Peter 2

Michael MiloroEditorG. E. Ghali �Peter E. Larsen �Peter D.
WaiteAssociate
Editors2004BC Decker Inc Hamilton�LondonPETERSON'SPRINCIPLESOFORAL AND
MAXILLOFACIALSURGERSecond EditionY
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To Beth and Macy,my two reasons for being,for your love and support.To Pete,my
teacher,for making me a better surgeon and person.Michael MiloroTo my wife,Hope,for
being my best friend and the love ofmy life.To my parents,Elias and Linda,and my
brother Fred,for their support,inspiration,devotion,and love.G.E.GhaliTo my
wife,Patty,and my sons,Michael,Matthew,and Mark.You are the most important people
inmy life,yet always understand and are patient with my absence.To my father who
inspired me toenter medicine.Lastly,to my former and current residents who teach me
every day.Peter LarsenTo my wife,Sallie,and my children,Allison,Eric,and Jon.To my
father who inspired my interest inoral and maxillofacial surgery and to my
residents who have continued to teach me.Peter WaiteDEDICATIONS
vCONTENTSPreface. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . ixEncomium. . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
xContributors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . xiiiVOLUME
1PART1:PRINCIPLESOFMEDICINE,SURGERY,ANDANESTHESIASection Editor:Peter
E.Larsen,DDS1.Wound HealingVivek Shetty,DDS,Dr.Med.Dent.; Charles N.Bertolami,DDS;
D.Med.Sc.. . . . . . . . . . . . . . . . . . . . . 32.Medical Management ofthe
Surgical PatientJames R.Hupp,DMD,MD,JD,MBA; David
N.Duddleston,MD. . . . . . . . . . . . . . . . . . . . . . . . . . . . .
173.Perioperative ConsiderationsNoah
A.Sandler,DMD,MD. . . . . . . . . . . . . . . . . . . . . . . . . . . .
474.Preoperative Patient AssessmentJoel M.Weaver,DDS,PhD. . . . . . . . . . . . . .
. . . . . . . . . . . . . . . 655.Pharmacology ofOutpatient Anesthesia
MedicationsM.Cynthia Fukami,DMD,MS; Steven I.Ganzberg,DMD,MS. . . . . . . . . . . .
. . . . . . . . . . . . . . 836.Pediatric SedationJeffrey D.Bennett,DMD; Jeffrey
B.Dembo,DDS,MS; Kevin J.Butterfield,DDS,MD. . . . . . . . . . . . . . . . . . . . .
. . . . 103PART2:DENTOALVEOLARSURGERYSection Editor:Peter
D.Waite,MPH,DDS,MD7.Management ofImpacted Teeth Other than Third MolarsDeborah
L.Zeitler,DDS,MS. . . . . . . . . . . . . . . . . . . . . . . . . . 1318.Impacted
TeethGregory M.Ness,DDS; Larry J.Peterson,DDS,MS�. . . . . . . . . . . . .
1399.Preprosthetic and Reconstructive Surgery Daniel B.Spagnoli,DDS,PhD; Steven
G.Gollehon,DDS,MD; Dale J.Misiek,DMD. . . . . . . . 15710.OsseointegrationMichael
S.Block,DMD; Ronald M.Achong,DMD,MD. . . . . 18911.Soft Tissue Management in
Implant TherapyAnthony G.Sclar,DMD. . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . 20512.Bone Grafting Strategies for Vertical Alveolar AugmentationOle
T.Jensen,DDS,MS; Michael A.Pikos,DDS; Massimo Simion,DDS; Tomaso
Vercellotti,MD,DDS. . . . . . . 22313.The Zygoma ImplantSterling R.Schow,DMD;
Stephen M.Parel,DDS. . . . . . . . . . . 23514.Implant ProsthodonticsThomas
J.Salinas,DDS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
251PART3:MAXILLOFACIALINFECTIONSSection Editor:Peter E.Larsen,DDS15.Principles
ofManagement ofOdontogenic InfectionsThomas
R.Flynn,DMD. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27716.Sinus
InfectionsRakesh K.Chandra,MD; David W.Kennedy,MD. . . . . . . . . .
29517.Osteomyelitis and OsteoradionecrosisGeorge M.Kushner,DMD,MD; Brian
Alpert,DDS. . . . . . . . . 313PART4:MAXILLOFACIALTRAUMASection Editor:Peter
E.Larsen,DDS18.Initial Management ofthe Trauma PatientMichael P.Powers,DDS,MS;
Michael S.Scherer,DDS,MD. . . . 32719.Soft Tissue InjuriesAlan S.Herford,DDS,MD;
G.E.Ghali,DDS,MD. . . . . . . . . 35720.Rigid versus Nonrigid FixationEdward Ellis
III,DDS,MS. . . . . . . . . . . . . . . . . . . . . . . . . . . . 37121.Management
ofAlveolar and Dental FracturesRichard D.Leathers,DDS; Reginald E.Gowans,DDS. . . .
. . . 38322.Principles ofManagement ofMandibular FracturesGuillermo E.Chacon,DDS;
Peter E.Larsen,DDS. . . . . . . . . . 40123.1 Management ofMaxillary FracturesLarry
L.Cunningham Jr,DDS,MD; Richard H.Haug,DDS. . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . 43523.2 Management ofZygomatic Complex FracturesJonathan
S.Bailey,DMD,MD; Michael S.Goldwasser,DDS,MD. . . . . . . . . . . . . . . . . . . .
. . . 44524.Orbital and Ocular TraumaMark
W.Ochs,DMD,MD. . . . . . . . . . . . . . . . . . . . . . . . . . . .
46325.Management ofFrontal Sinus and Naso-orbitoethmoid Complex FracturesLarry
L.Cunningham Jr,DDS,MD; Richard H.Haug,DDS. . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . 49126.Gunshot InjuriesJon
D.Holmes,DMD,MD. . . . . . . . . . . . . . . . . . . . . . . . . . . . 509�Deceased
viContents27.Pediatric Craniomaxillofacial Fracture ManagementJeffrey
C.Posnick,DMD,MD; Bernard J.Costello,DMD,MD;Paul
S.Tiwana,DDS,MD,MS. . . . . . . . . . . . . . . . . . . . . . . . .
52728.Management ofPanfacial FracturesPatrick J.Louis,DDS,MD. . . . . . . . . . . .
. . . . . . . . . . . . . . . . 547PART5:MAXILLOFACIALPATHOLOGYSection
Editor:G.E.Ghali,DDS,MD29.Differential Diagnosis ofOral DiseaseJohn
R.Kalmar,DMD,PhD; Carl M.Allen,DDS,MSD. . . . . 56330.Odontogenic Cysts and
TumorsEric R.Carlson,DMD,MD. . . . . . . . . . . . . . . . . . . . . . . . . . . .
57531.Benign Nonodontogenic Lesions ofthe JawsM.Anthony
Pogrel,DDS,MD. . . . . . . . . . . . . . . . . . . . . . . . . . 59732.Oral
Cancer:Classification,Staging,and DiagnosisG.E.Ghali,DDS,MD; M.Scott Connor,DDS,MD.
. . . . . . . . 61733.Oral Cancer TreatmentJon D.Holmes,DMD,MD; Eric
J.Dierks,DMD,MD. . . . . . . 63134.Lip CancerJames W.Sikes Jr,DMD,MD;
G.E.Ghali,DDS,MD. . . . . . . 65935.Salivary Gland Disease and TumorsRobert
A.Ord,MD,DDS,MS; Alex E.Pazoki,MD,DDS. . . . . . 67136.Management ofMucosal and
Related Dermatologic DisordersMichael W.Finkelstein,DDS,MS; Steven
D.Vincent,DDS,MS. . . . . . . . . . . . . . . . . . . . . . . . . . . 67937.Head
and Neck Skin CancerMichael F.Zide,DMD; Yan Trokel,MD,DDS. . . . . . . . . . . . .
697Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . 723VOLUME 2PART6:MAXILLOFACIALRECONSTRUCTIONSection
Editor:G.E.Ghali,DDS,MD38.Local and Regional FlapsAlan S.Herford,DDS,MD;
G.E.Ghali,DDS,MD. . . . . . . . . 76939.Bony Reconstruction ofthe JawsRandall
M.Wilk,DDS,PhD,MD. . . . . . . . . . . . . . . . . . . . . . . 78340.Microvascular
Free Tissue TransferJoseph I.Helman,DMD; Remy H.Blanchaert Jr,MD,DDS. . . . . . . .
. . . . . . . . . . . . . . . 80341.MicroneurosurgeryMichael Miloro,DMD,MD. . . . .
. . . . . . . . . . . . . . . . . . . . . . 81942.Cleft Lip and
Palate:Comprehensive Treatment Planning and Primary RepairBernard
J.Costello,DMD,MD; Ramon L.Ruiz,DMD,MD. . . . . . . . . . . . . . . . . . . . . . .
. . . . . 83943.Reconstruction ofthe Alveolar CleftPeter
E.Larsen,DDS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
85944.Reconstruction ofCleft Lip and Palate:Secondary ProceduresRamon
L.Ruiz,DMD,MD; Bernard J.Costello,DMD,MD. . . . . . . . . . . . . . . . . . . . . .
. . . 87145.Nonsyndromic CraniosynostosisG.E.Ghali,DDS,MD; Douglas
P.Sinn,DDS. . . . . . . . . . . . . 88746.Craniofacial Dysostosis Syndromes:Staging
ofReconstructionJeffrey C.Posnick,DMD,MD; Ramon L.Ruiz,DMD,MD; Paul
S.Tiwana,DDS,MD,MS. . . . . . . . . . . . . . . . . . . . . . . . .
901PART7:TEMPOROMANDIBULARJOINTDISEASESection Editor:G.E.Ghali,DDS,MD47.Anatomy and
Pathophysiology ofthe Temporomandibular JointMark C.Fletcher,DMD,MD; Joseph
F.Piecuch,DMD,MD; Stuart
E.Lieblich,DMD. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
93348.Nonsurgical Management ofTemporomandibular DisordersVasiliki Karlis,DMD,MD;
Robert Glickman,DMD. . . . . . . . . 94949.Temporomandibular Joint Arthrocentesis
and Arthroscopy:Rationale and TechniqueJeffrey J.Moses,DDS. . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . . 96350.Surgery for Internal Derangements
ofthe Temporomandibular JointLeslie
B.Heffez,DMD,MS. . . . . . . . . . . . . . . . . . . . . . . . . . . .
98951.Management ofthe Patient with End-Stage Temporomandibular Joint
DiseaseStephen B.Milam,DDS,PhD. . . . . . . . . . . . . . . . . . . . . . . . .
101552.Hypomobility and Hypermobility Disorders ofthe Temporomandibular
JointMeredith August,DMD,MD; Maria J.Troulis,DDS,MSc; Leonard B.Kaban,DMD,MD. . . .
. . . . . . . . . . . . . . . . . . . . 1033PART8:ORTHOGNATHICSURGERYSection
Editor:Peter D.Waite,MPH,DDS,MD53.Craniofacial Growth and Development:Current
Understanding and Clinical ConsiderationsPeter
M.Spalding,DDS,MS,MS. . . . . . . . . . . . . . . . . . . . . . 1051
Contentsvii54.Database Acquisition and Treatment PlanningMarc B.Ackerman,DMD; David
M.Sarver,DMD,MS. . . . . 108755.Orthodontics for Orthognathic SurgeryLarry
M.Wolford,DMD; Eber L.L.Stevao,DDS,PhD; C.Moody Alexander,DDS,MS; Joao Roberto
Goncalves,DDS,PhD. . . . . . . . . . . . . . . . . . . . . 111156.Principles
ofMandibular Orthognathic SurgeryDale S.Bloomquist,DDS,MS; Jessica J.Lee,DDS. . . .
. . . . . 113557.Maxillary Orthognathic SurgeryVincent J.Perciaccante,DDS; Robert
A.Bays,DDS. . . . . . . . 117958.Management ofFacial AsymmetryPeter
D.Waite,MPH,DDS,MD; Scott D.Urban,DMD,MD. . . . . . . . . . . . . . . . . . . . . .
. . . . . 120559.Soft Tissue Changes Associated with Orthognathic SurgeryNorman
J.Betts,DDS,MS; Sean
P.Edwards,DDS,MD. . . . . . . . . . . . . . . . . . . . . . . . . . .
122160.Prevention and Management ofComplications in Orthognathic SurgeryJoseph
E.Van Sickels,DDS. . . . . . . . . . . . . . . . . . . . . . . . . . .
124761.Orthognathic Surgery in the Patient with Cleft PalateTimothy A.Turvey,DDS;
Ramon L.Ruiz,DMD,MD; Katherine W.L.Vig,BDS,MS,D.Orth.; Bernard J.Costello,DMD,MD. .
. . . . . . . . . . . . . . . . . . . . . . 126762.Distraction OsteogenesisSuzanne
U.Stucki-McCormick,MS,DDS. . . . . . . . . . . . . . . . 127763.Surgical and
Nonsurgical Management ofObstructive Sleep ApneaB.D.Tiner,DDS,MD; Peter
D.Waite,MPH,DDS,MD. . . . 1297PART9:FACIALESTHETICSURGERYSection Editor:Peter
D.Waite,MPH,DDS,MD64.BlepharoplastyHeidi L.Jarecki,MD; Mark J.Lucarelli,MD,Bradley
N.Lemke,MD. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131765.Basic
Principles ofRhinoplastyJames Koehler,DDS,MD; Peter D.Waite,MPH,DDS,MD. . . .
134566.RhytidectomyG.E.Ghali,DDS,MD; T.William Evans,DDS,MD. . . . . . .
136567.Forehead and Brow ProceduresAngelo
Cuzalina,MD,DDS. . . . . . . . . . . . . . . . . . . . . . . . . .
138368.Liposculpting ProceduresMilan J.Jugan,DMD. . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . 140769.Skin Rejuvenation ProceduresGary D.Monheit,MD. . .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . 141970.Alloplastic Esthetic
Facial AugmentationBruce N.Epker,DDS,MSD,PhD. . . . . . . . . . . . . . . . . . . .
. . 143571.Otoplastic Surgery for the Protruding EarTodd G.Owsley,DDS,MD. . . . . .
. . . . . . . . . . . . . . . . . . . . .
1449Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . 1461
The Second Edition ofPeterson�s Principles ofOral and Maxillofacial
Surgery,reflects the efforts ofmany people made in a very short period oftime.The
timefrom the decision to undertake a second edition until publication release
totaledless than 2 years.This is a monumental accomplishment considering the
currentstate ofaffairs in the specialty oforal and maxillofacial surgery and the
difficul-ties in pursuing scholarly activity,even for the academic
practitioner.Although itis certainly not a simple task to assemble an author list
as extensive as the one inthis text,it was perhaps made easier because editors and
authors were inspired byfeelings oftribute to Larry Peterson to deliver on short
notice.When Larry Peterson decided to publish the first edition ofthis book over
adecade ago,he recognized the need in our specialty for a comprehensive andcomplete
reference textbook in oral and maxillofacial surgery that was practicaland
readable.Oral and maxillofacial surgery encompasses an ever-expandingrange
ofdiverse topics that makes it unique among the medical and dental
specialties.There was no concise textbook that dealt with the full scope
ofthespecialty that was available for residents and surgeons to use as a reference
forclinical practice.The textbook Contemporary Oral and Maxillofacial
Surgeryappropriately covers the requisite information for the dental student and
general dental practitioner,but Peterson�s Princi-ples ofOral and Maxillofacial
Surgeryprovides an organized and systematic approach to the specialty for residents
and clin-icians practicing full-scope oral and maxillofacial surgery.The first
edition ofthis text was the only reference ofits kind.Itis now continued with the
second edition,which is unique in many respects,among them the inclusion
ofcontributionsfrom more than 100 oral surgeons and other dental and medical
specialists,500 pieces oforiginal artwork,and a CD-ROM.The clear purpose ofthis
textbook is to provide a concise,authoritative,easy-to-read,currently
referenced,contempo-rary survey ofthe specialty oforal and maxillofacial surgery
that contains the information that a competent surgeon shouldpossess and
understand.Although some ofthe information may be outside ofthe scope ofthe
individual practitioner,thematerial contained in this text is definitely within the
scope ofthe specialty.This textbook should be considered a referencefor the oral
and maxillofacial surgeon during residency and into clinical practice.It will be an
excellent resource for exam-ination preparation purposes as well;in fact,the first
edition was adopted in some European countries as a required text-book for oral
surgery board certification.As with the first edition,the authors,primarily oral
and maxillofacial surgeons,were chosen because oftheir broad ex-perience and
expertise in each specific area ofthe specialty.The contributions from these
national and international authorscertainly reflect their knowledge and
specialization.Whenever appropriate,each chapter attempts to review etiology,diag-
nosis,patient assessment,treatment plan development,surgical and nonsurgical
treatment options,and recognition andmanagement ofcomplications.The information
contained in this textbook is based upon a thorough evaluation ofthe cur-rent
literature,as well as clinical expertise,and is free from commercial and personal
bias.Ifadditional information isrequired,references have been provided so that
other specialty textbooks may be consulted.Considering the rapid advance-ments and
developments in the fields ofmedicine and surgery,a nearly constant survey ofthe
current published literatureis required to maintain a working knowledge ofthe
standards ofdiagnosis and treatment.Future editions ofthis text willreflect these
changes in clinical practice.This text would not have been possible without the
help and support ofmany people,including Ghali,Pete,and Peter;the outstanding
authors who contributed their practice-defining knowledge;and the group at BC
Decker Inc,includingCatherine Travelle,Susan Cooper,and Paula Presutti,who sent a
seemingly endless number ofe-mails in an attempt toensure deadlines were
met.Certainly a debt ofgratitude is owed to Brian Decker for his
vision,dedication,and commit-ment to publish this textbook.Peterson�s Principles
ofOral and Maxillofacial Surgeryis theauthoritative textbook for the specialty
oforal and maxillo-facial surgery.PREFACEixMICHAELMILORO,DMD,MD
Dr.Larry J.(�Pete�) Peterson is easily the smartest person I have ever known,and I
do not mean with regard to medicineand surgery alone.Pete certainly forgot more
information in his life than most people ever know.He made everyone aroundhim want
to be better than they were,and he helped them to reach their potential.Peterson�s
Principles ofOral and Maxillo-facial Surgery,Second Edition,is dedicated to this
man.Unfortunately,the majority ofreaders will never have had theopportunity to meet
him and to experience his imposing presence.The fact that this book will continue
to educate manysurgeons for years to come would have pleased him very much since
his greatest passion in life was,perhaps,teaching.Pete obtained his doctor ofdental
surgery degree at the University ofMissouri,Kansas City,in 1968.He completed
histraining in oral and maxillofacial surgery at Georgetown University,where he
also received his masters ofscience degree.Pete served on the faculty at the
Medical College ofGeorgia and,subsequently,at the University ofConnecticut as the
direc-tor ofOral and Maxillofacial Surgery Residency Training.However,he is best
known for his academic accomplishments atOhio State University,where he served as
chairman ofOral and Maxillofacial Surgery,Pathology,and Anesthesiology from1982
through 1999.To experience the full range ofour specialty,Pete entered private
practice in 1999 and continued in thatarea until his death on August 7,2002.Pete�s
professional and personal accomplishments and his contributions to our specialty
are innumerable.In 1993 Peteassumed the role ofeditor-in-chiefofOral Surgery,Oral
Medicine,Oral Pathology,Oral Radiology and Endodontics,uponthe retirement
ofDr.Robert Shira.Pete demanded excellence in the manuscript submissions and
maintained high standardsfor this journal during his tenure.Pete also edited
Contemporary Oral and Maxillofacial Surgery,which,like its predecessorfrom his
mentor Dr.Gustav O.Kruger,defined dental undergraduate education in oral and
maxillofacial surgery nation-wide.Pete�s dedication to education was further
demonstrated in his role as chair ofthe American Association ofOral
andMaxillofacial Surgeons Committee on Residency Education and Training.He lectured
and published extensively bothnationally and internationally,with a particular
emphasis on the topics ofodontogenic infections and dental implantology,and his
contributions to the literature are many and varied.Pete was a loving husband and
father and enjoyed life to the fullest at each and every opportunity.To Pete,life
was ajourney.The answer to any problem was inconsequential;the long arduous path
from question to answer was the only pur-pose for the question in the first
place.Dr.Peter Larsen and I had the privilege ofworking closely with Pete and
experienc-ing his talents and benefiting from his wisdom and guidance at Ohio State
University for several years.We had the uniqueopportunity to observe Pete in and
out ofthe hospital�the phrase �work hard,play hard�epitomizes the Peterson philos-
ophy.Peter Larsen remembered Pete at his funeral;here is a portion ofthat
eulogy:xENCOMIUM
When I tried to decide what to say about this amazing man,I started by making a
list.What I discovered was a man ofwhat I like to call�wonderful
contradiction.�Pete was perhaps one ofthe most successful men I have known,yet he
would have listed his Eagle Scout Award as being more important thanmany ofthe
prestigious professional honors he received.He was our most vigorous critic and yet
our strongest advocate.He was the teacher ofteachers but also the perpetual
student.He wasnot an OSU alumnus but bled scarlet and gray.He demanded hard work
but taught me that it isn�t really work ifyou love what you do.He was a teacher
who,when honored,thanked his students for teaching him.Although surrounded by
personal success,he found the greatest satisfaction in the success ofothers.He was
our boss but was more comfortable as our partner in a raft on the New River.He
would argue with you,not to get you to agree,but to get you to disagree and
defend.He trained many to reach great financial success but placed the reward
gained by teaching higher than any financial reward.He had much ofwhich to boast
and be proud,but instead practiced humility.He was perhaps the smartest man I have
ever known but was always first to admit when you had a good idea,and was gracious
enough notto point out that he had thought ofit himself,perhaps even years prior.I
never heard him speak on a topic when I was not totally impressed with the insight
and knowledge he seemed to have,but he was oftenmore content listening to what
others had to say.He was more interested in finding the truth than about being
right himself.He was 15 years older than me but looked younger.He would often tell
residents,much to their dismay,I might add,that it is not the answer that is
important,but the question.Many ofhis accomplishments could easily be ranked on a
1-to-10 scale as a �10.�Yet,I can still hear him say,�There is no such thing as a
�10.��He had the same enthusiasm for a giant rope swing as he did for a new
operation.He knew more than many ofthe speakers at the lectures he attended,but he
always took notes.He built what is perhaps the best Oral and Maxillofacial Surgery
Department in the country,but,for me,his finest hour as our leader waswhen he
tenderly took care ofVicki,Arden Hegtvedt�s wife,when Arden died.He was a man most
deserving ofa long and wonderful life,yet we are here today because this wonderful
life has been tragically cut short.If,as said by William James,�the greatest use
oflife is to spend it for something that will outlast it,�then Pete spent his life
well.For,as I lookaround,I see scores ofus who owe so much ofwhat we are to this
one life well spent.Pete died too young,and he will be missed,but through this
textbook his teachings will continue.MICHAELMILORO,DMD,MDEncomiumxi
CONTRIBUTORSRonald M.Achong,DMD,MDDepartment ofOral and Maxillofacial
SurgeryLouisiana State University School ofDentistryNew Orleans,LouisianaMarc
B.Ackerman,DMDPrivate PracticeOrthodonticsBryn Mawr,PennsylvaniaC.Moody
Alexander,DDS,MSDepartment ofOrthodonticsBaylor College ofDentistry,Texas A&M
University SystemDallas,TexasCarl M.Allen,DDS,MSDSection ofOral and Maxillofacial
Surgery,Pathology,and Dental AnesthesiologyThe Ohio State University,College
ofDentistryColumbus,OhioBrian Alpert,DDS,FACDDepartment ofSurgical and Hospital
DentistryUniversity ofLouisville School ofDentistryLouisville,KentuckyMeredith
August,DMD,MDDepartment ofOral and Maxillofacial SurgeryHarvard
UniversityBoston,MassachusettsJonathan S.Bailey,DMD,MDDepartment
ofSurgeryUniversity ofIllinois College ofMedicine atUrbana-
ChampaignUrbana,IllinoisRobert A.Bays,DDSDepartment ofSurgeryEmory University
School ofMedicineAtlanta,GeorgiaJeffrey D.Bennett,DMDDepartment ofOral Surgery and
Hospital DentistryIndiana University School ofDentistryIndianapolis,IndianaCharles
N.Bertolami,DDS,D.Med.Sc.Department ofOral and Maxillofacial SurgeryUniversity
ofCaliforniaSan Francisco,CaliforniaNorman J.Betts,DDS,MSDepartment ofOral and
Maxillofacial SurgeryUniversity ofMichigan School ofDentistryAnn Arbor,MichiganRemy
H.Blanchaert Jr,MD,DDSDepartment ofOral and Maxillofacial SurgeryKansas City
Schools ofDentistry and MedicineUniversity ofMissouriKansas City,MissouriMichael
S.Block,DMDDepartment ofOral and Maxillofacial SurgeryLouisiana State University
School ofDentistryNew Orleans,LouisianaDale S.Bloomquist,DDS,MSDepartment ofOral
and Maxillofacial SurgeryUniversity ofWashington School
ofDentistrySeattle,WashingtonKevin J.Butterfield,DDS,MDDepartment ofOral and
Maxillofacial SurgeryUniversity ofConnecticut Farmington,ConnecticutEric
R.Carlson,DMD,MDDepartment ofOral and Maxillofacial SurgeryUniversity ofTennessee
Graduate School ofMedicineKnoxville,TennesseeGuillermo E.Chacon,DDSDepartment
ofOral and Maxillofacial SurgeryThe Ohio State University Medical
CenterColumbus,OhioRakesh K.Chandra,MDDepartment ofOtolaryngology-Head and Neck
SurgeryUniversity ofTennessee Health Science CenterMemphis,TennesseeM.Scott
Connor,DDS,MDDepartment ofOral and Maxillofacial SurgeryLouisiana State University
Health SciencesCenterShreveport,LouisianaBernard J.Costello,DMD,MDDepartment ofOral
and Maxillofacial SurgeryUniversity ofPittsburghPittsburgh,PennsylvaniaLarry
L.Cunningham Jr,DDS,MDDepartment ofOral Health ScienceUniversity ofKentucky,College
ofDentistryLexington,KentuckyAngelo Cuzalina,MD,DDSDepartment ofOral and
Maxillofacial SurgeryUniversity ofOklahoma Health Science CenterOklahoma
City,OklahomaJeffrey B.Dembo,DDS,MSDepartment ofOral Health ScienceUniversity
ofKentucky College ofDentistryLexington,KentuckyEric J.Dierks,DMD,MDDepartment
ofOral and Maxillofacial SurgeryOregon Health Sciences
UniversityPortland,OregonDavid N.Duddleston,MDDepartment ofMedicineUniversity
ofMississippi Medical CenterJackson,MississippiSean P.Edwards,DDS,MDDepartment
ofOral and Maxillofacial SurgeryUniversity ofMichigan School ofDentistryAnn
Arbor,MichiganEdward Ellis III,DDS,MSDepartment ofSurgeryUniversity ofTexas
Southwestern Medical CenterDallas,TexasBruce N.Epker,DDS,MSD,PhDAesthetic Facial
Surgery CenterWeatherford,TexasT.William Evans,DDS,MD,FACSDepartment ofOral and
Maxillofacial SurgeryThe Ohio State UniversityColumbus,Ohio;Department ofOral and
Maxillofacial SurgeryUniversity ofMichiganAnn Arbor,MichiganMichael
W.Finkelstein,DDS,MSDepartment ofOral Pathology,Radiology,andMedicineUniversity
ofIowa,College ofDentistryIowa City,Iowaxiii
xivContributorsMark C.Fletcher,DMD,MDDepartment ofOral and Maxillofacial
SurgeryUniversity ofConnecticut School ofDentalMedicineFarmington,ConnecticutThomas
R.Flynn,DMDDepartment ofOral and Maxillofacial SurgeryHarvard School ofDental
MedicineBoston,MassachusettsM.Cynthia Fukami,DMD,MSSection ofPediatric DentistryThe
Ohio State University,College ofDentistryColumbus,OhioSteven
I.Ganzberg,DMD,MSSection ofOral and Maxillofacial Surgery,Pathology,and
AnesthesiologyThe Ohio State University,College
ofDentistryColumbus,OhioG.E.Ghali,DDS,MD,FACSDepartment ofOral and Maxillofacial
SurgeryLouisiana State University Health Sciences CenterShreveport,LouisianaRobert
Glickman,DMDDepartment ofOral and Maxillofacial SurgeryNew York University College
ofDentistryNew York,New YorkMichael S.Goldwasser,DDS,MDDepartment
ofSurgeryUniversity ofIllinois College ofMedicine atUrbana-
ChampaignUrbana,IllinoisSteven G.Gollehon,DDS,MDDepartment ofOral and Maxillofacial
SurgeryLouisiana State University Health Sciences CenterNew Orleans,LouisianaJoao
Roberto Goncalves,DDS,PhDDepartmento de Cl�nica InfantilFaculdade de Odontologia de
Araraquara-UNESPAraraquara,Sao PaoloBrazilReginald E.Gowans,DDSDepartment ofOral
and Maxillofacial SurgeryCharles R.Drew University ofMedicineand ScienceLos
Angeles,CaliforniaRichard H.Haug,DDSDivision ofOral and Maxillofacial
SurgeryUniversity ofKentucky College ofDentistryLexington,KentuckyLeslie
B.Heffez,DMD,MS,FRCDDepartment ofOral and Maxillofacial SurgeryUniversity
ofIllinois,College ofDentistryChicago,IllinoisJoseph I.Helman,DMDDepartment ofOral
and Maxillofacial SurgeryUniversity ofMichiganAnn Arbor,MichiganAlan
S.Herford,DDS,MDDepartment ofOral and Maxillofacial SurgeryLoma Linda University
School ofDentistryLoma Linda,CaliforniaJon D.Holmes,DMD,MD,FACSDepartment ofOral
and Maxillofacial SurgeryUniversity ofAlabamaBirmingham,AlabamaJames
R.Hupp,DMD,MD,JD,MBA,FACS,FACDDepartments ofOral and Maxillofacial
Surgery,Otolaryngology,and SurgeryUniversity ofMississippi Medical Center
SchoolofDentistryJackson,MississippiHeidi L.Jarecki,MDDepartment ofOphthalmology
and Visual SciencesUniversity ofWisconsin School ofMedicineMadison,WisconsinOle
T.Jensen,DDS,MSUniversity ofColorado School ofDentistryDenver,Colorado Milan
J.Jugan,DMDDental DepartmentNaval Medical CenterSan Diego,CaliforniaLeonard
B.Kaban,DMD,MDDepartment ofOral and Maxillofacial SurgeryHarvard
UniversityBoston,MassachusettsJohn R.Kalmar,DMD,PhDSection ofOral Surgery,Oral
Pathology,andDental AnesthesiaThe Ohio State University,College
ofDentistryColumbus,OhioVasiliki Karlis,DMD,MDDepartment ofOral and Maxillofacial
SurgeryNew York University College ofDentistryNew York,New YorkDavid
W.Kennedy,MD,FACS,FRCSIUniversity ofPennsylvania School
ofMedicinePhiladelphia,PennsylvaniaJames Koehler,DDS,MDDepartment ofOral and
Maxillofacial SurgeryUniversity ofAlabamaBirmingham,AlabamaGeorge
M.Kushner,DMD,MDDepartment ofSurgical and Hospital DentistryUniversity
ofLouisvilleLouisville,KentuckyPeter E.Larsen,DDSDepartment ofOral and
Maxillofacial SurgeryThe Ohio State University,College
ofDentistryColumbus,OhioRichard D.Leathers,DDSDepartment ofOral and Maxillofacial
SurgeryCharles R.Drew University ofMedicine andScienceLos Angeles,CaliforniaJessica
J.Lee,DDSDepartment ofOral and Maxillofacial SurgeryUniversity ofWashington School
ofDentistrySeattle,WashingtonBradley N.Lemke,MDDepartment ofOphthalmology and
Visual SciencesUniversity ofWisconsin School ofMedicineMadison,WisconsinStuart
E.Lieblich,DMDDepartment ofOral and Maxillofacial SurgeryUniversity ofConnecticut
School ofDentalMedicineFarmington,ConnecticutPatrick J.Louis,DDS,MDDepartment
ofOral and Maxillofacial SurgeryUniversity ofAlabamaBirmingham,AlabamaMark
J.Lucarelli,MDDepartment ofOphthalmology and Visual SciencesUniversity ofWisconsin
School ofMedicineMadison,Wisconsin
ContributorsxvStephen B.Milam,DDS,PhD,FACDDepartment ofOral and Maxillofacial
SurgeryUniversity ofTexas Health Science CenterSan Antonio,TexasMichael
Miloro,DMD,MDDepartment ofOral and Maxillofacial SurgeryThe Nebraska Medical
CenterOmaha,NebraskaDale J.Misiek,DMDDepartment ofOral and Maxillofacial
SurgeryLouisiana State University Health Sciences CenterNew Orleans,LouisianaGary
D.Monheit,MDDepartments ofDermatology and OphthalmologyUniversity
ofAlabamaBirmingham,AlabamaJeffrey J.Moses,DDS,FACD,FICD,FAACSDepartment
ofDentistryUniversity ofCaliforniaLos Angeles,CaliforniaGregory
M.Ness,DDSDepartment ofOral and Maxillofacial SurgeryThe Ohio State
University,College ofDentistryColumbus,OhioMark W.Ochs,DMD,MDDepartment ofOral and
Maxillofacial SurgeryUniversity ofPittsburgh School ofDental
MedicinePittsburgh,PennsylvaniaRobert.A.Ord,MD,DDS,MS,FRCS,FACSDepartment ofOral
and Maxillofacial SurgeryUniversity ofMarylandBaltimore,MarylandTodd
G.Owsley,DDS,MDCarolina Surgical Arts,PAGreensboro,North CarolinaStephen
M.Parel,DDS,FACD,FICDDepartment ofOral and Maxillofacial SurgeryBaylor College
ofDentistry,Texas A&M University SystemDallas,TexasAlex E.Pazoki,MD,DDSDepartment
ofOral and Maxillofacial SurgeryUniversity ofMarylandBaltimore,MarylandVincent
J.Perciaccante,DDSDepartment ofSurgeryEmory University School
ofMedicineAtlanta,GeorgiaLarry J.Peterson,DDS,MS�Department ofOral and
Maxillofacial SurgeryThe Ohio State University,College ofDentistry
Columbus,OhioJoseph F.Piecuch,DMD,MDDepartment ofOral and Maxillofacial
SurgeryUniversity ofConnecticut School
ofDentalMedicineFarmington,ConnecticutMichael A.Pikos,DDSDepartment ofOral and
Maxillofacial SurgeryUniversity ofMiami School ofMedicineMiami,FloridaM.Anthony
Pogrel,DDS,MD,FRCS,FACSDepartment ofOral and Maxillofacial SurgeryUniversity
ofCaliforniaSan Francisco,CaliforniaJeffrey
C.Posnick,DMD,MD,FRCS(C),FACSDepartments ofSurgery and PediatricsGeorgetown
University Medical CenterWashington,District ofColumbiaMichael
P.Powers,DDS,MSDepartment ofOral and Maxillofacial SurgeryCase Western Reserve
University School ofDental MedicineCleveland,OhioRamon L.Ruiz,DMD,MDDepartments
ofOral and Maxillofacial Surgeryand PediatricsUniversity ofNorth CarolinaChapel
Hill,North CarolinaThomas J.Salinas,DDSDepartment ofOtolaryngologyUniversity
ofNebraska Medical CenterOmaha,NebraskaNoah A.Sandler,DMD,MDDepartment ofDiagnostic
and Surgical SciencesUniversity ofMinnesotaMinneapolis,MinnesotaDavid
M.Sarver,DMD,MSDepartment ofOrthodonticsUniversity ofNorth CarolinaChapel
Hill,North CarolinaMichael S.Scherer,DDS,MDDepartment ofOral and Maxillofacial
SurgeryCase Western Reserve University School ofDental
MedicineCleveland,OhioSterling R.Schow,DMDDepartment ofOral and Maxillofacial
SurgeryBaylor College ofDentistry,Texas A&M University SystemDallas,TexasAnthony
G.Sclar,DMDDepartment ofSurgeryUniversity ofMiami School
ofMedicineMiami,FloridaVivek Shetty,DDS,Dr.Med.Dent.Department ofOral and
Maxillofacial SurgeryUniversity ofCaliforniaLos Angeles,CaliforniaJames W.Sikes
Jr,DMD,MDDepartment ofOral and Maxillofacial SurgeryLouisiana State University
Health Sciences CenterShreveport,LouisianaMassimo Simion,DDSDepartment
ofPeriodontologyUniversity ofMilanMilan,ItalyDouglas P.Sinn,DDSDepartment
ofSurgeryUniversity ofTexas Southwestern Medical CenterDallas,TexasDaniel
B.Spagnoli,DDS,PhDDepartment ofOral and Maxillofacial SurgeryLouisiana State
University Health Sciences CenterNew Orleans,LouisianaPeter
M.Spalding,DDS,MS,MSDepartment ofGrowth and DevelopmentUniversity ofNebraska
Medical Center CollegeofDentistryLincoln,NebraskaEber L.L.Stevao,DDS,PhDDepartment
ofOral and Maxillofacial SurgeryBaylor College ofDentistry,Texas A&M Univer-sity
SystemDallas,Texas�Deceased
xviContributorsSuzanne U.Stucki-McCormick,MS,DDSPacific Center for Jaw and Facial
SurgeryEncinitas,CaliforniaB.D.Tiner,DDS,MDDepartment ofOral and Maxillofacial
SurgeryUniversity ofTexas Health Science CenterSan Antonio,TexasPaul
S.Tiwana,DDS,MD,MSDepartment ofOral and Maxillofacial SurgeryUniversity ofNorth
CarolinaChapel Hill,North CarolinaYan Trokel,MD,DDSDepartment ofOral and
Maxillofacial SurgeryUniversity ofTexas Southwestern Medical
CenterDallas,TexasMaria J.Troulis,DDS,MScDepartment ofOral and Maxillofacial
SurgeryHarvard UniversityBoston,MassachusettsTimothy A.Turvey,DDSDepartment ofOral
and Maxillofacial SurgeryUniversity ofNorth CarolinaChapel Hill,North CarolinaScott
D.Urban,DMD,MDDepartment ofOral and Maxillofacial SurgeryUniversity
ofAlabamaBirmingham,AlabamaJoseph E.Van Sickels,DDSDepartment ofOral Health
ScienceUniversity ofKentuckyLexington,KentuckyTomaso Vercellotti,MD,DDSDepartment
ofEar,Nose,and ThroatUniversity ofStudies ofGenova (Italy)Genova,ItalyKatherine
W.L.Vig,BDS,MS,D.Orth,FDS(RCS)Department ofOrthodonticsThe Ohio State
University,College ofDentistryColumbus,OhioSteven D.Vincent,DDS,MSDepartment ofOral
Pathology,Radiology,andMedicineUniversity ofIowa,College ofDentistryIowa
City,IowaPeter D.Waite,MPH,DDS,MD,FACDDepartment ofOral and Maxillofacial
SurgeryUniversity ofAlabama School ofDentistryBirmingham,AlabamaJoel
M.Weaver,DDS,PhD,FACD,FICDDepartment ofAnesthesiologyCollege ofMedicine and Public
Health The Ohio State UniversityColumbus,OhioRandall M.Wilk,DDS,PhD,MDDepartment
ofOral and Maxillofacial SurgeryLouisiana State University Health Sciences
CenterNew Orleans,LouisianaLarry M.Wolford,DMDDepartment ofOral and Maxillofacial
SurgeryBaylor College ofDentistry,Texas A&M University SystemDallas,TexasDeborah
L.Zeitler,DDS,MSDepartment ofOral and Maxillofacial SurgeryUniversity ofIowa
College ofDentistryIowa City,IowaMichael F.Zide,DMDDepartment ofOral and
Maxillofacial SurgeryUniversity ofTexas Southwestern MedicalSchoolDallas,Texas
Part 1PRINCIPLESOFMEDICINE,SURGERY,ANDANESTHESIA
CHAPTER 1Wound HealingVivek Shetty,DDS,Dr.Med.Dent.Charles
N.Bertolami,DDS,D.Med.Sc.The healing wound is an overt expressionofan intricate and
tightly choreographedsequence ofcellular and biochemicalresponses directed toward
restoring tissueintegrity and functional capacity followinginjury.Although healing
culminatesuneventfully in most instances,a variety ofintrinsic and extrinsic
factors can impedeor facilitate the process.Understandingwound healing at multiple
levels�bio-chemical,physiologic,cellular,and molec-ular�provides the surgeon with a
frame-work for basing clinical decisions aimed atoptimizing the healing
response.Equallyimportant it allows the surgeon to critical-ly appraise and
selectively use the growingarray ofbiologic approaches that seek toassist healing
by favorably modulating thewound microenvironment.The Healing ProcessThe
restoration oftissue integrity,whetherinitiated by trauma or surgery,is a phylo-
genetically primitive but essential defenseresponse.Injured organisms survive
onlyifthey can repair themselves quickly andeffectively.The healing response
dependsprimarily on the type oftissue involvedand the nature ofthe tissue
disruption.When restitution occurs by means oftis-sue that is structurally and
functionallyindistinguishable from native tissue,regenerationhas taken
place.However,iftissue integrity is reestablished primarilythrough the formation
offibrotic scar tis-sue,then repairhas occurred.Repair byscarring is the body�s
version ofa spotweld and the replacement tissue is coarseand has a lower cellular
content thannative tissue.With the exception ofboneand liver,tissue disruption
invariablyresults in repair rather than regeneration.At the cellular level the rate
and quali-ty oftissue healing depends on whetherthe constitutive cells are
labile,stable,orpermanent.Labile cells,including the ker-atinocytes ofthe epidermis
and epithelialcells ofthe oral mucosa,divide throughouttheir life span.Stable cells
such as fi-broblasts exhibit a low rate ofduplicationbut can undergo rapid
proliferation inresponse to injury.For example,boneinjury causes pluripotential
mesenchymalcells to speedily differentiate intoosteoblasts and osteoclasts.On the
otherhand permanent cells such as specializednerve and cardiac muscle cells do
notdivide in postnatal life.The surgeon�sexpectation of�normal healing�should
becorrespondingly realistic and based on theinherent capabilities ofthe injured
tissue.Whereas a fibrous scar is normal for skinwounds,it is suboptimal in the
context ofbone healing.At a more macro level the quality ofthe healing response is
influenced by thenature ofthe tissue disruption and the cir-cumstances surrounding
wound closure.Healing by first intention occurs when aclean laceration or surgical
incision isclosed primarily with sutures or othermeans and healing proceeds rapidly
withno dehiscence and minimal scar forma-tion.Ifconditions are less favorable,wound
healing is more complicated andoccurs through a protracted filling ofthetissue
defect with granulation and connec-tive tissue.This process is called healing
bysecond intention and is commonly associ-ated with avulsive injury,local
infection,or inadequate closure ofthe wound.Formore complex wounds,the surgeon
mayattempt healing by third intentionthrough a staged procedure that
combinessecondary healing with delayed primaryclosure.The avulsive or
contaminatedwound is d�brided and allowed to granu-late and heal by second
intention for 5 to 7 days.Once adequate granulation tissuehas formed and the risk
ofinfectionappears minimal,the wound is suturedclose to heal by first
intention.Wound Healing ResponseInjury ofany kind sets into motion a com-plex
series ofclosely orchestrated and tem-porally overlapping processes directedtoward
restoring the integrity oftheinvolved tissue.The reparative processesare most
commonly modeled in skin1;however,similar patterns ofbiochemicaland cellular events
occur in virtually everyother tissue.2To facilitate description,thehealing
continuum ofcoagulation,inflam-mation,reepithelialization,granulation
4Part 1: Principles ofMedicine,Surgery,and Anesthesiatissue,and matrix and tissue
remodeling istypically broken down into three distinctoverlapping
phases:inflammatory,prolif-erative,and remodeling.3,4Inflammatory Phase The
inflammatory phase presages thebody�s reparative response and usuallylasts for 3 to
5 days.Vasoconstriction ofthe injured vasculature is the spontaneoustissue reaction
to staunch bleeding.Tissuetrauma and local bleeding activate factorXII (Hageman
factor),which initiates thevarious effectors ofthe healing cascadeincluding the
complement,plasminogen,kinin,and clotting systems.Circulatingplatelets
(thrombocytes) rapidly aggregateat the injury site and adhere to each otherand the
exposed vascular subendothelialcollagen to form a primary platelet plugorganized
within a fibrin matrix.The clotsecures hemostasis and provides a provi-sional
matrix through which cells canmigrate during the repair process.Addi-tionally the
clot serves as a reservoir ofthecytokines and growth factors that arereleased as
activated platelets degranulate(Figure 1-1).The bolus ofsecreted pro-
teins,including interleukins,transforminggrowth factor �(TGF-�),platelet-
derivedgrowth factor (PDGF),and vascularendothelial growth factor (VEGF),main-tain
the wound milieu and regulate subse-quent healing.1Once hemostasis is secured the
reac-tive vasoconstriction is replaced by a morepersistent period ofvasodilation
that ismediated by histamine,prostaglandins,kinins,and leukotrienes.Increasing
vascu-lar permeability allows blood plasma andother cellular mediators ofhealing to
passthrough the vessel walls by diapedesis andpopulate the extravascular
space.Corre-sponding clinical manifestations includeswelling,redness,heat,and
pain.Cytokines released into the wound pro-vide the chemotactic cues that
sequential-ly recruit the neutrophils and monocytesto the site ofinjury.Neutrophils
normallybegin arriving at the wound site withinminutes ofinjury and rapidly
establishthemselves as the predominant cells.Migrating through the scaffolding
provid-ed by the fibrin-enriched clot,the short-lived leukocytes flood the site
with pro-teases and cytokines to help cleanse thewound ofcontaminating
bacteria,devital-ized tissue,and degraded matrix compo-nents.Neutrophil activity is
accentuatedby opsonic antibodies leaking into thewound from the altered
vasculature.Unless a wound is grossly infected,neu-trophil infiltration ceases
after a few days.However,the proinflammatory cytokinesreleased by perishing
neutrophils,includ-ing tumor necrosis factor a(TNF-a) andinterleukins (IL-1a,IL-
1b),continue tostimulate the inflammatory response forextended periods.5Deployment
ofbloodborne mono-cytes to the site ofinjury starts peaking asthe levels
ofneutrophils decline.Activatedmonocytes,now termed macrophages,continue with the
wound microd�bride-ment initiated by the neutrophils.Theysecrete collagenases and
elastases to breakdown injured tissue and phagocytose bac-teria and cell
debris.Beyond their scaveng-ing role the macrophages also serve as theprimary
source ofhealing mediators.Once activated,macrophages release a bat-tery ofgrowth
factors and cytokines(TGF-a,TGF-�1,PDGF,insulin-likegrowth factor [IGF]-I and
-II,TNF-a,andIL-1) at the wound site,further amplifyingand perpetuating the action
ofthe chemi-cal and cellular mediators released previ-ously by degranulating
platelets and neu-trophils.6Macrophages influence allphases ofearly wound healing
by regulat-ing local tissue remodeling by proteolyticenzymes (eg,matrix
metalloproteases andcollagenases),inducing formation ofnewextracellular matrix,and
modulatingangiogenesis and fibroplasia through localproduction ofcytokines such as
throm-bospondin-1 and IL-1b.The centrality ofFibrin clotGrowthfactorsPlatelet
plugBlood vesselBlood
vesselEpidermisEpidermisDermisDermisFibroblastFibroblastFatFGF-2MMPPDGFPDGFTGF-
3TGF- 2TGF- 1TGF- 1TGF- 1MacrophageFIGURE1-1Immediately following
wounding,platelets facilitate the formation ofa blood clot that secureshemostasis
and provides a temporary matrix for cell migration.Cytokines released by activated
macrophagesand fibroblasts initiate the formation ofgranulation tissue by degrading
extracellular matrix and promot-ing development ofnew blood vessels.Cellular
interactions are potentiated by reciprocal signaling betweenthe epidermis and
dermal fibroblasts through growth factors,MMPs,and members ofthe TGF-�family.FGF =
fibroblast growth factor; MMP = matrix metalloproteinase; PDGF = platelet-derived
growth factor;TGF-�= transforming growth factor beta.Adapted from Bissell MJ and
Radisky D.70
Wound Healing5macrophage function to early wound heal-ing is underscored by the
consistent find-ing that macrophage-depleted animalwounds demonstrate diminished
fibropla-sia and defective repair.Although thenumbers and activity ofthe
macrophagestaper offby the fifth post injury day,theycontinue to modulate the wound
healingprocess until repair is complete.Proliferative Phase The cytokines and
growth factors secretedduring the inflammatory phase stimulatethe succeeding
proliferative phase (Figure1-2).7Starting as early as the third day postinjury and
lasting up to 3 weeks,the pro-liferative phase is distinguished by the for-mation
ofpink granular tissue (granula-tion tissue) containing inflammatory
cells,fibroblasts,and budding vasculatureenclosed in a loose matrix.An
essentialfirst step is the establishment ofa localmicrocirculation to supply the
oxygen andnutrients necessary for the elevated meta-bolic needs ofregenerating
tissues.Thegeneration ofnew capillary blood vessels(angiogenesis) from the
interrupted vas-culature is driven by wound hypoxia aswell as with native growth
factors,particu-larly VEGF,fibroblast growth factor 2(FGF-2),and TNF-� (see Figure
1-2).Around the same time,matrix-generatingfibroblasts migrate into the wound
inresponse to the cytokines and growth fac-tors released by inflammatory cells
andwounded tissue.The fibroblasts start syn-thesizing new extracellular matrix
(ECM)and immature collagen (Type III).Thescaffold ofcollagen fibers serves to sup-
port the newly formed blood vessels sup-plying the wound.Stimulated fibroblastsalso
secrete a range ofgrowth factors,thereby producing a feedback loop andsustaining
the repair process.Collagendeposition rapidly increases the tensilestrength ofthe
wound and decreases thereliance on closure material to hold thewound edges
together.Once adequate col-lagen and ECM have been generated,matrix synthesis
dissipates,evidencing thehighly precise spatial and temporal regula-tion ofnormal
healing.At the surface ofthe dermal woundnew epithelium forms to seal offthedenuded
wound surface.Epidermal cellsoriginating from the wound marginsundergo a
proliferative burst and begin toresurface the wound above the basementmembrane.The
process ofreepithelializa-tion progresses more rapidly in oralmucosal wounds in
contrast to the skin.In a mucosal wound the epithelial cellsmigrate directly onto
the moist exposedsurface ofthe fibrin clot instead ofunderthe dry exudate (scab)
ofthe dermis.Once the epithelial edges meet,contactinhibition halts further lateral
prolifera-tion.Reepithelialization is facilitated byunderlying contractile
connective tissue,which shrinks in size to draw the woundmargins toward one
another.Wound con-traction is driven by a proportion ofthefibroblasts that
transform into myofi-broblasts and generate strong contractileforces.The extent
ofwound contractiondepends on the depth ofthe wound andits location.In some
instances the forcesofwound contracture are capable ofdeforming osseous
structures.Remodeling Phase The proliferative phase is progressivelyreplaced by an
extended period ofpro-gressive remodeling and strengthening ofthe immature scar
tissue.The remodel-ing/maturation phase can last for severalyears and involves a
finely choreographedbalance between matrix degradation andformation.As the
metabolic demands ofthe healing wound decrease,the rich net-work ofcapillaries
begins to regress.Under the general direction ofthecytokines and growth factors,the
collage-nous matrix is continually degraded,resynthesized,reorganized,and
stabilizedby molecular crosslinking into a scar.Thefibroblasts start to disappear
and the colla-gen Type III deposited during the granula-tion phase is gradually
replaced bystronger Type I collagen.Correspondinglythe tensile strength ofthe scar
tissue Fibrin clotBlood vesselBlood
vesselEpidermisEpidermisDermisDermisFibroblastFatu-PAt-PAMMPsFIGURE1-2The cytokine
cascade mediates the succedent proliferative phase.This phase is distin-guished by
the establishment oflocal microcirculation and formation ofextracellular matrix
andimmature collagen.Epidermal cells migrate laterally below the fibrin clot,and
granulation tissuebegins to organize below the epithelium.MMPs = matrix
metalloproteinases; t-PA = tissue plas-minogen activator; u-PA = urinary
plasminogen activator.Adapted from Bissell MJ and Radisky D.70
6Part 1: Principles ofMedicine,Surgery,and Anesthesiagradually increases and
eventuallyapproaches about 80% ofthe originalstrength.Homeostasis ofscar collagen
andECM is regulated to a large extent by ser-ine proteases and matrix metallopro-
teinases (MMPs) under the control oftheregulatory cytokines.Tissue inhibitors ofthe
MMPS afford a natural counterbal-ance to the MMPs and provide tight con-trol
ofproteolytic activity within the scar.Any disruption ofthis orderly balance
canlead to excess or inadequate matrix degra-dation and result in either an
exuberantscar or wound dehiscence.Specialized HealingNerve Injury to the nerves
innervating the orofa-cial region may range from simple contu-sion to complete
interruption ofthe nerve.The healing response depends on injuryseverity and extent
ofthe injury.8�10Neu-ropraxia represents the mildest form ofnerve injury and is a
transient interrup-tion ofnerve conduction without loss ofaxonal continuity.The
continuity oftheepineural sheath and the axons is main-tained and morphologic
alterations areminor.Recovery ofthe functional deficit isspontaneous and usually
complete within3 to 4 weeks.Ifthere is a physical disrup-tion ofone or more axons
without injuryto stromal tissue,the injury is described asaxonotmesis.Whereas
individual axonsare severed,the investing Schwann cellsand connective tissue
elements remainintact.The nature and extent ofthe ensu-ing sensory or motor deficit
relates to thenumber and type ofinjured axons.Mor-phologic changes are manifest as
degener-ation ofthe axoplasm and associatedstructures distal to the site ofinjury
andpartly proximal to the injury.Recovery ofthe functional deficit depends on
thedegree ofthe damage.Complete transection ofthe nervetrunk is referred to as
neurotmesis andspontaneous recovery from this type ofinjury is
rare.Histologically,changes ofdegeneration are evident in all axons adja-cent to
the site ofinjury.11Shortly afternerve severance,the investing Schwanncells begin
to undergo a series ofcellularchanges called wallerian degeneration.The
degeneration is evident in all axons ofthe distal nerve segment and in a fewnodes
ofthe proximal segment.Within 78 hours injured axons start breaking up and are
phagocytosed by adjacentSchwann cells and by macrophages thatmigrate into the zone
ofinjury.Once theaxonal debris has been cleared,Schwanncell outgrowths attempt to
connect theproximal stump with the distal nervestump.Surviving Schwann cells
prolifer-ate to form a band (B�ngner�s band) thatwill accept regenerating axonal
sproutsfrom the proximal stump.The proliferat-ing Schwann cells also promote
nerveregeneration by secreting numerous neu-rotrophic factors that coordinate
cellularrepair as well as cell adhesion moleculesthat direct axonal growth.In the
absenceofsurgical realignment or approximationofthe nerve
stumps,proliferatingSchwann cells and outgrowing axonalsprouts may align within the
randomlyorganized fibrin clot to form a disorga-nized mass termed neuroma.The rate
and extent ofnerve regener-ation depend on several factors includingtype
ofinjury,age,state oftissue nutri-tion,and the nerves involved.Althoughthe
regeneration rate for peripheral nervesvaries considerably,it is generally consid-
ered to approximate 1 mm/d.The regen-eration phase lasts up to 3 months andends on
contact with the end-organ by athin myelinated axon.In the concludingmaturation
phase both the diameter andperformance ofthe regenerating nervefiber increase.Bone
The process ofbone healing after a fracturehas many features similar to that
ofskinhealing except that it also involves calcifica-tion ofthe connective tissue
matrix.Bone isa biologically privileged tissue in that itheals by regeneration
rather than repair.Left alone,fractured bone is capable ofrestoring
itselfspontaneously throughsequential tissue formation and differentia-tion,a
process also referred to as indirecthealing.As in skin the interfragmentarythrombus
that forms shortly after injurystaunches bleeding from ruptured vessels inthe
haversian canals,marrow,and perios-teum.Necrotic material at the fracture
siteelicits an immediate and intense acuteinflammatory response which attracts
thepolymorphonuclear leukocytes and subse-quently macrophages to the fracture
site.The organizing hematoma serves as a fibrinscaffold over which reparative cells
canmigrate and perform their function.Invad-ing inflammatory cells and the
succeedingpluripotential mesenchymal cells begin torapidly produce a soft fracture
callus thatfills up interfragmentary gaps.Comprisedoffibrous tissue,cartilage,and
youngimmature fiber bone,the soft compliantcallus acts as a biologic splint by
bindingthe severed bone segments and dampinginterfragmentary motion.An orderly pro-
gression oftissue differentiation and matu-ration eventually leads to fracture
consoli-dation and restoration ofbone continuity.More commonly the surgeon
choosesto facilitate an abbreviated callus-freebone healing termed direct healing
(Figure1-3).The displaced bone segments are sur-gically manipulated into an
acceptablealignment and rigidly stabilized throughthe use ofinternal fixation
devices.Theresulting anatomic reduction is usually acombination ofsmall
interfragmentarygaps separated by contact areas.Ingrowthofmesenchymal cells and
blood vesselsstarts shortly thereafter,and activatedosteoblasts start depositing
osteoid on thesurface ofthe fragment ends.In contactzones where the fracture ends
are closelyapposed,the fracture line is filled concen-trically by lamellar
bone.Larger gaps arefilled through a succession offibrous
Wound Healing7tissue,fibrocartilage,and woven bone.Inthe absence ofany
microinstability at thefracture site,direct healing takes placewithout any callus
formation.Subsequent bone remodeling eventual-ly restores the original shape and
internalarchitecture ofthe fractured bone.Func-tional sculpting and remodeling
oftheprimitive bone tissue is carried out by atemporary team ofjuxtaposed
osteoclastsand osteoblasts called the basic multicellu-lar unit (BMU).The
osteoblasts developfrom pluripotent mesenchymal stem cellswhereas multicellular
osteoclasts arise froma monocyte/macrophage lineage.12Thedevelopment and
differentiation oftheBMUs are controlled by locally secretedgrowth
factors,cytokines,and mechanicalsignals.As osteoclasts at the leading edge ofthe
BMUs excavate bone through prote-olytic digestion,active osteoblasts move
in,secreting layers ofosteoid and slowly refill-ing the cavity.The osteoid begins
to miner-alize when it is about 6 �m thick.Osteo-clasts reaching the end oftheir
lifespan of2 weeks die and are removed by phagocytes.The majority (up to 65%) ofthe
remodel-ing osteoblasts also die within 3 monthsand the remainder are entombed
inside themineralized matrix as osteocytes.While the primitive bone
mineralizes,remodeling BMUs cut their way throughthe reparative tissue and replace
it withmature bone.The �grain�ofthe new bonetissue starts paralleling local
compressionand tension strains.Consequently theshape and strength ofthe reparative
bonetissue changes to accommodate greaterfunctional loading.Tissue-level
strainsproduced by functional loading play animportant role in the remodeling
oftheregenerate bone.Whereas low levels oftis-sue strain (~2,000 microstrains) are
con-sidered physiologic and necessary for celldifferentiation and callus
remodeling,high strain levels (> 2,000 microstrains)begin to adversely affect
osteoblastic dif-ferentiation and bone matrix forma-tion.13,14Ifthere is excess
interfragmentarymotion,bone regenerates primarilythrough endochondral ossification
or theformation ofa cartilaginous callus that isgradually replaced by new bone.In
con-trast osseous healing across stabilized frac-ture segments occurs primarily
throughintramembranous ossification.Major fac-tors determining the mechanical
milieu ofa healing fracture include the fracture con-figuration,the accuracy
offracture reduc-tion,the stability afforded by the selectedfixation device,and the
degree and natureofmicrostrains provoked by function.Ifafracture fixation device is
incapable ofsta-bilizing the fracture,the interfragmentarymicroinstability provokes
osteoclasticresorption ofthe fracture surfaces andresults in a widening ofthe
fracture gap.Although bone union may be ultimatelyachieved through secondary
healing bycallus production and endochondral ossi-fication,the healing is
protracted.Fibroushealing and nonunions are clinical mani-festations ofexcessive
microstrains inter-fering with the cellular healing process.Extraction Wounds The
healing ofan extraction socket is a spe-cialized example ofhealing by
secondintention.15Immediately after the removalofthe tooth from the socket,blood
fills theextraction site.Both intrinsic and extrinsicpathways ofthe clotting
cascade are activat-ed.The resultant fibrin meshwork contain-ing entrapped red
blood cells seals offtheGap healingContact healingOsteoblastBasic multicellular
unit OsteoclastOsteocyteBlood vesselFIGURE1-3Direct bone healing facilitated by a
lag screw.The fracture site shows both gap healing and contact healing.The internal
archi-tecture ofbone is restored eventually by the action ofbasic multicellular
units.
8Part 1: Principles ofMedicine,Surgery,and Anesthesiatorn blood vessels and reduces
the size ofthe extraction wound.Organization oftheclot begins within the first 24
to 48 hourswith engorgement and dilation ofbloodvessels within the periodontal
ligamentremnants,followed by leukocytic migrationand formation ofa fibrin layer.In
the firstweek the clot forms a temporary scaffoldupon which inflammatory cells
migrate.Epithelium at the wound periphery growsover the surface ofthe organizing
clot.Osteoclasts accumulate along the alveolarbone crest setting the stage for
active crestalresorption.Angiogenesis proceeds in theremnants ofthe periodontal
ligaments.Inthe second week the clot continues to getorganized through fibroplasia
and newblood vessels that begin to penetratetowards the center ofthe
clot.Trabeculae ofosteoid slowly extend into the clot from thealveolus,and
osteoclastic resorption ofthecortical margin ofthe alveolar socket ismore
distinct.By the third week the extrac-tion socket is filled with granulation
tissueand poorly calcified bone forms at thewound perimeter.The surface ofthewound
is completely reepithelialized withminimal or no scar formation.Active
boneremodeling by deposition and resorptioncontinues for several more weeks.Radi-
ographic evidence ofbone formation doesnot become apparent until the sixth toeighth
weeks following tooth extraction.Due to the ongoing process ofbone remod-eling the
final healing product oftheextraction site may not be discernible onradiographs
after 4 to 6 months.Occasionally the blood clot fails toform or may
disintegrate,causing a local-ized alveolar osteitis.In such instanceshealing is
delayed considerably and thesocket fills gradually.In the absence ofahealthy
granulation tissue matrix,theapposition ofregenerate bone to remain-ing alveolar
bone takes place at a muchslower rate.Compared to a normal socketthe infected
socket remains open or par-tially covered with hyperplastic epitheliumfor extended
periods.Skin GraftsSkin grafts may be either full thickness orsplit thickness.16A
full-thickness graft iscomposed ofepidermis and the entire der-mis;a split-
thickness graft is composed ofthe epidermis and varying amounts ofder-mis.Depending
on the amount ofunderly-ing dermis included,split-thickness graftsare described as
thin,intermediate,orthick.17Following grafting,nutritional sup-port for a free skin
graft is initially providedby plasma that exudes from the dilated cap-illaries
ofthe host bed.A fibrin clot forms atthe graft-host interface,fixing the graft
tothe host bed.Host leukocytes infiltrate intothe graft through the lower layers
ofthegraft.Graft survival depends on theingrowth ofblood vessels from the host
intothe graft (neovascularization) and directanastomoses between the graft and the
hostvasculature (inosculation).Endothelial cap-illary buds from the host site
invade thegraft,reaching the dermoepidermal junc-tion by 48 hours.Concomitantly
vascularconnections are established between hostand graft vessels.However,only a
few oftheingrowing capillaries succeed in developinga functional
anastomosis.Formation ofvas-cular connections between the recipient bedand
transplant is signaled by the pinkappearance ofthe graft,which appearsbetween the
third and fifth day postgraft-ing.Fibroblasts from the recipient bedbegin to invade
the layer offibrin andleukocytes by the fourth day after trans-plantation.The
fibrin clot is slowlyresorbed and organized as fibroblasticinfiltration
continues.By the ninth day thenew blood vessels and fibroblasts haveachieved a firm
union,anchoring the deeplayers ofthe graft to the host bed.Reinnervation ofthe skin
graft occursby nerve fibers entering the graft throughits base and sides.The fibers
follow thevacated neurilemmal cell sheaths to re-construct the innervation pattern
ofthedonor skin.Recovery ofsensation usuallybegins within 2 months after
transplanta-tion.Grafts rarely attain the sensoryqualities ofnormal skin,because
theextent ofre-innervation depends on howaccessible the neurilemmal sheaths are
tothe entering nerve fibers.The clinicalperformance ofthe grafts depends ontheir
relative thickness.As split-thicknessgrafts are thinner than full-
thicknessgrafts,they are susceptible to trauma andundergo considerable
contraction;how-ever,they have greater survival rates clin-ically.Full-thickness
skin grafts do not�take�as well and are slow to revascular-ize.Nevertheless full-
thickness grafts areless susceptible to trauma and undergominimal shrinkage.Wound
Healing ComplicationsHealing in the orofacial region is oftenconsidered a natural
and uneventfulprocess and seldom intrudes into the sur-geon�s
consciousness.However,thischanges when complications arise andencumber the wound
healing continuum.Most wound healing complications mani-fest in the early
postsurgical periodalthough some may manifest much later.The two problems most
commonlyencountered by the surgeon are woundinfection and
dehiscence;proliferativehealing is less typical.Wound InfectionInfections
complicating surgical outcomesusually result from gross bacterial contam-ination
ofsusceptible wounds.All woundsare intrinsically contaminated by
bacteria;however,this must be distinguished fromtrue wound infection where the
bacterialburden ofreplicating microorganismsactually impairs
healing.18Experimentalstudies have demonstrated that regardlessofthe type
ofinfecting microorganism,wound infection occurs when there aremore than 1
�105organisms per gram oftissue.19,20Beyond relative numbers,thepathogenicity ofthe
infecting microorgan-isms as well as host response factors deter-mine whether wound
healing is impaired.
Wound Healing9The continual presence ofa bacterialinfection stimulates the host
immunedefenses leading to the production ofinflammatory mediators,such
asprostaglandins and thromboxane.Neu-trophils migrating into the wound
releasecytotoxic enzymes and free oxygen radi-cals.Thrombosis and
vasoconstrictivemetabolites cause wound hypoxia,leadingto enhanced bacterial
proliferation andcontinued tissue damage.Bacteriadestroyed by host defense
mechanismsprovoke varying degrees ofinflammationby releasing neutrophil proteases
andendotoxins.Newly formed cells and theircollagen matrix are vulnerable to
thesebreakdown products ofwound infection,and the resulting cell and collagen
lysiscontribute to impaired healing.Clinicalmanifestations ofwound infection
includethe classic signs and symptoms
oflocalinfection:erythema,warmth,swelling,pain,and accompanying odor and
pus.Inadequate tissue perfusion and oxy-genation ofthe wound further compro-mise
healing by allowing bacteria to prolif-erate and establish infection.Failure
tofollow aseptic technique is a frequent rea-son for the introduction
ofvirulentmicroorganisms into the wound.Trans-formation ofcontaminated wounds
intoinfected wounds is also facilitated byexcessive tissue trauma,remnant
necrotictissue,foreign bodies,or compromisedhost defenses.The most important
factorin minimizing the risk ofinfection ismeticulous surgical
technique,includingthorough d�bridement,adequate hemo-stasis,and elimination ofdead
space.Careful technique must be augmented byproper postoperative care,with an
empha-sis on keeping the wound site clean andprotecting it from trauma.Wound
DehiscencePartial or total separation ofthe woundmargins may manifest within the
firstweek after surgery.Most instances ofwound dehiscence result from tissue fail-
ure rather than improper suturing tech-niques.The dehisced wound may beclosed again
or left to heal by secondaryintention,depending upon the extent ofthe disruption
and the surgeon�s assess-ment ofthe clinical situation.Proliferative ScarringSome
patients may go on to develop aber-rant scar tissue at the site oftheir
skininjury.The two common forms ofhyper-proliferative healing,hypertrophic scarsand
keloids,are characterized by hyper-vascularity and hypercellularity.Distinc-tive
features include excessive scarring,persistent inflammation,and an overpro-duction
ofextracellular matrix compo-nents,including glycosaminoglycans andcollagen Type
I.21Despite their overtresemblance,hypertrophic scars andkeloids do have some
clinical dissimilari-ties.In general,hypertrophic scars ariseshortly after the
injury,tend to be circum-scribed within the boundaries ofthewound,and eventually
recede.Keloids,onthe other hand,manifest months after theinjury,grow beyond the
wound bound-aries,and rarely subside.There is a clearfamilial and racial
predilection for keloidformation,and susceptible individualsusually develop keloids
on their face,earlobes,and anterior chest.Although processes leading to hyper-
trophic scar and keloid formation are notyet clarified,altered apoptotic behavior
isbelieved to be a significant factor.Ordinar-ily,apoptosis or programmed cell
death isresponsible for the removal ofinflammato-ry cells as healing proceeds and
for the evo-lution ofgranulation tissue into scar.Dys-regulation in apoptosis
results in excessivescarring,inflammation,and an overpro-duction ofextracellular
matrix compo-nents.Both keloids and hypertrophic scarsdemonstrate sustained
elevation ofgrowthfactors including TGF-� ,platelet-derivedgrowth factor,IL-1,and
IGF-I.22Thegrowth factors,in turn,increase the num-bers oflocal fibroblasts and
prompt exces-sive production ofcollagen and extracellu-lar
matrix.Additionally,proliferative scartissue exhibits increased numbers
ofneoangiogenesis-promoting vasoactivemediators as well as histamine-secretingmast
cells capable ofstimulating fibroustissue growth.Although there is no effec-tive
therapy for keloids,the more commonmethods for preventing or treating theselesions
focus on inhibiting protein synthe-sis.These agents,primarily corticosteroids,are
injected into the scar to decreasefibroblast proliferation,decrease angiogen-
esis,and inhibit collagen synthesis andextracellular matrix protein
synthesis.Optimizing Wound HealingAt its very essence the wound representsan
extreme disruption ofthe cellularmicroenvironment.Restoration ofcon-stant internal
conditions or homeostasis atthe cellular level is a constant undertow ofthe healing
response.A variety oflocal andsystemic factors can impede healing,andthe informed
surgeon can anticipate and,where possible,proactively address thesebarriers to
healing so that wound repaircan progress normally.23Tissue TraumaMinimizing
surgical trauma to the tissueshelps promote faster healing and shouldbe a central
consideration at every stage ofthe surgical procedure,from placement ofthe incision
to suturing ofthe wound.Properly planned,the surgical incision isjust long enough
to allow optimum expo-sure and adequate operating space.Theincision should be made
with one cleanconsistent stroke ofevenly applied pres-sure.Sharp tissue dissection
and carefullyplaced retractors further minimize tissueinjury.Sutures are useful for
holding thesevered tissues in apposition until thewound has healed
enough.However,sutures should be used judiciously as theyhave the ability to add to
the risk ofinfec-tion and are capable ofstrangulating thetissues ifapplied too
tightly.
10Part 1: Principles ofMedicine,Surgery,and AnesthesiaHemostasis and Wound
D�bridementBleeding from a transected vessel or dif-fuse oozing from the denuded
surfacesinterfere with the surgeon�s view ofunder-lying structures.Achieving
completehemostasis before wound closure helpsprevent the formation ofa
hematomapostoperatively.The collection ofblood orserum at the wound site provides
an idealmedium for the growth ofmicroorgan-isms that cause
infection.Additionally,hematomas can result in necrosis ofover-lying
flaps.However,hemostatic tech-niques must not be used too aggressivelyduring
surgery as the resulting tissue dam-age can prolong healing time.Postopera-tively
the surgeon may insert a drain orapply a pressure dressing to help eliminatedead
space in the wound.Devitalized tissue and foreign bodiesin a healing wound act as a
haven for bac-teria and shield them from the body�sdefenses.23The dead cells and
cellulardebris ofnecrotic tissue have been shownto reduce host immune defenses
andencourage active infection.A necrotic bur-den allowed to persist in the wound
canprolong the inflammatory response,mechanically obstruct the process ofwound
healing,and impede reepithelial-ization.Dirt and tar located in traumaticwounds not
only jeopardize healing butmay result in a �tattoo�deformity.Byremoving dead and
devitalized tissue,andany foreign material from a wound,d�bridement helps to reduce
the numberofmicrobes,toxins,and other substancesthat inhibit healing.The surgeon
shouldalso keep in mind that prosthetic graftsand implants,despite refinements in
bio-compatibility,can incite varying degrees offoreign body reaction and
adverselyimpact the healing process.Tissue PerfusionPoor tissue perfusion is one
ofthe mainbarriers to healing inasmuch as tissue oxygen tension drives the
healingresponse.24,25Oxygen is necessary forhydroxylation ofproline and
lysine,thepolymerization and cross-linking ofpro-collagen strands,collagen
transport,fibroblast and endothelial cell replication,effective leukocyte
killing,angiogenesis,and many other processes.Relative hypox-ia in the region
ofinjury stimulates afibroblastic response and helps mobilizeother cellular
elements ofrepair.26Howev-er,very low oxygen levels act together withthe lactic
acid produced by infecting bac-teria to lower tissue pH and contribute totissue
breakdown.Cell lysis follows,withreleases ofproteases and glycosidases
andsubsequent digestion ofextracellularmatrix.27Impaired local circulation
alsohinders delivery ofnutrients,oxygen,andantibodies to the wound.Neutrophils
areaffected because they require a minimallevel ofoxygen tension to exert their
bac-tericidal effect.Delayed movement ofneu-trophils,opsonins,and the other media-
tors ofinflammation to the wound sitefurther diminishes the effectiveness
ofthephagocytic defense system and allows col-onizing bacteria to
proliferate.Collagensynthesis is dependent on oxygen deliveryto the site,which in
turn affects woundtensile strength.Most healing problemsassociated with diabetes
mellitus,irradia-tion,small vessel atherosclerosis,chronicinfection,and altered
cardiopulmonarystatus can be attributed to local tissueischemia.Wound
microcirculation after surgerydetermines the wound�s ability to resist
theinevitable bacterial contamination.28Tissuerendered ischemic by rough
handling,ordesiccated by cautery or prolonged air dry-ing,tends to be poorly
perfused and sus-ceptible to infection.Similarly,tissueischemia produced by tight
or improperlyplaced sutures,poorly designed flaps,hypo-volemia,anemia,and
peripheral vasculardisease,all adversely affect wound healing.Smoking is a common
contributor todecreased tissue oxygenation.29After everycigarette the peripheral
vasoconstrictioncan last up to an hour;thus,a pack-a-daysmoker remains tissue
hypoxic for mostpart ofeach day.Smoking also increasescarboxyhemoglobin,increases
plateletaggregation,increases blood viscosity,decreases collagen deposition,and
decreas-es prostacyclin formation,all ofwhich neg-atively affect wound
healing.Patient opti-mization,in the case ofsmokers,mayrequire that the patient
abstain from smok-ing for a minimum of1 week before andafter surgical
procedures.Another way ofimproving tissue oxygenation is the use ofsystemic
hyperbaric oxygen (HBO) therapyto induce the growth ofnew blood vesselsand
facilitate increased flow ofoxygenatedblood to the wound.DiabetesNumerous studies
have demonstrated thatthe higher incidence ofwound infectionassociated with
diabetes has less to do withthe patient having diabetes and more to dowith
hyperglycemia.Simply put,a patientwith well-controlled diabetes may not beat a
greater risk for wound healing prob-lems than a nondiabetic
patient.Tissuehyperglycemia impacts every aspect ofwound healing by adversely
affecting theimmune system including neutrophil andlymphocyte
function,chemotaxis,andphagocytosis.30Uncontrolled blood glu-cose hinders red blood
cell permeabilityand impairs blood flow through the criti-cal small vessels at the
wound surface.Thehemoglobin release ofoxygen is impaired,resulting in oxygen and
nutrient deficien-cy in the healing wound.The woundischemia and impaired
recruitment ofcells resulting from the small vessel occlu-sive disease renders the
wound vulnerableto bacterial and fungal infections.ImmunocompromiseThe immune
response directs the healingresponse and protects the wound frominfection.In the
absence ofan adequateimmune response,surgical outcomes are
Wound Healing11often compromised.An important assess-ment parameter is total
lymphocyte count.A mild deficit is a lymphocytic levelbetween 1,200 and 1,800,and
levels below800 are considered severe total lymphocytedeficits.Patients with
debilitated immuneresponse include human immunodefi-ciency virus (HIV)-infected
patients inadvanced stages ofthe disease,patients onimmunosuppressive therapy,and
thosetaking high-dose steroids for extendedperiods.31Studies indicate that HIV-
infected patients with CD4 counts oflessthan 50 cells/mm3are at significant risk
ofpoor wound outcome.32Although newerimmunosuppressive drugs,such
ascyclosporine,have no apparent effect onwound healing,other medications canretard
the healing process both in rate andquality by altering both the
inflammatoryreaction and the cell metabolism.The use ofsteroids,such as
prednisone,is a typical example ofhow suppression ofthe innate inflammatory process
alsoincreases wound healing complications.Exogenous corticosteroids diminish
prolylhydroxylase and lysyl oxidase activity,depressing fibroplasias,collagen
formation,and neovascularity.33Fibroblasts reach thesite in a delayed fashion and
wound strengthis decreased by as much as 30%.Epithelial-ization and wound
contraction are alsoimpaired.The inhibitory effects ofgluco-corticosteriods can be
attenuated to someextent by vitamin A given concurrently.Most antineoplastic agents
exert theircytotoxic effect by interfering with DNAor RNA production.The reduction
in pro-tein synthesis or cell division reveals itselfas impaired proliferation
offibroblastsand collagen formation.Attendant neu-tropenia also predisposes to
wound infec-tion by prolonging the inflammatoryphase ofwound healing.Because
oftheirdeleterious effect on wound healing,administration ofantineoplastic
drugsshould be restricted,when possible,untilsuch time that the potential for
healingcomplications has passed.Radiation InjuryTherapeutic radiation for head and
necktumors inevitably produces collateraldamage in adjacent tissue and reduces
itscapacity for regeneration and repair.Thepathologic processes ofradiation
injurystart right away;however,the clinical andhistologic features may not become
appar-ent for weeks,months,or even years aftertreatment.34The cellular and
molecularresponses to tissue irradiation are imme-diate,dose dependent,and can
cause bothearly and late consequences.35DNA dam-age from ionizing radiation leads
to mitot-ic cell death in the first cell division afterirradiation or within the
first few divi-sions.Early acute changes are observedwithin a few weeks oftreatment
and pri-marily involve cells with a high turnoverrate.The common symptoms
oforalmucositis and dermatitis result from lossoffunctional cells and temporary
lack ofreplacement from the pools ofrapidlyproliferating cells.The
inflammatoryresponse is largely mediated by cytokinesactivated by the radiation
injury.Overallthe response has the features ofwoundhealing;waves ofcytokines are
producedin an attempt to heal the radiation injury.The cytokines lead to an
adaptive responsein the surrounding tissue,cause cellularinfiltration,and promote
collagen deposi-tion.Damage to local vasculature is exac-erbated by leukocyte
adhesion to endothe-lial cells and the formation ofthrombi thatblock the vascular
lumen,further depriv-ing the cells that depend on the vessels.The acute symptoms
eventually startto subside as the constitutive cells gradual-ly recover their
proliferative abilities.However,these early symptoms may notbe apparent in some
tissues such as bone,where cumulative progressive effects ofradiation can
precipitate acute breakdownoftissue many years after therapy.The lateeffects
ofradiation are permanent anddirectly related to higher doses.36Collagenhyalinizes
and the tissues become increas-ingly fibrotic and hypoxic due to oblitera-tive
vasculitis,and the tissue susceptibilityto infection increases correspondingly.Once
these changes occur they are irre-versible and do not change with time.Hence,the
surgeon must always anticipatethe possibility ofa complicated healingfollowing
surgery or traumatic injury inirradiated tissue.Wound dehiscence iscommon and the
wound heals slowly orincompletely.Even minor trauma mayresult in ulceration and
colonization byopportunistic bacteria.Ifthe patient can-not mount an effective
inflammatoryresponse,progressive necrosis ofthe tis-sues may follow.Healing can be
achievedonly by excising all nonvital tissue andcovering the bed with a well-
vascularizedgraft.Due to the relative hypoxia at theirradiated site,tissue with
intact bloodsupply needs to be brought in to provideboth oxygen and the cells
necessary forinflammation and healing.The progres-sive obliteration ofblood vessels
makesbone particularly vulnerable.Followingtrauma or disintegration ofthe soft
tissuecover due to inflammatory reaction,heal-ing does not occur because
irradiatedmarrow cannot form granulation tissue.In such instances the avascular
bone needsto be removed down to the healthy por-tion to allow healing to
proceed.Hyperbaric Oxygen TherapyHBO therapy is based on the concept thatlow tissue
oxygen tension,typically a par-tial pressure ofoxygen (PO2) of5 to 20 mm Hg,leads
to anaerobic cellularmetabolism,increase in tissue lactate,anda decrease in pH,all
ofwhich inhibitwound healing.64HBO therapy entails thepatient lying in a hyperbaric
chamber and breathing 100% oxygen at 2.0 to 2.4 atmospheres for 1 to 2 hours.TheHBO
therapy is repeated daily for 3 to 10 weeks.HBO increases the quantity ofdissolved
oxygen and the driving pressurefor oxygen diffusion into the tissue.Corre-
spondingly the oxygen diffusion distance
12Part 1: Principles ofMedicine,Surgery,and Anesthesiais increased threefold to
fourfold,andwound PO2ultimately reaches 800 to 1,100 mm Hg.The therapy stimulates
thegrowth offibroblasts and vascularendothelial cells,increases tissue vascular-
ization,enhances the killing ability ofleukocytes,and is lethal for anaerobic bac-
teria.Clinical studies suggest that HBOtherapy can be an effective adjunct in
themanagement ofdiabetic wounds.65Animalstudies indicate that HBO therapy could
bebeneficial in the treatment ofosteomyelitisand soft tissue
infections.66,67Adverseeffects ofHBO therapy are barotraumas ofthe ear,seizure,and
pulmonary oxygentoxicity.However,in the absence ofcon-trolled scientific studies
with well-definedend points,HBO therapy remains a con-troversial aspect ofsurgical
practice.68,69AgeIn general wound healing is faster in theyoung and protracted in
the elderly.Thedecline in healing response results fromthe gradual reduction
oftissue metabo-lism as one ages,which may itselfbe amanifestation ofdecreased
circulatoryefficiency.The major components ofthehealing response in aging skin or
mucosaare deficient or damaged with progressiveinjuries.37As a result,free
oxidative radi-cals continue to accumulate and are harm-ful to the dermal enzymes
responsible forthe integrity ofthe dermal or mucosalcomposition.In addition the
regional vas-cular support may be subjected to extrin-sic deterioration and
systemic diseasedecompensation,resulting in poor perfu-sion capability.38However,in
the absenceofcompromising systemic conditions,dif-ferences in healing as a function
ofageseem to be small.NutritionAdequate nutrition is important for nor-mal
repair.39In malnourished patientsfibroplasia is delayed,angiogenesisdecreased,and
wound healing and remod-eling prolonged.Dietary protein hasreceived special
emphasis with respect tohealing.Amino acids are critical for woundhealing with
methionine,histidine,andarginine playing important roles.Nutri-tional deficiencies
severe enough to lowerserum albumin to < 2 g/dL are associatedwith a prolonged
inflammatory phase,decreased fibroplasia,and impaired neo-vascularization,collagen
synthesis,andwound remodeling.As long as a state ofprotein catabolism exists,the
wound willbe very slow to heal.Methionine appears tobe the key amino acid in wound
healing.Itis metabolized to cysteine,which plays avital role in the
inflammatory,proliferative,and remodeling phases ofwound healing.Serum prealbumin
is commonlyused as an assessment parameter for pro-tein.40,41Contrary to serum
albumin,which has a very long half-life ofabout20 days,prealbumin has a shorter
half-life ofonly 2 days.As such it provides amore rapid assessment
ability.Normalserum prealbumin is about 22.5 mg/dL,alevel below 17 mg/dL is
considered amild deficit,and a severe deficit would bebelow 11 mg/dL.As part ofthe
perioper-ative optimization process,malnour-ished patients may be provided
withsolutions that have been supplementedwith amino acids such as glutamine
topromote improved mucosal structureand function and to enhance whole-bodynitrogen
kinetics.An absence ofessentialbuilding blocks obviously thwarts nor-mal repair,but
the reverse is not neces-sarily true.Whereas a minimum proteinintake is important
for healing,a highprotein diet does not shorten the timerequired for
healing.Several vitamins and trace mineralsplay a significant role in wound
healing.42Vitamin A stimulates fibroplasia,collagencross-linking,and
epithelialization,and willrestimulate these processes in the steroid-retarded
wound.Vitamin C deficiencyimpairs collagen synthesis by fibroblasts,because it is
an important cofactor,alongwith a-ketoglutarate and ferrous iron,inthe
hydroxylation process ofproline andlysine.Healing wounds appear to be moresensitive
to ascorbate deficiency than unin-jured tissue.Increased rates ofcollagenturnover
persist for a long time,and healedwounds may rupture when the individualbecomes
scorbutic.Local antibacterialdefenses are also impaired because ascorbicacid is
also necessary for neutrophil super-oxide production.The B-complex vitaminsand
cobalt are essential cofactors in anti-body formation,white blood cell function,and
bacterial resistance.Depleted serumlevels ofmicronutrients,including magne-
sium,copper,calcium,iron,and zinc,affectcollagen synthesis.43Copper is essential
forcovalent cross-linking ofcollagen whereascalcium is required for the normal
functionofgranulocyte collagenase and other colla-genases at the wound milieu.Zinc
deficien-cy retards both fibroplasia and reepithelial-ization;cells migrate
normally but do notundergo mitosis.44Numerous enzymes arezinc
dependent,particularly DNA poly-merase and reverse transcriptase.On theother
hand,exceeding the zinc levels canexert a distinctly harmful effect on healingby
inhibiting macrophage migration andinterfering with collagen cross-linking.Advances
in Wound CareAn increased understanding ofthe woundhealing processes has generated
height-ened interest in manipulating the woundmicroenvironment to facilitate
healing.Traditional passive ways oftreating surgi-cal wounds are rapidly giving way
toapproaches that actively modulate woundhealing.Therapeutic interventions
rangefrom treatments that selectively jump-start the wound into the healing
cascade,to methods that mechanically protect thewound or increase oxygenation and
perfu-sion ofthe local tissues.45,46Growth FactorsThrough their central ability to
orches-trate the various cellular activities thatunderscore inflammation and
healing,
Wound Healing13cytokines have profound effects on cellproliferation,migration,and
extracellularmatrix synthesis.47Accordingly newerinterventions seek to control or
modulatethe wound healing process by selectivelyinhibiting or enhancing the tissue
levels ofthe appropriate cytokines.The more common clinical approachhas been to
apply exogenous growth fac-tors,such as PGDF,angiogenesis factor,epi-dermal growth
factor (EGF),TGF,bFGF,and IL-1,directly to the wound.However,the potential ofthese
extrinsic agents hasnot yet been realized clinically and mayrelate to figuring out
which growth factorsto put into the wound,and when and atwhat dose.To date only a
single growth fac-tor,recombinant human platelet-derivedgrowth factor-BB (PDGF-
BB),has beenapproved by the United States Food andDrug Administration for the
treatment ofcutaneous ulcers,specifically diabetic footulcers.Results from several
controlled clin-ical trials show that PDGF-BB gel was effec-tive in healing
diabetic ulcers in lowerextremities and significantly decreasedhealing time when
compared to the placebogroup.48,49More recently,recombinanthuman keratinocyte
growth factor 2 (KGF-2) has been shown to accelerate woundhealing in experimental
animal models.Itenhanced both the formation ofgranula-tion tissue in rabbits and
wound closure ofthe human meshed skin graft explanted onathymic nude
rats.50,51Experimental studiessuggest potential for the use ofgrowth fac-tors in
facilitating peripheral nerve healing.Several growth factors belonging to
theneurotrophin family have been implicatedin the maintenance and repair
ofnerves.Nerve growth factor (NGF),synthesized bySchwann cells distal to the site
ofinjury,aids in the survival and development ofsensory nerves.This finding has led
someinvestigators to suggest that exogenousNGF application may assist in
peripheralnerve regeneration following injury.52Newer neurotrophins such as brain-
derivedneurotrophic factor and neurotrophin-3 aswell as ciliary neurotrophic factor
appear tosupport the growth ofsensory,sympathet-ic,and motor neurons in
vitro.53�55Insulin-like growth factors have demonstrated sim-ilar neurotrophic
properties.56Althoughmost ofthe investigations hitherto havebeen
experimental,increasing sophistica-tion in the dosing,combinations,and deliv-ery
ofneurotropic growth factors will leadto greater clinical
application.Osteoinductive growth factors holdspecial appeal to surgeons for their
abilityto promote the formation ofnew bone.Ofthe multiple osteoinductive
cytokines,thebone morphogenetic proteins (BMPs)belonging to the TGF-� superfamily
havereceived the greatest attention.Advances inrecombinant DNA techniques now
allowthe production ofthese biomolecules inquantities large enough for routine
clinicalapplications.In particular,recombinanthuman bone morphogenetic protein-
2(rhBMP-2) and rhBMP-7 have been stud-ied extensively for their ability to
induceundifferentiated mesenchymal cells to dif-ferentiate into osteoblasts
(osteoinduc-tion).Yasko and colleagues used a rat seg-mental femoral defect model
to show thatrhBMP-2 can produce 100% union rateswhen combined with bone
marrow.57Theunion rate achieved with the combinationapproach was three times higher
than thatachieved with autologous cancellous bonegraft alone.Similarly,Toriumi and
col-leagues showed that rhBMP-2 could healmandibular defects with bone formed bythe
intramembranous pathway.58Thewidespread application ofosteoinductivecytokines
depends in large part on a betterunderstanding ofthe complex interactionofgrowth
factors and the concentrationsnecessary to achieve specific effects.Gene TherapyThe
application ofgene therapy to woundhealing has been driven by the desire
toselectively express a growth factor for con-trolled periods oftime at the site
oftissueinjury.59Unlike the diffuse effects ofabolus ofexogenously applied growth
fac-tor,gene transfer permits targeted,consis-tent,local delivery ofpeptides in
high con-centrations to the wound environment.Genes encoding for select growth
factorsare delivered to the site ofinjury using avariety
ofviral,chemical,electrical,ormechanical methods.60Cellular expressionofthe
proteins encoded by the nucleicacids help modulate healing by regulatinglocal
events such as cell proliferation,cellmigration,and the formation ofextracel-lular
matrix.The more popular methodsfor transfecting wounds involve the in vivouse
ofadenoviral vectors.Existing genetherapy technology is capable ofexpress-ing a
number ofmodulatory proteins atthe physiologic or supraphysiologic rangefor up to 2
weeks.Numerous experimental studies havedemonstrated the use ofgene therapy
instimulating bone formation and regenera-tion.Mesenchymal cells transfected
withadenovirus-hBMP-2 cDNA have beenshown to be capable offorming bone wheninjected
intramuscularly in the thighs ofrodents.61,62Similarly bone marrow cellstransfected
ex vivo with hBMP-2 cDNAhave been shown to heal femoral defects.63Using
osteoprogenitor cells for the expres-sion ofbone-promoting osteogenic
factorsenables the cells to not only express bonegrowth promoting factors,but also
torespond,differentiate,and participate inthe bone formation process.These
earlystudies suggest that advances in gene ther-apy technology can be used to
facilitatehealing ofbone and other tissues and maylead to better and less invasive
reconstruc-tive procedures in the near future.Dermal and Mucosal
SubstitutesImmediate wound coverage is critical foraccelerated wound healing.The
coverageprotects the wound from water loss,drying,and mechanical injury.Although
autolo-gous grafts remain the standard for replac-ing dermal mucosal surfaces,a
number ofbioengineered substitutes are finding their
14Part 1: Principles ofMedicine,Surgery,and Anesthesiaway into mainstream surgical
practice.Thehuman skin substitutes available aregrouped into three major types and
serve asexcellent alternatives to autografts.The firsttype consists ofgrafts
ofcultured epider-mal cells with no dermal components.Thesecond type has only
dermal components.The third type consists ofa bilayer ofbothdermal and epidermal
elements.The chiefeffect ofmost skin replacements is to pro-mote wound healing by
stimulating therecipient host to produce a variety ofwound healing cytokines.The
use ofcul-tured skin to cover wounds is particularlyattractive inasmuch as the
living cellsalready know how to produce growth fac-tors at the right time and in
the rightamounts.The ultimate goal ofbioengineersis to develop engineered skin that
containsall ofthe components necessary to modu-late healing and allow for wound
healingwith a surrogate that replicates native tissueand limits scar
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1998;3 Suppl1:S1�23.47.Rumalla VK,Borah GL.Cytokines,growth fac-tors,and plastic
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CHAPTER 2Medical Management ofthe Surgical PatientJames R.Hupp,DMD,MD,JD,MBADavid
N.Duddleston,MDOral-maxillofacial surgery frequentlycauses temporary but clinically
significantalteration ofthe anatomy and physiologyofthe upper aerodigestive
tract,but hasminor direct impact on vital organ sys-tems.Therefore,the surgery
itselfis gener-ally safe to perform even on relativelyunhealthy
individuals.However,the phys-iologic stresses produced by surgery andthe anesthetic
techniques necessary forthese procedures can lead to serious mor-bidity and
mortality.This is especially truein patients with various organs on thebrink
ofdecompensation due to disease orcomorbid conditions.This chapter presents the
commonmedical situations that can compromisethe successful outcome oforal or
maxillo-facial surgery.Emphasis is given to themeans ofdetecting health problems
pre-operatively and preparing patients withvarious medical disorders so that
compli-cations in the perioperative period areavoided or minimized.The liberal use
ofmedical consultations is highly recom-mended for all situations in which a sur-
geon has concerns for the medical well-being ofa surgical patient.Most commonly
oral-maxillofacialsurgery is performed on healthy patients.A quick screen ofhealth
conditions maygive additional data in the evaluation ofthe healthy patient.A
preoperative patientquestionnaire has been used in determin-ing whether any further
risk should beascertained.1The questions in Table 2-1have been valuable in
preoperative patientevaluation.In addition to this group ofquestions,other
questionnaire-type screening toolscan be valuable.Exercise capacity,such asthe 6-
minute walk test,use ofmedicationsand herbal supplements,and age can beimportant
determinants ofperioperativerisks.2Exercise tolerance has been shown topredict
long-term mortality as well asshort-term perioperative risks.3All patientsshould be
questioned regarding their exer-cise tolerance with a question such as,�IfIasked
you to walk as far as you could,howfar would that be?�This may be answeredas a
function oftime or distance.It is help-ful to ask,�When was the last time youwalked
that far?�Ifthere is a limitation ofexercise,then ask,�What is the reason forthe
limitation?�It may be due to orthopedicor other musculoskeletal problems thatlimit
exercise,or cardiac or pulmonaryinsufficiency.Medication use is important,and
withthe use ofa plethora ofover-the-countermedications and dietary
supplements,Table 2-1Preoperative Patient Questionnaire1.Do you feel unwell?2.Have
you ever had any serious illnesses in the past?3.Do you get any more short ofbreath
on exertion than other people ofyour age?4.Do you have any coughing?5.Do you have
any wheezing?6.Do you have any chest discomfort on exertion?7.Do you have any ankle
swelling?8.Have you taken any medicine or pills in the past 3 months (including
excess alchol)?9.Do you have any allergies?10.Have you had an anesthetic in the
past 2 months?11.Have you or your relatives had any problems with a previous
anesthetic?12.What is the date ofyour last menstrual period?13.Do you observe any
serious abnormality from �end ofbed�that might affect anesthetic? (Clinician�s
observation)
18Part 1: Principles ofMedicine,Surgery,and Anesthesiaspecific questioning is in
order.Aspirin or other nonsteroidal anti-inflammatorydrug use may exacerbate
bleeding duringmajor surgery.Some herbal supplementsare known to increase the risk
ofbleedingas well.4Finally age can be used as a surrogatefor underlying disease or
decreased reserve.There are no absolute cutoffs for age in esti-mation ofrisk;age
of70 years is used as abenchmark for a separate risk factor in sur-gical
mortality.Laboratory testing may behelpful in a small subset ofpatients.Rou-tine
testing requirements may vary fromoperative center,office,or hospital,but ingeneral
there is often overtesting andunder-review ofthe results.Ifguidelines ata
particular center have been established,itis important to use a checklist ofthe
tests,including their results.Many ofthese testsare arbitrary and not supported by
evi-dence-based research.However,it is notunreasonable to establish a schedule
ofrou-tine testing in unselected patients.Whilemost young and apparently healthy
patientsdo not need any preoperative laboratorytesting,unselected adults over the
age of40 years may benefit from a preoperativehematocrit and tests ofrenal function
andblood glucose.A blood count may revealanemia or serve as a benchmark
whenexcessive blood loss or anemia is foundafter surgery.Glucose determination
ishelpful in those patients with diabetes orobesity,and serves as a useful
screening toolfor diabetes in the general population.5The preoperative evaluation
ofhealthypatients should include the following6,7:1.A screening questionnaire for
allpatients (see Table 2-1)2.A history ofexercise tolerance for allpatients3.Blood
pressure and pulse for allpatients4.History and physical examination ifone ofthe
above is abnormal,inpatients over 60 years,or in thoseundergoing major
surgery5.Pregnancy test for women who may bepregnant6.Hematocrit for surgery with
expectedmajor blood loss7.Serum creatinine concentration ifundergoing major
surgery,hypoten-sion is expected,nephrotoxic drugswill be used,or the patient is
over age50 years8.Electrocardiogram (ECG) recommen-dations as above,unless
obtainedwithin the previous month9.Chest radiograph for patients over 60 years,or
for those with suspectedcardiac or pulmonary disease,ifsuchimaging has not been
performedwithin the past 6 months10.Other tests only ifthe clinical evalua-tion
suggests a likelihood ofdiseaseCardiac DiseaseCardiac disease is common in the
NorthAmerican and other populations,and thepatient is usually well aware ofany
existingcardiac problem.Thus,it is essential toscreen for cardiovascular
disease,and recentinterventions have shown the ability togreatly reduce
perioperative risks in patientswith known or suspected cardiac disease.Preservation
ofcardiac health is anessential element ofany perioperative pro-tocol.The proper
match ofoxygen supply tooxygen use in myocardial tissue is the key tomaintaining
normal contractility and elec-trical activity.In the patient with a healthyheart
and lungs,the myocardium is protect-ed in the perioperative period by
avoidinghypovolemia,ensuring adequate oxygen-carrying capacity ofthe
blood,keepingserum electrolytes within physiologic limits,and supplying the lungs
with adequate oxy-gen.Cardiac output also depends on prop-erly functioning
valves.Finally the loadagainst which the ventricles must workshould stay within
reasonable limits to pre-serve optimal myocardial function.Several cardiac
conditions can existpreoperatively that have the potential tocompromise the heart�s
ability to maintainadequate blood pressure intra- or postop-eratively.These
conditions include coro-nary artery disease,valvular disease,vari-ous processes
predisposing the heart tocongestive failure,and abnormalities ofelectrical impulse
generation or conduc-tion.In the discussion ofthe four condi-tions that
follows,emphasis is on themeans ofassessing the degree ofcardiaccompromise and
reserve,ofimproving thesituation preoperatively,and ofmanagingthe condition
perioperatively.Coronary Artery DiseaseThe two principal processes that cause
aninsufficient blood supply to the myocardi-um are coronary artery obstruction
andspasm.Myocardial ischemia will occurwhen the supply ofoxygen is inadequateto
meet the demand for oxygen.Myocar-dial oxygen need is increased when theheart has
increased rate or mass,or isforced to work against an increased after-load that
increases end-diastolic wall ten-sion.In these situations symptoms ofischemia will
occur ifoxygen supply to themyocardium cannot be increased becausethe coronary
arteries are critically nar-rowed by fixed atheromatous lesionsand/or
spasm;clinically this is manifestedby exercise-induced angina pectoris.Coronary
artery disease is one ofthemost studied diseases in humans.Over thepast several
years new paradigms regard-ing coronary artery disease have emergedand have been
validated.The idea ofahard plaque slowly encircling the lumen ofa coronary artery
until occlusion hasoccurred has been replaced by the conceptofplaque rupture.Many
plaques in thelumen ofthe coronary vessels are consid-ered to be soft,with a
membrane or thincell layer covering a highly thrombogeniclipid core.This membrane
may ruptureeven in small lesions,exposing thrombo-genic materials into the
blood.This sets upan immediate clotting cascade resulting inthrombus
formation,occluding the vessel
Medical Management ofthe Surgical Patient19and precipitating myocardial infarction
orunstable angina.8,9Coronary artery disease includes theprogression ofan
endothelial lesion froma fatty streak to an occlusive lesion orplaque rupture as
noted above.Several riskfactors for coronary artery disease havebeen
identified,including family history ofearly coronary disease (under age 65 yr),male
gender,diabetes mellitus,and elevat-ed cholesterol,including total
cholesteroland/or low-density lipoprotein (LDL)cholesterol.High levels ofLDL
cholesterol,low levels ofhigh-density lipoprotein cho-lesterol,hypertension,and
cigarette smok-ing are the most predictive risk factors ofcoronary artery
disease.Additional riskfactors such as elevated levels ofhomocys-teine,C-reactive
protein,myeloperoxidaseand others are being evaluated.10Interest-ingly a large
percentage ofpatients withfirst-time myocardial infarction do nothave known risk
factors for coronaryartery disease.11,12As noted above,a plaque may progressto
cause a limitation offlow ofbloodthrough the coronary artery to themyocardial
tissue.Myocardial ischemiaproduces decreased myocardial contractil-ity rapidly
leading to systemic hypoten-sion and pulmonary vascular congestion.The limitation
offlow leads to the symp-tom ofangina.Patients may complain ofasqueezing,choking,or
tight feeling in thesubsternal region radiating to the throat,jaw,shoulders,or
arms.The patient mayalso experience dyspnea,diaphoresis,andnausea.Anginal symptoms
will dissipatesoon after the provoking activity ceases orafter transmucosal
nitroglycerin is admin-istered.Infarction symptoms will usuallypersist despite
nitroglycerin use or rest.It is important to ask patients suspectedofhaving
coronary artery disease iftheyhave discomfort with exertion,rather thanfocusing on
pain.A patient may give a his-tory ofdyspnea and chest tightness,amongother
symptoms,after exertion,eating aheavy meal,or entering a cold environment.Typically
these symptoms are reproducible.Patients who have angina symptoms thatare
progressive with less precipitating forces,angina with increasing frequency,or
anginaat rest are considered to have unstable angi-na and require evaluation by a
qualified car-diovascular specialist.There are no standard physical signsofcoronary
artery insufficiency so preop-erative screening relies on historic infor-mation and
electrocardiography.A cardio-vascular examination may show evidenceofvascular or
valvular disease,or somedegree ofcardiac decompensation.Symp-toms ofcompromised
coronary or carotidarteries should be sought preoperatively inall adult males,as
well as in menopausaland postmenopausal females.Physical ExaminationThe
physicalexamination in patients with coronaryartery disease is frequently
unrevealing.The history is the most important deter-minant ofrisk.However,a
cardiovascularexamination may show evidence ofvascu-lar disease,valvular disease,or
evidence ofcardiac decompensation.Patients with findings ofperipheralvascular
disease should be considered athigh risk for underlying coronary arterydisease.On
heart examination an S4maybe present,reflecting reduced compliancein an ischemic
myocardium.Auscultationofthe neck,periumbilical area oftheabdomen,and inguinal
areas should beused to detect bruits.In addition,pedalpulses and inguinal pulses
should bechecked.Diminished or absent pulses,cool feet,and skin changes such as
hairloss in the ankles and feet may indicateperipheral vascular disease.Specific
ques-tioning about problems occurring duringphysical activity or postprandially
shouldbe included.It must be remembered thatmany patients with first time
myocardialinfarction have no known risk factors.A resting ECG should be done
withina month ofa planned elective generalanesthetic and surgery in all males age
35 years and older,all females age 45 yearsand older,and all other patients with a
his-tory suggestive ofcardiac disease.13Moreelaborate routine cardiac testing is
unwar-ranted.Although it is unlikely to see rest-ing ECG changes suggestive
ofacuteischemia,old silent infarcts (representing20 to 60% ofall infarctions) or
conductionblocks due to coronary disease may bedetected.14It should be noted that
30% ofpatients with a history ofmyocardialinfarction have a normal resting
ECG.15ECG after controlled treadmill exercise is amore sensitive means
ofdetectingischemic tendencies as evidenced by STdepression or T-wave
inversion.Patientswith a past history ofcardiac diseaseshould have preoperative
posteroanteriorand lateral chest radiographs to detectearly signs ofcongestive
heart failure.Finally a thallium stress test can be used,but only in the case ofan
equivocal tread-mill test,or coronary angiography can beperformed to identify areas
ofnarrowing,which predispose the patient to periopera-tive myocardial ischemia
ifclinical indica-tions for angiography are present.All patients with a documented
historyofangina may have an increased risk ofperioperative infarction.This risk
varieswith the severity ofthe coronary diseaseand the degree ofphysiologic stress
in theperioperative period.Patients with stableangina have only a slightly raised
risk dur-ing anesthesia and surgery compared to thenormal population.Angina that is
worsen-ing with respect to frequency,duration,response to medication,or ease
ofproduc-tion is,by definition,unstable angina.Surgery in such a situation should
only pro-ceed ifrequired emergently.Patients withstable but poorly controlled
angina needmedical intervention to improve their car-diac status before most
elective surgery.The American College ofCardiologyhas produced a listing
ofmajor,intermedi-ate and minor cardiovascular risk factorsand matched these with a
listing ofhigher-risk operations.These risks are then entered
20Part 1: Principles ofMedicine,Surgery,and Anesthesiainto a straightforward
algorithm directed todecisions on invasive testing,noninvasivetesting,intervention
or progression tosurgery (Table 2-2 and Figure 2-1).16Riskreduction strategies have
also evolved,withreduced emphasis on preoperative testing.The newest risk reduction
strategy includesthe use of�-blockade in patients withknown coronary artery disease
or with riskfactors for coronary artery disease.17Patients with stable,well-
controlledangina,or who have delayed surgery after anuncomplicated myocardial
infarction for aperiod dictated by their cardiologist,canusually undergo elective
maxillofacial pro-cedures safely ifintraoperative hyper- orhypotension is
avoided.Although somestudies indicate the risk ofinfarctionincreases with the
duration ofsurgery,thishas only been well documented in the caseofmajor thoracic or
upper abdominal pro-cedures.18,19In general,nonurgent surgeryshould be postponed
for at least 6 weeksafter myocardial infarction.Patients whoneed nonurgent surgery
in this 6-week win-dow should be co-managed by a cardiolo-gist.Modern day general
anesthesia mayactually be protective ofthe myocardium,because supraphysiologic
levels ofoxygenare administered and cardiac work is mini-mized through maintenance
ofmusclerelaxation,sympathetic nervous systemantagonism,blood pressure
control,andprompt dysrhythmia recognition and man-agement.To assist with these
goals consider-ation should be given to radial artery cannulation for blood gas and
pH measure-ment and precise blood pressure monitor-ing.The presence ofsigns
ofchronic con-gestive failure following a myocardialinfarction increases operative
risk,as is dis-cussed later in this chapter.The risk ofgeneral anesthesia after
arecent myocardial infarction is due to pos-sible extension ofthe earlier
myocardialinfarction and the development ofcardiacdysrhythmias.A target-like zone
isdescribed in myocardial infarction,withthe center being infarcted tissue.It is
azone surrounding this infarcted tissue thatis considered to be stunned or
vulnerable.This zone is the area into which themyocardial infarction may extend
andfrom which dysrhythmias can be generat-ed.After the 6-week window has passed,the
patient can be evaluated as any othercoronary artery disease patient.20Patients
with coronary artery diseasehave their greatest risk ofcardiac problemsin the early
postoperative period.The car-diorespiratory system is no longer con-trolled by
general anesthesia,and the nor-mal stresses that occur in the earlyrecovery period
exist.There is usually aneed for increased cardiac output,whichthe diseased heart
may not be able todeliver or tolerate,and ischemia can result.Therefore,these
patients need frequentcardiopulmonary physical examinationsand close monitoring
ofvital signs,urineoutput,jugular venous pressure,and elec-trolytes.An immediate
postoperative ECGshould be obtained in patients with a his-tory ofcoronary artery
disease,particular-ly ifthey have any ofthe following:�Unexplained hypotensive or
syncopalepisode�Signs ofheart failure�Dysrhythmias�AnginaTable 2-2Clinical
Predictors ofIncreased Perioperative Cardiovascular Risk (Myocardial
Infarction,Heart Failure,Death)MajorUnstable coronary syndromesAcute or recent
myocardial infarction* with evidence ofimportant ischemic risk by clinical symptoms
or noninvasive studyUnstable or severe�angina (Canadian Class III or
IV)133Decompensated heart failureSignificant dysrhythmiasHigh-grade
atrioventricular blockSymptomatic ventricular dysrhythmias in the presence
ofunderlying heart diseaseSupraventricular arrhythmias with uncontrolled
ventricular rateSevere valvular diseaseIntermediateMild angina pectoris (Canadian
Class I or II)Previous myocardial infarction by history or pathological Q
wavesCompensated or prior heart failure Diabetes mellitus (particularly insulin-
dependent)Renal insufficiencyMinorAdvanced ageAbnormal electrocardiogram (left
ventricular hypertrophy,left bundle-branch block,ST-T abnormalities)Rhythm other
than sinus (eg,atrial fibrillation)Low functional capacity (eg,inability to climb
one flight ofstairs with a bag ofgroceries)History ofstrokeUncontrolled systemic
hypertension*The American College ofCardiology National Database Library defines
recent myocardial infarction as greater than 7 days but less than or equal to 1
month (30 days);acute myocardial infarction is within 7 days.�May include
�stable�angina in patients who are unusually sedentary.Adapted from Eagle KA et
al.16
Medical Management ofthe Surgical Patient21Need for noncardiac
surgeryOperatingroomPostoperative riskstratification and riskfactor
managementCoronaryrevascularizationwithin 5 years?Recurrentsymptoms or signs?Recent
coronaryevaluation?Recent coronaryangiography or stress test?Operating
roomClinicalpredictorsMajor clinicalpredictors*Intermediateclinical
predictors�Minor or noclinical predictors�Consider delayor cancel
noncardiacsurgeryConsider coronaryangiographyGo to step 6Go to step 7Medical
managementand risk factormodificationSubsequent care dictated by findings and
treatment resultsNoNoYesYesYesFavorable resultand no changein
symptomsEmergencysurgerySTEP 1STEP 2STEP 3STEP 4Undesirable result orNochange in
symptomsUrgent orelective surgerySTEP 5IntermediateSTEP 6clinical predictors�Poor(<
4 METs)Moderate orexcellent(> 4 METs)Lowsurgical riskprocedureIntermediatesurgical
riskprocedureHighsurgical riskprocedureNoninvasivetestingOperatingroomPostoperative
riskstratification and risk-factor reductionConsidercoronaryangiographySubsequent
caredictated by findingsand treatment resultsClinical predictorsFunctional
capacitySurgical riskNoninvasive testingInvasive testingSTEP 8LowriskHigh riskMinor
or noSTEP 7clinical predictors�Poor(< 4 METs)Moderate orexcellent(> 4
METs)Intermediate orlow surgical
riskprocedureNoninvasivetestingOperatingroomPostoperative riskstratification and
risk-factor reductionConsidercoronaryangiographySubsequent caredictated by
findingsand treatment resultsClinical predictorsFunctional capacitySurgical
riskNoninvasive testingInvasive testingSTEP 8LowriskHigh riskHighsurgical
riskprocedureFIGURE2-1Stepwise approach to preoperative cardiac assessment.Steps
are discussed in the text.Note that subsequent care may include cancellation or
delay ofsurgery,coronary revascularization followed by noncardiac surgery,or
intensified care.MET = metabolic equivalent.*Major clinical predictors include
unstablecoronary syndromes,decompensated congestive heart failure,significant
dysrhythmias,and severe valvular disease.�Intermediate clinical predictors include
mildangina pectoris,prior myocardial infarction,compensated or prior congestive
heart failure,diabetes mellitus,and renal insufficiency.�Minor clinical
predictorsinclude advanced age,abnormal electrocardiogram,rhythm other than
sinus,low functional capacity,history ofstroke,and uncontrolled systemic
hypertension.Adapted from from Eagle KA et al.16
22Part 1: Principles ofMedicine,Surgery,and AnesthesiaCare in the postoperative
periodshould be taken to maintain normalintravascular volume,avoid hyper-
orhypotension,keep serum electrolytes intheir physiologically normal ranges,man-age
patient anxiety and pain,give supple-mental oxygen when needed,and
resumepreoperative cardiac medications.Signs ofinfections or pulmonary problems
shouldbe pursued aggressively.Left Ventricular DysfunctionLeft ventric-ular
dysfunction can result from myocardialinfarction or primary
cardiomyopathy.Leftventricular dysfunction can be separatedinto systolic or
diastolic dysfunction.Sys-tolic dysfunction occurs after myocardialinfarction or
other direct muscle injury,causing either wall motion abnormalities ordecreased
cardiac output.Diastolic dysfunc-tion results from stiffness or reduced com-pliance
ofthe left ventricle.21Concepts ofpreload,afterload,andcompliance are useful to
know when dis-cussing left ventricular dysfunction.Pre-load is thought ofas volume
being pre-sented to the right heart.The right heart isa low-pressure
chamber,handling theinflux ofblood via the right atrium.Excessvolume may be
presented to the pul-monary vasculature,resulting in pul-monary congestion or
pulmonary edema.Preload problems can occur from leftheart failure causing fluid to
back up intothe pulmonary arterial tree,or may also bedue to reduced compliance in
the left ven-tricle.Rarely isolated right-sided ventricu-lar failure occurs,such as
from pulmonaryhypertension or right ventricular infarc-tion.Excess preload is
usually managedwith diuretic therapy or fluid restriction.Afterloadrefers to the
pressure in theaorta against which the left ventricle mustpump.This arterial
resistance or afterloadmay be increased in hypertension and aor-tic
stenosis.Afterload may also be relativeto the pumping capacity ofthe left ventri-
cle;hence normal blood pressures mayimpair a failing heart.Afterload reductionusing
vasodilators,especially angiotensin-converting enzyme (ACE) inhibitors,is
animportant treatment in heart failure,cer-tain valvular abnormalities,and
hyperten-sion.For instance,afterload reduction insystolic dysfunction reduces the
work ofthe left ventricle against the normal arter-ial pressure.This reduces demand
on theheart.Compliancerefers to the ability ofthe heart to distend.Reduced
compliancein the left ventricle is described as a stiff-ness or alteration in the
diastolic filling ofthe left ventricle.Ifthe left ventricle doesnot fill properly
during the cardiac cycle,pulmonary congestion can occur,eventhough the apparent
forward flow ofblood is not impaired.Left ventricular systolic dysfunctioncan be
tolerated within the reserve capaci-ty ofthe individual,or may manifest itselfas
congestive heart failure.As noted aboveit can be due to insults,such as
myocardialinfarction,viral myocarditis,or directtrauma to the heart.In addition
there maybe global dysfunction due to more wide-spread ischemia,idiopathic
cardiomyopa-thy,or valvular abnormalities.Symptoms suggesting congestive
heartfailure include dyspnea on exertion,paroxysmal nocturnal dyspnea
(PND),nighttime cough,and ankle swelling.Patients with PND may sit up on the
sideofthe bed for a moment and then get upto drink a glass ofwater.Patients
withsevere heart failure may sleep in a sittingposition or slumped against a
countertop.On physical examination ofthe heartthere may be an S3gallop rhythm and
thepoint ofmaximal impulse (PMI) may beshifted laterally and inferiorly.In
additiona diffuse PMI may be present.A murmurofmitral insufficiency may be present
dueto dilated annulus ofthe heart.The neckveins,which should be flat with
thepatient�s chest being elevated 30�,may bedistended.On lung examination rales
maybe present from pulmonary congestionand there may be dullness to percussionfrom
pleural effusions.Diagnostic testing for patients withheart failure includes an
ECG,which mayshow Q waves ofa previous myocardialinfarction,elevated QRS amplitude
ofleftventricular hypertrophy,or low QRS ampli-tude in some patients with severe
myocar-dial dysfunction.An echocardiogram mayshow evidence ofdiastolic
dysfunctionthrough measurements ofcompliance,ormay show wall motion abnormalities
andreduced ejection fraction.Management ofcongestive heart fail-ure is indicated
when evidence ofdecom-pensation is present.Decompensation ismanifested by increased
symptoms ofdys-pnea on exertion or PND,the presence ofan S3gallop rhythm,distended
neck veins,or an increase in peripheral edema.22Thedecision is then made whether or
not toadmit the patient to the hospital for treat-ment or to advanced treatment as
an out-patient.This is determined more by theseverity ofthe heart failure than
theurgency ofthe surgery.In either case themanagement includes starting or increas-
ing diuretic therapy,reducing afterload,and in some cases,increasing
contractilityofthe heart.Ifa diuretic has not been pre-scribed,furosemide 20 mg
daily for 3 to 4days should suffice in reducing total bodysalt and water.Ifa
diuretic has alreadybeen prescribed,doubling ofthe dose isindicated.Rarely a second
diuretic such asmetolazone would be added to boost theloop diuretic.Afterload
reduction is a key tenet in thetreatment ofcongestive heart failure.23AnACE
inhibitor is first-line treatment forcongestive heart failure and would beadded or
increased in dose during anepisode ofdecompensated congestive
heartfailure.Typically the systolic blood pressureis lowered to between 90 and 110
mm Hgunless significant hypertension was in-volved in the decompensation.After
appro-priate diuretic therapy and ACE inhibition,attention may be turned to
systolic contrac-tility.In cases ofdilated cardiomyopathythe addition ofdigoxin can
be helpful.Its
Medical Management ofthe Surgical Patient23applicability in other types ofheart
failureis questionable.Digoxin therapy should beguided by serum digoxin levels.In
addition,treatment ofdecompensated congestiveheart failure should include
monitoring ofelectrolytes.Ifa patient�s known congestiveheart failure is
compensated,the patient�ssurgical risk is greatly reduced toward nor-mal.24Ifthe
patient has reasonable func-tional capacity,for instance is able to walktwo blocks
or more without shortness ofbreath,the risk factor ofheart failure can
bediscounted,and the patient can come tosurgery.In summary a patient with decom-
pensated heart failure is at high risk formajor cardiac events,but this risk can
begreatly reduced with appropriate manage-ment,including diuretic
therapy,afterloadreduction,and digoxin therapy when need-ed.Diastolic
decompensation is usuallytreated acutely with diuretic therapy alone,using
afterload reduction and the use of�-blockers ifhypertension is present or fur-ther
treatment is needed.While �-blockersare often used in dilated cardiomyopathy,acute
use in the treatment ofdecompensa-tion is not recommended.Valvular Heart
DiseaseMost patients with valvular heart diseasewho have few symptoms or
limitations ofactivity can safely undergo most electivemaxillofacial
surgery.Diseased cardiacvalves pose two general risks:precipitationofcardiac
failure and susceptibility toinfective endocarditis.The likelihood ofcausing
failure or worsening preexistingcardiac failure is dependent on the loca-tion and
severity ofvalve pathology.Pro-phylactic antibiotics should be used for allpatients
with a cardiac value abnormalitywith a resultant murmur who undergomaxillofacial
procedures in which bleed-ing occurs (Tables 2-3 and 2-4 ).Mitral StenosisMitral
stenosis is almostalways a sequela ofchildhood rheumaticheart disease,although a
definite historycan be obtained in only halfofsuch cases.Fortunately the incidence
ofnew cases ofthis problem has decreased substantiallysince the use ofantibiotics
to managestreptococcal infections became commonpractice.The rheumatic disease
processcauses valve fibrosis,fusion,and calcifica-tion.These changes limit valve
motion,thus restricting the flow ofblood into theleft ventricle.The latency period
is usually15 to 20 years.Once valve obstructionoccurs the patient will begin to
suffergradually worsening exertional dyspneaand fatigue due to pulmonary
vascularcongestion and progressive right heartfailure.Left arterial enlargement may
leadto the appearance ofatrial fibrillation (AF)with possible atrial thrombus
formationand systemic arterial embolization.25,26Examination ofthe patient with
clini-cally significant mitral stenosis may revealan early diastolic opening snap
followedby a low-pitched murmur and a loud firstheart sound.Patients in AF will
character-istically have an irregularly irregular pulse.A chest radiograph will
reveal an enlargedleft atrium,pulmonary vascular enlarge-ment,and in more severe
cases right ven-tricular hypertrophy.An ECG may revealAF,left atrial
enlargement,and right ven-tricular hypertrophy.Echocardiography isTable 2-3Cardiac
Conditions Associated with Infectious EndocarditisHigh-Risk Category: Prophylaxis
RecommendedProsthetic cardiac valvesPrevious infectious endocarditisComplex
cyanotic congenital heart diseaseModerate-Risk Category: Prophylaxis
RecommendedMost other congenital malformationsAcquired valvular
dysfunctionHypertropic cardiomyopathyMitral valve prolapse with valvular
regurgitationNegligible-Risk Category: Prophylaxis NOT RecommendedCoronary artery
bypass graftMitral valve prolapse without regurgitationPhysiologic,functional,or
innocent heart murmurIsolated secundum atrial septal defectSurgical repair ofatrial
septal defect;patent ductus arteriosusPrevious rheumatic fever without valvular
dysfunctionOral Procedures in which Prophylaxis is RecommendedDental extractions
and biopsiesPeriodontal proceduresDental implant placementPeriapical endodontic
proceduresIntraligamentary local anesthetic injectionsDental prophylaxis when
bleeding is expectedOther procedures causing intraoral bleedingOral Procedures in
which Prophylaxis is NOT RecommendedRoutine local anesthetic injectionIntracanal
endodontic therapySuture removalTaking impressions
24Part 1: Principles ofMedicine,Surgery,and Anesthesiausually the definitive test
used to detectand characterize mitral stenosis.Patients with severe mitral stenosis
whorequire elective surgery may need preopera-tive mitral valve commissurotomy or
valvereplacement.AF may be managed by preop-erative digitalization or �-sympathetic
block-ade;pulmonary congestion is treated withdiuretic therapy.Patients with a
known orsuspected atrial thrombus are usually onchronic anticoagulant therapy,which
mayneed temporary alteration.Surgeons shouldnote the compromised cardiac output
ofpatients with mitral stenosis.Acute pulmonary edema is notuncommon following
noncardiac surgeryon patients with significant mitral steno-sis,particularly
ifexcess fluid replacementwas given.An additional problem facingthese patients is
diminished pulmonarycompliance that may require postopera-tive mechanical
ventilation longer than isusually necessary.Mitral RegurgitationMitral regurgita-
tion or insufficiency is most commonlythe result ofdamage or dysfunction due
tocoronary artery disease or from priorrheumatic heart disease.The incompetentvalve
prompts left ventricular enlarge-ments as the heart works and expands tomaintain
cardiac output.Symptoms ofcongestive failure appear as regurgitationworsens and the
enlarging heart transi-tions to the decompensation (right) sideofthe Frank-Starling
curve.Physical examination ofthe patientwith significant mitral regurgitation
willreveal an apical point ofmaximal impactdisplaced inferolaterally,an
apical,high-pitched,holosystolic murmur,and a thirdheart sound (gallop rhythm).Left
ventricu-lar hypertrophy and AF may appear on anECG.Echocardiography will help
define theextent ofvalve disease and,with a measure-ment ofend-systolic left
ventricular dimen-sion,the prognosis can be determined (adimension ofmore than 55
mm indicatesleft ventricular dysfunction).Doppler stud-ies or cardiac angiography
can be used todetermine the severity ofdysfunction.Patients with failure secondary
to initialregurgitation are medically managed withsodium
restriction,digoxin,diuretics,andpreload- and afterload-reducing vasodila-
tors.Eventually surgical valve repair orreplacement may be necessary.There is
little increased risk duringmaxillofacial surgery for patients withwell-controlled
mitral regurgitation.Thesurgeon and anesthesiologist must guardagainst the
pulmonary edema to whichthese patients are prone.Monitoring ofpulmonary capillary
wedge pressure willhelp guide therapy.Mitral Valve ProlapseMitral valve prolapse is
a common form ofmitral regurgitation,most frequently seenin young women,in which
one or both ofthe mitral valve leaflets prolapse into theleft atrium during
systole,allowing varyingdegrees ofregurgitation to occur.It is char-acterized by a
midsystolic click followed bya late systolic murmur.Symptoms includepalpitations
and chronic fatigue,but it canbe asymptomatic;echocardiography isdiagnostic.The
prevalence ofmitral valveprolapse in women and the general popula-tion has been
overestimated,with morerecent study showing a prevalence ofabout3%,equally
distributed among men andwomen;symptoms have been overestimat-ed as well.27Mitral
valve prolapse is usuallymanaged symptomatically,using �-sympa-thetic antagonists
to control palpitations.28As with other causes ofmitral regurgi-tation,with medical
management there islittle increased risk for anesthesia andsurgery.Patients should
have ECG monitor-ing to detect intraoperative dysrhythmias,and those with a murmur
should be givenantibiotics to prevent infective endocarditis.Aortic
RegurgitationAortic regurgita-tion or insufficiency occurs when the Table 2-
4Antibiotic Regimen for Prophylaxis ofInfectious
EndocarditisSituationAntibioticRegimenStandard AmoxicillinAdults:2 g orally 1 h
before procedureprophylaxisChildren:50 mg/kg orally 1 h before procedure*Penicillin
allergicClindamycinAdults:600 mg orally 1 h before procedureorChildren:20 mg/kg
orally 1 h before procedure*azithromycinAdults:500 mg orally 1 h before
procedureorChildren:15 mg/kg orally 1 h before procedure*clarithromycinAdults:500
mg orally 1 h before procedureChildren:15 mg/kg orally 1 h before procedure*Unable
to take AmpicillinAdults:2 g IM or IV within 30 min before oral
medicationprocedureChildren:20 mg/kg IV within 30 min before procedure*Unable to
take oral ClindamycinAdults:600 mg IV within 30 min before proceduremedication and
orChildren:20 mg/kg IV within 30 min before pencillin
allergiccefazolinprocedure*Adults:1 g IM or IV within 30 min before
procedureChildren:25 mg/kg IM or IV within 30 min before procedure*IM =
intramuscularly;IV = intravenously.*Total children�s dose should not exceed adult
dose.
Medical Management ofthe Surgical Patient25aortic valve becomes partially incompe-
tent,resulting in a backflow ofaorticblood into the left ventricle during dias-
tole.This causes left ventricular volumeoverload resulting in hypertrophy
andincreased wall thickness,both ofwhichincrease myocardial oxygen
requirements.Patients with clinically significant aor-tic regurgitation will report
unusualawareness oftheir heartbeat,prominentneck pulsations,and symptoms ofpul-
monary congestion at rest that resolveduring exercise.Examination reveals awidened
pulse pressure,a bisferious(bifid) carotid pulse,an inferolaterally dis-placed and
prolonged apical PMI,anddiastolic decrescendo murmur at the base.In severe cases
there may be a third heartsound and apical low-pitched diastolic(Austin Flint)
murmur.The ECG will reveal left ventricularhypertrophy,and a chest radiograph
willshow left ventricular and aortic rootenlargement.Echocardiography with
orwithout a Doppler is used to diagnose andcharacterize aortic
regurgitation.Patientswith significant aortic regurgitation will betreated with
vasodilators such as calciumchannel blockers or ACE inhibitors.�-Blockers should be
avoided since they canprolong diastole,increasing the regurgitantflow.Eventually
aortic valve replacementmay be necessary.Low-risk patients have anear-normal sized
left ventricular cavity,while high-risk patients nearing the time foraortic valve
replacement show enlargementofend-systolic left ventricular dimensions,corrected
for body surface area.29,30Typically bradycardia or vasodilationcannot be
tolerated;thus measures to pre-vent these changes should be used.TheECG lead
V5should be monitored periop-eratively for signs ofsubendocardialischemia.Pulmonary
artery catheterizationis useful in the perioperative period formeasuring left-sided
pressure and cardiacoutput.Afterload reduction may be helpfulin patients with
normal left ventricularfunction by reducing the regurgitant frac-tion,increasing
stroke volume,and decreas-ing left ventricular end-diastolic volumeand
pressure.Care must be taken whenusing afterload reducers to not allow
aorticdiastolic pressure to drop so low as to com-promise coronary perfusion.Aortic
StenosisAortic stenosis can involvethe valve itselfor be supra- or
infravalvular.Valve stenosis is most often due to either acongenitally bicuspid
valve (which occurs inabout 2% ofthe population) or an aging-related degeneration
ofa normal trileafletvalve.In either situation valve fibrosis andcalcification
occur and cause varying degreesofleft ventricular outflow obstruction.Symptoms
classically include exer-tional angina,syncope,or dyspnea.How-ever,many patients
can be asymptomaticuntil surgical stress unmasks problems.Physical examination
ofthe patient withsignificant aortic stenosis will typicallyreveal a weak
pulse,narrow pulse pressure,and a nondisplaced but accentuated andprolonged PMI.A
diamond-shaped sys-tolic murmur is heard at the base while afourth heart sound is
heard at the apex.Patients typically have little pulmonaryhypertension so that many
ofthe classicnoncardiac symptoms and signs ofheartfailure are not present.But
because the leftventricle depends on the end-diastolicboost from the left
atrium,the develop-ment ofAF can be catastrophic and shouldbe suspected in a
patient with aortic steno-sis who suddenly deteriorates.An ECG shows left
ventricular hyper-trophy,while the chest radiograph revealsleft ventricular and
ascending aorticenlargement and calcification.Echocar-diography can be used to
define the valvu-lar pathology,and cardiac angiography isused to determine the
pressure gradientacross the valve and to check the status ofthe coronary
arteries.Severely stenoticvalves may require surgical replacement.Patients with
mild-to-moderate dys-function requiring maxillofacial surgerytypically require
little modification in sur-gical or anesthetic management.The aor-tic valve opening
must be narrowed to75% ofits normal size before obstructivesigns occur.Ifaortic and
mitral stenosescoexist,the problems due to mitral steno-sis will
predominate.Perioperative risks inpatients with isolated aortic stenosis arehighest
ifthe history includes exertionaldizziness,syncope,or angina and the pres-ence
ofcoronary artery disease.The preservation ofsinus rhythm isimportant in these
patients.Tachydysrhyth-mias must be avoided since the atrial �kick�supplies needed
left ventricular filling.Supraventricular tachycardias should betreated immediately
with direct current car-dioversion.Sinus tachycardia may requireadministration ofa
�-sympathetic antago-nist.Bradycardia is also harmful,and ratesbelow 45 bpm should
be increased withatropine.Anesthetics that cause myocardialdepression should be
used cautiously,ifatall,and systemic vascular resistance shouldbe maintained.The
ECG lead V5 should bemonitored for signs ofischemia;ifdetected,coronary obstruction
must be differentiatedfrom insufficient coronary filling pressuredue to aortic
stenosis.Prosthetic Heart ValvesPatients withprosthetic heart valves represent a
specialsituation in which properly functioningvalves have essentially normal
cardiacfunction but may have new problemsdirectly related to the artificial valve
itself.These patients are susceptible to endo-carditis (particularly
staphylococcal),redcell destruction by the valve,prostheticvalve obstruction by
thrombosis or pan-nus formation,and paravalvular regurgi-tation.Serum
bilirubin,lactate dehydroge-nase,and reticulocytes should bemeasured to detect
occult hemolysis.Patients with mechanical (not biopros-thetic) valves are on
chronic anticoagulanttherapy that needs perioperative manage-ment.Patients with
prosthetic valvesshould be given antibiotics to preventinfective endocarditis.
26Part 1: Principles ofMedicine,Surgery,and AnesthesiaCongestive Heart Failure The
normal myocardium responds toincreased physiologic demands by increas-ing the
frequency ofcontractions and bydilating through the Frank-Starling mecha-nism,which
increases contractility (the end-diastolic wall tension).Heart failure occurswhen
the heart�s compensatory mecha-nisms fail to handle the hemodynamic load,causing
blood to back up into the pul-monary vasculature,right heart,and majorvenous beds
such as the portal system.Failure can be produced in two basicways.First,the heart
can be overwhelmedby excessive loads,such as elevated preload(venous return;eg,by
hypervolemia) orincreased afterload (resistance to ejection;eg,by elevated total
peripheral resistanceor aortic stenosis).Second,the heart�s abil-ity to compensate
for increased demandscan be compromised,such as by myocar-dial infarction or
cardiomyopathy.Long-term management requires thatboth excessive preload and
afterload bemodulated.Preload is lessened by limitingintravascular volume through
the use ofdietary sodium restriction and diuretics,and by venodilation with drugs
such asnitrates.Afterload is reduced through theadministration
ofvasodilators.Cardiaccontractility is augmented by digoxin.Angiotensin-converting
enzyme inhibitorsare another common therapeutic drug forfailure.Finally,physiologic
demands onthe heart are controlled by advising thepatient to get adequate rest and
avoidstrenuous exercise.A failing heart produces many signsand symptoms that vary
according to theseverity ofthe decompensation.Dilationofthe heart as it tries to
compensate canbe detected on a posteroanterior chestradiograph.The chest film will
also showincreased pulmonary vascular markingsthat occur as pressure forces fluid
intointerstitial spaces and alveoli,producingpulmonary edema.The signs ofrales
anddecreased breath sounds in dependentportions ofthe lungs,and symptoms suchas
dyspnea at rest or on exertion,paroxys-mal nocturnal dyspnea,and orthopneacommonly
occur.Failure ofthe heart topropel blood out ofthe systemic venoussystem can
produce increased interstitialfluid in the lower legs which is revealed aspitting
edema ofthe feet,ankles,and evenshins,increased central venous pressuregiving
jugular venous distention,and por-tal hypertension causing hepatomegaly.When
surgery is contemplated for apatient with a history ofcongestive
heartfailure,preoperative steps should be takento optimize the patient�s physical
status.The patient should be questioned about theamount ofexertion necessary to
producedyspnea and about how many pillows arenecessary while sleeping to prevent
orthop-nea,in order to quantitate the severity ofthe cardiac disability.Nocturnal
cough andrestlessness and easy fatigability can beearly symptoms ofproblems.Signs
ofcon-gestive failure include jugular venous dis-tention,presence ofa third heart
sound(gallop rhythm),pulsus alternans,basilarrales,and pitting edema.A chest radi-
ograph and ECG should be used to mea-sure heart size,to visualize the lung
fields,and to help detect AF.Ifpoorly compensat-ed failure is detected,the risk
ofpostopera-tive pulmonary edema is raised by 25%.31Patients prone to failure can
beimproved by increased attention to sodiumand water restriction and to their
compli-ance with medications such as diuretics,digoxin,and preload and afterload
reduc-ers.Potassium levels should be normalized.Mild preoperative hypokalemia can
bemanaged by oral replacement therapy orintravenous administration at a rate ofupto
10 mEq/h in concentrations up to 30 mEq/L.Patients taking digoxin shouldhave serum
levels measured.Signs andsymptoms ofdigoxin toxicity such as nau-
sea,diarrhea,anorexia,and new dysrhyth-mias should prompt postponement ofsurgery
until levels are normalized.Con-sideration should be given to placement ofa central
venous line for monitoring peri-operative central venous pressure or forplacing a
Swan-Ganz catheter.Anindwelling arterial line can also be usefulfor monitoring mean
arterial pressure andfor obtaining samples for blood gas analy-sis.After intubation
the patient�s lung com-pliance should be monitored closely,because decreased
compliance is an earlysign ofpulmonary edema.Mini-doseheparin and elastic stockings
can be usedpostoperatively to decrease the likelihoodofdeep vein thrombosis and
pulmonaryembolization.Passive leg exercises andearly ambulation postoperatively
also helpprevent these problems.An early postoper-ative chest radiograph can reveal
earlysigns ofpulmonary edema,as does an ele-vation ofpulmonary capillary wedge
pres-sures.During recovery the patient�s physi-cal activity and emotional stress
should bekept low to reduce unnecessary demandson the heart.Cardiac
DysrhythmiasPatients with diagnosed or occult cardiacrhythm disturbances present a
manage-ment challenge to the surgeon and anes-thesiologist in the perioperative
period.Dysrhythmias can compromise cardiacoutput leading to myocardial
ischemia,cerebral ischemia,congestive failure,orshock.In addition,dysrhythmias can
pre-dispose towards the formation ofintracar-diac thrombi and subsequent
systemicembolization.Patients with significant dysrhythmiasmay or may not have
symptoms.The ten-dency ofdysrhythmias to compromisecardiac function frequently
depends onoverall cardiac health.For example,anotherwise healthy individual can
easily tol-erate heart rates at the extremes oftherange of40 to 180,whereas someone
witha diseased heart would be less tolerant.Anesthesia and surgery are capable
ofunmasking a tendency toward dysrhythmiasthrough vagal stimulation,stress-
relatedrelease ofcatecholamines,drug-induced his-tamine release,dysrhythmogenic
drugs such
Medical Management ofthe Surgical Patient27as inhalational anesthetics,and hypoxia
dueto inadequate ventilation.Statistically,peri-operative dysrhythmias,particularly
duringintubation,are most common in patientswith preexisting dysrhythmias or heart
dis-ease,or who are on digoxin medication orundergo surgery and anesthesia for
longerthan 3 hours.In addition,surgery near thecarotid sinus can cause
atrioventricular con-duction disturbances due to the stimulationofintercostal
nerves.The presence ofsignificant cardiac dys-rhythmias can often be detected based
onsymptoms reported during a medical histo-ry,such as intermittent
palpitations,unex-plained syncopal episodes,and transientischemic
attacks.Determination ofpulserate and rhythm should be obtained duringthe physical
examination.An ECG shouldbe obtained in all patients with either sus-pected or
diagnosed dysrhythmias.Atrial DysrhythmiasThe most commondysrhythmia is sinus
tachycardia with a heartrate of100 to 180.Such an elevated ratecompromises cardiac
ouput by lesseningdiastolic filling time and increasing myocar-dial oxygen
consumption.Sinus tachycardiacan have many etiologies including
fever,hypovolemia,anemia,hypoxia,drug use,and hyperthyroidism.Therapy is directed
atthe underlying cause.32Paroxysmal Atrial TachycardiaParoxys-mal atrial
tachycardia (PAT) is a frequentdysrhythmia with an atrial rate of140 to 240and a
lower ventricular response rate.PATcan be due to digoxin toxicity or
myocardialischemia,but is usually due to reentrantpathways between the atria and
ventricles.The rhythm is unstable,reverting backto sinus in almost all cases.Risk
ofsurgicalprocedures is not elevated with a history ofPAT;however,ifthere have been
frequentor recent episodes ofPAT,a �-blocker mayhelp prevent tachycardia.Ablation
ofreen-trant pathways via electrophysiology pro-cedures is the treatment ofchoice
and isusually curative.33Atrial FlutterAtrial flutter (rate 250�300)commonly
appears with a 2:1 block produc-ing a ventricular rate of125 to 150.Patientsin
atrial flutter who undergo surgery have a50% mortality rate.It is therefore incum-
bent on the surgeon to identify and seekcorrection ofthis dysrhythmia preopera-
tively,with direct-current low-energy (25 to50 watt-seconds) cardioversion.Atrial
FibrillationAtrial fibrillation isthe second most common cardiac dys-rhythmia.It is
commonly asymptomaticbut characteristically produces an irregu-larly irregular
pulse rhythm and a fibrilla-tion pattern on ECG.The atrial rate isgreater than
350,whereas the ventricularrate varies from 140 to 180 bpm.Etiologiesinclude any
cause ofleft atrial hypertro-phy,thyrotoxicosis,and coronary arterydisease,and may
result from the excessiveuse ofcaffeine,cocaine,ethanol,diet pills,or nicotine,even
in healthy hearts.The physiologic compromise pro-duced by AF depends on the
ventricularresponse,myocardial health,and durationofthe dysrhythmia.A rapid
ventricularresponse increases perioperative mortalityby about 15%.Congestive heart
failure ormyocardial ischemia can appear abruptlyin susceptible patients going into
AF.Long-standing AF can allow the formationofan atrial thrombus and
subsequentthromboembolic complications.Preoperative management ofpatientswith a
history ofAF should include con-sideration ofdigitalization that by itselfmay
convert AF to a normal sinus rhythm.Intravenous verapamil can also be usedbut is
less successful in converting AF.Both digoxin and calcium channel antago-nists
decrease chronotropy,thus helping toslow the ventricular response rate to
morephysiologic levels.Amiodarone has beenshown to have prophylactic
value.34Careshould be taken to not allow the ventricu-lar rate to fall below
70.Acute onset ofAFis most effectively managed with directcurrent cardioversion
starting at about200 watt-seconds.Patients with chronicAF should be on
anticoagulants,whichmust be adjusted perioperatively.Premature Ventricular
ContractionsPre-mature ventricular contractions (PVCs) canbe due to many causes
including fever,hypoxia,drugs (including digoxin,amino-phylline,and inhalational
anesthetics),pul-monary artery catheters,electrolyte distur-bances,and myocardial
ischemia,or theymay be idiopathic.The significance ofPVCactivity,including more
complex ectopicventricular disturbances such as nonsus-tained ventricular
tachycardia,is controver-sial.Long-term mortality is not reduced inPVC patients
without apparent heart disease,but PVCs postmyocardial infarction or
withcardiomyopathy do carry increased risk.Thisis more a function ofunderlying
cardiomy-opathy rather than the dysrhythmia itself.The discovery ofsignificant
PVCactivity on a preoperative ECG warrants acomplete cardiac evaluation,and identi-
fied causes ofPVCs should be correctedpreoperatively.Development ofPVCs orruns
ofventricular tachycardia duringsurgery may signal cardiac ischemia orelectrolyte
abnormalities,which should beinvestigated and corrected.35,36The causeofPVCs should
be sought and corrected,but note that lidocaine is no longer used tosuppress
ectopic activity.Ventricular TachycardiaThe appearanceofthree or more PVCs in a row
is definedas ventricular tachycardia.It has a varietyofetiologies including
hypoxia,acidosis,myocardial ischemia,digoxin toxicity,hyper- or hypokalemia,and
hypercal-cemia.Prompt therapy consists ofintra-venous lidocaine or low-energy
direct-current cardioversion.37,38Heart BlocksAtrioventricular blockstake several
forms.A P�R interval greaterthan 20 ms constitutes a first degree atri-oventricular
block and is oflittle signifi-cance perioperatively in the absence of
28Part 1: Principles ofMedicine,Surgery,and Anesthesiaother cardiac
abnormalities.In seconddegree block,some atrial impulses are notconducted into the
ventricles.The Mobitztype I (Wenckebach) second degree blockhas a P�R interval that
progressivelylengthens until a nonconducted P waveoccurs and the cycle begins
again.Mobitztype I rhythms are usually due to digoxinexcess,myocardial ischemia,or
degenera-tion ofcardiac conduction tissue.Treat-ment with atropine is necessary
only forexcessively slow ventricular rates.Mobitztype II second degree blocks have
a con-stant P�R interval but frequent P waveswithout a ventricular response.This is
aworrisome dysrhythmia and perioperativeventricular pacing should be
considered.39Third degree atrioventricular blocksimply a complete block ofatrial
impulsesinto the ventricle.The ventricles thereforebeat at their low intrinsic rate
ofabout 45.Therapy usually requires the use ofapacemaker.Bundle branch blocks
present no directcontraindication to anesthesia and surgerybut usually signal some
underlying cardiacdisease.Pacing for bundle branch blocks isnecessary only
ifsymptomatic bradycardiaor complete heart block occurs.Patients who have permanent
cardiacpacemakers pose little increased risk dur-ing surgery over and above the
underlyingcardiac problem.Ifelectrocautery is neces-sary special care should be
taken to ensurethat it is properly grounded.A magnet toconvert a demand pacemaker
to the fixedrate mode should be available in the oper-ating suite.Surgery in the
Patient with Respiratory ProblemsGeneral Assessment ofAirway and LungsMaxillofacial
surgery itselfhas minimaleffect on pulmonary function comparedwith general thoracic
or abdominalsurgery,except when tissue is being trans-ferred from the thorax to the
maxillofacialregion.However,maxillofacial surgery doessometimes involve prolonged
general anes-thesia,and procedures can compromise theupper airways.Therefore,it is
important todiscover and treat airway and lung abnor-malities preoperatively
or,when not possi-ble,make necessary compensations in sur-gical and anesthetic
plans.The medical history should ascertainthe following about the status ofthe
venti-latory system:the presence ofsymptomssuch as wheezing,productive cough,andlow
exercise tolerance;the use ofpul-monary medications;cigarette smoking;prior
thoracic surgery or trauma;and pre-viously diagnosed pulmonary diseasesincluding
asthma,pneumonia,chronicobstructive pulmonary disease (COPD),or tuberculosis.In
physical examination,points ofsignificance to the assessment ofthe respiratory
system include a carefulinspection ofthe nasal airways,ausculta-tion oflung fields
for abnormal sounds,inspection ofmucosa and nail beds forsigns ofcyanosis or
clubbing,and mea-surement ofthe respiratory rate.40,41A plain chest radiograph is
useful fordetecting diffuse or localized parenchymaldisease,pulmonary
edema,hyperinflation,and consolidations such as pneumonia orneoplasms.However,the
yield from rou-tine preoperative chest radiographs is lowin patients without a
history or examina-tion suggestive ofpulmonary disease.Some pulmonary function
testing canbe performed at bedside,such as thebreath-holding test.The breath-
holdingtest involves having a patient make a max-imum inspiration and then hold
thebreath for as long as possible.Inability tohold one�s breath for at least 15
seconds isindicative ofsignificant pulmonary prob-lems.Spirometry is another useful
bedsidetest for assessing pulmonary functionalthough a delay in surgery is
usuallyunwarranted.Surgeons should requestformal pulmonary function testing
(PFT)for all patients in whom lung disease issuspected.PFTs help gauge
respiratoryreserve and measure the potentialresponse to measures taken to
improvelung function.42,43Measurement ofarterial blood gases(ABGs) is frequently a
part ofpulmonaryfunction testing.ABG determinationserves both as a baseline for
intra- andpostoperative measurements,and helpsassess the status ofpulmonary
gasexchange.A low partial pressure ofoxygen(PaO2)may be due to
hypoventilation,diffu-sion impairment,shunting,or a ventilation-perfusion
inequality,the last being the mostcommon cause.Anelevated partial pressureofcarbon
dioxide (PaCO2)is a sign ofhypoventilation either due to an inadequaterespiratory
rate or depth,or to a ventilation-perfusion inequality.Intraoperative capnog-raphy
and intra- and postoperative oximetryhave reduced the need for frequent
ABGsampling.Oximetry is also beneficial duringthe first few hours after
maxillofacial surgery,when respiratory insufficiency is most likelyto
occur.44AsthmaAsthma is characterized by episodes ofwheezing,cough,and production
ofmucous plugs.It is more common in chil-dren,although some adults will have newor
relapsed asthma later in life.Chronicuncontrolled asthma can lead to COPD,and
asthma complicated by cigarettesmoking can lead to COPD as well.Ques-tions
regarding history ofasthma,fre-quent or nocturnal coughing,shortness
ofbreath,dyspnea on exertion,and produc-tion ofmucous plugs are helpful in diag-
nosing asthma.Physical examination mayshow wheezing,particularly with
forcedexpiration.45,46Well-controlled asthma does not pose asignificant
perioperative risk.Patients withwell-controlled asthma should have a
doseofalbuterol by inhaler or nebulization priorto general anesthesia to prevent
intraopera-tive bronchospasm or larynogospasm.47,48The patient with a recent
history ofproblematic asthma is at significant risk
Medical Management ofthe Surgical Patient29when having general anesthesia
andsurgery.The bronchospasm that charac-terizes asthma can develop precipitouslyand
compromise ventilation,even withpositive pressure,and may be difficult toreverse in
time to prevent complications.As with most conditions ofthis nature,recognition and
prevention are the bestmanagement strategies.The airway narrowing in asthma isdue
to smooth muscle contraction,edemain airway walls,or mucous plugging ofair-
ways.Whereas bronchospasm is rapidlyreversible with muscle relaxants,edemaand
plugging are not.The likelihood ofan asthmatic episodeoccurring during surgery can
be judged bya few pieces ofhistoric information.Thefrequency,severity,duration,and
responseto therapy ofrecent asthma attacks willhelp gauge how well an individual�s
asthmais controlled and therefore the safety ofproceeding with surgical plans.When
questioning a patient with asth-ma,key factors are the frequency andnature
ofattacks,current medication use,last use ofsteroids,and an indication ofthe
severity ofasthma.A history ofmulti-ple emergency room visits for
asthma,hospitalization for asthma,history ofmechanical ventilation for
asthma,andsteroid dependency are indicators ofsevere asthma (Table 2-5).For many
years aminophylline-liketreatment was the mainstay ofasthma andCOPD
treatment.Several medicationshave replaced aminophylline and theo-phylline
treatment.For acute treatmentalbuterol by inhaler or nebulized adminis-tration is
used.The usual dose is 1 to 2actuations ofa metered-dose inhaler or anebulization
treatment every 4 to 6 hoursas needed,although hospitalized patientsmay receive
dosing more frequently.Inaddition,oral or parenteral steroid treat-ment is used
more liberally than in pastyears.Patients who are wheezing and areto undergo
surgical treatment are usuallygiven steroids to reduce wheezing and thechance
ofanesthesia-induced laryn-gospasm and bronchospasm.Steroids arethen rapidly
tapered and discontinuedover 3 to 7 days postoperatively.49Maintenance therapy in
asthma hasalso broadened to include inhaled steroids,long-acting �-
agonists,antileukotrienedrugs,and theophylline.50�52Inhaledsteroids using metered-
dose inhalers ordry-powder inhalation devices are givenon a regular dosing schedule
and are notabsorbed,preventing systemic complica-tions ofsteroid use.Prolonged
corticosteroid use carriesits own risks as is discussed later in thischapter.The
surgeon should confer withthe physician managing a patient�s asthmato ensure that
the patient has recently beenevaluated and that the steroid regimenprovides the
least amount ofdrug that isstill effective.Ifpossible the patient maybenefit from a
switch to inhaled cortico-steroid use through metered-dose inhalersthat may help
minimize systemic effects.Intra- and postoperatively asthmaticpatients should be
monitored for theappearance ofincreased airway resistance,wheezing,pulsus
paradoxus,tachycardia,fever,hypoxemia,hypercapnia,and acido-sis.Atelectasis is
common in asthmaticsand causes an increased risk ofbacterialpneumonia,which is why
thorough pul-monary examinations must be given atfrequent intervals during
recovery.49Chronic Obstructive Pulmonary DiseaseChronic obstructive pulmonary
disease(COPD) is an all-encompassing term forlung diseases characterized by loss
oflungtissue and its surface area.It includeschronic bronchitis,emphysema,and
otherconditions,but these distinctions are rathervague and do not result in
differing man-agement.Alveolar loss from destruction inCOPD results in less surface
area toexchange gases and in lower smooth muscletone ofthe
bronchioles.Emphysematousblebs may replace normal lung tissue.Mid-dle- and large-
sized bronchi have lost theircilia and muscle tone,and exude excessmucus,causing
pooling ofsecretions andreduced clearance ofdust,smoke,and bac-teria.Symptoms and
signs ofCOPDinclude chronic cough,sputum produc-tion,shortness ofbreath,decreased
exercisetolerance,wheezing,and increased antero-posterior thoracic
diameter.Patients withadvanced disease may purse their lips toincrease
intrathoracic pressure duringexhalation,thus holding open airways thatwould
otherwise close prematurely.53A chest radiograph may show hyperlu-
cency,kyphosis,and depressed and flat-tened diaphragms.Pulmonary functiontests show
a reduced forced expiratory vol-ume in the first second ofexhalation(FEV1) and a
reduced forced vital capaci-ty/FEV1ratio.FEV1is compared to age,gender,and racial
norms,and an FEV1ofless than 80% ofpredicted normal is abnor-mal,with readings
ofless than 60 indicatingsevere obstructive disease.Arterial bloodgases may show a
loss ofoxygenation andelevated carbon dioxide,due to reduced gasexchange and an
alteration in the usual res-piratory drive.As the term implies,bron-chospasm in
COPD may be less responsiveto bronchodilators than in asthma.Surgery and anesthesia
for patientswith significant COPD usually brings fewintraoperative risks due to the
lung diseaseitself.However,the likelihood ofpostoper-ative pulmonary complications
is high inCOPD patients.Therefore,proper preop-erative identification and
preparation areimportant.Preparing COPD patients for surgeryusually involves
reversing pathology ableto be altered medically.Hydration toTable 2-5Questions for
Asthma PatientsFrequency and nature ofattacksUse oforal steroidsEmergency room
visitsHospitalizationMechanical ventilation
30Part 1: Principles ofMedicine,Surgery,and Anesthesiamobilize mucus
secretions,inhaled �-agonists by metered-dose inhaler or nebu-lization,and inhaled
ipratropium are usedto optimize preoperative therapy.Oral orparenteral steroids are
used ifwheezing isdetected prior to surgery.Production ofmucopurulent sputummay
indicate the need for preoperativeantibiotics to help improve COPD symp-
toms.Ampicillin,trimethoprim/sulfacombinations,or erythromycin are usedmost
commonly and are given in 7- to 10-day courses.54Cigarette smoking is the most
commoncause ofCOPD and further exacerbatessymptoms ifcontinued after
irreversiblelung pathology occurs.Reversible problemsthat smoking causes include
the release ofnicotine,production ofcarbon monoxide,mucus hypersecretion,impaired
ciliaryfunction,and impaired local lung immuni-ty.Preoperative cessation ofsmoking
for 24 hours allows a significant decline in plas-ma carboxyhemoglobin and nicotine
levels,but the rate ofpulmonary complicationsdue to smoking takes weeks to fall
aftersmoking is stopped.In the case ofcoronaryartery bypass grafting,the percentage
ofpostoperative pulmonary complications informer smokers does not begin to
approachthe rate seen in nonsmokers until after atleast 8 weeks ofabstinence from
smoking.55Other preoperative measures that canprevent postoperative problems in
patientswith COPD include good nutrition and cor-rection ofhypokalemia to improve
respira-tory muscle strength and familiarization ofthe patient with incentive
spirometry.Pre-operative teaching in the use ofincentivespirometry,cough/deep
breathing exercises,and early ambulation help the patient pre-pare for recovery
before the pain and recov-ery period from anesthesia occur.There are several
anesthetic considera-tions for patients with COPD.Volatileanesthetics provide
bronchodilatoryeffects and thus are useful.Nitrous oxide,on the other hand,may
cause problemsdue to its accumulation in bullae potenti-ating rupture and
production ofpneu-mothorax.The respiratory depressiveeffects ofnarcotics makes
their use inCOPD patients hazardous,especially ifitis likely that their effects
will outlast theduration ofneeded anesthesia.The techniques ofcontrolled ventila-
tion must be altered in patients withobstructive airway disease.Ventilatory
ratesneed to be slow enough (typically 6 to 10per minute) to allow sufficient
exhalationtime and to compensate for slower diffu-sion ofgases across
membranes.Careshould be taken to avoid high pressures tolessen the potential
ofruptured bullae.Generally COPD patients do best with largetidal volumes at slow
rates and do not needpositive end-expiratory pressure.56Surgery in the Patient
withRenal and Urinary Tract DiseaseThe kidneys play several roles in
helpingmaintain physiologic normalcy;they aretherefore important for continuing
orregaining homeostasis during and aftersurgery and anesthesia.The renal system
isnecessary to support the processes offluid,electrolyte,and acid-base
balance,drugmetabolism and elimination,blood pres-sure control through the renin-
angiotensinsystem,red blood cell production througherythropoietin production,and
vitamin Dhydroxylation.There are several diseases that canaffect one or more
aspects ofkidney func-tion.However,for the maxillofacial surgeona better gauge
ofthe degree to which thepatient�s ability to tolerate anesthesia andsurgery is
compromised is the adequacy ofrenal function.The glomerular filtrationrate
(GFR),normally 100 to 125 mL/minper 1.73 m2ofbody surface area in an adult,is the
single most useful measure ofrenalhealth.The GFR is measured clinically
bydetermining the clearance ofendogenouscreatinine.The body�s serum creatinine(SC)
load is highly dependent on musclemass,and the clearance ofcreatinine fromthe serum
depends on the number offunc-tioning glomeruli,a number that graduallydecreases
with age.Also,SC varies inverselywith creatinine clearance (CCR).Thus,anestimation
ofthe CCR in males involvesobtaining the level ofSC and then multi-plying its
reciprocal by factors that are cor-rect for muscle mass and age.CCR =(140 � Age in
yr) (Weight in kg) (SC) (72 kg)For females,the above result is multipliedby
0.85.Although much less accurate,measurement ofSC (normal is < 1.5mg/dL) can be
used to help gauge renalfunction.Although measurement ofbloodurea nitrogen is used
commonly to testrenal health,it is a crude measure and maybe misleading,especially
in patients withpoor nutrition or who have been bleedinginto the intestinal
tract.Serum electrolyte abnormalities cansignal significant renal disease.Poor
renalfunction will often result in decreased secre-tion ofpotassium causing
hyperkalemia ora concentrating defect leading to urinarysodium wasting and hydrogen
ion retentionwith resultant hyperchloremic metabolicacidosis.Other indications
ofrenal prob-lems include proteinuria,pyuria,and hema-turia,all detectable on
routine urinalysis.Chronic Renal InsufficiencyThe risks ofanesthesia and surgery in
thepatient with known renal insufficiencyvary according to the severity
ofrenalcompromise.Patients with mild to moder-ate renal insufficiency (GFR of25�50
mL/min) usually tolerate the perioper-ative period well ifproperly managed.When
renal function is severely impaired(GFR of10�25 mL/min) or frank failure ispresent
(GFR < 10 mL/min),complica-tions ofrenal origin are much more likely.Patients with
severe renal insufficiencyhave a 60% increase in perioperative mor-bidity and a 2
to 4% increased mortalitycompared to healthy patients.57Extrarenal problems can be
producedby renal insufficiency.Normochromic or
Medical Management ofthe Surgical Patient31normocytic anemia frequently occurs
dueto several factors,including decreased ery-thropoietin,decreased red cell
survivaltime,and bone marrow depression.Inaddition,uremia can also cause
decreasedplatelet aggregating ability and depressedplatelet factor 3
release.58Pericardial inflammation or effusionis commonly associated with chronic
ure-mia or hemodialysis,as is myocardial dys-function.End-stage renal disease is
almostalways complicated by systemic hyperten-sion.Patients with renal
insufficiency haveimpairment oftheir immune systems withheightened susceptibility
to bacterial,viral,and fungal infections.The causeseems to be faulty neutrophil and
lympho-cyte production and function.Many oftheother problems caused by renal
dysfunc-tion affect the gastrointestinal tract.Symp-toms
ofnausea,vomiting,diarrhea,andanorexia frequently accompany uremia.Acute stomatitis
and salivary adenitis canoccur,as can pancreatitis.The stomachand intestine linings
may undergo inflam-matory changes.Hepatitis C is present inabout 19% ofdialysis
patients.59Excessive water retention is most easi-ly managed by fluid
restriction,whichusually helps improve the hypo-osmolarstate,and sodium and
hydrogen ion bal-ance.Hyperkalemia before elective surgerycan be managed with
dietary potassiumrestriction and potassium-wasting diuret-ics.More acute potassium
control maynecessitate the use ofcation-exchangeresins,strategies to drive
potassium intra-cellularly,or dialysis.Hypertension andfluid retention may
necessitate diuretic usepreoperatively.In cases ofrenal failure,hemodialysis is
recommended to reversefluid,electrolyte,and acid-base problems,as well as
extrarenal disorders such as ure-mic immunodepression.Dialysis shouldbe performed
no more than 24 hours pre-operatively.Platelet counts are helpful toidentify
heparin-induced thrombocytope-nia.60The lower heparin requirements innewer dialysis
techniques prevent many ofthe residual anticoagulation problems ofthe
past.However,surgeons shouldremember the capability ofheparin toinduce
thrombocytopenia.Preoperativechest radiographs and an ECG can be usedto detect
myocardial dysfunction or peri-cardial problems due to uremia or chronicfluid
overload.Plans should include theuse ofprophylactic antibiotics even forminimally
invasive procedures.61�63Intraoperative management ofthepatient with severe renal
insufficiencyshould include careful cardiac monitoringfor dysrhythmias and fluid
overload.Intravenous fluids should be administeredin quantities only sufficient to
replaceinsensible fluid and blood losses,and befree ofpotassium.Ifa hemodialysis
vascu-lar access (shunt) is in place,it should beprotected from
trauma.Intraoperativehemostasis should be especially meticu-lous ifthe patient will
be dialyzed imme-diately after surgery.64,65After surgery,steps should be taken
tomaintain proper fluid and electrolyte bal-ance,particularly until dialysis can
bedone.Most surgeons delay postoperativehemodialysis for at least 2 to 3 days
tolessen the chance ofwound bleeding dur-ing heparinization.However,patients
withoral or nasal procedures commonly swal-low a significant amount
ofblood,whichincreases the blood�s nitrogen load andmay prompt earlier dialysis
than wouldotherwise be necessary.Extended nasogas-tric suctioning may help prevent
bloodswallowing when the likelihood ofswal-lowing large amounts is high.A
significant problem that the anesthe-siologist and surgeon face when managinga
patient with renal insufficiency is drugelimination and the toxic effects
ofsomedrugs on the kidney.Drugs commonlyused during maxillofacial surgery thatneed
to be avoided or used with care in thepatient with renal compromise
includecephalosporins,penicillin,and sulfa antibi-otics,nonsteroidal anti-
inflammatorydrugs,nondepolarizing muscle relaxants,and enflurane.Many references
are avail-able that list drugs and dosing modifica-tions needed in renal failure
patients.HypertensionEssential hypertension is one ofthe mostcommon disorders
ofadults,so it is notsurprising that a large percentage ofadultpatients who require
surgery have hyper-tension.With more people aware ofthehazards ofuntreated
hypertension,manypatients seeking the type ofcare offered byspecialty surgeons have
had their hyper-tensive status evaluated and a manage-ment regimen prescribed.Two
basic problems can arise in thehypertensive patient requiring anesthesiaand
surgery.The first is that untreatedchronic hypertension can damage manyorgan
systems,particularly the heart,kid-neys,and brain.The damaged organs maybe less
able to tolerate demands placed onthem during the perioperative period.Thesecond
problem is that for many hyperten-sive patients,the medications prescribedfor
controlling hypertension may dullsome ofthe natural responses the bodyuses to
counteract anesthetic and surgicalchallenges.66Statistically there is no increase
in theincidence ofadverse effects from untreat-ed hypertension as long as the
diastolicpressure is less than 110 mm Hg and noconcurrent medical problems
exist.Whenconferring with a patient the surgeon canusually gain an idea ofthe
likelihood ofhypertensive organ damage by attemptingto learn ofthe patient�s
compliance withantihypertensive regimens.The patient�sphysician can often supply
this informa-tion.Target organ damage can also bedetected by various physical and
laborato-ry examinations.Cardiac damage usuallymanifests initially with left
ventricularhypertrophy (LVH).This causes a pro-longed and displaced point
ofmaximalimpact ofthe heart apex on palpation.Inaddition LVH shows on ECG,chest
radi-ographs,and echocardiograms.With time,
32Part 1: Principles ofMedicine,Surgery,and Anesthesiasigns and symptoms
ofcongestive heartfailure arise predisposing the heart to dys-
rhythmias,ischemia,and the appearanceofpulmonary edema.67,68The renal damage caused
by chronichigh blood pressure usually consists ofnephrosclerosis.This may be
detectableby routine urinalysis,on which protein-uria,hematuria,or pyuria is
seen.Renaldamage may also cause serum creatininelevels to rise.Cerebral damage due
to hyperten-sion usually manifests later in life with anincreased incidence
ofstroke.In additionthe cerebral vascular system�s ability toautoregulate is
impaired so that a greaterperfusion pressure must be maintainedthan would otherwise
be necessary.Someclinicians also believe chronic hyperten-sion promotes the
progress ofcarotidatherosclerosis and therefore recom-mend that the surgeon
auscultate forcarotid bruits.Many ofthe vascular changes thatoccur because
ofchronic hypertension caneasily be seen in the one site where thesmall vessels are
visible;that is,the fundusofthe eye.Hemorrhages and exudatesseen on fundoscopic
examination typical-ly indicate similar changes in other vascu-lar beds.69There is
a variety oftreatment optionsavailable for hypertensive patients,includ-ing
diuretics,ACE inhibitors,angiotensinreceptor blockers (ARBs),�-blockers,calci-um
channel blockers,selective a1-blockers,and central a-blockers.The surgeon shouldbe
familiar with these drugs and their sideeffects and risks in surgery.70�72Diuretics
can cause hypokalemia andhyponatremia,necessitating screening ofelectrolytes prior
to surgery.ACEinhibitors and,less likely,ARBs can causehyperkalemia and decreased
renal perfu-sion.�-Blockers reduce heart rate andcontractility,although beneficial
effects ofdecreased myocardial demand and preser-vation ofnormal sinus rhythm
generallyoutweigh perioperative risks ofuse.Calci-um channel blockers may cause
bradycar-dia but are usually well tolerated.Selectivea-blockers may cause first-
dose hypoten-sion,but are also usually well tolerated.Central a-blockers may cause
drowsiness,depression,and dry mouth.73,74For the patient with poorly
controlledhypertension (systolic pressure over 200 mmHg,diastolic pressure over 110
mm Hg),thesurgeon should defer elective surgery untilbetter control is obtained and
any end-organdamage is detected;appropriate compensa-tions should be made in the
treatment plan.Acute treatment ofhypertension can includeclonidine given in 0.1 mg
increments,orintravenous antihypertensives such as enala-prilat,labetalol,or
nicardipine infusion.Sub-lingual nifedipine should not be used.Patients whose blood
pressure is wellcontrolled preoperatively usually exhibitlarge swings in their
blood pressure duringand after surgery.Hypotension usuallyresponds to fluid
administration.Hyper-tension can usually be tolerated ifit doesnot reach severe
levels.Excessive increasesin blood pressure can be managed withshort courses
ofadditional antihyperten-sive medications until anesthetic drugs orsurgery-related
stresses have stopped,allowing patients to return to their preop-erative
status.75Surgery in the Patient with Endocrine DisordersDiabetes MellitusThe impact
ofdiabetes mellitus on theanesthetic and surgical management ofapatient is highly
dependent on the type,severity,and degree ofcontrol ofthe dia-betes.Type 1
(insulin-dependent) dia-betes mellitusis due to impaired produc-tion by or an
insufficient mass ofpancreatic islet �-cells.Type 2 (non�insulin-dependent)
diabetesmellitusoccurs due to an altered number andaffinity ofperipheral insulin
receptors.Total insulin production may also bedepressed but might be elevated.76The
usual daily production ofinsulinby a lean adult is 33 U;approximately 3 to 5 U are
needed for each meal while the basalinsulin requirement is about 1 U/h.Theketosis-
prone diabetic patient produces lessthan 10% ofthe average daily
insulinrequirement,but the typical type 2 diabeticpatient produces an average of15
U/24 h.Type 1 diabetes presents the more sig-nificant challenge to the well-being
ofasurgical patient.Patients are usually leanand have had this disease since their
youth.Those with long-standing type 1 diabetescannot go without their insulin for
morethan 48 hours without diabetic ketoacido-sis (DKA) occurring.Hormones
thatincrease during periods ofphysiologicstress,including
cortisol,catecholamines,and glucagon,act to counter the effects ofinsulin,producing
a stress-induced glu-cose intolerance,even in many healthynondiabetic patients.This
is why type 1patients who depend on exogenousadministration oftheir insulin
commonlyhave increased insulin requirements frompreoperative emotional
stress,intraopera-tive anesthetic stress,and postoperativewound,physiologic,and
emotional stress.Studies have shown that elevated bloodglucose not only impairs
wound healing,but can also depress leukocyte and pancre-atic �-cell function.These
are reasons,inaddition to prevention ofDKA,for appro-priate insulin supplementation
during andafter surgery.43,77Type 1 patients,in contrast to type 2diabetics,have a
high rate ofsystemicproblems.Peripheral neuropathies arecommon,predisposing these
individualsto chronic lower leg and foot lesions,which should be detected and noted
pre-operatively and prevented perioperatively.Long-standing diabetics are also
atincreased risk for coronary artery diseaseand may suffer silent (painless)
ischemicepisodes due to myocardial neuropathy.78Insulin-dependent
diabetics,particularlythose with poor control,handle
infectionspoorly.Therefore,vigilance should be
Medical Management ofthe Surgical Patient33especially high for breaks in aseptic
tech-niques and consideration given to the useofprophylactic antibiotics.Type 1
patientsalso have enhanced platelet stickiness thatmay promote unwanted clotting in
surgi-cal flaps.The formation ofglycosylatedhemoglobin A1Cinterferes with
oxygenrelease into tissues.79A rational approach to managementofdiabetes assists in
maintaining glycemiccontrol perioperatively.Care should begiven to avoid
hypoglycemia at any timeduring surgery,and to prevent severehyperglycemia as
well.The general rangeofadequate control is between 120 and200 mg/dL.This would
involve decreasingthe usual morning insulin by one-halftoallow plasma glucose to
rise during thesurgery,but providing enough basalinsulin to prevent DKA.80,81Ifa
patient is to have relatively short-duration ambulatory surgery and isrequired to
consume nothing by mouththe morning ofsurgery,only halfthe usualmorning dose
ofinsulin should be given atthe time when intravenous access isgained.Surgery
should be early in themorning and intravenous glucose shouldbe given
intraoperatively.During surgerythe clinician should watch for signs ofhypoglycemia
such as tachycardia anddiaphoresis.The patient should then beencouraged to consume
some caloriesource by mouth within 3 hours aftersurgery is completed.Portable
glucosemonitoring is useful for intra- and postop-erative serum glucose
monitoring.82Patients requiring more major surgeryand longer duration general
anesthesia areusually best managed in a setting in whichan anesthesiologist can
monitor bloodglucose levels in the operating room andadminister insulin on an as-
needed basis.The morning insulin should be withhelduntil intravenous glucose is
available;then one-halfto three-quarters oftheusual dose can be administered and
sup-plemented intraoperatively by the anes-thesiologist.83,84When patients are
unlikely to enteral-ly receive their usual caloric supply post-operatively,their
insulin should be givenbased on periodic (every 6 h) plasma glu-cose
sampling.Insulin doses should begauged to keep the plasma glucose at 150 to 250
mg/dL until normal dietaryhabits and activity levels return.Thepatient�s primary
care physician can helpguide dietary decisions.Type 2 patients usually have fewer
sys-temic abnormalities due to diabetes andare less likely to suffer perioperative
com-plications.But when major surgery andgeneral anesthesia are
performed,thesepatients usually become hyperglycemic.Not uncommonly patients who
are wellmanaged on diet and oral hypoglycemicswill need temporary insulin
supplementa-tion in the intra- and postoperative peri-ods.As in type 1
patients,blood glucoseshould be kept at 150 to 250 mg/dL,withinsulin
supplementation based on period-ic sampling.85Thyroid DisordersThe need for normal
levels ofthyroid hor-mones to maintain the function ofmanyofthe body�s physiologic
functions makesproper thyroid gland function importantto the surgeon.The gland is
composed offollicles,each ofwhich is a lumen filledwith thyroglobulin,which is
produced bya single layer ofepithelial cells lining thefollicle.Thyroid
hormones,thyroxine (T3)and triiodothyronine (T4),are producedand stored in the
gland in a ratio of10 to15:1 (T3:T4) and are released on stimula-tion by thyroid-
stimulating hormone,ananterior pituitary hormone.Between thefollicles
parafollicular cells exist whichsecrete calcitonin,whose function is tohelp lower
serum calcium by blocking itsrelease from bone.The majority ofT3 and T4
releasedfrom the gland are bound to various carri-er proteins.Most circulating T3
is pro-duced by conversion from T4 in the liverand kidney.T3 is much more potent
thanT4,but only the unbound form ofeitherhormone is active,and in the case ofT3
aninactive form called reverse T3 (rT3) canbe formed.In normal states 35% ofT4
isconverted to T3 and 40% to rT3.However,in times ofphysical illness or
emotionalstress,or ifcertain drugs (such as cortico-steroids) are used,a higher
percentage ofT3 conversion to rT3 can occur.The most common laboratory
testsofthyroid function are (1) measure-ments oftotal thyroid hormone (T) lev-els
by radioimmunoassay (normal is5,012 pg/dL),in which high values indi-cate
hyperthyroidism and low values indi-cate hypothyroidism;and (2) T3 resinuptake,in
which unoccupied thyroid hor-mone binding sites on thyroid-bindingglobulin are
measured.High values ofT3resin uptake are associated with hypothy-roidism,whereas
low values are consistentwith hyperthyroidism.86HyperthyroidismSymptoms ofhyper-
thyroidism include weight loss,palpita-tions,and restlessness.Exophthalmosoccurs in
more severe cases owing toincreased amounts ofretro-orbital fat.Once
diagnosed,therapy usually beginswith antithyroid drugs such as propylth-iouracil or
methimazole.�-adrenergicantagonists can be used to control symp-toms until thyroid
hormone levelsdecrease.Autoimmune thyrotoxicosis canbe allowed time to resolve
spontaneously,or treatment with radioactive iodine canablate the gland.Total
thyroidectomy isseldom indicated,except for adenomas ormalignancy.87,88Surgery in
the face ofhyperthyroidismcarries high risks ofcardiac dysrhythmiasor failure,and
the potential for causing athyroid crisis.Therefore,elective surgeryshould be
deferred until thyroid hormonelevels are properly managed.Ifemergencysurgery is
necessary on a patient withpoorly controlled hyperthyroidism,�-sympathetic
antagonists can be used to help control the effects ofthyroid
34Part 1: Principles ofMedicine,Surgery,and Anesthesiahormones on the heart while
intravenoussodium iodide (1 g) can be administeredto help block hormone release
from thethyroid gland.The �-antagonist should becontinued postoperatively until
theadministered antithyroid drugs have takeneffect.Palpation ofthe thyroid
glandshould be gentle in patients with knownhyperthyroidism to avoid increasing
hor-mone release,and infections should beaggressively managed because they toomay
precipitate a thyroid crisis.89�91HypothyroidismThe hypothyroid patientpresents a
lesser surgical and anesthetic riskwhen compared with the hyperthyroidpatient.The
insufficiency ofthyroid hor-mones causes cardiac depression,respiratorydepression
with weakening ofthe muscles ofrespiration,hyponatremia,constipation,neurologic
problems with memory loss anddepression,and several other metabolicproblems.Signs
ofhypothyroidism includeweight gain,periorbital edema,bradycardia,slowed deep
tendon reflexes,generalizedmuscle weakness,and hair loss.The potential surgical
problems in apatient with untreated hypothyroidisminclude intra- or postoperative
heart fail-ure,hypotension,ileus,mental confusion,and delayed wound
healing.Therefore,thyroid replacement therapy is advisableprior to elective
surgery.In an emergencythe surgeon must remain alert to potentialproblems due to
the hypothyroidism andcompensate for them ifthey occur.92Adrenal Gland DisordersThe
adrenal gland,responsible for the pro-duction ofa variety ofhormones
includingcortisol,aldosterone,and androgens,playsa central role in regulating many
metabol-ic processes.The gland usually comes tothe attention ofsurgeons because
ofabnormalities in cortisol production.Theaverage daily secretion ofcortisol in
theadult is 15 to 17 mg (range 8�28 mg).Secretion follows a diurnal pattern,peak-
ing at about 3:00 or 4:00 am,and falling tolow levels at about 8:00 or 9:00
pm.Releaseofcortisol is regulated by adrenocorti-cotropic hormone (ACTH) secreted
by thepituitary,with ACTH release normallyincreased in time ofphysiologic stress.It
isnot unusual for plasma cortisol levels toremain elevated for up to 19 days
aftermajor surgery.Excessive release ofcortisol from theadrenal cortex (Cushing�s
disease) is rare.These patients show truncal obesity,hypertension,thin skin that
heals poorly,and glucose intolerance.These problemscan also be seen in patients on
long-termtherapeutic corticosteroids for problemssuch as inflammatory joint or
bowel dis-ease.Increased surgical risks faced bypatients with hypercortisolism
includedelayed wound healing and a tendency forinfections.Delay ofelective surgery
is war-ranted until excessive cortisol levels areunder control.Ifsurgery cannot
wait,techniques designed to compensate forpoor wound healing such as better vascu-
larized flaps and the use ofprophylacticantibiotics will be helpful.Adrenal
insufficiency is more com-monly seen due to exogenous therapeuticsteroid
administration than to primaryadrenal glandular disease.Exogenous cor-ticosteroids
will inhibit ACTH release.Current concepts ofsteroid supplementa-tion for surgery
hold that briefperiods ofsteroid use,low-dose steroid use,andalternate-day steroid
use do not suppressthe hypothalamic-pituitary axis.Thus,ifsteroids have been used
for less than 3 con-secutive weeks within the past year,thedose ofchronic steroids
is 5 mg ofpred-nisone or less,or ifalternate-day steroidadministration is used,no
supplemental(stress-dose) steroids are needed.93Onceadrenal suppression has
occurred,apatient is at great risk for problems duringmajor surgery due to their
inability tomount a significant cortisol response tothe stress.This may precipitate
an adrenalcrisis,signaled by the onset oflethargy,tachycardia,flank or abdominal
pain,vomiting,fever,restlessness,delirium,hypotension,or coma.Because mineralo-
corticoid production is not controlled byACTH,its levels remain normal.Prevention
ofproblems remains thefocus ofmanagement ofpatients prone toadrenal
insufficiency.For those patientsrequiring higher doses ofsteroids,it is pru-dent to
use stress-dose steroids periopera-tively.A typical dose is hydrocortisone 100 mg
intravenously on call to the operat-ing room,followed by 50 mg every 8 hoursfor 48
hours postoperatively.The usualdose oforal steroids or its equivalent intra-venous
dose can then be resumed.Notethat more minor procedures usually do notrequire
steroid supplementation.94,95Surgery in the Patient with Hepatogastrointestinal
DisordersLiver DiseaseSurgeons are well aware ofthe liver�s vitalroles in
processing nutrients,synthesizingprotein,and metabolizing drugs.Fortu-nately the
liver has a tremendous reservecapacity for maintaining function in theface ofeven
severe hepatic pathology.Protein synthesis is one ofthe princi-pal liver
activities.Ofproteins produced,the ones ofparticular concern to surgeonsand
anesthesiologists are albumin and sev-eral ofthe clotting factors.Hepatic pro-
duction ofalbumin is in the range of10 to15 g daily.Albumin helps maintain
theoncotic force necessary to restrict excessiveloss ofintravascular fluid into the
intersti-tium.Albumin also has a large number ofreactive sites and can therefore
reversiblybind to most drugs.Ifalbumin productionslows sufficiently that serum
levels fallbelow 2.5 g/dL,then edema,ascites,and anelevation in the free-to-bound
ratio ofadministered drugs can result.The vitamin K�dependent coagulationfactors
II,VII,IX,and X are made in theliver.A significant fall in their levels can beseen
with either severe hepatocellular dis-
Medical Management ofthe Surgical Patient35ease or with impaired vitamin K absorp-
tion due to biliary problems.The liver is responsible for the properfunction
ofseveral enzyme systems thathelp to limit drug actions.Plasmacholinesterase is
produced by the liver;bybreaking ester linkages it inactivates drugssuch as
succinylcholine and ester-typelocal anesthetics.The hepatic microsomalenzyme system
converts lipid solubledrugs into more water soluble ones thatcan be excreted by the
kidney.Agents suchas some benzodiazepines,lidocaine,meperidine,morphine,and
alfentanildepend on this system for elimination.The most common insults to the
liverthat affect the performance ofmaxillofacialsurgery are ethanol and infectious
hepatitis.In the first case many liver functions can becompromised,whereas in the
second case,not only is proper liver function jeopar-dized,the surgeon must also
help preventthe spread ofthe infection to others.96Other important consequences
ofliver disease include impaired glycogenstorage and gluconeogenesis;hyper-splenism
due to obstructed portal bloodflow,causing thrombocytopenia;and poorhandling
oflarge gastrointestinal nitrogenloads such as swallowed blood,whichalters the
level ofconsciousness in patientswith severe liver dysfunction.Significant liver
problems cause alarge number ofsigns and symptoms sothat detection is usually
straightforward.Laboratory tests ofliver function tend tobe nonspecific indicators
oftissue damagebut are commonly used to evaluatepatients with suspected liver
disease.Serum aspartate transaminase levels risebecause ofdamage to either
liver,heart,kidney,or skeletal muscles.Changes inserum alanine aminotransferase
(ALAT)levels,on the other hand,are more specif-ic for hepatocellular
disease.Lactate dehy-drogenase is commonly measured but isanother nonspecific
indicator oftissuedamage,although its isoenzyme-5 fractionis believed to be more
specific for liverdamage.Elevations in serum alkalinephosphatase indicate
obstructed bileducts.Measurement ofserum albuminhelps gauge the severity ofliver
disease,with levels ofless than 2.5 g/dL being sig-nificant;however,malnutrition
can alsocause hypoalbuminemia.Severe liver dis-ease is indicated by a prolonged
pro-thrombin time (PT) and a decreasedplatelet count.Suspicion ofan infectiouscause
ofhepatic disease mandates the useofimmunologic tests for signals
ofviraldisease.Hepatitis A,typically due to fecalcontamination offood and water,is
evi-denced by hepatitis A antibodies.Acutehepatitis B,transmitted parenterally
orvenereally,will stimulate production ofsurface and core antigen
antibodies;thechronic form is revealed by the presence ofonly surface antigen
antibodies.Non-A,non-B hepatitis,caused by several differ-ent viruses and usually
transmitted byinfected blood products,causes elevatedALAT but no hepatitis A or B
antibodies.Finally,hepatitis C (d-agent),seen mostcommonly in illicit drug users
and multi-ply transfused patients,causes the appear-ance ofd-agent antibodies and
in its acuteform coexists with hepatitis B.97�99Maxillofacial surgery in the
patientwith mild to moderate liver disease usual-ly presents few problems because
ofhepat-ic reserve.Borderline severe cases requirespecial perioperative attention
to preventcomplications or a deterioration ofliverfunction.Liver function
tests,especiallyserum ALAT measurement,are useful.APT and platelet count are
necessary todetect a potential coagulopathy.Intra-venous vitamin K (5 to 10 mg over
3 to 5 min) can be administered ifa deficiencyis suspected and will shorten an
abnormalPT in 4 to 12 hours.Fresh frozen plasmacan be used temporarily to make up
for avitamin K deficiency until the parenterallyadministered vitamin is
effective.Because patients with severe liver dis-ease have problems with improper
gluco-neogenesis,the surgeon should closelymonitor serum glucose
levels.Patientslikely to handle nitrogen poorly,particu-larly those with a history
ofhepaticencephalopathy,should be placed ondietary protein restriction.Ifit is
likelythat blood will be swallowed,the patientmay need measures to reduce
nitrogenabsorption in the intestines,such asadministration ofnonabsorbable antibi-
otics or the use ofa cathartic such as lac-tulose;consciousness should be
closelymonitored.Drugs used for anesthesia and analge-sia may need to be modified
in the patientwith hepatic disease.Drugs to avoid inpatients with severe liver
disease include allnonsteroidal anti-inflammatory
drugs,tetracyclines,pentazocine,and atenolol.Drugs for which dosages need to
bereduced include diazepam,chlordiazepox-
ide,meperidine,morphine,propoxyphene,theophylline,lidocaine,verapamil,andmost �-
sympathetic antagonists.Mostanesthetics are generally safe to use inpatients with
hepatic disease,althoughsome feel halothane,fentanyl,and nitrousoxide should be
avoided because oftheirpotential for causing liver toxicity.Peptic Ulcer
DiseasePeptic ulcers and gastritis are two ofthemost common afflictions
ofadults,butthey are usually easily controlled with H2receptor antagonists,which
reduce acidsecretion,or sucralfate that forms a pro-tective coat over lesions
shielding themfrom the effects ofpepsin and acid.Although many patients still use
antacids,side effects such as diarrhea (in magne-sium-based antacids),constipation
(inaluminum-based antacids),and sodiumoverload make them less desirable.Signs
ofactive gastrointestinal bleed-ing include unexplained anemia and aguaiac-positive
stools,but the process isusually diagnosed based on the presence ofepigastric pain
temporarily relieved byfood or antacids.Endoscopy is used toconfirm clinical
suspicions.
36Part 1: Principles ofMedicine,Surgery,and AnesthesiaBefore maxillofacial surgery
can beperformed in patients with a history ofgastritis or peptic ulcer disease or
predis-posed to these problems due to prolongedphysiologic stress,the surgeon
mustensure that the patient�s gastrointestinalproblem is being addressed
properly.Theclinician should verify that the patient iscompliant with either their
H2receptorantagonist regimen (cimetidine,800 mghs;ranitidine,150 mg bid;or
famotidine,40 mg hs) or with sucralfate (1 g qid).When the patient is unable to
take oralmedication,cimetidine (300 mg q8h),ran-itidine (50 mg q8h),or famotidine
(20 mgq12h) can be given intravenously or intra-muscularly.Patients with a
predisposition to gas-tritis or peptic ulcer disease should not begiven non-
steroidal anti-inflammatorydrugs (NSAIDs).The use ofcorticos-teroids in these
patients is controversial.There is no strong scientific evidence
thatcorticosteroids can cause peptic ulcers inmost patients,but many clinicians
avoidtheir use in these patients.Surgery in the Patient with Disorders ofConnective
Tissue and JointsRheumatoid ArthritisRheumatoid arthritis (RA) is a chronicdisease
causing not only polyarthritis butalso problems in serosal
surfaces,bloodvessels,muscle,skin,and bone marrow.Maxillofacial surgery in patients
with RArequires careful evaluation to discoverthe extent ofthe patient�s
abnormalitiesand to attempt to have those problemsunder reasonable control.Classic
signsand symptoms ofRA include morningstiffness ofinvolved
joints,symmetricinvolvement ofproximal hand joints,subcutaneous (rheumatoid)
nodulesover bony prominences or extensor sur-faces,elevated serum rheumatoid
factor,and marked bony erosions visible onradiographs.Nonarticular problems seen
with RAinclude pericarditis,pleuritis,pneumoni-tis,myopathies,vasculitis,bone
marrowdepression,and skin ulcers.Rheumatoid arthritis patients aretreated with five
classes ofdrugs:analgesics(NSAIDs),glucocorticoids,slow-actingantirheumatic drugs
(SAARDs),or dis-ease-modifying antirheumatic drugs(DMARDs),and
anticytokines.Analgesicsinclude acetaminophen,tramadol,andnarcotics.NSAIDs range
from over-the-counter ibuprofen to newer selectivecyclooxygenase-2 (COX-2)
inhibitors suchas celecoxib,rofecoxib,and valdecoxib.NSAIDs relieve pain and reduce
inflamma-tion but do not alter the course ofrheuma-toid arthritis.COX-2 inhibitors
do nothave any inherent benefit over olderNSAIDs other than less
gastrointestinaltoxicity.Glucocorticoids effectively sup-press inflammation,often
at low doses,butcarry their own substantial risks.SAARDsand DMARDs include
hydroxychloro-quine,sulfasalazine,methotrexate,andleflunomide.Methotrexate is now
consid-ered to be first-line treatment for activerheumatoid
arthritis.Penicillamine,aza-thiaprine,cyclosporine,and gold salts areseldom
used.Anticytokines include etaner-cept,infliximab,adalimumab,and anakin-ra.These
drug classes are often used incombination to control inflammation andslow the
progression ofthe disease.100�103Patients with RA who require endo-tracheal
intubation should be evaluatedpreoperatively for their ability to extend atthe
neck,open their mandible,and movetheir cricoarytenoid joints.An early symptom
ofneck involve-ment in RA is neck pain with radiation tothe occiput.Preoperative
cervical spinefilms should be considered to evaluate forsubluxation ofthe cervical
spine.104Thesurgeon needs to remain more vigilantthan usual to prevent long periods
ofoverextension or flexion ofinvolved joints.Patients with Raynaud�s phenomenonneed
their fingers and toes kept warmintraoperatively.Patients with Sj�gren�ssyndrome
will require special care to pre-vent eye desiccation.The skin ofRApatients is
commonly thin and easily dam-aged,so additional padding ofpressurepoints is
indicated.Preoperative PT andpartial thromboplastin time (PTT) mea-surement will
help detect circulating anti-coagulants due to the RA.Early postoper-ative
ambulation,heat treatments,andpossibly physical therapy ofaffected jointswill help
prevent prolonged stiffness.Other Connective Tissue DisordersThe patient coming to
surgery may haveother connective tissue disorders such assystemic lupus
erythematosus (SLE),pso-riatic arthritis,ankylosing spondylitis,der-
matomyositis,and scleroderma,whichhave similar perioperative concerns.Preoperative
assessment ofpatientswith SLE and other connective tissue disor-ders should include
a thorough history andphysical examination,a urinalysis,elec-trolyte panel
including blood urea nitrogenand creatinine,a complete blood count,and a PT and
PTT.Blood typing or screen-ing should be done in advance ofsurgery toevaluate for
blood compatibility.A chestradiograph and ECG are indicated for evi-dence ofpleural
or pericardial disease.105Patients who have taken glucocorti-coid therapy should be
screened for useofstress-dose steroids,as noted above.Consider stopping NSAID
therapy,ifpossible,to allow return ofplatelet func-tion.The time needed for this
varies from7 to 10 days for aspirin to 1 day foribuprofen.Generally NSAIDs other
thanaspirin should be stopped 3 to 4 days pre-operatively,and acetaminophen or nar-
cotics can be used to control pain duringthis time.There is no evidence that stop-
ping SAARDs or DMARDs prior tosurgery conveys any benefit.Anticytokinescan limit
immune response in severeinfections,and in maxillofacial surgerythese drugs should
be discontinued
Medical Management ofthe Surgical Patient371 week before surgery and resumed 2
weeks postoperatively.Sj�gren�s syndrome patients shouldhave artificial tears or
lubricating gel placedin the eyes during anesthesia.Pilocarpine,ifused,should be
held to avoid confusionover anesthetic complications ofbron-
chospasm,bradycardia,and tremor.Patients with ankylosing spondylitishave similar
spine concerns as RA patients.Scleroderma patients may have limitedmandibular
movement as a consequenceoftheir disease,causing difficulty withendotracheal
intubation.SLE patients mayhave low platelets,which is generally welltolerated
without excessive bleeding.Forcounts less than 50,000,intravenousimmunoglobulin may
be used to improvethe platelet count.SLE patients may alsohave evidence ofthe lupus
anticoagulant,manifest by an elevated PTT.The lupusanticoagulant,also referred to
as antiphos-pholipid antibodies,can produce throm-boembolism.Patients may be
treated withaspirin ifantibodies are present and therehave been no previous
thromboembolicevents,or may be fully anticoagulated,requiring adjustment
perioperatively.106Surgery in the Patient with Neurologic and
NeuromuscularDisordersSeizure DisordersSeizures are typically recurrent
transientparoxysms ofhyperactive brain function,which can appear as impaired
conscious-ness,involuntary movement,autonomicdisturbance,or psychic
experiences.Theycan result from known causes such asfever,ethanol
withdrawal,hypoglycemia,hypoxia,or brain damage,or be idiopath-ic.Most
investigators feel the fundamentalsite ofpathology is in the cerebral cortex,which
can be detected on an electroen-cephalogram (EEG).The reconstructive maxillofacial
sur-geon is likely to encounter patients whosuffer seizures secondary to head
trauma(Chronic recurrent seizures occur in 30%ofpatients with cerebral
hematomas,15%ofthose with depressed skull fractures,and 5% ofpatients hospitalized
withclosed head injuries).Chronic postheadtrauma seizures usually do not occur
until6 to 12 months from the time ofinjury.Patients providing a past history ofany
form ofseizure disorder (except per-haps febrile seizures in childhood) shouldbe
under the care ofor evaluated by a neu-rologist before undergoing major
electivesurgery.107Patients with well-documentedseizures and who are under good
controlcan safely have general anesthesia andsurgery.Control is usually obtained by
theuse ofantiseizure medications such asdilantin,phenobarbital,valproic acid,car-
bamazepine,ethosuximide,and clo-razepate.Most ofthese drugs can causesedation,which
can be additive with anes-thetic drugs.Side effects ofcarbamazepineand dilantin
include nausea,dizziness,diplopia,and rarely bone marrow depres-sion.Valproic acid
can inhibit liverenzymes,potentially causing oversedationwith barbiturates.Newer
drugs include lamotrigine,gabapentin,tiagibine,and topiramate.Mostofthese drugs can
cause sedation,which canbe additive with anesthetic drugs.Other sideeffects vary
with each drug.When evaluating a patient with aseizure disorder for surgery,the
clinicianshould learn ofthe frequency,type,dura-tion,and sequelae ofseizures to
gauge thedegree to which control ofthe seizures hasbeen obtained.Serum drug levels
oftheseagents can be obtained to help check com-pliance and predict the appearance
ofseizures,ifsubtherapeutic,or possibletoxic reactions.Cerebrovascular
DiseasePatients with a history ofcerebrovascularaccidents,such as transient
ischemicattacks (TIAs) or strokes,requiring max-illofacial surgery need evaluation
by theirprimary physician before surgery.In mostcases little can be done
preoperatively todiminish the risk ofa stroke duringsurgery.A careful neurologic
examinationshould be performed preoperatively todocument residual damage,and
againpostoperatively to detect evidence ofintraoperative problems.108Two situations
in which preoperativeimprovement may be possible are in thepatient with either
poorly controlled hyper-tension or severe carotid stenosis.Essentialhypertension is
a known risk factor for thedevelopment ofa stroke;therefore,institu-tion
ofsuccessful antihypertensive therapybefore elective surgery is recommended.The
preoperative management ofpatientswith carotid lesions is controversial.Part ofthe
problem is that the finding ofa carotidbruit by itselfdoes not correlate with
thedegree or even presence ofcarotid stenosis.Thus,angiography is necessary
ifstenosis issuspected,to document the severity oftheprocess.The question is
whether to per-form a carotid endarterectomy only ifa TIAoccurs or ifcarotid artery
occlusion isgreater than 70%.109Patients with a history ofstroke orTIA frequently
harbor coronary artery dis-ease as well.A thorough assessment oftherisk for
coronary disease is indicated,asnoted in the above section.Patients with a history
ofcerebrovas-cular disease are often placed on inhibitorsofplatelet aggregation
such as aspirin ordipyridamole.Most physicians will permitthese drugs to be stopped
at least 1 weekpreoperatively to prevent bleeding prob-lems perioperatively.Stroke
patients mayalso have trouble clearing secretions orcontrolling saliva.Malignant
HyperthermiaMalignant hyperthermia is the leadingcause ofunexpected anesthetic
deaths inNorth America.It is a rare genetic disorderthat manifests following
treatment withanesthetic agents,most commonly suc-cinylcholine and halothane.The
onset ofmalignant hyperthermia is usually within
38Part 1: Principles ofMedicine,Surgery,and Anesthesiaan hour ofthe administration
ofgeneralanesthesia but rarely may be delayed aslong as 11 hours.Approximately one-
halfofcasesappear to be inherited in an autosomal-dominant fashion;the remainder
ofcasesare inherited in different patterns.Susceptible patients with autosomal-
dominant disease have any one ofeightdistinct mutations in the ryanodine recep-
tor.This receptor is a homotetrameric cal-cium channel found in the
sarcoplasmicreticulum ofskeletal muscle.In the presence ofanesthetic
agents,alterations in the hydrophilic,amino-terminal portion ofthe ryanodine recep-
tor result in uncontrolled efflux ofcalciumfrom the sarcoplasmic reticulum with
sub-sequent tetany,increased skeletal musclemetabolism,and heat
production.Forunclear reasons,overexpression ofthewild-type ryanodine receptor does
notablate abnormal myocyte responses tohalothane,although overexpression ofamutated
ryanodine receptor can inducethe malignant hyperthermia phenotype inmyocytes from
normal individuals.Typically malignant hyperthermiapresents soon after induction
ofanesthesiawith a rapid rise in body temperature andmuscle rigidity.Difficulty in
ventilatingthe patient or opening the mandible forintubation are common early
manifesta-tions.Other signs include
diaphoresis,tachypnea,tachycardia,hyperkalemia,hypocalcemia,elevated temperature
andcarbon dioxide content ofexpired air,andcardiac dysrhythmias.Renal failure
canoccur due to rhabdomyolysis and myoglo-binuria.110Consumptive coagulopathy
canalso be triggered.Mortality in patients inwhich the disorder was not
suspectedbefore anesthesia ranges from 63 to 73%.A predisposition to malignant
hyper-thermia should be suspected in patientswith the following
characteristics:�Unusual muscle
hypertrophy�Ptosis,ophthalmoplegia,strabismus�Pectus deformities or
kyphoscoliosis�Limb girdle weakness�Hip dislocation,dislocated patella,malaligned
feet�Known central core myopathy�Young males with previously describedappearance
�Any history ofmyopathy ofunknownetiologyPatients with a known or suspectedtendency
should be considered for local orregional anesthetic techniques.Ifgeneralanesthesia
is necessary a technique thatuses nitrous oxide,barbiturates,benzodi-
azepines,narcotics,or neuroleptic drugs isadvisable.Nondepolarizing muscle relax-
ants should be used ifnecessary.Drugssuch as succinylcholine,amide local anes-
thetics,ketamine,and volatile anestheticsshould be avoided.Premedication
withdantrolene (1 mg/kg) orally the day beforesurgery or as an intravenous bolus
the dayofsurgery is appropriate when malignanthyperthermia is a high
probability.Inaddition a set protocol for its manage-ment,should it occur,should be
in placebefore starting anesthesia for patients atrisk for malignant
hyperthermia.111,112Spinal Cord Disorders Paraplegia due to spinal cord damage
cancause a number ofproblems ofwhich thesurgeon needs to be
cognizant.Abnormalbladder emptying predisposes thesepatients to urinary tract
infections andchronic pyelonephritis.Paraplegia affect-ing the diaphragm can lead
to pneumonia,and inability to exercise the lower extrem-ities and pelvic region
setting up a situa-tion in which thromboembolism to thelungs is common.Inability to
move canalso cause the development ofdecubitusulcers.Renal and adrenal functions
areoften impaired due to amyloidosis,andanemia ofchronic disease is frequent
inparaplegics.Maxillofacial surgery for these indi-viduals can be accomplished
safely withgood patient preparation.Preoperativechecks ofpulmonary and renal
functionwill reveal patients at high risk for periop-erative complications.The
sputum andurine should be checked for evidence ofinfection and blood count obtained
to dis-cover ifanemia is present.Special careneeds to be taken to properly position
andpad vulnerable parts ofthe body duringand after surgery.Minidose heparin
willhelp prevent pulmonary embolism,as willkeeping the legs elevated during
surgeryand providing proper physical therapyafter surgery.Physical therapy is also
nec-essary to the upper extremities to preventcontractures.Continuous
urinarycatheterization is needed during surgery,returning to the intermittent
bladdercatheterization regimen (in place preoper-atively) as soon as possible after
surgery.Surgery in the Patient with a Psychiatric DisorderAffective
DisordersAffective disorders such as depression arecommon problems in modern
society.Patients with this disorder need specialcare during any surgical
treatment.Major depression is characterized by adepressed mood and an inability to
enjoylife.Symptoms include sleep disturbancesuch as early morning
wakening,appetitedisturbance,fatigue,decreased libido,lowself-esteem,and a feeling
ofhopelessness.Many patients are able to mask or deny theirsymptoms when under no
undue stress,butfacing a surgical procedure will usuallyuncover hidden symptoms
ofdepression.In addition to the emotional problemsthat patients with depression
incur in theperioperative period,problematic druginteractions can occur between
anestheticagents and many ofthe agents used tocontrol depression.Selective
serotoninreuptake inhibitors are in widespread usefor depression,anxiety,and panic
disorder,and are well tolerated perioperatively.Tri-cyclic antidepressants are in
common use
Medical Management ofthe Surgical Patient39for depression,chronic pain,and sleep
dis-orders.They can carry unwanted anti-cholinergic and hypotensive side
effects,which should be remembered when anes-thesia is given.An additional problem
withtricyclic antidepressants is their tendencyto cause increased conduction delays
inpatients with preexisting heart blocks.Monoamine oxidase inhibitors (MAOIs)are
also used to manage depressive symp-toms.They also have anticholinergic
andorthostatic hypotensive effects.Drugs withsympathomimetic action should be
avoidedin patients on MAOIs.Lithium carbonate is used for patientswith bipolar
(manic-depressive) disorders.It induces the characteristic ECG changes ofinverted
and flattened T waves.It can alsoproduce sinus node dysfunction and ven-tricular
irritability.Serum levels should bechecked preoperatively in these
patients.Benzodiazepines used for depressionpose little risk for safe anesthesia as
long asthe anesthesiologist is aware oftheir use.Abrupt discontinuation should be
avoidedto prevent the appearance ofa withdrawalphenomenon.Conditions such as
anorexia nervosaand bulimia should be addressed prior tomajor surgical procedures
due to theimpairment to nutritional health and elec-trolyte balance they
produce.113Psychotic DisordersPsychotic disorders are characterized bydelusions and
hallucinations.Psychoticpatients are usually easily recognized bythe results ofa
comprehensive mental sta-tus examination.Antipsychotic drugs suchas
phenothiazines,thioxanthenes,buty-rophenones,and indalones control manyofthe
symptoms ofpsychosis and causelittle increased risk ofproblems with anes-
thesia.They do have the tendency to causesedation and extrapyramidal symptoms
inmany patients.Introduction ofatypicalantipsychotic medications has resulted ina
large number ofpatients being convert-ed to these drugs,including
respiradone,olanzapine,quetiapine,ziprasidone,andaripiprazole.These medications
havemany drug-drug interactions,and consul-tation with a drug reference manual
orpharmacist would be prudent to avoidsuch complications.Surgery in psychotic
patients carriesno increased risk ofcomplications as longas the disorder is well
controlled.Acute psychosis,combativeness,andagitation can be disruptive as well
asunsafe for the patient and medical staff.After ruling out serious medical
complica-tions such as hypoxia,drug or alcoholwithdrawal,serious
infection,andmyocardial infarction,administration ofloraze-pam 1 to 2 mg PO or
IV,orhaloperidol 1 to 2 mg PO,IM,or IV,can beused for control ofsymptoms
acutely.Haloperidol also comes in a flavorless liq-uid formula.Substance
AbuseAlcoholismPatients who regularly con-sume large amounts ofethanol must
beallowed to withdraw from the effects ofthealcohol before they undergo
electivesurgery and anesthesia.Failure to followthis strategy risks the appearance
ofminoralcohol withdrawal syndrome,with itscompensatory neuronal excitability
andcatecholamine release,or the severe syn-drome delirium tremens (DT) with hallu-
cinosis,hyperpyrexia,hypertension,andlife-threatening cardiac dysrhythmias
andseizures.114,115The following four questions have ahigh sensitivity and
specificity for detect-ing alcoholism.116�Have you ever felt the need to cutdown on
drinking?�Have you ever felt annoyed by criti-cism ofyour drinking?�Have you ever
had guilty feelingsabout your drinking?�Have you ever taken a morning eyeopener?
Previous history ofDT and drinking amorning �eye opener�denote a high riskofalcohol
withdrawal.Two strategies are available for thealcoholic patient coming to
surgery:con-tinuation ofalcohol perioperatively,oravoidance ofalcohol with
vigilance forwithdrawal syndromes.While it seemscounterintuitive to continue
alcohol use ina hospital or postoperative setting,thisstrategy can prevent
withdrawal;mostpatients will resume drinking as soon asthey can anyway.For patients
newlyabstaining,those with a prior history ofDT may be given scheduled benzodi-
azepines,such as lorazepam 1 to 2 mgevery 8 hours,but most patients should
beobserved for evidence ofDT and treatedbased on symptoms.Early symptomsinclude
restlessness and tremulousness,followed by agitation,combativeness,fever,and
seizures.Symptoms should betreated as soon as they emerge,withoxazepam 15 to 30 mg
PO every 6 to 8 hours as needed,or lorazepam 1 to 2 mgPO,IV,or IM every 6 to 8
hours as needed.Most ofthe anesthetic hazards in thesober alcoholic patient are due
to ethanol-induced hepatic changes (see �Liver Dis-ease�).Chronic ethanol use
increases anes-thetic requirements for halothane andisoflurane.Clearance
ofbenzodiazepinesis also increased,so that larger doses maybe necessary in
alcoholic patients.Patientswith ethanol-induced liver disease areprone to
hypoglycemia and need frequentserum glucose determinations during andafter
surgery.Opioid and Illicit Drug AbusersIfsurgery is urgently necessary in opioid-
dependent patients,it is usually prudentfor the surgeon to avoid precipitating
thewithdrawal syndrome by substitutingmethadone (2.5 mg equals 10 mg ofmor-phine)
for the abused opioid.Usually 20 to40 mg ofmethadone is needed daily,administered
orally or intramuscularly in4 to 6 divided doses.Clonidine has also
40Part 1: Principles ofMedicine,Surgery,and Anesthesiabeen found useful for helping
preventsymptoms ofopioid withdrawal.117Hypotension is a common problem inopioid
abusers during the perioperativeperiod.They also are likely to have difficultveins
in which to gain access,necessitatingplacement ofcentral lines.Intravenousillicit
drug abusers also have a high inci-dence ofhepatitis B and C and
humanimmunodeficiency virus positivity.Cocaine use potentiates problemssuch as
coronary vasospasm,myocardialischemia/infarction,and dysrhythmias.The rapid
metabolism ofcocaine in apatient�s system prior to presenting forsurgery makes it
unlikely that acutelyintoxicated patients will be placed undersedation or general
anesthesia.118,119Surgery in the Special Patient Obese PatientsObesity is a common
affliction in modernsociety due to a combination ofpoordietary habits and general
lack ofphysicalactivity.The excessive weight in an obeseindividual is due to an
overabundance ofadipose tissue.Morbid obesity is definedas when a patient is 100%
over ideal bodyweight due to fat accumulation.Calcula-tion ofthe body mass index
(BMI) assistsin the diagnosis ofobesity,with a BMI of30 kg/m2and above defining
obesity.BMI =Body weight in kgSquare ofstature(height in m)Obesity by itselfdoes
not increase sur-gical mortality until it becomes severe,butthen the risk rises
exponentially.The pon-deral index has been used to quantitate theincreased risk
faced by obese individuals.The index is calculated by dividing anindividual�s
height in inches by the cuberoot oftheir weight in pounds.A resultgreater than 12.5
correlates highly with asignificantly heightened risk ofcomplica-tions in the
perioperative period.TheChase method is another means ofgaugingrisk in obese
individuals in which surgicalrisk is determined by the ratio ofweightversus
height.Pulmonary problems are the most fre-quent complications in the
perioperativeperiod in obese patients.These includepulmonary
embolism,bronchospasm,atelectasis,and pneumonia.Obesity cre-ates a form
ofrestrictive lung disease,especially when these patients are supine,due to
excessive weight on the thorax andabdomen that restricts full inspiration.Before
elective surgery in obesepatients a careful history and physicalexamination are
necessary to determinehow the obesity may affect anesthesia andto detect a
concurrent disease.Specificquestions about a history ofdaytimesomnolence and
snoring are needed tofind ifa patient�s airway is easily compro-mised.Past history
oflung disease,heartproblems,thrombophlebitis,or pul-monary embolism should also be
elicited.Obese patients should also be askedabout any previous problems in
theestablishment ofvenous access.The use-fulness ofphysical examination ofthechest
and abdomen is commonly limitedin obese patients.Therefore,ancillaryexamination
techniques such as PFTs,ECG,and plain chest radiography areusually
warranted.Because obese patients have height-ened risks ofpulmonary
problems,thosewho smoke should be helped to quit,hopefully for as long as possible
beforesurgery.A reasonable program ofweightreduction should also be
recommended.Many patients may benefit from a consul-tation about potential
gastrointestinalsurgery for weight control.When planning surgery the
possibilityofregional anesthesia should be consid-ered.Deep sedation should be
avoided ifthe airway is likely to be difficult to main-tain.Ifgeneral anesthesia is
selected as themethod ofpain and anxiety control,thepatient can be given
preoperative instruc-tion in incentive spirometry techniques.The increased risk
ofthrombophlebitis inthese patients can be lessened by the use ofa minidose heparin
or enoxaparin regi-men.Finally,a lowered threshold is appro-priate for placement
ofinvasive monitorssuch as a central venous pressure line or aSwan-Ganz
catheter.Obese patients are difficult anestheticcases.They are typically more ofa
problemto mask ventilate during the induction ofanesthesia.This should be
anticipated bybeing ready to quickly intubate the patientifnecessary even though
intubation itselfcan be challenging.120The excess weightusually decreases pulmonary
complianceand the functional residual and vital capac-ities.It should be kept in
mind that squeez-ing the bag connected to the endotrachealtube will not give an
accurate feel ofpul-monary compliance due to the weight ofthe chest
wall.Furthermore,the loweredlung capacities will cause an increasedshunt
fraction,which should be monitoredby frequent measurements ofarterial
bloodgases.Chest weight effects on the lungs canbe lessened by elevating the upper
body 15to 20�from the horizontal.The pharmacokinetics ofdrugs differin obese versus
lean individuals.Thewashout offat-soluble anesthetic agentsneeds to begin earlier
in the surgery toallow the patient to be awakened whendesired.When calculating the
dose ofwater-soluble drugs,the estimated leanbody mass ofthe obese individual
shouldbe used.Postoperative management ofobesepatients should include elevation
ofthehead ofthe bed,early ambulation,incen-tive spirometry,deep venous
thrombosisprophylaxis,and frequent physical exami-nation for signs ofpulmonary
problems ordeep vein thrombophlebitis.Geriatric PatientsAlthough many clinicians
are concernedthat there will be medical complicationswhen treating elderly
patients,studies sub-
Medical Management ofthe Surgical Patient41stantiate the fact that most elective
surgeryis safe in healthy geriatric patients.Howev-er,geriatric patients with
chronic diseasessuch as COPD,diabetes,and coronaryartery disease are certainly
susceptible tothe same problems as younger individualswith these same
processes.Therefore,when older patients have chronic diseases,preoperative
preparation should includeefforts to minimize the detrimental effectofthe disease
process on the patient�sphysiology.121Even though elderly patients canappear frail
and sick,a large percentage areactually well.Conversely the appearance ofhealth can
be deceiving,because all olderindividuals experience various changes inphysiologic
function that can affect theirresponse to the stress ofan operation.Statistically
the most common compli-cations that follow major surgery in theelderly are
pulmonary embolism,myocar-dial infarction,pneumonia,and congestiveheart failure.The
surgeon should be espe-cially vigilant for a past history or perioper-ative signs
ofthese problems.Furthermore,although geriatric patients usually are ableto
withstand the initial physiologic stressesofsurgery,ifa complication
occurs,theyhave less reserve to aid with recovery.The heart undergoes age-
relatedchanges that decrease the maximal heartrate (220 � age in yr).Cardiac output
falls(about 1% each year after age 20 yr)because ofincreased afterload anddecreased
elasticity ofarteries secondaryto atherosclerosis.This decreased elasticityalso
causes any small increase in bloodvolume to result in sharp increases inblood
pressure.Total circulation time atage 20 years is 48 seconds;this rises to 65
seconds at age 70 years.The cardiovas-cular system also loses much ofits respon-
siveness to catecholamines with age,sothat postural hypotension is common.Maximum
coronary flow capacity in theelderly is about 65% ofthat in teenagers.Pulmonary
function also falls as peo-ple get older.Loss oflung elasticity andincreased
stiffness ofthe chest wall predis-pose lungs to atelectasis and ventilation-
perfusion imbalances,as does theincreased residual volume in older lungs.Whereas
the PaO2 on room air at age 30 years averages about 94 mm Hg,it nor-mally falls to
about 74 mm Hg above age60 years.Vital capacity and expiratory flowrate begin to
fall when individuals reachage 30.Muscle weakness prevents forcefulcoughing,and
degeneration ofbronchialepithelium leads to less efficient lungcleansing.All
ofthese changes help toaccount for the relatively high incidence ofpulmonary
complications followingsurgery in older patients.Renal function decreases 20 to
30%between the ages of30 and 80 yearsbecause ofnatural loss ofglomeruli andfibrosis
ofinterstitial tissue.Creatinineclearance falls,but because lean body massalso
decreases there is usually no change inmeasured serum creatinine.An approxi-mation
ofexpected age-related changes inrenal function can be gained by the fol-lowing
equation:Creatinine clearance = 133 � (0.84 �Age)(mL/min)This formula can be used
to judge dosagesofdrugs dependent on renal clearance.Geriatric patients also suffer
a loss ofrenalconcentrating and diluting abilities astubules become less responsive
to antidi-uretic hormone.For that reason they caneasily have intravascular volume
distur-bances and electrolyte abnormalities.Thirst perception also becomes a
problemand thirst cannot be relied on to helpgauge fluid requirements in these
patients.Prostatic hypertrophy occurs in 80% ofmen with age,causingurinary
problemsthat are commonlyworsened by generalanesthesia.122,123The loss ofmuscle
mass and plasmavolume with age may affect drug actionsand necessitate changes in
drug doses.Older white females are also predisposed toloss ofbone strength owing to
osteoporosis;extra care should be taken when transport-ing these patients to and
from the operatingtable.Thinning ofskin in older patientsalso makes them more
susceptible to pres-sure damage,heightening the need forproper intraoperative
padding.Geriatric patients tend to mount poorfever responses to
pyrogens.Therefore,other signs ofproblems such as malaise oraltered states
ofconsciousness may need tobe used to detect infections.The hearingand visual
problems ofolder patients pre-dispose them to states ofconfusion own-ing to sensory
deprivation;providingappropriate sensory stimulation helps pre-vent this problem.A
decrease in gastroin-testinal motility leads to frequent consti-pation,and aging
often causes impairedglucose tolerance.Evaluation ofelderly patients beforeelective
maxillofacial surgery should beginwith a careful medical history.Old recordsand
consultation with the patient�s prima-ry care provider are usually excellentsources
ofneeded information.During thephysical examination specific note shouldbe made
ofthe patient�s state ofhydration,signs ofage-related problems such ascarotid or
aortic stenosis,and any pul-monary and mental status problems.AnECG and chest
radiograph are useful fordetecting occult problems and provide abaseline for later
comparisons.124,125Intraoperatively the patient should bekept from excessive loss
ofheat and over-or underhydration.Postoperatively,theclinician should be alert to
possible respi-ratory depression due to narcotics andsigns ofmyocardial damage such
as sud-den dyspnea or worsening ofcongestiveheart failure.Drug modifications in the
elderlyinclude reducing benzodiazepine dosagesby at least 50%,recognizing the
dysrhyth-mogenic potential ofatropine,and beingaware that narcotics such as
morphine andmeperidine have prolonged duration ofaction,and that water-soluble
drugs willhave a heightened pharmacologic effect
42Part 1: Principles ofMedicine,Surgery,and Anesthesiawhile lipid-soluble drugs
such as barbitu-rates will have a long elimination time.123Pediatric Patients The
surgical challenges in pediatricpatients are usually due to their small
size.However,it is hazardous to consider chil-dren as just small adults when
consideringtheir anesthetic needs for surgery.The physiology ofpediatric patients
iswhat makes them differ from adults intheir response to drugs and
anesthesia.Newborns and infants are obligate mouthbreathers.Children have
relatively smallnasal airways,large tongues,smallmandibles,short necks,and an
abundanceofpharyngeal lymphoid tissue;all oftheseserve to create an airway that is
easily com-promised.Dead space in children is about2 mL/kg,and tidal volume is
about threetimes the dead space.The heart ofinfants has a fixed strokevolume,so
that cardiac output is entirelydependent on heart rate.Blood volume inrelation to
body weight is high in infants,but ratio decreases with age.Fluid require-ments
ofchildren vary with weight asshown in Table 2-6.Normal urine outputalso varies
(Table 2-7).Children have relatively large surfaceareas that can quickly allow
excessive heatloss ifthey are left uncovered in an operat-ing room.Dosing ofdrugs
to children is usuallybest decided based on the
manufacturer�srecommendations.126Pregnant and Lactating PatientsPregnancy and
lactation are relative con-traindications to elective maxillofacialsurgery because
ofthe negative effects onthe mother and developing child ofvari-ous
drugs,irradiation from imaging stud-ies,and psychological stress associatedwith
surgery.127�129Ifsurgery cannot be deferred,thepatient�s obstetrician should be
consultedfor guidance with respect to safe drugs touse (Table 2-8).When feasible
the surgeryshould be conducted under local anesthe-sia.Steps to minimize anxiety
are alsoappropriate.During later stages ofpreg-nancy,patients cannot tolerate long
proce-dures without being allowed to emptytheir bladder.In addition,pressure
fromthe uterus compromises venous return tothe heart by placing pressure on the
venacava when patients are in a supine posi-tion.130Therefore,allowing patients
toassume a more left lateral position is nec-essary.A late-term pregnant
patient�sblood pressure or urinary protein must becarefully monitored to detect any
earlysign ofpreeclampsia.131,132Lactating patients need to avoid theuse ofdrugs
capable ofpassing into breastmilk and potentially harming the infant(Table 2-
9).References1.Hilditch WG,Asbury AJ,Crawford JM.Pre-operative screening:criteria
for referring toanesthetists.Anesthesiology 2003;58:117�27.2.Wu G,Sanderson
B,Bittner V.The 6-minutewalk test:how important is the learningeffect? Am Heart J
2003;146:129�33.3.Reilly DF,McNeely MJ,Doerner D,et al.Self-reported exercise
tolerance and the risk ofserious perioperative complications.ArchIntern Med
1999;159:2185�92.4.Ang-Lee MK,Moss J,Yuan C.Herbal medicineand perioperative
care.JAMA 2001;286:208�16.5.Mukherjee D,Eagle KA.Perioperative cardiacassessment
for noncardiac surgery.Circula-tion 2003;107:2771�4.6.Smetana,Up To
Date;2003.7.Linton MF,Fazio S.A practical approach torisk assessment to prevent
coronary arterydisease and its complications.Am J Cardiol2003;92
Suppl:19i�26i.8.Falk E,Shah PK,Fuster V.Coronary plaquedisruption.Circulation
1995;92:657�61.9.Cannon CP,Turpie AG.Unstable angina andnon-ST-elevation myocardial
infarction.Circulation 2003;107:2640�5.10.Dibra A,Mehelli J,Braun S,et
al.Associationbetween C-reactive protein level and subse-quent cardiac events among
patients withTable 2-8Medication to Avoid during Pregnancy*Aspirin and other
nonsteroidal anti-inflammatory agentsCarbamazepineChloral hydrate (ifchronically
used)ChlordiazepoxideCorticosteroidsDiazepam and other
benzodiazepinesDiphenhydramine hydrochlorideMorphineNitrous oxide (ifexposure
greater than 9 hours per week)Pentazocine
hydrochloridePhenobarbitalPromethazinePropoxypheneTetracyclines*All medications
should be used with care in pregnantpatients.The patient�s obstetrician should be
consulted ifthere is any question concerning the safety ofa drug for a pregnant
patient or the fetus.Table 2-7Urine Output Age (yr)Urine Output0�23 mL/kg/h2�52
mL/kg/h5 to adult1 mL/kg/hTable 2-6Fluid Requirements for ChildrenWeight (kg)Fluid
Requirements1�10100 mL/kg daily10�201,000 mL + 50 mL/kg over 10 kg daily201,500 mL
+ 20 mL/kg over 20 kg dailyTable 2-9Medications for Breast-Feeding
MothersSafePotentially
HarmfulAcetaminophenAmpicillinAntihistaminesAspirinCephalexinBarbituratesCodeineChl
oral
hydrateErythromycinCorticosteroidsFluorideDiazepamLidocaineMetronidazoleMeperidineP
enicillinOxacillinPropoxyphenePentazocineTetracyclines
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CHAPTER 3Perioperative ConsiderationsNoah A.Sandler,DMD,MDMany factors need to be
considered whenevaluating a patient prior to oral and max-illofacial
procedures.Whether a surgery isbeing performed in an office or operatingroom,the
practitioner must acknowledgethe impact ofthe surgery and the stress
theperioperative period potentially entails.Inaddition,the pathophysiology ofcon-
comitant medical ailments that may mod-ify therapy needs to be considered.Preop-
erative assessment,intraoperativemonitoring,and postoperative care needto be
modified based on individual patientrequirements.The following discussiondoes not
attempt to answer all questionsregarding perioperative patient care.Com-mon
clinical scenarios and diseaseprocesses are presented.Despite our bestefforts to
prevent problems throughassessment and monitoring,problems oremergencies can
arise;therefore,thischapter also addresses patient monitoringand emergency
management ofcommonclinical situations.Cardiac AssessmentSince the 1970s risk
assessment has beenperformed in an attempt to identify indi-viduals who may
encounter a significantcardiac event (ie,myocardial infarction[MI] or death) in the
perioperative period.In their often-referenced article,Goldmanand colleagues
identified nine indepen-dent factors associated with increasedperioperative cardiac
risk (Table 3-1).1These were assigned a point system basedon their relative
contribution to cardiacrisk.The more points,the higher the riskofsignificant
morbidity or mortality,pri-marily in the immediate postoperativeperiod (Table 3-
2).Since 1980 the American College ofCardiology in association with the Ameri-can
Heart Association (ACC/AHA) hasproduced guidelines for the
managementofcardiovascular disease.In 1996 a com-mittee was developed to assess
guidelinesin the perioperative evaluation for noncar-diac surgery.Expanding on the
factorsidentified by Goldman and colleagues,patient daily function and surgical
riskwere also considered.Recent evidence based on 4,315patients over the age of50
years undergoingelective noncardiac procedures suggests sixmajor risk factors
exist.These are includedin a revised cardiac risk index:high-risktype
ofsurgery,history ofischemic heartdisease,congestive heart failure,cerebrovas-cular
disease,preoperative treatment withinsulin,and preoperative serum creatinine> 2.0
mg/dL.2Based on these findings aswell as support from similar studies andrecent
technologic advances in coronarytesting and therapies,the ACC/AHA Table 3-1Risk
Factors Commonly Associated with Perioperative Morbidity and Their Point Value*
Risk FactorPoint ValueThird heart sound or jugular venous distention11Recent
myocardial infarction10Rhythm other than sinus or premature atrial contractions on
last echocardiogram7> 5 premature ventricular contractions per minute at any
time7Intraperitoneal,intrathoracic,or aortic operation3Age > 70 yr5Important aortic
stenosis3Emergent operation4Poor general medical condition3Partial pressure
ofoxygen < 60 or ofcarbon dioxide > 50 mm HgK < 30 mEq/LCreatinine > 3 mg/dL or
blood urea nitrogen > 50 mg/dLChronic liver diseaseBedridden from noncardiac
causes*As determined in Goldman L et al.1Adapted with permission from Goldman L et
al.1
48Part 1: Principles ofMedicine,Surgery,and Anesthesiapractice guidelines were
updated in 2002.3As part ofthese guidelines,consideration isgiven to cardiac
testing for individualsdetermined to be at risk for a perioperativeevent.The
following factors are assessed:�Is the surgery urgent? Ifdelay ofthesurgery may be
detrimental,cardiacassessment may need to be performedat a later time.�Has the
patient undergone coronaryrevascularization in the past 5 years orpercutaneous
coronary interventionfrom 6 months to 5 years previously?Ifthe patient has remained
free fromsymptoms ofischemia,the risk ofperioperative cardiac death or MI
isextremely low.�Has the patient undergone a coronaryevaluation in the past 2
years? Ifinva-sive or noninvasive testing was nega-tive and the person has
remainedsymptom free,no further periopera-tive testing is indicated.�Does the
individual have an unstablecardiac condition or major clinicalpredictor ofrisk?
These include acute(within 7 d) or recent (7�30 d) MI,unstable or severe
angina,decompen-sated heart failure,significant arrhyth-mias,and severe valve
disease.Theseconditions warrant delay ofthe proce-dure when possible,and usually
coro-nary angiography is performed.�Are there intermediate clinical predic-tors
ofrisk? These include angina pec-toris,prior MI as indicated by historyor
electrocardiography,compensatedor prior heart failure,preoperativecreatinine > 2
mg/dL (ie,renal insuffi-ciency),and diabetes mellitus (DM),particularly insulin-
dependent DM.In addition to these risks,the func-tional capacity ofthe individual
isdetermined.This is recorded in meta-bolic equivalents (METs),where 1 MET is the
oxygen consumption ofa70 kg 40-year-old man at rest.Func-tional capacity is
classified as excellent(> 10 METs),good (7�10 METs),mod-erate (4�7 METs),poor (< 4
METs)(Table 3-3).�What are the specific risks ofthesurgery? Considerations include
thetype ofsurgery (eg,vascular surgery ishigh risk) and hemodynamic changesthat
occur with certain surgeries (eg,significant bleeding or hypotension).Most oral and
maxillofacial surgeryprocedures are considered to be ofintermediate risk.In
general,patients with no major andfew intermediate predictors ofclinical riskand
moderate or excellent functionalcapacity can undergo oral and maxillofa-cial
surgery procedures with little risk ofperioperative death or MI.On the
otherhand,individuals with poor functionalcapacity who are to undergo higher-
risksurgery (eg,head and neck cancer resec-tion) are often considered for further
non-invasive testing (eg,stress test,echocardio-graphy).This approach has been
demon-strated in recent studies to be efficaciousand cost-effective.4�7Since most
oral and maxillofacial sur-gical procedures are considered to beintermediate
risk,the primary cardiac riskfactor is the existence ofone or more ofthe major
clinical predictors ofrisk (ie,recent MI,unstable or severe angina,decompensated
heart failure,significantdysrhythmias,and severe valve disease).The primary method
ofinitial identifica-tion ofthese factors is a history taking andphysical
examination.Patients with identi-fiable risks warrant deferment ofsurgerywith a
referral for consideration for a thor-ough cardiac evaluation.Myocardial
Ischemia/AnginaThe stress ofelective surgery begins wellbefore the incision is
made.Activation ofthe hypothalamic-pituitary-adrenal axis isinitiated by just
scheduling the procedureand persists through the surgical perioduntil at least a
week after the surgery.Con-comitant with the release ofcortisol isstimulation ofthe
adrenal medulla and theactivation ofthe sympathetic nervous sys-tem with
catecholamine release.Theseresponses may have served an evolutionarypurpose and/or
aid in aspects ofhealing;however,they can be detrimental in adebilitated patient
with poor reserve.Surgery,itself,necessitates myocardialwork.Patients with
atherosclerosis andcoronary artery disease with narrowing ofTable 3-2Assessment
ofMorbidity and Mortality Based on Cardiac Risk Factors* No or Minor Life-
ThreateningComplications� Complications�Cardiac DeathsClassPoint Total(n = 943)(%)
(n = 39)(%)(n = 19)(%)I (n= 537)0�5532 (99)4 (0.7)1 (0)II (n= 316)6�12295 (93)16
(5)5 (2)III (n= 130)13�25112 (86)15 (11)3 (2)IV (n= 18)> 264 (22)4 (22)10 (56)*As
determined in Goldman L et al.1�Documented intraoperative or postoperative
myocardial infarction,pulmonary edema,or ventricular tachycardia.Adapted with
permission from Goldman L et al.1Table 3-3Metabolic Equivalents forCommon
ActivitiesFunctional Metabolic CapacityEquivalentsTake care ofyourself1Walk a block
or twoClimb a flight ofstairs4Heavy workModerate recreation>10Strenuous sports
Perioperative Considerations49the coronary vessels may be unable to meetthis
increased demand.Myocardialischemia within 48 hours ofsurgery resultsin a ninefold
increase in the risk ofunsta-ble angina (defined as angina at rest orincreasing
angina symptoms) and/or MI.Myocardial work is primarily deter-mined by four factors
related to myocar-dial oxygen demand:heart rate,preload,afterload,and
contractility.Preloadrepre-sents all factors that contribute to passiveventricular
wall stress (tension) at the endofdiastole.It is approximately equal toend-
diastolic volume or pressure (ie,thevolume ofblood left in the heart
afterdiastole).Preload is generally a reflectionofthe volume status ofa patient.It
ismeasured via the central venous pressureor the pulmonary capillary wedge pres-
sure.Additionally,the left ventricularend-diastolic volume determines the car-diac
output according to Starling�s law.Clinically,this means increasing precon-traction
muscle fiber length by increasingleft ventricular end-diastolic volumethrough
volume administration leads toan increase in the force ofcontraction.Afterload,in
turn,represents all ofthe fac-tors that contribute to total ventricularwall stress
(tension) during systole.Theprimary determinants ofafterload are thetotal
peripheral resistance against whichthe heart muscle must pump and changesin
intrathoracic pressure.Afterload isindirectly measured through blood pres-sure and
mean arterial pressure.Contrac-tilityis the ability ofthe heart muscle toshorten
itselfin the face ofappropriatestimuli.8Ofthese factors,heart rate andafterload are
the major contributors tocardiac work and myocardial oxygen con-sumption.Elevated
heart rate is alsopotentially harmful in that it decreases thetime that oxygen and
nutrients can bedelivered to the myocardial cells (diastolicperfusion time).This is
the basis for thegoal ofmaintaining the blood pressureand pulse within 10% ofthe
preoperativevalue during anesthesia.9Patients with coronary artery diseaseoften
have a history ofhypertension.Blood pressure is measured using theproper cuffsize
with patients quiet andcomfortable (with back support,ifseat-ed) for at least 5
minutes prior to mea-surement.Hypertensionis defined as twoelevated blood pressure
readings separat-ed by at least 2 minutes of=140/90 mmHg on two or more separate
visits.Healthy patients with persistent elevatedpressures =160/100 mm Hg and
thoseconsidered to be at high risk (diabetics orpatients with clinical
cardiovascular dis-ease) should be considered for antihyper-tensive therapy.10
Preoperatively,elevated blood pres-sure should be managed by deferringtreatment for
elective procedures.Intraop-erative or postoperative hypertensionrarely requires
treatment.Hypertensivecrisis or emergency is a sudden increase insystolic and
diastolic blood pressure asso-ciated with end-organ damage ofthe cen-tral nervous
system,heart,or kidneys.Headache,altered level ofconsciousness,and less severe
manifestations ofcentralnervous system dysfunction are classicfindings in
hypertensive encephalopathy.Advanced retinopathy with
arteriolarchanges,hemorrhages,and exudates aswell as papilledema are seen on
fundus-copic examination.Angina,acute MI,orsigns ofheart failure can be present
inhypertensive crisis.Renal failure with olig-uria and/or hematuria is present
withdamage to the kidneys.Less than 1% ofpatients with a diagnosis
ofhypertensionexperience a crisis.In the United States theincidence is higher among
African Ameri-cans and the elderly.The majority havepreviously been diagnosed with
hyperten-sion and many have been prescribed anti-hypertensive therapy but with poor
con-trol.The incidence ofpostoperativehypertensive crisis varies depending onthe
population studied and has beenreported in 4 to 35% ofpatients.Reduc-tion ofblood
pressure in a hypertensivecrisis should be performed with intra-arterial blood
pressure monitoring.The term hypertensive urgency is char-acterized by severely
elevated blood pres-sure without acute end-organ damage.Postoperative hypertension
has beendefined arbitrarily as systolic blood pres-sure > 190 mm Hg and/or
diastolic bloodpressure =100 mm Hg.It should beappreciated that most patients
withseverely elevated blood pressure (diastolic> 110 mm Hg) have no acute end-
organdamage.The elevated blood pressureshould be treated in a controlled fashionin
an intensive care unit.The use ofsub-lingual nifedipine is strongly discouragedas
this may result in a precipitous fall inblood
pressure.Similarly,intravenoushydralazine may result in severe uncon-trolled
hypotension.Rapid and uncon-trolled reduction ofblood pressure mayresult in
cerebral,myocardial,and renalischemia or infarction.Table 3-4 describescommonly
recommended medicationsand dosages should it be determined thatreduction ofblood
pressure is necessary.11Recent Myocardial InfarctionIt is important to attempt to
avoid thestress ofsurgery ifthe patient is experienc-ing acute ischemia or has a
history ofrecent infarction.Traditionally a 6-monthinterval between the initial
incidence ofMI and elective noncardiac surgery hasbeen advocated to avoid stress
and the riskofre-infarction.However,recently theimportance ofthis time interval has
beencalled into question.The use ofthrom-bolytics,angioplasty,and risk stratifica-
tion after an acute MI has been the impe-tus for this change.Although somepatients
may continue to have myocardi-um at risk with subsequent ischemicepisodes,others
may have critical stenosisconverted to widely patent vessels.TheAHA/ACC Task Force
on PerioperativeEvaluation ofthe Noncardiac Surgery hasadvocated that the group at
highest risk isthose who have had an MI within 6 weeks;
50Part 1: Principles ofMedicine,Surgery,and Anesthesiaafter this period risk
stratification is basedon the presentation ofthe disease (ie,those with persistent
symptoms consistentwith active ischemia remain at the highestrisk level).12During
severe ischemic episodes therelease ofintracellular potassium frominjured cells may
result in partial repolar-ization ofthe surviving cardiac cells,partic-ularly along
the infarct border.These cellsmay then initiate areas ofectopia,poten-tially
leading to arrhythmias,especiallywith concurrent sympathetic
stimulation,electrolyte abnormalities,and ventricularhypertrophy.�-
Blockers,nitroglycerin,andamiodarone as well as high vagal tone canbe protective in
this circumstance.In addi-tion,intra-aortic balloon pumps,ventricu-lar assist
devices,coronary angioplasty,andrevascularization may be indicated.Acute Episode
ofChest Pain Suggestive ofMyocardialIschemia/InfarctionImmediate intervention
includes the assess-ment ofvital signs and the administration ofoxygen and
nitroglycerin tablets or spray at0.4 mg/dose (to be repeated in 5 min inter-vals
for three doses or until the pain is elim-inated).Ifthe pain is
persistent,intravenousmorphine (2�5 mg q5min or until pain reliefis achieved) and
aspirin 325 mg should begiven.The local Emergency Medical Serviceshould be
contacted early as the protocolcalls for the performance ofan early 12-
leadechocardiography (preferably by EmergencyMedical Service personnel) and
screening ofthe patient for an antifibrinolytic or reperfu-sion (ie,an angioplasty
with stent placementor coronary artery bypass graft) procedure.13Decompensated
Congestive Heart FailureA history ofworsening shortness ofbreath
(dyspnea),difficult ventilationwhen assuming the supine position(orthopnea),or
gasping for oxygen whenassuming the supine position when asleep(paroxysmal
nocturnal dyspnea) shouldalert the practitioner to the possibility ofacute
congestive heart failure.Signs ofcardiac failure include raised jugularvenous
pressure,added heart sounds (S3[the presence ofa third heart
sound],inparticular),pulmonary crackles (indicat-ing pulmonary
edema),hepatomegaly,and peripheral edema.The presence ofany ofthese signs or
symptoms warrants acomplete cardiac evaluation prior to initi-ating any elective
procedure.1,3Table 3-4Common Antihypertensive Agents Used to Actively Lower Blood
Pressure in Hypertensive CrisisDrugMechanismDosageCommentsClonidineCentral a2-
agonist0.1 mg PO q20minUseful in hypertensive urgency;graduallydecreases
BPDiazoxideSmooth muscle relaxant1�3 mg/kg IV,maximum single dose Causes rapid BP
decreaseof150 mgEnalaprilatAngiotensin converting 1.25 mg over 5 min q6hBlocks
angiotensin IIenzyme inhibitorEsmolol�1-selective blocker0.5 mg/kg followed by
infusion ofRapid onset (60 s),short duration25�300 �g/kg/min(10�20
min)FenoldopamDopamine agonistInitial dose 0.1 �g/kg/min titrate;Short
acting,increases renal perfusionmaximum 1.6 �g/kg/minLabetalola- and �-blocker
Loading dose of20 mg followedAvoid larger bolus doses;can cause (a:�= 1:7)by 20�80
mg dose at 10 minhypotensionintervals or 1�2 mg/min infusionNicardipineCa channel
blocker5 mg/h increasing 2.5 mg/h q5minUseful for cardiac and cerebral ischemia;
(maximum 15 mg/h)dose independent ofweightNitroprussideArterial/venous
Infusion;usually < 2 �g/kg/minRapidly decreases BP;risk
ofcyanidedilatationtoxicityPhentolaminea-blockerIV 1�5 mg bolusesCan cause
tachyarrhythmias,anginaTrimethaphan Nondepolarizing IV infusion 0.5�1
mg/min;maximum Adrenergic block is therapeutic effect;camsylateganglionic block15
mg/mincholinergic block ofside effectsBP = blood pressure.
Perioperative Considerations51ArrhythmiasThe normal pattern ofelectric transmis-
sion ofthe heart starts with the initiationofthe impulse in the sinoatrial (SA)
node,spreading through the atria with a conver-gence ofthe impulse at the
atrioventricu-lar (AV) node.There is a delay ofconduc-tion through the AV
node,accounting forthe P�R interval on the echocardiogram(ECG;100 ms).This interval
is prolongedby parasympathetic (vagal) stimulationand shortened by sympathetic
activity.Activation ofthe ventricles starts on theleft side ofthe interventricular
septum,crossing over to the right at the midpointofthe septum.The impulse
spreadsthrough the Purkinje system to the apex.The wave ofdepolarization then
movesalong the walls ofthe ventricles from theendocardium to the epicardium to
reachthe AV groove.Perioperative cardiac arrhythmias arecaused by abnormalities
ofcardiacimpulse formation,impulse conduction,or a combination ofboth.There is a
high-er incidence ofarrhythmias in the periop-erative setting,and anesthetic agents
areknown to alter cardiac impulse generationand conduction.Perioperative cate-
cholamines owing to exogenous adminis-tration or endogenous release in the pres-
ence ofischemia set the stage for newarrhythmia during this period.14,15Volatile
agents directly decrease SA andAV node automaticity,but increasing extra-cellular
calcium can antagonize this phe-nomenon.A common occurrence with theuse ofvolatile
agents is isorhythmic AV disso-ciation,in which the AV node generates thepacemaker
at a modestly higher rate than theSA node.This is a result ofdirect depressionofthe
SA node by the volatile agent and somestimulation ofthe AV node by
sympatheticactivity.Serious hemodynamic consequencesare not usually seen in healthy
individualsbut are a concern with ventricular noncom-pliance such as ventricular
hypertrophy as aresult ofatherosclerosis ofthe aorta orperipheral
vessels.Inhalation agents in gener-al are not otherwise
arrhythmogenic,butarrhythmias can be produced in the presenceoftriggering agents
and clinical situationsthat generate a high catecholamine state.Thisincludes light
anesthesia levels (with hyper-tension and tachycardia),hypoxemia,hyper-carbia,and
the use ofexogenous epinephrineor aminophylline (the latter ofwhich indi-rectly
causes the release ofendogenous cate-cholamines).The arrhythmogenic dose
inmicrograms per kilogram ofepinephrineadministered by infiltration with
variousinhaled agents are 2.1 with halothane,3.7with halothane and lidocaine,6.7
with isoflu-rane,and 10.9 with enflurane.16Paroxysmal supraventricular tachy-
cardias (PSVTs) arise from the SA or AVnode,atrium,or an accessory AV connec-
tion.They are common arrhythmias thatare usually seen in cardiac surgicalpatients
(20�40%) but can develop inpatients undergoing noncardiac surgery(usually major
vascular,cancer,or ortho-pedic procedures).The onset and termi-nation ofthese
rhythms are usuallyabrupt,with rates between 120 and 300 beats per minute (bpm).The
ECGtypically identifies the area oforigin ofthe ectopic conduction with a positive
Pwave being present in SA-node reentryPSVTs,absent or inverted P waves in AV-node
origin PSVTs,and altered P wavemorphology in intra-atrial reentry PSVTs.The most
common PSVT is atrial fibril-lation (> 90% ofSVTs in the postoperativeperiod).It
can occur as the result ofcardiacdisease,such as mitral valve disease,conges-tive
heart failure,coronary artery disease,orpericarditis.It can also be the result
ofsys-temic processes such as thyrotoxicosis,pul-monary embolus,chronic obstructive
pul-monary disease (COPD),alcohol or caffeineexcess,or electrolyte
disturbances.Changesseen on the ECG are most evident in lead IIas an irregular
rhythm.Untreated PSVT can result in ventricu-lar rates that exceed 120 to 200
bpm,whichcan cause significant hemodynamic insta-bility.Ifuncontrolled ventricular
ratesoccur acutely in the perioperative period,prompt treatment is necessary.Rate
con-trol is achieved with verapamil (a calciumchannel blocker noted for decreasing
con-duction at the AV node),digoxin,oresmolol (a �1-selective blocker).Ifpatientsdo
not convert to sinus rhythm with theseagents,electrocardioversion with
prioranticoagulation is attempted.It is interesting to note that a
recentlyperformed meta-analysis has demonstrat-ed that �-blockers reduce the
incidence ofpostoperative atrial fibrillation,whereasdigoxin and verapamil have no
effect.IfaPSVT is detected upon routine monitor-ing,patients should be referred for
furtherevaluation.Acute evaluation is required ifthe individual is symptomatic
and/or therate is poorly controlled.A complete dis-cussion ofthe causes and
treatment proto-cols ofPSVTs is beyond the scope ofthischapter.The reader is hereby
referred tothe most recent advanced cardiac life sup-port protocols released by the
AmericanHeart Association.13Abnormal conduction pathways canpresent as an irregular
rhythm.Wolff-Parkinson-White syndrome is a condi-tion in which such a pathway
connectsthe atria to the ventricles,bypassing theAV junction through the bundles
ofKent.As a result ofimpulses traveling throughthis accessory pathway,the
electrocardio-gram demonstrates a shortened P�Rinterval (< 0.12 s),a wide QRS
complex(> 0.10 s),and a characteristic slurring ofthe upstroke ofthe R wave (called
a deltawave) (Figure 3-1).This extra or accesso-ry electric pathway is present in
approxi-mately 1.5 per 1,000 people.It runs infamilies in < 1% ofcases.In the
majorityofindividuals,it is completely silent andis only detected on a routine
ECG.In asmall proportion ofpatients,the extraelectric pathway generates an electric
cir-cuit that produces a very rapid heart rate.Most patients tolerate this well,but
someexperience very troublesome palpitations,
52Part 1: Principles ofMedicine,Surgery,and Anesthesialight-headedness,and
blackouts.A verysmall minority ofpatients may die sud-denly from ventricular
fibrillation.Theideal treatment in patients with symp-toms is to destroy the extra
electric path-way using radiofrequency ablation.Younger patients (< 25 yr) are most
atrisk ofsudden death and require furthertests to assess their possibility
ofdevelop-ing life-threatening electric disturbances.This is best done with an
exercise testunder the supervision ofa cardiologist.The abrupt disappearance ofthe
deltawave on the ECG as the heart rateincreases is a good sign,obviating theneed
for further investigation.Ifthis doesnot happen,further electrophysiologictesting
is recommended.17Ventricular arrhythmias can be clas-sified as benign,potentially
malignant,and malignant.Benign ventricular ectopy(ie,premature ventricular
contraction)occurs in a normal heart with or withouta previous history
ofarrhythmias,isasymptomatic,and generally does notwarrant treatment unless
hemodynamicperturbations are noted.Nonspecific car-diac challenges such as
hypoxemia,hypercarbia,acidemia,sympatheticsurge,drug effects,and electrolyte
distur-bances should be investigated and treatedas necessary.A recently completed
studydemonstrated a 6.3% incidence ofpre-mature ventricular beats,but only
0.62%suffered severe adverse outcomes,which,according to the author,may have
beenrelated more to the aggressive treatmentemployed in these cases.More than
sixpremature ventricular contractions perminute,especially ifthey are
multifocal,are considered to be ventricular tachycar-dia and should be treated
accordingly.16Ventricular tachycardia with a pulse istreated using cardioversion or
antiar-rhythmia medication in a controlledmonitored setting.Pulseless
ventriculartachycardia is managed in the same man-ner as ventricular
fibrillation,asdescribed below.After assessing anunconscious victim for
responsiveness,breathing,and a pulse,the airway shouldbe opened,two rescue breaths
given,andcardiopulmonary resuscitation initiateduntil a defibrillator is
obtained.Therhythm should be assessed,and ifven-tricular tachycardia without a
pulse orventricular fibrillation is detected,pro-gressive electric shocks should be
admin-istered at 200 J,200 to 300 J,and 360 Jusing a conventional defibrillator or
anautomatic external defibrillator.Lessenergy is needed for a biphasic defibrilla-
tor (eg,120 J,150 J,and 200 J).Iftherhythm is persistent,epinephrine in 1 mgdoses
every 3 to 5 minutes or vasopressinas a single 40-unit dose should be admin-
istered.Defibrillation at maximum dose(360 J or the biphasic equivalent) shouldbe
repeated after the catecholamine (epi-nephrine or vasopressin dose).Ifunsuc-
cessful,doses ofamiodarone,lidocaine,procainamide,or magnesium may beattempted
followed by defibrillation at amaximal dose.For the most part,thesedrugs have only
preventive roles in case ofrecurrence ofthe arrhythmia.13,17Automatic Implantable
Cardioverter Defibrillators and PacemakersThe first automatic implantable
cardiovert-er defibrillator (AICD) was placed in 1980and became commercially
available in1986.In recent years the use ofAICDs hasbecome widespread and has
significantlyreduced cardiac death in this susceptiblepopulation from 40 to 60% to
< 2 to 3%over a 3-year postimplantation period.They are primarily used in cases
ofventric-ular ectopy or spontaneous/recurrentepisodes ofventricular
tachycardia/fibrilla-tion despite drug therapies.For the practi-tioner treating an
individual with an AICD,it is important to realize that basic andadvanced cardiac
resuscitation should pro-ceed as ifthe individual does not have thedevice.The shock
delivered by the appli-ance may be discernible but does not poseany risk to the
caregiver.The proper func-tioning ofthe device should be checkedafter
resuscitation.In addition,the use ofmagnetic resonance imaging (MRI) is con-
traindicated when the device is in place.Since electrocautery can cause the device
toadminister an inappropriate shock,thedevice should be inactivated prior to
usingany electrosurgical equipment.Presently there are over 1,500 types
ofpacemakers working in over two millionindividuals.In general,they are used
forbradycardia and to prevent resultantlow�cardiac output states.Modern
devicesadapt the rate to the metabolic needs ofthepatient.Sensors ofoxygen
saturation,rightventricular pressure,central venous bloodtemperature,and body
movements help toadapt the rate.No pacemaker beats areobserved ifthe intrinsic rate
is greater thanthe threshold ofthe pacemaker.Ifthe pace-maker is functioning,there
should be apacemaker spike on the down slope ofthe Rwave,ST segment,or T wave with
a QRScomplex following in a one-to-one rela-tionship.Pacemaker failure in the
perioper-ative period can occur as a result ofhypo-or hyperkalemia,hypo- or
hyperventila-tion,or acute ischemia.Some pacemakergenerators can be affected by
electro-cautery.It is advisable to use bipolar cauterywith the lowest possible
current and toavoid using cautery within 13 cm oftheP wave123Delta
waveFusionFIGURE3-1Demonstration ofthe delta wave in Wolff-Parkinson-White
syndrome.
Perioperative Considerations53pacemaker (usually located in the subpec-toral region
or �beltline�ofthe anteriorabdominal wall).Avoidance ofthe use ofMRI is advisable
as well.A discussion withthe patient�s cardiologist prior to surgery
isprudent.17Electrolytes and Acid-Base DisturbancesWith any arrhythmia,coexisting
acid baseand electrolyte disturbances should beidentified and corrected.Part ofthe
periop-erative assessment ofhypoxia is the mainte-nance ofacid-base balance.Normal
pH ofarterial blood is 7.4 and is maintained towithin 0.05 (ie,the normal pH range
oftheblood is 7.35 to 7.45).The main bufferingofacids occurs through the lungs
(throughthe conversion ofcarbonic acid [H2CO3] toCO2 and H2O) and the kidney
(through thebase bicarbonate [NaHCO3]).Respiratory acidosis occurs when thelungs
are not exhaling CO2adequately.This can occur with emphysema or respi-ratory
depressive states such as overseda-tion,respiratory insufficiency,and
arrest.Conversely,respiratory alkalosis occurswhen too much CO2is expelled as
inhyperventilation,neurogenic disorders,and salicylate toxicity (which,interesting-
ly,is accompanied by metabolic acidosis).Metabolic acidosis is caused by adeficit
ofthe base bicarbonate.Normallythere is an H2CO3-to-NaHCO3ratio of1:20.H+is
excreted in the urine,and bicar-bonate is reabsorbed into the renal tubulesto
maintain this ratio.With the presence ofexcess acid,the bicarbonate combines
withthis source ofH+,is excreted,and is there-fore no longer available for its
usualbuffering role.This results in an upset ofthe 1:20 ratio and acidosis.Lactic
acidfrom muscle activity or anaerobic condi-tions,diabetic ketoacidosis,renal
failure,or exogenous sources such as methanol,ethanol,or paraldehyde can all serve
as thealternative acid source.A method to deter-mine whether metabolic acidosis is
pre-sent is to calculate an anion gap (ifinfor-mation on electrolytes is
available):Anion gap = Na+� ([C1�] + [HCO3�])A normal range is 10 to 14
mEq/L.Metabolic alkalosis is caused by a rel-ative increase in bicarbonate.Only
rarelyis this caused by the exogenous adminis-tration ofbicarbonate since the
kidneynormally excretes excess bicarbonate inan individual who is well hydrated
andhas good kidney function.More com-monly this condition occurs owing
toelectrolyte disturbances such as occur as aresult ofvomiting,nasogastric
suctioning,or diuretic use.Primarily this can occurthrough shifts in intracellular
potassium.Hypokalemia increases the excitabilityand automaticity ofcardiac
muscle,increasing the possibility ofarrhythmias.Hypomagnesmia can potentiate this
effectby decreasing the extrusion ofintracellularcalcium,which is also
arrhythmogenic incardiac conduction cells.Assessment ofelectrolytes and their
correction is there-fore warranted in acid-base perturbations.Examples ofAcid-Base
Analysis 1.Note the pH value:pH < 7.35 = acido-sis;pH > 7.45 = alkalosis.2.Note the
value ofpartial pressure ofcarbon dioxide in arterial blood(PaCO2value).Ifit is the
same sign as the pH,thecondition is metabolic in nature.Ifitis the opposite in
sign,the condition isrespiratory.Therefore,pH < 7.35 andPaCO2< 40 mm Hg indicate
metabol-ic acidosis;pH < 7.35 and PaCO2> 40 mm Hg signify respiratory acidosis.This
represents a method ofanalysis that is easy to remember.Thebasis involves the
underlying cause ofeach condition.Respiratory acidosis isprimarily caused by an
elevation ofCO2,causing a compensatory eleva-tion ofcarbonic acid in the lung witha
resultant decreased pH.Metabolicacidosis is caused by the addition ofanacid source
to the normal acid-basebuffering system.This acid sourcelowers the pH.One ofthe
methods ofbuffering this acid is the carbonic acidsystem in the lung.Respiration
rateand depth increase in an attempt toeliminate the additional CO2pro-
duced,lowering the CO2.Ultimately,however,this system cannot eliminateall ofthe
additional acid and maintainthe normal acid-base ratio.18The cause ofalkalosis can
bedetermined in a similar manner:pH > 7.45 and PaCO2 > 40 mm Hg indi-cate a
metabolic condition;pH > 7.45and PaCO2< 40 mm Hg signify respi-ratory
alkalosis.3.Confirm the acid-base relationshipthrough analysis ofthe
bicarbonatelevel (assuming normal kidney com-pensations are present).In respiratory
acidosis the kidneyshould retain bicarbonate and reestab-lish the normal 1:20 acid-
to-base ratio(ie,the bicarbonate level should remainat its normal value of24
mEq/L).Inmetabolic acidosis there is usually abicarbonate deficit
(ie,bicarbonatelevel < 24 mEq/L).Case Example 1A 54-year-old man isreferred for
lethargy.A review ofsystemsreveals polydypsia,polyphagia,and polyuria.His
laboratory results are as follows:arterialblood gases reveal a pH of7.22,PaCO2of24
mm Hg,and HCO3�of12 mEq/L.Serumchemistries reveal Na =130 mEq/L,Cl� = 94 mEq/L,K =
4.5 mEq/L,and glucose = 600 mg/dL.In this example,the pH is < 7.35;therefore,it is
a case ofacidosis.The PaCO2is < 40 mm Hg;therefore,the process ismetabolic
acidosis.The bicarbonate level(12 mEq/L) confirms a relative bicarbonatedeficiency
consistent with metabolic acido-sis.An anion gap analysis is as follows:
54Part 1: Principles ofMedicine,Surgery,and AnesthesiaNa+� ([C1�] + [HCO3�])130 �
(12 + 94)= 31.5This reveals the presence ofan anion gapmetabolic
acidosis,consistent with dia-betic ketoacidosis based on the clinicalpresentation
and elevated glucose level(600 mg/dL).Case Example 2A 75-year-old womanwas recently
started on furosemide to treatpedal edema.She describes a loss ofener-gy and a
light-headed sensation when aris-ing from a seated position.Her arterialblood gases
indicate a pH of7.53,PaCO2of52 mm Hg,and HCO3�of32 mEq/L.Serum chemistries show the
following lev-els:Na = 129 mEq/L,Cl� = 90 mEq/L,K = 3.0 mEq/L,and glucose = 120
mg/dL.In this case,the pH (7.53) and PaCO2(52 mm Hg) reveal the presence
ofanalkalotic state.This is confirmed by thebicarbonate level (32
mEq/L).Metabolicalkalosis is often caused by secondary vol-ume depletion with
resultant electrolyteshifts.The loss ofintracellular potassiumcan cause the shift
ofprotons (H+) into thecell to maintain neutrality.Renal InsufficiencyIt is
interesting to note that an elevated cre-atinine is presently included as a factor
inrisk assessment for surgery.2Acute renalfailure is primarily a result
ofintraopera-tive renal hypoperfusion.It is usually seenin cardiopulmonary bypass
proceduresand thoracoabdominal and abdominalaortic aneurysm repairs,where its inci-
dence is reported to be as high as 15%,25%,and 5.4%,respectively.19�21In addi-tion
to surgical type,preoperative renalinsufficiency is the single consistent pre-
dictor ofpostoperative renal failure.19Additional insults that may further predis-
pose a patient to perioperative kidney fail-ure are the presence ofan already
ischemicstate caused by renal artery stenosis,vol-ume depletion,and diabetes,or a
recentacute ischemic event caused by hemor-rhage or exposure to radiocontrast
agents.Many other conditions can predispose thekidneys to ischemic injury,including
sep-sis,cirrhosis,jaundice,hepatorenal syn-drome,congestive heart
failure,shock,malignant hypertension,preeclampsia,sickle cell anemia,collagen
vascular dis-eases,and multiple myeloma.Many drugsalso potentiate the risk
ofischemic renalinjury through alterations in intrarenalhemodynamics,including
angiotensin-converting enzyme inhibitors,nonsteroidalanti-inflammatory
drugs,cyclosporine,tacrolimus,and amphotericin B.19,22The most susceptible area to
ischemicinjury is the tubular cells ofthe thickascending loop ofHenle and a portion
ofthe proximal convoluted tubules located inthe renal medulla (Figure 3-2).The
cells inthis region are rich in mitochondria andare responsible primarily for
chloride ionabsorption.A combination oflow bloodflow (compared with that in the
renal cor-tex) and high metabolic demand accountsfor this susceptibility.Initially
there is aloss ofurine-concentrating ability as thenormal medullary gradient
dissipates,fol-lowed by a decline in urine output astubules become obstructed and
denuded.Traditionally,the management ofacute renal failure has been the mainte-
nance ofurine output through the use ofintravenous hydration and diuretics suchas
furosemide and mannitol in addition tolow-dose dopamine to maintain renal per-
fusion.Recently this practice has come intoquestion since increasing renal blood
flowelevates the oxygen demand at the medullaand may lead to further
injury.19Presentresearch is directed at regulating renalvasoactive substances
discovered in animalmodels including prostaglandins (especial-ly prostaglandin
E2),angiotensin II,nitricoxide,endothelin,and adenosine.23Since volume depletion
and hypoten-sion are risk factors for the development ofacute renal
failure,preoperative testing ofblood urea nitrogen and creatinine shouldbe
conducted in patients with a known his-tory ofrenal insufficiency or a
diseasemechanism (eg,diabetes mellitus) in whichkidney damage may be present and
signifi-cant volume loss or hypotension may occur.In addition,the use
ofintraoperative inva-sive monitoring (ie,central venous pressureor pulmonary
capillary wedge pressure)may be warranted in these cases.19Pulmonary
AssessmentAsthmaAsthma is a disease characterized by anepisodic variable airflow
obstruction withincreased airway reactivity.Recently theimportance ofsubmucosal
inflammationand its control in managing asthma hasbeen stressed.Bronchoconstriction
in asth-matics is triggered by a stimulus such as anantigen,exercise,or exposure to
cold.Thetrigger elicits an acute inflammatory cas-cade,characterized by
degranulation ofmast cells and activation ofeosinophils andmacrophages in the
airway.Releasedleukotrienes,histamines,and bradykininsincrease vascular
permeability and resul-tant edema.The airways fill with mucusand inflammatory
cells,and smooth mus-cles contract as a response to released medi-ators and an
increased cholinergic tone.24,25Heightened airway responsiveness canincrease the
likelihood or severity ofbron-chospasm under anesthesia.Aspects ofthepatient�s
history that may indicate the poten-tial for problems to arise include
frequentnocturnal awakenings from bronchospasm,increased necessity for inhaler
use,recenthospitalizations or emergency departmentvisits,a change in the amount or
quality ofsecretions,or a recent viral illness or coldsymptoms.Spirometry is
helpful in the ini-tial diagnosis and chronic management ofreactive airway
disease.Its routine use addslittle information to the preoperative assess-ment that
cannot be ascertained by therecent history and physical examination.Repeat
assessments over time can be helpful,however,as subtle changes in flow rates canbe
detected by spirometry before they
Perioperative Considerations55become symptomatic;this allows preventivetreatment to
be initiated.The most common parameters thatare assessed over time are the forced
expi-ratory volume generated in the first sec-ond ofexhalation and the peak
expiratoryflow rate (Figure 3-3).26 These parameterscan be measured with
inexpensive hand-held devices.A 20% variation in peakexpiratory flow rates is
normal.Rates thatfall to 50 to 80% below normal are consid-ered a moderate
exacerbation.Flow rates< 50% ofbaseline are considered severeand require prompt
medical attention.The term reactive airway diseaseisconsidered by some individuals
to be syn-onymous with asthma.However,airwayreactivity is also increased owing to
aller-gic rhinitis,bronchitis,emphysema,andrespiratory viral
infections.Bronchospasmis a physical sign ofacute increased airwayresistance.It is
associated with tachypnea,wheezing,air trapping,and worsened gasexchange.Under
anesthesia wheezing andbronchospasm can occur with or withouta prior history
ofreactive airway disease.Most wheezing is self-limited and requiresno
intervention,but it can indicate the ini-tiation ofa more severe
bronchospasm.Patients with symptoms ofbronchospasmpreoperatively should have
elective proce-dures postponed.26Whereas asthmatics have chronichyperactivity ofthe
airways,patients withupper respiratory tract infections (URIs)have acute airway
reactivity that can last upto 6 weeks after recovery from the
initialinfection.Airway hyperactivity in URIs isneurally mediated with an increase
invagal-mediated bronchoconstriction.Chil-dren with a concomitant URI are especial-
ly susceptible to bronchospasm.These chil-dren are two to seven times more likely
tohave adverse events in the perioperativeperiod,and there is an increased risk
ofpostoperative desaturation in thesepatients.The risks are highest in
thosepatients undergoing endotracheal intuba-tion (in whom there is an 11-fold
increasein perioperative respiratory complica-tions).Definitive criteria for
canceling asurgery to be performed under sedation orgeneral anesthesia have not
been estab-lished,and the decision is often subjective.Suggested criteria for
cancellation includethe necessity ofendotracheal intubation,parental observation
that the child is acute-ly ill the day ofsurgery,the presence ofnasal congestion
and cough,concomitantexposure to passive smoke,and active spu-tum production.Most
surgeons agree thatthe planned surgery,ifelective,should bepostponed until after
the acute symptomshave resolved and have not recurred for a3-week period after the
initial evaluation.27Treatment ofa Reactive AirwayInhaled short-acting �2-
adrenergic agonistsare the drug offirst choice for the
treatmentProximalconvolutedtubuleDistalconvolutedtubuleInitial portionof
corticalcollecting
ductConnectingtubuleCorticalcollectingtubuleMedullarycollectingtubuleMedullaryductM
aculadensaStraightproximaltubuleDescendingthin limbof Henle'sloopAscendingthin
limbof Henle'sloopAscendingthick limbof
Henle'sloopBowman'scapsuleEfferentarteryAfferentarteryBowman's
capsuleRenalcortexProximalconvolutedtubulesLoop of HenleCortexMedullaCollecting
ductRenalmedullaFIGURE3-2Normal renal architecture.
56Part 1: Principles ofMedicine,Surgery,and Anesthesiaofacute bronchospasm.�2-
Agonists direct-ly relax smooth muscle,aid in the stabiliza-tion ofmast cells,and
inhibit the release ofacetylcholine from postganglionic choliner-gic nerves.The
inhibition ofthe cholinergicresponse is important because bron-chospasm during a
surgery is often mediat-ed by a vagal response.Doses should be lim-ited by side
effects rather than by anarbitrary number ofinhalations.In general,intubated
patients require twice the drugdose since the delivery ofdrug through
theendotracheal tube is inefficient.Ifthepatient is unconscious,the �2-agonist can
bedelivered subcutaneously or intravenously,usually as epinephrine.Intravenous epi-
nephrine can be used safely in low doses,but dysrhythmias and other
undesirableeffects may occur in older individuals.Glucocorticoids are useful in
asthma inpatients who have not adequately respond-ed to �2-agonists.Their reported
benefitsinclude reduction ofinflammation,hista-mine,and arachidonic acid
metabolites.Anticholinergic drugs such as ipratropiumcause bronchodilation directly
and bluntbronchoconstriction from cholinergic-mediated triggers.Both steroids and
anti-cholinergic agents enhance the activity of�2-agonists but are not indicated
for acuteexacerbations ofbronchospasm.In the past theophylline was fre-quently
recommended for acute exacer-bations ofbronchospasm;however,thishas been encouraged
less in recent yearssince its potency as a bronchodilator isless than the �2-
agonists and it frequentlyproduces toxicity and undesirable sideeffects including
dysrhythmias.In somepatients with chronic asthma or COPD,theophylline can decrease
the severityand frequency ofattacks and decreasesteroid requirements.Its mechanism
ofaction also has been questioned recently.Although it does increase
concentrationsofcyclic nucleotides (ie,cyclic adenosinemonophosphate) in airway
smooth mus-cle and inflammatory cells by inhibitingthe phosphodiesterase isozyme,it
alsohas been demonstrated in dogs to pro-duce bronchodilation by increasing
therelease ofendogenous catecholamines.(Halothane appears to block this effect.)The
drug also acts as an adenosine-recep-tor antagonist,which may help to medi-ate its
effects on ventilation and mediatorrelease.28 Cromolyn sodium reduces
thedegranulation ofmast cells,inhibiting therelease ofhistamine and
leukotrienes.Assuch,it is useful as a prophylaxis againstacute attacks in patients
with asthma.Ithas no beneficial value in the manage-ment ofacute
bronchoconstriction.Thelatest approach in reactive airway man-agement is to block
the conversion ofarachidonic acid to leukotrienes.Similarto other measures that are
directed atreduction ofthe inflammatory response,these medications prevent acute
exacer-bations ofasthma or bronchospasm butare not appropriate for acute
attacks.Anexample ofa leukotriene inhibitor ismontelukast sodium,which
specificallyblocks the leukotriene D4receptor.Respiratory arrest in the
perioperativeperiod is commonly caused by airwayobstruction,laryngospasm,or a
foreignbody in the airway.A further differentialdiagnosis and treatment algorithm
is pro-vided in Figure 3-4.29,30Perioperative Effects ofTobaccoSmokingCigarette
smoke contains over 3,000 con-stituents,some ofwhich are toxic ortumorigenic.Carbon
monoxide,producedas an end product ofburning tobacco,hasTime (s)Time (s)Maximum
inspirationMaximum inspirationFEV1FEV14321043210123456123456FVCFVCFEV1/FVC =
50%FEV1/FVC = 80%Lung Volume (L)Lung Volume (L)FIGURE3-3Comparison offorced
expiratory volume in 1 second (FEV1) and forced vital capacity(FVC) in a patient
with obstructive lung disease (A) and a normal individual (B).
Perioperative Considerations57a 200 times greater affinity than oxygen forthe
hemoglobin (Hb) molecule.Carboxy-hemoglobin,which can be as high as 15%,predisposes
a patient to perioperativehypoxia.Pulse oximetry fails to recognizethe presence
ofcarboxyhemoglobin(COHb) as distinct from oxyhemoglobin.Therefore,a patient with
10% COHb maydisplay a saturation of100% when,in fact,the actual saturation may be
closer to 90%.In addition,carboxyhemoglobin has theeffect ofshifting the oxygen
dissociationcurve to the left (ie,less oxygen is deliveredto tissues;Figure 3-
5).The relative hypoxiadetected by the body (more specifically,thekidneys) results
in an increased release oferythropoietin with a resultant thrombo-cytosis.In
addition,carbon monoxide hasa direct effect on the myocardium withincreased
automaticity and a lower thresh-old for ventricular fibrillation.31The pulse
oximeter functions by posi-tioning a pulsating arterial bed between atwo-wavelength
light-emitting diode and adetector (photodiode).One wavelength is660 nm (red),and
the other is 940 nm(infrared).Oxygenated hemoglobinabsorbs more ofthe 940 nm
wavelengththan does reduced hemoglobin,which,inturn,absorbs more ofthe 660 nm wave-
length.The percent saturation reading(SpO2%) is determined from the ratio
ofoxygenated hemoglobin to the total hemo-globin.A common difficulty in determin-
ing SpO2occurs secondary to changes inthe strength ofthe arterial pulse or
patientmovement,resulting in either no signal orartificially low readings.Causes
oftheseerrors include hypothermia,hypotension,the use
ofvasopressors,electrocautery,artificial or opaque nail finishes,and addi-tional
monitors such as an automaticblood pressure cuffor arterial line on thesame arm.The
effects ofother potentialsources oferror in SpO2measurement aregiven in Table 3-
5.32Nicotine as a vasoconstrictor can havea significant effect on the
cardiovascularsystem.Similar to other vasoconstrictors,increases in heart
rate,blood pressure,andperipheral vascular resistance are seen sec-ondary to the
activation ofthe sympathet-ic nervous system and the release ofcate-cholamines from
the adrenal medulla.This effect persists for 30 minutes aftersmoking a
cigarette.Coronary artery vas-cular resistance is similarly affected,potentially
leading to further limitedblood flow in areas predisposed toischemia.Nicotine can
also lower thethreshold for ventricular fibrillation.Car-bon monoxide and nicotine
have a rela-tively short half-life (carbon monoxide t1/2= 4 h;nicotine t1/2= 30�60
min).Withregard to potential cardiac complications,there is a direct benefit
ofabstinence fromsmoking for 12 to 24 hours.Able to ventilate?Support
ventilationVentilation�none or partialOxygenation�falling SpO2In all
cases:Supplemental O2Jaw repositioningConsider laryngospasm:Positive pressure
O2Suction pharynxSuccinylcholine IV� 10 mg; 20�40 mg (0.15�0.3 mg/kg)� 0.6�1.5
mg/kg IV; 4 mg/kg IMSupport ventilationAble to ventilate?Able to ventilate?Consider
bronchospasm:Inhaled �2-agonistIntubationEpinephrine 0.3�0.5 mg� IV: 3�5 cc of
1:10,000� SQ: 0.3�0.5 cc of 1:1,000Other considerations:Foreign body� Heimlich�
Laryngoscopy� Transtracheal catheter� Cricothyrotomy� TracheostomyEndotracheal tube
position"Stiff chest" syndrome (fentanyl)Tracheal
stenosisHematomaHypocalcemiaNoYesYesYesNoNoFIGURE3-4Respiratory arrest
algorithm.Adapted from American Association ofOral and MaxillofacialSurgeons29;
American Heart Association.30100806040200020406080100O2 unloaded from hemoglobin
duringnormal metabolismShift to right:H+CO2Temperature2,3 DPGO2 reserve that can be
unloaded from hemoglobin to tissues with high metabolismTissuesduring
exerciseTissuesat restPartial Pressure of Oxygen(mm Hg)LungsSaturation of O2
(%)FIGURE3-5 Oxygen dissociation curve.DPG = 2,3-diphosphoglycerate.
58Part 1: Principles ofMedicine,Surgery,and AnesthesiaUnfortunately,detrimental
effects onciliary function and mucus overproduc-tion by respiratory mucosa as a
responseto tobacco can last for months after smok-ing cessation.Additional
detrimentaleffects include increased bronchial reactiv-ity,macrophage
dysfunction,and changesin pulmonary surfactant.Assuming asmoker has not had long-
term deleteriouseffects related to COPD,these changesrequire 6 to 8 weeks for
complete reversal.Postoperative pulmonary complicationsincluding
atelectasis,pneumonia,andbronchospasm are much more likely tooccur in individuals
who smoke.Interestingly,increased pulmonarycomplications have been demonstratedwhen
a patient ceases smoking < 8 weeksprior to a planned surgery.Therefore,rec-
ommendations to the smoking patientshould include at least a 12- to 24-hoursmoking
�fast�or,more desirably,a cessa-tion ofsmoking for 8 weeks or more.Patients should
be counseled that cessa-tion for periods < 8 weeks may actuallypredispose the
individual to increased pul-monary complications.33In recent studies the effects
ofsecond-hand or passive smoke have been ana-lyzed.The risks ofchronic
bronchitis,asthma,and wheezing were all higher inpatients exposed to involuntary
tobaccoexposure,especially in the workplace witha daily exposure of> 8 h/d.The
exposurelevels in the workplace have been estimat-ed to be higher than at home,and
the timespent at work is usually longer.It is pru-dent to determine secondhand
smokeexposure in the perioperative manage-ment ofthe surgical patient.34ObesityThe
difference between normality and obesi-ty is arbitrary,but an individual
withincreased fat tissue to such an extent thatphysical and mental health are
affected andlife expectancy is reduced should be consid-ered obese.Body mass index
(BMI) is wide-ly used in clinical and epidemiologic studies.It is the ratio ofbody
weight (in kilograms)to height(in meters squared).A patient witha BMI of< 25 kg/m2
is considered normal.Apatient with a BMI of25 to 30 kg/m2is over-weight but at
relatively low risk for seriousmedical complications;one with a BMI of> 30 kg/m2 is
obese with a higher risk ofmorbidity and mortality.Morbidly obeseindividuals have
an increased risk ofdeathfrom cardiorespiratory and
cerebrovasculardisorders,diabetes mellitus,and certainforms ofcancer in addition to
many otherdiseases.These risks are proportional to theduration ofobesity.Weight
loss reduces therisks but only over time;weight reductionimmediately prior to
surgery has not beenshown to reduce perioperative risk.35,36Approximately 5%
ofobese individu-als have obstructive sleep apnea (OSA),which is characterized by
episodes ofapnea or hypopnea during sleep.Obstruc-tive apnea is characterized by
apneadespite a continuous respiratory effortagainst a closed airway.Central apnea
ischaracterized by the loss ofventilatoryeffort.Many patients diagnosed with OSAcan
have periods ofcentral apnea duringsleep as well.Apneais typically defined as10
seconds or more oftotal cessation ofairflow.Hypopneais defined as a reduc-tion in
airflow (typically 30�50%) or areduction sufficient to lead to a 4%decrease in
arterial oxygen saturation.Thenumber ofapneic or hypopneic episodesbelieved to be
significant is five or moreper hour.The exact number is arbitrary,as are the
definitions ofapnea and hypop-nea used by various sleep laboratories.Often
individuals with OSA are noted tohave nocturnal snoring and
daytimehypersomnolence.OSA can lead to hyper-capnia,systemic and pulmonary hyper-
tension,and cardiac arrhythmias.In the perioperative period,episodesofOSA are most
frequent during rapid eyemovement sleep,the extent ofwhich is rel-atively low in
the initial postoperativeperiod but in excess on the third to fifthpostoperative
nights.Caution shouldtherefore be exercised any time anestheticagents are used in a
patient with a historyor signs and symptoms consistent withOSA.In addition,the
continued use ofmedical therapies including continuouspositive airway pressure
should be stressedin the perioperative period.37Morbid obesity is characterized
byreductions in functional residual capacity(the volume remaining in the lungs
after anormal quiet expiration),expiratoryreserve volume (the volume ofair that
canforcefully be expired after a normal restingexpiration),and total lung
capacity.Thesechanges have been attributed to massloading and splinting ofthe
diaphragm(Figure 3-6).Anesthesia compounds theseproblems and impairs the ability
oftheobese to tolerate periods ofapnea.30,31Table 3-5Some Sources ofError in Pulse
OximetrySourceEffect on SpO2ActionCarboxyhemoglobinemiaFalsely high SpO2Increase
ventilation,eliminate rebreathingMethemoglobinemiaFalsely low readings,Administer
methylene blueapproaching 85%Hyperbilirubinemia,Overestimation ofSpO2Eliminate
causative agenthyperalimentation,owing to interference hyperlipidemiaoflight
transmissionVenous pulsationsFalsely low SpO2Change siteSpO2= percent saturation
ofoxygen.� 1992.Reproduced with permission ofAlliance Communication Group,a
division ofAllen Press,Inc.,from Mardirossan Gand Schneider RE.32
Perioperative Considerations59Ventilation and CapnographyCapnographyis defined as
the measure-ment and display ofexhaled carbon diox-ide.Increases in end-tidal
CO2combinedwith decreases in the respiratory rate oftheindividual have been
demonstrated to bean effective way to detect hypoventilationand respiratory
depression.Pulse oximetry,in contrast,indirectly measures oxygena-tion (partial
pressure ofoxygen in arterialblood).Based on the oxygen-hemoglobindissociation
curve (see Figure 3-5),therecan be a significant decline in oxygen satu-ration that
can go initially undetected bythe pulse oximeter.Capnography,bydetecting
hypoventilation,may be used toprevent hypoxia;upon noting hypoventila-tion,the
practitioner can take measures toimprove patient ventilation.Proponents
ofcapnography for non intubated sedationadvocate its use over other forms ofventi-
latory monitors that can experience inter-ference from operatory
noise,clothing,orsurgical drapes.These methods includeobservation ofchest wall
movements,plethysmography,auscultation ofbreathsounds (precordial stethoscope),or
palpa-tion or movement ofthe reservoir bag.Opponents to the use ofcapnography
fornonintubated sedation cite samplingerrors,particularly in individuals who
aremouth breathing when nasal sampling isbeing used.38�40Endocrine
AssessmentDiabetes MellitusPerioperative care ofthe diabetic patientdepends on
identification and assessmentofthe current status ofend-organ disease.Long-standing
diabetics frequently havecompromise in one or more organ system.Commonly associated
diseases includeatherosclerosis,coronary artery
disease,hypertension,cardiomyopathy,cerebrovas-cular disease,peripheral vascular
disease,peripheral and autonomic neuropathy,and/or renal
insufficiency.Preoperativeevaluation should focus on these concerns,and events
ofprior surgeries should bereviewed.For more complex procedures,laboratory values
that may be reviewedinclude blood glucose,blood urea nitro-
gen,creatinine,urinalysis (for glucose,ketones,and proteins),and
glycosylatedhemoglobin (Hb A1c) levels.Hb A1clevelsreflect the adequacy ofglucose
controlduring the previous 1 to 3 months.Levelsin nondiabetics range from 5 to 7%
ofhemoglobin.Levels in diabetics with poorlong-term glucose control exceed
8%.41With more procedures being per-formed on an outpatient basis and thelength
ofhospital stays being shorteneddramatically,perioperative managementofthe diabetic
patient has become morecomplicated.Many factors are presentthat determine the
glycemic response,including insulin secretion,insulin sensi-tivity,overall
metabolism,and nutrition-al intake in addition to the stress andlength ofthe
procedure.Surgical stressand some general anesthetic agents,themselves,are
associated with increasesin the counter-regulatory hormones epi-
nephrine,norepinephrine,glucagon,growth hormone,and cortisol.The effectofthese
hormones is to elevate insulinresistance,which increases hepatic glu-cose
production and decreases peripheralglucose use.Patients receiving pharmaco-logic
therapy to control their diabetesmay also be susceptible to hypoglycemia,especially
when fasting preoperatively.Although hypoglycemia can cause signif-icant
morbidity,marked hyperglycemiashould also be avoided since it can lead
todehydration and electrolyte disturbancesand impaired wound healing and predis-
pose to infection or diabetic ketoacidosisin the patient with type 1 DM.This is
notto say that patients with historically poorcontrol oftheir disease should be
rapidlynormalized presurgically;little evidencesupports this approach.In
general,thegoal for glucose control during surgeryshould be between 150 and 200
mg/dL.The more unstable the diabetes,the morefrequently this level should be
assessed inthe perioperative period.As in all patients,underlying
cardiac,pulmonary,renal,and electrolyte distur-bances and anemia should be
evaluated.Assessment should include a focus on themicrovascular (ie,renal
insufficiency,Maximal inspiratory levelResting expiratory levelMaximal expiratory
level TLCVCRVFRCICTVRVIRVERVFIGURE3-6Summary oflung volumes and capacities.ERV =
expiratory reserve volume; FRC =functional residual capacity; IC = inspiratory
capacity; IRV = inspiratory reserve volume; RV = resid-ual volume; TLC = total lung
capacity; TV = tidal volume; VC = vital capacity.
60Part 1: Principles ofMedicine,Surgery,and Anesthesiaretinopathy),macrovascular
(includingatherosclerosis,coronary artery disease,hypertension),and neuropathic
signs relat-ed to poor diabetes control.Medicationuse and insulin regimen should be
record-ed.Management ofthe patient should becoordinated with the individual who
man-ages the patient�s daily protocol.The fol-lowing are recommended guidelines in
themanagement ofpatients with diabetes whorequire a period ofnothing by mouth
priorto their planned procedure.Type 2 DM Controlled by Diet OnlyMeasurement
ofblood glucose should beconsidered prior to the procedure,afterthe procedure,and
intraoperatively forlonger surgeries.Hyperglycemia is treatedwith short-acting
insulin (regular orlispro),usually administered subcuta-neously.It is prudent to
remind patientsprior to discharge ofthe signs and symp-toms ofhyperglycemia
(discussed below)and to reinforce guidelines for contactingtheir physician.Type 2
DM Treated with Oral Hypo-glycemic AgentsOral hypoglycemicagents are generally
administered the dayprior to surgery and withheld the day ofsurgery.Ifpatients
manifest markedhyperglycemia,supplemental insulin maybe indicated;the surgery may
be per-formed ifelectrolyte levels are acceptable.Table 3-6 provides information on
com-mon oral hypoglycemic agents.Types 1 and 2 DM Treated with InsulinFor
individuals who take long-acting insulin(ie,extended zinc suspension or
glargine;Table 3-7),a switch to an intermediate-actingtype is initiated a day or
two prior to surgery.The regulation ofintermediate insulin is thenadjusted based on
the likelihood ofthepatient eating lunch.Ifthe likelihood oforalintake at lunch
time is high,two-thirds ofthenormal intermediate dose is given on themorning ofthe
procedure.Ifthe patient istreated with a twice-daily dose ofinsulin,then one-
halfofthe total morning dose ofinsulin (including short-acting) should
beadministered in the morning as intermediateinsulin.Ifthe likelihood ofconsuming
lunchis low,one-halfofthe total morning dose ofinsulin (including short-acting)
should beadministered as intermediate-acting insulinfor the patient treated with a
single insulindose and one-third for those on a twice-dailyregimen.For the patient
taking multipledoses ofshort-acting insulin,one-third ofthepre-meal dose ofshort-
acting insulin isadministered.Patients treated with continu-ous insulin infusion
therapy (with an insulinpump) are treated with their usual basal infu-sion
rate.Individual modifications ofinsulintherapy may be required,and it is
advisableto discuss the management with thepatient�s physician.Procedures
scheduledlater in the day can be more complex tomanage,and intravenous glucose
infusionand/or supplemental short-acting insulinmay be necessary.Long complex
operativeprocedures may require intravenous insulinregimens.Table 3-7 reviews the
commontypes ofinsulin and their onset,peak activ-ity,and duration.Hypoglycemia and
Hyper-glycemia: Identification andManagementDirect neurologic symptoms and
anadrenergic response characterize themanifestations ofhypoglycemia.Neuro-
glycopenia generally begins with confu-
sion,irritability,fatigue,headache,andsomnolence.Prolonged severe hypo-glycemia can
cause seizures and even focalneurologic deficits,coma,and death.Therefore,any new
neurologic symptomin the postoperative period should beinvestigated for
hypoglycemia becauseprolonged deficit ofglucose can result inirreversible
neurologic deficits.Theadrenergic symptoms include
anxiety,restlessness,diaphoresis,tachycardia,hypertension,arrhythmias,and
anginaowing to catecholamine release inresponse to hypoglycemia.Recognition
ofperioperative hypoglycemia can be diffi-cult initially because presenting symp-
toms can be altered or absent as a result ofthe effects ofanesthetic
agents,analgesics,and sympatholytic agents.In addition,diabetics with autonomic
neuropathyhave blunting ofthe adrenergic responseassociated with
hypoglycemia.Hypoglycemia is defined as glucose < 50 mg/dL in adults and < 40 mg/dL
inTable 3-6Mechanism ofAction ofCommon Oral Hypoglycemic AgentsDrug
ClassExample(s)MechanismNotesa-Glucosidase inhibitorsAcarbose,miglitolInhibit
intestinal brush border oligo-No efficacy until patient is eatingand
disaccharidasesBiguanidesMetforminSensitize target tissue (muscle,fat) toMay
potentiate the risk ofdevelopinginsulin actionlactic acidosis
perioperativelyThiazolidinedionesPioglitazone,rosiglitazone,Improve peripheral
glucose uptakeNo increased incidence oflactic
troglitazoneacidosisSulfonylureasGlipizide,chlorpropamideStimulate insulin
secretionHigher potential for developing perioperative hypoglycemia
Perioperative Considerations61children.Its treatment is a glucose sourceiforal
intake is possible;however,to avoidthe risk ofaspiration and delay in absorp-
tion,50 mL of50% (25 g) ofglucoseshould be administered intravenously.Each
milliliter ofD50 raises the blood glu-cose approximately 2 mg/dL.Glucagon(1�2
mg),diazoxide,and octreotide havebeen used but are typically reserved forsulfonyl
urea�induced hypoglycemia.Perioperatively many regulatory hor-mones that oppose
insulin action arereleased.Catecholamines,glucocorticoids,growth hormone,and
glucagons can causeplasma glucose levels of> 180 mg/dL,exceeding the capacity ofthe
kidney andresulting in glycosuria.Glucose-induceddiuresis can occur,resulting in
dehydra-tion or the formation ofketone bodies,which,in turn,results in diabetic
ketoaci-dosis.Treatment includes the use ofintra-venous insulin and appropriate
rehydra-tion.One unit ofregular insulin typicallylowers the glucose 25 to 30 mg/dL
in a 70 kg individual.Subcuticular injectionshould be avoided in the
perioperativeperiod owing to unpredictable cutaneousblood flow.42Adrenal
AssessmentAdrenal insufficiency is classified as eitherprimary,owing to disease
ofthe adrenalglands themselves,or secondary,owing todecreased adrenocorticotropic
hormone(ACTH) because ofpituitary or hypothala-mus disorders.Primary adrenal
insufficien-cy is also known as Addison�s disease and isthought to be the result
ofan autoimmuneprocess.Other causes ofprimary adrenalinsufficiency include chronic
granuloma-tous disease including tuberculosis.Secondary adrenal insufficiency is
mostcommonly seen in patients on chronic glu-cocorticoid therapy.Patients on
steroidtherapy may have ACTH suppression a fullyear after steroid
therapy.Symptomsinclude fatigue,weakness,anorexia,nauseaand vomiting,and weight
loss.Only in pri-mary adrenal insufficiency is ACTH elevat-ed,indirectly resulting
in increased skinpigmentation,especially in skinfolds.Inprimary adrenal
insufficiency,aldosteronelevels are low,resulting in dehydration withhyponatremia
and hyperkalemia since therole ofaldosterone in the kidney is resorp-tion ofsodium
(and water) and excretionofpotassium.In secondary adrenal insuffi-ciency,there are
often other endocrineabnormalities present.In individuals with an intact hypo-
thalamic-pituitary-adrenal axis undergo-ing a stressful event such as a surgical
pro-cedure,the adrenal glands increase theirbaseline secretion
ofcortisol.Increasingcortisol helps maintain hemodynamic sta-bility in the face
ofstress.Patients withlong-term exogenous steroid use have ablunted response to
surgical stress com-pared to that ofnormal controls,withresultant lower cortisol
levels.Adrenal crisis is usually seen in patientswith adrenal suppression and is
precipitat-ed by a stressor,typically surgery,trauma,or sepsis.Patients may
experienceintractable nausea and vomiting,abdomi-nal pain,fever,lethargy,and
coma.Hypotension and a narrow pulse pressure(the difference between systolic and
dias-tolic pressure) are evident as shock ensues.Based on these potential risks and
anecdo-tal reports published,supraphysiologic cor-ticosteroid regimens have been
recom-mended for patients on exogenous steroids.Recent evidence suggests that
patientson long-term steroids who receive no peri-operative coverage suffer a 1 to
2% risk ofincurring a hypotensive crisis.Studies sup-port maintaining patients on
their dailysteroid dosage throughout the periopera-tive period or providing smaller
steroiddosages rather than the supraphysiologicdosages once routinely
recommended.Anexception to this practice is the critically illpatient,in whom
supraphysiologic dosagesare often administered.An example ofasuggested steroid
regimen based on thedegree ofstress is provided in Table 3-8.43,44Thyroid
AssessmentHyperthyroidism primarily affectswomen,with a female-to-male ratio
ofapproximately 8:1.Common causes ofhyperthyroidism include Graves�disease (atoxic
diffuse goiter secondary to anautoimmune reaction caused by stimula-tory antibodies
to the thyroid-stimulatinghormone receptor),toxic nodular goiter,exogenous thyroid
hormone (iatrogenic),and iodine administration.The effects ofexcess thyroid hormone
include tachycar-dia,atrial fibrillation,premature ventricu-lar
contractions,worsening ofangina pec-toris,and high-output cardiac failureTable 3-
7Onset,Peak,and Duration ofCommon Insulin PreparationsType
ofInsulinExampleOnsetPeakDurationRapid-actingLispro5�15 min30�75 min2�4 hAspart5�15
min1�2 h3�6 hShort-actingRegular30�45 min2�3 h4�8 hIntermediate-actingNPH2�4 h4�8
h10�16 hZinc suspension2�4 h4�8 h10�16 hProlonged intermediate-Extended zinc 3�5
h8�12 h18�20 hactingsuspensionLong-actingGlargine4�8 hNo peak24 hPremixed
combination70/30 or 50/50 30�60 minEarly�lateAbout 18
hinsulin(NPH/regular)peak:2�12 h
62Part 1: Principles ofMedicine,Surgery,and Anesthesiaowing to increased �-receptor
sensitivity.Respiratory complications include impair-ment and weakness
ofrespiratory muscleswith associated tachypnea,and hypercar-bia owing to the
associated hypermetabol-ic state.Patients may be hypovolemic sec-ondary to diarrhea
and hyperthermia.Exophthalmos secondary to fatty infiltrateand edema can occur
(ie,Graves�orbitopathy) and,ifsevere,can lead toblindness.Bone resorption with
secondaryhypercalcemia may occur as well.It is important to assess the degree
ofthyroid control through a history takingand physical examination (and confirma-
tory laboratory examination,ifneeded).There is a direct correlation between
theseverity ofhyperthyroidism and intraop-erative risk.Patients scheduled for elec-
tive surgery should be made euthyroidbefore surgery (this usually
requiresweeks),and cardiovascular control,asdemonstrated by stable vital
signs,shouldbe confirmed.Ifthe surgery cannot bedelayed and the patient is
hyperthyroid,�-blockers are used to slow the heart rateand decrease the potential
for arrhyth-mia.�-Blockers also inhibit the deiodina-tion ofthyroxine to the more
active tri-iodothyronine.This latter effect alsooccurs with the use
ofpropylthiouracil,which additionally inhibits the synthesisofthyroid
hormones.Iodine inhibits therelease ofthyroid hormones but is onlygiven after
antithyroid drugs to avoid athyroid hormone surge.Failure to recognize that a
patient hasuncontrolled hyperthyroidism can resultin a thyroid storm,which can
manifesteither during the procedure or in thepostoperative period.It is
characterizedby marked tachycardia,hyperthermia,weakness,and an altered level
ofcon-sciousness.Untreated,the result can becongestive heart failure and/or cardio-
vascular collapse.Treatment includes air-way and ventilatory support withincreased
minute ventilation to controlexcessive CO2production.Body temper-ature should be
aggressively managedwith cool intravenous fluids,coolingblankets,and decreased
ambient temper-ature.�-Blocker administration shouldbe started immediately to
interrupt theadrenergic response.Traditionally,anonselective �-
blocker,propranolol,hasbeen used.More recently the use ofesmolol,a shorter-acting
�1-selectiveblocker has been advocated.Patientswith COPD,asthma,and congestiveheart
failure are more likely to toleratetherapy with a �1-selective agent.Hemo-dynamic
monitoring and the correctionoffluid and electrolyte imbalancesshould be
performed.The differentialdiagnosis ofa thyroid storm includesmalignant
hyperthermia (MH;seebelow),neuroleptic malignant syn-drome,and
pheochromocytoma.Women are ten times more likely todevelop hypothyroidism than are
men.Themost common cause is iatrogenic,sec-ondary to surgical resection or
radioactiveablation ofthe thyroid gland.Hashimoto�sthyroiditis,an autoimmune
disorder char-acterized by the presence ofantimicrobialantibodies,is the most
common noniatro-genic cause ofhypothyroidism.Hypothyroidism is usually insidious
inonset and often goes unrecognized despitemultisystem effects.The most commonsigns
and symptoms include lethargy,con-stipation,cold intolerance,weight gain,and
anorexia.Although severe hypothy-roidism can result in increased morbidityand
mortality,most experts agree that mildto moderate hypothyroidism poses noincreased
surgical risk.Elective surgeryshould be postponed in hypothyroidpatients until
adequate replacement thera-py is administered.Usually this can beaccomplished by
oral thyroxine supple-mentation.Two weeks are required beforethe patient has
symptomatic improvement.Triiodothyronine,which is the active hor-mone,can be
administered for a moreacute response,but it usually takes morethan 2 weeks until
the thyroid-stimulatinghormone,the marker for adequate
thyroidfunction,normalizes.42Malignant HyperthermiaMH is a rare autosomal dominant
trait inwhich individuals inherit hypersensitivityto specific trigger agents that
cause therapid accumulation ofcalcium into thesarcoplasmic reticulum ofskeletal
muscle.This causes sudden hypermetabolic reac-tions,leading to hyperthermia and
mas-sive rhabdomyolysis.Trigger agentsinclude potent volatile anesthetic agentsand
succinylcholine (a depolarizing mus-cle relaxant).Halothane has traditionallybeen
described as a causative agent andforms the basis ofthe diagnostic test toconfirm
MH.However,all volatile agents,including sevoflurane according to recentreports,can
induce MH.45The reaction that typically occurs isabrupt and severe,requiring
immediateattention.Elevation ofend-tidal CO2is anearly sign,prior to temperature
elevation.The main treatment is dantrolene,a non-specific muscle relaxant.Its
mechanism islikely the blockade ofthe release ofcalci-um from the sarcoplasmic
reticulum.Inan acute episode ofMH,a supply ofatleast 36 vials ofdantrolene should
be avail-able for immediate use;this correspondsto a maximum dose of10 mg/kg in a
70 kgadult.In an acute attack dantrolene isadministered repeatedly in 2 to 3
mg/kgdoses every 5 to 10 minutes.Each vialneeds to be reconstituted with 60 mL
ofTable 3-8Suggested Preoperative Surgical Steroid Coverage in Patients onChronic
Corticosteroid RegimensSurgicalSteroidStress(Hydrocortisone) DoseLow25 mg on day
ofsurgeryModerate50�75 mg on day ofsurgery,1 or 2 d taper Major100�150 mg on day
ofsurgery,1 or 2 d taperAdapted from Salem M et al.44
Perioperative Considerations63sterile water.Although the use ofdantro-lene has
reduced the mortality risk from50% prior to its use,there still is approxi-mately a
10% mortality rate.There is an estimated occurrence ofMH in 1 of15,000 children and
1 of50,000 adults.Those at risk for an attackinclude survivors ofan MH reaction
andindividuals with muscular dystrophy.Theclinical sign ofmasseter muscle
spasmduring anesthesia with halothane or suc-cinylcholine may also indicate a
suscepti-bility to MH.The in vitro caffeinehalothane contracture test is used to
eval-uate individuals susceptible to developingMH when exposed to triggering
agents.Diagnostic tests based on deoxyribonucle-ic acid are currently available for
MH-sus-ceptible individuals.In addition to triggeragents,phenothiazines (such as
prochlor-perazine) should be avoided since there isa possible association between
MH andneuroleptic malignant syndrome (NMS).NMS is a rare,occasionally
lethal,idiosyn-cratic complication associated with neu-roleptic antipsychotic
drugs.NMS is char-acterized by high temperature and musclerigidity.Anxiety and
agents with sympath-omimetic activity,especially a-agonists,have been demonstrated
to aggravate MHexperimentally.Agents that some authorshave recommended to be
avoided owingto sympathomimetic effects include keta-mine and atropine.The use
ofdantroleneprophylaxis in MH patients is uncommonin view ofthe low likelihood
(0�0.62%) ofan MH reaction when a trigger-free anes-thetic regimen is
used.Dantrolene is asso-ciated with a high frequency ofmuscleweakness and
postoperative nausea.In thepast,outpatient surgery was discouraged.It is now
recommended that careful post-operative monitoring be continued for atleast 4
hours.However,most oral andmaxillofacial surgeons likely avoid per-forming
outpatient sedation for someonewith a personal or family history ofmalig-nant
hyperthermia owing to the factorsdescribed.45,46References1.Goldman L,Caldera
DL,Nussbaum SR,et al.Multifactorial index ofcardiac risk in non-cardiac surgical
procedures.N Engl J Med1977;297:845�50.2.Lee TH,Marcantonio ER,Mangione CM,et
al.Derivation and prospective validation ofasimple index for prediction ofcardiac
riskofmajor noncardiac surgery.Circulation1999;100:1043�9.3.Eagle KA,Berger
PB,Calkins H,et al.ACC/AHAguideline update for perioperative cardio-vascular
evaluation for noncardiacsurgery�executive summary a report oftheAmerican College
ofCardiology/AmericanHeart Association Task Force on PracticeGuidelines (committee
to update the 1996guidelines on perioperative cardiovascularevaluation for
noncardiac surgery).Circula-tion 2002;105:1257�67.4.Bartels C,Bechtel JF,Hossman
V,Horsch S.Cardiac risk stratification for high-risk vas-cular surgery.Circulation
1997;95:2473�5.5.Glance LG.Selective preoperative cardiacscreening improves five-
year survival inpatients undergoing major vascularsurgery:a cost-effective
analysis.J Cardio-thorac Vasc Anesth 1999;13:265�71.6.Rubin DN,Ballal RS,Marwick
TH.Outcomesand cost implications ofa clinical-basedalgorithm to guide the
discriminate use ofstress imaging before noncardiac surgery.Am Heart J
1997;134:83�92.7.Shaw LJ,Hachamovitch R,Cohen M,et al.Costimplications ofselective
preoperative riskscreening in the care ofcandidates forperipheral vascular
operations.Am JManag Care 1997;3:1817�27.8.Norton JM.Toward consistent definitions
ofpreload and afterload.Adv Physiol Educ2001;25:53�61.9.Selzman CH,Miller
SA,Zimmerman MA,Harken AH.The case for [beta]-adrenergicblockade as prophylaxis
against periopera-tive cardiovascular morbidity and mortali-ty.Arch Surg
2001;136:286�90.10.Garg J,Messerli A,Bakris G.Evaluation andtreatment ofpatients
with systemic hyper-tension.Circulation 2002;105(1):2458�61.11.Varon J,Marik P.The
diagnosis and manage-ment ofhypertensive crisis.Chest
2000;118(1):214�27.12.Fleisher L.Evaluation ofthe patient with cardiacdisease
undergoing noncardiac surgery:anupdate on the original AHA/ACC guidelines.Int
Anesthesiol Clin 2002;40(2):109�120.13.Cummins RO,editor.Advanced cardiac
lifesupport.Dallas (TX):American HeartAssociation;1997.14.Forrest J,Cahalan
M,Rehder K,et al.Multi-center study ofgeneral anesthesia II.Results.Anesthesiology
1990;72:262�8.15.Forrest J,Rehder K,Cahalan M,Goldsmith C.Multicenter ofgeneral
anesthesia III.Pre-dictors ofsevere perioperative adverse out-comes.Anesthesiology
1992;76:3�15.16.Elamana V.Anesthetic considerations inpatients with cardiac
arrhythmias,pace-makers and AICDs.Int Anesthesiol Clin2001;39(4):21�42.17.Al-Khatib
SM,Pritchett EL.Clinical features ofWolff-Parkinson-White syndrome.AmHeart J
1999;138(3 Pt 1):403�13.18.Horne C,Derrico D.Mastering ABGs.Am JNurs
1999;99(8):26�32.19.SadovnikoffN.Perioperative acute renal fail-ure.Int Anesthesiol
Clin 2001;39(1):95�109.20.Godet G,Fleron MH,Vicaut E,et al.Risk fac-tors for acute
postoperative renal failure inthoracic or thoracoabdominal aorticsurgery:a
prospective study.Anesth Analg1997;85:1227�32.21.Johnston KW.Multicenter
prospective study ofnonruptured abdominal aortic aneurysm:part II.Variables
predicting morbidity andmortality.J Vasc Surg 1989;9:437�47.22.Thadvani R,Pascual
M,Bonventre JV.Acuterenal failure.N Engl J Med 1996;334:1449�60.23.Solomon
R.Radiocontrast-induced nephropa-thy.Semin Nephrol 1998;18:505�18.24.Moudgil G.The
patient with reactive airwaysdisease.Can J Anaesth 1997;44(5):R77�83.25.Kersjens
H,Groen HJ,van der Bij W.Respira-tory medicine.BMJ 2001;323:1349�53.26.Hurford
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children need a preoperativeassessment that is different from adults?
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cardiovascular care.Circulation2000;102 Suppl 1:143�308.31.Woehlck HJ,Connoly
LA,Cinquegrani MP,etal.Acute smoking increases ST depressionin humans during
general anesthesia.Anesth Analg 1999;89:856�63.
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RE.Limitations ofpulse oximetry.Anesth Prog 1992;39:194�6.33.Kotani N,Kushikata
T,Hashimoto H,et al.Recovery ofintraoperative microbicidaland inflammatory
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risk factor for chronicbronchitis and asthma in adults?
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obese patient.Br JAnaesth 1993;70:349�59.36.Adams JP,Murphy PG.Obesity in
anesthesiaand intensive care.Br J Anaesth 2000;85:91�108.37.BenumofJL.Obstructive
sleep apnea in theadult obese patient.J Clin Anesth 2001;13:144�56.38.Bennett
J,Petersen T,Burleson JA.Capnogra-phy and ventilatory assessment duringambulatory
dentoalveolar surgery.J OralMaxillofac Surg 1997;55:921�5.39.Vascello LA.A case for
capnographic monitor-ing as a standard ofcare.J Oral MaxillofacSurg
1999;57:1342�7.40.Bennett J.A case against capnographic moni-toring as a standard
ofcare.J Oral Maxillo-fac Surg 1999;57:1348�52.41.Jacober SJ,Sowers J.An update on
periopera-tive management ofdiabetes.Arch InternMed 1999;159:2405�11.42.Graham
GW,Unger BP,Coursin DB.Perioper-ative management ofselected endocrinedisorders.Int
Anesthesiol Clin 2000;38(4):31�67.43.Brown CJ,Buie WD.Perioperative stress
dosesteroids:do they make a difference? J AmColl Surg 2001;193:678�86.44.Salem
M,Tainish RE,Bromberg J,et al.Periop-erative glucocorticoid coverage:a reassess-
ment 42 years after emergence ofa prob-lem.Ann Surg 1994;219:416�25.45.Ducart
A,Adnet P,Renaud B,et al.Malignanthyperthermia during sevoflurane adminis-
tration.Anesth Analg 1995;80:609�11.46.Abraham RB,Cahana A,Krivosic-Horber RM,Perel
A.Malignant hyperthermia suscepti-bility:anesthetic implications and
riskstratification.QJM 1997;90(1):13�8.
CHAPTER 4Preoperative Patient AssessmentJoel M.Weaver,DDS,PhDThe primary purpose
ofpreoperativepatient assessment is to provide sufficientinformation to the
surgical and anestheticteam members to permit them to formu-late the most
appropriate surgical andanesthetic plans.The same process shouldbe used for both
office and hospitalizedpatients,including trauma victims;med-ically,mentally,or
physically compro-mised patients;and healthy patients hav-ing elective surgery with
either localanesthesia alone,conscious sedation,deepsedation,or general
anesthesia.Dependingon the variables discovered in the assess-ment,modifications to
the usual surgicaland anesthetic regimens may be necessaryto improve the chances
ofattaining a satis-factory outcome.The components ofthe preoperativeassessment are
(1) a review ofthe previousmedical records ifavailable,including
allmedical,surgical,and medication informa-tion;(2) a personal interview with
thepatient or knowledgeable guardian toobtain additional past medical and
surgicalhistories;(3) a focused physical and psy-chological examination ofthe
patient,withemphasis on the cardiovascular and respi-ratory systems and the
adequacy ofthe air-way in regard to the potential for difficultyin attaining and
maintaining its patencyduring deep sedation or general anesthesia;(4) a review
ofresults ofthe medical testsand referral for consultation ifneeded;(5)a
determination ofthe patient�s periopera-tive risk;and (6) a thorough explanation
ofthe various treatment options in discus-sion with the patient or guardian to
assistwith their treatment decisions and toobtain their informed
consent.Information such as current medica-tions,drug allergies,the likelihood
ofpreg-nancy,family history ofmalignant hyper-thermia,a significant medical or
surgicalhistory,and,ifthe procedure is scheduledat the time ofevaluation,an
assessment offluid or food ingestion may influence thesurgeon�s choice on how to
proceed.A review ofthe previous medicalrecords can provide a wealth ofinforma-tion
that the patient may not know or beable to relate during their
interview.Forexample,ifthere is previous documenta-tion ofa �difficult
airway�whereby ananesthesiologist had significant difficultywith mask ventilation
and needed multi-ple attempts to intubate a severely retrog-nathic patient,an oral
surgeon might notchoose to administer deep sedation orlight general anesthesia to
that patient inthe office.Better alternatives mightinclude light conscious sedation
in theoffice with only those drugs for whichpharmacologic antagonists exist,or
possi-bly an awake fiberoptic intubation in theoffice,surgicenter,or hospital prior
to theinduction ofgeneral anesthesia.Forpatients who are poor
historians,previousmedical records may be the sole source ofinformation concerning
previous surg-eries and medical problems.Unfortunate-ly,timely access to previous
medicalrecords may be difficult or impossible.Usually,information concerning
thepatient�s past medical,surgical,and anes-thetic history can be gathered by a
per-sonal or telephone interview.Althoughcompletion ofa health questionnaire
ormedical history form by the patient maybe a starting point for the
interview,italone does not meet the important goal ofestablishing a personal
dialogue with thepatient to ensure that this information isas complete and accurate
as possible.Thetrue value ofthe medical history form isto alert the interviewer as
to which areasneed further explanation.For example,apositive indication ofasthma by
thepatient on a health screening question-naire is relatively worthless
informationby itself;it must be followed up with fur-ther questioning concerning
the frequen-cy ofattacks,its precipitating factors,suc-cessful measures for
treatment,the mostrecent attack,and the degree ofseverity ofsymptoms,including
previous emergencyroom treatments for severe asthmaticepisodes,hospital
admissions,or evenendotracheal intubation in the intensivecare unit for status
asthmaticus.Onlyafter appropriate questioning has beencompleted for each positive
item on thepast medical history form can thepatient�s past medical,surgical,and
anes-thetic history be considered adequate.
66Part 1: Principles ofMedicine,Surgery,and AnesthesiaObviously,the additional
informationgleaned from the patient must be writtenon the form for review at the
time oftheprocedure as well as for proper medicole-gal documentation.Once the
information is gathered,thesurgeon should categorize the surgicalpatient according
to the American SocietyofAnesthesiologists (ASA) ClassificationofPhysical Status
(Table 4-1),even ifonlylocal anesthesia is to be used.ASA PS-1patients would be
expected to have a lowerrisk ofperioperative complications thanASA PS-4
patients.Despite a lack ofabsolute precision in accurately classifyingthe
perioperative risk for all patients,thisindex is,nevertheless,commonly used tohelp
identify certain risk factors so thatmodifications in the treatment plan can
beaccomplished.For instance,ambulatorygeneral anesthesia in a dental office forASA
PS-1 and many ASA PS-2 patients isconsidered safe and cost effective,whereasASA PS-
4 patients would only receive localanesthesia and perhaps light levels ofanx-
iolysis in an office setting.Assessment ofCardiovascularDiseaseCardiac
DiseaseCardiac disease can be subdivided intoischemic and nonischemic
disease.Ischemic disease includes atheroscleroticheart disease,angina pectoris,and
previousmyocardial infarction.Nonischemic diseaseincludes a wide variety
ofetiologies,such asvascular (polyarteritis nodosa),congenital(tetralogy
ofFallot),infectious
(bacterialendocarditis),inflammatory/autoimmune(scleroderma),traumatic (cardiac
contu-sion),toxic (alcoholic cardiomyopathy),pulmonary (cor
pulmonale),metabolic(obesity),neoplastic (carcinoid),andendocrine
(hyperthyroidism).In a landmark article,Goldman andcolleagues developed a
multifactorialindex to assess cardiac risk associated witha variety ofnoncardiac
procedures such asorthopedic and general surgery.1Thisprospective study followed
1,001 patientsolder than 40 years at Massachusetts Gen-eral Hospital until
discharge and recordedall complications.Various potential riskfactors for cardiac
complications were cor-related with actual complications,and arisk index based on a
points system wassubsequently formed.Ofthe 537 Class Ipatients,with 0 to 5
points,only 0.7% hadlife-threatening complications and 0.2%experienced cardiac
death.Patients with 6 to 12 points were placed into Class II,whereas those with 13
to 25 points com-prised Class III.Class IV patients,with 26or more points,had a 22%
incidence oflife-threatening complications and 56%experienced cardiac death.Ofall
these fac-tors,a previous history ofcongestive heartdisease was the most predictive
ofcompli-cations,followed by a myocardial infarc-tion within the previous 6
months.Detsky and colleagues modified theGoldman Index by including unstableangina
and remote myocardial infarctionas additional risk factors for perioperativecardiac
complications in vascular surgerypatients.2They simplified the scoring sys-tem
ofGoldman and colleagues into threeclasses,improving predictive accuracy.Table 4-2
represents Goldman and col-leagues�and Detsky and colleagues�factorsfor
perioperativecardiac risk.Although anesthetic and surgical carehave markedly
improved in the last 25 years and risks may be less in someareas,Kenchaiah and
colleagues recentlyreported that in both men and womenwho are obese,the risk
ofheart failure wasdoubled.3With the increasingly highprevalence ofobesity in the
United States,this risk factor,among others,will provemore important in determining
the risk ofpoor outcomes in the future.Ischemic Heart DiseaseAngina Pectorisand
Coronary Artery DiseaseAnginapectoris is typically a substernal chest painor
pressure that may radiate to either arm,the neck,or the mandible that is
initiatedby exercise,mental stress,pain,or otherfactors that produce increased
myocardialoxygen demand in the presence ofreducedoxygen delivery to the
myocardium.It ismost often caused by coronary artery dis-ease,although other
precipitating factorsinclude severe anemia,hypotension,vaso-constrictor
overdose,and coronary arteryspasm.Angina pectoris may be classifiedas
stable,unstable,or variant.Unfortunately,the symptoms ofanginapectoris may be
confused with mitral valveprolapse,esophageal reflux,esophagealspasm,peptic ulcer
disease,biliary disease,hyperventilation,musculoskeletal disease,and pulmonary
disease.The diagnosis ofangina pectoris is therefore not necessarilyeasy for the
clinician to establish.Stable angina pectoris is diagnosedwhen there is minimal
change over 2 months regarding precipitating
factors,frequency,intensity,duration,and treat-ments for successful termination
oftheattacks.Unstable angina pectoris relates toTable 4-1American Society
ofAnesthesiologists Physical Status ClassificationClassificationDescriptionPS-
1Normal healthy patientPS-2Patient with mild systemic diseasePS-3Patient with
severe systemic diseasePS-4Patient with severe systemic disease and a constant life
threatPS-5Moribund patient who is not expected to survive without the operationPS-
6Declared brain-dead donor patient for organ harvestAdapted from American Society
ofAnesthesiologists.Relative value guide,2003.Park Ridge (IL):American Society
ofAnesthesiologists;2003.
Preoperative Patient Assessment67recent changes in some or all the above fac-
tors.Thus,unstable angina is defined bychest pain encountered during less thanthe
usual exercise,or that lasts longer,ismore intense,more frequent,or requiresmore
than normal measures to terminateit.Unstable angina is also termed prein-farction
angina since it may be the harbin-ger ofan impending myocardial infarction.Variant
angina,also known as Prinzmetal�sangina,may occur in patients who have nodetectable
coronary artery disease but inwhom coronary vasospasm occurs period-ically,even at
rest or with ordinary exercise.Cardiac dysrhythmias are frequently pre-sent during
such spasms.These patientsare frequently prescribed calcium channelantagonists
prophylactically.Patients who elicit a history ofanginapectoris must be thoroughly
interviewedto permit the practitioner to properlyplace them into the appropriate
category.Patients who are judged to have reasonablecardiac reserve and are
considered stableare certainly good candidates for relativelysimple office
procedures while being care-fully monitored.Light to moderate levelsofconscious
sedation may prove beneficialin preventing an angina attack,particular-ly in the
anxious patient,by reducing thestress ofthe procedure and decreasingmyocardial
oxygen demand.Using pro-found local anesthesia with no more than40 �g ofepinephrine
has been recom-mended by Malamed for medically com-promised dental patients.4These
patientsshould be told to take their usual prophy-lactic medications such as �1-
adrenergicantagonists perioperatively,and to bringtheir nitroglycerin sublingual
tablets orspray on the day ofsurgery to abort anattack ifit were to occur.Common
risk factors for coronaryartery disease include advanced age,dia-betes
mellitus,hypertension,peripheralvascular
disease,hypercholesterolemia,obesity,cigarette smoking,sedentarylifestyle,and
family history ofcoronaryartery disease.According to Tarhan and col-leagues,the
perioperative risk ofan acutemyocardial infarction in patients without ahistory
ofmyocardial infarction is 0.13%.5Numerous retrospective studiesinvolving large
groups ofpatients indicatethat the risk ofa second myocardial infarc-tion in the
perioperative period seems tostabilize at approximately 6% after 6 months from the
initial infarction.5�8However,the 6% re-infarction rate is con-siderably higher
than the 0.13% incidenceofperioperative infarction for the sameprocedures in
patients without previousmyocardial infarction.Congestive Heart DiseaseMultiple
stud-ies indicate that the presence ofcongestivefailure is the single most
important riskfactor for perioperative cardiac morbidityindependent ofthe presence
ofdysrhyth-mias,cardiomyopathy,valvular disease,orcoronary artery
disease.1,9,10Appropriatestrategies for perioperative managementinclude
optimization with careful atten-tion to fluid management and maximizingtherapies
such as inotropes,diuretics,vasodilators,and antidysrhythmics.The New York Heart
Association(NYHA) functional classification ofpatients with heart disease (Table 4-
3) isuseful in categorizing patients who haveTable 4-2Index ofCardiac
RiskConditionGoldman et al1Detsky et al2Myocardial infarction< 6 mo1010> 6
mo�5Angina pectorisUnstable angina < 3 mo�10Class III angina�10Class IV�20Symptoms
ofcongestive heart failure11�< 1 wk prior�10> 1 wk prior�5DysrhythmiaPreventricular
contractions > 5/min75Rhythm other than sinus rhythm75Valvular
disease:significant/critical aortic stenosis320MiscellaneousAge > 70 yr55Emergency
operation410Major invasive surgery3�Poor general health:obstructive pulmonary
35disease,major electrolyte disturbance,renalfailure,liver
disease,nonambulatoryAdapted from Goldman L et al1;Detsky A et al.2Table 4-3New
York Heart Association Classification ofCardiac Patients ClassSymptomsIAsymptomatic
cardiac diseaseIISymptomatic with ordinary activity,comfortable at
restIIISymptomatic with minimal activity,comfortable at restIVSymptomatic at rest
68Part 1: Principles ofMedicine,Surgery,and Anesthesiaheart failure.It has been
shown to be pre-dictive ofcardiac morbidity and mortalityin the perioperative
period.In Goldmanand colleagues�study,NYHA Class Ipatients (asymptomatic cardiac
disease)had a 3% risk ofdeeloping perioperativepulmonary edema,whereas the
riskincreased to 25% in NYHA Class IVpatients (symptomatic at rest).10
Similarly,patients with signs ofcongestive heart fail-ure by examination or
radiograph weremore likely to develop pulmonary edemathan those without such
signs.Identification ofswollen ankles,ascites,and distended neck veins
duringphysical examination may help identifyright-sided heart failure,whereas a
persis-tent cough,three-pillow orthopnea,andrales on auscultation ofthe chest may
besignificant signs and symptoms ofleft-sided failure.Nonischemic Heart
DiseaseValvularDiseaseWhen valvular heart disease isrecognized through history or
physicalexamination,the surgeon must judge thepotential impact that this condition
mighthave in relation to the proposed procedureand the need for antibiotic
prophylaxis tohelp prevent endocarditis.The extent towhich the patient�s physical
activity is lim-ited by the cardiac condition usually servesas a useful guide to
determine whetherfurther consultation or testing is needed.The surgeon must
understand the poten-tial cardiac risks associated with the specif-ic problem and
know the physiologic con-sequences associated with changes incardiac
rate,rhythm,blood pressure,pre-load,afterload,and inotropy that anesthe-sia and
surgery may produce.Aortic StenosisAortic stenosis is recog-nized by its
characteristic systolic murmurin the second intercostal space.A chestradiograph may
demonstrate a prominentascending aorta owing to poststenoticdilatation.Symptoms
include angina pec-toris,dyspnea on exertion,and a history ofsyncopal
episodes.Although syncope canbe caused by central nervous systempathology
(epilepsy,stroke,or transientischemic attack),metabolic pathology(hyperventilation
or hypoglycemia),orautonomic pathology (orthostatichypotension,carotid sinus
hypersensitivi-ty,or micturition syncope),episodes ofsyncope in the presence
ofcardiac pathol-ogy such as heart block,ventricular tachy-cardia,and aortic
stenosis are an ominoussign.The incidence ofsudden death isincreased with aortic
stenosis.Ofall the valvular conditions encoun-tered in practice,aortic stenosis
appears tobe the most significant.Goldman and col-leagues recognized critical
aortic stenosisas an independent risk factor for poor out-come.It increased the
risk ofperioperativecardiac death by a factor of14.1,10Criticalaortic stenosis is
generally defined as anorifice of< 0.75 cm2and/or > 50 mm Hggradient across the
valve during normalcardiac output.This markedly increasesthe resistance to normal
aortic flow,andthe increased load on the left ventriclecauses a concentric left
ventricular hyper-trophy and decreased compliance.Myocardial oxygen demand is
thereforemarkedly increased,and ischemia-relatedchest pain can occur even without
coro-nary artery disease.These patients do nottolerate increases in heart rate
because ofdecreased ejection time,filling time,anddiastolic coronary artery
perfusion time ofthe left ventricle.Thus,�-adrenergic ago-
nists,anticholinergics,vasodilators,hypo-volemia,pain,and anxiety are poorly tol-
erated,particularly for patients whoseend-stage disease involves angina,syn-
cope,and congestive heart failure.The consulting cardiologist shoulddefine the
disease and the degree ofhemo-dynamic significance and optimize thepatient prior to
surgery.Echocardiographycan be a useful tool to demonstrate abnor-mal valve
leaflets and a constricted orifice.The amount offlow reduction and thevalvular area
can be calculated with Dopplerechocardiography.Although an
invasiveprocedure,cardiac catheterization is moreaccurate in assessing aortic
stenosis and hasa dual advantage ofassessing coexistingcoronary artery
disease.Therefore,it is mostimportant to carefully assess the significanceofaortic
stenosis for a patient who presentswith this diagnosis or in whom the practi-tioner
suspects it may exist.Aortic RegurgitationAortic regurgita-tion produces a
diastolic murmur heardbest in the right second intercostal spaceand is associated
with a widened pulsepressure,decreased diastolic pressure,andbounding peripheral
pulses.It is oftenseen in combination with left ventricularhypertrophy on a chest
radiograph andelectrocardiogram.Aortic regurgitationassociated with chronic aortic
insufficien-cy is not associated with increased periop-erative cardiac death
according to Gold-man and colleagues.1However,aorticinsufficiency increases the
perioperativerisk ofcongestive heart failure,which mayresult from factors that
decrease the for-ward flow ofblood.The use ofvasocon-strictors and the presence
ofanxiety,pain,and poorly controlled hypertension mayincrease peripheral vascular
resistance andcontribute to pulmonary congestion.Reduced inotropy and
bradycardiaincrease diastolic filling from aortic regur-gitation,whereas
tachycardia and vasodi-lation help maintain forward flow.Mitral StenosisMitral
stenosis is usuallythe result offusion ofthe valve leaflets atthe commissures
during the healingprocess from rheumatic fever.A normal-sized orifice is 4 to 6
cm2,but the patientbecomes symptomatic when the areadecreases by 50%.The condition
producesan opening snap early in diastole and arumbling diastolic murmur heard best
atthe cardiac apex.It may be associated withleft atrial enlargement on a chest
radi-ograph and notched P waves on the elec-trocardiogram.
Preoperative Patient Assessment69Mitral stenosis without regurgitationcauses left
atrial enlargement and ulti-mately congestive heart failure.Criticalmitral stenosis
is usually defined as an area< 1 cm2.Because the atrial outflow
isreduced,tachycardia reduces the flow intothe left ventricle,which increases pul-
monary congestion and decreases cardiacoutput.Thus,heart rate must remain rea-
sonably normal,and the atrial �kick�asso-ciated with sinus rhythm may be
necessaryfor maintaining cardiovascular stability.Mitral InsufficiencyMitral
insufficiencyis frequently associated with mitral steno-sis as the result
ofrheumatic heart disease.It produces a holosystolic blowing mur-mur heard best at
the apex.It is often tol-erated until the patient begins to developsigns and
symptoms ofcongestive heartfailure.Mitral insufficiency is associatedwith an
increased mortality rate ifpresentwith other risk factors such as congestiveheart
failure or recent myocardial infarc-tion.1,10As in aortic insufficiency,atten-tion
must be given to preventing excessivefluid administration and to maintainingforward
blood flow with moderateincreases in heart rate and vasodilation.Mitral Valve
ProlapseMitral valve pro-lapse,or Barlow�s syndrome,is associatedwith a bulging or
prolapse ofthe mitralvalve leaflets into the left atrium duringsystole.Typically,it
produces a nonejec-tion click cardiac murmur,often called�click-murmur
syndrome,�heard best atthe cardiac apex and may be associatedwith a regurgitant
murmur.The diagnosisis normally confirmed with echocardiog-raphy.Although not a
benign condition,itis less likely to be problematic than manyofthe above valvular
diseases.It is oftenassociated with a history ofchest pain,anxiety
attacks,dizziness,supraventriculartachycardia,and palpitations.Thesepatients are at
risk ofparoxysmal tachy-dysrhythmias and sudden death.Occa-sionally,mitral valve
prolapse is associatedwith significant regurgitation and endo-carditis.Appropriate
care includes mea-sures to prevent significant positiveinotropic and chronotropic
responses tostress by adequate control ofanxiety andpain,judicious use of�-
adrenergic ago-nists such as epinephrine,and carefulmonitoring ofcardiovascular
parametersduring surgery.CardiomyopathyCardiomyopathy mayresult from a variety
ofcauses not relatedto valvular or coronary disease,such assystemic
disease,infection,or drug andalcohol abuse.The degree ofcardiacimpairment can be
estimated by invasiveor noninvasive measurement ofthe car-diac ejection fraction
(percent EF);this isthe percentage ofleft ventricular bloodvolume ejected into the
aorta during eachcontraction.The normal value is approxi-mately 70% and should
increase with exer-cise or stress,whereas an EF of30% is usu-ally associated with
decreased exercisetolerance.Patients with an EF of15% orless have significant
physiologic impair-ment and may be candidates for cardiactransplantation.There are
three classes ofcardiomy-opathy:dilated,nondilated,and hyper-trophic.The typical
findings associatedwith dilated cardiomyopathy include amarked increase in left
ventricular end-diastolic volume.The perioperative impli-cations ofdilated
cardiomyopathy includeoptimization offunction including carefulfluid management and
maximizing thera-pies such as inotropes,diuretics,vasodila-tors,and
antidysrhythmics,as in the man-agement ofcongestive heart failure.Patients with
nondilated cardiomyopa-thy,also known as restrictive cardiomyopa-thy,present with
rigid ventricles that impairdiastolic filling,although the contractilefunction may
remain somewhat intact.Right ventricular failure and elevatedvenous pressures are
common.Dysrhyth-mias are a common cause ofdeath in thesepatients;therefore,careful
monitoring ofcardiovascular parameters is essential tofacilitate rapid
recognition,diagnosis,andtreatment oflife-threatening dysrhythmiasduring any
surgical procedure.Hypertrophic cardiomyopathy,alsoknown as idiopathic hypertrophic
subaor-tic stenosis (IHSS),is usually an inheritedautosomal dominant
characteristic,although it can also be a result oflong-standing hypertension.The
intraventricu-lar septum may be greatly thickened inasymmetric septal
hypertrophy,or thehypertrophy may be concentric.Depend-ing on the area
ofhypertrophy,left ven-tricular outflow obstruction may occurduring
systole.Furthermore,the septalleaflet ofthe mitral valve may not functionproperly
owing to the hypertrophy oftheseptum,and mitral regurgitation mayresult.Fatal
ventricular dysrhythmias mayresult in sudden death even in apparentlyhealthy
teenagers with undiagnosedhypertrophic cardiomyopathy.Ischemiawithin the
hypertrophic segment may alsoresult in myocardial infarction.Prepara-tion for
surgery would include carefulmonitoring ofvital signs and minimiza-tion ofthose
factors associated withincreases in cardiac inotropy and rate,such as
hypotension,vasodilation,�-adrenergic drugs,pain,and anxiety.Pre-operative �1-
blockade,adequate hydra-tion,and local anesthetics withoutepinephrine,unless
absolutely necessary,are the usual components ofgood opera-tive
planning.HypertensionHypertension is a very common disease.Although it can occur
secondarily as aresult ofa definable cause such as hyper-thyroidism or
pheochromocytoma,it ismost often a multifactorial primary dis-ease ofpoorly
understood origin,termedessential hypertension.11In their seventhreport,the Joint
National Committee onPrevention,Detection,Evaluation andTreatment ofHigh Blood
Pressure recent-ly revised their definition ofhypertension
70Part 1: Principles ofMedicine,Surgery,and Anesthesiafrom previous
reports,recognizing thatearly detection and treatment ofprehy-pertension and
hypertension is impor-tant and ultimately reduces risk.Impor-tant key messages in
the joint committee�slatest report are as follows:(1) forpatients < 50 years
ofage,systolic bloodpressure > 140 mm Hg is a much moreimportant risk factor for
cardiovasculardisease than is diastolic pressure eleva-tion;(2) beginning with a
pressure of115/75 mm Hg,the risk ofcardiovasculardisease doubles with every
incrementalincrease of20/10 mm Hg;and (3) a systolic pressure ofbetween 120 and 139
mm Hg or a diastolic pressure ofbetween 80 and 89 mm Hg is prehyper-tension,and
lifestyle modifications arerecommended to prevent cardiovasculardisease (Table 4-
4).11Major risk factors for hypertensioninclude
smoking,dyslipidemia,diabetesmellitus,age > 60 years,gender (men andpostmenopausal
women),and familyhistory ofcardiovascular disease inwomen > 65 and men > 55
years.Ifuntreated,it commonly causes coronaryartery
disease,cardiomegaly,congestiveheart failure,and end-organ damage tovital tissues
such as the heart,kidneys,retina,and brain.Elevated systolic bloodpressure in the
elderly appears to be abetter predictor than elevated diastolicblood pressure
ofterminal end-organdamage,such as coronary artery/cardio-vascular
disease,stroke,renal failure,postoperative myocardial ischemia,andoverall
death.11,12Because the increased peripheral vas-cular resistance produces a
contractedintravascular volume,hypertensive patientsare highly susceptible to the
vasodilatoreffects ofsedative and anesthetic agents thatmay result in a relative or
absolute severehypotensive episode.Prolonged excessive hypotension in apatient with
significant peripheral vasculardisease who needs a relatively high pressureto
perfuse vital organs may be more detri-mental during surgery than permitting
amodest degree ofhypertension to continue.For patients planning for elective
surgerywho are found to be significantly hyperten-sive at the preoperative
assessment,it is bestto postpone the procedure until their physi-cian can optimize
their pressure and vol-ume status.It is recommended that surgerybe
delayed,ifpossible,for poorly controlledhypertensive patients with blood pres-sure
above the mild to moderate range (> 180/110 mm Hg).11,13Acute treatment
ofhypertension atthe time ofelective surgery may produceblood pressure numbers that
initiallymake the practitioner more comfortablebefore starting anesthesia and the
proce-dure,but the less-than-optimized patientis much more likely to have
significantlabile hypertensive and/or hypotensiveepisodes during the course,and
this mayincrease their risk ofmorbidity or mortal-ity.As a general rule,patients
with hyper-tension should take all oftheir normalantihypertensive medications at
their nor-mal times with a sip ofwater prior tosurgery.Indeed,patients who skip a
doseofdrugs such as clonidine or propranololmay develop severe rebound hyperten-
sion,tachycardia,and angina pectoris.Maintaining pharmacologic homeostasis,with
only a few exceptions,such as holdingor halving the usual dose ofinsulin
ifthepatient is fasting preoperatively,is just asimportant on the day ofsurgery as
for anyother day.Assessment ofExercise Tolerance The Duke University Activity
Status Index(Table 4-5) uses the rate ofoxygen con-sumption necessary to accomplish
vari-ous physical tasks to quantify the degreeofphysical activity
performed.14Onemetabolic equivalent (MET) consumes3.5 mL/kg/min
ofoxygen.Hollenbergindicated that patients who could undergo> 7 METs had excellent
functional capaci-ty,whereas those able to perform only 4 to7 METs had only
moderate capacity.Patients who could do < 4 METs had poorfunctional
capacity.15Experienced clinicians usually relatethat they have confidence in
judging apatient�s overall capacity to safely undergoanesthesia and surgery by
inquiring aboutthe degree ofexercise that the patient isable to accomplish.Those
who can walkup several flights ofsteps without stoppingto rest are much less
worrisome than arethose who can manage only a few stepswithout developing severe
dyspnea orchest pain.Perioperative Cardiovascular Evaluation Algorithm The most
recent update ofperioperativecardiovascular evaluation guidelines bythe American
College ofCardiology andthe American Heart Association providesa framework for
determining the need foradditional cardiac consultation forpatients with
cardiovascular disease,depending on the presence ofvariouspredictors ofrisk for
perioperative car-diac death and nonfatal myocardialTable 4-4Classification
ofHypertensionSystolic BPDiastolic BPCategory< 120and<
80Normal120�139or80�89Prehypertension140�159or90�99Stage 1 hypertension (mild)>
160or> 100Stage 2 hypertension (moderate)Adapted from the seventh report ofthe
Joint National Committee on Prevention,Detection,Evaluation and Treatment ofHigh
Blood Pressure.11BP = blood pressure.
Preoperative Patient Assessment71infarction and the risk stratification forvarious
noncardiac surgical procedures.13Using these guidelines,the oral and max-illofacial
surgeon can estimate the cardiacrisks associated with the surgical proce-dure and
decide whether the patient�smedical condition warrants further car-diac
consultation.For instance,accordingto the algorithm in Figure 4-1,a cardiacpatient
with intermediate predictors ofcardiac risk (mild angina or controlledcongestive
heart failure) with good exer-cise tolerance (equal to or greater than 4 METs) who
is scheduled for a low-risksurgery (tooth extraction or toriremoval) should not
need an extensivecardiac work-up.However,that samepatient scheduled for
hemimandibulecto-my,partial pharyngectomy,laryngecto-my,or radical neck dissection
with flapreconstruction that would entail largefluid shifts while under anesthesia
formany hours (high surgical risk) and whohas poor exercise tolerance (< 4
METs)should receive cardiac testing prior tosurgery.Likewise,a patient with
minorpredictors ofcardiac risk (advanced ageor previous stroke) scheduled for
theabove high-risk surgery would not needcardiac consultation ifhis or her
exercisetolerance was good but should be referredifthe exercise tolerance was
poor.Although the guidelines in Figure 4-1do not specifically define the surgical
riskcategory ofthe most common oral surgi-cal procedures,the surgeon shouldattempt
to compare the severity oftheirproposed surgery with that ofthe exam-ples
provided.Perhaps a Le Fort III frac-ture would be similar in risk to an inter-
mediate-risk acetabular fracture,whereasa dental implant would be considered alow-
risk superficial procedure.Assessment ofPulmonary Disease Patients with pulmonary
disease must becarefully assessed preoperatively becauseeven healthy patients may
develop pul-monary complications as a direct resultofsurgery and
anesthesia.Pulmonarydisease can be classified as either restric-tive or
obstructive.Restrictive diseasemay be the result of,for instance,severescoliosis or
morbid obesity and results ina decrease in all measured lung volumes.Obstructive
disease is usually the result ofsmoking or asthma and may be charac-terized by
marked increases in residualvolume and functional residual capacity.A thorough past
medical history andphysical examination related to the pul-monary system prior to
sedation or gen-eral anesthesia is mandatory.Unfortu-nately,many
patients,particularly smok-ers,are not aware that they have signifi-cant pulmonary
compromise until it isvery advanced.As first reported by Morton in 1944,smoking is
a risk factor for postoperativepulmonary complications,even amongsmokers without
signs or symptoms ofchronic obstructive pulmonary disease.16,17The risk declines
from 33 to 14.5% afteronly 8 weeks following cessation ofsmok-ing,whereas those who
stop smoking for < 8 weeks have a higher risk ofcomplica-tions than do current
smokers.18The assessment should start withquestions regarding dyspnea on
exertionand functional level ofphysical activitythat can be accomplished,such as
howmany flights ofstairs can be managedwithout rest.Patients with mild or
onlyoccasional symptoms usually need nofurther investigation,whereas those
withfrequent or severe symptoms may needfurther evaluation and managementprior to
surgery.Although physical limi-tations may also be indicative ofcardio-vascular
disease or pulmonary disease,they often present simultaneouslybecause smoking is a
major risk factor forcardiovascular disease.Physical examination ofthe patientwith
obstructive pulmonary disease mayreveal an increased anteroposteriordiameter ofthe
chest,a depresseddiaphragm,a hyperresonant thorax onpercussion,and
wheezing,particularlyduring expiration.The chest radiographmay demonstrate
hyperinflated lungs.The forced expiratory volume in 1 sec-ond (FEV1) is usually <
80% ofthe vitalcapacity.Obstructive disease may bereversible,as in bronchial
asthma,or itmight have a reversible component.Common irreversible diseases
includeemphysema,chronic bronchitis,andbronchiectasis.However,antibiotics
andbronchodilator therapy may reverse atleast some ofthe components ofacutesymptoms
ofchronic bronchitis.Table 4-5Duke Activity Status IndexActivityMETsFunctional
CapacityWalk in house1.75PoorPersonal care (dress,bath,toilet)2.75PoorWalk 1�2
blocks2.75PoorLight work:dusting,washing dishes2.7PoorModerate
work:vacuuming3.5PoorYard work:raking,mowing4.5ModerateSexual relations
5.25ModerateClimb
stairs5.5ModerateGolf,bowling6ModerateSwim,basketball,ski7.5ExcellentRun8ExcellentA
dapted from Hlatky MA et al14;Hollenberg SM.15MET = metabolic equivalent;1 MET =
3.5 mL/kg/min oxygen use.
72Part 1: Principles ofMedicine,Surgery,and AnesthesiaAsthmaBronchial asthma is a
common pul-monary condition that must be respectedfor its potential to cause life-
threateningcomplications during surgery and anes-thesia.In addition to taking a
careful his-tory with regard to asthmatic triggers,fre-quency,severity,emergency
room visits,and hospitalizations,one can also assessthe potential for an acute
event by notingthe number ofdifferent asthma medica-tions required to control
symptoms andthe frequency and efficacy oftheir use.Wheezing from asthma immediately
priorto the induction ofanesthesia and surgeryStep 1: Emergency surgeryStep 2:
Revascularization < 5 yr, and no problemsStep 3: Evaluation < 2 yr was normal and
no new problemsStep 4: Major predictor of riskStep 5: Intermediate predictor of
riskStep 7: Minor predictor of risk: assess METsGood (> 4)Poor (< 4)To ORLow-risk
surgeryTo ORCancel surgery; fix problemStep 6: Assess METs for intermediate-high-
risk surgeryTo ORPoor (< 4)Good (> 4)Intermediate-risk surgeryIntermediate-low-risk
surgeryHigh-risksurgeryStep 8: CardiactestingHigh-risksurgeryTo ORCardiac
catheter�fixYesYesYesYesNoNoNoNoNoYesNegativePositiveFIGURE4-1Preoperative cardiac
assessment algorithm for surgical risk ofcardiac death/nonfatal
myocardialinfarction.Major predictors ofrisk: unstable angina,decompensated heart
failure,significant dysrhythmias,andsevere valvular disease; intermediate
predictors ofrisk: mild angina,prior myocardial infarction,controlled
heartfailure,diabetes,and renal insufficiency; minor predictors ofrisk: advanced
age,abnormal electrocardiogram,nonsinus rhythm,poor functional capacity,prior
stroke,and uncontrolled hypertension.High-risk surgeries:emergent major
surgery,major vascular surgery,and prolonged cases/major blood loss/fluid shifts;
intermediate-risk surgeries: carotid endarterectomy,head and
neck,intraperitoneal,intrathoracic,orthopedic,and prostate;low-risk surgeries:
endoscopic,superficial,cataract,and breast.METs = metabolic equivalents; OR =
operatingroom.Adapted from Eagle K et al.13
Preoperative Patient Assessment73is an ominous sign and is reason to post-pone all
but the most urgent procedures.EmphysemaEmphysema is characterized by irre-versible
enlargement ofthe alveolar airducts and by destruction ofthe walls ofthese air
spaces.The loss ofelasticity ofthese structures permits collapse oftheairways
during exhalation,resulting inincreased airway resistance.To keep theirairways from
collapsing,patients withsevere emphysema can be observed topurse their lips during
exhalation to attainpositive end-expiratory pressure in theirairways.The chest
radiograph typicallydemonstrates low flat diaphragms andextremely hyperlucent lung
fields,consis-tent with gas trapping and loss oflungparenchyma.Preoperative
management may decreasethe incidence ofpostoperative pulmonarycomplications.19Those
with suspected sig-nificant obstructive disease may be candi-dates for preoperative
pulmonary functiontesting and analysis ofarterial blood gases.Many emphysema
patients,commonlyknown as �pink puffers,�have reasonablynormal arterial blood gases
as they are ableto increase their minute ventilation andcardiac output to
compensate for increasedairway resistance.With increasing pul-monary artery
pressures above a mean of20 mm Hg,cor pulmonale develops as theright ventricle
begins to fail,resulting inhypoxemia,venous congestion,and sys-temic
edema.Measurement ofthe ratio ofFEV1toforced vital capacity (FVC) may help
todiscern the severity ofthe disease and pre-dict the chance for respiratory
failure iftheratio is < 50%.20Carbon dioxide retentiontypically occurs when the
FEV1:FVC ratiois < 35%.Chronic BronchitisChronic bronchitis,characterized by
achronic excess ofmucus in the bronchi-oles,is due to enlarged mucous glandsthat
reduce the luminal diameter oftheairways and increase resistance to airflow.Chronic
bacterial infections are commonand produce inflammation and fibrosisthat further
contribute to increased resis-tance.Patients with chronic bronchitisdevelop
hypoxemia and carbon dioxideretention relatively early in the course ofthe disease
compared with emphysemapatients.Cor pulmonale,manifested byhepatojugular reflux and
peripheraledema,also develops comparatively earlyand results in the patient being
termed a�blue bloater.�The preoperative evalua-tion and management ofchronic
bronchi-tis is similar to that for emphysema.Bronchiectasis Bronchiectasis occurs
when there is anabnormal enlargement ofthe bronchi thatare frequently filled with
purulent sputumand highly vascularized granulation tissue.There is risk
ofsignificant hemoptysis andan increased risk ofpulmonary edema,pulmonary
hypertension,and cor pul-monale.SummaryThe surgeon must complete a careful
andthorough past medical history and physi-cal examination to assess the risk
ofpul-monary disease.Recognition ofpoor exer-cise tolerance,clubbing ofthe
fingertips,chronic cough and dyspnea with minimalexertion,decreased breath
sounds,wheezes,rhonchi,and excessive expiratoryeffort are ominous signs
ofsignificant pul-monary disease that may warrant furtherevaluation and treatment
prior to surgeryand anesthesia.Many patients with severe pulmonarydisease require
continual administrationofsupplemental oxygen via a nasal can-nula at home.This
should be continuedduring dental treatment.In the event ofamedical emergency such
as chest pain,giving of100% oxygen by face mask andmonitoring ofthe respiratory
rate arehighly recommended for all suchpatients.Should the respiratory rate
ofapatient who is a chronic carbon dioxideretainer decrease because ofloss ofrespi-
ratory drive caused by the additional oxy-gen,the practitioner may simply need
toremind the conscious patient to breathe,or manually ventilate the
unconsciouspatient with positive pressure oxygen.Only ifa severely compromised pul-
monary patient is left unmonitored whilebreathing 100% oxygen by face maskwould
there be danger ofoxygen causinghypoventilation in the dental office that
isproperly equipped with airway adjunctsneeded for artificial
ventilation.Assessment ofthe Airway Assessment ofthe airway is one ofthemost
important facets ofthe preanesthesiaevaluation process because the inability
tomaintain a patent airway and provide ade-quate ventilation and oxygenation is
fre-quently responsible for anesthesia-relatedmorbidity and mortality.In a
closedclaims study by the American Society ofAnesthesiologists,Caplan and
colleaguesreported that 34% of1,541 liability claimswere for adverse respiratory
events.21Thiswas the largest source ofadverse outcomesin their study.Ofthese cases
approximate-ly 75% were related to either inadequateventilation (38%),esophageal
intubation(18%),and difficult intubation (17%).Although the current universal use
ofthepulse oximeter and end-tidal carbon diox-ide monitoring have
undoubtedlydecreased some ofthese events,at leastsome ofthe difficult intubations
couldhave been situations in which the anesthe-siologist could neither intubate nor
maskventilate an apneic patient.Thus,the oraland maxillofacial surgeon must
carefullyassess the potential for this type ofcata-strophic failure to maintain the
airwayduring any sedation or anesthesia admin-istered in the office or other
surgical venueand be prepared to properly manage thatcircumstance should it occur
despite care-ful assessment and planning to avoid it.
74Part 1: Principles ofMedicine,Surgery,and AnesthesiaThe American Society
ofAnesthesiol-ogists has developed and updated an algo-rithm for management ofthe
difficult air-way.22As seen in Figure 4-2,theseguidelines enable
anesthesiologists,nurseanesthetists,dentist anesthesiologists,andoral and
maxillofacial surgeons to have adetailed series ofplans and alternatives
tofacilitate the management ofthe difficultairway.This reduces the likelihood
ofadverse outcomes such as death,braindeath,myocardial injury,and airway trau-
ma.These guidelines recommend that acareful airway history and examination
beconducted prior to the induction ofanes-thesia to detect
medical,surgical,andanesthetic factors including previous anes-thetic
records,ifavailable,that may identi-fy the difficult airway.Congenital and acquired
diseases orconditions,for instance,may alter the air-way anatomy to such an extent
that attain-ing and maintaining a patent airway dur-ing anesthesia may be difficult
orimpossible.Congenital conditions such asPierre Robin,Treacher Collins,Golden-
har�s,Klippel-Feil,and Down syndromesare associated with abnormalities such
asrestricted movement ofthe neck andmandible,micrognathia,maxillary andmandibular
hypoplasia,and macroglossia.Examples ofacquired conditions
includeobesity,oropharyngeal space infections,epiglottitis,tonsillitis,rheumatoid
arthri-tis,tumors,temporomandibular joint dis-orders,head and neck cancer
surgery,andoropharyngeal radiation therapy.A careful physical examination
oftheairway must be accomplished.Anatomiccharacteristics associated with
difficultintubation include a short large-diameterneck,retrognathia with obtuse
mandibularangles,protruding maxillary incisors,decreased mobility ofthe temporo-
mandibular joint,and a high-arched palate.Although there is no airway rating sys-
tem that can accurately predict a difficultairway with high sensitivity and
specifici-ty,the modified Mallampati classificationis widely used.23The hypothesis
ofMal-lampati and colleagues is that the base ofthe tongue in certain individuals
is dispro-portionately large,which makes directlaryngoscopy difficult.The tongue
base istherefore compared with other anatomicfeatures that it may obscure.To
performthis test correctly,the patient should be sit-ting or standing upright and
asked toopen their mouth as widely as possiblewithout phonating.In Class I patients
theuvula,faucial pillars,and soft palate arevisible.In Class II patients only the
faucialpillars and soft palate are visible,whereasin the Class III patients,only
the softpalate is observed.Class I patients areexpected to have normal
airways,whereaspatients in Class II are somewhat morelikely to be difficult to
intubate.Intubationin Class III patients is even more likely tobe difficult.Samsoon
and Young later added afourth category to the original
Mallampaticlassification.24Their fourth class includedvisualization ofthe hard
palate but not thesoft palate or other structures.Class IVpatients have the highest
risk for a difficultintubation (Figure 4-3).Although difficult intubation does
notalways coincide with difficult mask venti-lation,one must recognize that
patients inmodified Mallampati Classes III and IVpose an increased risk ofloss ofa
patentairway during nonintubated deep sedationor general anesthesia.When
compoundedwith other risk factors such as mandibularretrognathia,obesity,or
postradiationtherapy,the practitioner may elect toadminister only light conscious
sedationwith drugs that are pharmacologicallyreversible or to secure the airway via
awakefiberoptic intubation prior to induction ofgeneral anesthesia.In certain
instances additional evalua-tion ofthe airway may be prudent.Forexample,fiberoptic
pharyngoscopy,softtissue radiography,computerized tomog-raphy,and magnetic
resonance imagingmay be helpful in identifying the extent ofairway compromise and
tracheal deviationassociated with severe dentofacial andneck infections.Patients
with a severeinfection and significant trismus,orthop-nea,dysphagia,drooling,and
dyspnea mayeasily lose the patency oftheir tenuous air-way with even modest doses
ofsedative,anxiolytic,or opioid analgesic medicationsgiven prior to attempted
fiberoptic intuba-tion.Preparations for an immediate surgi-cal airway must be made
well in advance.Assessment ofEndocrine Disease Any ofthe major endocrine disorders
canimpact the course ofanesthesia andsurgery and should be considered in
thepreoperative assessment.Adrenal GlandA lack ofadrenal cortical activity,as
inAddison�s disease,may decrease the pro-duction ofcortisol and aldosterone
andalter cardiovascular stability.Patients whotake supplemental
glucocorticosteroidsmay have a suppression ofadrenocorti-cotropic hormone from
their pituitarygland and may need preoperative supple-mentation ofcortisol.An
overproductionofepinephrine and norepinephrine in theadrenal medulla from a
pheochromocy-toma may create a hypertensive-tachycardiaccrisis
intraoperatively.Thyroid GlandHypothyroidismHypothyroidism hasmany potential causes
and is usually deter-mined by an assessment oflevels ofthyroidstimulating hormone
(TSH),triiodothyro-nine (T3),and thyroxin (T4).Patients whocomplain offatigue and
intolerance to coldand who are hypotensive may suffer
frommyxedema.Theoretically,myxedematouspatients may be more susceptible to
thedepressant effects ofanesthetics and lessresponsive to adrenergic vasopressors
andcardiac inotropes.However,a retrospectivestudy demonstrated no significant
difference
Preoperative Patient Assessment75DIFFICULT AIRWAY ALGORITHMAWAKE
INTUBATIONINTUBATION ATTEMPTS AFTERINDUCTION OF GENERAL ANESTHESIA1. Assess the
likelihood and clinical impact of basic management problems:A. Difficult
VentilationB. Difficult IntubationC. Difficulty with Patient Cooperation or
ConsentD. Difficult Tracheostomy2. Actively pursue opportunities to deliver
supplemental oxygen throughout the process of difficult airway management.3.
Consider the relative merits and feasibility of basic management choices:4. Develop
primary and alternative strategies:* Confirm ventilation, tracheal intubation, or
LMA placement with exhaled CO2a. Other options include (but are not limited to):
surgery utilizing facemask or LMA anesthesia, local anesthesia infiltration or
regional nerve blockade. Pursuit of these options usually implies that
maskventilation will not be problematic. Therefore, these options may be of limited
value if this step in the algorithm has been reached via the Emergency Pathway.b.
Invasive airway access includes surgical or percutaneoustracheostomy or
cricothyrotomy. c. Alternative non-invasive approaches to difficult intubation
include (but are not limited to): use of different laryngoscope blades, LMAas an
intubation conduit (with or without fiberoptic guidance), fiberoptic intubation,
intubating stylet or tube changer, light wand, retrograde intubation and blind oral
or nasal intubation.d. Consider re-preparation of the patient for awake intubation
or canceling surgery.e. Options for emergency non-invasive airway ventilation
include (but are not limited to): rigid bronchoscope, esophageal-tracheal
combitubeventilation, or transtracheal jet ventilation.Airway Approached byNon-
Invasive IntubationInitial IntubationAttempts Successful*Initial IntubationAttempts
UNSUCCESSFULFROM THIS POINT ONWARDS CONSIDER:FACE MASK VENTILATION NOT
ADEQUATECONSIDER / ATTEMPT LMANON-EMERGENCY PATHWAYEMERGENCY PATHWAYLMA
ADEQUATE*LMA NOT ADEQUATEOR NOT FEASIBLEIF BOTH FACE MASKAND LMAVENTILATION BECOME
INADEQUATEFACE MASK VENTILATION ADEQUATE1. Calling for Help2. Returning to
SpontaneousVentilation3. Awakening the PatientCancelCaseAlternative Approachesto
Intubation(c)Ventilation Not AdequateIntubation UnsuccessfulCall for HelpEmergency
Non-Invasive Airway Ventilation(e)SuccessfulIntubation*FAIL AfterMultiple
AttemptsInvasiveAirway Access(b)*Consider Feasibilityof Other
Options(a)AwakenPatient(d)EmergencyInvasive AirwayAccess(b)*Successful
Ventilation*FAILVentilation Adequate, Intubation UnsuccessfulConsider Feasibilityof
Other Options(a)Invasive Airway Access(b)*Succeed*FAILInvasive Airway
Access(b)*A.Awake IntubationA.B.B.C.Intubation Attempts After Induction ofGeneral
AnesthesiaNon-Invasive Technique for InitialApproach to IntubationInvasive
Technique for Initial Approach to IntubationPreservation of Spontaneous
VentilationAblation of Spontaneous Ventilationvs.vs.vs.FIGURE4-2Algorithm for
management ofa difficult airway.LMA = laryngeal mask airway.Reproduced with per-
mission from the American Society ofAnesthesiologists.22
76Part 1: Principles ofMedicine,Surgery,and Anesthesiain hemodynamic
instability,imbalance influid and electrolytes,necessity for vasopres-
sors,myocardial infarction,sepsis,bleeding,extubation time,or time to discharge
com-pared with matched controls.25The conclu-sion ofthe study was that mild
hypothy-roidism is not a contraindication for surgery.However,severe myxedema can
lead tocoma,cardiovascular collapse,and heart fail-ure and necessitates a
postponement ofsurgery until it can be corrected.26HyperthyroidismGraves�disease is
themost common type ofprimary hyperthy-roidism.Symptoms include hyperexcitabil-
ity,weight loss,hypertension,and tachycar-dia.Thyroid storm during anesthesia
canresemble malignant hyperthermia.Propyl-thiouracil or methimazole is
frequentlyprescribed to reduce thyroxin secretionprior to surgery,and �-adrenergic
antago-nists are used to stabilize the adrenergicactivity prior to and during
surgery.GoiterEnlargement ofthe thyroid glandmay adversely influence the patency
oftheairway.Substernal goiter may be difficult torecognize on physical examination
withouta chest radiograph,but it may producesymptoms ofdyspnea and dysphagia.Large
superficial goiters may increase thedifficulty ofendotracheal intubation.Pituitary
GlandThe pituitary gland has a wide influence onmany glands and organs.Increased
pro-duction ofhypophyseal pituitary tropichormones can produce secondary hyper-
thyroidism (TSH),secondary Cushing�ssyndrome (adrenocorticotropic hormone),and
acromegaly (growth hormone).Acromegaly predisposes the patient
tocardiomyopathy,dysrhythmias,and sud-den death.27,28The excessive growth hor-mone
increases the production ofinsulin-like growth factor I (IGF-I) by the liver
andother tissues.Excessive levels ofIGF-I canproduce headaches,profuse
sweating,jointdisorders,soft tissue swelling,and over-growth ofthe
hands,feet,mandible,andviscera.The patient with acromegaly maytherefore present
with a difficult airway,particularly for endotracheal intubation.Diabetes
MellitusDiabetes mellitus is a common diseasewith far-reaching
implications,primarilyowing to the microangiopathy-relatedimpairment ofnormal blood
flow andsubsequent end-organ damage.Patientsdiagnosed with insulin-dependent dia-
betes at a young age are less commonlyseen than those diagnosed withnon�insulin-
dependent diabetes later inlife,who are generally able to control itwith oral
hypoglycemic agents.Insulin-dependent diabetics generally have moresevere signs and
symptoms related to theirdiabetes and have increased potential tosuffer the
consequences for a longer peri-od oftime than non�insulin-
dependentdiabetics.Preoperative evaluation ofalldiabetics includes an assessment
ofthedegree ofblood glucose control and asearch for evidence ofend-organ damage.As
the degree ofend-organ damage pro-gresses,the likelihood
ofperioperativecomplications,often cardiovascular innature,increases.Blood sugar is
usually measured sever-al times a day when insulin therapy isneeded.Although blood
sugar concentra-tions can vary widely throughout the day,a measurement at the
preoperative assess-ment appointment can give the practition-er an idea ofthe
degree ofcontrol that thepatient might have at that time.The prac-titioner may also
discern that the patient isin optimal control by measuring the glyco-sylated
fraction ofadult hemoglobin(HbA1c) for a long-term picture
ofoverallcontrol.Hemoglobin A1binds with glu-cose to form HbA1c,which is a
relativelystable complex that provides more ofanaverage blood glucose level over a
periodof1.5 to 2 months.Thus,taken together,these two measurements provide the
prac-titioner with information on both short-and long-term control.A well-
controlled diabetic is expectedto have fewer perioperative complicationsincluding
reduced incidences ofwoundinfection and diabetic ketoacidosis.Although long-term
tight control shouldreduce end-organ damage,tight controlin the immediate
perioperative periodmay predispose the patient to hypo-glycemia,which can result in
central ner-vous system damage.A rational approach to properly man-aging diabetic
patients is based on knowl-edge ofthe type ofdiabetes present,thedegree ofits
control by the patient,thestress associated with the surgical proce-dure,and the
likelihood ofthe patientquickly resuming a normal diet and hypo-glycemia medication
postoperatively.29Short-term control by the sliding scale maybe best in the
perioperative period for manypatients;however,others may do welladministering their
insulin after surgery inClass IClass IIClass IIIClass IVFIGURE4-3Mallampati
classification.Adapted from Samsoon GLT and Young JRB.24
Preoperative Patient Assessment77their usual manner,as ifsurgery never hap-pened.An
individualized approach to dia-betic management is essential.End-organ damage from
diabetes mayresult in problems that directly affectsurgery and anesthesia.Renal
failure maybe the result ofdiabetic nephropathy,which may alter fluid and
electrolyte bal-ance and drug elimination.The lack oferythropoietin production by
the kidneymay result in significant anemia.Diabeticsensory neuropathy may permit
myocar-dial ischemia and silent myocardial infarc-tion to go unrecognized by the
patient andis an independent predictor ofperiopera-tive cardiac
morbidity.30Diabetic auto-nomic neuropathy may also increase therisk ofaspiration
ofgastric contents dur-ing deep sedation or general anesthesia bydelaying gastric
emptying.In addition,itmay cause unpredictable cardiovascularresponses to
anesthetic drugs and to othercardiovascular-active drugs.Metabolic acidosis with
hyperglycemia> 300 mg/dL in the diabetic definesketoacidosis.Insulin-resistance
owing totrauma,surgery,or infection may be a con-tributing factor.The conversion
offattyacids to acetoacetic acid,�-hydroxybu-tyrate,and acetone in the absence
ofinsulin produces metabolic acidosis andthe fruity smell on the breath that may
berecognized during the preoperative assess-ment.Extracellular potassium increases
asit leaves the cells,and this results in intra-cellular depletion ofpotassium in
the pres-ence ofhyperkalemia.Significant hypo-volemia results from the osmotic
diureticeffect ofglucose in the urine.All ofthesedeviations must be corrected with
insulin,fluid,and electrolytes before proceedingwith all but the most urgent
surgery.Assessment ofLiver Disease Preoperative assessment for liver disease
isparticularly important for those individu-als with cirrhosis or acute
hepatitisbecause morbidity and mortality rateswith these diseases are markedly
increased.When the practitioner suspects liver dis-ease during the perioperative
assessment,several screening tests are available.Acuteor chronic hepatocellular
damage is indi-cated with elevations ofaspartate amino-transferase (AST) and
alanine amino-transferase (ALT).Acute damage canproduce very high enzyme
elevations,whereas chronic damage may produceonly mildly elevated levels.ALT is
morespecific to hepatocytes.Unconjugated bilirubin from normalred cell destruction
may increase in the pres-ence ofsevere liver disease ifthe hepatocytescannot
conjugate it with glucuronide.Ele-vated serum bilirubin is responsible for
theyellow jaundiced appearance.Serum albumin and nearly all oftheclotting factors
such as prothrombin areproduced in the liver.Severe liver diseasecan decrease the
synthesis ofmany impor-tant proteins,as reflected in decreasedserum albumin
levels.Additionally,because many anesthetic drugs are nor-mally highly bound to
albumin,reducedserum albumin levels over a period ofmany weeks may permit unusually
highlevels offree drug to exist in the plasma,which could produce a
markedlyenhanced effect from a relatively smalldose.Reduced prothrombin levels
wouldbe reflected in an increased prothrombintime (PT) and International
NormalizedRatio (INR) and serve as additional mark-ers for the severity ofhepatic
disease.Because significant liver disease influencesso many bodily functions,only
necessarysimple procedures under local anesthesiaand perhaps nitrous oxide�oxygen
con-scious sedation should be attempted in anoffice setting for those patients with
signif-icant hepatic compromise.Assessment ofRenal Disease Renal disease has a
great impact on peri-operative morbidity and mortality.Themortality rate associated
with acute renalfailure ranges from 42 to 88%.31Levy andcolleagues demonstrated
that acute renalfailure is an independent risk factor formortality,regardless
ofother risk factors.32He also noted that because the mortalityofcontrast
medium�associated acuterenal failure is above 30%,elective surgeryshould be
postponed ifpossible until renalfunction returns to baseline in
thesepatients.Although newer less toxic con-trast agents are now available,acute
renalfailure can still occur.As previously discussed,renal failureis often a
consequence ofdiabetes andlong-standing hypertension.It can beresponsible for
congestive heart failure,fluid and electrolyte imbalance,anemia,hypertension,and
azotemia.When renaldisease is suspected from the history andphysical
examination,several tests can becompleted to assess its presence and thedegree
ofimpairment.Because urea andcreatinine are excreted by glomerular fil-tration and
their blood levels are thereforeinversely proportional to the glomerularfiltration
rate,blood urea nitrogen andserum creatinine levels are commonlyobtained to
initially assess renal function.Creatinine serum levels are normally inthe range
of0.6 to 1.5 mg/dL.Approxi-mately a 50% loss in kidney function isindicated by a
creatinine level > 2.0,whereas a 75% loss offunction would beindicated by a
creatinine level > 4.8.Crea-tinine levels > 10.0 are consistent withend-stage renal
disease (ESRD).Patients with ESRD who depend onhemodialysis often present for
periopera-tive assessment in either a hypervolemicor hypovolemic state,depending
onwhether they need dialysis soon or havejust completed it.Chronic hyperkalemiaand
anemia are commonly seen.Patientson hemodialysis are usually treated on theday
after dialysis,when they have some-what stabilized their physiology and whenthe
effects oftheir dialysis-associatedheparin are no longer present.Many ofthese
patients are quite sensitive to smalldoses ofsedatives and anxiolytics;there-
fore,slow careful intravenous titration of
78Part 1: Principles ofMedicine,Surgery,and Anesthesiathese drugs prior to dental
procedures ishighly recommended.Assessment ofBleeding Disorders A careful history
regarding bleeding prob-lems is essential prior to surgery.Excessivebleeding may
result from a variety ofcauses.For instance,drugs such as acetyl-salicylic acid and
other nonselective non-steroidal anti-inflammatory analgesicsmay inhibit platelet
function.Liver dis-ease may decrease the production ofclot-ting factors.A family
history ofbleedingmay be the result ofautosomal dominanttransmission ofvon
Willebrand�s diseaseto males and females,whereas hemophiliaA and B are both
inherited as sex-linkedrecessive traits.These patients may be tak-ing various
factors to bring their levels tothe normal range or may have had a his-tory
ofintravenous desmopressin admin-istration to acutely elevate levels offactorVIII
and von Willebrand�s factor prior tosurgery.A decreased ristocetin cofactoractivity
is the most sensitive and specificscreening test for von Willebrand�s
diseasebecause large multimers ofvon Wille-brand�s factor are important in
ristocetin-induced platelet aggregation.To help uncover previously unrecog-nized
bleeding disorders prior to majordental surgery,Holtzman and colleaguesrecommend
preoperative laboratoryassessment ofhemostasis prior to orthog-nathic
surgery.33However,there are a largenumber ofstudies that generally concurthat
routine hemostatic testing ofasymp-tomatic patients does not significantlyalter
treatment and is not cost-effective forthe low yield.34�39Wahl reviewed more than
950 patientscontinuously receiving anticoagulantswho underwent more than 2,400
dentalsurgical procedures,and only 12 (< 1.3%)required more than local measures to
con-trol bleeding.40Conversely,ofthe 526patients who stopped their
anticoagulanttherapy,5 suffered serious embolic com-plications and 4 ofthe 5
died.Wahl rec-ommends that most dental surgerypatients should remain at therapeutic
lev-els oftheir anticoagulant during the peri-operative period.When a bleeding
disorder is suspect-ed,the usual screening tests include the PTor INR to test the
activity ofthe extrinsicand final common pathways and the acti-vated partial
thromboplastin time to testthe intrinsic and final common pathways.Platelet counts
may be important whenthrombocytopenia is suspected and bleed-ing time is
prolonged.Assessment ofNeurologic and Neuromuscular Disorders The oral and
maxillofacial surgeon mayencounter a variety ofpatients with neu-rologic
disorders.Neurologic examina-tion may reveal important findings thatmay alter
treatment planning.Forinstance,head-injured trauma patientsare classified according
to the GlasgowComa Scale (Table 4-6).41Protection ofthe airway withoutincreasing
the chances ofworsening anyexisting neurologic impairment is ofprime importance in
severely trauma-tized patients.The preoperative assess-ment ofsome ofthese patients
may be,bynecessity,quite limited during resuscita-tive procedures.Nevertheless,it
isabsolutely necessary to accomplish towhatever degree is possible.Neuromuscular
disorders such asParkinson�s disease or multiple sclerosismay increase the risks
ofventilatory insuf-ficiency during spontaneous breathingand aspiration during
sedation or anesthe-sia when the airway is relatively unprotect-ed.Duchenne�s
muscular dystrophy maybe a risk factor for development ofmalig-nant hyperthermia or
neuroleptic malig-nant syndrome in response to variousanesthetic
drugs.EpilepsyEpilepsy is a common neurologic disorderthat requires careful
assessment.Patientswith a history ofseizure should maintaintheir antiseizure
therapy during the peri-operative period.The practitioner shouldbe aware ofthe
frequency and duration ofthe seizures,including the most recentone,and what to
expect should a seizureoccur.Despite maximal doses ofmultiplemedications,some
patients remain poorlycontrolled,and the surgeon must thendetermine the most
appropriate venue forsurgical treatment,while considering thatthe risks ofpulmonary
aspiration and res-piratory insufficiency during seizureepisodes are
increased.Transient Ischemic Attack and StrokePatients with a history
oftransientischemic attacks (TIAs) or stroke should beevaluated in the same manner
as thosewith angina pectoris and myocardialinfarction.Those who are deemed to
haveunstable TIAs or who have had a strokewithin the previous 6 months are
managedTable 4-6Glasgow Coma ScaleActionScoreEye openingSpontaneously4To speech3To
pain2None1Motor responseObeys6Localizes pain5Withdraws from pain4Flexion to
pain3Extension to pain2None1Verbal
responseOriented5Confused4Inappropriate3Incomprehensible2None1Adapted from Teasdale
G,Jennett B.41Patient�s score determines category ofneurologic impair-ment:15 =
normal;13 or 14 = mild injury;9�12 =moderate injury;3�8 = severe injury.
Preoperative Patient Assessment79similarly to those with unstable angina andrecent
myocardial infarction,respectively.The hypercoagulable state associated withthe
stress ofsurgery is more likely to man-ifest itselfin patients with preexisting
dis-ease in coronary and cerebral arteries.Preoperative Screening Tests
forAsymptomatic Patients With the advent ofhigh-tech automatedequipment in the past
several decades thatcan quickly complete a large number ofpreoperative screening
tests,practitionerswho wished to gather as much informa-tion as possible about
their patient to opti-mize care and reduce poor outcomesbegan to order �universal
testing,�even forapparently healthy asymptomatic patients,in a futile attempt to
�leave no stoneunturned.�Unfortunately,the indiscrimi-nate ordering ofmultiple
laboratory testshas many drawbacks and usually does notuncover diseases that
normally should bediscovered by other means such as a thor-ough history and
physical examination.For instance,Rabkin and Horne identified165 patients who had
been diagnosed as having �new electrocardiographicchanges.�42However,ofthat
number,163were identified as having changes consis-tent with their history and
physical exam-ination,so these changes were not unex-pected.Ofthe 2 patients whose
newelectrocardiographic changes were notconsistent with the basic
informationrecorded in their chart,1 patient wasfound to be in atrial
fibrillation,whichshould most likely have been discovered bypalpation ofan
irregular pulse during theexamination process.The other patienthad no physical
examination performed.Thus,this study indicated that a thoroughhistory and physical
examination shouldbe the key to determining whether thepractitioner should look for
new electro-cardiographic changes.Domoto and colleagues performed 19 screening
tests in 70 asymptomatic elder-ly patients whose mean age was > 80 years.43Most
abnormalities were minimally outsidenormal ranges,and only 0.1% ofthepatients had a
resulting change in treat-ment.Most importantly,no patient receivedan important
benefit from the tests.Like-wise,Dzankic found that the prevalence ofabnormal
preoperative electrolyte valuesand thrombocytopenia was small and had alow
predictive value in elderly surgicalpatients.44Although more prevalent,abnor-mal
hemoglobin,creatinine,and glucosevalues were also not predictive ofpostoper-ative
adverse outcomes.Thus,the routinepreoperative testing in geriatric patients
forhemoglobin,creatinine,glucose,and elec-trolytes on the basis ofage alone may not
beindicated.Selective laboratory testing,asindicated by history and physical
examina-tion,determines a patient�s comorbiditiesand surgical risk.Narr and
colleagues studied 3,000ASA PS-1 and PS-2 patients who receivedelective surgery and
found no benefit fromthe tests.45Archer and colleagues complet-ed a meta-analysis
ofover 14,000 patientsand concluded that the practice ofobtain-ing routine
preoperative chest radiographsshould be abandoned.46It is important to understand
that the�normal values�ofvarious tests are oftenset around a normal distribution
thatwould include values ofperhaps 95% ofahealthy population.However,somehealthy
individuals may fall above orbelow the normal range yet still be
withoutdisease.When one considers the variableselectivity ofindividual tests,it is
notunreasonable to expect that from a largebattery oftests,at least one may reveal
afalsely positive result.Such a result mayprompt the clinician to seek
additionalinformation from more invasive tests,which may result in a severe
complication.Therefore,indiscriminate testing can actu-ally do more damage than the
potentialharm ofsome unrecognized disease that itis designed to
discover.Additionally,in anera ofcost containment,testing asympto-matic patients in
hopes ofimproving out-comes is generally not cost-effective forthe resulting low
yield.47�50Althoughmany patients with significant diseasessuch as diabetes and
coronary artery dis-ease,as well as women ofchild-bearing agewho are not sure
oftheir pregnancy status,need certain laboratory testing preopera-tively,routine
testing ofhealthy asympto-matic patients with no complicating fac-tors is
unwarranted.51�53A carefully taken medical history and athorough physical
examination remain themost important aspects ofoptimal patientcare when
supplemented by specific teststhat are indicated by this information.Summary Having
obtained and evaluated all oftheappropriate information from the abovesources,the
oral and maxillofacial surgeonmust,in the end,judge whether the bene-fit-to-risk
ratio ofcompleting a procedurefor a particular patient,using a
particularsedative/anesthesia technique in a specificvenue (office,ambulatory
surgical center,or hospital),is acceptable.For some med-ically,physically,or
mentally complexpatients,an alternative surgical procedure,surgeon,anesthesia
provider,anesthesiatechnique,and/or venue may be deemedmore appropriate than for
those samevariables with the healthy patient.Soundprofessional judgment ofthe
surgeon isthe hallmark ofsuccessful oral surgicalpractice,and a complete
preoperativeassessment ofeach patient provides anopportunity to influence that
judgmentfor a safe and successful operation.Theoft-mentioned statement �never treat
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RD,editor.Anesthesia.2nd ed.NewYork:Churchill Livingstone;1986.p.225�53.53.Kaplan
EB,Sheier LB,Boeckmann MS,et al.The usefulness ofpreoperative
laboratoryscreening.JAMA 1985;253:3576�81.
CHAPTER 5Pharmacology ofOutpatient Anesthesia MedicationsM.Cynthia
Fukami,DMD,MSSteven I.Ganzberg,DMD,MSIntravenous sedation has a long history ofuse
in oral surgery practice.Oral sur-geons have been the historical leaders inthe
development ofoffice-based ambula-tory anesthesia practice.The develop-ment ofnewer
intravenous agents andtechniques have led to the increasedacceptance ofthese
practices as being safeand cost effective.Currently,the vastmajority (> 70%)
ofsurgical proceduresare performed on an ambulatory basis,and at least 20%
ofsurgical proceduresare performed with office-based sedationor general
anesthesia.While it is neither possible nor theintention ofthe authors to present
the fullscope ofanesthetic medications includingemergency medications in this
chapter,we will review the pharmacology ofmanyagents used in office-based sedation
andgeneral anesthesia practice.Where applic-able the use ofthese agents in oral
surgicalpractice is highlighted.Pharmacodynamics and
PharmacokineticsPharmacodynamicsPharmacodynamics is the study ofthepharmacologic
actions and clinical effectsofa drug in the body.1The clinicalresponse ofmost
anesthetic and sedativemedications derives from their actions inthe central nervous
system (CNS).At a cellular level the most frequentmechanism by which drugs exert
theirpharmacologic effects is through interac-tions with specific protein
receptorsembedded in cell membranes,which theninitiate a specific set
ofintracellularactions.These protein receptors can becharacterized as ion channels
or trans-membrane receptors.Ion channels allowthe passage ofspecific ions into or
out ofthe cell,including chloride,potassium,sodium,and calcium.Alterations in
theintracellular concentration ofthese ionsinitiate characteristic cellular effects
suchas depolarization ofa cell membrane ormovement ofstorage vesicles.Opening ofion
channels may be triggered by eitherchanges in membrane voltage or bindingby a
specific ligand.Voltage-sensitive ionchannels open and close depending on
cellmembrane voltage,whereas a ligand-gatedion channel undergoes
conformationalchanges when a drug or natural ligandbinds to it,altering ion channel
openingand closing.The ?-aminobutyric acid(GABA) receptor is an example ofa ligand-
gated chloride ion receptor.Transmembrane receptors are also lig-and regulated and
typically rely on secondmessenger systems to carry out the phar-macodynamic
effect.When a specific ligandbinds to the extracellular portion
ofthesetransmembrane receptors,a conformation-al change in the domain ofthe
receptorexposed towards the cytoplasm activateseither a specific enzyme or a second
mes-senger system.Second messenger systems,such as G proteins and cyclic
adenosinemonophosphate,are complex cascades ofsignaling proteins that,once
triggered,willproduce the intended effect.An example ofan enzyme-activated system
is insulin,which binds to its specific receptor,activat-ing an intracellular enzyme
called tyrosinekinase,resulting in increased glucoseuptake.Muscarinic acetylcholine
(ACh)receptors also use a second messenger cas-cade involving intracellular
calcium.Some lipid-soluble drugs do notengage membrane receptors,but insteadexert
their pharmacodynamic effect intra-cellularly via receptors found in the cyto-
plasm.Hormones and steroid medicationscross the cell membrane and bind to cyto-
plasmic receptors,which then alter cellularfunctions such as gene
transcription.Asmall number ofmedications may alsoalter enzyme activity outside
ofcells,suchas anticholinesterase drugs that block theactivity
ofacetylcholinesterase.Drugs are commonly classified aseither agonists or
antagonists for a specific
84Part 1: Principles ofMedicine,Surgery,and Anesthesiareceptor.Agonistdrugs
function to exertthe normal property associated withreceptor activation.GABA A
agonists likebenzodiazepines activate GABA receptors,allowing an influx
ofchloride,hyperpolar-izing the cell,and reducing neuronal activ-ity,thus promoting
the normal activityassociated with GABA activation.Antago-nistdrugs exert the
opposite effect ofthenatural ligand or agonist drug activity.Competitive
antagonistsbind at the normalligand-binding site but exert no pharma-cologic
effect.Instead the antagonist �takesup space�at the binding site,thus
blockingagonist drug activity.The higher the con-centration ofantagonist,the
greater theblocking effect.Agonist activity returnsonce the antagonist
concentrationdecreases or ifadditional agonist is admin-istered to overcome the
antagonist con-centration.Nondepolarizing neuromus-cular blockers are competitive
antagonistsfor the acetylcholine receptor.Noncompet-itive antagonistsdo not bind at
the ligandsite but instead attach to a different loca-tion on the receptor,altering
the configu-ration ofthe binding site and preventingnormal ligand
binding.Administration ofan additional agonist does not affect non-competitive
antagonist activity,as they donot compete for the same binding site.Many pesticides
are an example ofnon-competitive antagonist agents.PharmacokineticsPharmacokinetics
is the study ofthe fac-tors that affect the plasma concentrationofa drug in the
body,encompassing theprocesses ofabsorption,distribution,metabolism,and
elimination.1Commonlyidentified by the route ofadministration,such as per oral
(PO),intravenous (IV),intramuscular (IM),or inhalation,absorption describes the
point ofentry ofthe drug into the body.Orally adminis-tered agents undergo first-
pass metabolism;PO medications are absorbed by theintestinal mucosa and carried via
the por-tal circulation to the liver where theyundergo partial metabolism prior
toentrance into the central circulation.Thisprocess potentially reduces the
plasmaconcentration ofdrug that reaches theeffector site,such as the CNS.Since
thedegree ofgastrointestinal absorption andfirst-pass metabolism is
unpredictable,POsedative drugs can have less reliable clini-cal effects.Most
anesthetic agents used inoral surgical practice are delivered intra-
venously,intramuscularly,or by inhala-tion.In contrast to oral agents these
routesofadministration do not undergo first-pass metabolism.Both intravenous
andinhalation administration provide directentry into the central
circulation,reachingpeak plasma concentration very quicklyfollowing drug
administration.Inhalationpharmacokinetics will be discussed in thefollowing section
�Inhalation Anesthetics.�Distribution describes the movementofthe drug between body
compartments.The main factors influencing distributioninclude the allocation
ofblood flow to aspecific compartment,the concentrationgradient ofthe drug between
compart-ments,the chemical structure ofthe drug,and plasma protein binding ofthe
drug.Following administration the majority ofthe drug initially redistributes to
the vessel-rich compartments.This vessel-richgroup includes the
brain,heart,kidney,and liver,representing 10% oftotal bodymass but 75% ofcardiac
output.Since themajor site ofanesthetic agent activity isthe brain,early
distribution to the CNSresults in early anesthetic effects.The transfer ofthe drug
from the cen-tral circulation to the brain is also deter-mined by the concentration
gradientbetween the two compartments.A lowerconcentration in one compartment
favorsthe transfer from a region ofhigher con-centration.Following initial
intravenousadministration the initial drug concentra-tion in the brain is low
relative to the plas-ma concentration;thus,the drug willrapidly transfer into the
brain based onthis differential concentration gradient.Asthe plasma concentration
falls by contin-ued redistribution to other vessel-richorgans,and later to less
vessel-rich organssuch as skeletal muscle (approximately20% ofcardiac
output),anesthetic drugnot bound to receptors in the brain willtransfer back into
the central circulationfor further redistribution to other tissuesites.As the brain
concentration ofseda-tive agent falls,the clinical effects ofseda-tion also
decrease.Characteristics ofthe drug itselfaffectits distribution throughout the
body.Lipophilic drugs readily cross the blood-brain barrier and cellular
membranes,andgenerally exert their effects rapidly.Like-wise lipophilic drugs can
quickly exit theCNS,shortening the duration oftheireffects.Hydrophilic medications
eithercross very slowly or must be transportedby specific mechanisms.The size or
mole-cular weight ofthe drug molecules influ-ences movement across capillary
walls;smaller molecules will cross more readily.The degree to which the drug binds
toplasma proteins such as albumin and a1-acid glycoprotein will affect the amount
offree drug available to cross into the brain.Most sedative agents are highly
plasma-protein bound.For example,initial dosesofdiazepam are 98% bound to
plasmaprotein and unavailable to cross into theCNS.As the free drug plasma
concentra-tion decreases through further redistribu-tion,and later metabolism and
elimina-tion,plasma�protein-bound drug isreleased back into the plasma as free
drugand is able to cross the blood-brain barri-er.In this way drug bound to plasma
pro-tein may be thought ofas a reservoir ofdrug that may contribute to
prolongedsedative effects.Once plasma-proteinbinding sites have been filled,an
addition-al consequence is that further administra-tion ofsmall quantities ofdrug
can haveprofound effects as the majority oftheadditional administered agent will be
freedrug that is able to cross the blood-brainbarrier.Careful titration
ofintravenous
Pharmacology ofOutpatient Anesthesia Medications85agents,especially after initial
administra-tion and filling ofprotein binding sites,isimportant to avoid
oversedation due tothis mechanism.Hypoproteinemia sec-ondary to advanced age or
severe liver fail-ure can also dramatically increase the con-centration offree
drug,and dosereduction may be required.As redistribution continues,a fractionofthe
plasma concentration is delivered tothe liver,the primary organ ofdrug metab-
olism,undergoing transformation from alipid-soluble entity to a water-
solubleform.There are four main pathways ofhepatic
metabolism:oxidation,reduction,hydrolysis,and conjugation.Phase I reac-tions
include the first three pathways,con-verting the drug into a water-
solublemetabolite or intermediate form.Phase IIreactions involve most forms
ofconjuga-tion,in which an additional group is addedonto the metabolite in order to
increase itspolarity.Subsequent elimination via thekidney,the main excretory
organ,requireshydrophilicity to avoid reabsorption oftheexcreted drug.Water-soluble
drugs andmetabolites are eliminated chiefly by thekidney,but also via the
bile,lungs,skin,and other organs.Phase I hepatic reactions,includingthe cytochrome
P-450 (CYP-450) group ofenzymes which carry out the oxidationand reduction
reactions,occur in thehepatic smooth endoplasmic reticulum(hepatic microsomal
enzymes).The CYP-450 group ofenzymes has been character-ized into several
isoforms,including CYP-3A4,CYP-2D6,and CYP-1A2.Theconjugation reaction
ofglucuronidation isalso conducted by the hepatic microsomalenzymes.The hepatic
microsomalenzymes are unique in that certain chemi-cals and drugs,including those
used inanesthesia,can stimulate their activity.This is termed enzyme inductionand
gen-erally requires chronic exposure ofthedrug to the enzyme system for at least
sev-eral days or weeks.An isolated exposure toanesthetic agents is unlikely to
inducehepatic enzyme activity.However,ifthepatient�s daily medications induce
hepaticenzymes,then increased metabolism ofadditional medications is
possible.Induc-tion is isoform specific;a coadministereddrug will only be affected
by enzymeinduction ifboth drugs are metabolized bythe same enzyme system.Hepatic
micro-somal enzymes can also be inhibited bycertain drugs,thus reducing
metabolismofdrugs by a specific enzyme system.Forexample,patients taking cimetidine
fortreatment ofgastric ulcers may experienceprolonged residual CNS effects
fromdiazepam,as cimetidine inhibits thehepatic enzymes that normally
metabolizediazepam.Various tables have been pub-lished which list drugs that are
substrates,inducers,and inhibitors ofthe variouscytochrome enzyme
systems.Nonhepatic forms ofmetabolism areimportant for certain anesthetic medica-
tions,and are useful in patients with signif-icant liver or kidney disease.Drugs
suscepti-ble to Hofmann elimination spontaneouslydegrade at body pH and
temperature.Esterhydrolysis by nonspecific and specific (eg,pseudocholinesterase)
esterases is also lessdependent on renal and hepatic
functions.Redistribution,metabolism,and elim-ination reduce the plasma
concentrationofthe drug,increasing the transfer ofdrugfrom tissue sites (eg,brain)
back into thecentral circulation for further redistribu-tion,metabolism,and
elimination.Differ-ent mathematical models involving theseprocesses have been
developed thatdescribe the offset ofactivity ofanestheticagents.The fall of50%
ofthe plasma con-centration ofthe drug secondary to redis-tribution is termed the
alpha half-life.Theremoval of50% ofthe drug from the bodydue to metabolism and/or
elimination istermed the beta half-life,or eliminationhalf-life.Offset ofclinical
effects andawakening from a bolus ofan IV anesthet-ic agent is more dependent on
redistribu-tion ofthe drug away from the brain andis therefore better approximated
by thealpha half-life than the beta half-life.Insome cases residual CNS effects can
bepredicted by a long elimination half-life.The beta half-life has more use for
orallyadministered agents and particularlydescribes central compartment concentra-
tion in a one-compartment model.The pharmacokinetics ofa continu-ous infusion
ofintravenous anestheticagents may be better described by thecontext-sensitive
half-time.This valuerepresents the time necessary for theplasma drug concentration
to decreaseby 50% after discontinuing a continuousinfusion,depending on how long
theanesthetic agent has been administered.2Figure 5-1 describes the context-
sensitivehalf-time for a number ofcommon anes-thetic agents.Currently computer-
controlled pumps administer continuousinfusions based on a specific amount ofdrug
per time,but the newest infusionpumps can be programmed to calculateand provide
target plasma concentra-tions ofan agent to a specified anesthet-ic or analgesic
level.In the future thesepumps will likely be integrated with con-current
electroencephalogram con-sciousness monitoring to individualizeanesthetic drug
delivery.BenzodiazepinesBenzodiazepines are the most commonlyused sedative and
anxiolytic medicationsin oral surgery.Their relatively high mar-gin ofsafety as
compared to other sedative-hypnotic medications,in addition to the avail-ability
ofan effective reversal agent,makestheir use attractive during operator-
anesthetistprocedures in an outpatient setting.Benzodiazepines are composed
ofabenzene and diazepine ring fused together.3Agonist agents contain a 5-aryl
substitutionwhich is not present on the antagonistreversal agent (Figure 5-2).This
structurebinds to inhibitory GABA receptors foundthroughout the brain,particularly
in thecerebral cortex.Binding to the GABA Asubunit increases the frequency ofpore
86Part 1: Principles ofMedicine,Surgery,and Anesthesiaopening in the chloride-gated
channel,thusincreasing inward chloride flow,hyperpo-larizing cell membranes,and
reducing neu-ronal transmission.Characteristics shared by benzodi-azepines include
sedation,anxiolysis,anterograde amnesia,muscle-relaxingproperties,and
anticonvulsant activity.Indeed,any intravenous benzodiazepineagonist may be used to
suppress acuteseizure activity.These drugs do not pro-duce
analgesia.Benzodiazepines are commonly usedfor preoperative sedation both immedi-
ately prior to the procedure and as asleep adjunct the night before
surgery.Inclinical practice they are also used forconscious sedation,and at higher
dosescan produce deep sedation and even gen-eral anesthesia.In a nervous patient
anxiolysis frombenzodiazepines can produce noticeablereduction in blood pressure
and heartrate,but these medications have littledirect effect on cardiovascular
parame-ters.Given alone in slowly titrated doses,benzodiazepines also have minimal
effectson ventilation.Large bolus doses will,however,induce unconsciousness
andapnea.Additionally,even smaller doseswhen given in combination with an opi-oid
can synergistically enhance opioid-induced respiratory depression.Benzodiazepines
are metabolized byhepatic enzymes into hydrophilic forms.These metabolites are then
excreted by thekidney in urine.Side effects ofbenzodiazepines arefew,but
paradoxical excitement,in whichpatients may become overly disinhibitedand
disoriented,is a possible complica-tion.Flumazenil is useful in the reversal
ofparadoxical excitement and benzodi-azepine-related respiratory
depression.DiazepamDiazepam is lipid soluble and is carried inan organic solvent
such as propylene glycolor a soybean oil emulsion.Intravenousinjection can be
painful,although injectinginto a larger vein or pre-administration oflidocaine or
an opioid can reduce discom-fort.Intramuscular injection is painful andabsorption
can be unpredictable.Diazepam is still used for intra-venous conscious
sedation,given in 2.5 to 5 mg increments every few min-utes.Onset ofsedation occurs
in severalminutes and recovery from clinical seda-tion by diazepam is similar
compared tomidazolam.However,the much longerelimination time ofdiazepam may con-
tribute to lingering sedative effects.Diazepam can also be given orally (5 to10 mg)
for preoperative anxiolysis andmild sedation.This highly lipid-soluble drug accu-
mulates in fat tissues with slow reentry ofvery small quantities into the central
cir-culation,leading to an elimination half-life of24 to 96 hours.Diazepam is
alsometabolized into two pharmacologicallyactive metabolites,desmethyldiazepamand
oxazepam,each with long elimina-tion half-lives as well.The active meta-bolites and
parent drug are partially eliminated in bile and can result
in3002502001501005000123456789FentanylThiopentalMidazolamAlfentanilSufentanilContex
t-Sensitive Half-Time (min)Infusion Duration (h)PropofolFIGURE5-1Context-sensitive
half-time ofa number ofanesthetic agents.Adapted from HughesMA et
al.2CH3CH3COOC2H5OFNNNCH3CIONNCCCINNNOHOCICIFNNDiazepamLorazepamMidazolamFlumazenil
FIGURE5-2Chemical structure ofbenzodiazepine agonists and antagonist.
Pharmacology ofOutpatient Anesthesia Medications87reemergence ofsedation several
hoursafter completion ofthe procedure,due toenterohepatic metabolism.Upon inges-
tion ofa fat-rich meal,bile is releasedinto the gut,and active drug componentsin
the bile are reabsorbed by the intesti-nal mucosa and undergo first-
passmetabolism.These still active drugs arethen re-introduced into the central cir-
culation and into the CNS,resulting inpossible resedation.MidazolamMidazolam has an
imidazole ring attachedto its diazepine ring.The imidazole ring isopen,rendering
the compound water solu-ble at pH less than 4,but the ring closes atphysiologic pH
producing the lipid-solublebenzodiazepine.Midazolam can thereforebe delivered in an
aqueous solution,ratherthan propylene glycol,resulting in less painon intravenous
and intramuscular injec-tion.4It is 2 to 3 times as potent atdiazepam,with a faster
onset,much fasterelimination,and shorter duration oflin-gering effects.Its active
metabolites are notthought to produce significant sedativeeffects.Respiratory
depression is more ofaconcern with midazolam than diazepamafter bolus intravenous
administration.Midazolam is currently more popularthan diazepam for intravenous
sedation forshort oral surgical procedures.For con-scious sedation 0.05 to 0.15
mg/kg IV individed doses is titrated to effect,typicallygiven in 1 or 2 mg boluses
every few min-utes.Peak effect is seen in approximately 5minutes.Dosage should be
adjusted down-ward when given concurrently with othermedications such as opioids or
propofol.An intramuscular injection of0.5 mg/kg toa maximum of10 to 15 mg depending
onpatient age is also possible.As an alterna-tive midazolam may be given orally at
0.5to 1 mg/kg (maximum 15 mg),usuallymixed into a flavored syrup or in a com-
mercially available premixed product;thisroute may be better accepted by
pediatricpatients.5Clinical effect from PO adminis-tration will be seen after 15 to
20 minutesin the pediatric patient.LorazepamLorazepam is a long-acting benzodi-
azepine with a slow onset.Its use for POand IV sedation is therefore limited but
isan option for oral preoperative anxioly-sis,particularly the night before
surgeryor for long operative appointments.Dosage for an adult is 0.05 mg/kg,not
toexceed 4 mg total.TriazolamTriazolam is only available in an oral for-mulation as
0.125 mg and 0.25 mg tablets.This sleep adjunct can be used off-label foranxiolysis
and sedation at a dose of0.25 to0.5 mg for an adult.It is a very short-
actingbenzodiazepine and its effects are observedin 30 to 45 minutes with
clinically effectivesedation lasting from 30 to 90 minutes.FlumazenilFlumazenil is
a highly specific competitiveantagonist for the benzodiazepine receptorand is used
as a reversal agent for benzodi-azepine agonists.6It will reverse benzodi-azepine
sedation,excessive disinhibition,and the additive ventilatory depressionrelated to
benzodiazepines when combinedwith opioids.Flumazenil is given 0.2 mg
IVinitially,followed by 0.1 mg at 1-minuteintervals as necessary,to a total of1
mg.Inemergency situations,0.5 to 1 mg or moremay be administered in a bolus
dose.Reversal effects may take several minutes tomanifest.The effect offlumazenil
will last30 to 60 minutes and may require redosingsince agonist drug activity may
outlast thereversal effects.Flumazenil should not beadministered to epileptic
patients usingbenzodiazepines for seizure control andshould be used cautiously with
otherepileptic patients.OpioidsOpioid medications are used in oralsurgery primarily
for analgesia and mildsedation or euphoria.It is important tonote that narcotic
medications do not pro-duce amnesia or classic sedation,nor dothey induce loss
ofconsciousness or sensa-tion oftouch at clinically relevant doses.Patients given
opioid medications alonewill retain awareness and memory.Instead,opioids are often
used in combi-nation with sedative-hypnotic medica-tions such as benzodiazepines
and barbi-turates to provide analgesia and augmentthe desired level
ofanesthesia.While the term opiaterefers to anydrug derived from
opium,opioidmedica-tions include all substances,natural andsynthetic,which bind to
the opioid recep-tors.7Common opioid medications areshown in Figure 5-3.Endogenous
opioidssuch as endorphins and enkephalins,andadministered opioid medications
likemorphine,bind to opioid receptors locat-ed in presynaptic and postsynaptic neu-
rons throughout the CNS as well as inperipheral afferent nerves.Agonist activityat
these receptors either modifies ordecreases neuronal transmission
ofpainsignals.Several subtypes ofopioid recep-tors (eg,�,?,d) with differential
effectshave been identified.The �and ?recep-tors are predominantly responsible
foranalgesia,and most clinically used opioidsare agonists for the �receptor.A
subset ofopioids,termed agonist-antagonistopioids,are agonists at ?receptors and
antagonistsat �receptors.Thus agonist-antagonistopioids are contraindicated for
patients onlong-term opioids,such as those usingthese agents for chronic pain or
those onmethadone maintenance for treatment ofopioid substance abuse.Respiratory
depression is the mostcommon and pronounced side effect of�receptor agonists as
used in anestheticpractice.This effect can be significantlyexacerbated with
concurrent administra-tion ofother medications such as benzodi-
azepines,barbiturates,propofol,and otheropioids.Respiratory depression is
dosedependent,resulting from a decrease in
88Part 1: Principles ofMedicine,Surgery,and Anesthesiathe respiratory response to
arterial carbondioxide (CO2) levels in the brainstem res-piratory centers.Decreased
respiratoryrate and arterial hypoxemia may resultwithout supplemental oxygen (O2)
andappropriate monitoring (eg,pulse oxime-try).Opioids are often titrated incremen-
tally to balance the analgesic effect againstrespiratory depression.Bradycardia as
a direct effect is moreapparent with high doses ofopioids and isdue to centrally
mediated vagal response.This effect is common with opioids suchas
morphine,fentanyl,and the syntheticderivatives,but less common with meperi-dine.A
mild decrease or stabilization ofthe heart rate may be desirable in patientswith
cardiovascular disease.Most opioids are metabolized by hepat-ic enzymes and
excreted into the urine andbile.The exception is remifentanil,which ismetabolized
by plasma esterases.Opioids suppress the cough reflex andare a common ingredient in
cough medi-cines.These antitussive effects can be bene-ficial during
sedation,especially when usedin patients with hyperreactive airways
(eg,smokers).However,several opioids cancause the release ofhistamine and
cautionshould be used when histamine-triggeringopioids are administered to an
asthmaticpatient.Other manifestations ofhistaminerelease include a decrease in
blood pressuresecondary to vasodilation,and pruritus anderythema,especially at the
site ofinjection.Other adverse effects such as nauseaand
vomiting,constipation,urinaryretention,and biliary tract spasm mayincrease patient
discomfort postopera-tively,particularly with repeated oral orneuraxial
administration.These reactionsare frequently misinterpreted by thepatient and other
health care providers asan �allergic�reaction.MorphineMorphine is the standard
agent by whichother opioids are compared.It has poorlipid solubility and therefore
has a slowonset.Peak effect following IV administra-tion occurs in 15 to 30 minutes
and theanalgesic effect lasts approximately 4 hours.Because ofits slow onset and
longerduration ofactivity,it is commonly used inanesthesia for postoperative pain
manage-ment rather than intravenous sedation.Morphine is normally given in 1 to 2
mg IVincrements for postoperative analgesia.Morphine has several notable charac-
teristics.Histamine release from morphinecan result in skin flushing and a
decreasein blood pressure and may be ofconcernin an asthmatic patient.Morphine
ismetabolized by hepatic enzymes into twometabolites that are subsequently elimi-
nated by the kidney.One ofthese metabo-lites,morphine-6-glucuronide,is morepotent
than morphine itself,and pro-longed opioid effects in patients with renalfailure
can be significant.MeperidineMeperidine is a synthetic opioid with a rel-atively
rapid onset time and duration ofaction between 2 and 3 hours.It is used forboth
intravenous sedation and postopera-tive pain control.Meperidine is usuallygiven in
12.5 to 25 mg IV increments titrat-ed to effect.The drug has several identifying
char-acteristics.Like morphine,it also has anactive metabolite,normeperidine,which
ishalfthe potency ofmeperidine.Whenmixed with monoamine oxidase
inhibitors,meperidine administration may produce adangerous excitatory hyperthermic
reac-tion.With repeated dosing,particularly inrenally compromised
patients,accumula-tion ofnormeperidine may lead toseizures.Meperidine is also
associated withthe release ofhistamine;thus,appropriateprecautions should be
taken.Unlike theother opioids it is not associated withbradycardia;its structure
resemblesatropine and it possesses mild anticholin-ergic effects such as a mild
increase in heartrate (offset by direct vagal stimulation) andxerostomia.Meperidine
is commonly usedto reduce shivering postoperatively,anaction likely associated with
partial agonistactivity at the ?receptor.FentanylFentanyl is a synthetic opioid,and
itshigh lipid solubility leads to its highpotency,rapid onset (1 min),and
shorterduration ofaction (10 to 20
min).WithH3CCH3CH3CH3CH2CH2CH3CH2CH2CH2CH3CH2CCH2CH2CH2OCH3CH2CH3OCNCCH2CH3CH2OCH3N
CCH2CH3CNNNSNNNOONNNNNOOOOOOOOCCRemifentanilAlfentanilSufentanilFentanylMeperidineF
IGURE5-3Chemical structure ofsynthetic opioidagonists.
Pharmacology ofOutpatient Anesthesia Medications89such characteristics fentanyl is
a frequentchoice for intravenous conscious seda-tion for short office-based
procedures.Itis typically given in 25 to 50 �g incre-ments towards a total dose
ofapproxi-mately 1 to 2 �g/kg.It is also given duringinduction ofgeneral
anesthesia,both for analgesia and attenuation ofairwayreflexes during
intubation.Fentanyl does not induce histaminerelease and is therefore not
associated withvasodilatory or bronchospastic effects.However,at higher doses,it
can cause morepronounced bradycardia than morphine.Fentanyl is a potent respiratory
depressant.At high doses and with rapid bolus admin-istration,fentanyl and other
synthetic deriv-atives have been associated with chest walland glottic
rigidity,making ventilationimpossible;there are reports that even lowerdoses
(eg,100 �g) can trigger this centrallymediated effect.Fentanyl-associated chestwall
rigidity is treated with either naloxoneor succinylcholine (SCh),and positive pres-
sure O2and other resuscitation equipmentshould be immediately available.The inci-
dence offentanyl rigidity is reduced by apreceding dose ofa benzodiazepine or
otherhypnotic drug.Remifentanil,Sufentanil,andAlfentanilRemifentanil,sufentanil,and
alfentanil aresynthetic fentanyl derivatives used primar-ily for analgesia during
general anesthesia.Remifentanil in particular is associatedwith a rapid onset and
extremely shortduration ofaction,resulting in a signifi-cantly shorter recovery
time.Metabolizedby nonspecific plasma esterases,its clear-ance is very rapid and
independent ofbothhepatic and renal functions.It has a veryshort context-sensitive
half-time of4 min-utes with virtually no cumulative effect,even following hours
ofcontinuous infu-sion.These features make remifentanilideal for use in a
titratable continuousinfusion.Ofnote is the fact that becausethe actions ofthis
medication are so short-lived,postoperative pain will not beaddressed by
intraoperative remifentanil,and alternative pain control with anothernarcotic such
as a nonsteroidal anti-inflammatory drug (NSAID) or localanesthesia should be
considered towardsthe end ofthe procedure.Remifentanil is used in a total intra-
venous infusion anesthetic technique tomaintain anesthesia during dental
surgery,often in combination with propofol.Foranalgesia during general anesthesia
it is usedat 0.25 to 1 �g/kg or 0.5 to 2 �g/kg/min.Dur-ing sedation the dose ranges
from 0.05 to0.10 �g/kg/min.Remifentanil,like fentanyl,can causechest wall rigidity
and caution should beused during bolus administration.It isalso a highly potent
respiratory depres-sant,and even at lower doses,apnea maybe
pronounced.Ifspontaneous ventilationis desired the remifentanil infusion is usu-
ally titrated to maintain an adequate respi-ratory rate.None ofthese synthetic
deriv-atives cause the release ofhistamine.Sufentanil and alfentanil are shorter-
acting agents than fentanyl but not asrapid in offset as remifentanil.Theseagents
are commonly used as a continuousinfusion adjunct for intubated generalanesthesia
during cardiac or prolongedsurgery,particularly when residual opioideffects are
desirable postoperatively.Theyare not as commonly used for office-basedoral
surgical anesthesia.NalbuphineNalbuphine is the most frequently usedintravenous
agonist-antagonist opioid.Ithas a relatively short onset and duration ofaction of2
to 4 hours at sedation doses of5 to 10 mg for the adult patient.Althoughnalbuphine
and other agonist-antagonistopioids do possess a ceiling effect for res-piratory
depression at higher doses,atequianalgesic and clinically relevant seda-tion
doses,the respiratory depressanteffects are similar to �agonist opioids.Nalbuphine
does not release histamine.Unlike all the other agents notedabove which are US Drug
EnforcementAgency Schedule II controlled substances,nalbuphine is not currently a
scheduledcontrolled substance and does not requirestate and federal documentation
ofuse.NaloxoneNaloxone is a pure opioid antagonist thatis active at all opioid
receptor subtypes.Itwill reverse both the ventilatory depressiveand analgesic
effects ofopioids.It can alsobe used to reverse chest wall or glotticrigidity from
fentanyl and its derivatives.In patients taking opioids chronically (eg,chronic
pain management,illicit opioidusers,methadone therapy for opioidabuse),naloxone
must be used with cau-tion as the antagonist effect may precipi-tate acute opioid
withdrawal and acutecongestive heart failure may result.The initial dose is 0.4 to
2 mg IV foracute reversal.Naloxone can also be titrat-ed in 0.04 mg increments when
gradualadjustment ofmild respiratory depressionis required.Because the duration
ofnalox-one activity is 30 to 45 minutes,reemer-gence ofrespiratory depression may
occurand additional dosing may be needed.BarbituratesBarbiturates are sedative-
hypnotic med-ications that have long been employed asinduction agents ofgeneral
anesthesia.Barbiturates produce sedation,loss ofconsciousness,and amnesia.These
drugsdo not provide analgesia and may actuallyreduce pain threshold at lower
doses.Sev-eral barbiturates such as IV pentobarbitaland oral phenobarbital are
commonlyused as anticonvulsants for both preven-tion and treatment ofseizures.High
dosesofany intravenous barbiturate can alsosuppress acute seizure
activity.Barbiturates are derivatives ofbarbi-turic acid (Figure 5-4).The
characteristicsofthe individual barbiturate are deter-mined by the side chains
attached to thebarbiturate ring (Figure 5-5).For example,
90Part 1: Principles ofMedicine,Surgery,and Anesthesiasulfur substitution on the
no.2 carbon inthiobarbiturates increases the lipid solu-bility ofthese drugs and
hence decreasesonset ofaction and duration ofactivity.The methyl group attached to
the nitrogenatom ofthe ring in methohexital results ina more rapid onset for this
oxybarbiturateand increased susceptibility to cleavage,producing a shorter duration
than otheroxybarbiturates.Barbiturates act on GABA receptors ata specific binding
site (different from ben-zodiazepines),causing the chloride chan-nel to remain open
for a longer duration.The increased negative inward flow hyper-polarizes the
membrane,decreasing neu-ronal transmission.Awakening from intravenous barbitu-rates
is dependent on redistribution fromthe brain.These medications are metabo-lized by
hepatic enzymes without the for-mation ofactive metabolites and are thencleared
renally.Because these drugs arehighly protein-bound,hypoproteinemiasecondary to
liver failure or malnutritionincreases the plasma concentration offreedrug.Chronic
use ofbarbiturates cancause induction ofliver enzymes.Barbitu-rates are also
contraindicated in patientswith acute intermittent porphyria as theymay precipitate
an attack.Barbiturates are associated with adose-dependent decrease in
respiratoryrate and tidal volume with apnea observedat higher doses.Centrally
mediatedperipheral vasodilation leads to a transientdrop of10 to 30% in systemic
blood pres-sure,particularly when a full inductiondose is administered.This is
partiallyattenuated by a compensatory increase inheart rate as baroreceptor
reflexes remainintact.Hypotension is more evident in theelderly or medically
compromised,hypo-volemic patients.Thiopental can causehistamine release,which is
clinicallyinsignificant with methohexital.Intra-arterial injection
ofbarbituratescauses painful spasm ofthe vessel fromprecipitation ofbarbiturate
crystals,whichdamage the endothelium and may resultin occlusion ofthe artery.At
worst,decreased distal perfusion may result intissue necrosis ofa limb or nerve
damageand must be addressed immediately.Theintravenous catheter should be left
inplace,IV cardiac lidocaine or procaine(without epinephrine) administered,andthe
patient should be transported to anemergency department where medicationsor
regional blockade may be given torelieve the spasm and reduce the occlu-
sion.Although also uncommon,venousirritation and thrombosis secondary tocrystal
formation is also possible with con-centrations ofbarbiturates above 1%methohexital
and 2.5% thiopental.These medications are stored in pow-der form and reconstituted
in saline priorto use as sodium salts.The alkalinity ofthesolutions prevents
bacterial growth andensures a longer refrigerated shelflife ofup to 2 weeks for
thiopental and 6 weeksfor methohexital.ThiopentalThiopental is an ultrashort-acting
barbi-turate that is commonly used at 3 to 5 mg/kg IV to induce loss ofconscious-
ness for general anesthesia prior to endo-tracheal intubation.It is associated with
alonger recovery than methohexital due toits decreased plasma clearance and is gen-
erally not used as a continuous infusionto maintain anesthesia due to
significantstorage in multiple drug compartments.A 2.5% solution ofthiopental is
lessN162534CCH2 + 2H2ONCOOHOCHFIGURE5-4Chemical structure
ofbarbituricacid.PhenobarbitalOOOOOOOOOCH3CH2CH3CH3CH3CH3CH3CH2CH2CH2CH=CH2CH2CH3CH
2CH=CH2CH2CH=CH2CHC=CCH2CH3CHCH2CH2CH3CHCH2CH2CH3CHCH2CH2CH3CHCH2CH2CH3Pentobarbita
lSecobarbitalMethohexitalThiopentalThiamylalNNNHHNOOOHHHHNNHNNCH3SOOSOOHNNHNNFIGURE
5-5Chemical structure ofbarbiturates.
Pharmacology ofOutpatient Anesthesia Medications91expensive than other induction
agents,but when rapid recovery is desired duringoutpatient anesthesia,other agents
suchas methohexital and propofol haveproven more popular.Thiopental canrelease
histamine,which is a concern inasthmatic patients.MethohexitalMethohexital is an
ultrashort-acting bar-biturate that is commonly employed foroutpatient oral
surgical procedures,pri-marily for its more rapid recovery com-pared to thiopental
and its lower costcompared to propofol.As an oxybarbitu-rate,methohexital is less
lipid solublethan thiopental but is associated with amore rapid awakening because
ofitsincreased hepatic clearance.8Psychomo-tor function returns more quickly
withmethohexital than thiopental,allowingfor earlier discharge following an outpa-
tient procedure.Methohexital is reconstituted into a1% solution and given at 1.5 to
2 mg/kg IVfor induction ofgeneral anesthesia.Withthese doses blood pressure may
drop by upto 35% and heart rate increases up to 40%ofbaseline.In a common deep
sedationtechnique used in oral surgical practice,10 to 30 mg increments
ofmethohexitalare periodically administered after obtain-ing baseline conscious
sedation with abenzodiazepine and opioid to produce astate ofdeep sedation for
local anestheticadministration and other stimulating por-tions ofdentoalveolar
surgery.Methohexital is associated with invol-untary movements such as myoclonusand
hiccuping.These excitatory phenom-ena are dose dependent and may bereduced by prior
administration ofopi-oids.Low doses ofmethohexital can acti-vate seizure foci and
should be used cau-tiously,ifat all,for epileptic patients.Shivering upon awakening
is also com-mon following methohexital anesthesia.Methohexital exhibits clinically
insignifi-cant histamine release.PentobarbitalPentobarbital is an intravenous
short-acting barbiturate with a duration ofactionof2 to 4 hours.It is generally
used for con-scious sedation in doses of100 to 300 mg,combined with opioids and
possibly benzo-diazepines,for longer operative procedures.Cardiovascular effects
are more modestthan the ultrashort-acting agents.Nonbarbiturate
InductionAgentsOther medications are available for seda-tion and induction
ofgeneral anesthesia.These include propofol,etomidate,andketamine,all ofwhich can
produce uncon-sciousness but with several differing char-acteristics from
barbiturate medications.PropofolPropofol has become one ofthe most pop-ular
sedative-hypnotic drugs used forambulatory surgery.Propofol,2,6-diisopropylphenol
(Figure 5-6),is highlylipid soluble and available as a milky white1% suspension in
soybean oil,glycerol,andegg phosphatide.Like benzodiazepines
andbarbiturates,propofol is thought to interactwith the GABA receptor,causing
increasedchloride conductance and hyperpolariza-tion ofneurons.At higher doses
propofolcan produce amnesia and loss ofconscious-ness.It is also an
anticonvulsant,althoughspontaneous excitatory movements may benoted following
administration.9Depending on the dose and technique,propofol is used for all levels
ofsedationand general anesthesia.For induction ofgeneral anesthesia a bolus of1.5
to 2.5 mg/kg IV produces unconsciousnesswithin 30 seconds.In the intermittent
bolustechnique frequently used for deep sedationin oral surgery,small increments
ofpropo-fol (10 to 30 mg) are periodically adminis-tered after a baseline conscious
sedationwith a benzodiazepine and opioid isobtained,in order to produce a state
ofdeep sedation for local anesthetic adminis-tration and other stimulating portions
ofdentoalveolar surgery.Propofol can also beused as a continuous intravenous infu-
sion.10The dosages for conscious sedationrange from 25 to 100 �g/kg/min,deep seda-
tion from 75 to 150 �g/kg/min,and generalanesthesia from 100 to 300
�g/kg/mindepending on the use ofintubation.Theoverlap ofdose ranges,from
conscioussedation to general anesthesia,highlightsthe lower margin ofsafety ofthis
drug,especially ifthe intended level ofsedation isconscious sedation.US Food and
DrugAdministration labeling prohibits use ofpropofol by those involved in the
conductofthe surgical or diagnostic procedure.Propofol is extensively metabolized
byhepatic enzymes.In addition,extensiveredistribution and other mechanisms
ofmetabolism and elimination most likelyoccur,as the rate ofpropofol clearancefrom
the plasma exceeds hepatic bloodflow.This rapid plasma clearance mayaccount for the
decreased cumulative effectofthis drug in the body,contributing torapid
awakening.The context-sensitivehalf-time for this drug is short,reaching amaximum
of40 minutes even after 2 to 6 hours ofcontinuous infusion.Context-sensitive half-
times are even shorter withbriefinfusions.Propofol decreases systemic bloodpressure
by as much as 20 to 40% frombaseline through centrally
mediatedvasodilation.Propofol also blocks sympa-thetic tone and allows
parasympatheticvagal responses to predominate,therebyblunting the reflex
tachycardia that would(CH3)2CHCH(CH3)2OHFIGURE5-6Chemical structure ofpropofol.
92Part 1: Principles ofMedicine,Surgery,and Anesthesianormally be associated with
such a drop inblood pressure.Hypotension may there-fore be very significant
following bolusadministration ofpropofol,particularly inthe elderly,medically
compromised,andhypovolemic patients.Propofol also leads to dose-
dependentrespiratory depression and can produceapnea at higher doses.It is not
associatedwith histamine release and has bron-chodilatory properties.Recovery from
anesthesia with propo-fol has several unique characteristics.Com-pared to other
induction agents propofol isassociated with a more rapid awakeningand recovery,with
less residual CNS effects.Many patients also experience mild eupho-ria on
awakening,which enhances reportedsatisfaction with the anesthesia postopera-
tively.Even at subhypnotic doses propofolis associated with decreased
postoperativenausea and vomiting.9All these featuresmake propofol an attractive
choice for out-patient procedures where decreased time todischarge is
desirable.Even with an available generic formu-lation the higher cost compared to
barbi-turates is still apparent.The increased costcan overshadow the advantages
ofusingpropofol infusions,especially ifthe surgi-cal time is long (> 2 h),or
ifquick dis-charge is not required.Several considerations should betaken when using
propofol.The solutioncan cause significant pain on injection,especially in smaller
vessels.This may beattenuated with pre-administration ofopioids or 1% cardiac
lidocaine.Unlikebarbiturates,however,it does not causevasospasm when inadvertently
injectedinto an artery.Anaphylaxis is rare but has beenreported in patients with a
history ofallergic reactions to other medications,especially neuromuscular blocking
drugs.A history ofegg allergy does not necessar-ily preclude the use ofpropofol,as
the eggprotein contained in the suspension islecithin,whereas most egg allergies
con-sist ofa reaction to egg albumin.The original proprietary agent,Diprivan,uses
ethylenediaminetetraacetic acid as anantibacterial agent,whereas the genericversion
contains a sulfite.Although thisgeneric agent should not be used inpatients with
known sulfite sensitivity,itappears that allergic reactions and bron-chospasm are
very unlikely,although notcompletely unheard of,in other patientsincluding
asthmatics.Both drug suspen-sions are pH neutral and can support bac-terial
growth;therefore,the observationofsterile technique and discarding ofanopened vial
or filled syringe after 6 hoursare recommended.Cracked glass contain-ers or
discolored contents should be dis-carded,as sepsis is a possibility.EtomidateLike
midazolam,etomidate contains animidazole structure (Figure 5-7).It iswater soluble
but available in a 0.2% solu-tion in propylene glycol.In the same wayas the other
induction medications,etomi-date interacts at the GABA receptor.Etomidate is used
primarily as aninduction agent for general anesthesia at0.2 to 0.4 mg/kg IV.Its
main advantageover barbiturates and propofol is cardio-vascular stability.Although
systemic bloodpressure can decrease by up to 15% withetomidate,changes in heart
rate are mini-mal.It also does not depress myocardialcontractility.Etomidate is
usually reservedfor patients with unstable cardiac diseasebecause it is more
expensive than otherinduction agents.Spontaneous respiration may
bemaintained.Respiratory depression is lesspronounced with etomidate compared
tobarbiturates,although apnea is still possi-ble with higher doses.Etomidate is
metabolized by bothhepatic enzymes and plasma esterases.This rapid clearance leads
to awakeningand recovery that is faster than withthiopental but slower than with
metho-hexital or propofol.Myoclonus is common in over 50% ofpatients and may be
partially preventedwith pre-administration ofa benzodi-azepine or opioid.Many
patients experi-ence pain on injection secondary to thepropylene glycol.Etomidate
has been asso-ciated with adrenocortical suppression butthis is less profound when
only a singleinduction dose is administered.KetamineKetamine is a phencyclidine
derivative(Figure 5-8) that induces a state of�disso-ciative anesthesia.�This is
characterized asa �dissociation�between the thalamocorti-cal and limbic
systems,producing acataleptic state during which the patientmay appear awake but
does not respond tocommands.11The eyes may be open andnystagmic.Ketamine does
produce antero-grade amnesia,and unlike other inductionagents,it can produce
intense analgesia.Unlike other hypnotic agents keta-mine does not interact with
GABA recep-tors.The exact mechanism ofaction isunclear but ketamine is a
nonselectiveantagonist ofsupraspinal N-methyl-D-aspartate receptors,which involve
the exci-tatory neurotransmitter glutamate.Inhibi-tion ofthese receptors decreases
neuronalsignaling and is likely responsible for someanalgesic effects.Ketamine may
also inter-act with pain receptors in the spinal cordas well as opioid
receptors,which may alsoaccount for analgesia.12Ketamine is highly lipid soluble
andredistributes quickly,which accounts forONNCH3CHCH3CH2OCFIGURE5-7Chemical
structure ofetomidate.
Pharmacology ofOutpatient Anesthesia Medications93its rapid onset ofaction and
relativelyshort duration.It is metabolized by hepat-ic enzymes and has an active
metabolite,norketamine.Ketamine does have a signif-icant abuse potential and
chronic use canlead to enzyme induction.The cardiovascular effects
ofketaminereflect its indirect activation ofthe sympa-thetic nervous
system.Ketamine causes anincrease in norepinephrine by inhibitingreuptake at
postganglionic sympatheticneurons.Sympathetic stimulation increas-es heart rate and
systemic blood pressure.Ketamine should therefore be used withcaution in patients
with uncontrolledhypertension or in whom tachycardiashould be
avoided.However,ketaminemay be chosen for induction ofgeneralanesthesia at 1 to 2
mg/kg IV when cardio-vascular stimulatory effects are desired,asin emergent trauma
surgery.Practitionersshould note that ketamine is actually adirect myocardial
depressant,an effectnormally masked by the indirect sympa-thetic stimulation.In
severely compro-mised patients,however,catecholaminestores may be exhausted and
hypotensionsecondary to myocardial depression canbecome significant.Respiratory
depression is not signifi-cant with ketamine,although apnea willoccur with rapid
bolus administration.Upper airway reflexes remain largely butnot reliably
intact;aspiration is still possi-ble,especially as ketamine increases sali-vary
secretions and postoperative nauseaand vomiting.Ketamine does not causehistamine
release and is a potent bron-chodilator secondary to sympathetic acti-vation as
well as direct bronchial smoothmuscle relaxation.In oral surgical practice a
primaryindication for ketamine is intramuscularinjection for uncooperative adult
patients,such as the mentally challenged or thosewith severe psychiatric illness,or
for chil-dren who will not tolerate IV placement.The intramuscular dose for
induction ofgeneral anesthesia is 3 to 7 mg/kg,whereas2 to 3 mg/kg is usually
sufficient to obtainadequate control for IV placement.Awater-soluble benzodiazepine
like mida-zolam is commonly added to reduce thepossibility ofuncomfortable
dreamingassociated with ketamine.An anticholin-ergic medication like glycopyrrolate
is alsogiven to reduce the production ofsalivarysecretions secondary to
ketamine.Gly-copyrrolate may be preferred overatropine or scopolamine for its
superiorantisialagogue effects,less pronouncedcardiac effects,and poor CNS
penetration.The other main use in oral surgicalpractice is in an IV deep-sedation
tech-nique.Conscious sedation is first achievedwith a benzodiazepine,followed by
sub-anesthetic doses of10 to 30 mg ofketa-mine until a state that is similar to
deepsedation is achieved.Although ketamine isquite analgesic some surgeons also add
anopioid in the baseline sedation.Alterna-tively,ifa standard deep-sedation tech-
nique with methohexital has been applied(see �Methohexital,�above) and largedoses
ofthe barbiturate become necessaryto achieve adequate sedation,or unwantedpatient
movement persists despite highmethohexital doses,the addition ofsmallboluses
ofketamine can often enhance thequality ofsedation.�Emergence delirium�can occur
dur-ing awakening.The patient may experi-ence visual and auditory
hallucinationsthat can be perceived as either pleasant(euphoria) or unpleasant
(dysphoria),lasting for up to several hours.Deliriumoccurrence is less common in
children andwith doses less than 2 mg/kg IV.It may beattenuated with prior or
concurrentadministration ofbenzodiazepines,whichshould be routine when intravenous
seda-tion techniques are used.Inhalation AnestheticsInhalation anesthetics include
nitrousoxide (N2O) as well as the potent volatilehalogenated agents,such as
halothane,isoflurane,sevoflurane,and desflurane.N2O alone is commonly used in
dentaloffices for anxiolysis and mild sedation,but it is also used in combination
withother medications to induce and maintainboth sedation and general
anesthesia.Thehalogenated agents are extremely potentand are used for induction and
mainte-nance ofgeneral anesthesia.The pharmacokinetics ofthese anes-thetic agents
differ from those ofintra-venous medications.These drugs areinhaled and cross from
the alveoli intothe pulmonary vasculature,entering thegeneral circulation.They are
able tocross the blood-brain barrier and exertanesthetic effects within the
brain.Except for halothane most oftheseagents are minimally metabolized andare
subsequently excreted unchangedback into the alveoli.Once exhaled thesegases are
deposited into the anesthesiacircuit and eventually scavenged.Plasma concentrations
ofthe inhaledanesthetics are dependent on the concen-tration ofthe gas within the
alveoli,solu-bility characteristics ofthe individualgases,and cardiac
output.13,14Cardiac out-put influences the rate ofuptake from thealveoli.Main
factors affecting alveolar gasconcentration include the inspired con-centration
ofgas,alveolar ventilation,andthe total gas flow rate.Administering ahigher
concentration ofgas will increaseintra-alveolar concentration,whereasaltering the
total gas inflow or alveolarOCINHCH3FIGURE5-8Chemical structure ofketamine.
94Part 1: Principles ofMedicine,Surgery,and Anesthesiaventilation (respiratory
rate,tidal volume)will affect how quickly the concentrationofgas within the alveoli
changes.Each agent varies in its solubility inblood and other tissues such as the
brainand fat,and these characteristics determinethe ease with which the gas crosses
into thedifferent tissues.Ofthese,the blood:gas sol-ubility coefficient (Table 5-1)
is the mostuseful in describing the onset and offset ofaction ofan anesthetic
gas.The blood:gassolubility coefficient expresses the extent towhich the anesthetic
gas molecules fromthe alveolar spaces will dissolve into plasmabefore the plasma
solution becomes satu-rated.Conceptually,a lower coefficientmeans that the gas is
less soluble in bloodand will saturate the plasma compartmentquickly.Additional
�overflow�moleculeswill then be free to move into other highlyvascular tissues such
as the brain,where theCNS anesthetic effect takes place.A lowerblood:gas
coefficient therefore translatesinto faster onset ofaction at the brain.Oncethe gas
is discontinued and the alveolar andplasma concentrations decrease,the gasmolecules
move down their concentrationgradient from the tissues back into theblood stream
and then into the alveoli.Gases with lower blood:gas coefficients willlikewise
�offload�from the blood streaminto alveoli more quickly and can translateinto a
faster offset ofaction.Unlike intravenous medications theseinhaled drugs are not
administered indoses ofmg/kg.The equivalent oftheeffective dose (ED50) ofinhaled
anestheticagent is the minimum alveolar concentra-tion (MAC).The MAC value ofany
givenagent is the inhaled concentration (vol-ume %) ofthat agent required to
preventmovement in 50% ofpatients to a surgicalstimulus.MAC values for different
agentsare given in Table 5-1.MAC values providea useful dosage guide for anesthetic
gases.In adults a level of1.3 MAC will preventmovement in 95% ofpatients,whereas
1.5 MAC (MAC-BAR) will block anadrenergic response in 95% ofpatients.Below 0.3 MAC
(MAC-Awake),patientawareness is more likely.MAC values areadditive;for
example,if0.5 MAC ofN2Oand 1.0 MAC ofisoflurane are givensimultaneously,the total
MAC ofanes-thetic agent administered to the patient is1.5 MAC.It should be noted
that MACvalues are general guidelines,and individ-ual anesthetic requirements can
be influ-enced by a variety offactors such as age ormedical status.Neonates have
the lowestMAC requirement,whereas children havethe highest requirement.MAC require-
ments subsequently decrease in the elderlypatient.MAC values are typically listed
foradult (30- to 35-year-old) patients at 1 atmpressure and 20�C.The exact
mechanism ofaction ofinhaled anesthetic agents at the CNS is
stillcontroversial.Earlier theories have sug-gested that anesthetic molecules
insertinto and disrupt the lipid bilayer ofneu-ronal cell membranes,thus
interferingwith the cellular function.More currenttheories suggest that anesthetic
moleculesmay instead directly interact with cellularproteins,possibly with membrane
ionchannels or even specific receptors.Whereas N2O has mild or
minimalsympathomimetic effects,all ofthe halo-genated agents produce generalized
car-diovascular depressant effects.The potentvolatile agents block peripheral
vasocon-striction thus lowering mean arterialblood pressure.At lower doses below 1
MAC the baroreceptor sympathetic reflexis activated,which leads to a
compensatoryincrease in heart rate.The exception ishalothane,which in addition to
directlydepressing myocardial contractility,blocksthe baroreceptor reflex.This
resultingdecrease in cardiac output can lead to aprecipitous drop in systemic blood
pres-sure with higher doses ofhalothane.Halothane also has the highest associa-tion
with cardiac dysrhythmias.Halothaneinduction commonly suppresses sinoatrialnode
activity,leading to the developmentofjunctional rhythms.It also sensitizes
themyocardium to catecholamine-relatedTable 5-1Different Properties ofNitrous Oxide
and Potent Volatile AgentsGeneral Properties ofInhalation Anesthetics �
AdultsNitrous OxideIsofluraneEnfluraneHalothaneDesfluraneSevofluraneMolecular
weight44184.5184.5197.4168218Vapor pressure 20�CGas238172243664160MAC in
O21051.21.60.776.02.0% recovered metabolites00.22.4200.023Partition Coefficients at
37�CBlood:gas0.471.461.912.50.420.69Brain:blood1.11.61.41.91.31.7Muscle:blood1.22.9
1.73.423.1Fat:blood2.34536512748MAC = minimum alveolar concentration.
Pharmacology ofOutpatient Anesthesia Medications95ventricular dysrhythmias (Figure
5-9),par-ticularly under conditions ofhypercar-bia.15Isoflurane,sevoflurane,and
desflu-rane are not significantly associated withan increased incidence
ofepinephrine-associated dysrhythmias.Epinephrine con-tained in local anesthetic
solutions shouldbe limited to a maximum dose of1 to 2 �g/kg during halothane
anesthesiawhereas up to 3 to 4.5 �g/kg is consideredsafe with the other three
agents.Underhalothane anesthesia,administration of1.0to 1.5 mg/kg cardiac lidocaine
IV immedi-ately prior to intubation reduces the inci-dence ofventricular
dysrhythmias duringthis stimulating period when endogenousepinephrine release may
occur.Hypoxiaand hypercarbia also lower the thresholdfor dysrhythmias and should be
especiallyavoided with halothane anesthesia.Treat-ment ofthe presenting
dysrhythmiashould be managed as required,includinghyperventilation,deepening
ofanestheticlevel and,ifindicated,discontinuation ofhalothane with administration
ofan alter-native anesthetic agent.At usual doses N2O does not appre-ciably affect
respiration.However,thehalogenated agents produce a character-istic �rapid and
shallow�spontaneousbreathing pattern.A decrease in tidal vol-ume is accompanied by
an increase in thefrequency ofbreaths,but the faster respi-ratory rate does not
fully compensate forthe smaller tidal volumes.Therefore,minute ventilation is
reduced and arterialCO2levels will be elevated in patientsspontaneously breathing
while undergeneral anesthesia with these agents.Thehalogenated agents also cause a
dose-dependent decrease in airway resistanceand produce
bronchodilation.Hypoxicpulmonary vasoconstriction is attenuatedat 0.1 MAC for all
volatile agents.Although hepatic blood flow decreaseswith these agents,hepatic
damage,ifany,resulting from hypoxia is usually subclini-cal and
transient.Hepatotoxicity is more ofa concern with halothane administration.Renal
blood flow and urine output arereduced secondary to the decreased meanarterial
pressure.The release offluoridefrom the halogenated gases does notappear to cause
clinically significant dam-age to renal tissues.With sevoflurane,freshgas flows
should be at least 2 L/min to min-imize compound A accumulation in theCO2absorber
which can lead to very rarehepatic or renal damage.Malignant hyperthermia (MH)
isanother rare but very dangerous reactiontriggered by the halogenated agents as
wellas SCh.N2O,nondepolarizing neuromus-cular blockers,opioids,benzodiazepines,and
other intravenous anesthetic agentsdo not trigger MH.Exposure to thesemedications
causes an abnormal receptorin skeletal muscle cells to release
excessiveintracellular calcium,leading to uncon-trolled muscle contractions.As a
resultCO2production increases quickly andexhaled CO2rises sharply.Initial
signsinclude tachycardia and tachypnea,alongwith muscle stiffness.Metabolic
acidosisand hyperkalemia develop next and car-diac arrest is a
possibility.Increasing bodytemperature is a relatively late sign.Thehalogenated
agent must be discontinued atonce and 100% O2given,preferablythrough a different
circuit and machine.Dantrolene at 2.5 to 10 mg/kg IV must begiven as soon as
possible.Cooling mea-sures including cooled IV fluids should beinstituted.Emergency
help must beobtained immediately and the patient willrequire medical management and
moni-toring for at least 24 hours following theepisode.Reemergence ofthe reaction
iscommon,requiring re-administration ofdantrolene,and acute renal failure is
themost common morbidity secondary tomyoglobinemia.A mortality rate of10%
isassociated with an acute MH episode,evenwith immediate proper management.Nitrous
OxideN2O is commonly administered in dentaloffices for anxiolysis and mild
sedation.Itis a colorless and odorless gas,available inblue cylinders.In the dental
setting it iscommonly administered with a nasal hoodand appropriate scavenger
system.Con-centration ratios ofN2O:O2range up to70:30 on most N2O and
anesthesiamachines.High levels ofN2O:O2alone canproduce sedation and significant
analge-sia.Unexpected respiratory depression orairway obstruction can occur when
N2O isadded to other sedative agents.N2O in O2is likely the most commonlyused
sedative agent in dental offices andenjoys the unique advantage ofnot requir-ing an
escort after completion ofthe proce-dure provided adequate recovery time
haselapsed.The drug can be titrated,usuallystarting at 20% N2O and gradually
increas-ing to 50% as needed.Doses above thatlevel are associated with increased
nauseaand dysphoria,although the briefapplica-tion ofdoses higher than 50% is
useful dur-ing local anesthetic administration andother short stimulating surgical
episodes.At the conclusion ofN2O sedation,3 to 5 minutes of100% O2is administered
toprevent diffusion hypoxia;ifroom air O2isgiven instead,the rapidly exiting N2O
canPatients Exhibiting Ventricular Extrasystoles (%)100 80 60 40 20 0 12Epinephrine
per Body Weight
(�g/kg)Halothane(saline)Halothane(lidocaine)Isoflurane345710EnfluraneFIGURE5-
9Halothane sensitizes the myocardi-um to dysrhythmias following administration
ofepinephrine in saline.Addition of0.5% lido-caine to the epinephrine solution
decreases theincidence ofdysrhythmias,but the incidence isstill higher than during
isoflurane use.Adaptedfrom Johnston RR et al.15
96Part 1: Principles ofMedicine,Surgery,and Anesthesiadilute the O2concentration in
the alveoli tohypoxic levels during recovery.With a low blood:gas solubility
coeffi-cient of0.47,N2O has a very quick onsetand recovery.While N2O lacks the
potencyofthe halogenated agents at a MAC valueof105,it also lacks the respiratory
and car-diovascular side effects.During generalanesthesia it is often administered
to anintubated patient in combination withother medications such as
halogenatedgases and opioids.Using this combinationcan reduce the dose required
ofeach drugifgiven singly and will lessen the incidenceofpotential side effects.N2O
is also inex-pensive and can reduce the total cost ofadministered drugs.There are a
few contraindications forthe use ofN2O.It can enter closed spacesfaster than
nitrogen can exit,leading todistention ofthe closed space.13In oralsurgical
practice the implication ofthisproperty is to avoid N2O use in patientswith current
otitis media and sinus infec-tions and with emphysema
(blebs).Othercontraindications ofN2O use include cur-rent respiratory disease and a
history ofsevere postoperative nausea.Several precautions should be exer-cised when
using N2O.It has been impli-cated in producing sexual hallucinationsin some
patients,predominantly youngwomen.An additional person such as anassistant should
always be present whenthis gas is being administered.Patientswith preexisting
psychiatric disorders mayexperience exacerbated symptoms whileundergoing N2O
sedation.Because lowlevels ofN2O in room air have beendemonstrated to increase
spontaneousabortion rates in pregnant anesthesiaproviders,proper scavenging is
essential tominimize room air levels so that surgicalpersonnel are not at increased
risk.Fre-quent recreational use ofN2O has beenreported to lead to peripheral
neuropathyand other deleterious effects.As with allanesthetic agents anesthesia
providersmust never use these drugs for personaluse and should be alert to
potential misuseby other providers ofthese drugs.Potent Inhalation AgentsThe
halogenated inhalation agents com-monly in use today in the United Statesinclude
halothane,isoflurane,sevoflurane,and desflurane.As seen in Figure 5-10,allare
derivatives ofether except forhalothane.Unlike the original anestheticgas,diethyl
ether,these agents are halo-genated and nonflammable.The newerhalogenated
agents,sevoflurane and desflu-rane,are unique in that all ofthe side chainhalogen
atoms are fluorine.The gases arestored and released by gas-specific vaporiz-ers
that control the concentration (volume%) allowed into the anesthesia circuits
andinto the patient.They must also be scav-enged effectively so that room air
levels donot affect health care personnel.HalothaneHalothane has a sweet non-
pungent odor that does not irritate theairway mucosa to the extent ofisofluraneand
desflurane,and is therefore usefulfor inhalation induction ofgeneral anes-
thesia.Halothane is very potent,with aMAC value at 0.75 but a relatively
highblood:gas solubility of2.54.Therefore,halothane will have a slow onset
ofinhalation induction unless high dosesare used.Recovery from anesthesia willbe
slower than with other agents withlower solubility coefficients.Halothane is the
oldest and most inex-pensive ofcurrently available potent gasesbut presents with
the most deleterious sideeffects.As noted above,halothane is asso-ciated with
significant cardiovascularchanges and dysrhythmias.These shouldbe monitored closely
during inductionand epinephrine administration,such aswith local anesthesia,when
dysrythmiasare more commonly encountered.Unlikethe other agents,at least 15%
ofthehalothane molecules are metabolized bythe liver,and hepatotoxicity is more
signif-icant with halothane,especially afterrepeated and prolonged
administration.Halothane hepatitis is very rare but canresult in hepatic necrosis
and death.Ofallthe halogenated agents it also appears tobe the most potent trigger
for MH.IsofluraneIsoflurane is more pungentthan halothane and is not a good
choicefor inhalation induction.It has an inter-mediate potency (MAC 1.2) and
blood:gaspartition coefficient (1.46).This agent is acommon choice for maintenance
ofanes-thesia,as recovery time is in the interme-diate range and shorter than
halothane.Isoflurane is also much more cost-effectivefor longer periods
ofanesthesia comparedto two other popular agents,sevofluraneNNitrous
oxideHalothaneEnfluraneNOFCCFCIFBrHHCCFFCIFFFOCHIsofluraneFCCFHFCIFFOCHDesfluraneFC
CFHFFFFOCHSevofluraneHCCF3CF3FFOCHFIGURE5-10Chemical structure ofinhalation agents.
Pharmacology ofOutpatient Anesthesia Medications97and desflurane;its cost per
bottle is signif-icantly lower and the total amount used isless due to the lower
MAC.Isoflurane may be associated with anincrease in coronary steal phenomena,lead-
ing some practitioners to avoid using thisanesthetic in patients with significant
ather-osclerotic cardiac disease.Otherwise,con-traindications for using isoflurane
are few.SevofluraneSevoflurane is nonpungentand a common choice for
inhalationinduction.It has an intermediate potency(MAC 2.0),and at higher
doses,inductionwill be rapid.Recovery from sevofluranefollowing a short anesthetic
(< 1 h) is morerapid than either isoflurane or halothanedue to the lower blood:gas
solubility coef-ficient (0.69).For longer procedures,how-ever,the advantage
offaster recovery is off-set by the much greater cost ofsevofluranecompared to
isoflurane.The recovery timeis also not significantly improved com-pared to
isoflurane,as both gases similarlyredistribute into fat during longer anesthe-sia
periods,and offset ofthese gases fromfat storage is not different.All ofthe side
chain halogen atoms insevoflurane are fluorine,contributing to itslow blood:gas
solubility and recovery pro-file.Unlike earlier inhaled agents the smallamount
ofinorganic fluorine released dur-ing sevoflurane use has not been associatedwith
renal damage.16Sevoflurane and CO2absorbers (soda lime,barium lime) pro-duce a
degradation product called com-pound A,an olefin,which is nephrotoxic inrats but
has not been associated with signif-icant permanent renal damage in
humans.Regardless,sevoflurane is not usually theagent ofchoice for patients with
renal dis-ease.Even in healthy patients many practi-tioners recommend limiting
sevofluraneuse to less than 2 hours and maintaining atotal gas flow ofat least 2
L/min,to reducethe production ofcompound A.DesfluraneDesflurane is extremely pun-
gent and can be so irritating to nonanes-thetized airways that it may
precipitatecoughing and laryngospasm.It is to beavoided for inhalation
inductions.Duringinitial administration ofdesflurane,tachy-cardia can also occur
until deeper levels ofanesthesia are realized.Desflurane is delivered from
speciallyheated vaporizers as its vapor pressure isclose to atmospheric pressure.It
also pos-sesses only fluorine substitutions which,like sevoflurane,confer a low
blood:gassolubility.In fact,desflurane has the lowestblood:gas solubility
coefficient (0.43) ofany inhalation agent,lower than even N2O.This confers a quick
onset and offset,andrecovery can be very rapid following ashort anesthetic with
desflurane.Likesevoflurane,desflurane is more expensivethan the other gases,and
considering itshigher MAC value (6.0),much more ofthegas will be used per
minute,resulting in asignificantly higher cost ifdesflurane isused for a longer
procedure.Perioperative Analgesic MedicationsOpioid medications,which have been
dis-cussed previously,are the classic intraoper-ative and postoperative analgesic
medica-tions.In the operating room opioids areoften given concurrently with other
anes-thetic agents in a balanced technique tosupplement intraoperative
analgesia.Anopioid with a long duration ofaction likemorphine or hydromorphone is
common-ly administered by the practitioner prior tothe end ofthe procedure,in
anticipation ofpostoperative pain.During the initial phaseofpostoperative care
these medicationsmay be given either by the nursing stafforpatient,administered via
computer-aidedpatient-controlled analgesia pumps.Another option is ketorolac
trometh-amine,currently the only available intra-venous NSAID medication in the
UnitedStates.This agent can provide effective anal-gesia for many dentoalveolar
procedures atIV and IM doses of30 to 60 mg or 0.5 to 1.0 mg/kg.Onset time is 10 to
15 minutes,with an analgesic duration ofapproximate-ly 6 hours.Ketorolac 30 mg IM
is the anal-gesic equivalent of10 mg ofparenteral mor-phine and does not produce
opioid-relatedrespiratory depression,nausea,or sedation.3NSAID use does have
several cautions,how-ever.Because ofpossible NSAID-inducedinhibition ofplatelet
aggregation,the drugis normally administered after bleeding hasbeen controlled,and
should be avoided forsurgeries associated with postoperativehemorrhage.Patients
with bleeding-relateddisorders (gastrointestinal ulcers,inflam-matory bowel
disease,blood dyscrasias,liverfailure,etc) should not be given ketorolac.Life-
threatening bronchospasm can alsooccur with NSAIDs,particularly in thosewith a
history ofasthma or aspirin allergy.Because NSAIDs block prostaglandin pro-
duction,patients who depend on renalprostaglandins for adequate renal
functionshould be administered ketorolac cautious-ly.Patients with congestive heart
failure,hypovolemia,or cirrhosis,and those takingangiotensin-converting enzyme
inhibitorsor angiotensin II receptor antagonists,mayrequire renal perfusion to
maintain ade-quate renal perfusion,and NSAID adminis-tration can result in acute
fluid retention.This drug is also associated with a highercost than other analgesic
medications.The most commonly used agents forpostoperative pain control in oral
surgeryare likely the local anesthetics.Long-actinglocal anesthetics,like
bupivacaine and etido-caine,provide several hours ofanalgesia forinferior alveolar
nerve block anesthesia aswell as soft tissue anesthesia in the maxilla.Lidocaine
with epinephrine given intraoper-atively can also provide adequate
analgesicduration until postoperative oral NSAIDs oropioid/acetaminophen
combinations canachieve reliable plasma levels for generallypredictable
postoperative pain control.Neuromuscular-Blocking MedicationsSkeletal muscle
relaxation is often requiredduring surgery when patient movement
98Part 1: Principles ofMedicine,Surgery,and Anesthesiainterferes with procedures
involving anes-thesia or surgery.For example,paralysismay be required to facilitate
tracheal intu-bation,relax abdominal wall muscles foraccess during gastrointestinal
surgery,orcompletely inhibit patient movement dur-ing ocular surgery.Whereas
relaxation canbe achieved with deeper anesthetic levels orappropriate peripheral
neural blockade,neuromuscular-blocking agents are com-monly used to provide the
necessaryamount and duration ofrelaxation.The potential ofthese drugs
duringanesthesia and surgery was not recognizeduntil the middle ofthe twentieth
century.Many ofthe current neuromuscular-blocking agents used are derivatives
ofcurare,one ofthe oldest paralyzingagents,used by ancient hunters to para-lyze
prey.All are competitive antagoniststhat bind to the nicotinic ACh receptorslocated
at the postsynaptic membrane ofthe neuromuscular junction ofskeletalmuscle,thus
interfering with proper con-traction ofthe muscle.Neuromuscular-blocking agents
canbe classified as either depolarizing or non-depolarizing,and within the latter
groupcan be divided based on structure,speed ofonset,duration ofaction,and
metabolism.SuccinylcholineSCh,two joined ACh molecules,was intro-duced for surgical
muscle relaxation in the1950s and is the only depolarizing agentused today.Once SCh
binds to the AChreceptor,the postsynaptic membranedepolarizes,an action potential
is generat-ed,and the muscle contracts.Subsequentmuscle contractions are delayed
until SChdissociates from the receptor and ismetabolized by
pseudocholinesterase.SCh has the fastest onset (30�60 s) andshortest duration (5�10
min) ofthe neuro-muscular-blocking agents and is typicallyused to treat
laryngospasm not relieved withpositive pressure (20 to 40 mg,or 0.1 to 0.2
mg/kg).It is also given to facilitate tra-cheal intubation (1 to 1.5 mg/kg IV) or
whenemergent tracheal intubation is required totreat laryngospasm.It is no longer
used tomaintain intraoperative paralysis.SCh has several notable side
effects.Tachycardia can result upon initial admin-istration but sinus bradycardia
may devel-op,especially with repeated administra-tion.Widespread muscle
contractions canresult in postoperative myalgia,which canat times be prevented by
prior administra-tion ofa small dose ofa nondepolarizingmuscle blocker.The
contractions mayincrease intraocular and intragastric pres-sure and can also cause
a transient ele-vation in plasma potassium levels by 0.5 mEq/L.Plasma potassium
levels mayrise even higher than 0.5 mEq/L in patientswith certain neuromuscular
disorders,stroke,spinal cord injury,or significantburn injury.SCh is therefore
contraindi-cated in these patients,along with patientsin renal failure.SCh is a
trigger for MH (seesection on malignant hyperthermia).Itsuse should also be avoided
in patients withpseudocholinesterase abnormalities,as therecovery from this drug
will be prolonged.Nondepolarizing AgentsAll ofthe remaining neuromuscularblocking
agents are nondepolarizing anddo not initiate muscle contraction
uponadministration.The chemical structures ofthese drugs fall into two
classes:benzyliso-quinolines and aminosteroids.13Charac-teristics ofcurrently
available nondepolar-izing muscle relaxants are outlined inTable 5-2.Although it is
not as rapid in onset asSCh,rocuronium has the fastest onset ofthe nondepolarizing
agents,with paralysisoccurring at approximately 1 minute withhigher doses.It is
often chosen for facili-tating intubation when SCh cannot beused,particularly in an
emergent situa-tion.Onset time for most other agents isapproximately 3 minutes.Drug
selection for maintenance ofmuscle relaxation is often based upon theanticipated
need for continued paralysis.Pancuronium has the longest duration,whereas
mivacurium has the shortest.With any ofthese agents paralysis will lastlonger than
that produced with SCh andcontrolled ventilation must be provided.Return ofskeletal
muscle function is usu-ally monitored by a nerve stimulator,andthe degree
ofparalysis is gauged by thenumber oftwitches produced by stimula-tion ofspecific
muscles,such as adductorpollicis and orbicularis orbis.Paralysismay need to be
reversed by an anti-cholinesterase to ensure adequate recoveryofairway and
respiratory muscle functionprior to extubation.Adverse effects may also affect
thechoice ofneuromuscular-blocking agentand can be categorized by
structure.Thebenzylisoquinoline compounds may trig-ger histamine release thus
causing flush-ing and peripheral vasodilation.Amino-steroid structures may block
vagalactivity,causing a noticeable increase inheart rate.Histamine release may
beundesirable in asthmatic patients.Increased heart rate can be problematic
inpatients with cardiovascular disease.Most ofthe nondepolarizing agentsare
metabolized by the liver and excretedby the kidney.Three ofthese are lessdependent
on hepatic or renal function.Mivacurium,like SCh,is metabolized
bypseudocholinesterase and is affected by itsdeficiency.Atracurium and
cisatracuriumare removed by Hofmann elimination,whereby the drug spontaneously
degradesat body pH and temperature.AnticholinesterasesAnticholinesterases,or anti-
acetyl-cholinesterases,block the action ofacetyl-cholinesterase,the enzyme that
breaksdown ACh.In anesthesia,anticholinesteras-es such as
neostigmine,edrophonium,andpyridostigmine are used to reverse theeffects
ofnondepolarizing muscle relaxantsonce partial muscle function has returnedand
paralysis is no longer necessary,usuallyat the conclusion ofsurgery.By increasing
Pharmacology ofOutpatient Anesthesia Medications99the amount ofACh available at the
neuro-muscular junction,more ofthe neurotrans-mitter can bind to nicotinic ACh
receptors,overcoming the competitive inhibition ofthe neuromuscular blocker and
aiding inthe return ofmuscle function.Increased ACh will also bind to mus-carinic
ACh receptors at the heart,lungs,salivary glands,and smooth muscle.Thiscan lead to
undesirable side effects includ-ing bradycardia,bronchospasm,abdomi-nal
cramping,and excessive salivation.17Toprevent these effects anticholinergic med-
ications such as atropine or glycopyrrolate,which block muscarinic but not
nicotinicACh receptors,are given together withanticholinesterases.The
anticholinesteraseand anticholinergic medications are pairedaccording to similar
time ofonset andduration.Glycopyrrolate is generallyadministered with
neostigmine,whereasatropine is more commonly used withedrophonium.Doses ofthese
agents arelisted in Table 5-3.Anticholinergic MedicationsACh is a neurotransmitter
that binds totwo types ofreceptors.Nicotinic receptorsare located at autonomic
ganglia and theneuromuscular junctions ofskeletal mus-cle.Muscarinic receptors are
found atpostganglionic sites ofthe parasympathet-ic nervous system at the
heart,salivaryglands,and smooth muscle.Anticholiner-gic medications specifically
block mus-carinic receptors but do not affect nico-tinic receptors.Clinical uses in
anesthesia ofatropine,glycopyrrolate,and scopolamine are definedby their varied
effect at the muscarinicreceptor sites ofdifferent organs (Table 5-4).Atropine has
the fastest onset ofincreasingheart rate by blocking vagal nerve receptorsat the
heart and is used to treat emergentbradycardia.Both atropine and glycopyrro-late
are used to counteract bradycardia sec-ondary to anticholinesterase use
duringreversal ofmuscle relaxation.All three anti-cholinergic medications decrease
salivarysecretions.Glycopyrrolate is a quaternaryammonium compound,which cannot
crossthe blood-brain barrier.Atropine andscopolamine,both tertiary amines,cancross
the blood-brain barrier and causesedation.Scopolamine is also used for man-agement
ofnausea and prevention ofmotion sickness.Central anticholinergic syndrome is
aconcern with higher doses ofcentrallyacting anticholinergic medications,mani-
festing as restlessness and confusion.Itmay be reversed by physostigmine,anTable 5-
2Common Neuromuscular-Blocking Medications and Their PropertiesTSI Characteristics
ofCommonly Used Intubating Dose Time to Intubate25% Twitch RecoveryMetabolism
andHistamineNeuromuscular-Blocking Agents(mg/kg)(min)
(min)EliminationReleaseVagolysisDepolarizingSuccinylcholine115�10Plasma
cholinesterase�0NondepolarizingAminosteroidsRocuronium0.6�1.21�1.540�150Liver;kidne
y00Vecuronium0.1�0.122�325�30Liver;kidney00Pancuronium0.08�0.13�580�100Liver;kidney
0+Pipecuronium0.07�0.0853�550�120Liver;kidney0�BenzylisoquinolinesMivacurium0.15�0.
251.5�2.016�20Plasma cholinesterase+0Atracurium0.4�0.52�325�30Hofmann
elimination+0Cisatracurium0.15�0.21.5�250�60Hofmann
elimination00Doxacurium0.05�0.084�5100�160Liver;kidney00d-
Tubocurarine0.5�0.63�580�100Liver;kidney++0Table 5-3Reversal Doses
ofAcetylcholinesterase and Anticholinergic MedicationsCholinesterase Dose
Anticholinergic DoseCholinesterase(mg/kg)Anticholinergic(mg/mg
ofcholinesterase)Neostigmine0.4�0.8Glycopyrrolate0.2Edrophonium0.5�1.0Atropine0.014
The two most commonly used acetylcholinesterase medications are
listed.Acetylcholinesterase and anticholinergic medications are given in
recommended combinations according to similar onset time and duration ofaction
ofthe two types ofdrugs.The maximum dose ofcholinesterase is not always
necessary,but should be given based on thedegree ofrecovery from muscle
relaxation.The dose ofthe anticholinergic drug is determined by the amount
ofcholinesterase given.
100Part 1: Principles ofMedicine,Surgery,and Anesthesiaanticholinesterase that can
cross theblood-brain barrier.Antiemetic MedicationsPostoperative nausea and
vomiting(PONV) is one ofthe most commoncomplaints following surgery.Certaingroups
ofpatients (female,obese,previ-ous history ofnausea and vomiting)appear to be more
susceptible.Certainsurgeries (ear,ocular,tonsillar,gyneco-logic) are likewise
associated withincreased PONV.Nausea and vomitingafter oral surgery is not
uncommon.Swallowed blood and secretions stimu-late the gag reflex and are potent
gastricirritants.Drugs used during sedation andanesthesia,such as N2O,opioids,and
ket-amine,may trigger nausea postoperative-ly.Other �nonchemical�triggers ofnau-sea
include smell,gastric distention,motion,and even stress.Chemical triggers in the
bloodstreamcome into contact with an area in themedulla lacking an intact blood-
brain bar-rier called the chemoreceptor trigger zone(CTZ).18The CTZ (Figure 5-11)
containsreceptors for serotonin,histamine,mus-carinic ACh,and dopamine.Opioids,tox-
ins,and chemotherapy agents,as well asinput from the middle ear,also stimulatethis
area.Stimulation ofthe CTZ will acti-vate vomiting.Many antiemetic medications act
byblocking these receptors at the CTZ.Med-ications that block the dopamine
receptorinclude phenothiazines (eg,prochlorper-azine),and butyrophenones
(eg,droperi-dol).They effectively reduce PONV butare associated with adverse
effects such assedation and extrapyramidal reactions.5-HT3antagonists including
ondansetronand dolasetron are expensive,but produceless sedation and other adverse
effects thanthe dopamine antagonists.Antihistaminessuch as promethazine (which also
possess-es a phenothiazine structure) and diphen-hydramine can cause significant
sedation.Anticholinergic medications (eg,scopo-lamine) are rarely used for
PONV,although the antihistamines promethazineand diphenhydramine also possess anti-
cholinergic effects.Recently,dexamethasone has beenshown to decrease the incidence
ofPONVwhen given shortly after induction ofgen-eral anesthesia.A minimum adult dose
of8 mg IV appears to be required for thiseffect to be realized.19Selection
ofanesthetic agents mayhelp prevent PONV.Propofol appears tohave antiemetic effects
as well,particu-larly when administered for maintenanceofanesthesia.Additional
antiemetictreatment may be unnecessary followingthe use ofpropofol infusions,even
inpatients with a previous history ofPONV.Avoidance ofknown nausea trig-gering
agents such as N2O,ketamine,andlonger-acting opioid medications mayalso reduce
PONV.Table 5-4Varied Effects ofAnticholinergic MedicationsAnticholinergic
Medication
CharacteristicsTachycardiaBronchodilationSedationAntisialagogueAtropine????????
Glycopyrrolate????0???Scopolamine?????????= mild effect;??= moderate effect;???=
strong effect.OndansetronPromethazineAtropineDroperidol5-HT3HistamineMuscarinic
AChDopamine (D2)Nitrogen mustardCisplatinDigoxin glycosideOpioid,
analgesicsVestibular portionof nerve VIII MediastinumVagusGastrointestinal tract
distentionHigher centers (vision,
taste)PharynxReceptorsiteAreapostremaParvicellularreticularformationAntagonistAgoni
stChemoreceptortriggerzone(CTZ)EmeticcenterN2O?FIGURE5-11Diagrammatic
representation ofthe chemoreceptor trigger zone (CTZ).Adapted fromWatcha MF and
White PF.18 5-HT3= 5-hydroxytryptamine (serotonin); N2O = nitrous oxide.
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CHAPTER 6Pediatric SedationJeffrey D.Bennett,DMDJeffrey B.Dembo,DDS,MSKevin
J.Butterfield,DDS,MDThe anesthetic management ofthe pedi-atric patient presents the
oral and max-illofacial surgeon with unique and differ-ent challenges from those
with an adultpatient.The surgeon must be aware ofanatomic and physiologic
differences,different pharmacokinetics and pharma-codynamics ofmost
medications,andthe unique psychological development ofthe child and his or her
correspondingability to cope with the stress ofthe sur-gical experience.As the
child matures,changes in these parameters occur;there-fore,an understanding ofthe
growth andmaturation ofthe pediatric patient dic-tates the selection ofthe
anesthetic tech-nique and medications used in thepatient�s management.Anatomic and
Physiologic Considerations Respiratory SystemMuch ofthe uniqueness regarding anes-
thetic management ofchildren in oraland maxillofacial surgery is focused
onanesthesia delivered during intraoral pro-cedures in which the patient is not
intu-bated.Intraoral surgery in the anes-thetized nonintubated patient presents
aformidable and unique challenge.Theforemost concern is that the surgicalsite�the
oral cavity�is in close proxim-ity to the pharynx,thereby rendering thepatient
susceptible to airway obstructionand irritation.These factors can result ina
significant degree ofhypoxia.1,2Sucheffects can be exacerbated by a decreasedminute
ventilation and airway tone sec-ondary to sedative medication used dur-ing the
anesthetic administration.There are anatomic differencesunique to the pediatric
upper airway thatincrease the risk ofairway obstruction.Inthe young child the
tongue is large rela-tive to the size ofthe oral cavity.It is posi-tioned higher in
the oral cavity impingingon the soft palate secondary to the ros-trally positioned
larynx.Lymphoidhypertrophy with enlargement ofthetonsils and adenoids between the
ages of4 and 10 years can also contribute toupper airway obstruction.The lower
airway,consisting ofthetrachea,bronchi,and alveoli,also differsbetween pediatric
and adult patients.Thetrachea and bronchi are conduits in whichgas is transported
from the environmentto the alveoli.The pediatric airway diam-eter is relatively
smaller than that oftheadult.Since resistance is inversely propor-tional to the
radius ofthe lumen to thefourth power,there is an increased resis-tance.Narrowing
ofthe airway secondaryto secretions or edema will have a moreprofound adverse
effect on airwayexchange.The pediatric trachea is alsomore compliant.The increased
complian-cy makes the airway susceptible to col-lapse secondary to increased
negativeinspiratory pressure.This is significantbecause ofthe potential for
airwayobstruction in the nonintubated patient.When patients become obstructed
theyattempt to overcome the obstruction byincreasing the respiratory effort.In
thechild an attempt to compensate for upperairway obstruction with increasing
respi-ratory effort can cause collapse ofthe tra-chea and bronchial passages,which
mayparadoxically worsen the obstruction.Thefrightened child may already be at risk
forairway collapse since crying tends toincrease negative inspiratory
pressure.Anatomic differences between pedi-atric and adult patients diminish the
effica-cy ofventilation.In the child each rib isangled more horizontally relative
to thevertebral column;adults�ribs have a caudalslant.3Additionally,the accessory
musclesare less developed in the child.This resultsin a less effective thoracic
expansion and agreater dependence on diaphragmaticbreathing.Upper airway
obstruction in theyoung child occurring with sedation canresult in a paradoxic
chest wall movement,characterized by an inward movement ofthe chest opposing the
expansile down-ward movement ofthe diaphragm.Greater
104Part 1: Principles ofMedicine,Surgery,and Anesthesiaenergy is required,which can
lead tofatigue and subsequent hypoxia.Exchange ofgas takes place within
thealveoli.Closing volume,which is the vol-ume ofthe lung at which dependent air-
ways begin to close,is greater in the pedi-atric patient.The increased closing
volumein the pediatric patient results in increaseddead space ventilation.Thus,more
energymust be expended to adequately ventilatethe alveoli.The alveoli are also both
small-er and fewer in number in the pediatricpatient than in the adult.The
alveoliincrease in number until around 8 years oflife and continue to increase in
size untilfull adult growth is reached.The numberofalveoli may increase more than
10-foldfrom infancy to adulthood,with a resul-tant increase in surface area that
can be asgreat as 60-fold.4�6Functional residual capacity (FRC) isthe volume ofgas
in the lung after a nor-mal expiration and is related to the sur-face area ofthe
lung.The pediatricpatient has a diminished FRC expressedon a basis ofweight.7This
is illustrated bya minute ventilation to FRC ratio ofapproximately 5:1 in a 3 year
old and 8:1in a 5 year old compared to approximate-ly 2:1 in an adult.7FRC
decreases furtherin the sedated patient.The FRC providesa pulmonary oxygen
reserve.8Becausechildren have a higher metabolic demandand greater oxygen
consumption,thedecreased FRC results in a more rapiddesaturation ofhemoglobin
during peri-ods ofrespiratory depression.9�11Onemodel comparing the child to the
adultconcluded that an apneic period of41seconds in the pediatric patient
wouldresult in an arterial oxyhemoglobin satu-ration of85%,compared with an
apneicperiod of84 seconds in the adult.12Endotracheal IntubationThere are
alsoanatomic differences between the pedi-atric and adult airways that influence
intu-bation.A large tongue,rostral larynx,andlong and narrow epiglottis make laryn-
goscopy and visualization ofthe glotticopening more difficult in the
pediatricpatient.Adenoidal hypertrophy can alsoresult in hemorrhage or obstruction
ofanendotracheal tube,particularly duringnasal intubation.The narrowest part ofthe
trachea inthe pediatric patient is the cricoid carti-lage,in contrast with the
glottis in theadult.It is not until the age ofapproxi-mately 10 to 12 years that
the pediatricairway matures to that ofthe adult.Inthe pediatric patient care must
be takenwhen placing and securing an endotra-cheal tube to prevent impingement
ofthetip ofthe tube on the narrow subglotticregion.Such impingement ofthe endo-
tracheal tube on the tracheal mucosa canresult in edema and tracheal
narrowingcausing increased airway resistance postextubation.Uncuffed tubes are used
bymost anesthesiologists for patients lessthan 8 to 10 years ofage.13The argu-ments
against cuffed tubes are that theyincrease the risk ofairway mucosalinjury and that
an appropriately sizeduncuffed endotracheal tube can providean adequate seal at the
level ofthe cricoidcartilage.Formulas exist for calculatingthe appropriate size
ofendotracheal tube([age (yr) +16]/4) and the appropriatelength ofendotracheal
insertion ([age(yr)/2 + 12]).14However,28% ofthetime the initially selected
uncuffed endo-tracheal tube does not provide an ade-quate seal,and re-intubation
may be nec-essary.15An additional benefit in usingthe uncuffed tube is that a
larger tubemay be inserted,which causes less airwayresistance and less breathing
work.Theargument for a cuffed endotracheal tubeis that the fit can be adjusted and
it canprotect against aspiration.Ensuring thatthe cuffpressure does not exceed 25
cmH2O,which is believed to be the mucosalcapillary pressure,can minimize injuryto
the mucosa.When using an uncuffedtube,an air leak of25 cm H2O should be allowed.The
trachea is also shorter in the pedi-atric patient.It is not uncommon thathead
position is frequently changed dur-ing an oral and maxillofacial surgery pro-
cedure;this can cause the tube to becomedisplaced out ofthe trachea or pass
furtherinto the trachea and impinge on themucosa overlying the cricoid
cartilage.Change in head position,use ofan endo-tracheal tube that is too large,and
patientage between 1 and 4 years are three factorscontributing to the reported 1%
incidenceofpostintubation croup.16Certain congenital anomalies are wellrecognized
for their altered anatomy.Someofthe most commonly encountered disor-ders are
Crouzon syndrome (hypoplasticmaxilla�obligate mouth breather),Gold-enhar�s syndrome
(micrognathia,vertebralanomalies),hemifacial microsomia (hypo-plasia ofmandibular
condyle and ramus),M�bius sequence (micrognathia and limit-ed mandibular
movement),Pierre Robin�sanomalad (micrognathia,glossoptosis),and Treacher Collins
syndrome (mandibu-lar hypoplasia).These craniofacial anom-alies may complicate
ventilation and/orendotracheal intubation.For example,maxillary or mandibular
hypoplasia mayincrease the difficulty in achieving a satis-factory mask
fit.Anatomic differences inthe nasal cavity may impair nasal ventila-tion.This can
potentiate respiratoryobstruction during an intraoral procedurein which a
pharyngeal curtain is placed andthe patient is dependent on nasal respira-tion.The
tongue may be displaced posteri-orly by either maxillary or
mandibularhypoplasia,increasing the potential forobstruction.Cardiovascular
SystemThe pediatric cardiovascular system hassome significant differences
comparedwith that ofthe adult.Each relevant phys-iologic difference is outlined
below.Cardiac OutputPerfusion is dependenton cardiac output and peripheral resis-
Pediatric Sedation105tance.Cardiac output is dependent onheart rate and stroke
volume.The pedi-atric heart has less compliance than that ofthe adult,with minimal
ability to alterstroke volume.Thus,pediatric cardiacoutput is largely dependent on
heart rate(Table 6-1).Neural InnervationThe myocardium isinnervated by both the
sympathetic andparasympathetic nervous systems,with theparasympathetic nervous
system having agreater influence in the pediatric patientthan in the adult.In one
retrospectivestudy the incidence ofbradycardia duringanesthesia was reported to be
age related.The incidence ofbradycardia was approxi-mately threefold less in the 3-
to 4-year-oldcompared with the 2- to 3-year-old.17Blood PressureBlood pressure is
theproduct ofcardiac output and peripheralvascular resistance.The pediatric
patienthas less ability to alter peripheral vascularresistance;therefore,blood
pressure is large-ly dependent on cardiac output.A brady-cardia with resultant
decreased cardiac out-put thus results in a decrease in bloodpressure since the
child cannot compensateby increasing peripheral vascular resistance.SummaryThese
fundamental concepts clearly illus-trate the increased potential risks associat-ed
with sedating the pediatric patient:�The airway is more susceptible
toobstruction,and the patient has lessventilatory reserve;these result in amore
rapid oxygen desaturation (andhypoxia causes bradycardia).�The pediatric patient
has increasedparasympathetic innervation,result-ing in a more rapid onset
ofbradycar-dia (which may be influenced indi-rectly by respiratory impairment
ordirectly by the sedative drugs).�There is less cardiovascular compen-satory
ability,which results in hemo-dynamic instability.Preoperative Evaluation
ofthePatientThe purpose ofa preoperative evaluationis to compile information about
thepatient to establish the most optimal treat-ment plan.One needs to assess the
psy-chological and behavioral development ofthe patient,obtain a medical history
thatidentifies both acute and chronic diseaseprocesses,and determine the
patient�spreparation for surgery (eg,cardiovascularstatus),while performing an
appropriatephysical examination dictated largely bythe patient�s medical
history.Psychological AssessmentThe perioperative period can be verystressful for a
child.The child is confront-ed with an unfamiliar environment,unfa-miliar
people,apprehension about theunknown,and loss ofcontrol.The childfears separation
from the parents,thethreat ofneedles,the perception ofimpending pain,and the fear
ofmutila-tion.Younger children frequently cannotverbalize these concerns.Behavioral
mani-festations ofperioperative anxiety mayinclude hyperventilation,trembling,cry-
ing,agitation,and/or physical resistance.Children < 6 years ofage frequently
cannotcomprehend the need for or benefits ofthesurgical procedure.Children > 6
years oldor those who have better-developed socialskills (eg,acquired from daycare
programs)may be more capable ofunderstanding thesituation and expressing their
concerns.18Ifpossible,an older child should beallowed to participate in determining
theanesthetic treatment and should beexposed to the various induction tech-
niques:intravenous,intramuscular,oral,and inhalation.Adolescents may be more
capable ofcomprehending the planned surgery andanesthetic
management.However,theyare not adults.They have the ability todemonstrate myriad
behaviors and rapidmood changes.A paradoxic reaction tosedation in which the
adolescent appearsto become agitated after the administra-tion ofanxiolytic
medication may neces-sitate a deeper level ofanesthesia thanwhat may have
originally been planned.Another concern in the adolescentpatient is the use
ofillicit substances.Thishas reached epidemic proportions withan estimated 10.8%
of12- to 17-year-oldyouths reported to be current illicit drugusers in 2001.19The
presence ofparents during theadministration ofthe sedative agent mayreduce the
stress ofthe procedure andimprove the child�s cooperation.Con-versely,a parent�s
anxiety may be sensedby the child,further exacerbating thechild�s own level
ofanxiety.20Clear,sim-ple,and succinct explanations appropriatefor the age ofthe
child may minimizeadverse behavior.Preoperative FastingThe risk ofpulmonary
aspiration ofgas-tric contents in the pediatric patient dur-ing anesthesia is
reported to be up to 10 incidents per 10,000 cases.21�23Mor-bidity secondary to
aspiration includesobstruction from particulate material aswell as aspiration
pneumonitis that isdependent on both the quantity andTable 6-1Means and Ranges
ofNormal Cardiovascular Function Age (yr)Function2�67�1314�18Heart rate
(beats/min)100 (80�120)90 (70�110)80 (55�95)Systemic arterial pressure (mm
Hg)75�115/50�7595�125/60�80105�140/65�85Cardiac output
(mL/kg/min)150�170100�14090�115
106Part 1: Principles ofMedicine,Surgery,and Anesthesiaacidity ofthe
aspirate.Establishing para-meters that minimize the risk ofparticu-late gastric
contents as well as decreasethe quantity and acidity ofresidual gas-tric fluids can
decrease the incidence ofthis morbidity.Gastric emptying ofsolids is variable.A 6-
to 8-hour fast from solids is recom-mended to allow gastric emptying andminimize
the risk ofparticulate aspira-tion.Alternatively,gastric emptying timefor clear
liquids is approximately 10 to 15 minutes.After a 1-hour fast
ofclearliquids,approximately 80% ofthe con-sumed liquid is usually absorbed fromthe
stomach.Numerous studies haveshown that consumption ofunlimitedvolumes ofclear
liquids by pediatricpatients up to 2 hours prior to surgerydoes not significantly
increase the quanti-ty ofgastric volume or gastric acidity.24�28Guidelines have
thus been established forhealthy pediatric patients that allowunlimited amounts
ofclear liquids to beconsumed up to 2 to 3 hours prior tosurgery.This
recommendation avoids theneed for an extended fast,which has thepotential to make
the patient irritableand uncomfortable and to increase theincidence ofhypotension
secondary todehydration.However,in most cases itstill may be simplest to state that
the childshould have nothing by mouth (NPO)after midnight and to schedule the
proce-dure as the first case in the morning.Children who are scheduled in the
after-noon may have a light breakfast at least 6 hours prior to the
surgery.Emergency Treatment: Full Stomach Patients may present to the office
oremergency room requiring urgent care.The injury or the patient�s ability
tocooperate may be such that the necessarytreatment cannot be completed on
thepatient while he or she is awake and non-medicated,despite the fact that
thepatient is not NPO.The durationbetween the last food ingestion and theinjury is
the critical time period that isimportant in assessing a patient�s risk ofgastric
aspiration.Each patient and situa-tion must be assessed individually.Ifsedation or
general anesthesia is required,patient management may necessitate theplacement ofan
endotracheal tube tominimize the risk ofgastric aspiration.The following
interventions may min-imize the risk ofaspiration and/or theensuing injury that may
result from gastricaspiration:an H2-antagonist such as cime-tidine to decrease
gastric acidity,a clearantacid such as sodium citrate to decreasegastric
acidity,and metoclopramide topromote gastric emptying and increase thetone ofthe
lower esophageal sphincter.Glycopyrrolate also reduces the acidityand volume
ofgastric contents.29Atropine,alternatively,decreases the toneofthe lower
esophageal sphincter and pre-disposes to gastroesophageal reflux ofstomach
contents.Upper Respiratory InfectionIt is not uncommon for children to presentfor
surgery with a runny nose.Reports ofchildren presenting to surgery with or hav-ing
recently had such symptoms state inci-dences as high as 22.3% and 45.8%,respec-
tively.30Rhinitis is not a contraindicationto general anesthesia.Alternatively,a
childwith a severe upper respiratory infection(URI;symptoms include a
productivecough,fever,and mucopurulent discharge)should not be
anesthetized.However,it isunclear whether a child with a mild URI ora child
recovering from a URI should beanesthetized;therefore,it is important
todifferentiate between the diagnosis ofrhinitis and an infective
process.Pathophysiologic changes in the pul-monary system secondary to a URIinclude
increased nasal and lower airwaysecretions,increased airway edema
andinflammation,and increased airwaytachykinins.These pathophysiologicchanges can
result in laryngospasm,bron-chospasm,severe coughing,airway hyper-activity,breath
holding,diminished diffu-sion capacity,increased closing volumes,atelectasis,and
postintubation croup.31�34The elevated hyperactivity with
associatedbronchoconstriction and the increasedclosing volume compounded by a
greateroxygen uptake (secondary to the inflam-matory response ofthe infection) and
adecreased FRC (which normally occurswith general anesthesia) increases the
riskofhypoxemia.35�42Oxygen desaturationcan occur both intraoperatively and post-
operatively;the latter indicates the needfor continued postoperative
monitoring.URIs have also been demonstrated tocause respiratory muscle weakness
thatcan persist for up to 12 days.43The patho-physiologic changes that contribute
tothese adverse respiratory events can persistfor 4 to 6 weeks after the
URI.Traditional office-based ambulatoryanesthesia in oral and maxillofacialsurgery
is dependent on spontaneous ven-tilation in the nonintubated patient.Thisis
significant since the incidence ofadverserespiratory events is less in a patient
anes-thetized with a face mask or laryngealmask airway than in those with an endo-
tracheal tube.However,surgery involvingthe airway has been shown to increase
therisk ofadverse respiratory events.Although intraoral surgery is not truly air-
way surgery,it encroaches on the airwayand can cause airway irritability.The non-
intubated patient undergoing oral ormaxillofacial surgery is also susceptible
toperiods ofhypoventilation and apnea,which cannot be corrected without inter-
rupting the surgery.Kinouchi and col-leagues demonstrated that a patient withan
active or recent URI requires approxi-mately 30% less apneic time to desaturatethan
does a healthy patient.44In conclusion,the patient who pre-sents for elective
surgery with allergicrhinitis or a mild URI that is not ofacuteonset may be
anesthetized in the officewithout an endotracheal tube.Ifthe
Pediatric Sedation107patient has a significant URI,the proce-dure should be
rescheduled.Traditionalguidelines suggest that the procedureshould be rescheduled
for 4 to 6 weekslater ifthe patient is to be intubated,butbecause many children
have several URIsper year,trying to reschedule the surgeryfor a date when the child
is without symp-toms may be difficult.45Considering theabove,a delay of2 weeks is
probablyacceptable before performing a shortoffice-based minor dentoalveolar proce-
dure in which the patient is not intubated.Cardiovascular EvaluationThe child who
presents for surgery with apreviously undiagnosed cardiac murmurposes a diagnostic
challenge.Innocentmurmurs are heard in up to 50% ofnor-mal pediatric patients at
some point dur-ing childhood.The cause ofthese mur-murs is usually turbulent blood
flowthrough any ofthe great vessels.Featuresthat commonly identify innocent mur-
murs include those that are crescendo-decrescendo and ofshort duration andlow
intensity,and those that occur earlyin systole.All diastolic murmurs
arepathologic.The patient�s history may alsosuggest signs and symptoms
ofcardiacpathology.These may include limitedexercise tolerance,pale
color,frequentrespiratory problems,hypoxemia,palpi-tations,or dysrhythmias.A murmur
in anasymptomatic child is frequently notpathologic,and no special
anestheticconsiderations are required.However,ifthere is uncertainty regarding the
signifi-cance ofa murmur,a consultation with acardiologist is
recommended.Forpatients with congenital heart disease,prophylaxis against bacterial
endocarditisis necessary.Pregnancy Testing in the Adolescent PatientThe incidence
ofpregnancy detected byroutine universal testing in the ambulatorysurgical
adolescent between 12 and 21 yearsofage has been reported to be approxi-mately
0.5%.46Because ofthe severity ofthe potential consequences ofanesthetizinga
pregnant patient,it is important to reli-ably detect a pregnancy.An accurate
andreliable history in the educated patient canbe effective.47However,many patients
inthis age group may not provide an accuratehistory,especially in the presence
oftheirfamily.This is not an acceptable rationalefor routine testing.Ifroutine
testing isimplemented,there is the potential for afalse-positive test result,which
may havesignificant emotional consequences.Theissue remains controversial.Sedative
TechniquesIt is generally agreed that managing theanxious,uncomfortable,and
uncoopera-tive pediatric patient is one ofthe moredifficult anesthetic tasks.The
primarygoals in the management ofthe pediatricpatient include reducing
anxiety,establish-ing cooperation,ensuring comfort,estab-lishing amnesia and
analgesia,and ensur-ing hemodynamic stability.Although thegoals ofsedation are
similar for both thechild and the adult,reducing anxiety in theadult may enhance
cooperation,whereas inthe child it may not.To achieve a satisfac-tory result and
facilitate completion oftheplanned surgical procedure,the child mayrequire a
greater depth ofsedation.Sedation should be accomplished inas nonthreatening a
manner as possible.Because some children may be intenselyafraid
ofneedles,establishing intra-venous access may not be possible.Thesurgeon must be
familiar with alternativetechniques that allow for a safe satisfacto-ry induction
and recovery from anesthe-sia.Each case must be considered indi-vidually to select
both the mostappropriate drug and the route ofadmin-istration.The surgeon must take
intoconsideration the following factors indeveloping the anesthetic plan:(1) theage
ofthe patient,(2) the level ofanxietyand ability to cooperate withmedical/dental
staff,(3) the medical his-tory ofthe patient,(4) the patient�s priorsurgical or
anesthetic experience,(5) theinfringement ofthe procedure on the air-way,and (6)
the duration ofprocedure.The selected technique should ideally bepainless,be
accepted by the patient andparents,be rapid in onset,be appropriatein duration with
rapid recovery,and haveminimal side effects and a broad marginofsafety.Ifdrug
administration is associ-ated with pain or adverse memories,thebenefit ofthe
sedation may be decreased.The anesthetic must also provide an envi-ronment in which
the procedure can becompleted.In certain clinical situations amoderate degree
ofmovement may beacceptable,whereas in other situations nomovement is
acceptable.Also,the induc-tion agent may establish a depth such thatthe treatment
may be completed,but inother cases the goal ofthe inductionagent may be to
establish sufficient seda-tion to allow intravenous access andmaintenance
ofanesthesia with intra-venous agents.Lastly,and ofextremeimportance,one is
cautioned not tosedate a young child who will be trans-ported in a car seat prior
to arrival in theoffice.The respiratory depressant effectofthe medication combined
with thepositioning ofthe unattended child in thecar can result in unrecognized
upper air-way obstruction or respiratory impair-ment,with resultant death or
significantneurologic impairment.48Routes ofAdministrationSedative medication may
be administeredby many routes,including
oral,intranasal,transmucosal,rectal,intramuscular,inhalational,and
intravenous.49Theadvantage ofthe intravenous route is thatit results in the most
rapid onset,rapid off-set,and predictable effect.The disadvan-tage is that it
entails establishing intra-venous access.A percentage ofchildren donot cooperate
and allow an intravenouscatheter to be inserted.Many children
108Part 1: Principles ofMedicine,Surgery,and Anesthesiareport the needle puncture
from eitherintravenous placement or intramuscularinjection as the worst part
oftheir care.Even with a cooperative or an anes-thetized child,gaining peripheral
intra-venous access can present a challenge.Proper knowledge ofvenous anatomywith a
controlled organized approachgives the best chance for success.Com-monly accepted
sites for venous cannula-tion include the dorsum ofthe hand,volaraspect ofthe
wrist,antecubital fossa,andgreater saphenous vein.Even when analternative route
(eg,inhalation or intra-muscular) is used to induce the anesthetic,we recommend the
establishment ofintra-venous access.This can be achieved oncethe child is
sedated.Even ifthe procedurecan be accomplished without the adminis-tration ofan
intravenous agent,an estab-lished intravenous line can be used toadminister
intravenous agents ifneeded toaugment the initial anesthetic agent or toprolong the
duration ofthe anesthesia.The line can additionally be used toadminister other
medications required tomanage adverse events.In an emergent situation,ifthe tradi-
tional peripheral cannulation technique isnot successful,the clinician has two
possi-ble access sites that allow for a high degreeofpredictability.These sites are
thefemoral vein and intraosseous access,which are associated with a higher inci-
dence ofmorbidity.The femoral vein usu-ally requires a 20-gauge or 22-
gaugeangiocatheter.The intraosseous needle isrecommended primarily for children < 6
years ofage because they still have redbone marrow (Figure 6-1).In this tech-nique
a bone marrow needle or a no.14through 18 Cook intraosseous infusionneedle is
percutaneously inserted into theflat portion ofthe proximal tibia.Entry ismade in
the tibial plateau 1.5 cm below theknee joint and 2 cm medial to the
tibialtuberosity.The special bone marrow-stiletted needle is inserted with a
rotarymotion into the bone until the cavity isreached.The depth ofthe needle
insertionshould be planned.Ifit is advanced toofar,the needle penetrates the
posteriorcortex and does not allow infusion.Theneedle should be firmly set in the
bone.Often bone marrow may be aspirated toconfirm the placement.A syringe or intra-
venous line can be attached;ifit runs eas-ily,placement is confirmed.Slight
extrava-sation around the placement site shouldnot prevent the use ofthe
needle.Thecatheter can serve as a conduit for allintravenous fluids and drugs.The
inhalational induction ofanesthe-sia with a potent anesthetic agent also pro-vides
rapid onset,rapid offset,and a pre-dictable effect.The advantage
ofthistechnique,similar to the intravenous route,is the option to use short-acting
agentsenabling the anesthetic state to be rapidlyterminated at the end ofthe
procedure.The traditional inhalation induction isaccomplished by administering
oxygen ora mixture ofoxygen (minimum concentra-tion of30%) and nitrous oxide using
a fullface mask.Induction can be achieved usingone oftwo techniques.The potent
vaporagent can be increased gradually every fewbreaths until the induction is
complete.Alternatively,the patient may be immedi-ately administered a high
concentration ofthe potent inhalational agent.A modifica-tion ofthe latter
technique is to ask thepatient to exhale completely and then takea deep inspiration
ofthe vapor agent andhold his or her breath.Induction will beachieved with a single
breath,and sponta-neous ventilation will resume once a stateofgeneral anesthesia is
achieved.For briefprocedures (eg,extraction ofa deciduoustooth),once general
anesthesia is achieved,the face mask can be removed,the proce-dure performed,the
face mask reapplied,and the patient allowed to awaken breath-ing 100% oxygen.Some
clinicians advocatemaintaining the general anesthesia by con-Tibial
tuberosityFIGURE6-1For intraosseous infusions a bone marrow needle or specially
made intraosseous needle isinserted into the tibial plateau (just medial and down
from the tibial tuberosity).The catheter is thensecured and intravenous solutions
and medications may be administered.Adapted from American HeartAssociation.Textbook
ofpediatric advanced life support.Dallas: American Heart Association; 1994.
Pediatric Sedation109tinuing the administration ofthe potentvapor agent via a
traditional nasal hood.This can result in the delivery ofa dilutedconcentration
ofanesthetic agent to thealveoli,resulting in a lightening ofthepatient�s
anesthetic depth.Such an occur-rence would necessitate the interruption ofthe
procedure to replace the full face maskto increase the alveolar concentration ofthe
inhalational agent.Although the con-tinued administration ofthe vapor agentvia a
nasal hood is not contraindicated,itmay result in excessive environmental pol-
lution,even with a scavenger device that isa component ofthe nasal hood.A
circuitthat scavenges the vapor agent must also beused with the face mask.To avoid
thesepotential problems,especially for longerprocedures,the establishment ofintra-
venous access is recommended.Thevasodilatory effects ofthe potent agentmay optimize
conditions for establishingintravenous access.Once access is set,anes-thetic depth
can be maintained with intra-venous anesthetic agents.There are a few disadvantages
toinhalation induction.The vapor agent has ascent that may be objectionable to
some.Applying a scent (eg,scented lip gloss)selected by the child to the face mask
mayalter the odor ofthe agent.The odor mayalso be minimized ifthe child
breathesthrough the nose as opposed to themouth.18In addition,inhalation
inductionis also dependent on the child accepting theface mask.Techniques such as
asking thechild to inflate a balloon may be employedto distract the child.Any need
for mildrestraint should be explained to the parentand may be used to facilitate
induction inthe younger child.However,in older chil-dren or extremely uncooperative
children,the technique is dependent on the child�sacceptance ofthe face
mask.Ifexcessivephysical restraint is necessary,an alternativetechnique should be
considered.The intramuscular route ofadminis-tration approximates the rapidity and
pre-dictability ofonset ofintravenous admin-istration.Its primary disadvantage is
thediscomfort associated with the injection.However,for the uncooperative
child,itmay be the least traumatic method ofinducing anesthesia.Four
anatomicregions are used for intramuscular admin-istration ofdrugs:the deltoid
muscle,thevastus lateralis muscle,the ventroglutealarea,and the superior lateral
aspect ofthegluteus maximus muscle.These sites havebeen identified because they
have minimalnumbers ofnerves and large blood vessels,as well as adequate bulk to
accommodatethe volume ofthe injected medication.The rapidity ofonset ofthe drug is
depen-dent upon the perfusion ofthe muscle.Absorption and onset are also affected
bythe ionization ofthe drug and the vehiclein which it is dissolved.Oral
administration is considered bymany to be the least-threatening
inductiontechnique.Children are generally familiarwith and readily accept oral
medications.Oral administration also is generally wellaccepted by the mentally
impaired or autis-tic patient.However,oral techniques havelimitations.In one study
ofchildrenbetween the age of20 and 48 months,one-third ofthe children required that
the med-ication be administered into the back oftheir throat with a needle-free
syringe.50Although frequently used as a sole sedativeagent by many surgeons,an oral
sedativeagent can be used as a premedicant prior toestablishing intravenous access
or inducinggeneral anesthesia by a different route (eg,inhalation or
intramuscular).The limitedvolume offluid administered with the oralmedication is
not associated with anincreased risk for aspiration pneumonitis.51The primary
disadvantages oforalsedation are the slow onset,variableresponse,and prolonged
recovery.Inject-ing a sedative agent into the back ofthethroat with a needle-free
syringe (whenthe child does not otherwise accept themedication) has also been
associated withadverse consequences.It has been theo-rized that the drug intended
for orogastricadministration can be inadvertently aspi-rated by the crying
child.Bronchialabsorption can result in an excessive plas-ma level ofdrug.The
intranasal route was initially pro-posed for pediatric sedation because it wasfelt
to avoid first-pass degradation,berapid in onset,and be less traumatic thanthe
other routes that possessed these samebenefits.52Medications
administeredintranasally do result in a rapid rise in theplasma level ofa drug.This
occurs becausethe nasal cavity,which functions to warmand cleanse nasal
respirations,has a rela-tively extensive surface area with a thinnasal mucosa and
an abundance ofcapil-laries that facilitate the absorption ofdrug.The nasal mucosa
also provides a directconnection to the central nervous system(CNS) through the
cribriform plate.Med-ication may be absorbed through the crib-riform plate directly
into the CNS throughthe capillary beds or the olfactory neu-rons,or directly into
the cerebrospinalfluid.53Rhinitis or a URI may impair theabsorption ofa drug via
this route.54The intranasal route,although initiallyfelt to be less traumatic than
alternativeroutes,is frequently not well accepted bychildren.55,56The volume
ofmedicationused frequently results in a portion passinginto the pharynx and being
swallowed.Therefore,the unpleasant taste ofthe med-ication is not avoided,and the
drug is sub-ject to first-pass hepatic degradation.Mida-zolam is the most commonly
intranasallyadministered medication,but the acidic pHis irritating to the nasal
mucosa.Transmucosal absorption has alsobeen considered.The oral epithelium isthin
with a rich vascular supply.The min-imum epidermal barrier and the vascularsupply
provide an environment that pro-motes relatively rapid absorption ofdrugs.Oral
transmucosal administration ofadrug also has the advantage ofavoidinghepatic first-
pass degradation.Transmu-cosal administration requires cooperationofthe patient to
keep the drug in contact
110Part 1: Principles ofMedicine,Surgery,and Anesthesiawith the oral mucosa.The
medication maybe administered as a solution placed sub-lingually or as a lozenge.At
the presenttime the only available lozenge that has anacceptable flavor and is
commerciallyavailable is fentanyl citrate.Other sedativemedications are
bitter.Palatability can beimproved by mixing these medicationswith a flavored
solution that increasestheir volume;thus,the solution will be bit-ter or the volume
will be excessive,neitherofwhich is advantageous for the transmu-cosal
administration ofa liquid/solution.Many,ifnot most,pediatric patientsexpectorate
the medication or premature-ly swallow the liquid medication that isplaced within
the oral cavity as opposed tokeeping it there.Rectal drug administration has
beenused for the administration ofantiemet-ics,antipyretics,and analgesics to
bothadults and pediatric patients.Many seda-tive drugs that are usually
administeredIV,IM,or orally can be administered rec-tally.Rectal administration may
also beused in the management ofemergencies.For example,rectal administration
ofdiazepam is an acceptable route for thetreatment ofseizures.57,58The rectum is a
flat organ that is usu-ally empty.Its blood supply is derivedfrom the inferior
rectal arteries and isdrained via the superior,middle,and infe-rior rectal
veins.The superior rectal veindrains into the hepatic portal circulationvia the
inferior mesenteric vein.The mid-dle and inferior rectal veins drain into
theinternal iliac vein.The internal iliac veindrains into the vena cava,thus
bypassingthe hepatic-portal circulation and avoid-ing first-pass metabolism by the
liver.The absorption ofa drug that is admin-istered per rectum is affected by
several fac-tors.The variable absorption ofthe drugmay be partially influenced by
the venousdrainage ofthe rectum.Therefore,someindividuals feel that absorption and
subse-quent peak plasma level ofmedication isdependent on the location ofdeposition
ofdrug within the rectum.However,there aresignificant anastomoses between the
threerectal veins,and peak drug blood level hasnot clearly been shown to be
dependent onthe location ofagent deposition within therectum.Solutions are absorbed
more rapid-ly than are suppositories.A more dilutesolution with greater volume
provides morerapid onset and prolonged duration.59Stoolwithin the rectal vault as
well as expulsion ofan unmeasurable quantity ofdrug results indelayed or decreased
absorption.Alterationin the integrity ofthe mucosa or the pres-ence ofhemorrhoids
results in greaterabsorption.Ifa child is uncooperative,he orshe may tightly close
the anal sphincter dur-ing any aspect ofthe administrationprocess.Excessive force
both in placing orremoving the catheter may result in a lacer-ation ofthe mucosa
and cause a greaterabsorption ofdrug.Pharmacologic AgentsThe objective in selecting
a pharmacologicagent is to choose an agent that establishesan appropriate
environment to completethe surgical procedure.The effects soughtin the pediatric
patient include anxiolysis,amnesia,analgesia,immobilization,seda-tion,and
hypnosis.There are numerousagents that are currently used by oral andmaxillofacial
surgeons and other practi-tioners.In this section we discuss what wefeel to be the
most appropriate anestheticagents and the routes by which theyshould be
delivered.KetamineKetamine is a pharmacologicagent that induces a distinct
anestheticstate that resembles catalepsy.The patientappears awake but is
noncommunicative.Nonpurposeful movements may occur butare not disruptive.The eyes
are commonlyopen with a blank stare and intact cornealand light reflexes.60A
lateral nystagmus isalso very characteristic.Ketamine alsoproduces amnesia and
analgesia.The clinical effect created by ketamineresults from a dissociation
between thethalamoneocortical and limbic systems,which disrupts the brain from
interpretingvisual,auditory,and painful stimuli.61Theanalgesic effect,which occurs
at subanes-thesia plasma levels,is partially mediatedby ketamine binding to the �-
opioid andNMDA receptors.This is significantbecause the effect persists into the
postop-erative period and may decrease the needfor postoperative
analgesia.62Ketamine is also unique in its effectson the respiratory system.In
clinical dosescommonly used in oral and maxillofacialsurgery,ketamine usually
preserves upperairway musculature tone,spontaneous res-pirations,and FRC.This
minimizes theincidence ofupper airway obstruction andhypopneas/apneas,and maintains
the pul-monary oxygen reserve.63,64In contrast,most other anesthetics contribute to
adecrease in muscular tone,respirations,and FRC.In addition to maintaining
upperairway muscular tone,ketamine tends tobetter maintain the pharyngeal and
laryn-geal airway reflexes.This allows the patientto maintain the ability to
swallow andcough,which minimizes the risk ofpul-monary aspiration.Ketamine has also
beenshown to relax bronchial smooth muscleand cause bronchial dilatation.It has
beenused in the management ofwheezing dur-ing anesthesia.65Despite these benefits
the practitionermust respect the inherent dangers associ-ated with the anesthetic
management ofapatient.Respiratory depression character-ized by a decrease in
respiratory rate andtidal volume can occur with ketamine.Respiratory arrest has
been reported in a4-year-old child following the intra-muscular administration
ofketamine 4 mg/kg.66However,respiratory depres-sion is not common,and the
occurrence ofapnea is more likely to occur in infants orwith the rapid intravenous
infusion ofaninduction dose greater than 2 mg/kg.Slowintravenous infusion over 30
to 60 secondsofdoses between 0.5 mg/kg and 1 mg/kgshould minimize the incidence
ofsignifi-
Pediatric Sedation111cant respiratory depression.Aspiration ofgastric contents can
also occur despite thefact that ketamine better preserves theprotective airway
reflexes allowing apatient the ability to swallow andcough.67,68The protective
reflexes,although less impaired than with otherdrugs,are diminished.We feel that
apatient who is considered not to have anempty stomach should not be
sedated,anddisagree with those who feel that preserva-tion ofthe airway reflexes
justifies sedatingsuch patients.69The preservation ofthelaryngeal reflexes is a
protective mecha-nism;this may also contribute to airwaycomplications.Ketamine
produces anincrease in salivary and tracheobronchialsecretions,and the preservation
ofthelaryngeal reflexes may predispose thepatient to laryngospasm.Ketamine has both
direct and indirecteffects on the cardiovasculature.The directmyocardial depressant
effects are generallynot seen in the healthy patient anesthetizedin the office.The
indirect effects,which area result ofa sympathetic stimulation,pro-duce an increase
in heart rate and bloodpressure.The former may be more com-mon in the pediatric
patient.These effectsare well tolerated in the healthy pediatricpatient.These
hemodynamic changes maybe reduced when ketamine is combinedwith an anesthetic agent
that tends to bluntsympathetic stimulation (eg,benzodi-azepines,propofol).A
disadvantage ofketamine is its stimu-lation ofdreams and hallucinationsdescribed as
�out ofbody�experiences,sen-sations offloating,and delirium.70Althoughthe incidence
is less in children < 16 years ofage,the incidence may be as high
as10%.71,72Ketamine is also contraindicatedin patients who may have a globe
orintracranial injury as ketamine increasesboth intraocular and intracranial
pressure.Ketamine can be administered IV,IM,orally,intranasally,and rectally.We
discussonly the intravenous,intramuscular,andoral administrations ofketamine.The
advantage ofintramuscularadministration is that it does not requirepatient
cooperation.The mild distressassociated with the injection is briefas thedrug has a
rapid onset,within 3 to 5 min-utes.Dosing recommendations up to 10 mg/kg IM have
been described in vari-ous papers and texts.The larger dose clear-ly produces a
general anesthetic state.Foroffice-based or emergency-departmentprocedures
performed by oral and maxillo-facial surgeons,however,a dose of4 to 5 mg/kg IM
should provide effective disso-ciation.One investigation prospectivelyassessed
pediatric patients requiring seda-tion for minor procedures in an
emergencydepartment and found that a 4 mg/kg doseprovided effective sedation and
immobi-lization for 86.1% ofthe children.A satis-factory quality ofsedation was
achievedwith adjunctive local anesthesia for 97.2%ofthese patients,although 3.7%
requiredmild restraint despite adequate sedationand an absent withdrawal response
to pain.Only 2.8% ofthe patients required a repeatdose secondary to inadequate
sedation.73Local anesthesia is an important compo-nent ofany sedative technique
used by oraland maxillofacial surgeons.Although thisstudy demonstrated that it is
not alwaysrequired,incorporation oflocal anesthesiainto the anesthetic plan
minimizes theamount ofother anesthetic agentsrequired.The working time achieved
froma 4 mg/kg dose ofketamine was 15 to 30 minutes.A disadvantage ofintramuscu-lar
ketamine is that recovery is variable andcan be quite long.Although the
meanrecovery time in the above study was 82 minutes,recovery from injection to dis-
charge at times took up to 3 hours.Benzodiazepines can be administeredconcomitantly
with ketamine.The purposefor coadministering a benzodiazepine is toreduce the
amount ofketamine adminis-tered,reduce the incidence ofketamine-induced
hallucinations,attenuate the car-diovascular effects ofketamine,andprovide
additional amnesia.74Coadminis-tration ofa benzodiazepine with ketaminemay prolong
recovery.75Midazolam pro-duces a better reduction in unpleasantdreams than does
diazepam.76The favor-able pharmacokinetics ofmidazolam com-pared with diazepam also
provide a morerapid recovery.In a prospective investiga-tion,ketamine 3 mg/kg with
midazolam0.5 mg/kg was administered to pediatricpatients requiring sedation for
minor sur-gical procedures in the emergency depart-ment.77Although 30% ofthe
patients whoreceived this regimen manifested �inter-mittent crying,�only 14%
required addi-tional medication to establish a satisfactoryanesthetic state to
allow completion oftheplanned treatment.Recovery for this regi-men was at times
prolonged.The level ofsedation and immobiliza-tion is dependent on the planned
proce-dure.Although the intent is to provide anatraumatic experience for the
child,amildly dissociative sedative and analgesicstate compared with a deeper
dissociativeanesthetic state may be acceptable for abriefdentoalveolar
procedure.The intentis to modify the patient�s perception oftheprocedure.In this
situation the patient isnot profoundly sedated and the practi-tioner has to
tolerate some movement andpossibly some vocalization.Ketamine 2mg/kg to 3 mg/kg IM
should provide thisdesirable sedative depth.The lower dose of2 mg/kg is
advantageous in that recoveryfrom injection to discharge approximates60 minutes.For
many children the lowintramuscular dose ofketamine provides adepth ofsedation that
allows the place-ment ofan intravenous line.Ifnecessary,the depth ofsedation can
then be modi-fied using intravenous medications.Incre-mental doses ofketamine 5 to
10 mg IVcan be administered to the sedated patient,with onset occurring within 30
to 60 sec-onds.The duration ofsedation is 10 to 15 minutes.Although we have found
thatketamine 2 mg/kg generally facilitatesintravenous placement,one study report-ed
that 31% ofthe children resisted intra-
112Part 1: Principles ofMedicine,Surgery,and Anesthesiavenous placement with a dose
of3mg/kg.78For the patient who remainscombative and for whom intravenousaccess
cannot be established,an additionaldose ofketamine 1 to 2 mg/kg IM can
beadministered.Ifthe child allows placementofan intravenous catheter (without
anypremedicant),a dose ofketamine 0.5 to 1 mg/kg IV administered over 30 to 60 sec-
onds will establish dissociation.An anticholinergic agent (eg,glyco-pyrrolate or
atropine) is frequently coad-ministered with ketamine to
decreasehypersalivation.Tachycardia and postop-erative psychomimetic effects are
prob-lems associated with ketamine.Atropine,when combined with ketamine,producesa
significantly higher heart rate comparedwith the effect ofglycopyrrolate.As a ter-
tiary amine,atropine crosses the blood-brain barrier and
can,itself,producepostoperative delirium.A higher inci-dence ofadverse emergence
phenome-non,however,was not identified in stud-ies comparing glycopyrrolate
withatropine.79,80Both drugs can be mixed inthe same syringe with ketamine for
anintramuscular injection.The peak effectofintramuscular glycopyrrolate
occurswithin 30 minutes,at which time the pro-cedure is frequently completed and
thepatient is in the recovery phase oftreat-ment.Ifan intravenous line is to be
estab-lished after the onset ofsedation,glyco-pyrrolate can be administered IV with
apeak effect in approximately 1 minute.The dose ofatropine is 0.1 to 0.2 mg/kg,with
a minimum dose of0.1 mg and amaximum dose of0.6 mg.Glycopyrrolateis twice as potent
as atropine.The dose isthe same for both drugs,regardless oftheroute
ofadministration.Ketamine can also be administeredorally.81Bioavailability is
approximately17% following oral administration com-pared with 93% after
intramuscularadministration.82,83Onset ofsedationoccurs in approximately 20
minutes.Although doses reported have ranged from3 to 10 mg/kg,a more consistent
effect isachieved with doses > 6 mg/kg.In oneinvestigation oral ketamine 6 mg/kg
wasadministered for sedating anxious pediatricdental patients with a mean duration
ofsedation of36 minutes.84The quality ofsedation was reported as good for 65% ofthe
patients,and 100% ofthe treatment wascompleted.Mean recovery time was 56 minutes
with one child sleeping for 3 hours.Creating a state ofdeep sedation isdependent on
using larger doses ofmedica-tions.Ketamine 10 mg/kg PO was used as apremedicant in
the management ofpedi-atric patients undergoing invasive oncolog-ic
procedures.Approximately 50% ofthepatients were unresponsive at 60 minutes.This
dose was ineffective in < 10% ofthepatients.85Recovery,however,generallytook 2 to 4
hours,with 20% ofthe patientsbeing deeply sedated at 120 minutes
postadministration.Several authors have shownthat the anxiolytic and sedative
propertiesofmidazolam 0.5 mg/kg result in a moreclinically effective sedation than
does keta-mine 5 or 6 mg/kg.86,87The combination oforal midazolamand ketamine has
also been described.Thisdrug combination may provide effectivesedation when oral
midazolam has beenineffective.One study that demonstrated agreater efficacy with
this combination usedketamine 4 mg/kg with midazolam 0.4 mg/kg.88The reported
dosing regimenshave varied from ketamine 4 to 10 mg/kgwith midazolam 0.25 to 0.5
mg/kg.Situations may occur in the manage-ment ofa mentally
impaired,autistic,orolder child in whom an intravenous line oran intramuscular
injection cannot beadministered without harm to the patientor the healthcare
provider,and who willnot accept a face mask.Oral ketaminealone or combined with
oral midazolamcan be used to establish a cataleptic state,facilitating treatment
ofthe combativepatient.89,90It may be helpful to solicitassistance from the
patient�s caregiver orparent,as these individuals may be awareofstrategies to
ensure that the full oraldose is taken.Atropine or glycopyrrolatecan be orally
administered with ketamine;however,the time to peak decrease in sali-vation is 2
hours.91Regardless ofthe route ofadministra-tion,ketamine can establish a
clinicaleffect described as a �chemical straight-jacket.�The catatonic state
created by ket-amine is different from that with othergeneral anesthetic
agents;ketamine,whenused at the doses discussed above,may notbe considered to be a
true general anes-thetic.However,the anesthetic depth cre-ated by ketamine is not
consistent withconscious sedation,and airway problemscan
occur.Therefore,appropriate anes-thetic standards for deep sedation or gen-eral
anesthesia must be followed.MidazolamMidazolam is a water-solubleshort-acting
benzodiazepine.As a class ofagents,the benzodiazepines provide anxiol-
ysis,sedation,and amnesia.Midazolam canbe administered
IV,IM,orally,sublingually,intranasally,or rectally.Because ofits
watersolubility,intramuscular injection ofmida-zolam is pain free,and absorption is
pre-dictable.Unlike ketamine,however,as asingle agent there is no unique
anestheticbenefit to the intramuscular administrationofmidazolam.Intranasal
administration ofmidazo-lam was popular in the past.It was oncethe most common
intranasally adminis-tered medication.However,because ofanacidic pH,it produces
irritation to thenasal mucosa.The medication ifadminis-tered slowly is
discomforting and ifadministered rapidly passes through thenose into the nasal
pharynx and is swal-lowed.In a study that compared oral tointranasal administration
ofmidazolam,children were found to be less tolerant ofthe intranasal
administration.92Oral midazolam is probably the mostwidely used premedicant in
children.Therecommended dose ofmidazolam is 0.5 to1.0 mg/kg to a maximum of20
mg.Mida-
Pediatric Sedation113zolam 0.5 mg/kg achieves anxiolysis in 70to 80% ofpatients.The
anesthetic depthmay be potentiated by the administrationofnitrous oxide.The
combined adminis-tration of40% nitrous oxide with midazo-lam 0.5 mg/kg has produced
deep sedationin 12% ofpatients.93Unlike ketamine,midazolam causesloss ofairway
muscle tone.Although air-way obstruction is not common withdoses of0.5 to 1.0
mg/kg,airway obstruc-tion has been reported after 0.5 mg/kg oralmidazolam.94The
incidence ofairwayobstruction may increase with the admin-istration ofnitrous
oxide.In one study thecombined administration of50% nitrousoxide and 0.5 mg/kg oral
midazolamresulted in a 56% incidence ofupper air-way obstruction in children with
enlargedtonsils.95With maintenance ofairwaypatency,however,oral midazolam doses
of0.5 to 0.75 mg/kg generally do not result ina change in oxygen saturation,heart
rate,or blood pressure.96The onset ofeffect oforal midazolamis within 20
minutes,and the duration ofsedation is 20 to 40 minutes.Patients cangenerally be
discharged within 60 to 90 minutes from the time at which themedication is
administered.Midazolam is metabolized by thecytochrome oxidase system.Oral mida-
zolam is subject to hepatic first-passmetabolism.Erythromycin,clarithro-
mycin,protease inhibitors,azole antifun-gal medications,fluvoxamine maleate,and
grapefruit juice alter this cytochromeoxidase system and result in a higher anda
more sustained midazolam plasmalevel.97,98Higher doses oforal midazolam (0.75 to1.0
mg/kg)are associated with a greaterincidence ofside effects.These includeloss
ofhead control,blurred vision,and/or dysphoria.A paradoxic reactionmay also occur
in which the patientbecomes more excited as opposed tosedated.This is more common
in chil-dren and adolescents.99Induction AgentsMethohexital andpropofol are rapid-
onset short-actingagents that are effective for induction andmaintenance
ofanesthesia.These are theprimary anesthetic agents for generalanesthesia in oral
and maxillofacialsurgery performed in an office.The phar-macology ofthese agents is
discussed inChapter 5,�Pharmacology ofOutpatientAnesthesia Medications.�There are
someimportant points to make relative to theiruse in the pediatric
patient.Methohexital is an ultrashort-actingoxybarbiturate.It can be administered
rec-tally,IM,and IV.The advantage to the rec-tal administration ofmethohexital is
thatthe drug is administered in the presence ofthe parents,and,thus,the child is
asleepprior to parental separation.Rectal admin-istration,however,can be
distressing,asdiscussed above.Methohexital can also beadministered
intramuscularly.Administra-tion is quite painful,and there is no advan-tage to its
use in office-based anesthesiacompared with other available intramus-cular
agents.Neither rectal nor intramus-cular administration is generally employedin
ambulatory oral and maxillofacialsurgery offices.Most frequently methohex-ital is
administered IV.Interestingly,despite years ofsafe administration in
thisenvironment,the manufacturer�s packageinsert states that the use ofmethohexital
inthe pediatric patient is not adequatelystudied and thus not recommended.Propofol
is an alkylphenol.Its charac-teristics include rapid onset and shortduration
ofclinical effect,similar tomethohexital.Its high clearance rate andminimal
tendency for drug accumulationmake it a more ideal anesthetic agent forambulatory
surgery in both adult andpediatric patients.In one study comparingpropofol to
methohexital for anesthesia inpediatric patients undergoing proceduresin a dental
chair,propofol was associatedwith a 9% incidence ofventriculararrhythmias compared
with a 32% inci-dence associated with methohexital.100Clinical trials and case
series have demon-strated propofol�s efficacy in pediatricpatients.101�107The
proprietary formula-tion ofpropofol (Diprivan) is licensed bythe US Food and Drug
Administration(FDA) for use in children > 3 years ofagein the surgical
setting.Transient pain at the site ofinjection isreported in approximately 10 to
20% ofpatients given propofol.In the pediatricpatient this discomfort may result in
gra-dations ofmovement,which may requirerestraint ofthe patient until induction
isfully achieved.Propofol may also causehypotension and bradycardia.The inci-dence
is reported to be higher in the pedi-atric patient (17%) compared with that inthe
adult patient (3�10%).This usually isnot detected in the adult oral and maxillo-
facial surgery patient when a relatively lowinitial dose (< 1 mg/kg) is typically
used toachieve deep sedation or general anesthe-sia.Pediatric patients frequently
need tobe more profoundly anesthetized.Thisrequires the administration ofa
greaterdose ofpropofol,which may result in ahigher occurrence ofhypotension
orbradycardia in pediatric oral and maxillo-facial surgery patients.Propofol may
alsocause excitatory movement or myoclonus,the incidence ofwhich is greater in
thepediatric patient (17% vs 3�10%).The greatest potential concern withthe use
ofpropofol in the pediatricpatient is that cases offatal metabolic aci-dosis and
cardiac failure,termed propofol-infusionsyndrome,have been reported inover a dozen
children.108�112These inci-dents have all been associated with pro-longed
intubation and propofol infusions.A review by the FDA concluded thatpropofol had
not been shown to have adirect link to any pediatric deaths.113Although the causal
relationship betweenpropofol and metabolic acidosis remainsunproven,clinicians
should be aware ofthe risk for this reaction in children andlimit the dose and
duration ofpropofoltherapy accordingly.
114Part 1: Principles ofMedicine,Surgery,and AnesthesiaInhalational AgentsThe
origin ofanes-thesia is rooted within dentistry.The firstanesthetic was nitrous
oxide.Nitrous oxidehas anxiolytic,analgesic,amnestic,andsedative
effects.114,115Although not apotent anesthetic agent,nitrous oxide pos-sesses a
wide margin ofsafety and has few(ifany) residual side effects.Anotheradvantage
ofnitrous oxide is its low solu-bility.An anesthetic agent that has low sol-ubility
has rapid equilibration between thealveoli and the blood,and the blood andthe
brain.This results in both rapid onsetand anesthetic emergence.Also,nitrousoxide
may be combined with other anes-thetic agents.A deep sedative or generalanesthetic
state may be established with thecoadministration ofnitrous oxide and anoral or
parenteral agent.This may result inrespiratory impairment.Although nitrousoxide may
potentiate the effect ofanotheragent,the discontinuance ofit can,like-wise,reverse
the anesthetic depth and pro-mote a more rapid emergence.116�118Although nitrous
oxide lacks sufficientpotency to solely induce general anesthe-
sia,halothane,sevoflurane,desflurane,andisoflurane have sufficient potency toinduce
and maintain general anesthesia(Table 6-2).The primary benefit ofaninhalational
agent is for mask induction,and ofthe potent inhalational agents,onlyhalothane and
sevoflurane are nonpun-gent.These agents can be administered toan awake patient
with minimal respiratorycomplications (eg,coughing,breath hold-
ing,laryngospasm),whereas desfluraneand isoflurane tend to irritate the airway
ifused for mask induction.119�121The blood and tissue solubility ofaninhalational
agent is also important.Theseproperties influence the speed ofinduc-tion and
emergence from anesthesia.Agents that have a low solubility in bloodhave a more
rapid induction and shorteremergence time.The blood gas solubilitycoefficients
ofdesflurane,nitrous oxide,sevoflurane,isoflurane,and halothane
are0.42,0.47,0.6,1.4,and 2.3,respectively.These figures imply a more rapid onsetand
emergence for desflurane,sevoflu-rane,and nitrous oxide.Since all anesthetic agents
affect thepulmonary and cardiovascular systems,itis important to understand these
effects.All potent inhalational agents depressminute ventilation in a dose-
dependentmanner,with a resulting increase in partialpressure ofcarbon dioxide in
arterialblood (PaCO2).Clinically the practitionerwill observe a decrease in tidal
volume anda slight increase in respiratory rate.Although acceptable respiratory
parame-ters can be maintained during sponta-neous ventilations,ofthe two agents
usedfor mask induction,halothane producesless respiratory depression than
doessevoflurane.122Not all respiratory effectsare detrimental.All inhalational
agents arebeneficial in that they produce bronchialdilatation and are advantageous
in themanagement ofthe patient with bron-chospastic disease.All potent
inhalationalagents have myocardial depressant effects.The cardiovascular depressant
effects aregreatest with halothane use,which canresult in hypotension and
bradycardia.However,ofgreater significance is the abil-ity ofhalothane to sensitize
the heart tocatecholamines with resultant dysrhyth-mias.One study reported that 48%
ofpediatric patients anesthetized withhalothane had arrhythmias compared with16%
ofthose induced with 8% sevoflu-rane.Patients who had an incrementalinduction
ofsevoflurane had even fewerarrhythmias.Furthermore,ofthe arrhyth-mias associated
with halothane,40% wereventricular arrhythmias (consisting ofven-tricular
tachycardia,bigeminy,and cou-plets);with sevoflurane,only 1% were ven-tricular
arrhythmias (consisting ofsingleventricular ectopic beats).123The occur-rence
ofthese arrhythmias may also beassociated with the administration
oflocalanesthetics containing epinephrine.Halothane is the only inhalational
agentthat is associated with arrhythmias withclinical doses ofepinephrine.A limit
of1 �g/kg ofepinephrine in patients receiv-ing halothane is recommended.124�126Use
ofinhalational agents is advanta-geous in the oral and maxillofacial sur-geon�s
office because they provide a gener-al anesthetic state without
intravenousaccess.Therefore,only agents that arepleasant and nonirritating to the
airwaycan be used.Halothane has traditionallybeen the agent used by both
anesthesiolo-gists in the operating room and oral andmaxillofacial surgeons in
their offices.Sevoflurane appears to have the character-istics that most
approximate the idealinhalational agent,in that it is ofsufficientpotency,is
nonpungent,has a low bloodand tissue solubility,and has limited car-diorespiratory
effects.Sevoflurane hasreplaced halothane in the operating rooms.There are several
variations in mask-induction techniques.First,the inhala-tional agent may be
administered with aTable 6-2Inhalational Anesthetic AgentsBloodMaximum Acceptable
Concentration (%)AgentGas Solubility1�12 yrAdultNitrous
oxide0.47�105.00Halothane2.400.870.76Sevoflurane0.692.51.70Desflurane0.427.98�8.727
.30Isoflurane1.401.601.20Adapted from Cauldwell CB.Induction,maintenance and
emergence.In:Gregory GA,editor.Pediatric anesthesia.2nd ed.New York:Churchill
Livingston;1989.
Pediatric Sedation115combination ofnitrous oxide and oxygenor 100% oxygen.The
combination ofnitrous oxide with the potent vapor agentdecreases the percentage
ofvapor agentrequired to achieve an anesthetic depth.The decrease in minimum
alveolar con-centration (MAC) for halothane is signif-icantly clinically greater
for halothanethan for sevoflurane.This most likely isrelated to the difference in
solubility ofthe two potent inhalational agents.Another variation in mask induction
per-tains to the concentration ofinhalationalagent administered.The practitioner
mayadminister an incrementally increasingconcentration ofan agent (eg,increasingan
agent by 0.5�1% after a few breaths) ora high initial concentration ofan
agent(eg,sevoflurane 8%).Although onewould expect that sevoflurane wouldhave a more
rapid speed ofinduction,thedifferences between sevoflurane andhalothane have not
been consistentlydemonstrated.121,127The difference inspeed ofinduction appears to
be less dis-tinguishable when a high concentrationofhalothane is used.Similar to
speed ofinduction,anes-thetic emergence is dependent on severalvariables.Agents
that have a low bloodsolubility coefficient should have a short-er emergence
time.Several studies haveshown that desflurane,which has the low-est blood
solubility coefficient,has a veryrapid anesthetic emergence (5�7 min),and
halothane,which has the highestblood solubility coefficient,has a moreprolonged
recovery (10�21 min).128�132Sevoflurane has been shown,although notconsistently,to
have a more rapid anes-thetic emergence for intermediate- andlong-duration
anesthetics compared withhalothane.However,typically therequired state ofanesthesia
for a pediatricdental procedure in the office is brief,last-ing < 10
minutes.Recovery from anesthe-sia is also dependent on the duration ofthe
anesthesia.Clinical studies comparingsevoflurane and halothane for pediatricdental
extractions lasting between 4 and 6 minutes have not demonstrated a morerapid
recovery with sevoflurane.133In onestudy,in which children were subject to a4-
minute anesthesia,time to eye openingwas 102 seconds with halothane and 167 seconds
with sevoflurane.134The last factor that needs to be consid-ered both in comparing
sevoflurane andhalothane and in selecting an anestheticagent for the office is the
toxicity ofeachdrug.Halothane is metabolized in the liverto a trifluoroacetylated
product,whichbinds liver proteins promoting animmunologic response that can result
inhepatic injury.135,136The incidence,whichmay be as high as 1 in 6,000 cases
ofanes-thesia in adults,is significantly lower in thepediatric
population.Sevoflurane,although not associated with liver toxicity,has been
associated with the potential forrenal toxicity.137,138The drug undergoeshepatic
metabolism,which produces inor-ganic fluoride.However,the rapid elimi-nation
ofsevoflurane minimizes the renalfluoride exposure,which probablyaccounts for the
lack ofclinical renal dys-function,despite some reports ofserumfluoride levels > 50
�mol.Renal injury hasalso been associated with the formation ofcompound A,which is
a product ofthereaction between sevoflurane and CO2absorbents.Most ofthe
data,however,suggest that compound A does not inducerenal toxicity in humans.Other
MedicationsChloral hydrate isan alcohol-based sedative.It produces asleep from
which one is easily roused,inwhich the cardiorespiratory effects areconsistent with
those that occur with nat-ural sleep.The onset ofchloral hydrate isslow (30�60
min),its duration is variable(2�5 h),and it lacks the anxiolytic
effectsofbenzodiazepines.The sedative effect ofchloral hydrate does not produce
asfavorable a work environment as the anx-iolytic effect ofa
benzodiazepine.50Another disadvantage ofchloral hydrateis that it is a gastric
irritant and is associ-ated with nausea and vomiting.Antihistamines are commonly
used inmedicine and dentistry for their anti-pruritic and antiemetic effects.When
usedfor these conditions,sedation is frequentlyan unwanted side
effect.However,thesedative effects can be used to advantage,and antihistamines such
as promethazineand hydroxyzine are frequently combinedwith other drugs such as
chloral hydrateand meperidine to potentiate the sedativeeffect ofthe primary
anesthetic agent andto provide antiemetic effects.The sedativeeffects
ofantihistamines may last between3 and 6 hours,and when used alone do notprovide
anxiolysis.The oral transmucosal administrationofa sedative medication is
appealing.Fen-tanyl citrate is available as a lozenge on astick.The recommended
dose is between10 and 20 �g/kg.Bioavailability is between33% in children and 50% in
adults.139The difference in bioavailabilityresults from the amount ofdrug that
isswallowed and the amount ofdrug that isabsorbed through the oral mucosa.Thedrug
provides both analgesia and sedation.Onset ofanalgesia precedes the onset
ofsedation.Analgesia also lasts for 2 to 3 hours,providing some postoperativepain
control.Adverse side effects associat-ed with the fentanyl lozenge include a
highincidence ofnausea and vomiting,andpruritus.The major adverse effect associ-
ated with the use offentanyl citrate is ahigher incidence ofrespiratory
depressionthan that seen with other sedative medica-tions.The respiratory
depression associatedwith the fentanyl lozenge may last beyondthe sedative
effect.140Perioperative ComplicationsLaryngospasmIntraoral surgery in the
anesthetized non-intubated patient renders the patient sus-ceptible to airway
obstruction and airwayirritation.Such irritation can result in a
116Part 1: Principles ofMedicine,Surgery,and Anesthesialaryngospasm,which is the
apposition ofthe supraglottic folds,the false vocal cords,and the true vocal
cords.The laryn-gospasm may be sustained and maybecome progressively worse as the
supra-glottic tissues fold over the vocal cordsduring forceful inspiratory
efforts.Theincidence oflaryngospasm is 8.7 per 1,000 patients in the total
population and17.4 per 1,000 in patients < 9 years ofage.39The treatment
oflaryngospasmdepends on whether the airway obstruc-tion is complete or
incomplete.The singlediagnostic feature that distinguishes com-plete from
incomplete airway obstructionis simply the absence or presence ofsound.Ifthere are
inspiratory or expiratorysqueaks,sounds,grunts,or whistles,thenchances are the
child has incomplete air-way obstruction.Airway obstruction ofeither type requires
initial treatment witha patency-preserving maneuver such asthe jaw-thrust/chin-lift
maneuver.Because incomplete airway obstruc-tion may rapidly become
complete,signsand symptoms ofobstruction (eg,tra-cheal tug,paradoxic respiration)
shouldbe treated aggressively.The first maneu-ver is to apply gentle continuous
positiveairway pressure with 100% O2by facemask.An effective technique to
delivergentle positive pressure is to �flutter thebag.�In this technique the
reservoir bag isvery rapidly squeezed and released in astaccato rhythm,similar to
what onewould see with an atrial flutter oftheheart.In essence,one performs a
manualhigh-frequency oscillatory ventilationwith this technique.Ifthe
patientimproves,anesthesia and normal ventila-tion may be resumed.Overuse
ofthehigh-pressure flush valve to fill thebreathing circuit and anesthetic bag
maydilute potent anesthetic gases (ifbeingused) and lead to a lighter plane ofanes-
thesia in the child.In addition,high pres-sure applied to the airway may force
gasdown the esophagus and into the stom-ach,reducing ventilation even more.Pos-
itive airway pressure cannot �break�laryngospasm in the presence ofcom-plete airway
obstruction and may,in fact,worsen laryngospasm by forcing supra-glottic tissues
downward to occlude theglottic opening.For the laryngospasm that is refracto-ry to
continuous positive airway pressure,a neuromuscular blocking agent should
beadministered.The ideal agent should haverapid onset.For the nonintubated
patient,rapid recovery is also desirable.Succinyl-choline is the only neuromuscular
block-ing agent that provides these effects.SuccinylcholineIfintravenous access is
available,suc-cinylcholine 0.5 to 1.0 mg/kg is adminis-tered.Ifthe child is
hypoxemic,atropine0.02 mg/kg should preceed the adminis-tration ofthe
succinylcholine to prevent abradycardia secondary to the muscariniceffect
ofsuccinylcholine.Ifintravenousaccess is not available,succinylcholinemay be
administered intralingually or IM(succinylcholine 4 mg/kg).141There are several
potential complica-tions associated with the use ofsuccinyl-choline.These include
myalgias,malignanthyperthermia,masseter muscle rigidity,and hyperkalemic cardiac
arrest in patientswith undiagnosed myopathies.In somechildren the administration
ofsuccinyl-choline can result in masseter musclespasm.Masseter muscle spasm may
indi-cate a susceptibility to malignant hyper-thermia,but it can also be isolated
and notprogress to malignant hyperthermia.Theanesthetic team needs to
differentiatebetween an isolated spasm and a prodromalsign ofan impending emergency
to make adecision regarding the continuation oftheanesthetic and surgical course.In
a tertiaryenvironment with appropriate monitoring,the anesthesia may be continued
withobservation for the development ofothersystemic signs reflective ofthe
hypermeta-bolic state ofmalignant hyperthermia.Tachycardia is usually the earliest
sign,whereas end-tidal CO2is the most sensitivesign ofmalignant
hyperthermia.142,143Another potential life-threateningcomplication following the
administrationofsuccinylcholine is hyperkalemic cardiacarrest.Hyperkalemic cardiac
arrest followsthe administration ofsuccinylcholine inpatients with undiagnosed
myopathies;succinylcholine induces rhabdomyolysis,which causes hyperkalemia leading
tobradycardia/asystolic rhythm.Several casereports have appeared in the
literatureemphasizing this potential risk in thepediatric patient,which exists
becauseDuchenne�s and Becker�s muscular dystro-phies may go undiagnosed until the
agesof6 and 12 years,respectively.144,145Alternative neuromuscular agentshave been
developed that can providerapid onset and should be used for
electivesituations.Rocuronium may be used whensuccinylcholine is
contraindicated.Itsonset is rapid,however,with a consider-ably longer duration.The
administrationoflidocaine topically to the vocal cordsmay also be
effective.Succinylcholineremains the most ideal drug for the man-agement
oflaryngospasm and emergenttracheal intubation and is the essentialdrug for
managing laryngospasm in theoral and maxillofacial surgery
office.CricothyrotomyThree approaches to emergency surgicalopening ofthe airway are
mentioned inthe literature:emergency tracheotomy,emergency cricothyrotomy,and emer-
gency transtracheal ventilation.146 In theexperience ofmost,emergency tracheoto-my
cannot be performed rapidly enoughin dire situations.Likewise,transtrachealjet
ventilation is extremely hazardous inchildren because barotrauma may occurowing to
the restricted egress ofventilato-ry gas.Therefore,when endotrachealintubation
cannot be accomplished,themost rapid method for oxygenating thepatient in an
emergency situation iscricothyrotomy.147
Pediatric Sedation117Nausea and VomitingPostoperative nausea and vomiting(PONV) is
a cause ofmorbidity in pediatricpatients.Even mild PONV is associatedwith delayed
discharge,decreased parentalsatisfaction,and increased use ofresources.More severe
complications associated withPONV include dehydration and
electrolytedisturbances,or hypoxemia secondary toairway obstruction or
aspiration.PONVoccurs in 6 to 42% ofall pediatric surgicalpatients.The incidence is
variable depend-ing on age ofthe patient,the sex ofthepatient (there is a greater
incidence infemales > 13 yr),the anesthetic agents used,and the surgical
procedure.Fortunately,severe or intractable PONV is less common,occurring in 1 to
3% ofpediatric patients.148Anesthetic drug selection can have aneffect on the
incidence ofPONV.Pre-operative midazolam has been associatedwith reduced PONV in
children.149Sub-sedative doses ofpropofol also provideantiemetic effects.This
contrasts withmethohexital,which is associated with ahigher incidence ofPONV than
is propo-fol in adults.Studies are lacking compar-ing the incidence ofPONV ofthese
twoagents in a pediatric population.Pre-medication with opioid analgesicsincreases
the risk ofPONV.Oral trans-mucosal fentanyl citrate in doses of5 to20 �g/kg is
associated with PONV inalmost all patients.140As discussed above,ketamine is an
excellent agent for pedi-atric sedation.An unfortunate adverseeffect associated
with ketamine is areported incidence ofPONV that is ashigh as 50%.Nitrous oxide
also has emet-ic effects.However,concentrations < 40%are less likely to cause
PONV.Vomiting is a complicated responsemediated by the emetic center located inthe
lateral reticular formation ofthemedulla.This center receives input fromseveral
areas within the CNS,including thechemoreceptor trigger
zone,vestibularapparatus,cerebellum,higher cortical andbrainstem centers,and
solitary tract nucle-us.These structures are rich in dopamin-
ergic,muscarinic,serotoninergic,hista-minic,and opioid receptors.Blockade ofthese
receptors is the mechanism oftheantiemetic action ofdrugs.At the presenttime there
are no drugs known that actdirectly on the emetic center.Routine administration
ofantiemeticagents to all children undergoing surgeryis not justifiable as the
majority do notexperience PONV or have,at most,one ortwo episodes.The agents used
are the sameas those used to manage PONV in theadult.The following discussion
identifiespoints significant to the management ofPONV in the pediatric
patient.PhenothiazinesThe phenothiazines arebelieved to exert their antiemetic
effectsprimarily by antagonism ofcentraldopaminergic receptors in the chemore-
ceptor trigger zone.Low doses ofchlor-promazine,promethazine,and per-phenazine are
effective in preventing andcontrolling PONV.These drugs are fre-quently combined
with opioids (whenadministered orally by pediatric dentists)to decrease the emetic
effect ofthe opioid.All phenothiazines are capable ofprodu-cing extrapyramidal
symptoms and seda-tion,which may complicate postoperativecare.The degree ofsedation
variesbetween phenothiazines,with little seda-tion produced by perphenazine
comparedwith the other phenothiazines.150BenzamidesThe benzamide
derivativemetoclopramide has antiemetic and pro-kinetic effects and is the most
effectiveantiemetic ofthis class.Its antiemeticeffects are mediated by antagonism
ofcen-tral dopaminergic receptors,and at highdoses it also antagonizes serotonin-
3receptors.In the gastrointestinal tractmetoclopramide has significant dopamin-
ergic and cholinergic actions and increasesmotility from the distal esophagus to
theileocecal valve.High doses ofmetoclo-pramide are well tolerated by
adults,butchildren are prone to dystonic reactions.For this reason,metoclopramide
is com-bined frequently with diphenhydramine todecrease this incidence.Although
metoclo-pramide has been used successfully toreduce the incidence ofPONV in high-
riskchildren,it is not as effective as droperidolor the newer serotonin
antagonists.151,152Histamine AntagonistsThe histaminereceptor antagonists are
weakly antiemeticdrugs with profound sedative effects,which make them less suitable
for use inpostoperative patients.They are frequent-ly combined with other
anesthetic agentsin an oral cocktail for their sedative andantiemetic effects.These
drugs may beuseful for controlling emesis resultingfrom vestibular stimulation,as
occurs inpatients with motion sickness or aftermiddle ear surgery.They also
counteractthe extrapyramidal effects ofthe more effi-cacious dopamine receptor
antagonists.Muscarinic Receptor AntagonistsThevestibular apparatus and the nucleus
ofthe tractus solitarius are rich in mus-carinic and histaminic receptors.Mus-
carinic receptor antagonism is effective inpreventing emesis related to
vestibularstimulation,which may be the mecha-nism ofmorphine-induced PONV.Inadults
the use ofglycopyrrolate,a drugthat does not cross the blood-brain barri-er,has
been associated with three timesthe need for rescue antiemetic therapycompared with
atropine.153Transdermalscopolamine has been used successfully toreduce PONV in
children receiving mor-phine but is associated with a significantincrease in
sedation and dry mouth.154Other potential side effects include dys-
phoria,confusion,disorientation,halluci-nations,and visual disturbances.Serotonin
Receptor AntagonistsSero-tonin antagonists were discoveredserendipitously when
compounds struc-
118Part 1: Principles ofMedicine,Surgery,and Anesthesiaturally related to
metoclopramide werefound to have significant antiemetic effectsbut lacked dopamine
receptor affinity.These drugs produce pure antagonism ofthe serotonin-3
receptor.Ondansetron wasthe first drug ofthis class to become avail-able for
clinical use in 1991.Since that timegranisetron,and dolasetron have
beenintroduced.This class ofpure serotonin-3receptor antagonists is not associated
withthe side effects ofdopamine,muscarinic,orhistamine receptor antagonists.The
mostserious side effects ofondansetron are rarehypersensitivity
reactions.155Gastric emp-tying and small bowel transit time were notaffected by
ondansetron.Asymptomaticbriefprolongation ofthe P�R interval andthe QRS complex
ofthe electrocardiogramhave been reported in adults,but rapidintravenous infusion
ofondansetron inchildren was not associated with changes inheart rate,arterial
pressure,or oxyhemo-globin saturation.156Psychomotor and res-piratory function were
unaffected byondansetron.Prophylactic ondansetron0.05 to 0.15 mg/kg IV or orally
reduced theincidence ofPONV in children after a vari-ety ofsurgical
procedures.157Glucocorticoids (dexamethasone,methylprednisolone) exert
antiemeticproperties by a mechanism as yet un-known.These drugs have been used suc-
cessfully in the postoperative setting to pre-vent PONV.Dexamethasone in doses up
to1 mg/kg IV (maximum dose 25 mg) waseffective in reducing postoperative vomit-ing
in children after tonsillectomy.158How-ever,low-dose dexamethasone 0.15 mg/kgIV was
not as effective as perphenazine 70 �g/kg IV in preventing emesis after ton-
sillectomy in children.159This class ofdrugs is better used in combination
withanother antiemetic than as the sole agent toprevent PONV.Special
ConsiderationsOral and maxillofacial surgeons treat adiverse group
ofpatients.Simplistically,the pediatric patient differs from the adultpatient
anatomically,physiologically,andbehaviorally.Beyond these differences thepediatric
population is a diverse groupwithin itself.Oral and maxillofacial sur-geons are
involved with the managementofpatients with craniofacial syndromes aswell as other
physical or mental impair-ments.The craniofacial syndromes mayresult in anatomic
and physiologic alter-ations as well as mental disabilities.Poten-tial airway
abnormalities include macro-glossia,micrognathia,choanal atresia,limited mouth
opening,kyphoscoliosis,orcervical spine abnormalities.These abnor-malities may make
the patient more sus-ceptible to upper airway obstruction andcompromise spontaneous
ventilation,oxygenation,mask ventilation,or laryn-goscopy and intubation.Many
ofthesepatients may have significant cardiovascu-lar disease associated with their
syndrome.Mental impairment may also be associatedwith several congenital
syndromes.Alter-natively,physical disabilities are not alwaysassociated with mental
impairments.Thehealth care provider must avoid treatingthese patients as ifthey
were mentallyimpaired because oftheir inability to com-municate
normally.Lastly,substanceabuse among children and teens hasreached epidemic
proportions.This section reviews the clinical pre-sentation and anesthetic
management ofsome patients with special considerations.Attention Deficit
HyperactivityDisorder Attention deficit hyperactivity disorder(ADHD) is defined as
a persistent severepattern ofinattention or hyperactivity-impulsivity symptoms
compared withother children at a comparable develop-mental level.Three subtypes
ofADHD areidentified:a predominantly hyperactive-impulsive type,a predominantly
inatten-tive type,and a combined type.It is esti-mated to affect up to 5%
ofchildren.Medical therapy frequently includespsychostimulants such as methyl-
phenidate,dextroamphetamine,or pemo-line.Methylphenidate is the most com-monly
prescribed drug for ADHD.Inaddition to its use in the management ofADHD,1 to 2%
ofthe US high-schoolpopulation without a diagnosed medicalcondition is reported to
abuse thisdrug.160These drugs increase the bioavail-ability ofneurotransmitters.The
drugstend to cause an increase in blood pres-sure and heart rate.Adverse effects
aresimilar to that ofother sympathomimeticagents.CNS effects include
restlessness,dizziness,tremor,hyperactive reflexes,weakness,insomnia,delirium,and
psy-chosis.Cardiovascular effects may
includeheadaches,palpitations,arrhythmias,hypertension followed by hypotension,and
circulatory collapse.161Perioperative management ofa patienton a psychostimulant
(such as methyl-phenidate) includes recognizing signs andsymptoms suggestive
ofinappropriate use.Ifthere is a suggestion regarding overdose ofthe medication,the
surgery should be post-poned.However,when the medication isused appropriately,it is
generally well toler-ated.Ifthere are no indications ofadverseevents,the medication
should be continuedthroughout the perioperative period.Chronic use ofthe medication
may decreaseanesthetic requirements.The anesthetic management ofthesepatients is
dependent on the level ofco-operation ofthe patient.Preoperativesedatives may be
used.Many ofthese indi-viduals allow the placement ofan intra-venous
catheter.However,for the patientin whom intravenous access cannot
beestablished,ketamine (with or withoutmidazolam) administered orally or IM
iseffective and not contraindicated owing tothe chronic use ofa
psychostimulant.AutismAutism is a complex developmental dis-ability that typically
appears during thefirst 3 years oflife.The result ofa neuro-logic disorder that
affects the functioning
Pediatric Sedation119ofthe brain,autism is the third most com-mon developmental
disability in the Unit-ed States and occurs in approximately 2 to4 per 10,000 live
births.162Autism is fourtimes more prevalent in boys than in girlsand knows no
racial,ethnic,or socialboundaries.Family income,lifestyle,andeducational levels do
not affect the chanceofautism�s occurrence.Autism impacts the normal develop-ment
ofthe brain in the areas ofsocialinteraction and communication skills.Children and
adults with autism typicallyhave difficulties in verbal and
nonverbalcommunication,social interactions,andleisure or play activities.The
disordermakes it difficult for them to communi-cate with others and relate to the
outsideworld.163,164 In some cases aggressive and/orself-injurious behavior may be
present.Persons with autism may exhibit repeatedbody movements (hand flapping,rock-
ing),unusual responses to people,orattachments to objects and resistance tochanges
in routines.Children with autisticdisorders may include a subgroup ofindi-viduals
with associated psychiatric symp-toms,including aggression,self-abusivebehavior,and
violent tantrums,and often-times necessitate the use
ofpsychiatricmedications;antipsychotics are the mostprevalently prescribed
medications in thisgroup.165The autistic patient may also beprescribed medications
similar to thoseprescribed for ADHD.Management ofthese patients in theoral and
maxillofacial surgery settingrequires respect for the autistic child�s needfor
ritualistic behavior,which may result intantrum-like rages with any disruptions
ofroutine.Providing a calm environmentwith minimal stimulation and considera-tion
ofall associated pharmacologic influ-ences aids in the management
ofthesepatients.Premedication with a benzo-diazepine may be
beneficial.However,establishing an intravenous access still maynot be possible,and
an alternative tech-nique may be required.A mask inductionwith a potent vapor agent
or intramuscularketamine may be considered;however,theindividual may be too
physically strongand combative for these techniques.Analternative that should be
considered (evenin the noncombative individual) is oraladministration ofa
premedicant ofketa-mine or ketamine and midazolam.89Alter-ations in management must
be carriedover into the postoperative period,inwhich many patients with behavioral
ormental impairments are more agitated.Restraint may be necessary to prevent pre-
mature removal ofthe intravenous line,wound disturbance,or self-injury.Cerebral
PalsyCerebral palsy is a group ofneurologicdisorders that are characterized
byimpaired control ofmovement.The clini-cal manifestations are variable and
aredependent on the site and extent ofinjury.There are four
classifications:spastic,athetoid,ataxic,and mixed.Spastic cere-bral palsy is the
most common form andaffects up to 80% ofthe patients.Patientswith spastic cerebral
palsy present withmuscle hypertonicity,hyperreflexia,musclecontractures,muscle
rigidity,and muscleweakness.The pattern ofdysfunction canbe further classified into
monoplegia (onelimb),diplegia (both arms or both legs),hemiplegia
(unilateral),triplegia (threelimbs),and quadriplegia (all limbs).Theseverity ofthe
contractures may result inspinal deformities such as scoliosis.Athetoid or
dyskinetic cerebral palsy ischaracterized by choreiform,tremor,dys-tonia,and
hypotonia.The involuntarymovements seen with athetoid cerebralpalsy often increase
with emotional stress.Ataxic cerebral palsy is characterized bypoor coordination
and jerky movements.Associated medical conditions includemental retardation,speech
abnormalities,seizures,drooling,dysphagia,and gastro-esophageal reflux.166Mental
impairment ismost common in patients with spasticcerebral palsy.It is important to
recognizethat > 50% ofpatients with cerebral palsydo not demonstrate mental
impairment.Dysarthria or speech abnormalities sec-ondary to a lack ofcoordination
in musclemovement ofthe mouth can be seen inathetoid cerebral palsy.This
muscleabnormality should not be confused withmental impairment.Seizures are seen
inup to 35% ofpatients with spastic cerebralpalsy.The lack ofmuscle
coordinationcontributes to drooling and dysphagia.The inability to handle the
secretions andthe incompetent pharyngeal swallowreflex increase the risk
oflaryngospasm.Individuals with impaired neurologicfunction may also have an
increased inci-dence ofgastroesophageal reflux.Several factors must be taken into
con-sideration in treating these patients.Thespasticity and lack ofcoordination
cancontribute to a hyperactive gag reflex.Anx-iety can aggravate the involuntary
move-ments.Nitrous oxide sedation may beeffective in reducing these
responses.167Severe contractures may make positioningthe patient
difficult.Contractures,whichmay result in scoliosis,can result in arestrictive lung
disorder.The patient�shypotonia may necessitate stabilization ofthe head (even for
the nonsedated patient).Ifthe patient is to be sedated,muscle weak-ness may
predispose the patient toimpaired respirations.This may be com-pounded by
medications prescribed tocontrol the spasticity or seizure disorder.Conscious
sedation may be contraindicatedbecause ofthe inability to handle oralsecretions and
the risk ofgastroesophagealreflux.It may be necessary to protect theairway with the
placement ofan endo-tracheal tube.In the event that the airwayrequires emergent
intubation,the use ofsuccinylcholine is not contraindicated.168Down SyndromeDown
syndrome,or trisomy 21,is a com-mon chromosomal disorder occurring at arate of1.5
per 1,000 live births and is usu-ally characterized by mild to moderate
120Part 1: Principles ofMedicine,Surgery,and Anesthesiamental
retardation,cardiovascular abnor-malities,and craniofacial
abnormalities.Craniofacial abnormalities that have animpact on the anesthetic
management ofthese patients include macroglossia,micrognathia,and a short
neck,puttingthese patients at increased risk for airwayobstruction during
sedation.Enlargementofthe lymphoid tissue may also placethese patients at risk for
upper airwayobstruction.In addition,these patientshave generalized joint laxity
that may beassociated with subluxation ofthe tem-poromandibular joint during
airwaymanipulation.Intubation is usually notdifficult,but subglottic stenosis,which
ispresent in up to 25% ofDown syndromeindividuals,may necessitate a smaller-
diameter endotracheal tube.Atlantoaxial instability occurs inapproximately 20%
ofpatients with Downsyndrome,and airway maneuvers,such asneck positioning during
anesthesia for air-way opening or intubation,may induce aserious cervical injury
(C1-2 subluxation).This cervical spine instability is a con-traindication for
routine treatment untilboth the patient and the treatment risks arefully
evaluated.Sequelae to neurologicinjury are usually characterized by signifi-cant
symptoms or declining neurologicfunction without other neurologic dis-
order.Specific symptoms may include apositive Babinski sign,hyperactive deeptendon
reflexes,ankle clonus,neck discom-fort,and gait abnormalities.Down syndrome is
associated withcongenital heart disease in approximately40% ofits patients,and
consideration ofthese abnormalities (endocardial cushiondefect,ventricular septal
defect,tetralogy ofFallot,patent ductus arteriosus,and atrialseptal defect) in
conjunction with their pri-mary care physician is mandatory prior toproceeding with
a surgical procedure.Muscular DystrophyMuscular dystrophy is a group
ofdiseasesofgenetic origin,characterized by the pro-gressive loss ofskeletal muscle
function.There are nine types ofmuscular dystro-phies,the most common and
dramaticbeing Duchenne�s disease (pseudohyper-trophic muscular
dystrophy).Symptomstypically begin between the ages of2 to 5 years,often with the
patient becomingwheelchair-bound by age 12 years.Deathusually occurs between ages
15 and 25 years,usually secondary to pneumoniaor congestive heart failure.Becker�s
mus-cular dystrophy is the next most commonform ofmuscular dystrophy.Its manifes-
tations are similar,although milder,tothose ofDuchenne�s disease.Its onset
islater,and the progression ofthe disease isslower.Time to onset
ofdisease,beingwheelchair-bound,and death are 12,30,and 42
years,respectively.169The anesthetic management ofthesepatients is complicated by
muscle weak-ness contributing to poor respiratoryfunction.Atrophy ofthe paraspinal
mus-cles also leads to kyphoscoliosis (restric-tive lung disease),which further
restrictsrespiratory function.Pulmonary functiontests should be considered as part
ofthepreoperative assessment.Patients withfunctional vital capacities < 35% ofnor-
mal are at increased risk.Muscle weaknessalso contributes to obtunded
laryngealreflexes and an inability to clear tracheo-bronchial secretions.Patients
are atincreased risk for aspiration secondary tothe obtunded laryngeal reflexes
anddelayed gastric emptying.Patients with muscular dystrophy mayalso have
cardiovascular disorders.Theseinclude degenerative cardiomyopathy,car-diac
arrhythmias,and mitral valve pro-lapse.It is frequently difficult to assess car-
diovascular function in these patientsbecause they are usually wheelchair-boundand
not sufficiently stressed.However,car-diac compromise must be considered,espe-
cially in an older individual.Anestheticconsiderations must take into considera-
tion the potential for underlying respira-tory and cardiovascular disease.Succinyl-
choline is contraindicated because it cancause rhabdomyolysis with a
resultanthyperkalemia.Although all patients mayhave a slight increase in
extracellular potas-sium after the administration ofsuccinyl-choline,the increase
in a patient with mus-cular dystrophy can cause hyperkalemiccardiac arrest.The
avoidance ofsuccinyl-choline and volatile inhalational agents isalso recommended
because ofthe associa-tion ofDuchenne�s disease with increasedmalignant
hyperthermia.Nondepolarizingmuscle relaxants may be used;however,aprolonged
recovery time is seen in patientswith muscular dystrophy.The response toreversal
agents is also variable.Additional-ly,patients are susceptible to an un-explained
late respiratory depression.Ambulatory surgery may be unadvisablebut at a minimum
requires prolongedobservation prior to discharge.170Substance AbuseSubstance abuse
amongst children andteens has reached epidemic proportions,regardless
ofsocioeconomic status.In2001 an estimated 15.9 million Americansages 12 or older
were current illicit drugusers,meaning they had used an illicitdrug during the
month prior to the surveyinterview.This estimate represents 7.1% ofthe population
ages 12 years old or older.Among youths ages 12 to 17 years,approx-imately 10% were
current illicit drugusers.Data from 1999 to 2001 identifymarijuana as the most
popular abuseddrug,with a use approximating 7% ofthispopulation.Other abused
substancesincluded psychotherapeutic agents(approximately 3%),cocaine (approxi-
mately 0.5%),hallucinogens (approxi-mately 1%),and inhalants (approximately1%).An
adequate history taking prior toanesthesia regarding substance use andabuse is
therefore mandatory with allpatients.This history allows for a saferselection
ofanesthetic agents andimproved management ofany periopera-tive complications.
Pediatric Sedation121AlcoholAlcohol is the most commonlyused and abused substance
amongteenagers.Most alcohol use by USteenagers is in the form ofbinge drinking.Most
long-term systemic effects ofchron-ic alcohol abuse,including hepatic
injury,pancytopenia,and the neurotoxic effects(seizures,Wernicke-
Korsakoffsyndrome)are not present in the pre-adult abuser.Nonetheless,laboratory
examinationsmay reveal elevation of?-glutamyltrans-ferase,which is usually the
first liverenzyme to increase as a result ofheavyethanol ingestion.Hepatic damage
owingto alcohol frequently results in an aspar-tate transaminase�to�alanine amino-
transferase ratio > 1.A mean corpuscularvolume > 100 is strong confirmatory evi-
dence ofalcoholism.Aspiration risk is significantlyincreased in the chronic
alcoholic as alco-hol stimulates gastric acid secretion anddelays gastric emptying
time.In addition,the alcoholic patient may consume alcoholthe morning ofthe
procedure to quell thesigns ofwithdrawal,thus negating theNPO status.Cardiovascular
changes asso-ciated with chronic alcohol abuse result inalcoholic
cardiomyopathy,with resultanttachycardia and unexplained atrial or ven-tricular
ectopy.Alcohol abuse influences the choiceofanesthetic agents used in an
outpatientsetting.Tolerance to anesthetic agentsappears to develop in the chronic
alco-holic.Altered liver function results in anincreased toxicity with anesthetic
agentsthat undergo hepatic metabolism.Pro-longed activity and increased serum
levels ofboth succinylcholine and local anesthetic agents are the result
ofdecreased activity ofplasmacholinesterase.Nondepolarizing para-lytics are also
prolonged in chronic alco-hol abuse secondary to an increased
levelofacetylcholine.Intravenous agentsshould also include a benzodiazepine
thatcompensates for the lack of?-aminobu-tyric acid (GABA)-ergic
stimulation.AmphetamineAmphetamine,a racemicmixture of�-phenylisopropylamine,is
anindirect sympathomimetic drug.It is apowerful CNS stimulant with peripheral aand
�actions.The CNS mechanism ofamphetamine appears dependent on thelocal release
ofbiogenic amines such asnorepinephrine from storage sites in nerveterminals.Acute
amphetamine use dramat-ically increases anesthetic requirement andhas been
implicated in a case ofsevere intra-operative intracranial
hypertension.171,172Chronic amphetamine use is associatedwith a markedly diminished
anestheticrequirement.173This results from chronicstimulation ofadrenergic nerve
terminalsin the peripheral nervous system andCNS that depletes CNS
catecholamines.Refractory hypotension can result bothintra- and
postoperatively,requiringprompt pharmacologic intervention.There can be a
diminished pressorresponse to ephedrine after chronicamphetamine use.This is due to
cate-cholamine depletion in central andperipheral adrenergic neurons.CocaineCocaine
is an alkaloid derivedfrom the leaves ofa South Americanshrub.The drug is snorted
(intranasal),injected (intravenous),or smoked(inhaled).Its administration provides
anintense euphoria.Cocaine use amongst12- to 17-year-olds in the United States
isapproximately 0.8%.174The medical effects from cocaineresult from both acute
intoxication as wellas chronic use.CNS stimulation,hyper-vigilance,anxiety,and
agitation are com-mon in the acutely intoxicated individual.Cardiovascular effects
may include tachy-cardia,arrhythmias,hypertension,andischemia.Ischemic myocardial
injury mayoccur,even in the young patient.Theseeffects result from the inhibition
ofneuralreuptake ofdopamine,serotonin,andtryptophan;increased adrenergic
activity;and blockade ofthe sodium conductionchannels.Chronic cocaine abuse has
beenassociated with ventricular hypertrophy,myocardial depression,and cardiomyopa-
thy.Long-term use may also lead to con-traction band necrosis.This phenomenonis
associated with hypermetabolic condi-tions,such as cocaine abuse,hyper-
thyroidism,and pheochromocytomaresulting from continuous catecholamineconcentration
elevation.This conditionpredisposes the patient to dysrhythmias.175Patients may
also manifest neurologiceffects.A decrease in seizure threshold hasbeen
demonstrated in young adults.Ischemic cerebral vascular accidents mayresult from
the hypertensive crisis potenti-ated by the cerebral vasoconstriction result-ing
from the increased serotonin levels.Respiratory complications associatedwith
intranasal administration includesneezing,sniffing,and acute rhinitis.Pul-monary
complications associated withinhalational administration includecocaine-induced
asthma,chronic cough,pulmonary edema,and pneumoperi-cardium.Acute intoxication may
result inhypoxia owing to pulmonary vasculaturevasoconstriction.High levels
ofcocaine may persist for6 hours after nasal administration.Electiveanesthetic
management should bedeferred for at least 24 hours after thepatient has last used
cocaine.Electro-cardiographic monitoring is recommend-ed in all patients owing to
the potential forsilent ischemia and arrhythmias.Anes-thetic management may include
control ofpreoperative anxiety with benzo-diazepines.Consideration should be
givento avoiding adrenergic stimulants such asketamine and epinephrine-
containinglocal anesthetics.�Ecstasy�3,4-Methylenedioxymeth-amphetamine (MDMA) is a
stimulant thathas psychedelic effects that can last for 4 to6 hours and is usually
taken orally in pillform.The psychological effects ofMDMAinclude
confusion,depression,anxiety,sleeplessness,drug craving,and paranoia.
122Part 1: Principles ofMedicine,Surgery,and AnesthesiaAdverse physical effects
include muscletension,involuntary teeth clenching,nau-sea,blurred vision,feeling
faint,tremors,rapid eye movement,and sweating orchills.There is also an added risk
involvedwith MDMA ingestion by people with cir-culatory problems or heart disease
becauseofMDMA�s ability to increase heart rateand blood pressure.In 2001 an
estimated 8.1 million(3.6%) ofAmericans ages 12 or older hadtried ecstasy at least
once in their lifetime.The principle constituent ofecstasy(MDMA) can produce robust
deleteriouseffects on serotonergic functioning in ani-mals,including serotonin
depletion andthe degeneration ofserotonergic nerve ter-minals.176Although MDMA has
beencharacterized as a hallucinogenic amphet-amine because ofits structural
similarityto mescaline and amphetamine,it rarelyinduces hallucinatory
experiences,nor is itas potent a psychostimulant as ampheta-mine.Whether
neurotoxicity also occursin humans is unknown,but emerging evi-dence indicates that
repeated ecstasy expo-sure results in performance decrements inneurocognitive
function,which may be amanifestation ofneurotoxicity.177,178Most ecstasy tablets
contain MDMA;other commonly identified ingredientsinclude ketamine,methylenedioxy-
amphetamine,amphetamine,dextrometh-orphan,and combinations ofthese drugs.Some
tablets contain inert ingredients,whereas others contain phencyclidinehydrochloride
(PCP).Perioperative management mayinvolve addressing several complications,the most
common being syndrome ofinappropriate antidiuretic hormone,andhyperthermia.Other
less common butwell-known potential complicationsinclude tachycardia,agitation,and
nauseaand vomiting.Monitoring for the stigma-ta ofhyponatremia and
hyperthermiasupplements a well-performed preopera-tive history to determine which
patientsare at risk.Inhalational SubstancesInhalation sub-stance abuse is a problem
usually associatedwith young patients including preteens.The1997 Monitoring the
Future nationwidesurvey reported that inhalant use is mostcommon in the eighth
grade,in which 5.6%ofstudents used inhalants on a past-monthbasis and 11.8% on a
past-year basis.179They may present with
photophobia,eyeirritation,diplopia,tinnitus,sneezing,anorexia,chest pain,and
dysrhythmia.Before administering anesthesia one musttake into consideration
hepatic,renal,bonemarrow,and other organ pathology causedby halogenated and impure
chemicals.Lysergic Acid DiethylamideApproxi-mately 1% of16-year-olds in the
UnitedStates used lysergic acid diethylamide(LSD) in 2001.LSD,also known as
�acid,�isodorless and colorless,has a slightly bittertaste,and is usually taken by
mouth.OftenLSD is added to absorbent paper such asblotter paper and divided into
small deco-rated squares,with each square represent-ing one dose.The effects ofLSD
are unpre-dictable.They depend on the amounttaken;the user�s
personality,mood,andexpectations;and the surroundings inwhich the drug is
used.Usually the userfeels the first effects ofthe drug 30 to 90minutes after
taking it.Physical manifesta-tions include
mydriasis,hyperthermia,tachycardia,hypertension,diaphoresis,anorexia,and
tremors.Extreme emotionalvariability may occur,with extreme delu-sions and visual
hallucinations.LSD effectsare prolonged,typically lasting for > 12
hours.�Flashbacks�with auditory andvisual hallucinations may recur suddenlywithout
reuse ofthe drug and may occurwithin a few days or more than a year afterLSD
use.Flashbacks usually occur in peoplewho have used hallucinogens chronically orwho
have an underlying personality prob-lem.However,otherwise healthy peoplewho use LSD
may also experience flash-backs.Long-term effects ofchronic LSDinclude psychiatric
disorders (schizophre-nia,severe depression).It is difficult todetermine the extent
and mechanism oftheLSD involvement in these illnesses.Periop-erative anesthetic
practice involves recogni-tion ofthe potential psychiatric effects ofLSD on
patients and avoidance ofpoten-tially aggravating agents.MarijuanaMarijuana is the
most com-monly used nonalcohol illicit drug forpeople < 18 years old.In 2001 it was
usedby 76% ofcurrent illicit drug users.Approximately 56% ofcurrent illicit
drugusers consumed only marijuana,20% usedmarijuana and another illicit drug,and
theremaining 24% used an illicit drug but notmarijuana in the past month.Patients
whouse marijuana may present with anxiety,panic attacks,and sympathetic
discharge.Adverse effects ofmarijuana includeimmunodeficiency and upper
airwayhyperreactivity.Cases oflaryngospasmswithin 36 hours ofits use have
beenreported.180A �2-adrenergic agonist suchas albuterol may be considered to treat
thisincreased airway reactivity.Other periop-erative considerations include that
mari-juana potentiates opioid-induced respira-tory depression,and barbiturate
andketamine recovery time may be prolonged.Myocardial depression can occur,and
thethreshold for sympathomimetic-induceddysrhythmias is lowered.PCPPCP is a
dissociative anesthetic thatoriginally was synthesized for intravenoususe.Because
ofits postoperative emer-gence reactions (ie,hallucinations,pro-longed abnormal
level ofconsciousness,agitation),it fell out offavor,and its use asan anesthetic in
humans was discontinuedin 1963.PCP subsequently emerged as anoral drug ofabuse.PCP
is a commonlyabused street drug that is sold under manydifferent names and in
various forms.Itmay be sold on the street in tablet or cap-sule form,as a powder,or
as a solution.The PCP content in each form differswidely,commonly from 10 to
30%.�Angel
Pediatric Sedation123dust,�the powdered form ofPCP,general-ly has a higher PCP
content,occasionallyreaching 100%.Angel dust may be sniffed,smoked,ingested,or
injected IV.Percuta-neous absorption also has been reportedto occur in individuals
handling PCP (eg,law enforcement officers).Smokingremains the desired method
ofuse;thesubstance commonly is sprinkled ontodried leafmaterial
(eg,marijuana,tobac-co,oregano,mint) and then smoked.Perioperative anesthetic
considera-tions include its sympathomimetic effects,similar to its
congener,ketamine,with thepotential for tachycardia,tachyarrhyth-mias,and a true
hypertensive emergency.Maintaining normotension and avoidingsympathomimetics,which
may exacerbatePCP�s effects,are the standard for anes-thetic
management.SummaryAmbulatory anesthesia in the pediatricpatient can be safely
achieved in the oraland maxillofacial surgery office.The sur-geon has an array
oftechniques that areavailable.A technique has to be selectedthat is appropriate
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Part 2DENTOALVEOLARSURGERY
CHAPTER 7Management ofImpacted Teeth Other than Third MolarsDeborah
L.Zeitler,DDS,MSThe management ofimpacted teeth is abasic component ofmost oral and
max-illofacial surgery practices.Although themajority ofimpacted teeth are
thirdmolars,any other tooth may be impacted.The usual care for impacted third
molarsis removal;however,the care for impact-ed teeth other than third molars
mayinclude exposure (with or withoutattachment ofan orthodontic
bracket),uprighting,transplantation,or removal.These teeth often pose challenges in
treat-ment planning and surgical care.Thischapter includes information on inci-
dence,etiology,evaluation,and surgicaltreatment options.IncidenceThe incidence
ofimpacted permanentteeth has been addressed in several stud-ies.Grover and Lorton
examined 5,000army recruits and found a high frequencyofimpacted teeth (Figure 7-
1).1Althoughmaxillary and mandibular third molarswere the teeth most commonly
impacted,212 teeth excluding third and fourthmolars were impacted.This study
identi-fied the maxillary canine as the toothmost likely to be impacted following
max-illary and mandibular third molars.Impactions ofevery permanent toothwere
identified except the mandibularincisors and first molars.Thilander andMyrberg
examined more than 6,000Swedish school children and found a 5.4%prevalence
ofimpacted teeth excludingthird molars.2In an evaluation of3,874full-mouth
radiographs,Dachi and How-ell found the incidence ofimpactedcanines in the maxilla
to be 0.92% and ofother non�third molar teeth to be 0.38%.3This study also
identified maxillarycanines as the most commonly impactedteeth after maxillary and
mandibularthird molars.In a study ofmiddle-agedand older Swedish
women,Grondahlfound approximately 25 non�third molarimpacted teeth in 1,418 women
evaluat-ed.4Again,the canine tooth was the mostfrequent non�third molar
impactionidentified,followed by premolars and sec-ond molars.This study examined an
olderpopulation than did most ofthe otherstudies and had a lower incidence
ofnon�third molar impacted teeth.Presum-ably symptomatic teeth and those
withpathologic findings were removed at ear-lier ages in this population.4These
studiesare all similar in identifying the maxillarycanine as the tooth most likely
to beimpacted following third molars.Thenext most likely teeth to be impacted
aremandibular bicuspids,followed by maxil-lary bicuspids and second
molars.Impactions offirst molars and incisors arerelatively uncommon (Figure 7-
2).5Although impaction ofpermanentteeth is a relatively common finding,thelack
oferuption ofa primary tooth isapparently quite rare.When it occurs it isalmost
always a mandibular molar.Sub-merged teeth are common in the primarydentition but
generally reflect teeth thaterupted into a normal position and laterbecame
ankylosed and secondarily sub-merged.Bianchi and Roccuzzo have iden-tified 10 cases
in the literature ofthe past20 years that appear to illustrate primaryimpaction
ofdeciduous teeth.6A recentreview suggests that primary toothimpaction is usually
associated withdefects in the development and eruptionofthe permanent
successor,suggesting theneed for long-term follow-up.7FIGURE7-1Multiple impacted
teeth.
132Part 2: Dentoalveolar SurgeryEtiologyThe definition ofan impacted tooth is
�atooth that can not,or will not,erupt into itsnormal functioning positions,and
is,there-fore,pathologic and requires treatment.�8Causes ofimpacted permanent teeth
includesystemic and local factors.Impaction ofteethin the hereditary syndrome
ofcleidocranialdysplasia (Figure 7-3) is more properlytermed primary
retention.5Endocrine defi-ciencies (hypothyroidism and hypopitu-itarism),febrile
diseases,Down syndrome,and irradiation are other systemic factors thatmay influence
impaction ofpermanentteeth.9,10In all ofthese systemic conditions,multiple teeth
are generally involved.Morecommonly local factors are the cause ofper-manent tooth
impaction.These factorsinclude prolonged deciduous tooth reten-tion,malposed tooth
germs,arch-lengthdeficiency,supernumerary teeth,odonto-genic tumors abnormal
eruption path,andcleft lip and palate.5,11,12Because the maxillary canine is rela-
tively commonly impacted,it has beenstudied to identify the causes ofthis
toothimpaction.Jacoby separates labiallyunerupted maxillary canines from palatal-ly
impacted canines in his evaluation ofthe cause offailure oferuption
oftheseteeth.11Labially unerupted canines tend toshow a degree ofarch-length
deficiency,whereas palatally impacted canines do not.He stated that a canine might
appear in apalatal position ifextra space is availablein the maxillary bone owing
to eitherexcessive growth,agenesis,or peg shape ofthe lateral incisor,or stimulated
eruptionofa lateral incisor or first premolar.11In areview ofimpacted maxillary
canines,Bishara stated that the presence ofthe lat-eral incisor root with normal
length at thenormal time is important to guide thecanine in a proper eruptive
direction.9Impacted second molars have beenstudied to determine the cause
oftheseimpactions.Although maxillary secondpermanent molars are
infrequentlyimpacted,in a study ofthese impactions,Ranta found that the third molar
was gen-erally positioned occlusally and palatallyin relation to the second
molar,acting asan obstruction (Figure 7-4).13In a similarstudy Levy and Regan
identified the mostprobable cause ofimpaction ofdevelop-ing second molars as
malposition ofthetooth germs ofthe maxillary thirdmolars.10A typical finding was
deforma-tion ofthe mesial surfaces ofthe crownsand roots ofthe third
molars.Raghoebarand colleagues stated that impaction offirst molars is often
diagnosed as ectopiceruption,whereas impaction ofsecondmolars is usually associated
with arch-length deficiency.5Clinical problems have been identifiedassociated with
impacted permanentteeth.Failure ofteeth to erupt into theirnormal position in the
arch may result inproblems that include malocclusion,lossofarch length,migration or
loss ofneigh-boring teeth,periodontal disease,rootresorption ofadjacent
teeth,resorption(internal or external) ofthe impactedFIGURE7-2Unusual case ofan
impacted mandibular incisor.Reproduced with permission from Zeitler D.Management
ofimpacted teeth other than third molars.Oral Maxillofac Surg Clin North Am
1993;5:95�103.FIGURE7-3Multiple impacted teeth in a case ofcleidocranial
dysplasia.FIGURE7-4Impacted maxillary second andthird molars.
Management ofImpacted Teeth Other than Third Molars133tooth,dentigerous cysts or
odontogenictumors,and pericoronitis.5,9EvaluationClinical diagnosis ofimpacted
permanentteeth is straightforward,involving clinicalinspection that discloses the
absence ofthetooth in its normal position combinedwith the radiographic assessment
showingthe unerupted position ofthe tooth.Radiographic assessment oftheimpacted
teeth is important in the prepa-ration for surgical or orthodontic treat-ment.Most
techniques for localization ofan impacted tooth have been studied pri-marily with
maxillary canines.These tech-niques,however,can be generalized toother teeth in the
oral cavity.Ericson andKurol have studied the radiographicappearance ofectopically
erupting maxil-lary canines and have found that a palpa-ble canine generally erupts
in a relativelynormal position.14Most canines can beevaluated with accuracy from
convention-al periapical films.Axial or panoramicfilms were less useful.14When
polytomo-grams were used,root resorption wasdiagnosed with greater
accuracy.Thisstudy indicated that the optimal age forevaluating an ectopically
positionedcanine was 10 to 13 years,depending onindividual development.15A study
com-paring plain film radiography with com-puted tomography (CT) showed CT to
besuperior in showing tooth and root shape,crown-root relationship,and tooth incli-
nation.16However,the higher cost andradiation dose ofCT limits its use toimpacted
teeth in unusual positions or inproximity to vital structures.Standard radiographic
techniquesmay be used to localize the uneruptedteeth.These include the tube shift
method,buccal object rule,and periapical occlusalmethod.17The tube shift method
uses twoperiapical radiographs,shifting the tubehorizontally between
exposures.Iftheunerupted tooth moves in the same direc-tion in which the tube is
shifted,it is local-ized on the lingual or palatal side.A facialor buccally located
tooth moves in theopposite direction to the tube shift.17Thebuccal object rule uses
two radiographstaken with different vertical angulations ofthe x-ray beam.An object
located on thebuccal side moves inferiorly with the beamdirected inferiorly,whereas
an objectlocated in a lingual or palatal positionmoves superiorly.The periapical
occlusalmethod uses the periapical radiographtaken with a standard technique and
anocclusal radiograph to give two differentviews ofthe impacted tooth.17Panoramic
films can be used to assessmaxillary canine position (Figure 7-5).18This technique
uses the property that anobject closer to the tube (palatal) is rela-tively
magnified,and is most accuratewhen the tooth is close to the alveolarcrest.A study
comparing magnificationfrom a panoramic radiograph with a verti-cal parallax from
occlusal and panoramicfilms showed a slight superiority for thevertical parallax
method.Both methodswere better at localizing palatal cuspidsthan labial
cuspids.19Surgical TreatmentTreatment ofimpacted permanent teethmust be based on
clinical and radiograph-ic evaluation as well as a determination offuture
risks.Clearly,teeth that are sympto-matic,have caused infection in the sur-rounding
tissues,or have radiographic evi-dence ofdevelopment ofchanges
(cystformation,resorption ofadjacent teeth,orroot resorption ofthe impacted
teeth)require surgical treatment.Treatment ofthe asymptomatic tooth must take
intoaccount many factors,including age,spe-cific prevalence ofpathologic
conditions,severity ofpotential pathology associatedwith impacted teeth,progression
ofuntreated conditions,frequency andseverity ofpotential complications
oftreatment,potential patient discomfortand inconvenience associated with
eithertreatment or nontreatment,and economicconsequences oftreatment.4Methods
oftreatment ofimpacted permanent teethinclude orthodontic assistance
throughsurgical exposure with or without attach-ment ofthe tooth,surgical
uprighting,transplantation,and surgical removal.ExposureSurgical exposure is a
procedure thatallows natural eruption ofimpactedteeth.9,20�hman and �hman studied
542impacted teeth in 389 patients.20In thisstudy the crowns ofthe teeth were surgi-
cally exposed with removal oftissues inthe direction most appropriate for
crownmovement.The wounds were packed untilthey were totally epithelialized.The
teethwere allowed to erupt for up to 24 monthsor until the greatest diameter ofthe
crownreached the level ofthe mucosal surface.Of542 teeth only 16 were failures
(failureto erupt after 24 mo or with other compli-cations).This study found that
the teethtended to show a change ofinclination ofthe longitudinal access by
rotation alongthe root.Age did not appear to be a factorin success,although most
patients were < age 19 years.20In a study ofimpacted premolars,Thi-lander and
Thilander showed that surgicalexposure alone resulted in eruption,pro-vided that
space was present in the arch.21However,mesially tipped premolars had apoor
prognosis and required orthodonticFIGURE7-5Panoramic films can be used tolocalize
maxillary canines.
134Part 2: Dentoalveolar Surgeryguidance.Laskin and Peskin believe that ifexposure
ofteeth is to result in successfulspontaneous eruption,it should be doneas soon as
it is determined that the tooth isnot going to erupt spontaneously.22More
commonly,the technique ofsurgical exposure is combined with attach-ment ofan
orthodontic appliance to thetooth,allowing active guidance oftheimpacted tooth into
an ideal position.Important factors in this technique areprior orthodontic
treatment to provideadequate space within the dental arch forthe impacted tooth,and
anchorage.Manyappliances have been advocated,includingpolycarbonate crowns and pins
insertedinto the structure ofthe tooth.Both ofthese techniques are used rarely
because ofthe problems ofavailability ofbondedorthodontic brackets/buttons.Wires
placed around the cervical lineofthe tooth have been a common methodoforthodontic
guidance;however,thistechnique has been regarded as relativelyinvasive.A clinical
report in 1981 identi-fied external resorption as a possiblesequela ofthe wide
exposure at the cemen-toenamel junction (CEJ) that is necessaryfor placement ofa
cervical wire.23Thiscomplication was studied by Kohavi andcolleagues in 1984 in 23
patients who hadsurgical exposure and attachment ofa cer-vical wire to the
tooth.24The teeth wereseparated into two groups;one had �lightexposure�for
placement ofa band notexposing the CEJ,and the second had�heavy exposure�involving
the removal ofbone,complete removal ofthe follicularsac,and full exposure ofthe
CEJ.Thisstudy showed significantly more damagingeffects ofthe heavy exposure
technique,and the authors recommended avoidingexposure ofthe neck ofthe tooth
forplacement ofa cervical wire.24Although the use ofattachments suchas rare earth
magnets has been advised forthe movement ofteeth,the most commonmethod is the
placement ofa bondedorthodontic bracket.25This can usually bedone with a
conservative exposure ofthetooth,removing only enough soft tissueand bone to place
the bonded bracket,andavoiding exposure ofthe CEJ.9Studies have compared simple
expo-sure with packing to maintain a gingivalpath for eruption,with exposure
andbonding ofa bracket.Iramaneerat andcolleagues found that there was no differ-
ence in total orthodontic treatment timefor the two techniques.26Pearson and col-
leagues found that bracketing was morecostly and more likely to require reopera-
tion.27Nonetheless,placing a bracket isthe more popular technique,perhapsowing to
orthodontist preference andpatient comfort.For the most common type ofnon�third
molar impaction,the maxillarypalatal cuspid,the typical surgical exposureinvolves
reflection ofthe full-thicknesspalatal flap,conservative exposure ofthetooth,and
bonding ofa bracket to itspalatal surface (Figure 7-6).Ifthe tooth isnear the free
edge ofthe flap,soft tissuemay be removed to leave the crownexposed;the wound is
then packed gentlyduring the initial healing period.Ifthetooth is deeply
impacted,it may be moreappropriate to replace the soft tissue flap,bringing a wire
attached to the bondedbracket through the soft tissues near thecrest ofthe
ridge.The technique ofreplac-ing the flap has been examined for its peri-odontal
consequences.The clinical out-comes show minimal effects ofthe closederuption
technique on the periodontium.28Management ofthe cuspid that isimpacted on the
labial side follows thesame general principles as for the palatallyimpacted
cuspid.A position in the archmust be established by preliminary ortho-dontic
treatment prior to cuspid exposure.An additional important factor for thelabially
impacted cuspid is preservation ofattached mucosa adjacent to the cervicalline
ofthis tooth.Generally the mostappropriate technique is to begin with afull-
thickness mucoperiosteal flap to iden-tify the position ofthe impacted tooth.The
crown ofthe tooth is conservativelyuncovered,and a bonded bracket isattached;then
vertical releasing incisionsare made to provide a broadly based flapthat is
superiorly repositioned to cover theCEJ ofthe tooth.The bonded brackethelps to
support the attached gingiva inthis apical relationship (Figure 7-7).As theFIGURE7-
6A,Right maxillary canine isunerupted.B,Radiograph showing impactedcanine.C,Bracket
placed.Reproduced with per-mission from Zeitler D.Management ofimpact-ed teeth
other than third molars.Oral Maxillo-fac Surg Clin North Am 1993;5:95�103.ABC
Management ofImpacted Teeth Other than Third Molars135tooth is orthodontically
moved into posi-tion,an adequate band ofkeratinized gin-giva is present.Techniques
that involveremoval ofthe attached gingiva,leavingalveolar mucosa surrounding the
cervicalarea ofthe tooth,are to be avoided.These basic principles ofexposure
ofcanines can be generalized to many otherimpacted teeth.Exposure and orthodon-tic
attachment ofmaxillary and mandibu-lar bicuspids can be similar to those
formaxillary canines.Often mandibularbicuspids are located relatively centrally
inthe alveolar process.This may also be trueofmandibular molars.When this is
thecase,exposure from the coronal aspect ofthe tooth may be indicated.A
bondedbracket may be placed on the occlusal sur-face ofthe tooth and orthodontic
forcesapplied in a relatively vertical directionuntil the tooth is exposed
sufficiently toplace the orthodontic bracket in a moretraditional
position.UprightingSurgical uprighting ofteeth has beenapplied most commonly to
impactedmolars.Reynolds identifies several reasonsfor uprighting lower molar
teeth,includ-ing providing occlusion with opposingteeth and proximal contacts with
adjacentteeth,minimizing the risk ofcaries andperiodontal disease,and assisting
inorthodontic treatment.29Paleczny addsthat avoiding treatment ofunerupted
orsubmerged teeth may result in occlusaland periodontal problems for adjacentand
opposing teeth.30An important factor in the treatmentofimpacted molars is removal
ofthe thirdmolars that prevent the second molars�normal eruption (Figure 7-8).Ranta
stat-ed that it is typical for impacted secondmolars to erupt normally when
theoffending third molar is removed.13Although removal ofthe second molar toallow
eruption ofthe third molar into thesecond molar position may occasionallyhave a
satisfactory outcome in the maxilla,this is not likely to happen in
themandible.31Vig also recommends routineremoval ofthe third molar when a
secondmolar is impacted.32Consequently,surgical repositioningofimpacted mandibular
second molarteeth and occasionally first molars is theusual treatment
ofchoice.Whenimpaction ofa second molar is identified,consideration should be given
to correct-ing the impaction before the roots are fullyformed.31The optimal time
for uprightinga molar tooth is when two-thirds oftheroot has formed;molars with
fully formedroots have a poor prognosis.5The tech-nique for second molar uprighting
beginswith the removal ofthe third molar (Fig-ure 7-9).This generally creates the
neces-sary space for posterior tipping ofthe sec-ond molar.Ifno third molar is
present,itwill likely be necessary to remove boneposterior to the second
molar.Whendoing so,it is important to avoid damageto the CEJ ofthe second
molar.After ade-quate distal space is obtained,the secondmolar may be gently lifted
superiorly andposteriorly to clear the height ofcontact ofthe adjacent first
molar.Most second molars are relatively sta-ble after being lifted past the height
ofcontour ofthe first molar.Usually it isnot necessary to fix the tooth into posi-
tion (see Figure 7-9B).An extremelyFIGURE7-7Labially impacted canine
exposedimportant part ofthis surgical procedureusing an apically repositioned
flap.FIGURE7-8Third molar in path ofsecond molareruption.FIGURE7-9A,Impacted second
molar.B,Sec-ond molar lifted into position.C,Six-month fol-low-up radiograph
ofrepositioned second molar.ABC
136Part 2: Dentoalveolar Surgeryis ensuring that there are no occlusalforces on the
repositioned second molar.This generally does not require equilibra-tion on the
opposing tooth,but anocclusal adjustment can be performed ifnecessary.Antibiotics
are prescribed fol-lowing this procedure.An endodontic evaluation should
beperformed 3 weeks following the upright-ing ofthe tooth.When a tooth with
fullydeveloped roots is repositioned,endodon-tic treatment,ifindicated,should
beundertaken approximately 6 to 8 weeksfollowing the surgery.Radiographsshould be
taken at 6-month intervals for 2years to evaluate the postoperative course(see
Figure 7-9C).31TransplantationTransplantation ofteeth has been advocat-ed as an
alternative to other methods oftreatment ofimpacted teeth.It may beappropriate for
the adult patient who can-not undergo conventional orthodonticmovement ofa canine
or premolar.Sagneand Thilander studied 47 patients with 56canines that were
surgically transplanted.33The advocated technique is a careful wideexposure ofthe
impacted tooth.The toothis then moved into its position within thedental arch and
stabilized with a segmentalorthodontic appliance.Endodontic treat-ment begins with
calcium hydroxide paste6 to 8 weeks after the surgical procedure.Conventional root
canal filling is per-formed at 1 year following surgery.Thisstudy showed a
successful outcome in 54 of56 transplanted canines.Their concludingrecommendation
is to perform conven-tional orthodontic treatment for impactedcanines in children
and young individuals.However,when extraction would other-wise be performed,they
recommendtransalveolar transplantation as a soundalternative (Figure 7-
10).33RemovalSurgical removal ofimpacted permanentteeth may be performed when other
meth-ods oftreatment are unavailable.Basicsurgical principles ofradiographic
assess-ment and careful surgical technique mustbe followed.Conservation
ofbonethrough conservative exposure andremoval with sectioning ofthe toothshould be
considered.Impacted caninesshould be approached from the surface ofthe maxilla with
which they are mostclosely associated.Labially impactedcanines are frequently
removed with anelevator technique,but palatal caninesgenerally require removal
ofthe crownfollowed by sectioning ofthe root.Longi-tudinal sectioning ofthe root
ofthe palatalcanine often is useful and may conservebone.When a large palatal flap
has beenreflected,maintaining a palatal splint tosupport the soft tissues for
several daysprevents hematoma formation.Impacted maxillary bicuspids may beremoved
much like canines.Mandibularbicuspids are generally approached fromthe labial
surface ofthe mandible.Caremust be taken to preserve the integrity ofthe mental
nerve when the impacted toothis nearby.When the impacted lower bicus-pid is
lingually positioned,it is sometimesuseful to identify the tooth through a lin-gual
exposure;a labial flap then may beraised and a small hole placed in the
labialsurface ofthe bone to allow the bicuspidto be pushed through to the
lingual.Removal ofimpacted molars is similar toremoval ofimpacted third
molars.SummaryImpacted teeth other than third molars arerelatively common
findings.Much can bedone to preserve these teeth and allowtheir functional
positioning within thedental arch.Surgical exposure with orwithout orthodontic
guidance,surgicaluprighting,and transplantation ofteethare valuable techniques that
can be mas-tered by oral and maxillofacial surgeons.Although some studies have
indicated thatroutine removal ofimpacted teeth is notnecessary,removal is indicated
in manydifferent situations.FIGURE7-10A,Geminated tooth no.8.B,After removal
ofabnormal tooth no.8and transplantation oferupted tooth no.9,the unerupted tooth
no.9 is expected toerupt.C,Radiograph ofgeminated tooth no.8.D,Radiograph
ofduplicated tooth no.9.ABCD
Management ofImpacted Teeth Other than Third Molars137References1.Grover PS,Lorton
L.The incidence ofunerupted permanent teeth and relatedclinical cases.Oral Surg
Oral Med OralPathol 1985;59:420�5.2.Thilander B,Myrberg N.The prevalence
ofmalocclusion in Swedish schoolchildren.Scand J Dent Res 1973;81:12�20.3.Dachi
SF,Howell FV.A survey of3,874 routinefull-mouth radiographs:II.A study ofimpacted
teeth.Oral Surg Oral Med OralPathol 1961;14:1165�9.4.Grondahl AM.Prevalence
ofimpacted teethand associated pathology in middle-agedand older Swedish
women.CommunityDent Oral Epidemiol 1991;19:116�9.5.Raghoebar GM,Boering G,Vissink
A,Stegen-ga B.Eruption disturbances ofpermanentmolars:a review.J Oral Pathol Med
1991;20:159�66.6.Bianchi SD,Roccuzzo M.Primary impaction ofprimary teeth:a review
and report ofthreecases.J Clin Pediatr Dent 1991;15:165�8.7.Ostuka Y,Mitomi
T,Tomizawa M,Noda T.Areview ofclinical features in 13 cases ofimpacted primary
teeth.Int J Paediatr Dent2001;11:57�63.8.American Association ofOral and Maxillofa-
cial Surgery.Impacted teeth.Oral Health1998;88:31�2.9.Bishara SE.Impacted maxillary
canines:areview.Am J Orthod Dentofacial Orthop1992;101:159�71.10.Levy I,Regan
D.Impaction ofmaxillary per-manent second molars by the third molars.J Paediatr
Dent 1989;5:31�4.11.Jacoby H.The etiology ofmaxillary canineimpaction.Am J Orthod
1983;84:125�32.12.Moyres RE.Handbook oforthodontics.4th ed.Chicago:Year Book
Medical Publishers;1988.p.387.13.Ranta R.Impacted maxillary second perma-nent
molars.J Dent Child 1985;52:48�51.14.Ericson S,Kurol J.Radiographic assessment
ofmaxillary canine eruption in children withclinical signs oferuption
disturbance.Eur JOrthod 1986;8:133�40.15.Ericson S,Kurol J.Radiographic examination
ofectopically erupting maxillary canines.Am JOrthod Dentofacial Orthop
1987;91:483�92.16.Bodner L,Bar-Ziv J,Becker A.Image accuracy ofplain film
radiography and computerizedtomography in assessing morphologicalabnormality
ofimpacted teeth.Am J OrthodDentofacial Orthop 2001;120:623�8.17.Langland OE,Sippy
FH,Langlais RP.Textbookofdental radiology.2nd ed.Springfield(IL):Charles C
Thomas;1973.18.Chaushu S,Chaushu G,Becker A.The use ofpanoramic radiographs to
localize dis-placed maxillary canines.Oral Surg OralMed Oral Pathol Oral Radiol
Endod1999;88:511�6.19.Mason C,Papadakou P,Roberts GJ.The radi-ographic localization
ofimpacted maxillarycanines:a comparison ofmethods.Eur JOrthod
2001;23:25�34.20.�hman I,�hman A.The eruption tendencyand changes ofdirection
ofimpacted teethfollowing surgical exposure.Oral Surg OralMed Oral Pathol
1980;49:383�9.21.Thilander B,Thilander H.Impacted premolars.In:Transactions ofthe
European Ortho-dontic Society.Gothenburg,Sweden:Euro-pean Orthodontic
Society;1976.p.167�75.22.Laskin DM,Peskin S.Surgical aids in orthodon-tics.Dent
Clin North Am 1968;July:509�24.23.Shapiro Y,Katine MM.Treatment
ofimpactedcuspids:the hazard lasso.Angle Orthod1981;51:203�7.24.Kohavi D,Becker
A,Silverman Y.Surgicalexposure,orthodontic movement,and finaltooth position as
factors in periodontalbreakdown oftreated palatally impactedcanines.Am J Orthod
1984;85:72�7.25.Vardimon AD,Graber TM,Drescher D,Bourauel C.Rare earth magnets
andimpaction.Am J Orthod DentofacialOrthop 1991;100:494�512.26.Iramaneerat
S,Cunningham S,Horrocks E.The effect oftwo alternative methods ofcanine exposure
upon subsequent durationoforthodontic treatment.Int J PaediatrDent
1998;8:123�9.27.Pearson MH,Robinson SN,Reed R,et al.Man-agement ofpalatally
impacted canines:thefindings ofa collaborative study.Eur JOrthod
1997;19:511�5.28.Becker A,Brim I,Ben-Basset Y,et al.Closederuption surgical
technique for impactedmaxillary incisors:a post-orthodontic peri-odontal
evaluation.Am J Orthod Dentofa-cial Orthop 2002;122:9�14.29.Reynolds LM.Uprighting
lower molar teeth.Br J Orthod 1976;3:45�51.30.Paleczny G.Treatment ofthe
ankylosedmandibular permanent first molar:a casestudy.J Can Dent Assoc
1991;57:717�9.31.Johnson JV,Quirk GP.Surgical repositioningofimpacted mandibular
second molarteeth:case report.Am J Orthod DentofacialOrthop 1987;91:242�51.32.Vig
KW.Some methods ofuprighting lower sec-ond molars�II.Br J Orthod
1976;3:39�44.33.Sagne S,Thilander B.Transalveolar transplan-tation ofmaxillary
canines.A follow-upstudy.Eur J Orthod 1990;12:140�7.
CHAPTER 8Impacted TeethGregory M.Ness,DDSLarry J.Peterson,DDS,MS�Removal ofimpacted
teeth is one ofthemost common surgical procedures per-formed by oral and
maxillofacial sur-geons,and most surgeons cite thirdmolar removal as the operation
mostlikely to humble them.Extensive training,skill,and experience are necessary to
per-form this procedure with minimal trau-ma.When the surgeon is untrainedand/or
inexperienced,the incidence ofcomplications rises significantly.1�3Determining the
need for removal ofasymptomatic teeth is no less problemat-ic.In many situations
this decision ismade based on clinical experience andprofessional judgment;in
others thedecision is clear cut based on availablescientific data.Contemporary
medicaland dental practices demand evidence-based decision-making,and the surgeonis
called on more and more frequently tojustify surgical procedures,including
theremoval ofthird molars.This chapter reviews and discussesthe indications and
contraindications forthe removal ofimpacted teeth,the classi-fication ofimpacted
teeth and the deter-mination ofthe degree ofdifficulty ofsurgery,the parameters
ofperioperativepatient care,and the likely complicationsand their management
following thirdmolar surgery.Development ofthe MandibularThird MolarThe mandibular
third molar is the mostcommonly impacted tooth.It also presentsthe greatest
surgical challenge and invitesthe greatest controversy when indicationsfor removal
are considered.When the sur-geon is determining whether a specificthird molar will
become impacted andwhether it should be removed,he or sheneeds to have a clear
understanding ofthedevelopment and movement ofthe thirdmolar between the ages of7
and 25 years.A number oflongitudinal studieshave clearly defined the development
anderuption pattern ofthe third molar.4�7The mandibular third molar tooth germ
isusually visible radiographically by age 9 years,and cusp mineralization is com-
pleted approximately 2 years later.At age11 years,the tooth is located within
theanterior border ofthe ramus with itsocclusal surface facing almost
directlyanteriorly.The level ofthe tooth germ isapproximately at the occlusal plane
oftheerupted dentition.Crown formation isusually complete by age 14 years,and
theroots are approximately 50% formed byage 16 years.During this time the body
ofthe mandible grows in length at theexpense ofresorption ofthe anterior bor-der
ofthe ramus.As this process occursthe position ofthe third molar relative tothe
adjacent teeth changes,with the thirdmolar assuming a position at approxi-mately
the root level ofthe adjacent sec-ond molar.The angulation ofthe crownbecomes more
horizontal also.Usually theroots are completely formed with an openapex by age 18
years.By age 24 years 95%ofall third molars that will erupt havecompleted their
eruption.The change in orientation oftheocclusal surface from a straight
anteriorinclination to a straight vertical inclina-tion occurs primarily during
root forma-tion.During this time the tooth rotatesfrom horizontal to mesioangular
to verti-cal.Therefore,the normal developmentand eruption pattern,assuming the
toothhas sufficient room to erupt,brings thetooth into its final position by age 20
years.Most third molars do not follow thistypical eruption sequence
and,instead,become impacted teeth.Approximately halfdo not assume the vertical
position andremain as mesioangular impactions.Thereare several possible
explanations for this.The Belfast Study Group claims that theremay be differential
root growth between themesial and distal roots,which causes thetooth to either
remain mesially inclined orrotate to a vertical position depending onthe amount
ofroot development.7,8In theirstudies they have found that underdevelop-ment ofthe
mesial root results in amesioangular impaction.Overdevelopmentofthe same root
results in over-rotation�Deceased.ofthe third molar into a distoangular
140Part 2: Dentoalveolar Surgeryimpaction.Overdevelopment ofthe distalroot,commonly
with a mesial curve,isresponsible for severe mesioangular or hor-izontal
impaction.The Belfast Group hasnoted that,whereas the expected normalrotation is
from horizontal to mesioangularto vertical,failure ofrotation from themesioangular
to the vertical position is alsocommon.To a lesser extent,they docu-mented
worsening ofthe angulation frommesioangular to horizontal impaction andover-
rotation from mesioangular to dis-toangular.These over-rotations frommesioangular
to horizontal and frommesioangular to distoangular occur duringthe terminal portion
ofroot development.A second major reason for the failureofthe third molar to rotate
into a verticalposition and erupt involves the relation ofthe bony arch length to
the sum ofthemesiodistal widths ofthe teeth in the arch.Several studies have
demonstrated thatwhen there is inadequate bony length,there is a higher proportion
ofimpactedteeth.6,9,10In general,patients with impact-ed teeth almost invariably
have larger-sized teeth than do those withoutimpactions.10Even when the tooth-
bonerelationship is favorable,a lower thirdmolar that is positioned lateral to the
nor-mal position almost always fails to erupt.6This may also be the result ofthe
densebone present in the external oblique ridge.A final factor that seems to be
associ-ated with an increased incidence oftoothimpaction is retarded maturation
ofthethird molar.When dental development ofthe tooth lags behind the skeletal
growthand maturation ofthe jaws,there is anincreased incidence ofimpaction.This
ismost likely a result ofa decreased influ-ence ofthe tooth on the growth
patternand resorption ofthe mandible.This phe-nomenon results in the rather
counterin-tuitive observation that in a 20-year-old,an impacted third molar with
partiallydeveloped roots is less likely to erupt thana similarly positioned tooth
with fullydeveloped roots.Impacted versus Unerupted TeethNot all unerupted teeth
are impacted.Atooth is considered impacted when it hasfailed to fully erupt into
the oral cavitywithin its expected developmental timeperiod and can no longer
reasonably beexpected to do so.Consequently,diagnos-ing an impaction demands a
clear under-standing ofthe usual chronology oferup-tion,as well the factors that
influenceeruption potential.It is important to remember thateruption oflower third
molars is completeat the average age of20 years but that itcan occur up to age 24
years.A tooth thatappears impacted at age 18 years may haveas much as a 30 to 50%
chance oferuptingfully by age 25 years,according to severallongitudinal
studies.11�13 It is fairly wellestablished that the position ofretainedthird molars
does not change substantiallyafter age 25 years,14although there is someevidence
ofcontinued movement as late asthe fourth decade.11Many patients areevaluated for
third molar removal in theirlate teens,and the surgeon must thereforeattempt to
discern the probable outcomeofthe eruption process based on morethan tooth position
alone.Numerous studies have evaluated theinfluence ofvarious factors on the erup-
tion potential ofa lower third molar.Twofactors consistently emerge as most prog-
nostic:angulation ofthe third molar andspace available for its emergence.15�19Byage
18 to 20 years,lower third molars thatare horizontal or strongly mesioangularhave
much less eruption potential than dothose that are oriented more
vertically.Distoangular teeth are intermediate intheir likelihood to erupt
fully.However,the strongest hope offuture eruption lieswith those third molars that
can be seenradiographically to have space at least aswide as their crown between
the distal ofthe second molar and the ascendingmandibular ramus.At age 20
years,unerupted lower third molars that arenearly vertical and have adequate
horizon-tal space are more likely to erupt than toremain impacted.However,ifthe
crown-to-space ratio is > 1 or ifthe tooth orien-tation diverges substantially from
vertical,the tooth is unlikely ever to erupt fully.Indications for Removal
ofanImpacted ToothAn impacted tooth can cause the patientmild to serious problems
ifit remains inthe unerupted state.Not every impactedtooth causes a problem
ofclinical signif-icance,but each does have that potential.A body ofinformation has
been collect-ed based on extensive clinical experienceand clinical studies from
which indica-tions for removal ofimpacted teeth havebeen developed.For some
indications,there is lack ofevidence-based datagained from long-term prospective
lon-gitudinal studies.Pericoronitis Prevention orTreatmentWhen a third
molar,usually the mandibu-lar third molar,partially erupts throughthe oral
mucosa,the potential for theestablishment ofa mild to moderateinflammatory response
similar to gingivi-tis and periodontitis exists.In certain situ-ations the patient
may actually experiencea severe infection,which may require vig-orous medical and
surgical treatment.Thebacteria that are most commonly associat-ed with
pericoronitis are Peptostreptococ-cus,Fusobacterium,and Bacteroides (Por-
phyromonas).20�22 Initial treatment ofpericoronitis is usually aimed at d�bride-
ment ofthe periodontal pocket by irriga-tion or by mechanical
means,disinfectionofthe pocket with an irrigation solutionsuch as hydrogen peroxide
or chlorhexi-dine,and surgical management by extrac-tion ofthe opposing maxillary
third molarand,occasionally,ofthe offendingmandibular third molar.Severe cases
ofpericoronitis with systemic symptomsmay warrant antibiotic therapy.
Impacted Teeth141Prevention ofrecurrent pericoronitisis usually achieved by removal
oftheinvolved mandibular third molar.Although operculectomy has been recom-mended
for management ofthis problem,the soft tissue redundancy usually recursowing to the
relationship between theanterior border ofthe ramus and the fullyor partially
erupted mandibular thirdmolar.Pericoronitis can occur wheneverthe involved tooth is
partially exposedthrough the mucosa,but it occurs mostcommonly around mandibular
thirdmolars that have soft or hard tissue lyingover the posterior aspect ofthe
crown.23Approximately 25 to 30% ofimpactedmandibular third molars are
extractedbecause ofpericoronitis or recurrent peri-coronitis.14,24�27 Pericoronitis
is the mostcommon reason for removal ofimpactedthird molars after age 20
years.Withincreasing age,the incidence ofpericoro-nitis as an indication for
removal ofimpacted teeth also increases.Prevention ofDental DiseaseDental caries
can occur in the mandibularthird molar or in the adjacent secondmolar,most commonly
at the cervical line.Owing to the patient�s inability to effec-tively clean this
area and because the thirdmolar is inaccessible to the restorativedentist,caries in
the second and thirdmolars are responsible for extraction ofimpacted third molars
in approximately15% ofpatients.14,24�27As with pericoroni-tis,the presence ofcaries
and eventual pul-pal necrosis are responsible for an increas-ing percentage
ofextractions with age.The presence ofthe partially impactedthird molar and the
patient�s inability toclean the area thoroughly may result in earlyadvanced
periodontal disease.This is theprimary reason for removal ofapproxi-mately 5%
ofimpacted third molars.14,24�27Even young patients in otherwise good gen-eral
periodontal health have a significantincrease in periodontal pocketing,attach-ment
loss,pathogen activity,and inflamma-tory markers at the distal ofthe secondmolar
and around the third molar.28�30 Inpatients whose dental health is poor andwho have
partially erupted third molars,theperiodontal condition around the secondmolar and
partially erupted third molar canbecome extremely severe at an early
age.Orthodontic ConsiderationsThe presence ofthe impacted third molar,especially in
the mandible,may be respon-sible for several orthodontic problems.These problems
fall into three generalareas,which are outlined below.Crowding ofMandibular
IncisorsPer-haps one ofthe most controversial issuesregarding mandibular third
molars hasbeen the issue oftheir influence on anteri-or crowding ofmandibular
incisor teeth,especially after orthodontic therapy.Avariety ofstudies have been
reported thatsupport both sides ofthe controversy.Many ofthese studies have been
reviews ofsmall numbers ofpatients or ofanecdotalinformation.31,32More recent
literatureincludes longitudinal reviews ofortho-dontically treated patients in
larger num-bers,33,34and the preponderance ofevi-dence now suggests that impacted
thirdmolars are not a significant cause ofpost-orthodontic anterior crowding.In
fact,anterior incisor crowding is associatedwith deficient arch length rather than
themere presence ofimpacted teeth.Obstruction ofOrthodontic TreatmentIn some
situations the orthodontistattempts to move the molar teeth distally,but the
presence ofan impacted thirdmolar may inhibit or even prevent
thisprocedure.Therefore,ifthe orthodontistis attempting to move the buccal
segmentsposteriorly,removal ofthe impacted thirdmolar may facilitate treatment and
allowpredictable outcomes.Interference with Orthognathic SurgeryWhen maxillary or
mandibular osteotomiesare planned,presurgical removal oftheimpacted teeth may
facilitate the orthog-nathic procedure.Delaying removal ofthirdmolars until
mandibular osteotomy,espe-cially in mandibular advancement surgery,substantially
reduces the thickness andquality oflingual bone at the proximalaspect ofthe distal
segment,where fixationscrews are usually applied.Ifthird molarsare to be removed in
advance,sufficienttime must be allowed for the extraction siteto fill with mature
bone.On the other hand,following maxillary down-fracture a deeplyimpacted upper
third molar is often easilyapproached superiorly through the maxil-lary sinus and
may be safely removed in thismanner without compromising the soft tis-sue vascular
pedicle ofthe maxilla.Although these circumstances involve asmall percentage ofall
impacted thirdmolars,the surgeon must plan well inadvance (6�12 mo) for patients
undergoingthese procedures.Prevention ofOdontogenic Cysts and TumorsIn the impacted
third molar that is leftintact in the jaw,the follicular sac that wasresponsible
for the formation ofthe crownmay undergo cystic degeneration andform a dentigerous
cyst.The follicular sacmay also develop an odontogenic tumoror,in quite rare
cases,a malignancy.Thesepossibilities have frequently been cited as areason for
removal ofasymptomatic teeth;although rare,when pathology occurs,itmay pose a
serious health threat.35Thegeneral incidence ofneoplastic changearound impacted
molars has been estimat-ed to be about 3%.36,37In retrospectivesurveys oflarge
numbers ofpatients,between 1 and 2% ofall third molars thatare extracted are
removed because ofthepresence ofodontogenic cysts andtumors.14,24�27These
pathologic entitiesare usually seen in patients under age 40 years,suggesting that
the risk ofneo-plastic change around impacted thirdmolars may decrease with age.
142Part 2: Dentoalveolar SurgeryRoot Resorption ofAdjacent TeethThird molars in the
process oferuptionmay cause root resorption ofadjacentteeth.The general view is
that misalignederupting teeth may resorb the roots ofadja-cent teeth,just as
succedaneous teeth resorbthe roots ofprimary teeth during their nor-mal eruption
sequence.The actual occur-rence ofsignificant root resorption ofadja-cent teeth is
not clear,although it may be ashigh as 7%.38Ifroot resorption is noted onadjacent
teeth,the surgeon should considerremoving the third molar as soon as it
isconvenient.In most cases the adjacenttooth repairs itselfwith the deposition
ofalayer ofcementum over the resorbed areaand the formation ofsecondary
dentin.However,ifresorption is severe and themandibular third molar displaces
signifi-cantly into the roots ofthe second molar,both teeth may require
removal.Teeth under Dental ProsthesesBefore construction ofa removable orfixed
prosthesis,the dentist should makesure that there are no impacted teeth inthe
edentulous area that is being restored.Ifsuch teeth are present,the general rec-
ommendation is that they be removedbefore the final placement ofthe prosthe-
sis.Teeth that are completely covered withbone,that show no pathologic changes,and
that are in patients more than 40 yearsold are unlikely to develop problems ontheir
own.However,ifa removable tissue-borne prosthesis is to be constructed on aridge
where an impacted tooth is coveredby only soft tissue or 1 or 2 mm ofbone,itis
highly likely that in time the overlyingbone will be resorbed,the mucosa
willperforate,and the area will become painfuland often inflamed.Ifthis
occurs,theimpacted tooth will often need to beremoved and the dental prosthesis
eitheraltered or refabricated.Each situation must be viewed individ-ually,and the
risks and benefits ofremov-ing the impacted tooth must be given care-ful
consideration.In older patients withtooth- or implant-borne fixed
prostheses,asymptomatic deeply impacted teeth can besafely left in
place.However,ifa removableprosthesis is to be made and the bone over-lying the
impacted tooth is thin,the toothshould probably be removed before thefinal
prosthesis is constructed.Prevention ofJaw FracturePatients who engage in contact
sports,such as football,rugby,martial arts,andsome so-called noncontact sports such
asbasketball,should consider having theirimpacted third molars removed to
preventjaw fracture during competition.Animpacted third molar presents an area
oflowered resistance to fracture in themandible and is therefore a common sitefor
fracture.39�41 Additionally,the presenceofan impacted third molar in the line
offracture may cause increased complica-tions in the treatment ofthe
fracture.Management ofUnexplained PainOccasionally patients complain ofjawpain in
the area ofan impacted thirdmolar that has neither clinical nor radi-ographic signs
ofpathology.In these situ-ations removal ofthe impacted thirdmolar frequently
results in resolution ofthis pain.At this time there is no plausibleexplanation as
to why this reliefofpainoccurs.Approximately 1 to 2% ofmandibular third molars that
are extractedare removed for this reason.14,24�27When a patient presents with this
typeofcomplaint,the surgeon must make surethat all other sources ofpain are ruled
outbefore suggesting surgical removal ofthethird molar.In addition,the patient
mustbe informed that removal ofthe thirdmolar may not relieve the pain
completely.SummaryThe preceding discussion has dealt withthe indications for
removal ofsympto-matic impacted third molars.Most clini-cians agree that ifa
patient presents withone or more ofthe above pathologic prob-lems or symptoms,the
involved teethshould be removed.It is much less clearwhat should be done
prophylactically withteeth that are impacted before they causethese problems.Most
ofthe symptomaticpathologic problems that result from thirdmolars occur as a result
ofa partiallyerupted tooth.There is a lower incidenceofproblems associated with a
completebony impaction.Contradictions for Removal ofImpacted TeethThe decision to
remove a given impactedtooth must be based on a careful evalua-tion ofthe potential
benefits versus risks.In situations in which pathology exists,thedecision to remove
the tooth is uncompli-cated because it is necessary to treat thedisease
process.Likewise,there are situa-tions in which removal ofimpacted teethis
contraindicated because the surgicalcomplications and sequelae outweigh
thepotential benefits.The general contraindi-cations for removal ofimpacted teeth
canbe grouped into three primary areas:advanced patient age,poor health,andsurgical
damage to adjacent structures.42Extremes ofAgeHealing generally occurs more rapidly
andmore completely in younger patients;however,surgical removal ofuneruptedthird
molars in the very young is con-traindicated.Although some cliniciansreport that
removal ofthe tooth bud ofthedeveloping third molar at age 8 or 9 yearscan be
accomplished with minimal surgi-cal morbidity,43the general consensus isthat this
is not a prudent approach.Theoriginal view was based on the beliefthataccurate
growth predictions could bemade and,therefore,that an accuratedetermination could
be establishedregarding whether a given tooth would beimpacted.Ifsuch a
determination were thecase,then the tooth bud could be removed
Impacted Teeth143relatively atraumatically in the very youngpatient.The evidence at
this time,howev-er,is contradictory to that opinion,andthe general consensus is
that removal ofthe tooth bud at this stage may,in fact,beunnecessary because the
involved thirdmolar may erupt into proper position.As a patient becomes older there
isdecreased healing response,44which mayresult in a greater bony defect postopera-
tively than was present because oftheimpacted tooth.Additionally,the
surgicalprocedure grows more and more difficultas the patient ages owing to more
denselycalcified bone,which is less flexible andmore likely to fracture.As a
patient ages,the response to surgical insult is toleratedless easily and the
recuperation periodgrows longer.There is overwhelming clin-ical evidence to support
the fact that thenumber ofdays missed from work andother normal activity following
thirdmolar extraction is much higher in thepatient over age 40 years compared
withpatients under age 18 years.As a general rule,ifa patient has a fullyimpacted
third molar that is completelycovered with bone,has no obvious potentialsource
ofcommunication with the oral cav-ity,and has no signs ofpathology such as
anenlarged follicular sac,and ifthe patient isover age 40,the tooth probably should
notbe removed.Long-term follow-up by thepatient�s dentist should be performed peri-
odically,with radiography performed everyseveral years to ensure that no
adversesequelae are occurring.Ifsigns ofpathologydevelop,the tooth should be
removed.Iftheoverlying bone is very thin and a removabledenture is to be placed
over that tooth,thetooth should probably be removed beforethe final prosthesis is
constructed.Compromised Medical StatusPatients who have impacted teeth mayhave some
compromise in their health sta-tus,especially ifthey are elderly.As ageincreases,so
does the incidence ofmoder-ate to severe cardiovascular disease,pul-monary
disease,and other health prob-lems.Thus,the combination ofadvancedage and
compromised health status maycontraindicate the removal ofimpactedteeth that have
no pathologic processes.Other factors may compromise thehealth status ofyounger
people,such ascongenital coagulopathies,asthma,andepilepsy.In this group
ofpatients,it maybe necessary to remove impacted teethbefore the incipient
pathologic processbecomes fulminant.Thus,not only in theolder compromised patient
but also theyounger compromised patient,the sur-geon occasionally needs to remove
symp-tomatic as well as asymptomatic thirdmolars.The compromised medical
statusbecomes a relative contraindication andmay require the surgeon to work
closelywith the patient�s physician to manage thepatient�s medical
problems.Surgical Damage to Adjacent StructuresOccasionally an impacted tooth is
posi-tioned such that its removal may seriouslycompromise adjacent
nerves,teeth,andother vital structures (eg,sinus),making itprudent to leave the
impacted tooth insitu.The potential complications must beweighed against the
potential benefits ofsurgical removal ofthe tooth.When fullydeveloped,totally bone-
impacted thirdmolars are present around the inferioralveolar nerve;it may be best
to leave thatimpacted tooth in place and not risk per-manent anesthesia ofthe
inferior alveolarnerve.In such situations the potential riskofdevelopment
ofpathologic problemswould be relatively small,and,therefore,the advantage
ofremoval ofsuch a toothwould not outweigh the potential risks.Surgical extraction
ofimpacted thirdmolars can result in significant bonydefects that may not heal
adequately inolder patients and,in fact,may result inthe loss ofadjacent teeth
rather than theimprovement or preservation ofperi-odontal health.This also would be
viewedas a contraindication to removal oftheimpacted tooth.Surgery and
Perioperative CareDetermining Surgical DifficultyPreoperative evaluation ofthe
third molar,both clinically and radiographically,is acritical step in the surgical
procedure forremoval ofimpacted teeth.The surgeonpays particular attention to the
variety offactors known to make the impactionsurgery more or less difficult.A
variety ofclassification systems have been developedto aid in the determination
ofdifficulty.The three most widely used are angulationofthe impacted tooth,the
relationship ofthe impacted tooth to the anterior borderofthe ramus and the second
molar,andthe depth ofthe impaction and the type oftissue overlying the impacted
tooth.It is generally acknowledged that themesioangular impaction,which accountsfor
approximately 45% ofall impactedmandibular third molars,is the least diffi-cult to
remove.The vertical impaction(40% ofall impactions) and the horizon-tal impaction
(10%) are intermediate indifficulty,whereas the distoangularimpaction (5%) is the
most difficult.The relationship ofthe impactedtooth to the anterior border ofthe
ramusis a reflection ofthe amount ofroomavailable for the tooth eruption as well
asthe planned extraction.Ifthe length ofthealveolar process anterior to the
anteriorborder ofthe ramus is sufficient to allowtooth eruption,the tooth is
generally lessdifficult to remove.Conversely,teeth thatare essentially buried in
the ramus ofthemandible are more difficult to remove.The depth ofthe impaction
under thehard and soft tissues is likewise an importantconsideration in determining
the degree ofdifficulty.The most commonly used schemefor determining difficulty
involves consider-ation ofthe soft tissues and partial or com-plete bony
impaction.It is widely employedin part because it may be the most useful
144Part 2: Dentoalveolar Surgeryindicator ofthe time required for
surgeryand,perhaps even more importantly,because it is the system required to
classifyand code impaction procedures to all com-mercial insurance
carriers.Surprisingly,fac-tors such as the angulation ofimpaction,therelationship
ofthe tooth to the anterior bor-der ofthe ramus,and the root morphologymay have
little influence on the time thatsurgery requires.45Other factors have been
implicated inmaking the extraction process more diffi-cult.Roots can be either
conical and fusedroots or separate and divergent,with thelatter being more
difficult to manage.Alarge follicular sac around the crown ofthetooth provides more
room for access tothe tooth,making it less difficult to extractthan one with
essentially no space aroundthe crown ofthe tooth.Another important determinant
ofdifficulty ofextraction is the age ofthepatient.When impacted teeth areremoved
before age 20 years,the surgeryis almost always less difficult to perform.The roots
are usually incompletelyformed and thus less bone removal isrequired for tooth
extraction.There isusually a broader pericoronal spaceformed by the follicle ofthe
tooth,whichprovides additional access for toothextraction without bone
removal.Becausethe roots ofthe impacted teeth are incom-pletely formed,they are
usually separatedfrom the inferior alveolar nerve.In contradistinction,removal
ofimpacted teeth in patients ofolder agegroups is almost always more
difficult.Theroots are usually completely formed andare thus longer,which requires
more boneremoval,and closer to the inferior alveolarcanal,which increases the risk
ofpostsur-gical anesthesia and paresthesia.The fol-licular sac almost always
degenerates withage,which makes the pericoronal spacethinner;as a result,more bone
must beremoved for access to the crown ofthetooth.Finally,there is increasing
densityand decreasing elasticity in the bone,necessitating greater bone removal
todeliver the tooth from its socket.In summary,the degree ofdifficulty ofthe
surgery to remove an impacted tooth isdetermined primarily by two major fac-tors:
(1) the depth ofimpaction and typeofoverlying tissue and (2) the age
ofthepatient.Full bony impactions are alwaysmore difficult to remove than are soft
tis-sue impactions and,given two impactionsofthe same depth,the impaction in
theolder patient is always more difficult thanthe one in the younger patient.A
corollary ofsurgical difficulty is dif-ficulty ofrecovery from the surgery.As
ageneral rule,a more challenging and time-consuming surgical procedure results in
amore troublesome and prolonged postop-erative recovery.It is more difficult to
per-form surgery in the older individual,and itis harder for these patients to
recover fromthe surgical procedure.Technique The technique for removal
ofimpactedthird molars is one that must be learnedon a theoretic basis and then
performedrepeatedly to gain adequate experience.There is more variety in
presentation ofthe surgical situation ofimpacted thirdmolars than in any other
dental surgicalprocedure.Therefore,extensive experienceis required to master their
removal.A vari-ety oftextbooks are available that describein detail the technique
for removal ofthedifferent types ofimpactions.46,47In general,the surgeon�s
approachmust gain adequate access to the underly-ing bone and tooth through a
properlydesigned and reflected soft tissue flap.Bone must be removed in an
atraumatic,aseptic,and non�heat-producing tech-nique,with as little bone removed
anddamaged as possible.The tooth is thendivided into sections and delivered
withelevators,using judicious amounts offorceto prevent
complications.Finally,thewound must be thoroughly d�bridedmechanically and by
irrigation to providethe best possible healing environment inthe postoperative
period.The initial step in removing impactedteeth is to reflect a mucoperiosteal
flap,which is adequate in size to permit access.The most commonly used flap is the
enve-lope flap,which extends from just posteri-or to the position ofthe impacted
toothanteriorly to approximately the level ofthefirst molar (Figure 8-1A and
B).Ifthe sur-geon requires greater access to remove adeeply impacted tooth,the
envelope flapmay not be sufficient.In that case,a releaseincision is done on the
anterior aspect ofthe incision,creating a three-cornered flap(Figure 8-1C and
D).The envelope inci-sion is usually associated with fewer com-plications and tends
to heal more rapidlyand with less pain than the three-corneredflap.The buccal
artery is sometimesencountered when creating the releasingincision,and this may be
bothersome dur-ing the early portion ofthe surgery.The posterior extension ofthe
inci-sion must extend to the lateral aspect ofthe anterior border ofthe
mandibularramus.The incision should not continueposteriorly in a straight line
because themandibular ramus diverges laterally.Iftheincision were to be extended
straight,theblade might damage the lingual nerve.High-resolution magnetic
resonanceimaging has demonstrated that the lingualnerve may be intimately
associated withthe lingual cortical plate in the third molarregion in 25% ofcases
and be above thelingual crest in 10%.48The mucoperiostealflap is reflected
laterally to the externaloblique ridge with a periosteal elevatorand held in this
position with a retractorsuch as an Austin or Minnesota.The most commonly used
incisionused for the maxillary third molar is alsoan envelope incision (Figure 8-2A
and B).It extends posteriorly from the distobuccalline angle ofthe second molar and
anteri-orly to the first molar.A releasing incisionis rarely necessary for the
maxillary thirdmolar (Figure 8-2C and D),although it
Impacted Teeth145may be useful when the occlusal surface ofthe third molar is at or
superior to themidportion ofthe second molar root.The second major step is bone
removalfrom around the impacted tooth.Mostsurgeons use a high-speed low-torque air-
driven handpiece,although a few surgeonsstill choose to use a chisel for
boneremoval.The most recent advance is therelatively high-speed high-torque
electricdrill,which has some significant advan-tages in reducing the time required
forbone removal and tooth sectioning.It isessential that the handpiece exhaust the
airpressure away from the surgical site to pre-vent tissue emphysema or air
embolism,and that the handpiece can be sterilizedcompletely,usually in a steam
autoclave.The bone on the occlusal,buccal,andcautiously on the distal aspects
oftheimpacted tooth is removed down to thecervical line.The amount ofbone thatmust
be removed varies with the depth ofthe impaction.It is advisable not toremove any
bone on the lingual aspectbecause ofthe likelihood ofdamage to thelingual nerve
(Figure 8-3).A variety ofburs can be used to remove bone,but themost commonly used
are the no.8 roundbur and the 703 fissure bur.For maxillary teeth,bone removal
isdone primarily on the lateral aspect ofthetooth down to the cervical line to
expose theentire clinical crown.Frequently,the boneon the buccal aspect is thin
enough that itcan be removed with a periosteal elevator ora chisel using manual
digital pressure.Once the tooth has been sufficientlyexposed,it is sectioned into
appropriatepieces so that it can be delivered from thesocket.The direction in which
the impact-ed tooth is divided is dependent on theangulation ofthe impaction.Tooth
sec-tioning is performed either with a bur orchisel,but with the advent ofhigh-
speeddrills,the bur is most commonly usedbecause it provides a more
predictableplane ofsectioning.The tooth is usuallydivided three-quarters ofthe way
throughto the lingual aspect and then split theremainder ofthe way with a straight
eleva-tor or a similar instrument.This preventsinjury to the lingual cortical plate
andreduces the possibility ofdamage to thelingual nerve.The mesioangular impaction
is usu-ally the least difficult to remove.Aftersufficient bone has been
removed,thedistal halfofthe crown is sectioned offfrom the buccal groove to just
below thecervical line on the distal aspect ofthetooth.This portion ofthe tooth is
deliv-ered,and the remainder ofthe tooth isremoved with a small straight
elevatorplaced at a purchase point on the mesialaspect ofthe cervical line (Figure
8-4).Analternative is to prepare a purchase pointin the tooth with the drill and
use a cranepick or a Cryer elevator in the purchasepoint to deliver the tooth.The
horizontal impaction usuallyrequires the removal ofmore bone thandoes the
mesioangular impaction.Thecrown ofthe tooth is usually sectionedfrom the roots and
delivered with a CryerFIGURE8-1A,The envelope incision is most commonly used to
reflect the soft tissue ofthe mandiblefor removal ofan impacted third
molar.Posterior extension ofthe incision should diverge laterally toavoid injury to
the lingual nerve.B,The envelope incision is reflected laterally to expose bone
overly-ing impacted tooth.C,When a three-cornered flap is used,the release incision
is made at the mesialaspect ofthe second molar.D,When the soft tissue flap is
reflected by means ofa release incision,greater visibility is possible,especially
at the apical aspect ofthe surgical field.Adapted from PetersonLJ.Principles
ofmanagement ofimpacted teeth.In: Peterson LJ,Ellis E III,Hupp JR,Tucker MR,edi-
tors.Contemporary oral and maxillofacial surgery.4th ed.St Louis: CV Mosby;
2003.p.184�213.ABCD
146Part 2: Dentoalveolar Surgeryelevator.The roots are then displaced intothe
socket that was previously occupied bythe crown and are delivered into
themouth.Occasionally,they may need to besectioned into separate portions and
deliv-ered independently (Figure 8-5).The vertical impaction is one ofthemore
difficult ones to remove,especially ifit is deeply impacted.The procedure forbone
removal and sectioning is similar tothat for the mesioangular impaction inthat
occlusal,buccal,and judicious distalbone is removed first.The distal halfofthecrown
is sectioned and removed,and thetooth is elevated by applying a smallstraight
elevator at the mesial aspect ofthecervical line (Figure 8-6).The option
ofpreparing a purchase point in the tooth isalso frequently used,as for the
mesioangu-lar impaction.The most difficult tooth to remove isone with a
distoangular impaction.Afterthe removal ofbone,the crown is usuallysectioned from
the roots just above thecervical line and delivered with a Cryerelevator.A purchase
point is then preparedin the tooth,and the roots are deliveredtogether or sectioned
and delivered inde-pendently with a Cryer elevator (Figure 8-7).Extraction ofthis
impaction is moredifficult because more distal bone must beremoved and the tooth
tends to be elevat-ed posteriorly into the ramus portion ofthe mandible.Impacted
maxillary third molars arerarely sectioned because the overlying boneis thin and
relatively elastic.In patients withthicker bone,the extraction is
usuallyaccomplished by removing additional bonerather than by sectioning the
tooth.Thetooth should never be sectioned with a chis-el because it may be displaced
into the max-illary sinus or infratemporal fossa whenstruck with the chisel (Figure
8-8).Once the impacted tooth is deliveredfrom the alveolar process,the surgeonmust
pay strict attention to d�briding thewound ofall particular bone chips andother
debris.The best method to accom-plish this is to mechanically d�bride thesocket and
the area under the flap with aperiapical curette.A bone file should beused to
smooth any rough sharp edges ofthe bone.A mosquito hemostat is usuallyused
carefully to remove any remnant ofFIGURE8-2A,The envelope flap is the most commonly
used flap for the removal ofmaxillaryimpacted teeth.B,When soft tissue is
reflected,the bone overlying the third molar is easily visualized.C,Iftooth is
deeply impacted,a release incision can be used to gain greater access.D,When the
three-cornered flap is reflected,there is greater visibility ofbone�s more apical
portions.Adapted from Peter-son LJ,Ellis E III,Hupp JR,Tucker
MR,editors.Contemporary oral and maxillofacial surgery.4th ed.St Louis: CV Mosby;
2003.ABCDFIGURE8-3A,After the soft tissue has been reflected,the bone overlying the
occlusal surface oftoothis removed with a fissure bur.B,Bone on the buccal and
distal aspects ofimpacted tooth is thenremoved with bur.Adapted from Peterson
LJ,Ellis E III,Hupp JR,Tucker MR,editors.Contemporaryoral and maxillofacial
surgery.4th ed.St Louis: CV Mosby; 2003.AB
Impacted Teeth147the dental follicle.Finally,the socket andwound should be
thoroughly irrigatedwith saline or sterile water (30 to 50 mL isoptimal).49Within
certain limitations,themore irrigation that is used,the less likelythe patient is
to have a dry socket,delayedhealing,or other complications.The incision should
usually be closedby primary intention.The flap is returnedto its original
position,and the initialresorbable suture is placed at the posterioraspect ofthe
second molar.Additionalsutures are placed as necessary.Use ofPerioperative Systemic
AntibioticsOne ofthe primary goals ofthe surgeon inperforming any surgical
procedure is to pre-vent postoperative infection as a result ofsurgery.To achieve
this goal,prophylacticantibiotics are necessary in some surgicalprocedures.Most
ofthese procedures fallinto the clean-contaminated or contaminat-ed categories
ofsurgery.The incidence ofpostoperative infections in a clean surgery isrelated
more to operator technique than tothe use ofprophylactic antibiotics.Surgery for
the removal ofimpactedthird molars clearly fits into the category ofclean-
contaminated surgery;however,theFIGURE8-4A,When removing a mesioangular
impaction,buccal and distal bone are removed to expose crown oftooth to its
cervical line.B,The distalaspect ofthe crown is then sectioned from
tooth.Occasionally it is necessary to section the entire tooth into two portions
rather than to section the distalportion ofcrown only.C,After the distal portion
ofcrown has been delivered,a small straight elevator is inserted into the purchase
point on mesial aspectofthird molar,and the tooth is delivered with a rotational
and level motion ofelevator.Adapted from Peterson LJ,Ellis E III,Hupp JR,Tucker
MR,edi-tors.Contemporary oral and maxillofacial surgery.4th ed.St Louis: CV Mosby;
2003.ABCABCDFIGURE8-5A,During the removal ofa horizontal impaction,the bone
overlying the tooth�thatis,the bone on the distal and buccal aspects oftooth�is
removed with a bur.B,The crown is sec-tioned from the roots ofthe tooth and is
delivered from socket.C,The roots are delivered togetheror independently with a
Cryer elevator used with a rotational motion.The roots may need to beseparated into
two parts: occasionally the purchase point is made in the root to allow the Cryer
ele-vator to engage it.D,The mesial root ofthe tooth is elevated in similar
fashion.Adapted from Peter-son LJ,Ellis E III,Hupp JR,Tucker
MR,editors.Contemporary oral and maxillofacial surgery.4thed.St Louis: CV Mosby;
2003.
148Part 2: Dentoalveolar Surgeryexact incidence ofpostoperative infectionis
unknown.In the usual sense ofthe word,infection probably is a rare occurrence fol-
lowing third molar surgery.This meansthat it is unusual to see pain,swelling,anda
production ofpurulence that requiresincision and drainage or antibiotic therapy.The
incidence ofsuch infections is very lowfor most surgeons.In general,a
competentexperienced surgeon would expect to havean infection rate in the range of1
to 5% forall third molar procedures.50It is difficult,and probably impossible,to
reduce infec-tion rates below 5% with the use ofpro-phylactic
antibiotics.Therefore,it isunnecessary to use prophylactic antibioticsin third
molar surgery to prevent postoper-ative infection in the normal
healthypatient.Although the literature containsmany articles that discuss the use
ofpro-phylactic perioperative antibiotics,there isessentially no report oftheir
usefulness inthe prevention ofinfection following thirdmolar surgery.51,52A more
subtle type ofwound healingproblem that occurs after the surgicalremoval ofthe
impacted mandibular thirdABCFIGURE8-6A,When removing a vertical impaction,the bone
on the occlusal,buccal,and distal aspects ofthe crown is removed,and the tooth is
sectioned intomesial and distal portions.Ifthe tooth has a fused single root,the
distal portion ofthe crown is sectioned offin a manner similar to that depicted for
a mesio-angular impaction.B,The posterior aspect ofthe crown is elevated first with
a Cryer elevator inserted into a small purchase point in the distal portion ofthe
tooth.C,A small straight no.301 elevator is then used to lift the mesial aspect
ofthe tooth with a rotary and levering motion.Adapted from Peterson LJ,Ellis E
III,HuppJR,Tucker MR,editors.Contemporary oral and maxillofacial surgery.4th ed.St
Louis: CV Mosby; 2003.FIGURE8-7A,For a distoangular impaction,the
occlusal,buccal,and distal bone is removed with a bur.It is important to remember
that more distalbone must be taken offthan for a vertical or mesioangular
impaction.B,The crown ofthe tooth is sectioned offwith a bur and is delivered with
straightelevator.C,The purchase point is put into the remaining root portion ofthe
tooth,and the roots are delivered by a Cryer elevator with a wheel-and-
axlemotion.Ifthe roots diverge,it may be necessary in some cases to split them into
independent portions.Adapted from Peterson LJ,Ellis E III,Hupp JR,Tucker
MR,editors.Contemporary oral and maxillofacial surgery.4th ed.St Louis: CV Mosby;
2003.ABC
Impacted Teeth149molar is so-called alveolar osteitis or drysocket.This disturbance
in wound healingis most likely caused by the combination ofsaliva and anaerobic
bacteria.The use ofprophylactic antibiotics in third molarsurgery does,in
fact,reduce the incidenceofdry socket.Other techniques that reducebacterial
contamination ofthe socket,suchas copious irrigation,preoperative rinseswith
chlorhexidine,and placement ofantibiotics in the extraction socket,are
alsoeffective.53�60Once again,the issue ofrisksversus benefits becomes
important.Although systemic antibiotics are effectivein the reduction
ofpostoperative dry sock-et,they are no more effective than are localmeasures.The
increase ofantibiotic-relat-ed complications,such as
allergy,resistantbacteria,gastrointestinal side effects,andsecondary infections,is
not outweighed bythe benefits.Therefore,the use ofperioper-ative systemic
antibiotic administrationdoes not seem to be valid.Use ofPerioperative SteroidsJust
as the oral and maxillofacial surgeondesires to minimize the incidence ofinfec-tion
following third molar surgery,he orshe also has a major interest in reducingthe
perioperative morbidity.The use ofcorticosteroids to help minimize
swelling,trismus,and pain has gained wide accep-tance in the oral and maxillofacial
surgerycommunity.The method ofusage,howev-er,is extremely variable,and the
mosteffective therapeutic regimen has yet to beclearly delineated.There is little
doubt that an initialintravenous dose ofsteroid at the time ofsurgery has a major
clinical impact onswelling and trismus in the early postoper-ative
period.However,ifthe initial intra-venous dose is not followed up with addi-tional
doses ofsteroids,this earlyadvantage disappears by the second orthird postoperative
day.Maximum controlofswelling requires that additionalsteroids be given for 1 or 2
days followingsurgery.The two most widely used steroidsare dexamethasone and
methylpred-nisolone.Both ofthese are almost pureglucocorticoids,with little
mineralocorti-coid effect.Additionally,these two appearto have the least depressing
effect onleukocyte chemotaxis.Common dosagesofdexamethasone are 4 to 12 mg IV at
thetime ofsurgery.Additional oral dosages of4 to 8 mg bid on the day ofsurgery and
fortwo days afterward result in the maximumreliefofswelling,trismus,and
pain.Methylprednisolone is most commonlygiven 125 mg IV at the time ofsurgery fol-
lowed by significantly lower doses,usually40 mg PO tid or qid,later on the day
ofsurgery and for two days after surgery.High-dose short-term steroid use
isassociated with minimal side effects.It iscontraindicated in the patient with
gastriculcer disease,active infection,and certaintypes ofpsychosis.The
administration ofperioperative steroids may increase theincidence ofalveolar
osteitis after thirdmolar surgery,but the data are lacking asto the precise degree
ofincrease.61�65 Expected Postoperative CourseSurgical removal ofimpacted third
molarsis associated with a moderate incidence ofcomplications,around
10%.66,67Thesecomplications range from the expectedand predictable outcomes,such
asswelling,pain,stiffness,and mild bleeding,to more severe and permanent complica-
tions,such as inferior alveolar nerve anes-thesia and fracture ofthe
mandible.Theoverall incidence ofcomplication and theseverity ofthese complications
are associ-ated most directly with the depth ofimpaction,that is,whether it is a
completebony impaction,and to the age ofthepatient.68�70 Because offactors already
dis-cussed,removal ofimpacted teeth in theolder patient is associated with a
higherincidence ofpostoperative complications,especially alveolar
osteitis,infections,mandible fracture,and inferior alveolarnerve anesthesia.The
removal ofcompletebony impactions is likewise associatedwith increased
postoperative pain andmorbidity and an increase in the incidenceofinferior alveolar
nerve anesthesia.Another determinant ofthe incidenceofcomplications ofthird molar
surgery isthe relative experience and training ofthesurgeon.The less experienced
surgeon willhave a significantly higher incidence ofcomplications than the trained
experiencedsurgeon.1,2After the surgical removalofanimpacted third molar,certain
normalphysiologic responses occur.These includeFIGURE8-8Delivery ofan impacted
maxillarythird molar.A,Once the soft tissue has beenreflected,a small amount
ofbuccal bone isremoved with a bur or a hand chisel.B,Thetooth is then delivered by
a small straight eleva-tor with rotational and lever types ofmotion.The tooth is
delivered in the distobuccal andocclusal direction.Adapted from Peterson LJ,Ellis E
III,Hupp JR,Tucker MR,editors.Con-temporary oral and maxillofacial surgery.4th
ed.St Louis: CV Mosby; 2003.AB
150Part 2: Dentoalveolar Surgerysuch things as mild bleeding,swelling,stiffness,and
pain.All ofthese are inter-preted by the patient as being unpleasantand should
therefore be minimized asmuch as possible.With experience,most oral and max-
illofacial surgeons develop a clear under-standing ofthird molar surgery�s impacton
their patients�lives.However,despite itsextreme importance,this topic hasreceived
little significant study.Severalauthorities have published data on theshort-term
impact ofthird molar removalon quality oflife.71,72As expected,thirdmolar removal
often has a profoundlynegative impact for the first 4 to 7 daysafter surgery,but
longer follow-up revealsimproved quality oflife,mostly resultingfrom the
elimination ofchronic pain andinflammation (usually pericoronitis).Alarge
multicenter prospective study,theThird Molar Project,has recently pro-duced
detailed data on the postoperativequality oflife in patients who undergothird molar
removal.73 The performingsurgeon must be intimately familiar withthis information
ifhe or she is to provideproper preoperative counseling.BleedingBleeding can be
minimized by using a goodsurgical technique and by avoiding thetearing offlaps or
excessive trauma to theoverlying soft tissue.When a vessel is cut,the bleeding
should be stopped to preventsecondary hemorrhage following surgery.The most
effective way to achieve hemosta-sis following surgery is to apply a moistgauze
pack directly over the site ofthesurgery with adequate pressure.This isusually done
by having the patient bitedown on a moist gauze pad.In somepatients,immediate
postoperative hemo-stasis is difficult.In such situations a vari-ety oftechniques
can be employed to helpsecure local hemostasis,including oversu-turing and the
application oftopicalthrombin on a small piece ofabsorbablegelatin sponge into the
extraction socket.The socket can also be packed with oxi-dized cellulose.Unlike the
gelatin sponge,oxidized cellulose can be packed into thesocket under pressure.In
some situationsmicrofibrillar collagen can be used to pro-mote platelet plug
formation.Patients whohave known acquired or congenital coagu-lopathies require
extensive preparation andpreoperative planning (eg,determinationofInternational
Normalized Ratio,factorreplacement,hematology consultation)before third molars are
removed surgically.SwellingPostsurgical edema or swelling is anexpected sequela
ofthird molar surgery.As discussed earlier,the parenteral admin-istration
ofcorticosteroids is frequentlyemployed to help minimize the swellingthat
occurs.The application ofice packs tothe face may make the patient feel
morecomfortable but has no effect on the mag-nitude ofedema.74The swelling
usuallyreaches its peak by the end ofthe secondpostoperative day and is usually
resolvedby the fifth to seventh day.StiffnessTrismus is a normal and expected out-
come following third molar surgery.Patients who are administered steroids forthe
control ofedema also tend to have lesstrismus.Like edema,jaw stiffness
usuallyreaches its peak on the second day andresolves by the end ofthe first
week.PainAnother postsurgical morbidity expectedafter third molar surgery is
pain.The post-surgical pain begins when the effects ofthelocal anesthesia subside
and reaches itsmaximum intensity during the first 12 hours postoperatively.75A
large varietyofanalgesics are available for managementofpostsurgical pain.The most
commonones are combinations ofacetylsalicylicacid or acetaminophen with codeine
andits congeners,and the nonsteroidal anti-inflammatory analgesics.Women may bemore
sensitive to postoperative pain thanmen76;thus,they require more
analgesics.Analgesics should be given before theeffect ofthe local anesthesia
subsides.Inthis manner,the pain is usually easier tocontrol,requires less drug,and
mayrequire a less potent analgesic.The admin-istration ofnonsteroidal analgesics
beforesurgery may be beneficial in aiding in thecontrol ofpostoperative pain.The
most important determinant ofthe amount ofpostoperative pain thatoccurs is the
length ofthe operation.Nei-ther swelling nor trismus correlate withthe length
oftime ofthe surgery.There is,however,a strong correlation betweenpostoperative
pain and trismus,indicatingthat pain may be one ofthe principal rea-sons for the
limitation ofopening after theremoval ofimpacted third molars.77Complications
ofImpactionSurgeryInfectionAn uncommon postsurgical complicationrelated to the
removal ofimpacted thirdmolars is infection.The incidence ofinfection following the
removal ofthirdmolars is very low,ranging from 1.7 to2.7%.78 Infection after
removal ofmandibular third molars is almost alwaysa minor complication.About 50%
ofinfections are localized subperiostealabscess-type infections,which occur 2 to4
weeks after a previously uneventfulpostoperative course.These are usuallyattributed
to debris that is left under themucoperiosteal flap and are easily treatedby
surgical d�bridement and drainage.Ofthe remaining 50%,few postoperativeinfections
are significant enough to war-rant surgery,antibiotics,and hospitaliza-
tion.Infections occur in the first postop-erative week after third molar
surgeryapproximately 0.5 to 1% ofthe time.Thisis an acceptable infection rate and
wouldnot be decreased with the administrationofprophylactic antibiotics.
Impacted Teeth151FractureOne ofthe most frequent problemsencountered in removing
third molars isthe fracture ofa portion ofthe root,whichmay be difficult to
retrieve.In these situa-tions the root fragment may be displacedinto the
submandibular space,the inferioralveolar canal,or the maxillary sinus.Uninfected
roots left within the alveolarbone have been shown to remain in placewithout
postoperative complications.79The pulpal tissues undergo fibrosis,andthe root
becomes totally incorporatedwithin the alveolar bone.Aggressive anddestructive
attempts to remove portions ofroots that are in precarious positionsseem to be
unwarranted and may cause more damage than benefit.Radiographic follow-up may be
all that is required.Alveolar OsteitisThe incidence ofalveolar osteitis or
drysocket following the removal ofimpactedmandibular third molars varies between
3and 25%.Most ofthe variation is mostlikely a result ofthe definition ofthe syn-
drome.When dry socketis defined in termsofpain that requires the patient to
returnto the surgeon�s office,the incidence isprobably in the range of20 to
25%.2,80�87The pathogenesis ofalveolar osteitishas not been clearly defined,but the
condi-tion is most likely the result oflysis ofafully formed blood clot before the
clot isreplaced with granulation tissue.This fibri-nolysis occurs during the third
and fourthdays and results in symptoms ofpain andmalodor after the third day or so
followingextraction.The source ofthe fibrinolyticagents may be tissue,saliva,or
bacteria.80The role ofbacteria in this process can beconfirmed empirically based on
the factthat systemic and topical antibiotic prophy-laxis reduces the incidence
ofdry socket byapproximately 50 to 75%.The periodontalligament may also play a role
in the devel-opment ofalveolar osteitis.The incidence ofdry socket seems tobe
higher in patients who smoke and infemale patients who take oral contracep-
tives.81,82Its occurrence can be reduced byseveral techniques,most ofwhich areaimed
at reducing the bacterial contami-nation ofthe surgical site.Presurgical irri-
gation with antimicrobial agents such aschlorhexidine reduces the incidence
ofdrysocket by up to 50%.2Copious irrigationofthe surgical site with large volumes
ofsaline is also effective in reducing drysocket.49Topical placement ofsmallamounts
ofantibiotics such as tetracyclineor lincomycin may also decrease the inci-dence
ofalveolar osteitis.83�86 The goal oftreatment ofdry socket isto relieve the
patient�s pain during thedelayed healing process.This is usuallyaccomplished by
irrigation ofthe involvedsocket,gentle mechanical d�bridement,and placement ofan
obtundent dressing,which usually contains eugenol.The dress-ing may need to be
changed on a dailybasis for several days and then less fre-quently after that.The
pain syndromeusually resolves within 3 to 5 days,although it may take as long as 10
to 14 days in some patients.There is someevidence that topical antibiotics such
asmetronidazole may hasten resolution ofthe dry socket.87In summary,alveolar
osteitis is a dis-turbance in healing that occurs after theformation ofa mature
blood clot butbefore the blood clot is replaced with gran-ulation tissue.The
primary etiologyappears to be one ofexcess fibrinolysis,with bacteria playing an
important but yetill-defined role.Antimicrobial agents deliv-ered by perioperative
mouthrinses,topical-ly placed in the socket,or administered sys-temically all help
to reduce the incidence ofdry socket.Mechanical d�bridement andcopious saline
irrigation ofthe surgicalwound also are effective in reducing theincidence ofdry
socket.A rationalapproach may be to provide preoperativechlorhexidine rinses for
approximately 1 week before surgery,irrigate the woundthoroughly with normal saline
at the con-clusion ofsurgery,place a small square ofgelatin sponge saturated with
tetracyclinein the socket,and continue chlorhexidinerinses for 1 additional
week.This combina-tion approach should substantially reducethe incidence ofdry
socket.Nerve DisturbancesSurgical removal ofmandibular thirdmolars places both the
lingual and inferioralveolar branches ofthe third division ofthe trigeminal nerve
at risk for injury.Thelingual nerve is most often injured duringsoft tissue flap
reflection,whereas the infe-rior alveolar nerve is injured when theroots ofthe
teeth are manipulated and ele-vated from the socket.The generallyaccepted incidence
ofinjury to the inferi-or alveolar and lingual nerves followingthird molar surgery
is about 3%.66�69,88�90Only a small proportion ofthese anesthe-sia and paresthesia
problems remain per-manent.However,there is a significantincidence ofsome minor
alterations ofsensation after injury caused by thirdmolar surgery.As many as 45%
ofnervecompression injuries,which are typical inthird molar surgery,result in a
permanentneurosensory abnormality.91Inferior alveolar nerve injury is mostlikely to
occur in specific situations.Thefirst and most commonly reported predis-posing
factor is complete bony impactionofmandibular third molars.The angula-tion
classifications most commonlyinvolved are usually mesioangular and ver-tical
impaction.In some cases,nerve prox-imity to the root is indicated by an appar-ent
narrowing ofthe inferior alveolarcanal as it crosses the root or severe
rootdilaceration adjacent to the canal.Otherwell-documented radiographic signs
arediversion ofthe path ofthe canal by thetooth,darkening ofthe apical end
oftheroot indicating that it is included withinthe canal,and interruption
oftheradiopaque white line ofthe canal.92Insurgically verified inferior alveolar
nerveinjuries,the presence ofmore than one of
152Part 2: Dentoalveolar Surgerythese signs was highly sensitive but nothighly
specific for the risk ofinjury,whereas the absence ofall ofthese signshad a strong
negative predictive value.93When they are noted on a preoperativeevaluation ofthe
radiograph,the surgeonshould take extraordinary precautions toavoid injury to the
nerve,such as addition-al bone removal or sectioning ofthe toothinto extra
pieces,and the patient should becounseled in advance regarding his or herincreased
risk ofnerve injury.When an injury to the lingual or infe-rior alveolar nerve is
diagnosed in thepostoperative period,the surgeon shouldbegin long-term planning for
its manage-ment including consideration ofreferralto a neurologist and/or
microneurosur-geon.These issues are dealt with elsewherein this textbook.Rare
Complications The complications already discussed are themore common
occurrences,accounting forthe great majority ofcomplications insurgery to remove
impacted third molars.Several additional complications occuronly rarely and are
mentioned briefly.Maxillary third molars that are deeplyimpacted may have only thin
layers ofboneposteriorly separating them from theinfratemporal fossa,or anteriorly
separatingthem from the maxillary sinus.Smallamounts ofpressure in an errant
directioncan result in displacement ofthe maxillarythird molar into these adjacent
spaces.Whena maxillary third molar is displaced posteri-orly into the infratemporal
fossa,the sur-geon should try to manipulate the toothback into the socket with
finger pressureplaced high in the buccal vestibule near thepterygoid plates.Ifthis
is unsuccessful,thesurgeon can attempt to recover the tooth byplacing the suction
tip into the socket andaiming it posteriorly.Ifboth ofthese maneu-vers are
unsuccessful in recovering the tooth,the most effective technique is to allow
thetooth to undergo fibrosis and to return 2 to4 weeks later to remove it.Ifthe
tooth isasymptomatic,is not causing any restrictionin jaw movement,and is not
causing pain,the surgeon should consider leaving thetooth in place.Ifthe decision
is made toremove the tooth,three-dimensional local-ization ofthe tooth should be
made beforesurgery is initiated.Ifthe tooth is displaced into the max-illary
sinus,retrieval is usually done by aCaldwell-Luc procedure at the
sameappointment.The surgeon should localizethe tooth with at least a one-
dimensionalradiographic view and preferably a three-dimensional study before
performing theretrieval surgery.94Fracture ofthe mandible during theremoval
ofimpacted mandibular thirdmolars is a rare occurrence.The typicalsituation is a
deeply impacted third molar,most commonly in an older individualwith dense bone.The
surgeon placesexcessive pressure on the tooth with anelevator in an attempt to
deliver the toothor tooth section into the mouth;the frac-ture occurs,and the
remaining portion ofthe tooth is easily retrieved.The surgeonshould then perform an
immediate reduc-tion and fixation ofthe fracture.Ifthe sur-geon has the experience
and the arma-mentarium available,rigid internalfixation with miniplates is an
excellentchoice in this unfortunate situation.Wirefixation and application
ofintermaxillaryfixation is an acceptable alternative.Latemandible fractures
usually occur 4 to 6 weeks following extraction in patientsover age 40
years.Periodontal Healing after ThirdMolar Surgery Two ofthe important reasons for
remov-ing impacted third molars is to preserveperiodontal health or,in some
situations,to treat a periodontitis that alreadyexists.23A relative
contraindication to theremoval ofimpacted third molars is a sit-uation in which
there is good periodontalhealth and a complete bony impaction inan older
patient.Removal is contraindicat-ed because the healing response in olderpatients
would likely result in a large per-sistent postsurgical defect.After third molar
surgery,the boneheight distal to the second molar usuallyremains at the
preoperative level,95�97although some studies have indicated a netgain in bone
level after surgery.98Ifthebone level on the distal aspect ofthemandibular second
molar is compromisedby the presence ofthe third molar,it usual-ly remains at that
level following the heal-ing ofthe bone.There is universal agree-ment that bone
healing is better ifsurgeryis done before the third molar resorbs thebone on the
distal aspect ofthe secondmolar and while the patient is young.99�101The greatest
bony defect occurs in situa-tions in which the third molar has resorbedextensive
amounts ofbone from the sec-ond molar in an older patient,which com-promises bony
repair and bone healing.The other periodontal parameter ofimportance is attachment
level or,lessaccurately,sulcus or pocket depth.As withbone levels,ifthe
preoperative pocketdepth is great,the postoperative pocketdepth is likely to be
similar.In most studiesthe attachment level has been found to be atessentially the
same level as it is preopera-tively.95,102,103In older patients with com-plete bony
impactions,pocket depth andattachment levels may be significantlylower than
preoperative levels.However,inpatients younger than age 19 years,removalofcomplete
bony impactions results in nocompromise in attachment level or pocketdepth.Initial
healing after third molarsurgery usually results in a reduction inpocket depth in
young patients.97The long-term healing in this group continues for upto 4 years
after surgery,with continuingreduction in probable pocket depths.100However,long-
term follow-up ofolderpatients clearly demonstrates that this long-term healing
does not occur.98,100 Usually,the surgeon makes an attempt to mechani-cally d�bride
the distal aspect ofthe secondmolar root area with a curette to encourage
Impacted Teeth153improved bone regeneration followingthird molar extraction.In
summary,periodontal healing fol-lowing third molar surgery is clearly bestwhen the
impacted tooth is removedbefore it becomes exposed in the mouth,before it resorbs
bone on the distal aspectofthe second molar,and when the patientis as young as
possible.95�100,102,103Ifthethird molar is partially impacted and ispartially
exposed in the mouth,it shouldbe removed as soon as possible.The rea-son for this
is that there is already a deepand potentially destructive periodontallesion that
is difficult for the patient tomaintain hygienically.Even ifthe patient
isasymptomatic,the impacted tooth shouldbe removed as soon as possible to allowthe
best periodontal healing after surgeryas possible.In these situations the peri-
odontal healing is compromised becauseofthe fact that there was already a destruc-
tive lesion caused by the presence ofthepartially impacted third molar.The
completely impacted third molarin a patient older than age 35 years shouldbe left
undisturbed unless some pathologydevelops.Removal ofasymptomatic com-pletely
impacted third molars in theseolder patients results in pocket depths thatare
significant and the potential loss ofalveolar bone on the posterior aspect ofthe
second molar.SummaryThe issue ofwhether to remove impactedthird molars has
generated much contro-versy over the past three decades.The rea-son for this
controversy has been the lack oflong-term prospective studies that have fol-lowed
up large groups ofpatients withimpacted teeth to determine the eventualoutcome
ofleaving impactions in situ.Recently there has been intense interest
inestablishing clear scientifically valid evi-dence regarding the role ofthird
molarremoval in patient health care,especiallywith respect to predicting the
likelihood oferuption or the risk offuture pathology inasymptomatic
patients.Ongoing studiesare already greatly improving our knowl-edge in these
areas,and significant advancesmay be expected to appear in the scientificliterature
for the next several years.Clearly,impacted third molars associ-ated with or
contributing to adjacentpathology require removal as early as isreasonably
possible.The major controver-sy regarding proper care centers aroundasymptomatic
unerupted third molars.Itis clear that although incompletely erupt-ed mandibular
third molars will continueto erupt beyond age 18 or 20 years,in thevast majority
ofthese situations,there willbe a soft tissue or bone tissue flap over thedistal
aspect ofthe erupted third molar,which has the potential to cause
recurrentpericoronitis.In fact,the tooth that is mostlikely to be involved in
pericoronitis is theerupted vertically positioned third molarwith a soft tissue
flap (operculum) overthe distal aspect ofthe tooth.Althoughmost attempts at very
early prediction ofimpaction and removal oftooth buds atage 8 or 9 years have now
been generallyabandoned,it is reasonable that by age 17or 18 years the dentist and
surgeon canreasonably predict whether there will beadequate room for the tooth to
erupt withsufficient clearance ofthe anterior ramusto prevent soft tissue
overgrowth (as inpatients with large arch length and rela-tively small teeth).Soft
tissue and bone tissue healingwill occur at a maximum level ifthesurgery to remove
impacted third molarsis done as early possible.By age 17 years,ifthe diagnosis
ofinadequate room forfunctional eruption can be made,thenthe asymptomatic third
molar should beremoved.Even though the tooth may becompletely covered with soft and
hardtissue,removing the third molar at thatage will eliminate the future
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Surg1973;2:273�8.55.Kariro GSN.Metronidazole (Flagyl) and Arnicamontanain the
prevention ofpost-surgicalcomplications;a comparative placebo con-trolled clinical
trial.Br J Oral MaxillofacSurg 1984;22:42�9.56.Krekmanov L,Nordenram
A.Postoperativecomplications after surgical removal ofmandibular third molars.Int J
Oral Max-illofac Surg 1986;15:25�9.57.Krekmanov L,Hallander HO.Relationshipbetween
bacterial contamination and alve-olitis after third molar surgery.Int J OralSurg
1950;9:274�80.58.Krekmanov L.Alveolitis after operativeremoval ofthird molars in
the mandible.Int J Oral Surg 1981;10:173�9.59.Macgregor AJ,Addy A.Value
ofpenicillin inthe prevention ofpain,swelling and tris-mus following the removal
ofectopicmandibular third molars.Int J Oral Surg1980;9:166�72.
Impacted Teeth15560.Rood JP,Murgatroyd JM.Metronidazole in theprevention of�dry
socket.�Br J Oral Surg1979;17:62�70.61.Hooley JR,Francis FH.Betamethasone in
traumat-ic oral surgery.J Oral Surg 1969;27:398�403.62.Huffman GG.Use
ofmethylprednisolone sodi-um succinate to reduce postoperativeedema after removal
ofimpacted thirdmolars.J Oral Surg 1977;35:198�9.63.Pedersen A.Decadron phosphate
in the reliefofcomplaints after third molar surgery.IntJ Oral Surg
1985;14:235�40.64.Beirne OH,Hollander B.The effect ofmethyl-prednisolone on
pain,trismus,and swellingafter removal ofthird molars.Oral
Surg1986;61:134�8.65.Bustedt H,Nordenram A.Effect ofmethylpred-nisolone on
complications after removal ofimpacted mandibular third molars.SwedDent J
1985;9:65�9.66.Nordenram A.Postoperative complications inoral surgery.Swed Dent J
1983;7:109�14.67.Goldberg MH,Nemarich AN,Marco WP.Complications after mandibular
thirdmolar surgery:a statistical analysis of500consecutive procedures in private
practice.J Am Dent Assoc 1985;111:277�9.68.Bruce RA,Frederickson GC,Small CS.Age
ofpatients and morbidity associated withmandibular third molar surgery.J AmDent
Assoc 1980;101:240�5.69.Osborn TP,Frederickson C,Small IA,Torger-son TS.A
prospective study ofcomplica-tions related to mandibular third molarsurgery.J Oral
Maxillofac Surg 1985;43:767�9.70.Hinds EC,Frey KF.Hazards ofretained thirdmolars in
older persons:report of15 cases.J Am Dent Assoc 1980;101:246�50.71.McGrath
C,Comfort MB,Lo ECM,Luo Y.Changes in life quality following thirdmolar surgery�the
immediate postopera-tive period.Br Dent J 2003;194:265�8.72.Shafer DM,Frank ME,Gent
JF,Fischer ME.Gustatory function after third molarextraction.Oral Surg Oral Med
Oral PatholOral Radiol Endod 1999;87:419�28.73.White RP,Shugars DA,Shafer DM,et
al.Recovery after third molar surgery:clinicaland health-related quality oflife
outcomes.J Oral Maxillofac Surg 2003;61:535�44.74.Forsgren H,Heimdahl AN,Johansson
B,Krek-manov L.Effect ofapplication ofcolddressings on the postoperative course
inoral surgery.Int J Oral Surg 1985;14:223�8.75.Seymour RA,Blair GS,Wyatt FAR.Post-
operative dental pain and analgesic effica-cy.Br J Oral Surg
1983;23:298�303.76.Seymour RA,Meechan JG,Blair GS.An inves-tigation into post-
operative pain after thirdmolar surgery under local analgesia.Br JOral Maxillofac
Surg 1985;23:410�8.77.Pedersen A.Interrelation ofcomplaints afterremoval ofimpacted
mandibular thirdmolars.Int J Oral Surg 1985;14:241�4.78.Nordenram A,Grave
S.Alveolitis sicca dolorosaafter removal ofimpacted mandibular thirdmolars.Int J
Oral Surg 1983;12:226�31.79.Knutsson K,Lysell L,Rohlin M.Postoperativestatus after
partial removal ofthe mandibu-lar third molar.Swed Dent J 1989;13:15�22.80.Nitzan
DNW.On the genesis of�dry socket.�JOral Maxillofac Surg 1983;41:706�10.81.Sweet
JB,Butler DP.The relationship ofsmok-ing to localized osteitis.J Oral
Surg1979;37:732�5.82.Meechan JG,MacGregor IDM,Rogers SN,etal.The effect ofsmoking
on immediate post-extraction socket filling with blood and theincidence ofpainful
socket.Br J Oral Max-illofac Surg 1988;26:402�9.83.Swanson AE.A double-blind study
on theeffectiveness oftetracycline in reducing theincidence offibrinolytic
alveolitis.J OralMaxillofac Surg 1989;47:165�7.84.Nordenram A,Sydens G,Odegaard
J.Neomycin-bacitracin cones in impacted third molarsockets.Int J Oral Surg
1973;2:279�83.85.Goldman DR,Kilgore DS,Panzer JD,AtkinsonWH.Prevention ofdry socket
by localapplication oflincomycin in Gelfoam.OralSurg 1973;35:472�4.86.Hall
HD,Bildman BS,Hand CD.Prevention ofdry socket with local application oftetra-
cycline.J Oral Surg 1971;29:35�7.87.Mitchell L.Topical metronidazole in the treat-
ment of�dry socket.�Br Dent J 1984;156:132�4.88.Kipp DP,Goldstein BH,Weiss WW
Jr.Dyses-thesia after mandibular third molarsurgery:a retrospective study and
analysisof1,377 surgical procedures.J Am DentAssoc 1980;100:185�92.89.Wofford
DT,Miller RI.Prospective study ofdysesthesia following odontectomy ofimpacted
mandibular third molars.J OralMaxillofac Surg 1987;45:15�9.90.Mason DA.Lingual
nerve damage followinglower third molar surgery.Int J Oral Max-illofac Surg
1988;17:290�4.91.Robinson PP.Observations on the recovery ofsensation following
inferior alveolar nerveinjuries.Br J Oral Maxillofac Surg 1988;26:177�89.92.Rood
JP.The radiological prediction ofinfe-rior alveolar nerve injury during thirdmolar
surgery.Br J Oral Maxillofac Surg1990;28:20�5.93.Blaeser BF,August MA,DonoffRB,et
al.Panoramic radiographic risk factors forinferior alveolar nerve injury after
thirdmolar extraction.J Oral Maxillofac Surg2003;61:417�21.94.Oberman M,Horowitz
I,Ramon Y.Acciden-tal displacement ofimpacted maxillarythird molars.Int J Oral
Maxillofac Surg1986;15:756�8.95.Osborne WH,Snyder AJ,Tempel TR.Attach-ment levels
and crevicular depths at thedistal ofmandibular second molars fol-lowing removal
ofadjacent third molars.JPeriodontol 1982;53:93�5.96.Meister F Jr,Nery EB,Angell
DM,MeisterRC.Periodontal assessment following sur-gical removal ofmandibular third
molars.Gen Dent 1986;34�Apr:120�3.97.Kugelberg CF,Ahlstrom U,Ericson S,Hugo-son
A.Periodontal healing after impactedlower third molar surgery.Int J Oral
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following extractionofimpacted mandibular third molars.Oral Surg 1985;60:324.99.Ash
MM Jr,Costich ER,Hayward JR.A studyofperiodontal hazards ofthird molars.J
Periodontol 1962;33:209�19.100.Kugelberg CF.Periodontal healing two andfour years
after impacted lower thirdmolar surgery.Int J Oral Maxillofac
Surg1990;19:341�5.101.Kugelberg CF,Ahlstrom U,Ericson S,et al.The influence
ofanatomical,pathophysi-ological and other factors on periodontalhealing after
impacted lower 3rd molarsurgery a multiple-regression analysis.J Clin Periodontol
1991;18:37�43.102.Grondahl HG,Lekholm U.Influence ofmandibular third molars on
related sup-porting tissues.Int J Oral Surg 1973;2:137�42.103.Chin Quee TA,Gosselin
D,Miller EP,StammJW.Surgical removal ofthe fully impactedmandibular third molar.J
Periodontol1985;56:625�30.
CHAPTER 9Preprosthetic and Reconstructive SurgeryDaniel B.Spagnoli,DDS,PhDSteven
G.Gollehon,DDS,MDDale J.Misiek,DMDPreprosthetic surgery in the 1970s andearly 1980s
involved methods to prepare orimprove a patient�s ability to wear com-plete or
partial dentures.Most procedureswere centered around soft tissue correc-tions that
allowed prosthetic devices to fitmore securely and function more comfort-ably.In
severe cases bony augmentationwas incorporated and included such proce-dures as
cartilage grafts,rib grafts,alloplas-tic augmentation,visor osteotomies,andsandwich
grafts.Patients who were poorcandidates for surgery were often left withless-than-
satisfactory results both func-tionally and esthetically.In the late 1970s
Br�nemark and col-leagues demonstrated the safety and effica-cy ofthe implant-borne
prosthesis.1In the1990s implantology,distraction osteogene-sis,and guided tissue
regeneration signifi-cantly expanded the capabilities oftoday�sreconstructive and
preprosthetic surgeon.Genetically engineered growth factors willsoon revolutionize
our thoughts aboutreconstructive procedures.As a result,more patients are able to
tolerate proce-dures because they are given increasedfreedom and satisfaction with
regard totheir prosthetic devices and,in many cases,undergo less-invasive
techniques.In spite ofthe fact that routine dentalcare has improved over the past
century,approximately 10% ofthe population iseither partially or completely
edentulousand > 30% ofpatients older than 65 yearsare completely
edentulous.2Althoughthese figures are predicted to decrease overthe next several
decades,the treatment ofpartial and total edentulism will never becompletely
eliminated from the oral andmaxillofacial surgeon�s armamentarium.Since the primary
goal in preprosthet-ic reconstructive surgery is to eliminatethe condition
ofedentulism,one mustconsider the etiology ofthe edentulousstate when evaluating
patients and plan-ning treatment.In many cases the etiologyofa patient�s edentulism
has a major bear-ing on the reconstructive and restorativeplan.Edentulism arising
from neglect ofthe dentition and/or periodontal diseaseoften poses different
reconstructive chal-lenges than does that resulting from trau-ma,ablative
surgery,or congenital defects.Although restoration ofa functional den-tition is the
common goal,each specificetiology poses its own unique set ofchal-lenges.The goal
ofpreprosthetic andreconstructive surgery in the twenty-firstcentury is to
establish a functional biolog-ic platform for supportive or retentivemechanisms
that will maintain or supportprosthetic rehabilitation without con-tributing to
further bone or tissue loss.This environment will allow for a prosthe-sis that
restores function,is stable andretentive,preserves the associated struc-tures,and
satisfies esthetics.3Characteristics ofAlveolar Bonein the Edentulous PatientNative
alveolar bone responds to the func-tional effects (or lack thereof) caused
byedentulism.Increased resorption owing totraditional methods oforal
rehabilitationwith complete and partial dentures oftenresults in an overall
acceleration oftheresorptive process.The mandible is affect-ed to a greater degree
than the maxillaowing to muscle attachments and func-tional surface area.4As a
result,there isproportionally a qualitative and quantita-tive loss
oftissue,resulting in adverseskeletal relationships in essentially all spa-tial
dimensions (Figure 9-1).General systemic factors,such asosteoporosis,endocrine
abnormalities,renal dysfunction,and nutritional defi-ciencies,play a role in the
overall rate ofalveolar atrophy.Local factors,including
158Part 2: Dentoalveolar Surgeryjaw function,vascular changes,increasedphysical
demands owing to decreasedmandibular plane angle,adverse prosthet-ic
loading,mucosal inflammation,vascu-lar changes,and the number and extent ofprevious
surgeries involving mucoperi-osteal elevation,also contribute to pro-gressive
alveolar bone loss.5Although the factors contributing tobone loss and the resulting
patterns arewell understood,the rate ofbone lossvaries significantly from
individual toindividual.The consistent factor is theoverall duration ofthe
patient�s edentu-lous state.Functional Effects ofEdentulism The maxillomandibular
relationship isaltered in all spatial dimensions as a resultofthe loss
ofphysiologic function andteeth.There is a progression towarddecreased overall
lower facial height,lead-ing to the typical overclosed appearance,decreased
alveolar support for traditionalprostheses,encroachment ofmuscle andtissue
attachments to the alveolar crestresulting in progressive instability ofcon-
ventional soft tissue�borne prostheticdevices,neurosensory changes secondary
toatrophy,and an overall reduction in sizeand form in all three
dimensions.Thesechanges result in an overall decrease in fitand increase in patient
discomfort with theuse ofconventional dentures.The pro-longed effects ofedentulism
compoundedwith systemic factors and functional physi-cal demands from prosthetic
loading pro-duce atrophy that,in severe cases,places thepatient at significant risk
for pathologicfracture.As a result ofthe above effects,agoal-oriented approach to
treatment is themost appropriate.The overall objectivesinclude the following6:(1)
to eliminate pre-existent or recurrent pathology;(2) to reha-bilitate infected or
inflamed tissue;(3) toreestablish maxillomandibular relation-ships in all spatial
dimensions;(4) to pre-serve or restore alveolar ridge
dimensions(height,width,shape,and consistency)conducive to prosthetic restoration;
(5) toachieve keratinized tissue coverage over allload-bearing areas;(6) to relieve
bony andsoft tissue undercuts;(7) to establish prop-er vestibular depth and
repositioning ofattachments to allow for prosthetic flangeextension ifnecessary;(8)
to establishproper notching ofthe posterior maxillaand palatal vault proportions;
(9) to pre-vent or manage pathologic fracture oftheatrophic mandible;(10) to
prepare the alve-olar ridge by onlay grafting,corticocancel-lous augmentation,sinus
lift,or distractionosteogenesis for subsequent implant place-ment;and (11) to
satisfy facial esthetics,speech requirements,and masticatory chal-lenges.To satisfy
these goals,a treatmentplan directly addressing each existing con-dition is
indicated.Such a plan shouldinclude correction
ofmaxillomandibularrelationship,restoration ofridge form andFIGURE9-1The diagrams
show patterns and varying degrees ofseverity ofmandibular atrophy.A,Mandible shows
minimal alveolar bone resorption.B,Cross-section oflarge alveolar ridgeincluding
mucosal and muscular attachments.C,Mandible shows severe loss ofalveolar bone
thathas resulted in residual basal bone only.D,Cross-section shows resorbed
alveolar ridge,with mus-cular attachments.Adapted from Tucker MR.Ambulatory
preprosthetic reconstructive surgery.In:Peterson LJ,Indresano AT,Marciani RD,Roser
SM.Principles oforal and maxillofacial surgery.Vol 2.Philadelphia (PA): JB
Lippincott Company; 1992.p.1104.ABCD
Preprosthetic and Reconstructive Surgery159soft tissue relationship including
histologictype and condition,bone and/or soft tissuegrafting/repositioning,options
regardingimplant-supported or -stabilized prosthetictreatment,immediate versus
delayedimplant placement,preservation ofexistingalveolar bone with implants,and
correctionor minimization ofthe effects ofcombina-tion syndrome in cases involving
partiallyedentulous patients.Prior to developing a plan one mustconsider the amount
and source ofboneloss.Common causes ofprimary boneloss include trauma,pathology
such asperiodontal disease,destructive cysts ortumors,and bone loss associated
withextraction and alveoloplasty.Secondarybone loss,ifnot prevented,can follow
allofthe primary types listed above.Sec-ondary maxillary/mandibular bone lossis an
insidious regressive remodeling ofalveolar and even basal bone that is asequela
oftooth loss.This secondaryprocess is referred to as edentulous boneloss and varies
in degree based on anumber offactors.The pathophysiologyofedentulous bone loss
relates to anindividual�s characteristic anatomy,metabolic state,jaw function,and
prioruse ofand type ofprosthesis.Anatomi-cally,individuals with long dolicho-
cephalic faces typically have greater ver-tical ridge dimensions than do those
withshort brachycephalic faces.In addition,those with shorter faces are capable
ofahigher bite force.Metabolic disorderscan have a significant impact on apatient�s
potential to benefit fromosseous reconstructive surgery.Nutri-tional or endocrine
disorders and anyassociated osteopenia,osteoporosis,andespecially osteomalacia must
beaddressed prior beginning bone recon-struction.5Mechanical influences on
themaxilla and mandible have a variableeffect on the preservation ofbone.Thenormal
nonregressive remodeling ofbone essentially represents a balancebetween breakdown
and repair thatmaintains bone osteons,the functionalunit ofbone,and consequently
the via-bility ofbone shape and form.Bonerequires stimulation often referred to
as�the minimum essential strain�to main-tain itself.Both insufficient strain
andexcessive loads can lead to regressiveremodeling ofbone,with the classicexample
being denture compressionleading to an anterior-posterior andtransverse deficient
maxilla opposing awide mandible that is excessive in itsanterior-posterior
dimension.Residual ridge form has beendescribed and classified by Cawood
andHowell7(Figures 9-2 and 9-3) as follows:�Class I�dentate�Class
II�postextraction�Class III�convex ridge form,withadequate height and width
ofalveolarprocess�Class IV�knife-edge form with ade-quate height but inadequate
width ofalveolar process�Class V�flat-ridge form with loss ofalveolar process�Class
VI�loss ofbasal bone that maybe extensive but follows no
predictablepatternModifications to this classification thatmay be relevant to
contemporary recon-structive methods include subclassifica-tions in II and VI:Class
II�no defect,buccal wall defect,or multiwall defect ordeficiency;and Class
VI�marginal resec-tion defect or continuity defect.Medical ConsiderationsDuring the
patient evaluation process,particular attention to the patient�s chiefcomplaint and
concerns is imperative;athorough understanding ofthe past med-ical history is
mandatory in the treatmentand evaluation ofany patient.A currentor previous history
regarding thepatient�s success or failure at maintainingprevious prosthetic devices
is also neces-sary.Careful attention to patient�s func-tional,cognitive,and
physical ability toparticipate with the reconstructive plan iscrucial to the
success offuture restora-tions and overall patient satisfaction.Theevaluation
process should include a com-prehensive work-up ofthe patient�spredilection for
metabolic disease,including serum calcium,phosphate,albumin,alkaline
phosphatase,and calci-tonin levels.5Decreased renal functionand the presence ofa
vitamin D deficien-cy should also be ruled out.The mainte-nance ofbone mass
requires a balancedcalcium metabolism,a functionalendocrine system,and physiologic
load-ing ofbone tissue.Secondary medicalcomplications affecting edentulouspatients
include candidiasis,hyperkerato-sis,fibrous inflammatory
hyperplasia,dysplasia,papillomatosis,breathingchanges,and diet compromise away
fromnatural foods high in fiber and toward anincrease in processed foods.Hard and
Soft Tissue ExaminationA problem-oriented physical examinationshould include
evaluation ofthe maxillo-mandibular relationship;existing
alveolarcontour,height,and width;soft tissueattachments;pathology;tissue
health;palatal vault dimension;hamular notch-ing;and vestibular
depth.Identification ofboth soft tissue and underlying bone char-acteristics and/or
deficiencies is essentialto formulate a successful reconstructiveplan.This plan
should be defined and pre-sented to the patient both to educate thepatient and to
allow him or her to play arole in the overall decision-making processwith all
members ofthe dental team.The soft tissue evaluation shouldinvolve careful
visualization,palpation,and functional examination ofthe overly-ing soft tissue and
associated muscleattachments (Figure 9-4).Retraction ofthe upper and lower lips
help one identifymuscle and frenum attachments buccally.A mouth mirror can be used
lingually to
160Part 2: Dentoalveolar Surgerytent the floor ofmouth to evaluate
themylohyoid�alveolar ridge relationship.Careful palpation with manipulation ofboth
upper and lower alveolar ridges is thebest diagnostic determinant ofloose
andexcessive soft tissue.One must be aware ofoccult bony abnormalities obscured
bysoft tissue excess,especially in cases whereadequate alveolar ridge height and
width isimperative for implant placement (Figure9-5).Such abnormalities can lead
toembarrassing and unexpected changes inthe restorative plan at the time ofmucope-
riosteal reflection ofthe overlying soft tis-sue.Ifconventional prosthetic
restorationsare planned,attention to bony and soft tis-sue undercuts that oppose
the prostheticpath ofinsertion must be addressed.Crit-ical attention should be
given to deficien-cies in the palatal vault or buccal/lingualvestibule,defects in
the alveolar ridge,andthe presence ofbuccal,palatal,or lingualexostoses.During this
evaluation process,final decisions should be made regardingthe prognosis ofany
existing teeth andtheir role in the overall rehabilitation andcontribution to the
long-term success ofthe treatment plan.Finally,careful neu-rosensory evaluation
ofthe patient withsevere regressive remodeling may play asignificant role in the
determination offuture grafting or repositioning proce-dures aimed at maintaining
proper neu-rosensory function in conjunction withprosthetic
rehabilitation.Radiographic EvaluationTo date,the panoramic radiograph pro-vides
the best screening source for theoverall evaluation and survey ofbonystructures and
pathology in the maxillofa-cial skeleton.From examination radi-ographs,one can
identify and evaluatepathology,estimate anatomic variationsand pneumatization ofthe
maxillarysinus,locate impacted teeth or retainedroot tips,and gain an overall
appreciationofthe contour,location,and height ofthebasal bone,alveolar ridge,and
associatedinferior alveolar neurovascular canal andmental foramina.8Calibration
ofradiographs for magnifi-cation is necessary to determine the spatialdimensions
needed to plan implant restora-tions adjacent to neurovascular structuresor the
maxillary sinus,to determine defectsize and shape in distraction osteogenesis,and
to predict the necessary dimensions ofplanned augmentation
materials.AlveolarBasalGreater palatine foramenGreater palatine foramenWidest part
ofalveolar processWidest part of alveolar processCrest of alveolar processCrest of
alveolarprocessIncisive foramen0102010 mm0 mmIIIIIIVVVIIncisive foramenResorption
(mm)01010 mm0 mmIIIIIIVVVIGreater palatine foramenResorption (mm)FIGURE9-2Maxillary
horizontal measurements (A).Classification ofresorption ofmaxillary alveolar
ridge:anterior (B) and posterior (C).Adapted from Cawood JI,Howell RA.7ABC
Preprosthetic and Reconstructive Surgery161Posteroanterior and lateral cephalo-
metric radiographs can be used to evaluateinterarch space,relative and absolute
skele-tal excesses or deficiencies existing in themaxilla or mandible,and the
orientation ofthe alveolar ridge between arches.Theseare exceptionally useful when
the presenceofskeletal discrepancies may necessitateorthognathic correction to
provide accept-able functional relationships for
prostheticrehabilitation.Cephalometric analysis incombination with mounted dental
modelshelps one establish the planned path ofinsertion offuture prosthetic devices
aswell as identify discrepancies in interarchrelationships that affect the
restorative plan(Figure 9-6).9In recent years computed tomography(CT) has played an
increased role in thetreatment planning ofcomplex cases.Detailed evaluation
ofalveolar contour,neurovascular position,and sinus anato-my is available for the
subsequent plan-ning ofadvanced implant applications.Zygomatic implants that
obviate the needfor sinus lifting can be used in casesinvolving edentulous atrophic
maxillarysinuses (Figure 9-7).Careful evaluation ofthe path ofinsertion is easily
accom-plished using coronal CT examination ofthe maxillary sinuses.CT can also
providethe clinician with information regardingbone quantity and volume as well as
den-sity (Figure 9-8).In many cases the combination ofimaging modalities and
mounted modelswith diagnostic wax-ups can be helpful indetermining the
reconstructive plan.Theseelements are also useful in the fabrication ofsurgical
stents guiding implant placementor grafting procedures.Surgical stents fab-ricated
from CT-based models combineesthetic and surgical considerations;bridgethe gap
between the model surgery and theoperation;and allow cooperation betweenthe
surgeon,laboratory technician,peri-odontist,prosthodontist,and orthodontist,which
results in a cost-effective prostheticreconstruction with improved estheticresults
(Figure 9-9).In addition,accuracyofthe surgical procedure can be greatlyincreased
with an overall decrease in theduration ofthe procedure.Treatment Planning
ConsiderationsThe conventional tissue-borne prosthesishas given way to implant-
borne devicesthat have proven superior in providingincreased patient
function,confidence,and esthetics.Preprosthetic surgicalpreparation ofareas
directly involved withdevice support and stability are ofprima-ry importance and
should be addressedearly in the treatment plan.Overlying soft tissue procedures
neednot be attempted until satisfactory posi-tioning ofunderlying bony tissues is
com-plete.As a general rule,one should alwaysmaintain excessive soft tissue
coveragewhere available until the final bony aug-mentation is
complete.Complicationssuch as dehiscence,loss ofkeratinizedmucosa,and obliteration
ofvestibulardepth can be avoided ifrespect is given tooverlying soft tissue.Once
bony healing iscomplete,ifthe overlying tissue is clearlyexcessive,removal ofthe
excess soft tissuecan proceed without complication.Usingthe classification
ofedentulous jawsaccording to Cawood and Howell,7thereconstructive surgeon can plan
treatmentfor his or her patients accordingly.Many excellent reconstructive
plansachieve less-than-satisfactory resultsbecause ofinadequate anesthetic manage-
ment ofthe patient during the procedure.Although many procedures can be accom-
plished under local anesthesia or sedation,the clinician must have a low threshold
toprovide general anesthesia in a controlled25351555 mm15
mmIIIIIIIVVVIVIIVIII25351555 mm15 mm25351555 mm15
mmSymphysisParasymphysisMolarResorption (mm)FIGURE9-3Modified Cawood and Howell
classification ofresorption.The thicker line illustrates the amountofattached
mucosa,which decreases with progressive resorption.Adapted from Cawood JI,Howell
RA.7
162Part 2: Dentoalveolar Surgeryoperative setting to allow for
appropriatemanipulation ofthe surgical site to achievethe necessary goals ofthe
surgical proce-dure.Patient desires,health issues,surgeoncomfort,and the magnitude
ofthe defor-mity should all be considered when mak-ing decisions regarding
anesthetic type.The loss ofmaxillary and mandibularbone can have mild to severe
effects on anindividual�s well-being.Interestingly,thesize ofthe defect does not
always correlatewith the level ofdebilitation perceived bythe patient.Individuals
missing a singleanterior tooth with an associated buccalwall defect can feel quite
compromised,whereas,although it is rare,we haveencountered totally edentulous
patientswho live and function without even aremovable denture.This variability
under-scores the need for the dental team tounderstand the patient�s
chiefcomplaintand desired restorative goals.After obtain-ing a medical dental
history and diagnos-tic database,time spent educating thepatient about his or her
problem may helpthe patient refine goals and make it easierto develop a
satisfactory treatment plan.Since acceptable prosthetic reconstructioncan be
achieved with a variety oftreat-ments that vary in complexity,invasive-ness,time to
completion,simplicity ofmaintenance,functional attributes,esthet-ic attributes,and
cost,it is reasonable todevelop more than one treatment planthat can address the
patient�s needs.The patient�s overall health status,com-pliance
potential,patience,and ability tomaintain the final prosthesis/prosthesesmust be
considered when planning recon-structive preprosthetic surgical proceduresas well
as future prosthetic rehabilitation.Moreover,a multidisciplinary approachinvolving
the patient�s input is imperative forlong-term success and patient
satisfaction.3Principles ofBone RegenerationThere are many approaches available
forreconstructing a deficiency or defectiveosseous anatomy ofthe alveolar
portionsofthe facial skeleton.These include bio-logically viable autogenous bone
grafts,nonviable homologous allogeneic or het-erogeneic bone
implants,recombinanthuman bone morphogenetic protein-2(rhBMP-2),and tissue
regeneration bydistraction histogenesis.These techniquescan be used alone or in
combination andABFIGURE9-4A,Example ofmandible with muscular attachments at or near
the crest ofthe ridge.Also notethe absence offixed keratinized tissue over the
alveolar ridge area.B,Example ofmaxilla with inadequatevestibular depth
anteriorly,frenal attachments near the crest ofthe alveolar ridge,and flabby soft
tissue overthe alveolar ridge crest.Reproduced with permission from Tucker
MR.Ambulatory preprosthetic recon-structive surgery.In: Peterson LJ,Indresano
AT,Marciani RD,Roser SM.Principles oforal and maxillofa-cial surgery.Vol
2.Philadelphia (PA): JB Lippincott Company; 1992.p.1107.FIGURE9-5A,Evaluation ofthe
bone in themandible reveals contour irregularities oftheanterior region and a
vertical alveolar deficiencyin the posterior mandible area
bilaterally.B,Grossirregularities are evident along the maxillaryalveolar
ridge,with bilateral contour defects in thecanine-premolar area.C,Mounted casts are
usedto evaluate mandibular alveolar ridge deficiencyand anteroposterior skeletal
deficiency ofthemandible.Reproduced with permission fromTucker MR.Ambulatory
preprosthetic reconstruc-tive surgery.In: Peterson LJ,Indresano AT,Mar-ciani
RD,Roser SM.Principles oforal and max-illofacial surgery.Vol 2.Philadelphia (PA):
JBLippincott Company; 1992.p.1106.ABC
Preprosthetic and Reconstructive Surgery163often are enhanced by the application
ofadjunct procedures such as rigid fixationand guided bone regeneration.The
choiceofa reconstructive technique is influencedby many variables,including the
location,ridge relationships,dimensions ofthedefect,dimensions ofunderlying
bonestock,soft tissue availability and viability,and esthetic goals.Beyond choosing
a reconstructivetechnique,one must also consider inher-ent properties offacial bone
and its natur-al growth and remodeling characteristics.For bone to grow or
regenerate in directpressure areas,it must go through anendochondral replacement
process such asthat in active long bones or the mandibu-lar condyle.Areas ofthe
skeleton that areunder pressure must be covered by carti-lage�a tissue adapted to
this functionbecause it grows interstitially;is minimal-ly
calcified,avascular,turgid,and nour-ished by diffusion;and does not require
amembrane for nutrition.In contrast,bonecannot withstand significant
pressurebecause ofcompression closure ofthe vas-cular bed in the periosteum.Because
bonematrix is calcified,it must be vascularizedto grow,regenerate,or be
sustained.InFIGURE9-6A,Panoramic radiographshows anapparently adequate alveolar
ridge height.B,Lat-eral cephalometric radiograph ofthe same patientshows a
concavity in the anterior area ofthe alve-olar ridge,which produces a knife-edge
ridgecrest.This type ofalveolar ridge deformity cannotbe fully appreciated except
on a cephalometricradiograph.Reproduced with permission fromTucker MR.Ambulatory
preprosthetic recon-structive surgery.In: Peterson LJ,Indresano AT,Marciani
RD,Roser SM.Principles oforal andmaxillofacial surgery.Vol 2.Philadelphia (PA):JB
Lippincott Company; 1992.p.1107.ABFIGURE9-7A,Preoperative computed tomog-raphy (CT)
scan ofthe maxillary sinuses toallow for angulation and size measurement
ofatransantral implant restoration.B,The informa-tion gained from the CT evaluation
is applied tothe surgical placement ofimplants.C,Postoper-ative panoramic
radiograph ofthe implantplacement traversing the maxillary sinus.ABCFIGURE9-
8Computed tomography-based imaging used to evaluatebone density,quality,contour,and
volume.This information,whichhas cross-sectional tomographic and three-dimensional
components,can be used to plan treatments for complex cases ofimplant place-ment.
(Courtesy ofSimPlant Technologies)
164Part 2: Dentoalveolar Surgeryaddition,calcification ofthe matrix pre-cludes
interstitial growth,so bone can onlygrow by the appositional activity
ofitsmembranes.Periosteum has a dense con-nective tissue component and is struc-
turally adapted to transfer tensile forcesthat are generated by muscles,tendons,and
ligaments to bone.The majority ofthe facial skeleton isnot under load during
development;thusit does not require an endochondral phase,so it develops by an
intramembranousprocess.In the natural state,alveolar boneis protected from load by
the dentitionand is actually stimulated by strain forcestransferred to the alveolus
via the peri-odontal ligament.Although technology todate has not been able to
exactly replicatethis interface,osseointegrated implantshave a similar protective
effect on underly-ing bone,native or reconstructed,and thusshould be a component
ofall alveolarbone reconstructive plans.Another aspect offacial bone growthand
development relevant to reconstruc-tion that needs to be clearly understood isthe
regional differences in periosteumactivity that exist in association with
facialbones.It is a misconception that the cor-tices ofgrowing facial bones are
producedonly by periosteum.In fact,at least halfofthe facial bone tissue is formed
by endos-teum,the inner membrane lining themedullary cavity.Ofgreat significance
tothe placement ofalveolar ridge or alveolardefect bone grafts are the findings
thatabout halfofthe periosteal surfaces offacialbones are resorptive in nature and
halfaredepository.These properties exist becausefacial growth is a complex balance
betweendeposition and resorption that adds to thesize and shape ofa bone while it
is beingdisplaced to achieve its final position andrelationships to the bones ofthe
facial cra-nial skeleton.One can study the works anddiagrams ofEnlow and colleagues
to gain abetter understanding ofthese concepts andthe regional variations
ofnaturally resorp-tive and depository surfaces ofthe facialskeleton.10This
understanding should helpone better determine the most efficaciouslocation for
graft placement.For example,the anterior surface ofthe maxillary andmandibular
alveolar ridges are resorptiveand thus are best treated by the
placementofinterpositional grafts in association withthe endosteal aspects ofthese
bones,as seenin Figure 9-10.Interestingly,the periosteallining ofthe maxillary
sinus is also mostlyresorptive.Successful bone grafting via thesinus lift technique
has been demonstratedby numerous authors using a variety ofgraft techniques.It has
been our experiencethat sinus lift grafts ofautogenous cancel-lous bone,and bone
induced to grow byrhBMP-2,secondarily treated with osseo-integrated implants
remodel over time.A follow-up of> 5 years ofsome ofourpatients has shown that the
grafts becomescalloped over the surfaces ofthe implants,similar to the relationship
seen when natur-al roots extend above the floor ofa pneu-matized sinus.This finding
suggests thatthe capacity for remodeling by theperiosteal membrane exists even
after theface is mature,and that viable bone estab-lished by autogenous grafts or
rhBMP-2-mediated induction responds to thisprocess.11Another concept offacial
growth thatbears relevance to contemporary methodsofreconstruction is the
functional matrixconcept that has largely been described byMoss.12This concept
states that bone,itself,does not regulate the rate ofbonegrowth.Instead,it is the
functional softtissue matrix related to bone that actuallydirects and determines
the skeletal growthprocess.The vector and extent ofbonegrowth are secondarily
dependent on thegrowth ofassociated soft tissue.Bone,byvirtue ofits matrix
maturity,gives feed-back to this process by either inhibiting itor allowing it to
accelerate.Thus,the vol-ume ofbone generated is based on geneticproperties ofthe
soft tissue and a mechan-ical equilibration between bone and itssoft tissue
matrix.These principles are vis-ited when distraction forces are applied
toosteotomized bone.In 1989 Ilizarov forwarded the theoryoftension-stress applied
to bone as amechanism oflengthening bone.13,14Hestated that controlled
mechanicallyapplied tension-stress allows bone and softtissue to regenerate in a
controlled,reli-able,and reproducible manner.During thelatency phase
ofdistraction,there is aperiosteal and medullary revascularizationand
recovery.Simultaneously a relativelyhypovascular fibrous interzone developsthat is
rich in osteoprogenitor cells andserves as a pseudo�growth plate.Adjacentand
connected to the interzone are areas ofhypervascular trabeculae aligned in
thedirection ofthe distraction.Osteoprogen-itor cells in the interzone
differentiate intoosteoblasts and line the trabeculae.As dis-traction
progresses,appositional bonegrowth enlarges the trabeculae.Thisunderscores the idea
that mechanicalFIGURE9-9A,Computer-generated surgicalstent for implant
placement.B,Clinical photo-graph ofimplants placed with the use ofa com-puter-
generated surgical stent.AB
Preprosthetic and Reconstructive Surgery165stress applied to the soft tissue matrix
ofosteotomized bone can reactivate thesenative growth processes.It is interesting
to note that ifthe dis-traction device lacks sufficient mechanicalstability or
ifthe rate ofdistraction pro-gresses too rapidly,the tissue establishedmay mature
very slowly or not at all.On theother hand,ifdistraction progresses tooslowly,the
regenerate may mature prema-turely or there may be increased pain duringthe
procedure.We have found that ifthere isrecurrent pain associated with the activa-
tion ofa distractor,a slight increase in therate ofdistraction usually reduces the
pain.In many ways distraction histogenesis reca-pitulates the process ofnative bone
growthdirected by the influence ofthe soft tissuematrix.Premature maturation ofthe
matrixincreases resistance to distraction necessitat-ing increased distraction
force and the per-ception ofpain by the patient.This suggeststhat even the feedback
role ofthe bonematrix is active during this process.In mostcases the net result
ofdistraction histogene-sis is the formation ofa bone ossicle that isvascular and
rich in osteolysis,has a shapesimilar to the native bone,and has anappropriate soft
tissue envelope.Often dis-traction histogenesis alone is sufficient toregenerate
deficient alveolar ridge anatomy.In other cases distraction can be used
inassociation with bone grafting,especiallywhen the associated bone stock is
ofless-than-ideal shape or volume.In some cases,particularly in the posterior
mandible,thedistraction osteotomy can be extendedbeyond the area ofintended
implants sothat the distraction process actually growsthe bone needed for the
graft.Bone graftsplaced adjacent to regenerate typicallymature very rapidly owing
to the vasculari-ty,cellularity,and high concentration ofnatural BMP in
regenerate.Bone GraftsBone graft principles are discussed inChapters 12,�Bone
Grafting Strategies forVertical Alveolar Augmentation,�39,�Bony Reconstruction
ofthe Jaws,�40,�Microvascular Free Tissue Transfer,�and43,�Reconstruction ofthe
Alveolar Cleft.�Nonetheless,some ofthe characteristics ofgrafts and bone implants
pertinent to pre-prosthetic surgery are examined here.Byfar the most common graft
type is the freeautogenous viable bone graft.Since thesegrafts are from the
patient,they do notelicit an immune-rejection response.Common areas for procurement
includethe maxilla,mandible,cranium,tibialplateau,iliac crest,and rib.The
shape,form,and volume ofthe graft procuredare linked to the defect to be
reconstruct-ed.These grafts are used as corticocancel-lous blocks or particulate
cancellous graftscompacted and shaped by various mem-branes or trays.In many
instances purelycancellous blocks or cancellous particulatebone is used again with
membranes or traysor sandwiched in unloaded osteotomies ordefects.A third form
includes purely corti-cal grafts,primarily used to form a wall orstrut in
association with a defect that issimultaneously packed with particulatecancellous
bone.Cortical grafts revascu-larize very slowly and have minimal to nocell
survival;thus,they are not ideal forimplant placement.15Cancellous grafts have the
greatestconcentration ofosteogenic cells,and theparticulate form ofthese grafts has
thegreatest cell survival owing to better diffu-sion and rapid
revascularization.Thesegrafts must completely undergo a two-phase mechanism ofgraft
healing.16Osteoblasts that survive transplantationproliferate and form osteoid.This
processis active in the first 2 to 4 weeks,and thedefinitive amount ofbone formed
is relat-ed to the quantity ofosteoid formed inphase one.Phase two starts around
the sec-ond week after grafting,and although itpeaks in intensity at approximately
4 to 6 weeks,it continues until the graftmatures.The initiation ofphase two
ismarked by osteoclastic cell activity withinFIGURE9-10Growth and remodeling field
ofthe craniofacial skeleton.Resorptive fields are shadedand depository fields are
free ofshading.
166Part 2: Dentoalveolar Surgerythe graft.Osteoclasts remove mineral,forming
Howship�s lacunae along the tra-beculae.This resorptive process exposesthe
extracellular matrix ofbone,which isthe natural location ofthe bone-
inductiveglycoprotein BMP.Exposure ofBMP initi-ates an inductive process
characterized bychemotaxis ofmesenchymal stem cells,proliferation ofcells in
response to mito-genic signals,and differentiation ofcellsinto
osteoblasts.17Inducible cell popula-tions may be local or distant from the
graftsite.Examples oflocal cell populations thatmay contribute to the graft include
osteo-progenitor cells in the graft endosteum,stem cells ofthe transplanted
marrow,orcells in the cambium layer ofadjacentperiosteum.Additional inducible
pluripo-tent cells may arrive at the graft site withbudding blood vessels.During
phase twothere is progressive osteoclastic resorptionofphase one osteoid and
nonviable grafttrabeculae;this continues to expose BMP,which perpetuates the
differentiation ofosteoblasts,leading to the formation ofmature vascular osteocyte-
rich bone.This two-phase bone graft healingprocess is the one that most reliably
andquickly can regenerate bone with charac-teristics suitable for implant
placement.When choosing a bone graft,one mustconsider its ultimate purpose;since
mostgrafts associated with preprostheticsurgery are designed to support
implants,these grafts must provide the biologicenvironment necessary for
osseointegra-tion.Osseointegration is a biologicprocess,and its long-term success
requiresvascular osteocyte-rich bone.Another adjunct to preprostheticbone
reconstruction is the use ofallo-geneic bone.Since these grafts are nonvi-able,they
are technically implants.Allo-geneic bone is procured in a fresh sterilemanner from
cadavers ofgeneticallyunrelated individuals.American Associa-tion ofTissue Bank
standards require thatall donors be screened,serologic tests beperformed,and all
specimens be sterilizedand verified by culture prior to release.Processing
ofallogeneic bone is designedto achieve sterility and reduce immuno-genicity.Bone
cell membranes have bothclass I and II major histocompatibilitycomplexes on their
surfaces.These are themain sources ofimmunogenicity withinallogeneic bone
grafts.Allogeneic boneimplants are processed to remove theorganic matrix and only
retain the miner-al components;architecture is generallyconsidered to be
nonimmunogenic.Implants retaining both mineral andorganic components or
demineralizedimplants with only the organic compo-nent are washed and then
lyophilized toreduce immunogenicity.In most casesthis process reduces the immune
responseto clinically insignificant levels.In addi-tion to this
treatment,allogeneic bankbone is irradiated with ?-rays,a processthat assures
sterility and further reducesantigenicity.Unfortunately,this requires 2 to 3 Mrad
per radiation dose,whichdestroys BMP and thus the ability oftheseimplants to be
osteoinductive.18Common applications ofallogeneicbone implants for preprosthetic
surgeryinclude mandibles,iliac crest segments,andcalcified or decalcified ribs that
can be pre-pared and used as biologic trays for the place-ment and retention
ofcancellous bone grafts.Additional uses include mineral matrix ordemineralized
particulate implants used asosteoconductive graft extenders or forextraction-site
shape and form preservation.Research on particle size suggests that parti-cles in
the range of250 to 850 �m are themost useful.Although the current carrier sys-tem
used for rhBMP-2 bone induction is acollagen membrane,Becker and colleaguesshowed
that BMP extracted from the bonecan be added to particulate 200 to 500
�mdemineralized freeze-dried bone allograftsobtained from four American tissue
banks;this resulted in the transformation ofnon-inductive particles to particles
with osteoin-ductive properties.19Heterogeneous bonegrafts,or xenografts,are
specimens trans-ferred from one species to another.Implantsofthis type contain an
organic componentthat would elicit a strong immuneresponse;thus,they are not used
in con-temporary practice.Bovine implants thathave undergone complete
deproteinizationto remove the organic component havebeen shown to be
nonimmunogenic.Theseimplants remain as an inorganic mineralscaffold that can be
used for their osteocon-ductive properties as graft extenders or forextraction-site
preservation.The above discussion has identifiedtwo reconstructive methods that can
reli-ably restore bone with the characteristicsnecessary for maintaining
osseointegratedimplants.These methods include autoge-nous cancellous bone grafts
and distrac-tion histogenesis alone or with graft sup-plementation.A third approach
alluded toabove is the use ofrhBMP-2.20rhBMP-2has been studied extensively in
animalmodels,and human clinical trials in theareas oforthopedic surgery,spine
surgery,and maxillofacial surgery have been ongo-ing during the past decade.rhBMP-
2/ACS,which is the clinical combination ofBMPwith an absorbable collagen sponge
carrierplaced with a metal cage,received US Foodand Drug Administration (FDA)
approvalfor spine fusion surgery in 2002.To date,US human clinical trials related
to maxillo-facial reconstruction include complete fea-sibility studies,safety and
efficacy studies,and dose-response studies involving eitheralveolar ridge buccal
wall defects or poste-rior maxillary alveolar bone deficiency atsinus lift bone
sites.Safety has been estab-lished,and a dose of1.5 mg/mL,the samedose used for
spine fusion,was chosen formaxillofacial applications after completionofa sinus
lift dose-response study.A 20-center study ofpivotal sinus lifts is
nearcompletion;its dual end points include theevaluation ofbone regeneration at
endpoint one and the evaluation of2-yearloaded implant data at end point
two.Todate,a time frame for submitting this datafor FDA approval has not been
established.
Preprosthetic and Reconstructive Surgery167At our center 9 patients were enrolled
inthe pivotal study,with 21 evaluated sinuslifts sites.All study sites were
confirmedbefore treatment by CT scan to have 5 mmor less ofnatural bone.Six months
aftergraft placement,comparative CT scanswere obtained from all study sites and
thepresence ofgraft and graft dimensionswere assessed.All sites had enough bonefor
placement ofimplants at least 4 mm indiameter and 12 mm high.Trephine-procured
biopsy specimens obtained at thetime ofimplant placement were used toverify the
presence ofhomogeneous vascu-lar osteocyte-rich bone with a normal tra-becular and
marrow-space architecture.Atour center all 21 implants have remainedfunctionally
loaded for at least 36 months.These results are preliminary and may notreflect the
findings ofall centers.Similar tonatural BMP,rhBMP-2/ACS has beenshown to stimulate
the cascade ofbone-regeneration events,including chemotaxis,induction ofpluripotent
cells,and prolifer-ation.Our results to date show that thistechnique has the
potential to significantlyenhance patient care by providing anunlimited supply
ofnonimmunogenicsterile protein that can induce de novobone formation.Bone
regenerated by thisprocess has characteristics ofbone desir-able for implant
placement (Figure 9-11).Hopefully,the discussion ofhostproperties and regenerative
or graft tech-niques in this section will aid one in deter-mining the best graft
for sites to be recon-structed as part ofa preprosthetic surgicaltreatment
plan.Hard Tissue RecontouringCurrent Trends in Alveolar PreservationAs dental
implants continue to grow inpopularity and play a major role in pros-thetic
reconstruction,the need for tradi-tional bony recontouring at the time ofextraction
has been de-emphasized.Cur-rent trends tend to lean toward preserva-tion ofalveolar
bone and overlyingperiosteal blood supply,which enhancesand preserves future bone
volume.Alterna-tives to traditional alveoloplasty haveemerged in an effort to
maintain boneheight and volume for the placement ofimplants to provide a stable
platform forprosthetic reconstruction.Such alternativesinclude orthodontic guided
tooth/rootextraction,conservative extraction tech-niques using periosteotomes to
maintainalveolar continuity,immediate grafting ofextraction sites,reliefofundercuts
usingbone grafts or hydroxylapatite (HA) aug-mentation,and guided tissue
regeneration.In cases where bony abnormalities orundercuts require
attention,selective alveo-lar recontouring is indicated.Advances in implant
technology haveplaced a greater emphasis on planning foralveolar ridge
preservation.Beginning atthe initial consultation,all extraction sitesshould be
considered for implant recon-struction.Regardless ofthe reason forextraction
(ie,pulpal disease,periodontaldisease,or trauma),every effort should bemade to
maintain alveolar bone,particu-larly buccal (labial) and lingual
(palatal)walls.However,even with alveolar bonemaintenance,there can be
unpredictableresorption in a short period oftime.21Multiple adjacent extractions
may alsocontribute to extensive alveolar bone lossprecluding implant
reconstruction.Historically,techniques for alveolarridge preservation were
developed tofacilitate conventional denture prostheses.HA materials were the first
materials notFIGURE9-11Stages ofbone maturation are evident in these
photomicrographs ofautogenous bone grafts,autogenous grafts with bone morphogenetic
protein(BMP),and distraction-regenerate.A,Autogenous tibial plateau with no filler
was placed in this sinus lift site with < 5 mm ofnative bone,procured by
trephine,and sampled at 6 months after the graft.Viable osteocyte-rich bone
trabeculae are evident with normal marrow spaces with a few residual foci
ofnonviable graft(�100 original magnification; hematoxylin and eosin stain).B,BMP
was placed in an identical site to that shown in Figure A (�75 original
magnification:hematoxylin and eosin stain).This specimen reveals viable trabeculae
with normal haversian canals,de novo bone growth,and no nonviable
components.C,Regenerate was procured at the time ofthe distractor removal at this
mandibular distraction site.The regenerated growth represents woven bone with
somemature haversian systems (�128 original magnification: hematoxylin and eosin
stain).ABC
168Part 2: Dentoalveolar Surgeryplagued by host rejection and
fibrousencapsulation.Previously,the use ofpoly-methyl methacrylate,vitreous
carbon,and aluminum oxide had led to poorresults.Root form and particulate HAboth
were adapted and successful in pre-serving alveolar ridge form.22The
obviouslimitation with nonresorbable materials isthat they preclude later implant
recon-struction.Tricalcium phosphate is aresorbable ceramic that was
originallythought would solve this problem,but itproved not to be truly
osteoconductive asit promoted giant cell rather than osteo-clastic
resorption.23This resulted in limit-ed osteogenic potential.Another alloplastthat
has been used for this purpose isbioactive glass,which consists
ofcalcium,phosphorus,silicone,and sodium,but,again,the biologic behavior
ofthereplacement bone was never felt to be sat-isfactory for implant
reconstruction.24The gold standard for use for bonyreconstruction anywhere has
always beenautogenous grafts.The dilemma with auto-genous grafts involves donor
site morbidi-ty:whether from an intraoral or extraoralsource,the additional surgery
and inconve-nience to the patient has precluded its gen-eral use.To avoid the use
ofa donor site,various allogeneic bone preparations havebeen advocated.Stringent
tissue bank regu-lations have provided the public withgreater confidence in the use
ofthese mate-rials.Anorganic bone has most recentlybeen adapted for use in alveolar
ridgepreparation.Two products are currentlyavailable commercially.The first is
axenograft derived from a bovine source.The main advantage ofthis type ofmateri-al
is that it is available in an almost unlim-ited supply and is chemically and
biologi-cally almost identical to human bone.Minimal immune response is
elicitedbecause ofthe absence ofprotein;however,the resorption rate ofbovine
cortical boneis slow.In both animal and human studies,remnants ofnonvital cortical
bone havebeen shown to be present 18 months orlonger in the grafted site.25A second
prod-uct,derived from human bone,is processedby solvent extraction and
dehydration.Ani-mal studies have shown that there is near-complete remodeling with
little or no rem-nant ofthe human anorganic bone left inthe specimen.26Both the
deproteinized bovine boneand the solvent dehydrated mineralizedhuman bone appear to
have great potentialin alveolar ridge preservation.These materi-als take a long
time to resorb,so a ridge formis maintained over an extended period oftime,and are
resorbed and remodeled viaan osteoclastic process that results in boneideally
suited for implant placement.The technique for alveolar ridge preser-vation at the
time ofextraction has beendescribed by Sclar.27Atraumatic extractionis
essential.Preservation ofbuccal or labialbone may be facilitated by the use
ofmicro-osteotomes,and,whenever possible,buccalor labial mucoperiosteal elevation
is to beavoided or limited.The socket should begently curetted and irrigated,and in
thepresence ofperiodontal infection,topicalantibiotics may be
helpful.Tetracyclinepowder mixed with the deproteinizedbovine bone or the solvent
dehydrated min-eralized human bone may allow for the useofeither ofthese types
ofbone in almostany clinical situation.It is not essential thatthe graft have
complete watertight mucosalcoverage.Collagen membrane is used toprevent spillage
ofthe material from thesocket,particularly in maxillary extractions.When temporary
restorations are employedat the time ofsurgery,an ovate pontic pro-visional
restoration helps to support theadjacent mucosa during soft tissue matura-tion.In
selected instances immediate place-ment ofimplants in the extraction site canbe
done in conjunction with the use ofthesedeproteinized bone
preparations.Becauseofthe slow resorptive nature ofboth ofthese bone
preparations,they may be ideal-ly suited for buccal or labial defects thatwould
otherwise be grafted with autoge-nous cortical bone.AlveoloplastyOften hard and
soft tissues ofthe oralregion need to undergo recontouring toprovide a healthy and
stable environmentfor future prosthetic restorations.Simplealveolar recontouring
after extractionsconsists ofcompression and in-fracture ofthe socket;however,one
must avoid over-compression and over-reduction ofirreg-ularities.Current trends
endorse a selec-tive stent-guided approach to site-specificbony
recontouring,eliminating bonyabnormalities that interfere with prosthet-ic
reconstruction or insertion.Multipleirregularities produce undercuts that
areobstructions to the path ofinsertion forconventional prosthetic
appliances.Theseobstructions need a more complex alve-oloplasty to achieve desired
results.Inmany cases the elevation ofmucoperi-osteal flaps using a crestal incision
withvertical releases is necessary to preventtears and to produce the best access
to thealveolar ridge.During mucoperiosteal flapresection,periosteal and Woodson
eleva-tors are the most appropriate tools to pre-vent excess flap
reflection,devitalization,and sequestrum formation.These condi-tions increase pain
and discomfort for thepatient and increase the duration neededbefore prosthetic
restoration can proceed.The use ofa rongeur or file for advancedrecontouring is
preferred to rotary instru-ments to prevent over-reduction.For largebony
defects,rotary instrument recon-touring is preferred.Normal saline irriga-tion is
used to keep bony temperatures < 47�C to maintain bone viability.Owing to the
physiology ofbone andcurrent restorative options available,interseptal
alveoloplasty is rarely indicat-ed.The main disadvantage ofthis proce-dure is the
overall decrease in ridge thick-ness,which results in a ridge that may betoo thin
to accommodate future implantplacement.9Removal ofinterseptal boneeliminates
endosteal growth potential,which is necessary for ridge
preservation.Therefore,ifthis technique is to be used,
Preprosthetic and Reconstructive Surgery169one must be cognizant ofridge
thicknessand reduce the labial dimension onlyenough to lessen or eliminate
undercuts inareas where implants are not anticipated.After hard tissue
recontouring,exces-sive soft tissue is removed to relieve mobiletissue that
decreases the fit and functionalcharacteristics ofthe final prosthesis.Clo-sure
with a resorbable running/lock-stitchsuture is preferred because fewer knots
areless irritating for the patient.Treatment ofExostosesUndercuts and exostoses are
more commonin the maxilla than in the mandible.In areasrequiring bony
reduction,local anestheticshould be infiltrated.This produces ade-quate anesthesia
for the patient as well as anaid in hydrodissection ofthe overlying tis-sues,which
facilitates flap elevation.In themandible an inferior alveolar neurovascularblock
may also be necessary.A crestal inci-sion extending approximately 1.5 cmbeyond each
end ofthe area requiring con-tour should be completed.A full mucoperi-osteal flap
is reflected to expose all the areasofbony protuberance.Vertical releasingincisions
may be necessary ifadequateexposure cannot be obtained since traumaofthe soft
tissue flap may occur.Recontour-ing ofexostoses may require the use ofarotary
instrument in large areas or a handrasp or file in minor areas.Once removal ofthe
bony protuberance is complete andvisualization confirms that no irregularitiesor
undercuts exist,suturing may be per-formed to close the soft tissue
incision.Ifnonresorbable sutures are used,they shouldbe removed in approximately 7
days.In areas likely to be restored withimplants or implant-supported prosthe-
ses,irregularities and undercuts are besttreated using corticocancellous grafts
froman autogenous or alloplastic source.Thiscan be done using a vertical incision
onlyadjacent to the proposed area ofgrafting.A subperiosteal dissection is used to
createa pocket for placement ofthe graft mater-ial.Visual inspection and palpation
ofthearea should be done at the conclusion ofthe procedure to verify the
reliefofthedefect.The incision can be closed withresorbable sutures.In areas that
require alarge amount ofgraft material,scoring ofthe periosteum can assist in
closure ofsofttissue defects.In addition,the use ofaresorbable collagen membrane
can beused to prevent tissue ingrowth into thesurgical site.Tuberosity
ReductionExcesses in the maxillary tuberosity mayconsist ofsoft tissue,bone,or
both.Sound-ing,which is performed with a needle,candifferentiate between the causes
with a localanesthetic needle or by panoramic radi-ograph.Bony irregularities may
be identi-fied,and variations in anatomy as well as thelevel ofthe maxillary
sinuses can be ascer-tained.Excesses in the area ofthe maxillarytuberosity may
encroach on the interarchspace and decrease the overall freeway spaceneeded for
proper prosthetic function.Access to the tuberosity area can be obtainedeasily
using a crestal incision beginning inthe area ofthe posterior tuberosity and pro-
gressing forward to the edge ofthe defectusing a no.12 scalpel blade.Periosteal
dis-section then ensues exposing the underlyingbony anatomy.Excesses in bony
anatomy areremoved using a side-cutting rongeur.Care-ful evaluation ofthe level
ofthe maxillarysinus must be done before bony recontour-ing is attempted in the
area ofthe tuberosity.Sharp undermining ofthe overlying soft tis-sue may be
performed in a wedge-shapedfashion beginning at the edge ofa crestalincision to
thin the overall soft tissue bulkoverlying the bony tuberosity.Excess overly-ing
soft tissue may be trimmed in an ellipticfashion from edges ofthe crestal incision
toallow a tension-free passive closure (Figure9-12).Closure is performed using a
nonre-sorbable suture in a running fashion.Smallsinus perforations require no
treatment aslong as the membrane remains intact.Largeperforations must be treated
with a tension-free tight closure as well as antibiotics,preferably a
penicillinase-resistant penicillinsuch as an amoxicillin/clavulanate potassi-um
preparation or a second-generationcephalosporin.The patient is instructed totake
sinus medications including antihista-mines and decongestants for approximately10
to 14 days and not to create excessivetransmural pressure across the incision
siteby blowing his or her nose or suckingthrough straws.Genial Tubercle
ReductionThe genioglossus muscle attaches to thelingual aspect ofthe anterior
mandible.Asthe edentulous mandible resorbs,thistubercle may become significantly
pro-nounced.In cases in which anteriormandibular augmentation is indicated,leaving
this bony projection as a base forsubsequent grafting facilitates augmenta-tion
ofmandibular height.During conven-tional mandibular denture fabrication,thisbony
tuberosity as well as its associatedmuscle attachments may create displace-ment
issues with the overlying prostheses.In these cases it should be relieved.Floor-of-
mouth lowering procedures should alsobe considered in cases in which genioglos-sus
and mylohyoid muscle attachmentsinterfere with stability and function
ofconventional mandibular prostheses.Bilateral lingual nerve blocks in thefloor
ofthe mouth are necessary to achieveadequate anesthesia in this area.A
crestalincision from the midbody ofthe mandibleto the midline bilaterally is
necessary forproper exposure.A subperiosteal dissectionexposes the tubercle and its
adjacent muscleattachment.Sharp excision ofthe musclefrom its bony attachment may
be per-formed with electrocautery,with carefulattention to hemostasis.A
subsequenthematoma in the floor ofthe mouth maylead to airway embarrassment and
life-threatening consequences ifleft unchecked.Once the muscle is detached,the
bonytubercle may then be relieved using rotaryinstrumentation or a rongeur.Closure
isperformed using a resorbable suture in a
170Part 2: Dentoalveolar Surgeryrunning fashion.The genioglossus muscleis left to
reattach independently.Tori RemovalThe etiology ofmaxillary and mandibulartori is
unknown;however,they have anincidence of40% in males and 20% infemales.28Tori may
appear as a single ormultiloculated bony mass in the palate oron the lingual aspect
ofthe anteriormandible either unilaterally or bilaterally.In the dentate patient
they are rarely indi-cated for removal.Nevertheless,repeatedoverlying mucosal
trauma and interfer-ence with normal speech and masticatorypatterns may necessitate
treatment.In thepatient requiring complete or partial con-ventional prosthetic
restoration,they maybe a significant obstruction to insertion orinterfere with the
overall comfort,fit,andfunction ofthe planned prosthesis.In the maxilla,bilateral
greater palatineand incisive blocks are performed toachieve adequate
anesthesia.Local infiltra-tion ofthe overlying mucosa helps withhemostasis and
hydrodissection that facili-tates flap elevation.A linear midline inci-sion with
posterior and anterior verticalreleases or a U-shaped incision in thepalate
followed by a subperiosteal dissec-tion is used to expose the
defect.Rotaryinstrumentation with a round acrylic burmay be used for small
areas;however,forlarge tori,the treatment ofchoice is sec-tioning with a cross-cut
fissure bur.Oncesectioned into several pieces,the torus iseasily removed with an
osteotome.Caremust be taken not to over-reduce the palateand expose the floor ofthe
nose.Final con-touring may be done with an egg-shapedrecontouring bur (Figure 9-
13).Copiousirrigation is necessary throughout the pro-cedure.Closure is performed
with aresorbable suture.Presurgical fabricationofa thermoplastic stent,made from
dentalmodels with the defect removed,in combi-nation with a tissue conditioner
helps toeliminate resulting dead space,increasepatient comfort,and facilitate
healing incases in which communication occurs withthe nasal floor.Soft tissue
breakdown is notuncommon over a midline incision;how-ever,meticulous
hygiene,irrigation,andtissue conditioners help to minimize
thesecomplications.Mandibular tori are accessed usingbilateral inferior alveolar
and lingualnerve blocks as well as local infiltration tofacilitate dissection.A
generous crestalincision with subsequent mucoperiostealflap elevation is
performed.Maintenanceofthe periosteal attachment in the mid-line reduces hematoma
formation andmaintains vestibular depth.Nevertheless,when large tori encroach on
the midline,maintenance ofthis midline periostealattachment is impossible.Careful
flapelevation with attention to the thin fri-able overlying mucosa is necessary as
thistissue is easily damaged.Small protuber-ances can be sheared away with a
malletand osteotome.Large tori are dividedsuperiorly from the adjacent bone with
afissure bur parallel to the medial axis ofthe mandible and are out-fractured
awayfrom the mandible by an osteotome,which provides leverage (Figure 9-14).The
residual bony fragment inferiorlymay then be relieved with a hand rasp orbone
file.It is not imperative that theentire protuberance be removed as longas the
goals ofthe procedure areachieved.Copious irrigation during thisprocedure is
imperative,and closure iscompleted using a resorbable suture in arunning
fashion.Temporary denturedelivery or gauze packing lingually maybe used to prevent
hematoma formationand should be maintained for approxi-mately 1 day
postoperatively.Wounddehiscence and breakdown with exposureFIGURE9-12A,Area ofsoft
tissue to be excisedin an elliptic fashion over the tuberosity.B,Removal oftissue
and undermining ofbuccal andpalatal flaps completed.C,Final tissue closure.ABC
Preprosthetic and Reconstructive Surgery171ofunderlying bone is not uncommonand
should be treated with local irriga-tion with normal saline.Mylohyoid Ridge
ReductionIn cases ofmandibular atrophy,the mylo-hyoid muscle contributes
significantly tothe displacement ofconventional den-tures.With the availability
ofadvancedgrafting techniques and dental implants,there are fewer indications for
the reduc-tion ofthe mylohyoid ridge.In severe casesofmandibular atrophy,the
externaloblique and mylohyoid ridges may be theheight ofcontour ofthe
posteriormandible.In these cases the bony ridgemay be a significant source
ofdiscomfortas the overlying mucosa is thin and easilyirritated by denture flanges
extending intothe posterior floor ofthe mouth.As aresult,reduction ofthe mylohyoid
ridgemay accompany grafting techniques toprovide greater reliefand comfort for sub-
sequent restorations.Historically,this pro-cedure has been combined with
loweringofthe floor ofthe mouth;however,withthe advanced armamentarium
availabletoday,there are few,ifany,indications forthese procedures alone or in
combination.Anesthesia is achieved with buccal,inferior alveolar,and lingual
nerveblocks.A crestal incision over the heightofcontour is made,erring toward
thebuccal aspect to protect the lingualnerve.Subperiosteal dissection along
themedial aspect ofthe mandible reveals theattachment ofthe mylohyoid muscle tothe
adjacent ridge.This can be sharplyseparated with electrocautery to mini-mize muscle
bleeding.Once the overly-ing muscle is relieved,a reciprocatingrasp or bone file
can be used to smooththe remaining ridge.Copious irrigationand closure with
particular attention tohemostasis is completed.Placement ofastent or existing
denture may also aid inhemostasis as well as inferiorly reposi-tioning the
attachment.Again,these pro-cedures are rarely indicated and areincluded here
essentially for historic ref-erence,not for routine use.Soft Tissue
RecontouringWith the eventual bony remodeling thatfollows tooth loss,muscle and
frenumattachments that initially were not in aproblematic position begin to create
com-plications in prosthetic reconstruction andto pose an increasing problem with
regardto prosthetic comfort,stability,and fit.Often these attachments must be
alteredbefore conventional restoration can beattempted.As dental implants
becomecommonplace in the restoration ofpar-tially and totally edentulous
patients,sur-gical alteration ofthese attachments isindicated less
often.Nevertheless,inflam-matory conditions such as inflammatoryfibrous hyperplasia
ofthe vestibule orepulis,and inflammatory hyperplasia ofthe palate must be
addressed before anytype ofprosthetic reconstruction can pro-ceed.Obviously,any
lesion presentingpathologic consequences should undergobiopsy and be treated
accordingly beforereconstruction commences.In keepingwith reconstructive surgery
protocol,softtissue excesses should be respected andshould not be discarded until
the finalbony augmentation is complete.Excesstissue thought to be unnecessary may
beFIGURE9-13A,Preoperative view ofa maxillary torus with the midline incision
indicated (dashed line).B,Removal ofsectioned elements ofthe torus with an
osteotome.C,Final smoothing ofirregularities with a rotarybur.D,Final closure.ABCD
172Part 2: Dentoalveolar Surgeryvaluable after grafting or augmentationprocedures
are performed to increase theoverall bony volume.Hypermobile TissueWhen excess
mobile unsupported tissueremains after successful alveolar ridgerestoration,or when
mobile tissue exists inthe presence ofa preserved alveolar ridge,removal ofthis
tissue is the treatment ofchoice.Usually infiltrative local anesthesiacan be
performed in selected areas.Sharpexcision parallel to the defect in
asupraperiosteal fashion allows for removalofmobile tissue to an acceptable
level.Beveled incisions may be needed to blendthe excision with surrounding
adjacent tis-sues and maintain continuity to the sur-rounding soft tissue.Closure
withresorbable suture then approximates resid-ual tissues.Impressions for
prosthesis fabri-cation should proceed after a 3- to 4-weekperiod to allow for
adequate soft tissueremodeling.In cases in which dentureflange extension is
anticipated,the clinicianmust be careful to preserve the vestibulewhen undermining
for soft tissue closure.Granulation is a better alternative ifresid-ual tissues
cannot be approximated becauseit maintains the vestibule and increases thewidth
ofthe attached keratinized mucosa.Fibrous Inflammatory HyperplasiaFibrous
inflammatory hyperplasia is oftenthe result ofan ill-fitting denture that pro-duces
underlying inflammation ofthemucosa and eventual fibrous proliferationresulting in
patient discomfort and adecreased fit ofthe overlying prosthesis.Early management
consists mainly ofadjustment ofthe offending dentureflange with an associated soft
reline oftheprosthesis.When there is little chance ofeliminating the fibrous
component,surgi-cal excision is necessary.In most caseslaser ablation with a carbon
dioxide laseris the method ofchoice.When the treat-ment oflarge lesions would
result in sig-nificant scarring and obliteration ofthevestibule,sharp excision with
undermin-ing ofthe adjacent mucosa and reapproxi-mation ofthe tissues is
preferred.Again,maintenance ofa supraperiosteal planewith repositioning ofmucosal
edgesallowing for subsequent granulation ispreferred over approximation
ofwoundedges that results in the alteration ofvestibular depth.This is
accomplishedwith local anesthetic infiltrated into theproposed tissue bed,which is
closed only ifnecessary with resorbable sutures.Inflammatory Papillary Hyperplasia
Once thought to be a neoplastic process,inflammatory papillary hyperplasia
occursmainly in patients with existing prostheticappliances.29An underlying fungal
etiolo-gy most often is the source ofthe inflam-matory process and appears to
coincidewith mechanical irritation and poorhygiene practices.The lesion appears
asmultiple proliferative nodules underlyinga mandibular prosthesis likely
colonizedwith Candida.Early stages are easily treat-ed by an improvement ofhygiene
practicesand by the use ofantifungal therapy suchas nystatin tid alternating with
clotrima-zole troches intermittently.Nocturnalsoaking ofthe prosthesis in an
antifungalsolution or in an extremely dilute solutionofsodium hypochlorite helps
decrease theoverall colonization ofthe prosthesis.In proliferative cases
necessitating sur-gical treatment,excision in a supraperi-osteal plane is the
method ofchoice.Many methods are acceptable,includingsharp excision with a
scalpel,rotaryd�bridement,loop electrocautery asdescribed by Guernsey,and laser
ablationwith a carbon dioxide laser.30�32Becauseofthe awkward access needed to
removethe lesions,laser ablation is the methodwe employ.Treatment proceeds suprape-
riosteally to prevent exposure ofunder-lying palatal bone.Subsequently,place-ment
ofa tissue conditioner and adenture reline is helpful to minimizepatient
discomfort.Treatment ofthe Labial and Lingual FrenumLabial FrenectomyLabial frenum
attachments consist ofthinbands offibrous tissue covered withFIGURE9-14A,Rotary
trough exposes a mandibular torus and creates a cleavage plane between thetorus and
mandible.B,Osteotome shears the remaining attachment ofthe torus from mandible.AB
Preprosthetic and Reconstructive Surgery173mucosa extending from the lip and
cheekto the alveolar periosteum.The height ofthis attachment varies from individual
toindividual;however,in dentate individualsfrenum attachments rarely cause a prob-
lem.In edentulous individuals frenumattachments may interfere with fit and sta-
bility,produce discomfort,and dislodgethe overlying prostheses.Several surgical
methods are effectivein excising these attachments.Simple exci-sion and Z-plasty
are effective for narrowfrenum attachments (Figures 9-15 and 9-16).Vestibuloplasty
is often indicatedfor frenum attachments with a wide base.Local anesthetic
infiltration is per-formed in a regional fashion that avoidsdirect infiltration
into the frenum itself;such an infiltration distorts the anatomyand leads to
misidentification ofthefrenum.Eversion ofthe lip also helps oneidentify the
anatomic frenum and assistswith the excision.An elliptic incisionaround the
proposed frenum is completedin a supraperiosteal fashion.Sharp dissec-tion ofthe
frenum using curved scissorsremoves mucosa and underlying connec-tive tissue
leading to a broad base ofperiosteum attached to the underlyingbone.Once tissue
margins are under-mined and wound edges are approximat-ed,closure can proceed with
resorbablesutures in an interrupted fashion.Suturesshould encounter the
periosteum,espe-cially at the depth ofthe vestibule to main-tain alveolar ridge
height.This alsoreduces hematoma formation and allowsfor the preservation
ofalveolar anatomy.In the Z-plasty technique,excision ofthe connective tissue is
done similar tothat described previously.Two releasingincisions creating a Zshape
precedeundermining ofthe flaps.The two flapsare eventually undermined and rotated
toclose the initial vertical incision horizon-tally.By using the transposition
flaps,thistechnique virtually increases vestibulardepth and should be used when
alveolarheight is in question.FIGURE9-15A,Retracted lip exposes a
frenalattachment.B,Isolation and excision ofthe fre-nal attachment.C,Complete
excision revealingthe underlying periosteum.D,Closure ofunder-mined edges ofthe
incision.ACBDFlaps forclosing incisionFlaps forclosing incisionFlaps forclosing
incisionFIGURE9-16A,Excision ofa frenum withproposed Z-plasty
incisions.B,Underminedflaps ofthe Z-plasty.C,Transposed flapslengthening the
incision and lip attachment.ABC
174Part 2: Dentoalveolar SurgeryWide-based frenum attachments maybest be treated
with a localized vestibulo-plasty technique.A supraperiosteal dissec-tion is used
to expose the underlying perios-teum.Superior repositioning ofthe mucosais
completed,and the wound margin issutured to the underlying periosteum at thedepth
ofthe vestibule.Healing proceeds bysecondary intention.A preexisting dentureor
stent may be used for patient comfort inthe initial postoperative period.Lingual
FrenectomyHigh lingual frenum attachments mayconsist ofdifferent tissue types
includingmucosa,connective tissue,and superficialgenioglossus muscle fibers.This
attach-ment can interfere with denture stability,speech,and the tongue�s range
ofmotion.Bilateral lingual blocks and local infiltra-tion in the anterior mandible
provide ade-quate anesthesia for the lingual frenumexcision.To provide adequate
traction,asuture is placed through the tip ofthetongue.Surgical release ofthe
lingualfrenum requires dividing the attachmentofthe fibrous connective tissue at
the baseofthe tongue in a transverse fashion,fol-lowed by closure in a linear
direction,which completely releases the ventralaspect ofthe tongue from the
alveolarridge (Figure 9-17).Electrocautery or ahemostat can be used to minimize
bloodloss and improve visibility.After removalofthe hemostat,an incision is
createdthrough the area previously closed withinthe hemostat.Careful attention must
begiven to Wharton�s ducts and superficialblood vessels in the floor ofthe mouth
andventral tongue.The edges ofthe incisionare undermined,and the wound edges
areapproximated and closed with a runningresorbable suture,burying the knots
tominimize patient discomfort.Ridge Extension Procedures inthe Maxilla and
MandibleSubmucous VestibuloplastyIn 1959 Obwegeser described the submu-cous
vestibuloplasty to extend fixed alve-olar ridge tissue in the
maxilla.33Thisprocedure is particularly useful inpatients who have undergone
alveolarridge resorption with an encroachmentofattachments to the crest ofthe
ridge.Submucous vestibuloplasty is ideal whenthe remainder ofthe maxilla is
anatomi-cally conducive to prosthetic reconstruc-tion.Adequate mucosal length must
beavailable for this procedure to be success-ful without disproportionate
alteration ofthe upper lip.Ifa tongue blade or mouthmirror is placed to the height
ofthe max-illary vestibule without distortion orinversion ofthe upper
lip,adequatelabiovestibular depth is present (Figure 9-18).9Ifdistortion occurs
then maxil-lary vestibuloplasty using split-thicknessskin grafts or laser
vestibuloplasty is theappropriate procedure.Submucous vestibuloplasty can be per-
formed in the office setting under outpa-tient general anesthesia or deep
sedation.Amidline incision is placed through themucosa in the maxilla,followed by
mucosalundermining bilaterally.A supraperiostealseparation ofthe intermediate
muscle andsoft tissue attachments is completed.Sharpincision ofthis intermediate
tissue plane ismade at its attachment near the crest ofthemaxillary alveolus.This
tissue layer maythen be excised or superiorly repositioned(Figure 9-19).Closure
ofthe incision andplacement ofa postsurgical stent or den-ture rigidly screwed to
the palate is neces-sary to maintain the new position ofthesoft tissue
attachments.Removal ofthedenture or stent is performed 2
weekspostoperatively.During the healing peri-od,mucosal tissue adheres to the
underly-ing periosteum,creating an extension offixed tissue covering the maxillary
alveo-lus.A final reline ofthe patient�s denturemay proceed at approximately 1
monthpostoperatively.FIGURE9-17A,Lingual frenum attachment encroaching on an
atrophic mandibular alveolus.B,Excision ofthe frenum with underminingofmucosal
edges.Note: Care must be taken to avoid causing damage to Wharton�s ducts.C,Final
closure ofmucosal edges.ABC
Preprosthetic and Reconstructive Surgery175Maxillary VestibuloplastyWhen a
submucous vestibuloplasty is con-traindicated,mucosa pedicled from theupper lip may
be repositioned at the depthofthe vestibule in a supraperiosteal fashion.The
exposed periosteum can then be left toepithelialize secondarily.Split-thicknessskin
grafts may be used to help shorten thehealing period.In addition,placement
ofarelined denture may minimize patient dis-comfort and help to mold and adapt
under-lying soft tissues and/or skin grafts.Another option in this situation
islaser vestibuloplasty.A carbon dioxidelaser is used to resect tissue in a
supraperi-osteal plane to the depth ofthe proposedvestibule.A denture with a soft
reline isthen placed to maintain vestibular depth.Removal ofthe denture in 2 to 3
weeksreveals a nicely epithelialized vestibule thatextends to the desired depth
(Figure 9-20).Lip-Switch VestibuloplastyBoth lingually based and labially
basedvestibuloplasties have been described.34,35In the former an incision in the
lower lipand submucosa undermining to the alveolusis followed by a supraperiosteal
dissection tothe depth ofthe vestibule (Figure 9-21).The mucosal flap is then
sutured to thedepth ofthe vestibule and stabilized with astent or denture.The
labial denuded tissueis allowed to epithelialize secondarily.In the transpositional
vestibuloplasty,the periosteum is incised at the crest ofthealveolus and transposed
and sutured to thedenuded labial submucosa.The elevatedmucosal flap is then
positioned over theexposed bone and sutured to the depth ofthe vestibule (Figure 9-
22).These procedures provide satisfactoryresults provided that adequate
mandibularheight exists preoperatively.A minimumof15 mm is acceptable for the above
pro-cedures.Disadvantages include unpre-dictable results,scarring,and
relapse.Mandibular Vestibuloplasty and Floor-of-Mouth LoweringProceduresAs with
labial muscle attachments and softtissue in the buccal vestibule,the mylohyoidand
genioglossus attachments can precludedenture flange placement lingually.In a com-
bination ofthe procedures described byTrauner as well as Obwegeser and MacIn-
tosh,both labial and lingual extension proce-dures can be performed to effectively
lowerthe floor ofthe mouth (Figure 9-23).36�38This procedure eliminates the
componentsinvolved in the displacement ofconven-tional dentures and provides a
broad baseoffixed tissue for prosthetic support.Again,adequate mandibular height
ofat least 15 mm is required.Split-thickness skingrafting is used to cover the
denudedperiosteum and facilitate healing.Today,with the incorporation ofendosteal
implants and the fabrication ofimplant-borne prostheses,lingual and buc-colabial
flange extensions to stabilizemandibular prostheses are not
necessary.Consequently,attention is directed towardpreservation or preparation
ofthe alveolusfor implants rather than extension ofthefixed tissue attachments.As a
result,theseprocedures are rarely used today.Hard Tissue AugmentationAs stated
previously,the overall goals ofreconstructive preprosthetic surgery are toprovide
an environment for the prosthesisthat will restore function,create stabilityand
retention,and service associatedstructures as well as satisfy esthetics andprevent
minor sensory loss.There aremany classification systems ofrigid defi-ciencies
associated with many treatmentoptions;nevertheless,each patient must beevaluated
individually.When atrophy ofthe alveolus necessitates bony augmenta-
tion,undercuts,exostoses,and inappro-priate tissue attachments should be identi-
fied and included in the overall surgicalplan prior to prosthetic
fabrication.Maxillary AugmentationIn the past,vestibuloplasties were theprocedure
ofchoice to accentuate thealveolus in the atrophic maxilla.Unfortu-nately,poor
quality and quantity ofbonecombined with excessive occlusal loadingby conventional
prostheses continued toaccelerate the resorptive process.Eitheraugmentation or
transantral implantcross-arch stabilization must be consid-ered when anatomic
encroachment ofthepalatal vault or zygomatic buttress andloss oftuberosity height
affect overall fitand function ofa conventional prosthe-sis.This section discusses
conventionalaugmentation procedures ofthe maxillato restore acceptable alveolar
form anddimensions.There is a fourfold increase in resorp-tion in the mandible
compared with thatin the maxilla,combination syndromesnot withstanding.When severe
resorptionresults in severely atrophic ridges(Cawood and Howell Classes IV�VI),some
form ofaugmentation is indicated.Onlay,interpositional,or inlay grafting arethe
procedures ofchoice to reestablishacceptable maxillary dimensions.FIGURE9-18A
mirror presses the vestibularmucosa to the desired height to evaluate the ade-quacy
oflip mucosa.In this example,extension ofthe vestibular mucosa superiorly on the
alveolarridge does not result in thinning or intrusion ofthelip.Reproduced with
permission from Tucker MR.Ambulatory preprosthetic reconstructive surgery.In:
Peterson LJ,Indresano AT,Marciani RD,RoserSM.Principles oforal and maxillofacial
surgery.Vol 2.Philadelphia (PA): JB Lippincott Company;1992.p.1126.
176Part 2: Dentoalveolar SurgeryRidge Split OsteoplastyRidge-splittingprocedures
geared toward expanding theknife-edged alveolus in a buccolingualdirection help to
restore the crucialendosteal component ofthe alveolus thatis associated with
preservation andresponse to transligamentary loading andmaintains the alveolus
during the dentatestate.Replacement ofthis tissue allows fordental implant
stimulation ofthe sur-rounding bone that can best mimic thissituation and preserve
the existing alveolusMucosaShallow submucosal tissueand muscle attachmentsFIGURE9-
19Maxillary submucosal vestibuloplasty.A,Following the creation ofa vertical
midline inci-sion,scissors are used to bluntly dissect a thin mucosal layer.B,A
second supraperiosteal dissection is created using blunt dissection.C,Interposing
submucosal tissue layer created by submucosal andsupraperiosteal
dissections.D,Interposing tissue layer is divided with scissors.The mucosal
attachmentto the periosteum may be increased by removal ofthis tissue
layer.E,Connected submucosal andsupraperiosteal dissections.F,Splint extended in to
the maximum height ofthe vestibule,placing themucosa and periosteum in direct
contact.G,Preoperative appearance ofthe maxilla with muscularattachments on the
lateral aspects ofthe maxilla.H,Postoperative view.A,B,E,F adapted from
TuckerMR.Ambulatory preprosthetic reconstructive surgery.In: Peterson LJ,Indresano
AT,Marciani RD,RoserSM.Principles oforal and maxillofacial surgery.Vol
2.Philadelphia (PA): JB Lippincott Company;1992.p.1126�7.C,D,G,H reproduced with
permission from Tucker MR.Ambulatory preprostheticreconstructive surgery.In:
Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal andmaxillofacial
surgery.Vol 2.Philadelphia (PA): JB Lippincott Company;
1992.p.1127.DABCSubmucosalincisionsSubmucosalincisionMucosaSplintEFGH
Preprosthetic and Reconstructive Surgery177and possibly stimulate future
bonegrowth.Adequate dimensions,however,should exist that allow for a
midcrestalosteotomy to separate the buccal and lin-gual cortices (Figures 9-24 and
9-25).Alabial incision originates just lateral to thevestibule and continues
supraperiosteallyto a few millimeters below the crest ofthealveolus.A subperiosteal
flap then origi-nates exposing the underlying crest.Copi-ous irrigation accompanies
an osteotomycircumferentially anterior to the maxillarysinus from one side to the
other.Mobiliza-tion ofthe labial segment can be achievedwith careful manipulation
with anosteotome,taking care to maintain thelabial periosteal attachment.An
interposi-tional cancellous graft can then be placedin the resulting
defect,replacing the lostbony mass.Closure ofthe incision is awayfrom the graft
site and usually requiressuturing ofthe flap edge to the periosteumwith subsequent
granulation oftheremainder ofthe exposed tissue bed.Endosteal implants can be
placed approxi-mately 3 to 4 months later;waiting thislength oftime has been shown
to increaseoverall long-term implant success.Onlay GraftsWhen clinical loss
ofthealveolar ridge and palatal vault occur(Cawood and Howell Class
V),verticalonlay augmentation ofthe maxilla is indi-cated.Initial attempts at
alveolar restora-tion involved the use ofautogenous ribgrafts;however,currently
corticocancellousblocks ofiliac crest are the source ofchoice.39,40In a similar
approach to thatdescribed above,the crest ofthe alveolus isexposed and grafts are
secured with 1.5 to2.0 mm screws.Studies show increased suc-cess with implant
placement in a second-stage procedure rather than using them asFIGURE9-20Open
submucosal vestibuloplasty.A,Submucosal dissection between two anterior vertical
incisions followed by an incision on the crest ofthe alve-olar ridge.B,Preoperative
appearance ofthe maxilla; hydroxylapatite augmentation had been performed but
resulted in inadequate vestibular depth.C,Intra-operative photograph after
elevation ofthe mucosal flap and removal ofsubmucosal tissue.D,Appearance at the
time ofsplint removal.A adapted from and B�Dreproduced with permission from Tucker
MR.Ambulatory preprosthetic reconstructive surgery.In: Peterson LJ,Indresano
AT,Marciani RD,Roser SM.Principlesoforal and maxillofacial surgery.Vol
2.Philadelphia (PA): JB Lippincott Company; 1992.p.1128.BCDA
178Part 2: Dentoalveolar SurgeryFIGURE9-21Kazanjian flap vestibuloplasty.A,An
incision is made in the labial mucosa,anda thin mucosal flap is dissected from the
under-lying tissue.A supraperiosteal dissection is per-formed on the anterior
aspect ofthe mandible.B,The labial mucosal flap is sutured to thedepth ofthe
vestibule.The anterior aspect ofthelabial vestibule heals by secondary
intention.Adapted from Tucker MR.Ambulatory prepros-thetic reconstructive
surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser SM.Princi-ples oforal and
maxillofacial surgery.Vol 2.Philadelphia (PA): JB Lippincott
Company;1992.p.1120.ABFIGURE9-22Transpositional flap (lip-
switch)vestibuloplasty.A,After elevation ofthe mucosal flap,the periosteum is
incised at the crest ofthe alveolarridge and a subperiosteal dissection is
completed onthe anterior aspect ofthe mandible.B,The periosteumis then sutured to
the anterior aspect ofthe labialvestibule,and the mucosal flap is sutured to
thevestibular depth at the area ofthe periosteal attach-ment.C,Elevation ofthe
mucosal flap.D,Periostealincision along the crest ofthe alveolar ridge.E,Mucosa is
sutured to the vestibular depth at the areaofthe periosteal attachment.Note amount
ofvestibu-lar depth extension compared with the old vestibulardepth,which is marked
by the previous dentureflange.A,B adapted from and C�E reproduced fromTucker
MR.Ambulatory preprosthetic reconstructivesurgery.In: Peterson LJ,Indresano
AT,Marciani RD,Roser SM.Principles oforal and maxillofacialsurgery.Vol
2.Philadelphia (PA): JB Lippincott Com-pany; 1992.p.1121.ABDEC
Preprosthetic and Reconstructive Surgery179sources ofretention and stabilization
ofthegraft and alveolus at the time ofaugmenta-tion.Implant success ranges from >
90%initially and falls to 75% and 50%,respec-tively,at 3 and 5 years
postoperatively.41�45Implant success may be directly propor-tional to the degree
ofgraft maturation andincorporation at the time ofimplant place-ment.As a result,4
to 6 months ofhealingis an acceptable waiting period when long-term implant success
may be affected.Interpositional GraftsInterpositionalgrafts are indicated when
adequate palatalvault height exists in the face ofseverealveolar atrophy (Cawood
and HowellClass VI) posteriorly,resulting in anincreased interarch space.Because
thismethod involves a Le Fort I osteotomy,true skeletal discrepancies between
themaxilla and mandible can be corrected atthe time ofsurgery.The improvement
ofmaxillary dimensions as a result ofinter-positional grafts may obviate the need
forfuture soft tissue recontouring to provideadequate relieffor prosthetic
rehabilita-tion (Figure 9-26).Although early studiesentertained the simultaneous
placementofdental implants at the time ofaugmen-tation,recently several authors
havedemonstrated better success rates forimplants placed in a second-stage proce-
dure;this alleviates the need for excessivetissue reflection for implant
placementand allows for a more accurate placementat a later date.41A relapse of1 to
2 mm hasbeen demonstrated in interpositionalgrafts using the Le Fort I technique
withrigid fixation.46�50More data are needed todetermine long-term overall success
andrelapse with these procedures.Sinus Lifts and Inlay Bone GraftsSinuslift
procedures and inlay bone graftingplay a valuable role in the subsequentimplant
restoration ofa maxilla that hasatrophied posteriorly and is unable toaccommodate
implant placement owingto the proximity ofthe maxillary sinus toFIGURE9-23Floor-of-
mouth lowering.A,Mucosal and muscular attachments near the crest ofthealveolar
ridge.B,Inferior repositioning ofthe mucosal flap after the mucosal incision and
sectioningofmylohyoid muscle have been performed.C,Bolsters placed percutaneously
to secure the flap inferi-orly.D,Inferior mandibular �sling�sutures provide
inferior traction on the mucosal flap.E,Buttonssecure the mucosal flap
sutures.F,Postoperative appearance ofthe floor-of-mouth extension.A,B,E,Freproduced
with permission from Tucker MR.Ambulatory preprosthetic reconstructive surgery.In:
Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal and maxillofacial
surgery.Vol 2.Philadelphia (PA): JB Lippincott Company; 1992.p.1122�3.C,D adapted
from Tucker MR.Ambulatory preprosthetic reconstructive surgery.In: Peterson
LJ,Indresano AT,Marciani RD,RoserSM.Principles oforal and maxillofacial surgery.Vol
2.Philadelphia (PA): JB Lippincott Company;1992.p.1122.ABCDEF
180Part 2: Dentoalveolar Surgerythe alveolar crest.Incisions just palatal tothe
alveolar crest are created,followed bysubperiosteal exposure ofthe
anteriormaxilla.A cortical window 2 to 3 mmabove the sinus floor is created with
theuse ofa round diamond bur down to themembrane ofthe sinus.Careful
infractureofthe window with dissection ofthe sinusmembrane offthe sinus floor
creates thespace necessary for graft placement;thelateral maxillary wall is the
ceiling for thesubsequent graft (Figure 9-27).Cortico-cancellous blocks or
particulate bone maybe placed in the resulting defect.Tears inthe membrane may
necessitate coveragewith collagen tape to prevent extrusionand migration
ofparticulate graftsthrough the perforations.Althoughimplant placement can proceed
simulta-neously when 4 to 5 mm ofnative alveolusexists,we have found few cases
where thealveolus meets these requirements andtherefore elect to place implants
approxi-mately 6 months later.Block and Kenthave reported an 87% success rate
withsinus-grafting procedures.They also havestated that in the literature there is
anoverall success rate ranging from 75 to100%.51,52As these procedures gain popu-
larity and are routinely incorporated intomainstream preprosthetic surgery treat-
ment plans,more accurate data and long-term follow-up will be available.Treatment
ofSkeletal and Alveolar Ridge DiscrepanciesSupraeruption ofteeth and associated
alve-olar bone into opposing edentulous spacesin partially edentulous patients
precludesprosthetic rehabilitation owing to function-al loss offreeway space and
the fact that theopposing arch cannot be restored withoutthe extraction ofthe
offending supraerupt-ed dentition.With segmental alveolarsurgery,these teeth can be
repositioned toachieve a more appropriate relationshipwith the adjacent dentition
and to increasethe interarch space to allow for properprosthetic restoration ofthe
opposing den-tition.A preoperative work-up shouldinclude a thorough extraoral and
intraoralexamination.Cephalometric analysis andstudy models should be
obtained.Closecommunication with the restorative dentistis necessary to determine
expectationsregarding the final position ofthe tooth-bearing segment
postoperatively.MountedFIGURE9-24A,Diagram shows bone cuts and the position ofthe
buccal fragment after the osteoto-my.The bone grafts are already in
position.Adapted from Stoelinga PJW.61B,Handpiece in positionwith small crosscut
fissure bur performing osteotomy along the crest ofthe alveolar ridge.C,Osteoto-my
completed and buccal plate outfractured to complete ridge split.The defect is now
ready for inter-positional graft to maintain the increased buccolingual
width.D,Completed ridge split with interpo-sitional corticocancellous and
allogeneic bone used to fill the defect and maintain the increasedbuccolingual
dimension.ABCDFIGURE9-25A,Schematic drawing ofthe bone graft position in relation
to the nasalfloor.Note the reflected buccal periosteum after palatal
incisions.B,Position ofendosteal implants after the bone graft has healed.Adapted
from Stoelinga PJW.61AB
Preprosthetic and Reconstructive Surgery181models,model surgery to reposition
thesegment,and diagnostic wax-ups oftheproposed opposing dentition help one
toverify the feasibility and success ofthefuture prosthetic
reconstruction.Surgicalsplint fabrication is necessary to supportand stabilize the
segment postoperatively.Increased stability is obtained ifas manyteeth as possible
are included in the splintto help stabilize the teeth in the reposi-tioned
segment.The splint can be thick-ened to the opposing edentulous alveolarridge to
prevent relapse and to maintain thenew vertical alignment ofthe
repositionedsegment.Techniques for segmental surgeryare discussed Chapter
57,�MaxillaryOrthognathic Surgery,�and in other texts.An adequate healing period
ofapproxi-mately 6 to 8 weeks should precede pros-thetic rehabilitation.In totally
edentulous patients withskeletal abnormalities that prevent suc-cessful prosthetic
reconstruction owing toan incompatibility ofthe alveolar arches,orthognathic
surgical procedures may cre-ate a more compatible skeletal and alveolarridge
relationship.This can aid therestorative dentist in the fabrication offunctional
and esthetic restorations (Fig-ure 9-28).46During the evaluation andtreatment
planning stage,the restorativedentist should play a major role in deter-mining the
final position ofthe maxillaryand mandibular arches.Clinical examina-
tion,radiographic and cephalometricexaminations,and articulated modelsshould be
attained to determine appropri-ate presurgical vertical and
horizontaldimensions.This information should becombined with a cephalometric
predictionanalysis to determine the overall problemlist and surgical treatment
plan.Indexedsurgical splints that can be rigidly fixed tothe edentulous arches
should be fabricatedpreoperatively at the time ofmodelsurgery;these splints aid in
surgical repo-sitioning ofthe maxilla,mandible,orboth.Surgical procedures
describing repo-sitioning ofthe maxilla and mandible withrigid fixation are
discussed in Chapter 56,�Principles ofMandibular OrthognathicSurgery�and Chapter
57,�MaxillaryOrthognathic Surgery.�Prosthetic recon-struction can usually proceed
at 6 to 8 weeks postoperatively.Mandibular AugmentationOne ofthe most challenging
procedures inreconstructive surgery remains the recon-struction ofthe severely
atrophic mandible(Cawood and Howell Classes V and VI).Patients exhibiting these
deficits are charac-teristically overclosed,which creates anaged appearance,are
usually severely debil-itated from a functional perspective,andFIGURE9-26Graphic
(A) and clinical presentation (B) ofinterpositional iliac crest grafts tothe
maxilla.ABFIGURE9-27A,Sinus lift procedure with an inward trapdoor fracture
oflateral sinus wall.B,Graft materi-al is placed on the floor ofthe sinus.The sinus
lining should not be perforated during the elevation ofthe bone.Adapted from Beirne
OR.Osseointegrated implant systems.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM.Principles oforal and maxillofacial surgery.Vol 2.Philadelphia (PA): JB
Lippincott Company;1992.p.1146.AB
182Part 2: Dentoalveolar Surgeryoften present with significant risk forpathologic
fracture ofthe mandible.Because the ideal graft should be vascular-ized and
eventually incorporated into thehost bone through a combination ofosteo-conduction
and induction,autogenousbone grafts consistently meet these require-ments and offer
the most advantages to thereconstructive plan.Unfortunately,graftresorption and
unpredictable remodelinghave complicated grafting procedures;however,rigid fixation
and later incorpora-tion ofdental implants have allowed forthe needed stability
postoperatively withregard to resorption and have promotedbeneficial stimulation to
preserve existinggraft volume.Initially,mandibular aug-mentation with autogenous
rib and ileumenjoyed little long-term success.However,recent incorporation ofrigid
fixation,delayed implant placement 6 months aftergrafting (allowing for the initial
stage ofgraft resorption),guided tissue regenera-tion,and BMP have all contributed
toincreased success rates in onlay augmenta-tion ofthe mandible.53�57Inferior
Border AugmentationInferiorborder augmentation has been demon-strated using
autogenous rib or compositecadaveric mandibles combined with auto-genous cancellous
bone (Figure 9-29).58�60The following describes our technique forinferior
augmentation ofthe atrophicmandible using the latter method.Incisions are placed as
inconspicuous-ly as possible from one mandibular angleto the other and proceed
circumferentially3 to 4 mm below the inferior border ofthemandible and anteriorly
to the contralat-eral side.The superficial layer ofthe deepcervical fascia is
sharply dissected.The fas-cia is then incorporated in the reflection;anerve tester
is used to perform a carefulevaluation for the marginal mandibularbranch ofthe
facial nerve.ReflectionFIGURE9-29A,Cadaveric mandible tray rigid-ly fixed to an
atrophic mandible with autoge-nous cancellous bone sandwiched between nativeand
cadaveric bone.Note that bur holes havebeen created to facilitate the
revascularization ofthe graft.B,Cadaveric tray filled with autoge-nous bone before
insetting.C,Graft and cadav-eric tray inset for inferior border
augmentation.ABCABCDFIGURE9-28A and B,Preoperative views ofa 52-year-old patient
show severely collapsed circumoral tissues.C andD,The same patient 6 months
postopera-tively.Note the improvement ofthe sagging chin and support for circumoral
muscles.Better support for the lower lip also favorably affects the position ofthe
upperlip.The patient is not wearing dentures in any ofthe photographs.Reproduced
with permission from Stoelinga PJW.61
Preprosthetic and Reconstructive Surgery183superficial to the capsule ofthe sub-
mandibular gland allows dissection to theinferior border.Facial blood vessels
arelocated and managed with surgical tiesaccordingly.The inferior border is
exposedin a subperiosteal dissection with greatcare to avoid intraoral
exposure.Cadaver-ic mandibular adjustment involves reliev-ing the condyles and
superior rami,thin-ning the bone to a uniform thickness ofapproximately 2 to 3
mm,and creating ascalloped tray to incorporate the autoge-nous bone.Repeated try-
ins are necessaryto evaluate the overall adaptation to thenative mandible.Osseous
interfaces as wellas form and symmetry as they relate to theoverall
maxillomandibular relationshipare evaluated.Once appropriate dimen-sions have been
reached,the atrophicmandible fits securely inside the cadavericspecimen without
creating a Class IIIappearance,and flap closure is attainable,bur holes are drilled
throughout the spec-imen to facilitate vascularization.Autoge-nous bone is then
obtained from theileum,morselized,and placed in thecadaveric specimen.BMP soaked in
colla-gen is placed in the recipient bed as well asin a layered fashion over the
autogenousgraft.The entire specimen is fixed rigidlyto the native mandible using
screw fixa-tion posterior to the area offutureimplant placement and in the
mandibularmidline,where implants are usually notplaced.Postoperatively patients can
func-tion with their preexisting prosthesis andenjoy increased stabilization
ofthemandible.When combined with implantplacement at 4 to 6 months,this proce-dure
results in an overall resorption rateof< 5% and is associated with low rates
ofinfection and dehiscence intraorallyowing to the maintenance ofmucosal bar-riers
during reconstruction.Pedicled and Interpositional GraftsPlacement ofpedicled or
interpositionalgrafts in the mandible is based on themaintenance ofthe lingual
periosteum.The lingual periosteum maintains ridgeform and its presence results in
minimalresorption ofthe transpositioned basalarbone,as described by
Stoelinga.61Petersonand Slade as well as Harle described thevisor osteotomy in the
late 1970s (Figure9-30).62,63Unfortunately,labial bone graft-ing ofthe superiorly
repositioned lingualsegment was necessary to reproduce alveo-lar dimensions that
were compatible withprosthesis use.Schettler and Holtermannand then Stoelinga and
Tideman describeda horizontal osteotomy with interposi-tional grafts to augment
mandibularheight,with repositioning ofthe inferioralveolar neurovascular bundle
(Figures 9-31 and 9-32).64,65Unfortunately,neu-rosensory complications and collapse
ofthe lingual segment became significantdisadvantages to this technique.With
theincorporation ofmandibular implantsand the success offull mandibular pros-theses
that are supported by four or fiveanterior implants between mental forami-na,many
ofthese pedicled and interposi-tional procedures are in decline today.Alveolar
Distraction OsteogenesisAs alluded to previously,growing bone viathe application
oftension or stress has beenshown to be a viable solution to defects ofthe long
bone,mandible,and midface.Application to alveolar bone has been limit-ed only by
technologic advancement inappliances�the principles are still thesame.Alveolar
distraction offers some dis-tinct advantages over traditional bone-grafting
techniques.No donor site morbidi-ty is involved,and the actual distractionprocess
from the latency period throughactive distraction and consolidation is actu-ally
shorter than Phase I and Phase II boneremodeling and maturation.The quality ofthe
bone grown in response to this ten-sion/stress application is ideal for
implantplacement.The vascularity and cellularity ofthe bone promote
osseointegration ofden-tal implants.The greatest successes are relat-ed to the
achievement ofvertical graft sta-bility.One ofthe biggest problems inalveolar bone
grafting historically has beenmaintaining vertical augmentation ofbonegraft
sites.When distraction is used,thetransported alveolar segment does notundergo any
significant resorptive processbecause it maintains its own viabilitythrough an
intact periosteal blood supply.The intermediate regenerate quickly trans-forms into
immature woven bone andmatures through the normal processes ofactive bone
remodeling.The sequencing ofFIGURE9-30Visor osteotomy devised by Harle F.Adapted
from Stoelinga PJW61 and Harle F.63FIGURE9-31Sandwich osteotomy designed
bySchettler and Holtermann.Adapted from Stoelin-ga PJW61 and Schettler D and
Holtermann W.64
184Part 2: Dentoalveolar Surgeryevents is crucial to maintaining the newlyaugmented
bone and is definitely applicablein cases in which the alternatives are
limited.Diagnosis and treatment planning ofatypical case for alveolar distraction
osteo-genesis involves good clinical and radi-ographic examinations,primarily
usingpanoramic radiographs.Anatomic struc-tures such as adjacent teeth,the
sinusfloor,the nasal floor,and the inferior alve-olar canal are all easily
identifiable in thesesituations.It is rare that CT or other moresophisticated
imaging studies are required.The prosthetic work-up for these cases isalso
important.The ideal placement ofthenew alveolar crest both vertically and buc-
colingually determines the success ofthedistraction.The final position ofthe alve-
olus determines the exact alignment ofthetransport device and how it should
bepositioned in the bone.The shape ofthe residual alveolar boneis also important to
identify.Often verticalbone defects are accompanied by a signifi-cant horizontal
bone loss.This bone lossmust be dealt with either by further reduc-tion ofthe
vertical height to achieve ade-quate horizontal width or by some type ofpre- or
postdistraction bone graft augmen-tation to achieve an adequate width.Although the
success rates with alveo-lar distraction are very high when cases areproperly
planned,there are surgical pitfallsto be avoided to ensure that alveolar dis-
traction succeeds.First and foremost ismaintenance ofthe blood supply
ofthedistracted or transported segment.Manytimes this is difficult when access to
theosteotomies is limited.Although there isno minimum height or width for
thetransport segment,it should not exceedthe distance across which the segment
isbeing transported.Mistakes are oftenmade related to the application ofthe dis-
traction appliances.In the posteriormandible,the appliances are ofteninclined too
far lingually for implantreconstruction.Similarly,in the anteriormaxilla,an
adequate labial projection ofbone is difficult to achieve unless theappliance is
proclined to transport thealveolus inferiorly and labially.Additional-ly,care must
be taken when handling softtissues at alveolar ridge distraction sites.Mucosal
flaps maintained with a substan-tial vascular supply are necessary toachieve
predictable wound healing.Inaddition,we recommend both periostealand mucosal
closure to prevent segmentaldehiscence during the distraction process.There are
both intraosseous and extra-osseous devices that have been designed foralveolar
distraction.The Lead R Systemdevice designed by Chin is a simple oneconsisting
oftwo bone plates and a distrac-tion rod.66A horizontal osteotomy is creat-ed,and
the distraction rod is inserted froma crestal direction.The transport boneplate is
then engaged and positioned on thetransport section with a bone screw;thebasal bone
plate is engaged and likewisesupported on the bone with a screw.Thereare some
limitations with this devicebecause the distraction rod may limit itsuse in areas
where the vertical dimensionofocclusion is compromised.The rod isalso visible
anteriorly,which may be anesthetic issue.Finally,the rod may interferewith future
implant placement unless theimplant can be placed directly into the sitevacated by
the rod.The Robinson Inter-Oss alveolardevice was designed to be used in a one-
stage procedure in which the transportappliance actually becomes the implantwhen
the regenerate has matured.Anatomic limitations require a fairly sig-nificant
crestal bone height and width foruse.A similar device,the ACE distractiondental
implant system,allows for a distrac-tor that can be placed and then replacedwith a
dental implant once the distractionhas been completed.Again,this is a simpleand
easy implant to be placed,butanatomic constraints limit its use to cer-tain
situations.Both the ACE device andthe Robinson Inter-Oss device have limita-tions
in that they must be externallydirected or the distraction may veer offcourse.Other
devices available commer-cially that are similar to those above arethe DISSIS
distraction implant and theVeriplant.The Lead device mentionedabove provides
relatively rigid stabilizationofthe transport segment,but these otherdevices may
violate one ofthe primerequirements ofsuccessful alveolar dis-traction,namely,rigid
fixation ofthetransport segments.Extraosseous devices are much moresuccessful and
practical for distraction andrigid fixation ofthe segments.The TrackPlus System
manufactured by KLS MartinABFIGURE9-32Sandwich-visor osteotomy according to
Stoelinga and Tideman.A,Bone cut is outlined(dotted line).B,Cranial fragment is
lifted,supported by bone struts,and secured by a wire tied in afigure
ofeight.Adapted from Stoelinga PJW61 and Schettler D and Holtermann W.64
Preprosthetic and Reconstructive Surgery185and the bone plate device manufacturedby
Walter Lorenz Surgical are two devicesthat adhere to the principles
ofdistractionand rigid fixation (Figure 9-33).After placement ofa
distractiondevice,a latency period must be observed,the duration ofwhich is 4 to 7
days,depending on the age ofthe patient andthe quality oftissue at the transport
site.The latter is significant in patients whohave previously undergone
irradiation,multiple surgical procedures,or trauma,resulting in scar tissue and
compromisedblood supply.The active distraction peri-od varies depending on the
distance thesegment is transported.Standard princi-ples must be followed.The rate
andrhythm oftransport is 1 mm/d in dividedsegments�0.25 mm four times a day isthe
most practical for appliances as well asthe patient.The consolidation phase com-
mences when the distraction is complete.Generally the consolidation period shouldbe
three times the length ofthe distractionperiod.The extraosseous appliances pro-vide
rigid fixation to promote faster matu-ration ofthe regenerated bone.At the con-
clusion ofthe consolidation phase,theappliance can be removed.Rather thanwaiting
for full mineralization oftheregenerate,one can place the implants,which then
provide further rigidity to thetransport segment and allow for healing ofboth the
implant and the immature regen-erate simultaneously.The total treatmenttime is thus
much shorter than with con-ventional bone grafting with either auto-genous or
allogeneic bone,and in mostcases the appliance does not interfere withday-to-day
function.Other than theinability to wear a transitional prosthesis,there is minimal
disruption ofthe normalactivity and diet.Morbidity is generallyminimal and is
related strictly to manage-ment ofsoft tissue flaps,maintenance ofadequate
transport segment blood supply,and proper positioning ofosteotomies.ConclusionWith
the evolution and success ofdentalimplant technology,guided tissue regener-
ation,and genetically engineered growthfactors such as BMP,current indicationsfor
grafting and augmentation are usuallyrelated to facilitation ofimplant place-
ment.Time-honored reconstructive pro-cedures including bone grafting and aug-
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WR,White RP Jr.Surgical cor-rection ofdentofacial deformities.Philadel-
phia:W.B.Saunders;1980.47.Piecuch J,Segal D,Grasso J.Augmentation ofthe atrophic
maxilla with interpositionalautogenous bone grafts.J Maxillofac
Surg1984;12:133�6.48.Cawood JI,Stoelinga PJW,Brouns,JJ.A recon-struction ofthe
severely resorbed,Class VIin maxilla.A two step procedure.Int J OralMaxillofac Surg
1994;23:219�25.49.Piecuch JF,Silverstein K,Quinn PD.Bonegrafts in preprosthetic
surgery.Oral Max-illofacial Surgery Knowledge Update,Vol II.Chicago (IL):American
Association ofOraland Maxillofacial Surgeons;1998.p.11�3150.Locher MC,Sailer
HF.Results after a LeFort Iosteotomy in combination with titaniumimplants:sinus
inlay method.Oral Maxillo-fac Surg Clin North Am 1994;6:679�88.51.Block MS,Kent
JN.Sinus augmentation for den-tal implants:the use ofautogenous bone.J Oral
Maxillofac Surg 1997;55:1281�6.52.Thoma KH,Holland DJ.Atrophy ofthemandible.Oral
Surg 1951;4:1477�81.53.Curtis T,Ware W.Autogenous bone graft pro-cedures for
atrophic edentulous mandibles.J Prosthet Dent 1977;38:366�79.54.Saunders B,Cox
R.Inferior border rib graftingfor augmentation ofthe atrophic edentulousmandible.J
Oral Surg 1976;34:897�900.55.Davis WH,Delo RI,Ward WB.et al.Long term
Preprosthetic and Reconstructive Surgery187ridge augmentation with rib graft.J Max-
illofac Surg 1975;3:103�6.56.Bell WH,Buche W,Kennedy J III,et al.Surgi-cal
correction ofthe atrophic alveolar ridge:a preliminary report on a new concept
oftreatment.Oral Surg 1977;43:485�98.57.Baker RD,Connole PW.Preprosthetic aug-
mentation grafting:autogenous bone.JOral Surg 1977;35:541�51.58.Quinn PD.The
atrophic mandible:an alterna-tive to superior border grafting.In:Wor-thington
P,Evans J,editors.Controversiesin oral and maxillofacial surgery.Philadel-
phia:W.B.Saunders;1994.p.460�6.59.Quinn PD,Kent JN,MacAfee KA.Reconstruct-ing the
atrophic mandible with inferiorborder grafting and implants:a preliminaryreport.Int
J Oral Maxillofac Implants1992;7:87�93.60.Miloro M,Quinn PD.Prevention
ofrecurrentpathologic fracture ofthe atrophicmandible using inferior border
grafting:report oftwo cases.J Oral Maxillofac Surg1994;52:414�20.61.Stoelinga
PJW.Preprosthetic reconstructivesurgery.In:Peterson LJ,Indresano AT,Mar-ciani
RD,Roser SM,editors.Principles oforal and maxillofacial surgery.Philadel-phia:JB
Lippincott Co;1992.p.1169�207.62.Peterson LJ,Slade E.Mandibular ridge augmenta-tion
by a modified visor osteotomy:a prelim-inary report.J Oral Surg
1977;35:999�1004.63.Harle F.A follow up investigation ofsurgicalcorrection ofthe
atrophied alveolar ridgewith visor osteotomy.J Maxillofac
Surg1979;7:283�93.64.Schettler D,Holtermann W.Clinical and exper-imental results
ofa sandwich-technique formandibular alveolar ridge augmentation.JMaxillofac Surg
1977;5:199�202.65.Stoelinga PJW,Tideman H.Interpositionalbone graft augmentation
ofthe atrophicmandible:a preliminary report.J Oral Surg1978;36:30�2.66.Chin
M.Alveolar distraction osteogenesis.In:Samchucov ML,Cope JB,Cherkashin
AM,editors.Craniofacial distractionosteogene-sis.St.Louis:Mosby;2001.p.387�92.
CHAPTER 10OsseointegrationMichael S.Block,DMDRonald M.Achong,DMD,MDHistory ofDental
ImplantsReplacement oflost dentition has beentraced to ancient Egyptian and South
Amer-ican civilizations.1In ancient Egyptian writ-ings implanted animal and carved
ivoryteeth were the oldest examples ofprimitiveimplantology.In eighteenth and
nineteenthcentury England and colonial America,poor individuals sold their teeth
for extrac-tion and transplantation to wealthy recipi-ents.2The clinical outcomes
ofthese trans-planted dentitions were either ankylosis orroot resorption.Continued
research pro-longed allotransplant survival but did notappreciably improve
predictability.In 1809 Maggiolo placed an immedi-ate single-stage gold implant in a
freshextraction site with the coronal aspect ofthe fixture protruding just above
the gin-giva.3Postoperative complications includ-ed severe pain and gingival
inflammation.Since then various implant materials wereused ranging from roughened
lead rootsholding a platinum post to tubes ofgoldand iridium.3�6Adams in 1937
patented asubmergible threaded cylindrical implantwith a ball head screwed to the
root forretention for an overdenture in a fashionsimilar to that done today.7Up to
this point implant success wasmarginal with a maximum longevity ofonlya few
years.Strock placed the first long-termendosseous implant at Harvard in 1938.8This
implant was a threaded cobalt-chrome-molybdenum screw with a cone-shaped head for
the cementation ofa jacketcrown.The implant remained stable andasymptomatic until
1955,at which time thepatient died in a car accident.Strock wrote,�The histological
sections ofimplants in thedog study showed remarkable complete tol-erance ofthe
dental implant and the pathol-ogist report so indicated to our gratifica-
tion.�Strock demonstrated for the first timethat metallic endosteal dental implants
weretolerated in humans,with a survival rate ofup to 17 years.8Due to inadequate
alveolar bone heightin certain sites ofthe jaws,subperiostealimplants were
developed.In 1943 Dahlplaced a metal structure on the maxillaryalveolar crest with
four projecting posts.9Multiple variations to this initial designwere fabricated
but these devices oftenresulted in wound dehiscence.Bladeimplants were introduced
by Linkow andby Roberts and Roberts.10,11There werenumerous configurations with
broad appli-cations,and the implants became the mostwidely used device in
implantology in theUnited States and abroad (Figure 10-1).A two-staged threaded
titanium root-form implant was first presented in NorthAmerica by Br�nemark in
1978.12Heshowed that titanium oculars,placed inthe femurs ofrabbits,osseointegrated
inthe femurs ofrabbits after a period ofhealing.Two-staged titanium implantswere
first placed in patients in 1965 andstudies showed prolonged survival,free-standing
function,bone maintenance,andsignificant improvement in benefit-to-riskratio over
all previous implants.13Thisbreakthrough has revolutionalized max-illofacial
reconstruction.Subsequently,various implant designs have been manu-factured and
research in implantology hasgrown exponentially.The frontiers ofimplantology are
rapidly being advancedand esthetics continue to be an integralpart ofthis
progress.Implant Materials and SurfaceImplant materials have undergone a num-ber
ofdifferent modifications and devel-opments over the past 40 years.Commer-cially
pure titanium has excellentbiocompatibility and mechanical proper-ties.When
titanium is exposed to air,a 2 to 10 nm thick oxide layer is formedimmediately on
its surface.14This layer isbioinert.However,strength issues withpure titanium have
led manufacturers touse a titanium alloy to enhance strengthofthe implant.Most
abutments are madeoftitanium alloy.The use ofalloy signifi-cantly increases
strength,which can be anissue with small-diameter and internalconnections.Titanium
alloy (Ti-6Al-4V)is becoming the metal ofchoice forendosseous dental implants.
190Part 2: Dentoalveolar SurgerySeveral attempts have been made toimprove implant
anchorage in bone bymodifying the surface characteristics oftitanium implants
(Figure 10-2).In orderto enhance the bone connection to theimplant,a thin coating
ofhydroxylapatite(HA) has been plasma-sprayed onto aroughened and prepared titanium
implant.HA coatings usually range from 50 to 70 �m and are applied to the implant
sur-face with plasma-spray technology.15Apressurized hydrothermal postplasma-
sprayincreases the crystalline HA content from 77to 96%,with an amorphous content
of4%.This coating offers an improved bone adhe-sion as shown in several
studies.16,17Because ofthe success in orthopedicswith roughened titanium surfaces
forendosteal appliances,dental implant man-ufacturers have modified the titanium
sur-face either by adding titanium to the sur-face through plasma-spray technology
orby reduction procedures involving etchingand blasting the surface.The
titaniumplasma-sprayed surface was the first roughtitanium surface introduced into
implantdentistry.The titanium plasma-sprayed(TPS) surface process is characterized
byhigh-velocity molten drops ofmetal beingsprayed onto the implant body to a thick-
ness of10 to 40 �m.18Its original intentwas to obtain a greater surface area
forbone attachment.TPS implants demon-strated satisfying long-term results in
fullyand partially edentulous patients.Roughened titanium surfaces can alsobe
produced by reduction techniques suchas sand- or grit-blasting,titanium
oxideblasting,acid etching,or combinations ofthese techniques.In 2000 Cordioli and
col-leagues reported mean bone-to-implantcontact values at 5 weeks of72.4% for
theacid-etched surface,56.8% for TPS,54.8%for grit-blasted,and 48.6% for
machinedsurface implants.19Reduced healing timeshave been documented which are
believedto result in the need for less time fromimplantation to loading and better
resultsin poorer-quality bone.20Despite the success with machinedsmooth titanium
implants,the use ofaroughened surface has been substituted byall manufacturers and
clinicians as thecurrent surface ofchoice.With rare excep-tions most endosseous
implants have aroughened surface texture.Surgical Protocol Generic for All
ImplantsPlacement without Trauma tothe Soft and Hard Tissues Heat generation during
rotary cutting is oneofthe important factors influencing thedevelopment
ofosseointegration.It is wide-ly accepted that heat increases in proportionto drill
speed,and that byextension,FIGURE10-1A,Blade
implants.B,Subperiostealimplant.C,Threaded implants with smooth tita-nium or
hydroxylapatite-coated surface.ACBFIGURE10-2A,Titanium plasma-sprayed sur-face at
high magnification.B,Acid-etched tita-nium surface at low magnification.C,Hydroxyl-
apatite-coated surface at low magnification.ABC
Osseointegration191high-speed drilling causes physiologicdamage to bone.In 1983
Eriksson andAlbrektsson demonstrated the occurrenceofirreversible histologic damage
in therabbit tibia when heat exposure at a tem-perature of47�C was longer than 1
minute.21An even greater injuryoccurred after heating the bone to 53�C for1
minute,and heating to temperatures of60�C or more resulted in permanent cessa-tion
ofblood flow and obvious necrosisthat showed no sign ofrepair over follow-up period
of100 days.21Minimal heat during implant sitepreparation has been recommended
toachieve optimal healing conditions.Although the relationship between speedand
heat generation is still under debate,the consensus has been to recommendspeeds
ofless than 2,000 rpm with copiousirrigation for preparation ofimplant sites.21In
1986 Eriksson and Adell showed that theBr�nemark drilling system had a meanmaximum
temperature of30.3�C duringdrilling,with a maximum temperature of33.8�C.22The
duration ofmaximum tem-perature never exceeded 5 seconds.Watanabe and colleagues
measuredheat distribution to the surrounding bonewith three different implant drill
systems,in 1992.23Generation ofheat in the pres-ence or absence ofirrigation when
drillingwith spiral or spade-type drills wasobserved in the pig rib via
thermography.The maximum temperature generatedwithout irrigation was significantly
greaterthan with irrigation for each drill.The heatgenerated continuously spread to
the sur-rounding bone even after the bur or drillwas removed from the bone,and the
origi-nal temperature returned in about 60 sec-onds.The spiral drill required the
longesttime to generate heat,with gradual increaseoftemperature.The round bur and
cannonor spade drill could finish cutting in a shorttime,with rapid generation
ofheat.Maxi-mum temperature without irrigation washigher than with irrigation for
any drill.With irrigation at proper speed,minimalheat was generated.When cortical
bone wasprepared using the spiral drill,irrigationdecreased the maximum temperature
by10�C or more.It is recommended by allmanufacturers that the bur be moved upand
down while preparing the implant site,to allow accessibility ofirrigation to
thecutting edges ofthe bur,neutralizing heatgeneration and removing bone
debris.Time for IntegrationHistorically a nonloading healing periodofmachined-
surfaced dental implants hasbeen 4 to 6 months for the mandible and 6 months for
the maxilla.24The 4- to 6-month recommendations were made toprevent the development
ofa fibrousencapsulation ofthe implant fixtures thatoccurs with premature
loading.Theseearly recommendations for implant surgi-cal protocol were developed
based on clin-ical observations and not necessarily basedon an understanding ofthe
biologic prin-ciples ofimplant integration.The originalBr�nemark protocol has been
greatlymodified due to the advances in implantmicrotopographic surfaces and
design.Inrecent years histologic and experimentalstudies have shown that
specificallydesigned microtopographic implant sur-faces can result in increased
bone-to-implant contact at earlier healing timesthan obtained with machined-
surfaceimplants.Over the years histologic andclinical studies investigating early
andimmediate implant loading revealed thatimplants can be placed into function
earli-er than previously recommended.In 1998Lazzara and colleagues evaluated the
effi-cacy ofloading Osseotite dental implantsat 2 months to determine the effect
ofearly loading on implant performance andsurvival.25The cumulative implant sur-
vival rate was 98.5% at 12.6 months.Thecumulative postloading implant survivalrate
was 99.8% at 10.5 months.Testori andcolleagues investigated the clinical out-come
of2 months ofloaded Osseotiteimplants placed in the posterior jaws,witha follow-up
period of3 years.26The over-all cumulative implant survival rate afterfunctional
loading was 97.7% in themandible and 98.4% in the maxilla.Coop-er and colleagues
investigated the earlyloaded implants in clinical function with-out risking the
result ofosseointegration.27They demonstrated a 96.2% implant sur-vival rate with
loaded unsplinted maxil-lary anterior single-tooth implants 3 weeks after one-stage
surgical place-ment.27The majority ofthe taperedthreaded implants were placed in
type 3 bone with a minimal length of11 mm.The mean change in marginal bone levelwas
0.4 mm with a mean gain in papillalength of0.61 mm at 12 months.In arecent report
unsplinted implants placedby a single-stage procedure were successfulwhen loaded by
a mandibular overdentureprosthesis.28Further developments inimplant surfaces will
greatly reduce inte-gration time (Figure 10-3).Key Reasons for FailureEndosseous
dental implants have beenused successfully throughout the past
fewdecades.Unfortunately implants are notalways successful.Improper
implantplacement can result in a frameworkdesign that compromises esthetics
anddistribution offorce on implants.Endosseous implants distribute occlusalload
best in an axial direction,but iftheocclusal load is in a lateral
direction,manydamaging stresses,including shear stress-es,are generated directly at
the crest ofbone.Lazzara proposed that off-angleimplant positioning requiring over
25�ofangle correction will cause an implant to fail.29Overheating bone during
place-ment will result in a fibrous tissue againstthe implant surface rather than
the bone.Placing implants into bone ofpoor quali-ty without consideration to the
mechani-cal forces ofloading can result in early or late failure.Lack ofbone
contact at the time ofplacement is also a factor lead-ing to lack ofintegration or
marginal
192Part 2: Dentoalveolar Surgeryintegration.The presence ofinfectionwhen placing an
implant can lead to sub-optimal healing and eventual lack ofinte-gration,infection
within a week ofplace-ment,or lack ofbone formation thatresults in early failure
after loading.Keratinized gingiva has been shown topromote soft tissue health
around teeth.However,around dental implants,the pres-ence ofkeratinized gingiva may
or may notbe important for preservation ofcrestalbone.Krekeler and colleagues
suggestedthat there is a strong correlation ofkera-tinized gingiva with implant
failure and theabsence ofan adequate band ofkeratinizedmucosa surrounding the
abutment.30Thissuggested relationship was based on theability ofthe keratinized
mucosa to with-stand bacterial insult and ingression,whichcan lead to
periimplantitis.Clinical trials with HA-coatedimplants indicate that the presence
ofker-atinized gingiva is important for long-term success ofendosseous
implants.There was a significant relationshipbetween implant survival and crestal
bonelevel maintenance with posteriormandible implants in the presence ofa 1 to 2 mm
thick band ofattached kera-tinized gingiva.31The early Br�nemarkreports indicate
that crestal bone levelswere not affected by the presence ofkera-tinized gingiva in
the anterior mandible,although the presence oftransient gingivi-tis was increased
in patients without theprotective effect ofkeratinized gingiva.Thus,keratinized
gingiva is important foroverall periimplant health.31Procedures tocreate and
preserve keratinized gingiva arerecommended when placing and exposingimplants.When
placing a one-stageimplant,incision design should result inkeratinized gingiva
labial to the implant.The most important factors for implantsuccess,identified by
Block and Kent in1990,are surgery without compromise intechnique,placing implants
into soundbone,avoiding thin bone or implant dehis-cence at the time ofimplant
placement,established balance restoration,and ensur-ing appropriate follow-up
hygiene care.31Implants placed into thin ridges or that haddehiscence oftheir
surface did not uniform-ly gain bone attachment levels during thehealing
period.Labial bone implant defectsshould be grafted with particulate hydroxyl-
apatite.In the posterior maxilla,verticalbone loss seems to be due to excessive
cantilever-type forces placed on theimplants.The use ofsinus grafting is recom-
mended to provide adequate bone supportin the atrophic posterior maxilla.The pres-
ence ofkeratinized gingiva strongly correlat-ed with bone maintenance in the
posteriormandible.Consequently,implant surgicaltechniques should preserve all
keratinizedgingiva.Most patients who receive implantsfor dental restorations have
lost teeth due tocaries or periodontal disease.Patients needto maintain meticulous
oral hygiene.Ifpocket probing greater than 3 mm aroundthe implant occurs,additional
antibacterialsolution application or pocket elimination isrecommended for hygiene
purposes.Wound HealingBone healing is a physiologic cascade ofevents in which
complex regenerativeprocesses restore original skeletal structureand function.Bone
is generated by twoseparate mechanisms:endochondral andmembranous bone
formation.Endochon-dral bone formation occurs at the epiphy-seal plates in long
bones and condylar headofthe mandible and accounts for growthin length.32It entails
the laying down ofapreformed cartilaginous template,which isgradually resorbed and
replaced by bone.Membranous bone formation or primarybone healing requires
differentiation ofmesenchymal cells into osteoblasts,whichproduces osteoid.The
osteoid is then min-eralized to form bone.32This type ofboneformation occurs in the
calvaria,mostfacial bones,the clavicle,and the mandible.Osseointegration belongs to
the categoryofprimary bone healing.The wordosseointegrationwas defined as �a
directstructural and functional connectionTime to Integration (mo)654321SLAITI
SystemSmoothHA-coatedmachinedtitaniumOsseotiteFIGURE10-3Chart showing relative
healing times for different implant surfaces.HA = hydroxylap-atite; SLA type =
sandblasted and acid-etched.
Osseointegration193between ordered,living bone and the sur-face ofa load carrying
implant.�24Wound healing consists ofthree fun-damental
phases:inflammation,prolifera-tion,and maturation.The induction ofbone formation at
surgical interfacesreflects a major alteration in cellular envi-ronment.These
crucial events involve aninflammatory phase,a proliferative phase,and a maturation
phase.Phase One: Inflammatory PhaseBone healing around implants results in awell-
defined progression oftissueresponses that are designed to remove tis-sue debris,to
reestablish vascular supplyand produce a new skeletal matrix.Plateletcontact with
implant surfaces causes liber-ation ofintracellular granules that,whenreleased,are
involved in the early eventsassociated with tissue injury.33Release ofadenosine
diphosphate,serotonin,prosta-glandins,and thromboxane A2promotesplatelet
aggregation,resulting in a hemo-static plug.Platelets continue to degranu-late
during the formation ofthe hemosta-tic plug and release constituents thatincrease
vascular permeability (serotonin,kinins,and prostaglandins) and con-tribute to the
inflammatory responseaccompanying tissue injury.33Acute wound healing consists ofa
cel-lular inflammatory response dominatedmainly by neutrophils.Migration
oftheneutrophils to the site ofinjury generallypeaks during the first 3 to 4 days
followingsurgery.34These cells are attracted to thelocal area by chemotactic
stimuli and thenmigrate from the intravascular space tothe interstitial space by
diapedesis.Therole ofthese cells is primarily phagocytosisand digestion ofdebris
and damaged tis-sue.Digestion oftissue is feasible via therelease ofdigestive
enzymes such as colla-genase,elastase,and cathepsin.34By thefifth day macrophages
predominate andremain until the reparative sequence iscompleted.32These cells are
derived fromcirculating monocytes that originate fromthe bone marrow via monoblast
differenti-ation.Macrophages can be activated byproducts ofactivated lymphocytes
and thecomplement system.Macrophages havethe ability to ingest inflammatory
debrisby phagocytosis and to digest such parti-cles by releasing hydrolytic
enzymes.32Phase Two: Proliferative PhaseMicrovascular ingrowth from the adja-cent
bony tissues during this phase iscalled neovascularization.35Cellular dif-
ferentiation,proliferation,and activationresult in the production ofan
immatureconnective tissue matrix that is laterremodeled.The local inflammatory
cells(fibroblasts,osteoblasts,and progenitorcells) proliferate within the wound
andbegin to lay down collagen.36This combi-nation ofcollagen and a rich
capillarynetwork forms granulation tissue with alow oxygen tension.This hypoxic
state,combined with certain cytokines such asbasic fibroblast growth factor (bFGF)
andplatelet-derived growth factor,is respon-sible for stimulating
angiogenesis.bFGFseems to activate hydrolytic enzymes,such as
stromelysin,collagenase,and plas-minogen,which help to dissolve the base-ment
membranes oflocal blood vessels.32Reestablishment oflocal microcirculationimproves
tissue oxygen tension and pro-vides essential nutrients necessary forconnective
tissue regeneration.Local mesenchymal cells begin to dif-ferentiate into
fibroblasts,osteoblasts,andchondroblasts in response to local hypoxiaand cytokines
released from platelets,macrophages,and other cellular elements.32These cells begin
to lay down an extracellu-lar matrix composed ofcollagen,gly-
cosaminoglycans,glycoproteins,and glyco-lipids.The initial fibrous tissue and
groundsubstance that are laid down eventuallyform into a fibrocartilaginous
callus.Theinitial bone laid down is randomly arranged(woven type) bone.36Woven bone
forma-tion clearly dominates wound healing at thispoint for the first 4 to 6 weeks
after surgery.Phase Three: Maturation PhaseAfter the establishment ofa well-
vascularized immature connective tissue,osteogenesis continues by the recruit-
ment,proliferation,and differentiation ofosteoblastic
cells.32Differentiatedosteoblasts secrete a collagenous matrixand contribute to its
mineralization.Osteoid-type bone within a vascularizedconnective tissue matrix
becomesdeposited at dental implant surgicalinterfaces.16Eventually this
matrixenvelops the osteoblastic cells and is sub-sequently mineralized.This cell-
rich andunorganized bone is called woven bone.Loading ofthe dental implant
stimulatesthe transformation ofwoven bone tolamellar bone.16Lamellar bone is
anorganized bone displaying a haversianarchitecture.Bone remodeling occursaround an
implant in response to loadingforces transmitted through the implant tothe
surrounding bone.The lamellaearound the implant are remodeledaccording to the
exposed load,whichwith passage oftime,shows a characteris-tic pattern ofwell-
organized concentriclamellae with formation ofosteons in thetraditional
manner.16Under normal circumstances healingofimplants is usually associated with
areduction in the height ofalveolar margin-al bone.Approximately 0.5 to 1.5 mm
ofvertical bone loss occurs during the firstyear after implant insertion.35The
rapidinitial bone loss is attributed to the gener-alized healing response resulting
from theinevitable surgical trauma,such asperiosteal elevation,removal
ofmarginalbone,and bone damage caused by drilling.Options for the
EdentulousMandibleOptions for patients with an edentulousmandible include a
conventional denture,a tissue-borne implant-supported pros-thesis,or an implant-
supported prosthesis(Figure 10-4).
194Part 2: Dentoalveolar SurgeryPhysical Examination oftheEdentulous PatientThe
depth ofthe vestibule and the mental-is muscle attachments are noted to deter-mine
the necessity ofa vestibuloplasty.The width ofkeratinized gingiva on thealveolar
crest and the distance from thealveolar crest to the junction oftheattached and
unattached mucosa arenoted.Identification ofthe mental fora-men by digital
palpation is useful to deter-mine subsequent implant location.In arelaxed vertical
position ofthe jaws,therelationship ofthe anterior mandible tothe maxilla is
observed to determine thebenefits ofpositioning the implants tocorrect or mask a
Class II or Class IIIskeletal jaw relationship.Alveolar ridgepalpation will
determine the slopes ofthelabial and lingual cortices and the alveolarheight.The
location ofthe genial tuberclesshould also be noted.Radiologic Examination
oftheEdentulous PatientRadiologic evaluation ofthe patient priorto placing implants
is focused on thedetermination ofvertical height and theslopes ofthe cortices in
relation to theopposite arch.A panoramic radiograph isthe baseline radiograph used
to evaluatethe implant patient.The lateral cephalo-gram is useful to demonstrate
the slopesofthe cortices ofthe anterior mandibleand the skeletal ridge
relationships ofthemandible to the maxilla,and to provide asimple and inexpensive
radiographicassessment ofanterior alveolar height.Additional radiographic
techniquesinclude the use ofcomplex motiontomography or reformatted
computedtomography (CT) scans.CT has a lessthan 0.5 mm error when reformattedcross-
sectional images are examined.Asclinical experience increases most sur-geons agree
that there is less need forthese more expensive radiographic tech-niques for
preparation ofplacingimplants.CT scans are becoming popularin combination with
models ofthe bonefor accurate treatment planning and thefabrication offinal
prostheses prior to theactual surgical procedure.Incision Design
ConsiderationsBased on the location ofthe muscleattachments and the height
ofthemandible,the surgeon makes the deci-sion regarding which incision to use
toexpose the bone and subsequently placeimplants into the edentulous mandible.Ifthe
attachment ofthe mentalis muscleis 3 mm or more labial to the location ofthe
attached gingiva on the alveolarcrest,a crestal incision can be used.Ifthe mentalis
muscle is in close proximityto the alveolar crest,resulting in mobileunattached
gingiva directly against theimplant abutment,a �lipswitch�vestibu-loplasty is
performed to inferiorly repo-sition the muscle attachments.FIGURE10-4A,Two-implant
bar for clip overdenture retention.B,Two-implant locator for
overdentureretention.C,Hybrid prosthesis retained by five implants.D,Panoramic
radiograph showing position offive implants for hybrid prosthesis.E,Milled bar for
fixed/removable prosthesis.F,Inner aspect ofpros-thesis showing metal substructure
with plunger attachments.G,The patient pushes the plunger attach-ments to engage
the milled bar and thus retains the prosthesis to the bar.C,D reproduced with
permis-sion from Block MS.Color atlas ofdental implant surgery.Philadelphia (PA):
W.B.Saunders Company,2001.p.5.ABDEGCF
Osseointegration195Two ImplantsIn general,when placing two implants foran
overdenture,one should take into con-sideration the potential need for addition-al
implants at a later time.Some patientsenjoy the overdenture prosthesis but
maycomplain offood getting caught under thedenture,mobility ofthe prosthesis
whenspeaking,swallowing,or chewing,and adesire to eliminate changing clips,O
rings,or locator-type attachments.Thesepatients may then desire the retention
ofafixed or fixed-removable prosthesis.Forthese patients three additional
implantsmay be placed to result in a total offiveimplants in the anterior
mandible,whichis sufficient to support an implant-borneprosthesis.Taking this into
considerationwhen placing two implants into the anteri-or mandible,locating the
implants 20 mmapart,each 10 mm from the midline ofthemandible,allows for later
implant place-ment ifneeded.Implant placement at the correctheight in relation to
the alveolar crest iscrucial.Ifthe implant is placed such thatthe cover screw is
superficial to the adja-cent bone,a chance ofincisional dehis-cence or mucosal
breakdown may occur.Itis advantageous to countersink implantsin the anterior
mandible sufficiently (1 to2 mm depending on the type ofexternalor internal
connection ofthe specificimplant used) to allow the height ofthecover screw to be
in a flush relationshipwith the adjacent alveolar bone.The sur-geon should follow
the guidelines for thespecific implant system being used.Forone-stage implants
temporary healingabutments are placed as recommended bythe manufacturer.Accidental
loading frompoorly relined dentures can lead to traumato the implants and eventual
loss.Thus itis prudent to excessively relieve and useappropriate soft liners for
the transitionaldenture during the healing period.The anterior mandible may have
adense cortical plate with an abundantmarrow space,or it may have very mini-mal
marrow with an abundance ofcorti-cal bone.The smaller the mandible,themore cortical
bone and less cancellousbone is available.When encounteringvery dense bone it is
important to period-ically clean the drill bits to keep the cut-ting surfaces clean
ofdebris during thepreparation ofthe implant site.For coat-ed implants a
threadformer type ofbur isused to create threads in the bone.Forself-tapping
implants the surgeon mayneed to use a slightly larger bur than iscustomarily used
in other areas ofthemouth.For example,rather than using a3.0 mm bur prior to
selftapping a 3.75 mm implant,a 3.25 mm diameterdrill may be necessary to allow for
ease ofimplant insertion into very dense bone.Four or More ImplantsFour or more
implants are placed whenconsidering an implant-borne prosthesis.Implant-borne
prostheses include hybridscrewed-retained,crown-and-bridge type,or fixed/removable
with milled bars andretentive devices (see Figure 10-4).Theincision design is
similar for placement offour or more implants into the anteriormandible.The
subperiosteal reflectionshould be sufficient to expose the lingualand labial
cortices and the mental foramenbilaterally.After the periosteal reflection
iscompleted,the surgeon has an excellentview ofthe operative site,the contours
ofthe bone,and the location ofthe mentalforamen.A caliper is used to mark
thealveolar ridge at no less than 5 mm anteri-or to the mental foramen.This
distance isusually the anterior extent ofthe nerve,asit loops forward in the bone
prior to exit-ing the bone at the mental foramen.Asmall round bur is used to place
a depres-sion in the bone to locate the implant siteon one side ofthe mandible.A
similarmark is placed on the opposite side ofthemandible,no less than fivemm
anterior tothe mental foramen.The caliper is then setto 7 or 8 mm and the next
implant loca-tions are marked in a similar manner ante-rior to the two distal
locations.Ifa fifthimplant is to be used,then a mark is madein the midline ofthe
mandible.By usingthe caliper,the implant bodies are placed asufficient distance
apart to ensure ade-quate space for restoration and hygiene.The use ofCT-generated
models ofthemandible can result in surgical templatesthat can be secured to the
jaws with pins orthe implants themselves,resulting in pre-cise implant location by
preoperativeplanning.As the planning process matureswith CT-generated applications
and tem-plates,incisions will be needed less often.After the implant locations are
identi-fied,the first drill in the implant drillingsequence is used.Ifavailable a
surgicalstent is placed in order to correctly locatethe implants in relation to the
teeth.ForClass III mandibles the implants can beangled slightly lingually,for Class
IImandibles the implants can be angledslightly anteriorly,and for Class Imandibles
the implants are placed verti-cally in relation to the inferior border ofthe
mandible.Regardless ofthe angulationofthe implants,the crestal location
oftheimplants is the same,with the implantsexiting the crest midcrestally
withoutexcessive labial or lingual location.Augmentation ofthe Atrophic Mandible
Ifthe patient is in satisfactory health for abone graft harvest procedure,the
indica-tion for bone augmentation ofthe anteri-or mandible is a patient with less
than 6 mm ofbone height.Patients with greaterthan 6 mm ofbone height can do
wellwith implants without bone augmenta-tion.37Most clinicians will use iliac
crestcorticocancellous blocks to augment theheight in an atrophic mandible.The pro-
cedure can be performed through eitheran intraoral or an extraoral
incision,depending on clinician preference (Figure10-5).The placement ofimplants at
the time ofbone graft placement is also
196Part 2: Dentoalveolar Surgeryclinician dependent.Ifimplants are placedat the
time ofbone graft placement,thenthe patient�s time to restoration isdecreased,the
graft can be secured to themandible with threaded implants,and theshorter time to
functional loading may pre-vent graft resorption.The disadvantages ofplacing
implants at the time ofbone graftplacement include possible partial resorp-tion
ofthe graft and exposed portions ofthe implants,which is difficult to treat,mal-
position ofthe implants due to lack ofproper angulation at placement,which canbe
technically challenging from an extrao-ral approach,and potential lack ofintegra-
tion secondary to poor graft remodeling.Technically the graft procedures are
similar,with the exception ofthe surgical prepara-tion ofthe sites for the
implants.Intraoral incisions for placement ofblocks ofbone can be made either
crestal-ly or within the vestibule.The crestal inci-sion places the incision over
the bonegraft,but it also allows the surgeon to havethe best chance to avoid
incisional dehis-cence secondary to vascular insufficiency.A vestibular incision
places the incisionaway from the bone graft;however,bloodsupply to the edge ofthe
vestibular inci-sion travels through the dense fibrous tis-sue over the crest and
thus may be proneto breakdown secondary to vascular insuf-ficiency.Both ofthe
intraoral incisionsand their subsequent release will result inobliteration ofthe
vestibule,which willrequire secondary soft tissue grafting.Oneshould note that the
mental foramen isoften palpable on the alveolar crest,withsome portion ofthe
inferior alveolar nervedehisced from the mandible secondary toresorption ofthe
alveolar crest bone.The bone grafts are harvested andtrimmed as necessary.The goal
ofthe graftshould be to restore the mandible toapproximately 15 mm ofvertical
height;however,for a 3 mm mandible,gainingthis amount ofbone may be
excessive.Forthe extremely small 1 to 5 mm tallmandible,restoring the mandible to
10 to13 mm is considered a great success.Twoor three pieces ofcorticocancellous
boneblocks are trimmed and placed over thesuperior aspect ofthe mandible.The
edgesare smoothed and the grafts are stabilizedin position with screws placed
through thegrafts,engaging the inferior border ofthemandible.Ifimplants are placed
at thetime ofgraft placement,the clinician mustweigh the possibility ofpartial
graftresorption and subsequent implant fail-ure.Implants can be placed 4 months
afterthe graft was performed,and combinedwith a simultaneous vestibuloplasty.The
disadvantage ofusing an extraoralapproach is the scar that results and diffi-culty
placing implants at the time ofgraftplacement.Most implants,when placedinto a bone
graft performed through anextraoral incision,are flared to the labialaspect.The
advantages ofusing an extrao-ral approach to graft the atrophicmandible include
avoidance ofintraoralincision breakdown,avoidance ofanintraoral communication with
the bonegraft and potential infection,maintenanceofthe vestibular attachments,which
mayeliminate the need for vestibuloplasty,andease ofreflection ofthe inferior
alveolarnerve from the alveolar crest withoutincising over the nerve (Figure 10-
6).These advantages often are significant andoffer the patient the least chance
ofinci-sional dehiscence;hence,this approach isthe method ofchoice for these
authors.From this approach bone grafts can beplaced in either block or particulate
form,with implants used as �tent poles�tomaintain space over the graft.38Most
clinicians will allow at least 4 months to healing ofthe iliac crest cor-
ticocancellous bone graft prior to placingimplants.Iliac crest
corticocancellousFIGURE10-5A,Iliac crest corticocancellousblock graft augmentation
ofthe atrophicmandible,through an extraoral approach withsimultaneous placement
oftwo implants.B,Panoramic radiograph offinal prosthesis retainedby two overdenture
attachments.Reproducedwith permission from Block MS.Color atlas ofdental implant
surgery.Philadelphia (PA): W.B.Saunders Company,2001.p.28.BAFIGURE10-6A,Atrophic
mandible in a 75-year-old female.B,A 5-year follow-up radi-ograph of10 mm long
implants placed withoutbone graft.Reproduced with permission fromBlock MS.Color
atlas ofdental implant surgery.Philadelphia (PA): W.B.Saunders
Company,2001.p.29�30.BA
Osseointegration197grafts heal well but start resorbing after 3 to 4 months,so the
surgeon may need toplace the implants at 3 months,dependingon consolidation and
remodeling ofthebone graft,which is determined radi-ographically.Ifnecessary a
split- thicknessdissection can be made intraorally and apalatal or split-thickness
dermis or skingraft can be placed to restore some sem-blance ofvestibule.At the
time ofvestibu-loplasty,rigid fixation screws can beremoved and implants
placed,engagingthe inferior border ofthe mandible.Whensimultaneously performing a
vestibulo-plasty with implant placement,one shouldcountersink the implants below
the levelofthe periosteum so that the graft can layflush and not be tented up
offthe host tis-sue bed by the dome-like prominence ofthe cover screws
ofimplants.Placement ofImplants intoAtrophic Mandibles withoutGraftingThe majority
ofpatients with atrophicmandible with less than 10 mm ofboneheight and at least 5
to 6 mm ofheight arenot good candidates for bone grafting sec-ondary to health-
related issues.For thesepatients four implants can be placed,with1 to 2 mm ofthe
implant through the infe-rior border ofthe mandible,and 1 to 2 mmsupracrestal as
necessary.It is important togently prepare the bone with new sharpdrills and pretap
these bones since they canbe brittle and have minimal blood supply.The implants
should be placed to avoidlabial protrusion (see Figure 10-6).37Options for the
Edentulous MaxillaTreatment planning for the edentulousmaxilla is usually initiated
at the restorativedentist�s office.This includes establishmentofthe patient�s goals
ofwhat he/she desiresat the completion ofimplant therapy.Oncethese goals are
established the surgeon isseen and an assessment ofbone availabilityis performed.A
panoramic radiograph and a physi-cal examination are often all that arerequired to
delineate satisfactory bonebulk for the placement ofimplants intothe maxilla.From
the panoramic radi-ograph one can estimate the amount ofvertical bone available
throughout theentire maxilla.Occasionally a reformattedCT scan is obtained to
confirm the pres-ence ofbone prior to implant placement.Ifcross-sectional
radiography is planned,using a radiopaque stent at the time oftheradiography
significantly increases theamount ofinformation gathered.Theteeth in the patient�s
prosthesis are maderadiopaque by using a radiopaque mater-ial,typically 20 to 30%
barium sulfatecombined with clear acrylic so that theteeth are included in the
cross-sectionalimage.This provides information con-cerning the relationship ofthe
bone to thedesired teeth.Parel�s classification ofthe edentulousmaxilla is useful
for conceptualization ofthe prosthetic plan (personal communica-tion,1991).The
Class I maxilla involves thepatient who seems to be missing only themaxillary
teeth,but has retained the alveo-lar bone almost to its original level (Figure10-
7).The Class II maxilla has lost theteeth and some ofthe alveolar bone,andthe Class
III maxilla has lost the teeth andmost ofthe alveolar bone to the basal level.For
the Class I patient a fixed restora-tion,borne by implants,can be fabricatedbecause
the patient has adequate alveolarbone for support ofthe soft tissues and ismissing
only the teeth.There is usuallygreater than 10 mm ofbone height inboth the anterior
and posterior maxilla.For a fixed crown-and-bridge restoration,implants need to be
placed within theconfines ofthe teeth ofthe plannedrestoration.The implants should
beFIGURE10-7A,Edentulous Class I maxilla treatment planned for fixed crown-and-
bridge maxillaryprosthesis.Reproduced with permission from Block MS.Color atlas
ofdental implant surgery.Philadelphia: W.B.Saunders Company,2001.p.65.B,Final
anterior dentition demonstrating excel-lent gingival contours on implants in the
endentulous maxillary patient.Reproduced with permissionfrom Block MS.Color atlas
ofdental implant surgery.Philadelphia (PA): W.B.Saunders Company,2001.p.66.C,Milled
bar for implant-retained fixed/removable prosthesis.D,Fixed/removable pros-thesis
retained by �swing-lock�attachments to the milled bar.Reproduced with permission
from BlockMS.Color atlas ofdental implant surgery.Philadelphia (PA): W.B.Saunders
Company,2001.p.19.CADB
198Part 2: Dentoalveolar Surgeryplaced to avoid the embrasure regions inorder to
promote esthetics and oralhygiene.For a fixed crown-and-bridgerestoration,the
implants should be placed3 mm apical to the gingival margin oftheplanned
restoration in order to allow therestorative dentist to develop a naturalemergence
ofthe crowns from the gingi-va.Ifthe Class I patient desires a tissue-borne
overdenture on four implantsbecause offinancial constraints,then thedesign ofthe
overdenture bar must besuch as to avoid excessive space-occupy-ing designs,since
the patient is missingonly their teeth,not the alveolus.The Class II patients
rarely can beesthetically managed with a fixed crown-and-bridge prosthesis since
they requirethe labial flange ofthe maxillary prosthe-sis to support the nasal-
labial soft tissues.In order to distinguish the need foracrylic to support the soft
tissues,it isuseful to duplicate their maxillary den-tures and remove the labial
flange,leavingonly the teeth.The resultant soft tissueprofile with the modified
duplicatedmaxillary denture will easily help theimplant team and patient decide on
atreatment plan.Ifthe patients look goodwithout the flange oftheir denture,indi-
cating sufficient nasal-labial support,afixed crown-and-bridge restoration canbe
fabricated using pink porcelain oracrylic to decrease apical gaps from lostalveolar
bone.In addition the deficiencyofalveolar bone necessitates placing theimplants
more apical than is ideal,result-ing in excessively long teeth,teeth withpink
acrylic,a removable lip �plumper,�or a hybrid-type prosthesis with spacebetween the
prosthesis and the implants.A fixed crown-and-bridge,fixed/removable (spark erosion
or milled pros-thesis),or removable overdenture-typeprosthesis may be
prescribed.The implant-borne fixed and fixed-removable prosthesesrequire at least
six,or preferably eight,endosseous implants to adequately supporta maxillary
implant-borne prosthesis.Theexception is the use ofthe Zygomaticusimplant
fixtures.These prostheses requireposterior maxillary vertical height ofbonefor
implants placed in the first molarregion.The removable prosthesis requirestwo to
four implants placed into the anteri-or maxilla to support a bar that has reten-
tive vertical stress-breaking attachments.Edentulous maxillary prostheses are
usual-ly fabricated with cross-arch stabilization ofthe left and right
implants.Cross-arch sta-bilization significantly increases implantsurvival long
term.Placement ofFour Implants into the Anterior MaxillaFor the patient with
adequate anterior ver-tical bone height,and for whom a treat-ment plan has been
made for anteriorimplants for overdenture support,fourimplants can be placed.It is
recommendedto place at least four implants for a tissue-supported overdenture in
the maxilla.Fourimplants in the anterior maxilla are used tosupport a rigid
bar,often combined withvertical stress-broken attachments placedat the distal
aspects.Implants for overden-tures are typically placed with their centersslightly
palatal to the crest to avoid dehis-cence and thin bone over the facial aspectofthe
implants.The incisive canal shouldbe avoided as a site for implant
placement.Specifically,implants for overdentures areplace in the canine and
premolar locations,dependent on the availability ofbone.Animplant can be placed in
the lateral incisorposition ifnecessary.However,implantsplaced in the central
incisor locations com-plicate the prosthetic rehabilitation sincethe presence ofthe
abutments and a barnear the midline may result in excessivepalatal bulk in the
denture,which may bebothersome to the patient.Placement ofEight Implantswithout a
GraftIfthe goals ofthe patients are to have a den-ture or prosthesis that will
enable them tohave a palateless prosthesis and allow themto chew all textured foods
without the pros-thesis depending on the tissues for support,then a sufficient
number ofimplants isrequired to resist the forces ofmastication.For these patients
it is recommended to usesix to eight implants for an implant-supported fixed or
fixed/removable prosthe-sis,with an adequate number ofimplantslocated posteriorly
to support the molars.Eight implants in the anterior andposterior maxilla are used
to support asuprastructure for a totally implant-borne restoration with tissue
contact onlyfor speech.Ifa bar-type structure isplanned,the implants should be
placedwithin the confines ofthe borders oftheplanned prosthesis,and not labial or
out-side the borders ofthe teeth.Theimplants should be placed to avoidimpingement
ofthe teeth in the overden-ture and to allow space for the fabricationofthe bar.For
many ofthese implant-borne cases,implants are placed from thecanine region
extending posteriorly,witha minimal number ofimplants placedinto the incisal
region.This pattern ofplacement makes the design ofthe anteri-or portion ofthe
prosthesis easier.The implants for fixed/removableoverdentures are typically placed
withtheir centers slightly palatal to the crest inorder to avoid dehiscence and
thin boneover the facial aspect ofthe implants.Theimplants can be positioned from
secondmolar to central incisor;however,mostrestorative dentists prefer to avoid
ofthecentral incisor and second molar sites.Thesecond molar site can be used in
selectcases,but it does make the placement ofscrews,abutments,and transfer
copingsdifficult.In addition the bars may need thespace ofthe second molar site for
attach-ments,depending on the prosthetic designofthe retentive bar.Placement
ofEight Implantswith Sinus GraftsPatients who have received a treatment planor an
implant-borne restoration but who
Osseointegration199have insufficient vertical bone for the place-ment ofimplants in
the maxilla posterior tothe canines are considered for a combina-tion ofsinus
grafting and implant place-ment.The sinus grafts can be performed asone
surgery,followed 6 to 12 months laterwith implant placement,or the sinus graftcan
be performed and the implants placedat the time ofthe sinus graft.Ifthe sinusgraft
is performed prior to implant place-ment,the surgeon should verify that bonehas
formed within the graft.We and our colleagues perform sinusgrafting with immediate
placement ofimplants.Currently,the recommendedsinus graft material is autogenous
bone,harvested from the jaws,tibia,or iliaccrest.Ifnecessary the autogenous
bonevolume can be augmented with deminer-alized bone in a ratio not to exceed
1:1.Hydroxylapatite-coated implants are usedfor immediate placement into sinus
grafts.Single- and Multiple-UnitRestorationsThere are different surgical concerns
whenplacing single- or multiunit restorations inthe anterior maxilla or other areas
whereesthetics are less ofa concern.Placementofimplants into premolar and molar
loca-tions can usually be performed with lessconcerns ofpapilla and root
eminencemorphology (Figure 10-8).Premolar or Molar RestorationsDiagnosis and
treatment planning willindicate whether there is sufficient spaceand bone available
for implant placement.Periapical radiographs are necessary forsingle-tooth
restorations to confirm thatthe roots ofthe adjacent teeth do notimpinge in the
space that will be used bythe implant.Ifroot angulation is a prob-lem,then
preoperative orthodontics willneed to be performed prior to implantplacement,or a
fixed bridge can be maderather than placement ofan implant.Careful attention should
be directedto the final restorations and the mechan-ical loading that the
restoration andhence implants will feel.Canine guid-ance or group function is
usually presentand can affect the position oftheimplants.Canine discursion is
recom-mended when placing posterior implantsfor fixed restorations.The ideal
singlepremolar or molar restoration has a bal-anced occlusion that will result in
atrau-matic forces upon the implant.Single-tooth implants should be placed suchthat
the implant is under the workingcusp ofthe tooth,to avoid excessive can-tilever
forces.Maximal length implantsshould be used whenever possible.Shortimplants in the
posterior jaws tend tohave less long-term survival than longerimplants.The crown-
to-root ratio needsto be addressed.Complete treatmentplanning,which includes
knowledge ofthe final restoration,will increase successand limit complications.The
surgical incision is made slightlypalatal to the crest,with vertical
releasingincisions flaring into the vestibule in orderto keep the base ofthe flap
wider than thecrestal incision width.Full-thickness sub-periosteal labial and
palatal flaps are reflect-ed to expose the crest and to provide visu-alization
ofthe vertical cortices ofbone.The implant should be placed with its axisparallel
to the occlusal forces,with theemergence ofthe implant angling to meetthe buccal
cusps ofthe mandibular teeth.Multiple Implant�BorneRestorations for the
PosteriorMaxillaSince these restorations commonlyinvolve the distal
teeth,assessment oftheavailability ofbone in relation to thesinus is critical.If10
mm ofbone is notavailable,then a sinus augmentation isindicated.Iftwo long implants
can beFIGURE10-8A,This patient required a single implant for replacement ofa
premolar in the maxil-la.A tissue punch was used to access the crestal bone.The
implant site was prepared and the implantplaced through this circular soft tissue
hole.This implant has an internal connection.B,A fixed abut-ment was placed
immediately into the implant and prepared.A provisional crown,not in occlusion,was
fabricated.C,This is the final crown.Note the excellent soft tissue reaction to the
crown,abut-ment,implant complex.ABC
200Part 2: Dentoalveolar Surgeryplaced without the need for a sinus graft,along
with sinus elevation ofa third siteby the use ofosteotomes,then 8 mm ofbone for the
third implant is acceptable.However,the use ofosteotomes to elevatethe sinus floor
by 2 mm is not a proce-dure that has abundant scientific valida-tion.Therefore the
patient must beapprised ofthe risks and potential failure.When in doubt a sinus
elevation is per-formed.The mechanics ofthe finalrestoration need to be taken into
consid-eration when placing multiple implantsfor a full quadrant restoration.There
are patients who have suffi-cient vertical bone but are deficient inthe width
projection ofthe bone.Aftermaxillary teeth are extracted for a
varietyofreasons,facial bone resorption canoccur,leaving the palatal bone
intact,with the alveolus thin and deficient.Plac-ing the implant in the ideal
position mayresult in facial bone dehiscence.For thethin ridge in the posterior
maxilla,withsufficient bone height,several surgicaloptions are available.These
include theuse ofparticulate bone grafting withmembrane coverage,the use
ofonlaybone grafts harvested from the symph-ysis or ramus,and ridge expansion
usingosteotomes or osteotomies.Restorative Options for Single-Unit Restorations in
theAnterior MaxillaEsthetic implant restorations represent achallenge to reproduce
normal-appearingrestorations with normal-appearing softtissue profile and
integrity.Most implantsites that require esthetics have deficien-cies in the ideal
bone and overlying softtissue,and must be enhanced with a vari-ety ofsurgical
techniques.A tooth may bemissing because oflack oftooth develop-
ment,caries,external or internal resorp-tion ofteeth following trauma,root
canalcomplications,bone loss from periodontaldisease,or recent dentoalveolar
trauma.Each ofthese etiologies has secondaryeffects on the proposed implant site.It
iscommon to find a deficiency in labial bonewith loss ofthe previous root
eminenceform ofthe ridge.In addition,the overly-ing soft tissue at the level ofthe
alveolarcrest may be thin,resulting in a lack ofstippling,variations in gingival
color,andincreased translucency resulting in parts ofthe implant and abutment
showingthrough the gingiva.The majority ofanterior maxillarysingle-tooth sites
present with inadequatebone and soft tissue,requiring both boneand soft tissue
augmentation.The heightofthe papilla reflects the underlying cre-stal bone height
on the adjacent teeth.37Careful assessment ofthe bone levels onthe adjacent teeth
enables the surgeon andrestorative dentist to inform patients ofthe realistic
expectations ofretaining orcreating papilla for an esthetic single-tooth
restoration.The presurgical assessment,using theesthetic tooth wax-up,results in
the abilityofthe surgeon to estimate the height andwidth ofa bone graft,ifone is
indicated.For severe bone deficiency,which preventsimplant stabilization,a bone
graft shouldbe placed at least 4 months prior toimplant placement,allowing
futureimplant placement in the ideal locationhorizontally and vertically.When
thedeficit ofthe bone is such that the implantcan be placed and is mechanically
stable,with a portion ofits surface exposedthrough the bone,then a hard tissue par-
ticulate graft is placed at the same time asthe placement ofthe implant.The materi-
al used for grafting depends on the extentofthe implant bone fenestration.Autoge-
nous bone is used for larger fenestrations,with a gradual increase in
hydroxylapatiteused as the implant bone dehiscencedecreases in size.Incision
Considerations forEsthetic Sites When placing an implant in the centralincisor
location,careful attention to thedetail ofgaining access to the underlyingbone is
critical for obtaining a perfectresult,without ablation ofthe papilla orvertical
scars from poor incision designand technique.Ifthere is 5 mm from thecontact point
ofthe teeth to the crestalbone ofthe adjacent tooth,then the use ofsulcular
incisions is indicated.Ifthere arepapillae present but the teeth are long,with an
excess of5 mm between the con-tact point to the crestal bone ofthe adja-cent
tooth,then the patient needs to bewarned that papillae may not be presentafter
implant placement.When necessary,vertical incisions should be beveled toallow for
esthetic scar healing.When thebone anatomy permits,the use ofa tissuepunch and
avoidance ofincisions willallow for no scars and no loss ofpapilla.Angulation ofthe
implant shouldresult in the axis ofthe implant being ori-ented to emerge slightly
palatal to the inci-sive edge ofthe planned restoration.Ifplaced at or anterior to
the incisive edge ofthe tooth,there may be difficulty in devel-oping the emergence
profile ofthe restora-tion.Ifthe implant is placed too far labial,with the anterior
edge ofthe implant at theedge ofthe gingival margin ofthe plannedtooth,then with
addition ofthe abutmentand porcelain,the gingival contour will beexcessive and
gingival recession results.Asthe platform (ie,diameter ofthe implant)increases,the
clinician must be cautious toensure that the labial edge ofthe implant isnot
excessively labial,or emergence ofthecrown will be compromised and will resultin an
obese crown form.Most restorationsrequire more than 1 mm ofclearance fromthe labial
surface ofthe implant to theeventual clinical crown,secondary todevelopment ofthe
emergence profile ofthe restoration from the subgingival por-tion ofthe implant
restoration.The depth ofthe implant in relation tothe planned gingival margin is
also critical.Ifthe implant is placed too shallow,with 2 mm or less from the top
ofthe implant tothe gingival margin,then several adverse
Osseointegration201events can occur.The metal from theimplant may be visible
through the gingivalmargin.Because the distance from the topofthe implant to the
gingival margin isminimal,metal showing through the gingi-va is difficult to
camouflage.A minimal dis-tance between the gingival margin and thetop ofthe implant
may also result in diffi-culty in adjusting the margins ofthe abut-ment,with
porcelain extending to theimplant itself.It is then difficult to develop anatural
appearance since the gingival mar-gin region ofthe restoration is excessivelybulked
or round in shape.The use ofceram-ic abutments may help in these adverse situ-
ations.However,proper implant placementis a simple means to avoid these
problems.Immediate Loading and One-Stage ProtocolThe evolution ofimplant-related
therapiesin the modern era was based on the workofBr�nemark and colleagues,who
scien-tifically validated the process ofplacing animplant into bone,waiting a
period oftime for bone to heal to the implant,fol-lowed by long-term functional
loading.13During the 1970s and early 1980s a one-stage threaded titanium plasma-
coatedimplant was used for overdenture reten-tion with immediate loading.The
�Swissscrew�was placed into the anteriormandible and had excellent long-
termsuccess.Other one-stage implant systemswere slow to develop,but as they
haveemerged with data to support a one-stageprocess (ie,with no need for
exposuresurgery),the concept ofa one-stageendosseous implant therapy has
gainedcredibility.The Strauman system has long-term data indicating that a one-
stageunloaded implant system can work in allareas ofthe mouth,in distinction to
theSwiss screw and the Br�nemark proto-cols.14Recently,more interest has arisenfor
placement ofimplants into the esthet-ic zone ofthe maxilla,with either immedi-ate
loading or the use ofa healing abut-ment that mimics the natural shape
ofthetooth.The hypothesis is that by placing ahealing abutment with natural
contours,the soft tissue response will be enhanced,potentially resulting in a more
estheticfinal restoration.Treatment planning for a one-stage orimmediately
temporized anterior maxil-lary restoration begins with a list ofcon-
traindications.Ifa tooth is present andneeds to be extracted,a one-stage
exposedimplant placement at the time ofextrac-tion will require the following:�No
purulent drainage or exudate fromthe site�Excellent gingival tissue quality with-
out excessive granulation tissue�Lack ofperiapical,uncontrolled radi-
olucency�Adequate bone levels circumferential-ly without the need for additional
softor hard tissue graftingThe clinician has several options (Table10-1).At the
time oftooth extraction,ifthere are any ofthe contraindications pre-sent as
described above,either a graft can beplaced into the extraction socket,or nograft
is placed.The decision to avoid a graftis based on the thickness ofthe labial
boneand the prior healing patterns ofthepatient,ifknown.However,in our institu-
tion,an anterior extraction site without asocket graft is more prone to labial
boneresorption and hence less-than-ideal boneis available at the time ofimplant
place-ment.Ifa graft is placed into the socket,then after 3 to 6 months,depending
on thematerial placed,the implant can usually beplaced in an ideal location.Ifthere
is ideal bone and soft tissuepresent at the time ofextraction,animplant can be
placed at the time ofextrac-tion.The clinician should decide prior toextraction ifa
provisional restoration is tobe placed at the time ofimplant placement,or ifthe
implant is to have a healing abut-ment placed for a one-stage protocol,orsubmerged
for a two-stage protocol.Preoperative planning for immediatetemporization after
implant placementinvolves fabrication ofa surgical guidethat precisely locates the
implant in oneposition.The surgeon must work closelywith the restorative dentist to
ensure thatthe planned placement ofthe implant willindeed be able to be
performed.Therestorative dentist should be available dur-ing surgery to guide the
surgical place-ment and be able to adapt the temporaryrestoration after implant
placement.After the implant is placed and the ori-entation approved by the
restorative den-tist,the abutment is placed,and removedas necessary so that changes
in its heightand contours can be accomplished outsideTable 10-1Options When
Extracting Anterior Maxillary ToothProcedureAdjunctive
TreatmentsAdvantageDisadvantageExtract toothNo graft;wait 8 wkShort time to implant
placementLabial bone loss and need for adjunctive tissue graftsExtract
toothImmediate placement ofimplantLess time for overall treatmentIncreased chance
for infection;may not haveideal bone support upon placementExtract toothGraft
extraction site;wait 4 moProvides ideal placement siteExtended time for
treatmentfor implant placement
202Part 2: Dentoalveolar Surgeryofthe mouth.The abutment and tempo-rary crown may
be prepared on a modelprior to surgery in selected cases.The abut-ment is placed
and tightened to theimplant and the temporary crown com-pleted.The occlusion should
be relieved toavoid loading the implant during the heal-ing period.In some patients
who may beprone to loading the implant because ofathletics,weight lifting,or their
occlusion,an anatomic healing abutment or a customhealing abutment can be placed in
order topreserve the morphology ofthe gingiva,without the presence ofa tooth
form.Procedures performed during the inte-gration or healing period are delayed
untilimplant integration has occurred,in orderto avoid disturbance ofthis critical
aspectofimplant success.Approximately 2 months after the implants have
beenplaced,the patients are seen by the restora-tive dentist and surgeon to
decide,basedon the esthetic set-up,whether the implantsite requires additional
augmentation ofthe ridge.The goal is to achieve a convexridge profile and develop
the site�s shape toallow for the restoration to emerge fromthe gingiva,similar to a
natural tooth.Ourexperience indicates that 70% oftheimplant sites that required
hard tissuegrafts also benefited from subepithelialconnective tissue grafts placed
31/2monthsafter implant placement.SummaryThe successful restoration ofthe
patientwith dental implants can result in a changein dental function and
health,with a happypatient.The basis for the use ofdentalimplants is initiated by
the normalsequence ofwound healing,the translationofsurface engineering to implant
design,and evidence-based trials that verify andconfirm efficacy oftreatment
methods.References 1.Lemons J,Natiella J.Biomaterials,biocompati-bility and peri-
implant considerations.Dent Clin North Am 1986;30:3�23.2.Shulman LB.Transplantation
and replantationofteeth.Laskin:Oral and maxillofacialsurgery.Vol 2.St.Louis
(MO):C.V.MosbyCo.;1985.p.132�6.3.Driskell TD.History ofimplants.J CalifDentAssoc
1987;15:16�25.4.Bonwell,AC.First District Dental Society.In:Greenfield
EG,editor.Implantation ofarti-ficial bridge abutments.Dent
Cosmos1913;55:364.5.Greenfield EJ.Implantation ofartificial crownand bridge
abutments.Dent Cosmos1913;55:364.6.Harris SM.An artificial tooth.Dent
Cosmos1887;55:433.7.Adams PB,inventor.Anchoring means for falseteeth.US patent
2,112,007.1938 March 22.8.Strock EA.Experimental work on a method forthe
replacement ofmissing teeth by directimplantation ofa metal support into
thealveolus.Am J Orthodont Oral Surg1939;25:457�72.9.Dahl GSA.Om impijlighenten for
implanta-tion i Keken au metaliskelett som has ellerrention for fastoc eller
avatagbara prostesor.J Odontol Tidskr 1943;51:440.10.Linkow LI.The blade-vent:a new
dimension inendosseous implants.Dent Concepts1968;11:3�12.11.Roberts HD,Roberts
RA.The ramusendosseous implants.J South CalifDentAssoc 1970;38:571�7.12.Proceedings
ofthe Toronto Consensus Devel-opment Conference on Dental Implants.JProsthet Dent
1983;49:50.13.Br�nemark PI.Introduction to osseointegra-tion.In:Br�nemark PI,et
al,editors.Tissueintegrated prostheses.Chicago (IL):Quin-tessence Publishing
Co.Inc.;1985.p.29.14.Schenk RK,Buser D.Osseointegration:a reali-
ty.Periodontology.2000;17:22�35.15.Sykaras N,Iacopino A,Marker V,et
al.Implantmaterials,design and surface topographies:their effect on
osseointegration [review].Int J Oral Maxillofac Implants 2000;15:675�90.16.Buser
D,Schenk RK,Steinemann S,et al.Influ-ence ofsurface characteristics on bone inte-
gration oftitanium implants.A histometricstudy in miniature pigs.J Biomed MaterRes
1991;25:889�902.17.Thomas KA,Kay JF,Cook SD,Jarcho M.Theeffect ofsurface
macrotexture andhydroxylapatite coating on the mechanicalstrengths and histologic
profiles oftitaniumimplant materials.J Biomed Mater Res1987;21:1395�414.18.Brunski
JB,Puleo DA,Nanci A.Biomaterialsand biomechanics oforal and
maxillofacialimplants:current status and future devel-opments.Int J Oral Maxillofac
Implants.2000;15:15�46.19.Cordioli G,Zajzoub Z,Piatelli A,ScaranoA.Removal torque
and histomorphometricstudy offour different titanium surfaces.IntJ Oral Maxillofac
Implants 2000;15:668�74.20.Cochran DL,Buser D,ten Bruggenkate C,et alThe use
ofreduced healing times on ITIimplants with a sandblasted and acid-etched (SLA)
surface:early results fromclinical trials on ITI SLA implants.ClinOral Implants Res
2002;13:144�53.21.Eriksson RA,Albrektsson T.Temperaturethreshold levels for heat-
induced bone tis-sue injury:a vital-microscopic study in therabbit.J Prosthet Dent
1983;50:101.22.Eriksson RA,Adell R.Temperatures duringdrilling for placement
ofimplants using theosseointegration technique.J Oral Maxillo-fac Surg
1986;44:4�7.23.Watanabe F,Tawanda Y,Komatsu S,Hata Y.Heat distribution in bone
during prepara-tion ofimplant sites:heat analysis by real-time thermography.Int J
Oral MaxillofacImplants 1992;7:212�9.24.Adell R,Lekholm U,Br�nemark
PI.Surgicalprocedures.In:Br�nemark PI,Zarb GA,Albrektsson T,editors.Tissue
integratedprostheses:osseointegration in clinical den-tistry.Chicago
(IL):Quintessence Publish-ing Co.Inc.;1985.p.211�32.25.Lazzara R,Porter S,Testori
T,et al.A prospec-tive multicenter evaluation loading ofOsseotite implants two
months after place-ment:one-year results.J Esthet Dent1998;10(6):280�9.26.Testori
T,DelFabbroCH,Feldman S,et al.Amulticenter prospective evaluation of2-months loaded
Osseotite implants placedin the posterior jaws:3 year follow-upresults.Clin Oral
Implants Res 2001;12:1�7.27.Cooper L,Felton D,Kugelberg C,et al.A mul-ticenter 12
month evaluation ofsingle-tooth implants restored 3 weeks after 1stage surgery.Int
J Oral MaxillofacImplants 2001;16:182�92.28.Cooper LF,Scurria MS,Lang LA,et
al.Treat-ment ofedentulism using Astra Techimplants and ball abutments to
retainmandibular overdentures.Int J Oral Max-illofac Implants
1999;14:646�53.29.Lazzara RJ.Esthetic and restorative benefits ofnon-axillary
loaded implants.ImplantDent 1995;4:282�3.30.Krekeler G,Schilli W,Diemer J.Should
the exitofthe artificial abutment tooth be posi-tioned in the region on attached
gingival?Int J Oral Surg 1985;14:504�8.
Osseointegration20331.Block MS,Kent JN.Factors associated with softand hard tissue
compromise ofendosseousimplants.J Oral Maxillofac Surg 1990;48:1153�60.32.Feinberg
SE,Steinberg B,Helman J.Healing oftraumatic injuries.In:Fonseca RJ,WalkerRV,Betts
NJ,Barber HD,editors.Oral andmaxillofacial trauma.Vol 1.2nd Ed.Philadelphia (PA):WB
Saunders Co.;1997.p.13�59.33.Shetty V,Bertolami CN.The physiology ofwound
healing.In:Peterson LJ,IndresanoAT,Marciani RD,Roser SM,editors.Prin-ciples oforal
and maxillofacial surgery.Philadelphia (PA):JB Lippincott;1992.p.3�18.34.Black
J.Reaction ofbiological molecules withbiomechanical surfaces.In:Black
J,editor.Biologic performance ofmaterials.Funda-mentals ofbiocompatibility.New
York(NY):Marcel Dekker;1981.p.45.35.Adell R.A 15 year study
ofosseointegratedimplants in the treatment ofthe edentulousjaw.Int J Oral Surg
1981;10:387�416.36.Cooper LF.Biologic determinants ofbone for-mation for
osseointegration:clues forfuture clinical improvements.J ProsthetDent
1998;80:439�49.37.Higuchi KW,Block MS.Current trends inimplant reconstruction.J
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CHAPTER 11Soft Tissue Management inImplant TherapyAnthony G.Sclar,DMDSoft Tissue
Integration The term soft tissue integrationdescribesthe biologic processes that
occur duringthe formation and maturation ofthe struc-tural relationship between the
soft tissues(connective tissue and epithelium) and thetransmucosal portion ofan
implant.Although experimental and clinicalresearch have only recently begun to
focuson improving our understanding ofthefactors that can affect this soft tissue
envi-ronment,our current knowledge indicatesthat the maintenance ofa healthy soft
tis-sue barrier is as important as osseointegra-tion itselffor the long-term
success ofanimplant-supported prosthesis.As such,theimplant surgeon must be well
acquaintedwith various surgical techniques andapproaches for successfully managing
peri-implant soft tissues in commonly encoun-tered clinical
situations.Furthermore,when an inadequate quantity or quality ofsoft tissue is
available to secure a stableperiimplant environment,the implant sur-geon must know
the principles and tech-niques to successfully reconstruct thesecomponents.This
chapter focuses on basicprinciples and surgical techniques to man-age and,when
indicated,reconstruct peri-implant soft tissues to enhance the long-term
predictability and esthetic outcomesachieved in implant therapy.Flap Management
ConsiderationsThe primary goal ofimplant soft tissuemanagement is to establish a
healthy peri-implant soft tissue environment.This goal isaccomplished by obtaining
circumferentialadaptation ofattached tissues around thetransmucosal implant
structures,therebyproviding the connective tissue and epithe-lium needed for the
formation ofa protec-tive soft tissue seal.1In addition,whenimplant therapy is
performed in estheticareas,re-creating natural-appearingsoft tis-sue architecture
and topography at theprosthetic recipient site is often necessary.To achieve these
goals,the surgeon mustcarefully preserve and manipulate existingsoft tissues at the
implant site and performsoft tissue augmentation,when indicated.The
quantity,quality,and positioning ofthe existing attached tissues relative to
theplanned implant emergence should beevaluated prior to implant surgery.Theflap
should be designed to ensure that anadequate band ofattached,good-qualitytissue is
always available lingual or palatalto the planned implant emergence.Design-ing the
flap in this fashion is practicalbecause subsequent correction ofsoft tis-sue
problems occurring in lingual andpalatal areas is difficult.Preoperative eval-
uation using a surgical template helps thesurgeon visualize whether adequate
tissuequality and volume are available in the areacritical for prosthetic
emergence.The sur-geon can then decide where the incisionswill have to be made or
how the existingsoft tissues must be manipulated with spe-cific surgical maneuvers
to establish a sta-ble periimplant soft tissue environment ineach individual
case.Design for Submerged Implant PlacementWhen placing a submerged
implant,thebuccal flap must be designed to preserveboth the blood supply to the
implant siteand the topography ofthe alveolar ridgeand mucobuccal fold.The access
flap isoutlined by a pericrestal incision and oneor more linear or curvilinear
verticalreleasing incisions that extend onto thebuccal aspect ofthe alveolar
ridge.Thepericrestal incision is beveled to the lin-gual or palatal aspects (Figure
11-1).Theincision is initiated over the lingual orpalatal aspects ofthe ridge
crest,and thescalpel blade is angled to make contactwith the underlying
bone.Typically,linearvertical releasing incisions are used inedentulous situations
and curvilinearbeveled incisions are used in partiallyedentulous situations.In
either case,reflection ofthe buccal flap exposes the
206Part 2: Dentoalveolar Surgeryentire ridge crest and provides ampleaccess for
implant instrumentation.This isaccomplished with minimal lingual orpalatal flap
elevation,thus preservingperiosteal circulation and providingattached tissue to
anchor the buccal flapduring subsequent wound closure.Thestability ofthe
postoperative wound com-plex is improved,and the topography ofthe alveolar ridge
and mucobuccal fold ispreserved.As a result,wound dehiscence isdecreased and the
use ofa provisionalprosthesis during the osseointegrationperiod is
facilitated.Design for Abutment Connection and NonsubmergedImplant PlacementExcept
for the location and bevel ofthepericrestal incisions,the same flap designis used
for an abutment connection tosubmerged implants as for placement ofnonsubmerged
implants (see Figure 11-1).The pericrestal incision is initiated in aposition that
ensures the maintenance ofapproximately a 3 mm apicocoronaldimension ofattached
lingual tissue orgood-quality palatal mucosa (free ofrugae) for re-adaptation
around theemerging implant structures.The quantityand position ofthe existing soft
tissuesguide the location ofthe incision.In gen-eral,this incision is located
closer to themidcrestal position than the one made forsubmerged implant
placement.The scalpelblade is held so as to create a buccal bevelto facilitate
abutment connection andimplant placement while preservingperiosteal blood supply by
minimizing theneed for a lingual or palatal flap reflection.Additionally,the buccal
bevel maximizesthe amount ofattached tissue reflectedwith the buccal flap (see
Figure 11-1).As suggested above,by adjusting thelocation and bevel ofpericrestal
incisionsand precisely locating linear or curvilinearvertical releasing
incisions,the implantsurgeon is equipped with practical flapdesigns for submerged
implant placement,abutment connection,and nonsubmergedimplant placement in
edentulous and par-tially edentulous and esthetic case types(Figures 11-2�11-
6).Surgical Maneuvers for Management ofPeriimplant Soft TissuesOnce the flap has
been outlined in a man-ner that ensures an optimal lingual andpalatal soft tissue
environment,the surgi-cal maneuvers that are used for managingthe resulting buccal
flap during abutmentconnection and nonsubmerged implantplacement can be
determined,for themost part,by the apicocoronal dimensionofthe attached tissue
remaining on thebuccal flap margin.There are three dis-tinct soft tissue surgical
maneuvers thatare commonly used during abutment con-nection or nonsubmerged implant
place-ment to achieve the desired outcome ofobtaining primary closure with
circumfer-ential adaptation ofattached tissuesaround emerging implant
structures:resective contouring,papilla regeneration,and lateral flap
advancement.Although the minimum width ofattached tissue necessary to establish
astable periimplant soft tissue environ-ment has yet to be established,the follow-
ing guidelines for using each ofthe softtissue maneuvers provide consistentresults
in most clinical situations.It isimportant to note that the use ofa specif-ic
maneuver is based primarily on theapicocoronal dimension ofthe attachedtissue
remaining along the buccal flapmargin at each implant site.A combina-tion ofthese
surgical maneuvers is oftenindicated because the width ofattachedFIGURE11-1Beveled
pericrestal incisions: the black arrowsrepresent the path ofthe palatal and lin-
gual beveled pericrestal incisions recommended for submerged implant placement in
the maxilla andmandible.The blue arrowsrepresent the buccal beveled incisions
recommended for abutment con-nection and nonsubmerged implant placement in the
maxilla and mandible.Adapted from Sclar A.3FIGURE11-2The flap design for implant
place-ment in the edentulous mandible incorporates amidline vertical releasing
incision and distal ver-tical releasing incisions made well beyond thearea planned
for the implant placement.Theblack arrowindicates the location ofthe peri-crestal
incision used for submerged implantplacement.The location ofthe incision used
forabutment connection and nonsubmergedimplant placement is indicated by the
straightblue arrow.Adapted from Sclar A.3
Soft Tissue Management in Implant Therapy207tissue remaining on the buccal flap
variesas a result ofnecessary adjustments madein the path ofthe crestal incision to
main-tain an adequate width ofattached tissueon the lingual or palatal
flap.Resective ContouringWhen the widthofthe gingival tissues remaining on
thebuccal flap is 5 to 6 mm,resective con-touring facilitates circumferential adap-
tation ofthe soft tissues around theemerging implant structures.A finescalpel blade
held in a round handle isused to perform a gingivectomy on thebuccal flap
corresponding in shape andposition to the anterior-most abutmentor nonsubmerged
implant neck.Afterresective contouring the tissue is adaptedaround the emerging
implant structure;this process is then repeated sequentiallyaround each implant
(Figure 11-7).Thecontoured flap is then repositioned api-cally and secured around
the abutmentswith a suture passing through each inter-implant area,and additional
sutures areplaced to close the curvilinear releasingincisions.Papilla
RegenerationWhen the width ofthe gingival tissues remaining on the buc-cal flap is
4 to 5 mm,use ofthe papillaregeneration maneuver is indicated.Advo-cated by Palacci
and colleagues,2thismaneuver facilitates primary closure andcircumferential
adaptation around thetransmucosal implant structures whilepreserving an adequate
band ofattachedtissue around the emerging implant struc-tures.In addition,attached
mucosa istaken from the top ofthe ridge and movedin a buccal direction while
approximately3 mm ofattached lingual or palatal tissuesis preserved.A fine scalpel
is subsequentlyused to sharply dissect the tissues to createpedicles in the buccal
flap,which are pas-sively rotated to fill the interimplantspaces (Figure 11-
8).Passive adaptation ofthe pedicles in the interimplant space mayrequire reverse
cutback incisions madeaway from the base ofthe pedicle.The tis-sues are
sutured,avoiding tension withinthe pedicles,usually using a figure-of-eight
horizontal mattress suture.Alterna-tively,a simple interrupted suture passedthrough
the buccal flap in a fashion thatFIGURE11-3The flap design for implant place-ment
in the partially edentulous mandible isoutlined by pericrestal and curvilinear
beveledvertical releasing incisions.The black arrowindicates the location ofthe
pericrestal incisionused for submerged implant placement.Thelocation ofthe incision
used for abutment con-nection and nonsubmerged implant placement isindicated by the
straight blue arrow.Adaptedfrom Sclar A.3FIGURE11-4The flap design for implant
place-ment in the edentulous maxilla incorporatesparamidline vertical releasing
incisions and dis-tal vertical releasing incisions made well beyondthe area planned
for the implant placement.Theblack arrowindicates the location ofthe peri-crestal
incision used for submerged implantplacement.The location ofthe incision used
forabutment connection and nonsubmergedimplant placement are indicated by the
straightblue arrow.Adapted from Sclar A.3FIGURE11-5The flap design for an
implantplacement in the partially edentulous maxilla isoutlined by pericrestal and
curvilinear beveledvertical releasing incisions.The black arrowindicates the
location ofthe pericrestal incisionused for submerged implant placement.Thelocation
ofthe incision used for abutment con-nection and nonsubmerged implant placement
isindicated by the straight blue arrow.Adaptedfrom Sclar A.3FIGURE11-6The flap
design for estheticimplant therapy is outlined by pericrestal andcurvilinear
beveled releasing incisions.The verti-cal legs ofthe releasing incisions are made
in theadjacent interdental areas,thereby providing theopportunity to camouflage
within interdentalgrooves and the mucogingival junction.This flapdesign
incorporates greater amounts ofmucosaltissues,improving the overall elasticity
oftheflap.When combined with tension-releasing cut-back incisions,coronal
advancement is facilitat-ed without an embarrassment ofcirculation tothe flap
margin.The flap design is exaggeratedby moving the releasing incisions farther
awayfrom the site when reconstruction oflarge-volume esthetic ridge defects is
necessary or forimplant placement at sites where vestibulardepth is
inadequate.Adapted from Sclar A.3
208Part 2: Dentoalveolar Surgerypassively advances the pedicle into theinterimplant
space is effective in many sit-uations.Care must be taken to avoidplacement ofthe
suture through the pedi-cle as this would reduce circulation to thepedicle.Another
variation ofthis tech-nique uses pedicles created in the palatalflap,which can also
be rotated to fill theinterimplant spaces,and is especially use-ful in maxillary
situations where thickpalatal tissues exist.3Lateral Flap AdvancementWhen thewidth
ofthe gingival tissues remaining onthe buccal flap is 3 to 4 mm,the use
ofthelateral flap advancement maneuver facili-tates primary closure and
circumferentialadaptation ofattached tissues around theemerging implant structures
(Figure 11-9).3This maneuver is especially suited forcompletely edentulous or
posterior par-tially edentulous implant case types,wherean adequate band ofattached
tissue existsadjacent to the implant site.Attached tis-sues available from adjacent
areas are sim-ply repositioned to obtain primary closurewith attached tissues
around the emergingimplant structures.This maneuver requires that the flapbe
designed to extend beyond the area ofimplant placement to include theattached
tissues present in adjacent eden-tulous areas.As the closure progresses,the flap
advances,resulting in primaryclosure around the implants and the cre-ation ofa
denuded area that will heal bysecondary intention at the distal extent ofthe
dissection.This surgical maneuver isuseful in edentulous situations and inKennedy
Class I and II partially edentu-lous situations.Rationale for Soft Tissue Grafting
with ImplantsThe rationale for soft tissue augmentationaround dental implants is
related to theneed for soft tissue around natural denti-tion.In general,experienced
cliniciansagree that an adequate zone ofattachedtissue around a natural tooth or
implantprosthesis is desirable to better withstandthe functional stresses resulting
from mas-tication and oral hygiene.Moreover,a cer-tain amount ofattached tissue is
needed towithstand the potential mechanical andbacterial challenges presented by
estheticrestorations that extend below the freegingival margin.Potential
mechanicalchallenges include tooth preparation,softtissue retraction,impression
procedures,cementation ofprovisional and perma-nent restorations,removal
ofimplanthealing abutments,replacement ofhealingabutments with permanent
abutments,taking ofimplant-level impressions,andplacement ofprovisional and
permanentimplant restorations.After the final restoration the intra-crevicular
esthetic restorative margins maycontinue to present a permanent inflamma-tory
challenge to the surrounding soft tissueattachment apparatus.Some implant prac-
titioners believe that the microgap at the siteofthe abutment connection to two-
pieceimplants may present a similar challenge.Whether these challenges result in an
initialapical displacement ofthe marginal tissuesor possibly even progressive loss
ofattach-ment depends on multiple factors,includ-ing the following3:�Age ofthe
patient �General health ofthe patient�Host resistance factors�Effects ofsystemic
medications�Periodontal phenotype�Technique and effectiveness
oforalhygiene�Frequency and technique ofprofes-sional oral hygiene care5�6
mmFIGURE11-7Resective contouring maneuver.When the apicocoronal dimension ofthe
attachedtissue remaining on the buccal flap used for theabutment connection or a
nonsubmerged implantplacement is between 5 and 6 mm,resective con-touring is used
to facilitate circumferential adap-tation ofthe soft tissues around the
emergingimplant structures.Adapted from Sclar A.34�5 mmFIGURE11-8Papilla
regeneration maneuver.When the apicocoronal dimension oftheattached tissue
remaining on the buccal flap usedfor an abutment connection or a
nonsubmergedimplant placement is between 4 and 5 mm,thepapilla regeneration
maneuver is used to facili-tate circumferential adaptation ofthe soft tissuesaround
the emerging implant structures.Adapt-ed from Sclar A.33�4 mmFIGURE11-9Lateral flap
advancement maneu-ver.When the apicocoronal dimension oftheattached tissue
remaining on the buccal flap usedfor an abutment connection or a
nonsubmergedimplant placement is between 3 and 4 mm,lateralflap advancement is used
to facilitate circumferen-tial adaptation ofthe soft tissues around the emerg-ing
implant structures.Adapted from Sclar A.3
Soft Tissue Management in Implant Therapy209�Operative technique�Choice
ofrestorative materials�Initial location ofrestorative marginvis-�-vis
circumferential biologicwidth requirements�Prominence ofthe implant position inthe
alveolus�Pre-existing bony dehiscence�Design and surface characteristics ofthe
implant�Depth ofimplant placement�Thickness and apicocoronal dimen-sion ofthe
attached tissueBecause multiple factors influence thehealth ofthe marginal
tissues,prospectiveor retrospective experimental or clinicalstudies are difficult
to design and conduct,much less interpret.Certainly,studies thatprimarily consider
the apicocoronaldimension ofattached tissue and its effecton marginal soft tissue
health,withoutconsidering the other factors,are incon-clusive at best.Therefore,the
rationale forsoft tissue augmentation around naturaldentition or a dental implant
prosthesisshould be based on clinical experiencerather than on results from
experimentalor clinical studies.3Clinical Guidelines for Soft Tissue
AugmentationWhen the apicocoronal dimension ofattached tissue remaining on the
buccalflap will be < 3 mm,the surgeon shouldconsider soft tissue
augmentation.Otherfactors to consider include tissue thick-ness,tissue quality,the
presence ofsoft tis-sue inflammation or pathology,the type ofimplant restoration
planned,and theesthetic importance ofthe site.In a nones-thetic area the surgeon
can use the varioussurgical maneuvers described above toobtain primary closure and
then reevalu-ate the need for soft tissue grafting basedon the health and volume
ofperiimplantattached tissues obtained after initial heal-ing.In contrast,when the
total width ofattached tissue present is < 3 mm in anesthetic area,soft tissue
augmentation isindicated prior to implant placement.Inmost instances this can be
accomplishedwith an epithelialized palatal mucosalgraft,which quickly provides an
improve-ment in the quality ofthe soft tissues.Similarly,in esthetic areas,small-
volume soft tissue esthetic ridge defectscan be corrected simultaneously with sub-
merged or nonsubmerged implant place-ment with subepithelial connective
tissuegrafting,whereas large-volume soft tissueesthetic ridge defects are most
predictablyreconstructed prior to implant placementwith a series ofsubepithelial
connectivetissue grafts.Large-volume soft tissuedefects can also be corrected with
the useofa vascularized interpositional periostealconnective tissue (VIP-CT)
flap,which,inideal circumstances,allows for predictablereconstruction synchronous
with implantplacement.Principles ofOral Soft Tissue GraftingThe first principle
oforal soft tissue graft-ing is that the recipient site must providefor graft
vascularization.It is understoodthat free grafts initially survive by plasmat-ic
diffusion and are subsequently vascular-ized as capillaries and arterioles form a
vas-cular network providing the permanentcirculation for the graft.When a
recipientsite is partially avascular (eg,a denudedroot surface,an exposed implant
abutment,or an area recently reconstructed with ablock bone graft),the dissection
should beextended to provide a peripheral source ofcirculation to support the free
graft over theavascular or poorly vascularized areas.Although pedicle grafts and
flaps maintaintheir blood supply,it is also good surgicalpractice to prepare a
recipient site that cancontribute circulation to ensure optimalresults in the event
ofa reduction ofcircu-lation to a portion (most commonly,themargin) ofthe pedicle
graft or flap.The second principle oforal soft tissuegrafting is that the recipient
site must pro-vide a means for rigid immobilization ofthe graft tissue.Initial
graft survivalrequires that the graft be immobilized andintimately adapted to the
recipient site.Mobility ofthe graft during initial healingcan interfere with its
early nourishmentthrough plasmatic diffusion or can disruptthe newly forming
circulatory supply tothe graft,resulting in excessive shrinkageor sloughing ofthe
graft.The third principle is that adequatehemostasis must be obtained at the
recipi-ent site.Active hemorrhage at the site pre-vents the intimate adaptation
ofthe graft tothe recipient site.Hemorrhage also inter-feres with the maintenance
ofthe thin layeroffibrin between the graft and recipientsite,which serves to
physically attach thegraft to the recipient site and provides forthe plasmatic
diffusion that initially nour-ishes the graft before its
vascularization.Preparation ofa recipient site with a uni-form surface enhances the
intimate adapta-tion with the graft.The periosteum is gen-erally considered to be
an excellentrecipient site for oral soft tissue graftsbecause it fulfills all ofthe
requirementsdiscussed above.In addition,decorticatedalveolar bone can support and
nourish afree soft tissue graft,although immobilizingthe graft at the site is more
troublesome.The fourth principle oforal soft tissuegrafting involves the size and
thickness ofthe donor tissue.The donor tissue must belarge enough to facilitate
immobilizationat the recipient site and to take advantageofperipheral circulation
when root orabutment coverage is the goal.The graftalso must be large enough and
thickenough to achieve the desired volume aug-mentation after secondary contraction
hasoccurred.In addition,the donor tissueshould be harvested to ensure a
uniformgraft surface that facilitates intimate adap-tation to the recipient
site.Thicker grafts(> 1.25 mm) are especially useful for rootand abutment coverage
when graft healingover the central portion ofthe avascularsurface is characterized
by necrosis.The
210Part 2: Dentoalveolar Surgerynecrotic graft is gradually overtaken bygranulation
tissue from the periphery andultimately forms a scar.Thicker grafts arebetter able
to maintain their physicalintegrity during this process,which cantake as long as 4
to 6 weeks.In summary,harvesting a graft that is too small or toothin should be
avoided by evaluating thedonor site prior to surgery and by apply-ing the foregoing
principles during recipient- and donor-site surgery.Although failure to adhere to
thesesurgical principles may not result in theloss ofthe soft tissue
graft,increased com-plications such as inadequate volumeyield,graft sloughing,wound
breakdown,infection,and patient discomfort can beexpected.Epithelialized Palatal
GraftTechnique for Dental ImplantsGeneral ConsiderationsThe use ofan epithelialized
palatal graftfor the treatment ofa mucogingival defecthas enjoyed a long history
ofpredictablesuccess.4�6This versatile technique can beused not only to increase
the dimensionsofattached tissue around the natural den-tition and dental implants
but also as apredictable method for covering denudedroot or abutment
surfaces.Although theterm free gingival graftis a misnomer,it iscommonly used to
describe the transfer ofepithelialized tissue harvested from thepalate.When the
contemporary surgicaltechnique is used as described below,thicksplit-thickness
grafts (> 1.25 mm) or full-thickness grafts are preferred around bothnatural
dentition and dental implants.Contemporary Surgical Technique The surgical
technique for gingival graftingaround dental implants is essentially thesame as the
technique used around naturaldentition.3�7When gingival grafting is per-formed
after implant abutment connectionor delivery ofthe final restoration,a hori-zontal
incision is made through the inter-implant papilla coronal to the desired
finaltissue position.This facilitates abutmentcoverage with the gingival graft.When
gin-gival grafting is performed at second-stagesurgery or simultaneously with
nonsub-merged implant placement,the horizontalincision is made at the mucogingival
junc-tion,and any existing gingival tissues arerepositioned to the lingual or
palatal aspectofthe implants (Figure 11-10A).This stepis extremely important when
implants areplaced in the mandible because subsequentlingual soft tissue defects in
this area are dif-ficult to correct.A split-thickness dissectionis then carried
apically to create a uniformperiosteal site.In the edentulous mandible,care must be
taken to avoid damage to theFIGURE11-10Surgical technique for gingival grafting
simultaneous with abutment connection ornonsubmerged implant placement.A,A full-
thickness horizontal incision is made at the mucogingi-val junction,and a partial-
thickness vertical releasing incision is made at the midline.B,Full-thickness
elevation ofthe flap lingually exposes the ridge crest and allows repositioning
ofthe kera-tinized tissues lingually for abutment connection or nonsubmerged
implant placement.C,Split-thickness dissection on the buccal aspect ofthe alveolar
ridge provides a recipient site for rigid immo-bilization ofthe donor graft,which
is adapted around the emerging implant structures and secured tothe lingual tissues
and to the periosteum peripherally.The dissection is limited distally to
avoidunwanted injury to the mental nerve.Adapted from Sclar A.3ABC
Soft Tissue Management in Implant Therapy211mental nerve with the vertical
releasingincisions that typically outline the mesialand distal extents ofthe
recipient site in thedentate patient.Instead,in these instances amidline vertical
releasing incision andsharp dissection are used to create an ade-quate recipient
site (> 5 mm apicocoronaldimension) with a half-moon shape,asshown in Figure 11-
10B.Subsequently,themucosal flaps are excised and residual elas-tic or muscular
tissue are removed with tis-sue scissors or nippers.When working in aseverely
atrophic mandible,the mucosalflaps are preserved and sutured to theperiosteum at
the base ofthe dissection.The technique for graft immobilization isthe same
regardless ofwhether gingivalgrafting is performed around natural denti-tion,at
second-stage surgery for submergedimplants,or at the time ofnonsubmergedimplant
placement.The graft is sutured toeach papilla or interimplant area coronallyand
then to the periosteum peripherally torigidly immobilize the graft at the
recipientsite (Figures 11-10C,11-11,and 11-12).The following graft immobilization
pres-sure is applied with a moistened salinegauze for 10 minutes.Although a
periodon-tal dressing is not necessary for the recipi-ent site,a protective
dressing for the donorsite is recommended.Gingival grafting is indicated prior
toimplant placement in the severely atrophicmaxilla or mandible that is < 10 mm
inheight and has < 3 mm ofattached tissue.In this clinical situation the surgeon
shouldavoid significant dissection ofthe palatal orlingual tissues.Instead,a large
recipientbed is created on the buccal aspect ofthesite,extending far enough
apically from themidcrest to re-create the buccal vestibularfold.The graft is then
harvested and rigid-ly immobilized with sutures placedapproximately 5 mm apart to
avoid unnec-essary trauma and hematoma formation atthe periphery.During subsequent
implantsurgery,a 3 mm or greater portion ofthemature grafted tissue is repositioned
lin-gually,providing good-quality gingival tis-sue for wound closure over
submergedimplants and circumferential adaptation ofattached tissue around emerging
implantabutments or nonsubmerged implants.Subepithelial Connective TissueGrafting
for Dental Implants General ConsiderationsThe subepithelial connective tissue graft
isan extremely versatile procedure that canbe used to enhance soft tissue
contoursaround the natural dentition and dentalimplants (Figures 11-13�11-15).The
pro-cedure combines the use ofa free soft tis-sue autograft harvested from the
palateFIGURE11-11A,Preoperative view offour submerged implants ready for abutment
connection.The amount ofattached tissue is inadequate to ensure astable periimplant
soft tissue environment.B,Split-thickness dissection is performed to create a
uniform periosteal recipient site.C,Full-thickness elevationofthe attached tissues
exposes the implants for abutment connection; the existing keratinized tissue has
been repositioned to the lingual aspect ofthe emerg-ing abutments.D,A palatal
mucosal graft (gingival graft) is harvested from each side ofthe palate.E,The
grafts have been contoured for precise adaptationaround the abutments and secured
to the lingual tissues and periosteum peripherally.F,This 2-month postoperative
view demonstrates a tremendous vol-ume yield from the gingival grafting procedure.A
stable periimplant soft tissue environment has been obtained.Reproduced with
permission from Sclar A.3ABCDEF
212Part 2: Dentoalveolar Surgerythat is interposed beneath a partial-thickness
pedicle flap at the recipient site(ie,open approach).Alternatively,the graftcan be
secured in a split-thickness pouchprepared at the recipient site
(ie,closedapproach).The graft is harvested internal-ly from the palate,resulting in
a partial-thickness donor-site pouch that allows forprimary closure and thus a more
comfort-able palatal wound.Because the graft ispositioned between the periosteum
and apartial-thickness cover flap or pouch at therecipient site,it enjoys the
advantage ofadual blood supply to support graft revascu-larization.Because ofthe
abundant bloodsupply available for healing,the connectivetissue graft is less
technique sensitive,easi-er to perform,and more predictable thanthe gingival
graft.The connective tissuegraft also results in superior color match-ing and
esthetic blending at the recipientsite.The subepithelial connective tissuegraft can
be used during initial implant-site development prior to implant place-ment or
simultaneous with submergedimplant placement for the correction ofsmall-volume soft
tissue esthetic ridgedefects.Similarly,the connective tissuegraft can be performed
simultaneous withan abutment connection or nonsubmergedimplant placement to
reconstruct thesesmall-volume soft tissue defects or for thecorrection ofsoft
tissue recession defectsthat develop in the recall period.Finally,whenever a large-
volume soft tissue esthet-ic ridge defect is present,a series ofcon-nective tissue
grafts is usually required forreconstruction ofthese esthetic ridgedefects prior to
implant placement.3Surgical Technique: Donor-Site SurgeryThe technique for
harvesting subepithelialconnective tissue grafts from the premolarregion ofthe
palate has two variations:thesingle-incision approach and the dual-incision
approach.7,8In either case,thedonor-site surgery begins with a full-thickness
curvilinear incision madeFIGURE11-12A,Preoperative view ofa partial-ly edentulous
mandibular site planned for simul-taneous gingival grafting with the placement
ofnonsubmerged implants.B,Gingival graft adapt-ed around the transmucosal portion
ofnonsub-merged implants and secured to the lingual tissuesand the periosteum
peripherally.C,Final restora-tion in place.Note that a healthy periimplant
softtissue environment has been created.Reproducedwith permission from Sclar
A.3ACBFIGURE11-13A andB,Progressive soft tissue recession involving the mandibular
bicuspids and afirst molar tooth was successfully corrected with a root coverage
procedure using a subepithelial con-nective tissue graft.Reproduced with permission
from Sclar A.3ABFIGURE11-14A,The progressive soft tissue recession around this
lateral incisor implant restorationjeopardized its long-term success.B,A
subepithelial connective tissue graft was performed via a closedpouch recipient
site,resulting in the restoration ofsoft tissue esthetics and stability for this
patient witha thin scalloped periodontium.Prophylactic soft tissue grafting would
have prevented the recessionfrom occurring and is indicated when intracrevicular
restorations are planned for patients who pre-sent with thin periodontal
tissues.Reproduced with permission from Sclar A.3AB
Soft Tissue Management in Implant Therapy213through the palatal tissues
approximately2 to 3 mm apical to the gingival margin ofthe premolars (Figure 11-
16A).This inci-sion can be made perpendicular to thesurface ofthe palatal tissue,or
it can beslightly beveled.When it is made perpen-dicular to the palatal tissues,the
thicknessofthe coronal portion ofthe graft is max-imized;however,this usually
prevents pas-sive primary closure.In contrast,bevelingthe first incision limits the
thickness ofthecoronal portion ofthe graft but,in manycases,enables a passive
primary closure.When using the dual-incision approach,a partial-thickness
curvilinear incision isthen made approximately 2 mm apical to thefirst incision to
complete an ellipse (Figure11-16B).This incision defines the thicknessofthe
subepithelial connective tissue graft tobe harvested.The incision should be approx-
imately 1 mm deep to ensure adequatethickness ofthe remaining cover tissue andto
minimize the incidence ofsloughing atthe donor site.The scalpel is then
orientedparallel to the surface ofthe palatal tissue,and sharp dissection is used
to create a rec-tangular pouch.The apical extent ofthe dis-section is determined by
the height ofthepalate.The mesiodistal extent ofthe dissec-tion is determined by
the length ofthe firstand second incisions,which,in turn,aredetermined by the
overall size ofthe palateand the width ofthe premolars.The scalpelblade is then
used to complete the outline ofthe donor connective tissue graft with inci-sions
that pass through the underlying con-nective tissue and periosteum just short ofthe
mesial and distal extent ofthe pocket.Unnecessary trauma to the overlying
palataltissues is thus avoided when the scalpel isturned perpendicular to the
surface ofthedonor tissue.A Buser periosteal elevator andmembrane-placement
instrument are thenused to carefully begin subperiosteal eleva-tion ofdonor tissue
at the coronal aspect ofthe dissection.Once the coronal aspect ofthe graft has been
elevated,it is carefully sup-ported with tissue forceps and the subperi-osteal
elevation is extended to the apical por-tion ofthe pouch.Next,gentle traction
isplaced on the elevated tissue with forceps,FIGURE11-15A,Preoperative view
ofcentral incisor implant site with a small-volume soft tissue esthetic ridge
defect.B,An open flap approach involv-ing full thickness dissection at the ridge
crest and partial thickness dissection on the buccal aspect ofthe alveolar ridgewas
used for the implant placementand synchronous subepithelial connective tissue
grafting.Coronal advancement ofthe cover flap enabled further soft tissue volume
enhancement via sub-mersion ofthe one-piece nonsubmerged implant,thus expanding the
�soft tissue envelope.�C,Following conservative exposure and insertion ofa
customabutment and provisional restoration,the soft tissues were allowed to
stabilize prior to the delivery ofthe final restoration,which demonstrates
pleasingsoft tissue esthetics.Reproduced with permission from Sclar A.3FIGURE11-
16Subepithelial connective tissue grafting donor-site surgery via a dual-
incisionapproach.A,The occlusal view demonstrates the location and orientation
ofthe full-thickness andpartial-thickness incisions.B,The cross-sectional view
demonstrates the pathways ofthe incisions fordonor-site harvest via the dual-
incision approach.The shaded arearepresents the resultant donorgraft,consisting
ofboth connective tissue and periosteum.Adapted from Sclar A.3ABABC
214Part 2: Dentoalveolar Surgeryand a horizontal incision is made throughthe apical
aspect ofthe donor tissue fromwithin the pouch.The harvested tissue,which contains
epithelium,connective tis-sue,and periosteum,is then transferred withtissue forceps
to the recipient site or tem-porarily placed on sterile gauze moistenedwith
saline.Ifthe graft is submerged underthe recipient�s site flap,curved Iris tissue
scis-sors should be used to remove the epithelialtissue.Hemostasis is then obtained
at thedonor site by placing an absorbable collagendressing,such as CollaPlug,and
applyingpressure with saline-moistened gauze.Thedonor site is closed using
interrupted 4-0chromic gut sutures on a P3 needle passedthrough the interproximal
areas.The single-incision technique differs inthat only one incision is used to
establishaccess to both the subperiosteal and subep-ithelial planes
ofdissection.This approachbegins with a full-thickness curvilinearincision,as
described above.Next,thescalpel is reoriented within the incisionuntil it is
parallel to the surface ofthepalatal tissue.Subepithelial dissection thatparallels
the external surface ofthe palataltissue is accomplished to create a rectangu-lar
pouch.After making the first incision,the surgeon may find it useful to
performsubperiosteal elevation coronally.Thisimproves visualization ofavailable
soft tis-sue thickness (Figure 11-17),thereby aidingthe surgeon to establish the
appropriatesubepithelial plane ofdissection.Theremainder ofthe surgical procedure
isidentical to the procedure described abovefor the dual-incision technique.The
advantage ofthe dual-incisionapproach is that it is easier to perform.Since the
thickness ofthe donor tissue isdefined by the second incision,the result isthe
harvesting ofa graft ofuniform thick-ness.The disadvantage ofthis approach isthat
primary closure is seldom possible,and,therefore,the palatal wound can
beuncomfortable.Nevertheless,this approachis usually recommended for the novice
sur-geon.Although harvesting a donor graft ofuniform thickness is technically more
chal-lenging when the single-incision approachis used,primary closure ofthe
palatalwound results in greater patient comfort.As a result,most experienced
surgeons pre-fer this approach.Surgical Technique: Recipient-Site
SurgeryPreparation ofthe recipient site involveseither the elevation ofa split-
thickness flapthrough supraperiosteal dissection (opentechnique) or a
supraperiosteal dissection,which avoids vertical releasing incisions tocreate an
envelope or pouch (closed tech-nique).The decision ofwhich technique touse when
grafting around a natural toothor an implant restoration depends on sev-eral
factors.The open technique allowsdirect visualization during dissection,which
ensures the preparation ofa uniformrecipient site.This approach also allows
forsignificant coronal advancement when ver-tical soft tissue augmentation is
neededover an exposed root or abutment surface.The vertical releasing incisions
used in theopen technique sacrifice some circulation.However,the use ofa
curvilinear beveledflap with tension-releasing cutback inci-sions avoids
embarrassment ofcirculationto the flap margin and allows for greatercoronal flap
advancement than do tradi-tional trapezoidal flaps that requireperiosteal releasing
incisions to allow evenlimited coronal advancement.In contrast,the closed technique
avoidsthe need for vertical incisions,thus preserv-ing the blood supply to the site
and opti-mizing esthetic results.However,as a�blind�technique,it can be
technicallymore demanding.Also,because it does notallow for significant coronal
advancementofthe cover flap,this technique is oflimit-ed use when significant
vertical soft tissueaugmentation is needed,and it is con-traindicated whenever
vestibular depthlimits the preparation ofan adequatelysized recipient site.In
general,the closedrecipient site is preferred when the abut-ment or root exposure
is < 4 mm apico-coronally or when there is a significant riskofsloughing ofthe
cover flap because ofpoor vascularity at the site.Closed TechniqueThe technique
forclosed recipient-site preparation is the samewhether it is performed around a
naturaltooth or an implant restoration.A horizon-tal incision is extended to the
mesial anddistal aspects ofthe soft tissue defect justcoronal to the level ofthe
root or abutmentcoverage desired (Figure 11-18).Using a no.15C scalpel,the surgeon
makes thisincision at a right angle to the epithelium ata depth ofapproximately 1
mm.The hori-zontal incisions not only mark the graft�sfinal coronal position but
also facilitate thepouch dissection and subsequent immobi-lization ofthe
graft.Next,the scalpel is oriented parallel tothe tissue surface,and the horizontal
inci-sions are extended into the sulcus to createthe entrance to the recipient
site.The split-thickness dissection is extended apicallybeyond the mucogingival
junction at theFIGURE11-17Subepithelial connective tissuegrafting donor-site
surgery via the single-incisionapproach.The cross-sectional view demonstratesthe
pathways ofthe incision and the dissectionfor the donor-site harvest.The shaded
area rep-resents the resultant donor graft consisting ofboth connective tissue and
periosteum.Adaptedfrom Sclar A.3
Soft Tissue Management in Implant Therapy215mesial and distal aspects ofthe site
beforecrossing the midline.To ensure that therecipient site can contribute
adequateperipheral blood supply to sustain the graft,the dissection must extend
well beyond thewidth ofthe soft tissue defect being correct-ed.As a general
rule,the width ofthe recip-ient site should be three times that oftheexposed root
or abutment,which can beaccomplished by extending the defectmesially and
distally.The surgeon musttake care to avoid perforating or tearing theoverlying
tissues with the scalpel;a meticu-lous technique is required to ensure a uni-form
recipient-site surface.The blunt end ofa membrane-placement instrument is then used
toprobe the resultant pouch and confirmthat the dissection is complete.Occasional-
ly,strands or webs oftissue extending fromthe overlying tissues to the periosteum
aredetected in the apical extent ofthe dissec-tion.Ifnot released with sharp
dissection,these tissue strands prevent proper posi-tioning and passive adaptation
ofthe con-nective tissue graft within the pouch.Aperiodontal probe is then used to
measurethe dimensions ofthe recipient pouch andto guide the surgeon in the donor
harvest,and pressure is applied with saline-moistened gauze to obtain
hemostasis.Once the recipient site has been pre-pared and the donor tissue has been
har-vested,the donor tissue should be intimate-ly adapted and rigidly immobilized
at therecipient site.When a closed recipient site isused,the dimensions ofthe donor
connec-tive tissue should closely match those oftherecipient-site pouch.Curved Iris
tissue scis-sors are used to size the graft prior to secur-ing it in the pouch.The
graft should alwaysbe oriented so that the periosteal side facesdown at the
recipient site.A 4-0 chromicsuture on a P3 or FS2 needle is used to placea
horizontal mattress suture that enters theapical portion ofthe recipient
pouch,engages the graft,and exits the pouch api-cally.This suture is used to gently
�pull�thegraft into the recipient pouch and secure thegraft apically,thereby
resisting subsequentcoronal displacement.First,the suture nee-dle is passed through
the vestibular mucosainto the recipient pouch and retrieved withforceps.The suture
needle is then passedthrough the connective tissue side ofthegraft and back through
the periosteal side ofthe graft.Next,the membrane-placementinstrument is used to
identify the apicalextent ofthe recipient site,and the sutureneedle is passed back
through the mucosaltissue to exit the pouch several millimeterslateral ofwhere it
entered.A fine hemostat isclamped across equal lengths (approximate-ly 7.5 cm)
ofthe suture material,and suturescissors are used to cut away the remainingsuture
and needle.Subsequently,the surgeon uses theclamped suture material to slowly pull
thegraft into the recipient pouch,taking carenot to tear the overlying tissue.The
paddleend ofthe membrane-placement instru-ment is used like a shoehorn to guide
thegraft into the entrance ofthe recipientpouch.The flat portion ofthe instrumentis
moistened with saline and placedbetween the graft and the overlying tissueas the
graft is gently pulled into the pouch.This technique prevents bunching ofthegraft
at the entrance ofthe recipient pouchas well as excessive stretching of,and dam-age
to,the overlying tissues.The spikedend ofthe membrane-placement instru-ment is then
used to gently �push�thegraft further into the pouch entrance,while the clamped
suture material is usedto �pull�the graft apically.A triple tiesecures the graft in
the pouch.The graft is secured coronally,eitherwith interrupted sutures that pass
throughthe graft and interproximal tissues (see Fig-ure 11-18) or with a sling
suture.Interrupt-ed sutures in the papillary area are thenused to secure the cover
tissue pouch.Addi-tional sutures can be carefully placed toapproximate the coronal
margins ofthepouch in an effort to cover more oftheexposed
graft.Nevertheless,because signif-icant coronal advancement ofthe overlyingtissues
is not possible,a portion ofthe graftwill remain uncovered.Whenever possible,it is
recommended that two-thirds or moreofthe graft be secured within the recipient-site
pouch.Gentle pressure is applied overthe graft site with saline-moistened gauzefor
a minimum of10 minutes.Open TechniqueAgain,the technique foropen recipient-site
preparation is the essen-tially the same whether it is performedaround a natural
tooth or an implantrestoration,or to improve soft tissue con-tours during implant-
site development.This approach is useful for a moderateamount ofvertical soft
tissue augmentation,making it applicable for abutment coverageFIGURE11-18Closed
�pouch�technique for the preparation ofa recipient site for a subepithelial con-
nective tissue graft to improve soft tissue contours around a natural tooth or an
implant restoration.A,Split-thickness dissection (shaded area).B,Graft mobilization
apically and coronally.Adaptedfrom Sclar A.3AB
216Part 2: Dentoalveolar Surgeryprocedures and for improving soft tissuecontours
during implant-site developmentor when performed over a submergedimplant (Figure
11-19).The dissectionbegins by outlining the recipient site withpartial-thickness
horizontal and verticalincisions using a no.15C scalpel blade on around handle.The
horizontal incision,which is performed first,extends mesial anddistal to the soft
tissue defect at a level justcoronal to the final soft tissue positiondesired after
augmentation.Exaggeratedcurvilinear beveled incisions with tension-releasing
cutback incisions are then initiatedapically well beyond the mucogingival junc-tion
to outline the cover flap.Next,sharpdissection is used to elevate a split-
thicknessflap.The dissection is initiated coronallywith a no.15C scalpel blade.Flap
elevationis continued apically under direct visionwith sharp dissection under
tension,whichis carefully maintained with the use ofmicro-Adson tissue forceps.The
goal is tomaximize the thickness ofthe overlying tis-sue flap,leaving only a thin
layer ofimmo-bile periosteum.When coronal advance-ment ofthe cover flap is
performed,theadjacent papillary areas are de-epithelializedwith a fresh no.15C
scalpel.This furtherextends the wound margin,thereby reduc-ing flap retraction and
greatly enhancingincision line esthetics.It also eliminates thepossibility that the
undersurface ofthecoronally advanced flap will be coapted overan epithelial
surface,which would preventinitial wound healing and could result indehiscence
along the incision.The dimen-sions ofthe recipient site are then measuredwith a
periodontal probe,and hemostasis isobtained by applying gentle pressure withsaline-
moistened gauze.Once the donor graft has been har-vested,it is usually trimmed to
be slightlysmaller than the open recipient site.Thisfacilitates immobilization
ofthe graft andsuturing ofthe cover flap into positionwithout unwanted engagement
oftheunderlying graft,which can cause graftdislodgment secondary to swelling
orretraction ofthe cover flap.Whether graft-ing around natural dentition or
animplant restoration(s),the graft is firstsecured coronally with sutures
passedthrough the adjacent papillary areas usinga 4-0 chromic gut suture on a P3
needle.Alternatively,sling sutures can be used forthis purpose.Next,the graft is
secured lat-erally and apically to the periosteum withadditional sutures.The goal
is to gentlystretch the tissue,thus improving its adap-tation to the recipient
site.Next,the cover flap is secured coronallywith interrupted sutures passing
through thepapillae.These sutures should pass throughthe facial flap and the de-
epithelialized pap-illary tissue and then return under the con-tact points,where
they are tied facially.Alter-natively,a sling suture can be used.In thiscase,the
suture passes through the flap andthe papillary tissue on the first pass;it
thenpasses under the contact points as it returnsto the facial aspect,where it is
tied.Depend-ing on the thickness ofthe cover flap tissue,4-0 or 5-0 chromic gut
suture on a P3 needleis used.Next,the cover flap is secured later-ally.The use
ofexaggerated curvilinearbeveled incisions to outline the cover flapnot only
extends the recipient site,providingadditional circulation to sustain the
graft,italso facilitates immobilization ofthe graftand closure ofthe cover flap.The
suture needle should be perpen-dicular to the beveled incision as it
passesFIGURE11-19Open flap technique for the preparation ofa recipient site for a
subepithelial connec-tive tissue graft to improve soft tissue contours at an
implant site.This approach is useful at the timeofabutment connection (A and B) and
over a submerged implant (C and D).Adaptedfrom Sclar A.3ABCD
Soft Tissue Management in Implant Therapy217through the tissue.It also should be
orient-ed in an apicocoronal direction as it ispassed through the flap and adjacent
tissue.A single pass is recommended to ensureprecise positioning ofthe cover
flap.Theattached tissue contained in the flap is firstprecisely repositioned and
secured withsutures placed laterally.The sutures thenare placed apical to the
mucogingival junc-tion.When performed as part ofimplant-site development or when
grafting over asubmerged implant,the recipient site isextended further onto the
palatal or lingualsurface ofthe alveolar ridge via split-thickness dissection,and
the graft issecured in a similar fashion before closingthe cover flaps,as described
above.Moist-ened saline gauze is used to apply gentlepressure at the site for 10
minutes;a peri-odontal dressing is not usually needed.Vascularized
InterpositionalPeriosteal Connective Tissue FlapGeneral ConsiderationsThe
vascularized interpositional periostealconnective tissue flap (VIP-CT) flap is
aninnovative technique that provides forreconstruction oflarge-volume soft
tissueesthetic ridge defects with a single proce-dure.3In addition,the pedicled
blood sup-ply derived from the connective tissue�periosteal plexus within the flap
providesthe biologic basis for predictable simulta-neous hard and soft tissue
grafting proce-dures during esthetic implant-site devel-opment,even at compromised
sites.Additional advantages ofthe techniqueinclude negligible postoperative soft
tissueshrinkage;enhanced results realized fromhard tissue grafting procedures owing
tothe supplemental source ofcirculation andthe contribution to phase-two bone
grafthealing provided by the mesenchymal cellstransferred with the flap;and,when
hardand soft tissue site-development proce-dures are necessary,a reduction in
treat-ment time and patient inconvenience.Although the amount ofhorizontalsoft
tissue augmentation obtained with theVIP-CT flap is consistently greater thanthat
obtained with free soft tissue graftingtechniques,the amount ofvertical soft tis-
sue augmentation typically obtainedexceeds that obtainable even when severalfree
soft tissue grafts are performed,whichhas allowed the re-creation ofpositive gin-
gival architecture,even in situations whereprevious hard and soft tissue site
develop-ment techniques have fallen short.Thistechnique has also proven useful in
thetreatment ofcompromised sites in whichexisting soft tissues were poor in
qualityand severely scarred,rendering them inad-equate to support required hard
tissueimplant-site development (Figure 11-20).It is a predictable means
ofresubmergingan implant in the anterior area when anunexpected soft tissue
dehiscence compro-mises the final esthetic result.The volume oftissue transfer
routine-ly obtained with the VIP-CT flap has alsoallowed the camouflaging ofsmall-
volumecombination hard and soft tissue ridgedefects,as well as the correction
oflarge-volume soft tissue defects simultaneouslywith implant placement (Figures
11-21and 11-22),as previously discussed.Ofgreatest significance,this
techniqueprovides the implant surgeon with aproven technique for predictable
simulta-neous hard and soft tissue estheticimplant-site development at compro-mised
anterior sites with large-volumecombination esthetic ridge defects (Figure11-
23).These enhanced results are direct-ly related to maintenance ofintact circula-
tion to the flap and decreased postsurgicalcontraction.Surgical Technique As in the
previously described techniques,the surgeon begins by outlining and prepar-ing the
recipient site and then proceeds todonor-site preparation.An exaggeratedFIGURE11-
20Use ofthe vascularized interpositional periosteal connective tissue (VIP-CT) flap
to restore soft tissue volume and health at a severelycompromised
site.A,Preoperative view ofa severely compromised lateral incisor site following a
failed bone graft that resulted in the loss ofcol and papil-la on the adjacent
central incisor and severely scarred and inelastic soft tissue cover at the
site.B,A VIP-CT flap was performed to provide sufficient vol-ume ofgood-quality
tissue to support the subsequent bone graft.C,The final result after subsequent
bone grafting demonstrates the complete recon-struction ofnatural ridge contours
and the successful restoration ofthe adjacent col and papilla,a remarkable result
that is not always obtainable evenwith the VIP-CT flap.Reproduced with
permissionfrom Sclar A.3ABC
218Part 2: Dentoalveolar Surgerycurvilinear beveled flap design is used at
therecipient site.Abbreviated vertical releasingincisions are extended over the
alveolar crestonto the palatal surface at both the mesialand distal aspects ofthe
recipient site.Thisallows full exposure ofthe ridge crest forhard tissue grafting
or implant placement.The palatal incision at the distal aspect ofthe recipient site
parallels the gingival mar-gin on the oral aspect ofthe adjacent tooth(Figure 11-
24A).After recipient-site preparation,donor-site preparation begins by extending
thisincision horizontally to the distal aspect ofthe second premolar.To facilitate
subse-quent closure ofthe donor site,the orienta-tion ofthis incision should be
slightlybeveled and follow a path approximately 2mm apical to the free gingival
margins ofthe canine and premolar teeth (see Figure11-24A).Sharp dissection is then
usedinternally to create a split-thickness palatalflap in the premolar area.The
subepithe-lial dissection is carried mesially towardthe distal aspect ofthe
canine.The sur-geon should be careful to maintain an ade-quate thickness ofthe
palatal cover flap toavoid sloughing.In most cases the dissec-tion has to be deeper
in the area ofthepalatal rugae to avoid perforating thecover flap.Next,a vertical
incision is madeinternally through the connective tissueand periosteum at the
distal extent ofthesubepithelial dissection,as far apically as ispossible without
damaging the greaterpalatine neurovascular structures.Thisincision defines the
margin ofthe flap.Using a Buser periosteal elevator and amembrane-placement
instrument,thesurgeon then carefully elevates the resul-tant periosteal�connective
tissue layer,beginning in the second premolar area andworking toward the anterior
extent ofthedissection.Usually,this careful subpe-riosteal dissection yields intact
periosteumon the undersurface ofthe pedicle,whichaids in subsequent rigid
immobilization ofthe graft.Furthermore,intact periosteumpotentially provides
osteoblastic activity ifapplied over a bone graft when simultane-ous hard and soft
tissue site developmentis performed.A second incision is theninitiated under
tension internally at theapical extent ofthe previous vertical inci-sion and
extended horizontally anterior tothe distal aspect ofthe canine.The outlineofthe
periosteal�connective tissue pedicleis now complete.Limiting the incisions tothe
anatomic landmarks given ensuresthat the margin ofthe pedicle is safely har-vested
from the palatal area,where thethickest amount ofconnective tissue
isavailable,without risk ofdamage to adja-cent neurovascular structures.Next,aBuser
periosteal elevator is used to careful-ly elevate the periosteal�connective
tissuepedicle and undermine the full thicknessofthe palatal mucosa and periosteum
atthe base ofthe pedicle,just beyond themidline ofthe palate (Figure 11-
24B).Thissubperiosteal elevation or underminingFIGURE11-21Use ofthe vascularized
interpo-sitional periosteal connective tissue (VIP-CT)flap for the correction ofa
small-volume combi-nation hard and soft tissue esthetic ridge defect.A,Preoperative
view ofa maxillary canine sitewith a ridge lap pontic attempting to disguise
anobvious ridge contour defect.B,After implantplacement,a VIP-CT flap is rotated
and inter-posed underneath the donor- and recipient-siteflaps,which are closed
primarily.C,The finalrestoration demonstrates a natural estheticemergence and
successful camouflaging ofthesmall-volume combination esthetic ridge
defect.Reproduced with permissionfrom Sclar A.3ABFIGURE11-22Use ofthe vascularized
interpo-sitional periosteal connective tissue (VIP-CT)flap for the correction ofa
large-volume soft tis-sue esthetic ridge defect simultaneous with a sub-merged
implant placement.A,Preoperative viewofa lateral incisor implant site with
removablepartial denture with a tissue-colored flange usedto disguise the large-
volume soft tissue defect atthe site.B,The final restoration demonstrates anatural
emergence and soft tissue esthetics fol-lowing the implant placement and
synchronoususe ofthe VIP-CT flap.Typically,several free softtissue grafts are
necessary to restore a large-volume soft tissue defect.Reproduced with per-
missionfrom Sclar A.3BAC
Soft Tissue Management in Implant Therapy219begins at the distal aspect ofthe
dissectionin the area ofthe second premolar and iscarried anteriorly toward but
short oftheincisive foramen so as to avoid compro-mise to the neurovascular
structures inthis area.Doing so provides additionalelasticity at the base ofthe
pedicle to allowpassive rotation to the recipient site with-out the need for a
tension-releasing cut-back incision.Essentially,the two distinctplanes ofdissection
performed define theinterpositional periosteal�connective tis-sue pedicle flap
without disrupting its cir-culation.The subepithelial plane is super-ficial to the
greater palatine vessels butdeep enough to avoid sloughing ofthepalatal cover
flap.The subperiosteal planeis deep to the greater palatine vessels and islimited
anteriorly and posteriorly to avoiddamage to the neurovascular structures asthey
course through the palate.Tension-releasing cutback incisionsextended into the base
ofthe pedicle flapare rarely necessary when subperiostealundermining is
performed.When un-avoidable,these relaxing incisions are initi-ated at the pivot
point offlap rotationalong the line ofgreatest tension.Althoughthe line ofgreatest
tension is the radius ofthe rotation arc created by the apical hori-zontal
incision,the pivot point may notcoincide with the termination ofthat inci-sion.This
is because the periosteal under-mining causes a favorable displacement ofthe flap�s
pivot point and in most casesallows for tension-free rotation ofthe flapinto the
maxillary anterior area withoutthe need for a tension-releasing
cutbackincision.Nevertheless,when a tension-FIGURE11-23Simultaneous reconstruction
ofa large-volume combination hard and soft tissue esthetic ridge defect for
thereplacement offour maxillary incisors.A,Preoperative view ofthe compromised site
secondary to multiple interventionsleading to tooth loss and a previously failed
attempt at bone graft reconstruction.B,Intraoperative view following rigid fix-
ation ofcorticocancellous block bone grafts and condensation ofparticulate bone
graft material.The vascularized interpo-sitional periosteal connective tissue (VIP-
CT) flaps have been prepared and are ready for rotation over the block bone
graft,thereby improving the volume ofthe soft tissue in the areas critical for
prosthetic emergence and supplementing the circula-tion ofthe soft tissue cover for
enhanced bone graft healing.C,Nonsubmerged central and lateral incisor implants
wereplaced after 4 months ofhealing with customized tooth-form healing
abutments.The final restorative abutments,picturedin this clinical photograph,were
delivered after an additional 4 months.Note that use ofthe VIP-CT flap simultaneous
withthe block bone grafting procedure resulted in a significant vertical soft
tissue augmentation and the restoration ofthe nat-ural soft tissue architecture at
the site.D,The final restorations are harmonious in appearance,and pleasing
gingival esthet-ics are evident.Reproduced with permissionfrom Sclar A.3ABCD
220Part 2: Dentoalveolar Surgeryreleasing cutback incision is necessarydespite
undermining,the surgeon must becareful to limit the length ofthe incision toavoid
embarrassing the circulation.Anintraoperative assessment ofthe area ofgreatest
tension will guide the placement ofreleasing incisions.Next,the flap is rotatedinto
the recipient site and rigidly immobi-lized with sutures placed apically
and/orlaterally (Figure 11-24C).Alternatively,theflap can be secured directly to a
block bonegraft using sutures passed through tran-sosseous perforations in the bone
graft.Anabsorbable collagen dressing,such as Col-laPlug,is used as an aid to
hemostasis andto eliminate dead space in the donor har-vest area.Finally,the donor
and recipientsites are closed primarily with absorbablesutures,and gentle pressure
is applied withsaline-moistened gauze for 10 minutes.Oral Soft Tissue Grafting with
Acellular Dermal Matrix General ConsiderationsAcellular dermal matrix (AlloDerm)
hasbeen used as an alternative to harvestingautogenous epithelialized palatal
grafts andsubepithelial connective tissue grafts inperiodontal surgery since
1996.AlloDermgrafts are composed offreeze-dried allo-graft skin processed to remove
all immuno-genic cellular components (epidermis anddermal cells),leaving a useful
acellular der-mal matrix for soft tissue augmentation.AlloDerm can be used to
increase the widthofattached tissue around the natural denti-tion and
implants,obtain root or abutmentcoverage,and correct small-volume soft tis-sue
ridge defects.The advantages ofusingAlloDerm include the elimination ofdonor-site
surgery for greater patient com-fort,unlimited tissue supply,excellent han-dling
characteristics,and decreased surgicaltime.Disadvantages include greater sec-ondary
shrinkage and slower healing at therecipient sites when used as an onlay graftor
when complete coverage ofan interposi-tional AlloDerm graft is not
obtainable.Predictable root or abutment coveragerequires coverage ofthe AlloDerm
graftwith good-quality cover flap tissue.Surgical TechniqueThe surgical technique
for using AlloDermis essentially the same as that describedabove for the gingival
and subepithelialconnective tissue grafts.The AlloDermgraft must be rehydrated for
10 minutesbefore use.Two distinct sides ofthe Allo-Derm graft are identified by
applying thepatient�s blood to each surface and rinsingwith sterile saline.The
connective tissueside will retain the red coloration,whereasthe basement membrane
side will appearwhite.The connective tissue side containspreexisting vascular
channels that allow forcellular infiltration and revascularization.When used as an
onlay graft to increase thewidth ofattached tissues,the connective tis-sue side
should be oriented toward and inti-mately adapted to the recipient site (Figure11-
25).When used for root or abutmentcoverage,the basement membrane side ofthe graft
should be oriented toward theexposed root or abutment (Figure 11-26).The basement
membrane side ofthe Allo-Derm graft facilitates epithelial cell migra-tion and
attachment.Wherever possible,the author recommends preparing a largerrecipient site
(6�8 mm apicocoronaldimension) and immobilizing a larger Allo-Derm graft compared
to what is used whenan autogenous gingival graft is performed.FIGURE11-24Surgical
technique for the vascularized interpositional periosteal connective tissue (VIP-
CT) flap.A,Occlusal view ofincisions that out-line the donor and recipient
sites.Note that the preparation ofthe recipient site involves de-epithelialization
ofthe adjacent col and papillary areas.B,After split-thickness recipient-site
preparation,de-epithelialization ofthe attached tissue on the buccal aspect ofthe
ridge as well as the adjacent col andpapillary areas is performed,and implant
placement is completed.Subsequently,the VIP-CT flap is developed via subepithelial
and subperiosteal dissec-tions performed within the bicuspid region ofthe
palate.C,Subperiosteal undermining is extended to the midline,allowing the flap to
passively rotate tothe midline,where it is secured to the de-epithelialized areas
and periosteum at a split-thickness recipient site,or over a block bone graft when
simultane-ous reconstruction is performed.Adaptedfrom Sclar A.3ABC
Soft Tissue Management in Implant Therapy221This offsets the additional
shrinkageobserved with AlloDerm onlay grafts.Improvement has been observed in
therate ofincorporation ofAlloDerm onlayand interpositional grafts when platelet-
rich plasma (PRP) is incorporated into thesurgical protocol.3In these instances
theAlloDerm graft is first rehydrated in non-activated anticoagulated PRP
solutionprior to its immobilization at the recipientsite.Subsequently,activated PRP
is usedtopically at the recipient site as a growthfactor�enriched wound
dressing.Whenev-er PRP is used with AlloDerm or autoge-nous soft tissue grafts,care
must be takento avoid the formation ofa PRP blood clotbetween the soft tissue graft
and theperiosteal recipient site or the cover flap.3ConclusionThis chapter provides
the implant surgeonwith the basic information necessary forsuccessful management
ofperiimplant softtissues in the most common clinical sce-narios.In addition,it
presents principles oforal soft tissue grafting and surgical detailsofthe most
commonly used oral soft tissuegrafting techniques.However,as limitedinformation
concerning the indications,advantages,and expected outcomes oftheindividual
surgical approaches and tech-niques has been presented,further study bythe reader
is encouraged.References1.Schroeder A,van der Zypen E,Stich H,SutterF.The reaction
to bone,connective tissue,and epithelium to endosteal implants withtitanium-sprayed
surfaces.J MaxillofacSurg 1981;9:15�25.2.Palacci P,Ericsson I,Engstrand P,Rangert
B.Optimal implant positioning and soft tissuemanagement for the Br�nemark
System.Chicago:Quintessence Publishing Co.;1995.p.59�70.3.Sclar A.Soft tissue and
esthetic considerationsin implant
therapy.Chicago:Quintessence;2003.p.52�54.4.Sullivan HC,Atkins JH.Free autogenous
gingi-val grafts,I.Principles ofsuccessful graft-ing.Periodontics
1968;6:121�9.5.Gordon HP,Sullivan HC,Atkins JH.Free auto-genous gingival
grafts,II.Supplementalfindings�histology ofthe graft site.Peri-odontics
1968;6:130�3.6.Sullivan HC,Atkins JH.Free autogenous gingi-val
grafts,III.Utilization ofgrafts in thetreatment ofgingival recession.Periodon-tics
1968;6:152�60.7.Langer B,Calagna L.The subepithelial connec-tive tissue graft:a new
approach to theenhancement ofanterior cosmetics.Int JPeriodontics Restorative Dent
1982;2(2):23�34.8.Reiser C,Bruno JF,Mahan PE,Larkin LH.Thesubepithelial connective
tissue graft palataldonor site:anatomic considerations forsurgeons.Int J
Periodontics RestorativeDent 1996;16:131�7.FIGURE11-25Use ofAlloDerm (a freeze-
dried allograft skin processed to remove all immunogeniccellular components
[epidermis and dermal cells]) to increase the width ofattached tissue around
animplant restoration.A,Intraoperative view ofthe use ofan AlloDerm graft
simultaneous with theplacement offour nonsubmerged implants in an edentulous
mandible to improve the periimplant softtissue environment and to eliminate mobile
mucosal tissues in the area,while increasing vestibulardepth.B,The 2-month
postoperative view demonstrates a sufficient area ofattached nonmobile peri-implant
soft tissues to ensure a healthy soft tissue environment and ample access for oral
hygienemaintenance.Reproduced with permissionfrom Sclar A.3ABFIGURE11-26Use
ofAlloDerm (a freeze-dried allograft skin processed to remove all
immunogeniccellular components [epidermis and dermal cells]) for root- or abutment-
coverage procedures.A,Pre-operative view ofgeneralized progressive periodontal soft
tissue recession treated with AlloDerm grafts.B,The postoperative view demonstrates
successful root coverage at sites amenable to such a result andan increased width
ofattached tissue at those sites not amenable to complete root coverage.AB
CHAPTER 12Bone Grafting Strategies forVertical Alveolar AugmentationOle
T.Jensen,DDS,MSMichael A.Pikos,DDSMassimo Simion,DDSTomaso Vercellotti,MD,DDS
Strategies to increase alveolar verticaldimension fall into six general categories:
(1) guided bone graft augmentation,(2)onlay block grafting,(3)
interpositionalveolar bone graft,(4) alveolar distractionosteogenesis,(5) iliac
corticocancellousaugmentation bone graft,and (6) thesinus bone graft.The difficulty
in gaining and main-taining alveolar vertical augmentation iswell established in
the literature,but thevarious procedures that have been usedhave been complicated
by relapse andresorption.1�3Augmentations without theplacement ofimplants generally
resorbunless a nonresorbable grafting materialsuch as hydroxylapatite is
used.4�6This chapter reviews the indicationsand contraindications for the above
proce-dures,all ofwhich have found their nichein oral and maxillofacial surgery
recon-struction using osseointegrated implants.Alveolar vertical defects have
beenclassified according to the size ofthedefect.7Deficiencies can range from 1 or
2 mm to more than 20 mm in height.Ingeneral monocortical grafts or guided bonegraft
augmentations are useful for smalleraugmentations.Interpositional grafts workwell
for moderate-sized defects,whereasdistraction osteogenesis is reserved formore
extensive alveolar defects.Large bonemass deficiencies,where there is notenough
bone to distract,require iliac bonegraft reconstruction,though a vertical gainof10
mm is difficult to achieve in these set-tings.Finally,there is the sinus bone
graft,which functions as an �endosteal�expan-sion ofalveolar vertical bone
mass.Guided Bone Graft AugmentationVertical bone augmentation ofdeficientalveolar
ridges can be obtained with guid-ed bone regeneration techniques.Thesetechniques
allow vertical augmentation ofup to 10 mm both in the posterior andanterior maxilla
and mandible.A barriermembrane is placed and stabilized withtacks or screws in
order to protect an auto-genous bone graft usually harvested fromthe retromolar
area in the mandible.Themembrane is maintained in the site com-pletely covered by
the soft tissues for aperiod ofat least 6 months.The implants can be placed either
atthe time ofbone regeneration or at themembrane removal surgery.Figure 12-1
illustrates a posteriormandible atrophy in which 7 mm ofverti-cal bone height is
required.After fullthickness flap elevation,a couple of10 mm long tenting screws
have beenplaced in order to avoid the membranecollapse toward the bone ridge.The
corti-cal bone has been perforated with a roundbur (see Figure 12-1A).Autogenous
bonechips have been placed and covered with atitanium-reinforced expanded
polytetra-fluoroethylene (ePTFE) membrane (seeFigure 12-1B).After 6 months
ofunevent-ful healing,a mucoperiosteal flap has beenelevated (see Figure 12-1C),and
the mem-brane has been removed to expose theregenerated bone (see Figure 12-
1D).TwoBr�nemark implants have been placed (seeFigure 12-1E).Figure 12-1F and 12-
1Gshow the final porcelain-fused-to-metalprosthesis and the periapical x-ray after
3 years ofocclusal loading.Mandibular Block Autograftsfor Localized Vertical
RidgeAugmentationMandibular block autografts have beenused extensively for alveolar
ridge aug-mentation with great success and include
224Part 2: Dentoalveolar Surgerythe symphysis and ramus buccal shelfasdonor
sites.8�16The vertically deficientridge presents the greatest challenge
forreconstruction,and success with thesegrafts can be achieved with defects ofup
to6 mm.The posterior maxilla andmandible are the most common areas ofthe mouth
where this type ofdeficiencyoccurs.This section focuses on posteriormaxillary and
mandibular reconstructionin a staged manner prior to implant place-ment.Implants
are placed in a submergedor nonsubmerged mode after appropriatehealing time with
the block grafts.Typically,there is loss ofalveolar boneheight in the posterior
maxilla andmandible secondary to periodontal diseaseand after tooth removal.Tooth
loss resultsin buccal plate compromise and a reduc-tion in alveolar width.This bone
resorp-tion process continues in a medial direc-tion until a knife-edged ridge
forms.Thismay then result in a deficiency ofalveolarheight that would preclude
implant place-ment.The cortical plate may be minimalor absent,further complicating
implantplacement.Finally,occlusal forces aregreater in the posterior than in the
anteri-or area ofthe mouth,necessitating appro-priate surgical and prosthetic
treatmentplanning for long-term implant success.Treatment planning in these
areasmust include solutions to reduce stress.Aprimary plan includes increasing
thenumber ofimplants.No pontics are used,so one implant per buccal root is the
treat-ment planned for each case.In addition,no cantilevers are allowed.Splinting
ofallcrowns is also indicated for biomechanicalforce distribution.Occlusal
considerationsinclude eliminating lateral interferencesduring any excursive
movements.Thefinal factors involved in decreasing unde-sirable stress to the
implants are interrelat-ed.They include increasing the bone den-sity and maximizing
the diameter ofimplants.These two goals are accom-plished with mandibular block
grafts.Thequality ofbone from the ramus buccalshelfis typically type 1,and the
symphysisnormally exhibits type 2 and occasionallytype 1 quality bone.These grafts
createareas for the use oflarger diameterimplants that increase the surface
areaover which the stresses ofocclusal forcesare distributed.17,18There are four
key principles thatshould be followed for mandibular blockgraft
success.First,recipient site prepara-tion must be done to allow access for tra-
becular bone blood vessels and osteogeniccells,which is critical for predictable
boneincorporation.Also,platelet release fromFIGURE12-1A,An edentulous posterior
mandible isflapped open,and perforations are made through thecortex in preparation
for the bone graft.�Tent pole�bone screws are placed at the desired height,up to
10mm.B,Reinforced membrane is tacked into place.C,Six months later,the membrane is
exposed.D,Boneformation after membrane removal.E,Placement oftwo dental
implants.F,Final restoration.G,Periapi-cal x-ray after 3 years ofloading.ABCDEFG
Bone Grafting Strategies for Vertical Alveolar Augmentation225damaged blood vessels
produces platelet-derived growth factor and transforminggrowth factor (TGF-�),which
acceleratewound healing.Site preparation facilitatesintimate adaptation ofthe graft
to itsunderlying bony bed.Second,two-pointfixation ofeach block is important to
pre-vent microrotation ofthe graft resulting inincomplete bone incorporation.Low-
pro-file self-tapping screws are recommended.Third,primary closure without tension
ofthe wound site is critical to prevent dehis-cence,which is the primary
complicationofmonocortical block grafts.Carefulattention to undermining the flap
willallow for complete relaxation prior to clo-sure.Prosthesis contact with the
ridge isnot allowed for the entire duration ofhealing.Finally,implant placement
mustfollow graft incorporation and shouldnever be done simultaneously.This stag-ing
provides predictable bone volume andoptimal bone density to be created prior
tostage 1 surgery.The symphysis can provide a range ofdense cortical cancellous
bone rangingfrom 4 to 11 mm,in contrast to a typicalramus buccal shelfblock graft
that is 3 to4 mm.These grafts can be used for pre-dictable horizontal augmentation
of5 to 7 mm and vertical augmentation ofup toand including 6 mm.Symphysis Block
Graft HarvestA sulcular incision design is preferred forthe symphysis block graft
harvest asopposed to the more conventionalvestibular design.This approach can
besafely used ifthe periodontium is healthyand no crowns are present in the
anteriordentition.Also,a highly scalloped thingingival biotype is
contraindicated.The incision begins in the sulcusfrom second bicuspid to second
bicuspid.An oblique releasing incision is made atthe mesial buccal line angle
ofthese teethand continues into the depth ofthe buc-cal vestibule.A full thickness
mucope-riosteal flap is reflected to the inferiorborder ofthe mandible.This allows
forgood visualization ofthe entire symph-ysis,including both mental
neurovascularbundles.It also provides easy retractionat the inferior border and
results in a rel-atively dry field.Contrast this with thevestibular approach,which
results inmore limited access,incomplete visual-ization ofthe mental neurovascular
bun-dles,and more difficulty in superior andinferior retraction ofthe flap
margins.Also,there is typically bleeding secondaryto the mentalis muscle incision
resultingin the need for hemostasis.Finally,wound dehiscence from the
sulcularapproach is rare.The vestibular incisioncan result in wound dehiscence and
scarband formation.A 702L tapered fissure bur in astraight handpiece is used to
penetrate thesymphysis cortex via a series ofholes thatoutline the graft.It is
important to notencroach within 5 mm ofthe apices oftheincisor and canine teeth as
well as themental neurovascular bundles.Also,theinferior osteotomy is made no
closer than4 mm from the inferior border.All holesare then connected to a depth
ofat leastthe full extent ofthe bur flutes (7 mm).The graft is then harvested using
straightand curved osteotomes or modified bonespreaders.The donor site is packed
withgauze soaked in either saline or platelet-poor plasma.Closure ofthe site is
doneafter graft fixation and includes a particu-late graft.This graft is not
critical to theesthetic outcome;however,grafting ofthedonor site to allow for a
secondary blockharvest can be done.Ramus Buccal ShelfBlock Graft HarvestA full
thickness mucoperiosteal incision ismade distal to the most posterior tooth inthe
mandible and continues to the retro-molar pad and ascending ramus.Anoblique release
incision can be made intothe buccinator muscle at the posteriorextent ofthis
incision.The incision con-tinues in the buccal sulcus opposite thefirst bicuspid
where an oblique release ismade to the depth ofthe vestibule.A fullthickness
mucoperiosteal flap is thenreflected to the inferior border allowingfor
visualization ofthe external obliqueridge,buccal shelf,lateral ramus and body,and
mental neurovascular bundle.Theflap is further elevated superiorly from
theascending ramus and includes stripping ofthe temporalis muscle attachment.There
are three complete osteotomiesand one bone groove that need to be pre-pared prior
to graft harvest.A superiorosteotomy is created with a 702L fissurebur in a
straight handpiece.It beginsopposite the mandibular second molarand continues
posteriorly to the ascend-ing ramus approximately 4 to 5 mmmedial to the external
oblique ridge.Thelength ofthis osteotomy depends on thegraft size.The anterior
extent ofthisbone cut can approach the distal aspectofthe first molar,depending on
the ante-rior location ofthe buccal shelf.A modi-fied channel retractor is used for
idealaccess to the lateral ramus body area toallow for two vertical bone
cuts.Theosteotomies begin at each end ofthesuperior bone cut and continue inferior-
ly approximately 12 mm.All osteotomiesjust barely penetrate cortical bone.Finally,a
no.8 round bur is used to cre-ate a groove connecting the inferioraspect ofeach
vertical osteotomy.Thegraft is then harvested using modifiedbone spreaders that are
malleted alongthe superior osteotomy.The graft willfracture along the inferior
groove andshould be carefully harvested so as toavoid injury to the inferior
alveolar neu-rovascular bundle.The sharp ledge thatis created at the superior
extent oftheascending ramus is then smoothed witha large round fissure bur.Gauze
moist-ened with either saline or platelet-poorplasma is then packed into the
woundsite.Closure ofthe donor site can bedone after graft fixation.
226Part 2: Dentoalveolar SurgeryCase 1A healthy 59-year-old white female
wasreferred for implant evaluation.Clinicaland radiographic examination revealed
amissing right maxillary second bicuspidand all molars (Figure 12-2A).The edentu-
lous space exhibited a deficiency in alveolarheight ofapproximately 4 mm,along
withminimal sinus pneumatization precludingthe need for sinus grafting (Figure 12-
2Band C).The treatment plan included verti-cal bone augmentation using a right
ramusbuccal shelfblock graft prior to implantplacement for a three-unit fixed
bridge.The recipient site was exposed via afull thickness buccal flap reflection
(Fig-ure 12-2D).Site preparation includedslight decortication and perforationprior
to block grafting (Figure 12-2E).Aright ramus buccal shelfgraft was har-vested in
the conventional manner (Fig-ure 12-2F�H) and contoured to size (Fig-ure 12-2I and
12-2J).Platelet-richplasma was then placed on the recipientsite prior to block
graft fixation (Figure12-2K and L).Particulate demineralizedfreeze-dried bone
allograft was mortisedsuperior to the graft (Figure 12-2M),andadditional platelet-
rich plasma wasplaced over the graft complex (Figure 12-2N).Primary closure without
tensionwas accomplished prior to particulategrafting and administration ofplatelet-
rich plasma.A posterior vertical releaseincision was also made to allow
foradvancement ofthe full thickness flap(Figure 12-2O and P).Five months laterthe
site was reentered revealing excellentblock incorporation (Figure 12-2Q).Implants
were placed in a nonsubmergedmode because ofthe excellent type 1quality bone
(Figure 12-2R and S).FIGURE12-2A,Clinical photograph indicating edentulous right
posterior maxilla.B,Radiograph depicting vertical deficiency and minimal sinus
pneumatiza-tion.C,Model depicting vertical alveolar deficiency.D,Full thickness
buccal flap reflection.E,Site preparation including decortication and
perforation.F,Rightramus buccal shelfblock graft harvest.G,Ramus buccal
shelfgraft�cortical surface.H,Ramus buccal shelfgraft�marrow surface.I,Contouring
ofblock graft.(CONTINUEDONNEXTPAGE)ABCDEFGHI
Bone Grafting Strategies for Vertical Alveolar Augmentation227Case 2A healthy 62-
year-old white female wasreferred for implant evaluation.Thispatient was unhappy
with her existingbilateral distal extension partial dentureand desired fixed
prosthetic work inboth edentulous areas (Figure 12-3A andB).Clinical and
radiographic examina-tion revealed missing mandibularmolars bilaterally (Figure 12-
3A�C).Also noted was a vertical deficiency ofmore than 5 mm in the right
posteriormandible and 4 mm in the left posterioredentulous mandible.The
treatmentplan included vertical ridge augmenta-tion ofthe right side with a
symphysisgraft and ofthe left side with a rightramus buccal shelfblock graft.The
right edentulous site was exposed,appropriate crestal decortication and per-
foration was done,and a symphysis blockFIGURE12-2 (CONTINUED)J,Block graft
contoured within confines ofsurgical stent.K,Platelet-rich plas-ma applied to
recipient site.L,Screw fixation completed.M,Particulate demineralized freeze-dried
boneallograft mortised.N,Platelet-rich plasma impregnated collagen covering entire
wound site.O,Buccal flaprelease.P,Tension-free primary closure.Q,Excellent block
graft incorporation at 5 months.R,Stage 1surgery.S,Stage 1 nonsubmerged implant
placement completed.JKLMNOPQRS
228Part 2: Dentoalveolar Surgerygraft was fixated to the crest (Figure 12-3Dand
E).Platelet-rich plasma was applied tothe recipient site prior to graft
fixation.Five months later both sites were reenteredand revealed no evidence ofbone
resorp-tion (Figure 12-3F and G).The right siderevealed vertical augmentation of5
mm.Three threaded Spline implants wereplaced in a nonsubmerged mode becauseofthe
excellent type 1 quality bone (Figure12-3H and I).The left edentulous spacewas
augmented 4 mm with a right ramusbuccal shelfblock graft in the same fash-ion and
three threaded implants were alsoplaced nonsubmerged (Figure 12-3J�L).Both sites
were ultimately grafted withepithelial palatal tissue for enhanced kera-tinized
gingiva (Figure 12-3M and N),andthree-unit fixed bridgework was fabricatedfor each
site (Figure 12-3O).Mandibular block autografts for verti-cal alveolar ridge
augmentation are pre-dictable and offer many advantages.Thesegrafts are primarily
cortical in nature,exhibit minimal resorption,and tend toincorporate exceptionally
well with recipi-ent bone in a relatively short time.Theyalso maintain post-implant
placementbone volume and retain their radiograph-ic density to the augmented
site.Despitethe many advantages block grafts offer foralveolar ridge
augmentation,there arecomplications with posterior mandibularautografts when used
for horizontal andvertical augmentation.Morbidity with thisgrafting protocol is
associated with bothdonor and recipient sites.This includesexperience with 434
grafts harvestedbetween August 1991 and December 2002:208 symphysis grafts and 226
ramus buc-cal shelfgrafts.Symphysis donor site morbidityincludes intraoperative
complicationssuch as bleeding;mental nerve injury;softtissue injury
ofcheeks,lips,and tongue;block graft fracture;and potential bicorti-cal
harvest.Bleeding episodes are intra-bony and can be taken care ofwithcautery,local
anesthesia,and collagenplugs.Injury to the mental neurovascularbundle is avoidable
with proper surgicaltechnique,especially in the use ofthe sul-cular approach for
bone harvest.Blockfracture and bicortical block harvest canalso be prevented by
following good surgi-cal technique.Pain,swelling,and bruisingoccur as normal
postoperative sequellaeand are not excessive in nature.Use ofplatelet-rich plasma
has decreased overallsoft tissue morbidity.Infection rate is min-imal (<
1%).Neurosensory deficitsinclude altered sensation ofthe lower lip,chin (temporary
19%;permanent < 1%),and dysesthesia ofthe anterior mandibu-lar dentition (transient
53%;permanent < 1%).No evidence ofdehiscence wasseen using the sulcular
approach.The ramus buccal shelfharvest canalso result in intraoperative
complicationsincluding bleeding,nerve injury,soft tis-sue injury,block fracture,and
mandiblefracture.Intrabony bleeding and soft tis-sue bleeding can be handled with
cautery.Injury to the inferior alveolar neurovascu-lar bundle and the lingual
neurovascularABCDEFFIGURE12-3A,Right posterior edentulous mandible.B,Left posterior
edentulous mandible.C,Radiograph indicating bilateral posterior mandibular
verticaldeficiency.D,Block graft fixation with platelet-rich plasma
application.E,Block graft fixation.Note butt joint at anterior recipient donor
interface.F,Excellentblock graft incorporation at 5 months.(CONTINUEDONNEXTPAGE)
Bone Grafting Strategies for Vertical Alveolar Augmentation229bundle can be avoided
with proper soft tis-sue manipulation and meticulous osteoto-my preparation.Block
fracture is also anavoidable problem with proper surgicaltechnique.Postoperative
morbidityincludes trismus (approximately 34%) butis certainly transient and can
take up to 2 weeks to resolve.Pain,swelling,andbruising are typically mild to
moderateand,again,are minimal with use ofplatelet-rich plasma.Infection rate is
lessthan 1%.Altered sensation ofthe lower lipor chin occurs approximately 8%
ofthetime,with less than 1% being permanent.Altered sensation ofthe lingual nerve
hasalso been reported but has been transientonly.No incidence ofaltered sensation
ofmandibular dentition has been found.Infection rate is less than 1%.Recipient site
morbidity includes tris-mus,bleeding,pain,swelling,bruising,infection,neurosensory
deficits,boneresorption,dehiscence,and graft failure.Trismus can be expected,as the
surgicalprotocol for reconstruction ofthe posteri-or mandible includes manipulation
oftheposterior mandibular musculature.Inci-dence is less than 40% and is
transient.Bleeding ofthe recipient bed is intentionalsecondary to meticulous site
preparation(decortication and perforation),but exces-sive bleeding,although
rare,can occur sec-ondary to both intrabony and soft tissuevessel
transection.Pain,swelling,andbruising are mild to moderate and areminimized with
platelet-rich plasma.Infection rate is less than 1% and is usual-ly secondary to
graft exposure.Nerve neu-rosensory deficits can occur secondary tosite preparation
and block fixation becausenormal anatomy is violated.Dehiscenceand graft failure
(approximately 2.5%) areseen secondary to soft tissue closure withtension or
prosthesis contact with the graftsite.(Strong recommendation:avoid theuse ofany
type ofprosthesis secondary toposterior mandibular block graft recon-struction.)
Finally,block graft resorption atJKLMNOFIGURE12-3 (CONTINUED)G,Excellent block
graft incorporation at 5 months.H,Stage 1 implant surgery.I,Nonsubmerged implant
placement.J,Ramus buccalshelfblock graft with fixation.K,Radiograph indicating
block graft in fixation.L,Completed stage 1 nonsubmerged implant
placement.M,N,Completed epithelialpalatal graft.O,Completed restorations.GHI
230Part 2: Dentoalveolar Surgerystage 1 surgery is minimal (0 to 1.5 mm)but can be
excessive ifdehiscence ofthegraft occurs.In summary,overall morbidi-ty ofmandibular
block autografts foratrophic posterior mandibular reconstruc-tion is minimal.Most
complications arepreventable.Those that occur can be han-dled predictably with
minimal adverseeffects to the patient.Interpositional Bone GraftThe interpositional
bone graft is placedbetween a mobilized segmental osteotomyand the basal bone.A
typical vertical gainis 4 or 5 mm in the maxilla but 5 to 10 mmin the mandible.The
indication for theprocedure is an alveolar defect where thereis insufficient
vertical height for placementofimplants such as in the anterior maxillaor in the
posterior mandible when a stablevertical augmentation is required,usuallyover a
three- or four-tooth segment.Figure 12-4A to C illustrates an anteri-or maxillary
defect treated with interposi-tional grafting.Figure 12-4D shows a poste-rior
mandibular deficiency with 6 mm ofbone available above the inferior
alveolarnerve.An osteotomy was done (Figure 12-4E) through a vestibular incision
tomaintain both lingual and crestal bloodsupply.An interpositional cortical
bonegraft harvested from the ramus was placedat the osteotomy site,raising the
alveolusabout 7 mm (Figure 12-4F).The raised seg-ment rotated slightly
lingually,but this wascompensated for by using a bone plate toestablish both the
final vertical height andthe crestal axis ofthe osteotomized segment(Figures 12-4G
and H).Alveolar Distraction OsteogenesisA deficient alveolus can be distracted
toimprove vertical dimension for implantplacement.Sufficient width (5 mm)
andvertical height (8 to 10 mm) ofa distrac-tion site are needed in order to ensure
suf-ficient (5 �5 mm) bone mass ofthe seg-ment to be translated.Figure 12-5A to G
illustrates a casewhere severe atrophy ofboth soft and hardtissues left a
significant alveolar retrog-nathia and a vertical defect ofat least 10 mm (see
Figure 12-5A and B).Using aABCDEFGHFIGURE12-4A,A temporary bridge demonstratesa
vertical deficiency.B,An alveolar segmentedosteotomy using a 5 mm interposed block
combinedwith particulate autograft.C,The final dentalrestoration 1 year
later.D,Posterior alveolar atro-phy.E,An alveolar osteotomy curves upward poste-
riorly and stays above the nerve.F,A cortical graftis placed to ensure vertical
height.G,Particulateautograft is used with a bone plate to establish thedesired
alveolar position.H,X-ray findings of�sandwich�bone graft.
Bone Grafting Strategies for Vertical Alveolar Augmentation231vestibular approach,a
flared osteotomy wasmade (see Figure 12-5C).Then a biphasedistractor plate was
placed in order to gainvertical and horizontal displacement (seeFigure 12-
5D).Following a vertical distrac-tion of12 mm (see Figure 12-5E),horizon-tal
movement was achieved by tighteningthe nut on the horizontally placed screwsfor a 5
mm horizontal movement.Fourmonths later,,implants were placed (seeFigure 12-5F).The
final restoration wasplaced an additional 4 months later.A 1-year postrestorative
finding is shown inFigure 12-5G to J,indicating a stable bonepattern and reasonable
esthetic restoration.Iliac Corticocancellous Grafting When the jaw is too deficient
to do mono-cortical grafting or osteotomies,bone graftaugmentation with iliac
corticocancellousgraft is needed.Major grafting is usuallyrequired when bone mass
needs to beexpanded in order to gain enough bonefor osseointegration.Figure 12-6A
to G shows a patientwho had severe maxillary atrophy inwhich iliac bone graft was
combined withsinus augmentation and Le Fort Iadvancement.Figure 12-6A shows the
pre-operative finding ofsevere bone lossincluding maxillary retrognathia.A 5
mmmaxillary advancement with a Le Fort Iosteotomy fixated with resorbable
boneplates was done.The anterior reconstruc-tion relied on onlay
corticocancellousblock graft supported by particulate mar-row.Graft preservation
strategies such asbarrier membrane and titanium meshmay be helpful,but in this case
a corticalABCDEFFIGURE12-5A,Severe maxillary vertical deficiency.B,Marked alveolar
retrog-nathia.C,Distraction osteotomy.D,Placement ofbiphase distraction
device.E,Twoweeks after distraction.F,Implants are exposed a total of8 months after
the distrac-tion surgery.G,H,Final restoration.I,J,Implant findings 1 year after
restorationindicating a stable bone pattern.JGHI
232Part 2: Dentoalveolar Surgerygraft was placed laterally,which minimizesthe need
for a barrier membrane.Figure12-6B shows the down-fractured maxilla,where both
sinus and nasal membranesare elevated and preserved.The advancedmaxilla augmented
laterally and verticallyaround the arch is shown in Figure 12-6C.Figure 12-6D shows
the augmentation 6 months after grafting just prior toimplant placement.Figure 12-
6E showsexposure ofthe implants 6 months afterthat for a total of1 year ofbone
graft con-solidation.A final fixed-hybrid restorationis shown in Figure 12-6F and
G.Two yearsafter dental restoration bone levelsremained stable,but there is some
varia-tion in graft consolidation and resorptionwithin the graft (Figure 12-
6H).Prosthet-ic loading (temporary dentures) degradedthe final vertical
augmentation dimension,but not significantly.Typically,6 to 8 mmofvertical gain is
judged a success in theseverely atrophic case.Sinus Bone GraftThe sinus bone graft
is well established asone ofthe most stable vertical augmenta-tion procedures in
the surgeon�s arma-mentarium.Three techniques are used,including:1.Sinus intrusion
osteotomy2.Lateral approach sinus membrane ele-vation3.Alveolar augmentation
combinedwith sinus elevation (shown above)The sinus intrusion osteotomy can bedone
on the day ofextraction ifthe woundis clear ofsoft tissue and infection.In thecase
shown in Figure 12-7A,the intrusionwas done with a bone graft and implantplacement
6 weeks after the dental extrac-tion.At this stage epithelial closure ofthewound
was present,and a residual infec-tion had resolved.A bone graft was takenfrom the
mandible and intruded into thesinus floor using an osteotome.Bone graftwas also
placed into defects within theextraction socket.Figure 12-7A to C showthe sinus
grafting and implant procedure.Figure 12-7D show the final bone graftconsolidation
1 year after final restoration.The lateral sinus graft is done througha Caldwell-
Luc approach by elevating theABCDEFGHFIGURE12-6A,Preoperative edentulous maxilla
with severe atrophy.B,Thedown-fractured maxilla with preserved sinus and nasal
membranes.C,Theadvanced maxilla augmented laterally and vertically around the
arch.D,Sixmonths after grafting the area is exposed for implants indicating modest
shrink-age ofthe graft,still adequate for implant placement.E,Implant exposure
6months later (1 year after the initial iliac graft).F,G,The final prosthesis
andrestoration.H,Implant findings 2 years after placement into iliac graft indicat-
ing a stable bone loss pattern to 1st and 2nd screw thread.
Bone Grafting Strategies for Vertical Alveolar Augmentation233sinus membrane in
order to preserve a�closed wound.�Bone graft material ispacked against the sinus
floor,taking careto remove all soft tissue that might be pre-sent there.This
approach can be used forboth simultaneous and delayed implantplacement.Barrier
membranes are usuallynot required but benefit over the graftedsite ifa large
�window�is made.Smallwindows and the use ofautogenous boneas graft material
generally lead to primaryosseous healing ofthe osteotomy site.The use
ofpiezoelectric surgery ishelpful in avoiding perforation ofthemembrane.The
technique is particularlyhelpful in areas where a robust thickness ofbone is
present or when the membrane isextremely thin.The advantage ofusing thistechnology
is that piezoelectric surgerydoes not �cut�soft tissue,so sinus mem-brane
perforation is much less likely tooccur.Figure 12-8 demonstrates the piezo-electric
procedure leading to elevation ofthe membrane without perforation.After
grafting,the period for consoli-dation ofthe bone graft varies with thegrafting
material used.Allogeneic boneactually slows down the consolidationprocess.The use
ofcombination graftsincluding bovine xenograft,algipore,orvarious other alloplasts
all form bone ade-quate for osseointegration.18Though bone quality varies consider-
ably as shown by human trephine biopsyresults ofthe various grafting materials,the
capabilities ofthe sinus graft to gainenough bone to form load-
bearingosseointegration are remarkable.The 5-year failure rate ofimplants by
almostany grafting technique is less than 20%.19,20Though grafting material must
beosseoconductive,inductivity is notrequired in order for bone to form.Thesinus
floor grows bone with blood clotalone.Whatever the technique,bonemigrates
�endosteally�up the side oftheimplant.Ifonly a few millimeters ofmigration
occurs,in addition to theresidual bone,there is often enough gainto form and
maintain osseointegration.Therefore,the principal success ofthesinus grafting is
not one ofimplantmacro- or microarchitecture or even thetype ofgraft material,be it
alloplast,allo-graft,or autograft,but the intrinsicbone-forming capacity ofthe
sinus flooritselfand to a lesser degree the investingsinus membrane.21In cases
ofsevere atrophy the surgeonmust make every effort to use the best avail-able
technique and bone graft material ABCDFIGURE12-7A,B,An osteotome intrusion
andsimultaneous implant placement.C,D,Theintrusion osteotomy with simultaneous bone
graftand implant placement leads to a final restorationwith a bone graft level well
above the apex oftheimplant 1 year after final restoration.ABCFIGURE12-
8A,B,Piezoelectric sinus windowmade by instrumentation that does not disturbthe
membrane.C,The membrane is elevatedwithout perforation.
234Part 2: Dentoalveolar Surgerypossible in a highly compromised site.Thissetting
argues for the use ofparticulatebone marrow harvested from the tibia orilium and
possibly adjuncts such asplatelet-rich plasma.SummaryThe difficulty oftreating
alveolar verticaldefects requires the surgeon to be skilledin all ofthe above
modalities.In skilledhands,various approaches can be used intreating the same type
ofdefect.In most cases defect sites are notstrictly vertically deficient.Skill in
alveolarwidth augmentation,or combined treat-ment,is needed as well.With all
ofthesemeasures,the ultimate restorative goal isto obtain orthoalveolar form,a
conceptthat now encompasses a broad array ofsurgical innovation.References1.Davis
WH,Delo RI,Ward B,et al.Long termridge augmentation with rib graft.J Max-illofac
Surg 1975;3:103�6.2.Baker RD,Terry BC,Connole PW.Long termresults ofalveolar ridge
augmentation.JOral Surg 1979;37:486�91.3.Keller EE.The maxillary interpositional
compos-ite graft.In:Worthington P,Branemark P-I,editors.Advanced osseointegration
surgery:application in the maxillofacial region.Chica-
go:Quintessence;1992.p.162�74.4.Ayers R,Simska S,Nunes C,Wolford L.Long-term bone
ingrowth and residual micro-hardness ofporous block hydroxyaptiteimplants in
humans.J Oral Maxillofac Surg1998;56:1297�301.5.Tinti C,Parma-Benefenati S.Vertical
ridge aug-mentation:surgical protocol and restrospec-tive evaluation of48
consecutively insertedimplants.Int J Periodontics Restorative
Dent1998;18:434�43.6.Nystrom E,Kahnberg K-E,Gunne J.Bonegrafts and Branemark
implants in the treat-ment ofthe severely resorbed maxilla:a twoyear longitudinal
study.Int J Oral Maxillo-fac Implants 1993;8:45�53.7.Jensen OT,Shulman L,Block
M,Iacono V.Report ofthe sinus consensus conference of1996.Int J Oral Maxillofac
Implants1998;13 Suppl:11�45.8.Misch CM,Misch CE,Resnik R,et al.Recon-struction
ofmaxillary alveolar defects withmandibuar symphysis grafts for dentalimplants:a
preliminary procedural report.Int J Oral Maxillofac Implants 1992;7:360�6.9.Misch
CM.Comparison ofintraoral donorsites for onlay grafting prior to
implantplacement.Int J Oral Maxillofac Implants1997;12:767�76.10.Sindet-Pedersen
S,Enemark H.Reconstruc-tion ofalveolar clefts with mandibular oriliac crest bone
grafts:a comparative study.J Oral Maxillofac Surg 1990;48:554�8.11.Pikos
MA.Buccolingual expansion ofthe max-illary ridge.Dent Implantol Update
1992;3:85�7.12.Pikos MA.Facilitating implant placement withchin grafts as donor
sites for maxillary boneaugmentation:part I.Dent ImplantolUpdate
1995;6:89�92.13.Pikos MA.Facilitating implant placement withchin grafts as donor
sites for maxillary boneaugmentation:part II.Dent ImplantolUpdate
1996;7:1�4.14.Pikos MA.Alveolar ridge augmentation withramus buccal shelfautografts
and impactedthird molar removal.Dent ImplantolUpdate 1999;4:27�31.15.Pikos MA.Block
autografts for localized ridgeaugmentation:part I.The posterior maxil-la.Implant
Dent 1999;8:279�84.16.Pikos MA.Block autografts for localized
ridgeaugmentation:part II.The posteriormandible.Implant Dent 2000;9:67�75.17.Bidez
MW,Misch CE.Force transfer in implantdentistry:basic concepts and principles.Oral
Implantol 1992;18:264�74.18.Kummer BKF.Biomechanics ofbone:mechan-ical
properties,functional structure,func-tional adaptation.In:Fung YC,Perrone H,Anliker
M.Biomechanics:foundations andobjectives.Englewood Cliffs (NJ):Prentice-Hall;1972.p
273.19.Jensen OT,Greer R.Immediate placement ofosseointegrating implants into the
maxil-lary sinus augmented with mineralizedcancellous allograft and Gore-
Tex:second-stage surgical and histological findings.In:Laney WR,Tolman
DE,editors.Tissue inte-gration in oral,orthopedic,and maxillofa-cial
reconstruction.Chicago:Quintessence;1992.p 321�33.20.Jensen OT,Ueda M,Laster Z,et
al.Alveolardistraction osteogenesis.Select ReadingsOral Maxillofac Surg
2002;10:1�40.21.Jensen OT,Sennerby L.Histologic analysis ofclinically retrieved
titanium microimplantsplaced in conjunction with maxillary sinusfloor
augmentation.Int J Oral MaxillofacImplants 1998;13:513�21.
CHAPTER 13The Zygoma ImplantSterling R.Schow,DMDStephen M.Parel,DDSSeverely
resorbed edentulous maxillaepresent very complex problems for thesurgeon and
restorative dentist.1Lack ofinternal osseous stimulation and nonphys-iologic
crestal bone loading results in con-tinued resorption ofan already
atrophicedentulous maxilla.The end result is aninability to use a conventional full
dentureprosthesis.In 1999 Dr.Per-Ingvar Br�nemark andcolleagues introduced the
zygoma implant(P-I Br�nemark,personal communication,1999).In their initial study
over a 10-yearperiod,110 implants were placed.Eachpatient had an additional two to
four con-ventional implants placed in the anteriormaxilla,which was restored with
crossarch stabilization.Ofthe zygoma fixturesplaced and restored in the initial
study,only two were lost in the first year ofocclusal loading,and three failed in
thesubsequent 8 years for a long-term successrate of> 95%.The availability ofthe
zygoma implanthas provided a viable alternative for treat-ment ofpatients with
extreme resorptionofthe edentulous maxilla or large pneu-matized maxillary
sinuses.1,2Before theintroduction ofthis fixture,implant-supported or -retained
fixed or removableprostheses in the atrophic maxilla couldonly be considered after
extensive ridgepreparation.This preparation usuallyincluded major autologous bone
grafting,prolonged treatment times,long-terminability to wear any prosthesis,and
ahigher failure rate for conventionalimplants placed in large bone grafts.Zygoma
ImplantThe zygoma implant is an extended-length(30�52.5 mm) machined titanium
fixturethat is placed through the crestal (slightlypalatal) aspect ofthe resorbed
posteriormaxilla transantrally into the compactbone ofthe zygoma.In addition to two
tofour conventional fixtures in the anteriormaxilla,initial stability ofthis
elongatedfixture is assured by its contact with fourosseous cortices (Figure 13-
1)3�5:1.At the ridge crest2.The sinus floor3.The roofofthe maxillary sinus4.The
superior border ofthe zygomaThe zygoma implant provides posteri-or maxillary
anchorage when the existingosseous structures do not allow standardimplant
placement.The alternative in thissituation includes bone graft augmenta-tion (sinus
lifts and onlay grafts) with theirattendant costs,discomfort,prolongedtreatment
times,and higher complicationrates.The zygoma fixture is suggested inthe following
circumstances:�When full maxillary edentulism isaccompanied by advanced
posteriorresorption that would otherwiserequire grafting.At least two andpreferably
four anterior standardimplants are needed in combinationwith bilateral zygoma
implants.�In partial or incomplete maxillectomypatients when additional implantscan
be placed in other sites such as theFIGURE13-1A,Schematic representation ofmin-imal
recommended zygoma and standard implantfixtures for restoration with cross-arch
stabilizationand fixed restoration.B,Schematic representationofideal zygoma and
standard implant fixtures forrestoration with cross-arch stabilization and
fixedrestoration.AB
236Part 2: Dentoalveolar Surgerypiriform sinus,orbital rims,palatalshelves,or
pterygoid plates to supportcross-arch stabilization.IndicationsWhile the zygoma
implant is most oftenused in cases ofmoderate to severe atrophy,it can be
considered a valuable procedurefor any patient in need ofposterior maxil-lary
implant support with or without sig-nificant atrophy.The ability to avoid graft-ing
in many patients,along with thecontinuous use ofan interim maxillaryprosthesis also
makes the zygoma implantapproach appealing as a treatment option.Moderate
AtrophyThe majority ofpatients who present witha medium- to long-term history
ofden-ture wear will have a moderate degree ofatrophy (Figures 13-2 and 13-3).This
cat-egory ofdenture experience constitutesthe majority ofpatients who seek
implanttherapy to reverse the effects ofcontinuingbone loss and prosthesis
instability.Manywill be candidates for grafting procedures,such as sinus
augmentation or block onlaytechniques,as a means ofcreating addi-tional osseous
structure to allow enoughimplant sites for predictable support.Theability to avoid
such grafting is one oftheprincipal benefits ofconsidering the zygo-ma implant
alternative (Figure 13-4).Severe AtrophyAlthough most ofthese patients will essen-
tially be graft candidates,there are somewho,because ofhistory or physical circum-
stances,cannot or will not undergo theseprocedures.A history ofconsistent
graftfailure or a systemic compromise that con-traindicates grafting are examples
ofmiti-gating factors that may require consideringan alternative approach such as
use ofthezygoma implant (Figure 13-5A�D).Experi-ence to date with these patients is
notextensive,but early indications ofimplantsurvival are seen as encouraging,even
withthe most severely compromised maxillae(Figures 13-5E and 13-6).Prosthesis
design for the severelyatrophic maxilla with implant supportmay be influenced by
the relative size dis-parity between the two jaws.Most suchatrophy results in an
undersized maxillarelative to the corresponding mandible,even in cases where both
arches are equal-ly resorbed.Cantilever considerations andimplant stress
distribution may mandatethe use ofan overdenture prosthesis ratherthan a fixed
restoration in order to manageocclusal alignment and lateral spacing(Figure 13-
7).Inadequate Posterior SupportOccasionally patients will present withadequate bone
for anterior or premaxil-lary implants but have sinus extensionsthat eliminate the
potential for posteriorimplants without augmentation (Figure13-8).Ifsuch grafting
is indicated butcountermanded by patient request orhealth considerations,the
zygomaapproach can be equally effective.Syndrome PatientsAnother less frequent
indication for thezygoma approach can present in patientswith various anodontias
from syndromessuch as cleidocranial dysostosis or ecto-dermal dysplasia.Radiographs
may showeither impacted and unerupted teeth ormissing dentition,resulting in growth
pat-terns ofthe maxilla that are disrupted andminimized (Figures 13-9 and 13-
10).These individuals often present withinsufficient bone for adequate numbers
ofimplants and can be difficult to graftbecause ofspace or soft tissue
limitations.Zygoma implants can be valuable in theseinstances when combined with
conven-tional fixtures to provide the basis forFIGURE13-2Most edentulous maxilla
patientswith a history ofdenture use will have somedegree ofmoderate atrophy as
depicted here.Grafting procedures for augmenting existingbone levels is a commonly
recommended therapyfor patients with this level ofbone loss.FIGURE13-3Posterior
bone volumes are inade-quate for conventional fixture placement,mak-ing this
patient a candidate for grafting.Thisprospect was eliminated by the use
ofzygomaimplants.Stable anterior implants are alsorequired to complete the cross-
arch effect.FIGURE13-4A,The completed fixed partial den-ture,facial view.B,Occlusal
view illustrating thecantilever dimensions and screw retention sites.AB
The Zygoma Implant237long-term prosthetic support at a relative-ly early age
(Figures 13-11 and 13-12).Acquired and Congenital DefectsMaxillary defects created
by secondaryintervention,such as tumor removal or bytrauma,can often be treated
with zygomaimplant therapy to provide retention foran obturating prosthesis
(Figures 13-13).Similarly,congenital defects such as anunrepaired adult cleft
palate (which areFIGURE13-5A,Severe maxillary atrophy is demonstrated on this
survey film.The patient had a history ofseveral failed onlay bone graft
procedures.B,At one point,these implants were placed in graft and native bone.All
failed,with a resultant destruction offunctional support bone.C,Maxillarydimensions
from continuous lateral atrophy resulted in a residual anatomy that did not require
sinus invasion for implant placement.Even though this isunusual,it did not affect
the structural integrity ofthe implants.D,Implants were placed on either side ofthe
two zygoma fixtures for stability.E,Allimplants were successfully integrated and
were positionally suitable for prosthesis construction.BCDEAFIGURE13-6A,A
definitive restoration has been functioning for over 5 years with no evidence
ofsig-nificant implant challenge.B,Radiographically,the 5-year follow-up shows
normal bone response.ABFIGURE13-7A,An overdenture bar splint was constructed with
lateral extensions to keep the retentive elements aligned with the occluding
surfaces.B,The undersurfaceofthe overdenture illustrates the mechanical retention
provided.C,Frontal view ofthe finished prosthesis.ABC
238Part 2: Dentoalveolar Surgeryincreasingly rare owing to early surgicalclosure)
can often be treated with conven-tional implants in combination with zygo-ma
fixtures to support a removable pros-thetic appliance.Situations such as theseare
rarely the same because ofthe widevariations in residual soft tissue and
boneanatomy,and each case will require carefulindividual planning to assess the
potentialfor implant placement or zygoma use.Formany,however,the ability to use
remotebone anchorage with implants around thedefect periphery can create excellent
sup-plemental retentive possibilities for theseoften large and otherwise poorly
support-ed prosthetic devices.Immediate LoadingLiterature citations supporting the
possi-bility ofimmediate loading ofmaxillaryimplants increasingly support this con-
cept.6�9The criteria for attempting thisapproach are generally the same as
forimmediate loading anywhere in the oralcavity:adequate initial stability,good
bonereceptor sites,and initial cross-arch splint-ing with rigid materials (Figure
13-14Aand B).In situations where these criteriacan be met,the survival prospects
for bothconventional and zygoma fixtures appearto be equivalent to the rates
attained withthe delayed approach.The benefits inpatient
comfort,convenience,andenhanced function make this a desirableoption in
appropriately selected cases(Figure 13-14C�F).Partial EdentulismThe original
concept ofthe zygomaimplant,used with anterior implants andcross-arch
stabilization,would theoretical-ly not have application for posterior max-illary
partial edentulism (Figure 13-15A).In practice,however,there is potential forusing
the zygoma implant through thesinus,with additional fixtures on eitherside,to
support a fixed partial denture(Figure 13-15B�E).This approach has notbeen
thoroughly investigated,and clinicaltrials do not provide enough longevity tomake a
definitive statement regarding theefficacy ofthis technique.Being able togain
strong intermediate support throughsinus areas that would otherwise have tobe
grafted does have enough merit,how-ever,to warrant further
investigation.ContraindicationsOther than the most obvious contraindica-tions,such
as systemic compromise orsinus disease,there are only two specificsituations that
would complicate the use ofthe zygoma implant or make it unneces-sary.First,where
adequate maxillary boneexists for implant placement in numbersFIGURE13-8A,This
patient initially presentedwith good bone and five anterior implants,which had not
been loaded,opposing an intactrestored lower dentition.His physical
staturepresented the possibility ofheavy loading poten-tial to the upper arch,and
grafts were recom-mended posteriorly for additional implant place-ment.B,The
patient refused grafting,so 52 mmzygoma implants were placed bilaterally to pro-
vide the necessary support posteriorly.ABFIGURE13-9This ectodermal dysplasia
patientpresents with partial anodontia and associatedfindings typical ofthis
syndrome.FIGURE13-10The effects oflong-term overden-ture use without adequate
caries control are evi-dent intraorally.FIGURE13-11A,The arches were treated with
astaged approach,which included mandibularextractions,implant placement,and
immediateloading ofseveral fixtures.The maxilla wasdebrided at the same time,with
no implantplacement.Tooth bud removal was incomplete.B,Eventual maxillary implant
placement afterhealing included zygoma fixtures bilaterally inlieu ofgrafting
procedures.AB
The Zygoma Implant239and positions to support a prostheticappliance,the zygoma
implant is not need-ed.The second situation is where there isnot enough
premaxillary support for atleast two stable implants with good poten-tial
longevity.Differential diagnosis,infact,often depends more on the volumeand
condition ofanterior bone than exist-ing posterior anatomy to determinewhether some
edentulous patients may becandidates for this procedure.In suchinstances,bone-
grafting procedures shouldbe considered preprosthetically,to createan adequate
osseous base for effectivecross-arch stabilization.ComplicationsThe most
significant complication tozygoma implant therapy is the loss oftheimplant (Figures
13-16A�C).Our expe-rience to date indicates this is a relativelyinfrequent
occurrence,but the impact onthe original treatment plan is significant.Without this
support element,posterioranchorage may be severely compromisedand cantilever
extensions to the firstmolar region may overstress the remain-ing
components.Correcting the resultantimbalance using a zygoma approach willrequire a
healing period for bone regen-eration in the original site and eventualFIGURE13-
12Both constructions used porcelain-fused-to-metal technology.A,The completed max-
illary fixed partial denture.B,Frontal view ofboth restorations in
occlusion.ABFIGURE13-13A,Gunshot trauma created significant maxillomandibular
discontinuities.B,Recon-structive efforts over several years have resulted in
effective osseous restructuring in both arches.C,Traditional anatomic landmarks are
difficult to identify,and normal arch contours are signifi-cantly disrupted in the
repaired maxilla.D,While anchorage in the zygoma was adequate,absence ofalveolar
bone was noted on one side.The ability to use zygoma implants in this situation was
signif-icantly advantageous.E,Maxillomandibular relationships were lateralized as
depicted by the mount-ed casts ofeach arch.While not ideal,this was still a
workable situation.F,Radiographic view ofthecompleted prosthesis.G,Clinical view,in
occlusion,ofthe completed rehabilitation.Lateral jaw rela-tionship discrepancies
required a lingual cantilever and crossbite on the lower bridge.FGABCDE
240Part 2: Dentoalveolar Surgeryreplacement ofa second implant.Inter-im therapy may
include the use ofa pro-visional restoration on the remainingintegrated implants
but should notinclude a cantilever extension on theaffected side (Figure 13-16D).To
date,this rescue approach has proven effectivein the two instances that we have
experi-enced in zygomatic implant failure.Bothhave ultimately been restored to com-
plete function using both the originaland rescue zygoma fixtures for
posteriorsupport (Figure 13-16E�G).Presurgical Assessment:ClinicalCurrent use ofthe
zygoma implant dic-tates ultimate restoration with cross-archstabilization ofthe
fixtures with addi-tional implants.Adequate bone must beavailable to place and
retain at least twobut preferably four anterior maxillaryconventional implant
fixtures,which arejoined to the zygoma fixtures with a castbase.The patient must
have pathology-free maxillary sinuses and have accept-able soft tissues in the area
in which theimplants will be placed.The patient�streatment planning should be
completedbefore insertion ofthe implants for boththe maxillary and mandibular
arches.Patients should be physically and med-ically stable enough to withstand a
surgi-cal procedure approximately 2 hours longand to tolerate a general anesthetic
ordeep intravenous sedation.The patient�smandibular range ofmotion must beadequate
to provide access for placementoffixtures 30 to 52.5 mm longtranspalatally in the
area ofthe zygomat-ic buttress.The opposing mandibularteeth,ifpresent,may limit
access to thesite ofthe zygoma fixture placement.Ifusing deep sedation,local
anesthesia inthe mandibular arch,as well as in the sur-gical site itself,is
advisable.Presurgical Assessment:RadiographicAdequate radiographic examination
isneeded prior to surgery to identify or ruleout sinus or other pathology and to
evalu-ate the osseous anatomy ofboth the zygo-ma and maxilla.The thickness
oftheremaining alveolar bone inferior to thesinus in the second premolar�first
molarregion should be sufficient to providesome support for the long implant
nearthe abutment connection.The apex ofthesinus just lateral to the orbital floor
shouldbe identified and the quality and quantityofthe bone that will support the
apicalend ofthe zygoma implant evaluated.Theanterior maxillary alveolus should also
beevaluated to determine ifenough residualbone is available to place two to four
ante-rior implants.Panoramic,periapical,cephalometric,and plain tomography
orcomputerized exposures are all helpful inthis evaluation.FIGURE13-14A,These five
anterior and two zygoma implants were loaded immediately with a rein-forced resin
bridge converted from the original denture.B,The cantilever extensions are limited
at theprovisional stage,but the reinforced bridge provides a rigid cross-arch
effect.This prosthesis was deliv-ered immediately following
surgery.C,Radiographically,all implants appear integrated at 5.5 months.The
provisional fixed partial denture has not been removed during that time
period.D,The soft tissue response viewed at removal ofthe provisional prosthesis
shows relatively good epithe-lial recovery.The deep tissue response in the zygoma
regions results from the long-term resin connectionsubgingivally.E,The definitive
prosthesis was completed approximately 8 months after stage I
surgery.F,Radiographically all implants appear well integrated and functioning
normally.EFABCD
The Zygoma Implant241FIGURE13-15A,Sinus graft procedures wererecommended for this
patient,but were declined.As an alternative approach,zygoma implantswere considered
for the support needed to createfixed partial dentures bilaterally.B,The
zygomafixtures are augmented mesially and distally withconventional implants.A
delayed approach torestoration was used.C,The radiographic presen-tation
immediately after stage I surgery.D,Thecompleted right-side fixed partial denture
wasconstructed using porcelain-fused-to-metal tech-nology.E,The occlusal view shows
the bilateralrestorations,each with a central zygoma implant.BCDEAFIGURE13-16A,An
impression coping has been attached to the zygoma implant at the final impres-sion
appointment.B,It was noted that there was rotational instability ofthis fixture
with movementofthe coping.C,The implant was removed without resistance.There was no
sign ofbone adherenceto any ofthe implant surface.D,A provisional restoration was
created for interim use while the fail-ure site healed and during the healing
period for another zygoma implant.The cantilever extensionto the affected side has
been reduced to only premolar occlusion.E,Occlusal view ofthe completedrestoration
on healthy zygoma implants bilaterally.F,Frontal view ofceramometal
restoration.G,Radiographic view.The right side zygoma implant side shows an
integrated replacement fixture.ABEGFCD
242Part 2: Dentoalveolar SurgerySurgical ProtocolSurgery for zygoma implant
placement isbest performed using deep intravenoussedation or a general
anesthetic.Localanesthesia with vestibular infiltration,second-division nerve
blocks,and percu-taneous blocks or infiltration lateral andsuperior to the
zygomatic notch just later-al to the orbital rim should be adminis-tered.Bilateral
inferior alveolar nerveblocks are also helpful ifthe procedure isperformed with
sedation because signifi-cant retraction ofthe tongue,lower lip,and mandible are
needed to ensure ade-quate access for the procedure.A crestal incision,placed
slightly tothe palatal aspect ofthe ridge in the firstmolar�second bicuspid region
is madefrom the right- to left-tuberosity regionswith bilateral releasing incisions
at theincision ends.A releasing incision at themaxillary midline is also helpful
for flapdevelopment and retraction.The lateralmaxilla is exposed by elevating full-
thickness mucoperiosteal flaps sufficientto visualize the zygomatic buttress
fromridge crest to the superior surface ofthezygoma at the zygomatic notch,just
later-al to the orbit.The anterior maxilla isexposed to the piriform rims to avoid
tear-ing the flap during retraction and to allowplacement ofconventional anterior
maxil-lary implants.The entire lateral surface ofthe zygomatic buttress is exposed
using apalpating finger extraorally at the zygo-matic notch to ensure that the
dissection isnot directed into the orbital floor.Duringthe dissection,the
infraorbital nerveshould be identified and protected.A fissure bur,usually a 703 or
702,in astraight surgical handpiece is used to makea �slot�exposure vertically in
the lateralwall ofthe sinus near the height ofthezygomatic buttress.3The slot
should paral-lel the planned course ofthe zygomaimplant just medial to the lateral
sinuswall.The slot should extend from near thesinus floor at the planned site
ofimplantplacement superiorly to near the roofofthe sinus.Preparation ofthe slot in
thesinus wall allows the surgeon to visualizedirectly the passage ofall drill
prepara-tions and implant insertion through thelateral sinus.When preparing the
slot,theschneiderian membrane in the sinus isremoved to allow good visualization
andto prevent its interference with site prepa-ration and implant
insertion.Ifportionsofthe membranes are �picked up�by theimplant and carried into
the implantpreparation in the body ofthe zygoma,they could interfere with
osseointegration.A series oflong drills are used forincremental preparation ofthe
implantsite.The zygoma implant varies in lengthfrom 30 to 52.5 mm (Figures 13-17
and13-18).The apical two-thirds oftheimplant is 4 mm in diameter and the alve-olar
one-third is 5 mm in diameter.Theinitial drill is a round bur,which is used tostart
the implant preparation at the secondbicuspid�first molar area as near the
crestofthe residual alveolar ridge as possible�usually slightly to the palatal
aspect.Thesurgeon must preserve enough bone later-al to the site to fully surround
the alveolarportion ofthe implant.The round bur isdirected through the sinus floor
andthrough the lateral sinus superiorly fol-lowing the axis ofthe lateral wall
slotpreparation to the top ofthe sinus where itindents the site ofthe preparation
in thezygoma body.The slot preparation allowsdirect visualization ofthe passage
ofthedrill and the subsequent instrumentationand implant insertion (Figures 13-
19�13-21).A custom-designed zygoma retrac-tor with a toe-out tip is kept in
positionover the zygomatic notch throughout thesite preparation to provide good
visualiza-tion and protect the surrounding anato-my.The retractor also has a
midline mark-er that parallels the site preparation andassists in orientation ofthe
drills in theproper direction (see Figure 13-20).Sub-sequent drills to complete the
preparationare,in sequence,long 2.9 mm diametertwist drills,a 2.9 mm to 3.5 mm
pilot drill,and a 3.5 mm twist drill.The preparationis carried through the body
ofthe zygoma,through the cortical bone ofthe sinusroof,and through the cortex at
the superi-or border ofthe zygoma body at the notch.The soft tissues at the
superior portion ofthe preparation are protected by the zygo-ma retractor (Figure
13-22).Each fissurebur has incremental markings from 30 to52.5 mm,which help the
surgeon deter-mine the needed implant length.When theFIGURE13-17Zygoma implant
armamentari-um.From left to right:zygomatic retractor,round bur,2.0 mm fissure
bur,depth gauge,3.5 mm pilot drill,3.5 mm twist drill,50 mmzygoma implant,mandrel
and cover screw dri-vers,manual implant driver,final depth gaugechuck,chuck
changer.FIGURE13-18Zygoma implant.Apical two-thirds ofimplant is 4 mm in
diameter.Alveolarone-third is 5 mm in diameter.Note 45�-angledabutment platform.
The Zygoma Implant243preparation is complete,final determina-tion ofimplant length
is made using thezygoma implant depth gauge.Lastly,iftheresidual alveolar bone is
substantial,a 4 mm twist drill is used to complete thealveolar portion ofthe
preparation.Iftheresidual alveolar bone is spongy,this stepis usually
eliminated.The zygoma implant has an angulatedabutment platform.The
45�angulationallows the platform ofthe implant toemerge in the same plane as that
oftheconventional implants that will be placedin the anterior
maxilla.Premountedimplant carriers are already attached to thezygoma implants for
handling ofthe fix-ture with the handpiece.The implant isinserted with copious
irrigation,directlyvisualizing its passage through the lateralsinus through the
slot preparation (Figure13-23).During insertion,the implantmust stay in the same
plane as the drills inorder to ensure its engagement in thepreparation site at the
zygoma body.Theslot preparation should be extended supe-riorly far enough to allow
visualization ofthe preparation.When site preparationhas been adequately
performed,the hand-piece will stall when the apical portion ofthe implant engages 2
to 3 mm ofdensezygomatic bone.When this occurs,a man-ual driver is used to complete
implantinsertion.Proper angulation ofthe abut-ment platform is determined by
placing ascrewdriver in the implant carrier screwhead and seating the implant until
thescrewdriver is perpendicular to the crest ofthe edentulous ridge.The implant
carrieris removed and a cover screw is placed(Figure 13-24).After placement ofthe
zygomaimplants,two to four regular platformMark III or Mark IV Nobel
Biocareimplants are placed in the anterior maxilla(Figure 13-25).The flaps are
repositionedand sutured.The maxillary denture isrelieved,hollowed out at the
implantemergence sites,and soft-lined with a tis-sue conditioner.Prior to
closure,implant-level impressions are made.This allows forfabrication ofa rigid bar
to be placed atsecond-stage surgery about 6 months later.The patient�s denture
prosthesis isrelined as often as is necessary over the 6-month osseointegration
period.At second-stage surgery,the cast rigid bar isattached to the implant
fixtures,providingimmediate cross-arch stabilization.Thedenture is further hollowed
out andrelined or a transitional fixed prosthesis isconstructed and attached.Four
to 6 weekslater,after the soft tissues are healed,FIGURE13-19Diagrammatic
representation ofzygoma fixture placement from original protocol.Implant fixture
platform is positioned palatal toalveolar crest.Fixture passes along lateral wall
ofmaxillary sinus into the zygomatic body.Implantstabilization is supported by four
cortical plates ofbone and apically in the dense zygomatic body.FIGURE13-20Zygoma
retractor positioned onanatomic model.The ventral surface oftheretractor is scored
in the midline,vertically,toassist the surgeon in directing the drills andimplant
parallel to the retractor.FIGURE13-21Laboratory model illustratingthe �sinus
window�in the zygomatic buttress.The window allows visualization ofthe drillsand
implant as they pass through the lateral por-tion ofthe maxillary sinus.FIGURE13-
23Surgical view ofzygoma implantbeing inserted using a modified �sinus slot�tech-
nique.The sinus window is narrower and larger.Through the slot,the implant
preparation can bevisualized in the zygomatic body as the implantenters.The
45�abutment platform will be near-ly centered on the alveolar crest�not to
thepalatal side.FIGURE13-22Surgical view ofexposed implantsite.The zygoma retractor
is in position,thesinus slot is developed and the initial penetrationofthe round
bur at the site ofimplant insertionhas been completed.
244Part 2: Dentoalveolar Surgeryimpressions are made and the definitiveprosthesis
is constructed.Prosthetic ProcedureHealing PhaseThe maintenance ofthe zygoma
implantpatient is an ongoing process from thecompletion ofstage I surgery through
theentire healing phase (Figure 13-26).Asnoted earlier,the existing or
provisionalupper denture can be modified for imme-diate use (Figures 13-27�13-
30),giving thepatient a continuous esthetic presentation.There will be some
significant limitationsfor functional use,such as changes inretention or chewing
capability,but theoption ofhaving teeth throughout theentire process is usually far
more appeal-ing than the transitional periods ofnoprosthesis use that accompany
many graftprocedures.Protective SplintingOne ofthe unique features ofthese
implantsis the strength they provide when usedwith splinting and cross-arch
stabilization.When used or loaded independently,how-ever,it is felt that the off-
axis load transfercan be detrimental and possibly counter-productive for
maintenance ofosseointe-gration.10Immediately following stage IIsurgery,or exposure
ofall implants withabutment connections,it is recommendedthat some protective
measures be used toprevent independent stress transfer fromthe denture base to the
implants individu-ally.To this end,the current protocol callsFIGURE13-24Zygoma
implant fully inserted.Note the cover screw on the abutment platformpositioned near
the crest ofthe alveolar process.The implant �hugs�the lateral wall ofthe
sinus.FIGURE13-25Near ideal positioning ofthezygoma implants.A,Presurgical
panoramicradiograph.B,Postsurgical panoramic radi-ograph.C,Posterior-
anteriorradiograph.D,Lateral head radiograph.ABCDFIGURE13-26Immediately after
implantplacement cover screws are attached to all ofthefixtures used in the
maxillary arch,and the tis-sues are sutured to create a watertight
primaryclosure.This radiograph shows the implant posi-tions immediately after
placement.FIGURE13-27The patient�s original denture ishollow ground in the area
ofthe premaxillaryridge crest and distally onto the alveolar ridgeand palatal
mucosa areas where the two zygomaimplants will eventually exit.It is also
importantto relieve the intaglio surface ofthe labial flangeto prevent unnecessary
apical pressure in thevestibular area.
The Zygoma Implant245for splinting all ofthe newly exposedimplants with a soldered
bar within 24 hours ofabutment connection (Figures13-31 and 13-32).This is
accomplished bymaking an impression immediately afterthe abutments are delivered
and sending itto the dental laboratory for rapid turn-around (Figure 13-33).A gold
bar ofapproximately 2 mm in diameter is bent tocontour so that it touches a set
ofgoldcylinders attached to the abutmentanalogs on the cast (Figure 13-34).With
amicrowelding device the bar and cylinderscan be soldered together and within
ashort time period a passive protectivesplint can be fabricated.The bar splint
isdelivered,usually the next day,and thedenture is hollow ground to allow com-plete
seating without bar interference (Fig-ure 13-35).At this time,a complete softliner
can be applied to the upper prosthe-sis to enhance comfort and retention (Fig-ures
13-36 and 13-37).The bar splint maynot be necessary in situations where thepatient
is not wearing an upper prosthesis,but for all other cases where continuousdenture
wear is desirable,the bar splintprotocol should be used.Final Prosthesis
ConstructionFinal impressions can be made following anadequate healing
period,usually 3 to 4 weeks(Figures 13-38�13-40).The procedure forthis and ensuing
steps is the same as for allFIGURE13-28Denture conditioning material ismixed and
allowed to set for approximately 8 to10 minutes,at which time it will have a
viscousconsistency.The material is carefully applied tothe borders ofthe modified
denture and is thenplaced in the mouth and allowed to set whileborder
molding.FIGURE13-29With border molding move-ments intraorally,the conditioning
material isphysiologically formed to create a peripheral seal.Any excess material
is removed from the cham-ber so that no pressure is placed on the areasimmediately
over the implant sites.FIGURE13-30At the time ofstage II surgery thepatient should
present with well-healed maxil-lary mucosal surfaces and may occasionallyexhibit a
proliferative reaction into the denturebase chamber space as seen here.This excess
tis-sue is not detrimental.FIGURE13-31Radiographic analysis at approx-imately 5
months ofhealing shows the implants inboth arches appear to be
osseointegrated.Clinicalvalidation ofsuccessful osseointegration is com-pleted once
the implants have been exposed andabutments have been connected.FIGURE13-
32Abutments are selected at stageII surgery with as low a profile as possible
inorder to minimize extension ofthe provisionalsplint into the denture base area.In
this case two3 mm standard abutments have been selected forthe right side,both
ofwhich terminate at the gin-gival tissue.The left side implants are coveredwith
healing abutments since the tissue depththere is too shallow for 3 mm
connections.FIGURE13-33A,Tapered impression copings (right side)and fixture level
impression copings (leftside)are placed according to fixture and abutment locations
at the time ofstage II surgery.B,Thetapered impression copings are transferred into
the impression in their appropriate sites and the com-pleted impression is sent to
the laboratory.AB
246Part 2: Dentoalveolar Surgeryfixed bridge construction on implants.Jawrelation
records are obtained usingimplant-stabilized record bases and waxrims (Figure 13-
41).The try-in with teethfollows the trial set-up done in the labora-tory,and
patient approval ofthe estheticpresentation is confirmed (Figures 13-42�13-
44).Silicone putty indexes are madeofthe approved wax-up and are used toprovide a
matrix for creation ofa metal barstructure (Figures 13-45 and 13-46).Fol-lowing a
second try-in appointment forevaluation ofpassive fit and esthetics,theprosthesis
is processed with heat polymer-izing resin (Figure 13-47).Delivery isFIGURE13-34The
surgical cast is poured indental stone,and appropriate gold cylinders areattached
to the abutment and fixture level repli-cas.The gold baris bent to a shape that
contactseach gold cylinder,and the connection is com-pleted with a soldering
procedure using amicrowelding torch.FIGURE13-35The protective splint is
deliveredwithin 24 to 48 hours ofstage II surgery andserves to provide immediate
protection andcross-arch stabilization ofall ofthe implantsduring the final bridge
construction.FIGURE13-36The previous denture conditioningmaterial is removed from
the patient�s denture,and a disclosing material is used to identify anyareas
ofexcessive contact against the denture base.FIGURE13-37Soft tissue conditioning
materialcan then be used over the entire denture basearea to create tissue contact
and a peripheral sealretention.FIGURE13-38Following several weeks ofheal-ing,final
impressions are made using squareimpression copings,which will eventually bejoined
together with a low distortion resin mate-rial prior to impressing.FIGURE13-40The
master cast should be anabsolute replica ofthe patient�s presentationintraorally.It
is usually necessary to use a verifi-cation jig to assure that the positions and
orien-tation ofthe individual implant components areduplicated from the
mouth.FIGURE13-41Stabilized record bases are usedto record the centric jaw relation
position at thepatient�s appropriate vertical dimension ofocclusion.FIGURE13-39The
final impression is made usinga custom tray,to control material thickness,andan
open top technique,which allows the individ-ual copings to be picked up rather than
transferredinto the impression material.FIGURE13-42The mounted casts should be
anarticulated representation ofthe patient�s jawrelationships.
The Zygoma Implant247accomplished using appropriate screws andscrew torques to
provide even and completeseating (Figures 13-48 and 13-49).The bar structures are
generally waxedand cast in precious metals but can also bemilled from solid blocks
oftitanium withexcellent passive fit properties (Figures 13-50�13-54).11In select
situations,such asminimal interocclusal distance or highload forces,it may be
beneficial to use aporcelain-fused-to-metal restoration.Theprocedure for
constructing these prosthe-ses is essentially the same up to the point ofthe
patient-approved wax-up.The metalsubstructure will be designed to provideFIGURE13-
43The teeth are waxed to contourin positions dictated by the record base
procedureand are sent to the clinic for try-in and patientapproval.FIGURE13-44Final
approval for esthetic dis-play,occlusion,and vertical dimension are allobtained at
this clinical visit.FIGURE13-45The cast framework design isbased on available space
and tooth position as dic-tated by the wax set-up from the trial denturebase.These
dimensions are captured using a buc-cal index that keys to the master
cast.FIGURE13-46For greatest accuracy,the castingtechnique for these long-span
restorations usuallyrequires a runner bar and multiple sprue attach-ments to
minimize distortion.FIGURE13-47Using the buccal index,teeth arewaxed to the gold
casting for try-in.it isusuallydesirable to have a second try-in appointment
toverify the casting accuracy intraorally and toobtain final approval for
esthetics.FIGURE13-48The completed restoration hasbeen processed and is delivered
using the manu-facturer�s recommended torque at each ofthescrew sites.The screw
access holes can be coveredwith provisional materials for an interim periodbut will
eventually be filled with cotton over thescrews and a composite cover at the
surface.FIGURE13-49Radiographically,the definitiverestoration appears to fit
passively with allimplants functioning successfully after 4 years.FIGURE13-50An
alternative to the gold-castingtechnique is available using Procera technologythat
allows the creation ofa metal substructureout ofa single piece ofmachined
titanium.FIGURE13-51By entering scanning informa-tion into a computer
bank,computerized latheswith precisely controlled cutting heads attack thetitanium
blank to create the milled bar structure.
248Part 2: Dentoalveolar Surgerysupport for the veneering material and
willtherefore have a completely different archi-tecture from the hybrid denture
toothdesign.It may be especially advantageousto use the milled titanium technology
forthese restorations,since they do not tend todistort through the thermocycling
phasesofveneering to the same degree as the pre-cious metal alloy cast
substructures (Fig-ures 13-55 and 13-56).SummaryThe placement ofimplants and
restora-tion ofthe extremely atrophic maxilla is achallenge to both the surgeon
andprosthodontist.Ifconventional implantsare to be used exclusively in this
setting,extensive bone grafting is usually neededbefore implant insertion and
usuallyincludes sinus lifts and onlay grafts withlarge amounts ofdonor bone
required.The inconvenience,prolonged treatment,costs,potential
complications,lowerimplant success rates,and donor site mor-bidity are important
considerations.Thisis further compounded by the patient�sinability to wear a
prosthesis for extendedperiods oftime�a factor that keeps manypatients from
pursuing treatment.Withthe zygoma implant,bone grafts often maybe avoided,treatment
time is shortened,donor sites are unnecessary,and thepatient may continue to wear a
transition-al prosthesis.This results in greater patientacceptance while providing
the patientwith a well-tolerated,stable,and estheticfixed or removable prosthesis
at comple-tion oftreatment.The advantages ofconsidering thezygoma implant include
the following:1.Donor site morbidity is reduced oreliminated entirely.2.Treatment
time is markedly reducedor eliminated entirely.3.Bone graft survival and
consolidationare not considerations.4.The total number ofimplants to sup-port a
prosthesis is reduced.5.The treatment is more affordable andless invasive than
alternative treatments.The disadvantages ofthe zygomaimplant include the
following:1.Technically demanding surgery�should only be performed by well-trained
surgeons capable ofdealingwith any surgical situation or compli-cations that might
arise2.Risk ofinjury to adjacent struc-tures�that is,orbit,orbital contents,facial
nerve,lacrimal apparatus,infra-orbital nerve3.Risk ofpostoperative
sinusitis,althoughless than with sinus lift procedures4.Fixture failure�although
rare,moredifficult to retreatFIGURE13-52The milling process is completedat the fit
surfaces with a very precise secondarycutting tool that creates fit tolerances in
the rangeofsingle digit microns.These frameworks arevery lightweight and fit with a
degree ofpreci-sion that is difficult to duplicate with conven-tional casting
procedures.FIGURE13-53The completed restoration illus-trated here uses the same
hybrid denture toothprocessing concept as previously illustrated,withthe exception
that the bar structure is now tita-nium rather than cast alloy.FIGURE13-54Procera
technology can also beused to create porcelain-fused-to-metal restora-tions with a
degree ofpassivity that is equivalentto that found with resin processing on cast
sub-structures.FIGURE13-55This porcelain-fused-to-metalfixed partial denture was
indicated on the zygo-ma and standard implants because oftherestricted vertical
space available for bridge con-struction.FIGURE13-56The principal advantage
oftheProcera titanium framework approach over con-ventional porcelain-fused-to-gold
technology isthe apparent absence ofdistortion as the porce-lain is veneered
through multiple firing cycles.The integrity offit does not seem to be affectedwith
these titanium restorations to the samedegree as that found in comparable gold
alloyceramic restorations.
The Zygoma Implant2495.Surgical access difficult�deep seda-tion or general
anesthetic requiredAs with all properly planned and exe-cuted implant prosthetic
procedures,extensive coordination between the sur-geon and the prosthodontist is
necessarybefore initiating treatment.Ideally,theprosthodontist should be available
atsurgery.Similarly,the surgeon shouldbecome familiar with the prosthetic needsand
techniques involved with fixture posi-tioning and
restoration.Finally,patienteducation,preparation,evaluation,andinformed consent are
major parts oftheprocedure and its ultimate success.Patientunderstanding,before
treatment is initiat-ed,should include the need for meticuloushygiene and
maintenance.The zygoma implant,when under-stood and appropriately used,provides
atreatment alternative for many patientswith atrophic edentulous
maxillae.References1.Bedrossian E,Stumpel L,Beckely M,IndersanaT.The zygomatic
implant:preliminary dataon treatment ofseverely resorbed maxillae.A clinical
report.Int J Oral MaxillofacImplants 2002;17:861�5.2.Bedrossian E,Stumpel
LJ.Immediate stabiliza-tion at stage II ofzygomatic implants:ratio-nale and
technique.J Prosthet Dent2001;86:10�4.3.Stella JP,Warner MR.Sinus slot technique
forsimplification and improved orientation ofzygomaticus dental implants:a
technicalnote.Int J Oral Maxillofac Implants2000;15:889�93.4.Parel SM,Br�nemark
PI,Ohrnell LO,SvenssonB.Remote implant anchorage for the reha-bilitation
ofmaxillary defects.J ProsthetDent 2001;86:377�81.5.Higuchi KW.The zygomaticus
fixture:an alter-native approach for implant anchorage inthe posterior maxilla.Ann
R Australas CollDent Surg 2000;15:28�33.6.Schnitman PA,Wohrle PS,Rubenstein JE,et
al.Ten-year results for Br�nemark implantsimmediately loaded with fixed prostheses
atimplant placement.Int J Oral MaxillofacImplants 1997;12:495�503.7.Jaffin RA,Kumar
A,Bermann CL.Immediateloading ofimplants in partially and fullyedentulous jaws:a
series of27 case reports.J Periodontol 2000;71:833�5.8.Salama H,Rose LF,Salama
M,Betts NH.Immediate ofbilaterally splinted titaniumroot-form implants in
prosthodontics � atechnique reexamined:two cases.Int J Peri-odontol Rest Dent
1995;15:344�60.9.Tarnow DP,Emtiaz S,Classi A.Immediateloading ofthreaded implants
at stage 1surgery in edentulous arches:ten consecu-tive case reports with 1- to 5-
year data.IntJ Oral Maxillofac Implants 1997;12:319�24.10.Zhao R,Skalak R,Br�nemark
PI.An analysis ofa fixed prosthesis supported by the zygo-matic fixture.(In
press).11.Parel SM.The single-piece milled titaniumimplant bridge.Dent Today
2003;21:106�8.
CHAPTER 14Implant ProsthodonticsThomas J.Salinas,DDSBiomechanical
ConsiderationsPeriimplant BiologyConsiderations for tooth replacementwith
osseointegrated dental implantsinclude the biologic principles ofsoft andhard
tissues ofadjacent teeth to theimplant site.The placement ofan implantbetween two
periodontally healthy teeth isa unique situation whereby the bone andsoft tissue is
maintained in part by theteeth.Original studies by Waerhaug andGargiulo and
colleagues showed the widthofthe dentogingival complex surroundingnatural teeth
approaching 3 mm.1,2Com-parably,a similar study by Cochran andcolleagues
assimilated the periimplant tis-sues to a similar dimension.Based onthese
principles,the suggested depth ofplacement ofan implant below the freemargin ofsoft
tissue is approximately 3 to4 mm (Figure 14-1).3This distance pro-vides room for
biologic width,properemergence ofrestoration,and estheticsand also should allow for
remodeling ofthe soft tissue and bone,which occursbetween 6 months and 1 year.4It
has beenpostulated by some that the type ofperi-odontium influences how extensive
thisremodeling process is.In other words,thinscalloped gingiva recedes more
extensivelythan does thick nonscalloped gingiva.5,6Restorative interfaces with
metal shouldbe kept below the free margin oftissues inanticipation ofthis
remodeling.Tarnowand colleagues have shown that there is arelationship ofthe
underlying bone to softtissue in the interdental spaces betweennatural teeth.7Also
a relationship fromboth implant to natural tooth and implantto implant as well has
been demonstrated.8Therefore,the distance suggested from theside ofthe implant to
the adjacent toothshould be about 2 mm to avoid horizontalbone loss affecting the
adjacent tooth.Similarly,Tarnow and colleagues showedthe critical distance between
implant sur-face and implant surface approachedabout 3 mm before the mutually
destruc-tive process oflateral bone resorptionaccelerated each other�s processes
(Figure14-2).Typically,each implant loses peri-implant bone within the first year
andthen stabilizes�one criterion ofsuccess asoutlined by Albrektsson and
colleagues.9Patient FactorsSoft tissue evaluation prior to implantplacement is
critical for long-term successand maintenance.A sufficient volume ofkeratinized and
fixed tissue is needed toproperly maintain hygiene around animplant,just as it is
needed around a nat-ural tooth.Occasionally it may be neces-sary to incorporate
subepithelial connec-tive tissue or full-thickness soft tissuegrafts to prospective
implant sites.Whenrestoring single missing teeth,the inter-proximal bone between
the remaining3�4 mmFIGURE14-1Osseointegrated implant placed ata depth of3 to 4 mm
for biologic width andemergence profile.2 mm3 mm2 mmFIGURE14-2Suggested minimum
distances ofimplant to natural tooth and implant to implant.
252Part 2: Dentoalveolar Surgeryteeth is a good prognostic indicator
ofthelikelihood ofcreating and preservinginterdental papilla.Generally,the
distancefrom the residual alveolar bone to the con-tact area ofthe restoration can
be assessedon a periapical film.The likelihood ofhav-ing a papilla is depicted in
Table 14-1.Bone volume is best assessed by radi-ographic techniques,although a
rudimen-tary estimate can be made clinically by pal-pation and inspection.Assessing
a patientfor mandibular implant reconstructionmay include intraoral/extraoral
palpationas well as panoramic,occlusal,and lateralcephalometric radiographs.Single-
toothreplacement in the esthetic zone also canbe assessed by comparison ofthe
bonytopography ofthe adjacent teeth as well asperiapical/panoramic radiographs.Bone
isa scaffold for soft tissue,and it is typicalfor bone loss to occur on a scale
of0.2 mm/yr after implant placement.Therefore,it is not unusual that soft
tissuerecession occurs in this period oftime.This recession should be
anticipated,espe-cially when considering placing implantsin the esthetic zone and
elsewhere.It is well documented that local andsystemic factors such as cigarette
smokinghave a deleterious effect on the long-termsuccess ofdental implants.10�13It
is alsowell documented that smoking decreasesbone density.14In one study failure
rates ofimplants placed in type 4 bone approached35% in smokers;placement
ofimplantsinto types 1,2,and 3 bone ofsmokersresulted in a failure rate approaching
3%.15Although osteoporosis can be a negatingfactor to bone density,this disease
seems toaffect the hip and spine ofthose afflicted.No clear correlation can be
demonstratedthat osteoporosis is a contraindication tothe placement ofdental
implants.16Periodontal disease is a local factorthat should be under control to
avoidadverse effects ofa unique population ofmicrobiota affecting these
diseasedsites.17�19Bruxism is another local factor thatcan compromise long-term
success.Gen-erally,bruxism promotes micromovementofthe implant bone interface.In
bonetypes 3 and 4,bruxism may have a morepronounced effect on the long-
termosseointegration.Off-axis and lateralloading ofdental implants by bruxism
orother parafunctional forces can be delete-rious in the long term with respect
toaccelerated bone loss and prosthetic fail-ure.Self-awareness and occlusal
splinttherapy may provide appropriate protec-tion.Ifthese factors cannot be
controlledpreoperatively,alternative treatmentshould be considered.Radiation to the
head and neck inexcess of50 Gy is considered a contraindi-cation to dental implant
placement inmost cases.There are instances in whichthe radiation has created a
significantdegree ofxerostomia,which is incompati-ble with retaining natural teeth
or stabiliz-ing prostheses.Given the risks ofosteora-dionecrosis,hyperbaric oxygen
should beconsidered ifplacement ofimplants wouldsignificantly improve the oral
health andquality oflife in these individuals.20�22However,there are several
studies thatrefute the benefit ofhyperbaric oxygen tothe long-term survival
ofdentalimplants.23,24Standard protocol suggestedby Marx and Ames is 20
preoperative divesand 10 postoperative dives.25Systemic factors such as
diabetes,con-nective tissue diseases,autoimmune dis-eases,and HIV are considered
relativecontraindications to treatment withosseointegrated implants.26�31Ifthese
dis-ease processes are well controlled,it maybe advisable to treat the patient
toimprove the overall quality oflife.Chemotherapy given to patients
duringosseointegration has not been shown tobe subtractive in
success.32�34Radiographic EvaluationPeriapical radiographs are an excellentway to
evaluate single missing teeth sincethey depict a minimally magnifiedamount ofbone
and root topography.Adjacent root angulation,pulp chambersize,periodontal
defects,interproximalbone,and residual pathology are some ofthe factors critical to
the treatment plan-ning ofsingle-tooth implant restorations(Figure 14-3).Occlusal
radiographs for mandibulararch assessment also can give an apprecia-tion ofthe size
ofthe inner and outer cor-tices as well as the position ofthe mentalforamina
(Figure 14-4).It may be also feasi-ble to incorporate a radiographic marker onthe
patient�s denture to give a perspective ofthe relationship ofthe mental foramina
tothe overlying prosthesis.This can be donewith either lead foil from a film packet
tapedto the underside ofthe patient�s denture ora stainless steel wire attached
with stickyTable 14-1Potential ofCreating/Preserving Papilla Distance from Bone to
Chance ofContact Area (mm)Creating Papilla (%)4.01005.01006.0567.027Adapted from
Tarnow DP et al.7FIGURE14-3Presurgical planning for placementofan implant into site
no.10.Minimal magnifi-cation is noted from the periapical radiograph.
Implant Prosthodontics253wax to the buccal or occlusal portion ofthemandibular
denture.Panoramic radiographs are excellentscreening examinations that give a
broadperspective on the inferior alveolar canal,maxillary sinus,mental
foramina,andnasal floor;they are used for treatmentplanning ofsingle and multiple
missingteeth.The panoramic film generally has amagnification factor ofabout
25%,which should be anticipated on thework-up to gain a better appreciation ofthe
actual position ofvital structures andthe size ofimplant to be selected.Methods
ofstandardizing the magnifica-tion factor include the use ofknown-diameter
stainless steel shots incorporat-ed in a vacuum-formed stent worn at thetime
ofradiography (Figure 14-5).Thisvaries from patient to patient,by loca-tion,and
also with the machine used.Panoramic radiographs are also usefulfor verifying
complete seating ofimpres-sion and restorative components.Use ofthis film over a
standard periapical radi-ograph is preferable since the incidentbeam ofthe tube is
more likely to be per-pendicular to the long axis oftheimplant.Also,many edentulous
patientshave a shallow floor ofmouth and flatpalatal vault owing to resorption.It
is fareasier to obtain a perpendicular view ofthe implant platform in these circum-
stances,which is critical to the accurateperformance in the treatment
stages.Lateral cephalograms assess the max-illomandibular relationship as well
asthat ofthe maxilla and mandible to thecranial base.A lateral cephalogram maygive
an appreciation ofthe concavity ofthe lingual surface ofthe anteriormandible
vitally important to surgicalconsideration ofimplants in the anteriormandibular
area.Development ofantici-pated implant occlusion is well assessedwith lateral
cephalography,whichbecomes especially useful when recreat-ing anterior guidance and
posteriorocclusal schemes (Figure 14-6).Linear tomography is a useful adjunctwhen
considering a single-tooth implant ordefinitive positioning ofthe inferior alveo-
lar canal,concavity ofthe nasal fossa,andthe maxillary sinus.This feature is an
exten-sion ofmost modern panoramic radi-ographic units.It gives a three-
dimensionalperspective ofthe primary radiograph,which can help one anticipate
grafting pro-cedures or select an implant length andconfiguration (Figure 14-
7).Computed tomography (CT) can behelpful when considering maxillary reha-
bilitation with a full complement ofimplants or when other craniofacial land-marks
are planned for use.CT may beused in conjunction with computerizedtechnology to aid
implant placement.These images may be reformatted to con-struct a three-dimensional
image oftheselected part ofthe craniofacial skeleton.CT scans are useful in
assessing the healthofthe maxillary sinus prior to augmentiveprocedures (Figure 14-
8).A radiographic or imaging stent can beused when there is a need to join the
pros-thetic information to the bony topograph-ic information.In creating these
stents,acrylic resin can be mixed with 30% or lessbarium sulfate as a radiographic
marker tocreate the contour ofthe intended restora-tion.Some denture teeth are true
toanatomic form and create a radiopaqueappearance when included in the stent.Asan
alternative,access channels can be filledwith gutta-percha as a radiographic mark-
er.Ifverified radiographically,this imagingstent may double as a surgical
stent.Surgical StentsFabrication ofsurgical stents for implantplacement should be
part ofevery casesince the placement is permanent andFIGURE14-4Occlusal radiograph
gives the rel-ative position ofmental foramina and the taperofmandible.FIGURE14-
5Aand B,Five-millimeter stainlesssteel shots in vacuum-formed stent to calculatethe
magnification factor.ABFIGURE14-6Lateral cephalograms may assistin the work-up for
determining maxillo-mandibular relationships and occlusal schemes.
254Part 2: Dentoalveolar Surgeryirrevocable after integration.Planning ofeach case
includes the collection ofalldiagnostic data as previously mentioned.Once this data
has helped create a thor-ough treatment plan,fabrication ofa sur-gical stent can
begin from the diagnosticmodels and other information from thework-
up.35Construction ofprostheses beginswith a confirmation ofocclusal relation-ships
and the need to direct occlusal forcesover the long axes ofthe implants.Thisbecomes
exceptionally critical when afixed restoration is to be used.On thisbasis,a site is
selected and a stent made toguide the surgeon at placement (Figure14-9).This
information may also be trans-lated from radiographic findings to a sur-gical stent
in the position ofthe mentalforamina (previously described).Thisinformation can be
used to place implantsfar enough away from the foramina andeach other to be
mechanically advanta-geous.Again,parallelism is ofparamountimportance ifa stud-
retained overdentureis used.This stent can be as simple as avacuum-adapted
thermoplastic sheet overan edentulous cast or a clear processedduplicated
denture.Implant-supported overdenture con-struction may incorporate the use
ofthesurgical stent to keep the implant fixturesaway from the peripheral confines
oftheprosthesis.This may be beneficial to avoidencroaching on the peripheral seal
ineither esthetic or functional areas.Also,occlusal forces may be better directed
overthe long axes ofthe implants.The stentcan be either a duplicate ofa
diagnosticwax-up in clear resin or simply a duplicateofthe patient�s
denture,ifacceptable.Astent may be critical in this situation sinceit will be
supported with a splinted struc-ture in which cantilevering may be used.Implant
hybrid dentures mandate theuse ofa surgical stent since the occlusalaccess channels
are desired to be throughthe posterior teeth and the lingual aspectsofthe anterior
teeth.In these situations aslot can be created through these areas toprovide the
surgeon with latitude in siteselection.A clear processed duplicate ofthe patient�s
denture may be the best tech-nique in surgical stent design.Surgical stent design
for fixed prosthe-ses is mandated in that selection ofa specif-ic prosthetic design
may be entirely depen-dent on implant position and orientation.In the esthetic zone
the cemented designmay be the preferred method ofprosthesis,and placement ofan
implant in an orienta-tion just palatal through the incisal edge isoptimal.Also,the
implant platform shouldbe approximately 3 to 4 mm below the freeedge ofthe gingival
margin.Two vital piecesofinformation contained on a surgical stentare the
occlusal/incisal plane and gingivalmargin ofthe proposed restoration (Figure14-
10).To obtain this information a wax-upis performed in the desired occlusal posi-
tion.Once completed,this model should beduplicated into another cast.A vacuum-
adapted stent can be made on this duplicatecast.The matrix can be trimmed with a
hotknife and rotary instrument.Guide chan-nels can be created with old surgical
drills orlaboratory burs.The constant access diame-ter ofthese stents is based on
the concentricenlargement ofeach succeeding drill diam-eter.These stents are
usually easily made,arecost effective,are self-retaining,and do notrequire
prefitting.Since these stents fit well,it is only necessary to extend the stent two
tothree teeth on either side ofthe edentulousspaces for partially dentate
cases.Crown-to-Implant RatioIdeally,a crown-to-implant ratio of1:1 orless is
desired (Figure 14-11).For this rea-son,the minimum length needed approach-es 10 to
12 mm since the clinical crownFIGURE14-7Linear tomograms give cross-sec-tional data
when used with other films and radi-ographic stents.FIGURE14-8Three-dimensional
reconstruc-tion with computer software manipulation ofcomputed tomographic data ofa
patient with amaxillectomy.FIGURE14-9Stent used to place the implantswithin the
confines ofthe denture base.FIGURE14-10Surgical stent showing proposedgingival
margin and incisal/occlusal plane.(Surgery performed by Michael S.Block,DMD)
Implant Prosthodontics255length frequently approaches this measure-ment.Standard
implant diameters withshorter lengths have been shown to have ahigh failure
rate.36,37Often,replacement ofteeth in a compromised site gives rise to sin-gle or
multiunit restorations that have pooror unfavorable crown-to-implant ratios.Ifthe
restoration participates in anterior guid-ance,it should be splinted to other
implants.Ifthe restoration participates in posteriorocclusion,it should be
protected by naturalcanine teeth to limit lateral loads in excur-sions.Ifit is
placed in conjunction withother implants in the posterior,it may besplinted for
mutual support.OcclusionThere are several axioms in implant den-tistry relating to
occlusion:�Avoid lateral component forces when-ever possible.38�Establish occlusal
forces along thelong axis ofthe implant.�For added stability,splint implantswhen
possible.�When restoring occlusion ofan entirearch,favor the weaker ofthe two arch-
es.(In other words,an implant-bornerestoration opposing a complete den-ture should
be restored with bilateralbalanced occlusion.)One additional consideration is
that,unlike natural teeth,implants have no pro-prioception.In fact,many
patientsrestored with dental implants have a sig-nificantly increased bite force
within thefirst year.39�41In partially dentate cases,theimplant restoration should
have equal orslightly less occlusal loading than the nat-ural tooth (Figure 14-
12).Also,theocclusal contacts should preferably beplaced over the platform ofthe
implant tominimize the possibility ofscrew loosen-ing.Although this often may not
be possi-ble,it should be striven for to minimizecomplications.Full-Arch
RestorationsFull-arch reconstructions ofthe maxillashould be based on placement of8
to 10 implants splinted for cross-arch stabili-ty.42,43Reasonable length implants
(> 12 mm) should be considered especial-ly in the posterior maxilla as
shorterimplants into this relatively soft bone havebeen shown to do poorly in the
longterm.44The maxillary sinuses may pre-clude placement ofa full complement
ofimplants,and sinus augmentation or per-haps the use ofextended-length
implantsinto the zygomatic bones bilaterally mayallow an optimum force distribution
forfull-arch prostheses (Figure 14-13).Full-arch reconstruction ofthemandible can
involve different considera-tions as the mandible is a dynamic bonethat flexes and
rebounds as it opens andcloses.Traditionally,mandibular full-archreconstruction has
involved placement offour to six implants between the mentalforamina with a minimal
cantilever to theposterior.45The greater the anterior poste-rior spread,the greater
the amount ofcan-tilever possible.On average,a 16 mm dis-tal cantilever is
permitted (Figure 14-14).To avoid using a cantilever,it may be nec-essary to place
implants distal to the men-tal foramen.In such a case,division oftheprosthesis into
two components preventsunfavorable stress transfer.Anotheroption is to use the
distal fixtures for ver-tical support and not engage the abut-ment-implant junction
with an abutment-coping screw.46This allows some flexure ofthe mandible without
transferring stressto the prosthesis and/or implants.Pros-thetic screw or implant
failure may resultifa solid prosthetic connection spans thesplinted first molar
regions.Implant Selection Historically,osseointegrated dentalimplants were
introduced in their originalconfiguration as a machined parallel walledscrew.The
implant possessed a platformwith a 4.1 mm diameter,an external heximplant platform
(originally used to drivethe implant into position),and a 3.75 mmdiameter body;this
has been the most com-mon implant type placed worldwide (Fig-ure 14-15).The
original applications wereXYFIGURE14-11Ideal crown-to-implant ratiooccurs when X
=Y.FIGURE14-12Contact ofthe implant occlusionshould be over the platform ofthe
implant andslightly less intense than that ofnatural teeth.FIGURE14-13Full-arch
reconstruction usingtwo zygomatic implants and three endosseousimplants.
256Part 2: Dentoalveolar Surgerypiloted for the edentulous patient,and lim-ited
restorative options were available in thefirst years ofits introduction.In later
yearsthe use ofsurface-textured press-fit typeimplants also became popular because
theirsurgical installation was simplistic andachieved earlier integration into
softertypes ofbone (Figure 14-16).At this timethe connection ofabutments or
prosthesesto the surface ofthe implant was character-ized as a butt-joint
connection.Abutmentstability with single- and multiple-toothreplacement using
standard externallyhexed implants has a history ofcyclicfatigue with abutment screw
loosening.47,48As extended applications developed for theuse ofreplacements for
single and multipleteeth and with immediate loading,anincreased need for secure
abutment con-nections,esthetic versatility,and improvedsurgical stability in
trabecular bone becamemore apparent.Significant mechanicalimprovement in abutment
and screw-retained components occurred in the early1990s and markedly decreased
complica-tions.49Current trends are toward the use oftapered macroretentive implant
configura-tions,based on the fact that tapered screw-type implants have increased
surgical sta-bility in soft bone.An example ofthesetypes ofimplants is shown in
Figure 14-17.With these trends it is apparent that inter-nal connections are
preferable for fixedtooth replacement since abutment screwloosening appears
significantly less withinternal connections than with butt-jointimplants.The Morse
taper,a cone within acone attachment mechanism,is a feature ofsome implant systems
that allow the abut-ment-prosthetic connection to facilitateinstallation and to
maintain stability (Fig-ure 14-18).This taper creates a seating effectofthe
connection to the internal aspects ofthe implant;therefore,fewer lateral
stressesare transferred to the abutment screw,resulting in a less frequent
incidence ofscrew loosening and fracture.Morse tapersare measured in percentage
units that reflectthe shaft length relative to the radius oftheshaft.Thus,iffor
every centimeter ofshaftthe radius increases 0.01 cm,this would bydefinition be a
1% Morse taper.MostMorse tapers are anywhere from 0 to 7%,and dentistry most
commonly employs the4 to 7% series.Use ofspecific implantsresistant to the problems
ofabutmentscrew loosening and immediate stability isprobably more critical in cases
ofsinglemissing teeth or in which a cementedimplant crown and bridge are
planned.Thetraditional parallel walled screw continuesto enjoy success in the
general populationofedentulous patients restored withimplants50,51;the vast
majority ofprospec-tive and retrospective studies have conclud-ed that this
specific implant is highly suc-cessful for restorations in
edentulouspatients.52�54Long-term development hasresulted in an increased number
ofcompo-nents for edentulous applications.Thedevelopment ofan extensive
armamentari-um ofabutment connections and restora-tive components currently exists
forrestoration with esthetic fixed prostheses.Many well-known systems have this
versa-tility available,which is especially impor-tant when considering implant
restorationsin the esthetic zone.It is advisable for thesurgeon to become familiar
with therestorative components available whentreatment planning for implants
cases.Consideration ofthe components makes iteasier to select the appropriate
system forboth surgical installation and restoration.FIGURE14-14Cantilevering is
about 16 mm.FIGURE14-15Standard externally hexed implant.FIGURE14-16Press-fit
cylinder-type implant.FIGURE14-17Tapered-wall screw implant.
Implant Prosthodontics257Implant ComponentsThere is a wide array ofdental
implantcomponents for impression procedures,laboratory fabrication,and direct
restora-tive dentistry.The various types ofosseoin-tegrated implants are discussed
above.Abutments are simply transmucosalextensions for the attachment ofprosthe-
ses.Abutments can be used to provide arestorative connection above soft tissuesand
to provide for the biologic width.Abutments can be used for attachment ofscrew-
retained or cemented connectionsand can be made ofmetal or ceramic.Themost commonly
used abutment materialis machined titanium,which has beenshown to be strong and
resistant to plaqueretention,and to react favorably to softtissues.Titanium
abutments have beenused historically for the attachment ofscrew-retained
connections.Two ofthesetypes ofabutments are shown in Figure14-19.Titanium
abutments are also usedin many cases in which a cemented pros-thetic connection is
desired.With thingingiva,the gray hue ofthese abutmentscan be problematic in
esthetic areas.Castyellow gold has been used for abutmentconnections owing to its
blend withtranslucent gingival tissues.Although nohemidesmosomal attachment is
foundwith cast alloys or dental porcelain,55yel-low gold creates a warm appearance
inesthetically critical areas.In esthetic areasceramic abutments have also been
used incemented designs for single and multiple-unit crowns (Figure 14-20).Similar
totitanium,these abutments manifest a bio-logic attachment.The material used
inthese products has been mainly alu-minum oxide and zirconium.The decision to use
an abutment forscrew-retained restorations can be madebased on the depth
oftissue.Generally 3 mm or more oftissue depth necessitatesthe use ofan abutment.As
with anyrestorative procedure,biologic width isthe driving force between the
alveolarbone and the prosthetic margin.Ifthe tis-sue depth is < 3 mm,biologic width
isprobably created from a portion oftheimplant;therefore,the prosthesis may
beconnected directly to the implant,bypass-ing the need for an
abutment.Iftherestorative dentist is unsure ofwhichabutment to use,a fixture level
impres-sion can be recorded and the selectionprocess completed in the
laboratory.Impression procedures used for den-tal implants are based on
transferringeither the abutment position or theimplant position to the
laboratory.Ifabutments are to be used for a screw-retained restoration,an
impression FIGURE14-18Morse taper internal connection.FIGURE14-19A,Premachined
abutment for screw-retained restorations.B,Abutment for cement-retained
restorations.ABFIGURE14-20Aand B,Aluminum oxidecemented abutment with an all-
ceramic crown.(Prostheses prepared in collaboration withAvishai Sadan,DMD)AB
258Part 2: Dentoalveolar Surgerycoping is placed on the abutment andeither a
closed- or an open-tray techniquecan be used (Figure 14-21).The open-traytechnique
is considerably more accurateand is indicated for multiple splintedunits.At this
point an abutment analog orreplica is attached in the impression and acast is
poured in the laboratory to simu-late the oral situation.Ifno abutment is to be
used or ifacemented design is to be employed,a fix-ture level impression with an
impressionpost can be made in a similar open- orclosed-tray technique.Subsequently
animplant analog or replica is attached to theimpression post in the impression
andsimulated gingival material is placed;thena cast is poured to create a soft
tissue mas-ter model (Figure 14-22).The simulatedgingival material allows the
dentist or tech-nician to select an appropriate abutmentand/or design the
prosthesis while preserv-ing the actual position ofthe gingiva.Single-Tooth
ReplacementThe Nonrestorable ToothReplacement ofa single missing toothshould start
with an evaluation ofthe peri-odontium and structural support.Peri-odontal
defects,periapical pathology,bone loss,mobility,and pain are indica-tions for
periodontal/endodontic treat-ment or extraction.Other factors thatrequire
assessment prior to considerationfor either restoration or extraction are
theremaining coronal tooth structure,rootfracture,and restorative space.The deci-
mated tooth may have only one wall ofthecoronal structure
missing.Horizontaldeficits ofthis type can be restored byusing intracoronal
anchorage methods (ie,elective endodontics or post and core).However,vertical
deficits that encroachupon the biologic width may necessitatecrown elongation to
provide enough toothstructure necessary for a ferrule or exter-nal bevel,which
provides encasement ofremaining tooth structure.A 2 mmamount ofcoronal tooth
structure hasbeen shown to improve long-term struc-tural resistance to
failure56�58;in total,bio-logic width plus a 2 mm ferruled toothstructure
necessitates about 4 to 5 mm ofsuprabony tooth structure.Ifthis is notavailable,it
may be created by either ortho-dontic extrusion or crown elongation,which may
sometimes create unfavorablecrown-to-root ratios or furcation expo-sure.In this
scenario it may be prudent toconsider extraction and either replacementwith a fixed
partial denture (FPD) or a single-tooth implant-supportedrestora-tion.The longevity
ofan FPD has beenexamined by a number ofstudies and isfavorable over extended
periods oftime.59�61Much ofthe literature indicatesstandard FPD survival to be in
the higheightieth percentile at 10 years and seven-tieth percentile at 15
years.62,63However,typical complications occurring are relat-ed to
endodontics,recurrent caries,peri-odontal factors,and failures in retention.Single-
tooth implant studies reveal com-plications as well.64�67The incidence
ofcomplications for single-tooth implantrestorations appears to be significant
incomparison with other types ofimplantprostheses68;however,in comparison
withLaboratoryreplicaStoneAbutment master castFIGURE14-21A,Abutment transfer
impression using closed-tray technique.B,Abutment transferimpression using open-
tray technique.ABImplantreplicaSoft tissueimplant castFIGURE14-22A,Implant level
transfer impression using open-tray technique.B,Implant leveltransfer impression
using closed-tray technique.AB
Implant Prosthodontics259other implant restorations,the implantsingle crown is the
most successful.Ifsuf-ficient bone,soft tissue,and restorativedimension
exist,replacement with animplant-supported single-tooth restora-tion is considered
the standard ofcare andshould be offered to the patient.69,70The success
ofremovable prosthesesrelies on the combination ofretention,support,and
stability,which can be defi-cient.Implant dentistry today is rootedhistorically
from treatment ofmandibularedentulism,71,72which is currently the mostpredictable
form ofdental implant thera-py.73�76This success is primarily owing tothe high
degree ofsuccess ofosseointegra-tion in the anterior mandible.53A conven-tional
mandibular prosthesis should beevaluated for retention,support,and sta-
bility.Difficulty with speech,swallowing,and mastication should be consideredwhen
evaluating prostheses.Patient accep-tance ofconventional prostheses may
becontingent on stability and comfort whenmasticating.A patient�s
chiefcomplaintshould be closely scrutinized and correlat-ed with the clinical
examination to helpformulate the proper treatment;the com-plaint is the foundation
for a wide array ofconsiderations that determine avenuespossible for a candidate
considering treat-ment with osseointegrated implants.Manyofthese considerations
help to determinewhich imaging studies,preparatory treat-ment,and number
ofancillary proceduresare needed;ifthe treatment goals are feasi-ble;and what time
and cost commitment isinvolved.Treatment should be targeted atspecific goals to
achieve a predictable out-come that addresses the patient�s function-al and/or
esthetic problem.The treatmentmay encompass several different routespaying
attention to time,cost,longevity,and levels ofinvasiveness.The amount
ofkeratinized/fixed tis-sue,vestibular depth,available bone,andopposing occlusion
are all important fac-tors to consider prior to implant treatment(ie,natural
dentition,edentulous arch,and implant-borne occlusion).It may beappropriate to
recommend only animplant-retained overdenture for a favor-able mandibular
arch.However,mandibu-lar arches with limited support,vestibularextension,and
extensive bone resorptionmay require an implant-borne prosthesis.The Esthetic Zone
Esthetic considerations encompass addi-tional complex concerns such as
gingivaldisplay,proportion ofteeth in the estheticzone,and bone density
support.Theesthetic zone is generally considered to bethe maxillary anterior
area.When consid-ering replacement ofa single tooth in theesthetic zone,the
adjacent dentitionshould also be evaluated for proportional-ity and position.From a
frontal plane thelateral incisor should be about two-thirdsthe width ofthe central
incisor.Likewise,the width ofthe canine when viewed fromthe same vantage point
should be abouttwo-thirds the width ofthe lateral incisor,and so on.The width-to-
length ratio ofesthetically pleasing central incisorsshould be about 66 to
80%.77The axiomsare ranges found in nature and are consid-ered pleasing to the
human eye.Iftheseproportions are not present,they may becreated by surgical
periodontics,restora-tive dentistry,orthodontics,and,ifappro-priate,osseointegrated
implants.Occasionally,replacement ofmaxil-lary or mandibular canines may present
acompromise in either occlusion or esthet-ics for the functional goal
ofeliminatinglateral forces on the restoration/ implant.Esthetic and/or functional
correction maydictate the need for pretreatment ortho-
dontics,endodontics,periodontics,andconcurrent restorative dentistry.A com-plete
examination that includes diagnosticmodels,radiographs,and clinical pho-tographs
can be invaluable.Esthetic considerations for removableprosthodontics may be a
concern forlower edentulous arches when restoringthe facial contours typically lost
inmandibular resorption.This is especiallytrue when restoring the skeletal Class
IIpatient.The use ofa flange may be neces-sary to eliminate the labiomental
foldusually apparent in these cases.Likewisethe use ofa flange in the edentulous
max-illary arch may be beneficial to restoreupper lip support as well as the
estheticintegrity so critical to this area.A func-tional lingual maxillary alveolar
seal isessential for correct labiodental conso-nant production;in cases
ofadvancedresorption ofthe maxilla,an overdenturemay be the appropriate
treatment.Cemented Single UnitsCemented prostheses may be preferable toscrew-
retained designs for single-unitcrowns in the anterior areas.They tend toprovide
minimized bulk ofthe restoration.Overcontoured bulky restorations are nothygienic
and are detrimental to the main-tenance ofperiimplant tissues.The axis ofimplant
placement should be aimedthrough the incisal edge for standard-diameter implants
(Figure 14-23).Thisresults in predictable esthetics and man-ageable soft
tissues.Ifa comparably widerimplant is placed (4.3,5.0,or 6.0 mm) inan esthetic
site,the long axis should tra-verse just palatal through the incisal edge.Errors in
placement to the facial oftheincisal edge produce not only difficultieswith
angulation correction,but also a softFIGURE14-23Long axis ofimplant
placementthrough the incisal edge ofthe stent for cement-retained prostheses.
(Surgery performed byMichael S.Block,DMD)
260Part 2: Dentoalveolar Surgerytissue problem because the bone supportin this area
is lost owing to the osteotomy(Figure 14-24).Errors in placement too farpalatally
create ridge-lapping and hygienedifficulties.The superior/inferior place-ment ofthe
implant platform should be 3 to 4 mm below the anticipated free gin-gival
margin.The use ofa surgical stent inplacement aids in creating an optimal sitefor
implant restoration.The choice ofcemented restorations for a posteriortooth is
plausible and becomes especiallyuseful when angulation in placement isless than
ideal.However,the resistanceand retention form ofthe abutmentshould be sufficient
to resist dislodgment.The choice ofspecific abutments can beplanned in advance
ifplacement is basedon an ideal scenario.Anatomy should notdictate placement ofthe
implant posi-tion,but rather the placement should bebased on restorative
parameters.Thisinformation can be obtained by the use ofsurgical stents,which may
provide criticalinformation about where to develop theocclusion and where to
recreate the emer-gent path as the restoration exits the gin-gival sulcus.Screw-
Retained Single UnitsThe treatment plan for replacement ofasingle tooth with screw
retention is theprofessional preference ofthe restorativedentist.There are
advantages and disad-vantages to using this design for singleand multiple missing
teeth (Table 14-2).Screw-retained prostheses are simplisticto retrieve,easy to
trial fit,and can beshaped to the desired emergence witheither porcelain or
metal.This designalso eliminates the uncertainties ofloos-ening and incomplete
debris removalassociated with cemented prostheses.However,using screw-retained
prosthe-ses requires strict attention to placementand confines the axis ofthe
implantthrough the desired area ofemergencewithin the restoration.Screw
retentionfor single units in the esthetic area maybe problematic with respect to
hygiene asthese sites frequently have a full comple-ment ofbone and soft tissue on
adjacentteeth (Figure 14-25).This can create analmost unavoidable situation
ofridgelapping to provide the palatal accesschannel needed.Screw-retained prosthe-
ses are especially useful in the posteriordentition as retrievability is much
easierthan with the cemented prostheticdesign,and a controlled degree ofreten-tion
is afforded as well.Restorations for the Partially Edentulous Patient:FPDsFPDs
require the first assessment ofsiteplanning as with other types ofrestora-tions.It
is ofprime importance to under-stand that the implant bridge should besupported
entirely by dental implants.Combining the support with natural teethhas been shown
to involve prosthetic com-plications and intrusion ofthe abutmentteeth for a number
ofreasons.78,79Although these studies may use the specif-ic scenario ofa three-unit
FPD supportedby a natural tooth and implant,otherstudies have advocated strategic
teeth incombination with implants for full-archprostheses.80,81It is prudent to
keep therestoration supported entirely by dentalimplants to avoid problems
concerningabutment fracture,screw loosening,toothintrusion,malocclusion,and other
com-plications.82,83Designing the FPD to bescrew retained as opposed to
cementretained is largely based on personal FIGURE14-24Aand B,Implant placed too
far facially resulting in compromised periimplant softtissues.ABTable 14-2Screw
Retention versus Cement RetentionAdvantagesDisadvantagesScrew RetentionCement
RetentionScrew RetentionCement RetentionRetrievabilityEstheticImplant placement
criticalCement removal subgingivallyPorcelain emergenceAngle correction
possibleScrew access channel visibleAbutment selection critical in anteriorCost
effectiveLess bulk ofrestorationin Deep channels should be sealedProvisional
restoration needed inElimination ofcement anterior areasanteriorretrievalBuilt in
load indicator byCost factor with abutment/restorationtwo interfacesProblematic
retrievability
Implant Prosthodontics261preference but may be tailored to what canbe serviced and
maintained most easily.FPDs in the Esthetic ZonePlacement ofmultiunit restorations
in theanterior maxilla should bring to mindseveral anatomic considerations for
surgi-cal planning:�Length ofthe residual alveolar ridge tothe nasal
floor�Buccolingual width ofthe bony ridgeto provide for implant placement
�Available bone for angulation ofimplants to provide for either screwretention or
cement retention�Participation ofthe restoration inanterior guidance Anterior FPDs
or any restoration in theesthetic zone should first begin with a diag-nostic wax-up
or template (Figure 14-26).This will give an idea as to the incisal edgeposition as
well as the available restorativedimension,and should be verified in thepatient�s
mouth to correspond with faciallandmarks such as the center ofthe face
andinterpupillary line.Also,a proportionalrelationship should exist from the
centralincisor to the canine from an anterior per-spective.This proportionality
becomes crit-ical in esthetically prominent areas.Thewax-up may also indicate how
much tissuehas been lost as a result ofthe missing teeth,soft tissue,and associated
alveolar process.In these cases it may be necessary to con-sider horizontal or
vertical bone augmen-tive procedures as a first phase followed byplacement
ofimplants in a second phase.Insome cases it may not be feasible to per-form bone
grafting owing to local or sys-temic factors.Making precision detachablebridgework
that replaces teeth,soft tissues,and alveolar bone may be more predictablein these
circumstances.Ifthe surgical work-up determines implant placement will bedone
concomitantly with or without a bonegraft,the diagnostic wax-up should be usedto
fabricate a surgical guide or stent forimplant placement.Ifa bone graft is neces-
sary,the surgical guide references the incisaledge and gingival aspect ofthe
futurerestoration to aid in establishing the properamount and positioning ofthe
bone graft(Figure 14-27).Superior/inferior position-ing ofimplants is virtually the
same as forsingle units,described above.However,themesiodistal assessment
ofrestorative spaceshould be done first to determine theappropriate implant number
and dimen-sion to be placed.Using a 2 mm rule fromeach adjacent tooth and a 3 mm
rule fromimplant to implant,the appropriateimplant number and dimension can be cal-
culated (see Figure 14-2).Ifthe availablespace does not allow an appropriate num-
ber ofimplants or encroachment upon theimplant-implant proximity,either restora-
tive dentistry and/or orthodontics may beindicated.Occasionally,use ofa can-
tilevered bridge design can be advantageouswhere space constraints or
insufficientbone prohibits placement.Ifit becomesnecessary to cantilever the FPD
eithermesially or distally,a screw-retained designpermits a framework that better
withstandsthe cyclic loading ofocclusion and subse-quent problems with porcelain
fracture orother material failure.Screw-retained pros-theses require an entirely
passive fit.It isconsiderably more difficult to create a pas-sive-fitting screw-
retained framework thana cemented framework that has intimate fitwith the
supporting abutments.Conversely,it becomes occasionally necessary to per-form angle
correction as there is frequentdisparity between the long axes oftooth tothe long
axis ofbone available in the anteri-or maxilla.An intimate fit ofFPDs is fareasier
to achieve with a cemented prosthet-ic design than with a screw-
retainedrestoration.The subtle inaccuracies ofimpression making,alloy
casting,andFIGURE14-25Screw-retained restorations inthe esthetic area require more
attention to place-ment orientation and hygiene.FIGURE14-26Aand B,Diagnostic cast
and wax-up ofmissing maxillary anterior teeth.ABFIGURE14-27Surgical stent gives an
indicationofthe location and amount oftissue loss.
262Part 2: Dentoalveolar Surgeryporcelain application make the simultane-ous and
coincident fit ofscrew-retainedFPDs difficult;thus,a cemented prostheticdesign is a
more appropriate choice.With acemented design,the creation ofa surgicalstent is
critical for accurate placement andesthetic success ofthe implant restoration.After
placement and uncovering oftheimplants,it is prudent to create
provisionalrestorations to develop soft tissues.84Onlyin this way can an acceptable
esthetic out-come become predictable in the estheticzone.FPDs in the Anterior
MandiblePlacement ofmultiple-unit restorations inthe anterior mandible requires
similarforethought as with the anterior maxilla.Placement ofmultiple implants in
theanterior mandibular area presents aunique challenge in that one-to-
onereplacement ofteeth with implants cancreate proximity concerns (Figure 14-
28).Tarnow and colleagues have outlined thepattern ofbone loss to be about 3 mmfrom
the edge ofthe implant to an adja-cent implant.8Therefore,placement ofimplants
closer than 3 mm to each othercreates accelerated bone loss patterns inthese
areas.This pattern seems to be some-what less (about 2 mm) when the implantabuts a
natural tooth.Since the anteriormandible is mostly composed ofdensecompact bone,an
implant-to-toothreplacement ratio of1:2 may be acceptableas long as the crown-to-
implant lengthratio is 1:1.Gingival adaptation in theanterior mandible is not as
critical as it isin the anterior maxilla because phoneticsare primarily made in
relation to the max-illa.Screw-retained designs for FPDs inthe anterior mandible
seem to work well(Figure 14-29).Implant proximity shouldalso be assessed prior to
placement forhygiene procedures as the placement ofeven an appropriate number
ofsmall-diameter implants in this area can createhygiene difficulties.FPDs in the
Posterior MaxillaPlacement ofimplants in the posteriormaxilla requires sufficient
bone buccallyand lingually as well as inferior to the max-illary sinus.In
general,12 mm ofbone inactual height is the minimum required for amacroretentive
screw-type implant to ade-quately support occlusal forces.After theloss ofa tooth
in the posterior maxilla,thisrequired dimension might not be available(Figure 14-
30).Progressive enlargement ofthe maxillary sinus is often seen after toothloss as
well as residual ridge resorption.Diagnosis ofeither ofthese problems helpsone
determine the appropriate treatment.Ifpneumatization has taken place,sinus aug-
mentation procedures can be indicatedeither with concomitant or delayed
implantplacement.Residual ridge resorption ortraumatic destruction ofalveolar bone
bytrauma or periodontal disease may alsohave taken place.In these cases,onlay
bonegrafting may be a more appropriate treat-ment (Figure 14-31).The decision
toreplace a posterior maxillary quadrant withindividual crowns versus fewer
splintedimplants acting as an FPD may be related tothe length ofimplant or the
presence ofnatural canine teeth with cuspid-protectedocclusion (Figure 14-32).85In
general,hor-izontal forces acting on implants are con-sidered destructive.86,87It
is desirable to usethese implants as a vertical stop in thechewing cycle.Iflateral
components ofthechewing cycle are unavoidably placed onthe implant
restorations,they should besplinted together.Other strategies place theimplants in
a slightly staggered configura-tion from buccal to lingual and then splintthem
together.Screw-retained designs seemto allow retrievability and offer advantagesfor
modifying hygiene and performingreparative ceramometal procedures.FPDs in the
Posterior MandibleAs with the posterior maxilla,tooth lossfor an extended time can
result in residualridge resorption.In such cases onlay bonegrafting may provide an
appropriate bonevolume for implant installation.A limitingfactor for implant
placement in the poste-rior mandible is not only residual ridgeresorption but also
relative position oftheinferior alveolar canal.Panoramic radi-ographs may give a
full appreciation oftheposition ofthe inferior alveolar canal.Insome patients this
may assume a relativelyhigh position making placement ofFIGURE14-28Placement oftwo
implants instrategic locations to permit hygiene access andforce
distribution.FIGURE14-29Aand B,Screw-retained prosthesis permits hygiene access.AB
Implant Prosthodontics263implants ofreasonable length impossible.In these cases
lateral positioning oftheinferior alveolar nerve with implant place-ment may be the
only option for treatmentother than a removable partial denture.Nerve repositioning
is an effective adjunctin implant placement,but the techniquecan have significant
adverse nerve injury(Figure 14-33).88Cantilevered FPDsCantilevered fixed prostheses
may be usedin implant dentistry provided there is ade-quate length to the
supporting implantsand limited distance to the cantilever.Thismay be especially
useful when there is aninsufficient amount ofbone or when sig-nificant site
morbidity may result.Posteri-or cantilevering probably is a more com-mon
scenario,typically owing to a greateravailability ofbone in the anterior area ofthe
jaws.Anterior cantilevering may beused in areas where posterior anchorage
issuperior to anterior anchorage (Figure 14-34).Cantilevering requires that a
frame-work be connected at a maximum clampforce;such stability is best achieved
withscrew-retained frameworks.Occlusal con-tact created on the pontic should be
verylight to coincident.Restorations for the EdentulousPatientImplant-Retained
OverdenturesThose over 65 years ofage are said to rep-resent a significant
proportion ofthe USpopulation,and the average life expectan-cy has risen by 30
years since 1900.89Thisis due mostly to the increase in medicaladvances and
critical care.A sizable por-tion ofthis group is edentulous or partial-ly dentate
in at least one arch.90Many inthis age group have difficulty wearingmandibular
complete dentures owing topoor support and retention precipitatedby advanced bone
resorption,xerostomia,loss ofattached keratinized tissue,andneuromuscular
degeneration.The use ofimplants for these edentulous patients hasbeen shown to
actually preserve existingbone as opposed to results with conven-tional
dentures.91Increased support andanchorage can be improved with the use ofat least
two osseointegrated implants inthe anterior mandible.The use ofstudattachments
connected to the implantscan be a cost-effective measure to
improveretention,stability,and support (Figure14-35).Ifa stud-retained denture
isplanned,the implants should be as parallelFIGURE14-31Cranial onlay bone graft in
theposterior maxilla.(Image courtesy ofLeon F.Davis,DMD,MD)FIGURE14-32Individual
fixed units protect-ed from canine rise in lateral excursions.FIGURE14-33Placement
oftwo implants in theposterior mandible after inferior alveolar
nervetranspositioning.FIGURE14-35Stud-retained overdenture usingO-ring
attachments.FIGURE14-30Alveolar bone loss resulting inthe need for an onlay bone
graft prior to implantplacement.FIGURE14-34Anterior cantilever fixed
partialdenture.
264Part 2: Dentoalveolar Surgeryas possible to avoid premature wear oftheattachment
mechanism.The verticalheight ofthe attachment should be con-sidered as some
edentulous mandibulararches do not provide > 4 mm ofrestora-tive dimension for the
mandibular den-ture.Preoperative planning calls for theevaluation ofthe patient�s
present difficul-ty.Reasonable esthetics,occlusion,andextension should be evaluated
first.Ifthese factors seem to be appropriate,panoramic radiographs and possibly
anocclusal radiograph are helpful in deter-mining the position ofthe mental forami-
na.A prime objective is to place at leasttwo implants as far apart as possible
with-in this area.The anterior loop ofthe infe-rior alveolar nerve can extend as
far for-ward as 7 mm prior to exiting the mentalforamen;thus,consideration should
begiven to proper site selection.92A radi-ographic marker such as a piece
offoiltaken from a film packet or a standardizedstainless steel shot can be secured
to thepatient�s denture and placed in the mouthprior to panoramic and/or occlusal
radi-ography.This will give an indication ofthecorrect site selection for implants
in theanterior mandible.After the site has beenselected,an open channel can be
created inthe stent to allow surgical latitude.Eitherduplication ofthe patient�s
denture or awax trial tooth subsequently processed inclear acrylic resin can be
helpful in deter-mining the position.In general,taperedarch forms with extensive
resorption maydirect placement ofimplants in closeproximity to each other.In other
words,implants placed < 20 mm apart may notbe mechanically advantageous for
useindependently as stud attachments.Inthese cases,it may be desirable to
connectthe implants with a bar attachment to cre-ate a wider base ofanchorage
(Figure 14-36).There are several reasons to plan theimplant-retained denture for a
bar attach-ment.First,short (10 mm or less)implants or implants placed in
cancellousbone or types 3 and 4 bone,not typicallyseen in the anterior mandibular
area,maybe better supported by the splinting effectofa bar attachment.Second,non-
parallelimplants create different paths ofinser-tion,which subsequently serve to
wear anddisable the stud attachment prematurely.In these cases the bar attachment
can cor-rect this problem by providing a singlepath ofinsertion.Third,implants
placedin close proximity to each other may pro-vide better anchorage to the
overdenture ifa bar attachment is incorporated thatplaces the attachment mechanism
at awider base than the interimplant distance.There are some spatial
considerationsofusing a bar attachment that should beevaluated prior to treatment
planning.The vertical height needed for a barattachment can approach 11
mm.Thismeasurement is taken from the occlusalplane to the highest point ofthe
alveolarprocess.This distance will provide for theheight ofthe bar (2 to 4 mm),2 mm
underthe bar for maintenance ofhygiene,and atleast 7 to 8 mm ofrestorative material
inthe overdenture (usually acrylic resin)(Figure 14-37).Implant-retained
overdentures for themaxilla should always incorporate the useofbar attachments.The
literature citespoor long-term success for lone-standingimplants supporting
overdentures in themaxilla.A minimum offour implants inthe anterior maxilla
splinted with a barseems to be appropriate treatment.When-ever possible,cross-arch
stabilization ispreferred for maxillary implant-retainedor supported
overdentures.In these casesit may be prudent to also incorporate fullpalatal
coverage to assist with some resid-ual load transfer to the hard
palate.Theprosthetic treatment ofthese implantcases is assimilated to the Kennedy
Class Ipartially edentulous arch in that stress-breaking attachments and stress
distribu-tion to the soft tissue support posteriorlyare important
considerations.Implant-Supported OverdenturesImplant-supported overdentures may
beindicated when a patient has significant dif-ficulty in all factors
ofsupport,retention,and stability.Anatomically there may because to suspect that
extensive resorptionhas taken place that has resulted in the lossofalveolar
structure.Consequently,implantanchorage can be used to aid in the supportand
retention ofoverdenture prostheses.Historically,most ofthe literatureavailable on
implant-supported restora-tions in the mandible has been planned forfour to six
implants intraforaminally.93,94More contemporary literature suggests theuse offour
widely spaced implants in thisregion opposing an edentulous arch withequally
successful rates.95,96The strategy forusing implants in the anterior
mandibularFIGURE14-36Bar-retained denture using dis-tal attachments to widen the
retentive base.4�5 mm2�4 mm1�2 mmFIGURE14-37Minimum clearances needed fora bar-
attached overdenture.
Implant Prosthodontics265area allows segments to be cantileveredposteriorly in
accordance with the antero-posterior spread ofthe implants.97On aver-age,this
equates to 10 to 20 mm or to thearea ofthe lower first molar.98,99The deci-sion to
extend the cantilever can be basedon the arch form ofthe
fixtures,fixturelength,anterior cantilevering,natural max-illary dentition,and
parafunctionalhabits.100Favorable factors for extension ofthe cantilever are a
tapered arch with longfixtures,no anterior cantilevering,edentu-lous maxillary
arch,and no parafunctionalactivity.The most posterior implant sup-ports a load
typically ofcompression incomparison to the anterior fixtures,whichare placed under
tension.Also,themandible may be viewed as a dynamic bonystructure undergoing
flexure.101This canapproximate 2 mm at the mandibular angleupon maximum opening.For
this reason,implants placed distal to the foramenshould not be rigidly connected to
the con-tralateral side.102,103Implants planned forsupport ofa prosthesis in the
edentulousmaxilla should involve at least eight fix-tures.This may require the use
ofsinusaugmentation or extended-length implantsinto the zygomatic process.The use
ofcan-tilever extensions in the maxilla should belimited to 10 mm.104Attachment
mechanisms for implant-supported overdentures can range fromthe simple to the
sophisticated.Bar-clipattachments are a cost-effective and pre-dictable means
ofconnecting implants.More sophisticated milled-bar andplunger attachments can be
precisionmethods in telescopic placement ofaremovable prosthesis.The milled bar
canbe machined to a 2�taper,allowing a pre-cise path ofplacement (Figure 14-
38).Theunderside ofthis overdenture has a castmetallic housing that acts as a guide
overthe milled-bar attachment (Figure 14-39).Usually this restoration contains
eitherplunger or swivel attachments that lockthe overdenture as it comes to
completeplacement over the bar attachment.Thistechnique is very effective but can
allow asmall degree ofmicromovement.An additional method ofelectricaldischarge
machining,also known as sparkerosion,can be used in these cases;itresults in a
precise fit between the super-structure and bar.This technology,whichresults in an
essentially detachable fixedbridgework,may be prohibitive in costs.This three-level
treatment in an edentu-lous patient has predictable results.Fixed Detachable
ProsthesesOne alternative treatment method for anedentulous mandible is the use ofa
hybriddenture also known as a fixed removablerestoration.This restoration contains
ascrew-retained metal framework with aveneer ofacrylic resin and denture teeth,thus
earning the term hybrid.Suchrestorations are fixed and are not remov-able by the
patient;however,they do allowadequate room for oral hygiene proce-dures (Figure 14-
40).As might be expect-ed,no denture flange is present and aminimum vertical
restorative space of15mm is necessary for structural integrityand hygiene
access.Placement ofimplantsfor a hybrid denture must incorporate theuse ofa
surgical stent as the exit sites forthe access channels are critical.The sur-geon
may be cautioned against using ahybrid denture in those patients with askeletal
Class III or severe Class II rela-tionship as revealed by
cephalometricradiography.Access to channel locationand cantilevering and
maintenance ofhygiene would be the resultant problems ifused in these
patients.Recently,applicationofthis immediate-load and immediate-restoration
technique has become popu-lar.Prefabricated versions ofthe tech-nique have also
enjoyed widespreadsuccess.Chapter 13,�The ZygomaImplant,�elaborates on this
topic.Ofcourse,a full-arch ceramometalrestoration could also be used in these cir-
cumstances in which a minimal restorativedimension exists.In this
circumstancescrew-retained prostheses would offer sta-ble occlusal support while
allowing somedegree ofposterior cantilevering.Treating patients with an
edentulousmaxilla is dependent upon a number offactors.The primary determining
factor isFIGURE14-38Bar attachment milled to a 2�taper for implant-supported
overdenture.FIGURE14-39Precision detachable overden-ture with attachments for
engaging the bar.(Prostheses courtesy ofNorthshore Dental Labo-
ratory,Lynn,MA)FIGURE14-40Mandibular hybrid denture.
266Part 2: Dentoalveolar Surgeryone ofavailable space.Generally,the morespace
available (13+ mm vertically),themore indication there is for an overden-ture
prosthesis.Incipient resorption orminimal space availability (9�12 mm ver-tically)
may indicate the use ofa ceramo-metal design (Figure 14-41).Implant-supported
maxillary overdentures arefrequently used in cases ofmoderate tosevere resorption
as they replace not onlymissing mastication and esthetics but alsophonetic
physiology as well.Speech pro-duction may rely heavily on adaptation ofthe
prosthesis to the palatal gingiva.Thisis best accomplished with an
overdentureprosthesis to seal this linguoalveolar areaphonetically.Attachment
mechanisms forthe maxillary implant-supported over-denture are the same for the
mandibularoverdenture with the exception ofplungeror locking attachments placed
palatally(Figure 14-42).Contemporary TechniquesImmediate PlacementImmediate
placement ofimplants intoextraction sockets has been considered forsome
time.Although it has been per-formed successfully,inflammation andinfection should
be eradicated for pre-dictable osseointegration to occur.Con-siderations for using
immediate placementcapitalize on the osteogenic potential ofarecent extraction site
and the chance topreserve what bone remains.105,106The useoftapered implants in
these sites hasbecome popular to obliterate the socketdefect while being firmly
anchored in themajority ofthe bony walls.A word ofcau-tion is advised for those
teeth that havedrifted or are not in an ideal location astooth position influences
implant posi-tion.Indications for placement into arecent extraction socket are
freedom frominfection and reasonable orientation ofthe existing tooth.Ways
offacilitating thistechnique may incorporate orthodonticextrusion to create a
smaller socket in thebone,facilitating extraction,and overcor-recting bone
apposition to recreate miss-ing architecture (Figure 14-43).107Theextrusion should
take place slowly,usuallyover 3 to 6 months.Surgical Installation
StabilityInstallation ofimplants into bone usuallyis characterized by minimizing
the inher-ent gap between the implant and bonesurface.Although this can be accom-
plished with both screw-type and press-fitimplants,parallel- and tapered-
walledscrews are uniquely suited to providingfirm stability at surgical
placement.108�110This becomes an important considerationwhen achieving
osseointegration underplacement either in an extraction site,where a provisional
restoration will also beinserted,or where other implants will bejoined for an
immediate-load prosthesis.For immediate placement after extraction,the socket
should be obliterated by theimplant and/or grafting materials.Micro-movement in
excess of50 to 75�m hasbeen shown to inhibit osseointegration toa fibrous tissue
deposition instead ofboneapposition111;therefore,occlusion placedon a provisional
restoration during thecritical period ofosseointegration must becarefully
controlled to eliminate this sce-nario.Interproximal contact with adjacentteeth
should also be eliminated.Ifthismodality is desired,a more controlledtechnique
ofprotecting the occlusion witha centric relation splint orthotic may
beappropriate.Immediate loading for singleteeth mandates more data before it can
berecommended for routine use.However,controlled immediate loading
ofmultipleconnected implants in the anteriormandible has been favorably surveyed
andcan be cautiously recommended as long asthere are careful control ofocclusion
andpassive splinting frameworks.112Immediate RestorationImmediate restoration ofa
single-toothimplant may be incorporated in theesthetic zone (Figure 14-44).The
indica-tions are freedom from occlusal overloadand lateral forces.Sometimes,it is
difficultto control occlusion,and the creation ofan occlusal splint may be a
prudent way toprotect the implant while osseointegrationFIGURE14-41Full-arch
ceramometal fixedprosthesis cemented on custom fixed abutments.(Prostheses courtesy
Steven LoCascio,DDS )FIGURE14-42Swivel latches placed to thepalatal aspect for a
maxillary spark erosion over-denture prosthesis.FIGURE14-43Orthodontic extrusion
ofa non-restorable tooth to aid with migration ofthesoft/hard tissue as well as
atraumatic rootremoval.
Implant Prosthodontics267takes place (Figure 14-45).The advantagesofimmediate
restoration are the establish-ment and preservation ofthe periimplanttissues.It is
easier to preserve this tissuethan to recreate it by using a stagedapproach.Usually
provisional restorationsare placed upon single or multiple unitsduring
osseointegration.Immediate LoadSingle-Tooth ProsthesesStudies ofimmediately loaded
single-toothimplants are not widespread.However,data taken from a selected number
ofstudies indicate an 85% success rate onsingle-tooth prostheses in the
anteriormaxilla and other areas.113�115More dataare needed before this can be
recom-mended as a standard treatment.Protec-tion ofthe implant from overloading
iscritical as osseointegration is interruptedat 50 to 150 �m ofrepeated move-
ment.111,116Therefore immediately loadedimplants should be kept free from inter-
proximal contacts as deflection mesiodis-tally can also promote micromovement.Fixed
or Overdenture ProsthesesTheuse ofsplinted implants immediatelyloaded in the
mandibular anterior regionhas been discussed by Schnitman and col-leagues,117Henry
and Rosenberg,118Randow and colleagues,119and others.120Results indicate a
favorable response.Infact,the Novum System (Nobel Biocare,Yorba Linda,CA) is a
prefabricated imme-diate-load fixed denture system that enjoyswidespread success
(Figure 14-46).121TheNovum System is discussed in Chapter 13,�The
ZygomaImplant.�Controlled load-ing ofsplinted implants in the mandibleusing other
techniques has producedfavorable results,especially when theinstallation torque
exceeds 45 Ncm.Pas-sive retentive bar attachments are the req-uisite because
loading is accomplishedmore effectively with mutual support ofmultiple
implants.Maxillofacial ProsthesesPatients treated for tumor ablative surgeryofthe
oropharyngeal area may have a sig-nificant deficit ofanatomic structures nec-essary
for oral function.The incidence oforal cancer approaches about 5% ofallnew cancers
diagnosed in the US generalpopulation.122A significant number ofthese patients are
treated for malignantneoplasms ofthe lip,tongue,oropharynx,mandible,maxilla,soft
palate,larynx,external ear,orbit,and external nose.Tosuccessfully eradicate
disease,thesetumors are treated with multimodal ther-apy oftumor ablative
surgery,radiothera-py,and chemotherapy.The highest inci-dence ofthis disease
afflicts thoseindividuals with significant risk factors ofexcessive use ofalcohol
and tobacco,andother factors such as ultraviolet light expo-sure and infection with
human papilloma-virus.A common site ofdevelopment ofsquamous cell carcinoma is seen
in thelower lip and ventrolateral tongue.Occa-sionally,this disease expands by
directextension to involve structures ofthemandible and maxilla.Mandible
DefectsResection ofa portion ofthe mandiblemay be necessary to control disease
andmay create a discontinuity defect.Sincethe mandible is so integral to oral
physiol-ogy,it is desirable to preserve function asmuch as possible.Ifa marginal
mandibulectomy isperformed,the remaining mandible maybe reconstructed with
osseointegrateddental implants.Preservation ofthe infe-rior alveolar nerve may
preclude place-ment ifthere is minimal bone availableabove the canal position to
stabilizeimplants (Figure 14-47).In these casesFIGURE14-44Aand B,Nonrestorable
fractured tooth replaced with an immediate implant.ABFIGURE14-45Use ofocclusal
splint to protectan immediately placed implant/restoration insite no.9.Note that
the splint is relieved fromcontacting tooth no.9.FIGURE14-46Novum restoration
(Nobel Biocare,Yorba Linda,CA) installed into an edentulousmandible.
268Part 2: Dentoalveolar Surgeryeither nerve transposition or onlay bonegrafting
may serve to provide osseointe-grated rehabilitation.Ifmandibular con-tinuity is
not preserved with resection,itmay be desirable to reconstruct the areawith an
autologous or alloplastic graft.Autologous grafts offer a greater volumeofviable
bone with progenitor cells capa-ble ofcreating a more favorable environ-ment for
osseointegration.Nonvascular-ized or vascularized osteomyocutaneousflaps can be
used for reconstruction.Inpreviously operated fields it may bepreferable to use a
vascularized flap thatmay offer a secure opportunity for thegraft to remain viable
since the bloodsupply is preserved.The iliac crest hasbeen used with some degree
ofsuccessfor mandibular defects and some maxil-lary defects as well.Introduced by
Hidal-go,the use offibular grafts has alsoshown a promising degree ofsuccess
inreconstruction ofthese complexmandibular defects.123,124Being anon�weight-bearing
bone,the fibula is ofreasonable dimension to functionallyand cosmetically
reconstruct themandible.Bicortical stability for con-comitant or delayed implant
placementcan be also well obtained at surgicalinstallation,and long-term success
hasbeen observed (Figure 14-48).125Thechoice ofwhether to use either a section-al
overdenture design or a screw-retainedfixed prosthesis may be based on theamount
oftissue missing,the function ofthe tongue,peri-oral scarring,and adja-
cent/opposing occlusion.Frequently,thecrown-to-implant ratio is seen to be > 1:1
(Figure 14-49).Passive splinting ofthese implants is crucial to their long-term
success,and close attention must bepaid to development ofthe
occlusalscheme.Occasionally,it may be neces-sary to perform soft tissue revision
pro-cedures ifthe skin pedicle is thick or ifagreater vestibular depth is
needed.Thisensures soft tissue health and visibilityfor hygiene
procedures.Maxillary DefectsThe maxilla may require resection fortumor
control,which creates a host ofproblems related to speech and esthetics.Traditional
resection ofthe maxillainvolves an infrastructure procedure,ormay involve the
medial portion or a totalremoval ofthe maxilla.Infrastructuremaxillectomies are
used to control incip-ient disease ofthe oral cavity and havebeen classified by
Aramany based on fre-quency ofoccurrence.126Obviously,themore teeth,bone,and soft
tissue avail-able,the easier prosthetic rehabilitationcan be
employed.However,edentulouspatients requiring this operation mayhave significant
difficulty in obtainingstability with their prosthesis,and inthese cases a
consideration for the use ofimplants is warranted.The use ofsinus augmentation has
beenwell documented and deemed to be success-ful with the incorporated use
ofimplants.127,128This technique may be usedon a nondefect side where a unilateral
or pos-terolateral defect ofthe opposite side is pre-sent.Splinting ofapproximately
four or fiveimplants with a stress-breaking bar is gener-ally suggested and
provides the patient with aretentive stable prosthesis that may offerimproved
support as well (Figure 14-50).Recently the use ofzygomatic implants hasbeen
suggested as an alternative to sinus lift-ing.129,130The implant protocol for
zygomat-ic implants mandates bilateral placement,and preservation ofthe defect side
oftheinfraorbital rim may improve surgical stabil-ity.131Both ofthe techniques
require a screw-retained bar attachment to be made with theobturator (Figure 14-
51).Craniofacial DefectsResection ofportions ofthe craniofacialskeleton for disease
control can result inFIGURE14-47A,Mandible with insufficient supracanal height for
implant installation.B,Iliac crest graft tomandible stabilized by placement
ofosseointegrated implants.(Surgery performed by Michael Miloro,DMD,MD)ABFIGURE14-
48Implants placed into a vascular-ized fibula graft to the mandible.(Surgery per-
formed by Perry Johnson,MD,and MichaelMiloro,DMD,MD)FIGURE14-49Mandibular fixed
partial den-ture supported by a vascularized fibular graft inthe patient viewed in
Figure 14-48.
Implant Prosthodontics269both functional and esthetic defects.Thesedefects may not
be suited to plastic surgi-cal reconstruction owing to local orregional
factors.Traditional roles for pros-theses are to replace architecture with allo-
plastic materials that mimic the color andtextures ofadjacent skin.A method
ofretaining these prostheses can be attach-ment by medical-grade adhesives,whichmay
be unpredictable in holding and irri-tate underlying soft tissues.In suchinstances
the use ofosseointegrated tech-nology can provide similar anchorageused
intraorally.The rates ofsuccess in thecraniofacial skeleton ofimplants are alsowell
documented and should be plannedout with specialized imaging.132�134Three-
dimensional reconstruction techniquesmay provide valuable information to max-imize
success ofplacement exclusively inthe confines ofintended site
selection.Thetemporal bone is probably the best pre-dictable site for the placement
ofimplantsin comparison to frontal nasal areas.135This is true even ifradiation has
been usedto treat malignant tumors in this area.Thechoice ofa minimum oftwo
splintedimplants in the temporal bone can servewell to provide a bar-retained
prosthesis.Work-up should include computed tomo-graphic images with 2 mm axial cuts
whilea radiographic stent is worn (Figure 14-52).136This should affirm site
selection aswell as placement into sound bone.Bone-anchored hearing aids (BAHAs)
can beused as well in treating patients withTreacher Collins syndrome or other
formsofauditory agenesis.Placement ofimplants into frontalnasal bone is possible
with the use ofspe-cialized computer software to delineatethe frontal
sinus,anterior cranial fossa,orbit,and other vital structures adjacentto proposed
site selection.Extraoralanchorage can in some cases assist withanchorage ofan
intraoral prosthesis aswell (Figure 14-53).Radiotherapy ConcernsUnlike elective
implant placement,thereare particular concerns when providing apatient with
osseointegrated anchorage incases in which optimal oral function isessential
following tumor ablative surgery.Judicious use ofinterdisciplinary preop-erative
planning helps in deciding whichcases may be appropriate for osseointe-grated
implants.This becomes criticalwhen consideration is given to the relativerisks
ofcomplications after radiotherapyto the head and neck.As with any onco-logic
case,radiation therapy may beincorporated to improve long-term sur-vival.Because
ofabsorptive changes in theosseous tissues,osteoblast populations aretypically
affected by dosages exceeding 50 Gy.The possibility ofcreating osteora-dionecrotic
wounds increases with bonemanipulation above this dosage.However,osseointegrated
implants have been suc-cessfully employed in previously radiatedfields without
undue complications.137Hyperbaric oxygen therapy has beenobjectively shown to
reduce the risk ofosteoradionecrotic complications in boththe craniofacial skeleton
and intraoralregions.138As with any hypoxic wound,increasing oxygen tension above
40 PO2incomparison to a nonradiated control siteincreases the likelihood
ofhealing.Withthis increase ofO2concentration comesangioneogenesis and the
subsequenteffect ofpleuripotential cell differentia-tion into
osteoblasts.ComplicationsSoft Tissue Complications Soft tissue complications with
dentalimplants can be seen in areas where thequantity ofkeratinized soft tissue is
FIGURE14-50Aand B,Implants placed in the nondefect side ofa sinus-lifted
maxilla.Reproducedwith permission from Salinas TJ,Guerra LR,Rogers WA.Aesthetic
considerations for maxillary obtu-rators retained by implants.Pract Proced Aesthet
Dent 1997;9:265�76.ABFIGURE14-51Aand B,Implant-retained obturator using two
zygomatic and one pterygoid implant.AB
270Part 2: Dentoalveolar Surgeryminimal.As with natural teeth,implantrestorations
rely on attached and kera-tinized tissue for long-term maintenance.Soft tissues may
also be compromised insites where implant angulation is not idealin an esthetic
area.Finally,soft tissuedepths surrounding implants exceeding 5 to 6 mm may present
problems withlong-term maintenance.This can be espe-cially true for areas grafted
with soft tis-sues or in osteomyocutaneous flaps wheredermis is quite thick.In
these cases it maybe wise to reduce the soft tissue thicknesssurgically prior to
making a restoration oreven placing the implants.Radiographic Bone LossBone loss is
expected with the placementofany implant;however,this loss shouldnot exceed 1.5 mm
in the first 12 to 18 months.Bone loss in excess ofthisvalue exposes a significant
portion oftheimplant surface,making hygiene proce-dures difficult.Ifthe choice
ofimplant is amachined titanium screw,this problem isless than with implants having
a texturedsurface,but in either case it is desirable tosee bone loss ofno more than
0.2 mm/yr.Evaluation ofimplants in edentulouspatients by panoramic radiography
maybe more formidable than when using peri-apical
examinations.However,partiallydentate patients may benefit from periapi-cal
radiographs made with a silicone puttystandardized bite block.In this way radi-
ographs would be standardized at eachexposure,allowing interpretation at a con-
sistent incident beam angle.Screw LooseningAbutment and prosthetic screw
looseningcan be a recurrent problem seen often withsingle-tooth restorations.The
incidence ofscrew loosening is sizable in cases restoredwith standard external hex
platforms andgold screws.A method ofreducing screwloosening is to use a new
abutment orprosthetic screw,torque once to the rec-ommended torque application,wait
5 minutes,and then torque again.139Inthese circumstances screw loosening
isminimized.Repeated loosening ofscrewsshould bring to mind occlusal overload,heavy
contact in lateral excursions,orimplant mobility.Abutment FractureAbutment fracture
is a relatively uncom-mon occurrence but can be problematic,particularly for
cemented restorations.Material choices for implants subjected toheavy occlusion or
unavoidable lateralloads should be carefully selected.Although strong,ceramic
materials areused with caution in areas ofhigh stressapplication.Pre-machined
abutmentsused for screw-retained restorations canusually be replaced ifthey
fracture.Porcelain FracturePorcelain fracture is sometimes seen withimplant
prostheses owing to dynamicfatigue or contact overload.140Propriocep-tive feedback
is not present with implantrestorations and impacts during the chew-ing cycle
should be slightly less than thoseofnatural teeth.This can be verified using0.001-
inch stainless steel shimstock.Resin Base FractureResin base fractures are fairly
commonoccurrences because ofunfavorable stressdistribution,occlusal overload,and a
lackofproprioception.The incidence canrange from 1 to 16% over 5 years.141Waysto
combat this problem are to reinforce thebase with a cast metallic
housing.141Maintenance Patients restored with osseointegratedimplants should
receive regular and fre-quent follow-ups in the first year followingimplant
placement.Factors to evaluateFIGURE14-52Stent (A) and computed tomog-raphy scan
showing site selection (B) for implantplacement into temporal bone.ABFIGURE14-
53Facial and intraoral prosthesisanchored with two zygoma and three
endosseousimplants.
Implant Prosthodontics271include bone loss,mobility,and pain.Clinical examination
should include lightpercussion and gentle evaluation ofsofttissue,which may include
a standardizedperiimplant probing using nonmetallicstandardized force
probes.Radiographicevaluation includes both periapical andpanoramic
radiographs.Ifthe restorationis screw retained,it can be removed every2
years,cleaned,and resecured,or cleanedin position.Cleaning ofimplant and tita-nium
abutment surfaces should be donewith either gold or polyethylene
(Teflon)instruments so as not to scratch these bio-logically critical surfaces and
make themprone to plaque accumulation (Figure 14-54).142Any scratches or crevices
created bythis or other processes impose a nidus forplaque and calculus
accumulation.Aftercleaning,polishing with either toothpasteor a light prophylaxis
paste is recommend-ed.Since a perimucosal seal exists betweenthe implant and
abutment and tissue,it isnot suggested that cemented restorationsbe removed
routinely as this may jeopar-dize the integrity ofthe restoration andsurrounding
tissues.However,iftherestoration is retrievable,the prosthesisand/or attachment
should be removedevery 18 to 24 months for d�bridement,inspection,and
polishing.143Ifabutmentor coping screws have been torqued previ-ously,it is
generally suggested that they bereplaced to avoid future fatigue fracture.Success
CriteriaHistorically,the criteria ofsuccess haveinvolved one ofquantification
ofpain,mobility,and peri-implant radiolucency.These criteria were established by
Albrek-tsson and colleagues and remain one ofthe standards in long-term evaluation
ofdental implants.144Recently additional cri-teria have been added for the
assessmentofhard and soft tissue responses.Margin-al bone loss of< 4 mm or probing
depth of< 4 mm and a crevicular fluid flow rate of< 2.5 mm are considered
indicators ofsuc-cess.141Mobility,ifpresent,should be test-ed on an individual
basis to best assess atrue measure.Therefore,removing theprosthesis (especially
ifit is splinted withother implants) and gently percussingwith either a blunt
instrument or a stan-dardized torque instrument will give anindication
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Part 3MAXILLOFACIALINFECTIONS
CHAPTER 15Principles ofManagement ofOdontogenic InfectionsThomas R.Flynn,DMDThe
incidence,severity,morbidity,andmortality ofodontogenic infections havedeclined
dramatically over the past 60 years.In 1940 Ashbel Williams published a seriesof31
cases ofLudwig�s angina in which54% ofthe subjects died.1Only 3 yearslater,he and
Dr.Walter Guralnick pub-lished the first prospective case series inthe field ofhead
and neck infections,inwhich the mortality rate ofLudwig�s angi-na was reduced to
10%.2This dramaticreduction in mortality from 54 to 10% wasnot due to the first use
ofpenicillin in thetreatment ofthese infections.Rather,Dr.Guralnick applied the
principles ofthe ini-tial establishment ofairway security,fol-lowed by early and
aggressive surgicaldrainage ofall anatomic spaces affected bycellulitis or
abscess.Since then,with theuse ofantibiotics and advanced medicalsupportive
care,the mortality ofLudwig�sangina has been further reduced to 4%.3Dentistry has
made great progress inthe prevention and early intervention ofodontogenic
infections.Oral and maxillo-facial surgeons,as noted above,have madegreat strides
in managing and preventingmortality in severe odontogenic infec-tions.These
accomplishments,however,impose upon the oral and maxillofacialsurgeon the
obligation to remain intellec-tually prepared for the always unscheduledoccurrence
ofsevere odontogenic infec-tions by keeping one�s knowledge oftherelevant anatomy
and surgery fresh,andby remaining abreast ofcurrent develop-ments in the
microbiology and antibiotictherapy ofodontogenic infections.The late Dr.Larry
Peterson,whobrought the first edition ofthis text tofruition,articulated the
principles ofman-agement ofodontogenic deep fascial spaceinfections.These are eight
sequential stepsthat,iffollowed with thoroughness andgood judgment,will ensure a
high level ofcare for these increasingly uncommon,yetoccasionally life-threatening
infections.These principles outline the structureofthis chapter.The eight steps in
themanagement ofodontogenic infectionsare as follows:1.Determine the severity
ofinfection.2.Evaluate host defenses.3.Decide on the setting ofcare.4.Treat
surgically.5.Support medically.6.Choose and prescribe antibiotic
therapy.7.Administer the antibiotic properly.8.Evaluate the patient frequently.This
chapter will examine each ofthese principles in order and discuss andrelate current
knowledge to them.Step 1:Determine the Severity ofInfectionWithin the first few
minutes ofthe presen-tation ofa patient with a significant odon-togenic
infection,the surgeon should haveaccomplished the first three steps listedabove.A
careful history and a briefbutthorough physical examination shouldallow the
treating surgeon to determine theanatomic location,rate ofprogression,andthe
potential for airway compromise ofagiven infection.The host defenses,includ-ing
immune system competence and thelevel ofsystemic reserves that can be calledupon by
the patient to maintain homeosta-sis,are largely determined by history.Giventhis
initial database the surgeon must thendecide upon the setting ofcare,which willhave
a great influence on the outcome.The clinical presentation and relevantsurgical
anatomy ofinfections ofthe vari-ous deep fascial spaces ofthe head and neckhave
been well described in other texts.4,5The borders,contents,and relations
ofthevarious anatomic deep spaces that are like-ly to be invaded by odontogenic
infectionsare described in Tables 15-1 and 15-2.Three major factors must be consid-
ered in determining the severity ofaninfection ofthe head and
neck:anatomiclocation,rate ofprogression,and airwaycompromise.Anatomic LocationThe
anatomic spaces ofthe head and neckcan be graded in severity by the level towhich
they threaten the airway or vitalstructures,such as the heart and medi-astinum or
the cranial contents.The buccal,infraorbital vestibular,and subperiosteal
278Part 3: Maxillofacial Infectionsspaces can be categorized as having lowseverity
because infections in these spacesdo not threaten the airway or vital struc-
tures.Infections ofanatomic spaces thatcan hinder access to the airway due
toswelling or trismus can be classified as hav-ing moderate severity.Such
anatomicspaces include the masticatory space,whose components may be considered
sep-arately as the submasseteric,pterygo-mandibular,and superficial and deep tem-
poral spaces,and the perimandibularspaces
(submandibular,submental,andsublingual).Infections that have highseverity are those
in which swelling candirectly obstruct or deviate the airway orthreaten vital
structures.These anatomicspaces are the lateral pharyngeal andretropharyngeal,the
danger space,and themediastinum.Cavernous sinus thrombosisand other intracranial
infection also havehigh severity.In 1999 Flynn and colleaguesdevised a severity
score (SS) that assigned anumerical value of1 to 4 for involvementofeach ofthe
low,moderate,severe,orextreme severity anatomic spaces,respec-tively.6Table 15-3
lists the severity score foreach ofthe various deep fascial spaces.Thus,a patient
with cellulitis or abscess ofthe right buccal (SS = 1),right pterygo-mandibular (SS
= 2),and right lateral pha-ryngeal (SS = 3) spaces would have a totalseverity score
of6,which is the sum ofthevalues assigned to each ofthe threeanatomic spaces.Flynn
and colleagueswere able to explain by correlation analysis66% ofthe length
ofhospital stay with amodel that used the initial SS and the whiteblood cell count
on admission.6Table 15-1Borders ofthe Deep Spaces ofthe Head and
NeckBordersSpaceAnteriorPosteriorSuperiorInferiorSuperficial or Medial*Deep or
Lateral�BuccalCorner ofmouthMasseter m.,Maxilla,MandibleSubcutaneousBuccinator
m.pterygomandibular infraorbital spacetissue and skinspaceInfraorbitalNasal
cartilagesBuccal spaceQuadratus labii Oral mucosaQuadratus labii Levator anguli
oris m.,superioris m.superioris m.maxillaSubmandibularAnt.belly Post.bellyInf.and
med.Digastric tendonPlatysma m.,Mylohyoid,digastric m.digastric,surfaces
ofinvesting fasciahyoglossusstylohyoid,mandiblesup.constrictor mm.stylopharyngeus
mm.SubmentalInf.border ofHyoid boneMylohyoid m.Investing fasciaInvesting
fasciaAnt.bellies mandibledigastric m.�SublingualLingual surface
ofSubmandibularOral mucosaMylohyoid m.Muscles oftongue*Lingual surface
ofmandiblespacemandible�PterygomandibularBuccal spaceParotid glandLateral
Inf.border ofMed.pterygoidAscending ramus ofpterygoid
m.mandiblemuscle*mandible�SubmassetericBuccal spaceParotid glandZygomatic
archInf.border ofAscending ramus Masseter m.�mandibleofmandible*Lateral
pharyngealSup.and mid.Carotid sheathSkull baseHyoid bonePharyngealMedial pterygoid
m.�pharyngeal and scalene fasciaconstrictors andconstrictor mm.retropharyngeal
space*RetropharyngealSup.and mid.Alar fascia Skull baseFusion ofalar and� Carotid
sheath andpharyngeal prevertebral fasciaelateral pharyngealconstrictor mm.at C6-
T4space�PretrachealSternothyroid-RetropharyngealThyroid
cartilageSuperiorSternothyroid-Visceral fascia overthyrohyoid
fasciaspacemediastinumthyrohyoid fasciatrachea and thyroid glandAdapted from Flynn
TR.5ant.= anterior;inf.= inferior;lat.= lateral;m.= muscle;mm.= muscles;med.=
medial;mid.= middle;post.= posterior;sup.= superior.*Medial border;�lateral border.
Principles ofManagement ofOdontogenic Infections279Table 15-2Relations ofDeep
Spaces in InfectionsNeighboring Approach for SpaceLikely
CausesContentsSpacesIncision and DrainageBuccalUpper bicuspids Parotid
ductInfraorbitalIntraoral (small)Upper molars Ant.facial a.and
v.PterygomandibularExtraoral (large)Lower bicuspidsTransverse facial a.and
v.InfratemporalBuccal fat padInfraorbitalUpper cuspidAngular a.and
v.BuccalIntraoralInfraorbital n.SubmandibularLower molarsSubmandibular gland
SublingualExtraoralFacial a.and v.Submental Lymph nodesLateral pharyngeal
BuccalSubmentalLower anteriors Ant.jugular v.SubmandibularExtraoralFracture
ofsymphysisLymph nodes(on either side)SublingualLower bicuspids Sublingual
glandsSubmandibularIntraoralLower molars Wharton�s ductsLateral
pharyngealIntraoral-extraoralDirect traumaLingual n.Visceral (trachea andSublingual
a.and v.esophagus)PterygomandibularLower third molars Mandibular
div.ofBuccalIntraoralFracture ofangle oftrigeminal n.Lateral pharyngeal Intraoral-
extraoralmandibleInf.alveolar a.and v.SubmassetericDeep
temporalParotidPeritonsillarSubmassetericLower third molars Masseteric a.and
v.BuccalIntraoralFracture ofangle ofPterygomandibular Intraoral-
extraoralmandibleSuperf.temporal ParotidInfratemporal and Upper molars Pterygoid
plexusBuccalIntraoraldeep temporalInternal maxillary a.and
v.Superf.temporalExtraoralMandibular div.oftrigeminal n.Inf.petrosal
sinusIntraoral-extraoralSkull base foraminaSuperfical temporalUpper molars Temporal
fat padBuccalIntraoralLower molarsTemporal branch offacial n.Deep temporalExtraoral
Intraoral-extraoralLateral pharyngealLower third molars Carotid
a.PterygomandibularIntraoralTonsillar infection in Internal jugular
v.SubmandibularIntraoral-extraoralneighboring spacesVagus n.SublingualCervical
sympathetic chainPeritonsillar RetropharyngealAdapted from Flynn TR.4a =
artery;div.=division;inf.= inferior;n = nerve;superf.= superficial;v = vein.
280Part 3: Maxillofacial InfectionsRate ofProgressionUpon interviewing the patient
with aninfection,the surgeon can appraise therate ofprogression by inquiring about
theonset ofswelling and pain and comparingthose times to the current signs and
symp-toms ofswelling,pain,trismus,and airwaycompromise.In their study
ofhospitalizedodontogenic infections,Flynn and col-leagues found that the number
ofdays ofswelling prior to admission correlatednegatively with the initial severity
score.6This is probably because patients withmore severe and rapidly progressive
infec-tions were frightened enough to seek hos-pital care early on.Odontogenic
infections generally passthrough three stages before they resolve,the
characteristics ofwhich are listed inTable 15-4.During the first 1 to 3 days
theswelling is soft,mildly tender,and doughyin consistency.Between days 2 and 5
theswelling becomes hard,red,and exquisitelytender.Its borders are diffuse and
spread-ing.Between the fifth and seventh days thecenter ofthe cellulitis begins to
soften andthe underlying abscess undermines theskin or mucosa,making it
compressibleand shiny.The yellow color ofthe underly-ing pus may be seen through
the thinepithelial layers.At this stage the term fluc-tuanceis appropriately
applied.Fluctuanceimplies the palpation ofa fluid wave by onehand as the abscess is
compressed by theother hand.The final stage ofodontogenicinfection is
resolution,which generallyoccurs after spontaneous or surgicaldrainage ofan abscess
cavity.The swellingthen begins to decrease in size,redness,andtenderness.The
resolving swelling may stayfirm for some time,however,as the inflam-matory process
is involved in removingnecrotic tissue and bacterial debris.Table 15-4Stages
ofInfectionCharacteristicInoculationCellulitisAbscessDuration0�3 days3�7 daysOver 5
daysPainMild�moderateSevere and generalizedModerate�severe and
localizedSizeSmallLargeSmallLocalizationDiffuseDiffuseCircumscribedPalpationSoft,do
ughy,mildly tenderHard,exquisitely tenderFluctuant,tenderAppearanceNormal
colorationReddenedPeripherally reddenedSkin qualityNormalThickenedCentrally
undermined and shinySurface temperatureSlightly heatedHotModerately heatedLoss
offunctionMinimal or noneSevereModerately severeTissue
fluidEdemaSerosanguineous,flecks ofpusPusLevel
ofmalaiseMildSevereModerate�severeDegree
ofseriousnessMildSevereModerate�severePredominant
bacteriaAerobicMixedAnaerobicAdapted from Flynn TR.29Table 15-3Severity Scores
ofFascial Space InfectionsSeverity ScoreAnatomic SpaceSeverity score = 1 Vestibular
(low risk to airway or vital structures)SubperiostealSpace ofthe body ofthe
mandibleInfraorbitalBuccalSeverity score = 2Submandibular (moderate risk to airway
or vital structures)Submental Sublingual PterygomandibularSubmasseteric Superficial
temporal Deep temporal (or infratemporal)Severity score = 3 Lateral pharyngeal
(high risk to airway or vital structures)RetropharyngealPretrachealSeverity score =
4 Danger space (space 4)(extreme risk to airway or vital
structures)MediastinumIntracranial infectionThe severity score for a given patient
is the sum ofthe severity scores for all ofthe spaces involved by cellulitis or
abscess,based on clinical and radiographic examination.
Principles ofManagement ofOdontogenic Infections281A special note should be made
ofanespecially rapidly progressive infectioncalled necrotizing
fasciitis.Occasionallyfound in the head and neck,frequently dueto odontogenic
sources,necrotizing fasci-itis is a rapidly spreading infection that fol-lows the
platysma muscle down the neckand onto the anterior chest wall.Diabetesand
alcoholism have been shown to be sig-nificant predisposing factors,whereasmedical
compromise,delay in surgery,andmediastinitis are associated with
increasedmortality.7It can rapidly result in necrosisoflarge amounts
ofmuscle,subcutaneoustissue,and skin,resulting in severe recon-structive defects
(Figure 15-1).Similarprocesses may be involved in descendingnecrotizing infections
ofthe neck,whichfrequently progress to the mediastinum.The earliest signs
ofnecrotizing fasciitis aresmall vesicles and a dusky purple discol-oration ofthe
involved skin (Figure 15-2).Soon thereafter the skin may become anes-
thetic.Thereafter frank necrosis occurs.8A suspicion ofnecrotizing fasciitis is a
surgical emergency,requiring broad-spectrum antibiotics,repeated
surgicaldrainage,antiseptic wound packing,andintensive medical supportive
care,includ-ing fluids,calcium,and possibly bloodtransfusion.8Repeated surgical
d�bride-ment is the rule,not the exception.Hyperbaric oxygen therapy may also
beofbenefit.9Airway CompromiseThe most frequent cause ofdeath inreported cases
ofodontogenic infection isairway obstruction.Therefore,the surgeonmust assess
current or impending airwayobstruction within the first few momentsofevaluating the
patient with a head andneck infection.Complete airway obstruction is,ofcourse,a
surgical emergency.In such casesinsufficient or absent air movement inspite
ofinspiratory efforts will be apparent.In highly skilled hands one briefattempt
atendotracheal intubation may be made,buta direct surgical approach to the airway
bycricothyroidotomy or tracheotomy is morepredictably successful.In such extreme
cir-cumstances the presence ofinfection over-lying the trachea is less important
than theabsence ofventilation.Therefore,infectionin the region ofsurgical airway
access isnot a contraindication to an emergencycricothyroidotomy or tracheotomy.In
partial airway obstruction,abnor-mal breath sounds will be evident,consist-ing
ofstridor or coarse airway sounds sug-gestive offluid in the upper
airways.Thepatient may assume a special posture thatstraightens the airway,such as
the �sniffingposition,�in which the head is inclined for-ward and the chin is
elevated,as ifone weresniffing a rose.Other such postures includea sitting patient
with the hands or elbowson the knees and the chest inclined for-ward with the head
thrust anterior to theshoulders,which also straightens the air-way and may allow
secretions to drool out-ward onto the floor or into a pan.Occa-sionally a patient
with a lateral pharyngealspace infection will incline the neck towardthe opposite
shoulder in order to positionthe upper airway over the laterally deviatedtrachea
(Figure 15-3).Trismus is an ominous sign in thepatient suspected ofodontogenic
infection.A maximum interincisal opening that hasdecreased to 20 mm or less in a
patient withacute pain should be considered an infec-tion ofthe masticator space
until provedotherwise.Infections ofthe pterygo-mandibular space are sometimes
missedbecause trismus hinders the examiner�sview ofthe oropharynx.Therefore,it
isimportant for the examiner to position thepatient�s occlusal plane parallel to
the planeofvision and to orient a light coaxial to thatplane ofview.Then the
patient is asked tomaximally open the mouth in spite ofpain,and the tongue is
depressed with a mirroror tongue blade.This should allow theexaminer to get at
least a glimpse oftheposition ofthe uvula and the condition ofthe anterior
tonsillar pillars.The affectedtonsillar pillar will usually be edematousand
reddened,and it will displace the uvulato the opposite side (Figure 15-
4).Ifthesuspected site ofinfection is touched withthe mirror or tongue blade,acute
pain maybe elicited,especially as compared to theopposite side.The patient�s report
ofpainshould be distinguished from the gaggingthat is likely to occur.Various
clinical tests have been pro-posed with the aim ofpredicting
difficultintubation.The Mallampati test has beencorrelated with difficult
intubation by itsFIGURE15-1Necrotizing fasciitis.Large granu-lating skin defect
extending from the inferiorborder ofthe mandible to the clavicle,2 weeksafter
d�bridement.Reproduced with permissionfrom Flynn TR.15FIGURE15-2Necrotizing
fasciitis.Early stage,with swelling extending from the inferior borderofthe
mandible onto the anterior chest wall in a7-year-old boy.The chalky material on the
neckis calamine lotion that his mother used to treatthe vesicles ofpresumed contact
dermatitis due topoison ivy.Reproduced with permission fromFlynn TR.15
282Part 3: Maxillofacial Infectionsinitial proponent,as have trismus oflessthan 20
mm and decreased thyromental dis-tance.10,11These results,however,have notbeen
confirmed by independent examiners,although the combination ofan abnormalMallampati
test and a thyromental distanceofless than 5 cm has been correlated withdifficult
intubation in one study.11In airway obstruction,the respiratoryrate may be
increased or decreased;yet onefunctional method ofassessing the effec-tiveness
ofrespiratory efforts readily avail-able to the oral and maxillofacial surgeonis
the pulse oximeter.12An oxygen saturation ofbelow 94% inan otherwise healthy
patient is indeed anominous sign because it indicates insuffi-cient oxygenation
ofthe tissues due tohypoperfusion or hypooxygenation.Giventhe patient with
clinically apparent partialairway obstruction,an abnormally low oxy-gen saturation
is an indication for immedi-ate establishment ofa secure airway.Soft tissue
radiographs ofthe cervicalairway and chest can be quite valuable inidentifying
deviation ofthe airway laterallyon a posteroanterior film or anterior dis-placement
ofthe airway on a lateral view.These films can be taken fairly quickly,which can be
an advantage for radiographicexamination ofthe patient with a significantcervical
swelling.During prolonged periodsin the supine position,as required by theolder
generation ofcomputed tomography(CT) scanners,an infected swelling mayobstruct the
airway.On the other hand,thenewer high-speed CT scanners can obtain acomputerized
CT examination within sec-onds to minutes,which,ifavailable,wouldmake conventional
soft tissue radiographsobsolete (Figure 15-5).In a prospectivestudy Miller and
colleagues found 89%accuracy,95% sensitivity,and 80% specifici-ty in identifying
�drainable pus�by the com-bined use ofcontrast enhanced CT and clin-ical
examination.13By �drainable pus,�theauthors meant a collection of2 mL or
moreofpus.The high diagnostic yield thereforeofcontrast-enhanced CT and clinical
exam-ination makes this combination the methodofchoice for evaluation ofpotential
airwayobstruction,as well as characterizing thelocation and quality ofinfections in
thehead and neck.13Step 2:Evaluate Host DefensesImmune System CompromiseTable 15-5
lists the medical conditionsthat can interfere with proper function ofthe immune
system,which is,ofcourse,essential to the maintenance ofhostdefense against
infection.Diabetes is list-ed first because it is the most commonimmune-
compromising disease.Diabet-ics have the combination ofa whiteblood cell migration
defect,whichinhibits successful chemotaxis ofwhiteblood cells to the infected site
from theblood stream,and a vascular defect thatimpairs blood flow to small vessel
tissuebeds,especially in end organs such as thefoot.Orally,diabetics have an
increasedsusceptibility to periodontal infections.FIGURE15-5Axial computed
tomographyimage at the level ofthe hyoid bone,demonstrat-ing a cellulitis ofthe
left lateral pharyngeal spacethat is deviating the airway to the opposite sideand
spreading into the retropharyngeal space.Reproduced with permission from Flynn
TR.5Table 15-5Factors Associated withImmune System CompromiseDiabetesSteroid
therapyOrgan transplantsMalignancyChemotherapyChronic renal
diseaseMalnutritionAlcoholismEnd-stage AIDSFIGURE15-4Right pterygomandibular
spaceabscess.Note the swelling ofthe anterior tonsillarpillar and the deviation
ofthe edematous uvula tothe opposite side.Reproduced with permission fromFlynn TR
and Topazian RG.30FIGURE15-3Left lateral pharyngeal spaceabscess.Note the swelling
just anterior to thesternocleidomastoid muscle above the level ofthe hyoid bone and
the deviation ofthe headtoward the right shoulder,in an attempt toplace the upper
airway directly over the deviat-ed trachea.Reproduced with permission fromFlynn TR
et al.29
Principles ofManagement ofOdontogenic Infections283This disease also appears to
decrease hostresistance to more severe odontogenicinfections such as necrotizing
faciitis anddeep fascial space infections.The iatrogenic use ofsteroids
hasincreased over recent years with the use ofthese medications to treat
asthma,skin con-ditions,autoimmune diseases,cancer,andother inflammatory
conditions.Cortico-steroids appear to stabilize the cell mem-branes
ofimmunocompetent cells,therebydecreasing the immune response.Patientswith organ
transplants are often treatedwith corticosteroids,as well as otherimmunosuppressive
medications such ascyclosporine and azathioprine,to suppressorgan rejection
reactions.It has been postulated that everypatient with malignant disease has
somedefect ofthe immune system.The mecha-nisms ofimmune compromise in malig-nancy
are variable and not well identified,but the surgeon treating the patient
withongoing cancer should assume that thereis some defect ofthe immune
system.Cancer chemotherapy directly suppressesthe immune system along with
rapidlydividing cancer cells.Therefore,allpatients who have received
cancerchemotherapy within the past year shouldbe considered immunocompromised.Other
conditions that impairimmune function include malnutrition,alcoholism,and chronic
renal disease.The role ofhuman immunodeficiencyvirus (HIV) infection in
diminishinghost resistance to odontogenic infectionsis somewhat unclear and
paradoxical.HIV infection first and primarily dam-ages the T cell.On the other
hand,mostodontogenic infections are due to extra-cellular bacteria,which are
attacked by Bcells,the white blood cells that elaborateantibodies.Although HIV
infection maydamage B cells early in the course ofthedisease,its most devastating
effects areseen on the T cells,which explains theincreased rate ofcancers and
infectionsby intracellular pathogens in patientswith acquired immunodeficiency syn-
drome (AIDS) and pre-AIDS.Althoughpatients with HIV seropositivity maysuffer a more
intense and/or prolongedhospital course than other patients,HIVseropositivity does
not seem to increasethe incidence ofsevere odontogenicinfections.14Systemic
ReserveThe host response to severe infection canplace a severe physiologic load on
thebody.Fever can increase sensible andinsensible fluid losses and caloric require-
ments.A prolonged fever may cause dehy-dration,which can therefore decrease car-
diovascular reserves and deplete glycogenstores,shifting the body metabolism to
acatabolic state.The surgeon should alsobe aware that elderly individuals are
notable to mount high fevers,as often seenin children.Therefore,an elevated tem-
perature at an advanced age is not only asign ofa particularly severe
infection,butalso an omen ofdecreased cardiovascularand metabolic reserve,due to
thedemands placed on the elderly patient�sphysiology.15In several studies,the white
blood cellcount at admission has been a significantpredictor ofthe length
ofhospital stay.6,16Therefore,evaluation ofleukocytosis isimportant in determining
the severity ofinfection as well as in estimating thelength ofhospital stay.The
physiologic stress ofa seriousinfection can disrupt previously well-established
control ofsystemic diseasessuch as diabetes,hypertension,and renaldisease.The
increased cardiac and respira-tory demands ofa severe infection maydeplete scarce
physiologic reserves in thepatient with chronic obstructive pul-monary disease or
atherosclerotic heartdisease,for example.Thus,an otherwisemild or moderate
infection may be a sig-nificant threat to the patient with systemicdisease,and the
surgeon should be carefulto evaluate and manage concurrent sys-temic diseases in
conjunction with directmanagement ofthe infection.Step 3:Decide on the Setting
ofCareTable 15-6 lists the indications for hospi-tal admission ofthe patient with a
severeodontogenic infection.As previouslystated,an elevated fever increases meta-
bolic needs and fluid losses,which canlead to dehydration.In addition to
theclinical signs ofdry skin,chapped lips,loss ofskin turgor,and dry
mucousmembranes,dehydration can be assessedin the presence ofnormal serum creati-
nine by an elevated urine specific gravi-ty (over 1.030) or an elevated blood
ureanitrogen (BUN),which indicates prere-nal azotemia.Infections in deep spaces
that have aseverity score of2 or greater (see Table 15-3) can hinder access to the
airway for intu-bation by causing trismus,directly com-press the airway by
swelling,or threatenvital structures directly.Thus,an odonto-genic infection
involving the masticatorspace,the perimandibular spaces,or deep-er spaces indicates
hospital admission.Occasionally general anesthesia isrequired for patient
management due toinability to achieve adequate local anesthe-sia,the need to secure
the airway,or theinability ofthe patient to cooperate,as in ayoung child.Sometimes
concurrent sys-temic disease indicates hospital admissionand may even delay
surgery,as in the needto reverse warfarin anticoagulation.Table 15-6Indications for
HospitalAdmissionTemperature > 101�F (38.3�C)DehydrationThreat to the airway or
vital structuresInfection in moderate or high severityanatomic spacesNeed for
general anesthesiaNeed for inpatient control ofsystemic disease
284Part 3: Maxillofacial InfectionsIn deciding whether to admit thepatient with a
serious odontogenic infec-tion,it is generally safer to err on the sideofhospital
admission.The inpatient set-ting affords the patient with continualprofessional
monitoring,supportive med-ical care,the availability ofradiologic andmedical
consultative services,and,mostimportantly,a team that can rapidlysecure the airway
should it become com-promised.Step 4:Treat SurgicallyAirway SecurityThe dramatic
reduction in the mortalityofLudwig�s angina from 54 to 10% inonly 3 years,afforded
by Williams andGuralnick,was made possible by theirchanged surgical policy
ofimmediateestablishment ofairway security by earlyintubation or
tracheotomy,followed byaggressive and early surgical inter-vention.2No antibiotics
were used in theirpatients,except sulfa drugs in some cases.In the antibiotic era
mortality has beenfurther reduced to about 4%.3It is there-fore apparent that
immediate establish-ment ofairway security and early aggres-sive surgical therapy
are the mostimportant intervention steps in the man-agement ofsevere odontogenic
infections.Table 15-7 lists the indications for anoperating room procedure.The
para-mount indication is ofcourse to establishairway security.The involvement
ofmod-erate or high severity anatomic spaces gen-erally necessitates a more
complicated air-way management procedure,as well assurgical intervention in
anatomic loca-tions that are not amenable to profoundlocal anesthesia.An infection
that is rapid-ly progressing through the anatomic fas-cial planes,as in necrotizing
fasciitis,indi-cates the prompt establishment ofa secureairway,even iffor
anticipatory reasons,aswell as the possible need to extend theanatomic dissection
into regions that hadnot been contemplated preoperatively.Sometimes general
anesthesia is requiredfor patient management reasons alone,especially in the
patient who is not able tocooperate,such as a young child or men-tally handicapped
individual.Successful airway management in dif-ficult situations requires a
teamapproach.Preoperatively the surgeonshould communicate with the anesthesi-
ologist to establish the airway manage-ment plan.The anesthesiologist shouldbe
interested in understanding theanatomic location ofthe infection,as wellas its
implications for airway manage-ment.The anesthesiologist will value theopportunity
to see any effacement,dis-placement,or deviation ofthe airway asdemonstrated on
clinical examinationand CT.The airway management planshould include the projected
initial man-agement,as well as secondary proceduresshould the initial approach
fail.An infrequently used surgical tech-nique that may aid in protecting the air-
way during intubation or tracheotomy isneedle decompression.In this technique,under
local anesthesia an abscess ofthepterygomandibular,lateral
pharyngeal,submandibular,or sublingual space isaspirated with a large-bore needle
in orderto decompress the surrounding tissues.This maneuver may decrease the risk
ofabscess rupture through taut,distendedoropharyngeal tissues during instrumen-
tation ofthe airway.Additional benefits ofthis procedure are the redirection
ofpusdrainage into the oral cavity or onto theskin,where it can easily be
removed,andobtaining an excellent specimen for cul-ture and sensitivity
testing.Surgical DrainageIn general,surgery for management ofsevere odontogenic
infections is not diffi-cult.Given a thorough knowledge oftheanatomy ofthe deep
fascial spaces ofthehead and neck,the surgeon should be able,by using appropriate
anatomic landmarks,to use small incisions and blunt dissectionwithout direct
exposure and visualizationofthe entire infected anatomic space.Fig-ure 15-6
illustrates the appropriate loca-tions for extraoral incision placement fordrainage
ofthe various anatomic deepspaces.In addition a vertical incision overthe
pterygomandibular raphe can be usedto drain the pterygomandibular space aswell as
the anterior compartment ofthelateral pharyngeal space,as illustrated inFigure 15-
7.Lest the surgeon crush a vitalstructure within the beaks ofa hemostatduring blunt
dissection,it is crucial toinsert the instrument closed,then open itat the depth
ofpenetration,and then with-draw the instrument in the open position.A hemostat
should never be blindly closedwhile it is inside a surgical wound.Anoth-er
important principle ofsurgical incisionand drainage is the need to dissect a path-
way for the drain that includes the loca-tions where pus is most likely to be
found.This can be guided by the preoperative CTexamination and by knowledge
ofthepathways that odontogenic infection ismost likely to take.For
example,indrainage ofthe submandibular space,ifincisions are placed over the
anterior andposterior bellies ofthe digastric muscle atthe
submandibular,submental,and sub-lingual location and at the
submandibular,sublingual location as shown in Figure 15-6,then the dissection must
pass superiorlyand medially until the medial (lingual)plate ofthe mandible is
contacted.Themost likely pathway for odontogenicinfections to enter the
submandibularspace is through the thin lingual plate ofthe mandible,which also
approximates theroot apices ofthe lower molar teeth.ByTable 15-7When to Go to the
Operating RoomTo establish airway securityModerate to high anatomic
severityMultiple space involvementRapidly progressing infectionNeed for general
anesthesia
Principles ofManagement ofOdontogenic Infections285exploring this location,the
surgeon mayfind a collection ofpus that would other-wise have been missed.In order
to pass adrain through the submandibular spaceeffectively,the surgeon should
thereforepass a large curved hemostat from oneincision upward to the medial side
ofthemandible and then down to the other inci-sion.A Penrose drain can then be
graspedin the tip ofthe hemostat and pulledthrough the dissected pathway from
oneincision to the other,thus draining theentire submandibular space.The
resultingpathway for a through-and-through drainin the submandibular space is
illustratedin Figure 15-8.The advantages ofthrough-and-through drainage are the
provision oftwopathways for the egression ofpus,place-ment ofthe incisions in
healthy tissue incosmetically acceptable areas,and the abil-ity to irrigate the
infected wound with uni-directional flow from one incision to theother.Wound
irrigation is facilitated espe-cially by the use ofa Jackson Pratt�typedrain,which
is noncollapsible and perfo-rated.Such unidirectional superior-to-inferior drainage
ofthe pterygomandibu-lar space using intraoral and extraoralincisions and a Jackson
Pratt drain is illus-trated in Figure 15-9.There is little evidence to indicate
thatfrequent wound irrigation hastens the res-olution ofinfection.However,it does
makeclinical sense to remove by irrigation bac-teria,pus,clots,and necrotic tissue
frominfected wounds as they accumulate.Simi-larly the use ofbulky occlusive
dressingshas not been shown to substantially alterthe outcome ofcases ofodontogenic
infec-tion.Nonetheless the use ofsuch a dress-ing,as illustrated in Figure 15-
10,may bemore comfortable over the long run than adressing that is taped to the
skin,and it cer-tainly helps to prevent the contaminationofthe hospital by
pathogenic organisms.The need for this type ofhygiene is boundto increase in coming
years,as both antibi-otic-resistant organisms and critically ill,sometimes
immunocompromised patientsincreasingly inhabit hospitals.Drains should be
discontinued whenthe drainage ceases.They may be advancedgradually or removed all
at once.There isno evidence in favor ofeither technique.Pus usually stops flowing
from surgicallydrained abscesses in 24 to 72 hours,butthis process may take
somewhat longerwhen only cellulitis has been encountered.It should be kept in mind
however thatlatex Penrose drains can be antigenic,andafter several days they may
cause exuda-tion due to foreign body reaction alone.Timing ofIncision and
DrainageMuch ofthe surgical literature on the man-agement ofdeep fascial space
infections ofSuperficial and deeptemporal, submassetericSubmandibular,submental,
sublingualLateral pharyngeal,retropharyngealLateral
pharyngeal,retropharyngealcarotid sheathSubmandibular, sublingualpterygomandibular,
submassetericFIGURE15-6Incision placement for extraoral drainage ofhead and neck
infections.Incisions at thefollowing points may be used to drain infections in the
indicated spaces: superficial and deep tempo-ral,submasseteric;
submandibular,submental,sublingual; submandibular,sublingual,pterygo-
mandibular,submasseteric; lateral pharyngeal,retropharyngeal; lateral
pharyngeal,retropharyngeal,carotid sheath.Adapted from Flynn TR.31FIGURE15-
7Intraoral incision placement fordrainage ofthe anterior compartment ofthe lat-eral
pharyngeal space (curved arrow) and thepterygomandibular space (straight
arrow).Adapted from Flynn TR.31
286Part 3: Maxillofacial Infectionsthe head and neck advocates an expectantapproach
to surgical drainage ofdeep neckinfections.The overall strategy ofthisapproach is
to use parenteral antibiotictherapy as a means ofcontrolling,localiz-ing,or even
eradicating the soft tissueinfection.Failure ofthe medical approachis determined by
patient deterioration,impending airway compromise,and theidentification ofan
abscess by CT or clini-cal examination or both.Only then is sur-gical drainage
undertaken.17�19 The expec-tant approach to management ofsevereodontogenic
infections has not been sup-ported by empiric investigation.The alternative
strategy,successfullydemonstrated by Williams and Gural-nick,is the immediate
establishment ofairway security as necessary,and aggres-sive early surgical
intervention.2 Identifi-cation ofan abscess is not required beforesurgical
intervention.The approach byWilliams and Guralnick is predicated onthe concept that
early incision anddrainage aborts the spread ofinfectioninto deeper and more
critical anatomicspaces,even when it is in the cellulitisstage.In a prospective
case series of34 patients hospitalized with severeodontogenic infections,Flynn and
col-leagues performed surgical drainage onall patients as soon as possible
afteradmission.6In none oftheir cases didincision and drainage seem to hasten
thespread ofinfection.The need for reoper-ation was not significantly
differentbetween those patients in whom abscessand those in whom cellulitis was
found.6Culture and Sensitivity TestingInfections that present in the low
severityanatomic spaces (see Table 15-3) are not inan anatomic position that is
likely tothreaten the airway or vital structures.Inthe absence ofimmunologic or
systemiccompromise,such infections are veryunlikely to become serious or life
threaten-ing.Straightforward treatments,such asremoval ofthe involved
teeth,intraoralJackson Pratt drainpasses through thepterygomandibular
spaceFIGURE15-9Jackson Pratt irrigating drain placed from an intraoral inci-sion
through the pterygomandibular space to an extraoral incision,allowingunidirectional
irrigation and drainage.Adapted from Flynn TR.31Swelling in thesubmandibular
spaceDrainPosteriordigastric muscleAnteriordigastric muscleFIGURE15-8Pathway ofa
through-and-through drain ofthe submandibularspace.Note that the drain passes deep
to the medial surface ofthe mandible,below the attachment ofthe mylohyoid
muscle.Adapted from Flynn TR.31
Principles ofManagement ofOdontogenic Infections287incision and drainage,and
empiric antibi-otic therapy,are almost always successful.In this setting it can be
hard to justify theincreased cost ofroutine culture andantibiotic sensitivity
testing.Furthermore,since most odontogenic pathogens areslow-growing
species,identification canbecome an expensive and time-consumingtask for the
microbiology laboratory.Thisexpense is hard to justify,given the factthat at least
until recently,the oral flora isroutinely sensitive to penicillin.Therefore,most
microbiology laboratories,whengiven a specimen that grows out a-hemolytic
streptococci mixed with short,anaerobic,weakly gram-negative rods,willreport the
growth ofnormal oral flora,thus avoiding the necessity for speciesidentification
and subsequent antibioticsensitivity testing.For these reasons rou-tine culture and
sensitivity testing forminor oral infections does not appear tobe justified.When an
infection involves anatomicspaces ofmoderate or greater severity,orwhen there is
significant medical orimmune system compromise,culture andsensitivity testing as
early as possible in thecourse ofinfection is important becausethe final result
ofantibiotic sensitivity test-ing can be delayed for as much as 2 weekswhen
fastidious or antibiotic-resistantorganisms are involved.Culture and sensitivity
testing is alsojustified when the surgeon is dealing withinfections that have been
subjected tomultiple prior courses ofantibiotic thera-py or in chronic infections
that are recalci-trant to therapy.Immunocompromisedpatients also tend to harbor
unusualpathogens,such as Klebsiella pneumoniaein diabetes,methicillin-resistant
Staphylo-coccus aureusin intravenous-drug abusers,and intracellular pathogens,such
asmycobacteria in HIV/AIDS.In summary,culture and sensitivity testing should
beperformed in unusual infections,the med-ically and immune compromised,and cer-
tainly in all cases severe enough to requirehospitalization.Proper culture
technique involves theharvesting ofthe specimen in a mannerthat minimizes
contamination by normaloral or skin flora.Ideally the skin ormucosa should be
prepared with antisep-tic and isolated,and the culture should beobtained by
aspiration from the point ofmaximum inflammation,where abscess ismost likely to be
found.Ifthis is not pos-sible,then at surgery a swab and culturettesystem can be
used,although the surgeonmust be careful to avoid contamination ofthe specimen by
saliva or skin flora.Fur-thermore the culture transport systemshould be designed to
maintain the viabil-ity ofanaerobic organisms,which do notsurvive in commonly
available aerobicculturette systems.Even though the sur-geon may not encounter pus
during aspi-ration attempts or surgical drainage,fluidaspirates and swab cultures
ofinfectedsites do yield valid cultures with readilyinterpretable
results.Therefore,specimensshould be sent for culture and sensitivitytesting even
when pus is not obtained.Step 5:Support Medically Medical supportive care for the
patientwith a severe odontogenic infection iscomposed
ofhydration,nutrition,andcontrol offever in all patients.Mainte-nance or
reestablishment ofelectrolytebalance and the control ofsystemic dis-eases may also
be a crucial part ofthenecessary supportive medical care forsome cases,and the
reader is referred toappropriate texts for a more comprehen-sive discussion ofthese
matters.Initial temperature has been shownto be a significant predictor ofthe
lengthofhospital stay with severe odontogenicinfections.6,20Fever below 103�F
(39.4�C)is probably beneficial.Mild temperatureelevations promote
phagocytosis,increase blood flow to the affected area,raise the metabolic rate,and
enhanceantibody function.Above 103�F,howev-er,fever can become destructive
byincreasing metabolic and cardiovasculardemands beyond physiologic
reservecapacity.Energy stores can be rapidlydepleted and the loss offluid is
signifi-cantly increased.Adequate hydration is perhaps the bestmethod for
controlling fever.Daily sensiblefluid loss,consisting primarily ofsweat,isincreased
by 250 mL per degree offever.Insensible fluid loss,consisting mainly ofevaporation
from lungs and skin,isincreased by 50 to 75 mL per degree offever per
day.Therefore,a 70 kg patientwith a fever of102.2�F would have a dailyfluid
requirement ofabout 3,100 mL.Thiswould translate to a required intravenousinfusion
rate ofapproximately 130 mL perhour,assuming no oral intake and no
otherextraordinary fluid losses.21The next approach to controlling feveris usually
taken by the administration ofacetaminophen or aspirin.Fevers are oftenexaggerated
in children and decreased inFIGURE15-10A properly placed Barton dress-ing,which
avoids taping ofthe skin.It canocclude and absorb the drainage ofa maxillofa-cial
infection.Reproduced with permission fromFlynn TR.15
288Part 3: Maxillofacial Infectionsthe elderly.Thus,an older patient with
arelatively mild elevation oftemperaturemay have a fairly significant
infection.Atthe same time the surgeon may wish tocontrol fever in the elderly at a
lower tem-perature level than in the younger patientbecause ofa fever�s increased
cardiovascu-lar and metabolic demands.21 Fever can becontrolled or reduced by a
variety ofothermethods when necessary.These includecool water or alcohol sponge
baths,chilleddrinks when practical,or even an immer-sion bath using tepid
water.Fever also increases metabolicdemand by 5 to 8% per degree offever
perday.21Therefore,it may be necessary tosupplement the infected patient�s
oralintake,which is likely to be significantlyinhibited by the local effects ofthe
infec-tion and surgery,by using supplementaryfeedings or even enteral nutrition via
afeeding tube.Step 6:Choose and Prescribe Antibiotic Therapy It is beyond the scope
ofthis chapter todiscuss the topic ofantibiotic selection forhead and neck
infections comprehensively.This matter has been recently covered indetail
elsewhere.22The empiric antibioticsofchoice for odontogenic infections
are,however,listed in Table 15-8.These antibiotic choices are separatedby severity
ofinfection.Mild or outpatientinfections have been shown in a numberofstudies to
respond well to the oral peni-cillins.There was no significant differencein pain or
swelling at 7 days oftherapybetween penicillin and various
otherantibiotics,including clindamycin,amoxi-cillin,amoxicillin-clavulanate,and
cephra-dine,although these parameters improvedmore rapidly during the first 48
hours oftherapy with the alternative antibi-otics.23�25In one pediatric study pain
andswelling were significantly better at 7 dayswith amoxicillin.26In all ofthe
above ref-erenced studies the involved tooth or teethwere treated with extraction
or root canaltherapy.Incision and drainage was per-formed as
necessary.Therefore,penicillincontinues to be a highly effective antibiot-ic for
uncomplicated odontogenic infec-tions,owing to its low cost and low inci-dence
ofunwanted side effects.For severe infections warranting hos-pital admission the
antibiotics ofchoice forodontogenic infections do not includepenicillin.In 1999
Flynn and colleaguesfound a 26% failure rate ofpenicillin whenused empirically in a
series of34 hospital-ized cases ofodontogenic infection.6Ofthe31 patients who were
placed on penicillin(3 were allergic),8 experienced clinicaltherapeutic failure
ofpenicillin,which wasdetermined by failure ofimprovement
inswelling,temperature,and white blood cellcount after adequate surgical drainage
wasverified by postoperative CT.This highclinical failure rate ofpenicillin in
hospital-ized odontogenic infections is clinicallyunacceptable because ofthe
seriousness ofthese cases.Therefore,clindamycin hasbecome the empiric antibiotic
ofchoice forodontogenic infections that are seriousenough to warrant hospital
admission.Most resistance to penicillin thatoccurs among the oral pathogens is due
tosynthesis of�-lactamase.Approximately25% ofthe strains ofthe Prevotella
andPorphyromonasgenera are able to synthe-size this enzyme.�-Lactamase can also
befound in some strains ofFusobacteriumand Streptococcus
species.Importantly,however,the oral strains ofstreptococcithat synthesize �-
lactamase are generallyamong the S.mitis,S.sanguis,and S.sali-variusspecies.These
species are membersofthe Streptococcus viridansgroup that areresponsible for many
cases ofendocarditis.They are not frequently found in odonto-genic
abscesses.Streptococcus anginosus,S.constellatus,and S.intermediusare theviridans
streptococci that comprise theStreptococcusmilleri group.The S.millerigroup is most
commonly found in odonto-genic abscesses,and fortunately it remainsTable 15-
8Empiric Antibiotics* ofChoice for Odontogenic InfectionsSeverity
ofInfectionAntibiotic ofChoiceOutpatientPenicillin Clindamycin Cephalexin (only
ifthe penicillin allergy was not the anaphylactoid type;use caution)Penicillin
allergy:Clindamycin Moxifloxacin Metronidazole aloneInpatientClindamycin Ampicillin
+ metronidazole Ampicillin + sulbactamPenicillin allergy:Clindamycin Third-
generation cephalosporin IV (only ifthe penicillin allergy was not the
anaphylactoid type;use caution) Moxifloxacin (especially for Eikenella corrodens)
Metronidazole alone (ifneither clindamycin nor cephalosporins can be
tolerated)*Empiric antibiotic therapy is used before culture and sensitivity
reports are available.Cultures should be taken in severeinfections that threaten
vital structures.IV = intravenous.
Principles ofManagement ofOdontogenic Infections289sensitive to the natural and
semisyntheticpenicillins,such as penicillin V and amoxi-cillin.Therefore,it is
reasonable to usepenicillin plus a �-lactamase inhibitor suchas ampicillin-
sulbactam or a penicillin plusmetronidazole as alternative antibiotics forserious
odontogenic infections.The peni-cillins and metronidazole have the advan-tage
ofcrossing the blood-brain barrierwhen the meninges are inflamed.Clin-damycin,on
the other hand,does not crossthe blood-brain barrier.Therefore,it isappropriate to
use penicillin plus metro-nidazole or ampicillin-sulbactam whenthere is a risk ofan
odontogenic infectionentering the cranial cavity.22Few cephalosporins are able to
crossthe blood-brain barrier.Some third-generation cephalosporins,such as cef-
tadizime,can do so.In addition,ceftadiz-ime is effective against the oral strepto-
cocci and most oral anaerobes.Among thecephalosporins,therefore,ceftadizime isthe
alternative antibiotic ofchoice.A new fluoroquinolone antibiotic,moxifloxacin has
great promise in thetreatment ofhead and neck infections.Itsspectrum against oral
streptococci andanaerobes is excellent.Its absorption isvirtually complete via
either the oral orintravenous routes,and it penetratesbone readily.Therefore,this
new antibi-otic may become a significant addition tothe oral and maxillofacial
surgeon�sarmamentarium.Even though metronidazole is activeonly against obligate
anaerobic bacteria,itsuse alone in the treatment ofodontogenicinfections,when
combined with appropri-ate surgical therapy,may be effective.In
onestudy,ornidazole,a member ofthe nitroim-idazole family,was effective when
usedalone in the management ofodontogenicinfections.27Thus,the use
ofmetronidazolealone may be an appropriate stratagemwhen all ofthe other
appropriate antibioticsare contraindicated.As with all antibiotics,the surgeon
should be aware ofthe sideeffects and drug interactions ofthe antibi-otics he or
she uses.Metronidazole has adisulfiram-like reaction with alcohol,andshould be used
with caution in pregnancy.Step 7:Administer the Antibiotic Properly The tissue
level ofantibiotics determinestheir effectiveness.Those tissue levels areofcourse
dependent on the antibiotic�slevel in serum,through which the antibi-otic must pass
in order to achieve thera-peutic levels in soft tissues,bone,brain,and abscess
cavities.Administration ofantibiotics by the oral route requires thatthe drug
successfully navigate the vagariesofthe highly acidic stomach,the chemicalqualities
ofingested foods,and the basicintestinal tract.Once an antibiotic isabsorbed by the
gastric or intestinalmucosa,it may then be subject to first-pass metabolism in the
liver and subse-quent excretion though the bile.Part ofthe excreted antibiotic may
then be reab-sorbed by the intestine,resulting inenterohepatic recirculation.For
these rea-sons orally administered antibioticsachieve much lower serum levels at a
slow-er rate than when they are injected direct-ly into the vascular system
intravenously.Some antibiotics,however,are equallywell absorbed intravenously and
orally.Thefluoroquinolones,such as ciprofloxacin andmoxifloxacin,are the best
examples ofthis.For this reason the fluoroquinolones arenot given intravenously
unless use oftheoral route is contraindicated.The minimum inhibitory concentra-tion
(MIC) is the concentration ofanantibiotic that is required to kill a
givenpercentage ofthe strains ofa particularspecies,reported as 50% or 90%
ofstrains(MIC50or MIC90,respectively).The effec-tiveness ofsome antibiotics is
determinedby the ratio ofthe serum concentration ofthe antibiotic to the MIC
required to kill aparticular organism.For example,with thefluoroquinolones and the
aminoglyco-sides,ifthe serum concentration achievedis three to four times the MIC
for theorganisms involved,then maximum killingpower will be achieved.These are
examplesofconcentration-dependent antibiotics.22With time-dependent
antibiotics,such as the �-lactams and vancomycin,antibiotic effectiveness is
determined bythe duration for which the serum concen-tration ofthe antibiotic
remains above theMIC.With time-dependent antibiotics,itis necessary to know the
serum elimina-tion half-life (t1/2) ofthe antibiotic inorder to determine its
proper dosage inter-val.The dosage interval can then bedesigned in order to
maintain the serumconcentration above the MIC for at least40% ofthe dosage
interval.22Fortunately,the mathematics involvedin these calculations have already
beendetermined by the drug manufacturer.Dosage intervals should not be changedfrom
published guidelines by the surgeon.Nonetheless,the surgeon must be aware ofthe
greater effectiveness ofintravenousantibiotics over their oral counterparts.For
example,when penicillin G is givenevery 4 hours intravenously,a peak serumblood
level of20 �g/mL is achieved.Sincethe serum elimination half-life ofpeni-cillin G
is 0.5 hours,after 3 hours (6 half-lives) the serum concentration will
beapproximately 0.3 �g/mL.Since the MIC90ofStreptococcus viridansis 0.2
�g/mL,theserum concentration ofpenicillin G afteran intravenous dose of2 million
units willremain above the MIC90for approximate-ly 75% ofthe dosage
interval.Therefore,penicillin G,2 million units given intra-venously every 4
hours,should be highlyeffective against the viridans group
ofstreptococci,especially the abscess-forming S.millerigroup.By the same method the
peak serumlevel that can be achieved with an oraldose of500 mg ofamoxicillin is 7.5
�g/mL,and its t1/2is only 1.2 hours.Since amoxicillin�s MIC90for
viridansstreptococci is 2 �g/mL,the serum con-centration ofamoxicillin will fall
belowthe MIC90at approximately 2 hours after
290Part 3: Maxillofacial Infectionsthe peak serum level has been achieved,which is
only 25% ofthe 8-hour dosageinterval.Therefore,oral amoxicillin,eventhough it is
considered by many to be amore effective antibiotic,is less likely to beeffective
against the viridans streptococcithan intravenous penicillin G.Another practical
matter that mustalways be considered in administeringantibiotics is their
cost,especially theircost to the patient.When a patient doesnot have prescription
drug insurance cov-erage,such as in the working poor and theelderly,the retail cost
ofthe antibiotic canbe a significant factor in whether the pre-scribed antibiotic
is indeed followed.In2003 the retail cost of1 week�s supply ofpenicillin V 500 mg
taken 4 times per daywas US$12.09 at a large pharmacy chain inthe northeastern
United States.The retailcost of1 week�s supply ofclindamycin 300 mg taken 4 times
per day was US$58.59.These prices reflect generic medications,not brand name
antibiotics,which are sig-nificantly more expensive.Thus,an indi-gent patient may
not be able to pay for amore expensive antibiotic,and thereforehe or she may be
forced to either takereduced amounts ofthe antibiotic,toextend the dosage
interval,or to forgo tak-ing the antibiotic entirely.Accordingly theastute
clinician will take the cost factorinto account.When appropriate,a frankdiscussion
ofthe cost ofthe antibiotic ascompared to the patient�s means appearsto be the best
policy.Step 8:Evaluate the Patient Frequently In outpatient infections that have
been treat-ed by tooth extraction and intraoral incisionand drainage,the most
appropriate initialfollow-up appointment is usually at 2 dayspostoperatively for
the following reasons:1.Usually the drainage has ceased and thedrain can be
discontinued at this time.2.There is usually a discernible improve-ment or
deterioration in signs andsymptoms allowing the next treat-ment decisions to be
made.For odontogenic deep fascial spaceinfections that are serious enough for hos-
pitalization,daily clinical evaluation andwound care are required.By 2 to 3 postop-
erative days the clinical signs ofimprove-ment should be apparent,such as decreas-
ing swelling,defervescence,cessation ofwound drainage,declining white bloodcell
count,decreased malaise,and adecrease in airway swelling such that extu-bation can
be considered.Also at this timepreliminary Gram�s stains and/or culturereports
should be available,which mayprovide some guidance as to the appropri-ateness ofthe
empiric antibiotic therapy.Ifthe above signs ofclinical improve-ment are not
apparent,then it may be nec-essary to begin an investigation for possi-ble
treatment failure.The causes oftreatment failure in odontogenic infec-tions are
listed in Table 15-9.One ofthebest methods ofreevaluation is the post-operative
CT.A postoperative CT canidentify continued airway swelling thatmay preclude
extubation,or furtherspread ofthe infection into previouslyundrained anatomic
spaces,or it may con-firm adequate surgical drainage ofall theinvolved anatomic
spaces by the visualiza-tion ofradiopaque drains in all oftheinvolved fascial
spaces.Sometimes it is difficult to determinewhether the inability to extubate a
patient isdue to antibiotic resistance or inadequatesurgical drainage.Figure 15-11
illustratestwo such cases in which a postoperative CTwas able to identify the most
likely cause forthe lack ofclinical improvement.In Figure15-11A,oropharyngeal
swelling surroundsthe endotracheal tube in spite ofthe pres-ence ofsurgical drains
in all ofthe infectedspaces.This lack ofimprovement at 4 post-operative days was
due to therapeutic failureofpenicillin,which was treated by changingthis patient�s
antibiotic to clindamycin.Sub-sequently the patient improved.In Figure15-11B,there
is continued oropharyngealswelling surrounding the endotracheal tubeat 5
postoperative days.On the other handthe infection has progressed from the suc-
cessfully drained left pterygomandibularspace to the left and right lateral
pharyngealspaces,as well as the retropharyngeal space.This patient was taken back
to the operatingroom for repeated drainage ofall oftheinfected spaces.It should be
noted,however,that inthis author�s experience the use ofCTscanning to determine
whether a patientcan be extubated gives a late positive sig-nal.The best available
clinical test for theability to extubate in the case ofupper air-way swelling is
the air leak test (Figure 15-12).The air leak test is performed in thefollowing
manner in the spontaneouslyventilating patient:1.The endotracheal tube and trachea
aresuctioned.2.The oxygen supply is reconnected andany coughing that was stimulated
bythe tracheal suctioning is allowed tosubside.3.The oropharynx and oral cavity
aresuctioned free ofdebris,hemorrhage,and secretions.4.The cuffofthe endotracheal
tube isdeflated while the oxygen supply ismaintained.5.After waiting for any
coughing to sub-side,the oxygen supply is disconnectedTable 15-9Causes ofTreatment
FailureInadequate surgeryDepressed host defensesForeign bodyAntibiotic
problemsPatient noncomplianceDrug not reaching siteDrug dosage too lowWrong
bacterial diagnosisWrong antibioticAdapted from Peterson LJ.32
Principles ofManagement ofOdontogenic Infections291and the surgeon�s thumb is
placed toocclude the opening ofthe endotra-cheal tube.6.The patient is then
instructed tobreathe spontaneously around theendotracheal tube,and ifthis can
bedone,a positive air leak test isobtained.Ifthe patient cannot breathearound the
occluded endotrachealtube,then a negative result is obtained,and extubation should
be delayed.Given a positive air leak test result,thebest method for patient
extubationinvolves extubation over a stylet or prefer-ably an endotracheal tube
changer.Con-sideration may be given to performing theextubation procedure in an
operatingroom,where the best facilities for handlingan airway emergency are
available.Onemethod for extubation over a tube chang-er is described as
follows:1.The patient is preoxygenated for 3 to 5 minutes.2.The endotracheal tube
and trachea aresuctioned.3.Five milliliters of1% lidocaine with-out epinephrine is
administered viathe endotracheal tube,followed byoxygenation and then repeated tra-
cheal suctioning.4.The oral cavity and oropharynx aresuctioned free
ofdebris,hemorrhage,and secretions.5.The oxygen supply is disconnectedand a tube
changer then is intro-duced into the trachea via the endotracheal tube.6.The
cuffofthe endotracheal tube isdeflated and the endotracheal tube iswithdrawn over
the tube changer untilits tip is in the oropharynx.7.Ifthe patient is able to
breathe aroundthe tube changer as it remains in thetrachea,then extubation can be
com-pleted.8.Ifthe patient is not able to breathearound the tube changer,then
theendotracheal tube is re-inserted overthe tube changer into the trachea.9.The
endotracheal tube cuffis re-inflated,the tube changer is with-drawn,and oxygen is
reconnected.After extubation,the patient is closelymonitored clinically and with
pulse oxime-try.Arterial blood gases may be drawn 1 hour after extubation in order
to verifyadequate oxygenation and ventilation.Occasionally,the infecting
flora,espe-cially in a particularly severe infectionwith a prolonged course,will
change dur-ing the course oftreatment.This may bedue to the selection pressure
exerted byintensive antibiotic therapy,or it may bedue to the subsequent
introduction ofhospital-acquired pathogens,resulting in anosocomial
infection.Therefore,in pro-longed treatments and in especially severecases it may
be prudent to reculture infect-ed sites,so that any new or previouslyundetected
pathogens can be identified.In cases where there is continuedchronic drainage from
an infected site,such as in diagnosed or suspectedosteomyelitis,the surgeon�s
mnemonicfor the causes ofa fistula can be used.�FETID�stands for foreign
body,epithe-lium,tumor,infection,and distalobstruction.In the maxillofacial
region,FIGURE15-11A,Four-days postoperative computed tomography (CT) image ofa
patient with a rightpterygomandibular and lateral pharyngeal space abscess.Note the
intraoral drains in the pterygo-mandibular and anterior compartments ofthe lateral
pharyngeal space,and the extraoral drain in theposterior compartment ofthe lateral
pharyngeal space (arrow).B,Five-days postoperative axial CT ofa patient with a
previously placed drain in the left pterygomandibular space (arrow).Note the exten-
sion ofthe infection into the right and left lateral pharyngeal spaces and the
retropharyngeal space,withconstriction and deviation ofthe airway.Reproduced with
permission from Flynn TR.31ABFIGURE15-12Air leak test,performed byoccluding the
endotracheal tube with a finger,todetermine whether the patient can breathearound
the outside ofthe endotracheal tube.Reproduced with permission from Bennett JDand
Flynn TR.33
292Part 3: Maxillofacial Infectionsthis mnemonic can be used to provide
adifferential diagnosis for the chronicdrainage ofpus.Foreign bodies may
berepresented by bone plates and screws,ordental or cosmetic facial
implants.Epithelium may cause chronic drainagesimply because an epithelialized
fistuloustract has not been completely excised orbecause an epithelium-lined cyst
hasdrained externally.Tumors (especiallymalignant ones) that become infected donot
heal,which may result in chronicdrainage.Infection can ofcourse
drainchronically,which should alert the sur-geon to suspect osteomyelitis or a
chron-ic periapical abscess that is draining ontothe skin,as in Figure 15-
13.Distalobstruction classically refers to intestinalobstructions,but the concept
can still beapplied to the salivary ducts and to thenatural sinus drainage
pathways,such asthe ostium ofthe maxillary sinus.Whenthese openings for natural
drainage ofsaliva or mucus become obstructed,theninfection may result and drainage
mayoccur by an alternate pathway,such asproximal fistulization ofthe sub-mandibular
salivary duct due to a salivarystone blocking the natural opening ofWharton�s
duct.Ifa thorough search for previouslyundetected pathogens turns up negative oror
ifanother cause for treatment failurecannot be found,then the surgeon
shouldconsider the possibility ofantibiotic fail-ure,such as microbial resistance
to empir-ic antibiotic therapy or the use ofan incor-rect dosage or route
ofadministration forthe antibiotic.The criteria for changingantibiotics are listed
in Table 15-10.Because ofthe necessary time delay inobtaining culture and
sensitivity reports,itis occasionally necessary to change fromone empiric
antibiotic to another.Ideallythe surgeon should consider another ofthe empiric
antibiotics ofchoice listed inTable 15-8.The input ofan infectious dis-ease
consultant may also be valuable inthis situation.Summary Severe odontogenic
infections can be themost challenging cases that an oral andmaxillofacial surgeon
will be called on totreat.Often the patient with a severe odon-togenic infection
has significant systemicor immune compromise,and the constantthreat ofairway
obstruction due to infec-tions in the maxillofacial region raises therisk ofsuch
cases incalculably.Further-more,the increasing rarity ofthese casesand the ever-
changing worlds ofmicrobi-ology and antibiotic therapy make stayingabreast ofthis
field difficult for the busysurgeon.Therefore,the eight steps in thetreatment
ofsevere odontogenic infec-tions,first outlined by Dr.Larry Peterson,remain the
fundamental guiding principlesthat oral and maxillofacial surgeons mustuse in
successful management ofthesecases.The application ofthe eight stepsmust be
thorough and the surgeon�s mindmust always remain open to the
possibilityoftreatment failure,an error in initial diag-nosis,antibiotic
resistance,and previouslyundiagnosed medically compromisingconditions.Although
adherence to theseprinciples cannot always guarantee a suc-cessful result,it can
assure the oral andmaxillofacial surgeon that he or she ispracticing at the highest
standard ofcare.AcknowledgmentThe author wishes to thank Lisa Lavargna forher
expert assistance in the preparation ofthismanuscript.References1.Williams
AC.Ludwig�s angina.Surg GynecolObstet 1940;70:140.2.Williams AC,Guralnick WC.The
diagnosisand treatment ofLudwig�s angina:a reportoftwenty cases.N Engl J Med
1943;228:443.3.Hought RT,Fitzgerald BE,Latta JE,Zallen,RD.Ludwig�s angina:report
oftwo cases andreview ofthe literature from 1945 to January1979.J Oral Surg
1980;38:849�55.4.Flynn TR.Anatomy and surgery ofdeep fascialspace
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1994.Rosemont (IL):AmericanAssociation ofOral and Maxillofacial Sur-
geons;1994.p.79�107.5.Flynn TR.Anatomy oforal and
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ChangingAntibioticsAllergy,toxic reaction,or intoleranceCulture and/or sensitivity
test indicatingresistanceFailure ofclinical improvement,givenRemoval ofodontogenic
causeAdequate surgical drainage (suggest postoperative imaging)Other causes for
treatment failure ruled out48�72 h ofthe same antibiotic therapyFIGURE15-
13Adraining sinus tract onto the faceresulting from an untreated periapical
abscess.Reproduced with permission from Flynn TR andTopazian RG.30
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CHAPTER 16Sinus InfectionsRakesh K.Chandra,MDDavid W.Kennedy,MDChronic sinusitis is
a disease with highprevalence in the American population,affecting up to 13.4%
ofthe populationand accounting for almost 2% ofallambulatory diagnoses
rendered.1Thiscondition is important not only because ofits frequency but because
complications ofsinusitis may carry severe neurologic,oph-thalmologic,and systemic
consequences.Therefore it is incumbent on all practi-tioners,particularly those who
managestructures ofthe maxillofacial complex,tobe familiar with the features
ofsinonasaldisease.Technologic advances in diagnos-tic imaging,endoscopy,and
surgicalinstrumentation have revolutionized thediagnosis and treatment
ofsinusitis.Fur-thermore,both clinical experience andbasic science knowledge have
modifiedour perspective ofsinusitis such that wenow understand it as an
inflammatory dis-order,rather than a purely infectiousprocess.This chapter attempts
to synthe-size a framework for understanding theetiology,clinical
presentation,diagnosis,medical treatment,and surgery forsinonasal inflammatory
disease.These ele-ments are discussed in the context ofourcurrent knowledge base
and the latesttechnologic innovations.The diagnosis and management ofsinusitis has
traditionally been based onpatient symptomatology and plain filmimaging.The advent
ofsinonasalendoscopy and the wide availability ofcomputed tomography (CT)
haveenhanced diagnostic accuracy,treatmentplanning,and surgical
capabilities.Priorto these developments,management pri-marily consisted
ofantibiotic therapy,with surgery (often performed via facialincisions) reserved
for complications.Endoscopy and CT have permitted electivemanagement ofsinusitis
for symptomaticimprovement and the prevention ofcom-plications.Advances in our
understandingofmicrobiology,allergy,and pharmacolo-gy have complemented these
modalities.The first fiber-optic nasal examinationwas performed by Hirshman using a
mod-ified cystoscope.Instrumentation wasthen refined after World War II,permit-ting
the development ofsmaller scopeswith improved illumination.Hopkinsdesigned a series
ofrigid endoscopes inthe early 1950s.They were relatively smallin diameter and had
wide field high-contrast optics and bright illumination.This technology was used by
Professor W.Messerklinger ofGraz,Austria,for system-atic nasal airway
evaluation.Importantly,Messerklinger observed that primaryinflammatory processes
ofthe lateral nasalwall,particularly the middle meatus,resulted in secondary
disease ofthe maxil-lary and frontal sinuses.2This led to thedefinition ofthe
osteomeatal complex(OMC;Figure 16-1) as the site ofcommondrainage for the
maxillary,frontal,andanterior ethmoid sinuses.Messerklingerdemonstrated that even
small anatomicvariations or inflammatory processes inthis location may impair
ventilation anddrainage ofthe adjacent sinuses,with sub-sequent development
ofsignificantinflammatory disease in these regions.This observation led him to
employ endo-scopes for the surgical management ofsinusitis such that disease
processes affect-ing the natural sinus drainage pathwayscould be
addressed.Particularly,heshowed that even limited surgical proce-dures directed
toward the OMC and ante-rior ethmoid sinuses can result inimprovement ofventilation
and drainageofthe frontal and maxillary sinuses.During the 1980s
Stammberger,alsoofGraz,and Kennedy,in the UnitedStates,further refined and
popularizedthese techniques.3Since that time nasalendoscopy has been employed in
the sur-gical management ofsinonasal neoplasmsas well as a multitude ofboth skull
baseand orbital pathologies.Although indica-tions do exist for external approaches
tothe paranasal sinuses,endoscopicapproaches are typically first line in
thesurgical management algorithm.Recentadvances in surgical instrumentation
haveincluded the development ofangled for-ceps,drills,and
telescopes.Additionally,the availability ofstereotactic navigation-al imaging has
permitted more compre-hensive surgery to be performed safely.The practices
ofoptimal medical therapy,
296Part 3: Maxillofacial Infectionsboth pre- and postoperatively,and metic-ulous
postoperative care have furtherimproved our treatment success.Theremainder ofthis
chapter highlights thestate ofthe art in the diagnosis and man-agement
ofsinusitis.Clinical PresentationSinusitis is a clinical diagnosis that is con-
firmed by physical examination,includingnasal endoscopy,and radiographic imag-
ing.The Task Force on Rhinosinusitissponsored by the American Academy
ofOtolaryngology�Head and Neck Surgeryhas established criteria to define a
historyconsistent with sinusitis.3These are basedon patient signs and symptoms and
aregrouped into major and minor criteria,asoutlined in Table 16-1.The presence
oftwo or more major factors,or one majorplus at least two minor factors,is consid-
ered a �strong history for sinusitis.�Ofnote,purulent nasal drainage alone is con-
sidered diagnostic for sinusitis.This find-ing is clearly visible on nasal
endoscopyand may manifest as purulence in themiddle meatus or within a sinus
cavityitself.This is described in greater detailbelow under �Diagnosis.�It also
deservesclarification that fever is only considered amajor factor in the setting
ofacute sinusi-tis but is otherwise a minor factor.Although the term sinusitisis
commonlyin use,the process may more accurately bedescribed by the term
rhinosinusitisbecause the nasal and sinus mucosal sur-faces are contiguous and it
would beimpossible to have sinusitis without acoexisting rhinitis.The terms are
usedinterchangeably in the present chapter.Rhinosinusitis is classified as
eitheracute,subacute,recurrent acute,orchronic.The distinctions are based
solelyupon the time course or temporal patternin which the patient has
symptoms.Patients may also have episodes ofrecur-rent acute sinusitis superimposed
on abaseline state ofchronic sinusitis.A diag-nosis ofacute sinusitis requires that
crite-ria satisfying a strong history for sinusitisare present for 1 to 4
weeks.Patientsshould exhibit signs and symptoms for atleast 1 week before sinusitis
is diagnosedbecause sinusitis typically involves a bac-terial process,and the vast
majority ofpatients with symptoms for < 1 weekhave simple viral upper respiratory
infec-tions.Strictly speaking,however,a viralupper respiratory infection is synony-
mous with an acute viral rhinosinusitis.Subacute sinusitis requires that these
Nasal septumEthmoid bullaInfundibulumConcha bullosaUncinate processInfraorbital
ethmoidal cellFIGURE16-1Diagram ofcoronal section through the region ofthe
osteomeatal complex.Note theuncinate process,ethmoid bulla,infundibulum,nasal
septum,infraorbital ethmoidal cell,and conchabullosa.(Courtesy ofTina
Bales,MD,resident,Department ofOtorhinolaryngology�Head and NeckSurgery,University
ofPennsylvania [with adaptations])Table 16-1Factors Associated with a History
ofRhinosinusitis*Major FactorsMinor FactorsFacial pain/pressureHeadacheFacial
congestion/fullnessMaxillary dental painNasal drainage/dischargeCoughPostnasal
dripHalitosis (bad breath)Nasal obstruction/blockage FatigueHyposmia/anosmia
(decreased or absent sense ofsmell)Ear pain,pressure,or Fever (acute sinusitis
only)fullnessPurulence on nasal endoscopy (diagnostic by itself)Fever*Either two
major factors,or one major and two minor,are required for a diagnosis
ofrhinosinusitis.Purulence on nasalendoscopy is diagnostic.Fever is a major factor
only in the acute stage.
Sinus Infections297criteria have existed for 4 to 12 weeks,andin chronic sinusitis
the criteria are pre-sent for at least 12 weeks.In recurrentacute
sinusitis,episodes last < 4 weeks,but the patient is asymptomatic
betweenepisodes.Rhinosinusitis may also havesignificant fungal components and maybe
influenced by environmental,generalhost,and local host factors (see
below).EtiologyAnatomy and Physiology oftheNose and Paranasal SinusesThe
pathophysiology ofsinusitis must beunderstood in the context ofthe normalanatomy
and physiology ofthe nose andparanasal sinuses.The paranasal sinusesare formed
early in development asevaginations ofrespiratory mucosa fromthe nose into the
facial bones.Cavity for-mation begins in utero,and pneumatiza-tion continues into
early adolescent life.The ethmoid sinus develops into a bonylabyrinth of3 to 15
small air cells on eachside.In contrast,the other sinus cavitiesdevelop as a single
bony cavity on eachside ofthe facial skeleton,although vari-ations may exist.The
ostium ofeachsinus represents the point at which out-pouching initiated.The lateral
nasal wall on each side islined by three turbinate bones designatedas
inferior,middle,and superior (Figure16-2).The space under each is known aseither
the inferior,middle,or superiormeatus,respectively.The OMC is a spacewithin the
middle meatus into which themaxillary,anterior ethmoid,and frontalsinuses drain
(see Figure 16-1).It is thisregion where pathology such as anatomicvariation or
inflammatory disease is mostlikely to impair sinus ventilation
anddrainage,resulting in the development ofsinusitis.The posterior ethmoid
sinusesdrain into the superior meatus.The sphe-noid sinus drains into an area known
asthe sphenoethmoidal recess,which lies atthe junction ofthe sphenoid and
ethmoidbones in the superior portion ofthe poste-rior nasal cavity (see Figure 16-
2).The remaining discussion details theanatomy ofthe middle meatus and theOMC,for
this is the critical region in thedevelopment ofsinusitis.These structuresare
mainly derived from the ethmoidbone,a T-shaped structure,ofwhich thevertical part
contributes to the nasal sep-tum,middle (and superior) turbinate,eth-moid air cell
system,and the lateral nasalwall (see Figure 16-1).The horizontal por-tion forms
the cribriform plate ofthe skullbase.The uncinate is a sickle-shapedprocess
ofethmoid bone that lies along thelateral nasal wall.The cleft-like space later-al
to this structure is known as theinfundibulum,and this is the region intowhich the
maxillary sinus drains.Themedial opening ofthe infundibulum,where it opens into the
middle meatus,isknown as the hiatus semilunaris.The eth-moid bulla is a prominence
ofanteriorethmoid air cell(s) along the lateral nasalwall that hangs just superior
to theinfundibulum.The drainage tract fromthe frontal sinus courses inferiorly
fromthe sinus medial to the medial orbital wall,lateral to the middle turbinate,and
anteri-or to the ethmoid bulla.This tract,knownas the frontal recess,is highly
variable andis often lined with variant anterior eth-moid air cells.It is apparent
that even min-imal inflammatory disease in the OMCcan impair sinus ventilation and
drainageofthe adjacent ethmoid,maxillary,andfrontal sinuses.The paranasal sinuses
and the majori-ty ofthe nasal cavity itselfare lined withpseudostratified columnar
ciliated epithe-lium (respiratory type).The cilia suspenda mucous blanket,which is
secreted bygoblet cells in the mucous membrane (Fig-ure 16-3).The cilia propel this
blanket in apredetermined direction (Figure 16-4),ina manner similar to the
�mucociliary esca-lator�ofthe tracheobronchial tree.Thisphenomenon is important
because in theSuperiorturbinateMiddleturbinateInferiorturbinateFIGURE16-2Structures
ofthe lateral nasal wall.Note the position ofthe inferior,middle,and superior
turbinates.(Courtesy ofTina Bales,MD,resident,Department ofOtorhino-
laryngology�Head and Neck Surgery,University ofPennsylvania [with adaptations])
298Part 3: Maxillofacial Infectionsparanasal sinuses cilia propel mucustoward the
natural ostium.This meansthat in the maxillary sinus cilia must pro-pel mucus
against gravitational forces.Anysurgical procedures intended to promotesinus
drainage must,however,beaddressed to the natural ostium.One or more ofthe following
local fac-tors may create a predisposition for sinusi-tis:(1) mechanical
obstruction ofmucocil-iary flow,particularly in the OMC region,(2) defects in
ciliary capability to propelthe mucous blanket,and (3) abnormalquantity or quality
ofsecretions.A combi-nation ofthese factors results in the devel-opment ofsinusitis
by allowing stasis ofsecretions,resulting in bacterial coloniza-tion and infection
with associated inflam-mation.4In turn,this results in furtherostial
obstruction,stasis,and exacerbationofthe inflammatory
process.Furthermore,impairment ofsinus ventilation createsacidic anaerobic
conditions that cause cil-iary damage and ineffective mucus clear-ance.5A variety
oflocal and systemic dis-ease processes may promote sinusitis byinfluencing
mucociliary clearance at theanatomic,histologic,immunologic,andbiochemical levels
(Figure 16-5).Anatomic FactorsPost-traumatic,congenital,or iatrogenicconditions
involving the craniofacialskeleton may physically obstruct sinusostia,contributing
to the development ofsinusitis.These may include abnormalitiesofthe nasal
septum,such as spurs anddeviations,or variants ofthe middleturbinate including
turbinate pneumatiza-tion (concha bullosa) or hypertrophy.These entities may narrow
the middlemeatal cleft,thus impairing mucus out-flow with subsequent bacterial
coloniza-tion and inflammation.Variations oftheethmoidal air system may also
obstructmucociliary outflow.Such examplesinclude the infraorbital cell (Haller
cell)and pneumatized middle turbinate (con-cha bullosa;see Figure 16-1).Sinonasal
tumors and polyps may alsopromote sinusitis by impairing the out-flow
ofsecretions.A discussion ofsinonasal neoplasia is beyond the scope ofthis
chapter.Nasal polyps by themselvesare not a disease but a manifestation ofadvanced
sinonasal inflammation.Theorigin ofnasal polyps is therefore multi-factorial and
may include any combina-tion ofthe infectious,allergic,immuno-
logic,metabolic,and/or genetic conditionsdescribed below.The presence ofaccessory
ostia,either congenital or iatrogenic,may pro-mote the development ofchronic
sinusi-tis by the mucus recirculation phenome-non.This is most apparent in
themaxillary sinus.Mucus is physiologicallypropelled around accessory ostia
andtoward the natural ostium (see Figure 16-4).However,the presence ofan
accessoryostium allows mucus reentry into thesinus lumen.Earlier surgical
techniquesattempting to augment sinus ventilationand drainage included the creation
ofa�nasoantral window�in the inferior mea-tus,with the rationalization that
thiswould permit drainage in a gravity-dependent manner.This approach,how-ever,is
suboptimal because cilia attemptto direct mucus around the iatrogenicostium to the
natural one.In children adenoid hypertrophy is afrequent underlying cause ofsinus
infec-tions.This impairs the outflow ofsecretionsfrom the posterior nasal cavity
into thenasopharynx.The diagnosis is suspected inchildren presenting with nasal
obstruction,mouth breathing,and rhinorrhea.A nasalforeign body may also be observed
in chil-dren with these findings and may eithermimic or be the cause
ofrhinosinusitis.TheMucousblanketFIGURE16-3Histology ofthe sinonasal mucosa.Note
the pseudostratified ciliated cells and the gobletcells.The cilia suspend and
propel the mucous blanket.(Courtesy ofTina Bales,MD,resident,Depart-ment
ofOtorhinolaryngology�Head and Neck Surgery,University ofPennsylvania [with
adaptations])Left frontalsinusRight frontalsinusLeft maxillarysinusRight
maxillarysinusAccessoryostiumFIGURE16-4Cilia beat in a predeterminedmanner to
direct mucus flow to the naturalostium and around accessory ostia.(Courtesy ofTina
Bales,MD,resident,Department ofOtorhinolaryngology�Head and Neck Surgery,University
ofPennsylvania [with adaptations])
Sinus Infections299classic finding in these patients is unilateralfoul-smelling
rhinorrhea.Miscellaneous anatomically relatedconditions that may increase the risk
fordeveloping sinusitis include the presenceofnasotracheal or nasogastric tubes
andbarotrauma.Nasal intubation may impairsinonasal drainage,but other mechanismsmay
be involved as studies have observedsinusitis on the side opposite tube place-
ment.6Barosinusitis results from tissueedema induced by rapidly changing
airpressures during diving,air travel,orhyperbaric oxygen therapy.Any preexist-ing
anatomic narrowing ofthe OMC pre-disposes to barosinusitis as air pressurewithin
the sinus cannot effectively equili-brate with the ambient pressure duringascent or
descent.Inflammatory Conditions The most common inflammatory condi-tion that
predisposes to sinusitis is a viralupper respiratory infection,or the com-mon
cold,during which approximately80% ofpatients have decreased patency ofthe
maxillary sinus ostium secondary totissue edema.7Mucociliary clearance isalso
impaired secondary to destructionand shedding ofciliated epithelial cells.Influenza
virus appears to be the mostdestructive in this regard.8Rhinovirus isthe most
common cause,with over 100serotypes identified,and respiratory syn-cytial
virus,parainfluenza virus,and coro-navirus may also be implicated.Regardlessofthe
offending virus,conditions ofostialobstruction and impaired mucociliaryflow permit
bacterial overgrowth.Dental conditions may cause maxillarysinusitis secondary to
direct extension ofinfectious or inflammatory processesthrough the apices
ofmaxillary teeth intothe sinus.Infection following a sinus liftprocedure appears
to be more likely whenthere is preexisting osteomeatal inflamma-tion.Dental implant
and root canal materi-als may also extrude into the sinus,initiatinginflammation
via a foreign body reaction or by acting as a nidus for bacterial colo-
nization.Specifically,paraformaldehyde-containing pastes have been
implicated.9Chronic inflammatory disordersaffecting the respiratory mucosa appear
tocorrelate with sinusitis.Patients with aller-gic rhinitis frequently exhibit
sinusmucosal disease,and,conversely,a largeproportion ofpatients with
chronicsinusitis have positive responses to allergyskin testing.This is thought to
be animmunoglobulin E (IgE)-mediated (typeI) immediate hypersensitivity,with cell-
mediated late-phase responses.Ourunderstanding ofthe mechanistic rela-tionship
between allergy and sinusitis isfar from complete,however,and the exactconcordance
between the disorders isunknown.10Nonetheless,it appears thatatopic patients have
an underlying predis-position for mucosal inflammation.Ostialobstruction and
impaired mucociliaryflow from allergen exposure may result inbacterial overgrowth
and exacerbation ofthe inflammatory process.The effect ofallergic disease persists
even after surgicalprocedures that enlarge the natural sinusostia.In fact,surgery
may increase mucos-al inflammation by enhancing allergenexposure to susceptible
mucosa within thesinus,despite anatomic improvements inthe drainage
pathway.Patients with asthma are also predis-posed to sinusitis secondary to a
general-ized reactivity ofthe respiratory mucosa.Again,the exact relationship
betweenthese entities is unclear.However,there isevidence that asthma symptoms
mayeven improve after surgical managementofcomorbid chronic
sinusitis.11,12Oneatopic syndrome that deserves discussionis the Aspirin-
sensitivity triad (Samter�striad).These patients develop asthma inassociation with
sinusitis and nasal poly-posis,and Aspirin precipitates
acutebronchospasm.Overall,it is estimatedthat up to 25% ofpatients with
nasalpolyposis develop bronchoconstriction inresponse to Aspirin
administration.13Aspirin-sensitivity triad is a defect ofarachidonic acid
metabolism and mayhave a genetic basis.14Host factors(allergy, anatomy,
genetics)Environmental factors(allergens, viral infections)Sinus ostial
obstructionMucosal inflammationStasis of secretionsHypoxiaCiliary
dysfunctionImmunologic reactionBacterial colonizationand infectionFungi?FIGURE16-
5Sinusitis is a multifactorial process,ofwhich bacterial infection is a component.
300Part 3: Maxillofacial InfectionsOver 100 chemicals have been found tocause nasal
irritation,many ofwhich arefound in cigarette smoke.Pollutants maycontribute to
sinusitis through severalmechanisms.Deposition ofirritant parti-cles in the mucous
blanket during respira-tion can increase the relative concentrationto which the
mucous membrane isexposed,resulting in direct chemical andphysical irritation,which
subsequently pro-motes the inflammatory process.15The irri-tant effects ofthese
chemicals may alsoinduce neurogenic inflammation throughvasodilation,tissue
edema,and leukocyteinflux.Specifically,neuropeptides such assubstance P from
unmyelinated sensoryfibers have been implicated.16Pollutantsmay also impair
mucociliary clearancethrough alterations in mucus viscosity,inhibition ofciliary
function,and increasesin epithelial permeability.The typicalchemical components
ofoutdoor pollutionhave been shown to increase neutrophilcounts in nasal lavage
specimens.17A studyin Finland also correlated the increase innasal polyposis and
frontal sinusitis with airpollution.These studies provide circum-stantial but
objective evidence that pollu-tants play a significant role in the
increasingprevalence ofchronic sinusitis.18Recently there has been
investigationinto a possible role for gastroesophagealreflux disease (GERD) in
sinonasalinflammation,particularly in the pediatricpopulation.19,20In fact,GERD has
beenassociated with a multitude ofinflamma-tory processes ofthe upper
aerodigestivetract including esophagitis,pharyngitis,and laryngitis.Evidence for
its role insinusitis,however,is circumstantial,andmany feel that it is not a
significant predis-posing factor.20Nonetheless,GERDshould be suspected in children
whoseinflammation appears refractory to med-ical and surgical
management.Bacteriology ofSinusitisThe type ofbacteria involved in a sinusinfection
depends on multiple factors,including the immune or metabolic statusofthe host,the
duration ofthe diseaseprocess,whether the infection is commu-nity or hospital
acquired,and antibioticresistance patterns.In uncomplicatedacute
sinusitis,Streptococcus pneumoniaeand Haemophilus influenzaeare the mostcommonly
isolated pathogens;Moraxellacatarrhalismay also be a
significantorganism,particularly in the pediatricpopulation.Staphylococcus
aureus,Strep-tococcus pyogenes,coagulase-negativestaphylococci,anaerobes,and gram-
negative organisms are found in varyingproportions.The pathogenic roles
ofstaphylococcal species in acute sinusitis areunclear as these are found near the
maxil-lary ostium in 60% ofhealthy asympto-matic adults.21Anaerobes,when
isolated,are typically a component ofa mixed bac-terial infection and may be the
result ofanextension ofa dental abscess.22It shouldalso be noted that up to 50%
ofpatientsdiagnosed clinically with acute sinusitishave sterile sinus aspirates.The
reason forthis is unclear,but it may reflect viral orallergic processes diagnosed
as bacterialsinusitis.Nosocomial acute sinusitis maybe caused by nasal
intubation,nasal pack-ing,patient immobility,chronic debilita-tion,and/or
immunosuppression.Themost common species isolated in thesecases is
Pseudomonas,although S.aureusisalso frequently isolated,and the bacteriolo-gy may
be unpredictable.Patients with chronic sinusitis typical-ly represent a population
with severalmonths to years ofsymptoms who havereceived multiple antibiotic
courses.Thusthe bacterial profile in these patients dif-fers from that ofacute
sinusitis.Polymi-crobial infections and antibiotic-resistantorganisms are often
found.In general,ahigher proportion ofS.aureus,coagulase-negative
staphylococci,gram-negativebacilli,and streptococci are isolated inaddition to the
typical pathogens ofacutesinusitis.23,24The roles ofS.aureusandcoagulase-negative
staphylococci are con-troversial as these organisms are known tocolonize the
anterior nose and are less fre-quently isolated when the anterior nose
isdisinfected.25Most authors agree,howev-er,that S.aureusis a significant
pathogenand should be treated when identified.26,27Gram-negative organisms that may
be iso-lated include Pseudomonas,Klebsiella,andProteus.Viridans
streptococci,organismscommonly found among oral flora,areobserved in up to one-
third ofcases.24Interestingly,one study identified anaer-obes in 93% ofspecimens in
children withchronic sinusitis.28However,because theupper aerodigestive tract is
highly colo-nized with anaerobes,29their role in theinfectious process is
unclear.Postsurgical-ly,the sinonasal mucosa is frequently colo-nized or infected
with Pseudomonasand/or S.aureus,and patients may still besusceptible to acute
exacerbations by thepathogens involved in acute sinusitis.Role ofFungiMuch has
evolved in our understanding ofthe role offungi in sinusitis,and differentpatterns
offungal sinusitis exist.Fungaldisease can be classified as noninvasive
orinvasive.Both fungal balls and allergicfungal sinusitis are part ofthe
noninvasivegroup,although recently it has been sug-gested that fungus has a wider
role as anactive factor in the pathogenesis ofeosinophilic chronic
rhinosinusitis.Inva-sive fungal disease is typically a fulminantdisease in
immunocompromised individ-uals but can also occur occasionally as anindolent
disease in patients who areimmunocompetent.Fungal balls are typi-cally seen in
immunocompetent individu-als with chronic (or recurrent acute)symptomatology that
is often subtle andrestricted to a single sinus.Patients maycomplain about the
perception ofa foulodor and occasionally report expellingfungal debris with nose
blowing.Mostcommonly,a fungal ball consisting ofAspergillus fumigatusis found in
the max-illary sinus with scant inflammatory cell
Sinus Infections301infiltration in the surrounding mucosa.30The condition is
indolent,and cure isoften achieved after surgical removal ofthe fungus ball and
assurance ofpatencyofthe natural sinus ostium.Allergic fungal sinusitis (AFS) is
aform ofnoninvasive fungal sinusitis seenin immunocompetent patients,whoexhibit a
hypersensitivity reaction to fun-gal organisms in the nose and sinuses.Thedisease
typically presents with unilateralnasal polyposis and thick tenacious secre-
tions.31The most commonly implicatedfungi are those ofthe Dematiaceae fami-ly,32but
Aspergillusspecies are also seen.The exact pathophysiology is controversialbut is
thought to involve IgE-mediated(type I) responses.IgE-sensitized mastcells are
activated by exposure to fungalantigens resulting in
degranulation,influxofeosinophils,and exacerbation ofinflammation via the release
ofmajorbasic protein.Immune complex (type III)reactions involving IgG have also
beenidentified.Patients have a severe inflam-matory reaction with nasal polyposis
andinspissated �allergic mucin�consisting ofeosinophil breakdown products (Charcot-
Leyden crystals) and fungal forms.AFS-like conditions have also been described
inwhich mucin is observed,but fungal formsare not identified microscopically or
byculture.33Recent studies by Ponikau andcolleagues and Taylor and colleagues,how-
ever,revealed that fungi can be demon-strated with increased sensitivity usingnovel
culture and staining techniques.34,35In fact,this group showed that fungi
arepresent in 93% of101 patients with chron-ic sinusitis.34 This has led to the
hypothesisthat the fungi,themselves,may induce aneosinophilic response,and that
fungi mayplay a prominent role in chronic sinusitis,even in the absence offrank
AFS.This areaofresearch is progressing rapidly.Patients with AFS may present
withthe typical signs and symptoms ofchron-ic sinusitis.Underlying AFS must be sus-
pected in a chronic sinusitis patient whosecourse is unusually refractory to
medicaltherapy.Additionally,advanced nasalpolyposis with inspissated mucin
andfungal debris may cause thinning ofboneofthe adjacent orbit and skull
base.Thegoals for treatment ofAFS are to eliminatethe fungal antigenic load and to
reestab-lish sinus ventilation,drainage,andmucociliary clearance.Surgery has
aprominent role in these regards but mustbe complemented with medical therapiesto
both reduce inflammation and elimi-nate the fungal load.Immunocompromised patients
are atrisk for developing fulminant invasive fun-gal sinusitis.This patient
population iscomposed ofdiabetics,transplant patients,those receiving cancer
chemotherapy,burnvictims,the elderly,and patients with con-genital or acquired
immunodeficiency.Inaddition to the typical symptoms ofsinusi-tis,patients with
invasive fungal diseasemay present with severe pain,fever,prop-tosis,visual
impairment,cranial neuropa-thy,other focal neurologic findings,seizures,and altered
mental status.Invasivefungal sinusitis may begin as a noninvasiveform with
subsequent tissue invasion in asusceptible patient.Aspergillus and fungi ofthe
Mucoraceae family are often implicat-ed,with the latter being more common
indiabetics.Black necrotic eschars ofthenasal mucosa are noted during
nasalendoscopy,with bone destruction on CTscans.Biopsy ofthe border ofthe eschar
isessential to confirm the diagnosis.Biopsy isalso necessary when pale insensate
mucosais discovered in a patient with a strong his-tory and risk factors for
invasive fungalsinusitis.Treatment requires aggressivesurgical d�bridement
ofinfected and devi-talized tissues,topical and systemic anti-fungal
medications,and management ofpredisposing conditions.The chronic indolent form
ofinvasivefungal sinusitis is more commonlyobserved in immunocompetent patientsand
is endemic in Sudan,but it has alsobeen observed in type II diabetics.Aspergillus
flavusis the most commonorganism encountered.Symptoms ofchronic sinusitis are
initially present,butthese progress to cause visual and neuro-logic signs.Nasal
endoscopy may revealgranulomatous inflammation.31Bonedestruction ultimately
occurs.Treatmentincludes surgical removal offungal debrisand affected tissues,as
well as systemic andlocal antifungal therapy.Genetic DisordersLittle is known
regarding genetic influ-ences on the risk ofdeveloping sinusitis,and the exact
contribution ofhereditaryvariables is difficult to quantify given themultifactorial
nature ofthe disease.How-ever,recently the ADAM33gene has beenidentified as being
associated with theclosely related disease asthma.Many ofthepredisposing
inflammatory conditionsdiscussed previously,particularly thoseinvolving an atopic
response,also tend tocluster in families,suggesting a
geneticcomponent.Additionally,several definedcongenital syndromes are associated
withsinusitis.These include defects ofmetabo-lism,ciliary structure/function,and
theimmune system.Some ofthe more com-mon pathologies with a primary geneticbasis
are outlined below.Cystic fibrosis (CF) is an autosomalrecessive disorder affecting
epithelial trans-port ofchloride and water via mutations inthe CFTRgene.This
results in abnormallyviscous secretions,which become inspis-sated in the
lung,pancreas,and sinonasaltract,ultimately leading to chronic inflam-mation and
fibrosis.In the sinonasal tract,patients exhibit florid polyposis and colo-nization
with Pseudomonas.A sweat test todetect elevated chloride levels is diagnosticand
should be performed on any child pre-senting with nasal polyposis.Recent dataalso
suggest that heterozygous carriers maybe at increased risk for developing
chronicsinusitis.36Aggressive medical manage-ment against Pseudomonas is
necessary;treatment also includes surgery to remove
302Part 3: Maxillofacial Infectionspolyps and chronically infected tissue andto
provide sinus ventilation.Pulmonarydisease is typically the life-limiting mani-
festation ofCF,but in the era oflung trans-plantation,patients may live well into
thefourth or fifth decade.Inherited disorders ofciliary struc-ture or function also
are associated withchronic sinus disease.Kartagener�s triadis a syndrome involving
sinusitis,bronchiectasis,and situs inversus.37Sinus,middle ear,and pulmonary dis-
eases are observed in nearly all cases,andmale patients are usually infertile sec-
ondary to sperm immobility.These man-ifestations are a consequence ofstructur-al
defects in the dynein arms ofcilia.Light microscopy reveals a reduction inciliary
beat frequency,and structuralabnormalities can be observed underelectron
microscopy.Primary ciliarydyskinesia (or immotile cilia syndrome)is twice as common
as Kartagener�s syn-drome and has similar sinopulmonarymanifestations without situs
inversus.38These patients often live a normal lifespan with timely management
ofsinopulmonary infections and prophylac-tic measures such as avoidance ofenvi-
ronmental pollutants.Young�s syndrome is also associatedwith chronic sinusitis,lung
disease,andmale infertility.39The etiology ofmaleinfertility,however,is secondary
toobstruction ofthe epididymis,and spermmotility is normal.There is no
associationwith situs inversus.Sinus and lung diseaseusually do not progress beyond
childhood,and few require sinus surgery.40Multiple inherited
immunodeficiencydisorders may be associated with sinusitis.These typically involve
defects ofantibody-mediated immunity,particularly IgG sub-class deficiency,for
which the inheritancepattern is unknown.41Common variableimmunodeficiency (dominant
or reces-sive),IgA deficiency (dominant),X-linkedagammaglobulinemia,and
complementdeficiencies are among the disorders iden-tified.42�44The particular type
ofimmun-odeficiency involved may dictate thenature ofthe superinfecting
organism.45For example,complement defects areassociated with gram-negative
infections.Difficult-to-manage sinus disease shouldinspire an investigation into
this area,including the quantitative measurement ofimmunoglobulins and possibly
comple-ment levels.DiagnosisRoles ofEndoscopy and CTSinus infections are typically
diagnosedbased on clinical criteria described previ-ously (see Table 16-1).Symptom
severityand effect on quality oflife can be scoredon multiple different
scales.46,47Acutesinusitis is frequently diagnosed and man-aged by the primary care
practitionerlargely based on history,but recurrentacute sinusitis,chronic
sinusitis,or thatwhich has failed medical managementrequires endoscopic evaluation
and radi-ographic imaging.This is importantbecause over two-thirds ofpatients
whomeet the criteria for rhinosinusitis havenegative results on endoscopy,and
over50% have negative results on CT scans.46Sinusitis can be diagnosed
regardlessofsymptomatic criteria ifpus is noted inthe middle meatus during
nasalendoscopy (Figure 16-6).In patients whohave had surgical antrostomy,pus may
beseen within the maxillary sinus.This canbe cultured during the
examination,withthe results being useful in antibiotic selec-tion.In addition to
purulence,nasalendoscopy can detect mucosal inflamma-tion,edema,polyposis (Figure
16-7),andanatomic variations such as a deviatedseptum.A recent study demonstrated
thatthe findings ofpurulence,polyps,ormucosal edema correlate with sinusitis
byCT,but anatomic variation was not a sig-nificant predictor.Also,negativeendoscopy
was a good predictor for CTscan results that were normal or indicatedFIGURE16-
6Purulent discharge from themiddle meatus draining into the nasopharynxadjacent to
the eustachian tube orifice.Repro-duced with permission from Joe SA,Bolger
WE,Kennedy DW.Nasal endoscopy: diagnosis andstaging ofinflammatory sinus
disease.In:Kennedy DW,Bolger WE,Zinreich SJ,editors.Diseases ofthe sinuses:
diagnosis and manage-ment.Hamilton: BCDecker Inc; 2001.p.120.FIGURE16-7View into
left nasal cavity demon-strates a polyp (P) extending from the middlemeatus.S =
septum; M = middle turbinate; I =inferior turbinate.Reproduced with permissionfrom
Joe SA,Bolger WE,Kennedy DW.Nasalendoscopy: diagnosis and staging ofinflammato-ry
sinus disease.In: Kennedy DW,Bolger WE,Zinreich SJ,editors.Diseases ofthe sinuses:
diag-nosis and management.Hamilton: BCDeckerInc; 2001.p.123.MPIS
Sinus Infections303minimal disease.46Overall,these resultsunderscore the need for
endoscopy in thediagnostic evaluation ofcases other thanisolated episodes
ofuncomplicated acutesinusitis.Approximately one-third ofrandomlyselected
asymptomatic people have somemucosal changes on CT scans,but patientswith symptoms
and some endoscopicfindings do not necessarily have positivefindings on CT
scans.48Thus,although CTis a good predictor ofmoderate mucosalthickening,it
probably should not be con-sidered a gold standard for diagnosis.Thedecision to
treat medically may be basedrationally on endoscopic findings becausesuch normal
findings are associated withnormal or near-normal CT results in over75%
ofcases.46CT is necessary,however,when surgery is anticipated,complicationsare
suspected,or when there is a signifi-cant discrepancy between history andendoscopic
examination.In these situa-tions CT not only helps to confirm thediagnosis but also
aids in surgical plan-ning.The coronal plane provides the bestview ofthe OMC
(Figure 16-8) and can beused to detect opacification,mucosalthickening,and neo-
osteogenesis,all ofwhich are indicative ofchronic inflamma-tion.Anatomic variations
such as a conchabullosa (pneumatized middle turbinate)can be also detected.Scans
can additional-ly be obtained in the axial plane,andimages may be reconstructed in
threeplanes:coronal,axial,and sagittal.Thistechnology allows for precise
anatomiclocalization ofdisease processes and intra-operative stereotactic
navigational imag-ing (see �Surgery,�below).It should benoted that although plain
films are widelyavailable and inexpensive,much more pre-cise data is obtained with
a coronal CT,whose use has comparable costs and radi-ation exposure.Although plain
films maydetect complete sinus opacification or air-fluid levels,chronic
inflammatory diseasecorrelates with as little as 2 mm ofmucos-al thickening,which
cannot be identifiedon plain films.49In an effort to reduce both costs andradiation
exposure,protocols have beendesigned involving lowered radiation doses.These allow
adequate bony detail and donot appear to cause diagnostic errors,50although soft
tissue contrast is slightlyreduced.For diagnostic purposes and forroutine elective
sinus surgery,images in thecoronal plane alone are sufficient.Theseshould be
obtained at 3 mm cuts,althoughsome centers attempt to further reducecosts by using
thicker sections.51Special ConsiderationsFungal SinusitisFungal sinusitis,as out-
lined previously,may manifest in a spec-trum ofboth invasive and
noninvasiveforms.Endoscopically,with noninvasiveor chronically invasive
disease,fungalforms may be evident (Figure 16-9),alongwith mucosal edema and/or
polyposis.Inallergic fungal sinusitis the allergic mucinthat is inspissated among
the nasal polypsand fungal debris has a peanut butter�likequality.Histologically
this contains fungalforms,eosinophils,and Charcot-Leydencrystals (breakdown
products ofeosinophil granules;Figure 16-10).Themucous membranes ofinvasive
fungalsinusitis typically contain black necroticeschars but may be pale or gray in
earlierphases.These findings are secondary toischemic necrosis induced by fungal
inva-sion ofthe mucosal vasculature and mayextend to the gingivae and palate.Suspi-
cion ofinvasive fungal sinusitis requiresbiopsy confirmation (Figure 16-11),fol-
lowed by aggressive d�bridement ofinfect-ed and devitalized
tissues.Typically,noninvasive fungal diseaseappears on CT scans as areas
ofincreaseddensity within the sinuses (Figure 16-12).FIGURE16-8Coronal computed
tomographyscan ofthe sinus through the osteomeatal com-plex.An infraorbital ethmoid
cell (Haller cell; H)is demonstrated.Also,see Figure 16-1.Repro-duced with
permission from Zinreich SJ,Got-wald T.Radiographic anatomy ofthe
sinuses.In:Kennedy DW,Bolger WE,Zinreich SJ,editors.Diseases ofthe sinuses:
diagnosis and manage-ment.Hamilton: BCDecker Inc.; 2001.p.24.FIGURE16-9Examples
offungal balls ofthe maxillary sinus.Note the fungal debris andmucosal
edema.Reproduced with permission from Dhong HJ,Lanza DC.Fungal rhinosi-nusitis.In:
Kennedy DW,Bolger WE,Zinreich SJ,editors.Diseases ofthe sinuses: diagno-sis and
management.Hamilton: BC Decker Inc; 2001.p.181.
304Part 3: Maxillofacial InfectionsThis may be secondary to the affinity offungi
for magnesium,calcium,manganese,or ferromagnetic elements,52although theexact
mechanism for this finding isunclear.CT images may also reveal exten-sive soft
tissue thickening or opacificationsecondary to polyposis or postobstructivemucus
retention.Bone thinning ordestruction may be observed from theexpansile nature
ofthe inflammatoryprocess or owing to tissue invasion.Complications
ofSinusitisBecause ofthe proximity ofthe paranasal sinuses tothe eyes and
brain,complications ofsinusitis are divided into two broad cate-gories:orbital and
intracranial.Infectionextending into the orbit and associatedsoft tissues usually
originates from the eth-moids and occurs through one oftwomechanisms:(1) direct
extension throughthe orbital wall or (2) retrograde spreadthrough veins between the
sinuses and theorbit.Lymphatic spread is not a significantfactor because lymphatics
are absent in theorbit.The spectrum oforbital complica-tions ofsinus infections has
been classifiedin five categories (Figure 16-13).53Preseptal cellulitis,or
periorbital cel-lulitis,is edema and inflammation oftheskin and muscle anterior to
the orbitalseptum secondary to impairment ofvenous drainage from these
tissues.54There are no visual symptoms,restrictionsofextraocular movement,or signs
ofchemosis as the infection has not invadedthe intraconal soft tissues.In
contrast,orbital cellulitis indicates edema andinflammation ofthe intraconal
contentsresulting in ophthalmoplegia,proptosis,and chemosis secondary to
obstruction ofvenous outflow via the ophthalmic veins.Subperiosteal abscess (Figure
16-14) isa collection ofpurulent material betweenthe bony orbital wall and the
orbitalperiosteum,usually from direct spread ofacute infection in the ethmoid
sinusesthrough the lamina papyracea.Dependingon the size ofthe abscess and the
associat-ed mass effect,and the degree ofinflam-mation,ocular muscles and visual
acuityare variably affected.Progression ofthissubperiosteal process may
subsequentlyresult in an abscess ofthe orbital tissues.An orbital abscess may also
occur withprogression oforbital cellulitis.At thisstage,restriction ofextraocular
mobility,proptosis,chemosis,and visual loss areoften observed.When orbital
cellulitis orsubperiosteal or orbital abscesses are sus-pected,contrast-enhanced CT
examina-tion is necessary.55Cavernous sinus thrombosis is a gravecomplication that
occurs from directextension or retrograde thrombophlebitis(via the ophthalmic vein)
ofethmoid orsphenoid infections.56,57In addition torestriction ofextraocular
mobility,prop-tosis,chemosis,and visual loss,cranialneuropathies and signs
ofmeningitis maybe observed.Given the frequency ofocularfindings,this entity is
often categorizedwith the orbital complications ofsinusitis,but ifthis or another
intracranial compli-cation is suspected,magnetic resonanceimaging must be
performed.Lumbarpuncture may also be indicated.Intracranial complications occur
lessfrequently than do orbital complicationsand are most commonly related to
thefrontal or sphenoid sinuses (Figure 16-15).58,59These complications may occurvia
either direct spread or retrogradethrombophlebitis.Pott�s puffy tumor is
acollection ofpus under the foreheadperiosteum with inflammatory changesofthe
overlying skin and soft tissues.FIGURE16-10Allergic mucin ofallergic
fungalsinusitis.Microscopic evaluation reveals eosino-phils and Charcot-Leyden
crystals (�400 originalmagnification; stained with hematoxylin-eosin).Reproduced
with permission from Dhong HJ,Lanza DC.Fungal rhinosinusitis.In: Kennedy DW,Bolger
WE,Zinreich SJ,editors.Diseases ofthesinuses: diagnosis and management.Hamilton:
BCDecker Inc; 2001.p.186.FIGURE16-11Silver-stained histopathologicsection revealing
tissue invasion in invasive fun-gal (Aspergillus) sinusitis (�400 original magni-
fication).Reproduced with permission fromDhong HJ,Lanza DC.Fungal
rhinosinusitis.In:Kennedy DW,Bolger WE,Zinreich SJ,editors.Diseases ofthe sinuses:
diagnosis and manage-ment.Hamilton: BC Decker Inc; 2001.p.182.FIGURE16-12Pre-and
postoperative comput-ed tomography ofthe paranasal sinuses in thismiddle-aged woman
with Bipdaris speciferaallergic fungal rhinosinusitis.Note the hyper-plastic mucosa
with the hyperdensities seen onthe bone windowing ofthe sinuses and the pre-
operative absence ofturbinates.Reproducedwith permission from Dhong H-J,Lanza
DC.Fungal rhinosinusitis.In: Kennedy DW,BolgerWE,Zinreich SJ,editors.Diseases ofthe
sinuses:diagnosis and management.Hamilton: BCDecker Inc; 2001.p.185.
Sinus Infections305This develops secondary to the spread ofinfection through
emissary veins intothe cranial bone marrow,and thusessentially represents
osteomyelitis ofthe frontal bone.An epidural abscess develops fromosteitis ofthe
posterior table ofthe frontalsinus extending into the space between thefrontal bone
and the dura.Patients presentwith low-grade fever and worseningheadache from
elevated intracranial pres-sure.This complication may be surpris-ingly indolent
because there are no focalneurologic signs and examination ofthecerebrospinal fluid
(CSF) is often nor-mal.59In a manner analogous to theorbital abscess,subdural and
brainabscesses can occur from the direct spreadofan epidural abscess or from
retrogradethrombophlebitis.Increased intracranialpressure is significant in these
cases andmay lead to herniation and death.Subdur-al abscess may cause septic venous
throm-bosis and venous infarction.60Brainabscess is associated with brain
necrosis.In contrast to the above intracranialconditions,which usually arise from
thefrontal sinus,meningitis typically arisesfrom infection ofthe ethmoid or
sphenoidsinus.61The typical presenting symptomsand signs are high
fever,headaches,seizures,and delirium.Lumbar punctureis necessary to establish the
diagnosis andobtain culture results.TreatmentMedical ManagementThe principle
oftherapy for sinusitis isto break the cycle ofimpaired mucocil-iary
clearance,stasis,infection,andcccFIGURE16-13Orbital complications ofsinusitis:
A,preseptal cellulitis (c); B,orbital cellulitis (c); C,orbital subperiosteal
abscess (a); D,orbital abscess (a); E,septic thrombosis ofthe cavernous sinus
(t).Adapted from Lusk RP,Tychsen L,Park TS.Complications ofsinusitis.In: Lusk
RP,editor.Pediatric sinusitis.NewYork: Raven Press;
1992.p.127�46.ccaatABCDEFIGURE16-14Axial computed tomography scandemonstrating a
subperiosteal abscess adjacent tothe right medial orbital wall secondary to
acuteinfection in the ipsilateral ethmoid sinuses.Reproduced with permission from
Choi SS,Grundfast KM.Complications in sinus disease.In: Kennedy DW,Bolger
WE,ZinreichSJ,editors.Diseases ofthe sinuses: diagnosis and manage-ment.Hamilton:
BC Decker Inc; 2001.p.170.badebfcgFrontalsinusFIGURE16-15Intracranial complications
ofsinusitis.These include osteomyelitis (a),periorbital abscess (b),epidural
abscess (c),subdural abscess (d),brain abscess(e),meningitis (f),and septic
thrombosis ofthe superi-or sagittal sinus (g).Adapted from Choi
SS,GrundfastKM.Complications in sinus disease.In: Kennedy DW,Bolger
WE,ZinreichSJ,editors.Diseases ofthe sinuses:diagnosis and management.Hamilton: BC
Decker Inc;2001.p.172.
306Part 3: Maxillofacial Infectionsinflammation.Treatment for uncompli-cated acute
sinusitis is primarily med-ical,with antibiotics representing themainstay
oftherapy.In most primarycare settings,it is acceptable to initiateantibiotic
therapy when the criteria foracute sinusitis are met.First-line drugsfor acute
rhinosinusitis recommended bythe Agency for Health Care Policy andResearch
Institute include amoxicillin(500 mg PO tid) and trimethoprim/sulfamethoxazole
(double strength tablets,one PO bid).It has been further recom-mended that
cephalosporins,macrolides,penicillinase-resistant penicillins,andfluoroquinolones
should be reserved forfailures offirst-line therapy or for com-
plications.However,some have ques-tioned whether,given the high
incidenceofpneumococcal and H.influenzaeresis-tance in many areas,this
graduatedantibiotic response is really appropriate.Treatment duration should be at
least 10to 14 days,and antibiotic doses must beadjusted for patient weight (in
children)and for hepatorenal function,whereappropriate.Recent trends have
includedthe use ofculture-directed therapy,which,at least theoretically,allows
long-term cost effective management.This canbe performed safely and accurately
usinga middle meatal swab under endoscopicguidance.62Oral decongestants such as
pseu-doephedrine and topical decongestantssuch as phenylephrine and
oxymetazolinemay be useful by decreasing tissue edemaby a-adrenergic
vasoconstriction.Thisallows sinus ventilation and symptomaticrelief.Topical
decongestants must be usedjudiciously,however,as continuance ofthese medications
beyond 3 to 5 days isassociated with reduced duration ofactionand rebound
vasodilation,a conditionknown as rhinitis medicamentosa.Theroles for antihistamines
and topical nasalsteroids in the management ofacute infec-tions are
controversial.Ifallergy is thoughtto be a significant predisposing or coexist-ing
factor,antihistamines may be indicat-ed.Topical steroids,although useful inchronic
rhinosinusitis,have no provenefficacy in the treatment ofacute sinusitisbut may
have a prophylactic effect in pre-venting recurrent acute episodes.Oralsteroids
(eg,prednisone or methylpred-nisolone) are not typically prescribed foracute
sinusitis when a significant bacterialcomponent is expected because
theimmunosuppressive effects may promotethe development ofcomplications.How-
ever,oral steroids are useful in the man-agement ofacute exacerbations
ofchronicsinusitis to control the baseline inflamma-tory tendencies ofthe sinonasal
mucosa.Nasal saline irrigations and mucolytics(eg,guaifenesin 600 mg PO bid�qid)
mayhave a role in the treatment ofboth acuteand chronic sinusitis by assisting
themobilization ofsecretions.Antibiotic therapy is also a major com-ponent in the
treatment ofchronic (andsubacute) sinusitis.The principles oftreat-
ment,however,differ from those for acutesinusitis.First,the appropriate duration
oftherapy may be as long as 3 to 6 weeks.27,63Additionally,empiric therapy requires
reg-imens with coverage ofStaphylococcusandanaerobes in addition to the
commonpathogens ofacute sinusitis (S.pneumoni-ae,H.influenzae,and
M.catarrhalis).26Culture-directed therapy is essential asantibiotic resistance is a
significant prob-lem in this patient population.Virtually allstrains
ofM.catarrhalisand over 50% ofthose ofH.influenzaeare penicillin resis-
tant.64Commonly employed regimensinclude clindamycin (150 mg PO qid) pluseither
trimethoprim/sulfamethoxazole or afluoroquinolone.Amoxicillin-clavulanateand
selected oral second- and third-generation cephalosporins may be usefulas single-
agent therapy.New-generationmacrolides (clarithromycin,azithromycin)and other
cephalosporins may be effective,depending on culture and sensitivityresults.26Each
antibiotic has a unique pro-file oftoxicities and side effects that mustbe
considered.Recent trends have includedthe use ofantibiotic-containing
irrigationsand nebulized aerosols,particularly in con-junction with endoscopic
sinus surgery.65Steroids are also a mainstay in thetreatment ofchronic
sinusitis.Steroidsdecrease inflammation nonspecifically viaa variety
ofmechanisms.Primarily theyinhibit cell-mediated immunity by block-ing lymphocyte
migration and prolifera-tion.66,67Eosinophil and basophil countsare reduced,68and
the release ofhistamineand leukotriene from basophils is inhibit-ed.Also,steroids
decrease both vascularpermeability and the secretory activity ofsubmucosal
glands.69Topical nasal steroids are effective inreducing mucosal inflammatory
changesand are considered safe for long-term use.70With initiation ofthe
medication,sympto-matic improvement is not realized until > 1 week ofuse.71Patients
must be coun-seled in this regard because most patientsexpect the immediate
reliefprovided bytopical decongestants,which cannot beused long-term without
rebound vasocon-gestion.Potential risks associated with nasalsteroids include
epistaxis and septal perfo-ration.The complications ofsystemicsteroid use,although
possible,are rare withtopical nasal steroids.Studies have demon-strated increased
risk ofacute open-angleglaucoma and ocular hypertension withinhaled but not
intranasal steroid use.72Suppression ofthe adrenocortical axis hasbeen observed
with higher-than-recom-mended dosages,73but other studies haveshown that routine
daily use is not associat-ed with axis suppression.74Oral steroid therapy can be
used inter-mittently in patients with chronic sinusitisto manage acute
exacerbations.Severaldifferent steroid compounds are available,and each has its own
relative potencies andside effects.Most often either prednisoneor
methylprednisolone is used.Doses usu-ally begin at 30 mg daily (or equivalent)and
are tapered over 2 to 3 weeks.Taperingdoses are required after 5 to 7 days ofther-
Sinus Infections307apy secondary to suppression oftheadrenocortical axis.Severe
acute exacerba-tions may require higher dosages,andsome patients with recalcitrant
chronicrhinosinusitis may necessitate long-termsteroid regimens.Often,protracted
steroidcourses are necessary for management ofcoexisting asthma in this patient
popula-tion.12Systemic steroid therapy is poten-tially associated with serious side
effects.Long-term use may result in osteopenia orosteoporosis,which may be
reversible inearly phases.75Patients on long-term oralsteroids should therefore
undergo bone-density studies regularly.Steroid use is alsoassociated with
cataracts,hyperglycemia,glaucoma,sodium retention,fat accumu-lation,and
psychosocial changes.Patients with chronic sinusitis with sig-nificant atopic
components may be difficultto manage.The most important strategy inthis population
is avoidance.Antihistamineuse should be limited to those with docu-mented allergy
by testing or clear allergicstigmata such as frequent sneezing or itchywatery
eyes.Antihistamines may cause dry-ing and thickening ofnasal secretionsresulting in
impaired mucociliary flow;therefore,they must be used judiciously.Afull discussion
ofallergy management isbeyond the scope ofthis chapter,but it mayinclude topical
and oral steroids,antihista-mines,and mast cell stabilizers.There isalso mounting
evidence supporting the useofimmunotherapy,particularly in caseswith an allergic
fungal component.76Antifungal agents may also have a rolein the treatment
ofsinusitis.Invasive formsoften require intravenous therapy withamphotericin B.Use
ofthis medication islimited by renal toxicity.Chronic sinusitiswith an allergic
fungal component mayalso be treated with antifungal agentsincluding itraconazole
(200 mg PO bid).Topical nasal irrigation with solutions con-taining amphotericin B
or nystatin has alsobeen employed in the treatment offungalsinusitis.The efficacy
ofthese treatments isan area ofactive research.SurgeryIndications for surgery
include (1) acutesinusitis with a pending or evolving com-plication,(2) chronic
sinusitis that hasfailed maximum medical managementincluding at least 3 weeks
ofbroad-spectrum antibiotics,and (3) most formsoffungal sinusitis.In cases
ofcomplicatedacute sinusitis and invasive fungal disease,surgery should be
performed on an urgentor emergent basis.In uncomplicated chronic sinusitis thegoals
ofsurgery are to eliminate mechani-cal obstruction ofmucociliary flow,remove
chronically inflamed mucosa andbone,manage/prevent complications,andrule out other
disorders such as neoplasia.The determination that �maximal medicalmanagement�has
failed must be individu-alized.It should be noted that the indica-tions for surgery
are more stringent in thepediatric population,for whom someadvocate 3 weeks
ofintravenous antibiotictherapy prior to consideration ofsurgery.77Children with
severe chronic sinusitisshould first have thorough work-up andappropriate treatment
for conditionssuch as allergy,GERD,CF,and immun-odeficiency.Simple measures such
asavoidance ofpollutants (eg,secondhandcigarette smoke78) and
environmentalallergens may avert the need for surgery.One study demonstrated
allergies in 80%ofchildren with sinusitis.79Children inday-care centers may be
prone to upperrespiratory infections and consequentlychronic sinusitis.80Other
series haveshown that medical treatment ofGERDmay eliminate the need for sinus
surgeryin 90% ofchildren otherwise consideredsurgical candidates.81Prior to surgery
it is important to eval-uate the CT scan to assess the extent ofinflammatory
disease and the patient�sanatomy.A mental checklist is developedto assess the depth
ofthe ethmoid skullbase and the position and integrity ofthemedial orbital
walls.The presence ofacces-sory ethmoid air cells,such as the infraor-bital cell or
concha bullosa,and anatomicanomalies such as maxillary sinus hypopla-sia are
noted.Triplanar reconstructions ofthinly cut CT scans are used as part
ofastereotactic imaging protocol (Figure 16-16).This is useful to assess anatomy
andpathology in the axial,coronal,and sagittalplanes both preoperatively and
intraopera-tively,where the surgeon can correlateendoscopic and CT findings during
dissec-tion.Use ofthis technology is indicatedwhen normal anatomic landmarks
havebeen altered,as in patients who have hadprevious surgery and in cases
ofmassivepolyposis.Patients with advanced chronicinflammatory disease,particularly
thosewith nasal polyposis,are treated with oralsteroids for up to 2 weeks before
surgery.Courses oforal and occasionally intra-venous antibiotics are required in
selectedcases preoperatively.Surgery is performed under the visu-alization
ofendoscopes (Figure 16-17),often with angled lenses,and with a vari-ety offorceps
and punches (Figure 16-18).Powered tissue shavers similar to thoseused in
arthroscopic surgery are also used(Figure 16-19).The goals ofsurgery are toremove
chronically inflamed tissue and torestore sinus ventilation,drainage,andmucociliary
clearance.Evidence exists thatin chronic sinusitis the inflammatoryprocess involves
the underlying bone.82,83Thus,it is especially important to resectthe bony ethmoid
partitions underlyingchronically inflamed mucosa.Diseasedmucosa is resected,whereas
normalmucosa is preserved.It is critical to avoidstripping ofnormal mucosa
becausedenuded bone results in delayed healing,84and the regenerated mucosa does
notregain normal ciliary density.In performing maxillary antrostomy,the uncinate
process is completely resectedand the natural ostium (see Figure 16-19)is
identified and subsequently enlarged.The opening must communicate with thenatural
ostium in a manner that permits
308Part 3: Maxillofacial Infectionsphysiologic mucociliary clearance patterns.The
bone ofthis structure frequentlyexhibits osteitis.To avoid intracranial com-
plications,special care is necessary duringthe removal ofdiseased tissue along
theskull base as well as during sphenoid andfrontal sinus surgery.Intraoperative
stereo-tactic navigational imaging is useful in per-forming more comprehensive
surgery inthese regions (see Figure 16-16).Prior to the widespread use ofendo-
scopes,ethmoidectomy was performedwith a headlight,surgical loupes,or
amicroscope.Endoscopic technology hasgreatly improved our ability to
performethmoidectomy safely and comprehen-sively.In addition,external
approachesincluding the Caldwell-Luc operation,external ethmoidectomy,and frontal
sinustrephination were performed more com-monly.The Caldwell-Luc operation,origi-
nally described in the late 1800s,is anapproach to the maxillary sinus throughthe
labiogingival sulcus and canine fossa(Figure 16-20).In the classically
describedoperation to treat chronic maxillarysinusitis,mucosa ofthe maxillary
sinuswas curettaged,and an inferior meatalantrostomy was created.Our knowledge
ofthe mucociliary clearance patterns and ourability to now address the natural
ostiumhave made the classic Caldwell-Luc proce-dure obsolete in the primary
surgicalmanagement ofchronic maxillary sinusi-tis.Occasionally a sublabial approach
isstill required to the maxillary sinus inunusual circumstances;however,givenour
current understanding ofthe ability ofthe mucosa to respond to medical therapyand
the long-term problems associatedwith mucosal stripping,only a very limit-ed
mucosal resection is performed whenthis is required.Overall,externalapproaches may
have a limited role in themanagement ofcomplicated sinusitis,butendoscopic surgery
is preferred whentechnically possible to address the impli-cated pathology.Major
complications specific to sinussurgery occur in 0 to 5% and include bleed-ing,CSF
leak and visual problems.85Intra-operative blood loss may range from 20 to500
cc,depending on the extent ofdiseaseand surgery.Hemostasis is usually achievedin
surgery with localvasoconstrictorsFIGURE16-16Aand B,Devices for intraoperative
stereotactic navigation.A selected point is identifiedin the coronal,sagittal,and
axial planes using reconstructed computed tomographic data.Reproducedwith
permission from Kennedy DW.Functional endoscopic sinus surgery: concepts,surgical
indications,and instrumentation.In: Kennedy DW,Bolger WE,Zinreich
SJ,editors.Diseases ofthe sinuses: diagno-sis and management.Hamilton: BC Decker
Inc; 2001.p.206.ABFIGURE16-17Nasal endoscope shown with itsassociated sheath used
for irrigation.Reproducedwith permission from Kennedy DW.Functionalendoscopic sinus
surgery: concepts,surgical indica-tions,and instrumentation.In: Kennedy
DW,BolgerWE,Zinreich SJ,editors.Diseases ofthe sinuses: diag-nosis and
management.Hamilton: BC Decker Inc;2001.p.203.FIGURE16-18Surgical forceps ofvarious
sizes,angles,and cutting action are available for endo-scopic surgery.Reproduced
with permission fromKuhn FA.Surgery ofthe frontal sinus.In: KennedyDW,Bolger
WE,Zinreich SJ,editors.Diseases ofthe sinuses: diagnosis and management.Hamil-ton:
BC Decker Inc; 2001.p.294.
Sinus Infections309and/or cautery.Although a small amountofbleeding is typical in
the first few daysfollowing surgery,excess bleeding is rareand,ifit does
occur,seldom reaches trans-fusable quantities.The incidence andseverity
ofpostoperative hemorrhage maybe increased in patients with
acquiredimmunodeficiency syndrome,diffusepolyp disease,and revision cases.86CSF
leak is a risk ofsurgery performedon the ethmoid bone.This occurs in 0.01to 1.4%
ofcases.85,86Ifrecognized intraop-eratively,a CSF leak should be repaired inthe
same operative setting.Patients diag-nosed with an iatrogenic CSF leak postop-
eratively may present with meningitis,which requires medical treatment and sur-
gical repair.The risk oforbital penetrationduring endoscopic sinus surgery is 2
to4%,and in one-third ofthese cases,orbitalemphysema is also
observed.Fortunatelythe risk ofblindness is low,approachingzero in several
series.85,86This devastatingcomplication is usually secondary to anexpanding
intraorbital hematoma,although optic nerve injury is possibleduring surgery ofthe
sphenoid and poste-rior ethmoid.Ifblindness is encounteredpostoperatively,initial
management is toremove any nasal packing and performorbital massage to evacuate any
bleeding.Emergent ophthalmologic consultationshould be obtained,and lateral
canthoto-my or endoscopic orbital decompressionmay be required.Another complication
ofsinus surgery affecting the eye is naso-lacrimal duct
injury.Postoperatively,thepatient presents with epiphora,or tearing.The
nasolacrimal duct courses anterior tothe natural ostium ofthe maxillary sinusand
can be injured when the antrostomy isenlarged anteriorly.The most common
complication afterendoscopic sinus surgery is the formationofsynechiae,observed in
approximately8%.86Although these may be asympto-matic,they may also contribute to
ostialstenosis and obstruction and,ultimately,the need for revision
surgery.Postopera-tively,the surgically opened sinus cavitiesare d�brided under
endoscopic visualiza-tion in the office setting.Patients are askedto use nasal
saline sprays and/or irriga-tions to reduce crusting and facilitate thed�bridement
process.Recalcitrant casesmay benefit from the addition ofantibi-otics to these
irrigation solutions.87Postoperative medical managementand long-term follow-up care
is criticallyimportant.Patients are usually put on acourse oforal antibiotics to
prevent bacte-rial proliferation in the blood and mucusthat may collect in the
sinus cavities post-operatively.Antibiotic selection and theduration oftreatment
are individualizedFIGURE16-19A powered tissue shaver is used toresect the inferior
portion ofthe uncinate process,exposing the natural ostium ofthe
maxillarysinus.Reproduced with permission from ParsonsDS,Nishioka G.Pediatric sinus
surgery.In:Kennedy DW,Bolger WE,Zinreich SJ,editors.Diseases ofthe sinuses:
diagnosis and manage-ment.Hamilton: BC Decker Inc.2001.p.275.Infraorbital
foramenand nerveBony canine fossaIntrasinus portion ofinfraorbital nerveMedial wall
of maxillary cavityFIGURE16-20Caldwell-Luc approach.The maxillary sinus is entered
throughits anterior wall in the canine fossa.Adapted from Mabry RL,Marple BF.Open
maxillary sinus procedures.In:Kennedy DW,Bolger WE,Zinreich SJ,editors.Diseases
ofthe sinuses: diagnosisand management.Hamilton: BC Deck-er Inc.2001.p.387.AB
310Part 3: Maxillofacial Infectionsaccording to culture results and the
degreeofinflammation observed.Antibiotics canbe discontinued once the mucosa
hasrecovered and ciliary activity can offset thestagnation ofsecretions.Topical and
oralsteroids are often prescribed postopera-tively to decrease inflammation
andreduce scar formation during the healingprocess.Although some patients
requirelong-term oral steroid therapy,it is prefer-ably avoided,when possible,given
the sideeffects.In contrast,patients almost univer-sally require long-term
treatment withtopical nasal steroids.This is usually welltolerated and is
considered safe.Overall endoscopic sinus surgery isconsidered successful in 80 to
90% ofpatients after at least 2 years follow-up.86,88The natural history for
patients with nasalpolyps undergoing surgery alone is recur-rence since polyposis
is multifactorial andis associated with a tendency towardmucosal inflammatory
reactivity.Onestudy demonstrated recurrent polyp dis-ease in 55% ofpatients after a
mean follow-up of3 years and 5 months.Nonetheless,surgery has a clear role inthese
patients as is evidenced by the obser-vation that over halfwere asymptomaticor
significantly improved,and none wereworse.88Diligent postoperative careincluding
d�bridement,medical manage-ment,and possibly allergy therapy isessential to reduce
or eliminate the ten-dency toward recurrence,and long-termendoscopic follow-up is
required to evalu-ate for and treat even asymptomatic dis-ease.Studies have also
demonstrated thatsinus surgery in patients with both asthmaand nasal polyposis may
decrease bothpulmonary and nasal symptoms andreduce the dependency on oral
steroids.ConclusionsUltimately,additional advancements in ourmanagement ofsinus
disease will requireadvancements in our understanding ofthepathophysiology.At this
time,a �commonpathway,�through which patients with var-ious risk factors develop
sinusitis has notbeen defined.Sinusitis can be managedeffectively,however,with
medical therapyin most cases.There are clear roles for sur-gical intervention in
acute sinusitis withcomplications (or pending complications),chronic sinusitis that
has failed medicalmanagement,and the various forms offun-gal disease.Combined with
appropriatemedical management,surgical outcomescan be maximized in these
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CHAPTER 17Osteomyelitis and OsteoradionecrosisGeorge M.Kushner,DMD,MDBrian
Alpert,DDSOsteomyelitisOsteomyelitis is defined as an inflamma-tion ofthe bone
marrow with a tendency toprogression.This is what differentiates it inthe jaw from
the ubiquitous dentoalveolarabscess,�dry socket�and �osteitis,�seen ininfected
fractures.It involves adjacent cor-tical plates and often periosteal tissues.In the
preantibiotics era,osteomyelitisofthe mandible was not uncommon.Withthe advent
ofantibiotics,it became a raredisease.In recent years antimicrobials havebecome
less effective and there has been are-emergence ofthe disease,presentingmajor
diagnostic and therapeutic chal-lenges for practicing surgeons.Despitemodern
therapy it can still remain a majorsource ofmorbidity to the patient,requir-ing
multiple surgeries and resulting inprolonged treatment with loss ofteethand/or
jawbone.The incidence ofosteomyelitis is muchhigher in the mandible due to the
densepoorly vascularized cortical plates and theblood supply primarily from the
inferioralveolar neurovascular bundle.It is muchless common in the maxilla due to
theexcellent blood supply from multiple nutri-ent feeder vessels.In addition the
maxillarybone is much less dense than the mandible.Diminished host defenses,both
localand systemic,can contribute significantlyto the emergence and clinical course
ofthedisease.Osteomyelitis has been associatedwith multiple systemic diseases
includingdiabetes,autoimmune states,malignan-cies,malnutrition,and acquired immun-
odeficiency syndrome.1The medicationslinked to osteomyelitis are
steroids,chemotherapeutic agents,and bisphos-phonates.1�3Local conditions that
adverse-ly affect the blood supply can also predis-pose the host to a bony
infection.Radiation therapy,osteopetrosis,and bonepathology can alter the blood
supply to thearea and provide a potential foothold forosteomyelitis to set in
(Figure 17-1).PathogenesisIn the maxillofacial region,osteomyelitisprimarily occurs
as a result ofcontiguousspread ofodontogenic infections or as aresult
oftrauma.Primary hematogenousosteomyelitis is rare in the
maxillofacialregion,generally occurring in the veryyoung.The adult process is
initiated by aninoculation ofbacteria into the jawbones.This can occur with the
extraction ofteeth,root canal therapy,or fractures ofthe max-illa or mandible.This
initial insult results ina bacteria-induced inflammatory processFIGURE17-
1A,Panoramic view ofcemento-ossifying fibroma ofthe right mandible,a
poorlyvascularized bone tumor.The patient had atransoral biopsy to establish the
diagnosis.Afterthe biopsy,the patient had repeated episodes ofswelling and
drainage.B,Close-up ofpanoramicview.Note the area ofosteomyelitis seen withinthe
center ofthe pathologic lesion.C,Three-dimensional computed tomography scan recon-
struction showing multiple bony sequestrum fromlow-grade osteomyelitis within bony
pathology.ACB
314Part 3: Maxillofacial Infectionsor cascade.In the normal healthy
host,thisprocess is self-limiting and is a
componentofhealing.Occasionally,however,in thenormal host,and certainly in the
compro-mised host,there is the potential for thisprocess to progress to the point
where it isconsidered pathologic.With inflammationthere is hyperemia and increased
bloodflow to the affected area.Additional leuko-cytes are recruited to this area to
fight offinfection.Pus is formed when there is anoverwhelming supply ofbacteria and
cellu-lar debris that cannot be eliminated by thebody�s natural defense
mechanisms.Whenthe pus and subsequent inflammatoryresponse occur in the bone
marrow,an ele-vated intramedullary pressure is createdwhich further decreases the
blood supply tothis region.The pus can travel via haversianand Volkmann�s canals to
spread through-out the medullary and cortical bones.Oncethe pus has perforated the
cortical bone andcollects under the periosteum,theperiosteal blood supply is
compromisedand this further aggravates the local condi-tion.The end point occurs
when the pusexits the soft tissues either by intraoral orextraoral
fistulas.MicrobiologyMore than 500 bacterial taxa have beenidentified in the
mouth.4�6The mouthand the anus are opposing ends ofthesame alimentary tube,and many
clini-cians consider them to be the most high-ly contaminated areas ofthe
humanbody.In the past,staphylococcal specieswere considered the major pathogen
inosteomyelitis ofthe jaws.However,withrefinements in the collection and pro-
cessing ofmicrobiologic specimens,weare able to get a true picture ofthe disease-
causing organisms.As with mostoral infections the prime pathogenicspecies are
streptococci and anaerobicbacteria.The anaerobes responsible aregenerally
bacteroides or peptostreptococ-ci species.Often,the infections are mixed,growing
several pathogens on final cul-ture.The clinician must begin empiricantibiotic
treatment based on the mostlikely pathogens.This could include peni-cillin and
metronidazole as dual-drugtherapy or clindamycin as a single-
drugtreatment.Definitive antimicrobial ther-apy should be based on the final
cultureand sensitivities for optimal medicalmanagement results.ClassificationOver
the years many ways ofclassifyingosteomyelitis have been presented.Arather complex
classification system wasproposed by Cierny and colleagues.7Osteomyelitis was
classified as beingeither suppurative or nonsuppurative byLew and Waldvogel.8This
classificationwas modified by Topazian.9Additionalauthors classified osteomyelitis
as beingeither hematogenous or secondary to acontiguous focus
ofinfection.10Anothersystem proposed by Hudson essentiallydivided the presentation
ofosteomyelitisinto acute and chronic forms.11With themultitude ofclassification
systems,thecontroversy involved in adequately clas-sifying osteomyelitis is clearly
evident.However,for simplicity�s sake,theclassification system offered by Hudsonis
the most advantageous to the clinician.Osteomyelitis is divided into acute
orchronic forms based on the presence ofthe disease for a 1-month
duration.111.Acute osteomyelitisa.Contiguous focus (Figure 17-
2)b.Progressivec.Hematogenous 2.Chronic osteomyelitisa.Recurrent multifocal (Figure
17-3) b.Garr�s (Figure 17-4)c.Suppurative or nonsuppurative(Figure 17-
5)d.Sclerosing (Figure 17-6)Clinical PresentationVery often,as with any
infection,thepatient with osteomyelitis ofthe maxillo-facial region will present
with classicsymptoms:�Pain�Swelling and erythema
ofoverlyingtissues�Adenopathy�Fever�Paresthesia ofthe inferior
alveolarnerve�Trismus�Malaise�FistulasThe pain in osteomyelitis is oftendescribed
as a deep and boring pain,which is often out ofproportion to theclinical picture.In
acute osteomyelitis it isvery common to see swelling and erythe-ma ofthe overlying
tissues,which areindicative ofthe cellulitic phase oftheinflammatory process ofthe
underlyingbone.Fever often accompanies acuteosteomyelitis,whereas it is relatively
rarein chronic osteomyelitis.Paresthesia ofthe inferior alveolar nerve is a classic
signofa pressure on the inferior alveolarnerve from the inflammatory processwithin
the medullary bone ofthemandible.Trismus may be present ifthere is inflammatory
response in themuscles ofmastication ofthe maxillofa-cial region.The patient
commonly hasmalaise or a feeling ofoverall illness andfatigue,which would accompany
any sys-temic infection.Lastly both intraoral andextraoral fistulas are generally
presentwith the chronic phase ofosteomyelitis ofthe maxillofacial region.Often
these patients will have a labo-ratory work-up as part oftheir
initialexamination.In the acute phase ofosteomyelitis it is common to see a leuko-
cytosis with left shift,common in anyacute infection.Leukocytosis is
relativelyuncommon in the chronic phases ofosteomyelitis.The patient may also
exhib-it an elevated erythrocyte sedimentationrate (ESR) and C-reactive protein
(CRP).Both the ESR and CRP are very sensitive
Osteomyelitis and Osteoradionecrosis315indicators ofinflammation in the bodyand
they are very nonspecific.Therefore,their main use is to follow the
clinicalprogress ofthe osteomyelitis.Nearly all patients will have someform
ofmaxillofacial imaging.Theorthopanoramic view is indispensable inthe initial
evaluation ofosteomyelitis.This view is easily obtainable in mostdental offices and
can yield valuableinformation as to the radiographicchanges with
osteomyelitis,potentialsources ofthe disease,and predisposingconditions such as
fractures and underly-ing bone disease.One must bear in mindthat radiographic
images lag behind theclinical presentation since corticalinvolvement is required
for any change tobe evident.Therefore,it may take severalweeks before the bony
changes appearradiographically.Hence,it is possible tosee a patient with acute
osteomyelitis thathas a normal-appearing orthopantomo-gram.However,one can often
see theappearance of�moth-eaten�bone orsequestrum ofbone,which is the
classicappearance ofosteomyelitis.Computerized tomography (CT)scans have become the
standard in evalu-ating maxillofacial pathology such asosteomyelitis.They provide
three-dimensional imaging not available on anorthopanoramic view.The CT scan
cangive very detailed images as to early cor-tical erosion ofbone in
ostemyelitis.Onecan often see the extent ofthe lesion andbony sequestra along with
pathologicfractures.CT scanning,like plain films,requires 30 to 50%
demineralization ofbone before changes can be seen,thuspresenting an essential
delay in diagnosisofosteomyelitis.12Magnetic resonance imaging (MRI)is generally
considered more valuable inthe evaluation ofsoft tissue lesions ofthemaxillofacial
region.However,MRI canassist in the early diagnosis ofosteo-myelitis by loss ofthe
marrow signalbefore cortical erosion or sequestrum ofthe bone appears.Thus,MRI may
benefitin identifying the earlier stages ofosteomyelitis.12Nuclear medicine has
evolved to aid inthe diagnosis ofosteomyelitis.Technetium99 has been the workhorse
ofnuclearmedicine imaging ofthe maxillofacialregion.The technetium 99 bone scan
isvery sensitive in highlighting areas ofincreased bone turnover;however,thescan is
not very specific to areas ofinfec-tion.With the addition ofgallium 67 orindium 111
as contrast agents,one can dif-ferentiate areas ofinfection from traumaor
postsurgical healing as these agentsspecifically bind to white blood
cells.FIGURE17-2A,Panoramic view ofextractionsite oftooth no.32 in an otherwise
healthy 32-year-old patient.The patient experiencedmultiple episodes ofpain and
swelling in theright posterior mandible after tooth no.32 wasremoved.B,Close-up
ofthe panoramic view ofthe no.32 site.C,Axial computed tomographyscan ofthe no.32
site.D,Coronal computedtomography scan ofthe no.32 site.Note themoth-eaten bone and
bone sequestrum.E,Transoral d�bridements ofthe right posteriormandible.F,Bone
d�brided and adjacent toothno.31 removed.Tissue eas sent for culture andsensitivity
and histopathology.ABCDFE
316Part 3: Maxillofacial InfectionsTreatmentThe management ofosteomyelitis
ofthemaxillofacial region requires both medicaland surgical interventions.In rare
cases ofinfantile osteomyelitis,intravenous antibi-otic therapy alone may eradicate
the dis-ease.Antibiotic therapy is rarely curativein later-onset cases,and the
overwhelmingmajority ofosteomyelitis cases requiresurgical intervention.Clearly the
first step in the treatment ofosteomyelitis is diagnosing the
conditioncorrectly.The tentative diagnosis is madefrom clinical
evaluation,radiographic eval-uation,and tissue diagnosis.The clinicianmust be aware
that malignancies can mimicthe presentation ofosteomyelitis and mustbe kept in the
differential diagnosis untilruled out by tissue histopathology (Figure17-7).Tissues
from the affected site shouldbe sent for Gram stain,culture,sensitivity,and
histopathologic evaluations.The clini-cal response to the treatment ofany
patientwill be compromised unless altered hostfactors can be optimized.Medical
evalua-tion and management in defining andtreating any immunocompromised state
isindicated and often helpful.For example,glucose control in a diabetic patient
shouldbe stabilized for best response to therapy.FIGURE17-3A,Panoramic view taken
ofa 55-year-old female before extraction ofsymptomatic tooth no.17.The patient had
a history ofunusual infections andrecurrent infections without a specific
diagnosis.The patient began having pain and swelling in the left mandible after
tooth no.17 was extracted.B,Panoramic viewofno.17 site postoperatively.C,Panoramic
view after intraoral d�bridements ofthe left mandible and extraction ofteeth
no.18,29,20.Histopathology confirmeddiagnosis ofosteomyelitis.The patient was
treated with antibiotics based on culture and sensitivity reports.D,Panoramic view
shows radiographic worsening ofdis-ease.Note the classic appearance ofmoth-eaten
bone and impending pathologic fracture ofthe left mandible.Medical work-up revealed
hypogamma globulinemia,achronic immunocompromised state.E,Bone specimen showing
osteomyelitis resected.F,Panoramic view after left mandible resection
ofosteomyelitis with pathologicfracture.Rigid internal fixation with a
reconstruction plate allowed maintenance ofspace and facial form with continuous
jaw function and mobility.G,The patientwas asymptomatic for 2 years before having
pain and swelling in the anterior mandible.D�bridement revealed necrotic moth-eaten
bone.H,The patient eventuallyrequired removal ofthe remainder ofthe right mandible
due to uncontrollable osteomyelitis.The patient was hospitalized and received
intravenous antibiotics basedon multiple specific culture and sensitivity
reports.She also received intravenous gamma globulin to correct
hypogammaglobulinemia.Hyperbaric oxygen treatmentswere also used to treat
refractory osteomyelitis.The patient had a prolonged in-patient hospital course
with multiple surgeries.I,Panoramic view with subtotalmandibulectomy for
osteomyelitis.Only the left ramus and condyle remain intact.The patient is
currently on daily antibiotic immunosuppressive therapy for life,aswell as monthly
infusions ofgamma globulin.Despite aggressive medical management by infectious
disease experts,she still has bouts ofrecurrent pneumonia.ABCDEFGHI
Osteomyelitis and Osteoradionecrosis317Empiric antibiotic treatment shouldbe
started based on Gram stain results ofthe exudate or the suspected pathogenslikely
to be involved in the maxillofacialregion.Definitive culture and sensitivityreports
generally take several days orlonger to be obtained but are valuable inguiding the
surgeon to the best choice ofantibiotics based on the patient�s specificcausative
organisms.13Infectious diseaseconsultation may illustrate the most cur-rent
antimicrobials and/or regimens.Surgical OptionsClassic treatment is sequestrectomy
andsaucerization.The aim is to d�bride thenecrotic or poorly vascularized
bonysequestra in the infected area and improveblood flow.Sequestrectomy
involvesremoving infected and avascular pieces ofbone�generally the cortical plates
in theinfected area.Saucerization involves theremoval ofthe adjacent bony cortices
andopen packing to permit healing by sec-ondary intention after the infected
bonehas been removed.Decortication involvesremoval ofthe dense,often
chronicallyinfected and poorly vascularized bony cor-tex and placement ofthe
vascular perios-teum adjacent to the medullary bone toallow increased blood flow
and healing inthe affected area.The key element in theabove procedures is
determined clinicallyby cutting back to good bleeding bone.Clinical judgment is
crucial in these stepsbut can be aided by preoperative imagingthat shows the bony
extent ofthe patholo-gy.It is often necessary to remove teethadjacent to an area
ofosteomyelitis.Inremoving adjacent teeth and bone theclinician must be aware that
these surgicalprocedures may weaken the jaw bone andmake it susceptible to
pathologic fracture(see Figure 17-6).Supporting the weakened area with afixation
device (external fixator or recon-struction type plate) and/or placing thepatient
in maxillomandibular fixation isfrequently used to prevent pathologic frac-
ture.Indeed,we have primarily graftedsuch areas when the sequestrectomy
andsaucerization have been deemed adequate.Some authors have proposed adjunc-tive
treatment methods that deliver highdoses ofantibiotic to the area usingantibiotic
impregnated beads or woundirrigation systems.14�16This therapyworks on the premise
that high local lev-els ofantibiotics are made available andthe overall systemic
load is very low,thusreducing the possible side effect and complication
rate.Hyperbaric oxygen (HBO) treatmenthas also been advocated for the
treatmentofrefractory osteomyelitis.This treat-ment method works by increasing
tissueoxygenation levels that would help fightoffany anaerobic bacteria present
inthese wounds.The widespread use ofHBO treatment ofosteomyelitis stillremains
controversial.Resection ofthe jaw bone has tradi-tionally been reserved as a last-
ditch effort,generally after smaller d�bridements havebeen performed or previous
therapy hasbeen unsuccessful or to remove areasinvolved with pathologic
fracture.Thisresection is generally performed via anextraoral route,and
reconstruction can beeither immediate or delayed based on thesurgeon�s
preference.Rigid internal fixationFIGURE17-4A,Facial view ofa 13-year-old
male,otherwise healthy.Note the swelling ofthe right mandibleposterior
body.B,Close-up ofthe panoramic view ofthe right mandible.Note the proliferative
periostitis at theinferior border that is characteristic ofGarr�s
osteomyelitis.C,Close-up ofthe right mandible inferior borderwith classic �onion
skin�appearance.D,Occlusal view ofthe right mandible showing �onion
skin�appearance.(Courtesy ofDr.Mark Bernstein)ABCD
318Part 3: Maxillofacial Infectionshas simplified the postoperative course
byproviding a means for immediate functionofthe jaws.We believe that early
resection andreconstruction shorten the course oftreat-ment.Once the patient
develops paresthe-sia in mandibular osteomyelitis,resectionand immediate
reconstruction are indicat-ed.At this point preservation ofthemandible is highly
unlikely and oneshould attempt to shorten the course ofthe disease and treatment
(Figure 17-8).OsteoradionecrosisRadiation therapy is a valuable treatmentmodality
in treating cancer ofthe maxillo-facial region.Radiation therapy can beused alone
or as adjunctive therapy incombination with surgery and chemother-apy.Radiation
therapy like any treatmentmodality has deleterious side effects,including mucositis
and xerostomia.Oneofthe most dreaded side effects is osteora-dionecrosis
(ORN).Historically,ORN wasfelt to represent a radiation-
inducedosteomyelitis.However,Marx has shownthat osteoradionecrosis represents
achronic nonhealing wound that is hypox-ic,hypocellular,and hypovascular.17Inyears
past,the radiation therapist usedorthovoltage therapy and there was a highincidence
ofORN.However,the modernradiation therapists use megavoltage,which is felt to be
kinder to the bone andsoft tissues.In addition,collimation andshielding oftissues
in conjunction withcareful dental evaluation preoperativelyhave greatly decreased
the incidence ofORN.The effects ofradiation last a life-time and do not decrease
over time.ORN is generally caused by trauma tothe radiated area,usually by dental
extrac-tion,but it can also occur spontaneously.The clinical picture ofORN is most
com-monly seen with pain and exposed bone inthe maxillofacial region (Figures 17-9
and17-10).ORN is more common in themandible than in the maxilla for
reasonsdescribed earlier in this chapter.A dosage ofFIGURE17-5A,Panoramic view
taken ofa 42-year-old male with pain and swelling ofthe leftmandible.Problems
started after failed root canaltreatment on tooth no.18.Teeth no.18 and 17
wereextracted.The left mandible was d�brided and oralantibiotic treatment was
prescribed.Note the gener-alized osteolysis ofthe left mandible with
dissolutionofthe inferior border.B,Technetium 99 bone scan�lighting up�the left
mandible.C,Patient withextraoral fistula,paresthesia,and painful dysesthesiaofthe
left mandible that was scheduled for resection.D,Specimen showing bony destruction
ofthe leftmandible.Tissue was sent for culture and sensitivityand histopathologic
diagnoses.E,Surgical site show-ing defect and normal bleeding bone
margins.F,Lefthemimandible with reconstruction plate in place tomaintain space and
facial form and provide imme-diate function.The patient�s mandible was to
bereconstructed in a second-stage procedure.G,Post-operative anteroposterior view
ofthe mandible.H,Postoperative panoramic view ofthe mandible.ABCDEFGH
Osteomyelitis and Osteoradionecrosis319radiation above 5,000 to 6,000 rads is gen-
erally felt to make the mandible susceptibleto ORN.Radiographically,the
appearanceon the orthopantomogram or CT scanresembles conventional osteomyelitis
withareas ofosteolysis and bony sequestrum.Often there is an appearance ofmoth-
eatenbone present on these films.The treatment ofORN is aimed atremoving the
nonviable (necrotic) tissueand allowing the body to heal itself.Theclinician must
always be aware that tissueremoved in a prior cancer patient shouldbe sent to
pathology to rule out occult orrecurrent malignant disease that is mas-querading as
a bony infection.Minord�bridements ofexposed bone may workin the most minor cases
ofORN.Currenttherapy calls for augmentation oftissuehealing response by the use
ofHBO.HBOtherapy consists of100% oxygen deliveredin a pressurized manner.Tissues
treatedwith HBO have increased levels ofoxygen,which has a negative effect on
bacteria andFIGURE17-6A,Panoramic view taken ofa 70-year-old male with pain and
swelling in the rightmandible.Note the sclerotic lesion in the right
mandible.B,Close-up ofa panoramic view showingsclerotic lesion in the right
mandible.Incisional biopsy revealed osteomyelitis.C,Axial computedtomography (CT)
scan showing sclerotic lesion ofthe right mandible.D,Axial CT scan showinglesion
ofthe right mandible.E,Coronal CT scan showing sclerotic lesion ofthe right
mandible withareas of�moth-eaten�bone.F,Panoramic view ofthe right mandible after
d�bridement back to goodbleeding bone.G,Close-up ofa panoramic view showing a
weakened area ofthe right mandible.H,Panoramic view ofthe mandible 3 months
postoperatively.The patient had heard a �pop�whilechewing.I,Close-up ofa panoramic
view showing pathologic fracture ofthe right mandible.J,Openreduction and rigid
internal fixation ofpathologic fracture ofthe right mandible.GECABDFHIJ
320Part 3: Maxillofacial Infectionsa positive effect on angiogenesis andincreased
blood flow to the area.HBO hasbeen used effectively to treat ORN and asan
adjunctive treatment with maxillofacialreconstructive procedures such as
dentalextractions,dental implants,and jawreconstruction in the radiated patient.HBO
treatment consists ofdives ortreatment sessions for 90 minutes based at2.4 atm
ofpressure.Twenty to 30 dives aregiven preoperatively before any
surgicalintervention is performed.The area ofORN is then d�brided and followed
with10 additional HBO treatments.Recon-struction ofthe maxillofacial region isbased
on the patient�s response to thetreatment protocol.HBO treatments areexpensive and
facilities are often scarce,available only in larger cities with medicalcenters or
academic health science centers.With the addition ofmicrovascularsurgery to the
surgical armamentarium,there now exists an excellent surgicaloption in treatment
ofthe patient withORN.Microvascular surgery (free flaps)allows the surgeon to bring
in hard andsoft tissues that have their own indepen-dent blood supply.The
fibula,iliac crest,scapula,and radius are all consideredapplicable donor
sites.18,19The fibula isvery popular in maxillofacial reconstruc-tion as the
surgeon can bring an excellentlength ofbone which can be osteotomizedand fabricated
into a new mandible.20,21There is an excellent skin paddle to pro-vide soft tissue
coverage (see Figure 17-7).The microvascular flap is plugged into thefacial vessels
or the carotid artery andjugular vein system for blood supply anddrainage.The
clinical advantage ofmicrovascular surgery is that the surgeondoes not have to rely
on a compromisedhost bed from radiation therapy or a lackofsoft tissue,which very
often occur inablative cancer surgery.In addition HBOtreatments are not necessary
withmicrovascular surgery.Lastly dentalimplant reconstruction has been used
withfree tissue transfer techniques and hasFIGURE17-7A,Malignancy masquerading
asosteomyelitis.Panoramic view taken from a 17-year-old male.Pain,swelling,and
paresthesiadeveloped around erupting wisdom tooth no.17.Note the bony changes at
the left mandibular angle.B,Close-up ofa panoramic view.Note the osteoly-sis,moth-
eaten bone,and dissolution ofthe inferi-or border.C,Axial computed tomography
scanshows osteolysis and swelling ofadjacent tissues.Exploration and biopsy
revealed Ewing�s sarcoma.The patient underwent aggressive chemotherapyand radiation
therapy.D,Panoramic view 2 yearspost-treatment.Pathologic fracture ofthe
leftmandibular angle with osteoradionecrosis.Biopsiesrevealed no recurrent
malignancy.E,Fibula beingprepared for free tissue transfer after resection
oftheleft mandibular angle region.F,Fibula withosteotomies to create mandibular
contour.Note thehealthy soft tissue skin paddle attached.G,Panoramic view ofthe
free fibula flap recon-struction ofthe left mandible.ABCDEFG
Osteomyelitis and Osteoradionecrosis321FIGURE17-8A,Panoramic view taken ofa 64-
year-old female with symptomatic tooth no.32 scheduled for extraction.B,Close-up
ofa panoramic viewshowing decay in partially impacted tooth no.32.C,Panoramic view
ofthe mandible with pain,swelling,and paresthesia ofthe right mandible.D,Close-up
ofa panoramic view showing pathologic fracture with bone sequestrum at the right
mandibular angle region.E,Right angle d�brided via an extraoralapproach.F,Rigid
fixation applied to a �defect fracture.�No bony contact is present after
osteomyelitis is d�brided to normal bleeding time.G,The patientreceives an
autogenous bone graft as part ofprimary surgery.H,Panoramic view ofd�bridements and
reconstruction as a one-stage procedure.ABCDEFGHABCFIGURE17-9A,Panoramic view ofthe
mandible post-radiation in a patient with oral squamous cell carcinoma.Note the
large bony sequestrum.B andC,Intraoral views ofthe right and left mandible showing
exposed bone.(CONTINUEDONNEXTPAGE)
322Part 3: Maxillofacial Infectionsproven successful in the dental reconstruc-tion
ofthese patients.22ConclusionOsteomyelitis and osteoradionecrosis pre-sent an
ongoing and potentially difficultclinical scenario to manage.Many patientswill
receive a combination ofsurgery andmedical management to adequately healfrom these
diseases.Some patients will berequired to undergo extensive and poten-tially
disfiguring surgery to manage theirdisease.The medical management,includ-ing
antibiotic therapy and HBO treat-ment,may be expensive,time consuming,and
disruptive to the patient�s life.Both ofthese conditions can be started with some-
thing as innocuous and common as a den-tal extraction.Clinicians must always be
vigilant forpost-treatment complications,includingosteomyelitis and
osteoradionecrosis.Despite advances in both medical manage-ment and surgical
therapy,the absoluteanswer to the prevention and/or oral man-agement
ofosteomyelitis and osteora-dionecrosis has yet to be found.References1.Marx
RE.Chronic osteomyelitis ofthe jaws.Oral Maxillofac Surg Clin North
Am1991;3:367�81.2.Marx RE.Pamidronate and zoledronateinduced avascular necrosis
ofthe jaws.JOral Maxillofac Surg 2003;61:1115�8.3.Migliorati CA.Bisphosphonates and
oral cavi-ty avascular bone necrosis.J Clin Oncol2003;21:4253�4.4.Schuster
GS.Microbiology ofthe orofacialregion.In:Topazian G,Goldberg H,HuppJR,editors.Oral
and maxillofacial infec-tions.4th ed.Philadelphia (PA):W.B.Saun-ders;2002.5.Flynn
TR.Anatomy and surgery ofdeep spaceinfections ofthe head and neck � knowl-edge
update.Rosemont (IL):AmericanAssociation ofOral and Maxillofacial Sur-
geons;1993.p.30�42.6.Peterson LJ.Microbiology ofhead and neckinfections.Oral
Maxillofac Clin North Am1991;3:247�57.7.Cierny G,Mader J,Pennick J.A clinical
stagingsystem for osteomyelitis.Contemp Orthop1985;10:17.8.Lew DP,Waldvogel
FA.Osteomyelitis.N Engl JMed 1997;336:999�1007.9.Topazian RG.Osteomyelitis ofthe
jaws.In:Topazian G,Goldberg H,Hupp JR,editors.Oral and maxillofacial infections.4th
ed.Philadelphia (PA):W.B.Saunders;2002.10.Vighagool A,Calhoun J,Mader J,et
al.Thera-py ofbone and joint infections.Hosp For-mul 1993;28:66.11.Hudson
JW.Osteomyelitis and osteora-dionecrosis.In:Fonseca RJ,editor.Oral andmaxillofacial
surgery.Vol 5.Philadelphia(PA):W.B.Saunders;2000.12.Schuknecht B,Carls
F,Vulavanis,et al.Mandibular osteomyelitis:evaluation andstaging in 18 patients
using magnetic reso-nance imaging,computed tomography andconventional radiographs.J
Craniomaxillo-fac Surg 1997;25:26.13.Peterson L,Thomson R.Use ofthe clinical lab-
oratory for the diagnosis and managementofinfectious diseases related to the oral
cav-ity.Infect Dis Clin North Am 1999;13:775.14.Alpert B,Colosi T,vonFraunhofer
JA,et al.The in-vivo behavior ofgentamicinPMMA beads in the maxillofacial region.J
Oral Maxillofac Surg 1989;47:46.15.Chisholm B,Lew D,Sadasivan I.The use
oftobramycin impregnated polymethyl-methracrylate beads in the treatment
ofosteomyelitis ofthe mandible.J Oral Max-illofac Surg 1993;51:444.FGDFIGURE17-9
(CONTINUED)D,Transoral d�bridements ofosteoradionecrosis.E,Specimen ofthe
mandible,essentially �lifted out�ofthe tissue bed.F andG,Lateral and frontal views
afterremoval ofthe mandible involved with osteoradionecrosis.The remaining
deformity is com-monly known as �Andy Gump�deformity.EFIGURE17-10Rare case
ofmaxillary osteora-dionecrosis.Clinical presentation is one ofexposed bone and
pain.
Osteomyelitis and Osteoradionecrosis32316.Grime P,Bowerman J,Weller
P.Gentamicinimpregnated PMMA beds in the treat-ment ofchronic osteomyelitis
ofthemandible.Br J Oral Maxillofac Surg1990;28:367.17.Marx RE.Osteoradionecrosis:a
new concept ofits pathophysiology.J Oral Maxillofac Surg1983;41:283.18.Disa
JJ,Pusic Al,Hidalgo DA,et al.Simplifyingmicrovascular head and neck reconstruc-
tion:a rational approach to donor siteselection.Ann Plast Surg
2001;47:385�9.19.Hidalgo DA,Disa JJ,Cordeiro PG,et al.A reviewof716 consecutive
free flaps for oncologicsurgical defects:refinement in donor siteselection and
technique.Plast Reconstr Surg1998;102:722�32.20.Hidalgo DA,Pusic AL.Free flap
mandibularreconstruction:a 10 year follow-up study.Plast Reconstruct Surg
2002;110:438�9.21.Cordeiro PG,Disa JJ,Hidalgo DA,et al.Recon-struction ofthe
mandible with osseous freeflaps:a 10 year experience with 150 consec-utive
patients.Plast Reconstr Surg 1999;104:1314�20.22.Disa JJ,Winters RM,Hidalgo DA.Long
termevaluation ofbone mass in free fibula flapmandibular reconstruction.Am J
Surg1997;174:503�6.
Part 4MAXILLOFACIALTRAUMA
CHAPTER 18Initial Management ofthe Trauma PatientMichael P.Powers,DDS,MSMichael
S.Scherer,DDS,MDThe initial assessment and management ofa patient�s injuries must
be completed inan accurate and systematic manner toquickly establish the extent
ofany injuryto vital life-support systems.Nearly 25 to33% ofdeaths caused by injury
can beprevented when an organized and system-atic approach is used.1Significant
data exist to suggest thatdeath from trauma has a trimodal distrib-ution.2The first
peak on a linear distribu-tion ofdeaths is within seconds or minutesofthe
injury.Invariably these deaths aredue to lacerations ofthe brain,brainstem,upper
spinal cord,heart,aorta,or otherlarge vessels.Few ofthese patients can
besaved,although in areas with rapid trans-port,a few ofthese deaths have
beenavoided.The second death peak occurswithin the first few hours after
injury.Theperiod following injury has been called the�golden hour�because these
patients maybe saved with rapid assessment and man-agement oftheir injuries.Death
is usuallydue to central nervous system (CNS)injury or hemorrhage.Recent analysis
oftrauma system efficacy suggests that trau-ma deaths could be reduced by at
least10% through organized trauma systems.These patients,whose numbers are signif-
icant,benefit most from regionalized trau-ma care.3The third death peak occurs
daysor weeks after the injury and is usually dueto sepsis,multiple organ failure,or
pul-monary embolism.4Patients are assessed and treatmentpriorities are established
based onpatients�injuries and the stability oftheirvital signs.In any emergency
involving acritical injury,logical and sequentialtreatment priorities must be
establishedon the basis ofoverall patient assessment.Injuries can be divided into
three generalcategories:severe,urgent,and nonur-gent.2Severe injuries are
immediately lifethreatening and interfere with vital phys-iologic
functions;examples are compro-mised airway,inadequate breathing ,hemorrhage,and
circulatory systemdamage or shock.These injuries consti-tute approximately 5%
ofpatient injuriesbut represent over 50% ofinjuries associ-ated with all trauma
deaths.Urgentinjuries make up approximately 10 to15% ofall injuries and offer no
immedi-ate threat to life.These patients may haveinjuries to the abdomen,orofacial
struc-tures,chest,or extremities that requiresurgical intervention or repair,but
theirvital signs are stable.Nonurgent injuriesaccount for approximately 80%
ofallinjuries and are not immediately lifethreatening.This group ofpatients even-
tually requires surgical or medical man-agement,although the exact nature
oftheinjury may not become apparent untilafter significant evaluation and observa-
tion.Laboratory studies,additional phys-ical findings,radiographic examinations,and
observations for several days orweeks may be required.5The goal ofini-tial
emergency care is to recognize life-threatening injuries and to provide life-saving
and support measures untildefinitive care can be initiated.Assessment ofthe
Severity ofInjuryThe primary goal oftriage is to prioritizevictims according to the
severity andurgency oftheir injuries and the availabil-ity ofthe required care.With
regionaltrauma centers in modern trauma sys-tems,the goal oftriage is to rapidly
andaccurately identify patients with life-threatening injuries and to treat
thosepatients appropriately,while at the sametime avoiding unnecessary transport
ofless severely injured patients (Figure 18-1).6�8Over the past three decades
manyscales and scoring systems have beendeveloped as tools to predict outcomesbased
on several criteria.
328Part 4: Maxillofacial TraumaGlasgow Coma ScaleThe Glasgow Coma Scale (GCS)
wasdeveloped in 1974 by Teasdale and Jennet.9It was the first attempt to quantify
theseverity ofhead injury.The three variablesincluded were best motor
response,bestverbal response,and eye opening (Table18-1).Best motor response is a
reflectionofthe level ofCNS function,best verbalresponse shows the CNS�s ability to
inte-grate information,and eye opening is afunction ofbrainstem
activity.Scoresrange from 3 to 15,with a higher numberrepresenting an increased
degree ofcon-sciousness.The use ofthe letter Tdesig-nates that the patient was
intubated at thetime ofthe examination.In a prospective multicenter study,patients
with a head injury who had anadmission GCS of9 or less correlated withhigher
mortality rates,regardless ofcentervolume,mechanism ofinjury,or treat-
ment10;therefore,this system can be usedto predict outcomes.The GCS has weak-nesses
in that it does not take into accountfocal or lateralizing signs,diffuse metabol-ic
processes,or intoxication.Trauma Score and Revised Trauma ScoreThe Trauma Score was
developed byChampion and colleagues to quickly assessthe extent ofinjury to vital
systems andthe severity ofthe injury to provide prop-er triage and treatment ofthe
patient.11Itwas later modified by Champion and col-leagues to become the Revised
TraumaScore in 1989.12The Trauma Score provided a means ofcharacterizing the
physiologic status ofinjured patients�cardiovascular,respiratory,and neurologic
systems.The Trauma Scoreincorporated five variables:GCS,respirato-ry
rate,respiratory expansion,systolicblood pressure,and capillary refill.TheRevised
Trauma Score omitted respiratoryexpansion and capillary refill owing to dif-ficulty
assessing these elements in the fieldand the wide margin for interpretation.� GCS <
14 or � Systolic BP < 90 or � RR < 10 or > 29 or � RTS < 11 or � PTS < 9Measure
vital signs and level of consciousness Yes, take to trauma center;alert trauma
teamNo, evaluate for mechanism of injury and evidence of high-energy impact � Flail
chest � Limb paralysis� Two or more proximal long-bone fractures � Pelvic
fractures� Amputation proximal to wrist/ankle � Combination trauma with burns� All
penetrating traumas to head, neck, torso, and extremities proximal to elbow and
kneeYes, take to trauma center;alert trauma team� Ejection from auto � Extrication
time > 20 min� Death in same passenger compartment � Falls > 6m� Pedestrian thrown
or run over � Roll over� High-speed auto crash � Auto-pedestrian injury with > 8
km/h impact� Initial speed > 64 km/h � Motorcycle crash > 32 km/h or with � Major
auto deformity > 50 cm separation of rider and bike� Intrusion into passenger
compartment > 30 cm Yes, contact medical control; considertransport to trauma
center; considertrauma team alertNo� Age < 5 or > 55 yr� Pregnancy�
Immunosuppressed patients � Cardiac disease; respiratory disease� Insulin-dependent
diabetes, cirrhosis, morbid obesity, coagulopathyYes, contact medical control;
considertransport to trauma center; considertrauma team alertNo, reevaluate with
medical control Step 1Step 2No, assess anatomy of injuryStep 3 Step 4 When in
doubt, take to a trauma center! FIGURE18-1Triage decision scheme.BP = blood
pressure; GCS = Glasgow Coma Scale; PTS = PediatricTrauma Score; RR = respiratory
rate; RTS = Revised Trauma Score.Adapted from American College ofSur-geons
Committee on Trauma.Advanced trauma life support for doctors: student course
manual�.6th ed.Chicago: American College ofSurgeons; 1997.
Initial Management ofthe Trauma Patient329With the original trauma score,the
totalpoints added to give a trauma score of1 to15,the higher the score,the better
the prog-nosis.Thus,an injured patient who exhibitseye opening to painful stimulus
(score 2),averbal response that is incomprehensible(score 2) and withdrawal from a
painfulstimulus (score 4) would have a GCS of8 points and would contribute 3 points
tothe trauma score.The Revised Trauma Score has a codedvalue for each ofthree
variables (Table 18-2).A value of0 to 4 is assigned for eachvariable to give a
total range of0 to 12,with lower scores representing an increas-ing severity
ofinjury.Trauma scores ofaround 8 indicate an approximate 33%probability for
mortality (Table 18-3).13,14In 1989 Champion and colleagues per-formed the Major
Trauma OutcomeStudy,consisting ofan analysis of33,308trauma patients whose cases
were submit-ted by 89 hospitals across the United Statesand Canada,with survival
probabilitiesassociated with admission trauma scoresdetermined for 25,327
patients.They con-cluded that patients likely to benefit fromprompt diagnosis and
definitive care atlevel I trauma centers are those with anoriginal trauma score
of12 or less.12Injury Severity ScoreThe Injury Severity Score was developedto deal
with multiple traumatic injuries.It compares death rates from blunt trau-ma using
data that rate the severity ofinjury in each ofthe three most severelyinjured organ
systems.Each injury isevaluated and categorized according tothe injured organ
system (respiratory,CNS,cardiovascular,abdominal,extrem-ities,and skin) and graded
according tothe severity ofthe injury:1 is minor;2moderate;3 severe non�life
threatening;4 life threatening,survival probable;5survival not probable;6 fatal
cardiovas-cular,CNS,or burn injuries.The threehighest scores for organ systems are
thensquared and added;the highest injuryseverity score possible is 108 (62+
62+62).Mortality rates have been found toincrease with greater severity ofinjuryand
age (Table 18-4).15In addition to the field scales thatmeasure abnormal physiologic
signs forassessment ofinjury for triage decisions,mechanism-of-injuryfactors and
anatom-ic factors are also important considerations.Mechanism-of-injury factors can
provideinsight to a possible significant injury thathas not yet resulted in
significant changesin vital signs.Those such factors that have ahigh correlation
with life-threateninginjuries include the following16:�Evidence ofa collision
involving high-energy dissipation or rapid deceleration�A fall of6 m or
more�Evidence that the patient was in a dan-gerous environment when injured (eg,a
burning building or icy water)�An automobile accident in which ittakes > 20 minutes
to remove thepatient,there is significant damage tothe passenger
compartment,rearwarddisplacement ofthe front axle hasoccurred,the patient is
ejected fromthe vehicle,a rollover occurs,or otherpassengers have died Anatomic
factors that correlate withmortality include penetrating trauma to
thehead,neck,torso,groin,or thigh;flail chest;major burns;amputations;two or
moreproximal long bone fractures;and paralysis.Concurrent disease or factors such
as age of< 5 years or > 55 years and known cardiacor respiratory disease may
sharply worsen apatient�s prognosis,even in the presence ofonly a moderately severe
injury.17Table 18-1Glasgow Coma ScaleActionScoreEye openingSpontaneously4To
speech3To pain2None1Motor responseObeys6Localizes pain5Withdraws from pain4Flexion
to pain3Extension to pain2None1Verbal
responseOriented5Confused4Inappropriate3Incomprehensible2None1Adapted from Teasdale
G and Jennett B.9Patient�s score determines category ofneurologic impair-ment:15 =
normal;13 or 14 = mild injury;9�12 =moderate injury;3�8 = severe injury.Table 18-
2Revised Trauma Score Variables Glasgow Coma ScaleSystolic Blood Pressure (mm
Hg)Respiratory RateCoded Value13�15> 8910�2949�1276�89> 2936�850�756�924 or
51�491�513000Adapted from Champion HR et al.12 Table 18-3Predicting Mortality
Usingthe Revised Trauma ScoreTrauma ScoreMortality Rate (%)12< 110128336374662700>
99Adapted from Senkowski CK and McKenney MG.14
330Part 4: Maxillofacial TraumaThe American College ofSurgeonsCommittee on Trauma
Subcommittee onAdvanced Trauma Life Support has devel-oped a schematic orderly
assessment ofinjured patients.The Advanced TraumaLife Support (ATLS) system
consists ofrapid primary evaluation,resuscitation ofvital functions,a detailed
secondaryassessment,and,finally,the initiation ofdefinitive care (see Figure 18-
1).7Other Scoring SystemsMany other scoring systems and tools havebeen created in
attempts to accurately aidtriage and to predict outcomes,includingthe Pediatric
Trauma Score,18the Traumaand Injury Severity Score,19and A SeverityCharacteristic
ofTrauma score20;recentlyscales using the ninth edition ofInterna-tional
Classification ofDiseases nomen-clature have been implemented includingan
International Classification ofDisease-Based Injury Severity Score.21Primary
Survey:ABCsAn algorithm for the initial systemic evalu-ation and stabilization
ofthe multiplyinjured patient is presented in Figure 18-2.During the primary
survey,life-threateningconditions are identified and reversedquickly.This period
calls for quick and effi-cient evaluation ofthe patient�s injuries andalmost-
simultaneous lifesaving interven-tion.The primary survey progresses in alogical
manner based on the ABCs:airwaymaintenance with cervical spine control,breathing
and adequate ventilation,and cir-culation with control ofhemorrhage.Let-ters D and
E have also been added:a briefneurologic examination to establish
degreeofconsciousness,and exposure ofthepatient via complete undressing to
avoidinjuries being missed because they are cam-ouflaged by clothing.Airway
Maintenance with Cervical Spine ControlThe highest priority in the initial assess-
ment ofthe trauma patient is the estab-lishment and maintenance ofa patent air-
way.In the trauma patient,upper airwayobstruction may be due to bleeding fromoral
or facial structures,aspiration offor-eign materials,or regurgitation ofstom-ach
contents.Commonly,the upper air-way is obstructed by the position
ofthetongue,especially in the unconsciouspatient (Figure 18-3).Initially a chin-
liftor jaw-thrust procedure may position thetongue and open the airway.The chin-
liftprocedure is performed by placing thethumb over the incisal edges
ofthemandibular anterior teeth and wrappingthe fingers tightly around the
symphysisor the mandible.The chin is then liftedgently anteriorly and the mouth
opened,ifpossible.This method should nothyperextend the neck.8The other handcan be
used to assist with access to the oralcavity,using the fingers in a sweepingmotion
to remove such things as debris,vomitus,blood,and dentures that may beresponsible
for the obstruction.A tonsil-lar suction tip is helpful to remove accu-mulations
from the pharynx.Patientswith facial injuries who may have basilarskull fractures
or fractures ofthe cribri-form plate may,with the routine use ofasoft suction
catheter or nasogastric tube,be compromised as these tubes may inad-vertently be
passed into the contents ofthe cranial vault during attempts at a pha-ryngeal
suction.The jaw thrust procedure requires theplacement ofboth hands along
theascending ramus ofthe mandible at themandibular angle.The fingers are
placedbehind the inferior border ofthe angle,and the thumbs are placed over the
teethor chin.The mandible is then gentlypulled forward with the fingers at theangle
and rotated inferiorly with pressurefrom the thumbs.The elbows may beplaced on the
surface alongside thepatient to assist with stability.The jaw-thrust procedure is
the safest method ofjaw manipulation in a patient with a sus-pected cervical
injury.The jaw-thrustprocedure does require two hands,andassistance must be
available to clear thedebris and other obstructions.After thejaw is opened,it may
be possible to placea bite lock or large suction device towedge the teeth open.An
oral or nasalairway should be placed to elevate thebase ofthe tongue and to
maintain thepatent airway.With any patient sustaining injuriesabove the
clavicle,one should assumethere may be a cervical spine injury andavoid
hyperextension or hyperflexion ofthe patient�s neck during attempts toestablish an
airway.Excessive movementofthe cervical spine can turn a fracturewithout neurologic
damage into a frac-ture that causes paralysis.Maintenanceofthe cervical spine in
the neutral posi-tion is best achieved with the use ofabackboard,bindings,and
purpose-builthead immobilizers.The use ofsoft orsemirigid collars allows,at
best,only50% stabilization ofmovement.22Cervi-cal spine injury should be assumed
pre-sent and protected against until thepatient can be stabilized and
cervicalinjury can be ruled out during the sec-ondary survey.Table 18-4Mortality
Rates for Various Injury Severity Scores by Age GroupsMortality Rates for Scores
(%)Age (yr)n15253545550�491,5403832618950�69316521566810070+109164582100100Adapted
from Powers M.15
Initial Management ofthe Trauma Patient331YesNoYesNoNoYesNoNoYesNoYesYesIntubate or
secureoral airway.*Airway patentand secure?1. Administer oxygen.2. Maintain
cervical spine immobilization.Unilaterally diminishedbreath sounds (after
endotracheal tube repositioning)?1. Intubate.2. Assist ventilation.Tube or needle
thoracostomyHead injury withunconsciousness or pupil asymmetry?Pneumothorax
orhemothorax?Head injury?Check ventilation:1. Hypoventilation?2. Flail chest? 3.
Respiratory distress?1. Open chest.�Pulse present?2. Relieve cardiactamponade. 3.
Cross-clamp sorts.1. Stop gross externalhemorrhage.2. Insert two or morelarge-bore
intravenous lines. 3. Draw blood for cross-matching cbc.4. Rapidly infuse
crystalloid solution.5. Maintain cardiac monitoring.Shock present(hypotension,
delayedcapillary refill, cool palemoist skin)?1. Check vital signs and insert
intravenous line(s); draw blood for cbc and blood gasdeterminations.2. Obtain
radiographs (portable chest radiographs, anteroposterior view of pelvis, cervical
spine).3. Remove clothing; perform head-to-toe examination.4. Insert Foley
catheter�; obtain urine for analysis.�1. Intubate.2. Hyperventilate. 3. Administer
mannitol 1 g/kg intravenously.Cardiac tamponade(distended neck veins, high central
venouspressure, penetratingtrauma near heart)?Abdominal trauma (abdominal
tenderness,penetrating abdominal trauma, or multiple blunttrauma with
alteredconsiousness)?Aortic injury (widenedmediastinum, apical cap, first rib
fracture, aortic nob obscuration)?Insert chest tube.Obtain head CT scan.1. Confirm
diagnosiswith echocardiogramor needle aspiration,if time permits.2.. Perform
thoracotomy.Obtain CT scan or perform peritoneallavage.Obtain aortic
archarteriogram.Multiple traumaFIGURE18-2Multiple trauma algorithm.cbc = complete
blood count; CT = computedtomography.*Maintain cervical spine
precautions.Nasotracheal intubation (preferred) ororotracheal intubation with axial
head traction.�Unlikely to be ofbenefit for blunt traumawith asystole.Perform only
ifexperienced with the procedure and ifthere is adequate surgicalsupport.�Ifnot
contraindicated (ie,high-riding prostate,meatal blood,scrotal hematoma).�Ifnot
contraindicated (ie,midface or cribriform plate fracture).Adapted from Trunkey
DDIn: Ho M,Saunders CE,editors.Current emergency diagnosis and treatment.3rd
ed.Norwalk (CT): Lange Publishing Co.; 1990.
332Part 4: Maxillofacial TraumaBreathingWith establishment ofan adequate airway,the
pulmonary status must be evaluated.Ifthe patient is breathing
spontaneously�confirmed by feeling and listening for airmovement at the nostrils
and mouth�supplemental oxygen may be delivered byface mask.The exchange ofair does
notguarantee adequate ventilation.The chestwall ofa patient with a
pneumothorax,flail chest,or hemothorax may move butnot ventilate
effectively.Also,shallowbreaths with minimal tidal volumes do notventilate the
lungs effectively.Very slow orrapid rates ofrespiration usually suggestpoor
ventilation.The patient�s statusshould be reevaluated constantly.Ifsignsofadequate
ventilation deteriorate,asecure airway should be placed (ideally anendotracheal
tube) and assisted ventila-tion should be started.Ifthe patient is notbreathing
after establishment ofan airway,artificial ventilation should be providedwith a
bag-valve mask or a bag attached toan endotracheal tube.The patient whorequires
assisted positive pressure ventila-tion from an Ambu bag or ventilator mustbe
carefully monitored ifthe chest statushas not been completely evaluated.Changes in
intrathoracic pressure mayconvert a simple pneumothorax into atension
pneumothorax.The chest shouldbe exposed and inspected for obviousinjuries and open
wounds.There shouldbe equal expansion ofthe chest wall with-out intercostal and
supraclavicular muscleretractions during respiration.The rate ofbreathing should be
evaluated for tachyp-nea or other abnormal breathing patterns.Signs ofchest injury
or impending hypox-ia are frequently subtle and include anincreased rate
ofbreathing and a change inbreathing pattern,frequently toward shal-lower
respirations.7The chest wall shouldalso be inspected for bruising,flail chest,and
bleeding,and the neck should be eval-uated for evidence oftracheal
deviation,subcutaneous emphysema,and distendedjugular veins.The chest should be
palpat-ed for the presence ofrib or sternal frac-tures,subcutaneous
emphysema,andwounds.Auscultation ofthe chest mayreveal a lack ofbreath sounds in an
area,suggestive ofinadequate ventilation.Dis-tant heart sounds and distended
neckveins are suggestive ofcardiac tamponade.Arterial oxygen tension (PaO2) should
bemaintained between 70 and 100 mm Hg.Aside from airway obstruction,the
causesofinadequate ventilation in the traumavictim result from altered chest
wallmechanics.Open pneumothorax,flailchest,tension pneumothorax,and mas-sive
hemothorax are immediate life-threatening conditions and should bequickly
identified and treated.Open PneumothoraxAn open pneumo-thorax is due to a defect in
the chest wall,allowing the air to be moved in and out ofthe pleural cavity with
each respiration(Figure 18-4).Because ofthe loss ofchest wall integrity,equilibrium
developsbetween intrathoracic pressure andatmospheric pressure.The involved
lungcollapses on inspiration and slightlyexpands on expiration,causing air to
besucked in and out ofthe wound;this isreferred to as a sucking chest wound.Ifthe
opening in the chest wall is approxi-mately two-thirds ofthe diameter
ofthetrachea,air will pass through the path ofleast resistance�the chest wall
defect.With the collapse ofthe involved lung anda loss ofnegative pleural
pressure,theexpired air from the normal lung passes tothe involved lung instead
ofout ofthe tra-chea,and it returns to the normal lung oninspiration.This
eventually results in alarge functional dead space in the normallung and,combined
with loss oftheinvolved lung,may develop into a severeventilation-perfusion
problem.An open pneumothorax should betreated with coverage ofthe defect with
asterile occlusive dressing that is secured onthree sides ofthe dressing to the
chest.Theunsecured side ofthe dressing acts as aone-way valve,allowing air to
escape thepleural cavity on expiration.Secure tapingofalledges ofthe dressing
results in anaccumulation ofair within the thoracicFIGURE18-3A,Commonly in the
unconsciouspatient,the tongue drops posteriorly to occlude theairway.This may be
especially true in the patientwith mandibular fractures because the tongueloses
support.A patient with a suspected maxillo-facial or head trauma must have the head
stabi-lized at all times to prevent hyperflexion ofaninjured cervical spine until
the possibility ofinjuryhas been ruled out.B,With the cervical spine sta-bilized,a
jaw-thrust may be used.C,A Chin-liftprocedure also may be helpful to open the
airway.Adapted from Powers M.15ABC
Initial Management ofthe Trauma Patient333cavity and a subsequent tension pneu-
mothorax.Occlusive dressings such aspetrolatum gauze may be used as a tempo-rary
measure during initial examinationor over large defects.A chest tube must beplaced
in a distant site on the affectedchest wall to avoid development ofa ten-sion
pneumothorax,and the wound musteventually be closed in the operatingroom.Ifthe lung
does not expand afterclosure ofthe defect or ifsigns ofpoorventilation persist,the
patient should beplaced on a ventilator with positive end-expiratory pressure
(PEEP) to expand thelung.The patient should be carefully mon-itored and have a
chest tube in place toavoid the development ofa tension pneu-mothorax caused by a
tear in one ofthebronchi or in the lung parenchyma.Signsofa tension pneumothorax in
patients onventilators include increased airway resis-tance and diminished tidal
volume.A closed pneumothorax may developfrom blunt trauma to the chest or a
lunglaceration,possibly from a fractured rib.Air from the lung to the pleural
spaceequalizes the pressures,and the lung col-lapses.A ventilation-perfusion
deficitoccurs because the blood circulated to theaffected lung is not
oxygenated.With apneumothorax,percussion ofthe chestshows hyperresonance.Breath
sounds areusually distant or absent.Management ofthe pneumothorax is confirmed and
eval-uated with upright chest radiographs.Anopen pneumothorax that has a
dressingplaced over the chest wound becomes aclosed pneumothorax.Pneumothoraces
that are traumaticallyinduced are usually treated with a tubethoracostomy to
correct any respiratorycompromise.A small pneumothorax maybe treated by
hospitalization and carefulobservation ifthe patient is otherwisehealthy,is symptom
free,and does notneed general anesthesia or positive pres-sure ventilation and
ifthe size ofthe pneu-mothorax is not increasing as measured onserial 24-hour chest
radiographs.23,24Thisis rarely the case with the trauma victim,and a chest tube
should be placed immedi-ately in the multiply injured patient with apneumothorax
(Figure 18-5).A moderate-sized chest tube (32�40Fin adults or 26�30F in children)
is general-ly placed either anteriorly in the secondintercostal space midclavicular
line or inthe fourth or fifth intercostal space midax-illary line.The midaxillary
line is general-ly preferred for cosmetic reasons,and ifthe tube is positioned
properly superiorlytoward the apex ofthe lung,it can effec-tively remove both fluid
and air.A skin incision ofapproximately 3 cmin length is made one intercostal
spacebelow the intended placement ofthe tube.Ifthe tube is to be placed through
thefourth intercostal space,an incision is madethrough the skin along the fifth
intercostalspace.A gloved finger is used to tunneltransversely through the
subcutaneous tis-sue to the inferior margin ofthe fourth rib.The intercostal
muscles are separated with alarge Kelly clamp,and the chest tube isinserted
superiorly and posteriorly into thepleural cavity.The tube should be securedto the
skin with sutures,and an occlusivedressing should be used to cover the defectaround
the tube.The tube is then connect-ed to an underwater sealed drainage toremove the
air or fluid.Upright posteroan-terior and lateral chest radiographs shouldbe taken
to confirm the position ofthechest tube,the position ofthe last drainagehole on the
tube,and the position andamount ofair or fluid remaining in thepleural cavity.Daily
physical examinationAirCollapsed lungChest walldefectFIGURE18-4A,A pneumothorax
develops from damage to the chest wall or laceration ofthe lung pleura,with a
resulting loss ofnegative intrapleural pres-sure.A pneumothorax may be graded as
small (15�60%) or large (> 60%).Band C,An open or communicating chest wound occurs
when there is an openwound in the chest wall.Air can often be heard moving in and
out ofthe wound during respirations; the condition may be referred to as a sucking
chest wound.An open pneumothorax may be converted to a simple pneumothorax with the
use ofan occlusive dressing over the chest wall wound.Care must be taken not
tocreate a trapdoor effect and cause a tension pneumothorax to develop.Adapted from
Powers M.15ABC
334Part 4: Maxillofacial Traumaand radiographs should be performed tomonitor
progress ofremoval ofair or fluid.Ifthe tube becomes blocked and significantfluid
or air remains,a new chest tubeshould be placed.Tension PneumothoraxA tension pneu-
mothorax develops when the injury acts asa one-way valve through the chest wall
orfrom the lung into the pleural cavity with-out equilibration with the outside
atmos-phere (Figure 18-6).A dangerous progres-sive increase ofintrapleural
pressuredevelops as air enters the pleural cavity oninspiration but cannot escape
on expira-tion,causing complete collapse oftheaffected lung.As the pressure
increases,thetrachea and mediastinum are displaced tothe opposite pleural cavity
and impinge onthe normal lung.The positive intrapleuralpressure compresses the vena
cava,leadingto decreased cardiac output.The compres-sion ofthe normal lung causes
shunting ofblood to nonventilated areas and severeventilatory disturbances.These
changesdevelop into a rapid onset ofhypoxia,aci-dosis,and shock.24The most common
causes oftensionpneumothorax are mechanical ventilationwith PEEP,spontaneous
pneumothoraxin which emphysematous bullae havefailed to seal,and blunt chest trauma
inwhich the parenchymal lung injury hasfailed to seal.Occasionally,traumaticdefects
in the chest wall may lead to ten-sion pneumothorax.7The presence ofapneumothorax
should be considered inpatients who rapidly become acutely ill;develop severe
respiratory distress;andexhibit decreased breath sounds,hyper-resonance on one side
ofthe chest,dis-tended neck veins,and deviation ofthetrachea away from the involved
side.Ifuntreated,a tension pneumothoraxresults quickly in death.Ifa
developingtension pneumothorax is suspected,thepositive intrapleural pressure
should bereleased as quickly as possible.The pres-sure can be released by inserting
a large-bore needle (14�16 gauge) anteriorly intothe affected hemithorax through
the sec-ond or third intercostal space in the mid-clavicular line.This quickly
converts thetension pneumothorax to a pneumotho-rax,which can be treated with
placementofa chest tube (Figure 18-7).HemothoraxHemothoraxis the collec-tion
ofblood in the pleural cavity.It iscommonly the result ofpenetratinginjuries that
disrupt the vasculature,but itcan result from blunt trauma that tears
thevasculature.The initial loss ofblood col-lected in the pleural cavity may come
fromlung injuries,but because oflow pul-monary arterial pressure,the blood loss
isusually slowed.Massive hemothorax usu-ally results from injuries to the aortic
archor pulmonary hilum;it may also resultfrom injuries to the internal
mammaryarteries or intercostal arteries,which arebranches ofthe aorta.A hemothorax
maydangerously reduce the vital capacity ofthe lung and contribute to
hypovolemicshock.A hemothorax is usually associatedwith a pneumothorax,and the
subsequentblood loss causes hypotension,a decreasedcardiac output,and metabolic
acidosis,which,when combined with the ventilato-ry compromise,results in hypoxia
and res-piratory acidosis.123456654FIGURE18-5Chest tube placement.The patient
should be supine with the arm positioned superiorly toassist with access to the
midaxillary line.A,An incision is made through the skin and subcutaneous
tissuealong the inferior aspect ofthe fifth rib.B,A large Kelly clamp is used,with
the tips placed inferiorly,tobluntly dissect over the fifth rib into the
intercostal space between the fourth and fifth ribs.C,A gloved fin-ger should be
used to enter the pleural space to avoid possible laceration ofstructures,within
the pleuralspace,such as the lung,or possible disruption ofabdominal contents in
case ofa ruptured diaphragm.D,The chest tube is then passed along the
finger,superiorly and posteriorly within the pleural cavity.Thetube should be
secured to the chest with sutures,covered with an occlusive dressing,and then
connected toan underwater sealed drainage,which creates suction,following
verification oftube position by chest radi-ographs.Adapted from Powers M.15ABCD
Initial Management ofthe Trauma Patient335A hemothorax should be suspectedfollowing
penetrating or blunt chest trau-ma ifthe patient is in shock with reducedbreath
sounds and with a chest dull topercussion on one side.The neck veinsmay be flat
because ofsevere hypovolemiaor distended as a result ofthe mechanicaleffects ofa
chest full ofblood.7With theloss ofa small amount ofblood(< 400 mL),the diagnosis
is difficultbecause there may be little or no change inthe patient�s
appearance,vital signs,orphysical findings.Fluid collections > 200 to300 mL can
usually be seen on a goodupright chest radiograph with a bluntingofthe costophrenic
angle.The supineradiograph is less accurate.24Treatment ofa hemothorax consists
ofrestoration ofthe circulating blood vol-ume with transfusion
offluids,volumeexpanders,blood,or blood productsthrough large-bore intravenous
lines;con-trol ofthe airway and support ofthe ven-tilation as required;and drainage
oftheaccumulated blood from the pleural cavi-ty.A large chest tube (36�40F) should
beinserted in the fifth or sixth intercostalspace in the midaxillary line and
directedposteriorly and superiorly to avoid dam-age to a possibly elevated
diaphragm.Thechest tube should be connected to anunderwater seal and steady suction
(20�30 cm ofwater).Ifthe chest tube becomesclotted and fails to drain,another
chesttube should be put in place rather than anattempt made to irrigate the first
tube.With massive bleeding,autotransfusion ofthe drained blood is possible until
bankblood is available.25A persistent hemorrhage requires sur-gical
exploration.Thoracotomy forintrathoracic bleeding is indicated for
thefollowing:initial thoracostomy tubedrainage > 20 mL/kg
ofblood;persistentbleeding at a rate > 7 mL/kg/h;increasinghemothorax seen on chest
radiographicstudies;or the patient remaining hypoten-sive despite adequate blood
replacement,and other sites ofblood loss have beenruled out,or the patient
decompensatingafter an initial response to resuscitation.24In a few
instances,emergency thoracoto-my in the emergency room may be neces-sary for
control ofblood loss.However,mortality from this procedure is very high.Flail
ChestA flail chest results when thereare multiple rib fractures,usually at
severalsites along the rib (Figure 18-8).The result-ing unstable segment ofchest
wall movesparadoxically during respirations�inwardwith inspiration and outward with
expir-ation.A flail chest may affect respiratoryability to the point at which
hypoxemiaoccurs.The pain associated with the One-way valvein chest
wallInspirationExpirationFIGURE18-6A tension pneumothorax develops as air enters
the pleural cavity on inspiration butcannot leave during expiration (A),resulting
in a progressive increase in intrapleural air pressure (B).The injury in the chest
wall or trachea acts like a one-way valve,and the increasing intrapleural pres-sure
results in a shift ofthe trachea and mediastinal structures away from the
injury.The pressure onthe vena cava does not allow for an adequate return ofblood
to the heart,and compression oftheopposite lung (added to the injured lung) causes
severe ventilatory disturbance.Adapted from VukichDJ,Markovchick VJ.Pulmonary and
chest wall injuries.In: Rosen R,editor.Emergency medicine:concepts and clinical
practice.St.Louis: CV Mosby Co.; 1988.ABFIGURE18-7A,Right pneumothorax.A closed
pneumothorax may develop from blunt trauma to thechest or a lung
laceration,possibly from a fractured rib.Air from the lung to the pleural space
equal-izes the pressures,and the lung collapses.A ventilation-perfusion deficit
occurs because the blood cir-culated to the affected lung is not oxygenated.With a
pneumothorax,percussion ofthe chest showshyperresonance.Breath sounds are usually
distant or absent.Management ofthe pneumothorax isconfirmed and evaluated with
upright chest radiographs.B,Right pneumothorax following chest tubeplacement.A
chest tube should be placed immediately in the multiply-injured patient with a
pneu-mothorax.A moderate-sized chest tube (32�40�in adults or 26�30�in children) is
generally placedeither anteriorly in the second intercostal space midclavicular
line or in the fourth or fifth intercostalspace midaxillary line.AB
336Part 4: Maxillofacial Traumarespiratory effort may also compromise
theventilatory compliance ofthe patient.Thefractured ribs may have punctured
thelung,causing a tension pneumothorax orhemithorax.A problem with flail chest
andhypoxemia is the underlying pulmonarycontusion from the injury.The contusedlung
may be asymptomatic in the initialpresentation but develop complicationslater with
gas exchange.Little abnormalbreathing may be apparent immediatelyafter the
injury.Later,as fluid moves intothe lung with the developing contusion,lung
compliance falls,and more pressure isneeded to inflate the lungs.The
pulmonarycontusion underlying major chest wallinjuries may be the primary cause
ofhypoxia and morbidity in patients with flailchest.Mortality in patients
sustainingsevere blunt chest trauma remains relative-ly high at 12 to 50%.26A flail
chest is usually apparent onvisual examination ofthe unconsciouspatient.It may not
be initially apparent inthe conscious patient because ofsplintingofthe chest
wall.The patient moves airpoorly as a result ofparadoxic breathing,and movement
ofthe thorax is asymmet-ric and uncoordinated.The region ofthefractures may be
tender to palpation.Recommended management offlailchest involves three stages.The
first stageis initial stabilization ofthe loose seg-ment with an external
splint,such as asandbag,rolled sheet,or intravenousbag,taped over the location
ofthe para-doxic movement to both stabilize thatsegment and to reduce the pain
associat-ed with its movement.Although thistends to reduce the vital capacity
ofthelung,it increases the efficiency ofventila-tion.This form oftreatment can
produceatelectasis ifused for a prolonged period,but it is adequate for the first
30 minutesuntil more definitive treatment can beobtained.The next step for
prolongedreliefis intercostal nerve blocks to blockthe pain from the fractured
ribs,therebyallowing the patient to breathe deeplyand cough.The final step involves
the useofa volume-cycled respirator with endo-tracheal intubation to provide PEEP
andintermittent mandatory ventilation.This�internal splinting�with ventilatory sup-
port effectively manages the inadequatedepth ofventilation,improves
oxygenabsorption in the segments ofpul-monary contusion,and decreases atelec-
tasis.Ifproper management with ventila-tory assistance is initiated
early,therespiratory support may be required foronly 2 to 4 days.Ifmanagement
isdelayed until the patient demonstratesrespiratory difficulty,prolonged therapyfor
up to 14 days may be necessary.26OxygenationAfter establishment ofapatent airway
and sustained breathing,thepatient should be given supplemental oxy-gen to assist
reversing ofdecreased tissueoxygenation during the immediate post-traumatic
period.The patient will havediminished oxygen-carrying capacity as aresult
ofinjuries to the pulmonary or car-diovascular system:respiratory
compromiseInspirationExpirationInspirationFIGURE18-8A flail chest occurs when three
or more adjacent ribs are fractured in at least two locations,result-ing in a
freely moving segment ofthe chest wall during respirations.The chest wall moves
paradoxically duringinspiration and expiration owing to the flail segment.A,Upon
inspiration the flail segment sinks inward as thechest wall expands,impairing the
ability to produce negative intrapleural pressure.B,The heart and other con-tents
ofthe mediastinum shift toward the noninjured side.Cand D,During expiration the
flail segment ispushed outward,and the chest wall cannot efficiently force air from
the lungs.Air may shift uselessly from lungto lung.Adapted from Vukich
DJ,Markovchick VJ.Pulmonary and chest wall injuries.In: Rosen P,editor.Emer-gency
medicine: concepts and clinical practice.St.Louis: CV Mosby Co.; 1988.p.477.ABCD
Initial Management ofthe Trauma Patient337may be due to a head injury and
disruptionofcerebellar reflex systems,airway distressfrom maxillofacial or neck
injuries,or pul-monary injuries such as pulmonary contu-sion,flail chest,and a
tension or open pneu-mothorax that mechanically does notprovide for proper delivery
ofoxygen to thecardiovascular system.Oxygen can be deliv-ered through a nasal
cannula,face mask,orendotracheal tube.A person breathing100% oxygen can move five
times moreoxygen into the alveoli with each breath aswhen breathing normal
air.Oxygen therapycan increase available oxygen by as much as400% above
normal.27Administered oxygen can increase theinspired oxygen to 8 L/min and
canincrease the fraction ofinspired oxygen(FiO2).A higher FiO2can be delivered by
aVenturi mask,with the proper applicationofa bag and mask system.The greatest dif-
ficulty with this system is maintaining anadequate seal between the mask and
face.The thumb and index finger are placedover the mask to hold the mask
securelyover the mouth and nose,and the otherfingers are curled beneath the
inferior bor-der ofthe mandible.The FiO2can beincreased in a bag and mask system
with arebreathing mask and an oxygen accumu-lator to deliver a high concentration
ofoxygen.Ventilation with the bag and masksystem is difficult in patients with
possiblemaxillofacial,cervical spine,or thoracicinjuries,and the patient should be
intu-bated ifoxygen resuscitation is required.Endotracheal intubation helps to pro-
tect the airway and facilitates adequatelung inflation with high FiO2in theinjured
patient.Oxygen administeredthrough the endotracheal tube shouldincrease the FiO2 by
100% (especially ifthepatient is comatose) until arterial bloodgas measurements
confirm hemoglobinsaturation (PaO2> 60�70 mm Hg),atwhich point FiO2can be lowered
tobetween 40 and 60%.28Pulmonary oxygentoxicity may result if100% oxygen
isadministered continuously for 24 hours;therefore,100% oxygen delivery is accept-
able only until PaO2levels can be ascer-tained.Some concern exists about the sup-
pression ofthe respiratory drive withoxygen therapy,but the hypoxic drive canbe
reestablished following stabilization ofthe injured patient.The most important
mechanism ofdelivery ofoxygen to the tissues is thehemoglobin within the
erythrocytes in thecardiovascular system.In a traumatizedpatient,hemorrhage may
decrease theavailable hemoglobin to the point ofhypooxygenation ofvital organ
tissues andcell death.A normal hemoglobin of15 g/100 mL provides transport
of20%volume ofoxygen,whereas a hemoglobinof7 g/100 mL carries only a 10%
volumeofoxygen,which is the critical reserve levelofoxygen consumption for most
tissues,especially the myocardium and brain.27The treatment ofshock in the patient
withmultisystem injuries is directed towardrestoring cellular and organ
perfusionwith adequately oxygenated blood,ratherthan merely restoring the patient�s
bloodpressure and pulse rate.8CirculationFollowing establishment ofan
adequateairway and breathing in the injuredpatient,the cardiovascular system
ofthepatient must be assessed and control ofbaseline circulation to the tissues
must bequickly restored.The most common causeofshock in the traumatized patient
ishypovolemia caused by hemorrhage,either externally or internally into
bodycavities.Assessment ofthe degree ofshockis important because inadequate
tissueperfusion can cause irreversible damage tovital organs such as the brain or
kidneys ina short time period.During the primaryassessment a minimum oftwo large-
bore(14�16 gauge) intravenous cathetersshould be placed peripherally
iffluidresuscitation is required.At the time ofplacement ofan intravenous
catheter,blood should be drawn from the catheterto allow for typing,cross-
matching,andbaseline hematologic and chemical stud-ies.Ifthere is any doubt
ofadequate venti-lation,arterial blood should be obtainedfor blood gas
analysis.Tissue perfusion and oxygenation aredependent on cardiac output and
arebest initially evaluated by physical exam-ination ofskin perfusion,pulse
rate,uri-nary output characteristics,and themental status ofthe patient.Blood pres-
sure levels are commonly used to mea-sure cardiac output and to define hypov-
olemia,but in the emergency situationtime does not permit blood pressurelevel
measurement and the physical signsofhypovolemia are more sensitive todeveloping
shock.The response oftheblood pressure level to intravascular lossis nonlinear
because compensatorymechanisms ofincreased cardiac rateand contractility,along with
venous andarteriolar vasoconstriction,maintain theblood pressure in the young
healthyadult during the first 15 to 20% ofintravascular blood loss.After a
bloodloss of20%,the blood pressure level maydrop significantly.(In the elderly
patientwith less-efficient compensating mecha-nisms,the decline in blood pressure
lev-els may begin to develop after a 10 to15% blood loss.) The patient may arrestat
an intravascular blood loss of40%.29Blood pressure level may be insensitiveto the
early signs ofshock,and a patient�sblood pressure level may quickly drop following
the initial assessment as the com-pensating mechanisms can no longer pro-vide for
the intravascular volume loss.Also,the usual baseline blood pressure level ofthe
patient is often unknown.A patientwho has a systolic pressure of120 mm Hgbut is
normally hypertensive may have asignificant loss,whereas a healthy youngathlete may
have a normal systolic pressureof90 mm Hg and the blood loss might beassumed to be
greater than it is.Skin perfusion is the most reliableindicator ofpoor tissue
perfusion during
338Part 4: Maxillofacial Traumathe initial evaluation ofthe patient.Theearly
physiologic compensation for vol-ume loss is vasoconstriction ofthe vesselsto the
skin and muscles.The cutaneouscapillary beds are one ofthe first areas toshut down
in response to hypovolemiabecause ofstimulus from the sympatheticnervous system and
the adrenal glandthrough epinephrine and norepinephrinerelease.The release ofthe
catecholaminescauses sweating,and during palpation theskin may feel cool and
damp.The lowerextremities are usually first to be affected,and the first indication
ofintravascularloss may be paleness and coolness oftheskin over the feet and
kneecaps.A check ofthe capillary filling time by performing ablanch test gives an
estimate oftheamount ofblood flowing to the capillarybeds.In this test,pressure is
placed on thefingernail,toenail,or hypothenar emi-nence ofthe hand (to evacuate
blood fromthe capillary beds),followed by a quickrelease ofthe pressure.The time
requiredfor the blood to return to the capillarybeds,represented by the restoration
ofnormal tissue color,is usually < 2 secondsin the normovolemic patient.This indi-
cates that the capillary beds are receivingadequate circulation.30The rate and
character ofthe pulse is agood measure ofthe cardiac rate.The pulserate is a more
sensitive measure ofhypo-volemia than is the blood pressure,but it isaffected by
other factors commonly associ-ated with the trauma situation,such as thepatient�s
pain,excitement,and emotionalresponse,resulting in tachycardia withoutunderlying
hypovolemia.However,inadults with tachycardia > 120 beats/min,hypovolemia should be
expected and inves-tigated further.Older patients generally areunable to exceed
rates of140 beats/min in ahypovolemic state,whereas youngerpatients may present
rates of160 to 180 beats/min with severe intravascularloss.In patients who have
pacemakers,aretaking heart-blocking medications such aspropranolol or digoxin,or
have conductionabnormalities within the heart,hypo-volemic status may not be
represented byincreased pulse rates.The location ofthe pulse may give
someindication ofthe cardiac output.Generally,ifthe radial pulse is palpable,the
patient�ssystolic blood pressure is > 80 mm Hg;ifthefemoral pulse is palpable,the
patient�s sys-tolic blood pressure is 70 mm Hg or higher;and ifthe carotid pulse is
noted,the systolicblood pressure is > 60 mm Hg.Pulserhythm and regularity may also
provideclues to increasing hypovolemia and car-diac hypoxia.Cardiac dysrhythmias
such aspremature ventricular contractions or arte-rial fibrillations produce an
irregular rateand rhythm,signaling the loss ofcompen-sating mechanisms maintaining
myocardialoxygenation.Decreased intravascular volume isimmediately reflected in
decreased urinaryoutput because the compensatory mecha-nisms ofthe body decrease
blood flow to thekidneys in favor ofblood flow to the heartand brain.Any patient
with significant trau-ma should always have an indwelling uri-nary catheter
inserted to monitor urine vol-ume every 15 minutes.29A minimallyadequate urine
output is 0.5 mL/kg/h,andfluid therapy should be initiated to main-tain at least
this level ofurinary output.Ifthe patient�s injuries include pelvic frac-tures or
blunt trauma to the groin,a uri-nary catheter should not be placed until
aurethrogram can be evaluated for urethralinjury.Ifurethral injury is unlikely,the
uri-nary catheter may be placed with minimalconcern.Classic signs ofurethral
injuryinclude blood at the meatus,scrotalhematoma,or a high-ridding boggyprostate
on rectal examination.Alterations in the mental status ofthetrauma patient caused
solely by hypo-volemia are uncommon,except in themost progressive preterminal
stages ofintravascular fluid loss.Compensatorymechanisms maintain blood flow to
thebrain,and hypoperfusion to the braindoes not develop until the systolic
bloodpressure falls below 60 mm Hg.The men-tal changes usually seen are
agitation,con-fusion,uncooperativeness,anxiety,andirrationality.These alterations
in mentalstatus can also be seen in a patient withhead trauma,spinal injury,drug or
alcoholintoxication,hypoxia,or hypoglycemia.Inthe emergency situation these other
causesofmental status changes should be inves-tigated when hypovolemia is suspected
inthe agitated patient who has or possiblyhas suffered substantial blood
loss.29Hypovolemia caused by hemorrhagemay commonly cause flat neck veins.Dis-
tended neck veins,however,suggest eithertension pneumothorax or cardiac dys-
function.As discussed earlier,with tensionpneumothorax an examination ofthechest
may reveal absent breath sounds anda hyperresonant chest.Cardiac dysfunc-tion
results from cardiac tamponade,myocardial contusion or infarction,or anair
embolus.Cardiac tamponade presents a clinicalpicture that is similar to that
oftensionpneumothorax�distended neck veins,decreased cardiac output,and hypoten-
sion.Blunt or penetrating trauma maycause blood to accumulate in the pericar-dial
sac.The blood in the pericardial sacresults in inadequate cardiac filling
duringdiastole,diminished cardiac output,andcirculatory failure.Cardiac
tamponadeusually is associated with penetratingwounds to the chest that have
injured thetissues ofthe heart.The classic Beck�s triadofdecreased systolic blood
pressure levels,distended neck veins,and muffled heartsounds may be observed.The
expected dis-tended neck veins caused by increased cen-tral venous pressure may be
absent becauseofhypovolemia.The neck veins,ifdistend-ed,may become distended
further duringinspiration (Kussmaul�s sign),and the pul-sus paradoxus (lowering
ofthe systolicpressure by > 10 mm Hg on normal inspi-ration) may be accentuated or
absent.Ten-sion pneumothorax may mimic cardiactamponade or,because ofthe nature
ofthe
Initial Management ofthe Trauma Patient339penetrating injury,may develop at thesame
time as cardiac tamponade,thus pre-senting a confusing clinical
presentation.Cardiac tamponade is initially man-aged by prompt pericardial
aspirationthrough the subxiphoid route (Figure 18-9).Because radiographs and
physicalexamination are not helpful,a positivepericardial aspiration along with a
historyofchest trauma is frequently the onlymethod ofmaking a correct
diagnosis.Because ofthe self-sealing qualities ofthemyocardium,aspiration
ofpericardialblood alone may temporarily relieve symp-toms.All trauma patients with
a positivepericardial aspiration require open thora-cotomy and inspection ofthe
heart.Peri-cardial aspiration may not be diagnostic ortherapeutic ifthe blood in
the pericardialsac has clotted,as occurs in 10% ofpatientswith cardiac
tamponade.29Ifaspirationdoes not lead to diagnosis or improvementofthe patient�s
condition,only emergentthoracotomy can solve the problem.Pericardial aspiration
through thesubxiphoid route involves the insertion ofa needle,preferably covered by
a plasticcatheter (angiocatheter),at 90�slightly tothe left ofthe xiphoid
process.The needleis inserted until it clears the sternal borderand is then
directed at 45�toward the leftscapula to directly enter the pericardium.Suction is
placed on the needle hub toidentify by blood return when the needlehas entered the
pericardial sac.Ifthe nee-dle is properly placed,as little as 50 cc ofblood from
the pericardial sac shouldresult in a marked improvement in thepatient�s
condition.Control ofBleedingHemorrhage isdefined as an acute loss ofcirculating
blood.Normally the blood volume is approximate-ly 7% ofthe adult ideal body
weight.A 70 kgmale has approximately 5 L ofcirculatingblood.The blood volume does
not increasesignificantly in obese patients,and in chil-dren the blood volume is
usually between 8and 9% ofbody weight (80�90 mL/kg).7Bleeding may be external or
internal intobody cavities.Most external hemorrhagecan be controlled with direct
pressure to thewound.Ifan extremity is involved,it shouldbe elevated.Firm pressure
should be contin-uous,and ifthe dressings become soakedthey should not be removed
but,rather,cov-ered with additional dressings.Removal ofadressing may disrupt clot
formation andpromote further bleeding.Firm pressure onthe major artery in the
axilla,antecubitalspace,wrist,groin,popliteal space,or anklemay assist in control
ofhemorrhage distal tothe site.Pressure points should only be usedifdirect wound
pressure is not effectivealone.Pressure bandages include the use ofair-pillow
splints and blood pressure cuffs.Pneumatic antishock garments (PASGs)and medical
(military) antishock trousers(MASTs) previously used to increase bloodpressure in
cases ofhypotension have beenfound to be detrimental in some situationssuch as
instances ofvascular injuries.31ThePASG/MAST garments are still used bysome to
stabilize pelvic fractures.Scalp orskin wounds may best be managed withimmediate
closure with large monofilamentsutures (without cosmetic closure consider-ations)
and direct pressure until the hemor-rhage is controlled.Because ofthe rich blood
supply tothe face and neck,significant hemorrhagemay be associated with large
scalpwounds,nasal or midface fractures,andpenetrating neck wounds.In a short peri-
od oftime the scalp may lose a largeamount ofblood,which oozes from thegalea and
loose connective tissue layers.The wound can be approximated rapidlywith 2-0
nonresorbable sutures withoutregard to cosmetic closure.Direct pressureshould then
be placed over the wound tocontrol the hemorrhage and minimizehematoma
formation.After the patienthas been stabilized,the sutures may beremoved and a more
cosmetic
approachPericardiumHeart45#PericardiumXiphoidprocessManubriumHeartFIGURE18-
9Pericardiocentesis can be transiently lifesaving when a significant cardiac
tamponade develops.Aand B,The patient is placed in a supine position,and a 16- or
18-gauge needle on a 60 cc syringe is introducedjust to the left side ofthe xiphoid
process.The needle should be introduced at a 45�angle to the chest wall,45�offthe
midline and directed toward the posterior aspect ofthe left shoulder.A popping
sensation may be felt asthe pericardium is entered.Ifthe blood within the
pericardial sac is slightly clotted,it may interfere with theeffectiveness ofthe
procedure.Reliefofa depressed systolic blood pressure level should be
immediate,resultingfrom an increased stroke volume.The procedure may be required
several times until definitive treatment can beinitiated.Adapted from Powers M.15AB
340Part 4: Maxillofacial Traumawith resorbable sutures may be used toclose the
galeal layer and to achieve goodapproximation and orientation ofthehair-bearing
dermal and skin layers.Nasal or midface fractures may hem-orrhage from tears ofthe
ethmoidal arter-ies that arise from the internal carotid sys-tem or from branches
ofthe maxillaryartery system (Figure 18-10).Most hemor-rhages from facial injuries
can be con-trolled with direct pressure or packing(Figure 18-11).Internal maxillary
arterybleeding from posterior maxillary wallfractures associated with Le Fort I or
IIlevel fractures usually can be controlled bypressure with gauze packing for
extendedperiods.Liquid thrombin or epinephrinemay be added to the gauze
packing,andthe patient�s head may be elevated to assistwith hemostasis.Ifdirect
control is neces-sary,good visualization ofthe damagedvessel is required.Blind
clamping maycause further bleeding from vessels andsoft tissues,as well as nerve
damage.Anterior ethmoidal arteryPosterior ethmoidal arterySphenopalatine
arteryGreater palatinearteryFacial arteryAnterior ethmoidal arteryPosterior
ethmoidal arterySeptal branch of thesphenopalatine arterySeptal branch of superior
labial arteryGreater palatinearteryKiesselbach'sor Little's areaFIGURE18-10The
lateral wall ofthe nasal cavity (A) and the nasal septum (B) receive a rich blood
supply fromboth the internal and external carotid artery system.The superior aspect
ofthese structures receives a blood sup-ply through the internal carotid system
from the anterior and posterior ethmoidal arteries.The middle and infe-rior aspects
are supplied by vessels from the external carotid artery: the facial artery and the
nasopalatine,greaterpalatine,and sphenopalatine arteries from the maxillary
artery.The region commonly referred to as Kiessel-bach�s or Little�s area,in the
anterior inferior portion ofthe nasal septum,receives an abundant blood supplyfrom
all the vessels and is the region where most epistaxis originates.Adapted from
Powers M.15ABForcepsRubber catheterSutureGauze packCatheterGauze
pack(posterior)Nasal pack(anterior)FIGURE18-11A combined technique used for
anterior and posterior packing ofthe nasal cavity involves the following: A,A small
red rubber catheter is intro-duced through the nostrils and carefully passed
posteriorly along the floor ofthe nose until visualized in the oropharynx.Care must
be taken with Le Fort II level,nasoethmoid,or other fractures involving the
cribriform plate that the catheter does not pass through the fracture site into the
cranial vault.Once the catheter isvisualized,a forceps may be used to grasp the
catheter and pull it into the oral cavity.B,The catheter is then sutured to a tape
that is secured to a wad ofgauzepacking material.The catheter is drawn from the
nasal cavity through the nostril,pulling the gauze pack into position in the
nasopharynx against the posterioraspect ofthe nasal cavity.C,Once the posterior
pack is in place,the anterior pack (consisting of1 cm ribbon gauze) is packed in an
orderly fashion along the nasalfloor,building superiorly; this allows for easy
removal and efficient packing ofthe nasal cavity.Adapted from Leigh JM.Primary
care.In: Rowe NC,Williams JC,editors.Maxillofacial injuries.Edinburgh: Churchill-
Livingston; 1985.p.54�74.ABC
Initial Management ofthe Trauma Patient341Ligation ofthe external carotid artery
maybe required only in extreme cases;usuallyit is ineffective when used alone and
with-out direct control ofhemorrhage becauseofthe collateral circulation ofthe
face.The potential internal sites ofhemor-rhage are the thoracic
cavity,abdomen,retroperitoneum,and extremities.A com-plete physical examination
with radiogra-phy and computed tomography (CT) isuseful to identify hemorrhages
into theseareas (Figures 18-12 and 18-13).Whenthere is no evidence ofexternal or
intratho-racic bleeding,continued severe hypo-volemia is usually the result
ofbleeding intothe abdomen or at fracture sites.Blood losswith fractures should be
considered to be atleast 1,000 to 2,000 mL for pelvic fractures,500 to 1,000 mL for
femur fractures,250 to500 mL for tibia or humerus fractures,and125 to 250 mL for
fractures ofsmallerbones.A hematoma the size ofan appleusually contains at least
500 mL ofblood.Control ofhemorrhage into internal spacesis not done in the primary
survey unless thehemorrhage may have damaging effects onthe cardiovascular or
pulmonary system.Aslow internal hemorrhage may be con-trolled by secondary fixation
offractures;by the defense mechanisms ofvascularocclusion,refraction,and clot
formation;orby open exploratory surgery.Hypovolemic Shock in the Patient
withMultisystem InjuriesThe most commoncause ofshock seen in the patient with mul-
tisystem injuries is hypovolemia caused byhemorrhage.Virtually all
multisystemicinjuries are accompanied by a degree ofhypovolemic shock that presents
as a grad-ed physiologic response to hemorrhage.This response can be classified
based on thepercentage ofacute blood loss (Table 18-5).Class I Hemorrhage: Blood
Loss ofUp to 15%The clinical symptoms ofbloodloss ofup to 750 mL in the 70 kg
adultmale are minimal.A mild tachycardia isnoted,but the compensatory
mechanismsofthe body retain normal blood pressurelevels,pulse pressure,respiratory
rate,andtissue perfusion.Class II Hemorrhage: Blood Loss of15 to 30%Blood loss of15
to 30% repre-sents an 800 to 1,500 mL loss in the 70 kgadult male.Clinical symptoms
commonlyexpected with this level ofblood loss aretachycardia,tachypnea,and a
decrease inthe difference between systolic and dias-tolic blood pressure or pulse
pressure.Thedecrease in pulse pressure level is due tothe elevation
ofcatecholamines andincreased peripheral vascular resistance inresponse to the
decreased intravascularcomponents.The increase in diastolicpressure suggests
hypovolemia becausethere is no noticeable increase in the sys-tolic pressure in the
early stages ofbloodloss.The peripheral vasoconstriction mayshow an elongated
capillary refill time,and the skin may feel cold and moist.Class III Hemorrhage:
Blood Loss of30 to 40%In the 70 kg adult male,a 30to 40% blood volume loss
represents a1,500 to 2,000 mL loss,which is fairlydetrimental to the survival
ofvital organtissues.Patients present with the classicsigns ofinadequate tissue
perfusion,including marked tachycardia (120 to 140 beats/min),tachypnea,marked
vaso-constriction,a decreased systolic
pressurelevel,diaphoresis,anxiety,restlessness,anddecreased urinary output.Class IV
Hemorrhage: Blood Loss of> 40%Blood losses approaching halfoftheintravascular
volume produce an immedi-ately life-threatening situation.Symptomsinclude marked
tachycardia,a significantdecrease in the systolic blood pressurelevel to < 60 mm
Hg,marked vasocon-striction with a very narrow pulse pres-sure,marked
diaphoresis,obtunded men-tal state,and no urinary output.ManagementIn managing the
traumapatient in shock,the speed with whichresuscitation is initiated and the
timeFIGURE18-12Pelvic fracture.Pelvic fractures,fractures ofthe femur,and multiple
fractures ofother long bones may cause hypovolemic shockand life-threatening blood
loss,the primary siteofwhich may be difficult to determine.Typicalclosed fractures
ofthe pelvis may lose 1 to 5 L ofblood,femur fractures 1 to 4 L,and arm frac-tures
0.5 to 1 L from the vasculature.FIGURE18-13Femur fracture.Fat embolismsyndrome is
usually associated with major frac-tures oflong bones,especially ofthe
femur.Thepatient typically does well for 24 to 48 hours andthen develops
progressive respiratory and centralnervous system deterioration.Concomitant lab-
oratory value changes include hypoxemia,thrombocytopenia,fat in the urine,and a
slightdrop in hemoglobin.Fat enters the venous sinu-soids at the fractured site and
becomes lodged inthe lung alveoli.
342Part 4: Maxillofacial Traumarequired to reverse shock are the factorscrucial to
the patient�s outcome.32Thefocus should again always be on control-ling the
hemorrhage,whether it bethrough basic measures such as pressureand elevation or
through rapidimaging/surgical intervention.Two large-bore (16 gauge or larger)
short angio-catheters are a minimum for beginningfluid therapy.Initial attempts
should bemade to place percutaneously thecatheters in the basilic or cephalic veins
inthe antecubital fossa ofboth arms.Percu-taneous placement
offemoral,jugular,orsubclavian vein catheters may also be usedifthere are no
abdominal injuries orpelvic or femur fractures.When thepatient is in an extreme
hypovolemicstate,placement ofpercutaneouscatheters may be difficult;venous cut-down
procedures to expose the saphenousvein provide venous access for fluid resus-
citation.Flow is directly dependent on thecatheter�s internal diameter and is
inverse-ly dependent on its length.Therefore,twocatheters ofthe same length and
diameter,whether inserted peripherally or centrally,give the identical flow
rate,but a longercentral catheter delivers a lower possiblemaximum flow rate than
does a shorterperipherally placed catheter.A central linethrough the subclavian or
internal jugularvein routes usually takes longer to placethan does a peripheral
line and mayrequire disruption ofother resuscitationmeasures such as chest
compressions dur-ing placement.Furthermore,a central linemay complicate
resuscitation ofthe trau-ma victim by causing or aggravating adeveloping
pneumothorax or hemotho-rax or other potential complications asso-ciated with its
placement.Therefore,peripheral intravenous lines are the accessofchoice in the
primary management ofthe trauma patient.Circulatory support and proper oxy-genation
oftissues require adequate sys-tolic and diastolic blood pressure levels,pulse
pressure levels,pulse rate character-istics,and capillary refill times.The clini-
cal observations ofthese parameters aredifficult to quantitate,as is
measuringimprovement ofstabilization ofthe circu-latory system.Adequate urine
production is a pre-dictable sign ofrenal function,except incases in which urine
production may beenhanced by the use ofdiuretics.For thisreason,urinary output is a
prime indicationofresuscitation and patient response.AFoley catheter should be
placed in the blad-der as soon as possible to measure urinaryflow.There are three
contraindications forthe insertion ofa Foley catheter,and thecatheter should not be
placed until all havebeen ruled out.These contraindications inthe traumatized
patient are the presence ofblood at the urethral meatus,ofhemor-rhage into the
scrotum,and ofa high-riding prostate (Figure 18-14A).33�35Attempts to pass a
catheter up an injuredurethra can convert an incomplete lacera-tion into a complete
laceration and canintroduce infection into the perineal andretropubic hematoma.A
rectal examinationshould be performed in all trauma patientswith suspected pelvic
trauma before place-ment ofa catheter.With posterior urethraldisruption,the
prostate may be forced supe-riorly by a hematoma;ifthe prostate cannotbe palpated,a
urethral injury should be sus-pected (Figure 18-14B).36The initial intravenous
resuscitationfluid used in most hospitals is a balancedelectrolyte solution such as
lactatedRinger�s solution or 0.9% normal saline.During prolonged shock,isotonic
fluid islost from the intravascular and interstitialspaces to the extracellular
space.Initially,the patient should be given 2 L ofintra-venous fluid (20 mL/kg for
a pediatricpatient) rapidly over 10 to 15 minutes andthen observed.Ifthis maneuver
does notraise the systolic blood pressure to at least80 to 100 mm Hg,the patient
requiresadditional fluid,blood,and control ofblood loss.There is still controversy
aboutthe use ofcolloids (albumin,plasma pro-tein fractions) and artificial
plasmaTable 18-5Estimated Fluid and Blood Losses*Class I Class IIClass IIIClass
IVBlood loss (mL)Up to 750750�1,5001,500�2,000> 2,000Blood loss (% vol)Up to
1515�3030�40> 40Pulse rate< 100> 100> 120> 140Blood
pressureNormalNormalDecreasedDecreasedPulse pressureNormal or
DecreasedDecreasedDecreasedincreasedRespiratory rate14�2020�3030�40> 35Urine output
(mL/h)> 3020�305�15NegligibleMental statusSlightly Mildly
Anxious,Confused,anxiousanxiousconfusedlethargicFluid
replacement�CrystalloidCrystalloidCrystalloid Crystalloid and bloodand bloodAdapted
from American College ofSurgeons Committee on Trauma.Advanced trauma life support
for doctors:studentcourse manual�.6th ed.Chicago:American College
ofSurgeons;1997.p.98.*Based on the initial presentation ofa 70 kg man.�The
guidelines in the table are based on the �3-for-1�rule.This rule is derived from
the empiric observation that mostpatients in hemorrhagic shock require as much as
300 mL ofelectrolyte solution for each 100 mL ofblood loss.Appliedblindly,these
guidelines can result in excessive or inadequate fluid administration.For example,a
patient with a crushinjury to the extremity may have hypotension out ofproportion
with his or her blood loss and requires fluids in excess ofthe 3:1 guidelines.In
contrast,a patient whose ongoing blood loss is being replaced by blood transfusion
requires < 3:1.The use ofbolus therapy with careful monitoring ofthe patient�s
response can moderate these extremes.
Initial Management ofthe Trauma Patient343expanders (dextran,hetastarch) to
treathypovolemia secondary to trauma.Thecost ofthese materials does not appear tobe
justified by clinical data.37,38Extensivemeta-analysis shows a trend
towardincreased mortality with the use ofcol-loids over
crystalloids.39However,there isstill support for their use,particularly ifblood
replacement is delayed or inade-quate or in patients with severe headinjuries that
require fluid restriction ther-apy to control rising intracranial pressure(ICP)
levels.Most patients respond to initial fluidadministration,but this improvement
maybe transient�especially in patients whohave lost > 20% oftheir blood
volume.7With excess hemorrhage,red blood cellsmust be replaced in the intravascular
cir-culation to maintain an optimum oxygen-carrying capacity.The safest type
ofbloodto administer is blood that has been fullycross-matched.Obtaining fully
cross-matched blood may require 30 minutes ormore and is usually not possible
immedi-ately in the trauma situation.Type-specificblood is a safe alternative and
can usuallybe ready within 5 to 15 minutes.Withwhole blood loss and requirements
forearly blood replacement,O-negative bloodmay also be given in patients with
excessivehemorrhage.5The O blood group is themost common and contains no
cellularantigens.Theoretically,O-negative bloodcan be given to persons regardless
oftheindividual�s blood group with minimal riskofantigen-antibody hemolytic
reaction.However,no more that 4 U ofO-negativeblood should be given.40Fresh frozen
plasma (FFP) is frequent-ly used as a volume expander and providesall ofthe
clotting factors except platelets.Italso provides opsonins and some comple-ment
factors,which may be deficient inpatients with severe trauma or shock.Dur-ing
massive transfusions,a unit ofFFP isoften given after every 5 U ofblood,espe-cially
ifpacked red blood cells are admin-istered in an attempt to prevent coagula-tion
abnormalities.Additionally,plateletlevels below < 100,000/mm3may be anindication
for a platelet transfusion.41The restoration and maintenance ofbody temperature is
also important in thetrauma patient.Appropriate body temper-ature increases the
response to resuscita-tive measures and decreases the risk ofworsening coagulopathy
with massivetransfusion.The use ofbody warmers andfluid warmers is strongly
recommended.Ifthe patient initially responds totherapy,blood may not be required
imme-diately,but the patient will require bloodas hypovolemic shock continues to
devel-op.A blood sample should be sent to theblood bank as soon as possible for
fullcross-matching.The patient who is resus-citated initially with O-
negativeunmatched blood or type-matched bloodshould be switched to fully cross-
matchedblood as soon as is reasonably possible tolimit the risks ofhemolytic
reactions.42Such blood is compatible within the AB-positive and Rh blood groups but
maycontain minor antigenic incompatibilities.Ideally,the amount ofblood given
shouldbe equal to the amount lost by the patient,but this is difficult to assess in
the traumapatient.In critically ill or injured patients,the ideal hemoglobin is
12.5 g/dL (hemat-ocrit of38% or higher).Although a hema-tocrit of30 to 35% has been
recommend-ed in the past,higher levels improve theoxygen-carrying capacity,and
theincreased viscosity seems to cause relative-ly little reduction in cardiac
output untilthe hematocrit exceeds 45 to 50%.Ifthe patient does not respond to
initialfluid resuscitation and blood transfusions,either surgical intervention is
required tocontrol continued hemorrhage or the initialdiagnosis ofhypovolemia is
incorrect.Mea-surement ofthe central venous pressurewith a catheter or evaluation
ofthe neckveins may assist with the assessment ofhypovolemic shock.Those patients
withexsanguinating hemorrhage should have alow central venous pressure,and those
withother causes ofshock should have a normalor elevated central venous
pressure.7Theultimate hemodynamic criterion in thetreatment ofhypovolemic shock is
thepatient�s response.Adequate resuscitation isachieved when adequate circulation
andurine output are restored.A patient being treated for hypo-volemic shock is
usually placed in a head-down or Trendelenburg�s position toempty the venous side
ofthe peripheralProstate displacedsuperiorlyHematomaUrethral disruptionsuperior
tourogenital diaphragmUrogenitaldiaphragmPerforation of urethraBuck's fasciaUrine
escapes intoscrotum uponurinationFIGURE18-14A,The contraindications for placement
ofa Foley catheter in the trauma patient arethe presence ofblood at the urethral
meatus,hemorrhage into the scrotum,and a high-riding prostate.Blood at the urethral
meatus may be a significant enough disruption ofthe urethra to prohibit pas-sage
ofa catheter safely.B,The development ofa hematoma or urine collection within the
scrotumtypically results from an anterior urethral disruption from perineal blunt
trauma with a perforationofBuck�s fascia.With a posterior urethral disruption,the
prostate may be forced superiorly by thedeveloping hematoma.Adapted from Powers
M.15AB
344Part 4: Maxillofacial Traumacirculation back to the heart.Frequently,the patient
with multisystem trauma hasinjuries to the abdomen or chest that mayinterfere with
the respiratory capacity ifthe patient is in the Trendelenburg�s posi-
tion.Alternatively,both ofthe patient�slegs can be elevated while the
patient�strunk is maintained in a supine position.43Neurologic ExaminationUpon
completion ofthe assessment ofthecardiovascular system and control ofanyexternal
hemorrhage,a briefneurologicevaluation is performed to establish thepatient�s level
ofconsciousness and pupil-lary size and reaction.This briefneuro-logic examination
quickly identifies anysevere CNS problems that require imme-diate intervention or
additional diagnos-tic evaluation.A lack ofconsciousnesswith altered pupil reaction
to lightrequires an immediate CT scan ofthehead and management with mannitol
orfluid restrictions.Be aware ofany medica-tions that the patient may have received
ordrugs he or she may have taken that mayaffect the pupils.The Committee on Trauma
oftheAmerican College ofSurgeons recom-mends the use ofthe mnemonic AVPU.7,8In this
system,each letter describes a levelofconsciousness in relation to thepatient�s
response to external stimuli:alert,responds to vocal stimuli,respondsto painful
stimuli,and unresponsive.A more detailed quantitative neuro-logic examination is
part ofthe secondarysurvey ofthe trauma patient.The primarysurvey establishes a
baseline;ifthepatient�s neurologic condition varies fromthe primary to the
secondary survey,achange in intracranial status may be pre-sent.A decrease in the
level ofconscious-ness may indicate decreased cerebral oxy-genation or
perfusion.The reactivity ofthe pupils to lightprovides a quick assessment
ofcerebralfunction.The pupils should react equally.Changes represent cerebral or
optic nervedamage or changes in ICP.Furtherchanges in pupil reactivity or levels
ofcon-sciousness may be due to alterations inventilation or oxygenation
status.Themost common causes ofcoma ordepressed levels ofconsciousness
arehypoxia,hypercarbia,and hypoperfusionofthe brain.42Depressed levels ofcon-
sciousness and narrow pinpoint pupilsmay result after an opiate overdose.Afteran
overdose with meperidine hydrochlo-ride,the pupils may appear normal ordilated.In
both cases,treatment requiresthe narcotic antagonist naloxonehydrochloride,0.4 mg
initially.Careshould be taken to avoid a quick violentwithdrawal phase in the
opiate abuser;thisis accompanied by profound distress,nau-sea,agitation,and muscle
cramps.Both hypoglycemia and hyper-glycemia can cause depressed levels
ofconsciousness.Ifa quick blood glucoselevel cannot be obtained (and dependingon
other injuries),the patient can begiven and immediate bolus of25 g ofglu-cose to
manage critical hypoglycemia.Abenefit ofthe glucose load is the hyperos-molar
status that may,for a short time,reduce cerebral edema.44Exposure ofthe PatientThe
patient should be completely disrobedso that all ofthe body can be
visualized,palpated,and examined for injuries orbleeding sites.The clothing must be
com-pletely removed,even ifthe patient issecured to a spinal backboard.The
easiestmethod is to cut the clothing down themidline ofthe torso,arms,and legs
tofacilitate the examination and assessment.Frequent careful reevaluation
oftheinjured patient�s vital signs is important tomonitor the patient�s ability to
maintainan adequate airway,breathing,and circu-lation (Figure 18-15).Secondary
AssessmentThe secondary assessment does not beginuntil the primary assessment has
been com-pleted and management oflife-threateningconditions has begun.During the
secondaryassessment the patient�s vital signs andcondition should be constantly
monitoredto evaluate the therapeutic interventionsinitiated during the primary
assessmentand to further assess the patient for anyother life-threatening problems
not evi-dent during the primary survey.Changesin the patient�s vital
signs,respiratory andcirculatory status,and neurologic func-AirwayCervical
collarIntravenouslinesChest tubeFoley catheterFIGURE18-15The primary assessment
ofthepatient with multiple injuries requires evalua-tion and maintenance ofan
adequate airwaywith cervical protection,adequate breathing(including the placement
ofchest tubes to cor-rect alterations in normal lung and chest wallphysiologic
conditions),and adequate circula-tion and hemodynamics,with the placement oftwo
large-bore intravenous lines peripherallyand the insertion ofa Foley catheter after
pos-sible urethral damage is ruled out.The patientshould be totally exposed so that
the entirebody can be examined for injuries.Adaptedfrom Powers M.15
Initial Management ofthe Trauma Patient345tions are expected in the first 12
hours.7The secondary assessment includes a sub-jective and objective evaluation
oftheinjured patient.A subjective assessment shouldinclude a briefinterview with
the patient,ifpossible.A briefhealth history can beuseful,including
medications;allergies;previous surgery;a history ofthe injury;and the
location,duration,time frame,and intensity ofthe chiefcomplaint.Obvi-ously,the
comatose patient cannot pro-vide useful subjective information,butfamily
members,bystanders,or other vic-tims may provide some details.The objective
assessment shouldinvolve inspection,palpation,percussion,and auscultation ofthe
patient from headto toe.Each segment ofthe body (headand skull,chest,maxillofacial
area andneck,spinal cord,abdomen,extremities,and neurologic condition) is evaluated
toprovide a baseline ofthe patient�s presentcondition.Special procedures such
asperitoneal lavage,radiographic studies,and further blood studies may be done
atthis time.Head and SkullPrimary injuries to the head and skullmay involve
lacerations,abrasions,avul-sions,and contusions ofthe scalp;frac-tures ofthe
cranium and cerebral contu-sions;and intracranial bleeding to thebrain from
lacerations or shearinginjuries.The brain may also suffer sec-ondary insults from
intracranial bleed-ing,hypoxia,and ischemia.Hypoxia isdue to an impaired delivery
ofoxygen tothe brain,whereas ischemia can resultfrom arterial hypotension,elevated
ICP,or pressure on intracranial vessels fromexpanding hematomas resulting in a her-
niation ofthe brain from the cranialvault (Figure 18-16).The secondaryinsults
ofhypoxia and various forms ofischemia are usually preventable.Aboutone-
halfofpatients with head injurieshave some degree ofreversible injurycaused by
increased ICP that can be con-trolled with aggressive management.Failure to prevent
increased ICP is themost frequent cause ofdeath in hospital-ized patients with a
severe head injury.Hypertension with concomitant brady-cardia may indicate
increasing ICP(Cushing�s phenomenon).Hypotensionwith tachycardia usually indicates
bloodloss.Shock is rarely associated with theprimary neurologic injury,and
systemicsources ofblood loss should be investi-gated.The classic findings
ofCushing�sphenomenon are usually present < 25%ofthe time,even when the ICP is
foundto be > 30 mm Hg and a value > 15 mmHg is considered abnormal.Accurate
continual neurologic assess-ment and examination for mass lesionswith CT scans are
rapid noninvasive tech-niques that are not life threatening for thepatient with a
head injury and that estab-lish a baseline examination for futurestudies.When an
intracranial injury is sus-pected,CT scans can quickly and easily beused to
diagnose localized intracranialhemorrhage (Figure 18-17),contusion,foreign
bodies,and skull fractures.Inaddition,secondary effects oftrauma suchas
edema,ischemia,infarction,brain shift,and hydrocephalus can be seen on CTscans.In
the acutely traumatized patient,CT scans can be used to diagnose intra-cerebral and
extracerebral blood collec-tions with nearly 100% accuracy.A signif-icant mass
lesion can cause cerebralischemia by elevating ICP or by compress-ing vascular
structures.A CT scan shouldbe done immediately following stabiliza-tion ofthe
injured patient,rather thanwaiting for signs ofan expanding intracra-nial
hematoma.Indications for a CT scaninclude seizure activity,unconsciousnesslasting
for more than a few minutes,abnormal mental status,abnormal neuro-logic
evaluation,and evidence ofa skullfracture found on physical examination.There is
still controversy regarding when ahead CT is appropriate.It has been sug-gested
that a CT ofthe head be obtained inall patients with blunt head trauma whohave
experienced a loss ofconsciousnessor mild amnesia,even those with normalneurologic
findings.45Extreme care should always be takenwhen moving a patient with a head
traumato the CT machine because ofthe highincidence ofassociated cervical spine
frac-tures in patients with head and facial trau-mas.46Iftrauma to the spine is
suspected,the cervical spine should be immobilizedbefore the patient is moved and
the CTexamination should be extended to studythe cervical spine as well.In
addition,anysuspected facial injuries should be exam-ined by extending the CT
examinationinferiorly�as low as the inferior border ofthe mandible.Unfortunately,in
many casesFalx cerebriDuraDuraCraniumSubdural
hematomaIntracerebralhematomaEpiduralhematomaDuraMiddle meningealarteryFIGURE18-
16Mass lesions commonly associated withhead trauma include epidural
hemorrhage,subduralhemorrhage,and intracerebral hemorrhage.A subduralhematoma is
usually caused by venous bleeding withprogressive loss ofneurologic function.The
epiduralhematoma is usually associated with skull fractures nearthe temporoparietal
region,with tearing ofthe middlemeningeal artery.Adapted from Powers M.15
346Part 4: Maxillofacial Traumaevaluation and treatment offacial injuriesmust be
delayed for a significant time,which means that the patient is
needlesslytransported back to the radiology depart-ment for further studies because
offailureto initially extend the CT examination.As ICP increases above normal,a
fair-ly standard progression ofneurologicabnormalities ensues,involving sections
ofthe brain sequentially:the cerebral cortex,producing an altered state
ofconscious-ness;the midbrain,producing dilation andthen fixation ofthe
pupils,initially on theside ofthe lesion,with varying degrees ofbilateral
hemiparesis;the pons,resultingin a loss ofthe corneal reflex and theoccurrence
ofthe doll�s eye reflex (Figure18-18);and the
medulla,producing,insequence,apnea,hypotension,and death.The physical examination
ofthe headshould include an examination ofthe scalpfor lacerations and foreign
bodies.Because ofthe rich vascular supply ofthe scalp,especial-ly in children,scalp
injuries may result in sig-nificant blood loss.Lacerations may overlie aninjury to
the cranium,or intracranial hemor-rhage may be present.An untreated scalpwound with
a cranial injury may eventuallyact as a port for bacteria to enter the
injuredarea,causing meningitis or a brain abscess.The head should be examined for
signs ofabasilar skull fracture:hematoma over themastoid process behind the ears
(Battle�ssign);hemotympanum;cerebrospinal fluid(CSF),rhinorrhea,or otorrhea;and
subscler-al hemorrhage.Whenever a basilar skull frac-ture is suspected,a
nasogastric tube shouldnot be used because the tube may inadver-tently pass into
the cranial vault.The neurologic examination shouldbe briefand should evaluate the
level ofconsciousness,motor and cranial nervefunction (suggestive ofdeveloping
masslesions),brainstem findings,and trends inthe neurologic status.Alcohol and
drugintoxication are frequently associated withinjured patients in the trauma
situationand may complicate the neurologic exam-ination.A decreased level
ofconsciousnessshould not be attributed to alcohol orother drugs until intracranial
pathologicconditions have been ruled out.The GCS (discussed above) provides asimple
method ofgrading consciousnessand functional capacity ofthe cerebralcortex (see
Table 18-1).It can be usedboth in the field and as a reassessmenttool to assess
brain function,brain dam-age,and patient progress,based on thethree behavioral
responses:eye opening,best verbal response,and best motorresponse.Two regions ofthe
brain,ifinjured,can produce unconsciousness;the cerebral cortices bilaterally and
thebrainstem reticular activation systemregardless ofthe cause ofinjury,can
alsodepress the level ofconsciousness.7Examination ofthe motor function ispart
ofthe GCS,which gives informationabout any asymmetry offunction.The con-scious
patient should be asked to move theextremities in response to commands.Aninability
to do so may represent damage tothe limb or spinal cord.In the
unconsciouspatient,deep tendon reflex and plantarresponse testing can assess both
sensoryinput and motor output.Ofspecial concernis abnormal posturing and
nonpurposefulmovement to stimulus.Abnormal flexoractivity (decorticate) involves
flexion oftheforearms on the chest with flexion ofthewrists and fingers;in abnormal
extensorposturing,the arms,hands,and fingers areextended with the hands abducted.In
bothcases the lower extremities are extendedand no attempt is made to localize the
pointofstimulation.Although bilateral extensorplantar responses are nonspecific,a
unilat-eral Babinski sign points to corticospinaltract damage.FIGURE18-17Computed
tomography scans demonstrating anatomic variances associated with intracranial
bleeding.A,Subarachnoid hemorrhage isdefined as blood within the cerebral spinal
fluid and meningeal intima and probably results from tears ofsmall subarachnoid
vessels.Blood is spread diffusely through the arachnoid matter and usually does not
cause mass effect,but may predispose a patient to cerebral
vasospasm.B,Intracerebral hem-orrhage is formed deep within the brain tissue and is
usually caused by shearing or tensile forces that mechanically stretch and tear
deep small-caliber arte-rioles as the brain is propelled against irregular surfaces
in the cranial vault.Note the surrounding edema and mass effect.C,Subdural
hematomas areblood clots that form between the dura and the brain.They are usually
caused by the movement ofthe brain relative to the skull,as is seen in
acceleration-deceleration injuries.Note the considerable shift ofmidline to the
right.ABC
Initial Management ofthe Trauma Patient347Pupillary function,eye movements,and eye
opening can provide informationabout the level ofconsciousness,as well asabout
brainstem function.The size,shape,and reactivity ofthe pupil to light
provideinformation about second and third nervefunction and midbrain activity.A
sluggishreactive or a dilated nonreactive (blown)pupil on one side indicates
compression ofthe third cranial nerve by brain herniationin the unconscious
patient.The pupillarylight reflex can be used to evaluate cranialnerve function and
possible elevated ICPwith brain herniation.In normal activity,when light is shone
in one eye,both pupilsconstrict equally.The optic or second cra-nial nerve carries
both visual and pupillaryfibers.The optic nerves connect shortlyafter they leave
the retina to form the opticchiasm.At the optic chiasm,the nasalfibers cross to
join the temporal fibersfrom the other eye,and the visual fiberscross to the visual
occipital cortex.Thepupillary fibers are relayed bilaterally tothe Edinger-Westphal
nucleus ofthe ocu-lomotor or third cranial nerve.The cranialnerve supplies the
sphincter muscle oftheiris,allowing it to contract.There is alsoautonomic
innervation ofthe eyes.Theiris is supplied by both sympathetic andparasympathetic
fibers.Stimulation ofthesympathetic fibers causes the pupil todilate and upper
eyelid to elevate.Thus,significant information aboutthe trauma patient can be
obtained bylooking into the eyes.Ifa light is shoneinto the right eye and the left
eye does notrespond,there may be a disruption oftheright optic or left oculomotor
nerves.Ifthe light is then shone into the left eye andit does not respond,a
disruption ofthethird cranial nerve should be suspected.Pupillary dilatation ofone
eye may be dueto a developing brain herniation on theipsilateral side,with
bilateral pupillarydilatation suggestive ofsignificant mid-brain injury or loss
ofparasympatheticfunction.Conversely,pinpoint pupils afterhead trauma may indicate
drug overdoseor loss ofsympathetic tone as seen inHorner�s syndrome.The function
ofthe brainstem mayalso be assessed with evaluation ofthecorneal reflex,which
involves sensoryinput from the trigeminal (fifth) nerve.The oculocephalic
maneuver,or test ofthedoll�s eye reflex,requires an intact vestibu-lar or acoustic
(seventh) nerve to permithead rotation to evaluate reflexive move-ment ofthe eyes
(see Figure 18-18).Obvi-ously this maneuver is not to be used withpatients who have
a suspected cervicalspine injury.The oculovestibular responsetest evaluates the
third,fourth,sixth,andeighth cranial nerves,as well as brainstemactivity.In this
test the external auditorycanal is irrigated with cold water;thereshould be full
eye movement toward theear canal lavaged with cold water.Ifnot,there may be a
disruption along any oftheneural tracts or ofthe tympanic mem-brane (see Figure 18-
18).A lumbar puncture should not beperformed in patients with acute
headinjuries.The change in pressure associat-ed with the removal ofCSF from the
lum-bar region may precipitate cerebral herni-ation in the patient with an elevated
ICP.CSF emerging from the nose or ear iscommonly associated with a basilar
skullfracture.Clear or red-tinged fluid thatdrains from the nose or ear should
beconsidered to be CSF.There is no reliablemethod available in the
emergencyFIGURE18-18Responses that test the third,sixth,and eighth cranial
nerves,as well as ascending brainstem pathways from the pontomedullary junction to
themesencephalon.A,The caloric response (oculovestibular maneuver) involves the
placement ofcold water into the ear.In a comatose patient,the eyes should ton-
ically deviate toward the irrigated ear.B,Patient at rest.C,In the oculocephalic
response (doll�s eye reflex) in comatose patients,the head is turned from the mid-
line and there is a reflex movement ofthe eyes in the opposite direction ofhead
rotation.Adapted from Powers M.15ABC
348Part 4: Maxillofacial Traumadepartment for distinguishing CSF fromnasal
mucosa.The use ofglucose indicatorsticks is associated with a high incidence
offalse-positive results.A useful aid may be a�ring sign.�A drop ofthe fluid from
thenose or ear is placed on a piece offilterpaper.Ifthe fluid is CSF,the blood
compo-nents ofthe fluid remain in the center andrings ofclear fluid form around
them.7A CT scan should be performed todetermine whether there is a fracturesite.The
head ofthe bed should be ele-vated to 90�.Ifindicated,the fractureshould be
reduced.The leakage shouldcease after 7 days;ifit does not,neuro-surgical
procedures may be indicated torepair the dural tear.A rectal examination is an
essentialpart ofthe examination ofthe patient witha head injury.Rectal sphincter
tone is pre-sent ifthe injury is intracranial only;ifthere is no rectal tone,a
coexisting spinalcord injury is present.Coexisting head andspine injuries should be
suspected untilproven otherwise.A head injury is initially classified asmild (GCS
13�15),moderate (GCS 9�12),or severe (GCS =8).Patients with headinjuries who
experience no loss ofcon-sciousness,no amnesia,no palpable frac-tures,and a GCS
score of15 can be dis-charged home to a reliable caretaker;brainimaging is
unnecessary,although it is gen-erally recommended that CT imaging beperformed due
to its low cost and its con-venience.Patients who experience a loss ofconsciousness
or amnesia,or have a GCSscore of13 or 14 must undergo an imme-diate head CT.Ifthis
noncontrast studyfinding is negative,the patient can be dis-charged to a reliable
caretaker.Ifthere is afocal neurologic finding on examination,aGCS score of< 13,or
an intracraniallesion seen on the head CT,the patientshould be admitted to an
intensive careunit or neurologic observation unit forcontinuing care.The
administration ofprophylactic phenytoin at a loading doseof18 mg/kg IV is used by
some for controlofpossible seizure activity.Ongoingseizures may be controlled with
a benzodi-azepine.Neurosurgical consultationshould be obtained early in the manage-
ment ofany obvious head trauma.Patientswith severe head injuries (GCS < 8)should
undergo rapid sequence intubationtechnique for airway protection and bettercontrol
ofICP.The patient�s ICP is con-trolled using various techniques,includingreverse
Trendelenburg position,osmoticdiuresis (mannitol),hyperventilation ofthe intubated
patient (although there islittle or no documented benefit to
thisprocedure),sedation,pharmacologicparalysis,and phenobarbital coma
(lastresort).Judicious use ofresuscitative fluidsand control ofsystemic
hypertension alsohelp to control ICP.ChestThroughout the secondary assessment ofthe
multiply injured patient,the primaryevaluation ofairway,breathing,and circu-lation
must be monitored for developmentofdifficulties or overlooked
problems.Pneumothorax,open pneumothorax,hemothorax,flail chest,and cardiac tam-
ponade may develop after the primaryassessment and must be treated according-ly.It
is estimated that chest injuries areresponsible for 20 to 25% ofall traumadeaths
per year in the United States.26The secondary assessment ofchesttrauma involves the
evaluation ofanupright chest radiograph for the presenceofair in the mediastinum or
under thediaphragm,widening ofthe mediastinumwith a shift toward the
midline,thoracicinjuries and fractures that alter lung expan-sion,and the presence
offluid.Figure 18-19 shows a chest radiograph ofa patientwithout chest trauma.In
most instancesthe trauma patient needs to be immobi-lized on a backboard (Figure
18-20),and asupine film is substituted for an uprightone.Ifa chest injury is
suspected,a CTscan should also be obtained.An electro-cardiogram,arterial blood gas
analysis,hematocrit,and urinalysis should beobtained.Six potentially lethal
injuries toconsider in the secondary assessment arepulmonary contusion,aortic
disruption,tracheobronchial disruption,esophagealdisruption,traumatic diaphragmatic
her-nia,and myocardial contusion.7Pulmonary contusions are treated inthe same
manner regardless ofwhetherthere is an accompanying flail chest injury.Pulmonary
contusions are common inblunt chest trauma because the capillarydamage within the
lungs results in intersti-tial and intra-alveolar edema and shunting.Pulmonary
contusions and adult respira-tory distress syndrome (ARDS) are themost common
potentially lethal chestinjuries seen in the United States becausethe resulting
respiratory failure does notoccur instantaneously but develops in 24 to72
hours.24The patient may complain ofpain and dyspnea,and blood gas levelstend to
deteriorate progressively over theinitial 48 to 72 hours as increasing
edemadevelops in the alveoli.Chest radiographsreveal a developing opacification
oftheinvolved areas.Treatment involves ade-quate ventilation ofthe
lungs,includingchest physiotherapy,supplemental oxygen,coughing with deep
breathing,and nasotracheal suction.Ifventilatory assis-tance is
required,spontaneous ventilation with intermediate mechanical ventilation FIGURE18-
19Normal upright chest radiograph.
Initial Management ofthe Trauma Patient349provides much better ventilation-perfu-
sion matching,better hemodynamics,andquicker weaning than does assisted ventila-
tion.The use ofsteroids is controversial.47Injury to intrathoracic large arteries
orveins may develop with blunt or penetrat-ing trauma;this is the most commoncause
ofsudden death after an automobileaccident or a fall from a great height.7Common
sites ofinjury are the aortic rootand the descending aorta at the origin ofthe
ductus arteriosus and at thediaphragm.These injuries are fatal withina few
minutes�only 15% ofpatients withthoracic aortic injuries are still alive onarrival
at a hospital.It is not uncommonfor the aorta intima and media to be frac-tured
circumferentially,with only theadventitia and surrounding mediastinaltissues
preventing fatal hemorrhage.Thepatient may appear clinically stable;yet,failure to
recognize this vascular injuryleads to eventual death.Adjunctive signson chest
radiographs that are suggestive ofthoracic vascular injury include a
widenedmediastinum,fractures ofthe first andsecond ribs,obliteration ofthe
aorticknob,deviation ofthe trachea to the right,the presence ofa pleural
cap,deviation ofthe esophagus to the left,and a downwarddisplacement ofthe left
mainstreambronchus.7Ifan aortic rupture is suspect-ed on clinical or radiographic
examina-tion,an aortography should be performed.While waiting for the aortogram,it
isimportant not to let the patient becomehypertensive or cough or gag
excessively(eg,as may occur with the placement ofanasogastric tube).Maxillofacial
Area and NeckMaxillofacial injuries may cause airwaycompromise from blood and
secretions,from a mandibular fracture that allows thetongue to fall against the
posterior wall ofthe pharynx,from a midface injury thatcauses the maxilla to fall
down and backinto the nasopharynx,and from foreigndebris such as avulsed teeth or
dentures.Alarge tonsillar suction tip should be usedto clear the oral cavity and
pharynx.Anoral airway assists with tongue position;however,care must always be
taken toavoid manipulation ofthe neck and toprovide for access to the oral cavity
anddentition for reduction and fixation ofanyfractures requiring some period
ofinter-maxillary fixation.Neither midface frac-tures nor cerebrospinal rhinorrhea
arecontraindications to nasal intubation.Care should be taken to pass the tubealong
the floor ofthe nose into the phar-ynx,and the tube should be visualizedbefore
intubation ofthe trachea.The physical examination shouldbegin with an evaluation
for soft tissueinjuries.Lacerations should be d�bridedand examined for disruption
ofvitalstructures such as the facial nerve orparotid duct.The eyelids should be
elevat-ed so that the eyes can be evaluated forneurologic and possible ocular
damage.The face should be symmetric without dis-colorations or swelling suggestive
ofbonyor soft tissue injury.The bony landmarksshould be palpated,beginning with
thesupraorbital and lateral orbital rims,infra-orbital rims,malar eminences,and
zygo-matic arches,and nasal bones should bepalpated.Any steps or irregularities
alongthe bony margin are suggestive ofa frac-ture.Numbness over the area
ofdistribu-tion ofthe trigeminal nerve is usuallynoted with fractures ofthe facial
skeleton.The oral cavity should be inspectedand evaluated for lost
teeth,lacerations,and alterations in the occlusion.Any teethlost at the time
ofinjury must be account-ed for because the tooth may have beenaspirated or
swallowed.The neck should also be examined forinjury.Subcutaneous air may be
visualizedifmassive injury is present;ifsubtle,itmay be detected only by
palpation.Thepresence ofair in the soft tissues may bethe result oftracheal
damage.Any exter-nally expanding edema or hematoma ofthe neck must be observed
closely for con-tinued expansion and airway compromise.Carotid pulses should be
assessed.Palpa-tion for abnormalities in the contour ofthe thyroid cartilage and
for the midlineposition ofthe trachea in the suprasternalnotch should be
performed.Spinal CordThere are > 10,000 spinal cord injuries peryear in the United
States,usually caused byFIGURE18-20Stabilization ofthe trauma vic-tim for
transportation is best achieved with theuse ofa long backboard with bindings and
sand-bags to control the head in a neutral position.Adapted from Powers M.15
350Part 4: Maxillofacial Traumamotor vehicle accidents.Multiple studieshave
reported a 10 to 20% association ofcervical spine injuries with
maxillofacialinjuries in the multiply traumatizedpatient although recent data
suggest noincrease in cervical spine injury when facialtrauma is
present.48,49Approximately 55%ofspinal injuries occur in the cervicalregion,15% in
the thoracic region,15% inthe thoracolumbar junction,and 15% inthe lumbosacral
area.8Identification ofcervical spine injury is essential in themanagement ofblunt
trauma because amissed injury can result in catastrophicspinal cord
damage.Tetraplegia as a resultofcervical spine injury is not only atragedy for the
patient;it also represents atremendous financial burden to society.50According to
the National Spinal CordInjury Center Databank,in July 1996,theaverage medical cost
ofthe first year ofacord injury involving C1 through C4 was$417,000 (US).50Patients
can be expectedto have medical costs of$1,350,000 overthe course oftheir lifetime
as well as lostwages and productivity.Patients can thenexpect a greatly shortened
life span,whichvaries according to the age ofthe patient atthe time ofinjury.48A
description ofthe mechanism ofinjury,especially high-velocity accident,may give
clues to a possible injury ofthespine such as a whiplash injury.Thepatient may
experience little discomfortfrom major injury to the chest,abdomen,and extremities
as a result ofsensory lossfrom a spinal injury.Because ofthe loss ofsympathetic
tone with cervical injuries,the patient may present with a systolicblood pressure
level of70 to 80 mm Hgwithout the tachycardia,cool extremities,poor perfusion,and
decreased urinaryoutput noted in the patient with hypo-volemic shock.The neurologic
shock isdue to dilatation ofthe arterial system,lossofmuscle tone,and loss
ofreflexes.Theabsence ofneurologic deficit does notexclude injury to the cervical
spine.Acomplete series ofcervical radiographsshould be obtained and read prior to
theremoval ofstabilization.Ifa helmet isworn by the victim,the helmet should
besecured to the long spine board with 8 cmcloth tape,and cervical spine
radiographsshould be taken and cleared for cervicalspine injury before the
attempted removalofthe helmet.Physical examination ofthe patientwith a suspected
spinal injury should bedone carefully,with the patient in a neutralposition and
with minimal movement ofthe spine and head (see Figure 18-20).Thepresence ofan
unstable cervical spineinjury must be considered in the evalua-tion and
resuscitation ofevery patient withinjuries associated with blunt
trauma.Thecatastrophic physical consequences ofirre-versible quadriplegia,as well
as the hugeeconomic costs required to care for thislifelong disability,require that
great caremust be taken to rule out unstable cervicalspine injury.The patient
should be treatedas ifthere has been an unstable injury tothe
nerves,bone,muscles,and other struc-tures ofthe neck until there is positive clin-
ical and radiographic evidence that there isno injury.The neck and spine should
becarefully examined for deformity,edema,ecchymosis,muscle spasm,and
tendernesswhile being carefully supported to avoidfurther damage associated with an
unsta-ble cervical neck injury.The neurologic examination ofthepatient with a
spinal injury is similar tothat ofthe patient with closed head trau-ma.The mental
status,motor function,sensation over dermatomes,brainstemreflex,and spinal reflexes
should all beevaluated and charted.The patient shouldbe carefully examined for
rectal tone andbladder control as evidence ofautonomicfunction.Hypoventilation
caused byparalysis ofthe intercostal muscles resultsfrom injury to the lower
cervical or upperthoracic spinal cord.Ifthe upper or mid-dle cervical spin is
injured,the diaphragmwill also be paralyzed as a result ofinvolve-ment ofthe C3
though C5 spinal cord seg-ments.Abdominal breathing and the useofthe respiratory
accessory muscles willbe evident.7Bachulis and colleagues evaluated4,941 trauma
victims between February1981 and July 1985 and found that 1,923(39%) had
radiographs taken oftheir cer-vical spines.51Injuries to the cervical spinewere
detected in 94 patients (5%).Ninetyofthese patients had cervical spine frac-
tures;four had a disruption ofthe cervicallongitudinal ligaments without bonyinjury
and were quadriplegic.In the studythe overall incidence ofcervical spineinjury in
the trauma patient was 2%.Neu-rologic deficit did not develop in anypatient with a
neurologically intact spinalcord at the time ofadmission.Theresearchers found
that,ofthe 94 patients,there were 65 alert patients with no neuro-logic deficits
who had unstable cervicalspine injuries.Without exception,thesepatients either
complained ofneck pain orofpain on palpation ofthe neck.Otherstudies have reported
that no alert patientwithout neck pain was found to have anycervical
injury.51Fischer concluded that ascreening radiographic examination ofthecervical
spine is not indicated in the alert,sober,and cooperative patient with nocomplaints
ofneck pain and no tender-ness to palpation ofthe neck,even whensignificant injury
is present;however,theauthor does recommend screening for allpatients with
decreased levels ofcon-sciousness and a history ofan injury thatcould have
conceivably injured the cervicalspine,for all patients with neurologicdeficits
compatible with cervical origin,and for all patients with neck pain or ten-
derness.51Cervical spine injuries mayresult from axial loading,flexion,exten-
sion,rotation,lateral bending,and distrac-tion or combinations ofthese
mechanismsofinjury (Figure 18-21).In the study by Bachulis and col-leagues,lateral
cross-table cervical spineradiographs were obtained in all injuredpatients and
demonstrated cervical spine
Initial Management ofthe Trauma Patient351injury in 70 patients but not in the
other24,for an unacceptable false-negative rateof26%.The authors recommended
thatall patients at risk for cervical spine injurymust have a complete initial
radiographicexamination,including lateral,anteropos-terior,odontoid,and right and
leftoblique views ofthe cervical spine.CTscanning was found to be the most
usefulmodality to confirm a cervical spineinjury in those patients with a
suspectedinjury to the cervical spine not confirmedon plain film radiographs.They
recom-mend the use ofCT scans ofthe neck forpatients with a possible neck injury
andassociated head injury that requires a CTscan ofthe brain,for patients in
whomradiographic visualization ofC6 or C7 aredifficult,and for patients with a
suspectedcervical injury that is not detected inscreening radiographs.46A recent
study byGriffen and colleagues concluded that CTscanning ofthe cervical spine
shouldreplace plain film studies in blunt traumapatients completely.52Visualization
ofall seven cervical ver-tebrae is important (see Figure 18-21).The shoulders must
be distracted inferior-ly by pulling down on the arms to providea clear view ofthe
spinal anatomy from C6through T1.It is important that a clearview ofthe spine at
the C6 and C7 level beobtained without obstruction by theshoulders to obtain a
proper diagnosticstudy.Ifvisualization ofC6 and T1 cannotbe obtained,the
radiographic view may beimproved by placing the arms in a �swim-mer�s
position,�with downward tractionon one arm and upward traction on theother and the
radiograph beam aimedthrough the axilla ofthe upward arm.Radiographs should be
examined for frac-tures and fracture dislocations ofthe spineby evaluation the
anteroposterior diame-ter ofthe spinal canal;the contour andalignment ofthe
vertebral bodies;dis-placement ofbony fractures ofthe lami-nae,pedicles,or neural
fascicles;and softtissue swelling.18Three-way cervical
views(anteroposterior,oblique cervical,and lat-eral cervical) plus an open-mouth
odon-toid view or a CT scan ofthe neck coupledwith adequate cervical spine
immobiliza-tion during evaluation and resuscitationshould allow the cervical spine
to beviewed safely.On a lateral cervical spine radiograph,the soft tissue thickness
between the phar-ynx and osseous C3 should be < 5 mm.Anincrease in this area
suggests a fracture.Thedistance may vary with inspiration or expi-ration.7On the
lateral view the features tobe examined are the general contour ofthespine,the
vertical alignment ofthe anteri-or and posterior margins ofthe vertebralbodies,the
midlaminar line,the width ofthe spinal column,and evidence ofcom-pression or
fracture ofindividual verte-brae.On anteroposterior views the heightand alignment
ofthe spinous processesand the interspinous distances are exam-ined.The discovery
ofany findings sug-gesting the presence ofa cervical spinalinjury mandates the use
ofprotective mea-sures.It has been demonstrated that a sta-bilization device such a
cervical collarallows significant movement ofthe cervicalspine.53The recommended
stabilizationfor patients with cervical fractures is a cer-vical collar in
combination with a longspinal board.Appropriate head holders orsandbags should be
used bilaterally to sup-port the neck laterally,and the head shouldbe secured with
an 8 cm cloth tape acrossthe forehead and around the board (seeFigure 18-
20).Obviously,maintaining astable airway is critical in patients whohave suffered
significant head and necktrauma.Cervical neck protection as well asa nasal trumpet
or similar airway protec-tion device may be indicated to maintain apatent
airway.Ifthe airway becomes unsta-ble,nasotracheal intubation or cricothy-roidotomy
should be performed,in thatorder,always ensuring that the cervicalspine continues
to be stabilized.CT should be used for further evalua-tion ofdetected or suspected
fractures,evaluation ofquestionable plain films,andto complete radiographic
examination ofareas not well visualized by plain films.FIGURE18-21Normal cervical
radiographs: A,lateral; B,anteroposterior.Radiographs should beexamined for
prevertebral edema,subluxation,widening ofthe interspinous distance,widening
oftheatlantodental interval,bony fractures,malalignment,or jumped facets.AB
352Part 4: Maxillofacial TraumaThe lower cervical spine often is not wellvisualized
on radiographs,even with useofthe swimmer�s position,and a CT scanis frequently
required.AbdomenWith abdominal trauma,the physicalexamination is an informative
portion ofthe diagnostic evaluation.Penetratingwounds must be identified,and many
sur-geons believe that the safest managementofpenetrating wounds is a
laparotomy.7The abdominal girth should be measuredat the umbilicus soon after
admission toestablish a baseline against which to evalu-ate possible intra-
abdominal bleeding.Abdominal rigidity and tenderness areimportant signs
ofperitoneal irritation byblood or internal contents,and they maybe the main
indications for a laparotomyofa patient injured by blunt trauma.Rec-tal and pelvic
examinations are essential ifthere is a question ofpelvic or perinealinjury.A
nasogastric tube should bepassed,ifpossible,into the stomach toremove gastric
contents.Plain films have limited value inabdominal trauma.They can be useful
inlocalizing foreign bodies,bony structures,and free air with the use
ofanteroposteri-or and cross-table views.The use ofdiagnostic peritoneal
lavage(DPL),once a standard diagnostic test usedin blunt and occasionally
penetratingabdominal traumas,has decreased signifi-cantly with the advancement in
CT andultrasonography.DPL is indicated inpatients with a history ofblunt
abdominaltrauma and increasing pain,patients withunexplained hypovolemia following
multi-ple trauma,patients who are candidates forlaparotomy but who have
questionable find-ings,and patients who have experiencedsevere trauma and who may
require anextended period under general anesthesia.7Absolute contraindications to
DPL are a his-tory ofmultiple abdominal operations andobvious indications for an
exploratorylaparotomy�free air and penetrating trau-ma.A DPL is usually performed
with a ster-ile intravenous catheter inserted percuta-neously through a small
midline incisionabout 2.5 to 4 cm below the umbilicus.Thecatheter is advanced into
the pelvis after thebladder has been emptied.Ifno blood,bile,or intestinal fluid is
aspirated,the abdominalcavity is irrigated with 1 L ofsaline.The fluidis then
drained from the abdomen throughthe intravenous tubing.It is generally feltthat the
presence of100,000 red blood cellsor 500 white blood cells per cubic
millimeterafter blunt trauma is sufficient to make alaparotomy mandatory (Table 18-
6).CT scanning ofthe abdomen is alsoacceptable ifthe patient is stable andemergent
laparotomy is not indicated.Theadvantages to CT include that it is nonin-vasive;it
is capable ofdiscerning the pres-ence,source,and approximate quantity
ofintraperitoneal hemorrhage;and it occa-sionally can demonstrate active
bleeding.CT scanning coincidentally evaluates theretroperitoneum�an area not
sampled byDPL�as well as the vertebral column andcan be readily extended above or
below theabdomen to visualize the thorax or pelvis.It is helpful in the evaluation
ofhematuriaand,ifused early enough,in determiningrenal artery injury.Disadvantages
includesuboptimal sensitivity for injuries ofthepancreas,diaphragm,small
bowel,andmesentery.Injuries ofthe small bowel andmesentery can have profound
morbidityand even mortality ifnot diagnosed early.In the absence ofhepatic or
splenicinjuries,the presence offree fluid in theabdominal cavity suggests an injury
to thegastrointestinal tract and/or its mesenteryand mandates early surgical
intervention.Complications also can result from intra-venous contrast
administration.The costcan also be significant,especially ifestab-lished
indications are not followed.Ultrasonography or focused assess-ment with sonography
for trauma is rapid-ly becoming an integral diagnostic compo-nent in trauma
centers.Ultrasonographyhas undergone a large number ofclinicalevaluations in
Europe,Asia,and the UnitedStates.Its primary role is detecting freeintraperitoneal
blood after blunt trauma.This is accomplished by a focused exami-nation ofspecific
anatomic areas whereblood or fluid is most likely to accumulate.Ultrasonography can
also evaluate theTable 18-6Parameters for Evaluation ofPeritoneal Lavage
FluidPositive20 mL gross blood on free aspiration (10 mL in children)=100,000
RBCs/mm3=500 WBCs/mm3(ifobtained =1 h after the injury)=175 U amylase/100
mLBacteria (determined with Gram�s stain)Bile (by inspection ofchemical
determination ofbilirubin content)Food particles (microscopic analysis ofstrained
or spun specimen)IntermediatePink fluid on free aspiration50,000�100,000
RBCs/mm3100�500 WBCs/mm375�175 U amylase/100 mLNegativeClear aspirate=50,000
RBCs/mm3=100 WBCs/mm3< 75 U amylase/100 mLAdapted from Powers M.15RBC = red blood
cell;WBC = white blood cell.
Initial Management ofthe Trauma Patient353pericardial space and
intraperitonealspaces.Ultrasonography carries a host ofadvantages:�It is a portable
instrument that can bebrought to the bedside in the traumaresuscitation
area.�Studies ofthe pericardial andintraperitoneal spaces can be accom-plished in <
5 minutes.�Sensitivity in detecting as little as 100mL to,more typically,500 mL
ofintraperitoneal fluid ranges from 60to 95% in most recent studies,andspecificity
for hemoperitoneum isexcellent.54�Unlike DPL,ultrasonography canrapidly gauge the
mediastinum,isnoninvasive,and can be performedserially and by multiple
technicians.�Unlike CT scanning,ultrasonographydoes not pose a potential
radiationhazard and does not require adminis-tration ofcontrast agents.�Performing
focused ultrasonographicexaminations with an abdominaltrauma patient does not
require theskill ofa board-certified radiologist,which allows ultrasonography to
bemore readily accessible to injuredpatients.Accuracy correlates withlength
oftraining and experience,butexpertise can be readily accomplishedin emergency
medicine and surgicaltraining programs.55�Overall,ultrasonography can serve asan
accurate and rapid test and is a lessexpensive diagnostic screening toolthan are
DPL and CT.However,there are disadvantages to the useofultrasonography,including
the following:�It does not image solid parenchymaldamage,the
retroperitoneum,ordiaphragmatic defects very well.�It is technically compromised by
theuncooperative agitated patient,as wellas by obesity,substantial bowel gas,and
subcutaneous air.�Indeterminate studies require follow-up.�Ultrasonography is less
sensitive andmore operator dependent than is DPLin revealing hemoperitoneum
andcannot distinguish blood from ascites.�Ultrasonography (as well as DPL)does not
detect the presence ofsolidparenchymal damage iffree intraperi-toneal blood is
absent,as in subcapsu-lar splenic injury.56�Finally,ultrasonography is poor
fordetecting a bowel injury in whichhemorrhage tends to be inconsequen-tial,and
failure to diagnose hollow vis-cus perforation in a timely mannercan have
catastrophic results.Table 18-7 presents indications,advan-tages,and disadvantages
ofultrasonogra-phy,DPL,and CT in blunt abdominaltrauma.Genitourinary TractWhen an
injury to the genitourinary tractis suspected,urologic consultation isrequired to
further evaluate and diagnosethe extent ofinjury.The major cause ofurethral
ruptures is blunt trauma.Over95% ofpatients with a pelvic fracture havean
associated posterior urethral rupture.The force ofthe injury causes a
shearingeffect between the urethra and the urogen-ital diaphragm.34Anterior
urethral rup-tures are also commonly associated withblunt trauma.Most ofthese
injuries occurin men.57Blood at the urethral meatus is the sin-gle best indicator
ofurethral trauma.35Themeatus must be carefully inspected foreven the slightest
amount ofblood beforeinserting a urethral catheter.As is discussedabove,attempts to
introduce a Foleycatheter up an injured urethra can convertan incomplete laceration
into a completelaceration with a subsequent retropubic orperineal hematoma.33A
rectal examinationmust be performed on all patients with asuspected pelvic
injury.With posterior ure-thral disruption,the prostate may beforced superiorly by
a hematoma.Iftheprostate is not palpable,a genitourinaryinjury should be
suspected.33Absence ofblood at the meatus andpalpability ofthe prostate on rectal
exam-ination are sufficient evidence to allow thepassage ofa urethral
catheter.Ifresistanceis noted,the catheter should be removed.Retrograde
urethrography is the bestmethod to establish continuity ofor dam-age to the
urethra.33Urine should be obtained and evaluat-ed for the presence ofblood.A
urinalysisof10 or more red blood cells on a high-power field is suggestive ofa
urinary sys-tem injury.Hematuria is the best indicatorofrenal injury,and the degree
ofhema-turia may not correlate with the degree ofinjury.Ifthe patient with a blunt
injury isstable but has hematuria,a CT scan can beused to accurately visualize the
genitouri-nary system and abdominal and retroperi-toneal contents.Extremities
Pelvic fractures,fractures ofthe femur,and multiple fractures ofother long bonesmay
cause hypovolemic shock and life-threatening blood loss,the primary site ofwhich
may be difficult to determine.Typi-cal closed fractures ofthe pelvis may lose 1 to
5 L ofblood,femur fractures 1 to 4 L,and arm fractures 0.5 to 1 L from the vas-
culature.58Certain extremity injuries areconsidered life threatening because
ofassociated complications�massive openfractures with ragged dirty wounds;bilat-
eral femoral shaft fractures (open orclosed);vascular injuries,with or
withoutfractures,proximal to the knee or elbow;crush injuries ofthe abdomen and
pelvis;major pelvic fractures;and traumaticamputations ofthe arm or leg.7Physical
examinations should consistofinspection and palpation ofthe
chest,abdomen,pelvis,and all four extremities.Areas
oftenderness,discoloration,swelling,and deformity should be inspect-ed,and proper
radiographs should be
354Part 4: Maxillofacial Traumaobtained.All peripheral pulses should beexamined for
evidence ofvascular injury.Pulse rates should be equal;any abnormal-ity ofdistal
pulse rates suggests a vascularinjury and must be explained.Dopplerexamination
ofthe extremity is useful,butangiography is the best test for
definitivelyevaluating a suspected vascular injurywhen the diagnosis is in
doubt.7Direct pressure should be used to con-trol hemorrhage,and fractures should
besplinted as quickly as possible.Splintsshould generally include joints above
andbelow the site ofinjury.Prompt orthope-dic consultation should be obtained.Fat
embolism syndrome is usuallyassociated with major fractures oflongbones,especially
ofthe femur.The patienttypically does well for 24 to 48 hours andthen develops
progressive respiratory andCNS deterioration.Concomitant labora-tory value changes
include hypoxemia,thrombocytopenia,fat in the urine,and aslight drop in
hemoglobin.Fat enters thevenous sinusoids at the fractured site andbecomes lodged
in the lung alveoli.Fatembolism syndrome has been reported tooccur with 30 to 50%
ofmajor long-boneand pelvis fractures.59However,with thecurrent coordinated
management ofmul-tiply injured patients,the incidence ofboth fat embolisms and ARDS
is decreasedby expeditious femoral shaft and pelvicfracture treatment.56The primary
treat-ment is ventilatory assistance.Therapywith steroids and acetylsalicylic acid
hasbeen shown to be helpful,possibly becauseofa reduction ofplatelet
aggregation.With a better understanding offluidand electrolyte therapy,an early
aggressivemanagement ofhemorrhagic shock andprompt surgical treatment are now
possi-ble.However,in the interest ofacute resus-citation,orthopedic injuries are
often over-looked initially and are treated at a latertime.When these injuries
involve the spine,pelvis,or femur,immobilization ofthepatient is necessary for the
purpose oftrac-tion.In immobilized patients with unstablefractures,there is an
increased morbiditycaused by respiratory failure or sepsis withrelated multiple
organ failure.The severelyinjured patient with orthopedic fractureswho survives the
acute phase oftreatmentgenerally undergoes a prolonged course inthe intensive care
unit.This leads to mor-bidity secondary to decreased muscu-loskeletal function
(eg,muscle wasting,stiffjoints,loss oflimb length) caused by delaysin fracture
stabilization and subsequentpatient mobilization.60Studies have shownthat early
fracture stabilization can signifi-cantly decrease
mortality,musculoskeletalmorbidity,and cardiopulmonary andmetabolic consequences
commonly associ-ated with multiple trauma.58Long-bone fractures are a commoncause
offat embolisms and ARDS.Opera-tive fixation oflong-bone fractures inpatients with
multiple injuries within thefirst few days ofinjury can minimize thedevelopment
offat embolisms.56Primaryrigid fixation allows the patient to get outofbed and
assume an upright position,thus improving pulmonary and muscu-loskeletal
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trauma.New York:Theime Stratton;1985.p.285�301.36.Devine PC,Devine CJ Jr.Posterior
urethralinjuries associated with pelvic fractures.Urology 1982;20:467�70.37.Bell
RM,Krantz BE.Initial assessment.In:Mattox KL,Feliciano DV,Moore EE,edi-tors.Trauma
4th ed.New York:McGraw-Hill;2000.p.153�70.38.Velanovich V.Crystaloid versus colloid
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RL,TrunkeyDD.Blood component supplementationduring massive transfusion ofAS-1 red
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position on bloodpressure and carotid flow.Surg GynecolObstet
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indications for cervical spineradiographs in the traumatized patient.AmJ Surg
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EE,Feliciano DV,edi-tors.Trauma.Norwalk (CT):Appleton &Lange;1988.p.115�23.48.Ivy
ME,Cohn SM.Addressing the myths ofcervical spine injury management.Am JEmerg Med
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increased risk ofcervicalspine injury? J Trauma 1993;34:549�57.50.National Spinal
Cord Injury Statistical Center(NSCISC).Spinal cord injury:facts and fig-ures at a
glance.Birmingham (AL):NSCISC:July 1996.51.Fischer RP.Cervical radiographic
evaluation ofalert patient following blunt trauma.AnnEmerg Med
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SJ,Fry WR,Helmer SD.Insti-tutional learning curve ofsurgeon-
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CHAPTER 19Soft Tissue InjuriesAlan S.Herford,DDS,MDG.E.Ghali,DDS,MDIn the United
States over 11 million trau-matic wounds are treated in emergencydepartments each
year.Facial lacerationscomprise approximately 50% ofthesewounds.1Facial injuries
impact both func-tion and esthetics.There is often a psycho-logical aspect
associated with the injurysecondary to patient�s concern regardingpermanent
scarring and subsequent facialdisfigurement.According to a recent sur-vey,cosmetic
outcome is the single mostimportant aspect ofcare to the patient.2Principles
ofManagementThe initial examination involves evaluat-ing and stabilizing the trauma
patient.Anylife-threatening conditions should beidentified and managed
immediately.Theconditions ofthe airway,breathing,andcirculation are
examined,followed by ageneral neurologic assessment with partic-ular attention to
cervical spine and cranialinjuries.It is important to achieve hemostasiswhen
stabilizing and evaluating thepatient who has sustained trauma.Mostbleeding will
respond to application ofapressure dressing.Occasionally surgicalexploration and
packing ofthe woundunder general anesthesia may be indicat-ed.In rare instances
vessels in the neckmay need to be ligated.Indiscriminateclamping inside the wound
should beavoided because damage to importantstructures such as the facial nerve
orparotid duct may result.It is unusual forbleeding from soft tissue injuries to
theface to result in a shock state.Lacerationsinvolving the scalp can occasionally
bedifficult to control with pressure and mayrequire clamping,ligation,or electro-
cautery.In soft tissue injuries not involving theface the length oftime from
initial injuryto treatment is important.Secondary riskofinfection increases with
the lapse oftime.3Because ofthe rich vascularity ofthe face there is no �golden
period�forsuture repair offacial wounds.In fact heal-ing offacial wounds is
unaffected by theinterval between injury and repair.4Patients who are immunized and
havereceived a booster injection within the last10 years do not require tetanus
prophylax-is ifthe wound is not tetanus prone.Tetanus-prone wounds are those
withheavy contamination from soil or manure,devitalized tissue,or deep
puncturewounds.Ifthe wound is tetanus prone andthe patient has not received a
boosterinjection within 5 years prior to the injury,a 0.5 mL tetanus toxoid boost
injectionshould be given.Ifthe patient has notreceived a booster within 10 years
prior,they should receive a booster injection forany wound.Patients who are not
immu-nized should receive both a booster injec-tion and 250 units
oftetanusimmunoglobulin,followed by a full courseofimmunization.5Treatment ofsoft
tissue injuriesinvolves early reconstructive proceduresaddressing both the soft
tissue and theunderlying bony injury in a minimumnumber ofstages.6,7Occasionally it
is bet-ter to delay soft tissue repair until the facialfractures have been
addressed.In patientswith large avulsion oftissue,definitiveearly reconstruction
ofthe tissue loss withregional or microvascular flaps may berequired.8,9Anatomic
EvaluationFollowing the initial evaluation and resus-citation,injuries to the soft
tissues shouldbe evaluated during the secondary survey.Patients sustaining trauma
often haveassociated soft tissue injuries.Facialinjuries can be superficial but may
extendto involve adjacent structures
includingbones,nerves,ducts,muscles,vessels,glands,and/or dentoalveolar
structures.Associated injuries,including vascularinjury,may develop acutely or days
afterthe injury.10,11A thorough head and neck examina-tion determines the extent
ofassociatedfacial wounds.Peripheral cranial nerves arecommonly involved with
lacerations thatinvolve the face.The facial nerve dividesthe parotid gland into
deep and superficialportions (Figure 19-1).Any injury to thegland should raise
suspicion for associatedfacial nerve injury.12The facial nerve exitsthe
stylomastoid foramen and divides into
358Part 4: Maxillofacial Traumafive branches within the parotid gland(Figure 19-
2).Proximal facial nerveinjuries posterior to a vertical line drawnfrom the lateral
canthus should be repairedusing microsurgical techniques.Because ofthe significant
peripheral anastomoses,repair offacial nerve injuries involving dis-tal branches
anterior to the canthal plane isunnecessary (Figure 19-3).Injury to the parotid
gland can lead toleakage ofsaliva into the soft tissue.Theparotid duct is
approximately 5 cm inlength and 5 mm in diameter.It exits thegland and runs along
the superficial surfaceofthe masseter muscle and then penetratesthe buccinator
muscle to enter the oral cav-ity opposite the upper second molar.Treat-ment
ofparotid duct injuries depends onthe location ofthe injury.These injuresshould be
repaired in the operating roomwith the aid ofmagnification.Ifthe injuryinvolves the
proximal duct while it is still inthe gland,the parotid capsule should beclosed and
a pressure dressing placed.Iftheinjury is located in the midregion oftheduct,the
duct should be repaired.Injuriesinvolving the terminal portion ofthe ductshould be
drained directly into themouth.Lacrimal probes are useful in can-nulating the duct
and identifying injuries.Cervical branchMarginal mandibular branchBuccal
branchBuccal branchParotid (Stenson's) ductParotid glandFrontozygomatic
branchFIGURE19-1The facial nerve divides the parotid into a deep and superficial
lobe.Cervical branchStylohyoid branchBuccal branch Parotid ductParotid
glandGeniculate ganglionMarginal mandibular branchBuccal branch Stylomastoid
foramenPosterior auricular branchZygomatic branches (orbital)Temporal
branchesDigastric branchFIGURE19-2Anatomy ofthe facial nerve.FIGURE19-3Zone
ofarborization ofthe facial nerve.
Soft Tissue Injuries359A polymeric silicone (Silastic) catheter isplaced to bridge
the defect.The severed endsare then sutured over the catheter,which isleft in place
for 10 to 14 days (Figure 19-4).The parotid capsule should be closed to pre-vent
formation ofa parotid duct fistula orsialocele.Lacerations are closed primarilyand
a pressure dressing is placed to preventfluid accumulation.There are several
protocols for evalua-tion and treatment ofpenetrating injuriesto the neck,face,and
temporal bone.Ifthere is suspicion that deep critical struc-tures have been
injured,the appropriateprotocol should be followed.Sequence ofRepair and Basic
TechniqueA decision is made to repair the wound inthe emergency department or to
performthe repair in the operating room under ageneral anesthetic.Large complicated
lac-erations demand ideal lighting andpatient cooperation.In injuries wherethere is
a concern that deep structureshave been damaged,a general anestheticaffords the
best opportunity for explo-ration and repair.The patient mayrequire repair ofother
traumatic injuriesin the operating room,and on manyoccasions,definitive repair
ofassociatedfacial soft tissue injuries can be per-formed at the same
time.Lidocaine is a popular local anestheticand ranges in strength from 0.5 to
2%.It isusually administered with epinephrine1:100,000.Lidocaine has a rapid onset
ofaction,a wide margin ofsafety,and a lowincidence ofallergic sensitivity.A thor-
ough evaluation ofthe seventh cranialnerve should be undertaken prior to injec-tion
ofanesthetic or administration ofageneral anesthetic.Injecting local anes-thetic
prior to cleaning the wound willallow more effective preparation.Localanesthetics
containing epinephrine havebeen used successfully in all areas oftheface but may
not be optimal in areas wheretissue monitoring is critical or whereextensive
undermining ofthe soft tissue isnecessary.13One should avoid injectingdirectly into
the wound when importantlandmarks could be distorted.Regionalnerve blocks are
beneficial in minimizingthe amount oflocal anesthesia requiredand also prevent
distortion ofthe tissues.14After adequate anesthesia has beenobtained,the wound is
thoroughlyd�brided.Nonvital tissue is conservative-ly excised in an attempt to
salvage most ofthe tissue.Devitalized tissue potentiatesinfection,which inhibits
phagocytosis.Persistent infection at a wound site leadsto the release
ofinflammatory cytokinesfrom monocytes and macrophages,whichdelays wound healing.An
anaerobic envi-ronment results and limits leukocytefunction.15Soft tissue wounds
are oftencontaminated with bacteria and foreignmaterial.Treatment ofthese
injuriesinvolves copious irrigation and is aimedat minimizing the bacterial wound
floraand removing any foreign bodies.Withrespect to infection rates,studies
haveshown no statistical difference in woundsirrigated with normal saline when com-
pared to other solutions.Pulsatile-typeirrigation devices may be helpful toremove
debris,necrotic tissue,and loosematerial.Hydrogen peroxide impedeswound healing and
has poor bactericidalactivity.A good rule is to avoid irrigatingthe wound with any
solution that wouldnot be suitable for irrigating the eye.Careful and meticulous
cleaning ofthewounds primarily will avoid unfavorableresults such as
�tattooing,�infection,hypertrophic scarring,and granulomas.A scrub brush and
detergent soap may benecessary to remove deeply imbeddedforeign
material.However,soaps maycause cellular damage and necrosis.Asurgical blade may be
helpful to scrapeforeign material that is deeply embedded.Polymyxin B sulfate can
be used toremove residual grease or tar in wounds.Proper cleaning and good
surgicaltechnique are imperative in minimizinginfection.Infections are rare when
theFIGURE19-4A,This laceration shows the parotid duct severed and cannulated with a
polyethylene tube.B,The duct is suturedover the tubing.AB
360Part 4: Maxillofacial Traumawound is closed so that no dead space,devi-talized
tissue,or foreign bodies remainbeneath the sutured skin.Hydrogen perox-ide is
minimally bactericidal and toxic tofibroblasts even when diluted to 1:100.16Diluted
hydrogen peroxide is useful in thepostoperative period in cleaning crustsaway from
incision lines in order to mini-mize scarring.Common methods for closingwounds
include suturing,applying adhe-sives,and stapling.It is preferable to suturecomplex
facial lacerations secondary toesthetic considerations.A layered closureis almost
always necessary and eliminatesdead space beneath the wound.Ifthe deadspace is not
obliterated,accumulation ofinflammatory exudates may occur.Thisleads to
infection,which in turn may causetension across the epidermis.Tension cancause
necrosis ofthe skin edges due toimpairment ofthe vascular supply andmay cause an
increase in scarring.17Injuries involving anatomic borderssuch as the vermilion
ofthe lip must bereapproximated precisely.Examples ofthese landmarks include
eyebrows,lipmargins,and eyelids.Lacerations shouldbe closed by placing a suture in
the centerofthe laceration to avoid creating exces-sive tissue on the end ofthe
laceration(dog-ear).Deep layers should be reap-proximated with 3-0 or 4-0
buriedresorbable sutures.The superficial skin isclosed with 5-0 or 6-0 suture.It is
impor-tant to avoid causing puncture markswhen grasping the wound
edges.Marginsshould be undermined to allow slighteversion ofthe wound
margin.Skinsutures should be removed 4 to 6 daysafter placement.By this time the
woundhas regained only 3 to 7% ofits tensilestrength and adhesive strips help
supportthe wound margins.18At 7 to 10 days following sutureremoval the collagen has
begun to cross-link.The wound is now able to tolerateearly controlled motion with
little risk ofdisruption (Figure 19-5).19As the woundheals it will contract along
its length andwidth and become inverted due to colla-gen and fibroblast
maturation.Initialmanagement is aimed at producing aslightly everted wound edge.The
woundcontinues to remodel up to a year follow-ing injury but never regains greater
than80% ofthe strength ofintact skin.Tissue adhesives are gaining in popu-
larity.Some studies have suggested similarcosmetic outcomes in wounds treated
withoctylcyanoacrylate when compared tostandard wound closure techniques
fornon�crush-induced lacerations treated lessthan 6 hours after injury.20�22Closure
oflacerations with octylcyanoacrylate isfaster than standard wound closure meth-
ods.However,its use should be avoided incomplex lacerations involving the
face,where there are esthetic concerns.Suture materials and different
surgicaltechniques do not show substantial differ-ences in relation to
outcome.Generalcharacteristics ofthe patient (ie,sex andage) and ofthe wound
(ie,length and site)seem to be important predictors ofadversetissue
reaction.23,24Suboptimal appear-ance is associated with wounds that
areinfected,wide,incompletely approximat-ed,or have sustained a crush
injury.Thetotal number ofbacteria is more impor-tant that the species ofbacteria
contami-nating a wound.Greater than 105aerobicorganisms per gram oftissue are
neededfor contamination,and crush-typewounds are 100 times more susceptible
toinfection.25Delayed primary closure may be neces-sary in some instances.Patients
who maybenefit from a delayed procedure includethose with extensive facial edema,a
subcu-taneous hematoma,or those with woundsthat are severely contused and
containdevitalized tissue.Secondary revision pro-cedures are usually undertaken
monthslater to allow for scar maturation.Clinical examination and radiographsare
used to diagnose fractures ofthe face.Facial fractures are ideally treated prior
tosoft tissue repair.Ifrepair ofthe facialbones is delayed,it is optimal to close
thelacerations initially.The wounds can bereentered and revised ifneeded to
accessthe fracture site.Types ofInjuriesAbrasionsShear forces that remove a
superficial layerofskin cause abrasions.The wound shouldbe gently cleansed with a
mild soap solu-tion and irrigated with normal saline.These superficial injuries
usually heal withlocal wound care.It is important to deter-mine whether foreign
bodies have beenembedded in the wound.Failure to removeall foreign material can
lead to permanent�tattooing�ofthe soft tissue.After thewound is cleansed the
abrasion is coveredwith a thin layer oftopical antibiotic oint-ment to minimize
desiccation and sec-ondary crusting ofthe wound.Reepithelialization without
significantscarring is complete in 7 to 10 days iftheepidermal pegs have not been
completelyremoved.Ifthe laceration significantlyextends into the reticular dermal
layer,sig-nificant scarring is likely.ContusionsContusions are caused by blunt
traumathat causes edema and hematoma forma-tion in the subcutaneous tissues.The
asso-ciated soft tissue swelling and ecchymosiscan be extensive.Small hematomas
usuallyresolve without treatment;hypopigmenta-tion or hyperpigmentation ofthe
involvedtissue can occur,but is rarely permanent.Large hematomas should be drained
toprevent permanent pigmentary changesand secondary subcutaneous
atrophy.LacerationsLacerations are caused by sharp injuries tothe soft tissue
(Figure 19-6).Lacerationscan have sharp,contused,ragged,or stel-late margins.The
depth ofpenetrationshould be carefully explored in the acute
Soft Tissue Injuries361setting.Closure is performed using a lay-ered
technique.Ifthe margins are beveledor ragged they should be conservativelyexcised
to provide perpendicular skinedges to prevent excessive scar formation.Rarely is
there an indication for changingthe direction ofthe wound margins by Z-plasty at
the time ofprimary woundrepair.Flap-like lacerations occur when acomponent ofthe
soft tissue has been ele-vated secondary to trauma.Eliminatingdead space by layered
closure and pressuredressings is especially important in
these�trapdoor�injuries.Avulsive InjuresAvulsive injures are characterized by
theloss ofsegments ofsoft tissue.Undermin-ing the adjacent tissue,followed by
prima-ry closure,can close small areas.When pri-mary closure is not possible,other
optionsare considered.These include local flaps orInjuryCoagulation
ofplateletsInflammationGranulocytesCollagen
lysisEpitheliumFibroblastContractionProcollagenCollagen fibrilCollagen
fiberD�bridementResistance toinfectionProteoglycansynthesisNeovascular
growthRemodelingHealed woundFIGURE19-5Stages ofwound healing.
362Part 4: Maxillofacial Traumaallowing the wound to heal by secondaryintention
followed by delayed soft tissuetechniques.Ifa significant amount ofsofttissue is
missing,then a skin graft,localflaps,or free-tissue transfer may be neces-sary
(Figure 19-7).Animal and Human BitesDog bites are most common in children andthe
midface is frequently involved.26,27Canines can generate 200 to 450 psi
whenbiting,and examination for fractures shouldbe performed.28Management
ofbiteinjuries involves liberal amounts ofirriga-tion and meticulous primary
closure.29Wound irrigation and d�bridement areimportant in reducing
infection.Animal and human bites are mostoften polymicrobial,containing aerobicand
anaerobic organisms.Dog bites areoften open and lend themselves to vigor-ous
irrigation and d�bridement.Catshave a large quantity ofbacteria in theirmouth,with
the most frequent andimportant pathogen being Pasteurellamultocida.30Cat bites are
associated witha twofold higher risk ofinfection than themore common dog bite
wounds.Becausetheir bites usually cause puncturewounds,they are difficult to
clean.Hav-ing the patient follow up 24 to 48 hoursafter the initiation oftherapy
allows thesurgeon to monitor the wound for anysigns ofinfection.Antibiotic
prophylaxis for animal bitescontinues to be debated with few goodprospective
studies available.26,31Amoxicillin-clavulanate is the current drug ofchoice forbite
wounds.Antibiotic prophylaxis shouldbe directed at Pasteurella multocidafor infec-
tions presenting within 24 hours ofinjury.For wounds that present after 24 hours
ofinjury,Streptococcus and Staphylococcusspecies are more common,and
antibioticprophylaxis with a penicillinase-resistantantibiotic should be
chosen.32Immediate closure ofbite injuries issafe,even with old injuries.33There
isapproximately a 6% rate ofinfection whenbite wounds are sutured primarily in
lacera-tions where there are cosmetic concerns.34Extensive animal bite wounds
involving theface should be treated according to the crite-ria ofesthetic
reconstructive surgery.Rabiesprophylaxis should be given for bite woundsthat
occurred from an unprovoked domes-tic dog or cat that exhibits bizarre behavioror
from an attack by a wild animal such as araccoon,skunk,bat,fox,or
coyote.35FIGURE19-6A,Patient with multiple lacerations.B,Closure
oflacerations.ABFIGURE19-7A,Patient with avulsive injuries including the upper and
lower eyelids.B,Elevation ofmultiple advancement and rotation flaps to gain
coverage.C,Securing the flaps into position.D,Closure oflacerations and flaps.ABCD
Soft Tissue Injuries363Gunshot Wounds to the FaceGunshot wounds require careful
attentionand evaluation for associated facial frac-tures.Both entry and exit wounds
should beevaluated.Exit wounds often producemarked tissue destruction and require
acuted�bridement.Regional flaps can be useful intreating facial soft tissue defects
caused bygunshot wounds (Figure 19-8).8Ballistic facial injuries are grouped
byetiology:gunshot,shotgun,and high-energy avulsive injuries.36Over the past
20years advances in imaging and the intro-duction ofcraniofacial approaches
withrigid fixation have led to an evolution oftreating facial injuries.The esthetic
andfunctional results offacial injury areimproved dramatically by the combina-tion
ofa definitive open reduction ofbonewith early replacement ofsoft tissue intoits
primary position.Immediate definitivereconstructions with rigid fixation
ofthefacial fractures and closure ofthe lacera-tions are recommended.Standard inci-
sions often need to be modified because ofthe soft tissue wounds.Regional
ConsiderationsCertain anatomic areas deserve special con-sideration.Reestablishment
ofanatomiczones with proper orientation is critical inachieving optimal esthetic
results.Scalp and ForeheadScalp wounds can occasionally cause alarge amount ofblood
loss due to the richvascular supply in this region and theinelasticity ofthe scalp
preventing con-traction and closure ofthe vessels.The lay-ers ofthe scalp (SCALP)
include the skin,subcutaneous tissue,aponeurosis layer,loose subepicranial
space,and pericraniallayer.In patients sustaining scalp injuries itis important to
evaluate for associatedintracranial injuries.Careful inspectionshould be performed
to look for evidenceofskull fractures.Because the scalp has anexcellent blood
supply in the subcuta-neous tissues as well as the pericranial lay-ers,avulsed
tissue,skin grafts,and variousflaps have a high rate ofsurvival.Hollan-der and
colleagues found no significantdifference in rate ofinfection in scalp lac-erations
that were irrigated compared tothose that were not.37In avulsive defects in which
the peri-cranium is intact and primary closure isnot possible,a split-thickness
skin graftcan be used.A secondary reconstructiveprocedure involving various
rotationaland advancement flaps or tissue expansioncan be undertaken after healing
ofthedefect.38Ifthe cranial bone is exposedwith large avulsive defects,then
variousflap procedures are indicated primarily.Reconstruction ofthe eyebrow is dif-
ficult secondarily,and efforts to repairlacerations primarily without distortionare
important.Eyebrows should never beshaved,as regrowth ofthe hair is unpre-
dictable.Closure oflacerations shouldattempt to salvage as much tissue as pos-
sible.Care should be taken to avoid dam-age to the remaining hair
follicles.Scarscan be removed 6 to 12 months later withFIGURE19-8A,Patient who
sustained a shotgun wound with avulsion oftissue.B,Preoperativeradiograph showing
associated comminuted facial fractures.C,Reapproximation ofthe bone and
softtissue.D,Postoperative radiograph showing the reduction ofmultiple facial
fractures.ABCD
364Part 4: Maxillofacial Traumaincisions made parallel to the hair folli-cles to
avoid injury.Eyelid and Nasolacrimal ApparatusA thorough ophthalmologic
examinationis important to assess for injuries to theglobe and to evaluate and
document visu-al acuity.Closure oflacerations involvingthe eyelids is done in a
layered fashion(Figure 19-9).Care should be taken to pre-cisely reapproximate the
eyelid marginsand the tarsus (Figure 19-10).The con-junctiva and tarsus are closed
withresorbable sutures with the knot buried toavoid irritating the cornea.The
orbicularmuscle is then closed followed by closureofthe skin.Injuries involving the
uppereyelid may include detachment ofthe lev-ator aponeurosis and M�ller�s
musclefrom the tarsal plate.The muscles shouldbe identified and reattached to the
tarsalplate in order to prevent ptosis and restorelevator function.The lacrimal
gland produces tears,which flow across the cornea and draininto canaliculi via the
puncta ofthe upperand lower eyelid margins (Figure 19-11).From the canaliculi the
tears enter thenasolacrimal duct and drain into the infe-rior meatus ofthe nose.Any
lacerationsthat involve the medial third ofthe eyelidshould be carefully inspected
for damageto the canaliculus.39Repair is accom-plished by introducing a lacrimal
ductprobe into the puncta and into the wound(Figure 19-12).The ends ofthe
laceratedduct are identified and approximated overa polymeric silicone tube
(Crawford tube).The tube is left in place for 8 to 12 weeks.Ifonly one canaliculus
is intact and func-tioning,the patient most likely will haveadequate
drainage.40Ifthe patient exhibitschronic epiphora postoperatively,then
adacryocystorhinostomy is indicated.Avulsive injuries to the eyelids aretreated
with skin grafts and/or local flaps.Defects ofup to 25% ofthe eyelid lengthcan be
closed primarily.Skin grafts har-vested from the opposite eyelid provideexcellent
texture and color match.NoseThe nose occupies a prominent positionon the face and
is often injured.Injuries ofthe internal nose should be evaluatedusing a nasal
speculum.The septumshould be evaluated for the presence ofahematoma,which appears
as a bluish ele-vation ofthe mucosa.Hematomas involv-ing the nasal septum should be
evacuatedwith a small incision or needle aspiration.Nasal packing or polymeric
silicone nasalsplints can be placed to prevent recurrenceofthe hematomas and are
removed in 7 to10 days.A running 4-0 chromic gut mat-tress suture placed in and
through the sep-tum can prevent recurrence.Untreatedhematomas can lead to infection
andnecrosis ofthe cartilage,which may causecollapse ofthe septum and a
resultant�saddle nose.�FIGURE19-9Surgical repair ofthe eyelid.A,Excision ofouter
lamina on one side and inner lamina on the other.B,After excision.C,Closure.Inner
sutures areburied to avoid suture material irritating the conjunctiva.ABCFIGURE19-
10A,Pentagonal resection ofthelower lid allows straight closure ofthe
tarsalplate.B,Closure is made with no suture materi-al through the conjunctiva.AB
Soft Tissue Injuries365There is an excellent blood supply tothe nose.Lacerations
ofthe external noseshould be closed with 6-0 nonabsorbablesutures.Key sutures
should be placed toreapproximate anatomic landmarks toensure proper
orientation,especiallyaround the nasal rim.Bone,cartilage,and/or skin grafts may be
required toreconstruct avulsive defects ofthe nose.Skin grafts harvested from the
periauricularregions provide excellent color and texturematch.41Local flaps may be
required torestore missing tissue (Figure 19-13).EarInjuries involving the external
ear shouldalert one to the possibility ofother injuries.An otoscopic examination
ofthe externalauditory canal and tympanic membranecombined with a hearing
assessmentshould be performed prior to treatment.Injuries to the auricle include
ecchymosis,abrasion,laceration,hematoma,and par-tial or total avulsion.Hematomas
involving the ear usuallyoccur when the ear sustains a glancingblow.These should be
drained with aneedle or incision.An incision is oftenpreferable to simple
aspiration becausethere is less ofa chance ofreaccumula-tion ofthe
hematoma.42Evacuation ofthe hematoma prevents fibrosis anddevelopment ofa
�cauliflower ear�defor-mity.A bolster dressing should be placedto prevent
recurrence ofthe hematoma.Astent can also be fabricated from poly-siloxane
impression material and kept inplace for 7 days.43The ear has a very good vascular
sup-ply and can maintain tissue on a smallpedicle.Injuries involving the
cartilageoften do not require sutures.Ifsuturesare required a minimal amount are
usedto avoid devitalizing the region ofcarti-lage (Figure 19-14).Avulsive injuries
ofthe ear can involve a portion ofthe ear orthe entire ear (Figure 19-
15).Iftheavulsed segment is 1 cm or less,it can bereattached and allowed to
revascularize.44Lacrimal canaliculi(superior and inferior)Medial canthusLacrimal
sacDrainage beneathinterior turbinateFIGURE19-11Nasolacrimal system
anatomy.FIGURE19-12A,Lacrimal probe identifies the disrupted canaliculi.B,A
polymeric silicone tube is cannulated through the canaliculi.AB
366Part 4: Maxillofacial TraumaFor larger avulsive injuries the ear shouldbe
examined for vessels for the possibilityofmicrovascular reattachment.A
morepredictable method is to use the �pocketprinciple�described by Mladick and col-
leagues (Figure 19-16).45The detachedear is dermabraded to remove the super-ficial
dermis and reattached to the stump.It is then buried underneath a skin flapelevated
in the posterior auricular regionto provide vascular supply to the reat-tached
ear.Approximately 2 to 3 weekslater the revascularized ear is uncoveredand allowed
to reepithelialize.Ifsalvage ofthe ear is not possibleother alternatives include
staged recon-struction with rib cartilage,skin flaps,orsilicone implants.The
introduction ofosseointegrated implants has made pros-thetic reconstruction an
appealing treat-ment option (Figure 19-17).LipThe lip anatomy involves a transition
ofmucosal tissue to skin.Scars that affectthe orbicularis oris may result in func-
tional difficulties.Nerve blocks are help-ful in wounds involving the lip to
preventdistortion caused from injecting directlyinto the wound.A single suture
should beplaced initially to reapproximate the ver-milion border exactly.Deep
tissues areclosed in layers,followed by closure ofthemucosa with 4-0 chromic and
skin clo-sure with 6-0 nylon suture.Avulsive defects ofthe lips requirespecial
attention.Up to one-fourth ofthelip can be closed primarily with accept-able
functional and esthetic results.Injuries that involve a greater amount oftissue
loss can be reconstructed with avariety offlaps such as Abbe-Estlander
orKarapandzic (Figure 19-18).NeckSuccessful management ofpenetratinginjuries ofthe
neck depends on a clearunderstanding ofthe anatomy oftheregion.Injuries can involve
deep structuresFIGURE19-13A,Nasal tip defect resulting from a bite.B,Elevation and
advancement oflocal internalnasal flaps to provide mucosal coverage.C,Placement
ofcartilage and bone grafts to reconstruct theinternal anatomy ofthe nose.D,The
pedicled flap is sutured into place.The flap is divided 3 weeks later.ABCDFIGURE19-
14A,Auricle injury with lacerations involving the cartilage.B,Postoperative
appearance.AB
Soft Tissue Injuries367affecting the vascular,respiratory,diges-
tive,neurologic,endocrine,and skeletalsystems.46The neck is divided into
threeanatomic zones.47Zone I extends from thelevel ofthe clavicles and sternal
notch tothe cricoid cartilage.Zone II is from thelevel ofthe cricoid cartilage to
the angle ofthe mandible.It is the most surgicallyaccessible and is the easiest to
evaluateintraoperatively without the aid ofpreoper-ative diagnostic testing.Zone
III extendsfrom the angle ofthe mandible to the base ofthe skull.There is
controversy regarding which pen-etrating neck wounds require
exploration.46�50Preauricular flapDenuded areaPostauricular flapWedgedefectStar
defectAfterclosureBurow's trianglesand advancementof helical rimAfter
closureAfterclosureFIGURE19-15A,Conversion ofa defect to a wedge.B,The use
ofBurow�s triangles.C,Conversion ofa defect to a star.ABC
368Part 4: Maxillofacial TraumaSerial physical examinations alone havebeen shown to
be effective.In cases whereserial physical examinations are not possi-ble,mandatory
exploration ofneck woundsmay be more beneficial.There should be ahigh index
ofsuspicion for esophagealinjuries because complications can be dev-astating
ifrepair is delayed.Primary repairis most often indicated in tracheal and vas-cular
injuries.Postoperative Wound CareCareful postoperative care and follow-upare
important to optimize results.Wounds should be monitored closely todetermine
whether early intervention isindicated to minimize scar contractureor hypertrophic
scarring.Local flaps andgrafts may be indicated secondarily.Local injection
ofsteroids provides anFIGURE19-17A,Osseointegrated implantsare placed in the area
ofthe defect.B,The pros-thesis secured in place with magnets.BFIGURE19-16A,Avulsed
ear.B,The ear is thoroughly dermabrad-ed to remove the superficial layer ofthe
dermis.C,Reimplantation oftheear.D,A posterior auricular �pock-et�is created.E,The
ear is buriedbeneath a skin flap and allowed torevascularize for 3 weeks prior
touncovering.ABCDEA
Soft Tissue Injuries369adjunct in the management ofspecifictypes ofinjuries.Facial
scars continue tomature over a period of12 to 18 months.A recent study found no
difference inoutcome ofsurgical scars treated withpulsed carbon dioxide laser when
com-pared with dermabrasion.51Keeping a wound clean and scab freeallows for more
rapid reepithelialization.52Epithelial cells survive and migrate betterin a moist
environment.Antibiotic oint-ment can enhance this migration.It is
notepithelialization that provides strength tothe wound but rather the collagen
fiberssupporting the surface.Rebuilding offibers takes time,and suturing a
woundsplints the skin together until new connec-tive tissue is built.Cleaning daily
with dilute hydrogenperoxide and dressing with antibiotic oint-ment is
standard.Patients should avoidsun exposure for the first 6 months afterthe injury
to prevent hyperpigmentationofthe areas.SummarySoft tissue injuries involving the
face canbe devastating to the patient.Primaryrepair ofthese wounds is almost
alwaysadvantageous over delayed secondaryprocedures.The primary goals oftreat-ment
are to restore patients to their pre-operative state offunction and to achievean
esthetic result.References1.Hollander JE,Singer AJ,Valentine S,et al.Wound
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closed under tensionwith PGA (Dexon) and polydioxanne(PDS).Br J Plast Surg
1989;687�9118.Thomas DW,O�Neill ID,Harding KG,et al.Cuta-neous wound healing:a
current perspective.JOral Maxillofac Surg 1995;53:442�7.19.Key SJ,Thomas
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1995;33(2):76�85.20.Singer AJ,Hollander JE,Valentine SM,et
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vsstandard wound closure techniques for lac-eration repair.Stony Brook Octylcyano-
acrylate Study Group.Acad Emerg Med1998;5:94�9.21.Singer AJ,Quinn JV,Clark RE,et
al.Closure oflacerations and incisions with octylcyano-acrylate:a multicenter
randomized con-trolled trial.Surgery 2002;131:270�6.22.Singer AJ,Quinn JV,Thode HC
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repair.Plast ReconstrSurg 2002;110:429�35.23.Gabrielli F,Potenza C,Puddu P,et
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wound dehis-cence among plastic surgery outpatients.Plast Reconstr Surg
2001;107:38�45.FIGURE19-18A,Avulsive lip resulting from a dog bite.The lower lip
flap is outlined.B,The pedicled Abbe flap is sutured into place and divided 3
weekslater.C,After division ofthe flap.ABC
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factors for infection in patients withtraumatic lacerations.Acad Emerg
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bite injuriesofthe face:experience with 94 patients.JOral Maxillofac Surg
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antimicrobial therapy.Vol32.Hyde Park (VT):Antimicrobial Thera-
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wounds:a controlled study.Ann Emerg Med 1980;9:410�4.33.Donkor P,Bankas DO.A study
ofprimary clo-sure ofhuman bite injuries to the face.JOral Maxillofac Surg
1997;55:479�81.34.Chen E,Hornig S,Shepherd SM,et al.Primaryclosure ofmammalian
bites.Acad EmergMed 2000;7:157�61.35.Krebs JW,Strine TW,Childs JE.Rabies surveil-
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CHAPTER 20Rigid versus Nonrigid FixationEdward Ellis III,DDS,MSInternal
fixationsimply implies the place-ment ofwires,screws,plates,rods,pins,and other
hardware directly to the bonestohelp stabilize a fracture.Internal fixationcan be
rigidor nonrigiddepending on thenature ofthe fracture,and the
type,strength,size,and location ofthe hard-ware placed.Since various degrees
andmany types ofnonrigidfixation exist,it isuseful to first define rigidinternal
fixa-tion.By default any technique that doesnot satisfy this definition can then be
con-sidered nonrigid.Rigid Internal FixationThe term rigid internal fixationhas
manydefinitions.For instance,one definition is�any form ofbone fixation in which
other-wise deforming biomechanical forces areeither countered or used to advantage
tostabilize the fracture fragments and to per-mit loading ofthe bone so far as to
permitactive motion.�1This definition,althoughadmittedly long and perhaps
confusing,encompasses the essence ofthe techniqueas practiced today and includes
clues tothe methods ofapplying the appropriatehardware.A more basic definition
whichincludes the same objectives is �any formoffixation applied directly to the
boneswhich is strong enough to prevent inter-fragmentary motion across the
fracturewhen actively using the skeletal struc-ture.�2Most ofthe differences in
techniqueare in the application ofthe fixation.Inherent in these definitions is the
prereq-uisite for surgical exposure to anatomical-ly align the fragments (open
reduction)and secure the fixation hardware.To rigid-ly stabilize fractures,an
operative proce-dure is necessary.Examples ofrigid fixation in themandible are the
use oftwo lag screws orbone plates across a fracture,the use ofareconstruction bone
plate with at leastthree screws on each side ofthe fracture,and the use ofa large
compression plateacross a fracture (Figure 20-1).Properlyapplied,these fixation
schemes are ofsuf-ficient rigidity to prevent interfragmen-tary mobility during the
healing period.An inseparable corollary to the pre-vention ofinterfragmentary
mobility byrigid fixation is a peculiar type ofbonehealing where no callus
forms.The bonesinstead go on to heal by a process ofhaver-sian
remodeling.Histologically,osteoclastscross the fracture gap and are followed
byblood vessels and osteoblasts (Figure 20-2).New bone is laid down by
theosteoblasts,forming osteons which crossthe gap and impart microscopic points
ofbony union to the fracture.3A remodelingphase then converts the entire area to
mor-phologically normal bone.This type ofbone healing is termed primaryor
directbone union,and it requires absoluteimmobilization between the osseous frag-
ments,that is,rigidfixation,and minimaldistance (gap) between them.Nonrigid
Internal FixationAny form ofbone fixation that is notstrong (rigid) enough to
prevent inter-fragmentary motion across the fracturewhen actively using the
skeletal structureis considered nonrigid.The basic differ-ence between rigid and
nonrigid fixationcenters on interfragmentary mobility.Ifthere is mobility ofthe
osseous frag-ments during active use ofthe skeletalstructure following application
ofinter-nal fixation devices,internal fixation isnonrigid.An example ofnonrigid
fixa-tion is a transosseous wire placed acrossa mandibular fracture.The wire can
onlyprovide stability by virtue ofits (limited)ability to prevent spreading ofthe
gap,but by itself,the wire cannot neutralizetorsion and/or shear
forces.Additionalfixation measures then become neces-sary,such as the use
ofmaxillomandibu-lar fixation (MMF) (Figure 20-3).However,various forms
ofnonrigidfixation are recognized,and there is acontinuum between rigid fixation
andno fixation at all.There are some formsofnonrigid fixation that are strongenough
to allow active use ofthe skele-ton during the healing phase but not ofsufficient
strength to prevent interfrag-mentary mobility.These types offixa-tion have been
called functionally stablefixation,indicating that there is adequatestability to
allow function even though
372Part 4: Maxillofacial TraumaTension band plateStabilization plateFIGURE20-
1Examples ofrigidfixation schemes for mandibular fracture.A,A large compression
plate incombination with an arch bar for a symphysis fracture (two-point
fixation).B,Two lag screws insertedacross a symphysis fracture (two-point
fixation).C,Two bone plates for a symphysis fracture (two-pointfixation).These may
or may not be compression plates.Typically the larger one at the inferior border is
acompression plate and the one located more superiorly is not.D,Two bone plates for
a mandibular bodyfracture (two-point fixation).These may or may not be compression
plates.Typically the larger one at theinferior border is a compression plate and
the one located more superiorly is not.E,A lag screw placed atthe inferior border
combined with a smaller bone plate located more superiorly (may or may not be com-
pression plate; two-point fixation).The use ofan arch bar offers a third point
offixation.F,A large com-pression plate placed at the inferior border ofa body
fracture combined with an arch bar (two-point fixa-tion).G,A compression plate at
the inferior border ofan angle fracture combined with a noncompressionplate at the
superior border (two-point fixation).The upper plate could also be a compression
plate.H,Twononcompression miniplates applied to an angle fracture (two-point
fixation).I,Reconstruction bone plateapplied to the inferior border ofan angle
fracture (one-point fixation).Rigidity is provided by virtue ofthethickness
(strength) ofthe plate and the use ofat least three bone screws on each side ofthe
fracture.ABCDEFGHI
Rigid versus Nonrigid Fixation373there is not adequate stability to allowdirect
bone union.Many ofthe fixationschemes that are being used clinically inthe
maxillofacial area are not truly rigidfixation,but functionally
stablefixation.Functionally stable fixation in maxillo-facial surgery is a spectrum
that variesfrom one region ofthe facial skeleton toanother,from one fracture to the
next,and from one patient to the next.Exam-ples offunctionally stable
fixationinclude the single miniplate technique oftreating mandibular angle or body
frac-tures (Figure 20-4).4In spite oftheinterfragmentary motion that
thesetechniques may permit,the clinical out-comes are excellent,indicating
thatabsolute immobility ofthe fragments isunnecessary for satisfactory recovery.In
the late 1950s the Swiss Associationfor the Study ofInternal Fixation(AO/ASIF)
promulgated four biomechan-ical principles in fracture management5:1.Accurate
anatomic reduction2.Atraumatic operative technique pre-serving the vitality ofbone
and softtissues3.Rigid internal fixation that produces amechanically stable
skeletal unit4.Avoidance ofsoft tissue damage and�fracture disease�by allowing
early,active,pain-free mobilization oftheskeletal unit These principles had as
their aim therigid fixation offractures.In recognitionofthe finding that
functionally stable fixa-tion is very effective clinically,in 1994,theAO/ASIF
changed its third biomechanicalprinciple from rigid internal fixation
tofunctionally stable fixation.Bone healing under the condition ofmobility between
the osseous fragmentsis termed indirector secondarybone heal-ing.In such
circumstances there is depo-sition ofperiosteal callus,resorption ofthe fragment
ends,and tissue differentia-tion through various stages from fibrousto osseous
(Figure 20-5).Bone cannotFIGURE20-2Types ofprimary bone healing.A,When there is
minimal distance between the frag-ments,and the fragments are rigidly
immobilized,osteoclasts from one fragment �drill�their way intothe fracture gap and
into the opposite fragment.Behind them come fibrovascular tissue
andosteoblasts,which begin to lay down new bone.With maturation these become new
haversian canals.This process is usually called contact healing.B,When a small gap
exists between the rigidly immo-bilized fragments,lamellar bone is laid down within
the fracture gap.Then the process described above(A)occurs,with new haversian
canals crossing the gap.This process is sometimes called gap healing.With either
ofthese types ofprimary bone healing,no external callus would be found along the
out-side ofthe fragments ifthey were rigidly immobilized.Adapted from Schenk
R,Willenegger,H.3ABFIGURE20-3Internal wire fixation ofsymph-ysis and left angle
fractures.Note that these wiresare not sufficiently stable to allow use
ofthemandible during the healing process,so maxillo-mandibular fixation is applied
for at least 5weeks (in an adult) to maintain stability.FIGURE20-4The Champy method
oftreatingangle fractures using a single,noncompressionminiplate attached with 2.0
mm monocorticalscrews.Because this plate is placed in the mostbiomechanically
advantageous area for thisregion (superior border),a small plate can neu-tralize
the functional forces and permit active useofthe mandible during the healing
process.How-ever,although this technique is functionally sta-ble,interfragmentary
motion probably occurs tosome extent during function.It is therefore
notrigidfixation.Adapted from Champy M et al.4
374Part 4: Maxillofacial Traumaform across a mobile gap.The formationofa callus can
be thought ofas nature�sinternal fixation,providing stability tothe osseous
fragments so that boneunion can proceed.The appearance ofacallus on a radiograph
indicates thatthere is mobility between the fragments,requiring the deposition
ofthe callus to�immobilize�the fragments to allowossification to proceed.Selection
ofFixation Schemes:How Much Fixation (Rigidity) is Enough?With that prelude into
definitions offixa-tion types,the remainder ofthis chapterwill discuss some ofthe
variables in theselection offixation schemes for fracturesofthe mandible.Because
the mandible isthe only bone in the face that is mobile andsubjected to deforming
forces from power-ful muscles,not much will be said aboutthe
midface.However,whether in traumaor orthognathic surgery,the type offixa-tion that
is required in the midface is func-tionally stable �adaptation�osteosynthesis.The
bones are simply placed into a certainposition and the fixation devices areapplied
to maintain that position.Onewould therefore not use compressionplates in the
midface (with the possibleexception ofthe frontozygomatic suturearea) because
oftheir ability to change thespatial relationship ofthe bones by apply-ing an
active force across the fracture orosteotomy.However,bone plates ofsuffi-cient
strength must be applied across afracture or osteotomy gaps to allow
thetransmission offunctional forces acrossthe gap without an alteration in the
occlu-sion.The application ofvery thin boneplating systems seems to be able to
providesuch stability in most fractures orosteotomies when placed in multiple loca-
tions.For instance,at the Le Fort I level,four thin bone plates (1.3 or 1.5 mm sys-
tems) provide functionally stable fixationunder most
circumstances.However,whenthere has been a large movement ofthemaxilla such as in a
maxillary advancementor inferior repositioning procedure,thick-er and stronger bone
plates would usuallybe required (Figure 20-6).Biomechanic Studies versus Clinical
OutcomesWhen selecting a fixation scheme for agiven fracture,one has to consider
manythings,such as the size and number offix-FIGURE20-5Secondary or indirect bone
healing.A,After a fracture occurs,a subperiosteal hematoma isformed followed by
initial invasion ofgranulation tissue.B,A thin rim ofbone forms under the
periosteumby membranous ossification.Hyaline cartilage is formed progressing toward
and eventually penetrating thefracture gap.C,The cartilage cells form
columns,increase in size,and narrow the intercellular matrix.Smallfingerlike
extensions ofvessels penetrate these columns.The cartilage is replaced with woven
bone.D,As theosseous matrix matures,remodelling and replacement ofwoven bone
continues until a lamellar pattern is pre-sent.Adapted from Muller ME et al.5ABCD
Rigid versus Nonrigid Fixation375ation devices,their location,the
surgicalapproach,and the amount ofsoft tissuedisruption necessary to expose the
frac-ture and place the fixation devices.Inchoosing the fixation scheme for the
frac-ture,one might intuitively feel that morerigid fixation is better than less
rigid fixa-tion.However,it is clear from the litera-ture on outcomes ofmandibular
fracturesthat the stability ofthe fracture constructis only one variable in
determining a suc-cessful outcome for the patient.Theresults from every study ever
performed inthe laboratory or in computer modelinghave shown that two bone plates
appliedto a fracture are more stable than one.6�8However,there has never been any
statisti-cally significant evidence from clinicalstudies that two plates perform
better thanone.In fact,the results ofmy own studiesfor fractures ofthe angle ofthe
mandibleshow that two plates perform much morepoorly than does one plate in that
loca-tion.9�13One must therefore be very care-ful in applying treatment recommenda-
tions from laboratory studies to thepatient.Fracture stability is only one fac-tor
in the treatment equation.There aremany others,such as maintenance ofblood
supply,that must also be consideredwhen determining treatment recommen-
dations.Load-Bearing versus Load-Sharing FixationThe most simplistic way to discuss
fixationschemes for fractures is to break themdown into those fixation devices that
areload-bearing and those that share theloads with the bone on each side
ofthefracture (load-sharing).Load-bearing fix-ation is a device that is
ofsufficientstrength and rigidity that it can bear theentire load applied to the
mandible duringfunctional activities.Injuries that requireload-bearing fixation are
comminutedfractures ofthe mandible,those fractureswhere there is very little bony
interfacebecause ofatrophy,or those injuries thathave resulted in a loss ofa
portion ofthemandible (defect fractures).In such casesthe fixation device must
bridge the area ofcomminution,minimal bone contact,orbone loss,and bear all ofthe
forces trans-mitted across the injured area that are gen-erated by the masticatory
system.Load-bearing fixation is sometimes calledbridging fixation because it
bridges areasofcomminution or bone loss.The mostcommonly used load-bearing device
is amandibular reconstruction bone plate(Figure 20-7).Such plates are
relativelylarge,thick,and stiff.They use screws thatare generally greater than 2.0
mm in diam-eter (most commonly 2.3 mm,2.4 mm,or2.7 mm).When secured to the
fragmentson each side ofthe injured area by a mini-mum ofthree bone
screws,reconstructionbone plates can provide temporary stabili-ty to the bone
fragments.The bone platesare not prosthetic devices and will usuallyfail in time
(several months to years later)by either loosening ofthe screws or frac-ture ofthe
plate,but can provide stabilityuntil the comminuted fragments haveconsolidated
and/or the missing bone hasbeen replaced with grafts.Load-sharing fixation is any
form ofinternal fixation that is ofinsufficient sta-bility to bear all ofthe
functional loadsapplied across the fracture by the mastica-tory system.Such a
fixation device(s)requires solid bony fragments on each sideofthe fracture that can
bear some ofthefunctional loads.Fractures that can be sta-bilized adequately with
load-sharing fixa-tion devices are simple linear fractures,and constitute the
majority ofmandibularfractures.Fixation devices that are consid-ered load-sharing
include the variety of2.0 mm miniplating systems that are avail-able from a number
ofmanufacturers.Examples ofload-sharing fixation forangle fractures are
demonstrated in Figure20-1A�H.Lag screw techniques are alsoload-sharing in that the
bone that is com-pressed is sharing the functional loadswith the screws.Simple
linear fracturescan also be treated by load-bearing fixa-FIGURE20-6Use offour bone
plates across theLe Fort I level ofa fracture.These plates can bequite thin (ie,1.3
or 1.5 mm) iffour are used.However,stronger plates (ie,2.0 mm) should beused where
bone interfaces are less favorable,orwhen the maxilla is placed into a position
that isresisted by soft tissue forces (ie,maxillaryadvancement or inferior
repositioning).FIGURE20-7Example ofload-bearing fixation.The application ofa large
reconstruction boneplate across an area ofcomminution or bone lossallows active use
ofthe mandible.The plate bearsall ofthe loads applied across the
fracture.Ittherefore is unnecessary for the intervening bonyfragments to share any
ofthe load.
376Part 4: Maxillofacial Traumation.Comminuted or defect fractures,orthose where a
minimum ofbone contact ispresent,cannot be treated by load-sharingfixation because
there is insufficient bonestock adjacent to the fracture to resist dis-placement by
functional forces.Regional Dynamic ForcesDifferent regions ofthe mandible under-go
different magnitudes and direction offorces.In simplistic terms fractures ofthe
angle under most functional situa-tions tend to �open�at the superior bor-der
(Figure 20-8Aand B).Therefore,theapplication offixation devices at thesuperior
border is more effective in pre-venting this separation offragmentsunder function
than applying them atthe inferior border (Figure 20-8CandD).There is little
tendency for isolatedfractures ofthe angle to have medial orlateral displacement
during function,sothe fixation requirement is mainly toprevent separation ofthe
superior bor-der.Relatively small plates can thereforeadequately control this
fracture.TheChampy miniplate technique functionsextremely well for this fracture
and con-sists ofa 2.0 mm miniplate applied withmonocortical screws along the
superiorborder (see Figure 20-4).4Because metal-lic plates have high tensile
strength,eventhin plates work adequately at the angleto prevent the tendency for a
gap to format the superior border under function.13Isolated fractures ofthe
mandibularbody behave similarly under function,witha tendency for a gap to form at
the superi-or surface,but the more anterior the frac-ture,the more tendency for
torquing ofthefragments to occur,causing mediolateralmisalignment ofthe inferior
border.Whilethe arch bar may provide sufficient resis-tance to the tendency for a
gap to formbetween the teeth under function,a plate---------------+++++++++++++
+Elevator muscle forcesTensionCompressionDepressor musclesand occlusal
forcesFIGURE20-8Functional forces acting across the intact mandibular angle or body
region (A) and after a fracture (B).Note that a gaptends to form at the superior
border ofa fractured mandibular angle secondary to muscle and occlusal forces.The
superior border istherefore called the zone oftension (separation),whereas the
inferior border is under compressive force during function (compressionzone).C,A
small bone plate applied along the zone oftension (separation) is very effective in
countering the forces ofmastication,andeffectively neutralizes the
forces,maintaining closure ofthe fracture gap.D,A small plate applied in the zone
ofcompression (inferiorborder) is very ineffective in neutralizing the muscle
forces,and a gap will easily form superiorly in the zone oftension.ABCD
Rigid versus Nonrigid Fixation377or lag screws somewhere else on the bodyofthe
mandible is necessary to prevent themediolateral displacement that accompa-nies the
torquing motion under function.For isolated body fractures,this can be arelatively
small plate,such as a 2.0 mmminiplate or even a single lag screw com-bined with a
solid arch bar (Figure 20-9).The directions offorces that are dis-tributed through
the anterior mandiblevary with the activity ofthe mandible.Thismeans that the
classical zones oftension onthe superior and compression on the infe-rior surfaces
ofthe mandible are notabsolute.7.8Instead,the anterior mandibleundergoes shearing
and torsional (twist-ing) forces during functional activities.4,14Application
offixation devices must there-fore take these factors into consideration.This is
why most surgeons advocate twopoints offixation in the symphysis:eithertwo bone
plates,two lag screws,or possiblyone plate or lag screw combined with anarch bar
(see Figure 20-1A�H).14One-Point versus Two-PointFixationMandibular fractures can
be treated by theapplication offixation devices at one placealong the fracture or
at more than onepoint,generally two.There is no doubt thatthe addition ofa second
point offixationprovides more stability to the fracture.However,to take mechanical
advantage ofmore than one point offixation,the fixationdevices should be placed as
far apart fromone another as possible.Because fixationdevices are applied to the
lateral surface ofthe mandible,the ability to use two-pointfixation requires that
there be sufficientheight ofbone so that the fixation devicescan be placed far
apart from one another.For instance,an atrophic mandibular frac-ture,where there is
a vertical height ofonly15 mm,would not gain much mechanicaladvantage from placing
two bone plates onthe lateral surface (Figure 20-10).In suchinstances a single
stronger bone plate shouldbe applied below the inferior alveolar canal(Figure 20-
11).For the majority offracturesin the dentulous mandibular body and sym-
physis,there is sufficient height ofbone toplace one load-sharing plate along the
infe-rior and one along the superior aspect ofthelateral cortex.However,the ability
to do sowill depend on the local anatomy.Ifonechooses to use two load-sharing bone
platesto provide rigid fixation,one must be cog-nizant ofthe position ofthe tooth
roots andthe inferior alveolar/mental nerves.Ifthereis insufficient room between
the roots oftheteeth and the inferior alveolar/mentalnerves,one might choose to use
a singlebone plate along the inferior border ratherthan to risk injury to the tooth
roots or infe-rior alveolar/mental nerves when placingthe second bone plate (see
Figure 20-1F).Depending on the size ofthe plate andwhether or not an arch bar will
also be usedto provide another point offixation,the fix-ation could be rigid or
functionally stable.FIGURE20-9Example ofa simple isolatedmandibular body fracture
treated by the applica-tion ofarch bars and a single 2.0 miniplate.LoadHt a LoadHt
b LoadHt b LoadHt a FIGURE20-10Biomechanical effectiveness ofdifferent constructs.A
and B demonstrate biomechanicaleffectiveness oftwo plates when placed at different
distances from one another.A,The load is applied to afracture construct where there
is a large fragment (Ht a) and a great separation between the two boneplates.This
is a very stable construct.B,The load is applied to a fracture construct where the
bone fragmentis small(Ht b) and there is little distance between the two bone
plates.This construct is much less stablethan the one in A because ofthe limited
space between the two plates,in spite ofthe fact that the same twobone plates are
applied.C andD demonstrate biomechanical effectiveness oftwo constructs when only
oneplate is applied.C,A single plate is applied to a construct with little vertical
height (Ht a).D,A single plateis applied to a construct with a greater vertical
height (Ht a).The construct with a greater vertical dimen-sion(D)is much more
stable because ofthe greater buttressing effect provided by the longer moment
armofthe increased vertical dimension ofbone.ABCD
378Part 4: Maxillofacial TraumaCompression versus Noncompression Plate
OsteosynthesisThere are many types ofbone plates thatare available for clinical
use.In their mostsimplistic forms plates are either compres-sion plates or
noncompression plates.Compression plates have the ability tocompress the fractured
bony margins,helping to bring them closer together,andimparting additional
stability by increas-ing the frictional interlocking betweenthem (Figure 20-
12).While these proper-ties might be advantageous,the applica-tion ofcompression by
a plate creates adynamic force that can work to one�s dis-advantage ifthe plate is
not perfectlyapplied.Compression plates are safest touse in fractures where there
is minimalobliquity,and where there are sound bonybuttresses on each side ofthe
fracture thatcan be compressed by the plate.One should only use compressionplates
ifone desires absolute rigidity acrossthe fracture.Ifmicromotion across thefracture
occurs,compression plateosteosynthesis will often fail by
becomingloose.Therefore,ifcompression plateosteosynthesis is desired,rigid
fixationmust also be desired.Ifthis means that twoplates are necessary to achieve
absoluterigidity,they should be used.Ifit meansthat a larger compression plate need
beapplied,then that should also be done.Locking Plate�Screw SystemsOver the past 10
years,there has been anintroduction oflocking plate�screw sys-tems into
maxillofacial surgery.Theseplates function as internal fixators,achiev-ing
stability by locking the screw to theplate.There are several potential advan-tages
to such fixation devices.Convention-al bone plate�screw systems require pre-cise
adaptation ofthe plate to theunderlying bone.Without this
intimatecontact,tightening ofthe screws will drawthe bone segments toward the
plate,resulting in alterations in the position ofthe osseous segments and the
occlusalrelationship.Locking plate�screw systemsoffer certain advantages over other
platesin this regard.The most significant advan-tage may be that it becomes
unnecessaryfor the plate to intimately contact theunderlying bone in all areas.As
the screwsare tightened they �lock�to the plate,thusstabilizing the segments
without the needto compress the bone to the plate (Figure20-13).This makes it
impossible for thescrew insertion to alter the reduction.Thistheoretical advantage
is certainly moreimportant when using large bone plates,such as reconstruction
plates,which canFIGURE20-11Use ofa single strong bone plate (reconstruction plate)
when the vertical height ofthemandible is small.A,Atrophic mandible fractured
through the body region.B,Reconstruction boneplate applied to the fracture to
provide rigid fixation.Even ifthere were room to place two smallerbone plates on
the lateral cortex,they would be so close to one another that their mechanical
effec-tiveness would be minimal.ABFIGURE20-12Compression plates help to minimize
the fracture gap and to impart stability by thefrictional interlock they induce.The
screw holes in at least one ofthe oval bone plate holes is/are
drilledeccentrically,that is,away from the fracture,so that as the screw(s) is/are
tightened (A),the V-shapedundersurface ofthe screw head contacts the plate and
forces the plate away from the fracture (B),imparting compression to the bone
fragments and closing the gap (C).ABC
Rigid versus Nonrigid Fixation379be very difficult to perfectly adapt to
thecontours ofthe bone.Another theoreticaladvantage to the use oflocking
boneplate�screw systems is that the screws areunlikely to loosen from the
bone.Thismeans that even ifa screw is inserted intoa fracture gap,loosening ofthe
screw willnot occur.The possible advantage to thisproperty ofa locking plate�screw
system isa decreased incidence ofinflammatorycomplications from loosening ofthe
hard-ware.It is known that loose hardwarepropagates an inflammatory response
andpromotes infection.For the hardware or alocking plate�screw system to
loosen,loosening ofa screw from the plate orloosening ofall ofthe screws from
theirbony insertions would have to occur.Bothofthese are unlikely.A third advantage
toa locking screw�plate system is that theamount ofstability provided across
thefracture gap is greater than when standardnonlocking screws are used.15,16While
the possible advantages to alocking plate�screw fixation system
aretheoretical,whether clinical results can beimproved is not clear from the
literature.However,given the potential advantagesthat locking plate�screw systems
provide,such systems should be considered when-ever noncompression plates are
chosenfor a fracture.Lag Screw FixationThe lag screw fixation technique consists
ofusing screws to compress fracture frag-ments without the use ofbone
plates.Toapply the lag screw technique,two soundbony cortices are required because
thistechnique shares the loads with the bone.The hole in the cortex under the head
ofthescrew is called the gliding hole.It is thesame diameter as the external
diameter ofthe screw threads,so the threads will notengage this cortex.The screw
threads on theterminal end ofthe screw engage the oppo-site cortex.By tightening
the screw a tensileforce is created within the screw that com-presses the bony
cortices together,tightlyreducing the fracture (Figure 20-14).As with using
compression boneplates,lag screw fixation is a techniquethat should only be used to
provideabsolute rigid fixation.Micromotionacross a fracture secured with lag
screwswill likely result in dissolution ofthe bonearound the screws,with loss
ofstability.Therefore,lag screws should only beselected when there is sufficient
boneavailable to place at least two screws intosound bone that can,in all
likelihood,cre-ate rigidity across the fracture.The use oflag screws has
severaladvantages over the use ofbone plates.Ituses less hardware when compared to
theuse ofplates thus making it more costeffective.When properly applied,lagscrews
are a very rigid method ofinternalfixation.Because there is no plate to bebent,the
insertion ofa lag screw is quick-er and easier,and the reduction moreaccurate than
when bone plates are used.One must understand completely that thelag screw
technique offixation is one thatrelies on compression ofbone fragments.Ifthe
intervening bone is unstable due tocomminution or is missing,compressingacross this
area will cause displacement ofthe bone fragments,overriding ofseg-ments,and/or
shortening ofthe fracturegap,resulting in problems with the occlu-sion.One should
always place the lagscrew in a direction that is perpendicularto the line
offracture to prevent overrid-ing and displacement during tightening ofthe screws
(Figure 20-15).Plate FatigueBone plates may break under function,resulting in
possible loss offixation,infec-tion,nonunion and/or malunion.Platesbreak for a
number ofreasons,but mostfracture in vivo because offatigue.Platesused in
maxillofacial surgery today areusually made oftitanium.Titanium is arelatively
biocompatible material and hasmaterial properties that are consideredadequate for
internal fixation when appro-priate plates are selected.One ofthe unde-sirable
properties oftitanium is its brittle-ness (or lack ofductility) when comparedto
bone.One only has to bend a miniplateback and forth a couple oftimes to seehow
readily it will fracture.Placement ofbone plates on areas ofthe mandible thatare
constantly and repeatedly deformedunder function can result in fatigue frac-ture
ofthe plates.Examples are 2.0 mmFIGURE20-13A locking plate�screw system.Note the
second set ofthreads just under the headofthe screw that will lock into receptacle
threadsinside the hole ofthe bone plate.FIGURE20-14Technique oflag screw place-
ment.A,The outer cortex is drilled to the exter-nal diameter ofthe screw
threads,and is coun-tersunk to receive the head ofthe screw.Theinner cortex is
drilled to the internal diameter ofthe screw.B,Screw tightening creates compres-
sion ofthe bony interfaces because the head ofthe screw compresses the outer cortex
against theinner cortex that is engaged by the screw threads.AB
380Part 4: Maxillofacial Traumaminiplates or 2.0 mm adaptation platesapplied to the
condylar process,or similarplates applied to the atrophic mandible(Figure 20-
16).The condylar process isconstantly undergoing mediolateral tiltingduring opening
and closing movements ofthe mandible.The atrophic mandible sim-ilarly undergoes
�wishboning�duringfunction (Figure 20-17).17The less theamount ofbone stock
present,the higherthe magnitude ofthese movements.Thus,atrophic mandibles undergo
much morewishboning than do large dentulousmandibles.Because ofthe small cross-sec-
tional area ofthe condylar process,thisarea ofthe mandible similarly flexes dur-ing
function.Bone plates applied to such areas ofthe fractured mandible have to be able
tonot only acutely withstand the deformingforces applied,but must also withstand
thechronically applied cyclic loading untilsuch time that the bone has healed.This
iswhy several authors have recommendedthicker,stronger 2.0 mm plates (mini-dynamic
compression plates) (Figure 20-18) or two2.0 mm miniplates for condylarprocess
fractures,and reconstruction boneplates for atrophic mandibular frac-
tures.18�21This problem with the atrophicmandible is the reason the AO/ASIF
hasrecommended,�The weaker the bone,thestronger the plate must be.�21Single versus
MultipleMandibular FracturesBecause ofthe shape ofthe mandible,frac-tures ofthe
mandible are often multiple.Most surveys show that just under 50% areisolated,the
same amount are doubly frac-tured,and a small percentage have morethan two
fractures.Fixation requirementsfor double (or multiple) fractures differfrom
isolated fractures.One can use lessrigid forms offixation on isolated
fractures,because the forces generated during func-tion are less complex than when
a second orthird fracture is present.For instance,thereis minimal tendency for
fractures ofthesymphysis,body,or angle to result in widen-ing ofthe mandible unless
fixation devicesare incorrectly applied.The application ofasingle 2.0 mm miniplate
along the lowerPerpendicular to long axis of bonePerpendicular to fractureFIGURE20-
15Improper (A) and proper (B) methods ofplacing lag screws.The screw should
alwaysbe drilled perpendicular to the line offracture to prevent sliding ofthe
fragments during tightening ofthe screws.ABFIGURE20-16A standard 2.0 mm miniplate
(A)and adaptation miniplates (B) (the 2.0 mm refers tothe size ofthe screw that
this plate accommodates,not the size ofthe plate).These plates have very
goodtensile strength,but readily fracture under cyclicloading because oftheir thin
cross section.BAFIGURE20-17Under function,the mandible�wishbones�in and
out.FIGURE20-18Example ofa stronger 2.0 mmbone plate than the miniplate shown in
Figure 20-16.The mini-dynamic compression plate shown inthis photograph has a
thicker cross-sectional areaand a broader strap between the holes.This plateis
useful for fractures ofthe mandibular condylarprocess and rarely fractures for that
application.
Rigid versus Nonrigid Fixation381border ofthe mandible combined with anarch bar is
usually adequate fixation for iso-lated simple linear fractures ofthe symph-ysis
and body regions (two-point fixation).Ifan arch bar is not used or the teeth are
notsound,one should use either a strongerplate at the inferior border or add
another2.0 mm miniplate more superiorly alongthe lateral cortex.The application ofa
single2.0 mm miniplate along the superior borderis also adequate fixation for most
isolatedsimple linear fractures ofthe angle region.4Lag screws can also be used
instead ofor inaddition to plates,where appropriate.When two fractures are present
there isa greater tendency for the segments to dis-place because ofthe bilateral
loss ofsupportthat occurs.Widening ofthe mandiblemust be prevented by applying
adequateinternal fixation to resist that tendency.With bilateral simple linear
fractures oneshould always consider using a more rigidform offixation on at least
one ofthe frac-tures.For instance,when an angle fractureis combined with a
contralateral body orsymphysis fracture,one should considertreating the body or
symphysis fracturewith either two 2.0 mm miniplates,or astronger bone plate at the
inferior border,aswell as using the arch bar as another pointoffixation (Figure 20-
19).The angle frac-ture can then be treated with a single supe-rior border 2.0 mm
miniplate.Similarly ifan angle fracture is combined with a con-tralateral condylar
process fracture,oneshould consider the application ofmorestable fixation at the
angle ifthe condylarprocess is going to be treated closed usingno MMF and
functional therapy (Figure20-20).In that case two 2.0 mm miniplates(or an
alternative rigid treatment) shouldbe considered.Ifthe condylar process weregoing
to undergo open reduction and inter-nal fixation,or ifseveral weeks ofMMFwere going
to be used,then the angle frac-ture could be treated with a single superiorborder
2.0 mm miniplate (functionally sta-ble but not rigid fixation).4The fracture
pattern that has the mosttendency for widening is the midsymphysisfracture combined
with condylar processfractures,especially when both condyles arefractured.In such
cases the musculatureattached to the lingual surface ofthemandible pulls the
mandible posteriorly,and because there is no posterior supportvia the
temporomandibular joints,the lat-eral mandibular fragments open like abook.Such
fractures must be carefullymanaged to first restore the mandibularwidth and then to
maintain it.A short thinbone plate,like a 2.0 mm miniplate,or eventwo 2.0 mm
miniplates,may not offer suffi-cient resistance to the tendency to widen(Figure 20-
21A).Ifone chooses to treat thecondylar process fracture(s) closed,verystable
fixation must be applied across thereduced mandibular symphysis to retainthe normal
width ofthe mandible.This canbe achieved by several techniques,but themost stable
is to either use a reconstructionplate applied across the symphysis (Figure20-
21B),or ifthe fracture is linear,twowell-placed lag screws (see Figure 20-1B).The
application oftwo thicker 2.0 mmbone plates (thicker than miniplates) wouldalso
suffice (see Figure 20-1C).Ifone choseto open the condylar process
fractures,thenthe symphysis fracture can be treated as anisolated symphysis
fracture,with whatevertechnique the surgeon usually
chooses.Nonrigid(functionallystable)RigidFIGURE20-19Possible fixation scheme for
right angle and left body frac-tures ofthe mandible.The more accessible body
fracture is treated with amore rigidform offixation (eg,a thicker bone plate at the
inferior borderor twominiplates).The angle fracture can then be treated with a
function-ally stable form offixation,which is easier to apply than would be a
rigidtechnique at the angle.The angle fracture is thus treated as ifit were an iso-
lated fracture,with a single 4-hole 2.0 mm miniplate.GapFIGURE20-20Demonstration
ofhow widening ofthe mandible can occurafter an angle fracture treated without
rigid fixation is combined with closedtreatment ofa contralateral condylar process
fracture.The single 4-hole 2.0 mm miniplate that works very well in this location
for isolated fracturesofthe mandibular angle may not be able to prevent the
tendency for widen-ing.With the loss ofthe articulation at the temporomandibular
joint on theright side,the entire right side ofthe mandible can also cause torquing
at theleft angle fracture under function,leading to displacement and malocclusion.
382Part 4: Maxillofacial TraumaSummaryWhile the number ofplating sets and fixa-tion
schemes are numerous,one can usuallytreat most fractures with very few instru-ment
sets.It is possible to treat the majorityoffractures ofthe mandible either with
lagscrews,2.0 mm miniplates,or reconstruc-tion bone plates.There are,however,frac-
tures where one may wish to use 2.0 mmscrews but thicker plates than
miniplates,forinstance,condylar process fractures or frac-tures ofthe atrophic
mandible.In thosecases one can use thicker and stronger boneplates that accommodate
2.0 mm screws.Forthese situations a locking 2.0 mm bone plat-ing set that has
plates ofvarying lengths andthicknesses allows one to choose the appro-priate bone
plate for almost any location.References1.Allg�wer M,Spiegel PG.Internal fixation
offractures:evolution ofconcepts.ClinOrthop 1979;138:26�9.2.Ellis E.Rigid skeletal
fixation offractures.JOral Maxillofac Surg 1993;51:163�73.3.Schenk R,Willenegger
H.Morphological find-ings in primary fracture healing.Symp BiolHung
1967;7:75.4.Champy M,Lodd� JP,Schmitt R,etal.Mandibular osteosynthesis by
miniaturescrewed plates via a buccal approach.JMaxillofac Surg 1978;6:14�9.5.M�ller
ME,Allg�wer M,Willenegger H.Man-ual ofinternal fixation.New York:Springer-
Verlag;1970.6.Choi BH,Kim KN,Kang HS.Clinical and invitro evaluation ofmandibular
angle frac-ture fixation with two-miniplate system.Oral Surg 1995;79:692�5.7.Kroon
FH,Mathisson M,Cordey JR,Rahn BA.The use ofminiplates in mandibular frac-tures.An
in vitro study.J CraniomaxillofacSurg 1991;19:199�204.8.Rudderman RH,Mullen
RL.Biomechanics ofthe facial skeleton.Clin Plast Surg1992;19:11�29.9.Ellis E,Karas
N.Treatment ofmandibularangle fractures using two mini-dynamiccompression plates.J
Oral Maxillofac Surg1992;50:958�63.10.Ellis E,Sinn DP.Treatment ofmandibularangle
fractures using two 2.4 mm dynamiccompression plates.J Oral Maxillofac
Surg1993;51:969�73.11.Ellis E,Walker L.Treatment ofmandibular anglefractures using
two noncompression mini-plates.J Oral Maxillofac Surg 1994;52:1032�6.12.Ellis
E,Walker LR.Treatment ofmandibular anglefractures using one noncompression mini-
plate.J Oral Maxillofac Surg 1996;54:864�71.13.Potter J,Ellis E.Treatment
ofmandibular anglefractures with a malleable non-compres-sion miniplate.J Oral
Maxillofac Surg1999;57:288�92.14.Niederdellmann H.Fundamentals ofhealingoffractures
ofthe facial skull.1.Biome-chanics.In:Kruger E,Schilli W,editors.Oral and
maxillofacial traumatology.Vol 1.Chicago (IL):Quintessence Publishing
Co.;1982.p.125�8.15.S�derholm A-L,Lindqvist C,Skutnabb K,Rahn B.Bridging
ofmandibular defectswith two different reconstruction systems:an experimental
study.J Oral MaxillofacSurg 1991;49:1098�105.16.Gutwald R,B�scher P,Schramm A,et
al.Bio-mechanical stability ofan internal mini-fixation-system in maxillofacial
osteosyn-thesis.Med Biol Eng Comp 1999;37 Suppl2:280.17.Hylander WL,Johnson KR.Jaw
muscle func-tion and wishboning ofthe mandible dur-ing mastication in macaques and
baboons.Am J Phys Anthrop 1994;94:523�47.18.Ellis E,Dean J.Rigid fixation
ofmandibularcondyle fractures.Oral Surg 1993;76:6�15.19.Hammer B,Schier P,Prein
J.Osteosynthesis ofcondylar neck fractures:a review of30patients.Br J Oral
Maxillofac Surg1997;35:288�91.20.Choi B-H,Kim K-N,Kim H-J,Kim M-K.Eval-uation
ofcondylar neck fracture platingtechniques.J Craniomaxillofac
Surg1999;27:109�12.21.Schilli W,Stoll P,B�hr W,Prein J.Mandibularfractures.In:Prein
J,editor.Manual ofinternal fixation in the cranio-facial skele-
ton.Chapt.3.Techniques recommended bythe AO/ASIF Maxillofacial
Group.Berlin:Springer-Verlag;1998.p.87.GapFIGURE20-21A,Combination ofa symphysis
fracture treated with a single short bone plate and concomitant closed treatment
ofacondylar process fracture can result in widening ofthe mandible.Because the bone
plate is applied along the buccal cortex,it has amechanical disadvantage in
preventing widening ofthe mandible.To prevent this,a longer,thicker,stronger plate
should be appliedthat �yolks�the mandible (B).AB
CHAPTER 21Management ofAlveolar andDental FracturesRichard D.Leathers,DDS Reginald
E.Gowans,DDSHistoryAlthough there is speculation about whomthe first dental
surgeons were,dentoalveo-lar trauma has existed since humans beganto walk the
earth.Altercations withhumans and animals,accidents,as well asdental treatment
misadventures each havea part in the development oftoday�s den-toalveolar treatment
protocols.Arguably,Hippocrates ofCos,wholived during the Greco-Roman period(350
BC�AD750 ) was the first to documenttreatment regimens for dentoalveolartrauma in
his writings.He discussed bind-ing teeth together in mandible fractures.Gold wire
or linen thread was used as �bri-dle wire.�He alluded to various
splintingtechniques that involved teeth that weredistant to the fractured or
subluxed area(Figure 21-1).In the same way,to expeditethe healing process,he
stressed recaptur-ing proper occlusion,a concept that is stillpracticed today.We
could theoretically think ofHip-pocrates as one ofthe first investigators tosee the
value in �evidenced-based�treat-ment protocols;he is credited with sepa-rating the
obscure religious beliefs fromtrue medical observation.1,2Archigenes (~ 59
BC�AD17),a Romanphysician and dentist,believed that a bro-ken tooth should
initially be treated with amedieval endodontic procedure by intra-pulpal cautery
with a hot iron instrument.3Claudius Galen (~ AD130�200),aGreek physician,also
subscribed to thebeliefthat reestablishing occlusion wasessential in treating
dentoalveolar frac-tures (see Figure 21-1).3Etiology and IncidenceDentoalveolar
injuries commonly occur inthe pediatric,teenage,and adult popula-tions.Each group
has specific etiologiesthat pertain to age,sex,and demographics.In the pediatric
group,the primarycause ofthese injuries is falls.Possibly dur-ing the first years
oflife,the early anatom-ic development and skeletal weight distri-bution cause the
poor coordination thatleads to falls.In the larger surveys,thepediatric population
accounts for 5% ofall facial fractures.4Andreasen reported abimodal trend in the
peak incidence ofdentoalveolar trauma in children aged 2 to4 years and 8 to 10
years.Likewise,therewas an overall prevalence of11 to 30% inthe children with
primary dentition.Those with permanent or mixed dentitionranged from 5 to 20%.The
ratio ofmen towomen was 2:1.5Children and adolescents overlap withrespect to the
etiology ofdentoalveolarinjury.Contact sports and playgroundactivities lead to most
injuries.In fact,approximately one-third ofall dental trau-ma is secondary to
sporting accidents.6FIGURE21-1Mandible found at the ancient site ofSidon in Lebanon
(dated 500 BC).Gold wire wasused to splint periodontally involved anterior
incisors.A,Frontal view.B,Lingual view.Reproducedwith permission from The
Archaeological Museum,American University,Beirut,Lebanon.AB
384Part 4: Maxillofacial TraumaThe use ofmouthguards and appropriatehead
gear,however,has helped to decreasesport-related injuries.7Child abuse appears to
be another signif-icant cause ofdentoalveolar and facial injury.An alarming census
ofchild abuse is docu-mented in the literature.In the year 2000 anestimated 879,000
children were abused.Ofthese,19.3% were physically abused.8In theUnited States,over
50% ofphysical trauma inchild abuse occurs in the head and
neckregion.Internationally,about 7% ofall phys-ical injuries involve the oral
cavity,with 9%between ages 0 and 19 years.9,10Generally,adult injuries are caused
bymotor vehicle collisions,contact sports,altercations or assaults,industrial acci-
dents,and iatrogenic medical or dentalmisadventures.Demographic and behavioral
researchhas increased the profession�s understand-ing ofpsychosocial issues that
relate tofacial trauma.Leathers and colleagues reported onorofacial injury profiles
in an inner-cityhospital.They found that most orofacialinjuries resulted from
intentional violence,and the victims were primarily sociallyand economically
disadvantaged groups inthe minority populations.11,12Black and colleagues related
substanceabuse�specifically alcohol and �streetdrugs��with orofacial
injuries.Theyfound that a significantly greater propor-tion ofpatients who screened
positive fordrug and alcohol abuse at the time ofinjuryhad a previous history
ofhead injuryand/or orofacial injury.Further,we shouldconsider the high rate
ofrecidivism in thispopulation as another behavioral factor.13Other groups that are
at increased riskofdentoaveolar trauma are those withseizure disorders,mental
disorders,andcongenital maxillofacial abnormalities.Lockhart and colleagues
reported find-ings,by the Risk Management Foundation,indicated that damage to the
teeth was themost frequent anesthesia-related claim,often resulting in
litigation.14Poor laryn-goscopy technique and the unmonitoredbiting force ofthe
comatose patient alsopotentially caused dentoalveolar injury.15,16With direct
trauma,maxillary incisorsare the most frequently traumatized teeth,especially
ifthey are associated with a Class IIDivision 1 malocclusion.Trauma to the pri-mary
dentition usually results in variousluxations (~ 75%),whereas in
permanentdentition,crown or crown-root fracturesare the normal (39%).17Indirect
trauma tothe dentition usually results from the force-ful impact ofthe mandible
with the maxil-la,following a blow to the chin region.These traumas will often
result in injury tothe posterior teeth (Figure 21-2).5History and Physical
ExaminationObtain a thorough history ofthe patientand the traumatic
incident.Preinjury data,such as biographic,demographic,past med-ical history,time
ofincident,occlusion,location ofincident,loss ofconsciousness,and nature ofthe
incident could potentiallyexpedite the treatment process.18,19The potential for
aspiration,airwaycompromise,and neurosensory deficitdictates that the clinician
should thor-oughly evaluate all dentoalveolar-injuredpatients prior to managing
dental injuries.The initial examination should be system-atic,methodic,and
comprehensive (seeFigure 21-2).Equally,an injury that couldinvolve tooth or
alveolar fracture may besubstantial enough to cause a briefloss ofconsciousness.The
clinical presentation ofclosed head injuries,such as basal skullfractures and
epidural hematomas,may beoccult.Hence,ifthese are not recognizedearly,they may have
devastating conse-quences.Davidoffand colleagues reportedthat it was not uncommon
for a closedhead injury to result when a loss ofcon-sciousness ofless than 1 hour
occurred,along with facial trauma.20Signs ofconfu-sion followed by �lucid
intervals�mayrequire further radiographic and/or com-puted tomography (CT) scan
studies.21Unaccounted for avulsed teeth,freetooth fragments,or dislodged
restorationsraise the suspicion ofaspiration.For thisreason,auscultation ofthe
chest to ruleout wheezing or labored breathing isessential.Owing to its anatomic
position,the right mainstem bronchus is often thesite offoreign body
dislodgment.Supportany positive finding with proper neck,chest,and abdominal
radiographs.22Iffor-eign bodies exist in the abdomen,arrangefollow-up for the
patient with radi-ographs,and monitor for the risk ofgas-trointestinal (GI)
obstruction until theforeign body is cleared.Maxillofacial ExaminationFor
medicolegal purposes,consider preop-erative photographs prior to
invasivetreatment.Include the following in the patientexamination23:� Extraoral
soft tissue� Intraoral soft tissue� Jaws and alveolar bone� Teeth (displacement and
mobility)� Percussion and pulp testingEnsure that the patient is cleanedextraorally
with a mild antiseptic soap,while taking care not to further inoculateinjury sites
with debris or foreign bodies.Consider tetanus prophylaxis,dependingon previous
immunization complianceand wound presentation.(Table 21-1).24FIGURE21-2Blunt facial
trauma resulting insoft tissue lacerations and dental and alveolarcompromise.
Management ofAlveolar and Dental Fractures385Thoroughly inspect superficial and
deeplacerations,abrasions,or any soft tissuecompromise.The mechanism
ofinjuryelicited in the history and the soft tissuedefect alerts the surgeon to
suspect under-lying hard-tissue damage,such as to themaxilla,the mandible,the
temporo-mandibular joint (TMJ),and alveolar frac-tures.Success rates are time-
dependentwith dentoalveolar trauma,and generallyperioral soft tissue lacerations
(lips)should be repaired after intraoral treat-ment,except in cases ofpoor
hemorrhagecontrol.In children,women,and theelderly,ifthe injury observed fails to
cor-relate well with the history given,suspectand subsequently rule out
abuse.Authori-ties,such as social services representatives,initiate proper legal
protocols,ifnecessary.Prior to any intraoral manipulations,obtain initial
radiographic studies (eg,in thepediatric patient,knowledge ofthe errantdeciduous
tooth root to the permanenttooth bud position).The chance offurtherdamage could be
exponentially disastrous toboth the future eruption and the morphol-ogy ofthe
developing permanent tooth.25�27Approach intraoral soft tissue exami-nation with
caution.Carefully manipulateand handle traumatized tissues to avoidfurther
compromise.Depending on themechanism ofinjury,bone or tooth frag-ments may have
penetrated these delicateareas.Closely inspect hematoma forma-tion or ecchymotic
areas.Buccal mucosallacerations should raise the suspicion forStensen�s duct or
orifice injuries.The lips,the floor ofthe mouth,and the tongueregions are all areas
at risk for penetratingor secondary injury and thus should beinspected
accordingly.Account for all frac-tured or missing teeth and restorations orassume
they were swallowed,aspirated,orlodged within adjacent structures.Similar-
ly,arrange for radiographic evaluation ofthe maxillary and nasal sinuses prior
tofurther treatment.28�30While examining for jaw and alveolarbone fractures,the
presence ofgross mobil-ity or pericoronal bleeding ofthe involvedteeth may be
noted.Sublingual ecchymosisat the floor ofthe mouth is pathognomon-ic for an
underlying mandible fracture.Stepdefects,crepitation,malocclusion,and gin-gival
lacerations all raise suspicion ofpossi-ble underlying bony defects.Assess all
fractured teeth for enamel,dentin,and pulpal involvement.Completemobility ofthe
crown may indicatecrown-root fracture.Superficial crazing orinfractions may be
identified with a directlight source,transilluminating perpendic-ular to the long
axis ofthe tooth from theincisal edge.Inspect and consider eachtooth at risk,even
at sites distal to the ini-tial traumatic impact.Indirect trauma ofthe chin may
cause posterior dentitiondefects,such as vertical or cusp fractures.Check occlusion
and note any displace-ments,intrusions,or luxations.The direc-tion offorce is most
commonly in a buccal-lingual direction.Test percussion sensitivity and pulpvitality
to rule out periodontal ligamentinjury or one ofthe many forms offrac-tures.Gentle
tapping ofthe injured andnoninjured control teeth is the techniqueofchoice.Use the
handle ofa mouth mir-ror or a specially designed calibrated per-cussion
instrument.Tactile,auditory,andvisual senses are used.Dullness may alertthe surgeon
to the possibility ofa luxa-tion injury or alveolar fracture.The qual-ity ofthis
sound indicates that the teethare not in optimal contact with the adja-cent bony
structure.Ifthe enamel is frac-tured or infraction has occurred,thesound is
reminiscent ofa �cracked teacup.�31The typical sound ofthe unin-jured tooth is that
ofsolid metallic reso-nance.Percussion testing,in and ofitself,can add insult to
injury;thus,control andcaution are warranted.Evaluate tooth vitality via various
pulptesting modalities.Mechanical,thermal,and electrical noxious stimuli are
used.These tests use various stimuli to check forconduction disturbances at the
sensoryreceptors ofthe pulp.The pulp comprisesboth nonmyelinated and myelinated
nervefibers,which regulate vascular changes andrespond to pain
stimuli,respectively.As thetooth develops,the pain fibers (ie,myeli-nated)
increase,while simultaneously low-ering the electrometric pulp stimula-
tion.32,33This concept sheds light on someofthe treatment differences in open
andclosed apices ofthe permanent dentition.Pulp testing in the acute phase ofden-
toalveolar fracture is controversial andheavily based on the cooperation and com-
munication ofthe patient as well as therepair process ofthe injured pulp tissue.The
fear ofpossibly experiencing increasedpain during testing,especially in
children,limits verbal objectivity and may renderpulp testing too
unreliable.Also,acutelyinjured teeth may revascularize in approxi-mately 1
month,thus increasing the risk offalse-negative results during pulp testing.The
development stage ofthe involvedTable 21-1Summary ofTetanus ProphylaxisNontetanus-
Prone WoundsTetanus-Prone WoundsHistory ofAdsorbed TetanusTd*TIGTd*TIG (250 U
IM)Unknown or =3 dosesYesNoYesYes=3 doses�No�NoNo�NoTd = tetanus and diphtheria
toxoids adsorbed�for adult use;TIG = tetanus immune globulin�human.*For children <
7 yr old:DTP (DT,ifpertussis vaccine is contraindicated) is preferred to tetanus
toxoid alone.For persons =7 yr old,Td is preferred to tetanus toxoid alone.�Ifonly
three doses offluid toxoid have been received,a fourth dose oftoxoid,preferably an
adsorbed toxoid,should be given.�Yes,if> 10 yr since last dose.�Yes,if> 5 yr since
last dose.(More frequent boosters are not needed and can accentuate side
effects.)Adapted from Alexander RH and Proctor HJ.24
386Part 4: Maxillofacial Traumateeth also plays a significant role in therepair
process.Incomplete apical develop-ment increases the chances ofpulp repairand
revascularization.As the toothmatures and apical width constrictionstarts,the
chances ofpulp repair decrease.Bacterial invasion in the pulp injury zoneincreases
the risk oftotal pulp necrosis.Paradoxically,occasionally uninjured teethmay not
respond as expected.Even withthis controversy in mind,pulp testing con-tinues.Some
ofthe testing paraphernaliaare listed as follows34:�Mechanical stimulation�Dental
probe�Cavity prepping with drills�Saline-laden cotton pledget (fractured
teeth)�Thermal test�Heated gutta-percha�Ice�Ethyl chloride�Carbon dioxide
snow�Dichlorodifluoromethane�Electrometric test�Electric pulp testersLaser Doppler
flowmetry (LDF),a rela-tively new pulp testing apparatus,hasshown promise.A laser
beam,which isdirected at the coronal-labial aspect ofthepulp,is scattered by pulp
blood cells that inturn produce a Doppler frequency shift.Thefraction oflight
scattered back is detectedand processed to elicit a signal.The basictheory is that
the pulp revascularizationprocess can be monitored.Studies haveshown that,in cases
wherein electrometrictests were negative and LDF displayed vascu-lar perfusion,the
LDF accuracy ofpulp vital-ity reached 100%.The drawbacks to thisform oftesting are
poor light transmissionwhen blood pigments from discolored teethare
encountered,complexity ofequipmentuse,and poor price containment.35,36To ensure
completeness,generate astandardized treatment record during theevaluation
process,which systematicallyculminates in a diagnosis,treatment plan,and
prognosis.Figure 21-3 provides thedentoalveolar trauma record,which
shouldinclude,but is not limited to,these entities.Radiographic
ExaminationRadiographic examination is essential todetermine whether any underlying
struc-tures are damaged and should includeperiapical,occlusal,and panoramic radi-
ographs.The periapical radiograph pro-vides the most detailed information aboutroot
fractures and the dislocation ofteeth.Following treatment,periapical films
canconfirm the proper positioning ofanavulsed or luxated tooth into the
alveolus.Occlusal radiographs,however,pro-vide a larger field ofview,and the detail
isalmost as sharp as a periapical radiograph.Dentoalveolar Trauma
RecordName:_____________________________________
Date:_____________________Age:Sex:Incident:CauseLocationTimeNeurologic status:Locus
of controlConsciousnessHeadacheNausea, vomitingExtraoral findings:Intraoral
findings:Radiographic findings:PosteroanteriorOcclusalPanoramicOtherTooth vitality
findings (pulp testing):Tooth mobility (+1, +2, +3):Ellis classification (I, II,
III, IV):Luxation:Yes ___No ___Type ________________Avulsion:Yes ___No ___Storage
medium _______Time ______Supporting structure trauma:Diagnosis:Treatment
plan:Prognosis:Good ___Fair ___Guarded __Examined by:FIGURE21-3Dentoalveolar trauma
record.
Management ofAlveolar and Dental Fractures387When occlusal radiographs or
periapicalfilms are used to examine soft tissues forthe presence offoreign
bodies,reduce theradiographic exposure time.The panoramic radiograph is a
usefulscreening view and can demonstrate frac-tures ofthe mandible and maxilla as
wellas fractures ofthe alveolar ridges andteeth.In the hospital setting,dental
radi-ographs may not be available.Althoughnot ideal,plain films,such as
themandibular series and the Caldwell views,may reveal tooth and alveolar
injuries.In the trauma patient whose tooth hasnot been accounted for at the
accidentscene,arrange for chest films to rule outthe possibility
ofaspiration.Abdominalradiographic films can determine whetherdisplaced teeth or
prosthetic applianceshave been ingested.Classification ofDentoalveolar Injuries
Once the diagnosis ofdentoalveolarinjury is made,the injury is classified forease
ofcommunication and treatmentplanning.Many classification systemshave been proposed
over the years basedon the anatomic site ofinjury,the cause,the treatment
alternatives,or a combina-tion ofthese.The two most common sys-tems are those
developed by Ellis andDavey (Figure 21-4) and Andreasen (Fig-ures 21-5�21-7).The
most commonlyused simple and comprehensive classifi-cation ofdentoalveolar injuries
is onethat was developed by Andreasen andoriginally adopted by the World
HealthOrganization system for disease classifi-cation,using the International
Classifica-tion ofDiseases codes.The classificationcan be applied to both permanent
andprimary dentition.It includes descrip-tions ofinjuries to
teeth,supportingstructures,and gingival and oral mucosa.Injuries to the teeth and
supportingstructures are divided into dental tissues,pulp,periodontal tissues,and
supportingbone as follows:�Dental tissues and pulp�Crown infraction (ie,a craze
line orcrack in the tooth without loss oftooth substance)�Crown fracture that is
confined toenamel,or enamel and dentin,withno root exposure (uncomplicated) �Crown
fracture producing a pulpexposure (complicated) �Fracture involving the
enamel,dentin,and cementum without pulpexposure (uncomplicated crownroot
fracture)�Fracture involving the enamel,dentin,and cementum with pulpexposure
(complicated crown-rootfracture)�Root fracture involving the dentinand cementum and
producing apulp exposure (root fracture)�Injuries to periodontal tissuesare divid-
ed into six categories and encompasswhat are commonly referred to as sub-luxations
and avulsions.�Concussion:defined as an injury tothe periodontium producing sensi-
tivity to percussion without loosen-ing or displacement ofthe tooth�Subluxation:the
tooth is loosenedbut not displaced�Luxation (ie,lateral,intrusion,andextrusion)
dislocation,or partialavulsion:the tooth is displacedwithout an accompanying com-
minution or fracture ofthe alveolarsocket�Injuries to the supporting
bone�Comminution ofthe alveolar hous-ing,often occurring with an intru-sive or
lateral luxation�Fracture ofa single wall ofan alveolus�Fracture ofthe alveolar
process,en bloc,in a patient having teethbut without the fracture line nec-essarily
extending through a toothsocket�Fracture involving the main bodyofthe mandible or
maxilla Categories ofinjuries to the gingival ororal mucosa area include the
following:�Abrasion�Contusion�LacerationTreatment ofInjuries to theHard Tissues and
PulpEnamel Fractures (Crown Infraction)These injuries include
fractures,chips,andcracks that are confined to enamel,notcrossing the enamel-dentin
border but ter-minating at the border.The cracks or frac-tures can be seen by
indirect light or trans-illumination.Treatment involves smoothing therough edges or
repairing with compositeresin.It is difficult to predict future pulpalvitality;for
this reason,perform pulp test-ing immediately after the injury and againin 6 to 8
weeks.IVIIIIIIFIGURE21-4Ellis classification:I�fracturewithin enamel; II�fracture
ofenamel-dentin;III�fracture involving pulp; IV�fractures involv-ing the roots.
388Part 4: Maxillofacial TraumaCrown Fracture without Pulp InvolvementCrown
fractures are the most frequentinjuries in the permanent dentition.Crown fractures
that expose dentinaltubules potentially may lead to contami-nation and inflammation
ofthe pulp,eventually resulting in pulpal necrosis ifuntreated.Luxation injury
concomitant tocrown fractures,with or without pulpexposure,is the primary source
ofpulpalcomplications following injury.Prognosisis better ifthe enamel-dentin
fractureinvolves a tooth that has not been luxatedbecause the blood supply to the
pulp hasnot been disturbed,and the immunologicdefense systems in the pulp will
combatbacterial invasion (Figure 21-8).Treatment is directed at protecting thepulp
by sealing the dentinal tubules.Although zinc oxide�eugenol cement hasbeen one
ofthe best agents for producinga hermetic antibacterial seal,it is generallynot
recommended at the site where a com-posite resin restoration is placed becausethe
eugenol component may interfere withpolymerization,at least with some com-posites.A
similar effect has been seen witha hard-setting calcium hydroxide paste,resulting
in bond strength reduction inFIGURE21-5Diagram ofinjuries to dental tissue and
pulp.A,Crown infraction.B,Crown fracture confined to enam-el and dentin
(uncomplicated crown fracture).C,Crown fracture directly involving pulp
(complicated).D,Uncompli-cated root fracture.E,Complicated crown-root
fracture.F,Horizontal root fracture.Adapted from Andreasen JO,editor.Traumatic
injuries ofthe teeth.1st ed.Philadelphia (PA): W.B.Saunders; 1972.ABCDEF
Management ofAlveolar and Dental Fractures389certain dental-bonding agents.In
fractureswith dentin exposure only,we recommenda dental bonding agent,followed by
acomposite restoration.With pulp expo-sure,the preferred treatment is
calciumhydroxide placed directly over the expo-sure and sealed in place with a
glassionomer cement followed by a dentinbonding agent and composite.37Crown
Fracture with PulpInvolvementCrown fractures involving the enamel,dentin,and pulp
are called complicatedcrown fractures by Andreasen and Class IIIfractures by
Ellis.Prognosis depends onthe length oftime that has elapsed sincethe injury
occurred,the size ofthe pulpexposure,the condition ofthe pulp (vitalor
nonvital),and the stage ofroot devel-opment.Make every effort to preserve thepulp
in immature teeth.Conversely,inmature teeth with extensive loss
oftoothstructure,pulp extirpation and root canaltherapy are prudent before
post,core andcrown restoration.The prognosis is bestfor teeth with a vital pulp
exposure ifthefracture is treated within the first 2 hours.Treatment requires
direct pulp cap-ping for small pinpoint exposures.Ifapatient�s tooth has an open
apex and asmall pulp exposure is seen within 24 hours,it should be directly pulp-
capped with calcium hydroxide.Performcalcium hydroxide pulpotomies for
largerexposures and for small exposures in teethwith open apices over 24 hours
old.Thedirect pulp cap ofcalcium hydroxidepulpotomy is designed to allow a
toothwith an open apex to complete root devel-opment.Teeth that have calcium
hydrox-ide pulpotomies usually require root canaltherapy along with a post and core
andultimately coronal coverage.In fractures with a vital pulp and aclosed
apex,perform a direct pulp cap ifthere is a small pulp exposure and ifthepatient is
seen within 24 hours.Ifthe pulpexposure is larger then 1.5 mm or ifit hasbeen
present for over 24 hours,carry outroot canal therapy.Crown-Root FractureA fracture
that is longitudinal and followsthe long axis ofthe tooth or ifthe coronalfragment
constitutes more than one-thirdofthe clinical root,extraction is
generallyrecommended.However,with a fractureline that is above or slightly below
the cer-vical margin,appropriate forms ofconser-vative therapy can usually be used
torestore the tooth.Crown lengthening ororthodontic elevation ofthe involvedtooth
may be necessary.Root FractureThis type offracture is limited to fracturesinvolving
the roots only (Ellis IV).Mostroot fractures occur in the apical and mid-dle one-
third and rarely in the cervicalone-third.Root fractures are not
alwayshorizontal;in fact,they are often diagonalin angulation.Radiographs taken
immedi-ately after an injury may not show a hori-zontal or diagonal root
fracture.After 1 or2 weeks when inflammation,hemorrhage,and resorption have caused
the fragmentsFIGURE21-6Diagram ofinjuries to periodontal tis-sues.A,Periodontal
concussion.B,Subluxation.C,Lux-ation,dislocation,or partial
avulsion.D,Exarticulationor avulsion.Adapted from Andreasen JO,editor.Trau-matic
injuries ofthe teeth.1st ed.Philadelphia (PA):W.B.Saunders; 1972.ABCD
390Part 4: Maxillofacial Traumato separate,the radiograph will show thedamage more
conclusively.Root fractures in the apical or middleone-third are usually not
splinted unlessthere is excessive mobility (Figure 21-9).Treatment ofmobile root
fractures con-sists ofapposition ofthe fractured seg-ments with rigid splinting for
12 weeks.Treatment for cervical one-third�rootfractures usually involves extraction
ofthetooth or orthodontic extrusion ofthe root.Periodontal Tissue Injury and
TreatmentInjury to the periodontal tissue presentsitselfin many
ways.Radiographically,thisinjury usually involves an evident disloca-tion or a
movement ofthe tooth,and nar-rowing or loss ofperiodontal space may beseen.The fate
ofthe tooth that has sus-tained a periodontal injury is twofold.Pri-marily,we see
the injury from the localizedimpact and the late complication ofthesecondary
resorptive process.The likelyresult ofdisplacement injuries is the devel-opment
ofsome type and degree ofresorption.Thus,to better treat thesetypes ofinjuries,it
would behoove the sur-geon to understand this process,both clin-ically and
conceptually.This processaffects both primary and permanent den-tition.The etiology
and pathogenesis isessentially identical to that seen in avul-sion injuries,which
we discuss later in thischapter in �Exarticulations (Avulsions).�Classification
ofRoot ResorptionRootresorption is classified as either root sur-face resorption or
root canal resorption.Root surface resorption,also known asexternal root
resorption,is most common-ly seen after intrusive injuries and less insubluxation
injuries.It is classified intothree types:(1) surface resorption,(2)replacement
resorption,and (3) inflam-matory resorption.Root Surface ResorptionSURFACERESORP-
TIONSurface resorption indicates that theluxated or avulsed tooth root
displayssuperficial resorption lacunae,which arerepaired with newly formed
cementum.Although not usually seen on radiographs,these may appear as vague
excavations orcavities on the lateral root surface.A nor-mal lamina dura is usually
present.Thisdevelopment is a response to localizedperiodontal ligament and/or
cementuminjury.The process is less aggressive andself-limiting compared with the
otherresorption processes.REPLACEMENTRESORPTIONReplace-ment resorption also known
as ankylosis,presents as an indistinguishable mergingofbone and root substance.The
rootFIGURE21-7Diagram ofinjuries to supporting alveolar bone.A,Fracture ofsingle
wall ofthe alveolus.B,Fracture ofthe alveolar process.Adapted from Andreasen
JO,editor.Traumatic injuries ofthe teeth.1st ed.Philadelphia (PA): W.B.Saunders;
1972.ABFIGURE21-8Crown fracture without pulpinvolvement.The fracture ofthe central
incisorinvolved both enamel and dentin.Treatmentinvolved sealing the dentinal
tubules with adentinal bonding agent followed by an estheticcomposite
restoration.FIGURE21-9Mandibular central incisors withfractures ofthe apical one-
third.No stabilizationwas used.Vital pulp testing was noted after 8 weeks.Note the
interposition ofconnective tissueat the fracture site(arrow).(Courtesy
ofDr.ThomasG.Dwyer and Dr.James R.Dow,Roseville,CA.)
Management ofAlveolar and Dental Fractures391substance is being ultimately replaced
bybone,and radiographically a loss oftheperiodontal space and progressive
rootresorption is seen.INFLAMMATORYRESORPTIONInflam-matory resorption appears as
well-circumscribed areas ofcementum anddentin resorption.The localized
adjacentperiodontal tissue is markedly inflamed.The onset ofinflammation is a
result ofthe infected and necrotic pulp tissue with-in the root canal.The
radiograph shows anappearance ofroot resorption with lines ofadjacent bone
radiolucency.Root Canal ResorptionRoot canalresorption,also known as internal
rootresorption,presents less often than rootsurface resorption.Studies found that
itappears in both permanent and primaryteeth.Radiographic imaging may
beequivocal;labial or lingual presentationsofsurface resorption may be
erroneouslysuperimposed over the root canal.Toavoid a misdiagnosis supplemental
radi-ographic views are warranted.Root canalresorption is classified as two types:
(1)internal replacement resorption and (2)internal inflammatory
resorption.INTERNALREPLACEMENTRESORPTIONInternal replacement resorption
showsmetaplastic replacement ofnormal pulptissue into cancellous bone,resulting in
awidened pulp chamber.This is a character-istic process that is seen in root
fracturesand,to a lesser extent,in luxation
injuries.INTERNALINFLAMMATORYRESORPTIONInternal inflammatory resorption
oftenlocated at the cervical region ofthe pulp,presents radiographically as an
irregularor oval-shaped radiolucent enlargementwithin the pulp chamber.This
conditionrelates to the ingression ofbacteria viadentinal tubules within a necrotic
pulpdelineated as the necrotic pulp zone.Pos-sibly,this zone is responsible for the
pro-gression ofthe process.Normal pulp tissueis altered and transformed into
granula-tion tissue with giant cells that resorb thedentinal walls ofthe root
canal,giving thechamber an enlarged appearance.The ces-sation ofthis process will
require rootcanal therapy (Figure 21-10).The potential devastating effects
oftheresorptive process require immediate andproper treatment ofperiodontal
injuries.Classification ofPeriodontal InjuriesPeriodontal injuries are classified
as con-cussions and displacements.Displace-ments include
subluxations,intrusiveluxations,extrusive luxations,and
lateralluxations.ConcussionOften this injury is over-looked because no acute
clinical or radi-ographic evidence oftrauma is seen.Noabnormal
mobility,displacement,or bleed-ing is apparent;only minimal injury to thetissues
was acquired.Frequently,the historyofthe insult guides the surgeon to the sus-
pected tooth or teeth.The hallmark to diag-nosis is a marked reaction to percussion
inboth the horizontal and vertical directions.The discomfort is similar to that ofa
�hottooth,�hyperemic quality.Because a con-cussed tooth may take on a chronic
courseor exhibit progressive problematic seque-lae,it warrants close
monitoring.Treatment includes taking the sus-pected tooth out ofocclusion to
avoidfunction.Ifat all plausible,considerocclusal adjustments on the opposing den-
tition,thereby limiting further trauma tothe involved
tooth.DisplacementsDisplacement injuries,orluxations,principally involve the
primaryand permanent maxillary central incisors.The mandibular teeth are less at
risk,unless a Class III malocclusion exists.Gen-erally,displacement injuries are
moreprevalent in primary dentition owing tothe increased elasticity and resilience
ofthe bony supporting structures.Converse-ly,permanent teeth will have an
increasedrisk oftooth fracture.38,39The specific lux-ation classification depends
on the forceand direction oftraumatic impact.Fifteento 61% ofluxation injuries
occur in thepermanent dentition and 62 to73% in theprimary dentition.Multiple teeth
are usu-ally involved in luxation injuries.40SubluxationSubluxation injuries
occurwhen there is an injury to the tooth-supporting structures that causes abnor-
mal loosening;however,there is no clinicalor radiographic displacement
oftheinvolved tooth.The tooth is sensitive topercussion testing and occlusal
forces.Rupture ofthe periodontal tissues is usu-ally evident by bleeding at the
gingivalmargin crevice (Figure 21-11).Treatment is similar to that for concus-sion
injuries with occlusal adjustments andvitality testing.Excessive mobility
maynecessitate nonrigid stabilization.Continuefollow-up evaluation and vitality
testing for6 to 8 weeks.Approximately 26% ofinjuries withthis classification result
in pupal necrosis,and endodontic treatment is indicated.Studies show that external
resorption willFIGURE21-10Maxillary lateral incisor with ahistory ofperiodontal
injury (subluxation).Evi-dence ofinternal root resorption,specifically,inter-nal
inflammatory resorption(arrow),is seen.
392Part 4: Maxillofacial Traumaoccur in 4% ofthese injuries.41Subluxationhas the
lowest frequency ofperiodontal tis-sue injury resorption.Intrusive
LuxationIntrusive luxationsmay cause marked displacement ofthetooth into the
alveolar bone,with possiblecomminution or fracture ofthe alveolarsocket.Percussion
sensitivity is limited,and decreased mobility is noted becausethe tooth is
essentially locked in.A high-pitched metallic sound is elicited on per-
cussion,reminiscent ofan anklyosedtooth.The intrusive injury is more com-monly seen
in the maxilla because ofitsless dense anatomy and irregular premax-illary
configuration.The superiorly placedhollow cavities and thin floors ofthe nasaland
maxillary sinuses create a formula forrelative ease ofdislodgement ofteeth tothese
sites when intrusive forces areencountered.Intrusive injuries are themost severe
ofthe luxation injuries thatinvolve the pediatric patient.The intrudedprimary tooth
may be impinging on thetooth bud ofthe permanent successors ina buccal-occlusal
position.26�28The inci-dence ofpupal necrosis is relatively high(96%).Inflammatory
resorption inci-dence may reach 52% as a result ofthenecrotic pulp (Figure 21-
12).Treating intrusive injuries depends onroot development.Ifincomplete
rootdevelopment exists,allow the intrudedtooth to re-erupt.Continue this processfor
approximately 3 months.Ifre-eruption does not occur,to facilitate thisprocess,place
an orthodontic extrudingappliance.Ifpulp necrosis occurs,seekendodontic therapy.In
cases ofcompleteroot development with closed apices,re-position the tooth
atraumatically,andstabilize with a nonrigid splint.Then,ini-tiate endodontic
therapy in approximately10 to 14 days after injury.Use CaOH as acanal filler in
this therapy to retard orinhibit the inflammatory or replacementresorption
process.42�44In fact,use CaOHin any intrusive luxation injuries thatresult in the
displacement ofthe tooth inexcess of3 to 5 mm,and initiate within 2
weeks.This,along with instrumentationofthe canal,will eradicate the
bacterialcontamination and allow for the repair ofthe periodontal ligament.Replace
the CaOH filler ifit resorbsduring the healing process.Arrange forfrequent
radiographic follow-up at 3-month intervals,and continue for 6 to12 months.Perform
conventional rootcanal therapy with gutta-percha obtura-tion when signs
ofresorption have ceased.Extrusive LuxationExtrusive luxationsare the partial
displacement ofthe toothout ofthe socket in a coronal or incisaldirection with
lingual deviation ofthecrown.This results in the rupture and sev-erance ofthe
neurovascular and periodon-tal ligament (PDL) tissues,respectively.There is gross
mobility and bleeding at thegingival margin.Further,radiographically,the PDL space
is widened.A dull sound isheard on percussion testing.Pulp necrosisoccurs
approximately 64% ofthe time,and a relatively low frequency ofexternalresorption is
seen at 7%.41It is treated by delicately placing theextruded tooth back into the
proper posi-tion in the socket.Check and re-checkocclusion to ensure no rotation
hasoccurred.Then,stabilize the tooth with anonrigid splint for approximately 2 to 3
weeks.Ifsigns ofpulp necrosis occur,employ endodontic therapy.Lateral
LuxationsLateral luxations mayresult from traumatic forces that displace
thetooth,or teeth,in many directions;however,the lingual direction appears to be
the mostprevalent.These luxations often involve thebony alveolar socket.The
radiographicappearance is similar to the extruded toothon occlusal views,with the
PDL spacewidening in the apical direction.Linear orcomminuted fractures are the
norm.Lingualand buccal plate expansion may render thetooth mobile.Localized soft
tissue compro-mise is often apparent.When bony defectsexist beneath the gingiva,it
is common to seecomplex lacerations and step defects.Because the tooth is often
locked in an errantposition,the percussion resonance andmobility resemble the
intruded tooth.FIGURE21-11Patient with subluxed left max-illary central
incisor.Bleeding andecchymosis atthe gingival margin crevice denotes rupture ofthe
periodontal tissues.Treatment involved sta-bilization with a custom-fabricated
nonrigidsplint for 2 weeks.FIGURE21-12A,Panorex view depicting
extentofintrusion.B,Teeth extruded,aligned,and sta-bilized with nonrigid
splint.Soft tissue gingivalwound repaired.AB
Management ofAlveolar and Dental Fractures393The key to treatment is to
reestablishpreinjury occlusion.Delay soft tissue repairuntil this is
completed.Manipulate thetooth or teeth back into the socket.Ifanalveolar segment is
involved,reposition it.Digitally apply buccal and lingual pressurein cases
oftraumatic bony expansion toensure early PDL repair.Apply a nonrigidsplint that is
extended to and is supportedby the presumably uninjured adjacentteeth.Leave the
splint in place for 2 to 8 weeks,depending on bony healing,whichmay require longer
stabilization time.Avoidthe use ofdisimpaction devices,such as for-ceps or
hemostats,while attempting toreestablish proper alignment ofteeth
orsegments.Excessive fulcruming forces mayfurther compromise the tooth and/or sup-
porting structure.In persons who may have experienceddelayed treatment in excess
of48 hours,reestablishing occlusion may be difficult andtraumatic.Consider
spontaneous or ortho-dontic realignment.Continue frequent radi-ographic follow-up
and vitality testing forseveral months.Adjacent teeth that mayhave become
devitalized warrant vitalitytesting.Any signs ofpulp necrosis should bemet with
immediate endodontic therapy.Another complication to consider isthe loss ofmarginal
bone support in bothlateral and intrusive luxation injuries,which can occur as a
temporary or perma-nent condition.It is seen clinically as aningrowth ofgranulation
tissue at the gin-gival crevice,resulting in a loss ofattach-ment.This is the
normal process ofperi-odontium healing and takes up to 6 to 8 weeks.When this
process occurs,contin-ue maintenance ofthe splint and pay closeattention to oral
hygiene compliance toprevent further bone loss.The frequency ofthis bony loss
reach-es 5% for lateral luxations and 31% inintruded luxations.45Exarticulations
(Avulsions)Seemingly,avulsion injuries are the worstofthe dentoalveolar injuries.By
defini-tion,these injuries involve tooth,or teeth,that are completely dislodged
from thesocket for a period oftime.Owing to thehigher risk
ofaspiration,supportingstructure damage,or actual physical loss ofthe tooth,these
injuries require specialattention.Old ideology and myths stillplague the use
ofnewer proven protocols.Avulsion injuries occur from 0.5 toabout 16% in the
permanent dentition andoccur less in the primary dentition (7 to13%),with children
ages 7 to 9 years beingmost associated with this injury.Theseinjuries usually
involve a single tooth,withthe maxillary central incisor most often atrisk,which is
due to the relative instabilityofthe periodontal ligament during theprogressive
eruption ofthese teeth.46The treatment ofsuch injuries mustbe geared toward early
reestablishment ofperiodontal ligament cellular physiology.The fate ofthe avulsed
tooth depends onthe cellular viability ofthe periodontalfibers that remain attached
to the root sur-face prior to reimplantation.Althoughextraoral time is a
factor,newer physiolog-ically compatible solutions are availablethat can maintain
and/or replenish peri-odontal ligament cell metabolites.Twosuch solutions are
Hank�s balanced saltsolution and ViaSpan (Figures 21-13 and21-14).47�49Both Hank�s
solution and ViaSpan arephysiologic with compatible pH andosmolality (Table 21-
2).ViaSpan is thesolution ofchoice for organ storage dur-ing transport for
transplantation.The rel-ative availability and cost effectiveness ofHank�s solution
makes it the medium ofchoice in storage ofavulsed teeth.Com-mercially available by
Phoenix LazarusInc.,Save-A-Tooth,an emergency toothpreserving system that contains
Hank�ssolution as its active ingredient,is a main-stay in many athletic first aid
kits.Other methods for temporarily storingan avulsed tooth are milk,saliva,and
saline;however,their ability to replenish cellularmetabolites has not been
documented.Milkis a readily available medium for the lay per-son,and,because time
is ofthe essence,it isthe medium ofchoice in the absence ofHank�s solution or
ViaSpan.Milk will onlyprevent further cellular demise;thus,it isused specifically
when teeth have beenextraoral for < 20 minutes.Any periodontalligament extraoral
exposure > 15 minuteswill deplete most ofthe cell metabolites;forthis reason,a
longer period ofextraoral timelimits milk�s effectiveness to maintain cellu-lar
viability.Unlike Hank�s solution andViaSpan,which can store avulsed teeth
andreplenish cellular metabolites for 24 hoursand 1 week,respectively,milk as a
storagemedium becomes ineffective after approxi-mately 6
hours.50,51TreatmentConsidering the root matura-tion,the extraoral time,and the
generalFIGURE21-13Hank�s balanced salt solution,commercially available as Save-A-
Tooth(Phoenix Lazarus,Inc.).FIGURE21-14ViaSpan,cold storage solutioncurrently
available as an organ transport solution.
394Part 4: Maxillofacial Traumahealth ofthe tooth preinjury determines theroute
oftreatment.The idea ofearly orimmediate replantation should be adopted.Teeth that
are in poor condition froma hygiene standpoint are generally notreplanted.Those
that present with moder-ate to severe periodontal disease,grosscaries involving the
pulp,apical abscessformations,infection at the replanting site,and bony defects
and/or alveolar injuries,in which supporting bone is lost are lesslikely to be
considered for replantation.To optimize success oftreatment,replant and stabilize
avulsed teeth within 2 hours (120 minutes);periodontal liga-ment cells become
irreversibly necroticafter this time frame.Attempt to salvageavulsed teeth,even
ifthe critical 2-hourperiod has passed,but the prognosisbecomes progressively
worse.Teeth with open apices > 1 mm diame-ter have a prognosis that is much
betterthan that ofthe more mature or closed-rootapex.Treat the tooth with an open
rootwithin the 2-hour time frame by placing itin Hank�s solution for about 30
minutes.Next,place the tooth in a 1 mg/20 mL doxy-cycline bath for 5
minutes,followed byimmediate replantation and splint stabi-
lization.47,52Ifradiographic or clinical evi-dence ofpathology is noted,perform
anendodontic apexification procedure with aCaOH filling.The CaOH should be period-
ically replaced until the apex is closed,fol-lowed by conventional root canal
therapy.Newer materials for apexification pro-cedures are on the market that
decreasethe need for multiple CaOH replace-ments�one ofwhich is ProRoot MTA(Mineral
Trioxide Aggregate),marketed byDensply Tulsa Dental.Contrary to CaOH,MTA provides a
hard-setting nonre-sorbable surface with cavity adaptation.Itprovides excellent
tissue biocompatibilityand allows for immediate apical seal.53,54The increased
potential for reestab-lishment ofpulpal circulation in teethwith open apices has
been shown toimprove prognosis ofsurvival ofthe pulpand PDL in the avulsed tooth
(Figures 21-15 and 21-16).This revascularizationprocess is optimized by the topical
appli-cation ofdoxycycline.Individuals whohave avulsed teeth with mature or
closedapices and who present within the 2-hourtime frame are treated by placing
thetooth in Hank�s solution for about 30 minutes,followed by replantation
andsplinting for 7 to 10 days.Carry outendodontic cleansing and shaping
ofthecanal,and place a CaOH filling just priorto splint removal.Final gutta-
perchaobturation is contingent on resolvingcanal and/or root pathology (6 to 12
months).Late failure ofthe replanta-tion process is manifested as
eitherinflammatory or replacement resorptionowing to a necrotic pulp or
compromisedPDL,respectively.In individuals who experience an extra-oral period that
exceeds 2 hours,apical rootmorphology plays little role in the
successrate.Eliminate the necrotic periodontal lig-ament strands manually or
chemically in asodium hypochlorite wash for approxi-mately 30 minutes.Perform root
canal ther-apy extraorally with conventional cleansingand shaping ofthe
canal.Withhold finalobturation until the canal,dentinal tubules,and root surface
have been treated with var-ious chemicals in a stepwise fashion.First,acitric acid
bath for 3 minutes,followed byrinsing with 0.9% NaCl,will open anddebride the
dentinal tubules,thus allowingunimpeded ingrowth ofconnective tissue tothe root
surface.Second,the tooth shouldbe moved to a 1% stannous fluoride solu-tion for 5
minutes.This will decrease therisk ofthe resorption process.Finally,set up a 5-
minute bath of1 mg/20 mL doxycycline,which will ridthe root surface ofresidual
bacterial rem-nants and facilitate pulpal revasculariza-tion.Complete the final
obturation withgutta-percha.The tooth is then replantedinto preinjury alignment and
splinted for7 to 10 days (Tables 21-3 and 21-4).50,52,55Table 21-2Solutions to
Replenish Periodontal Ligament Cell MetabolitesSolutionCharacteristicsHank�s
balanced pH = 7.2salt solutionOsmolality = 320 mOsmViaSpanpH = 7.4Osmolality = 320
mOsmCow�s milkpH = 6.5�6.7Osmolality = 225 mOsmPulp Survival (%)Time (yr)Closed
apexOpen apex10090807060504030201001 510FIGURE21-15Studies by Andreasen and
colleagues support theincreased potential for pulpal healing after replantation
related to stageofroot development (closed vs open apex).Adapted from Andreasen
JOand Andreasen FM.34
Management ofAlveolar and Dental Fractures395Splinting Protocol and
TechniqueSplint-ing after avulsion and displacement injuriesimmobilizes the tooth
or segment into prop-er preinjury alignment and allows for the ini-tial pulpal
revasculature and periodontal lig-ament healing course.Several techniqueshave been
advocated in the past;however,theacid-etch/resin splint (or variants
ofthistechnique) is the treatment ofchoice.56,57This technique fulfills the
requirements ofacceptable splint utilization in a maxillofacialtraumatic injury
(Table 21-5).The acid-etch technique is the onlysystem that most closely adheres to
theserecommendations (Figure 21-17).Thearch bar,self-curing,Essig,intracoronal,and
circumferential splints may rarely pre-sent with an indication but are not rou-
tinely recommended.Each has beendemonstrated to violate one or many ofthe basic
splint requirements.The archbar,in particular,produces an eruptive orextrusive
force because ofthe placement ofthe wire beneath the height ofcontour ofthe
tooth.Also the rigid nature ofthesetechniques will facilitate the
externalresorption process (Table 21-6).Treatment ofFractures oftheAlveolar
ProcessOwing to the exposed anatomy,alveolarfractures usually occur at the incisor
andpremolar regions.Treatment involves earlyreduction and stabilization ofthe
involvedsegments.Depending on the fracture�sPeridontal Ligament Healing/Survival
(%)Closed apexOpen apex1009080706050403020100Time (yr)1 510FIGURE21-16Periodontal
healing/survival after replantation relat-ed to stage ofroot development (closed vs
open).Adapted fromAndreasen JO and Andreasen FM.34Table 21-3Treatment Summary for
Avulsed Teeth< 2 h;open apex1.Replant immediately ifpossible2.Transport in Hank�s
solution or milk3.Present to nearest qualified facility (decrease time call
first)4.Check ABCs;evaluate for associated injuries (history and physical
examination)5.Store in Hank�s Solution for about 30 min6.Transfer to a 1 mg/20 mL
doxycyline bath for about 5 min7.Perform radiography
(posteroanterior,occlusal,panoramic,chest)8.Initiate local anesthesia9.Irrigate
socket with saline solution10.Perform tetanus prophylaxis as needed11.Initiate
antibiotic coverage12.Replant tooth13.Splint for 7�10 d14.Perform apexification
with CaOH in cases ofpathosisClosed apex1.Store in Hank�s solution for about 30
min2.Replant3.Splint for 7�10 d4.Perform endodontic cleansing and shaping ofcanal
at time ofsplint removal5.Fill canal with CaOH (6�12 mo)6.Perform final gutta-
percha obturation (~6�12 mo)ABC = airway,breathing,and circulation.Table 21-
4Treatment Summary forTeeth Avulsed > 2 Hours*1.Replant
immediately,ifpossible2.Transport in Hank�s solution or milk3.Present to nearest
qualified facility(decrease time call first)4.Check ABCs;evaluate for
associatedinjuries (history and physical examination)5.Bathe tooth in sodium
hypochlorite for ~30 min vs manual d�bridement ofthe periodontal ligament6.Perform
extraoral RCT7.Bathe tooth in citric acid (~3 min)8.Bathe tooth in 1% stannous
fluoride(~5 min)9.Transfer to a 1 mg/20 mL doxycylinebath for ~5 min10.Perform
radiography (posteroanterior,occlusal,panoramic,chest)11.Initiate local
anesthesia12.Perform tetanus prophylaxis as needed13.Initiate antibiotic
coverage14.Replant tooth15.Splint for 7�10 dABC = airway,breathing,circulation;RCT
= root canaltherapy*Open or closed apex.
396Part 4: Maxillofacial Traumaseverity,use either an open or closed tech-
nique.Digital manipulation and pressure,along with rigid splint
stabilization,willusually be sufficient in the closed tech-nique.Leave the splint
in place for approx-imately 4 weeks.A gross displacement and/or imped-ance to
reduction may necessitate theopen technique.Inability to freely reducefracture
segments may be due to root orbony interferences or impaction (apicallock) (Figure
21-18).Access to the areainvolves an incision that provides ade-quate exposure and
is located apical to thefracture lines.The segment is then disim-pacted or freed
up.Proper alignment andocclusion are then attained,and the seg-ments are stabilized
with suitable trans-osseous wire or a small (2.0 mm) mono-cortical plate.Ensure
that the closure ofthe wound is meticulous to prevent expo-sure ofbone and/or
hardware to theingress ofbacteria.Stabilize teeth that may be mobilein the
fractured segment with anappropriate secondary splint after
bonystabilization.Likewise,avoid removingteeth that are considered nonsalvage-able
and that are within the bony seg-ment until the bony healing phase iscompleted (~ 4
weeks).Obvious infec-tion and inadequate bony envelopmentindicate early
removal.Successful treatment ofalveolar frac-tures is associated with the pupal
healingafter the injury.When the fracture level isapical to the root tips,the
vascular supplyto the pulp is less at risk;however,iftheline ofthe fracture and
root apices are incontact,the teeth in the alveolar segmentare at a higher risk for
internal or externalresorption.In concomitant injuries,such asmaxillary or
mandibular fractures,earlymaxillomandibular fixation is accom-plished with a
technique that will allowfor dual treatment ofthe dental and/oralveolar injury and
the jaw injury (eg,arch bars and maxillomandibular fixa-tion).Perform the more
invasive openreduction ifindicated.Avulsive injuries will often exposebone and
jeopardize tooth support.Aimtreatment at soft tissue coverage in theform
ofjudicious mucosal advancementflaps.Consider early removal for teethwithout bony
support.Treatment ofTrauma to the Gingiva and Alveolar MucosaTraumatic injury to
the oral soft tissuemainly consists ofabrasion,contusion,and laceration.Ifthese
injuries are notaddressed,they can place the underlyingbony tissue at risk for
devitalization.Fre-quently these injuries may alert the sur-geon to underlying
trauma.The ultimategoal oftreatment is to reestablish vital softtissue bony
coverage.AbrasionAn abrasion is a superficialwound wherein the epithelial or
gingivaltissue is rubbed,worn,or scratched.Treat-ment consists oflocal cleansing
with amild disinfectant soap for the skin andsaline rinsing and/or irrigation ofthe
gin-giva.Antibiotic coverage is seldom neces-sary.Inspect the wound for possible
for-eign body (asphalt) accumulation,whichTable 21-5Splint RequirementsThe splint
should1.Be able to be applied directly in the mouth without delay owing to
laboratory procedures2.Stabilize the injured tooth in a normal position3.Provide
adequate fixation throughout the entire period ofimmobilization4.Neither damage the
gingiva nor predispose to caries and should allow for a basic oralhygiene
regimen5.Not interfere with occlusion or articulation6.Not interfere with any
required endodontic therapy7.Preferably fulfill esthetic demands8.Allow a certain
mobility (nonrigid) to aid periodontal ligament healing in cases offixation after
luxation injuries and replacement ofavulsed teeth;however,after root fracture,the
splint should be rigid to permit optimal formation ofa dentin callus to unite the
root fragments9.Be easily removed without re-injury to toothAdapted from Andreasen
JO,Andreasen FM.Textbook and color atlas oftraumatic injuries to the teeth.3rd
ed.Munksgaard;1994.p.347�8.FIGURE21-17Acid-etch splinting technique.A,Subluxed
tooth and alveolar fracture associated withmaxillary left central
incisors.B,Nonrigid passive placement ofsplint.Traumatized teeth are placedinto
preinjury alignment,acid-etched,and stabilized with composite resin.Splint is free
ofocclusionand soft tissue trauma.AB
Management ofAlveolar and Dental Fractures397could lead to unsightly accidental
tattoo-ing.Ifpresent,carry out meticulousremoval within 12 hours,with care not
tofurther inoculate the patient.58Theremoval process includes a technique
thataligns the surgical blade perpendicular tothe direction ofthe
abrasion.ContusionA contusion,a hemorrhageofsubcutaneous tissue without
lacerationor break ofoverlying soft tissue,is similarto a bruising injury caused by
blunt trau-ma.Treating gingival contusion includeslocal cleansing and
observation.Thisinjury may be associated with an underly-ing hematoma or ecchymotic
formation,which is generally self-limiting.Antibioticcoverage is usually
unnecessary.LacerationLacerations are the mostcommon form offacial
injury.Gingivallacerations may involve an underlyingbony defect.Treatment involves
earlycleansing and reapproximation.Removedevitalized tissue in a conservative man-
ner,and suture in a manner that limitswound tension.Consider antibiotic andtetanus
prophylaxis.More serious avulsivegingival wounds warrant close
inspectionofremaining tissue and underlying bonyintegrity.Exposure ofany underlying
bonydefect may indicate localized keratinizedsliding or advancement
flaps.Ifnonkera-tinized tissue is used for coverage,futuregrafting may be
indicated.Pediatric Dentoalveolar Trauma TreatmentThe poor coordination
ofpediatricpatients who are learning to walk,as wellas their relatively large pulp
chamber-to-tooth ratio,accounts for most pediatricdentoalveolar injuries.Managing
thepatient may require sedation and restraint;thus,additional factors must be dealt
withduring the treatment regimen.Displacement injuries are more preva-lent than are
tooth fractures in the prima-ry dentition secondary to the relativeresilience ofthe
surrounding bone.Simi-larly,these injuries are more common inthe pediatric
dentition than in the perma-nent dentition.Treating the primary dentition is dic-
tated by the likelihood that the perma-nent tooth bud may be compromised,secondary
to the buccal-occlusal positionofthe primary teeth to the permanenttooth bud
(Figure 21-19).TransmissionTable 21-6Sequence ofAcid-Etch Splinting
Technique*1.Perform alveolar bony reduction and/or replantation2.Perform localized
cleansing and d�bridement3.Isolate and dry area4.Custom fabricate wire (~26
Ga),double-stranded monofilament nylon line,or paper clipExtend wire to at least 1
or 2 teeth on either side ofthe involved tooth or teeth5.Etch the incisal halfofthe
labial surface ofthe involved and adjacent teeth with gelled phosphoric acid for
30�60 s6.Remove etchant with water stream for ~20 s7.Air dry etched surface;surface
should appear chalky white8.Passively place prefabricated wire to involved
teeth9.Stabilize splint with fast-setting autocure or light-cure composite
resin10.After resin is set,smooth rough edges with a fine acrylic or diamond
finishing bur(Check occlusion)11.Perform soft tissue and gingival repair as
needed12.Remove splint in 7�10 d *It may be prudent to use a composite shade that
differs from the natural color ofthe involved teeth as this will facilitate ease
ofremoval and prevent trauma to enamel.FIGURE21-18A,Blunt facial trauma resultingin
alveolar fracture and perioral soft tissue lacer-ations.B,Occlusal radiograph
confirming alveo-lar fracture with lingual displacement (�apicallock�) ofmandibular
central incisors and left lat-eral incisors(arrow).C,Alveolar fracture disim-
paction,reduction,and stabilization with archwire.D�bridement and repair ofperioral
soft tis-sues(arrow).ABC
398Part 4: Maxillofacial Traumaofforce to the developing tooth is possi-ble in
displacement injuries,which maycause interference with odontogenesis,ultimately
resulting in enamel discol-oration and/or hyploplasia (Figure 21-20).Table 21-7
provides a summary ofthetreatment regimen.Andreasen and Raven reported on
thegeneral prognosis ofthe traumatized per-manent successors,secondary to
forcesapplied by the primary dentition.Theyfound that the individual�s age at the
timeofinjury and the type ofluxation play amajor role in the errant development
ofthepermanent dentition (Figure 21-21).21,22,59FIGURE21-19Anatomic position ofthe
prima-ry dentition to the developing permanent toothbud.Note the �buccal-
occlusal�and �buccal-incisal�position ofthe primary roots(arrow).Table 21-
7Treatment ofPediatric InjuriesType ofInjuryTreatmentCrown fracturesClass I (enamel
only)Smooth rough edgesClass II (enamel and dentin)1.CaOH or glass ionomer liner
over dentin2.Composite resin restorationClass III (pulpal involvement)Vital
pulp1.Formocresol pulpotomy2.Coronal coverageNonvital pulp1.ZnOH-eugenol
pulpectomy2.Coronal coverage Class IV (root fracture)Apical thirdNo
treatment;follow-up Cervical third1.Remove tooth fragments2.Allow apical third to
resorb ifcompromise to permanent tooth bud is expectedLuxations
SubluxationMonitor/follow-upLateral luxationsRealign/remove
prnExtrusionRealign/remove prnIntrusion1.Allow to re-erupt 4�6 wk 2.Remove ifin
contact with permanent successor3.Remove ifinfection presentsprn = as
needed.FIGURE21-20A,Normal position ofprimary tooth to permanent tooth bud.B,Apical
intrusion ofpri-mary root impinging on permanent tooth bud.Blue arrowsdenote
permanent tooth bud.C,Hypoplasiaofpermanent tooth secondary to apical intrusion.ABC
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teeth dur-ing the administration ofgeneral anesthe-sia.Anesth Anal
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EE.Soft tissue and dentoalveo-lar injuries.In:Peterson LJ,Ellis E,HuppJR,Tucker
MR,editors.Contemporary oraland maxillofacial.2nd ed.St.Louis (MO):C.V.Mosby
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head injury infacial trauma victims:incidence andimpact.Ann Emerg Med
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microscopic study of117injured permanent teeth.Scand J Dent
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teeth on their perma-nent successors.II.A clinical and radi-ographic follow-up
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associated withtreatment oftraumatic injuries ofthe oralcavity-aspiration
ofteeth:report ofa case.JOral Surg 1953;11:242�342.29.Snawder KD,Bastawni
AE,O�Toole TJ.Toothfragments lodged in unexpected areas.JAMA
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maxillofacial injury:report ofa case.J Oral Surg 1972;30:839�40.31.Rowe NL,Killey
HC.The clinical examinationoffractures ofthe middle third ofthe facialskeleton
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J,Andreasen JO.Influence ofmatu-ration status and tooth type ofpermanentteeth upon
electrometric and thermal pulptesting.Scand J Dent Res 1976;84:286�90.33.Johnsen
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thenon-invasive measurement ofpupal bloodflow.Int Endod J
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thetreatment ofavulsed teeth.Oral Surg OralMed Oral Path Oral Radiol
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CHAPTER 22Principles ofManagement ofMandibular FracturesGuillermo E.Chacon,DDSPeter
E.Larsen,DDSManagement oftrauma has always beenone ofthe surgical subsets in which
oraland maxillofacial surgeons have excelledover the years.More
particularly,ourexperience with dental anatomy,head andneck physiology,and
occlusion providesus with unparalleled skills for the manage-ment ofmandibular
fractures.The mandible is the second mostcommonly fractured part ofthe maxillofa-
cial skeleton because ofits position andprominence.1,2The location and pattern
ofthe fractures are determined by the mech-anism ofinjury and the direction
ofthevector ofthe force.In addition to this,thepatient�s age,the presence
ofteeth,and thephysical properties ofthe causing agentalso have a direct effect on
the characteris-tics ofthe resulting injury.3Bony instability ofthe
involvedanatomic areas is usually easily recognizedduring clinical
examination.Dental mal-occlusion,gingival lacerations,andhematoma formation are
some ofthemost common clinical manifestations.In the management ofany bone frac-
ture,the goals oftreatment are to restoreproper function by ensuring union
ofthefractured segments and reestablishingpreinjury strength;to restore any
contourdefect that might arise as a result oftheinjury;and to prevent infection at
the frac-ture site.Restoration ofmandibular func-tion,in particular,as part ofthe
stomatog-nathic system must include the ability tomasticate properly,to speak
normally,andto allow for articular movements as ampleas before the trauma.In order
to achievethese goals,restoration ofthe normalocclusion ofthe patient becomes para-
mount for the treating surgeon.Basic principles oforthopedic surgeryalso apply to
mandibular fractures includ-ing reduction,fixation,immobilization,and supportive
therapies.It is well knownthat union ofthe fracture segments willonly occur in the
absence ofexcessivemobility.Stability ofthe fracture segmentsis key for proper hard
and soft tissue heal-ing in the injured area.Therefore,the frac-ture site must be
stabilized by mechanicalmeans in order to help guide the physio-logic process
toward normal bony healing.Reduction ofthe fracture can beachieved either with an
open or closedtechnique.In open reduction,as the nameimplies,the fracture site is
exposed,allow-ing direct visualization and confirmationofthe procedure.This is
typically accom-panied by the direct application ofa fixa-tion device at the
fracture site (Figure 22-1).A closed reduction takes place whenthe fracture site is
not surgically exposedbut the reduction is deemed accurate bypalpation ofthe bony
fragments and byrestoration ofthe functioning segments,for example,restoration
ofthe dentalocclusion by wiring the teeth together,using splints,or employing
external pins(Figure 22-2).Fixation must be able to resist the dis-placing forces
acting on the mandible.Itcan take one oftwo forms:direct or indi-rect.When direct
fixation is used,the frac-ture site is opened,visualized,and reduced;then
stabilization is applied across the frac-ture site.The rigidity ofdirect fixation
canrange from a simple osteosynthesis wireacross the fracture (ie,nonrigid
fixation) toa miniplate at the area offracture tension(ie,semirigid fixation) or a
compressionbone plate (ie,rigid fixation) to compres-sion screws alone (lag screw
technique).Indirect fixation is the stabilization oftheproximal and distal
fragments ofthe boneat a site distant from the fracture line.TheFIGURE22-1Open
reduction with internal fix-ation implies surgical exposure,visualization,and
manipulation with the placement ofa stabi-lization device directly along the bone
segmentsinvolved in the fracture.A locking reconstructionplate has been placed on
this injury via a sub-mandibular approach.
402Part 4: Maxillofacial Traumamost commonly used method formandibular fractures is
the use ofinter-maxillary fixation (IMF).A further ex-ample ofindirect fixation is
the use ofexternal biphasic pin fixation in combina-tion with an external frame
(Figure 22-3).Over the past three decades many dif-ferent techniques and approaches
havebeen described in the literature to surgi-cally correct facial fractures.More
recentlythe use ofinternal fixation utilizing plateshas shown the highest success
rates withthe lowest incidence ofnonunions andpostoperative infections.4�6The
origin ofplating as a treatment option for fracturescan be traced to Dannis and
colleagues,who reported the successful use ofplatesand screws for fracture repair
in 1947.7Later refinement ofthis technique is cred-ited to Allgower and colleagues
at the Uni-versity ofBasel,who successfully used thefirst compression plate for
extremity frac-ture repair in 1969.8However,it was notuntil 1973 that Michelet and
colleaguesreported on the use ofthis treatmentmodality for fractures ofthe facial
skele-ton.9In 1976 following Michelet�s success,a group ofFrench surgeons headed
byChampy developed the protocol that isnow used for the modern treatment
ofmandibular fractures.But it was not until1978 that these findings were published
inthe English literature.10Basically,there are two categories ofplating
systems:rigid compression platessuch as the AO/ASIF (Arbeits-gemein-schaft fur
Osteosynthesefragen/Associa-tion for the Study ofInternal Fixation)and the
semirigid miniplates.The advan-tages and disadvantages ofeach systemhave been
extensively discussed;however,the question remains:does compression offractures
really offer a clinically significantadvantage in terms ofbetter bone healingand
fewer complications? Proponents ofthe AO system state thatprimary or direct bone
healing is the mainadvantage offered by this system.When afracture is
compressed,absolute interfrag-mentary immobilization is achieved withno resorption
ofthe fragment ends,no cal-lus formation,and intracortical remodel-ing across the
fracture site whereby thefractured bone cortex is gradually replacedby new
haversian systems.11However,inother studies it has been shown thatabsolute rigidity
and intimate fractureinterdigitation is far from mandatory foradequate bony
healing.Compression is notnecessary at the fracture site for healing,and it is
questionable whether compressionstimulates osteogenesis.12,13Biomechanical
ConsiderationsStudies ofthe relationship between thenature,severity,and direction
oftraumaticforce on the resultant mandibular injurywere made by Huelke and
colleagues.14�19Before this,few experimental studies hadbeen done with regard to
the mechanism ofmandibular fracture.Most literature regard-ing the mechanism
offracture was based onclinical impressions and opinions.Early investigators showed
that linearfractures in long bones were initiated bybone failure resulting from
tensile strainrather than compressive strain.20Huelkeand Harger applied forces
ofvarying mag-nitudes and direction to dried mandiblesand observed the resultant
production oftension and compression.17They foundthat > 75% ofall experimentally
producedfractures ofthe mandible were in primaryareas oftensile strain,which
supported asimilar observation made earlier in longFIGURE22-2This panoramic
radiographdemonstrates the use ofwires to perform a closedreduction with
intermaxillary fixation ofa min-imally displaced right parasymphysis
fracture.FIGURE22-3Superior (A) and lateral (B) views ofa mandibular external
fixator.In this particular sys-tem,biphasic pins are applied transcutaneously
andare secured to one another using a universal jointsystem and rigid metal rods.BA
Principles ofManagement ofMandibular Fractures403bones.A notable exception was that
com-minuted condylar head injury that wasproduced by a load parallel to
themandibular ramus was primarily theresult ofcompressive force.In response to
loading,the mandible issimilar to an arch because it distributes theforce ofimpact
throughout its length (Fig-ure 22-4).However,unlike the arch,themandible is not a
smooth curve ofuni-form bone,but rather it has discontinu-ities such as
foramina,sharp bends,ridges,and regions ofreduced cross-sectionaldimension like the
subcondylar area.As aresult,parts ofthe mandible developgreater force per unit
area,and conse-quently,tensile strain is concentrated inthese locations.When a
force is directed along theparasymphysis-body region ofthemandible,compressive
strain developsalong the buccal aspect,whereas tensilestrain develops along the
lingual aspect.This produces a fracture that begins in thelingual region and
spreads toward the buc-cal aspect.17The mobile contralateralcondylar process moves
in a directionaway from the impact point until it is lim-ited by the bony fossa and
associated softtissue.At this point,tension developsalong the lateral aspect ofthe
contralater-al condylar neck,and a fracture occurs.Ifgreater force is applied to
the parasymph-ysis-body region,not only will tensiondevelop along the contralateral
condylarneck leading to fracture in this area,butcontinued medial movement ofthe
small-er ipsilateral mandibular segment will leadto bending and tension forces
along thelateral aspect and subsequent fracture ofthe condylar process on the
ipsilateral side.Force applied directly in the symphysisregion along an axial plane
is distributedalong the arch ofthe mandible.Becausethe condylar heads are free to
rotate with-in the glenoid fossa to a certain degree,tension develops along the
lateral aspect ofthe condylar neck and mandibular bodyregions,as well as along the
lingual aspectofthe symphysis.This leads to bilateralcondylar fractures and a
symphysis frac-ture (Figure 22-5).Variation from these standard fracturepatterns
occurs for two general reasons.First,there is a wide range in the possiblemagnitude
and direction ofthe impactand in the shape ofthe object deliveringthe
impact.Second,the condition ofthedentition,position ofthe mandible,andinfluence
ofassociated soft tissues couldnot be controlled in these studies.Early observers
felt that the presence ofposterior dentition tended to reduce theincidence
ofcondylar injury.21�23Theimplication was that,as the mandible wasforced
posteriorly and superiorly,the denti-tion would meet and absorb some
oftheforce,thereby diminishing the forcereceived at the condyle.This was
supportedRotational
movementpermittedCompressionCompressionCompressionCompressionCompressionTensionTens
ionTensionForceFIGURE22-4The effect ofa load on an arch where ends are free to
rotate.Adapted fromLarsen PE.Traumatic injuriesofthe condyle.In: Peterson
LJ,Indresano AT,Marciani RD,Roser SM,editors.Principles oforal and
maxillofacialsurgery.Vol 1.Philadelphia (PA): JB Lippincott Company; 1992.p.444.
404Part 4: Maxillofacial Traumaby the clinical observation that the posteri-or
dentition was often fractured on the sideofthe condylar fracture.However,morerecent
findings do not support this theoryand show that all types offractures
occur,irrespective ofthe occlusion,and that nocorrelation exists between the degree
ofdis-location,level offracture,or type offrac-ture with the presence ofa distal
occlu-sion.24Although the presence or absence ofa posterior dentition does not
correlatewith the incidence offracture,the presenceofspecific teeth,particularly
impacted thirdmolars,has been shown to markedly affectthe incidence ofmandibular
fractures.Itwas shown that,when impacted thirdmolars are present,this area
represented aregion ofinherent weakness and the inci-dence ofcondylar fractures
decreases,whereas the incidence ofmandibular anglefractures increases.25Although
unable to show that theocclusion played any role in the type offracture
produced,investigators havefound that the relative degree ofmandibu-lar opening at
the time ofimpact does playan important role in the type offracturethat
occurs.23,26More recent studies haveshown that not only is the incidence offracture
higher when the mouth is open,but the level offracture varies with
degreeofopening.When the mouth is opened,the fractures tend to be located more
inthe condylar neck or condylar head region,whereas when it is closed,fractures are
inthe subcondylar area.25Evaluation ofMandibular FracturesTraumatic craniofacial
and skull baseinjuries require a multidisciplinary teamapproach.Trauma physicians
must evalu-ate carefully,triage properly,and maintaina high index ofsuspicion to
improve sur-vival and enhance functional recovery.Frequently,craniofacial and skull
baseinjuries are overlooked while treatingmore life-threatening injuries.27Unno-
ticed complex craniofacial and skull basefractures,cerebrospinal fluid
fistulas,andcranial nerve injuries can result in blind-
ness,diplopia,deafness,facial paralysis,ormeningitis.Following the principles
ofAdvancedTrauma Life Support,during the initialassessment in the emergency
department,the first and most critical obligation is tomake sure that the airway is
patent andfree ofpotential obstruction.The tongue,which may have a tendency to fall
back,must be controlled,and objects obstruct-ing the airway must be
removed.Ifanobstruction cannot be removed,a new air-way must be established by
endotrachealintubation (remembering possible cervicalspine injuries) or
cricothyrotomy.Afterthe airway has been secured and respira-tion is occurring,vital
signs must beassessed,including pulse rate and bloodpressure.Any significant blood
loss is like-ly to be coming from injuries apart fromthose ofthe face.Other
critical injuriesmust be ruled out,including intracranialhemorrhages,cervical and
other spinalinjuries,chest injuries,abdominal trauma,and fractures ofthe long
bones.Local examination ofthe face and jawsshould be conducted in a logical
sequence.The first objective is to obtain an accuratehistory from the patient,or
relative ifthepatient cannot cooperate.Pertinent to
aCompressionCompressionTensionCompressionTensionTensionFIGURE22-5Force directed at
the symphysis along an axial plane is distributed along the arch
ofthemandible.Tension is dissipated along the mandible,and the fracture occurs
bilaterally in the area ofleast stability,the condylar neck.As in other fractures,a
symphysis fracture may develop caused bytension from the blow.Adapted fromLarsen
PE.Traumatic injuries ofthe condyle.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM,editors.Principles oforal and maxillofacial surgery.Vol 1.Philadelphia (PA): JB
Lippincott Company; 1992.p.445.
Principles ofManagement ofMandibular Fractures405fractured mandible examination is
nota-tion ofthe size,number,and force ofanyblows to the face.Patients often
complain ofthe following:�Pain or tenderness is often present atthe site ofimpact
with the possibilityofa direct fracture,or at a distant sitein the case ofan
indirect fracture.�Difficulty chewing.Pain could be lim-iting mandibular function
or theremay be a malocclusion or mobility atthe fracture site.�Malocclusion.The
patient may be ableto tell the clinician ofan alteration inthe bite from
normal;however,patients are not always reliable andmay claim that the bite feels
normalwhen it is not and vice versa.�Numbness in the distribution oftheinferior
alveolar nerve.This usuallyindicates a displaced fracture in theregion ofthe body
or angle ofthemandible on the affected side.Anondisplaced fracture often does
notgive rise to numbness in the distribu-tion ofthe inferior alveolar
nerve.Clinical ExaminationThe clinical examination should consist ofinspection and
palpation.It is best to pro-ceed in an orderly fashion and to performthis
evaluation as a component part oftheentire head and neck examination ofthetrauma
patient.The skin ofthe face and,inparticular,the area around the mandibleshould be
inspected for swelling,hematomas,and lacerations.A commonsite for a laceration is
under the chin,andthis should alert the clinician to the possi-bility ofan
associated subcondylar or sym-physis fracture.Typically,the patient whohas suffered
a fracture ofthe mandibularcondyle will present with facial asymmetry(Figure 22-
6).This is owing to the loss ofthe vertical height ofthe ramus on the sidewith the
fracture,resulting in a shift ofthemandible to the ipsilateral side.The best
routine to evaluate facialfractures is to start at the top and workdown,assessing
the stability oftheanatomic structures in a mediolateralfashion.It is best to begin
the examina-tion from behind the seated or supinepatient (Figure 22-7).The
clinicianshould palpate the movement ofthecondyle both over the lateral aspect
ofthejoint and through the external acousticmeatus and observe the movement
ofthemandible itself.Ifa unilateral condylarfracture is present,a subjective
assessmentcan then be made between the palpablemovement ofone side compared with
theother.Failure to detect the translation ofthe condyle,especially when
associatedwith pain on palpation,is highly indica-tive ofa fracture in this
area.Palpationwill frequently confirm tenderness overthe lateral pole ofthe injured
condylewith associated crepitation.However,inthe case offracture
dislocations,thecondyle may not be palpable.Any significant deviation on openingmay
be indicative ofsubcondylar fractureon the side to which the mandible devi-ates.To
better evaluate this area,the fifthfinger is placed in each acoustic meatusand the
patient is asked to open and closethe mouth.On opening,the mandible fre-quently
shifts even more toward the side ofthe fracture as a result ofdecreased trans-
lation ofthe condyle on the injured side.As mentioned before,in unilateral frac-
tures,there is deviation ofthe occlusiontoward the fractured side,with
prematureocclusal contact in the posterior region onthat side.This results because
the lateralpterygoid muscle on the fractured sidepulls on the fractured segment and
doesnot have any protruding influence on themandible.The lateral pterygoid muscle
onthe contralateral side is unopposed andthus causes deviation to the fractured
side.The midlines no longer coincide,andthere is an open bite in the body region
onthe contralateral side.This is often accom-panied by fracture ofthe posterior
denti-tion on the same side as the condylar frac-ture (Figure 22-8).Ifbilateral
condylar fractures are pre-sent,the occlusion may not be deviated.The midlines are
often coincident,andFIGURE22-6Patient with significant lower faceecchymosis and
asymmetry as a result ofa sym-physis fracture,bilateral subcondylar fractures,and a
Le Fort I fracture resulting from a directimpact to the chin during a
fall.FIGURE22-7Bimanual palpation ofthemandible by the surgeon in a cephalad
positionallows excellent evaluation and comparison ofthe anatomic structures.
406Part 4: Maxillofacial Traumapremature contact is present bilaterally onthe
posterior dentition with an anterioropen bite.The posterior dentition may
befractured on both sides in these situations.Often the patient with a fracture
ofthecondylar process also has a limited rangeofmotion.This limitation,however,is
pri-marily caused by voluntary restriction as aresult ofpain.One has to keep in
mindthat any limitation ofmandibular move-ment may also be a result ofreflex
musclespasm,temporomandibular effusion,ormechanical obstruction to the
coronoidprocess resulting from depression ofthezygomatic arch.Other less common
find-ings include blood within the externalauditory canal and,in the case
offracturedislocation,development ofa prominentpreauricular depression.Careful
otoscopicevaluation ofthe external auditory canal isofparticular importance in
patients sus-pected to have suffered an injury at thislevel.Occasionally a fracture
ofthe condy-lar process will produce a tear in theepithelial lining ofthe anterior
wall ofthecanal,which produces bleeding from theacoustic meatus.It is important to
deter-mine that this bleeding is not coming frombehind a ruptured tympanic
membrane,which may signify a basilar skull fracture.A detailed intraoral
examinationshould be undertaken with good lightingand immediate availability
ofsuction.Themost common intraoral findings are mal-occlusion,fracture ofthe
dentition,anddecreased interincisal opening.Continuing with the systematic evalu-
ation ofthe patient,it is suggested thatexamination ofthe soft tissues be under-
taken next.The gingival tissue should beinspected for tears or lacerations.With
theaid ofa tongue blade,the floor ofthemouth is examined;sublingual ecchymosisis
almost pathognomonic ofa fracture ofthe mandible.Next the dentition is exam-ined
for evidence ofbroken teeth and forsteps or irregularities in the dental arch.The
patient is asked to lightly bite the teethtogether and to say whether the bite
feelsdifferent from normal,following which theocclusion is inspected.Premature
occlusalcontacts are noted.The three causes ofanaltered occlusion in the trauma
patient area displaced fracture,a dental injury such asa displaced tooth,and a
temporomandibu-lar joint effusion or dislocation.Ifthe patient is edentulous and
hasintact dentures with him,these can bereplaced in the mouth and the
occlusioninspected (Figure 22-9).The mandibleshould then be grasped on each side
ofanysuspected fracture and gently manipulatedto assess mobility.Ifno fracture can
befound but clinical suspicion remains high,the mandible may be compressed
byapplying pressure over both angles (Figure22-10).This nearly always gives rise
topain at a fracture site.In the case ofsub-condylar fractures,firm posterior
pressureon the chin will cause pain in the pre-auricular region.Radiographic
EvaluationTo adequately screen for the presence ofamandibular fracture,at least two
views atright angles to each other are necessary.Apanoramic radiograph and a
reverseTowne�s view (Figure 22-11) are adequatescreening studies for this
purpose.Ifonlyone view is used,fractures can easily bemissed.28In the multiple-
trauma patientfor whom panoramic radiographs are notpossible,lateral oblique views
may be sub-stituted.Other radiographic views thatmay be useful depending on the
circum-stances are posteroanterior mandibular,mandibular occlusal,and
periapical.Lineartomographies ofthe temporomandibularjoints can also be useful in
the evaluationoffractures at the level ofthe condylarprocess.However,intracapsular
fracturesFIGURE22-8Significant midline deviationtoward the fracture side along with
buccal cusptip fractures ofboth mandibular bicuspids andfirst molar.FIGURE22-9The
patient�s own dentures oftenbecome very useful instruments in the assessmentand
management ofmandibular fractures in theedentulous patient,ifthey are intact or can
bereasonably repaired.FIGURE22-10The application ofgentle biman-ual pressure over
the angle regions can unmask aminimally displaced fracture in the anteriorregion
ofthe mandible.
Principles ofManagement ofMandibular Fractures407ofthe condylar head are often
difficult tovisualize accurately on plain films.The typical radiographic
findingswhen a condylar fracture is present are thefollowing:a shortened condylar-
ramuslength;the presence ofa radiolucent frac-ture line or,in the case ofoverlapped
seg-ments,the presence ofa radiopaque double density (Figure 22-12);and evi-dence
ofpremature contact on the side ofthe fracture ifthe radiograph was takenwith the
patient in occlusion.Ifmoreaccurate information ofthe involvementofthe
temporomandibular joint isrequired,axial and coronal computedtomography (CT) scans
offer an excellentopportunity to study the fracture details.Indications for CT
scans are the following:1.Significant displacement or disloca-tion,particularly
ifopen reduction iscontemplated2.Limited range ofmotion with a suspi-cion
ofmechanical obstruction causedby the position ofthe condylar segment3.Alteration
ofthe surrounding osseousanatomy by other processes,such asprevious internal
derangement ortemporomandibular joint surgery,tothe degree that a pretreatment
base-line is necessary4.Inability to position the multiple-trauma patient for
conventional radi-ographs (CT scans may be the only useful radiograph that can be
obtained)Chayra and colleagues reviewed theneed for a complete series
offilms.29Theyconcluded that the initial screening ofpatients could be effectively
undertakenwith a panoramic radiograph alone.Ninety-two percent offractures were
seen on apanoramic radiograph alone,comparedwith only 66% on a routine
radiographicseries without a panoramic view.However,in order to accurately
visualize displace-ment it is recommended that the standardmandibular views consist
ofa panoramicradiograph,a posteroanterior mandibularview,and reverse Towne�s view
(Figure 22-13).The latter view allows for visualizationofthe degree ofmedial or
lateral displace-ment ofthe fracture and unveils injuries inwhich only subtle
deviation is present,suchas is seen in greenstick fractures,which arenot readily
evident on panoramic view.The panoramic radiograph usuallyrequires the patient to
be able to standupright and also requires accurate patientpositioning for good-
quality films.In theseverely traumatized patient,this may bedifficult to achieve
with some machines.Further,mesiolateral displacement in theramus and body and
anteroposterior dis-placement in the symphyseal regions mayalso be difficult to
visualize.The traditionallateral oblique views ofthe mandible can beused when
panoramic films are not pos-sible.They require accurate positioning ofthe patient
and film to obtain useful views,particularly in the condylar area.A trans-cranial
temporomandibular view may be agood addition in these circumstances.Accurate
assessment ofsymphysealfractures may be problematic with thestandard views.A
mandibular occlusalview is particularly useful in this scenario.It also aids in the
assessment ofthe frac-ture ofthe lingual plate,particularly invery oblique
fractures.Periapical viewsmay also be necessary for evaluation oftheteeth on either
side ofthe fracture line toassess root fractures,periapical and peri-odontal
pathology,and the relationship ofthe fracture line to the periodontal liga-ment
ofeach tooth.ClassificationThe first step in the development ofanappropriate
treatment plan is to establisha clear understanding ofthe type ofinjury the patient
has suffered,in orderto provide an adequate surgical solution.In the diagnostic
work-up phase,the lackofstandardized ways to assess and FIGURE22-11Obtaining at
least two radiographic viewsofthe mandible facilitates identification ofdiscreet
injuriesand also allows for a better assessment ofthe degree ofdis-placement ofthe
fracture segments.A significantly rotatedproximal segment ofthe right angle
fracture is apparent inthe panoramic radiograph (A),whereas the same
fractureappears almost nondisplaced in the Towne�s view (B).ABFIGURE22-12Panoramic
radiograph showingclear findings ofa right condylar neck fracture.
408Part 4: Maxillofacial Traumacharacterize the nature and severity ofthe orofacial
injury engenders variationin practice patterns.30Probably the mostbasic question
one should ask at the ini-tial evaluation is whether the fracturesare displaced or
nondisplaced.Depend-ing on the amount ofenergy transmittedto the facial skeleton
and the vector inwhich such force is directed,there will bemore or less disruption
ofthe normalanatomic structures.Muscle attachmentand their counteracting forces
also play aprimary role in the pattern and directionofthe fractures.It is the
displacing forcesofthe muscles ofmastication that influ-ence favorableness (Figures
22-14 and22-15).The principle offavorableness isbased on the direction ofa fracture
lineas viewed on radiographs in the horizon-tal or vertical plane.A horizontally
favor-able fracture line resists the upward dis-placing forces,such as the pull
ofthemasseter and temporalis muscles on theproximal fragment when viewed in
thehorizontal plane.A vertically favorablefracture line resists the medial pull
ofthemedial pterygoid on the proximal frag-ment when viewed in the vertical
plane.In the parasymphyseal region ofthemandible,the combined action
ofthesuprahyoid and digastric muscles on abilateral fracture can pull on the
distalfragment inferiorly in unfavorable frac-tures,putting the patient at risk for
acuteupper airway obstruction.The first concern is whether there areindeed
fractures present,and ifthere are,where they are located anatomically.Mandibular
fractures may be further clas-sified by the pattern offracture (Figure 22-16)
present and by anatomic location.Many systems ofclassification havebeen applied to
fractures involving themandibular condyle.24,31�35The recom-mended classification
parallels the com-prehensive classification set forth by Lin-dahl.24As mentioned
before,it isimperative that radiographs be taken ofthe suspected injury in two
planes at rightangles to each other.The following majorrelations are noted:the
level ofthe frac-ture;the relation ofthe condylar frag-ment to the mandible,termed
the degreeofdisplacement; and the relation ofthecondylar head to the fossa,or the
degree ofdislocation.FIGURE22-13Mandible series ofa patient with a left subcondylar
fracture.The series consists ofpos-teroanterior (A),Towne�s (B),left lateral
oblique,(C) and right lateral oblique (D) views.Ifapanoramic radiographic machine
is readily available,the lateral oblique shots can be replaced by apanoramic
view.ABCDFIGURE22-14Diagram ofhorizontally unfa-vorable(left) and favorable(right)
fracturelines.Arrowsindicate displacing forces.AdaptedfromLuyk NH.88p.410.
Principles ofManagement ofMandibular Fractures409Anatomic LocationThe following
classification has been mod-ified from Kelly and Harrigan�s epidemio-logic study in
which they dividedmandibular fractures based on theiranatomic
location36:�Dentoalveolar fracture:Any fracturethat is limited to the tooth-
bearingarea ofthe mandible without disrup-tion ofcontinuity ofthe underlyingosseous
structure�Symphysis fracture:Any fracture inthe region ofthe incisors that runsfrom
the alveolar process through theinferior border ofthe mandible in avertical or
almost vertical direction�Parasymphysis fracture:A fracture thatoccurs between the
mental foramen andthe distal aspect ofthe lateral mandibu-lar incisor extending
from the alveolarprocess through the inferior border �Body fracture:Any fracture
that occursin the region between the mental fora-men and the distal portion ofthe
sec-ond molar and extends from the alveo-lar process through the inferior
border�Angle fracture:Any fracture distal tothe second molar,extending from
anypoint on the curve formed by thejunction ofthe body and ramus in theretromolar
area to any point on thecurve formed by the inferior border ofthe body and
posterior border oftheramus ofthe mandible�Ascending ramus fracture:A fracture
inwhich the fracture line extends hori-zontally through both the anterior
andposterior borders ofthe ramus or thatruns vertically from the sigmoid notchto
the inferior border ofthe mandible�Condylar process fracture:A fracturethat runs
from the sigmoid notch tothe posterior border ofthe ramus ofthe mandible along the
superioraspect ofthe ramus;fractures involv-ing the condylar area can be
classifiedas extracapsular or intracapsular,depending on the relation ofthe frac-
ture to the capsular attachment Pattern ofFractureThe following classification is
based on pat-tern offracture (see Figure 22-16):�Simple fracture:A simple fracture
con-sists ofa single fracture line that doesnot communicate with the
exterior.Inmandibular fractures this implies afracture ofthe ramus or condyle or
afracture in an edentulous portion withno tears in the periosteum.�Compound
fracture:These fractureshave a communication with the externalenvironment,usually
by the periodontalligament ofa tooth,and involve all frac-tures ofthe tooth-bearing
portions ofthe jaws.In addition,ifthere is a breachofthe mucosa leading to an
intraoralcommunication or a laceration oftheFIGURE22-15Diagram ofvertically
favorable(left) and unfavorable(right) fracture lines.Arrow indicates displacing
force.Adapted fromLuyk NH.88p.410.FIGURE22-16Types offractures: A,simplefracture;
B,compound fracture; C,comminutedfracture; D,impacted fracture in right subcondy-
lar area and pathologic fracture in the left anglearea; E,direct and indirect
fractures.AdaptedfromLuyk NH.88p.411.ABCDE
410Part 4: Maxillofacial Traumaskin communicating with the fracturesite,edentulous
portions ofthemandible may be involved.�Greenstick fracture:This type offrac-ture
frequently occurs in children andinvolves incomplete loss ofcontinuityofthe
bone.Usually one cortex is frac-tured and the other is bent,leading todistortion
without complete section.There is no mobility between theproximal and distal
fragments.�Comminuted fractures:These arefractures that exhibit multiple frag-
mentation ofthe bone at one fracturesite.These are usually the result ofgreater
forces than would normally beencountered in simple fractures.�Complex or
complicated fracture:Thistype ofinjury implies damage to struc-tures adjacent to
the bone such as majorvessels,nerves,or joint structures.Thisusually implies damage
to the inferioralveolar artery,vein,and nerve inmandibular fractures proximal to
themental foramen and distal to themandibular foramen.On rare occasionsa peripheral
branch ofthe facial nervemay be damaged or the inferior alveolarnerve injured in
subcondylar fractures.�Telescoped or impacted fracture:Thistype ofinjury is rarely
seen in themandible,but it implies that one bonyfragment is forcibly driven into
theother.This type ofinjury must be dis-impacted before clinical movementbetween
the fragments is detectable.�Indirect fracture:Direct fractures ariseimmediately
adjacent to the point ofcontact ofthe trauma,whereas indi-rect fractures arise at a
point distantfrom the site ofthe fracturing force.An example ofthis is a
subcondylarfracture occurring in combinationwith a symphysis fracture.�Pathologic
fracture:A pathologic frac-ture is said to occur when a fractureresults from normal
function or mini-mal trauma in a bone weakened bypathology.The pathology
involvedmay be localized to the fracture site,such as the result ofa cyst or
metasta-tic tumor,or as part ofa generalizedskeletal disorder,such as
osteopetrosis.�Displaced fracture:Fractures may benondisplaced,deviated,or
displaced.A nondisplaced fracture is a linearfracture with the proximal
fragmentretaining its usual anatomic relation-ship with the distal fragment.In
adeviated fracture,a simple angulationofthe condylar process exists in rela-tion to
the remaining mandibularfragment,without development ofagap or overlap between the
two seg-ments.Displacementis defined asmovement ofthe condylar fragmentin relation
to the mandibular segmentwith movement at the fracture site.The fragment can be
displaced in a lat-eral,medial,or anteroposterior direc-tion.In displaced fractures
the articu-lar surface ofthe condyle remainswithin the glenoid fossa and does
notherniate through the joint capsule.�Dislocated fracture:A dislocationoccurs when
the head ofthe condylemoves in such a way that it no longerarticulates with the
glenoid fossa.When this is associated with a fractureofthe condyle,it is termed a
fracturedislocation.Fracture dislocations arediscussed more completely later in
thischapter.The mandibular condyle mayalso be dislocated as a result
oftraumawithout an associated condylar frac-ture.Dislocations can occur anterior-
ly,posteriorly,laterally,and superiorly.�Special situations:Other types offrac-
tures that do not readily fit the aboveclassification include grossly commin-uted
fractures or fractures involvingadjacent bony structures,such as theglenoid fossa
or tympanic plate;openor compound fractures;and fracturesin which a combination
ofseveral dif-ferent types offractures exist.Openfractures ofthe condyle are
usuallycaused by missiles such as bullets.Nonfracture Injuries ofthe Articular
ApparatusThe most commonly documented result oftrauma to the articular apparatus
andmandibular condyle is fracture.Otherinjuries occur as well and must be
consideredin the differential diagnosis (Table 22-1).Anterior dislocationoccurs
when thecondyle moves anterior to the articulareminence.This is by far the most
commonsituation and represents a pathologic for-ward extension ofthe normal
translationalmovement ofthe condylar head.Unlikesubluxation,which is also a forward
exten-sion ofthe condyle,dislocation is not self-reducing.Dislocation may be caused
byyawning,oral sex,phenothiazine use,andtrauma.Traumatically induced
anteriordislocation is most commonly bilateral,but it may occur unilaterally
(particularlyifassociated with a concomitant fractureelsewhere in the mandible).The
diagnosisofan anteriorly dislocated mandible ismade by the following clinical
features:ananterior open bite with the inability toclose the mouth;severe pain in
the regionTable 22-1Injuries ofthe ArticularApparatusEffusionHemorrhagic or
serousSoft tissue injuryDiskCapsuleLigamentsDislocation ofthe condyle from the
fossaWithout fractureWith fracture other than condyleWith associated condylar
fractureFractureNondisplacedDeviatedDisplacedDislocatedComminutedInvolving adjacent
bony structuresCombinations ofthe above
Principles ofManagement ofMandibular Fractures411anterior to the ear;absence ofthe
condylefrom the glenoid fossa with a visible andpalpable preauricular
depression;inabilityto move the mandible except to open themouth slightly in a
purely rotational man-ner;difficulty in speaking;and a prognath-ic lower
jaw.Finally,ifunilateral disloca-tion is present,the chin will be deviated tothe
opposite side (Figure 22-17).Patientswith anterior dislocation ofthe mandibu-lar
condyles without other mandibulartrauma should be approached using thefollowing
treatment protocol:2 cc oflocalanesthetic solution should be depositedinto the
joint capsule followed by manualreduction.Ifthis is unsuccessful or thepatient is
overly apprehensive,diazepamshould be carefully titrated intravenouslyfollowed by
further attempts at manualreduction.Ifthese measures fail,then gen-eral anesthesia
with the use ofa musclerelaxant may be necessary.37It is usuallypossible to reduce
an acute dislocation withthese maneuvers.In refractory cases or incases associated
with mandibular body andangle fractures in which the dislocated seg-ment is
difficult to control by manipula-tion,surgical intervention may be required.A
percutaneous bone hook placed throughthe sigmoid notch or wires placed throughthe
angle ofthe mandible allow for addi-tional downward
traction.38,39Followingsuccessful reduction,the patient should beinstructed to
refrain from opening his orher mouth widely and to support the jawwith a hand under
the chin when yawningfor a period of3 weeks to allow for healingofthe injured soft
tissue in and around thejoint.IMF is not necessary for a first-timeacute anterior
dislocation ofthe jaw,unless it persistently dislocates
afterreduction.Inpersistent,recurrent dislo-cation,contributing factors,such as
phe-nothiazine use,should be identified.Asoft diet may also be recommended
forseveral days along with a nonsteroidalanti-inflammatory analgesic.When a blow to
the mandible pro-duces primarily a posterior vector offorceand does not result in
fracture ofthecondylar neck,the head ofthe condylemay be forced into a posterior
dislocation.This injury is frequently associated withlaceration and fracture ofthe
externalauditory canal leading to hemorrhage thatis visible at the external
acoustic meatus.26In most cases maintenance ofthe patient�socclusion and treatment
ofthe associatedear injuries are the only management pro-cedures necessary.Lateral
dislocationofthe condylar headis always associated with a concomitantfracture
either ofthe condyle or elsewherewithin the mandible.The diagnosis ofthiscondition
is straightforward.The condylarhead is palpable as a hard mass either in
thepreauricular region or in the lower part ofthe temporal space.This type ofinjury
isassociated with a marked crossbite,which isnot attributable solely to the
mandibularfracture but instead is secondary to the dis-placed condyle.Treatment
requires reduc-tion ofthe dislocation through manipula-tion ofthe dislocated
segment by graspingit with a thumb on the dentition and withthe fingers extraorally
along the body ofthemandible.Ifthe proximal segment size isinadequate for this
maneuver,a percuta-neous towel clip through the angle or asmall incision with
placement ofa wirethrough the angle (as described for anteriordislocation) may be
necessary.After reduc-tion ofthe dislocation,treatment oftheassociated fracture is
accomplished,prefer-ably with rigid internal fixation.Superior dislocationinto the
middlecranial fossa without associated fracture ofthe mandibular condyle has
beendescribed.The patient is predisposed tothis type ofdislocation when the
condylarhead is small and rounded.40This injury ismore common when the mouth is
open atthe moment ofimpact.41This type ofinjury usually occurs with
concomitantmidface fractures that are telescoped,causing shortening ofthe vertical
dimen-sion ofthe face and allowing superior dis-location ofthe mandibular
condyle.Supe-rior dislocation ofthe mandibular condyleis associated with cerebral
contusion andbasilar skull fracture with facial nerveparalysis and deafness.These
patients pre-sent with severe restriction ofinterincisalopening,pain in the area
ofthe temporo-mandibular joint,bleeding from the exter-nal auditory canal or
hemotympanum,and deviation ofthe jaw to the affectedside.A variety oftreatment
modalities arerecommended,including observation,condylotomy,elastic
traction,condylecto-my,and manual reduction.42Neurosurgi-cal consultation is
required.Effusion and hemarthrosisofthetemporomandibular joint after traumaoccur
similarly as in other joints.23Inmost cases this leads to a distention ofthe joint
capsule with varying amountsofdiscomfort.Frequently deviation ofthe mandible away
from the affected sideoccurs as a result ofdownward pressureon the condyle from the
production ofFIGURE22-17Prognathic appearance,chindeviation,and a large amount
ofswelling on theright side ofthe face as a result ofa right unilat-eral condylar
dislocation,which occurred as aresult ofa blow to the chin during a motor ve-hicle
crash.
412Part 4: Maxillofacial Traumafluid within the joint.This producesfacial asymmetry
and malocclusion (Fig-ure 22-18).The treatment oftraumaticallyinduced effusions
ofthe temporo-mandibular joint is aimed at the restora-tion ofpreinjury occlusion
with return tofunction and reliefofpain.Ifthe patientpresents with the subjective
symptoms ofajoint effusion but has a stable and repro-ducible occlusion,the
condition may bemanaged with close daily observation,nonsteroidal anti-inflammatorv
medica-tions,and a soft diet.Frequently the con-dition will resolve in a matter
ofdays.If,however,the malocclusion is significantenough that the patient is unable
toachieve a stable occlusion without manip-ulation ofthe jaw,Ivy loop wiring or
archbars should be placed and guiding elasticsused to produce a stable
occlusion.Arthrocentesis,arthroscopy,or both arecommon therapies for hemarthrosis
inother joints and may also be considered.43Regardless ofthe therapy
chosen,careshould be taken to avoid excessive IMFbecause this may result in a long-
term lim-itation offunction.It has been suggestedthat this limitation in function
is a resultoforganization ofthe blood within thejoint space with development
offibrosisand subsequent ankylosis.Many authorshave emphasized the importance
ofthisproposed mechanism in the developmentofankylosis.44,45Aspiration or
arthroscop-ic lavage may alleviate this.It is possible,however,that the development
oflimitedfunction and ankylosis is more dependenton the inability to maintain a
full range ofmotion during the IMF period rather thanon the hemarthrosis.This
theory is sup-ported by the failure ofexperimentallyinduced hemarthroses to produce
ankylo-sis,46and by the absence ofankylosis andlimited function after
iatrogenicallyinduced hemarthroses during joint injec-tions or arthroscopy.47Most
likely,decreased range ofmotion after joint effu-sion is the result ofintra-
articular fibrosispotentiated by prolonged IMF.Treatment ofMandibular
FracturesFractures ofthe mandible have been report-ed to comprise between 40 and
62% ofallfacial fractures,36,48,49although these figuresmay not represent the true
incidencebecause isolated nasal fractures are seldomincluded in such
surveys.Ifthese injuries aretaken into account,the occurrence ofmandibular
fractures decreases to anywherebetween 10 and 25% ofall facial fracturesdepending
on the mechanism ofinjury.50The literature is consistent on the fact thatabout one-
halfofall patients who suffermandibular fractures are involved in amotor vehicle
accident.2,48,51�53Males areoverwhelmingly reported to be affectedmore frequently
than females in a ratio rang-ing from 3:1 to 7:1 depending on the surveyand
especially the country involved.48,54,55Predictably,such studies reveal the most
sus-ceptible age group for both sexes is between21 and 30 years ofage.54,56,57In
most cases,mandibular fracturesare encountered in isolation from anyother facial
fractures.But different studieshave revealed that almost 20% ofthesepatients have
concomitant fractures inother anatomic structures ofthe facialskeleton,58�60with
the most common onebeing the zygomaticomaxillary complex.61Further injury away from
the facial regionmay also be present,including multiple-system trauma.In the study
by Ellis andcolleagues of2,137 patients with mandibu-lar fractures,10.5% ofsubjects
sustainedother injuries outside the maxillofacialregion.48Injury patterns are
largely depen-dent on the mechanism ofinjury,withpatients involved in motor vehicle
acci-dents sustaining a great percentage ofotherinjuries.The distribution
ofprincipal frac-ture sites has been reported as 33% involv-ing the body,29% in the
condylar region,23% the angle,and 8% in the symphysisregion (Figure 22-19).It is
not unusual tosustain more than one fracture site in themandible.Mandibular
fractures are mul-tiple in more than 50% ofthe cases.48,62,63The left side is more
commonly involved,in particular the left angle,probablybecause most assailants are
right-handedand the left side ofthe jaw would be theside most likely to be
struck.57Falls show agreater proportion ofsubcondylar frac-tures,as high as 36.3%
in one study.49When multiple fractures ofthe mandibleare considered,the most common
combi-nations are angle and opposite body,bilat-eral body,bilateral angle,and
condyle andopposite body (Figure 22-20).36The site offracture is also determinedby
the size,direction,and surface area ofthe impacting blow.An impact to the
chinFIGURE22-18Significant facial asymmetry (A)and malocclusion (B) resulting from
a large lefttemporomandibular joint hemarthrosis.AB
Principles ofManagement ofMandibular Fractures413with a line offorce through the
symphysisand temporomandibular joints will pro-duce a single subcondylar fracture
at 193 kg (425 lb.) and a bilateral subcondy-lar fracture at about 250 kg (550
lb.),whereas symphyseal fractures requireforce between 250 and 408 kg (900
lb.).64An impact to the lateral aspect ofthemandibular body using a 2.5 �10 cm (1
�4 in.) impact surface will produce amandibular fracture at 136 to 317 kg(300�700
lb.).When an impact force isdelivered to the mandible,the bone
bendsinward,producing compressive forces onthe impacted (lateral) surface and
tensileforces on the lingual (medial) surfaces ofthe bone opposite the impact
site.18Frac-ture results when the tensile strain over-comes the resistance ofthe
bone,begin-ning on the medial side ofthe mandibleand progressing through the bone
towardthe impact point.Direct fracture may occur at the site ofimpact,but
additional indirect fracturesmay result when higher forces areinvolved.An example
would be a blow tothe left angle,causing a direct fracture atthe left-angle region
and an indirect frac-ture in the right body.Occasionally,onlyindirect fracture
results,usually in the sub-condylar area as,for example,when a blowon the chin
results in a fracture ofeithercondylar neck.Indirect fractures demon-strate the
opposite tensile strain patternsand fracture outcomes from those ofthedirect
fracture;that is,the tensile straindevelops on the side opposite to theimpact.In
the case ofgreenstick fractures,the fracture occurs on the tension side andbending
occurs on the compression side.General Approach and Goals ofTherapyDeciding on the
correct treatment is oftenmore difficult than administering thetreatment itself.The
dilemma concerningthe appropriate management offracturesofthe mandibular condyle is
most exem-plary ofthis.Technically easy proceduressuch as closed reduction have
experiencedlong-term successful results,whereas morecomplicated and technically
demandingprocedures ofopen reduction have con-tinually and cyclically been employed
inan attempt to improve on the resultsobtained with closed
reduction.Althoughanatomic reduction with rigid internalstabilization ofthe
fracture segments maybe desirable,it is essential that the surgeonclearly define
the goals oftherapy andchoose the simplest and most effectivesurgical method
available to reach them.The goals to be achieved in treatmentoffractures ofthe
mandible are listed inTable 22-2.Maintenance ofa stable occlu-sion is necessary for
both functional andesthetic reasons.Complete range ofmotionalso allows normal
mastication and pre-vents the development ofcontralateral tem-poromandibular joint
dysfunction.A nor-mal range ofmotion is most dependent onpostoperative retraining
ofthe muscles andelimination ofpain.Ideally,the disk-condylar relationship should
remain intactwithout evidence ofinternal derangement.Some clinical signs ofinternal
derangementsuch as joint noise can be tolerated ifnotassociated with pain or
decreased range ofmotion.Growth disturbance can resultfrom ankylosis or from injury
to the carti-laginous head ofthe condyle.A goal oftreatment should include early
mobilizationto prevent ankylosis and close follow-up toidentify growth changes
early in their devel-opment.Attainment ofan anatomic bonyunion is not a primary
goal in treatment of29.34.823.11.433.08.4FIGURE22-19Percentage ofmandibular
fracturesite distribution.Adapted fromLuyk NH.88p.411.ABCDFIGURE22-20Most common
multiple mandibular fracture sites:A,angle and opposite body;B,bilateral
body;C,bilateral angle; andD,condyle and opposite angle.Adapted fromLuyk
NH.88p.413.
414Part 4: Maxillofacial Traumacondylar fractures,particularly ifit must bedone at
the expense ofother more impor-tant goals.A malunion or fibrous unionthat functions
normally without pain ispreferable to a radiographically excellentreduction that
does not eliminate pain orlimitsmotion.Treatment OptionsClosed ReductionIfthe
principle ofusing the simplest method to achieve opti-mal results is to be
followed,the use ofclosed reduction for mandibular fracturesshould be widely
used.According to Bern-stein,�It is safe to say that the vast majori-ty offractures
ofthe mandible may betreated satisfactorily by the method ofclosed reduction.�65May
and colleagues gofurther66:�Many fractures are probablyovertreated by open
reduction.It is impor-tant to realize that the majority offrac-tures can be
successfully managed by con-servative means (closed reduction).�Thisconcept becomes
critical when one con-siders the economic significance ofinflat-ed
hospital,operating room material,andpersonnel costs.Even more important,theneed for
general anesthesia is obviated.Apatient with a mandibular fracture man-aged by
closed technique can be success-fully treated as an outpatient with eitherlocal
anesthesia or conscious sedation.Therefore,the indications for closedreduction may
simply be stated as all casesin which an open reduction is either notindicated or
is contraindicated.Severalconditions deserve specific mention.Grossly comminuted
fractures are,as ageneral rule,best treated by closed reduc-tion,because using open
reduction tech-niques would jeopardize the blood supplyto the small bone fragments
and lead to anincreased likelihood ofinfection.This cat-egory also includes gunshot
wounds,which are particularly prone to infection.Fractures in the severely
atrophicedentulous mandible represent a difficultclinical situation.On the one
hand,there islimited osteogenic potential;the majorityofthe blood supply comes from
theperiosteum,so an open reduction furtherdisrupts the blood supply.On the
otherhand,a stable,nonmobile reduction andfixation ofthese fractures is difficult
withclosed reduction techniques.Open reduc-tion with limited dissection ofthe soft
tis-sue and rigid fixation may be the preferredtechnique.Later in this chapter we
reviewin more detail the management ofthisgroup ofpatients.In situations where
there is a lack ofsoft tissue overlying the fracture site,softtissue flaps have to
be transposed to covera fracture site (particularly ifa through-and-through
communication existsbetween the skin and oral cavity).Thepresence ofbone
plates,screws,and wiresmay increase the likelihood ofinfectionunder these
circumstances.Fractures in children involving thedeveloping dentition are difficult
to man-age by open reduction because ofthe pos-sibility ofdamage to the tooth buds
orpartially erupted teeth (Figure 22-21).Closed reduction offractures ofthemandible
together with indirect fixationcan be achieved by either the applicationofIMF or by
applying a technique to themandible only.The overwhelming majority ofpub-lished
clinical series over the past 50 yearsstrongly promote closed reduction for
themanagement offractures ofthe mandibu-lar condyle in both adults and chil-
dren.21,22,33,34,67�70These uniformly excel-lent results were obtained in all ages
ofpatients treated.71Conclusions drawn byvarious authors are the following:no cor-
relation exists between the degree ofradi-ographic displacement and the severity
ofclinical symptoms;no correlation existsbetween the radiographic alignment
ofthefracture segments and postoperative func-tion;growth complications and
ankylosisare exceedingly rare;open reduction withinternal fixation is fraught with
complica-tions;and evidence supports the choice ofclosed reduction as the primary
treatmentmodality for condylar fractures regardlessofthe degree
ofdisplacement.Although the majority ofthe large stud-ies reviewed patients in
allage groups,someauthors specifically studied children andtheir response to
conservative managementofcondylar fractures.72�78All obtainedTable 22-2Goals
ofTherapy1.Obtain stable occlusion.2.Restore interincisal opening and mandibular
excursive movements.3.Establish a full range ofmandibular excursive
movements.4.Minimize deviation ofthe mandible.5.Produce a pain-free articular
apparatus at rest and during function.6.Avoid internal derangement ofthe
temporomandibular joint on the injured or the contralateral side.7.Avoid the long-
term complication ofgrowth disturbance.FIGURE22-21Posteroanterior mandibularview
ofa 4-year-old child with a symphysis frac-ture.Management ofthis injury through
anopen reduction with internal fixation poses a sig-nificant risk ofdamaging the
developing perma-nent dentition.
Principles ofManagement ofMandibular Fractures415excellent results with minimal
complica-tions when fractures ofthe condyle in chil-dren were treated with closed
methods.The superiority ofclosed reduction ofcondylar fractures is also supported
bynumerous animal studies.Experimentallyinduced fracture dislocation in rhesus mon-
keys has resulted in �a workable,usablemandibular articulation regardless ofwhether
the condyle was left remaining atright angle to the ramus,pushed medially
oranteriorly,or reduced and maintained viatransosseous wire.There was little
sacrificeofmandibular growth or symmetry.�79Fur-ther studies compared three methods
oftreatment for fracture dislocations in rhesusmonkeys.80,81No difference existed
betweenthose treated with internal fixation usingwire ligature,those treated with
maxillo-mandibular fixation,or those who receivedno treatment.No incidents
ofnonunionwere reported with any closed technique.Length ofFixationTraditionally
thelength ofIMF used for adult mandibularfractures has been 6 to 8
weeks.However,this length ofIMF is not without penalty.Often patients continue to
lose weightduring this period,they may not be able toreturn to work,and there is
some evidenceofhistologic changes in the temporo-mandibular joint.82,83Juniper and
Awtywere able to demonstrate that 80% ofmandibular fractures treated by open
orclosed reduction and IMF were clinicallyunited in 4 weeks.84They were also able
todemonstrate a clear relationship betweenthe age ofthe patient and the
predictabili-ty ofearly fracture union.These resultswere confirmed by
Amaratunga.85Hefound that 75% ofmandibular fractureswere clinically stable by 4
weeks,thatalmost all fractures in children healed in 2 weeks,and that a significant
number offractures in older patients took 8 weeks toheal.It appears that each
individual casemust be judged on its merits but that mostuncomplicated fractures in
children areunited in 2 to 3 weeks,in adults 3 to 4 weeks,and in older patients in
6 to 8 weeks.Several other factors should betaken into account when deciding on
theappropriate regime for a particular patient.The following situations generally
requirelonger periods ofIMF:comminuted frac-tures;fractures in
alcoholics,particularlythose with nutritional problems;fracturesin patients with
psychosocial handicaps;fractures treated late;and fractures withteeth removed in
the line ofthe fracture.Length ofFixation for Condylar FracturesIdeally,the period
ofIMF should allow forreestablishment ofthe preinjury occlusionand should not be
longer.Increased lengthofthe time offixation may result in limita-tion in function
or ankylosis ofthe joint.Inpractice,a wide variety ofopinions existsover the length
oftime that constitutes anadequate period offixation.Differencesdepend on the age
ofthe patient,the type offracture,and the presence ofother fractures.Most
clinicians agree that a shorter period isneeded in children,but they are no closer
inagreement over what this time should be.Animal studies have shown excellent
occlu-sion and postoperative function even infracture dislocations when no IMF
isused.79�81Some studies in humans alsoagree with this.However,the inability
toocclude the teeth without pain is frequentlypresent in patients with condylar
fracturesand does require some period offixation.Attempts to predetermine which
fractureswill need longer IMF than others have beenmade.85The length oftime has
been basedon the presence or absence ofteeth,the typeoffracture,and the age ofthe
patient.How-ever,Walker has suggested that a relativelyshort period
ofintermaxillary fixation isrequired for all patients regardless
ofage,occlusion,and type offracture.86,87Intermaxillary Techniques
DENTATEPATIENTSIntermaxillary techniques indentate patients include application
ofarch bars (Figure 22-22),direct wiring,Ivyloop wiring (interdental eyelet wiring)
(Figure 22-23),continuous wire loop tech-nique (Stout�s
method,Obwegeser�smethod),cast cap splints,and IMF screws(Figure 22-24).Methods for
dentate patients usuallyinclude 0.5 mm (25-gauge) soft stainlesssteel wires around
the teeth.In general,thewires should be handled in a similar fash-ion for all
methods,following certainprinciples:1.Tighten the wires with a
continuoustension.2.Direct the force apically when tighten-ing the wires.3.Tighten
all wires in a clockwise direc-tion.4.At the end oftightening,turn only halfa turn
at a time.5.Turn the end ofthe wire into the inter-proximal embrasure.These
additional rules apply whenarch bars are used:1.Adapt the arch bar closely.2.Use a
cuspid wrap wire where indicated.3.Avoid placing the wire across theintermaxillary
stabilization lugs.4.Use circumferential wires when singleteeth stand alone,and
intraosseoussuspension or circum-mandibularwires in edentulous areas.5.In the area
ofthe fracture,reductionshould be accomplished prior to stabi-lization ofthe arch
bar on both sidesofthe fracture.FIGURE22-22Placement ofErich arch bars
fornoninvasive treatment ofa mandibular fracture.
416Part 4: Maxillofacial TraumaWhen IMF is used it may be appliedwith either
elastics or wires.Elastics canbe used for fracture reduction and
forIMF;however,they apply a constant pres-sure,which can lead to muscle spasm
andpain,particularly in the masseter muscle,and they are difficult to keep
clean.Wires,on the other hand,are easier to keep cleanand are passive.However,they
do loosenover time and may need to be tightenedor replaced over the period
offixation.LINGUALORLABIALSPLINTTo con-struct a lingual splint,an impression
istaken ofthe lower arch and a stone modelis poured (Figure 22-25).Ifthere is dis-
placement ofthe fracture site,an upperimpression will also need to be
taken.Thelower stone model is then sectioned at thefracture site,and using the
upper model asa guide (Figure 22-26),the correct occlu-sion is reconstructed.Then
the sectionedmodel is waxed together in the correctrelationship,and the lingual
surface isrelieved with a 1 mm thickness ofwax.Ahard acrylic splint is then made
and holesdrilled so that it can be wired to the teeth(Figure 22-27).Just before
placement athin coating ofsoft liner is applied.Thefracture is reduced,and the
splint is wiredinto position.EXTERNALPINFIXATIONIn externalpin fixation usually two
pins on both theproximal and distal fragments are placed,ifpossible.The biphasic
extraoral tech-nique uses a special transbuccal trocar set.This is used for each
hole through indi-vidual skin incisions.A 2.2 mm twist drillis used to drill
through both corticalplates at slow speed with constant irriga-tion.Specially
designed self-tapping,coarse-threaded screws are then placedwith a socket wrench.A
series oflockingplates and bars are secured to the four ormore pins,and then a
self-curing acrylicsecondary splint is constructed (Figure22-28).External pin
fixation can be usedin edentulous fracture sites in whichthere is bone loss
secondary to gunshotinjuries,pathologic fractures,or osteo-myelitis,or in cases in
which a bone-grafting procedure has been performed.It can also be used in fractures
oftheatrophic edentulous mandible or inmandibular fractures associated withmidface
fractures when a quick and sim-ple method offixation is required.FIGURE22-23In
patients with a full and stableocclusion,Ivy loops can be applied to
achieveintermaxillary fixation after closed reduction.A,Frontal view.Note there is
also an Essig wirein the anterior dentition to help maintain thereduction ofthe
right parasymphysis fracture.B,Right buccal view.C,Left buccal view.ACBFIGURE22-
24An option to obtain intermaxillary fixation in patients with a reliable occlusion
is theuse ofintermaxillary fixation screws.In most cases two screws placed on each
side is sufficient tomaintain the reduction.A,Right buccal view.B,Left buccal
view.ABFIGURE22-25For the fabrication ofa lingualsplint,the cast must be carefully
sectioned alongthe areas where the fractures are located.
Principles ofManagement ofMandibular Fractures417EDENTULOUSPATIENTSClosed reduc-
tion in edentulous patients is achieved withGunning�s splints or splints made from
thepatient�s own dentures (Figure 22-29).Open ReductionOpen reduction ofmandibular
fractures has developed tobecome a more frequent treatment optionfor the management
ofthese injuries over thelast decade.With the development ofimproved fixation
systems,which directlytranslates into reduced IMF times or no IMFat all,both
surgeons and patients havebecome more comfortable with this treat-ment option.Luyk
stated that the signifi-cance ofthe rather large number ofsuccess-fully managed
patients using closed reduc-tion was magnified when one considers thatat the time
there were no large studies onopen reduction showing any improvementin the result
or any decrease in the rate ofcomplications.88Today,we know that thisstatement has
to be dissected carefully andthat depending on the time elapsed betweenthe injury
and treatment,and whether thepatient is taking antibiotics,this will changethe
outcome tremendously.In contrast,thoserecommending open reduction
ofcondylarfractures have failed to report complicationrates for the proposed
technique or,whencited,reported complication rates that aregreater than those seen
historically withclosed reduction;they experienced complica-tions that have not
been seen with closedtechniques;and they allowed inadequate follow-up before
assessing the outcome.The major indications for open reduc-tion ofa fractured
mandible are summa-rized below.Unfavorable or Unstable FractureUnfa-vorable or
unstable fractures arise in sev-eral circumstances.When an angle frac-ture is
displaced at the time ofinjury andis horizontally or vertically unfavorable,itis
unlikely that simple IMF will maintainthe proximal segment in the correct posi-
tion.Under the influence ofthe medialpterygoid or the powerful mandibular ele-vator
muscles (temporalis and masseter),the proximal segment most likely will
bedisplaced.This could lead to delayed heal-ing and possibly permanent disruption
ofthe inferior alveolar nerve.When the frac-ture is both horizontally and
verticallyunfavorable,an extraoral approach is rec-ommended.Also,most fractures in
theparasymphyseal region cannot be routine-ly treated satisfactorily by closed
reductionbecause ofthe pull ofthe suprahyoid anddigastric muscles.Fractures in this
regiontend to open at the inferior border andalong the lingual surface with the
superioraspects ofthe mandibular segments rotat-ing medially at the point
offixation whenclosed reduction and IMF are used.Withthe medial rotation ofthe
horizontalramus the lingual cusps ofall premolarsand molars move out ofocclusal
contact.This results in masticatory inefficiency,and untoward periodontal changes
willFIGURE22-27A,The splint is fabricated,trimmed,and polished to guarantee a
passive fit in themodified cast.B,Drill holes are placed in the interdental areas
to allow for wires to be passed andsecured around the teeth.ABFIGURE22-28A Joe Hall
Morris external fixa-tor is used to manage a severe mandibular frac-ture resulting
from a gunshot wound.This sys-tem consists ofbiphasic transcutaneous pins andan
acrylic frame fabricated intraoperatively.FIGURE22-26Once the fracture segments
havebeen manually realigned,the cast is waxedtogether and fast-setting stone is
added to rebuildthe base and allow for mounting and fabricationofthe splint.
418Part 4: Maxillofacial Traumafollow.89If,in addition to a fracture in
thisarea,the patient also has a concomitantangle or condylar fracture,the risk
oflat-eral flaring ofthe mandibular angles is avery real possibility.This negative
resultcan be much worse in cases in which bilat-eral condylar fractures are present
and inpatients with associated midfacial frac-tures,when the mandible is used as
thebase for the reconstruction.Prolonged Delay in Treatment ofthe Frac-ture with
Interpositional Soft TissueOccasionally when there has been anexcessive delay in
treating a fracturedmandible,interpositional tissue betweenthe two bone ends can
prevent a satisfac-tory closed reduction.In this situation anopen reduction is
necessary to remove thesoft tissue between the fragments.Complex Facial
FracturesThe satisfacto-ry reduction ofcomplex facial fracturesrequires two stable
reference points towhich the maxillary complex can bereduced.These include a stable
supraorbitalbar ofbone and also a stable mandible.Thisoften necessitates open
reduction and fixa-tion ofthe mandibular fractures.Openreduction and fixation ofa
subcondylarfracture are indicated when there are bilat-eral subcondylar fractures
in the presenceofcomplex middle third fractures,so that astable vertical platform
is provided onwhich the face can be reconstructed.Medically Compromised
PatientsSomepatients with special medical conditionsare best treated without
IMF.They may bebetter treated with an open reduction.This group ofpatients includes
those withdecreased pulmonary function.Williamsand Cawood have demonstrated
signifi-cant decrease in pulmonary function asso-ciated with IMF.90Patients with
gastroin-testinal disorders who are on a liquid diet,particularly one based on milk
products,may have difficulties.Those with severeseizure disorders in which airway
difficul-ties may arise with IMF and patients withpsychiatric or neurologic
problems may becandidates for open reduction.Concurrent Condylar Fracture
Associatedwith Fractures Elsewhere in the MandibleIt is often advantageous to be
able to mobi-lize condylar fractures early to prevent pos-sible ankylosis.This is
particularly true incases ofintracapsular fractures in whichimmobilization is more
likely to lead toankylosis.In this situation open reductionand fixation
ofangle,body,or symphysealfractures will allow early mobilization ofan associated
condylar fracture.There are certain contraindications tothe use ofopen reduction
ofmandibularfractures.As a general principle,when asimpler means oftreating a
fracture can beused,it should be.This is often more cost-effective for the
community at large andoften results in fewer complications.How-ever,each individual
case must be judgedon its merits.The periosteal blood supply ofmulti-ple small
fragments ofbone can be jeopar-dized when an open reduction is attempt-ed for
comminuted fractures.This canlead to an increased likelihood ofinfectionand delayed
healing.Gunshot wounds arebest managed by closed reduction when-ever
possible,because often the bone iscomminuted and there is a greater risk
ofinfection in these fractures.Atrophicedentulous mandibles must be treatedwith
care.When an open reduction is nec-essary,the maximal blood supply to thefracture
site should be preserved.Ifclosed reduction is used for thetreatment ofa condylar
process fracture,itis best that intermaxillary fixation be dis-continued in all
patients at approximately10 to 14 days.Ifother mandibular frac-tures are associated
with the fracturedcondyle,it is desirable to treat them withsome form ofadditional
stabilization,such as a lingual splint,external pins,orrigid internal fixation.This
allows for theearly release ofIMF without compromis-ing the healing ofthese other
fractures.Open Reduction ofCondylar FracturesA variety ofuseful techniques for
openreduction have been described.73,91�94Thereason for employing open reduction
ineach case was to avoid the complicationsfound in closed reduction.No data or
follow-up ofpatients was presented todocument this.Tanasen and Lamberg,Zide and
Kent,and Raveh and colleaguesfollowed patients with open reduction forup to 37
months.95�97Complication ratesof85,50,and 10% were seen,respectively,including
facial nerve dysfunction andkeloid formation.No comparison wasmade with patients
treated with closedreduction during the same time period.Chuong and Piper attempted
to compareclosed reduction with open reduction,including concomitant disk repair in
theirstudy.98Eight ofnine open reductionpatients who were studied for an
averageof11months experienced complications(89%).Six of12 patients receiving
closedreduction were found to have malocclu-sion at the end oftreatment (50%).It
ispossible that the high incidence ofmaloc-clusion in the closed reduction
groupmight be a result ofprolonged fixation,inadequate follow-up,and lack ofsuper-
vised postoperative rehabilitation.87There is a lack ofany controlled clinicaldata
to indicate the superiority ofopenreduction techniques as a primary mode
ofmanagement ofcondylar fractures in FIGURE22-29Intermaxillary fixation in
anedentulous patient using Gunning�s splints witharch bars imbedded into the
acrylic.
Principles ofManagement ofMandibular Fractures419children or adults.Although it is
apparentthat,in some situations,an unacceptableincidence ofcomplications results
whenclosed reduction is employed,it is inappro-priate to assume that an open
techniquecan avoid these complications until this isborne out in controlled
clinical trials.Despite the evidence in favor ofclosedreduction as the treatment
ofchoice forthe majority offractured condyles in bothchildren and adults,there are
indicationsfor the performance ofopen reduction(Table 22-3).In the past the
indication for openreduction ofa condylar fracture was pri-marily a radiographic
one.Essentially,itwas thought that the condyle behaved likeother areas ofthe
mandible or otherbones in the body and that it wouldrespond better and heal with
more satis-factory function ifan ideal anatomicreduction were
obtained.93,95,99,100It hasbeen shown that there is little ifany cor-relation
between the degree ofdisplace-ment or dislocation ofthe fracture andthe ability to
obtain satisfactory functionwith a closed reduction.A more func-tional approach in
assessing the need foropen reduction was taken by Zide andKent.96,101According to
these investiga-tors,indications for open reduction ofcondylar fractures should
rely on theidentification ofspecific clinical entitiesthat,when treated with closed
reduction,would result in a high degree offailure.They also take into account an
objectiveevaluation offunction at the time oftheplanned reduction,the presence and
con-dition ofthe patient�s dentition,the like-lihood ofsuccessfully performing
aclosed reduction,and the presence ofother modifying factors such as thepatient�s
medical condition or the exis-tence ofother facial fractures.Absolute
IndicationsAbsolute indica-tions for open reduction are present in thosesituations
in which limitation in function ishighly probable ifa closed reduction is per-
formed or in those situations in which aclosed reduction is not
possible.Limitationoffunction may be caused by fracture withdislocation ofthe
proximal segment intothe middle cranial fossa,by invasion ofthejoint by a foreign
body,by lateral extracap-sular dislocation ofthe condylar head,or bythe presence
ofany fracture dislocation thatproduces a mechanical stop,preventingmandibular
movement.Inability to per-form a closed reduction may result whenthe fracture is
displaced so that it is impos-sible to manipulate the teeth into an appro-priate
occlusion.Possible or Relative IndicationsPossibleor relative indications for open
reductionalso exist and should be assessed on thebasis ofbenefit as opposed to
risk:1.Bilateral condylar fractures with com-minuted midfacial fractures.The ratio-
nale for open condylar reduction inthese situations is that it allows for
theestablishment ofa horizontal and verti-cal dimension ofthe midface when
thiscannot be achieved by other means.Ifrigid internal fixation ofthe midface
ispossible,then open reduction ofthecondyle may no longer be indicated.2.Situations
in which IMF is not feasible.Certain medical conditions,such aspoorly controlled
seizures,psychiatricdisorders,or severe mental retarda-tion,make maxillomandibular
fixationdifficult and possibly dangerous.Also,patients with multiple trauma,partic-
ularly head injury or chest injury,areat increased risk for complications ifplaced
in maxillomandibular fixationunless tracheostomy is
planned.Inaddition,maxillomandibular fixationis extremely difficult in those
patientsTable 22-3Indications for Open Reduction ofFractures ofthe Mandibular
Condyle1.Absolute indicationsA.Limitation offunction secondary to the
following:1.Fracture into middle cranial fossa2.Foreign body within the joint
capsule3.Lateral extracapsular dislocation ofcondylar head4.Other fracture
dislocations in which a mechanical stop is present on opening,which is confirmed
radiographicallyB.Inability to bring the teeth into occlusion for closed
reduction2.Relative indicationsA.Bilateral condylar fractures with comminuted
midface fractures in which rigid internal fixation ofthe midface is not
possibleB.Situations when intermaxillary fixation is not feasible as a result ofthe
following:1.Medical restrictionsa.Poorly controlled seizure disorderb.Psychiatric
disordersc.Severe mental retardationd.Concomitant injuries such as head injury or
chest injury (unless tracheostomy is planned)2.Displaced fractures where dentures
or splints are not feasible because ofsevere mandibular atrophyC.Bilateral
fractures in which it is impossible to determine what the proper occlusion is as a
result ofloss ofposterior teeth or the presence ofa preinjury skeletal
malocclusionD.In fracture dislocation in adults to restore the position and
function ofthe meniscus (controversial)
420Part 4: Maxillofacial Traumawith displaced condylar fractures inwhom dentures
are not present andsplints are not feasible because ofsevere mandibular
atrophy.3.Bilateral fractures in which it isimpossible to determine the
properocclusion.Occasionally,a patient withbilateral fractures will have such
anambiguous occlusion that,even withthe use ofstudy models and carefulclinical
examination,it is not possibleto determine the appropriate maxillo-mandibular
relation.This may lead toinappropriate placement ofthemandible into malocclusion or
toplacement ofa preexisting malocclu-sion into a normal
relation,therebypredisposing the patient to nonunionor long-term functional
disability.4.Fracture dislocation in an adultpatient to restore position and func-
tion ofthe disk.Previous emphasis onindications for open reduction havecentered
around the need for bonyreduction and fixation without con-sideration ofdisk
position.Theunstated implication ofmost oftheliterature is that the position
ofthedislocated disk is not critical for opti-mal functional results after
condylefracture.98However,this is contradic-tory,given the present emphasis onthe
importance ofcorrect condylardisk alignment for management ofthose patients with
internal derange-ment ofthe temporomandibularjoint.The disk is important in
theprevention ofpost-traumatic ankylo-sis.47An interesting concept has beenraised
about the possible necessity fordisk repositioning,especially in frac-ture
dislocations,to allow for optimaltemporomandibular joint function.Some clinicians
have suggested that�open reduction and internal fixationofcondylar fractures in
conjunctionwith disk repair is a biologicallysound approach�.�98Based on
theirexperience,it might be recommendedthat,in fracture dislocations in whichopen
reduction is indicated,anattempt should be made to repositionthe disk at the time
ofthe reduction.However,inadequate data exist tosuggest that open reduction per-
formed solely for the purpose ofdiskrepositioning is valid.Surgical
ApproachCONDYLARFRACTURESA variety ofsurgical approaches to the frac-tured condyle
have been suggested,includ-ing intraoral,submandibular,retro-
mandibular,preauricular,and,morerecently,endoscopic.The most importantfactor in
determining the approach used isthe level at which the fracture has
occurred.Modifying factors such as the degree ofdis-placement or dislocation and
the plannedmethod offixation may also have a bearingon the approach
selected.Traditionally fractures in the condylarneck and above were best
approachedthrough a preauricular or endaural inci-sion.101This approach also has
the addedadvantage ofallowing for surgical manip-ulation ofthe soft tissues within
the joint,ifdesired.Subcondylar fractures and frac-tures extending into the upper
ramusregion are best approached using a retro-mandibular or Hinds
approach.102Theincision begins approximately 1 cm belowthe lobe ofthe ear and 1 cm
posterior tothe ramus ofthe mandible.The dissectionis carried down to the parotid
gland,which is retracted anteriorly,providingaccess to the vertical fibers ofthe
massetermuscle overlying the ramus.These fibersare not stripped but instead are
separatedbluntly along their vertical course,allow-ing access to the underlying
ramus.Accesscan easily be gained to relatively high sub-condylar fractures through
this approach,and a variety offixation techniques arepossible without additional
percutaneouspuncture,as may be needed ifa sub-mandibular approach is used.Low sub-
condylar fractures,especially those with-out a significant degree
ofdisplacement,may be easily approached from an intra-oral incision.103In severe
anteromedialfracture dislocations in which the condylarhead is not retrievable
despite the choiceofapproach,a vertical ramus osteotomy,followed by removal ofthe
osteotomizedsegment,has been recommended.104�106This allows for access to the
proximalcondylar head,which is located mediallyand is also removed.Rigid fixation
withplates or screws is carried out between theramus segment and condylar
head.Theunit is returned as a free autogenous bonegraft,and the osteotomy is
plated.Thistechnique is useful for high dislocatedfractures and may be
accomplishedthrough a retromandibular approach.OTHERMANDIBULARFRACTURESOpen
reduction ofmandibular fracturesprior to the advent ofantibiotics was asso-ciated
with a high incidence ofinfection.Following the introduction ofantibiotics,most
clinicians used the extraoralapproach to the fracture site.This tech-
nique,however,is time-consuming,resultsin a visible surgical scar,and can
damageadjacent structures,particularly the mar-ginal mandibular branch ofthe
facialnerve.Transoral open reduction has beenadvocated as an excellent
alternative.107�110The technique is claimed to be quicker toperform,results in no
extraoral scar,anddoes not damage the facial nerve.Lesspostoperative wound care is
required,andit is simple to perform the techniquesunder local anesthesia.Transoral
openreduction ofmandibular fractures is use-ful in tooth-bearing portions ofthe
jaw(ie,in symphyseal,body,and angle frac-tures).Complications rates and
infectionrates appear to be similar between the twotechniques when large numbers
ofcasesare studied.111,112Occasionally,a combination ofap-proaches is
necessary,particularly in frac-ture dislocations in which a preauricularapproach
may be necessary to retrieve theproximal segment,while fixation is per-formed
through another approach.113
Principles ofManagement ofMandibular Fractures421Throughout the past
decade,surgeonshave become interested in the concept ofminimally invasive surgical
approaches toavoid potential patient morbidity frommore traditional open surgical
techniques.With the development ofthese techniques,management ofthese injuries via
an endo-scopic approach has gained great popular-ity among surgeons.In 1994 Ma and
Fangwere the first ones to describe the use ofanendoscope to access the mandibular
angleregion.114Later Jacobovicz and colleaguesmodified this technique for the
manage-ment ofcondylar fractures.115Recently,more authors have also described
theirexperience with this approach.116�118The surgical approach,as described
byMiloro,118requires a 15 to 20 mm modifiedRisdon incision to gain access to the
lateralramus.A subperiosteal dissection is thenperformed blindly to create an
�optical cav-ity�on the lateral aspect ofthe ramus onthe fracture side from the
sigmoid notch tothe inferior border and from the mandibu-lar notch anteriorly to
the posterior borderofthe ascending ramus posteriorly.A mod-ified Storz retractor
with a curved end isthen placed through the incision and belowthe periosteum to
engage the sigmoidnotch.A 4 mm,30�endoscope is used forretraction and visualization
ofthe surgicalsite.Following irrigation and the use ofasuction elevator,the sigmoid
notch,inferi-or border,mandibular notch,posteriorborder,and the fracture site can
be clearlyidentified endoscopically.The fracturedsegments are then repositioned
andreduced.Inferior traction on the angle ofthe mandible,although limited by
IMF,canbe helpful in the mobilization ofthe seg-ments.Fixation is achieved with a
2.0 mmtitanium miniplate and screws through apreauricular stab incision and trocar
(Fig-ure 22-30).Following reduction and stabi-lization,the IMF is released for
evaluationofthe occlusion.Methods ofFixationOnce access to thefracture has been
achieved,any number offixation devices may be employed (Figure22-31).In a given
situation,any one ofthese techniques may have certain advan-tages over the
other.With the developmentofsophisticated rigid internal fixation sys-tems and
instrumentation for their place-ment,miniplate fixation ofthese fractureswill be
the technique most readilyemployed in most cases.Miniature boneplates can be
applied using any ofthe pre-viously discussed approaches.These plateshave the
advantage ofbeing available in awide variety ofshapes and sizes;they arenow readily
available in most operatingrooms;and they provide a more stableform offixation than
do wires or Kirschn-er wires.Theoretically,bone plates haveanother advantage�they
can be placed ona relatively small proximal fragment first,allowing for the
creation ofa handle tomore effectively manipulate the proximalsegment into an
appropriate reduction.Should the incision selected not allow fortotal access to the
fracture,currently avail-able bone-plating systems are equippedwith instrumentation
for percutaneousplacement ofscrews.WIREIntraosteal wiring (wireosteosynthesis) can
be placed either by anintra- or extraoral route using one ofthreebasic
techniques:1.A simple straight wire across the frac-ture site (Figure 22-32A).This
shouldbe placed so that the direction ofpull ofthe wire is perpendicular to the
fracturesite.This technique can be eitherthrough both the buccal and
lingualcortical plate or it may be used on thebuccal cortical plate only.This is
usefulin the angle region,where a third molarsocket can be quickly and easily
usedfor a simple straight buccal cortex wire.2.Figure-of-eight wire (Figure 22-
32B).This wiring technique has beenshown to have increased strengthcompared with
simple techniques atboth the inferior and superior bordersin angle
fractures.1193.Transosseous circum-mandibularwiring (Obwegeser�s technique) (Fig-
ure 22-32C).This is a useful wiringtechnique when the fracture runsobliquely
compared with the inferiorborder ofthe mandible.Ifthe fractureline is too vertical
the wire couldbecome displaced into the fracture line.The wire used should be a
pre-stretched soft stainless steel,and the frac-ture should be held in a reduced
positionwhile the wire is being tightened so thatthe wire does not reduce the
fracture andpossibly lead to wire breakage.FIGURE22-30Endoscopic management
ofcondylarfractures offers excellent reduction and fixation ofthefracture
segments,while reducing the morbidity ofconventional open approaches to this
site.A,Visual-ization ofthe condylar neck fracture.B,Titaniumminiplate in place
after reduction.(Photographscourtesy ofMichael Miloro,DMD,MD)AB
422Part 4: Maxillofacial TraumaFIGURE22-31Previously reported techniques for direct
stabilization ofcondyle fractures: A,Silverman (1925); Band C,Thoma (1945);
D,Stephenson(1952); E,Robinson (1960); F,Robinson (1962); G,Messer (1972); H,Kobert
(1978); I,Petzel (1982).(CONITINUEDONNEXTPAGE)ABCDEFGHI
Principles ofManagement ofMandibular Fractures423RIGIDFIXATIONDissatisfaction
withthe use ofIMF as a means oftreatment ofmandibular fractures has resulted in
thedevelopment ofopen reduction and fixa-tion techniques that do not require the
teethto be wired together.Criticism ofthe disad-vantages ofprolonged immobilization
ofthe jaws has included patient complaints ofpanic,insomnia,social
inconvenience,pho-netic disturbance,loss ofeffective worktime,physical
discomfort,weight loss,histo-logic changes in the condylar head,and dif-ficulty
recovering a normal range ofjawmovement.This has led some clinicians toseek
alternative methods oftreatment,including the use ofrigid internal fixation.The
principal disadvantages ofthe com-pression plating systems for mandibularfractures
are the use ofan external approach,thus giving rise to facial scarring and
thepotential for damage to the mandibularbranch ofthe facial nerve,and the use
ofvery rigid plates,giving rise to �stress shield-ing,�although this has never been
shown tobe a problem in mandibular fractures.Also,the position ofthe teeth and
inferior alveolarnerve and the use ofbicortical screw fixationnecessitate that the
compression plates beplaced in areas ofcompression rather thantensile forces,and
therefore,additional tech-niques are required to overcome the tensionforces.Another
disadvantage is that removalofthe plates is advocated.The second major group
ofplate fixa-tion techniques is the monocortical mini-plate osteosynthesis,which
was firstdescribed by Michelet and colleagues andthen modified and popularized
byChampy and colleagues.9,10The principaladvantages ofthis technique over compres-
sion plating systems are the use oftheintraoral approach and the positioning ofthe
plates in the juxta-alveolar area wheretensile strain occurs when the mandible
isloaded.The healing that results from theuse ofthis system in humans has not
beendemonstrated clearly.At least one group ofauthors claims that the system gives
rise torigid fixation and that it results in primarybone healing,although no
evidence is pro-vided to support this assertion.120In viewofthe small malleable
nature oftheseplates and the fact that the system is mono-cortical,it would seem
more1ikely that thetechnique is only semirigid and wouldresult in callus formation
and secondarybone repair.This is not to imply that it is aninferior
technique,because callus forma-tion generally gives rise to quicker andstronger
early bone repair.121Special SituationsEdentulous FracturesThe edentulousmandible
in the trauma patient has severalfactors modifying its behavior that the den-tate
mandible does not.The loss ofthe teethresults in resorption ofthe alveolar
bone,which weakens the mandible.The loss ofbone also means that there is less
cross-sectional area ofbone in contact in fracturepatients and less periosteum and
endos-teum to supply the osteogenic cells for frac-ture healing.Because ofthe aging
processthe majority ofthe blood supply to theedentulous mandible is from the
perios-teum rather than the inferior alveolarFIGURE22-31 (CONTINUED)J,Brown (1984);
K,Fernandez (1987); L,Kitayama (1989); M,Ellis(1989).Adapted fromLarsen
PE.Traumatic injuries ofthe condyle.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM,editors.Principles oforal and maxillofacial surgery.Vol 1.Philadelphia(PA): JB
Lippincott Company; 1992.p.460.JKLM
424Part 4: Maxillofacial Traumaartery.122A larger percentage offractures inthe
edentulous patient are not compoundbecause ofthe lack ofteeth.Minor displace-ment
ofthe bones can be easily accommo-dated in the construction ofnew dentures.The
edentulous population also tends tohave more health problems resulting
fromconditions such as osteoporosis,diabetesmellitus,and steroid therapy,which
maydirectly affect bone healing.The site distrib-ution offractures tends to be
different in theedentulous patient,with a higher percent-age ofbody fractures
(43.5%) and lowerpercentages ofangle (15.2%) and symphy-seal (4.3%) fractures
(Figure 22-33).123A20% incidence ofnonunion has beenreported in the treatment
ofedentulousfractures,particularly when nonrigid fixa-tion was applied in open
reduction cases.111Longer periods ofimmobilization have alsobeen shown to be
necessary to achieve satis-factory healing.124,125The anatomic site influences
treat-ment.Ifthe location ofthe fracture is pos-terior to the denture-bearing
area,theneither additional fixation (eg,external pinfixation) or open reduction and
fixationmay be necessary to control the proximalfragment.Muscle pull on the
edentulousjaw is considerably weaker than in a den-tate mandible and undisplaced
fracturesare often closed injuries.Therefore,ifthefragments are undisplaced or
minimallydisplaced and not mobile,conservativetherapy may be all that is
necessary.Moredefinitive treatment will be necessary ifthefragments are displaced
or excessivelymobile.The bilateral body fracturedeserves special mention because
the pullofthe suprahyoid muscles tends to displacethis fracture inferiorly.These
usually occurin the pencil-thin atrophic mandible.Avariety oftreatment modalities
have beensuggested to treat these difficult fracturesincluding open reduction with
rigid inter-nal fixation,closed reduction with andwithout bone grafts,and external
pin fixa-tion.When the edentulous mandible iscomminuted again because ofthe
poorblood supply to the bone fragments,thosefragments are best managed by
closedreduction.The use ofsemirigid fixationsystems without some form ofIMF is
notindicated in this patient subset.External pin fixation by the biphasictechnique
is often used in edentulous frac-tures.It obviates the need for IMF,thusallowing
early mobilization ofthe jaw andimproving feeding in some patients.It canbe used in
comminuted fractures withoutjeopardizing blood supply to the fractures,and it can
also bridge a bone loss gapbefore bone grafting.Fractures in ChildrenAs previously
men-tioned,fractures in children are less commonthan in adults.Their management is
compli-cated by the presence ofdeciduous teeth,which may be mobile during the mixed
den-tition stage and whose shape has little in theway ofundercut areas,which means
that theydo not retain wire as well as adult teeth.Thepresence oftooth buds reduces
the area avail-able for interosteal fixation,and there exists agreater potential
for ankylosis and growthdisturbances in the younger population.Also,children do not
tend to tolerate IMF aswell as adult patients.On the other hand,fractures tend to
heal quicker in children andslight malocclusion problems can be com-pensated for by
growth ofthe patient.Children make up about 5% ofallmandibular fractures.These
fractures arerare in children under 5 years ofage becauseofthe greater elasticity
ofthe bone andlighter weight ofchildren,which lowers theFIGURE22-32A,Simple wiring
technique.B,Figure-of-eight wire.C,Transosseous circum-mandibular wire.Adapted
fromLuyk NH.88p.427.ABC37.00 15.243.54.3FIGURE22-33Percentage offracture sites
inedentulous patients.Adapted fromLuyk NH.88p.429.
Principles ofManagement ofMandibular Fractures425forces ofimpact during
falls.Condylar frac-tures appear to be common,affecting about46% ofpatients either
alone or in combina-tion with other fractures.126Mandibular fractures in children
canoften be successfully managed by acrylicsplint therapy ofthe mandible only
orwith eyelet wires and IMF.126,127A short-ened period ofIMF,2 to 3 weeks,is all
thatis required.When an open reduction isrequired,it has been successfully accom-
plished by the extraoral route using inferi-or border wiring in order to avoid
thetooth buds.128,129Ifadequate bone height is availablebelow the area where the
tooth buds arelocated,the use ofresorbable plates offersa great advantage to fixate
these fractures(Figure 22-34).Complications are rare in this group
ofpatients.Malunion,nonunion,and infec-tion tend to have a low
incidence.67Twoserious complications that can occur,how-ever,are ankylosis and
growth distur-bances.Both ofthese tend to be more com-mon with intracapsular
condylar fracturesand when the damage is ofa crushingnature.130The incidence and
severity ofthese complications can be reduced byshorter periods ofIMF and close
follow-up.Management ofTeeth in the Line ofFrac-tureIn the past,teeth in the line
ofthefracture were always removed.23,131,132Their removal was advocated because
frac-tures ofthe dentate portion ofthe jaws arecompound via the periodontal
ligamentand it was believed that this communica-tion fostered
infection,osteomyelitis,andnonunion.However,Neal and colleagues,Kahnberg and
Ridell,Schneider and Stern,and Amaratunga have all been able toshow that the
majority ofteeth in the frac-ture line can be saved ifappropriateantibiotic therapy
and fixation techniquesare used.133�136The impacted mandibularthird molar tooth
deserves special men-tion.Most authors have advocated leavingthe tooth in situ
ifthe tooth is not in directcommunication with the mouth,no peri-coronitis
exists,and reduction ofthe frac-ture is achievable without removal.Shettyand
Freymiller reviewed the indicationsfor removal ofteeth in the line ofthe frac-ture
as follows137:1.Teeth grossly loosened,showing evi-dence ofperiapical pathology or
sig-nificant periodontal disease2.Partially erupted third molars withpericoronitis
or associated cyst3.Teeth that prevent reduction offractures4.Teeth with fractured
roots5.Teeth with exposed root apices orentire root surface from the apex tothe
gingival margin6.An excessive delay from the time offracture to definite
treatmentUse ofAntibioticsZallen and Curry demonstrated that withcompound
mandibular fractures,an infec-tion rate of50% can be expected in thosepatients who
do not receive antibiotic ther-apy.138A prospective trial was undertaken inwhich
only dentate compound mandibularfractures were evaluated.One-halfofthepatients in
this study received �prophylacticantibiotics,�usually penicillin.It was notstated
for how long the antibiotic therapywas continued or when it started in relationto
the injury.One-halfthe patients who didnot receive antibiotics had infections at
thefracture site as opposed to only 6% ofthosewho did receive antibiotics.It seemed
tomake little difference whether the fractureswere treated by open or closed
reduction.All fractures in this study were treated within36 hours.Another study has
confirmed theseresults in facial fractures and has suggestedthat short-term
prophylaxis as is used in elec-tive surgery may be as effective as the moreusual 5-
day course ofantibiotics.139Thisgroup also found little difference in the inci-
dence ofinfection whether there was a delayin treatment ofmandibular fractures or
not.Penicillin should remain the antibioticofchoice for compound mandibular frac-
tures whether closed reduction or openreduction is contemplated.The
antibioticprophylaxis should begin preoperativelyand be continued for not more than
24 hours postreduction.ComplicationsDelayed Union and NonunionNonunion is
distinguished from delayedunion by the potential ofthe bone to heal.Delayed union
is a temporary condition inwhich adequate reduction and immobiliza-tion eventually
produces bony union.Onthe other hand,nonunion may persistindefinitely without
evidence ofbone heal-ing unless surgical treatment is undertakento repair the
fracture.Nonunion is general-ly characterized by pain and abnormalmobility
following treatment.Malocclusionmay be present in dentate cases and mobil-ity
exists across the fracture line.Radi-ographs demonstrate no evidence ofheal-ing and
in later stages show rounding offofthe bone ends.Delayed and nonunionoccur in about
3% offractures.140There are several causes and contribut-ing factors.The most
common reason ispoor reduction and immobilization.141This is more likely in
edentulous fractures.Infection is often an underlying cause,andany tooth in the
line ofthe fracture must becarefully assessed for root fracture andvitality.A
decreased blood supply can leadto delays in healing.Excessive stripping ofFIGURE22-
34Use ofa resorbable plate for fixa-tion ofa symphysis fracture in a 4-year-old
child.
426Part 4: Maxillofacial Traumathe periosteum,especially in comminutedand
edentulous fractures,can lead todelayed healing.Metabolic deficiencies
andalcoholism are also significant contributorsto delayed healing.Cannell and
Boydshowed a high incidence ofdelayed unionand nonunion in a group
ofalcoholicpatients.142These patients were probablyalso at increased likelihood to
sustain amandibular fracture.Although the exactreasons for delayed healing in this
group ofpatients is not known,they are known tohave metabolic and vitamin
deficiencies,poor compliance particularly with IMF,poor bony quality,and impaired
localblood supply,all ofwhich could be con-tributing factors.These patients should
betreated whenever possible with closedreductions,because this treatment has alower
incidence ofcomplications in thisgroup ofpatients.142Treatment ofdelayed union
andnonunion is aimed at eliminating theunderlying cause ofthe problem.Wheninfection
is present it must be managedwith d�bridement ofsequestra,drainage,and antibiotic
therapy.Loose fixation suchas wires and plates must be removed,andadequate fixation
with IMF,extraoral pinfixation,or even rigid plate fixation shouldbe applied across
the fracture site.143Ifthere is a gap between the bone ends,abone graft may be
necessary.InfectionInfection and osteomyelitis appear to bethe most common
complications (Figure22-35).In some studies,particularly with-out antibiotics,it
may occur in over 50%ofcases.144Some ofthe underlying causeshave already been
discussed.These can bedivided into systemic factors,such as alco-holism and no
antibiotic coverage,andlocal factors,such as poor reduction andfixation,fractured
teeth in the line offrac-ture,and comminuted fractures.Most infections appear to be
mixed innature,with a-hemolyticStreptococcusand Bacteroides spp organisms found
mostcommonly.58Treatment has already beenoutlined as for delayed and nonunion
offractures.MalunionMalunions can be defined as a bone unionofthe fracture in which
some displace-ment ofthe bones still exists.Not allmalunions offractured mandibles
areclinically significant.Often malunions inedentulous patients or those involving
theramus and condylar area ofthe mandibleresult in no clinically detectable
alterationin appearance or function.When,thedentate portion ofthe jaw is
involved,however,a malocclusion can result.Therates ofmalocclusion in patients
treatedwith IMF tend to be very low.In oneprospective trial between rigid
internalfixation and standard techniques the rateofmalocclusion with the rigid
fixationwas three times higher.However,as theauthors concede,they were initially
inex-perienced with the technique and othershave reported a low incidence ofmaloc-
clusion.145,146Malocclusion can be cor-rected by further or prolonged IMF in
theearly stages ofhealing,and selective toothgrinding,orthodontics,or
osteotomiesafter complete bony union.Malocclusion that does not resultfrom growth
alterations but from a mal-union ofthe condyle fracture occurs infre-quently ifan
adequate follow-up regimenis followed.Ifmalocclusion does persist,its management is
similar to the manage-ment ofmalocclusion from other causes.Judicious use
ofequilibration,orthodon-tics,and orthognathic surgery allows forrestoration ofa
functional occlusion.Before reconstructing the occlusion to thisnew articulation,it
is necessary to allow aperiod of6 to 12 months for completehealing and for any
remodeling ofthearticular apparatus to occur.Nerve InjuryTraumatic injury to the
inferior alveolarnerve is common in displaced fractures ofthe body and angle ofthe
mandible.ThereFIGURE22-35A,Sinus tract from an infected anterior mandibular
fracture after open reductionwith internal fixation.B,After hardware removal and
bony d�bridement,a large defect can beobserved in the left parasymphysis region.AB
Principles ofManagement ofMandibular Fractures427are few studies documenting
recovery ofthe nerve.Larsen and Nielsen reported apermanent disturbance in mental
nervefunction in 8% of229 patients studied.147Return ofnerve function depends on
thedegree ofinitial trauma to the nerve and anaccurate reduction and adequate
fixationofthe mandibular fracture.Rarely otherbranches ofthe mandibular division
ofthetrigeminal nerve can be affected.Theseinclude the masseteric
nerve,auriculotem-poral nerve (both with condylar fractures),and the buccal and
lingual nerves associat-ed with intraoral lacerations with body orangle
fractures.Also rare is damage to themarginal mandibular branch ofthe facialnerve
with fractures ofthe condyle,ramus,and angle ofthe mandible.It is more com-mon to
see this nerve damage caused by alaceration along its course.Most fractures ofthe
mandible healwith relatively simple management.Allclinicians must be wary
ofovertreatmentofsimple cases that can lead to an increasein cost oftreatment for
both the patientand society and also an increase in compli-cation rates.Growth
AlterationGrowth alterations as the result ofcondylar injury may occur as the
resultoftwo mechanisms.Over- or understim-ulation ofnormal growth may resultfrom
direct injury to the condyle,or arestriction ofnormal growth may occursecondary to
fibrosis or scarring ofthesurrounding tissue.It was once thought that fracture
ofthe condyle produced a growth deficit inproportion to the age ofthe patient at
thetime ofinjury:the younger the child,thegreater potential growth
problem.120However,although it is true that childrenundergo several periods ofrapid
growthduring their development and that aninjury during one ofthese growth peri-ods
may be associated with a higher inci-dence ofgrowth alteration,78other fac-tors are
involved that alter this simplistictheory.Frequently,complete regenerationofthe
condyle occurs in young patients,with no residual deficit following frac-ture,and
better regeneration occurs inactively growing patients,particularlythose under the
age of12 years.148,149Thisclinical observation is supported byexperimental
studies,104which foundthat,following surgically created fracturedislocations in
young monkeys,excellentregeneration occurred with no growthdisturbance in any ofthe
animals.Thisability for restitution ofgrowth in chil-dren under the age of12 years
appears toaccount for the lack ofdirect correlationbetween the age ofinjury and the
degreeofgrowth disturbance�a correlationthat would be expected ifthe sole deter-
minant were the amount ofgrowth left atthe time ofinjury.The concept that the
condylar carti-lage acts as a growth center has beenreplaced by the theory that the
cartilageacts as a remodeling center.150The resti-tution ofgrowth seen after
condylarinjury (which at times may actually leadto overgrowth ofthe affected
condyle) isa direct result ofthis remodeling centerwithin the condylar cartilage
reacting to atraumatic episode.It is not unusual for anew condylar apparatus to
develop,withresorption ofthe displaced or dislocatedcondylar head.This
compensatorygrowth seems to depend on the potentialspace created by the
displacement ofthestump ofthe condylar process.150For thisreason,it is important to
maintain themandible in its original occlusion,notonly for a few weeks during
healing,butalso for the next several months whilebony regeneration and
compensatorygrowth occur.Even when occlusion ismaintained and the patient is ofthe
idealage,25% ofsubjects experience a growthdisturbance.148,149,151Because
ofthis,ade-quate patient education and long-termfollow-up for several years is
necessary inchildren with fractures ofthe condyle(Figure 22-36).Temporomandibular
Joint DysfunctionA wide range oftemporomandibularjoint problems may result from
injuriesto the condylar apparatus.Internalderangement and ankylosis are perhapsthe
two most common.Internal DerangementA correlationexists between previous condylar
fractureand the development ofinternal derange-ment ofthe temporomandibular
joint.There is a greater incidence oftemporo-mandibular joint pain,deviation on
open-ing and joint noise in patients with previ-ous condylar fractures.71The
resultantinternal derangement primarily occurs inadults and is oftwo broad
types.The firstis internal derangement that occurs on theside ofthe fracture and
results from softtissue injury within the joint.Open reduc-tion with direct repair
ofthe injured softFIGURE22-36Significant mandibular hypopla-sia in a 12-year-old
boy,resulting from bilateralintracapsular condylar fractures suffered shortlyafter
birth.
428Part 4: Maxillofacial Traumatissues has been advocated by some as apossible
means ofpreventing this prob-lem.98,99No long-term data have estab-lished that this
is effective.The other formofinternal derangement occurs contralat-eral to the
condylar injury.This derange-ment was described by Gerry as the�condylar
postfracture syndrome.�32Patients who develop a unilateral hingetype ofjoint after
a fracture can rapidlydevelop overfunction ofthe contralateraljoint with
hypermobility and,ultimately,anterior dislocation ofthe disk.AnkylosisAnkylosis is
a rare complica-tion ofmandibular fractures.It is more like-ly to occur in children
and is associated withintracapsular fractures and immobilizationofthe mandible.The
most commonlyaccepted etiology is ofintra-articularhemorrhage,leading to abnormal
fibrosisand ultimately ankylosis.141In children,ifleft untreated,it results in
disturbedgrowth and underdevelopment oftheaffected side.Prevention is easier than
cure,and the use ofonly short periods ofIMF inchildren can help reduce the
occurrence ofthis complication.Management once thecondition is established is
surgical with atemporomandibular joint arthroplasty,wide resection ofthe ankylotic
portion ofbone,coronoidectomy,and reconstructionwith a costochondral rib graft,with
activeearly and prolonged mobilization andexercises.152Although development
ofinternalderangement seems to occur solely inadult patients,ankylosis is much
morecommon in children (Figure 22-37).Factors contributing to the develop-ment
ofankylosis have been outlined.35They include the site and type offracture,the age
ofthe patient at the time ofinjury,the duration ofIMF,and the extent ofdamage to
the disk.The site and type offracture may playan important role in whether or not
anky-losis occurs.It is widely accepted that intra-capsular fractures are more
likely to devel-op ankylosis.The postinjury relation ofthecondylar stump with the
glenoid fossa isalso a factor.With fractures ofthe condylarhead,a greater
likelihood exists that therewill be intimate contact between the prox-imal portion
ofthe distal segment and theglenoid fossa,predisposing the patient
toankylosis.48Failure to produce ankylosisafter experimentally induced
condylarfractures,81coupled with the clinical obser-vation that the incidence
ofintracapsularfracture is much higher than that ofanky-losis,leads one to believe
that other factorsbesides the site offracture must be opera-tive in the production
ofankylosis.The condyle ofa young child is moreeasily crushed than
fractured,153,154possiblybecause the cortical bone ofthe child is rel-atively thin
and the condylar neck broad.155The immediate subarticular layer is alsoextensively
vascularized.An impact leadingto a crush injury is more common in a childbecause
ofthese anatomic differences,andthe resulting fragments ofhighly vascular-ized
osteogenic material that are dispersedthroughout the joint space may be thecause
ofankylosis.155This theory helps toexplain the clinical observation that there isa
greater predisposition for post-traumaticankylosis in patients sustaining
suchinjuries before the age of10 years.156It is widely accepted that the length
ofthe maxillomandibular fixation may playa role in the development
ofankylosis.Markey was unable to produce ankylosisafter experimentally induced
fracturewith prolonged maxillomandibular fixa-tion.157In studies performed by
Beeklerand Walker,ankylosis occurred with pro-longed fixation,while no ankylosis
couldbe created in a moving jaw.81This con-firms the observation that the duration
ofimmobilization is contributory to thedevelopment ofankylosis,although it isnot
the primary determinant.The loca-tion and condition ofthe disk may beanother
determinant in the occurrence oftemporomandibular joint ankylosisbecause one never
finds the disk in thearea oftemporomandibular joint ankylo-
sis.48Experimentally,ankylosis has beencreated in a baboon by a combination
ofbilateral fractures ofthe condyloidprocess,diskectomy,and
prolongedimmobilization,while the same procedurewithout diskectomy did not
produceankylosis.48Thus far,this discussion hasbeen limited to the development
oftrueankylosis with the formation ofa bony orfibrous union within the joint
itself.Thereis also the potential for the developmentofpseudo ankylosis ifsoft
tissue traumasurrounding the joint leads to fibrosis andscarring or (in the case
ofzygomatic archand coronoid fractures) a bony uniondevelops between other
fractured areasand not within the joint itself.In summary,it is likely that the
follow-ing groups ofpatients will be at high risk fordevelopment
ofankylosis:patients underthe age of10 years at the time ofinjury;patients with
intracapsular fractures andfracture dislocations with gross telescoping;FIGURE22-
37Coronal computed tomographyscan ofthe patient in Figure 22-36 showing truebony
ankylosis ofboth temporomandibular joints.
Principles ofManagement ofMandibular Fractures429and patients with compound
comminutedfractures,particularly ifthe coronoidprocess and zygoma are also
involved.35Prevention oftemporomandibularjoint ankylosis is accomplished by recog-
nition ofthose patients at risk,briefimmobilization periods,and
aggressivepostoperative physiotherapy and long-term follow-up.Other Complications
Associatedwith Condylar FracturesWhen the condylar head is forced posteri-orly in
the process offracture,some forceis directed against the posterior and supe-rior
walls ofthe glenoid fossa.Fracture ofthe tympanic plate may occur.In
addition,partial obstruction ofthe external audito-ry canal may result,causing a
conductivehearing loss because ofthe close proximi-ty ofthe middle ear.Patients
with a histo-ry ofa condyle fracture should undergo acareful otoscopic examination
to evaluatethe condition ofthe anterior wall oftheexternal auditory canal,as well
as toobserve for signs ofpotential middle earinjury.Appropriate consultation must
beobtained ifinjuries ofthis nature are indi-cated by clinical examination or
history.Basilar skull fracture along the floor ofthemiddle cranial fossa may also
occur from asimilar mechanism,resulting in cerebralcontusion.The fracture may also
spreadthrough the petrous portion ofthe tempo-ral bone,resulting in injury
ofcranialnerves VII and VIII and a neurosensoryhearing deficit (as opposed to a
conduc-tion deficit),facial nerve paralysis,andpossibly Battle�s sign.Ifeither
ofthe fracture segmentsencroaches on the infratemporal fossa,trauma to the nerves
or vessels in this areamay occur.Damage ofa large vessel canresult in hematoma
formation or develop-ment ofa false aneurysm.158This expand-ing hematoma or false
aneurysm may alsocause injury to the seventh cranial nerve.The third division ofthe
cranial nerve Vmay also be injured by the displacedcondylar
segments.159,160Ifaberrant rein-nervation occurs from this injury,the
latecomplication ofauriculotemporal syn-drome may result.160,161Postoperative
ManagementRegardless ofthe technique employed fortreatment ofthe mandibular
fractures,thepostoperative management ofthe patientis critical for long-term
successful rehabil-itation and return to function.In cases in which open reduction
inter-nal fixation is employed without the use ofpostoperative IMF,follow-up visits
shouldbe used as reinforcement sessions to remindthe patient about proper diet and
progres-sive increase in function.It has been ourexperience that in many respects
this groupofpatients should be monitored moreclosely than those treated with IMF to
pre-vent possible postoperative complicationssecondary to their injudicious or
untimelyreturn to normal diet and function.The proper length ofmaxillo-mandibular
fixation (ifused),the dura-tion and frequency ofevaluation by thesurgeon,the early
detection ofpotentialcomplications,the judicious use ofphysio-therapy,and proper
patient education areall necessary.In most cases some form ofIMF will have been
employed.The lengthofthe fixation period,as previously dis-cussed,varies between 2
to 8 weeksdepending on many factors.At the end ofthis period,a systematic approach
forremoval ofthe fixation is desirable.A follow-up regimen similar to that
describedby Walker must then be instituted.87,88Thisallows for wound healing
monitoring,oralhygiene reinforcement,and observation ofadequate dietary intake.It
also gives theclinician the opportunity to control theocclusion in those patients
who need fur-ther stabilization,while encouraging earlymovement in those patients
who have sta-ble occlusions.It is impossible to predicton the basis ofthe type
offracture whichpatients will need continued aggressiveelastic guidance to maintain
their occlu-sion.Children ofless than 12 years ofagerarely require more
fixation,but patientsover the age of12 years show extremevariability,regardless
offracture type.Ifthe occlusion is stable and reproducible atthe time ofIMF
release,then jaw-openingexercises are begun.Ifaggressive physio-therapy is
initiated after release ofIMF fortreatment ofa condylar process fracture,the
patient should be evaluated in 24 hours to confirm the presence ofa stable
occlusion.The arch bars are left inplace and training elastics are used.Thepurpose
ofthese elastics is to permit func-tion,while maintaining the occlusion.Aneffective
way to accomplish this is to grad-ually reduce the use ofelastics over a peri-od
oftime.Initially,elastics should be used24 hours a day.They should be placedlightly
during the daytime to assist inguiding the mandible into occlusion,par-ticularly
ifsignificant deviation is present,and applied more tightly at night.After 1
week,it may be possible to completelyabandon daytime elastic fixation and con-tinue
with relatively tight elastic fixation atnight.After another 1 to 2 weeks
ofthistherapy,assuming that continued mainte-nance ofa normal occlusion is
present,thepatient should be allowed to functionwithout any guiding elastic
fixation forapproximately 1 week.If,at that time,there continues to be a stable
occlusion,further evaluation should continue forother problems,such as limited
mouthopening or pain,and the arch bars may beremoved.If,on the removal ofthe IMF
orat any time during the training period,theocclusion becomes unstable and nonre-
producible,an additional period oftightintermaxillary fixation with wires or elas-
tics is indicated for 1 or 2 weeks.Clinicalexperience seems to indicate that a
longerperiod ofcontrolled elastic traction is oftenneeded in adults with displaced
or dislo-cated fractures,particularly ifthese arebilateral.Even with judicious use
ofguid-ing elastic fixation,patient education,andcareful continued
evaluation,malocclusion
430Part 4: Maxillofacial Traumapersists in some patients.In these cases onemust
consider equilibration,orthodontics,osteotomies,or a combination ofthese tocorrect
the malocclusion.Throughout the post-IMF period,aggressive maintenance ofrange
ofmotion is necessary.In some patients thismay be as simple as instructing them
toopen their mouths as wide as possible in asymmetrical manner.Other patients
mayinitially require daily evaluations andforced opening by the
surgeon.Manuallyforcing the teeth apart,use ofa ratchet,mouth props,progressive
wedging oftongue blades between the teeth,or othermore sophisticated physiotherapy
devicesare all effective means ofregaining pre-injury interincisal opening.The
success or failure ofany pro-posed treatment for the fracturedmandible,whether by
open or closedreduction,will necessarily hinge on thecareful adherence to sound
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CHAPTER 23.1Management ofMaxillary FracturesLarry L.Cunningham Jr,DDS,MDRichard
H.Haug,DDSThe results ofepidemiologic surveys onmaxillary fractures differ with the
politicsand population density ofthe geographicregion studied,the era in which the
sur-veys were performed,the socioeconomicstatus ofthe population,and the institu-
tion whose experience was reviewed.1�5Itis difficult to make generalized
statementsabout the findings ofthese studies,buttrends do exist,and these trends
make itclear that maxillary fractures are more fre-quently associated with motor
vehicleaccidents and motorcycle accidents thanwith any other cause.Maxillary
fracturesmost often occur in conjunction withother facial fractures and are most
oftenassociated with injuries such as lacera-tions,other facial
fractures,orthopedicinjury,and neurologic injury.1,2,5,6Mostmaxillary fractures
occur in young menaged 16 to 40 years;they are most com-mon among patients between
21 and 25 years ofage,and the risk ofsustainingfacial bone fractures increases as
the age ofthe patient increases.6HistoryAlthough maxillary fractures are com-monly
classified according to the Le Fortsystem,these fractures were describedand treated
thousands ofyears beforeRen� Le Fort was born.The first clinicalexamination ofa
maxillary fracture wasrecorded in 2500 BCin the SmithPapyrus.7Many other early
recordsdescribe treatments for maxillary frac-tures or the iatrogenic fracture
ofthemaxilla for therapeutic purposes.In 1822Charles Fredrick William Reiche
provid-ed the first detailed treatise ofmaxillaryfractures,entitled De Maxillae
SuperiorsFractura.7In 1823 Carl Ferdinand vanGraefe described the use ofa head
framefor treating a maxillary fracture.7Hisdevice was as technically complex
asthose currently in use.In 1859 BernhardR.K.Von Langenbeck described a tech-nique
for the osteoplastic resection ofthemaxilla.8In 1867 David Cheever dis-cussed
complete mobilization ofthemaxilla with the use ofchisels for theremoval ofa
nasopharyngeal tumor.9In1893 Otto Lanz also described the cre-ation ofan iatrogenic
maxillary fracturefor access to a tumor.It was not until 1901 that Ren� Le
Fortpublished his landmark works,a three-partexperiment using 32 cadavers that
wereeither intact or decapitated.10�12The headsofthe cadavers were subjected to
varioustypes oftrauma;the soft tissue was thenremoved and the bones were
examined.LeFort noted that,generally,ifthe face wasfractured,the skull was not.He
then statedthat fractures occurred through three weaklines in the facial bony
structure:those thatprotect the cranial cavity,those that cir-cumscribe the
midface,and those that cutacross the face.From these three lines theLe Fort
classification system was developed(Figure 23.1-1).Le Fort Classification SystemIn
his description ofmaxillary fractures LeFort considered several factors:the
vectorType IIIType IIType IFIGURE23.1-1Anteroposterior and lateral views ofthe
skull showing the Le Fort classification sys-tem ofmaxillary fractures.
436Part 4: Maxillofacial Traumaofforce overcoming the inertia ofthe face;the
thickness ofthe bone and buttressescounteracting the mass,velocity,and
pointofapplication;and the maxilla,which henoticed was unaffected by muscle
pull,unlike the long bones.These considera-tions resulted in a classification
ofthreelevels offracture.Le Fort I LevelMaxillary fractures at the Le Fort I
leveltraverse the lateral antral wall,the lateralnasal wall,and the lower third
ofthe sep-tum,and they separate at the pterygoidplates.Thus,the entire mobilized
segmentconsists ofthe maxillary alveolar bone,thepalatine bone,the lower third
ofthe nasalseptum,and the lower third ofthe ptery-goid plates.The superior two-
thirds ofthese bones remain associated with theface.Le Fort II LevelMaxillary
fractures at the Le Fort II levelinvolve most ofthe nasal bones,the max-illary
bones,the palatine bones,the lowertwo-thirds ofthe nasal septum,the den-
toalveolus,and the pterygoid plates.Unlike the horizontal separation noted inthe Le
Fort I fracture,the Le Fort II frac-ture is pyramidal in shape.The fractureextends
from below the nasofrontal suturethrough the nasal bones along the maxillato the
zygomaticomaxillary suture andincludes the medial inferior third oftheorbit.The
fracture then continues alongthe zygomaticomaxillary suture to andthrough the
pterygoid plates.The septumis also separated superiorly.The segmentsmay be intact
below this line offracture,but they are most often comminuted.Le Fort III
LevelFractures at the Le Fort III level involve thenasal bones,the zygomas,the
maxillae,thepalatine bones,and the pterygoid plates.These fractures essentially
separate theface along the base ofthe skull.The frac-ture line extends from the
nasofrontalsuture along the medial wall ofthe orbitthrough the superior orbital
fissure.Itthen extends along the inferior orbital fis-sure and the lateral orbital
wall to thezygomaticofrontal suture.The zygomati-cotemporal suture is also
separated.Thefracture then extends along the sphenoidbone,separating the pterygoid
plates.Theseptum becomes separated at the cribri-form plate ofthe ethmoid.Le Fort
III frac-tures are most often comminuted.Withhighly comminuted
fractures,patientsmay sustain fractures at more than onelevel.Virtually all
combinations ofLe FortI,II,and III fractures are possible on eitherside ofthe
face.In Garretson�s 1898 treatise the pri-mary method oftreating fractures
ofthemaxillae was to construct a bandage ordressing that elevated the mandible
intoocclusion and secure it there.13A numberofmaterials were used to add stability
tothese bandages,including plaster ofParis,wood,gutta-percha,and vulcan-ized
rubber.In addition to splinting thejaws Garretson advocated the use ofinterdental
splints,stating �As a means ofdressing in any complicated jaw fracture,the
interdental splint is as invaluable andreliable as it is simple ofconstructionand
easy ofapplication.�13Blair gave a very good description ofthe anatomy ofmaxillary
fractures and ofthe examination for diagnosing such frac-tures.14He noted that
mandibular ban-dages were insufficient to stabilize maxil-lary fractures and
advocated a maxillarysplint,quoting an authority ofthe day,Dr.John
L.Marshall:Impressions ofthe upper andlower teeth were taken with themodeling
compound by firstmolding it upon the upper teethand while it was yet soft
forcingthe lower jaw upward until a cor-rect occlusion ofthe teeth wasobtained.This
impression wastrimmed to the desired shape;aone-eighth-inch steel wire wasimbedded
in the sides on a linewith the ends ofthe teeth,thenbent backward upon itselfoppo-
site the cuspid teeth....Fromthis was constructed a hard-rub-ber splint,with the
wiresattached....The splint is held inposition by means ofdoubleelastic straps
attached to the wireon each side and buckled to aclose-fitting leather or net
cap,which is reinforced with leatherand laced firmly on the head....The object
of[the splint] was tofurnish a sure guide to the nor-mal position ofthe
superiormaxillae.Without this the cor-rectness ofthe adjustment ofthebones could
not have been veri-fied.Its importance thereforecannot be overestimated.14Similar
treatment modalities werepresented by Brophy in 1918;he present-ed illustrations
ofthe splints as well aspreoperative and postoperative images ofa
patient.15AnatomyThe two maxillae are paired structuresconnected by a midline
suture;the bonestogether compose a five-sided pyramid.The anterior surface slopes
downwardfrom its superior contact with the frontaland nasal bones at an angle
ofapproxi-mately 15�.The most prominent point atthe anterior surface is the
anterior nasalspine.A number ofprotuberances exist onthe maxilla,formed by the
alveolar baseand origins ofthe small facial muscles.The lateral surface ofthe
maxillae formsthe infratemporal fossae and buccalvestibule and attaches to the
zygoma.Mostofthe superior surface forms the majorityofthe orbital floor.The medial
surface ofeach maxillaforms the midline suture and lateral nasalwalls.This includes
the nasal concha and
Management ofMaxillary Fractures437sinus ostia.The ostium ofthe naso-lacrimal duct
is beneath the inferior con-cha.The ostia ofthe maxillary sinus andmiddle
ethmoids,as well as the opening ofthe nasofrontal duct,lie beneath the mid-dle
concha.The inferior border composes thepalatal vault and alveolus,which containthe
teeth.The posterior border abuts thesphenoid bone and the
pterygomaxillarysuture.16Within the maxilla is the maxil-lary sinus.This 34 �33 �25
mm air cavi-ty is responsible for the weakness ofthemaxilla.The sinus is present at
birth butdoes not pneumatize to its mature extentuntil the patient reaches 14 to 15
years ofage.Minor changes in the sinus continuethroughout life.17The strong
buttresses ofthe maxilla are the lateral piriform but-tress,the zygomatic
buttress,the greaterpalatine buttress,and the floor ofthe nose.The palatine bone is
Lshaped andabuts the posterior maxilla as a pairedstructure.These bones assist the
maxilla informing the posterior sinus,the posteriorlateral nasal wall,and the
pterygomaxillarysuture.When joined to the maxilla the fourbones represent one unit
(Figure 23.1-2).16The nasal bones are paired structuresthat abut the frontal bone
superiorly,themaxilla laterally,the septum posteriorlyand medially,and each other
anteriorlyand medially.The bones are thicker supe-riorly;therefore,fractures at the
Le Fort IIlevel may occur inferior to the nasofrontalsuture.The nasal septum is a
thin trape-zoidal bone lying perpendicular to andjoining the maxillae and palatine
bones.The superior border is thick and articu-lates with the ethmoid bone.16The
ethmoid bone is cuboidal andextremely pneumatized;thus,it can beeasily fractured
and comminuted.Thecribriform plate ofthe ethmoid composesthe roofofthe nasal cavity
and communi-cates with the anterior cranial fossaethrough multiple foramina for the
olfacto-ry nerves.Lateral to the crista galli is a slitthrough which dura mater is
exposed.Pos-terior and superior movements ofthemidface can easily comminute this
bone,thus disrupting the dura mater and result-ing in a cerebrospinal fluid
leak.16The zygoma abuts the frontal bone atthe frontozygomatic suture and the tem-
poral bone at the zygomaticotemporalsuture.The maxilla and zygoma form two-thirds
ofthe orbital rim and,along withthe palatine bone,one-third ofthe wallsand floor
ofthe orbit.The infraorbital nerve traverses theorbital floor and exits through the
infraor-bital foramen.The maxillary bone,alongwith the zygoma,forms the inferior
orbitalfissure.Through this fissure run the max-illary nerve,the infraorbital
vessels,andthe ascending branches ofthe ptery-gopalatine ganglion.The frontal
process ofthe maxilla contains the lacrimal appara-tus,which is housed between the
medialcanthal ligaments.The blood supply to the maxillae andpalatine bones is
through the periosteum,the incisive artery,and the greater andlesser palatine
arteries.The internal maxil-lary artery,a source ofpotentially devas-tating
hemorrhage,lies posterior to themaxillae and palatine bones and anteriorto the
pterygoid plates ofthe sphenoid.18The blood supply to the nasal septum andthe
lateral nasal walls is provided by theanterior and posterior ethmoidal arteries,the
sphenopalatine artery,and the greaterpalatine and superior labial
arteries.16DiagnosisClinical ExaminationAdvanced trauma life-support
protocolsshould be followed for all patients whohave suffered trauma.Detailed
examina-tion ofmaxillofacial fractures is complet-ed in the secondary survey,after
the pri-mary survey and successful resuscitationhave been completed.As has been
donehistorically the clinical examinationshould begin with the initial
observationofthe patient,followed by palpation ofthe fractures.14,19As was written
by Blairin 1914,��In all cases ofinjury oftheface the dental arches and the
palateshould be inspected,and the facial bonesoutlined
digitally.�14Lacerations,abra-sions,and ecchymotic areas should
berecorded.Periorbital ecchymosis andfacial edema should be noted and are
verytypical ofthese fractures.Epistaxis withany evidence ofcerebrospinal fluid
leak-age (clear fluid mixed with blood,�tramlines�) should be
identified.Asymmetryofthe nose,traumatic telecanthus,a flatnasal bridge,and a dish-
shaped face shouldall be noted.Intraorally the examiner maysee fractured
teeth,vestibular ecchymosisand edema,palatal ecchymosis,mucosalNasal boneNasal
septumZygomatic bonePalatine boneMaxillaFIGURE23.1-2Disarticulated midfacial
skeleton demonstrates the anatomy ofthe maxilla,the zygo-ma,the nasal bones,and the
nasal septum.
438Part 4: Maxillofacial Traumalacerations and bleeding,steps ordiastema in the
maxillary teeth,and mal-occlusion.The skeletal framework ofthe faceshould be
carefully palpated.With respectto the maxilla,the alveolus should be pal-pated and
any fractures or mobility noted.The examiner should also observe themaxilla for
movement as a unit,while pal-pating the forehead,the nasal bridge,andthe
zygomaticofrontal sutures.The noseshould be examined grossly for
contourirregularity (Figure 23.1-3).A nasal specu-lum should be used to identify
compoundfractures ofthe septum or septalhematoma.Both hands should be used
topalpate the orbital rims and in particularthe zygomaticomaxillary
suture.Theintraoral examination should be complete,and the examiner should note
accumula-tion ofblood,debris,or avulsed teeth thatcould compromise the airway,as
well asthe presence oflaceration,abrasion,orecchymosis.Abnormal occlusion with
ananterior open bite and posterior prematu-rities should be noted and correlated
withpretraumatic occlusion ifpossible (familymembers,photographs,dental
records).ImagingFractures are identified clinically and con-firmed
radiographically.In the past theWaters�view and lateral facial radiographswere used
in identifying maxillary frac-tures and may still be used today in remoteareas
without access to a computedtomography (CT) scanner (Figure 23.1-4).Fine details
ofthe fracture sites are diffi-cult to visualize.Axial and coronal CTscans ofthe
midface should be obtained ifa scanner is available (Figure 23.1-5).Ifclinical
evidence strongly indicates maxil-lary fracture (midface mobility and mal-occlusion
with intact mandible),then CTimaging is a confirmatory test for maxil-lary
fractures.Important indications forCT scanning are suspected orbital floorfractures
(best diagnosed in the coronalview) and surgical planning.CT scans canalso
demonstrate the soft tissue differencesofhematoma or edema ofthe subcuta-neous
tissue,muscle,and fat.For severemidface trauma or maxillary displace-ment,the
three-dimensional CT scan is avaluable tool (Figure 23.1-6).TreatmentPatients do
not die ofmaxillary fractures,but they may die ofconcomitant injury orfailure to
manage the sequelae ofmaxillaryfractures.As is true for all injuries
initialattention should be directed at establishingan airway and controlling
hemorrhage.The most frequent cause ofhemorrhage inLe Fort level fractures is a
fractured sep-tum.This bleeding may be addressed byplacing nasal packs ofone ofa
number ofmaterials,including gauze packing,Mero-cel packing (Medtronic Xomed),Rhi-
norocket (Shippert Medical TechnologiesCorp.),and Epistat (Medtronic
Xomed).Bleeding from sites oflaceration or abra-sion may be controlled by
tamponade.Exsanguinating hemorrhage is rarelyencountered with facial
fractures;however,its occasional occurrence has long beennoted:�Hemorrhage,which is
not readilyamenable to successful treatment,as in thecase ofrupture ofthe internal
maxillaryartery or its terminal branches,may be FIGURE23.1-3A,B,When the maxilla is
examined for fracture the head is stabilized and the den-toalveolar process is
manipulated so that gross movements offractured segments can be detected.Checking
for Le Fort II or III fractures requires that one hand holds the bridge ofthe nose
while theother manipulates the maxilla.Movement at the nasofrontal suture suggests
a Le Fort II or III fracture.ABFIGURE23.1-4Waters�radiograph for evalua-tion
ofmaxillary fractures.
Management ofMaxillary Fractures439followedby fatal results.�15Should uncon-
trollable bleeding be encountered,thepatient should undergo angiographic evalu-
ation with embolization ofthe injured arteryifindicated.20�24At least one group has
sug-gested caution in the use ofembolizationbecause ofthe possible crossover
oftheembolic material between the external andinternal carotid
circulation.25Maxillary fractures isolated to thedentoalveolar process and
involving boneshould be manually reduced and rigidlyfixated with arch bars and
ligature wires.Ifthe segment is too large to be stabilizedwith arch bars
alone,acrylic can be addedto the facial surface ofthe arch bar,or anocclusal splint
can be constructed andsecured in place.Complications includebone
resorption,ankylosis ofteeth,exter-nal root resorption,and tooth loss.26,27In more
extensive injuries thesequence oftreatment ofmaxillary frac-tures depends largely
on the associatedinjuries.Nasotracheal intubation is pre-ferred when it is not
contraindicated by theneed for complicated repair ofnasal andnasoethmoidal
injuries.In such cases asubmental intubation technique can beused28�32;tracheotomy
is a final option(Figure 23.1-7).After the airway has beensecured and general
anesthesia has beenadministered,arch bars should be placed,along with any required
splints or stents.Ifteeth are deemed unsalvageable theyshould be removed at this
time.Thesequence oftreatment depends on the sur-geon�s philosophy and the presence
ofother facial fractures.Whether the surgeonprefers to work from the �bottom
up�orfrom the �outside in,�anterior projectionofthe maxilla is most easily obtained
whenthe mandible is intact.For this reasonstrong consideration should be given to
therepair ofany mandible fracture before themaxilla is stabilized.Intermaxillary
fixa-tion (to an intact mandible) is the mostreliable technique for establishing
anteriorprojection ofthe maxilla (Figure 23.1-8).Although many wiring
techniqueshave been described in the past,rigidinternal fixation is the standard
ofcare.19,33�36The maxilla should be stabi-lized to the next highest stable facial
struc-ture,which varies with Le Fort fracturelevel.At the Le Fort I level,fixation
isplaced along the vertical buttresses ofthemaxilla at the piriform and zygomatic
but-tresses.At higher Le Fort levels it may benecessary to use fixation to the
nasalbones,the orbital rims,or the zygomati-cofrontal sutures.Although Le Fort
levelsare frequently referred to in discussions ofpatient treatment,high-quality CT
scansand widespread use ofrigid fixation haveled to the treatment ofmultiple facial
frac-tures as separate units.For example,a LeFort I/II fracture would be treated as
a LeFort I fracture,a left orbital fracture,or aleft zygomaticomaxillary complex
frac-ture.In these cases it is advisable to restoremidface projection with the
repair oforbital or zygomatic fractures before fixa-tion ofthe maxilla.Contemporary
bone plates and screwsare made oftitanium.For maxillary recon-struction these
plates must be ofsufficientrigidity to overcome the effects ofgravity;the forces
ofmastication are resisted bybone contact.For this purpose screws withan outer
diameter of1.5 mm are adequate.FIGURE23.1-5Computed tomography scan ofmidface
trauma,including maxillary fracture.FIGURE23.1-6Three-dimensional
computedtomography scans give an overall view oftheinjuries and offer valuable
information.FIGURE23.1-7The patient�s airway is protect-ed by using a submental
intubation technique.FIGURE23.1-8Arch bars and intermaxillaryfixation are shown.
440Part 4: Maxillofacial TraumaIn areas such as the orbital rim or nasalbone,1.3 mm
or 1.0 mm systems may beused.In cases in which bone contact is decreased because
ofcomminution,1.7 mm or 2.0 mm systems may be used.Ifresistance is encountered
duringmobilization ofthe maxilla,Rowe disim-paction forceps may be used to
helpreduce the fracture (Figure 23.1-9).Thepaired forceps are placed with the fat
endin the nose and the bowed end on thepalate.The surgeon stands over thepatient�s
head and in an inferior-anteriormovement disimpacts the maxilla.Furtherassistance
may be provided with Hayton-Williams forceps used in conjunction withthe Rowe
disimpaction forceps.Ifthe maxillary fracture is incomplete(eg,greenstick
fracture),the surgeon mayhave difficulty in mobilizing the maxilla.The fractured
hemimaxilla may beimpacted or telescoped,causing severemalocclusion with minimal
mobility.In acase such as this,severe difficulty with dis-impaction ofLe Fort level
fractures can beeasily overcome by completing the frac-ture with an osteotomy.This
concept isnot as novel as it might sound;in 1914,Blair wrote,��ifthe impaction
cannot bebroken up ...resort may be had to a small,sharp chisel.�14After down-
fracture themaxilla can easily be moved into appropri-ate occlusion and stabilized
without fur-ther difficulty (Figure 23.1-10).Immediate bone grafting has
beenadvocated for the severely comminutedmaxillary antrum.37This treatment pre-
vents prolapse ofthe facial soft tissue intothe maxillary sinus and the facial
deforma-tion that results.Titanium mesh works wellfor this procedure;it is
malleable,can bequickly fixated,resists pressure ofthe softtissues ofthe
face,becomes osseointegrated,and allows regrowth ofthe native tissue (ie,ciliated
respiratory epithelium,goblet cells,squamous epithelium) (Figure 23.1-
11).38Surgical SplintsIn cases ofgross comminution,periodon-tal disease,or
inadequate partial dentition(less than three occluding teeth per sex-tant),occlusal
wafers or palatal splints areuseful.These splints are fabricated afterimpressions
have been taken and modelsurgery has been completed.When anocclusal wafer is
fabricated it should coverthe occlusal surfaces and the heights ofcontour,but it
should not encroach on thesoft tissues.Holes should be placedbetween occlusal
surfaces in the splint sothat it may be ligated separately to the archbar,as might
be done with an orthognath-ic surgical splint.The Gunning�s splint has been used
toestablish intermaxillary fixation for eden-tulous patients;this splint is
essentially adenture baseplate fabricated to the existingedentulous or partially
edentulous ridgewith arch bars or suspension brackets.39Dentures can also be
secured to the jawsFIGURE23.1-9A,Rowe disimpaction forceps.B,Application ofthe
forceps.BAFIGURE23.1-10A,B,Clinical images showing an unfractured right maxillary
antrum and a com-minuted telescoped left maxillary fracture that was very difficult
to reduce.C,D,After an osteotomy wasperformed at the Le Fort I level on the right
side,the maxilla could be easily mobilized,and the fracturewas reduced and fixated
without further difficulty.ABCD
Management ofMaxillary Fractures441with bone screws before intermaxillaryfixation
is attempted.Special ConsiderationsHigh-Force or Avulsive InjuriesHigh-caliber
high-velocity gunshot wounds,blast injuries,and high-speed motor vehi-cle accidents
with unrestrained victimscause most avulsion injuries associatedwith maxillary
fractures.The priority intreating these injuries is to preserve asmuch ofthe
remaining tissue as possible.Consideration and administration ofanarrow-spectrum
antibiotic directed atoral and nasal contaminants,as well astetanus prophylaxis,are
a priority in theseinjuries.As is true for all injuries thesewounds should be
thoroughly evaluatedfor bleeding,foreign bodies,and extent ofdamage.Extensive
irrigation with pulsedfluids should be used to remove debris.Life-threatening
hemorrhage shouldbe addressed early for homeostasis andfor airway
management.40Hemorrhagethat cannot be controlled by local mea-sures such as packing
(anterior and pos-terior) and electrocautery is an indica-tion for angiography and
embolizationofthe injured artery or arteries.Becauseofthe collateral blood supply
ofthe face,most tissues remain viable with only asmall isthmus ofblood
supply.Fracturesshould be repaired with rigid fixation.Voids in bone should be
addressed with asecondary reconstruction.Multiple lac-erations with comminuted
fractures willbe associated with edema and substantialvenous congestion.This tissue
may pro-vide satisfactory blood supply to existingsegments but not to large bone
grafts.Next the soft tissue lacerations should beaddressed.Advancement flaps should
beused only to cover exposed bone or tocorrect oronasal or oroantral fistulas.Iftoo
little soft tissue exists,flaps shouldnot be advanced;such repairs should
beaddressed during a secondary recon-struction.Consideration should be givento the
use ofvascularized free flaps inthis situation.20For cases ofavulsion,whether free
flapsare used or not,implant reconstructionshould be considered.Implants with obtu-
rators can be used,as is often seen in partialmaxillectomy after tumor
resection.Implant restorations can also be placed inbone from composite flap
reconstructions.41Injuries to Geriatric PatientsGeriatricpatients who suffer a Le
Fort injury pose aspecial concern.Additional medical ill-nesses and disabilities
may render generalanesthesia quite risky for these patients.The surgeon should
exercise judgmentwhen morbid medical conditions coexistwith minimally displaced
fractures inedentulous patients.A new prosthesis maybe more effective than
reduction and fixa-tion ofthe fracture.The geriatric maxilla is less vascularand
has more pneumatized antra,less alve-olar bone,and less dense trabeculation.Should
reduction and fixation be required,existing dentures may be modified byrelining and
affixing arch bars or intermax-illary fixation buttons.A Gunning�s splintmay also
be fabricated.Such a splint maybe fixed to the zygoma,the anterior nasalspine,the
piriform rim,or the palate,eitherwith wires or cortical bone screws.Pediatric
Maxillary FracturesPediatricmaxillary fractures occur infrequently.Because the
pediatric sinuses are not high-ly pneumatized,these fractures tend to beless
comminuted in children than inadults.No long-term studies have beenundertaken with
populations large enoughto determine what alterations in maxillarygrowth will occur
after pediatric maxillaryfractures.When fixation is undertaken,consideration should
be given to the con-tour and the root length ofthe primarydentition.The use
ofocclusal splints andskeletal fixation should be entertained.Resorbable plating
systems have beenadvocated for use in pediatric patients sothat potential
complications oftransloca-tion,extrusion,and growth restriction canbe
avoided.42,43Triana and Shockleyreported the use ofan L-lactic acid andglycolic
acid resorbable plating system;advantages ofthe system include ease ofcontouring
the plates,appropriate rigidityofthe systems,resorption within 12 months,no
increased risk ofpostoper-ative wound infection,and the apparentabsence ofgrowth
restriction.42ComplicationsComplications associated with maxillaryfractures and
their repair are listed inTable 23.1-1.A number ofthese complica-tions may not be
readily apparent untilweeks or months after injury,but thepotential for their
occurrence should beborne in mind during evaluation andtreatment ofthe
patient.Perioperative and postoperative air-way obstructions are unusual in cases
ofmaxillary fracture alone.However,theseconditions may occur in association
withFIGURE23.1-11A,Titanium mesh is preformedbefore it is sterilized and used in
maxillary recon-struction.Reproduced with permission from HaugRH et
al.51B,Intraoperative view ofthe use oftita-nium mesh.AB
442Part 4: Maxillofacial Traumaextubation while the patient is obtunded,with a
septal hematoma or nasal packing,and with excessively edematous soft tissuesthat do
not allow breathing through thenasal airways.Patients with intermaxillaryfixation
and complete dentition may havedifficulty breathing during this time.Rein-
tubation,opening nasopharyngeal air-ways,or merely removing the intermaxil-lary
fixation may be effective.Uncorrectednasal septal fractures can lead to postoper-
ative airway obstruction that remains afterall soft tissue swelling has
resolved.Acutesinusitis can result from prolonged naso-tracheal intubation.44Acute
or chronicsinusitis may also occur in the ethmoid,sphenoid,frontal,and maxillary
sinusesbecause fractures may obliterate orobstruct the sinus ducts or
ostia.Postoperative hemorrhage occurs ifarterioles and veins are not ligated
whenlacerations are repaired,ifinadequatebone reduction allows continued
oozingofblood,ifan aneurysm is present,or ifanartery is partially
transected.Lacerationsshould be reexplored so that hemorrhagecan be
controlled.Hematomas should bedrained.Oozing ofblood from bonerequires re-reduction
or the use ofbonewax.Hemorrhage from a major arteryrequires emergency
tamponade;ifthesource cannot be identified,then arteriog-raphy and embolization are
indicated.Aneurysms and pseudoaneurysms arecomplications ofmaxillofacial trauma
butrarely occur as the result ofisolated maxil-lary fractures.They can also result
in post-operative bleeding and are indications forangiography and
embolization.45Because ofthe proximity ofthe maxil-la to the orbits,complications
associatedwith vision can occur.Blindness is rarelyassociated with midface
fractures and ismost often seen in fracture patternsinvolving the orbit,often with
a moresevere mechanism ofinjury.46Immediatepostoperative blindness can be a compli-
cation ofthe reduction ofhigh Le Fortfractures (Le Fort III or fractures
involvingthe orbits) and occurs because ofincreased intraorbital hemorrhage
orpressure,a retinal artery spasm,retrobul-bar hemorrhage,or the impingement ofbone
fragments on the optic nerve.47Anundiagnosed or inadequately treatedorbital floor
fracture (alone or in combi-nation with a zygomatic component) canlead to
enophthalmos and diplopia.The most obvious postoperative com-plications are
misplaced bone segments orfixation devices.These complications arereadily
identified by clinical examination(eg,malocclusion) or postoperative radi-ographic
examinations.A second surgicalprocedure will correct such complications.Other
complications related to rigid inter-nal fixation include
palpability,infection,extrusion or exposure,translocation,stress shielding,cortical
osteopenia,andnonunion.48,49Nonunion ofthe fracturedsegments can occur as the
result ofinade-quate blood supply,inaccurate position,movement
ofsegments,infection,ornutritional deficiencies.50Infections maybe caused by
contaminated soft tissue lac-erations or foreign bodies,hematomas,orodontogenic
infections from previouslydiseased or fractured teeth.Infectionaround bone plates
and screws can occuryears after their placement.Malunion ofmaxillary fractures
canobstruct the nasolacrimal ducts.Thisobstruction causes epiphora and may leadto
episodes ofdacryocystitis.Bone seg-ments from fractured or improperlyreduced
maxillary fractures can alsoimpinge on the infraorbital nerve,causingnumbness ofthe
distribution ofthe sec-ond division ofthe trigeminal nerve.Although the reduction
and fixationofmaxillary fractures may at times seemstraightforward,the proximity
ofcompli-cated anatomic structures and the conse-quences ofinaccurate repair make
itincumbent on the surgeon to follow soundsurgical principles in the management
ofthese fractures.AcknowledgmentsThe authors thank Flo Witte,MA,ELS,forher expert
editorial assistance.References1.Haug RH,Prather J,Indresano AT.An epi-demiologic
survey offacial fractures andconcomitant injuries.J Oral MaxillofacSurg
1990;48:926�32.2.Turvey TA.Midfacial fractures:a retrospectiveanalysis of593
cases.J Oral Surg 1977;35:887�91.3.Kelly DE,Harrigan WF.A survey offacial frac-
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FracturesInfraorbital nerve paresthesiaEnophthalmosInfectionExposed hardware
Deviated septumNasal obstructionAltered visionNonunionMalunion or
malocclusionEpiphoraForeign body reactionsScarring SinusitisAdapted from Haug RH et
al.52
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CHAPTER 23.2Management ofZygomatic Complex FracturesJonathan S.Bailey,DMD,MDMichael
S.Goldwasser,DDS,MDThe zygoma articulates with the frontal,sphenoid,temporal,and
maxillary bonesand contributes significantly to thestrength and stability ofthe
midface.Theforward projection ofthe zygoma causes itto be injured frequently.1The
zygoma maybe separated from its four articulations.This is called a zygomatic
complex frac-ture.The terms trimalaror tripod fractureare therefore
inaccurate.These termsreflect an inability to easily identify theorbital
(zygomaticosphenoid) portion ofthe injury before the advent ofcomputedtomography
(CT).The zygomatic archmay be fractured independently or as partofa zygomatic
complex fracture.The cause ofzygomatic injuries varieswith patient demographics and
the locationofthe reporting institution.Matsunaga andSimpson at Los Angeles
County/UniversityofSouthern California Medical Centerfound that a majority ofthe
1,200 zygo-matic fractures studied were the result ofmotor vehicle accidents
(MVAs).2In con-trast,Ellis and colleagues found that 80% ofzygomatic fractures in
Glasgow,Scotland,resulted from assaults,falls,or sportsinjuries.Only approximately
13% offrac-tures in this series involved MVAs.3In this chapter,the anatomic fea-
tures,diagnosis,management,and com-plications ofzygomatic complex frac-tures are
discussed.Surgical AnatomyThe zygoma has four projections,whichcreate a
quadrangular shape:the frontal,temporal,maxillary,and the infraorbitalrim.The
zygoma articulates with fourbones:the frontal,temporal,maxilla,andsphenoid.A
zygomatic complex fractureincludes disruption ofthe four articulat-ing
sutures:zygomaticofrontal,zygomati-cotemporal,zygomaticomaxillary,andthe
zygomaticosphenoid sutures (Figure23.2-1A and B).All zygomatic complex
fracturesinvolve the orbital floor,and therefore anunderstanding oforbital anatomic
featuresis essential for those treating these injuries.The orbit is a quadrilateral
pyramid that isbased anteriorly.The orbital floor slopesinferiorly and is the
shortest ofthe orbitalwalls,averaging 47 mm.4It is composed ofthe orbital plate
ofthe maxilla,the orbitalsurface ofthe zygomatic bone,and theorbital process ofthe
palatine bone.The medial and lateral walls con-verge posteriorly at the orbital
apex.Themedial wall consists ofthe frontalprocess ofthe maxilla,the lacrimal
bone,the orbital plate ofthe ethmoid,and asmall portion ofthe sphenoid
body.Thelateral orbital wall is the thickest and isformed by the zygoma and the
greaterwing ofthe sphenoid.The orbital roofis composed ofthefrontal bone and lesser
wing ofthe sphe-noid (Figure 23.2-1C).The zygomatic arch includes the tem-poral
process ofthe zygoma and the zygo-matic process ofthe temporal bone.Theglenoid
fossa and articular eminence arelocated at the posterior aspect ofthe zygo-matic
process ofthe temporal bone.The sensory nerve associated withthe zygoma is the
second division ofthetrigeminal nerve.The zygomatic,facial,and temporal branches
exit the foraminain the body ofthe zygoma and supplysensation to the cheek and
anterior tem-poral region.The infraorbital nerve pass-es through the orbital floor
and exits atthe infraorbital foramen (see Figure23.2-1C).It provides sensation to
theanterior cheek,lateral nose,upper lip,and maxillary anterior teeth.Muscles
offacial expression originating from thezygoma include the zygomaticus majorand
labii superioris.They are innervatedby cranial nerve VII.The masseter mus-cle
inserts along the temporal surface ofthe zygoma and arch and is innervated by
446Part 4: Maxillofacial Traumaa branch ofthe mandibular nerve (seeFigure 23.2-
1A).The temporalis fascia attaches to thefrontal process ofthe zygoma and zygo-
matic arch (Figure 23.2-1D).The fasciaproduces resistance to inferior displace-ment
ofa fractured fragment by thedownward pull ofthe masseter muscle.The position ofthe
globe in relationto the horizontal axis is maintained byLockwood�s suspensory
ligament.Thisattaches medially to the posterior aspectofthe lacrimal bone and
laterally to theorbital (Whitnall�s) tubercle (which is 1 cm below the
zygomaticofrontal sutureon the medial aspect ofthe frontalprocess ofthe zygoma).The
shape andlocation ofthe medial and lateral canthiofthe eyelid are maintained by the
can-thal tendons.The lateral canthal tendonis attached to Whitnall�s
tubercle.Themedial canthal tendon is attached to theanterior and posterior lacrimal
crests.Zygomatic complex fractures are oftenTemporalis muscleMasseter
muscleZygomaticus major muscleTemporalis fasciaZygomaticus minor
muscleZygomaticomaxillary sutureZygomaticotemporal suture Levator labii superior
muscleFrontozygomatic suture Zygomatic process, maxillaTemporal process,
zygomaGreater wing, sphenoidZygomatic archZygomatic process, temporalMedial
canthalligamentLateral canthalligamentPalpebral fissureInferior tarsusInfraorbital
nerveand vesselsLacrimal glandFrontomaxillarysutureOptic foramenSuperior
orbitalfissurePosteriorlacrimal crestAnteriorlacrimal crestLacrimal
boneInfraorbital foramenSkinSubcutaneoustissueLateral
skullTemporalismuscleSuperficialtemporal fasciaDeeptemporal fasciaPotential
spaceformed bydivision oftemporal fasciaZygomatic archCoronoidprocessFIGURE23.2-
1A,Relation ofmuscles and cranial bones to the zygomatic complex as seen in frontal
or lat-eral view.B,Relation ofthe skull to the zygomatic complex as seen from a
submental view.C,Relation ofsoft tissues,muscle,and nerves to the orbit as seen
from a frontal view.D,Frontal view offascia and muscleattachment to the
skull,zygomatic arch,and coronoid process.Adapted from Perrott DH,Kaban LB.Man-
agement ofzygomatic complex fractures.In: Peterson LJ,Indresano AT,Marciani
RD,Roser SM.Principlesoforal and maxillofacial surgery.Vol.1.Philadelphia (PA):
J.B.Lippincott Company; 1992.p.490�491.ABCD
Management ofZygomatic Complex Fractures447accompanied by an
antimongoloid(downward) cant ofthe lateral canthalregion caused by displacement
ofthezygoma (see Figure 23.2-1C).DiagnosisZygomatic fractures are not life
threaten-ing and are usually treated after more seri-ous injuries are stabilized
and swelling hasresolved 4 to 5 days after injuries.Initial evaluation ofthe
patient with azygomatic fracture includes documenta-tion ofthe bony injury and the
status ofsurrounding soft tissue (eyelids,lacrimalapparatus,canthal tendons,and
globe)and cranial nerves II to VI.Visual acuityand the status ofthe globe and
retinashould be established;an ophthalmologistshould be consulted for suspected or
ques-tionable ophthalmic injury.HistoryThe nature,force,and direction oftheinjuring
blow should be determined fromthe patient and any witnesses.A direct lat-eral
blow,as in an assault,often results in anisolated zygomatic arch or an
inferomedial-ly displaced zygomatic complex fracture.Afrontal blow usually produces
a posteriorlyand inferiorly displaced fracture.The patient with a zygomatic
complexfracture complains ofpain,periorbitaledema,and ecchymosis.There may
beparesthesia or anesthesia over the cheek,lateral nose,upper lip,and maxillary
ante-rior teeth resulting from injury to thezygomaticotemporal or
infraorbitalnerves.This occurs in 18 to 83% ofallpatients with zygomatic
trauma.3,5�7Whenthe arch is medially displaced,the patientmay complain
oftrismus.Epistaxis anddiplopia may be present.3Physical ExaminationEcchymosis and
edema are the most com-mon early clinical signs and are present in61% ofall
zygomatic injuries.2Depressionofthe malar eminence and infraorbitalrim produce
flattening ofthe cheek.Sub-conjunctival hemorrhage is often noted.Downward
displacement ofthe zygomaproduces an antimongoloid slant to thelateral
canthus,enophthalmos,and accen-tuation ofthe supratarsal fold ofthe uppereyelid
(Figure 23.2-2).Lacerations in thefacial region should lead the surgeon tosuspect
underlying fracture.Palpation ofthe zygomaticofrontalsuture,the entire 360�ofthe
orbital rim,and the zygomatic arch should be carriedout in an orderly
fashion.Tenderness,astep-off,or separation at the sutures areindicative ofa
fracture.Intraorally,disrup-tion at the zygomaticomaxillary buttressarea is
palpable,and ecchymosis in theregion ofthe canine fossa may be visible.The range
ofmandibular motion is evalu-ated to rule out impingement ofthe zygo-matic arch on
the coronoid process.In isolated zygomatic arch fractures,adepression is observed
and palpated ante-rior to the tragus (Figure 23.2-3).Pain anddecreased mandibular
motion are com-monly present with these injuries,whereasorbital signs are usually
absent.Evaluation ofthe eye includes docu-mentation ofvisual
acuity,pupillaryresponse to light,fundoscopic examination,ocular movement,and globe
position.Lim-itation ofmotion ofthe extraocular mus-cles,diplopia,and enophthalmos
may benoted ifsignificant fractures ofthe orbitalfloor or medial or lateral walls
are present.Lack ofpupillary response and ptosis arepresent ifcranial nerve III has
been injured.Injuries to the optic nerve,hyphema,injuryto the globe,retro-orbital
hemorrhage,reti-nal detachment,and disruption ofthelacrimal ducts may also be
present.Neurologic examination includescareful evaluation ofall cranial nerves,with
special attention directed toward cra-nial nerves II,III,IV,V,and VI.Radiographic
EvaluationThe diagnosis ofzygomatic fractures isusually established by history and
physicalexamination.CT scan ofthe facial bones,in axial and coronal planes,is
standard forall patients with suspected zygomatic frac-tures.8�10Radiographs are
helpful for FIGURE23.2-2A,A 22-year-old male who sustained a blow to the right
cheek.Frontalphotograph illustrates the typical signs ofzygomatic complex fracture:
periorbital ecchy-mosis,edema,antimongoloid slant,and subconjunctival
hemorrhage.B,A 38-year-oldmale who sustained a blow to the left cheek 2 weeks prior
to presentation.Frontal pho-tograph demonstrates resolving periorbital ecchymosis
and malar depression.AB
448Part 4: Maxillofacial Traumaconfirmation and for medicolegal docu-mentation and
to establish the extent ofthe bony injury.Computed TomographyCT is the gold
standard for radiographicevaluation ofzygomatic fractures.Axialand coronal images
are obtained to definefracture patterns,degree ofdisplacement,and comminution and
to evaluate theorbital soft tissues.Specifically,CT scansallow for visualization
ofthe buttresses ofthe midfacial skeleton:nasomaxillary,zygo-
maticomaxillary,infraorbital,zygomati-cofrontal,zygomaticosphenoid,and zygo-
maticotemporal buttresses.Coronal viewsare particularly helpful in the evaluation
oforbital floor fractures (Figure 23.2-4A).9Soft tissue windows,in the coronal
plane,are useful to evaluate the extraocular mus-cles and to evaluate for
herniation oforbitaltissues into the maxillary sinus.Plain RadiographsCT scans have
replaced plain films for thediagnosis and management ofzygomaticcomplex
fractures.However,a fundamentalworking knowledge ofthis technique isrequired.In
many emergency rooms andhospitals,trauma patients will still have plainfilm
radiographic evaluation.The ability toread and interpret these films to diagnoseand
treat these patients is mandatory.Waters�ViewThe single best radiographfor
evaluation ofzygomatic complex frac-tures is Waters�view.It is a
posteroanteriorprojection with the head positioned at a27�angle to the vertical and
the chin rest-ing on the cassette.This projects thepetrous pyramids offthe
maxillary sinus-es,permitting visualization ofthe sinuses,lateral orbits,and
infraorbital rims (Figure23.2-4B).When this is combined with anerect Waters�view,a
stereographic view ofthe fracture can be obtained.In patientswho are unable to
assume a facedownposition,a reverse Waters�projection pro-vides similar
information.Caldwell�s ViewCaldwell�s view is a pos-teroanterior projection with
the face at a15�angle to the cassette.This study is help-ful in the evaluation
ofrotation (around ahorizontal axis).Submentovertex ViewThe submen-tovertex (jug-
handle) view is directedfrom the submandibular region to the ver-tex ofthe skull.It
is helpful in the evalua-tion ofthe zygomatic arch and malar pro-jection (Figure
23.2-4C).Classification ofFracturesHistorically,the classification
ofzygomaticfractures was used to predict which fractureswould remain stable after
reduction.Clini-cally,this would allow the surgeon to identi-fy those fractures
that would require openreduction and some method offixation.In 1961 Knight and
North classifiedzygomatic fractures by the direction ofdis-placement on a
Waters�view radiograph.11With the advent ofCT scans and theincreased use ofrigid
internal fixation,more modern classification schemes aimto identify those fractures
that requireaggressive surgical approaches.In 1990,Manson and colleagues pro-posed
a method ofclassification based onthe pattern ofsegmentation and displace-
ment.8Fractures that demonstrated littleor no displacement were classified as low-
energy injuries.Incomplete fractures ofone or more articulations may be
present.Middle-energy fractures demonstratedcomplete fracture ofall articulations
withmild to moderate displacement.Com-minution may be present (Figure 23.2-5).High-
energy injuries were characterizedby comminution in the lateral orbit andlateral
displacement with segmentation ofthe zygomatic arch (Figure 23.2-6).FIGURE23.2-3A
36-year-old male who sustained a blow to the left cheek.A,Frontal photograph
illustrates the typical findings ofa zygomaticarch fracture: preauricular
depression.B,Worm�s-eye view.C,Axial CT scan demonstrating isolated depressed left
zygomatic arch fracture.ABC
Management ofZygomatic Complex Fractures449Gruss and colleagues proposed a sys-tem
that stressed the importance ofrecog-nizing and treating zygomatic arch frac-tures
in association with the zygomaticbody.12Like Manson and colleagues,Grussstressed
the importance ofidentifying andtreating segmentation,comminution,andlateral bowing
ofthe zygomatic arch.Zingg and colleagues,in a review of1,025 zygomatic
fractures,classified theseinjuries into three categories.7Type A frac-tures were
incomplete low-energy frac-tures with fracture ofonly one zygomaticpillar:the
zygomatic arch,lateral orbitalwall,or infraorbital rim.Type B fractureswere
designated complete �monofrag-ment�fractures with fracture and dis-placement along
all four articulations.Type C �multifragment�fractures includ-ed fragmentation
ofthe zygomatic body.Although all three classificationschemes vary to some
degree,eachmethod notes that as the amount ofdis-placement and comminution
increases,the role ofopen reduction and internalfixation
increases.TreatmentTreatment ofzygomatic fractures must bebased on a complete
preoperative evalua-tion.This includes a CT scan with axial andcoronal images to
fully appreciate the natureofthe injury.Classification techniques,FIGURE23.2-
4A,Coronal CT scan demonstrating aright zygomaticomaxillary buttress and orbital
floorfracture with herniation oforbital contents into themaxillary
sinus.B,Waters�view demonstrating rightzygomatic complex fracture.C,Submentovertex
viewdemonstrating displaced left zygomatic arch fracture.CABFIGURE23.2-5Middle-
energy fracture.A,Axial CT scan demonstrating displacement ofthe lateral orbital
wall.B,Coronal CT scan demonstrating frac-ture and minimal displacement ofthe
infraorbital rim.C,Coronal CT scan demonstrating mild displacement ofthe
zygomaticomaxillary buttress.ABC
450Part 4: Maxillofacial Traumaifthey are accepted,are helpful to standard-ize
terminology,to plan treatment,and topredict prognosis.However,the surgeonmust
individualize treatment based on acombination ofhistory,physical examina-
tion,radiographic findings,and sound clin-ical judgment.Management ofzygomatic
complexand zygomatic arch fractures depends onthe degree ofdisplacement and the
resul-tant esthetic and functional deficits.Treat-ment may therefore range from
simpleobservation ofresolving swelling,extraoc-ular muscle dysfunction,and
paresthesiato open reduction and internal fixation ofmultiple fractures.Zygomatic
Arch FracturesNondisplaced and minimally displacedzygomatic arch fractures may
require nosurgical correction.Because these injuriesusually do not result in
significant func-tional deficits,it may be appropriate sim-ply to observe the
patient.Duverney was the first surgeon todescribe an operative technique for treat-
ment ofa fractured zygomatic arch.13Heused intraoral finger pressure to elevatethe
depressed arch.Alternatively in thistechnique,the patient is instructed to biteon a
block ofwood,which results in tem-poralis muscle and tendon tension.Thisforce,along
with finger pressure in an out-ward direction,reduces the fracture.13Goldthwaite in
1924 was the first todescribe an intraoral approach to the zygo-matic arch through
a stab wound in thebuccal sulcus.14A sharp elevator is passedsuperiorly through the
vestibule andbehind the maxillary tuberosity,and for-ward pressure is applied to
reduce the arch.Quinn modified this technique bymaking an incision in the mucosa at
thelevel ofthe maxillary alveolus and extend-ing it inferiorly along the anterior
borderofthe ramus.The dissection continuesalong the lateral aspect ofthe
coronoidprocess,ending at the level ofthe maxil-lary alveolus and extending it
inferiorlyalong the anterior border ofthe ramus.The dissection continues along the
lateralaspect ofthe coronoid process,ending atthe level ofthe zygomatic arch at the
site ofthe fracture.An elevator is placed betweenthe coronoid processes and
zygomaticarch,and the fracture is reduced.15The standard technique for
treatmentofzygomatic arch fractures,first describedby Gillies,Kilner,and Stone in
1927,can alsobe used to reduce zygomatic complex frac-tures.16A temporal incision
(2 cm in length)is made behind the hairline.The dissectioncontinues through the
subcutaneous andsuperficial temporal fascia down to the glis-tening white deep
temporal fascia (Figure23.2-7A).The temporal fascia is incised hor-izontally to
expose the temporalis muscle.Asturdy elevator,such as a urethral sound orRowe
zygomatic elevator,is inserted deep tothe fascia,underneath the temporal
surfaceofthe zygoma.The elevator must passbetween the deep temporal fascia and tem-
poralis muscle or it will be lateral to thearch.The bone should be elevated in an
out-ward and forward direction,with care takennot to put force on the temporal bone
(Fig-ure 23.2-7B).The arch should be palpated atall times as a guide to proper
reduction.Thewound is closed in layers.An alternative technique uses a J-shaped
curved hook elevator.This isinserted just below the zygomatic archanterior to the
articular eminence througha preauricular stab incision.The tip ofthehook is
directed under the displaced frag-ments,and reduction is achieved withcontrolled
lateral traction.7In a series of2,067 zygomatic frac-tures,Ellis found 10 of136
isolated zygo-matic arch fractures required some formoffixation.3Numerous methods
ofstabi-lization for zygomatic arch fractures havebeen proposed.These include
temporarilypacking the temporal fossa with 1/2-inchgauze,a nasogastric tube,or a
urinarycatheter.17�19More conveniently,a transcu-taneous circumzygomatic arch wire
can bepassed and tightened over a foam-backedaluminum eye shield to suspend the
arch.Although not a support technique,analuminum foam-rubber-backed fingersplint
has been used to prevent the patientfrom placing undue force on the arch.Thesplint
is formed into a Ushape,taped tothe face,and maintained for 3 to 5
days.20FIGURE23.2-6High-energy fracture.A,Axial CT scan demonstrating lateral
bowing and segmentation ofthezygomatic arch.B,Coronal CT reconstructions
demonstrate comminution ofthe zygomaticomaxillary buttress,infraorbital rim and
orbital floor.This patient was unable to be positioned for true coronal scans
because ofacervical spine injury.Note disruption ofthe right globe on coronal
images resulting from orbital globe rupture.AB
Management ofZygomatic Complex Fractures451Open reduction with internal fixationis
seldom necessary for treatment ofiso-lated zygomatic arch
fractures.Internalfixation with miniplates may be requiredas part ofthe management
ofhigh-energycomminuted zygomatic complex or panfa-cial fractures.Zygomatic Complex
FracturesLow-Energy Zygomatic Complex Frac-turesLow-energy,nondisplaced orminimally
displaced zygomatic complexfractures may require no operative cor-rection.The
patient should be observedlongitudinally for signs ofdisplacement,extraocular
muscle dysfunction,andenophthalmos after swelling resolves.Sta-ble,minimally
displaced zygomatic com-plex fractures without significant clinicalfindings may
require no treatment.Thepatient should be made to appreciate therisk ofresidual
asymmetry ofthe cheek,orbit,and eyelid ifthe fracture is
notreduced.Documentation,including pho-tographs,is recommended.21Middle-Energy
Zygomatic Complex Frac-turesMiddle-energy,displaced zygo-matic complex fractures
require reductionand internal fixation.Over the past 20 years there has been an
increase in theuse ofopen reduction and internal fixa-tion.In 1984,Zachariadis and
colleaguesmanaged 45% ofall zygoma fractures withthe Gillies technique.At the same
institu-tion,in 1995,only 2.5% ofthese fractureswere treated by this same
method.22In 1996,Ellis and Kittidumkerng pro-posed an algorithm oftreatment for
isolat-ed middle-energy zygomatic complex frac-tures that did not require
orbitalreconstruction (Figure 23.2-8).23The initialstep in this algorithm is
reduction ofthefracture.Ellis and others recommend theuse ofa Carroll-Girard
screw,which isinserted transcutaneously into the malareminence (Figure 23.2-9).The
Carroll-Girard screw provides excellent three-dimensional control to reduce the
fracture.Ifthe reduction is unstable,or ifthereis question regarding the accuracy
ofthereduction,the author recommends pro-ceeding to open reduction and
internalfixation.The zygomaticomaxillary but-tress is exposed first and stabilized
with aplate ifnecessary.The zygomaticofrontal buttress isexposed next and also
stabilized with aplate ifrequired.This method requiresproper patient
selection,experience,andmeticulous technique to ensure accuratereduction and
stabilization.Other authors recommend routineexposure oftwo or more ofthe three
ante-rior buttresses for middle-energy injuries:the zyomaticomaxillary
buttress,zygo-maticofrontal buttress,and the infraorbitalrim (Figures 23.2-10�23.2-
12).In this manxner,multiple buttresses are visualized andthe three-dimensional
accuracy ofthereduction can be confirmed.24�27High-Energy Zygomatic Complex Frac-
turesA more aggressive surgical approachshould be planned to treat high-energy
frac-tures (Figure 23.2-13).12,23,24,28There is oftensignificant comminution ofthe
anteriorbuttresses,making anatomic reduction Superficial fasciaand
subcutaneoustissue retractedDeep temporalis fasciaoverlying muscleFIGURE23.2-
7Gillies�s approach to reduce zygomatic arch fracture.A,Temporal incision through
subcutaneous and superficial fascia down tothe deep temporal fascia.B,Reduction
offracture with elevator.Adapted from Perrott DH,Kaban LB.Management ofzygomatic
complex frac-tures.In: Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principles
oforal and maxillofacial surgery.Vol.1.Philadelphia (PA): J.B.Lippincott Company;
1992.p.498.AB
452Part 4: Maxillofacial Traumadifficult.With segmentation ofthe zygo-matic arch,it
is impossible to control thisposterior buttress.Additionally,these frac-tures often
require orbital reconstruction.To restore proper projection,facialwidth,and orbital
volume,exposure ofthezygomatic arch and orbital floor is oftenrequired in addition
to exposure oftheanterior buttresses.A coronal flap is usedto gain access to the
zygomatic arch.Atranscutaneous or transconjunctival inci-sion is used to explore
and reconstruct theinternal orbit.With wide intraorbitalexposure,the broad
sphenozygomaticsuture may also be visualized to aid inanatomic
reduction.12,23,24,28,29Surgical Approach to the Zygomaticomax-illary ButtressAfter
a throat pack isplaced and local anesthesia infiltrated,anincision is made in the
maxillary vestibule 3 to 5 mm above the mucogingival junc-tion.The incision extends
from the caninearea to the first or second molar region.Theuse ofelectrocautery may
reduce bleeding.The periosteal incision is made,and amucoperiosteal flap is
elevated to exposethe infraorbital nerve,piriform rim,andzygomaticomaxillary
buttress (see Figure23.2-10).Additional superior dissection isused to visualize the
infraorbital rim.30,31Surgical Approach to the Zygomati-cofrontal ButtressAccess
and exposurefor open reduction ofthe zygomati-cofrontal buttress can be achieved
througha supratarsal fold or lateral eyebrow inci-sion (Figure 23.2-14A and
B).Ifpresent,apreexisting laceration may be used forexposure ofthis region.In
1996,Kung and Kaban described theuse ofa supratarsal fold incision forapproach to
the lateral orbit (see Figures23.2-11 and 23.2-14B).32The incision isplaced in a
skinfold parallel to the superiorpalpebral sulcus above the tarsal plate.It
isplaced approximately 10 to 14 mm abovethe margin ofthe upper eyelid.A 2.0 cm
incision is usually adequate but maybe extended laterally into the crow�s-foot
forincreased exposure.Blunt dissection parallelto the orbicularis oculi muscle
fibers sepa-rates them and exposes the lateral orbitalrim.The dissection is
continued,superficialto the orbital septum and over the lateralorbital rim.A
vertical periosteal incision ismade,and subperiosteal dissection willexpose the
fracture.The incision providesaccess to the frontozygomatic suture andresults in a
less noticeable scar.A lateral brow incision is performedby first palpating the
frontozygomaticsuture.A 2.0 cm incision is made withinReduce fracture(Carroll-
Girard screw)Reduced and stableUnsure of reductionand/or unstableReduced but
unstableReduced and stableTransoral openreductionReduced but unstableOpen reduction
lateral orbit and wire/plate frontozygomatic areaBone plate zygomaticomaxilla
buttressReduced but unstableReduced and stableSTOPSTOPSTOPSTOPFIGURE23.2-8Zygomatic
complex fracture without need for internal orbitreconstruction.Adapted from Ellis E
and Kittidumkerng W.23FIGURE23.2-9Carroll-Girard screw placedtranscutaneously for
reduction ofa zygomaticcomplex fracture.
Management ofZygomatic Complex Fractures453the confines ofthe lateral eyebrow
parallelto the superior lateral orbital rim (see Fig-ure 23.2-14A).Dissection is
continuedthrough the orbicularis oris and theperiosteum to the fracture
site.Surgical Approach to the Infraorbital Rimand OrbitAccess and exposure for
openreduction ofthe infraorbital rim and orbitalfloor can be achieved through a
transcuta-neous subciliary or transconjunctival inci-sion.Protection ofthe globe
with a scleralshield or tarsorrhaphy is recommended.A subciliary incision is made 1
to 2 mmbelow and parallel to the lower eyelashmargin (see Figures 23.2-13 and 23.2-
14A).It should extend from lateral to the punc-tum in a natural skinfold.The fibers
oftheorbicularis muscle are separated horizon-tally at the same level as the skin
incision,and a composite skin-muscle flap is elevat-ed anterior to the orbital
septum.Aperiosteal incision is made on the anteriorsurface ofthe infraorbital
rim.Subpe-riosteal dissection is then completed toexpose the orbital rim and
floor.31,33Multi-ple variations ofthis technique have beendescribed including a
skin-only flap,astepped skin-muscle flap,and a subtarsalapproach.These have been
compared toeach other and to the transconjunctival inci-sion.34�36Regardless
oftechnique,trans-cutaneous approaches are associated with ahigher incidence
ofectropion,increasedscleral show,and cutaneous scarring.37�40To avoid the problems
associated withcutaneous incisions,many authors recom-mend the transconjunctival
approach.37�42Tessier described this approach in 1973(Figures 23.2-14C and 23.2-
15).43Thelower lid is retracted,and an incision ismade below the lower border ofthe
tarsus.Dissection is extended inferiorly,and apreseptal dissection (superficial to
theorbital septum) is used to expose theinfraorbital rim.Variations ofthis tech-
nique include a retroseptal dissection.Thisapproach maintains the integrity
ofthelower lid but requires retraction oftheorbital fat during fracture reduction
andfixation (Figure 23.2-16).31A lateral canthotomy can be used toincrease
exposure.Meticulous repair ofthe lateral canthotomy is required to pre-vent
asymmetry.31,38,40,41Manson and colleagues described amethod to expose the entire
lateral orbit,infraorbital rim,and orbital floor througha single incision.This may
be performedwith a subciliary or transconjunctivalapproach and requires extended
subpe-riosteal dissection with mobilization ofthelateral canthal tendon.44Pitfalls
in Surgical Approach to the Infra-orbital Rim and OrbitAll approaches tothe
infraorbital rim may result in complica-tions.The subciliary and
transconjunctivalincisions may result in ectropion,entropi-on,and increased scleral
show.Advocates ofthe transconjunctival approach citeincreased rates ofectropion and
scleralshow with transcutaneous incisions (seeFigure 23.2-13J).37�40In
1993,Applingfound a 12% rate oftransient ectropionand 28% rate ofpermanent scleral
showwith a subciliary approach.In comparison,the transconjunctival approach had
notransient ectropion and a 3% rate ofper-manent scleral show.39Multiple factors
have been cited as thecause ofincreased scleral show and ectro-pion.During the
dissection to the orbitalrim,care should be taken to ensure thatthe placement ofthe
periosteal incision ison the anterior surface ofthe maxilla.Anincision placed on
the superior rim orposterior to the orbital rim may violate theorbital
septum.Subsequent scarring andcontracture ofthe septum may result inincreased
scleral show or ectropion.44Improper wound closure may alsocontribute to lower lid
complications.FIGURE23.2-10Intraoral exposure and fixa-tion ofzygomaticomaxillary
buttress fracture.FIGURE23.2-11Exposure and fixation ofzygo-maticofrontal buttress
fracture via a supratarsalfold incision.FIGURE23.2-12Exposure and fixation ofinfra-
orbital rim fracture via a subciliary incision.
454Part 4: Maxillofacial TraumaFIGURE23.2-13A 36-year-old female sustaining a high-
energy right zygomatic complex fracture from a motorvehicle accident.A,Note
periorbital ecchymosis and flat-tening ofright malar eminence.The widened
intercanthaldistance results from a concomitant hemi-nasoethmoidfracture with
lateral dislocation ofthe medial canthal lig-ament.B,Axial CT scan demonstrating
zygomatic archfracture.C,Axial CT scan demonstrating posterior dis-placement
ofmalar prominence and comminution ofthezygomaticomaxillary buttress.D,Coronal CT
scan ofhemi-nasoethmoid fracture.E,Coronal CT scan ofcom-minution
ofzygomaticofrontal and zygomaticomaxillarybuttresses.Note orbital floor fracture
and significantenlargement ofthe orbital volume.F,Coronal flap torestore sagittal
projection ofthe zygomatic arch.Because ofcomminution ofthe
zygomaticofrontal,zygomaticomaxil-lary,and infraorbital rim,and hemi-nasoethmoid
frac-ture this was required to ensure anatomic reduction.Noteexposure oftemporal
fat pad to protect the facial nerveand exposure ofzygomatic arch.G,Anatomic
reduction ofthe hemi-nasoethmoid fracture via a preexisting lacera-tion.Note the
insertion ofthe medial canthal ligament.H,Anatomic reduction ofthe orbital rim via
a subciliaryincision.I,Intraoral exposure
ofzygomaticomaxillarybuttress.J,Postoperative frontal photograph demonstrat-ing
restoration offacial width,intercanthal distance,andmalar projection.Note increased
scleral show secondary tosubciliary incision.K,Postoperative coronal CT
scandemonstrating restoration oforbital floor and zygomati-cofrontal and
zygomaticomaxillary buttresses.ABCDEFGHIJK
Management ofZygomatic Complex Fractures455Following wide subperiosteal
exposure,which is often required for complex frac-ture repair,the facial soft
tissues maydescend caudally,resulting in loss ofante-rior projection,accentuation
ofthenasolabial fold,increased scleral show,andectropion.Phillips and colleagues
recom-mend resuspension ofthe periosteum,muscle,and subcutaneous
tissue.Multipleholes are drilled in the inferolateral orbitalrim.The edge ofthe
periosteum,muscle,and subcutaneous tissue is sutured to theorbital rim.This may
minimize tractionon the infraorbital tissue and subsequentectropion or increased
scleral show.33Lastly,postoperative support for thelower eyelid with a frost stitch
has beenproposed as a technique to prevent ectro-pion.This may encourage re-draping
ofthe lower eyelid tissues.23,44Surgical Approach to the Zygomatic ArchIn high-
energy zygomatic complex frac-tures or secondary correction ofzygomat-ic
deformities,access is limited with con-ventional incisions.To obtain
adequateexposure,a coronal incision combinedwith a lower eyelid approach is recom-
mended (see Figure 23.2-13F).The initial incision is through the skin,subcutaneous
tissue,and galea ofthe scalp.Elevation ofthe coronal flap proceeds in thesubgaleal
loose areolar connective tissuesuperficial to the pericranium.The tempo-ral and
preauricular plane ofdissection isalong the temporal fascia,which can beidentified
by its characteristic glisteningwhite appearance.A horizontal periostealincision is
made 2 to 3 cm above the supra-orbital rim,and a subperiosteal plane ofdis-section
is developed to the superior and lat-eral orbit.An incision is made in
thesuperficial layer ofthe temporal fascia fromthe posterior zygomatic arch to the
previ-ously exposed supraorbital region.The tem-poral fat pad should be identified
(see Fig-ure 23.2-13F).The dissection is extendedinferiorly at this depth to the
zygomatic archand anteriorly to the lateral orbital rim.Thefacial nerve is
protected within the flap.12,31Internal FixationHistorically,manymethods have been
used for stabilization ofzygomatic complex fractures.These haveincluded antral
packing,percutaneous wirefixation,and wire osteosynthesis.It is nowaccepted that
miniplate or microplate fixa-tion provides the best results and
minimalcomplications.22,45�47LateraleyebrowSubciliaryPercutaneousTemporal(Gillies)S
upratarsal foldConjunctivalFIGURE23.2-14Frontal view illustrating periorbital
incision sites.A,Four different incisions for repair ofzygoma fractures.B,Upper
eyelid incision within the lateralsupratarsal fold.C,Transconjuctival incision
below the lower border ofthe tarsus.Adapted from Perrott DH,Kaban LB.Management
ofzygomatic complex fractures.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM.Principles oforal and maxillofacial surgery.Vol.1.Philadelphia (PA):
J.B.Lippincott Company; 1992.p.500.ABCFIGURE23.2-15Transconjunctival incision
forapproach to the infraorbital rim.ConjunctivaOrbital fatSkinTarsal plateOrbital
septumOrbicularisoculi muscleMaxillary sinusFIGURE23.2-16Sagittal view ofeye
illustrating relation ofconjunctiva,orbital septum and fat,and orbicularis muscleto
the eye and infraorbital rim.Adapted from Perrott DH,Kaban LB.Management
ofzygomatic complex fractures.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM.Principles oforal and maxillofacial surgery.Vol.1.Philadelphia (PA):
J.B.Lippincott Company; 1992.p.501.
456Part 4: Maxillofacial TraumaControversy exists regarding the bestlocation for
internal fixation and the num-ber and type ofplates required.Multiplestudies have
tried to characterize the forcesplaced on the zygomatic complex and theamount
offixation required to achieve�stability.�23,24,29,48�54These forces includethe
masseter and temporalis muscles andfascia and soft tissue contracture,whichcause
rotational movements in multipleaxes around the zygomatic buttresses.Internal
fixation must provide enoughstrength to resist these forces.For low- and middle-
energy fractures,stable fixation can be achieved at one ormore ofthe anterior
buttresses.The loca-tion offixation and number ofsites offix-ation depends on the
fracture pattern,location,vector ofdisplacement,anddegree
ofinstability.Occasionally one-point fixation may be adequate.7,23,26,50,52More
commonly two- or three-point sta-bilization is required.7,23,24,26,27,45,50,55For
high-energy injuries,a fourthpoint offixation is required.The zygomat-ic arch is
typically comminuted and later-ally displaced.Open reduction and inter-nal fixation
is required to restore properfacial width and projection.7,12,23,24,45,55Internal
Fixation ofthe Zygomaticomax-illary ButtressThe zygomaticomaxillarybuttress
provides an ideal location forinternal fixation for middle- and high-energy
fractures.53,54Anatomic reductionofthis fracture assists in restoring
malarprojection,but is difficult ifthe buttress iscomminuted.The overlying soft
tissue isthick,and plate palpability is not a con-cern.Therefore,this fracture
should bestabilized with 1.5 or 2.0 plates.23,26,55,56Internal Fixation ofthe
ZygomaticofrontalButtressThe zygomaticofrontal buttresscontains excellent bone for
fixation and canaccommodate a 2.0 plate.55The reductionand fixation ofthis fracture
will reestablishthe vertical height ofthe zygomatic com-plex.However,because ofits
narrow inter-face,this buttress may not be as helpful inevaluating reduction ofa
rotated frac-ture.12,54The thickness ofthe soft tissueoverlying this region is
variable.In someinstances it may be quite thin and a largeplate may be
palpable.Ifstable fixation canbe achieved at other sites,a smaller platemay be
used.55Internal Fixation ofthe Infraorbital RimUnlike the zygomaticofrontal
buttress,theinfraorbital rim has poor quality bone forinternal
fixation.55Additionally,the lowereyelid skin is quite thin,and large plates
areeasily palpable.Despite these concerns,fix-ation ofthis site is required to
define theorbital volume and facial width.57�59Theinfraorbital rim is typically
displaced poste-riorly and inferiorly.28The fracture shouldbe mobilized anteriorly
and superiorly andstabilized.Typically a 1.0 or 1.5 microplateis used to stabilize
the infraorbitalrim.26,27,30,55A potential pitfall in reductionofthis fracture is
an unappreciated hemi-nasoethmoid fracture (see Figure 23.2-13D).Ifthe infraorbital
rim is secured tothis undiagnosed displaced segment,post-operative facial widening
may occur.23,54,60Internal Fixation ofthe Zygomatic ArchInternal fixation ofthe
zygomatic arch isrequired for high-energy fractures thatdemonstrate comminution and
lateral dis-placement.12,23,24,28,55Restoration ofthissagittal buttress assists in
restoring facialprojection and facial width.When exposed,the zygomatic arch is
often reduced and sta-bilized first in the sequence ofrepair ofhigh-energy
injuries.Caution must be usedin restoring a �straight�arch and not
a�curved�arch,which will decrease facialprojection.This fracture typically requires
alarge plate to resist deformational forces.55,56Sequence ofInternal FixationAs in
thetreatment ofpanfacial fractures,a system-atic approach is helpful to ensure
accuraterestoration offacial height,width,andprojection.28,53For middle-energy
injuries with expo-sure ofall three anterior buttresses,thezygomaticofrontal
fracture may be stabi-lized temporarily with an interosseouswire.26,28This is
followed by fixation ofthezygomaticomaxillary fracture and theinfraorbital rim.The
temporary wire at thezygomaticofrontal fracture is replaced witha plate.The orbital
floor is reconstructedafter the zygoma has been restored to itscorrect three-
dimensional position.26,53In high-energy fractures,the zygomaticarch should be
reconstructed first.12,24,28,45,53Management ofthe Orbital FloorPatients with
middle-energy zygomaticcomplex injuries and no clinical or radi-ographic evidence
oforbital disruption donot require exploration.23Middle-energyinjuries with
displacement ofthe orbitalrim or floor or herniation ofsoft tissueinto the sinus
should be explored (see Fig-ure 23.2-4A).Clinical indications fororbital
exploration include enophthalmos,limitation ofextraocular muscle functionwith a
positive forced duction test,andpersistent diplopia.High-energy fracturesrequire a
more aggressive approach,andthe orbital rim and floor should beexplored and
reconstructed.23,24,26,45,53,61Fujino and Makino classified orbitalfloor injuries
as linear and pure blow-outfractures (Figure 23.2-17).A linear frac-ture occurs
when the infraorbital rim isstruck,displacing the orbital contents andfloor
posteriorly.62The orbital septum istorn,herniating soft tissue into the maxil-lary
sinus.When the force is removed,theorbital floor returns to its original
positionand the soft tissues are entrapped in thefracture site.Comminution ofthe
orbitalfloor is produced by a force ten timesgreater than that required for a
linear frac-ture.Fragments are forced inferiorly intothe sinus,producing bony
discontinuity.Indications for exploration ofisolatedorbital floor fractures include
CT scan evi-dence ofa fracture and herniation oforbital
tissue,enophthalmos,dystopia,
Management ofZygomatic Complex Fractures457disabling diplopia that does not
improveover 7 to 14 days,and a positive forcedduction
test.45,60,61,63�65TreatmentAccess to the floor is accom-plished by a subciliary or
transconjuncti-val incision.Simple linear fractures mayrequire only removal
ofentrapped tissue.Larger defects require reduction ofthe softtissue and bone
fragments from the sinusand reconstruction ofthe floor with abone graft or
implant.Exploration oftheorbital floor is completed prior to reduc-tion ofthe
fracture.Reconstruction ofthefloor is completed after reduction and sta-bilization
ofthe orbital rim.26,55,61The orbital floor may be reconstruct-ed with an
autograft,an allograft,or aprosthetic implant.Autograft sourcesinclude
calvaria,iliac crest,or nasal septalcartilage.66,67Allograft sources
includelyophilized dura and cartilage.68Alloplas-tic material such as titanium
mesh27,66,69offers a strong,malleable material that canaccurately be adapted to
span the orbitaldefect.Porous polyethylene implants andresorbable polydioxanone
sheets have alsobeen used for orbital reconstruction.45,70,71Regardless ofthe
technique,anatomicrestoration ofthe orbital volume isrequired to prevent
postoperative enoph-thalmos.57�59,66In complex fractures,a sig-nificant portion
oforbital floor may becomminuted or missing.The defect mustbe completely
defined,and the graft orimplant must be placed on an intact pos-terior
�ledge,�which may be 35 to 38 mmposterior to the rim.72,73Forced duction tests
should be performed before and after the orbitalfloor exploration,as well as after
recon-struction.55,61Role ofBone GraftingEarly bone graft-ing is indicated for
severe injuries in whichthere is loss ofbone or extensive comminu-tion.Comminution
ofthe orbital floor andzygomatic buttresses is common in high-energy injuries.These
zygomatic complexfractures are often associated with othersevere midface fractures
that require treat-ment.Grafts may help to achieve anatomicreduction and
stability,as well as to preventsoft tissue contraction.74,75Postoperative Care
Zygomatic complexfractures violate the maxillary sinus.For thisreason,antibiotics
and decongestants arerecommended.Ampicillin,amoxicillin,clindamycin,or
cephalosporin may beused.61A decongestant such as pseu-doephedrine is also used to
clear the airway.Incisions are observed carefully forsigns ofinfection,and the eye
is examinedto document visual acuity and to rule outcomplications such as corneal
abrasion.Postoperative radiographs (Waters�viewand submentovertex view) are
obtained todocument reduction ofthe fracture.A CTscan may be obtained in comminuted
frac-tures to evaluate the zygomatic complexreduction and orbital
reconstruction.54,61ComplicationsAlthough complications ofzygomatic com-plex and
zygomatic arch fractures areuncommon,the surgeon must recognizetheir signs and
symptoms to provideappropriate care.Complications may occurin the early
postoperative period or mayonly become manifest later in recovery.Infraorbital
ParesthesiaThe incidence ofsensory alterations oftheinfraorbital nerve following
zygomatictrauma ranges from 18 to 83%.3,5�7Studiesby Vriens and colleagues and
Taicher andcolleagues have found improved recoveryofinfraorbital sensation
following openreduction and internal fixation at thezygomaticofrontal suture
compared withreduction without fixation.5,6Presumably,anatomic reduction ofthe
fracture mayminimize compression ofthe nerve andallow for recovery.However,in
Vriens�sstudy,the same degree ofimprovementwas not seen in patients requiring
orbitalfloor exploration and reconstruction.Malunion and AsymmetryInadequate
reduction or stabilization ofzygomatic fractures may result in malunionor
asymmetry.7,12,23,28Poor malar projec-tion is the result ofuncorrected inferior
andposterior rotation ofthe zygoma.Increasedfacial width,in addition to decreased
malarprojection,results from inadequate reduc-tion ofthe zygomatic arch as part ofa
high-energy orbitozygomatic injury.28Malunion that is recognized up to 6 weeks
after injury may be correctedusing routine zygomatic reduction tech-
niques.Correction ofmild late deformitiesincludes autogenous onlay grafts or place-
ment ofalloplastic implants such asporous polyethylene.24Severe late post-traumatic
deformities may require zygo-matic osteotomy and repositioning.Cra-nial bone
grafting may also be required.Scarring and contraction ofthe periorbitalsoft tissue
may also occur.76Lid retraction,entropion,ectropion,and canthal reposi-tioning may
need to be addressed in addi-tion to osseous
reconstruction.EnophthalmosEnophthalmos is one ofthe most troublingcomplications
following orbitozygomaticFIGURE23.2-17Isolated blow-out fracturewith herniation
oforbital contents into themaxillary sinus.
458Part 4: Maxillofacial Traumafractures.An increase in orbital volume isthe most
common etiology.57�59Grant and colleagues described thisclinical problem eloquently
by comparingthe shape ofthe orbit to that ofa cone.Thevolume ofa cone is 1/3(pr2)
h.The orbitalrim position determines the radius ofthecone and the anteroposterior
orbitallength is the height ofthe cone.In thisequation,the radius is squared and
smallincreases in the radius result in dramaticincreases in volume.Clinically,poor
align-ment ofthe orbital rim may significantlyincrease the orbital volume and
result inenophthalmos.58Orbital floor blow-out fracture alsomay result in
enophthalmos by increasingthe orbital volume (Figure 23.2-18).Withimproved CT
technology,calculation oforbital volume and its implication regard-ing orbital
floor fractures is possible.73,77�80Raskin and colleagues demonstrated that a13%
increase in orbital volume,at 4 weeks,results in significant enophthalmos (> 2
mm).79The critical size ofthe orbitaldefect and herniation oforbital tissues
havealso been studied.In 2002,Ploder and col-leagues reported that a mean fracture
areaof4.08 cm or a mean displaced tissue vol-ume of1.89 mL,was associated with
greaterthan 2 mm ofenophthalmos.80In general,approximately 1 cm3ofdisplaced
tissueequals 1 mm ofenophthalmos.81Late repair ofenophthalmos is techni-cally
challenging.Wide access with osteoto-my ofthe zygoma,repositioning,and grafting is
usually required.Re-draping ofthe periorbital soft tissue including a can-thopexy
may be required.57�59DiplopiaDiplopia is a common sequela ofmidfacialfractures.The
incidence varies between 17and 83% and depends on the time ofpre-sentation
following the injury and the pat-tern and severity ofthe injury.3,68,82�84In
areview of2,067 zygomatic complex frac-tures,Ellis and colleagues noted a 5.4
to74.5% incidence ofdiplopia.3Nondisplacedzygomatic complex fractures and
isolatedzygomatic arch fractures had the lowestincidence ofdiplopia,while pure
blow-outfractures had the highest incidence.The principal causes ofdiplopiainclude
edema and hematoma,entrap-ment ofthe extraocular muscles andorbital tissue,and
injury to cranial nervesIII,IV,or VI.Histologic studies by Iliffandcolleagues have
shown post-traumaticfibrosis ofthe extraocular muscles inresponse to injury.They
hypothesize thatthis may impair contractility and decreaseexcursions ofthe
muscles.45,82,85�87Axial and coronal CT scans and oph-thalmologic consultation are
recommendedto assist in evaluation.45,82Diplopia relatedto edema,hematoma,or
neurogenic causesmay resolve without intervention.Diplopiaresulting from entrapment
requires explo-ration and reduction ofherniated orbitaltissue (Figure 23.2-
19).45,60,61,63�65,82FIGURE23.2-18A,A 27-year-old female presented with late
enophthalmos and diplopia afteran undiagnosed orbital floor fracture.Note vertical
dystopia and prominent supratarsal fold.B,Coronal CT scan demonstrating
displacement ofthe orbital floor.C,One-year postopera-tive frontal photograph after
transconjunctival reconstruction ofthe orbital floor with titani-um mesh.Note the
symmetry ofthe vertical globe position and the supratarsal fold.D,Post-operative
coronal CT scan demonstrating titanium mesh reconstruction ofthe orbital floor.ABCD
Management ofZygomatic Complex Fractures459Persistent bothersome diplopia thatdoes
not resolve may require treatment byan ophthalmologist.The condition mayrespond to
exercise or surgery.45,61Traumatic HyphemaTrauma to the eye may result in
bleedinginto the anterior chamber�the areabetween the clear cornea and the colored
iris(Figure 23.2-20).Ophthalmology consulta-tion is recommended.Goals
oftreatmentinclude prevention ofrebleeding,which mayoccur in 5 to 30%
ofpatients,and mainte-nance ofnormal ocular tension.88.89Management ofhyphema
consists ofsupportive therapy including elevation ofthe head ofbed and patching
ofthe injuredeye.Medical management includes
topicalcycloplegics,corticosteroids,and �-blockers.Systemic
antifibrinolytics,carbonic anhy-drase inhibitors,and osmotic agents mayalso be
required.Rarely,surgical interven-tion by the ophthalmologist is required.Repair
offractures may be delayed.Traumatic Optic NeuropathyTraumatic optic neuropathy may
manifestas conditions ranging from mild visualdeficit to complete visual loss.An
ophthal-mologic consultation is mandatory.Treat-ment varies depending on the cause
butmay include systemic steroids or surgerywith orbital or optic nerve
decompression.Treatment offacial fractures may bedelayed.45,90Superior Orbital
Fissure SyndromeSuperior orbital fissure syndrome is anuncommon complication
following facialtrauma.Presentation may include ptosis,ophthalmoplegia,forehead
anesthesia,anda fixed dilated pupil.Proptosis may be pre-sent.Treatment may include
reduction offractures,steroids,orbital apex explo-ration,and aspiration
ofretrobulbarhematoma ifpresent.91Retrobulbar HemorrhageRetrobulbar hemorrhage is a
rare but severecomplication that may be the result ofeither the initial injury or
the operative cor-rection.Disruption ofthe retinal circula-tion may lead to
irreversible ischemia andpermanent blindness.In a review of1,405orbitozygomatic
fractures,Ord reported a0.03% incidence ofpostoperative retrobul-bar hemorrhage
with visual loss.92Anemergent ophthalmologic consultation
isnecessary;however,decompression withlateral canthotomy and cantholysis shouldnot
be delayed (see Figure 23.2-20).TrismusPatients with zygomatic fractures com-monly
present acutely with a complaint oftrismus.However,there are few cases
ofFIGURE23.2-20Retrobulbar hemorrhage.A,This patient presented with periorbital
pain,fixedand dilated pupil,proptosis,and acute progressiveloss ofvision.Note
hyphema.B,Immediate later-al canthotomy and cantholysis were
performed.ABFIGURE23.2-19A,A 45-year-old male suffered a fall and presented with
right orbital floor blow-out fracture and significant restric-tion ofthe inferior
rectus and diplopia.B,Coronal CT scan demonstrating large orbital floor blow-out
fracture with herniation oftheorbital contents into the maxillary
sinus.C,Postoperative view after transconjunctival reconstruction ofthe orbital
floor with titani-um mesh and return ofnormal extraocular muscle function.Note
projection ofthe globes without evidence ofenophthalmos.ABC
460Part 4: Maxillofacial Traumalong-term reduced mandibular range ofmotion
following zygomatic complexfractures reported in the literature.Themost likely
cause is impingement ofthezygomatic body on the coronoid processofthe
mandible.Trismus may also occursecondary to fibrous or fibro-osseousankylosis ofthe
coronoid to the zygomat-ic arch.A CT scan should be obtained toconfirm the
diagnosis.Coronoidectomy isthe most common treatment.Ifthe zygo-ma is improperly
reduced,zygomaticosteotomy and repositioning may be nec-essary to restore
unrestricted motion ofthe mandible.61,93AcknowledgmentThe authors gratefully
acknowledge Drs.Kaban and Perrott,the authors ofthechapter on zygomatic complex
fractures inthe first edition ofPrinciples ofOral andMaxillofacial Surgery,whose
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CHAPTER 24Orbital and Ocular TraumaMark W.Ochs,DMD,MDOrbital FracturesAnatomyThe
orbit is the bony vault that houses theeyeball,or globe.It is a quadrangular-
basedpyramid that has its peak at the orbital apex.The average adult orbit has a
volume of30 cc;the globe averages 7 cc (Figure 24-1).Even a modest change in the
position ofoneofthe bony walls can have a significantimpact on the orbital volume
and,thus,globe position.The orbit serves to houseand protect the globe.By age 5
years orbitalgrowth is 85% complete,and it is finalizedbetween 7 years ofage and
puberty.1,2The orbital rim is composed ofdensecortical bone that generally protects
theorbital contents and globe from directblunt trauma.Seven bones form the
orbit:maxillary,zygomatic,frontal,ethmoidal,lacrimal,palatine,and
sphenoid.Besidesforming a protective socket for the globe,these bones also provide
origins for theextraocular muscles,and foramina and fis-sures for cranial nerves
and blood vessels.3The orbital walls vary considerably intheir thickness.Whereas
the superior later-al and inferior rims tend to be rather thick,the bones just
posterior to these and themedial rim are usually fairly thin (< 1 mm).Fractures
ofthe anterior andmiddle thirds ofthe bony orbit are fairlycommon.The orbital floor
and medial wallare most frequently fractured owing totheir thinness and lack
ofsupport.This isfortunate since inward or medial displace-ment ofmidfacial or
zygomatic bones canreduce the orbital volume and be accom-panied by orbital
hemorrhage.The subse-quent increased intraorbital pressure ismost often relieved by
traumatic expan-sion ofthe walls with herniation oforbitaltissue into the maxillary
sinus and/or eth-moid air cells adjacent to these walls.Inessence,the paranasal
sinuses and ethmoidair cells serve as air bags or shock absorbersto the globe and
orbital contents.This pro-tective mechanism explains why globe per-foration is
relatively uncommon followingSites of potentialvisual
impairmentGlobeRuptureIntraocular hemorrhageOrbitRetrobulbar hematomaBlow-in
fractureOptic nerveEdemaBleedingVasospasmOptic canalShearing of nerveContusionBone-
fragment injuryIntracranialCentral injuriesOptic tractOccipital cortexOrbital
anatomy4 cm4.0 � 4.5 cm5 � 6 cm2.5 cm2 cm3 cm1 cm4.4 � 5 cmFIGURE24-1Orbital
configuration with potential sites for traumatic injuries leading to
visualimpairment.Adapted from Ochs MW,Johns FR.Orbital trauma.In: Fonseca
RJ,Marciani RD,Hendler BH,editors.Oral and maxillofacial surgery: trauma.Vol
3.Philadelphia (PA): W.B.Saun-ders; 2000.p.207.
464Part 4: Maxillofacial Traumamidfacial trauma.Orbital fractures thatinvolve the
frontal sinuses more common-ly result in serious eye
injuries.4,5Thesefractures,following blunt trauma,and theassociated blindness are
probably not seenas often owing to the severity offorces andconcomitant
neurologic,cervical spine,and multisystem trauma.In short,theygenerally are not
survivable events.The orbital roofconsists mainly ofthe frontal bone,with the
anterior cranialfossa superior to it.The lesser wing ofthesphenoid has a minor
contribution poste-riorly.The superior orbital rim is general-ly rather thick and
then rapidly becomesquite thin (< 1 mm) posterior from theedge.In elderly patients
the orbital roofmay be resorbed in select areas,allowingthe dura to become
confluent with theperiorbita.This should be kept in mindduring orbital dissection
and elevation inthis region for both trauma and tumorwork.Generally,the anterior
portion ofthe orbital roofis occupied by the supra-orbital extension ofthe frontal
sinus.Thefrontal sinus begins to form around theage of6 years and is unilateral in
5% ofadults and lacking in another 5%.Anterolaterally there is a smooth broadfossa
that houses the lacrimal gland.Atthe most medial extent is the
trochlea,approximately 4 mm behind the rim.There the cartilaginous pulley has a
dualinsertion for the superior oblique muscletendon.At the junction ofthe
medialone-third and lateral two-thirds ofthesuperior rim is the supraorbital
notch.Inone-fourth ofadults,a supraorbital fora-men is found,secondary to the
ossifica-tion ofthe ligament crossing the inferiorextent.6When reflecting bicoronal
flaps,asmall triangular wedge ostectomy shouldbe performed in these individuals
torelieve the encased supraorbital nerveand vessels and to allow for a
relaxedreflection oftissues at the rim.The orbital floor is bordered laterally
bythe inferior orbital fissure.However,there isno distinct border medially (Figure
24-2).The orbital floor is formed primarily by theorbital process ofthe
maxilla�anterolater-ally by a portion ofthe zygomatic bone,andposteriorly by a
small portion ofthe pala-tine bone.The maxillary sinuses are presentat birth and
reach the orbital floor andinfraorbital canal by age 2 years.7The inferi-or orbital
fissure gives rise to the infraorbitalgroove from its midportion,which is about2.5
to 3 cm from the infraorbital rim.Theinfraorbital fissure converts to a
canalhalfway forward,carrying the infraorbitalnerve and vessels and opening
approximate-ly 5 mm below the rim ofthe maxilla as theinfraorbital foramen (Table
24-1).8Theinfraorbital nerve provides sensory innerva-tion to the upper lip,lateral
nose,and ante-rior maxillary teeth and mucosa.The orbitalfloor can be as thin as
0.5 mm,with itsweakest portion just medial to the infraor-bital groove and
canal.This explains thephenomenon that most blunt traumasresulting in orbital floor
blow-outs are man-ifested primarily with injury and sagging ofthe medial orbital
floor and orbital contentsinto the underlying maxillary sinus withextension
laterally to the infraorbital canal.The lateral wall ofthe orbit is formedmainly by
the greater wing ofthe sphenoidand portions ofthe zygoma.Although thistends to be
the strongest wall,it is fairlycommonly fractured along the front-ozygomatic
junction,extending slightly FIGURE24-2Right bony orbit.The inferiororbital fissure
can be seen converting to a canalangling medially at the Y-shaped
divide.Thelacrimal fossa is characteristically thin.The lam-ina papyracea occupies
the majority ofthe medi-al wall,with the frontoethmoidal suture at thesuperior
extent.Table 24-1Orbital Fissures/Canals and Their ContentsLocationContentsSuperior
orbital fissure�lesser and Motor nerves:III (superior and inferior greater wings
ofsphenoiddivisions),IV (trochlear),V (abducens)Sensory
nerves:V1(frontal,lacrimal,nasociliary),sympathetic fibersVessels:superior
ophthalmic vein,anastomosis ofrecurrent lacrimal and middle meningeal
arteriesInferior orbital fissure�greater wingSensory nerves:V2(infraorbital and
zygomatic),ofsphenoid;palatine,zygomatic,parasympathetic branches
ofpterygopalatineand maxillary bonesganglionVessel:inferior ophthalmic vein and
branches topterygoid plexusOptic canal�lesser wing ofsphenoidOptic
nerve,meninges,ophthalmic artery,sympathetic fibers Anterior ethmoid canal�frontal
and Nerve:anterior ethmoid becomes dorsal nasalethmoid bonesVessel:anterior ethmoid
arteryPosterior ethmoid canal�frontal and Nerve:posterior ethmoidethmoid
bonesVessel:posterior ethmoid arteryNasolacrimal fossa�lacrimal and Nasolacrimal
sac and ductmaxillary bones
Orbital and Ocular Trauma465posteriorly and then running verticallyalong the
thinnest portion ofthe sutureline,where the greater wing ofthe sphe-noid and zygoma
meet.This wall separatesthe orbit from the temporalis muscle.Owing to the heavy
nature ofthis muscleand the direction ofblunt forces,generallythere is some mild
degree ofinward dis-placement.The lateral orbital walls,iftheywere to be extended
posteriorly,wouldform a 90�angle to each other.Each later-al orbital wall forms a
45�angle at theorbital apex,with its medial wall counter-part.This is important to
bear in mindwhen attempting to realign or reconstructfractured walls.The superior
orbital fis-sure separates the greater and lesser wingsofthe sphenoid and serves as
the delin-eation between the orbital roofand lateralwall.At the orbital apex the
lesser wing ofthe sphenoid forms the lateral portion ofthe ring ofthe optic
canal.One centimeterbelow the frontozygomatic suture,and justinternal (3�4 mm) to
the lateral orbitalrim,is Whitnall�s tubercle (lateral orbitaltubercle).This gentle
outcropping ofbonefunctions as the insertion point for the lat-eral retinacular
structures.The lateral reti-naculum is composed ofthe lateral hornofthe levator
aponeurosis;the lateral can-thal tendon ofthe eyelids;and the inferiorsuspensory
(Lockwood�s) ligament andmultiple fine check ligaments ofthe later-al rectus
muscle.These soft tissue attach-ments are found anatomically in this
orderproceeding inferiorly and posteriorly fromthe rim.These multiple structures
becomeconfluent to form the common lateral reti-naculum,which is the actual
insertion tothe tubercle.6Clinically the point toremember is that reattachment
ofthe lat-eral canthal tendon should be to the later-al orbital tubercle.The medial
wall ofthe orbit is by farthe most complex and potentially prob-lematic to manage
in severe trauma.Themedial orbital wall is composed anterior-to-posterior by a
portion ofthe maxillary,lacrimal,ethmoid,and sphenoid bones.The majority ofthe
medial wall is formedby the extremely thin (0.2�0.4 mm) lami-na papyracea ofthe
ethmoid bone.Housed along the frontoethmoidal junc-tion are the anterior and
posterior eth-moidal foramina.The anterior ethmoidalforamen is 20 to 25 mm behind
the medi-al orbital rim,and 12 mm beyond this isthe posterior ethmoidal
foramen.Theforamina can be found approximatelytwo-thirds ofthe way up the
medialorbital wall,within the frontoethmoidalsuture line,and serve as important
surgi-cal landmarks identifying the level ofthecorresponding cribriform
plate.Orbitalsurgeons use these arteries as the land-marks for the superior extent
oforbitalwall decompression.The anterior eth-moidal foramen transmits the
anteriorethmoidal artery and anterior ethmoidalbranches from the nasociliary nerve
fromthe orbit coursing into the nasal cavity.This is why otolaryngologists
sometimesuse a medio-orbital approach to ligate orcauterize the anterior ethmoidal
artery tocontrol recalcitrant nasal bleeding.Although the anterior ethmoidal
vesselcan be cauterized with few ill effects,thecontents ofthe posterior ethmoidal
fora-men (posterior ethmoidal artery and,vari-ably,a sphenoethmoidal nerve from
thenasociliary nerve) are generally allowed toremain intact since they serve as a
usefuldelineation to the posterior extent ofsafemedial wall dissection.Once beyond
the orbital rims,subpe-riosteal dissection generally proceeds fair-ly easily,except
for points ofnerves or ves-sels perforating through foramina,orbitalfissures,or
muscle origins such as that ofthe inferior oblique.When
encounteringresistance,surgeons should attempt toidentify the exact anatomic reason
for theresistance,such as structures that mayneed to be preserved or periorbital
tissuesthat have become entrapped in fracturelines.Knowledge ofthe limits ofsafe
sub-periosteal dissection is mandatory.Alsoimportant is knowing the distance
fromthe intact orbital rim,where vital struc-tures can be identified.Generally,a
subpe-riosteal dissection from the inferior lateralrims can be safely extended for
25 mm.Anexploration distance of30 mm from thesuperior orbital rim or anterior
lacrimalcrest (found on the frontal process ofthemaxilla) can be safe.5A high
medial walldissection places the orbital apex and opticcanal at risk.One caveat to
these �safe sur-gical exploration distances�is that they areaverages ofknown
landmarks to intactadult orbital rims.When traumatic forcesdisplace a portion ofa
rim,it is generallyin a posterior or medial direction,whicheffectively reduces
these distances.Knowl-edge ofthe bony orbital anatomy,with itsforamina,fissures,and
attachment areas,helps the surgeon to avoid injuries to vitalstructures contained
within them.1Aver-age distances for locating these criticalstructures as they
relate to identifiablebony landmarks are contained in Table 24-2.Surgeons should
avoid disrupting themedial canthal tendon,lacrimal appara-tus,pulley ofthe superior
oblique muscle,supraorbital nerves and vessel,attach-ments to Whitnall�s
tubercle,and the ori-gin ofthe inferior oblique muscle.Table 24-2Distance ofVital
Orbital Structures from Bony LandmarksStructureReference LandmarkMean Distance
(mm)Midpoint ofinferior orbital fissureInfraorbital foramen24Anterior ethmoidal
foramenAnterior lacrimal crest24Superior orbital fissureZygomaticofrontal
suture35Superior orbital fissureSupraorbital notch40Optic canal (medial
aspect)Anterior lacrimal crest42Optic canal (superior aspect)Supraorbital notch45
466Part 4: Maxillofacial TraumaThe anterior boundary ofthe orbit isdefined by the
orbital septum.The upperand lower eyelids are anatomically similarin their
composition,with correspondinglayers anteriorly to posteriorly.When oneis looking
downward,the lid retractorsenable the lower eyelid to roll with theglobe,thus
avoiding a visual field cut.Thelids have a very thin keratinized epitheli-um that
is loosely attached to the underly-ing orbicularis oculi muscle (Table 24-3).The
orbicularis oculi muscle is innervatedby cranial nerve VII and acts as a
sphincterand closing force for the eyelids.In therelaxed state the orbicularis
oculi isopposed in the upper eyelid by the levatorpalpebrae superioris,which is
innervatedby cranial nerve III.The resting tone andlevel ofthe upper eyelid are
partly deter-mined by the amount ofsympatheticinput to M�ller�s muscle.The
orbicularisoculi has two distinct layers:the outersuperficial fibers (orbital
portion) and thedeeper fibers (palpebral portion).Thepalpebral section medially has
intricateinsertions and envelops the lacrimal sac bydividing into intertwined deep
and super-ficial heads.The superficial portion insertsonto the anterior lacrimal
crest.The innerdeep head inserts into the fascia ofthelacrimal sac and posterior
lacrimal crest.The medial canthal tendon is formed bythe condensation ofthe
orbicularis musclefibers.It is the superficial head ofthe can-thal tendon that has
a tenacious insertioninto the anterior lacrimal crest.This isbeneficial during
orbital approaches sincethe anterior insertion offers considerableresistance to
dissection,which helps oneavoid inadvertent injury to the lacrimalsac.At the
lateral edge ofthe orbicularisoculi,the superficial fibers form an indis-tinct
raphe,and it is the deeper fibers thatcomprise the lateral canthal tendon,inserting
onto Whitnall�s tubercle.9Theupper and lower lids should form a 30 to40�angle at
the lateral canthus,which issituated 1 cm below the
frontozygomaticsuture.Typically,the lateral canthus is sit-uated 2 to 4 mm above
the medial canthus.Just posterior to the orbicularis oculiis the orbital septum.The
orbital septumis continuous with the orbital periosteumand the periosteum ofthe
facial bonesoverlying the rims.One to two millimetersbelow the inferior rim,where
these layersconverge on the facial aspect,is aperiosteal thickening called the
arcus mar-ginalis.5This is a useful landmark whenperforming an infraciliary or
preseptaltransconjunctival approach to the inferiorrim.Ifone stays in front ofthe
orbital sep-tum and incises below the arcus margin-alis,then orbital contents and
fat do notherniate into the field.The distal edges ofthe orbital septum insert into
the superioredge ofthe tarsal plates.The orbital sep-tum and these insertions
prevent the pre-aponeurotic orbital fat from herniatingout into the
eyelids.Superiorly there is acentral and medial fat pad,and inferiorlythere are
three distinct fat pads (medial,central,and lateral).With aging,theorbital septum
can become lax and,partic-ularly in the lower lids,result in �baggylids.�Severe
sagging ofthe lower lids isreferred to as festooning.The primary elevator ofthe
upper eye-lids is the levator palpebrae superiorismuscle.Inferiorly it forms an
aponeurosisbelow Whitnall�s ligament that attachesbroadly over the anterior tarsal
plate.Approximately 15 to 20 mm above thetarsal plate,the aponeurosis consists
ofathickened fascial band,which is termedWhitnall�s ligament.This is a
suspensoryligament ofthe lid.M�ller�s muscle arisesbeneath the levator muscle and
inserts intothe superior border ofthe tarsal plate.M�ller�s is a smooth muscle that
receivessympathetic input for its tone and helpsregulate the resting position ofthe
uppereyelids while the eyes are open.Increasedstimulation or sympathetic input
causes a�wide-eyed�look and a more alert appear-ance.10The capsulopalpebral fascia
and theinferior tarsal muscle in the lower eyelidsare also termed the lower lid
retractors.The lid retractors are formed from thefibrous attachments ofthe inferior
rectusand inferior oblique muscles,and fuse withLockwood�s inferior suspensory
ligament.The tarsal plate is formed by densefibrous connective tissue and is
primarilyresponsible for the convex form ofeach ofthe lids.The tarsal border
parallels the freemargin ofthe eyelid.The horizontallength ofeach tarsus is
approximately 30 mm.The height is greatest in the mid-portion ofthe lid.The height
ofthe uppertarsus is 10 mm,whereas in the lower lid itis 4 mm.Embedded within the
tarsalplates are a fine network ofmeibomian(sebaceous) glands.When obstructed
andchronically inflamed,these glands canform a cyst-like mass called a
chalazion.The lacrimal system is responsible forthe lubrication and wetting ofthe
globe.Accessory lacrimal glands perform normalwetting ofthe eye,and the lacrimal
glandproduces reflex tearing.The lacrimalgland,which is situated in the
anterioraspect ofthe superior lateral orbit,isdivided into two lobes by the
levatoraponeurosis.The larger orbital lobe liesabove the levator aponeurosis,and
its tearducts traverse the palpebral lobe,whichhas 6 to 12 tear ductules that empty
intothe superior lateral fornix.When drillingin this region,such as during a repair
ofafrontozygomatic fracture,one must takecare not to injure the palpebral lobe or
toinadvertently remove it,thinking that it isherniated fat;this error often results
in aproblematic dry eye.Lacrimal secretions,Table 24-3Eyelid Layers:Cutaneous
(Anterior) to Conjunctival (Posterior)SkinSubcutaneous areolar tissueStriated
muscle (orbicularis oculi)Submuscular areolar tissue (contains main sensory nerves
to lids)Fibrous layer with tarsal platesNonstriated smooth muscleMucous membrane or
conjunctiva
Orbital and Ocular Trauma467or tears,traverse medially and inferiorlyacross the
globe,wetting the cornea,andaccumulate at the medial inferior aspect ofthe eye.The
fluid is then either drawn orpumped into the lacrimal puncta oftheupper and lower
eyelids.These puncta areonly 0.2 to 0.3 mm in diameter.The upperpunctum is usually
just slightly medial inrelation to the lower punctum.When thelids close,the puncta
come into contact.The upper and lower canaliculi travelwithin the lids,first
vertically (2 mm),then horizontally for 8 to 10 mm,parallel-ing the lid margin.They
join to form acommon canaliculus just before enteringthe lateral aspect ofthe
lacrimal sac,whichis one-third ofthe way down from theupper portion ofthe
sac.Typically,thelacrimal sac is 1 cm in length and 5 mm indiameter.The palpebral
portion oftheorbicularis oculi has dense intertwinedinsertions that envelope the
lacrimal sac.Inferiorly,the sac drains into the naso-lacrimal duct,which has a 12
mm intra-bony canal coursing inferiorly and posteri-orly that opens into the
inferior meatus ofthe nasal cavity below the inferior concha.This opening is 30 to
35 mm from the edgeofthe external nares.Reflux oftears andnasal mucus back up into
the nasolacrimalduct is prevented by a mucosal fold calledHasner�s valve.With
persistent epiphorafollowing trauma or surgical intervention,it is important to
establish the precisepoint ofmechanical obstruction thatexists within the lacrimal
drainage system.Irrigation ofthe inferior canaliculus mayrelieve temporary
obstruction owing todry or thickened secretions.A dye disap-pearance test,Jones I
or II,nasolacrimalirrigation,or dacryocystography can helpone determine the precise
point ofobstruction and guide surgical planning.Following trauma or operative
interven-tion,epiphora may be due to hypersecre-tion from a corneal abrasion,lash
ptosis,foreign bodies,or entropion,all ofwhichserve as persistent stimuli leading
to reflexlacrimal gland secretion.Fracture ConfigurationsIsolated orbital wall
fractures account for4 to 16% ofall facial fractures.Iffracturesthat extend outside
the orbit are included,such as those ofthe zygomatic complex(ZMC) and naso-
orbitoethmoid (NOE),then this accounts for 30 to 55% ofallfacial fractures.11,12ZMC
fractures are the most common-ly occurring facial fracture,second only tonasal
fractures.By definition,ZMC frac-tures are the most common fracture withorbital
involvement.13The ZMC,or tri-pod,often hinges about the frontozygo-matic suture
with a medial,inferior,andposterior vector ofrotational displace-ment.This is due
to the direction andforce ofblunt trauma and the variablethicknesses ofthe
components oftheZMC.The frontozygomatic area offers thethickest pillar.When
fractured there isusually a slight vertical displacement witha reasonable
anteroposterior alignment.The much thinner anterior maxillary andlateral orbital
floor offers little resistanceto fracture and displacement.Fractures ofthe NOE are
most oftendue to severe blunt midface trauma.Thesefractures create cosmetic
deformities with aflattening ofthe nasal dorsum and a widen-ing ofthe intercanthal
distance;they canalso be accompanied by a violation oftheunderlying dura with a
cerebrospinal fluid(CSF) leak.Any persistent or copious clearnasal drainage should
be tested to deter-mine a �2-transferrin level to rule out a CSFleak.It is uncommon
for the canthal ten-dons to become disinserted from the bones.This is particularly
true ofthe lateral can-thal tendon.Traumatic telecanthus withNOE fractures is a
result ofa flattening ofthe nasal bridge and a lateral splaying oftheorbital rims
and anterior lacrimal crest.Reduction and fixation ofthese bony seg-ments and,less
frequently,direct transnasalwiring are necessary for adequate restora-tion ofmedial
intercanthal distance andalignment.In adult Caucasians this is typi-cally 29 to 32
mm;it is slightly more inblack and Asian individuals.Lacrimaldrainage problems can
also arise fromsevere NOE fractures owing to canalicularor lacrimal sac disruption
or scarring.Internal orbital fractures occur innumerous patterns.These fractures
aretypically described by their location andthe size ofthe defect.Three basic
patternsofinternal orbital fractures have beendescribed:linear,blow-out,and com-
plex.14Linear internal orbital fracturesmaintain periosteal attachments and typi-
cally do not result in a defect with orbitalcontent herniation;however,they
canresult in a significant enlargement oftheorbital volume with a resulting late
enoph-thalmos.Blow-out fractures are the mostcommon.By definition,these are
limitedto one wall and typically are 2 cm or less indiameter.The most commonly
involvedwall with a blow-out fracture is the anteri-or medial orbital
floor,followed by themedial wall and,less frequently,the orbitalroof,which can
present as ablow-infrac-ture.Exploration,repair,or reconstructionofan orbital
rooffracture may be indicat-ed ifa dural tear is suspected or to preventa
�pulsatile globe.�This rhythmic inwardand outward movement ofthe eye is dueto the
cerebrovascular pulsation and theinfluence ofrespiration on the overlyingcerebral
hemispheres.This phenomenonis typically not present acutely but occursafter
resolution ofedema,with the recov-ered patient complaining ofpersistentblurred or
double vision.Complex inter-nal orbital fractures consist ofextensivefractures
affecting two or more orbitalwalls;they often extend to the posteriororbit and may
involve the optic canal.These complex fractures are usually asso-ciated with more
severe trauma and sur-rounding fractures such as Le Fort II,LeFort III,and frontal
sinus fractures.Clinical ExaminationEven in the most severely injured patient,the
mechanism ofinjury and surrounding
468Part 4: Maxillofacial Traumahistory should be ascertained before per-forming a
clinical examination ofthe orbitand globe.A systematic approach assessingboth the
globes and orbits further definesfunctional and cosmetic defects.The
initialophthalmologic evaluation should includeperiorbital examination,visual
acuity,ocu-lar motility,pupillary responses,visualfields,and a fundoscopic
examination.Visual acuity should be independent-ly tested on each eye using a
Snellen chartat a standard 6 m (20 ft.) distance or withreading ofstandard-type
print at 40 cm(16 in.).The patient should wear theircorrective lenses during this
examination.Ifover 40 years ofage,the patient shouldbe wearing his or her reading
glasses.Theeyelids and periorbital region should beinspected for
edema,chemosis,ecchymo-sis,lacerations,ptosis,asymmetric liddrape,canalicular
injury,and canthal ten-don disruption.With significant acuteperiorbital
ecchymosis,there should be anincreased suspicion ofa direct blunt globeinjury or an
internal orbital wall fracture.A lid retractor (Desmarres) is useful forseparating
swollen tight lids so that theglobe and pupil can be adequately exam-ined.Also,this
retractor may serve to liftthe edge ofthe lid to examine its inneraspect.With an
upper eyelid laceration,any fat that is herniating below the level ofthe brow
through the wound should causeconcern that an underlying injury hasoccurred to the
levator muscle.Likewise,ifthe palpebral conjunctiva has been vio-lated,it is
prudent to consult an ophthal-mologist to rule out a globe perforation.With a
medial vertical laceration ofthelids,particularly the lower,gentle
lateralretraction may reveal a cut canaliculus ormedial canthal tendon
disinsertion.Canalicular disruption warrants anurgent ophthalmology consult and
usual-ly requires surgical reanastomosis and sil-icone tube placement into the
naso-lacrimal system and surroundingsupportive repair to prevent outflowobstruction
and epiphora.Extraocular movements are evaluatedto rule out mechanical entrapment
or pare-sis.Diplopia,and the field ofgaze in whichit occurs,should be noted (Figure
24-3).Ofgreatest concern is diplopia in the primary(straight-ahead) and downward
gazes.These are the two fields that are used mostoften.Mild or equivocal
restriction (< 5�)in extreme fields ofgaze is common in thesetting ofsevere orbital
trauma with hem-orrhage or edema.Computed tomography(CT) scan findings should be
correlatedwith any clinically noted entrapment.Ifmechanical entrapment is
suspected,thenthe eye should be topically anesthetized anda forced duction
performed with a fine-toothed forceps.Typically,an Adson forcepsis used at the
inferior fornix with the beaksopen,pressing inward against the depth ofthe fornix
and toward the globe side,untilthe globe rolls downward slightly.Thebeaks are then
pressed together,graspingthe insertion ofthe inferior rectus.Upward,downward,and
lateral motions can be eval-uated.The point ofdoing a forced ductiontest is to
determine whether the diplopia isdue to a restriction ofa muscle or paresis ofa
muscle.Pupillary light reactivity,size,shape,and symmetry should all be assessed
andnoted.Ifunequal pupils (anisocoria) or anirregularly pointing pupil is
found,thenthe patient should be queried regardingprevious ocular trauma or eye
surgery(cataracts).An irregular pupil often pointstoward the site ofa globe
penetration orinjury.This is often teardrop shaped,withthe narrow portion pointing
toward theperforated side ofthe globe,which is usu-ally concealed beneath the lid
(Figure 24-4).An ophthalmologist should be consult-ed immediately and
precautionarymeasures instituted,including protectiveFox shield over the eye,head-
of-bed eleva-tion,bed rest,analgesics,and antiemeticsto avoid sudden increases in
intraocularpressure owing to Valsalva forces.Both globes should be evaluated forany
acute enophthalmos,exophthalmos,orvertical dystopia.This is often ascertainedfrom
above or by standing directly in frontofthe patient.Visual fields are tested
foreach eye,one at a time,by confrontation.The examiner and patient faces should
bepositioned directly toward each other,0.6 m apart.The patient is asked to
staredirectly into the examiner�s eyes,while theexaminer�s hand is held in their
ownextreme field ofgaze,midway between thepatient and the examiner.The patient
isthen asked to detect numbers offingersshowing,motion,or the digit
displayed.Inessence,the examiner�s peripheral field ofgaze is serving as a control
for the patient.Quadrant defects are indicative ofpost-chiasm injury.A fundoscopic
exami-nation should be performed in a dimly litroom to help maximize pupillary
dilata-tion and ease ofthe examination.Lens dis-location,vitreous
hemorrhage,retinaldetachment,and foreign bodies may benoted or may be the cause for
not beingable to view the fundus.Ifhistory and ini-tial clinical findings warrant a
dilated fun-doscopic examination,then neurologicstatus should be reevaluated and
con-firmed,and clearance from the primarytreating physician or neurosurgeon
firstobtained.A dilated fundoscopic examina-tion with indirect ophthalmoscopy is
gen-erally performed by an ophthalmologist torule out more occult injuries or
examine agreater portion ofthe globe toward theequator.The ophthalmologist may
elect toperform tonometry or a slit-lamp exami-nation.Tonometry indirectly
measuresintraocular pressure by placing the instru-ment on the surface ofthe
eye.Normal(10�20 mm Hg) or symmetric bilateralreadings are reassuring.However,this
doesnot rule out a penetrating injury.With ele-vated pressures but an otherwise
unre-markable examination,a history ofglau-coma should be elicited.An
acuteabnormally high intraocular pressure withexophthalmos,limited globe
movement,and resistance to retropulsion is indicativeofa retrobulbar hematoma,which
may
Orbital and Ocular Trauma469ABCDETo change the side,swing index along this lineTo
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lineObjectNo0I1/161/4II1III4IV16VI0IIIIIIVV6410,031520,100mm2NoRelat.Intens.30,3154
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____________________________________________12010590908 07 06 05 04 03 02 0101 02
0304 05 06 07 08 0907 07 06 06 05 0 5 04 04 03 03 02 02 01 01
075602402552702853003153303451952102254513530150165151800___________ mmDiameter
pupilObjectWRGBColorCorrection___________ mmDiameter pupilRelat.
Intens.WRGBColorCorrectionOS.OD.Vision: __________sph O __________ cyl ________ � =
________Date: ________________________________________Diagnosis:
______________________________Name:
____________________________________________Date:
________________________________________Diagnosis:
______________________________No4321I0IIIIIIVVObjectRelat. Intens.OS.OD.Vision:
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03 02 0101 02 03 04 05 06 07 08 0907 07 06 06 05 0 5 04 04 03 03 02 02 01 01
075602402552702853003153303451952102251354515030165151800FIGURE24-3This 9-year-old
child presented with complaint of�double vision and cheek numbness�after being
struck in the left orbital region with a hardball.A,Note the lateral
subconjunctival hemorrhage and that there was no difficulty in the upgaze.B,In
downgaze he had severe firm fixed restriction ofthe left eyethat was positive to a
forced duction test.C,The right lateral gaze had trace restriction.D,The left
lateral gaze was unremarkable.E,Direct coronal computedtomography (CT) scan ofthe
bony window revealed a trapdoor fracture ofthe left orbital floor with herniation
and a probable impingement ofthe inferior obliquemuscle and fascial
framework.F,Diploic visual fields (Goldman visual field test).With binocular
testing,patients are asked to look at the grid and track a point-ed light that is
shown from behind the chart.When patients experience double vision,they respond to
the examiner who charts the abnormality.In this case,theupper grid was recorded at
the initial presentation.Diplopia was experienced in all areas below the line
(10�12�).This child�s severely limited downgaze,corre-lated with the CT
findings,prompted surgical exploration and orbital floor repair within 12 hours.The
lower grid was recorded at 10 days postoperatively andshowed marked improvement in
the downgaze,with diplopia occurring at 40�inferiorly.F
470Part 4: Maxillofacial Traumarequire acute evacuation via a lateral can-thotomy.A
�soft eye�with a relatively lowpressure or deep anterior chamber is sug-gestive ofa
posterior scleral rupture.A slit-lamp examination is generallyperformed with the
patient in an uprightposition;ifthe patient is confined to abed,a modified
examination can be per-formed with a penlight.A handheldportable slit lamp can be
used in the trau-ma setting.The purpose ofthis examina-tion is to evaluate the
surface contour ofthe globe and cornea to rule out conjunc-tival chemosis
(swelling),hemorrhage,emphysema,and foreign bodies.Theanterior chamber should be
evaluated fordepth,clarity,and hyphema (blood in theanterior
chamber).Hyphema,iffound,should be evaluated by an ophthalmolo-gist so that
surgical evacuation or medicalmanagement may be instituted in aneffort to avoid
occlusion ofthe trabecularmeshwork,which may lead to glaucomaor a fixed iris.The
iris�s shape and reactiv-ity should also be noted.Ifa corneal abra-sion or
laceration is suspected,this may bemore thoroughly evaluated with fluores-cein dye
and a Wood�s lamp (cobalt bluelight).The fluorescein dye pools in thelaceration or
abrasion and fluoresces witha bright lime-green hue under the lamp-light (Figure
24-5).Finally,the bony orbital rim should bepalpated for steps,crepitus,and
mobility.The patient should be queried aboutaltered or lack ofsensation,and
neurosen-sory testing should be performed to evalu-ate the
supraorbital,supratrochlear,andinfraorbital nerves.Imaging Once a complete
ophthalmologic and oralexamination has been performed,selectedstudies such as CT or
magnetic resonanceimaging (MRI) can be ordered withdefined parameters to provide
meaningfulresults.Imaging is essential for properdiagnosis and treatment oforbital
trauma.Noncontrasted CT is the primary imagingmodality currently used for
evaluatinginjuries from blunt or penetrating trauma,as well as for localizing most
orbital foreignbodies.15Other imaging modalities,such asplain
radiography,reconstructed three-dimensional CT,MRI,ophthalmic ultra-
sonography,color Doppler imaging,andangiography,may provide necessary addi-tional
information in select instances.CTscans have become the standard ofcare
inevaluating acute orbital injuries.Standardradiography is a readily available and
inex-pensive method for primary evaluations oforbital fractures.Plain
radiography,how-ever,is inadequate when used in evaluatinginternal orbital
fractures,and it is difficultto localize foreign bodies with plain
filmsalone.Waters�projection allows visualiza-tion ofthe orbital roofand floor and
isparticularly useful for evaluating orbitalfloor blow-out fractures (Figure 24-
6).With this 23�(preferably posteroanterior)view,the petrous portion ofthe
temporalbones is projected below the maxillarysinuses and indirect signs offracture
canbe noted,such as a teardrop formation orair-fluid levels.This is also an
excellentview to assess a ZMC fracture.Ifplain films reveal an internal
orbitalfracture that possibly warrants surgicalintervention,then CT scans should
beobtained.The fracture can then be fully eval-uated for surgical treatment
planning.CTallows excellent visualization oforbital softtissues and permits one to
simultaneouslyassess the cranial vault and brain during a�trauma scan.�A trauma CT
scan series gen-erally involves 10 mm axial cuts ofthe crani-um and 5 mm cuts
through the facial region.Iffiner detail or three-dimensional recon-structed images
are desirable,then 1 mmfine cuts can be ordered.Internal orbitalfractures are best
evaluated when the imag-ing plane is perpendicular to the fractureline.Thus,images
are usually obtained inFIGURE24-4Laceration ofthe right lowermedial eyelid that
extends through the margin.At first the examiner thought there was simplya strand
ofclotted blood on the medial globe.Recognition ofthe irregular-pointing pupil
ledto the suspicion ofa globe perforation,whichwas confirmed with a dilated
ophthalmologicexamination.FIGURE24-5A broad corneal abrasion oftheright eye
illustrated with the pooled fluoresceindye under a cobalt blue (Wood�s)
lamp.FIGURE24-6Waters�view demonstrating opaci-fication ofthe left maxillary sinus
and a mediallydisplaced left zygomatic buttress and arch.
Orbital and Ocular Trauma471both the axial and coronal planes to fullyevaluate the
fracture lines,patterns,andvolume changes.This is particularly usefulfor comparison
to the contralateral oruninjured side.The standard imagingapproach for facial
trauma is to obtaindirect (non-reformatted) 3 to 5 mm sec-tions in the axial and
coronal planes.Intra-venous contrast offers no advantages to theevaluation ofacute
bony facial injuries.Direct coronal views with 3 mm sectionsare preferred for
evaluating orbital rooforfloor fractures;however,they may be unob-tainable owing to
cervical spine precautionsor the patient�s inability to extend the neckand
adequately position him- or herselfforthe coronal CT.In these patients,reformat-ted
coronal images can be obtained basedon the axial image data set.However,withthis
technique,there can be a loss ofspatialresolution on the reformatted
images.Theaxial images with fine detail (1 mm slices)must be obtained to allow for
meaningfulreformatted image quality.Ifan optic canalfracture is suspected,then 1 to
1.5 mm axialcuts should be obtained.16,17This allows abetter determination and
correlation ofanyafferent visual defect owing to possiblebony impingement.Although
MRI is generally accepted asa superior soft tissue imaging modality,CTscans
adequately assess lens dislocation,vit-reous hemorrhage,ruptured globe,retrob-ulbar
hemorrhage,or avulsion ofthe opticnerve.CT is the imaging ofchoice in local-izing
metallic and most nonmetallic foreignbodies in relation to the globe,muscularcone
(area inside the extraocular muscles),and the optic nerve.15,18The location
andextent ofany subperiosteal hematoma for-mation,with possible mass effects,can
alsobe adequately assessed with CT imaging.Computer-generated three-dimensionalCT
imaging can provide superior views andspatial orientation offragments for com-plex
orbital and facial fractures.In themajority ofacute facial fractures,three-
dimensional CT scanning is unnecessary.However,with complex facial trauma
withsevere displacement,or for secondaryreconstruction,three-dimensional CTscanning
is invaluable for surgical treat-ment planning.19Generally,1 to 1.5 mmfine axial
cuts are obtained;the patientmust remain motionless for the entire scan,which may
include more than 100 slices.CT imaging has some drawbacks.Aspreviously
mentioned,patients may beunable to position themselves comfortablyfor direct
coronal imaging.Sedation maybe warranted in pediatric or uncoopera-tive trauma
patients.However,with facialbleeding,possible concomitant mandiblefractures,or
obtundation from alcohol orstreet-drug use,a secure airway must bemaintained
throughout the radiology pro-cedure.This may require endotrachealintubation.CT
scans may fail to revealradiolucent foreign bodies such as woodor vegetative
matter.20In these instancesultrasonography and MRI are most usefulin detecting the
radiolucent foreign bodyand localizing it.These studies should beobtained when the
CT scans are equivocalor when physical examination suggests thepresence offoreign
bodies.MRI can be useful in the setting oforbital trauma to assess soft tissue
injuryor entrapment ofextraocular muscles inthe area ofthe orbital suspensory
frame-work.Standard radiographs or CT scansshould be obtained before MRI is per-
formed on patients with suspectedintraocular or intraorbital ferromagneticbodies
because ofthe potential for dis-placement ofthe metallic fragments,resulting in
further significant ocular orbrain injury.21,22With CT imaging,woodcan appear
isodense with fat or mimicintraorbital air.Ifthe history or clinicalexamination
indicates that fragments ofwood may have penetrated the orbit orglobe,then an MRI
should be ordered.AnMRI should also be performed when anapparent orbital emphysema
(focal air col-lection) fails to resorb rapidly (within sev-eral days);this may
suggest a space-occupying foreign body.23Ophthalmic ultrasonography is sel-dom used
but is a readily available,safe,inexpensive,and noninvasive
imagingmodality.24Foreign bodies located in theorbit can be identified with
ultrasonog-raphy but are much more difficult todetect when located in the orbital
apexowing to signal reflection.Wood andother radiolucent materials can bedetected
with ultrasonography.25ColorDoppler imaging is an ultrasound tech-nique that
provides simultaneous two-dimensional images and visualization ofblood flow.26It
can be useful in evaluat-ing a post-traumatic high-flow carotidcavernous
fistula.However,angiographyremains the study ofchoice for defini-tively
establishing this diagnosis.Ocular Injuries and DisturbancesPatients who sustain
midfacial trauma,particularly in motor vehicle accidents,often have concomitant
neurologic andmultisystem injuries.A neurologicallyimpaired or uncooperative
patient pre-sents additional challenges in performingan adequate orbital and
ophthalmologicexamination.It is paramount that the pri-mary tenets ofadvanced
trauma life sup-port be adhered to in securing the airwayand protecting the
cervical spine.Whenorbital fractures caused by severe bluntforce trauma are
detected,additional asso-ciated injuries should be sought,such asorbital canal or
apex involvement,retro-bulbar hematoma,or globe perforation.When there are multiple
midface frac-tures,such as those ofthe ZMC,NOE,andfrontal sinus,and Le Fort II or
Le Fort IIIfractures,then more severe intraorbitalinjury,bleeding,and globe
perforation arelikely.Basilar skull fractures,as evidencedby clinical signs such as
CSF otorrhea orrhinorrhea,Battle�s sign,or CT evidencesuch as fracture lines or
intracranial air,are generally caused by high-velocityimpact and are often
associated withsevere neurologic injury.
472Part 4: Maxillofacial TraumaSuperior orbital fissure syndrome ischaracterized by
impairment ofcranialnerves III,IV,V,and VI secondary to com-pression by a fractured
bony segment orhematoma formation in the region.Orbitalapex syndrome has all the
hallmarks ofsuperior orbital fissure syndrome,with theaddition ofoptic nerve
(cranial nerve II)injury.Between 0.6 and 4% ofpatients suf-fering orbital fractures
have a globe injuryor optic nerve impairment,resulting in asignificant or total
loss ofvision in oneeye.27,28This fact highlights the need for athorough initial
ophthalmologic and visu-al acuity assessment,with follow-up serialexaminations as
indicated.Visual ImpairmentVisual impairment or total vision loss canoccur at
various levels along the opticpathway.Direct injury or forces transmit-ted to the
globe by displaced fracture seg-ments can result in retrobulbarhematoma,globe
rupture,hyphema,lensdisplacement,vitreous hemorrhage,reti-nal detachment,and optic
nerve injury.Patients with orbital fractures and anydegree ofvisual impairment who
com-plain ofsevere ocular pain should be eval-uated for retrobulbar hematoma.It
isoften the �less impressive�orbital fracturethat leads to retrobulbar hematoma
for-mation (Figure 24-7).This is due to bleed-ing within a relatively closed
compartmentand the lack ofa potential drainage path-way through paranasal
sinuses,such as theethmoids or maxillary sinus.In essence,there is a compartment
syndrome result-ing from elevation ofintraorbital pressure,which leads to central
retinal artery com-pression,or ischemia ofthe optic nerve.The increased
intraorbital pressures cansecondarily raise the intraocular pressure,which,in
turn,compromises the ocularblood supply.29�31In most instancesrequiring emergent
treatment,there is adegree ofexophthalmos and excessive ten-sion ofthe
lids.Although CT scanning toconfirm the diagnosis is desirable,thereshould not be
unnecessary delay in thesurgical management.The immediate orurgent surgical
management for retrobul-bar hematoma evacuation consists ofa lat-eral
canthotomy,with or without inferiorcantholysis,and disinsertion ofthe sep-tum along
the lower eyelid in a medialdirection.A small Penrose drain is left inplace for 24
to 48 hours to ensure adequatedrainage and to prevent reaccumulation.Additional
maneuvers to lower theintraocular pressure include administra-tion ofintravenous
mannitol or acetazo-lamide or application ofvarious
glaucomamedications.Typically,blow-in fracturesor inward rotation ofthe ZMC does
notresult in increased intraorbital or intraoc-ular pressures with visual
impairment.This is most likely due to pressure reliefand volume expansion provided
by addi-tional orbital wall fractures such as themedial wall into the ethmoid or
the floorsagging into the maxillary sinus.A penetrating globe injury can resultfrom
what appears to be an innocuoussmall laceration or from horrific blunt-force
trauma.When an eyelid laceration isaccompanied by an asymmetric pupil,without a
prior history ofsurgery,then aglobe perforation likely exists (Figure 24-8).Blunt
trauma can lead to globe perfo-ration owing to a scleral rupture from thesudden
instantaneous increased intraocu-lar pressure.The most common site forscleral
rupture is at the site ofpreviouscataract surgery,at the limbus,or just pos-terior
to the insertion ofthe rectus mus-cles onto the globe,which is 5 to 7 mmfrom the
edge ofthe limbus.The areaunder the muscle insertion is anatomicallythe weakest and
thinnest portion ofthesclera.With suspected globe perforation,pupillary dilatation
and inspection by anophthalmologist is mandatory.Theinspection may be difficult�the
injurymay not be visible on fundoscopic exami-nation since it is anterior to the
equator ofthe globe and externally may be hiddenunderneath the rectus muscle
insertion.Detection and surgical access for repairmay require dissection ofthe
bulbar con-junctiva with retraction ofthe extraocularmuscles and external globe
inspection.The penetrating injuries should be treatedemergently,or within 12
hours,to decreasethe risk ofinfection or ocular content her-niation.The ultimate
visual outcomedirectly correlates with the presentingvisual acuity.Few eyes that
cannot detecthand motions or have no light perception(NLP) regain useful
vision.Globe injuriesshould be addressed before any facial lac-erations are
repaired.The exception is sig-nificant active blood loss from a
severedvessel.Hyphema is blood in the anteriorchamber ofthe eye.It can be as severe
ascomplete obliteration ofthe anteriorchamber,termed �eight-ball
hyphema,�orFIGURE24-7Axial computed tomography scanofa right retrobulbar
hematoma.This diffuseinfiltrative pattern is characteristic,whereas thediscreet
clot mass is less common.FIGURE24-8A full-thickness corneal lacerationand an
irregular pupil ofthe right eye is seenduring a slit-lamp examination.
Orbital and Ocular Trauma473more commonly a thin 1 to 2 mm layeringat the inferior
margin in the upright posi-tion (Figure 24-9).Some hyphemas aretermed
microhyphemas,with red bloodcells floating in the anterior chamber andnot layering
out.The level and severity ofthe hyphema should be noted and record-ed.The bleeding
is from the rupture ofaniris or ciliary body vessel and usually is theresult
ofblunt trauma.Patients often com-plain ofeye pain and,occasionally,visualloss
ifthe amount ofbleeding is severe.Medical management ofhyphema isaimed at
preventing rebleeding andvenous congestion and promoting clear-ance ofthe existing
blood.This mayinclude hospitalization,bed rest,head-of-bed elevation,and longer-
acting cyclo-plegics (topical agents such as scopo-lamine or
atropine).Cycloplegicsmaintain a dilated pupil and thus immobi-lization ofthe
iris,which discourages fur-ther rebleeding.Topical steroids may beadministered to
decrease further rebleed-ing and reduce intraocular inflammation.Oral aminocaproic
acid is an antifibri-nolytic recommended to reduce the inci-dence ofrebleeding into
the anteriorchamber.In moderate to severe cases thereshould be daily monitoring
ofintraocularpressures and control ofany high pressureincreases with intravenous
carbonic anhy-drase inhibitors (acetazolamide,whichlimits aqueous humor production)
orhyperosmotics (mannitol).With severehyphema,intraocular surgery to
irrigate,aspirate,and evacuate the clot may be nec-essary to prevent optic atrophy
owing toelevated pressures,or to avoid permanentcorneal blood staining.32The
anteriorchamber washout is the most commonlyperformed procedure for this
purpose.Vitreous hemorrhage can result fromblunt trauma with the rupture
ofciliary,retinal,or choroidal vessels.If,during fun-doscopic examination,the
retina cannotbe visualized despite a normal-appearinganterior chamber and
lens,vitreous hem-orrhage is most likely present.As withhyphema,initial management
typicallyinvolves hospitalization,bedrest withhead-of-bed elevation,and serial
clinicalexaminations.Vitreous hemorrhage isslow to resolve,and it may take months
forthis to clear,with symptomatic visualimprovement.33A vitrectomy may berequired
after 6 months ifsatisfactoryresorption has not occurred.Lens dislocation may be
detected byfundoscopic or slit-lamp examination.Thelens,in its normal anatomic
position,phys-ically separates the anterior and posteriorchambers,but it can be
dislocated eitherpartially or totally into either one.Symp-toms include monocular
diplopia andblurred vision;thus,it is important to checkeach eye�s visual acuity
independently.Pos-terior dislocation may be well tolerated;however,complete
anterior dislocation canresult in glaucoma and usually requiresemergency extraction
ofthe lens.Rhegmatogenous retinal detachmentand peripheral tears result from
bluntforce trauma.Characteristic symptomsinclude flashing lights and a field loss
bestdescribed as a curtain or window shadecoming over the eye.On
fundoscopicexamination,the retina may not be clearlyvisualized,or undulations may
be present.Retinal detachments require surgery.33Anemergency consultation with an
ophthal-mologist and initial maneuvers should beinstituted.Maneuvers involve
bedrest in ahead-up position and assurance that thereis no Valsalva-type
exertion;these preventfurther extension ofthe detachment.Operative management may
include anyor all ofthe following:a scleral buckle,cryotherapy a vitrectomy,or
endolaser.In-office pneumatic retinopexy works wellwith superior detachments:an
inertexpandable gas is injected into the vitreousand indirect laser treatment is
applied.Optic nerve injury or compromise canresult from orbital fractures in the
posteri-or region or optic canal.Optic nerveinjury or vascular compromise is
charac-terized by decreased visual acuity,dimin-ished color vision,and a relative
afferentpupillary defect.It is possible to retainvery good vision and yet still
have an opticnerve injury manifested by color deficits,afferent papillary
defect,and visual fieldloss.Detection ofearly subtle changesrequire that a
cooperative patient under-goes visual acuity testing,consisting oftesting with a
Snellen chart,finger count-ing,detection ofmotion,or light percep-tion.Patients may
present with NLP,which mandates an emergency consulta-tion with an ophthalmologist
and a fineaxial CT imaging ofthe orbital apex.IfNLP persists > 48 hours,then rarely
doesany meaningful vision return to the affect-ed eye.Patients with NLP or
severelydecreased visual acuity may be sufferingfrom traumatic optic neuropathy
andshould be given high-dose systemicmethylprednisolone therapy for at least 48 to
72 hours (initial loading dose of30 mg/kg IV methylprednisolone
sodiumsuccinate,followed by 15 mg/kg IV 2 hlater and q6h thereafter).34�36Ifthe
patientis uncooperative,heavily sedated,orunconscious,pupillary reaction can
bemonitored and followed as a sensitive testofoptic nerve (cranial nerve II)
function.This is best achieved in a dimly lit room;apenlight is moved alternating
from oneeye to the other every 2 to 3 seconds,andthe pupillary response is
observed.WithFIGURE24-9This partial hyphema ofthe righteye resulted from a punch to
the face; a comput-ed tomography scan showed a minimally dis-placed orbital floor
fracture.The slit-lampexamination shows early layering.This patientreceived
nonoperative management.
474Part 4: Maxillofacial Traumathe light shining into the normal eye,bothpupils
should exhibit a brisk constriction.Ifthe light is then directed from the unin-
jured to the injured eye the pupil on theinjured eye will dilate.This is indicative
ofan optic nerve injury (relative afferentpupillary defect).A
unilateral,fixed,dilat-ed pupil is usually due to an efferent path-way injury
(cranial nerve III),or someform ofintracranial injury or bleed,whichis usually
accompanied by other neurolog-ic lateralizing signs.DiplopiaWhen a patient
complains ofseeing a dou-ble image ofthe same object,the examin-er should first
test each eye independentlyby covering the opposite eye to determinewhether the
diplopia is monocular orbinocular.Monocular diplopia is usuallydue to lens
dislocation or opacification,oranother disturbance in the clear mediaalong the
visual axis.Acute binoculardiplopia,secondary to trauma,derivesfrom one ofthree
basic mechanisms:edema or hematoma,restricted motility,or neurogenic injury.The
most commoncause ofbinocular diplopia followingtrauma is orbital edema and
hematoma.This is usually found in peripheral fields ofgaze,and,ifother findings are
absent,diplopia in the primary and downwardgazes usually resolves along with
theedema in 7 to 10 days.Slight diplopia inextreme peripheral fields ofgaze may
per-sist for months but is rarely problematicsince individuals seldom require
theseextreme views for everyday function.Alsothe patient may complain that the phe-
nomenon is transitory and that suddenlooking �upward and outward�(superior-ly and
laterally,such as when looking in arearview mirror) may cause instantaneousbut
briefdiplopia.Binocular vision with-out diplopia is most important in the pri-mary
(straight-ahead) and downwardfields ofgaze.The majority ofour dailyactivities,such
as conversing,reading,andwalking,use these visual fields.Ifdiplopiapersists,an
ophthalmologic consultationshould be sought.Systemic corticosteroidshasten the
resolution oforbital edema andthe resulting diplopia,which is fairly com-mon
following blunt trauma to the orbit.Persistent post-traumatic diplopia isbest
evaluated by an ophthalmologist.It isimportant to establish an accurate diagno-sis
and precise etiology.The basic evalua-tion should include assessing symmetry ofthe
corneal light reflexes and testing ofductions (following a finger in all
eightfields ofgaze) including a selective forcedduction.The forced duction helps
distin-guish between restricted motion fromentrapment,scarring,or fibrotic contrac-
tures versus a neurogenic motility disorder(cranial nerves III,IV,or
VI).Ophthalmol-ogists use diploic visual fields (see Figure24-3F) to quantify and
categorize thediplopia;serial examinations allow accu-rate tracking ofspontaneous
recovery orpostsurgical progress.In the acute setting,restrictive disorders are
managed withearly bony orbital surgery and reconstruc-tion,whereas neurogenic
disorders aremanaged with the injection ofbotulinumtoxin into select extraocular
muscleswhose forces are unopposed by the injuredor restricted muscles.Following
bonyorbital reconstruction or selective botu-linum toxin injections,there should be
a6- to 12-month waiting period for thediplopia to stabilize.Then,any residualand
stable diplopia can be addressed withstrabismus (extraocular muscle)
surgery.Strabismus surgery has two basic maneu-vers:a repositioning ofmuscle
insertionsonto the sclera or a weakening oftheopposing muscles.After a period
ofheal-ing,selective botulinum toxin injectionsor more minor revision
strabismussurgery may be required to fine-tune theresult.The important point to
stress is thata healed abnormal bony wall position ororbital volume
changes,resulting inenophthalmos or vertical dystopia,typi-cally do not cause
stable significantdiplopia.In fact,vertical dystopia ofup to1 cm can be
accommodated by the brainand should not result in diplopia in theprimary fields
ofgaze.Therefore,any bonywall revision or reconstruction should beperformed to
correct a cosmetic or otherfunctional defect without promise ofcor-rection or
improvement in any coexistingdiplopia.These reconstruction proceduresshould be
performed and allowed to heal,and the diplopia allowed to stabilize for 6 months
prior to the strabismus surgery,which would address the diplopia.In the trauma
setting,diplopia may bedue to restricted ocular motility from aprolapse ofthe
periorbital contents intothe medially fractured ethmoid air cells orunderlying
maxillary sinus.Such diplopiamay also be due to entrapment or directimpingement on
the fine suspensory liga-mentous system ofthe orbit or,less fre-quently,ofthe
extraocular muscles.Restricted motility or entrapment is com-monly found with
orbital floor and medi-al wall fractures,less frequently with rooffractures,and
rarely with lateral wall frac-tures.Significant medial wall fractures aremanifested
primarily by enophthalmosowing to volume expansion.When testing range
ofmotion,ifthereis repeatedly a firm fixed limited stop ofunilateral eye motion,the
eye should beanesthetized topically and a forced ductiontest performed.Occasionally
the entrap-ment or incarceration ofthe supportingstructures or muscles is mild,and
duringthe forced duction,initial resistance maybe encountered and then relieved.In
suchan instance,the positive forced duction testwas both diagnostic and
therapeutic.How-ever,ifthe forced duction test is positiveand mimics the voluntary
active point ofrestricted motion,this should be correlatedwith CT scan findings
(see Figure 24-3).37A repeatable fixed point oflimitation isusually due to direct
entrapment oftheextraocular muscles or the capsulopalpe-bral fascia (fascia
ofTenon).This is morecommon in linear floor fractures than incomminuted multiple
wall fractures.
Orbital and Ocular Trauma475Patients with muscle or Tenon capsuleincarceration
confirmed by CT are candi-dates for urgent exploration and repair(within 12
h).Prolonged muscle entrap-ment with ischemia can lead to fibrosis(Volkmann�s
contracture) with permanentdiplopia,despite surgical release oftheentrapped
tissues.When exploring thesefractures,the entrapped fascia or musclecan be
difficult to release.This classicallyoccurs in the pediatric patient with
ananteroposterior linear fracture oftheorbital floor with no accompanying
rimfracture.When an area ofresistance isencountered initially and correlates to
thissame anatomic location on CT,then con-sideration should be given to inserting
aninstrument within the anterior fractureline and gently twisting or prying to
openup the fracture,or taking a fine osteotomeor instrument to fracture away a
smalladjacent strip oforbital floor so that a thinblunt malleable retractor on
either side ofthe entrapped area can gently lift andreduce the entrapped soft
tissues back intothe orbit.Direct grasping ofthe tissues andtugging to reduce them
back into the orbitmay result in further contusion and injury.Diplopia can be due
to a central oph-thalmoplegia owing to impairment ofcra-nial nerves III,IV,or
VI.The fourth nerveis the most commonly injured at the pointwhere it passes over
the petrous ridge ofthe temporal bone.This results in verticaldiplopia and a
compensatory head tilt tothe opposite shoulder.These nerves havefairly long
intracranial tracts and can beinjured by direct skull fractures or be com-pressed
by intracranial bleeds or diffusecerebral edema after blunt head trauma.Cranial
nerve palsies often spontaneouslyrecover within 6 to 9 months.Recovery isquite
variable and is dependent on severi-ty and the type ofinjury.Eyelid
LacerationsEyelid lacerations,particularly thoseextending to the lid margin and
gray line,should be thoroughly evaluated forlacrimal drainage system
injury,canthaltendon disruption,or injury to the tarsalplate and levator
aponeurosis.Afterantibiotics and tetanus prophylaxis havebeen administered as
necessary,the woundshould be cleansed and d�brided,takingcare to protect the
globe,possibly with acontact lens.The eyelid laceration shouldbe repaired in a
layered fashion,startingwith the tarsal plate repair (with 6-0polyglycolic
acid),lid margin (two to threeinterrupted sutures with 6-0 silk,which
isnonirritating to the cornea),orbicularismuscle re-apposition (multiple 6-0
plaingut sutures),and finally skin (with 6-0nylon or 6-0 fast-absorbing
gut).Topicalophthalmic ointment should be pre-scribed since these agents come in
contactwith the globe frequently,and suturesshould be removed in 5 or 6
days.Patientsshould be followed up and monitored forpotential complications such as
scar con-tracture or lid notching.Several weekspost repair,ifsignificant lid
contracture orfocal thickening is noted,then selectivejudicious steroid injections
(triamci-nolone acetonide,40 mg/mL) can beadministered with accompanying
dailymassage by the patient.In my experience,avulsion or loss ofeyelid soft tissue
is rare.When thisoccurs,it is usually from an abrasivecrushing macerated-type
laceration sus-tained in such accidents as a rollover inan all-terrain vehicle or
ejection from amotor vehicle.In evaluating theseinjuries,the examiner should
moisten therolled edges ofthe laceration and attemptto gently realign them.One
should notabnormally align the tissues,borrowingthem from the periphery and
shorteningthem in the vertical dimension.This canresult in lid retraction or
lagophthalmos,with risks ofcorneal exposure and ulcer-ation.It is best either to
leave a smallamount ofdenuded underlying tissues,which will reepithelialize
secondarily,andpossibly perform a temporary tarsorrha-phy,or,for larger defects,to
harvest a thindefatted skin graft for primary recon-struction (Figure 24-
10).Lacrimal InjuriesInjuries to the lacrimal drainage systemmost often result from
direct eyelid lacera-tions at the medial edge ofthe lid,whichtraverse the lid
margin and disrupt the infe-rior canaliculus.Canalicular lacerationsalso occur
indirectly when strong forces areapplied to the lateral aspect ofthe
lids.Thistension directed laterally causes the eyelidto split at the weakest
point,which is justmedial to the punctum (Figure 24-11).Damage to the lacrimal
drainage systemcan also be seen with severe medial rim andorbital wall fractures.A
disruption in thelacrimal system can be detected by passinga lacrimal probe through
the punctum andvisualizing the blunt-tipped probe withinthe laceration or wound.It
is especiallyimportant to detect this with the inferiorcanaliculus since this
system is dominant inthe vast majority ofpatients.Repair involves reanastomosis
ofthecanaliculus and either mono- or bicanalic-ular intubation.With bicanalicular
intu-bation,repair is performed by passing asilicone intubation tube through
thepuncta into the laceration and then locat-ing the distal cut end ofthe drainage
sys-tem for passing the tube into the nose,which is retrieved with a hook beneath
theinferior turbinate.Typically both the supe-rior and inferior canaliculi are
intubated(usually one is uninjured);both siliconetubes are passed into the nose and
are tiedto each other.This allows for retention ofthe looped tube for 6 to 12
weeks.Intraop-eratively,the silicone tubes are stretchedtoward the external
nares,tied together,and typically oversewn or tied with a finesilk suture to allow
for long-term reten-tion.Ifno tension is applied to the cutends ofthe silicone
tubing while tying,then,postoperatively,the loop formed atthe canaliculi puncta
will migrate laterallytoward the cornea,causing irritation or anannoying visual
field disturbance.
476Part 4: Maxillofacial TraumaTelecanthusTraumatic telecanthus typically results
fromsevere midfacial trauma (NOE) with dis-placement and splaying ofthe bones
thatserve as attachments for the medial canthaltendons.It is less frequently due to
lacera-tion and actual physical disruption anddisinsertion ofthe canthal tendons
from theunderlying bone.Therefore,traumatic tele-canthus from these injuries is
best treatedearly (within 7�10 d) following injury toprevent scarring and secondary
maladaptivechanges that compromise the reestablish-ment ofthe more normal narrow
intercan-thal distance.Preoperatively,one shoulddetermine whether the increased
intercan-thal distance is due to either a unilateral or abilateral injury.Treatment
typically includesan approach via a coronal incision,a Lynch(lateral nasal)
approach,or a combination,with reduction and fixation ofthe displacedbones or
direct transnasal wiring.Externalsplinting rarely yields satisfactory results.I
have found that direct canthal tendonreattachment with transnasal wire fixationis
best performed by passing a doubled-endloop of30-gauge stainless steel
wiretransnasally from the contralateral medialorbital wall and then suturing the
medialcanthus to the wire loop.The wire is thendrawn to the opposite side by
graduallytwisting the two ends around a short sec-tion oftitanium microplate
situated in theopposite medial orbital wall (Figure 24-12).Nonoperative Management
ofOrbital FracturesIndications for nonoperative or,as it haspreviously been
termed,conservativeman-agement oforbital fractures has been con-troversial for many
years.Some historicFIGURE24-10A,This young male sus-tained a macerated forehead,and
eyelidand nasal lacerations after being ejectedfrom a motor vehicle in an
accident.B,After moistening,redraping,andsuturing the soft tissues,it was
apparentthat there was a significant defect (8 �10 mm) ofskin on the right upper
lid.C,A full-thickness skin graft was harvestedfrom the right posterior auricular
area,which was closed primarily with the aidofreleasing Z-plasty
incisions.D,Theundersurface (dermal side) ofthe graftwas thinned and defatted.E,The
graftwas first perforated and inset over theskin defect.A temporary tarsorrhaphywas
maintained for 1 week to minimizemotion and shearing forces.F,Facialappearance 3
months after repair.G,Passive lid patency was achieved.There was no further
revision surgery.ABCDEFG
Orbital and Ocular Trauma477perspective and review is warranted sinceit provides
insight into the evolution andcurrent thinking regarding nonoperativeorbital
fracture treatment.In 1957 Smithand Regan coined the term blow-out frac-ture and
advocated early surgical interven-tion for orbital floor fracture repair.38Fol-
lowing this,Converse and Smith endorsedsurgical exploration and repair ofallorbital
fractures within the first 3 weeks ofinjury.39Even with surgical explorationand
repair,they found that enophthalmosor functional difficulties would develop,and
they attributed this to the blunt trau-ma forces and tissue damage rather thanthe
surgical intervention.Crikelair andcolleagues in 1972 promoted the conceptthat
orbital floor fractures were overdiag-nosed on plain films and,thus,were over-
operated.40They introduced the conceptofrepairing only select orbital floor frac-
tures,which were confirmed by tomogra-phy and only ifdiplopia or
enophthalmospersisted after an observational period of2 weeks.This marked an
importantchange in thinking toward a more selectiveapproach for surgical
intervention oforbital floor fractures.This change was,inpart,prompted by reports
and articlesdocumenting unacceptable complicationssuch as a total loss ofvision
following sur-gical exploration ofasymptomatic floorfractures.41In 1974 Putterman
and col-leagues reported on a series of57 patientswhom they had observed and on
whomthey had performed no surgical interven-tion whatsoever.42Only a few
oftheseindividuals had any persistent diplopia,and there were no visual acuity
distur-bances 4 months following the trauma.This landmark article created a
drasticshift in thinking�nonsurgical treatmentofall orbital fractures was
advocated.Put-terman and colleagues proposed thatpatients with persistent diplopia
should bemanaged by contralateral eye musclesurgery,or contralateral fat
resection,tomask the enophthalmos or altered visualaccess ofthe injured
side.Although thisretrospective study and series ofpatientsreceived much criticism
from both theophthalmology and facial trauma special-ties,it did reveal that many
orbital floorfractures healed uneventfully without sur-gical intervention and with
the perfor-mance ofeye-movement exercises.Following Putterman and colleagues�report
were a series ofarticles by variouspractitioners who attempted to refine
anddelineate the indications for surgicalexploration and repair oforbital
floorfractures.Dulley and Fells reported thatonly 50% ofall patients with orbital
floorfractures required surgical intervention.43All patients underwent a 2-week
observa-tional period;an individual would thenundergo surgical intervention ifone
ofthefollowing criteria was present:enophthal-mos > 3 mm,large herniation
oftissueinto the antrum,entrapment with limitedupward gaze,or significant
diplopia.Nev-ertheless,these criteria were somewhatsubjective and were limited by
the currentimaging techniques.Crumley and col-leagues used similar indications
forsurgery to those ofthe Putterman group,but based on these criteria,almost 90%
ofall their patients with orbital floor frac-tures underwent surgical repair.44Con-
verse and Smith developed and furtherrefined these same indications for
orbitalfloor surgery and reinforced the need andimportance ofserial clinical
examinationsin patients who had shown no initial indi-cations for surgery.45This
group promot-ed the concept that serial examinationsrevealing the development
ofenophthal-mos should be the criterion for surgicalintervention and not simply
that a large orcomminuted floor fracture existed.Theyproposed that the development
ofsignifi-cant postinjury enophthalmos is variableand could be due to either
resolving hem-orrhage and edema or orbital fat atrophy.In 1982 a survey by the
American SocietyFIGURE24-11A,Innocuous-appearing small left lower medial lid
laceration sustained from an inci-dental grab along the cheek during a touch
football game.B,Slight lateral traction on the lower lidand probing ofthe inferior
punctum revealed a full-thickness lid laceration medial to the punctumwith
severance ofthe inferior canaliculus.An oculoplastic surgeon repaired and managed
this injurywithin 8 hours.ABFIGURE24-12Reattachment and repositioningofthe left
medial canthus is fine-tuned by twist-ing a 30-gauge wire over a section
ofmicroplatesituated along the right medial orbital wall justbehind and above the
posterior lacrimal crest.
478Part 4: Maxillofacial TraumaofOphthalmic,Plastic and ReconstructiveSurgery
revealed that two-thirds ofoculo-plastic surgeons were operating within 2 weeks
ofinjury with few serious compli-cations or sequelae.46Although this wasreassuring
that current surgical approach-es and techniques were safe,there was noinquiry into
what the criteria or determi-nates were for undertaking surgical repair.What was
helpful was that several ensu-ing studies began to delineate which
patientsexhibiting functional deficits might benefitfrom surgical exploration as
opposed toobservation.Koorneef,in an anatomic study,showed that fine connective
tissue septa sur-rounded the extraocular muscles.47He advo-cated eye movement
exercises in patientswith mild or moderate restrictive motility aslong as there was
demonstrated serialimprovement in motility.He purported thatedema,hemorrhage,and
connective tissueentrapment were responsible for the majori-ty oflimited motility
in patients with orbitalfloor injuries.In 1984 Smith and colleagues intro-duced the
concept that Volkmann�s con-tracture might occur as a result ofelevatedintraorbital
compartment pressures.48Although this phenomenon was well-known,documented,and
proven in theorthopedic literature to occur with extrem-ities,it was unproven to
occur in the orbit.Volkmann�s contracture is a paresis frommuscle shortening and
fibrosis that resultsin limited mobility.Applying this conceptto the orbit,Smith
and colleagues recom-mended surgical intervention in the elderly,in individuals who
are hypotensive,and forsmall or linear orbital floor fractures withcoexisting
diplopia.They felt that these sit-uations left patients at an increased risk
fororbital compartment syndrome,thusdeveloping permanent limited mobilityowing to
Volkmann-like contractures.Con-current with these theories and recommen-dations was
the report by Hawes andDortzbach that emphasized the need forsurgical repair within
2 weeks followinginjury in patients with persistent diplopiawithin a 30�range ofthe
primary visual(straight-ahead) gaze.49They based this ontheir findings that there
were poor resultswhen late repairs were performed in thispatient group.Clearly the
advent and ready availabil-ity ofCT for use in diagnosing �trapdoor�fractures with
mechanical impingement ofthe orbital structures helped to refinediagnostic
capabilities and to aid treat-ment planning.Several groups ofauthorsemphasized the
need for correlating a pos-itive forced duction test with CT
evidenceofincarceration or impingement.50,51Without specific evidence ofa
trapdoorphenomenon or direct impingement,orbital floor fractures with limited
motili-ty were observed for 2 weeks.Persistentsymptoms or findings then prompted
sur-gical intervention.Trapdoor fractures orfine linear breaks without rim
fractures aremuch more common in pediatric patients.When severe limitation
ofmovement isencountered (typically upward or down-ward gaze,or both) and is
correlated withCT findings,this is a true emergency thatshould be treated
surgically to relieve theentrapment as soon as possible.Since his initial
controversial 1974article,Putterman has revised his indica-tions for surgical
intervention.52Putter-man and his colleagues indications arenow comparable to those
ofother sur-geons.They advocate 7 days ofsystemiccorticosteroids to speed the
resolution ofdiplopia within the first 3 weeks.This mayaid in resolving edema and
helping deter-mine who might benefit from surgery.Although persistent functional
limitationsare usually clear indications for surgery,controversy remains in
treating thosepatients who demonstrate a steady butslow resolution oftheir diplopia
that per-sists beyond 3 weeks.When the surgeon is confronted withany orbital
fracture,it is helpful to catego-rize the clinical deficits and goals ofsurgi-cal
treatment as being either functional orcosmetic.Simply operating on a radi-ographic
finding because it exists is notsatisfactory.The surgeon,with the assis-tance ofhis
ophthalmology colleagues,should determine what,ifany,functionaldeficits and
cosmetic deformities exist.Aspecific anatomic reason for these shouldbe
sought.Then,ifthe magnitude ofthefunctional deficit or cosmetic deformitywarrants
surgery,the type ofsurgicalapproach,repair,and materials shouldspecifically address
the structural causes.In a patient with the clinical findings ofonly
�soft�indications for surgery,a 2-week observational period seems pru-dent.Several
studies have addressed cos-metic deformities as they relate to orbitalfloor
fractures,offering indications forsurgery versus observation.Hawes andDortzbach
used tomography and felt thatorbital floor fractures involving > 50% ofthe surface
area should be reconstructedwithin the first 2 weeks to avoid the pre-dictable
development ofenophthalmos.49They also stated that patients with smallerorbital
floor fractures but with > 2 mm ofenophthalmos present at 2 weeks postin-jury
should undergo orbital floor recon-struction.This recommendation is basedon the
fact that later repair is technicallymore difficult with less optimal outcomesowing
to scar contracture and muscleshortening.Parsons and Mathog were ableto
demonstrate,using a laboratory model,that orbital floor fracture and displace-ment
ofequal magnitude with the medialwall fracture and displacement had amuch greater
effect on globe position.53This study supports the practice ofmostsurgeons,which is
nonsurgical and obser-vational management ofisolated displacedmedial wall
fractures.When orbital fractures are associatedwith other facial fractures such as
Le Fort orZMC fractures,several authors have advo-cated orbital floor exploration
and repairwith any evidence ofprolapse ofthe orbitalcontents into the sinus.54,55In
1991 Putter-man and colleagues advocated followingpatients closely for the
development of
Orbital and Ocular Trauma479enophthalmos,using objective measure-ment with a Hertel
exophthalmometer,orserial measurements for vertical dystopia byaligning the top ofa
clear ruler to bothundisturbed medial canthi and notingwhere the ruler bisects each
eye.52Despitenumerous reports,clinical series,andauthor suggestions,controversy
stillremains regarding the management ofthose patients who develop only mild
enophthalmos or hypo-opthalmos (1�2 mm) without any functional deficitsduring the
acute observational period.Operative Management ofOrbital FracturesIndicationsIt is
imperative that the surgeon has a com-plete understanding ofthe mechanism ofinjury
and potential complications to makea full diagnosis and an appropriate treat-ment
plan in each type oforbital fracture.Patients with a suspected or known
orbitalfracture should undergo thorough clinicalexamination,including fundoscopic
exam-ination;visual acuity;pupillary reactivity;detection ofdiplopia,extraocular
move-ment with any limitations noted,enoph-thalmos,and vertical dystopia;forced
duc-tion testing;and recording ofparesthesias.Radiographic studies should determine
thefull extent ofthe orbital fracture and anysurrounding and associated facial
fractures.CT scans,especially in the direct coronalplane,are the gold standard for
use inorbital surgery treatment planning.Con-traindications for surgery are
hyphema,retinal tears,globe perforation,the patientsees only with the eye on the
injured side,and life-threatening instability.Indications for surgery can be
dividedinto functional and cosmetic categories.Alogical systematic approach is
prudent inselecting patients who are suitable foracute or early surgical repair
versus thosewho deserve an observational period withintervention when signs or
symptomswarrant it (Figure 24-13).With regard tofunction,diplopia and decreased
visualacuity are the two main areas ofconcern.The majority ofsurgeons and articles
inpublished literature support early surgicalintervention in a patient with an
orbitalfloor fracture that has mechanical restric-tion ofgaze and a positive forced
ductiontest with a CT scan that has a trapdoorappearance or suggestions ofinferior
rec-tus muscle incarceration.56,57This phe-nomenon occurs more in children
withlinear fractures owing to the elasticity oftheir bones.58Pediatric or adult
patientswith these findings warrant early interven-tion to free up the tissues and
hopefullyprevent any permanent restriction owingto ischemic necrosis or scar
contracture.Inpatients with less impressive restrictivemotility (10�15�),a positive
forced duc-tion test,and no CT evidence ofmuscleentrapment,an observational period
ofseveral weeks is reasonable.These patientsmay only have entrapment ofsome
ofthefine connective tissue septa supporting theglobe,and with routine daily
functionand/or eye exercises,this restriction typi-cally steadily improves.Clinical
follow-upwith a series ofexaminations (two orthree) within the first 14
days,steroid ther-apy,and eye movement exercises shouldoptimize the outcome.In any
patient withan orbital fracture that has persistentmechanical restriction or
diplopia within30�oftheir primary gaze,especially thedowngaze (used during
reading),surgicalexploration is warranted.Prior to under-taking surgery,however,any
neurogenic orcentral component should be ruled out.Although infrequently
employed,elec-tromyography can be used to distinguishneurogenic diplopia from
mechanicalrestriction in problematic or brain-injuredpatients.Neurogenic or
neuromuscularinjuries are more suitably treated by stra-bismus surgery.With regard
to decreasedvisual acuity,an ophthalmologist shouldassess the patient serially for
resolution orimprovement.In more severe cases�patients who can only see shadows or
fig-ures or who have NLP�the fine-cut axialCT scans ofthe orbital apex and
canalshould be reviewed with the radiologist todetermine whether there is bony
mechan-ical impingement,hematoma,and/oredema compressing the optic nerve or vas-
cular supply.With the increasing popular-ity ofendoscopic approaches to the
cranialbase (typically for tumor removal),mostmajor medical centers have
neurosurgeonsand/or otolaryngology head and neck spe-cialists that are competent in
performingtransnasal endoscopic optic canal decom-pression.Ifat all possible,this
should per-formed within 12 to 24 hours ofthe con-firmed diagnosis ofexternal optic
nervecompression within the canal proper.Cosmetic deformities such as enoph-thalmos
or hypo-ophthalmos result from abony orbital volume increase,extrusion ofintraconal
fat into extraconal spaces,orprolapse oforbital contents into the maxil-lary sinus
or ethmoid air cells.Contrary tolong-standing dogma,post-traumatic fatatrophy does
not play a significant role inthe development ofthese deformities.59Most surgeons
currently undertake surgi-cal intervention in orbital floor reconstruc-tion ifthere
is 2 to 3 mm or greater ofenophthalmos or hypo-ophthalmos in thepresence oforbital
edema or hematoma.The rationale is that early repair offers themost favorable
outcome and that the cos-metic deformity only worsens as the edemaand hematoma
resolve.Orbital floordefects ofgreater than halfofthe surfacearea with concomitant
CT evidence ofthedisruption or prolapse into the underliningantrum generally should
be repaired.Again,the rationale for this is that as theedema resolves,eventually
there is somedegree ofenophthalmos or verticaldystopia that creates a cosmetically
unac-ceptable or,less frequently,functional prob-lem requiring surgery.With minimal
floordisruption (< 50%) and no entrapment orsignificant herniation,observation for
2weeks is prudent.Ifthe patient developsany functional problems or enophthalmos
480Part 4: Maxillofacial Trauma> 2 mm,then surgery can be undertaken totreat the
functional or cosmetic defect.Unnecessary delays approaching 6 weeksand beyond make
the surgical repair moredifficult and the ultimate outcome lessdesirable owing to
scarring and muscleshortening.Surgical ApproachesOnce it has been determined a
patientrequires surgical intervention,a well-thought-out plan and sequential
approachshould be developed.Ofparamountimportance is the determination ofwhichofthe
anatomic areas need to be accessedwith direct visualization and which intactbony
edges or landmarks need to be foundor fixated to accomplish the repair.Thishelps
the surgeon determine which softtissue incision should be employed.Ingeneral,most
surgeons prefer to firstgrossly reduce and usually fixate all perior-bital and
facial fractures prior to accom-plishing internal orbital repairs.The mostcommonly
used surgical approaches andmethods ofreconstruction are presentedhere so that the
surgeon can make an indi-vidualized and informed decision.Inferior and Lateral
Orbital ApproachesThere are three basic incisions used foraccessing the orbital
floor:the infraorbital,subciliary,and transconjunctival (Figure 24-14).Although
there are three basicapproaches,there are numerous technicalvariations based on
surgical training andindividual preference.Clearly the subciliaryand
transconjunctival incisions are the mostpopular owing to their superior
estheticsand generous access,and the fact that sur-geons are familiar with their
use.It is myopinion that the infraorbital or rim incisionresults in the worst
esthetics and offers noOrbital floor fractureFunctional deficitCosmetic
deformity(�) Forced duction test(+) Forced duction testEnophthalmos orinferior
dystopiaNormal globe positionMuscle entrapmenton CT
scanEmergentexplorationYoungernormotensivepatientSerial examinations,eye exercises,
andsteroids for 7�10 dConnective tissueimpingement only on CT scanMechanical
restrictionor persistent diplopia within 30#of primary gazeNo evidence of
neuromuscularinjuryEvidence of neuromuscularinjury (by forcedgeneration
andretraction test)StrabismussurgerySurgicalexplorationResolution of
mechanicalrestriction and diplopiawithin 30#of primarygazeElderly
orhypotensivepatientYoungernormotensivepatientSurgicalexplorationFollowclinicallywi
th serialexaminationsNo surgeryNo surgery> 50% floordefect or softtissue prolapse<
50% floordefectSteroids and follow-upclinically for 14 dEnophthalmosor
inferiordystopiaNo globepositionchangesOrbital floor reconstructionFIGURE24-
13Orbital floor fracture evaluation and treatment decision diagram.CT = computed
tomography; (�) = negative; (+) = positive.
Orbital and Ocular Trauma481advantages over the two former approaches;therefore,it
should not be employed.The subciliary incision was popular-ized by Converse in
1944.60Typically agently curved linear skin incision is madeseveral millimeters
below the lid edge oreyelash margin,preferably in a skin crease.The skin flap is
then undermined in aninferior direction for several millimetersbefore traversing
deeper inward directlythrough the orbicularis oculi muscle fibersand stopping when
the orbital septum isencountered.The rationale for the divi-sion ofthe skin and
muscle at differentlevels (stepping the incision lines) is that ithelps to prevent
direct or full-thicknessscarring and tethering ofthe eyelid.Oncethe orbital septum
has been encountered,the preseptal approach is then carried outinferiorly to the
orbital rim,and theperiosteum is incised just below the arcusmarginalis.The
periosteum ofthe orbitalrim is then reflected upward and inward,and dissection is
carried out over theorbital rim.One must bear in mind thatthe orbital floor drops
offseveral millime-ters toward the inferior direction prior toheading straight
posteriorly.The orbitalfloor dissection can then be extended pos-teriorly for a
safe distance of30 mm.Withan intact adult rim,the optic canal is only40 mm from the
anterior lacrimal crest,and with any rim displacement inward,this margin ofsafety
is further decreased.A modification ofthe subciliary approachis the �skin
only�incision.This techniqueis comparable to the technique justdescribed,except
that after dividing theskin,the inferior dissection is carried outsuperficially to
the orbicularis oculi mus-cle fibers until the inferior orbital rim isreached,and
then the muscle is divided atthe same level as the periosteal incision.This
approach is used less often owing tothe amount ofstretching on the unsup-ported
large skin flap and the resultanthigh rate ofectropion (permanent in 8%)and
potential skin necrosis,particularly inthe elderly patient who has a history
ofheavy smoking.61These complicationsprompted the development ofan alterna-tive
technique called the �skin-muscleflap.�With this procedure a similar inci-sion is
accomplished 1 to 2 mm below thelid margin but is carried through both theskin and
muscle at the same level down tothe tarsal plate.Again,the plane ofdissec-tion is
carried out anterior or superficial tothe orbital septum (preseptal) until
theorbital rim is encountered.This approachresults in excellent esthetics,a
simplifieddissection,and a decreased incidence ofhematoma formation or skin
necrosis.Subciliary incisionLower lid�crease incisionRim incisionSubtarsal
incisionFornix incisionTarsal plateOrbicularis oculi muscleOrbital
septumCapsulopalpebral fascial extension(inferior lid retractors)Extraconal orbital
fatWhitnall's inferiorsuspensory ligamentFIGURE24-14Cross-sectional view ofthe
inferior lid and various floor approach incisions.Adapted fromOchs MW,Johns
FR.Orbital trauma.In: Fonseca RJ,Marciani RD,Hendler BH,editors.Oral and max-
illofacial surgery: trauma.Vol 3.Philadelphia (PA): W.B.Saunders; 2000.p.208.
482Part 4: Maxillofacial TraumaThis skin-muscle flap still carries a 6% rateofearly
ectropion62;however,it is general-ly temporary and resolves within severalweeks
with gentle massage.This was con-firmed by several investigators who corre-lated
preoperative periorbital edema andincreased age positively with the develop-ment
ofthis temporary ectropion with thesubciliary approach.63A revision ofthisapproach
or technique is to use a relaxedskin tension line incision.The transconjunctival
approach fororbital floor fractures was first popular-ized by Tessier and Converse
and col-leagues in 1973 for orbital floor frac-tures.64,65The two basic variations
ofthisapproach to the orbital rim are retroseptalor preseptal approaches.Although
the ret-roseptal approach is a more directapproach to the rim,it exposes the
orbitalfat,which herniates into the surgical fieldand may interfere with the
surgery andresult in more fat atrophy,especially withcautery,and hence
enophthalmos.For thisreason,the preseptal approach is generallyfavored.66The
preseptal approach (see Fig-ure 24-14) as described by Tessier involvesan incision
through the palpebral con-junctiva just 2 to 3 mm below the inferioredge ofthe
tarsus that is extended throughthe inferior lid retractors and orbital sep-
tum.64Next,a preseptal vertical dissectionis carried out down several
millimetersbelow the orbital rim,and the periosteumis incised.The dissection ofthe
facialaspect ofthe rim and the floor is then car-ried out.This obviates orbital fat
hernia-tion in a fairly bloodless field.The necessi-ty for a periosteal closure is
controversialowing to the possibility ofentropion orectropion with inadvertent
suturing oftheperiosteum to the orbital septum or otherlayers.64,67Some surgeons
advocate a Frostsuture for a period of24 to 48 hours toallow for proper lower lid
redraping dur-ing early healing.Most surgeons find thisunnecessary.Ifthere is any
difficulty inidentifying opposing edges ofthe cutperiosteum,then no suturing should
beperformed rather than an inappropriatetethering ofmore superficial or
superioreyelid layers and structures to the underly-ing rim.Many instances of�early
ectropi-on�or a �shortened lid�are the result ofimproper suturing.The
transconjunctivalpreseptal approach enjoys a low incidenceofunfavorable scarring
with ectropion orentropion (1.2%).55However,one draw-back to this approach remains
a some-what-limited view during the preseptaldissection and limited exposure once
theorbital floor has been accessed.For thisreason,the lateral canthotomy and com-
plete severance ofthe lower limb ofthelateral canthal tendon (inferior cantholy-
sis) was introduced by McCord and Mosesin 1979.68This procedure allows for a gen-
erous tension-free exposure to the orbitalfloor,lateral orbital wall,and medial
area.The surgical exposure obtained with thetransconjunctival approach with the
infe-rior cantholysis is superior to that ofasubciliary incision.Also,the much
smallercutaneous incision is placed in a morefavorable area ofthe crow�s-feet.The
majority ofsurgeons currentlyuse the transconjunctival incision with orwithout
canthotomy or the subciliary inci-sion (preseptal approach) for orbital rimand
floor access.69Both ofthese basic inci-sions provide good exposure with excel-lent
esthetics and an extremely low rate ofcomplications.Each surgeon�s own train-
ing,familiarity,and personal preferenceshould guide which rim approach is
used.Superior and Medial Orbital ApproachesAccess to the superior orbital rim
andzygomaticofrontal (ZF) suture can beaccomplished via a lateral eyebrow inci-
sion,upper blepharoplasty incision,coro-nal incision,or lateral canthotomy inci-
sion that is an extension ofa subciliary ortransconjunctival incision with a
superiorcantholysis.The eyebrow incision,ifper-formed properly,results in
excellentesthetics and is quickly and easily per-formed;therefore,it is one ofthe
morecommon approaches used for the lateralorbital rim or ZF suture area.The
otherincisions described are used more oftenwhen extensive facial fractures are
presentthat require extensive skeletal exposure ofthe superior rim,cranial vault,or
zygo-matic arch.The lateral brow incision is placed onthe extreme outer aspect
ofthe eyebrow,usually just superior to the ZF suture.TheZF suture line is usually
approximately 1 cm above the lateral canthus.Generally,the skin ofthe lateral brow
is tented overthe superior lateral orbital rim,and a 1.5 cm curvilinear incision is
made in abeveled fashion paralleling the hair folli-cles.Double-pronged skin hooks
are thenplaced on the skin margins,and traction ismaintained with digital palpation
oftheinternal edge ofthe orbital rim.The skinincision opening is then gently
retractedinferolaterally more directly over the ZFsuture,and a needle-tipped Bovie
cauteryis used to divide the orbicularis oculi mus-cle fibers overlying the rim and
ZF suture.Additional undermining and dissection iscarried out in an inferolateral
direction toprovide full and adequate access to thefracture and enough adjacent
bone toallow for rigid fixation.The advantages ofnot extending the skin incision
beyond thebrow obviously involve esthetics (placingit in the well-camouflaged and
hidden areaofthe hair follicles) but also include thatthe skin is stepped and
muscle incisionsare made in distinct layers,which providefor more favorable
healing.This incisionalso allows access for placing a bluntcurved instrument deep
to the zygomaticarch for the reduction ofthe ZMC or archfractures.Closure should be
accomplishedin three distinct layers ofperiosteum,sub-cutaneous tissue,and skin.The
periosteal,muscle,and deep subcutaneous closuresare particularly important in that
theyprovide the bulk ofsoft tissue over anyplates and screws in the region.The
upper blepharoplasty incision canalso be used for access to the ZF suture.
Orbital and Ocular Trauma483The incision is placed in one ofthe uppereyelid skin
creases,preferably the deepestcrease (which can be marked preopera-tively,with the
patient awake).The skinincision is then carried down through sub-cutaneous
tissue,retracted somewhat lat-erally,and extended through the orbicu-laris oculi
and periosteum by sharpdissection.Generally a 1 cm length ofthelateral
blepharoplasty incision is all that isrequired for complete access to the
lateralorbital rim.This is due to the supplenessand mobility ofthe thin eyelid
skin.Careshould be taken to not over-retract the tis-sue,and the skin incision
should beextended slightly laterally ifexcessiveretraction forces are
apparent.Separatesuturing ofthe periosteum and skin are allthat is required.The
coronal incision allows for excel-lent access to the entire supraorbital
rim,roof,frontal sinus,superior aspects ofthenasal bone,lateral orbital rim and
wall,medial orbital rim and wall,and zygomat-ic arch.70This approach is generally
neces-sary for extensive facial fractures involvingthe zygoma,frontal sinus,and NOE
com-plex and for Le Fort III fractures.Numer-ous variations ofthe incision design
exist,but generally a curvilinear incision isplaced at least 2 cm posterior to the
hair-line (in the midline) and then extendedposteriorly,paralleling the
hairline,andfinally inferiorly into the preauricularregion.It is generally helpful
to carry thevertical component ofthe coronal incisionoverlying the temporalis
muscle just pos-terior to the junction ofthe superior helixand the scalp.It is then
sharply angled for-ward,hugging the anterior helix andpreauricular skin crease down
to the pre-tragal area.By doing so,the superficialtemporal vessels are generally
not encoun-tered or violated and retracted forwardwith the flap,allowing for a much
drierfield.It is not necessary to shave the scalp,but a 1 cm area ofhair can be
trimmed atthe incision to allow for ease ofclosure,postoperative hygiene,and
sutureremoval.Local anesthesia with vasocon-strictors is helpful for hemostasis
andoften obviates the need for compression(Raney) clips.The incision is carried
outthrough the skin,subcutaneous connec-tive tissue,and galea aponeurotica into
theloose areolar tissue in the midline.Thesubgaleal plane ofdissection is
contiguouswith a plane deep to the parietotemporalfascia in the area ofthe
temporalis muscle.The incision is then extended laterally inthe supraperiosteal
plane;it is helpful toinsert a Metzenbaum or curved Mayo scis-sors in this plane
prior to extending theincision laterally.This prevents inadver-tent incising or
nicking ofthe temporalisin an otherwise dry field.The dissection iscarried out
laterally to the superior tem-poral line bilaterally.Dissection is thencarried
anteriorly to the frontal bone,anda horizontal incision is made through
theperiosteum approximately 2 cm above thesuperior orbital rim.The incision is car-
ried laterally to the superior temporal lineand joined with the preauricular area
infe-riorly through the superficial layer ofthedeep temporal fascia to protect the
tempo-ral and frontal branches ofthe facialnerve.71The facial nerve courses in a
planesuperficial to the deep temporal fasciaapproximately 1 to 3 cm from the
tragusalong the zygomatic arch.72This approachprovides complete access to the
medial,lateral,and superior orbital rims.When amore extensive view ofthe medial
orbitalwall is required,subperiosteal dissectionand release ofthe superior trochlea
can beperformed�the flap is retracted moreinferiorly over the nasal dorsum,with
adirect view ofthe medial wall.No attemptsshould be made to re-attach the
trochleasince,when the soft tissues are re-draped,the trochlea re-adheres on its
own.Sutur-ing may actually pierce or violate thetrochlear tendon and result in
ocularmotility disturbances.Closure ofthe coro-nal flap should include suspending
thedeep temporal fascia over the temporalismuscle,deep closure ofthe galea aponeu-
rotica,subcutaneous buried suturing,andclosure ofthe skin.It is important
toremember that when a hemicoronal inci-sion is employed,the medial extent
oftheincision should be carried beyond themidsagittal plane and extended complete-
ly to the hairline.This allows for adequatereflection and retraction over the
entirezygoma and orbital rim structures.When a transconjunctival incision isused
with a lateral canthotomy,an exten-sion ofthe dissection superiorly can beused for
access to the ZF suture by severingthe superior limb ofthe canthal tendon.67This
approach provides good access to thelateral and infraorbital skeleton;however,itis
less frequently used because it requires amore complex closure and re-anchoring
ofthe lateral canthal tendon complex.Anymisalignment results in canthal
dystopia,usually in an inferior direction,and arounded-out �almond-shaped�eye
appear-ance.Ifthe superior canthal tendon and itsorigin to the internal rim are
allowed toremain intact,it provides a highly reliablelandmark to which the inferior
canthallimb can be sewn,resulting in excellentsharp-angled (30�40�) esthetics.The
entire lateral wall and rim is easi-ly accessed through a standard blepharo-plasty
incision that extends only to the lat-eral orbital rim.This approach iscommonly
used for lateral orbital decom-pressions in cases ofsevere thyroidorbitopathy and
it affords excellent expo-sure also to portions ofthe orbital roofand to the apex
ofthe orbit laterally.Medial Orbital ApproachesAccess tothe medial orbital rim and
superior aspectofthe medial orbital wall can be accom-plished through a coronal
incision,as pre-viously described.However,a separate lat-eral nasal incision can be
used for isolatedmedial wall exploration or to access theinferior aspect ofthe
medial orbital floor.This can be a transconjunctival or subcil-iary approach to the
inferior rim and floor.The entire medial wall can be visualized by
484Part 4: Maxillofacial Traumaextending the transconjunctival incisionthrough the
caruncle.The medial orbitalwall and rim,by definition,are involved infractures
ofthe NOE complex,Le Fort IIand III fractures,extensive frontal
sinusfractures,and,occasionally,large blow-outfractures.The lateral nasal incision
is mostoften used for access to the medial orbitalrim to reconstruct a detached
medial can-thal tendon with direct transnasal wiring.This type ofinjury often
occurs with NOEfractures and Le Fort III fractures.As stat-ed earlier,medial
orbital wall fracturesgenerally do not result in any entrapmentor ocular mobility
problems.Generally theupper one-third ofthe medial orbital wallis uninvolved or
nondisplaced,simplybecause it is the very thick extension ofthecranial base.The
lower two-thirds ofthemedial orbital wall overlie the ethmoid aircells and can be
displaced inward,result-ing in volume expansion.Unless there isextensive
involvement,generally theresulting increase in orbital volume doesnot result in the
development ofenoph-thalmos.Ifthe inferior two-thirds ofthemedial wall or orbital
floor are involvedand require surgical repair,then the previ-ously described
approaches to the orbitalfloor should suffice.However,fracturesthat extend farther
superiorly (above thefrontoethmoidal suture/anterior eth-moidal foramen) may
require a lateralnasal approach or coronal incision.Thelateral nasal approach
involves a verticalgentle curvilinear 1 cm incision approxi-mately 5 to 10 mm
medial to the insertionofthe medial canthus.Care should betaken not to place this
incision too close tothe medial canthus as this can result in ascar contracture
with �webbing�and anabnormal epicanthal fold postoperatively.The incision should be
placed over the lat-eral nasal structures properly,and after theskin incision is
made,the dissectionshould be carried straight mediallythrough skin,subcutaneous
tissue,and arudimentary portion ofthe orbicularisoculi muscle and periosteum.There
is noneed to step these layers.The periosteumcan then be reflected posteriorly and
supe-riorly to the medial orbital rim and wall.The medial canthal tendon and
lacrimalsac lie posterior and just inferior to theincision.The anterior ethmoidal
vessels lieposteriorly and superiorly approximately24 mm from the anterior lacrimal
crest.These vessels can be gently divided withbipolar cautery,providing excellent
hemo-stasis and improved access for identifyingan intact bony ledge.However,one
shouldbear in mind that any bony violation orentry superior to this line carries
thepotential risk for entry into the anteriorcranial fossa.When an orbital implant
isrequired along the medial wall,anteriorfixation ofthe implant is
recommended.Acute Repair Internal orbital fractures have varied pat-terns and
degrees ofseverity.It is helpfulto attempt to classify them either as linear,blow-
out,or complex fractures.Linearfractures are those in which the bone frag-ments and
walls remain intact.However,owing to angulation or overlap,they mayresult in either
a bony orbital volumeincrease or decrease.Overlap fracturesgeneral result in a bony
defect ofoneorbital wall (typically the medial orbitalfloor) and are the most
common orbitalfracture.Blow-in fractures can occur inany orbital wall but most
commonly occurin the roofand are associated with frontalsinus fractures.Blow-in and
blow-outfractures ofthe orbital roofoccur withequal frequency.Complex fractures
arethose that involve two or more walls,are > 2 cm in diameter,or are
comminutedwith displaced and unretrievable segments.Often these complex fractures
are associat-ed with fractures that extend beyond theorbital frame such as Le Fort
II or III andfrontal sinus fractures.These are termedcombined fractures.The goals
ofacute orprimary reconstruction ofprimary orbitalfractures are to alleviate any
functionaldeficit and to restore the facial esthetics.Linear fractures are
generally causedby blunt forces directly to the globe or par-tially to the rim and
most often result in anesthetic deformity such as enophthalmosor hypo-
ophthalmos.Functional deformi-ties with entrapment are less common withlinear
orbital fractures.However,isolatedlinear fractures can have an
instantaneoustrapdoor effect owing to momentaryexpansion and entrap the edge ofsoft
tis-sues including the inferior rectus.Oncetightly pinched between these bony seg-
ments,this manifests itselfas severe ocularmotility restriction that is
reproducible onserial examinations at the same point oflimitation.There is also a
positive result tothe forced duction test.This type offrac-ture necessitates
immediate surgical inter-vention to prevent the ischemic necrosis ofthe extraocular
muscles.The majority oflinear fractures in the orbit do not result inesthetic
deformities such as enophthalmosor hypo-ophthalmos unless there is anassociated
facial fracture such as a frac-tured ZMC with a medial and downwardrotation.It is
the volume changes thataccount for the abnormal globe position.The goal
ofreconstruction is to restore theanatomic position ofthe bony rim andassociated
facial bones and to reapproxi-mate,to the best ofone�s ability,the nor-mal bony
orbital volume with a recon-structive material.Numerous materialshave been
described in the literature forthese purposes,such as porous polyethyl-
ene,bioresorbable polydioxanone,nylon,gelatin film,titanium mesh,and autoge-nous
bone grafts (split-thickness calvariumand,less frequently,iliac
crest).73�79Eachmaterial has advantages and disadvantagesrelated to the
strength,application,reactiv-ity,infection rate,biointegration,and com-plication
rate associated with its use.For linear and blow-out fractures,Iprefer to use thin
(0.85 mm) porous poly-ethylene sheeting.This alloplastic materialis extremely
biocompatible and nonresorp-tive.It has more than adequate tensilestrength and does
not cause any capsule
Orbital and Ocular Trauma485formation such as that seen with polymericsilicone
sheeting.It has considerable flexi-bility (which can be improved with place-ment in
an autoclaved saline) and littlememory properties.The pore size allowstissue
ingrowth,which reduces the risk ofmigration.80However,I still recommendanchoring
the porous polyethylene sheet-ing to the anterior lateral orbital floor witha
single titanium screw (Figure 24-15).Thegreatest advantages ofthis material are
itsease ofcontouring,in situ carving,burring,and that it can be layered
posteriorlybehind the orbital equator to achieve prop-er orbital volume and
contour.52Titanium mesh,with fixation to sur-rounding intact orbital rims,is quite
use-ful when there are severe or comminutedinjuries and a cantilevering is
requiredbecause intact internal medial or posteriorbony margins have not been
identified oraccessed.However,the possibility ofunac-ceptable postoperative
scarring to themesh may occur,resulting in limited ocu-lar motility.Therefore,when
titaniummesh is employed,I still prefer to overlay itwith either a split-thickness
calvarial graftor a sheet ofporous polyethylene sheeting.These materials are
secured to the under-lying mesh with either 30-gauge stainlesssteel wire or
suturing.Blow-out fractures typically involveone orbital wall (usually the anterior
ormedial portion ofthe orbital floor) andare < 2 cm in
diameter.Enophthalmosassociated with orbital blow-out fracturesis due to an
enlargement ofthe orbitalbony volume that allows the orbital fat tobe distributed
within a larger compart-ment.39Fat atrophy contributes little,ifanything,to the
development ofearly orlate enophthalmos.81The reverse mecha-nism,often referred to
as blow-in fracture,may result in a decreased orbital volume.Exophthalmos and
ocular motility distur-bances are uncommon unless there aresurrounding severe
associated fracturessuch as ZMC or frontal sinus fractures.In 1960 Converse and
Smith intro-duced the concept of�pure�(isolatedfloor) and �impure�(floor and rim)
blow-out fractures.39Pure fractures are thoughtto be caused by a sudden
instantaneousincrease in intraorbital pressures fromdirect blunt-force trauma to
the globeitself.Impure fractures are purported to becaused by direct trauma and
compressionofthe bony rim and collapse ofthe sur-rounding facial bones,and result
in the dis-ruption ofthe internal orbital walls.Whatis most disconcerting is the
finding ofasso-ciated globe trauma such as hyphema,iri-doplegia (ciliary body
paralysis),and reti-nal hemorrhage in 90% ofpatients withpure blow-out
fractures.This supports thenotion that pure blow-out fractures arecreated by
substantial instantaneous directglobe trauma.This fact should heightenone�s
awareness ofthe potential for seriousglobe injury when dealing with isolated orpure
blow-out fractures.The goal ofprimary reconstruction ofblow-out fractures is to
restore the config-uration ofthe orbital walls,return pro-lapsed orbital contents
to the orbit proper,and eliminate any impingement or entrap-ment oforbital soft
tissues.In contrast tothe orbital floor blow-out fractures,isolat-ed blow-out
fractures to the roofor medi-al walls usually do not contribute signifi-cantly to
the development ofcosmeticdeformities or result in entrapment orlimited ocular
motility.As a result,medialand roofdefects are managed by observa-tion,serial
examinations,and interventionwhen symptoms warrant.The most diffi-cult area ofthe
orbital floor blow-out frac-ture to repair is the posterior medialextent,which is
beyond the globe axis.Often,an intact bony ledge cannot beidentified or the graft
material is notextended posteriorly enough to supportthe orbital contents in this
region.Thisarea is often responsible for a failedenophthalmos repair in orbital
blow-outfractures.It is the reconstruction ofthisposterior medial floor to its
normal con-tour that is the key to restoring normalglobe position both
anteroposteriorly andvertically.It is this scenario that is prob-lematic in delayed
reconstructions sinceattempts to create a normal anteroposteri-or position ofthe
globe may result in inap-propriate overpositioning ofthe globe in asuperior
direction.I prefer to use gelatinfilm as a temporary barrier for small orlinear
defects,simply to prevent entrap-ment during normal active ocular motion.This film
is resorbed rather rapidly anddoes not provide much structural support;therefore,it
is not used for larger defects inwhich herniation ofcontents into theunderlying
sinus is a possibility.Generally,the orbital blow-out fracture is explored inall
ofthe intact bony walls identified.Oncethe malleable ribbon or globe retractorshave
supported the globe and orbital FIGURE24-15A,Right inferior orbital rim andfloor
fracture reduced and fixated with a 1.7 mmmicroplate.A portion ofthe mid-rim was
suc-tioned away from the antrum and was missing.B,The floor defect was
reconstructed with 0.85 mmthick porous polyethylene sheeting secured with asingle 4
mm long 1.7 mm screw at the anteriorlateral intact floor.A tab extension ofthe
sheetingwas fashioned at the rim defect,curved,andsecured with a 5-0 nylon mattress
suture.AB
486Part 4: Maxillofacial Traumacontents superiorly,then the reconstruc-tive
material can be slid underneath themand overlap the intact bony marginsslightly at
the majority ofareas to provideadequate support.I prefer to use porouspolyethylene
for moderate to large blow-out fractures.The porous polyethylenesheeting can be
secured with a single posi-tional screw (usually 1.7 mm externalthread diameter) or
an extended tab ofthis material can be sutured to the orbitalrim orbital plate(see
Figure 24-15).Careshould be taken to not extend the grafts upto the orbital rim or
over the edge sincethese will be palpable and would improp-erly reconstruct the
normal anatomic con-tour to the floor,which should dip downbehind the rim for
several millimetersbefore proceeding posteriorly.Also,theextension ofsemirigid
grafts onto theorbital rim has an undesirable rampingeffect,which tends to position
the globe inan abnormal posterior direction,resultingin enophthalmos.After the
floor graft isplaced and secured,trimming or smooth-ing should be accomplished and
a forcedduction test performed prior to anywound closure to ensure that no impinge-
ment ofthe soft tissues has occurred.Complex orbital fractures are general-ly
associated with additional surroundingmidfacial and frontal sinus fractures.Pri-
mary reconstruction ofthese defects ischallenging owing to the extent
oftheseinjuries,the lack ofany normal identifi-able anatomy,and poor surrounding
bonysupport for rigid fixation and anchoringofreconstructive materials.However,it
isin this group ofindividuals that primaryrepair with normal anatomic realignmentis
critical for acceptable esthetic and func-tional outcomes.Delaying the
primaryrepair beyond 7 to 10 days usually resultsin some secondary soft tissue
changes,theinability to completely retrieve small bonysegments,and a less-than-
desirable out-come.The initial step in the reconstruc-tion ofcomplex facial
fractures is adequateexposure ofall midfacial structures withadequate alignment and
reduction prior torigid fixation ofany components withplates and screws (Figure 24-
16).Thishelps one avoid misalignment,over-reduction,or improper angulation ofthese
segments.Achieving adequate expo-sure requires more extensive
subperiostealdissection than is done for most otherorbital fractures.It may be
desirable toalso completely dissect and expose allinternal orbital fractures prior
to fixationofthe surrounding periorbital or midfa-cial fractures.Generally the
orbital rim isplated with 1.7 mm or finer plating sys-tems.Care should be taken at
the inferiororbital rim and especially the lateralorbital rim to keep the plates
several mil-limeters from the edge ofthe rim;other-wise,they will be annoyingly
palpableonce the soft tissue edema has subsided.Once the orbital rims and midfacial
boneshave been fixated,the moderate to largeorbital floor defects are generally
repairedwith porous polyethylene and anchored tothe anterior inferior floor with a
singlescrew.Sometimes layering ofthis materialwith an additional sheet posteriorly
isrequired to achieve correct anteroposteri-or globe positioning.More
extensivedefects may require titanium mesh ororbital floor plates with screw
fixation tothe rims and autogenous bone grafts.Sev-eral bone grafts can be secured
to themetallic mesh framework to independent-ly reconstruct the floor,medial
wall,and,less frequently,the lateral orbital walls.The advantage ofhaving bone
overlie themetallic mesh is that remodeling canFIGURE24-16A,An elderly female
sustained a severely displaced left zygomatic complex (ZMC) fracture with > 75%
orbital floor disruption.She was onwarfarin sodium and had moderately decreased
left visual acuity with increased ocular pressures.B,Axial CT scan revealed a ZMC
fracture with a severe pos-terior,medial,and moderate inferior displacement.C,The
patient was taken urgently (within 12 h) for surgical treatment to reduce the
fracture and re-expandthe orbital volume.Serial examination and ocular pressure
checks were performed every 2 hours pre- and postoperatively.Owing to cardiac risk
factors,theanticoagulation was not reversed,nor was the patient treated with fresh
frozen plasma.The zygomaticofrontal (ZF) suture area was first approached througha
lateral brow incision.After the intraoral vestibular and then transconjunctival
approaches were accomplished,the ZF fracture was plated.(CONTINUED)ABC
Orbital and Ocular Trauma487occur�secondary revision surgery isenhanced when
dissecting along a healedbony surface versus bare mesh.In severe orlarge defects
with comminution,overcor-rection ofthe enophthalmos component(but not a hyper-
ophthalmic deformity)by several millimeters is often necessary totake into account
the orbital edema thatexists.In addition,with bone grafts,someFIGURE24-16
(CONTINUED)D,The infraorbitalrim was fixated with a 1.2 mm titanium plate,andthe
floor was reconstructed with 0.85 mm porouspolyethylene sheeting.E,The left
maxillary sinusanterior wall defect visualized through the vestibu-lar incision
along the edentulous ridge.Note theherniated orbital soft tissues.F,After retrieval
oftheorbital soft tissues from above and insertion oftheporous polyethylene floor
graft,the repair wasinspected from below ensuring that there was notissue prolapse
or entrapment.The fracture wasthen spanned from the buttress to the intact
medialmaxilla with a 1.7 mm plate.The anterior maxil-lary wall defect was not
grafted.G,The eye positionwas assessed with the contralateral side,and aforced
duction test revealed a free and full range ofmotion.H,The patient had a routine
24-hour fol-low-up computed tomography scan ofthe head,asper the request ofthe
neurosurgeon.The images ofthe patient�s face demonstrated excellent realign-
ment.Postoperatively she had greatly improvedvision and no neurologic
impairment.She was dis-charged home on postoperative day two on
warfarinsodium.I,The reformatted coronal images showgood orbital floor support
ofthe globe.J,Facialappearance at 1 week postoperatively.K,Six weekspostoperatively
this patient had no complaints andher baseline visual acuity had returned.HIJKDEFG
488Part 4: Maxillofacial Traumamild resorption can take place with
subtlesettling.However,it is the resolution oftheedema that accounts for the
majority ofpostoperative globe position changes.ZMC fractures are second only
tonasal fractures in incidence.These frac-tures are described in greater detail
inChapter 23.2,�Management ofZygomat-ic Complex Fractures�and Chapter 25,Management
ofFrontal Sinus and Naso-orbitoethmoid Complex Fractures.�Some discussion is
warranted here,asZMC fractures relate to orbital involve-ment and appropriate
intraoperativesequencing.Nonfragmented or single-piece ZMC fractures are generally
dis-placed in an inferior,medial,and posteri-or direction,with a pivot-point
rotationabout the ZF suture.As a result,the orbitalfloor suffers the most
disruption.On ini-tial inspection,the coronal CT scans maynot reveal the degree
oforbital floor dis-ruption,but ifone envisions the outwardreduction ofthe
zygomatic buttress andthe resulting medial floor void,the magni-tude ofthe injury
can be appreciated.Onlyafter reduction and stabilization oftheentire external
orbital framework and sur-rounding facial bones should the internalorbital defects
be repaired (see Figure 24-16C�G).The internal orbital injuries asso-ciated with
fragmented ZMC fracturesusually involve multiple orbital walls andlarger
defects.Therefore,more extensiveexposure is generally necessary and morerigid
materials are usually required forreconstruction.NOE injuries result mainly
fromextreme blunt force trauma and have a highdegree ofassociated intracranial and
neu-rologic injuries.Additionally,injuries to thenasal airway and lacrimal system
canoccur.82Injuries to the lacrimal system canbe managed by the placement ofsmall
sili-cone tubes.Even though canalicular dis-ruption is more common with laceration-
type injuries,these tubes can still beinserted with blunt trauma when a fairamount
ofedema is present and the sur-rounding anatomy is obscured.This pro-phylactic
intubation ofthe superior andinferior canaliculi and the lacrimal systemhelps to
avoid iatrogenic injury during theextensive dissection required to treat thistype
ofinjury.The tubes can be allowed toremain in place several weeks postopera-tively
during the resolution ofedema.Repair ofNOE injuries is recommendedwithin the first
7 to 10 days after injury,before the soft tissues have had the chanceto re-adapt
with significant scarring con-tracture and generally a flattened andsplayed
appearance to the orbits and mid-face.NOE injuries generally do not causeentrapment
simply because ofthe orbitalwalls involved and the degree ofcomminu-
tion.However,entrapment ofthe medialrectus can occur during reconstruction,fix-
ation,and suturing;therefore,a forced duc-tion test should be performed at the com-
pletion ofthese phases.The primary defectsassociated with NOE injuries are
medialcanthal disruption with telecanthus andincreased bony volume resulting in
enoph-thalmos.Ifthere are no other indicationsfor coronal dissection,such as
frontal boneor zygomatic arch fractures,then the medi-al orbital component ofthe
NOE fracture isbest approached directly through a lateralnasal (Lynch)
incision.Often accessing theinferior medial wall or positioning the infe-rior edge
ofthe medial wall graft requiresan additional inferior rim and orbital
floorapproach,such as the subciliary ortransconjunctival
approach.Traumatictelecanthus should be treated by direct fix-ation
techniques,using 1.0 to 1.7 mm plat-ing systems.External splinting may providesome
reasonable nasal bone molding,but itgenerally does little to improve
traumatictelecanthus.Generally,the medial canthalligament heals in a position that
is toosuperficial and inferior.Postoperatively theentire area fills with dense scar
tissue,and itis difficult to secondarily dissect and reposi-tion the canthus in its
normal position.With NOE fractures the medial canthal ten-dons usually maintain
their attachment tothe bony segments.Therefore,properreduction and fixation ofthe
bony skeletonto the surrounding stable bone (maxilla,orbital,and frontal) often
corrects the tele-canthus deformity.This should be accom-plished and the medial
canthal positionreassessed.Ifthe canthal position is stillunacceptable,then a fine
stainless steel wire(30-gauge) can be secured directly to thecanthal tendon or
preferably,sutured to thewire that has been passed transnasally.The double-armed
wire is insertedfrom the contralateral orbit to the side thatwill be anchored,with
the entry point onthe medial wall being just posterior andsuperior to lacrimal
fossa.This can beaccomplished by prethreading the double-armed wire into a gently
curved 16-gaugeneedle,passing it transnasally throughsmall burr holes,retrieving
the double-armed wire on the side to be fixated,andwithdrawing the needle
canula.The can-thus is then sutured to the wire loop with ahalf-round needle (4.0
Mersilene S-2 nee-dle),and the wire is drawn to the contralat-eral side and the
limbs twisted graduallyaround a short section ofplate to fine-tunethe canthal
position (see Figure 24-12).This is a much easier way to accomplishprecise canthal
positioning than are directsuturing techniques.SummaryOrbital fractures are often
associated withocular injuries and midfacial fractures.Athorough ophthalmologic
evaluation ismandatory to detect ocular injuries and topreserve vision.Surgical
interventionshould be based on either a functionaldeficit or a cosmetic
deformity.The surgicalsequencing and timing ofthe repair shouldbe well thought
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treatment oforbitalfloor fractures.J Oral Maxillofac Surg1981;9:81�4.55.Zingg
M,Chowdhury K,Ladrach K.Treatmentof813 zygoma-lateral orbital complex frac-
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W.Exploration oftheorbital floor:an indicated procedure? JCraniomaxillofac Surg
1990;1:187�90.57.Sacks A,Friedland J.Orbital floor fractures:should they be
explored early? Plast Recon-str Surg 1979;64:190�3.58.deMann K,Hes WJ,deJong
PT,Wijingaarde R.Influence ofage on the management ofblowout fractures ofthe
orbital floor.Int JOral Maxillofac Surg 1991;20:330�6.59.Manson PN,Clifford CM,Su
CT,IliffNT.Mechanisms ofglobal support and post-traumatic enophthalmos.I.The
anatomy ofthe ligament sling and its relation to intra-muscular cone orbital
fat.Plast ReconstrSurg 1986;77:193�202.60.Converse JM.Two plastic operations for
repairofthe orbit following severe trauma andextensive comminuted fracture.Arch
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ofconjunctival and subciliaryincisions for orbital fractures.Br J PlastSurg
1983;10:309�13.62.Heckler F,Songcharoen S.Subciliary incisionand skin-muscle eyelid
flap for orbital frac-tures.Ann Plast Surg 1983;10:309�13.63.Pospisil OA,Fernando
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and trauma.J Oral MaxillofacSurg 1973;1:3�8.65.Converse JM,Firmin F,Wood-Smith
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reconstruction surgery[discussion].J Oral Maxillofac Surg 2001;59:291�2.67.Manson
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CHAPTER 25Management ofFrontal Sinus and Naso-orbitoethmoid Complex FracturesLarry
L.Cunningham Jr,DDS,MDRichard H.Haug,DDSFractures ofthe frontal bone and the naso-
orbitoethmoid (NOE) complex are infre-quent,occurring among 2 to 15% ofpatients
with facial fractures.1�4Whenthese fractures occur,they can cause devas-tating
complications because oftheir prox-imity to the brain,eyes,and nose.Compli-cations
include blindness or other forms ofvisual disturbance,orbital cellulitis
orabscess,meningitis,brain abscess,andfacial deformation.Although reports
ofthesurgical management ofthe diseasedfrontal sinus have existed for > 100
years,5no consensus has yet been reached on idealcare after traumatic
injury.5�7Most victims are male (66�91%) andyoung (usually 20�30 yr ofage,range
6�72 yr),1,7�20and most frontal sinus and NOEinjuries are sustained in motor
vehicle ormotorcycle collisions (44�85%).1,3,7,8,10,11,14�24NOE fractures can occur
in isolation,butthey most often occur in association withother midface
fractures.23,25As many as 60%ofpatients with NOE fractures have associat-ed
nonfacial injuries.24The distribution between fractures ofthe supraorbital rim and
fractures ofthefrontal sinus is almost equal.The pub-lished frequency offractures
ofthe anteri-or wall,the posterior wall,and the floor ofthe frontal sinus varies
rather widely:43 to61% ofreported patients had anteriortable fractures only,19 to
51% had anteri-or and posterior table fractures,2.5 to 25%had injuries to the
nasofrontal duct,and0.6 to 6% had posterior fractures only.2,3,8Anatomy and
Physiology Embryology ofthe SinusThe frontal bone is an intramembranousbone that
develops from two paired struc-tures that begin to ossify at the eighth orninth
week in utero.10,26The ossificationbegins in the frontal processes ofthe squa-mous
regions,progresses to the orbitaland squamous regions,and reaches thefrontal and
temporal regions by thetwelfth week.The metopic suture in themidline closes during
the second year oflife.27The forehead is displaced anteriorlyby sutural
growth,inner table resorption,and outer table deposition.28The frontal sinus is a
small outpouch-ing at birth and undergoes almost all ofitsdevelopment
thereafter.The sinus maydevelop from one or several different sites:as a rudiment
ofthe ethmoid air cells,as amucosal pocket in or near the frontalrecess,as an
evagination ofthe frontalrecess,or from the superior middle mea-tus.20Initial
pneumatization begins duringthe fourth month in utero.Secondarypneumatization
begins at the age of6 months to 2 years and develops laterallyand vertically.The
sinus is radiographical-ly identifiable by the time the child reach-es the age of6
years.29Most pneumatiza-tion is completed by the time the child is12 to 16 years
old,but it continues untilthe age of40 is reached.5,20,26,30The config-uration
ofthe sinus and the position ofthesepta are extremely variable.Physiology ofthe
SinusThe entire surface area ofthe frontal sinusis covered with respiratory
epitheliumranging in thickness from 0.07 to 2.0 mm.31The mucosa consists ofpseu-
dostratified ciliated epithelium,mucus-producing goblet cells,a thin
basementmembrane,and a thin lamina propria thatcontains seromucous glands.31When
themucosa is healthy,a blanket ofmucin
492Part 4: Maxillofacial Traumaoverlies the epithelium.The cilia flow at250
cycles/min.The mucin blanket flowsin a spiral fashion in a medial-to-
lateraldirection;the flow is slowest at the roofand fastest at the nasofrontal
duct.32Themucin empties at the nasofrontal duct at arate of5.0 g/cm2.The
physiologic charac-teristics ofthe sinus and the status ofthenasofrontal duct
dictate the treatment ofthe frontal sinus in trauma.33OsteologyThe frontal bone is
shaped as a concavedisk with a horizontal table forming theorbital rim.From the
nasion the boneextends approximately 12.5 cm superiorly,8.0 cm laterally,and 5.5 cm
posteriorly.Two frontal tuberosities are noted lateral tothe midline and superior
to the supraor-bital run.The thickest area ofthe bone isthe supraorbital rim from
the frontozygo-matic process to the nasal bones.The eth-moid plate is bound on
three surfacesalong the floor ofthe frontal bone in themidline.As the floor ofthe
frontal boneextends laterally,it becomes concave andforms the orbital roof.The
supraorbitaland frontal foramen are located at the mostsuperior portion ofthe
orbital rim.Thesupratrochlear foramen is located medialto the supraorbital foramen
or notch andlateral to the nasal bones.A spine or con-cavity exists on the frontal
bone along themedial anterior orbital roof;the trochlea ofthe superior oblique
muscle is attached tothis spine (Figure 25-1).34,35Paired triangular sinuses are
foundwithin the frontal bone.These sinusesare asymmetric and are separated by
afrontal septum.The average height ofthesinuses is 32 mm,and their average widthis
26 mm.29,35The surface area is approx-imately 720 mm2.32The frontal bone isthinnest
in the region ofthe glabella atthe anterior wall and floor ofthe sinus.The duct
ofthe frontal sinus emptiesinto the ethmoid air cells ofthe middlemeatus ofthe
nose.Frontal sinusCribriform plateEthmoid sinusSuperior conchaMiddle
conchaMaxillary sinusInferior conchaNasofrontal ductFrontal sinusMucosal
liningFrontal sinusSuperior concha(turbinate)Nasofrontal ductEthmoid sinusMiddle
concha(turbinate)Lower concha(turbinate)FIGURE25-1A,Frontal bone and frontal sinus
showing therelation ofthe nasofrontal duct and nose.The arrows representthe flow
from the sinuses to the nose.B,Lateral view ofthe nor-mal nasofrontal duct.The
arrows represent the flow from thesinuses to the nose.C,Superior view ofthe normal
nasofrontalduct.Adapted from Zide MF.Nasal and nasoorbital ethmoidfractures.In:
surgery.Vol.2.Philadelphia(PA): JB Lippincott Company: 1992.p.576�7.ABC
Management ofFrontal Sinus and Naso-orbitoethmoid Complex Fractures493The internal
concave surface ofthefrontal bone forms the anterior cranialfossa that houses the
brain.The floor ofthe frontal bone outlines the roofoftheorbit.The convex outer
table is boundedby the scalp and the frontalis,orbicularis,and procerus muscles.The
osseous struc-tures that abut the frontal bone are thelacrimal and ethmoid bones
inferiorly,thesphenoid inferiorly and posteriorly,theparietal posteriorly and
superiorly,thezygoma laterally,the nasal bones anterior-ly,and the maxilla
anteriorly and inferior-ly.The ethmoid air cells and nasal appara-tus are situated
inferiorly.The nasal part ofthe frontal boneextends inferiorly deep to the nasal
bonesand the frontal process ofthe maxilla,adding support to the NOE
complex.Thenasal bones and the maxilla make up thepiriform rim.The articulation
ofthenasal bones forms a crest posteriorly andinferiorly;this crest articulates
with thefrontal bone,the perpendicular plate ofthe ethmoid (forming the upper third
ofthe nasal septum),and the septal carti-lage.The NOE region is supported struc-
turally by a vertical buttress�the frontalprocess ofthe maxilla�and two horizon-tal
buttresses:the supraorbital and infra-orbital rims.36The medial walls ofthe orbit
beginbehind the frontal process ofthe maxilla.The thin lacrimal bone and a frail
laminapapyracea in the anterior are weak andsusceptible to fracture.Higher
up,thefrontoethmoid suture delineates the levelofthe cribriform plate and crista
galli.Neurovascular StructuresThe arterial blood supply to the frontalsinus is from
the supraorbital and anteriorethmoid arteries.Two foramina are pre-sent along the
suture line:the anterior eth-moid foramen,through which course thenasociliary nerve
and the anterior eth-moidal artery;and the posterior eth-moidal foramen,through
which pass thevessel and nerve ofthe same name.Further posterior along the
medialorbital wall,the optic nerve exits throughthe body ofthe sphenoid bone,3.5 to
5 mm behind the posterior ethmoidal fora-men in a line parallel to the two
foramina.The frontal bone is supplied by the supra-orbital,anterior superficial
temporal,ante-rior cerebral,and middle meningeal arter-ies.27,34,35Venous drainage
is transosseousthrough the anastomosis ofvessels ofthesubcutaneous,orbital,and
intracranialstructures.The primary venous drainage isthrough the
supratrochlear,supraorbital,superficial temporal,frontal diploic
(veinsofBreschet),superior ophthalmic,andsuperior sagittal sinuses.27,34The
relation-ship ofthe diplo� to the anterior cranialfossae is important to understand
becausethese structures can become a conduit forthe spread ofinfection.Interorbital
SpaceThe nasofrontal suture is the continuationofthe frontoethmoid suture and
corre-sponds to the plane ofthe base ofthe skullor frontal sinus.The interorbital
space isbounded laterally by the medial wall oftheorbits.In the middle is the
perpendicularplate ofthe ethmoid and nasal septum.The anterior wall is composed
ofthepaired nasal bones,the frontal processes ofthe maxilla,and the nasal processes
ofthefrontal bone.The ethmoid air cells within theinterorbital space occupy the
upper halfofthe wall lateral to the nasal fossa.Thedimensions ofthe anterior end
ofthe eth-moid labyrinth are approximately 2.5 cmvertically and 1 cm
transversely.The pyra-mid-shaped sinus measures 3.5 to 5 cmfrom front to back.The
ethmoid air cells drain into themiddle meatus,as does the nasofrontalduct.The
nasofrontal duct is located in theposterior medial floor ofthe frontal sinusat the
junction ofthe ethmoid and nasalportions ofthe floor,and it coursesthrough the
anterior ethmoid in the mid-dle meatus or just anterior to the middleturbinate.The
length ofthe duct may varyfrom a few millimeters to a centimeter ormore (Figure 25-
2).Medial Canthal TendonThe orbicularis oculi muscle has threeportions:the
orbital,the preseptal,and thepretarsal.The pretarsal portions oftheupper and lower
lids unite at the canthusto form the medial canthal tendon (MCT).The MCT may be
subdivided into asuperficial portion and a deeper portionwith the lacrimal sac
between them.Thesuperficial portion has two �legs�andinserts into the frontal
process ofthe max-illa,providing support to the eyelids andmaintaining the
integrity ofthe palpebralfissure.36,37The anterior leg attaches to
theposterolateral surface ofthe nasal bones,and the superior leg inserts at the
junctionofthe frontal process ofthe maxilla andthe angular process ofthe frontal
bone.The deeper portion (also known asHorner�s muscle or the pars
lacrimalis)attaches to the posterior lacrimal crest.NOE injuries may cause avulsion
ofthe tendons from the bone or,more com-monly,fractures ofthe bone that containsthe
attachment oftendons.This portion ofthe orbital rim is an important anatomicregion
with regard to reconstruction ofNOE fractures.36Lacrimal ApparatusThe lacrimal
drainage system is intimatelyrelated to the NOE region and can be dam-aged during
trauma to or reconstruction ofthis area.The system removes any excesstears that
accumulate after lubrication ofthe surface ofthe globe.The superior andinferior
lacrimal canaliculi drain thelacrimal lake.The puncta ofthe canaliculiopen just
lateral to the lacrimal lake andare surrounded by Horner�s muscle.Theorifice ofthe
upper punctum faces down-ward and backward,and the orifice ofthelower punctum faces
upward and back-ward.The superior punctum is approxi-mately 3 mm medial to the
inferior
494Part 4: Maxillofacial Traumapunctum.The two canaliculi pierce thelacrimal fascia
and enter the lacrimal sacat or very near a common point.Thecanaliculi lie mostly
behind the medialpalpebral ligament and are surrounded bythe pars
lacrimalis.38,39The lacrimalcanaliculi are lined with nonkeratinizedand non�mucin-
producing stratifiedsquamous epithelium.The epithelium is75 to 150 �thick and
consists ofa few lay-ers ofsquamous cells,polyhedral cells,and a basal cell
layer.39The lacrimal sac lies in a fossa on theanteromedial wall ofthe bony
orbit.It islined with pseudostratified columnarepithelium and is approximately 12
mmlong.39The apex ofthe sac ends blindly ina superior fundus,and the sac
continuesinferiorly into the nasolacrimal duct,which is housed in a bony canal.The
ductempties into the inferior meatus in thenasal cavity.38Patient Evaluation
Clinical FindingsPeriorbital ecchymosis and pain are themost common signs and
symptoms asso-ciated with fractures ofthe frontalbone.5,40�44When the bone bleeds
and theperiosteum is interrupted,leakage ofblood into the adjacent facial
planesresults in periorbital ecchymosis.Throughthis same
mechanism,subconjunctivalhemorrhage may occur.Ifthe nose andzygomas are
unaffected,a finding ofsub-conjunctival hemorrhage is sufficient forthe diagnosis
offrontal bone fracture.Fractures ofthe NOE complex can pro-duce the following
signs:nasal deformity,edema and ecchymosis ofthe eyelids,sub-conjunctival
hemorrhage,cerebrospinalfluid (CSF) leakage,hyposmia,traumatictelecanthus,increased
canthal angles,andblindness (Figure 25-3).23,45Soft tissue lacerations in the
region ofthe glabella and the supraorbital rims arealso commonly found in
association withfrontal bone fractures and may be associ-ated with anesthesia or
paresthesia ofthedistribution ofthe supraorbital and supra-trochlear
nerves.5,40�44Depression ofthebone with flatness and cosmetic deformityis noted
ifthe patient is examined soonafter injury.Examination ofa patient withNOE
fractures detects mobility ofthenasal bones,traumatic telecanthus,Frontal
sinusNasofrontal ductCribriform plateVomer (sectioned)Palate (sectioned)FIGURE25-
2A,Section through the intraorbital space revealing the rela-tionship ofthe frontal
sinus and the ethmoid sinuses to the nose.The arrowsrepresent the flow from the
sinuses to the nose.B,The drainage ofthenasofrontal duct into the nose is located
in the posterior medial floor ofthefrontal sinus and at the junction ofthe ethmoid
and nasal portions ofthefloor.The arrows represent the flow from the sinuses to the
nose.Adapted fromZide MF.Nasal and nasoorbital ethmoid fractures.In: Peterson
LJ,IndresanoAT,Marciani RD,Roser SM.Principles oforal and maxillofacial
surgery.Vol.2.Philadelphia (PA): JB Lippincott Company; 1992.p.560.OrbitEthmoid
sinus (aircells)Cribriform plateFrontal sinusNasofrontal ductPerpendicular plateof
ethmoidSuperior turbinateMaxillary sinusInferior turbinateMiddle
turbinateInfraorbital neurovascularbundleAB
Management ofFrontal Sinus and Naso-orbitoethmoid Complex Fractures495depression
ofthe radix,a wide and flat-tened nasal dorsum,and an upturnednasal tip (Figure 25-
4).From 1 hour to 5 days after injury,there may be enoughedema to hide the contour
depression.Pal-pation may reveal crepitation and tender-ness over the fracture
site.40�44Fractures involving the posterior tableofthe frontal sinus or the
cribriform platemay cause CSF leakage.40�43,46Confirmationofthe presence ofCSF can
be made by col-lecting this fluid and comparing its concen-trations ofglucose and
chloride with thepatient�s serum concentrations.Concentra-tions ofchloride and
glucose can be deter-mined in as little as 0.1 mL offluid.Chlorideconcentrations in
the collected fluid that aregreater than concentrations in serum andglucose
concentrations less than those inserum indicate the presence ofCSF.Collect-ed fluid
can also be tested for the presence of�2-transferrin;a positive result confirms
thepresence ofCSF (Table 25-1).47The depression ofbone fragmentsinto the orbit may
cause exophthalmos,proptosis,or ptosis.A depressed injuryalso causes restricted
ocular movement ifthe superior rectus muscle,the superioroblique muscle,or the
trochlea is dam-aged.43,44Medial orbital wall fracturesassociated with NOE
fractures can alsocause enophthalmos.A thorough examination is importantto
distinguish between a nasal fracture andan unstable NOE fracture.The examinershould
place the thumb and index fingerover the medial canthus
bilaterally.MobilityFIGURE25-3Initial appearance ofa patientwith a frontal sinus
fracture.Note the bilateralperiorbital ecchymosis and forehead laceration.FIGURE25-
4Pre- (A) and postoperative (B) images ofa patient with an NOE fracture showing
aseverely depressed radix.ABTable 25-1Normal Values ofConstituents ofCSF,Serum,and
Nasal SecretionsConstituentCSFSerumNasal SecretionsOsmolarity295 mOsm/L295
mOsm/L277 mOsm/LSodium140 mEq/L140 mEq/L150 mEq/LPotassium2.5�3.5 mEq/L3.3�4.8
mEq/L12�41 mEq/LChloride120�130 mEq/L100�106 mEq/L119�125 mEq/LGlucose58�90 mg/100
mL80�120 mg/100 mL14�32 mg/100 mLAlbumin 50�75%55%57%Total protein5�45 mg/dL6.0�8.4
mg/dL335�636 mg/dL(% oftotal protein)Immunoglobulin G3.5 mg/100 mL1,140 mg/100 mL51
mg/100 mL�2-Transferrin (% of15%0%0%total transferrin)Adapted from Brandt MT et
al.47 CSF = cerebrospinal fluid.
496Part 4: Maxillofacial Traumaofthese fragments may vary,but any move-ment implies
instability and requires openreduction and stabilization.36A ruler orcaliper should
be used to measure the inter-canthal distance.The normal distance is28.6 mm to 33.0
mm for adult women;itis 28.9 mm to 34.5 mm for adult men.Increased widths suggest
an NOE fracture.Two tests that can aid in the diagnosis ofinstability ofthe medial
canthus are the�bowstring�test and the bimanual exami-nation.The bowstring test
involves pullingthe lid laterally while palpating the tendonarea to detect movement
offracture seg-ments.48,49The Furness test may also beperformed by grasping the
skin overlyingthe medial canthus with a small-tissue for-ceps (Figure 25-5).A lack
ofcreasing orresistance by the underlying bone isindicative ofan underlying
fracture.50Thebimanual examination requires placing aninstrument (eg,a Kelly clamp)
high intothe nose,with its tip directly beneath theMCT.Gentle lifting with the
contralateralfinger palpates the canthal tendons andallows an assessment ofthe
instability ofthe tendon attachment and the necessityfor open
reduction.51ImagingPoor outcomes after the treatment ofNOEfractures and frontal
sinus fractures typi-cally result from misdiagnosis,inadequateplanning,lack
ofexposure,inadequatereduction or fixation ofsoft tissue or bone,stripping ofthe
medial canthi,or loss ofnasal contour with insufficient primarygrafting.36,52In the
past,Waters�projec-tions,reverse Towne�s projections,lateralskull films,and laminar
tomograms wereused to visualize midface and upper-facefractures.It is clear that
appropriate preop-erative imaging can help to prevent misdi-agnosis and can aid in
proper treatmentplanning.Today computed tomography(CT) scans are the gold standard
for imag-ing these fractures (Figure 25-6).5,10,36,52�56The plane ofchoice for
frontal sinusimaging is the axial view,preferably withslice thicknesses of1.0 or
1.5 mm.22,26,30Thehigh degree ofdetail required for imagingNOE fractures
necessitates axial and coro-nal views with slice thicknesses of1.0 or 1.5
mm.25,36Indeed,it has been shown thatfor severe fractures ofthe NOE region,two-and
three-dimensional CT scans providethe most information about the medialorbital
wall,the medial maxillary buttress,and the piriform aperture.36,57Patency ofthe
Nasofrontal DuctAlthough the newest CT scanners provideexceptional views and can
often provideslices through the nasofrontal duct,evi-dence oftheir reliability in
detectingobstruction ofthe ducts is scant.54,55Ductobstruction should be suspected
with frac-tures involving the medial supraorbital rimor the frontal bone with nasal
ethmoidalcomponent fractures,and it should alwaysbe considered when a CSF leak is
present.12In these situations an open or intraopera-tive evaluation ofpatency is
indicated.Thisevaluation is important because the condi-tion ofthe nasofrontal duct
has the mostinfluence on the health ofthe frontal sinus(Figure 25-
7).12,20,22,33,54,58�62Classification ofNOE FracturesAs with all fractures,NOE
fractures areclassified as unilateral or bilateral,open orclosed,and simple or
comminuted.Threetypes ofNOE fractures have been welldescribed.25,36,38,63A type I
fracture main-tains the attachment ofthe MCT to a largesingle nasoethmoidal
fracture segment;repairing this type offracture is straight-forward.A type II
fracture shows morecomminution yet maintains the attach-ment ofthe medial canthus
to a sizablebony segment.Type III fractures displaysevere comminution with possible
avul-sion ofthe MCT from its bony attachment(Figure 25-8).Classification ofFrontal
SinusFractures Traditional fracture classifications can beused with reference to
frontal bone fracturesBimanual palpationMedial canthus moveslaterally if fractured
Kelly forceps in nasal vaultFIGURE25-5Illustrations ofthe bowstring (A) and biman-
ual examination (B) for possi-ble NOE fractures.Adaptedfrom Zide MF.Nasal
andnasoorbital ethmoid fractures.In: Peterson LJ,Indresano AT,Marciani RD,and Roser
SM.Principles oforal and maxillo-facial surgery.Vol.2.Philadel-phia (PA): JB
Lippincott Com-pany; 1992.p.562.Palpable "bow"AB
Management ofFrontal Sinus and Naso-orbitoethmoid Complex Fractures497(eg,open or
closed).Numerous other classi-fication schemes have been proposed in thesurgical
literature in an attempt to simplifysurgical decision making.Although theseschemes
are well intended,some are socomplex that they actually complicatedecision making
and are ofno value.Con-sideration must always be given to the con-dition ofthe
anterior table,the posteriortable,and the nasofrontal ducts and to thepresence
ofcomorbid intracranial injuryand concomitant
craniomaxillofacialinjuries.5,8,14,20,64The simplest and mosthelpful classification
schemes distinguishpossible complications and treatments onthe basis oftypes
offractures.Isolated anterior table fracturesshould be treated so that cosmetic
defor-mities can be prevented.Posterior tablefractures,alone or in combination
withanterior table fractures,should be treatedso that neurologic
sequelae,includingmeningitis and brain abscess,can beavoided.Combinations
offractures thatcompromise the nasofrontal duct shouldbe treated so that the
development ofmucoceles and pyoceles can be prevented.These fracture combinations
include frac-tures ofthe anterior table and the posteri-or table,fractures ofthe
anterior table andthe NOE,and fractures ofthe anteriortable and the medial superior
orbital rim.Treatment Surgical AccessThe coronal approach to surgery providesthe
greatest access to the frontal bone andsinus and produces the most desirable cos-
metic results.5,10,22,61Although lacerationsmay be considered as an approach to
thefracture,their size and shape rarely pro-vide enough access without undue
andunsightly extension.Gullwing or spectacleincisions result in unattractive scars
thatare highly visible because oftheir promi-nence on the brow and the resulting
reflec-tion oflight.These scars can be camou-flaged only with wide-rimmed
glasses.The�open sky�approach is equally deforming,leaving an H-shaped scar over
the browsand nasion.Although the coronal approach hasbeen well described,65the
preparationrequired for a coronal incision varies.Ifaneurosurgical procedure is
anticipated,the hair may be shaved and the skindegreased with alcohol and then
preparedwith an antimicrobial skin preparationagent,preferably povidone-iodine
solu-tion.Ifa neurosurgical procedure is notanticipated,the hair should be
partedcoronally from preauricular region topreauricular region.Water soluble lubri-
cant is helpful in maintaining the part.The hair may then be braided in
multiplepigtails and gathered anteriorly and pos-teriorly on either side ofthe
part.Localanesthetic with a vasoconstrictor is usedto aid in
hemostasis.Electrocauteryshould not be used for the initial incisionbecause it may
damage hair follicles.Theincision is made to the depth ofthe looseaponeurotic
layer.The flap is underminedalong this plane and above the periosteumin an anterior
direction.Raney clips arehelpful in achieving hemostasis;however,hemorrhage may
recur when they areremoved,and electrocautery may need tobe used carefully at the
end ofthe proce-dure as the individual clips are removed.Again,care must be taken
to avoid hairfollicles to preserve scar camouflage.The flap is elevated to within
2.0 cm ofthe fracture or within 3.0 cm ofthe supra-orbital rims.The pericranium is
thenFIGURE25-6The detail offracture anatomy is clearly superior in computed
tomographic (CT) scanswhen compared with traditional radiography.A,Initial
appearance ofa patient with an NOE frac-ture.B,Axial CT scan showing the fracture.C
and D,Axial and coronal CT scans ofanother patientillustrating detailed fracture
anatomy.ABCDFIGURE25-7Intraoperative view ofthe floor ofthe frontal sinus with
nasofrontal ducts.
498Part 4: Maxillofacial Traumaincised,and the reflection ofthe flap con-tinues
deep to the pericranium so that thebranches ofthe facial nerve can be pro-
tected.Further reflection can be obtainedwith greater exposure by extension
ofthepreauricular incision,galeal splitting (ifavascularized galeal flap is not
anticipated),or release ofthe supraorbital nerve fromits foramen or notch.Osseous
Recovery and AccessRecovery ofbony fragments in comminut-ed fractures is best
undertaken during thereflection ofthe coronal flap.Fragments ofthe anterior table
should be released fromthe periosteum and removed one at a time.Some method
oforganizing the fragmentsshould be used.For example,the frag-ments could be
numbered and their posi-tions recorded on a map.They should bearranged in the same
order on a back table(Figure 25-9).Ifcontaminated,segmentsofbone may be cleansed
with copious irri-gation,scrubbing,and even povidone-iodine solution,and then used
for recon-struction as free grafts.66Once the anteriortable has been removed,access
should beadequate for sinus exploration,posteriortable inspection,and sinus
floor(nasofrontal duct) evaluation.Ifa more extensive neurosurgical pro-cedure is
anticipated,osseous recoverymay be performed in concert with a cran-iotomy bone
flap.Before small fragmentsare recovered,the osseous flap designshould be mapped
out on the frontal bone(with care taken to avoid the sagittalsinus).Bur holes are
created at three orfour corners ofthe frontal bone.The ten-uous and adherent dura
is releasedthrough the bur holes,and a craniotome isused to connect the bur
holes.The dura iscarefully reflected as the bone flap isremoved.Recovery ofthe rest
oftheosseous fragments can then be completed.A perimeter-marking technique canbe
used for removal ofthe anterior tablethat is unfractured.67The removal oftheentire
anterior table is important whenobliteration ofthe sinus is anticipatedbecause this
procedure requires thoroughremoval ofsinus mucosa.One side ofahemostat or pick-up
instrument can beinserted into the sinus,and a small burhole can be made at the tip
ofthe superfi-cial arm ofthe instrument.Fixation platescan be adapted before the
removal oftheremaining anterior table segment.Intraoperative Evaluation
oftheNasofrontal DuctAfter access has been obtained and oss-eous exploration and
recovery have been performed,the condition ofthe frontalsinus floor and the
nasofrontal ducts can be assessed by direct visualization (see Figure 25-7).The
relative patency oftheduct can then be evaluated by placing an FIGURE25-8Naso-
orbitoethmoid fracture classification.Type I fractureType II fractureType III
fractureFIGURE25-9Comminuted frontal sinus seg-ments arranged prior to
reconstruction.
Management ofFrontal Sinus and Naso-orbitoethmoid Complex Fractures499angiocatheter
into the nasofrontal duct andintroducing an appropriate fluid mediumso that flow
can be assessed.A 3.8 cm (1.5 inch) 18-gauge angiocatheter is thebest instrument
for this purpose.Patency ofthe nasofrontal duct can be confirmed byintroducing
normal saline and observingits emergence from beneath the medialturbinate or its
collection in the posteriorpharynx (Figure 25-10).Because ofits dra-matic
hue,methylene blue dye has beenoffered as an appropriate fluid for evaluat-ing
patency.However,this blue dye can dis-rupt visualization ofthe surgical
fieldbecause completely removing the dye is dif-ficult during a surgical procedure
(Figure25-11).Fluorescein is an excellent alterna-tive because it is
clear,colorless,water solu-ble,and radiolucent.68However,its visual-ization
sometimes requires using anultraviolet light source and then dimmingthe operating
room lights.Radiopaque dyehas been suggested for use as a diagnosticmedium for
nasofrontal duct fractures,butits visualization requires a C-arm fluo-roscopy
unit.60Moreover,any spilledradiopaque dye must be completely clearedbefore
additional radiographs or computedtomographic images are obtained.Indigocarmine is
another acceptable dye,butCongo red is neurotoxic.Anterior Table FracturesThe
thinnest area ofthe frontal bone isthe region ofthe glabella,the anterior wallofthe
frontal sinus,and this region ishighly susceptible to fracture.These frac-tures may
seem straightforward but stilldeserve careful attention.Simple green-stick or
nondisplaced anterior wall frac-tures do not require operative treat-
ment.69Displaced anterior table fracturesrequire open reduction.The surgeonshould
closely inspect the sinus floor,theposterior wall,and the patency ofthenasofrontal
duct.Ifthe posterior wall andthe floor are free ofinjury,the pieces ofthe anterior
wall may be fixated with low-profile bone plates.64,66,70,71Any voidremaining in
the anterior wall after recon-struction can be closed by placing titani-um
mesh,methylmethacrylate,or otherbone substitutes.The soft tissue injuriesmay then
be repaired.Posterior Table FracturesFractures to the posterior table ofthefrontal
sinus are more concerning becauseofthe proximity to the anterior cranialfossae
(Figure 25-12).Posterior table frac-tures can be subclassified into three cate-
gories:nondisplaced,displaced,and dis-placed with gross neurologic injury.Eachofthe
subclassifications is invariably asso-ciated with anterior wall penetration.Eachis
treated differently,and each requiresneurosurgical consultation or joint man-
agement with a neurosurgeon.Antibioticcoverage is particularly important in pre-
venting infection.16FIGURE25-10Technique ofidentifying apatent nasofrontal
duct.Adapted from Zide MF.Nasal and nasoorbital ethmoid fractures.In:Peterson
LJ,Indresano AT,Marciani RD,RoserSM.Principles oforal and maxillofacial
surgery.Vol.2.Philadelphia (PA): JB Lippincott Compa-ny: 1992.p.582.ABFIGURE25-
11Aand B,Intraoperative evaluation ofnasofrontal duct patency by injection
ofmethyleneblue.In B,note the methylene blue coming from thepatient�s
nostril.Reproduced with permission fromHaug RH and Cunningham LL.64FIGURE25-12CT
scan demonstrating anteriorand posterior table fractures ofthe frontal sinus.
500Part 4: Maxillofacial TraumaThe surgeon should check carefullyfor displacement
ofthe fracture,CSF leak,entrapment ofsinus membranes,anddural tears.Ifthe injury is
not substantialand the nasofrontal duct is patent,theanterior table is replaced and
fixed and thesoft tissue injuries are repaired.Com-minution ofthe posterior
table,penetrat-ing injury,CSF leak with extensive duraldamage,or frontal lobe
damage requiresfrontal sinus cranialization:completeremoval ofthe posterior
table,therebyeffectively increasing the size ofthe anteri-or cranial
fossa.5,20,58,59,62,64In one reviewofcases,as many as 16% ofpatientsundergoing
frontal sinus surgery requireda cranialization procedure.5In such a casethe
posterior table would be gentlyremoved,either with a diamond bur orwith
rongeurs.Care should be taken in thearea ofthe sagittal sinus to avoid
severebleeding.All irregularities ofthe sinus aresmoothed with a bur.After bone
removalthe dura should be repaired with primaryclosure,a fascia or synthetic
patch,or agaleal or pericranial flap.5,64The wound is closed in
layers.Strictattention must be given to meticulousremoval ofall ofthe mucosal
elementsfrom the walls,cul-de-sacs,and septa ofthe sinus and from all bone frag-
ments.72�74Failure to remove such ele-ments may result in a mucocele orpyocele.The
mucosa is then reflecteddown into the nasofrontal duct,and theorifice is obstructed
by local bone or mus-cle.The harvested fat is placed into thesinus and packed until
the sinus is full.Finally,the outer table is reassembled andrestored as would be
done for a simpleanterior wall fracture.Orbital Roofand SupraorbitalBar
ReconstructionOnce the posterior wall and the sinus floorhave been
explored,inspected,and evalu-ated for damage,the orbital roofandsupraorbital bar
may be reconstructed.After these procedures have been complet-ed,a galeal flap
should be reflected,thesinus obliterated,and the nasofrontal ductobstructed.The
free osseous fragmentsthat have been recovered,mapped,andarranged on a back table
should be rigor-ously curetted for removal ofany respira-tory epithelium that could
becomeentrapped between them during recon-struction.Every remnant
ofrespiratoryepithelium should be removed from everycrevice and cul-de-sac so that
the possibil-ity offuture mucocele formation is mini-mized.This procedure is
followed withlocal ostectomy with a no.8 round dia-mond bur and copious amounts
ofsaline.The arranged bone fragments should beconsolidated with titanium
microscrews(1.0�1.3 mm) and with appropriate plates,mesh,or both.75,76 Mesh has an
advantagein that it provides support and consolida-tion ofthe segments in three
planes ofspace (Figure 25-13).75,76Titanium meshhas been shown to be compatible
with softtissue,undergoing incorporation withindigenous cells.77Resorbable
technologycontinues to show promise,even forfrontal bone
injury78;however,theresorbable systems currently available arenot as versatile as
titanium mesh in theirability to be contoured or to stabilize smallbone
fragments.Before final placement ofthe consolidated titanium and bone seg-ments,the
sinus should be copiously irri-gated and hemostasis achieved.Once thisphase ofthe
procedure has been complet-ed,the nasofrontal ducts may be obstruct-ed
(ifindicated),the sinus obliterated,thebrain isolated with a galeal flap
(ifindicat-ed),and,finally,the anterior table replaced.Nasofrontal Duct
ObstructionNasofrontal duct obstruction should notbe confused with sinus
obliteration.Sinusobliteration is the elimination ofdeadspace by the introduction
ofanothermaterial.Duct obstruction is one ofthemethods ofisolating the sinus (or
brain)from nasal contamination,basically byplugging it with another material.As
stated above,the condition ofthenasofrontal duct is the most important fac-tor in
maintaining the health ofthe frontalsinus.12,20,22,33,54,58�62This duct permits
theexit ofmucin,seroma,or hematoma afterinjury.Ifthe duct is injured and obstruct-
ed,sinusitis,meningitis,or osteomyelitismay develop.The condition ofthe ductshould
be considered in the evaluation offractures ofthe NOE complex,the supraor-bital
rim,or the sinus floor.Ifthe duct isnot patent,thorough removal ofevery pos-sible
remnant ofsinus mucosa is performedby curettage.20,58,68,73,74This procedure
isFIGURE25-13Reconstruction ofthe frontal barand frontal sinus with titanium
mesh.A,Themesh is adapted to a dried skull and then steril-ized prior to
surgery.B,Intraoperative view ofreconstruction ofthe frontal bar and nasal dor-sum
with mesh.AB
Management ofFrontal Sinus and Naso-orbitoethmoid Complex Fractures501followed by
removal ofadditional mucosafrom every cul-de-sac and crevice with asmall (no.8 or
larger) diamond bur undercopious amounts ofirrigation and with theaid
ofmagnification.Any remaining rem-nants ofthe nasofrontal duct mucosa arethen
inverted into the nose.A number ofmaterials can be used toobstruct the nasofrontal
duct.Temporalfascia,temporal muscle,or both can beharvested from the adjacent
temporalregion through a bitemporal flap.Tensorfascia lata is another
alternative,but it mayproduce morbidity at the second surgicalsite.Estimating the
surface area to be cov-ered is an important technical point.Asuture package is a
good template for mea-surement and recording.Because fasciashrinks,it is important
to harvest approx-imately 20% more graft material than isindicated by the
template.Bone graftmaterial can be harvested from the sinusseptum,the inner
table,or elsewhere onthe cranium.79Commercial tissue sealantsprepared from human
plasma and con-taining bovine-derived aprotinin are avail-able.These sealants have
been shown to beeffective tissue adhesives and hemostaticagents.80�82Autologous
platelet gel andautologous fibrin glue have also been usedfor similar
indications.83,84In addition,anew fibrin sealant from the American RedCross has
been reported to show promiseas a hemostatic agent without the additionofbovine
aprotinin.85Whatever products are chosen,theorganization and arrangement
oftheobstructive media are important.Forexample,a tissue sealant may be placedafter
inversion ofthe sinus mucosa.Fasciaor muscle may then be introduced into
theremnants ofthe duct to block passage ofnasal contaminants,followed by inner-
table cranium or remnants ofseptal bonefrom the sinus,followed by another
layeroftissue sealant.Tissue sealants can beused effectively to seal offthe sinus
fromthe nasal cavity when they are appliedlayer by layer as described above.Sinus
ObliterationNasofrontal duct obstruction is necessaryto seal offthe frontal sinus
from nasal con-taminants.Sinus obliteration adds onemore layer to the seal but also
eliminatesthe �dead space�or air within the sinus thatmay permit fluids to
accumulate,thus caus-ing a seroma or a hematoma.Furthermore,after
cranialization,sinus obliteration cush-ions and protects the
brain.Historically,sinus obliteration has been accomplished ina number
ofways,including inserting nosubstance or object (theoretically permit-ting bone
fill after curettage) or hydroxyla-patite,glass
wool,bone,cartilage,muscle,absorbable gelatin sponge,absorbable knit-ted
fabric,acrylic,or fat.16,73,74,86�92The useoffat has been reported most
frequently,and this method historically has providedthe most desirable
results.Harvesting fat is simple and may beperformed by liposuction or an
openapproach.89With the open approach theskin is first cleansed with an
antimicrobialagent from below the umbilicus to abovethe escutcheon ofthe
genitalia.A transversesemilunar incision is made within the�bikini�line,5.0 cm
superior to the symph-ysis pubis (Pfannenstiel�s incision);an inci-sion 5.0 to 8.0
cm long is adequate.Analternative to this approach is a verticalincision from below
the umbilicus to abovethe symphysis pubis.The incision is carriedthrough skin and
subcuticular tissue to thefat.The fat is grasped with an Allis clampand
retracted.Scissors are used to dissectthe fat subcutaneously,moving
laterally,inferiorly,superiorly,and caudally to thefascia overlying the abdominis
rectus mus-cles,which are then connected,releasingthe fat.Irrigation and meticulous
attentionto hemostasis are important before closureofthe incision to avoid hematoma
andinfection (Figures 25-14 and 25-15).NOE ReconstructionEarly surgical management
is important inthe reduction ofNOE fractures.25,38,45Thedeformities that result
from unrepairedNOE fractures are severe and difficult to correct,requiring NOE
osteotomies and grafting,and satisfactory results arerarely achieved.In addition to
the coronal approach,complete exposure ofthe NOE area oftennecessitates lower
eyelid incisions(transconjunctival or subciliary) and amaxillary vestibular
incision.36Theseapproaches aid in the treatment ofdis-placed infraorbital rims and
maxillaryantrum or piriform rims.Type I fractures are less difficult to treatand
can at times be reduced transnasallyand treated without fixation.More often,single-
segment NOE fractures are reducedthrough a coronal incision and secured atthe
nasofrontal junction,the maxillary but-tress,and the infraorbital
rims.36,38Transnasal wiring is recommended forfractures graded as Markowitz type II
orhigher.22Although we are truly in an era ofrigid fixation (bone plates and
screws),FIGURE25-14A,Abdominal fat graft harvestshowing the amount offat
obtainable.B,Subse-quent hematoma formation,which necessitateda return to the
operating room for evacuation.AB
502Part 4: Maxillofacial Traumacomplete reduction ofthe NOE area andreattachment
ofthe MCT,or replacementofa small bone segment,seem never to beadequate with
microplates alone.For NOEfractures including avulsion ofthe MCT orin which the MCT
is attached to a smallbone segment,transnasal wiring should beconsidered.The point
offixation ofthewires should be directed posterior andsuperior to the lacrimal
fossa so that themedial canthal distance is decreased andwidening ofthe nasal bones
and bluntingofthe medial canthal area can be avoided.22Wires must be passed through
the medialorbital bone and the superior nasal septumor the perpendicular plate
ofthe ethmoid.Their passage can be facilitated with theuse ofa spinal needle or a
wire-passing awl.Drill holes can also be used to aid in wirepassing.Some clinicians
have advocatedtemporary removal ofthe nasal bone foridentification ofthe �canthal
bearingbone�and for facilitation ofthe passage oftransnasal wires.22,36The MCT and
itsbony segment can be incorporated into thetransnasal wire fixation,or an
avulsedMCT can be attached to the transnasalwire with sutures.Slight overcorrection
ofthe medial canthal distance is desired.Incases in which fracture comminution pre-
vents adequate fixation ofthe MCT to abone segment,stabilization with fixationto a
calvarial bone graft has been advocat-ed.36In cases in which sufficient
medialorbital wall remains,placing a microplateand screw for attaching the MCT
behindthe lacrimal crest has been suggested.38Bone grafting may often be
necessaryin cases ofsevere comminution ofthenasal bones or the medial orbital
walls.Onlay ofcranial bone grafts to maintaindorsal height and nasal tip projection
canbe performed through a coronal incision,and these grafts can be fixated rigidly
orwith wire.Medical Therapy ofthe Sinus PostoperativelySaline solution nasal spray
can reducesymptoms ofrhinosinusitis.93This therapycan prevent crusting ofthe
nasolacrimalduct as well as the frontonasal duct and theostia ofthe maxillary
sinus.Because thistreatment is inexpensive and involves littleor no risk,it can be
made a part ofreason-able postoperative care regimens.There have been no clinical
trials relatedto post-traumatic medical treatment ofthesinus.However,for patients
in whom thefrontal sinus has been left intact,there maybe at least a temporary
decrease in functionofthe mucociliary apparatus.94�96In addi-tion,the trauma
ofsurgery causes edema inthe sinus tissues.Mucolytics have been advo-cated for use
in patients with rhinosinusitisto thin the mucus secretions and to
improveclearance.93During the post-traumatic orpostoperative period,the use
ofmucolyticssuch as guaifenesin may be beneficial.Decongestants may also be
consideredin the immediate postoperative period.Decongestant medications (eg,pseu-
doephedrine or oxymetazoline hydrochlo-ride) act by stimulating a-
adrenergicreceptors in the mucosa ofthe upper respi-ratory tract.This action causes
vasocon-striction in the respiratory mucosa,therebyshrinking the mucosa and
increasing thesize ofthe airways or ducts.93,97,98Topicalagents have fewer systemic
side effects butare known to have a rebound potential andshould be used for no more
than 3 days.Because there is no consensus regardingthe use ofpostoperative
antibiotics,theiruse should be based on the individualpatient and type ofinjury.The
extent ofsofttissue injury,presence ofwound contami-nation,a concomitant CSF
leak,and otherassociated injuries should all be considered.Current recommendations
regarding theuse ofprophylactic antibiotics for head andneck injuries include a
duration oftherapyofno more than 24 hours.99,100In cases ofcontamination by a
foreign body,this treat-ment may be continued for 10 days.In theabsence ofgross
contamination ofthewound,a limited number ofpostoperativedoses can be considered,or
none at all.Antibiotics used to treat acute rhinosinusitisinclude
amoxicillin,amoxicillin-clavulanate,azithromycin,cefpodoxime proxetil,cef-
prozil,cefuroxime axetil,clarithromycin,lev-ofloxacin,loracarbef,and trimethoprim-
sulfamethoxazole.93Penicillin is still the drugofchoice for treating facial
fractures.101FIGURE25-15Aand B,Elevated pericranialflap to be inset into the
frontal sinus for oblit-eration.C,A second patient undergoing thesame procedure;
here,the fat is being placedinto the sinus.ABC
Management ofFrontal Sinus and Naso-orbitoethmoid Complex Fractures503Complications
Complications offrontal bone injuryvary in severity and may occur manyyears after
the injury.The principal typesofcomplications are those that occurdirectly at the
time ofinjury,those ofaninfectious nature,and those that arechronic problems.The
most devastating complicationsare neurologic problems resulting fromdisplacement or
penetration ofthe frontalbones into the brain.These injuries canresult in
concussion,severe brain injury,ordeath.Displacement ofthe floor ofthefrontal bone
can cause orbital damage.Themost frequent ocular complication isdiplopia.Damage to
the superior obliquemuscles or trochlea may result in limitedrange ofmotion ofthe
globe.Severing ofthe supraorbital nerve by the injury or dur-ing reflection ofthe
osteoplastic flap leavesa permanent anesthesia ofthe distributionofthe
forehead.102Trauma to the floor ofthe frontal sinus or displacement ofthemedial
supraorbital rim may cause a CSFleak.Generally,reduction ofthe fracturescorrects
this problem.Ifit is persistent,however,neurosurgical repair is
indicated.Infectious complications most fre-quently arise from occlusion
ofthenasofrontal duct or contamination ofthesinus by penetrating foreign
bodies.Themost frequently encountered infection ismeningitis.88Ifthe nasofrontal
duct isoccluded,blood may accumulate in thesinus,creating an environment that
isconducive to the growth ofanaerobic bac-teria.13,103Frontal sinus abscess is
spreadby direct extension through small frac-tures ofthe frontal bone or through
tran-sosseous anastomotic vessels.59The resultis brain
abscess,meningitis,cavernoussinus thrombosis,or (ifthe abscess is longterm)
osteomyelitis.Mucoceles are the most commonchronic problems.104�106Respiratory
mucosatrapped between fracture segments or leftbehind during obliteration
procedures maycontinue to grow.This continued growthmay lead to the formation
ofmucoceles orpyoceles.The size ofthe growth determineshow much damage occurs to
adjacent boneand neurologic tissue.Frontal sinus imag-ing (CT or magnetic resonance
imaging)should be ordered to detect a postoperativemucocele or pyocele.Imaging
studiesshould be performed at 1,2,and 5 yearsafter surgery or whenever
symptomsappear.107Complications can occur as lateas up to 20 years
postoperatively,andpatients should be encouraged to have rou-tine yearly follow-
ups.59Pain and headache may be chronic andmay persist without an identifiable
cause.13Cosmetic deformities such as contourdeficits and irregularities stem from
sever-al causes.Bone loss at the time ofinjurymay not be noticed for
months.Osteomyelitis with subsequent d�bride-ment leaves voids in bone.Even ifthe
frac-tures are properly treated at the time ofinjury,remodeling may leave
irregularities.Anosmia�the loss ofthe sense ofsmell�and hyposmia are known
complica-tions ofNOE fractures and can occur in asmany as 38% ofpatients with high
centralmidface fractures.108In addition,23% ofpatients with high midface fractures
reporta decreased sense oftaste
(hypogeusia).108DacryocystorhinostomyDacryocystorhinostomy (DCR) is therepair ofthe
lacrimal drainage systemthrough the creation ofa new �ostomy�ortrack from the
lacrimal canaliculi to thenasal cavity.Techniques that have beendescribed include
open (external),endonasal,and soft tissue conjuctivorhi-nostomy.109�111Perhaps the
best-described techniqueis the open DCR.This procedure is per-formed through a 10
mm vertical incisionplaced 10 to 12 mm medial to the medialcanthus ofthe affected
eye.Blunt dissec-tion is then used to approach the lacrimalcrest.A periosteal
incision is followed bycareful dissection ofthe lacrimal sac awayfrom the bony
fossa,and an osteotomy isplaced posterior to the lacrimal crest.Thedeep surface
ofthe bone in this region islined with nasal mucosa,which shouldremain intact
during the osteotomy.Place-ment ofa lacrimal probe can facilitatevisualization
ofthe lacrimal sac.After thesac has been freed,it is incised on its medi-al
surface,and superior and inferiorreleasing incisions are made on the super-ficial
side ofthe sac (posterior flap).Thisprocedure is followed by a vertical
incisionofthe nasal mucosa and anterior releasingincisions (anterior flap).At this
pointCrawford tubes are used to intubate boththe superior and the inferior
canaliculi.When intubation is complete,the ends ofthe Crawford tubes are visible in
thelacrimal sac and can be inserted throughthe lacrimal osteotomy and
retrievedintranasally inferior to the middleturbinate.These ends are then cut
toextend to the nasal vestibule and aresutured in place to the lateral nasal
wall(Figure 25-16).39,110Closure is then begun with anastomo-sis ofthe lacrimal sac
and the nasalmucosa.The anterior flap ofthe nasalmucosa is closed to the posterior
flap ofthe lacrimal sac.Often this is technicallychallenging,and an alternative is
to suturethe anterior lacrimal sac flap to perios-teum to maintain the opening
between thelacrimal sac and the nasal mucosa.Careshould be taken to avoid suturing
theretained polymeric silicone tubing duringflap closure.The remainder ofthe
incisionis closed in two layers.The tubing is left inplace for 4 to 6 months,and
patientsshould use saline nasal sprays to preventcrusting ofthe tubes (Figure 25-
17).The endonasal approach is conceptu-ally the same procedure,except that
thedissection is performed from inside ofthenose with the aid ofendoscopic instru-
ments and a fiber-optic light,which areintroduced into the sac through
thecanaliculi.The nasal mucosa is incisedand reflected over an area transilluminat-
ed from above.The illuminated area is
504Part 4: Maxillofacial Traumamost commonly seen beneath the middleturbinate,which
may need to be displacedmedially so that appropriate exposure canbe obtained.The
transilluminating lightcan be seen most readily through thelacrimal bone posterior
to the frontalprocess ofthe maxilla.The frontal processcan be removed with a Freer
elevator orwith a 2 mm Kerrison rongeur.Thelacrimal sac is then gently lifted free
fromthe lacrimal bone with a Freer elevator.The thin lacrimal bone overlying the
sac isthen removed.An opening is then madeinto the lacrimal sac,and the
Crawfordtubing is inserted as before.Polymeric sil-icone tubes are left in place
for 1 month,and saline spray and lacrimal irrigationare recommended.111Correction
ofPost-traumatic Deformity Six months to 1 year after the initial surgi-cal
correction,secondary deformities ofthe frontal bone may be addressed.Con-tour
defects result from failure to fully ele-vate depressed fractures,from voids inbone
lost at the time ofthe trauma,andfrom infection.A multiplicity ofmaterialshas been
used to correct contour defects,including bone from the adjacent calvaria,ileum,or
rib;cartilage;titanium or stain-less steel;polymeric silicone,methyl-
methacrylate,hydroxylapatite granules,silver,a cobalt-chromium
alloy,polytef,polyethylene terephthalate fiber,nylon,polyethylene,and
aluminum.112,113Theprocedures for correcting such defectsinvolve one-stage indirect
prosthetic tech-niques,two-stage techniques,single-stagedirect techniques,or
computer-generatedsingle-stage techniques.114�116The one-stage indirect technique
requires that animpression be taken ofthe defect throughthe skin.The impression
negative is thenfilled with plaster to form a positive imageon which an onlay
prosthesis may be fab-ricated.Acrylic,polyethylene,tantalum,titanium,and cobalt-
chromium prosthe-ses may be fabricated with this technique.A full-thickness flap is
then reflected,andthe prosthesis is secured.The single-stage direct
techniquerequires that a full-thickness flap bereflected beyond the margins ofthe
defect.FIGURE25-16A,Incision oflacrimal sac.B,Osteotomy,made with a round
bur,through which the polymeric silicone tubesare placed.C,View ofthe polymeric
sili-cone tubes exiting through the nasalmucosa into the nose.D,The lacrimal
sacflap is shown being held in the forceps overthe polymeric silicone tubing that
exits intothe nasal cavity.ABCD
Management ofFrontal Sinus and Naso-orbitoethmoid Complex Fractures505Onlay
cartilage or bone grafts then may besecured ifan autograft is desired.Other-wise,an
acrylic resin may be used.Thebone is moistened,and acrylic is mixedand placed on a
glass or polytefslab androlled to a uniform thickness.The acrylicis placed directly
over the bone and cov-ered with a sheet ofseparating foil.Thefull-thickness flap is
replaced to ensureproper contour and then is again reflected.A copious amount
ofsaline is used to irri-gate the area so that the material does notcause thermal
damage to the skull.Theflap is then replaced and sutured.Improvements in computer
designand technology now enable the fabrica-tion ofprostheses for one-stage recon-
structions.The patient undergoes a three-dimensional CT before the
operativeprocedure is performed.114A computer-assisted diagnosis/computer-
assistedmanufacturing (CAD/CAM) protocol isthen used to create a model ofthe
frontalbone and defect.A prosthesis may be cre-ated from polymeric
silicone,acrylic,acobalt-chromium alloy,or hydroxylap-atite-coated metals.During
the operativeprocedure,the prosthesis is inserted asdescribed
above.AcknowledgmentThe authors thank Flo Witte,MA,ELS,forher expert editorial
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CHAPTER 26Gunshot InjuriesJon D.Holmes,DMD,MDThe greater the ignorance,the greater
the dogmatism.�William OslerManagement ofgunshot injuries to the faceled in many
ways to the development ofmodern maxillofacial surgery,and itremains a cornerstone
ofthe specialty oforal and maxillofacial surgery.There is anaura that surrounds the
management ofthese complex wounds that affects residentsas well as experienced
clinicians.The mys-tique that developed in the earliest accountsofmanagement
ofgunshot wounds(GSWs) persists with the passing along ofmyths and dogma to
subsequent genera-tions ofresidents.Readers are encouragedto use the information in
this chapter as aguide,to combine it with their own experi-ence,and hopefully to
continue the evolu-tion in treatment ofthese unique wounds.HistoryThe introduction
ofChinese gunpowderto Europe around the thirteenth centurywas quickly followed by
the developmentofprojectile weapons based on its explo-sive properties.The first
recorded use ofacannon was by Edward III against theScots in 1327,and small arms
carried byone or two soldiers began appearing in thefourteenth century.1Early
weapons thatused modified arrows were replaced withmore efficient stone
and,ultimately,metallic projectiles.Improvements in pro-jectiles and firearms led
to increasingnumbers ofmore devastating wounds.Surgeons accustomed to dealing with
avariety ofwounds from blunt,bladed,andpointed weapons were faced with blast
andprojectile injuries ofa completely differentnature.Contamination and devitalized
tis-sues led to increasing numbers ofinfec-tions,which surgeons ofthe day
incorrect-ly attributed to the gunpowder itself,andto the anticipation of�laudable
pus.�Sub-sequent advances in surgical knowledgewent on to closely parallel the
evolution offirearms.Knowledge gained on the battle-field by famed military
surgeons such asAmbroise Par� (1510�1590) elevated theart ofsurgery to a learned
profession.1Unfortunately,the battlefield has movedto the urban areas with
increasing num-bers ofcivilian gunshot injuries.DemographicsGSWs are second only to
motor vehicleaccidents as a source ofinjury and death,and rank as the eighth
leading cause ofdeath in the United States.2Recently thenumber offirearm-related
deaths andinjuries in children and adolescents hasdeclined.3According to the
National Cen-ter for Injury Prevention and Control,firearm-related deaths have
shown a con-tinual decline from approximately 15 per100,000 in 1993 to
approximately 11 per100,000 in 1998.4Because ofpast difficul-ties with
surveillance,however,mostreports likely underestimate unintentionalfirearm-related
deaths and injuries over-all.5,6Interestingly,Patton and Woodwardreported that
although GSW admissionsdecreased at the Henry Ford Hospital inDetroit by 45%,the
number ofpatientswho required operations actuallyincreased by 17%.The number
ofgunshotvictims dead on arrival remained steady.Apossible explanation is that an
increasednumber ofpatients are discharged fromthe emergency department after
signifi-cant injury requiring admission has beenruled out;these patients are
therefore notcounted as admissions.7The demographics ofgunshot injuriesare
telling.Most victims are young males(< 38 yr).Suicides and assaults far out-number
unintentional and accidentalshootings.Firearms are implicated in 58%ofmale suicides
and 37% offemale sui-cides.Importantly,the number ofpatientssurviving and requiring
treatment ofgun-shot injuries outnumber firearm fatalitiesby approximately
5:1.8,9Currently there are an estimated135,000 GSWs treated annually in the Unit-ed
States.The incidence offirearm-relatedinjury and death in the United Statesexceeds
that ofother developed countries.10Although there appears to be a
relationshipbetween the rate ofhousehold firearm own-ership and the homicide
rate,most agreethat other social factors are required toexplain the number
offirearm injuries in
510Part 4: Maxillofacial Traumathe United States in comparison with otherdeveloped
countries.9Indeed,in countriesin which firearm ownership is required formilitia
duty,firearm injuries are lower on aper-capita basis than in the United States.The
majority ofcivilian firearm injuries aresustained from handguns (86%),followedby
shotguns (8%) and rifles (5%).Approxi-mately 12 to 14% ofunintentional andassault
gunshot injuries involve the headand neck,whereas 51% ofself-inflicted gun-shot
injuries involve the head and neck.4Clark and colleagues reported on
theirexperience at the Maryland Shock TraumaCenter and found that of178 GSWs to
theface,40% involved the frontal bone and cra-nium,9% involved the orbits,14%
involvedthe lower midface (maxilla),13% involvedthe mandible,and 24% involved
multiplesites.Shotgun injuries more commonlyinvolved the mandible and
midface.11Demetriades and colleagues reported on theextensive experience ofthe
University ofCalifornia at Los Angeles.Of4,139 patientsadmitted with gunshot
injuries over a 4-year period,6% (247) had GSWs to theface.Thirty-eight percent
ofthese had iso-lated wounds to the face,whereas theremaining 62% had associated
injuries toother body areas.They reported that themandible was the most commonly
involvedfacial bone (54 cases),followed by the max-illa and zygoma (21 cases
each).The orbitsand nasal bones were involved in 18 and
15cases,respectively.Thirty-six patients diedfollowing admission.All ofthe deaths
weresecondary to injuries to the chest,abdomen,or brain.There were no deaths
associatedwith isolated facial injuries.12Aside from the tragedy offirearm-related
injuries and the emotional toll suchinjuries take on victims,their
families,andcommunities,the financial burden to soci-ety offirearm-related injuries
is significant.This is especially true with regard to thelong-term rehabilitation
and multiplereconstructive surgeries that many victimsoffacial GSWs require.Cook
and col-leagues reported approximately 115,000firearm-related injuries in the
UnitedStates yearly,with an annual cost oftreat-ing firearm injuries
ofapproximately $2.3billion;ofthis,taxpayers pay $1.1 billion.Although this cost
represents only one-quarter of1% ofthe US health care budgetof$950 billion,it is
significant consideringthat the group most affected typicallyinvolves younger
healthier patients thatusually require very little medical
care.13BallisticsBallisticsis the science ofprojectile motion.A prerequisite to
understanding the injuriescaused by various firearms is knowledge ofthe language
ofballistics.The potentialproblems ofa wound caused by a projectilecan be better
anticipated ifone has someknowledge ofthe weapon and projectiletype that caused the
wound.For example,ifthe surgeon is aware that a patient suffered ahigh-energy wound
caused by a high-power,high-velocity cartridge,he can betterappreciate the
potential for extensive areasofdevitalized tissue that may declare later.In
addition,an understanding offirearmnomenclature allows the surgeon some abil-ity to
predict the types ofweapons that arecommonly involved in various types ofcivilian
gunshot injuries.For this reason,theclinician dealing with gunshot injuriesshould
be conversant in the rudiments ofballistics,types offirearms,and
projectiles.Ballistic science seeks to explain thebehavior ofthe projectile and is
typicallydivided into three stages:1.Internal (or interior) ballisticsdescribesthe
forces that apply to a projectile fromthe time the propellant is ignited to thetime
the projectile leaves the barrel.Animportant consideration is barrellength.In
general,longer barrels (rifles)allow the force ofthe propellant to acton the
projectile longer and generatehigher velocities than do shorter-bar-reled
weapons.In addition,a longerbarrel serves to stabilize the bullet overlonger
distances.2.External ballisticsrefers to forces thatact on the bullet in flight.The
primaryfactors that govern external ballisticsare the weight and shape ofthe
bullet.3.Terminal ballisticsis the study ofbulletbehavior once it impacts the
target andis primarily concerned with how muchenergy is transferred to the target
mate-rial and the resultant damage.The sci-ence ofterminal ballistics is
mostimportant to the surgeon and is themost common source ofcontroversywhen
discussing ballistic wounding.Attempts to reproduce the interactionofbullets with
living tissue by usingvarious target media such as ballistic gelhave led to many
myths surroundingwounding and the �stopping power�ofvarious bullets and
weapons.Similarly,surgeons have passed on many myths oftheir own regarding GSWs and
thefirearms that cause them.Energy and Wounding PowerTraditionally,kinetic energy
has been usedas the basis to explain wounds caused by agunshot.Simple physics can
be applied tothe projectile using the following formula:KE= mv2where KEis kinetic
energy,mis the massofthe projectile,and vis the velocity oftheprojectile.Wounding
power is typically related tothe amount ofkinetic energy transferredto the
target:P= m(Vimpact � Vexit)2where Pis power,mis mass ofthe projec-tile,and Vis
velocity.Based on these formulas,the velocityofa projectile has traditionally been
con-sidered far more important than its mass inwounding power.Indeed,often guns
areclassified as low velocity (< 350 m/s),medium velocity (350�600 m/s),and
highvelocity (> 600 m/s).Considering a typi-cally sized projectile,a velocity
ofapproxi-
Gunshot Injuries511mately 50 m/s is required to penetrate theskin,and a velocity
ofaround 65 m/s willfracture bone.14See Table 26-1 for a com-parison ofcommonly
encountered pistoland rifle cartridges.In general,there is an inverse relation-ship
between a bullet�s diameter (caliber)and velocity.Unfortunately,the realities
ofwounding are not as clear cut,and theemphasis on velocity and kinetic energy
ofthe weapon as it relates to treatmentstrategies is excessive.15In an
excellentreview,Fackler debunks many ofthe com-monly held beliefs ofballistic
injury,including the idolatry ofvelocity,the exag-geration ofthe effects
oftemporary cavita-tion and pressure,bullet tumbling,theexaggerated role ofkinetic
energy transfer,and,most importantly,the emphasis onextensive wound
d�bridement.16The het-erogeneity ofthe human body,which iscomposed oftissues
ofvarying densitiesand elasticities,does not allow formulas toexplain all ofthe
nuances ofwoundingcaused by projectiles ofdifferent velocities,sizes,and
weights.Practically,there is abalance between velocity,projectile mass,and
projectile size that governs theamount ofenergy transferred to the targetand
resultant tissue wounding.These fac-tors govern the four components ofpro-jectile
wounding:penetration,permanentcavity formation,temporary cavity forma-tion,and
fragmentation.Penetration allows the projectile totransmit kinetic energy and
destroy tissue.A bullet must penetrate to a sufficientdepth to cause
damage.Likewise,a projec-tile that over-penetrates or passes com-pletely through
nonvital tissue may resultin little damage.The permanent cavity describes thespace
that results from direct tissue dis-ruption and destruction.It is a function ofthe
penetration and size ofthe projectile.It is generally considered to be the
mostimportant factor in the wounding andstopping power ofa particular cartridgeand
bullet.The temporary cavity is produced asthe projectile travels through the
targettissue.Transfer ofkinetic energy results ina stretching ofelastic
tissues.Althoughthey may remain intact,some ofthese tis-sues may be irrecoverably
damaged.Arteries may suffer pseudoaneurysm for-mation and rupture,and nerves may
failto recover function.Fragmentation,which may not be pre-sent in a GSW,refers to
the projectile (cer-tain projectiles are designed to fragment;see below) or
secondary fragments such asclothing or bone that develop from beingstruck by the
projectile.Despite claims by many bullet manu-facturers,fragmentation ofthe
projectiledoes not reliably occur in most handgunwounds.Bullets specifically
designed asfragmentation rounds typically suffer fromlow-penetration ability.High-
velocity riflerounds are known,however,for their dev-astating fragmentation.The
effects ofthe temporary cavity onwounding are often exaggerated in ballis-tic
literature.Because most tissue has anelastic nature and ability to recover
fromstretching (certain tissues such as brain areexceptions),damage from temporary
cav-itation is not as important as manyexpound.The massive zones ofnecrotictissue
that were felt to develop from tem-porary cavitation do not exist in reality.The
most important factors in projectilewounding remain penetration and the sizeofthe
permanent cavity.A very small pro-jectile traveling at high velocity striking
anarea oflow density (eg,fat) may impart farless damage than a larger projectile
travel-ing at a lower velocity and striking an areaofhigh density (eg,bone).The
realities ofstopping power further call into questionmany ofthe claims promulgated
throughballistic literature as well as surgical prac-tices.In reality,the power
transferred tothe victim is the same as what the recoilimparts on the
shooter.Again,simplephysics explains that the impact ofa 9 mmpistol round (see
below) is the same as thatcreated by a 0.45 kg weight dropped froma height of1.82 m
or ofa 4.53 kg weightdropped from a height of1.82 cm.In morepractical terms,the
amount ofenergydelivered to a body by a bullet is approxi-mately equivalent to that
transmittedwhen one is hit with a baseball.17Table 26-1 Comparison ofApproximate
Cartridge Velocities and Muzzle Energy* Bullet WeightVelocityMuzzle
EnergyCartridge(grains)�(ft./s)(ft./lb.).22 LR291,225140.32 auto71900129.380 auto
(9 mm short)95955190.38 special145680170.357 magnum1101,565 5359 mm1241,100345.45
auto230790370.44 magnum2401,420741.223 (NATO 5.56 �45)553,1001,280.308 (NATO 7.62
�51)1103,0002,650.300 magnum1802,9003,50020-gauge shotgun5471,1851,40012-gauge
shotgun8201,2502,600Adapted from Federal Ammunition Company high power ammunition
handbook.Minneapolis;1983.*Velocities and muzzle energy can vary within different
cartridges depending on the weight ofbullet,powder type,and othervariables such as
barrel length.�1 oz.= 437.5 grains.
512Part 4: Maxillofacial TraumaIt is important to understand that thescience
ofwounding power is more thansimple physics;it is a complex interplay ofprojectile
and target tissue characteristicsthat makes each wound unique.For this rea-
son,categorization ofwounds based onprojectile characteristics such as
velocity,although useful,should not promote dog-matic management schemes but
insteadshould serve as guides.Surgeons should bewary ofstrict categorization
schemes andtreatment algorithms based only on velocityor another bullet
characteristic and shouldbear in mind Lindsey�s statement,�I willkeep treating the
wound,not the weapon.�15Firearm TerminologyAs with ballistics,some knowledge
offirearms is necessary for surgeons manag-ing GSWs.It is a prerequisite for commu-
nicating with law enforcement officers andother clinicians.Firearms are generally
classified ashandguns,rifles,and shotguns.Handgunsare also referred to as pistols
and revolvers,depending on their mechanical actions.With few exceptions,most are
low ormedium velocity,typically < 600 m/s,andusually cause tissue damage along the
bul-let tract only.Rifles range from low to highvelocities.Shotguns typically are
smooth-bore weapons that fire shells filled withlead shot ofvarious sizes.Some
shotgunsmay be modified with rifled barrels to fireshells containing a solid lead
projectilereferred to as a slug.Although they are oflow velocity,close-range
shotgun injuriesare devastating,especially with larger leadshot such as buckshot
(see below).Rifles and handguns are classified bycaliber.The caliber ofa weapon is
thediameter ofthe muzzle bore,which is thesame as the diameter ofthe projectile
(bul-let).Cartridgeor round refers to the casecontaining the ignition system
(primer),the propellant,and the projectile (bullet).Measurements for American
firearms aretypically in inches.For example,the .45caliber pistol bullet is 0.45
in.(1.14 cm) indiameter.Firearms ofEuropean origin,such as the 9 mm,have
classically used themetric system.The American militaryround for the M-16 (military
version ofthe AR-15) is usually the 223,which is0.223 in.(0.57 cm) in
diameter,whereasthe Soviet AK-47 fires a 30-caliber projec-tile,or 7.62 �39
(39refers to the length ofthe case containing the propellant in mil-limeters;Figure
26-1).Shotguns were originally designed tobe used on small fast-moving game
andtypically fired small pellets that dispersedin flight to form a pattern.Typical
muzzlevelocities range from 335 to 427 m/s.Theyare usually referred to by
gauge,which is anEnglish measurement that describes howmany lead balls equaling 1
lb.(0.45 kg)would fit into a particular diameter ofthebarrel.For example,it would
take 12 leadballs equal in diameter to the internaldiameter ofa 12-gauge shotgun
barrel tomake 1 lb.A 12-gauge shotgun has aninternal barrel diameter of1.85
cm,where-as a 28-gauge shotgun has an internal bar-rel diameter of1.41 cm.It is
clear that thehigher the gauge,the smaller the diameterofthe barrel (Figure 26-
2A).There aresome exceptions to this classificationscheme.For example,a 410 shotgun
has aFIGURE26-1A,Representa-tive rifle cartridges.From leftto right:.300 Winchester
mag-num,30-06,.308 (7.62 �51NATO),.223 (5.56 �45NATO),7.39 (AK-47 round),and .17
rimfire.B,Representa-tive pistol cartridges.From leftto right:.44
magnum,.357magnum,.38 special,.45 auto,.40 auto,9 mm auto,.380 auto(9 mm short),.22
rimfire.BA
Gunshot Injuries513barrel whose internal diameter is 0.410 in.(1.04 cm).In
general,the lower the gauge,the more powder and shot the shell can contain.Shot is
also classified by size.Com-monly encountered shot sizes range from8 shot (0.23
cm),with approximately 500pellets in a 12-gauge shell,to number 00buckshot (0.83
cm),with 9 to 15 pellets ina 12-gauge shell.Shells come in differentlengths within
the same gauge as well.Forexample,a 12-gauge shell may be a 23/4in.(6.99 cm) or 3
in.(7.62 cm) shell.Longershells hold a larger charge ofpowder andshot,which can be
used for larger game orgame at further distances.As a generalrule,longer-barreled
shotguns and thosewith a full choke (a constriction ofthe endofthe barrel) keep the
pellets in a tighterpattern over longer distances.Finally,some shotguns may be
modified withrifled barrels to fire shells containing asolid lead projectile
referred to as a slug.Shot is usually selected based on the size ofgame.Buckshot
refers to larger pelletsmeant for large game or human targets;it isparticularly
devastating because its impactis similar to multiple low- to medium-velocity
handgun wounds,depending onthe range.18It is also important to note thedifferent
makeup ofa shotgun shell (seeFigure 26-2A).The pellets are typically sep-arated
from the propellant by waddingthat helps to contain and transfer thepower ofthe
charge to the pellets.Thispartition can be made offelt or plastic andmay be found
embedded in close-rangewounds (Figure 26-2B).Most handguns and rifles have
barrelswith internal grooves referred to as riflingthat impart a spin to the
bullet.This keepsthe projectile stable in flight over longerdistances.In early
firearms that wereloaded from the muzzle (muzzleloaders),the tight fit between the
bullet and the bar-rel that resulted from rifling significantlyslowed loading.For
this reason,most earlymilitary weapons were smoothbore.Sacri-fices in long-range
accuracy were a trade-offfor rapid rates offire.This obstacle wasovercome in 1847
by Captain Mini�,whodeveloped a projectile with a hollow coni-cal base that loaded
easily but expandedfor a tight fit when the propellant enlargedbehind it (Figure
26-3).Ultimately,breech-loading weapons,in which a self-contained round enclosing
the ignitionsystem (primer),propellant,and projectilewas loaded from the beginning
ofthe bar-rel instead ofthe end,overcame these dif-ficulties.The development
ofrifling,how-ever,allowed high-velocity projectiles thatwould remain stable in
flight over longdistances.Eventually,all projectilesbecome unstable in flight
because the cen-ter ofgravity lies well behind the center ofFIGURE26-
2A,Representative shotgun shells.From left to right:10 gauge; 3 in.12 gauge;
23/4in.12 gauge; 20 gauge �Demonstrator�shell withshot,wadding,and powder
visible; .410 gauge.B,Plastic and felt shotgun wadding.ABFIGURE26-3Left,Earlyround
projectile and Mini�ball with expanding base.Right,Modern full-jacketedand soft
point rounds with�boat tail�to improve flightcharacteristics.
514Part 4: Maxillofacial Traumaresistance (the bullet tip) causing them totake on
various motions during flight.Oscillation around the long axis ofthebullet is
referred to as yaw.Rifling seeks tostabilize yaw but imparts its own
motion,referred to as precession(circular yawing),around the center
ofgravity,creating adecreasing spiral and nutation,which is arotational movement in
small circles.19These motions occur during flightthrough air.Bullets may be
modified in anattempt to decrease these motions inflight;an example is a �boat
tail�bullet,intended to be stable over longer distances.Upon encountering a denser
substancesuch as tissue,the projectile immediatelystarts tumbling.Increased
tumbling caus-es more tissue wounding because it pre-sents a larger surface
area.Bullets haveundergone a variety ofmodifications in anattempt to control these
motions andincrease wounding and stopping power.The simplest and earliest
projectilewas a stone or lead ball (see Figure 26-3).Over time the projectile
evolved to theconical-shaped Mini� ball.The lead coni-cal bullet remains in
use.Modifications aremade based on intended use.In general,military rounds are
restricted by theHague convention (1899) to the full-metaljacket.Fragmentation
rounds have beenoutlawed,although some countries con-tinue to use flechette rounds
(designed tofire small metal spikes or fragments).Sim-ple lead bullets referred to
as wadcuttersare inexpensive and often used as targetrounds.Jacketed bullets with
exposed leadtips (soft points) are designed to expandon impact for maximum tissue
destruc-tion (maximum permanent cavity) andare typically designed for hunting.A
vari-ety ofmodifications have been made tohandgun bullets in an attempt to make
upfor their lack ofvelocity and to increasewounding (Figure 26-4).Because
oftheirlow velocity,handgun bullets have diffi-culty expanding reliably in
tissue.Attempts to overcome this have centeredon the creation ofbullets with
variousopen ends,so-called hollow points (seeFigure 26-4).Some ofthese are
partiallycovered with a metal jacket in attempt tocontrol expansion.As noted
earlier,despite manufacturers�claims to the con-trary,reliable expansion is
difficult toobtain in low-velocity rounds.Some man-ufacturers have created +P
ammunition,which contains different gunpowder toobtain a higher velocity.Also,some
bulletsare designed to explode on impact byincorporating an explosive into a
hollowcavity in the bullet (devastator rounds).The ignition ofmost cartridges
isaccomplished by a firing pin striking aprimer.Some cartridges use a primer
builtinto the case and are referred to as rimfirebecause the firing pin strikes the
edge ofthecartridge rim to discharge the propellant.Mention should be made ofother
pro-jectiles that have been associated withinjury.Modern airguns can achieve
veloci-ties sufficient to cause tissue damage.Theproliferation ofpaint-ball guns
has led toan increase in the number ofophthalmo-logic injuries.20Finally,unorthodox
bulletssuch as wooden,rubber,and �bean bag�projectiles are being used increasingly
incrowd-control situations.Although meantto be nonlethal methods ofdeterrence,these
rounds can cause significant tissuedamage and even death.They are frequent-ly
associated with facial fractures.21Classification SchemesClassification oftraumatic
injuries ishelpful in guiding treatment and,moreimportantly,tracking outcomes for
vari-ous treatment modalities.A number oftrauma scoring systems and classifica-
tions for various injuries have beendeveloped and validated.Similarly,attempts have
been made to classifyGSWs to assist the surgeon in selectingappropriate management
strategies.Many ofthese classification schemeswere developed on the
battlefield.Dis-similarities between civilian and militarygunshot injuries,such as
ammunition,wounding potential ofmilitary weapons,and treatment objectives,make
these clas-sification schemes oflittle use in the urbantrauma center,which most
commonlydeals with low- to medium-velocity hand-gun injuries.22,23Trauma systems
have attempted toincorporate gunshot injuries into existingclassification and
trauma scoring systems.Unfortunately,current schemes have notproven beneficial in
guiding treatment andjudging outcomes to develop idealapproaches.Attempts to
distinguish GSWsas low or high velocity have suffered fromthe shortcomings noted
above.In addi-tion,velocity is less critical than bullettype,mass,distance to
target,and specificvital organs involved because most civilianFIGURE26-4Full-
jacketedbullet compared with varioushollow-point rounds designedto aid the
expansion oflower-velocity bullets.
Gunshot Injuries515injuries are caused by low- or medium-velocity weapons.One ofthe
earliest and simplest classi-fication schemes classifies GSWs as non-penetrating
(grazing or blast wound),penetrating (bullet does not exit),perfo-rating (in and
out),and avulsive.TheInternational Committee ofthe Red Crossintroduced the armed
conflict classifica-tion system to improve information gath-ering and communication
regarding warwounds.Because ofthe diversity ofbattle-field weaponry,by necessity
the systemignores weapon type and instead concen-trates on wound severity in terms
oftissuedamage and anatomic structuresinvolved.22,23 Gugala and Lindsey suggest-ed
a civilian gunshot injury classificationscheme.It takes into account energy (highor
low),involvement ofvital structures(neural and vascular),wound type (non-
penetrating,penetrating,perforating),fracture (intra-articular and extra-articu-
lar),and contamination.Primarily used inorthopedics,its usefulness in
gunshotinjuries to the head and neck is limited.23Shotgun WoundsBecause oftheir
unique ballistic profile,shotgun injuries are often classified basedon the distance
to the target.Shotgun pel-lets have significant aerodynamic resis-tance and give up
substantial amounts ofkinetic energy during flight.In type I shot-gun injuries (< 5
m),the pellets strike thetarget as a single mass,resulting in massivekinetic energy
transfer,tissue avulsion,anda high mortality rate (85�90%).Patientsthat survive
suicide attempts with shotgunstypically survive because,in an attempt toreach the
trigger with the muzzle under thechin or in the mouth,the head is hyperex-
tended,which causes the pellets to createdevastating injuries to the face but
avoidthe cranium.Fragments ofpaper or plasticwadding may be found in the
wound.TypeII injuries (5�12 m) usually result in muchless tissue destruction.At
these distancesthere is significant dispersal ofthe pelletsand loss
ofenergy.Penetration may occurthrough deep fascia,but fractures are rare.Ocular
injuries can occur as well asembolization oflead pellets,but mortalityis less
(15�20%).At distances > 12 m (typeIII),usually only the skin is penetrated
andmortality is rare (0�5%).24,25Because spe-cific information on shooting
distances isnot often available to the clinician,a systemwas suggested that
evaluated the maximumdistance ofpellet scatter.Type I injurieshad > 25 cm ofpellet
scatter.Type IIinjuries had 10 to 25 cm ofscatter.Type IIIinjuries had < 10 cm
ofscatter and wouldroughly correspond to a type I injury in theclassification
ofSherman and Parrish.24This classification scheme was developedand applied to
abdominal shotgun woundsin an attempt to guide therapy.26Again,thedifficulty lies
in applying this scheme,orany scheme,universally to GSWs involvingdifferent
anatomic sites and weapon types.It should be noted that rifle and shot-gun
injuries,although rare in assaults,arefrequently encountered in attempted sui-cide
patients.A characteristic wound pro-file is seen because ofthe head positionassumed
when the patient places the barrelofthe weapon in the mouth or under thechin and
subsequently hyperextends toreach the trigger.Characteristic powderburns are seen
at the entrance wound (Fig-ure 26-5).The face frequently takes the fulleffect ofthe
blast,whereas lethal intracra-nial involvement is avoided.27Ifa high-energy weapon
such as a shotgun or rifle isused,the injury can be devastating withsignificant
tissue loss.Although classification schemes canserve useful purposes in research as
well asclinical practice,strict adherence to treat-ment algorithms based on wound
classifi-cation can lead to mismanagement.Importantly,information regarding
typesoffirearm and other details ofthe shoot-ing are frequently not available,and
clini-cal assessment ofthe wound remains themost reliable method for
determiningtreatment approaches.ManagementGeneral PrinciplesOn admission victims
ofgunshot injuriesare best managed by standard advancedtrauma life support (ATLS)
protocols.Even seemingly innocuous woundsdeserve attention,given the erratic
natureofthe wounds.Specific attention must begiven to the possibility
ofmultipleinjuries;it is imperative to thoroughlyinspect the patient for multiple
entranceand exit wounds.Visually disturbing butnonlife-threatening facial gunshot
injuriescan distract medical personnel from othermore subtle lethal injuries such
as a pene-trating thoracic wound that enteredthrough the back.Ophthalmologic
andneurosurgical consultations are obtainedwhen indicated.Approximately 17%
ofpatients with a GSW to the face have asso-ciated brain injuries,and 8% have
associ-ated C-spine injuries.12,28Eye injuries arepresent in approximately 13%
(Figure 26-6).28Certain considerations for gunshotinjuries should be
emphasized.AirwayLoss ofthe airway is the single most likelycause ofdeath in an
isolated GSW to theface.When confronted with a patient witha facial GSW,surgeons
should have a lowFIGURE26-5Submental entrance wound withpowder burns characteristic
ofa suicide attemptby placing a gun under the chin.
516Part 4: Maxillofacial Traumathreshold for establishing a definitive air-way
through intubation or a surgical air-way ifintubation is not possible.Intuba-tion
either in the field or the emergencydepartment is required in 25 to 36%
ofpatients.Wounds involving the mandiblehave the highest rate
ofintubation(37�53%),followed by those ofthe mid-face (18�36%).28�31Excluding
patients thatrequire airway control for associated braininjuries,Demetriades and
colleaguesfound that 17.4% ofpatients requiredurgent airway control for facial
injuries.12Gunshot injuries to the neck may result intracheal damage and require an
emergentsurgical airway (cricothyroidotomy).Intu-bation with fiber-optic assistance
is possi-ble,but paralytics should be avoidedowing to the risk ofexpanding
hematomasor massive edema.Cricothyroidotomy oran awake tracheostomy is more
appropri-ate in this setting.The need to convert anintubated airway to a
tracheostomydepends on several factors.Tracheostomycan make repair ofinjuries
involving themandible and midface easier.Patients whowill require multiple return
trips to theoperating room for wound d�bridementsand �second looks�will benefit
from thedecreased risk ofmultiple intubations.Delayed swelling can be anticipated
withtrauma to the upper aerodigestive tractincluding the tongue (Figure 26-
7A);thismay influence the decision to proceedwith tracheostomy.Associated
trachealinjuries are another indication for tra-cheostomy (Figure 26-
7B).Lastly,multiplesystem injuries with anticipated long-termventilation is an
indication for early tra-cheostomy.Most experienced surgeonswould agree that it is
rare to regret havingperformed a tracheostomy,but tragic toregret not performing
one.Hemorrhage ControlLife-threatening hemorrhage is unusual incivilian gunshot
injuries.Low-velocityhandgun injuries typically do not involvethe great
vessels.Demetriades and col-leagues in Los Angeles reported only 7.5%ofpatients
with isolated gunshot wounds tothe face to be in shock upon admission(systolic
blood pressure < 90 mm Hg).Intheir report 70 patients (28.3% ofthe total)required
angiography,and 10 oftheserequired embolization.12Overall the litera-ture reports
angiography in 17 to 63% ofpatients with a GSW to the face,with posi-tive findings
in 15 to 51%.Indications forangiography include expanding hematomaand bleeding that
persists despite localmeasures.29,32,33The most commonlyinvolved vessels in these
cases were themaxillary and facial arteries.Gunshotinjuries associated with high-
velocityweapons or fractures,however,can result insignificant blood loss.Initial
attempts tocontrol hemorrhage in the emergencydepartment center on direct pressure
andpacking.Blind clamping should be avoidedbecause ofthe attendant risk ofdamage
toother structures (Figure 26-8).Standardmethods for epistaxis control such as
Foleycatheters or specially designed ballooncatheters will control most midface
bleed-FIGURE26-6Perforated globe with shotgunpellet.FIGURE26-7A,Massive late tongue
edema.B,Trachealinjury from a gunshot wound.(Courtesy ofEric
J.Dierks,MD,Portland,OR)ABFIGURE26-8Blind clamping in the emergencydepartment
management ofa facial gunshotwound.
Gunshot Injuries517ing (Figure 26-9).In cases ofmandible frac-tures,temporary
reduction ofthe fracturemay be required.Penetrating injuries canrequire that the
surgeon make difficultchoices.Injuries at the skull base may ben-efit from
angiography and embolization(see �Penetrating Neck
Injuries,�below).Unfortunately,the time necessary to mobi-lize the angiography
suite often makes thisan impossible choice for the unstable trau-ma patient in the
middle ofthe night.Forthis reason,control oflife-threateninghemorrhage is typically
best performed inthe operating room.Ligation ofmultiplevessels is required.�Tying
off�the carotid isusually ineffectual and dangerous;anattempt should be made to
control specificvessels.Lacerations ofthe internal jugularartery are best
controlled with ligation orrepair (Figure 26-10).Packing and reduc-tion offractures
should be performed tocontrol bleeding from the midface ifpossible.There is
possibility oflatepseudoaneurysm formation and delayedhemorrhage,and selective
angiographyshould be performed as indicated.Addi-tionally,the possibility ofbullet
or frag-ment embolization should be considered.Penetrating Neck InjuriesGunshot
wounds involving the face may beassociated with an entrance or exit woundin the
neck,which is divided into threezones originally described by Monson andcolleagues
from Cook County Hospital34:�Zone I is most commonly defined asthe area from the
clavicles to thecricoid cartilage.It contains the inferi-or aspect ofthe trachea
and esophagusalong with the major vessels ofthethoracic inlet:the common
carotidarteries,thyrocervical trunk,internaljugular veins,brachiocephalic
trunk,subclavian arteries and veins,thoracicduct,thyroid gland,and spinal cord.Risk
ofinjury to the great vessels iscommon in this area,and,conse-quently,injuries to
zone I carry a highmortality rate (approximately 12%).Some authors place the
junction ofzones I and II at the cricoid cartilage,whereas others define it as
being at thetop ofthe clavicles.�Zone II represents the area from thecricoid
cartilage to the angle ofthemandible.It contains the commoncarotid
arteries,internal and externalcarotid arteries,internal
jugularveins,larynx,hypopharynx,and cra-FIGURE26-9Nasal packing with anterior
andposterior balloon catheters.FIGURE26-10A,Gunshot wound to zone II associated
with a mandible fracture.B,Plain film demon-strating the bullet in zone
II.C,Computed tomographic angiography failing to demonstrate tamponadedlaceration
in internal jugular vein but showing subcutaneous air and edema ofneck
injury.D,Laceratedinternal jugular vein (clamped) found on neck exploration.ACBD
518Part 4: Maxillofacial Traumanial nerves X,XI,and XII.It is thelargest area and
therefore the mostcommonly involved zone in penetrat-ing neck trauma.�Zone III
spans the region from theskull base to the angle ofthe mandible.It contains the
carotid arteries,theinternal jugular veins,and the pharynxalong with multiple
cranial nervesexiting the skull base.It should beappreciated that gunshot wounds
thatinvolve mandibular fractures areaccompanied by injuries to zone III.Van As and
colleagues reported on 116patients shot in the neck in South Africa.Ofthese,70
suffered a direct hit to theneck;in 46 patients the bullet traversed theface or
chest first.Ofthe 116 patients 85suffered some vascular injury,althoughmost were
minor branches,61 had someinjury to the airway,and 32 had an injuryto the pharynx
or esophagus.35Manypatients had more than one injury.Man-agement strategies for
penetrating neckinjuries are typically based on the zone(s)involved.36,37Gunshot
wounds to the headand neck frequently involve projectilesthat traverse or involve
more than onezone.For this reason,surgeons may haveto modify management plans based
on thesituation at hand.Although a completediscussion ofpenetrating neck trauma
isbeyond the scope ofthis chapter,generalprinciples should be understood by sur-
geons managing facial gunshot injuries.Initially the patient�s stability froman
airway and hemodynamic statusguides the decision-making for pene-trating neck
injuries (Figure 26-11).Inthe stable patient,a complete examina-tion is part ofthe
secondary survey ofATLS.Signs oftracheal injury,such assubcutaneous
emphysema,stridor,hoarseness,dysphonia,or hemoptysisrequire urgent
intervention.Hard signsofvascular injury,such as expandinghematoma,and pulse or
neurologicdeficit,also signal the need for urgentmanagement.In the absence
ofurgentmanagement needs,the surgeon mustrule out occult injuries based on thezones
involved.Injuries to zone I can be associatedwith significant bleeding because
ofthelarge vessels in this area.This is especiallytrue with regard to injuries
caused by high-energy weapons.Although serving to pro-tect the vessels,the
clavicles are a hindranceto the application ofdirect pressure to thearea and to
rapid surgical exposure.In thestable patient most surgeons advocate rou-tine
angiography and an evaluation oftheesophagus via rigid esophagoscopy or abarium
swallow.The choice between bari-um swallow and esophagoscopy variesaccording to the
surgeon�s preference asboth are reasonably accurate at diagnosinginjury (90% and
86%,respectively).Inaddition,there is some controversy regard-ing the appropriate
contrast media.Although meglumine diatrizoate causesless inflammatory response than
does bar-ium when it extravasates into tissues owingto an esophageal perforation,it
results in asevere chemical pneumonitis ifaspirated.For this reason,barium should
be used ifthere is any impairment to the gag andcough reflexes;ifthere is a
leak,early oper-ative intervention allows it to be washedout during
surgery.Penetrating injuries tothe left neck,and rarely to the right,canresult in a
chyle leak (Figure 26-12).Thesurgeon should take care to exclude this atthe initial
exploration,ifpossible,and torepair it by oversewing the duct with localtissues.It
is useful to have the anesthesiol-ogist apply positive pressure and to placethe
patient in Trendelenburg�s position.Delayed management is much more diffi-cult
after the tissues have been exposed tochyle.Conservative management with adiet
ofmedium-chain triglycerides,whichare not carried by the gut lymphatics,anddrainage
should be attempted initially ifthe leak presents in the postoperative set-
ting.Exploration is indicated for leaks of> 400 to 500 cc/d for a week.Penetrating
injuries to zone II are themost common and are most amenable tosurgical
exploration,ifwarranted.Forasymptomatic patients,computed tomo-graphic angiography
is becoming an impor-tant tool for screening and can assist indetermining whether
operative explorationis warranted.Patients can undergo serialexaminations over 24
hours ifthe angiogra-phy results are negative.Computed tomo-graphic angiography is
faster and less inva-sive than angiography but is oflowerspecificity.It should also
be noted thatinjuries that have �tamponaded�themselvescan be missed on either (see
Figure 26-10C).Some surgeons recommend the use ofabarium swallow or rigid
esophagoscopy,whereas others recommend observationonly ifthe index ofsuspicion for
injury islow,as with wounds from low-energy guns.Ifpatients have associated
mandible frac-tures,the neck can be explored while themandible fractures are
exposed for fixation.Imaging is required in zone III injuriesifthe patient is
stable.Diagnosis ofvascularinjuries at the skull base typically
requiresangiography,which can also allow interven-tion ifindicated.Injuries to zone
III arerarely amenable to surgical intervention.Overall,angiography remains thegold
standard for exploration ofvascularinjuries ofthe neck.In Van As and col-
leagues�report,89 patients underwentangiography for GSWs to the neck;resultswere
positive in 12 patients,with mostlesions occurring in the common carotidfollowed by
the internal and externalcarotids (3 cases each),the vertebralartery (2 cases),and
the subclavian artery(1 case).35Currently ultrasonography isgaining popularity as a
rapid noninvasivetechnique for the evaluation ofa varietyoftraumatic injuries in
the emergencydepartment.Ginzburg and colleaguesevaluated the usefulness ofduplex
ultra-sonography to evaluate vascular injuriesin a double-blind study using
angiogra-phy as a control.They reported a 100%true-negative rate,100%
sensitivity,and
Gunshot Injuries51985% specificity in detection ofarterialinjury.Ultrasonography
will most likelycontinue to grow in popularity as ascreening tool because ofits
cost and thespeed at which it can be performed.38Fur-ther improvements in
noninvasive vascu-lar evaluation techniques,such as helicalcomputed tomographic
angiography andultrasonography,will reduce the numberofpatients undergoing
traditionalangiography and improve patient selec-tion for nonoperative
management.NutritionThe majority ofcivilian gunshot woundsaffect young healthy
males.Nutritional sta-tus becomes an issue only in patientswhose injuries preclude
oral alimentationfor an extended period (> 4 or 5 d).Feed-ing via nasogastric
intubation allowsbypass ofthe oral cavity and improvedhygiene in the early days
following injury.Consideration should be given to percuta-neous endoscopic
gastrostomy iflong-term bypass ofthe oral cavity is necessary,the patient will be
unable to eat,or thepatient has a preexisting nutritional deficit.ImagingFollowing
the ATLS protocol,standard C-spine and chest radiographs should beobtained.These
can be valuable for visual-izing the bullet fragments and in gainingsome insight
into the path ofthe bullet(see Figure 26-10B).It is important torecall,however,that
projectiles rarely fol-low a straight path once they enter tissue.The ability to
obtain accurate three-dimensional images in a rapid fashion hasbeen one ofthe most
important advancesin dealing with gunshot injuries to the face.Spiral computed
tomography combinedwith three-dimensional reconstructionsallows the surgeon an
unparalleled view ofPenetrating neck woundFollow ATLS protocol for airway control
and primary surveyPerform secondary survey, which includes the following:Detailed
examination to rule out hard signs of vascularor laryngotracheal injury (shock,
expanding hematoma, active hemorrhage, bruit or thrill, pulsedeficit, neurologic
deficit, subcutaneous emphysema,a "sucking" wound, stridor, dyspnea,
hoarseness,dysphonia or hemoptysis)Anteroposterior/lateral soft tissue neck wound
with markersProtocol for symptomatic patientsProtocol for asymptomatic patients
Symptomatic patientShockStable vital signsZone IPerformangiographyZone IICheck
hardsignsPerforminterventionalradiologyPerform neck exploration� Direct
laryngoscopy� Bronchoscopy� Esophagoscopy vs postoperative barium swallowZone
IIIPerformangiographyFIGURE26-11A,Initial decision tree for penetrating neck
trauma.B,Management ofthe symptomatic patient with a penetrating neck wound.ATLS =
advanced trau-ma life support.ABFIGURE26-12Chyle leak following penetratinginjury
to zone I ofneck oversewn with nonab-sorbable suture and covered with a flap from
thesternocleidomastoid muscle.
520Part 4: Maxillofacial Traumathe extent ofdamage to the
maxillofacialskeleton,which lies beneath the skin (Fig-ures 26-13 and 26-
14).Although it doesnot accurately demonstrate the amount ofsoft tissue
damage,clinical inspectioncombined with three-dimensional imagingallows an accurate
assessment.As discussedpreviously,the importance oftemporarycavitation and emphasis
on the amount ofdevitalized tissue distant from the primarywound has probably been
overstated in thepast.Computed tomographic angiographycan also be useful in certain
situations forevaluating vascular damage,especially incases ofpenetrating neck
injuries.It shouldbe remembered,however,that angiogra-phy remains the gold standard
to evaluatethe vasculature.Also,angiography allowsthe ability to intervene with
embolizationofactive bleeding vessels that are difficultto approach surgically (see
�PenetratingNeck Injuries�above).Patients who are notsufficiently stable for
imaging should bestabilized in the operating room,anddefinitive repair should be
deferred untilappropriate imaging can be obtained.Operative ProcedureParalleling
the evolution offirearms hasbeen development in the management ofgunshot injuries
to the head and neck.Theearliest surgeons dealing with gunshotinjuries blamed
complications on gunpow-der that would later be ascribed to contam-ination and
infections.The mystique thatsurrounded gunshot injuries persists insome ways to
modern times in surgicaldogma that is passed down.During WorldWar I,high-energy
close-range gunshot andshrapnel wounds to the face necessitated thedevelopment
ofmaxillofacial surgery.Kazanjian and Converse described theirapproach to gunshot
wounds as three phas-es consisting ofinitial d�bridement andsuturing,immobilization
ofbony fragmentswith splints and ligatures,and,finally,reconstruction following
healing ofthe softtissue.39Many ofthe principles developed atthat time persist
today,with surgeons advo-cating a phased approach with delayed clo-sure
ofwounds,d�bridement oftissue,andsecondary reconstruction.40Many surgeonsstill
advocate closed reduction and divisionofcare into early (first 10
d),intermediate(10�60 d),and late (> 60 d) phases.28Thedifferent nature ofcivilian
gunshotwounds and improved management tech-niques have led to a reappraisal
ofstagedapproaches,and current managementprinciples should more properly be consid-
ered a continuum that is based on thewound and patient profile.11,41,42 The suc-
cessful application ofrigid fixation princi-ples to blunt traumatic injuries
resulted inincorporation ofthese techniques to gun-shot injuries.Early surgeons
understoodthe importance ofimmobilization on thehealing ofGSWs but lacked the
ability totruly immobilize bony structures oftheface.The development ofrigid
fixationtechniques and their application to GSWswas an important advance.Early
concernsregarding placement ofhardware into con-taminated sites proved
unfounded.Byallowing the early stabilization ofbone seg-ments,percolation
ofcontaminated oralfluids was prevented,primary bone healingwas made possible,and
the effects ofscarcontracture were minimized.This has ledmost surgeons to advocate
early definitiverepair ofthe majority ofcivilian gunshotFIGURE26-13Three-
dimensional computedtomography scan demonstrating fragmentationofthe mandible
resulting from a gunshotwound.(Courtesy ofJames
R.Koehler,MD,Birmingham,AL)FIGURE26-14A,High-velocity entrance wound oftheright
cheek.B,High-velocity exit wound ofleft cheek.C,Three-dimensional computed
tomography scandemonstrating extensive bony comminution associatedwith a high-
velocity gunshot wound.(Courtesy ofJames R.Koehler,MD,Birmingham,AL)ABC
Gunshot Injuries521wounds,which generally are inflicted withlow-velocity weapons.An
operative plan for a gunshot injuryto the face is best formulated after charac-
terization ofthe wound as low or highenergy (Figures 26-15 and 26-16).Thesurgeon
facing a gunshot injury shouldconsider the concept introduced by Man-son for
evaluation offour components:soft tissue injury,bone injury,soft tissuesloss (true
avulsion),and bone loss.43Afterevaluation ofthe wound,a decision ismade regarding
early definitive repair ver-sus the need for delayed repair.The major-ity
ofcivilian gunshot wounds resultingfrom assaults can be managed with
earlydefinitive repair because these injuriesusually result in injury to the soft
tissueand bone but rarely loss ofthese tissues.Impressive soft tissue injuries are
usuallynot avulsive,and most can be closed pri-marily (see Figure 26-
15).Extensived�bridement ofsoft tissue is not indicated.Wound debris should be
removed,andwounds should be lavaged with normalsaline.Antibiotic solutions such as
salineand bacitracin (50,000 U/L) have not beenshown to be more effective than
normalsaline but are still popular.A pulsatingirrigator is useful to mechanically
agitatedebris from the tissue.Obvious devitalizedand loose teeth should be
removed.Frac-tures are reduced and fixed rigidly.Other-wise,teeth should be
maintained ifpossi-ble to aid in restoration ofocclusion andproper jaw
relations.Drains are often indi-cated;whether closed suction or Penrose isused
depends on the wound.Pressuredressings can also be used to minimizedead space.In
cases oftrue soft tissueavulsion,a decision must be made regard-ing whether primary
flaps or grafting isindicated.In wounds that are relativelyclean,local flaps and
skin grafts may beappropriate.In grossly contaminatedwounds,delayed closure or
grafting maybe necessary.Closing mucosa to skin canbe a useful technique,but many
cases canbe managed with dressing changes andincorporation ofan early flap
procedure.Free tissue transfer,although useful,should be delayed until the initial
phase ofwound healing,when its accompanyingvascular spasm and attendant hypercoagu-
lable state has decreased.In wounds with extensive soft andhard tissue damage and
true loss ofsoftand hard tissue,an approach using earlystabilization ofbone
fragments with max-illomandibular fixation,external fixation,or internal fixation
with reconstructionplates combined with conservative man-agement ofsoft tissue is
indicated.In thisera ofrigid internal fixation,the utility ofmaxillomandibular
fixation should not beoverlooked.12,28In addition,external fixa-tion devices are
still useful in select cases.Second-look operations with conservativewound washouts
and d�bridement ofonlyobviously dead tissue,which have gainedpopularity in
orthopedics,have great util-ity in injuries to the maxillofacial skeleton.Second
d�bridements should be per-formed 24 to 48 hours after the initialsurgery.This
allows for the maintenanceoftissue considered �borderline,�whichcan be excised ifit
truly becomes devital-ized.Skin grafts can be used as permanentor temporary
replacement for missing tis-sue to reduce deformity from scar contrac-FIGURE26-
15A,Gunshot wound resulting from the placement ofa low-velocity handgun into the
mouth.B,Initial closure demonstrating no true tissue loss.C,Three-month
postoperative photograph demonstrat-ing minimal residual deformity following
closure.The facial nerve is intact.ABCFIGURE26-16Extensive wound resulting from a
high-velocity weapon.
522Part 4: Maxillofacial Traumature.Once the soft tissues have stabilized,adecision
can be made regarding earlyreplacement oflost tissues with free tissuetransfer or
delayed reconstruction.In general,earlier repair leads to improved outcomes with
less scar contracture andresultant deformity.Bone grafts at thetime ofinitial
surgery may be indicated inthe midface (see below).Again,manage-ment strategies
should be considered acontinuum that is modified as necessaryrather than strict
distinct stages.ContaminationIt should be remembered that projectilesfrom firearms
are not sterile.This fact iswell known to those who have dippedtheir bullets in
feces prior to assassinationattempts but lost on clinicians who havetaught that
gunshot wounds are indeedsterile.The heat generated by the dischargeofthe
propellant as well as the frictionbetween the bullet and barrel is not suffi-cient
to sterilize the bullet.44,45Contamina-tion can occur from the bullet and alsofrom
skin flora and foreign bodies (cloth-ing) carried into the
wound.Historically,streptococcal bacteremia was the mostimportant cause ofdeath on
the battlefieldin the preantibiotic era.46Wounds inwhich the bullet traverses the
aerodigestivetract or paranasal sinuses are at particularrisk.Devitalized tissue
and vascular con-gestion leads to an ideal environment forbacterial
growth.Prophylactic coveragewith broad-spectrum antibiotics,typicallya second-
generation cephalosporin,andtetanus prophylaxis,when indicated,should be initiated
in all gunshot wounds.Extensive surgical d�bridement is rarelyindicated in wounds
consistent with low-velocity projectiles to prevent infection.Removal
ofprojectiles,a well-worntradition in Hollywood,is less commonlyindicated in
reality.The need for theremoval ofbullets must be balancedagainst the real risk
ofincreasing damage.Lead toxicity is a rare complication thatdoes not typically
justify the routineremoval ofbullet fragments.47Removal ofintra-articular bullet
fragments should beconsidered when the increased risk ofleadtoxicity is associated
with fragments with-in joint spaces and the potential for long-term deterioration
ofthe joint.48Finally,consideration may be given to the removalofbrass- or copper-
jacketed bullets thatare in close proximity to central or majorperipheral nerves
because ofpotentialneurotoxicity.49,50It is important to remember that bul-let
fragments are potential evidence andan appropriate chain ofcustody isrequired.Most
hospitals have a protocol inplace to ensure that this chain is unbrokenfrom the
time they are retrieved to whenthey are logged in as evidence.This usual-ly
involves a police officer or otherdesignee taking direct possession ofthebullet or
fragments in the operating roomor nearby.Documentation ofinjuries withphotographs
can aid in reconstructing theevents leading to the injury and recordingwhere
fragments were retrieved.Sincesome assaults have injury patterns similarto
suicides,it is important to consider thischain ofcustody because
subsequentinvestigations may reveal that an apparentsuicide was actually an
assault.51Specialized StructuresFacial NerveDamage to the facial nerve is present
inonly 3 to 6% ofcivilian GSWs to theface.12,28This is most likely because low-
energy weapons are involved in most ofthese cases.However,such damage is
notuncommon in injuries inflicted by higher-velocity firearms.Careful
documentationat the earliest possible opportunity isimportant.Ifa functioning nerve
becomesnonfunctional secondary to swelling,thesurgeon can be reasonably confident
thatfunction will return.Obvious transectionofthe nerve requires repair.In
heavilycontaminated wounds,repair should bedelayed for 48 to 72 hours,given the
pos-sibility that grafts will be required to spandamaged segments.Beyond 72 hours
dis-tal branches ofthe facial nerve will notrespond to a nerve
stimulator,makingtheir identification difficult.Ifpossible,tagging the branches
with suture at theinitial surgery is invaluable.Extensivedamage to the proximal
nerve mayrequire a temporal bone dissection toidentify a viable proximal nerve for
graft-ing.Injuries distal to a line dropped verti-cally from the lateral canthus
(zone ofarborization) do not typically requirerepair because ofthe multiple
intercon-nections distal to this line and the reason-able expectation ofreturn
offunction,even ifthe nerve is temporarily nonfunc-tioning (see Figure 26-
15).Salivary DuctsTransected salivary ducts may be repairedor ligated depending on
the amount ofdamage.The parotid duct can be repairedover an intravenous catheter or
polymericsilicone tubing,which is then sutured tothe buccal mucosa.It is best to
avoidbringing the tubing out ofthe mouthbecause ofthe tendency for it to be dis-
lodged.In injuries that penetrate theparotid-masseteric fascia,there is a poten-
tial for development ofa sialocele or fistu-la.These typically resolve with
drainageand pressure dressings.Aspiration may berequired multiple
times,and,rarely,anti-sialagogues may be indicated.In addition,removal ofany
associated foreign bodiesmay be necessary to resolve the fistula andhasten
healing.Dermal grafts can be usedat the time ofrepair (Figure 26-
17).Controversies:Delayed versus Early Management and Closed versus Open Fracture
ManagementProponents exist both for closed manage-ment offractures with delayed
reconstruc-tion as well as aggressive early managementwith open reduction
offractures andreplacement ofmissing tissue as soon as
Gunshot Injuries523possible.Both groups point to failures andshortcomings ofthe
other to justify theirapproach.Advocates ofdelayed repairpoint to a higher
incidence ofinfection andto benefits ofclosed treatment,whereasthose advocating
more aggressive manage-ment report improved functional andesthetic
outcomes.52,53Since neitherapproach is likely to ever be subjected to arandomized
trial measuring outcomes,surgeons must base their treatment deci-sions on a
critical review ofthe literatureand their own experience.As with mostarguments in
surgical science,the truthmost likely lies somewhere in the middle.Certainly the
advantages ofaggressive earlymanagement are appealing (Figure 26-18).Early return
to function and decreasednumbers ofrevision surgeries are laudablegoals.Currently
techniques involving openreduction and fixation offractures result-ing from GSWs
seem to be gaining in pop-ularity,and patients are less likely to betreated with
closed reduction.Given thatmost ofthese injuries are low energy,this
isacceptable.The main disadvantage ofopenreduction is infection,which
primarilyaffects the mandible.The reported rate ofinfection with open reduction and
fixationofmandible fractures resulting from agunshot is around 16 to
17%.54However,rigid fixation can frequently be maintainedin the event ofwound
problems and stillserves to stabilize mandibular segments.Surgeons should avoid the
application ofaset protocol to every GSW situation andshould instead rely on a
careful appraisal ofthe wound and decide on the amount ofearly repair that is
indicated.Bone GraftingBone grafts are frequently required in themanagement ofGSWs
to the face,whether for replacement oftrue loss ofbone (avulsive injuries) or in
cases inwhich comminuted and misplaced frag-ments need to be replaced or
reinforced.Reconstruction with bone grafts gainedpopularity in World War I,and much
ofwhat we know about the healing offreebone grafts was learned following
theirintroduction for late reconstruction ofgunshot injuries in wartime.Iliac
bonegrafts were popular for late reconstruc-tion.Surgical dogma was against early
orFIGURE26-17A,Salivary-cutaneous fistula associated with a retained bullet
fragment.B,The bullet wasremoved and a dermal graft was placed.ABFIGURE26-
18A,Grazing shotgun facial wound,sus-tained in hunting accident,associated with
avulsionofthe upper third ofthe nose,including the skin,nasalbones,a portion ofthe
upper lateral cartilages,and theskin ofupper eyelid.B,Use ofimmediate cranial
bonegrafting to replace the lost nasal support.C,Develop-ment ofa pericranial flap
to envelope the cranial boneand provide a vascularized tissue bed to support afull-
thickness skin grafting.D,Early postoperativephotograph demonstrating the full take
ofskin graft.E,Late (1 yr) postoperative photograph demonstrat-ing good nasal
support and prosthetic rehabilitation ofthe left globe; photograph was taken prior
to thereconstruction ofthe ala with a graft from the helix.ABCDE
524Part 4: Maxillofacial Traumaprimary bone grafting and stipulatedwaiting until
soft tissue healing hadoccurred.More recently the use ofbonegrafts in the early
setting has gained popularity.Gruss and colleagues have published extensively on
their successwith early bone grafting to stabilize andsupport soft tissues,and to
decrease scarcontracture and distortion.55The use ofcranial bone in blunt injuries
was extend-ed to include GSWs with some success.Currently many surgeons advocate
the useofprimary bone grafting in the midface.Some surgeons also advocate
immediatebone grafting ofmandible defects.56Mostagree,however,that delayed grafting
ofdiscontinuity defects ofthe mandible isstill indicated because ofthe high risk
ofexposure and loss ofbone grafts in thissite,and that immediate grafting in
themandible should be avoided.11,52Clarkand colleagues reported a 35%
incidenceofwound complications in patientsundergoing immediate reconstruction
ofsignificantly comminuted mandible frac-tures resulting from
GSWs.Conversely,primary bone grafting was uniformly suc-cessful in the cranium and
midface.11Rigid fixation maintains the mandibularsegments.Even ifthe titanium
platebecomes exposed,wound care will allow itto be maintained until definitive
recon-struction.43,55In summary,primary bonegrafting in the early phase
ofgunshotwound management can be useful,but itshould be limited to the upper and
mid-face.Maintenance ofmandibular seg-ments with rigid reconstruction
platescombined with delayed grafting or freeflap reconstruction offers a
predictableresult,and in most cases primary graftingofthe mandible is not
indicated.Late ReconstructionDelayed bone reconstructions frequentlysuffer from a
scarred hypovascular envi-ronment that does not support the graft.In addition,there
is typically a deficiencyin soft tissue that becomes more pro-nounced when wounds
are opened.Inthese cases vascularized tissue transferoffers the ability to import
soft tissueand/or bone into the site.As noted previ-ously,free tissue transfer is
usually delayeduntil after the acute setting to decrease theincidence offlap loss
secondary to clottingofthe vascular pedicle.Preoperativeangiography often is
beneficial to identifyappropriate vessels in the neck.Vascular-ized bone grafts can
support osseointe-grated implants to complete the recon-struction.Anthony and
colleaguesreported on the use ofthe fibula inpatients in whom previous
reconstructiveattempts for gunshot injuries had failed.57Both cases involved
secondary reconstruc-tions.Some surgeons have advocateddelayed reconstruction in
gunshot woundsthat resulted from suicide attemptsbecause ofthe potential for repeat
suicideattempts,arguing that there is a high rateofrecidivism and that patients
should bestabilized psychologically for some periodoftime prior to undertaking an
extensive(and expensive) reconstructive effort.However,Cusick and colleagues found
anincidence ofonly 8% confirmed mortalityin the follow-up of91 patients who
hadattempted suicide.58All were patients whohad long-standing chronic mental
illness.De Leo and colleagues found a higher ratein an elderly European
population.In a 1-year follow-up,they found 24% hadattempted suicide again,with
approxi-mately halfbeing successful in their sec-ond attempt.59With modern
techniques,however,primary reconstruction hasbecome more attractive in most
patientswho have self-inflicted gunshot wounds.1,60It should be noted,however,that
someauthors still recommend delayed recon-structive efforts.Siberchicot and col-
leagues reviewed 165 patients with self-inflicted gunshot injuries between 1982and
1996 and suggested that delayeddefinitive reconstruction was more likelyto achieve
satisfactory results in appear-ance and function.53ConclusionsThe development
offirearms heralded anew era in surgery as well as warfare.Evo-lution ofmore
efficient weapons contin-ues to force surgeons to improve tech-
niques.Similarly,improvement in themanagement ofGSWs to the face has par-alleled
the advancement oforal and max-illofacial surgery.Advances by VaraztadKazanjian,the
�miracle man ofthe West-ern front�during World War I,continuedthrough the wars
ofthe twentieth century.Improvements in casualty managementand triage in the Korean
and Vietnamconflicts led to increased survival ofthosewith devastating facial
injuries.Tech-niques and skills developed by oral andmaxillofacial surgeons in the
manage-ment ofthese injuries translated directlyto other areas such as bone
grafting,andpromoted the growth and expandingscope ofthe specialty.These efforts
arecontinued today in urban trauma centersdealing with gunshot injuries to the
face.Improvements in imaging and fixationtechniques have resulted in an evolutionin
management,with an emphasis on ear-lier repair and a focus on improvement inquality
oflife.AcknowledgmentSpecial thanks to David H.Holmes,DDS,for his assistance and
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RD,Browne JD,Phipps CD.Gunshotwounds to the mandible and midface:eval-
uation,treatment,and avoidance ofcom-plications.Otolaryngol Head Neck
Surg1994;111:739�45.31.Chen AY,Stewart MG,Raup G.Penetratinginjuries to the
face.Otolaryngol Head NeckSurg 1996;115:464�70.32.Yao ST,Vanecko RM,Corley RD,et
al.Gunshotwounds ofthe face.J Trauma 1972;12:523�8.33.May M,Cutchavaree
A,Chadaratana P.Mandibular fractures from gunshotwounds:a study of20
cases.Laryngoscope1973;83:369�73.34.Monson DO,Saletta JD,Freeark
RJ.Carotidvertebral trauma.J Trauma 1969;9:987�99.35.Van As AB,van Deurzen
DF,Verleisdonk EJ.Gunshots to the neck:selective angiographyas part ofconservative
management.Injury2002;33:453�6.36.Holmes JD,Koehler JR.Management ofpene-trating
neck trauma:current practices andreport ofa case.J Oral Maxillofac Surg2003.
[Submitted]37.Biffl WL,Moore EE,Rehse DH,et al.Selectivemanagement ofpenetrating
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GovernmentPrinting Office;1929.47.Selbst SM,Henritig F,Fee MA,at al.Lead poi-soning
in a child with a gunshot wound.Pediatrics 1986;3:413�6.48.Kent JN,Neary JP,Silvia
C,Zide MF.Openreduction offractured mandibularcondyles.Oral Maxillofac Surg Clin
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nervous system.Neuroradiol-ogy 1976;12:121�9.50.Sherman IJ.Brass foreign body in
the brainsystem.J Neurosurg 1960;17:483�5.51.Azmak D,Altun G,Koc S,et al.Intra-
andperioral shooting fatalities.Forensic Sci Int1999;101:217�27.52.Deveci
M,Sengenzer M,Selmanpakoglu M.Reconstruction ofgunshot wounds oftheface.Gazi Med J
1998;9:47�56.53.Siberchicot F,Pinsolle J,Majoufre C,et al.Gun-shot injuries ofthe
face.Analysis of165 casesand reevaluation ofthe primary treatment.Ann Chir Plast
Esthet 1998;43:132�40.54.Neupert EA,Boyd SB.Retrospective analysis of
526Part 4: Maxillofacial Traumalow-velocity gunshot wounds ofthemandible.Oral Surg
Oral Med Oral Pathol1991;72:383�97.55.Gruss JS,Mackinnon SE,Kassell EE,CopperPW.The
role ofprimary bone grafting incomplex craniomaxillofacial trauma.PlastReconstr
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CHAPTER 27Pediatric CraniomaxillofacialFracture ManagementJeffrey
C.Posnick,DMD,MDBernard J.Costello,DMD,MDPaul S.Tiwana,DDS,MD,MSHistoric
PerspectivesThe management ofcraniomaxillofacialtrauma,and the treatment offacial
fracturesin children in particular,has evolved gradu-ally.A review ofthe historic
landmarks in itstreatment is important for understandingwhat has yet to be
accomplished.At the turn ofthe century Rene Le Fortwas the first to document a
tendency for theoccurrence ofspecific patterns ofmidfacefractures after direct
facial trauma.1Withina few years thousands ofcombined soft andhard tissue facial
injuries resulted from thetrench warfare ofWorld War I and requiredurgent treatment
and secondary recon-struction.Two physicians in particular,V.H.Kazanjian and
H.Gillies,stand out for theirwork during this period.2,3During and afterWorld War
Iand again during World WarII,these men laid the foundation for whatwe now know as
craniomaxillofacialsurgery.Rowe and Killey,Dingman andNatvig,and others refined the
basic princi-ples laid down by their mentors,set out toeducate their peers,and
brought thesetreatment principles to the civilian popula-tion after the two world
wars.4,5At the sametime,the use ofantibiotics and improvedairway and metabolic
management ofthetrauma patient increased survival rates.6The extensive surgical
procedures that wereoften required to improve the quality oflifeofthe multiply
traumatized patient alsobecame a reality.Knowledge ofthe successful repair
oftraumatic facial injuries brought hope topeople with congenital facial
deformities.Gillies and Harrison pioneered the elective(extracranial) total midface
advancement(Le Fort III osteotomy) for Crouzon syn-drome.3In 1967 Tessier described
a cranialbase approach to the management ofskeletal deformities associated
withCrouzon syndrome and Apert syndrome.His landmark presentation and publica-tions
were the beginning ofmodern cranio-facial surgery.In 1968,Hans Luhr,a
youngmaxillofacial surgeon,proposed thatminiature (metal) bone plates and
screwscould be constructed and used effectivelyto fixate a mandibular fracture
togetherfor improved healing.7Despite hisenthusiasm these concepts
ofinternalfixation for the craniomaxillofacial skele-ton were not put into wide
practice untilthe mid-1980s.The concept ofa hospital-based civiliantrauma service
that functioned 24 hoursa day,7 days a week,coupled with imme-diate �in-the-
field�emergency recon-struction ofthe trauma patient followedby rapid transport to
the trauma center,was pioneered by R.A.Cowley with thedevelopment ofthe University
ofMary-land�s shock trauma center.8This conceptofaccurate and rapid verification
ofinjuries by the trauma surgeon,combinedwith well-trained and immediately avail-
able surgical subspecialists,hospital sup-port staff,and technology,led to remark-
able patient recoveries in otherwisehopeless situations.The importance ofmanaging
the facialinjuries ofthe multiple-trauma patientbecame evident early in the trauma
center�sexperience.Following the basic philosophyoftotal patient
rehabilitation,Gruss andcolleagues in Canada and Manson and col-leagues in the
United States developed newconcepts for the management ofcran-iomaxillofacial
trauma.9�13Their basicapproach incorporated the early accuratepreoperative
diagnosis ofall skeletalinjuries by clinical examination with verifi-cation using
computed tomography (CT)scanning techniques,wide (direct) surgicalexposure ofall
fractures for open reductionofdisplaced and mobile segments,use ofstable internal
fixation techniques (platesand screws),and primary autogenous bone
528Part 4: Maxillofacial Traumagrafting to replace missing or irreversiblydamaged
skeletal units.The rapid dissemi-nation oftheir concepts and basic clinicalapproach
to everyday surgical practicearound the world is a tribute to Gruss andManson,who
remain dedicated to thehighest standards ofclinical care,research,and
education.Children with facial injuries have notbenefited equally from this rapid
refine-ment in the management offacial traumain adults.In 1943 Waldron and
colleagueswere the first to bring to the maxillofacialsurgeon�s attention the often
unique facialinjuries in the traumatized child.14MacLennan,and then Rowe,wrote
aboutthe rarity offacial fractures in childrenand suggested a basic approach with a
phi-losophy toward conservatism.15,16Otherpublished articles have also tended
towardconservatism,with only limited incorpo-ration ofthe principles described
earlierby Gruss and Manson.17�39Only recentlyhave the distinct advantages
ofaccurateprimary repair and the stable fixation offacial fractures been applied to
the rehabil-itation ofinjuries in children.40�47Also,resorbable materials have been
madeavailable as a fixation option for pediatriccraniomaxillofacial fracture
management.Special Considerations in ChildrenThe general principles for
resuscitatingmultiply injured patients follow theadvanced trauma life-support
principlescreated by the American College ofSur-geons.48This systematic approach to
traumain adult patients has been modified for themanagement oftrauma in the
child,takinginto account several critical differences:�Infants are obligate nasal
breathers;atthe same time their nasal air passages arerelatively narrow and easily
obstructed.�The chest wall in children is pliable;major thoracic injuries may
existwith fewer than expected signs ofexternal trauma.�Children frequently swallow
air whenthey are injured or frightened,resultingin gastric dilatation.This may be
asource ofconfusion when evaluating thepatient to rule out an acute
abdomen.�Abdominal girth and the volume ofthe peritoneal cavity in infants andyoung
children are relatively small.Significant intra-abdominal bleedingresults in a
rapid change in girth.�Children may maintain a normal orborderline blood pressure
level despitesignificant fluid loss and then decom-pensate rapidly.�Children have a
larger body surface area-to-overall mass ratio than adults and aretherefore more
prone to hypothermia.Children are generally injured in low-velocity accidents
secondary to falls fromlow heights,playground equipment,orriding toys.Most commonly
they arrive atthe emergency room in a state ofhemody-namic stability.With regard to
the fre-quency oforgans injured,the kidney is thesolid organ that is the most
frequentlyinjured,followed by the spleen,liver,andpancreas.Hollow viscus
perforations aremuch less common compared with adultinjury patterns.In contrast
nonaccidentaltrauma is more insidious and devastating.The pattern oforgans
injured,especially inthe toddler,is the reverse ofthat seen inaccidental
trauma.With child abuse thehistory is often vague and inconsistent.49,50A history
ofprior injuries and hollow vis-cus perforation is common.Airway management in
children withfacial trauma has undergone significantchange.With the widespread use
ofsoftendotracheal tubes in the 1960s,the numberoftracheostomies carried out for
periopera-tive airway management decreased.51,52Useoffiberoptic laryngoscopy has
furtherdecreased the incidence oftracheostomyfor acute airway management in the
pedi-atric trauma patient.Kaban and Posnickand colleagues reported no
tracheostomiesfor airway management in their series con-sisting of262 and 137
pediatric facial trau-ma patients,respectively.30,53Also cervicalspine injuries are
exceedingly rare.30,53,54Anatomic ConsiderationsMaxillofacial injuries are much
less com-mon in younger children than in adoles-cents and adults.This lower
incidence offacial trauma in infants and young chil-dren is a result
ofsocioenvironmental,general physical,and craniomaxillofacialanatomic
factors.55,56Before the age of5 years most childrenlive a relatively protected
existence,withclose adult supervision,strict limitationson their physical
environment,and con-stant safeguards to limit injury.Althoughfalls from limited
heights are frequent themomentum gained by the child�s smallbody is ofa low
velocity.These low-impactforces can usually be absorbed by theirwell-padded
skin,elastic skeleton,and car-tilaginous growth centers.After the age of5 to 7
years,rapid pro-gression ofneuromotor developmentresults in a general desire for
independentactivity,more frequent social interactionswith other children,and a
wider range ofactivities outside ofthe house,with lessstringent parental and adult
supervision.These factors result in increased opportu-nity for direct facial
trauma.Additionally,increasing numbers ofautomobiles on theroad and participation
in pedestrian activ-ities in public areas result in competitionfor space with
motorized vehicles.Ongoing craniomaxillofacial growthresults in a changing anatomy
(Figure 27-1).57For the first several years oflifethe cranium follows the rapid
pace ofbrain growth and results in a relativelylarge and prominent forehead.The
ocularglobes and orbits also develop rapidlyearly in life and join the forehead in
theirrelative prominence early in life.Thisearly period oflife is marked by a lack
ofparanasal sinus and dental development,resulting in limited vertical height,hori-
zontal projection,and transverse width of
Pediatric Craniomaxillofacial Fracture Management529the maxillomandibular regions
early inchildhood.These factors result in a highskull-to-face ratio,leaving the
frontal andupper orbital regions more exposed totrauma while the lower face remains
rela-tively protected.The mandible defines the lower bor-der ofthe facial
skeleton.Its evolvinganatomy throughout growth and develop-ment significantly
affects the pattern ofinjuries that occur in the lower facethroughout
childhood.During infancyand early childhood,the condylar processofthe mandible has
a well-vascularizedmarrow space with a thick and short neck.The condylar injuries
seen involve com-pression,whereas neck fractures are morerare.This is in contrast
with the condylarprocess�s tall and cortical characteristicslater in childhood and
adolescence,whichleave it vulnerable to neck fractures.Themandible and maxilla
continue to growthroughout childhood,maintaining a highcancellous-to-cortical-bone
ratio andresulting in greater elasticity ofthe jaws,with more greenstick and
nondisplacedfractures than are seen in adulthood.Dur-ing the first few years oflife
the developingpermanent tooth buds are small,and thetooth-to-bone ratio ofthe jaws
is relative-ly low.In the mixed dentition phase (6 to12 years) a higher tooth-to-
bone ratioweakens the mandible in specific locationsand encourages fracture through
thedeveloping tooth crypts when traumaoccurs.After 5 years ofage the
paranasalsinuses develop gradually,resulting inareas ofskeletal weakness,which
results inease ofseparation ofthe midface from thebase ofthe skull when facial
traumaoccurs.Another factor in children is thehighly osteogenic
periosteum,whichresults in early healing ofa fracture withmore extensive remodeling
after boneunion has occurred.PreventionThe increased use ofage- and weight-specific
protective restraints,lower speedlimits,more strict alcohol abuse laws,anduse ofair
bags have greatly diminished theincidence ofmotor vehicle�related trau-ma.58,59For
the infant and young child(less than 100 lb) release ofthe automo-bile�s air bag
may in itselfcause traumaand even death (suffocation).The recogni-tion that
conventional lap belts do notproperly restrain or protect infants andyoung children
is a relatively recent find-ing.Special harness restraints,marketedsince 1967,are
required for children weigh-ing less than 44 lb to prevent forwardmovement,to
support the head,and to dis-tribute the force ofinjury over a larger sur-face
area.Current recommendations statethat children weighing less than 100 lboryounger
than 12 years should not beplaced in an air bag�equipped seat.Infantsshould face
the rear ofthe vehicle untilthey are at least 1 year ofage.Vehicle safe-ty belts
are not to be used until the shoul-der belt can be positioned across the chestwith
the lap belt low and snug across thethighs.Larger children may use
boosterseats,which have been shown to be pro-tective in many motor vehicle
crashes.58Abooster seat is used until the standardshoulder and lap belts fit
appropriately.Public acceptance,with mandatory laws,has progressively increased
their use.Adults have a particular obligation toensure that children riding in
their auto-mobiles are properly restrained in devicesthat are appropriate for their
size and age.Popular multispeed bicycles,dirtbikes,and off-road vehicles placed in
thehands ofuntrained or unprotected chil-dren and adolescents have contributed toan
increasing number ofmaxillofacialinjuries in these users.Demas and Braunreviewed
the injuries ofall-terrain vehicleaccident victims at a major pediatric trau-ma
center and found that 37% ofthesepatients sustained facial injuries.60Partici-
pation in everyday sport activities isanother source ofpediatric facial frac-
tures.Proper helmets,mouth protectors,and face guards are not always
mandatoryequipment,even in many organized con-tact sport leagues.The awareness and
recognition ofchild abuse and parental and family vio-lence as a cause offacial
trauma is anotherconsideration that must not be overlookedby the pediatric or
general dentist,pedia-trician,and emergency room or traumaphysician.61Diagnostic
StudiesWhen facial trauma is suspected in thechild,either by history or physical
exami-nation,radiographic documentation ismandatory.For the isolated
mandiblefracture the panoramic tomogram pro-vides an excellent image ofthe
entiremandible.However,for many patientswith significant mechanisms
oftrauma,unclear history,or other factors,CT scan-ning provides the necessary
informationto make a complete diagnosis ofany facialfractures.CT scanning has for
the mostFIGURE27-1Oblique view ofdry skulls ofvarious ages.Ages ofskulls(left
toright) are approximately 6 months,11 years,and 20years.Reproduced with permission
from Posnick JC.132
530Part 4: Maxillofacial Traumapart supplanted standard radiography asthe preferred
method ofimaging pediatricfacial trauma.62,63Multiple CT scan planarviews
(coronal,axial,sagittal) performedwith spiral scanning through all ofthefacial
structures ofinterest,with three-dimensional reformation ofthe CT scandata,confirm
the location and extent ofskeletal,soft tissue,and visceral injuries(ie,brain or
eye trauma).The patient isplaced in the CT gantry and when neces-sary given
sedation or,occasionally,gener-al anesthesia.The radiation doses requiredfor
imaging are generally much lower thanthat for standard tomograms and havemore
limited scatter.Spiral and multislicetechniques have reduced the dose ofradi-ation
significantly when compared witholder CT methods.64These techniques alsoallow for
reformatted images in otherplanes (eg,coronal views) that are ofexcel-lent
quality.This is helpful in patients whohave been immobilized in a cervical
collar.For isolated mandibular injury thepanoramic tomogram still gives the
bestoverall perspective ofdentoalveolar andcondylar head (ofthe mandible)
anatomyand injuries and can be taken with a cervi-cal collar in place.Epidemiology
and GeneralTreatment ConceptsThe patterns offacial injury in the pedi-atric
population are considerably differentthan those for adults.Understanding
thesedifferences in injury presentation helps thesurgeon during the evaluation and
treat-ment phases.The objectives ofthe studypreviously published by Posnick and
col-leagues were to record the pattern offacialinjuries treated over a 4-year
period at apediatric tertiary trauma unit and to doc-ument the treatment provided
and anycomplications that occurred (Tables 27-1�27-4).53The information gainedfrom
this study remains pertinent becauseit illustrates the common injury patternsseen
in pediatric facial trauma at a majorreferral center for acute treatment.All
patients with acute facial fracturesevaluated at a single tertiary care
pediatrichospital over a 4-year period and treatedby the author (J.C.P.) were
enrolled in thestudy.53The mechanism ofinjury,locationand pattern offacial
fractures,and extentofassociated soft tissue injuries were eval-uated.For each
fracture the method ofreduction,the type offixation,and theneed for primary bone
grafts were record-ed.Patients were placed into two groups:(1) those requiring
acute care who receivedtheir primary treatment and evaluation ata single
hospital,by Posnick;and (2) thosetreated for secondary (or residual) defor-mity,who
were referred to Posnick formanagement at varying times after theirinjuries.All
perioperative complicationswere catalogued.Follow-up ofthe patientgroup ranged from
1 to 5.5 years at theclose ofthe study.Fracture patterns were classifiedaccording
to their complexity.Group 1included all isolated fractures limited toone bone,group
2 included all multiplefractures occurring in a single bone,andgroup 3 included
multiple fractures occur-ring in multiple anatomic regions withinthe facial
skeleton.Because ofthe hospi-tal�s entrance restrictions the oldest childin this
population was 18 years.The facial trauma population con-sisted of137 patients (318
fractures) seenover a 4-year period.53Most ofthe patients(42%) were between 6 and
12 years ofage,and the total population averaged 10.2 years ofage.Boys (63%)
outnum-bered girls (37%) in the study (see Table27-2).Ofthe 137 patients,81 were
treatedfor acute fractures (171 fractures) and 56were evaluated for reconstruction
ofsec-ondary deformities resulting from the ini-tial fractures (147
fractures).Ofthe 171acute fractures,121 were treated surgically.Fifty percent ofthe
patients wereinjured in traffic accidents,followed in fre-quency by falls and
injuries related tosports and altercations (see Table 27-1).Causal mechanisms
appeared to be dis-tributed similarly between sexes,except fora slightly higher
number ofmales withfractures attributable to an altercation orTable 27-1Mechanism
ofPediatric Facial Fracture by Age CategoryAge Group Sports-Related (year)Traffic
AccidentFallsand AltercationsOther< 319023 to 5128416 to
1232129413+233152Total6832289Adapted from Posnick JC et al.53Table 27-2Patient Age
and Occurrence ofPediatric Fractures by RegionAge Group
(year)CraniumOrbitZygomaMidfaceMandible< 1010031 to 2221043 to 52523196 to
12816982713+41791222Total1641212375Adapted from Posnick JC et al.53
Pediatric Craniomaxillofacial Fracture Management531to recreational vehicle
accidents.The like-lihood ofhigh-velocity injuries increasedwith age (10% in the 1-
to 2-year agegroup,increasing to 55% in the 6- to 12-year age group).Falls as a
causedeclined with age (55% in the 1- to 2-yearage group,dropping to 8% in the 13+
yearage group).The number offacial fracturestended to increase in the summer
months;45% ofall fractures occurred between themonths ofMay and August.Ofthe 137
children with facial frac-tures,66 (48%) sustained isolated frac-tures (group 1),27
(20%) had multiplefractures in a single bone (group 2),and44 (32%) had multiple
fractures in multi-ple sites within the craniofacial skeleton(group 3).Children
younger than 3 yearswere more likely to sustain only singlefractures (see Tables
27-2 and 27-3).Thechildren experienced one or more frac-tures in the following
craniofacial regions:mandibular (55%),orbital (30%),den-toalveolar (23%),midface
(17%),nasal(15%),zygoma (14%),and cranium(12%).Fracture pattern profiles were sim-
ilar in both the acute care and secondarytreatment groups.Midface (20 of23)
andzygoma (18 of21) fractures were morelikely to occur in children older than 6
years ofage (see Table 27-2).The distribution offractures byanatomic region and
degree ofcomplexityis presented in Table 27-3.Similar anatom-ic patterns were seen
in both the acute andsecondary cases.Most ofthe fracturesoccurred as part ofa
complex injury pat-tern,with the exception ofmandibularfractures,which occurred as
isolated frac-tures with nearly equal frequency.Eighty-one patients with
acuteinjuries were seen for evaluation duringthe period ofthe study.These patients
sus-tained 175 fractures,requiring 121 opera-tive interventions.Injuries occurring
athigh velocity,such as traffic-related events(74%),more frequently required
interven-tions than those occurring at low velocity,such as falls (51%).Boys did
not requiresignificantly more operations than girls.Necessity for operative
interventionincreased significantly with the increasingcomplexity offacial
fractures (group 1 togroup 3) but not with age.Open or closed reduction
techniqueswere used with approximately the same fre-quency.When closed reduction
was used,most patients (93%) underwent reductionand stabilization ofthe fracture
with maxil-lomandibular fixation (eg,Erich arch bars,skeletal suspension
wires,Stout wires).Anexternal fixation device was used for onlyone patient.Only
four fractures werereduced and not stabilized.Thirteen frac-tures (20%) were opened
and exploredwithout any form offixation.Most ofthesewere orbital floor fractures
with associatedbone-grafting procedures.Ofthe fracturestreated by open reduction,35
(55%) weremanaged with only one form offixation tostabilize the reduction and 14
(21%) withmultiple forms.Use ofplates (miniplates ormicroplates) and screws
accounted for 82%(40 of49) ofthe internal fixation methodsused.Although age was not
a factor in thechoice ofplate-and-screw fixation,reviewofthe data indicated that
this method wasnot used on any patient younger than 3 years (only three ofthe
children in ourpopulation were younger than 3 years).Plates and screws were used
most often inthe mandible (40%) and orbits (26%).Bone grafts (21) were used for
fractures ofthe orbit (16),cranial vault (2),mandible(2),and nose (1).The preferred
donor sitesincluded cranium (10),anterior maxillarywall (4),and hip
(2).Complications in treating pediatricfacial trauma are rare ifgood principlesare
adhered to and precise surgical execu-tion is achieved.This is due,at least
inpart,to the excellent healing capabilities ofmost children.Nonunion is very rare
dueto the excellent healing potential ofpedi-atric bone.Malunion may occur but
isTable 27-3Pediatric Fracture Pattern by Anatomic Region and ComplexityFracture
Complexity*Anatomic RegionNo.ofSubjectsNo.ofFracturesGroup 1Group 2Group
3Cranium25279115Orbit41737529Zygoma21224017Midface23312021Nose1723647Mandible751073
81720Dentoalveolar324481113Adapted from Posnick JC et al.53*Fracture complexity
resulting from trauma was represented by three groups:group 1,trauma involving a
single fracture in a single anatomic region;group 2,trauma involving multiple
fractures in a single anatomic region;and group 3,trauma involving multiple
fractures in multiple anatomic regions.Table 27-4Management ofAcute Pediatric
Fractures*No Surgical Closed Reduction Open Reduction Treatment(No.ofFractures)
(No.ofFractures)50Reduction only (4)Exploration only (13)Maxillomandibular
fixationSingle fixation method (35)External fixationMore than 1 fixation method
(14)*N= 171.Adapted from Posnick JC et al.53
532Part 4: Maxillofacial Traumausually due to inadequate reduction.InPosnick and
colleaguesstudy no deaths,tooth loss,or injuries to the eye or brainwere directly
attributable to any operativeprocedure.Two patients developed soft tis-sue
infections that responded to treatmentby incision,drainage,and
administrationofantibiotics.Another developed a smallarea ofalopecia after a
coronal flap proce-dure.One patient,in whom a fractureextended through a tooth
root,developed aperiapical tooth abscess.This conditionwas treated with extraction
and systemicantibiotic therapy.One miniplate wasremoved 1 year later because it was
palpa-ble and visible below thin forehead skin.Ofthe 137 patients in this series,77
(56%) had associated soft tissue injuries.These included lacerations to the
scalp(31%),and injuries to the ear (20%),chin(13%),tongue (8%),forehead
(6%),andeyelid (6%).Thirty-three percent in thefacial fracture group had injuries
to otherorgan systems.Associated head injuriesaccounted for 42% ofthis
group,followedby damage to the extremities (24%),eyes(22%),thorax (10%),and abdomen
(2%).None ofour patients sustained injuries tothe cervical spine.As expected,the
morecomplex the facial injury,the greater thelikelihood ofassociated injury (p= .
03);19% ofgroup 1,26% ofgroup 2,and 36%ofgroup 3 patients had an associated
injury.Six percent required emergency endotra-cheal intubation when first
evaluated;noemergency tracheostomies were required.Patterns ofPediatric Facial
Fracture Injury and Methods ofManagementAnterior Cranial Vault andSupraorbital
Ridge FracturesFractures ofthe forehead and upper orbitalregions,combined with
brain injury anddural tears with cerebrospinal fluid (CSF)leakage,constitute a
frequent pattern ofinjury in infants and in children youngerthan 5 years when major
anterior craniofa-cial trauma occurs (Figure 27-2).53Isolatedcranial vault
fractures (18 of318 fractures,6%) occurred infrequently in this series.When they
did occur,the anterior cranialvault was the most common location (13),followed by
the posterior vault (4) andfrontal sinus (1).Complete evaluationusing CT scanning
ofthe brain,eyes,andcraniofacial skeleton,combined with neu-
rosurgical,ophthalmologic,and craniofa-cial assessment,should be performed
toevaluate the injuries completely.A com-bined neurosurgical and
craniofacialreconstructive procedure is necessary forrepair ofthe injured
brain,dura,andskeleton.A coronal (skin) incision pro-vides the best exposure ofthe
fracturedregions and surrounding normal struc-tures.Once the brain and dural
injurieshave been managed by the neurosurgeon,reduction and stable fixation
(microplatesand screws) ofall fractures are completedby the craniofacial
surgeon.When massivecomminution exists,bony defects are pre-sent,or complete
orbital roofreconstruc-tion is required,then autogenous cranialbone is harvested
and used.In a normallydeveloping child the skull will mature intothree clinically
reliable layers (outer table,medullary cavity,inner table) between theages of2 and
5 years.In these instances thebone ofthe cranial vault is suitable
forsplitting,yielding bone for grafting.Thesetechniques and a team approach to
theearly diagnosis and management ofcom-bined injuries are cost effective and
resultin a rapid facial rehabilitation for theinjured child.Naso-orbitoethmoid and
Frontal Sinus FracturesThe prevalence ofnaso-orbitoethmoidfractures closely follows
the developmentofthe paranasal sinuses.They are rarelyseen in children younger than
5 years,butthey become progressively more commonin adolescents and adults (Figure
27-3).Rowe reviewed his series ofpediatric frac-tures and found that injuries to
the middlethird ofthe face made up only 0.5% ofallpediatric fractures.16Kaban and
colleaguesreported no midface fractures in 109 pedi-atric facial fracture patients
from 1965 to1975.31During the next 10 years,withanother 184 fractures,they reported
only 5 midface fractures,all Le Fort III levelinjuries.Posnick and colleagues
reportedthat midface injuries seen at a major pedi-atric trauma center during a 4-
year periodmade up 17% ofa series of318 fractures in137 patients.53Kaban associated
thisincreased prevalence ofmidface injurieswith the increase in survival
ofpersonsinvolved in serious motor vehicle acci-dents,which may result in more
extensivefacial injuries in the survivors.65When dis-placed naso-orbitoethmoid
fractures dooccur in children,we have adopted thesame open reduction and internal
fixation(ORIF) techniques generally accepted foradult-type injuries.Stable internal
fixationtechniques (micro- and miniplates andscrews) and primary autogenous
cranialbone grafts when indicated,result in theanatomic healing required to achieve
satis-factory rehabilitation ofthe child withfacial injury.28,33,66�74As in the
adult,when the medial can-thal ligament is displaced,it usuallyremains attached to
a bone fragment.Themedial canthal ligament and bone frag-ment are repositioned and
fixed withoutthe need for a direct medial canthopexy.Formal medial canthopexies
often con-tribute to an unnatural appearance andshould be avoided ifpossible.Often
thebony fragment(s) can be repositioned withthe aid ofmicroplates and screws with
orwithout the use ofa transnasal wire.Frontal sinus injuries in children
areapproached in a similar way to those intheir adult
counterparts.75,76Anteriorfrontal sinus wall fractures are
anatomicallyreconstructed and stabilized to preventcontour deformity.When the
fracture com-ponents are severely comminuted,autoge-nous cranial bone grafts can be
used toreplace the entire unit.Depending on the
Pediatric Craniomaxillofacial Fracture Management533extent offrontal sinus
development andinjury,the mucous membranes may required�bridement with maintenance
ofa patentfrontonasal duct or,in cases offractures ofthe ducts,sinus obliteration
with sealing ofthe duct.Ifthe posterior frontal sinus wallis injured,neurosurgical
consultation helpsdetermine whether cranialization ofthesinus through an
intracranial approach isrequired.77Since CSF leaks are commonwith dural tears in
these injuries,it is oftenhelpful to place bone,fibrin glue,and apericranial flap
in the defect to prevent CSFleaking.A double-ring sign is seen on filterpaper when
CSF is present within nasalFIGURE27-2A 16-year-old girl sustained frontal and upper
orbital trauma when she hit her forehead on the dashboard in a motor vehicle
accident.Initially the cere-brospinal fluid (CSF) leak was repaired through a local
scalp laceration; minimal attention was given to her frontal and orbital
fractures.Ongoing CSF leak withmeningitis and loss ofthe frontal bone flap
occurred,after which she was referred to Posnick and colleagues,and a delayed
combined neurosurgical/craniofacialapproach was carried out.A,Frontal view before
the delayed surgery.B,Frontal view 1 year after reconstruction.C,Oblique view
before the delayed surgery.D,Obliqueview 1 year after reconstruction.E,Three-
dimensional computed tomography (CT) scan offrontal bone defect.F,Intraoperative
view ofdural tear resulting in trau-matic encephalocele.Access
craniotomy/osteotomies allow exposure for reconstruction oforbital roof/medio-
orbital wall defects.G,CT scan ofthe anterior cranial baseand orbital roof/medio-
orbital wall defects.H,Intraoperative view offrontal bone defect and displaced
orbital rim fractures.(CONTINUEDONNEXTPAGE)ABCDFHEG
534Part 4: Maxillofacial Traumafluid.Alternatively,�2-transferrin can bemeasured
within the nasal fluid to deter-mine ifnasal leaking is indeed CSF.Endo-scopic
techniques with imaging guidancecan be used to effectively repair persistentleaking
that may occur postoperatively.Le Fort (Midface) FracturesThe prevalence ofLe Fort
midface frac-tures increases rapidly once aeration ofthemaxillary and ethmoid sinus
cells hasoccurred.The rapid development ofthesinuses takes place between 6 and 12
yearsofage.Consequently maxillary fracturesin children do not follow the patterns
seenin adults.Displaced midface fracturesshould be treated with ORIF
techniquessimilar to those used in adults.13,78This isnecessary to achieve and
maintainanatomic restoration.Closed reductiontechniques may be preferred in
specificclinical situations to avoid injury to theunerupted permanent dentition,but
thedental injuries are generally the result ofthe trauma event rather than
ofreductionand fixation techniques that have beencarried out by an experienced
surgeonfamiliar with the dentition.In Posnick and colleagues study 23patients
sustained 31 fractures in the midfa-cial region.These included nasofrontoeth-moid
fractures (13 of31,42%),Le Fort I (8 of31,26%),Le Fort II (5 of31,16%),andLe Fort
III (5 of31,16%).Midfacial frac-tures generally occurred as part ofa com-plex
facial fracture pattern;only 2 of31 (6%) occurred in isolation.Although fewacute
midfacial fractures occurred,themajority (9 of12) required surgery (Figure27-
4).Unstable or displaced fractures weretreated with open reduction and internal
fix-ation.The surgical goals in such cases are torestore midface projection,facial
width,andorbital volume,and to normalize occlusalrelationships.Seven ofnine
midfacial frac-tures were stabilized with plates and screws.A circumvestibular
intraoral mucosalincision provides ideal exposure ofmaxil-lary fractures through
the zygomatic but-tress,anterior maxillary wall,and piriformnasal aperture
regions.When additionalaccess to the zygomatic arch,frontozygo-matic
suture,supraorbital ridge,and fron-tonasal junction is required,a coronal(skin)
incision is also used.Ifspecificexploration ofthe infraorbital rims,orbital
floors,and lower aspects ofthemedial orbital walls is required,a subcil-iary,lower
lid,or transconjunctival inci-sion is added.Palatal incisions are to beavoided,and
preservation ofthe gingiva isimportant to the child�s periodontalhealth.As in the
case ofadults the restora-tion ofnormal anatomic position ofthemidfacial skeleton
generally requires openreduction,stable fixation (miniplates andmicroplates and
screws) and may rarelyrequire autogenous cranial bone grafts orthe placement
ofalloplastic materials.Zygomatic Complex FracturesA zygomatic complex fracture
describes afracture through the frontozygomaticsuture,zygomatic arch,infraorbital
rim,and zygomatic buttress.Fracture throughthe orbital floor and lateral orbital
wallcompletes the quadripod injury.The extentofdisplacement ofthe zygomatic
complexfracture is best clarified through CT scan-ning in the axial and coronal
planes anddefines the extent ofsurgery necessary torestore and maintain preinjury
anatomy.The child�s presenting physical findings aresimilar to those seen in the
adult.Theygenerally include periorbital ecchymosis;paresthesia over the zygomatic
arch,lateralnose,cheek,upper lip,and anterior maxil-lary teeth;and subconjunctival
hemor-rhage.79Ophthalmologic consultation isessential to determine baseline
ocularglobe and extraocular muscle injury anddysfunction.Since the base ofthe
lateralorbit is made up ofthe zygomatic bone,FIGURE27-2 (CONTINUED)I,Intraoperative
view offronto-orbital reconstruction with split cranialgrafts and plate/screw
fixation.Note the right parietal donor site with split cranial
reconstruction.J,Intraoperative view ofcranial vault after reconstruction.K,Three-
dimensional CT scan views ofreconstructed cranial vault and orbits.Reproduced with
permission from Posnick JC et al.133JKI
Pediatric Craniomaxillofacial Fracture Management535fractures within the orbital
floor frequentlyrequire management in conjunction withrepositioning ofthe
zygoma.Some injuriesrequire reconstruction ofthe orbital floorwith autogenous bone
or synthetic materi-als.Ofthe eight acute zygoma fracturesobserved in Posnick and
colleagues�study,three were minimally displaced and man-aged without surgery.The
five displacedfractures were comminuted injuries thatwere treated with open
reduction and inter-nal fixation.Three ofthese fractures werestabilized with plates
and screws.Most zygomatic complex fractures canbe approached and reduced using
multipleapproaches such as maxillary vestibular,lower eyelid,and brow incisions.Ifa
badlycomminuted zygomatic arch is associatedwith a displaced zygomatic complex
frac-ture,a coronal (scalp) incision may be usedwith intraoral and subciliary (or
lower lidor transconjunctival) incisions to expose,explore,reduce,graft,and
internally fix allfractured regions.78With a minimally dis-placed or incomplete
fractured zygoma,more limited treatment is used to achieveadequate fracture
reduction.This can beFIGURE27-3A 5-year-old girl who was in a motor vehicle
accident sustained orbitonasal,ethmoid,and frontal bone fractures with associated
brain and duralinjury with cerebrospinal fluid leak.She required a combined
neurosurgical/craniofacial procedure.A,Frontal view 6 days after surgery.B,Frontal
view 2 yearsafter (single-stage) reconstruction.C,Oblique view 6 days after
surgery.D,Oblique view 2 years after reconstruction.E,Worm�s-eye view 6 days after
surgery.F,Worm�s-eye view 2 years later.G,Intraoperative view ofreconstructed
orbitonasal and frontal fractures.Stabilization is with titanium plates and
screws.H,Intraoperative close-up view ofreduced orbitonasal and frontal fractures
stabilized with titanium plates and screw fixation.Medial canthopexies were also
car-ried out (note location ofwires).Reproduced with permission from Posnick
JC.134ABCDEFGH
536Part 4: Maxillofacial Traumadone through a Gillies�approach withinthe temporal
scalp,an eyebrow incision,ora Keene approach from an intraoralvestibular
incision.Blow-Out and Blow-In Fractures ofthe OrbitBlow-in and blow-out fractures
ofone ormore orbital walls and/or floor may beassociated with more complex
fractures(eg,anterior cranial vault/upper orbital,naso-orbitoethmoid,Le Fort
midface,orzygomatic complex fractures) or mayoccur as isolated injuries.80�83The
key tothorough evaluation is complete clinical,ophthalmologic,and CT scan assess-
ments.84A thin-sliced axial and coronal CTscan is completed to visualize all
fourorbital walls and/or floors to ensure thatthe presence and extent ofall blow-in
orblow-out fractures are recognized.Theophthalmologic assessment may
requirepupillary dilatation and slit-lamp evalua-tion in the ophthalmologic
suite.Orbital fractures are common in chil-dren and were frequent in Posnick
andcolleagues�study;41 patients sustained 73separate fractures ofthe orbit.The
distrib-ution offractures within the orbit includ-ed the floor (23 of73,32%),medial
wallFIGURE27-4A 14-year-old boy sustained combined Le Fort I and II fractures with
bilateral orbital blow-out fractureswhen he was accidentally kicked in the face
while playing competitive soccer.A,Frontal view before repair.B,Frontal view1 year
after (single-stage) reconstruction.C,Occlusal view before repair.D,Occlusal view 1
year after reconstruction.E,Illustration before and after reduction and fixation.
(CONTINUEDONNEXTPAGE)ABCDE
Pediatric Craniomaxillofacial Fracture Management537(14 of73,19%),and orbital
roof(13 of73,18%).Only 7 ofthese orbital fractureswere sustained as isolated
injuries.Oftheacute fracture group,21% ofthe fractureswere orbital fractures.These
were treatedboth surgically (59%) and nonsurgically(41%) (see Table 27-4).Most
ofthe orbitalinjuries that were managed operativelywere minimally displaced floor
fractures.Thirty�two percent oforbital fractureswere managed by
exploration,reduction,and grafting with autogenous material butwithout graft
fixation (Figure 27-5).Plate-and-screw fixation was used in six orbitalrim
fractures and three rooffractures.With the collaboration ofa neurosurgeon,displaced
rooffractures (blow-in frac-tures) were routinely treated with openreduction via an
intracranial approach.The roofwas reconstructed with con-toured calvarial bone
grafts fixed withplates and screws.Once a clinically and
radiographicallysignificant orbital wall and/or floor injury isrecognized,early
exploration and reposi-tioning ofthe soft tissues back into the orbitwith
simultaneous reconstruction ofinjuredorbital walls and/or floor to
appropriatedimensions and overall intraorbital volumeis carried out.80,85Because
the complicationsofextraocular muscle entrapment,diplopia,and enophthalmos are
difficult to treat later,early evaluation ofpatients at high risk,fol-lowed by
prompt surgical intervention,isencouraged.Orbital wall and/or floor frac-tures heal
rapidly in children and result in ahigher incidence ofscar cicatrization
oftheherniated orbital soft tissues than in adults.Nasal FracturesNasal fractures
are also common in thepediatric population.Ofthe few acute nasalfractures that
occurred in the author�s series(12 of171,7%),58% were minimally dis-placed and did
not require surgery,and33% were treated by closed means.Onlyone fracture required
open reduction.Many isolated nasal fractures were treatedon an outpatient basis.The
nasal fracturesseen by Posnick and colleagues in this studywere generally
associated with other facialfractures and were therefore not represen-tative
ofnasal fractures seen in general atthe hospital (emergency department).Development
ofthe nasal septum isthought to be a major factor in midfacegrowth.In theory,trauma
to the nasalregion early in childhood will negativelyimpact on midface
growth.86Although thenose is the most frequently fractured partofthe face in a
child,extensive midfacegrowth retardation after trauma has onlyrarely been
documented.86Nasal injuries are often recognized butthen ignored as unimportant.Two
seriouspitfalls in treating nasal fractures in chil-dren are (1) failure to
recognize adjacentbony injuries extending outside the noseand (2) septal hematoma
after nasal trau-ma (which may in theory result in septalnecrosis and
perforation).Diagnosis ofnasal and septal fractures is usually basedFIGURE27-4
(CONTINUED)F,Computed tomography (CT) scan demonstrating nasofrontal bone
separation and com-minuted medial orbital walls.G,Three-dimensional CT views
demonstrate Le Fort II fracture with nasofrontal separa-tion and location ofthe
infraorbital rim and maxillary fractures.H,CT scans demonstrating the morphology
ofthe mid-face after reconstruction.A�D,F�H reproduced with permission,E adapted
from Posnick JC.132FHG
538Part 4: Maxillofacial Traumaon clinical examination.Radiographicconfirmation can
be made with CT scansor plain films ofthe nose,but these areusually not necessary
for clinically appar-ent and isolated nasal septal fractures.Dis-placed nasal bone
and nasal septal frac-tures should be reduced and stabilizedwith splints in a
similar manner as is donein adults.This should be completed with-in several days
ofthe injury,as childrenheal more quickly than adults,makingrepositioning ofthe
small nasal bone frag-ments more difficult with time.Mandibular FracturesThe lower
jaw ofa child represents anevolving anatomy that affects the patternoffractures
seen at varied ages (Figures27-6 and 27-7).Mandibular fracture pat-terns are
affected by the fact that thechild�s jaws are filled with teeth at variousstages
ofdevelopment at differentages.15,18,40�46,64,87�91Injury to the develop-ing bone
and tooth buds may result fromthe trauma ofthe fracture,the surgicaltechnique,or
complications oftreatment(eg,nonunion,malunion,infection).47In Posnick and
colleagues�studymandibular fracture sites included thecondyle (59
of107,55%),parasymphysis (29of107,27%),body (10 of107,9%),and angle(9
of107,8%).Thirty-nine percent ofall frac-tures in the study were ofthe
mandible.Ofthose treated,18 of28 (64%) were treatedwith closed reduction,most
ofwhich werecondylar process fractures with an element ofmalocclusion.Only two
condylar processfractures were opened.Both were low sub-condylar mandibular neck
fractures associat-ed with other injuries in the mandible.Mini-mally displaced body
and angle fractures witha satisfactory occlusal relationship were fre-quently
treated with maxillomandibular fixa-tion.Displaced or comminuted fractureswere
treated with open reduction and internalfixation,and this treatment was used
mostfrequently for parasymphyseal injuries (53%)and angle fractures (24%) (see
Table 27-4).A surgeon familiar with the evolvingdentition is able to apply arch
stabilizationand maxillomandibular fixation,whenindicated,in dentulous children
ofall ages.Obstacles to the usual application ofsurgi-cal arch bars are overcome
with the use ofskeletal fixation:circum-mandibular,cir-
cumzygomatic,infraorbital,anterior nasalspine,and piriform aperture wires areused
for additional support.When inter-nal fixation techniques are required,care-ful
application ofmicroplate or miniplateand screw fixation,generally with unicor-tical
screws strategically placed along thethick cortical inferior border combinedwith
arch bar stabilization,is often theleast traumatic and most stable option.Knowledge
ofthe location ofdevelopingteeth allows the surgeon to place internalfixation as
needed,with minimal trauma.The general principles oftreatingmandibular fractures
are the same in chil-dren and adults:anatomic reduction iscombined with
stabilization adequate tomaintain it until bone union has occurred.With the
exception ofmandibular condylefractures,we frequently find that the judi-cious use
ofORIF is preferable to the closedreduction and immobilization techniqueswith
splints when treating fractures in thedeciduous and mixed dentition.Some sur-geons
believe that minor degrees ofmalu-nion may be self-correcting in children orat
least amenable to orthodontic alignment.This margin ofsafety should not be used
asan excuse for inadequate treatment.Mandibular Condyle and Subcondyle Frac-
turesInjury to the mandibular condylarprocess may affect jaw growth and temporo-
mandibular joint (TMJ) function.18,31,33,92�109The mandible is the final facial
bone to com-plete normal growth,and injury to thecondylar growth center before
skeletal matu-rity may lead to growth retardation on theFIGURE27-5A 4-year-old boy
sustained an isolated blow-out fracture ofthe left orbital floor withentrapment
ofthe inferior rectus muscle through the floor defect.He underwent explorative
surgerywith repositioning ofthe orbital contents back into the orbit.Reconstruction
ofthe orbital floor defectwas with a split cranial graft taken from the
temporoparietal region.A,Frontal view with eyes inupward gaze demonstrating left
inferior rectus entrapment.B,Close-up view early after reconstruc-tion
demonstrating improved upward gaze ability.C,Comparison oftwo-dimensional coronal
slicedcomputed tomography scans through the midorbits before (left) and after
(right) reconstruction.Reproduced with permission from Posnick JC.132ABC
Pediatric Craniomaxillofacial Fracture Management539ipsilateral side,resulting in
facial asymmetryand malocclusion.Once a mandibular condylar fractureoccurs,a degree
ofTMJ degenerativechanges or growth restriction is a likely sce-nario despite the
treatment option selected.Condylar injuries represent a wide spec-trum
offractures,dislocations,and com-pression injuries.They may be intracapsularor
extracapsular,displaced or nondisplaced,comminuted or noncomminuted,open
orclosed,located low or high in the condylarneck,medial or lateral pole
fractures,andisolated injuries or associated with morecomplex facial fractures.The
treatment ofa fracture ofthemandibular condyle remains controver-sial.110�124Most
authors and clinicians con-tinue to advocate a nonoperative approach,whereas a few
prefer the use ofopen reduc-tion techniques.The frequency ofless thanideal results
seen with varied treatmentsgiven for similar injuries is a reflection ofthe
irreversible injury that may occur tothe highly differentiated and specializedTMJ
structure.Despite a great deal ofsur-geon interest and experience over the
yearswith open reduction techniques,its propo-nents have not been able to
convincinglydemonstrate a lower incidence ofgrowthdisturbance,TMJ
ankylosis,internalderangement ofthe TMJ,loss ofposteriorfacial height,or
malocclusion in theirpatients.Although endoscopic techniqueshave been reported,a
detailed analysis ofoutcomes is lacking and the benefitsremain to be seen.125Open
reduction ofa condyle fracturemay be warranted in a child in
someinstances.122�124Indications may includethe following:�Displacement into the
middle cranialfossa�Unacceptable occlusion after a closedtechnique trial has
failed�Avulsion ofthe condyle from thecapsule�Bilateral fractures ofthe condyles
withcomminuted midface fracturesWe continue to advocate a nonopera-tive approach
for most condylar and sub-condylar fractures in young children.Ashort period
ofpartial immobilization withelastics is generally useful for patient com-fort,to
encourage soft tissue healing,and tolimit the conversion ofa greenstick or min-
imally displaced fracture into a complete orfully displaced one.Ten to 14 days
ofuse offirm elastics is generally enough to accom-plish these goals and still
allow earlyincreased range ofmotion to limit the like-lihood ofthe development
ofTMJ fibrosisor ankylosis.Instituting a regimen ofphysi-cal therapy for several
months is importantto avoid TMJ fibrosis or ankylosis.When a condyle fracture
occurs and theuse offirm elastics needs to be limited toreduce the incidence ofTMJ
sequelae,thefixation technique selected for additionalsimultaneous maxillary and
mandibularFIGURE27-6Illustration ofthree skulls ofvarious ages(A,2 years;B,6
years;C,12 years).Different methods ofachieving arch bar stabilization at dif-
ferent ages including circum-mandibular,circumzygomatic,infraorbital,and piriform
aperture wires.Adapted from Posnick JC.135ABC
540Part 4: Maxillofacial Traumafractures should be carefully considered.The common
occurrence ofa combinedparasymphyseal and condylar fracture willwarrant a more
stable form ofparasymphy-seal fracture fixation (miniplates andscrews) so that
early active mandibularrange ofmotion with TMJ function canoccur.Instituting a
liquid diet for a limitedtime period even after firm elastic use maybe helpful in
preventing displacement ofparasymphysis or body fractures.When amandibular angle
fracture occurs in thepresence ofa condyle fracture,the com-bined forces may be
significant enough tocause displacement unless ORIF at the anglefracture is carried
out.The advantages ofcontinuous passivemotion (CPM) for the healing ofinjuredjoint
surfaces have been well documented inexperimental animals.126�128Salter and col-
leagues concluded that chondrogenesis inthe healing offull-thickness defects in
therabbit femur occurs through differentiationofthe pluripotential cells ofthe
subchondralFIGURE27-7An 11-year-old boy sustained multiple facial trauma in a
waterskiing accident.Theinjuries included a left intracapsular condyle fracture,a
right low condylar neck fracture,a rightparasymphyseal fracture,dentoalveolar
injuries,and multiple facial lacerations.A,Frontal viewbefore fracture
reduction.B,Full-face view 2 years after reconstruction,with facial symmetry
andgood facial nerve function.C,Oblique view 2 years after
reconstruction.D,Demonstration of40 mm ofvertical opening 2 years after
reconstruction.E,Occlusal view 2 years after reconstruc-tion.F,Illustration
offractures before and after reduction and fixation.G,Intraoral view ofdis-placed
right parasymphyseal fracture.(CONTINUEDONNEXTPAGE)ABCDFEG
Pediatric Craniomaxillofacial Fracture Management541bone to chondrocytes as a
result ofthe stim-ulation provided by CPM ofthe joint.126,127They documented
improved healing ofintra-articular fractures with the use ofCPMcompared with
immobilization.128The useofCPM in the treatment ofTMJ disordersand for the early
management ofacute TMJinjuries seems to have promise but has notbeen used
often.Conversely the use ofextended periods ofimmobilization oftheacutely injured
TMJ appears to be counter-productive.A regimen ofphysical therapyfor the TMJ after
an initial phase ofimmo-bilization is recommended for optimal reha-
bilitation.Also,functional appliances havebeen used in an attempt to reestablish
verti-cal height to foreshortened fracture sites inthe early injury phase.Although
case serieshave shown good results,no outcome dataare available that show a clear
advantage tousing this technique.104Since growth distur-bance is a concern with
these injuries,long-term follow-up is necessary to evaluate thepossible development
ofasymmetry.Parasymphyseal FracturesWhen mar-ginal reduction and fixation
techniquesare used for parasymphyseal or symphy-seal fractures,a small
dentoalveolar gapoften occurs between the two teeth adja-cent to the fracture
site.Using open reduc-tion techniques with stable (miniplate andscrew) fixation at
the inferior border,com-bined with reduction and stabilization atthe dentition with
an arch bar,gives amore reliable bony union ofthe injurywithout
displacement.Plating at the tension-band zone is not recommended inthe mixed
dentition.Body FracturesBody fractures ofthemandible usually have favorable
�musclepull�vectors on the segments,whichencourage reduction rather than displace-
ment.In these situations closed reductiontechniques with maxillomandibular fixa-
tion generally suffice.Alternatively theskilled surgeon can place inferior
borderplates and screws with the aid ofa trans-cutaneous trocar and intraoral
incision.When extended maxillomandibular fixa-tion must be avoided
(eg,associatedcondyle fracture or severe trauma),morestable forms ofinternal
fixation (platesand screws) are indicated.Dentoalveolar InjuriesAnterior maxil-lary
and mandibular teeth and their sup-porting alveolar structures often bear thebrunt
oflower face injuries,and as a resultdentoalveolar injuries are very commonin the
pediatric population.43,111,129�131The teeth may be concussed,subluxed,FIGURE27-7
(CONTINUED)H,Intraoral view ofreduced and plate/screw stabilized right
parasymphyseal fracture.I,Computed tomography (CT) scans demonstrating left
intracapsular condyle fracture and right condylar neck fracture.J,CT scans
demonstrating right parasymphyseal fracture.K,Postoperative Panorex radiograph
demonstrating reductionand fixation offractures.A�E,G�K reproduced with
permission,F adapted from Posnick JC.135HIKJ
542Part 4: Maxillofacial Traumapartially or totally avulsed,or intruded.InPosnick
and colleagues�study dentoalveo-lar fractures were evenly distributedbetween the
mandible and the maxilla.Thirty-two children sustained 44 fractures,8 ofwhich were
isolated.Teeth that areloosened should be returned to their nor-mal position in the
tooth socket and alveo-lar segments reduced to their preinjuryposition.The reduced
teeth and alveolarsegments should be immobilized untilhealing occurs.Isolated
dentoalveolarinjuries may be adequately reduced underlocal anesthesia and then
stabilized withthe application ofacid-etch bonding tech-niques and a braided
wire.Arch bars can behelpful in select cases but often will extrudethe teeth.The
selected splinting techniquesmust meet certain criteria,including
easyfabrication,maintenance ofonly passiveforces on the teeth,lack ofirritation to
thesoft tissues,maintenance ofnormal occlu-sion,allowance ofgood oral
hygiene,accessfor subsequent endodontic treatment,andeasy removal.Longitudinal
reassessmentwith a pediatric or general dentist isimportant because ankylosis
ofprimaryteeth may prevent the normal eruption ofpermanent teeth.Resorbable
Fixation MaterialsTitanium alloy plates and screws are thestandard for
craniomaxillofacial fixation.The use ofplate and screw titanium fixa-tion in the
craniomaxillofacial skeletonhas consistently resulted in low compli-cation rates
and excellent biocompatibil-ity.However,controversy associated withtheir use in
growing bones has led to thedevelopment ofresorbable fixationmaterials.Issues
ofbiocompatibility,strength,bulk,inflammatory response,and predictable resorption
rates contin-ue to be discussed.Most resorbable plateand screw fixations use isomer
configu-rations ofalpha-hydroxy polylactic andpolyglycolic acids.Possible
advantages ofresorbable fixa-tion include the following:�Degradation ofthe material
by the cit-ric acid cycle into CO2and H2O�No interference with imaging (CT,magnetic
resonance imaging,standardradiographs)�No effect on postoperative
radiationtreatment�The possibility ofintegrating sub-stances such as antibiotics
within thefixation materialPossible disadvantages ofresorbablefixation include the
following:�Less mechanical strength when com-pared with titanium alloys
ofsimilarsizes ��Memory�ofthe material,which maydistort reduction offracture
�Increased reactivity during the degra-dation phase�Increased operative working
timeSummaryThe pattern ofcraniomaxillofacial frac-tures seen in children and
adolescentsvaries with evolving skeletal anatomyand socioenvironmental
factors.Facialfractures in children may go unrecog-nized as a result oflimited
communica-tion,incomplete radiographic examina-tion,or the late presentation
ofthepatient by the family.Recognition ofthedifferences between children and
theiradult counterparts is important in facialrehabilitation.Consideration should
begiven to open reduction ofthe fractures,primary autogenous cranial bone graft-
ing,and the use ofstable forms offrac-ture fixation (miniplates and microplatesand
screws).Late sequelae ofpediatricfractures occur even when appropriateand prompt
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CHAPTER 28Management ofPanfacial FracturesPatrick J.Louis,DDS,MD Management
ofpatients with multipledisplaced and comminuted fractures canbe extremely
challenging not only forthose who are inexperienced but also forexperienced
surgeons.Improper diagno-sis,treatment planning,and sequencingproduce inadequate
results and canlengthen procedure time.However,withthe availability ofdetailed
imaging,1�3ridged fixation,4�6bone grafting tech-niques,7�9and proper
sequencing,4,10,11outcomes can be optimized.All facets offacial form and
functionare important,and one should strive to pre-serve them.The importance
ofproperocclusion cannot be underestimated sinceacute changes in the way teeth come
togeth-er can be readily detected by the individ-ual.12Such alterations can result
in myofas-cial or temporomandibular joint pain.13Reestablishing the patency ofthe
nasal cav-ity is important in the prevention ofnasalobstruction and potential
problems such assinusitis and obstructive sleep apnea.14,15Itis also required to
establish the proper qual-ity ofspeech.16Small changes in orbital vol-ume can
result in enophthalmos and/ordiplopia.17,18The reestablishment
offacialheight,width,and projection is importantfor the prevention offacial
deformities andfor the psychological and social well-beingofthe individual.19�21No
one ofthese fac-tors can be considered more importantthan the other;together they
constitute theface and its associated functions.In this chapter,discussion is
presentedon some ofthe historic perspectives,etiol-ogy,anatomic
considerations,imaging,bone grafting,soft tissue resuspension,sequencing
oftreatment,and complica-tions as they relate to the management ofpanfacial
fractures.Historic PerspectivePanfacial fracturesare defined as thoseinvolving the
upper,middle,and lowerthirds ofthe face.4These complex injuriesare fractures that
involve the frontal bones,zygomaticomaxillary complex,naso-orbitoethmoid
region,maxilla,andmandible.Complex facial injuries such asthese are generally the
result ofhigh-velocity trauma.22Prior to the advent ofrigid fixation
techniques,23�25these frac-tures were treated with wire fixation andhead
frames.26�28With these techniques itwas difficult to establish and maintain
thethree-dimensional stability ofthe facialskeleton.There have been several
importantadvances in the management ofmaxillo-facial trauma that have resulted
inimproved outcomes.These include thedevelopment ofhigh-resolution comput-ed
tomography,rigid fixation techniques,soft tissue resuspension,and primarybone
grafting.All ofthese have made asignificant impact on the diagnosis andtreatment
ofpanfacial injuries;each isdiscussed later in this chapter.EtiologyPanfacial
fractures result from motor vehi-cle collisions,assault,sports-related acci-
dents,industrial accidents,and gunshotwounds.22,29�32Since gunshot wounds
areaddressed in Chapter 26,and becausethere is usually associated soft tissue dam-
age causing them to generally require dif-ferent principles ofmanagement,they
arenot discussed in this chapter.Anatomic ConsiderationsFacial ButtressesMany
authors have described the buttressesofthe face both in vertical and
horizontalplanes.10,32�34The vertical buttresses includethe
nasomaxillary,zygomaticomaxillary,andpterygomaxillary buttresses (Figure 28-1).The
nasomaxillary buttress includes themaxillary process ofthe frontal bone andthe
frontal process ofthe maxilla,extendinglateral to the piriform rim.The zygomati-
comaxillary buttress is composed ofthezygomatic process ofthe frontal bone,lat-eral
orbital rim,lateral zygomatic body,andzygomatic process ofthe
maxilla.Thepterygomaxillary buttress includes thepterygoid plates ofthe sphenoid
and maxil-lary tuberosities.Usually the nasomaxillaryand zygomaticomaxillary
buttresses arereconstructed,but the pterygomaxillarybuttress is not because
ofinaccessibility.The condyle and posterior mandibular
548Part 4: Maxillofacial Traumaramus make up yet another buttress estab-lishing
posterior facial height.The horizontal buttresses are alsodescribed as anterior
posterior buttresses.10These include the frontal,zygomatic,maxillary,and mandibular
buttresses(Figure 28-2).The frontal buttress iscomposed ofthe supraorbital rims
andthe glabellar region.The zygomatic but-tress consists ofthe zygomatic arch,zygo-
matic body,and infraorbital rim.Themaxillary and mandibular buttresses arecomposed
ofthe basal bone ofthe maxil-la and mandible arches.None ofthese buttresses exists
in avacuum.Together they give the facialskeleton its structural integrity.The
boneis generally thicker over these describedareas to neutralize the forces
ofmastica-tion or impact.With the proper reductionofthese buttresses,we are able to
recon-struct the height,width,and projection ofthe face.Key LandmarksWhen there are
multiple facial fracturesinvolving the upper,middle,and lowerface,reconstruction
should be approachedas a puzzle.Known landmarks and anato-my can be used to
reconstruct more pre-cisely those areas that have been damaged.Some key landmarks
that may help inestablishing the proper positioning ofthefacial skeleton include
the dental arches,mandible,sphenozygomatic suture,maxil-lary buttress,and
intercanthal region.Dental ArchesWhen one or both ofthe dental arches
areintact,they can be used as guides.Forexample,ifthe patient has suffered a LeFort
fracture but no midpalatal split,themaxilla,as an intact arch,can be used toset the
mandibular arch and establishproper width.Particularly problematic isthe situation
in which there is a mid-palatal split and the mandible is also frac-tured along the
tooth-bearing region,with associated condyle fractures.Thiscan easily lead to
widening ofthe entirefacial complex ifthese segments are notproperly reduced.One
approach to thisproblem is to reestablish the maxillarywidth by exposing the
palatal fracture,then reducing and fixating the region(Figure 28-3).34�37This
approach workswell ifthere is a solitary midpalatal frac-ture without comminution
or avulsion.Asecond approach is to obtain impressionsfor fabrication ofdental
models.Simulat-ed surgery can then be performed on theupper and lower casts and a
surgical splintfabricated (Figure 28-4).38,39This is by nomeans a foolproofmethod
when both theupper and lower arches are fractured.Themore severe the injury
(ie,multiple seg-ments),the more difficult it is to establisha preinjury
occlusion.Ifthe patient hasdental models ofhis preinjury occlusionPosterior
mandibularramus/condylePterygomaxillaryZygomaticomaxillaryNasomaxillaryFrontalZygom
aticMaxillaryMandibularFIGURE28-1Vertical buttresses ofthe face.FIGURE28-2The
horizontal buttresses ofthe face.
Management ofPanfacial Fractures549from previous orthodontic or
prostheticrehabilitation,these can provide invalu-able clues to establishing the
proper archform.A third option is to reconstruct themandible since this is
generally a robustbone that can undergo anatomic reduc-tion ifattention is paid to
detail.The MandibleAnatomic reduction at the symphysisand/or body can be achieved
with anextraoral exposure ofthe fracture.Suchexposure allows for direct
visualizationofthe inferior border and,to a lesserdegree,the lingual cortex.The
reductionofboth the buccal and lingual corticalsurfaces prior to fixation yields
betterresults (Figure 28-5).40,41When bilateralsubcondylar fractures are
present,theymust be treated to establish the posteriorfacial height and facial
width.Whenbilateral subcondylar fractures are pre-sent and there is an associated
fracturealong the symphysis and/or body region,the mandible may undergo
splaying,with a resultant increase in facial width.The lateral pterygoid muscle
attachmentat the pterygoid fovea,as well as the lat-eral capsular ligament ofthe
temporo-mandibular joint,acts to preventextremes ofmovement laterally.Themandibular
condyle can be reconstitutedto the mandibular ramus to help estab-lish facial
height and width.Sphenozygomatic SutureThe sphenozygomatic suture,along theinternal
surface ofthe lateral orbital wall,has been shown in cadaver studies to be akey
landmark for both the reduction andfixation ofthe zygomaticomaxillary com-
plex.42�44Ifother aspects ofthe facialskeleton are ignored,use ofthis suturealone
can result in errors;however,iftheorbital roofand superior lateral orbit
areintact,this suture can be an importantlandmark for the proper positioning
ofthezygoma and zygomatic arch.The sphe-nozygomatic suture is usually exposedalong
the internal surface ofthe lateralorbital wall (Figure 28-6).Once reduced,a small
plate is placedacross this fracture for fixation.Since theFIGURE28-3Reduction and
fixation ofapalatal fracture using a miniplate.FIGURE28-4Dental models from one
patient: postorthodontic models (A),post-trauma models (B).Model surgery has been
performed on these casts using the postorthodontic models as a guide
(C).ABCFIGURE28-5Nonreduced mandibular fractureinvolving the symphysis and condylar
process(A).Poorly reduced mandibular symphysis frac-ture with nonreduced lingual
cortex and lateraldisplacement ofthe mandibular angles (B).Well-reduced mandibular
symphysis and condy-lar process fractures (C).Note the approxima-tion ofthe lingual
cortex in the symphysis region.ABC
550Part 4: Maxillofacial Traumaorbital roofand superior lateral orbit arerarely
fractured,they are usually accuratelandmarks.Likewise,the zygomatic but-tress is
important in establishing theproper position ofthe zygoma and/ormaxilla.Once the
zygoma is in the prop-er place,the location ofthe maxilla canbe verified.This broad
area ofsurfacecontact aids in the reduction and fixationprocess.Ifthere is
significant bone loss inthis region,consideration should begiven to primary
grafting to reestablishthis buttress.Intercanthal RegionThe intercanthal region may
also be used toreestablish midfacial width since the inter-canthal distance is
fairly constant in theadult facial skeleton.45Restoration oftheproper intercanthal
distance via reductionofthe naso-orbitoethmoid complex canhelp to determine facial
width (Figure 28-7).10 This depends mainly on the fracturetype.Ifthere is minimal
or no comminu-tion in the region,proper reduction can aidin reestablishment
offacial form.Unfortu-nately,many times this area is severely com-minuted and is
oflittle help.Establishingthe proper intercanthal distance throughmeasurement is
usually performed in caseswith severe comminution.ImagingImaging ofthe facial
skeleton has gonethrough a gradual evolution in the area offacial trauma.Plain film
radiography andlinear tomography were the gold standarduntil the advent ofcomputed
tomography(CT).46�49CT has improved our ability toimage the facial skeleton and
obtain detailsnot possible with plain films (Figure 28-8).1It allows the clinicians
to determine not onlythe location offractures but also the degreeand direction
ofdisplaced segments.2,3Sincethe introduction ofCT,it has undergone anevolution
both in the quality ofthe imagesand its application.In a previous articleauthors
reported on �sophisticated CT,�inwhich 5 mm cuts through the facial skeletonwere
presented.2It is now a routine practiceat the University ofAlabama at Birminghamto
obtain 0.75 mm axial cuts with coronalreconstructions.This allows for three-
dimensional reconstruction (Figure 28-9),ifneeded,and decreases the number
ofrepeatscans.50,51The scans are loaded onto the hos-pital information system and
can be viewedon computers throughout the medical cen-ter and at remote
locations.This decreasescosts by avoiding the production ofmultiplehard copies,and
it improves efficiency.With current CT technology,the max-illofacial trauma surgeon
can evaluate thefracture pattern by viewing individual cutsor the three-dimensional
reconstructions.3This allows the surgeon to view necessaryFIGURE28-6Reduction and
fixation ofthesphenozygomatic suture.FIGURE28-7A,Clinical photograph ofpatientwho
has a naso-orbitoethmoid fracture with anintercanthal distance of43
mm.B,Intraopera-tive photograph showing exposure ofthe naso-orbitoethmoid
fracture.ABFIGURE28-8Computed tomography showing midfacial fractures and a left
condylar head fractureon the axial view (A),and a left condylar head fracture on
the coronal view (B).AB
Management ofPanfacial Fractures551details or the overall injury
pattern.Bymanipulating the image windows on amonitor,the surgeon can view hard
andsoft tissue details.Soft tissue details thatcan be viewed on CT are not
readilyapparent on plain films.These includeintracranial injuries,injuries to the
globe,presence and location offoreign bodies,extraocular muscle entrapment,soft
tissueavulsion,displaced teeth,and the airway.Ifa cervical spine injury is
suspected,it maybe imaged at the time ofcranial and max-illofacial imaging.The
combination ofphysical exami-nation and current CT imaging allows aclear treatment
plan to be generated.Thishelps greatly with sequencing at the
timeofsurgery.Surgical ApproachesApproaches to the facial skeleton in panfa-cial
trauma should permit wide exposureofthe fracture to allow for anatomicreduction.The
location and extent ofexposure are dependent on fracture sever-ity and
combination.The followingdescribes which fractures can be accessedthrough the
various surgical approaches(Figure 28-10):�Bicoronal flap
procedure:frontalsinus,naso-orbitoethmoid (superioraspect),medial canthal
tendon,supra-orbital rim,orbital roof,superioraspect ofthe medial and lateral
orbitalwall,zygomatic arch,and mandibularcondyle (with preauricular
extension)�Subciliary and transconjunctival inci-sion with lateral
canthotomy:infraor-bital rim,medial and lateral orbitalwall,and orbital floor.The
transcon-junctival incision with lateral cantho-tomy does allow access to the fron-
tozygomatic suture.This requiresdetachment ofthe lateral canthal ten-don and
incision through the orbicu-laris oculi muscle and periosteumdeep to the lateral
periorbital skin.The subciliary approach may allowbetter access to the lateral
nasal region�Upper eyelid crease incision:superiorand lateral regions ofthe
orbit.It is gen-erally used to expose the frontozygo-matic suture.This incision is
not need-ed when the bicoronal incision is used�Perinasal incisions:naso-orbitoeth-
moid region,medial canthal tendon,and nasolacrimal sac.These incisionsare generally
avoided because ofthepotential for significant scarring.Thisincision is not needed
when thebicoronal incision is used�Maxillary vestibular incision:maxillaand
zygomaticomaxillary buttress�Mandibular vestibular incision:mandible from the ramus
to the sym-physis.This approach is not usually rec-ommended for comminuted
fractures �Cervical incisions:mandible,except forwhen there is a high condylar
neckfracture.The approach is generallyindicated when anatomic reduction
iscrucial.It allows the surgeon to visual-ize the reduction ofthe lingual cortex.It
is also indicated for comminuted andcomplicated fractures such as a fractureofthe
atrophic edentulous mandibleBone Grafting and Soft Tissue ResuspensionTwo
procedures have improved outcomesin the management ofpanfacial trauma:ABFIGURE28-
9Aand B,Three-dimensional computed tomography images ofpatient with
extensivemidface injuries.Note the detail and quality ofthe
images.abcdefghFIGURE28-10Surgical approaches to the facial skeleton:bicoronal with
preauricular extension (a),paranasal (b),superior tarsal crease (c),subciliary
(d),transconjuncti-val with lateral canthotomy (e),maxillary vestibule
(f),mandibular vestibule (g),cervical crease (h).
552Part 4: Maxillofacial Traumaprimary bone grafting and resuspension ofthe soft
tissue after extensive exposure ofthe facial skeleton.7�9As previously dis-
cussed,the facial buttresses are areas thatcan serve as guides in the reduction
ofthefacial skeleton and provide stabilization offractures.With high-velocity
trauma,com-minution and loss ofbony segments canoccur in the buttress and
�nonbuttress�areas ofthe face.When these defects aresignificant,the surgeon may
consider theuse ofbone grafting to prevent soft tissuecollapse and to allow for
structural supportofthe facial skeleton.Previous articles havereported on primary
bone grafting withfew complications.7�9Even when the bonegraft becomes
exposed,secondary woundhealing generally occurs.Common areasthat may require
primary bone graftinginclude the frontal bone,nasal dorsum,orbital floor,medial
orbital wall,and zygo-maticomaxillary buttress.There are many potential sources
ofbone for a graft,but calvarial bone may bethe best.Access is often achieved
througha bicoronal flap that has already been cre-ated during the management ofthe
frac-tures.These grafts have been shown toresist resorption better than endochon-
dral bone.8Rigid fixation ofthese graftshas been shown to decrease
resorption(Figure 28-11).8Soft tissue resuspension after surgicalaccess to facial
fractures is important forlong-term facial esthetics.42,52,53Resuspen-sion may be
especially beneficial in themidface region.For repair ofmidface frac-tures,the
region is usually exposed transo-rally and from a periorbital approach.52The soft
tissue attachment over the mid-face is customarily completely stripped.This
frequently results in sagging ofthesoft tissue,with reattachment at a moreinferior
position.Manson and colleaguesstated that there are two steps to placingthe soft
tissue back into proper positionafter exposure ofthe facial skeleton:refixa-tion
ofthe periosteum or fascia to theskeleton,and closure ofthe periosteum,muscle
fascia,and skin where incisionshave been made.42The periosteum isinflexible and
limits soft tissue lengtheningand migration.Its reattachment is usuallyaccomplished
by drilling holes in key loca-tions to fix the periosteum to the bone.Areas where
periosteal closure should beobtained include the frontozygomaticsuture,infraorbital
rim,deep temporal fas-cia,and muscular layers ofmaxillary andmandibular
incisions.32,42,52,54Areas whereperiosteal reattachment should beobtained include
the malar eminence andinfraorbital rim,temporal fascia over thezygomatic
arch,medial and lateral canthi,and mentalis muscle.42Sequence ofTreatmentAirway
ManagementHow to maintain the airway is a crucialdecision in the management
ofpanfacialfractures.There are several options that aredictated by the fracture
pattern and extentofother injuries.When there are extensivehead injuries and
prolonged intubation isanticipated,tracheostomy should be con-sidered.55�57
Likewise,tracheostomy is anappropriate option to facilitate the man-agement
ofmultiple facial fractures.10,56,57In many cases there are extensive injuriesto
the naso-orbitoethmoid region,makingnasal intubation difficult and haz-
ardous.58,59With nasal intubation,access tothe frontal sinus and naso-
orbitoethmoidregion is hindered.Oral intubation may be an option
whenmaxillomandibular fixation is either notpossible or not indicated.When
prolongedintubation is not anticipated,optionsinclude submental intubation60,61or
passingthe tube behind the dentition,ifspace per-mits.Ifan extraoral approach is
indicated tomanage a mandibular body/angle fractureor a symphysis
fracture,submental intuba-tion may hinder access.Fracture Management Much has been
written about the propersequencing oftreatment for panfacial frac-
tures.10,28,42,52,62Sequences such as �bottomup and inside out�or �top down and
out-side in�have been used to describe two ofthe classic approaches for the
managementofpanfacial fractures.To my knowledgethere have been no randomized
studies toascertain whether one approach is superiorto the other.The bottom up and
inside outapproach predates the use ofrigid fixationbut it is still a valid
approach.It establishesthe mandible as a foundation for setting therest ofthe face
and includes open reductionand internal fixation ofsubcondylar frac-tures,as well
as the remainder ofthemandible.The occlusion is set by placingthe patient in
maxillomandibular fixation;then,the maxilla should be in the
properposition.Realignment ofthe zygomaticbuttresses follows in this
sequence;howev-er,fixation at this point may lead to inaccu-racies in upper midface
position.Instead,abreak in the sequence is usually preferredhere.The
zygomaticomaxillary complex isreduced and fixated first.This allows for amore
accurate repositioning ofthe uppermidface before fixation at the
zygomaticbuttress.The maxilla is now fixated alongthe zygomaticomaxillary
buttress.Last,thenaso-orbitoethmoid fracture is reducedand stabilized (Figure 28-
12).62The opposite approach,top down andoutside in,starts at the zygomatic
region.The sphenozygomatic suture is reducedFIGURE28-11Primary bone graft
rigidlyfixed into position to reconstruct the anteriormaxillary sinus wall
including the nasomaxil-lary and zygomaticomaxillary buttress.(Cour-tesy ofJames
Koehler,DDS,MD.)
Management ofPanfacial Fractures553FIGURE28-12Bottom up and inside out
surgicalapproach.Aand B,Sequencing ofpanfacial frac-tures can begin with
maxillomandibular fixation.This is followed by reduction and fixation
ofthesubcondylar fractures followed by the symphysis,body,or angle fracture.Cand
D,The zygomas arereduced and fixated next using the sphenozygomat-ic
suture,zygomatic arch,and zygomaticomaxillarysutures as guides.Eand F,The maxilla
can now bestabilized in along the zygomaticomaxillary but-tress.Gand H,The naso-
orbitoethmoid fracturecan now be reduced and fixated at the nasofrontaland
frontomaxillary sutures and the infraorbitaland piriform rims.ABCDEFGH
554Part 4: Maxillofacial TraumaFIGURE28-13Top down and outside in
surgicalapproach.Aand B,Sequencing ofpanfacial frac-tures can begin with the
zygomas using the sphe-nozygomatic suture and the zygomatic arches asguides.Cand
D,The naso-orbitoethmoid fracturescan be reduced next and fixated at the
nasofrontalsuture and maxillofrontal sutures and infraorbitalrim.Eand F,The maxilla
is reduced and fixated.Stabilization is achieved at the nasomaxillary
andzygomaticomaxillary buttresses.Gand H,Themandible is reduced last in this
sequence.This isaccomplished with the use ofmaxillomandibularfixation followed by
reduction and fixation ofthemandibular fractures.ABCDEFGH
Management ofPanfacial Fractures555and fixated inside the orbit.The zygomaticarch
is reduced and plated.Ifthe arches arenot properly reduced,underprojection ofthe
midface can result.The alignment ofthe arch can be verified by the proper posi-tion
ofthe sphenozygomatic suture.Fromthis point the zygomas can be further posi-tioned
and fixated at the frontozygomaticsuture.The naso-orbitoethmoid complex isthen
positioned to the supraorbital rims,infraorbital rims,and maxillary process ofthe
frontal bones.The maxilla is addressednext using the position ofthe zygomatico-
maxillary buttress and piriform rim as aguide.Maxillomandibular fixation can thenbe
established (Figure 28-13).52Reductionand fixation ofthe mandibular condyle andthe
symphysis/body/angle fractures arethen performed.Some surgeons feel that there is a
sig-nificant advantage to the top down andoutside in approach because open treat-
ment ofthe condyles may not be neces-sary.The patient is treated with
varyingperiods ofmaxillomandibular fixation,which may be a valid approach in the
caseofcomminuted intracapsular fractures.Although this is a viable option in
somecases,there are two potential complica-tions.One is an unrecognized rotation
ofthe body or ramus ofthe mandible,result-ing in widening.A second complication
istemporomandibular joint ankylosiscaused by the inability to begin early phys-ical
therapy.One author reviewed closedtreatment ofmandibular condyle fracturesand
showed compromised results.63Earlyfunction ofpatients with condylar headfractures
is usually indicated,along withguiding elastics to maintain the range ofmotion
ofthe temporomandibular joint.Neither one ofthese techniques willachieve optimal
results in every situation.Instead,an approach that goes fromknown to unknown is
certainly moreaccurate.For example,ifthere is a signifi-cant calvarial injury,it
may be difficult tostart from the cranium and proceed cau-dally.In this case,a
sequence that startscaudally and proceeds cranially mayachieve more optimal
results,allowing thesurgeon to reconstruct the damaged cra-nial portion last.On the
other hand,ifthere is significant comminution ofthemandible or ifkey segments are
missing,itmay be more appropriate to start craniallyand proceed caudally.Thus,the
maxillofa-cial trauma surgeon must be comfortablewith both approaches and use
knownlandmarks to achieve optimal results.In Tables 28-1 and 28-2,two
commonsequences ofmanagement offacial frac-tures are illustrated.Other
sequencesexist,but they are variations ofthese twomajor approaches.Complications
There are many complications that areassociated with various fractures;these
arediscussed elsewhere in the text,with refer-ence to the specific fracture
type.However,a significant complication associated withpanfacial fractures that I
will discuss here iswidening ofthe facial complex.This occurswhen the surgeon fails
to properly reducekey areas that guide in establishing facialwidth.42Ifthe first
area approached is fix-ated in an improper location,subsequentfragments will be
reduced and fixed in animproper spatial arrangement,resulting ina series oferrors
and,usually,a widenedfacial complex.To prevent this,the surgeonmust use stable
segments,known land-marks,and anatomic reduction in themanagement ofpanfacial
fractures.Ifthe complication does occur,thesurgeon must assess the patient and
deter-mine the severity and location ofthe prob-lem.This is done through physical
exami-nation and CT imaging (Figure 28-14).Insevere cases three-dimensional
computedtomographic reconstruction ofthe entirefacial skeleton can be obtained
and,ifindi-cated,a three-dimensional stereolitho-graphic model can be made.64,65The
modelallows the surgeon to identify and recreatethe fractures during model
surgery.Thefracture may be reduced anatomically andstabilized with plates,which can
then besterilized and used at the time ofsurgery.This technique and the use
ofproper land-marks can aid in the proper reduction andfixation ofthe
fractures.ConclusionsThe management ofpanfacial fractures isextremely complex.There
are,however,many technologic advances that can aid thesurgeon in the proper
management ofthesefractures.The most important oftheseadvancements is imaging.With
the adventofhigh-resolution scanners,the surgeonhas a more accurate picture ofthe
fractureTable 28-2Sequence B:Top Down and Outside In*1.Tracheostomy2.Repair
offrontal sinus fracture3.Repair ofbilateral zygomati-comaxillary complex
(including arch)fracture4.Repair ofnaso-orbitoethmoid fracture5.Repair ofLe Fort
fracture (including midpalatal split)6.Maxillomandibular fixation7.Repair
ofbilateral subcondylar fractures8.Repair ofmandibular
fracture(symphysis/body/ramus)*See Figure 28-13.Table 28-1Sequence A:Bottom Up and
Inside Out* 1.Tracheostomy2.Repair ofpalatal fracture3.Maxillomandibular
fixation4.Repair ofcondyle fracture5.Repair ofmandibular fractures
(body/symphysis/ramus)6.Repair ofzygomaticomaxillary complex fracture (including
arches)7.Repair offrontal sinus fracture8.Repair ofnaso-orbitoethmoid complex
fracture9.Repair ofmaxilla*See Figure 28-12.
556Part 4: Maxillofacial TraumaGHFIGURE28-14Aand B,Twenty-one-year-old male who
fell from a height oftwo stories.Facial fractures included the frontal sinus,naso-
orbitoethmoid,bilateral zygomaticomaxillary complex,Le Fort I with midpalatal split
and avulsion oftooth no.9,mandibular symphysis,and bilateral intracapsularcondyle
fractures.In this photograph it is evident that the patient has significant facial
widening owing to a failure to establish proper facial width.He alsohas bilateral
bony ankylosis ofthe condyles secondary to a closed reduction ofthe condyle
fractures.Cand D,Three-dimensional stereolithographic mod-els generated from CT
imaging.Note the significant widening ofthe mandible and midface.Eand F,Simulated
surgery was performed on this model andmandibular plates were prebent.Note the
significant narrowing ofthe model.Mandibular condyles are now positioned in the
fossae.Gand H,Modelsurgery was performed on the dental cast,based on the
preorthodontic models that were brought in by the family.A surgical splint was
fabricated.(CONTINUEDONNEXTPAGE)ADEBCF
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maxil-lary vestibular incision,and the use ofthe previous chin scar.The hardware
was removed.The previous fractureswere recreated by performing bilateral condylar
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decrease in facial width and increase in facial height.Patient also had zygomatic
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canthopexy,midface resuspension,and genioplasty.(Courtesy ofDr.Patrick Louis and
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Part 5MAXILLOFACIALPATHOLOGY
CHAPTER 29Differential Diagnosis ofOral DiseaseJohn R.Kalmar,DMD,PhDCarl
M.Allen,DDS,MSDOne ofthe major roles ofthe oral andmaxillofacial surgeon is that
ofdiagnosti-cian.From private practices in small com-munities to large tertiary
care medical cen-ters,these specialists are called upon toevaluate and diagnose a
wide variety ofconditions affecting the face,jaws,head,and neck as well as the
tissues ofthe oralcavity.The term diagnosecomes from theGreek words
dia(�through,��apart�) andgnosis(�knowledge�),meaning literally toknow apart or to
distinguish.Indeed,although the ability to correctly diagnoseis important to
virtually all professions,itis perhaps most strongly linked to the clin-ical
practice ofmedicine and dentistry.Forhealth care practitioners,a diagnosisisdefined
as the determination ofthe natureofa disease or pathologic condition.Anaccurate
diagnosis is obviously importantand occasionally critical to the patient sothat the
most appropriate treatment canbe initiated as soon as possible.Earlydetermination
ofthe true diagnosis canfurther benefit the patient by avoiding theneed for
expensive unnecessary laboratorystudies,the use ofineffective or
impropermedications,and the inconvenience ofadditional costly consultation(s).A
variety ofterms related to the diag-nostic process may be used during theevaluation
ofthe patient.Occasionally thediagnosis is relatively
straightforward.Usually,however,a variety ofconditionswith similar clinical
features need to beconsidered,and a differential diagnosisisprepared.The
differential diagnosis repre-sents a listing ofthe more likely
diagnosticconsiderations for a particular pathologicfinding or condition,ranked in
descend-ing order ofprobability.Therefore,thenumber one consideration from the
initialdifferential diagnosis should represent theculmination ofthe clinician�s
evaluationand is termed theclinical diagnosis(ie,working or tentative
diagnosis,clinicalimpression).Although construction ofthedifferential is initially
based upon clinicalsigns,symptoms,and history,this list ofdiagnoses is subject to
modification orrefinement following additional studiessuch as radiographic imaging
and hemato-logic or serum analysis (Figure 29-1).1,2Asis discussed below,the
differential listingmay vary widely depending upon theexperience and knowledge base
ofthetreating clinician.The designation offinaldiagnosisis used when the
clinicianbelieves that the nature ofthe disease hasbeen identified to a reasonable
degree ofcertainty.This progression from informa-tion to possible diagnoses to
final diagno-sis is known as the diagnostic processormethod.A case example is
provided below.Although the determination ofa finaldiagnosis often represents the
end ofthediagnostic phase ofpatient care,it is worthremembering that the
�final�diagnosis isnot always correct.As is stressed below,observation ofthe
patient�s response totherapy and careful monitoring ofthesubsequent disease course
are essentialaspects ofcomprehensive patient manage-ment.Should a lesion or
condition notbehave in the expected manner,reevalua-tion and revision ofthe final
diagnosismay ultimately be required.The Diagnostic ProcessThe clinician begins the
diagnostic processby gathering or accumulating informa-tion.In some instances this
informationincludes a significant historic component,whereas in other cases
(eg,asymptomaticlesions discovered upon routine examina-tion) the data may be
limited strictly to thefindings ofthe physical examination,together with any
necessary diagnosticstudies or tests.Depending upon the expe-rience and expertise
ofthe practitioner,aconfident final diagnosis may requirenothing more than clinical
inspection.Inmany cases,however,even the most
564Part 5: Maxillofacial Pathologyexperienced diagnostician requires addi-tional
information from appropriateimaging or laboratory studies.Case Study: From
DifferentialDiagnosis to Final DiagnosisA 25-year-old male presents with a 3-month
history ofgradual painlessenlargement ofthe right anterior lowerjaw.His medical
history is unremarkable,and he denies recent trauma to the area.Clinical
examination reveals a 1.5 cm bonyfirm swelling ofthe right mandibular alve-olus in
the area ofteeth no.26 and 27causing primarily buccal expansion withan unremarkable
overlying mucosa.Thearea is nontender to palpation,and theadjacent teeth are
vital.Initially,the clinical differential diagno-sis focuses on the most common
conditionsthat could present in a fashion similar tothe lesion in this
patient.Likely considera-tions include central giant cell granuloma,central
ossifying fibroma,ameloblastoma,and odontogenic keratocyst.Important additional
information iseasily obtained in this case with routinedental radiography.A
panoramic filmreveals a 2 cm unilocular radiolucentlesion ofthe right mandible with
a well-defined sclerotic border that containsscattered small particles
ofradiodensematerial.With this additional informa-tion,the differential diagnosis
is revisedto exclude conditions not usually associ-ated with calcification and
possibly toinclude other less common conditionsthat have a radiopaque
component:cen-tral ossifying fibroma,desmoplasticameloblastoma,and calcifying
epithelialodontogenic tumor.A biopsy ofthe lesional tissue reveals awell-
circumscribed cellular proliferationofbenign spindle cells containing scat-tered
trabeculae ofosteoid and bone.Thefinal diagnosis is central ossifying
fibroma.HistoryMost attempts at formulating a differentialdiagnosis begin with data
gathering thatincludes the history ofthe specific problembeing investigated as well
as the patient�smedical and social history.The patient�sperception ofthe duration
ofthe lesion canbe important as long-standing lesions maysuggest a developmental or
benign process,whereas rapidly evolving problems oftenrepresent
reactive,infectious,or malignantdisease.Exceptions to these generalizationsare
numerous,however,since mycobacterialinfections may develop slowly,as do
someneoplasms that are considered malignant(eg,basal cell
carcinoma).Furthermore,thereliability ofthe patient to provide an accu-rate history
is occasionally compromisedowing to the patient�s inattention,limitedmental
capacity,or denial ofdisease.Lesion detection or presentationInitial differential
diagnosisCytology, culture, other laboratory or imaging studiesNonsurgical
management, 10�14 dLarge lesion or high indexof suspicion for malignancyHistory,
physical examination, routine radiographsLesion improvementor resolutionLesion
persistenceor progressionRecommend biopsyPerform biopsyRefer to specialist for
biopsy"Final" diagnosisNo further treatment requiredFurther treatment requiredTreat
patientRefer patient to specialistfor treatmentPatient follow-up in coordination
with other specialist(s)Revision of final diagnosis as indicatedFIGURE29-1The
diagnostic process.Adapted from Ellis E III.1
Differential Diagnosis ofOral Disease565Symptoms,particularly related to painor
tenderness,are important in developinga differential diagnosis.Pain and tender-ness
(pain on palpation) are often signs ofan inflammatory or infectious
process,although malignancies can also producesuch symptoms,particularly late in
theircourse.A notable exception to this is ade-noid cystic carcinoma,which is
infamousfor the early onset oflow-grade intractablepain.Other symptoms such as
paresthesiaor numbness can also be significant andmay be related to pressure on
nervescaused by a cystic lesion or tumor mass.Reported changes in the lesion may
alsoprovide important insights.Ifa mass gradu-ally enlarges,the possibility
ofneoplasia hasto be entertained,whereas a mass that fluc-tuates in size is more
suggestive ofa reactiveprocess.In addition,changes in symptomsmay be
significant.Decreasing pain or ten-derness likely represents a resolving inflam-
matory or infectious process,whereas painthat develops in a long-standing
previouslyasymptomatic mass may be an indication ofmalignant transformation
(eg,carcinomaarising in pleomorphic adenoma).Clinical ExaminationFollowing a review
ofthe patient�s medicalhistory and history ofthe present lesion orcondition,the
clinician typically proceedswith gathering objective data throughcareful clinical
examination.A variety oflesional parameters should be evaluatedand
recorded,including (1) site,(2) size,(3) character (eg,macule,ulcer,mass),
(4)color,including an assessment ofitshomogeneity,(5) surface morphology
(eg,smooth,pebbly,granular,verrucous),(6)the border (eg,smooth,irregular,indis-
tinct,sharply defined),(7) consistency onpalpation,(8) local symptoms,and (9)
thedistribution ifmultiple or confluentlesions are observed.The precise anatomic
site or locationofa lesion can provide essential diagnosticinformation and is
discussed later ingreater detail.Lesion size can have diagnostic impli-
cations,particularly when combined withan estimate oflesion duration to give
anapproximate rate ofgrowth or enlarge-ment.The finding ofa large lesion
mayindicate a locally aggressive or malignantneoplasm ifthe history suggests a
relative-ly recent onset.Yet,even when abnormaltissue has been noted for several
monthsor years,a history ofprogressive increasein the size ofthe affected area
should beviewed suspiciously (Figure 29-2).Asmentioned above,relying on the
accuracy(or veracity) ofthe patient history can beproblematic and should be
weightedaccordingly in the differential diagnosis.Confirmation ofthe clinical
historythrough other health care practitionerscan be helpful in this
regard.Establishing the character ofthe lesionis an essential aspect ofthe clinical
evalua-tion.Ulcers can be seen with traumatic,infectious,or neoplastic
conditions,where-as masses or swellings more commonlyindicate neoplasms,reactive
proliferations,cysts,or enlarged lymph nodes.A historyor evidence ofvesicle or
bulla formationmight be suggestive ofa viral condition,animmunobullous disorder,or
possibly aninherited mucocutaneous disease.Macular lesions,which are completelyflat
by definition,usually represent an areaofcolor change.A brown or black maculeis
often the result ofmelanin pigment;ared or purple macule usually
representshemoglobin in either its oxygenated orreduced form,respectively.A dull
flatwhite implies keratin production,an areaoftranslucent whitish change may
meanincreased epithelial edema,and a shinycreamy yellow-white appearance is
usuallya sign ofan ulcer�s fibrinous pseudomem-brane.A blue or grayish macule is
fre-quently associated with exogenous (amal-gam,foreign body) or
endogenous(melanin) pigmented material that isdeposited within the connective
tissuebelow the level ofthe epithelium.Although additional information regard-ing
the margin or border ofa lesion is pro-vided below,it should be mentioned thatmost
pigmented lesions in the oral cavityare relatively homogeneous in color andhave a
smooth well-defined margin.Bycontrast,a pigmented lesion that exhibitssignificant
border irregularity and colorvariegation should be considered as suspi-cious for
melanoma (Figure 29-3).The surface morphology ofa lesioncan be virtually diagnostic
for certain con-ditions.Examples include the �tapiocapudding�appearance ofthe
surface ofalymphangioma or the papillary epithelialfronds ofsquamous
papilloma.Similarly,FIGURE29-2A,Asymptomatic papillary epithelial lesion in a 50-
year-old male that has been pre-sent for approximately 2 years without apparent
increase in size.Clinical diagnosis: squamouspapilloma.B,Asymptomatic epithelial
lesion in a 65-year-old male with a papillary or granularsurface that has been
present for approximately 2 years with slow progressive
enlargement.Clinicaldiagnosis: verrucous carcinoma.AB
566Part 5: Maxillofacial Pathologyan irregularly papular or granular
surfacearchitecture can be seen with malignanttumors as well as granulomatous
process-es that can range from deep fungal ormycobacterial infections to foreign-
bodyreactions to immune-mediated conditionssuch as Crohn�s disease or
sarcoidosis.Palpation ofthe lesion is necessary toassess its consistency,the
lateral or deepmargins,and the presence or absence oftenderness.When assessing
consistency,detection ofa doughy soft mass suggests acystic lesion or a benign
fatty tumor.Arubbery-firm character may be detectedwith a variety ofbenign or
neoplastic dis-orders,whereas an even firmer consistencycan reflect metastatic
disease within alymph node.A hard or bony consistencynaturally indicates a
mineralized or calci-fied component to the lesion.The border or margin ofa
primarilysubmucosal or subcutaneous lesion is usu-ally described as
encapsulated,well-demarcated,or infiltrative.An encapsulat-ed process is often
freely movable withinthe deep soft tissues,a finding common toa variety ofbenign
neoplasms and cysts.The margins ofsome benign lesions (eg,neurofibroma) and some
low-grademalignancies (eg,acinic cell carcinoma)may be well-demarcated,but they are
gen-erally less mobile compared with encapsu-lated lesions.The margins ofmany
malig-nancies are indistinct,as the tumorinvades and blends with the
surroundinghost tissues.As noted earlier,the finding ofa localsymptom such as
tenderness is usuallyassociated with an inflammatory process,especially acute
inflammation.Althoughmalignant neoplasms may also presentwith tenderness or
dysesthesia (eg,adenoidcystic carcinoma),this feature is usually alater-stage
development secondary totumor invasion oflocal nerves or
surfaceulceration.Tenderness may also be aprominent clinical feature
ofcertainbenign tumors such as traumatic neuroma.Finally,the presence ofmultiple
iden-tical or similar lesions can suggest a num-ber ofconditions,depending upon
theirparticular character (eg,ulcerations,papules,vesicles) and distribution.Multi-
ple small painful recurrent ulcerationsbilaterally on the ventrolateral surface
ofthe tongue in a young adult female patientare most suggestive ofthe
herpetiformvariant ofrecurrent aphthous stomatitis.On the other hand,the finding
ofa focusofseveral small relatively painless ulcera-tions in a unilateral
distribution on the lefthard palate would be more consistent witha recurrent
intraoral herpes infection.Similarly,multiple purplish plaquesinvolving the oral
mucosa and skin ofa35-year-old male who is positive for thehuman immunodeficiency
virus would bestrongly suggestive ofKaposi�s sarcoma.Developing the
DifferentialDiagnosisAfter collecting the historic and clinicalinformation,the
final diagnosis may beobvious;however,in many instances thediagnosis is not readily
apparent and theformulation ofa differential diagnosis isappropriate.Several
approaches haveevolved over the centuries ofmedical prac-tice to assist in the
categorization or group-ing ofdiseases.These grouping techniquespermit the large
number ofpossible diag-nostic considerations for a given lesion tobe reduced to the
more probable condi-tions.The resultant narrowing ofthe dif-ferential diagnosis,in
turn,aids in theselection ofadditional diagnostic tests thatare most useful in
securing a final diagno-sis.The major diagnostic strategies orapproaches that have
been used to groupor organize the differential are based on (1) the history and
clinical presentation,(2) the potential disease histogenesis,and(3) the disease
location (more specifically,the frequency ofa given condition in a par-ticular
location).In actual practice,moreexperienced clinicians typically employ allofthe
categories simultaneously.As a con-sequence,the specialist is able to
rapidlyproduce a much narrower and usuallymore precise list ofinitial diagnostic
con-siderations (see the case study below).Evaluation ofthe physical characteris-
tics ofa given lesion in the context ofthehistory and clinical setting often
permitsthe clinician to arrive at a reasonable list ofdiagnostic possibilities.For
example,afirm fixed painless 2 cm nodule ofuncer-tain duration in the anterior
cervical areaofthe neck is suspicious for possiblemetastatic disease or lymphoma.By
con-trast,ifthe nodule were soft,mobile,andABFIGURE29-3A,Macular grayish 0.8 cm
pigmentation with well-defined borders ofright posteriorbuccal mucosa in a 52-year-
old female.The patient reported that it had been present for years.Clin-ical
diagnosis: amalgam tattoo.B,Ulcerated area ofmacular pigmentation affecting
posterior maxil-lary left alveolar mucosa in a 65-year-old male.Note the border
irregularity and color variegation.Clinical diagnosis: melanoma.
Differential Diagnosis ofOral Disease567tender to palpation,an inflammatoryprocess
would be more likely.Another useful approach to develop-ing a differential
diagnosis is to considerwhether the clinical and historic aspectsofthe lesion can
be explained by any,some,or all ofthe broad categories ofdis-ease
histogenesis.These categories includedevelopmental,inflammatory/immune-
mediated,infectious,neoplastic,andmetabolic conditions.This is a time-honored
systematic method ofdiagnosis,and many clinicians find it useful to criti-cally
consider diagnostic possibilitiesfrom each category.For example,anasymptomatic
lesion that has been pre-sent for several years and feels encapsulat-ed upon
clinical palpation would be mostconsistent with a developmental orbenign neoplastic
process.Althoughinflammatory conditions,malignant neo-plasms,and metabolic
conditions mightnot be excluded completely,they wouldnot receive primary
consideration in theinitial differential.Similarly,ifthe lesionpresented as a
chronic ulceration ofthelateral tongue in an adult patient,disor-ders from the
neoplastic (especially malig-nancies),infectious (eg,mycobacterial ordeep fungal
infections),and immune-mediated (eg,Wegener�s granulomatosisor regional enteritis)
categories wouldhave to be considered.The third diagnostic grouping strate-gy
relies on the identification oflesionsthat most commonly present in a partic-ular
anatomic location.The tendency forcertain conditions to occur withincreased
frequency at certain sites is wellrecognized.For example,a nontenderbluish
fluctuant mass ofrecent onsetinvolving the lower labial mucosa verylikely
represents a mucocele.By contrast,mucocele would not be included in thedifferential
diagnosis ofa painless persis-tent bluish mass ofthe attached gingivaas salivary
gland tissue is not normallypresent at that site.This latter clinicalfinding
would,however,be completelyconsistent with a gingival cyst oftheadult.A nonhealing
relatively insensitiveulceration ofthe lateral tongue in anadult patient that has
no identifiablesource ofirritation or trauma would behighly suspicious for squamous
cell carci-noma.Salivary gland neoplasia would bea strong consideration for a
rubbery firmmass ofthe posterior hard palate.Case Study: Neophyte versusExpert
Clinician An otherwise healthy 72-year-old womancomplains ofsores in her mouth for
thepast year.Her medical history is unre-markable and she is not taking any med-
ications.She has not been aware ofanyblisters,and she feels the problem is get-ting
worse.The lesions tend to wax andwane in severity and have affected severalareas
ofthe mouth,including the hard andsoft palates,the labial mucosa,and theventral
tongue.Examination shows several shallowerosions and ulcerations with
raggedmargins.The lesions range from 0.5 to1.0 cm in diameter and involve the
lowerlabial mucosa,the ventral tongue bilater-ally,and the anterior soft palate.No
vesi-cles or bullae are seen,and no white stri-ae are evident.The inexperienced
diagnostician whois not very familiar with oral lesions mightprovide a differential
diagnosis based onconditions that are primarily ulcerative:herpesvirus
infection,aphthous ulcers,erosive lichen planus,squamous cell carci-noma,and
candidiasis.On the basis ofthislist,the patient would likely be placed onone or
possibly more courses ofantiviralmedication.The patient�s condition wouldnot
improve,and she might then beswitched to antifungal medication(s).After that
approach has failed to resolvethe problem,topical corticosteroids mightbe
prescribed.Following several weeks oftopical corticosteroid use with little or
noimpact on the patient�s oral sores,thediagnostician may recommend that abiopsy be
performed.In this situation,thepatient has invested several months�timeand spent
hundreds ofdollars on inappro-priate or ineffective medications�all inthe absence
ofa clear diagnosis.For the experienced diagnosticianwho is more familiar with oral
conditions,the differential would be much smaller:cicatricial pemphigoid or
pemphigus vul-garis.With a greater understanding oforaldisease,the specialist
should be able toeliminate many ofthe considerations thatthe first clinician
entertained.For exam-ple,recurrent herpesvirus infection doesnot typically affect
nonkeratinized mucosain an immunocompetent patient andwould not wax and wane in
severity.Although aphthous ulcers often exhibit awaxing-and-waning course,the
lesionalmargins are usually smooth,not ragged.Erosive lichen planus would be
consideredunlikely owing to the lack ofradiatingwhite striae at the periphery ofthe
orallesions,as well as the lack ofbuccalmucosa involvement.Squamous cell carci-noma
would not be reasonable because ofthe multifocal presentation and the histo-ry
ofwaxing and waning.Finally,althoughcandidiasis is occasionally associated
withtenderness or irritation ofthe oralmucosa,it does not induce true ulcerationand
would therefore have a low probabili-ty ofrepresenting the actual diagnosis.Based
on the patient�s age,the distrib-ution ofthe lesions,the history oftheprocess,and
the clinical appearance ofthelesions,a differential diagnosis that cen-ters on
immune-mediated disease wouldbe most appropriate.In this situationbiopsies for
examination with both lightmicroscopy and direct immunofluores-cence (DIF) would be
requested or per-formed after the initial consultation.Histopathologic evidence
ofacantholysisand DIF findings ofinterepithelialdeposits ofimmunoglobulin G (IgG)
andcomplement component 3 (C3) wouldestablish the final diagnosis
ofpemphigusvulgaris in a relatively rapid and
568Part 5: Maxillofacial Pathologycost-effective manner.Besides the mone-tary
savings,a more timely and correctdiagnosis often saves the patient fromunnecessary
suffering and mentalanguish,both by initiating effective treat-ment earlier and by
relieving the anxietythat many patients experience when theydo not know the nature
oftheir disease.Early diagnosis and treatment ofcondi-tions such as pemphigus
vulgaris may alsoreduce disease progression or the need formore aggressive
therapy.Determining the Final Diagnosis:Additional Diagnostic MethodsIfthe final
diagnosis cannot be deter-mined based on historic findings andphysical examination
alone,a variety ofprocedures and tests can be used to assistin the diagnostic
process.Generally,diag-nostic tests should be ordered so that themost likely
diagnosis can be either con-firmed or eliminated.The methodic appli-cation ofthis
process together with aproper rationale for selecting each testtypically leads to
the correct diagnosis inthe most rapid cost-effective manner.Teststhat do not
address the most likely diag-nostic possibilities should be delayed asthe
probability that they will provide use-ful information is small,yet they can dra-
matically increase costs to the patient.Anexception to this statement would be a
sit-uation in which a particular test is per-formed to rule out a rare or unusual
con-dition ofserious clinical significance.Finally,diagnostic tests should be
inter-preted by individuals with specialty train-ing in that area whenever possible
toensure the most timely and accurate resultor final diagnosis.Diagnostic studies
are not necessarilycomplex or expensive.For example,aputative vascular lesion can
be evaluatedeasily by pressing it with a glass slide to testfor possible blanching
(diascopy).Thebruit ofa vascular malformation may beheard upon auscultation using a
stetho-scope.Operative findings at the time ofsurgery occasionally provide
importantdiagnostic clues,such as the presence ofcheesy keratotic debris within a
cysticlesion associated with an impacted tooth,suggestive ofan odontogenic
keratocyst,or the empty bone cavity seen with trau-matic bone cyst.Finally,follow-
up evalua-tion ofa lesion is a straightforward proce-dure that can provide
importantdiagnostic insight with respect to biologicbehavior.Those conditions that
persist orprogress 2 weeks after initial inspectionoften require additional tests
to establishthe diagnosis.Diagnostic ImagingDepending on the clinical
setting,imagingstudies may be both appropriate and nec-essary to the work-up ofan
oral lesion.Additional information on this topic isavailable in an excellent
radiology textedited by White and Pharoah.3Briefly,imaging studies can include
plain radi-ographic films,sialography,ultrasonogra-phy,computed tomography
(CT),magnet-ic resonance imaging (MRI),radionuclideimaging,and positron emission
tomogra-phy (PET).Plain FilmsFor evaluation ofbonelesions,plain films are the most
commonlyemployed imaging modality and,togetherwith CT,are often the most
useful.Withthe increased use ofpanoramic radi-ographs as a screening study in many
cur-rent dental practices,it is not unusual forthese films to detect a previously
unidenti-fied skeletal abnormality.Evaluation ofsuch a lesion includes an
assessment offea-tures such as localization (single,multifo-
cal,generalized),margins (well defined,poorly defined),internal structure (radi-
olucent,radiopaque,mixed),effects onsurrounding structures (teeth,inferioralveolar
canal,cortical bone),and whetherthere have been any associated symptoms.For
example,a single radiolucent lesion atthe apex ofa nonvital tooth most
likelyrepresents a periapical cyst or granuloma.A similar-appearing radiolucency
belowthe level ofthe inferior alveolar canal in theposterior mandible more likely
representsa Stafne defect.Sharply defined marginsindicate a benign process in
mostinstances,whereas poorly defined marginscan sometimes signify
malignancy.Notableexceptions to this rule include osteo-myelitis and fibrous
dysplasia,both ofwhich typically have borders that blendwith the surrounding
bone.Radiolucentlesions are produced by conditions that donot generate a calcified
product.Radiopaque and mixed lesions representconditions that can produce a
mineralizedproduct,such as bone,cementum,dentin,or enamel.It is generally safe to
assumethat the vast majority oflesions associatedwith the crown ofan impacted tooth
areodontogenic in origin.Ifthe teeth areerupted,however,determining whether alesion
is ofodontogenic origin can beproblematic since there are few areas in thejaws in
which a 2 cm lesion does notappear to be tooth-related.Symptoms suchas pain or
paresthesia may suggest infec-tion or malignancy,but benign conditionscan
occasionally present in this fashion.SialographySialography has almostbecome a lost
art.This technique relies onretrograde injection ofa radiopaque fluid,also known as
contrast medium,into theduct system ofeither the parotid or sub-mandibular salivary
gland.A plain radi-ograph is made,and the pattern ofdistri-bution ofthe contrast
medium is assessed.Many ofthe previous indications forsialography such as
evaluation ofsalivarygland neoplasia have been supplanted bynewer imaging
modalities such as MRI.Nonetheless,sialography can be useful inassessing chronic
obstructive salivarygland disease and gland function.Thecharacteristic sialographic
finding ofpunctate sialectasis (�blossoms on abranchless tree�pattern) seen in
patientsaffected by Sj�gren�s syndrome is helpfulin supporting that diagnosis.
Differential Diagnosis ofOral Disease569UltrasonographyUltrasonography ismost
useful in the evaluation ofdeeplyseated masses and is often helpful in dis-
tinguishing a solid mass from one that iscystic.This technique relies on the
factthat different tissue densities result in dif-ferent degrees ofreflection or
echo pro-duction ofa beam ofhigh-frequencysound waves.Although ultrasonographydoes
not expose the patient to ionizingradiation,the tissue resolution is typicallyless
than that achieved with either CT orMRI technology.CTCT is a cross-sectional
radiologicimaging technique that is particularly use-ful in the evaluation ofbone
lesions.Notonly can the density and margins ofthelesion in question be evaluated
with thistechnique but cortical expansion and fineinternal details can often be
more readilyappreciated compared with plain filmimages.Use ofcontrast media has
extend-ed the utility ofthis technique in areas ofsoft tissue
pathology.Furthermore,morerecent designs such as spiral CT scannershave made data
acquisition much morerapid and have reduced radiation dose tothe patient while
maintaining or improv-ing resolution.MRIMRI is a newer form ofcross-sectional
imaging that does not exposepatients to ionizing radiation.Although pri-marily used
in the evaluation ofsoft tissuelesions,it is also capable ofproviding diag-nostic
information regarding bony lesions.Two distinct views are typically generated:T1
and T2.Adipose tissue has the highestsignal in the T1-weighted image,and thisview
is often used for identifying anatomicstructures.By comparison,the T2
imagehighlights tissues with high water contentand is especially useful in
depicting inflam-matory processes and neoplasms.Radionuclide
ImagingRadionuclideimaging relies on the specific uptake ofany one ofseveral
isotopes by varioustypes oftissues or cells.Localization oftheisotope is determined
by examining thepatient with a gamma scintillation camera.The most commonly used
isotope,tech-netium 99m pertechnetate,can demon-strate areas ofhigh metabolic
activity.It isuseful in identifying inflammatory condi-tions such as
osteomyelitis,areas ofactiveskeletal lesions offibrous dysplasia orosteitis
deformans,and metastatic disease.PET ScanPET scan is the most recentlydeveloped
cross-sectional imaging tech-nology.This technique relies on the iden-tification
ofmetabolically active cells,suchas metastatic deposits ofsquamous
cellcarcinoma,that exhibit preferential uptakeofradionuclide-labeled glucose.In
con-junction with CT/MRI,preoperative PETimaging ofpatients with head and
neckcancer has lead to increased sensitivity andspecificity for detection oforal
cavity car-cinoma,esophageal carcinoma,and clini-cally occult metastatic disease in
theneck.4�8PET scans have proved particular-ly useful in the post-treatment follow-
upby helping to distinguish altered anatomiclandmarks or areas offibrosis from
recur-rent tumor as well as the detection ofdis-tant metastases from head and neck
pri-maries.6�8The technique is notrecommended for neoplasms that are rela-tively
inactive metabolically (eg,low-grademucoepidermoid carcinoma).In addition,the lower
limit oftumor mass detection bycurrent technology is no better than
thatofCT/MRI,and false-positives owing toinflammatory changes are reported.Analysis
ofLesional Tissue: Histopathologic,Immunopatho-logic,and Molecular EvaluationIn a
large number ofcases,the final diag-nosis depends on the results ofhistopathologic
examination oflesionaltissue.In some situations the diagnosis
isstraightforward,whereas in others adefinitive diagnosis cannot be made
untilsophisticated immunohistochemical orcomplementary DNA studies are per-
formed.As with imaging,a variety oftechniques are available to the patholo-gist,and
their selection varies on a case-by-case basis,depending on the diagnos-tic
challenges posed by the individualpatient specimen.Exfoliative CytologyExfoliative
cytol-ogy is a relatively inexpensive noninva-sive technique that may be used to
pro-vide additional information related tolesions ofsurface origin.The utility
ofthis technique in the diagnosis ofcondi-tions such as
candidiasis,herpesvirus(herpes simplex virus,human her-pesviruses 1 and 2)
infections,and pem-phigus vulgaris is well documented.More recently a modified form
ofcytologic sampling that employs an oralbrush instrument to collect epithelial
cellsfollowed by automated histopathologicevaluation has been introduced to den-
tistry.Suggested advantages includeimproved sampling ofall epithelial layersand
increased sensitivity and specificity inthe detection ofprecancerous and cancer-ous
lesions versus results with routineexfoliative cytology.This new techniquedoes not
provide a definitive diagnosis,however,and cannot be used as a substi-tute for
scalpel biopsy and routinehistopathologic examination (see below).Therefore,in a
clinical setting where theindex ofsuspicion for possible precancer-ous or cancerous
change is high,such asthe high-risk areas for oral cancer (ie,ven-trolateral
tongue,floor ofmouth,tonsillarpillars,soft palate),or in a patient with sig-
nificant risk factors (ie,heavy smoking,heavy alcohol use,or both),use
ofbrushcytology would not be recommended dueto the inherent delay in definitive
diagno-sis ofthe lesional tissue and any subse-quent treatment.In cases in which a
per-sistent mucosal lesion is identified but theindex ofsuspicion is low,the brush
cytol-ogy technique may be useful in excludingthe presence ofprecancerous or
malignant
570Part 5: Maxillofacial Pathologyepithelial changes.For such innocuouslesions,a
finding ofabnormal cells couldtrigger scalpel biopsy (and definitive diag-nosis)
before the surgical procedure mightotherwise have been deemed necessary.Fine-Needle
AspirationFine-needle aspi-ration (FNA) is a useful method for evalu-ating
subcutaneous or more deeply situatedmass lesions,although obtaining a diagnos-tic
sample and interpreting the results accu-rately requires specialized
training.Thistype ofprocedure is most widely used indetermining the nature
ofsalivary gland orneck masses.Currently FNA is available inmost large urban areas
throughout theUnited States,usually in conjunction withtertiary care medical
centers.Incisional BiopsyIncisional biopsy isgenerally indicated for large lesions
(> 2 cm) and those that could representunencapsulated or potentially
malignantneoplasms.By definition an incisionalbiopsy is a diagnostic surgical
procedure inwhich a sample or portion ofa lesion isremoved for histopathologic
review,leav-ing the remainder ofthe lesion at the biop-sy site.In cases ofsuspected
malignancy,anincisional biopsy is usually the procedureofchoice unless the
clinician performingthe biopsy will also be involved in defini-tive treatment ofthe
cancer (see below).Excisional BiopsyExcisional biopsy istypically used to manage
clinically benignlesions that are < 2 cm in diameter.Anexcisional biopsy is defined
as a diagnosticsurgical procedure in which all clinicallyabnormal tissue is removed
for microscop-ic analysis.Excision ofa small but poten-tially malignant lesion
(eg,squamous cellcarcinoma with a primary tumor [T],regional nodes [N],and
metastasis [M]staging ofT1N0M0) may be appropriate insettings in which the surgeon
performingthe biopsy is also responsible for final treat-ment.With rare
exceptions,an excisionalbiopsy should not be performed on a sus-pected malignant
lesion unless the per-forming clinician is involved in
definitivetreatment.Otherwise,the surface mucosamay be completely healed by the
time thepatient is referred to the oncologist,obscuring the extent ofthe original
lesionand unnecessarily hindering definitivetreatment planning.Specimen orientation
is recommendedwhenever a clinician suspects that a neo-plastic process may have
recurrent ormalignant potential,including conditionssuch as epithelial dysplasia or
pleomorphicadenoma.This can be accomplished bycareful identification ofthe anatomic
mar-gins ofthe biopsy specimen with suture(s),an accompanying sketch ofthe
specimen,and its orientation to the surrounding tis-sues or both.Such anatomic
orientation ofthe tissue sample allows the pathologist toproperly subdivide and
process the speci-men so that the adequacy ofexcision canbe assessed at all
surgical margins.Theterms negativeor clearmarginsare usedwhen the surgical margins
appear freefrom tumor involvement.When tumor istransected or lies immediately
adjacent tothe surgical margin without evidence ofacapsule,proper specimen
orientation per-mits the location ofthe positivemargin(s)to be determined as
precisely as possible.With this information the surgeon canthen plan the most
conservative surgicalapproach that will also accomplish the pri-mary goal
oftherapy:complete removal ofresidual neoplastic tissue.Specimen
InformationAlthough obtain-ing an adequate biopsy specimen is animportant result
ofproper surgical tech-nique,proper diagnostic techniquerequires that the surgeon
also transmitadequate clinical information to thepathologist through use ofthe
specimen orbiopsy data sheet.Inflammatory,reactive,and even neoplastic conditions
can haveoverlapping histopathologic features thatare difficult (ifnot impossible)
to distin-guish without an adequate description ofthe clinical setting.Lacking this
informa-tion,the pathologist may not be able toprovide a completely accurate or
specificdiagnosis.Pertinent details from the med-ical or dental history,the history
ofthelesion,the location and physical character-istics ofthe lesional
tissue,and,whenapplicable,the radiographic features canassist with the
histopathologic analysis.Clinical findings at the time ofbiopsy canalso provide
essential information.A goodexample is the discovery ofan empty cavi-ty during the
exploration ofa radiolucentlesion ofbone.This situation often meansthat only
minimal tissue can be submittedfor review;however,the operative findingis virtually
pathognomonic for traumaticbone cyst.Quality close-up clinical pho-tographs
including digital images can behelpful,particularly for specialists whohave dental
training such as oral and max-illofacial pathologists.Biopsies ofbonypathology
should be accompanied by radi-ographs (originals or copies),wheneverpossible,as
correlation may be needed tohelp distinguish conditions such as
fibrousdysplasia,ossifying fibroma,and focalcemento-osseous dysplasia.A final piece
ofinformation thatshould always be submitted together withthe biopsy specimen is
the clinical diagno-sis.The clinical diagnosis is important attwo levels.First,it
helps the pathologist byproviding an educated �best guess�as towhat the lesional
tissue was thought tomost likely represent by the clinician.Should the initial
histopathology ofthesubmitted specimen appear substantiallydifferent from the
clinical diagnosis,thepathologist may request deeper sections,rotation ofthe
specimen,or special stud-ies to ensure that all aspects ofthe biopsymaterial have
been thoroughly examined.Second,in cases where the final histo-pathologic diagnosis
varies significantlyfrom the working diagnosis,it is the clin-ician who should
proceed cautiously.After discussing the case directly with thesign-out
pathologist,the surgeon may be
Differential Diagnosis ofOral Disease571satisfied with the unexpected diagnosisand
plan accordingly.Ifnot,the clinicianmay request a second opinion on the orig-inal
biopsy material or choose to performa second biopsy procedure.In
essence,theclinical diagnosis serves as a �litmus test�for both the pathologist and
surgeon,animportant function that ultimately bene-fits the patient.For the oral and
maxillofacial sur-geon,this type ofdiscordance may beminimized ifthe tissue
specimen is ini-tially reviewed by an oral and maxillofa-cial pathologist.The oral
and maxillofa-cial pathologist receives highlyspecialized training in the pathology
ofthe head and neck,including odonto-genic cysts and tumors and salivarygland
diseases.The typical general surgi-cal pathologist,by comparison,has amodest degree
ofexperience withrespect to oral conditions and may beunfamiliar with the unique
microscopicfeatures oflesions from this area.To givesome perspective,individuals
trained inoral and maxillofacial pathology pro-grams review tens ofthousands
oforalbiopsy specimens prior to graduation.By contrast,it is unusual for general
sur-gical (anatomic) pathology residents toexamine more than a few hundred spec-
imens from the orofacial region duringtheir training.Furthermore,the oral
andmaxillofacial pathologist has a com-mand ofthe terminology used by thedental
profession to describe oral diseaseand can more readily correlate the clini-cal and
radiographic features with themicroscopic findings.Just as a generalsurgeon may be
able to remove a set ofimpacted third molars,the generalpathologist may be able to
provide anadequate diagnosis for an oral biopsy.Inmost situations,however,the
profes-sionals who are trained specifically tomanage problems related to the oral
andmaxillofacial region are able to accom-plish their respective tasks more effi-
ciently and accurately.The Microscopic Differential DiagnosisOn occasion a final
diagnosis cannot bemade after examining routine hema-toxylin and eosin�stained
sections ofalesion.In such a situation,the pathologistis faced with a microscopicor
histopatho-logic differential diagnosis.For some cases,special chemical stains may
be useful inthe detection ofsuspected microorgan-isms or the identification
oftissue prod-ucts such as mucin or amyloid.In othercases,particularly spindle-cell
malignan-cies and a group ofundifferentiated neo-plasms termed small blue-cell
tumors,thefinal diagnosis can be even more challeng-ing.Thankfully,even though
these tumorsmay appear undifferentiated at the lightmicroscopic level,they often
continue toproduce molecules that relate either totheir cellular origin or to their
newlyacquired form ofdifferentiation.To moreaccurately classify such tumors,these
mol-ecular products oforigin or differentiationare routinely assessed in the
lesional cellsthrough the use ofimmunohistochemical(IHC) studies.These techniques
employ awide variety ofmonoclonal and polyclon-al antibodies that are directed
against spe-cific cellular or integrated viral antigens(eg,those produced by the
Epstein-Barrvirus) that are usually expressed even inotherwise
�undifferentiated�neoplasms.The antibodies are linked to an enzymethat is capable
ofcleaving a selected chem-ical substrate.This activity produces a pig-mented
product (often brown;hence theterm �brown stains�) that is deposited inthe tissues
wherever the target antigens areexpressed.The diagnosis ofa particulartumor often
requires the analysis ofanumber ofantigens to fully explore thehistopathologic
differential.In cases ofmalignant lymphoma,for example,it isnot uncommon for a
panel of10 or more�probes�to be used to characterize theneoplastic process and
permit a therapythat is optimized for that particular tumor.Although routine
formalin-fixedparaffin-embedded tissue sections cangenerally be used to perform
most IHCstudies,an important exception involvestumors that require analysis by flow
cytom-etry.Typically used to permit rapid andhighly specific subclassification
oflym-phomas and leukemias,flow cytometryemploys IHC probes,but the tissue sam-ples
must not be fixed and should be ana-lyzed immediately following collection.Another
exception to this rule concerns thedefinitive diagnosis ofimmunobullous dis-orders
such as cicatricial pemphigoid.When such conditions are consideredwithin the
differential,perilesional tissueshould be obtained and submitted in a spe-cial
holding medium known as Michel�ssolution (Michel�s Media).A holdingmedium is
necessary because the molecu-lar structure ofthe diagnostic antigens inthese
conditions (eg,immunoglobulins,complement,and fibrinogen) is usuallydestroyed by
formalin fixation.These spec-imens are processed as frozen sections andare
evaluated by DIF,a special form ofIHCthat employs antibodies tagged with fluo-
rescent markers.When a special ultraviolet-capable microscope is used,these
markersreveal the presence and pattern ofimmunoreactants necessary to confirm
orrefute a potential autoimmune diseaseprocess.Indirect immunofluorescence(IIF)is
used for conditions such as pemphigusvulgaris,in which elevated levels ofcircu-
lating autoantibody are often seen.Forindirect immunofluorescent studies,patient
serum is incubated with a segmentofcontrol substrate (typically
monkeyesophagus).The serum is removed and thesubstrate is then incubated with
antibodyprobes similar to those used in DIF studies.As with DIF,ultraviolet
microscopy is usedto examine the substrate for evidence ofserum-derived antibody
binding to epithe-lial or basement membrane components.In a few instances even the
moresophisticated immunohistochemical tech-niques cannot provide a definitive
diagno-sis.In those situations newly developedmolecular techniquesare being used
with
572Part 5: Maxillofacial Pathologygreater frequency.These techniquesinclude
sophisticated cytogenetic studiessuch as fluorescence in situ hybridization(FISH)
as well as molecular probes thatuse complementary deoxyribonucleic acid(cDNA) to
identify disease-specific DNAsequences in human tissue samples.Exam-ples include
restriction fragment lengthpolymorphism analysis with Southernblot or antigen
receptor gene rearrange-ment analysis by polymerase chain reac-tion for the
determination ofclonality inB- or T-cell proliferations.Patient Follow-Up One ofthe
most important aspects in thediagnosis and management ofa given orallesion or
condition is the follow-up evalu-ation.This appointment permits the clini-cian to
assess the abnormality for physicalor symptomatic changes,gain insight intothe
kinetics ofgrowth or rate ofresolu-tion,and assess the impact ofinitial con-
servative treatment measures or recom-mendations to the patient.Theseadditional
pieces ofinformation may sup-port the working diagnosis,and no furtherwork-up may
be required (see Figure 29-1).Alternatively,the follow-up findingsmay indicate that
further investigation ofthe differential considerations is warrant-ed such as
biopsy and histopathologicreview.Finally,careful follow-up shouldbe considered
mandatory for patients whohave been previously diagnosed with ortreated for oral
dysplasia or carcinoma.Although an important part ofthepractice ofdentistry and
medicine,formalguidelines for the management oforallesions that are not clearly
premalignant orcancerous have only recently been suggest-ed.9Such guidelines are
helpful to cliniciansas they provide systematic protocols for themanagement oforal
pathologic conditionsand serve to reduce the medicolegal riskassociated with this
important aspect ofpatient care (Table 29-1).After the initial evaluation and
carefuldocumentation ofan oral lesion,a follow-up examination should be scheduled
for 7to 14 days later,with or without any treat-ment.Ifthere is evidence oflesion
enlarge-ment or other physical or symptomaticchanges that do not suggest normal
healingor resolution,then biopsy is indicated.Ifthe lesion remains relatively
unchangedand the index ofsuspicion for malignancyis low,the clinician should help
the patientdecide the next course ofaction basedupon experience,advanced
training,orboth.Whenever available,referral to anoral and maxillofacial pathologist
may behelpful in this regard.Ifthe patient andclinician decide to defer biopsy,this
deci-sion should be documented and re-evalua-tion ofthe area should be scheduled at
1,3,6,and 12 months following the initialexamination.During the follow-up
period,diagnostic options include the brush cytol-ogy technique (to identify
evidence ofatypical epithelial cells in surface lesions)or incisional biopsy (to
establish a firmdiagnosis).The need for these optionsvaries depending on the
concerns ofthepatient or the experience and expertise ofthe clinician.At any time
point,however,evidence ofsignificant lesional changeshould immediately trigger a
recommen-dation ofbiopsy.After a year mostunchanged lesions can be monitored
atroutine semiannual or annual dental visits.Finally,it should be recognized
thatthese recommendations,althoughsound,do not represent rigid guidelinesor
medicolegal standards ofcare thatcover every clinical scenario.Eachpatient and
abnormality deserves indi-vidual attention and management thatmay vary from the
protocol above,basedupon training,experience,and the clini-cal judgement ofthe
practitioner.References1.Ellis E III.Principles ofdifferential diagnosisand
biopsy.In:Peterson LJ,Ellis E,HuppJR,Tucker MR,editors.Contemporary oraland
maxillofacial surgery.4th ed.St.Louis:Mosby,Inc.;2003.p.458�78.2.Halstead CL,Blozis
GG,Drinnan AJ,Gier RE,editors.Diagnostic process.In:Physicalevaluation ofthe dental
patient.St.Louis:The C.V.Mosby Company;1982.p.8�12.3.Frederiksen NL.Specialized
radiographic tech-niques.In:White SC,Pharoah MJ,editors.Oral radiology:principles
and interpreta-tion.4th ed.St.Louis:Mosby,Inc.;2000.p.217�41.4.Hlawitschka M,Neise
E,Bredow J,et al.FDG-PET in the pretherapeutic evaluation ofprimary squamous cell
carcinoma oftheoral cavity and the involvement ofcervicallymph nodes.Mol Imag Biol
2002;4:91�8.Table 29-1Follow-Up Protocol for Oral Pathology 1.Initial re-
evaluation:7�14 d following lesion detection/examination2.Ifno evidence oflesional
progression or suspicious clinical alterations,reevaluate at 1,3,6,and 12 mo
intervals;thereafter,re-examine in conjunction with normal recall visits (every
6�12 mo)3.Iflesional progression or suspicious clinical changes noted,incisional or
excisional biopsyshould be performed as soon as possible,and specimen should be
reviewed by oral and maxillofacial pathologist4.Ifno evidence ofpreneoplastic
change (dysplasia) or malignancy (carcinoma or sarcoma)reported,schedule follow-up
as in step 2 and document subsequent findings in patient record5.When diagnosis
ofdysplasia (premalignancy) or malignancy is reported,refer or scheduleimmediately
for appropriate work-up and therapy;following definitive treatment,begin follow-up
evaluations as in step 2 or similar protocol Adapted from Alexander RE et al.9
Differential Diagnosis ofOral Disease5735.Kato H,Kuwano H,Nakajima M,et al.Com-
parison between positron emission tomog-raphy and computed tomography in theuse
ofthe assessment ofesophageal carci-noma.Cancer 2002;94:921�8.6.Hubner KF,Thie
JA,Smith GT,et al.Clinicalutility ofFDG-PET in detecting head andtumors:a
comparison ofdiagnostic meth-ods and modalities.Clin Positron
Imaging2000;3:7�16.7.McGuirt WF,Greven K,Williams D III,et al.PET scanning in head
and neck oncology:areview.Head Neck 1998;20:208�15.8.Schmid DT,Stoeckli
SJ,Bandhauer F,et al.Impact ofpositron emission tomographyon the initial staging
and therapy in locore-gional advanced squamous cell carcinomaofthe head and
neck.Laryngoscope2003;113:889�91.9.Alexander RE,Wright JM,Thiebaud S.Evalu-
ating,documenting and following up oralpathological conditions:a suggested proto-
col.J Am Dent Assoc 2001;132:329�35.
CHAPTER 30Odontogenic Cysts and TumorsEric R.Carlson,DMD,MDOdontogenic cysts and
tumors are rela-tively uncommon lesions ofthe oral andmaxillofacial region that
must be consid-ered whenever examining and formulatinga differential diagnosis ofan
expansileprocess ofthe jaws.The clinical presenta-tion,radiographic appearance,and
natur-al history ofthese lesions varies consider-ably,such that odontogenic cysts
andtumors represent a diverse group oflesions ofthe jaws and overlying soft tis-
sues.Collectively speaking,their occur-rence is frequent enough to warrant
athorough discussion.As a whole,thesepathologic entities have been studied
andreported on extensively.Purely defined,odontogenicrefers toderivation from a
tooth-related apparatus.Tooth formation is a complex process thatinvolves both
connective tissues andepithelium.Three major tissues areinvolved in odontogenesis
including theenamel organ,the dental follicle,and thedental papilla.The enamel
organ is anepithelial structure that is derived fromoral ectoderm.The dental
follicle and den-tal papilla are considered ectomesenchy-mal in nature because they
are in partderived from neural crest cells.For each tooth,odontogenesis beginswith
the apical proliferation from the oralmucosa ofepithelium known as the dentallamina
(Figure 30-1).The dental lamina,in turn,gives rise to the enamel organ,acap-shaped
structure that subsequentlyevolves into a bell shape.After forming theenamel
organ,the cord ofdental laminanormally fragments and degenerates;however,small
islands ofthe dental lami-na may remain after tooth formation andare believed to be
responsible for thedevelopment ofseveral ofthe odontogeniccysts and tumors.The
enamel organ has four types ofepithelium.The innermost lining isreferred to as the
inner enamel epitheliumand becomes the ameloblastic layer thatforms tooth
enamel.The second layer ofcells adjacent to the inner enamel epitheli-um is the
stratum intermedium.Adjacentto this layer is the stellate reticulum,fol-lowed by
the outer enamel epithelium.Sur-rounding the enamel organ is loose con-nective
tissue known as the dental papilla.Contact with the enamel organ epitheliuminduces
the dental papilla to make odonto-blasts that form dentin.As the odonto-blasts
deposit dentin,they induce theameloblasts to begin forming enamel.Following the
initial formation ofthecrown,a thin layer ofthe enamel organepithelium known as
Hertwig�s rootsheath proliferates apically to provide thestimulus for odontoblastic
differentiationin the root portion ofthe developingtooth.This epithelial extension
laterbecomes fragmented but leaves behindsmall nests ofepithelial cells known
asrests ofMalassez in the periodontal liga-ment space.The rests ofMalassez
arebelieved to be the source ofepithelium formost periapical cysts but generally
are notbelieved to give rise to any ofthe odonto-genic neoplasms,with the possible
excep-tion ofthe squamous odontogenic tumor.In the development ofa tooth,follow-ing
completion ofenamel formation,theFIGURE30-1The enamel organ is seen emanat-ing from
the dental lamina (hematoxylin andeosin; original magnification�20) Reproducedwith
permission from Cawson RA,Eveson JW,editors.Oral pathology and diagnosis.Coloratlas
with integrated text.Philadelphia (PA):W.B.Saunders; 1987.
576Part 5: Maxillofacial Pathologyenamel organ epithelium atrophies toform a thin
flattened layer ofcells that cov-ers the enamel ofthe unerupted tooth.This layer
ofepithelium is known as thereduced enamel epithelium.In the normalsequence
ofevents,this reduced enamelepithelium later merges with the surfaceepithelium and
forms the initial gingivalcrevicular epithelium ofthe newly
eruptedtooth.However,iffluid accumulatesbetween the reduced enamel epitheliumand
the crown ofthe tooth before tootheruption,a cyst is formed that is known asa
dentigerous or follicular cyst.An understanding ofthe progressionofodontogenic
cysts and tumors withinthe oral and maxillofacial region requires athorough
knowledge ofthe cell cycle ofthese lesions and an appreciation oftheconcept
ofproliferation versus apoptosis(programmed cell death).Most ofthepathogenetic
mechanisms ofodontogeniccysts and tumors can be explained via thecell cycle (Figure
30-2).Normally cell divi-sion is divided into four phases:G1(gap1),S
(deoxyribonucleic acid synthesis),G2(gap 2),and M (mitosis).A key event is
theprogression from G1to the S phase.Genet-ic alterations,ifunrepaired in the
G1phase,may be carried into the S phase andperpetuated in subsequent cell
divisions.The G1-S checkpoint is normally regulatedby a well-coordinated and
complex systemofprotein interactions whose balance andfunction are critical to
normal cell divi-sion.1As can be seen in Figure 30-2,oncegenetic change occurs that
encourages thedevelopment ofan odontogenic cyst ortumor,a series ofevents mediated
by theodontogenic lesion occur that may pro-mote proliferation.Such events
supportthe pathogenetic mechanism involved inthe progression ofthe cyst or tumor.It
is the purpose ofthis chapter toreview the clinically significant and morecommonly
encountered odontogenic cystsand tumors.In so doing,salient clinicaland
radiographic features are discussed,asare the pathogenetic mechanisms support-ing
proliferation ofsome ofthe moreaggressive odontogenic cysts and
tumors.Recommendations for treatment andprognostic information are also
offered.Odontogenic Cysts With rare exceptions,epithelium-linedcysts in bone are
seen only in the jaws.2Other than a few cysts that may resultfrom the inclusion
ofepithelium alongembryonic lines offusion,most jaw cystsare lined by epithelium
that is derivedfrom odontogenic epithelium,hence theterm odontogenic cysts.These
cysts are sub-classified as developmental or inflamma-tory in nature.Although the
cell type isoften known,developmental cysts are ofunknown origin;however,they do
notseem to be the result ofan inflammatoryreaction.Inflammatory cysts,on the
otherhand,are the result ofinflammation(Table 30-1).Dentigerous CystBy definition,a
dentigerous cyst occurs inassociation with an unerupted tooth,mostcommonly
mandibular third molars.Other common associations are with max-illary third
molars,maxillary canines,andmandibular second premolars.2They mayalso occur around
supernumerary teethand in association with odontomas;how-ever,they are only rarely
associated withprimary teeth.2,3Although dentigerouscysts occur over a wide age
range,they aremost commonly seen in 10- to 30-year-olds.There is a slight male
predilection,and their prevalence appears to be higherin Whites than in Blacks.Many
dentiger-ous cysts are small asymptomatic lesionsthat are discovered
serendipitously onroutine radiographs,although some maygrow to considerable size
causing bonyexpansion that is usually painless until sec-ondary infection
occurs.Radiographically,the dentigerous cystpresents as a well-defined unilocular
radi-olucency,often with a sclerotic border(Figure 30-3).Since the epithelial
lining isderived from the reduced enamel epitheli-um,this radiolucency typically
and prefer-entially surrounds the crown ofthe tooth.A large dentigerous cyst may
give theimpression ofa multilocular processbecause ofthe persistence ofbone trabec-
ulae within the radiolucency.However,dentigerous cysts are grossly
andhistopathologically unilocular processesCell cycle(PCNA, Ki-67)G1SG2MG0BCL2,
BCLXL,ApoptosisothersBAK, BCLXS,othersBAX, P53Inhibitor proteins(p16, p21,
p27)E2FpRbProliferation(cyclins + kinases)Growth/mitogenicfactorsFIGURE30-2The cell
cycle�a concept ofproliferation versus apoptosis.PCNA = proliferating cellnuclear
antigen.
Odontogenic Cysts and Tumors577and probably are never truly
multilocularlesions.2Three types ofdentigerous cysthave been described
radiographically,including the central variety,in which theradiolucency surrounds
just the crown ofthe tooth,with the crown projecting intothe cyst lumen.In the
lateral variety,thecyst develops laterally along the tooth rootand partially
surrounds the crown.Thecircumferential variant ofthe dentigerouscyst exists when
the cyst surrounds thecrown but also extends down along theroot surface,as ifthe
entire tooth werelocated within the cyst.One diagnostic dilemma for oral
andmaxillofacial surgeons is distinguishingbetween a dentigerous cyst and
anenlarged dental follicle.This distinctionbecomes clinically significant when
thesurgeon considers whether to submit tis-sue removed with an impacted third
molarfor histopathologic examination asopposed to clinical designation as a folli-
cle,with simple disposal ofthe tissue.Theradiographic distinction becomes some-what
arbitrary;however,any pericoronalradiolucency that is > 4 or 5 mm is con-sidered
suggestive ofcyst formation andshould be submitted for microscopicexamination.It is
noteworthy that pathol-ogists also struggle with the distinctionbetween dental
follicles associated withdeveloping teeth and odontogeniclesions.4,5It seems that
odontogenic cysts,odontogenic fibroma,and odontogenicmyxoma are the lesions most
often inap-propriately diagnosed by surgical patholo-gists owing to a general
unfamiliarity withthe normal process ofodontogenesis.4Ofperhaps even greater
concern is thelarge unilocular radiolucency.Althoughmost commonly classified
radiographicallyas dentigerous cysts,it is incumbent uponthe surgeon to section
these excised speci-mens in the operating room and to consid-er frozen-section
analysis.In fact,somespecimens may contain a focus ofunicysticameloblastoma and
therefore require con-sideration ofmore extensive treatment.The histologic features
ofdentigerouscysts may vary greatly depending mainly onwhether or not the cyst is
inflamed.In thenoninflamed dentigerous cyst,a thin epithe-lial lining may be
present with the fibrousconnective tissue wall loosely arranged (Fig-ure 30-4).In
the inflamed dentigerous cyst,the epithelium commonly demonstrateshyperplastic rete
ridges,and the fibrous cystwall shows an inflammatory infiltrate.Treatment and
PrognosisMost dentiger-ous cysts are treated with enucleation ofthe cyst and
removal ofthe associatedtooth,often without a preceding incisionalbiopsy (Figure
30-5).Larger cysts that aretreated in the operating room should prob-ably undergo
frozen-section diagnosis andappropriate treatment that might be dic-tated by other
diagnoses.Curettage ofthecyst cavity is usually advisable at the timeofremoval
ofthe cyst in the event that amore aggressive cyst is diagnosedhistopathologically
following removal inan office setting.Such diagnoses wouldinclude odontogenic
keratocyst and uni-cystic ameloblastoma.Large dentigerous cysts may be treatedwith
marsupialization (Figure 30-6) whenenucleation and curettage might otherwiseresult
in neurosensory dysfunction or pre-dispose the patient to an increased
chanceofpathologic fracture.Some patients whoare not candidates for general
anesthesiamay also be treated with a marsupializationprocedure in an office setting
under localanesthesia.This permits decompression ofthe large dentigerous cyst with
a resultantreduction in the size ofthe cyst and bonydefect.At a later date the
reduced cyst canbe removed in a smaller-scale surgery.I emphasize the need for
histopatho-logic examination ofall radiolucencies thatare empirically diagnosed as
dentigerouscysts.This includes those that are enucleat-ed as well as those that
undergo marsupial-ization,during which it is important to inspect the cyst lumen
and submit a Table 30-1Classification ofOdontogenic CystsDevelopmentalDentigerous
cystEruption cystOdontogenic keratocystOrthokeratinized odontogenic cystGingival
(alveolar cyst ofthe newborn)Gingival cyst ofthe adultLateral periodontal
cystCalcifying odontogenic cystGlandular odontogenic cystInflammatoryPeriapical
(radicular cyst)Residual periapical (radicular cyst)Buccal bifurcation
cystFIGURE30-3This unilocular radiolucency oftheleft mandibular ramus associated
with impactedtooth no.17 was discovered serendipitously whenthe patient was
evaluated for routine dental work.FIGURE30-4The biopsy ofthe radiolucency inFigure
30-3 shows an atrophic stratified squamousepithelium without significant associated
inflam-mation.The diagnosis is dentigerous cyst (hema-toxylin and eosin; original
magnification �40).
578Part 5: Maxillofacial Pathologyrepresentative piece for
histopathologicexamination.Support ofthis statementstems from the occasional
formation ofasquamous cell carcinoma,mucoepider-moid carcinoma,or ameloblastoma
fromor in association with a dentigerous cyst.6�8The prognosis for most
histopathologicallydiagnosed dentigerous cysts is excellent,with recurrence being a
rare finding.Odontogenic KeratocystThe odontogenic keratocyst is a distinctiveform
ofdevelopmental odontogenic cystthat deserves special consideration becauseofits
specific histopathologic features andaggressive clinical behavior.Two variants
ofthis cyst are well known;the sporadic cystand the cyst associated with the nevoid
basalcell carcinoma syndrome.Both variants ofthe odontogenic keratocyst are
believed tobe derived from remnants ofthe dental lam-ina.This cyst shows a
different growthmechanism and biologic behavior from thepreviously described
dentigerous cyst.Mostauthors believe that dentigerous cysts con-tinue to enlarge as
a result ofincreasedosmotic pressure within the lumen ofthecyst.This mechanism does
not appear tohold true for odontogenic keratocysts,andtheir growth may be related
to unknownfactors inherent in the epithelium itselfofenzymatic activity in the
fibrous wall.9Adequate diagnosis and treatment ofthe odontogenic keratocyst is
importantfor three reasons:(1) this cyst is recog-nized as being more aggressive
than otherodontogenic cysts,10(2) the odontogenickeratocyst has a higher rate
ofrecurrencethan other odontogenic cysts,11and (3) theassociation with nevoid basal
cell carcino-ma syndrome requires that the clinicianexamine a patient with multiple
cysts ofthe jaws for physical findings that mightdiagnose this
syndrome.12�14Odontogenic keratocysts may be foundin patients ranging in age from
infancy toold age;however,60% ofcases are seen inpeople between 10 and 40 years
old.15In hisseries of312 cases,Brannon found a meanage ofnearly 38 years.16The peak
preva-lence was in the second and third decadesoflife,with only 15% occurring past
the ageof60 years.Woolgar and colleaguesreviewed 682 odontogenic keratocysts
from522 patients and found a mean age of40 years for patients with single nonrecur-
rent cysts and 26.2 years for patients withmultiple cysts ofthe nevoid basal cell
carci-noma syndrome.17A slight male predilec-tion is usually seen,and 60 to 80%
ofcasesinvolve the mandible,particularly in theposterior body and ascending
ramus.2Although it is rare for a dentigerous cyst toappear multilocular on
radiographs,it ismost common for odontogenic keratocyststo appear multilocular
(Figure 30-7).ManyFIGURE30-5A,The dentigerous cyst in Figure30-3 is treated with
enucleation and curettage ofthe cyst and removal ofthe etiologic tooth.B,The5-year
postoperative radiograph shows anAacceptable bony fill.BFIGURE30-6A,This large
biopsy-proven dentigerous cyst occurred in an elderly patient who had coronary
artery disease.Owing to the size ofthe cyst and thecompromised cardiac status ofthe
patient,a relatively noninvasive marsupialization was performed.B,An acrylic plug
with a wire handle was placed in a smallsurgical entrance into the cyst cavity.The
cyst shrunk considerably,after which time the etiologic impacted tooth was removed
with a small remnant ofdentiger-ous cyst.C,The 5-year postmarsupialization
radiograph shows an excellent fill ofbone.ABC
Odontogenic Cysts and Tumors579appear unilocular and can therefore be con-fused
with dentigerous cysts.It is clear,therefore,that the differential diagnosis
ofaunilocular radiolucency must include bothentities and that treatment should
includecurettage in the event that the diagnosis isodontogenic keratocyst.When
multiplemultilocular radiolucencies are noted on apanoramic radiograph,the
clinician mustperform an incisional biopsy and investi-gate the possibility
ofnevoid basal cell car-cinoma syndrome (Table 30-2).Histologically,the odontogenic
kera-tocyst is readily recognized.A uniformlayer ofstratified squamous
epithelium,usually six to eight cells in thickness,ispresent (Figure 30-8).The
parakeratoticsurface is characteristically corrugated.The wall is usually thin and
friable,whichcan pose problems for removal in onepiece intraoperatively.Epithelial
buddingand the presence ofdaughter cysts may benoted in the connective tissue
wall.It isgenerally advisable to ask the pathologistto examine the sections
carefully for thesetwo features as they generally impart amore aggressive character
to the cyst.Treatment and PrognosisLike the treat-ment ofmost odontogenic
cysts,theodontogenic keratocyst may be treatedwith enucleation and curettage and
mustbe removed in one piece,which requiresacceptable access and lighting (Figure
30-9).As such,many patients are suitablytreated in an operating room setting
undergeneral anesthesia.This is particularlyhelpful when removing large cysts.It is
myexperience and that ofothers that a largemajority ofsporadic odontogenic kerato-
cysts may be effectively managed with athorough enucleation and
curettagesurgery.18,19MacIntosh has advocated theresection ofodontogenic
keratocysts with5 mm linear margins as the preferred pri-mary method
oftreatment,and hasreported on 37 patients with 43 lesionsemphasizing the efficacy
and superiorresults ofresection over all other thera-peutic undertakings.20The
reported frequency ofrecurrenceofthe odontogenic keratocyst ranges from2.5% to
62.5% in various studies.11Thiswide variation may be related to the totalnumber
ofcases studied,the length offol-low-up periods,and the inclusion orexclusion
oforthokeratinized cysts in thestudy group.Several reports that includelarge
numbers ofcases indicate a recur-rence rate ofapproximately 30%.2Regeziand
colleagues point out that the recur-rence rate for solitary odontogenic kerato-
cysts is 10 to 30%.21They indicate thatapproximately 5% ofpatients with odon-
togenic keratocysts have multiple sporadicjaw cysts (nonsyndromic) and that
theirrecurrence rate is greater than that for soli-tary lesions.21Brannon has
suggested threemechanisms responsible for recurrence:(1) remnants ofdental lamina
within thejaws not associated with the originalodontogenic keratocyst being
responsiblefor de novo cyst formation;(2) incompleteremoval (persistence) ofthe
original cystsecondary to a thin friable lining and cor-tical perforation with
adherence to adja-cent soft tissue;and (3) remaining rests ofdental lamina and
satellite cysts followingenucleation.22Vedtofte and Praetoriusreviewed 72 patients
with 75 odontogenickeratocysts and observed remnants ofdental lamina between the
cyst membraneFIGURE30-7This multilocular radiolucency,pre-sent in a 54-year-old
man,should suggest anodontogenic keratocyst when formulating a differ-ential
diagnosis.Table 30-2Clinical Features oftheBasal Cell Nevus Syndrome=50%
frequencyMultiple basal cell carcinomasOdontogenic keratocystsEpidermal cysts ofthe
skinPalmar/plantar pitsCalcified falx cerebriEnlarged head circumferenceRib
anomalies (splayed,fused,partially missing,bifid)Mild ocular hypertelorismSpina
bifida occulta ofcervical or thoracic vertebrae15�49% frequencyCalcified ovarian
fibromasShort fourth metacarpalsKyphoscoliosis or other vertebral anomaliesPectus
excavatum or carinatumStrabismus (exotropia)< 15% frequency (but not
random)MedulloblastomaMeningiomaLymphomesenteric cystsCardiac fibromaFetal
rhabdomyomaMarfanoid buildCleft lip and/or palateHypogonadism in malesMental
retardationAdapted from Gorlin FJ.14FIGURE30-8The classic histologic appearanceofan
odontogenic keratocyst from the incisionalbiopsy ofthe lesion in Figure 30-7
(hematoxylinand eosin; original magnification �40).
580Part 5: Maxillofacial Pathologyand overlying mucosa.23As such,theyadvocated the
excision ofoverlyingmucosa in conjunction with removal ofthe cyst.Williams and
Connor recom-mended a primary enucleation and curet-tage surgery for odontogenic
keratocysts,including the use ofmethylene blue as amarking agent,followed by a 3-
minuteapplication ofCarnoy�s solution.11Theyindicated that resection should be
consid-ered for the treatment ofa recurrentodontogenic keratocyst,with inclusion
ofappropriate bone and soft tissue margins.Pathogenetically,the odontogenic ker-
atocyst expresses cell cycle phenomena thatsupport its proliferation.21These
includethe release ofthe cytokines interleukin 1a(IL-1a) and IL-6 as well as
parathyroidhormone�related protein that encourageresorption
ofbone.21,24Moreover,theexpression ofproliferating cell nuclearantigen (PCNA) in
odontogenic cysts hasbeen assessed.It is hypothesized that theidentification ofthe
proliferative activity inodontogenic cysts and tumors may be use-ful to predict
their biologic behavior.Thesame may be true ofthe Ki-67 antigen.Infact,two studies
have been performed thathave quantified these parameters.25,26Theconclusion ofboth
studies is that anincreased proliferative activity for theodontogenic keratocyst in
comparisonwith the dentigerous cyst is noted consis-tently.These results are in
agreement withthe more aggressive behavior seen with theodontogenic keratocyst.The
orthokeratinized odontogeniccyst,once thought to be a variant oftheodontogenic
keratocyst,is now generallywell accepted as being a different clinico-pathologic
entity from the more commonparakeratinized odontogenic keratocyst;itshould
therefore be placed in a differentcategory.These cysts usually appear asunilocular
radiolucencies,but occasionalexamples have been multilocular.A major-ity ofthese
cysts are encountered in alesion that appears clinically and radi-ographically to
represent a dentigerouscyst,most often involving an uneruptedmandibular third molar
tooth.Histologi-cally,the epithelium is thin and orthoker-atinized,and a prominent
palisaded basallayer,characteristic ofthe odontogenickeratocyst,is not
present.Enucleation andcurettage ofthe orthokeratinized cyst iscurative in most
cases.The reported rateofrecurrence of2% is far lower than thepreviously quoted
statistics for recurrenceofthe odontogenic keratocyst.2Nevoid Basal Cell Carcinoma
SyndromeThe nevoid basal cell carcinoma syndrome(basal cell nevus syndrome,Gorlin�s
syn-drome) is an autosomal-dominant inher-ited condition that exhibits high pene-
trance and variable expressivity.It iscaused by mutations in the
PTCHtumorsuppressor gene,mapped to chromosome9q22.3-q31.Affected patients (Figure
30-10A) may demonstrate frontal and tem-poroparietal
bossing,hypertelorism,andmandibular prognathism (see Table 30-2).14Other frequent
skeletal anomaliesinclude bifid ribs and lamellar calcificationofthe falx cerebri
(Figure 30-10B).14TheFIGURE30-9A,A very thin cyst lining wasencountered when
performing the enucleationand curettage ofthe odontogenic keratocyst inFigure 30-
7.B,The 7-year postoperative radi-ograph shows an excellent fill ofbone.A recon-
struction bone plate was placed at the time oftheenucleation and curettage to
prevent a patholog-ic fracture ofthe mandible.ABFIGURE30-10A,This 18-year-old shows
some ofthe clinical features ofthe nevoid basal cell carci-noma syndrome including
frontal bossing andmandibular prognathism.B,The radiograph fromanother patient
shows a calcified falx cerebri.AB
Odontogenic Cysts and Tumors581most significant clinical feature is the ten-dency
to develop multiple basal cell carci-nomas that may affect both exposed andnon�sun-
exposed areas ofthe skin.Pittingdefects on the palms and soles can befound in
nearly two-thirds ofaffectedpatients (Figure 30-11).The discovery ofmultiple
odontogenic keratocysts is usual-ly the first manifestation ofthe syndromethat
leads to the diagnosis.For this reason,any patient with an odontogenic kerato-cyst
should be evaluated for this condi-tion.Although the cysts in patients withnevoid
basal cell carcinoma syndromecannot definitely be distinguished micro-scopically
from those not associated withthe syndrome,they often demonstratemore epithelial
proliferation and daughtercyst formation in the cyst wall.The treatment ofthe
odontogenickeratocyst in patients with nevoid basalcell carcinoma syndrome can be
difficultowing to the large number of�recur-rences�in these patients.As a matter
ofpoint,I choose to refer to these as newprimary cysts owing to the autosomal-
dominant penetrance ofthe syndromeand cyst development.It is certainly pos-sible
that many ofthese cysts are persis-tent,particularly when considering howcommon it
can be to retain rests ofthedental lamina when enucleating an odon-togenic
keratocyst.Whatever the mecha-nism,a resection hardly seems to be war-
ranted.Marsupialization is a moredesirable procedure (Figure 30-12) andhas been
shown to result in complete res-olution ofthe sporadic cyst,with no his-tologic
signs ofcystic remnants,daughtercysts,or budding ofthe basal layer
oftheepithelium.27Although all ofthe eightcases in the series by Pogrel and
Jordanwere sporadic cysts,27a similar approachto syndrome patients with
odontogenickeratocysts that had been operated onmultiple times has been performed
withsuccess in a small sample size.18Glandular Odontogenic CystThe glandular
odontogenic cyst (sialo-odontogenic cyst) is a rare and recentlydescribed cyst
ofthe jaws that is capableofaggressive behavior and recurrence.Although it is
generally accepted as beingofodontogenic origin,it shows glandularor salivary
features that seem to point tothe pluripotentiality ofodontogenicepithelium as
cuboidal/columnar cells,mucin production,and cilia are noted inthese
cysts.Glandular odontogenic cystsoccur most commonly in middle-agedadults,with a
mean age of49 years at thetime ofdiagnosis.2Eighty percent ofcases occur in the
mandible,21and astrong predilection for the anteriorregion ofthe jaws has been
reported,with many mandibular lesions crossingthe midline (Figure 30-13).These
cystsmay appear either unilocular or multi-locular radiographically.There is a
histologic similarity betweenthe glandular odontogenic cyst and the pre-dominantly
cystic intraosseous mucoepi-dermoid carcinoma.However,the epitheliallining ofthe
glandular odontogenic cyst istypically thinner and does not show evi-dence ofthe
more solid or microcysticepithelial proliferations seen in mucoepi-dermoid
carcinoma (Figure 30-14).Wal-dron and Koh reviewed the similaritiesbetween the two
lesions and concluded thatit is entirely possible that some cases previ-ously
diagnosed as central mucoepidermoidFIGURE30-11Plantar pitting can be observedby
immersing the foot in povidone-iodine solu-tion followed by a conservative wash
ofthe footwith saline.The solution is taken up in the pitspresent in the plantar
surface ofthe foot.FIGURE30-12The patient in Figure 30-10A had previously undergone
three enucleation and curet-tage surgeries for bilateral maxillary odontogenic
keratocysts.A,Development ofnew large cysts inthis area led to additional treatment
with marsupialization.B,Six months later the axial computedtomography shows
regression ofthe cysts.AB
582Part 5: Maxillofacial Pathologytumors may be reclassified as examples
ofglandular odontogenic cysts.28Treatment and PrognosisMost glandu-lar odontogenic
cysts are treated with enu-cleation and curettage (Figure 30-15).Some
authors,however,point to a recur-rence rate ofapproximately 30% andtherefore
recommend resection.29Calcifying Odontogenic Cyst The calcifying odontogenic cyst
(COC),orGorlin�s cyst,is an uncommon lesion thatdemonstrates considerable
histopathologicdiversity and variable clinical behavior.Although designated as a
cyst,some investi-gators provide evidence for subclassifica-tion as a neoplasm as
well.30,31In addition,the COC may be associated with other rec-ognized odontogenic
tumors,most com-monly the odontoma.Adenomatoid odon-togenic tumors and
ameloblastomas havealso been associated with the COC.Ghostcell keratinization,the
characteristic micro-scopic feature ofthis cyst,is also a definingfeature ofthe
cutaneous lesion known asthe calcifying epithelioma ofMalherbe orpilomatrixoma.The
World Health Organi-zation�s classification ofodontogenictumors groups the COC with
all its variantsas an odontogenic tumor rather than anodontogenic cyst.The
commentary on thesecond edition by Kramer,Pindborg,andShear points out that some
COCs appear tobe non-neoplastic,but others show an infil-trative pattern
ofgrowth.32They furtherindicate that more experience with theCOC may provide
reliable criteria for theirreclassification.The review by Hong andcolleagues
designated 79 of92 cases ofCOC as cysts with the remaining 13 casesbeing neoplastic
in nature.30The COC is predominantly anintraosseous lesion,although 13 to 30%
ofreported cases occur as peripheral lesions.2Both the peripheral and central
lesionsoccur with about equal frequency in themaxilla and mandible.There appears to
bea predilection for the incisor and canineareas.Patients range in age from infant
toelderly,with a mean age ofoccurrence ofabout 30 years.COCs that are
associatedwith odontomas tend to occur in youngerpatients,with a mean age of17
years.2Themore rare neoplastic variant ofthe COCappears to occur in elderly
patients.MostCOCs appear radiographically as unilocu-lar well-defined lesions.The
radiopaquestructures within the lesions have beendescribed as either irregular
calcificationsor toothlike densities.Treatment and PrognosisThe standardtreatment
for the COC is enucleation andcurettage (Figure 30-16).A limited num-ber
ofrecurrences have been reported aftersuch treatment.When a COC is associatedwith
another recognized odontogenictumor such as an ameloblastoma,thetreatment and
prognosis are likely to bethe same as for the associated tumor.Although only a few
cases have beenreported,31a carcinoma arising in a COCmay occur.One such reported
case result-ed in multiple pulmonary metastases andwas referred to as an
odontogenic ghostFIGURE30-13Aand B,This glandular odonto-genic cyst presented with
a unilocular radiolucen-cy ofthe anterior mandible crossing the midline.ABFIGURE30-
14Histopathology ofthe lesion inFigure 30-13 shows a nonkeratinized
stratifiedsquamous epithelium with intraepithelialmucous cells and cilia
(hematoxylin and eosin;original magnification �40).FIGURE30-15A,The patient whose
radi-ograph appears in Figure 30-13 underwent anenucleation and curettage ofthe
cyst as well asremoval ofthe anterior mandibular teeth.B,The 3-year postoperative
radiograph showsacceptable bony fill.AB
Odontogenic Cysts and Tumors583cell carcinoma by the authors.33It has notbeen
demonstrated whether the malignantCOC arose from previously benign
lesionsand,ifso,whether that precursor was thecystic or neoplastic type.Odontogenic
Tumors Odontogenic tumors comprise a complexgroup oflesions ofgreat importance to
oraland maxillofacial surgeons.Many oftheselesions are true tumors,whereas some
arehamartomas.Like normal odontogenesis,odontogenic tumors demonstrate
varyinginductive interactions between odontogenicepithelium and odontogenic
ectomes-enchyme.This ectomesenchyme was for-merly referred to as mesenchymebecause
itwas thought to be derived from the meso-dermal layer ofthe embryo.It is now
accept-ed that this tissue differentiates from theectodermal layer in the cephalic
portion ofthe embryo;hence,the designation ectomes-enchyme.Odontogenic tumors are
typicallysubclassified by their tissues oforigin (Table30-3).Tumors ofodontogenic
epitheliumare composed only ofodontogenic epitheli-um without any participation
ofthe odon-togenic ectomesenchyme.Other odonto-genic neoplasms,referred to as
mixedodontogenic tumors,are composed ofodontogenic epithelium and ectomesenchy-mal
elements.A third group,tumors ofodontogenic ectomesenchyme,includesthose tumors
composed principally ofectomesenchymal elements.Although someodontogenic epithelium
may be includedwithin these lesions,it does not appear toplay an essential role in
their pathogenesis.The frequency ofodontogenic tumorsseems to be geographically
determined(Table 30-4).Studies from North Americaseem to indicate that odontogenic
tumorsrepresent approximately 1% ofall acces-sions in oral pathology
laboratories,34,35whereas African studies have a much high-er incidence
ofodontogenic tumors.36�41Moreover,the ameloblastoma is morecommonly encountered in
African andother underdeveloped countries than inNorth America.AmeloblastomaThe
ameloblastoma is the most commonclinically significant and potentially
lethalodontogenic tumor.Excluding odon-tomas,its incidence equals or exceeds
thecombined total ofall other odontogenictumors.These tumors may arise from
restsofthe dental lamina,a developing enamelorgan,the epithelial lining ofan
odonto-genic cyst,or the basal cells ofthe oralmucosa.2The ameloblastoma occurs
inthree different variants,each with specificimplications for treatment and a
uniqueprognosis:solid or multicystic,unicystic,and peripheral.In an analysis ofthe
inter-national literature,3,677 cases ofameloblastoma were reviewed,ofwhich92% were
solid or multicystic,6% wereunicystic,and 2% were peripheral.42Solid or Multicystic
AmeloblastomaThis variant ofthe ameloblastoma isFIGURE30-16A,This calcifying
odontogeniccyst appears as a mixed radiolucent/radiopaquelesion on the occlusal
radiograph.B,This patientunderwent enucleation and curettage ofthelesion.C,The
histopathology shows characteris-tic ghost cells (hematoxylin and eosin;
originalmagnification �40).ABCTable 30-3Classification ofOdontogenicTumors Tumors
ofodontogenic epitheliumAmeloblastoma�Malignant ameloblastoma�Ameloblastic
carcinomaCalcifying epithelial odontogenic tumorSquamous odontogenic tumorClear
cell odontogenic carcinomaPrimary intraosseous carcinomaTumors ofodontogenic
epithelium with odontogenic ectomesenchyme �dental hard tissue
formationAmeloblastic fibromaAmeloblastic fibro-odontomaAmeloblastic
fibrosarcomaOdontoameloblastomaOdontoma�Compound composite�Complex
compositeAdenomatoid odontogenic tumorTumors ofodontogenic ectomesenchyme�included
odontogenic epitheliumOdontogenic fibromaGranular cell odontogenic tumorOdontogenic
myxomaCementoblastoma
584Part 5: Maxillofacial Pathologyencountered in patients over a wide agerange.43It
is rare in children in their firstdecade oflife and relatively uncommon inthe
second decade.44The tumor shows arelatively equal rate ofoccurrence in thethird
through seventh decades.There isno gender predilection,and racialpredilection is
most controversial.About85% ofthis variant ofthe ameloblastomaoccur in the
mandible,most commonly inthe molar/ramus region.45About 15% ofmulticystic
ameloblastomas occur in themaxilla,usually in the posteriorregions.46�49A painless
expansion ofthejaws is the most common clinical presen-tation;neurosensory changes
are uncom-mon,even with large tumors (Figure 30-17).Slow growth is the
rule,withuntreated tumors leading to tremendousfacial disfigurement (Figure 30-
18).50The most common radiographic fea-ture is that ofa multilocular
radiolucency.Buccal and lingual cortical expansion iscommon,frequently to the point
ofperfo-ration.Resorption ofadjacent tooth rootsis common.Histologic patterns
includefollicular,in which the stellate reticulum islocated within the center ofthe
odonto-genic island (Figure 30-19);plexiform,inwhich the stellate reticulum is
located out-side ofthe odontogenic rest;acanthoma-tous,in which squamous
differentiation ofthe odontogenic epithelium is present;granular cell,in which the
tumor islandsexhibit cells that demonstrate abundantgranular eosinophilic
cytoplasm;desmo-plasticowing to extremely dense collage-nized stroma that supports
the tumor;andthe least common basal cellvariant,inwhich nests ofuniform basaloid
cells arepresent,with a strong resemblance to basalcell carcinoma.In this latter
tumor stellatereticulum is not present in the central por-tions ofthe nests.One
additional excep-tion surrounds the desmoplastic variant,which is generally not a
radiolucent tumorradiographically owing to its high contentofcollagenized
stroma.Pathogenetically,the proliferativecapacity ofameloblastomas has been stud-
ied.As might be conjectured,the recurrentameloblastoma is associated with the high-
est number ofPCNA-positive cells,fol-lowed by the previously
unoperatedameloblastomas.26The nuclear PCNA pos-itivity ofthe unicystic
ameloblastoma wasnotably lower than the positivity ofthesolid multicystic
ameloblastoma.26Othercell cycle features supporting the aggressivebehavior ofthe
ameloblastoma include theoverexpression ofBCL2and BCLX,as wellas the expression
ofIL-1 and IL-6.51Treatment and PrognosisThe ameloblas-toma continues to be a
subject offascina-tion in the international literature.Unfortu-nately,although most
agree that aggressivetreatment is essential for cure ofthis tumor,the fact remains
that a consensus has notbeen reached on the biologic behavior ofthis neoplasm and
how best to treat it.52 Theliterature is therefore paradoxically a sourceofboth
information and misinformation.Conflicting opinion,extending backward intime,has
served both to educate and to con-fuse,and it has been left to generations
ofsurgeons to sift and interpret what they con-sider to be clinically valid.It is
my strongopinion that this neoplasm is both highlyaggressive and curable.This
notwithstand-ing,numerous methods oftreatment haveTable 30-4Incidence ofOdontogenic
Tumors Study (yr)SpecimensRegezi JA et al.34Odukoya O36Daley TD et al.35(1978)
(1995)(1994) Total54,5341,51140,000Total odontogenic tumors706 (1.3%)*289
(19.1%)*445 (1.1%)*Ameloblastoma 78 (11.0%)�169 (58.5%)�79 (17.8%)�Adenomatoid
odontogenic tumor22 (3.1%)�18 (6.2%)�14 (3.1%)�Odontoma473 (67.0%)�12 (4.2%)�204
(45.8%)�Myxoma20 (2.8%)�34 (11.8%)�24 (5.4%)�*Percentage oftotal specimens in
respective study.�Percentage oftotal odontogenic tumors in respective study
specimens.ABFIGURE30-17A 17-year-old girl with obviousfacial expansion (A)related
to a multilocularradiolucency ofthe left mandible associatedwith impacted tooth
no.17 (B).Note theadvanced root resorption on teeth no.18 and19,indicative ofthe
aggressive nature ofthistumor.The incisional biopsy showed solid/mul-ticystic
ameloblastoma.
Odontogenic Cysts and Tumors585been recommended,ranging from simpleenucleation and
curettage to resection.53�59The solid or multicystic ameloblastomatends to
infiltrate between intact cancellousbone trabeculae at the periphery ofthetumor
before bone resorption becomesradiographically evident.Therefore,theactual margin
ofthe tumor often extendsbeyond its apparent radiographic or
clinicalmargin.60Attempts to remove the tumor bycurettage,therefore,predictably
leavebehind small islands oftumor within thebone,which are later determined to
berecurrent disease.These must be realized aspersistent diseaseas the tumor was
nevercontrolled from the outset.When a smallburden oftumor is left behind,it may
bedecades before this persistent diseasebecomes clinically and radiographically
evi-dent,and long after a surgeon falsely pro-claimed the patient to be cured.Owing
to the highly infiltrative andaggressive nature ofthe solid or
multicysticameloblastoma,I recommend resection ofthe tumor with 1.0 cm linear bony
margins(Figure 30-20).This linear bony marginshould be confirmed by
intraoperativespecimen radiographs.Soft tissue marginsare best managed according to
the anatom-ic barrier margin principles whereby oneuninvolved surrounding anatomic
barrieris sacrificed on the periphery ofthe speci-men.61When all soft and hard
tissue mar-gins are histologically negative,the patientis likely to be cured ofthis
neoplasm.Unfortunately,any less aggressive treatmentmodality may be fraught with
inevitablepersistence discovered at variable
timespostoperatively.62Moreover,although thepersistent and occasionally
nonresectableameloblastoma is radiosensitive,once thisotherwise benign tumor defies
curative sur-gical therapy,radiation is ofquestionableuse in salvaging these
patients.63,64Unicystic AmeloblastomaIn 1970 Vick-ers and Gorlin published their
findingsregarding the histologic alterations associ-ated with neoplastic
transformation ofameloblastomatous epithelium.65Thesehistologic changes were (1)
hyperchroma-tism ofbasal cell nuclei ofthe epitheliumlining the cystic cavities,(2)
palisading andpolarization ofbasal cell nuclei oftheepithelium lining the cystic
cavities,and (3)cytoplasmic vacuolization,particularly ofbasal cells ofcystic
linings.They referred tothese changes as early histopathologic fea-tures
ofneoplasia.Unicystic ameloblastomarefers to a pattern ofepithelial
proliferationthat has been described in dentigerous cystsofthe jaws that does not
exhibit the histo-logic criteria for ameloblastoma publishedby Vickers and
Gorlin.66�69This entitydeserves separate consideration based on
itsclinical,radiographic,and pathologic fea-tures.Moreover,in many cases it may
betreated more conservatively than the solidor multicystic ameloblastoma with
thesame degree ofcure.70Unicystic ameloblastomas are mostcommonly seen in young
patients,withabout 50% ofthese tumors being diag-nosed during the second decade
oflife.The average age ofpatients with unicysticameloblastomas has been reported as
22.1 years,compared with 40.2 years forthe solid or multicystic variant.42Morethan
90% ofthese tumors are found in theFIGURE30-18Twenty years ofundisturbedgrowth ofa
solid/multicystic ameloblastoma ledto significant facial disfigurement (A),with
animpressive radiographic appearance (B).A seg-mental resection ofthe right
mandible was per-formed (C).ABCFIGURE30-19The incisional biopsy ofthepatient in
Figure 30-17 shows follicular variantofthe solid/multicystic ameloblastoma (hema-
toxylin and eosin; original magnification �60).
586Part 5: Maxillofacial Pathologymandible,usually in the molar/ramusregion.71A
unilocular radiolucency,mim-icking a dentigerous cyst,is the most com-mon
radiographic presentation for theunicystic ameloblastoma (Figure 30-21).Most,ifnot
all,unicystic ameloblastomasare unilocular radiolucencies.2Threehistopathologic
variants ofunicysticameloblastoma have been described thatimpact treatment and
prognosis.In theluminal unicystic ameloblastoma,thetumor is confined to the luminal
surfaceofthe cyst (Figure 30-22).The lesion con-sists ofa fibrous cyst wall with a
liningthat consists totally or partially ofameloblastic epithelium.The
intraluminalunicystic ameloblastomacontains one ormore nodules ofameloblastoma
project-ing from the cystic lining into the lumenofthe cyst.These nodules may be
relative-ly small or largely fill the cystic lumen,and are noted to show a
plexiform patternthat resembles the plexiform pattern seenin conventional
ameloblastomas.As such,these tumors are referred to as plexiformunicystic
ameloblastomas.In the thirdvariant,known as mural unicysticameloblastoma,the
fibrous wall ofthe cystis infiltrated by typical follicular or plexi-form
ameloblastoma.The extent anddepth ofthe ameloblastic infiltration mayvary
considerably.Pathogenetically,the unicystic amelo-blastoma seems to have a
proliferativecapacity between that ofthe odontogenickeratocyst and the solid or
multicysticameloblastoma.26Treatment and PrognosisThe clinical andradiographic
findings in most cases ofuni-cystic ameloblastoma suggest that the lesionis an
odontogenic cyst,most commonly adentigerous cyst.Under the circumstancesthe surgeon
should routinely open a �cystic�lesion and look for luminal proliferation
oftumor.When able,histopathologic exami-nation ofsuch a process should occur
withfrozen sections.This is particularly impor-tant when dealing with large
cysts.With ahistologic diagnosis ofunicystic ameloblas-toma,the surgeon should
request thepathologist to obtain multiple sectionsthrough many levels ofthe
specimen toproperly subclassify the variant ofunicysticameloblastoma.When the
ameloblastic ele-ments are confined to the lumen ofthe cystwith or without
intraluminal tumor exten-sion,the enucleation has probably beencurative
treatment.When the cyst wall hasbeen violated by the tumor as in a muralvariant
ofunicystic ameloblastoma,themost appropriate surgical management isquite
controversial.Ifthis diagnosis is madepostoperatively,the surgeon may wish toadopt
close indefinite follow-up examina-tions ofthe patient.Ifa preoperative inci-sional
biopsy provides a diagnosis ofmuralunicystic ameloblastoma,the surgeon
mightrecommend a resection ofthe tumor owingto the fact that this variant ofthe
unicysticameloblastoma has a higher rate ofpersis-tence than do the luminal or
intraluminalunicystic ameloblastomas.The treatment ofa luminal or intralu-minal
variant ofthe unicystic ameloblas-toma is enucleation and curettage (Figure30-
23).In a collective sense,the �recur-rence�rate ofall unicystic
ameloblastomasFIGURE30-20A,Treatment ofthe ameloblas-toma ofthe patient in Figure
30-17 required adisarticulation resection ofthe left mandible.B,The effectiveness
ofthe bony linear marginshould always be evaluated by intraoperativespecimen
radiographs.ABFIGURE30-21This unilocular radiolucencyassociated with tooth no.17
should generate adifferential diagnosis ofdentigerous and otherodontogenic
cysts.FIGURE30-22The histopathology ofthe lesionin Figure 30-21 shows luminal
unicysticameloblastoma (hematoxylin and eosin; originalmagnification x40).
Odontogenic Cysts and Tumors587has been reported as 10 to 20% followingenucleation
and curettage.70This is signif-icantly lower than that ofenucleation andcurettage
ofthe solid or multicysticameloblastoma.The question then arisesas to when to
resect a unicystic ameloblas-toma.Three instances are likely to requiresuch
treatment.The first is the recurrentunicystic ameloblastoma.A tumor thatrecurs
following a well-performed enucle-ation and curettage should probably beapproached
with the more aggressiveresection.Second is the mural ameloblas-toma.This variant
ofthe unicysticameloblastoma is probably more aggres-sive than the luminal and
intraluminalvariants ofthe unicystic ameloblastomaowing to the presence oftumor in
the cystwall and therefore closer to the surround-ing bone.It seems logical to
approachthese tumors with a surgery similar to thatfor the solid or multicystic
ameloblastoma(Figure 30-24).The final indication forresection ofa unicystic
ameloblastoma isin the management ofvery large tumors(see Figure 30-24) with
significant expan-sion such that an enucleation and curet-tage surgery would
effectively result in aresection ofthe involved jaw.Peripheral AmeloblastomaThe
periph-eral or extraosseous ameloblastoma is themost rare variant ofthe
ameloblastoma.This tumor probably arises from rests ofdental lamina or the basal
epithelial cellsofthe surface epithelium and shows theFIGURE30-23A,The luminal
unicysticameloblastoma in Figure 30-21 is treated withan enucleation and curettage
surgery.B,The 5-year postoperative radiograph shows anacceptable bony
fill.BAACBDFIGURE30-24This 18-year-old presented with significant right facial
expansion (A)associated withthe destructive radiolucency ofthe right mandible noted
on the panoramic radiograph (B).The inci-sional biopsy documented the mural variant
ofunicystic ameloblastoma (hematoxylin and eosin;original magnification �20) (C).A
disarticulation resection was performed (D).
588Part 5: Maxillofacial Pathologysame features ofthe intraosseous form ofthe
tumor.72Clinically,these tumors pre-sent as nonulcerated sessile or peduncu-lated
gingival lesions (Figure 30-25).Most examples are < 1.5 cm and usuallyoccur over a
wide age range,with an aver-age reported age of52 years.Althoughthese tumors do not
infiltrate bone,theymay be seen to �cup out�bone in the jaws(Figure 30-
26).Treatment and PrognosisThe peripheralameloblastoma is most appropriatelytreated
with a wide local excision.Whensurgical margins are negative for tumor,cure is the
likely consequence.Malignanttransformation ofa peripheral ameloblas-toma is very
rare.73Malignant Odontogenic TumorsMalignant odontogenic tumors are veryrare.They
may arise from the epithelialcomponents ofthe odontogenic apparatus.The rests
ofMalassez,the reduced enamelepithelium surrounding the crown ofanimpacted
tooth,the rests ofSerres in thegingiva,and the linings ofodontogeniccysts represent
the precursor cells formalignant transformation.Odontogeniccarcinomas are
classified in Table 30-5.74Ingeneral,all ofthese tumors exhibit typicalmicroscopic
features ofmalignancy,withthe exception ofthe malignant (metasta-sizing)
ameloblastoma and the clear cellodontogenic carcinoma.Behaviorally,all ofthese
tumors have the potential for eitherregional nodal or distant metastases.Malignant
(Metastasizing) Ameloblas-tomaMalignant ameloblastomas arebest described as
neoplasms that have thehistologic features ofbenign ameloblas-toma as shown by the
primary growth inthe jaws and by any metastatic growth.75The most common sites
ofmetastatic dis-ease are the lungs (Figure 30-27),followedby the cervical lymph
nodes and visceralorgans.76�78Lung metastases have some-times been regarded as
aspiration phe-nomena,yet the peripheral location ofmany ofthese deposits
supportshematogenous spread.Eversole points outthat instances ofmetastasis have
arisenfrom solid or multicystic ameloblastomasrather than unicystic
tumors.74Ameloblastic CarcinomaAmeloblasticcarcinomas are malignant
epithelialodontogenic tumors that exist in thebackground ofbenign
ameloblastomas.This designation is reserved for anFIGURE30-25This lesion ofthe
right palatalmucosa (A) showed peripheral ameloblastoma onincisional biopsy
(hematoxylin and eosin; origi-nal magnification �40)(B).ABFIGURE30-26A �cupped
out�lesion in bone attooth no.4 is noted in the patient in Figure 30-25.Table 30-
5Classification ofOdontogenic Carcinomas Malignant (metastasizing)
ameloblastomaAmeloblastic carcinomaPrimaryDedifferentiatedPeripheralPrimary
intraosseous squamous cell carcinomaSolidCystogenic�Nonkeratinizing
cyst�Odontogenic keratocystClear cell odontogenic carcinomaMalignant epithelial
odontogenic ghost cell tumorAdapted from Eversole LR.74FIGURE30-27Histologically
benign ameloblas-toma is noted in the lung.This finding satisfies thedefinition
ofmalignant ameloblastoma (hema-toxylin and eosin; original magnification �20).
Odontogenic Cysts and Tumors589ameloblastoma that has cytologic
featuresofmalignancy in the primary tumor (Fig-ure 30-28),in a recurrence,or in
anymetastatic deposit.Although ameloblas-tic carcinomas have been reported
tometastasize to the lungs and distantorgans,79,80many cases do not metasta-size.In
Corio and colleagues�series ofeight cases ofameloblastic carcinoma,rapid growth and
pain were commonsymptoms.81These symptoms are recog-nized as being uncommon in
patientswith benign ameloblastomas.Primary Intraosseous Squamous
CellCarcinomaSquamous cell carcinomasthat are encountered in the jaws,lack
anycontinuity with the oral or antralmucosa,and occur in the absence ofaprimary
carcinoma located elsewhere aretermed primary intraosseous squamouscell
carcinomas.These cases are assumedto arise from odontogenic epithelium.They
typically occur in elderly patientsand tend to occur in the mandibularbody
region.The 5-year survival rate is30 to 40%.74Squamous cell carcinomasmay also
arise from the linings ofodon-togenic cysts.Cystogenic carcinomas areseen in
patients > 50 years ofage andtypically occur in the mandible.Finally,dentigerous
cysts can undergo glandularmetaplasia,and there are rare instancesofcentral
mucoepidermoid carcinomasreported to arise from odontogenic cyst lining.Clear Cell
Odontogenic CarcinomaAlthough the clear cell odontogenic carci-noma is ofputative
odontogenic origin,histologic similarities to the developingtooth germ are lacking
in manyinstances.74The differential diagnosisincludes metastasis from a distant
site,especially the kidney.The clear cell variantofrenal cell carcinoma is the
chiefentityto consider.The clear cell odontogeniccarcinoma is generally seen in
elderlywomen,with the maxilla and mandiblebeing affected equally.Malignant
Epithelial OdontogenicGhost Cell TumorThe epithelial odon-togenic ghost cell
tumor,also known asdentinogenic ghost cell tumor,is thesolid variant ofthe
calcifying odonto-genic cyst.Both epithelial and ectomes-enchymal odontogenic
elements are pre-sent;however,only the epithelialcomponent shows cytologic features
ofmalignancy.Ameloblastic FibromaThe ameloblastic fibroma is considered tobe a true
tumor in which the epithelialand mesenchymal tissues are both neo-plastic.This is
in distinction to theameloblastic fibro-odontoma and odon-toma that represent
developmental stagesofthe same hamartomatous lesion.82,83The ameloblastic fibroma
tends to occurin young patients in the first two decadesoflife.The posterior
mandible is affectedin 70% ofcases (Figure 30-29).Radi-ographically,either a
unilocular or multi-locular lesion is observed.FIGURE30-28A,The large destructive
radiolucencyofthe right mandible was present in a 22-year-oldman who complained
ofprecipitous growth andpain.The incisional biopsy showed benign solid/mul-ticystic
ameloblastoma.Band C,A segmental resec-tion was performed.Dand E,Final
histopathology ofthe resection specimen showed ameloblastic carcino-ma in a
background ofbenign ameloblastoma(hematoxylin and eosin; original magnification
�20[D] and �100 [E]).ABCDE
590Part 5: Maxillofacial PathologyTreatment and PrognosisThe ameloblas-tic fibroma
is recognized as an indolenttumor that is effectively treated by an enu-cleation
and curettage surgery (Figure 30-30).Although recurrence is rare underthe
circumstances,resection should bereserved for recurrent lesions.Approxi-mately 45%
ofameloblastic fibrosarcomasdevelop in the setting ofa recurrentameloblastic
fibroma.2Ameloblastic Fibro-odontomaThe ameloblastic fibro-odontoma,as previ-ously
discussed,probably represents ahamartoma.Moreover,some investigatorsbelieve that
this lesion is only a stage in thedevelopment ofan odontoma and does notrepresent a
separate entity.Slootweg pointsout that when one considers the data on age,site,and
sex,it seems that the ameloblasticfibro-odontoma is an immature
complexodontoma.82As with ameloblastic fibromas,the ameloblastic fibro-odontoma
occursmore frequently in the posterior regions ofthe jaws.This lesion is commonly
asympto-matic and is discovered serendipitously orwhen radiographs are exposed to
provide adiagnosis for asymmetric eruption ofthedentition in children (Figure 30-
31).Theselesions are distinctly well circumscribedand appear as mixed
radiopaque/radiolu-cent masses.Treatment and PrognosisThe ameloblas-tic fibro-
odontoma is treated effectivelywith an enucleation and curettage surgery(Figure 30-
32).Recurrence after thisapproach is very rare.Malignant transfor-mation
ofameloblastic fibro-odontomahas been reported but is exceedingly
rare.84OdontomaOdontomas are the most frequentlyoccurring odontogenic
tumors,withprevalence exceeding that ofall otherodontogenic tumors combined.As
statedFIGURE30-29A,A destructive unilocularradiolucency is present in a 15-year-old
boy.B,Incisional biopsy confirmed ameloblasticfibroma (hematoxylin and eosin;
originalmagnification �40).ABFIGURE30-30An enucleation and curettagesurgery is
performed in the patient in Figure 30-29.The associated permanent teeth are
removedwith the tumor.FIGURE30-31A panoramic radiograph ofa 9-year-old boy shows a
mixed radiolucent/radiopaque lesion ofthe left posterior mandible.Ameloblastic
fibro-odontoma is a likely diagno-sis owing to the patient�s age as well as the
radi-ographic character ofthe lesion.FIGURE30-32A,Enucleation and curettage
isperformed ofthe lesion in Figure 30-31.The per-manent tooth is removed with the
lesion.B andC,The histopathology shows ameloblastic fibro-odontoma (hematoxylin and
eosin; originalmagnification �20).ABC
Odontogenic Cysts and Tumors591previously,these lesions are generally wellaccepted
as representing hamartomas.Odontomas present centrally within thejaws in one oftwo
forms:compound,inwhich multiple small toothlike structuresexist;and complex,in
which irregularmasses ofdentin and enamel are presentwith no anatomic resemblance
to a tooth.Compound odontomas are predominant-ly seen in the anterior maxilla
(Figure 30-33),whereas complex odontomas are typ-ically seen in the posterior
maxilla ormandible (Figure 30-34).Treatment and PrognosisOdontomasare treated with
simple enucleation andcurettage and are not known to recur.Odontogenic MyxomaThe
odontogenic myxoma is an uncom-mon benign neoplasm ofthe jaws that isthought to be
derived from ectomes-enchyme and histologically resembles thedental papilla ofthe
developing tooth.These tumors are slow growing with apotential for aggressive
behavior and ahigh recurrence rate after subtherapeuticremoval.85They occur over a
wide agerange but seem to occur most commonlyin the third decade oflife.Although
thetumor can occur anywhere in the jaws,theposterior mandible is most common loca-
tion (Figure 30-35).Histologically,thetumor is composed ofhaphazardlyarranged
stellate,spindle-shaped,andround cells in an abundant loose myxoidstroma that
contains only a few collagenfibrils (Figure 30-36).Radiographically,the odontogenic
myxoma appears as aunilocular or multilocular radiolucencythat may displace or
cause root resorptionofteeth in the area ofthe tumor.Althoughnot pathognomonic
ofthe odontogenicmyxoma,the radiolucent defect may con-tain thin wispy trabeculae
ofresidualbone,which are often arranged at rightangles to one another in a
�stepladder�pattern (see Figures 30-35B and 30-37).Insome patients the tumor may
have agreater tendency to form collagen fibers;such lesions are designated
fibromyxomas.Pathogenetically,the proliferationand aggressive behavior ofthe
odonto-genic myxoma may be related to overex-pression ofantiapoptotic cytokines
BCL2and BCLX.51Treatment and PrognosisOdontogenicmyxomas should be treated with
resectionwith 1.0 cm bony linear margins as con-firmed with a specimen radiograph
(FigureFIGURE30-35A large soft tissue mass ofthe leftposterior mandibular gingiva
(A)associatedwith an underlying radiolucent lesion ofthemandible (B).ABFIGURE30-
33A,An expansile lesion oftheright maxilla.B,Multiple small toothlike calci-fied
structures are removed that represent com-pound odontoma.ABFIGURE30-34A complex
odontoma ofthe leftposterior mandible.FIGURE30-36The odontogenic myxoma showsa
loose myxoid stroma,in this case,eroding intothe cementum ofa tooth root
(hematoxylin andeosin; original magnification �40).
592Part 5: Maxillofacial Pathology30-37).These tumors are not encapsulatedand tend
to infiltrate the surrounding bonesuch that complete removal by curettage isnearly
impossible.Resection ofthe tumorwith a normal surrounding margin ofbone and soft
tissue that shows negativemargins should be curative.Calcifying Epithelial
Odontogenic TumorThe calcifying epithelial odontogenictumor,also known as the
Pindborgtumor,is an uncommon lesion thataccounts for < 1% ofall
odontogenictumors.It is particularly noteworthy thatthe three studies depicted in
Table 30-4reported only 15 cases ofthis odonto-genic tumor among a collective
series of1,440 odontogenic tumors.Fewer than200 cases have been reported in the
inter-national literature.Although this tumorhas been reported over a wide age
range,it is most often encountered in patientsbetween 30 and 50 years
ofage.86Approximately two-thirds ofthese neo-plasms occur in the mandible.87A pain-
less slow-growing mass is the most com-mon presenting sign.Radiographically,the
most common presentation is amixed radiopaque/radiolucent lesion,frequently
associated with an impactedtooth (Figure 30-38).Histologically,the Pindborg tumor
isquite unique.Discrete islands,strands,orsheets ofpolyhedral epithelial cells in
afibrous stroma are noted.Large areas ofamorphous eosinophilic hyalinized (amyloid-
like) material are also present.Calcifications,which are a distinctive fea-ture
ofthe tumor,develop within the amy-loid-like material and form
concentricrings,known as Liesegang rings (Figure30-39).The precise nature ofthe
amyloid-like material is unknown.The materialdoes stain as amyloid when stained
withCongo red or thioflavine T.After Congored staining,the amyloid exhibits apple-
green birefringence when viewed withpolarized light.It has been illustrated thatthe
amyloid-like material may actuallyrepresent amelogenins or other enamelproteins
secreted by the tumor cells.88Treatment and PrognosisAlthoughslow growing,the
Pindborg tumor ishighly infiltrative and destructive and iscapable ofaggressive
behavior.88,89Owingto the small number ofreported cases andlack ofconsistent
follow-up,evidence-based recommendations for treatment arenot
available.Nonetheless,the tumor isgenerally recommended to be treatedidentically to
the ameloblastoma andodontogenic myxoma,with 1.0 cm bonylinear margins and the
appropriate atten-tion to soft tissue anatomic barriers (Fig-ure 30-40).When this
treatment wasundertaken for Franklin and Pindborg�sseries oftumors,only one patient
under-going resection experienced recurrence.87FIGURE30-37A,The patient in Figure
30-35underwent a segmental resection ofhis odonto-genic myxoma.B,As with the
ameloblastoma,specimen radiographs should be obtained whenresecting an odontogenic
myxoma to verify thebony linear margin.A better depiction ofthe�stepladder�pattern
ofthe odontogenic myxomais noted on this specimen radiograph.ABFIGURE30-38A 40-
year-old woman with a 5-year history ofan expansile mass ofthe left max-illa
(A).The panoramic radiograph (B)and thecoronal computed tomography scan (C)show
amixed radiolucent/radiopaque lesion ofthe left pos-terior maxilla.ABC
Odontogenic Cysts and Tumors593Adenomatoid Odontogenic TumorThe adenomatoid
odontogenic tumor,regarded by many as a hamartoma,is anuncommon odontogenic
lesion,accountingfor 3 to 7% ofall odontogenic tumors.Thislesion was once believed
to be a variant ofameloblastoma and was previously desig-nated
adenoameloblastoma.90,91Its clinicalfeatures and biologic behavior permit dis-
tinction from the ameloblastoma (Figure30-41).These lesions are limited to
youngpatients,and two-thirds ofall cases are diag-nosed in the second
decade.92�95The tumor isextremely uncommon in patients > 30 years.It has a
predilection for the anterior regionofthe jaws and is found twice as often in
themaxilla than in the mandible.Females areaffected about twice as often as
males.Mostadenomatoid odontogenic tumors aresmall,rarely exceeding 3 cm in
diameter.Inabout 75% ofcases,the lesion appears as awell-circumscribed unilocular
radiolucencythat involves the crown ofan erupted tooth,frequently a
canine.Histologically,the adenomatoidodontogenic tumor is a well-definedlesion that
is usually surrounded by athick fibrous capsule (Figure 30-42).When the lesion is
bisected,the centralportion ofthe tumor may be essentiallysolid or may show varying
degrees ofcys-tic change with intraluminal prolifera-tion oftissue.The lesion is
composed ofspindle-shaped epithelial cells that formsheets,strands,or whorled
masses ofcells in a scant fibrous stroma.Theepithelial cells may form rosette-
likestructures about a central space that maybe empty or contain small amounts
ofeosinophilic material that may stain foramyloid.96�98Tubular or duct-like struc-
tures are characteristic for the adenoma-toid odontogenic tumor (see Figure 30-
42).These consist ofa central spacesurrounded by a layer ofcolumnar orcuboidal
epithelial cells whose nucleiexhibit reverse polarization.Treatment and
PrognosisOwing to thislesion being encapsulated,it separates eas-ily from the
surrounding bone.As such,anenucleation and curettage surgery is cura-tive (Figure
30-43).Ofthe 499 cases ofadenomatoid odontogenic tumor report-ed in the
literature,only 1 acceptable caseofrecurrence has been documented.99FIGURE30-
39Incisional biopsy ofthe patientin Figure 30-38 shows signs indicative
ofthePindborg tumor including discrete islands ofodontogenic
epithelium,calcification (Liesegangrings),and hyalinized material suggestive
ofamyloid (hematoxylin and eosin; original mag-nification �40).FIGURE30-40The
patient with the Pindborgtumor in Figure 30-38 is treated with hemimax-
illectomy.FIGURE30-41An expansile lesion ofthe lingualaspect ofthe left mandible
(A)associated with aunilocular radiolucency ofthe left mandible (B).ABFIGURE30-
42Incisional biopsy ofthe lesion inFigure 30-41 shows a well-encapsulated
lesion(hematoxylin and eosin; original magnification�10) (A)with duct-like
structures and rosettes(hematoxylin and eosin; original magnification�40) (B).These
findings are indicative oftheadenomatoid odontogenic tumor AB
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CHAPTER 31Benign Nonodontogenic Lesions ofthe JawsM.Anthony Pogrel,DDS,MDBenign
nonodontogenic lesions ofthejaws represent a mixed group oftumors,which in many
cases are difficult to classi-fy.Additionally,there are some lesionswithin this
group that actually only seemto occur in the jaws,and,therefore,although they do
not contain any histolog-ic or immunohistochemical evidence ofodontogenic
structures,the mere fact thatthey only occur in the jaws may mean thatthey are in
fact odontogenic.The subjects discussed in this chapterare fibro-osseous
disease,osteoblastomaand osteoid osteoma,aggressive mesenchy-mal tumors
ofchildhood,benign tumors ofbone-forming cells,synovial chondromato-sis and
osteochondroma,lesions containinggiant cells,vascular malformations,Langer-hans
cell histiocytosis,nonodontogeniccysts ofthe jaws,neurogenic
tumors,Paget�sdisease,massive osteolysis (Gorham�s dis-ease),and tori.Benign Fibro-
osseous Disease Differences remain in the classification anddiagnosis offibro-
osseous disease.1There isa general consensus that the common enti-ty for all ofthe
lesions is the replacement ofnormal bone with a tissue composed ofcol-lagen fibers
and fibroblasts that containvarying amounts ofmineralized substance,which can be
either bone or cementum-likematerial.It is difficult to differentiate con-clusively
between bone and cementum withlight microsurgery.For the purposes ofthis
chapter,theterm fibro-osseous diseaseis taken toinclude the following groups
oflesions:fibrous dysplasia,cemento-osseous dys-plasia,and fibro-osseous
neoplasms.Fibrous Dysplasia Fibrous dysplasia is considered to be adevelopmental
hamartomatous fibro-osseous disease ofunknown etiology.Itmay represent
developmental arrest in abenign fibro-osseous proliferation thatlacks the ability
to fully differentiate.2Somatic mutations in the GS a-genehave been proposed to
cause monostoticand polyostotic conditions and Albright�ssyndrome.3,4Fibrous
dysplasia is normally subdi-vided into four different forms:1.Monostotic fibrous
dysplasia affectingonly one bone2.Polyostotic fibrous dysplasia affectingmultiple
bones3.Albright�s syndrome in which multi-ple lesions are associated with hyper-
pigmentation and endocrine distur-bances,predominantly precociouspuberty and/or
hyperthyroidism54.Craniofacial fibrous dysplasia confinedto bones ofthe
craniofacial complexThe jaws are commonly associated with allforms offibrous
dysplasia.In the jaws theonset is usually during the first and seconddecades,and it
produces painless swellingofthe involved bones (Figure 31-1).Classi-cally,the
radiographic appearance shows aground-glass opacity without clearlydefined borders
(Figure 31-2).In its cranio-facial form the maxilla,zygoma,sphenoid,frontal
bones,nasal bones,and base oftheskull can be involved.Expansion can
causecompression ofnerves and blood vessels.The optic canal can be narrowed by
fibrousdysplasia,although it seems unlikely thatFIGURE31-1Swelling ofthe left
mandible andmaxilla owing to fibrous dysplasia.
598Part 5: Maxillofacial Pathologyany associated vision loss can be relieved
byorbital decompression.6The maxillaappears to be affected more often than
themandible,and females are affected morecommonly than males.Typically
lesionsundergo periods ofactivity and periods ofquiescence.When they are
active,they areoften symptomatic in that the patient mayperceive a throbbing or
discomfort,theswelling increases,and the lesions appearhot on a bone scan (Figure
31-3) and can,in fact,mimic osteomyelitis.7�11In a quies-cent phase they may be
totally asympto-matic.Teeth can be displaced by the lesion(Figure 31-4).Familial
cases offibrous dys-plasia have been noted.12The lesions offibrous dysplasia may
beunder hormonal control,particularly inAlbright�s syndrome,and cases
ofincreasedactivity and reactivation during pregnancyhave been noted.13,14Although
not normal-ly recognized as a premalignant lesion,sar-comatous change has been
noted in fibrousdysplasia.15,16Early cases appear to havebeen associated with the
use ofradiationtherapy for treatment,17,18but cases ofspontaneous sarcomatous
degenerationhave been noted.19Additionally,some caseshave been difficult to
diagnose and mayhave represented a low-grade osteosarcomafrom the
outset.20Classically,fibrous dysplasia appears tobe a lesion that �burns
itselfout�when thepatient is in the late teens or early twenties,although cases
ofactive fibrous dysplasiahave been noted much later than this.Treatment is
generally symptomatic;ifthe lesions are asymptomatic,a biopsydiagnosis alone may be
adequate withoutcarrying out any definitive treatment.Sur-gical treatment should be
limited during anactive phase because the lesions are vascularand can bleed quite
profusely.Treatment isbest reserved for quiescent periods,atwhich time cosmetic
recontouring is thenormal treatment ofchoice.Regrowth,however,can be expected
following thistreatment in 25 to 50% ofcases,particular-ly ifundertaken at a young
age.Some inves-tigators have suggested more aggressivesurgical procedures including
mandibularand maxillary resections.21Cemento-osseous Dysplasia The cemento-osseous
dysplasias represent apathologic process ofthe tooth-bearingareas and probably
represent the common-est manifestation offibro-osseous disease;however,since they
are frequently asympto-matic and require no treatment,they areless ofa diagnostic
and clinical dilemmathan are the other forms offibro-osseousdisease.In this
condition there is a disor-dered production ofbone and cementum-like tissue in the
jaws.The three formsinclude periapical,focal,florid osseous dys-plasias,and
familial gigantiform cemen-toma,which are probably variants ofthesame pathologic
process but which can bedifferentiated by clinical and radiographicfeatures.The
etiology ofthese lesionsremains in doubt,but local trauma mayplay some part,even
such benign trauma asabnormal occlusal forces.There is a pre-dominance ofcases
occurring in femalesand also in African Americans.22It is sus-pected that the
periodontal ligament maybe the origin ofthe fibrous tissue found inthe cemento-
osseous dysplasias.Histologi-cally the three types ofcemento-osseousdysplasia are
indistinguishable,showingnew woven bone trabeculae and/orspherules ofcementum-like
material,which often blend into the cortical bone.Afibrous tissue stroma is
present.There isvery little inflammatory component.Trau-matic bone cysts have been
reported in con-junction with this lesion.23Periapical Cemento-osseous
DysplasiaPeriapical cemento-osseous dysplasia pre-sents as circumscribed lesions in
periapicalareas associated with vital teeth,with theanterior mandible being most
usuallyFIGURE31-2A,Radiographic appearance ofpatient in Figure 31-1 showing ground-
glassappearance oflesions.B,Periapical view oftypi-cal ground-glass appearance
offibrous dysplasia.ABFIGURE31-3Bone scan ofpatient in Figures31-1 and 31-2 showing
area ofincreased uptakeofisotope in both sides ofthe mandible and theleft maxilla
(arrow).The isotope used was Tc99mdiphosphonate.FIGURE31-4Teeth displaced by
lesions offibrous dysplasia.
Benign Nonodontogenic Lesions ofthe Jaws599involved.African American females
arepredominantly affected.Radiographicallythe lesions can be
radiolucent,ofmixeddensity,or radiopaque,depending on theirstage ofdevelopment
(Figure 31-5).Stud-ies indicate that they may occur in around6% ofAfrican American
females.24Focal Cemento-osseous DysplasiaLesionsoffocal cemento-osseous dysplasia
have apredilection for middle-aged African Amer-ican females and present as
nonexpansileradiolucencies with associated opacities,often in edentulous areas
ofthe mandible.They frequently occur in sites ofpreviousdental extractions and may
represent sometype ofabnormal healing following dentalextraction.Since they are
usually asympto-matic,cases are often noted on routinepanoramic radiographs.They
are normallywell circumscribed and rarely exceed 2 cm.Differentiation from
ossifying fibroma maybe difficult.25Florid Cemento-osseous DysplasiaFloridcemento-
osseous dysplasia has a predilec-tion for middle-aged African Americanfemales and
presents as a painless nonex-pansile lesion often involving two or morejaw
quadrants.Radiographically it appearsas multiple confluent lobular radiopaquemasses
in tooth-bearing areas (Figure 31-6).Lesions may be associated withsuperimposed
infection and osteomyelitis,and have also been associated with idio-pathic bone
cysts.26Histologically they havean unencapsulated proliferation ofcellularfibrous
tissue with trabeculae or wovenbone and calcification.More mature lesionsmay become
acellular and avascular withcoalescent sclerotic bone masses.Althoughcommon in
African Americans,floridcemento-osseous dysplasia has been notedin all racial
groups.Many patients are par-tially or totally edentulous when the condi-tion is
first discovered.Cortical expansionis usually absent or oflimited degree.It hasbeen
suggested that chronic diffuse scleros-ing osteomyelitis may represent a variant
ofthis condition,but it probably represents adifferent condition,inflammatory
innature.The differences between the twoconditions have been noted
anddescribed.8,27,28However,the role ofbacte-ria in chronic diffuse sclerosing
osteo-myelitis has proven elusive,and,in general,even authorities who strongly
support aninfectious origin have had difficulty isolat-ing organisms.29,30Familial
Gigantiform CementomaFamil-ial gigantiform cementoma represents anautosomal
dominant variant ofosseousdysplasia usually involving multiple quad-rants with
variably expansile lesions,oftenin the anterior mandible.31This particularform
ofosseous dysplasia has no racialpredilection.The lesions often evolve dur-ing
childhood and can grow rapidly.Treat-ment is usually surgical and symptomaticand is
limited to cosmetic recontouring.Fibro-osseous Neoplasms Ossifying Fibroma
Ossifying fibroma(cemento-ossifying fibroma) usually pre-sents as a well-demarcated
mixed radiolu-cency/radiopacity with smooth and oftensclerotic borders (Figure 31-
7).The lesionsare usually solitary and most commonlyoccur in the
mandible.Histologically theycontain a relatively avascular cellular fibrousstroma
with reticular bone trabeculae andcementum-like spherules.Most authoritiesnow feel
comfortable clearly differentiatingthis lesion from fibrous dysplasia.Chromo-somal
abnormalities have been identified inan ossifying fibroma and a
cementifyingfibroma.32,33The ossifying fibroma is felt tobe a true neoplasm and
occurs at a later agethan does fibrous dysplasia,being mostcommon later in the
third and early in thefourth decades.Ossifying fibroma appearsto be confined to the
jaws and craniofacialcomplex,although similar lesions have beenreported in the long
bones.34�36There is,again,a female predominance but no racialpredominance,and
growth rates are vari-able.Since it is felt to be a neoplasm,thetreatment is
surgical;in fact,the lesionsoften shell out easily at surgery,althoughthere is
recurrence,the rate ofwhich hasvariously been reported from 1 to 63%.37�39For these
reasons,some authorities recom-mend aggressive treatment for more aggres-sive
lesions,including aggressive curettage,FIGURE31-5Periapical cemento-osseous dyspla-
sia ofthe left maxilla (an atypical site).All associ-ated teeth are vital.The
patient is a 48-year-oldAfrican American female.FIGURE31-6Florid cemento-osseous
dysplasiaofthe mandible in a 49-year-old African Ameri-can female.All associated
teeth are vital.FIGURE31-7Ossifying fibroma ofthe leftmandible.It appears as a
well-defined mixedradiolucency/ radiopacity.
600Part 5: Maxillofacial Pathologylocalized surgical resection,and
segmentalmandibular resection.40,41When present inthe craniofacial
complex,treatment mayhave to be more aggressive to protect thevital
structures.42Juvenile Aggressive Ossifying FibromaJuvenile aggressive ossifying
fibroma wasfirst described in 1952 as a variant ofossi-fying fibroma.43The lesions
classicallyoccur in younger children and adolescentsand present with an aggressive
behavior,but they have been noted in older patientsand are not always particularly
aggressive.The World Health Organization definesjuvenile aggressive ossifying
fibroma as �anactively growing lesion mainly affectingindividuals below the age
of15 years,which is composed ofa cell-rich fibroustissue containing bands
ofcellular osteoidwithout osteoblastic rimming togetherwith trabeculae ofmore
typical wovenbone.Small foci ofgiant cells may be pre-sent,and in some parts there
may be abun-dant osteoclasts related to the woven bone.Usually no fibrous capsule
can be demon-strated,but the lesion is well demarcatedfrom the surrounding
bone.�44Two vari-ants have been described:trabecular andpsammomatous.The trabecular
variantusually occurs in childhood,with a slightmaxillary predominance,and may
containclustered multinuclear giant cells.Thepsammomatous variant can occur
inadults as well as adolescents and oftenaffects the orbit and paranasal
tissues;fre-quently it contains a whorled pattern ofclosely packed spheric ossicles
and a myx-oid component with aneurysmal bonecyst�like areas.Although felt to be
more aggressivethan the commoner ossifying fibroma thatis found at a later age,this
condition is notconsidered to necessitate truly aggressivesurgery;conservative
excision is still therecommended treatment,although lesionsinvolving the
craniofacial structures mayrequire more extensive surgery.Recur-rence rates
ofbetween 20 and 50% havebeen reported,and recurrences may becommoner in younger
patients.1Osteoblastoma and Osteoid Osteoma Osteoblastoma and osteoid osteoma
aregenerally felt to be variants ofthe samelesion and are related to fibro-osseous
dis-ease.Cementoblastoma and gigantiformcementoma are the equivalent
cementallesions and are associated with teeth.Thealternative name for the
osteoblastoma isgiant osteoid osteoma,and it is generallyfelt to represent a larger
version oftheosteoid osteoma.Both are benign process-es and are felt to represent
true neoplasms.The osteoblastoma occurs primarily in thevertebrae and long
bones,but it has beendescribed in the jaws.45�47Clinically itoften grows rapidly
and the predominantclinical feature is pain,which is generallylocalized to the
lesion itself.Although feltto be a true neoplasm,there have beenreports
ofregression after biopsy orincomplete removal,which could point toit being a
reactive process ofsome kind.48Most cases ofosteoblastoma occur in thesecond decade
oflife;they rarely occurafter age 30 years.Males appear to beaffected more commonly
than females.Inthe head and neck,the mandible is themost common site.Radiographic
features are variable,usually consisting ofa combination ofradi-olucency and
radiopacity (Figure 31-8).The designation osteoblastomais normallyreserved for
lesions > 2 cm in diameter.They are well circumscribed radiographi-cally with a
thin radiolucency surroundingthe variably calcified contents.A sunraypattern ofnew
bone formation similar tothat described in malignant bone tumorsmay be evident.The
histologic appearance shows irreg-ular trabeculae ofosteoid and immaturebone within
a predominantly vascular stro-mal network.There are various degrees ofcalcification
present.Stromal cells are gen-erally small and slender.Differentiationmust be made
from the ossifying fibroma,fibrous dysplasia,and osteosarcoma.Treatment ofthe
osteoblastoma is gen-erally confined to conservative surgical exci-sion either with
curettage or local excision.Recurrences are rare but have been reportedand may
necessitate more aggressive treat-ment such as en bloc resection.49Rareexamples
ofmalignant transformation havebeen reported,50,51but some ofthese may berelated to
an incorrect initial diagnosis.45The osteoid osteoma represents asmaller version
ofthe osteoblastoma and isfelt to be a true neoplasm.It is normally < 2 cm in
diameter clinically and radi-ographically.It again occurs in the secondand third
decades oflife with a male pre-dominance.Pain is again the major
clinicalfeature.Classically,the pain is worse at nightand is relieved by
acetylsalicylic acid.Ifthelesion is located near the cortex,it may pro-duce a
localized tender swelling.Radi-ographically the lesion again shows a well-defined
mixed radiolucency/radiopacitywith a small radiolucent rim around thelesion,which
is walled by sclerotic bone.Histologically it resembles the osteoblas-toma with a
rich vascular stroma with tra-beculae ofosteoid and immature bone.Thebone is rimmed
by layers ofactiveosteoblasts.Histologically it is impossible todifferentiate it
from the osteoblastoma.Treatment is again conservative surgicalexcision.Spontaneous
regression has alsobeen reported clinically.FIGURE31-8Osteoblastoma ofthe left
mandiblein 24-year-old female.Note mixed radiolucen-cy/radiopacity with a
radiolucent rim.
Benign Nonodontogenic Lesions ofthe Jaws601ChondromaA chondroma is a benign tumor
ofmaturecartilage.The occurrence ofthese lesions inthe jaws is extremely rare52;in
fact,whetherthey ever occur in the jaws or whether theyare usually described as
chondromyxomasor chondromyxoid fibromas has been ques-tioned.53�57In many cases the
true diagnosisin those reported cases is actually low-gradechondrosarcoma.58Most
reports concernthe mandibular condyle,suggesting thatthese lesions may arise from
cartilaginousremnants.59,60The chondroma presents as apainless slowly progressive
swelling,whichmay result in mucosal ulceration.The gen-der distribution is
equal,and most tumorsoccur under the age of50 years.Radi-ographically they present
as irregular radi-olucent lesions,although foci ofcalcifica-tion may occasionally
be present.Resorption oftooth roots has been report-ed.Histologically the lesions
contain well-defined lobules ofmature hyaline cartilage.Treatment is localized,and
conservative sur-gical excision is normally recommended.Because ofthe doubtful
nature oftheselesions and the always-present possibility ofa lesion representing a
low-grade chon-drosarcoma,some authorities have suggest-ed wide excision for all
ofthese lesions as akind ofinsurance policy.58Osteoma Osteomas are benign tumors
consisting ofmature compact or cancellous bone.Theymay arise on the surface ofbone
(periostealosteomas) or centrally within the bone(endosteal osteomas).61They are
often dis-covered as asymptomatic radiopacities.Osteomas are most commonly discov-
ered during the second and fifth decadesoflife,although they have been noted inall
age groups.Males appear to be affectedmore frequently than females.Gardner�s
syndrome is an autosomaldominant condition in which patientshave intestinal
polyposis,multiple osteo-mas (usually endosteal) ofthe jaws,fibro-mas ofthe
skin,epidermal cysts,impactedteeth,and odontomas.62�65The specificgene associated
with the condition hasnow been identified on the long arm ofchromosome 5.66�68Many
cases ofincom-plete manifestation ofthe syndrome havebeen reported.The clinical
significance ofthis syndrome is that the intestinal polyps,which frequently occur
in the colon andrectum,are premalignant and have a veryhigh rate ofmalignant
transformation.The associated osteomas are often foundin the jaws,particularly in
the angle regionofthe mandible,as well as the facial bonesand long bones.It has
been suggested thatany patient with multiple mandibularosteomas should be
investigated for thepossibility ofGardner�s syndrome.Investi-gation should include
a detailed history ofgastrointestinal disturbance and,ifposi-tive,follow-up with
colonoscopy;ifthediagnosis is confirmed,a prophylacticcolectomy should be
performed.Periosteal osteomas usually present asasymptomatic slow-growing bony
masses.Endosteal osteomas are usually asympto-matic and are noted on routine radi-
ographs.Radiographically they appear aswell-circumscribed sclerotic
radiopaquemasses (Figure 31-9).Histologically theyconsist ofeither dense compact
bone withsparse marrow spaces or lamellar trabecu-lae ofcancellous bone with
fibrofatty mar-row spaces.Osteoblastic activity is oftenpredominant.Treatment
ofosteomas is surgical exci-sion (Figure 31-10).This is often necessaryto establish
the diagnosis.Asymptomaticcases may be followed up clinically andradiographically
without treatment.Fol-lowing excision,recurrences are very rare.Synovial
Chondromatosis and Osteochondroma Both synovial chondromatosis and osteo-chondroma
are conditions that occur inthe temporomandibular joints and may beconsidered
variants ofthe chondroma andosteoma.In synovial chondromatosisthere is a
proliferation ofsmall particulate,generally unattached chondromas withinthe
confines ofthe joint capsule.Althoughmost frequently found in the knee,theyhave
been reported in most joints.Well-recognized cases have occurred in the tem-
poromandibular joints with symptomsnormally consisting ofpain and swellingbut most
often with deviation ofthemandible toward the unaffected side (Fig-ure 31-
11).69,70The etiology is unknown,but trauma has been suggested.71WhenFIGURE31-
9Radiograph ofan endosteal osteo-ma in the ascending ramus ofthe left
mandible.FIGURE31-10Surgical specimen from theosteoma shown radiographically in
Figure 31-9.FIGURE31-11Panoramic radiograph showinga number ofradiopaque foreign
bodies in theright temporomandibular joint (arrow).
602Part 5: Maxillofacial Pathologythese lesions become symptomatic,theyshould be
removed via a standard preau-ricular approach.Since it is felt that theyarise from
metaplasia within the synoviallining cells ofthe joint,it is often advocat-ed that
the lining be removed at the sametime.72Cases have been reported in whichup to 200
ofthese bodies were presentwithin the temporomandibular joint (Fig-ure 31-
12).12Following removal,recur-rence has not been reported.The osteochondroma is
felt to be abenign lesion that arises predominantly inlong bones from a herniation
ofcartilagethrough the epiphyseal plate.It tends to pre-sent with a predominantly
osseous corewith a cartilaginous cap.The lesionbecomes symptomatic when function
isaffected,for example,a malocclusion ormandibular asymmetry develops (Figure31-
13).Cases have been reported in themandibular condyle.73Cases in the tem-
poromandibular joints appear identical inall respects to lesions in other bones
ofthebody.However,the association with the epi-physeal plate that occurs in the
long bones isnot present in the temporomandibularjoint.On magnetic resonance
imaging itappears as an extraneous appendage to thetemporomandibular joint and is
usuallymore radiopaque than the surroundingmandible (Figure 31-14).Treatment
issymptomatic;when symptoms occur,local-ized excision is recommended via the nor-
mal temporomandibular approach.Recur-rence has been reported but is
unusual.74�77Aggressive MesenchymalTumors ofChildhood It is recognized that
children and youngadults can develop an aggressive andrapidly growing tumor
ofbone,which,although often having a benign mesenchy-mal appearance,nevertheless
behaves veryaggressively.The exact nature oftheselesions remains unknown,but many
havebeen classified as desmoplastic fibromas,which is the hard tissue equivalent
offibromatosis in the soft tissues.Any bonecan be affected including the jaws.The
etiology and pathogenesis are indoubt since their aggressive behavior sug-gests a
neoplastic process,but genetic,endocrine,and traumatic factors have alsobeen
suggested.Most occur in personsunder the age of20 years,and there is nogender
predilection.The mandible is affect-ed more frequently than the maxilla.78Radi-
ographically a unilocular or multilocularradiolucency is noted with poorly
definedmargins,cortical perforation,and rootresorption often being present (Figures
31-15 and 31-16).Histologically the lesion con-sists ofinterlacing bundles in a
whirledaggregate ofcollagenous tissue with elon-gated and spindle
fibroblasts.Hypocellular-ity is often present.However,atypia andmitotic features
are not found.Osteoidmaterial is not produced by this lesion.In treating this
lesion,the adage �treatthe biology,not the histology�is ofpara-mount
importance.Although the lesionlooks benign histologically,it oftenbehaves
aggressively,79and the appropriatetreatment is aggressive surgery,whichoften
involves mandibular or maxillaryresection (Figure 31-17).This is psycho-logically
difficult for the surgeon to per-form in a young child without a
histologicdiagnosis ofmalignancy,but the recur-rence rate is very high following
more con-servative procedures.For lesions in inac-cessible areas such as the base
ofthe skull,radiation therapy and/or chemotherapyhas been attempted with variable
degreesofsuccess.80,81FIGURE31-12The synovial chondromas removedfrom the jaw ofthe
patient in Figure 31-11.FIGURE31-13A malocclusion caused by an osteo-chondroma
ofthe left temporomandibular joint.FIGURE31-14Magnetic resonance image
ofanosteochondroma ofthe left temporomandibularjoint (arrow)in the patient shown in
Figure 31-13.FIGURE31-15A desmoplastic fibroma present-ing as a well-defined
radiolucency at the lowerborder ofthe body ofthe left mandible in a 3-year-old
patient.
Benign Nonodontogenic Lesions ofthe Jaws603Lesions Containing Giant Cells There are
a number oflesions that occurin the jaws that contain giant cells withinthem.Their
relationship to each other,however,is ill defined.Histologically all ofthe giant
cell lesions appear similar,ifnotidentical,and they usually cannot be dis-
tinguished on light microscopy alone.Theclinical
history,immunohistochemistry,orgenetic markers have to be used to differ-entiate
the lesions.Central Giant Cell Granuloma Central giant cell granuloma is a
lesionoccurring almost exclusively in the jaws.(A similar lesion has been described
in thesmall bones ofthe fingers and toes,but itsrelationship to the central giant
cell gran-uloma is unknown.82) Although not nor-mally considered an odontogenic
lesion,the fact that it only occurs in the jawbonesprobably indicates some
relationship tothe teeth or tooth-bearing structures.Itoccurs primarily in the
anterior parts ofthe jaws in people in the second and thirddecades oflife,but it
has been recorded inall sites at all ages.Its histogenesis remainsspeculative.When
first described it wascalled a reparative giant cell granulo-ma,83�85and it was
considered a reparativelesion that was essentially self-healing.There was little
evidence ofthis,however,and only oblique references to its self-healing properties
can be found.Worthshowed in a study ofa number ofnon-treated lesions that
resolution often didoccur as seen radiographically;even whenthe lesions did not
resolve completelyradiographically,only a fibrous scar wasnoted on surgical
exploration.86The cur-rent consensus,however,is that these arenot reparative
lesions and that ifthey arenot treated,they are progressive.Mostappear to follow a
fairly benign course,butmore aggressive lesions have beennoted.87�89The true nature
ofthe centralgiant cell granuloma remains speculative.It has been suggested that it
may be aninflammatory lesion,a reactive lesion,atrue tumor,or an endocrine
lesion.It maybehave most like a reactive lesion.Older theories about the origin
ofthese lesions suggested that they may bederived from the odontoclasts that
wereresponsible for resorption ofthe decidu-ous teeth;this was said to explain why
theyare normally found in areas where decidu-ous teeth were present and are found
afterthe deciduous teeth have resorbed.Radiographically the central giant
cellgranuloma can take a number offormsfrom a well-defined radiolucency,a moreill-
defined radiolucency or a multilocularradiolucency.Teeth can be displaced bythe
lesion,although resorption ofteeth isuncommon (Figures 31-18 and 31-
19).Histologically these granulomas con-tain focal arrangements ofgiant cells with-
in a vascular stroma with thin-walled cap-illaries adjacent to the giant
cells.There isa spindle cell stroma.Immunohistochem-istry has shown that the giant
cells are infact osteoclasts,90and the spindle cells areprobably the cells oforigin
ofthis lesion.91Treatment is usually surgical and con-sists oflocal curettage,which
is usuallycurative.92However,there is a 15 to 20%recurrence rate,and ifthe lesions
are large,even conservative curettage may involvethe loss ofmany teeth and possibly
theinferior alveolar nerve in the mandible,and it may have sinus and nasal implica-
tions in the maxilla.With the aggressivevariants,more aggressive surgery has
beensuggested including mandibular resectionand appropriate reconstruction.93Since
the central giant cell granulomaand the brown tumor ofhyperparathy-roidism cannot
be separated histologically,it is advocated that hyperparathyroidismbe excluded
from the diagnosis by serumcalcium,phosphate,and parathormoneFIGURE31-16A
desmoplastic fibroma present-ing as an ill-defined radiolucency ofthe leftmandible
causing displacement ofteeth in apatient aged 8 years.FIGURE31-17A,Resected
specimen from the patient in Figure 31-15.B,Immediate reconstructionwith ribs can
often be performed in young children.Reconstruction plate and rib grafts in
place.ABFIGURE31-18A central giant cell granuloma ofthe anterior mandible causing
the displacementofteeth.
604Part 5: Maxillofacial Pathologyand parathormone-related protein assaysin all but
the single small and morebenign lesions.94A number ofnonsurgical treatmentshave
been suggested,all ofwhich have theiradvocates.Intralesional steroids
(usuallytriamcinolone injected into the lesion onceper week for 6 wk) have been
advocatedand have shown some success.95�98Theirmode ofaction is unknown,but they
maywork by suppressing the inflammatorycomponent ofthe lesion.They are probablybest
reserved for smaller lesions that can bemore easily treated by intralesional injec-
tions (Figure 31-20).Calcitonin given by subcutaneous injec-tion has also been
advocated and has metwith some success (Figure 31-21).99�106Thetheory behind this
treatment is that thelesion may be caused by an as-yet undiscov-ered parathormone-
like hormone,and thatthe use ofcalcitonin antagonizes its actionand allows the
lesion to heal.Since some ofthe giant cells have been shown to have cal-citonin
receptors on them,this may explaincalcitonin�s effectiveness.94a-Interferon given
by subcutaneousinjection has also been advocated in thetreatment ofthe central
giant cell granulo-ma and has again met with some suc-cess.106,107The rationale for
this therapy isthat the antiangiogenic action ofthe a-interferon suppresses the
angiogeniccomponent ofthis lesion,causing healingto occur.In most cases surgery is
stillrequired after the a-interferon treatment,but it may be less radical surgery
and theremay be a smaller chance ofrecurrence.It has again been suggested that
thecentral giant cell granuloma may,in fact,be a selfhealing lesion,with the
naturalhealing process stimulated by the nonsur-gical therapy employed.105Giant
Cell Tumor The giant cell tumor is normally found inthe long bones and its presence
in the jawsis not universally accepted;ifit does occur,it is extremely rare.This
lesion is an aggres-sive one and is felt by some to be a variantofa low-grade
osteosarcoma.The recur-rence rate after local curettage is high,andthe appropriate
treatment is in doubt.Some authorities advocate local curettage,whereas some have
advocated resection.Histologically it is very similar to the cen-tral giant cell
granuloma,except that thegiant cells are larger with more nuclei,andthey are more
evenly spread throughoutthe lesion and not as focally placed as in thecentral giant
cell granuloma.However,inany particular case it may be extremely dif-ficult to make
this distinction.45Hyperparathyroidism In hyperparathyroidism (primary,sec-
ondary,or tertiary),calcium is mobilizedfrom the bones into the blood stream
tomaintain homeostasis in the face ofincreased renal excretion.Mobilizationfrom
bone takes place focally and produceslesions in the bones (including the jaws)that
are known as brown tumors because oftheir fairly distinctive coloration on
surgicalexploration.108Clinically and histologicallythey are identical to the
central giant cellgranuloma and cannot be distinguished oneither clinical or
histologic grounds (Figure31-22).Therefore,whenever a lesion suchas this is
recurrent,aggressive,or multiple,hyperparathyroidism must be excluded bymeans
ofserum calcium,phosphate,andparathormone and parathormone-relatedprotein
assays.Ifthese confirm a diagnosisofhyperparathyroidism,it should be treat-ed
appropriately.The lesions normallyresolve without any further treatmentbeing
required.Cherubism Cherubism is a familial genetically domi-nant condition first
described by Jones in afamily in 1933.109Affected family membershave multiple
lesions mainly affecting thefacial bones.Because ofthe involvement ofthe maxilla
and orbital floor,the face has arounded appearance and the eyes tend tolook
upward,giving the patient a cherubicappearance (Figure 31-23).The geneticdefect in
this condition has been identifiedon chromosome 4p16.3.110,111Expression is
variable,with somepatients having subclinical lesions discov-ered only on
radiographs and some havingextensive and clinically obvious lesions.Spontaneous
mutations also occur.Radi-ographically the lesions appear honey-combed and can be
very extensive.Teethare often displaced,and in active periodsthe lesions are
extremely vascular (Figures31-24 and 31-25).FIGURE31-19A central giant cell
granulomaofthe left angle region ofthe mandible,appear-ing as an ill-defined
multilocular radiolucency,causing resorption ofthe distal root ofthe firstmolar
(unusual).FIGURE31-20A,A central giant cell granulomaofthe right mandibular
bicuspid region causingdisplacement ofthe root ofthe first bicuspid(arrow).B,One
year after a course ofsix intrale-sional injections oftriamcinolone (10 mg/cc).Note
that the area is now radiopaque.AB
Benign Nonodontogenic Lesions ofthe Jaws605Histologically the lesions are very sim-
ilar to central giant cell granuloma,withfocal accumulations ofgiant cells in
aspindle cell matrix.Perivascular cuffing isoften present,and in some cases can
beused to differentiate the two lesions.Because ofits histologic similarity
tocentral giant cell granuloma,calcitonin hasbeen used in an attempt to cause
resolution,but it has not met with success,suggestingthat they are,in
fact,different lesions.112Treatment ofcherubism is usuallyconservative and
expectant and into theteenage years is devoted to trying to aideruption ofthe
teeth,which is oftenabnormal.Later it is directed toward cos-metic recontouring
ofthe affected bones.The lesions normally become less activeand less vascular
toward the end ofthesecond decade and into the third decade,and it is at this time
that most cosmeticremodeling is carried out.Aneurysmal Bone Cyst Aneurysmal bone
cyst is most commonlyfound in the jawbones and appears to be acombination ofa
sinusoidal vascularlesion with a giant cell component.Radi-ographically the lesion
appears as a well-circumscribed soap bubble�type lesion(Figure 31-
26).Histologically the giant cellcomponent resembles the central giant
cellgranuloma,whereas the vascular compo-nent is thin-walled
sinusoids.Someauthorities consider this to be a vascularvariant ofa central giant
cell granuloma;others consider it a separate lesion.Itresponds well to moderately
aggressivecurettage,although hemorrhage can be aproblem.Recurrences are
rare.Vascular MalformationsVascular malformations can occur any-where in the body
and are felt to be devel-opmental lesions,which can occur in softtissue or
bone.Central vascular malforma-tions ofthe jaws are a rare but well-documented
entity.They are in contrast tothe true hemangioma,which is a neo-plasm ofvascular
endothelium and is nor-mally present at birth,often enlarges,andthen frequently
involutes.113The vascularmalformation generally is not present atFIGURE31-21A,A
central giant cell granulo-ma ofthe left posterior mandible (same case asFigure 31-
19).B,Same case 2 years after an 18-month course ofsubcutaneous
calcitonininjections.Note the continued development ofthe roots ofthe second
molar,the cessation ofresorption ofthe distal root ofthe first molar,and the
radiopacity replacing radiolucency.ABFIGURE31-22Hyperparathyroidism showing
arecurrent lesion ofthe left mandible with a patho-logic fracture and a lesion
ofthe right mandible.FIGURE31-23A 7-year-old female with cheru-bism affecting the
maxillofacial region.FIGURE31-24A panoramic radiograph ofthepatient shown in Figure
31-23.Note the exten-sive multilocular radiolucencies.FIGURE31-25A coronal computed
tomograph-ic scan ofthe patient in Figure 31-23,showingextensive involvement ofthe
mandible and max-illa by cherubism.
606Part 5: Maxillofacial Pathologybirth,appears later,and does not
involute.Vascular malformations can take a num-ber offorms.The most practical
classifica-tion is to divide them into high-flow andlow-flow vascular
malformations.Thehigh-flow vascular malformations areeither arterial lesions or
arteriovenous fis-tulas.The low-flow malformations aremainly venous in nature.The
clinical sig-nificance ofa vascular malformation isthat a central high-flow
vascular malfor-mation can cause torrential hemorrhagewhen surgical intervention
ensues.Thishas been fatal on occasion.114Many ofthese lesions are asymptomatic and
mayeven be difficult to detect preoperativelyon radiographs.Ifthere is a clinical
pre-sentation,it is often a slow-growing asym-metric expansile lesion ofthe jaw,and
ifitis high flow,it may be associated with abruit.Radiographically a high-flow mal-
formation may appear as an irregularpoorly defined soap bubble�type lesion,which
may cause resorption ofthe rootsofteeth and does not normally causenerve
involvement (Figure 31-27).Low-flow malformations are similar but areoften somewhat
better defined and maycontain calcifications or phleboliths with-in them.The
presence ofphleboliths isdiagnostic ofa low-flow malformation.Diagnosis is usually
confirmed by com-puted tomography.To avoid the possibility ofinadver-tently
carrying out a tooth removal or abiopsy in the presence ofa high-flow mal-
formation,a diagnostic needle aspirationshould be carried out
preoperatively.Ifbright red blood under pressure isencountered,surgery should be
aban-doned.Since the radiographic and clinicalappearances ofa vascular
malformationare not diagnostic,the differential diagno-sis normally includes a
number ofodonto-genic and nonodontogenic lesions,includ-ing the central giant cell
granuloma,theaneurysmal bone cyst,ameloblastoma,odontogenic keratocyst,and
odontogenicmyxoma.All ofthese lesions shouldundergo needle aspiration prior to
biopsyor surgical treatment to rule out a high-flow vascular malformation.When a
vas-cular malformation is suspected or diag-nosed,selective angiography is
normallyperformed via a femoral approach (Figure31-28).Ifa high-flow vascular
malforma-tion is diagnosed,treatment is normallypreoperative embolization followed
bywide resective surgery.The embolizationcan involve a number ofmaterials,includ-
ing muscle,polyvinyl,pellets,and plat-inum coils,which are inserted via
theangiography catheter or on direct punc-ture.On entering the lesion they
unwindand expand (Figure 31-29).115,116Postem-bolization angiography carried out
imme-diately after the embolization normallyshows a diminution in blood flow to
thelesion.However,because ofthe powerfulangiogenic effect ofthese lesions (proba-
bly by production ofangiogenesis growthfactor),reestablishment ofsmaller collat-
eral vessels usually occurs within a fewdays,and it is often impossible to reem-
bolize these smaller collateral vessels.Therefore,definitive surgery should
becarried out within a small number ofdaysofembolization.Definitive surgery nor-
mally takes the form ofresection underFIGURE31-26A,The �soap bubble�appearanceofan
aneurysmal bone cyst ofthe right maxilla.B,An axial computed tomographic scan
ofananeurysmal bone cyst ofthe angle ofthe rightmandible(arrow).ABFIGURE31-
27Radiograph ofa high-flow vascu-lar malformation ofthe left mandible crossing
themidline.It appears as an ill-defined �soap bubble�radiolucency causing some root
resorption.FIGURE31-28Subtraction angiogram ofahigh-flow vascular malformation
ofthemandible.Oblique lateral view with lowerincisors(arrow).
Benign Nonodontogenic Lesions ofthe Jaws607hypotensive anesthesia with
adequateresuscitative measures available.117�119Fol-lowing resection appropriate
reconstruc-tion can be performed.This can includethe re-insertion ofthe resected
portion ofbone after curettage,thinning,perfora-tion,and simultaneous bone grafting
(Fig-ure 31-30).Other approaches such asinjection ofa variety ofsubstances into
thelesion including glue,fibrin gel,and plat-inum coils,115for example,have
beenattempted;also,case reports exist oflesions being treated by means
oflocalcurettage following embolization,but thisis not normally recommended.Low-
flow or venous malformationsare not as life-threatening and are normal-ly treated
with direct puncture and anattempt to thrombose the lesion byintralesional
injection ofa variety ofagents,including sclerosing agents,anabsorbable gelatin
sponge,and platinumcoils.This may bring about thrombosis,allowing the necessary
dental or surgicaltreatment to be carried out.Oftenmandibular resection is not
necessary but,rather,a local surgical procedure.Langerhans Cell Histiocytosis
Langerhans cell histiocytosis is the term cur-rently employed for what was
previouslyknown as histiocytosis X,and before thatthe three separate conditions
Letterer-Siwedisease,Hand-Sch�ller-Christian disease,and eosinophilic
granuloma.Lichtensteinfirst suggested that the three diseases wererelated and that
the common factor was thepresence ofhistiocytes.120The cells oforiginofthis disease
have now been identified asthe Langerhans cells,which are dendriticcells in the
skin and mucosa that have amacrophage-like function.At the presenttime what causes
these cells to proliferate ina clonal fashion with phenotypic evidenceofactivation
and give rise to Langerhans celldisease is unknown.121The nature ofthisdisease also
eludes us.Some recent studieshave suggested that it may have some oftheproperties
ofa tumor or have a viral etiolo-gy.122,123Other studies propose that it maybe a
response to an overwhelming allergenicchallenge,and they report cases
ofeosinophilic granuloma that have resolvedspontaneously,further adding to the puz-
zle.121,124The Histiocyte Society has attempt-ed to define all ofthe histiocytic
diseases in alogical manner,125and Letterer-Siwe diseaseis now felt to represent
the acute disseminat-ed form ofLangerhans cell histiocytosis,whereas Hand-Sch�ller-
Christiandiseaserepresents the chronic disseminated form,and eosinophilic granuloma
represents thechronic localized form.The acute disseminated form usuallyaffects
young children.It is multisystem innature,affecting the skin,bones,and inter-nal
organs (especially lungs and liver),and isfrequently fatal.Treatment is
chemotherapy.The chronic disseminated form ofthedisease is classically associated
with a triadofpunched-out bone lesions (often affect-ing the skull and
jaws),diabetes insipidus(owing to posterior pituitary involve-ment),and
exophthalmos (owing todeposits in the posterior orbit).This nor-mally affects an
older age group,often inthe second and third decades but some-times much older.The
bone lesions oftenaffect the jaws.Although they usuallyappear as fairly well-
defined punched-outradiolucencies (Figure 31-31),they canalso be less well defined
and can affect theapices ofthe teeth only and lead to a pos-sible differential
diagnosis ofperiapicalinfection.A frequent aspect ofpresenta-tion is loose
teeth;radiographically theyoften appear as �floating teeth�(Figure 31-32).The
treatment ofthe chronic dis-seminated form ofthe disease is variable,and for well-
circumscribed lesions canconsist oflocal curettage.However,formore aggressive
forms,chemotherapy isfrequently employed as well.Low-doseradiation therapy has also
been used onisolated lesions,and it does remain one ofthe very few indications for
low-dose radi-ation therapy,often in the region ofa fewhundred centigray.The
chronic localized form ofthe dis-ease is commonly found in the jaws andusually
shows as a well-defined radiolu-FIGURE31-29A high-flow vascular malforma-tion
embolized with a platinum coil.FIGURE31-30A,Resected mandible containing a high-
flow vascular malformation that had beenembolized previously.B,The same resected
specimen reduced to a hollow perforated tray,filled withautogenous iliac crest
cancellous bone,and replaced for an immediate reconstruction.(Photographscourtesy
ofJ.S.Lee,DDS,MD.)AB
608Part 5: Maxillofacial Pathologycency,often in the bicuspid region andmore
frequently in the mandible.Differ-ential diagnosis in this case includes anyfairly
well-defined radiolucency.Treat-ment usually consists ofaggressive
localcurettage,and the recurrence rate is low.Teeth are sacrificed as
necessary.Intrale-sional steroids have also been employedwith some success,and
cases ofsponta-neous regression have been reported.124,126It is generally felt that
the occurrence ofLangerhans cell histiocytosis is sporadic,but clusters have been
noted and there are anumber ofreports ofa familial inci-dence.121I have seen the
disease in a fatherand son.The father was diagnosed with thechronic disseminated
form ofthe disease atage 53 years (see Figure 31-31),whereas hisson died from the
acute disseminated formofthe disease at age 11 years.Nonodontogenic Cysts ofthe
Jaws In this section the following are discussed:globulomaxillary lesion,nasolabial
lesion,median mandibular cyst,nasopalatineduct cyst,all ofwhich are also know as
fis-sural cysts,traumatic bone cyst,andStafne�s bone cyst.Aneurysmal bone cysthas
been discussed under �Lesions Con-taining Giant Cells,�above.Globulomaxillary
Lesion Globulomaxillary lesionwas initially definedas a globulomaxillary cyst and
was felt to bea fissural cyst caused by retained epithelialremnants at the fusion
ofthe maxillaryprocess with the globular process.It is nor-mally found in the
second or third decade.In the classic description,the lesion pre-sents as a pear-
shaped well-defined radi-olucency in the maxilla between the lateralincisor and
canine.Associated teeth areclassically vital,and the lesion is lined bycystic
epithelium with occasional globularor ciliated epithelia.Current thinking is that
although thislesion does exist as a radiographic and clin-ical entity (Figure 31-
33),it is not,in fact,afissural cyst since the proposed embryonicderivation is now
known to be flawed andthe supposed fusion line does not exist.It isfelt that most
lesions previously diagnosedas globulomaxillary cysts can now bereclassified as
odontogenic keratocysts,radicular cysts,periapical granulomas,lat-eral periodontal
cysts,central giant cellgranulomas,calcifying odontogenic cysts,and odontogenic
myxomas.45Tooth roots may be diverged by thelesion,and biopsy is usually necessary
toconfirm the diagnosis and enable appro-priate surgical treatment to be carried
out.Treatment normally consists ofenucle-ation and curettage.Nasolabial Cysts The
nasolabial cyst was felt to be the softtissue counterpart ofthe
globulomaxillarycyst.Again,it was felt to be formed at thelines offusion ofthe
globulomaxillaryprocesses.Similarly,this lesion does exist,but its true origin
remains in doubt.Itcould be derived from remnants that formthe nasolacrimal
duct.This cyst manifestsitselfas a soft tissue swelling in the lateralaspect ofthe
upper lip,fairly high in thesulcus (Figure 31-34).The cyst lining istypically a
pseudostratified columnar typewith numerous goblet cells.Treatment islocal
excision.Median Mandibular Cyst Median mandibular cyst is a rare cystfound in the
midline ofthe mandible.Itwas originally felt to form at the line offusion ofeach
halfofthe mandibular arch.Again,the embryologic theory behind thislesion is no
longer felt to be applicable,and it is believed that those lesions foundin the
anterior mandible represent someother type ofodontogenic cyst or tumor.Nasopalatine
Duct Cyst Nasopalatine duct cyst is also known as inci-sive canal cyst and is
generally located on thepalatal end ofthe nasopalatine duct.It fre-quently presents
as a soft swelling behind theupper anterior teeth.It is felt to be derivedfrom the
epithelial remnants ofthe pairedembryonic nasopalatine ducts within theincisive
canal,and that either infection ortrauma may be the stimulus for the cells
toproliferate and form a cyst.These cystsappear to occur more frequently in
malesthan in females and are commonest in thefourth to sixth decades oflife.Most
cases areasymptomatic and are either found bychance on radiograph or present as a
soft tis-sue swelling in the palate.Radiographicallythis cyst appears as a well-
defined radiolu-cency found in the midline ofthe anteriorpalate (Figure 31-35).In
many patients thenasopalatine duct can be identified on anocclusal radiograph;the
question then arisesas to when the diagnosis ofnasopalatineduct cyst should be
entertained.A fairly arbi-trary cutoffpoint of7 mm has been suggest-ed�ifthe
nasopalatine duct appears to be > 7 mm in diameter,the presence ofa cystshould be
suspected.127FIGURE31-31The multiple irregular radiolucentlesions ofchronic
disseminated Langerhans cellhistiocytosis in a 53-year-old male whose son diedofthe
acute form ofthe disease at age 11 years.FIGURE31-32The �floating teeth�ofLanger-
hans cell histiocytosis.
Benign Nonodontogenic Lesions ofthe Jaws609Diagnosis is by biopsy,which normal-ly
shows a pseudostratified columnarepithelium lining.Treatment,ifrequired,is surgical
and consists oflocal curettage.This almost inevitably requires the sacri-fice ofthe
nasopalatine vessels and nerves,which results in a small area ofanesthesiaover the
anterior palate behind the upperincisor teeth.Some patients (particularlymore
elderly patients) find this particular-ly troublesome in the articulation
ofsomewords.Recurrence rate is very low follow-ing treatment.Traumatic Bone Cyst
Traumatic bone cyst has been called anumber ofnames,including idiopathicbone
cyst,simple bone cyst,and latentbone cyst.It is almost always asympto-matic and a
chance finding on radi-ographs.It occurs most commonly in themandible,particularly
in the posteriormandible.It classically appears on a radi-ograph as a fairly well-
defined radiolucen-cy,which usually has a scalloped marginbeneath the tooth roots
(Figure 31-36).Itis not quite as well defined as an odonto-genic cyst,and the
description made byHowe was that it appears as a �pencilsketch for a final pen and
ink drawing.�128The etiology ofthis lesion is in doubt,and suggestions have
included that it mayresult from intramedullary hemorrhagefrom trauma,which can be
quite mild.Instead oforganization and new bone for-mation occurring,for some reason
theblood clot liquefies and is then resorbed,leaving an empty space.On surgical
explo-ration these lesions are normally found tohave either no lining whatsoever or
just avery thin filmy lining.They are normallyempty except,possibly,for a little
straw-colored fluid in the base ofthe lesion,which could represent the last
remnants ofan absorbing blood clot.Studies haveshown that the gaseous contents
ofthelesion are mainly nitrogen,and this is pre-sumably because they contain air
and theoxygen is absorbed preferentially into theblood stream.129Although these
lesions have beenshown to regress spontaneously,a biopsyis almost always performed
to determine adiagnosis.The biopsy is normally curativesince anything that causes
bleeding intothe lesion causes resolution.Suggestedtreatments have included
everything fromno treatment whatsoever to curettage orinjection ofautologous blood
or packingwith an absorbable gelatin sponge.130Recurrences are extremely rare but
havebeen reported,as have bilateral cases.130Stafne�s Bone Defect Stafne�s bone
defect is also known as staticbone cyst;it is always asymptomatic andfound by
chance on a radiograph.It FIGURE31-33A globulomaxillary cyst appear-ing as a pear-
shaped swelling between the later-al incisor and canine tooth.FIGURE31-34A,A
nasolabial cyst causing a swelling in the buccal sulcus in the lateral
incisorarea.B,The enucleated cyst,which was confined to the soft tissues with no
bony extension.Histol-ogy showed squamous epithelium with goblet cells.ABFIGURE31-
35A,Palatine duct cyst appearing as a well-defined midline radi-olucency.B,The same
cyst enucleated.AB
610Part 5: Maxillofacial Pathologypresents as a well-defined radiolucency onthe
lower border ofthe mandible,belowthe inferior alveolar nerve (Figure 31-37).The
appearance is so diagnostic that biop-sy is often not required.When this defect
isexplored surgically,one normally findsthat it is not a totally intrabony lesion
but,in fact,an indentation ofthe mandible onthe lingual side (Figure 31-38).The
inden-tation is normally filled with an offshootofthe submandibular salivary
gland.Thiscan be confirmed by sialography,whichshows filling ofthe defects with
theradiopaque media.Cases have also beenseen that include lymphoid tissue in
thecavity.It is felt that these may representdevelopmental lesions,although they
maynot present until adult life.Such lesionsmay represent the entrapment ofthe
sali-vary gland or lymphoid tissue duringdevelopment ofthe mandible or the sub-
sequent erosion ofthe lingual plate ofthemandible by the tissue.Treatment
isunnecessary,but enucleation is often per-formed as a process
ofdiagnosis.131Neurogenic Tumors Schwannoma The schwannoma is a benign tumor
oftheneurilemoma or nerve sheath.Althoughusually found in the soft tissues,it
canoccur in bone,where it usually exists as awell-defined
radiolucency.Followingbiopsy to confirm the diagnosis,treatmentusually consists
ofsurgical excision.Recurrences are rare.Histologically lesionsare well
encapsulated and predominantlyofspindle cells showing either an Antoni A(spindle
cells arranged in palisaded whorlsand waves) or Antoni B (spindle cells witha more
haphazard appearance).Neurofibroma Neurofibromas are felt to be derived fromthe
fibrous elements ofthe neural sheathand may exist as solitary lesions or as
partofgeneralized neurofibromatosis or vonRecklinghausen�s disease.This latter con-
dition is autosomal dominant,and twodistinct subsets have been defined associ-ated
with the NF1and NF2genes.Although most commonly reported insoft
tissues,neurofibromas do occur in boneand have been reported on the inferior alve-
olar nerve,where they appear as a fusiformswelling in continuity with the inferior
alve-olar canal (Figure 31-39).Other bonechanges associated with
neurofibromatosiscan include cortical erosion from adjacentsoft tissue lesions or
medullary resorptionfrom interosseous lesions.In cases associat-ed with the
inferior alveolar nerve,pain orparesthesia can result.The normally recommended
treatmentfollowing biopsy is localized excision.Thelesions are often vascular,and
extensiveblood loss has been reported from surgicalmanagement ofmandibular
lesions.Mandibular resection has been advocatedby some authorities.The malignant
trans-formation rate to neurogenic sarcoma ofFIGURE31-36A,Bilateral poorly defined
trau-matic bone cysts.(Bilateral cysts are unusual.) B,Same radiograph shown in
Figure A with cystsoutlined,showing the size and scalloped marginsaround
teeth.BAFIGURE31-37Appearance ofa Stafne�s bonedefect on panoramic radiograph below
the infe-rior alveolar nerve on the right body ofthemandible.FIGURE31-38Clinical
photograph ofa Stafne�sbone defect on the lingual side ofthe mandible.This defect
contained lymphoid tissue.FIGURE31-39A neurofibroma on the left infe-rior alveolar
nerve presenting as a large fairlywell-defined radiolucency in the
mandibularramus(arrow).The patient also had caf�-au-lait spots.
Benign Nonodontogenic Lesions ofthe Jaws6115 to 15% in the generalized form ofthe
dis-ease could be a further indication for surgi-cal removal ofthese
lesions.Traumatic Neuroma Traumatic neuroma represents a misguidedattempt at nerve
regeneration whereby fol-lowing an injury to a nerve,neurons sproutfrom the site
ofinjury but for anatomic orphysiologic reasons cannot result in a func-tional
nerve repair.Ifa nerve is sectioned,an amputation neuroma can develop onthe
stump;ifa nerve is injured along itslength,either an incontinuity or lateralneuroma
can result (Figure 31-40).In theoral cavity these latter neuromas are mostoften
noted on the lingual and inferior alve-olar nerves.On the inferior alveolar
nervethey can occur as a fusiform enlargement ofthe inferior alveolar canal and
result mostcommonly following mandibular trauma,resection ofpathologic lesions,and
nerveinvolvement following dentoalveolarsurgery (Figure 31-41).Ifthe symptoms are
severe,appropriatetreatment is resection ofthe neuroma andappropriate nerve
reconstruction.Since theinferior alveolar nerve cannot be stretchedsignificantly in
the canal,repair normallyinvolves a graft ofsome kind.Nerve graftsfrom the sural
nerve or great auricularnerve have been reported,as have veingrafts,with some
success.132The approachcan be either intraoral or extraoral,but theextraoral
approach generally gives betteraccess and clinical results.However,it doeshave a
higher morbidity,with possible risksofscarring and ofdamage to the mandibu-lar
branch ofthe facial nerve.Paget�s Disease First described by Sir James Paget
in1876,133this entity still carries his name.Itsalternative name is osteitis
deformans.It isa slowly progressive bone condition ofunknown etiology,predominantly
affect-ing males over the age of50 years.Oneunproven theory is that Paget�s
diseasemay be a delayed or slow reaction to amyxovirus stimulus.Clinically there is
hyperactive boneturnover with alternate resorption ofbone,a vascular phase,and
finally a scle-rosing phase.Most bones ofthe body areinvolved,and the disease can
result in con-siderable deformity.In the facial regionthe maxilla is affected more
often than themandible.Family histories have beenobtained in this disease,and the
geneticbasis ofthe condition is being defined.The classic presentation used to be
apatient whose hat or gloves no longer fit-ted correctly,or in whom false
teeth,par-ticularly the maxillary denture,did not fitowing to bone swelling.Today
these pre-sentations are much fewer since well-fitting hats,gloves,and dentures are
lesscommonly encountered.Initial presenta-tion is usually related to bone deformity
orpain.In the head and neck,headaches andsymptoms owing to vascular and
nervecompression have been noted.The classic radiographic appearance isofa �cotton-
wool�appearance in the skulland maxilla ofaffected patients (Figure31-42),with
hypercementosis around theroots ofteeth,and loss oflamina dura andobliteration
ofthe periodontal ligamentspace.This does make tooth extractionextremely difficult
in these patients.Rootresorption has also been noted.The histopathology shows the
typicalreversal lines ofalternate resorption andbone deposition (Figure 31-
43).Classical-ly,patients have markedly elevated serumalkaline phosphatase
levels.Treatment is both systemic and local.Systemic treatment currently consists
ofFIGURE31-40An excised lateral neuroma thatwas on the lingual nerve.FIGURE31-41An
incontinuity neuroma on theinferior alveolar nerve(arrow) as a result oftheremoval
ofa third molar.The nerve is exposed viaan extraoral approach and lateral
corticotomy.FIGURE31-42A,Lateral and B,frontal radi-ographs ofa patient with
Paget�s disease showingtypical �cotton wool�appearance.AB
612Part 5: Maxillofacial Pathologythe use ofsalmon calcitonin or diphos-phonates to
inhibit bone resorption.Calci-tonin can be taken either subcutaneouslyor by nasal
spray,and diphosphonates aretaken orally or by injection.Treatmentcauses
stabilization ofthe bone and a low-ering ofthe raised alkaline
phosphataselevels.Localized treatment is directed tocosmetic and/or functional
recontouringofbone.It should be noted that the boneofPaget�s disease is often
vascular,andbleeding during recontouring can beextensive.Somewhat
paradoxically,how-ever,healing is often delayed owing to theintervening sclerotic
areas ofbone.The classic causes ofdeath in patientswith Paget�s disease are heart
failure andosteosarcoma.Heart failure caused by theexcessive blood supply to the
remodelingbone can cause high output or left heartfailure in elderly
persons.Sarcomatouschange has been reported in 5 to 15% ofpatients with Paget�s
disease,which shouldbe considered a premalignant condition.134Gorham�s
DiseaseAlthough first described in 1838,135this dis-ease was named after
Gorham,whoreviewed the literature and added three newcases in 1954.136Its
alternative name is mas-sive osteolysis.Gorham�s disease is a raredisease ofunknown
etiology,usually occur-ring in the second to third decades oflife,although it has
been reported in all agegroups.There is no sex or racial predilec-tion,although an
autosomal dominantinheritance pattern has been suggested.Thediagnosis is usually
one ofexclusion.Anybone can be affected,and there is usuallymassive
osteolysis,which is generallyasymptomatic until a pathologic fractureoccurs
(Figures 31-44 and 31-45).The boneis usually replaced with fibrous
tissue.Themajority ofcases are monostotic,butpolyostotic cases have been
reported.135There is no specific treatment for this dis-ease;however,radiation
therapy and surgi-cal resection have been beneficial in selectedcases.Serum
biochemistry is usually nor-mal,and isotope bone scans do not showexcessive
activity.Osteoclasts are not aprominent feature ofthe condition.Thelong-term
prognosis is uncertain,but somelong-term remissions have been reported.135Tori
Torus Palatinus The palatine torus appears as a bony hardswelling along the midline
ofthe palate.Itcan be discrete or may be large and lobular(Figure 31-46).It usually
occurs in the sec-ond or third decade oflife,and has a ten-dency to grow throughout
life.It is tempt-ing to feel that these lesions may beembryologic in their
development andform at the line offusion ofthe two palatalplates,but this is
probably incorrect andthe true nature ofthese lesions remainsunknown.Larger
versions may requiresurgical removal because oftheir interfer-ence either with
speech or feeding or withprosthodontic reconstruction.The com-mon surgical approach
is via a double Y-shaped incision (Figure 31-47) and subse-quent bone removal.The
bone is virtuallyalways solid cortical bone and is actuallyfairly difficult to
remove.The recom-mended technique is to make a number ofvertical cuts in the bone
with a fissure bur(Figure 31-48).Then the interveningridges ofbone can be snapped
offand afinal smoothing ofthe residual bone car-ried out,taking care not to
perforatethrough into the nasal cavity (Figure 31-49).It may be advisable to insert
a dressingplate after the procedure to prevent exces-sive hematoma formation and
possiblerecurrence ofthe torus (Figure 31-50).FIGURE31-43Histology ofPaget�s
disease show-ing reversal lines ofnew bone deposition andresorption (�40 original
magnification; stainedwith hematoxylin and eosin).FIGURE31-44Early case ofGorham�s
syn-drome with a partial loss ofthe right body ofthemandible.FIGURE31-45Axial
computed tomographicscan ofpatient in Figure 31-44 2 years later; notethe complete
loss ofthe right mandible.FIGURE31-46Large bilateral torus palatinus.
Benign Nonodontogenic Lesions ofthe Jaws613Torus Mandibularis Mandibular tori are
bony exophyticgrowths that present on the lingual aspectofthe mandible opposite the
bicuspids(Figure 31-51).They are virtually alwaysbilateral.Again,they present in
earlymidlife and tend to grow with age.Largerversions may require removal because
theyinterfere with tongue positioning,speech,and prosthodontic reconstruction,as
wellas with oral hygiene around the lower pos-terior teeth.The etiology ofthese
lesions isin doubt;again,it is tempting to think ofthem as being embryologic
lesions formedat the junction ofthe original Meckel�scartilage and the
neomandible,but this isalmost certainly not correct.Ifsurgical removal is
required,it iscarried out via an extensive gingival mar-gin incision with a
possible lingual-releasing incision,followed by removal ofthe bone.This is carried
out by making anumber ofvertical cuts with a fissure bur,as with the maxillary
torus,and then snap-ping offthe intervening ridges ofbonewith a periosteal
elevator.The residualirregularities are then smoothed with alarger bur.Occasionally
mandibular toriare on a fairly narrow neck and can beremoved in toto with a well-
directionedblow from a mallet and chisel.Recurrence oftori is rare,and it hasoften
been noted that palatal andmandibular tori rarely occur in the
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image cytometry.Int JOral Maxillofac Surg 1989;18:3�6.89.Ficarra G,Kaban LB,Hansen
LS.Central giantcell lesions ofthe mandible and maxilla:aclinicopathologic and
cytometric study.Oral Surg Oral Med Oral Pathol1987;64:44�9.90.Flanagan AM,Nul
B,Tinkler SM,et al.,Themultinucleate cells in giant cell granulomasofthe jaw are
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RG,Regezi JA.Central giant cell granulomas ofthe jaws;phenotype and proliferation-
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1991;3:165�71.93.Whitaker S.Giant cell lesions ofthe jaws.OralSurg Oral Med Oral
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for central giant cellgranuloma.A case report.Int J Oral Max-illofac Surg
1994;23:366�8.98.Carlos R,Sedano HO.Intralesional cortico-steroids as an
alternative treatment for cen-tral giant cell granuloma.Oral Surg OralMed Oral
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ofthejaws regress with calcitonin therapy.Br JOral Maxillofac Surg
1993;31:89�94.100.O�Regan EM,Gibb DH,Odell EW.Rapidgrowth ofgiant cell granuloma in
pregnan-cy treated with calcitonin.Oral Surg OralMed Oral Pathol Oral Radiol
Endod2001;92:532�8.101.Lannon DA,Earley MJ.Cherubism and itscharlatans.Br J Plast
Surg 2001;54:708�11.102.de Lange J,Rosenberg AJ,van den Akker HP,etal.Treatment
ofcentral giant cell granulo-ma ofthe jaw with calcitonin.Int J OralMaxillofac Surg
1999;28:372�6.103.Rosenberg AJ,Bosschaart AN,Jacobs JW,et al.[Calcitonin therapy in
large or recurrent cen-tral giant cell granulomas ofthe lower jaw].Ned Tijdschr
Geneeskd 1997;141:335�9.104.Penfold CN,Evans BT.Giant cell lesions com-plicating
Paget�s disease ofbone and theirresponse to calcitonin therapy.Br J OralMaxillofac
Surg 1993;31:267.105.Pogrel MA.Alternative therapies for the central
616Part 5: Maxillofacial Pathologygiant cell granuloma.J Oral Maxillofac
Surg2003;61:649�53.106.Kaban LB,Mulliken JB,Ezekowitz RA,et al.Antiangiogenic
therapy ofa recurrent giantcell tumor ofthe mandible with interferonalfa-
2a.Pediatrics 1999;103:1145�9.107.Kaban LB,Troulis MJ,Ebb D,et al.Antiangio-genic
therapy with interferon alpha forgiant cell lesions ofthe jaws.J Oral Maxillo-fac
Surg 2002;60:1103�13.108.Hunter D.Hyperparathyroidism:generalisedosteitis
fibrosa.Br J Surg 1931;19:203�84.109.Jones WA.Familial multi-locular cystic
diseaseofthe jaws.Am J Cancer 1933;17:946�50.110.Tiziani V,Reichenberger E,Buzzo
CL,et al.Thegene for cherubism maps to chromosome4p16.Am J Hum Genet
1999;65:158�66.111.Mangion J,Rahman N,Edkins S,et al.Thegene for cherubism maps to
chromosome4p16.3.Am J Hum Genet 1999;65:151�7.112.Southgate J,Sarma U,Townend JV,et
al.Studyofthe cell biology and biochemistry ofcherubism.J Clin Pathol
1998;51:831�7.113.Kaban LB,Mulliken JB.Vascular anomalies ofthe maxillofacial
region.J Oral MaxillofacSurg 1986;44:203�13.114.Lamberg MA,Tasanen A,Jaaskelainen
J.Fatal-ity from central hemangioma ofthemandible.J Oral Surg
1979;37:578�84.115.Perrott D,Schmidt B,Dowd C,Kaban L.Treat-ment ofa high-flow
arteriovenous malfor-mation by direct puncture and coilembolization.J Oral
Maxillofac Surg1994;52:1083�6.116.Kaneko R,Tohnai I,Ueda M,et al.Curativetreatment
ofcentral hemangioma in themandible by direct puncture and embolisa-tion with N-
butyl-cyanoacrylate (NBCA).Oral Oncol 2001;37:605�8.117.Bunel K,Sindet-Pedersen
S.Central heman-gioma ofthe mandible.Oral Surg Oral MedOral Pathol
1993;75:565�70.118.Ozdemir R,Alagoz S,Uysal AC,et al.Intraosseous hemangioma ofthe
mandible:a case report and review ofthe literature.JCraniomaxillofac Surg
2002;13:38�43.119.Beziat J,Marcelino J,Bascoulergue Y,Vitrey D.Central vascular
malformation ofthemandible:a case report.J Oral MaxillofacSurg
1997;55:415�9.120.Lichtenstein L.Histiocytosis X.Integration ofeosinophilic
granuloma ofbone,�Letterer-Siwe disease�and �Schuller-Christian disease�as related
manifestations ofa single nosolog-ic.AMA Arch Pathol 1953;56:84�102.121.Arico
M,Danesino C.Langerhans�cell histio-cytosis�is there a role for genetics?
Haematologica 2001;86:1009�14.122.Willman C,Busque L,Griffith B,et al.Langer-
hans�cell histiocytosis (histiocytosis X)�aclonal proliferative disease.N Engl J
Med1994;331:154�6.123.Kawakubo Y,Kishimoto H,Sato Y,et al.Human cytomegalovirus
infection in fociofLangerhans cell histiocytosis.VirchowsArch
1999;434:109�15.124.Boutsen Y,Esselinckx W,Delos M,Nisolle JF.Adult onset
ofmultifocal eosinophilicgranuloma ofbone:a long-term follow-upwith evaluation
ofvarious treatmentoptions and spontaneous healing.ClinRheumatol
1999;18:69�73.125.Jaffe R.The histiocytoses.Clin Lab Med 1999;19:135�55.126.Watzke
IM,Millesi W,Kermer C,Gisslinger H.Multifocal eosinophilic granuloma ofthejaw:long-
term follow-up ofa novelintraosseous corticoid treatment for recal-citrant
lesions.Oral Surg Oral Med OralPathol Oral Radiol Endod 2000;90:317�22.127.Roper-
Hall HT.Cysts ofdevelopmental origin inthe premaxillary region,with special
referenceto their diagnosis.Br Dent J 1938;65:405�34.128.Howe GL.Hemorrhagic cysts
ofthe mandible.Br J Oral Surg 1965;3:55�76.129.Toller P.Radioactive isotope and
other investi-gations in case ofhaemorrhagic cyst ofthemandible.Br J Oral Surg
1964;2:86�93.130.Pogrel M.Bilateral solitary bone cysts:reportofcase.J Oral Surg
1978;36:55�8.131.Stafne EC.Bone cavities situated near the angleofthe mandible.J Am
Dent Assoc1942;29:1969�72.132.Pogrel MA.The results ofmicroneurosurgeryofthe
inferior alveolar and lingual nerve.J Oral Maxillofac Surg 2002;60:485�9.133.Paget
J.On a form ofchronic inflammation ofbone (osteitis deformans).Trans R
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treatment ofPaget�s disease ofbone.Am Fam Physician 2002;65:2069�72.135.Fisher
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Surg 1990;48:1222�5.136.Gorham LW,Wright AW,Schultz HH,et al.Disappearing bones:a
rare form ofmassiveosteolysis.Am J Med 1954;17:674�82.
CHAPTER 32Oral Cancer:Classification,Staging,and DiagnosisG.E.Ghali,DDS,MDM.Scott
Connor,DDS,MDEstimates indicate that more than 1.3 million new cancers will be
diagnosedin the United States this year,and 27,700will be located in the mouth
andoropharynx.1This number representsapproximately 3% ofall cancers and isthe
eighth most common cancer affectingmales in the United States.Globally,morethan
360,000 new cases oforal cancer willbe diagnosed this year.2Mortality ratesremain
high despite some advances inlocoregional control.There will beapproximately
200,000 deaths worldwide,ofwhich 7,200 will occur in the UnitedStates.Most patients
will present fordiagnosis with either regional or distantdisease.Data have shown a
trend forAfrican Americans to have moreadvanced disease compared with
whiteAmericans (68% vs 52%) at the time ofdiagnosis.Even more alarming is the
factthat,when compared with equal stages atthe time ofdiagnosis,African
Americanshave a poorer 5-year relative survival ratecompared with other races.A
review oftrends in 5-year relative survival ratesover the past three decades has
shown astatistical difference between the timeperiods of1974 to 1976 and 1992 to
1996(54% vs 59%);the improvement in sur-vival again fails to hold true for
theAfrican American population.1Approximately 85 to 95% ofall oralcancer is
squamous cell carcinoma(SCC).3,4However,multiple other malig-nant lesions can be
found in the oral cavi-ty such as sarcoma,minor salivary glandtumors,mucosal
melanoma,lymphoma,or metastatic disease from nearly any sitein the body.Risk
Factors for SCC ofthe Oral CavityThe etiology ofSCC ofthe oral cavity hasbeen
studied extensively.Numerous riskfactors have been suggested as etiologicagents for
the development ofthese malig-nancies.While no single causative agentcan be
attributed to the development ofalloral cancers,several carcinogens have
beenidentified,and ofthose tobacco and alco-hol appear to have the greatest impact
onmalignancy development.Both extrinsicand intrinsic factors likely play a role
inthe development ofSCC ofthe oral cavity.The risk oforal cancer associated
withtobacco use is noted to be 2 to 12 timeshigher than in the nonsmoking popula-
tion,and 90% ofindividuals with oralcancer will have a smoking
history.5�9Thecombination ofvarious carcinogens with-in tobacco,combined with the
heat,maylead to a variable number ofgenetic muta-tions in the epithelium ofthe
upperaerodigestive tract.At some point thesecontinued mutations,coupled with
thepatients�own inherent genetic susceptibil-ity,expressed in the hetero- or
homogene-ity ofcertain tumor suppressor genes oroncogenes (TP53,c-myc),may lead to
thedevelopment ofa cell line capable ofunregulated growth.Alcohol in itselfis not a
recognizedinitiator in the development oforal SCC.However,the role ofalcohol as a
promot-er in the development oforal cancerwhen coupled with the use
ofsmokingtobacco has been shown.10This may berelated to the effects ofcontaminants
inalcohol and its ability to solubilize car-cinogens and enhance their
penetrationinto oral mucosa.5,11A possible viral etiology has beendemonstrated in
oral cancers,especially bythe human papilloma virus (HPV).TheHPV subtypes 16 and
18,similar to thosecausing cervical cancer,have been implicat-ed.Smith and
colleagues showed that whenindividuals in his study had other risk fac-tors
adjusted,such as smoking,alcohol,and
618Part 5: Maxillofacial Pathologyage,the presence ofHPV in the oral cavitywas
associated with a 3.7 times greaterchance ofcancer development than in
thenoninfected individual.12Other authorshave noted a unique subset ofcharacteris-
tics in individuals that may develop SCC asa result ofHPV infection,showing
lessassociation with tobacco or alcohol abuse,frequently involving the tonsils,and
havingan improved prognosis.13The study ofthe tumor biology ofSCC has exploded in
the past decade.Theaccepted molecular theory concerninggenetic alterations ofSCC is
that ofa�multihit�tumorigenesis ultimately lead-ing to unregulated cell growth and
func-tion.14,15It is thought that multiple exoge-nous insults
(tobacco,alcohol,viral) canlead to activation ofoncogenes or inacti-vation oftumor
suppressor genes.Onco-gene dysregulation leads to a gain offunc-tion alteration,and
transforming growthfactor alpha (TGF-a) and eukaryotic initi-ation factor 4E
(eIF4E) are two examplesofwell-studied genes that have proven up-regulation in
SCC.16Loss oftumor sup-pressor gene function requires loss ofbothnormal
alleles,which leads to the inactiva-tion ofthe critical function ofthat gene.The
most studied ofthe tumor suppressorgenes are TP53and P16.15,17�19No singlegene
alteration is responsible for carcino-genesis,but rather a host ofaltered
genescontribute.Attempts have been made touse genes and their products to
identifyoncologically safe margins operativelywith minimal success.20Gene therapy
tri-als that target these specific genes holdbetter promise.Premalignant
DiseasePremalignant disease can be divided intothat occurring as an isolated lesion
or thatassociated with a condition.A precancer-ous lesion is defined as
morphologicallyaltered tissue in which the development ofmalignancy is more likely
than with nor-mal mucosa.A precancerous condition is acondition or generalized
disease that doesnot necessarily alter the appearance ofthemucosa but may be
associated with agreater risk for the development ofcan-cer.21Precancerous lesions
are broadlyclassified as leukoplakia and erythroplakia.Leukoplakia is defined as a
whitepatch or plaque that cannot be character-ized clinically or ascribed to any
otherpathologic disease.22Leukoplakia cannotbe scraped or rubbed offand is
thereforeprimarily a diagnosis ofexclusion.Lesionscaused by lichen planus,white
spongenevus,nicotine stomatitis,or otherplaque-causing diseases do not qualify
asleukoplakia.Leukoplakia is strictly a clini-cal diagnosis and does not imply any
spe-cific histologic diagnosis.Leukoplakia isgenerally asymptomatic and
clinicallyappears as a white or off-white lesion thatmay be flat,slightly
elevated,rugated,orsmooth (Figure 32-1).It may be found asisolated or multifocal
lesions and maychange in morphology over time.Morethan 70% ofthe time leukoplakia
occurson two or more surfaces and has a strongmale predilection.23,24A more
aggressivevariant exists and is referred to as prolifer-ative verrucous leukoplakia
(Figure 32-2).The lower lip vermilion,buccal mucosa,and gingiva account for most
oral cavityleukoplakia;however,lesions found on thetongue and floor ofthe mouth
account formost lesions exhibiting dysplasia or carci-noma.23�26These relative
frequencieschange with different geographic locationsand are based on local
habits.The only consistent histology found inall leukoplakia is the presence
ofhyperker-atosis.The underlying epithelium may rangefrom normal to invasive
carcinoma.The trueetiology for the development ofleukoplakiais
unknown;however,several causative fac-tors have been proposed.Tobacco use,whether
smoked or smokeless,is most close-ly associated with the development ofleuko-
plakia,and more than 70% ofpatients withleukoplakia are smokers.23While
severalstudies have shown elimination oftobaccouse to be associated with resolution
ordecrease in the size ofthe lesion,others haveshown poor improvement with its
cessation.Ultraviolet radiation to the lower lipis frequently observed in the
developmentoflower lip vermilion leukoplakia.Indi-viduals with chronic unprotected
expo-sure to sunlight are at highest risk fordevelopment.These leukoplakia
lesionsare frequently associated with actiniccheilitis (Figure 32-3).27FIGURE32-
1Typical appearance offloor-of-mouth leukoplakia.FIGURE32-2Common presentation
ofprolifer-ative verrucous variant ofleukoplakia on gingiva.FIGURE32-3Actinic
cheilitis ofthe lower lipsecondary to chronic unprotected sun exposure.
Oral Cancer: Classification,Staging,and Diagnosis619Trauma is also associated with
thedevelopment ofleukoplakic lesions.Ill-fitting dentures,sharp edges on oral pros-
theses or teeth,or parafunctional oralhabits with objects such as toothpicks canbe
associated with leukoplakia.Obvioustraumatic lesions to the buccal mucosasuch as
the development ofa linea alba arenot considered leukoplakia.The frequency
ofdysplasia and carci-noma within leukoplakia is most closelyassociated with the
lesion�s location andpatient�s habits.Waldron and Shafer intheir study of3,256
lesions submitted totheir respective oral pathology depart-ments as
�leukoplakia�found that 43% offloor-of-mouth lesions and 24% ofbothtongue and lip
lesions contained somedegree ofdysplasia or carcinoma.25Sever-al studies have also
looked at malignanttransformation over time and found it tovary from 0.13 to
17.5%.23�26,28The resultsofthese studies vary according to suspect-ed causes ofthe
leukoplakia (geographichabits) and the length offollow-up or timeto biopsy ofthe
lesion.The malignanttransformation ofthese lesions has beenstudied extensively by
Silverman and col-leagues.23They note that,while a definiterate oftransformation
cannot be stated,their 257 patients had a 17.5% transfor-mation rate with an
average follow-uptime of7.1 years.The second year offollow-up in their series
exhibited thegreatest rate ofmalignant transformationat 5%.Ifthose lesions
initially noted to bedysplastic on biopsy were followed,theyhad an even higher rate
ofmalignanttransformation,at 36.4%.Earlier studiesby Silverman and colleagues found
malig-nant transformation rates of0.13% and6%.26,28The variability in
transformationrates ofmost studies is attributed to differ-ences in
ethnicity,drinking alcohol andtobacco usage,location ofthe lesions,andduration
offollow-up.Erythroplakia is a red patch that can-not be scraped offor
characterized clini-cally or ascribed to any other pathologicdisease (Figure 32-
4).Almost all true ery-throplakia demonstrates dysplasia,carci-noma in situ,or
invasive carcinoma.Shafer and Waldron�s review ofbiopsiessubmitted under this
clinical diagnosisrevealed that 51% were invasive SCC,40%were carcinoma in situ or
severe dysplasia,and 9% were mild to moderate dysplasia.29The most common sites
ofoccurrence arethe floor ofthe mouth and retromolartrigone.Lesions appear as
bright red,arefrequently �velvety�in appearance,andhave a sharply demarcated
border.The eti-ology ofthese lesions is unknown butthought to be the same as that
for leuko-plakia.Frequently these lesions are notedto be nonhomogeneous in
appearancewith adjacent or intralesional leukoplakia.When observed with this
morphology,they are referred to as erythroleukoplakiaor �speckled
erythroplakia�(Figure 32-5).These lesions also harbor an ominouspotential as rates
ofmalignant transfor-mation have been noted ofup to 23%.23Oral submucous fibrosis
(OSF) is aprecancerous condition seen predomi-nantly in India and Southeast Asia.It
is achronic,progressive mucosal disordermost frequently associated with the
habitofchewing betel quids;however,there isevidence that this lesion is
multifactorialin nature with genetic,immunologic,nutritional,and autoimmune factors
pos-sibly involved.30,31The condition is charac-terized by a mucosal rigidity that
leads totrismus,odynophagia with spicy foods,and difficulty with speech and
swallowing.Unlike tobacco pouch keratosis,OSF doesnot regress with the cessation
ofbetel quiduse.Longitudinal studies have shown amalignant transformation rate
of7.6%over a 17-year period.32Cervical Lymph Node LevelsThe neck is divided into
six �surgical lev-els�based on anatomic structures (Figure32-6).Each anatomic area
ofthe oral cav-ity has a predictable lymphatic drainagepattern to the over 300
lymph nodes in theFIGURE32-4Typical appearance oferythro-plakia located on left
posterior soft palate.FIGURE32-5Typical appearance ofery-throleukoplakia on labial
and buccal mucosa.VIIIIIIVIVIFIGURE32-6Lymph node levels ofthe neck.Levels I toVI
are subdivided and described in text.
620Part 5: Maxillofacial Pathologyneck.33By grouping defined nodal groupsinto
surgical levels,clinicians are affordedthe ability to communicate with eachother.It
also allows clinicians to tailortheir surgical management ofthe neckbased on these
known drainage patterns.Level I includes the submental andsubmandibular nodal
groups.Level IA,the submental group,isbounded by the hyoid bone inferiorly,the
mandibular symphysis superiorly,and the anterior bellies ofthe digastricmuscles
laterally.Level IB,the submandibular group,isbounded by the posterior belly
ofthedigastric inferiorly,the mandibular bodysuperiorly,the anterior belly ofthe
digas-tric muscle anteriorly,and the stylohyoidmuscle posteriorly.34,35Level II
includes upper jugular lymphnodes surrounding the internal jugularvein and adjacent
spinal accessory nerve.Level IIA is bounded inferiorly by ahorizontal plane made by
the inferiorbody ofthe hyoid bone,superiorly by theskull base,anteriorly by the
stylohyoidmuscle,and posteriorly by a vertical planedefined by the spinal accessory
nerve.Level IIB is bounded inferiorly by ahorizontal plane made by the inferiorbody
ofthe hyoid bone,superiorly by theskull base,anteriorly by a vertical planedefined
by the spinal accessory nerve,andposteriorly by the lateral border
ofthesternocleidomastoid muscle (SCM).34,35Level III includes middle jugularlymph
nodes surrounding the internaljugular vein.It is bounded inferiorly by ahorizontal
plane defined by the inferiorborder ofthe cricoid cartilage,superiorlyby the
horizontal plane defined by theinferior body ofthe hyoid bone,anteriorlyby the
lateral border ofthe sternohyoidmusculature,and posteriorly by the lateralborder
ofthe SCM or sensory branches ofthe cervical plexus.34,35Level IV includes the
lower jugularlymph nodes surrounding the internaljugular vein.It is bounded
inferiorly by theclavicle,superiorly by the horizontal planecreated by the inferior
border ofthe cricoidcartilage,anteriorly by the lateral border ofthe sternohyoid
musculature,and posteri-orly by the lateral border ofthe SCM orsensory branches
ofthe cervical plexus.34,35Level V includes all the nodes in theposterior
triangle,the spinal accessory andtransverse cervical nodes,and all
oftheupper,middle,and lower jugular lymphnodes on the posterior aspect ofthe
SCM.Level VA is bounded inferiorly by thehorizontal plane created by the
inferiorborder ofthe cricoid cartilage,superiorlyat the apex found at the
convergence ofthe SCM and trapezius muscles,anterior-ly by the posterior belly
ofthe SCM orsensory branches ofthe cervical plexus,and posteriorly by the anterior
belly ofthetrapezius muscle.Level VB is bounded inferiorly by
theclavicles,superiorly by the horizontal planecreated by the lower border ofthe
hyoidbone,anteriorly by the posterior belly ofthe SCM or sensory branches ofthe
cervi-cal plexus,and posteriorly by the anteriorborder ofthe trapezius
muscle.34,35Level VI includes the pretracheal,paratracheal,and prelaryngeal or so-
calledDelphian lymph nodes.It is bounded infe-riorly by the suprasternal
notch,superior-ly by the hyoid bone,and laterally by thecommon carotid
arteries.This level is alsoknown as the anterior compartment.34,35Clinical
Correlation Based on SiteThe boundaries ofthe oral cavity extendfrom the
vermiliocutaneous junction ofthe lips to the junction ofthe hard and softpalate
posterior-superiorly and to the linecreated by the circumvallate papilla poste-
rior-inferiorly.Posterior-laterally theboundaries are represented by the
anteriorfaucial pillars.The American Joint Com-mittee on Cancer (AJCC) has divided
theoral cavity into seven distinct anatomiclocations from which primary lesions
maydevelop.36The sites have defined bound-aries,and in developing these sites
theAJCC has attempted to produce a meansofbetter studying and treating oral
cancer.Mucosal LipThe lip begins at the junction ofthe ver-milion border with the
skin and includesonly the vermilion surface or that portionofthe lip that comes
into contact with theopposing lip.It is well defined into anupper and lower lip
joined at the commis-sures ofthe mouth.26It is supported by theorbicularis oris
muscle and receives itsblood supply from branches ofthe facialartery.Sensory
innervation is provided bythe mental nerve and motor function viabranches ofthe
facial nerve.Mucosal lip cancers representapproximately 2 to 42% oforal
cavitycancers.4,37�41Mucosal lip cancer is seenalmost exclusively in older white
men asa result ofchronic sun exposure (Figure32-7).Its infrequent occurrence in
dark-skinned races is further evidence ofitsetiology.Nodal metastasis in lip cancer
isinfrequent,10% oflower lip cancers and20% ofcancers in the upper lip and com-
missure are found to metastasize to thenodes.42Metastasis from the lower lip isto
the submental,submandibular,andperifacial nodes (level I more commonlythan level
II).Preauricular,periparotid,and submandibular nodes drain cancersofthe upper lip
and commissure (level IImore commonly than level I).BilateralFIGURE32-7Neglected
carcinoma ofthelower lip.
Oral Cancer: Classification,Staging,and Diagnosis621neck metastasis may develop
ifthe lowerlip lesion is near or has crossed the mid-line;however,the upper lip
rarelyexhibits crossover between right- andleft-side lymphatics.43Buccal
MucosaBuccal mucosa includes all the lining oftheinner surface ofthe cheeks and
lips fromthe line ofcontact ofthe opposing lips(mucovermilion junction) to the line
ofattachment ofmucosa to the alveolar ridge(upper and lower) and
pterygomandibularraphe.36The buccal mucosa is supportedby the buccinator muscle
posteriorly andthe obicularis oris anteriorly.The vascularsupply to the posterior
aspect is derivedfrom the buccal artery,a branch oftheinternal maxillary
artery;innervation isfrom the buccal branches ofthe facialnerve along with the long
buccal branch ofthe third division ofthe trigeminal nerve.Carcinoma ofthe buccal
mucosa rep-resents 2 to 10% ofall SCC ofthe oralcavity (Figure 32-8).4,37,38,44In
Centraland Southeast Asia the use of�pan�(acombination oftobacco,betel nut,andlime)
has been linked to buccal mucosacarcinoma and represents more than 40%ofall oral
cavity SCC.45First-echelonlymphatic drainage from the buccalmucosa is level I
followed by level II.46Cervical metastases are observed in 10 to27% ofpresenting
patients.44,47,48Alveolar RidgeThe alveolar ridge mucosa may be dividedinto lower
(mandibular) and upper (max-illary) components.The mucosa overlyingthe alveolar
process ofthe mandibleextends from the line ofattachment ofmucosa in the buccal
gutter to the line offree mucosa ofthe floor ofthe mouth.Posteriorly it extends to
the ascendingramus ofthe mandible.36The mucosaoverlying the alveolar process ofthe
max-illa extends from the line ofattachment ofmucosa in the upper gingival buccal
gutterto the junction ofthe hard palate.Its pos-terior margin is the upper end
ofthepterygopalatine arch.36Alveolar ridge or gingival carcinomarepresents 2 to 18%
oforal cancers andoccurs predominantly on the mandibularalveolus (64 to
76%).4,37�41,49,50At diagno-sis,approximately one-third ofthesetumors exhibit some
bony involve-ment.50,51Lymph node metastasis tends tooccur more frequently in
mandibularridge tumors than in maxillary tumors.Nodal drainage is principally to
levels Iand II for both the maxillary andmandibular lesions and is found in 24
to28% ofpatients at diagnosis.46,49-51Alveo-lar ridge carcinomas are frequently
insidi-ous tumors masquerading as inflammato-ry lesions,periodontitis or
gingivitis,toothabscesses,or denture sores (Figure 32-9).Retromolar Gingiva
(Retromolar Trigone)The retromolar gingiva is a triangularregion ofattached mucosa
overlying theascending ramus ofthe mandible from thelevel ofthe posterior surface
ofthe lastmolar tooth superiorly to the tuberosity ofthe maxilla.Laterally this
area merges withbuccal mucosa and medially is in continu-ity with the soft
palate,anterior tonsillarpillar,and floor ofthe mouth.36Tumors ofthe retromolar
trigone fre-quently involve adjacent anatomic sites atthe time ofdiagnosis (Figure
32-10).Pri-mary symptomatic complaints with thesetumors are sore throat,otalgia,and
tris-mus.Tumors ofthe retromolar trigonerepresent 2 to 6% ofall oral cavity carci-
nomas.4,38,39Lymphatic drainage from thisarea is predominantly to the submandibu-
lar nodes (level IB) and the upper jugu-lodigastric nodes (level II).46,52Lesions
ofthis region tend to be more aggressive innature with regard to developing
cervicalmetastasis,because 27 to 56% ofindividu-als present with metastatic
disease.53�55Floor ofthe MouthThe floor ofthe mouth is a semilunarspace over the
mylohyoid and hyoglossusmuscles,extending from the inner surfaceofthe lower
alveolar ridge to the under-surface ofthe tongue.Its posterior bound-ary is the
base ofthe anterior faucial pillarofthe tonsil.It is divided by the frenulumofthe
tongue and contains the ostia ofthesubmandibular and sublingual
salivaryglands.36Anatomically it consists oftheFIGURE32-8Squamous cell carcinoma
oftheleft buccal mucosa.FIGURE32-9Biopsy-proven squamous cell car-cinoma ofthe
mandibular alveolar ridge result-ing in erosion ofunderlying bone and
looseningofdentition.
622Part 5: Maxillofacial Pathologyunattached mucosa overlying the mylohy-oid and
hyoglossus muscles.Carcinoma ofthe floor ofthe mouthrepresents 8 to 25% oforal
cavity SCC,andseveral studies have shown a fairly dramaticincrease in incidence
(Figure 32-11).4,38�41Two distinct lymphatic drainage systemshave been identified
in the floor ofthemouth.56The superficial system drainsbilaterally into the
submandibular nodes(level I),while the deep system drains intothe ipsilateral
submandibular,upper andmiddle jugulodigastric nodes (levels I,II,and III).Studies
have shown that nearlyone-halfofall patients presenting with afloor-of-mouth
carcinoma will havemetastatic disease at presentation.57�59Shaha and colleagues
demonstrated that60% ofindividuals with metastatic diseasewill have multiple levels
involved.57Hard PalateThe hard palate is between the upper alve-olar ridge and the
mucous membrane cov-ering the palatine process ofthe maxillarybones.It extends from
the inner surface ofthe posterior edge ofthe palatine bone andcan be divided into a
hard and soft com-ponent.36In the United States,only 25% ofpalatal SCC occurs in
the hard palate with75% occurring in the soft palate (anatom-ically a part ofthe
oropharynx).60�62InIndia and Southeast Asia,where reversesmoking is popular,the
proportion ofhard palate lesions is greater.The hard palate represents 3 to 6%
ofall oral cavity SCC (Figure 32-12).4,37�39There is a paucity oflymphatics to
thehard palate.Approximately 10 to 25% ofindividuals present with evidence
ofmetastasis,generally to levels I and II.61,63Hard palate lesions may also
metastasizeto retropharyngeal nodes or nodes that arenot palpable on a clinical
examination orreadily removable with a traditional neckdissection.Nonhealing ulcers
and poor-fitting dentures are common complaintsamong individuals who develop
disease atthis site.Anterior Two-Thirds oftheTongue (Oral Tongue)The anterior two-
thirds ofthe tongue isthe freely mobile portion that extendsanteriorly from the
line ofcircumvallatepapillae to the undersurface ofthe tongueat the junction ofthe
floor ofthe mouth.It has four areas:the tip,the lateral bor-ders,the dorsum,and the
undersurface(nonvillous ventral surface ofthe tongue).The undersurface ofthe tongue
is consid-ered a separate category by the WorldHealth Organization.36The tongue
isentirely a muscular structure composed ofthe extrinsic muscles,the
genioglossus,hyoglossus,styloglossus,and palatoglos-sus,as well as the intrinsic
muscles ofthetongue.Blood supply to the tongue is fromthe paired
lingual,sublingual,and deeplingual arteries.The tongue receives motorinnervation
via the hypoglossal nerve andtaste and sensation from lingual branchesofthe
trigeminal nerve.In the United States,SCC ofthetongue is found mainly on the
anteriortwo-thirds (75%),versus the posteriorone-third (25%).64Tongue carcinoma
rep-resents 22 to 49% ofall oral cancer diag-nosed (Figure 32-13).4,37�41Several
epi-demiologic reviews have shown theunfortunate trend ofan increase in
tonguecancer and an alarming increase in theFIGURE32-10Ulcerative carcinoma
ofleftretromolar trigone with extension towards theanterior tonsillar
pillar.FIGURE32-11Carcinoma ofanterior floor ofthe mouth presents with
induration,ulcera-tion,and mild tongue fixation.FIGURE32-12Carcinoma ofthe hard
palatewith extension to alveolar mucosa.FIGURE32-13Carcinoma proliferating
fromventral tongue to encompass full thickness ofthetongue.
Oral Cancer: Classification,Staging,and Diagnosis623incidence ofthose diagnosed
before 45years ofage.40,41,65�67Lymphatic drainageofthe oral tongue is principally
to level II,followed by levels III and I.46,52Carcinomaofthe lateral border
generally metastasizesipsilaterally,but SCC ofthe tip or body ofthe tongue may
exhibit bilateral metas-tases.Approximately 40% ofpatients haveevidence ofclinical
node metastasis at thetime ofdiagnosis.68StagingThe TNM system devised by the AJCC
isdesigned to stratify cancer patients intodifferent stages based on the
characteris-tics ofthe primary tumor (T),regionallymph node metastasis (N),and
distantmetastasis (M).It is an attempt to helpguide treatment and estimate
patients�5-year survivability.Trefers to the prima-ry lesion and is graded on
greatest dimen-sion and presence ofadjacent tissue infil-tration (Table 32-
1).Nrefers to regionallymph node involvement and is graded onthe presence
ofnodes,greatest dimension,and side ofinvolvement in relation to theprimary tumor
(Table 32-2).Mgrades dis-tant metastasis and is based simply on itspresence (M1) or
absence (M0).The AJCCstaging system (Table 32-3) is designed forclinical
use;however,the patient may berestaged based on final pathology afterresection and
designated with a pprefix(pTNM) or at autopsy with an a(aTNM).Ifsynchronous tumors
are found at pre-sentation,the higher stage tumor shouldbe used for stage
designation,and an msuffix may be used to denote the multipleprimary tumors
(TmNM).36,69Assessment ofPrimary LesionProper lesional assessment is based on
athorough clinical evaluation.Accuratemeasurement ofthe primary lesionbefore biopsy
is essential.Often,biopsiedSCCs are referred without accurate mea-surements,leaving
the treating surgeonin a difficult situation relative to proper-ly assigning a T
group.Additionally,postbiopsy inflammation could lead toover- or underestimates
ofthe lesion�strue dimensions.A complete evaluation ofall anatomiclocations within
the oral cavity must beperformed by visual examination and pal-pation to detect any
mucosal abnormality.The goal in evaluating the patient is todetect any abnormal
tissue and assess theextent ofdisease.Patients may present withmyriad complaints
such as a nonhealingsore in the mouth,loosening ofteeth,ill-fitting dental
prosthesis,trismus,otalgia,orweight loss.Examination ofthe oral cavityshould
include removal ofall dental appli-ances and use ofa dental mirror for indi-rect
evaluation ofthe nasopharynx andhypopharynx.Bimanual palpation is criti-cal to
assess any involvement ofstructuressuch as the deep musculature ofthetongue,floor
ofthe mouth,buccal mucosa,salivary structures,or bony mandibularTable 32-1Primary
Tumors (T)TumorDescriptionTXPrimary tumor cannot be assessedT0No evidence ofprimary
tumorTisCarcinoma in situT1Tumor 2 cm or less in greatest dimensionT2Tumor more
than 2 cm but not more than 4 cm in greatest dimensionT3Tumor more than 4 cm in
greatest dimensionT4a*Tumor invades adjacent structures (eg,through cortical
bone,into deep [extrinsic] muscle ofthe tongue,maxillary sinus,skin offace)
(resectable)T4bTumor invades masticator space,pterygoid plates,or skull base or
encases internal carotid artery (unresectable)*Superficial erosion alone ofbone or
tooth socket by an alveolar primary is not sufficient to classify a tumor as
T4.Adapted from Greene FL et al.35,36Table 32-2Regional Lymph Nodes
(N)NodeDescriptionNXRegional lymph nodes cannot be assessedN0No regional lymph node
metastasisN1Metastasis in a single ipsilateral lymph node,3 cm or less in greatest
dimensionN2Metastasis in a single ipsilateral lymph node,more than 3 cm but not
more than 6 cm in greatest dimension;or in multiple ipsilateral lymph nodes,none
more than 6 cm in greatest dimension;or in bilateral or contralateral lymph
nodes,none more than 6 cm in greatest dimensionN2aMetastasis in a single
ipsilateral lymph node more than 3 cm but not more than 6 cm in greatest
dimensionN2bMetastasis in multiple ipsilateral lymph nodes,none more than 6 cm in
greatest dimensionN2cMetastasis in bilateral or contralateral lymph nodes,none more
than 6 cmin greatest dimensionN3Metastasis in a lymph node more than 6 cm in
greatest dimensionAdapted from Greene FL et al.35,36
624Part 5: Maxillofacial Pathologystructures.Assessment ofthe lateral tongueand
posterior pharynx is assisted by anteri-or and lateral traction on the tongue
withcotton gauze (Figure 32-14).The AJCC describes the possiblegrowth patterns ofa
tumor as endophytic,exophytic,or ulcerated.36These character-istics play no part in
staging the primarytumor.While depth ofinvasion is not usedto clinically stage the
patient,several stud-ies have shown that depth ofinvasion doesplay a prognostic
role in the developmentofregional metastasis,especially in tongueand floor-of-mouth
cancers.70�72Thestudy performed by Spiro and coworkersat Memorial Sloan-Kettering
Cancer Cen-ter looked at primary tumor thickness inrelation to risk ofcervical node
metastasisin SCC ofthe tongue and floor ofthemouth.70They found that patients
withthin (< 2 mm) cancer ofthese respectiveareas had a failure rate of1.9% and
lymphnode metastasis present in 7.5% ofpatients versus patients whose primarytumor
was thick (> 2 mm),who had a45.6% failure rate and metastatic node dis-ease was
present in 38%.Rarely,primarytumors may be located in areas that aredifficult to
assess or may be painful toassess,requiring an evaluation under anes-thesia along
with panendoscopy.Panendoscopy,or �triple endoscopy,�involves the use ofa rigid
bronchoscope,esophagoscope,and laryngoscope tosequentially examine and take
biopsies,ifrequired,from the aerodigestive tract.Warren and Gates first described
thenotion ofsynchronous and metachronoustumors in 1932.73A synchronous tumor
isdescribed as a second histologically con-firmed malignancy.This malignancy mustbe
distinct and geographically separatedby normal non-neoplastic mucosa and
notofmetastatic origin from the index lesion.It must also be discovered at the time
ofinitial tumor evaluation.Ifthe second pri-mary tumor is discovered at a later
time itis considered a metachronous tumor.Slaughter and colleagues described
theconcept of�field cancerization�secondaryto the panmucosal effects ofsmoked
tobac-co irritants and alcohol.74This theoryexplains the relatively high prevalence
ofsecond primary malignancies in the upperaerodigestive tract and has been
describedon a molecular level.75Panendoscopybecame the gold standard for
discoveringan often asymptomatic synchronouslesion.McGuirt reported a
synchronousprimary lesion rate of16% in his prospec-tive study of100 head and neck
cancerpatients.76The discovery ofthe synchro-nous lesions frequently led to an
alterationin the treatment plan ofthe index lesion.Other reported incidences
ofsynchronousprimary tumors range from 2 to 9%.77�81Panendoscopy can be performed
quicklyand at a minimal price for the patient interms ofcost and added
morbidity.The availability offlexible endoscopes,especially nasopharyngoscopes,has
led totheir use in many institutions,along withthe conversion to flexible
bronchoscopesand esophagoscopes.Additionally with theadvent oftomographic
imaging,routinepreoperative panendoscopy is currentlyundergoing reevaluation in
many institu-tions.Many authors believe that the lowyield ofbronchoscopy compared
withchest imaging should preclude its use,while others have called for
selectiveendoscopy to investigate only symptom-driven complaints.81�84Should
multipleprimary tumors be discovered duringpatient evaluation,each lesion should
bestaged separately.Assessment ofRegional MetastasisEvaluation ofthe neck is
perhaps the mostcritical and difficult aspect ofstaging oralor any head and neck
cancer.The presenceofa single lymph node with metastatic dis-ease reduces the
patient�s 5-year survival by50%.In turn,the presence ofextracapsularspread
decreases this survival by another50%.85A retrospective study by Snow andcolleagues
showed a surprisingly high rateofextracapsular tumor spread in evensmall lymph
nodes.His analysis showedthat lymph nodes greater than 3 cm had a73.7% chance
ofextracapsular spread,2 to3 cm a 53.3% chance,1 to 2 cm a 44.3%,and less than 1 cm
a 28.8% chance.86Otherstudies have concurred with this high rateofextracapsular
spread.87,88These drasticTable 32-3Stage GroupingStageCharacteristicsStage
0TisN0M0Stage IT1N0M0Stage IIT2N0M0Stage IIIT3N0M0T1N1M0T2N1M0T3N1M0Stage
IVAT4aN0M0T4aN1M0T1N2M0T2N2M0T3N2M0T4aN2M0Stage IVBAny TN3M0T4bAny NM0Stage IVCAny
T Any NM1Adapted from Greene FL et al.35,36FIGURE32-14Anterior manual traction
ofthe tongue with the aid ofa cotton gauzeimproves visualization ofthis lateral and
ven-tral tongue mass.
Oral Cancer: Classification,Staging,and Diagnosis625reductions in long-term
survival under-score the importance ofpreoperative stag-ing for an appropriate
prognosis and treat-ment plan.It should be noted that stagingdepends not on
specific lymph node levelinvolvement,but rather on presence ofnodes,size,number,and
whether they areipsilateral,contralateral,or bilateral in rela-tion to the
lesion.Traditionally,the gold standard instaging the neck has been through
digitalpalpation ofall levels ofthe neck bilateral-ly.The neck has a large number
ofpalpa-ble structures and a large area to be sur-veyed for the presence oflymph
nodes.While there is no correct order in which toevaluate the neck,each clinician
shoulddevelop a sequence to use consistently toavoid missing any part ofthe
examination.Observation ofthe neck is important tonote any asymmetries or skin
changes.Most clinicians prefer to palpate the neckstanding behind the
patient,simultane-ously palpating each aspect ofthe neck.We find it helpful to
break the neck downinto muscular triangles and examine themsequentially from the
submandibular tri-angle to the posterior triangle.Lymphnode chains should be
evaluated for thepresence ofpalpable masses,noting theirsize,surgical neck
level,and whether themass is fixed or moveable.Bending thepatient�s head forward or
slightly to theside will ease taut tissues ofthe neck allow-ing for better
palpation.Other importantpalpable structures ofthe neck to be eval-uated in the
examination include theparotid gland,the thyroid gland,and
thepostauricular,occipital,and supraclavicu-lar lymph node chains.The parotid
glandshould be evaluated for the presence ofany palpable disease or masses and
thethyroid gland for any nodule,masses,orthyromegaly.The trachea should beinspected
for any deviation or fixation.The past decade has seen a relativelyhigh incidence
ofobserver error.89,90Deficiencies have been observed in boththe ability to
recognize the presence ofaclinically palpable node and also in theability to assess
its size.A study by Alder-son and colleagues showed that both res-idents and
staffinvolved in the treatmentofhead and neck malignancies consis-tently
underestimated the size ofsmallernodes,and accuracy ofassessment wasindependent
ofexperience.90With the advent ofadvanced imaging,both computed tomography (CT) and
mag-netic resonance imaging (MRI) have beenused as adjuncts to the physical
examinationfor both evaluating nodal disease and help-ing to delineate the nodes in
relation to vitalstructures such as the carotid artery.Studieshave shown that
clinically negative tumor-positive nodes may be detected on CT orMRI in 7.5 to 19%
ofcases.91�96Computed TomographyCT is generally performed preoperativelywith
intravenous contrast to help delineatevascular from lymph structures.The
scangenerally involves 3- to 5-mm slices fromthe skull base to the
clavicles.Importantradiographic markers for the presence ofsuspicious adenopathy
include lymph nodesize,shape,and central necrosis.A lymphnode is considered
abnormal when it isgreater than 1.5 cm in the jugulodigastricregion or greater than
1 cm in other regionsofthe neck.92,96Shape has been suggested asa criterion to help
distinguish pathologicnodes.The shape ofa normal or hyperplas-tic lymph node
resembles a bean,asopposed to round or sphere-like metastaticnodes frequently
present.Next to size,themost specific indicator ofmetastatic nodaldisease on
tomographic imaging is thepresence ofintranodal necrosis,indepen-dent ofsize and
shape (Figure 32-15).Onlyan intranodal abscess or fatty hilar metapla-sia can
simulate central tumor necrosis.Magnetic Resonance ImagingMRI is another method
ofneck imagingthat has gained popularity in the pastdecade.With superior soft
tissue detail,one would expect better delineation oflymph node
pathology;however,the fatthat surrounds the cervical lymph nodescan interfere with
imaging detection.TheT1-weighted,fat-suppressed contrast-enhanced image is perhaps
the optimalsequence to evaluate cervical metastaticdisease.92,97MRI provides the
distinctadvantage ofviewing the neck and prima-ry tumor in planes not available by
CT.Difficulty with the use ofMRI concernsboth the time and motionlessnessrequired
for an acceptable study to be per-formed.Individuals with oral cancer fre-quently
have large lesions that may com-promise the airway while supine forextended periods
oftime.When usingMRI for evaluating the neck the same cri-teria concerning nodal
size,shape,andcentral necrosis should be applied aswhen evaluating with
CT.Ultrasound Ultrasound (US) evaluation ofthe neckhas become increasingly popular
in Euro-pean countries.Sonography is relativelyinexpensive and is tolerated well.It
may beused as an initial study to help guide theclinician in deciding whether
further imag-ing studies ofthe neck may be required.This is especially true in the
clinically N0neck.Sensitivity ofsonography in thedetection ofcervical lymph node
metasta-sis is 89 to 95%,and specificity is 80 toFIGURE32-15Axial computed
tomographyscan with contrast demonstrates large right cer-vical node with criteria
for regional metastasis.
626Part 5: Maxillofacial Pathology95%.98�100This specificity can be increasedwith
the use ofUS-guided fine-needleaspiration.101Criteria for the evaluation
ofpotentially malignant cervical nodes withsonography also involve the assessment
ofnodal size,shape,and presence ofcentralnecrosis.Metastatic nodes are characteris-
tically round to spherical in shape and arefrequently hypoechogenic.In the
presenceofextracapsular spread,loss ofborder def-inition is observed.Normal lymph
nodesare frequently difficult to detect because oftheir high echogenicity mimicking
that ofthe surrounding fatty tissue.Positron Emission TomographyThe use of2-18F-
fluoro-2-deoxy-D-glucose (FDG) positron emission tomog-raphy (PET) relies on the
enhanced meta-bolic activity oftumoral tissue in thebody,ofwhich increased
glycolysis is usu-ally the biochemical hallmark.FDG,aradiolabeled glucose analog,is
preferen-tially taken up within tumor cells thatexhibit increased glycolysis;they
can bedetected from the increased signaling inthat tissue (Figure 32-16).This study
isunique in that it represents a functionalimaging scan as opposed to a morpholog-
ic imaging scan.A prospective study byAdams and colleagues showed a
highersensitivity and specificity for FDG-PET(90%,94%) compared with CT (82%,85%)
and MRI (80%,79%).102Severalother studies have produced similarresults.103�105As
with ultrasound,FDG-PET may have a unique role in the evalu-ation ofthe clinically
N0 neck.106FDG-PET has found a place in the evaluation ofan unknown primary with
success ratesreported from 10 to 60% in the identifica-tion ofthe index
lesion.107�109Drawbacks to the use ofFDG-PET forevaluation ofthe neck include the
inabili-ty to differentiate between cancerous andreactive inflammatory lymph nodes
andthe poor anatomic delineation ofthe pri-mary tumor and neck nodes in relation
tosurrounding structures,particularly thoseofa vascular nature.Assessment ofDistant
MetastasisFinal evaluation ofthe oral cancer patientinvolves a work-up for possible
distantmetastasis.Although the percentage ofindividuals who present with an
untreatedprimary tumor who already have distantmetastasis is low,it is prudent to
havethoroughly staged the individual for opti-mal treatment planning.Distant
metastasisfrom the oral cavity most frequentlyinvolves the lung,followed by liver
andbone.Therefore,routine posterior-anteriorand lateral chest radiographs and the
eval-uation ofliver function tests (LFTs) areconsidered the minimum metastaticwork-
up for head and neck cancerpatients.Depending on abnormalitiesfound in the chest
radiograph or LFTs,locoregional extent ofthe disease,anddegree ofclinical
suspicion,the surgeonmay also choose to obtain a CT ofthechest or abdomen and
pelvis.Obtainingother studies such as bone scans should besymptom-driven.An added
advantage ofan FDG-PET study in the evaluation ofdistant metastatic oral cancer is
its wholebody imaging ofpossible tumor spread.The infrequency ofdistant
metastasiswas recognized early by Crile.110Studiesproduced from the patient
database atMemorial Sloan-Kettering Cancer Centerhave also shown relatively low
rates in theeventual development ofdistant metasta-sis,ranging from 13% in
individuals withfloor-of-mouth cancer to 15% in patientswith carcinoma ofthe
tongue.57,111As newtherapies lead to better locoregional con-trol ofdisease,we can
expect to see agreater incidence ofdistant metastasis inlong-term follow-
up.DiagnosisA thorough clinical examination is thefirst line ofdefense in the
detection oforal cancer.Prognosis is directly depen-dent on the tumor stage at
diagnosis.Nearly one-halfofall oral cancers are notdetected until they are in
advanced stages.This delay may be because symptomsmay not develop until later in
the diseaseprocess or the socioeconomic group mostlikely to develop oral cancer is
unable toseek treatment until it has reached anadvanced stage.Studies have shown
thatonly 14% ofadults in the United States haveever had an oral cancer
examination.112A study by Holmes and colleagues showedthat detection oforal and
oropharyngealSCC during non�symptom-drivenexami-nations was associated with a lower
stageat diagnosis.113These detections occurredin the dental office,whether by a
dentist,dental hygienist,or oral and maxillofacialsurgeon.Toluidine BlueOral cancer
can have various clinicalappearances,ranging from subtle mucos-al color or texture
changes to gross ulcer-ation or a fungating lesion.These mucos-al alterations are
particularly difficult toassess in early cancers and dysplasia.Itwas recognized in
the 1960s that toluidineblue stained malignant cells in vivo.Tolu-FIGURE32-
16Preoperative positron emissiontomography scan demonstrates increased activityin
right tongue and right neck at levels II and III.
Oral Cancer: Classification,Staging,and Diagnosis627idine blue is a metachromic dye
that hasbeen used as a nuclear stain.The dyeuptake has been shown to aid in the
earlyrecognition and diagnosis oforal SCC.114While the dye�s exact mechanism
ofaction is unknown,theories have beenproposed that the dye selectively stainscells
with increased deoxyribonucleic acidsynthesis or quantitatively more nucleicacids
than other cells.115It has also beensuggested that the dye binds to
sulfatedmucopolysaccharides,found in higherquantities in actively growing
cells.Sever-al studies have borne out toluidine blue�ssensitivity (89 to 100%) and
specificity(62 to 90%) for oral SCC.115�117Thisspecificity increases when a
protocol isfollowed involving a second rinse 14 daysafter the initial application
to allow forresolution ofany inflammatory lesionsthat may be present.The
sensitivity oftoluidine blue in detecting dysplasticlesions is not as high as that
for SCC.Sen-sitivity rates have been recorded rangingfrom 74 to 84.6%.115,117These
dysplasticlesions stain inconsistently,and toluidineblue cannot be used as
reliably.Toluidine blue is currently marketedas a commercially available kit.Our
opin-ion is that its use should be limited to thescreening ofhigh-risk
individuals,andassisting in directing biopsies from a largearea ofabnormal-
appearing tissue.In theend,toluidine blue cannot be substitutedfor a thorough oral
examination and biop-sies when clinical suspicion is high.BiopsyOnce a clinically
suspicious lesion is iden-tified in the oral cavity,tissue diagnosismust be
obtained prior to rendering anytreatment.This biopsy can usually be donein an
office setting or rarely under generalanesthesia with panendoscopy ifthe lesionis
difficult to access and patient toleranceis low.The traditional
biopsy,whetherincisional or excisional (for small lesions),is the gold standard.It
should be empha-sized that an accurate dimension ofthelesion should be acquired
prior to biopsyin order to properly stage the lesion.Whenfaced with a large
lesion,it is best to takeseveral biopsies from different sites in anattempt to
decrease any sampling errorthat might be read as dysplasia,necrosis,or
inflammation.Brush cytology has gained acceptancein the dental community as a
safe,mini-mally invasive technique for use in thescreening ofclinically
suspiciouslesions.118Brush cytology differs fromexfoliate cytology in that it
removes anentire transepithelial layer for cytologicevaluation as opposed to the
sloughingsurface layer ofthe mucosa.Commerciallyavailable kits exist that include a
brushbiopsy instrument,glass slide,and fixative.The suspicious lesion is sampled by
rub-bing or rotating the sampling brushagainst its surface until pinpoint
bleedingat the biopsy site is obtained,indicatingsampling to the basement membrane
andan adequate specimen.This specimen isthen transferred to the slide,fixed in
theoffice,and sent to the corporation for eval-uation by both a computer and
oralcytopathologist.Brush biopsy results areclassified as �negative�when no
epithelialabnormality is noted,�positive�when def-inite cellular evidence
ofdysplasia or car-cinoma is found,�atypical�when abnor-mal epithelial changes
ofuncertaindiagnostic significance are observed,and�inadequate�when an
incompletetransepithelial specimen was submitted.The largest study ofbrush cytology
by Sci-ubba and colleagues found a sensitivityand specificity
of100%.119However,assome authors have pointed out,a lack ofinvestigation with
scalpel biopsy ofatypi-cal results in �innocuous-appearing�lesions has resulted in
a possible specifici-ty exaggeration ofthis technique;otherstudies have borne this
result out withreported sensitivities ofapproximately90% but a specificity ofonly
3%.120Brush biopsies�best value may lie inthe general dentist�s hand where he orshe
may encounter epithelial abnormali-ties on a daily basis and is reluctant torefer
the patient for biopsy.It is ouropinion that brush cytology is only ascreening
tool,and any atypical or posi-tive results must be confirmed by an inci-sional
biopsy.The same should be saidabout highly suspicious lesions read
as�negative.�Ifclinical suspicion remainshigh despite a negative cytology
result,abiopsy should be obtained.ConclusionsSCC ofthe oral cavity continues to be
acommon disease worldwide including inthe United States.Despite research
andadvances in surgical and adjuvant therapy,long-term survival remains poor.It is
a dis-ease all clinicians will be faced with,andearly recognition and diagnosis
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CHAPTER 33Oral Cancer TreatmentJon D.Holmes,DMD,MD Eric J.Dierks,DMD,MDOral cavity
cancers account for 30% ofhead and neck cancers and represent a sig-nificant
challenge to clinicians.Treatmentrequires multidisciplinary expertise and
iscomplicated by the complex role that theoral cavity plays in
speech,mastication,andswallowing.Oral squamous carcinomasaccount for 90%
ofmalignancies affectingthe oral cavity,and will be the focus
ofthischapter.Although discussion will be limitedto the treatment ofsquamous cell
cancers,oncologic principles outlined in this chap-ter can be applied to other
malignanciesaffecting the oral cavity.1�3Regardless ofadvances in diagnosisand
treatment,mortality from oral cancerhas not changed significantly in the past 50
years.Approximately 50% ofpatientsdiagnosed with oral cancer will ultimatelydie
oftheir disease.4,5Early detection andappropriate treatment ofcancers remainthe
most effective weapons against cancersofthe oral cavity.Unfortunately public
andprofessional awareness and knowledge oforal cancer is low.A recent
editorialreferred to oral cancer as �The ForgottenDisease.�6Incidence and mortality
for oralcancer is nearly double that ofcancer ofthecervix (30,300 vs 13,500 and
8,000 vs4,400,respectively);yet few adults canremember their last oral cancer
examina-tion,whereas most women are aware oftheir last gynecologic examination and
Papsmear.7Patient knowledge ofother can-cers,such as skin,breast,and
prostate,hasincreased in recent years because ofpublicawareness campaigns.Only
recently,how-ever,has oral cancer begun to receive someofthe same attention.The
American Can-cer Society recommends a cancer-relatedcheck-up,including examination
for can-cers ofthe oral cavity,every 3 years forasymptomatic men and women aged 20
to39 years and yearly for men and womenaged 40 years and older.8Although the
oralcavity is readily accessible for examination,results ofa study by Holmes and
colleaguesquestioned whether health care profession-als were screening for
asymptomatic can-cers.9Additionally,smaller symptomaticcancers often went
undetected in theirstudy and were ultimately detected at alater stage.Interestingly
all asymptomaticcancers were referred from dental prac-tices,and the average
clinical and patho-logic stage ofcancers referred from physi-cian offices were
statistically higher.9This isunfortunate since the population at high-est risk for
development ofan oral cancer isfour to six times more likely to seek carefrom a
physician than a dentist.10,11Clearlythere is a need for increasing the
public�sawareness oforal cancer and improvingscreening for early oral cancers in
order toimprove outcomes regardless oftreatmentmodality employed.HistologyJust as
the molecular events leading to thedevelopment ofsquamous cell carcinomaare a
multistep process,the histologic pro-gression ofbenign mucosa to invasive can-cer
typically follows an orderly progres-sion.Although squamous cell carcinoma isthe
most common,other variationsrequire alterations in treatment.Verrucous carcinoma is
generally con-sidered an uncommon variant ofsqua-mous cell carcinoma,representing
only 5%oforal cancers.12It has a predilection forthe buccal mucosa,and typically
appears asa thick white cauliflower-like growth (Fig-ure 33-1).The basement
membrane is typ-ically intact and the cells are very well dif-ferentiated.It is not
uncommon to findfocal areas ofinvasive squamous cell carci-noma within the excised
specimen,andpatients should be prepared for this even-tuality.The prognosis is
excellent followingadequate excision.FIGURE33-1Verrucous carcinoma ofbuccalmucosa
with extension onto the adjacent maxil-lary alveolus.
632Part 5: Maxillofacial PathologyBasaloid squamous cell carcinoma rep-resents a
rare aggressive form ofsquamouscarcinoma.It affects males predominately,and is
associated with a high rate ofcervicaland distant
metastases.13Histologicallybasaloid cells are arranged in nests or cords.Perineural
invasion and a high mitoticindex are common and coincide with itstendency to
recurrence and worse progno-sis,with a 38% mortality at 17-month follow-up.14Given
the aggressive nature ofbasaloid squamous cell carcinoma,electivetreatment ofthe
neck and postoperativeradiotherapy with or without adjunctchemotherapy are probably
indicated.It is helpful to request from the pathol-ogist a depth-of-invasion
measurement onmore superficial lesions,given its predic-tive value in regard to
occult metastases,and determining the need for elective neckdissection (see
discussion on elective neckdissection in this chapter).Depth ofinva-sion will not
influence treatment ofdeepindurated or fixed lesions.Slowly resorbingsutures,which
will serve as a marker ifanexcisional biopsy is performed,is best ifclosure is
required.Management ofPremalignant Lesions Leukoplakia is defined as a
predominatelywhite lesion ofthe oral mucosa that can-not be characterized as any
other definablelesion (Figure 33-2).15Worldwide esti-mates ofits prevalence range
from 1.5 to2.6%.16Lower socioeconomic status seemsto be associated with higher
prevalence.17The potential for malignant transforma-tion oforal leukoplakia to
invasive squa-mous cell carcinoma is well recognized,and leukoplakia can be
considered a pre-cancerous lesion (ie,�a morphologicallyaltered tissue in which
cancer is more like-ly to occur than in its apparent
normalcounterpart�).15Estimated rates oftrans-formation,however,vary
widely.Thismost likely relates to the heterogeneity ofthe lesions included in most
studies.Whilehomogeneous white leukoplakia has a rel-atively low
risk,erythroleukoplakia has ahigh incidence ofassociated dysplasia,car-cinoma in
situ,and frank carcinoma.Intheir oft-quoted study of257 patients fol-lowed for a
mean of8 years,Silverman andcolleagues found transformation rates forleukoplakia to
range from 6.5% for homo-geneous lesions to 23.4% in erythropla-sia.18Lesions
containing dysplasia had atransformation rate of36.4%.18The annu-al transformation
rate in one populationwas less than 1%,which still demonstrateda 36-fold risk
increase for squamous cellcarcinoma in patients with oral leuko-plakia over the
population in general.19Predicting which lesions will ultimate-ly transform is
currently not possible.Given its asymptomatic nature,the soleindication for
treatment ofleukoplakia isan attempt to prevent subsequent malig-nant
transformation.Treatment modali-ties include excision,ablation,and chemo-
prevention.Unfortunately no treatmentmodality has been shown to prevent sub-sequent
development ofsquamous cellcarcinoma.The first Cochrane review on therapyfor
leukoplakia did not find any reliabletherapy to prevent the transformation
ofleukoplakia to oral squamous cell carcino-ma.20Also,there were no effective
preven-tive measures to halt the development oforal leukoplakia.No surgical
procedureswere included in this review because ofthelack ofrandomized clinical
trials evaluat-ing surgical excision.Chemopreventiveagents including retinoids,beta
carotene,green tea,and bleomycin were evaluated.Retinoids held the most promise and
wereassociated with resolution oflesions.Theultimate goal remains prevention ofsub-
sequent malignant transformation,andunfortunately none ofthe agents demon-strated
this reliably.In addition associatedside effects were problematic (see
section�Chemoprevention�in this chapter).20,21Surgical excision remains an alterna-
tive for dealing with worrisome lesions.CO2laser excision has been used to
treatwidespread superficial lesions in anattempt to limit scarring and
morbidityassociated with large excisions.Laser abla-tion allows the destruction
oflarge super-ficial lesions.It does not provide a histo-logic specimen,however,and
biopsiesfrom any areas ofulceration or erythro-plasia are probably indicated prior
to abla-tion.Unfortunately recurrence followinglaser excision or ablation is not
uncom-mon,and it does not necessarily preventmalignant transformation.22Given the
high rates ofmultiplelesions and their propensity to recur,pho-todynamic therapy
(PDT) is gaining pop-ularity as a potential method for dealingwith multiple diffuse
lesions.PDT relieson a complex interaction ofa photosensi-tizing agent,which is
preferentially con-centrated in abnormal tissue,with light ofvarious
wavelengths,depending on thephotosensitizer,to create necrosis througha nonthermal
reaction.Tissue necrosis ismediated through the creation ofsingletoxygen,a highly
reactive species thatinduces cellular damage through severalmechanisms.Advantages
ofPDT includeminimal damage to surrounding tissuesand no cumulative damage,which
theo-retically allows unlimited treatments.Given the propensity for these patients
todevelop multiple lesions,this is an impor-tant advantage over excision or
ablationusing traditional methods.DisadvantagesFIGURE33-2Leukoplakia ofthe ventral
tongue.include marked photosensitivity,especially
Oral Cancer Treatment633with regard to sun exposure,for variablelengths oftime
after the administration ofthe agent.Areas treated undergo healingthrough
mucosalization with minimal orno scarring.Although a complete reviewofPDT is beyond
the scope ofthis chapter,excellent reviews are available.23�25PDT has been used
with some successin the endoscopic treatment ofdysplasticBarrett�s esophagitis to
prevent its trans-formation to adenocarcinoma.26Similarlyattempts have been made to
treat diffuseoral leukoplakia with PDT with some suc-cess.27In addition to its role
in the man-agement ofleukoplakia,initial trials ofPDT applied to invasive squamous
cellcarcinoma ofselected sites in the head andneck are being reported.Copper and
col-leagues reported on 25 patients with T1and T2 lesions ofthe oral cavity
andoropharynx treated with PDT.Completeremission was noted in 86%
oflesions.Recurrences were salvaged with conven-tional therapy.28In addition to its
applica-tion to mucosal lesions,interstitial deliv-ery oflight may allow treatment
ofmoredeeply situated tumors.Although resultsare promising,PDT for leukoplakia
andoral cavity cancers remains investigational,and its role in the management
ofleuko-plakia and squamous cell cancers ofthehead and neck awaits
clarification.Role ofPanendoscopy in Treatment PlanningOnce a histologic diagnosis
oforal cancerhas been made,a patient evaluation is initi-ated in an attempt to
define the extent ofthe locoregional disease,as well as the exis-tence ofdistant
metastases.The discussionthat was started with the patient when thebiopsy was
performed is now continuedwith the knowledge that a malignancy ispresent,but that
continued work-up is nec-essary to define the extent ofdisease.Patients frequently
feel a sense ofurgencyonce a diagnosis ofcancer is rendered.Theywant treatment
initiated quickly.It isimportant to convey that cancer is not asurgical emergency
and that the growthrate ofepithelial malignancies allows for anappropriate
evaluation that must be com-pleted prior to making treatment recom-mendations.It
should also be rememberedthat there is a high incidence ofdepressionin the head and
neck cancer patient popu-lation.The level offamily and communitysupport should be
gauged,and appropriatereferrals should be made ifdeemed neces-sary.The patient�s
overall medical condi-tion should also be assessed in preparationfor any planned
treatment.Aside from thestandard history and physical examination,including head
and neck examination,nasopharyngoscopy or indirect laryn-goscopy in the office
should be considered.This evaluation may be forgone ifpanen-doscopy or �triple
endoscopy�is planned tosearch for synchronous primary cancers.Following McGuirt�s
1982 study ofpanendoscopy,examination ofthe esoph-agus,larynx,and bronchus was
consideredmandatory in the work-up ofthe patientwith cancer ofthe head and neck.29A
mir-ror examination ofthe nasopharynx wasalso frequently included.McGuirt�s find-
ing ofsynchronous tumors in 16% ofpatients led most clinicians to
includepanendoscopy in their evaluation.29Recently its routine use has been
calledinto question for a variety ofreasons,including cost
containment,improvedimaging modalities,and lower rates ofsynchronous primary tumors
ofthe headand neck than previously expected.Someclinicians still feel there is a
role for anexamination ofthe primary cancer undergeneral anesthesia,along with
panen-doscopy.They argue that the ability toexamine some larger primary cancers
iscompromised in the clinical settingbecause ofpatient discomfort,and that
thepanendoscopy affords the clinician aninvaluable opportunity to examine
theprimary cancers without this constraint.Others argue that the low yield ofbron-
choscopy over chest radiographs and com-puted tomography (CT) scans and theability
to perform an examination ofthelarynx with flexible nasopharyngoscopymitigate
against the usefulness ofrigidlaryngoscopy and bronchoscopy.Also,themajority
ofpatients with cancer ofthehead and neck receive a flexibleesophagoscopy along
with placement ofapercutaneous endoscopic gastrostomytube.For these reasons
panendoscopyshould probably be symptom driven.30Choosing a TreatmentOnce the
initial evaluation,data collection,and staging are complete,a discussionregarding
treatment is undertaken.Theclinician and the patient are faced withdeciding which
treatment modality orcombination offers not only the best chancefor cure,but also
quality oflife.Quality-of-life issues are becoming increasingly impor-tant in
treatment planning.Despite mediahyperbole on cancer treatment �break-
throughs,�cancer treatment still falls intothree basic
categories:surgery,radiation,orchemotherapy,or some combination there-of.Choosing
the appropriate treatmentrelies on many factors,including thepatient�s medical
condition as well as themodalities available to the clinician.Certaintherapeutic
modalities,such as neutronbeam radiotherapy,may hold promise forcertain tumors,but
are limited in theiravailability.Although each will be discussedseparately in the
upcoming sections,mostpatients will ultimately receive more thanone form
oftreatment.SurgerySurgery remains the cornerstone ofmosttreatment regimens for
oral cavity cancer.Surgery offers several advantages,includ-ing the harvest ofa
specimen forhistopathologic analysis and the possibili-ty ofremoving the cancer
with one treat-ment modality at one session.For moststage I and stage II cancers
ofthe oral cavi-ty,surgical resection with frozen sectionanalysis ofthe margins is
advocated by mostclinicians.Although primary radiation to
634Part 5: Maxillofacial PathologyT1 and T2 lesions may offer similar dis-ease
control,the side effects ofradiationto the oral cavity outweigh those ofsurgery in
most situations.In addition,given the rate ofsecond primary cancersin the head and
neck cancer patient pop-ulation,it is often better to hold radiationifpossible in
case it is needed in thefuture.The oral cancer patient populationis prone to the
development ofsecondprimary cancers and some would arguethat radiation for
borderline indicationsmight be withheld for future use shouldthe need
arise.Reirradiation,althoughpossible in some circumstances,is associ-ated with a
high degree ofmorbidity.The importance ofobtaining clearhistologic margins has been
a foundationfor surgical treatment oforal cavity cancerand has been supported by
several studiesthat have demonstrated decreased survivalassociated with positive
margins,even iffollow-up radiation is given.Unfortunate-ly clear pathologic margins
are not alwaysan assurance ofa good outcome.Fieldcancerization is a concept that
was pro-posed by Slaughter and colleagues in 1953,after they reviewed resection
specimensfrom the oral cavity and oropharynx.Theyfound multiple foci ofcancer in
11% ofspecimens.Areas ofdysplasia also existeddistant from the primary
site.31Additionalstudies have shown that margins that areclear histologically may
still have cells atthe margin that demonstrate premalig-nant changes,and this can
be associatedwith recurrence.A recent study demon-strated that an altered P53gene
existed in52% ofreviewed patients and that recur-rence occurred in almost
halfofthesepatients.32Other markers have beenshown through molecular analysis to
existat margins that are clear histologically;specifically the proto-oncogene
eIF4Ehasbeen shown to be associated with adecreased disease-free interval when pre-
sent at the resection margin.32In an inter-esting study Thomson performed
biopsiesin patients with unilateral squamous cellcarcinomas or premalignant
lesions.33These biopsies were taken on the oppositeside ofthe mouth in the same
area as thecontralateral cancer or premalignantlesion.These so-called �mirror
image�biopsies revealed frank dysplasia or carci-noma in situ in 30%
ofpatients.33Thisconcept of�condemned mucosa�hascaused clinicians to question the
ability ofsurgeons to obtain clear margins in somecancers.Studies have clearly
shown,how-ever,a decreased local control and survivalin patients with positive
margins.Jacobs and colleagues analyzedpatients who had received
postoperativeradiation;patients with satisfactory mar-gins suffered an 11% relapse
rate,whereaspatients with unsatisfactory marginsrelapsed 26% ofthe time.34This is
mostlikely due to the inability ofradiation ther-apy to deal with the increased
tumor cellburden in some cases offinal positive mar-gins.34These studies have led
some toinvestigate addition ofbrachytherapy toexternal beam postoperative radiation
topatients with unsatisfactory margins,andto subsequently demonstrate
improvedsurvival in patients with positive marginswho received this intensive
radiation.35Itis agreed by most that surgeons shouldstrive for clear margins,given
this impactofpositive margins on survival.Excisionwith 1 to 1.5 cm ofnormal tissue
beyondthe obvious tumor edge is generally suffi-cient.Margins should then be
harvestedfrom either the specimen or the woundresection periphery depending on the
sur-geon�s preference.These thin strips are ori-ented for the pathologist using a
specimenmap (Figure 33-3).Mucosal margins aswell as deep margin specimens are
submit-ted;however,frozen-section analysis isaccurate but not infallible.Indeed the
roleoffrozen analysis ofmargins in oral cavitycancer has been heavily debated and
itscost effectiveness called into question,leading some surgeons to abandon
thepractice.Although frozen-section analysisis highly accurate and has a high
correla-tion with final histologic analysis ofthesubmitted tissue samples,its
ability to pre-dict whether the entire tumor surface ofthe final specimen will be
clear ofclose orinvolved margins is not as reliable.For thisreason frozen sections
appear to be morebeneficial in smaller localized tumors.36�38On occasion a surgeon
will be facedwith a situation where the frozen marginswere negative but the final
processed spec-imen shows involvement ofone or moremargins.This phenomenon can have
sev-eral explanations.First,sampling error canoccur.Secondly,ifthe margins analyzed
byfrozen technique were taken from thetumor resection bed,then it might lie
justbeyond the cancerous margin.Also,tumorshrinkage ofapproximately 25 to 30%occurs
when the tumor is removed fromthe body.Faced with this dilemma the sur-geon has
several options.Re-excision ofapositive soft tissue margin is difficult andrarely
productive.Wound closure orreconstruction ofthe defect distorts tissue,and it is
frequently impossible to deter-mine exactly where the positive marginwas.For this
reason a final positive marginmay represent an indication for postopera-tive
radiation therapy (see section �Radia-tion�below).Conversely clearance ofcan-cer
within bone with radiation is difficultFIGURE33-3Specimen map for
demonstrationofthe orientation offrozen section specimens tothe pathologist.
Oral Cancer Treatment635and recurrence rates are high,suggestingthat patients with
positive bone marginsshould be strongly considered for re-exci-sion.Recent reports
illustrate that patho-logic margins that are positive on finalanalysis are more
likely a reflection oftheaggressiveness ofthe particular cancerthan a reflection on
the surgical proce-dure.Sutton and colleagues found thatfinal positive margins had
a high correla-tion with aggressive histologic parameterssuch as perineural and
lymphovascularinvasion.39Thus,the biologic aggressive-ness suggested by positive
margins may initselfaccount for the poorer outcome ofpatients with positive
surgical margins,and be an indication for multimodalitytherapy instead ofattempts
at re-excision.Surgery in patients with head andneck squamous cancer presents
uniquechallenges that surgeons should be pre-pared to face.The following
discussionoffers an overview ofsome ofthe periop-erative issues facing patients and
surgeons.Subsequent sections will review surgicalpoints pertinent to specific sites
within theoral cavity.Perioperative Issues in Oral Cavity Cancer TreatmentThe
decision to operate on a patient withhead and neck cancer must involve consid-
eration ofpotential complications.Studieshave demonstrated that age itselfis
notassociated with increased complications,but comorbidities are associated
withincreased complications and lengthy hos-pital stays.This is especially true
regardingcomplex reconstructive efforts,such asvascularized tissue
transfer.40Several fac-tors deserve special attention in the patientundergoing
surgery for a malignancy ofthe upper aerodigestive tract.AirwayIfthere is any doubt
concerningthe ability ofa patient to maintain an air-way in the perioperative
period,a tra-cheotomy is advisable.A tracheotomy tubedoes not prevent
aspiration,and paradoxi-cally may actually increase its likelihoodbecause
oftethering ofthe trachea andimpaired glottic closure.Tracheotomy isnot without its
own risks,and the nursingstaffperforming tracheotomy care must bewell versed in
suctioning and maintenance.Decanulation can generally be performedsoon after edema
has decreased.Perioperative AntibioticsOperations onthe oral cavity are considered
�clean-contaminated,�and therefore,periopera-tive antibiotics are indicated.Several
well-controlled studies have demonstrated thatantibiotics started prior to the
incisionand continued for no more that 24 hoursserve to minimize perioperative
infectionsand emergence ofresistant strains.First-generation cephalosporins and
clin-damycin represent the most commonlyused prophylactic antibiotics in oral can-
cer surgery.Topical antimicrobials such aschlorhexidine and clindamycin rinses
havealso been shown to successfully reduce theincidence ofinfections.41,42Alcohol
WithdrawalMany patients withoral cavity cancer will be dependent onalcohol.Alcohol
withdrawal is common ifprecautions are not taken and can culmi-nate in delirium
tremens leading to car-diovascular collapse and death.Appropri-ate prophylaxis with
benzodiazepines isrecommended ifthe patient drinks daily.Lorazepam is commonly used
because ofits predictable onset and lack ofactivemetabolites.Intravenous alcohol (5
to10% alcohol with 5% dextrose in water)can be used in the postoperative periodand
slowly tapered as the patient recoversfrom surgery.Deep Venous ThrombosisPatients
whowill be immobilized for a significant timeduring surgery or following surgery
shouldreceive prophylaxis for deep venous throm-bosis.This prophylaxis most
commonlytakes the form ofmechanical compressiondevices that cause endothelial cells
torelease antithrombogenic factors and pre-vent stasis.It is important that these
beplaced and activated before surgery.Phar-macologic agents are generally reserved
forknown cases ofthrombosis because oftheirpropensity to cause bleeding in the
postop-erative setting.Low-molecular-weightheparin may be an option in this
setting.Ifthe patient has undergone microvascularreconstruction,aspirin or low-
molecular-weight dextran may be indicated.Fluid ManagementMost patientsundergoing
surgery for oral cavity cancerscan be managed without invasive moni-toring offluid
status.Colloids may beneeded to prevent undue amounts ofcrys-talloid leading to a
significant increase inedema.Preoperative and daily weights canbe used to track
fluid status.In patientswith compromised cardiovascular reserveor in those
undergoing large resectionsand free-flap reconstruction,invasivemonitoring with
central venous monitor-ing or via a Swan-Ganz catheter may benecessary.Although
uncommonly per-formed,patients requiring bilateral resec-tion ofthe internal
jugular veins will needfluid restriction.TransfusionOpinions regarding the needfor
transfusion vary.In general a hemat-ocrit less than 25 requires
transfusion,andthose between 25 and 30 may need transfu-sion based on clinical
parameters.NutritionMany patients with head andneck cancer will present with
decreasednutrition reserves.Even patients withoutweight loss are often faced with
therapiesthat will leave them unable to maintaintheir nutrition.The ability to
bypass theupper digestive tract during intense multi-modality therapy by the
endoscopic place-ment ofa gastric feeding tube (percuta-neous endoscopic
gastrostomy or PEGtube) is invaluable.This procedure offers aminimally invasive
�lifeline�for patientsundergoing intensive therapy to the head
636Part 5: Maxillofacial Pathologyand neck.Placement ofa PEG tube hasbecome
commonplace in head and neckcancer patients.Although rare there havebeen anecdotal
reports ofseeding squa-mous cell carcinoma to the abdominalwall ifthe PEG is placed
prior to resec-tion.43This complication,although rare,has led some surgeons to
recommendplacement in the postoperative period.Even ifa PEG is placed,the patient
shouldbe encouraged to continue some oralintake,as the risk ofesophageal
stenosisincreases ifthe patient completely stopsoral alimentation during radiation
treat-ment.This is especially true during com-bined chemoradiation
protocols.Complications ofSurgeryComplications ofsurgical resection aremany and
vary directly with the patient�scomorbidities,such as ischemic cardiac dis-
ease,chronic pulmonary disease,and alco-holism.Medical manifestations ofpreexist-
ing chronic disease states,such asmyocardial infarction,stroke,and pneumo-nia,can
be precipitated by major surgery,along general anesthetic,and a prolongedintensive
care unit stay.Significant morbid-ity or death can be the result.Technical sur-
gical complications,such as failure ofrecon-structive flaps,development
offistulas,andthe other myriad problems that may requirereturn to surgery for
management,pale insignificance to the greatest complication�locoregional recurrence
ofthe cancer.RadiationA complete review ofradiation physicsand medicine is beyond
the scope ofthischapter,and excellent reviews on the topicare available.44Surgeons
dealing with oralcancer should have an understanding ofradiation therapy and its
advantages anddisadvantages.This entails a familiaritywith radiation biology and
the interactionofradiation with living tissue,as well asthe biology ofcell
death.Cell death can bedivided into two types:reproductive celldeath,which results
from damage to cel-lular genetic material,or apoptosis,whichis programmed cell
death.Reproductivecell death can occur as a result ofsingleDNA strand breaks,which
are commonand easier for the cell to repair,or double-strand breaks,which are more
difficult forthe cell to recover.Apoptosis occurs whena cell enters a programmed
cell deathmode as a result ofdamage.Radiation cancause either type ofcell death and
alsoslows cellular division.Classically radia-tion is discussed in terms ofthe four
R�s:repair,reoxygenation,redistribution,andregeneration.Radiotherapy is primarily
given byexternal beam using electromagnetic radi-ation or particulate components.X-
raysand gamma rays represent photons.X-raysare produced by a man-made source
andgamma rays are produced by radioactivedecay,most commonly ofcobalt 60.Par-
ticulate radiation using electrons plays animportant role in head and neck
cancer.Another form ofparticulate radiation isneutron radiotherapy,which may have
aspecific role in salivary gland malignan-cy.45Regardless ofthe
source,radiationinteracts with tissue to produce severaltypes ofdamage to cells.The
radiationparticle-cell interaction may be eitherdirect,or more commonly impact
withH2O molecules to create secondary parti-cles that interact with cellular
DNA.Absorbed dose is reported as a gray (Gy),which is one joule ofabsorbed dose
perkilogram.Previously dose was reported asa rad,which was defined as 100
ergsabsorbed per gram.One gray is equal to100 rad and one centigray (cGy) equalsone
rad (1 cGy = 1 rad).In the early to mid-twentieth century,radiation was given as
orthovoltage (125to 500 KeV).Currently radiation is deliv-ered as megavoltage (> 1
MeV).Megavolt-age results in more radiation delivered todeeper tissues with less
superficial (skin)damage.In comparison a superficial radi-ograph unit (x-ray
machine) delivers 30 to125 KeV.Radiation therapy is typicallygiven in daily doses
of200 cGy,except inaltered fractionation schedules.Fractionationrefers to the
schedule onwhich the radiation dose is administered.Standard radiotherapy is
administereddaily,5 days a week,with weekends off.Inan effort to maximize damage to
the morerapidly dividing tumor cells while sparingnormal tissues as much as
possible,frac-tionation schedules have been altered.Although used primarily in
clinical trials,clinicians should be familiar with theadvantages and disadvantages
ofotherfractionation schedules because it is likelythat their use will become more
wide-spread.Accelerated fractionationrefers toan overall reduction in treatment
timeaccomplished by giving two or more daily-dose fractions ofclose to
conventionalsize.Hyperfractionationimplies that theoverall treatment time is
conventional orslightly reduced,but an increase in totaldose is achieved by giving
two or moresmall-dose fractions on each treatmentday.Each ofthese regimens is
associatedwith varying degrees ofearly and late tox-icities.For example,some
clinicians feelthat long-term effects such as osteora-dionecrosis are increased
with hyperfrac-tionated schedules,especially when com-bined with concomitant
chemotherapy.This view is not universal,however,and asmore experience is
gained,questionsregarding toxicity will be answered.46,47Aside from changes in
radiationschedules,other facets ofradiation deliv-ery technique have undergone
recentchanges.Radiation is delivered to a specif-ic target area that is limited by
shielding(defined as radiation portals or �ports�)that is placed to protect areas
that are notsuspected ofharboring tumor or that areless tolerant ofradiation
(ie,the spinalcord).The radiation treatment plan is typ-ically standardized for
each subsite in theoral cavity.Conformal radiation treatmentrefers to more
localized delivery ofradia-tion to the suspect site.By linking CTimages with the
ability to manipulate the
Oral Cancer Treatment637radiation beams,radiation therapists areable to more
accurately focus the radiationdose on the tumor bed and avoid adjacentuninvolved
areas that may be more sus-ceptible to radiation damage (Figure 33-4).There is
still concern that highly con-formal treatment plans may result inincreased
recurrence rates because ofthemore limited field ofradiation.Intensitymodulated
radiotherapy is an example ofaconformal treatment plan combined withvarying
radiation doses to limit the collat-eral damage to surrounding
areas.48,49Brachytherapy or interstitial radio-therapy is administered by placing
aradioactive source,typically radium(226Ra) or iridium (192Ir),directly in thetumor
mass using needles or loopcatheters.In this manner radiation isdelivered
continuously.This does notallow the tumor cells to �repopulate�between fractions as
in external beamtherapy.Unfortunately cells native to thearea cannot recover
either,resulting inextensive radiation-induced fibrosis andosteoradionecrosis.This
technique allowsa higher total dose ofradiation to be givento a primary site than
does external beambecause the radiation is placed directly inthe tumor
mass.Brachytherapy has devel-oped a reputation for creating chronicwounds and may
lead to osteoradionecro-sis when used adjacent to the mandible.Itscurrent use is
generally limited to treat-ment oftongue or tongue base primaries,and is usually
combined with externalbeam radiation.Brachytherapy has alsobeen advocated for
treatment ofclose orpositive margins following surgical exci-sion.35Brachytherapy
patients may requirea tracheotomy for airway control becauseofairway compromise
from edema.Wound healing is also severely compro-mised.Some clinicians have
recommend-ed only limited biopsies in the treated areaifrecurrence is suspected
because chronicnonhealing wounds can develop.50,51Radiation can be administered
withcurative intent in the preoperative settingor as an attempt to shrink a tumor
presur-gically (neoadjunct).When the primarytumor is to be treated with
radiation,theclinician must also consider elective radia-tion ofthe neck for
control ofoccultmetastases.Because ofits dependence onoxygen for
effectiveness,bulky neck diseasewith its attendant hypoxic core shouldprobably be
treated with neck dissection,either before radiation or as a planned pro-cedure
within 4 weeks ofcompletion ofradiation.Early-stage oral cavity cancer(T1 or T2)
responds equally well to radia-tion or surgery.The morbidity ofradiationand the
inability to use it again in the caseofa second primary cancer or recurrentdisease
makes surgery a more attractivemodality in most situations.Larger tumors(T3 and T4)
generally respond poorly toradiation alone.Preoperative radiationgiven in an
attempt to shrink larger tumorsis hampered by the fact that tumors do notshrink
concentrically.Viable islands oftumor cells can be left beyond the newclinically
evident margins.In theory sur-geons are committed to excising to theoriginal
margins,something that seldomhappens in clinical practice.The primary role for
radiation in oralcavity cancer is in the postoperative settingwhen there is
potential for persistent dis-ease.Clinical protocols vary among insti-tutions,but
there are accepted indicationsfor postoperative radiation therapy:�Two or more
lymph nodes containingmetastatic disease in a neck dissection(many clinicians
contend that onepositive node is an indication)�Extracapsular extension (ECS)
ofcan-cer beyond the confines ofa node�Poor histologic factors:extensive per-
ineural or perivascular invasion,posi-tive (close) soft tissue margins�Large (T3 or
T4) primary cancersReports have found ECS to be associat-ed with decreased
survival:disease limitedto the node was associated with a 70% sur-vival,whereas ECS
was associated with a27% survival at 5 years.52Million and col-leagues found that
35% ofpatients withclinically negative necks converted to posi-tive ifthe primary
cancer was treated withsurgery alone.53This dropped to 5% ifradi-ation therapy was
added.Even microscopicevidence ofextracapsular extension is asso-ciated with a
higher rate ofrecurrence anddeath.54The decision to add radiation treat-ment must
be made with a clear under-standing ofthe morbidity ofits use.In advanced
disease,clinicians are facedwith a choice ofpreoperative or postopera-tive
radiation treatment.Planned preopera-tive radiation treatment is rarely used butmay
lower the probability ofpositive mar-gins and may allow smaller surgery (con-
troversial).Lower doses ofradiation arerequired because ofthe improved oxygena-tion
in areas not disturbed by surgery.Post-operative radiation treatment allows
easiersurgery and better healing in tissues notdisturbed by radiation-induced
fibrosis.Frozen-section analysis ofmargins is easierin this setting,and surgery
allows improvedtreatment planning based on final patholo-gy.Postoperative radiation
therapy remainsthe mainstay in most cases ofresectablecancers ofthe oral cavity.A
study by theRadiation Therapy Oncology Group,FIGURE33-4Three-dimensional
conformalmapping ofpostoperative radiotherapy for esthe-sioneuroblastoma ofthe
olfactory bulb.Globesand optic nerves are depicted to ensure minimalradiation
damage to these structures.
638Part 5: Maxillofacial PathologyRTOG 73-03,compared 50 Gy
preoperativeradiotherapy to 60 Gy postoperative radio-therapy.The 10-year follow-up
demon-strated no survival advantage to either reg-imen,but postoperative
radiationtreatment demonstrated superior locore-gional control.55How much is
enough?Results from an MD Anderson CancerCenter (University ofTexas,USA)
studyshowed that 54 Gy was needed in the post-operative setting,and 57.6 Gy was
needed ifextracapsular extension was present.56Timing ofinitiation ofradiation
ther-apy following surgery is controversial.Vikram demonstrated a clear
survivaladvantage in patients whose radiationtherapy was started within 6 weeks
ofsurgery.57For this reason reconstructiveoptions that led to reliable healing in
thisamount oftime were advocated.57A morerecent study failed to replicate
Vikram�searlier findings,leading some to challengethe supposed impact oftiming on
ultimateoutcome.Other studies have reportedimproved outcomes when
postoperativeradiation begins within 6 weeks and endswithin 100 days ofsurgery for
oral cavitysquamous cancers.58,59The future direction for radiationtreatment may
include the development ofeffective radioprotectants and radiosensi-
tizers.Radioprotectants,such as amifos-tine,are given in an attempt to protect nor-
mal tissues.Amifostine was developed bythe military as a possible protection
fromnuclear attack and has recently beenapplied to head and neck cancer patients
toprotect salivary gland function duringradiation therapy.60Xerostomia is a long-
term problem that has a significant effecton patients treated with radiation
therapyto the head and neck,with 64% ofpatientsreporting moderate to severe
permanentxerostomia.61Decreased incidence ofcan-didiasis,a frequent side effect
observed inpatients with radiation-induced xerosto-mia,has been used as an end
point in ami-fostine therapy used for its protective effecton salivary gland
function.62Its use is asso-ciated with side effects,such as hypoten-sion,and some
patients do not tolerate it.Itis costly and there remains some fear thatits
radioprotective effects might extend tothe cancer cells as well,resulting in
higherrecurrence rates.Radiosensitizers arechemotherapeutic agents that enhance
thateffectiveness ofradiation (see section�Chemotherapy�below).ChemotherapyUntil
1991 the role ofchemotherapy inhead and neck cancer was limited to it usein the
management ofrecurrent and/ormetastatic disease.A landmark study thatchanged our
view ofchemotherapy wasreported by the Cooperative Studies Pro-gram ofthe
Department ofVeterans AffairsLaryngeal Cancer Study Group who report-ed a multi-
institutional trial on patientswith advanced laryngeal cancer.63Theirstudy
demonstrated larynx preservationand equivalent survival among patientswho received
induction chemotherapy fol-lowed by radiation,as opposed to tradition-al
laryngectomy and postoperative radia-tion.63Although criticized by some for itslack
ofa radiation-only control group,theresults fostered a renewed interest in use
ofchemotherapy in the management ofadvanced head and neck malignancy,including
squamous cell carcinoma oftheoral cavity.Several reviews are available onthe
evolving role ofchemotherapy in headand neck cancer.The following summarizesthe
basics ofchemotherapy in oral cavitycancer and discusses several potentialfuture
applications.Prior to analyzing the results ofchemotherapy in oral cavity
cancer,anunderstanding ofthe basic biology ofchemotherapy and the associated termi-
nology is necessary.In many wayschemotherapy for cancer is conceptuallysimilar to
chemotherapy for infections;however,the immune system in general isnot inherently
competent to destroy thecancer.Chemotherapeutic agents kill aconstant fraction
ofcancer cells leavingbehind a certain amount ofresistant cells.These resistant
cells subsequently divideand the tumor mass once again increases.In infectious
diseases the body�s immunesystem aids in the destruction ofthedecreased burden
ofcells,whereas in can-cer the patient usually does not have animmune system that
can deal with therogue cell line.Similar to infections withresistant
strains,multidrug protocols havebeen developed to counter the develop-ment
ofresistant cell lines in cancer.Prin-ciples ofchemotherapy have been devel-oped to
overcome the development ofresistant cell lines such as the use ofmulti-ple agents
that have demonstrated inde-pendent activity against the cancer type,the
combination ofdrugs with differingtoxicities to allow maximum dosing ofeach
agent,and the maintenance ofshortintervals between dosing agents whileallowing
adequate recovery ofnormal tis-sues.Solid tumor growth is governed byGompertzian
kinetics,which means thatgrowth slows as tumor bulk increases.Since
chemotherapeutic agents are mosteffective against cells undergoing replica-
tion,smaller and faster growing tumorsare more susceptible.64Assessment ofthe
literature regardingchemotherapy is complicated ifone doesnot understand the
definitions ofcom-plete response,partial response,stabledisease,and
progression.Each ofthese isdetermined by the sum ofthe product ofthe perpendicular
diameters ofall mea-surable tumors.Measurements areobtained at the beginning
oftreatmentand at completion.�Complete response:Defined as the dis-appearance ofall
evidence ofdisease�Partial response:At least a 50% reduc-tion in size as defined by
the formulaabove�Stable disease:Less than a 50% reduc-tion in tumor
size�Progression:An increase of25% orappearance ofnew lesions
Oral Cancer Treatment639An important point to remember isthat tumor regression must
only last for 4 weeks.It is understandable,therefore,that reports ofa complete
response oftenhave little impact on improved survival.The response rate represents
the total per-cent ofpatients achieving complete andpartial responses.An additional
problemwith chemotherapy trials is patient selec-tion bias.Increasingly the role
ofcomor-bidities in ultimate outcome and theimpact ofperformance status on
survivalare being recognized as important con-tributors to survival in head and
neck can-cer (see discussion below).Performancestatus is typically reported using
theKarnofsky performance status (PS),whichrates patients on a scale of0 (death) to
100(normal,no evidence ofdisease) or theEastern Cooperative Oncology
Groupscale,which rates patients on a scale ofPS0 (fully active) to PS 5
(death).65,66Mostclinical trials require a certain PS to quali-fy,leading to
enrollment ofhealthierpatients and improved outcomes.Timing ofchemotherapy has been
thesubject ofmuch investigation.Again,defi-nitions are the key to understanding
andinterpretation ofresults ofclinical trials.Palliative chemotherapyis given to
patientswith incurable disease to temporarilyreduce tumor volume in the hope
ofimproving quality oflife and lengtheningsurvival.This is typically the arena
thatserves as a testing ground for new thera-peutic agents.Adjuvant
chemotherapyisgiven to patients who have undergonetreatment oftheir primary cancer
site withsurgery and/or radiation.Goals oftreat-ment include elimination ofoccult
dis-ease,especially distant metastases.As thepatient no longer has visible or
palpabletumor with which to gauge response,agents must be selected that have
provenactivity against the cancer type.Neoadju-vant chemotherapy (also known as
induc-tion chemotherapy) is given to patientsprior to definitive treatment ofthe
prima-ry cancer site.64This tactic is generallychosen in an attempt to decrease the
sizeofthe primary cancer to make definitivetreatment possible.For example,a
tumordeemed unresectable may be �down-staged�by neoadjuvant chemotherapy to
aresectable tumor.As stated earlier tumorsdo not shrink concentrically and islands
oftumor may remain beyond the visiblemargin.An additional advantage toneoadjuvant
therapy is the ability to eval-uate response.Squamous cell carcinomasrepresent a
heterozygous population evenwithin the same tumor.Some will beexquisitely
responsive to a particular regi-men,whereas others will not.Medicaloncologists can
tailor their treatmentmore accurately ifvisible or palpabletumor is available to
evaluate response.The biggest criticism ofneoadjuvant ther-apy is that it delays
the definitive treat-ment ofthe primary cancer.Local failure isstill the biggest
cause ofdeath in oral cav-ity cancer,and delaying treatment oftheprimary site
increases the difficulty ofobtaining control ofthe primary cancer.In addition
initial chemotherapy can theo-retically select more hardy cell lines thatare
resistant to all therapy.Indeed critics ofthe Department ofVeterans Affairs Laryn-
geal Cancer Study Group larynx trial con-tend that neoadjuvant chemotherapy sim-ply
selected out less aggressive cancers thatwould respond to radiation
treatment.Currently the role ofchemotherapy thathas generated the most interest is
combi-nation with radiation treatment for an�organ sparing�approach.Chemotherapyin
combination with radiation treatmentcan be given in a sequential or a concur-rent
strategy.Concurrent therapy takesadvantage ofthe radiosensitization ofcer-tain
drugs and avoids delay in treating theprimary cancer site.The downside is amarked
increase in side effects and toxici-ty that can lead to breaks in
radiationtreatment,which have been shown to beassociated with a decrease in local
control.In an attempt to control some ofthese tox-icities,chemotherapy is usually
given atthe beginning ofradiation treatment andfrequently at the completion
ofradiation.Sometimes radiation therapy is interrupt-ed (split-course radiation) on
purpose,and chemotherapy is given.Again,radia-tion breaks are considered to be
associatedwith decreased control and are thereforenot recommended.Chemotherapeutic
agents are underconstant development and a complete dis-cussion ofavailable agents
is beyond thescope ofthis chapter.Several principlesdeserve mention.In general
drugs can bedivided into cell cycle�specific and noncellcycle�specific
agents,depending onwhether the particular agent requires thatthe target cell be in
a certain phase (G0,S,G1,or mitosis) to be effective.Agents canalso be categorized
based on their princi-ple mode ofaction.Antimetabolites,suchas methotrexate and 5-
fluorouracil,blockdevelopment ofcertain metabolites criti-cal for cell
metabolism.5-Fluorouracil is afluoridated pyrimidine analog thatinhibits
thymidylate synthetase,blockingthe generation ofthymidine,which is nec-essary for
DNA synthesis.It is frequentlyused in the treatment ofhead and necksquamous cell
carcinoma.Typically it iscombined with other agents,and it is
aradiosensitizer.Methotrexate,an analog offolic acid,blocks conversion ofdihydrofo-
late to tetrahydrofolic acid,which is a pre-cursor ofthymidylic acid and
purine.Thisresults in an interruption ofDNA,RNA,and protein synthesis.Once a
standard forhead and neck squamous cell carcinoma,methotrexate is now typically
only usedfor palliation.Its side effect profile andability to be administered
intramuscularlyon an outpatient basis make it a goodoption for this
purpose.Cisplatin and car-boplatin are alkylating agents that formcross-links in
DNA and arrest cell division.Cisplatin is more effective in squamouscell cancer but
is associated with morerenal and neurologic side effects than car-boplatin.Other
agents used less frequentlyin head and neck squamous cell cancer
640Part 5: Maxillofacial Pathologyinclude paclitaxel,which stabilizes micro-tubular
formation and arrests cells in G2,and bleomycin,which creates DNA breaks.Agents
under development includeflavopiridol,a cyclin-dependent kinaseinhibitor that has
been shown to induceapoptosis (programmed cell death) insquamous cell cancer lines
in vitro,and forwhich a phase 1 trial is underway.67,68Standard therapy for
resectable diseaseremains surgery followed by radiotherapy,ifindicated.To
date,induction chemother-apy followed by surgery has not shown asurvival benefit in
oral cavity cancer.Thequestion ofadding chemotherapy in thepostoperative setting
remains unanswered.Currently no study has shown definitiveimprovement.Cooper and
colleaguesreported on the results ofthe RTOG 95-01/Intergroup phase 3 trial that
evaluatedconcurrent chemoradiotherapy in postop-erative treatment ofhigh-risk
squamouscell carcinoma ofthe head and neck,defined as multiple lymph nodes
involved,extracapsular disease,and positive mar-gins.The locoregional control and
overall2-year survival were not improved signifi-cantly,and the small improvement
in disease-free survival was at the expense ofasignificant increase in
toxicity.69Addingchemotherapy following surgery and radi-ation has been shown to
decrease the inci-dence ofdistant metastases,but this hasnot been associated with
improved sur-vival.At this point chemotherapy in thepostoperative setting is not
indicatedexcept in cases ofknown metastatic dis-ease,and its use outside ofclinical
trialsshould probably be discouraged.70�72Currently the role for chemotherapyin
oral cavity cancer is limited to use inunresectable disease in which it is com-
bined with radiation treatment,metastaticdisease,or recurrence.Organ
preservation(not to be confused with organ function)through the use ofconcurrent
chemoradi-ation protocols has received much atten-tion.Meta-analyses by El-Sayed
and Nel-son,and Munro have demonstrated thatconcurrent treatment is better
thanneoadjuvant therapy.Locoregional controland survival were improved in
advancedhead and neck cancers.73,74In an attempt to avoid the systemiceffects
ofchemotherapy,investigators haveattempted to deliver agents topically,as wellas
intratumorally with both intra-arterialinjections and intratumoral depot formsvia
polymers and gels (see section in thischapter on recurrent tumors).A novel
formofconcurrent chemoradiation is the intra-arterial cisplatin and radiotherapy
(RAD-PLAT) protocol popularized by researchersat the University ofCalifornia,San
Diego,and University ofTennessee at Memphis,which has shown promise for
advancedcancers with bulky primary cancers andnodal disease.75Treatment involves
supra-dose cisplatin delivered directly into feedervessels ofthe tumor bed by
microarterialcatheters placed under angiography.Sodi-um thiosulfate,which is a
neutralizingagent for cisplatin,is administered systemi-cally,allowing doses five
times larger thanstandard protocols.Results ofpatients withT4 N2�3 disease treated
with the protocolrevealed 4-year local control of84%,disease-specific survival
of46%,and overallsurvival of29%.75Unfortunately,the proto-col is associated with
significant toxicity,including death.Use ofthe RADPLAT pro-tocol is currently
limited to centers thathave gained familiarity with the techniqueand management
ofthe toxicities associat-ed with it.Most ofthese concurrentchemoradiation
protocols involvedoropharyngeal and hypopharyngeal can-cers,and are plagued by
noncompliancebecause oftoxicity and side effects.Mucosi-tis is intense and
placement ofa PEG tubeis usually mandatory.75Other novel techniques for minimiz-ing
the systemic side effects ofchemother-apeutic regimens are under
development,including the PDT discussed above underthe management
ofleukoplakia.Trials ofchemotherapy limited to theoral cavity are few.At this time
the clearestindication for chemotherapy in oral can-cer is in metastatic and
recurrent disease.The most commonly used chemothera-peutic regimen for metastatic
or recurrentoral cavity squamous cell carcinomainvolves combinations ofcisplatin or
car-boplatin and 5-fluorouracil.Median sur-vival rates of5 to 7 months and 1-year
sur-vival of20% demonstrate the need forimproved regimens.Investigations contin-ue
to define a role for chemotherapy inadvanced squamous cell carcinomas oftheoral
cavity.Unfortunately early responsesto chemotherapy have not
demonstratedimprovement in overall survival and onlymodest gains in median survival
time.76Current research in chemotherapeuticagents focuses on agents that bind to
spe-cific receptors in an attempt to limit effectsto target cells.Similar to the
hormonaltherapy used in breast and prostate can-cers,investigators are
experimenting withagents such as epidermal growth factorinhibitors.77Gene therapy
that targetsknown alterations in head and neck squa-mous cell cancer lines,such as
TP53,is alsoan area ofgrowing research.78Restorationofthese altered genes,possibly
throughviral vectors,holds promise in certainpopulations.79A recent review by
Milasand colleagues at the MD Anderson Can-cer Center offers insight into the
currentstate ofchemotherapy in head and neckcancer,as well as newer
chemotherapeuticagents on the horizon.80ChemopreventionAn additional area
ofintensive research isdevelopment ofchemoprevention agents,which are defined as
agents that reverse orsuppress premalignant carcinogenic pro-gression to invasive
malignancy (see sec-tion �Management ofPremalignantLesions,�above).The role ofsuch
agentswould be twofold:(1) to treat premalig-nant lesions to prevent their
evolution toinvasive carcinoma,and (2) to preventdevelopment ofsecond primary squa-
mous cell cancers in patients who have
Oral Cancer Treatment641already undergone treatment ofcancer.Given its
accessibility to clinical observa-tion,leukoplakia has been used to
monitorresponsiveness to certain chemopreven-tion agents in clinical trials.Ofthe
agentsevaluated,including retinoids,betacarotene,and vitamin E
derivatives,retinoids have demonstrated the most effi-cacy in eliminating
leukoplakia.It isimportant to note,however,that reversalofthese lesions has not
been demonstrat-ed to reduce the risk ofdeveloping cancer,and the lesions soon
return after cessationoftreatment.13-Cis-retinoic acid,which ismore commonly used
to treat acne,hasbeen studied extensively in both the treat-ment ofpremalignant
lesions and in theprevention ofsecond primary cancers.Itmay act through the up-
regulation ofadistinct retinoic acid receptor,RAR-�,whose down-regulation is
associated withdevelopment ofhead and neck cancer.Results oftrials to date have
been mixed.Although effective in eliminating leuko-plakia,side effects limit its
use,and lesionsreturn after discontinuing the drug.Sec-ondary primary tumors occur
in 4 to 7%ofpatients treated for head and neck squa-mous cancer and are the major
concern-related cause ofdeath in early-stage can-cer.The prevention ofthese tumors
istherefore important.Studies of13-cis-retinoic acid have shown decreased inci-
dence ofsecond primary cancer but noeffect on primary disease
recurrence.Thissuggests that retinoids may prevent can-cerous development in
damaged cells butwill not treat fully transformed cancercells.Also,overall survival
was not affect-ed.Required doses ofretinoids have sideeffects,including
mucocutaneous toxicity(peeling and cheilitis) and elevation ofliver function
tests.Development ofsecond-generation retinoids may attenu-ate some ofthese side
effects.One studydemonstrated a worrisome increased inci-dence ofprimary lung
cancer in patientstreated with beta carotene.81,82In addition,Wang and colleagues
recently reported ona novel tretinoin biofilm that allows sus-tained topical
delivery to the oral cavity.83Investigators continue to search forchemotherapeutic
agents with moreacceptable side effect profiles.One ofthese agents is the Bowman-
Birkinhibitor,a protein derived from soybeansthat has shown clinical activity
againstleukoplakia without the attendant sideeffects ofretinoids.84Nonsteroidal
anti-inflammatory drugs have also being inves-tigated since chemoprevention
activitywas found in some cyclooygenase-2(COX-2) inhibitors.COX-2 influencesseveral
steps in the development ofmalig-nancies,such as
apoptosis,angiogenesis,invasiveness,and immune surveil-lance.85,86COX-2 expression
has beennoted in high-risk premalignant lesions.87In addition to their potential
role inchemoprevention,COX-2 inhibitors holdpromise in the treatment ofinvasive
squa-mous cell carcinomas.88Although chemo-prevention offers hope for patients at
highrisk for development ofsecond primarycancers and treatment ofpatients withhigh-
risk lesions (see discussion on pre-malignant lesions above),its use is cur-rently
restricted to clinical trials and off-label use.Further work is needed toestablish
a safe and effective chemopre-ventive regimen.Special Treatment Considerations by
Site The LipAlthough classified as an oral cancer,squa-mous cell carcinomas ofthe
lip typically fol-low a different clinical course than those oforal mucosal
cancers.The primary etiologicagent,sun exposure,is different from oralcancers,and
the location oflip cancers usu-ally leads to earlier discovery.The
behaviorofsquamous cell cancers ofthe vermilionborder is usually intermediate
betweensquamous cell carcinoma ofthe skin andthat ofthe mucosa.The vast majority
ariseon the lower lip where sun exposure isgreatest.Most lip cancers are treated by
sur-gical resection using 0.5 to 1.0 cm marginsand frozen-section control.Although
oftenreferred to as a �wedge�resection,the actualspecimen more closely resembles a
shieldwith parallel sides and a tapering base.�Wedge�excisions may be combined with
avermilionectomy or �lip shave�procedure,removing vermilion that has suffered
exten-sive actinic damage or contains carcinomain situ (Figure 33-5).CO2laser
ablation ofthe surface ofthe lip is also useful as analternative to vermilionectomy
for diffuseactinic changes.Squamous cell carcinomaofthe lip shares with squamous
cell carci-noma ofother cutaneous sites a potentialfor perineural invasion.A large
perineuraltumor deposition along the inferior alveolarnerve,several years after a
lip cancer,can bemistaken for primary intraosseous carcino-ma (Figure 33-6).Neck
dissection is usually not indicatedfor lip cancer unless there is clinical evi-
dence oflymph node involvement by exam-ination or imaging.Cancers ofthe upper
lipand commissure can metastasize to the peri-parotid lymph nodes,and
superficialparotidectomy may be required ifthere areclinically enlarged nodes.Some
largerlesions can be treated with radiation alone ifsurgical resection will result
in unacceptablecompromise in appearance and function.Five-year survival for lip
cancer isgood for early-stage disease (90% forstages I and II).89,90FIGURE33-
5Vermilionectomy combined withwedge resection oflip cancer associated with dif-fuse
actinic changes across the remainder ofthe lip.
642Part 5: Maxillofacial PathologyBuccal MucosaBuccal squamous cell carcinomas
repre-sent approximately 10% oforal cavity can-cers in the United States compared
to 41%in India.Squamous cell carcinomas ofthebuccal mucosa can be deceptive in
theirclinical course.Because ofthe intimacy tothe buccal space and deeper
structures,cancers that penetrate the buccinatormuscle can be difficult to
eradicate (Figure33-7).Patients may present with involve-ment ofthe pterygoid space
posteriorly orthe parotid gland laterally.Extensioneither superiorly or inferiorly
can lead toinvasion ofthe maxillary alveolus ormandibular alveolus
respectively.Thesecancers often arise in wide areas ofdam-aged mucosa,and adequate
excision ofthese lesions often results in complexdefects ofthe cheek that can be
difficult toreconstruct.Primary radiation may be anoption for smaller
lesions.Although up to50% ofpatients with buccal squamous cellcarcinoma can present
with neck metas-tases,the rate ofoccult disease in the neckis around 10%.91As with
other oral cancersites elective treatment ofthe neck withradiation or surgery is
indicated in T3 orT4 lesions.Consideration should also begiven to elective
treatment ofthe neck indeep T1 (> 4 mm) and larger T2 lesions.Vikram and Farr
concluded that com-bined therapy for large lesions withsurgery and radiation
offered the bestchance for cure.92Two-year overall survival rates forearly-stage
disease treated with a varietyoftreatment modalities range from 83 to100%.Stage III
survival rate is 41% andstage IV is 15%.Available survival statis-tics,however,are
often not accuratebecause ofthe inclusion ofverrucous car-cinoma in some ofthe
published reports.Diaz and colleagues at the MDAnderson Cancer Center reported on
119consecutive patients with buccal squa-mous cell carcinomas,the majority ofwhich
were treated with surgery followedby radiation ifindicated (positive mar-gins,nodal
involvement).93Five-year sur-vival rates for patients with stages I,II,III,and IV
disease were 78%,66%,62%,and 50% respectively.The significantimpact ofnodal
involvement was noted.Diaz and colleagues found 5-year survivalrates of69% with
nodal involvement,which decreased to 24% in cases withextracapsular
extension.93Retromolar TrigoneGiven their proximity to the pterygo-mandibular
space,tonsillar pillars,mandible,and tongue base,squamous cellcarcinomas ofthe
retromolar trigone(RMT) can behave in a more aggressivefashion,like an
oropharyngeal primarycancer (Figure 33-8).Smaller lesions areamenable to wide local
excision with orwithout a marginal mandibulectomydepending on the proximity to the
bone(see discussion below).Larger lesions mayinvade the pterygomandibular space
andextend cephalad towards the skull base.Such tumors require segmental
compositeresections with neck dissection.Signifi-cant trismus can be an indication
ofpterygoid involvement and may makeradiation treatment with or without con-
comitant chemotherapy a better optionthan surgery.Elective neck radiotherapyor
elective neck dissection with a selectiveneck dissection should be considered inT2
or greater lesions.As with other sites adepth ofinvasion greater than 4 mm in
T1lesions may be an indication for electivetreatment ofthe neck.Kowalski and
colleagues reported on114 RMT cases treated with surgery withor without radiation
and found 5-yearsurvivals of80% (T1),57.8% (T2),46.5%(T3),and 65.3% (T4).94Overall
5-yearsurvival was 55.3%.They recommendedadjunctive radiation in stages III and
IV.94In an excellent review ofthe managementofRMT cancers,Genden and colleaguesalso
suggested that the addition ofpreop-erative or postoperative radiation confersa
survival advantage.95FIGURE33-6Apparent intraosseous squamouscell carcinoma arising
from perineural spread ofa previous lip carcinoma.Review ofthe originallip
resection specimen demonstrated perineuralinvasion.FIGURE33-7Squamous cell
carcinoma ofthebuccal mucosa,deeply invading through the buc-cinator
muscle.FIGURE33-8Squamous cell carcinoma oftheretromolar trigone.
Oral Cancer Treatment643The TongueThe oral tongue,that portion anterior tothe
circumvallate papillae,is the mostcommon location for intraoral squamouscell
carcinomas.They typically present aspainless indurated ulcerations.Ifpain ispresent
it is usually due to secondaryinfection.The behavior and treatment oforal tongue
cancers is sufficiently differentthan that ofposterior tongue lesions(oropharyngeal
tongue or tongue base) toallow clinicians to determine the epicenterofthe tumor and
classify it correctly.Thismay be challenging in the case oflargercancers.The oral
tongue poses significantchallenges to clinicians.Seemingly smalllesions can
metastasize early and recurafter treatment.Control rates for smalllesions ofthe
tongue (60 to 80%) arepoorer than those ofsimilar size in otheroral cavity
subsites.There are minimalbarriers in the tongue to tumor invasion,and there is
frequent invasion into adja-cent or deeper structures at presentation.Although more
commonly associated withoropharyngeal primary cancers,referredotalgia is not
uncommon for cancers ofthe oral tongue,and limitation oftonguemobility with
resultant dysarthria is asso-ciated with invasion ofthe deeper muscu-
lature.Magnetic resonance imaging (MRI)can be useful in evaluating the depth
ofinvasion (Figure 33-9).Treatment oftongue lesions should be aggressive,andstrong
consideration for elective treatmentofthe neck should be given in all casesexcept
for the most superficial lesions (< 2 mm).Although Fakih and colleagueswere not
able to demonstrate a survivaladvantage in patients who underwent anelective neck
dissection versus a watch-and-wait policy,they did demonstrate thatdeeper lesions
were associated with a sig-nificant rate ofcervical metastases.96Up to10 to 12%
oftongue cancers with metas-tases to the neck can demonstrate �skip�metastases to
level IV.Considerationshould be given to extending the neck dis-section to include
level IV.97Postoperativeradiation should be considered in situa-tions where
multiple frozen-section speci-mens were sent before obtaining
clearmargins,perineural invasion,microvascu-lar or microlymphatic invasion,or
otherworrisome findings that are present.Smaller superficial tumors are amen-able
to wide local excision and reconstruc-tion via primary closure,split-thicknessskin
grafting,or healing by secondaryintention.Larger tumors are reconstructedwith
vascularized tissue transfer,andmandibulotomy may be needed for ade-quate access to
large or posterior lesions.Radial forearm or lateral arm microvascu-lar free flaps
allow excellent mobility andlittle bulk (Figure 33-10).Unilateral orbilateral
pedicled nasolabial flaps can occa-sionally be used for anterior
tonguelesions.Large oral tongue cancers thatcross the midline present the surgeon
witha difficult choice.Ifresection is chosen it isoften better to tailor the radial
forearm flapsmaller than the resected area to allow theremaining tongue musculature
less bulk tomove during excursions (Figure 33-11).Near total glossectomy (resection
oftheoral tongue with only tongue base remain-ing) almost always results in high
morbid-ity and is associated with a high incidenceofaspiration that may ultimately
requirelaryngectomy for aspiration control.Treat-ment with external beam radiation
alone isassociated with unacceptable failure rates.In this setting consideration
should begiven to organ-sparing protocols with con-comitant chemoradiation therapy
ifsurgery will be associated with unaccept-able morbidity.Brachytherapy
combinedwith external beam radiation is the treat-ment ofchoice at some
centers.Technicalexpertise is required,and most patientsrequire tracheotomy for
airway control.Tongue base tumors,although actuallyan oropharyngeal subsite and not
consid-ered an oral subsite,are discussed here forcompleteness.The tongue base
allowstumors to grow silently,and diagnosis at anearly stage is the exception
rather than therule.Most small (T1 and some T2) lesionsshould be treated with
combined therapy,typically surgery plus radiation treatment.Larger tumors are
typically treated with anorgan-sparing approach using chemoradia-tion therapy or
external beam therapy,sometimes combined with brachytherapy.Results with external
beam alone have beendisappointing.Reconstruction ofsmallerposterior tongue defects
is best accom-plished by radial forearm or lateral armflaps,ifprimary closure or
healing by sec-ondary intention is inappropriate.LargerFIGURE33-9Enhanced,T2-
weighted mag-netic resonance imaging ofa tongue showingright tongue tumor deeply
invading tonguemusculature.FIGURE33-10Radial forearm flap used toreconstruct large
tongue defect with nearly nor-mal speech and swallowing.
644Part 5: Maxillofacial Pathologyexcisions (75% to total) typically are recon-
structed with a free rectus flap.98Most treatment failures ofthe oraltongue involve
locoregional recurrence.Second primary cancer rates are high(30%) and this also
contributes to treat-ment failure and death.Three-year sur-vival for T1 and T2
lesions is 70 to 80%,but this decreases to 15 to 30% in patientswith lymph node
metastases.99,100Someclinicians have reported that tongue squa-mous cell carcinoma
arising in youngpatients may represent a more aggressivesubset and warrant more
aggressive thera-py.Overall survival for younger patients isactually similar to
those ofolder patientswith the same stage because oftheir lack ofintercurrent
illnesses.It was found,how-ever,that oral tongue cancers in youngerwomen did behave
more aggressively andwere associated with higher recurrencerates.This subset may
warrant moreaggressive initial therapy.101,102Floor ofMouth The floor ofmouth (FOM)
is the secondmost common location for oral cavitysquamous cell cancers (Figure 33-
12).FOM cancers can extend along the ventraltongue and cause fixation.In
additionFOM tumors can become fixed to themandible or extend into level I ofthe
neck.McGuirt and colleagues have demonstrat-ed improved outcome with elective
treat-ment ofthe neck,and elective treatment ofthe neck should be considered in all
butthe smallest thin lesions (< 3 mm).103Sagittal mandibulectomy may be consid-ered
in tumors that abut the mandiblewithout evidence ofinvasion (see discus-sion
below).Small primary cancers can beequally treated with surgery or
radiation,although surgery is the choice ofmostclinicians.Anterior lesions may
requiresialodochoplasty to reroute the sub-mandibular ducts ifthe
submandibulargland is not removed by ipsilateral neckdissection.Smaller FOM defects
can be closedprimarily or left to heal by secondaryintention.A partial closure
ofthe defectwill often suffice.Larger FOM defects,par-ticularly those that include
mylohyoidresection,benefit from a bulkier recon-struction,such as a vascularized
radialforearm flap or bilateral nasolabial flapsplaced in a one- or two-stage
operation.Local recurrence remains a problemwith FOM squamous cancers,and resultsin
high rates oflocoregional failure.Five-year survival rates are 64 to 80% (stage
I),61 to 84% (stage II),28 to 68% (stage III),and 6 to 36% (stage IV).104Alveolus
and GingivaGingival squamous cell cancers represent aunique subset in oral cavity
cancers thatarise on the attached gingiva and thatshould be differentiated from
those thatarise on the unattached mucosa ofthealveolus.Occult neck metastasis is
rare,and elective treatment ofthe neck is notnecessary in smaller lesions.Larger
lesionsmay require partial maxillectomy,or mar-ginal or segmental
mandibulectomy,ifbone invasion is suspected.Indicationsand variations on
mandibulectomy arediscussed below.In general control ratesare excellent for
gingival primary cancersiftreated with adequate margins.Alveolar cancer arises from
the unat-tached mucosa ofthe alveolar ridge andhas a different clinical behavior
than gin-gival carcinomas.It requires more aggres-sive therapy and more extensive
resectionofbone.Most anterior and some posteriormaxillectomies for alveolar and
gingivalsquamous cells can be accomplished via atransoral approach using techniques
oforthognathic surgery (Figure 33-13).105The pterygoid plates require removal
onlyifthere is evidence ofinvasion through theposterior maxilla.Posterior extension
mayindicate the need for a transfacial (Weber-Fergusson) approach for adequate
expo-sure.Reconstruction ofmaxillary defectscan be accomplished with local
flaps,suchas the temporoparietal fascial or tempo-ralis muscle flap,or free-flap
reconstruc-tion.The complex nature ofmaxillarydefects and the bulk ofsome ofthe
flaps,however,often leave a less-than-satisfactoryresult.Prosthetic obturation
ofthe defectFIGURE33-11A,Large deeply infiltrative squamous cell carcinoma ofthe
lateral tongue.B,Radialforearm flap tailored to the size ofthe resection,not the
apparent size ofthe defect.ABFIGURE33-12Advanced squamous cell carci-noma ofthe
anterior floor ofthe mouth.
Oral Cancer Treatment645offers several advantages,including a sim-pler
operation,easier early detection ofrecurrence,and replacement ofteeth.Most
maxillary alveolus and gingivalsquamous cells that invade the sinusinvolve the
infrastructure lying belowOhngren�s line,an artificial line that runsfrom the
medial canthus to the angle ofthe mandible and separates the maxillarysinus into an
infra- and supra-structure.Defects arising from cancers resectedbelow this line are
easily reconstructedwith obturators.Cancers that require truetotal maxillectomy
(resection ofone ofthepaired maxillas,including the orbitalfloor) tend to require
flap reconstruction.Ifdura mater is exposed as part ofa skullbase resection,flap
coverage is advisable.Overall 5-year survival for alveolarridge carcinoma is 50 to
65% for both theupper and lower alveolar ridge.Poor out-come is associated with
advanced stage,perineural spread,and positive margins.Adjunctive radiation is
recommended ifnodal metastases,perineural spread,orpositive margins are
present.106The Palate Squamous cell cancers ofthe palate,hardand soft,are rare.The
soft palate is consid-ered an oropharyngeal subsite (Figure 33-14).Cancers arising
from the hardpalate may extend onto the soft palate andvice versa.The periosteum
ofthe palateacts as a significant barrier,and smallerlesions can be treated with
wide local exci-sion.Healing by secondary intentionunder a protective stent secured
to thepalate is a viable reconstructive option ifthe palatal bony structure is not
removed.Oral-nasal communications in the hardpalate can be treated with an
obturator ora local flap,such as an anteriorly basedmidline tongue flap.Oral-nasal
fistulas inthe soft palate are best treated with tempo-rary obturation,as the
majority will closespontaneously.Occult cervical metastasesare rare among hard
palate cancers (10 to25%),and elective treatment ofthe neck isgenerally not
indicated except in T3 or T4lesions.107,108Also,metastases may occur tothe
retropharyngeal nodes,and considera-tion should be given to irradiation oftheneck
to include this area ifsuspected.Management ofthe Mandible in Oral Cavity
CancerManagement ofthe mandible in oral cavitycancer has been the subject ofmuch
con-troversy.In the past the mandible was rou-tinely sacrificed in the treatment
ofFOMand tongue cancers,as it was felt that theregional lymphatics coursed through
themandibular periosteum,necessitating anin-continuity resection ofthe
tongue,FOM,mandible,and neck dissection(Commando�s operation).The morbidityofthis
approach was felt necessary to erad-icate in-transit metastases,a beliefthat
waslikely based on mistranslation by McGregorofan article published by Polya and
vonNavratil in 1902,in which they actually rec-ommended removal ofthe periosteum
orrim ofmandible and not a segment.109Marchetta and colleagues subsequent-ly
demonstrated that lymphatics did notflow through the mandible,and that
theperiosteum ofthe mandible actuallyserved as a barrier to invasion.110It wasfound
that squamous cell carcinoma inva-sion occurs most commonly through theperiodontal
ligament in the dentatemandible and through the porous occlusalsurface ofthe
edentulous mandible.110O�Brien and colleagues also demonstratedthat an inflammatory
front preceded can-cer that stimulated subperiosteal resorp-tion and the creation
ofbony clefts thatallowed cancer to invade the cortex.111Once the cortex was
invaded,the inferioralveolar canal was usually involved,espe-cially in edentulous
mandibles.111,112Thisfinding has led to surgeons advocatingpreservation
ofmandibular continuitythrough the use ofa marginal mandibul-ectomy,in cases
without obvious bonyinvolvement.These principles apply onlyto the nonirradiated
mandible.Cancerinvasion ofa previously irradiatedmandible occurs through multiple
sites.The clinical and radiographic evaluationsofmandibular
involvement,however,arefrequently inaccurate.Clinical findingssuch as impairment
ofinferior alveolarnerve function or fixation ofthe tumor tothe mandible raise the
index ofsuspicion.The history ofan extraction ofa tooth inan area ofa cancer may
suggest localmandibular invasion.Although used bysome,bone scans are cumbersome
toobtain and interpret accurately.A high-quality panoramic radiograph is
probablythe most commonly used tool to decide onmandibular resection versus
segmentalresection.CT scanning using DentaScanFIGURE33-13Le Fort I island approach
to aposterior maxillary tumor,without Weber-Fergusson incision.FIGURE33-14Squamous
cell carcinoma oftheright soft palate invading posteriorly to involvethe anterior
pole ofthe tonsil.
646Part 5: Maxillofacial Pathologysoftware has also been used,althoughrecent
studies have shown that an MRIdemonstrating enhancement ofthe mar-row signal was a
better predictor ofmandibular involvement.Also,newertechniques that modulate the
magneticfield in an attempt to examine changes inthe bone marrow hold promise for
evalu-ating mandibular involvement.Tumorinvasion into the marrow space is accom-
panied by a lower intermediate signal.Astrong bright marrow signal associatedwith
normal marrow fat underlying thedark cortex typically excludes
mandibularinvolvement.38At this time the most accurate assess-ment ofmandibular
involvement occurs atthe time ofsurgery when the surgeon caninspect the bone.In
addition,some sur-geons send periosteum for frozen-sectionanalysis,whereas others
submit cancellousscrapings for frozen analysis.113Once adecision has been made to
perform a mar-ginal mandibulectomy,the surgeon hasseveral choices for osteotomy
design.Some surgeons advocate rim mandibulec-tomy,preserving at least a 1 cm
inferiorborder,whereas others advocate a sagittalmarginal mandibulectomy or a
variationthereof.114An important point is theavoidance ofright angles in the
osteotomydesign that serve as stress risers and maylead to fracture.We prefer an
osteotomythat begins in the sigmoid notch andsweeps inferiorly and anteriorly for
lesionslocated in the posterior mandible (Figure33-15).It is important to note that
thethick cortical bone along the posteriorramus is rarely involved,even when
themandible is invaded,and it can usually bepreserved and serves as an area for
plating.Edentulous mandibles are generally notcandidates for marginal
resectionalthough this is not an absolute rule.Waxand colleagues,and Shah have
publishedexcellent reviews ofthe topic ofsegmentaland marginal resection,and the
reader isdirected to their reviews for a more in-depth discussion.115,116Ifthe
surgeon isanticipating a marginal resection,and asegmental resection becomes
indicatedbased on operative findings,he or she isfaced with a surgery for which
both sur-geon and patient might not be prepared.Frank discussions before surgery
help pre-pare the patient and their family for thiseventuality.Mention should be
made ofthe possible return to the operating roomiffinal pathologic analysis reveals
an unex-pected amount ofbone involvementnecessitating a segmental resection andmore
elaborate reconstruction.Splitting the mandible,or mandibulo-tomy,is often
necessary for access to largecancers,especially ofthe posterior tongue(Figure 33-
16).Technical refinement ofmandibulotomy helps avoid complica-tions.Mucosal
incisions should not beplaced directly overlying the proposedosteotomy
site.Division ofthe mandibleat the parasymphysis or symphysis is pre-ferred over an
osteotomy in the bodyregion.Ifthe mandibular osteotomy isbeing performed for access
to the tongue,the cut should be made anterior to themental nerve to preserve
it.Preadaptationofplates will allow reestablishment ofthepreoperative occlusion and
contour.Management ofthe CervicalLymph Nodes in Oral CavitySquamous
CancerManagement ofthe regional lymphatics isa consideration in any cancer.The
abilityofa cancer to metastasize most commonlymanifests itselfby growth ofcancer
inlymph nodes.Surgical treatment oftheneck is justified for two reasons:theremoval
ofgross disease in patients withFIGURE33-15Outline ofmarginal mandibulec-tomy
suitable for resection oftumors ofthe retro-molar trigone and posterior maxillary
alveolus.FIGURE33-16A,Outline ofincision for lip-splitting approach to the
posterior oral cavity andoropharynx.B,Midline division ofthe tongue following
midline mandibulotomy.AB
Oral Cancer Treatment647clinical evidence ofnodal involvement(therapeutic neck
dissection) or a highenough index ofsuspicion ofoccult cervi-cal metastases to
justify an elective neckdissection (END).Some surgeons wouldalso suggest that
unreliable patients shouldundergo END as follow-up may be irregu-lar.Excluding the
hard palate and lip,approximately 30% ofpatients with oralcavity cancer will
present with cervicalmetastases.117The decision to treat the N0neck is based on the
probability ofnodalinvolvement.Evaluation ofthe neck forcervical metastases remains
a critical com-ponent ofthe evaluation ofthe patientwith oral cavity cancer.Manual
palpationis regarded as the first step in this processand is usually accomplished
before biopsyto avoid postbiopsy inflammatory nodalenlargement.In most necks a
lymph nodemust be at least 1 cm in diameter to be pal-pable.The accuracy and
reliability ofpal-pation is low,with an overall error ofapproximately 30% in
several studies.118Imaging modalities including CT,MRI,ultrasonography,and positron
emissiontomography (PET) have become increas-ingly important in the evaluation for
cer-vical metastases and in guiding therapy.A CT scan with contrast from the
skullbase to clavicles has become the most com-mon imaging modality used for
detectionofcervical metastases (Figure 33-17).Spe-cific criteria for nodal
metastases,includ-ing node size greater than 1 cm (except thejugulodigastric
node,which must begreater than 1.5 cm),central necrosis,andmorphology (round
instead ofoval) haveincreased sensitivity to over 90%.119MRIneck evaluation has
gained popularity inrecent years,and is typically used ifthe pri-mary site is being
imaged with MRI,suchas for a tongue cancer.CT and MRI,in thatorder,are the most
widely used imagingmodalities for detection ofoccult metas-tases in the United
States.The characteristics ofthe primarytumor may also predict metastases.Spiroand
colleagues demonstrated that depth ofinvasion in tongue cancer was a
reliablepredictor oflymph node metastases incancer ofthe oral tongue.120They
foundthat cancers with 2 to 8 mm depth ofinva-sion had a significantly higher rate
oflymph node metastases than those withinvasion ofless than 2 mm (25.7%
vs7.5%).Depth ofinvasion greater than 8 mm was associated with a 41% rate ofoccult
metastasis.Tumor thickness lessthan 2 mm has been associated with a 13%incidence
oflymph node metastases and3% would ultimately succumb to their dis-ease,whereas
greater than 9 mm ofinva-sion was associated with a 65% incidenceoflymph node
metastases and 35% woulddie oftheir disease.120,121O-charoenrat andcolleagues also
demonstrated an increasedrisk ofcervical metastasis in tongue can-cers with a depth
ofinvasion greater than 5 mm,and correlated this with poor out-come even in early
stage (I and II) tonguecancers.122Similar results were reported byKurokawa and
colleagues,who found thatdepth greater than 4 mm was associatedwith an increased
risk for development oflate cervical metastases in patients withmoderately
differentiated squamous cellcancers ofthe tongue,and diminishedoverall
survival.123This has led to recom-mendations that even in the absence ofevi-dence
oflymph node metastases,the neckshould receive elective treatment (eitherelective
neck dissection or irradiation) forthicker primary tumors.Other investiga-tors have
suggested that depth ofinvasionbe added to the staging oforal squamouscell
carcinomas.Aside from depth,clini-cians have looked at other characteristicssuch as
DNA aneuploidy and histologicgrade.At this time applications ofthistechnology have
not been adopted in theroutine clinical setting.Two additional imaging
modalitiesused for evaluating nodal metastasesdeserve mention.Ultrasonography
andPET with fluorodeoxyglucose are gaining inpopularity for initial staging and
follow-upstaging ofpatients with head and neck can-cer.Although not commonly used
in theUnited States,ultrasonography has beenused in outpatient clinics for
evaluation oforal cancer patients in Europe for sometime.Ultrasonography criteria
for malig-nant changes include nodal size andchanges in echogenicity,central
necrosisthat will lead to an echogenic hilum,and ahypoechogenic periphery.Its
ability toimprove on manual palpation ofcervicallymphadenopathy has led to its
increaseduse in the United States.It can also help toevaluate carotid or jugular
invasion.Whenperformed by an experienced clinician andcombined with aspiration
cytology,ultra-sonography is very accurate.124Knappe andcolleagues reported a
sensitivity of89.2%and a specificity of98.1% in 56 patientswho underwent
preoperative ultrasound-guided fine-needle aspiration followed byelective or
therapeutic neck dissections.125Recently PET has become increasinglypopular in the
staging and follow-up ofpatients with head and neck squamous cellcarcinoma.By
identifying areas ofhigh glu-cose uptake,PET scans allow clinicians toidentify
potential metastases in the preoper-ative work-up (Figure 33-18).Presence ofdistant
metastases may influence the choiceofinitial treatment.The role ofPET scans inthe
evaluation ofoccult cervical metastasesFIGURE33-17Computed tomography scanwith
contrast showing peripheral rim enhance-ment and central lucency oflymph node
harbor-ing metastatic squamous cell carcinoma.
648Part 5: Maxillofacial Pathologyis limited by the need for at least 5 to 10
mm3oftumor for detection.Their role in thework-up ofpatients with cervical
metastasesand unknown primaries continues to beexplored.126PET is also used to
examinepatients who have undergone chemoradio-therapy for recurrent
disease.127Thesepatients are notorious for their difficulty inexamination secondary
to extensive changesin the soft tissue.It is recommended that atleast 3 months pass
prior to obtaining a PETscan because ofthe persistent inflammationassociated with
radiation and the tumorici-dal effects that persist after radiation is com-
pleted.It should also be remembered thatcurrent technology requires that a focus
ofsquamous cell carcinoma be several mil-limeters to be detected.128In the past it
wasstated that distant metastases were a latefinding in head and neck cancer
patientsand most patients succumbed to locore-gional disease.It was felt that less
than 1% ofhead and neck cancer patients had distantdisease at presentation.As the
use ofPETscanning in the initial evaluation ofpatientswith oral cavity cancers
becomes morewidespread,detection ofdistant metastasesat the initial evaluation may
become morecommon.One result ofthese improve-ments in detection ofdistant disease
is stagemigration.In other words,as our ability todetect distant disease
improves,morepatients are staged higher.This does notmean that patients are being
diagnosedlater in the course oftheir disease than inthe past but simply that our
diagnostic abil-ities have improved.Neck Dissection in Oral Cavity Squamous Cell
CancerThe goals ofneck dissection are to removegross disease in patients with
clinical evi-dence ofnodal involvement (therapeuticneck dissection) or to remove
occultmetastases in patients whose tumor char-acteristics make one suspicious
ofoccultcervical metastases (elective neck dissec-tion or END).The importance
oftreatingthe cervical lymph nodes was stressed byCrile in his landmark 1906
paper,and waslater popularized by Martin and col-leagues.129,130Generations
ofsurgeonswere trained in the classic radical neck dis-section (Figure 33-
19).Improved under-standing ofthe regional lymphatic flowand nodal basins at risk
for metastasesfrom different primary locations has led toan increasing number
ofmodifications ofthe standard radical neck dissection.Theresultant,often
misused,terminology ofneck dissection was standardized by theAmerican Academy
ofOtolaryngology�sCommittee for Head and Neck Surgeryand Oncology in
1991.131Revisions wereproposed in 2002 to improve communica-tion among
clinicians.132These proposedchanges were primarily in regard to theselective neck
dissections,and specificnames such as supraomohyoid neck dis-section were
eliminated in favor ofthephrase �selective neck dissection�followedin parentheses
by the levels removed.Thedefinitions pertinent to oral cavity cancerare listed
below:�Radical neck dissection:Refers to theremoval ofall ipsilateral cervicallymph
node groups extending fromthe inferior border ofthe mandible tothe clavicle,from
the lateral border ofthe sternohyoid muscle,hyoid bone,and contralateral anterior
belly ofthedigastric muscle medially,to the ante-rior border ofthe
trapezius.Includedare levels I through V.This entails theremoval ofthree important
nonlym-phatic structures�the internal jugu-lar vein,the sternocleidomastoid mus-
cle,and the spinal accessory nerve.�Modified radical neck dissection:Refers to
removal ofthe same lymphnode levels (I through V) as the radi-cal neck
dissection,but with preserva-tion ofthe spinal accessory nerve,theinternal jugular
vein,or the sternoclei-domastoid muscle.The structures pre-served should be
named.Someauthors propose subdividing the mod-ified neck dissection into 3
types:Type I preserves the spinal accesso-ry nerve.Type II preserves the spinal
accesso-ry nerve and the sternocleidomas-toid muscle.FIGURE33-18Positron emission
tomographyscan showing recurrent cancer in the left neckwith three mediastinal
metastases.Note theheavy physiologic uptake in the brain,heart,kid-neys,and
bladder.FIGURE33-19Standard radical neck dissectionofthe right neck.Note the
communication withthe oral cavity where an oral cancer has also beenresected.
Oral Cancer Treatment649Type III preserves the spinal acces-sory nerve,the
sternocleidomas-toid muscle,and the internal jugu-lar vein.�Selective neck
dissection:Refers to thepreservation ofone or more lymphnode groups normally
removed in aradical neck dissection.In the 1991classification scheme there were
sever-al �named�selective neck dissections.For example,the supraomohyoid
neckdissection removed the lymph nodesfrom levels I to III (Figure 33-
20).Thesubsequent proposed modification in2001 sought to eliminate
these�named�dissections.The committeeproposed that selective neck dissec-tions be
named for the cancer that thesurgeon was treating and to name thenode groups
removed.For example,aselective neck dissection for oral cavi-ty cancer would
encompass thosenode groups most at risk (levels I toIII) and be referred to as a
selectiveneck dissection (levels I to III).�Extended neck dissection:Refers to
theremoval ofone or more additionallymph node groups,nonlymphaticstructures,or
both,not encompassedby a radical neck dissection.For exam-ple,mediastinal nodes or
nonlymphat-ic structures such as the carotid arteryor hypoglossal nerve.It is
important to remember that clas-sification schemes are continually chang-ing,and as
science evolves the indicationsfor different dissections will certainlychange.For
an oral cavity primary withoutevidence oflymph node metastases,aselective neck
dissection removing lymphnodes from levels I to III is the generallyaccepted
procedure.Shah and colleaguesdemonstrated supraomohyoid neck dis-section to
eradicate occult metastatic dis-ease in 95% ofpatients.133Some
surgeons,however,advocate including level IV(extended supraomohyoid neck dissec-
tion) to decrease the risk,however small,ofmissed occult metastases.Extension onthe
left side does entail an increased risk tothe thoracic duct and attendant
chyleleak.98Modifications ofneck dissectionshave been made in an attempt to
preventthe morbidity ofradical neck dissection(Figure 33-21).Preservation ofthe
spinalaccessory nerve decreases the incidence ofpainful shoulder
syndrome.Extensiveskeletonization ofthe nerve,however,canresult in significant
dysfunction even ifthenerve is preserved (Figure 33-22).Severalstudies have
suggested that dissection oflevel IIb (above the nerve) is unnecessaryin the
clinically negative neck because ofthe low incidence ofmetastases in this
area(1.6%),and is recommended only ifbulkydisease is present in level
IIa.134Ifthere is clinical evidence oflymphnode metastases,controversy exists
overthe proper type ofneck dissection (see sec-tion �Therapeutic Neck
Dissection,�below).The application ofsupraomohy-oid neck dissection to the N
positive neck(therapeutic neck dissection) has yieldedmixed results.135Previous
studies havedemonstrated that patients undergoingselective neck dissections for N0
neckshave a higher rate ofrecurrence in theneck ifpositive nodes are ultimately
foundin the pathologic specimen.This can beimproved by the addition
ofpostoperativeradiation treatment.136The questionremains as to whether this is due
to thetype ofneck dissection or simply the biol-ogy ofthe tumor.137,138Most
surgeonsadvocate some form ofneck dissection ifthere is demonstrable evidence
ofmetasta-tic disease in the neck,and a diminishingnumber ofsurgeons maintain that
the evi-dence oflymph node metastases is justifi-cation for nothing less than a
standardradical neck dissection.FIGURE33-20Supraomohyoid neck
dissection,orselective neck dissection,levels I to III.The stern-ocleidomastoid
muscle,nerve XI,and internaljugular vein are preserved.FIGURE33-21Denervation ofa
patient�s lefttrapezius following sacrifice ofspinal accessorynerve during radical
neck dissection.FIGURE33-22Dissection and skeletonization ofspinal accessory nerve
can produce shoulder dys-function even ifnerve is preserved.
650Part 5: Maxillofacial PathologyAnother controversy regarding theevolution ofneck
dissection concerns theconcept ofin-continuity versus discontin-uous neck
dissections.In the past it wasconsidered mandatory to remove the pri-mary tumor in
direct continuity with theneck dissection,in one specimen.Work bySpiro and Strong
found no adverse impacton survival when neck dissection was per-formed in a
discontinuous manner.Biasmight have occurred,however,as smallerlesions were in the
discontinuity group.139A study by Leemans and colleagues foundworse outcomes in
stage II cancer ofthetongue with discontinuous neck dissec-tion,with local
recurrence rates of19.1%versus 5.3% and a 5-year survival of63%versus 80%.140Most
surgeons prefer an in-continuity approach iftechnically feasible,without the
resection ofobviously unin-volved structures such as the mandible.The controversy
surrounding electiveneck dissection versus elective neck irradi-ation (without neck
dissection) continues.Advantages ofsurgery include the produc-tion ofa surgical
specimen that guides theneed for further treatment.Ifno lymphnodes are
identified,radiation can be held.The possibility offuture second,third,oreven
fourth primary cancer arising in thisat-risk population makes reserving radia-tion
attractive.A comprehensive discus-sion ofthe management ofcervical lymphnodes in
head and neck cancer is beyondthe scope ofthis chapter.Three excellentreviews are
available and recommend-ed.117,141,142Although several studies havefailed to
demonstrate a survival advantagein patients who undergo elective neck dis-section
versus careful follow-up and ther-apeutic neck dissection ifa
metastasisdevelops,most surgeons would agree thatthe morbidity associated with a
selectiveneck dissection is minimal and would havea low threshold for performing
it.Sentinel Node BiopsyAs the evolution toward less invasive surgi-cal modalities
proceeds,dissection oftheN0 neck (staging neck dissection or elec-tive neck
dissection) is becoming increas-ingly limited.The sentinel node technique,first
popularized for melanoma,has beeninvestigated for use in head and neck can-
cer.143,144Theoretically it allows the identi-fication and removal ofthe first-
echelonlymph node (�sentinel node�) that wouldfirst receive metastases from a given
site.The technique involves injecting the areasurrounding the primary site with
aradioactive-labeled material,99mTc-sulfurcolloid.Various molecular weights can
bechosen depending on the transit timedesired.A radiograph is then taken to iden-
tify and locate the sentinel node.Thepatient is then taken to the operating
roomwhere the surgeon may inject isosulfanblue dye around the primary tumor
site.The dye will also drain to the sentinel nodeand stain it blue,assisting the
surgeon inidentification during surgery (Figure 33-23).The surgeon will also use a
gammadetection probe counterprobe to identifythe node with the highest
concentration ofradioactive colloid.The node is thenremoved,and ifit is
histologically positive,further treatment such as radiation may beindicated.In
melanoma,sentinel nodebiopsy has a reported sensitivity of82 to100%,and very few
false-negatives.145,146The technique has been investigated inthe head and neck with
varying results.Problems with the application ofthe sen-tinel node technique to
squamous cell can-cer ofthe oral cavity relate to the rich lym-phatic drainage with
possible bilateraldrainage as well as the complex anatomy inthe neck,leading to
difficulty in dissectingout a single node.In addition close prox-imity ofthe
sentinel node to the primarycancer,for example,an FOM primary can-cer and submental
node,can lead to theaccumulation ofcolloid around the prima-ry cancer,which
obscures the sentinelnode.The rich lymphovascular networkcan also lead to drainage
to several nodes.Cevantos and colleagues used the sentinelnode technique in 18 oral
cavity cancerswith N0 necks.147They compared sentinelnode biopsy to CT images and
PET imagesby obtaining a CT and PET followed bysentinel node biopsy and neck
dissection.They found 10 true-positives,6 positivenodes identified on frozen
section,2 pos-tive notes on evaluation ofpermanentpathologic specimens,and 2 on
immuno-peroxidase staining for cytokeratin.In 6 specimens,the sentinel node was the
onlypositive node.They also found 7 true-negatives and 1 false-negative.In 1 case
thesentinel node identified by the radioactivecolloid did not contain cancer,but
anothercervical node did.They also found thattumor in the node can lead to
obstructionand redirection oflymphatic flow.147Pit-man and colleagues further
demonstratedthe use ofthe sentinel node biopsy tech-nique for the N0 neck.148Hyde
and col-leagues reported on 19 patients whoseradiographic and clinical test results
ontheir necks were negative and who under-went sentinel lymph node biopsy and
PETscanning followed by conventional neckdissection.149In 15 ofthe 19 patients
thesentinel node as well as the remainingnodes were negative.In 3 ofthe 19
patientsthe sentinel node was positive along withother nodes.In 1 patient the
sentinel nodewas negative,but another node removed inthe neck dissection was
positive.The nodewas located close to the primary cancer,which often leads to
difficulty discriminat-ing activity due to the tumor and that ofadjacent
nodes.Interestingly PET failed toFIGURE33-23Sentinel node biopsy.Note thedark
staining ofthe sentinel node.
Oral Cancer Treatment651reveal cancer in the 4 patients with subse-quently
identified cervical metastasis (seediscussion on PET scanning,above).149Inthe
future the sentinel node biopsy maybecome the operative procedure ofchoicefor
dealing with the N0 neck.In an excel-lent review Pitman and colleagues con-cluded
that sentinel lymph node biopsyremains an experimental technique in headand neck
cancers and has not become astandard ofcare.150Therapeutic Neck DissectionPatients
presenting with nodal disease willusually undergo some type oftherapeuticneck
dissection,the nature ofwhich varieswith surgeon�s preference.Some surgeonswill
treat all patients with suspected cervi-cal metastases with a radical neck dissec-
tion.Most consider a modified radicalneck dissection adequate,removing theinternal
jugular vein or sternocleidomas-toid muscle ifindicated.There is some evi-dence
that selective neck dissection may beadequate for the N positive neck in
certaincarefully selected patient populations (seediscussion ofselective neck
dissections,above).Anderson and colleagues reportedthe results ofthree academic
centers inwhich patients with previously untreatedclinically and pathologically N
positivenecks underwent neck dissection.151Theyreported a regional control rate
of94.3%.Their results were comparable to patientsundergoing more extensive neck
dissec-tions.151Patients presenting with massivenodal disease who are going to be
treatedwith chemoradiation therapy or combina-tion ofbrachytherapy and external
beamtherapy can present a challenge to sur-geons who are faced with the option
ofsurgery before or following radiation.Notinfrequently surgeons are faced with
com-plete clinical resolution ofdisease and theprospects ofa neck dissection in a
heavilyirradiated field.There is some variation inapproaches to this dilemma.Some
sur-geons recommend pretreatment neck dis-section to remove bulky
disease,whereasothers plan a neck dissection 4 to 6 weeksafter treatment regardless
ofresponse.Stillothers recommend a CT scan at 4 weeksand CT-guided biopsy ofany
suspiciousnodes.This is followed by neck dissectionifthe node biopsy is positive
for cancer.McHam and colleagues found that clinicalfactors did not predict patients
with resid-ual disease following chemoradiationtherapy and recommended neck dissec-
tion in all patients initially seen with N2 toN3 disease.152This recommendation
wasmade in light ofa 26 to 35% complicationrate in patients undergoing neck dissec-
tions following chemoradiation therapy.152The role ofPET scanning in this
situationis unclear,but patients with recurrent can-cer following multimodality
therapy typi-cally have a poor outcome,making salvagesurgery an unattractive
alternative.Surgical management ofcervicallymph node metastasis,both occult
andevident,continues to evolve.It is clear thatmetastases are an indication
ofaggressive-ness and portend a poorer prognosis.Once the cancer has developed the
neces-sary genetic mutations to break free andcolonize independent ofthe
primarytumor,the chance ofcure with singlemodality therapy diminishes.In his presi-
dential address to the New England Surgi-cal Society,Blake Cady referred to ��lymph
node metastases asthe speedome-ters ofthe oncologic vehicle,not
theengine.Indicators,not governors ofsur-vival.�153Clearly the role for the
radicalneck dissection has diminished greatlyover the past few decades,as less
invasivesurgical techniques for dealing with thecervical lymphatics have gained
populari-ty.This trend will likely continue,as therole ofsurgery in the control
ofmetastaticdisease is better defined.154�156Recurrence and Follow-Up
SurveillanceIn 1984 Vikram and colleagues published aseries ofreports that
discussed patterns offailure in patients treated with multi-modality therapy for
head and neck can-cer.157�159This classic series ofarticles out-lined failure
characteristics at the local site,neck,distant sites,as well as developmentofsecond
malignant neoplasms in patientstreated at Memorial Sloan-Kettering Can-cer
Center,NY,USA.136,157�159Ninety per-cent ofpatients who will suffer a recur-rence
oforal cavity cancer will do so in thefirst 2 years.For this reason patients
areplaced in a structured follow-up.Stage atrecurrence is the most important
predic-tor ofsurvival,with stage I at recurrenceassociated with a median survival
of24.3 months and a disease-free survival at2 years of73%,whereas stage IV recur-
rence was associated with a median sur-vival of9.3 months and a 2-year disease-free
survival of22%.160Follow-upprotocols vary widely and are intended todetect
recurrences early.De Visscher andManni suggested the following 161:1.Every 2 months
for 1 year2.Every 3 months for year 23.Every 4 months for year 34.Every 6 months
for years 4 and 55.Then yearlyDespite this and other suggested fol-low-up
protocols,the follow-up schedulemust be tailored to the individual patientand must
take into account the patient�slikelihood ofhaving a
recurrence,possiblecontinuation ofsmoking or other habits,ability to travel and
keep appointments,and the potential availability oflocal med-ical or dental care
that might assist in follow-up surveillance.Follow-up appoint-ments include an
update ofpatient historyand review ofsystems as well as clinicalexamination for
recurrence or detection ofnew primaries.Questions raised by physicalexamination
should prompt an appropriateimaging study,rebiopsy,or examinationunder
anesthesia.Caution should be used,however,in performing biopsies in patientswho
have received intensive multimodalitytherapy,such as RADPLAT,brachytherapy,or
hyperfractionated radiationschedules
652Part 5: Maxillofacial Pathologycombined with chemotherapy.Extensivebiopsy wounds
are notorious for slow heal-ing and can lead to chronic wounds.Appropriate
imaging,including abaseline CT or MRI at the completion ofmultimodality therapy,is
invaluable.Therole ofPET scanning in follow-up contin-ues to evolve.Failure at the
primary cancer site willultimately occur in approximately 20% ofpatients,and
regional recurrence in theneck will occur in 10%.Death from dis-tant metastases is
rare,occurring in onlyabout 1 to 4% ofcases in which locore-gional control is
maintained.An unfortu-nate consequence ofimproved control atthe primary cancer site
with multimodali-ty therapy is an increasing incidence ofdistant metastases.In
addition to recur-rences,prospective studies have demon-strated that second primary
cancers devel-op at a rate of4 to 7% annually in patientswho have had a head and
neck squamouscancer.Second primary cancers are theleading cause ofdeath among
patientswho have undergone treatment for early-stage oral cancers.136,157�159The
ability ofa cancer to metastasizedepends on the development ofa series ofgenetic
mutations,allowing for cells todisseminate from the primary tumor,arrest in the
microcirculation,extravagate,infiltrate into stroma,and survive andproliferate as a
new colony.Surveillancefor distant metastases therefore becomesan important
component ofthe follow-upevaluation.The lungs are the most com-mon site for distant
metastases,followedby the liver and bone.Yearly or biannualchest radiographs allow
for detection oflung metastases,the most common distantsite metastasized for oral
cavity cancer,and primary lung cancers,which are notuncommon in the population at
risk fororal cancer.162Given the current unavail-ability ofan effective treatment
regimen,however,some authors have questionedthe use ofannual or semiannual
chestradiographs.163PET scanning may proveto be a more valuable alternative for
detec-tion ofdistant disease.Yearly lab work toinclude liver function studies is
also rec-ommended.In patients who have receivedradiation as part oftheir
treatment,peri-odic thyroid function tests are helpful,asmany will ultimately
become hypothyroidwith attendant fatigue and decreasedwound healing ability.Collins
stated that patients with headand neck cancer are probably never cured,and that it
is better to consider that thehost-tumor relationship has been durablyaltered in
favor ofthe host.164It is impor-tant to realize that approximately one-third
ofpatients with presumed localizeddisease will relapse and die ofcancer.Inadvanced
head and neck squamous cellcarcinoma 20 to 30% will survive,40 to60% ofpatients
will suffer locoregionalrecurrence,and 20 to 30% will succumb todistant
metastases.Hence the majority oftreatment failures remain recurrence oflocoregional
disease.164Patients withrecurrent disease are restaged,whichrequires a similar
evaluation as the origi-nal.Panendoscopy and examination underanesthesia take on
greater importancewhen a clinician is faced with examinationoftissue scarred and
distorted by previoussurgery and radiation.Distant metastasesshould be ruled out to
the extent possibleprior to deciding on aggressive re-treatment.It the patient does
have recur-rence that is confined to the locoregionalarea,treatment decisions are
limited byprevious therapy.Reirradiation protocolsexist but are accompanied by
significantmorbidity.165Intensive reirradiation andchemotherapy protocols are being
investi-gated and show some promise.166Themorbidity ofsuch treatments is signifi-
cant,and their use should be restricted toclinical trials at this time.Surgical
salvageremains the primary option,but the extentofsalvage surgery must be
considerablybroader than might initially be considered.Goodwin reported on the
outcome ofsal-vage surgery for recurrent head and neckcancers,and found benefit in
stages I andII.160Success was limited in moreadvanced disease.160Clearly defined
goalsshould be established between surgeonand patient for salvage surgery.Is
theoperation for cure or palliation? Palliativesurgery should be undertaken very
cau-tiously as surgical complications maygreatly overshadow the palliative
goals.Patients and their families must have real-istic expectations as well as
understandthat there is no benefit from repeated sur-gical intervention for
recalcitrant cancer.Patients with inoperable cancer posea unique challenge to the
clinician.Ascure is no longer a realistic option,treat-ment modalities to prolong
life andimprove quality oflife assume a higherpriority.Pain control becomes a
signifi-cant issue in patients with recurrent headand neck cancer.Long-acting
sustainedrelease formulations such as transdermalnarcotic patches combined with
short-acting narcotics for breakthrough painare typically required.Rhizotomy is
anoption for intractable pain.Pain controlcan be a goal ofpalliative chemotherapyor
radiotherapy.Novel methods for thetargeted delivery ofchemotherapeuticagents into
the tumor are under develop-ment.A combination ofcisplatin andepinephrine gel
injected into recurrenttumors demonstrated significant pallia-tion without
significant side effects inmost.167Wound management becomes animportant issue,and
dealing with largemalodorous wounds can be taxing onpatients and families.Patients
presentingwith advanced head and neck cancer willtypically survive 6 to 12 months
withouttreatment,and patients with end-stagehead and neck cancer will have a
mediansurvival of101 days.164There is a natural tendency for clini-cians to avoid
the dying patient.There isa reluctance to face a disease whose biol-ogy has
resisted their best efforts andwhose treatment has left patients debili-tated and
frequently deformed.While
Oral Cancer Treatment653family members and clinicians are dis-cussing further
treatment options,patients are frequently simply concernedwith pain control and the
effects ofmas-sive doses ofnarcotics on bowel function.Frank,thoughtful discussions
must beheld with the patients and their familiesregarding end-of-life issues and
will helpsurgeons deal with these very real con-cerns.Hospice provides an
excellentresource,and once enrolled most familiesare appreciative ofthe support
offered bythese professionals in end-of-life care.In this era ofimproved
treatmentmodalities for local and regional disease,clinicians are finding that
factors unrelat-ed to the primary cancer and beyond theircontrol are influencing
survival.It isbecoming increasingly evident that factorsaffecting outcome in oral
cancer patientsare multiple and may relate more topatient characteristics than the
canceritselfor the treatment they receive.Researchers are finding that genetic
factorsofthe primary cancer have an impact onthe response ofthe particular tumor
toany treatment.168High expression ofepi-dermal growth factor receptors is
associat-ed with poor outcome,and may indicatethe need for more intensive
multimodalitytherapy.Alterations in TP53have beenassociated with recurrence in
squamouscell cancer ofthe head and neck that wasrefractory to radiation
treatment.Futuretreatments may include restoration ofTP53function.169Importantly
studies are also demon-strating that comorbidities and perfor-mance status predict
survival independentofstage at diagnosis.Performance statushas been shown to be a
predictor ofsur-vival independent oftumor,regionalnodes,and metastasis (TNM)
stage.Manyhead and neck cancer patients suffer othermedical problems related to
tobacco andalcohol use,and these can result indecreased overall survival despite
cancer-specific survival.Ribeiro and colleaguesfound that daily alcohol
consumption,smoking,poor body mass index,and othercomorbidities had an independent
impacton prognosis.170As discussed earlier theremay indeed be a more aggressive
form ofsquamous cell carcinoma that affectsyounger patients,but data from
theNational Cancer Data Base indicate thatyounger patients have a survival
advantagethat is most likely related to their lack ofcomorbidities.171Frequently 5-
and 10-year survival curves are impacted more bythese comorbidities than the tumor
char-acteristics recorded in the TNM system(see discussion below).172The TNM stag-
ing system will continue to undergo revi-sions to enhance its use.Future
TreatmentsIn the future,biologic markers hold outpromise as the key to treatment
ofheadand neck squamous cancers.Serving aspotential targets for gene
therapy,biologicmarkers may also determine appropriatetreatment strategies and may
select whichpatients should be treated with surgery,radiation
treatment,chemotherapy,orcombination treatment.Certain subpopu-lations ofsquamous
cancers,those withhigh levels ofTP53expression and low lev-els ofthe marker Ki-67
for example,havehigher relapse rates following initial thera-py.These patients may
benefit from moreaggressive combination treatments.168,169Every few years a new
cancer therapyis heralded as the end ofcancer surgery.For the present,surgery will
continue toplay the key role in management oforalcavity cancers,and surgeons must
beknowledgeable in all diagnostic and treat-ment modalities as they continue
theircaptainship ofthe oral cancer team.Thesurgeons treating oral cancer,regardless
oftheir discipline,must learn from the con-tributions and mistakes oftheir
forebearsand add the benefit oftheir own trainingand experience.They must then use
theirknowledge base and the input ofothertreating colleagues to synthesize a plan
oftreatment tailored to the patient who sitsbefore them.They must interact
effective-ly with colleagues ofother disciplines withthe patient�s benefit their
foremost con-cern.They must execute the surgical com-ponents ofthe treatment plan
with accu-racy and skill.They must be supportive totheir patients and their
patients�families ata time ofgreat stress in their lives andmust not turn away from
adversity orcomplication.They must accept the factthat not all patients can be
cured.Theyshould derive inspiration from those whosurvive and satisfaction from
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CHAPTER 34Lip CancerJames W.Sikes Jr,DMD,MD G.E.Ghali,DDS,MDLip cancer,one ofthe
most common can-cers ofthe head and neck region,is one ofthe most easily
diagnosed,with generally agood prognosis.In some individuals,lipcancer may behave
aggressively,manifest-ed by recurrence or mortality in up to 15%ofpatients.1�4The
most common malig-nancy ofthe lip is squamous cell carcino-ma,whereas basal cell
carcinoma accountsfor only 1% ofall lip carcinomas.4�6Othermalignancies ofthe lip
have been reportedbut are less common.7,8Epidemiology and EtiologyThe incidence
oflip cancer variesthroughout the world,resulting in 30% ofall malignant tumors
ofthe oral cavity incertain regions.In the sunbelt region ofthe United States,lip
cancer is the mostcommon cancer ofthe oral cavity,and itsincidence is second only
to skin malignan-cy ofthe head and neck.Australia,north-ern Spain,and Newfoundland
have areported annual incidence ranging from11 to 50 cases per 100,000
population.9In the United States,the incidence oflip cancer is 1.8 per 100,000
population,with the state ofUtah having the highestregional rate ofalmost 12 cases
per100,000.10Generally,the behavior oflipcancer resembles skin cancer more
thancarcinoma ofmucosal origin in the oralcavity proper.The lower lip is the
mostcommon site for lip cancer (88 to 98%),with only 2 to 7% arising from the
upperlip and 4% at the oral commis-sures.1,4�6,11�13The most common age atdiagnosis
is 54 to 65 years.4Although acondition seen in middle age,lip canceroccasionally
occurs in patients under age30 years.14Lip cancer has a predilectionfor men,with
men to women ratios rang-ing from 35:1 to 6:1,depending on thelocation ofthe
lesion.4The etiology oflip cancer is incom-pletely understood at present.Several
fac-tors have been associated with lip cancerdevelopment,but direct cause and
effecthas not been proven.Approximately one-third ofpatients with lip cancer have
out-door occupations,suggesting that sunexposure may be an etiologic factor.Because
ofits prominence,the lower lip isat a higher risk for exposure to the sun,compared
with the upper lip.Hence,thisresults in the discrepancy in the distribu-tion
between upper and lower lip can-cers.15,16Carcinoma ofthe lip principallyaffects
those individuals with fair skincomplexions.The prevalence oflip canceris at least
10 times higher in whites than inthose with darker skin and is extremelyrare among
Blacks.11,17Although it hasnever been proven,darker-skinned indi-viduals are
believed to have a protectivepigment in the vermilion ofthe lips thatprovides
protection from solar injury.10Multiple factors have been linked to
lipcancer,including tobacco use,pipe smok-ing,thermal injury,lip trauma,poor
oralhygiene,exposure to chemicals,mechanicalirritants,immunosuppression,and
chronicinfections.11�13,16,18�23Several case serieshave reported that a large
proportion oflipcancer patients regularly use tobacco,indi-cating that tobacco use
is etiologically asso-ciated with lip cancer develop-ment.5,11,15,19,24�28In
1984,Douglass andGammon reassessed the epidemiology oforal cancer and declared that
there wasinsufficient prooffor declaring tobacco asan etiologic factor in the
development oflipcancer.10Additional case-controlled studiesconcluded that no
statistically significantrelation exists between tobacco exposureand lip
carcinoma.29,30The smoking ofcig-ars and pipes is often considered an impor-tant
etiologic factor;however,no convinc-ing evidence exists that supports a
causalrelationship between tobacco use anddeveloping lip carcinoma.Cigar and
pipesmoking today,at best,are likely responsi-ble for only a small fraction oflip
cancers.Because alcohol and tobacco exposure�the two factors most strongly
associatedwith developing oral carcinoma�seem tohave limited influence on the
developing lipcarcinoma,the most consistently associatedfactor with lip cancer
appears to be pro-longed and cumulative exposure to ultravi-olet radiation from
sunlight.4,18�20,24,29,31Anatomic ConsiderationsEmbryologically,the upper lip forms
byfusing the two maxillary processes with a
660Part 5: Maxillofacial Pathologycentral median nasal process (Figure 34-1).As a
result,a central midline mass withtwo larger lateral segments is
formed.Theseparation ofthe lateral segments by thiscentral midline mass makes
metastasisfrom upper lip cancers to the contralateralneck exceedingly
rare.Conversely,thelower lip,formed by fusion in the midlineoftwo mandibular
processes,is at anincreased risk for contralateral neckmetastasis,particularly with
lesions nearthe midline.The lateral and superior bor-ders ofthe upper lip are well
defined at thenasolabial creases bilaterally and at thenasal base superiorly.The
inferior borderofthe lower lip is defined along the trans-versely oriented
labiomental crease.The formal definition oflip cancer,established by the American
Joint Commit-tee on Cancer for the purpose ofstaging lipcancer,describes the lip as
�beginning at thejunction ofthe vermilion border with theskin and including only
the vermilion sur-face or that portion ofthe lip that comesinto contact with the
opposing lip.It is welldefined into an upper and lower lip joinedat the commissures
ofthe mouth.�32Thisdefinition focuses on the unique epithelialsurface ofthe lip
vermilion and excludescancers that arise from the adjacent skin orlabial mucosa.In
statistical reporting,can-cers ofthe lip are commonly grouped withthose ofthe oral
cavity,because the lip isdefined as part ofthe oral cavity by theAmerican Joint
Committee on Cancer.9,32Lymphatic drainage ofthe lower liporiginates as an
interconnecting networkoflymph vessels beneath the submucosa ofthe vermilion.33It
subsequently gives riseto five or six lymphatic collecting trunksthat eventually
terminate into regionallymph nodes.The lymphatic trunks ofthecentral one-third
ofthe lower lip typicallydrain into the submental lymph nodes.The trunks that arise
from each lateral one-third ofthe lower lip typically drain intothe ipsilateral
submandibular lymphnodes.In certain individuals,the lymphat-ic trunks from the
central one-third ofthelip may drain to the submandibular lymphnodes on either
side.Cervical metastasis from lip canceroccurs in fewer than 10% ofpatients
withcancer ofthe lower lip and in up to 20% incancer ofthe upper lip and
commissure.5In the upper lip,crossover oflymphaticdrainage between the right and
left halvestypically does not occur.33The upper lipalso possesses five or six
collecting trunkson each side ofthe midline that originateas delicate lymphatic
vessels in the submu-cosa ofthe vermilion.The trunks ulti-mately terminate in the
submandibularlymph nodes but occasionally also drain tothe ipsilateral preauricular
or infra-auricular parotid lymph nodes.Metastasisthat results from cancer ofthe lip
mostcommonly involves the submandibularand submental lymph nodes (level
1).34�36Metastasis to level II ofthe jugular chainrarely occurs.Cancer involving
the upperlip may occasionally metastasize to theparotid lymph nodes,but
contralateralmetastasis is unusual for cancers oftheupper lip that do not cross the
midline andfor lower lip cancers that do not involvethe central one-third ofthe
lower lip.Metastasis from the lower lip is pri-marily to the
submental,submandibular,and perifacial nodes.Metastasis is found inthe
submandibular lymph nodes in about80 to 90% ofpatients with metastasis fromcancer
ofthe lower lip.5,37Although theupper lip is responsible for fewer than 10%oflip
cancer cases,its pattern ofmetastasisis fairly predictable,with the submandibu-lar
and parotid lymph node groups beingmost commonly involved.38Carcinoma ofthe
commissure and upper lip spreads tothe preauricular,periparotid,and sub-mandibular
nodes.Bilateral metastasismay develop ifthe lesion is near or hascrossed the
midline ofthe lip.Crossoverbetween the lymphatics ofthe right andleft sides ofthe
upper lip rarely occurs.4Cervical metastasis occurs late in thecourse oflip cancer
in fewer than 10% ofpatients with cancer ofthe lower lip andup to 20% in cancer
ofthe upper lip andcommissure.5Lymph node metastasis tothe upper jugular digastric
chain is seen inonly about 15% ofall patients who havelymph node metastasis and is
almostalways seen in conjunction with ipsilateralsubmandibular
metastasis.5,37ManagementEvaluationBecause carcinomas ofthe lip occur on ahighly
visible and constantly exposedregion ofthe body,a relatively early diagno-sis is
often feasible.The clinical presenta-tion oflip carcinomas is quite characteris-
tic,generally presenting as an exophytic orulcerated lesion on the vermilion
border,along with variable degrees ofinfiltration ofthe underlying musculature or
invasion ofthe overlying skin or labial mucosa (Figure34-2).Well-differentiated
squamous cellcarcinomas are often associated withhyperkeratosis and leukoplakia
ofthe ver-milion border ofthe lip.Any lip lesion thatMaxillary processMedial nasal
processMandibular processFIGURE34-1Developing upper lip,receiving contribu-tions
from a central medial nasal process and bilateralmaxillary processes.Developing
lower lip receiving con-tributions solely from bilateral mandibular processes.
Lip Cancer661the clinician views as a possible malignancyshould undergo an
incisional biopsy thatincludes both a portion ofthe lip lesion anda small portion
ofnormal appearing tissueat the margin.The factors that should beconsidered in
planning surgical resectionand reconstruction ofthe lips include thetumor stage,lip
subsite oforigin,patientpreference,and the histopathologic typeand grade ofthe
tumor.Staging oflip cancers is similar to thatemployed for tumors ofthe oral
cavity(Table 34-1).32Tumors less than 2 cm ingreatest dimension are staged as
T1,whereas massive tumors with invasion ofdeep soft tissues,adjacent bone,or
overly-ing skin are staged as T4(Table 34-2).Radiographic evaluation oftumors
detect-ed at an early stage that involve the lip isgenerally unnecessary.On the
other hand,advanced tumors that adhere to or invadethe adjacent mandible require
furtherradiologic evaluation.Detailed studies ofthe mandible,including panoramic
radi-ographs and computed tomography scans,may be necessary to delineate the extent
ofthe bony invasion,as well as any involve-ment ofthe inferior alveolar
canal.Melanomas and squamous cell carcinomasare known to be neurotropic and
mayspread along the inferior alveolar nerve viathe mental foramen.39�41Patients
whocomplain ofnumbness or paresthesia war-rant further radiologic
evaluation.Surgical TreatmentThe ultimate goal oflip cancer manage-ment is long-
term control ofthe carcinomawith preservation ofthe competency andesthetics ofthe
perioral region.Althoughexternal beam irradiation or surgical exci-sion can control
small primary tumors ofthe lip equally well,surgery is quicker andleaves little
esthetic or functional impair-ment.Larger lip cancers require plannedsurgical
resection,with reconstruction inmost cases.In the past 100 years,clinicianshave
employed many methods to managelip cancer.Some ofthe less effective meth-ods have
included direct applications ofcaustic agents,such as hydrochloric acid,arsenic
paste,or nitric acid.In addition,laser surgery,electrocoagulation,andcryotherapy
have been advocated by some.However,the two modalities that have beenthe most
thoroughly evaluated and thathave undergone the test oftime are surgeryand
radiation therapy.These two tech-niques yield excellent results for very
earlyFIGURE34-2Typical presentation ofa large exo-phytic squamous cell carcinoma
ofthe lower lip.Table 34-1Tumor Stage GroupingStage 0TisN0M0Stage IT1N0M0Stage
IIT2N0M0Stage IIIT3N0M0T1N1M0T2N1M0T3N1M0Stage
IVT4aN0M0T4aN1M0T1N2M0T2N2M0T3N2M0T4aN2M0Stage IVBAny TN3M0T4bAny NM0Stage IVCAny
TAny NM1Table 34-2Tumor Node Metastasis System for Lip CancerT = Tumor Size
TXPrimary tumor cannot be assessedT0No evidence ofprimary tumorTis Carcinoma in
situT1< 2 cmT2> 2 cm and =4 cmT3 > 4 cmT4Tumor invades through cortical bone
inferior alveolar nerve,floor ofmouth,or skin offace (ie,chin or nose)N = Nodal
Metastasis (regional)NXRegional lymph nodes cannot be assessedN0No regional nodes
palpableN1Single ipsilateral node < 3 cmN2Metastasis in a single ipsilateral lymph
node,> 3 cm but =6 cm;or in multiple ipsilateral lymph nodes,none > 6 cm;or in
bilateral or contralateral lymph nodes,none > 6 cmN2aSingle ipsilateral node > 3 cm
but =6 cmN2bMultiple ipsilateral nodes =6 cmN2cBilateral or contralateral nodes =6
cmN3Node > 6 cmM = Distant MetastasisMXDistant metastasis cannot be assessedM0No
distant metastasisM1Distant metastasis
662Part 5: Maxillofacial Pathologylip cancers,and surgery is the most com-mon
treatment selected for managing lipcarcinoma ofany size,particularly the larg-er T3
and T4 tumors.The determination ofan adequatesurgical margin around a lip cancer
issomewhat nebulous,and few objectivedata have been gathered to substantiateany
recommendations for adequate exci-sion margins.The size ofthe primarylesion is the
most common factor that weuse to determine the extent ofthe margin-al
excision.Larger cancers have typicallymandated wider margins than have small-er
cancers.Based on these general guide-lines,a minimum of8 to 10 mm ofnormaltissue
around a lip cancer is recommendedto facilitate its complete
removal.2,11,25,42�44Smaller lip cancers,less than 1 cm in great-est dimension,can
often be managed withslightly smaller margins of5 mm.44In ourexperience,the locally
advanced T4 squa-mous cell carcinomas ofthe lip are opti-mally treated with a
slightly larger marginofapproximately 15 to 20 mm.The lip shave,or vermilionectomy
pro-cedure,is ideal for those situations whereinareas ofleukoplakia,actinic
cheilitis,or car-cinoma in situ involve the vermilion ofthelips (Figure 34-
3).45�54These premalignantconditions require treatment but not com-plete full-
thickness excision ofthe lip.Thisoperation involves partial or entire excisionofthe
lip vermilion.The vermilionectomymay also be used,in conjunction with a full-
thickness lip excision,in individuals pos-sessing invasive lip carcinoma and prema-
lignant vermilion changes.Following thevermilionectomy,the residual defect is pri-
marily closed with labial mucosal advance-ment flaps.In situations with invasive
lesions,thelip shave procedure is contraindicated,andfull-thickness excision ofthe
involved por-tion ofthe lip is the traditional procedurefor management.The most
commonlyselected configuration oflip excision is aV,W,or a shield (Figure 34-4).The
defectsresulting from the Vand Wexcisions caneasily be closed primarily with no
addi-tional mobilization ofadjacent tissues(Figure 34-5).The rectangular form
ofexcision,however,requires advancementoflaterally based lip flaps to achieve a
sat-isfactory closure.These forms ofexcisionare selected purely on the basis
ofcosmet-ic and functional considerations for all T1and most T2 lip
carcinomas.Invasion ofthe mandible,involvementofthe mental or inferior alveolar
nerve,tumor sizes ofT3 or greater,or associatedregional lymph node metastasis
generallynecessitate a more aggressive resection.Aggressive treatment requires an
excisionand reconstruction that is more complexthan the standard full-thickness Vor
Wexcision,and will be discussed in detail inthe following section on lip
reconstruc-tion.Include a marginal mandibulectomywith the resection oflip cancers
thatapproximate the alveolar ridge or outerlabial cortex ofthe
mandible.Likewise,forrare lesions that actually demonstrateradiographic invasion
ofthe mandible,include a segmental mandibulectomy inthe treatment plan.Lip
ReconstructionLip reconstruction following surgical exci-sion ofcancer should
reestablish the func-tion and appearance ofthe lip.The key tofunctional restoration
is the reconstitutionofthe orbicularis oris muscle.Primarysurgical restoration
ofthe orbicularismuscle following resections that exceedtwo-thirds to three-
quarters ofthe liplength will create microstomia.Defects ofthe vermilion
resultingfrom a lip shave procedure are generallyrestored with labial mucosal
advancementflaps.55�57The labial mucosal flap developsby creating a plane between
the minor sali-vary glands and the inner surface oftheorbicularis oris muscle.This
flap may bemobilized into the buccal vestibule ifnec-essary.The flap is secured to
the anteriorcutaneous margin ofthe excision to createa new vermilion cutaneous
border (Figure34-6).Other less commonly used flaps forvermilion reconstruction
after a lip shaveinclude cross-lip buccal mucosa flaps andtongue flaps.57�59Closure
may be achieved primarilywhen a full-thickness excision ofthe upperor lower lip
results in a defect ofup to one-third ofthe lip length (Figure 34-7).TheFIGURE34-
3Actinic cheilitis involving thevermilion ofthe lower lip.FIGURE34-4The proposed
incisions for a shieldexcision oflower lip are delineated.FIGURE34-5Primary closure
ofa Wexcision ofthe lower lip.
Lip Cancer663V-shaped excision design is most com-monly used when a primary closure
isanticipated.Typically,the apex ofthe Visplaced at or slightly above the
nasolabialfold or labiomental crease.55�58,60�62A min-imum ofa three-layered
closure compris-ing mucosa,muscle,and skin is necessaryto avoid unesthetic notching
ofthe lip asthe scar matures.Lip cancers that extend more deeplyinto the lip
substructure but still involve asuperficial length ofvermilion that wouldotherwise
produce a defect may be closedprimarily via the W-shaped modification ofthe
Vconfiguration (Figure 34-8).Thisexcision uses an M-plasty in place ofthesingle
apex ofthe V.A three-layered closureofthe defect,with careful attention to detailin
the reconstruction ofthe orbicularis orismuscle layer is achieved (see Figure 34-
5).The need to reconstruct lip defectsgreater than one-third ofthe lip length ledto
the development ofvarious circumoralflap advancement techniques.56�58,60,62�64The
most popular ofthese techniquesincludes the Karapandzic reconstructionflap (Figure
34-9).This flap consists ofatransfer ofthe remaining lip tissue toreconstitute the
lips and mouth opening.The Karapandzic flap uses release inci-sions within the
labiomental crease,extending around the region ofthe oralcommissures and continuing
superiorlywithin the nasolabial creases bilaterally.Combining sharp and blunt
dissectionFIGURE34-7Good esthetic results followingshield excision and primary
closure ofa rightlower lip defect involving one-third the totallength ofthe lower
lip.FIGURE34-8A,Typical presentation ofsquamous cell carcinoma ofthe right lower
lip.B,Wexci-sion ofthe lesion sparing the right commisure.ABFIGURE34-6A,Actinic
chelitis ofthe lower lipwith atypia noted on biopsy.B,Completed exci-sion ofthe
lower lip vermilion.C,Completeundermining ofthe mucosa and removal ofadja-cent
minor salivary glands help prevent rolling ofthe lower lip and mucocele
formation,respective-ly.D,Mucosal advancement and primary closureofthe surgical
defect has been completed.E,Early postoperative results following the lipshave
procedure.ABCDE
664Part 5: Maxillofacial Pathologyseparates the orbicularis muscles from
thesurrounding facial expression muscles.Neurovascular structures are preservedand
transposed medially,along with theflap,and intraoral buccal mucosal
releaseincisions are often necessary.For this reason,the Karapandzic flap isideally
suited in situations where two-thirds to three-quarters,or more,ofthelower lip is
resected,particularly when theresection is centrally located and leaves thelateral
ends near the commissures intact.The incisions for elevation ofthe Kara-pandzic
flap require mobilization oftheskin and subcutaneous tissues that aresuperficial to
the orbicularis oris muscleand mucosa and deep to the orbicularisoris muscle.At the
same time,the muscleitselfmust be kept intact,with its nerveand blood supply
preserved as tissues arerotated and sutured medially.Among other reconstructive
optionsfor the lip,the cross-lip flaps are particu-larly useful in repairing
moderate lipdefects ofone-third the length ofonelip.60,65�67These techniques
transfer a full-thickness segment oflip tissue into adefect on the opposite
lip.Estlander andAbbe developed the most commonly usedcross-lip flap repair
techniques.66,67TheAbbe flap,as originally described,transferstissue from the lower
lip to a defect in thecentral component ofthe upper lip.It is,however,most often
used to reconstructlower lip defects by transferring tissuefrom the upper lip
(Figure 34-10).TheEstlander flap was used to reconstructdefects ofthe upper or
lower lip in a singlestage by transferring lip tissue around theoral commissure
(Figure 34-11).All cross-lip flaps are generally referred to as Abbe-Estlander type
flaps.The principle ofthe Abbe-Estlanderflap repair is that the width ofthe base
ofthe triangular flap is one-halfthat ofthewidth ofthe base ofthe triangular
surgicaldefect.The vertical length ofthe flapFIGURE34-9A,Defects greater than one-
third ofthe lip may require circumoral flaps,such as the Karapandzic flap depicted
by this schematic.B,Schematic depicting the closure ofthe Karapandzic
flap.C,Esthetic postoperative results ofa Karapandzic flap can be achieved.Note the
recurrence ofthe lesion in the midline.ABCFIGURE34-10A drawing ofthe two-stage
Abbeflap,demonstrating the cross-lip transfer that isdivided at approximately 3
weeks postoperatively.FIGURE34-11A schematic drawing oftheone-stage Estlander flap
with the classic round-ing ofthe commissure region.
Lip Cancer665should match that ofthe defect.The cross-lip flap includes and depends
on a smallpedicle that carries the labial artery fromthe donor lip.Generally,mark
out the flap on theupper lip on the same side as the plannedexcision (Figure 34-
12).Make a skin inci-sion at the previously marked outline ofthe Abbe-Estlander
flap on the lateralaspect ofthe upper lip.The lateral incisionis deepened through
both the musculatureand the mucosa,extending from the ver-milion border up to the
apex ofthe flap.With extreme caution,perform an inci-sion along the medial margin
ofthe flap,beginning at the apex ofthe flap andworking toward the vermilion border
toavoid injury to the labial artery.As mobi-lization ofthe flap toward the
vermilionborder proceeds,separate the musculatureofthe upper lip bluntly with a
hemostat,and divide a little at a time small segmentsofthe muscle fibers with
scissors.Once thelabial artery is identified,under directvision,divide the other
attachments ofthemusculature ofthe upper lip around thelabial artery,while keeping
the mucosa ofthe vermilion border intact.In addition,toallow flap rotation,divide
the intraorallabial mucosa on the medial aspect oftheflap,from the apex ofthe flap
toward thelip.Rotate the flap 180�to fill the surgicaldefect in the lower lip.Inset
ofthe flap begins by accurateapproximation ofthe vermilion edges ofthe flap and the
lower lip,followed bycareful multilayered closure.Bring the vas-cular pedicle
across the open mouth,andperform the second-stage release 3 weekslater (Figure 34-
13).Preoperatively,instruct the patient to avoid trauma to thisintervening pedicle
during the immediatepostoperative period.When one commissure ofthe lip mustbe
sacrificed along with the excision ofthelip cancer,then employ a nonbridged Est-
lander flap (Figure 34-14).This flap is cre-ated as a single-stage procedure
withoutthe need for secondary pedicle division.The downside ofthis type offlap is
thedevelopment ofa somewhat unnatural,rounded commissure.The Abbe-Estlanderflap can
be used in reverse when a lesion ofthe upper lip is excised by elevating theflap
from the lower lip.Alternatively,acheek advancement flap with Burow�s tri-angle is
often useful for repairing lateraldefects ofthe upper lip (Figure 34-15).Several
techniques designed for lipdefects are too extensive for reconstruc-tion using the
Karapandzic or Abbe-Estlander techniques.68�70 These tech-niques use adjacent cheek
tissue in theform oflaterally based advancement flaps.In the Bernard flap,the lower
lip may beexcised in its entirety,along with soft tis-sues ofthe mental region,and
the result-ing defect is closed by lateral cheek flaps toform a new lower lip
(Figure 34-16).To setback the commissure and to reduce theincidence ofa �fish-
mouth�deformity,excise triangles ofthe skin from both sidesofthe upper lip.Preserve
the mucousmembrane to help form a new vermilionborder.Excise the triangular wedges
ofskin from the nasolabial crease on bothsides,subsequent to excision ofthe prima-
ry tumor.The base ofthis triangular exci-sion extends from the commissure
oftheFIGURE34-12In the cross-lip flap,the transferportion in most cases need only
be 50% as largeas the defect.Care should be taken to preventinjury to the superior
labial artery.FIGURE34-13Typical appearance ofthecross-lip transfer flap at the
time ofsutureremoval,demonstrated in this lower to upperlip transfer.FIGURE34-14At
times an extension into thelabiomental crease may aid in closure ofthedefect,as
seen marked during this cross-liptransfer flap.FIGURE34-15In situations that do not
requirereconstruction ofthe vermilion surface ofthe lip,a cutaneous advancement
flap may be appropri-ate,as in this case with Burow�s triangles to aidin
advancement.
666Part 5: Maxillofacial Pathologymouth,up to the nasolabial crease,depending on
the width ofthe cheek flapto be mobilized (Figure 34-17A).Afterexcising the
triangular wedges,incise themucosae from their inner aspect,exceptfor the base,and
shift the triangular flapsofthe upper lip mucosa medially,alongwith the flaps
(Figure 34-17B).Make acounter incision in the lower mucogingi-val sulcus
bilaterally,and mobilize bothcheek flaps medially.Perform a closure ofthe lip
musculature on both sides withinterrupted sutures.The triangular wedgesofthe mucosa
from the upper lip areeverted and rolled inferiorly to provide anew vermilion
surface.Mucosal closure iscompleted inferiorly in the mucogingivalsulcus (Figure
34-17C and D).The main advantage ofthe Bernardflap is its ability to reconstruct
almost thewhole lower lip in a single-stage procedure.The main disadvantage is
reducing the sizeofthe orifice and creating a so-called per-manent smile deformity
ofthe lips,mostoften produced in edentulous individuals.The reconstruction ofmore
massivedefects that include total lip excision,aswell as excising the adjacent
floor ofthemouth,skin,or mandible,requires the useofdistant flaps,such as the
deltopectoral orpectoralis major myocutaneous flap.Alter-natively,use free
vascularized compositeflaps to reconstruct these large defects.Afree flap that has
recently shown to be par-ticularly useful is the composite radial forearm-palmaris
longus free flap.71,72Cervical LymphadenectomyPatients with early cancer ofthe lip
(stagesI and II) do not generally need electivetreatment ofthe cervical lymph
nodes,because the rate ofoccult metastasis is low.The risk for cervical metastasis
increaseswith poorly differentiated cancer,recur-rent cancer,or with cancer that
extendsinto the labial mucosa or that invades themandible.Given the infrequency
withwhich stage I and stage II lip cancersspread to regional lymph
nodes,electivetreatment ofthe neck is not alwaysrequired.One report indicated that
therewas delayed cervical metastasis between 35and 40% from lip cancer tumors 2 to
4 cmin size.4This report confirms a much larg-er rate ofmetastasis than that
usually seenin clinical practice.With advanced disease (stages III andIV),elective
neck dissection oflevels Ithrough III is recommended (Figure 34-18).Thus,even ifthe
patient has nopalpable adenopathy (N0 neck),the clini-cian should still use
elective radiationtherapy or elective neck node dissection inmanaging
patients,owing to the high rateofmicroscopic lymph node metastasis inthese
patients.In patients with lesions ofthe upper lip,commissure,or both,include a
superficial parotidectomy.Clini-cally apparent lymph nodes require eitherradiation
therapy or neck dissection for N1nodes and combined therapy (neck dissec-tion and
radiation) for N2 and N3 nodes.73Treatment Results The cure rate for T1 and T2 lip
cancerswithout regional metastasis is greater than90% with surgery or
radiation.4,48The FIGURE34-16In situations requiring completeexcision ofthe lower
lip,the Bernard flap mayprovide a means for reconstruction with circum-oral
tissues,depicted in this schematic drawing.FIGURE34-17A,Proposed incisions for a
classic Bernard flap reconstruction ofthe lower lip.B,Thedevelopment ofthe Bernard
flap after resection ofthe lower lip.C,Closure ofthe wound includes themucosal
layer,orbicularis oris layer,dermal layer,and the skin closure.D,Postoperative
follow-up at1 year demonstrates no recurrence and good esthetic results.ABCD
Lip Cancer6675-year determinate survival is approxi-mately 80%.1The cure rates for
cancer ofthe lips suggest a better prognosis than forother cancers ofthe oral
cavity.Cancerinvolving the oral commissure is moreaggressive,with a 5-year cure
rate rangingbetween 34 and 50%.Cancers that includeareas larger than 2 cm have cure
rates of< 80%,and those that invade deep enoughto involve the mandible have a cure
rate of< 50%.4,74The primary cause offailure islocal recurrence,rather than
regional nodemetastasis.Other adverse prognostic fac-tors include poor histologic
grade,tumorthickness > 6 mm,desmoplasia,stromalsclerosis,muscular invasion,and
perineur-al invasion.75�77Angiogenesis has not beenshown to have prognostic
significance.78While TP53mutations are seen in 50% oflip cancers,the clinical
significance ofthisobservation is unknown.79Generally,elective lymph node dis-
section in the N0 neck is reserved foradvanced stage disease (stage III andstage
IV).74,80About 5 to 10% ofpatientswith lip cancer will develop evidence ofnodal
involvement.1,81,82Without ques-tion,the presence ofcervical lymph nodemetastasis
affects survival.The average 5-year survival for patients with cervicalmetastasis
oflip carcinoma is approxi-mately 50%,with a range of29 to 68%.Recurrence rates in
the neck after treat-ment ofregional metastasis are 40% forN1 disease and up to
100% for N3 dis-ease.1The risk ofdeveloping a metachro-nous lip cancer is estimated
at about 20%by 10 years follow-up.83ConclusionsLip cancer accounts for a
significant per-centage ofall head and neck malignanciesin the United States.Lip
cancer arises fromthe lower lip in nearly 90% ofcases.Etio-logic factors associated
with lip cancerinclude sun exposure,alcohol,and tobac-co abuse.Commissure
involvement is anadverse prognostic factor.Regional cervi-cal lymph node metastasis
is directly relat-ed to a poor prognosis.With overall curerates of80 to 90%,lip
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reliefofdeformity due to double harelip.PlastReconstr Surg 1968;42:481�3
66.Estlander JA.Eine methode aus der linen lippesubstanzuerluste der anderen zu
ersetzen.Arch Klin Chirurg 1872;14:622.Reprintedwith English translation.Plast
ReconstrSurg 1968;442:361.67.Templer J,Renner G,Davis WE,et al.A modi-fication
ofthe Abbe-Estander flap fordefects on the lower
lip.Laryngoscope1981;91:153�6.68.Webster RE,Coffey RJ,Kellcher RE.Total andpartial
reconstruction ofthe lower lip withinnervated muscle-bearing flaps.PlastReconstr
Surg 1960;25:360�7.69.von Burow CA.Beschreibung einer neuenTransplantations-Methode
(Meth ode derseitlichen dreiecke) zum weiderersatz ver-lorengegangener Teile des
Gesichts.Berlin:Nauck;1855.70.Bernard C.Cancer de la leure inferieure operepar un
procede nouveau.Bull Mem SocChir Paris 1853;3:357.71.Sadove RC,Luce EA,McGrath
PC.Reconstruc-tion ofthe lower lip and chin with the com-posite radial forearm-
palmaris longus freeflap.Plast Reconstr Surg 1991;88:209�14.72.Furuta S,Sukaguchi
Y,Imasarva M,et al.Reconstruction ofthe lips,oral commissure,and full-thickness
cheek with a compositeradial forearm-palmaris longus free flap.Ann Plast Surg
1994;33:544�7.73.Duplechain G,Amedee RG.Carcinoma ofthelip.J La State Med Soc
1992;144:441�2.74.Zitsch RP.Carcinoma ofthe lip.OtolarngolClin North Am
1993;26:265�77.75.Saywell MS,Weedon D.Histological correlatesofmetastasis in
primary invasive squamouscell carcinoma ofthe lip.Australas J
Pathol1996;36:193�5.76.Breuninger H,Schaumburg-Lever G,Holzschuh J.Desmoplastic
squamous cellcarcinoma ofskin and vermilion surface:ahighly malignant subtype
ofskin cancer.Cancer 1997;79:915�9.77.Dos Santos LR,Cernea CR,Kowalski LP.Squa-mous
cell carcinoma ofthe lower lip:a ret-rospective study of58 patients.Rev PaulistaMed
1996;114:1117�26.78.Tahan SR,Stein AL.Angiogenesis in invasivesquamous cell
carcinoma ofthe lip:tumor
Lip Cancer669vascularity is not an indicator ofmetastaticrisk.J Cutan Pathol
1995;22:236�40.79.Ostwald C,Gogacz P,Hillmann T,et al.p 53Mutational spectra are
different betweensquamous-cell carcinoma ofthe lip and theoral cavity.Int J Cancer
2000;88:82�6.80.Krabel MR,Koranda FC,Panje WR.Squamouscell carcinoma ofthe upper
lip.J DermatolSurg Oncol 1982;8:487�91.81.Sack JG,Ford CN.Metastatic squamous
cellcarcinoma ofthe lip.Arch Otolaryngol1978;104:282�5.82.Nuutinen J,Karja J.Local
and distant metasta-sis in patients with surgically treated squa-mous cell
carcinoma ofthe lip.Clin Oto-laryngol 1981;6:415�9.83.McCombe D,MacGill K,Ainslie
J,Beresford J,Matthews J.Squamous cell carcinoma ofthelip:a retrospective review
ofthe Peter Mac-Callum Cancer Institute experience.ANZ JSurg 2000;70:358�61.
CHAPTER 35Salivary Gland Disease and TumorsRobert A.Ord,MD,DDS,MSAlex
E.Pazoki,MD,DDSThe salivary glands consist ofthree majorpaired glands (the
parotid,submandibular,and sublingual) as well as numerous minorsalivary
glands,situated mostly in the oralcavity but also found in the
pharynx,larynx,trachea,and sinuses.In the oral cavity 700 to900 minor salivary
glands are found,themajority ofwhich are located at the junc-tion ofthe hard and
soft palates.Theseglands produce saliva,which functions as alubricant for speech
and swallowing,assiststaste,has antibacterial and immunologicproperties,and
contains digestive enzymes.The salivary glands are affected by many dif-ferent
disease processes,some ofwhich aresurgical in nature while others have a med-ical
basis.Surgical diseases include tumors,stones,and cysts,whereas medical
diseasesinclude viral infections,autoimmune dis-eases,and sarcoidosis.This chapter
will con-centrate on the salivary gland diseases thatare ofmost interest to the
surgeon.TumorsTumors ofthe salivary glands show a widevariety ofpathologic types
varying frombenign to highly malignant.Salivary can-cers are comparatively rare and
comprise3% ofhead and neck cancers,which inturn account for 3% ofall
malignancies.These neoplasms will be discussedaccording to their histopathologic
diagno-sis and the surgical principles dictated bythe site ofthe
tumor.HistopathologyThe large variety oftumors that occur inthe salivary glands
make an exhaustive listofall types impossible in a chapter ofthislength.The most
common epithelial sali-vary gland tumors will be reviewed inorder to illustrate the
fundamentals ofmanagement ofsalivary neoplasia.Benign TumorsPleomorphic AdenomaThe
pleomorphic adenoma is the mostcommon benign salivary tumor at all
sites.Approximately 80% ofall pleomorphicadenomas (PSAs) occur in the parotid,and
despite their slow growth they canbecome extremely large ifneglected.Thistumor is
thought to arise from both sali-vary ducts and myoepithelial cells and is atrue
�mixed tumor.�Because ofits deriva-tion,histologically,many different pat-terns can
occur,from cellular,glandular,and myxoid types to cartilagenous andeven ossified
forms.These features can beseen in different areas ofthe same tumor,accounting for
its name,pleomorphic(Greek for many forms).The importantfeature from a surgical
standpoint is thepresence ofa �pseudo capsule,�which con-tains outgrowths or
pseudopodia ofthetumor.Attempts at �enucleation�ofthetumor from within its
�capsule�willinevitably leave viable tumor cell nests andpredispose the patient to
multifocal recur-rence.Some authorities believe thatyounger patients with
pleomorphic ade-nomas have a higher chance oftumorrecurrence and increased growth
duringpregnancy.Malignant change is rare andusually takes place in long-
standingtumors,the most common type being car-cinoma ex pleomorphic adenoma.Prog-
nosis will depend on the type ofmalig-nancy and involvement ofthe
capsule.Rarely,malignant change in both ele-ments ofthe pleomorphic adenoma (duc-
tal and myoepithelial) will occur givingrise to the carcinosarcoma or true
mixedmalignant (biphasic) pleomorphic adeno-ma.On rare occasions,an apparently his-
tologically benign tumor will metastasizeinto the so-called benign
metastasizingpleomorphic adenoma.Warthin�s TumorsThis benign tumor isalmost
exclusively found in the parotid.Itoccurs mostly in men and is more commonin
smokers.It is thought to derive from sali-vary duct cells that are entrapped in
lymphnodes during embryonic development.Thetumor consists oflarge cystic spaces
with asurrounding columnar epithelium and a
672Part 5: Maxillofacial Pathologystroma oflymphocytes.Surgically thesetumors may
be multiple in one parotidgland or bilateral,or involve lymph nodesadjacent to the
parotid gland.1,2HemangioendotheliomaIn children themost common cause ofparotid
mass is ahemangioma or hemangioendothelioma.3These are benign tumors that may
appearsoon after birth and grow rapidly.Usually,conservative treatment while
waiting forinvolution is recommended.Malignant
TumorsMucoepidermoidCarcinomaMucoepidermoid carcinoma(MEC) is the most common
malignantsalivary gland neoplasm in both adults andchildren,and the most common
salivarygland cancer ofthe parotid and minor sali-vary glands.This tumor can be
oflow gradeor high grade depending on its histology.Low-grade MECs have multiple
macrocystsand abundant mucus-producing cells.High-grade varieties have multiple
squa-mous cells and very few mucus-producingcells or cysts,and mucicarmine or
periodicacid�Schiffstains may be needed to identi-fy intracellular mucus to
characterize thistumor.There are three cell types ofMEC:mucus
producing,intermediate,and squa-mous.The respective ratio ofmucus-producing cells
to squamous cells willdetermine the clinical aggressiveness ofthetumor (see
above).Low-grade MECs canbe very slow growing and nonmetastasiz-ing,and can
generally behave like a benigntumor.High-grade MECs can exhibitaggressive growth
and invasion resulting inwidespread metastasis and death.High-grade tumors usually
show increased pleo-morphism and meiotic figures.High-gradelesions may metastasize
to cervical lymphnodes or spread hematogenously to thelung,liver,and bone.Adenoid
Cystic CarcinomaAlthough thistumor is very slow growing,its relentlesscourse,with
repeated recurrence and metas-tasis via the blood stream,gives low 20-yearsurvival
rates.4Adenoid cystic carcinoma isthe most common malignancy ofthe sub-mandibular
gland and is the secondmostcommon salivary gland cancer overall.Three histologic
types are seen:tubular,cribriform (the classic �Swiss cheese�pat-tern),and
solid.The solid type has the worstprognosis,especially when areas ofnecrosisare
present.The infiltrative nature ofthislesion and the frequency
ofperineuralinvolvement with spread along the nervemandate wide resection
margins.Perineuralspread is a bad prognostic sign for both localrecurrence and
distant metastasis.Clinicaland radiologic examination ofthis tumorfrequently
underestimate its true extent,andfollow-up of15 to 20 years is required as
laterecurrences occur.Low-Grade Polymorphous AdenocarcinomaLow-grade polymorphous
adenocarcinomaoccurs almost exclusively in the minor sali-vary glands and is second
only to mucoepi-dermoid carcinoma at these sites.It arisesfrom terminal duct cells
and is characterizedby cytologically bland monotonous cells thatcan assume many
different patterns (glan-dular,cribriform,and lobular) within thesame
tumor.Characteristically �Indian file�cells and perineural involvement are
seen.Although this tumor behaves in a very low-grade manner,local recurrence will
occurwith inadequate excision.5The importantpathologic features seen from the
surgeon�sviewpoint are frequent misdiagnosed on ini-tial biopsy,due to the
different patterns thatmay be sampled.Common misdiagnoses areadenoid cystic
carcinoma,pleomorphic ade-noma,and malignant pleomorphic ade-noma.It is also
important to be aware thatthe frequent presence ofperineural involve-ment does not
lead to a worse prognosis,asis the case for adenoid cystic carcinoma.Site
ofTumorParotid GlandThe surgical principlesoftreating parotid tumors are dictated
bythe histopathology ofthe tumor and theneed to preserve the facial nerve.Diag-
nostic imaging with computed tomogra-phy (CT) or magnetic resonance (MR)
isdesirable for superficial lobe tumors butis essential for suspected deep-lobe
neo-plasms,especially those with a parapha-ryngeal component.Since 80%
ofparotidtumors are benign and 80% ofthese arepleomorphic adenomas,a solitary
massin the parotid with no features ofmalig-nancy is most likely a PSA.Open
biopsyofsuch a mass is therefore contraindicat-ed as this will rupture the
�capsule�and�seed�the PSA,increasing the complexityofsubsequent surgery and chances
ofrecurrence.Fine-needle aspiration biopsy(FNAB) for cytology is the
preferredmethod ofdiagnosis.6Clinically onlyone-third ofmalignant tumors will
havesymptoms or signs ofmalignancy,such aspain,ulceration ofskin,facial nerve
palsy,or metastatic cervical nodes.7Thus virtu-ally all parotid tumors will
initially betreated as benign unless FNAB shows def-inite malignancy or there is
clinical evi-dence ofmalignancy (Figure 35-1).Themajority oftumors occur in the
superfi-cial lobe,and superficial lobectomy withpreservation ofthe facial nerve has
beenthe standard operation for many years.Recent minor modifications have includ-ed
the use ofa face-lift incision,the use ofthe superficial musculoaponeurotic sys-tem
to prevent Frey�s syndrome,the useofflaps or alloplasts to augment defects,and the
suggestion that �capsular dissec-tion�without the need to remove theentire
superficial parotid may be suffi-cient.8�10Superficial lobectomy is suitablefor
benign and low-grade malignanttumors,and even in high-grade malig-nancies only
branches ofthe nerve thatare actually infiltrated will be sacrificed.Ifthe nerve or
portions ofit have to beresected,immediate grafting is recom-mended.In deep-lobe
tumors a totalparotidectomy is performed,with thesuperficial lobe being dissected
first toexpose the nerve.Good margins with
Salivary Gland Disease and Tumors673surrounding normal salivary gland tissueare
more difficult to obtain on deep-lobetumors,which tend to be large as they areoften
detected late.In high-grade tumors,surrounding tissues such as skin,mas-seter,and
mandible may require sacrifice,as dictated by the need to obtain clearmargins.In
these instances considerationshould be given to neck dissection.Whereclinically
positive nodes are present,amodified radical neck dissection is usual-ly the
operation ofchoice.11Where thepatient is N0 clinically,but at high riskfor occult
nodal disease,a selective neckdissection oflevels I to IV or levels II toIV is
indicated.In high-grade tumorspostoperative radiation therapy is
usuallyindicated.Chemotherapy has not beenshown to convey a survival benefit
forthese lesions.Submandibular GlandIn suspected sub-mandibular neoplams,CT
imaging,MRimaging,and FNAB are all useful in thediagnostic work-up.Fifty percent
oftumors will be malignant,adenoid cysticcarcinoma being the most common.Inbenign
neoplasms (PSAs) removal ofthesubmandibular gland with an extracapsu-lar dissection
ofthe tumor and 2 to 3 mmofsurrounding soft tissue is sufficient.Formalignant
tumors the minimum resectionwill be an en bloc removal oflevel I.Ifindi-cated the
overlying platysma superficiallyand the mylohyoid muscle deeply will beexcised.In
most malignant tumors withN0 necks,the cervical incision necessaryfor removal
oflevel I will dictate extendingthis to a supraomohyoid neck removinglevels I to
III.The adenoid cystic carcinomadoes not usually metastasize via the lym-
phatics;instead it spreads hematogenouslyand neck dissection may not be
indicated.The mandibular branches ofthe facial,lin-gual,and hypoglossal nerves are
all in closerelation to the submandibular gland.Ifthese nerves appear to be
involved by can-cer,they should be traced until the nerveappears normal.After
resection,frozen sec-tions should be sent from the cut nervetrunk to confirm
clearance,although�skip�lesions do occur.Radiation may beuseful
postoperatively.Minor Salivary GlandsThe PalateThemajority ofminor salivary gland
tumorsoccur at the junction ofthe hard and softpalates.In this location 50% are
malignant,the most common being low-grademucoepidermoid carcinoma followed bylow-
grade polymorphous adenocarcinoma.Coronal and axial CT scans with bony win-dows are
helpful to demonstrate bonedestruction and involvement ofthe sinusesor nasal
cavity.Biopsy through the middleofthe lesion is indicated as the overlyingmucosa
will be excised.12In PSA,excisionwith a 5 mm margin is adequate.Theperiosteum is a
good deep margin ifthebone is uninvolved,as is usually the casewith PSA (Figure 35-
2).In low-gradelesions a 1 cm margin and similar approachFIGURE35-1A,Large
neglected pleomorphicadenoma ofthe left parotid gland.B,Axial com-puted tomography
scan showing tumor in thesuperficial lobe.C,Operative photograph show-ing
superficial parotidectomy with initial dissec-tion ofthe upper and lower branches
ofthe facialnerve trunk.ABCFIGURE35-2Large pleomorphic adenoma ofthe right palate.
674Part 5: Maxillofacial Pathologyare used.Local flap reconstruction or theuse ofa
palatal plate with subsequent sec-ondary healing by granulation is used
forreconstruction.Where bone invasion hasoccurred,as in adenoid cystic carcinoma
orhigh-grade tumors,a partial maxillectomywill be required.In the case ofadenoid
cys-tic carcinoma,attention must be given tothe greater palatine nerve,with frozen
sec-tion clearance obtained.Cranial extension,orbital involvement,and infiltration
poste-riorly into the pterygoids will increase theextent ofsurgery and its
morbidity,with adecrease in survival (Figure 35-3).Recon-struction is usually with
an obturator,although primary maxillary reconstructionhas been revisited with the
development ofinterosseous implants and compositemicrovascular free flaps.The
Retromolar FossaAlthough this is arelatively unusual site for minor salivarygland
tumors,virtually 100% are malig-nant and are low-grade mucoepidermoidcarcinomas.The
surgeon should be awarethat a cystic soft tissue mass distal to thethird molar,with
or without radiographicmandibular involvement,is unlikely to bea mucocele,and
incisional biopsy shouldbe undertaken to confirm the diagnosis.Intrabony
TumorsAlthough intrabony(central) salivary gland tumors are rare,the vast majority
are malignant low-grade mucoepidermoid carcinomas.13These are mostly seen in the
third molarregion ofthe mandible and are frequent-ly multilocular.The tumors are
oftendiagnosed radiologically as ameloblas-tomas,or odontogenic keratocysts.Resec-
tion with a 1 cm margin and sacrifice ofthe inferior alveolar nerve and
overlyingsoft tissue in areas ofperforation arerequired.Neck dissection is usually
notnecessary,but ifthe neck has beenopened widely for mandibular resection
asupraomohyoid neck dissection can beundertaken.A reconstruction plate isplaced and
either primary reconstructionwith a fibular or deep circumflex iliacartery
microvascular flap or secondaryposterior iliac crest
corticocancellousreconstruction may be used.Other Intraoral
SitesInterestingly,theproportion ofbenign to malignant tumorsvaries according to
site,with virtually allupper lip tumors being benign and a high-er proportion
oflower lip tumors beingmalignant.Salivary gland neoplasms ofthe tongue and buccal
mucosa tend to bemalignant and require wide soft tissue dis-section to obtain
margins.The Sublingual GlandLess than 1% ofall salivary gland tumors occur in the
sub-lingual gland but almost 100% are malig-nant.Surgical approach will be dictated
bythe histology and required access for mar-gins.In most cases we have preferred a
lipsplit and mandibulectomy to allow goodvisualization ofthe tumor,direct examina-
tion ofthe mandibular lingual corticalplate,and the ability to trace back the lin-
gual nerve when necessary.Obstructive DiseaseObstruction to the salivary glands is
usual-ly seen in the submandibular and parotidglands.It may be due to calcified
stones(most common in the submandibulargland) or mucous plugs (most common inthe
parotid) or strictures ofthe duct.Stoneformation is classically due to stasis
offlow,infection,and alteration ofthe ductcontents.Calcified stones are formed
bythe precipitation ofcalcium salts around anidus ofmucous plugs,epithelial
cells,ormicroorganisms.Approximately 80% ofsialoliths occur in the
submandibulargland.14Microliths in the minor salivaryglands have been described.As
calcified sialoliths increase in sizethey may give rise to symptoms,especiallywhen
they are present in the duct.Classi-cally the patient reports pain and swellingwhen
eating or drinking or sometimeseven from the smell offood (Figure 35-4).Examination
ofthe gland may show a ten-der swelling with inability to milk salivafrom the duct
orifice.Plain radiography is used to demon-strate calcified stones,the lower
occlusalfilm for the submandibular gland,and anocclusal or periapical dental film
held inthe cheek for the parotid.Lateral obliquemandibular films or panoramic radi-
ographs will show parotid duct stones andcalcified stones in the hilum or
glandularsubstance ofthe submandibular gland.CTFIGURE35-3Recurrent low-grade
polymorphousadenocarcinoma ofthe palate postmaxillectomywith invasion ofthe orbital
floor and orbital fat.FIGURE35-4Right submandibular glandswelling and sialadenitis
secondary to anobstructing sialolith.
Salivary Gland Disease and Tumors675scans and ultrasonography have also
beenused.When a noncalcified (mucous plug)obstruction is suspected,sialography
maydemonstrate a filling defect (Figure 35-5).Acute infection should be managed
withantibiotics prior to sialography.Treatmentofthe stone will depend on its
location.Submandibular GlandAnterior DuctIfthe stone is palpable inthe anterior
floor ofthe mouth close to theorifice ofWharton�s duct,an intraoralapproach may be
used.Although the ante-rior duct is traditionally regarded as a linebetween the
first molars,the floor ofthemouth slopes downward following themylohyoid muscle as
the premolars arereached,and technical difficulty isincreased as the stone is more
distal (Fig-ure 35-6).Initially a suture is passedbehind the sialolith around
Wharton�sduct to use as a traction suture,tenting theduct upward and preventing
posterior dis-placement ofthe stone during surgicalmanipulation.An incision in line
with theduct is made through the mucosa and dis-section carried down to the
duct.This isopened in its long axis allowing removal ofthe stone.The posterior
suture is removedand the gland is milked or explored with alacrimal probe to find
other stones.Theduct is sutured open to the edges ofthemucosa (fish tailed) to
prevent stricture.Posterior DuctStones in the posteriorsubmandibular duct are much
more tech-nically difficult to remove intraorally,requiring general
anesthesia,excellentlight,and retraction,as well as the help ofan assistant to push
the gland upward intothe mouth from extraorally.Even so,irri-tating bleeding can
occur and the lingualnerve must be visualized and protected(see Figure 35-6).Stones
in the Hilum or GlandWhen the stone is below the posterior edgeofthe mylohyoid
muscle,removal ofthegland is necessary.Although intraoral sub-mandibular gland
excision has beendescribed,the potential for bleeding frombranches ofthe facial
vein and artery andpossible scarring ofthe anterior pole ofthe gland to the
mylohyoid muscle canmake this a technically challenging andhazardous procedure.15We
believe that theconventional cervical approach gives thebest access and is the
safest procedure.Under general anesthesia an approxi-mately 5 cm incision is made
over the sub-mandibular gland at 11/2- to 2-fingerbreadths below the mandible.This
incisionshould be parallel to the neck skin creases,not to the lower border ofthe
mandible(Figure 35-7).The platysma is sectionedand the inferior pole ofthe
submandibulargland visualized.The gland is exposed bysubcapsular dissection at the
inferior poste-rior pole.Blunt finger dissection will releasethe deep surface ofthe
gland.The authorsdo not routinely tie the facial artery andvein at this stage as
these can usually be dissected offthe gland,although clipping FIGURE35-5A,Sialogram
showing a large cal-cified stone in the hilum,with dilated intraglan-dular
ducts.Note the filling defect at the proxi-mal duct from the mucous plug
(arrow).B,Thefilling defect is confirmed by this sialogram to beat the terminal
duct (arrow).ABFIGURE35-6Lateral oblique radiograph ofthemandible showing the
entire Wharton�s ductoccupied by calcified sialolith.Note how thestone passes
inferiorly and deeply,the fartherposteriorly it is placed (arrows).FIGURE35-
7A,Incision for submandibular glandexcision parallel to the neck crease.B,Sub-
mandibular gland mobilized and retracted throughthe wound.The arrowpoints to the
lingual nerve inthe superior part ofthe wound.AB
676Part 5: Maxillofacial Pathologymultiple arterial branches to the gland canbe
tedious.The anterior pole ofthe sub-mandibular gland is mobilized offthemylohyoid
muscle,and in cases ofchronicsialadenitis,sharp dissection may be neces-sary due to
dense fibrosis.The superiorpole ofthe gland is dissected in a subcapsu-lar plane
and the gland mobilized posteri-orly.The posterior edge ofthe mylohyoidmuscle is
retracted to expose the lingualnerve and the branch to the gland is tiedand
sectioned (see Figure 35-7B).The sub-mandibular duct is dissected superiorlyinto
the floor ofthe mouth as far as possi-ble,tied,sectioned,and the gland
removed.Parotid GlandMost obstructive symptoms in the parotidgland are associated
with noncalcifiedstones or mucous plugs.Although thesecan sometimes be removed with
tweezersfollowing duct dilatation or �milked�from the duct,they often cause
repeatedbouts ofpain and swelling.Sialography ishelpful in evaluating the extent
ofdamageto the ductal architecture.Sialograms mayshow changes varying from mild
sialecta-sis to gross dilatation ofStensen�s ductwith loss ofsecondary and tertiary
ducts(Figure 35-8).Sialograms are frequentlyhelpful symptomatically,with cure
orimprovement in many patients.Inadvanced cases with no improvement,parotidectomy
may be required.Stones in the Terminal DuctRadi-ographically opaque stones at
Stensen�spapilla can be managed intraorally in asimilar manner to those ofthe
anteriorportion ofWharton�s duct.Followingplacement ofa posterior traction
suture,the duct is opened with an incision run-ning in the long axis ofthe
duct.Stones in the Posterior DuctWhen thestone involves the extraglandular
portionofthe duct lateral to the buccinator mus-cle,both intraoral and extraoral
approach-esare described.16,17The intraoralapproach involves a Y-shaped
mucosalincision,dissection through the buccina-tor muscle,and the use ofa traction
sutureto pull the duct into the mouth.The extra-oral approach requires the duct to
be dis-placed laterally with a finger placed in themouth,with blunt dissection down
to thestone,avoiding the facial nerve.Parotid Gland StonesStones at thehilum ofthe
gland or intraglandularstones usually require a parotidectomy ifthey are
symptomatic.The facial nervedissection may be challenging due toextensive fibrosis
(Figure 35-9).Nonsurgical ApproachesMiniature endoscopes have been used tovisualize
sialoliths and remove them withbaskets.18Lithotripsy has also beenattempted either
via endoscopes (intracor-poreal) or extracorporeally.Intracorporeallithotripsy uses
shock waves produced bylasers,electrohydraulic sources,or a pneu-moballistic
source.In a review of6 seriesofextracorporeal lithotripsy ranging from33 to 104
stones,Escudier reported astone-free range of18.2 to 52.9% withresidual fragments
occurring in 47.1 to81.8% ofcases.19Mucoceles and RanulasMucoceles are mostly due
to extravasationofmucus from a salivary gland,although afew are true retention
phenomena.Themost common site is the lower lip,due totrauma (usually following an
accidentalbite in a child).Mucoceles are simple totreat and they should not recur
iftheunderlying damaged minor salivary glandhas been removed.Following a vertical
inci-sion through the mucosa over the muco-cele,a number ofminor salivary glands
areusually identified.As it may be impossibleFIGURE35-8Sialogram showing gross
destruc-tion ofthe parotid ductal architecture withdilatation ofthe glandular ducts
into largemucus-filled sacs.FIGURE35-9A,Computed tomography scanshowing a large
parotid stone at the hilum ofthegland.B,Parotid duct opened to show thesialolith in
situ,following parotidectomy.AB
Salivary Gland Disease and Tumors677to identify the damaged gland,all theseminor
glands should be removed beforecarefully suturing the mucosal incision.Ranulas are
large retention phenomenathat occur in the floor ofthe mouth in rela-tion to the
sublingual gland.They may belarge enough to elevate the tongue andinterfere with
speech and swallowing (Fig-ure 35-10).Where dehiscence in the mylo-hyoid muscle
occurs,the mucus can draininto the submandibular space as a �plung-ing ranula.�The
treatment ofranulas hasbeen reviewed at length in a classic paper byCatone.20He
concluded that definitivetherapy was removal ofthe sublingualgland.Several large
series have been report-ed comparing sublingual gland excisionwith so-called
marsupialization,demon-strating 100% cure for gland excision and43 to 63% cure for
marsupialization.21,22Despite this evidence some authoritiesstill plead the case
for marsupialization or�marsupialization with packing,�whichthey claim has a lower
recurrence rate of10 to 12%.23We subscribe to the view thatranulas should be
treated by sublingualgland excision.An intraoral approach is made with anincision
along the axis ofthe gland lateral tothe ductal orifices.The submandibular ductis
identified,either by dissection or follow-ing cannulation with a lacrimal
probe.Thegland is dissected in a subcapsular planewith meticulous hemostasis.At its
posteriorpole the lingual nerve is identified as itcrosses the duct and is
preserved.The sub-lingual gland is dissected from anteriorly,and the final excision
is the posterior poleafter visualizing the lingual nerve.References1.Lamelas
J,Terry JH,Alfonso JE.Warthins tumor;multicentricity and increasing incidence
inwomen.Am J Surg 1987;154:347�51.2.Snyderman C,Johnson JT,Barnes EL.Extra-parotid
Warthin�s tumor.Otolaryngol HeadNeck Surg 1986;94:169�75.3.Lack EE,Upton
MP.Histopathlogic review ofsalivary gland tumors in childhood.ArchOtolaryngol Head
Neck Surg 1988;114:898�906.4.Ampil FL,Misra PP.Factors influencing sur-vival
ofpatients with adenoid cystic carci-noma ofsalivary glands.J Oral MaxillofacSurg
1987;45:1100�10.5.Castle JT,Thompson LD,Frommelt RA,et al.Polymorphous low grade
adenocarcinoma:a clinicopathologic study of164 cases.Can-cer
1999;86:207�19.6.Lindberg LG,Ackerman M.Aspiration cytol-ogy ofsalivary gland
tumors � diagnosticexperience for 6 years oflaboratory work.Laryngoscope
1976;86:584�94.7.Ord RA.Surgical management ofparotidtumors.Atlas Oral Maxillofac
Surg Clin NAm 1995;7:529�64.8.Witt RL.The significance ofthe margin inparotid
surgery for pleomorphic adenoma.Laryngoscope 2002;112:2141�54.9.To EW,Pang PC,Chiu
GM.The use ofmodi-fied rhytidectomy for parotidectomy [let-ter].Br J Plast Surg
2000;531:80.10.Gooden EA,Gullane PJ,Irish J,et al.Role ofthesternocleidomastoid
muscle flap preventingFrey�s syndrome and maintaining facialcontour following
superficial parotidecto-my.J Otolaryngol 2001;30:98�101.11.Kaplan MJ,Johns
ME.Salivary gland cancer.Clin Oncol 1986;5:525�47.12.Pogrel MA.The diagnosis and
management ofsalivary gland tumors.Atlas Oral Maxillo-fac Surg Clin N Am
1993;5:319�30.13.Brookstone MS,Huvos AG.Central salivarygland tumors ofthe mandible
and maxilla:a clinicopathologic study of11 cases withreview ofthe literature.J Oral
MaxillofacSurg 1992;50:229�36.14.Berry RL.Sialadenitis and sialolithiasis:diag-
nosis and management.Atlas Oral Maxillo-fac Surg Clin N Am 1995;7:479�504.15.Miloro
M.The surgical management ofsub-mandibular gland disease.Atlas Oral Max-illofac
Surg Clin N Am 1998;6:29�50.16.Baily BJ,editor.Anatomy and physiology ofthesalivary
glands.In:Head and neck surgery �otolaryngology.Vol 1.Philadelphia
(PA):JBLippincott;1993.p.453.17.Ord RA.Salivary gland disease.In:Fonseca
RJ,editor.Oral and maxillofacial surgery.Vol 5.Philadelphia (PA):WB
Saunders;2000.p.279�80.18.Nahlieli O,Baruchin AM.Sialoendoscopy:three years
experience as a diagnostic andtreatment modality.J Oral Maxillofac
Surg1997;55:912�8.19.Escudier MP.The current status and possiblefuture for
lithotripsy ofsalivary calculi.Atlas Oral Maxillofac Surg Clin N
Am1998;6:117�31.20.Catone GA.Sublingual gland mucous escape.Pseudocysts ofthe oro-
cervical region.Atlas Oral Maxillofac Surg Clin N Am1995;7:431�77.21.Yoshimura
Y,Obara S,Kondoh T,Naitoh ST.Acomparison ofthree methods used for thetreatment
ofranula.J Oral Maxillofac Surg1995;53:280�2.22.Crysdale WS,Mandelsohn JD,Conley
S.Ranulas-mucocoeles ofthe oral cavity experience in 26children.Laryngoscope
1988;98:296�8.23.Baurmash HD.Mucocoeles and ranulas.J OralMaxillofac Surg
2003;61:369�78.FIGURE35-10Large ranula overlapping theocclusal plane in a 10-year-
old boy.
CHAPTER 36Management ofMucosal andRelated Dermatologic DisordersMichael
W.Finkelstein,DDS,MSSteven D.Vincent,DDS,MSFungal Disease ofthe Oral CavityFungal
diseases ofthe oral cavity can beclassified as superficial or deep in relationto
the primary tissue(s) involved in theinfection.Most oral fungal infections
areopportunistic in nature.Persons living ingeographic areas endemic to one or
moreofthese fungi may show immunologicreactivity to the surface antigens
withouthaving historic features ofactive disease.The deep fungi usually infect the
lungsbefore dissemination to other organ sys-tems,including the oral cavity.Deep
fun-gal diseases,including histoplasmosis,coc-
cidioidomycosis,blastomycosis,andcryptococcosis,present clinically as chron-ic
proliferative ulcerated granulomatoustissue lesions that may be single or multi-ple
and painful or asymptomatic.Theymay simulate clinical features ofa malig-nant
neoplasm.CandidosisAlthough numerous deep and superficialfungal diseases can
involve the oral cavity,candidosis is by far the most common.Theterm candidosisis
the correct nomencla-ture describing an infection with one ofseveral species
ofCandidaorganisms.However,many publications use the termcandidiasisto describe the
same disease,even though the suffix �-iasis�is character-istically used to describe
parasitic infec-tions such as schistosomiasis or amebiasis.One or more species
ofCandida can befound as a component ofthe normal oralflora in about 60% ofhealthy
adults.Theorganism can exist in one ofthree states:theyeast form consisting
ofblastospores mea-suring 1.5 �m to 5 �m in diameter,elongat-ed pseudohyphae,and
chlamydosporesmeasuring 7 �m to 17 �m in diameter.In itscommensal state,the
organism usuallyexists only as spores or pseudohyphae.Candidosis is usually an
opportunis-tic infection caused by a localized or sys-temic suppression ofthe
immune sys-tem.Commonly recognized causes ofcandidosis include the use ofbroad-
spectrum antibiotics,xerostomia,chron-ic diseases ofthe immune system,andtherapy
for malignant disease includingchemotherapy or radiation.Oral infections involving
Candidaspecies may appear as one ofthree clinicalforms:acute,chronic,and mucocuta-
neous.Candidosis characteristically showserythematous mucosa with or
withoutoverlying white plaques,which may berubbed away with light abrasive
pressure(Figure 36-1).The dorsum ofthe tongueusually shows diffuse patches
ofpapillaryatrophy (Figure 36-2).Occasional small orconfluent ulcerations may be
noted.Angu-lar cheilitis is a prominent clinical featureoforal candidosis.Patients
characteristi-cally complain ofan oral �burning�sensa-tion.Denture-sore
mouth(denture stom-atitis) is a clinical term used to describepatients with mucosal
erythema orinflammatory papillary hyperplasia,usu-ally related to a localized
candidosis undera removable prosthodontic appliance.Clinical features oforal
candidosisusually include foci ofmucosal erythema,which is the result
ofinflammation andmucosal atrophy,areas ofulceration,andsometimes white
pseudomembranousplaques,which are seen to consist ofcan-didal pseudohyphae and
spores ifexam-ined microscopically (Figure 36-3).Thesepseudomembranous
plaques,althoughusually present in acute-onset cases ofcandidosis,are frequently
absent in casesofchronic candidosis such as those relatedto prosthetic
appliances.The lack ofwhitepseudomembranes should not thereforepreclude
consideration ofcandidosis incases ofchronic mucositis.Candidosis hasalso been
noted in lesions characterized byfocal increases in keratinization such aslichen
planus,focal keratosis with or
680Part 5: Maxillofacial Pathologywithout dysplasia (leukoplakia),hairytongue,hairy
leukoplakia,and even squa-mous cell carcinoma.A recent study showedthe presence
ofcandidal hyphae and sporesin 31% ofbiopsy specimens showing orallichen
planus.However,a possible cause-and-effect relationship between candidosisand
increased keratinization ofthe epitheli-um is difficult to show.Cytologic
PreparationsClinical diag-noses oforal candidosis are easily andquickly confirmed
using exfoliative cytol-ogy studies.Cytologic specimens are pre-pared using a
wooden tongue blade toscrape the oral mucosa ofthe involvedareas;the exfoliated
material is smearedonto a glass slide.The slide is air dried for5 minutes and then
fixed in ethanol (hairsprays with a high alcohol content can beused as fixatives in
a clinical setting).Theslides are stained with potassium hydrox-ide,periodic
acid�Schiffmodified forfungi,or any one ofseveral other stainsthat delineate the
fungal hyphae andspores.The infection can be further delin-eated as a species using
cultures onSabouraud dextrose or blood agar.Oral candidosis is the most
commondiagnosis made in patients whose chiefcomplaint involves a chronic
nonspecificmucositis or burning sensation.Other dis-eases included in the clinical
differentialdiagnosis include lichen planus,pemphi-gus,pemphigoid,and medication-
relatedtoxic mucositis.As stated above,candido-sis may be a secondary component
ofother chronic oral diseases or localizedepithelial thickening
lesions.ManagementThe initial management oforal candidosis following confirmation
ofthe clinical impression with exfoliativecytology studies is the use ofone or
moreantimycotic agents.Ofgreatest therapeuticvalue in most patients is
ketoconazole,administered in one 200 mg tablet dailyfor 10 to 14 days.Ifsystemic
factors con-traindicate the use ofketoconazole,clotri-mazole troches,administered
in one 10 mgtablet dissolved in the oral cavity up to fivetimes daily,or
chlorhexidine in a 0.12%mouthrinse in a 5 to 10 mL dose twicedaily NPO for 1
hour,are usually effective.Nystatin powder or cream may be used toline dentures in
patients with denture soremouth.Ofvital importance is a review ofthe patient�s past
medical history and current medical status in an attempt toidentify the causative
factors for thisopportunistic infection.In patients whohave no identifiable
predisposing factorsor ifthe predisposing factors are not cor-rectable,multiple
recurrences may beanticipated.Median Rhomboid GlossitisAlthough the early reports
ofmedianrhomboid glossitis suggested an originfrom the tuberculum impar,many
investi-gators now favor classification ofthis lesionas a localized candidosis
(Figure 36-4).1Although the exact cause-and-effect rela-tionship is
unclear,Candidaspp are foundin association with many ofthese lesions,and recent
studies have shown the preva-lence ofmedian rhomboid glossitis to behigher in
adults than in children,a findingcontrary to the developmental theory oforigin.The
lesion appears clinically as anFIGURE36-1Ato C,Oral
candidosis.Whitepseudomembranous plaques that can be removedwith light abrasion
involving buccal,lateral-glossal,and soft palatal mucosa.ACBFIGURE36-2Oral
candidosis.Atrophy ofthefiliform papillae on the dorsal tongue.
Management ofMucosal and Related Dermatologic Disorders681erythematous patch,which
may be roughlyovoid or rhomboid in shape,is asympto-matic,and is located on the
dorsal midlineofthe tongue just anterior to the circum-vallate papillae.The area is
usually smoothand devoid offiliform papillae.Unless the lesion is
symptomatic,notreatment is indicated.For symptomaticcases,management with
antifungal regi-mens is usually beneficial.The lesionsare generally regarded as
having nomalignant potential.Bacterial Infections ofOralMucosaAcute Necrotizing
UlcerativeGingivitisAcute necrotizing ulcerative gingivitis is arare and clinically
painful ulcerative dis-ease that presents with progressive necro-sis ofthe
interdental papillae,usuallybeginning in the mandibular incisorregion.The
interdental papillae necrosismay spread or remain localized.Thenecrotic papillae
are usually covered with apseudomembrane ofnecrotic epithelialcells,plaque,and
microbial organisms.The patient may have systemic signs andsymptoms including fever
and regionallymphadenopathy.Patients have a charac-teristic rancid halitosis caused
in part bythe presence ofnecrotic material in theoral cavity.2,3The probable cause
ofthis diseaseinvolves a symbiotic infection by twobacteria,a fusiform bacillus and
a spiro-chete.However,inoculation ofthese bac-teria into healthy tissues does not
pro-duce disease,and because moderatenumbers ofthese organisms can befound in
otherwise clinically healthymouths,other factors such as stress andsmoking,both
ofwhich can affect thehost�s immune system,have been impli-cated as causative
factors.Local d�bridement by scaling andcurettage,sometimes under local anesthe-
sia,usually brings about a marked reliefofsymptoms.A therapeutic dose
ofanantibiotic such as tetracycline may be indi-cated for patients with extensive
disease orevidence ofregional lymph node enlarge-ment.The use oftopical antiseptics
suchas chlorhexidine or diluted hydrogen per-oxide is ofvalue for initial
management ofthe lesions.The lesions usually heal within2 to 3 weeks,and the
interdental papillaeoften regenerate,seldom requiring gingi-val surgery.Improved
oral hygienethrough use ofa soft-bristled toothbrushand floss is the best long-term
therapy andis aimed at recurrence prevention.SyphilisSyphilis is a venereal
infection that hasbeen documented extensively,beginningin about the fourteenth or
fifteenth centu-ry.Before the introduction ofpenicillin inthe early 1940s,over
500,000 new caseswere documented in the United Stateseach year.The Centers for
Disease Controland Prevention reported 6,657 cases ofprimary and secondary syphilis
in theUnited States in 1999.4The disease is caused by the spirocheteTreponema
pallidumand is acquired bycontact with an active lesion.The spiro-chete can also be
transmitted by trans-fused blood,and it crosses the placentalbarrier from maternal
to fetal circulation.In cases involving transmission froman active lesion,the site
ofinfection formsa chancre or ulceration,which is usuallyaccompanied by regional
lymphadenopa-thy.The ulcer and lymphadenopathy usu-ally persist for 3 to 10 weeks
and thenresolve spontaneously.This initial diseasemanifestation constitutes
primarysyphilis.Assuming no treatment is ren-dered,secondary syphilis develops
follow-ing a latency period ofseveral weeks.Inthis stage the now widely
disseminateddisease causes fever,malaise,a macu-lopapular rash,and multiple
ulcerationsor mucous patches on mucosal surfaces.Broad-based,proliferative slightly
raisedulcerations known as condyloma latummay occur during secondary syphilis.These
lesions also persist for 5 to 10 weeksand then resolve without
treatment.Ifthepatient is still untreated,several recur-rences ofthe manifestations
ofsecondarysyphilis may occur or the disease mayenter a prolonged latency period
lastingmonths or years.5�7Fortunately tertiary syphilis developsin only a few
patients.There are manymanifestations oftertiary syphilis,owingto the extensive
involvement oforgan sys-tems.Central nervous system involvementcan present as a
generalized paralysis ortabes dorsalis.Inflammation ofthe circu-latory system can
result in aneurysms,especially in the aorta.Intraoral manifes-tations include
granulomatous prolifera-tions known as gummas,as well as a poor-ly understood
generalized glossitis.FIGURE36-3Oral candidosis.Cytologic prepa-ration showing
hyphae and spore form charac-teristic ofCandidasp (�160 original magnifica-tion;
stained with periodic acid�Schiffstainmodified for fungal organisms).FIGURE36-
4Median rhomboid glossitis.A localized form ofatrophic candidosis.
682Part 5: Maxillofacial PathologyThe diagnosis ofsyphilis is usuallymade following
serologic studies,includ-ing Venereal Disease Research Laboratoryand fluorescent
treponemal antibodyabsorption tests.The treatment ofchoicefor syphilis remains 2.4
million U ofben-zathine penicillin.For patients allergic topenicillin,erythromycin
or tetracyclinemay be substituted.GonorrheaGonorrhea is currently the most wide-
spread human bacterial infection in theworld and is caused by Neisseria gonor-
rhoeae,a gram-negative diplococcus.Transmission is usually venereal,involving
genital,oral,or pharyngealmucosa.The incubation period is about 1 week with the
initial features ranging fromno evidence ofdisease to mucosal ulcers andregional
lymphadenopathy.These features,although reported in the oral cavity,are
rarecompared with the muchmore commonpharyngeal infection.Therefore,inpatients who
present with chronic apht-hous-like ulcerations and erythema pre-dominantly
involving the pharyngealmucosa rather than the oral mucosa,agonorrheal infection
should be part oftheclinical differential diagnosis.The micro-scopic features are
nonspecific,and theclinical features ofthe disease seldom indi-cate a biopsy.The
diagnosis is based ondemonstration ofthe organism in culturemedia or through the
use ofimmunofluo-rescent antibody techniques.8,9The treatment ofchoice for
gonorrheacontinues to be penicillin.Occasionalpenicillin-resistant strains are
noted dur-ing sensitivity cultures and require man-agement with alternative
antibiotics.Pigmented Lesions ofOralMucosa and Skin Pigmented lesions oforal mucosa
andskin can be divided into generalizedlesions,which are diffuse and multifocal,and
localized lesions involving one orseveral locations.Generalized PigmentationsSome
ofthe common causes ofgeneral-ized pigmentations are listed in Table 36-1.The most
common type ofgeneralizedpigmentation is hereditary or racial.Thepigmentation is
diffuse,symmetric,andmost commonly located on the gingiva andlabial
mucosa.Pregnancy and ingestion oforal contraceptives may produce
melaninpigmentation called chloasma or melasma.Pigmented macules occur on the
labialmucosa,forehead,malar prominences,andaround the eyes and lips.10�13Smokers
sometimes have melanin pig-mentation ofthe attached gingiva.Numer-ous medications
may cause pigmentationofskin and/or oral mucosa.Antimalarialssuch as
quinine,chloroquine,and amodi-aquine may cause pigmentation in approx-imately 25%
ofpatients taking them for > 3 to 4 months.Cancer chemotherapeuticdrugs such as
busulfan,cyclophosphamide,and bleomycin have been reported to
causepigmentation,primarily ofskin.Hydan-toin may produce facial
pigmentationresembling chloasma.Minocycline maycause pigmentation
ofskin,bones,teeth,oral mucosa,and the thyroid.Pigmenta-tion secondary to heavy
metals is due todeposition ofmetals in the skin and oralmucosa.This type
ofpigmentation is notcommonly seen today because oftheirdecreased value as
therapeutic agents.Peutz-Jeghers syndrome is character-ized by multiple pigmented
macules ofthehands and feet;areas surrounding themouth,eyes,and nose;and
intraorally onthe buccal mucosa,labial mucosa,gingiva,and palate.Multiple
hamartomatouspolyps are present in the gastrointestinaltract.Patients with this
syndrome have anincreased incidence ofcancer both withinand outside the
gastrointestinal tract.Patients with Addison�s disease haveincreased pigmentation
ofthe skin,lips,gingiva,buccal mucosa,and tongue.Sys-temic manifestations are
prominent andinclude malaise,weakness,nausea,vomit-ing,diarrhea,weight loss,and
hypotension.Neurofibromatosis is a relatively com-mon autosomal dominant inherited
syn-drome.Virtually all patients have six ormore brown cutaneous macules > 1.5 cmin
diameter known as caf� au lait spots.Numerous freckles 2 or 3 mm in diameterare
often present in the axilla and otherintertriginous regions.Other features
ofneurofibromatosis include multiple neu-rofibromas,central nervous
systemtumors,seizures,intellectual handicap,and speech impediments.Albright�s
syndrome consists ofpolyostotic fibrous dysplasia plus multiplecaf� au lait
spots.Endocrine abnormali-ties,most commonly precocious pubertyin young females,are
also present.Localized Pigmented LesionsLocalized pigmented lesions can be divid-ed
into four classes based on their causeand clinical features:(1) melanocytic,Table
36-1Generalized PigmentationsofSkin and Oral MucosaHereditary (racial)Pregnancy
(chloasma,melasma)Smoking (smoker�s melanosis)MedicationsAntimalarials Oral
contraceptivesBusulfanCyclophosphamideBleomycinPhenytoinPhenothiazinesMinocyclineHe
avy metals BismuthLeadSilverGoldArsenicMercurySyndromes and systemic diseasesPeutz-
Jeghers syndromeAddison�s disease Neurofibromatosis Albright�s syndrome
Management ofMucosal and Related Dermatologic Disorders683(2) vascular,(3)
extravasated blood,and(4) tattoos.Melanocytic LesionsMelanocytic lesionsare due to
increased amounts ofmelaninpigment in the tissue and/or a
proliferationofmelanocytes or nevus cells.Melanocyticlesions are
gray,brown,black,or blue anddo not blanch on pressure.EphelidesThe ephelis or
freckle is asmall circumscribed brown or black mac-ule that occurs on sun-exposed
areas ofskin.It appears in childhood and darkensin the summer and fades during the
win-ter.Microscopically,the ephelis showsincreased melanin in the basal cell layer
ofthe epidermis but no increase in the num-ber ofmelanocytes.Ephelides are not pre-
malignant and require no treatment oncethe diagnosis is established.Oral Melanotic
MaculesThe oral melan-otic macule is an oral mucosal pigmenta-tion with similar
microscopic features toephelis.The lesions are well-circumscribedflat macules that
are gray,brown,blue,orblack.Most are 1 to 3 mm in diameter.Themost common locations
are the vermilionborder ofthe lip,gingiva,and buccalmucosa.They are often confused
clinicallywith tattoos and nevi.14,15Microscopically,oral melanotic mac-ules show
increased melanin in the basal celllayer,lamina propria,or both.The cause oforal
melanotic macules is unknown,although they may be an atypical manifesta-tion
ofphysiologic pigmentation becausethe microscopic appearance is identical toracial
pigmentation.These macules do notrecur or undergo transformation intomelanoma,but
they may be difficult to dis-tinguish it from nevi or melanoma in situ.They should
be excised for microscopicdiagnosis or checked frequently.Lentigo SimplexLentigo
simplex is a mac-ular brown-to-black lesion that is not associ-ated with sun
exposure and may occur onany skin surface.It is not premalignant andrequires
excision only for microscopic diag-nosis.Microscopically,lentigo
simplexdemonstrates an increased number ofmelanocytes in the basal cell
layer,anincreased amount ofmelanin in themelanocytes and the basal
keratinocytes,andelongation ofthe rete ridges.Macrophagescontaining melanin
(melanophages) are pre-sent in the upper dermis.16NeviA nevus is a proliferation
ofnevuscells or melanocytes.Nevi are extremelycommon lesions on skin but are
relativelyuncommon on oral mucosa.Most nevi ofskin are absent at birth and appear
inchildhood.They progress through a seriesofstages,and then decline in number
withincreasing age.Nevi begin as junctionalnevi,with nests ofnevus cells at the
dermal-epidermal junction.Compoundnevi demonstrate nevus cell nests in the epi-
dermis and upper dermis.Intradermal nevihave nevus cell nests only in the
dermis.Clinically,junctional nevi are flat pig-mented macules.The compound nevus
isslightly elevated and sometimes has apapillomatous surface.Intradermal neviare
dome shaped and pedunculated.Com-pound and intradermal nevi may not
bepigmented.Normal nevi are round to oval,have a smooth border,and are
sharplydemarcated from the surrounding skin.They are most commonly found on sun-
exposed skin above the waist.17,18Dysplastic nevi are precursors tomelanoma.They
may occur sporadicallyor in an autosomal dominant inheritedsyndrome in which they
are quite numer-ous.Dysplastic nevi have irregular bordersthat are indistinct and
fade into the sur-rounding skin.They may demonstrate amixture ofcolors,including
tan,darkbrown,and pink.Dysplastic nevi are typi-cally larger than normal nevi.It is
not necessary to remove normalcutaneous nevi unless they are irritated
byclothing.Since dysplastic nevi have anincreased potential for developing
intomelanoma,they should be removed.Inpatients with numerous dysplastic nevi,the
lesions should be closely monitoredand excised ifthey change.Nevi ofthe oral mucosa
are usuallybetween 1 and 6 mm in diameter and aremost commonly located on the
hardpalate and buccal mucosa.They are occa-sionally nonpigmented.The majority
oforal nevi are raised and thickened,but asignificant number may be
flat.Microscopically,the majority oforalnevi have been reported as intramucosal,but
blue,compound,and junctional nevialso occur.17Because ofthe small number ofreported
cases oforal nevi,their potentialfor evolving into melanoma is not known.Because
ofthis,lesions in which nevus ispart ofthe clinical differential diagnosisshould be
completely excised.MelanomasMelanoma is a malignantneoplasm ofnevus cells or
melanocytes.Microscopically,melanomas begin at thedermal-epidermal junction and
then maydemonstrate two different patterns ofgrowth.In radial growth,or melanoma
insitu,melanoma cells grow laterally alongthe dermal-epidermal junction but do
notinvade the underlying dermis.A melanomamay remain in the radial growth phase
foryears,and during this time it does notmetastasize.During vertical growth
themelanoma cells grow into the dermis andare capable ofinvading vascular
channelsand nerves and metastasizing.19�22Microscopically,melanoma cells
aredescribed as epithelioid or spindleshaped.Epithelioid cells are round tocuboidal
and form nests.The spindle cellsare elongated and do not form nests.Thetumor cells
demonstrate nuclear pleo-morphism,anaplasia,and mitotic figures.The amount
ofmelanin within tumorcells is variable.The Fontana-Massonstain demonstrates
melanin in some ofthe amelanotic-appearing tumor cells.The dopa reaction is more
reliable for
684Part 5: Maxillofacial Pathologydemonstrating melanin,but it requiresfresh
tissue.There are four types ofcutaneousmelanoma:lentigo maligna
melanoma,superficial spreading melanoma,acral-lentiginous melanoma,and
nodularmelanoma.Lentigo maligna (melanotic freckle ofHutchinson) represents lentigo
malignamelanoma in situ.It presents as a brownmacule with black flecks and
irregularmargins located on sun-exposed surfacesofelderly persons.It may remain in
theradial growth phase for 10 to 15 yearsbefore progressing to invasive
lentigomaligna melanoma,indicated by the devel-opment ofnodularity.Superficial
spreading melanoma consti-tutes about 70% ofcutaneous melanomas.It occurs on both
exposed and unexposedsurfaces,most commonly on the upper backin men and lower legs
in women.Thismelanoma has irregular borders and greatvariation in color within one
lesion,includ-ing tan,brown,black,pink,blue,and whiteareas (Figure 36-5).It often
demonstratesnodularity and ulceration.Superficialspreading melanoma remains in the
radialgrowth phase for a shorter time than doeslentigo maligna melanoma and thus
has apoorer prognosis.Acral-lentiginous melanoma is themost common melanoma in
black per-sons.It occurs primarily on the palms,soles,and in association with
nails.It canmetastasize early.Nodular melanoma presents as arapidly growing darkly
pigmented nodulethat is often ulcerated.It is not associatedwith sun exposure.Since
it grows vertical-ly from the beginning,it is often deeplyinvasive by the time it
is diagnosed.Treatment ofcutaneous melanomausually consists ofwide surgical
excision.Chemotherapy is sometimes used,butradiation therapy has not proven
effective.Incisional biopsy is not thought to causemetastasis ofmelanomas.The most
important prognostic factorfor cutaneous melanoma is the thicknessofthe lesion.One
study reported a 10-yearsurvival rate of99.5% for patients withmelanomas < 0.76 mm
thick,as opposedto 48% survival for those with melanomas3 mm and greater in
thickness.23Melanoma oforal mucosa is a rareneoplasm most commonly located on
thehard palate and maxillary gingiva ofpatients > 50 years ofage.About one-third
ofpatients have preexistingmelanosis,or macular hyperpigmenta-tion,which probably
represents radialgrowth ofthe lesion.This may be presentfor years before vertical
growth occurs.Atthe time ofdiagnosis,many oralmelanomas are large,ulcerated,and
havecaused bony erosion.A significant num-ber oftumors are amelanotic.Treatment
oforal melanoma is widelocal excision with or without lymph nodedissection.The
prognosis is quite poor.The5-year survival in one series was only 13%.23This may be
due to the advanced stage oforal melanomas at the time ofdiagnosis.Vascular
LesionsVascular lesions aredue to increased numbers ofblood vessels,or blood
vessels ofincreased diameter.These lesions are compressible,blanch onpressure,and
are red,blue,or purple.HemangiomaHemangioma is a prolif-eration ofblood vessels
that is usually con-genital and may regress spontaneously.Itis commonly found on
the skin and in theoral cavity.Hemangioma ofskin may present as asoft tissue
enlargement or a flat surfacelesion.Nevus flammeus,or port-winestain,is a red-to-
blue macule present atbirth.Sturge-Weber syndrome (encephalo-trigeminal
angiomatosis) includes con-genital port-wine stain in the distributionofthe
trigeminal nerve,hemangiomas ofthe leptomeninges,and ipsilateral heman-giomas ofthe
face,skull,jaws,and oralcavity.The hemangiomas often containcalcifications and may
result in seizuredisorders and other neurologic problems.Hemangiomas ofthe oral
cavity arecompressible red or blue soft tissueenlargements that blanch on
pressure.They present most commonly in the lips,tongue,and buccal
mucosa.Microscopically,hemangiomas areclassified as cavernous or capillary.Cav-
ernous hemangiomas consist oflargevessels lined with a single layer ofendothelial
cells,whereas capillaryhemangiomas contain numerous smallervessels.During their
period ofgrowth,capillary hemangiomas demonstratemarked endothelial proliferation
andonly a few capillary lumina.Hemangiomas are unencapsulatedlesions and can be
difficult to remove sur-gically.Other treatment modalitiesinclude sclerosing
agents,cryotherapy,andlaser surgery.Treatment is not recom-mended unless lesions
are a functional orcosmetic problem.VarixA varix is a dilated vein.It occursmost
commonly on the lip,buccal mucosa,and ventral surface ofthe tongue.Itincreases in
frequency with increasing age.The typical varix is blue,compressible,and blanches
on pressure.A thrombosedvarix is firm to palpation,does not blanch,and resembles a
nevus.FIGURE36-5Melanoma.Alteration in color ofa nevocellular nevus with apparent
expansioninto the surrounding normal skin.
Management ofMucosal and Related Dermatologic Disorders685No treatment is necessary
for a varixunless nevus or melanoma is included inthe clinical differential
diagnosis.Kaposi�s SarcomaKaposi�s sarcoma is amalignancy ofendothelial cell origin
thatoccurs in three settings.It was first describedas a disease involving the skin
ofthe distalportion ofthe lower extremities in elderlymales ofMediterranean or
Jewish origin.Itis also endemic in black African childrenand adults.The African
form involves vis-cera and lymph nodes as well as skin.Recently it has become a
common lesion inpatients with immunosuppression sec-ondary to organ transplantation
or humanimmunodeficiency virus (HIV) infection.Kaposi�s sarcoma frequently
involvesthe oral cavity,especially in patients withHIV infection.Oral lesions are
most com-mon on the hard palate and gingiva.Thelesions may be single or
multiple,flat orexophytic,and red,blue,or brown.Theexophytic lesions blanch on
pressure.The microscopic appearance ofearlylesions ofKaposi�s sarcoma
resemblesgranulation tissue.Increased numbers ofdilated capillaries and a chronic
inflam-matory infiltrate are present.Advancedlesions have vascular and spindle cell
com-ponents.The vascular channels are linedwith prominent endothelial
cells.Strandsofpleomorphic spindle cells line narrowslits containing
erythrocytes.Extravasatederythrocytes and hemosiderin in the stro-ma help
distinguish Kaposi�s sarcomafrom fibrosarcoma.Treatment ofKaposi�s sarcoma
includesradiation therapy,surgery,and/orchemotherapy.African patients and
patientswith Kaposi�s sarcoma secondary toimmunosuppression have a poor
prognosis.The disease causes death in 10 to 20% ofelderly males with the
disease.Lesions Owing to Extravasated BloodBecause these lesions are due to the
pres-ence ofblood outside ofblood vessels,they do not blanch on pressure.HematomaA
hematoma is a blood blis-ter or a circumscribed pool ofblood out-side ofa vessel.It
is typically caused bytrauma and is most commonly found onthe buccal mucosa along
the occlusalplane.It appears blue to purple and iscompressible to palpation.A
hematomarequires no treatment and resolves sponta-neously in several
weeks.Ecchymosis and PetechiaeAn ecchymosis,or bruise,is caused by diffuse bleeding
intothe tissue secondary to trauma.It is not pal-pable.It is initially blue but
evolves throughmany color changes before resolving.Petechiae are multiple discrete
roundhemorrhagic spots < 2 mm in diameter.They are more reddish than are ecchy-
moses or hematomas.Petechiae are aresult ofcapillary bleeding.They may beassociated
with a viral disease or a blooddyscrasia.TattoosTattoos are the most commonoral
pigmentation.They are the result ofintentional or accidental implantation offoreign
material,such as amalgam,graphite,ink,or metal,into the skin ororal mucosa.A tattoo
on the hard palateis often a result ofa child falling on apencil held in his or her
mouth andpushing graphite into the tissue.Amal-gam tattoo is usually seen on the
gingiva,alveolar mucosa,buccal mucosa,andfloor ofthe mouth.The most common
presentation ofatattoo is an asymptomatic flat nonthick-ened blue-to-black
pigmentation.Occa-sionally,however,a tattoo may be thick-ened owing to fibrosis or
may enlargebecause ofphagocytosis ofthe foreignmaterial by macrophages or
incorporationofthe material into collagen fibers.Rarely,the foreign material may
incite a foreignbody granuloma with multinucleated giantcells and
macrophages.Radiographs maybe helpful in detecting foreign material inthe
tissue,but not all foreign material canbe visualized radiographically.Excision ofa
tattoo is necessary onlywhen a nevus or melanoma is included inthe clinical
diagnosis.Vesicular,Ulcerated,and Erythematous Lesions Numerous diseases cause
vesicles and/orulcers ofthe oral cavity.Some diseases suchas herpes simplex and
aphthous ulcers areimportant because they are frequentlyencountered in
practice.Other diseasessuch as epidermolysis bullosa and pemphi-gus are serious
life-threatening diseases.Because vesicles are so transient inthe oral cavity,it is
usually impossible todetermine ifan ulcer was preceded by avesicle.Ifa vesicle was
present,then aph-thous ulcers,ulcers ofinfectiousmononucleosis,traumatic
ulcers,andulcers owing to bacteria can be excludedfrom the clinical diagnosis.A
thorough history should be obtainedfrom patients with vesicular/ulcerative dis-
eases and should include the followingquestions:1.How long have the lesions been
present?2.Are the lesions recurrent?3.Ifyes,how often do they recur?4.Do they recur
in the same locations?5.Have you noticed vesicles?6.Have you noticed lesions on the
skin,eyes,or genitals?7.Have you been aware offever,malaise,and lymphadenopathy in
associationwith the lesions?8.What medications do you take?Since there are a large
number ofdis-eases that can cause vesicles or ulcers,one ofthe convenient ways to
classify the diseases isby their cause.The discussion ofvesicular,ulcerated,and
erythematous lesions belowis arranged by the cause
oflesions,forexample,hereditary,viral,or autoimmune.Hereditary
DiseasesEpidermolysis BullosaThe most impor-tant hereditary vesicular/ulcerative
disease
686Part 5: Maxillofacial Pathologyis epidermolysis bullosa (EB).There are atleast
18 types ofEB including some thatare not inherited.The current classification ofEB
isbased on where the split that forms theblisters occurs,inheritance,and
clinicalfindings.Intraepidermal forms are non-scarring and have autosomal dominant
orX-linked inheritance.The split occurswithin the epithelium and is associatedwith
defective tonofilaments ofthe basalsquamous epithelial cells.Junctionalforms ofEB
have autosomal recessiveinheritance and demonstrate skin atrophy.The split occurs
within the basementmembrane and is due to decreased num-bers ofhemidesmosomes and
tonofila-ments.Dermal forms have autosomaldominant or recessive inheritance
withatrophy and scarring ofskin and mucosa.The split occurs in the upper dermis
orlamina propria owing to defects inanchoring fibrils associated with the
basallamina.Typing ofpatients requires the useofelectron microscopy,immunofluores-
cence,and immunohistochemistry.24�26EB simplex Koebner type is anintraepidermal
form.Blisters mainlyinvolve the feet,hands,and neck.Theybegin in infants and are
exacerbated byheat.Abnormal nails are sometimes pre-sent.Oral blisters are
occasionally seen,but the teeth are normal.The diseaseimproves at puberty and is
compatiblewith a normal life span.EB atrophicans generalisata gravisHerlitz type is
a junctional form withautosomal recessive inheritance.Blistersbegin within a few
days after birth andinvolve the hands and feet,followed by thetrunk,face,and
scalp.The nails are lost ordystrophic.Death within the first fewmonths oflife is
common.Oral blistersand ulcers are found in almost all patients.Enamel is
hypoplastic,pitted,and exten-sively involved with caries.EB dystrophica Cockayne-
Tourainetype is a dermal form with autosomaldominant inheritance characterized
byblisters ofthe ankles,knees,hands,elbows,and feet that produce scars.Milia
(epider-mal cysts) are common.Nails are thickand dystrophic.Onset is birth to 5
years ofage,and the condition improves with age.Some patients have oral
bullae.Another dermal type is EB dystrophi-ca Hallopeau-Siemens.It has
autosomalrecessive inheritance.Blisters are presentshortly after birth and may
involve anyskin surface.Scars form and cause con-traction.Formation ofa clawhand
and/ormitten-like hand are common.Nails aredystrophic or absent.The
larynx,pharynx,and esophagus may be involved.Oral bul-lae and scarring may result
in diminishedoral opening,ankyloglossia,tongue atro-phy,loss ofbuccal and
vestibular sulci,andperioral stricture.Teeth have hypoplasticenamel,delayed
eruption,and retention.EB bullosa acquisita is a noninheritedtype that begins in
adulthood.Blistersform in areas oftrauma.Oral lesions havebeen reported but are
rare.27EB is a disease that cannot be cured.The treatment is supportive and sympto-
matic and includes corticosteroids andantibiotics to fight secondary
infections.5Viral InfectionsThe majority ofviral infections are sub-clinical and
asymptomatic.We know oftheir existence because ofthe developmentofantibodies in the
patients.Symptomaticviral vesicular and ulcerative diseases oftenhave systemic
manifestations ofmalaise,fever,tender lymphadenopathy,and lym-phocytosis.They
generally have an acuteonset and a vesicular stage,with the excep-tion ofinfectious
mononucleosis.Multiplelesions are present.The herpesvirus family consists ofherpes
simplex virus (HSV) types 1 and 2,varicella-zoster virus,Epstein-Barr
virus(EBV),and cytomegalovirus.Herpesvirus-es can assume a latent state in the
patient.Cytomegalovirus is important in neonatesand immunocompromised patients;it
isnot discussed further in this chapter.HSVThe primary infection with HSVmay occur
in seronegative patients ofanyage and results in acute herpetic gingivo-
stomatitis.The patient experiences theabrupt onset ofmalaise,fever,and
tendercervical lymphadenopathy.Multiple vesi-cles and ulcers can involve any oral
mucos-al surface and are accompanied by gingivalswelling and erythema.The fluid-
filledvesicles contain numerous virions and areinfectious.The mouth can
becomeextremely painful,resulting in difficultyeating and drinking (Figure 36-
6).After primary infection ofthe oralmucosa,HSVs travel centripetally
alongperipheral nerves to nerve cell bodies ofthe trigeminal ganglion.The
virusesremain latent in the ganglion.Reactivationofthe latent virus causes
transport ofviralFIGURE36-6Aand B,Primary herpetic gin-givostomatitis.Acute-onset
vesicles rupturealmost immediately leaving 1 to 2 mm ulcers ofkeratinized and
nonkeratinized oral mucosa.AB
Management ofMucosal and Related Dermatologic Disorders687genomes to the epithelial
surface,wherereplication occurs.Recurrent lesions mayresult.The most important
factors associ-ated with recurrent lesions are
ultravioletradiation,immunosuppression,and localtrauma.With regard to
immunosuppres-sion,patients with defects in cell-mediatedimmunity have herpes
infections that aremore frequent and severe.28�31The vesicles and ulcers
ofrecurrent(secondary) herpes occur in small clusterson the lip,gingiva,and hard
palate,andthey tend to recur in the same location.Thelesions are often preceded by
a prodrome oftingling,pain,or numbness in the area.Sys-temic manifestations are not
present.Recurrent herpetic lesions are oftenconfused with aphthous ulcers.Theyoccur
on the lip and keratinized oralmucosa,whereas aphthae occur onnonkeratinized
mucosa.Recurrent herpet-ic lesions consist ofmultiple small ulcersin a
group;aphthae consist ofone to sev-eral larger widely distributed ulcers.Herpes
simplex infection ofthe fingeris called herpetic whitlow (Figure 36-7).The primary
infection presents abruptlywith edema,erythema,vesicles,and painin the infected
finger,often accompaniedby fever and axillary and epitrochlear lym-phadenopathy.The
lesions may recur.Either HSV-1 or -2 can infect the oralmucosa and skin.HSV-1 has a
predilectionfor oral mucosa and skin outside ofthegenital area,whereas HSV-2
prefers thegenital region.Genital HSV-1 infectionsand oral HSV-2 infections have a
greatlydecreased incidence ofrecurrence.The diagnosis ofmucocutaneous her-pes is
usually apparent on the basis ofclin-ical features,so biopsy is rarely
done.Microscopic examination ofa fluid-filledherpetic lesion demonstrates an
intraep-ithelial vesicle with marked acantholysis.The epithelial cells have swollen
homoge-neous eosinophilic cytoplasm,known asballooning degeneration,and one or mul-
tiple nuclei.Inclusion bodies may be seenin the nuclei ofballoon cells
aseosinophilic structures surrounded by aclear halo.Cytologic preparation ofafluid-
filled vesicle can also demonstratemultinucleated epithelial cells,and thediagnosis
can be augmented by usingimmunoperoxidase techniques to showantibodies to HSV
(Figure 36-8).Thediagnosis can also be confirmed by isolat-ing the virus in tissue
culture.Lesions ofprimary and recurrent her-pes resolve spontaneously in 10 to 14
days,and treatment is often unnecessary.Whentreatment is required,acyclovir is the
cur-rent drug ofchoice.Acyclovir inhibits viralreplication but has no effect on
normalhost cell function.However,it does notprevent or eliminate the latent viral
state.Acyclovir is very useful in the treat-ment ofherpes simplex infections
inimmunocompromised patients.It hasbeen reported to decrease the duration ofviral
shedding from lesions,the durationofpain,the time to scabbing,and the timeto
healing oflesions.It can reduce thenumber ofrecurrences,but infection canrecur
after the medication is discontinued.Acyclovir can decrease viral shedding,time to
healing,new lesion formation,andduration ofsymptoms in primary genitalHSV
infections.Primary oral herpeswould be expected to respond in a similarmanner,but
the medication must beadministered during the first 3 days.The use oftopical
acyclovir in healthypatients with recurrent herpes labialis hasgiven conflicting
results.To have anyeffect,the medication must be used duringthe prodrome,or within
the first fewhours after onset oflesions.Topical sun-blocking agents are useful in
reducing thefrequency ofrecurrences ofherpes labialis.In summary,acyclovir is most
helpfulin the treatment ofherpes simplex infec-tions in immunocompromised
patientsand in patients with frequent or severerecurrences.It appears to have
little valuein healthy patients with infrequent minorrecurrences ofherpes
labialis.Varicella-Zoster VirusThe primaryinfection with varicella-zoster virus
causesvaricella,or chickenpox.Varicella typicallyhas mild systemic manifestations
accom-panied by papules,vesicles,and ulcers onthe skin and mucosa.Successive crops
oflesions begin on the trunk and move to theface and extremities.Lesions in
variousstages are present at the same time and arequite pruritic.Vesicles and
ulcers resem-bling primary herpes sometimes occur onoral mucosa.Therapeutic
management for varicellais symptomatic and is aimed at reducingthe
pruritus.Antihistamines and topicallotions are helpful in this
respect.Varicellatypically has a mild clinical course,andcomplications are
rare,except in neonates,FIGURE36-7Herpetic whitlow.Epidermal vesi-cles ofthe index
finger.FIGURE36-8Herpes cytology.Cytologic prepa-ration showing epithelial cells
with enlargednuclei resulting from viral replication (�160original magnification;
stained with Papanico-laou�s stain).
688Part 5: Maxillofacial Pathologythe elderly,and
immunocompromisedpatients.Complications include bacterialinfections
ofskin,encephalitis,Reye�s syn-drome,and pneumonia.Infection with the varicella-
zostervirus results in a latent state,as in herpessimplex.The recurrent disease is
calledherpes zoster,or shingles.Reactivation ofvaricella-zoster virus is not as
common aswith HSV,except in elderly or immuno-compromised patients.Zoster has a
prodrome ofpain,burn-ing,or paresthesia,followed by groupedvesicles on an
erythematous base.Thelesions are unilateral and follow the distri-bution ofa
peripheral sensory nerve.Theyare most common on the trunk and in thedistribution
ofthe trigeminal nerve (Fig-ure 36-9).Oral lesions can have a painfulprodrome that
mimics a toothache in somecases.The lesions in zoster resolve in sever-al weeks,but
severe pain in the nerve dis-tribution (postherpetic neuralgia) can per-sist for
weeks to months after the lesionshave resolved.The prevalence and durationofpain
increases with age.Involvement ofthe facial nerve can cause Bell�s palsy.The
microscopic features oftissuesinfected with varicella-zoster are identicalto those
infected with herpes simplex.Valacyclovir has been shown to be ofsome value in the
treatment ofzosterwhen the drug is started within the firstfew days ofonset
ofinfection.EBVThe EBV causes infectious mononu-cleosis and is also associated with
hairyleukoplakia,Burkitt�s lymphoma,nasopha-ryngeal carcinoma,and
lymphoblasticleukemia.EBV infects B lymphocytes andsalivary glands and persists
within these tis-sues for the lifetime ofthe host.The abilityofEBV to reactivate
depends on the com-petency ofthe cellular immune system.Infants and children
infected with EBVusually have an asymptomatic course,butabout one-halfofinfected
adolescents andadults develop acute infectious mononucle-osis.The clinical features
include malaise,fever,pharyngitis,and lymphadenopathy ofcervical,axillary,and
inguinal chains.Splenomegaly,hepatomegaly,and hepatitiswith abnormal liver function
tests may bepresent.Occasionally an erythematous skinrash is seen.Ulcers may
involve the oral mucosa,but a vesicular stage does not occur.Theulcers are
secondary to decreased host resis-tance and appear after the systemic mani-
festations.Petechiae occur on the palate inabout one-third ofpatients.The orophar-
ynx is inflamed and may be ulcerated.Laboratory features ofacute infectioninclude
an increase in relative and absolutenumbers oflymphocytes and monocytesexceeding
50%,with > 10% atypical lym-phocytes in the peripheral blood.Theatypical
lymphocytes are called Downeycells,and they have indented or horseshoe-shaped
nuclei and abundant basophilicfoamy cytoplasm.The total leukocytecount is between
10,000 and 20,000 by thesecond or third week ofthe illness.Sero-logic findings
include high titers ofhet-erophil antibodies,which clump red bloodcells ofsheep.The
antibodies may notappear until several weeks after the onset ofsigns and
symptoms,and they decline dur-ing the ensuing 3 to 6 months.Involved lymph nodes
microscopicallyshow reactive lymphadenitis.Lymphoidnodules in the inner cortex are
hyperplas-tic.The germinal centers are markedlyenlarged and contain macrophages
withnuclear debris and numerous mitoses.Sometimes very large cells with
multilobednuclei and prominent nucleoli resembleReed-Sternberg cells ofHodgkin�s
disease.32There have been reports ofa chronicfatigue syndrome associated with
EBV.Patients describe this as a flulike illnesswith muscle
aches,pharyngitis,tenderlymphadenopathy,low-grade fever,andpersistent severe
fatigue.Elevated titersofimmunoglobulin G (IgG) antibodiesto viral capsid or early
antigens ofEBVare present.Treatment ofinfectious mononucleo-sis is supportive.The
acute disease usuallyresolves within 2 to 4 weeks.Splenic rup-ture is one ofthe few
fatal complicationsofthe disease,but it is extremely rare.Group A CoxsackievirusThe
two mostimportant group A coxsackievirus infec-tions involving the oral cavity are
herpan-gina and hand,foot,and mouth disease.Herpangina begins with
fever,pharyngitis,and anorexia.Vesicles and ulcers occur pri-marily on the soft
palate,uvula,and anteri-or tonsillar pillar.The disease resolves inseveral days and
requires only sympto-matic treatment.Hand,foot,and mouth disease has aprodrome
offever,malaise,and headache,followed by macules and vesicles on thepalms and
soles.Vesicles and ulcers can belocated anywhere in the oral cavity.Treat-ment is
symptomatic,and the diseaseresolves within several weeks.MeaslesAlthough a vaccine
for measlesexists,outbreaks ofthe disease still occur,primarily on college
campuses.Measlesbegins with high fever,conjunctivitis,pho-tophobia,cough,and nasal
discharge.Leukopenia is common during this pro-dromal phase.Red vesicles with white
cen-ters (Koplik�s spots) appear on the buccalmucosa,followed in several days by an
ery-thematous maculopapular skin rash.Therash first appears on the face and
thenspreads to the trunk and extremities.31FIGURE36-9Herpes zoster.Acute-onset
ulcera-tion localized to left maxillary soft tissues.
Management ofMucosal and Related Dermatologic Disorders689Microscopic examination
ofthe oralmucosal vesicles reveals epithelial necrosis,intercellular
edema,cytoplasmic andnuclear inclusions,and multinucleatedepithelial giant
cells.Lymph nodes andtonsils show lymphoid hyperplasia andgiant cells (Warthin-
Finkeldey cells).Therapeutic management for measlesis symptomatic.It is usually a
self-limiteddisease but may have a number ofseriouscomplications,including
croup,bacterialpneumonia,otitis media,and encephalitis.RubellaRubella (German
measles) is amild infectious disease,but it can causeserious fetal malformations
when itoccurs in pregnant women.The pro-drome consists
ofmalaise,fever,mildconjunctivitis,and lymphadenopathy.Oral vesicles and ulcers may
be present,but they are not distinctive.A macu-lopapular skin rash begins on the
faceand spreads downward to the trunk andextremities.It usually lasts for about 3
days.Arthralgia may involve wrists,fin-gers,and knees.Rubella may be com-pletely
asymptomatic or consist oflym-phadenopathy without the rash.33,34Congenital rubella
syndrome usuallyresults from maternal infection during thefirst trimester
ofpregnancy.The classicparts ofthe syndrome include cardiacmalformations ofpatent
ductus arterio-sus,interventricular septal defect,or pul-monic stenosis;eye lesions
ofcataracts,chorioretinitis,and microphthalmia;men-tal retardation;and
deafness.Rubella is usually a benign diseaserequiring only symptomatic
treatment.Alive attenuated vaccine is effective,but itshould not be given to
pregnant women orto those who may become pregnant with-in 2 months
ofvaccination.HIVHIV infects and destroys helper T lymphocytes,resulting in
profoundimmunosuppression that predisposes toopportunistic infections and
malignanttumors.HIV is transmitted by sexual inter-course,through contact with
blood orblood products,and perinatally.It isfound in saliva,but transmission by
salivais unlikely.The clinical spectrum ofHIV infec-tion includes an acute viral
syndrome withmalaise,fever,and lymphadenopathy;anasymptomatic carrier state in
which thereare circulating antibodies to HIV,and awasting syndrome.Neurologic
disordersare common and range from subtle mem-ory loss to dementia.Numerous oppor-
tunistic infections,both fatal and nonfatal,and malignant neoplasms are a
character-istic part ofacquired immunodeficiencysyndrome (AIDS).Many ofthese can
bepresent in the oral cavity.35Oral ManifestationsOPPORTUNITISTICINFECTIONSA common
oral disease inHIV-infected patients is candidosis.Fourclinical types ofcandidosis
can be presentin HIV patients.Pseudomembranous can-didosis appears as white plaques
that ruboff,leaving an erythematous and/or bleed-ing base.Hyperplastic candidosis
presentsas white rough plaques that do not rub off.Erythematous candidosis is
characterizedby diffuse or localized patches ofredmucosa.Angular cheilitis presents
ascracks or fissures ofthe commissures,sometimes associated with white
plaques.Candidosis in HIV infection responds toantimycotic medications,but it is
chronicand recurrent.36Hairy leukoplakia consists ofunilater-al or bilateral white
rough plaques that donot rub off,most commonly found on thelateral surface ofthe
tongue.It is seenmainly in homosexual males but is alsofound in other HIV-risk
groups.Deoxyri-bonucleic acid (DNA) hybridizationdemonstrates EBV in epithelial
cells ofthelesion.Hairy leukoplakia is pathognomon-ic ofHIV infection and is highly
predictivethat the patient will develop AIDS.36,37Microscopically,hairy leukoplakia
is alesion ofsquamous epithelium demon-strating hyper-
keratosis,acanthosis,andswollen ballooning epithelial cells.Hairy leukoplakia is
usually an asymp-tomatic infection requiring no treatment.For those patients
requiring treatment,acyclovir 200 mg tablets 12 times per dayfor 3 weeks has been
used with some tem-porary success.In addition,cytologysmears for candidosis should
be performedand antifungal medication prescribed forpatients with candidal
organisms.Herpes simplex and herpes zoster aremore frequent and severe in
HIVpatients as are nonspecific aphthous-likeulcers.Prolonged postzoster
neuralgiacan be extremely painful.High-dose acy-clovir can be useful in the
treatment ofeither disease.38,39PERIODONTALDISEASEA unique formofperiodontal
disease is present in manyHIV patients.Clinical features includechronic gingival
erythema,severe pain,soft tissue necrosis,and rapid destructionofalveolar bone and
the periodontalattachment.Pocket formation is minimalor absent.The cause ofHIV
periodontitismay be an overgrowth ofvirulent organ-isms possessing tissue-damaging
capabili-ties.This is probably a result ofcompro-mised immunity owing to HIV
infection.HIV periodontitis does not respond toconventional therapy
alone.However,itdoes reportedly respond to twice-dailyrinsing with chlorhexidine
combined withconventional methods.40MALIGNANTNEOPLASMSThe mostcommon malignant
neoplasms involvingthe oral cavity in HIV patients are Kaposi�ssarcoma,non-
Hodgkin�s lymphoma,andsquamous cell carcinoma.Most HIVpatients with Kaposi�s
sarcoma have orallesions,and these may be the first sign ofthe disease.The lesions
are red,blue,orpurple and may be flat or elevated.They aremost common on the hard
palate and gin-giva.Treatment includes radiation therapy,laser surgery,and/or
chemotherapy.41�43Non-Hodgkin�s lymphoma ofthe oralcavity in HIV patients is
characterized by
690Part 5: Maxillofacial Pathologyrapid growth,tendency to occur on thepalate or
alveolar ridge,and poor progno-sis.Most ofthese lymphomas are ofB-cellorigin,and in
situ hybridization tech-niques often reveal Epstein-Barr virusDNA in the tumor
cells.Other oral manifestations ofHIVinfection include salivary gland enlarge-
ment,xerostomia,and ulcerations similarto aphthous ulcers.36Autoimmune
DiseasesAutoimmune diseases typically have agradual onset and a chronic
progressivecourse with exacerbations and remissions.Lymphadenopathy is rare.It is
important to perform an incision-al biopsy to establish a definitive diagnosis.A
gingival biopsy should be avoided,ifpossible,because nonspecific
gingivalinflammation makes microscopic diagno-sis difficult.Topical or systemic
cortico-steroids usually control but do not cureautoimmune diseases.PemphigusTwo
types ofpemphigus,vulgaris and vegetans,have oral manifesta-tions.Pemphigus
vulgaris is the mostcommon and is characterized by flaccidbullae that quickly
rupture formingpainful ulcers.Large areas ofskin andmucosa can be involved,causing
seriousproblems with infection.Oral mucosal lesions are almostalways present,and
they are the initiallesions in the majority ofcases.Extensiveareas ofmucosa may be
involved,makingeating extremely painful and difficult.Rubbing or blowing air on
clinically unin-volved mucosa creates a blister,a phenom-enon called Nikolsky�s
sign.A Nikolsky�ssign is most commonly associated withpemphigus vulgaris and benign
mucousmembrane pemphigoid,but it may also bepresent in bullous pemphigoid and
lichenplanus.In pemphigus vegetans the blistershave a rough warty
surface.44,45Pemphigus is caused by circulatingautoantibodies directed against
desmo-somes ofsquamous epithelium.Thisresults in loss ofepithelial cell cohesionand
formation ofan intraepithelial blisterin the lower spinous cell layer.The
basalepithelial cells remain attached to theunderlying connective
tissue.Acantholyticepithelial cells floating in the vesicle aretermed Tzanck
cells.They have roundedcytoplasm and large hyperchromaticnuclei.Cytologic
preparation made froman early blister and stained with Papanico-laou�s stain can
demonstrate Tzanck cells.A cytologic smear gives only a preliminarydiagnosis and
does not replace a biopsy.Direct immunofluorescent studies,using the patient�s own
skin or mucosa,reveal in vivo bound IgG antibody in theintercellular spaces ofthe
epithelium inalmost all cases (Figure 36-10).IgA,IgM,and C3 are present less
often.Indirectimmunofluorescence tests for autoantibod-ies in the patient�s
serum.In pemphigus,circulating IgG antibodies can be demon-strated in the serum in
most patients atsome time during the course ofthe disease.Indirect
immunofluorescence is not as sen-sitive as the direct technique.However,thetiter
ofantibodies in the serum is often pro-portional to the severity ofthe
disease.Early diagnosis ofpemphigus isimportant because it is a serious
diseaserequiring aggressive treatment with corti-costeroids.It is often fatal ifnot
treated.Even with treatment,10 to 15% ofpatientsdie owing to the effects
ofcorticosteroids.Cicatricial PemphigoidIn cicatricialpemphigoid (benign mucous
membranepemphigoid [BMMP]),autoantibodies areformed against components in the
epithe-lial basement membrane.This results inpainful vesicles and ulcers that may
healwith scarring.BMMP has a markedpredilection for females and adults pastmiddle
age.46BMMP initially involves oral mucosain almost all cases.The lesions consist
oferythema,vesicles,and ulcers,most com-monly involving the gingiva.Because
theepithelium becomes detached from theconnective tissue,BMMP is sometimescalled
chronic desquamative gingivitis,anonspecific clinical description that canbe
applied,less commonly,to pemphigusand lichen planus (Figure 36-11).BMMPcan also
involve conjunctiva;nasal,pha-ryngeal,esophageal,and vaginalmucosa;and
skin.Scarring and adhesionbetween the bulbar and palpebral con-junctivae
(symblepharon) causes visualimpairment.The microscopic features ofBMMPinclude
subepithelial vesicle formationand nonspecific inflammatory infiltrate inthe
connective tissue (Figure 36-12).Direct immunofluorescence reveals linearFIGURE36-
10Pemphigus antibodies.Immunoglobulin G antibodies revealed viaimmunofluorescence
in stratum spinosum (�160original magnification).FIGURE36-11Cicatricial
pemphigoid.A Nikol-sky�s sign caused by an air syringe directed atmarginal gingiva.
Management ofMucosal and Related Dermatologic Disorders691continuous deposits ofIgG
and C3 alongthe basement membrane zone.CirculatingIgG antibodies against the
basementmembrane zone are present in low titerand in only a minority
ofcases.Topical and/or systemic corticosteroidsusually control the disease.The most
seri-ous aspect ofBMMP is conjunctival scar-ring,which can lead to
blindness.47�52Bullous PemphigoidBullous pem-phigoid (BP) and BMMP have
similarcauses and microscopic features but a dif-ferent distribution oflesions.The
skin inall patients with BP demonstrates largethick-walled bullae,but oral
mucosallesions are less common.Direct immunofluorescent findings areidentical in
BMMP and BP.Indirectimmunofluorescence reveals circulatingIgG antibodies against
the basement mem-brane in the vast majority ofBP patientsbut only rarely in
patients with BMMP.There appears to be no correlation betweenantibody titer and
disease severity in BP.47,52Lupus ErythematosusLupus erythe-matosus is an
autoimmune disease in whichautoantibodies form to a wide variety oftis-sues
including skin and oral mucosa.Theautoantibodies can be directed against thecell�s
nuclear material (antinuclear antibod-ies [ANA]) or cytoplasmic
antigens.53,54Discoid lupus erythematosus (DLE) isa skin disease that most
commonlyinvolves the face,scalp,and ears.The skinlesions appear as erythematous
patches,often scaly and hyperpigmented.Olderlesions may have atrophic scarring
central-ly and hyperkeratosis at the periphery.Oral lesions ofDLE are uncommon
inthe absence ofskin lesions.They charac-teristically show central erythema
withwhite spots and a border zone ofwhitestriae surrounded by
telangiectases.Lesstypical oral lesions can resemble lichenplanus or
hyperkeratosis.Systemic lupus erythematosus (SLE)is a chronic multisystem disease
mostcommon in young women between theages of15 and 40 years.Arthritis is typi-cally
present,often at the onset.Centralnervous system manifestations includeseizures and
psychoses.The leading causeofdeath is renal disease,leading todestruction
ofglomeruli and hyperten-sion.Other manifestations include vas-culitis,Raynaud�s
phenomenon,pleurisy,and pericarditis.Numerous laboratory abnormalitiesmay be
present in SLE.The most impor-tant include elevated titers ofantibody tonative
DNA,positive LE cell preparation,persistent false-positive serologic test
forsyphilis,anemia,leukopenia,thrombocy-topenia,proteinuria > 0.5 g/d,and
cellularcasts in the urine.The classic skin lesion ofSLE is an ery-thematous rash
located on sun-exposedsurfaces such as the malar eminences.Theoral lesions are
similar to those ofDLE.Oral ulceration is a well-known manifesta-tion ofSLE.Oral
candidiasis secondary tocorticosteroid therapy is common in SLE.Certain medications
have been report-ed to cause lupus-like reactions.The mostcommon ofthese include
procainamide,hydralazine,phenytoin,penicillamine,methyldopa,trimethadione,primidone
,thiouracil,and carbamazepine.Systemicinvolvement is less common with thedrug-
induced syndrome,and the signsand symptoms usually resolve when thedrug is
withdrawn.The microscopic appearance oflupusis variable.The epithelium is
hyperkera-totic and shows alternating areas ofatro-phy and hyperplasia.The lamina
propria isedematous and has dense perivascular anddeep inflammatory
infiltrates.Periodicacid-Schiffstain demonstrates depositssubjacent to the
epithelium and thicken-ing ofblood vessel walls.Direct immunofluorescence on
orallesions reveals deposits ofIg and C3 in thebasement membrane zone ofthe
epitheli-um in the majority ofcases ofDLE and SLE.Therapeutic management
oforallesions oflupus includes topical and/orsystemic corticosteroids and
antimycoticmedications as necessary for candidiasis.DLE has a good prognosis.The
prognosisfor SLE depends upon the extent ofsys-temic involvement ofthe
disease.Idiopathic VesiculoulcerativeDiseasesIdiopathic diseases have causes that
areunknown or poorly understood.They donot have clinical characteristics commonto
the entire class,and they must be con-sidered individually when formulating
aclinical differential diagnosis.Aphthous UlcersAphthous ulcers arecommon painful
lesions that have period-ic recurrences.Most patients have only asingle ulcer
during a given episode,although occasionally two or three ulcersmay be present
(Figure 36-13).Vesicles donot occur.Unlike recurrent herpes,aph-thous ulcers are
found on nonkeratinizedoral mucosal surfaces.They have an acuteonset,and each ulcer
heals spontaneouslywithout scarring in 10 to 14 days.Thereare no systemic
manifestations and usual-ly no lymphadenopathy.55�61Major aphthae,also known as
peri-adenitis mucosa necrotica recurrens,orSutton�s disease,is characterized by
multi-ple large mucosal ulcers.A patient has atFIGURE36-12Cicatricial
pemphigoid.Uni-form separation ofepithelium from underlyingconnective tissue at the
level ofthe basementmembrane (�60 original magnification; stainedwith hematoxylin
and eosin).
692Part 5: Maxillofacial Pathologyleast one ulcer present all the time.Theulcers
may take up to 6 weeks to heal,andhealing is accompanied by scarring.Beh�et�s
syndrome is a systemic diseasethat can affect most organ systems.Themost common
lesions are recurrent oralaphthous ulcers,genital ulcers,skin lesions,and eye
lesions.The skin lesions consist oferythema nodosum�like eruptions
andthrombophlebitis.The eye may be affectedby recurrent iritis,uveitis,and
retinitis,which can lead to blindness.Other lesscommon problems include
arthritis,ilealand colonic ulcers,aneurysms,arterial andvenous occlusion,and a
variety ofcentralnervous system diseases.Aphthous ulcers have been associatedwith a
number offactors,but the cause isunclear.Aphthae do not appear to be causedby
deficiencies in serum vitamin B12,redblood cell folate,iron,or total iron-
bindingcapacity,or malabsorption enteropathies.An allergic response to certain
foods such aswalnuts,strawberries,and tomatoes doesnot appear to be
important.Genetic factors are significant as thefrequency ofhuman leukocyte DR7
anti-gen is significantly increased in aphthaepatients,and aphthae are more
commonin related persons.Women commonlystate that the ulcers appear with the
onsetofmenstruation,supporting the role ofendocrine factors.The microscopic
features ofaphthousulcers are those ofany nonspecific ulcerand are not
diagnostic.The history andclinical findings determine the diagnosis.The goal
oftherapeutic management isto decrease the inflammatory response;topical
corticosteroids accomplish this formost patients.Patients with major aphthaeusually
require systemic corticosteroids.Lichen PlanusLichen planus is a chron-ic disease
ofskin and mucosa.Skin lesionsare often extremely pruritic and appear asviolet-
colored flat-topped papules andplaques with a shiny surface.The lesionsare most
commonly located on the volarsurface ofthe wrists,anterior surface ofthe legs,and
penis.Oral lesions oflichen planus are mostcommon in adults > 40 years.The
lesionshave several forms.The reticular formpresents as a network oflacy white
linescalled Wickham�s striae (Figure 36-14).The plaque form appears as
whitehomogenous plaques.The white lesionsin both forms are nonpainful,rough
topalpation,and do not rub off.Theatrophic form consists oferythematousmucosa plus
a reticular keratotic patternalong the periphery.The erosive formcombines
ulcerations with atrophic fea-tures (Figures 36-15 and 36-16).Theatrophic and
erosive forms are typicallysymptomatic.Occasionally,vesicles areseen,which quickly
rupture to formpainful ulcers.Ulcers and erosions caninvolve the attached gingiva
producing adesquamative gingivitis pattern in 25% ofpatients.Candidosis is another
commonfinding in patients with lichen planus.Oral lesions oflichen planus are
multifo-cal and can involve any mucosal surface.The most common locations are the
buc-cal mucosa,followed by gingiva and thetongue.One-fifth ofpatients with
orallesions have skin lesions.62�68Drugs can cause lichenoid reactions ofskin and
mucosa that are clinically similarFIGURE36-13Aphthous stomatitis.Well-circumscribed
nonindurated ulcer ofthe ventralglossal mucosa.FIGURE36-14Lichen
planus.Hyperkeratoticstriations ofthe buccal mucosa.FIGURE36-15Aand B,Lichen
planus.Hyper-keratotic striations,erythema,and ulceration oflateroventral glossal
mucosa.ABFIGURE36-16Lichen planus.Dorsal tonguelichen planus often characterized by
hyperkera-totic plaques rather than striations.
Management ofMucosal and Related Dermatologic Disorders693to lichen planus.The
reactions resolvewhen the drug is discontinued.The mostcommonly implicated drugs
includemethyldopa,amiphenazole,chloroquine,hydroxychloroquine,quinacrine,chlor-
propamide,tolbutamide,tetracycline,chlorothiazide,practolol,dapsone,furosemide,phen
othiazines,quinidine,triprolidine,para-aminosalicylic acid,arsenicals,bismuth,gold
salts,and mercury.Lichenoid reactions also occur during thechronic phase ofgraft-
versus-host diseasefollowing bone marrow transplantations.Lichen planus is
considered a diseaseofthe cellular immune system involving
Tlymphocytes,Langerhans�cells,andmacrophages.The Langerhans�cells andmacrophages
process antigens and presentthe antigenic material to T lymphocytes.The lymphocytes
proliferate and becomecytotoxic for basal cells ofthe squamousepithelium.A similar
immune mechanismhas been reported in graft-versus-host dis-ease and erythema
multiforme.The microscopic features oflichenplanus are variable,and clinical
featuresare important in establishing the diag-nosis.The primary microscopic
featuresinclude hyperkeratosis and a band-likeinflammatory infiltrate,consisting
pri-marily oflymphocytes,subjacent to theepithelium (Figure 36-17).The epitheli-
um�connective tissue interface isobscured owing to liquefaction degen-eration ofthe
epithelial basal cell layerand/or infiltration with lymphocytes.An eosinophilic
band may be seenbetween the inflammatory infiltrate andthe epithelium.The spinous
cell layer isoften hyperplastic.Colloid or Civattebodies,representing necrotic
epithelialcells,are occasionally seen as eosino-philic bodies in the lower layers
oftheepithelium.Direct immunofluorescence revealsfibrinogen deposition in the
basementmembrane zone in almost all cases,andless commonly in colloid bodies and
wallsofblood vessels.Lichen planus is a chronic or recurrentdisease that only
rarely undergoes sponta-neous remission.The goal oftreatment iscontrol
ofsymptoms.Asymptomaticlesions require no treatment,whereassymptomatic cases are
usually controlledwith topical and/or systemic cortico-steroids.In one study of570
patients withoral lichen planus,63% experiencedimprovement and 29% experienced com-
plete remission while maintained on corti-costeroids.69Antifungal medication is
nec-essary ifcandidosis is present.It appears that oral carcinoma occursin lichen
planus patients at a slightly high-er rate than in the general
population.However,the frequency ofmalignanttransformation is unknown,and the clas-
sification oflichen planus as a premalig-nant lesion does not appear
justified.Peri-odic recall examinations are necessary.Erythema MultiformeErythema
multi-forme (EM) can involve skin and oralmucosa independently or simultaneously.It
has traditionally been described as acuteand self-limited,requiring an average
of3weeks for resolution.Some patients have avariable pattern ofrecurrence.In
otherpatients EM has a chronic course.The cause ofEM is unknown,althoughit appears
to be some type ofimmune dys-function.It may be related to immunecomplexes
deposited in walls ofblood ves-sels in the dermis or submucosa.In abouthalfthe
cases EM appears to be triggered byinfections or drugs.The most commoninfections
reported include herpes simplexviruses,tuberculosis,and histoplasmosis.The most
frequently implicated drugs aresulfonamides,barbiturates,phenylbuta-zone,oxy-
phenbutazone,phenazone,peni-cillins,chlorpropamide,phenytoin,andcarbamazepine.The
skin lesions ofEM include mac-ules,papules,vesicles,and bullae.Themost
characteristic lesion,known as theiris or target lesion,appears as a centralvesicle
surrounded by erythematous andskin-colored rings.The lesions are sym-metrically
distributed,most commonly onthe extremities and face.One-fourth to one-
halfofpatients withskin lesions have oral lesions (Figure 36-18).Ulcers are
present,most commonly on thelips,buccal mucosa,and tongue,as well aserythematous
mucosa.The oral lesions varyfrom mild to so severe that patients cannotspeak or
eat.The lesions may be accompa-nied by headache,fever,and malaise.70,71Stevens-
Johnson syndrome is a severeform ofEM with more serious
systemicmanifestations.Extensive skin lesions,conjunctivitis,and oral and
genitalmucosal lesions are present.The orallesions often begin as vesicles,which
rup-ture forming painful ulcers.Lesions on thelabial mucosa may have a bloody
crust.Toxic epidermal necrolysis is an evenmore serious form ofEM characterized
bylarge flaccid bullae and sloughing oftheepidermis in large sheets.Oral lesions
maybe prominent,especially on the buccalFIGURE36-17Lichen planus.Focal hyperker-
atosis,basal cell liquefaction degeneration,and asuperficial infiltration
oflymphocytes (�60 orig-inal magnification; stained with hematoxylinand eosin).
694Part 5: Maxillofacial Pathologymucosa.Toxic epidermal necrolysis is usu-ally
caused by drugs.The patient is acute-ly ill,and the disease is often fatal.The
microscopic features ofEM arenot diagnostic.The epithelium demon-strates edema and
necrosis ofker-atinocytes.The connective tissue containsperivascular infiltrates
oflymphocytes,plasma cells,and macrophages.Immuno-fluorescence reveals deposits
ofIgM andC3 in the vascular walls,suggestingimmune complex deposition is
importantin the pathogenesis.Treatment may not be necessary formild forms
ofEM,which have a goodprognosis,although they may be recur-rent.More serious types
respond well tocorticosteroids;however,Stevens-Johnsonsyndrome is occasionally
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CHAPTER 37Head and Neck Skin CancerMichael F.Zide,DMDYan Trokel,MD,DDSSkin cancer
is the most common cancerafflicting mankind.In the United Statesalone,an estimated
1 million new lesionsare diagnosed each year.1Skin cancer maybe grouped into two
subsets:nonmelanomaskin cancer (NMSC) and melanoma.NMSC comprises 95% ofall skin
cancers.Melanoma,ofwhich 1 to 8% occurs in thehead and neck,fills the remaining
5%.2�4Even with this low incidence,melanoma is responsible for about 75% ofskin
cancer-related deaths.The overallmortality for NMSC is relatively low,withan
estimated 5-year survival rate of95%.5,6Regardless,NMSC may be locally aggres-
sive,leading to significant morbidity,dis-figurement,loss offunction,and highhealth
care costs.7This chapter focuses onthe epidemiology,etiology,clinical charac-
teristics,and management (medical andsurgical) ofthese cutaneous
malignancies.Nonmelanoma Skin CancerEpidemiologyThe NMSCs include basal cell
carcinoma(BCC;75% ofNMSCs),squamous cellcarcinoma (SCC;20% ofNMSCs),and afew rarer
malignancies,such as Merkel celltumor,dermatofibrosarcoma protuberans,and adnexal
tumors.5Incidence data forthe United States should be interpretedskeptically as
most NMSCs are treated inoutpatient clinics or private offices and arenot routinely
reported to cancer reg-istries.3Reported yearly skin cancer ratesare approximately
2 in 1,000 in the conti-nental United States,1 in 100 on the islandofKauai,and > 2
in 100 in Australia.8Epidemiologic studies demonstrate apositive correlation
between ultraviolet(UV) radiation exposure and the inci-dence ofNMSC.NMSC is
predominantlya Caucasian disease (=98%) but doesoccur in Blacks and Hispanics.3The
risk ofdeveloping NMSC increases the closer onelives to the equator,and the more
one�soutdoor activities increase the concentra-tion ofsun exposure through
reflection.8,9Examples ofthe latter include workaround snow,water,cement,and
roofing.For all races 75% ofNMSCs appear onbody areas most chronically exposed to
sun-light,such as the head,face,neck,and dor-sum ofthe hands.5The incidence
ofBCCand SCC at early ages is comparable for menand women,but men > 45 years have a
threetimes greater incidence ofNMSC,specifi-cally SCC.10,11In men common sites are
theears and nose,whereas in women the noseand lower extremities are most common.The
incidence ofNMSC had beenincreasing for decades.The mortality rate,however,has
recently leveled offand isnow beginning to decrease,perhaps owingto public
information programs.12Overall,NMSC has an excellent prognosis,butapproximately
2,000 deaths occur annual-ly,three-fourths ofwhich are frommetastatic
SCC.13,14EtiologyThe etiology ofNMSC is multifactorialbut can be broadly
categorized into host-related and environmental causes.Hostfactors include an
individual�s phenotype,genetic syndromes,precursor lesions,andimmunologic
issues.Environmental vari-ables include exposure to UV radiation,ionizing
radiation,and chemicals.2Host FactorsTanning is the body�sdefense mechanism against
NMSC.One�sability to tan is directly related to theamount ofmelanin in the
skin,which isgenetically determined and cannot beinfluenced.Skin melanin determines
aperson�s photosensitivity.The moremelanin an individual has,the less damageUV
radiation inflicts.Deleterious effects ofUV radiation are attenuated by the stra-
tum corneum via refraction,reflection,and direct absorption by melanin.Fitzpatrick
classified skin into six dif-ferent groupings or types (Table 37-1).15Each group
was categorized based on theresults of30 minutes ofdirect sunlight tothe skin in
the northern hemisphere.Thegroups are based on the amount ofmelanin an individual
possesses,inherentpigmentation,and sensitivity to UV light.For example,a person in
type 1 is the clas-sic freckle-faced light-eyed redhead whoburns and never tans,a
Celtic type.Peoplein type 1 are highly susceptible to skincancer but remarkably
also heal from
698Part 5: Maxillofacial Pathologyreconstruction wounds with the least per-ceptible
scar.Type 2 is typified by theblond-haired blue-eyed person,a Scandi-navian type.A
type 3 person has olive skinand often dark eyes and occasionallyburns but tans
readily,a Mediterraneantype.The descent ofpeople in type 4 isHispanic,type 5 is
Arabic/Indian,andtype 6 is African.Remarkably,as resis-tance to skin cancer
increases,scarifica-tion becomes more obvious,often pig-menting or forming
keloids.Host factors contribute to a patient�songoing risk ofdeveloping new
cancers.A patient with a prior history ofNMSChas a 36 to 52% 5-year risk
ofanothercancer arising.16,17SyndromesGenetics plays a starring rolein determining
who gets skin cancer.Newer drugs to treat skin cancers,forexample,5% imiquimod
cream appliedtopically three times per week,show greatpromise in treating skin
cancers throughinherent immune responses.18There areseveral syndromes that
predispose a per-son to skin cancer:�Basal cell nevus syndrome (Gorlin�ssyndrome)
is an autosomal dominantdisorder characterized by multipleBCCs,odontogenic
keratocysts,bifidribs,scoliosis,brachymetacarpalism,palmar and plantar
pits,calcificationofthe falx cerebri,prominent supra-orbital ridges,and
hypertelorism.The BCCs that are produced look likesmall nevi (Figure 37-1) but act
justlike common nodular BCC.Controlwith a CO2laser or curettage
andelectrodesiccation (C and E) is criti-cal before enlargement destroysanatomic
structures.19�21 �Xeroderma pigmentosa is an autoso-mal recessive disorder
resulting indefects in repair ofdeoxyribonucleicacid (DNA).UV radiation results
inskin DNA damage;therefore,xeroder-ma pigmentosa is characterized
byhypersensitivity to sun exposure andthe development ofmultiple skin can-
cers.Children with this disorder mustmodify their lifestyles to function asnight
people.There are summer campsfor them,at which activities begin attheir wake-up
time�sundown�Albinism is an autosomal recessivedisorder resulting in the absence
ofmelanin with a subsequent increasein development ofskin cancer,espe-cially
SCC�Epidermodysplasia verruciformis is anautosomal recessive disorder.It resultsin
the development ofBCC from flatwarts in sun-exposed areas inhomozygous individuals
infected withhuman papillomavirus type 3 or 5Predisposing LesionsSeveral congeni-
tal and acquired lesions predispose toskin cancer:�Nevus sebaceus ofJadassohn is a
well-circumscribed slightly raised hairlesslesion on the scalp or face present
atbirth that becomes verrucous andnodular during puberty.Approxi-mately 10% ofsuch
lesions undergomalignant transformation to BCC(Figure 37-2) �Actinic keratosis
(AK),also known assolar or senile keratosis,is the mostcommon precancerous lesion
oftheepidermis.AK is characterized by red,yellow,brown,or colorless macules
orpapules with scaly irregular surfaces,ranging in size from a few millimetersto
several centimeters.Left untreated,there is a 10 to 13% risk
ofmalignanttransformation ofAK to SCC (Figure37-3);therefore,the American Acade-my
ofDermatology recommendstreatment.22�25All suspicious lesionsshould undergo
biopsy.Treatmentoptions include chemical peel,laser,cryotherapy,C and E,tangential
exci-sion,or 5-fluorouracil (5-FU) �Cutaneous horns are hard keratoticgrowths that
protrude from the skin.Histologically they are advanced AK.Approximately 10%
ofthese lesionshave an underlying SCC26Immunologic FactorsImmunosuppres-sion
predisposes a person to several typesofcancers including skin cancer.Immuno-
suppression alters the immune surveil-lance mechanism that typically
destroyspotentially malignant cells.3Humanimmunodeficiency virus infection,lym-
phoproliferative disease,occult malignan-cy,organ transplantation,and a variety
ofother medical conditions result inimmunosuppression.Renal transplanta-tion
patients on long-term immunosup-pressive therapy not only have a higherincidence
ofSCC and metastasis,theirTable 37-1Fitzpatrick Skin Types*
TypeCharacterization1Always burns easily,shows no immediate pigment darkening,and
never tans2Always burns easily,shows trace immediate pigment darkening,tans
minimally andwith difficulty3Burns minimally,+ immediate pigment darkening,tans
gradually and uniformly (light brown)4Burns minimally,++ immediate pigment
darkening,tans well (moderate brown)5Rarely burns,+++ immediate pigment
darkening,tans very well (dark brown)6Rarely burns,+++ immediate pigment
darkening,tans profusely (black)*Fitzpatrick skin phenotypes portray the outcomes
of30 min ofsun exposure at midday in the northern hemisphere.+ indicates a relative
level ofpigment darkening,with +++ being the highest.From Fitzpatrick TB.15
Head and Neck Skin Cancer699tumors appear years earlier than in anycontrol
population.27�30However,moststudies suggest that some other risk factorsuch as
ionizing radiation or viral infec-tion,along with a decreased immune sys-tem,is
necessary for the development ofthese tumors in this subset
ofpatients.3,31Environmental FactorsIonizing radia-tion,certain chemicals,and skin
damagefrom the environment can also cause skincancer.UV radiation has been fingered
asthe primary environmental culprit.Thereare three types ofUV radiation:UVA(320�400
nm),UVB (290�320 nm),andUVC (200�280nm).UVB rays are themost
carcinogenic,triggering skin cancervia photochemical damage to DNA,injuryto DNA
repair mechanisms,and partialsuppression ofcell-mediated
immunity.5,32UVA,originally thought to be harmless,isnow known to enhance the
effects ofUVBas a cocarcinogen.3Most UVC is filteredout by the ozone layer.As the
ozone layerthins,as it has over Antarctica and parts ofAustralia,UVC enhances the
developmentofskin cancer.The most common historicreports for NMSC as well as
melanoma aretwo to three childhood blistering sun-burns or =3 years ofintense sun
exposure.A comment must be made about thetwo methods oftanning used in
tanningparlors.The method using UVA light,inour estimation,enhances new skin can-
cers.32We have seen skin cancers even inteenagers who have used tanning parlors.The
�California�spray tan,a skin dye thatlasts for 3 to 5 weeks,is harmless.Chemicals
such as arsenic,polycyclicaromatic hydrocarbons,and psoralensused in combination
with UVA (a treat-ment for psoriasis) have all been implicat-ed as originators for
NMSC.33Patients suf-fering from chronic inflammatory skinconditions,such as chronic
radiation ker-atosis,burn scars,and ulcers,have anincreased risk ofdeveloping skin
cancers.PreventionAlthough a doctor may be capable oftreat-ing skin cancer
effectively,the informedpatient is the greatest resource against thedevelopment
ofnew cancers.Preventivemeasures can be classified into three
types:sunscreens,clothing,and education.Sunprotection is rated by sun protection
factorFIGURE37-1This 30-year-old woman was first seen 10 years prior for
treatmentofmultiple odontogenic keratocysts.A,The small pigmented dots are all
incipientor growing basal cell skin cancers,which are slow growing and less
aggressive thanmost cancers resulting from sun exposure.B,Intraoperatively.Excision
is indicat-ed for the larger lesions; curettage and electrodesiccation or CO2laser
is used forincipient lesions.C,Improvement is noted after 1 month.ABCFIGURE37-
2Nevus sebaceus.FIGURE37-3Scaly actinic keratoses on the scalp,some ofwhich have
progressed to squamous cellcarcinoma (in situ).
700Part 5: Maxillofacial Pathology(SPF).The SPF is a ratio ofthe smallestamount
ofradiation needed to produceerythema on protected skin comparedwith the same
degree ofredness producedon unprotected skin.Sunscreens functioneither chemically
or physically.Chemicalsunscreens,such as para-aminobenzoicacid,benzophenones,and
cinnamates,reduce UV skin penetration by absorbingsolar rays.Physical sunscreens
includingtitanium dioxide,zinc oxide,and kaolin,act as physical barriers.It is now
known that regular applica-tion ofSPF 30 sunblock may reduce theevolution ofnew
actinic keratoses by 50%after 3 years.Additionally,patients shouldbe told that the
application ofSPF 30 doesnot abrogate the need for behavioral mod-ification.For
example,a farmer whoapplies SPF 30 at the start ofthe day willhave the protection
wear offshortly after afew hours ofsweating.Clothing may provide some protec-
tion,but a wet T-shirt has an SPF of0 to1.33High SPF clothing is available,but it
isexpensive and not very comfortable.Basal Cell CarcinomaBasal cell tumors
originate from pluripo-tential cells in the epidermis and hair folli-cles.They are
often slow growing and maytake years to enlarge significantly.33Typically,patients
with BCC are cat-egorized as Fitzpatrick types 1 to 3 witha history ofsun
exposure.Eighty to 93%ofthe cancers occur on sun-exposedareas ofthe head and
neck,and 26 to30% occur on the nose.34BCCs can bedivided into several
subtypes:superfi-cial,nodulo-ulcerative (or nodular),pig-
mented,infiltrative,micronodular,morphea-like,and basosquamous.Superficial BCC
represents approxi-mately 10% ofall BCCs (Figure 37-4).35They present as slightly
elevated plaquesor discrete macules that may be scaly.Theycan resemble eczema or
fungal infections.Nodulo-ulcerative BCC is the mostcommon type,accounting for
approxi-mately 75% ofall BCCs (see Figure 37-4).35Clinically,they present as well-
definedtranslucent pearly nodules that are eitherround or oval with rolled borders
and occa-sional ulcerations.Telangiectasias are com-monly seen coursing through the
lesion.Pigmented BCCs range from brown toblue-black and can be mistaken
formelanoma.Morphea-like BCCs present asfirm plaques that are yellow or white
withan ill-defined border.They can be quitelarge and do not show more than 1 to 2
mm elevation.This tumor is likely tohave positive margins after
excision.Basosquamous carcinomas have bothbasal and squamous cell
differentiations.They have a higher growth rate as well asa higher metastatic
potential than doother BCCs.Micronodular,infiltrative,and morphea-like BCCs are the
more aggressive variantsofBCC and together account for 10% ofBCCs.7Death from BCC
is rare,with a rate ofmetastasis of0.0028 to 0.1%.36Size,depthofinvasion,and
histologic type are impor-tant predictors for metastasis.10Favoredsites
ofmetastasis include regional lymphnodes,liver,lung,bone,and skin.This
raremetastasis is twice as common in males asin females.36Squamous Cell
CarcinomaSCC is the second most common skin can-cer and accounts for 20% ofall
NMSCcases.SCC is a malignant proliferation ofepidermal
keratinocytes.HistologicallySCC is composed ofnests and cords ofatypical squamous
cells from the epider-mis infiltrating into the dermis;it oftencontains keratin
pearls.The lifetime risk ofdeveloping SCC is 4 to 14%,and the inci-dence has
increased by 20% in the pastdecade alone.11,37,38Men with a fair complexion who are
> 50 years and have had heavy sun expo-sure in the past several years typically
getmultiple actinic keratoses and SCC.SCCpresents as a painless poorly defined ery-
thematous nodule with raised borders(Figure 37-5).Cutaneous horns or
ahyperkeratotic crust with ulcerations maybe present.The surrounding skin mayreveal
signs ofchronic sun damage.Unlike BCC,SCC may grow rapidlyand
metastasize.Metastasis is most com-mon in lesions > 4 mm deep.The cumula-tive rate
ofmetastasis is between 2 and 6%,and the 5-year survival rate for metastaticSCC is
only 34%.11,38Metastasis can occureither through the lymphatics or byhematogenous
spread,with common sitesbeing the regional lymph nodes,the lungs,and the liver.The
location ofthe primarylesion influences the rate ofrecurrenceand metastasis.SCCs
occurring on the lip,ear,melolabial crease,and periorbital andpreauricular areas
have higher rates ofrecurrence and metastasis (10�14%).38,39The most common
precursor for SCCis AK.The rate oftransformation ofAK toSCC is 1 in 1,000 per
year.39Approximately40% ofpeople > 40 years have had at leastone AK.Keratoacanthoma
is a commonlyconfused with SCC,both clinically and histologically.Keratoacanthoma
is a self-healing raised growth lesion with a centralkeratin-filled plug.It grows
quickly butoften spontaneously involutes after 2 to 6months,leaving only a
depressed white scar.Bowen�s disease is an in situ SCC pre-senting as a slow-
growing erythematousscaling plaque with an irregular but sharpoutline.These lesions
rarely transforminto invasive SCC.SCC may evolve from chronicallyunhealed or
unstable wounds,burn scars,or ulcers.These lesions,sometimes calledMarjolin�s
ulcers,have a 20% higher rate oflymph node metastasis than does UV-induced
SCC.40,41Histologic features,such as the degreeofdifferentiation,depth
ofinvasion,andperineural involvement,as well as tumorsize are prognostic indicators
that maydictate selection ofwidth ofthe excision-al margin.More differentiated
lesionshave a lower invasive tendency and,hence,
Head and Neck Skin Cancer701a better prognosis.Larger tumors andthose that invade
deeply along tissueplanes have a greater risk ofrecurrenceand metastasis.Tumors > 2
cm have atwofold increase in recurrence rate andare three times more likely to
metastasize.Tumors arising in scars or wounds areusually more aggressive and have a
metas-tasis rate between 18 and 38%.7With SCCthe first shot at cure is crucial as
recurrentSCCs have a metastatic rate of24 to 45%;ifthey metastasize the 5-year
survival rateis around 50%.7MelanomaMelanoma is a potentially deadly andaggressive
neoplasm resulting from themalignant transformation ofmelanocytes.The incidence
ofmelanoma is increasingfaster than any other cancer.It is estimatedthat the
frequency ofmelanoma will dou-ble every 10 to 15 years,and that > 40,000new cases
ofmelanoma will be diagnosedthis year in the United States alone.7,41,42Melanoma
occurrence increases the closerone�s residence is to the equator,with resi-dents
ofQueensland,Australia,having thehighest rate ofmelanoma,approaching 1in 14.43An
estimated 1 in 75 people devel-op melanoma in their lifetime,up from 1in 150
persons in 1985.44Melanomaaccounts for over three times more deathsthan the
combined fatalities from all otherskin malignancies.45Risk FactorsPeople in
Fitzpatrick groups 1 and 2 arethe most susceptible to melanoma.Therole ofUV is not
precisely known forFIGURE37-4A,Superficial and nodulo-ulcerative basal cell
carcinomas (confirmed with biopsy) are excised under local anesthesia in the
office.The specimens aresent for permanent histopathology.B,Five days later,in the
operating room,the defects are ready for reconstructive closure.C,Finger pressure
(inherent elasticity)reveals that the largest defect is tight but amenable to
advancement flap closure.D,The upper defect is presutured with 3-0 nylon
(mechanical creep).E,Margins areexcised (0.5�1 mm sharp squaring ofthe rounded
edges with scraping ofdebris) and complex closures ofthe lower defects are
accomplished.F,The nylon sutures arereleased and the tension-free upper defect is
repaired with an advancement flap and M-plasty.G,Results at suture removal 1 week
later.ABCDEFG
702Part 5: Maxillofacial Pathologymelanoma,but lots offreckles and a histo-ry
ofthree or more blistering sunburns,the use ofa tanning bed,and havingundergone
psoralen plus UVA therapyhave been implicated.43,46Several additional risk factors
formelanoma have been identified.About10% ofpatients with melanoma have afirst-
degree relative with the disease.47�Common moles,�also known as acquiredmelanocytic
nevi,can be a risk factor.Individuals with > 100 ofthese moleshave a tenfold risk
ofdevelopingmelanoma.4,48When combined with afamily history
ofmelanoma,dysplasticnevi (atypical moles ),which are presentin approximately 10%
ofthe population,represent a significantly increased risk ofdeveloping
melanoma.Congenital (blackhairy) nevi have a 4% lifetime risk ofdeveloping into
melanomas.43Lentigomaligna,or melanotic freckle ofHutchin-son,is a precursor in
situ lesion thatbecomes malignant in approximately 5%ofcases (Figure 37-6).Thirty
percent ofmelanomas arise from preexisting lesions,whereas 70% arise de
novo.Clinical and Histologic DescriptionThe mnemonic ABCDis useful in cate-gorizing
the characteristics ofmelanomas:asymmetry,border irregu-larity,color changes or
variation,diame-ter oflesion (< or > 6 mm).The practi-tioner should not place the
patient underFIGURE37-5A,This 60-year-old has confirmed squamous cell cancer on his
nasal tip (and basal cell cancers elsewhere).B,Five days after excision ofthe can-
cers,with permanent histology assuring margin clearance,the patient undergoes
Doppler ultrasonography in preparation to identify the location ofthe axial ves-sel
for a paramedian forehead flap.C,The flap is designed on the right supratrochlear
vessels.D,The lower recipient site has been trimmed sharply,and the pinkvascular
flap is ready for inset.E,The flap in place.F,The sutured flap revascularizes for 3
weeks.At this time,it may be thinned again or divided and inset accord-ing to
topographic principles.G,Two months postoperatively,the results ofsurgery are
inconspicuous.ABCDEFG
Head and Neck Skin Cancer703casual observation (ie,not perform abiopsy) just
because these common indi-cators might be absent.Approximately40% ofboard-certified
dermatologistsand 50%+ ofother clinicians do notidentify melanoma correctly by
clinicalintuition alone.Other suspicious factorsinclude the color pink in a dark
lesionand persistent itching.Melanoma in situ is an intraepitheliallesion that can
progress to an invasivelesion.When it is still in the epithelium,itis described as
being in a horizontalgrowth phase,but when it invades dermisand approximates blood
vessels,it is in avertical growth phase and thickens.Hence,deeper melanomas are
more deadly.Histopathologically,malignant melanomapresents as a proliferation
ofatypicalmelanocytes.The tumor originates at theepidermal-dermal junction.The
cells theninvade upward into the epidermis orextend downward into the
dermis.Melanomas are categorized into fourmain clinical and histologic
subtypes:superficial spreading melanoma,nodularmelanoma,lentigo maligna
melanoma,and acral-lentiginous melanoma.Superfi-cial spreading melanoma accounts
for70% ofall melanomas.Clinically superfi-cial spreading melanoma is a flat or
slight-ly elevated dark lesion with asymmetricborders;it can be present for up to 5
yearsprior to invasion ofthe dermis.Nodular melanoma is the secondmost common
variant,accounting for 15to 30% ofmelanomas.It appears as araised
black,brown,blue,or red nodule,perhaps with ulcerations,bleeding,orcrusting.It may
look just like a BCC,butcontrary to BCC,the lesion grows rapidlyover a few
months.Around 5% ofnodu-lar melanomas lack pigmentation and arepinkish
�amelanotic�melanomas.Nodu-lar melanomas are thicker and metasta-size
rapidly.Lentigo maligna melanoma comprises4 to 10% ofmelanomas.It arises in sun-
exposed areas and occurs in the elderly.Acral-lentiginous melanoma accountsfor 2 to
8% ofall melanomas in Cau-casians but is the most common type inAfrican
Americans,Asians,and Hispanics.Clinically,they present as pigmentedlesions with
irregular borders.Papules andnodules are frequently seen within thelesion.Biopsy is
the only fail-safe method toprove or disprove melanoma.Ifmelanomais
suspected,incisional and excisionalbiopsies are much more diagnostic andprognostic
than is a shave biopsy.Regard-less,ifa shave biopsy is performed andmelanoma
returns as the diagnosis,thenext step is to obtain a full-thickness spec-imen (via
punch or incisional biopsy) toascertain the diagnosis and confirm truedepth.Neither
incisional nor excisionalbiopsy disseminates tumor.Incisional biopsy should be
reservedfor lesions > 2 cm or those located atanatomically restricted areas
(eg,eyelids,ears).The biopsy should be at the mostraised site or the darkest area
ofthe lesion(Figure 37-7).Full-thickness excisionalbiopsy with a 2 mm margin is the
pre-ferred method for lesions < 2 cm.Once the diagnosis has been estab-
lished,melanoma is staged either by mea-suring the tumor depth from the
granularcell layer ofthe epidermis to the farthestdepth oftumor invasion (Breslow
classifi-cation) or by determining the anatomiclevel ofinvasion (Clark
classification).Melanomas measuring < 0.76 mm have a5-year survival rate of>
93%,whereaslesions > 4 mm thick have a 5-year survivalrate of< 50%.49,50Melanomas
with ulcera-tion or histologically high mitosis ratespredictably worsen
prognoses.Discoveryoflocoregional or distant metastasis lowers5-year survival to
40% or 5%,respective-ly.51The most frequent sites ofmelanomametastasis include the
skin,lymph nodes,lung,liver,brain,bone,and gastrointestinaltract.On the other
hand,the presence ofaABCDFIGURE37-6A,This 65-year-old manhas a lentigo maligna on
his cheek anda basal cell cancer on his nose.Band C,After margin clearance by
permanenthistology (7 d later),the cheek defectand the nasal defect are each
repairedwith a rotational flap and back cut.D,An excellent esthetic result is
evident.
704Part 5: Maxillofacial Pathologygreat number oftumor-infiltrating lym-phocytes
and a lack ofvascular invasionimprove survival prognosis.7Controversy exists
regarding the valueofelective lymph node dissection (ELND),although it is well
accepted that there is nobenefit to ELND performed concurrentlywith primary tumor
resection.Our cur-rent management protocol is not to sug-gest ELND or sentinel node
biopsy forlesions measuring < 1 mm or > 4 mm.Intermediate depth tumors (1�4 mm)
arereferred for sentinel node biopsy based onstudies suggesting that it increases
the 5-year survival rate by 10% (ie,from 35 to45%) (Tables 37-2 and 37-
3).52Management ofNMSC LesionsRegardless ofthe obvious appearance ofsome cancers,a
biopsy should be per-formed for histologic confirmation andtyping.The histologic
characteristicsinfluence clinical behavior,recurrence,and metastatic
potential.Determinationofmargin size for tumor clearance shouldbe based on a
compilation ofall availableinformation.Biopsy techniques are personal.Anytechnique
that delivers adequate histologicmaterial for diagnosis is acceptable.Shavebiopsy
with a scalpel or curved razor bladeis simple.Shave biopsy leaves a 5 to 6
mmsaucer-shaped defect,removing epidermisand some dermis.The only drawback toshave
biopsy is that histologic and prognos-tic features may be deeper than the
shave.Thus,a shave biopsy might potentially be sosuperficial as to limit pathologic
differenti-ation between an in situ versus an invasivelesion.Shave biopsy is
contraindicated inpotential melanomas.A �pseudoshave�biopsy might be performed with
a curettedspecimen prior to electrodesiccation.Punch biopsy garners a full-
thicknessspecimen.The punch has a circular cut-ting edge,which is pushed and turned
intoa suspicious lesion just like a hole saw.Thepunched out defect may be sutured
or mayheal secondarily.Punch biopsies,althoughworthwhile for melanoma in which
depthdiscernment is critical,may be too aggres-sive for a superficial lesion as the
punchmay force the tumor deeper into tissue.Incisional and excisional biopsies
arewell known to surgeons.Deciding whetherto use one revolves around whether
thediagnosis is obvious (eg,a dysplastic nevusin a patient with a history
ofthem),thetumor size,and whether a small biopsywill influence the excision
clearance mar-gin.When indicated,excisional biopsiesshould be oriented with sutures
or dye fortumor margin clearance.Fine-needle aspiration (FNA) may alsobe used to
obtain specimens for histologicexamination ofdeep material.FNA isworthwhile to
differentiate a dermal cystfrom a parotid tumor in the periauricularregion.With FNA
the pathologist aspiratestissue with a 23- or 25-gauge needle andstains and fixes
the material on a glass slide.Once the pathologic diagnosis ofskincancer is
confirmed,the surgeon plans fortumor destruction by correlating
tumorcharacteristics with patient�s age,skin his-tory,medical history,social
history,andcosmetic expectations.Treatment optionsFIGURE37-7Large multicolored
pigmentedlesions should undergo biopsy with a full-thicknessincision at the darkest
area.Table 37-2Melanoma:Survival RatesTumor 5-YearBreslow ClassificationClark
ClassificationThickness (mm)Survival (%)No evidence ofprimary tumorI.Tumor in
epidermis (noninvasive)< 0.7699Thickness > 0.76 mmII.Melanoma cells in papillary
dermis0.76�1.5 94Thickness 0.76�1.5 mmIII.Melanoma cells fill papillary
dermis1.51�2.25 83Thickness 1.51�3.0 mmIV.Melanoma cells in reticular
dermis2.26�3.0 72Thickness > 3.0 mmV.Melanoma cells in subcutaneous fat> 3.0<
50Table 37-3Melanoma:Biopsy StrategiesTumor ThicknessMargin ExcisionLymph Node
Dissection?Lentigo maligna,in situ5 mm�1.0 cmNoMelanoma < 1.00 mm1 cmNoMelanoma
1.01�4.00 mm2 cmPossible sentinel lymph nodedissection 1.0�4.0 mmMelanoma > 4.01
mm2�3 cmFor diagnostic purposes
Head and Neck Skin Cancer705might include liquid nitrogen cryotherapy,standard
excision,Mohs�micrographicsurgery (MMS),radiation,C and E,topicalchemotherapy,laser
ablation,photody-namic therapy,interferon,and retinoids.We review most ofthese
options below.Standard ExcisionCommonly,skin cancers are excised andassessed for
margin clearance.Exceptionsinclude some AKs and some superficialSCCs or BCCs,which
may be treated byother modalities.52Excision may be doneunder local anesthesia or
in the outpa-tient surgery setting.Tables 37-4 and 37-5 outline acceptable margins
for clearingmost lesions.The lesion and indicated margin forclearance is outlined
with a marking pen.Local anesthesia with epinephrine doesnot affect pathologic
margin assessmentbut may reduce the surgeon�s ability tomonitor vascularity to an
adjacent ran-dom flap.Clearer delineation oftumormargins may be enhanced with
adjunctiveprocedures for melanoma,BCC,and AK.In the case
ofmelanoma,subcutaneousextension should be viewed with a Wood�slight.In the cases
ofBCC and AK,pre-excision curettage delineates tumor mar-gins more accurately.Some
BCCs,mor-phea-like and infiltrative,may not be ascurettable as soft tumors,but the
BCCsthat are curettable have a 25% higherchance ofbeing cleared with the first
exci-sion than ifexcised without curettage(Figure 37-8).52Ideally,specimens should
be examinedhistologically on the entire lateral and deepmargin.Circumstances may
reduce thelikelihood ofthis beneficial extensive eval-uation.For example,frozen
histologic eval-uations (while the patient is anesthetizedin the operating room)
are often three tofour representative �loaf-of-bread�slices.You can imagine how
much time would beconsumed should the pathologist sectionand examine a large tumor
in toto.2Toabrogate the inherent limitations offrozensections,many surgeons
routinely delayreconstruction until after all margins arecleared by permanent
histology,or sendthe patient to a specialist in MMS.Permanent histology after
office exci-sion and subsequent delayed reconstruc-tion provides benefits to
surgeon andpatient alike.Office excision allows thepatient to visualize the extent
ofthe defectand to add input into personal reconstruc-tive desires and
expectations.The surgeonhas the option to research effective meth-ods
ofreconstruction away from the oper-ating room and to subsequently go to
theoperating room with a plan;the patientwill know prior to the surgery
exactlywhere the scars will be located.Delayedreconstruction has been proven
beneficialfor patients receiving skin grafts as thedelay eliminates the potential
forhematoma and may allow buildup ofahigher granulation base.MMS offers the same
�delayed�opportunity.The patient�s entire tumor isresected prior to
reconstruction,whichmay be performed on an elective basisoften up to a week
later.The only surgicaldifference between immediate (within 24 h) and delayed
reconstruction (=48 h)is that defects reconstructed later are cir-cumferentially
excised for 0.5 to 1 mm toexpose a new distinct margin.Debris mayalso need to be
curetted from the base.Regardless,this step-by-step delayed tech-nique is almost
painless and does not fos-ter infection (Figure 37-9).51,53Antibioticsare not
necessary.Mohs�Micrographic SurgeryMMS is based on two principles:(1)most tumors
spread by contiguousgrowth and (2) all tumor cells must beexcised for
cure.Dermatologist FredericE.Mohs,MD,originated his method inthe 1930s and
published results in 1941.Mohs�technique evaluates the entire cir-cumference and
deep margins afterfrozen sections.Unlike the representativebreadloafmethod,in which
the patholo-gist might suggest further removal ofanentire positive superior margin
ofthetumor,Mohs�technique pinpoints theactual location oftumor extension.Iden-
tified tumor extensions are re-excisedTable 37-4Margin Control for Squamous Cell
CancersTumor DescriptionMargin ControlSmall,well differentiated5 mm with
orientation> 1 cmIncrease margin sizeLesion on upper
lips,eyelids,nose,ears,etc.Consider Mohs�micrographic surgeryTable 37-5Margin
Control for Basal Cell CancersTumor DescriptionMargin Control5 mm or less2 mm 5
mm�1 cm3�4 mm 1�2 cm5�7 mm > 2 cm,morphea-like,orunusual 7�10 mm margin
orMohs�micrographic pathologic behaviorsurgery or delayed reconstruction following
permanent histologyUnusual pathologic behavior,recurrent Mohs�micrographic surgery
ordelayed tumors,tumors on lips,ear,nose,reconstruction following permanentmedial
canthus,eyelidshistology
706Part 5: Maxillofacial Pathologyand rescrutinized until the tumor istotally
removed.Hence,MMS is morepredictable for total cure and tissue spar-ing as
well.54�56Over the years we have noted certainlimitations to Mohs�technique,such
asoverconservative treatment for someaggressive tumors.This deficiency,notinherent
in the Mohs�technique,is provedby the fact that not all microscopic exten-sions are
visible to the human eye;there-fore,even tumors excised with Mohs�tech-niques may
recur.As a result,we believethat a large SCC ofthe scalp is betterserved with an
aggressive non-Mohs�exci-sion.Controversy exists as to whetherMohs�technique is
justified for melanomaand dermatofibrosarcoma protuberans,for example.For a 1 cm
nodulo-ulcerative BCC,Mohs�technique proceeds as follows:thelesion is debulked with
a curette and thenexcised with a 2 to 3 mm margin angled at45�toward the center
ofthe tumor.Thespecimen is anatomically oriented,subdi-vided into numbered color-
coded sec-tions,and mapped.Mapped segments arepressed flat on their freshly cut
border,frozen,and sectioned so that the entirefresh border is visualized.The cure
rates for primary BCCs < 2 cm treated with MMS approach99% (vs 90�95% by routine
pathologicexamination).56,57Standard verticalbreadloafsections evaluate < 1%
ofthesurgical margins.Recurrent BCC curerates range from 94 to 96% with MMSversus
85% with other modalities.56,57For primary SCC,MMS boasts a cureFIGURE37-8A,This
50-year-old man has what appears to be an imposing basal cell cancer.B,Curettage
ofthe softtumor allows easy visualization and control ofperipheral and deep
margins.C,Seven days after resection and marginclearance by permanent histology,a
cervicofacial-type flap above the superficial musculoaponeurotic systemis
planned.D,The flap is advanced superiorly.E,Hairlines and sideburns are
realigned.F,At 2 weeks the results are very esthetic.ABCDEF
Head and Neck Skin Cancer707ADCBEHGFILKJFIGURE37-9A,In the office the
surgeon,donning nonsterile gloves,curettes (with a dermatologic curette,pictured)
thisbiopsy-proven nasal basal cell cancer.The patient is under local
anesthesia.B,Curettage reveals that the tumor is smalland superficial.C,After
tagging the tumor for margin identification (alwaysshort 12:00 superior and long
left or lateral),the wound is dressed very specifically.(Ifthere is any potential
bleeding,a piece ofsurgicel may be placed at the base).D,Bacitracin is swabbed only
within the defect.E,Mastisol or tincture ofbenzoin is wiped peripherally.F,A
nonadherentdressing covers the wound base; the overdressing has an absorbent piece
ofgauze within a conforming mesh bandage,whichis placed over the wound.One or 2
days later,in the office the surgeon,donning nonsterile gloves,removes the
dressing.Thisprocedure is performed without the use ofanesthesia.The area is
cleaned with 50:50 peroxide and water,and the patientis instructed how to redress
the wound daily after a shower (which includeswashing out the defect with mild soap
andwater).G,The patient dresses the wound with bacitracin,a nonadhesive
dressing,and tape only.No scabs should form.Inthis case the histology analysis
returned declaring that the superior tumor margin was within one high-power
field.H,Onthe day ofsurgery,a small amount oftissue is planned for excision
superiorly (and peripherally to square the margins),and a bilobed flap is planned
as the defect is < 1.5 cm in diameter.I,The excisions have been made.J,During the
closurethe entire nasal dorsum is undermined submuscularly and
supraperichondrally.K,The second lobe ofthe flap is orientedperpendicular to the
alar rim to avoid lifting the rim.L,After 2 months the result is excellent.
708Part 5: Maxillofacial Pathologyrate from 94 to 99% as opposed to 90%for non-
Mohs�techniques.39,54,58Recur-rent SCC cure rates with MMS approach90% as opposed
to 76% for other treat-ment modalities.54Under these circumstances MMS isindicated
for the treatment ofrecurrentBCC,histologically difficult BCC
(ie,micronodular,infiltrative,and morphea-like),and BCCs in which conservation
oftissue is critical (eg,on the nose,lip,ear).For SCC,MMS might be indicated
forlower lip cancer,some poorly differentiat-ed SCCs,and areas where maximum
tissuepreservation is essential.7Radiation TherapyRadiation therapy (RT) has been
men-tioned for treatment ofskin malignan-cies for almost a century,but currently
itplays a role as an adjunctive or salvagemeasure,rarely a curative role.The cura-
tive advantage ofradiation is preserva-tion ofnormal tissue next to the irradia-
tion site.RT might therefore beconsidered for the
eyelid,lip,nose,andear.Unfortunately,RT conveys someunwanted potential side
effects:cuta-neous erythema,necrosis,hypopigmen-
tation,telangiectasia,atrophy,fibrosis,hair loss,delayed healing,and risk
ofthedevelopment offuture NMSCs whenadministered to younger patients.59RT oftumors
< 2 mm has a cure rateof90% and 85 to 95% for BCC and
SCC,respectively.60,61However,larger lesionshave a much lower success
rate.Formelanoma,local recurrence rates ofup to50% have been reported.62Thus,RT
formelanoma is only a viable option for med-ically compromised patients who
cannotwithstand surgery or for patients whorefuse surgery.CryosurgeryCryosurgery
destroys skin cancers andsome adjacent tissue by freezing.Cryosurgery cure rates
for AK,BCC,SCC,and lentigo maligna range from 94 to99%.63,64Liquid nitrogen may be
sprayedon the lesion directly or through a cry-oprobe.Rapid freezing ofthe treated
skinoccurs as heat is transferred from the skinto the probe.Intracellular ice
crystalsform,and cell membranes disrupt as thetemperature is lowered to �50�C to
�60�C.When thawing occurs electrolytes recrys-tallize,resulting in vascular stasis
and localalterations in the microcirculation,thusproducing further tissue
damage.2,65Most doctors freeze lesions plus a 4 to6 mm margin to account for tumor
exten-sion.Freeze-thaw cycles may be repeatedfor maximal effect.Healing occurs by
sec-ondary intention,with a flat hypopig-mented scar.The side effects
ofcryosurgeryinclude pain,erythema,edema,blistering,exudation,and scarring.This
technique isinexpensive,and there are no costs forpathology.Hence,a lesion chosen
forcryotherapy should be relatively small andwell demarcated.Curettage and
ElectrodesiccationC and E is a cost-effective but technique-dependent therapy
ofNMSC.The lesionarea is cleaned with alcohol,outlined witha provisional margin by
a skin marker,andanesthetized.The lesion is curetted aggres-sively with the skin
tensed,after whichelectrodesiccation (hyfrecation) for hemo-stasis and adjacent
tissue kill occurs.Thiscycle may be repeated three to five times.The major
advantage to C and E isexpedience,fostering treatment ofmulti-ple lesions within a
single visit.Disadvan-tages include prolonged healing,oftenweeks depending on size
and care,hypopigmentation,and possibly hyper-trophic scar.Material from curettage
maybe sent for initial pathology,but margincontrol after C and E is not
possible(unless curettage is used as a precursor toexcisional pathology).The
clinician�s experience and thetumor�s anatomic site and size are prog-nostic
factors limiting success followingC and E.BCCs < 5 mm have an 8.5%recurrence rate
after C and E by an expe-rienced clinician.66Lesions ofthe nose,ear,and perioral
and periocular areasmay recur at a rate of16%.66This ratesoars to 26% for lesions >
20 mm.66Ther-apeutic C and E is therefore contraindi-cated for larger
lesions,poorly differenti-ated SCC,or melanoma.Topical ChemotherapyTopical 5-FU or
5% imiquimod medicallyeliminates surface lesions.Retinoids areoccasionally used
concurrently.5-FU is athymine analog that interferes with DNAsynthesis causing cell
death by acting as aninhibitor ofthymidylate synthase.Imiquimodinduces production
ofinterferon-aand mes-senger ribonucleic acid cytokines.Appli-cation of5-FU is
recommended twicedaily for 2 to 3 weeks for superficial AKand for 3 to 6 weeks for
more diffuse wor-risome lesions.Imiquimod is applied onlythree times per week but
currently ismuch more expensive than 5-FU.Curerates with 5-FU and imiquimod
rangefrom 92% for SCC in situ to 95% forsuperficial BCC and AK.2,67Patients need to
be warned that thereis an ugly inflammatory scabby reactionduring topical
therapy,but the cosmeticoutcome is usually very good as long ascompliance is
nurtured.LasersThe CO2laser focuses a beam oflight witha wavelength of10,600
nm.Laser light isabsorbed by water and nonselectivelyvaporizes the skin.The
CO2laser can beused as a cutting instrument (in thefocused mode) to excise or
ablate lesions(in a defocused mode) such as multipleAKs,superficial BCC,and SCC.We
havefound its greatest benefit in ablation ofsuperficial AK and superficial
SCC,bothon the skin and lower lips.Presurgical skinpreparation with retinoids may
foster morerapid healing.We have not prescribed pre-operative antibiotics or
antivirals for small
Head and Neck Skin Cancer709localized areas but continue to do so whenlarge areas
ofthe face are treated.Photodynamic TherapyPhotodynamic therapy is not
widelyaccepted for skin cancer therapy but hasbeen applied to
lung,breast,colon,andbladder cancers.Aminolevulinic acid iswiped on a lesion;it is
metabolized in can-cer cells to produce porphyrins,which actas
photosensitizers.Four to 6 hours later,the area is irradiated with visible
lightfrom a laser or noncoherent light source.Reactive O2species are generated
withinthe cells producing cell death.68Cure rates for photodynamic therapyfor
AKs,superficial SCC,and BCC arereported to be > 90% in some studies,but tumors
thicker than 2 mm are photoresistant.69InterferonsInterferons are cytokines that
may effectcell growth and differentiation and accentimmune responses and antiviral
activity.Intralesional injection ofinterferon-acanattain cure rates of> 80% for
superficialand nodulo-ulcerative BCC.70,71RetinoidsRetinoids are vitamin A
derivatives thatare crucial for control ofcell growth,dif-ferentiation,and
apoptosis.Topicalretinoids are somewhat effective againstAKs but much less so
against even superfi-cial BCCs and SCCs.Application ofretinoids as a skin cancer
preventative is along-term proposition as the effects ofthedrug plateau at around 6
months andreverse shortly after discontinuation.Retinoids do appear to act
synergistical-ly with 5-FU and may be applied in an exfo-liation regimen.Noted
complaints includedryness and flaking,minor side effects com-pared with the
clinical effects of5-FU.Applied Skin Anatomy The skin is composed oftwo
layers:thesuperficial epidermis and,beneath it,thedermis.The epidermis is composed
offour distinct layers.From deep to superfi-cial,they are as follows:basal cell
(stratumbasale),prickle cell (stratum spinosum),granular cell (stratum
granulosum),andkeratin (stratum corneum).Cells from thestratum basale divide and
migrate upwardtoward the stratum corneum.The dynam-ic epidermis turns over and
exfoliatesevery 30 days.This is why buried epitheli-um from a cyst might continue
to producesebaceous keratin.The epidermis contains four
celltypes:keratinocytes,Langerhans�cells,melanocytes,and Merkel cells.Ker-
atinocytes constitute 80% ofthe epider-mal cell makeup.Langerhans�cells are
antigen-presentingcells,which capture andprocess antigens and present them toskin-
specific lymphocytes.Aging andsignificant sun exposure both lessen thetotal number
ofLangerhans�cells.This isone partial explanation for the increaseofskin neoplasms
in the elderly.72Melanocytes are ofneural crest originand are found in the basal
layer.Melanocytes produce melanin,which,inturn,protects the nucleus ofthe ker-
atinocyte from UV radiation.Althoughnumbers ofmelanocytes are constant forall
individuals,the activity ofthemelanocytes differs from one race to thenext.For
example,melanocyte activity indarkly pigmented skin is higher than inlight-colored
skin.As with Langerhans�cells,numbers ofmelanocytes decreasewith age,another
explanation for moreskin cancers developing as we get older.73,74Merkel cells,found
in the epidermis anddermis,have an unclear function.The dermis,situated between the
epi-dermis and subcutaneous fat,adheres to theepidermis at the basement
membrane.Thebasement membrane mechanically sup-ports the epidermis and acts as a
mechani-cal barrier.The two dermal layers are thesuperficial papillary dermis and a
deeperthicker reticular layer.The dermis is com-posed ofcollagen,elastic tissue,and
groundsubstance.Collagen decreases by 1% a yearthroughout adulthood.75Topical
tretinoininhibits dermal collagenase,thus slowingthe degradation rate
ofcollagen.76,77Elastic fibers in the dermis provideskin with recoil.With
aging,elastic fibersdecrease causing skin laxity,bags,andjowls.Chronic sun exposure
thickens elas-tic fibers,and clumps form in the papil-lary layer.Chemical
peels,dermabrasion,and laser resurfacing can remove some ofthese clumps.78The
dermal ground substance is madeup ofglycosaminoglycans,hyaluronicacid,chondroitin
4-sulfate,fibronectin,and dermatan sulfate.These constituentshydrate the skin and
maintain tensile elas-ticity.78The principle cell ofthe dermis isthe
fibroblast,whose functions includeproduction ofcollagen,elastin,andground
substance.Fibroblasts enhancewound healing through contraction andproduction
ofscar.Aging affects skin quality.Fine wrin-kling,dermal atrophy,and a decrease
insubdermal adipose tissue are aging phe-nomena.Epidermal regeneration mayslow down
by up to 50%,retarding sec-ondary wound healing.79(Note:Isotretinoin retards
epithelial regenerationchemically;hence,elective surgery shouldbe limited on
patients having usedisotretinoin until the medication has beendiscontinued for 6�8
mo.) Natural colla-gen decreases in quality and quantity.Skinbecomes more compact
as the collagenrearranges itselfinto thick coarse bundlesor loosely woven straight
fibers.The der-mal blood vessels may be collapsed,disor-ganized,or absent in the
elderly,potentiat-ing a greater risk for flap necrosis.21,80Skin has a rich nerve
supply.In theepidermis the Merkel cell may providetouch perception.Meissner�s
corpuscles,located in the papillary dermis,providefine touch sensation.Pacinian
corpuscles,located in the deeper subcutaneous tissue,mediate deep pressure and
vibratory
710Part 5: Maxillofacial Pathologysensation.Autonomic efferent nervesinnervate
blood vessels and appendagealstructures.Hair-bearing skin is commonlyreferred to as
nonglabrous and smoothnon�hair-bearing skin as glabrous.Skinconditions vary between
individuals andfrom region to region with respect
tomobility,color,scars,Fitzpatrick type,tex-ture,thickness,and adnexal
structures.81The blood supply to the skin servestwo functions:nutrition and thermal
reg-ulation.Two major routes ofblood supplyexist�musculocutaneous and septocuta-
neous arteries.82The musculocutaneoussystem traverses the muscle and enters
thesubcutaneous tissue in a random pattern(the basis for random skin flaps).Random-
pattern blood flow to the tip ofthe flap is via the interconnecting subder-mal
plexus.The superficial vascular plexuslocated in the reticular dermis providesthe
capillary loops in the dermal papillae.The deeper vascular plexus,or
subdermalplexus,lies between the dermis and subcu-taneous fat.A septocutaneous
vessel trav-els through the septal fascia and coursesparallel to the skin surface
with an accom-panying vein.Named septocutaneous ves-sels (eg,supratrochlear)
provide an axiallybased flap with a rich blood supply.A largeinterconnecting
vascular arcade existsbetween the systems.83Understanding thefacial vascular
network is crucial to creat-ing flaps that survive.Flaps and Grafts and Secondary
Intention HealingDefinitions and ConceptsThe removalofany tumor leaves a defect.The
hole cre-ated after tumor excision may be called theprimary defect.The secondary
defect isthe wound created after tissue is trans-posed to close the primary
defect.Everyflap creates a potential secondary defect.Ideally,secondary defects
should be easy toclose,within relaxed skin tension lines(RSTLs),in areas ofloose
adjacent tissue,and within anatomic boundaries.84Options for defect repair include
(1)primary closure,(2) local or distant flap,(3) graft,and (4) healing by
secondaryintention.Elasticity and movability aretwo inherent skin characteristics
thatenable relocation and,perhaps,primaryclosure.Elasticity is the ability
oftheskin to stretch.Skin in the cheek andneck is very elastic.Movability is
notrelated to elasticity.Temple skin is lessmovable than cheek skin,and the scalp
isrelatively immobile.Flaps move tissue,skin and subcuta-neous from one area to
another with anaccompanying vascular supply.Flaps arecosmetic,use well-matched
skin,andfunctionally protect underlying struc-tures such as bone or
cartilage,whichmay not have adequate blood supply tosupport a graft.Three types
of�impure�flap movements are classically defined�advancement,rotation,and
transposi-tion�although some suggest there areonly two types ofmovement�slidingand
lifting.84�86Slidingrefers to stretch-ing or mobilizing tissue from one site
toanother (advancement and rotation).Liftingtissue across a bridge ofnormaltissue
to close a defect is similar to trans-position.84All flaps (except free flaps)have
some pivotal restraint,whether it beadjacent skin,subcutaneous tissue,orblood
vessels.Delay increases viability to a flap byenlarging and realigning the
subdermalvasculature plexus.It is now known thatskin flap reliability is based on
�angio-some�units;therefore,wide and thin ran-dom flaps run out ofblood supply
inroughly the same location.Delay may aug-ment survivability.Methods include rais-
ing and suturing tissue without disturbingthe pedicle,and tissue expansion.Subse-
quently (9�12 d later),the flap is mobi-lized.84,87The mechanisms that increasethe
blood flow with delay include thedepletion ofvasoconstricting substances,formation
ofvascular collaterals andreorientation ofvascular channels,stimu-lation ofan
inflammatory response,andrelease ofvasodilating substances.Esthetic flaps are not
mere hole fillers.They are designed to complement naturalesthetic units and facial
borders.Defectsthat trespass multiple esthetic units aredesigned to reproduce these
independentunits.For example,a cheek tumor defectthat encroaches on the nose might
bereconstructed with different flaps and/orgrafts for the cheek and nose.Grafts are
easy to position into recipi-ent defects and are ideal for monitoringtumors.Grafts
must be placed on a well-vascularized bed.Sometimes exposedbone should be allowed
to build a granu-lation base before grafting.Grafts may beoffull thickness or split
thickness.Har-vesting methods include punching,shav-ing with a dermatome,and
excision.Graftdonor sites are selected based on estheticand tumor
considerations.Ideally,graftsto the nose are well matched with preau-ricular
skin,but any supraclavicular facialgraft (from the blush area) matches thefacial
color better than does any torso orthigh graft.Healing by secondary intention is
apainless but time-consuming process.It isindicated for patients who do not
wantmore surgery,who can accept or obtainthe daily care,and who can accept ascarred
result.Secondary healing can beused for small defects (< 1 cm) or for larg-er
defects in areas where the resulting scarwould be inconspicuous or tumor obser-
vation is critical.Healing by secondary intention is sim-ilar to open-wound
therapy.Followingtumor excision and hemostasis,the woundis dressed with antibiotic
ointment (eg,bacitracin and/or polymyxin B sulfate).The outer edges ofthe wound are
coatedwith an adhesive (eg,adhesive bandage ortincture ofbenzoin).A
nonadherentdressing is applied over the wound and asmall rim ofperipheral
tissue.This istopped with a dry piece ofgauze to absorbany blood,which is then
covered with a
Head and Neck Skin Cancer711contour mesh tape.When the defect isatop bone,the raw
bone may be coveredwith two layers ofmoisture-retaining wetgauze,but any method
that abrogates des-iccation is acceptable (Figure 37-10).Three days later the
dressing isremoved and the wound inspected.Anyoozing and crusting should be
removedwith a 50:50 peroxide and water solution.The wound is redressed in three
layers�antibiotic ointment within the wound fol-lowed by a nonadherent
dressing,which isthen covered with mesh tape.The patientredresses the wound in this
fashion on adaily basis to keep the area moist and freeofscabs.Areas amenable to
secondaryepithelialization include the scalp,theretroauricular area,and some
concavitiesaway from mobile apertures.Secondaryepithelialization would be a poor
choicearound the mouth,for example,whereretraction might distort the lips.Three
caveats regarding secondaryhealing are useful to keep in mind.First,scabs should
not form.Scabs hinderepithelialization and harbor bacteria.Sec-ond,continuous
application ofantibioticointment can lead to allergic reactions andyeast
infections.This is more commonwith ointments that contain neomycinsulfate than with
bacitracin.Alternatively,petrolatum can be substituted for theantibiotic
ointment.Finally,some patientscan be so incapacitated by their medicalillnesses
that they cannot dress theirwounds.Home health care nursing can beenlisted to aid
in their daily wound care.Skin BiomechanicsSkin is a heteroge-neous material with
unique mechanicalproperties.As skin is stretched,the ran-domly oriented collagen
and elastic fibersare stretched in the direction oftheapplied force.This continues
until all ofthe available collagen and elastic fibers areFIGURE37-10A,This 60-year-
old patient (who has diabetes and congestive heart failure) has a very rapid-ly
growing forehead/scalp squamous cell carcinoma.B,In the operating room the tumor is
widely excised.C,The base shows tumor into the outer table ofthe skull,which is
removed.D,The wound is dressed openwith microfibrillar collagen peripherally to
prevent bleeding,and a compression bandage over two layers ofmoist ointment-
saturated mesh gauze.Permanent histology shows complete tumor clearance,but
thepatient�s medical problems delay reconstruction.E,The patient has an excellent
granulation base at 5 weeks.He elects to allow the defect site to epithelialize
secondarily with daily dressing changes at home.F,At 8 weeks50% epithelialization
is evident.G,Total epithelialization has occurred at around 3 months.He has had
notumor recurrence or metastasis after a 2-year follow-up and has deferred further
reconstruction.ABCDEFG
712Part 5: Maxillofacial Pathologyrecruited and no further lengtheningoccurs.After
the maximum amount ofstretch is reached,the skin may rupture.Permanent striae may
scar the skin sur-face,as is often noted in pregnancy.Over-stretching the skin
collagen effaces theblood vessels under tension;thus,necrosissecondary to decreased
perfusion to a dis-tal flap may occur (Figure 37-11).88Skin tension exists in all
directionson the face but is greatest along theRSTLs.Ideally,elective incisions
shouldbe placed parallel to the RSTLs.Incisionsmade perpendicular to RSTLs (or in
thelines ofmaximum extensibility [LME])gape and heal with more obtrusivescars.89The
rhombic flap,once consid-ered by many as the �workhorse�facialflap,has been used
less over time becausesome ofthe final legs lie within the LME.Today flaps are more
commonlydesigned with topographic units andRSTLs as primary
considerations,ratherthan just to fill a hole.Skin is elastic and stretches easily
atlow stress levels.This is related to theinherent extensibility ofthe skin.At
high-er forces skin may become viscoelastic,that is,it can extend out a little more
inspite ofits thick state.This phenomenonis explicable through the two time-
dependent characteristics:creep andstress relaxation.88Mechanical creeprefers to
the changein length that is seen when skin is heldunder a constant stress or
force.The forcethat is exerted to stretch skin decreaseswith time.88The surgeon
routinely notesthis mechanism at work after he tightlysutures an avulsive forehead
wound.Twodays later the forehead is relaxed again.High stress loads therefore
produce adegree ofcreep.The skin may not be total-ly relaxed for several
months.Serial exci-sion is a technique that harnesses therelaxation ofskin over
time.Wide defectsmay be closed sequentially over time.Stress relaxationis the
decrease instress that occurs over time when skin isheld under tension at a
constant strain oris cyclically loaded.88It may be effectedintraoperatively with
the placement ofaballoon under the skin or by scoring thescalp galea and pulling
the skin.Addition-ally,there are skin stretchers that are madefor this purpose
(Figure 37-12).Finally,biologic creepis a slowmethodic stretching
ofskin,yieldingbrand new skin.88Skin expanders do justthat (Figure 37-13).Flap
UnderminingSafe flap closure ofadefect is dependent on harnessing theinbred
stretchable bendable nature ofskinwithout exceeding the limits ofstretch orblood
supply.Some tissues can bestretched for centimeters without under-mining
occurring,whereas others must beseparated from tethering subcutaneoustissues.On the
other hand,a subcutaneousisland flap,totally separated from the teth-er
ofskin,depends on the mobile vascularsubcutaneous pedicle.Undermining releases the
verticalattachments between the dermis and sub-cutaneous planes,thereby reducing
shear-ing forces and allowing the skin to slideand redrape in another
position.78Themobilization benefits from underminingfacial skin usually occur
within the first 2cm.Animal studies reveal that undermin-ing beyond 4 cm produces
little skin edgeadvance and possibly a more difficultstretch oftissue.90,91A
correct undermining level providesthe critical balance between mobility andblood
supply.For example,simple randomflaps,undermined in the superficial fat,are easy to
raise on the cheek.Submuscu-lar flaps maintain a robust blood supply tosmall
relatively immobile nasal flaps.Flap DesignsAdvancement FlapsAnadvancement flap is
advanced linearlyover a defect.It consists ofa classic ellip-tic closure with
adjacent undermining;there are no rotational or pivotal move-ments.Tissue
elasticity provides ade-quate horizontal motion with a flat clo-sure effected as
Burow�s triangles areremoved from the ends.The length oftheellipse is three to four
times the width ofthe defect.Advancement flaps can be constructedwith multiple
modifications:simple,FIGURE37-11This large basal cell cancer was excised (A) and
closed with two flaps (B).The patient,a smoker,had excess tension placed on the
lower flap,leading ultimately to almost 1 cm oftip necrosis.AB
Head and Neck Skin Cancer713square,bilateral,Burow�s triangle reposi-tioning,and A-
or O- to T-shapeddesigns.92The experienced surgeon real-izes that the tethering
forces ofadvancingskin also constrict the size ofthe leadingedge.Modifications are
useful in specificinstances.All flaps,including simpleadvancement flaps,presuppose
that thesurgeon can disguise,adjust,transpose,oreliminate �dog-ears�or excess
tissue thatgathers as tissue is transposed.There are seven ways to deal withdog-
ears93�96:1.Do nothing;this approach works wellon the scalp as bunched up tissue
liesdown with time2.Close opposite lines ofuneven lengthsby spreading out the
problem�halv-ing (Figure 37-14A)3.Remove the excess to a hidden area�anend or
middle triangle (Figure 37-14B) 4.Lengthen the incision.This eliminatesbunching
(Figure 37-14C) 5.Perform an M-plasty (sometimescalled a T-plasty),which shortens
theproblem (Figure 37-14D) 6.Reverse the Sloop and hide the excesselsewhere (Figure
37-14E) 7.Advance the dog-ear as a flap (subcu-taneous �island�) or use it as a
free graft(Figure 37-14 F;also see Figure 37-6) Rotational FlapsCurvilinear
rotationflaps rotate from a tethered pivot point.These flaps fill triangular
defects.Thelength ofthe arc is dependent on manyvariables,such as existing
laxity,the size ofthe defect,the location,and blood supplyto the
flap.85,97�101Rotation flaps rarely fitFIGURE37-12A,This 95-year-old woman has a
relatively small scalp defect.B,Finger pressure shows that significanttension is
necessary to close it elliptically.C,After limited subgaleal undermining,two pins
are placed subcutaneously.D,A skin stretcher (courtesy ofLife Sciences Medical) is
hooked onto the pins.Slow loading is applied for 30 minutes.E,Afterthe end
triangles are excised,the wound is stapled closed.F,The site after 2 months.ABCDEF
714Part 5: Maxillofacial Pathologyperfected geometric schemes ofsuccess.Rather,the
surgeon often finds himselfadjusting to the specific variables ofagiven situation
(Figure 37-15).There aretwo exceptions to this complexity thathave been worked out
fairly precisely:1.The nasal bilobed flap ofZitelli hasexcellent results when
applied towardlower or middle nasal defects of1.5 cmor less.102This occurs as long
as thesecond lobe ofthe flap is perpendicu-lar to the alar rim and the first
lobedoes not cross deep concavities such asthe alar groove 2.The scalp rotation
method ofAhujafills defects ofup to 3 cm with mini-mal adjustments103Advantages to
rotational flaps includebroad-based reliable vascularity,flexibilityin design,and
easy placement ofscars intoesthetic/cosmetic zones or RSTLs.A majoradvantage is
that the flap can be rotatedagain should additional tissue need to beremoved
secondary to tumor concerns orshould laxity be lacking.98,104Disadvantages to
rotational flapsinclude the problems associated with anypivotal flap such as
standing cutaneousdeformities and the need for larger flaps.Regardless,rotational
flaps may be ideal-ly designed to reconstruct medium tolarge defects ofthe
cheek,neck,scalp,and forehead.Transposition FlapsTransposition flapstransfer
defined tissue along an arc ofrotation,often over normal tissue,torepair a primary
defect.Actual tissuemovement may be rotational,linear,orboth (Figure 37-
16).Transposition flapstend to be more confined than are rota-tion flaps,and design
is critical for suc-cess.The design/location ofthe pivotpoint is the most important
factor.Aftertissue is transposed,flap tensions shouldbe diffused to prevent
strangulation oftissue and distortion ofadjacent struc-tures.The regional
differences in tissuemobility impact the geometry ofthe flapdesign,with the classic
transpositionbeing a rhombus.The rhombic flap is an equilateral par-allelogram with
oblique angles.The (Lim-berg) rhombic flap,first described in 1963,was an
equilateral rhombus with 60�and120�internal angles.105According to the classic
(Borges)design,eight potential rhombic flaps mayclose a defect.These flaps are
constructedas umbrellas,drawn offthe obtuse side oftwo potential
parallelograms.These paral-lelograms each have two sides parallel tothe LME.These
LME are always perpen-dicular to RSTLs and run in the directionthat tissue
stretches most efficaciously.The rhombic flap,whose short diago-nal line parallels
the LME and whosemobilization does not interfere with adja-cent structures,is
usually chosen for therhombic transposition.The resulting ten-sion vector in
rhombic flaps lies 20�fromthe short diagonal in a loose tissue
plane.Dufourtmental,Webster,and othersmodified the classic rhombic design.106The
Dufourtmental flap was designed toclose rhombic defects with acute
anglesapproximating 90�or a square defect.AsFIGURE37-13A,This 45-year-old heavy
smoker had a squamous cell cancer removed fromhis midforehead and a basal cell
cancer from the left temple.Direct advancement closure wasimpossible.B,After
allowing some granulation tissue to form at the base,a split graft wasplaced on the
midforehead.An 8 �6 cm skin expander was placed laterally and expandedtwice weekly
for just over 2 months.C,The expanded rotation flap was mobilized to coverthe
midforehead defect.D,The result 1 month after closure.Note the well-healed direct
clo-sure ofthe right cheek defect and the depression ofthe left temple full-
thickness skin graft.ABCD
Head and Neck Skin Cancer7153231323TumorRSTLLengthenlineFIGURE37-14Six ofthe seven
ways to deal with dog-ears (the seventh being to do nothing).A,Halving.Close
opposite lines ofuneven lengths by spreading outthe problem.B,End or middle
triangle.Remove the excess in a hidden area.C,Lengthen the incision.This eliminates
bunching.D,M-plasty (sometimes called aT-plasty).This procedure shortens the
problem.E,Reverse the S.Hide the excess elsewhere.F,Advance the dog-ear as a flap
(subcutaneous island) or use it as afree graft (see also Figure 37-6).RSTL =
relaxed skin tension lines.ABDEFC
716Part 5: Maxillofacial Pathologywith the Limberg design,the peripherallines were
equal in length,but unlike therhombic flap,the short diagonal differedin angle
size.Dufourtmental designed twoisosceles triangles situated base to base.Once the
sides ofthe triangles weredrawn,the short diagonal was extended,as was one ofthe
adjacent sides.A thirdline bisecting these two lines creates thefirst flap.The
cutback line was drawn par-alleling the long diagonal completing thesecond flap.The
Webster 30�flap allowedfor easier closure by bisecting the 60�angle into two
30�angles via an M-plasty.Here,the short diagonal had to be at least110�to prevent
puckering and to main-tain flap viability.Rhombic,banner,note flaps,and oth-ers
have been modified to close circulardefects over all areas ofthe face.Axial Pattern
FlapsAxial pattern flapsare based on named vessels in the headand neck.Classic
designs include the Abbe(Figure 37-17) and Estlander flaps and theparamedian
forehead flap.97A full descrip-tion ofthese flaps is discussed in Chapter38,�Local
and Regional Flaps.�Skin GraftsSkin grafting involves theremoval ofdonor skin
(epidermis andvarying levels ofdermis,fat,or muscle)from one area to revascularize
at another.The success ofskin grafts is based on fac-tors that affect angiogenesis
and capillaryingrowth into the graft.Recipient bed vascularity and intimategraft-
host contact as well as overall hosthealth or condition affect graft success.Wounds
with a poor vascular supply maynot support a graft or may need to be pre-pared
before grafting.Cartilage base;irra-diated tissue;fibrosis;and foreign,crushed,or
nonviable tissue can compro-mise success.Additional procedures,suchas bringing in
vascular tissue from else-where,may be required to optimize therecipient bed prior
to skin grafting.98Bed vascularity may be compromisedby bleeding or cautery to
arrest bleeding.Thus,there is an inherent benefit to delay-ing grafting or placing
a pressure bolsterbandage on top ofthe graft to preventbleeding.We do not touch
full-thicknessgraft bolsters for 6 or 7 days.Mechanical shear forces may
disruptcontact between the graft and recipientbed,promoting graft
failure.Althoughthis may be minimized with appropriatesuturing techniques as well
as the place-ment ofdressings,the force ofa hardshower can dislodge a graft and
shouldbe avoided.Wound infections rarely jeopardizeskin grafts in the head and
neck.It is com-mon for surgeons to confuse the darkeschar ofa failing graft in a
smoker withinfection.Regardless,some local measuresthat decrease wound bacteria
includesaline dressings,sulfadiazine silver,mafenide acetate cream,acetic acid
solu-tions,sodium hypochlorite solutions,andvinegar and water.A patient�s overall
medical health caninfluence the success ofskin grafting.Autoimmune diseases such as
rheumatoidarthritis,systemic lupus erythematosus,hematologic disorders,diabetes
mellitus,FIGURE37-15A,This 70-year-old has anindiscreet temple basal cell
cancer,which isremoved by Mohs�micrographic surgery.B,Clo-sure includes a large
rotational scalp flapdesigned with the center ofthe arc ofrotation atthe 18-gauge
needle position,and a templeadvancement flap.Cand D,The flaps are mobi-lized and
stapled into position prior to final clo-sure.E,The result is excellent at 1
month.ACEBD
Head and Neck Skin Cancer717poor nutrition,and smoking as well asmedications such
as corticosteroids andchemotherapeutic agents may compro-mise graft
success.99�101Full-Thickness Skin GraftsFull-thicknessskin grafts (FTSGs) are
chosen when localor distant flaps are not feasible or whenthe FTSG would offer
acceptable cosmesisand function.Examples include the multi-operated face,upper
nasal surface defects,nasal lining tissue,and medial canthalarea.FTSGs resist
contraction and maypossess the texture and color ofnormalskin.In children FTSGs
have the potentialto grow.98The FTSG is preferred over the split-thickness skin
graft (STSG) in areaswhere a wound contracture may lead to afunctional deformity.An
example is thelower eyelid,where wound contracturewould result in ectropion.An
excellentFTSG for this example would includeupper eyelid skin and orbicularis
oculimuscle,which has been shown to pre-dictably revascularize.Selection criteria
for a head and neckFTSG directs the surgeon to carefully con-sider particulars ofa
variety ofsites�theupper eyelid,post- or preauricular skin,and the lateral neck or
supraclavicularregion.For example,postauricular skin isphotoprotected and has few
adnexal struc-tures,which may not be suitable for nasaldefects.Preauricular skin
grafts in malescan lead to sideburn asymmetry.Supra-clavicular and neck skin is
thin and may bemore photodamaged than the face.Inaddition,a supraclavicular scar
may be anuisance for women who wear clothingwith low necklines.The harvesting
ofmost FTSGsinvolves cutting out a simple template ofthe defect (eg,from suture
packaging)(Figure 37-18).Since an FTSG contractsby 10 to 15% after harvest,the
donor graftpattern must be enlarged by around20%.102This contracture issue is
critical inareas ofmobility such as in the lower eye-lid.Here,grafts should be
enlarged by 150to 200% vertically to avoid ectropion/con-traction
occurring.98,101The FTSG may be defatted with ser-rated scissors or by scraping
with a blade.Defatting is complete when the shiny der-mis is homogeneously
exposed.FTSGshould fit into a wound bed with maxi-mum surface contact without any
tenting.Basting sutures may be used to affix thegraft to the underlying bed to
squeeze outdead space prior to peripheral sutur-ing.98,103Peripheral sutures are
easier toinsert when passed from the graft throughthe host skin with a tapered
needle.Any nonadherent (to the graft) bolsterofcotton,gauze petrolatum
dressing,orplastic,for example,secured a few millime-ters outside the grafted
tissue is acceptable.Some surgeons prefer to remove the bolsterafter 48 hours to
inspect the surgical siteFIGURE37-16A,This 45-year-old woman hashad a basal cell
carcinoma for the past 3 years.B,It is repaired with a simple submental transposi-
tion flap.C,Perhaps the lateral submandibularbulkiness will need to be removed in
the future,butthe submental fat removal was highly esthetic.ABCFIGURE37-17A,This
70-year-old man has alarge basal cell cancer removed by Mohs�micro-graphic
surgery.B,Subsequently a midline axi-ally based Abbe flap is inserted.C,Three
weekslater,the Abbe flap is divided and inset as an in-office procedure.The
esthetic result 2 weeks latershows the flap is not exactly in the midline
butsimulates the philtral area effectively.ABC
718Part 5: Maxillofacial Pathologyand then replace the bolster with a
moreconventional dressing.FTSGs undergo an evolutionarysequence.Initially,a graft
is white followedby a period ofcyanosis or a bluish/viola-ceous hue.Subsequently
there is a periodofhyperemia or a red state,which fadesover time until the graft
assumes its nor-mal color.Ifthe graft fails,the entire epi-dermis turns black and
sloughs off,fol-lowed by reepithelialization.98Thenecrotic graft acts as a biologic
dressing,allowing healing to occur by secondaryintention from the wound edges as
well asfrom adnexal structures.Split-Thickness Skin GraftsAn STSG isdefined as thin
ifits thickness measures 0.02to 0.03 cm,medium from 0.03 to 0.046 cm,and thick from
0.046 to 0.076 cm.ThinnerSTSGs have improved survival rates com-pared with thicker
ones because there isgreater exposure ofthe graft to theunderlying vasculature,and
less tissue isneeded for revascularization.STSGs havea higher degree ofcontraction
than doFTSGs and do not grow in children.Thingrafts afford less protection to the
under-lying tissues and do not withstand repeat-ed trauma well.For example,an
STSGmay be chosen to cover a bare pericrani-um/skull after removal ofa scalp
tumor;subsequently,the patient may reportbreakdown sites or scabs from sleepingon
the grafted sites.STSGs are generally less pleasing cos-metically than are FTSGs
and areemployed for functional reconstruction(Figure 37-19).STSGs are worthwhile
for (1) woundstoo large to repair with a local flap or anFTSG,(2) wounds requiring
monitoringfor tumor recurrence,or (3) temporarycoverage ofa wound prior to
definitivereconstruction.Contraindications includeareas that might compromise
functionalor esthetic expectations.STSG donor sites for facial reconstruc-tions
include the �blush zone�ofthe later-al neck and supraclavicular area and
thescalp,owing to their similarity in color andtexture.The
hip,thigh,buttock,abdomen,torso,and inner aspect ofthe arm are alsoapplicable at
times.98,100,104There are varying types ofder-matomes ranging from machine to manu-
al.The Brown dermatome allows for pre-cise modification ofgraft thickness.Thegraft
dimensions should be at least 25%larger than the wound defect.98Other der-matomes
include the Padgett,Davol-Simon,Castroviejo,Reese,and Padgett-Hood dermatomes and
the Weck knife.The sterile donor site is lubricatedwith mineral oil.Traction and
counter-traction are applied,and the dermatome isengaged and advanced with a slight
down-ward and forward pressure.The donor sitebleeds ifit is cut in the correct
plane.Afterpressure or thrombin control,a semiper-meable occlusive dressing covers
thedonor site and is left in place for 1 week to10 days.Semipermeable membrane
dress-ings decrease the pain ofthe donor siteand enhance wound healing by maintain-
ing a moist environment.97Other dressing materials includeAllevyn and Nobecutane
spray.Allevyn is ahydrophilic polyurethane material that ishighly absorbable and
nonadherent.Itsouter layer is waterproofand bacteriaproof.The dressing is
soft,absorbent,andcomfortable for the patient.Nobecutanespray when applied on the
wound forms atransparent plastic film.Nobecutane con-tains a modified acrylic resin
in an organ-ic solvent along with the bactericidal-fungicidal agent
tetramethylthiuramdisulfide.Brodovsky and colleaguesshowed that this spray is an
effective tem-porary dressing that promotes rapid pain-less healing.The film is
shed spontaneous-ly with epidermal regeneration.107FIGURE37-18A,This 65-year-old
womanhas had a superficial basal cell cancerremoved from her upper lip.B,For
estheticpurposes,the entire philtral section was alsoexcised and replaced with a
full-thickness skingraft harvested preauricularly.C,The graftwas designed with a
template.D,The result at1 month is esthetically excellent.ABDC
Head and Neck Skin Cancer719Unlike for an FTSG,a tie-over dress-ing may not be
necessary for STSG.Agood compression dressing and/or bast-ing stitches may suffice
to promoteadherence between the graft and under-lying tissue and to prevent fluid
accumu-lation.A variation to placing interruptedbasting sutures is the spiral
bastingstitch.The suture is started at the edge ofthe graft with the �tail�left
long.108Thesuture is then run along the periphery ofthe graft,spiraling toward the
center,and then tied to the tail.The graft canthen be dressed in a similar fashion
tothat for an FTSG.Composite GraftsComposite graftscontain two or more tissue
layers.Com-posite grafts are ideal for reconstructingthe nasal ala rim,auricular
defects,andeyebrows.Composite grafts are able tomaintain the thinness and contour
ofthestructure with minimal contracture.Themost common donor site for
compositegrafts is the ear,including the crus ofhelix,rim,antihelix,tragus,and
earlobe.A major disadvantage to compositegrafts is the risk ofgraft failure,which
ishigher than for FTSG and STSG and isattributed to the high metabolic demandsofthe
grafts.Harvesting (donor) adjacentdermis attached to the composite graftand
inserting the de-epithelialized dermisinto adjacent subcutaneous tunnels(recipient)
may improve vascularity sub-stantially.109Cooling the composite graftwith ice for
24 hours also helps.Regardless,composite grafts are tech-nique
sensitive.Generally,compositegrafts should be no larger than 1.5 to 2.0 cm.Avelar
and colleagues have showncomposite grafts greater than 2.0 cmgrafted successfully
to nasal and auriculardefects.110Similarly,Skouge has effective-ly grafted larger
defects using a �tongueand groove�technique and turndownhinged flaps.104The
postoperativeappearance ofcomposite grafts is distinc-tive.At placement,the graft
is white orblanched.Within 6 hours it becomespink,and by 24 hours it is
cyanotic.Bypostoperative day 3,it resumes its pinkcolor.Grafts that fail develop an
escharwith subsequent necroses and sloughing.ComplicationsThere are risks to all
pro-cedures.Patients who receive skin cancerprocedures should be warned
ofthepotential for recurrence ofthe tumor aswell as revision ofany reconstructive
pro-cedure.Flap problems include necrosis,infection,hematoma,wound dehiscence,and
scarring.Smoking greatly increases the risk ofnecrosis.Patients who smoke one
packper day triple the risk offlap or graftnecrosis compared with
nonsmokers.Smoking affects the blood supply via twomechanisms.First,nicotine is a
potentvasoconstrictor that may lower tissueoxygenation by > 50%.Nicotine effectsare
visible within 10 minutes and can lastup to 50 minutes.Second,carbonmonoxide is a
competitor with oxygen forhemoglobin.It has a higher affinity forhemoglobin than
does oxygen,resultingin high levels ofcarboxyhemoglobin.This leads to tissue
hypoxia.FIGURE37-19A,This debilitated elderly man hashad a large basal cell cancer
removed from abovehis ear.B and C,The resection is controlled bycurettage ofthe
soft tumor mass.D,A split graft isharvested from his thigh,tacked,and basted
intoplace with multiple chromic sutures.A foam spongebolster is subsequently used
for 5 days.E,At 1 month,although the site is unesthetic,the man�stumor problems
have been resolved simply.ABCDE
720Part 5: Maxillofacial PathologyInfectionInfections are rare in vascular-ized
head and neck tissues,and necrosismay be mistaken for infection.More com-mon causes
ofredness include stitchabscesses,which are foreign body reac-tions,and allergies
to antibiotic ointment.Infections,handled by drainage
(whenindicated),irrigation,and antibiotics,usu-ally resolve
readily.BleedingBleeding may be caused bypatient factors or surgical
issues.Patientfactors include medical conditions such asrenal failure,liver
failure,collagen vasculardisease,various cancers (hematopoieticmalignancies),and
medications.Medica-tions that can cause bleeding include war-
farin,heparin,antithrombotics,non-steroidal anti-inflammatory drugs,acetylsalicylic
acid,and cold remedies.Fur-thermore,commonly used herbal medica-tions such as
garlic,feverfew,and vitamin Ecan inhibit thrombocyte function.The surgeon must
weigh the benefits ofdiscontinuing anticoagulants against therisks ofsurgery since
there have been sever-al documented cases ofstroke when antico-agulants were
stopped prior to dermatolog-ic surgery.Consultation and coordinationwith the
patient�s internist and appropriatepreoperative laboratory data are helpful.There
is no need to discontinue any antico-agulant prior to performing a biopsy.Surgical
issues may arise intraopera-tively or during the postoperative period.Decisions
must be made concerning judi-cious cautery,the use ofdrains,the
effectofvasoconstrictors,and postoperativepressure.Seepage may occur from anyfacial
flap,but hematoma may necrose theflap.A hematoma,in the space createdbetween the
flap and underlying tissue isdetrimental to flap circulation because itcreates
tension,and it acts as a physicalbarrier preventing cohesion to the under-lying
tissue base.Additionally,stagnatingblood may promote wound infection.An early
hematoma may often bepushed out and washed away,but areforming hematoma must be
explored.Likewise,late collections ofjellied bloodshould be manually extruded.Poor
Cosmetic ResultsFacial flapsshould restore anatomic continuity,maintain functional
integrity,and pro-vide an esthetically pleasing result.Inspite ofwell-executed
surgical tech-niques,less than optimal results mayoccur because ofunpredictable
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JK.Mohs�micrographic surgery.Clin Plast Surg 1993;20:149�56.56.Shriner DL,McCoy
DK,Goldberg DJ,et al.Mohs�micrographic surgery.J Am AcadDermatol
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Exp Dermatol1999;24:130�3.58.Holmkvist KA,Roenigk RK.Squamous cellcarcinoma ofthe
lip treated with Mohs�micrographic surgery:outcome at 5 years.JAm Acad Dermatol
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and current applica-tions.Dermatol Surg 1997;23:1089�93.60.Anscher M,Montano
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North Am1996;76:1383�98.63.Kuflik EG.Cryosurgery updated.J Am AcadDermatol
1994;31:925�44.64.Lindgren G,Larko O.Long term follow up ofcryosurgery ofbasal cell
carcinoma oftheeyelid.J Am Acad Dermatol 1997;36:742�6.65.Mallon E,Dawber
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1996;22:854�8.66.Spencer JM,Tannenbaum A,Sloan L,et al.Does inflammation contribute
to the eradi-cation ofbasal cell carcinoma followingcurettage and
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with 5-fluorouracil.J Am Acad Dermatol 1981;4:633�45.68.Allison RR,Mang TS,Wilson
BD.Photody-namic therapy for the treatment ofnon-melanomatous cutaneous
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and dura-tion ofphotosensitizer application onresponse.Arch Dermatol
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differences in healing ofsuperficial skin wounds in humans.ArchDermatol
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KW,Larabee WF.A study ofskin flapadvancement as a function ofundermin-ing.Arch
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for correction ofpostoncolog-ic surgical defects.J Oral Maxillofac
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in facial reconstruction.St.Louis:Mosby;1995.p.247�71.99.Rudolph R,Ballantyne
DL.Skin grafts.In:McCarthy JG,editor.Plastic surgery,Vol 1.General
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TJ.Reconstruction ofnasal defects usingfull thickness grafts:a personal
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SJ.Visualized basting suturesin the application offull thickness skingrafts.J
Dermatol Surg Oncol 1987;13:1236�9.104.Skouge JW.Techniques for split-thickness
skingrafting.J Dermatol Surg Oncol 1987;13:841�9.105.Bray DA.Clinical applications
ofthe rhomboidflap.Arch Otolaryngol 1983;109:37�42.106.Bray DA.Rhombic
flaps.In:Baker SR,editor.Local flaps in facial
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M.Nobe-cutane spray as temporary dressing ofskingraft donor sites.J Dermatol Surg
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thickness skin graftingtechnique.J Dematol Surg Oncol
1987;13:853�8.109.Chandawarkar RY,Cervino AL,Wells MD.Reconstruction ofnasal
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Part 6MAXILLOFACIALRECONSTRUCTION
CHAPTER 38Local and Regional FlapsAlan S.Herford,DDS,MDG.E.Ghali,DDS,MDFlap
Principles Over the past 50 years the developmentand application ofseveral
different flapshas led to reliable reconstruction offacialdefects.Most defects can
be reconstructedimmediately,leading to better restorationofform and function with
early rehabilita-tion.1Reconstructing facial defects can beboth challenging and
rewarding.Missingtissue most often results from either trau-ma or oncologic
surgery.Commonly thereis a wide range ofoptions for repairing agiven
defect,including healing by sec-ondary intention,primary closure,place-ment ofa
skin graft,or mobilization oflocal or regional tissue.Compared to skingrafts,local
flaps often produce superiorfunctional and esthetic results.2�6A greatadvantage
oflocal tissue transfer is thatthe tissue closely resembles the missingskin in
color and texture.These flaps canbe rotated,advanced,or transposed into atissue
defect.Regional tissue can also berecruited to repair facial defects.When deciding
which option to use,there should be a progression from simpleto complex
treatments.Considerationshould be given to primary closure or theuse ofskin grafts
first,followed by local,then regional,and finally distant pedicledor microsurgical
free tissue transfer.Flapsrequire additional incisions and tissuemovement,which
increase the risks ofpostoperative bleeding,hematoma,pain,and
infection.Confirmation oftumor-free margins should be done prior to
flapreconstruction ifa malignant lesion hasbeen excised.7Some defects are amenable
to closurewith a single flap,but others require acombination offlaps for optimal
results.8An advantage ofusing multiple flaps isthat they can be harvested from
separateesthetic units.This decreases the size ofthesecondary defect and may allow
placementofscars between esthetic units,thusimproving scar camouflage leading to
bet-ter cosmesis.Often,separated repair ofindividual facial subunits with
separateflaps provides a better cosmetic result thanifa single flap is used to
reconstruct theentire defect.Flaps differ from grafts in that theymaintain their
blood supply as they aremoved.Abundant dermal and subdermalplexus allow for
predictable elevation ofrandom cutaneous flaps.A cutaneous flapmay also have its
arterial supply based on adominant artery in the subcutaneous layer.Muscular
perforating arteries are impor-tant contributors to the cutaneous vascularbed.The
most important variable for flapviability is not the length-to-width
ratiobut,rather,the perfusion pressure and vas-cularity at the pedicle
base.9Because localflaps provide their own blood supply,theyare particularly useful
in patients withcompromised recipient sites such as thosethat have been
irradiated.As local flaps heal,regaining ofbloodflow and cutaneous sensibility
increases.The rate ofblood flow and two-point dis-crimination on the surface
oflocal flaps isstatistically no different when comparedwith the corresponding area
ofthe unop-erated side.10The recovery ofsensorynerve function in facial flaps is
dependenton the intimacy ofcontact between theflap and the recipient bed and on the
via-bility ofthe type ofrestoration.Relaxed skin tension lines (RSTLs)result from
vectors within the skin thatreflect the intrinsic tension ofthe skin atrest.They
are due to the microarchitec-ture ofthe skin and represent the direc-tional pull on
wounds.The RSTLs aregenerally parallel to the facial rhytids.Lines ofminimal
tension (rhytids) resultfrom repeated bending ofthe skin frommuscular contraction.A
permanentcrease results from the adhesions betweenthe dermis and deeper
tissues.These nat-ural skin creases run perpendicular to thedirection ofmuscle pull
and can guideincision orientation for optimal scarcamouflage and cosmesis.The face
is composed ofesthetic sub-units.11,12The areas where these subunitsmeet are
referred to as anatomic borders.The esthetic subunit principle is based onthe fact
that our eyes see objects as a seriesofblock images that are spatially orga-
nized.Scars that are located at the junctionoftwo adjacent anatomic subunits are
770Part 6: Maxillofacial Reconstructioninconspicuous because one expects to seea
delineation between these areas.Flap Nomenclature There are many methods described
forclassifying cutaneous flaps:by the arrange-ment oftheir blood supply,their
configu-ration,location,tissue content,andmethod oftransferring the flap.Blood
SupplyCutaneous flaps consist ofskin and subcu-taneous tissue and can be
characterized bytheir predominant arterial supply.Theseinclude random pattern,axial
pattern,andpedicle flaps (Figure 38-1).Random flapsare supplied by the dermal and
subdermalplexus alone and are the most common typeofflap used for reconstructing
facial defects.Axial pattern flaps are supplied by moredominant superficial vessels
that are orient-ed longitudinally along the flap axis.Pedicleflaps are supplied by
large named arteriesthat supply the skin paddle through muscu-lar perforating
vessels.Free tissue transferrefers to flaps that are harvested from aremote region
and have the vascular con-nection reestablished at the recipient
site.LocationAnother means ofclassification is by theregion from which the tissue
is mobilized.This includes local,regional,and distantflaps.Local flaps imply use
oftissue adjacentto the defect,whereas regional flaps refer tothose flaps recruited
from different areas ofthe same part ofthe body.Distant flaps areharvested from
different parts ofthe body.ConfigurationFlaps are often referred to by their
geomet-ric configuration.Examples ofthese flapsinclude bilobed,rhombic,and Z-
plasty.Tissue ContentThe layers oftissue contained within theflap can also be used
to classify a flap.Cutaneous flaprefers to those flaps thatcontain the skin
only.When other layersare incorporated into the flap they areclassified
accordingly.Examples includemyocutaneous and fasciocutanous flaps.Method
ofTransferThe most common method ofclassifyingflaps is based on the method
oftransfer.Advancement flaps are mobilized along alinear axis toward the defect
(Figure 38-2).Rotation flaps pivot around a point at thebase ofthe flap (Figure 38-
3).Althoughmost flaps are moved by a combination ofrotation and advancement into
the defect,the major mechanism oftissue transfer isused to classify a given
flap.Transpositionflaprefers to one that is mobilized towardan adjacent defect over
an incompletebridge ofskin.Examples oftranspositionflaps include rhombic flaps and
bilobedflaps (Figure 38-4).Interposition flaps dif-fer from transposition flaps in
that theincomplete bridge ofadjacent skin is alsoelevated and mobilized.An example
ofaninterposition flap is a Z-plasty.Interpolat-ed flaps are those flaps that are
mobilizedeither over or beneath a complete bridge ofintact skin via a pedicle.These
flaps oftenrequire a secondary surgery for pedicledivision.Microvascular free
tissue
transferRandomCutaneousAxialMyocutaneousMusculocutaneousbranchesPerforatorvesselsSe
gmentalvesselsIslandMusculocutaneousbranchesPerforatorvesselsSegmentalvesselsMuscul
ocutaneousbranchesPerforatorvesselsPerforatorvesselsSegmentalvesselsFIGURE38-
1Diagrammatic representation ofcutaneous blood supply in skin and myocutaneous
flaps.Adapted from Ariyan S.41
Local and Regional Flaps771from a different part ofthe body relies onreanastomosis
ofthe vascular pedicle.Designing the Flap There are many options for
reconstructingfacial defects.Often the optimal method isnot readily apparent.A
stepwise approachcan be helpful in selecting and designing aflap.The
characteristics ofthe defect andadjacent tissue must be analyzed.Theseinclude
color,elasticity,and texture ofthemissing tissue.The defect size,depth,andlocation
are evaluated as well as the avail-ability and characteristics ofadjacent
orregional tissue.It is important to deter-mine the mobility ofadjacent
structuresand to identify those anatomic landmarksthat must not be distorted.The
orienta-tion ofthe RSTLs and esthetic unitsshould by analyzed closely.Potential
flap designs should be drawnon the skin surface being careful to avoidthose designs
that obliterate or distortanatomic landmarks.The final location ofthe resultant
scar should be anti-cipated byprevisualizing suture lines and choosingflaps that
place the lines in normal creases.The secondary defect that is created asthe tissue
is transferred into the primarydefect must be able to be closed easily.When
designing a flap,it is important toavoid secondary deformities that
distortimportant facial landmarks or affect func-tion.Avoid obliterating critical
anatomiclines that are essential for normal functionand appearance.Proper surgical
technique involves gen-tle handling ofthe tissue by grasping the skinmargins with
skin hooks or fine-toothed tis-sue forceps.Avoid traumatizing the vascularsupply by
twisting or kinking the base oftheflap.Deep pexing sutures minimize tensionon the
flap and eliminate dead space.Exces-sive tension on the flap may decrease bloodflow
and cause flap necrosis.Meticuloushemostasis should be achieved prior to
finalsuturing so that a hematoma does not devel-op beneath the flap.It is important
to FIGURE38-2A,Double advancement flapswith Burow�s triangles.B,Closure ofthe
defect.ABFIGURE38-3A,Rotation flap for closure ofaforehead defect.B,Closure ofthe
defect.ABFIGURE38-4A,Bilobed flap for closure ofa nasal tip defect.B,Closure ofthe
defect.C,Rhombic flapfor closure ofa check defect.Note the 120 and
60�angles.D,Closure ofthe defect.ABCD
772Part 6: Maxillofacial Reconstructionadequately mobilize and extend the
flap,which should be ofadequate size to remainin place without tension to minimize
thechance ofdehiscence,scarring,or ectropion.Types ofFlapsLocal Flaps Advancement
FlapsAdvancement flapshave a linear configuration and are advancedinto the defect
along a single vector.Theseflaps can be single or double.Advancementflaps are often
chosen when the surroundingskin exhibits good tissue laxity and theresulting
incision lines can be hidden in nat-ural creases.Advancement flaps limit
woundtension to a single vector with minimal per-pendicular tension.They are often
helpful inreconstructing defects involving the fore-head,helical rim,lips,and
cheek.In theseareas advancement flaps capitalize on thenatural forehead furrows
without causingvertical distortion ofthe hairline superiorlyor the eyebrow
inferiorly (Figure 38-5).Advancement flaps are created by par-allel incisions
approximately the width ofthe defect.Standing cutaneous deformities(�dog ears�) are
usually created and aremanaged with excision.A Z-plasty inci-sion or Burow�s
triangle may be per-formed at the base ofthe flap,reducing thestanding cutaneous
deformities.A variation ofthe advancement flapis the V-Yflap.A triangular island
oftis-sue adjacent to the defect is isolated andattached only to the subcutaneous
tissue.It relies on a subcutaneous pedicle forblood supply.As it is advanced into
thedefect,the secondary defect is closed pri-marily in a simple V-
Ymanner.Theseflaps are especially amenable for cheekdefects along the alar facial
groove andare generally avoided where there aresuperficial nerves because ofthe
depth ofthe incisions.Intraoral uses ofadvancement flapsinclude covering oroantral
fistulas andalveolar clefts.A disadvantage ofbuccaladvancement flaps is the
decrease investibular sulcus depth (Figure 38-6).Rotation FlapsRotation flaps have
acurvilinear configuration.Defects recon-structed with rotation flaps should
besomewhat triangular or modified byremoving normal tissue to create a trian-gular
defect.These flaps have a large baseand are usually random in their vascular-ity
but may be axial.One or more rota-tion flaps are often used to reconstructscalp
defects.Because ofthe relativeinelasticity ofthe scalp tissue,these flapsmust be
large relative to the size ofthedefect.Scoring ofthe galea is helpful ingaining
additional rotation and advance-ment (Figure 38-7).The axial frontonasal flap is a
modifiedsimple rotation flap with a back cut.13�16It isuseful for closing nasal
defects (Figure 38-8).The flap is based on a vascular pedicle at thelevel ofthe
medial canthus.This pedicle con-sists ofa branch ofthe angular artery and
thesupraorbital artery.Rotated palatal flaps are helpful forclosing large oroantral
fistulas.8,17Fistu-las < 5 mm in diameter usually closeFIGURE38-5A,Advancement flap
for closure offorehead defect.B,Closure ofdefect with incisionlines placed in
natural forehead crease.ABFIGURE38-6Buccal advancement flaps can beused to cover an
oroantral fistula.A,A Moczair buc-cal sliding trapezoidal flap is slid (arrow)to
use thepapilla ofthe adjacent tooth to rotate into the defect.B,Rehrman�s buccal
advancement flap uses a flapthat has vertical extensions.To adequately mobilizethis
flap to cover the defect without tension,theperiosteum must be incised (broken
line)along itsbase and the flap advanced (arrow)over the defect.C,Ifthe fistula is
present along an edentulous region,a transverse flap or bipedicle flap can be
used.ABC
Local and Regional Flaps773spontaneously.18,19Local flaps or graftscan be used to
close larger fistulas.Two-layer closures are less prone to developingrecurrence
oforoantral fistulas.Approxi-mately 75% ofthe palatal soft tissue canbe rotated to
cover adjacent defects.Transposition FlapsThese flaps arerotated and advanced over
adjacent skin toclose a defect.Examples oftranspositionflaps include rhombic flaps
and bilobedflaps.These flaps are advantageous in areaswhere it is desired to
transfer the tensionaway from closure ofthe primary defectand into the repair ofthe
secondarydefect.Transposition flaps have a straightlinear axis and are usually
designed so thatone border ofthe flap is also a border ofthe defect.An advantage
ofthis type offlap is that it can be developed at variabledistances.Areas where
these flaps are oftenused include the nasal tip and ala,the infe-rior eyelid,and
the lips.The rhombic flap is a precise geomet-ric flap that is useful for many
defects ofthe face.20,21The traditional rhombic(�Limberg�) flap is designed with 60
and120�angles and equal-length sides.Theangle ofthe leading edge ofthe rhombicflap
is approximately 120�but may vary.The flap is begun by extending an incisionalong
the short axis ofthe defect that isequal to the length ofone side oftherhombic
defect.Another incision is thenmade at 60�to the first and ofequal length(Figure
38-9).Disadvantages ofthe rhom-bic flap are the significant tension at theclosure
point as well as the amount ofdis-carded tissue to transform a circular defectinto
a rhombus.The bilobed flap is a transpositionflap with two circular skin paddles
(seeFigure 38-4).22,23Esser is credited withthe design ofthe bilobed flap in
1918.ItFIGURE38-7A,A large scalp defect secondary to trauma.B,Outline ofscalp
flaps.C,Elevation offlaps with scoring ofthe galea.D,Closure ofthe
defect.ABCDABCFIGURE38-8A,Axial frontonasal flap for repair ofa nasal
defect.B,Elevation ofthe flap with thorough undermining.C,Closure ofthe defect
774Part 6: Maxillofacial Reconstructionis useful for skin repairing oflateral
noseand nasal tip defects up to 1.5 cm.Thebilobed flap has a random pattern
bloodsupply.The flap is primarily rotatedaround a pivot point and the paddles
aretransposed over an incomplete bridge ofskin.The second lobe allows the
transferoftension further from the primarydefect closure.The bilobed design
rotatesaround an arc that is usually 90 to 100�.In the bilobed flap the first lobe
closesthe defect and the second closes the firstlobe defect.The flap is designed
with apivot point approximately a radius ofthedefect away from the wound
margin.Thefirst lobe is usually the same size as thedefect,and the second lobe is
slightlysmaller with a triangular apex to allowfor primary closure.The axis ofthe
sec-ond flap is roughly 90 to 100�from theprimary defect and undermined widelyto
distribute the tension.An advantage ofthe bilobed flap isthat one can construct a
flap at some dis-tance from the defect with an axis that isindependent ofthe linear
axis ofthedefect.A disadvantage ofthis flap is that itleaves a circular scar that
does not blendwith the existing skin creases.During heal-ing the flap may become
elevated (�pincushioning�) because ofthe narrow pedi-cle that is prone to
congestion,scar tissuethat impedes lymphatic drainage,andcurvilinear scars that
tend to bunch theflap up as they shorten.Interpolation FlapsInterpolation
flapscontain a pedicle that must pass over orunder intact intervening tissue.A
disad-vantage ofthese types offlaps is that forthose passing over bridging skin,the
pedi-cle must be detached during a second sur-gical procedure.Occasionally it is
possibleto perform a single-stage procedure by de-epithelializing the pedicle and
passing itunder the intervening skin.Advantages ofinterpolation flaps include their
excellentvascularity,and also their skin color andtexture match.The forehead flap
(median and para-median) is a commonly used interpolationflap and remains the
workhorse flap forlarge nasal defects.24�27It is a robust anddependable flap.The
forehead flap is pri-marily based on the supratrochlear vessel,is relatively
narrow,and uses a skin paddlefrom the forehead region.The flap is sup-plied by a
rich anastomosis between thesupratrochlear and angular arteries.Because ofthe
marked vascularity,it ispossible to incorporate cartilage or tissuegrafts for nasal
reconstruction.The fore-head flap has abundant tissue available,allowing
resurfacing ofthe entire nasalunit with a single flap and provides a goodtexture
and color match to the native nose.The technique for elevating the fore-head flap
is straightforward.The flap canbe designed directly in the midline or in
aparamidline location.A template ofthedefect is used to outline the
flap.Elevationofthe flap proceeds in either a subgaleal orsubcutaneous plane.The
pedicle is alwayselevated in such a way as to incorporatethe frontalis muscle.The
width ofthepedicle is usually 1.0 to 1.5 cm,whichallows for easy rotation ofthe
pedicle.Prior to inset the skin paddle is selectivelythinned to match the native
skin thickness.The pedicle is divided approximately 3 weeks later,with the base
ofthe pedicleinset into the glabellar area to reestablishbrow symmetry.The
incision,and result-ing scar,is perpendicular to the RSTLs buttends to heal well
(Figure 38-10).The nasolabial flap (melolabial) isuseful for reconstructing defects
involv-ing the oral cavity and those involvingthe lower third ofthe nose (Figure
38-11).28�31It can be used as an interpo-lation flap with either a single or
stagedtechnique.The flap is supplied by theangular artery,intraorbital
artery,andinfratrochlear artery and can be basedeither superiorly or inferiorly.The
areaofrecruitment for nasal reconstructionis in closer proximity to the
primarydefect than is the forehead flap.A disad-vantage ofthe nasolabial flap is
thatthere is a limited amount oftissue avail-able,and asymmetry can occur along
theFIGURE38-9A,Outline for a rhombic flap.B,Resection ofthe lesion.C,The flap is
transposed intothe defect.D,Postoperative result with the incisions placed in the
relaxed skin tension lines.ABCD
Local and Regional Flaps775nasolabial flap folds.When the pedicle isdivided,the
defect can be closed primar-ily by placing the scar in the nasal facialjunction and
the nasolabial flap fold.The lip-switch flap (Abbe) can betaken from either lip,but
it is most com-monly switched from the lower to theupper lip.32�34This flap can be
used toreconstruct as much as one-third oftheupper lip.The lower lip can supply a
flapofone-quarter ofits length,and the Abbeflap offers immediate replacement
oftotallip anatomy (Figure 38-12).The labialartery supplies the flap and should
bemaintained with a small cuffofsubcuta-neous tissue and muscle surrounding
thevascular pedicle.The pedicle is dividedafter approximately 2 to 3 weeks.Tongue
flaps are excellent flaps forintraoral reconstruction.They use adjacenttissue,have
an excellent blood supply,andare associated with minimal morbidity.The tongue has
excellent axial and collater-al circulation,with the lingual artery pro-viding the
main blood supply.Up to one-halfofthe tongue can be rotated for tissuecoverage
without compromising speech,FIGURE38-10A,Nasal defect after excision ofsquamous
cell carcinoma lesion.B,Use ofDoppler ultrasonography to locate the supra-trochlear
artery.C,The forehead flap has been elevated.D,The flap is turned 180�and sutured
into place.E,The pedicle is divided 2 to 3 weeks later.F,Postoperative resultABCDEF
776Part 6: Maxillofacial Reconstructionmastication,or deglutition.35A variety
offlap designs have been described includinganterior- and posterior-based tongue
flaps(Figure 38-13).Some indications includerepair oforal defects and fistula
closure.These flaps are helpful for providing clo-sure oflarge oroantral
fistulas.Regional Flaps For large facial defects,local flaps maynot provide
sufficient tissue to adequate-ly restore the missing tissue.In these
casesconsideration should be given to using aregional flap.36,37Regional flaps
aredefined as those that are located near adefect but are not in the immediate
prox-imity.They are frequently harvested fromthe neck,chest,or axilla and can
providecoverage oflarge surface areas on theface.Selection ofa specific regional
flapdepends on the size and location ofthedefect and also on the intrinsic
propertiesofthe flap.Advantages ofregional flapsinclude the large amount ofsoft
tissueand skin available.Disadvantages ofthesetypes offlaps include poor color and
tex-ture match,excessive bulkiness oftheflap,and donor site morbidity.FIGURE38-
11A,Outline ofa nasolabial flap in apatient with a defect in the anterior floor
ofthe mouth.B,The pedicle is de-epithelialized and tunneled into themouth.C,The
flap is sutured into place to restore themissing soft tissue.D,The incision has
been hidden inthe nasolabial fold.ABCDFIGURE38-12A,Patient with a traumatic
lipdeformity with avulsion ofa portion ofhis upperlip.B,Reapproximation ofthe
orbicularis orismuscles and perialar advancement flaps toreestablish upper lip
length.C,An Abbe flap isused to restore the missing philtrum.D,Postop-erative
result.ABCD
Local and Regional Flaps777Pectoralis Major Myocutaneous FlapThe pectoralis major
myocutaneous flapremains a workhorse ofreconstructivesurgery.38�40The flap was
introduced byAriyan41and has provided a reliablemethod ofsoft tissue reconstruction
ofbone and soft tissue defects ofthemandible and maxilla.The pectoralismajor
myocutaneous flap can be rotatedaround a pivot point 180�and is suppliedby two
separate blood supplies (Figure38-14).The thoracoacromial artery aris-es from the
second portion ofthe axillaryartery and forms four branches as it pen-etrates the
fascia.The pectoral branch isthe major artery that supplies the pec-toralis major
myocutaneous flap.Theposition ofthe vascular pedicle can beapproximated by drawing
a line from theshoulder point to the xiphoid.The pec-toral branch descends at a
right anglefrom the middle ofthe clavicle until itmeets this line.Branches ofthe
internalmammary artery supply the medial por-tion ofthe muscle and skin over the
ster-num.The flap provides good coverageFIGURE38-13Aand B,Use ofan anteriorly based
tongue flap to cover the soft tissue deficit resulting from an alveolar
cleft.C,This type offlap isalso useful for closing large oroantral
fistulas..ABCInternal mammary arteryThoracoacromialarterySkin islandPecoralis major
muscleFIGURE38-14The pectoralismajor myocutaneous flap is divid-ed lateral to the
internal mamma-ry artery perforating vessels.Themuscle can be divided lateral tothe
skin island to leave the lateralportion ofthe muscle intact; thispreserves the
axillary fold.
778Part 6: Maxillofacial Reconstructionfor the carotid artery when combinedwith a
neck dissection.Deltopectoral FlapThe introduction ofthe deltopectoral flap by
Bakamjian andcolleagues represented a significantimprovement for reconstructing
largeablative resections for head and neck can-cer.42�44Currently it is used as an
alterna-tive to the pectoralis major myocutaneousflap for soft tissue
reconstruction ofthemandible and maxilla.This flap is com-posed
offascia,subcutaneous tissue,andskin but does not contain muscle (Figure38-
15).Perforators from the internalmammary artery provide vascular supplyto the
flap.The secondary defect is coveredwith a skin graft.Temporalis FlapThe temporalis
flap wasintroduced by Golovine in 1898 andremains useful for covering
intraoraldefects (Figure 38-16).45�48The outer por-tion ofthe muscle is invested by
the deeptemporal fascia.This fascia is supplied bythe middle temporal vessel,which
origi-nates just below the zygomatic arch.Thetemporalis muscle is supplied by both
theanterior and posterior deep temporal arter-ies,which arise from the second
portion ofthe internal maxillary artery.This dualblood supply allows for splitting
ofthemuscle into anterior and posterior flaps.When elevating the muscle,it
isimportant to remain on the deep tempo-ral fascia beneath the superficial
temporalfascia to avoid damage to the frontalbranch ofthe facial nerve.Elevation
ofthe inferior portion ofthe flap is per-formed in a subperiosteal plane to
avoiddamage to the deep temporal arteries,which lie on the undersurface ofthe mus-
cle.An osteotomy ofthe zygomatic archis often helpful to facilitate placement ofthe
muscle into the mouth.The arch canbe put back into place and secured
withIncisionsFIGURE38-15Incisions for a deltopectoral flap.ABCDFIGURE38-
16A,Temporalis muscle flap for repair ofa midface defect caused from a shotgun
wound.B,The temporalis muscle is divided,and the posterior portion is sutured into
place.C,Cranial boneis used to restore the missing tissue.D,The anterior portion
ofthe temporalis flap is sutured into placeto �sandwich�the bone grafts.
Local and Regional Flaps779plates and screws.A disadvantage ofthetemporalis flap is
the minimal cosmeticdeformity ofhollowing in the temporalregion;this can be
corrected with autoge-nous or alloplastic materials and can beminimized by using
either an anterior ora posterior flap.Sternocleidomastoid FlapFirst des-cribed by
Jinau in 1909 for facial reani-mation,the sternocleidomastoid flap wasrepopularized
by Owens.49�55The muscleis invested by the deep cervical fascia andis supplied by
three arteries.The domi-nant vessel is the occipital artery,whichenters the muscle
below the mastoid tipand supplies the superior portion ofthemuscle.The superior
thyroid artery sup-plies the middle portion,and the thyro-cervical trunk supplies
the inferior thirdofthe muscle.The muscle is elevated over the deepcervical fascia
superior to the carotidsheath.It is recommended to maintaintwo ofthe three vessels
when elevatingthe flap to enhance the viability oftheflap.The spinal accessory
nerve entersthe deep portion ofthe muscle approxi-mately at the carotid bifurcation
andshould be preserved to prevent denerva-tion atrophy ofthe muscle (Figure 38-
17).Advantages ofthe sternocleidomas-toid flap include its close proximity tothe
defect and minimal donor site defect(Figures 38-18 and 38-19).Trapezius
Myocutaneous FlapThetrapezius myocutaneous flap is supplied bythree
arteries,allowing several flaps to beused.The main vessel supplying the trapez-ius
muscle is the transverse cervical artery,which is a branch ofthe
thyrocervicaltrunk.The upper portion ofthe muscle issupplied by the occipital
artery.The trapez-ius myocutaneous flap is a ready source ofskin ofuniform
thickness without excessiveOccipital arterySuperior thyroid arteryThyrocervical
trunkFIGURE38-17Blood to the sternocleidomastoid muscle is supplied through three
arteries.FlapClosureFIGURE38-18A,Superiorly based flap with skin
pedicle.B,Transposition ofthe flap.C,Closure ofthe donor defect.ABC
780Part 6: Maxillofacial Reconstructionmuscle bulk.56The main disadvantage isthe
limited rotation and the short pedicle.Latissimus Dorsi Myocutaneous FlapQuillen
and colleagues first described theuse ofthe latissimus dorsi myocutaneousflap for
head and neck reconstruction in1978.57,58The flap is not commonly usedfor head and
neck reconstruction unlessother flaps are unavailable or there arevery large
defects requiring coverage.Themuscle is supplied by the thoracodorsalartery,which
is the dominant vessel,andalso by four to six perforators from theposterior
intercostals and lumbar vessels.The main advantage ofthe latissimus dorsiflap is
the large amount ofskin provided.The main disadvantages are the need toreposition
the patient during the opera-tion and morbidity from the donor site.Complications
Postoperative complications can be mini-mized with careful preoperative
planningofflap design and by early recognition ofproblems.59A medical history can
be usedto identify patients with risk factorsinvolving small vessels.These risk
factorsinclude smoking,diabetes,hypertension,previous radiation,and
preexistingscars.60,61Complications may be reversibleor irreversible.Early
recognition and treat-ment can minimize complications andprevent them from becoming
irreversible.Two main unwanted outcomes are flapfailure and unacceptable cosmetic
results.Flap survival depends on early recog-nition offlap compromise.Ischemia
isdefined as an inadequacy ofperfusion inproviding tissue needs.Signs
ofarterialischemia include a pale and cool flap thatdoes not blanch with pressure
and typical-ly does not bleed with a pinprick.Flaps aresomewhat ischemic initially
because theoriginal tissue perfusion has been com-promised by flap elevation.Most
tissuecan survive on 10% ofits average bloodflow.59Whether the flap will
undergonecrosis depends on patient-related andsurgery-related factors that
influence therisk ofnecrosis in facial flaps.Smoking isassociated with an increased
risk offlapfailure.The deleterious effects ofsmokingon flap survival include
hypoxemia andvasoconstriction.Patients should beadvised to quit smoking during the
peri-operative period.Common causes ofbleeding in facialreconstruction with local
flaps includeinadequate hemostasis and drug-inducedcoagulopathy.Hematoma
formationshould be identified and decompressedwithin 24 hours.62Decompression can
beaccomplished with aspiration using a 22-gauge needle or by taking out one or
twosutures and applying gentle compressionon the flap.Hematoma formation
maydiminish tissue perfusion and can lead toischemia or necrosis by
inducingvasospasm,stretching the subdermalplexus,or separating the flap from
itsrecipient bed.Patients should be ques-tioned carefully about the use ofmedica-
tions that affect coagulation such asacetylsalicylic acid,nonsteroidal anti-
inflammatory drugs,and vitamin E.Ifpossible,these medications should beavoided for
2 weeks prior to and 1 weekafter surgery.Congestion is the most common vas-cular
problem associated with facial flaps.Signs ofa congested flap include
warmth,edema,and a purple color that blancheswith pressure then immediately
refills.Apinprick will cause release ofdark venousblood.Venous congestion can lead
to arte-rial compromise and flap necrosis.Man-agement ofcongested flaps may
includetemporarily releasing sutures to allowdecompression at the flap edges or
possi-ble impingement involving the flap pedi-cle.Tight bandages around the flap
pedicleshould be removed.Medicinal leeches(Hirudo medicinalis)may be useful
indecompressing congested flaps.63,64Salivafrom the leech contains an
anticoagulantand a vasodilator that facilitate continuedoozing from the site even
up to 6 hoursafter they detach.Hyperbaric oxygen (HBO) has beenshown to be
beneficial in improving thevascularity ofmarginal tissues.65Prophy-lactic HBO
therapy in cutaneous flapsurgery in the irradiated tissue bed maybe particularly
helpful to combat thehypoxia and hypocellularity.HBO is ben-eficial in treating
both venous congestionand arterial ischemia by creating a localFIGURE38-19A,The
sternocleidomastoid flap iselevated with a superior base.B,The flap is rotat-ed in
place to provide soft-tissue coverage over thereconstruction plate.C,The flap is
sutured intoplace and the donor site closed primarily.ABC
Local and Regional Flaps781arterial vasoconstriction through the risein arterial
oxygen content,which reducesthe amount ofinflow.The tissue oxygenlevels continue to
rise owing to theimproved diffusion even though there isvasoconstriction and a
reduction in vas-cular perfusion.The flap can maintainviability while continued
neovasculariza-tion occurs.Other options include theuse ofheparin and dipyridamole
to helpincrease the survival ofan ischemic flap.66Infection can complicate flap
heal-ing.67The postoperative infection rate forclean wounds in facial surgery is as
low as2.8%,with higher rates in facial recon-struction with local flaps.68Tissue
oxy-genation is an important factor in preven-tion ofwound infection and is
closelyrelated to blood supply.Infections involv-ing local flaps may result in flap
failure orpoor cosmetic outcome secondary towound dehiscence and
scarring.Conclusion A variety offacial flaps are available to thereconstructive
surgeon for repairing facialdefects.The goal offlap surgery is torestore
form,function,and esthetics.There are many advantages to using localand regional
flaps,which can lead to opti-mal esthetic results.References 1.Schliephake
H,Furrert K,Schneller T.Prospec-tive study ofthe quality oflife ofcancerpatients
after intraoral tumor surgery.JOral Maxillofac Surg 1996;54:664�9.2.Kruger
E.Reconstruction ofbone and soft tis-sue in extensive facial defects.J Oral Max-
illofac Surg 1982;40:714�20.3.Summers BK,Siegle RJ.Facial cutaneous recon-structive
surgery:general aesthetic princi-ples.J Am Acad Dermatol 1993;29:669�81.4.Baker
SR.Resurfacing flaps in reconstructiverhinoplasty.Aesthetic Plast Surg 2002;26:17-
23.5.Baker SR.Local cutaneous flaps.OtolaryngolClin North Am 1994;27:139�59.6.Baker
SR.Regional flaps in facial reconstruc-tion.Otolaryngol Clin North
Am1990;23:925�46.7.Escobar V,Zide MF.Delayed repair ofskin can-cer defects.J Oral
Maxillofac Surg 1999;57:271�9.8.Ducic Y,Herford AS.The use ofpalatal islandflaps as
an adjunct to microvascular free tis-sue transfer for reconstruction
ofcomplexoromandibular defects.Laryngoscope 2001;111:1666�9.9.Milton S.Pedicled
skin-flaps:the fallacy ofthelength:width ratio.Br J Surg 1970;57:502-
8.10.Schliephake H,Schmelzeisen R,Neukam FW.Long-term results ofblood flow and
cuta-neous sensibility offlaps used for thereconstruction offacial soft tissues.J
OralMaxillofac Surg 1994;52:1247�52.11.Gonzalez-Ulloa M.Restoration ofthe face
cover-ing by means ofselected skin in regional aes-thetic units.Br J Plast Surg
1956;9:212�21.12.Burget GC,Menick FJ.The subunit principle innasal
reconstruction.Plast Reconstr Surg1985;76:239�47.13.Rieger RA.A local flap for
repair ofthe nasaltip.Plast Reconstr Surg 1967;40:147�9.14.Marchac D,Toth B.The
axial frontonasal flaprevisited.Plast Reconstr Surg 1985;76:686�94.15.Haneke
E.Surgical treatment ofdefects on the tipofthe nose.Dermatol Surg
1998;24:711�7.16.Herford AS,Zide MF.Reconstruction ofsuper-ficial skin cancer
defects ofthe nose.J OralMaxillofac Surg 2001;59:760�7.17.Millard DR.The island
flap in cleft palate surgery.Surg Gynecol Obstet 1963;116:197�8.18.Liposky
RB.Immediate repair ofthe oroantralcommunication:a preventative dental pro-cedure.J
Am Dent Assoc 1981;103:727-919.Yih WY,Merrill RG,Howerton DW.Secondaryclosure
oforoantral and oronasal fistulas:amodification ofexisting techniques.J
OralMaxillofac Surg 1988;46:357�64.20.Limberg AA.Planimetrie und Stereometrie
derHautplastik.Jena,Germany:Fischer Verlag;1967.21.Borges AF.Choosing the correct
Limberg flap.Plast Reconstr Surg 1978;62:542�5.22.Zitelli JA.The bilobed flap for
nasal recon-struction.Arch Dermatol 1989;125:957�9.23.Iida N,Ohsumi N,Tonegawa M,et
al.Simplemethod ofdesigning a bilobed flap.PlastReconstr Surg
1999;104:495�9.24.Shumrick KA,Smith TL.The anatomic basisfor the design offorehead
flaps in nasalreconstruction.Arch Otolaryngol HeadNeck Surg
1992;118:373�9.25.Burget GC,Medick FJ,editors.The paramedianforehead
flap.In:Aesthetic reconstruction ofthe nose.St.Louis:Mosby;1994.p.57�92.26.Burget
GC.Aesthetic restoration ofthe nose.Clin Plast Surg 1985;12:463�80.27.McCarthy
JG,Lorenc ZP,Cutting C,et al.The median forehead flap revisited:theblood
supply.Plast Reconstr Surg 1985;76:866�9.28.Ducic Y,Burye M.Nasolabial flap
reconstructionoforal cavity defects:a report of18 cases.JOral Maxillofac Surg
2000;59:1104�8.29.Kakinuma H,Iwasawa U,Honjoh M,Koura T.A composite nasolabial flap
for an entire alareconstruction.Dermatol Surg 2002;28:237�40.30.Maurer P,Eckert
AW,Schubert J.Functionalrehabilitation following resection ofthe floorofthe
mouth:the nasolabial flap revisited.JCraniomaxillofac Surg
2002;30:369�72.31.Lazaridis N,Zouloumis L,Venetis G,et al.Theinferiorly and
superiorly based nasolabialflap for reconstruction ofmoderate-sizedoronasal
defects.J Oral Maxillofac Surg1998;56:1255�9.32.Zide MF,Fuselier C.The partial-
thicknesscross-lip flap for correction ofpostoncolog-ic surgical defects.J Oral
Maxillofac Surg2001;59:760�7.33.Yih WY,Howerton DW.A regional approach
toreconstruction ofthe upper lip.J Oral Max-illofac Surg 1997;55:383�9.34.Schulte
DL,Sherris DA,Kasperbaurer JL.Theanatomical basis ofthe Abbe flap.Laryngo-scope
2001;111:382�6.35.Massengill R,Pickrell K,Mladick R.Lingualflaps:effect on speech
articulation andphysiology.Ann Otol Rhinol Laryngol1970;l79:853�7.36.Motamedi
MH,Behnia H.Experience withregional flaps in the comprehensive treat-ment
ofmaxillofacial soft-tissue injuries inwar victims.J Craniomaxillofac
Surg1999;27:256�65.37.Blackwell KE,Buchbinder D,Biller HF,UrkenML.Reconstruction
ofmassive defects inthe head and neck:the role ofsimultaneousdistant and regional
flaps.Head Neck1997;19:620�8.38.Ariyan S.The pectoralis major myocutaneousflap.A
versatile flap for reconstruction inthe head and neck.Plast Reconstr
Surg1979;63:73-81.39.Ariyan S.Further experiences with the pec-toralis major
myocutaneous flap for theimmediate repair ofdefects from excisionsofhead and neck
cancers.Plast ReconstrSurg 1979;65:605-12.40.Marx RE,Smith BR.An improved
techniquefor development ofthe pectoralis majormyocutaneous flap.J Oral Maxillofac
Surg1990;48:1168�80.41.Ariyan S.Pectoralis major,sternomastoid,andother
musculocutaneous flaps for head andneck reconstruction.Clin Plast Surg
1980;7(1):89-109.
782Part 6: Maxillofacial Reconstruction42.Bakamjian VY.Total reconstruction
ofphyar-ynx with medially based deltopectoral skinflap.NY State J Med
1968;68:2771�8.43.Sasaki K,Nozaki M,Honda T,et al.Deltopec-toral skin flap as a
free skin flap revisited:further refinement in flap design,fabrica-tion and
clinical usage.Plast Reconstr Surg2001;107:1134�41.44.Lazaridis N,Tilaverdis
I,Dalambiras S,et al.The fasciocutaneous cervicopectoral rota-tion flap for lower
cheek reconstruction:report ofthree cases.J Oral Maxillofac
Surg1997;55:1166�71.45.Golovine SS.Procede de cloture plastique del�orbite apr�s
l�exenteration.Arch Ophthal1898;18:679.46.Alonso del Hoyo J,Fernandez Sanroman
J,Gil-Diez JL,et al.The temporalis muscle flap:an evaluation and review of38
cases.J OralMaxillofac Surg 1994;52:143�7.47.Burggasser G,Happak W,Gruber
H,FreilingerG.The temporalis:blood supply and inner-vation.Plast Reconstr Surg
2002;109:1862�9.48.Abubaker AO,Abouzgia MB.The temporalismuscle flap in
reconstruction ofintraoraldefects:an appraisal ofthe technique.OralSurg Oral Med
Oral Pathol Oral RadiolEndod 2002;94:24�30.49.Jinau A.Die Chirurgishe behanolung
derfacialislachmung.Dtsch ZF Chin 1909;102:377�81.50.Owens NA.A compound neck
pedicle designedfor the repair ofmassive facial defects.PlastReconstr Surg
1955;15:369�89.51.Zhao YF,Zhang WF,Ahao JH.Reconstructionofintraoral defects after
cancer surgeryusing cervical pedicle flaps.J Oral Maxillo-fac Surg
2001;59:1142�6.52.Ariyan S.Further experience with the stern-ocleidomastoid
myocutaneous flap.PlastReconstr Surg 2003;111:381�2.53.Kerawala CJ,McAloney
N,Stassen LF.Prospec-tive randomized trial ofthe benefits ofasternocleidomastoid
flap after superficialparotidectomy.Br J Oral Maxillofac
Surg2002;40:468�72.54.Kierner AC,Zelenka I,Gstoettner W.The ster-nocleidomastoid
flap�its indications andlimitations.Laryngoscope 2001;111:2201�4.55.Marx
RE,McDonald DK.The sternocleido-mastoid muscle as a muscular or myocuta-neous flap
for oral and facial reconstruc-tion.J Oral Maxillofac Surg
1985;43:155�62.56.Papadopoulos O,Tsakoniatis N,Georgiou P,Christopoulos A.Head and
neck soft-tissuereconstruction using the vertical trapeziusmusculocutaneous
flap.Ann Plast Surg1999;42:457�8.57.Quillen CG,Shearing JG,Georgiade NG.Useofthe
latissimus dorsi myocutaneous islandflap for reconstruction in the head and
neckarea.Plast Reconstr Surg 1978;62:113�7.58.Posnick JC,McCraw JB,Magee W Jr.Use
ofalatissimus dorsi myocutaneous flap for clo-sure ofan orocutaneous fistula ofthe
cheek.J Oral Maxillofac Surg 1988;46:224�8.59.Vural E,Key
JM.Complications,salvage,andenhancement oflocal flaps in facial recon-
struction.Otolaryngol Clin North Am2001;34:39�51.60.Goldminz D,Bennett RG.Cigarette
smokingand flap and full-thickness graft necrosis.Arch Dermatol
1991;127:1012�5.61.Kinsella JB,Rassekh CH,Wassmuth ZD,et al.Smoking increases
facial skin flap compli-cations.Ann Otol Rhinol Laryngol
1999;108:139�42.62.Mulliken JB,Healey NA.Pathogenesis ofskinflap necrosis from an
underlying hematoma.Plast Reconstr Surg 1979;63:540�5.63.Utley DS,Koch RJ,Goode
RL.The failing flapin facial plastic and reconstructive surgery:role ofthe
medicinal leech.Laryngoscope1998;108:1129�35.64.Dabb RW,Malone JM,Leverett LC.The
use ofmedicinal leeches in the salvage offlapswith venous congestion.Ann Plast
Surg1992;29:250�6.65.Zamboni WA,Roth AC,Russell RC,et al.Theeffect ofhyperbaric
oxygen on reperfusionofischemic axial skin flaps:a laser Doppleranalysis.Ann Plast
Surg 1992;28:339�41.66.Kerrigan CL,Daniel RK.Pharmacologic treat-ment ofthe failing
skin.Plast Reconstr Surg1982;70:541�8.67.Bumpous JM,Johnson JT.The infected
woundand its management.Otolaryngol ClinNorth Am 1995;28:987�1001.68.Sylaidis
P,Wood S,Murray DS.Postoperativeinfection following clean facial surgery.Ann Plast
Surg 1997;39:342�6.
CHAPTER 39Bony Reconstruction ofthe JawsRandall M.Wilk,DDS,PhD,MDOverview and
GoalsBony reconstruction ofthe jaws representsone ofthe most daunting tasks
presentingto the oral and maxillofacial surgeon.Thedemands ofreconstruction ofthe
mandibleand maxilla represent challenges for the fol-lowing reasons.The
requirements for suc-cess follow a strict criterion for occlusion ofthe dentition
and oral rehabilitation.Minormalpositionings result in occlusal problemsthat are
both perceptible to the patient andprovide a formidable task to the
restorativedentist.Major malpositions may make oralrehabilitation near
impossible.The func-tional loads to be carried on the bone canchallenge both
hardware and the reconsti-tuted mandible and maxilla.The environ-ment ofthe oral
cavity can be hostile foradequate healing and regeneration.Indige-nous flora ofthe
oral cavity is one ofthemost diverse in the human body,and thebacterial load can be
considerable.Whenpathogenic flora is present,as is not uncom-mon in the compromised
host,healing canbe further challenging.The bones them-selves represent complex
morphologies,curved shapes,and complex relationshipswith adjacent
structures.Reproducing theseparameters adds to the complexity ofthetask.The jaws by
virtue oftheir prominentplacement on the exposed face impart con-siderable esthetic
requirements.Unlikeother parts ofthe body,which are hidden byclothing,the face is
rarely concealed.The goals ofreconstruction under theaforementioned conditions are
to providemorphology and position ofthe bone inrelation to its opposing jaw,provide
ade-quate height and width ofbone,restorecontinuity ofthe mandible and maxilla,and
provide facial contour and support forsoft tissue structures.While these
conceptsmay seem straightforward,surgeons havestruggled for centuries to achieve
them andsuccess is often elusive.Various success rateshave been described for bony
reconstruc-tion ofthe jaws,but criteria have usuallybeen incomplete and rates
uninspiring.The factors leading to the lack ofade-quate bone development or loss
ofbone inthe first place have a role in the types andmethods used to begin a
reconstruction.Ablative loss ofboth bone and associatedsoft tissue from treatment
ofneoplastic orother pathologic processes represent a fardifferent task from loss
ofbone from trau-ma or infection.Other modulating factorsinclude the presence
ofsystemic diseases,exposure to therapeutic doses ofionizingradiation,or failure
ofdevelopment ofnormal bony structures.Success rates inirradiated jaws are
typically lower by sig-nificant amounts,and rates ofcomplica-tions have been
reported as high as81.3%.1Complete graft loss in 30% ofirradiated patients
undergoing bone graft-ing to the jaws and an additional 50% ofpatients experiencing
partial graft lossafter reconstructive procedures have beenreported.2Use
ofhyperbaric oxygen ther-apy and microvascular reconstruction hasimproved these
rates.3,4Bony reconstruction begins withassessing the bone to be
reconstructed.Thelocation,size,and relationship to the otherstructures are the
prime factors in planninga reconstruction.A large defect ofthe angleregion is
managed differently than a smalldefect in the same region.A defect in thealveolus
ofthe maxilla is managed differ-ently than a similar-size defect in the
hardpalate.Defects in areas that are opposed bynatural dentition are managed
differentlythat those that are in areas that have littlefunctional
consequence.Anatomic Considerations inReconstruction ofthe JawsAnatomically the
mandible can be dividedinto four broad regions (Figure 39-1) withsomewhat
indistinct boundaries:condylarportion,ramus,body,and alveolus.Severalsubsets or
overlapping areas have beendescribed.The coronoid region can be con-sidered as part
ofthe ramus,the angleregion encompasses both part ofthe ramusand body,and the
symphysis is the anteriorpart ofthe body.Each ofthe areas presentsunique
characteristics,and the decision toreconstruct or repair certain areas is depen-
dent on the goals to be achieved.The condylar region is critical to themasticatory
functions ofthe jaws and over-all movements ofthe mandible.In the
784Part 6: Maxillofacial Reconstructionyoung and growing patient there are impli-
cations for growth ofthe jaw.The relation-ship ofthis area with the temporal
boneand the interarticular disk is beyond thescope ofthis chapter.Anatomic features
ofthe condylar region are the muscularattachments and morphologic support offacial
height.The lateral pterygoid muscleattaches to the condylar region and pro-vides
for translatory movement ofthemandible and its excursive movements.When
reconstructing large or entire por-tions ofthe condyle with grafts,failure
ofreattachment ofthe lateral pterygoid mus-cles will result in impairment or loss
ofthese functions.The condylar region con-tributes to the posterior vertical height
ofthe mandible.Loss ofthe condylar regionor insufficient reconstruction results
inreduced height with resulting malocclusionand esthetic contour deficiencies.Not
onlydoes the reconstructed condyle need tohave adequate bulk and form,but it
alsoneeds to be placed in appropriate relation-ship to the temporomandibular joint
fossa.The ramus area participates in masti-catory function as the site ofattachment
ofthe major muscles ofmastication.Themasseter,medial pterygoid,and tempo-ralis
muscles all attach here and providethe major input for developing bite force.These
muscles also serve as a potent bloodsupply for the reconstructed bone andserve as
an excellent recipient bed.Theramus region provides bulk,facial con-tour,and
continuity between major seg-ments ofthe mandible.Damage or loss ofbone structure
in this area can lead todecreased posterior mandibular heightwith resulting
malocclusion,facial contourdefects,and decreased masticatory func-tion.The major
sensory nerve ofthemandible enters this area and is prone toinjury during
reconstructive efforts.Thecoronoid process is considered part oftheramus,and its
loss can be considered to betrivial.There are no good reasons toreconstruct a
coronoid process.As in otherparts ofthe mandible,the relationship ofthe coronoid
process to the surroundingbones is critical.Malpositioning ofthecoronoid process
can impede opening ofthe jaw owing to interferences with thezygoma and zygomatic
arch.The body ofthe mandible is probablythe most complex area ofthe mandible
toreconstruct for several reasons.It has acomplex curved shape that makes recon-
struction difficult,it is along the lever ofthemandible and has the highest loads
placedon it,it contains a sensory nerve that isprone to injury,and it is the site
ofattach-ment ofa complex array
ofmuscles.Themylohyoid,geniohyoid,digastric,mentalis,buccinator,and tongue
musculature allhave attachment to this part ofthe bone.Their presence helps to
serve as an excellentrecipient bed,but the forces they exert onthe bone present
problems in reconstruc-tion and maintaining the contour ofthebone.In the anterior
region the muscleattachments serve a vital function in main-taining airway patency
through attachmentofthe tongue musculature and support ofthe hyoid complex.The body
ofthemandible supports the alveolus and tooth-bearing structures,and it has a
critical rela-tionship to the opposing jaw.The alveolus ofthe mandible is the
siteofthe functional component ofthemandible,the dental occlusion.This por-tion
ofthe mandible is dependent on theposition ofthe mandibular body for
itsrelationship to the maxillary arch.Thealveoli need proper height and width
tosubserve the functions ofthe dentition.Inthe maxilla the alveolus is in
relationshipto the maxillary sinus and nasal cavity,andthis relationship alters
reconstructiveefforts.In the anterior portion ofthe jawsthis alveolar component is
essential tomaintaining position ofthe overlying softtissue,especially the
lips.Loss in this areaor inadequate reconstruction can lead toboth functional and
esthetic deficiencies.The maxilla,or upper jaw (Figure 39-2),is a complex bone
comprising thebulk ofthe midface.It has relationshipswith the opposing mandible,the
orbitalcomplex,paranasal sinuses,zygoma,andnasal cavity.The palate forms the
roofofthe mouth and serves to partition the oraland nasal cavities.Incomplete
reconstruc-tion ofthe palate leads to hypernasalspeech and regurgitation ofthe oral
cavitycontents,unless obturated.The paucityand quality ofsoft tissue surrounding
thisregion makes bony reconstruction espe-cially difficult.At the posterior aspect
ofthe maxilla,a complex array ofmusclesattaches and subserves the functions
oftheCoronoidCondyleAlveolusRamusSymphysisBodyAngleFIGURE39-1Mandibular
regions.PyriformapertureZygomaticprocessAlveolusButtressPalateFIGURE39-2Maxillary
regions.
Bony Reconstruction ofthe Jaws785soft palate.These attachments are involvednot only
in speech and swallowing but alsoin eustachian tube function.In the alveo-lar
portion ofthe maxilla,the relationshipto the maxillary sinus is an often-
confounding factor in reconstruction.Highly pneumatized sinuses provide
littlesupport for grafting procedures.In theanterior region ofthe maxilla,support
fornasal and orbital structures is required formaintaining nasal airway support
andfacial contour and esthetics for the nose.Defects ofthe MandibleDefects ofthe
mandible can involve singlesubsets ofthe mandible,several segments,or the entire
mandible.Marginal defectsinvolve loss ofthe mandibular bone withthe inferior and
posterior portions leftintact.In marginal defects the continuityofthe mandible is
intact,and reconstruc-tive efforts are focused on maintainingbulk and
contour.Segmental defectsinvolve loss ofmandibular bone and eitherthe posterior or
inferior border and confera continuity defect ofthe mandible.Descriptions ofthe
size ofthe defect areusually expressed in centimeters,mea-sured at the inferior
border.This measure-ment will serve as a guide in estimating theamount ofbone
necessary to reconstructthe defect.Segmental defects can cause awide variety
ofreconstructive challenges,depending on their anatomic location.Small lateral
continuity defects are sur-prisingly well tolerated,and followingablative
procedures,it was not unusual todefer or omit reconstructive techniques.Segmental
defects ofthe anteriormandible,however,are not well toleratedbecause ofunfavorable
anatomic and bio-mechanical features.Maintenance oftongue position and interramal
width areseverely compromised with large anteriorsegmental defects.The defects need
to beinterpreted not only in terms oftheir rela-tionship to the rest ofthe mandible
butalso in relation to the opposing maxillarystructures,both dental and
nondental.Identifying and categorizing defects ofthemandible in terms ofboth size
and extentrepresent the first step in bony reconstruc-tion ofthe lower jaw.Defects
ofthe MaxillaDefects ofthe maxilla can be divided intothose that disrupt
partitioning ofcavitiesand those that represent inadequate bulkor position ofbone
in one ofthe subsets.Partitioning disruptions need to be evalu-ated in terms ofboth
size and location.Small defects in the bone interfering withpartitioning can be
managed by soft tissueprocedures only and may not necessarilyneed to undergo bony
reconstruction.Larger defects in bone interfering withpartitioning can be
successfully obturatedby maxillofacial prostheses and,similarly,may not need bony
reconstruction.Manyreconstructive options exist for these typesofdefects.The
demands ofocclusalrestoration or stability ofthe upper jawrepresent the majority
ofneeds for bonyreconstruction.Positioning ofthe upperjaw segments can be managed
throughorthognathic surgery,which is not thefocus ofthis chapter.With defects in
thealveolar portion ofthe jaws,evaluation ofadequate bone in terms
ofheight,width,and relationship to bone in the opposingmandible is the critical
first step in recon-struction ofthe upper jaw.Limitation ofBony ReconstructionBony
reconstruction ofthe jaws dependslargely on the amount ofsoft tissue avail-
able.Soft tissue coverage and recipient bednourishment need to be addressed prior
toany bony reconstruction.The soft tissueevaluation and management should pre-cede
any efforts at bony reconstruction.The limitations ofbony reconstruction lielargely
in the imagination and skills ofthepractitioner.Host limitations relate to
theexisting soft tissue envelope in terms ofboth bulk and blood supply and
systemicfactors in the patient.Identification ofallfactors influencing outcome will
be a crit-ical step in determining choice ofbestmethods for bony
reconstruction.Bone BiologyThe hallmark ofreconstruction ofthe jawsis the grafting
ofbone into sites ofloss orneed.Bone,unlike most other tissues ofthe body,heals not
by formation ofscartissue but by regeneration ofbone.Advances in the understanding
ofbonephysiology,immunologic concepts,andtechnology have made successful recon-
struction ofthe jaws possible and some-what predictable.The success
ofjawreconstruction today is several times whatit was only three decades ago.Bone
recon-struction on a physiologic level is accom-plished by combinations ofthree
process-es:osteogenesis,osteoconduction,andosteoinduction.Osteogenesis is the
forma-tion ofnew bone from osteocompetentcells.Osteoconduction is the formation
ofnew bone along a scaffold from the host�sosteocompetent cells.Osteoinduction
isthe formation ofnew bone from the dif-ferentiation and stimulation ofmesenchy-mal
cells by the bone-inductive proteins.The understanding ofthe basic bio-logic
processes in bone has blossomedover the past thirty years.Key discoveriesin the
bioactive molecules began with thefindings ofUrist and Strates relating to thebone
morphogenetic proteins (BMPs).5,6BMP is not a single protein but a family
ofproteins belonging to the transforminggrowth factor-�superfamily (TGF-�).Atleast
13 BMPs have been identified (BMP-1does not belong to the TGF-�superfami-ly).The
ones that are ofclinical interestand are involved in human bone metabo-lism are
BMP-2,BMP-4,and BMP-7 (alsocalled osteogenic protein 1 [OP-1]).7Aswith most
biologic systems,antagonists tothese molecules exist for biologic regula-
tion.7�14These antagonists called noggin,chordin,gremlin,dan,and cerberus
areproteins that bind to BMPs and thus governcartilage and skeletal
morpohogenesis.15
786Part 6: Maxillofacial ReconstructionBMPs 2,4,and 7 have effects on stemcells and
osteoblast precursor cells toconvert them to mineralizing osteoblasts.BMPs bind and
initiate a cell signalthrough a transmembrane receptor com-plex and generate an
intracellularresponse involving Smad proteins thatpromotes osteoblast
differentiation.TheSmad proteins function as inducibletranscriptional activators
associated witha component that binds deoxyribonucle-ic acid (DNA) when they enter
theosteoblast nucleus.Research into the spe-cific genes activated is an active area
ofwork and definitive elucidation ofthemechanisms is ongoing.Bone Grafting
BiologyAxhausen initially described the repair ofbone and divided it into two
phases.16Thefirst phase consists ofcellular proliferationand production ofosteoid
in a disorganizedfashion.The second phase is characterizedby resorption ofthe
osteoid and replace-ment by more organized lamellar bone.During the first phase
ofbone regenerationthe transplanted cells within the graft pro-liferate and form
new osteoid over thecourse ofa few weeks.The amount ofboneregeneration is dependent
on the amountofbone cells that survive the transplanta-tion procedure.These
cells�survival is inte-grally related to the nourishment from therecipient bed.For
the first 3 to 5 days diffu-sion by plasmatic circulation is the
sourceofnutrients;by day 5,capillary ingrowthfrom the surrounding soft tissue and
boneedges penetrate the graft.17Free grafts ofbone can be either can-
cellous,cortical,or corticocancellousblocks (Table 39-1).Within a graft,cancel-lous
bone revascularizes sooner than cor-ticocancellous or cortical block
grafts.Endosteal osteoblasts proliferate and formosteoid on the surface
ofcancellous bonetrabeculae.18Those cells within the trabec-ulae may die as a
result oftheir encase-ment in mineralized matrix and impaireddiffusion through
it.Osteocytes withintheir lacunae appear to survive ifthey areless than 0.3 mm from
the surface.19Incortical grafts,revascularization is muchslower because the process
follows preex-isting haversian systems from the periph-ery into the interior.20A
histologic differ-ence in cortical grafts is the initiation ofosteoclastic rather
than osteoblastic activi-ty.The osteoclasts will enlarge the haver-sian systems
peripherally,then centrally.The haversian systems ofa cortical graftwill undergo
significant resorption beforeosteoblastic activity will fill in the
resorbedareas.The process ofosteoclastic resorp-tion followed by osteoblastic
deposition istermed �creeping substitution.�New bonemay be deposited throughout the
graft,leaving areas ofnecrotic bone covered byviable bone.The necrotic bone areas
maypersist indefinitely.20The osteoid from thetransplanted cells and from the
endosteumfuse in a process called consolidation.A second phase ofbone growth fol-
lows the initial consolidation and begins atabout 2 weeks.Fibroblasts and other
mes-enchymal cells differentiate into osteo-clasts and begin a resorption
oftheosteoid.This differentiation ofcells isaccomplished by BMPs found in the
trans-planted bone.New bone is laid down in amore orderly fashion.The two-phase
the-ory ofbone healing applies to all types ofautogenous grafts.In summary:(1) can-
cellous grafts are revascularized morerapidly than cortical grafts,(2)
cancellousbone incorporates by an appositionalphase followed by a resorptive phase
butcortical grafts incorporate by a resorptivephase followed by an appositional
phase,and (3) cancellous grafts tend to repaircompletely whereas cortical grafts
remaina mixture ofnecrotic and viable bone.Bone grafts improve in their mechan-ical
properties over time.Cancellous bonegrafts tend to be strengthened over timewith
the addition ofnew bone.As thenecrotic cores are replaced,the strength ofthe bone
returns to normal.Cortical graftshave a different time course and actuallyundergo a
weakening ofthe bone duringthe osteoclastic phase.Cortical grafts havebeen shown to
be 40 to 50% weaker thannormal bone from 6 weeks to 6 monthsfollowing
transplantation,a period inwhich the porosity ofthe graft increasesapproximately
15%.21After 1 to 2 years themechanical strength becomes equal tonormal bone.Other
sources ofbone are available forgrafting,but none has surpassed autoge-nous grafts
(Table 39-2).Grafts can beeither homologous grafts (Table 39-3)(allografts) or
heterografts (xenografts).The ability to obtain grafted bone withoutdonor site
morbidity to the patient hasbeen a longtime goal ofreconstructive sur-
geons.Autogenous bone grafts have beenshown to be superior to allogeneic
bone,xenogeneic bone,bone substitutes,andalloplasts in terms ofthe
function,form,and adaptability.22The superiority is dueto the transfer ofa greater
number anddensity ofosteocompetent cells.23Homol-ogous grafts,also known as
allografts orallogeneic grafts come from another per-son.Allogeneic grafts are
genetically dis-similar and to avoid tissue rejection Table 39-2Bone
GraftsAutogenous grafts:free grafts,composite graftsHomologous grafts
(allografts)Heterogeneous grafts (xenografts)Table 39-
3AllograftsUndemineralizedPartially demineralizedTotally demineralizedTable 39-
1Free Autogenous GraftsCancellousCorticalCorticocancellous
Bony Reconstruction ofthe Jaws787phenomena must be rendered nonanti-genic.These
grafts serve a purpose merelyas a scaffold for reconstruction and do nottransfer
osteocompetent cells.Grafts ofthe mandible can be used in conjunctionwith an
autogenous cancellous graft withthe allogeneic bone used as a scaffoldingwith
desired contour,size,and shape.24There are many methods for rendering anallograft
less antigenic including boiling,deproteinizing,merthiolating,freezing,freeze-
drying,irradiating,and dry heat-ing.The most common method used isfreeze-drying
(lyophilization).The majorsource ofantigenicity in allografts is thecellular
elements ofbone.Boiling,drying,or chemically treating the bone will kill thecells
but has a deleterious effect on coagu-lation oforganic elements,reducing
oreliminating their inductive effects andmaking their removal by host
cellularprocesses difficult.25Heat in excess of80oCdestroys the biologic properties
ofthebone matrix.26Allograft materials have been used inseveral jaw reconstructive
procedures,buttheir volume and lack ofosteocompetentcells make their use
limited.27�30Alloplastic graft materials includehydroxylapatite crystals,bioactive
glasses,calcium sulfate,beta tricalcium phos-phate,and biphasic calcium phos-
phate.31�33Hydroxylapatites are the mostcommonly used alloplasts.Porous nonre-
sorbable hydroxylapatite found in coralhas been used but with only limited suc-
cess.New bone can grow into the pores,but the nonresorbable coral matrix shieldsthe
new bone from stress and prevents itfrom maturing as well as might be desired.Bone
Morphogenetic ProteinsBMPs are an attractive restorative material.Although
technically a graft,this materialderives its ultimate effect by bone formationin
the host.The role ofBMPs in reconstruc-tion ofthe jaws,indications for and limita-
tions oftheir use,and the ideal carrier todeliver the material have yet to
bedefined.34�37The safety ofBMPs has beenstudied extensively in orthopedic applica-
tions,with most ofthe studies having beenconducted with grafting to the spine
andreported in the orthopedic literature.38�40With a goal to increase the available
bonefor placement ofendosseous implants in themaxilla,BMPs have been placed into
themaxillary sinus with collagen sponges as acarrier to induce new bone
formation.41,42With a similar goal in mind BMP-7 has beenplaced in fresh extraction
sites prior to theplacement ofdental implants in dogs show-ing greater
amount,density,and degree ofremodeling ofbone.43They have beenplaced in alveolar
ridges with a resorbablecollagen sponge as a carrier;however,safetyand feasibility
was assessed in only onestudy.44,45They have also been placed with apoly(a-hydroxy
acid) carrier into alveolarcleft defects in dogs with equivocal results.46Large
mandibular defects (3 cm segmental)in animal studies have been reconstitutedwith
BMPs.47�49Only two human BMPstudies have been published.42,50Autogenous Bone
Grafting SitesIntraoral Bone GraftsGrafts that can be obtained from a local
orregional site are attractive in that they areeasily obtained,often in the same
surgicalfield (Figure 39-3).They are,however,usually limited in size,quality,or
cancel-lous bone content.Intraoral donor sitesinclude the symphysis
(chin),ramus,mandibular inferior border,mandibularbody,coronoid process,and
zygoma.51�64Limited amount ofbone is available fromthese sites,and the amount
ofcancellousbone is sparse.For harvesting ofgrafts from the chineither an
intrasulcular or vestibular inci-sion can be made.The periosteum andmentalis muscle
are stripped from the chinregion,and osteotomies are performed onthe buccal surface
beginning below theapices ofthe teeth.Alternatively a trephinecan be used to obtain
the graft.The mid-line is usually left intact,and grafts can beharvested from the
right and left sidessimultaneously ifnecessary;graft volumesof1 to 3 cc have been
reported.3A mildpressure dressing is applied to the chinregion for 5 days.Temporary
paresthesiaofthe chin has been reported in at least43% ofcases.65For harvesting
oframal grafts,severalincisions can be used.In the edentulouspatient a crestal
incision is used extendingposteriorly to the ascending ramus at thelevel ofthe
occlusal plane.With healthynatural teeth,an intrasulcular incision isused,extending
it posteriorly to theascending ramus.When prosthetic crownsare
present,consideration should be givento a submarginal incision along
themucogingival line,again extending to theascending ramus.Following any
oftheseincisions,a full thickness mucoperiostealflap is developed along the lateral
aspect ofthe mandible,exposing the lateral ramusofthe mandible.A rectangular block
ofcortical bone up to 4 mm in thickness,upto 3.5 cm in anteroposterior
dimension,and up to 1 cm superoinferiorly can beharvested.The medialmost osteotomy
cutis lateral to the teeth and 4 to 6 mm medi-al to the external oblique
line.Theosteotomies can be cut with burs,saws,ora small diamond wheel (especially
usefulfor the inferiormost cut).Using osteo-tomes and chisels the block can
beFIGURE39-3Intraoral bone graft donor sites.
788Part 6: Maxillofacial Reconstructionremoved.Alternatively,trephines can beused
to obtain bone.Morbidity from thisprocedure includes fracture ofthemandible,lingual
or inferior nerve neu-rosensory disturbance,bleeding,and inci-sion
dehiscence,although these events areconsidered rare.66Cranial Bone GraftsCranial
bone is a time-honored site forobtaining bone for grafting.Initiallydescribed for
use in facial reconstructionby Tessier and refined by Jackson and col-leagues,the
technique can yield consider-able amounts ofcortical bone but limitedamounts
ofcancellous bone.67,68There isan age-dependent relationship ofthedevelopment
ofdiploic space in the cal-varial bones:80% ofchildren have adiploic space by the
age of3 years,andwhen present it is less than 50% ofits adultthickness.69The grafts
can be harvestedfrom either the inner or outer corticaltables and the procedure is
well tolerated bypatients.Fearon looked at postharvest mag-netic resonance imaging
(MRI) ofthe brainin 20 patients and did not detect any abnor-malities,even though 3
ofthe patients hada full thickness breach.70The thickness ofthe bone should be at
least 6.0 mmto con-sider in situ harvesting.Koenig and col-leagues recommend not
performing insitu bone graft harvesting from this siteprior to 9 years
ofage.69Selection oftheside ofthe head to use should be in thenondominant
hemisphere.Grafts fromthe areas ofthe parietal bone are the mostuseful;although
harvest from the frontalor occipital regions has been described,thetemporal region
should be avoided.Theincision through the scalp for obtainingthe graft can be
either coronal (full or par-tial) or sagittal (Figure 39-4).The dissec-tion ofthe
scalp flap should proceed in thesubgaleal plane,and then the pericraniumofthe
calvaria should be incised sharply.The area ofthe graft is marked out with abur
staying at least 2 cm from the sagittalsuture to avoid overlying the sagittal
sinusor arachnoid granulations.The graftdonor site should also be chosen to
avoidother sutures.For harvest ofsmall areas ofbone,asingle block can be obtained
(Figure 39-5).A bur is used to make initial cuts throughthe outer cortex ofthe
calvaria.One side isbeveled to allow insertion ofa curvedosteotome in a plane
parallel to the outersurface and at the diploic level.For largerblock grafts
(Figure 39-6) it is advisable tobevel two or more sides to avoid inadver-tent
perforation ofthe inner cortex.Whenlarger amounts ofgraft are needed it maybe safer
to harvest the bone as severalstrips,rather than a single block (Figure39-7).Once
the graft has been harvestedthe donor bed is checked to assure integri-ty ofthe
inner cortex,and a piece ofgelatin foam is placed over the site.Theperiosteum is
reapproximated and thescalp closed in layers,with the galea beingreapproximated.The
skin can be closedwith either staples or sutures.For grafts from the inner table
oftheskull (internal table ofcalvaria),a formalcraniotomy is performed and the
boneflap is handled ex vivo (Figure 39-8).Thegraft is obtained from the inner
cortex,and the flap is replaced after resuspendingthe dura then fixated.In a series
of212 in situ cranial bonegraft harvests,Zins and colleagues noted a0.5% incidence
ofdural tear and a 2.4%incidence ofdural exposure without tear.71No
infections,seromas,or bleeding wereencountered in his series.In a large
seriesof12,672 cranial bone graft harvests,thetotal complications comprised
only0.18%.72Inadvertent exposure ofthe dura(not reported as a complication)
occurredin 11%.Costochondral GraftsGrafts from the rib are useful in that
theycontain both bony and cartilaginous tis-sues.The cartilaginous component is
usefulfor providing an articular surface for thetemporomandibular joint and for
provid-ing a growth center in growing patients.This source ofbone,however,is
limited bythe size,curvature,and strength ofthe rib.For reconstructing the
temporomandibularjoint the contralateral rib usually has themore favorable
contours.Ribs from eitherside can be harvested,but most surgeonsprefer to use the
right side over the left sideFIGURE39-4Exposure for cranial bone
graftharvest.FIGURE39-5A andB,Harvest ofsmall cranial bone graft.AB
Bony Reconstruction ofthe Jaws789because ofthe position ofthe heart.Anincision is
used that corresponds to thesubmammary crease (Figure 39-9).Thisincision is well
hidden in women and is aminor concern in men.The incision willusually overlie the
sixth rib.A curvilinearincision is used and the skin is incisedsharply;sharp
dissection is used to enterthe plane overlying the ribs from the costo-chondral
junction to the midaxillary line.Either the fifth or sixth rib can be harvest-
ed.The sixth rib is usually the inferiormostorigin ofthe pectoralis major
muscle,andits use will entail the least amount ofstrip-ping ofthe muscle.A
longitudinal incisionis made over the bony portion ofthe rib,and a careful
subperiosteal dissection isperformed circumferentially around therib.Care is to be
used at the inferior anddeep aspect ofthe rib to avoid the neu-rovascular
bundle.Either saws or rib cutterscan be used to divide the rib.The rib can
beharvested with a variable amount ofcarti-lage attached to the end.Once the rib
isharvested the cut edge ofthe residual ribremaining in the patient is rounded
toavoid sharp edges.Sterile saline is placed inthe donor site,and the patient�s
lungs areinflated to assess for pneumothorax.Thewound is closed in layers and a
long-actinglocal anesthetic is administered to the har-vest site.Iliac Crest Bone
GraftsThe ilium is the most preferred donor sitefor bone grafting.Grafts may be
obtainedfrom either the anterior or posterior por-tions ofthe bone.It contains the
greatestabsolute cancellous bone volume and hasthe highest cancellous-to-cortical
boneratio.Greater amounts ofbone can beobtained from the posterior ilium.From
asingle side,the maximum amount ofobtainable bone approaches 50 cc.Fromthe
posterior ilium,the maximum obtain-able bone approaches 90
cc.DocumentedABCDFIGURE39-6A toD,Harvest ofa larger cranial bone block
graft.FIGURE39-7A toC,Harvest ofseveral cranial strip grafts.ABC
790Part 6: Maxillofacial Reconstructiondonor site complications
includehematoma,seroma,nerve and arterialinjuries,gait disturbances,fractures
oftheiliac wing,peritoneal perforation,infec-tion,sacroiliac instability,and
pain.Majorcomplications have been reported to beless common (0.7�25%) than minor
ones(1.8�15.4%).The reported prevalence ofcomplications following anterior or
poste-rior iliac crest bone grafting has varied.73Harvest ofthe anterior iliac
crest bonegraft begins with site selection.Harvestingofthe graft from the
ipsilateral or con-tralateral side from the recipient site islargely determined by
positioning ofthepatient relative to the rest ofthe operatingroom team.A separate
field is used to avoidcontamination ofdonor and recipientsites,and the
contralateral side is usuallypreferred.The anatomic landmarks oftheanterior
superior iliac crest and relativeposition ofnerve structures are marked(Figure 39-
10).The nerve branches thatare most at risk are the lateral cutaneousbranch ofthe
subcostal nerve (T12) andthe lateral cutaneous branch ofthe iliohy-pogastric nerve
(L1).The lateral femoralcutaneous nerve is located anterior andmedial to the
anterosuperior iliac tubercle;careful delineation oflandmarks will avoiddamage to
this nerve.Anesthesia or pares-thesia ofthe skin following harvesting ofiliac crest
bone grafts has ranged from 8 to38% ofpatients.73�78The skin overlying theiliac
crest is gently pulled superiorly andmedially to allow the incision to rest in
aposition inferior and lateral to the promi-nence ofthe bone.The resultant
scarshould be in a position where it is notrubbed or chafed afterward by a belt
orclothing (Figure 39-11A).The incision ismade parallel to the crest ofthe iliac
boneand approximately 2 cm posterior to theanterosuperior iliac tubercle.A 3 cm
inci-sion is usually adequate to gain access tothe iliac bone.The skin is incised
sharplydown to the subcutaneous fat.Using elec-trocautery,the subcutaneous tissue
isincised down to the fascia overlying thefascia lata and external oblique
muscles.Anincision is made along the crest ofthe bonedown to and through the
periosteum.Thisincision can usually be made with minimalcutting into the muscle
fibers.Once theincision is made through the periosteum,the subperiosteal dissection
can proceedonto the medial or lateral surfaces oftheilium,depending on the approach
usedand the need for a multilaminar graft.Inthe anteromedial approach the subpe-
riosteal dissection continues onto themedial side ofthe bone (Figure 39-11B).Care
is taken not to strip muscle from thelateral surface ofthe ilium.Keeping thetendons
ofthe tensor fascia lata attached tothe ilium minimizes gait disturbances
andpain.Acute ambulation difficulty has beenreported in as many as 50%
ofpatientsimmediately following iliac crest bone har-vest,with long-term ambulation
difficultyranging from 3 to 12.7%.75,78,79A Bennettretractor is helpful to protect
the iliacusmuscle and peritoneal contents.In the anterolateral
approach,theperiosteum is stripped from the lateral FIGURE39-8A andB,Inner table
cranial bone graft (arrow).ABFIGURE39-9A,Incisions for access.B,Dividing the
rib.C,Harvested ribs.D,Assessing for entry intothe pleural space.ABCD
Bony Reconstruction ofthe Jaws791surface ofthe ilium for easier access but at acost
ofincreased incidence ofgait distur-bance.Once the ilium is exposed by
anyapproach,the bone can be harvested as acorticocancellous block graft,a cortical
graft,or a cancellous graft (Figure 39-11C�F).Thesize ofthe graft is outlined,and
usingsaws,osteotomes,or a bur,osteotomies areperformed.The cancellous graft can
beharvested with curettes,gouges,ortrephines.74,79�82Hemostasis is obtainedwith the
use ofgelatin foam or otherhemostatic agents ifnecessary.Use ofdrains at the donor
sites ofeither posteri-or or anterior approaches is not indicated;and no difference
has been shown inwound healing.83Injection ofa long-acting local anesthetic agent
into the over-lying soft tissue provides some comfort inthe immediate postoperative
period.84Harvest ofthe posterior iliac crest isanother well-documented source
forbone.85�88Patient positioning in the supineposition for most maxillofacial
proceduresinvolves a patient repositioning when poste-rior iliac crest bone is
harvested.Largeramounts ofbone available from thisapproach may make it worthwhile
to con-sider this option.The patient is positionedin the prone position with a
small amountofflexion and placement ofa hip roll.Thelandmarks identified are the
spinousprocesses ofthe vertebra and the posterosu-perior iliac crest and spine.A 5
cm curvilin-ear incision is made through the skin over-lying the iliac crest.Nerves
at risk are thesuperior and middle cluneal nerves (L1 toS3).Using sharp and blunt
dissectionthrough the subcutaneous tissues,the pos-terosuperior crest is identified
and the fasciadivided between the abdominal and glutealmuscles.A subperiosteal
dissection pro-ceeds,and the tissue is reflected laterally.Care is used to avoid
the sacroiliac liga-ments.Bone can be harvested as a cortico-cancellous block
graft,a cortical graft,or acancellous graft similar to the approach tothe iliac
crest.Complication rates for poste-rior iliac crest bone harvest are,in
general,lower than those for anterior harvest.73�77,79Tibial Bone GraftThe tibial
metaphysis is another importantsource ofautogenous bone.O�Keefe andcolleagues
reported the first large series(230 cases) using the tibia as a donor site.89They
found adequate bone for graftingLateral cutaneous branchof iliohypogastric
nerveLateral cutaneous branchof subcostal nerveLateral femoralcutaneous
nerveInguinal ligamentFIGURE39-10Diagram ofnerves.Adaptedfrom Lew D,Hinkle RM.Bony
reconstruction ofthe jaws.In: Peterson LJ,Indresano AT,Mar-ciano RD,Roser
SM.Principles oforal and max-illofacial surgery.Vol.2.Philadelphia: J.B.Lip-pincott
Company; 1992.p.923.FIGURE39-11A,Landmarks for obtaining graft.B,Osteotomies for
harvest.C,Corticocancellous grafts.D,Cortical surface ofgraft.E,Cancellous
graft.F,Cancellous graft applied.ABDECF
792Part 6: Maxillofacial Reconstructionand a low incidence (1.3%) ofcomplica-
tions,none ofwhich were long-term.Thetibial region heals exceptionally
well,butradiographic findings in the donor sitemay persist indefinitely.90The use
ofthissite is relatively contraindicated in grow-ing patients because ofthe risk
ofdistur-bance to a growth center site,although itsuse has been reported in the
repair ofalve-olar clefts.91Catone and colleaguesdescribed the use oftibial bone in
maxillo-facial surgery and was able to obtain up to42 mL ofuncompressed cancellous
boneper site.92Bone from the tibial site wassuccessfully used to graft
mandibularnonunions,in orthognathic surgery,as asinus augmentation,and in
mandibularreconstruction.Comparison oftibialgrafts against iliac crest grafts in
secondaryalveolar clefts shows similar bone densitiesat 6 months.91The graft is
usually harvested with thepatient in the supine position,although thegraft can be
harvested with the patient inthe prone position.89A 3 cm longitudinaland slightly
angled incision (Figure 39-12)is made through the skin overlying
Gerdy�stubercle.Gerdy�s tubercle is a prominenceofbone on the anterior surface
ofthe prox-imal end ofthe tibia located lateral to thetibial tuberosity.It is the
distalmost inser-tion ofthe iliotibial tract.Sharp dissectionis used to obtain a
supraperiosteal dissec-tion overlying and inferior to Gerdy�stubercle.The
dissection should be medialto the tibialis anterior muscle and lateral tothe
patellar ligament.Ifa cortical graft isdesired,the dissection can proceed in
asubperiosteal plane,exposing Gerdy�stubercle.89Ifno cortical bone is required,an
osteoperiosteal flap can be created byincising through the periosteum in a
�U�shape,leaving periosteum attached to thecortex.92A cortical window is made
withburs,saws,or osteotomes measuring 1 cmby 1 cm.The window should incorporatethe
crest ofthe tubercle at the superiorportion ofthe window.The crest repre-sents a
simple and reliable landmark toavoid the articular surface ofthe tibia andthe joint
space.It is recommended to keepat least a 2 cm distance from the articularsurface
ofthe tibia to avoid damage.93Amedial approach to the tibia has also beenadvocated
that avoids the insertion oftheiliotibial tract and several other
anatomiclandmarks.94,95In the medial approach,thelandmarks are two lines:one
vertical linedrawn through the patella and tibialtuberosity and the other
perpendicular tothe first,through the tibial tuberosity.It isrecommended that an
oblique skin incisionbe made centered over a point 15 mm supe-rior to the
horizontal line and 15 mm medi-al to the vertical line.95Dissection
continuesthrough the periosteum overlying the boneunderneath the incision.A bone
window ismade to provide access to the cancellousbone.Regardless ofthe approach
(medial vslateral) used,once the window has beenremoved or elevated,the cancellous
bonecan be harvested with curettes.Equalamounts ofbone are available from
eitherlateral or medial approaches.95For largervolumes ofgrafts,bilateral grafting
can bedone,with some possible impairment toearly ambulation.No attempt is made
tofill the metaphyseal dead space,and nodrains are used.The wound is closed in lay-
ers.Ifsmaller amounts ofbone are needed(< 15 cc),the procedure can continuethrough
a small stab incision and with useofa trephine or curettes.92,96van Dammereported
up to 40 cc ofcancellous boneobtained through this method.96Microvascular Free
FlapsMany microvascular free flaps have beendescribed for reconstruction
ofthemandible and maxilla,including the fibu-la,iliac crest,and scapula.Free
microvas-cular flaps have the advantage ofhavingtheir own blood supply independent
ofthe local tissue bed,and they behave as amicrovascular transfer
oftissue,exceptwhere they interface with the existingrecipient bone.In areas ofpoor
vascularsupply they have superiority over otherbone grafts.Additionally they may
betransferred as composite grafts includingsoft tissue components.A detailed
discus-sion ofmicrovascular free flap reconstruc-tion is presented in Chapter
40,�Microvascular Free Tissue Transfer.�Platelet-Rich PlasmaWith the advent ofblood
factor fractionationin hematology and the search for hemostaticagents,interest has
increased in platelet-richplasma (PRP) fractions.PRP is a volume ofautologous
plasma that has a platelet concen-tration higher than normal.In general,PRPcontains
> 1 �106platelets/�L.In clinicalpractice,PRP is applied to the site ofa bonegraft
to deliver a high concentration ofgrowth factors from platelets.97Once thePRP-
containing high concentrations offib-rinogen and platelets are mixed with throm-bin
and calcium,a gel is formed resulting inthe release ofgrowth factors from
theplatelet (a) granules.Within 10 minutestheplatelets secrete 70% oftheir stored
growthfactors and close to 100% within the firsthour.98The platelets then
synthesize addi-tional amounts ofgrowth factors for about8 days until they are
depleted and die.Theprecise content and concentration ofgrowth factor has yet to be
fully elucidated.The a-granules ofplatelets release at leastseven growth
factors,including platelet-derived growth factor,TGF-�,platelet-FemurPatellaMedial
harvestsiteLateral harvestsiteGerdy's tubercleFibulaTibiaFIGURE39-12Incision for
tibial bone graft.
Bony Reconstruction ofthe Jaws793derived epidermal growth factor,platelet-derived
angiogenesis factor,insulin-likegrowth factor-1,and platelet factor-4.99There is a
complex interplay between thegrowth factors that depends on their con-
centration,local microenvironment,andinteractions with other molecules.Many ofthese
growth factors can have effects thatare in opposite directions depending on
thecontext ofexpression.100The PRP constel-lation ofgrowth factors allows the
complexinterplay ofthese agents to be exploited tobetter advantage than relying on
a singlegrowth factor agent.PRP is an autologous preparation;therefore,the risk
ofdisease transmissionfrom its use should theoretically be nil.There has been some
concern about theantigenicity ofthe bovine thrombin used,although this has not been
a problem inmaxillofacial applications.101It is believedthat some ofthe
antigenicity attributed tothrombin results from contaminationfrom bovine factor V
in the thrombinpreparation.Another gelling agent,ITA,has been used in place
ofbovine thrombinbut its constituents are proprietary andunknown.102There are
several systems for prepar-ing PRP (Figure 39-13) ranging from thesimple to the
complex,from those thatrequire whole units ofblood to those thatrequire only 50
mL.The most complex arethe general-purpose cell separators thatare widely used by
blood banks and hospi-tals.Using a plasmapheresis technique,450 mL ofwhole blood is
drawn offinto acollection bag containing an anticoagu-lant,usually citrate
phosphate dextrose.Other anticoagulants are available;antico-agulant citrate
dextrose-A is also used andmay be preferred.98Edetic acid is avoidedsince it
fragments the platelets.102Thepreparation is then centrifuged first athigh speed to
separate the plasma from thered cells and the buffy coat.The centrifugeis then
slowed down and run for a periodoftime to further separate the PRP andthe platelet-
poor plasma (PPP).Approxi-mately 30 cc ofPRP can be obtained fromthe sample in
about 30 minutes.Plateletcounts of0.5 to 1.0 �106/�L can usually beattained with
this method.It is recom-mended that the PRP be used within 6 hours ofbeing
procured.Once devel-oped,PRP is stable and remains sterile inthe anticoagulated
state for 8 hours.98In a quest to achieve a concentrateddelivery ofplatelets at a
reasonable cost,sev-eral systems were developed that use small-er procurements
ofwhole blood,are faster,produce more concentrated product,andare less
expensive.97,102,103Two ofthe unitsthat are currently approved by the US Foodand
Drug Administration are the HarvestSmartPRep Platelet Concentrate Systemand the 3i
Platelet Concentrate CollectionSystem.These systems both use tailoredcentrifuge
containers to manipulate theblood cells to achieve the separation andsequestration
ofplatelets.They both havelong and short spin cycles.Average plateletcounts of1.4
to 1.8 �106/�L are obtained ina 5 mL sample.99Run times for the prepara-tion are
usually 15 to 20 minutes.Once the PRP has been prepared,thecoagulation process is
initiated using amixture of100 US units oftopical bovinethrombin (TBT) powder
suspended in 10 mL sterile saline and 10% calcium chlo-ride.In a 10 cc syringe,6 mL
ofPRP ismixed with 1 mL of10% CaCl2,1 mL TBT,and 1 mL air for mixing.The mixture
isapplied to the bone grafts in a layered fash-ion.Some ofthe newer systems have
special syringe tips that combine the con-stituents from several syringes simul-
taneously.Once applied,the mixture setsin a matter ofminutes.There is a paucity
ofstrong clinical datato support many ofthe claims being madefor PRP in the
jaws;only one prospectivetrial is published.104The majority ofthepublications are
case series or case reports.Marx and coworkers evaluated the effect ofPRP on bone
graft reconstructions ofmandibular continuity defects 5 cm orgreater,showing a
maturity index ofabouttwice actual maturity at 2 and 4 months.97In a case series
of15 patients,PRP has beenadded to freeze-dried demineralized boneto augment the
maxillary sinus and alveolarridge.105The authors posit that use ofPRPmay allow for
earlier implant placementand loading,but this conclusion willrequire further study
to be supported.Inanother cases,24 maxillary sinuses wereFIGURE39-13A,Machine for
harvest ofplatelet-rich plasma.B,Fractionated sample containing platelet-rich
plasma.AB
794Part 6: Maxillofacial Reconstructionaugmented with a combination ofPRP
anddeproteinized bovine bone along withsimultaneous insertion
ofendosseousimplants.104In three ofthese cases bonedensity measurements made at 4
monthsshowed increased density compared withthe surrounding native bone.Only
prelimi-nary data are available to date on the histo-logic evaluation ofthe PRP-
augmentedsinuses.106,107A case report ofuse ofPRPwith autogenous bone and a
titanium meshfor a large anterior maxillary defect has alsobeen
described.108Fourier and fractalanalysis ofradiographs ofmaxillary alveo-lar ridge
repair using PRP and inorganicbovine bone showed trabecular patterns ofthe
regenerated bone similar to but lower incomplexity than the native bone,which
theauthors attributed to the PRP.109Hyperbaric Oxygen TherapyAfter success with
treating osteora-dionecrosis ofthe mandible with hyper-baric oxygen therapy,the
modality wasapplied to patients undergoing mandibu-lar reconstruction.110Applying
fairly strin-gent success criteria,a rate of94% wasreported.Hyperbaric oxygen
therapy con-sists ofbreathing 100% O2at 2.4 atm for90 minutes,commonly referred to
as adive.Protocols for reconstructive proce-dures differ from those used to treat
oste-oradionecrosis and consist of20 dives pre-operatively and 10 dives
postoperatively.The mechanisms by which hyperbaricoxygen thereapy exerts its
effects are bio-chemical,cellular,and physiologic.111Dur-ing a dive,arterial oxygen
tensions in excessof2,000 mm Hg,and tissue oxygen ten-sions ofalmost 400 mm Hg have
beenattained.Physiologically at 2.4 atm,oxygennot only saturates the available
hemoglobinbut dissolves in the plasma to more than 10times the amount at sea level
(0.3 mL/dL).Tissue irradiated beyond 5,000 cGy exhibitshypoxia,hypovascularity,and
hypocellular-ity.This predisposes the tissue to infectionand poor wound healing in
addition tomaking it a poor donor bed for a bonegraft.Hypoxia inhibits and
decreases theneutrophil-mediated killing ofbacteria byfree radicals.Tissue
PO2levels in irradiatedpatients have been documented as low as 5 mm Hg and often
range between 5 and 15 mm Hg.During hyperbaric oxygen ther-apy the tissue PO2rises
to between 100 and250 mm Hg but falls to baseline within 10 minutes following a
dive in the initialperiod oftherapy.Improved collagen for-mation and fibroblast
proliferation occurwhen the tissue oxygen tension is raisedover 20 to 30 mm
Hg.112Capillary prolifer-ation occurs along collagen laid down fol-lowing
hyperbaric oxygen exposure.As thisneovascularization spreads,tissue oxygena-tion
improves between 20 and 35 mm Hgin the hours after treatment.The improve-ment
plateaus after 10 to 20 dives;divesbeyond this time do not marginallyimprove the
host bed.Complications ofhyperbaric oxygentherapy include reversible
myopia;barotrau-ma to the middle ear,lungs,teeth,and sinus-es from rapid pressure
changes;seizures(self-limited and causing no
permanentdamage);claustrophobia;reversible tracheo-bronchial symptoms (chest
tightness,sub-sternal burning sensation,and cough).Noevidence ofa tumorigenic
effect ofhyper-baric oxygen has been found to date.113Reconstruction ofthe
MandibleReconstruction ofthe mandible can occurimmediately at the conclusion ofan
abla-tive procedure ofthe jaw (primary recon-struction);delayed (secondary),after
anappropriate time ofprimary soft tissuehealing;or,in the case ofdevelopmental
orgradually acquired defects,at the time ofrecognition ofthe need for
reconstruction.The first step in reconstruction is to classifythe defect determined
by its size,location,and functional or cosmetic impairment.The size ofthe defect in
three dimensionswill define the magnitude ofthe recon-struction.Small defects ofthe
alveolus mayrequire limited bone grafting,while largerdefects may require more
extensive orstaged procedures.Some defects may notnecessarily be restored to the
original sizeand bulk ofthe missing part.Loss ofa sig-nificant portion ofa ramus
may be ade-quately managed by providing continuityfrom the condyle to the body
ofthemandible without restoring a coronoidprocess or several centimeters
ofanteropos-terior width.The bulk ofthe bone needonly be enough to provide for
adequatestrength to manage the functional loads.Location is important as some
defects maynot need to be restored,such as the veryposterior ofthe body ofthe
mandible (dis-tal to the first or second molar) where noplan is made for
restoration ofthe dentalocclusion ofthe mandible or opposingdental arch.The
functional deficits thatexist and those that are to be addressed playa role in the
choice ofreconstruction.Once the area ofbony defect has beendefined and the
assessment ofhow muchbone to reconstruct has been determined,attention should be
directed to how to bestachieve these goals.The available soft tis-sue in terms
ofquantity and quality isparamount in choosing a reconstructivemethod.Indeed the
soft tissue will deter-mine to a large extent the availableoptions.Ifthe soft
tissue is adequate inboth ofthese parameters,the options willbe many.If,however,the
soft tissue isinadequate in size or bulk,efforts will needto be made to provide
adequate soft tissuebefore undergoing bony reconstruction.This can be accomplished
by introducingmore soft tissue through local flaps,pedi-cled flaps,or microvascular
free flaps.Composite flaps are an option for simulta-neous hard and soft tissue
reconstruction.Techniques such as distraction osteogene-sis can provide increased
bone and soft tis-sue simultaneously like the compositegrafts.Ifthe quantity ofsoft
tissue is ade-quate but the quality ofthe soft tissue ispoor,the reconstruction
will be compro-mised or the options limited.Tissue thathas been irradiated or has
extensive scar-ring will provide a poor host bed for any
Bony Reconstruction ofthe Jaws795grafting procedures.Adjunctive proce-dures such as
hyperbaric oxygen therapyor soft tissue flaps may be necessary toprovide an
adequate donor bed.The functional and esthetic require-ments will dictate the goal
to be accom-plished;multiple-stage procedures are thenorm rather than the
exception.Reconstruction ofthe MaxillaThe same general parameters inapproaching the
mandibular reconstruc-tion are operative in the maxilla.Identi-fication ofthe goals
ofreconstructionwill dictate the course ofreconstructionto take.Once the goal has
been delineat-ed,attention is first given to the soft tis-sue envelope to support
bony recon-struction ofthe maxilla.Appropriategrafting procedures are
undertaken,andprovision is made for interim prosthet-ics.The following cases
illustrate specificpoints ofconsideration in reconstructionofthe areas ofthe
jaws.Case Example 1: Reconstruction ofLarge Traumatic Mandibular DefectThe patient
is a 17-year-old man who suf-fered a gunshot wound to the anteriormandible with
loss ofboth hard and softtissue (Figure 39-14).The maxilla wasunaffected.The first
step in this case is todefine the defect in terms ofboth hard andsoft tissue and
decide on a strategy forreconstruction.As this is a contaminatedwound with ill-
defined areas ofvital hardand soft tissue,delayed reconstruction isthe preferred
option.D�bridement offreebone fragments and grossly nonperfusedsoft tissue will
enhance the rapidity ofpri-mary healing (Figure 39-15).Once thed�bridement is
complete,the bone compo-nents are aligned using available dentallandmarks (Figure
39-16) and soft tissuecomponents are reapproximated (Figure39-17).To aid the ease
ofreconstruction,anatomic relations are maintained and sta-bilized with fixation
devices (Figure 39-18)to preserve interramal width.At this time amore accurate
assessment ofsoft tissue andbone deficits can be appreciated in
threedimensions.There is a segmental mandibu-lar defect with inadequate soft
tissues andan opposing dental arch.The functionalrequirements for reconstruction
include(1) restoration ofcontinuity ofthemandible,(2) adequate bone height andwidth
to allow restoration ofthe occlusion,and (3) restoration ofmandibular mor-phology
for esthetic and functional require-ments.Because ofthe avulsive nature
ofthedefect,the soft tissue is inadequate in termsofquality and quantity.A period
ofweeksto months may be required for the soft tis-sues to mature and heal.Before
bony recon-struction can begin,soft tissue must bebrought in to provide for an
adequaterecipient bed for grafting and restoration ofcontours.In this otherwise
healthy individ-ual,autogenous grafting will most effective-ly supply the adequate
bulk and form nec-essary to achieve the goals.A pedicledmyocutaneous graft
(pectoralis major)with a skin paddle will provide the bloodsupply to nourish the
graft and to provideadequate bulk ofskin in the chin region.The residual bilateral
condyle-ramal com-plexes will be stabilized with a titaniumreconstruction plate
(Figure 39-19).Anappropriately sized skin paddle will restoreFIGURE39-14Gunshot
wound to mandible.FIGURE39-15A andB,D�bridement ofnonviable hard and soft
tissues.ABFIGURE39-16Alignment using dental land-marks.FIGURE39-17Reapproximation
ofskin andmucosa.
796Part 6: Maxillofacial Reconstructionthe missing skin over the chin (Figure 39-
20).The muscle is positioned to restorebulk to the region and to approximate
thearea ofthe future bone graft.The soft tis-sues are then allowed to heal over
severalweeks prior to definitive bone grafting (seeFigure 39-20D).Both allografts
and auto-grafts will be used,with a cadavericmandibular crib (Figure 39-21) secured
tothe reconstruction plate used to maintainthe proper morphology ofthe
mandible.Acancellous marrow graft is obtained to pro-vide adequate bulk (Figure 39-
22).Restora-tion ofthe contours and functionality ofthe mandible results at the
completion ofthe reconstruction (Figure 39-23).Case Example 2: Delayed
Reconstruction ofan AblativeDefect ofthe MandibleA swelling with associated
radiolucency ofthe mandible is noted (Figure 39-24).Boththe medial and lateral
cortices have beendestroyed in the area ofthe lesion.Becauseofthe location and size
ofthe defect,recon-struction ofthe defect is indicated to restorebulk and strength
ofthe residual mandiblefollowing treatment.After adequate soft tis-sue healing,an
anterior iliac crest cancellousbone graft is obtained and placed in thedefect (see
Figure 39-24B).One year follow-ing reconstruction,the bone graft hasmatured with a
normal trabecular pattern.The graft is maintained and the bone is ade-quate for
oral rehabilitation 2 years aftergrafting (see Figure 39-24E).Case Example 3:
Reconstructionofthe Anterior MaxillaA 37-year-old man had undergone avulsivetrauma
to the anterior maxilla during amotor vehicle accident.The residual defectwas from
the loss ofanterior maxillary teethand a large portion ofthe alveolus (Figure39-
25A).Dental models were obtained,anda diagnostic wax-up was prepared to assessthe
ideal position ofthe restored teeth.Thebony reconstructive effort is therefore
guid-ed by the prosthetic plan so that adequatebulk and position ofthe grafted bone
can beassured.The defect in the upper jaw consist-ed ofinadequate bone in terms
ofheightand width and inadequate soft tissues.No oral�nasal cavity partitioning
defectexisted.A wide pedicled flap is raised FIGURE39-18A andB,Stabilization with
external fixator.ABFIGURE39-19Stabilization ofmandible withtitanium reconstruction
plate.FIGURE39-20A,Harvest ofpectoralismajor myocutaneous flap with skin
paddle.B,Flap is brought into chin region.C,Skinpaddle is inset into chin
region.D,Healedsoft tissue prior to bone grafting.ABCD
Bony Reconstruction ofthe Jaws797FIGURE39-21A,A freeze-dried allogeneic cadaver
mandible is obtained and hollowed out.B,Useful section ofthe crib is
perforated.C,The crib is securedto the plate (arrow)with the pectoralis major
muscle (arrow)nourishing the bone graft.ABCFIGURE39-22Occlusal radiograph in the
area ofthe graft.FIGURE39-23Restoration ofcontour ofchin.FIGURE39-24Radiographs
illustrating delayedreconstruction ofan ablative defect ofthemandible: A,prebiopsy;
B,immediately post-graft;C,2 weeks postgraft;D,1 year postgraft; E,2 years
postgraft.ABCDE
798Part 6: Maxillofacial Reconstruction(Figure 39-25B) to expose the bony
defect,and a stent prepared from the diagnosticwax-up is used to assess the bony
defectmore accurately (Figure 39-25C).Sterilebone wax is used to prepare a template
forthe graft dimensions (Figure 39-25D).Acorticocancellous graft is obtained from
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CHAPTER 40Microvascular Free Tissue TransferJoseph I.Helman,DMDRemy H.Blanchaert
Jr,MD,DDSReconstruction ofthe maxillofacial regionhas been a challenge due to the
significantcomplexity offunction and esthetics.Theintroduction offree tissue
transfer to thearmamentarium ofavailable techniqueshas facilitated this task,and
thereforeallowed for a better quality oflife for ourpatients.Following the
description ofthehistory offree flaps in this chapter,thesurgical techniques are
reviewed and dis-cussed along with the most common spe-cific donor sites:the radial
forearm flap,the free fibula flap,and the iliac crest withthe deep circumflex iliac
vessels.History ofthe Surgical MicroscopeThe development ofmicrosurgical free tis-
sue transfer resulted in a dramatic evolu-tion in head and neck
reconstruction,allowing for a significant increase in theavailable choices
ofanatomic and function-al rehabilitation.There is no doubt that theavailabilities
ofsurgical loupes and intraop-erative microscopes have been the facilitat-ing
factors to performing microvascularand microneurosurgical anastomoses.In 1590 Dutch
opticians Zacharias andHans Janssen aligned two lenses within asliding tube,thereby
inventing the micro-scope.Galileo Galilei independently devel-oped the same device
a decade later byinverting his �tubum opticum�or telescope.From the sixteenth to
the nineteenthcenturies many technical advances weremade,including the mathematical
formu-las ofErnst Abbe who predicted and stan-dardized optical qualities,allowing
Zeissto mass produce high-quality micro-scopes.Operating spectacles were intro-
duced in the 1860s and surgical loupeswere used for the first time in surgery bythe
German physician Saemisch in 1876.The first surgical microscope was built byDr.Carl
Nylen,a Swedish otolaryngologistwho used it for the first time in the oper-ating
theater in 1921.1History ofFree Tissue Transfer for Head and Neck
ReconstructionEarly attempts to achieve free tissuetransfer resulted in few
successes.Carrelfirst reported free vascularized transferofintestine into the
cervical region ofexperimental animals in 1907.2In thelate 1950s and early 1960s
Jacobson andSuarez performed successful anastomosisofcarotid arteries in dogs and
rabbitswith a 100% patency rate.3When Jacob-son presented the outcome ofhisresearch
at a national meeting,a leadingsurgeon at a prestigious institution stat-ed in
front ofthe audience,�This is verynice work,but it is simply ridiculous tobring a
microscope into the operatingroom.�1During the 1960s the art ofmicrosurgery was
promoted by neuro-surgeons and plastic surgeons withencouraging results.New flaps
were designed for recon-struction ofthe head and neck based onthe ability to
transfer distant tissues andprovide immediate viability through a vas-cular
anastomosis.In 1975 Taylor and colleaguesdescribed the free fibula flap,while
Hidalgoapplied the technique for mandibularreconstruction in 1989.4,5In 1981
Yangdeveloped the radial forearm flap,whileSoutar and colleagues popularized
thetechnique for intraoral reconstructionwith and without the addition ofa
portionofthe radius in the mid-1980s.6�8In 1978Taylor described the transfer ofthe
iliaccrest as an osteomyocutaneous flap basedon the blood supply from the
circumflexartery and vein.9,10Free flaps became popular in the headand neck region
due to the ability to trans-fer vascularized bone and soft tissue in onestage at
the time ofthe resection,with pre-dictable high success rates.It is also obvi-ous
that they increased the choices oftis-sue availability,as well as
pliability,texture,color,etc,in the quest to achieve an idealreconstruction and a
functional rehabilita-tion ofthe patient.Principles
ofMicrovascularAnastomosisInstrumentationThe microsurgery instruments require
thefollowing specifications:
804Part 6: Maxillofacial Reconstruction1.Their weight must not exceed 15 to20
g.Titanium instruments usuallyhave less weight.2.They must be at least 10 cm long
sothat they lie loosely in the hand.3.The closing pressure ofsome instru-ments such
as forceps or scissorsshould lie between 50 and 60 g.Tremorincreases with higher
closing pressure.4.The vascular clamps must exert an even-ly distributed pressure
over the wholelength ofthe jaw ofthe clamp.The jawsmust lie parallel with each
other.5.Microscissors should have an open-ing ofless than 4 mm.They can beeither
straight or curved,but it isimperative that they cut tissue in aclean fashion in
order to reduce therisk ofa thrombosis in a vascularanastomosis or the formation
ofaneuroma in a crushed nerve.6.Watchmaker forceps are extremelyuseful,either
straight or angled.Theycan be used as needle holders as longas there is no need to
exert a signifi-cant force on the needle,in which casea microneedle holder would be
theinstrument ofchoice.7.Microsurgical bipolar coagulationallows for concentrated
coagulationbetween the two ends ofthe forceps,avoiding unnecessary
devitalizationoftissues.8.Microscope and/or loupes.Surgicalmicroscopes were
developed by Zeissin the early days and presently thereare several similar
microscopes manu-factured by other companies.A mag-nification of10�is usually
enough foranastomosis.The zoom allows for reg-ulation from a magnification
of10�while performing the anastomosis,toa lower magnification (4�to 6�) whilethe
suture is being knotted.11Anastomosis TechniqueThe suture (usually 9-0) is passed
at a dis-tance from the margin ofthe vessel similarto that ofthe thickness ofthe
wall.It is rec-ommended to apply a counterforce whilepassing the needle through the
vessel byholding the forceps open inside the lumen(Figures 40-1A and B) instead
ofgraspingthe vessel wall which may damage the edgeofthe vascular structure (Figure
40-1C).After the suture has passed through bothends ofthe vessel,a small �tail�of2
to 3 mm is left in order that the knot can beperformed while seeing the suture
endwithin the field ofthe surgical microscope(Figures 40-1D and E).After the first
suture is placed the sec-ond suture is usually placed 180�from thefirst.The third
suture is placed in betweenthe first and the second,and two more inter-rupted
sutures are placed on the same side.After finishing one side the vascular clampsare
turned to expose the other side oftheanastomosis.The sutures should always beat the
same distance as the edges ofthe ves-sel as well as the same distance between
eachone ofthe sutures (Figure 40-2).When the vascular anastomosis cannotbe
performed �end-to-end�due to very significant differences in the diameter ofthe
lumen,an �end-to-side�anastomosis isa viable alternative (Figure 40-3).An
ovalexcision ofthe wall ofthe large-diameterartery is performed,and the sutures
areexecuted in a similar fashion as explainedin the end-to-end anastomosis.Radial
Forearm Free FlapMany types offree flaps have been used inhead and neck
reconstruction.The radialforearm flap is perhaps the most com-monly used soft
tissue microvascular flapfor intraoral and oropharyngeal defects.Ithas gained wide
acceptance because ofitsreliability,adaptability,ease ofharvest,andthe thin pliable
nature ofthe flap.The flapallows restoration ofthe complex three-dimensional
anatomy inherent in oral andoropharyngeal defects.This is demon-strated by the
commonplace reconstruc-tion ofcombined tongue and floor-of-mouth defects.Folding
the flap on itselftosimultaneously reconstruct the tongueand floor ofmouth creates
redundancyand allows the residual tongue to retainoutstanding mobility (Figure 40-
4).FIGURE40-1A and B,It is recommended to apply counterforce while suturing by
holding the forcepsopen inside the lumen.C,Grasping the vessel with the forceps may
damage the edge ofthe vessel.Whilepassing the needle the motion should be
circular,following the needle shape in order to avoid a tear ofthe vascular
structure.D andE,A small �tail�of2 to 3 mm should be left at the end ofthe suture
to per-form the knot within the microscope surgical field.Adapted from Medhorn HM
and Muller GH.11ABCDE
Microvascular Free Tissue Transfer805Clinically the skin paddle ofthe radialforearm
flap often takes on an appearancesimilar to that oforal mucosa following
itstransfer to the oral cavity.This change inappearance has been shown to be
reactivein nature and does not represent true metaplasia.12DevelopmentThe history
ofthe spread ofunderstandingofthe flap is interesting.Soutar and col-leagues
reported and referenced the intro-duction ofthe flap to German surgeons vis-iting
China in 1980.7Subsequently thesesurgeons published in the German lan-guage
literature on the use ofthe radialforearm as a donor site for the creation
ofneurofasciocutaneous and osteocutaneousflaps in neck and in hand
reconstructions.Soutar and colleagues reported the useofthe radial forearm flap in
primarymandibular reconstruction in 1983.7Cor-rigan and O�Neill published a report
ofthecases outlining the technique ofosteocuta-neous flap harvest and
transfer,andincluded a description ofcomplicationsencountered.13The most
devastating ofthese complications is distal radius frac-ture,which results in
significant deformi-ty.Vaughan documented extensive experi-ence with 120 radial
forearm flaps,prais-ing the adaptability and applicability ofthe flap in head and
neck reconstruc-tion.14,15Published reports have demon-strated it to be possible to
perform defini-tive mandibular reconstruction using theosteocutaneous radial
forearm flap anddental implants.16The volume and heightofthe bone compare poorly to
those ofother flaps.The fibula and deep circumflexiliac artery flap appear to have
the mostsuitable bone stock to facilitate dentalimplant�based mandibular
rehabilitationand are therefore more popular whenbone is necessary.17Refinement and
adaptation oftheradial forearm flap continued throughoutthe early 1990s.Urken and
colleaguesreported on the use ofthe neurofasciocu-taneous radial forearm flap in
head andneck reconstruction.18This report includ-ed a means ofmonitoring buried or
poor-ly accessible flaps that could be facilitatedby the inclusion ofa skin paddle
on theproximal fascial/subcutaneous element ofthe flap.Protection ofthe flap
vessels andaugmentation ofthe contour deformitycreated by neck dissection are
additionaladvantages ofthis modification.19,20Theliterature abounds with
descriptions ofsuitable adaptations ofthe radial forearmflap to specific sites
within the head andneck.Urken and Biller published a3rd suture6th suture1st
suture2nd sutureFIGURE40-2The first and secondsutures are performed 180�from
eachother.The third suture is placed betweenthe first two while holding the vessel
onboth sides with the tails ofthe first andsecond sutures.After interrupted
suturesare placed on one side ofthe vessel,themicrovascular clamps are turned
toexpose the other side ofthe anastomosisand proceed in a similar fashion as on
thefirst side.Adapted from Medhorn HMand Muller GH.11ABCDEFFIGURE40-3A�F,The end-
to-side anastomosis is performed after excision ofan oval segment ofthe�side�donor
vessel.The sequence ofsuturing is similar to the technique described in Figure 40-
2.Adapted from Medhorn HM and Muller GH.11
806Part 6: Maxillofacial Reconstructiondescription ofa bilobed neurofasciocuta-
neous flap for hemiglossectomy defectsthat allows preservation ofresidual
tonguefunction.21Oromandibular reconstructionhas been reported using the free
radialforearm flap alone or in combination witha fibula free flap.7,13,22,23Lower
lip recon-struction has been described wherein thepalmaris longus tendon provides
supportand suspension to the flap.24,25Simultane-ous lip and cheek,full-thickness
cheek,and soft palate reconstruction have alsobeen described.24�28Oral cavity
andpharyngoesophageal reconstruction withthe radial forearm flap has advantages
overother reconstructive modalities,demon-strating good functional
outcomes.29,30Reconstruction offacial defects (forehead,nasal) has also been
described as an appro-priate use ofthe radial forearm flap.31,32Extreme uses ofthe
flap include reports ofthe creation ofhybrid flaps,wherein thecephalic vein remains
pedicled for use incases with inadequate venous outflow andthe simultaneous use
ofbilateral flaps.33,34Throughout the development ofthefree radial forearm
flap,reinnervation ofthe flap has received considerable atten-tion.Many authors
have discussed therole ofsensory reinnervation in function-al outcomes in oral
cavity and oropharynxreconstruction.17,18,21,35,36Recall that someofthe earliest
descriptions ofthe use ofthe flap were neurofasciocutaneous flaps.7The
neurofasciocutaneous radial forearmflap is typically designed to include onlythe
median antebrachial cutaneous nerve(see Figure 40-6).Sensory nerve
mappingaccomplished by cadaveric microdissec-tion and selective nerve block
techniquein 8 forearms of4 human subjects hasrevealed that much ofthe skin
territoryharvested with the flap is supplied byeither the lateral antebrachial
cutaneousnerve or the superficial radial sensorynerve.37This brings into question
themeans by which the radial forearm flapachieves reinnervation.Many authorshave
postulated that reinnervation occursby ingrowth ofnerve fibers from therecipient
bed and peripheral or adjacenttissues.27,36,38�41Close and colleagues com-pared
spontaneous sensory recovery inmyocutaneous pectoralis major flaps andradial
forearm fasciocutaneous flaps andfound the forearm flaps to exhibit signifi-cantly
better sensation.35This supports theidea that the characteristics ofboth theflap
and the recipient bed influence thesensory recovery within non-
reinnervatedFIGURE40-4Clinical photos taken at a 3-month follow-up exami-nation
illustrating the excellent mobility achieved following rightpartial glossectomy and
free radial forearm flap (FRFF) reconstruc-tion.This degree ofmobility is common
and is the primary reason forthe minimal alteration in function following
hemiglossectomy recon-struction with the FRFF.A,Unlimited protrusion ofthe
tongue.B,Excellent lateral motion ofthe tongue is clearly demonstrated.C,Elevation
ofthe tongue tip is unimpaired.ACB
Microvascular Free Tissue Transfer807soft tissue flaps.Netscher and
colleaguesstudied 12 patients who underwent freeradial forearm flap reconstruction
ofthetongue and floor ofmouth.39Sevenpatients received reinnervated flaps and
5received flaps without intentional neuralanastomosis.Improved sensory recoveryin
the patients who received reinnervatedflaps was documented,but no
statisticallysignificant difference in function couldbe found.Santamaria and
colleagues reportedobjectively evaluated sensory recovery inreinnervated flaps to
be near normal whenneural anastomosis was accomplished tothe lingual or inferior
alveolar nerve.36Sensation was found to be poor iftheanastomosis was carried out to
otherrecipient nerves (posterior auricularnerve,cervical plexus,hypoglossal
nerve).The study also found the recovery ofsen-sation to be significantly
diminished inpatients who received postoperative radio-therapy.In summary the
decision to per-form the radial forearm flap as a neurofas-ciocutaneous flap must
be made on acase-by-case basis dependant on the defectcharacteristics and
location,recipient bed,and the ability to accomplish anastomosisto the lingual or
inferior alveolar nerve.Anatomic ConsiderationsBlood SupplyThe arterial blood
supplyofthe radial forearm fasciocutaneous flapis based on perforators ofthe radial
artery.The fascial plexus supplied by these perfo-rators supplies the skin ofnearly
the entireforearm.There are discrete groups oftheseperforators.The most clinically
relevant isthe small number ofperforators at the sitewhere the flexor carpi
radialis and brachio-radialis muscles overlap.One particularlyrelevant implication
ofthis is the ability todevelop multiple skin flap elements basedon a single
vascular pedicle without therequirement ofpreservation ofthe entirefascial
element.42,43The bone element ofthe flap is supplied by branches ofthe radi-al
artery within the lateral intramuscularseptum.Branches that form a
longitudinalplexus within the periosteum pass throughthe insertion ofthis
fascia.44The venous drainage ofthe radialforearm flap occurs through the intercon-
necting superficial (cephalic vein) anddeep (venae comitantes) systems.Thomaand
colleagues published an excellentdescription ofthe variation on the patternofvenous
drainage identified in 40 clinicalcases.22Five distinct patterns weredescribed.The
type I pattern,found 20%ofthe time,exhibits wide communicationofan anastomosing
vein ofthe venaecomitantes and the cephalic vein,whichsplit to separate cephalic
median andbasilic median veins.The type II patternexisted 43% ofthe time and was
similar totype I,with the exception that no divisionofthe fusion ofvessels
occurred.The typeIII pattern,seen 18% ofthe time,displayedan anastomosis ofthe
paired venae comi-tantes that remained separate from thecephalic vein.The type IV
patternoccurred 5% ofthe time and exhibited nofusion ofthe venae comitantes
ofnearequal size.Although pattern V,seen 15%ofthe time,also exhibited no fusion
ofthetwo systems,there was clearly a dominantvenae comitantes.45Thoma and
colleaguesmade a strong recommendation for com-pleting multiple venous
anastomoses.Their view appears to be common in earlyfree flap and replant
experiences.Howev-er,a single venous anastomosis has beenshown to be adequate in
the more recentliterature.Futran and Stack comparedoutcomes and operating time in
43 con-secutive radial forearm flaps.46Two anas-tomoses were performed in 16
patientsand one anastomosis was performed in 23patients.They reported no difference
inflap survival and no flaps were re-exploredfor venous complications.Twenty-one
to36 minutes less surgical time was docu-mented in cases in which a single
venousanastomosis was completed.Surgeon pref-erence and individual patient and
flapcharacteristics determine the most appro-priate vein for anastomosis.Clearly
incases with a superficial venous systemcompromised by trauma or
extensivevenipuncture,the deep system (venaecomitantes) must be used.The
reliabilityofthe deep system has been well docu-mented.47Netscher and colleagues
useddye injection to study the venous drainagesystem.48They found that careful
mappingofthe cephalic vein was necessary toensure its capture within the flap,occa-
sionally necessitating localization oftheflap skin paddle over a portion ofthe dor-
sum ofthe forearm.Venae comitantes ves-sel diameters were found to be less than 2
mm in several specimens.The study alsoconcluded that selection ofthe site forvenous
anastomosis significantly alters thevessel diameter.In order to obtain thegreatest
diameter,the confluence ofthevenae comitantes must be identified.Thismay result in
venous pedicle redundancyand kinking.The superficial venousdrainage system exhibits
a larger diameterthroughout its entire length and is signifi-cantly easier to
elevate,and its separationfrom the arterial pedicle increases optionsfor recipient
vein selection with acceptablevessel geometry.Vascular
AbnormalitiesPreoperativeevaluation ofthe arterial supply to thehand is required
prior to harvest ofthefree radial forearm flap.This is traditional-ly accomplished
by an Allen�s test.Accu-rate performance ofthe test involvesexsanguination ofthe
hand by clenchingand releasing the fist multiple times whileboth the radial and
ulnar arteries are com-pressed.Return ofcolor to the blanchedthenar eminence and
thumb followingrelease ofthe ulnar artery confirms ade-quate communication between
the super-ficial (ulnar) and deep (radial) palmararches.Thus harvest ofthe flap
would notcompromise the blood supply to the hand.A single published report ofacute
ischemiato the hand following radial forearm flap
808Part 6: Maxillofacial Reconstructionharvest despite a �normal�Allen�s test ini-
tiated further investigation into forearmvascular anatomy.49The subjective
natureofthe Allen�s test has led to the use ofadjunctive clinical aids such as
Dopplerand pulse oximetry to ensure adequateperfusion ofthe thumb with radial
arteryocclusion.In their description ofa methodfor preoperative vascular
assessment,Nukols and colleagues reported the use ofan �objective Allen�s test�in a
clinical seriesof65 patients.50Twenty-five patients werethought to have inadequate
flow by sub-jective testing,18 ofwhom were found tohave acceptable flow by
objective testing.The authors concluded that objective test-ing was more reliable
in identifying poten-tial problem donor sites.Color flowduplex assessment of18
patients revealed5 with unilateral or bilateral arteriopathy.This finding impacted
the site selection ofthe radial forearm harvest or resulted inthe use ofalternate
reconstructive modali-ties in those 5 cases.51Interestingly,colorflow duplex
quantifications ofthe flowrates in the upper extremities of11
patientspreoperatively and 4 to 5 months post-operatively revealed overall
increased flowrates (mean 162 mL/min to 215 mL/min).The increased flow resulted
from dramaticincreases in blood flow through the anteri-or and posterior
interosseous arteries.Infact the anterior interosseous artery wasfound to take on a
flow rate (33% ofthetotal) that was nearly equal to that oftheradial artery before
flap harvest (39%).51,52Many authors have published casereports ofvascular
abnormalities oftheradial artery.39,53�57Funk and colleaguespublished a review
ofthe literature onforearm vascular anomalies that includedclinical correlation
based on 52 patients.58The paper described six types ofanom-alies,the most common
ofthese being ahigh origin (proximal to the antecubitalfossa) ofthe radial artery
occurring inapproximately 15% ofall upper extremi-ties.The majority ofradial
arteries in thesepatients originate from the brachial artery,but 10 to 25% were
reported to arisedirectly from the axillary artery.Thisanomaly poses no problem for
safe radialforearm flap harvest.The second mostcommon anomaly reported was a
superfi-cial ulnar artery.The superficial locationofthe ulnar artery places the
vessel at riskin flaps involving the entire volar surfaceofthe forearm.Surgeons are
stronglyencouraged to palpate the entire antecu-bital fossa and volar forearm in
order torule out this anomaly.The abnormal vesselcourse is typically best palpated
overlyingthe flexor carpi muscle.The superficialulnar artery anomaly reported in
2.5% ofupper extremities should prompt the sur-geon to preferentially use other
sites forflap harvest because ofthe risk incurred inselection ofsuch a donor
site.The flap canbe done safely with this anomaly ifthe flapis positioned more to
the radial side oftheventral forearm.Distal takeoffofthe radi-al artery has been
reported once.No riskofvascular insufficiency is incurred withthis anomaly,and
there is no reason tobelieve it could be identified prior to flapelevation.The
other anomalies reportedresult in significant risk ofvascular insuf-ficiency to the
hand in the case ofradialartery flap harvest and should be easilyidentified on the
basis ofabnormal Allen�stests (Figure 40-5).ComplicationsIn general,patients
withhead and neck defects tend to be less thanideal surgical candidates because
ofmedicalcomorbidities.Comorbidities are commonand are related to advanced
age,alcoholabuse,and tobacco abuse.Complicationscan occur at the operative sites
directly orthey may be medically related.Singh andcolleagues analyzed a cohort
of200 consec-utive patients with head and neck defectswho had undergone free tissue
transfer,todetermine factors that influence both surgi-cal site and medical
complication rates.59Successful free tissue transfer was accom-plished in 98%
ofcases.Complicationsoccurred in 56 cases (28%) with 21 (10.5%)patients developing
multiple compli-cations.Using univariate analysis,statisticallysignificant factors
that increased the risk ofcomplication included prior radiation ther-apy,anesthesia
time >10 hours,andadvanced Charlson comorbidity grade.However,after multivariate
analysis onlyadvanced Charlson grade proved signifi-cant.Prior radiation therapy
appeared tohave no significant effect on flap survival,asreported in other
studies,although signifi-cant alteration in technique including veingrafting may be
required.60,61Surgical timehas also been shown to correlate signifi-cantly with
increased rates ofsurgical siteinfection,which is the most common factorin late
vascular compromise offree tissuetransfers through direct effect on the vascu-lar
pedicle.62,63The free radial forearm flap is a veryreliable reconstruction.The
internationalmicrovascular research group published amulti-institutional
prospective study of493 free flaps.64In a subgroup ofthereport,84 free radial
forearm flaps exhibit-ed a thrombosis rate of8.3% and a flapfailure rate
of3.6%,indicating a significantrole for flap monitoring and flap salvagesurgery in
head and neck reconstruction.Monitoring ofthe radial forearm flap isrequired in
order to identify early compro-mise ofthe flap vasculature.Conventionaltechniques
ofmonitoring have been shownto be adequate for this purpose.TheseFIGURE40-5An
abnormal Allen�s test.Notethe clearly delineated vascular territory oftheulnar
artery.
Microvascular Free Tissue Transfer809techniques include visual inspection
forcolor,capillary refill assessment,Dopplerprobe assessment,and needlestick
test.Flapdesign for deep or buried flaps in whichdirect observation is not possible
shouldinclude either a monitor skin paddle thatcan be directly evaluated or an
implantableDoppler probe.20,65An extensive review of750 consecutive microvascular
flapsdemonstrated a re-exploration rate of8.5%and a flap loss rate of2.3%.65The
majorityofthose flaps salvaged were re-explored at< 48 hours due to observed
changes in theparameters monitored.Late re-explorationat > 72 hours was most
commonly theresult ofwound infection causing compro-mise ofthe vascular pedicle by
pressure orthrombosis.Late re-exploration is associat-ed with high rates offlap
loss.Several assessments ofdonor site mor-bidity ofthe radial forearm flap
harvesthave been carried out.66�70Complete orpartial failure ofsplit thickness skin
graftat the donor site is the most commoncomplication encountered.This can leadto
flexor tendon exposure and prolongedhealing.Many methods have been devisedto
decrease the incidence ofthis compli-cation including coverage ofthe defectwith
rotation/advancement flaps,pre-operative tissue expansion and primaryclosure,full-
thickness grafting,suprafas-cial dissection,and the use ofvacuum-assisted wound
care.71�79A devastating complication ofosteo-cutaneous radial forearm flap harvest
ispostoperative radius fracture.Prophylacticplating is strongly recommended
whenbone is included in the flap.80,81Selectionofan alternative donor site seems a
moreprudent alternative provided that one isavailable.Overall,with the exception
ofcases in which a radius fracture occurs,donor site function,though
objectivelyaltered,is subjectively insignificant.62,66,68Flap TechniqueSimultaneous
clinical evaluation ofthetumor defect site by both the ablative andreconstructive
surgeons is particularlyuseful in design ofthe radial forearm flapand allows
planning for the most appro-priate vessel geometry.Careful examina-tion ofthe
proposed donor site is requiredto verify the patency ofthe superficialvenous system
and to document the arter-ial anatomy ofthe hand.An Allen�s test ismandatory and
should be supplementedwith Doppler or pulse oximetry wheneverthe examination is
inconclusive.Palpationofthe entire forearm to determine the vas-cular anatomy
should be done without atourniquet (arterial assessment) and withthe use ofa
venipuncture tourniquet anddependant positioning ofthe upperextremity (venous
anatomy).Preliminary planning is supplementedby the intraoperative examination
ofboththe resection specimen and the defect site.Occasionally modifications are
requireddue to extension ofthe planned resectionto achieve tumor margins or due to
vascu-lar insufficiency identified in access flapsfollowing a lip
split�mandibulotomy pro-cedure.Accurate determinations ofthepedicle length required
allow further tai-loring ofthe flap harvest to the specifics ofthe defect site.This
facilitates flap harvestbecause the surgeon need not dissect theentire available
vascular pedicle length.This also facilitates the anastomosis proce-dure because
the surgeon can skeletonizethe region ofthe pedicle at which the anas-tomosis will
be completed during a non-ischemic period.The donor site is prepared for surgeryby
removing hair in the surgical field withclippers.The radial artery is outlinedalong
its length with a surgical marker.Avenipuncture tourniquet is applied to dis-tend
the veins and the superficial venoussystem is outlined with a surgical marker.A
preliminary outline ofthe flap is thenmarked on the wrist that will be
refinedfollowing the completion ofthe resectionand identification ofthe most
appropriaterecipient vessels.For most cases a fascio-subcutaneous segment ofthe
flap proxi-mal to the skin paddle can be included tooptimize the blood
supply,resist vesselkinking,and protect the vascular pedicle.The surgical site is
prepared with achlorhexidine surgical scrub and isolatedusing extremity drapes.A
standard arm-board is sufficient for support oftheextremity throughout surgery.Care
istaken to ensure absolute isolation ofthearm from the head and neck field.Cross-
contamination has been implicated incausing suppurative tenosynovitis result-ing in
a frozen hand.82Upon completion ofthe resection orrefining ofthe defect site,the
neck is care-fully explored to identify likely recipientvessels.The selected
vessels should bechecked for patency,presence ofathero-sclerosis,and intimal
injury.Loupe mag-nification facilitates this process.Althoughany suitable vessel
can be used as a recipi-ent vessel,the facial artery and commonfacial vein are most
commonly selected asrecipient vessels in intraoral reconstruc-tion.Because these
vessels lie central in thelateral neck,less alteration ofthe flap ves-sel geometry
occurs on extreme headmovement when these vessels are used.The reader is reminded
ofthe transversecervical artery (a branch ofthe thyrocervi-cal trunk) because ofits
similar diameterto the radial artery.Because ofthe positionofthe transverse
cervical artery low in theneck,it is commonly available and in goodcondition
following prior selective neckdissection or radiotherapy.Although theavailable
pedicle length allows for use ofneck vessels,when performing an upperfacial
reconstruction the superficial tem-poral artery and vein or the facial arteryand
vein are often used.Daily aspirin therapy to decreaseplatelet aggregation is
initiated on theevening ofsurgery and continued for 6 weeks.Flap harvest is
accomplished fol-lowing exsanguination ofthe upper extrem-ity and inflation ofa
tourniquet to 250 mmHg.Tourniquet control facilitates the flapharvest by maximizing
visualization.This
810Part 6: Maxillofacial Reconstructioncreates an excellent environment forteaching
the microvascular flap harvesttechnique.Enough cannot be said aboutthe crucial role
that gentle tissue/vesselhandling plays in the ultimate viability ofthe
microvascular transfer.The distal flapis elevated first,requiring ligation
ofthedistal radial artery and cephalic vein.Asubfascial plane ofdissection allows
cap-ture ofall available communicationsbetween the elements ofthe vascular sup-ply
ofthe flap without significantlyincreased morbidity (Figure 40-6).The superficial
radial nerve is resectedto avoid violation ofthe fascial compart-ment.This can be
used as a free nerve graftof4 to 6 cm length ifneeded.The sensorydefect is limited
to the dorsal portion ofthe thumb and index finger.We havefound that skin graft
placement over a pre-served dorsal radial nerve provides insuffi-cient
protection.Severe pain can resultfrom stimulation ofthe nerve by a sleeveor
wristwatch.Continued dissection around the cir-cumference ofthe designed flap is
accom-plished deep to fascia laterally and deep tothe dermis proximally.Skin flaps
are thenelevated proximally coincident with thevolume ofthe planned
fasciosubcutaneouselement ofthe flap.Proximal to this thecephalic vein and
antebrachial cutaneousnerve are isolated.Proximal dissection ofthe arterial
vascular pedicle requires theseparation ofthe fascia joining the flexorcarpi
radialis and brachioradialis musclesand the lateral retraction ofthese
muscles(Figure 40-7).The venae comitantes are dissectedfrom the radial artery for a
few centime-ters either side ofthe planned arterialanastomosis and are
preserved.Where oneofthe venae comitantes is clearly domi-nant,only this vessel is
preserved.Numer-ous interconnections exist between thesetwo vessels and careful
dissection isrequired to achieve their separation.Withthe vascularity assured the
flap is then ele-vated distal to proximal.This requiresidentification and ligation
ofdeep branch-es ofthe radial artery.We prefer to use tita-nium vessel clips to
accomplish this.Thesefacilitate rapid flap harvest and are excel-lent markers ofthe
pedicle position in theevent that the neck must be explored at alater date.After
completion ofthe flapharvest,the tourniquet is released.Carefulexamination ofthe
flap during this reper-fusion interval should be accomplished toensure absolute
hemostasis because accessfollowing inset and reanastomosis will belimited.The
surgeon should examine thehand for adequate perfusion.Tourniquettime less than 45
minutes is the norm fol-lowing familiarity with the flap harvest.This can be
significantly less withincreased surgical experience.The vascular pedicle is then
transectedfollowing a suitable period ofreperfusion(30 minutes on average).The flap
vesselsshould be occluded with appropriatelysized microvascular clamps during
comple-tion ofthe inset.The flap is then transferredRadial arteryRadial arteryVenae
comitantesVenae comitantesCephalic veinMedial antebrachialcutaneous nerveFlexor
carpi radialis muscleBrachioradialis muscleCephalic veinFIGURE40-6Cross-sectional
anatomy ofthe radial forearm free flap donor site.The harvested flapdemonstrates
subfascial dissection ofthe flexor compartment.Adapted from Urken ML.99Radial
arteryUlnar arteryFloor of mouthLateral tongueCephalic veinFlexor carpiradialis
muscleBrachioradialismuscle retractedFIGURE40-7The harvest ofthe flap.Note the
retraction ofthe brachioradialis muscle required to dis-sect the radial artery.
Microvascular Free Tissue Transfer811to the defect site.Care must be taken toavoid
rotation or kinking ofthe flap vessels,particularly when the flap must be
passedthrough a tunnel to the defect site.Insettingshould be accomplished
completely priorto microvascular anastomosis to allowaccurate determination ofthe
vascularpedicle geometry.Meticulous closure withgentle eversion to achieve a
watertight sealis necessary because ofthe deleteriouseffects ofsaliva on the flap
vessels.Care istaken to achieve a flap vessel�recipient ves-sel geometry that
contains only slightcurves to prevent vessel kinking.We preferend-to-end
interrupted sutured anasto-moses with the vessels secured in Aclandframe clamps.The
artery is approximatedfirst because the recipient artery is general-ly deeper than
the venous structures.Heparinized saline (500 U/100 cc NS) isused to irrigate
during the anastomosis.Papavarine is occasionally used ifarterialspasm is noted.It
should be recognized thatgentle handling is the best defense againstspasm.Following
the release ofthe approx-imator clamps,the flap should be
carefullyevaluated.Evaluation ofcolor and capillaryrefill is generally adequate for
flap monitor-ing.In situations wherein this is difficult orthe status ofthe flap is
unclear,pricking theflap with a 25-gauge needle confirms flapperfusion.Color and
character ofthe bleed-ing are important.A venous-compromisedflap will bleed dark
blood that does not clotas well as serous fluid.Closed-suction drains are used in
theneck with care taken to prevent them beingdisplaced onto the vascular
pedicle.Theproximal skin flaps at the donor site areapproximated over a closed-
suction drain.The distal skin elements are sutured to themuscle to fixate them.A
split-thicknessskin graft is placed overthe donor sitedefect and secured.A
compressive dress-ing and volar splint or vacuum-assistedclosure dressing are
applied.Theseremain in place for 5 days.Active andpassive range-of-motion exercises
are ini-tiated at 2 weeks post flap harvest.The free radial forearm fasciocuta-
neous flap is extremely useful in head andneck reconstruction.The flap�s
reliability,adaptability,ease ofharvest,and the simi-lar character ofthe thin
pliable skin to thelining tissues ofthe oral cavity make itsuse commonplace in
modern maxillofacialreconstruction.Free Fibula FlapAnatomic ConsiderationsThe
fibula is ideal for large bony defectssince it offers up to 25 cm
ofvascularizedcortical bone.Ifwe view the fibula in across section,we can identify
a triangularshape established by three borders.Theanterior border is the area
ofattachment ofthe anterior intermuscular septum,and theinterosseous or medial
border is the pointofattachment ofthe interosseous mem-brane that binds the fibula
to the tibia.Theposterior intermuscular septum attaches tothe posterior border
(Figure 40-8).In the proximal aspect the fibula artic-ulates with the tibia and the
knee joint,whereas in the distal aspect it articulateswith the tibia and the
talus.Above the knee the popliteal arterydivides into the anterior and posterior
tib-ial arteries.Distal to the knee the posteriortibial artery has a collateral
branch,theperoneal artery.The blood supply to thefibula is delivered through
perforatorsoriginating in the peroneal artery which isusually between 2 and 4 mm in
diameter.The venae comitantes provide the venousdrainage;these are paired vessels
that runalong the artery (Figure 40-9).A significant limitation ofthe freefibula
flap is the common presence ofperipheral vascular disease in the
lowerextremities.In population-based studiesthat evaluated the incidence ofarterial
dis-ease in the lower extremity in patientsolder than 55 years,the parameter was
anankle-brachial index lower than 0.9.83Thevalue was obtained by dividing the
systolicblood pressure measured at the ankle bythat obtained at the brachial
artery.ADanish study that included 700 individu-als aged 60 years showed a
prevalence oflower extremity arterial disease of16% inmen and 13% in women.84A
similar studyfrom Edinburgh showed an overall inci-dence of17%.83Unfortunately the
same risk factors(age and tobacco) are a common denomi-nator for head and neck
cancer patients aswell as patients with peripheral vasculardisease;therefore,it is
indicated to per-form either a conventional angiography orInterosseous membraneDeep
peroneal nerve andanterior tibial artery and vein Extensor digitorum longus
muscleExtensor hallucis longus muscleSuperficial peroneal nerve and accessory
arteryAnterior intermuscular septumPeroneus brevis musclePeroneus longus
muscleFibulaPosterior intermuscularseptumFlexor hallucis longus muscleTransverse
intermuscular septum Peroneal artery and veinSoleus musclePosterior tibial artery
and vein and tibial nerve Crural fasciaGastrocnemius muscleFlexor digitorum longus
muscle TibiaTibialis posterior muscleTibialis anterior muscleFIGURE40-8Cross-
sectional view ofthe tibia and fibula with the surrounding anatomic
structures.Adapt-ed from Serafin D.93
812Part 6: Maxillofacial Reconstructiona magnetic resonance angiography toestablish
the safety ofharvesting the flap.In a recent retrospective study Smithand
colleagues reviewed 17 potential freefibula flap candidates (34 legs) evaluatedby
both a color flow Doppler (CDF) andangiography.Sixteen legs were normal byboth
studies,18 legs showed abnormalCFD study results,and the angiogramrevealed anatomy
that was considered torepresent a high risk for fibula flap har-vest in 16 legs and
considered safe in theother 2 legs.85The free fibula flap can be raised withor
without a skin paddle.The skin paddlehad a poor prognosis,based on the origi-nal
series by Hidalgo who harvested theattached skin based on
septocutaneousperforators.5Schusterman and colleagueslater performed an anatomic
study thatshowed more soleus musculocutaneousperforators than septal
perforators.86Fur-thermore the clinical success ofthe skinpaddle is above 90% when
the musculo-cutaneous perforators are incorporatedin the flap,whereas the viability
oftheskin is only 33% when the flap is based onseptal branches.Neurosensory
potential to the skin pad-dle was described by Hayden and colleaguesby
incorporating the lateral cutaneous nerveofthe calf(LCNC) and/or the sural com-
municating nerve (SCN) in order to restoreintraoral sensation by anastomosis
ofthelingual nerve to the LCNC and/or the infe-rior alveolar nerve to the
SCN.87,88Flap Technique The patient is placed in the supine posi-tion,the hip and
the knee are slightlyflexed,and a pneumatic tourniquet isplaced in the proximal
aspect ofthe leg.Aline is drawn from the lateral malleolus tothe fibular head.Ifa
skin paddle is includ-ed,it should be centered more posteriorlythan the axis ofthe
fibula in order toinclude both the septocutaneous and themusculocutaneous
perforators.The dissection is carried down to thecrural fascia that is incised.The
dissectioncontinues through the anterior border ofthe peroneal muscles while
maintaining acuffof2 to 3 mm ofmuscle surroundingthe bone.The extensor digitorum
longusand the extensor hallucis longus are elevat-ed anteriorly,exposing the
interosseousseptum that connects between the fibulaand the tibia.The peroneal
vessels and theanterior tibial vessels are located posteriorto the interosseous
septum;therefore,care-ful dissection with fine dissecting scissorsshould be
performed in order to avoiddamage to the vascular structures or to thedeep peroneal
nerve.At this stage,two hor-izontal incisions are performed in the prox-imal and
distal aspects ofthe fibula wherethe osteotomy is being planned.The bonycuts are
performed with a Gigli,a recipro-cating,or an oscillating saw while the medi-al
aspect is protected with a malleableretractor.The peroneal vessels are ligated
intheir distal aspect and the vascular pedicleis carefully dissected superiorly
until thebranching ofthe peroneal artery from theposterior tibial is identified.The
flexor hal-lucis longus muscle and part ofthe soleusmuscle are included in the
flap,especially ifa skin paddle is planned (Figure 40-10).It is recommended to
perform theosteotomies to shape the fibula while pedi-cled to the proximal vessels
in order tominimize the ischemia time as well aspreparation ofthe vessels in the
recipientsite before ligation ofthe proximal aspectofthe peroneal artery.The skin
defect in the leg can be closedprimarily or through the addition ofasplit-thickness
skin graft.An example ofthe application ofthistechnique is as follows:A patient
presented with a large massin the anterior aspect ofthe mandible withan obvious
clinical deformity due to sig-nificant buccal expansion ofthe buccalcortical
bone,with a progressive growthduring the 3 years previous to his clinicalevaluation
(Figure 40-11).Panoramicradiography showed a multilocular lesionextending from
tooth no.21 to tooth no.31 (Figure 40-12).A histopathologic diagnosis
ofameloblastoma was obtained through anincisional biopsy ofthe lesion.A
magneticresonance angiogram was obtained whichshowed a normal vascular pattern in
bothlower extremities.A segmental resectionofthe lesion was performed along withthe
mental and inferior alveolar nerves(Figure 40-13).The defect was immediately recon-
structed with a free fibula flap without theneed for a skin paddle since residual
mucosawas available for primary closure.Twoosteotomies were performed in the fibula
toallow for appropriate contour,resulting inthree bony segments that were fixated
to therecipient mandible by means ofa recon-struction plate (Figure 40-14).A
postopera-tive panoramic radiograph was obtainedRear view of
kneePoplitealarteryAnterior tibialarteryPeronealarteryNutrient branchPosterior
tibialarteryFIGURE40-9Vascular anatomy ofthe fibula,viewfrom a posterior view ofthe
leg.Adapted fromO�Leary MJ et al.88
Microvascular Free Tissue Transfer813which showed good continuity ofthe
bonysegments (Figure 40-15).In a previous ret-rospective study it was reported that
radi-ographic bony healing was achieved in 93%ofosteotomy sites offree fibula
flaps.89The amount ofbone available in freeflaps in order to place
osseointegratedimplants has been investigated in ananatomic study in 28 cadavers
evaluatingthe most commonly employed donorsites.90Implantability was
establishedbased on measurements ofheight,width,and cross-sectional area.The
resultsshowed that the iliac crest was the mostimplantable donor site
(83%),followed bythe scapula (78%),the fibula (67%),andthe radius (21%).90A
retrospective analysis ofpatientstreated with a free fibular flap formandibular
reconstruction was per-formed by Disa and colleagues evaluat-ing the long-term bone
mass ofthe fibu-la.89Only patients with at least 24 months offollow-up were
included inthe study.The comparative measure-ments offibular height revealed that
cen-tral segments underwent a meandecrease in height by 4%,body segmentsdecreased
by 7%,and ramus segmentsdecreased by 5%.The findings were notaffected by the site
ofreconstruction,patient age,length offollow-up,adjuvantradiation therapy,or
placement ofosseointegrated implants.Morbidity following Free FibulaFlapsA
retrospective analysis ofdonor site mor-bidity was performed by Shindo and col-
leagues on 53 consecutive patients whounderwent fibula osteocutaneous free tis-sue
transfer.91Donor site wound complica-tions occurred in 15 patients,4 ofwhom(8%) had
extensive wound breakdown,Deep peronealnervePeroneal arteryand veinExtensor
digitorumlongus muscleInterosseousmembrane (cut)Distal peronealartery and
veinPeroneus longusmuscleTibialisanterior muscleTibialisposterior muscleExtensor
hallucislongus muscleSoleus and flexorhallucis longusmusclesFIGURE40-10Elevation
ofthe free fibula flap after the osteotomy ofthe distal and proximal attach-
ments.The ligation ofthe feeding vessels is obvious in the distal aspect ofthe
flap,while the proximalblood supply is maintained until the osteotomies are
performed.Adapted from Serafin D.93FIGURE40-11Clinical aspect ofa patient
withbuccal expansion ofthe mandible due to a largeameloblastoma.FIGURE40-
12Radiographic view ofthe patientin Figure 40-11 with a large ameloblastoma ofthe
mandible.FIGURE40-13Mandibular specimen after sur-gical resection ofthe
ameloblastoma.
814Part 6: Maxillofacial Reconstructionmuscle necrosis,and/or exposure
oftendonand/or bone,whereas the other 11 patients(21%) had only minor wound
complica-tions limited to superficial skin slough.Shindo and colleagues
recommendedavoiding skin closure under tension since thegroup with the higher
complication rate hadprimary closure ofthe donor site.91Otherreported complications
have included weak-ness ofgreat toe dorsiflexion,reduced springaction ofthe donor
leg,ankle stiffness,andin a few cases,ankle instability.Despite thementioned
deficits,all patients were able toresume daily and recreational activities.92Iliac
Crest Osteomyocutaneous Free FlapAnatomic ConsiderationsThe blood supply to the
osteomyocuta-neous iliac crest flap is based on the deepcircumflex iliac artery
(DCIA) and vein.The DCIA takes origin from the externaliliac artery or femoral
artery in the regionofthe inguinal canal (42% below theinguinal ligament from the
femoralartery,41% behind the inguinal ligamentfrom the external iliac artery,and
17%above the inguinal ligament from theexternal iliac artery).93The artery courses
a distance ofabout5 to 7 cm between its origin and the ante-rior superior iliac
spine,following thereonthe inner aspect ofthe iliac crest.TheDCIA provides an
ascending branch thatperforates through the transversus abdo-minis muscle giving
blood supply to thetransversus as well as the internal andexternal oblique muscles
(Figure 40-16).Through its pathway the artery pro-vides multiple perforators to the
bone,muscle,and overlying skin.The deep cir-cumflex iliac vein follows the
arterialcourse.The lateral femoral cutaneous nervecrosses the DCIA near the
anterior supe-rior iliac spine.The nerve should be dis-sected,retracted,and
protected duringthe harvesting ofthe vascular pedicle andthe flap.Flap TechniqueThe
skin paddle is designed by drawing aline from the femoral artery to the
inferiorangle ofthe scapula.The skin paddle isthen designed with an axis on the
above-mentioned line and centered on the iliaccrest,including the myocutaneous
perfo-rators which enter the skin along the inneraspect ofthe crest.The external
oblique muscle (with theattached overlying skin) is incised,leaving acuffofabout 3
cm ofmuscle attached to theinner aspect ofthe iliac crest.Ifa significantportion
ofthe internal oblique muscle hasto be harvested in order to cover soft
tissuedefects in the oropharyngeal region,thenthe muscle is divided in a horizontal
fash-ion below the costal margin,and the dissec-tion is initiated in the
superior,medial,andlateral aspects while incorporating theascending branch ofthe
DCIA.After iden-tifying the ascending branch ofthe DCIA inthe inner aspect ofthe
internal obliquemuscle,the deep circumflex iliac vessels aredissected
proximally.The transversus abdo-minis muscle is incised parallel to the
crest,leaving a cuffofabout 3 cm attached to theinner aspect ofthe crest.The
peritoneum is then retractedmedially and the iliacus muscle is identi-fied.The
transversalis fascia fuses with theiliacus fascia,and the deep circumflex ves-sels
consistently travel lateral to this fascialfusion.A 1 to 2 cm incision is
performedmedial to the insertion ofthe iliacus fasciadown to the
periosteum.FIGURE40-14Reconstruction ofthe surgicaldefect with a free fibula
flap.The structureslocated superior to the reconstruction plate arethe spared
inferior alveolar and mental nerves.The vascular structures below the screws and
thereconstruction plate at the level ofthe angle ofthe mandible are the peroneal
vessels aftermicroanastomosis to the facial vessels.FIGURE40-15Radiographic view
ofthe recon-structed mandible with a free fibula flap.Iliacus muscleExternal
oblique muscleAscendingbranchof deepcircumflexiliac arteryAnteriorsuperioriliac
spineDeepcircumflexiliac arteryExternal iliac arteryInguinal ligamentFIGURE40-
16Anatomy ofthe deep circumflexiliac artery (DCIA).Adapted from Strauch
B,YuHL,editors.Atlas of microvascular surgery. NewYork: Thieme Medical Publisher
Inc.; 1993.p.142�58.
Microvascular Free Tissue Transfer815The lateral or lower aspect ofthe skinpaddle
is incised,proceeding through thedeep fascia ofthe thigh and the
gluteusmuscle,detaching them from the perios-teum ofthe lateral aspect ofthe iliac
crestuntil achieving the desired bone depth(Figure 40-17).When both the medial and
lateral cor-tices are exposed,the osteotomy is per-formed.Ifadditional osteotomies
are neces-sary in order to contour the bone,it is rec-ommended to proceed while the
tissue isstill pedicled to the feeding deep circum-flex vessels.After the flap is
harvested the musclesare approximated in layers to prevent thepotential
complication ofherniation ofthe abdominal contents.The transversalisfascia and
transverse abdominis muscleare sutured to the iliacus fascia and the ili-acus
muscle.The fascia lata and the glu-teus are sutured to the external
obliquemuscle.The inguinal ligament should bereattached ifit had been divided.In
most cases the inner aspect oftheiliac crest is sufficient to reconstruct
amandibular defect,having the advantagesofa less deforming defect and avoiding
thelateral dissection ofthe gluteus mediusmuscles (Figure 40-18).Morbidity
following Iliac Crest Free FlapsRogers and colleagues analyzed the associ-ated
morbidity and the quality oflife ofpatients who had undergone harvesting ofeither a
deep circumflex iliac or a fibulafree flap.94They used the University ofWashington
Quality ofLife questionnaire,which showed no statistical differencesbetween the
patients in their activity,anx-iety,mood,pain,recreation,or shoulderfunction.Rogers
reported that the patientsreconstructed with free fibula flaps hadlower scores for
swallowing and taste.Onthe other hand,for maxillectomy defects,they preferred the
deep circumflex iliacflap over the fibula free flap,the latterbeing almost
exclusively used formandibular continuity defects.Theknown incidence ofinguinal
hernia wasabout 10% for patients who underwentfree iliac flap harvesting.Overall
the conclusion is that bothflaps are viable options for complex recon-structive
needs in the head and neckregions requiring bone and soft tissue cov-erage.Donor
site morbidity should be pre-sented to the patient with emphasis on thepotential
impact on their quality oflife.DiscussionThe iliac crest provides a significant
seg-ment ofbone that may reach 4 cm inheight and 11 cm in length.The dimen-sions
ofthe flap may allow for a recon-struction ofa hemimandibulectomy oranterior
mandibular defect.There are two significant advantages tothe iliac crest/internal
oblique free flap:(1) the amount ofbone available forpotential reconstruction with
osseointe-grated implants;and (2) the availability ofa thin and broad muscle that
can be left toheal by secondary epithelization intraoral-ly.Brown and colleagues
developed theconcept ofreconstruction ofthe maxillaryalveolus with the iliac crest
while the palatewas reconstructed with the muscle.95,96The disadvantage ofthe flap
is the rel-atively short vascular pedicle and thepotential for herniation ofthe
abdominalcontents.Versatility ofFree Tissue TransferThe flaps described in the
current chapterare the most commonly used in head andneck reconstruction.The
ability to trans-fer vascularized tissues allows for a signifi-cant variety
ofoptions.The rectus abdominis free flap hasbeen used mostly for base ofskull
recon-struction and tongue reconstruction.It isbased on two vascular pedicles:the
deepsuperior epigastric vessels,which are acontinuation ofthe mammary
vessels;andFIGURE40-17Harvesting ofa full-thicknessiliac crest bone flap.Adapted
from Strauch B,Yu HL,editors.Atlas of microvascular surgery.New York: Thieme
Medical Publisher Inc.;1993. p. 142�58.FIGURE40-18Harvesting ofa split-thickness
iliaccrest bone flap.Adapted from Strauch B,Yu HL,editors.Atlas of microvascular
surgery. New York:Thieme Medical Publisher Inc.; 1993. p. 142�58.
816Part 6: Maxillofacial Reconstructionthe deep inferior epigastric
vessels,whichare branches ofthe external iliac artery.The deep inferior epigastric
vessels have alarger diameter and a longer vascular pedi-cle which makes them the
preferred choicefor anastomosis to the recipient vesselswith very high reliability
and success.97The free scapular flap has been usedfor mandibular and maxillary
reconstruc-tions.The flap can be elevated togetherwith the latissimus dorsi
muscle,adding alarge amount ofsoft tissue to large andcomplex defects ofthe
maxillofacialregion.The vascular supply to the scapularbone is provided by the
scapular vessels,whereas the blood supply to the latissimusdorsi muscle is provided
by the thora-codorsal vessels.Urken and colleagues have describedthis combination
offlaps as the subscapu-lar system and specified some ofits uniquefeatures98:�Long
length and large caliber ofthevascular pedicle�Abundant surface area ofthin
skinthat can be transferred�Separation between the soft tissue andbony flaps which
provides freedom forthree-dimensional insetting�The potential to combine the latis-
simus dorsi and the serratus anteriormuscles with overlying skin and adja-cent
segments ofribOther flaps have been used fororopharyngeal
reconstruction,includingfree omentum for oral lining,gracilis mus-cle free flaps
with the anterior obturatornerve for facial reanimation,and lateralthigh or lateral
arm free flaps for pharyn-geal reconstruction.Even free tem-poroparietal fascial
flaps have been usedbased on the superficial temporal vesselsfor intraoral lining
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reconstruction.New York (NY):Raven Press;1995.p.152.
CHAPTER 41MicroneurosurgeryMichael Miloro,DMD,MDInjuries to the terminal branches
ofthetrigeminal nerve may occur commonlyfollowing a variety ofroutine oral
andmaxillofacial surgical procedures,and theoverwhelming majority ofthese
injuriesundergo spontaneous recovery withouttreatment.Third molar surgery is
respon-sible for most ofthe injuries to both theinferior alveolar and lingual
nerves.Thereported incidence ofnerve injury variesin the literature,but generally
both tem-porary and permanent paresthesia mustbe considered.Nerve injury may occur
fol-lowing mandibular and maxillary orthog-nathic surgery,maxillofacial trauma,den-
tal implant placement,endodontictherapy,facial fractures,and treatment
ofpathology.The anatomy ofthe trigeminalnerve system is unique since it
carries,insome branches,both general sensoryinformation and special (eg,taste)
sensa-tion.Injury to a nerve may result in neu-roma formation,which can manifest in
avariety ofclinical signs and symptoms.Nerve injuries are classified by two popu-
lar classification schemes,which are basedon the likelihood ofan injured
nerverecovering spontaneously.A basic under-standing ofnerve terminology
(Appendix)and normal neural wound healing isessential to most appropriately
manageclinical situations.The initial evaluation ofpatients withnerve injuries must
proceed in an orderlyfashion,with several levels oftesting todetermine most
accurately the degree ofindividual nerve injury.A standardizedclinical neurosensory
test (CNT) may beemployed for most patients;however,someadvanced testing is
available for special cir-cumstances.A variety ofnonsurgical andpharmacologic
treatments are available forthe patient with nerve injury.For mostpatients with
dysesthesia,pharmacologictherapy is the mainstay oftreatment.Once the decision is
made to proceedwith microneurosurgery,a sequence ofsur-gical steps must be followed
meticulously.Specific surgical techniques depend onwhich specific nerve is
involved,as well asthe extent ofthe injury.In general,microneurosurgical repair ofa
trigeminalnerve injury involves neurolysis and prepa-ration ofthe nerve stumps to
perform neu-rorrhaphy.The deleterious effects often-sion on a nerve repair site
have been welldocumented,so the inability to perform aprimary tension-free repair
warrants con-sideration for an autogenous nerve graft oranother option for nerve
gap managementsuch as conduit repair.Following micro-neurosurgery,postoperative
sensory re-education may play a role in the regenera-tive process.The overall
success rates ofmicroneurosurgical repair ofthe trigeminalnerve vary
considerably;however,animportant factor in determining success isthe length oftime
from injury to repairsince this impacts on the degree ofganglioncell
death,wallerian degeneration,and cor-tical somatosensory reorganization.TheAmerican
Association ofOral and Maxillo-facial Surgeons Clinical Interest Group
onMaxillofacial Neurologic Disorders haspromulgated certain treatment time rec-
ommendations for the patient who sustainsa trigeminal nerve injury.1The field
ofmicroneurosurgery is inits infancy.As more surgeons becomefamiliar with the
diagnosis and manage-ment ofpatients with trigeminal nerveinjuries,more
laboratory,radiologic,andclinical information will become availableto guide
therapy.Also,residency programswill become more capable oftraining resi-dents in
the principles and practice ofmicroneurosurgery and will thus fosteraccess to this
aspect ofspecialty carethroughout the country and abroad.DemographicsTrigeminal
nerve injuries result from avariety ofroutine oral and maxillofacialsurgical
procedures,such as third molarodontectomy,management offacial trau-ma,orthognathic
surgery,endosseous den-tal implant placement,salivary duct andgland
surgery,treatment ofbenign andmalignant lesions ofthe head and neck,preprosthetic
surgery,and endodontic andperiradicular surgery.Complications ofthird molar removal
are responsible for themajority ofnerve injuries.2These can occurduring any phase
ofthird molar surgery,including local anesthetic injection,incision
820Part 6: Maxillofacial Reconstructionand flap design,the use ofa high-speeddrill
for bone removal or tooth sectioning,elevation ofthe tooth with trauma to
thelingual soft tissues,socket curettage withexposed neurovascular tissue,removal
ofremnants ofan assumed �dental follicle�that may contain neural or vascular
tissue,the use ofmedicaments in the extractionsite to aid healing or prevent
alveolar osteitis(eg,tetracycline-containing compounds3,4),and the placement
ofsutures.The effica-cy oflingual nerve retraction duringlower third molar surgery
has shownthat although the incidence oftempo-rary lingual nerve paresthesia
isincreased owing to a slight stretching ormanipulation (6.4% with retraction
vs0.6% without retraction),the differencein long-term dysfunction is not signifi-
cant (0.6% with retraction vs 0.2% with-out retraction).5Other studies
haveindicated a temporary paresthesia rate ofapproximately 10 to 15% with
lingualnerve retraction and protection,with apermanent rate of< 1%.The incidence
oftrigeminal nerveinjury may be estimated based on a reviewofthe available
literature.Overall the inci-dence ofinferior alveolar nerve (IAN)injury from third
molar surgery is 0.41 to7.5% and from sagittal split osteotomy is0.025 to
84.6%,whereas the lingual nerveis affected 0.06 to 11.5% ofthe time fol-lowing
third molar removal.However,themore important clinical distinction is
todifferentiate temporary from permanentparesthesia rates.For sagittal
splitosteotomies,temporary inferior alveolarparesthesia may be as high as 80 to
100%,but permanent rates are < 1 to 5%.Forthird molar surgery,both inferior
alveolarand lingual nerve temporary paresthesiasrange from 2 to 6% each,whereas
perma-nent rates are approximately 25% ofthetemporary rates,or 0.5 to 2%
overall.Many risk factors for nerve injury duringthird molar surgery have been
reportedand include advanced patient age,femalesex (recent animal studies indicate
thatgender may play a role in spontaneousneurosensory recovery following
injury),depth ofimpaction,mesiodistal angula-tion ofthe tooth
(distoangular),lingualangulation ofthe tooth,integrity ofthelingual cortex,the need
for tooth section-ing,removal ofbone distal to the thirdmolar,and surgeon
experience.Certainlythe risk ofan IAN injury may be influ-enced by so-called Rood
radiographic pre-dictors ofpotential tooth proximity to theinferior alveolar
canal.6These seven radi-ographic predictors on panoramic radi-ograph may indicate
the potential forincreased risk ofinjury to the IAN,andthey are listed in Table 41-
1.In cases witha high index ofsuspicion ofnerve injury(eg,deep impaction,advanced
age),inten-tional coronectomy with close observationshould be considered.7As
opposed to therelatively consistent course ofthe IAN,thelingual nerve position is
variable;and it isinjured less often than the IAN followingthird molar
surgery.8�12The position ofthe lingual nerve has been documentedclinically,13in
cadaveric dissections,14,15and radiologically.16On average,in thethird molar
region,the lingual nerve lies2.5 mm medial to the lingual plate ofthemandible and
2.5 mm inferior to the lin-gual crest.The lingual nerve may be indirect contact
with the lingual plate in25% ofcases (Kisselbach and Chamber-lain reported 62%13)
and may lie above thelingual crest in 10 to 15% ofcases (Kissel-bach and
Chamberlain reported 17.6%13)based on an undisturbed radiographicassessment ofthe
nerve.Mandibular blocks may result in infe-rior alveolar and lingual nerve
injuries;however,the incidence is unknown owingto unreported cases.An estimated 1
in100,000 to 1 in 500,000 blocks result inparesthesia.Perhaps the largest study
ofitskind,Harn and Durham�s study of9,587mandibular blocks showed a 3.62% inci-
dence oftemporary paresthesia and a1.8% incidence oflong-term paresthesialasting >
1 year.17Several theories havebeen proposed to explain the mechanismofinjury.Direct
neural trauma is unlikelyowing to abundant interfascicular neuralcomponents
resulting in separation ofthefascicles by a needle or suture withoutdirect neural
disruption.18The resultantedema may be responsible for the tran-sient paresthesia
that resolves sponta-neously.Local anesthetic toxicity may beresponsible for
prolonged paresthesia fol-lowing a mandibular block,especially ifthe solution is
deposited within the con-fines ofthe epineurium.Recent reportsindicate that
prilocaine and articaine maybe associated with an increased risk oflong-term
paresthesia compared withother local anesthetic solutions,but fur-ther
investigation is warranted.19�21Thethird potential mechanism ofinjuryinvolves the
formation ofan epineurialhematoma.The epineurium and per-ineurium contain a vast
plexus ofvesselsthat nurture the neural elements,and aneedle may cause disruption
ofone ormore vessels.The localized bleeding mostcertainly tamponades itselfowing to
thesurrounding epineurium,and the pressuremay impinge on select groups
offasciclescontained within the nerve.The resultantclinical signs and symptoms
oflocalizedparesthesia,not involving the entire distri-bution ofthe inferior
alveolar/ mentalnerve,nicely match the expected histolog-ic situation,making this
theory plausible.Also,lymphatic drainage ofthe localizedhematoma over the few days
to weeks Table 41-1Rood�s Radiographic Predictors ofPotential Tooth Proximityto the
Inferior Alveolar Canal1.Darkening ofthe root2.Deflection ofthe root3.Narrowing
ofthe root4.Dark and bifid root apex5.Interruption ofthe white line ofthe
canal6.Diversion ofthe canal7.Narrowing ofthe canalAdapted from Rood JP and Shehab
AAN.6
Microneurosurgery821following surgery coincides with the clini-cal resolution
ofsymptoms in most cases.The final theory is that ofthe needle-barbmechanism
ofinjury.22During a mandibu-lar block injection,the needle may beadvanced to the
medial ramus where asmall barb may form at the needle tip.Onwithdrawal,ifthe needle
has passedthrough or in the vicinity ofthe lingualnerve or IAN,fascicular
disruption mayoccur with potentially long-standing clini-cal consequences.Recent
trends in ourclinical understanding ofinjection-relatednerve injuries are the
following:�These injuries are difficult to predictand prevent�The classic electric-
shock sensation isreported uncommonly by patientswho sustain these
injuries�Injection injuries are more likely toresult in dysesthesia than are
othercauses ofnerve injuries�There may be a nonanatomic distribu-tion ofnerve
involvement (includingthe second and third divisions ofthetrigeminal
nerve)�Injection injuries occur more com-monly in females�The lingual nerve,which
is stretchedmore upon mouth opening than is theIAN,is more commonly affected�The
majority ofcases resolve within 8 weeks,and ifparesthesia persists for> 8
weeks,then only one-third ofthose injuries resolve spontaneouslyMicroneurosurgery
is a poor optionfor patients with injection-related nerveinjuries because surgical
access is difficult;therefore,most cases are managed withpharmacologic therapy.One
ofthe diffi-culties for microneurosurgeons is differ-entiating a mandibular block
injury froma third molar injury to the IAN.On rareoccasions the third molar site
ofthe IANhas been explored and found to be nor-mal,with the assumption that the
injuryoccurred as a result ofinjection ratherthan extraction.23It is well known
that orthognathicsurgery may result in nerve injury.TheIAN is affected more often
than is the lin-gual nerve,and rarely the facial nerve maybe affected (0.67% with
sagittal splitosteotomy in one study24).Certainly muchis known about the risks
ofIAN injuryassociated with sagittal split osteotomy,aswell as screw
overpenetration injury to thelingual nerve.25,26Unfortunately,thereported incidence
ofimmediate andlong-term neurosensory deficit varies con-siderably (from < 5% to >
90%) owing topoorly controlled factors inherent in thestudy designs,such as
individual operatorvariability and surgeon experience,lack ofstandardization
ofneurosensory testing,lack ofcontrol sites for normal cutaneousfacial
sensibility,and variation in the peri-ods ofneurosensory testing.Several stud-ies
have examined the specific parametersofneurosensory recovery after
bilateralsagittal split osteotomy by using objectiveand subjective assessment.27One
studyfound a 39% incidence ofneurosensorydysfunction following sagittal
ramussurgery,28and others have shown < 15%dysfunction at 6 months.29Although
theincidence ofnerve dysfunction varies,there are well-known risk factors for
nerveinjury,including the following30:patientage31;increased length ofthe surgical
pro-cedure;proximal or distal segment frac-ture (�bad splits�);concomitant
thirdmolar removal;concomitant genioplastyprocedures;compression during
fixation;inadvertent use ofchisels;nerve entrap-ment in the proximal
segment;nervemanipulation in the area ofthe osteotomyand,perhaps more
significantly,in the lin-gual region during medial dissection(based on
intraoperative recordings ofIAN somatosensory evoked potentials)32;the location
ofthe inferior alveolar canalclose to the inferior border;low corpusheight and
retrognathism (IAN closer tobuccal cortex)33;and frank nerve transec-tion during
surgery.Unfortunately,long-term neurosensory dysfunction followingorthognathic
surgery is not generallyamenable to surgical correction.However,most patients
tolerate the paresthesia wellfollowing correction ofa significantdentofacial
deformity.Two caveats are thatpatients tolerate mild paresthesia follow-ing major
surgery well (with informedconsent) and that the magnitude ofneu-rosensory
dysfunction decreases as thetime from injury increases.This certainlyapplies to
orthognathic nerve injuries.Maxillofacial trauma may result ininjury to any ofthe
terminal branches ofthe trigeminal nerve.Mandible fracturesthat violate the IAN
canal result in tempo-rary or permanent paresthesia.Treatmentofmandible fractures
with inadvertentplacement ofscrews may cause iatrogenicnerve injury.In
general,reduction ofthefracture aids in realigning the natural con-duit (ie,the IAN
canal) that will help toguide spontaneous neurosensory recoveryeven with a
transection injury.Also,the presence and/or treatment oforal pathologic lesions may
result in nerveinjury.The use ofCarnoy�s solution (ferricchloride 0.1 g/mL,absolute
alcohol 6 mL,chloroform 3 mL,glacial acetic acid 1 mL)following treatment
ofpathology has beenshown to have a critical exposure time inan animal model of5
minutes,after whichtime there may be long-term irreversibleneural
injury.34,35Following a resectionprocedure,consideration should be givento
immediate or delayed neural recon-struction using autogenous nerve grafts.Although
preprosthetic surgery is per-formed less frequently today than in
thepast,procedures such as torus mandibu-laris reduction and vestibuloplasty
placethe terminal branches ofthe mental nerveand infraorbital nerve at risk
ofinjury.Sur-gical repair ofsmall terminal nerve fibers isdifficult and often
results in scarring and apoor chance ofneurosensory recovery.Themaxilla and
mandible are excellent sourcesofautogenous bone grafts;however,theyare not without
potential morbidity.Themajority ofpatients who undergo genial
822Part 6: Maxillofacial Reconstructionbone graft harvest complain ofdesensitiza-
tion ofthe mandibular anterior teeth.Depending on the specific techniqueemployed
for posterior mandibular ramusgrafting,the IAN may be at risk ofiatro-genic
injury.Mandibular endodontic ther-apy and periapical surgery may result in aninjury
to the IAN,depending on the prox-imity ofthe root apex to the canal.Someendodontic
filling materials may be neuro-toxic,and to prevent irreversible paresthe-sia that
in many cases results in dysesthesia,consideration should be given to
promptexploration and d�bridement ofmedica-ments that have permeated through
theroot apex and are in direct contact with thenerve.Distraction osteogenesis
ofthemandible has been shown to induce tran-sient changes in neuronal
conductionwithout significant long-term nerve dys-function.36,37On a clinical
level,a youngerpatient would certainly tolerate a �stretch-type�ofinjury to the
nerve well.Recentdata indicate that with a corticotomy anddistraction rates of1
mm/d neural changesare unlikely but that rates greater than thismay be deleterious
to nerve function;how-ever,more studies are necessary.38Finally,implant-related
injuries to theIAN are common (30�40%) and problem-atic to manage
appropriately.Unfortu-nately there is a lack ofdata regardingappropriate patient
assessment and man-agement,with a lack ofconsensus ontreatment protocols.In the
posteriormandible the likely cause ofnerve damageis that the initial pilot (depth)
drill pene-trates the superior cortex ofthe canal andviolates the IAN vein (or
artery,which isless likely).This results in some bleedingthat,on placement ofthe
implant,tam-ponades itself.The resultant increasedpressure in the closed
environment createsa compartment syndrome,with harmfuleffects on neurosensory
function.Thistype ofinjury commonly results in long-term unpleasant altered
sensation (dyses-thesia) rather than simple decreased sen-sation (hypoesthesia).The
recognitionpostoperatively that the patient has pares-thesia and that the implant
is within theconfines ofthe canal warrant the clinicianto consider removal ofthe
implant,withor without immediate replacement with ashorter implant.If,however,the
injurywas due to a compartment syndromeeffect,then implant removal
withoutreplacement may be prudent.For patientswith persistent paresthesia,referral
to amicroneurosurgeon may be warranted.The procedure ofIAN repositioning (lat-
eralization and transpositioning) is anoption that theoretically would induce
a�controlled�injury to the nerve and pro-tect it during implant
preparation.Withlateral decortication ofthe mandible andnerve exposure,a
compartment syndromeis not possible.Despite the potentialadvantages ofnerve
repositioning,there isa high incidence oflong-term paresthesiaranging from 0 to
77%,with a mean ofapproximately 30 to 40%.39With appro-priate surgeon
experience,proper patientselection,and informed consent,this pro-cedure remains a
viable option in posteri-or mandibular reconstruction.Trigeminal Nerve Anatomy and
PhysiologyA briefreview ofthe trigeminal nerve isnecessary to understand clinical
diagnosisand management.The trigeminal nerve(Figure 41-1) is composed ofa
mesoneuri-um that suspends the nerve within thesurrounding tissues and is
continuouswith the outer epineurium that definesand surrounds the nerve
trunk.Theepineurium contains a vast plexus ofves-sels called the vasa nervorum,as
well aslymphatic channels.The epineurium isdivided into outer and inner
epineuriums,and the inner layer is composed ofa looseconnective tissue sheath with
longitudinalcollagen bundles that protect against com-pressive and stretching
forces imposed onthe nerve.Individual fascicles are definedby the perineurium,which
is a continua-tion ofthe pia-arachnoid layer ofthe cen-tral nervous system.It
functions to pro-vide structural support and act as a diffu-sion barrier,similar to
the blood-brainbarrier that prevents the transport ofcer-tain molecules.The
individual nerve fibersand Schwann cells are surrounded by theendoneurium,which is
composed ofcolla-gen,fibroblasts,and capillaries.There arethree types ofneural
fascicular patterns:monofascicular (one large fascicle),oligo-fascicular (2�10
fascicles),and polyfascic-ular (> 10 fascicles) (Figure 41-2).Theinferior alveolar
and lingual nerves arepolyfascicular in nature.Polyfascicularnerves have abundant
interfascicular con-nective tissue�the importance ofwhich isthat needle
penetrations rarely causedirect neural trauma and that nerve repairwith realignment
ofthe fascicles is chal-lenging.The nerve is composed ofa func-tional unit with
differing fiber types thattransmit a variety ofinformation (Table41-2).The A alpha
fibers are the largestmyelinated fibers with the fastest conduc-tion velocity;they
mediate position andfine touch through muscle spindle affer-ents and skeletal
muscle efferents.The Abeta fibers mediate proprioception.Thesmallest myelinated
fibers are the A deltaOuter epineuriumInner epineuriumPerineuriumEndoneuriumSchwann
cellSchwann cellAxonAxonFascicleUnmyelinated fibersMyelinated fiberFIGURE41-
1Trigeminal nerve anatomy.
Microneurosurgery823fibers that carry pain (�first�or �fast�pain)and temperature
information.The smaller-diameter and slower-conducting unmyeli-nated C fibers
mediate �second�or �slow�pain and temperature sensations.TheSchwann cells surround
both myelinated(one Schwann cell per nerve fiber) andunmyelinated (one Schwann cell
per sev-eral nerve fibers) nerves,and they play amajor role in nerve survival and
regenera-tion following injury.Although the myelinsheath may not survive a nerve
injury,theSchwann cells do,and they provide a sup-portive role in the production
ofneu-rotrophic and neurotropic factors (such asnerve growth factor) that enhance
neuralrecovery.The nodes ofRanvier are the 0.3to 2.0 �m unmyelinated segments
betweenthe myelin sheaths that are responsible forthe diffusion ofcertain ions that
causenerve depolarization and repolarizationand the saltatory conduction ofa
nerveimpulse along the nerve.Following nerve injury many changesoccur,but the basic
process ofnerve heal-ing involves both degeneration and regen-eration (Figure 41-
3).40,41The nerve cellbody responds with an increased metabol-ic phase with a
heightened production ofribonucleic acid and breakdown ofNissl�ssubstance for
export from the cell body.Atthe site ofinjury,there is edema and par-ticulate
cellular debris.In addition,there isa proliferation ofphagocytes,andmacrophages
begin to clean the area.Within days there are axonal sprouts thatextend from the
proximal nerve stump.Each axon may have as many as 50 collat-eral sprouts.There is
proliferation and ahigh level ofactivity ofSchwann cells aswell.These begin to lay
down new myelinfor the arrival ofthe new axons.Addition-ally,nerve growth factors
are producedthat influence the direction ofsproutingand guide the new axons into
the newlyFIGURE41-2Three types ofneural fascicular patterns: A,monofascicular;
B,oligofascicular; C,polyfascicular.Adapted from Lundborg G.The nerve trunk.In:
Lundborg G,editor.Nerve injury and repair.New York: Churchill Livingston;
1998.p.198.ABCTable 41-2Trigeminal Nerve FibersSize Conduction Fiber(�)Velocity
(m/s)FunctionA alpha (myelin)12�2070�120Position,fine touchA beta
(myelin)6.0�1235�170ProprioceptionA delta (thin myelin)1.0�6.02.5�3.5Superficial
(first) pain,temperatureC (unmyelinated)0.5�1.00.7�1.5Deep (second)
pain,temperatureCell bodyAxonSchwann cellEndoneuriumInjury siteMacrophages and
phagocytes clear debris Cell body swelling due toincreased metabolic activityAxonal
sproutsSchwann cells producenerve growth factorsSchwann cells align into bands of
B�ngner to guide axonal sproutsFIGURE41-3Ato E,Neural wound-healing
mechanisms.ACBDE
824Part 6: Maxillofacial Reconstructionformed myelin sheaths,known as thebands
ofB�ngner.In the event that all ofthese interrelated processes occur appro-
priately,then spontaneous neural regener-ation occurs.In the event that one or
moreofthe reparative processes fail,there maybe neuroma formation.A neuroma is sim-
ply a disorganized mass ofcollagen fibersand randomly oriented small nerve fasci-
cles (sprouts).Neuromas are classified bygross morphology into the following
types(Figure 41-4):amputation (stump) neuro-ma,neuroma-in-continuity (central
orfusiform neuroma),and lateral neuromasthat are either lateral exophytic
neuromasor lateral adhesive neuromas.Nerve Injury ClassificationThere are two
acceptable classificationschemes used to describe the histologicchanges that occur
following nerve injury.Seddon described a three-stage classifica-tion system in
1943,42and Sunderlandrevised and further subclassified nerveinjuries into five
grades in 1951 (Figure41-5 and Table 41-3).43A neurapraxia(Seddon) or first-degree
(Sunderland)injury is characterized as a conductionblock from transient anoxia
owing toacute epineurial/endoneurial vascularinterruption resulting from mild
nervemanipulation (traction or compression),with rapid and complete recovery ofsen-
sation and no axonal degeneration.Dam-age is confined to within the endoneuri-
um.Sunderland further subdividesfirst-degree injuries into types I,II,and III.Type
I results from mild nerve manipula-tion with rapid (hours) return ofsensa-tion when
neural blood flow is restored.Type II is due to moderate traction orcompression
with the formation oftran-sudate or exudate fluid and intrafascicularedema,with
return ofsensation followingedema resolution (days).Type III injuriesresult from
more severe nerve manipula-tion that may result in segmental demyeli-nation,with
recovery within days toweeks.An axonotmesis (Seddon) corre-Amputation
neuromaNeuroma-in-continuityLateral exophyticneuromaPeriosteumLateral adhesive
neuromaFIGURE41-4Neuroma types: amputation neuro-ma,neuroma-in-continuity,lateral
exophytic neu-roma,lateral adhesive
neuroma.NeurapraxiaAxonotmesisNeurotmesisEpineuriumPerineuriumEndoneuriumBasal
laminaAxonTo endoneuriumTo perineuriumThrough endoneuriumThrough perineuriumThrough
epineuriumFirst degreeSecond degreeThird degreeFourth degreeFifth degreeFIGURE41-
5Nerve injury classifications: A,Seddon classification; B,Sunderland
classification.AB
Microneurosurgery825sponds to second-,third-,and fourth-degree (Sunderland)
injuries,with the dif-ference being the degree ofaxonal damage.Second-degree
injuries are due again totraction or compression that results
inischemia,intrafascicular edema,ordemyelination.This damage extendsthrough and
includes the endoneuriumwith no significant axonal disorganization.Recovery is slow
and may take weeks tomonths,and it may not be complete.Third-degree injuries
continue the spec-trum ofmore advanced injury owing tomore significant neural
trauma with vari-able degrees ofintrafascicular architectur-al disruption and
damage extending to theperineurium.Recovery is variable;it maytake months and be
incomplete.Fourth-degree injuries result in damage to theentire fascicle that
extends through theperineurium to the epineurium,but theepineurium remains
intact.There is axon-al,endoneurial,and perineurial damagewith disorganization
ofthe fascicles.Spontaneous recovery is unlikely,but min-imal improvement may occur
in 6 to 12 months.Finally,neurotmesis (Seddon)and fifth-degree (Sunderland)
injuriesresult from complete or near completetransection ofthe nerve with
epineurialdiscontinuity and likely neuroma forma-tion.Spontaneous neurosensory
recoveryis unlikely.For completeness,in 1988 Del-lon and Mackinnon described a
sixth-degree injury,which recognizes that manynerve injuries exhibit features
ofdifferentdegrees ofinjury according to Sunderland(Table 40-4).44The Seddon and
Sunder-land classification schemes attempt to cor-relate histologic changes with
clinical out-come (see Table 41-3).Clinical Neurosensory TestingThe patient who
sustains an injury to thetrigeminal nerve may present with a vari-ety ofsigns and
symptoms.These may bedivided into nonpainful
anesthesia,hypoesthesia,hyperesthesia,or painfulanesthesia (anesthesia
dolorosa),hypoes-thesia,or hyperesthesia (allodynia�painfrom a nonpainful
stimulus�or hyper-pathia�increased pain owing to a painfulor nonpainful
stimulus).The history usu-ally indicates the etiologic event,and thechiefcomplaint
may include the followingdescriptive terms:numbness,itchy,crawl-
ing,stretched,drooling,painful,tingling,tickling,pulling,burning,stinging,pinsand
needles,hot sensation,cold sensation,inability to feel food on lip,inability
totaste,inability to shave,inability to smile,and loss ofconsortium.The history
ofpresent illness should be explored in depthwith a description ofthe onset and
pro-gression ofsymptoms,change in symp-toms,treatment received and
response,aggravating and alleviating factors,andpresent symptoms.The McGill Pain
Questionnaire(MPQ) may be used to assess pain andaltered sensation,and it is a
useful tool formonitoring progression ofneurosensoryrecovery.The MPQ uses three
classes ofdescriptive words to assess the level ofdys-function and interference
with activity:sensory class
(temporal,spatial,thermal,punctate,incisive,constrictive,tractionpressure),affectiv
e class (tension,fear,autonomic properties,punishment),andevaluative class (patient
perception).Per-haps the simplest and most reliable mea-sure ofsubjective patient
assessment is theuse ofa visual analog scale.Generally,thisis a 10 cm five-degree
scale,with a degreemarked every 2.5 cm (Figure 41-6).This isa useful tool for
monitoring subjectiveimprovement.It must be remembered thatsubjective and objective
nerve testings areTable 41-3Nerve Injury Classifications:Seddon versus Sunderland
SeddonSunderlandHistologyOutcomesNeurapraxiaFirst degreeNo axonal damage,no
demyelination,Loss ofsensation,rapid recoveryno neuroma(days to weeks),no
microneurosurgeryAxonotmesisSecond,third,and More axonal damage,demyelination,Loss
ofsensation,slow incomplete recoveryfourth degreespossible neuroma(weeks to
months),possible microneurosurgeryNeurotmesisFifth degreeSevere axonal
damage,epineurial Loss ofsensation,spontaneous recovery discontinuity,neuroma
formationunlikely,microneurosurgeryTable 41-4Sunderland Grade and Recovery
PatternsDegree ofInjuryRecovery PatternRate ofRecoveryTreatmentFirst
degreeCompleteFast (days to weeks)NoneSecond degreeCompleteSlow (weeks)NoneThird
degreeVariableSlow (weeks to months)Possible nerve explorationFourth
degreeNoneUnlikely recoveryMicroneurosurgeryFifth degreeNoneNo
recoveryMicroneurosurgerySixth degree*Varies�Varies�Varies�*Sixth-degree injury
data from Dellon AL and Mackinnon SE44�Depending on specific injury pattern.
826Part 6: Maxillofacial Reconstructionrarely at the same level.For example,inone
study ofnerve testing following sagit-tal split osteotomy,the subjective neu-
rosensory deficit was 26.0%,whereas theobjective tests revealed an 89.5%
deficit.45Treatment planning decisions must bebased on an assessment ofboth the
sub-jective and objective testing results.Also,aradiographic assessment may reveal
priorradiographic predictors ofroot proximityto the canal,retained root
fragments,dis-tal bone removal,or the presence offor-eign bodies in extraction
sites.Clinical examination begins withinspection ofthe oral cavity,which mayshow
signs ofself-induced trauma,a lin-gually placed third molar incision
scar,oratrophic changes ofthe tongue fungiformpapillae.46Palpation may induce a
Tinel�ssign,which is a provocative test ofregen-erating nerve sprouts that it is
performedby light palpation over the area ofsus-pected injury.This maneuver elicits
a dis-tal referred �tingling�sensation at the tar-get site.This sign is thought to
indicatesmall-diameter fiber recovery;however,itis poorly correlated with
functionalrecovery and is often confused with neu-roma formation.To perform the
CNTappropriately,the patient should be seat-ed comfortably in a quiet room,and
thespecific testing procedures should beexplained clearly to the patient,with con-
firmation that there is an understandingofwhat the patient is being asked to doand
what possible responses are accept-able.The specific tests are performedwith the
patient�s eyes closed,and thecontralateral uninjured side serves as thecontrol,when
appropriate.The CNT is performed at three levels:A,B,and C (Table 41-5).47The
CNTinvolves a dropout algorithm that attemptsto correlate the results ofthe test
with thelevel ofnerve injury (Figure 41-7).Iftheresults oflevel A testing are
normal,thenthe CNT is terminated and the patient isconsidered normal;this would
correspondto a Sunderland first-degree injury.Anabnormal result at level A
indicates theneed to proceed to level B testing.Iftheresults oflevel B testing are
normal,thenthe patient is considered mildly impaired(Sunderland second-degree
injury).IflevelB results are abnormal,then level C testingis performed.Iflevel C
results are normal,then the patient is moderately impaired(Sunderland third-degree
injury).Iflevel Cresults are abnormal,then the patient isconsidered severely
impaired (Sunderlandfourth-degree injury).Ifthe patient�s testresults are abnormal
at levels A,B,and Cand there is no response to any noxiousstimulus,the patient is
considered com-pletely impaired (Sunderland fifth-degreeinjury).Level A testing
includes brush-stroke directional and static two-point dis-criminations.These tests
assess function ofthe larger myelinated A alpha and betafibers.These fibers are the
most sensitive tocompression and traction injuries;there-fore,the CNT is terminated
iflevel A isnormal.Brush-stroke directional discrimi-nation is performed with a
fine sable orcamel hair brush.The brush is stroked gen-tly across the area
ofinvolvement at a con-stant rate,and the patient is asked to indi-cate the
direction ofmovement (ie,to theleft or right) and the correct number ofpatient
statements out of10 is recorded.Two-point discrimination is performed ina static
fashion (vs a moving two-point dis-crimination) and with blunt tips to avoid Adelta
and C fiber stimulation.This test canbe performed with any device that is capa-ble
ofallowing the distance between twopoints to be measured consistently (eg,aBoley
gauge).The closest distance (in mil-limeters) at which the patient can consis-
tently discern the two points is recorded.Atlevel B testing,contact detection is
per-formed with Semmes-Weinstein monofila-ments or von Frey
hairs,which,again,assess the A beta fiber integrity and func-tion.These devices are
acrylic resin or plas-tic transparent/translucent rods with nylonfilaments
ofvarying diameters.The stiff-ness ofeach filament determines the forcenecessary to
deflect or bend the filament.The narrowest diameter filament thatrequires the least
amount offorce to deflectthat is detected consistently is recorded.Atlevel C
testing,pinprick nociception andthermal discrimination assess the smaller Adelta
and C fibers,which are most resistantto injury.Pinprick nociception may be per-
formed simply with a 30-gauge needle;however,a pressure sensitive device is
moreappropriate.Thermal discrimination maybe performed with suprathreshold meth-ods
using ice or ethyl chloride or hot wateron a cotton swab,but other options
are1Completeabsence ofsensation2Almost no
sensation3Reducedsensation4Almostnormalsensation5FullynormalsensationRight1Complete
absence ofsensation2Almost no
sensation3Reducedsensation4Almostnormalsensation5FullynormalsensationLeftFIGURE41-
6Visual analog scale.Table 41-5Clinical Neurosensory TestingSubjective
assessment:visual analog scale Objective assessmentLevel A:static two-point
discrimination,brush-stroke directional discriminationLevel B:contact
detectionLevel C:pinprick nociception,thermal discriminationPlease indicate with an
�X�on each of the two lines your perception of your current level of sensation.
Microneurosurgery827available.Minnesota thermal disks made ofcopper,stainless
steel,glass,and polyvinylchloride can be used.Although the tests employed in theCNT
are considered objective tests,theyare,in reality,subjective since they requirea
patient response.There are few purelyobjective tests ofnerve function available,and
these include trigeminal somatosen-sory evoked potentials and magneticsource
imaging.48Unfortunately,thesetests are not readily available and are notconsidered
a part ofthe routine assess-ment ofa nerve-injured patient.Also,there is little
data on the trigeminal nerveand the patterns ofresponses based onspecific
injuries.Finally,taste can be assessed by a vari-ety ofmeans,but generally it is
performedas either whole-mouth or localized testing.Solutions such as 1 M sodium
chloride(salt),1 M sucrose (sweet),0.4 M aceticacid (sour),and 0.1 M quinine
(bitter)may be used.There are many difficultieswith taste assessment in the patient
with alingual nerve injury.The perception oftaste alteration is extremely variable
andhas little correlation with the degree oflin-gual nerve injury.For example,a
patientwith a fourth- or fifth-degree lingual nerveinjury may not report any taste
alterationsubjectively but may test abnormally withdifferent solutions.The complex
sense oftaste is mediated not only by the chordatympani branch ofthe facial nerve
but alsothrough feedback mechanisms in thenasopharynx,oropharynx,and hypophar-
ynx,as well as the nucleus tractus solitar-ius in the brainstem.49Regarding
lingualnerve repair,objective and subjective neu-rosensory recovery also is
inconsistent.50Diagnostic nerve blocks can be a usefulcomponent ofthe patient
evaluation whendysesthesia or unpleasant sensations pre-dominate the clinical
scenario.The primarypurpose ofthe diagnostic block is to local-ize the source
ofpain and determine theprognosis for recovery following eitherpharmacologic or
surgical therapy.Thepreferred local anesthetic solution is ofalow concentration
(eg,0.25% lidocaine) toselectively block the smaller A delta and Cfibers while not
affecting the larger myeli-nated fibers.Ifthe low concentration failsto relieve the
pain,a higher concentration isused in the same location.Diagnosticblocks begin
peripherally and proceed cen-trally with constant reassessment ofthearea
ofinvolvement both objectively andsubjectively.Ifpatients present with symp-toms
consistent with sympathetically medi-ated pain or causalgia,a stellate
ganglionblock may be performed.These symptomsindicate a problem not amenable to
periph-eral microneurosurgery.Other pain syn-dromes that generally are not relieved
withdiagnostic nerve blocks include anesthesiadolorosa and deafferentation
pain;thesealso are not managed surgically but,rather,pharmacologically.Nonsurgical
TreatmentPharmacologic management ofperipheralnerve injuries is reserved for
patients whopresent with unpleasant abnormal sensa-tions or dysesthesia.In the
majority ofcases,pharmacologic treatment should bemanaged with a consultation from
an expe-rienced individual such as a neurologist
orNormalMildlyimpairedAbnormalImpairedAbnormalModeratelyimpairedAbnormal?Threshold?
ResponseNo responseSeverely impairedAnestheticContact detection(level B)Pain
sensitivity(level C)NormalModeratelyimpairedBrush stroke direction and two-point
discrimination(level A)NormalFIGURE41-7Algorithm for objective clinical
neurosensory test.
828Part 6: Maxillofacial Reconstructionfacial pain specialist.Many systemic
(Table41-6) and topical (Table 41-7) medicationsare available.51Whereas the
systemic drugsmay have significant side effects,topicalagents offer the advantages
oflittle systemicabsorption,possibly only minor irritation(which can be relieved
with a period ofabstinence),and over-the-counter avail-ability in many cases.There
are also manycombinations oftopical agents that can beused,such as a eutectic
mixture oflocalanesthetics (EMLA) that contains 2.5%lidocaine and 2.5%
prilocaine.Many ofthetopical agents are prepared in a pleuroniclecithin organogel
base.For most oral sur-geons long-term pharmacologic manage-ment is not part
oftheir routine practice,sothe prompt referral to a microneuro-surgeon or
neurologist may offer the bestchance for long-term success.Considera-tion may be
given to a trial ofa topicalagent such as capsaicin cream 0.025% tidand/or a
systemic medication with few sideeffects,such as baclofen 10 mg tid orgabapentin
100 mg tid.Some oral surgeons manage perioper-ative paresthesia following third
molarremoval or implant placement with ashort course ofcorticosteroid therapy inan
attempt to decrease perineural edema.Although there is little evidence to
suggestthat systemic steroids actually provide anyeffect,the use ofsteroids when a
nerveinjury occurs,indicates that the surgeonhas recognized a problem and has taken
anaction to improve outcome,which isadvantageous when considering medico-legal
involvement issues.Perhaps the most important consider-ation should be prompt
referral,whenindicated,to a specialist for pharmacologicor surgical management
ofthe patientwith a nerve injury.The indications forreferral include but are not
limited tothose listed in Table 41-8.In the past,prior to consideration ofsurgical
management,a variety ofneuro-ablative techniques have been used to man-age painful
neuropathies.Some oftheseinclude radiofrequency thermal
neurolysis,cryoneurolysis,and alcohol and glycerolinjections at the site ofinjury
as well as atthe gasserian ganglion.Based on the com-plications and recurrence
rates ofdys-esthesia,caution should be employed when considering these
options.52,53The use ofalow-level laser (gallium-aluminum-arsenide,wavelength 820
nm) has promisein the area ofneural healing.Several stud-ies have shown improvement
in objectiveand subjective neurosensory recoverieswith the use oflaser therapy in
some ofthemore difficult cases,such as long-standinginjuries,orthognathic IAN
paresthesia,and prolonged dysesthesia unresponsive topharmacologic or surgical
therapy.54�56However,the current limited availabilityofthe low-level laser and the
lack ofapproval by the US Food and DrugAdministration preclude its routine usefor
patients with nerve injuries.Treatment AlgorithmsThe decision to proceed with
microneuro-surgery must be made following a carefulpatient assessment over a
defined periodoftime.The dilemma is that sufficienttime must be given to allow for
sponta-neous neurosensory recovery but thatprompt surgical intervention may
affordthe best chance for recovery.Time is a crit-ical issue for three main
reasons.First,atthe site ofinjury,distal nerve degeneration(wallerian
degeneration�named forAugustus Waller in 1892) occurs owing tothe interruption
ofaxonal transport.Thisprogressive loss ofneural tissue may com-promise future
repair attempts.Second,atthe nerve cell bodies there is ganglion celldeath that
occurs early following injury.57Third,as the time from nerve injuryincreases,there
is a higher likelihood thatcentral cortical changes may occur,andthese would make
peripheral repair inef-fective.58As a result,if30 to 50% ofgan-Table 41-7Topical
MedicationsCategoryExampleTopical anesthetics5% viscous lidocaine gel;20%
benzocaine gel;2.5% lidocaine with 2.5% prilocaineNeuropeptidesCapsaicin cream
(0.025% or 0.075%)Nonsteroidal anti-inflammatory drugsKetoprofen 10�20% PLO
base;diclofenac 10�20% PLO baseSympathomimeticsClonidine 0.01% PLO base or patchN-
methyl-D-aspartate blocking agentsKetamine 0.5% PLO
baseAnticonvulsantsCarbamazepine 2% PLO baseTricyclic antidepressantsAmitriptyline
2% PLO baseAntispasmodicsBaclofen 2% PLO basePLO = pleuronic lecithin
organogel.Table 41-8Microneurosurgeon Referral IndicationsObserved nerve
transectionComplete postoperative anesthesiaPersistent paresthesia (lack
ofimprovement in symptoms) at 4 wkPresence or development ofdysesthesiaTable 41-
6Systemic PharmacologicAgentsLocal anestheticsCorticosteroidsNonsteroidal anti-
inflammatory agentsAntidepressantsNarcotic analgesicsAnticonvulsantsMuscle
relaxantsBenzodiazepinesAntisympathetic agents
Microneurosurgery829glion cells have undergone necrosis,thebest possible success
rate from surgicalrepair may also be 30 to 50%.Microneurosurgery is indicated
forpersistent paresthesia that fails to improveover successive
examinations.Thisincludes both subjective and objectiveassessments.Surgery is not
indicated ifthere is continued improvement at eachsubsequent assessment.The current
rec-ommendations are to consider surgery forthe lingual nerve within 1 to 3 months
fol-lowing the injury,and for the IAN within3 to 6 months following the injury
(Figure41-8).The rationale for the difference intime is that the IAN lies within a
bonyTransection or Sunderland fourth or fifth degree (3rds,
BSSO)CleanAvulsiveImmediate primaryrepairDelayed primaryrepair(14�21
days)NSTNSTNSTConsider surgery,as indicatedChemical(RCT, tetracycline)NSTConsider
surgery,as indicatedCompression (root tip, implant, mandible fracture)Stretch or
Sunderlandfirst to third degreeObserved nerve injuryNSTImmediate
decompressionImmediated�bridementUnobservednerve injuryNSTLingual nerveInferior
alveolar nerveSurgery1�3 moSurgery3�6 moFIGURE41-8Nerve treatment algorithms:
A,unobserved nerve injury; B,observed nerve injury.BSSO = bilateral sagittal split
osteotomy; NST= neurosensory testing; RCT = root canal therapy.ABcanal that can
guide spontaneous regener-ation,so more time is allotted for thatprocess,whereas a
lingual nerve injuredwithin soft tissue does not have a �physio-logic conduit�to
guide regeneration.Ingeneral,the oral surgeon should have follow-up examinations
with the patientover a period ofapproximately 4 weeks.Ifthere is persistent
paresthesia or a worsen-ing ofsymptoms,referral should be madeto a
microneurosurgical specialist.For an unobserved nerve injury,theplan should be to
continue neurosensorytesting for 1 month and then to refer forsurgery in the 1- to
3-month (lingualnerve) or 3- to 6-month (IAN) time peri-ods.For an observed nerve
injury,treat-ment should focus on the specific etiology.For a suspected traction
injury (Sunder-land first-,second-,and third-degreeinjuries),the patient should be
tested for 1 month for signs ofexpected spontaneousrecovery.In the case ofnerve
compression,immediate decompression should be con-sidered.This includes removal ofa
rootdisplaced into the IAN canal,removal orreplacement when there is evidence
ofimplant impingement within the confines
830Part 6: Maxillofacial Reconstructionofthe IAN canal,or reduction and align-ment
ofa displaced posterior mandiblefracture including the IAN canal.Neu-rosensory
testing should be performed fol-lowing decompression,and microneuro-surgery should
be considered as indicated.Chemical injuries should be d�bridedpromptly.For
observed transectioninjuries (Sunderland fourth- or fifth-degree injuries),an
immediate primaryrepair may be performed for a clean tran-section injury
(eg,scalpel transection).Foran avulsive injury (eg,lingual nerve entan-gled in a
bur),consideration is given to adelayed primary repair performed at 3 weeks
following the injury.This allowstime for the proximal and distal nervestumps to
define the degree ofinjury,andto determine whether the surroundingenvironment is
conducive to nerve surgery,when there are high levels ofneurotropicand neurotrophic
factors.After surgery,patients should be followed up with repeatneurosensory
testing.The success rates ofmicroneurosurgi-cal reconstruction following nerve
injuryare variable in the literature.This is due tomany factors including the lack
ofstan-dardization with the following59:age,theetiology ofinjury,the time ofdelay
frominjury to repair,specific surgical techniquesused,the length ofthe nerve
gap,themethod ofneurosensory examination,theuse ofnormative values for control
sites,follow-up period variability,and criteria todefine success (Table 41-9).A
global reviewofthe literature might indicate a successrate of30 to 50% following
microneuro-surgery,including direct and gap repairs.Ingeneral,direct repair is
preferred over gaprepair (eg,using an autogenous nerve graft)and has higher
reported success rates.60Perhaps the largest study to date indicatesan overall
�success�rate of76.2% in 521 patients.61The success criteria weredefined as light
touch detected > 80% ofthe time and a 30% decrease in postopera-tive pain level.The
study results suggestedsome important trends in outcome.Hypoesthetic injuries
improved better fol-lowing microneurosurgery than did hyper-esthetic injuries,the
lingual nerve recoveredbetter than did the IAN overall,and therewas a decrease in
success associated with adelay of> 6 months.A recent report of51 microneurosurgical
reconstructions(direct and gap repairs) found that 10patients subjectively reported
goodimprovement,18 patients some improve-ment,22 patients no improvement,and 1
patient reported feeling worse followingsurgery.62This indicates that 55%
ofpatients showed some improvement.Inanother study of53 surgical patients,with
amean follow-up of13 months,light touchimproved from 0 to 51% and pinprick noci-
ception improved from 34 to 77%.Patientsalso experienced improved taste and
anincreased number offungiform papillae,and there was a decrease in incidence
ofaccidental tongue biting.Interestingly,therewas no correlation ofsuccess with
delayfrom time ofinjury to repair.No patientbecame completely normal,and there
wasno reduction in dysesthesia;however,mostpatients considered the surgery
worthwhile.There is certainly a need for standardizationin all aspects ofevaluation
and managementofmicroneurosurgical patients.Surgical TreatmentMicroneurosurgical
reconstructioninvolves a sequence ofsurgical proceduresincluding
exposure,dissection,assess-ment,manipulation,and repair.Many ofthe techniques
oftrigeminal nerve repairfollow those ofhand surgery and use sim-ilar
instruments.In general,surgical loupemagnification (�3.5 magnification) is ade-
quate.An operating microscope (�12magnification) is cumbersome and diffi-cult to
use with a transoral exposure,although it may be more useful with atransfacial
approach.ExposureSurgical access to the lingual or IAN maybe accomplished
transfacially or transoral-ly.The transfacial approach affords wideexposure and
access;however,it necessi-tates a facial incision with subsequent scarformation.The
intraoral approach pro-vides a more difficult surgical access andrequires more
diligence in microsurgery inthe posterior regions ofthe oral cavity,butit avoids a
facial incision.The decisionregarding surgical access depends on anindividual
patient�s anatomy,the site ofnerve injury,planned surgical procedures,patient
preference,and surgeon�s skill andexperience.External NeurolysisMicrodissection
ofthe nerve once exposedinvolves liberation ofthe nerve from thesurrounding tissues
to facilitate inspection.For the lingual nerve this procedure mayinvolve the
release ofthe nerve from a lat-eral adhesive neuroma in the area ofthelingual plate
in the third molar region,whereas for the IAN a corticotomy is gen-erally required
for external neurolysis.Sev-Table 41-9Classification ofSensoryRecoveryGrade
(Stage)Recovery ofSensibilityS0No recoveryS1Recovery ofdeep cutaneous
painS1+Recovery ofsome superficial painS2Return ofsome superficial pain and tactile
sensationS2+S2 with over-responseS3*Return ofsome superficial pain and tactile
sensation without over-response;two-point discrimination > 15 mmS3+S3 with good
stimulus localization;two-point discrimination = 7�15 mmS4Complete
recovery,S3+;two-point discrimination = 2�6 mm*S3 score indicates significant
clinical recovery (WyrickJD,Stern PJ.Secondary nerve reconstruction.HandClin
1992;8:587).Adapted from Mackinnon SE.Surgical management oftheperipheral nerve
gap.Clin Plast Surg 1989;16:587.
Microneurosurgery831eral techniques have been described for lat-eral decortication
in the area ofthe thirdmolar for IAN exposure,and these rangefrom a simple nerve
transpositioning to amodified buccal corticotomy or a unilater-al sagittal split
ramus osteotomy (Figure41-9).63The location ofthe injury and thesurgeon�s
preference frequently dictate thespecific approach used.The lingual nerve isusually
exposed via a modified incisionused for third molar surgery with a sulcu-lar
lingual extension (Figure 41-10).Forthe infraorbital nerve,external neurolysismay
be performed secondary to reductionand fixation ofa displaced zygomatico-maxillary
complex fracture impinging onthe neurovascular bundle at the infraor-bital
foramen.It has been suggested thatexternal neurolysis may provide
definitivetreatment for a nerve injury ifthe nervecompression is < 25% ofthe normal
diam-eter,ifthe paresthesia is ofshort duration(< 6 mo),and ifthere is no evidence
ofneuroma formation.64Internal NeurolysisThe term internal neurolysisrefers to sur-
gical manipulations within the epineuri-um to prepare the nerve for repair.Sophis-
ticated maneuvers may compromise repairby unnecessary removal oftissue andFIGURE41-
9Exposure techniques for the IAN: A,Lateral decortication ofthe mandible;
B,withexposure ofthe inferior alveolar neurovascular bundle.C,Sagittal ramus
osteotomy with anteriorextension via lateral decortication to the mental
foramen.D,Lateral mandibular decortication.E,Bone removal with chisels.F,Wide
exposure ofthe neurovascular bundle.ABDCEFDistal nerveNeuroma of right lingual
nerveDistal nerveProximal nerveSural graftFIGURE41-10Lingual nerve
exposure.A,Incision design via a distobuccal extension and lingual gingival sulcus
approach.B,Right lingual nerve exposure with neu-roma.C,Right lingual nerve repair
with an interpositional nerve graft.ABC
832Part 6: Maxillofacial Reconstructioninduction ofcicatrix formation owing
toexcessive manipulation.Several types ofinternal neurolysis have been
described,including epifascicular epineurotomy,epi-fascicular epineurectomy,and
interfascic-ular epineurectomy (Figure 41-11).Thefirst two prepare the epineurium
forrepair;any interfascicular surgery maycause further fascicular disruption
andscarring.Extensive internal neurolysisprocedures should be used with
caution.Nerve Stump PreparationPerhaps the most critical portion ofthesurgical
procedure involves the inspectionofthe proximal and distal nerve stumpsvia
magnification.The preparation ofthenerve stumps follows exposure;there mayalready
be an existing discontinuity from atransection injury.When a neuroma
ispresent,meticulous excision is required(Figure 41-12).It must be recognized
thatwith any neuroma,the clinical appearanceofneuronal edema or atrophy is less
thanthe internal fascicular changes (see Figure41-12A).Failure to resect enough
nervetissue to reach normal fascicles results in afailure ofneurosensory
recovery.Once thenerve is divided,ifnecessary,into proxi-mal and distal stumps,care
must be takento resect small (1 mm) portions ofthenerve trunk in both directions
(see Figure41-12B) until healthy glistening whitemushrooming fascicles are seen to
herni-ate through the edges ofthe epineurium(see Figure 41-12C).ApproximationThe
trigeminal nerve is similar to otherperipheral nerves in that it does not toler-ate
tension well;therefore,tension-free clo-sure is mandatory.65The deleterious
effectsoftension result from vascular compro-mise and subsequent fibrosis at the
nerverepair site.Approximation is the act ofbringing the nerve stumps into contact
andassessing the degree oftension that is pre-sent.At the time ofapproximation a
deci-sion must be made regarding whether touse an interpositional graft.In
general,mobilization with primary epineurialrepair is possible for lingual nerve
gaps < 10 mm and for IAN gaps < 5 mm.CoaptationCoaptation is the process ofaligning
theproximal and distal nerve stumps into thepremorbid cross-sectional fascicular
ori-EpineurotomyEpineurectomyFIGURE41-11Internal neurolysis: A,epifascicular
epineurotomy; B,epifascicular epineurectomy; C,interfascicular epineurectomy.A and
B adapted from LaBancJP.Reconstructive microneurosurgery ofthe trigeminal nerve.In:
surgery.Vol2.Philadelphia: J.B.Lippincott Company; 1992.p.1067.ABC1 mm1 mmFIGURE41-
12Nerve stump preparation.A,Neuroma; resection at the �clinical margin�ofthe
neuroma fails to complete nerve preparation.B,Neuroma resection in 1 mm
increments.C,Mushrooming fascicle.ABC
Microneurosurgery833entation.This is a difficult maneuver witha polyfascicular
nerve that has undergoneany degree ofdistal nerve changes indiameter or fascicular
pattern.This step isusually not performed painstakingly intrigeminal nerve repair
because ofthecomplex polyfascicular pattern.NeurorrhaphyNeurorrhaphy is the act
ofnerve suturingfor both direct and gap repairs.The trigem-inal nerve is repaired
using epineurialsutures,not perineurial sutures (Figure41-13).Generally,an 8-0
monofilamentnonresorbable nylon suture is chosensince a resorbable material would
invokeinflammation and disturb the area ofanticipated neural healing.At least
twosutures are used per anastomosis site toprevent rotation,but not more than
threeor four sutures should be used per anasto-mosis.The first suture is placed on
themedial side ofthe anastomosis since it ismore difficult to access.The epineurium
ispierced with the needle 0.5 to 1.0 mmfrom the edge ofthe nerve.The secondsuture
is placed 180�from the first suture,and then an assessment is made regardingthe
need for more sutures.Nerve GraftsWhen neurorrhaphy is not possible with-out
tension and a nerve gap exists,aninterpositional graft must be consideredfor
indirect neurorrhaphy.66The optionsfor autogenous nerve grafting include butare not
limited to the sural nerve,thegreater auricular nerve,and possibly themedial
antebrachial cutaneous nerve.67The sural nerve is the preferred nerve forgrafting
since it most appropriatelymatches the nerve diameter and the fasci-cular number
and pattern ofthe trigemi-nal nerve (Table 41-10).68The area ofthenerve superior to
the lateral malleolusexhibits less branching than at or belowthe lateral
malleolus.The sural nerve,ormedial sural cutaneous nerve,is a branchofthe sacral
plexus (S1,S2) and suppliessensory information to the posterior lowerextremity and
the dorsolateral foot.Suralgrafts up to 20 cm in length are possible,and patients
tolerate the donor site deficitwell.69The greater auricular nerve is apoor choice
for trigeminal repair.As abranch ofthe cervical plexus (C1,C2),thegreater auricular
nerve supplies sensationto the pre- and postauricular regions,thelower third ofthe
ear,and the skin overly-ing the posteroinferior border at the angleofthe
mandible.Patients are generally notamenable to sacrificing one facial regionfor
another.Additionally,the small diame-ter ofthe nerve makes it useful only whenused
as a cable graft (Figure 41-14).Thesole advantage ofa greater auricular graftover a
sural graft is in situations when itcan be harvested via the same incision
foranother procedure,such as the repair ofanextraoral mandibular fracture or
manage-ment ofpathology.The basic premise withgraft repair is that the graft
supplies theSchwann cells and growth factors neces-sary to support and encourage
axonalsprouting through the graft toward thetarget site.Entubulation TechniquesIn
an attempt to avoid donor site morbidi-ty,a variety ofentubulation techniqueshave
been proposed to create conduits dur-ing nerve regeneration (Figure 41-15).These
conduits involve both autogenousand alloplastic materials (Table 41-
11).Theautogenous options include vein,70�72colla-gen,73,74and muscle
grafts.75AlloplasticFIGURE41-13Direct epineurial neurorrhaphy.Table 41-10Size
ofDonor Nerve Grafts Relative to Injured NerveDonor NerveSural Greater
AuricularGreater Auricular Injured Nerve(2.1 mm)(1.5 mm)Cable (3.0 mm)Inferior
alveolar (2.4 mm)88%63%125%Lingual (3.2 mm)66%47%94%Adapted from Brammer JP and
Epker BN.68FIGURE41-14Greater auricular nerve cable graft.FIGURE41-15Entubulation
(conduit) nerverepair.
834Part 6: Maxillofacial Reconstructionmaterials include polyglycolic acid,76poly-
meric silicone,77and expanded polytetra-fluoroethylene.78�81It appears that the
useofthese alloplastic materials has a highsuccess in the animal model but poor
clin-ical outcomes.Further investigation is war-ranted as new materials are
developed.Postsurgical ManagementIn the majority ofcases,patients experiencea
variable period ofcomplete anesthesiafollowing nerve repair.In
general,nerveregeneration progresses at approximately 1 mm/d (about 3 cm/mo) from
the cellbody to the target site.For example,with adirect IAN repair,the approximate
distancefrom the trigeminal ganglion to the lowerlip and chin is 10
cm;therefore,completenerve regeneration takes about 100 days or12 weeks following
repair.With graft repairthe time frame is lengthened owing toslowed regeneration
through the graft site,but recovery is variable.A poor outcomefollowing
microneurosurgery may precludefuture surgical options;therefore,the bestchance for
microneurosurgical success is atthe first (and most likely,the last)
surgicalintervention.Medicolegal IssuesOral and maxillofacial surgeons
currentlypractice during a time of�malpractice cri-sis,�and nerve injuries
secondary to thirdmolar removal account for a large propor-tion ofthe
complaints.82Based on theinformation contained in this chapter andrecent trends in
malpractice,all oral andmaxillofacial surgeons should have a min-imum
ofunderstanding ofthe diagnosisand management ofnerve injuries accord-ing to the
so-called legal parameters ofcare.83These are summarized as follows:�Spontaneous
sensory recovery occursin most but not all patients.It is diffi-cult to predict
early,it may not be�complete,�and it may not be to thepatient�s satisfaction.Nerves
in softtissue (lingual nerve) have a lower rateofspontaneous regeneration than
dothose in bony canals (IAN)�All nerve injuries should be document-ed and evaluated
with a history,exami-nation,and neurosensory testing(objective and subjective).The
injuryshould be classified (Seddon or Sun-derland).In cases ofobserved orknown
nerve injury,prompt referralfor microsurgery provides the bestopportunity for
sensory recovery�Repeat examinations at frequent inter-vals may be
necessary.Patients shouldbe followed up for at least 1 month.Complete recovery in 1
month indi-cates neurapraxia,and no furthertreatment is
indicated.Neurosensorydysfunction that lasts > 1 month indi-cates a higher-grade
injury with uncer-tain spontaneous neurosensory recov-ery.Microneurosurgical
consultationshould be considered�Nerve injuries that show improvement(objective
and/or subjective) may befollowed up expectantly.Onceimprovement stops for a period
oftime,it usually does not begin again�Most nerve injuries resolve within 3 to9
months,but onlyifimprovementbegins prior to 3 months.Patientswho are anesthetic at
3 months usual-ly do not achieve significant neurosen-sory recovery.Prompt
microsurgery isusually indicated�Patients with partial sensory loss and/orpainful
sensations that they find unac-ceptableshould be considered formicrosurgery
ifobjective and subjectivefindings have not improved or returnedto normal by 4
months.Microsurgicaldelay decreases the chance ofsuccessbecause progressive distal
nerve degen-eration and/or the development ofacentral pain syndrome occur�Some
painful neuropathies may bemanaged nonsurgically under thesupervision ofa
microneurosurgeonor other experienced individual (eg,neurologist)�Angry uninformed
patients withnerve injuries are less likely to improvewith any treatment,surgical
or nonsur-gical.A discussion regarding optionsand the risk ofnerve injury should
beprovided so that the patient can giveinformed consent.Local anestheticinjections
carry a risk ofnerve injury�Early surgical intervention (ie,at 3�4 mo)is more
likelyto produce neurosensoryimprovement than is late intervention.Surgery delayed
beyond 12 months isseriously compromised by distal nervedegeneration and the
development ofchronic pain syndromes�Surgery is more likelyto improveresponses to
objective sensory testingand/or to reduce functional impair-ment than it is to
reduce pain or sub-jective feelings ofnumbnessReferences1.American Association
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acidPolyesterPolytetrafluoroethylene (PTFE)Expanded PTFE Silicone,polymeric
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following suralnerve harvest.J Oral Maxillofac Surg2002;60 Suppl 1:75.70.Miloro
M.Inferior alveolar nerve regenerationthrough an autogenous vein graft.J
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AE.The numbing truth.Monitor1998;9:1.
Microneurosurgery837APPENDIXNerve Terminology Review*allodynia:Pain due to a
stimulus that does not normally provoke pain.analgesia:Absence ofpain in the
presence ofstimulation that would normally be painful.anesthesia:Absence ofany
sensation in the presence ofstimulation that would normally be painful or
nonpainful.anesthesia dolorosa:Pain in an area or region that is
anesthetic.atypical neuralgia:A pain syndrome that is not typical ofclassic
nontraumatic trigeminal neuralgia.axonotmesis (Seddon) or second- sthrough fourth-
degree injuries (Sunderland):Nerve injury characterized by axonal injury with
subsequent degenerationand regeneration.causalgia:Burning pain,allodynia,and
hyperpathia after a partial injury ofa nerve.central pain:Pain associated with a
primary central nervous system lesion (spinal cord or brain trauma,vascular
lesions,tumors).chemoreceptor:A peripheral nerve receptor that is responsive to
chemicals,including catecholamines.deafferentation pain:Pain occurring in a region
ofpartial or complete traumatic nerve injury in which there is interruption
ofafferent impulses by destruction ofthe afferent pathway or other
mechanism.dysesthesia:An abnormal sensation,either spontaneous or evoked,that is
unpleasant.All dysesthesias are a type ofparesthesia but not all paresthesias
aredysesthesias.endoneurium:A connective tissue sheath surrounding individual nerve
fibers and their Schwann cells.epineurium:A loose connective tissue sheath that
encases the entire nerve trunk.fascicle:A bundle ofnerve fibers encased by the
perineurium.hyperalgesia:An increased response to a stimulus that is normally
painful.hyperesthesia:An increased sensitivity to stimulation,excluding the special
senses (ie,seeing,hearing,taste,and smell).hyperpathia:A painful syndrome
characterized by increased reaction to a stimulus,especially a repetitive
stimulus.The threshold is increased as well.hypoalgesia:Diminished pain in response
to a normally painful stimulus.hypoesthesia:Decreased sensitivity to
stimulation,excluding the special senses (ie,seeing,hearing,taste,and
smell).mechanoreceptor:A peripheral nerve receptor preferentially activated by
physical deformation from pressure and associated with large sensory
axons.mesoneurium:A connective tissue sheath,analogous to the mesentery ofthe
intestine,that suspends the nerve trunk within soft tissue.monofascicular
pattern:Characteristic cross-section ofa nerve containing one large
fascicle.neuralgia:Pain in the distribution ofa nerve or nerves.neurapraxia
(Seddon) or first-degree injury (Sunderland):Nerve injury characterized by a
conduction block,with rapid and virtually complete return ofsensation or function
and no axonal degeneration.neuritis:A special case ofneuropathy now reserved for
inflammatory processes affecting nerves.neurolysis:The surgical separation
ofadhesions from an injured peripheral nerve.neuroma:An anatomically disorganized
mass ofcollagen and nerve fascicles,and a functionally abnormal region ofa
peripheral nerve resulting from a failedregeneration following injury.neuropathy:A
disturbance offunction or a pathologic change in a nerve.neurotization:Axonal
invasion ofthe distal nerve trunk.neurotmesis (Seddon) orfifth-degree injury
(Sunderland):Nerve injury characterized by severe disruption ofthe connective
tissue components ofthe nervetrunk,with compromised sensory and functional
recovery.Third-degree injury:Characterized by axonal damage and a breach ofthe
endoneurial sheath,resulting in intrafascicular disorganization.The perineurium and
epineurium remain intact.The mechanism is typically traction or compression.Fourth-
degree injury:Characterized by disruption ofthe axon,endoneurium,and
perineurium,resulting in severe fascicular disorganization.The epineurium remains
intact.Possible mechanisms include traction,compression,injection injury,and
chemical injury.Fifth-degree injury:Characterized bycomplete disruption ofthe nerve
trunk with considerable tissue loss.Possible mechanisms include
laceration,avulsion,and chemical injury.nociceptor:A receptor preferentially
sensitive to a noxious stimulus or to a stimulus that would become noxious
ifprolonged.oligofascicular pattern:Characteristic cross-section ofa nerve
containing 2 to 10 rather large fascicles.paresthesia:An abnormal sensation,either
spontaneous or evoked,that is not unpleasant.A global term used to encompass all
types ofnerve injuries.perineurium:A thick connective tissue sheath surrounding
fascicles.polyfascicular pattern:Characteristic cross-section ofa nerve containing
> 10 fascicles ofdifferent sizes,with a prevalence ofsmall
fascicles.protopathia:The inability to distinguish between two different modes
ofsensation,such as a painful and nonpainful pinprick.sympathetically mediated
pain:A general term that refers to a family ofrelated disorders including
causalgia,reflex sympathetic dystrophy,minor causalgia,Sudeck�s atrophy,and
postherpetic neuralgia,which may be sympathetically maintained.synesthesia:A
sensation felt in one part ofthe body when another part is stimulated.wallerian
degeneration:The distal degeneration ofthe axon and its myelin sheath following
injury.*Adapted from LaBanc JP,Gregg JM.Glossary.Trigeminal nerve injury:diagnosis
and management.Oral Maxillofac Surg Clin North Am 1992;4:563.
CHAPTER 42Cleft Lip and Palate:Comprehensive Treatment Planning and Primary
RepairBernard J.Costello,DMD,MDRamon L.Ruiz,DMD,MDThe comprehensive treatment
ofcleft lipand palate deformities requires thoughtfulconsideration ofthe anatomic
complexi-ties ofthe deformity and the delicate bal-ance between intervention and
growth.Comprehensive and coordinated carefrom infancy through adolescence
isessential in order to achieve an ideal out-come,and surgeons with formal
trainingand experience in all ofthe phases ofcaremust be actively involved in the
planningand treatment.1�3Specific goals ofsurgicalcare for children born with cleft
lip andpalate include the following:�Normalized esthetic appearance ofthelip and
nose�Intact primary and secondary palate �Normal speech,language,and hearing �Nasal
airway patency �Class I occlusion with normal masti-catory function�Good dental and
periodontal health�Normal psychosocial developmentSuccessful management ofthe
childborn with a cleft lip and palate requirescoordinated care provided by a number
ofdifferent specialties including oral/maxillo-facial
surgery,otolaryngology,genetics/dys-morphology,speech/language
pathology,orthodontics,prosthodontics,and others.4In most cases care ofpatients
with con-genital clefts has become a subspecialtyarea ofclinical practice within
these differ-ent professions.In addition to surgery forcleft repair,treatment plans
routinelyinvolve multiple treatment interventionsto achieve the above-stated
goals.Becausecare is provided over the entire course ofthe child�s
development,long-term follow-up is critical under the care ofthese differ-ent
health care providers.The formationofinterdisciplinary cleft palate teams hasserved
two key objectives ofsuccessfulcleft care:(1) coordinated care providedby all ofthe
necessary disciplines,and (2)continuity ofcare with close interval follow-up ofthe
patient throughout periods ofactive growth and ongoing stages ofrecon-struction.The
best outcomes are achievedwhen the team�s care is centered on thepatient,family,and
community ratherthan a particular surgeon,specialty,orhospital.The idea ofhaving an
objectiveteam that does not revolve around thedesires ofone particular individual
or dis-cipline is sometimes impeded by competi-tive interactions between surgical
special-ties.Historic battles over surgical domainsbetween surgical specialties and
economicfactors contribute to these conflicts andnegatively affect the work ofthe
team.Healthy team dynamic and optimal patientcare are achieved when all members
areactive participants,when team protocolsand referral patterns are equitable and
basedon the surgeons�formal training and experi-ence instead ofspecialty
identity,and whenthe needs ofthe child are placed above theneeds ofthe team.This
chapter presents an overview oftheconcepts for reconstruction ofthe cleft lipand
palate deformity.The surgical recon-struction ofclefts requires that the
surgeonundertaking this important work maintain acognitive understanding ofthe
complexmalformation itself,the varied operativetechniques employed,facial growth
consid-erations,and the psychosocial health ofthepatient and family.The objectives
ofthischapter will be to present the overall stagedreconstructive approach for
repair ofcleft lipand palate from infancy through the time ofskeletal maturity,as
well as a focused discus-sion ofthe specific surgical proceduresinvolved in primary
cleft lip and palaterepair.Secondary revision procedures,bone
840Part 6: Maxillofacial Reconstructiongraft reconstruction ofthe cleft
maxilla,andorthognathic surgery for cleft-related dys-morphology are discussed in
Chapter 43,�Reconstruction ofthe Alveolar Cleft,�Chapter 44,�Reconstruction ofCleft
Lipand Palate:Secondary Procedures,�andChapter 61,�Orthognathic Surgery in
thePatient with Cleft Palate.�History ofCleft Lip and Palate RepairThe history
ofcleft lip and palate care hasalways been closely linked to dentistry andoral and
maxillofacial surgery.The birthand roots ofwhat is now the AmericanCleft Palate-
Craniofacial Association arestrongly rooted in dentistry.The first documented cleft
lip repairwas performed in AD390 on a patient wholater became the Governor General
ofsev-eral regions in China,although nothing isknown about the actual
surgeon.5,6JehanYperman is believed to have been the firstto describe unilateral
and bilateral cleft liprepair.6,7The first diagrammatic represen-tation ofcleft lip
repair and cleft palateobturator use is credited to Ambrose Parein the fourteenth
century.6,8Much later thefirst documented successful cleft palaterepair was
performed by a dentist,Le Mon-nier,in 1766 in Paris.6,9The concepts ofcleft lip and
palate repair have evolved fromstraight line repairs to a variety oftech-niques
using various cutbacks,triangles,and Z-plasties.6�14During the 1950s,Asen-sio,an
oral and maxillofacial surgeon fromGuatemala,developed a novel technique forcleft
lip repair,which involved the rotation ofthe philtral segment inferiorly and
advance-ment ofthe lateral segment medially using aquadrangular flap.Although he
used thisapproach in Guatemala throughout the1950s,he did not report it until
muchlater.15,16Ralph Millard ofMiami describedhis classic rotational-
advancementtech-nique in the mid-1950s,and his conceptschanged cleft repair
forever.17,18Millard iscredited with perhaps the most importanttechnical
development related to cleft liprepair,and today the majority ofsurgeonsuse his
original technique or some closemodification ofit.In the mid-nineteenth
century,Hulli-hen,recognized as the father ofAmericanoral and maxillofacial
surgery,published atreatise on comprehensive care ofcleft lipand palate
deformities.19Another pioneer,Truman Brophy,was the professor oforalsurgery and
dean ofthe Chicago CollegeofDentistry and contributed greatly to thecare ofmany
patients with clefts.Brophypublished a text detailing his experienceswith the
management ofvarious malfor-mations ofthe mouth and their surgicalrepairs including
the details ofcleftrepair.20One ofhis pupils was ChalmersLyons who started a
residency program inoral surgery at the University ofMichiganin 1917.20Lyons
developed the largest cleftpractice in America and contributedextensively to the
literature.20Many ofthe concepts related to inter-disciplinary care with a cleft
palate teamcare were introduced by Robert Ivy,an oraland maxillofacial surgeon who
laterbecame dually qualified in plasticsurgery.20Robert Ivy trained both in den-
tistry and medicine at the University ofPennsylvania.After his training in den-
tistry,Ivy further developed his interests inmaxillofacial surgery as an assistant
to hisuncle,Matthew Cryer,who was a professorin oral surgery at the University
ofPenn-sylvania.Robert Ivy became interested inclefts during his training as the
first dentalintern at Philadelphia General Hospital atthe University
ofPennsylvania.His inter-ests in maxillofacial injury led him to servein France in
World War I as an assistant toVilray Blair.After the war Ivy and
Blair�scollaboration resulted in two landmarkpublications by Ivy,Essentials
ofOralSurgeryand Fractures ofthe Jaws.Throughwork with his state representatives in
Har-risburg,Pennsylvania,he was able to startthe very first cleft palate clinics in
Lancast-er,Pittsburgh,Philadelphia,Erie,andScranton that provided
interdisciplinarycare to children for cleft lip and palatedeformities.When Reed
Dingman putforth a resolution ofthe American SocietyofMaxillofacial Surgeons
condemningoral and maxillofacial surgeons practicingin the hospital setting,Ivy
resigned hismembership and sent a letter ofprotest tothe organization that he
helped build insupport ofhis dental colleagues.20In the 1950s the concept ofprimary
orearly bone grafting ofthe cleft maxillarydefect was introduced by
Schmid.21Although the concept was initially met withenthusiasm from a number
ofsurgeons,pri-mary bone grafting was eventually aban-doned due to unfavorable
outcomes.Duringthe decades that followed,the negative skele-tal,dental,and growth-
related consequencesofprimary bone grafting became betterunderstood.22,23During the
early 1970s oraland maxillofacial surgeons Boyne and Sandswere the first to publish
their favorable out-comes using autogenous particulate bonegrafts for
reconstruction ofthe cleft maxil-la/alveolus later in childhood during themixed
dentition rather than earlier in life.24Although their work and results
representeda landmark discovery in the field ofcleftreconstruction,cleft palate
teams were slowto integrate his approach into their treat-ment protocols because
ofthe negative asso-ciations that lingered following the days ofprimary bone
grafting.Today their princi-ples ofsecondary bone grafting represent thestandard
approach for almost all oftheworld�s cleft centers.24,25Orthognathic reconstruction
ofthepatient with cleft deformities has been dis-cussed by many authors.26�36Early
tech-niques limited some surgeons�options toprocedures centered on mandibular set-
back.37During the 1970s the use oftotalmaxillary osteotomy was pioneered
byBell.38His novel ideas provided oral andmaxillofacial surgeons with an
understand-ing ofthe biologic basis for maxillaryosteotomy,described the vascular
supplythat allowed the procedures to be per-formed safely,and as a result
incorporated
Cleft Lip and Palate: Comprehensive Treatment Planning and Primary Repair841the Le
Fort I osteotomy into modern-daypractice.38Since that time a number oftechnical
refinements have been describedfor use ofthe Le Fort I osteotomy specifi-cally in
the cleft patient.Much ofthis workhas been done by two ofBell�s
formerpupils,Fonseca and Turvey,who went on tomake substantial contributions to the
skele-tal reconstruction ofpatients with clefts.39Another dual qualified oral and
maxillofa-cial surgeon,Posnick,has published themost complete descriptions
ofsurgicaltechnique modifications for patientsundergoing midfacial advancement in
theabsence ofprior bone graft reconstructionand his extensive experiences with the
long-term stability ofmidfacial advancementafter correction ofvarious types
ofcleftdeformities with orthognathic tech-niques.26�30Distraction osteogenesis
hasgained recent popularity for correction ofmidfacial hypoplasia but has yet to
showsignificant advantages over traditional tech-niques for the majority
ofpatients.32,33,40�42Comprehensive and coordinated carehas become more prevalent
across theworld,involving many different types ofspecialty care for children with
clefts.Pos-nick has provided the most comprehen-sive,succinct,and evidenced-based
discus-sions on the topic ofcleft lip and palatereconstruction from infancy through
ado-lescence.26These efforts as well as cranio-facial training programs associated
withoral and maxillofacial surgery have helpedto solidify the role oforal and
maxillofa-cial surgery in the comprehensive care ofpatients with
clefts.EmbryologyTo understand the goals oflip and palaterepair from an anatomic
standpoint thecleft surgeon must have an appreciation forthe failure
ofembryogenesis that results inclefting.There are critical points in thedevelopment
ofthe fetus when the fusion ofvarious prominences creates continuity andform to the
lip,nose,and palate.Anomaliesoccur when the normal developmentalprocess is
disturbed between these compo-nents.Each ofthese prominences is madeup
ofectomesenchyme derived from neuralcrest tissue ofthe mesencephalon
andrhombencephalon.Mesoderm is also pre-sent within these prominences as mes-
enchymal tissue.The prescribed destiny ofeach ofthese cells and tissues is
controlledby various genes to alter the migration,development,and apoptosis and
form thenormal facial tissues ofthe fetus.At the mol-ecular level there are many
interdependentfactors such as signal transduction,mechan-ical stress,and growth
factor productionthat affect the development ofthese tissues.Currently only
portions ofthis complexinterplay ofgrowth,development,andapoptosis are clear.At
approximately 6 weeks ofhumanembryologic development the mediannasal prominence
fuses with the lateralnasal prominences and maxillary promi-nences to form the base
ofthe nose,nos-trils,and upper lip.The confluence ofthese anterior components
becomes theprimary palate.When this mechanismfails,clefts ofthe lips and/or
maxillaoccur.At approximately 8 weeks thepalatal shelves elevate and fuse with
theseptum to form the intact secondarypalate.When one palatal shelffails to
fusewith the other components,then a unilat-eral cleft ofthe secondary palate
occurs.Ifboth ofthe palatal shelves fail to fuse witheach other and the midline
septum,thena bilateral cleft ofthe palate occurs.Fusion occurs when programmed
celldeath (apoptosis) occurs at the edges ofthe palatal shelves.The ectodermal com-
ponent disintegrates and the mes-enchyme fuses to form the intact palate.Soon after
this the anterior primarypalate fuses with the secondary palate andossification
occurs.At any point,iffailureoffusion occurs with any ofthe abovecomponents,a cleft
will occur ofthe pri-mary and/or secondary palates.Cleftsmay be complete or
incomplete based onthe degree ofthis failure offusion.Genetics and EtiologyClefts
ofthe upper lip and palate are themost common major congenital craniofa-cial
abnormality and are present in approx-imately 1 in 700 live
births.43Althoughinheritance may play a role,cleft lip andpalate is not considered
a single-gene dis-ease.Instead clefts are thought to be ofamultifactorial etiology
with a number ofpotential contributing factors.These fac-tors may include chemical
exposures,radi-ation,maternal hypoxia,teratogenic drugs,nutritional
deficiencies,physical obstruc-tion,or genetic influences.One prevailingtheory
relates the process ofclefting as athreshold in which multiple factors cometogether
to raise the individual above athreshold at which time the mechanism offusion
fails.44,45Recently multiple geneshave been implicated in the etiology
ofclefting.46�48Some ofthese genes includethe MSX,LHX,goosecoid,and
DLXgenes.Additional disturbances in growth factors ortheir receptors that may be
involved in thefailure offusion include fibroblast growthfactor,transforming growth
factor-�,platelet-derived growth factor,and epider-mal growth factor.Clefts ofthe
lip occur more com-monly in males than in females.49Inaddition left-sided cleft
lips are morecommon than right-sided cleft lips,andunilateral cleft lips are more
commonthan the bilateral cleft ofthe lip.50Bilater-al clefts ofthe lip are most
often associat-ed with clefting ofboth the primary andsecondary palates.Cleft
palate alone isseen in approximately 1 in 2,000 livebirths and this incidence is
similar in allracial groups.51Significant differences inthe prevalence ofclefts
exist when specif-ic ethnic/racial populations are exam-ined.For example,African
Americanshave a birth prevalence that is less com-mon than the total
population,butAsians tend to have a higher prevalence.In the majority ofcases
unilateral cleftlip and palate is an isolated nonsyndromic
842Part 6: Maxillofacial Reconstructionbirth defect that is not associated with
anyother major anomalies.43,52,53By compari-son a much greater proportion
ofpatientswith an isolated cleft palate will have anassociated syndrome or
sequence.43,53Some ofthe more common syndromesseen in this group include
Stickler�s,Vander Woude�s,or DiGeorge syndromes.Itis important to identify the
diagnosisearly,as functional issues may arise earlyin life and go unnoticed.For
example,patients with an isolated cleft palateshould be evaluated early by an
experi-enced pediatric ophthalmologist to eval-uate the possibility ofStickler�s
syn-drome.Patients with Stickler�s syndromemay have ocular abnormalities that
leadto retinal detachment.In an otherwisehealthy-appearing child these findingsmay
be difficult to diagnose and so earlyvisual loss may go unnoticed.In manycases
long-term genetics follow-up is nec-essary to make a definitive diagnosis andto
provide genetic counseling.The chances ofa recurrence ofcleft-ing within a family
are dependent onmany factors,including family history,severity,gender,degree
ofrelationship tothe affected individual,and the expres-sion ofa
syndrome.Predicting the inher-itance patterns offamilies who have a his-tory
ofcleft lip and/or palate can becomplicated.A skilled geneticist/dysmor-phologist
is best equipped to make thesedeterminations based on pedigree analy-sis and
genetic testing.Since most cleftsare sporadic the chances ofa family hav-ing
another child with a cleft after havinga child with a unilateral cleft lip
andpalate in which there was no family histo-ry ofclefting is approximately 2 to
4%.The chances are higher ifadditional fam-ily history is present or ifthe cleft is
bilat-eral.54,55The nature ofany genetic influ-ence will have an effect on the
presence ofa cleft.Such is the case in patients withautosomal dominant syndromes
such asStickler syndrome where 50% ofthe chil-dren may express the syndrome ifone
ofthe parents carries the altered gene.ClassificationThe typical classification
system used clin-ically to describe standard clefts ofthe lipand palate is based on
careful anatomicdescription.Clefts can be unilateral
orbilateral;microform,incomplete,or com-plete;and may involve the lip,nose,pri-mary
palate,and/or secondary palates(Figure 42-1).The presentation ofclefts isextremely
variable,and the individualrepairs are custom-tailored to achieve thebest symmetry
and balance.More severefacial clefting is most commonly describedusing Tessier�s
orbitocentric system ofnumbering (Figure 42-2).56Other systemsexist that are based
on embryologic fusionplanes,but these are cumbersome to use inroutine clinical
practice.57Prenatal CounselingRecent advances in ultrasound imaginghave
revolutionized prenatal care andmaternal-fetal medicine.Currently ultra-sound
images ofclefts ofthe lip can bevisualized as early as 16 weeks.58�60Diag-nostic
images ofthe palate are more diffi-cult to acquire,making the correct
prenataldiagnosis ofa cleft palate less predictable.Palatal structures may be
visualized usingsagittal and coronal views,but this current-ly requires the very
latest technology and askilled ultrasonographer with experienceperforming this type
ofstudy.FIGURE42-1Cleft lips come in a variety ofconfigurations,such that each
repair must be customized to establish the most normal morphology.A,Microform
leftunilateral cleft lip only,not requiring primary repair.B,Minor left incomplete
unilateral cleft lip only.C,Left incomplete unilateral cleft lip and palate with
aSimonart�s band.D,Wide left complete unilateral cleft lip and palate.ABCD
Cleft Lip and Palate: Comprehensive Treatment Planning and Primary Repair843When
the diagnosis ofcleft lip is madeduring pregnancy the family can then bereferred to
an experienced surgeon for aprenatal discussion.A prenatal consultationprovides an
excellent opportunity to explainthe diagnosis,review the different stages ofcleft
lip and palate reconstruction that maybe necessary,and prepare the parents
forpractical considerations such as feeding ofachild with a cleft palate.This gives
the fami-ly the opportunity to ask questions,calmfears,and learn about feeding
techniquesthat will be important during the first weekoflife for their baby.Parents
are empoweredwith this new knowledge,and the prepara-tions made during a prenatal
consultationallow them to anticipate the delivery oftheirbaby with a greater
comfort level regardingthe necessary care ofthe child during theearly postnatal
period.The family is thenreferred to a cleft and craniofacial team inorder to
undergo a more thorough interdis-ciplinary approach.Critical to this process is
consultationwith a geneticist/dysmorphologist to fur-ther discuss the issues
associated with thebirth and the possibility ofother
associateddeformities.Additional testing may be war-ranted to evaluate the
possibility ofassoci-ated deformities,syndromes,or sequencesthat could affect the
birthing process.Exceptionally skilled ultrasonographers canvisualize airway
development and otherabnormalities that may require early inter-vention with fetal
surgery,exit procedures,extracorporeal membrane oxygenation,orsurgical airway
management (tracheoto-my) at the time ofdelivery.In some medical centers fetal
diagno-sis and treatment teams are in place to dealwith issues associated with
various defor-mities diagnosed in the prenatal period.These teams foster a cohesive
environmentwhere information is exchanged throughconsultation.Much like in the
environ-ment ofa cleft and craniofacial team,fam-ilies can get the best information
availableto consider their child�s treatment deci-sions using an interdisciplinary
caremodel that is patient (mother and fetus),family,and community oriented.Feeding
Concerns Children born with isolated cleft lip canfeed quite well and even have the
opportu-nity to breastfeed in most instances.How-ever,infants with cleft palate can
have dif-ficulty feeding due to the inability to forman adequate seal between the
tongue andpalate for creation ofsufficient negativepressure to suck fluid from a
bottle.Nasalregurgitation and inefficient handling ofsecretions and foodstuffs may
also beobserved during early development.Spe-cialized nipples and bottles are
necessary toimprove feeding immediately after birth.The most useful devices combine
oversizednipples with reservoir spaces and largeopenings,a squeezable bottle to
push fluid01234576891011131214 14131211109874560012123FIGURE42-2A and B,Complex
facial clefts can be classified based on Tessier�s original orbitocentric system
ofnumbering.Cleftsmay involve all tissue planes including
skin,mucosa,bone,teeth,muscle,brain,peripheral nerve,and other specialized
tissues.AB
844Part 6: Maxillofacial Reconstructioninto the nipple assembly,and a one-wayvalve
that allows the bolus offluid to passfrom the bottle to the nipple only in orderto
minimize the amount ofwork the childmust perform to feed.These include a vari-ety
ofnipples with reservoirs that collect avariable volume ofliquid that can
beexpressed more easily when sucking is inef-ficient or not possible.Bottles that
can besqueezed to allow for manual flow ofliquidto the infant are helpful for
improvingfeeding.No single bottle and nipple com-bination tends to work better than
another,but trials with a variety oftypes using dif-ferent techniques are helpful
in optimizingfeeding early in life.Close attention toweight gain is necessary for
these children.Generally,in 24 hours each infant shouldhave approximately 2 to 3
ounces ofmilkfor each pound ofweight.Feeding sessionsshould last no longer than 35
minutes aslonger sessions are fatiguing and burnmore calories than the baby can
consume.Infants should be weighed at least weeklyusing the same scale,preferably at
theirpediatrician�s office.The subject ofbreast-feeding an infantwith a cleft
palate is controversial,withsome practitioners encouraging the prac-tice and others
strongly opposed to it.There are clear advantages to breast-feeding a
newborn,including passiveimmunologic contribution ofthe motherto the child in the
form ofsecretoryimmunoglobulin A and an experience thatenhances bonding between the
motherand child during such a critical period.61,62At the same time the infant�s
inability tocreate negative oral pressure will oftenmake successful nursing
difficult,ifnotimpossible.It is relatively common toencounter an exclusively
breast-fed infantwith severe dehydration and failure tothrive secondary to these
difficulties.Thisis especially a concern in infants that havea wide cleft ofthe
secondary palate,wherebreast-feeding may not be possible.Theauthors�approach with
regard to breast-feeding in the presence ofa cleft palate isto use a combined
protocol that includesintermittent feeding with the use ofa spe-cialized bottle (as
described above) andattempts at nursing.Breast milk may bepumped for use with the
specialized nip-ple and bottle that will provide the nutri-tional and immunologic
benefits desired.This also allows the parents to keep a morequantitative record
ofhow many ounceshave been ingested over the course oftheday since this is normally
difficult withbreast-feeding alone.At the same time themother and baby are not
deprived ofanopportunity to incorporate breast-feedinginto the daily regimen.This
approachobviously requires rigorous documenta-tion ofthe child�s
weight,consultationwith a lactation consultant and infantfeeding specialist,and
frequent follow-upevaluations through the surgeon and/orpediatrician.Treatment
Planning and Timing:OverviewThe timing ofcleft lip and palate repair
iscontroversial.Despite a number ofmean-ingful advancements in the care ofpatients
with cleft lip and palate,a lack ofconsensus exists regarding the timing
andspecific techniques used during each stageofcleft reconstruction.Surgeons
mustcontinue to carefully balance the function-al needs,esthetic concerns,and the
issue ofongoing growth when deciding how andwhen to intervene.In no other type
ofsur-gical problem is the issue ofearly surgery�seffect on growth more apparent
than inthe treatment ofcleft lip and palate defor-mities.The decision to surgically
manipu-late the tissues ofthe growing child shouldnot be made lightly and should
take intoaccount the possible growth restrictionthat can occur with early
surgery.Never-theless many patients with congenitaldeformities will benefit from
surgicalintervention based on functional or psy-chosocial reasons.Understanding
thegrowth and development ofthe craniofa-cial skeleton is critical to the
treatmentplanning process.33In many cases waitingfor a greater degree ofgrowth to
occur isadvantageous unless compelling function-al or esthetic issues are present
that cannot or should not wait.Due to many different treatmentphilosophies the
timing oftreatmentinterventions is considerably variableamongst cleft
centers.Therefore,it is diffi-cult to produce a timing regimen thateveryone agrees
on.Each stage ofsurgicalreconstruction and the suggested timingbased on the
patient�s age are presented inTable 42-1.Special considerations mayalter the
sequencing or timing ofthe vari-ous procedures based on individual func-tional or
esthetic needs.Cleft lip repair is generally undertakenat some point after 10 weeks
ofage.Oneadvantage ofwaiting until the child is 10 to12 weeks ofage is that it
allows a completemedical evaluation ofthe patient so that anyassociated congenital
defects affecting otherorgan systems (eg,cardiac or renal anom-alies) may be
uncovered.The surgical proce-dure itselfmay be easier when the child isslightly
larger and the anatomic landmarksmore prominent and well defined.Histori-cally the
anesthetic risk-related data sug-gested that the safest time period for surgeryin
this population ofinfants could be out-lined simply by using the �rule
of10�s.�Thisreferred to the idea ofdelaying lip repairuntil the child was at least
10 weeks old,10 pounds in weight,and with a minimumhemoglobin value of10
dL/mg.63,64Todaymore sophisticated pediatric techniques,advances in intraoperative
monitoring,andimproved anesthetic agents have all resultedin the ability to provide
safe general anes-thesia much earlier in life.65Despite the abil-ity to provide
safe anesthesia earlier in life,there is no measurable benefit to perform-ing lip
repair prior to 3 months ofage.64,66,67Some surgeons have advocated that liprepair
be carried out in the first days ofinfancy based on the idea ofcapitalizing onearly
�fetal-like�healing.Unfortunatelythese hoped-for benefits have not been
mechanism (velopharyngeal insufficiencyor VPI),and this may produce
hypernasalspeech.74These children are usually diag-nosed at 3 to 5 years ofage when
adetailed speech examination can beobtained by a skilled speech pathologistfamiliar
with clefts.When VPI is shown tobe consistent and due to a definableanatomic
defect,surgery is often helpfulin correcting this problem.A pharyngealflap or
sphincter pharyngoplasty may beused to treat VPI,with the goal ofimprov-ing closure
between the oral and nasalcavities and reducing nasal air escape dur-ing the
production ofcertain sounds.Thedetails ofassessment,diagnosis,and treat-ment ofVPI
associated with cleft palateare discussed in Chapter 44,�Reconstruc-tion ofCleft
Lip and Palate:SecondaryProcedures.�Approximately 75% ofpatients with any type
ofcleft will presentwith clefting ofthe maxilla and alveo-lus.24�26Bone graft
reconstruction ofthissite is performed during the mixed denti-tion prior to the
eruption ofthe perma-nent canine and/or the permanent lateralincisor.The timing
ofthis procedure isbased on dental development and notchronologic age.Based on work
by Boyneand Sands,most surgeons reconstruct thisarea during the mixed dentition
prior toeruption ofthe permanent canine.Earlierreconstruction ofthis area has been
asso-ciated with a high degree ofmaxillaryobserved,and problems with excessive
scar-ring and less favorable outcomes have beenencountered instead.68�70Children
mayhave more scarring at this early age,andtheir tissues are smaller and more
difficultto manipulate.Consequently the estheticoutcomes may be worse ifsurgery is
per-formed at an earlier age,and since there areno clear benefits to earlier repair
the recom-mendations for repair stand at approxi-mately 3 months ofage.Cleft palate
repair is usually performedat approximately 9 to 18 months ofage.Indeciding the
timing ofrepair the surgeonmust consider the delicate balance betweenfacial growth
restriction after early surgeryand speech development that requires anintact
palate.Most children will require anintact palate to produce certain speechsounds
by 18 months ofage.Ifdevelop-mental delay is present and speech will notlikely
develop until later,then the repair canbe delayed further.There is little evidence
tosuggest any benefit to palate repair prior to9 months ofage.71�73Repairs prior to
thistime are associated with a much higher inci-dence ofmaxillary hypoplasia later
in lifeand show no improvements in speech.Forthese reasons most surgeons will
performprimary palate repair at approximately 9 to12 months ofage.As the child
continues to develop,approximately 20% ofchildren will haveinadequate closure ofthe
velopharyngealCleft Lip and Palate: Comprehensive Treatment Planning and Primary
Repair845growth restriction requiring orthognathiccorrection later in life in a
much higherpercentage ofpatients.22,24The gold stan-dard for reconstruction in this
area isautogenous bone from the anterior iliaccrest.Cranial
bone,rib,tibia,symphysis ofthe mandible,zygoma,and allogeneicbone have all been
studied,but none havebeen shown to be appreciably better thanthe iliac
crest.26,75,76Orthognathic reconstruction ofmax-illary and mandibular discrepancies
is per-formed at 14 to 18 years ofage based onindividual growth
characteristics.26�36,38This is done in conjunction with ortho-dontics prior to and
after surgery.Howev-er,in some cases ofsevere maxillaryhypoplasia,early Le Fort I
osteotomy maybe performed to optimize facial estheticsand occlusion with the
supposition thatrevision osteotomies will likely be neces-sary.These early
osteotomies may compli-cate later treatment.Early orthognathiccorrection is
reserved for the most severedysmorphology,and in most cases theauthors prefer
standard orthognathictechniques.31�33Attempts at using distrac-tion osteogenesis
have been associatedwith a higher complication rate than withstandard orthognathic
techniques.32,42,77Orthognathic correction ofthe deformi-ties associated with cleft
lip and palatedefects is discussed in Chapter 61,�Orthognathic Surgery in the
Patient withCleft Palate.�As with the timing ofother interventions,lip and nasal
revision is best reserved untilafter the majority ofgrowth is complete.Mostofthe
lip and nasal growth is complete afterage 5 years.Lip revision can be
consideredprior to school age at about 5 years ofage.However,this may be performed
earlier ifthedeformity is severe.Nasal revision is per-formed after age 5 years as
most ofthe nasalgrowth is also complete by this time.Iforthognathic reconstruction
is likely,thenrhinoplasty is usually best performed afterorthognathic surgery as
maxillary advance-ment improves many characteristics ofnasalTable 42-1Staged
Reconstruction ofCleft Lip and Palate DeformitiesProcedureTimingCleft lip
repairAfter 10 weeks Cleft palate repair9�18 monthsPharyngeal flap or
pharyngoplasty3�5 years or later based on speech developmentMaxillary/alveolar
reconstruction 6�9 years based on dental developmentwith bone graftingCleft
orthognathic surgery14�16 years in girls,16�18 years in boysCleft rhinoplastyAfter
age 5 years but preferably at skeletal maturity;after orthognathic surgery when
possibleCleft lip revisionAnytime once initial remodeling and scar maturation is
complete but best performed after age 5 years
846Part 6: Maxillofacial Reconstructionsupport.However,when nasal deformity
isparticularly severe,rhinoplasty can be con-sidered earlier even iforthognathic
surgery isexpected.Multiple early revisions ofthe lip ornose should be avoided so
that excess scar-ring does not potentially impair ongoinggrowth.Secondary revisions
ofcleft lip andpalate deformities are discussed in Chapter44,�Reconstruction
ofCleft Lip and Palate:Secondary Procedures.�Cleft Lip and Palate RepairPresurgical
Taping and Presurgical OrthopedicsFacial taping with elastic devices is usedfor
application ofselective external pres-sure and may allow for improvement oflipand
nasal position prior to the lip repairprocedure.In the authors�opinions
thesetechniques often have greater impact incases ofwide bilateral cleft lip and
palatewhere manipulation ofthe premaxillarysegment may make primary repair techni-
cally easier.Although one ofthe basic sur-gical tenets ofwound repair is to
closewounds under minimal tension,attemptsat improving the arrangement ofthe seg-
ments using taping methods have notshown a measurable improvement.78�80Some
surgeons prefer presurgicalorthopedic (PSO) appliances rather thanlip taping to
achieve the same goals.81,82PSOappliances are composed ofa custom-madeacrylic base
plate that provides improvedanchorage in the molding oflip,nasal,andalveolar
structures during the presurgicalphase oftreatment (Figure 42-3).Althoughthe use
ofappliances probably makes foran easier surgical repair,there has been alack
ofclinical evidence to demonstratethat there is any measurable improve-ment in
esthetics ofthe nose or lip,den-tal arch relationship,tooth
survival,orocclusion.Studies have looked at the den-tal arch relationship outcomes
in patientswho have infant presurgical orthopedicdevices,and no improvement in
dentalarch relationship was seen.83,84Addition-ally no long-term improvement in
speechoutcome has be demonstrated in patientswho had PSOs.85Furthermore
concernsregarding potential negative conse-quences with these types
ofapplianceshave been raised.86PSOs also add signifi-cant cost and time to
treatment early inthe child�s life.Many appliances require ageneral anesthetic for
the initial impres-sion used to fabricate the device.Fre-quent appointments are
necessary formonitoring ofthe anatomic changes andperiodic appliance adjustment.The
Latham appliance was popular forexpanding and aligning the maxillary seg-ments
ofthe patient with a cleft palate.87Itis a pin-retained device that is inserted
intothe palate with acrylic extensions onto thealveolar ridges.A screw mechanism is
thenused to manipulate the segments as desired.The Latham appliance has been shown
tobe associated with significant growthrestriction ofthe midface when used
ininfancy to approximate the segments priorto definitive repair.86Children who
havehad Latham appliances have been shown tohave significant midfacial growth
restric-tion in adolescence 100% ofthe timewhereas children who have not had
theLatham appliance have midface hypoplasia25 to 35% ofthe time.42,80,86The
nasoalveolar molding appliancehas become popular with some surgeons inattempts to
manipulate the segments with-out pin retention prior to lip and noserepair (see
Figure 42-3).The appliancepopularized by Grayson is adjustable byremoving or adding
acrylic and manipu-lating protrusive elements that attempt tomold the nasal
cartilages.This deviceattempts to align the alveolar segments,lipstructures,and
nasal cartilages to optimizerepair.Unfortunately the hoped-for advan-tages ofthis
appliance have not been real-ized.Additionally no long-term data areavailable
regarding growth in the craniofa-cial skeleton after using this protocol.Thelimited
short-term data that are availablecannot be extrapolated to determine theultimate
outcome on growth,function,oresthetics.Some surgeons use gingivoperi-osteoplasty in
conjunction with the PSO,using limited flaps to close the alveoluscleft during the
primary repair ofthe lip orpalate.Many surgeons who use this appli-ance in
conjunction with their primary liprepairs will perform a gingivoperiosteo-plasty in
attempts to have bone form at theFIGURE42-3Frontal and lateral views ofthe Grayson
nasoalveolar moldingappliance showing the nasal projections that help to
theoretically mold thenasal cartilages and maxillary segments into a more
appropriate configura-tion prior to repair.
Cleft Lip and Palate: Comprehensive Treatment Planning and Primary
Repair847alveolus.This is more easily performedwith the segments aligned in close
proxim-ity as the flaps are small.82Experiences withsimilar techniques in the 1960s
involvingprimary bone grafting were poor withrespect to growth.22,23Additionally
therehas been no convincing long-term objec-tive data showing improvement in
eitherlip or nose esthetics.In their current state oftechnicalrefinement there is
no evidence that anyofthe PSOs offer an improved outcomewith respect to
esthetics,function,orgrowth in patients with cleft lip andpalate.Coupled with the
fact that appli-ances are time-consuming and have ahigh cost offabrication and
utilization,itis difficult to advocate their uniform use.As with other
interventions consideredfor patients with clefts,costly and un-proven interventions
should be avoided,although they may prove to be helpful insome select
cases.88Hopefully,long-termdata will be forthcoming and positive tohelp determine
which patients may bene-fit from PSO appliance treatment.Lip AdhesionSome surgeons
attempt to surgicallyapproximate the segments ofthe cleft lipprior to definitive
lip repair in an attemptto achieve a better relationship ofboth thelip structures
and the dental arches.89�91This is achieved by advancing small flapsoftissue across
the cleft site.While somesurgeons advocate the use ofthis tech-nique in wide
bilateral clefts,it is rarelyperformed in unilateral cases.When used,the lip
adhesion is usually completed at 3 months ofage.In most cases this willconvert a
wide complete cleft into a wideincomplete cleft as the scar will eventuallybe
excised from the cleft site recreating asimilar wide deformity.The definitive
liprepair is then completed 3 to 9 monthslater by excising the scar and reapproxi-
mating the remaining lip structures.Fur-thermore at the second procedure there
isusually less supple tissue to work withwhen performing the definitive repair
dueto scarring.As with most endeavors incleft surgery,repeated early
interventionstend to complicate later refinements dueto excessive scarring.In
general adequatemobilization ofthe flaps in one stage willmake tension-free skin
closure possible inalmost every case without the need fortaping,presurgical
orthopedic appliances,and/or lip adhesion.Unilateral Cleft Lip RepairClefts ofthe
lip and nose that are unilateralpresent with a high degree ofvariability,andthus
each repair design is unique (see Figure42-1).26,92The repair technique preferred
bythe authors for cleft lip and nasal deformities isshown in Figures 42-4 and 42-5
and is usuallyperformed after 10 weeks ofage.17,18,26,63Thebasic premise ofthe
repair is to create athree-layered closure ofskin,muscle,andmucosa that
approximates normal tissueand excises hypoplastic tissue at the
cleftmargins.Critical in the process is thereconstruction ofthe orbicularis oris
mus-culature into a continuous sphincter.TheMillard rotation-advancement
techniquehas the advantage ofallowing for each ofthe incision lines to fall within
the naturalcontours ofthe lip and nose.This is anadvantage because it is difficult
to achieve�mirror image�symmetry in the unilateralcleft lip and nose with the
normal sideimmediately adjacent to the surgical site.A Z-plasty technique such as
the Randall-Tennison repair may not achieve this levelofsymmetry because the Z-
shaped scar isdirectly adjacent to the linear noncleftedphiltrum (Figure 42-
6).Achieving symme-try is more difficult when the rotation por-tion ofthe cleft is
short in comparison tothe advancement segment.Primary nasal reconstruction may
beconsidered at the time oflip repair to repo-sition the displaced lower lateral
cartilagesand alar tissues.Several techniques areadvocated,and considerable
variation existswith respect to the exact nasal reconstruc-tion performed by each
surgeon.93,94Theprimary nasal repair may be achieved byreleasing the alar
base,augmenting the areawith allogeneic subdermal grafts,or even aformal open
rhinoplasty.Since lip repair isdone at such an early point in growth
anddevelopment,the authors prefer minimalsurgical dissection due to the effects
ofscar-ring on the subsequent growth ofthese tis-sues.McComb described a technique
thathas become popular,consisting ofdissect-ing the lower lateral cartilages free
from thealar base and the surrounding attachmentsthrough an alar crease
incision.93,95�97Thisallows the nose to be bolstered and/orstented from within the
nostril to improvesymmetry.Bilateral Lip RepairBilateral cleft lip repair can be
one ofthemost challenging technical proceduresperformed in children with clefts.The
lackofquality tissue present and the widelydisplaced segments are major challenges
toachieving exceptional results,but superiortechnique and adequate mobilization
ofthe tissue flaps usually yields excellentesthetic results (Figures 42-7�42-
10).Additionally the columella may be quiteshort in length,and the premaxillary
seg-ment may be significantly rotated.Ade-quate mobilization ofthe segments
andattention to the details ofonly usingappropriately developed tissue will
yieldexcellent results even in the face ofsignifi-cant asymmetry.Some surgeons have
used aggressivetechniques to surgically lengthen the col-umella and preserve
hypoplastic tissueusing banked fork flaps.98,99Early andaggressive tissue flaps in
the nostril and col-umella areas do not look natural after sig-nificant growth has
occurred and result inabnormal tissue contours.While surgicalattempts at
lengthening the columella maylook good initially,they frequently lookabnormally
long and excessively angularlater in life (Figure 42-11).Revision ofthese
iatrogenic deformities is difficult
848Part 6: Maxillofacial Reconstructionand some ofthe contour irregularities
willnot be able to be revised adequately.Usu-ally ifthe hypoplastic tissue is
excised andincisions within the medial nasal base andcolumella are avoided,the
long-termesthetic results are excellent.The authors prefer a primary
nasalreconstruction that can be performed in asimilar fashion to the unilateral
techniquedescribed by McComb.100This allows forrelease and repositioning ofthe
lower lat-eral cartilages and alar base on both sideswithout aggressive degloving
ofthe entirenasal complex.Other open rhinoplastytechniques have been suggested
usingeither direct incision on the nasal tip orthrough prolabial unwinding tech-
niques.100�103As with most early maneuversFIGURE42-4A,A complete unilateral cleft
ofthe lip is shown highlighting the hypoplastic tissue in the cleft site that is
not used in the reconstruction.Note the nasal deformities that are typical in the
unilateral cleft,including displaced lower lateral nasal cartilages,deviated
anterior septum,and nasalfloor clefting.B,The typical markings for the
authors�preferred repair are shown highlighting the need to excise the hypoplastic
tissue and approximategood vermilion and white roll tissue for the repair.C,Once
the hypoplastic tissue has been excised,the three layers oftissue are dissected
(skin,muscle,andmucosa).It is important to completely free the orbicularis oris
from its abnormal insertions on the anterior nasal spine area and lateral alar
base.Nasalflaps are also incorporated into the dissection to repair the nasal floor
(not shown).D,The orbicularis oris muscle is approximated with multiple inter-
rupted sutures,and the vermilion border/white roll complex is reconstructed.The
nasal floor and mucosal flaps are approximated.E,The lateral flap isadvanced and
the medial segment is rotated downward to create a healing scarline that will
resemble the natural philtral column on the opposite side.Theincision lines are
hidden in natural contours and folds ofthe nose and lip.ABCDE
Repair849aggressive rhinoplasty at this time mayincur early scarring that affects
the growthpotential ofthe surrounding tissues,mak-ing revision more difficult and
long-termesthetics less than ideal.Cleft Palate RepairThe term primary palateis
used to describethe anatomic structures anterior to the inci-sive foramen (eg,the
alveolar ridge,maxil-la,piriform rim).The termsecondary palaterefers to those
structures posterior to theincisive foramen.Therefore,when surgeonsrefer to the
initial or �primary�cleft palaterepair,they are actually describing the clo-sure
ofthe secondary palate structures thatinclude the hard palate,soft
palate,anduvula.The structures ofthe embryologicprimary palate are reconstructed
later inchildhood during the cleft maxillary/alveolar bone graft procedure.There
are two main goals ofcleft palaterepair during infancy:(1) the water-tightclosure
ofthe entire oronasal communica-tion involving the hard and soft palate;and(2) the
anatomic repair ofthe musculaturewithin the soft palate that is critical for nor-
mal creation ofspeech.The soft palate,orvelum,is part ofthe complex coupling
anddecoupling ofthe oral and nasal cavitiesinvolved in the production
ofspeech.Whena cleft ofthe soft palate is present there areabnormal muscle
insertions located at theposterior edge ofthe hard palate.Surgerymust not simply be
aimed at closing thepalatal defect but rather at the release ofabnormal muscle
insertions.Muscle conti-nuity with correct orientation should beestablished so that
the velum may serve as adynamic structure.The exact timing ofrepair ofa palatecleft
is controversial.Generally the velummust be closed prior to the developmentofspeech
sounds that require an intactpalate.On average this level ofspeech pro-duction is
observed by about 18 months ofage in the normally developing child.Iftherepair is
completed after this time,com-pensatory speech articulations may result.Repair
completed prior to this time allowsfor the intact velum to close
effectively,appropriately separating the nasopharynxfrom the orophayrynx during
certainspeech sounds.104�107FIGURE42-5A,Three-month-old child with a right-sided
incomplete unilateral cleft lip.Note the short philtrum near the midline that must
be rotateddownward to avoid notching and to improve symmetry.B,Nine-month-old boy
after the rotation-advancement repair ofhis cleft lip and nasal deformi-ties.C,The
same child inB 21/2years after his cleft lip and nasal repairs.ABCFIGURE42-6A
typical scar that may resultfrom a Z-type lengthening repair.Although thelength and
symmetry ofthe lip is good,anunnatural contour can occur due to the Zshapeofthe
closure.
850Part 6: Maxillofacial ReconstructionIn patients with cleft palate,concerns
fornormal speech development are frequentlybalanced with the known biologic conse-
quences ofsurgery during infancy;namely,the problem ofsurgery during the
growthphase resulting in maxillary growth restric-tion.33,72,73,108When repair
ofthe palate isperformed between 9 and 18 months ofage,the incidence ofassociated
growth restric-tion affecting the maxillary development isapproximately
25%.31,33,109�111Ifrepair iscarried out earlier than 9 months ofage,then severe
growth restriction requiringfuture orthognathic surgery is seen withgreater
frequency.22,26,31,33,109,112�114At theFIGURE42-7A,The bilateral cleft ofthe lip
and maxilla shown here is complete and highlights the hypoplastic tissue along the
cleft edges.The impor-tance ofthe nasal deformity is evident in the shorter
columella and disrupted nasal complexes.B,Markings ofthe authors�preferred repair
are shown withan emphasis on excision ofhypoplastic tissue and approximating more
normal tissue with the advancement flaps.C,A new philtrum is created by excis-ing
the lateral hypoplastic tissue and elevating the philtrum superiorly.Additionally
the lateral advancement flaps are dissected into three distinct
layers(skin,muscle,and mucosa).Nasal floor reconstruction is also performed.D,The
orbicularis oris musculature is approximated in the midline with multi-ple
interrupted and/or mattress sutures.This is a critical step in the total
reconstruction ofthe functional lip.There is no musculature present in the pre-
maxillary segment,and this must be brought to the midline from each lateral
advancement flap.The nasal floor flaps are sutured at this time as well.Thenew
vermillion border is reconstructed in the midline with good white-roll tissue
advanced from the lateral flaps.E,The final approximation ofthe skinand mucosal
tissues is performed leaving the healing incision lines in natural contours ofthe
lip and nose.ABDEC
Cleft Lip and Palate: Comprehensive Treatment Planning and Primary Repair851same
time proceeding with palatoplastyprior to 9 months ofage is not associatedwith any
increased benefit in terms ofspeechdevelopment so the result is an increase
ingrowth-related problems with an absence ofany functional benefit.115,116Using
only thechronologic age it seems that carrying outthe operation during the 9 to 18
monthstimeline best balances the need to addressfunctional concerns such as speech
develop-ment with the potential negative impact ongrowth.To date no case-controlled
rigorousclinical trial has examined what is likely themost critical factor in
dictating the exacttiming ofcleft repair�the individual child�strue language age.In
cases where significantdevelopmental delay is present surgeryshould be delayed
since speech formation isnot yet an issue and there is a likely benefit interms
ofgrowth ofthe maxilla.Delayingpalatal closure is relevant in situations wherethe
cleft palate is associated with other com-plex medical conditions,neurodevelopmen-
tal delay,complex craniofacial anomalies,and/or the presence ofa
tracheotomy.Another approach used to balancespeech issues with growth-related con-
cerns is to stage the closure ofthe sec-ondary palate with two operations.Gener-
ally this involves the repair ofthe softpalate early in life as an initial
step,fol-lowed by closure ofthe hard palate later ininfancy.The idea is that timely
repair ofthe soft palate,which is critical for speech,is accomplished while hard
palate repairwith mucoperiosteal stripping is delayeduntil growth is further
along.117,118Although this technique is not advocatedby the majority
ofsurgeons,some sur-geons may feel that repairing the hardpalate portion later may
offer the advan-tages ofless growth restriction,easierrepair oflarger clefts,and
less chance forfistula formation.No convincing data existto favor this approach
over a single-stagerepair,but the practice is continued bysome centers where
anecdotal evidencesuggests that there may be some benefit.Incontrast most North
American speech andlanguage pathologists prefer closure ofthepalate as a single
operation.117Cleft palate reconstruction requires themobilization ofmultilayered
flaps to recon-struct the defect due to the failure offusionofthe palatal
shelves.Generally when theinitial palate closure is performed,thisrefers to closure
ofthe tissues posterior tothe incisive foramen.This is done in a lay-ered fashion
by first closing the nasalmucosa and then the oral mucosa.Since themain function
ofthe palate is to close theFIGURE42-8A,Presurgical appearance ofthe incomplete
bilateral cleft lip ofa 3-month-old boy.B,Surgical markings for excision ofthe
hypoplastic tissue and the planned creation ofa new philtrum.Advancement flaps from
the lateral lip segments bring good white-roll to the midline via small cut-
backs.C,The same child at 1 year ofage after the repair ofhis bilateral cleft
lip.ABCFIGURE42-9A,Presurgical appearance ofa bilateral cleft lip and palate with
impressive asymmetryand rotation ofthe premaxillary segment.Note the significant
nasal asymmetry and bunching oftheorbicularis oris laterally.B,The same child at 14
months ofage.AB
852Part 6: Maxillofacial Reconstructionspace between the nasopharynx andoropharynx
during certain speech sounds,the surgeon must also reconstruct the mus-culature
ofthe velopharyngeal mechanism.The musculature ofthe levator palatini isabnormally
inserted on the posterior aspectofthe hard palate and therefore must bedisinserted
and reconstructed in the mid-line.26,119Therefore,the soft palate is closedin three
layers by approximating the nasalmucosa,levator musculature,and the oralmucosa.The
hard palate portion is closedin two layers using nasal mucosa flaps andthen oral
mucosa flaps.Both the hard andsoft palate repairs must be done in a tension-free
manner to avoid wound break-down and fistula formation.Adequatemobilization ofthe
flaps during the dissec-tion is essential to achieve tension-free closure.At times
some surgeons may electto incorporate vomer flaps into the repair ifthere is
difficulty in mobilizing the lateralflaps to the midline.Many techniques have been
describedfor repair ofthe palate.120�127The Bardachtwo-flap palatoplasty uses two
large full-thickness flaps that are mobilized with FIGURE42-10A,Presurgical frontal
view ofa wide bilateral cleft lip and palate with significant asymmetry and lack
ofcolumella length.B,Presurgicalleft lateral view ofa wide bilateral cleft lip and
palate with a protrusive premaxillary segment.Note the short columella length.C,The
same child at 10 months ofage after repair ofher bilateral cleft lip and palate.No
presurgical taping or orthopedic appliances were used.ABCFIGURE42-11A,Frontal view
ofa teenage girl who had undergone columella lengthening and banked fork flaps
during her initial repair and multipleattempts at secondary rhinoplasty by another
surgeon prior to orthognathic surgery.B,Frontal view ofa patient who underwent
columella lengtheningand banked fork flaps during her initial repair.C,Lateral view
ofthe patient fromB with a columella that is curved upwards and abnormally
angular.ABC
Cleft Lip and Palate: Comprehensive Treatment Planning and Primary Repair853layered
dissection and brought to the mid-line for closure (Figure 42-
12).26,120Thistechnique preserves the palatal neurovascu-lar bundle as well as a
lateral pedicle for ade-quate blood supply.The von Langenbecktechnique is similar
to the Bardach palato-plasty but preserves an anterior pedicle forincreased blood
supply to the flaps.26,121This technique is also successful in achiev-ing a layered
closure but may be more diffi-cult when suturing the nasal mucosa nearthe
anteriorly based pedicle attachments.The authors do not favor push-back tech-niques
as they may incur more palatal scar-ring,restrict growth,and do not show
ameasurable benefit in speech.Another common technique is the Fur-low double-
opposing Zplasty,whichattempts to lengthen the palate by takingadvantage ofa Z-
plasty technique on boththe nasal mucosa and the oral mucosa (Fig-ure 42-
13).26,124�127This technique can beeffective at closing the palate but has
beenreported by some to have a higher rate offistula formation at the junction
ofthe softand hard palates where theoretical length-ening ofthe soft palate may
compromisethe closure.26,128�133No benefit has beenconvincingly demonstrated with
any par-ticular repair technique when one looks atdental arch form,speech
outcome,feeding,or any other functional variable.At thispoint in our understanding
surgeons oftenconsider their own experiences and train-ing when repairing
clefts,since definitivedata suggesting that one repair is preferableover another
are lacking.In very wide clefts some surgeons willadvocate the consideration ofa
pharyn-geal flap at the primary palatoplasty pro-cedure to assist in closure since
revisionpalatoplasty is sometimes unsuccessful ineradicating fistulas.Those who use
thistechnique usually perform it in extremelywide clefts and do so very
selectively.Thisallows the central portion ofthe closure tobe filled with posterior
pharyngeal walltissue making the closure ofthe nasal andpalatal mucosa
easier.Patients with PierreRobin syndrome or Treacher Collins syn-drome may have
exceptionally wide cleftsthat are difficult to close with no tension,and this
technique may be considered.Thedrawbacks ofusing a pharyngeal flap dur-ing the
repair ofthe palate include a sig-nificantly increased risk for complicationssuch
as bleeding,snoring,obstructivesleep apnea,or hyponasality.The details ofpharyngeal
flap surgery and revisionpalatoplasty techniques are discussed inChapter
44,�Reconstruction ofCleft Lipand Palate:Secondary Procedures.�Complex Facial
CleftingClefting ofthe facial structures other thanthe typical nasolabial region is
rare andoften presents difficult challenges to thereconstructive cleft
surgeon.Therefore it isimportant to consider referring patientsFIGURE42-12A,A
unilateral cleft ofthe primary and secondary palates is shown with the
typicalinvolvement from the anterior vestibule to the uvula.B,The Bardach
palatoplasty technique requirestwo large full-thickness mucoperiosteal flaps to be
elevated from each palate shelf.The anterior por-tion (anterior to the incisive
foramen) ofthe cleft is not reconstructed until the mixed dentition stage.C,A
layered closure is performed in the Bardach palatoplasty by reapproximating the
nasal mucosa.The muscle bellies ofthe levator palatini are elevated offoftheir
abnormal insertions on the posteri-or palate.They are then reapproximated in the
midline to create a dynamic functional sling for speechpurposes.D,Once the nasal
mucosa and musculature ofthe soft palate are approximated,the oralmucosa is closed
in the midline.The lateral releasing incisions are quite easily closed primarily
due tothe length gained from the depth ofthe palate.In rare cases,in very wide
clefts a portion ofthe later-al incisions may remain open and granulate by
secondary intention.ABCD
854Part 6: Maxillofacial Reconstructionwith complex facial clefting to surgeonswith
experience in this particular area.Comprehensive interdisciplinary care ismandatory
to achieve the best resultsincluding involvement
ofneurosurgery,ophthalmology,orthodontics,speechpathology,and other members
ofthecraniofacial team.Some interventionssuch as eye lubrication may be
necessarywithin hours after birth,and accurate pre-natal diagnosis ofsevere facial
clefting ishelpful in planning for early care.The etiology ofthe various facial
cleftsmay be related to failure ofembryologicfusion,physical obstruction in fetal
life,association with an encephalocele ortumor,amniotic bands,or other
anatomicdisruptions during fetal life.55The vastmajority ofcomplex facial clefts
are spo-radic events and not related to a singlegene disease.Many complex facial
cleftsinvolve the orbit,and the classification sys-tem most often used is
orbitocentric indesign (see Figure 42-2).Paul Tessierdescribed a numbering system
for facialclefting phenomena to make descriptionand surgical planning more easily
dis-cussed.56Other systems exist but have amore cumbersome nomenclature.57Primary
repair ofsevere facial clefts isoften more difficult than even the mostdifficult
standard bilateral clefts.134�136While mobilization ofthe lip and nosestructures is
rather straightforward,theclosure ofclefts in the orbital region canbe challenging
due to the lack ofeyelidand adjacent tissue for advancementand/or rotation.Revision
surgery is thenorm in this group and should include askilled ophthalmologic surgeon
early inthe process for the best results.The staged reconstruction ofthesetypes
ofsevere facial clefts is similar to themore common cleft lip and palate
protocols.However,several functional issues are pre-sent in patients with complex
facial cleftingthat require more immediate attention.Forexample,patients with large
Tessier no.7clefts may have problems with retainingfoodstuffs in their oral
cavities due to thediscontinuity ofthe orbicularis oris (Figure42-14).This may
prompt early repair andreestablishment ofthe orbicularis oris mus-culature for
functional concerns.For those patients with orbital clefts askilled pediatric
ophthalmologist shouldevaluate the child early to avoid severecorneal abrasion and
desiccation.Immedi-ate lubrication ofthe globes is necessary toprevent severe
irreversible corneal damageuntil eyelid structures can be mobilized tocover the
globe adequately.Early afterbirth tarsorrhaphy stitches can be used togain adequate
closure ofthe lids forcorneal protection.Ignoring the need foreye protection may
result in severe cornealscarring that may cause blindness andprompt consideration
for corneal trans-plantation.Corneal transplants in infantsFIGURE42-13A,A complete
cleft ofthe secondary palate (both hard and soft) is shown from theincisive foramen
to the uvula.B,The Furlow double-opposing Z-plasty technique requires that sepa-
rate Z-plasty flaps be developed on the oral and then nasal side.Note the cutbacks
creating the nasalside flaps highlighted in blue.C,The flaps are then transposed to
theoretically lengthen the soft palate.A nasal side closure is completed in the
standard fashion anterior to the junction ofthe hard and softpalate.Generally this
junction is the highest area oftension and can be difficult to close.This con-
tributes to the higher fistula rate in this type ofrepair.D,The oral side flaps are
then transposed andclosed in a similar fashion completing the palate closure.ABCD
Cleft Lip and Palate: Comprehensive Treatment Planning and Primary Repair855are
often not successful but are possible inpatients with severe orbitofacial
clefts.Another concern is the support oftheglobes at the orbit floor that may
beinvolved in some facial clefts.The timingoforbital reconstruction is dependent
onthe functional needs ofthe cleft area ineach patient.These are just some
oftheconcerns present in complex facial cleft-ing,and a customized treatment plan
mustbe formulated for each patient.Outcome AssessmentDecision-making in cleft care
should bebased on evidenced-based research and acritical look at
outcomes.Unfortunatelythere is little evidenced-based researchavailable to guide
clinicians through themany treatment protocols for cleft care.113Although the
clinical experience ofthe sur-geon certainly has value,this must be inte-grated
with a constant review ofevidence-based research.Typically enthusiasm by asurgeon
or a particular group ofsurgeonsregarding a specific intervention because
ofpersonal experiences may help popularizethat intervention but with little
outcomedata to support its use.Too frequently thelong-term results are not
forthcoming,andthe treatment regimen may still persist.Unfortunately some ofthe
treatment regi-mens used today are based on the poor out-comes and mishaps
ofprevious surgeonsrather than regimens chosen as a conse-quence ofpublished
evidence ofthe actualsuccess ofa particular treatment.Additionally the pressures
ofa costlyhealth care system have made treatmentdecision questions even harder to
investi-gate.88A need to understand the outcomedifferences between treatment
philoso-phies will be critical to help determinewhich protocols will be most
beneficial tothe patient without extending valuablehealth care resources on
unproven or inef-fective methods.For this reason amongmany others,the need to
discardunproven and unnecessary interventionshas never been greater.Outcomes
studiesbased on functional results such asappearance,facial
growth,occlusion,patient satisfaction,and psychosocialdevelopment are all critical
in thisprocess.Surgeons involved in the care ofpatients with clefts must critically
reviewthe literature on a regular basis and not betempted by poorly evaluated
techniquespopularized by clinical reports.ConclusionsThe comprehensive care
ofpatients withclefts requires an interdisciplinaryapproach that demands precise
surgicalexecution ofthe various procedures neces-sary to correct cleft
deformities,as well asfrequent long-term follow-up.Cliniciansexperienced in the
comprehensive inter-disciplinary care ofpatients with clefts arebest equipped to
deal with these concerns.The treatment ofpatients with cleft andcraniofacial
deformities should be free ofbias and should demand team care that
ispatient,family,and community oriented.Only in this fashion can the overall treat-
ment be optimally successful.This type ofcare maximizes the patient�s ability
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(PA):W.B.Saunders;2000.p.487�502.
CHAPTER 43Reconstruction ofthe Alveolar CleftPeter E.Larsen,DDSIn the management
ofpatients with cleftlip and cleft palate,the decision regardingalveolar cleft
grafting is one ofthe mostcontroversial.Is grafting ofthe residualalveolar defect
indicated? Ifso,at what ageis it most appropriate,what material ismost ideal,and
should adjunctive proce-dures such as orthodontic expansion beused before or after
grafting? Lastly,whatare appropriate measures ofsuccess? Thischapter reviews what
is known,discussesthese controversies,and provides a ratio-nale for the approach to
the residual alve-olar cleft defect.Rationale for GraftingAlthough some authors
have advocatednongrafting techniques1or prosthodonticapproaches,the general
consensus is thatachieving continuity between the cleftalveolar segments has
significant advan-tages,regardless ofhow and when this isaccomplished.Potential
advantagesinclude the following2:1.Grafting achieves stability ofthe archand
prevents collapse ofthe alveolarsegments.This provides improvedorthodontic
stability2.Grafting preserves the health ofthedentition.Grafting provides room
forthe canine and lateral incisors to eruptinto the arch into stable alveolar
boneand maintains bony support ofteethadjacent to the cleft3,43.Grafting restores
continuity not onlyofthe alveolus,but also ofthe maxillaat the piriform rim.This
supports theala and provides improved stabilityand support for the nose.This
mayhave a direct esthetic benefit and mayalso prove to be oflong-term benefitwhen
formal rhinoplasty proceduresare performed34.Palatal and nasolabial fistulas are
oftenpresent even following palatoplasty.Grafting ofthe alveolar defect pro-vides
an opportunity for the surgeonto address the residual oronasal fistu-la.This may
have potential benefit forboth hygiene and speech.Many cleftpatients present with
chronic upperrespiratory and sinus disease,whichmay be related to reflux into the
nasalcavity and sinus.There is some evi-dence that the residual
fistula,whetherlabial or palatal can have an effect onspeech articulation and
nasality.Thereis evidence that closure ofthe fistulaand grafting the cleft defect
canimprove nasal emission and nasality5Measuring OutcomesPrior to discussing the
controversiesassociated with reconstruction oftheresidual alveolar cleft,it is
important toaccept some consistent measure ofsuc-cessful outcome.Most reports rely
ondescriptive data.This makes comparisonofdifferent approaches difficult.To eval-
uate bone graft success,Bergland andcolleagues described a semiquantitativeapproach
that divided grafts into fourtypes based on alveolar crest height.6While this is
effective,it has been sug-gested that occlusal alveolar bone heightdoes not
adequately measure success.7Support ofthe ala and opportunity forsuccessful tooth
movement into the siteor placement ofan endosseous implantalso requires apical bone
formation.Amodification ofthe Bergland scale thatmeasures both occlusal and basal
boneheight may be a better tool for evaluatinggraft success.Although the
Berglandscale and modifications ofit rely on atwo-dimensional radiograph to
evaluatebone fill within a three-dimensionalcleft,studies show good
correlationbetween bone volume as predicted bythese two-dimensional radiographs
andthat shown on three-dimensional com-puted tomography scans.8Timing ofthe
GraftPerhaps the most controversial topic inmanaging the alveolar cleft is when
graft-ing should be performed.In the tradition-al literature,terminology is not
consistent.Outcome measures for various approachesare also defined
inconsistently,whichmakes comparison difficult.Here,alveolargrafting will be
grouped according to tim-ing as defined below (Table 43-1).
860Part 6: Maxillofacial ReconstructionPrimary GraftingSome define primary alveolar
bone graft-ing as that which is performed simultane-ously with lip repair.9Others
have statedthat any grafting that is performed at lessthan 2 years ofage is
considered primarygrafting.Still others have defined primarygrafting as grafting
that is performedbefore the palate is repaired.10,11Primary grafting performed at
thetime oflip repair has failed to result inacceptable outcome.Long-term
studiesshow abnormal maxillary developmentwith maxillary retrognathia,concave pro-
file,and increased frequency ofcrossbitecompared with patients without
grafts.12,13Primary grafting performed after theclosure ofthe lip and before the
closure ofthe palate has proven successful in a limitednumber ofcenters when a very
specific pro-tocol is followed.10,11A prosthesis is placedbefore the lip is closed
to mold the alveolarsegments into close proximity.The lip isthen closed,and this
further aids in mold-ing the segments.The segments must be inclose proximity with
good arch form beforean onlay rib graft is placed across the labialsurface ofthe
cleft in a subperiosteal tunnelthat is developed by limited dissection.Advocates
ofthis approach have notexperienced problems with altered facialgrowth and
malocclusion,most likely theresult ofthe limited dissection used in thesecases.They
have reported improved occlu-sion and graft success in these patients,compared with
patients grafted at otherages.14It is still difficult to wholeheartedlyendorse this
approach.Several additionalanesthetics and surgeries are needed at ayoung age.This
technique may not be pos-sible in all patients,such as those with iso-lated
alveolar clefts without palatal cleftingor those patients in whom segments cannotbe
orthopedically aligned.In one center,because ofthese limitations,nearly one-
halfofpatients could not be treated withprimary grafting.10Outcomes may also notbe
as good as with other approaches.In onestudy,15there was an increased incidence
ofmalformation ofpermanent lateral incisorsin the primary graft group and
decreasedsuccess ofthe graft,with only 41% ofpri-mary grafts (54% ifpregrafting
orthopedicswas included) resulting in adequate boneheight when measured with a
Berglandscale.This was compared with 73% successofthose sites grafted in the mixed
dentitionstage (after eruption ofthe permanent cen-tral incisors and before
eruption ofthemaxillary canine).Early Secondary GraftingGrafting after the child
reaches 2 years ofage and before 6 years is considered earlysecondary grafting.The
literature does notsupport early secondary grafting.Secondary Grafting During the
Mixed Dentition (after Eruption ofthe Maxillary Central Incisors and beforeEruption
ofthe Canine)Alveolar reconstruction with grafting dur-ing the eruption ofthe
permanent denti-tion may be best for various reasons.Rationale for grafting and for
timing ofgrafting during this time period includethe following:1.There is minimal
maxillary growthafter age 6 to 7 years,and the effect ofgrafting at this time will
result in mini-mal to no alteration offacial growth16,172.Cooperation with
orthodontic andperioperative care is predictable.General anesthesia is not required
forroutine orthodontic procedures suchas expansion3.The donor site for graft
harvest is ofacceptable volume for predictablegrafting with autogenous bone4.Bone
volume may be improved byeruption ofthe tooth into the newlygrafted
bone185.Grafting during this phase allowsplacement ofthe graft before
eruptionofpermanent teeth into the cleft site,which achieves one ofthe primarygoals
ofgrafting � to enhance thehealth ofteeth in and adjacent to thealveolar cleftThe
landmark papers by Boyne andSands established that grafting in the mixeddentition
achieves many ofthe goals ofreconstruction ofthe cleft alveolus.19,20Theideal
patient is between the ages of8 and 12 years with a maxillary canine root that
isone-halfto two-thirds developed.This tim-ing is supported by several well-
documentedstudies.6,21�25However,some authors havesuggested that earlier grafting
should beconsidered as a means ofpreserving the lat-eral incisor as
well.12,26,27These authorshave suggested that grafting be consideredas early as 6
years ofage.There is some evi-dence that grafting between the ages of6 and 8
years,in addition to achieving theexpected goal ofpreserving the canine,canpreserve
the lateral incisor as well,but thisremains controversial.Despite clear indica-
tions that grafting in the mixed dentition ispreferable to either primary,early
sec-ondary,or late secondary grafting,it is notentirely clear whether this grafting
shouldbe performed early (age 6�8 years) or late(age 8�12 years).Various individual
factorsshould be evaluated when determining theideal time for grafting during the
mixeddentition (Table 43-2).Table 43-1Timing ofAlveolar BoneGrafting< 2 Years
ofAge: Primary GraftingAfter lip repairBefore palate repair=2 Years ofAge:
Secondary GraftingAge in years2�5:Early secondary 6�12:Mixed dentition secondary
(after central incisor eruption and before the canine erupts)6�8:Early mixed
dentition9�12:Late mixed dentition> 12:Late secondary grafting
Reconstruction ofthe Alveolar Cleft861Dental Versus Chronologic AgeManyoutcomes
ofgrafting are related to pre-serving health ofthe dentition adjacent toand
erupting into the cleft site.It makessense that the timing ofthe graft be deter-
mined on the basis ofdental rather thanchronologic age.When the maxillary cen-tral
incisors begin to erupt,regardless ofchronologic age,the patient should beevaluated
for grafting,taking into consid-eration the other factors discussed below.In some
patients this may be much earlierthan the traditionally recommended agefor
evaluation.Presence ofthe Lateral IncisorManyproponents ofearlier mixed
dentitiongrafting advocate this timing because ofthe opportunity to salvage the
lateralincisor.12,24,26During the evaluation,atten-tion should be directed to the
presence ofthe lateral incisor and to whether thistooth appears to be normally
formed.Theincidence ofcongenitally missing perma-nent lateral incisors within the
alveolarcleft is between 35 and 60%.15,28Ifa later-al incisor is present and
appears to be wellformed,earlier grafting may be beneficial.Even ifthe tooth is not
perfectly formed,itmay still be beneficial to attempt to pre-serve it.The grafted
alveolus will oftenthin to the point that alveolar width is notadequate for
definitive reconstructionwith an endosseous implant without addi-tional
grafting.29Retaining the lateralincisor will maintain bone width and per-haps
eliminate the need for yet anothergraft at the time ofimplant placement.Position
ofthe Lateral IncisorIfthe lat-eral incisor is mesial to the cleft it often
hasadequate space for eruption.However,ifthe lateral incisor is located in the
posteri-or segment,earlier grafting may be neces-sary to preserve the lateral
incisor.9In onereview,36% ofpatients with cleft lip andalveolus had missing lateral
incisors.Ofthe 64% who had lateral incisors,90% ofthe lateral incisors were located
distal tothe cleft.In the same series ofpatients,57% ofthose with cleft lip and
palate hadmissing lateral incisors,and ofthe remain-ing 43%,86% ofthe lateral
incisors werelocated distal to the cleft.28Therefore,asignificant number ofpatients
may benefitfrom earlier grafting to preserve the lateralincisor (Figure 43-
1).Rotation ofthe Central IncisorThemaxillary permanent central incisor willoften
erupt in a rotated and angled posi-tion (Figure 43-2).This reflects the mor-phology
ofthe underlying bone.Inextreme cases,the crowding ofthe twoincisors can preclude
normal oralhygiene methods,and this can lead todecay ofthe central incisor.The
patientor parent may also be concerned with theposition ofthe incisors for social
rea-sons.Ifa decision is made to rotate theseteeth into alignment,it may be
necessaryto graft the alveolar defect prior to thisorthodontic tooth
movement.30Failureto consider the morphology ofthe boneon the distal surface ofthe
erupted cen-tral incisor can result in bone loss andperiodontal defects as a result
ofortho-dontic tooth movement.Since the incisorteeth erupt around age 6 years,the
sur-geon may choose to graft at an earlier ageso that orthodontic movement
oftheincisors can be accomplished.Social IssuesThe window for mixeddentition
grafting is large (age 6�12 years).This is also during a period oftremendoussocial
development for the patient.Ifagraft is necessary,the timing ofsurgeryshould
respect the social and educationaldevelopment ofthe child.Slightly
earliergrafting,when it may cause less interfer-ence with education or other
importantopportunities for social development,maybe preferable to grafting at an
exact stageofdental development.Size ofthe Patient and ofthe CleftPetitepatients
with large cleft defects are chal-lenging.Adequate closure ofthe defectmay be
difficult,and harvesting an ade-quate amount ofgraft material may bechallenging as
well.This is particularly truefor large bilateral cleft defects.In
thesepatients,the lateral incisor is often absent,the oronasal communication is
often quiteTable 43-2Factors Contributing to Timing ofGrafting During the Mixed
DentitionDental age vs chronologic agePresence ofthe lateral incisorPosition ofthe
lateral incisor Degree ofrotation/angulation ofthe central incisorTrauma/mobility
ofpremaxillary segment (bilateral clefts)Social issuesSize ofthe patient and ofthe
cleftOcclusionNeed for adjunctive proceduresDynamic ofthe teamFIGURE43-1A,Occlusal
radiograph shows lat-eral incisor distal to the cleft.B,Grafting whichwas done at
age 7 years to facilitate eruption ofthe lateral incisor.AB
862Part 6: Maxillofacial Reconstructionlarge,and the premaxilla is frequently
inless than ideal position.In these largedefects,later grafting is often better,to
waitfor growth ofthe patient and orthodonticalignment ofthe cleft segments.Need for
Other ProceduresPatients areoften evaluated for velopharyngeal incom-petence,minor
esthetic revision ofthenose or the lip,and pressure-equalizingtubes for otitis
media.It is reasonable tocoordinate the timing ofsurgery for thealveolar cleft with
other procedures thatmay be necessary.Ifvelopharyngeal flapsurgery is planned
during the mixed denti-tion phase,it should take precedence overthe alveolar
graft.Improved speech is moreimportant to the child�s development thanachieving
continuity ofthe alveolus.Alveo-lar grafting would be compromised ifper-formed
simultaneously with velopharyn-geal flap surgery,and in these patients,it
isappropriate to delay the graft until thevelopharyngeal flap surgery is accom-
plished and speech therapy re-instituted.Minor soft tissue,nasal,and lip revision
areoften desired by the patient and parents.These can be accomplished with
alveolargrafting.The grafting process can distortthe nose and soft tissue;these
soft tissueprocedures should be performed first withalveolar grafting undertaken in
the samesetting and with care not to disrupt theesthetic procedures already
done.Dynamic ofthe TeamCleft manage-ment should always involve a multidisci-plinary
team,with the wide expertise todevelop a proper treatment plan.Difficul-ties may
arise when the priorities ofonespecialty compete with those ofanother.Ifthe
surgical team is faced with an ortho-dontic provider who feels strongly that it
isappropriate to align the maxillary centralincisors as soon as they erupt,it will
benecessary for the alveolar defect to begrafted earlier to prevent compromise
ofosseous support for the central incisors.Some orthodontists and surgeons
believethat palatal expansion is necessary prior tografting.These teams may find
that it ismore appropriate to graft patients at alater age,as it may take months to
achievethe desired expansion prior to the graft.Secondary Grafting after
Eruptionofthe Permanent Canine (Late Secondary Grafting)Late secondary grafting has
receivedsome support;however,data show thatwhen all the goals ofalveolar
reconstruc-tion are considered it has a less thanacceptable outcome.Patients older
than12 years ofage who undergo graftinghave been reported to have decreasedsuccess
when evaluated using the Berg-land scale,6,15,25,27,31,32loss ofosseous sup-port
ofteeth adjacent to the cleft,18andincreased morbidity.27There is lessopportunity
to salvage the lateral incisor,and there is a delay in correction oftheorthodontic
condition.This delayedgrafting does allow for increased optionswith regard to donor
site for graft mate-rial,as harvest ofthe mandibular symph-ysis becomes
possible.Such grafts aredifficult in the mixed dentition stage,where it is
difficult to obtain adequatebone without damaging unerupted teeth.Source ofBone
GraftThe selection ofthe ideal grafting materialis somewhat dependent on the timing
ofthe graft.In primary bone grafting,the ribis the only site for adequate quantity
ofbone with acceptable morbidity.In themixed dentition stage,the rib is not
asappropriate as other sites such as the cal-varia or iliac crest.These options
wouldalso be possible sources for bone for latesecondary grafting,as well as grafts
fromthe mandibular symphysis and possiblythe tibia.As the data suggest that
grafting dur-ing the mixed dentition is ideal,discussionwill focus on comparing
various sources ofgraft material for this group ofpatients.The advantages and
disadvantages ofvari-ous potential sources ofbone are outlinedin Table 43-3.Iliac
CrestPotential advantages ofthe iliac crest bonegraft include low morbidity and
high vol-ume ofviable osteoblastic cells (cancellousbone);two teams may work
simultaneous-ly,and this procedure is well accepted bythe patient.Bone can be
harvested from the iliaccrest through various approaches.Somehave suggested that a
lateral approach isappropriate in the growing patient.33Thisprocedure disrupts the
iliotibial tract andhas a higher incidence ofgait disturbanceand postoperative
pain.34In theory it maybe appropriate to avoid the anterior crest,which does not
complete its growth untilafter age 20 years.34However,the carti-FIGURE43-
2A,Photograph ofa typical unilateral cleft.There is rotation ofthe central incisor
andangulation ofthe crown toward the cleft.This maintains bone support for the root
ofthe tooth.B,Occlusal radiograph shows that the cleft defect is larger than it
appears clinically and support for theincisor root is provided by only a thin
margin ofbone.AB
Reconstruction ofthe Alveolar Cleft863laginous cap overlying the crest is reducedin
thickness to about 1cm by age 9 years.Damage to the crest at this time could leadto
disturbance in growth and cosmeticdeformity ofthe crest;however,splittingthe crest
longitudinally,which allowsaccess to the underlying cancellous mar-row,has been
used for harvest ofbone inthis age-group with no reported growthalteration and less
postoperative gait dis-turbance than with the lateral
subcrestalapproach.35,36Calvarial BoneCalvarial bone has been recommended bysome as
an alternative to iliac crest graft-ing.37,38Some authors have concerns aboutthe
potential for success when calvaria isused as a graft source.39,40 This may
berelated to the technique ofharvest.Bonegrafts consisting ofdiploic bone have
beenshown to be more successful than thosegrafts harvested using a high-speed
rotarydevice to shave offprimarily cortical bonefrom the surface ofthe
calvaria.40Howev-er,even when harvesting calvarial bone insuch a way as to maximize
diploic bone,results may not be as good as with iliaccrest bone.In one study where
primarilydiploic bone was carefully harvested fromthe calvaria,the results were
still less suc-cessful (80% graft success) than with tra-ditional iliac crest bone
(93% graft suc-cess).41It is likely that either source iseffective as long as
primarily diploic boneis used.This limitation may render cal-varia as a less useful
source for large cleftsand bilateral clefts.Calvarial grafts may have
decreasedmorbidity compared with iliac crest har-vest.There is less postoperative
pain andno gait disturbance.Other potentialadvantages include decreased
surgerytime.Cranial bone grafts can be harvest-ed more quickly than iliac crest
grafts.Ifasingle team is performing surgery,thismay be significant.However,it is
not pos-sible to harvest the cranial graft simulta-neously with the alveolar cleft
repair;grafting from the iliac crest iftwo teamsare used can decrease overall
operatingtime compared with calvarial grafting.Lastly,the incision for graft
harvest ishidden in the hairline,which may have acosmetic advantage.Grafting from
the calvaria has poten-tial disadvantages.There is a perceivedincreased risk by
patients and their fami-lies,although several studies show that themorbidity ofbone
harvest from the cal-varia is minimal.34As mentioned previous-ly,the volume
ofdiploic bone is limited,making this less predictable for large orbilateral
clefts.Allogeneic Bone and Bone SubstitutesIn an effort to eliminate the morbidity
andtime necessary to harvest bone from anyautogenous site,some authors have evalu-
ated allogeneic bone as a potential sourceofgraft material.Studies have shown
thatallogeneic bone can be used successfully tograft secondary alveolar cleft
defects andthat results can be compared favorablywith those achieved with
autogenousbone.42However,the demands ofbonehealing in the alveolar defect where
thereis potential communication between thegraft and the nasal and oral cavity
maymake this less predictable in large cleftdefects or bilateral clefts.In
general,bonehealing with autogenous bone is biologi-cally different than with
allogeneic bone.Autogenous bone grafts initiate anangioblastic response early in
the healingprocess,and some ofthe transplanted cellsremain viable,resulting in a
more rapidformation ofnew bone.In contrast,allo-geneic bone grafts demonstrate
slowerrevascularization,as there are no viablecells transferred with the
graft.42,43There isalso a theoretical risk ofdisease transmis-sion from allogeneic
sources ofbone.Mathematically the risk is quite small butmay be ofconcern to
patients and families.Table 43-3Comparison ofGraft
SourcesSiteAdvantageDisadvantageConsiderationsIliumLarge quantity cancellous
bone,Mild transient gait disturbanceAll clefts,particularly large and bilateral two
teamscleftsCalvariaMinimal postoperative discomfort,Limited cancellous/diploic
bone,Unilateral clefts,lower successincision hidden,low morbidityincreased
operative timeMandibular Same operative field,rapid procurement,Limited boneOlder
children with small defectssymphysisminimal painRibTwo teamsPoor source cancellous
bone,Not recommend except for primary postoperative pain,visible scar,graftingrisk
ofpneumothoraxProximal Abundant cancellous bone,easy procedure,�Not recommend in
patients that have nottibiamild postoperative pain,two teamscompleted growthAdapted
from Ochs MW.49
864Part 6: Maxillofacial ReconstructionPreliminary work suggests that
bonemorphogenic proteins and other tissue-derived growth factors could be useful
ineliminating the need for autogenousbone harvest in this patient
population;however,there are insufficient outcomedata and availability ofthese
productscommercially to make them the materialofchoice.In summary,autogenous bone
har-vested from either the iliac crest or calvariaremains the most predictable
techniquefor cleft reconstruction.The iliac crest hassome potential advantage over
the calvari-al graft;however,this certainly depends ontechnique and surgeon
preference.Pre- versus Postsurgical OrthodonticsControversy exists regarding the
use oforthopedic expansion ofthe cleft seg-ments and the relationship
betweenexpansion and grafting.This issue hasnot been entirely settled.Most
authorsprefer presurgical expansion,citing easierexpansion because ofless
resistance,improved access to the cleft for closure ofthe nasal floor,better
postoperativehygiene,and less chance ofreopening theoronasal
fistula.23,24Presurgical expan-sion may also allow orthopedic move-ment ofthe
premaxillary segment in thebilateral cleft patient,which can eliminatetraumatic
occlusion that can negativelyimpact graft success.Proponents ofexpansion following
grafting cite advan-tages ofimproved bone consolidationwhen the graft is placed
under a dynamicload during healing,a smaller soft tissuedefect to close,less
difficulty procuringan adequate volume ofbone,and a nar-rower defect,which will
regenerate bonemore quickly.26Both approaches havebeen used in conjunction with
autoge-nous grafting in the mixed dentition stagewith success.9In practice,both
approaches arevalid,and the decision should be basedon individual clinical
presentation.31Small unilateral clefts with collapse ofthe arch may be easier to
graft with somepresurgical expansion.In these cases,such expansion may not increase
the sizeofthe defect appreciably,and betteralignment ofthe segments can
improvehygiene ofthe teeth adjacent to the cleftand improve access (Figure 43-
3).Inthese cases,the end point ofpresurgicalexpansion is improved arch
form,notnecessarily resolution ofcrossbite.Bilat-eral clefts with collapse ofthe
lateral seg-ments may also benefit from presurgicalexpansion.Expanding the lateral
seg-ments may allow the premaxilla,which isoften anteriorly positioned,to bebrought
back into better relation withthe arch,improving arch form,and,insome
cases,eliminating traumatic occlu-sion (Figure 43-4).Ifthis is not doneprior to
grafting,it may be difficult toobtain ideal arch continuity,and posi-tioning ofthe
segments after graftingmay be difficult.In patients with reason-able arch form,good
alignment ofthesegments,and dental development corre-sponding to ideal timing for
grafting,itmakes little sense to delay grafting inorder to expand
preoperatively,even inthe presence ofa buccal crossbite.Thesecrossbites may be
related only to theanterior-posterior discrepancy,and evenifthey are truly
representative oftrans-verse deficiency,they can be treated easi-ly with expansion
following the graft.These clefts can be expanded withoutopening the oronasal
fistula or having anegative effect on the graft.Not only is there controversy
regardingpre- versus postsurgical expansion,thereare also two schools ofthought
regardingorthodontic movement ofthe eruptedteeth adjacent to the cleft.Some
authorssuggest that aligning the teeth adjacent tothe cleft produces better hygiene
and animproved result.23However,orthodonticmovement ofteeth adjacent to the cleft
isnot typically desired.44Orthodontic move-ment ofteeth adjacent to the cleft prior
tografting increases the risk ofmoving theseteeth into the cleft
site,compromisingosseous support.Studies have directly cor-related the success
ofgrafting with thepresence ofadequate bone on the distalsurface ofthe central
incisor preoperative-ly.45These defects cannot subsequently beFIGURE43-3A,Occlusal
photograph ofa typical unilateral cleft.There is rotation ofthe central incisors
and collapse ofthe lesser segment.Expansion ofthe less-er segment will bring the
arch into better form and facilitate grafting without widening the cleft.B,Similar
cleft that has been expanded.C,This cleft is alreadywide without any expansion.It
would not be appropriate to expand this cleft before grafting even ifa crossbite is
present.ABC
Reconstruction ofthe Alveolar Cleft865grafted as the bone graft will not adhere
tothe tooth surface.The central incisor adja-cent to the cleft site is usually
rotated andangled with the crown tipped toward thecleft.This rotation and
angulation decreas-es the mesial-distal dimension ofthe toothand allows for the
best bony support ofthetooth (see Figure 43-2).Orthodontic forcesofrotation and
tipping will have the unde-sirable effect ofincreasing the mesial-
distaldimension,encroaching on the bony sup-port at the cemento-enamel junction
ofthetooth.Orthodontic root torque to correctthe angulation ofthe tooth will have
theundesired effect ofpushing the apical por-tion ofthe root toward the cleft
site.Theunderlying osseous cleft is frequently muchlarger than the overlying soft
tissue defectmay indicate,giving a false sense ofsecuri-ty to the orthodontist who
may want tomove these teeth in the absence ofa graft(Figure 43-5).Surgical
Technique for Grafting the Cleft Alveolus The ideal technique will meet the follow-
ing criteria:1.Predictable closure ofthe nasal floorproduces a watertight barrier
betweenthe graft and the nasal cavity 2.There is access to closure
ofresidualpalatal and labial fistula 3.Keratinized attached tissue is main-tained
around the teeth adjacent to thecleft and in the site where the yetunerupted
lateral incisor and caninewill erupt 4.Mobilization oftissue is adequate toclose
large defects without tension,when such defects are present FIGURE43-4A,Occlusal
photograph ofbilateral cleft with collapse ofthe lateral segments and protrusion
ofthe premaxilla.B andC,Right and left obliqueocclusal radiographs show the cleft
defect.D,Expansion ofthe bilateral cleft allows the premaxilla to move posteriorly
and improves arch form and alignment ofthe segments.E andF,Occlusal radiographs
ofthe same patient following grafting with eruption ofthe canine.ADBCEFFIGURE43-
5Occlusal radiograph ofa patient that hadorthodontic rotation ofthe maxillary
central incisor adja-cent to the cleft prior to grafting the defect.There is loss
ofbone on the distal surface ofthe root to the apex.The toothrequired removal.
866Part 6: Maxillofacial Reconstruction5.The vestibule is not shortened,andscarring
is not excessive Given these requirements,the tech-nique most often used employs
advancingbuccal gingival and palatal flaps.Thisapproach has some
disadvantages,includ-ing the following:1.Difficulty obtaining closure in
largebilateral clefts,which heal by sec-ondary intention offull-thicknesswounds
created by the advancement 2.A four-corner suture line that approx-imates the flaps
directly overlying thegraft,which may lead to dehiscence3.The possibility that
elevating large fullthickness mucoperiosteal flaps leadsto growth alteration in
young patients.However,when compared with fingerflaps and trapezoidal flaps,which
canshorten the vestibule and placenonkeratinized tissue around the den-tition,this
approach remains the bestThe procedure can be broken down asfollows.The first step
requires developmentoffull-thickness mucoperiosteal buccal flaps(Figure 43-6).Some
authors may recom-mend papilla preservation.When grafting isdone in the mixed
dentition,especially ifearly,this is not necessary as the papilla
willregenerate.Palatal flaps are then developed,incorporating whatever residual
palataldefect may be present to allow for closure ofthe residual palatal
fistula.Some diagramsshow this incision being made from a palatalapproach.This may
be possible in wide cleftsbut in practice is more easily accomplishedby starting
reflection ofthe palatal flaps froma sulcular incision that is placed on thepalatal
side ofthe dentition followed byreflection offull-thickness palatal flapstoward the
palatal defect.The palatal flapscan then be separated from the nasal tissuealong
the cleft margin by sharp dissectionwith scissors from the anterior
extendingposteriorly as the flaps are elevated (Figure43-7A).In this manner,the
maximum palatalsoft tissue is preserved for closure,whileassuring adequate nasal
mucosa to obtain awatertight nasal closure.Once the buccal andpalatal flaps have
been developed,access isreadily obtained to the nasal mucosa,whichis then reflected
and sutured,burying theknots to obtain a watertight nasal closure(Figure 43-7B and
C).Most schematic dia-grams ofcleft closure show this portion ofthe procedure being
performed from thepalatal aspect.However,it is generally mostreadily accomplished
in narrow clefts fromthe anterior through the cleft defect.Oncethe nasal mucosa is
closed,the palatal defectis closed by first closing the palatal flaps,con-verting
the cleft palate into a single flap (Fig-ure 43-7D).The graft material is then
placedinto the cleft from the anterior,making cer-tain to fill all voids completely
to the piri-form rim.Graft material can be condensedusing an orthodontic band
pusher orperiosteal elevator (Figure 43-7E).It is help-ful to place a malleable
retractor to protectthe nasal floor as the bone is packed intoplace.Finally,the
labial flaps can beadvanced,and they are sutured to each otherand then to the
palatal flap producing theclassic four-corner closure over the crest ofthe ridge
(Figure 43-7F and G).In mostcases,the sliding flaps will be advanced onepapilla on
either side ofthe cleft,or,in somecases,only a single papilla advancementfrom the
posterior segment is necessary.Itmay be necessary to perform a small backcut or to
release or score the periosteum toobtain a tension-free closure.It is best to usea
resorbable monofilament suture.A palatal stent can be used to stabilizethe cleft
and protect the soft tissue closure.This may compromise hygiene and bloodsupply to
the palatal flaps and,in mostcases,is not required for success.In thebilateral
cleft,ifthere is a traumatic occlu-sion to the anterior maxillary
dentition,amandibular bite plane is helpful to open thebite and prevent mobility
ofthe premaxilla.It is appropriate to use intraoperativeantibiotics.Previous
studies show thatgraft success and incidence ofinfection arenot improved by the use
ofpostoperativeantibiotics.46Some surgeons feel morecomfortable with a 1-week
course ofantibiotics,particularly when the soft tis-sue closure is questionable.The
postoperative diet should be limit-ed to full liquids for approximately 5 days.This
can be advanced to a soft mechanicaldiet.However,it is critical that the
patientrefrain from incising food with the anteriordentition;rather the patient
should cut foodinto small pieces and masticate primarily onthe posterior teeth.In
bilateral cases,this isparticularly important as any trauma to thepremaxilla will
cause mobility ofthe seg-ment leading to graft failure.Radiographicevidence ofgraft
consolidation should bevisible within 8 weeks.The surgeon shouldconfirm successful
consolidation ofthegraft prior to any orthodontic manipulationofthe teeth adjacent
to the cleft.OverviewThis chapter has outlined historic
benefitsofgrafting,discussed many ofthe contro-versies,and provided data on the
benefitsand disadvantages ofseveral approaches.FIGURE43-6A andB,Sulcular incision
used todevelop sliding flaps for closure over the graft.Adapted from Hall HD and
Posnick JC.23AB
Reconstruction ofthe Alveolar Cleft867The following is a stepwise approachto
managing the alveolar cleft from oneperspective.1.At age 5 to 6 years an
orthodonticevaluation is performed.The ability ofthe patient to cooperate with
ortho-dontic treatment is assessed,the archis evaluated for collapse,and
eruptedsupernumerary teeth in the area ofthecleft are
identified.Radiographicexamination should include apanoramic film as well as an
intraoralview that allows detailed evaluation ofthe cleft site.Periapical films can
beused for this,but a lateral obliqueocclusal film is best.An occlusal film
isplaced in the standard position whiledirecting the beam obliquely to themidline
along the long axis ofthe cleft(Figure 43-8) FIGURE43-7A,Palatal flaps are
developed sharply with scissors.This also separates the nasal mucosafrom the
palatal tissue.B,Palatal closure.This can be done before or after the nasal mucosa
is closed.C,Nasal mucosal flaps are reflected from the bony walls ofthe
cleft.D,Nasal flaps are approximated withsutures burying the knots when
possible.E,Bone is packed into the defect with a periosteal elevator ororthodontic
band pusher.Digital pressure against the palatal flap facilitates packing and
protects thepalatal closure.F andG,The labial flaps are advanced toward each other
and closed.This provides attachedkeratinized tissue.Exposed areas distally where
the flaps have been advanced are left to granulate.Adapt-ed from Hall HD and
Posnick JC.23ABCDEFG
868Part 6: Maxillofacial Reconstruction2.Iferupted supernumerary teeth
areidentified in the area ofthe cleft,theseare extracted now or,at a minimum,8
weeks before the graft (Figure 43-9A)3.Orthodontic expansion is performedifthere
are specific goals that can bemet prior to grafting.These wouldinclude decreasing
traumatic occlu-sion to the premaxillary segment inbilateral cleft patients and
correctingarch collapse that will compromisegrafting.No attempt is made to cor-rect
the crossbite at this stage,andthere is no attempt to orthodonticallycorrect
rotation ofthe permanent cen-tral incisor (see Figure 43-9A) 4.The alveolar cleft
is grafted when thepatient is between 6 and 8 years ofage.Two teams perform the
surgery withgraft harvest from the iliac crestsimultaneous with the cleft
closure5.The graft is evaluated with a lateraloblique occlusal radiograph 3
monthsfollowing surgery (Figure 43-9B)6.Final orthodontic expansion is per-formed
ifindicated,and permanentincisor teeth are then rotated intoproper alignment
7.Conventional orthodontic treatment isperformed at a more traditional
age,following eruption ofthe remainingpermanent dentition.Patients are peri-
odically monitored for eruption ofthecanine in the cleft.Some authors haveindicated
that in 30 to 73% ofpatients,eruption ofthe canine into the alveolargraft requires
surgical uncovering ofthe tooth or uncovering and ortho-dontic
assistance.12,47,48Others havereported that nearly all ofthese teethcan be expected
to erupt without sur-gical intervention24(Figure 43-9C).FIGURE43-8A,Traditional
maxillary occlusal radiograph.The cleft is identifiable,but overlap ofthe bone
makes itdifficult to determine the size ofthe defect and relationship ofthe teeth
to the defect.B,Oblique occlusal radiograph isexposed by directing the beam
obliquely to the midline,along the long axis ofthe cleft.Note that the morphology
ofthecleft is better identified,as is the relationship ofunerupted teeth to the
defect.ABFIGURE43-9A,The cleft has been expanded.The canine is in position to begin
eruption.There is a supernumerary/malformed lateral incisor erupting
horizontallyinto the cleft.B,The supernumerary tooth has been removed.The defect
was grafted 2 months following extraction and the film shows good bone
consolidation.C,The maxillary canine can be seen erupting into the graft.ABC
Reconstruction ofthe Alveolar Cleft869Ifuncovering is necessary,techniquesto
preserve attached tissue are used aswould be appropriate for impactedcanines in
noncleft patients 8.Missing lateral incisors are managedwith space development and
implantplacement,as opposed to canine sub-stitution.This is accomplished follow-ing
definitive orthodontic treatmentand orthognathic surgery ifindicated,after
maxillary growth is complete.Even when bone height is adequateand teeth adjacent to
the graft havegood support,the graft undergoesresorption resulting in a narrow
ridge.This is not unlike the bone resorptionfound with congenitally absent
lateralincisors in noncleft patients.Success-ful implant restoration is
possible,butfurther grafting is likely needed beforeadequate labial-palatal width
is avail-able for implant placement30(Figure43-10).Attention to soft and hard tis-
sue is critical in these patients toachieve esthetic resultsConclusionRestoration
ofthe cleft alveolus and max-illa by grafting is a critical part ofthe over-all
management ofthe patient with cleftpalate.A systematic approach can
improvepredictability.This is best accomplishedduring the mixed dentition
stage.Adjunc-tive expansion may be accomplishedbefore or after grafting,depending
on theneeds ofthe patient.References1.Santiago PE,Grayson BH,Cutting CB,et
al.Reduced need for alveolar bone grafting bypre-surgical orthopedics and primary
gin-givoperiosteoplasty.Cleft Palate Craniofac J1998;35:77�80.2.Horswell
BB,Henderson JM.Secondary osteo-plasty ofthe alveolar cleft defect.J OralMaxillofac
Surg 2003;61:1082�90.3.Kalaaji A,Lilja J,Friede H.Bone grafting at thestage ofmixed
and permanent dentition inpatients with clefts ofthe lip and primarypalate.Plast
Reconst Surg 1994;93:690�6.4.Teja A,Persson R,Omnell ML.Periodontal sta-tus ofteeth
adjacent to nongrafted unilater-al alveolar clefts.Cleft Palate Craniofac
J1992;29:357�62.5.Bureau S,Penko M,McFadden L.Speech out-come after closure
oforonasal fistulas withbone grafts.J Oral Maxillofac Surg
2001;59:1408�13.6.Bergland O,Semb G,Abyholm RD.Eliminationofthe residual alveolar
cleft by secondarybone grafting and subsequent orthodontictreatment.Cleft Palate J
1986;23:175�205.7.Hynes PJ,Earley MJ.Assessment ofsecondaryalveolar bone grafting
using a modificationofthe Bergland grading system.Br J PlastSurg
2003;56:630�6.8.Dado DV,Rosenstein SW,Adler ME,KernahanDA.Long term assessment
ofearly alveolarbone grafts using three-dimensional com-puter assisted tomography:a
pilot study.Plast Reconst Surg 1997;99:1840�5.9.Vig KWL,Turvey TA,Fonseca
RJ.Orthodonticand surgical considerations in bone graft-ing in the cleft maxilla
and palate.In:Tur-vey TA,Vig KWL,Fonseca RJ,editors.FacialFIGURE43-10A,Occlusal
radiograph shows thin bridge ofbone with inadequate height.A malformed lateral
incisor was maintained to preserve as much width aspossible.B,The tooth was
removed.C,After 2 months ofhealing,an onlay bone graft was placed.D,Clinical view
after grafting.E andF,View following placement ofthe implant and
reconstruction.DEFABC
870Part 6: Maxillofacial Reconstructionclefts and craniosynostosis:principles
ofmanagement.Philadelphia:WB Saunders;1996.p.396.10.Eppley B.Alveolar cleft bone
grafting (part 1):Primary bone grafting.J Oral MaxillofacSurg
1996;54:74�82.11.Rosenstein SW.Early bone grafting ofalveolarcleft deformities.J
Oral Maxillofac Surg2003;61:1078�81.12.Kwon JK,Waite DE,Stickel FR,Chisholm T.The
management ofalveolar cleft defects.JAm Dent Assoc 1981;102:848�53.13.Robertson
NRE,Jolleys A.An 11 year follow upofthe effects ofearly bone grafting ininfants
born with complete clefts ofthe lipand palate.Br J Plast Surg
1983;36:438�43.14.Helms JA,Speidel M,Denis KL.Effect oftim-ing on long-term
clinical success ofalveolarcleft bone grafts.Am J Orthod DentofacialOrthop
1987;92:232�40.15.Brattstrom V,McWilliam J.The influence ofbone grafting age on
dental abnormalitiesand alveolar bone height in patients withunilateral cleft lip
and palate.Eur J Orthod1989;11:351�8.16.Daskalogiannakis J,Ross RB.Effect
ofalveolarbone grafting in the mixed dentition onmaxillary growth in complete
unilateralcleft lip and palate patients.Cleft PalateCraniofacial J
1997;34:455�8.17.Witsenburg B.The reconstruction ofanteriorresidual bone defects in
patients with cleftlip,alveolus and palate:a review.J Maxillo-fac Surg
1985;13:197�208.18.DempfR,Teltzrow T,Kramer FJ,HausamenJE.Alveolar bone grafting in
patients withcomplete clefts:a comparative studybetween secondary and tertiary bone
graft-ing.Cleft Palate Craniofac J 2002;39:18�25.19.Boyne PJ,Sands NR.Combined
orthodontics-surgical management ofresidual palato-alveolar cleft defects.Am J
Orthod 1976;70:20�37.20.Boyne PJ,Sands NR.Secondary bone graftingofresidual
alveolar and palatal clefts.J OralSurg 1972;30:87�92.21.Abyholm RE,Bergland E,Semb
G.Secondarybone grafting ofalveolar clefts.Scand JPlast Reconstr Surg
1981;15:127�40.22.Broude D,Waite DE.Secondary closure ofalveolar defects.Oral Surg
1974;37:829.23.Hall HD,Posnick JC.Early results ofsecondarybone grafts in 106
alveolar clefts.J OralMaxillofac Surg 1983;41:289�94.24.Turvey TA,Vig K,Moriarty
J.Delayed bonegrafting in the cleft maxilla and palate:amultidisciplinary
analysis.Am J Orthod1984;86:244�56.25.Yi-Lin J,James DR,Mars M.Bilateral
alveolarbone grafting:a report of55 consecutivelytreated patients.Eur J Orthod
1998;20:299�307.26.Boyne PJ.Bone grafting in the osseous recon-struction ofalveolar
and palatal clefts.OralMaxillofac Clin North Am 1991;3:589�97.27.Hall HD,Werther
JR.Conventional alveolarcleft bone grafting.Oral Maxillofac ClinNorth Am
1991;3:609�16.28.Suzuki A,Watanabe M,Nakano M,TakahamaY.Maxillary lateral incisors
ofsubjects withcleft lip and or palate:part 2.Cleft PalateCraniofac J
1992;29:380�4.29.Kearns G,Perrott DH,Sharma A,et al.Place-ment ofendosseous
implants in graftedalveolar clefts.Cleft Palate Craniofac J1997;34:520�5.30.Vig
KWL.Alveolar bone grafts:thesurgical/orthodontic management ofthecleft maxilla.Ann
Acad Med Singapore1999;28:721�7.31.Enemark H,Sindet-Pedersen S,Bundgaard M.Long-
term results after secondary bonegrafting ofalveolar clefts.J Oral MaxillofacSurg
1987;45:913�8.32.Paulin G,Astrand P,Rosenquist JB,Barthold-son L.Intermediate bone
grafting ofalveo-lar clefts.J Craniomaxillofac Surg 1988;16:2�7.33.Crockford
DA,Converse JM.The ilium as asource ofbone grafts in children.PlastReconstr Surg
1972;50:270�4.34.Larsen PE.Sources ofautogenous bone graftsin pediatric
patients.Oral Maxillofac ClinNorth Am 1994;6:137�52.35.Rudman RA.Prospective
evaluation ofmor-bidity associated with iliac crest harvest foralveolar cleft
grafting.J Oral MaxillofacSurg 1997;55:219�23.36.Wolfe SA,Kawamoto HK.Taking the
iliac bonegraft.J Bone Joint Surg 1978;60:411.37.Harsha BC,Turvey TA,Powers SK.Use
ofauto-genous cranial bone grafts in maxillofacialsurgery.J Oral Maxillofac Surg
1986;44:11�5.38.Turvey TA.Donor site for alveolar cleft bonegrafts (letter).J Oral
Maxillofac Surg 1997;45:834.39.Jackson IT,Helden G,Marx R.Skull bonegrafts in
maxillofacial and craniofacialsurgery.J Oral Maxillofac Surg
1986;44:949�56.40.Kortebein MJ,Nelson CL,Sadove MA.Retro-spective analysis of135
secondary alveolarcleft grafts using iliac or calvarial bone.J Oral Maxillofac Surg
1991;49:493�8.41.Sadove MA,Nelson CL,Epply BL,Nguyen B.An evaluation ofcalvearial
and iliac donorsitres in alveolar cleft grafting.Cleft PalateCraniofac J
1990;27:225�9.42.Maxson BB,Baxter SD,Vig KWL,Fonseca RJ.Allogeneic bone for
secondary alveolar cleftosteoplasty.J Oral Maxillofac Surg 1990;48:933�41.43.Marx
RE,Miller RI,Ehler WJ,et al.A compar-ison ofparticulate allogeneic and particu-late
autogenous bone grafts into maxillaryalveolar clefts in dogs.J Oral MaxillofacSurg
1984;42:3�9.44.Vig KWL,D�orth RCS,Turvey TA.Orthodontic-surgical interaction in the
management ofcleft lip and palate.Clin Plast Surg1985;12:735�48.45.Aurouze C,Moller
KT,Bevis RR,et al.Thepresurgical status ofthe alveolar cleft andsuccess ofsecondary
bone grafting.CleftPalate Craniofac J 2000;37:179�84.46.Larsen PE,Myers G,Beck
MF.Morbidity ofalveolar cleft grafting in the early mixeddentition (<8years).J Oral
Maxillofac Surg1997;55(Suppl 3):127.47.Eldeeb M,Messer LB,Lehnert MW,et al.Canine
eruption into grafted bone in max-illary alveolar cleft defects.Cleft Palate
J1988;19:9�16.48.Enemark H,Sindet-Pedersen S,Bundgaard M,Simonsen EK.Combined
orthodontic-sur-gical treatment ofalveolar clefts.Ann PlastSurg
1988;21:127�33.49.Ochs MW.Alveolar cleft bone grafting (part 2):secondary bone
grafting.J Oral MaxillofacSurg 1996;54:83�8.
CHAPTER 44Reconstruction ofCleft Lip and Palate:Secondary ProceduresRamon
L.Ruiz,DMD,MD Bernard J.Costello,DMD,MDA congenital cleft ofthe lip and
palaterepresents a complex malformationinvolving the hard and soft tissues
oftheface.Children born with cleft lip andpalate face several unique functional
andesthetic challenges requiring a combined(interdisciplinary) treatment approach
inorder to obtain an ideal outcome relativeto speech,occlusion,facial
appearance,and individual self-esteem.This success-ful reconstruction routinely
requiresmultiple phases ofsurgical intervention.Because treatment is carried out
duringperiods ofgrowth,the benefit-risk ratioofany planned surgical procedure
mustbe carefully considered in order to pro-vide the maximum benefit to
thepatient.1,2Surgeons caring for these chil-dren must maintain a firm
cognitiveunderstanding ofthe three-dimensionalanatomy ofthe cleft lip and palate
mal-formation and the complex interplay thatexists between the surgical
proceduresand ongoing facial growth.The various surgical proceduresinvolved in
staged reconstruction ofcleftlip and palate have been described exten-sively in the
literature and are presented inChapters 42,�Cleft Lip and Palate:Com-prehensive
Treatment Planning and Pri-mary Repair,�Chapter 43,�Reconstructionofthe Alveolar
Cleft,�and Chapter 61,�Orthognathic Surgery in the Patient withCleft Palate.�3�6In
addition,the AmericanCleft Palate�Craniofacial Association(ACPCA) has developed
parameters ofcare in order to facilitate the coordinatedinterdisciplinary treatment
ofindividualsaffected with cleft lip and palate deformi-ties.7The ACPCA document
summarizes amanagement protocol that is centeredaround thoughtful timing ofspecific
inter-ventions based on the patient�s dental,skeletal,speech,and psychological
devel-opment.The general staged approach tocleft lip and palate reconstruction
frominfancy through adolescence is presentedin Table 44-1.Contemporary
managementprotocols involve several phases ofsurgeryduring infancy (cleft lip
repair and palateclosure) and early childhood (bone graftreconstruction ofthe cleft
maxilla andalveolus) that are considered requiredoperations in all cases ofcomplete
unilat-eral or bilateral cleft lip and palate.In addi-tion to those primary stages
ofrepair,sev-eral children will go on to requireadditional procedures for
correction ofsecondary problems.Secondary recon-struction ofcleft lip and palate
may involveTable 44-1Stages ofCleft Lip and Palate Reconstruction:Infancy through
Adolescence Surgical Treatment AgeTiming ConsiderationsCleft lip repair*10 to 12
weeks Cleft palate repair*9 to 18 monthsExact timing ofrepair is based on child�s
speech/language ageSecondary palate surgery for VPI 3 to 5 yearsBone graft
reconstruction 6 to 9 yearsBased on dental developmentofcleft
maxilla/alveolus*Orthognathic surgery14 to 16 years for females,16 to 18 years for
malesDental implant placement16 to 18 years Lip/nasal revisionAfter age 5
yearsVaries widely depending on clinical findings and psychosocial
concerns.Definitive nasal surgery usually delayed until adolescence.*Reconstruction
stage is required for all patients with complete cleft lip and palate.VPI =
velopharyngeal insufficiency.
872Part 6: Maxillofacial Reconstructionsurgery for treatment
ofvelopharyngealdysfunction,bone graft reconstruction ofbony clefts ofthe
maxilla,correction ofresidual skeletal disproportion withmalocclusion,closure
ofpalatal fistulas,normalization oflip and nasal form,andprosthetic rehabilitation
ofthe cleft dentalgap.Although the indications for each oftheprimary and secondary
surgical undertak-ings are different and the decision-makingprocesses may vary,one
cannot view each ofthese procedures as isolated events.Thischapter reviews the
different phases ofsec-ondary cleft lip and palate reconstructionthat may be
required after primary cleft lipand palate repair with the purpose ofpro-viding an
organized description ofthe con-temporary philosophy and rationale forsurgical
interventions and specific timing.Fistula ClosureBackgroundWhen a child is born
with a cleft palate,there is an abnormal communicationbetween the oral and nasal
cavities.One ofthe principles essential to successful surgi-cal repair involves the
separation oforaland nasal side soft tissues from each otherand then reconstruction
ofthose distincttissue layers to establish separate nasal floorand oral mucosal
linings.The result is clo-sure ofthe hard palate in two layers (nasalmucosa and
oral mucosa) and closure ofthe soft palate in three layers (nasal side,levator
musculature,and oral side mucosa).Residual abnormal oronasal communi-cations,or
�fistulas,�following the initialrepair are relatively frequent problems thatrequire
subsequent surgical procedures inpatients with cleft palate.Before addressingthe
specific management approach to resid-ual fistulas,one must define the clinical
sit-uation based on the patient�s age,previoussurgical history,and the exact
location ofthe fistula.Another important considera-tion is the extent to which the
cleft defectinvolves the primary and secondary palates.The primary palate comprises
the anatom-ic structures anterior to the incisive fora-men
(alveolus,maxilla,piriform,lip).Thesecondary palate comprises the
anatomicstructures between the incisive foramenand the uvula.Using this
terminology,acomplete cleft ofthe primary and sec-ondary palates would involve the
maxilla,alveolus,hard palate,and soft palate.Anisolated cleft palate involving the
hard andsoft palate (without affecting the alveolarridge) would be described as a
completecleft ofthe secondary palate while a cleftinvolving only the soft palate
(and not thehard palate or alveolus) is described as anincomplete cleft ofthe
secondary palate.Even when a child is born with a com-plete cleft palate
(ie,affecting the primaryand secondary palate),the primary repairinvolves closure
ofthe secondary palateonly�those structures from the incisiveforamen to the
uvula.The goals ofcleftpalate repair during infancy are twofold:first,to establish
complete watertight clo-sure ofthe secondary palate for separationofthe oral and
nasal cavities and,second,to repair the levator musculature in orderto allow for
normal speech formation.Repair ofthe skeletal maxillary/alveolarcleft defect and
its associated oronasalcommunication are not generally under-taken at this
stage.Many surgeons consid-er this alveolar defect part ofthe originalcleft
deformity that has been purposely leftunrepaired instead ofa true
�fistula.�Definitive repair ofthe anterior alveolar ornasolabial fistula is instead
incorporatedinto the bone graft reconstruction per-formed during midchildhood based
onthe child�s dental development.5,6,8,9Bonegraft reconstruction ofthe cleft defect
ispresented in greater detail in Chapter 43,�Reconstruction ofthe Alveolar
Cleft.�Ideally,a child with a complete cleftpalate will undergo palate repair
duringinfancy with successful closure ofthe hardand soft (or secondary) palates and
thenbone graft reconstruction ofthemaxilla/alveolus (or primary palate) withclosure
ofany residual nasolabial fistuladuring childhood.Unfortunately,residualpalatal
fistulas are frequently encounteredafter the initial palate repair.The risk offis-
tula formation seems to be closely associat-ed with the size ofthe original
cleftdefect.10,11The type ofrepair used by thesurgeon may also affect the fistula
rate.Recent reports indicate that a two-flappalatoplasty technique is associated
with thelowest rate (3.4%) ofpalatal fistula forma-tion.12Another frequently
employed tech-nique,the Furlow double opposing Z-plasty,is associated with a higher
incidence oforonasal fistula.5This difference in the rateoffistula occurrence is
probably morenoticeable when the cleft defect beingrepaired is very wide.The most
commonlocation for development ofa residualpalatal fistula following cleft palate
repair isthe junction ofthe hard and soft palates fol-lowed by the anterior hard
palate and inci-sive foramen region.5,6,11,13The incidence ofpalatal fistula
following single-stage palato-plasty varies greatly,with the reported ratesas high
as 50%.11Indications for Fistula Repairand Timing ofSurgeryMost fistulas are noted
early on in the post-surgical period following palate repair andare the direct
result oflocal wound break-down owing to tension or vascular compro-mise.Another
time period when a palatalfistula may be encountered is during Phase I(pre-bone
graft) orthodontic treatment,especially ifmaxillary expansion has
beenundertaken.There is disagreement aboutthe causal relationship
oforthodonticexpansion and development ofa palatal fis-tula.However,most
experienced cleft sur-geons believe that fistula defects discoveredduring maxillary
expansion are preexistingoronasal communications and are not actu-ally caused by
the orthodontic treatment.Small fistulas present since infancy can behidden within
a narrow palate by collapsedmaxillary segments and then uncovered asthe maxillary
arch form is expanded byorthodontic or orthopedic means.
Reconstruction ofCleft Lip and Palate: Secondary Procedures873The recommended
timing offistulaclosure may vary significantly and remainsa controversial
topic.Some surgeons andcleft teams may advocate relatively aggres-sive management
with early closure ofanyfistula present after the initial palate repair.We prefer
to take a more long-range viewofthese problems and delay surgery forseveral years
whenever possible.In infants,the closure ofa small (1 to 4 mm),nonfunctional
fistula can generallybe deferred until later in childhood.Insuch cases,fistula
repair may be incorpo-rated into any future necessary proceduressuch as pharyngeal
surgery for velopharyn-geal insufficiency or bone graft reconstruc-tion ofthe cleft
maxilla and alveolus aslong as there are no functional speech orfeeding-related
concerns.When a larger (> 5 mm) fistula is present,there is agreater likelihood
that functional concernswill be encountered,such as nasal airescape which impacts
speech,nasal refluxoffood and liquids,and hygiene-relateddifficulties.In clinical
situations where sig-nificant functional problems exist,earlierclosure ofthe
persistent fistula is indicated.As part ofthe decision-making process,surgeons must
weigh the benefits offistularepair against the negative effects ofa sec-ond palatal
surgery involving stripping ofmucoperiosteum on subsequent maxillarygrowth.Another
consideration in planningthe exact timing offistula closure is thetype ofrepair
technique being used for therepair.Attempts to close a fistula with localflaps or
repeat palatoplasty may be under-taken during infancy and early childhood.On the
other hand,in cases in which theuse ofa regional (eg,tongue) flap isrequired,the
child must be old enough tocooperate with the perioperative regimen.Operative
Techniques for ClosureofPalatal FistulasThe repair ofresidual palatal fistulas fol-
lowing cleft palate repair has beendescribed using several different tech-
niques.5,10,14�16Current operations usedfor fistula repair include local palatal
flaps,modifications ofthe von Langenbeck andtwo-flap palatoplasty
techniques,palato-plasty with incorporation ofa pharyngealflap,and the use ofa
tongue flap.Otherregional flaps,including the tongue,buc-cal mucosa,buccinator
myomucosal,tem-poralis muscle,and vascularized tissuetransfer are less frequently
used but havebeen described.14,17�21One ofthe most frequently describedprocedures
for closure ofresidual fistulas isthe use oflocal soft tissue flaps created with-in
the palatal mucosa and rotated over thedefect for closure (Figure 44-1).The com-
ponents ofthis approach are the creation ofturnover flaps around the defect for
nasalside closure,elevation ofa palatal fingerflap,and rotation ofthe flap for
coverage ofthe defect.A significant area ofexposedbone is left at the donor
site,and this isallowed to heal by secondary intention.Unfortunately,this type
ofrepair is usefulonly for very small palatal defects and isassociated with a
relatively high failurerate.14Small rotational flaps within palataltissues that
contain extensive scarring fromprior surgical procedures are difficult tomobilize
without residual tension and mayhave diminished blood supply resulting in aless-
than-ideal healing capacity and agreater chance ofwound breakdown.Our preferred
approach to residualpalatal fistulas involves the modification ofone ofthe primary
palate repair techniques,namely the Bardach or von Langenbeckprocedures.5,22These
approaches allow ade-quate coverage ofeven large defects with theuse ofbulky soft
tissue flaps,a layered repairofthe nasal and oral sides,and a tension-free line
ofclosure (Figures 44-2 and 44-3).In addition,the amount ofbone that is leftexposed
after the repair is minimal to none.This is because the vertical depth ofthepalatal
vault translates into soft tissueextension medially,and so the result ispalatal
soft tissue flaps that adequatelycover the underlying bone with a layer ofdead
space between the palatal shelves andthe oral mucosa lining.The Bardach (two-flap)
palatoplasty is our preferred operationin cases where the fistula defect is 5 mm
orlarger.The primary advantage ofthisapproach is the ability to raise large soft
tis-sue flaps,which can be mobilized easily andallow for easy visualization and
closure ofFIGURE44-1The use ofa small,rotational flap for closure ofa residual
palatal fistula.This type ofrepair has a high failure rate.A,Turnover flaps are
used to establish a nasal side closure and a palatalmucosal flap is
outlined.B,Random pattern,full-thickness mucoperiosteal flap is elevated and mobi-
lized for coverage ofdefect.AB
874Part 6: Maxillofacial Reconstructionthe nasal mucosa.By comparison,one ofthe
theoretical advantages ofthe von Lan-genbeck procedure is the creation ofbipedicled
flaps that maintain anterior andposterior blood supplies.While the anteriorpedicles
do provide additional perfusion,they also result in less freely movable flapswith
limited access and visualization ofthenasal side tissues.For this reason,we use
thevon Langenbeck technique only for rela-tively small defects within the hard
palate.In situations where there is a muchlarger (> 1.5 cm) defect,successful
closuremay dictate that the surgeon recruit addi-tional soft tissue using a
regional flap.Fis-tula defects within the posterior hardpalate or soft palate may
be addressed withthe use ofa modified palatoplasty proce-dure as described above in
combinationwith a superiorly based pharyngeal flap.After the palatal flaps are
developed andthe nasal side dissection is complete,apharyngeal flap is
harvested.The pharyn-geal flap soft tissue is then incorporatedinto the nasal side
closure ofthe areawhere the fistula was present.Using thistechnique,a substantial
amount ofaddi-tional soft tissue can be recruited for tension-free repair ofa large
palatal defect.When the fistula is located within theanterior two-thirds ofthe hard
palate,theprocedure ofchoice for recruitment ofadditional soft tissue is the
anteriorlybased dorsal tongue flap (Figure 44-4).First,nasal side closure ofthe
palataldefect is performed using turnover flapswith multiple interrupted
sutures.Next,this technique calls for development ofananteriorly based tongue flap
that isapproximately 5 cm in length by one- totwo-thirds the width ofthe
tongue.Thetongue flap is elevated along the underly-ing musculature and then inset
using mul-tiple mattress sutures for closure oftheoral side.The recipient bed
within thetongue is closed primarily.After the initialsurgery,the tongue flap is
allowed to healfor approximately 2 weeks.At that time,the patient is returned to
the operatingroom.Nasal fiber-optic intubation is indi-cated for the second
procedure since thetongue is still sutured to the palate,restricting normal
visualization ofthe air-way.The flap is sectioned and the stump atthe donor site is
freshened and inset intothe tongue.The use oflaterally and poste-riorly based
tongue flaps has also beenFIGURE44-2Modification ofthe two-flap palatoplasty
technique for closure ofa residual palatal fistu-la.A,Two large mucoperiosteal
flaps are developed with dissection extended to a point posterior ofthe fis-tula
defect.The nasal mucosa is repaired as a separate layer.B,Closure ofthe oral
side.The midline isclosed first using multiple interrupted sutures,and then the
lateral incisions are reapproximated.ABFIGURE44-3Modification ofthe von Langenbeck
technique for closure ofa residual palatal fistula.A,Incisions are created at the
fistula defect along the junction oforal and nasal mucosa,and lateral-ly in order
to develop palatal flaps.Care is taken to maintain anterior soft tissue attachment
forimproved blood supply.This may make flap mobilization and visualization ofthe
defect difficult.B,The nasal side is closed first,and then oral side closure is
accomplished with interrupted sutures.AB
Reconstruction ofCleft Lip and Palate: Secondary Procedures875presented in the
cleft literature.23,24In ouropinion,however,an anteriorly based flapis better
tolerated by most patients andallows for the greatest degree oftonguemobility with
less risk oftearing the flapfrom its palatal insertion.Secondary Cleft Palate
Surgery for Management ofVelopharyngeal DysfunctionBackgroundThe secondary palate
is composed ofahard (bony) palate anteriorly and a softpalate or
�velum�posteriorly.Within thesoft palate,the levator veli palatini muscleforms a
dynamic sling that elevates thevelum toward the posterior pharyngealwall during the
production ofcertainsounds.Other muscle groups within thevelum,the tonsillar pillar
region,1and pha-ryngeal walls also impact resonance qualityduring speech formation
(Table 44-2).Thecombination ofthe soft palate and pharyn-geal wall musculature
jointly form what isdescribed as the velopharyngeal (VP)mechanism (Figure 44-
5A).The VP mech-anism functions as a sphincter valve inorder to regulate airflow
between the oraland nasal cavities and create a combinationoforally based and
nasally based sounds.Children born with a cleft palate have,by definition,a
malformation that dra-matically impacts the anatomic compo-nents ofthe VP
mechanism.Specifically,clefting ofthe secondary palate causesdivision ofthe
musculature ofthe veluminto separate muscle bellies with abnormalinsertions along
the posterior edge ofthehard palate (Figure 44-5B).The initialpalatoplasty is not
carried out simply forclosure ofthe palatal defect (oronasalcommunication)
itself,but is aimed also ataddressing these underlying anatomic dis-crepancies
involving the musculature.During surgery for palatal closure,caremust be taken to
sharply separate the mus-cles offofthe palatal shelves,realign them,and establish
continuity in order to createa functional palatal-levator muscle sling.Some
describe this primary repair ofthepalatal musculature as �intravelar velo-plasty,�a
component ofthe cleft palate clo-sure.Although this description helps toarticulate
the importance ofaddressingthe levator muscle,it may confuse someclinicians by
suggesting that muscle repairor intravelar veloplasty is a separate proce-
dure.Irrespective ofthe type ofcleft palateFIGURE44-4Use ofan anteriorly based
dorsaltongue flap for repair ofa large fistula within theanterior hard
palate.A,Diagram ofpalatal defectand elevation ofanteriorly based tongue
flap.Turnover flaps are first used to create a nasal siderepair and then the tongue
flap is developed.Thewidth ofthe flap may be as wide as two-thirds thewidth ofthe
tongue and approximately 4 to 6 cmin length.B,The donor site is closed using multi-
ple interrupted sutures and the tongue flap is insetand sutured to the palatal
mucosa surroundingthe defect.C and D,Intraoperative views oftongue flap harvest and
inset.A and B adaptedfrom Posnick JC.Cleft-orthognathic surgery: theisolated cleft
palate deformity.In: Posnick JC,RoseA,Ross A,editors.Craniofacial and
maxillofacialsurgery in children and young adults.1st ed.Philadelphia (PA):
W.B.Saunders; 2000.p.957�8.ACBD
876Part 6: Maxillofacial Reconstructionrepair technique employed (von Langen-
beck,Bardach,Furlow,etc),meticulousrelease ofabnormal muscle insertions andvelar
muscle reconstruction must beincorporated as a critical element ofthesurgical
procedure.Most children who undergo successfulcleft palate repair during infancy (9
to 18 months) will go on to develop speechthat is normal or to demonstrate
minorspeech abnormalities that are amenable totreatment with speech therapy.In a
small-er segment ofthis patient population,however,the velopharyngeal mechanismwill
not demonstrate normal functiondespite surgical closure ofthe
palate.25�Velopharyngeal insufficiency�(VPI) isdefined as inadequate closure
ofthenasopharyngeal airway port during speechproduction.The exact etiology ofVPI
fol-lowing successful cleft palate repair is acomplex problem that remains
difficult tocompletely define.Inadequate surgicalrepair ofthe musculature is one
cause ofVPI,but even muscles that have beenappropriately realigned and
reconstitutedmay fail to heal normally or function prop-erly because ofcongenital
defects withtheir innervation.The role ofpostsurgicalscarring and its impact on
muscle functionand palatal motion is poorly understood.When using a Furlow double
opposing Z-plastyprocedure for the initial palaterepair,the theoretical advantages
includebetter realignment ofthe palatal musclesand lengthening ofthe soft
palate,butthese benefits may be negatively balancedby a velum that demonstrates
less motionor elevation owing to the additional scar-ring associated with two
separate sets ofZ-plastyincisions.In addition,it must beconsidered that the
repaired cleft palate isTable 44-2Muscle Groups Contributing to the Velopharyngeal
Mechanism Muscle Insertion Origin Function Uvulus muscleMucous membrane ofsoft
palatePalatal aponeurosisVelar extensionTensor veli palatiniSoft and hard
palatesMedial pterygoid plateOpens auditory tubeSalpingopharyngeousPalatopharyngeal
aponeurosisTorus tubariusMotion ofthe lateral walls Superior constrictorMedial
pharyngeal rapheVelum;medial pterygoid platePosterior and lateral wall
sphincteringLevator veli palatiniSoft palateTemporal boneElevation ofthe
velumPalatopharyngeousSoft palate aponeurosisPharyngeal wallAdduction ofposterior
pillars;sphinctering ofvelum PalatoglossusTongueSoft palateRetracts
tongue;antagonistic to the levator during speechPterygoid hamulus and tensor
palatini musclePterygomandibular raphe andsuperior constrictor
musclePalatopharyngeus musclePalatoglossus muscleLevator veli palatini
musclePterygoid hamulus and tensor palatini musclePterygomandibular raphe
andsuperior constrictor musclePalatopharyngeus musclePalatoglossus muscleLevator
veli palatini muscleFIGURE44-5Anatomy ofthe velopharyngeal mechanism.A,Normal
anatomy.B,Anatomic distortions associated with complete cleft ofthe primary and
sec-ondary palate.Note abnormal insertions oflevator veli palatini muscle along the
posterior edge ofthe hard palate.AB
Reconstruction ofCleft Lip and Palate: Secondary Procedures877only one factor
contributing to VP function,and other abnormalities related to oropha-ryngeal
morphology,lateral and posteriorpharyngeal wall motion,and nasal airwaydynamics may
all contribute to VP dysfunc-tion.Certainly,these other structures mayalso play a
role in compensating for thepalatal deformity.For example,a short,scarred soft
palate that does not elevate verywell may be compensated for by the recruit-ment
and hypertrophy ofmuscular tissuewithin the posterior pharyngeal wall (�acti-vation
ofPassavant�s ridge�).26�28The audible nasal air escape withresultant hypernasal
speech that is associ-ated with VPI is perhaps the most debili-tating consequence
ofthe cleft palatemalformation.Approximately 20% ofchildren with VPI following
palatoplastywill go on to require management involv-ing additional palatal
surgery.25Leftuntreated,nasal air escape-related reso-nance problems will lead to
other speechabnormalities,namely,abnormal com-pensatory articulations.Warren�s
elegantaerodynamic demands theory providesthe best explanation ofwhat occurs
withsevere VPI.29His theory states that nasalair escape owing to inadequate VP clo-
sure will cause the patient to articulatepressure consonants at the level
ofthelarynx or pharynx instead ofwithin theoral cavity.These abnormal,compensato-
ry,misarticulations further complicateproblems with speech formation anddecrease
speech intelligibility in patientswith cleft palate�related VPI.Indications for
Surgery and TimingFollowing the initial cleft palate repair,peri-odic evaluations
are critical in order toassess the speech and language developmentofeach
child.Typically,this involves a stan-dardized screening examination performedby a
speech and language pathologist as partofan annual visit to the cleft palate
team.Inpatients with speech problems such as VPI,more detailed studies including
the use ofvideofluoroscopy and nasopharyngoscopymay be indicated.Videofluoroscopy
studiesare used to radiographically examine theupper airway with the aid ofan oral
contrastmaterial.These techniques allow dynamictesting ofthe VP mechanism with
views ofthe musculature in action.In addition,details ofthe upper airway anatomy
includ-ing residual palatal fistulas can be visualizedand their contribution to
speech dysfunc-tion evaluated during the study.For a video-fluoroscopy study to be
ofdiagnostic value,it must include multiple views ofthe VPmechanism and a speech
pathologist mustbe present in order to administer verbal test-ing in the radiology
suite.Nasopharyn-goscopy using a small,flexible,fiber-opticendoscope is routinely
used for the evalua-tion ofpatients with VPI.Nasopharyn-goscopy allows for direct
visualization oftheupper airway and specifically the VP mech-anism from the
nasopharynx.This tech-nique avoids the radiation exposure associ-ated with
videofluoroscopy but requirespreparation ofthe nose with a topical anes-
thetic,skillful maneuvering ofthe scope,and a compliant patient.Once the endo-scope
is inserted,observations ofpalatalfunction,airway morphology,and pharyn-geal wall
motion are made while the patientis verbally tested by the speech pathologist.5The
opportunity for direct visualization ofthe VP mechanism in action during
speechformation provides information that is crit-ical to clinical decision-making
related tosecondary palatal surgery in cases ofcon-firmed or suspected
VPI.Secondary palatal surgery in youngchildren is indicated when VPI
causeshypernasal speech on a consistent basisand is related to the anatomical prob-
lem.30�32The exact timing ofsurgery forVPI remains
controversial,however,withrecommendations ranging from 2.5 to 5 years ofage.In
children 2.5 to 4 years ofage,obtaining enough diagnostic informa-tion to make a
definitive decision regard-ing treatment is often difficult.In such ayoung age
group,variables such as thechild�s language and articulation develop-ment and a
lack ofcompliance during thespeech evaluation compromise the diag-nostic accuracy
ofpreoperative assess-ments.33�35By the time a child reaches 5 years
ofage,compliance with naso-pharyngoscopy is better,and there isenough language
development to allow fora more thorough perceptual speech evalu-ation.These factors
allow for more defini-tive conclusions regarding the status ofVPfunction or
dysfunction in the child with arepaired cleft palate.One final salientpoint is that
decisions regarding the advis-ability ofsurgery for VPI must be madeonly through
close collaboration with anexperienced speech and language patholo-gist.The
decision to go forward with addi-tional surgery for VPI simply is not an iso-lated
surgical judgment.The problem ofVPI with hypernasalspeech may also be encountered
later in lifein patients that require orthognathic surgeryfor correction ofcleft-
related maxillary defi-ciency.As discussed in Chapter 61,�Orthog-nathic Surgery in
the Patient with CleftPalate,�approximately 25% ofpatients whohave undergone cleft
palate repair duringinfancy will require additional surgery forcorrection
ofmidfacial deficiency duringadolescence when they are nearing
skeletalmaturity.36This usually involves midfacialadvancement at the Le Fort I
level with orwithout mandibular surgery in order to nor-malize skeletal
position,correct malocclu-sion,and improve facial form.Largeadvancements ofthe
maxilla in patients witha repaired cleft palate may worsen preexistingVPI or may be
the cause ofnew-onsetVPI.37�39A minority ofpatients with border-line VP closure
preoperatively will develophypernasal speech even after relatively smalldegrees
ofmaxillary forward displacement.Since predicting exactly how each patient
willrespond to maxillary advancement is diffi-cult,formal speech assessment and
detailedcounseling ofthe patient and family regard-ing the possibility ofdeveloping
post-operative VPI is recommended prior to
878Part 6: Maxillofacial Reconstructionundertaking any cleft orthognathic
surgeryinvolving maxillary advancement.Fortu-nately,most patients who develop VPI
fol-lowing maxillary advancement will recoveradequate VP closure without the need
foradditional palatal surgery.In a study byTurvey and Frost,pressure-flow
studieswere used to examine VP function aftermaxillary advancement in patients
withrepaired cleft palate.40In their study groupofpatients with adequate VP closure
beforesurgery,the VP apparatus demonstratedthree different responses following
midfa-cial advancement:(1) adequate VP closureafter surgery,(2) deterioration with
inade-quate VP function after surgery followed bya gradual improvement and recovery
ofnormal closure over a 6-month period,and(3) inadequate VP closure after
surgerywithout improvement necessitating pha-ryngeal flap surgery.When
maxillaryadvancement does result in clinically signif-icant VPI,additional
corrective surgeryshould be delayed at least 6 months.Inmost cases,postoperative
neuromuscularadaptation allows the VP mechanism torecover,and the patient returns
to a base-line level offunction with resolution ofhypernasal speech without the
need foradditional operative intervention.Operative Techniques Contemporary
surgical management ofVPI generally involves the use ofeither oftwo types
ofprocedures:(1) the superiorlybased pharyngeal flap,and (2) the sphinc-ter
pharyngoplasty.The use ofautogenousand alloplastic implants for augmentationofthe
posterior pharyngeal wall has beendescribed,but is not a commonly
usedprocedure.More recently,some surgeonshave advocated the use ofa second palato-
plasty operation as an attempt at palatallengthening in the patient with VPI;how-
ever,limited data exist to support this as apreferred technique.The superiorly
based pharyngeal flapremains the standard approach for surgi-cal management ofVPI
after palate repair.The procedure was initially described bySchoenborn in
1876.41�43Surgical maneu-vers are directed at recruiting tissue bydeveloping a
superiorly based soft tissueflap from the posterior pharyngeal wall(Figure 44-
6).The soft palate is thendivided along midsagittal plane from thejunction ofthe
hard and soft palate to theuvula and the flap from the posterior pha-ryngeal wall
is inset within the nasal layerofthe soft palate.As a result,a largenasopharyngeal
opening which cannot becompletely closed by the patient�s VPmechanism is converted
into two (rightand left) lateral pharyngeal ports.Closureofthese ports is easier
for the patient toaccomplish as long as adequate lateralpharyngeal wall motion is
present.Whenrandomly applied to patients with VPI,thesuperiorly based pharyngeal
flap proce-dure is effective 80% ofthe time.44Whenthe flap is applied using careful
preopera-tive objective evaluations,success rates ashigh as 95 to 97% have been
reported.45,46Shprintzen and colleagues have advocatedcustom tailoring ofthe
pharyngeal flapwidth and position based on the particularcharacteristics ofeach
patient as seen onnasopharyngoscopy.44,47The high overallsuccess rate and the
flexibility to designthe dimensions and position ofthe flapitselfare advantages
ofthe superiorlybased pharyngeal flap procedure.The dis-advantages ofthe pharyngeal
flap proce-dure are primarily related to the possibili-ty ofsevere nasal
obstruction resulting inmucous trapping and postoperativeobstructive sleep
apnea.Inferiorly based pharyngeal flaps formanagement ofVPI are rarely used.Previ-
ous reports have documented increasedmorbidity without better speech
outcomesassociated with inferiorly based flaps.48Inaddition,inferiorly based flaps
tend tocause downward pull on the soft palatefollowing healing and contracture
oftheflap.The result may be a tethered palatewith decreased ability to elevate
during theformation ofspeech sounds.The dynamic sphincter pharyngoplas-ty is
another option for the surgical man-agement ofVPI.This procedure wasdescribed by
Hynes in 1951 and modifiedby several other authors.49�54The operativeprocedure
involves the creation oftwosuperiorly based myomucosal flaps creat-ed within each
posterior tonsillar pillar(Figure 44-7).Each flap is elevated withcare taken to
include as much ofthepalatopharyngeal muscle as possible.Theflaps are then attached
and inset within ahorizontal incision made high on the pos-terior pharyngeal
wall.The goal ofthisprocedure is the creation ofa singlenasopharyngeal port
(instead ofthe twoports ofthe superiorly based pharyngealflap) that has a
contractile ridge posterior-ly to improve VP valve function.The mainadvantage ofthe
sphincter pharyngoplastyover the superiorly based flap is a lowerrate
ofcomplications related to nasal air-way obstruction as described
above.55�57Despite this advantage,there is no evi-dence that pharyngoplasty
proceduresachieve superior outcomes in the resolu-tion ofVPI.Also,the use ofa
sphincterpharyngoplasty technique may be associ-ated with increased scarring along
the ton-sillar pillar region.In the past,augmentation ofthe pos-terior pharyngeal
wall has been attemptedin order to facilitate closure ofthe nasalairway.Various
autogenous and alloplasticmaterials have been used including localtissue,rib
cartilage,injections ofTeflon,silicon,Silastic,Proplast,and
collagen.58,59Improvement in speech after augmenta-tion ofthe posterior pharyngeal
wall isunpredictable.Problems with migrationor extrusion ofthe implanted material
andan increased rate ofinfection added to theproblems with these techniques.For
thesereasons,pharyngeal wall implants arerarely used.Some surgeons advocate the use
ofarevisional palatoplasty instead ofa pharyn-geal flap or pharyngoplasty procedure
inthe management ofpatients with VPI after
Reconstruction ofCleft Lip and Palate: Secondary Procedures879cleft palate repair
in infancy.60Specifically,a Furlow double opposing Z-plastypalato-plasty is carried
out in order to lengthenthe soft palate and facilitate VP closure.Unfortunately,the
anticipated benefits ofthese second palatoplasties have never beenestablished.The
clinician also must consid-er the disadvantages ofthis type ofsurgicalprocedure and
weigh them against poten-tial benefits.The double opposing Z-plastyprocedure
requires a more aggressive dis-mantling ofthe palate than what isrequired during a
conventional pharyngealflap procedure.The result may be a slight-ly longer
palate,but one with more exten-sive scarring and less physiologic move-ment.Another
consideration is thesignificantly higher rate offistula forma-tion associated with
this type ofrepair.Complications Related to Surgical Procedures for VPISurgery
involving airway structures isalways associated with the potential forcomplications
related to postoperativehemorrhage and edema.As a result,patients who undergo
attachment ofapharyngeal flap require admission to thesurgical intensive care unit
with continu-ous airway monitoring during the first 24 hours following surgery.This
type ofsetting permits the rapid recognition andprompt management
ofcomplicationsthat may result in airway compromise.Ofall the procedures related to
cleft care,the pharyngeal flap and sphincteroplastyoperations carry the greatest
risk forearly airway compromise.Airway lossand compromise are not common butrequire
immediate management whenthey are encountered in order to avoidlife-threatening
consequences.Long-term postoperative complica-tions related to the superiorly based
pha-ryngeal flap are frequently associated withproblems related to increased airway
resis-tance.Insertion ofa pharyngeal flap willdecrease the size ofthe
nasopharyngealairway,facilitate VP closure,decrease nasalair escape,and make speech
more intelli-gible.At the same time,however,the pro-cedure may create a pathologic
level ofupper airway obstruction that leads to newproblems.In several
cases,patients whohave undergone pharyngeal flap surgeryFIGURE44-6Illustration
ofsuperiorly based pharyngeal flap operative procedure.A,Creation ofsuperiorly
based flap ofposterior pharyngeal wall soft tissues.The pharyngeal flap is
developed andelevated offofthe prevertebral fascia.Soft palate is divided with a
midline incision from the uvula tothe junction ofthe hard and soft palates.B,Soft
palate oral,nasal,and muscle layer dissection inpreparation for flap
inset.Nasopharyngeal airways are placed in order to help size each lateral pha-
ryngeal port.C,The flap is sutured into the nasal side ofthe soft palate before the
nasal side is repairedand the oral mucosa and underlying musculature are
repaired.D,Sagittal view demonstrating appro-priate vertical level offlap
inset.ABCD
880Part 6: Maxillofacial Reconstructionstart snoring.Snoring itselfdoes not rep-
resent any significant pathophysiology butmay concern parents or significant
otherswho observe the patient during sleep.When the degree ofupper airway resis-
tance is more severe,the result may bepostoperative obstructive sleep
apnea(OSA).OSA is a cessation ofbreathingduring sleep secondary to upper
airwayobstruction that disrupts the sleep cycle,compromises effective
oxygenation,andmay cause behavioral changes and day-time somnolence in affected
individuals.Left untreated,OSA is associated withsevere cardiac and pulmonary
conse-quences.When OSA is suspected in a childwho has previously undergone a
pharyn-geal flap procedure,a formal work-upincluding nasopharyngoscopy and
sleepstudy (polysomnography) is indicated.Care should be taken to evaluate the
entireairway in order to determine the level ofthe obstruction.Surgeons may
initiallyassume that the airway obstruction isrelated to the flap only to discover
that amore severe problem exists somewhereelse in the upper airway
tract.Often,athorough clinical evaluation yields abnor-mal findings that contribute
to the prob-lem ofOSA at multiple levels ofthe upperairway.Because ofthe complexity
oftheseclinical problems,the decision to modifyor take down a pharyngeal flap in a
childwith OSA must be made only after discus-sions between the surgeon,airway
expert(eg,pediatric otolaryngologist or pediatricpulmonologist),and speech and
languagepathologist.Interestingly,many patientswho have had pharyngeal flap
placementduring their childhood will tolerate surgi-cal division ofthe flap without
a recur-rence ofsevere VPI or hypernasal speech.On the rare occasion when VPI does
recurfollowing flap take-down,interval treat-ment with a prosthetic device such as
apalatal lift appliance for at least 6 monthsshould be considered prior to
embarkingon any further airway surgery.Management ofthe Submucous Cleft PalateA
submucous cleft palate is another formofthe congenital cleft palate malforma-tion
in which the overlying mucosal layeris intact,but the underlying soft
palatemusculature is divided.As described byCalnan,the classic clinical findings
witha submucous cleft palate are a triad ofbifid uvula,hard palate bony
notch,andseparation along the median raphe ofthesoft palate especially during
elevation ofthe velum.61When a submucous cleft palate is pre-sent,the levator
muscle is clefted andabnormally inserts into the posterior edgeofthe hard
palate.The primary functionalconcern related to submucous cleft palate isFIGURE44-
7Sphincteroplasty procedure.A,Incision ofthe posterior pharyngeal wall and the
poste-rior tonsillar pillars.B,Elevation ofbilateral myomucosal flaps within the
tonsillar pillars.Care istaken to include palatopharyngeous muscle.C,The mobilized
flaps are then sutured to each other atthe midline.D,Closure is then achieved by
insetting the joined flaps within the posterior pharyngealwall incision.The donor
site ofeach flap is also closed with interrupted sutures.ABCD
Reconstruction ofCleft Lip and Palate: Secondary Procedures881the possibility that
the patient will developVPI and resultant hypernasal speech asencountered in other
cleft palate patients.Despite this concern,the majority ofpatients with a submucous
cleft palate willnot require surgical intervention.In fact,44% ofpatients will
actually remain com-pletely asymptomatic until childhood.62As described above,the
bifid uvula isoften the most easily detected feature ofthesubmucous cleft palate
triad ofclinicalfindings.However,a bifid uvula may alsobe observed in the absence
ofany otherfeatures ofsubmucous clefting (eg,notched hard palate,velar
separation,hypernasality).In fact,the incidence ofbifid uvula is approximately 1:80
while theincidence ofsubmucous cleft palate is1:280.63Previous investigation has
suggest-ed a connection between the isolated find-ing ofa bifid uvula and VP
dysfunctionwhen otherwise asymptomatic patientswere evaluated using a
nasopharyngoscop-ic protocol.64As a result,the clinical findingofan isolated bifid
uvula may be consideredan indicator ofincreased risk for VPI in apatient who is to
undergo adenoidectomy.This underscores the value ofa thoroughclinical examination
before any ofthesesurgical procedures are undertaken and theimportance
ofpresurgical speech evalua-tion and family counseling regarding thepotential risks
ofpostsurgical VPI.A certain proportion ofchildren willpresent with an occult
submucous cleftpalate.The occult submucous cleft palatedoes not have any ofthe
classic triad ofphysical findings.In most cases,the reasonfor consultation is VPI-
related speech dif-ficulties that have been noted duringchildhood speech
development or thathave arisen following a surgical interven-tion
(eg,adenoidectomy).In our experi-ence,the proportion ofchildren withoccult
submucous cleft palate approaches10% and preoperative diagnosis is
oftendifficult.Prior reports have attempted todescribe characteristic facial
features,cephalometric findings,and voice studiesthat can assist in the presumptive
diagno-sis ofsubmucous cleft palate.65The vast majority ofpatients with asubmucous
cleft palate will require eitherno treatment or speech therapy only.Sur-gical
intervention is not undertaken simplybecause the diagnosis ofsubmucous cleftpalate
has been made.The speech oftheseindividuals is closely monitored duringchildhood
with interval speech evaluations,and surgery is reserved for only those caseswhere
VPI is diagnosed and not amenableto speech therapy.The type ofspecific sur-gical
procedure used to manage sub-mucous cleft-related VPI varies dependingon the
preference ofthe surgeon andspeech pathologist.Several early proce-dures emphasized
exploration ofthe softpalate through a limited midline incisionwith repair ofthe
levator muscle.Contem-porary methods primarily involve the useofa standard
palatoplasty (two-flap,push-back,or Furlow) and repair ofthe velarmusculature,with
or without a simultane-ous pharyngeal flap procedure.Bone Graft Reconstruction
ofthe Cleft Maxilla and PalateApproximately 75% ofall orofacial cleftswill involve
the maxilla.5Despite success-ful lip repair and closure ofthe hard andsoft palate
during infancy,a residualnasolabial fistula and bony cleft defect thatinvolves the
alveolar ridge,maxilla,andpiriform rim will remain.These residualdeformities are
addressed by secondarybone grafting performed during middlechildhood (6 to 9 years
ofage).The objec-tives ofbone graft reconstruction ofthecleft maxilla are to
establish adequate bonymatrix for eruption ofthe permanent cus-pid tooth,close any
residual alveolar fistu-la communication,establish bony conti-nuity ofthe maxillary
ridge,and improvethe underlying bony support ofthe nasalbase.In the case
ofbilateral cleft lip andpalate,an added benefit ofbone graftreconstruction is the
stabilization ofthepreviously mobile premaxilla segment.The details ofbone graft
reconstruction ofthe cleft maxilla are discussed in greaterdetail in Chapter
43,�Reconstruction ofthe Alveolar Cleft.�Orthognathic Surgery for Correction
ofMidfacial DeficiencyPatients who have undergone cleft palaterepair during infancy
will often exhibitsome degree ofmaxillary growth restric-tion.This disproportionate
jaw growth isthe biological consequence ofprior surgi-cal intervention and is not
related to thecongenital cleft deformity.Previousauthors have reported a 25%
incidence ofmaxillary hypoplasia that is severe enoughto produce a clinically
significant dento-facial deformity with negative effects onspeech and
occlusion.5,6,17,36The successfulcorrection ofthese secondary skeletaldeformities
frequently requires treatmentprotocols that include orthognathicsurgery in
conjunction with the final phaseoforthodontic treatment.Simultaneousbone grafting
is used for contouring thedysmorphic skeletal structures.The use oforthognathic
techniques to correct residualskeletal problems in the patient with cleftlip and
palate is discussed in greater detailin Chapter 61,�Orthognathic Surgery inthe
Patient with Cleft Palate.�Revisional Surgery for Cleft Lip and Nasal
DeformitiesReconstruction ofthe Cleft Nasal Deformity Congenital clefts that
involve the lip,nose,and underlying skeletal structure will causea complex three-
dimensional deformity ofthe nasal complex that affects both formand
function.66,67In the case ofa completeunilateral cleft,the typical nasal
deformityis characterized by splaying ofthe alar base,inferior displacement ofthe
alar rim,devi-ation ofthe nasal tip,and irregularity ofthe caudal nasal
septum.Abnormal fibrousinsertions exist between the lateral crus ofthe lower
lateral cartilage and the lateral
882Part 6: Maxillofacial Reconstructionpiriform rim on the cleft side.At the
timeofthe initial lip repair procedure,maneu-vers for primary nasal
reconstructioninclude dissection along the lower lateralcartilage in order to
separate the overlyingskin from the cartilage and sharp releaseofthe fibrous
insertions along the piri-form rim so that the nostril can be reposi-tioned
appropriately.Despite effectiveprimary cleft lip and nasal repair
duringinfancy,most patients will demonstrateenough residual nasal dysmorphologythat
secondary nasal surgery for correc-tion ofthe cleft-associated malformationor
improvement in nasal airflow will berequired later in life.The timing ofcleft nasal
revisionalsurgery also remains controversial.Somesurgeons take a more aggressive
approachand undertake extensive nasal reconstruc-tion during early childhood.Our
philoso-phy is to delay the definitive cleft rhino-plasty until the nasal complex
is close tomature size.Ifthe patient�s reconstructivetreatment plan also requires
maxillaryadvancement,then nasal surgery shouldbe delayed until approximately 6
monthsfollowing the orthognathic procedure.This allows for a more predictable out-
come and long-lasting improvement innasal function and facial
esthetics.Earlysurgery is reserved for individuals withsevere airway or nasal
airflow problems orchildren that have the potential to experi-ence psychosocial
consequences such asteasing at school.When possible,earlynasal surgery should be
timed after thebone graft reconstruction ofthe maxilla sothat a stable bony
foundation along thepiriform rim and nasal base exists first.Secondary cleft-nasal
reconstructionwill often require dorsal reduction,lowerlateral cartilage
sculpting,cartilage graft-ing,and nasal osteotomies.Cartilage graft-ing is a
critical component ofthe finalnasal reconstruction and is used for aug-mentation
ofthe dysmorphic lower lateralcartilage and improvement ofnasal
tipprojection5,68,69(T.J.Tejera,DMD,MD,personal communication,November2003).Several
different donor sites may beused including auricular cartilage,nasalseptum,and rib
cartilage.Ear cartilage ismost useful in situations where augmenta-tion
ofhypoplastic cleft-side lower lateralcartilage is required.Septal cartilage ismost
easily accessible and provides anexcellent scaffold for repositioning ofthelower
lateral cartilages and improvementofnasal tip symmetry and
projection.Unfortunately,patients may present fordefinitive nasal reconstruction
havingundergone previous septal cartilage har-vest and not have sufficient quantity
for asecond septal cartilage graft.In these cases,the use ofcostochondral cartilage
isanother excellent option.Rib cartilageprovides adequate amounts ofgraft mate-
rial,but requires a distant donor surgicalsite.We have found this type
ofcartilagegraft to provide excellent strength forstraightening the nasal tip and
alar com-plex.These techniques are best carried outthrough an open rhinoplasty
approach.5Atranscolumellar splitting incision is com-bined with marginal incisions
in order toprovide wide access and direct visualiza-tion ofthe nasal dorsum,upper
and lowerlateral cartilages,and nasal septum.A similar rationale is applied
whenconsidering the timing ofsecondary nasalreconstruction in the bilateral cleft
lippatient,but the specific dysmorphologyaddressed is somewhat different.General-
ly,nasal asymmetry is less problematic,and the dysmorphology is characterizedby
deficient columellar length.Previousliterature has focused on the
secondarylengthening ofthe columella through theuse ofbanked forked flaps or
columellarlengthening using soft tissue flaps from thefloor ofthe nose and alar
flaps.70,71Unfor-tunately,these types ofsurgical proceduresoften result in a
distorted columellar-labial angle,excessive �railroad�scars thatextend onto the
nasal tip,and additionaldistortion ofthe broad nasal tip.We findthat the approach
described by Posnickusing septal cartilage strut grafts attachedto the caudal nasal
septum and lower lat-eral cartilages yields the most natural-looking results.5,6The
objective is correc-tion ofthe underlying cartilaginousanatomy with stretching
ofthe overlyingsoft tissue envelope,instead ofdirect sur-gical manipulation ofthe
columellar skin.Secondary Surgery for Cleft LipScar RevisionEven when the initial
cleft lip repair proce-dure is considered to be successful,the vastmajority
ofchildren will go on to require anadditional operation for lip revision at
somepoint in their lifetime.4,72Although revision-al procedures are often viewed as
optionalphases ofcleft lip reconstruction,surgeonsmust advise families ofthis
likelihood.As a child grows,the hard and soft tis-sues ofthe maxillofacial complex
growand change,and the repaired lip is affect-ed.Ongoing growth often makes it
diffi-cult to predict which children will needadditional lip surgery.A child�s lip
mayinitially look satisfactory and over timedemonstrate unfavorable changes
necessi-tating revision.On the other hand,favor-able changes may occur during the
healingprocess that actually improve the appear-ance ofthe repaired cleft lip.At
approxi-mately 8 to 10 weeks following surgery,sig-nificant lip contracture may be
seen duringthe fibroblastic phase ofhealing.The resultis vertical shortening ofthe
repaired cleftside that will seemingly require furthersurgery.Ifthe same child is
reevaluated 6 months later,after additional woundmaturation,they may demonstrate
per-fectly acceptable lip esthetics and not beconsidered a candidate for
revision.Ideally,only one lip scar revision isundertaken,when the child is between
theages of5 and 15 years.The procedure isstaged for as late in childhood as
possible.When a severe deformity persists or psy-chosocial concerns exist,lip
revision maybe carried out earlier in life before thechild becomes school aged.
Reconstruction ofCleft Lip and Palate: Secondary Procedures883The surgical
objectives ofcleft lip revi-sion include excision ofresidual scar,re-approximation
ofkey anatomic landmarkssuch as the vermilion-cutaneous junctionand vermilion-
mucosal junction,and lev-eling ofvertical lip lengths (philtralcolumns).Critical to
an acceptable out-come is the meticulous repair ofthe orbic-ularis oris muscle as a
distinct layer.Thecleft surgeon must dissect and repair alllayers (skin or
vermilion,muscle,oralmucosa) in order to establish improved lipform and normalize
lip function and ani-mation (Figure 44-8).Often this requirescomplete take-down
ofthe lip and recre-ation ofa full-thickness defect.Comprehensive Dental
andProsthetic Rehabilitation In patients with a cleft ofthe primarypalate (maxilla
and alveolus),three possi-bilities exist with regard to the status ofthepermanent
lateral incisor:(1) the lateral ispresent and erupts normally,(2) the later-al is
congenitally missing,or (3) the lateralis present,but is dysmorphic and not
arestorable tooth.When the lateral incisoris this dysmorphic,extraction is
usuallyrequired prior to or at the time ofbonegraft reconstruction.In those cases
where a lateral incisor isnot present,management ofthe residualdental gap will
eventually be required.Treatment options include the placementofa three-unit fixed
prosthesis,replace-ment ofthe missing tooth with anendosseous dental implant,or
orthodonticsubstitution ofthe ipsilateral cuspid toothfor the lateral incisor.In
contemporary practice,the use ofathree-unit bridge for replacement ofacongenitally
missing incisor is generallyavoided,especially in young patients.Thisprosthetic
option has several disadvan-tages:it usually requires preparation oftwo otherwise
perfectly healthy teeth (cen-tral and cuspid),hygiene is more difficultaround the
pontic,and even in the best ofcircumstances the prosthetic restorationwill require
replacement several times dur-ing the patient�s lifetime.Over the course ofthe past
twodecades,the use oftitanium dentalimplants has revolutionized the
prostheticrehabilitation ofpatients with missingteeth.This technology has also
beenapplied to patients born with cleft lip andpalate (Figure 44-9).73�75The use
ofanimplant-supported crown provides a natural-looking restoration with
excellentlong-term viability and obviates the needfor instrumentation ofthe
surroundingteeth.When a dental implant is being con-sidered,pertinent treatment-
planningconcerns include the maintenance ofade-quate space for the implant and
restora-tion and the quantity ofalveolar boneavailable for placement ofthe
titaniumfixture.Our preferred approach involvesthe preservation ofapproximately 7
mmofinterdental space in order to allow forplacement ofa 3.5 mm dental
implant.Inmost patients who have undergone previ-ous successful bone grafting,the
verticaldimension ofthe alveolar ridge seems tobe well maintained until the time
ofimplant placement.Facial-palatal width ofthe ridge,however,may be more problem-
atic,and a significant number ofcleftpatients may require some additionalminor bone
grafting approximately 3 to 4 months prior to implant surgery.Inmost cases,the
width ofthe alveolus canbe nicely augmented with bone harvestedfrom the mandibular
symphysis or ramusregion.Implant placement requires thatthe patient be at or near
skeletal maturity.Another option for management ofthe cleft dental gap when the
lateral incisoris not present is the use oforthodontictherapy in order to
substitute the missinglateral incisor with the ipsilateral
cuspidtooth.Interestingly,this maneuver fre-quently results in very acceptable
dentalesthetics even ifprosthetic modification ofthe cuspid is not undertaken.Like
the useofa dental implant,this treatment optionalso obviates the need for
preparation ofthe adjacent healthy tooth structure.Inmost cases,the substitution
option alsoeliminates the need for any prostheticcomponent at all.Another advantage
ofthis treatment option is that it may beundertaken at a younger age than theother
prosthetic options.Limiting factorsFIGURE44-8A to C,Unilateral cleft lip revi-
sion.Pre- and immediate postoperative pho-tographs ofa patient undergoing revision
ofaunilateral cleft lip.The full-thickness cleft defectis recreated with care taken
to reconstitute theorbicularis oris muscle.The hypertrophic scarwas excised and
anatomic landmarks includingthe vermilion border,white roll,wet-dry line,and nasal
sill are reapproximated.ABC
884Part 6: Maxillofacial Reconstructionrelated to this option are primarily
relatedto issues oforthodontic anchorage.Summary Orofacial clefts are complex
malforma-tions that affect the three-dimensionalanatomy ofthe maxillofacial hard
and softtissues and have profound functional andesthetic consequences.Successful
recon-struction ofthese defects involves multiplestages ofsurgical
intervention.Primarysurgery is centered on initial closure ofthelip and palatal
defects.Secondary surgicalprocedures are then carried out in order toclose residual
oronasal communication,address VPI,reconstruct the bony maxil-lary cleft,normalize
maxillary skeletalposition and occlusion,improve lip andnasal esthetics and
function,and facilitatethe dental prosthetic rehabilitation ofthepatient.Because
multiple,separate surgi-cal interventions are carried out duringactive
growth,thoughtful timing ofeachstage ofreconstruction is critical in orderto
maximize the benefit for the patient andmitigate the potentially negative
biologicconsequences related to growth.Surgeonsmust maintain a thorough
understandingofthe anatomy,the intricacies ofthe cleftmalformation,and the
underlying pat-terns ofgrowth and development ofthecraniomaxillofacial
region.References 1.Leonard BJ,Brust JD,Abrahams G,et al.Selfconcept ofchildren and
adolescents withcleft lip and/or palate.Cleft Palate Cranio-fac J
1991;28:347.2.Strauss RP.Health policy and craniofacial care:issues in resource
allocation.Cleft PalateCraniofac J 1994;31:78.3.Bergstrom LV.Congenital and
acquired deaf-ness in clefting and craniofacial syndromes.Cleft Palate J
1978;15:254.4.Cohen SR,Corrigan M,Wilmot J,et al.Cumu-lative operative procedures
in patients aged14 years and older with unilateral or bilat-eral cleft lip and
palate.Plast Reconstr Surg1995;96:267.5.Posnick JC.The staging ofcleft lip and
palatereconstruction:infancy through adolescence.In:Posnick JC.Craniofacial and
maxillofacialsurgery in children and young adults.Philadelphia
(PA):W.B.Saunders;2000.6.Posnick JC,Ruiz RL.Stages ofcleft lip andpalate
reconstruction:infancy through ado-lescence.In:Wyszynski DF,editor.Cleft lipand
palate:from origin to treatment.NewYork;Oxford University Press;2002.7.American
Cleft Palate�Craniofacial Associa-tion.Parameters for the evaluation andtreatment
ofpatients with cleft lip/palate orother craniofacial anomalies.Cleft
PalateCraniofac J 1993;30(Suppl 1):4.8.Abyholm FE,Bergland O,Semb G.Secondarybone
grafting ofalveolar clefts.Scand JReconstr Surg 1981;15:127.9.Turvey TA,Vig
K,Moriarty J,et al.Delayedbone grafting in the cleft maxilla andpalate:a
retrospective multidisciplinaryanalysis.Am J Orthod 1984;86:244.10.Cohen
SR,Kalinowski J,LaRossa D,Randall P.Cleft palate fistulas:a multivariate statisti-
cal analysis ofprevalence,etiology,and sur-gical management.Plast Reconstr
Surg1991;87:1041.11.Ogle OE.The management oforonasal fistulasin the cleft palate
patient.Oral MaxillofacialSurg Clin North Am 2002;14:553�62.12.Wilhelmi BJ,Appelt
EA,Hill L,Blackwell SJ.Palatal fistulas:rare with the two-flappalatoplasty
repair.Plast Reconstr Surg2001;107:315�8.13.Stal S,Spira M.Secondary reconstructive
pro-cedures for patients with clefts.In:SerafinD,Georgiade NG,editors.Pediatric
plasticsurgery.St Louis (MO):C.V.Mosby;1984.14.Lehman JA.Closure ofpalatal
fistulas.Op TechPlast Surg 1995;2:255�62.15.Schendel SA.Secondary cleft
surgery.SelectRead Oral Maxillofac Surg 1992;3(6):1�27.16.Posnick JC.Cleft
orthognathic surgery:the iso-lated cleft palate deformity.In:Posnick
JC.Craniofacial and maxillofacial surgery inchildren and young
adults.Philadelphia(PA):W.B.Saunders;2000.17.Turvey TA,Vig KWL,Fonseca
RJ.Maxillaryadvancement and contouring in the pres-ence ofcleft lip and
palate.In:Turvey TA,Vig KWL,Fonseca RA,editors.Facial cleftsand
craniosynostosis:principles and man-agement.Philadelphia (PA):W.B.Saun-
ders;1996.18.Posnick JC,Ruiz RL.Invited discussion.Repairoflarge anterior palatal
fistulas using thintongue flaps:long-term follow-up of10patients.Ann Plast Surg
2000;45:115�7.19.Bozola AR,Ribeiro-Garcia ERB.Partial bucci-nator myomucosal
flap,posteriorly based.Op Tech Plast Surg 1995;2:263�9.20.Ninkovic M,Hubli
EH,Schwabegger A,AnderlH.Free flap closure ofrecurrent palatal fis-tula in the
cleft lip and palate patient.JCraniofac Surg 1997;8:491�5.21.Posnick JC.The
treatment ofsecondary andresidual dentofacial deformities in the
cleftpatient.Surgical and orthodontic treat-ment.Clin Plast Surg
1997;24:583�97.22.Bardach J.Two-flap palatoplasty:Bardach�stechnique.Op Tech Plast
Surg 1995;2:211�4.FIGURE44-9Prosthetic rehabilitation ofa 27-year-oldpatient with
previously unrepaired bilateral maxillary alve-olar clefts.She had undergone
primary lip and palate repairduring infancy but never underwent bone graft
reconstruc-tion.Treatment consisted ofbone graft reconstruction ofthebony clefts
using autogenous corticocancellous bone graftobtained from the anterior iliac crest
followed by dentalimplant placement 6 months later.A,Preoperativepanoramic
radiograph reveals large bilateral bony cleftdefects.B,Panoramic radiograph
following bone graftreconstruction and implant placement.C,Temporary pros-thetic
restoration.Implant placement was performed as asingle-stage procedure with
construction oftemporarybilateral three-unit bridges.ABC
Reconstruction ofCleft Lip and Palate: Secondary Procedures88523.Johnson PA,Banks
P,Brown AE.Use oftheposteriorly-based lateral tongue flap in therepair ofpalatal
fistula.Int J Oral Maxillo-fac Surg 1992;23:6�9.24.Kinnebrew MC,Malloy
RB.Posteriorly based,lateral lingual flaps for alveolar cleft bonegraft coverage.J
Oral Maxillofac Surg1983;41:555�61.25.Costello BJ,Ruiz RL,Turvey
TA.Velopharyngealinsufficiency in patients with cleft palate.Oral Maxillofac Surg
Clin 2002;14:539�51.26.Glaser ER,Skolnick ML,McWilliams BJ,Shprintzen RJ.The
dynamics ofPassavant�sridge in subjects with and without velo-phyngeal
insufficiency.A multiview video-fluoroscopic study.Cleft Palate
Journal1979;16:24�33.27.Passavant G.On the closure ofthe pharynx inspeech.Archiv
Heilk 1863;3:305.28.Passavant G.On the closure ofpharynx inspeech.Virchows Arch
1869;46:1.29.Warren DW.Compensatory speech behaviorsin cleft palate:a
regulation/control phe-nomenon.Cleft Palate J 1986;23:251�60.30.Henningsson
G,Isberg A.Velopharyngealmovements in patients alternating betweenoral and glottal
articulation:a clinical andcineradiographical study.Cleft Palate
J1986;23:1.31.Isberg A,Henningsson G.Influence ofpalatalfistula on velopharyngeal
movements:acineradiographic study.Plast Reconstr Surg1987;79:525.32.Lohmander-
Agerskov A,Dotevall H,Lith A,et al.Speech and velopharyngeal function in chil-dren
with an open residual cleft in the hardpalate,and the influence oftemporary cover-
ing.Cleft Palate Craniofac J 1996;33:324.33.Shprintzen RJ,Bardach J.The use
ofinforma-tion obtained from speech and instrumen-tal evaluations in treatment
planning forvelopharyngeal insufficiency.In:Cleftpalate speech management:a
multidiscipli-nary approach.St Louis (MO):Mosby YearBook;1995.p.257.34.Golding-
Kushner KJ,Argamaso RV,Cotton RT,et al.Standardization for the reporting
ofnasopharyngoscopy and multi-view vide-ofluroscopy:a report from an
internationalworking group.Cleft Palate J 1990;27:337.35.Warren DW,Dalston RM,Mayo
R.Hyper-nasality and velopharyngeal impairment.Cleft Palate Craniofac J
1994;31:257.36.Turvey TA,Ruiz RL,Costello BJ.Surgical cor-rection ofmidface
deficiency in the cleft lipand palate malformation.Oral MaxillofacSurg Clin
2002;14:491�507.37.Fonseca RJ,Turvey TA,Wolford LM.Orthog-nathic surgery in the
cleft patient.In:Fon-seca RJ,Baker SJ,Wolford LM,editors.Oraland maxillofacial
surgery.Philadelphia(PA):W.B.Saunders Co;2000.p 87�146.38.Posnick JC,Tompson
B.Cleft-orthognathicsurgery:complications and long-termresults.Plast Reconstr Surg
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cleft deformi-ties.In:Goldwyn RM,Cohen MM,editors.The unfavorable result in plastic
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function in the pres-ence ofcleft palate.Abstract ofpresenta-tions at the 38th
annual meeting oftheAmerican Cleft Palate Association,Lancast-er,Pennsylavania,May
1980.41.Bernstein L.Treatment ofvelopharyngeal incom-petence.Arch Otolaryngol
1967;85:67�74.42.Rosseli S.Divisione palatine 3 sua aura chirurgi-co.Alu Congr
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derStaphylorraphies.Arch Klin Chirurgie1876;19:528.44.Shprintzen RJ.The use
ofmultiview videofluo-roscopy and flexible fiberoptic nasopharyn-goscopy as a
predictor ofsuccess with pha-ryngeal flap surgery.In:Ellis F,Flack
E,editors.Diagnosis and treatment ofpalatoglossal
malfunction.London:CollegeofSpeech Therapists;1979.p 6�14.45.Argamaso
RV,Levandowski G,Golding�Kush-ner KJ,et al.Treatment ofasymmetricvelopharyngeal
insufficiency with skewedpharyngeal flap.Cleft Palate Craniofac
J1994;31:287.46.Shprintzen RJ,Lewin ML,Croft CB,et al.Acomprehensive study
ofpharyngeal flapsurgery:tailor�made flaps.Cleft Palate J1979;16:46.47.Shprintzen
RJ,McCall GN,Skolnick ML,Lencione RM.Selective movement ofthelateral aspects ofthe
pharyngeal walls dur-ing velopharyngeal closure for speech,blowing,and whistling in
normals.CleftPalate J 1975;12:51�8.48.Randall P,Whitaker LA,Noone RB,Jones WD.The
case for the inferiorly based pharyngealflap.Cleft Palate Craniofac J
1978;15:262�5.49.Hynes W.Pharyngoplasty by muscle transplan-tation.Br J Plast Surg
1951;3:128.50.Hynes W.The results ofpharyngoplasty bymuscle transplantation in
�failed cleftpalate�cases,with special reference to theinfluence ofthe pharynx on
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ofthe dynam-ic muscular sphincter ofthe pharynx.PlastReconstr Surg
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sphincter pharyn-goplasty as a secondary procedure in cleftpalates.Plast Reconstr
Surg 1983;71:180.54.Jackson IT.Sphincter pharyngoplasty.ClinPlast Surg
1985;12:711�7.55.Guilleminault C,Stoohs R.Chronic snoringand obstructive sleep
apnea syndrome inchildren.Lung 1990;168:912.56.Sirois M,Caouette�Laberge L,Spier
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Surg1994;93:943.57.Ysunza A,Garcia�Velasco M,Garcia�GarciaM,et al.Obstructive sleep
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PlastSurg 1954;6:264�82.62.McWilliams BJ.Submucous clefts ofthe palate:how likely
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deformity in clefts.In:Kernahan DA,Rosenstein SW,editors.Cleftlip and palate:a
system ofmanagement.Baltimore (MD):Williams and Wilkins;1990.p.68�73.67.Horswell
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and a primaryforked flap:a preliminary report.PlastReconstr Surg
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alae.Plast Recon-str Surg 1958;21:417.72.Harper DC.Children�s attitudes to physical
dif-ferences among youth from Western andnon-Western cultures.Cleft Palate Cranio-
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with congenital unrepairedcleft palate defects using free iliac crest bonegrafts
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ofresidual alveolar cleftdefects with one-stage mandibular bonegrafts and
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CHAPTER 45Nonsyndromic CraniosynostosisG.E.Ghali,DDS,MDDouglas P.Sinn,DDSIn its
basic form craniosynostosis repre-sents premature suture fusion.It occurs
inapproximately 1 per 1,000 live births in theUnited States.Craniosynostosis may
beclassified as nonsyndromic or syndromic.Most forms ofcraniosynostosis are isolat-
ed and not associated with any other con-ditions and are therefore
nonsyndromic.Syndromic craniosynostosis will be cov-ered in another chapter.The
pathogenesisofcraniosynostosis is complex and proba-bly multifactorial.Moss
theorized thatcraniosynostosis such as seen in Apert andCrouzon syndromes results
from abnor-mal tensile forces transmitted to the durafrom an anomalous cranial base
throughkey ligamentous attachments.1Thishypothesis fails to explain craniosynosto-
sis in patients with a normal cranial baseconfiguration.The cause ofcraniosynos-
tosis may be postulated to be the result ofeither primary suture
abnormalities,suffi-cient extremes offorces that overcome theunderlying expansive
forces ofthe brain,inadequate intrinsic growth forces ofthebrain,or various genetic
and environmen-tal factors.2Cranial vault growth achievesapproximately 80% ofthe
adult size atbirth and definitive size by 2.5 to 3 years ofage.3The existence ofthe
six major sutur-al regions allows for head expansion aswell as transvaginal head
deformation.4Recall that posterior fontanelle closure (3 �6 mo) generally precedes
anteriorfontanelle closure (9 � 12 mo).Functional ConsiderationsThe major
functional problems associatedwith craniosynostosis are
intracranialhypertension,visual impairment,limita-tion ofbrain growth,and
neuropsychiatricdisorders.5In general the functional prob-lems increase as the
number ofsuturesinvolved increases.5These functionalabnormalities are gradual in
their develop-ment,difficult to detect,and often irre-versible in
nature.Intracranial HypertensionIntracranial hypertension is defined as apressure
ofgreater than 15 mm Hg.Stud-ies by Marchac and Renier have demon-strated a 13%
incidence ofintracranialhypertension with single suture stenosisand up to a 42%
incidence in multisuture-stenosed children.6The clinical symptomsofintracranial
hypertension includeheadaches,irritability,and difficulty sleep-ing.The
radiographic signs may includecortical thinning or a l�ckensch�del (ham-mered
metal) appearance ofthe innertable ofthe skull;these clinical and radi-ographic
signs are relatively late develop-ments.Ifintracranial hypertension
goesuntreated,it affects brain function;ifper-sistent this may necessitate early
operativeintervention during the first few monthsoflife.Intracranial hypertension
mostlikely affects those with the greatest dis-parity between brain growth and
intracra-nial capacity and may occur in as many as42% ofuntreated children with
more thanone suture affected.Currently intracranialvolume is measured using
computedtomography (CT) scans,a noninvasivemethod appropriate for use in
childrenwith craniosynostosis.It might be possibleto identify individuals who are
at a greaterrisk for developing intracranial hyperten-sion and would benefit the
most fromearly surgery.Visual ImpairmentIntracranial hypertension,ifleft untreat-
ed,may lead to papilledema,typicallyacute.After chronic intracranial hyperten-
sion,eventually optic atrophy develops,which results in complete or partial blind-
ness.Some forms ofcraniosynostosis mayinvolve orbital hypertelorism and maylead to
compromised visual acuity andrestricted binocular vision.Limitation ofBrain
GrowthBrain volume in the normal child almosttriples during the first year
oflife.By 2years ofage the cranial capacity is fourtimes that at birth.Ifbrain
growth is toproceed unhindered,open sutures at thelevel ofthe cranial vault and
base mustspread during phases ofrapid growth formarginal ossification.In
craniosynostosis,premature suturefusion is combined with continuing
braingrowth.Depending on the number and
888Part 6: Maxillofacial Reconstructionlocation ofprematurely fused sutures andthe
timing ofclosure,the growth potentialofthe brain may be limited.Surgical inter-
vention can provide suture release andreshaping to restore a more
normalintracranial volume.In general this does notcompletely reverse
craniosynostosis,anddiminished volume is often the end result.Neuropsychiatric
DisordersNeuropsychiatric disorders are believed tobe secondary to cerebral
compression.Disorders range from mild behavioral dis-turbances to overt mental
retardation.Several studies have shown that childrenwith craniosynostosis and
associated neu-ropsychiatric disorders often improve aftercranial vault
reconstruction.DiagnosisOne should suspect craniosynostosis inany infant with an
abnormal head shape.Definitive diagnosis is based on clinicaland radiographic
evaluations.The clinicalevaluation involves the palpation oftheskull for any
movement,ridging,and pres-ence ofthe anterior and posteriorfontanelles.Quantitative
measurements ofthe superior orbital rims,relative to themost anterior aspect ofthe
cornea,alsomay help in planning treatment for supe-rior orbital rim
advancements.The radiographic evaluation ofcra-niosynostosis is used to define
quantitativelyaberrant anatomy,plan surgical procedures,and,most
importantly,provide a means todemonstrate to the parents the differencebetween
stenosed and nonstenosed sutures.Conventional skull radiographs,such as plainskull
films and lateral cephalograms,areinexpensive and widely available.The preop-
erative assessment ofpatients with suspectedor known craniosynostosis is based on
theseconventional radiographs.Most cases ofsyn-ostosis can be demonstrated on plain
skullfilms.Normal or patent cranial sutures man-ifest as a line.The absence ofa
radiolucentline in the normal anatomic position ofasuture may suggest
craniosynostosis.Currently,CT scans provide improvedhard tissue imaging.The
definition ofthese elements ofthe bony facial structureson high-resolution CT
images with orwithout three-dimensional reconstructionis unmatched by other imaging
techniques(Figure 45-1).The development ofCTscanning,particularly three-
dimensionalreformatting,and the maturation ofread-ily available means
ofcraniofacial surgeryhave led to a close dependence on CTscanning for preoperative
surgical plan-ning.CT scanning also has been used todocument surgical changes in
vivo and tofollow developments longitudinally.7�18ClassificationThe classification
ofcraniosynostosis isbased on the shape ofthe skull,which usu-ally reflects the
underlying prematurelyfused suture or sutures.19,20The major cra-nial vault sutures
that may be involvedinclude the left and right coronal,metopic,sagittal,and
lambdoid sutures.Unilateral Coronal SynostosisUnilateral coronal synostosis results
inflatness on the ipsilateral side ofthe fore-head and supraorbital ridge
region.Thehead is inherently asymmetric in shapewith a flattened or retropositioned
fore-head on the ipsilateral side,especiallywhen viewed from the top (Figure 45-
2).The term for this deformity is �anterior pla-giocephaly.�One should rule out
infantmolding or positional plagiocephaly andcongenital torticollis as other
possible diag-noses.Premature fusion ofthe unilateralFIGURE45-1Computed
tomographyscan withthree-dimensional reconstruction.Patency ofmetopicand coronal
sutures as well as anterior fontanelle;premature fusion ofsagittal
suture.Reproduced withpermission from Ghali GE et al.46p.3.FIGURE45-2Frontal and
superior views.Char-acteristic right anterior plagiocephaly.Adaptedfrom Ghali GE et
al.46p.4.
Nonsyndromic Craniosynostosis889coronal suture represents 20% ofthe iso-lated or
nonsyndromic cases ofsynostosisin the United States.Characteristic mor-phologic
features occur on the ipsilateralside.The frontal bone is flat,and thesupraorbital
ridge and lateral orbital rimare recessed (Figure 45-3).The orbit isshallow,and the
anterior cranial base isshort in the anteroposterior dimension.The root ofthe nose
may be constrictedand deviated to the affected side (Figure45-4).The ipsilateral
zygoma and infraor-bital rim also may be flat and recessed.Bilateral Coronal
SynostosisBilateral coronal synostosis is the mostcommon cranial vault suture
synostosispattern associated with Apert andCrouzon syndromes.Bilateral
coronalsynostosis results in recession ofthesupraorbital ridges,which causes
theoverlying eyebrows to sit posterior to thecorneas.In addition to the
recessedsupraorbital bone,the forehead appearsto be lower and there is sagittal
shorten-ing ofthe skull (Figure 45-5).The termfor this cranial vault deformity
is�brachycephaly.�The anterior cranialbase is short in the anteroposteriordimension
and wide transversely.Theoverlying cranial vault is high in thesuperior-inferior
dimension,with anteri-or bulging ofthe upper forehead thatresults from compensatory
growth ofthepatent metopic suture (Figure 45-6).Theorbits are also shallow
(exorbitism),withthe eyes bulging (exophthalmus) andabnormally separated (orbital
hyper-telorism).Brachycephaly represents 20%ofthe isolated craniosynostosis cases
inthe United States and is the most com-mon syndrome-associated synostosis.Metopic
SynostosisMetopic synostosis usually occurs in isola-tion and results in a
triangular shape to theskull (Figure 45-7).The term for this cra-nial vault
deformity is �trigonocephaly.�The associated cranial vault deformity con-sists
ofrelative hypotelorism,an elevatedsupraorbital ridge medially,and posterior-
inferior recession ofthe lateral orbital rimsand lateral aspect ofthe
supraorbitalridges.Palpation often reveals a prominentmidline keel in the region
ofthe metopicsuture.(Figure 45-8).The bitemporalwidth is decreased,which results in
anFIGURE45-3Superior view.Recessed frontalbone,supraorbital ridge,and lateral
orbital rimon patient�s right side.Reproduced with permis-sion from Ghali GE et
al.46p.5.FIGURE45-4Frontal view.Nasal bridge androot deviation to the affected
(right) side charac-teristic in plagiocephaly.Reproduced with per-mission from
Ghali GE et al.46p.5.FIGURE45-5Frontal and superior views.Char-acteristic
brachycephaly.Adapted from Ghali GEet al.46p.4.FIGURE45-6Frontal view.High cranial
vaultand transverse widening characteristic ofbrachy-cephaly.Note visible ridging
in the bicoronalsuture region.Reproduced with permission fromGhali GE et al.46p.7.
890Part 6: Maxillofacial Reconstructionabnormal anterior cranial vault shape
anddecreased anterior cranial vault volume.The overlying forehead is sloped
posterior-ly to approximately the level ofthe coronalsutures.Trigonocephaly
represents 10% ofthe nonsyndromic craniosynostosis casesin the United
States.Sagittal SynostosisSagittal synostosis,the most commonform,is rarely
associated with increasedintracranial pressure.The skull typicallyhas
anteroposterior elongation with acompensatory transverse narrowing(Figure 45-9).The
term for this cranialvault deformity is �scaphocephaly.�Thedeformity consists ofan
elongatedanteroposterior dimension and a narrowtransverse dimension to the cranial
vault(Figure 45-10).Usually,the midface andanterior cranial vault sutures are
notaffected.Scaphocephaly represents 50%ofall single-suture craniosynostosis
casesin the United States.Unilateral Lambdoid SynostosisUnilateral lambdoid
synostosis results inflatness ofthe affected ipsilateral parieto-occipital
region.The location ofthe earcanal and external ear are more posteriorand inferior
on the ipsilateral side com-pared with the contralateral side.Thisconfiguration is
more noticeable whenthe patient is examined from the superi-or view and is
relatively inconspicuousfrom the frontal or profile views.Theterm for this cranial
vault deformity is�posterior plagiocephaly.�One shouldrule out infant molding and
congenitaltorticollis (Figure 45-11).With position-al (or deformational)
plagiocephaly,theipsilateral ear and forehead are posi-tioned anteriorly,and the
ear is not infe-riorly displaced as it is with true unilater-al lambdoid fusion.The
use ofhead-molding helmet therapy hasreceived renewed interest in the pastdecade as
the preferred treatment ofchil-dren with positional head shape abnor-malities.21The
overall incidence oftrueunilateral lambdoid synostosis is lessthan 3% ofall
isolated synostosis cases inthe United States.FIGURE45-7Frontal and superior
views.Char-acteristic trigonocephaly.Adapted from GhaliGE et al.46p.8.FIGURE45-
8Intraoperative view followingshaving ofthe head demonstrates prominentmidline
ridging.Reproduced with permissionfrom Ghali GE et al.46p.9.FIGURE45-9Lateral and
superior views.Char-acteristic scaphocephaly.Adapted from Ghali GEet
al.46p.10.FIGURE45-10Intraoperative view followingshaving ofthe head demonstrates
prominentsagittal suture ridging associated with scapho-cephaly.Reproduced with
permission from GhaliGE et al.46p.11.
Nonsyndromic Craniosynostosis891Principles ofManagementMultidisciplinary
TeamApproachThe multidisciplinary team approach wasdeveloped in response to the
failures thatcommonly occurred when various aspectsofcare were not coordinated and
when therelationships among coexisting problemswere not known.3,22The objectives
ofthisapproach are diagnosis,formulation,andexecution oftreatment plans and
longitu-dinal follow-up for patients with craniofa-cial deformities;the team should
meet atleast monthly for regular outpatient evalu-ations.Transcripts ofthese
evaluations areforwarded with recommendations to pri-mary care providers and
appropriate agen-cies.Children under the age of5 years areusually evaluated
annually,whereas chil-dren over 5 years ofage are seen everyother year.The
frequency ofevaluationvaries with the stability ofthe deformityand its
consequences.The craniofacial team should consistofa pediatric anesthesiologist,a
pediatricophthalmologist,a surgeon,an audiolo-gist,a maxillofacial
prosthodontist,anorthodontist,a psychologist,a geneticist,an otolaryngologist,a
pediatrician,socialworkers,a speech pathologist,and anurse.23�27All these team
members haveintegral roles at various times in the child�sdevelopment.28,29Current
Surgical ApproachThe goals ofcraniosynostosis suturerelease are twofold.The first
goal is toallow the brain to grow and expand with-out restriction.The second goal
is toestablish a more normal contour to theforehead,supraorbital
ridges,andskull.30�32In most cases,an intracranialapproach is used for cranial
vault andorbital osteotomies,with reshaping andadvancement ofbony segments for
idealage-appropriate bony morphology.Whenplanning the time and type
ofsurgicalintervention,one must consider the func-tions,future growth,and the
developmentofthe craniofacial skeleton and the main-tenance ofnormal body
image.Simplecraniosynostosis can be managed success-fully with frontocranial
remodeling.Although the timing ofcraniosynos-tosis repair remains controversial
andindividualized,we prefer early surgicalrepair between the ages of4 and 8
months.33�35Early surgical repair allowsfor rapid frontal lobe growth,which sup-
ports the forehead and supraorbital ridgeadvancement.At this age,the cranium
ishighly malleable and therefore easier tocontour;a positive effect on facial
growthmay be achieved and future deformitiesmay be lessened.Also during this
periodofrapid growth,residual bony defectsheal more rapidly.In severe forms
ofcraniosynostosis,additional revision ofthe cranial vault and orbit is
necessaryduring infancy or early childhood toincrease intracranial volume
further,which allows for continued brain growthand avoids or reduces the likelihood
ofintracranial hypertension.A craniotomy is performed by a pedi-atric neurosurgeon
to remove thedeformed section ofcranium and provideaccess for osteotomies to be
performed inthe cranial base.The skeletal segments arereshaped and replaced into a
new posi-tion.Although many ofthe followingexamples ofsurgical repair depict trans-
osseous wiring and titanium plating,thecurrent trend includes the use ofresorbable
plates and screws.These plates,which are composed ofpolylactic andpolyglycolic
acid,are completely resorbedby hydrolysis within 9 to 14 months whilemaintaining
tensile strength for initial sta-bilization.36�38As a result,growth restric-tions
are minimized,as is the potential fortranscranial migration.Surgical
ConsiderationsUnilateral Coronal SynostosisMultiple surgical approaches for the
cor-rection ofunilateral coronal synostosis(Figures 45-12 and 45-13) have
beendescribed.39�41Good long-term resultsare obtained when treatment
ofcoronalsynostosis includes suture release alongwith cranial vault and orbital
osteotomiesfor reshaping and advancement in infan-cy.At the Louisiana State
UniversityHealth Sciences Center in Shreveport,unilateral orbital rim advancement
andFIGURE45-11Frontal(A) and superior(B)views ofa child with positional
plagiocephaly.Radiographic and clinical examination demon-strated no evidence
ofcraniosynostosis; noteAasymmetry ofexternal ear position.B
892Part 6: Maxillofacial Reconstructionfrontal bone reshaping are ideally per-
formed at 6 to 8 months ofage.Othercenters have reported good results whentreatment
is provided between the ages of2.5 and 3 years.To achieve optimal sym-metry,we
prefer to use a bilateral surgicalapproach.Symmetry ofthe cranial vaultand orbit
must be achieved duringsurgery,because results generally do notimprove over
time.Stabilization isachieved by using direct intraosseouswires or resorbable
plates and screws.Bilateral Coronal SynostosisThe treatment ofbilateral coronal
synos-tosis (Figures 45-14 and 45-15) requiressuture release and simultaneous
bilateralorbital rim and frontal bone advance-ments.42,43Surgery is performed when
thepatient is between 6 and 8 months ofage.Other centers have reported good
resultswith children treated between the ages of2.5and 3 years ofage.The
osteotomies for thebilateral orbital rim advancement are madesuperior to the
nasofrontal and frontozygo-matic sutures and extend to the squamousportion ofthe
temporal bone.Stabilizationis achieved with direct transosseous wires orresorbable
plates and screws.The more nor-malized shape providesthe needed increaseFIGURE45-
12A child with unilateral coronal synostosis resulting in left-sided anterior
plagiocephaly.A,Asymmetric forehead and orbit viewed from above.Notemarked left
supraorbital retrusion and right forehead and cranial vault bulging.B,Bur holes
prepared for bifrontal craniotomy at the level ofthe supraorbitalregion,allowing a
1 cm fronto-orbital unit (bandeau),which extends into the temporal fossa via
tongue-in-groove (tenon) extensions.Note that the degree ofextension into the
lateral and inferior orbital rims is variable based on esthetics.C,The removed
bandeau is contoured bilaterally via removal ofwedges from theleft orbital roofand
scoring the right orbital roof.D,The bandeau is reshaped to achieve symmetry by
bending the left side and straightening the right side.EandF,Stabilization
offorehead and bandeau achieved via resorbable plates and screws.Adapted from Ghali
GE et al.46p.14�15.CDEFAB
Nonsyndromic Craniosynostosis893FIGURE45-13A,Six-month-old patient with right
anterior plagiocephaly placed in supine positionand head secured in a Mayfield
headrest.A coronal incision is used and the anterior scalp flap is ele-vated
subperiosteally along with the temporalis muscle.Extension may be carried pre- or
postauricularas needed.B,Subperiosteal dissection is achieved bilaterally
circumferentially in the periorbital,lateralcanthal,lateral orbital,and zygomatic
buttresses.Care is taken to maintain the integrity ofthe medialcanthal
ligaments.Posterior scalp flap is dissected subperiosteally to between the coronal
and lambdoidsutures.Area ofproposed bifrontal craniotomy and bur holes are
marked.C,Neurosurgeon performsbifrontal craniotomy using Midas Rex drill.D,Frontal
and temporal lobes ofthe brain are gently repo-sitioned to perform upper orbital
and temporal osteotomies through the skull base.Reciprocating saw isused to perform
bilateral tongue-in-groove extensions from external approach to the level
ofpterion.E,Attention is turned to the anterior skull base osteotomy and the saw is
directed internally across theskull base anterior to the olfactory bulbs while
retracting the frontal lobe.F,In addition to frontal loberetraction,the orbital
contents must be protected via retraction at this time.The level ofthe osteotomyat
the lateral orbital rim is customized as needed from as high as the frontozygomatic
suture to as lowas the lateral aspect ofthe orbital floor into the inferior orbital
fissure.G,Bandeau has been removedand asymmetry noted prior to reshaping.H,Left
oblique view following remodeling and recontouringofthe bandeau but prior to
frontal bone placement.Resorbable plates and screws are used for fixation.
(CONTINUEDONNEXTPAGE)ACFHEBDG
894Part 6: Maxillofacial ReconstructionFIGURE45-13 (CONTINUED)I,Retraction
ofbifrontal lobes demonstrates differential degree ofadvancement on the right side
at anterior skull base.J,Supe-rior view ofanterior cranial vault prior to
reshaping.K,Superior view ofanterior cranial vault after osteotomies,reshaping,and
resorbable plate and screwfixation ofthe bone segments.Barrel-staving cuts may be
made in the temporal and parietal bones as needed for reshaping purposes.L,A 6-
month-old boywith right unilateral plagiocephaly.He underwent anterior cranial
vault and bilateral superior orbital rim osteotomies with reshaping and
advancementby the procedure described.Preoperative frontal view is shown.M,Frontal
view 6 weeks after reconstruction.N,Preoperative superior view.O,Superiorview 6
weeks after reconstruction.P,Frontal view 2 years after reconstruction.Q,Superior
view 2 years afterreconstruction.Reproduced with permissionfrom Ghali GE et
al.46p.16�24.LOPMNQIJK
Nonsyndromic Craniosynostosis895in intracranial volume within the anteriorcranial
vault.Metopic SynostosisSurgical treatment ofmetopic synostosis(Figures 45-16 and
45-17) involvesmetopic suture release,simultaneousbilateral orbital rim
advancements,andlateral widening via frontal boneadvancement.These procedures are
usu-ally performed at 6 to 8 months ofage.Orbital hypotelorism is corrected
bysplitting the supraorbital ridge unit verti-cally in the midline and placing
autoge-nous cranial bone grafts to increase theintraorbital distance.Stabilization
isachieved with direct transosseous wiresor resorbable microplate
fixation.Themicroplate fixation is usually placed atthe inner surface ofthe cranial
bone.Theabnormally shaped bone that has beenremoved is cut into sections
ofappropri-ate shape for the new forehead configura-tion.The anterior cranial
base,anteriorcranial vault,and orbit are given a moreesthetic shape,and the volume
oftheanterior cranial vault is increased,whichFIGURE45-14Brachycephaly before and
afteranterior cranial vault and bilateral superior orbitalrim
osteotomies,reshaping,and advancements.A,Site ofosteotomies as indicated.Dissection
andosteotomies are similar to that previously describedfor plagiocephaly
repair.B,After osteotomies,reshaping,and fixation ofbandeau and
frontalplates.Adapted from Ghali GE et al.46p.25.ABFIGURE45-15A female infant born
with bilateral coronal synostosis and apparent normal growthofher midface.She
underwent anterior cranial vault and bilateral superior orbital rim osteotomieswith
reshaping at 6 months ofage as previously described.A,Frontal view soon after
birth.B,Supe-rior view preoperatively at 6 months ofage.C,Intraoperative lateral
view ofanterior cranial vaultand orbits after osteotomies,reshaping,and fixation
ofsegments.D,Frontal view at 3 years ofage.E,Superior view at 1 year
ofage.Reproduced with permission from Ghali GE et al.46p.25�7.ADECB
896Part 6: Maxillofacial Reconstructionallows the brain adequate space.Autoge-nous
bone may be taken from the poste-rior cranium,when required,to enhancefrontal
reconstruction.Sagittal SynostosisHistorically,when premature closure ofasagittal
suture (Figures 45-18 and 45-19) wasrecognized in early infancy,most neurosur-geons
believed that simple release ofthesagittal suture through a strip
craniectomywithout simultaneous skull reshaping wasadequate treatment.4,36,44,45Our
results usingthis technique have been less than favorable,and a residual cranial
vault deformity usual-ly results.Ifimprovements in cranial vaultshape are to be
achieved,most cases requirea formal total cranial vault reshaping at theage of4 to
8 months.Variations in the degreeofthe scaphocephalic deformity are com-
mon,depending on the extent ofsagittalsuture stenosis.When the posterior
halfisfused,the patient is treated in the proneposition with the posterior two-
thirds ofthecranial vault reshaped.When the anteriorhalfis fused,the patient is
treated in thesupine position with the anterior two-thirdsofthe cranial vault
reshaped,with or with-out superior orbital rim reshaping.Whenthe entire suture is
fused,a combination ofFIGURE45-16Trigonocephaly repair after anterior cra-nial
vault and superior orbital rim osteotomies.For themost part,the surgical approach
is similar to that previ-ously described for anterior cranial vault and
superiororbital rim osteotomies and reshaping.A,As part ofthereshaping,the bandeau
is often split vertically at themidline and an interpositional autogenous cranial
bonegraft placed to correct hypotelorism.B,Resorbable formsoffixation lend
themselves to internal plating ofthebandeau as shown.Adapted from Ghali GE et
al.46p.28.ABABCDEFGHFIGURE45-17A 10-month-old girl with metopic synostosis
resulting in trigonocephaly.She underwent anterior cranial vault reshaping,bilat-
eral superior orbital rim advancements,and bitemporal widening via barrel-staving
osteotomies.A,Frontal view before surgery.B,Frontal viewafter
reconstruction.C,Superior view before surgery.D,Superior view after
reconstruction.E,Frontal view at 2 years ofage.F,Superior view at2 years
ofage.G,Frontal view at 4 years ofage.H,Inferior view at 4 years ofage.
(CONTINUEDONNEXTPAGE)
Nonsyndromic Craniosynostosis897PreoperativePostoperativeFIGURE45-18A child after
total cranial vault and upper orbital osteotomies for the treatment
ofscaphocephaly.A,Forehead is symmetrically tilted back.Theocciput is symmetrically
tilted forward.The anterior-posterior dimension is thereby shortened and secured
via resorbable plates and screws.Barrel-stave cuts aremade laterally to widen the
transverse dimension or the squamous portion ofthe temporal plates as
osteotomized,interchanged,and stabilized with resorbable platesand screws.Superior
view preoperatively (B) and postoperatively (C).Total cranial vault reshaping as
well as orbital rim alteration is accomplished to increase thebiparietal width and
decrease the frontal and occipital prominences.Adapted from Ghali GE et
al.46p.35.ABCFIGURE45-17 (CONTINUED)I,Intraoperative frontal view outlining
proposedosteotomy and bifrontal craniotomy sites.J,Superior view ofbandeau prior
toreshaping.K,Superior view ofbandeau after reshaping and resorbable plate andscrew
stabilization.L,Frontal view ofbandeau after reshaping and resorbableplate
fixation.M,View ofsame bandeau from cranial aspect.N,Superior viewafter fixation
ofbandeau.Pivoting point ofrotation is about the glabellar region.Observation ofthe
gap between the bandeau and anterior cranial base assists inassessing ideal
placement and bitemporal expansion.O,Superior-oblique view ofanterior cranial vault
prior to reshaping.P,Superior-oblique view ofanterior cra-nial vault after
osteotomies,reshaping,and fixation.Reproduced with permissionfrom Ghali GE et
al.46p.28�34.IJKLMNOP
898Part 6: Maxillofacial Reconstructionboth approaches may be necessary.Unless
asignificant concomitant supraorbital defor-mity exists,we prefer to treat full
sagittalsuture stenosis (anterior and posterior) atone operative setting in the
prone positionvia a total cranial vault reshaping.For olderchildren (older than 1
year) or childrenwith a need for upper orbital reconstruc-tion,we prefer the supine
position at oneoperative setting or,rarely,in two stages,with posterior
reconstruction precedinganterior and orbital reconstruction by 4 to6 months.Other
centers have reportedgood results when routinely staging fullsagittal
synostosis.FIGURE45-19A 6-month-old girl with anterior and posterior sagittal
suture synostosis resulting inscaphocephaly.She underwent total cranial vault
reshaping without the need for any orbitalosteotomies.A prone position was used
throughout the procedure.A,Lateral view before surgery.B,Lateral view after
reconstruction.C,Superior view before surgery.D,Superior view after recon-
struction.E,Prone positioning is necessary and requires careful protection ofboth
the airway andglobes.F,Intraoperative superior view ofproposed osteotomy sites for
total cranial vault reshaping.G,Intraoperative superior view ofthe
osteotomies,reshaping,and resorbable plate fixation.H,Intra-operative left lateral
view prior to reshaping.I,Intraoperative left lateral view after
osteotomies,reshaping,and resorbable plate fixation.Reproduced with permission from
Ghali GE et al.46p.36�40.ABCDEFGHI
Nonsyndromic Craniosynostosis899Unilateral Lambdoid SynostosisMany surgeons
consider simple stripcraniectomy ofthe involved suture or par-tial craniectomy
ofthe region to be ade-quate treatment.More extensive vaultcraniectomy and
reshaping are generallynecessary.Ifimprovements in cranial vaultshape are required
after 10 to 12 months ofage,formal posterior cranial vault reshap-ing is
performed.SummaryIn approximately 1 in 1,000 live births inthe United States,an
infant has some vari-ant ofa craniofacial deformity.Ifcleft lipand palate
deformities are included,theincidence is even greater.Surgical manage-ment ofthese
patients has been advocatedto occur from the first few weeks afterbirth until well
into the second decade.Many ofthese patients require multiple,staged procedures
that involve movementsofthe bone and soft tissue from both theintracranial and
extracranial approaches.The surgical approach to most ofthesecongenital deformities
was radicallychanged by techniques introduced to theUnited States by Paul Tessier
ofFrance in1967.From his imaginative intracranialand extracranial
approaches,numerousadvances have been made that facilitatethe biodegradable plating
systems,whichhave improved the management ofthesecomplex craniomaxillofacial
deformities.References 1.Moss ML.The pathogenesis ofpremature cra-nial synostosis
in man.Acta Anat (Basel)1959;37:351.2.Zeiger JS,Beaty TH,Hetmanski JB,et al.Genetic
and environmental risk factors forsagittal craniosynostosis.J Craniofac
Surg2002;13:602�6.3.Brodsky L,Ritter-Schmidt DH,Holt L.Cranio-facial anomalies:an
inter-disciplinaryapproach.St.Louis (MO):Mosby Yearbook;1989.4.Graham JM,de Saxe
M,Smith DW.Sagittalcraniosynostosis:fetal head constraint as onepossible cause.J
Pediatr 1979;95:747�50.5.Magge SN,Westerveid M,Pruzinsky T,PersingJA.Long-term
neuropsychologic effects ofsagittal craniosynostosis on child develop-ment.J
Craniofac Surg 2002;13:99�104.6.Marchac D,Renier D.Treatment ofcraniosyn-ostosis in
infancy.Clin Plast Surg 1987;14:61�72.7.Cutting C,Grayson B,Bookstein F,et
al.Computer-aided planning and evaluationoffacial and orthognathic
surgery.ClinPlast Surg 1986;13:449�62.8.Gault D,Brunelle F,Renier D,Marchac
D.Thecalculation ofintracranial volume using CTscans.Childs Nerv Syst
1988;4:271�3.9.Lo LJ.Craniofacial computer-assisted surgicalplanning and
simulation.Clin Plast Surg1994;21:501�16.10.Marsh JL,Gado M.The longitudinal
orbital CTprojection:a versatile image for orbital assess-ment.Plast Reconstr Surg
1983;71:308�17.11.Marsh JL,Vannier MW.Computer-assistedimaging in the
diagnosis,management andstudy ofdysmorphic patients.In:Vig KWL,Burdi
AR,editors.Craniofacial morphogene-sis and dysmorphogenesis.Ann Arbor:Uni-versity
ofMichigan Press;1988.p.109�26.12.Marsh JL,Vannier MW.The �third�dimensionin
craniofacial surgery.Plast Reconstr Surg1983;71:759�67.13.Marsh JL,Vannier
MW.Three-dimensionalsurface imaging from CT scans for thestudy ofcraniofacial
dysmorphology.JCraniofac Genet Dev Biol 1989;9:61�75.14.Marsh JL,Vannier MW,Stevens
WG,et al.Computerized imaging for soft tissue andosseous reconstruction in the head
andneck.Clin Plast Surg 1985;12:279�91.15.Marsh JL,Vannier MW,Bresina
S,HemmerKM.Application ofcomputer graphics incraniofacial surgery.Clin Plast
Surg1986;13:441�8.16.Posnick JC,Bite U,Nakamo P.Comparison ofdirect and indirect
intra-cranial volumemeasurements.In:Proceedings ofthe 6thInternational Congress on
Cleft Palate andRelated Craniofacial Anomalies.June15�18,1989.17.Posnick
JC.Indirect intracranial volume mea-surements using CT scans:clinical applica-tions
for craniosynostosis.Plast ReconstrSurg 1992;89:34�45.18.Vannier MW,Marsh JL,Warren
JO.Threedimension CT reconstruction images forcraniofacial surgical planning and
evalua-tion.Radiology 1984;150:179�84.19.Longacre JJ,Destafano GA,Holmstrand
K.Theearly versus the late reconstruction ofcon-genital hypoplasia ofthe facial
skeleton andskull.Plast Reconstr Surg 1961;27:489�504.20.Oakes
WJ.Craniosynostosis.In:Serafin D,Geargiade NG,editors.Pediatric
plasticsurgery.St.Louis (MO):C.V.Mosby Co.;1984.p.404�39.21.Seymour-Dempsey
K,Baumgartner JE,Teich-graeber JF,et al.Molding helmet therapy inthe management
ofsagittal synostosis.J Craniofac Surg 2002;13:631�35.22.Sinn DP,Ghali GE,Ortega
M.Major craniofa-cial surgery.In:Levin DL,Morriss FC,edi-tors.Essentials
ofpediatric intensive care.New York:Churchill-Livingstone;1997.p.636�43.23.Arndt
EM,Travis F,Lefebvre A,Munro IR.Psy-chological adjustment of20 patients
withTreacher Collins syndrome before and afterreconstructive surgery.Br J Plast
Surg1987;40:605�9.24.Barden RC,Ford ME,Jensen AG,et al.Effectsofcraniofacial
deformity in infancy on thequality ofmother-infant interaction.ChildDev
1989;60:819�24.25.Barden RC,Ford ME,Wilhelm W,et al.Thephysical attractiveness
offacially deformedpatients before and after craniofacialsurgery.Plast Reconstr
Surg 1988;82:229�35.26.Barden RC,Ford ME,Wilhelm W,et al.Emo-tional and behavioral
reactions to faciallydeformed patients before and after cranio-facial surgery.Plast
Reconstr Surg 1988;82:409�18.27.Lafebvre A,Travis F,Arndt EM,Munro IR.A psychiatric
profile before and after recon-structive surgery in children with
Apert�ssyndrome.Br J Plast Surg 1986;39:510�3.28.Arnaud E,Meneses P,Lajeunie E,et
al.Postop-erative mental and morphological outcomefor nonsyndromic brachycephaly.J
Cranio-fac Surg 2002;110:6�12.29.Warschausky S,Kay JB,Buchman S,et al.Health-
related quality oflife in childrenwith craniofacial anomalies.J CraniofacSurg
2002;110:409�14.30.Marchac D.Forehead remolding for craniosyn-ostosis.In:Converse
JM,McCarthy JG,Wood-Smith D,editors.Symposium ondiagnosis and treatment
ofcraniofacialanomalies.St.Louis (MO):C.V.Mosby Co.;1979.p.323.31.Edgerton MT,Jane
JA,Berry FA,et al.The fea-sibility ofcraniofacial osteotomies ininfants and young
children.Scand J PlastReconstr Surg 1974;8:164�8.32.Edgerton MT,Jane JA,Berry
FA.Craniofacialosteotomies and reconstruction in infantsand young children.Plast
Reconstr Surg1974;54:13�27.33.McCarthy JG,Epstein F,Sadove M,et al.Earlysurgery for
craniofacial synostosis:an 8-
900Part 6: Maxillofacial Reconstructionyear experience.Plast Reconstr Surg
1984;73:521�33.34.Whitaker LA,Barlett SP,Schut L,Bruce D.Craniosynostosis:an
analysis ofthe timing,treatment and complication in 164 patients.Plast Reconstr
Surg 1987;80:195�212.35.Whitaker LA,Schut L,Kerr LP.Early surgeryfor isolated
craniofacial dysostosis.PlastReconstr Surg 1977;60:575�81.36.Cohen SR,Holmes
RE.Immediate cranialvault reconstruction with bioresorbableplates following
endoscopically assistedsagittal synostectomy.J Craniofac
Surg2002;13:578�84.37.Pietrzak WS.Critical concepts ofabsorbableinternal fixation.J
Craniofac Surg 2000;11:335�41.38.Pietrzak WS,Kumar M,Eppley BL.The influ-ence
oftemperature on the degradationrate oflactosorb copolymer.J CraniofacSurg
2003;14:176�83.39.Jane JA,Park TS,Zide BM,et al.Alternativetechniques in the
treatment ofunilateralcoronal synostosis.J Neurosurg 1984;61:550�6.40.Mohr
G,Hoffman HJ,Munro IR,et al.Surgicalmanagement ofunilateral and bilateralcoronal
craniosynostosis:21 years ofexpe-rience.Neurosurgery 1978;2:83�92.41.Persing
JA,Babler WJ,Jane JA,Duckworth PF.Experimental unilateral coronal synostosis
inrabbits.Plast Reconstr Surg 1986;77:369�77.42.Hoffman HJ,Mohr G.Lateral canthal
advance-ment ofthe supraorbital margins:a new cor-rective technique in the
treatment ofcoronalsynostosis.J Neurosurg 1976;45:376�81.43.Marchac D,Renier
D,Jones BM.Experiencewith the �floating forehead.�Br J Plast
Surg1988;41:1�15.44.Shillito J,Matson DD.Craniosynostosis:areview of519 surgical
patients.Pediatrics1968;41:819�53.45.Weinzweig J,Baker SB,Whitaker LA,et al.Delayed
cranial vault reconstruction forsagittal synostosis in older children:an algo-rithm
for tailoring the reconstructiveapproach to the craniofacial deformity.J Craniofac
Surg 2002;110:397�408.46.Ghali GE,Sinn DP,Tantipasawasin S.Manage-ment
ofnonsyndromic craniosynostosis.Atlas Oral Maxillofac Surg Clin N Am2002;10:1�41.
CHAPTER 46Craniofacial Dysostosis Syndromes:Staging ofReconstructionJeffrey
C.Posnick,DMD,MD Ramon L.Ruiz,DMD,MD Paul S.Tiwana,DDS,MD,MSCranial sutures are a
form ofbone articula-tion in which the margins ofthe bones areconnected by a thin
layer offibrous tissue.The cranial vault is composed ofsix majorsutural areas and
several minor sutures,which serve two critical functions duringthe postnatal
period.Initially,the suturesallow head deformation during vaginaldelivery as part
ofthe birthing process.Later,during an infant�s postnatal develop-ment,cranial
vault sutures facilitate headexpansion to accommodate propulsivebrain growth.1Only
small amounts ofpres-sure (5 mm Hg) from the growing brain arerequired to stimulate
bone deposition atthe margins ofa cranial bone.2,3Under nor-mal conditions,the
brain volume will triplewithin the first year oflife,and by age 2 years,the cranial
capacity is four timesthat at birth.4Under normal circumstances,closure ofthe
cranial vault sutures occursearlier than closure ofthe membranousfacial bone
sutures,which often remainpatent until adulthood.The term craniosynostosisis
defined as apremature fusion ofa cranial vault suture.With rare exception,this is
an intrauterineevent.A more accurate description ofcraniosynostosis may be a
congenital absenceofthe cranial vault sutures.The result isfusion ofthe bones
adjacent to the sutureand arrested sutural growth ofthe adjacentbones.The classic
theory known as Vir-chow�s law states that premature fusion ofacranial vault suture
results in limited devel-opment ofthe skull perpendicular to thefused suture and a
compensatory �over-growth�through the sutures that remainopen.5The result is a
dysmorphology withcharacteristics depending on the suturesaffected,and potential
neurologic conse-quences related to underlying brain com-pression.Most forms
ofcraniosynostosisrepresent random,nonsyndromic malfor-mations limited to the
cranial vault andorbital regions.Management typicallyrequires a combined
neurosurgical andcraniofacial approach for release oftheinvolved suture and
reshaping ofthe dys-morphic skeletal components.For addition-al discussion ofthe
treatment ofnonsyn-dromic craniosynostosis,see Chapter 45,�Nonsyndromic
Craniosynostosis.�Cranio-facial dysostosis is the term applied to syn-dromal forms
ofcraniosynostosis.These dis-orders are characterized by suturalinvolvement that
not only includes the cra-nial vault but also extends into the skull baseand
midfacial skeletal structures.Craniofa-cial dysostosis syndromes have beendescribed
by Carpenter,Apert,Crouzon,Saethre-Chotzen,and Pfeiffer.6Although thecranial vault
and cranial base are thought tobe the regions ofprimary involvement,thereis also
significant impact on midfacialgrowth and development.7,8In addition tocranial
vault dysmorphology,patients withthese inherited conditions exhibit a charac-
teristic �total midface�deficiency that is syn-drome specific and must be addressed
aspart ofthe staged reconstructive approach.Functional ConsiderationsBrain Growth
and Intracranial Pressure Ifthe rapid brain growth that normallyoccurs during
infancy is to proceed unhin-dered,the cranial vault and base suturesmust remain
open and expand duringphases ofrapid growth,resulting in mar-ginal ossification.In
craniosynostosis,pre-mature fusion ofsutures causes limitedand abnormal skeletal
expansion in thepresence ofcontinued brain growth.Depending on the number and
location ofprematurely fused sutures,the growth ofthe brain may be
restricted.2,9�11In addi-tion,abnormal cranial vault and midfacialmorphology occurs
as determined by
902Part 6: Maxillofacial ReconstructionVirchow�s law.Ifsurgical release
oftheaffected sutures and reshaping to restore amore normal intracranial volume
andconfiguration are not performed,decreased cognitive and behavioral func-tion is
likely to be the end result.Elevated intracranial pressure (ICP) isthe most serious
functional problem asso-ciated with premature suture fusion.A�beaten-
copper�appearance along theinner table ofthe cranial vault seen on aplain
radiograph or the loss ofbrain cis-ternae as observed on a computed tomog-raphy
(CT) scan may suggest elevatedICP,12but these are considered soft radi-ographic
findings.Intracranial hypertension can beestablished invasively by means ofa bur-
hole craniotomy used to place either anepidural or intraparenchymal
pressuresensor.Increased ICP is most likely toaffect patients with great
disparitybetween brain growth and intracranialcapacity and may occur in as many as
42%ofuntreated children in whom more thanone suture is
affected.2,10,13Unfortunately,there is no absolute agreement on whatlevels ofICP
are normal at any given age ininfancy and early childhood.The clinical signs and
symptoms relat-ed to elevated ICP may have a slow onsetand be difficult to
recognize in the pediatricpopulation.Although standardized CTscans allow for
indirect measurement ofintracranial volume,it is not yet possible touse these
studies to make judgments as towho requires craniotomy for decompres-
sion.14,15Careful neurosurgical and pedi-atric ophthalmologic evaluation are
criticalcomponents ofthe data gathering requiredto formulate a definitive treatment
plan in apatient with craniosynostosis.VisionUntreated craniosynostosis with
elevatedICP will cause papilledema and eventualoptic nerve atrophy,resulting in
partial orcomplete blindness.Ifthe orbits are shal-low (exorbitism) and the eyes
are proptot-ic (exophthalmos),as occurs in the cranio-facial dysostosis
syndromes,the corneamay be exposed and abrasions or ulcera-tions may occur.An
eyeball extending out-side ofa shallow orbit is also at risk oftrauma.Ifthe orbits
are extremely shallow,herniation ofthe globe itselfmay occur,necessitating
emergency reduction fol-lowed by tarsorrhaphies or urgent orbitaldecompression.Some
forms ofcraniofacial dysostosisresult in a marked degree oforbital hyper-
telorism,which may compromise visualacuity and restrict binocular vision.Diver-gent
or convergent nonparalytic strabis-mus or exotropia occurs frequently andshould be
considered during the diagnos-tic evaluation.This may be the result ofcongenital
anomalies ofthe extraocularmuscles themselves.Paralytic or nonpara-lytic unilateral
or bilateral upper eyelidptosis also occurs with greater frequencywith craniofacial
dysostosis than in thegeneral population.HydrocephalusHydrocephalus affects as many
as 10% ofpatients with a craniofacial dysostosissyndrome.16�19Although the etiology
isoften not clear,hydrocephalus may besecondary to a generalized cranial
basestenosis with constriction ofall the cra-nial base foramina,which impacts
thepatient�s cerebral venous drainage andcerebrospinal fluid (CSF) flow
dynamics.Hydrocephalus may be identified withthe help ofCT or magnetic
resonanceimaging (MRI) to document progressive-ly enlarging ventricles.Difficulty
exists ininterpreting ventricular findings as seenon a CT scan especially when the
skulland cranial base are brachycephalic.Theskeletal dysmorphology seen in a
childwith severe cranial dysmorphology relat-ed to craniosynostosis may translate
intoan abnormal ventricular shape that is notnecessarily related to abnormal CSF
flow.Serial imaging and clinical correlation isindicated,and a great deal
ofclinicaljudgment is often required in makingthese assessments.Effects ofMidface
Deficiency on AirwayAll newborn infants are obligate nasalbreathers.Many infants
born with a cranio-facial dysostosis syndrome have moderateto severe hypoplasia
ofthe midface as acomponent oftheir malformation.Theywill have diminished nasal and
nasopha-ryngeal spaces with resulting increasednasal airway resistance
(obstruction).Theaffected child is thus forced to breaththrough the mouth.For a
newborn infantto ingest food through the mouth requiressucking from a nipple to
achieve negativepressure as well as an intact swallowingmechanism.The neonate with
severe mid-face hypoplasia will experience diminishednasal airflow and be unable to
accomplishthis task and breathe through the nose atthe same time.20�23Complicating
this clini-cal picture may be an elongated and ptoticpalate and enlarged tonsils
and adenoids.The compromised infant expends signifi-cant energy respiring,and this
may pushthe child into a catabolic state (negativenitrogen balance).Failure to
thrive resultsunless either nasogastric tube feeding isinstituted or a feeding
gastrostomy isplaced.Evaluation by a pediatrician,pedi-atric otolaryngologist,and
feeding special-ist with craniofacial experience can helpdistinguish minor feeding
difficulties fromthose requiring more aggressive treatment.Sleep apnea ofeither
central orobstructive origin may also be present.Ifthe apnea is found to be
secondary toupper airway obstruction based on a for-mal sleep study,a tracheostomy
may beindicated.In rare situations,�early�mid-face advancement is useful to improve
theairway and allow for tracheostomydecannulation.Central apnea may occurfrom
poorly treated intracranial hyper-tension and other contributing factors.Ifthis is
the case,the condition mayimprove by reducing the intracranial
Craniofacial Dysostosis Syndromes: Staging ofReconstruction903pressure to a normal
range throughcranio-orbital or posterior cranial vaultdecompression or
expansion.Dentition and OcclusionThe incidence ofdental and oral anom-alies is
higher among children with cran-iofacial dysostosis syndromes than in thegeneral
population.In Apert syndrome inparticular,the palate is high and constrict-ed in
width.The incidence ofisolated cleftpalate in patients with Apert
syndromeapproaches 30%.13Clefting ofthe sec-ondary palate may be submucous,incom-
plete,or complete.Confusion has arisenover whether the oral malformations
andabsence ofteeth that are often characteris-tic ofthese conditions are a result
ofcon-genital or iatrogenic factors (eg,injury todental follicles associated with
early mid-face surgery).The midfacial hypoplasiaseen in the craniofacial dysostosis
syn-dromes often results in limited maxillaryalveolar bone to house a full
complement ofteeth.The result is severe crowding,whichoften requires serial
extractions in order toaddress the problem.An Angle Class IIIskeletal relationship
in combination withanterior open bite deformity is typical.HearingHearing deficits
are more common amongpatients with the craniofacial dysostosissyndromes than in the
general popula-tion.24In Crouzon syndrome,conductivehearing deficits are common,and
atresiaofthe external auditory canals may alsooccur.Otitis media is more common
inApert syndrome,although the exact inci-dence is unknown.Middle ear disease maybe
related to the presence ofa cleft palatethat results in eustachian tube dysfunc-
tion.Congenital fixation ofthe stapedialfootplate is also believed to be
frequent.The possibility ofsignificant hearing lossis paramount in importance and
shouldnot be overlooked because ofpreoccupa-tion with other more easily
appreciatedcraniofacial findings.Extremity AnomaliesApert syndrome results in joint
fusion andbony and soft tissue syndactyly ofthe digitsofall four limbs.24These
Apert-associatedextremity deformities are often symmetric.Partial or complete
fusion ofthe shoulder,elbow,or other joints is common.Broadthumbs,broad great
toes,and partial softtissue syndactyly ofthe hands may be seenin Pfeiffer
syndrome,but these are vari-able features.Preaxial polysyndactyly ofthe feet may
also be seen in Carpentersyndrome.Morphologic ConsiderationsExamination ofthe
patient�s entire cranio-facial region should be meticulous and sys-tematic.The
skeleton and soft tissues areassessed in a standard way to identify allnormal and
abnormal anatomy.Specificfindings tend to occur in particular malfor-mations,but
each patient is unique.Theachievement ofsymmetry and normalproportions and the
reconstruction ofspe-cific esthetic units are essential to formingan unobtrusive
face in a child born with acraniofacial dysostosis syndrome.Frontoforehead Esthetic
UnitThe frontoforehead region is dysmorphicin an infant with craniofacial dysosto-
sis.25�30Establishing normal position oftheforehead is critical to overall facial
symme-try and balance.The forehead may be con-sidered as two separate esthetic
compo-nents:the supraorbital ridge�lateralorbitalrim region and the superior
forehead (Fig-ure 46-1A and B).31,32The supraorbitalridge�lateral orbital rim
region includesthe glabella and supraorbital rim extend-ing inferiorly down each
frontozygomaticsuture toward the infraorbital rim andposteriorly along each
temporoparietalregion.The morphology and position ofthe supraorbital ridge�lateral
orbital rimregion is a key element ofupper facialesthetics.In a normal forehead,at
the levelofthe frontonasal suture,an angle rangingfrom 90 to 110�is formed by the
supraor-bital ridge and the nasal bones whenviewed in profile.Additionally,the eye-
brows,overlying the supraorbital ridge,should be anterior to the cornea.When
thesupraorbital ridge is viewed from above,the rim should arc posteriorly to
achieve agentle 90�angle at the temporal fossa witha center point ofthe arc at the
level ofeachfrontozygomatic suture.The superiorforehead component,about 1.0 to 1.5
cmup from the supraorbital rim,should havea gentle posterior curve ofabout 60�,lev-
eling out at the coronal suture regionwhen seen in profile.Posterior Cranial Vault
Esthetic UnitSymmetry,form,and the appropriateintracranial volume ofthe posterior
cranialvault are closely linked.Posterior cranialvault flattening may result from
either aunilateral or bilateral lambdoidal synosto-sis,which is rare;previous
craniectomywith reossification in a dysmorphic flatshape,which is frequent;or
postural mold-ing because ofrepetitive sleep position-ing.33A short
anterior�posterior cephaliclength may be misinterpreted as an anteri-or cranial
vault (forehead) problem whenthe occipitoparietal (posterior) skull rep-resents the
primary region ofthe deformi-ty.Careful examination ofthe entire cra-nial vault is
essential to defining thedysmorphic region so that appropriatetherapy may be
carried out.Orbitonasozygomatic Esthetic UnitIn craniofacial dysostosis
syndromes,theorbitonasozygomatic regional deformity is areflection ofthe cranial
base malformation.For example,in Crouzon syndrome whenbilateral coronal suture
synostosis is com-bined with skull base and midfacial defi-ciency,the
orbitonasozygomatic regionwillbe dysmorphic and consistent with a
short(anterior�posterior) and wide (transverse)anterior cranial base.34In Apert
syndrome,the nasal bones,orbits,and zygomas,like
904Part 6: Maxillofacial Reconstructionthe anterior cranial base,are
transverselywide and horizontally short (retruded),resulting in a shallow
hyperteloric uppermidface (zygomas,orbits,and nose).34Advancing the midface without
simultane-ously addressing the increased transversewidth will not adequately
correct the dys-morphology.35Maxillary-Nasal Base Esthetic UnitIn the craniofacial
dysostosis patient withmidface deficiency,the upper anterior face(nasion to
maxillary incisor) is verticallyshort,and there is a lack ofhorizontalanterior-
posterior (A-P) projection ofthemidface.36,37These findings may be con-firmed with
cephalometric analysis thatindicates a sella-nasion angle (SNA) belowthe mean value
and a short upper anteriorfacial height (nasion to anterior nasalspine).The width
ofthe maxilla in thedentoalveolar region is generally constrict-ed with a high
arched palate.In order tonormalize the maxillonasal base region,multidirectional
surgical expansion andreshaping are generally required.Themaxillary lip-to-tooth
relationship andocclusion are normalized through Le FortI osteotomy and orthodontic
treatment aspart ofthe staged reconstruction.Quantitative AssessmentA quantitative
analysis ofmeasurementstaken from CT scans,surface anthropom-etry,cephalometric
analysis,and dentalcasts is critical to data gathering for evalu-ation
ofcraniofacial deformities.38�43Thisanalysis will confirm or refute
clinicalimpressions,aid in the treatment planningofintraoperative skeletal
movements andreshaping,and provide a framework forobjective assessment ofimmediate
andlong-term results.These methods ofassessment rely on the measurement oflinear
distances,angles,and proportionsbased on accurate,reliable,and repro-ducible
anatomic landmarks found to beuseful for patient evaluation.FIGURE46-1The
craniofacial skeleton ofa child with bilateral coronal synostosis before and
afteranterior cranial vault and three-quarter orbital osteotomies with
reshaping.A,Site ofosteotomies asindicated.B,After osteotomies and reshaping and
fixation ofthe cranio-orbital regions.Adapted fromPosnick JC.76AB
Craniofacial Dysostosis Syndromes: Staging ofReconstruction905CT Scan AnalysisThe
use ofCT scans has clarified ourappreciation ofthe dysmorphology ofachild born with
a craniofacial malforma-tion.44,45Accurate standardized points ofreference have
been identified in thecranio-orbitozygomatic skeleton based onaxial CT
images.42,43Knowledge ofdiffer-ential facial bone growth patterns andnormal
measurement values can now beused to improve diagnostic accuracy,assistin the
staging ofreconstruction by under-standing growth vectors,and offer theoption
ofmaking intraoperative measure-ments that correlate with the preoperativeCT scan
measurements and ideal dimen-sions.This information can effectivelyguide the
surgeon in the reconstruction ofan individual with a craniofacial malfor-mation and
also allows for accurate post-operative reassessment.Anthropometric Surface
MeasurementsCross-sectional studies ofthe patterns ofpostnatal facial growth based
on anthro-pometric surface measurements have beencarried out in growing Caucasian
chil-dren.38�41,46This published material hasproven useful in the quantitative
evalua-tion and recognition ofdiscrepancies inpostnatal development in the head
andface ofpatients with specific craniofacialsyndromes.This is particularly
usefulwhen evaluating basic distances,angles,and proportions ofthe
head,face,andorbits in patients affected with craniofacialdysostosis
syndromes.Cephalometric AnalysisCephalometric radiography,first intro-duced by
Broadbent in 1931,has been tra-ditionally used to study the morphologyand patterns
ofgrowth ofthe maxillofacialskeleton.47The large collection ofnorma-tive data
developed allows clinicians tomonitor an individual�s facial
growth.Theinterpretation ofcephalometric radi-ographs remains useful in the
analysis offacial heights and maxillary,mandibular,and chin positions and their
relationshipsto one another;the cranial base;and thedentition.30,36,48,49The
lateral cephalomet-ric radiograph offers an accurate viewfrom the midsagittal plane
ifthe facialskeleton being analyzed is relatively sym-metric.Unfortunately,the
number ofanatomic landmarks that can be identifiedaccurately in the cranio-
orbitozygomaticregion is limited because ofthe overlapofstructures,which makes
predictablylocating these anatomic landmarks moredifficult.Surgical
ManagementHistoric Perspectives: The PioneersThe first recorded surgical approach
tocraniosynostosis was performed by Lanne-longue in 189050and Lane in
1892,51whocompleted strip craniectomies oftheinvolved sutures.Their aim was to
controlthe problem ofbrain compression(intracranial hypertension) within a con-
genitally small cranial vault.The classic neurosurgical techniqueswere refined over
the ensuing decades andwere geared toward resecting the synostoticsutures in the
hope that the �released�skullwould reshape itselfand continue to growin a normal
and symmetric fashion.52Stripcraniectomy procedures were supposed toallow for
creation ofnew suture lines at thesite ofthe previous synostosis.With
therealization that this goal was not achieved,attempts were made to surgically
disassem-ble the involved cranial vault and thenreplace the pieces ofcalvaria as
free grafts toshape the cranial vault.Problems with thesemethods included
uncontrolled postopera-tive skull molding,resulting in reossifica-tion in
dysmorphic configurations.In someother children,when extensive craniec-tomies were
carried out,permanent skulldefects remained.After World War II,Gillies and Harri-
son reported experience with an extracra-nial Le Fort III osteotomy to improve
theanterior projection ofthe midface in anadult with Crouzon syndrome.53The
earlyenthusiasm for this technique later turnedto discouragement when the patient�s
facialskeleton relapsed to its preoperative status.In 1967,Tessier described a
new(intracranial�cranial base) approach to themanagement ofCrouzon
syndrome.54Hislandmark presentation and publicationswere the beginning ofmodern
craniofacialsurgery.55�63To overcome the earlier prob-lems encountered by Gillies
and Harrison,Tessier developed an innovative basic surgi-cal approach that included
new locationsfor the Le Fort III osteotomy,a combinedintracranial�extracranial
(cranial base)approach,use ofa coronal (skin) incision toexpose the upper facial
bones,and use ofanautogenous bone graft.He also applied anexternal fixation device
to help maintainbony stability until healing had occurred.The concept
ofsimultaneous suturerelease for craniosynostosis combinedwith cranial vault
reshaping in infants wasinitially discussed by Rougerie and col-leagues64and later
refined by Hoffman andMohr in 1976.65Whitaker and others pro-posed a more formal
anterior cranial vaultand orbital reshaping procedure for uni-lateral coronal
synostosis in 1987,66andthen Marchac and colleagues publishedtheir experience with
the �floating fore-head�technique for simultaneous suturerelease and anterior
cranial vault andorbital reshaping to manage bilateral coro-nal synostosis in
infancy.32The widespread use ofcranial bone asa graft option has virtually
eliminated theneed for rib and hip grafts when autoge-nous bone replacement is
required incranio-orbitozygomatic procedures.Thisrepresents another ofTessier�s
contribu-tions to craniofacial surgery that has stoodthe test oftime.In 1968,Luhr
introduced the use ofsmall metal plates and screws to stabilizemaxillofacial
fractures and then osteoto-mies.67In current practice,the use ofinternal plate and
screw fixation is the
906Part 6: Maxillofacial Reconstructionpreferred form ofstabilization for thethree-
dimensional reconstruction ofmul-tiple osteotomized bone segments andgrafts.The
development ofresorbableplates and screws as a form ofstable fixa-tion continues to
evolve as a fixation alter-native,especially for use in growing bonesand for
immobilization ofonlay bonegrafts.47The reliability ofresorbable fixa-tion to
withstand the compressive(relapse) forces after total midfacialadvancement
procedures and the normalloading forces ofocclusion during theactive bone healing
phase leave it a lessdesirable fixation option for the craniofa-cial dysostosis
patient.More recently,the intraoperativeplacement ofa distraction device as amethod
ofachieving advancement ofthemidface in patients with severe forms ofcraniofacial
hypoplasia has been added tothe surgeon�s armamentarium.47Ifused,distraction
osteogenesis is not applieduntil after successful completion ofstan-dard
osteotomies and disimpaction in theoperating room.The distraction apparatusis
either anchored to the �stable�skeletoninternally or externally (through a
�halo�head frame) and then to the palatal (intra-oral) and infraorbital rims or
zygomaticbuttresses.Advancement ofthe �total mid-face�can then proceed.Once
adequate(midface) advancement has been accom-plished (on an outpatient basis) over
aperiod ofseveral weeks,the patient is gen-erally returned to the operating room
forstabilization and final reconstruction.Thefinal reconstruction may require
addition-al segmental osteotomies,bone grafting,or placement ofplate and screw
fixation.The �distraction approach�to the midfacedeformity is a labor-
intensive,technique-specific,and relatively crude method ofaccomplishing horizontal
advancementwith difficulty in controlling the verticaldimension ofthe midface and
without theability to alter the transverse deformity ordeficiency.In our
opinion,the currentlevel ofdistraction technology leaves it anadjunctive rather
than primary technique.It is most useful when the midfacialhypoplasia is severe to
the extent that con-ventional techniques cannot reliably allowthe immediate (in the
operating room)desired advancement and when complexvertical and transverse
reconstruction isnot required.Philosophy Regarding Timing ofInterventionIn
considering the timing and type ofintervention the experienced surgeon willtake
several biologic realities into account:the natural course ofthe malformation(ie,Is
the dysmorphology associated withCrouzon syndrome progressively worsen-ing or is it
a nonprogressive craniofacialdeformity?);the tendency toward growthrestriction ofan
operated bone (estheticunit) that has not yet reached maturity (ie,we know that
operating on a palate ofachild born with a cleft in infancy will causescarring and
later result in maxillaryhypoplasia in a significant percentage ofindividuals);and
the uncertain relation-ship between the underlying growing vis-cera (ie,brain or
eyes) and the congenital-ly affected and surgically altered skeleton(ie,Ifthe
cranial vault is not surgicallyexpanded by 1 year oflife in a patient withmultiple
suture synostosis,will brain com-pression occur?).In attempting to limit
functionalimpairment and also achieve long-termideal facial esthetics,an essential
ques-tion the surgeon must ask is,�Duringthe course ofcraniofacial development,does
the operated-on facial skeletal ofthe child with craniofacial dysostosistend to
grow abnormally,resulting infurther distortions and dysmorphology,or are the
initial positive skeletal changes(achieved at operation) maintained dur-ing ongoing
growth?�Unfortunately,thetheory that craniofacial procedures car-ried out early in
infancy will �unlockgrowth�has not been documentedthrough the scientific
method.68�70Incision PlacementFor exposure ofthe craniofacial skeletonabove the Le
Fort I level,the approachused is the coronal (skin) incision.Thisallows for a
relatively camouflaged accessto the anterior and posterior cranial
vault,orbits,nasal dorsum,zygomas,uppermaxilla,pterygoid fossa,and temporo-
mandibular joints.For added cosmeticadvantage,placement ofthe coronal inci-sion
more posteriorly on the scalp andwith postauricular rather than preauricu-lar
extensions is useful.When exposure ofthe maxilla at the Le Fort I level
isrequired,a circumvestibular maxillaryintraoral incision is used.Unless compli-
cations occur that warrant unusual expo-sure,no other incisions are required
formanaging any aspect ofthe craniofacialdysostosis patient�s
reconstruction.Theseincisions (coronal [scalp] and maxillary[circumvestibular]) may
be reopened asneeded to further complete the patient�sstaged
reconstruction.Management ofCranial VaultDead SpaceThe management ofthe dead space
thatresults with cranial vault or cranial baseexpansion is critical to limiting
complica-tions.Dead space within the cranial vaultafter cranial expansion is
managed bybeing gentle to the tissues,achieving goodhemostasis,closure oftissue
layers,place-ment ofbone grafts,the stable fixation ofosteotomy segments,and
obliteration (ofdead space) with soft tissue flaps or graftswhen
indicated.Expansion ofthe cranial vault withforward advancement ofthe anterior cra-
nial base,orbits,and midface results inboth extradural (retrofrontal) dead spaceand
a communication ofthe anterior fossawith the nasal cavity.71Dead space withinthe
anterior cranial vault and the commu-nication ofthe frontal fossa with the
nasalcavity across the anterior skull base mayresult in hematoma formation,CSF
Craniofacial Dysostosis Syndromes: Staging ofReconstruction907leakage,infection,and
fistula forma-tion.72,73Management ofthis expandedspace in the anterior cranial
fossa follow-ing frontofacial or forehead advancementremains
controversial.Relatively rapid fill-ing ofthe expanded intracranial space bythe
frontal lobes has been documented ininfants and young children when theexpansion
remains in a physiologicrange.71,74This observation supports theconservative
management ofretrofrontaldead space in younger patients.Moregradual and less
complete filling isthought to occur in older children andadults.Ifso,this may be
particularly trou-blesome when the anterior fossa deadspace communicates directly
with thenasal cavity.When possible,closing offthenasal cavity from the cranial
fossa at thetime ofoperation is preferred.Insertion ofa pericranial flap can help
to separate thecavities and at the same time obliteratedead space.The use offibrin
glue to sealthe anterior cranial base also provides atemporary repair between the
cavities,allowing time for the reepithelialization ofthe nasal mucosa.75When
feasible,aftermidface advancement the anterior skullbase is reconstructed (ie,bone
grafts) tofacilitate healing across the skull base tolimit CSF leakage and prevent
fistula for-mation.Until the torn nasopharyngealmucosa heals,communication
betweenthe nasal cavity and cranial fossa is apotential for leakage
(air,fluid,bacteria)and nasocranial fistula formation.To pre-vent
this,postoperative endotracheal intu-bation may be extended for 3 to 5 days
andbilateral nasopharyngeal airways may beplaced after extubation.In
addition,sinusprecautions and restriction ofnose blow-ing further limit reflux
(nose to cranialfossa) ofair and fluid during the postoper-ative period.All ofthese
maneuvers areaimed at avoiding a pressure gradient andwill facilitate sealing ofthe
intracranialcavity from the upper aerodigestive tract.When anterior cranial vault
reconstructionis performed and aerated frontal sinusesare present,management ofthe
sinus is byeither cranialization or obliteration.When a craniofacial dysostosis
patientis to undergo intracranial volume expan-sion as part ofthe craniofacial
procedureand they also require hydrocephalus man-agement,the potential for
problemsincreases.Complications may arise fromexcessive CSF drainage
(�overshunting�).With overshunting there is decreased brainvolume and dead space
remains.Fronto-orbital advancement and cranial vaultexpansion procedures should be
carefullystaged with ventriculoperitoneal (VP)shunting procedures.Ultimately,the
deci-sion regarding the sequencing ofshuntingprocedures is based on neurologic
findingsand the neurosurgeon�s judgement.In apatient with a VP shunt in place
before thesurgery,careful neurosurgical evaluation,including CT scanning ofthe
ventricularsystem,is carried out to confirm that theshunt is functioning
appropriately.Soft Tissue ManagementA layered closure ofthe coronal incision(galea
and skin) optimizes healing and lim-its scar widening.Resuspension ofthe mid-face
periosteum to the temporalis fascia in asuperior and posterior direction
facilitatesredraping ofthe soft tissues.Each lateralcanthus should be adequately
suspended orreattached in a superior�posterior direc-tion to the lateral orbital
rim.The use ofchromic gut for closure ofthe scalp skin inchildren may be used to
obviate the needfor postoperative suture or staple removal.Crouzon Syndrome Primary
Cranio-orbital Decompression: Reshaping in InfancyThe initial treatment for Crouzon
syn-drome generally requires bilateral coronalsuture release and simultaneous
anteriorcranial vault and upper orbital osteotomieswith reshaping and advancement
(see Fig-ure 46-1).76�79Our preference is to carrythis out when the child is 9 to
11 months ofage unless clear signs ofincreased intracra-nial pressure are
identified earlier in life(Figure 46-2).Reshaping ofthe upperthree-quarters ofthe
orbital rims andsupraorbital ridges is geared towarddecreasing the bitemporal and
anteriorcranial base width,with simultaneous hor-izontal advancement to increase
the A-Pdimension.This also increases the depth ofthe upper orbits,with some
improvementofeye proptosis.The overlying forehead isthen reconstructed according to
morpho-logic needs.A degree ofovercorrection ispreferred at the level ofthe
supraorbitalridge when the procedure is carried out ininfancy.In our opinion,by
allowing addi-tional growth to occur (waiting until thechild is 9 to 11 months
old),the recon-structed cranial vault and upper orbitalshape is better maintained
with less needfor repeat craniotomy procedures butwithout risking compression ofthe
under-lying brain.The goals at this stage are to provideincreased intracranial
space in the anteri-or cranial vault for the brain;to increasethe orbital
volume,which allows the eyesto be positioned more normally for betterprotection
from exposure;and to improvethe morphology ofthe forehead andupper orbits.A
postauricular coronal (scalp) inci-sion is made,and the anterior scalp flap
iselevated along with the temporalis musclein the subperiosteal plane.Bilateral
circum-ferential periorbital dissection follows,withdetachment ofthe lateral
canthi,but withpreservation ofthe medial canthi and naso-lacrimal apparatus to the
medial orbitalwalls.The subperiosteal dissection is con-tinued down the lateral and
infraorbitalrims to include the anterior aspect ofthemaxilla and zygomatic
buttress.The neuro-surgeon then completes the craniotomy toremove the dysmorphic
anterior cranialvault.With protection ofthe frontal andtemporal lobes ofthe brain
(remaininganterior to each olfactory bulb),safe direct
908Part 6: Maxillofacial Reconstructionvisualization ofthe anterior cranial baseand
orbits is possible at the time oforbitalosteotomies.The orbital osteotomies are
then com-pleted across the orbital roofand superioraspect ofthe medial orbital
walls,laterallythrough the lateral orbital walls and inferi-orly just into the
inferior orbital fissures.The three-quarter orbital osteotomy units,with their
tenon extensions,are removedfrom the field.The orbital units arereshaped and
reinset into a preferred posi-tion.Orbital depth is thereby increased,andglobal
proptosis is reduced.Fixation is gen-erally achieved with 28-gauge
interosseouswires or suture at each infraorbital rim andwith plates and titanium or
resorbablescrews at the tenon extensions and fron-tonasal regions.The removed
calvaria is cut into seg-ments,which are placed individually toachieve a more
normally configured ante-rior cranial vault.The goal ofreshaping isto narrow the
anterior cranial base andorbital width slightly and provide moreforward projection
and overall normalmorphology.Repeat Craniotomy for Additional Cranial Vault
Expansion and Reshaping inYoung Children After the initial suture
release,decompres-sion,and reshaping are carried out duringinfancy,the child is
observed clinically atintervals by the craniofacial surgeon,pedi-atric
neurosurgeon,pediatric ophthalmol-ogist,and developmental specialist andundergoes
interval CT scanning.Shouldsigns ofincreased ICP develop,urgentbrain decompression
with cranial vaultexpansion and reshaping is performed.47When increased ICP is
suspected,the loca-tion ofbrain compression influences forwhich region ofthe skull
further expan-sion and reshaping is planned.Ifthe brain compression is judged to
beanterior,then further anterior cranial vaultand upper orbital osteotomies with
reshap-FIGURE46-2An 18-month-old girl with brachycephaly and midface deficiency
with a mild degree ofpapilledema was referred for evaluation.She was found to have
bilateral coronal synostosis and mid-face hypoplasia without extremity
anomalies.The diagnosis ofCrouzon syndrome was made.Sheunderwent cranio-orbital
reshaping (see Figure 46-1).Several months later,a ventriculoperitonealshunt was
placed for management ofhydrocephalus.Further staged reconstruction will include a
totalmidface advancement procedure later in childhood followed by orthodontic
treatment and orthog-nathic surgery in the early teenage years.A,Frontal view
before surgery.B,Frontal view at 3 years ofage,1.5 years after undergoing cranio-
orbital decompression and reshaping.C,Profile view beforesurgery.D,Profile view at
3 years ofage,1.5 years after undergoing first-stage cranio-orbital decom-pression
andreshaping.E and F,Three-dimensional CT scan views ofcraniofacial skeleton,just 1
week after cranio-orbital reshaping with advancement.Reproduced with permission
from PosnickJC.Crouzon syndrome: evaluation and staging ofreconstruction.In:
Posnick JC,editor.Craniofacial andmaxillofacial surgery in children and young
adults.Philadelphia (PA): W.B.Saunders Co.; 2000.p.275.CDABEF
Craniofacial Dysostosis Syndromes: Staging ofReconstruction909ing and advancement
are carried out.Thetechnique is similar to that described previ-ously.47,78Ifthe
problem is posterior com-pression,expansion ofthe posterior cranialvault,with the
patient in the prone posi-tion,is required (Figure 46-3).The �repeat�craniotomy
carried outfor further decompression and reshapingin the child with Crouzon
syndrome isoften complicated by brittle cortical bone(which lacks a diploic space
and containssharp spicules piercing the dura),the pres-ence ofpreviously placed
fixation devicesin the operative field (eg,Silastic sheeting,metal clips,stainless
steel wires,plates,andscrews),and convoluted thin dura com-pressed against (or
herniated into) theinner table ofthe skull.All ofthese issuesresult in a greater
potential for dural tearsduring the calvarectomy than would nor-mally occur during
the primary procedure.A greater potential for morbidity should beanticipated when
re-elevating the scalpflap,dissecting the dura free ofthe innertable ofthe skull
and cranial base,and thenremoving the cranial vault bone.Management of�Total
Midface�Deformity in ChildhoodThe type ofosteotomies selected to managethe �total
midface�deficiency or deformityand residual cranial vault dysplasia shoulddepend on
the extent and location ofthepresenting dysmorphology rather than on afixed
approach to the midface malforma-tion.47,53�57,78�84The selection ofa monobloc(with
or without additional orbital segmen-tation),facial bipartition (with or
withoutadditional orbital segmental osteotomies),or Le Fort III osteotomy to manage
the basichorizontal,transverse,and vertical orbital,and upper midface deficiencies
or deformi-ties in a patient with Crouzon syndromedepends on the patient�s
presenting midfaceand anterior cranial vault morphology.Theobserved dysmorphology
is dependent onthe original malformation,the previousprocedures carried out,and the
effects ofongoing growth (Figures 46-4 and 46-5).FIGURE46-3A child with Crouzon
syndromeis shown at 10 months ofage.His deformities are char-acterized by mild
bilateral coronal and marked bilateral lambdoid synostosis in combination
withmidface deficiency.He has diminished intracranial volume,resulting in brain
compression.The orbitsare shallow with resulting eye proptosis,and the midface is
deficient with malocclusion.He is shownbefore and after undergoing posterior
cranial vault decompression and reshaping to expand theintracranial volume.He later
underwent placement ofa ventriculoperitoneal shunt for managementofhydrocephalus.He
will require a total midface advancement (monobloc) with further anterior cra-nial
vault reshaping after 5 years ofage.This will be followed by orthognathic surgery
in combinationwith orthodontic treatment in the teenage years.A,Profile view before
surgery.B,Profile view afterposterior cranial vault reconstruction.C,Intraoperative
lateral view ofcranial vault (patient in proneposition) as seen with posterior
scalp flap elevated.D,Same intraoperative view after posterior cra-nial vault
decompression,reshaping,and fixation ofbone segments with microplates and
screws.E,Comparison ofthree-dimensional CT scan views before and after
reconstruction.F,Comparison ofthree-dimensional CT scan views ofcranial base before
and after reconstruction.Reproduced withpermission from Posnick JC.The craniofacial
dysostosis syndromes: secondary management ofcran-iofacial disorders.Clin Plast
Surg 1997;24:429.ABCDEF
910Part 6: Maxillofacial ReconstructionWhen evaluating the upper and midfacein a
child born with Crouzon syndrome,ifthe supraorbital ridge is in good positionwhen
viewed from the sagittal plane (thedepth ofthe upper orbits is adequate),themidface
and forehead have a normal arc ofrotation in the transverse plane (not con-
cave),and the root ofthe nose is ofnormalwidth (minimal orbital
hypertelorism),there is little need to reconstruct this region(the forehead and
upper orbits) any further.In such patients,the basic residual midfacedeformity is
in the lower halfofthe orbits,zygomatic buttress,and maxilla.Ifso,thedeformity may
be effectively managed usingan extracranial Le Fort III osteotomy.Ifthe
supraorbital ridges,anterior cra-nial base,zygomas,nose,lower orbits,andmaxilla all
remain deficient in the sagittalplane (horizontal retrusion),then amonobloc
osteotomy is indicated (see Fig-ures 46-4 and 46-5).In these patients,theforehead
is generally flat and retruded andwill also require reshaping and advance-
ment.Ifupper midface hypertelorism(increased transverse width) and
midfaceflattening (horizontal retrusion) with lossFIGURE46-4A child at 8 years
ofage with Crouzon syndrome who underwent a limited first-stage cranio-orbital
procedure at 6 weeks ofage.He thenunderwent anterior cranial vault and monobloc
(orbits and midface) osteotomies with advancement.A,Profile view before monobloc
procedure.B,Pro-file view after reconstruction.C,Craniofacial morphology before and
after anterior cranial vault and monobloc osteotomies with advancement as
carriedout.Osteotomy locations indicated.Stabilization with cranial bone grafts and
miniplates and screws.D,View ofinner surface offrontal bones afterbifrontal
craniotomy.Compression ofbrain against inner table has resulted in resorption ofthe
inner skull.This is an indication oflong-standing increasedintracranial
pressure.E,Frontal view before surgery.F,Frontal view after reconstruction.
(CONTINUEDONNEXTPAGE)ABCEFD
Craniofacial Dysostosis Syndromes: Staging ofReconstruction911ofthe normal facial
curvature (concavearc) are also present,then the monoblocunit is split vertically
in the midline (facialbipartition),a wedge ofinterorbital (nasaland ethmoidal) bone
is removed,and theorbits and zygomas are repositioned medi-ally while the maxilla
at the palatal level iswidened.The facial bipartition is rarelyrequired in Crouzon
syndrome,but themonobloc is.When a monobloc or facialbipartition osteotomy is
carried out as the�total midface�procedure,additional seg-mentation ofthe upper and
lateral orbitsfor reconstruction may also be required tonormalize the morphology
ofthe orbitalesthetic units.For most patients,a surgeon�s attemptto simultaneously
adjust the orbits andidealize the occlusion using the Le Fort III,monobloc,or
facial bipartition osteotomyin isolation,without completing a separateFIGURE46-4
(CONTINUED)G,Occlusal viewsbefore and after reconstruction.H,Comparisonofaxial CT
slices through midorbits before andafter reconstruction,indicating
resultingincreased intraorbital depth and decreased prop-tosis
achieved.I,Intraoperative bird�s-eye lateralview ofcranial vault demonstrating
Silastic stripthat had been placed by the neurosurgeon whenthe patient was 2 months
ofage (8 years earlier).J,Removing the Silastic strip along the sphenoidwing region
is difficult due to bone overgrowth.K,Intraoperative view of(Rowe) forceps in
noseand mouth after monobloc osteotomy but beforedisimpaction.L,Same view but with
coronalincision turned down,indicating degree ofadvancement at supraorbital ridge
level afterdisimpaction.(CONTINUEDONNEXTPAGE)HIKLJG
912Part 6: Maxillofacial ReconstructionLe Fort I osteotomy,is an error in judg-
ment.The degree ofhorizontal deficiencyobserved at the orbits and maxillary denti-
tion is rarely uniform.This further seg-mentation ofthe midface complex at theLe
Fort I level is required to establish nor-mal proportions.Ifa Le Fort I
separationofthe total midface complex is not carriedout and the surgeon attempts to
achieve apositive overbite and overjet at the incisorteeth,over-advancement ofthe
orbits withenophthalmos will occur.The Le Fort Iosteotomy is generally not
performed atthe time ofthe total midface procedure.This will await skeletal
maturity and thenbe combined with orthodontic treatment.Until then,an Angle Class
III malocclu-sion will remain.A major esthetic problem specific tothe Le Fort III
osteotomy when its indica-tions are less than ideal is the creation ofirregular
step-offs in the lateral orbitalrims.This will occur when even a moder-ate (Le Fort
III) advancement is carriedout.These lateral orbital step-offs are unat-tractive
and are visible to the casual observ-er at conversational distance.Surgical mod-
ification performed later is difficult,oftenwith less than ideal esthetic
results.Anoth-er problem with the Le Fort IIIosteotomy isthe difficulty in judging
an ideal orbitaldepth.A frequent result is either residualproptosis or
enophthalmos.Simultaneouscorrection oforbital hypertelorism or correction ofa
midface arc-of-rotationproblem is not possible with the Le Fort
IIIprocedure.Excessive lengthening ofthenose,accompanied by flattening
ofthenasofrontal angle,will also occur ifthe LeFort III osteotomy is selected when
theskeletal morphology favors a monobloc orfacial bipartition procedure.It is not
possi-ble to later correct the surgically createdvertical elongation ofthe
nose.Final reconstruction,as discussedabove,ofthe cranial vault deformities
andorbital dystopia in Crouzon syndrome canbe managed in patients as young as 5 to
7 years ofage.47By this age,the cranial vaultand orbits normally attain
approximately85 to 90% oftheir adult size.43When theupper midface and final cranial
vault pro-cedure is carried out at or after this age,thereconstructive objectives
are to approxi-mate adult dimensions in the cranio-orbitozygomatic region,with the
expecta-tion ofa stable result (no longer influencedby growth) once healing has
occurred (seeFigure 46-4).Psychosocial considerationsalso support the upper midface
and finalcranial vault procedure taking place inpatients 5 to 7 years ofage.When
the pro-cedure is carried out at this age,the childmay enter the first grade with
an opportu-nity for satisfactory self-esteem.Routineorthognathic surgery will be
necessary atthe time ofskeletal maturity to achieve anideal occlusion,facial
profile,and smile.Orthognathic Procedures forDefinitive Occlusal and LowerFacial
Esthetic Reconstruction Although the mandible has a normal basicgrowth potential in
Crouzon syndrome,the maxilla does not.An Angle Class IIIFIGURE46-4
(CONTINUED)M,Lateral view ofzygomatic arch and tenon extension ofsupraorbital
rimafter monobloc advancement just before miniplate fixation.N,Same view after
miniplate fixation ofzygomatic arch and tenon extension.O,Bird�s-eye view
ofstabilized monobloc unit after advancement.There is increased intracranial volume
(dead space) in the anterior cranial vault for brain expansion.P,Same view with
elevated pericranial flaps,which will be turned in to close the opening between the
noseand the anterior cranial base.A,B,D�P reproduced with permission and C adapted
from Posnick JC.98MNOP
Craniofacial Dysostosis Syndromes: Staging ofReconstruction913FIGURE46-5A 12-year-
old boy with unrepaired Crouzon syndrome who underwent total cranial vault and
monobloc osteotomies with reshaping and advance-ment.A,Oblique view prior to
surgery.B,The patient�s craniofacial morphology before surgery.Osteotomy locations
indicated.A second illustration afterosteotomies completed with
advancement,reshaping,and fixation.C,Three-dimensional CT scan views ofcranial
vault and cranial base prior to surgery.D,Intra-operative view with forceps placed
at orbital rims indicating extent ofproptosis.E,Lateral skull radiograph with
�fingerprinting�indicating long-standingincreased ICP.F,Inner table internal side
offrontal bone indicating compression ofbrain against inner table
ofskull.G,Intraoperative lateral view ofcranial vaultand orbits through coronal
incision before osteotomies.H,Same view after osteotomies,reshaping and
stabilization ofbone segments with miniplates and screws.
(CONTINUEDONNEXTPAGE)ACBDEFHG
914Part 6: Maxillofacial ReconstructionFIGURE46-5 (CONTINUED)I,Frontal view before
surgery.J,Frontal view after reconstruction.K,Profile view before surgery.L,Profile
view after reconstruction.M,Worm�s-eye view before surgery.N,Worm�s-eye view after
reconstruction.O,Comparison oflateral cephalometric radiographs before and after
reconstruction.P,Comparison ofthree-dimensional CT scan views before and after
reconstruction.A,C�P reproduced with permission and B adapted from Posnick
JC.98IJKLMNPO
Craniofacial Dysostosis Syndromes: Staging
ofReconstruction915malocclusion,resulting from maxillaryretrusion,with anterior
open bite oftenresults.A Le Fort I osteotomy to allow forhorizontal
advancement,transverse widen-ing,and vertical adjustment is generallyrequired in
combination with an osteo-plastic genioplasty (vertical reduction andhorizontal
advancement) to further correctthe lower face deformity.Secondary defor-mities
ofthe mandible should be simulta-neously corrected through sagittal
splitosteotomies.The elective orthognathicsurgery is carried out in conjunction
withorthodontic treatment planned for com-pletion at the time ofearly skeletal
maturi-ty (approximately 13 to 15 years in girlsand 15 to 17 years in boys) (Figure
46-6).Apert SyndromeApert syndrome has previously been classi-fied on the basis
ofits clinical findings.85,86Postmortem histologic and radiographicstudies suggest
that skeletal deficiencies inthe patient with Apert syndrome result froma cartilage
dysplasia at the cranial base,lead-ing to premature fusion ofthe midlinesutures
from the occiput to the anteriornasal septum.87�91In addition,a componentofthe
syndrome is four-limb symmetrycomplex syndactylies ofthe hands and feet(Figure 46-
7).Fusion and malformation ofother joints,including the elbows andshoulders,often
occur.The soft tissue enve-lope also varies from that in Crouzon syn-drome,with a
greater downward slant to thecanthi lateral and a distinctive,S-shapedupper eyelid
ptosis.The quality ofthe skinoften varies from normal,with acne andhyperhidrosis
being prominent features.Atthe molecular level,one oftwo fibroblastgrowth factor
receptor 2 (FGFR2)muta-tions involving amino acids (Ser252Trp andPro253Arg) have
been found to cause Apertsyndrome in nearly all patients studied.92�94Primary
Cranio-orbital Decom-pression: Reshaping in InfancyThe initial craniofacial
procedure forApert syndrome generally requires bilater-al coronal suture release
and anterior cra-nial vault and upper three-quarter orbitalosteotomies to expand
the anterior cranialvault and reshape the upper orbits andforehead (see Figure 46-
1).95,96Our prefer-ence is to carry this out when the child is 9 to 11 months
ofage,unless signs ofincreased intracranial pressure are identi-fied earlier in
life.The main goals at thisstage are to decompress the brain and pro-vide increased
space for it in the anteriorcranial vault and to increase the orbitalvolume to
decrease globe protrusion.Thefronto-orbital surgical technique is similarto that
described for Crouzon syndrome(Figure 46-8).Further Craniotomy for Additional
Cranial Vault Expansion and Reshaping inYoung ChildrenAs described for Crouzon
syndrome,afterthe initial suture release,decompression,and reshaping carried out
during infancy,the child is observed clinically at intervalsby the craniofacial
surgeon,pediatric neu-rosurgeon,pediatric ophthalmologist,anddevelopmental
pediatrician and under-goes interval CT scanning.76,97,98Shouldsigns ofincreased
ICP develop,furtherdecompression with reshaping ofthe cra-nial vault to expand the
intracranial vol-ume is performed (Figure 46-9).In Apertsyndrome the posterior
cranial vault morecommonly requires expansion.The tech-nique is similar to that
described forCrouzon syndrome.Management ofthe �Total Midface�Deformity in
ChildhoodIn Apert syndrome,for almost all patients,facial bipartition osteotomies
combinedwith further cranial vault reshaping per-mit a more complete correction
oftheabnormal craniofacial skeleton than canbe achieved through other midface
proce-dure options (ie,monobloc or Le Fort IIIosteotomies).When using the facial
bipar-tition approach,a more normal arc ofrotation ofthe midface complex isachieved
with the midline split.This fur-ther reduces the stigmata ofthe preopera-tive
�flat,wide,and retrusive�facialappearance.The facial bipartition alsoallows the
orbits and zygomatic buttressesas units to shift to the midline
(correctionofhypertelorism) while the maxillary archis simultaneously
widened.Horizontaladvancement ofthe reassembled midfacecomplex is then achieved to
normalize theorbital depth and zygomatic length.Theforehead is generally
flat,tall,and retrud-ed,with a constricting band just above thesupraorbital
ridge,giving the impressionofbitemporal narrowing.Reshaping oftheanterior cranial
vault is simultaneouslycarried out (see Figures 46-8�46-10).Seealso Figure 46-9H
for preoperative cranio-facial morphology and planned and com-pleted osteotomies
and reshaping.Notethat stabilization was achieved with cranialbone grafts and plate
and screw fixation.ALe Fort III osteotomy is virtually neveradequate for an ideal
correction oftheresidual upper and midface deformity ofApert syndrome.Orthognathic
Procedures forDefinitive Occlusal and LowerFacial Esthetic ReconstructionThe
mandible has normal basic growthpotential in Apert syndrome.The extent ofmaxillary
hypoplasia will result in anAngle Class III malocclusion with severeanterior open-
bite deformity.A Le Fort Iosteotomy is required to allow for hori-zontal
advancement,transverse widening,and vertical adjustment in combinationwith an
osteoplastic genioplasty to verti-cally reduce and horizontally advance
thechin,often combined with bilateral sagittalsplit osteotomies ofthe
mandible.Theelective orthognathic surgery is carriedout in conjunction with
detailed ortho-dontic treatment planned for completionat the time ofearly skeletal
maturity(approximately 13 to 15 years in girls and15 to 17 years in boys).
916Part 6: Maxillofacial ReconstructionFIGURE46-6A 19-year-old boy born with
Crouzon syndrome.When he was 11 years ofage,the patient was seen by another surgeon
and underwent a Le FortIII osteotomy with advancement through an extracranial
approach.He presentedin his late teenage years with asymmetric and dystopic
orbits,zygomatic hypopla-sia,a retrusive upper jaw,an asymmetric lower jaw,and a
long chin.He under-went a combined orthodontic and orthognathic approach,including
a Le Fort Iosteotomy (horizontal advancement),bilateral sagittal split osteotomies
ofthemandible (correction ofasymmetry),and an osteoplastic genioplasty
(verticalreduction and horizontal advancement).Stabilization was accomplished
withminiplates and screws.During the same general anesthesia procedure,he under-
went a reopening ofhis coronal (scalp) incision with harvesting ofsplit
cranialgrafts to recontour and augment the orbits and zygomas.A,Frontal view
beforesurgery.B,Frontal view after reconstruction.C,Profile view before
surgery.D,Profile view after reconstruction.E,Oblique view before
surgery.F,Obliqueview after reconstruction.G,Occlusal view before
surgery.H,Occlusal view afterreconstruction.I,Oblique occlusal view before
surgery.J,Oblique occlusal viewafter reconstruction.K,Articulated dental casts
before surgery.L,Articulated den-tal casts after model reconstruction.Reproduced
with permission from Posnick JC.Crouzon syndrome: evaluation and staging
ofreconstruction.In: Posnick JC,edi-tor.Craniofacial and maxillofacial surgery in
children and young adults.Philadelphia (PA): W.B.Saunders Co.;
2000.p.299�300.ABCDEFGIHJKL
Craniofacial Dysostosis Syndromes: Staging ofReconstruction917FIGURE46-7A 28-year-
old woman born withApert syndrome.She was raised in Athens,Greece,and was unable to
undergo craniofacialor extremity reconstruction.A,Frontal view.B,View
ofhands.C,View offeet.Reproduced withpermission from Posnick JC.Apert
syndrome:evaluation and staging ofreconstruction.In: Pos-nick
JC,editor.Craniofacial and maxillofacialsurgery in children and young
adults.Philadelphia(PA): W.B.Saunders Co.; 2000.p.308.ABCFIGURE46-8A 6-month-old
girl with Apert syndrome underwent anterior cranial vault and three-quarter orbital
osteotomies with reshaping asdescribed (see Figure 46-1).A,Frontal view before
surgery.B,Three-dimensional CT scan view ofcranial vault before surgery.C,Profile
view beforesurgery.(CONTINUEDONNEXTPAGE)ABC
918Part 6: Maxillofacial ReconstructionFIGURE46-8 (CONTINUED)D,Three-dimensional CT
scan view ofcranial basebefore surgery.E,Frontal view oforbital osteotomy unit
before reshaping.F,Frontal view oforbital osteotomy unit after reshaping.G,Bird�s-
eye view oforbital osteotomy unit before reshaping.H,Bird�s-eye view oforbital
osteotomyunit after reshaping.I,Frontal view before surgery.J,Frontal view 1 year
later.K,Profile view before surgery.L,Profile view 1 year later.M and N,Frontal
andprofile views 2 years after reconstruction.(CONTINUEDONNEXTPAGE)DEGFHIJKLMN
Craniofacial Dysostosis Syndromes: Staging ofReconstruction919FIGURE46-8
(CONTINUED)O and P,Frontal and profile views 3 years after firststage cranio-
orbital reshaping; further staged reconstruction is required.Q,Comparison
ofstandard axial CT slices through cranial vault before and 1year after cranio-
orbital reshaping.The cranial vault length (cephalic length)has increased from 115
to 158 mm.The anterior cranial vault width (intercoro-nal distance) has remained
stable at 115 mm.R,Comparison ofstandard axialCT slices through midorbits before
and 1 year after reconstruction.Marked globeprotrusion of16 mm has increased to 17
mm 1 year later.The anterior interor-bital distance diminished from 29 to 25
mm,which still represented 137% oftheage-matched control value.(Magnification ofthe
individual CT scan imageswas not controlled for.) Reproduced with permission from
Posnick JC et al.95 FIGURE46-9A child born with Apertsyndrome underwent bilateral
�lateral canthal advancement�procedures when she was 6 weeks ofage,carried out by
theneurosurgeon working independently.At 18 months ofage,she returned with
turricephaly and a constricted anterior cranial vault requiring further cranio-
orbitaldecompression and reshaping.At 5 years ofage,she underwent anterior cranial
vault and facial bipartition osteotomies with reshaping.As part ofher staged recon-
struction,she will require orthognathic surgery and orthodontic treatment planned
for the teenage years.A,Frontal view at 8 months ofage after lateral
canthaladvancement procedure with residual deformity.B,Axial-sliced CT scan through
midorbits indicating dystopia,hypertelorism,and proptosis.C,Lateral view at8 months
ofage.D,Axial-sliced CT scan through zygomatic arches indicating midface
deficiency.(CONTINUEDONNEXTPAGE)ABCDOPQR
920Part 6: Maxillofacial ReconstructionFIGURE46-9 (CONTINUED)E and F,Lateral and
bird�s-eye view ofcranio-orbital region after three-quarter orbital osteotomies and
reshaping and anterior advancement.G,Frontal view at 5 years ofagejust prior to
further anterior cranial vault and facial bipartition osteotomies.H,Craniofacial
morphol-ogy with planned and completed osteotomies and reconstruction.I and
J,Bird�s-eye view ofcranial vaultand close-up view ofupper orbits after osteotomies
with reshaping.(CONTINUEDONNEXTPAGE)EFGIHJ
Craniofacial Dysostosis Syndromes: Staging ofReconstruction921FIGURE46-9
(CONTINUED)K,Frontal view before surgery.L,Frontal view after facial bipartition
reconstruction.M,Oblique viewbefore surgery.N,Oblique view after
reconstruction.O,Profile view before surgery.P,Profile view after
reconstruction.Q,Worm�s-eye view before surgery.R,Worm�s-eye view after
reconstruction.S,Comparison ofaxial-sliced CT scans through zygomas beforeand after
reconstruction,indicating a normalization ofzygomatic arch length.T,Axial-sliced CT
scan views through midorbitsbefore and after reconstruction,indicating correction
oforbital hyperteleorism and proptosis.(CONTINUEDONNEXTPAGE)KLMNOPQRST
922Part 6: Maxillofacial ReconstructionPfeiffer SyndromeIn 1964,Pfeiffer described
a syndromeconsisting ofcraniosynostosis,broadthumbs,broad great toes,and
occasionallypartial soft tissue syndactyly ofthe hands.99This syndrome is known to
have an auto-somal dominant inheritance pattern withcomplete penetrance documented
in allrecorded two- and three-generation pedi-grees.100Variable expressivity ofthe
cranio-facial and extremity findings is common(Figures 46-11 and 46-12).Although
someauthors have found clinical similarities incertain patients with Pfeiffer
syndrome,Crouzon syndrome,and Jackson-Weisssyndrome,the three disorders are
nosolog-ically distinct.47,101According to Cohen,thephenotypes ofthe three
conditions do notcorrelate well with the known molecularfindings.102Patients with
these three syn-dromes may have similar or even identicalmutations in exon B
ofFGFR2,yet theybreed true within families,an observationthat is as yet unexplained
by the molecularfindings.102,103Current thinking suggests that Pfeiffersyndrome is
heterogeneous because it iscaused by a single recurring mutation(Pro252Arg)
ofFGFR1and by several dif-ferent mutations affecting FGFR2.104,105FIGURE46-9
(CONTINUED)U and V,Comparison ofthree-dimensional CT scan views ofcraniofacial
region before and after recon-struction,including improved morphology
oforbits.A�G,I�V reproduced with permission,and H adapted from Posnick JC.Apert
syn-drome: evaluation and staging ofreconstruction.In: Posnick
JC,editor.Craniofacial and maxillofacial surgery in children and
youngadults.Philadelphia (PA): W.B.Saunders Co.; 2000.p.316.FIGURE46-10A 5-year-old
girl with Apert syndrome who underwent decompression and forehead and upper orbital
reshaping at 6 months ofage.She then presented to us with residual deformity
requiring cranial vault and facial bipartition osteotomies with reshap-ing.She will
require orthognathic surgery and orthodontic treatment later in the teenage years
to complete her reconstruction.A,Frontalview before facial bipartition
surgery.B,Intraoperative lateral view ofcranial vault and orbits through coronal
incision after reshaping.C,Bird�s-eye view ofcranial vault after osteotomies and
reshaping and fixation ofbone segments.(CONTINUEDONNEXTPAGE)UVABC
Craniofacial Dysostosis Syndromes: Staging ofReconstruction923Cohen has reviewed
the literature and fur-ther subgrouped Pfeiffer syndrome accord-ing to clinical
features,associated low-frequency anomalies,and outcome.Accord-ingto Cohen,Type I
corresponds to theclassic Pfeiffer syndrome and is associatedwith satisfactory
prognosis.The Type IIsubgroup is associated with the cloverleafskull anomaly while
Type III is not.BothTypes II and III have a less favorable out-come,with frequent
death in infancy.TheType I variant frequently presents withbicoronal
craniosynostosis and midfaceinvolvement.The longitudinal evaluationand staging
ofreconstruction depend onindividual variations but is similar to thatdescribed for
Crouzon syndrome.Carpenter SyndromeCarpenter syndrome is characterized
bycraniosynostosis often associated withpreaxial polysyndactyly ofthe
feet,shortfingers with clinodactyly,and variable softtissue syndactyly,sometimes
postaxial ply-dactyly,and other anomalies such as con-genital heart defects,short
stature,obesity,and mental deficiency.24It was firstdescribed by Carpenter in 1901
and waslater recognized to be an autosomal reces-sive syndrome.In general,the
reconstruc-tive algorithm described for Crouzon syn-drome can be followed.Saethre-
Chotzen SyndromeSaethre-Chotzen syndrome has an auto-somal dominant inheritance
pattern withFIGURE46-10 (CONTINUED)D,Frontal view beforesurgery.E,Frontal view 2
years after reconstruction.F,Profile view before surgery.G,Profile view 2 years
afterfacial bipartition reconstruction.H,Occlusal view beforesurgery.I,Occlusal
view 6 months after reconstruction.J,Comparison ofaxial-sliced CT scan views
throughmidorbits before and after reconstruction,demonstrat-ing improvement in
orbital hypertelorism and orbitaldepth with diminished eye proptosis.K,Standard
axialCT scan slices through cranial vault 1 week after facialbipartition (note dead
space in the retrofrontal region),and at 1 year (notice that initial retrofrontal
dead spacehas been resolved by brain expansion).Reproduced withpermission from
Posnick JC.97HIJKDEFG
924Part 6: Maxillofacial ReconstructionFIGURE46-11A 2-month-old child born
withPfeiffer syndrome (Type I).She has bilateralcoronal synostosis resulting in
brachycephalywithout suggestion ofmidface deficiency.A,Frontal view.B,Frontal view
ofCT scan.C,Pro-file view.D,Profile view ofCT scan.E,Obliqueview.F,Oblique view
ofCT scan.G,Cranialbase view ofCT scan.H,Craniofacial view ofCTscan.Reproduced with
permission from PosnickJC.Pfeiffer syndrome: evaluation and staging
ofreconstruction.In: Posnick JC,editor.Craniofa-cial and maxillofacial surgery in
children andyoung adults.Philadelphia (PA): W.B.SaundersABCo.; 2000.p.344.CDEFGH
Craniofacial Dysostosis Syndromes: Staging ofReconstruction925a high degree
ofpenetrance and expres-sivity.106Its pattern ofmalformations mayinclude
craniosynostosis,low-set frontalhairline,ptosis ofthe upper
eyelids,facialasymmetry,brachydactyly,partial cuta-neous syndactyly,and other
skeletalanomalies.As part ofthe reconstruction,cranio-orbital reshaping will almost
cer-tainly be required and is similar to thatdescribed for Crouzon syndrome.Evalua-
tion and management ofthe total midfacedeficiency and orthognathic deformitiesas
decribed for Crouzon syndrome shouldbe followed.CloverleafSkull Anomaly
Kleeblattsch�del anomaly (cloverleafskull)is a trilobular-shaped skull secondary
toFIGURE46-12A 6-year-old girl born with Pfeiffersyn-drome (initially thought to
have Crouzon syndrome).She underwent cranio-orbital decompression early
inchildhood.She presented to us with a constricted anteri-or cranial vault,orbital
dystopia,and midface deficien-cy.She underwent anterior cranial vault and
monoblocosteotomies with reshaping (see Figure 46-4).A,Frontalview before
surgery.B,Frontal view after monoblocreconstruction.C,Profile view before
surgery.D,Profileview after monobloc reconstruction.E,Occlusal viewbefore
surgery.F,Occlusal view after reconstruction.Shestill requires orthodontic
treatment and orthognathicsurgery,which is planned for the early teenage years.G
and H,Comparison ofaxial CT slices through midor-bits before and after
reconstruction indicating decreasedproptosis.Reproduced with permission from
Posnick JC.Pfeiffer syndrome: evaluation and staging ofreconstruc-tion.In:Posnick
JC,editor.Craniofacial and maxillofa-cial surgery in children and young
adults.Philadelphia(PA): W.B.Saunders Co.; 2000.p.349.ABCDEFGH
926Part 6: Maxillofacial Reconstructioncraniosynostosis (Figure 46-
13).107,108Thecloverleafskull anomaly is known to beboth etiologically and
pathogeneticallyheterogeneous.This anomaly is also non-specific:it may occur as an
isolated anom-aly or together with other anomalies,mak-ing up various syndromes
(namely,Apert,Crouzon,Carpenter,Pfeiffer,and Saethre-Chotzen).The extent and timing
ofanteri-or cranial vault or upper orbital,posteriorcranial vault,and midface
reconstructionwill be dependent on individual variationin the presenting
deformity.In general,theprotocol described for Crouzon syndromecan be
followed.SummaryDetails ofthe timing and techniques forcorrection ofthe varied
forms ofcranio-facial dysostosis syndromes differ fromcenter to center.However,an
essentialelement ofsuccessful rehabilitation isthe delivery ofcare by
committed,expe-rienced,and technically skilled clini-cians.The combined expertise
ofanexperienced craniofacial surgeon andpediatric neurosurgeon working togeth-er to
manage the cranio-orbital malfor-mation and the experienced maxillofa-cial surgeon
and orthodontist workingtogether to manage the orthognathicdeformity are essential
to achieve maxi-mum function and facial esthetics foreach patient.Our preferred
approach for manage-ment ofthe craniofacial dysostosis syn-dromes is to stage the
reconstruction tocoincide with facial growth patterns,vis-ceral (brain and eye)
function,and psy-chosocial development.Recognition oftheneed for a staged
reconstruction serves toclarify the objectives ofeach phase oftreatment for the
craniofacial surgeon,team,and most importantly the patientand patient�s family.By
continuing to define our rationalefor the timing and extent ofsurgical inter-
vention and then evaluating both functionand esthetic outcomes,we will
furtherFIGURE46-13The craniofacial skeleton ofa 6-month-old child born with
cloverleafskull anomaly.Heunderwent tracheostomy and gastrostomy shortly after
birth and died ofpneumonia before craniofacialreconstruction could be
undertaken.A,Frontal view.B,Posterior view.C,Right oblique view.D,Leftoblique
view.E,Left profile view.F,Right profile view.Reproduced with permission from
Cloverleafskullanomalies:evaluation and staging ofreconstruction.In:Posnick
JC,editor.Craniofacial and maxillofa-cial surgery in children and young
adults.Philadelphia (PA): W.B.Saunders Co.; 2000.p.364.ABCDEF
Craniofacial Dysostosis Syndromes: Staging ofReconstruction927improve the quality
oflife for the manyhundreds ofchildren born with syndro-mal forms
ofcraniosynostosis.Our objec-tive is to see each individual achieve per-sonal
success in life without special regardfor the original
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Part 7TEMPOROMANDIBULARJOINTDISEASE
CHAPTER 47Anatomy and Pathophysiology ofthe Temporomandibular JointMark
C.Fletcher,DMD,MDJoseph F.Piecuch,DMD,MDStuart E.Lieblich,DMDClassificationThe
temporomandibular joint (TMJ) iscomposed ofthe temporal bone and themandible,as
well as a specialized densefibrous structure,the articular disk,sever-al
ligaments,and numerous associatedmuscles.The TMJ is a compound jointthat can be
classified by anatomic type aswell as by function.Anatomically the TMJ is a
diarthrodi-al joint,which is a discontinuous articula-tion oftwo bones permitting
freedom ofmovement that is dictated by associatedmuscles and limited by
ligaments.1Itsfibrous connective tissue capsule is wellinnervated and well
vascularized andtightly attached to the bones at the edgesoftheir articulating
surfaces.It is also asynovial joint,lined on its inner aspect bya synovial
membrane,which secretes syn-ovial fluid.The fluid acts as a joint lubri-cant and
supplies the metabolic and nutri-tional needs ofthe nonvascularizedinternal joint
structures.Functionally the TMJ is a compoundjoint,composed offour articulating
sur-faces:the articular facets ofthe temporalbone and ofthe mandibular condyle
andthe superior and inferior surfaces ofthearticular disk.The articular disk
dividesthe joint into two compartments.Thelower compartment permits hinge motionor
rotation and hence is termed gingly-moid.The superior compartment permitssliding
(or translatory) movements and istherefore called arthrodial.Hence the tem-
poromandibular joint as a whole can betermed ginglymoarthrodial.Bony StructuresThe
articular portion ofthe temporal bone(Figure 47-1) is composed ofthree parts.The
largest is the articular or mandibularfossa,a concave structure extending fromthe
posterior slope ofthe articular emi-FIGURE47-1A,The left temporomandibular joint
viewed from the sagittal aspect on a dry skull.B,The left temporomandibular joint
viewed from theoblique/coronal aspect on a dry skull.C,The left glenoid fossa and
articular eminence.ABC
934Part 7: Temporomandibular Joint Diseasenence to the postglenoid process,which is
aridge between the fossa and the externalacoustic meatus.The surface ofthe articu-
lar fossa is thin and may be translucent on adry skull.This is not a major stress-
bearingarea.The second portion,the articular emi-nence,is a transverse bony
prominence thatis continuous across the articular surfacemediolaterally.The
articular eminence isusually thick and serves as a major func-tional component
ofthe TMJ.The articulareminence is distinguished from the articu-lar tubercle,a
nonarticulating process onthe lateral aspect ofthe zygomatic root ofthe temporal
bone,which serves as a pointofattachment ofcollateral ligaments.Thethird portion
ofthe articular surface ofthetemporal bone is the preglenoid plane,aflattened area
anterior to the eminence.The mandible is a U-shaped bone thatarticulates with the
temporal bone bymeans ofthe articular surface ofitscondyles,paired structures
forming anapproximately 145�to 160�angle to eachother.The mandibular condyle
(Figure 47-2) is approximately 15 to 20 mm inwidth and 8 to 10 mm in
anteroposteriordimension.The condyle tends to be round-ed mediolaterally and convex
anteroposte-riorly.On its medial aspect just below itsarticular surface is a
prominent depression,the pterygoid fovea,which is the site ofattachments ofthe
lateral pterygoid muscle.Cartilage and SynoviumLining the inner aspect ofall
synovialjoints,including the TMJ,are two types oftissue:articular cartilage and
synovium(Figure 47-3).The space bound by thesetwo structures is termed the synovial
cavi-ty,which is filled with synovial fluid.Thearticular surfaces ofboth the
temporalbone and the condyle are covered withdense articular fibrocartilage,a
fibrousconnective tissue.This fibrocartilage cov-ering has the capacity to
regenerate and toremodel under functional stresses.Deep tothe
fibrocartilage,particularly on thecondyle,is a proliferative zone ofcells thatmay
develop into either cartilaginous orosseous tissue.Most change resulting
fromfunction is seen in this layer.Articular cartilage is composed ofchondrocytes
and an intercellular matrixofcollagen fibers,water,and a nonfibrousfiller
material,termed ground substance.Chondrocytes are enclosed in otherwisehollow
spaces,called lacunae,and arearranged in three layers characterized bydifferent
cell shapes (Figure.47-4A).Thesuperficial zone contains small flattenedcells with
their long axes parallel to thesurface.2In the middle zone the cells arelarger and
rounded and appear in colum-nar fashion perpendicular to the surface.The deep zone
contains the largest cellsand is divided by the �tide mark�belowwhich some degree
ofcalcification hasoccurred.There are few blood vessels inany ofthese areas,with
cartilage beingnourished primarily by diffusion from thesynovial fluid.Collagen
fibers are arranged in arcadeswith an interlocking meshwork offibrilsparallel to
the articular surface joiningtogether as bundles and descending to theirattachment
in the calcified cartilagebetween the tide mark (Figure 47-4B).Functionally these
arcades provide a frame-work for interstitial water and ground sub-stance to resist
compressive forces en-countered in joint loading.Formed byintramembranous processes
the TMJ�sFIGURE47-2The mandibular condyle.Repro-duced with permission from Piecuch
JF,LieblichSE.Anatomy and pathology ofthe temporo-mandibular joint.In: Peterson
LF,Indresano AT,Marciani RD,Roser SM.Principles oforal andmaxillofacial
surgery.Vol.3.Philadelphia (PA):J.B.Lippincott Company; 1992.p.1858.Articular
cartilageArticular diskCollateral (diskal) ligamentLateral capsular ligamentMedial
capsular ligamentSynovial membraneSuperior joint spaceInferior joint spaceFIGURE47-
3The temporomandibularjoint (coronal view).Adapted fromPiecuch JF,Lieblich
SE.Anatomy andpathology ofthe temporomandibularjoint.In: Peterson LF,Indresano
AT,Marciani RD,Roser SM.Principles oforal and maxillofacial
surgery.Vol.3.Philadelphia (PA): J.B.Lippincott Com-pany; 1992.p.1859.
Anatomy and Pathophysiology ofthe Temporomandibular Joint935articular cartilage
contains a greater propor-tion ofcollagen fibers (fibrocartilage) thanother
synovial joints,which are coveredinstead by hyaline cartilage.The ground substance
contains a vari-ety ofplasma proteins,glucose,urea,andsalts,as well as
proteoglycans,which aresynthesized by the Golgi apparatus
ofthechondrocytes.Proteoglycans are macro-molecules consisting ofa protein
coreattached to many glycosaminoglycanchains ofchondroitin sulfate and
keratansulfate.Proteoglycans play a role in the dif-fusion ofnutrients and
metabolic break-down products.Ground substance per-mits the entry and release
oflargequantities ofwater,an attribute thought tobe significant in giving cartilage
its charac-teristic functional elasticity in response todeformation and
loading.Lining the capsular ligament is thesynovial membrane,a
thin,smooth,richlyinnervated vascular tissue without anepithelium.Synovial
cells,somewhatundifferentiated in appearance,serve botha phagocytic and a secretory
function andare thought to be the site ofproduction ofhyaluronic acid,a
glycosaminoglycanfound in synovial fluid.Some synovialcells,particularly those in
close approxi-mation to articular cartilage,are thoughtto have the capacity to
differentiate intochondrocytes.The synovium is capable ofrapid and complete
regeneration follow-ing injury.Recently,synovial cells (as wellas chondrocytes and
leukocytes) have beenthe focus ofextensive research regardingthe production
ofanabolic and cataboliccytokines within the TMJ.3Synovial fluid is considered an
ultrafil-trate ofplasma.2It contains a high concen-tration ofhyaluronic acid,which
is thoughtto be responsible for the fluid�s high viscos-ity.The proteins found in
synovial fluid areidentical to plasma proteins;however,syn-ovial fluid has a lower
total protein content,with a higher percentage ofalbumin and alower percentage ofa-
2-globulin.Alkalinephosphatase,which may also be present insynovial fluid,is
thought to be produced bychondrocytes.Leukocytes are also found insynovial
fluid,with the cell count being lessthan 200 per cubic millimeter and with lessthan
25% ofthese cells being polymor-phonuclear.Only a small amount ofsyn-ovial
fluid,usually less than 2 mL,is presentwithin the healthy TMJ.Functions ofthe
synovial fluid includelubrication ofthe joint,phagocytosis ofparticulate debris,and
nourishment ofthearticular cartilage.Joint lubrication is acomplex function related
to the viscosity ofsynovial fluid and to the ability ofarticularcartilage to allow
the free passage ofwaterwithin the pores ofits glycosaminoglycanmatrix.Application
ofa loading force toarticular cartilage causes a deformation atthe location.It has
been theorized thatwater is extruded from the loaded area intothe synovial fluid
adjacent to the point ofcontact.The concentration ofhyaluronicacid and hence the
viscosity ofthe synovialfluid is greater at the point ofload,thusprotecting the
articular surfaces.As theload passes to adjacent areas the deforma-tion passes on
as well,while the originalpoint ofcontact regains its shape andthickness through
the reabsorption ofwater.Exact mechanisms offlow betweenarticular cartilage and
synovial fluid are asyet unclear.Nevertheless the net result is acoefficient
offriction for the normallyfunctioning joint�approximately 14 timesless than that
ofa dry joint.The Articular DiskThe articular disk (Figure 47-5) is com-posed
ofdense fibrous connective tissueand is nonvascularized and noninnervat-ed,an
adaptation that allows it to resistArcades ofcollagen fibersSuperficial zoneMiddle
zoneDeep zoneTide markCalcified zoneSubchondral zoneFIGURE47-4Articular
cartilage.Adapted from Albright JA and Brand RA.2AB
936Part 7: Temporomandibular Joint Diseasepressure.4Anatomically the disk can
bedivided into three general regions asviewed from the lateral
perspective:theanterior band,the central intermediatezone,and the posterior
band.The thick-ness ofthe disk appears to be correlatedwith the prominence ofthe
eminence.Theintermediate zone is thinnest and is gener-ally the area offunction
between themandibular condyle and the temporalbone.Despite the designation
ofseparateportions ofthe articular disk,it is in fact ahomogeneous tissue and the
bands do notconsist ofspecific anatomic structures.The disk is flexible and adapts
to function-al demands ofthe articular surfaces.5Thearticular disk is attached to
the capsularligament anteriorly,posteriorly,medially,and laterally.6Some fibers
ofthe superiorhead ofthe lateral pterygoid muscle inserton the disk at its medial
aspect,apparentlyserving to stabilize the disk to themandibular condyle during
function.Retrodiskal TissuePosteriorly the articular disk blends with ahighly
vascular,highly innervated struc-ture�the bilaminar zone,which is involvedin the
production ofsynovial fluid.Thesuperior aspect ofthe retrodiskal tissue con-tains
elastic fibers and is termed the superiorretrodiskal lamina,which attaches to
thetympanic plate and functions as a restraintto disk movement in extreme
translatorymovements.5The inferior aspect oftheretrodiskal tissue,termed the
inferiorretrodiskal lamina,consists ofcollagen fiberswithout elastic tissue and
functions to con-nect the articular disk to the posterior mar-gin ofthe articular
surfaces ofthe condyle.It is thought to serve as a check ligament toprevent extreme
rotation ofthe disk on thecondyle in rotational movements.LigamentsLigaments
associated with the TMJ arecomposed ofcollagen and act predomi-nantly as restraints
to motion ofthe condyleand the disk.Three ligaments�collateral,capsular,and
temporomandibular liga-ments�are considered functional liga-ments because they
serve as major anatom-ic components ofthe joints.Two
otherligaments�sphenomandibular and stylo-mandibular�are considered accessory liga-
ments because,although they are attachedto osseous structures at some distance
fromthe joints,they serve to some degree as pas-sive restraints on mandibular
motion.The collateral (or diskal) ligaments (seeFigure 47-3) are short paired
structuresattaching the disk to the lateral and medialpoles ofeach condyle.Their
function is torestrict movement ofthe disk away fromthe condyle,thus allowing
smooth synchro-nous motion ofthe disk-condyle complex.Although the collateral
ligaments permitrotation ofthe condyle with relation to thedisk,their tight
attachment forces the diskto accompany the condyle through itstranslatory range
ofmotion.6The capsular ligament (see Figures 47-3,47-5,47-6,and 47-7) encompasses
eachjoint,attaching superiorly to the temporalbone along the border ofthe
mandibularfossa and eminence and inferiorly to theneck ofthe condyle along the edge
ofthearticular facet.It surrounds the joint spacesand the disk,attaching anteriorly
and pos-teriorly as well as medially and laterally,where it blends with the
collateral liga-ments.The function ofthe capsular liga-ment is to resist
medial,lateral,and inferiorforces,thereby holding the joint together.Itoffers
resistance to movement ofthe jointonly in the extreme range ofmotion.A sec-ondary
function ofthe capsular ligament isto contain the synovial fluid within thesuperior
and inferior joint spaces.The temporomandibular (lateral) liga-ments (see Figure
47-7) are located on thelateral aspect ofeach TMJ.5Unlike the cap-sular and
collateral ligaments,which havemedial and lateral components within eachArticular
cartilageAnterior capsular ligamentArticular diskSuperior joint spaceSuperolateral
pterygoid muscleInferolateral pterygoid muscleSuperior retrodiskal laminaInferior
retrodiskal lamina Inferior joint spaceFIGURE47-5The temporomandibular joint
(lateral view).Adaptedfrom Bell WE.4FIGURE47-6Capsular ligament (lateral
view).Adapted from Piecuch JF,Lieblich SE.Anatomyand pathology ofthe
temporomandibular joint.In: Peterson LF,Indresano AT,Marciani RD,Roser
SM.Principles oforal and maxillofacialsurgery.Vol.3.Philadelphia (PA):
J.B.LippincottCompany; 1992.p.1861.
Anatomy and Pathophysiology ofthe Temporomandibular Joint937joint,the
temporomandibular ligaments aresingle structures that function in pairedfashion
with the corresponding ligament onthe opposite TMJ.Each temporomandibu-lar ligament
can be separated into two dis-tinct portions,that have different func-tions.6The
outer oblique portion descendsfrom the outer aspect ofthe articular tuber-cle ofthe
zygomatic process posteriorly andinferiorly to the outer posterior surface ofthe
condylar neck.It limits the amount ofinferior distraction that the condyle
mayachieve in translatory and rotational move-ments.The inner horizontal portion
alsoarises from the outer surface ofthe articulartubercle,just medial to the origin
oftheouter oblique portion ofthe ligament,andruns horizontally backward to attach
to thelateral pole ofthe condyle and the posterioraspect ofthe disk.The function
ofthe innerhorizontal portion ofthe temporo-mandibular ligament is to limit
posteriormovement ofthe condyle,particularly dur-ing pivoting movements,such as
when themandible moves laterally in chewing func-tion.This restriction ofposterior
movementserves to protect the retrodiskal tissue.The sphenomandibular ligament
(Fig-ure 47-8) arises from the spine ofthe sphe-noid bone and descends into the
fan-likeinsertion on the mandibular lingula,as wellas on the lower portion ofthe
medial sideofthe condylar neck.1The spheno-mandibular ligament serves to some
degreeas a point ofrotation during activation ofthe lateral pterygoid
muscle,thereby con-tributing to translation ofthe mandible.The stylomandibular
ligament (see Fig-ure 47-8) descends from the styloid processto the posterior
border ofthe angle ofthemandible and also blends with the fascia ofthe medial
pterygoid muscle.It functionssimilarly to the sphenomandibular liga-ment as a point
ofrotation and also limitsexcessive protrusion ofthe mandible.Vascular Supply and
InnervationThe vascular supply ofthe TMJ arises pri-marily from branches ofthe
superficialtemporal and maxillary arteries posterior-ly and the masseteric artery
anteriorly.There is a rich plexus ofveins in the poste-rior aspect ofthe joint
associated with theretrodiskal tissues,which alternately filland empty with
protrusive and retrusivemovements,respectively,ofthe condyle-disk complex and which
also function inthe production ofsynovial fluid.Thenerve supply to the TMJ is
predominantlyfrom branches ofthe auriculotemporalnerve with anterior contributions
fromthe masseteric nerve and the posteriordeep temporal nerve.1Many ofthe nervesto
the joint appear to be vasomotor andvasosensory,and they may have a role inthe
production ofsynovial fluid.MusculatureAll muscles attached to the mandible influ-
ence its movement to some degree.Onlythe four large muscles that attach to theramus
ofthe mandible are considered themuscles ofmastication;however,a total of12 muscles
actually influence mandibularmotion,all ofwhich are bilateral.1Musclepairs may
function together for symmetricmovements or unilaterally for asymmetricmovement.For
example,contraction ofboth lateral pterygoid muscles results inprotrusion and
depression ofthe mandiblewithout deviation,whereas contraction ofone ofthe lateral
pterygoid muscles resultsin protrusion and opening with deviationto the opposite
side.Muscles influencing mandibularmotion may be divided into two groups byanatomic
position.Attaching primarily tothe ramus and condylar neck ofthemandible is the
supramandibular musclegroup,consisting ofthe temporalis,mas-seter,medial
pterygoid,and lateral ptery-goid muscles.This group functions pre-dominantly as the
elevators oftheOuter oblique portion(Limits rotational openingmovement)Inner
horizontal portion(Limits posterior movement)FIGURE47-7Temporomandibular joint
(lateralaspect).Adapted from Okeson JP.Medial capsular ligamentStylomandibular
ligamentSphenomandibularligamentPterygoid plateStyloid processFIGURE47-
8Temporomandibular ligament (medial view).Adaptedfrom Piecuch JF,Lieblich
SE.Anatomy and pathology ofthe temporo-mandibular joint.In: Peterson LF,Indresano
AT,Marciani RD,RoserSM.Principles oforal and maxillofacial
surgery.Vol.3.Philadelphia(PA): J.B.Lippincott Company; 1992.p.1863.
938Part 7: Temporomandibular Joint Diseasemandible.The lateral pterygoid does havea
depressor function as well.7Attaching tothe body and symphyseal area ofthemandible
and to the hyoid bone is theinframandibular group,which functionsas the depressors
ofthe mandible.Theinframandibular group includes the foursuprahyoid muscles
(digastric,geniohyoid,mylohyoid,and stylohyoid) and the fourinfrahyoid muscles
(sternohyoid,omohy-oid,sternothyroid,and thyrohyoid).Thesuprahyoid muscles attach
to both thehyoid bone and the mandible and serve todepress the mandible when the
hyoid boneis fixed in place.They also elevate thehyoid bone when the mandible is
fixed inplace.The infrahyoid muscles serve to fixthe hyoid bone during depressive
move-ments ofthe mandible.Supramandibular Muscle GroupThe temporalis muscle (Figure
47-9) is alarge fan-shaped muscle taking its originfrom the temporal fossa and
lateral aspectofthe skull,including portions ofthe pari-etal,temporal,frontal,and
sphenoidbones.Its fibers pass between the zygomat-ic arch and the skull and insert
on themandible at the coronoid process andanterior border ofthe ascending ramusdown
to the occlusal surface ofthemandible,posterior to the third molartooth.1Viewed
coronally the temporalismuscle has a bipennate character in thatfibers arising from
the skull insert on themedial aspect ofthe coronoid process,whereas fibers arising
laterally from thetemporalis fascia insert on the lateralaspect ofthe coronoid
process.In ananteroposterior dimension the temporalismuscle consists ofthree
portions:the ante-rior,whose fibers are vertical;the middle,with oblique fibers;and
the posterior por-tion,with semihorizontal fibers passingforward to bend under the
zygomatic arch.The function ofthe temporalis muscle is toelevate the mandible for
closure.It is not apower muscle.In addition contraction ofthe middle and posterior
portions ofthetemporalis muscle can contribute to retru-sive movements ofthe
mandible.To asmall degree unilateral contraction ofthetemporalis assists in
deviation ofthemandible to the ipsilateral side.The masseter muscle (Figure 47-
10),ashort rectangular muscle taking its originfrom the zygomatic arch and
inserting onthe lateral surface ofthe mandible,is themost powerful elevator ofthe
mandibleand functions to create pressure on theteeth,particularly the molars,in
chewingmotions.The masseter muscle is com-posed oftwo portions,superficial
anddeep,which are incompletely divided,yethave somewhat different
functions.Thesuperficial portion originates from thelower border ofthe zygomatic
bone andthe anterior two-thirds ofthe zygomaticarch and passes inferiorly and
posteriorlyto insert on the angle ofthe mandible.Thedeep head originates from the
inner sur-face ofthe entire zygomatic arch and onthe posterior one-third ofthe arch
from itslower border.The deep fibers pass vertical-ly to insert on the mandible on
its lateralaspect above the insertion ofthe superfi-cial head.The superficial
portion in par-ticular has a multipennate appearancewith alternating tendinous
plates andfleshy bundles ofmuscle fibers,whichserve to increase the power ofthe
muscle.Both the superficial and deep portions ofthe masseter muscle are powerful
elevatorsofthe mandible,but they function inde-pendently and reciprocally in other
move-ments.Electromyographic studies showthat the deep layer ofthe masseter
isalways silent during protrusive move-ments and always active during
forcedretrusion,whereas the superficial portionis active during protrusion and
silent dur-ing retrusion.8Similarly the deep masseteris active in ipsilateral
movements but doesnot function in contralateral movements,whereas the superficial
masseter is activeduring contralateral movements but notin ipsilateral
movements.The medial pterygoid muscle (Figure47-11) is rectangular and takes its
originfrom the pterygoid fossa and the internalsurface ofthe lateral plate ofthe
pterygoidprocess,with some fibers arising from thetuberosity ofthe maxilla and the
palatinebone.Its fibers pass inferiorly and inserton the medial surface ofthe
mandible,Parietal boneFrontal boneTemporalismuscleTemporal boneFIGURE47-9The
temporalis muscle with the zygomatic arch and massetermuscle removed.Adapted from
Clemente CD.51
Anatomy and Pathophysiology ofthe Temporomandibular Joint939inferiorly and
posteriorly to the lingual.Like the masseter muscle the medial ptery-goid fibers
have alternating layers offleshyand tendinous parts,thereby increasingthe power
ofthe muscle.The main func-tion ofthe medial pterygoid is elevation ofthe
mandible,but it also functions some-what in unilateral protrusion in a syner-gism
with the lateral pterygoid to promoterotation to the opposite side.The lateral
pterygoid muscle (see Figure47-11) has two portions that can be consid-ered two
functionally distinct muscles.Thelarger inferior head originates from the lat-eral
surface ofthe lateral pterygoid plate.9Itsfibers pass superiorly and outward to
fusewith the fibers ofthe superior head at theneck ofthe mandibular
condyle,insertinginto the pterygoid fovea.The superior headoriginates from the
infratemporal surface ofthe greater sphenoid wing,and its fiberspass
inferiorly,posteriorly,and outward toinsert in the superior aspect ofthe
pterygoidfovea,the articular capsule,and the articulardisk at its medial aspect,as
well as to themedial pole ofthe condyle.Anatomic stud-ies have shown that the
majority ofthesuperior head fibers insert into the condylerather than the disk.The
inferior and superior heads ofthelateral pterygoid muscle function inde-pendently
and reciprocally.8,10The prima-ry function ofthe inferior head is protru-sive and
contralateral movement.Whenthe bilateral inferior heads functiontogether,the
condyle is pulled forwarddown the articular eminence,with the diskmoving passively
with the condylar head.This forward movement ofthe condyledown the inclined plane
ofthe articulareminence also contributes to opening ofthe oral cavity.When the
inferior headfunctions unilaterally the resulting medialand protrusive movement
ofthe condyleresults in contralateral motion ofthemandible.The function ofthe
superiorhead ofthe lateral pterygoid muscle is pre-dominantly involved with closing
move-ments ofthe jaw and with retrusion andipsilateral movement.A summary
ofthemovements ofthe lateral pterygoid muscleand the other supramandibular muscles
isgiven in Table 47-1.SuperficialportionDeepportionFIGURE47-10The masseter
muscle.Adapted from Piecuch JF,Lieblich SE.Anatomy and pathology ofthe
temporomandibular joint.In: Peterson LF,Indresano AT,Marciani RD,Roser
SM.Principles oforal and maxillofacialsurgery.Vol.3.Philadelphia (PA):
J.B.Lippincott Company; 1992.p.1865.MedialpterygoidInferior
lateralpterygoidSuperior lateralpterygoidFIGURE47-11Medial and lateral pterygoid
muscles.Adaptedfrom Clemente CD.51
940Part 7: Temporomandibular Joint DiseaseInframandibular Muscle GroupThe
inframandibular muscles can be subdi-vided into two groups:the suprahyoids andthe
infrahyoids.The suprahyoid group con-sists ofthe digastric,geniohyoid,mylohyoid,and
stylohyoid muscles;lies between themandible and the hyoid bone;and serves toeither
raise the hyoid bone,ifthe mandible isfixed in position by the
supramandibulargroup,or depress the mandible,ifthe hyoidbone is fixed in position
by the infrahyoids.The infrahyoid group,consistingofthe
sternohyoid,omohyoid,sternothyroid,andthyrohyoid muscles,attaches to the hyoidbone
superiorly and to the sternum,clavicle,and scapula inferiorly.This group ofmus-cles
can either depress the hyoid bone orhold the hyoid bone in position,relative tothe
trunk,during opening movements ofthe mandible.Biomechanics ofTemporomandibular
JointMovementComplex free movements ofthemandible are made possible by the rela-
tion offour distinct joints that areinvolved in mandibular movement:theinferior and
superior joints�bilaterally.Two types ofmovement are possible:rotation and
translation.The inferior joints,consisting ofthecondyle and disk,are responsible
for rota-tion,a hinge-like motion.The center ofrotation is considered to be along a
horizon-tal axis passing through both condyles.4,5Intheory pure hinge motion
ofapproximately2.5 cm measured at the incisal edges oftheanterior teeth is
possible.Nevertheless mostmandibular movements are translatory aswell,involving a
gliding motion between thedisk and the temporal fossa,which are thecomponents ofthe
superior joints.Themandible and disk glide together as a unitbecause they are held
together by the collat-eral ligaments.The maximum forward andlateral movement ofthe
upper joint intranslation is approximately 1.5 cm.All movements ofthe
mandible,whether symmetric or asymmetric,involveclose contact ofthe
condyle,disk,andarticular eminence.Pure opening,closing,protrusive,and retrusive
movements arepossible as a result ofbilaterally symmetricaction ofthe
musculature.Asymmetricmovements,such as those seen in chewing,are made possible by
unilateral movementsofthe musculature with different amountsoftranslation and
rotation occurring with-in the joints on either side.The positioning ofthe condyle
anddisk within the fossa,as well as the constantcontact between the
condyle,disk,and emi-nence,is maintained by continuous activityofthe muscles
ofmastication,particularlythe supramandibular group.The ligamentsassociated with
the TMJ do not move thejoint.Although they can be lengthened bymovements
ofmuscles,they do not stretch(ie,do not have an elastic recoil that returnsthem to
a resting position automatically).Instead the role ofthe ligaments is that
ofapassive restriction ofmovement at theextreme ranges ofmotion.During
normalfunction rotational and translational move-ments occur
simultaneously,permitting thefree range ofmotion necessary in speakingand
chewing.Pathology ofthe Temporomandibular JointThe demand for treatment oftemporo-
mandibular joint dysfunction (TMJD) iswell known.Most studies estimate
theprevalence ofclinically significant TMJ-related jaw pain to be at least 5%
ofthegeneral population.Approximately 2% ofthe general population seeks treatment
fora TMJ-related symptom.11,12TMJD maybe the result ofmuscular hyperfunction
orparafunction,and/or underlying primaryor secondary degenerative changes withinthe
joint.It is important to note howeverthat no single causative factor leading toTMJD
has been unequivocally demon-strated in scientifically based
studies.13Classification ofTMJD is separated intononarticular and articular
categories andhas been eloquently described by de Bontand colleagues.13Nonarticular
disorders include muscledisorders such as myofascial dysfunction,muscle spasm (with
splinting,pain,andmuscle guarding),and myositis.Articulardisorders,often
accompanied by internalderangement,include noninflammatoryand inflammatory
arthropathies,growthdisorders,and connective tissue disorders.In diagnosing and
treating TMJD it ishelpful to assess patients with the aboveclassification as a
frame ofreference Table47-2.Treatment modalities can vary sig-nificantly depending
on this classification.Nonarticular Temporomandibular DisordersNonarticular TMJ
disorders most com-monly manifest as masticatory muscle dys-function.Approximately
one-halfor moreofall TMJDs are forms ofmasticatoryTable 47-1Contributions ofthe
Supramandibular Muscles ofMastication to Movements ofthe Jaw as Confirmed by
ElectromyographyMusclesMovementMedial pterygoidClosure,protrusionLateral pterygoid
(inferior head)Protrusion,opening contralateralLateral pterygoid (superior
head)Retrusion,closure,ipsilateralMasseter,superficial layerProtrusion,closure
contralateralMasseter,deep layerRetrusion,closure ipsilateralTemporalis,anterior
portionClosureTemporalis,posterior portionRetrusion,closure ipsilateralAdapted from
Gay T and Piecuch J.8
Anatomy and Pathophysiology ofthe Temporomandibular Joint941myalgia.14,15They
include such conditionssuch as acute muscle strain and spasm,myofascial pain and
dysfunction (MPD),chronic conditions such as fibromyalgia,and less
commonly,myotonic dystrophiesand myositis ossificans.They invariablycontribute to
decreased mandibular rangeofmotion and pain.The important role ofthe
supramandibular and inframandibu-lar muscle groups on mandibular move-ment and
function is evident in these con-ditions.Other nonarticular disordersinclude growth
disorders affecting TMJfunction and miscellaneous factors such asheterotopic bone
formation leading toTMJD.MPD is most commonly related tomasseter or temporalis
muscle spasm.16Additionally it can involve the pterygoidsor any combination ofthe
supramandibu-lar or inframandibular muscle groups.Parafunctional habits such as
bruxism andjaw clenching are thought to be the maincontributors to MPD and have
also beenfound to be causative in acute closed-lockconditions.The literature is
replete withvarious treatment modalities for MPD.Such treatments include occlusal
adjust-ments (for gross discrepancies),night-guard appliances (for joint
unloading,jawrepositioning,and occlusal protection),nonsteroidal anti-inflammatory
medica-tions,muscle relaxants,and physical ther-apy.These treatment
modalities,alone orin combination,remain the standard ofcare for the treatment
ofnonarticularTMJD,particularly MPD.Fibromyalgia is a systemic conditionmarked by
poor sleep,generalized painwith absence oflocalization to joints,and a history
ofsomatization in otherorgan systems such as irritable bowelsyndrome and
headaches.17It is typicallyobserved in an older population thanMPD and has a female
predilection.Fibromyalgia is often difficult to differ-entiate from MPD and is
treated in simi-lar fashion;that is,nonsurgically,withanti-inflammatory
medications,dietarymodifications,home-care techniques,bite appliances,and physical
therapy.There appears to be a poorer overallresponse to the treatment offibromyal-
gia when compared with MPD.Rarely other nonarticular conditionssuch as myotonic
dystrophy and myositisossificans progressiva can lead to signifi-cant loss
offunction and pain in the TMJregion.Myotonic dystrophy is a domi-nantly inherited
multisystem disorder thatmay affect facial muscles in fully devel-oped disease
states.18This condition maycontribute to atrophy and fibrosis ofthesupramandibular
and inframandibularmusculature.Clinically there are a varietyoftypes ofmyotonic
dystrophies.Theytend to exert their pathologic effects insimilar fashion,sometimes
resulting intrismus,loss offunction,and pain.Myosi-tis ossificans progressiva is a
rare condi-tion resulting in fibrosis ofsoft tissuesafter apparent minor
trauma.This condi-tion has been reported to affect TMJ func-tion after local
trauma,including surgery,and can result in significant loss ofmandibular range
ofmotion,trismus,andpain.19Soft tissue ossification can some-times occur after head
trauma,severeburns,or neurogenic stimulus.In thesecases heterotopic bone formation
isobserved and can lead to ankylosis in mul-tiple joints throughout the body
includingthe TMJ.20Articular TemporomandibularDisordersNoninflammatory articular
disorders oftheTMJ,the most common ofwhich isosteoarthrosis,are often
idiopathic.Osteoarthrosis can manifest as chondroma-lacia (softening ofthe
cartilage),temporaryor permanent disk displacement,degenera-tive changes within
bone and cartilageoften with osteophyte formation andremodeling,fibrosis,or any
combination ofthe above.Noninflammatory articular dis-orders may also be secondary
to trauma,infection,previous surgery,crystal deposi-tion disorders (gout and
pseudogout),avas-cular necrosis,or structural damage to jointcartilage resulting in
disk displacementand/or perforation (Figure 47-12).TMJdisk displacement has been
categorizedthrough a widely accepted staging systemby Wilkes,using such criteria as
severity ofdisplacement and chronicity (Table 47-3).21Table 47-2General
Classification ofSynovial DisordersArticular DisordersNoninflammatory
arthropathiesPrimary osteoarthrosis (no clear predisposing factor)Secondary
osteoarthrosis (trauma,previous surgery,avascular necrosis)Mechanical
derangementsBone and cartilage disorders with articular manifestationsInflammatory
arthropathiesSynovitis CapsulitisRheumatoid arthritisJuvenile rheumatoid
arthritisSeronegative polyarthritisAnkylosing spondylitisPsoriatic
arthritisReactive arthritis (bacterial,viral,fungal)Growth disordersNon-
neoplastic:developmental (hyperplasia,hypoplasia,dysplasia)Non-neoplastic:acquired
(ie,condylolysis)NeoplasmPseudotumors (synovial chondromatosis)Benign
(chondroma,osteotoma)Malignant (primary,metastatic)Diffuse connective tissue
disordersMiscellaneous articular disordersNonarticular DisordersMuscle
disordersMuscle spasm (strain)Myofascial pain and dysfunction
(MPD)FibromyalgiaMyotonic dystrophiesMyositis ossificans progressivaGrowth
disordersAdapted from de Bont L et al.13
942Part 7: Temporomandibular Joint DiseaseNoninflammatory arthropathies
aredistinctly limited in their amount ofovertinflammation and may be clinically
silent orfocal in nature.Alternatively ifthe conditionbecomes more severe,symptoms
will ensue.Ifdegenerative changes progress to synovi-tis,joint effusion (secondary
to increasedvascular permeability),or capsulitis,it isthen considered to have
transformed intoan inflammatory arthropathy.Inflammatory arthropathies are pri-
marily due to such conditions as rheuma-toid arthritis,juvenile rheumatoid
arthritis,ankylosing spondylitis,psoriatic arthritis,or arthritis resulting from
infectious causes(see Table 47-2).Secondary causes ofinflammatory arthropathies
include syn-ovitis,capsulitis,traumatic arthritis,oracute inflamed crystal-induced
arthritis,such as gout.As discussed previously non-inflammatory arthropathies can
progress tothe inflammatory types through increasingconcentrations ofdegradation
productswithin the joint.Degenerative changesresulting in the release
ofinflammatorymediators have been demonstrated toworsen the degree oftissue
destruction anddysfunction within the TMJ.This patholog-ic inflammatory cascade has
been the pri-mary focus ofcurrent TMJ research.The past decade has shed new light
onthe cause and treatment ofarticular disor-ders (mainly,internal derangement)
oftheTMJ.Gross evaluation ofdisk position anddisk integrity has traditionally been
themainstay ofdiagnosis and surgical treat-ment.More recently the physiologic
activityofsynovial cells,chondrocytes,and inflam-matory cells in symptomatic joints
havebeen associated with pathogenesis.Thisfundamental shift in focus has changed
theprimary treatment approach from open-joint surgery aimed at restoring the func-
tional anatomy ofthe TMJ,to less invasivetechniques directed toward lysis ofadhe-
sions and intracapsular lavage.22TMJarthrocentesis and arthroscopy are thoughtto
achieve an alteration in the joint milieufavoring a reduction in symptoms
andimproved joint function.Open-jointsurgery nonetheless may still have a role
insevere degenerative disease when preopera-tive criteria are met and surgery is
indicated.Milam and Schmitz have proposed avariety ofmolecular biologic
mechanismsfor TMJD.23Synovoid cells,chondrocytes,and inflammatory cells in the TMJ
pro-duce a physiologic balance between ana-bolic and catabolic
cytokines.23Anaboliccytokines such as insulin-like growth factor-I and transforming
growth factorbeta are instrumental in the formation ofextracellular joint matrix
molecules.Col-lagen,proteoglycans,and glycoproteinsare essential in load-bearing
joints like theTMJ.Alternatively catabolic cytokinessuch as interleukin-1 (IL-
1),IL-6,andtumor necrosis factor alpha (TNF-a) havebeen identified with the
formation ofpro-teases within the TMJ.These proteases(aspartic,cysteine,serine,and
metallopro-teases,among others) operate at low andneutral pH to exert their
pathologic effectsleading to degenerative changes.Oxidative stress,often found
associatedwith pathologic joints,is thought to con-tribute to free radical
formation in the TMJ.The presence offree radicals has been pos-tulated as an
amplifying factor in the activa-tion ofcytokines,enzymes,neuropeptides,and
arachidonic acid metabolites leading todegenerative joint disease.24Nitric
oxide,afree radical involved in regulating vasculartone,has been observed at higher
concen-trations in arthritic joints.Nitric oxide hasdirect effects on prostaglandin
synthesis andcyclooxygenase-2 enzymes leading to syn-ovial inflammation and tissue
destruction.25In a normal functioning joint a delicate bal-ance is maintained
between anabolic andcatabolic mechanisms.In symptomaticjoints catabolic processes
have been foundto exert greater overall effects thus disrupt-ing the balance
between anabolic physiolog-ic maintenance and the negative effects ofcatabolic
cytokines.TMJ synovial fluid analysis has provento be an excellent vehicle for
evaluating theproposed contribution ofcytokines,pro-teinases,and other catabolites
to TMJD.Multiple independent studies support thehypothesis ofcatabolic imbalance
withinthe joint.Kubota and colleagues demon-strated increased levels ofIL-1�,IL-
6,andactive matrix metalloproteinases in TMJswith internal derangement and
osteoarthri-tis when compared with control samples.26This study suggests the
presence ofelevatedconcentrations ofthese cytokines and pro-teinases serving as
potential catabolic mark-ers for cartilage degradation in the humanTMJ.Murakami and
colleagues reportedhigh concentrations ofchondroitin-4 andchondroitin-6 sulfates
compared withhyaluronic acid in the TMJ synovial fluid ofpatients with internal
derangement suggest-ing glycosaminoglycan components asmarkers ofjoint
pathology.27Israel and col-leagues demonstrated the prevalence ofsyn-ovitis and
osteoarthritis through arthro-scopic evaluation in symptomatic TMJs.28These
findings correlated with increasedlevels ofkeratan sulfate in the synovial
fluidTable 47-3Wilkes ClassificationStage IEarly reducing disk displacementStage
IILate reducing disk displacementStage IIINonreducing disk
displacement:acute/subacuteStage IVNonreducing disk displacement:chronicStage
VNonreducing disk displacement:chronic with osteoarthritisFIGURE47-12Perforated
disk (Wilkes stage Vpatient).
Anatomy and Pathophysiology ofthe Temporomandibular Joint943ofthese joints
suggesting its role as a poten-tial biochemical marker for articular carti-lage
degradation.28Recently osteoclasto-genesis inhibitory
factor/osteoprotegerin(OCIF/OPG),a member ofthe TNF recep-tor family,has been
studied in synovial fluidsamples ofTMJD patients.29Increasedosteoclastic activity
has been seen histologi-cally in diseased mandibular condyles.Osteoclast
differentiation requires cell-to-cell contact between osteoclast progenitorsand
bone marrow stromal cells.The pres-ence ofOCIF/OPG is thought to inhibitosteoclast
differentiation by preventing thecell-to-cell contact needed for such
activity.Synovial fluid samples in this study demon-strated decreased amounts
ofOCIF/OPG inosteoarthritic and internally deranged jointssuggesting its
physiologically importantfunction in healthy joints.Although furtherinvestigation
ofsynovial fluid componentsin TMJD is necessary to formulate
definitiveconclusions,it continues to shed new lighton the pathogenesis and
treatment ofsuchdisorders.Treatment ofpatients with internalderangement ofthe TMJ
typically beginswith nonsurgical treatment modalities.Bite appliance therapy,diet
modifications,nonsteroidal anti-inflammatory medica-tions,muscle relaxants,moist
heat or ice,and physical therapy have been found tobe efficacious.30Surgical
intervention istypically employed only after failure ofnonsurgical treatment
objectives.A variety ofsurgical treatment modali-ties have been used in the
treatment ofartic-ular TMJD.Arthrocentesis and TMJarthroscopy have been found to be
mini-mally invasive effective treatments for artic-ular TMJD by decreasing pain and
increas-ing mandibular range ofmotion.(Surgicaltechniques for arthroscopy are
addressed inChapter 49,�Temporomandibular JointArthrocentesis and
Arthroscopy:Rationaleand Technique.�) Indications for thesemodalities include,but
are not limited to,acute closed-lock degenerative joint diseaseaccompanied by pain
and limited range ofmotion and joint effusion.Arthrocentesisand arthroscopy have
also been reported tobe useful in severe,often sudden onset,closed-lock disease due
to an anchored or�stuck disk�phenomemon.This proposedphenomenon involves the disk
becomingadherent to the glenoid fossa throughincreased intra-articular
friction,with orwithout the formation ofadhesions withinthe joint.Lysis ofadhesions
with joint lavagehas been reported efficacious in restoringmandibular range
ofmotion and decreasingpain in these clinical scenarios.31,32TMJarthrocentesis and
arthroscopy showpromising results using the above criteria ofpain symptoms and
mandibular range ofmotion.33Based on the pathophysiologydiscussed in this chapter,a
hypothesisexplaining the efficacy ofjoint lavage relatesto a proposed alteration in
the biochemicalconstituents ofthe joint fluid,thus shiftingthe balance toward
anabolic processes whilereducing the amount ofactive catabolitescontained within
the joint.34Indications for open arthrotomyinclude but are not limited to joint
ankylo-sis,the need for reconstruction due tocondylar resorption or growth distur-
bance,history ofprevious surgery,removalofforeign bodies,neoplasia,trauma,orsevere
degenerative disease precluding lessinvasive interventions.(Indications
andtechniques for open TMJ surgery areaddressed more thoroughly in Chapter
50,�Surgery for Internal Derangements oftheTemporomandibular Joint,�and
Chapter51,�Management ofthe Patient with End-Stage Temporomandibular Joint
Disease.�)Open-joint surgery is primarily based onrestoration ofthe functional
anatomy ofthe TMJ when less invasive techniques arenot feasible or
unsuccessful.Recent datasuggest comparable outcomes betweenopen and closed surgery
in the TMJ withlower morbidity associated with the lat-ter.35Open TMJ surgery
remains a viabletreatment option at the end ofthe surgicaltreatment algorithm.New
insight into thepathogenesis ofTMJD has opened thedoor to less invasive (albeit
equally effec-tive) treatment options for a large numberofTMJD patients.Infections
ofthe Temporomandibular JointInfections ofthe TMJ are not common.Prompt diagnostic
and therapeutic inter-vention is required when an infection ofthe TMJ is suspected
because joint disten-tion is usually painful and permanentchanges in joint function
can occur.Onexamination patients usually exhibit aposterior open bite on the
ipsilateral sideas a result ofthe increased joint fluid.Thepatient will also
maintain a posture towardthe contralateral side.36The surface overly-ing an
infected joint is often warm,andfluctuance is occasionally felt.The bacteria
causing an infected jointare usually spread through a hematoge-nous route.The
synovium is vascular andlacks a basement membrane,which per-mits bloodborne
bacteria to gain accessto the joint space.37Joints with underly-ing arthritic
disease tend to be more sus-ceptible to distant infection.Although thesource ofthe
bacteria is usually at a dis-tant site,spread from dental infections ofmaxillary
teeth has been reported inwhich the bacteria are thought to spreadthrough the
pterygoid plexus ofveins tothe joint.38Direct innoculation ofa jointarea following
a traumatic injury is alsopossible.Complications ofinfections ofthe TMJ include
fistula formation,fibro-sis or bony ankylosis,temporal boneosteomyelitis,and
intracranial abscessformation.A thorough history and review ofsys-tems aids in the
diagnosis ofacute infec-tious arthritis ofthe TMJ.Active infectionin adjacent
sites,especially the ipsilateralmaxillary molars,should be searched for.Other
joints must be assessed to determineifthey are involved.Initially aspiration ofthe
joint should be considered to bothrelieve the pain from the joint
capsulardistention and to help in the identification
944Part 7: Temporomandibular Joint Diseaseofthe infecting organism(s).The aspira-
tion is performed by using a 20-gauge orlarger needle under sterile
conditions.Thesynovial fluid should be Gram stained andcultured for both aerobic
and anaerobicbacteria.Sedation or general anesthesiamay be required for the
arthrocentesis.In sexually active adults 60% ofgen-eral acute infectious arthritis
is due toNeisseria gonorrhoeae.39The majority ofthese patients have a prodrome
ofmalaise,anorexia,headaches,fever,andchills.A few days ofmigratory
arthritisusually precedes the localization ofinfec-tion in one or two
joints.Markowitz andGerry reported a TMJ involvement rate of3% in patients with
disseminated gono-coccal arthritis.40In children under 2 years ofage almost 50%
ofacute infec-tious arthritis is due to Haemophilusinfluenzae.No reports ofTMJ
involve-ment are available.Other gram-positivecocci have been isolated from TMJ
infec-tions in all age groups,including staphy-lococci (particularly in the
elderly) and�-hemolytic streptococci.The adherencecharacteristics ofStaphylococcus
aureusand Neisseriagonorrhoeaeto synoviumaccount for their
prevalence.41Thus,thebest choice for initial empiric antibiotictherapy for an acute
infectious TMJarthritis is an agent that combines a peni-cillin with a �-lactamase
inhibitor.Thecombination ofampicillin and sulbactamwill cover infections from the
staphylo-coccal and streptococcal groups.Sulbac-tam,a derivative
ofpenicillin,inactivatesbacteria-produced �-lactamase and alsohas direct
bactericidal activity against theNeisseriaorganisms.Therefore,this com-bination may
have an advantage over thecombination ofa penicillin and clavulan-ic acid.It should
be noted that bacterialresistance has become increasingly moreproblematic.Reference
to up-to-dateantibiotic regimens is recommended.Effective treatment ofseptic
arthritisby oral antibiotics has not been well stud-ied,therefore the parenteral
administra-tion ofantibiotics should be used initial-ly.37Choices include
ampicillin and sulbac-tam (Unasyn) 3 g intravenous (IV) every 6 hours,or
clindamycin 600 mg IV every 6 hours in penicillin-allergic patients.Athird
generation cephalosporin,cefotaxime6 to 12 g IV per day,could be used for agram-
negative infection in a nonhospital-ized patient.37Tobramycin 3 mg/kg/day infour
doses should be considered to treat apossible presence ofPseudomonas aerugi-nosain
infections that develop in hospital-ized or immunocompromised patients.The duration
oftreatment depends onthe clinical response and the organism iso-lated.Based on
information available fortreatment ofseptic arthritis involvingNeisseria
gonorrhoeae,the patient with aseptic TMJ could be placed on oral ampi-cillin or
tetracycline after a 2-week courseofIV therapy.Reportedly infectionsinvolving
Staphylococcus aureusand gram-negative bacilli require 4 weeks oftotaltherapy,and 2
to 3 weeks oftherapy is ade-quate for streptococci and Haemophilusspecies.42Thus,it
appears that a 30-daytotal course ofantibiotic therapy for acuteTMJ infection is
appropriate.In addition to culture and sensitivitytesting,the aspirate from the
infected jointshould be submitted for white blood cell(WBC) count and
differential,and exam-ined for the presence ofcrystals and fibrin-ogen.Fibrinogen
is usually present in thesynovial fluid ofacutely infected joints.Therefore,some
ofthe synovial fluid col-lected should be placed into a heparinizedtube to prevent
clotting.It is important tonote that ethylenediaminetetraacetic acid(EDTA)
interferes with crystal analysis,therefore synovial fluid should not beplaced in
tubes containing it.The synovialfluid ofan inflamed joint commonly con-tains
greater than 2,000 WBC/mm3(normal < 200 WBC/mm3).Septic jointsnormally have WBC
counts greater than50,000/mm3.The cells are primarilymononuclear,as opposed to a
predomi-nance ofpolymorphonuclear cells ininfected joint fluid.An exception to
thisoccurs in fungal or mycobacterial jointinfections in which the synovial fluid
usu-ally contains less than 20,000 WBC/mm3and shows a greater proportion
ofmononuclear cells.43Following the institution ofantibiotictherapy,lavage ofthe
joint may be useful.Removing the joint fluid containing theproducts ofthe
inflammation,reducingthe bacterial load within the joint,andrelieving the joint
distention will usuallymarkedly relieve the patient�s symptomsand may also decrease
the likelihood ofspread to the temporal bone.Murakamiand colleagues have reported
on the use ofthe arthroscope for monitoring and treat-ing an acutely infected
TMJ.38Following the resolution ofan acuteTMJ infection,a program must be startedto
minimize joint disability and to moni-tor for recurrence ofinfection.The
acuteinflammatory process that accompaniesan infection can result in the deposition
offibrinogen and other products,which canpredispose the joint toward a fibrous
orbony ankylosis.Active range ofmotionexercises are started as soon as possible
toprevent intra-articular adhesions.Thepatient�s range ofmotion should be docu-
mented at weekly intervals.Ifthe range ofmotion is still limited 1 month
followingthe resolution ofthe infection,a brise-ment procedure or an arthroscopic
proce-dure to lyse intra-articular adhesionsshould be
considered.However,beforethis,extracapsular causes oflimited open-ing,such as
masseter muscle trismus,need to be differentiated from intracapsu-lar
disorders.Intracapsular restrictionsare usually accompanied by restriction
oflateral excursions to the contralateral sideand deviation on opening.Recurrence
ofjoint infection (ofall joints) has beenreported to occur at a rate
of10.5%.44Newman noted that infection recurred aslong as 1 year following the
initialepisode.44The patient should be advisedofthis possibility.
Anatomy and Pathophysiology ofthe Temporomandibular Joint945Neoplastic
DiseasesTumors affecting the TMJ area are exceed-ingly rare.The tissues from which
a neo-plasm may arise include the synovium,bone,cartilage,and associated muscula-
ture.Neoplasms ofthis region can presentwith signs and symptoms similar to
thoseoccurring with internal derangement(preauricular pain and dysfunction) andthus
can result in a delay in the diagnosis.The clinician should be aware ofthis
whentreating temporomandibular disorders,especially ifthe patient fails to respond
totraditional therapy.Benign TumorsThe most common benign bone tumors ofthe TMJ
include the osteoma and condylarenlargement or condylar hypertrophy.Both present
signs related to the increasein size ofthe condyle,a shift in themandible to the
contralateral side,and anipsilateral open bite.Often the range ofmotion is
decreased as the increased size ofthe condylar head prevents normal trans-
lation.Radiographs,including tomogramsand computed tomography scans,shouldbe
obtained to delineate the extent ofthecondylar growth and to determineinvolvement
ofthe glenoid fossa and asso-ciated structures.Radionuclide scansshould be
performed to determine iftheprocess is still active and bone is
beingproduced.Treatment includes a condylarhead resection (partial or complete)
foractive lesions or a condyloplasty to reducecondylar size and restore the
occlusion fornongrowing lesions.Condylar reconstruc-tion is usually not
necessary.The diskshould be preserved or replaced (ifit hasbeen damaged) with a
temporalis muscleflap or cartilage graft.Physical therapy isusually required to
reduce dysfunction.Postoperative maxillomandibular fixationis not usually
necessary,but guiding elas-tics may be helpful with muscle retraining.An active
physical therapy program toreduce joint adhesions prevents perma-nent restriction
ofthe joint.Virtually all other benign bone tumorshave been reported to occur in
the TMJ.These bone tumors behave as they wouldin other areas ofthe mandible and
there-fore should be treated in a similar fashion.Synovial TumorsSynovial
chondromatosis is the mostcommonly reported neoplasm ofthe TMJsynovium.Lustman and
Zelster reporteda series of50 cases in which the mean agewas 47 years.45This is in
contrast to syn-ovial chondromatosis involving otherjoints,which is more commonly
found inthe 20- to 30-year-old age group.46Painand swelling ofthe preauricular area
arethe most common initial signs.Depend-ing on the degree ofcalcification
present,radiographs may reveal the presence ofloose radiodense bodies within the
joint.These loose bodies are formed by meta-plastic synovial tissues.Foci
ofmetaplas-tic synovium detach from the synoviallining and remain viable while
suspendedin the synovial fluid.While suspendedthey form a perichondrium and
continueto grow and enlarge.Although the reasonis unknown this process most
frequentlyoccurs in the superior joint space.Theloose bodies are composed
ofcartilagecontaining multinucleated cells.Thepresence ofcellular atypia and hyper-
chromatism is common and a carefulreview ofall histologic material removedis
necessary to rule out the possibility ofchondrosarcoma.Treatment ofsynovial
chondromato-sis involves extirpation ofthe loose bodiesand removal ofthe synovial
lining.Lust-man and Zelster reported that a condylec-tomy was necessary in 13 of47
cases togain access to the anteromedial portion ofthe joint.45The condyle itselfis
notinvolved and therefore should only beremoved for access.Recurrence
ofsynovialchondromatosis is quite rare and isthought to be caused by an
incompleteexcision ofthe original lesions.No cases ofTMJ synovial chondromatosis
transform-ing into chondrosarcoma have beenreported,although this has been
reportedin the knee.47Ganglion CystsGanglion cysts have also been reported tooccur
in association with the TMJ.Theseare cystic structures that arise subcuta-neously
in association with the joint cap-sule or tendon sheaths.Histologic examina-tion
ofa ganglion reveals a true cyst,containing a mucinous fluid and hyaluron-ic
acid.These lesions present as a preauric-ular mass and may produce classic
�TMJsymptoms,�such as pain and limitation offunction.The swelling produced by
theganglion in the preauricular region can beconfused with a parotid mass.Surgery
isindicated to remove the cyst and reoccur-rences have not been
reported.48Malignant TumorsMalignancies ofthe TMJ are very rare andare usually the
result ofdirect extensionsofprimary lesions ofadjacent structures.Metastatic
disease has been reported toinvolve the TMJ,but is more commonlyfound in the
mandibular angle region.This may be due to the relative paucity ofcancellous bone
in the condylar headregion.49The most common lesions tometastasize to the condyle
are adenocarci-nomas ofthe breast,kidney,and lungs.Aswith benign tumors the early
signs ofmalignant disease ofthe TMJ are pain anddysfunction.Primary malignancies
oftheTMJ have been reported as intrinsictumors ofthe condylar bone,disk,synovi-
um,and cartilaginous linking.Typicallypatients with malignancies ofthe TMJ areolder
than the usual internal derangementpatient.Patients with a history ofpreexist-ing
malignant disease must undergo athorough search for metastasis ifTMJsymptoms
develop.Radionuclide scansmay be useful,although the inflammationfrom chronic
synovitis can result in activi-ty localizing in the condyle.50Patients pre-senting
with a fracture ofthe condyle
946Part 7: Temporomandibular Joint Diseasewithout a history oftrauma should be sus-
pect for the presence ofa malignant lesionin the condyle.Primary TMJ malignancies
requireaggressive therapy to prevent intracranialextension ofthe
disease.Radiation,surgery,and chemotherapy are all appro-priate means oftreatment
ofdiseases inthis region.Radiation therapy can also beused for palliation in
disseminated diseaseto control pain from the TMJ region andto prevent pathologic
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theo-retical concept.J Oral Maxillofac Surg2001;59:36�45.32.Rao VM,Liem MD,Farole
A,Razik A.Elusive�stuck�disk in the temporomandibularjoint:diagnosis with MR
imaging.Radiolo-gy 1993;189:823�7.33.Goudot P,Jaquinet AR,Hugonnet S,et
al.Improvement ofpain and function afterarthroscopy and arthrocentesis ofthe tem-
poromandibular joint:a comparative study.J Craniomaxillofac Surg
2000;28:39�43.34.Zardeneta G,Milam SB,Schmitz JP.Elution ofproteins by continuous
temporomandibu-lar joint arthrocentesis.J Oral MaxillofacSurg
1997;55:709�16.35.Holmlund AB,Axelsson S,Gynther G.A comparison ofdiskectomy and
arthro-scopic lysis and lavage for the treatment ofchronic closed-lock ofthe
temporo-mandibular joint:a randomized outcomestudy.J Oral Maxillofac Surg
2001;59:972�7.36.Bounds GA,Hopkins R,Sugar A.Septic arthri-tis ofthe
temporomandibular joint:a prob-lematic diagnosis.Br J Oral Maxillofac
Surg1987;25:61�7.37.Simpson ML.Septic arthritis in adults.In:Gustilo RB,Grumminger
RP,TsukayamaDT,editors.Orthopedic infection.Philadel-phia (PA):WB
Saunders;1900.p.286.
Anatomy and Pathophysiology ofthe Temporomandibular Joint94738.Murakami K,Matsumoto
K,Iizuka T.Suppu-rative arthritis ofthe temporomandibularjoint:report ofa case with
special referenceto arthroscopic observations.J MaxillofacSurg
1984;12(1):41�5.39.Parker RH.Acute infectious arthritis.In:Schlossberg
D,editor.Orthopedic infec-tion.New York (NY):Springer-
Verlag;1988.p.69�75.40.Markowitz HA,Gerry RG.Temporomandibu-lar joint disease.Oral
Surg Oral Med OralPathol 1950;3:75�9.41.Eisenstein BI,Masi AT.Disseminated gonococ-
cal infection and gonococcal arthritis.Semin Arthritis Rheum 1988;10:155�9.42.Smith
JW.Infectious arthritis.In:Mandell GL,Douglas RG,Bennett JE,editors.Principlesand
practice ofinfectious diseases.NewYork (NY):John Wiley &
Sons;1985.p.697.43.Mahowald ML,Messner RP.Chronic infectivearthritis.In:Schlossberg
D,editor.Ortho-pedic infection.New York (NY):Springer-Verlag;1988.p.76�95.44.Newman
JH.Review ofseptic arthritisthroughout the antibiotic era.Ann RheumDis
1976;35:198�204.45.Lustman J,Zelster R.Synovial chondromatosisofthe
temporomandibular joint.Int J OralMaxillofac Surg 1989;18:90�4.46.Orden A,Laskin
DM,Leu D.Chronic preauric-ular swelling.J Oral Maxillofac Surg1989;47:390�7.47.King
JW,Splut HJ,Fechner RE,VanderpoolDW.Synovial chondrosarcoma ofthe kneejoint.J Bone
Joint Surg 1967;49:1389�96.48.Copeland M,Douglas B.Ganglions ofthe tem-
poromandibular joint.Plast Reconstr Surg1988;69:775�6.49.Hartman GL,Robertson
GR,Sugg WE,et al.Metastatic carcinoma ofthe mandibularcondyle.J Oral Surg
1973;31:716�9.50.Mizukawa JH,Dolwick MF,Johnson RP,et al.Metastatic breast
adenocarcinoma ofthemandibular condyle.J Oral Surg 1980;38:448�9.51.Clemente
CD,editor.Gray�s anatomy ofthehuman body.30th ed.Philadelphia (PA):Lea &
Febiger;1985.p.451.
CHAPTER 48Nonsurgical Management ofTemporomandibular DisordersVasiliki
Karlis,DMD,MDRobert Glickman,DMDTemporomandibular disorder (TMD) isthe general term
used to describe the man-ifestation ofpain and/or dysfunction
ofthetemporomandibular joint (TMJ) and itsassociated structures.Up to 5% ofthe pop-
ulation are affected by TMD,with signifi-cantly more frequent and more severe
signsand symptoms appearing in women andolder adults.1,2The etiology ofTMD is pre-
sumed to include trauma,parafunctionalhabits,malocclusion,joint
overloading,arthritides,psychological factors,andergonomic positioning ofthe
head.Theimpact ofpsychological factors is difficultto calculate,but approximately
10 to 20%ofpatients with TMD also manifest someform ofpsychiatric illness.3As
symptoms ofTMD are quite variable and remain exceed-ingly difficult to attribute
exclusively to oneor more events (such as the true contribu-tion or extent
ofinvolvement ofmuscles ofmastication),the joint itselfor psychologi-cal factors is
best understood in terms ofinterdependence.When a diagnosis ofTMD is suspected or
confirmed,therapyshould be directed to improve function andreduce pain and
discomfort.There is ampleliterature to suggest that nonsurgical treat-ment
modalities may account for as muchas a 74 to 85% favorable response rate inpatients
with TMD.4,5In one study,Suvinenand colleagues reported that 81% oftheirpatients
showed 50% or greater improve-ment after conservative physical therapywith a 6-
month follow-up,attributing theimprovement to a possible placebo-typeeffect.6Other
sources report significantreliefin 30 to 60% ofpatients when undersome form
oftreatment.7Additionally,long-term follow-up studies have suggestedthat almost all
patients with TMD willimprove with time,regardless ofthe type oftreatment they may
receive.4,8�12Thus,itappears well established in the literaturethat the majority
ofpatients with TMDachieve some reliefofsymptoms with non-surgical therapy.The
dilemma for the sur-geon is exacerbated by the broad spectrumofresults and claims
that use a seeminglyendless variety ofsurgical and nonsurgicalstrategies.Since the
extent or severity ofsymptomatology is apparently unrelated toetiology,and the
overwhelming number ofsymptoms respond to conservative man-agement,the question
ofwhether and howto incorporate surgical and nonsurgicaltreatment into the care
ofthese patientsbecomes challenging for the attendingphysician.There are absolute
indicationswhere surgical intervention would be ofprimary benefit,and the questions
wouldbe whether there is still a role for nonsurgi-cal therapy in these
patients,and ifso,whenit should be instituted and for how long.One approach is to
consider the concept ofnonsurgical versus surgical therapy mis-leading and
incomplete.There are manytimes when it is inappropriate to considersurgery.At other
times nonsurgical therapyprecedes and almost always follows
surgicalintervention.Therefore,it is essential forthe surgeon to have a deep
appreciation ofthe available techniques and their limita-tions in order to know
when and how toproperly manage TMDs.The purpose ofthis chapter will be to delineate
those tech-niques that are adjunctive or discriminatingto surgical
considerations.Treatment ConsiderationsThe primary goal in treatment ofTMD isto
alleviate pain and/or mandibular dys-function.Pain and alterations in
function(ie,mastication and speech) can becomequite debilitating,greatly affecting
oralhealth care and diminishing the quality oflife for these individuals.Another
criticalobjective relates to patient counseling andeducation on the predisposing
factors forTMD.Depending on the degree ofimpair-ment,patients can often be assured
thatTMD is a benign condition and clinicalimprovement can be expected with appro-
priate therapy.However,it is prudent ifnot incumbent upon the surgeon toinform
patients that complete elimination
950Part 7: Temporomandibular Joint Diseaseofsymptoms is at times
unattainable.Nonsurgical techniques that can decreaseunintentional overloading
ofthe mastica-tory system,eliminate pain,reduce dys-function,decrease
chronicity,and pro-mote healing are essential in all phases oftherapy.A patient
home care program mayprevent further injury and allow for a peri-od ofhealing.In
general patients can beinstructed to limit mandibular function,modify habits,avoid
stress,and start ahome exercise program.8Clicking and popping ofthe TMJ isquite
common in TMD and normal joints.It is difficult to eliminate,usually reoccurs,and
there is inconclusive evidence to sug-gest whether this poses a problem for
thepatient.There is considerable support thatjoint sounds without pain or
dysfunctionshould not be treated (Table 48-1).Once a diagnosis ofTMD has
beenestablished,frequent follow-up appoint-ments are necessary once therapy is
insti-tuted,to determine whether there is anyimprovement.Initial impressions
mayrequire modification after several weeks oftherapy,and further diagnostic
proceduresmay be warranted to rule out
vascular,neurologic,neoplastic,psychological,orotolaryngologic abnormalities.TMD is
acomplex disorder that is molded by manyinteracting factors,and strong considera-
tion should be given to a multidisciplinaryapproach.The role ofthe
dentist,physicaltherapist,neurologist,psychologist/psy-
chiatrist,anesthesiologist,and oral andmaxillofacial surgeon cannot be under-
stated,and should be key constituents ofany facial pain/TMD center.We
cannotprecisely dictate timing or length ofthera-py.This must still be determined
by thesurgeon and based on severity ofsymp-toms and supporting diagnostic parame-
ters.As with other joints considerationmust be given to rule out pathology,decrease
inflammation,allow unimpededjoint motion,and restore range ofmotion.To accomplish
this in a ginglymoarthrodi-al joint that is permanently attached to theopposite
side and is intimately involved inoral health is indeed a challenge.The remainder
ofthis chapter pro-vides basic guidelines for nonsurgicaltherapeutics.It is not
intended to elimi-nate or preselect adjunctive dental or sur-gical
treatment.Nonsurgical TherapyDiet A soft diet is often overlooked in the man-
agement ofTMD.A soft diet preventsoverloading ofthe TMJ and decreasesmuscle
activity that may be hyperactive.The extent oftime that a patient should beplaced
on a soft food diet is dependent onthe severity ofsymptoms.Patients shouldbe
instructed to cut their food into smallpieces and abstain from eating chewy,hard,or
crunchy foods.Uncooked vegeta-bles and meats represent examples offoods that should
not be eaten by thesepatients.A strict liquid diet is reserved forthose patients
experiencing severe TMDsymptoms (Table 48-2).PharmacotherapyMedications are often
prescribed for man-aging the symptoms associated with TMD.Patients should
understand that thesemedications may not offer the cure to theirproblem but can be
a valuable adjunctiveaid when prescribed as part ofa compre-hensive program.With
pharmacotherapythere is always a danger ofdrug dependen-cy and abuse,particularly
with narcoticsand tranquilizers.Since many TMD symp-toms are periodic,there is a
tendency toprescribe medications on a �take as need-ed�philosophy.This can provide
briefperiods ofpain relief,but more frequentpain cycles can result in less
effectivenessofthe drugs and ultimate overuse or abuseofthe medications.12�15The
general rec-ommendation is that when pharma-cotherapy is employed,the
medicationsshould be prescribed at regular intervalsfor a specific period oftime
(eg,four timesdaily for 2 wk).The clinician must alwaysbe cognizant ofpotential
personality traitsthat may contribute to drug dependenceor abuse.Other obvious
factors are con-current medical ailments or medications,patient age,occupation,and
each patient�sattitude toward pharmacotherapy.The most common pharmacologicagents
used for the management ofTMDare analgesics,anti-inflammatory agents,anxiolytic
agents,antidepressants,musclerelaxants,antihistamines,and local anes-
thetics.Analgesics,corticosteroids,andanxiolytics are useful for acute TMD
pain.Anti-inflammatory medications and anti-depressants are primarily indicated
forchronic pain management.Muscle relax-ants,nonsteroidal anti-inflammatorydrugs
(NSAIDs),and local anesthetics canbe used for both acute and chronic
pain.AnalgesicsAnalgesic medications areeither opiate or nonopiate
preparations.Nonopiate analgesics (salicylates andacetaminophen) can be added to
the anti-inflammatory regimen to assist in painrelief.The salicylates (ASA) are
commonlyused in TMD and are the benchmark med-ications to which other analgesics
are usu-ally compared.Salicylates are antipyretic,analgesic,and anti-
inflammatory.ForTable 48-1Goals ofNonsurgical Therapyfor Temporomandibular
DisordersAlleviate painDecrease or eliminate jaw dysfunctionEducate and counsel
patientsTable 48-2Soft DietDecreases muscle activity and loading forces on
temporomandibular jointsControls range ofmotion�hinge and slidingRanges from liquid
diet to elimination ofhard chewy food;involves cutting food into small
piecesEliminates gum chewing
Nonsurgical Management ofTemporomandibular Disorders951those patients who cannot
take aspirin,anonacetylated aspirin such as choline mag-nesium trisalicylate or
salsalate may beeffective.As with all salicylates,however,choline magnesium
trisalicylate and sal-salate should not be prescribed for childrenor teenagers with
chickenpox,influenza,orflu symptoms or exposure.Opioid analgesics
(oxycodone,propoxyphene,and hydrocodone) shouldbe prescribed only for moderate to
severepain oflimited duration,due to the highpotential for addiction.These drugs
areoften administered in conjunction withNSAIDs or acetaminophen
(Vicodin,Lortab,Percocet,Darvocet,etc).They acton opioid receptors in the central
nervoussystem,producing analgesia and sedation.Because patients can quickly
becomedependant on the narcotic analgesics,it isrecommended that these drugs not be
pre-scribed for longer than 2 to 3 weeks.Otherside effects include constipation
secondaryto decreased gastric motility.Anti-inflammatory MedicationsThereare two
types ofanti-inflammatory medica-tions useful in treating TMD:NSAIDs
andcorticosteroids (Figure 48-1).Glucocortico-steriods prevent the release
ofarachidonicacid,a key component ofthe inflammationcascade.NSAIDs inhibit
cyclooxygenase,which inhibits prostaglandin synthesis fromarachidonic
acid.16�18NSAIDsThe advantages ofNSAIDs inTMD patients are analgesia and their
anti-inflammatory properties (Tables 48-3 and48-4).NSAIDs may offer relieffor
patientswith synovitis,myositis,capsulitis,sympto-matic disk displacement,and
osteoarthri-tis.19This type oftherapy helps alleviatethe inflammation,which thereby
causes adecrease in pain perception.Side effectsinclude gastric
irritation,allergies,and liverdysfunction.An ideal NSAID would be onethat has
minimal gastric irritation,a quickonset with long-lasting effects,low
dosagerequirements,is tolerated at high levels,and is low in cost.NSAIDs are
divided intoseven groups based on their chemicalstructure:salicylates
(ASA),propionicacids (ibuprofen,naproxen),acetic
acids(indomethacin,ketorolac),fenamic acids(meclofenamate),oxicams (piroxicam),and
the cyclooxygenase (COX)-2inhibitors (celecoxib,rofecoxib).The mostcommon NSAIDs
used are ibuprofen,diclofenac,and naproxen,but because ofpurported fewer
gastrointestinal (GI) sideeffects and minimal effect on platelets,COX-2 inhibitors
are becoming more pop-ular.Recent studies have found that COX-2,an important
inflammatory mediator,ispresent in the TMJ synovial tissue and fluidofpatients with
internal derangements.This offers the possibility that the COX-2inhibitors might be
more effective for TMJpain and arthralgias than other anal-gesics.20,21Enteric
coating,prodrugs(nabumetone ),taking agents after mealsor in conjunction with
antacids,and takinggastric protective agents (ranitidine andsucralfate) have been
reported to reducethe gastric irritation from NSAIDs.22CorticosteroidsBy completely
blockingthe arachidonic acid cascade,corticosteroidsproduce a greater anti-
inflammatory re-sponse than do NSAIDs.Systemic steroidsare indicated only for
short-term therapy (5to 7 d) due to their long-term possible com-
plications.Osteoporosis,diabetes,hyperten-sion,electrolyte changes,and clinical
Cush-ing�s disease are sequelae oflong-termsystemic corticosteroid
treatment.23Steroidshave also been directly injected into the TMJDisturbance ofcell
membraneRelease ofphospholipidsPhospholipaseArachidonic acidCyclooxygenase-2(COX-
2)Cyclooxygenase-1Leukotrienes(COX-1)ProstaglandinsNSAIDsCorticosteroidsFIGURE48-
1Inflammation cascade.The corticosteriods prevent the release ofarachi-donic acid
and thereby interrupt most ofthe inflammation cascade.The NSAIDsinhibit
cyclooxygenase,which inhibits prostaglandin synthesis from arachidonic acid.NSAID =
nonsteroidal anti-inflammatory drugs.
952Part 7: Temporomandibular Joint Diseasein an attempt to decrease inflammation
ormediate the inflammatory response (ie,following arthroscopy),but long-term
orexcessive use is associated with condylarhypoplasia by inhibiting osteoblastic
activi-ty and increasing loss ofcalcium in theurine and GI
tract.24AnxiolyticsAnxiolytic medicationsreduce the anxiety,insomnia,and
musclehyperactivity associated with TMD(Tables 48-5 and 48-6).These drugs oftenhelp
the patient reduce the perception of,or reaction
to,stress.Benzodiazepines(diazepam) decrease anxiety,relax skeletalmuscle,and cause
sedation and may beselected according to their more favorablecharacteristics
(ie,less sedation).The mus-cle relaxant properties may be used todecrease the
effects ofbruxism secondaryto hyperactivity ofmuscles ofmastication.It is
recommended that the benzodi-azepines not be used for more than a 2-week period
because ofthe high poten-tial for dependency,although this can beincreased up to 3
weeks only at bedtime tocontrol bruxism.19Buspar (azaspirode-canedione) is an
anxiolytic;however,itdoes not produce either sedation or mus-cle relaxation.It may
be used to controlanxiety in TMD patients without produc-ing
drowsiness.Antihistamines (promethazine andhydroxyzine) antagonize central
andperipheral H1receptors,and have a seda-tive effect as well as anxiolytic
properties.Antihistamines,unlike the benzodi-azepines,do not have the potential
forabuse.They can be used more safely inchildren and the elderly and for the treat-
ment ofvertigo and nausea that mayaccompany
TMD.25AntidepressantsAntidepressantsinclude monoamine oxidase
inhibitors(MAOIs),tricyclic antidepressants,andselective serotonin reuptake
inhibitors(Tables 48-7 and 48-8).They are pre-Table 48-3Commonly Used Nonsteroidal
Anti-inflammatory AgentsCategoryGenericBrandHalf-Life
(hours)SalicylatesAcetylsalicylic acid (aspirin)Bayer2.5Enteric
coatedEcotrin2.5Aspirin with buffering agentBufferin2.5Aspirin with
caffeineAnacin2.5DiflunisalDolobid8�12Choline magnesium
Trilisate9�17trisalicylateSalsalateDisalcid16Propionic
acidIbuprofenMotrin,Advil,1.8�2.5Nuprin,RufenFenoprofenNalfon2�3SuprofenSuprol2�4Na
proxenNaprosyn12�15Naproxen sodiumAnaprox12�15Acetic
acidIndomethacinIndocin4.5�6SulindacClinoril7.8 (16.4)*TolmetinTolectin1�1.5Fenamic
acidMeclofenamateMeclomen2 (3.3)*Mefenamic
acidPonstel2PyrazolonesPhenylbutazoneButazolidin84OxicamPiroxicam
olamineFeldene30�86COX-2 inhibitorsCelecoxibCelebrex11�12 RofecoxibVioxx17*Active
metabolite.Adapted from Syrop SB.25Table 48-4Nonsteroidal Anti-inflammatory
Drugs:Ideal PropertiesMinimal gastric irritationQuick onset with long-lasting
effectsLower dosageTolerated at high levelsLow costTable 48-5Commonly Used
BenzodiazepinesUsual Dosage Elimination Generic Brand(mg/d)(half-life
[h])AlprazolamXanax0.5�1.5 (ddd)12�15ChlordiazepoxideLibrium15�60
(ddd)5�30DiazepamValium2�40 (ddd)20�50FlurazepamDalmane30 (at
bedtime)47�100LorazepamAtivan2�6 (ddd)10�18OxazepamSerax30�60
(ddd)5�15PrazepamVerstran20�40 (ddd)30�100TemazepamRestoril15�30 (at
bedtime)10�20TriazolamHalcion0.25�0.5 (at bedtime)1.5�5ddd = divided daily
dosesAdapted from Syrop SB.25
Nonsurgical Management ofTemporomandibular Disorders953scribed for chronic
pain,headaches,sleepdisorders,obsessive-compulsive disorders,and central-mediated
pain disorders.Therelationship between pain and depressionis a challenge and often
necessitates treat-ing both simultaneously.Depression in theTMD or chronic pain
population isgreater than in the general population.Studies report that up to 30%
ofTMDpatients have major depression at the timeofpresentation for treatment,and up
to74% ofpatients with chronic TMD havehad an episode ofmajor depression.26,27MAOIs
are not routinely prescribed forTMD due to their numerous side effectsand dietary
restrictions.Benefits oftricyclicantidepressants have been well document-ed in
chronic pain or depression popula-tions and are probably due to analgesic
andantidepressant actions.The analgesic prop-erties are independent ofthe
antidepressanteffect,which requires higher doses.It hasbeen shown that low doses
ofamitriptyline(10 mg) before sleep can have an analgesiceffect on chronic pain but
have no relation-ship to the antidepressant actions thatrequire doses up to 20
times greater.28Tri-cyclic antidepressants may also help treatnocturnal bruxism and
any sleep distur-bance associated with TMD.29Side effectsare related to
anticholinergic activity caus-ing xerostomia,constipation,blurredvision,and urinary
retention.Selectiveserotonin reuptake inhibitors can also beused for treating the
depressed TMDpatient.These medications often need to betaken for several months and
patients mustbe counseled appropriately.Fluoxetine(Prozac) may increase bruxism and
anxietyand should be carefully monitored.Muscle RelaxantsCentrally acting mus-cle
relaxants (cyclobenzaprine,methocar-bamol,and carisoprodol) may be used torelax
hyperactive musculature associatedwith TMD (Tables 48-9�48-11).Theserelaxants may
also act as sedatives,and theyare commonly combined with NSAID use.Cyclobenzaprine
(Flexeril) has a similarchemical structure to the tricyclic antide-pressants and
ifgiven over an extendedperiod oftime will produce antidepressantand sedative
actions as well as the anti-cholinergic side effects ofthe tricyclics.Central
muscle relaxants can be very effec-tive for acute myofascial pain (ie,trauma).One
peripheral muscle relaxant,baclofen,has been used in myofascial painbut is best
reserved for severe musclespasm or neurogenic pain.Recently botu-linum toxin has
been used to treat severebruxism.By providing muscle relaxation,inflammation ofthe
masseter muscle andTMJ capsule can be reduced.30,31Local AnestheticsLocal
anesthetics acton the nerve cell membrane to preventgeneration and conduction
ofimpulses(Table 48-12).Local anesthetics can beused as diagnostic blocks intra-
articularlyand/or intramuscularly to alleviate painand increase range ofmotion.For
exam-ple,injection behind the maxillarytuberosity will permit the lateral ptery-
goids to be anesthetized,thereby allowingmaximal protrusion and retrusion
ofthemandible.There should be no vasocon-strictor used in conjunction with the
anes-thesia,as the decrease in blood flow mayincrease muscular pain.The
intrinsicvasodilation effect ofthe anesthesia mayimprove perfusion and thereby
furtheralleviate pain.It has been shown that anintra-articular injection
ofmepivacainealong with physiotherapy in patients withanteriorly displaced disks
has yieldedfavorable results in pain reliefand masti-catory efficiency.32Physical
Therapy There are many factors contributing to lim-ited range ofmotion.They include
muscu-lar pain,anterior disk displacement (closedlock),and fibrotic scar tissue
preventingrotation or translational movements.It iswell accepted that
immobilization has dele-terious effects on both joints and muscles.Table 48-
6Antianxiety Medications:BenzodiazepinesBind GABA receptorsSerotonergic (5-HT) in
the amygdalaBeneficial for treatment ofanxiety,insomnia,muscle
hypertonicityPotential abuseAvoid short-acting or high-potency drugs
(ie,triazolam,alprazolam,lorazepam)Taper gradually to avoid withdrawal,rebound
anxietyGABA = ?-aminobutyric acid;5-HT = 5-hydroxy-tryptamine (serotonin).Table 48-
7Commonly Used AntidepressantsGenericBrandDosage (mg/d)Side
EffectsAmitriptylineElavil10�300HighDesipramineNorpramin50�300ModerateDoxepinSinequ
an25�300HighImipramineTofranil20�300ModerateNortriptylinePamelor,25�150ModerateAven
tyl25�150FluoxetineProzac5�20ModerateTable 48-8Antidepressant MedicationsTricyclics
are most used and studied for chronic pain and depressionMonoamine oxidase
inhibitors (MAOIs) not first choice due to adversereactionsSelective serotonin
reuptake inhibitors (SSRIs) such as fluoxetine can increase anxiety and bruxism
954Part 7: Temporomandibular Joint DiseaseImmobilization may cause
degenerativechanges to the joint surfaces,synovial fluid,and surrounding
tissues.Reduced motionalso results in rapid muscle fatigue,muscleweakness,and
contractures.Synovial fluidgeneration is reduced or halted when jointsare
immobile.Additionally it has beenobserved that the synovial fluid ofpatientswith
pain and limited motion often con-tains inflammatory byproducts.Kaneyamaand
colleagues listed a variety ofcytokinessuch as interleukin (IL)-1�,tumor
necrosisfactor (TNF)-a,IL-6,and IL-8 in sympto-matic joints,not observed in
asymptomaticjoints.33This high level ofcytokine activityis believed to be related
to the underlyingpathogenesis ofTMD.Cytokines such asIL-6 and IL-1�may induce the
�inflamma-tory cascade.�As a result ofthe release ofproteinases,there may be
destruction ofarticular cartilage and bone resorption.Each cytokine has its unique
properties,notonly affecting the surrounding tissues butalso aiding in the release
ofothercytokines.33Thus,the role offunctionalmotion and the synovium may be an
inde-terminate factor in the health ofthe TMJ(Table 48-13).Exercise TherapyPhysical
therapy andexercise are an important part ofany TMDprogram.Mild or acute symptoms
can beinitially managed with soft diet,jaw rest,heat/ice packs,jaw/tongue posture
open-ing exercises,lateral jaw movements,andpassive stretching exercises.Once again
theexact sequence oftherapy is unknown butis usually based on degree ofpain and
lim-itation offunction.Further reduction ofpain and inflammation may require
anoffice-based physical therapy program.From our experience,ultrasonography,Table
48-9Commonly Used Muscle RelaxantsUsual Dosage Generic Brand(mg/d; divided
doses)CarisoprodolRela,Soma1,000�1,400ChlorzoxazoneParaflex,Parafon Forte
D.S.C.750�3,000MeprobamateMiltown,Equanil1,200�1,600MethocarbamolRobaxin1,500�4,500
CyclobenzaprineFlexeril5�30OrphenadrineNorflex,Disipal150�300DiazepamValium2�40Comb
ination Fixed DosageMeprobamateEquagesic1�2 tablets 3 or 4 Aspirintimes
dailyOrphenadrineNorgesic1�2 tablets 3 or 4 Aspirintimes dailyCaffeineAdapted from
Syrop SB.25Table 48-10Central Muscle Relaxantsand Their EffectsCentral Muscle
RelaxantsCarisoprodol (Rela,Soma)Chlorzoxazone (Paraflex)Methocarbamol
(Robaxin)Cyclobenzaprine (Flexeril) EffectsTranquilizing effectsGeneral sedative
effect on central nervoussystemNo specific neurotransmitterNo effect on skeletal
muscle,motor end plate,or nerve fiberTable 48-11Peripheral Muscle
RelaxantsPeripheral Muscle RelaxantsBaclofen (Lioresal) derivative ofGABA that
blocks spinal cord contraction reserved for severe muscle spasm,or neurogenic
painBotulinum toxin (Botox) is useful for management oforomandibular
dystoniaEffectsBlock synaptic transmission at neuro-muscular junctionBlock muscle
contractionGABA = ?-aminobutyric acid.Table 48-12Local AnestheticsAct on nerve cell
membrane to prevent generation and conduction ofimpulsesDiagnostic blocksMuscle
injection treatment to increase range ofmovementTable 48-13Physical TherapyHome
Treatment Program (good for mild acute symptoms)Soft dietDecrease functionHeat/ice
packsJaw/tongue posture opening exerciseLateral jaw movementControl passive motion
(ie,Therabite)Office Treatment (reduction ofpain and
inflammation)UltrasonographyTranscutaneous electrical nerve stimulationRange
ofmotionSoft tissue manipulationTrigger point injectionsAcupuncture (reestablishing
proper energy flow by adding electric current or heat to the placed acupuncture
needle)
Nonsurgical Management ofTemporomandibular Disorders955transcutaneous electrical
nerve stimula-tion (TENS),soft tissue manipulation,trigger point injections,and
acupuncturehave also been advocated as effective in themanagement ofthe TMD
patient.Jaw exercise therapy can be describedas passive,active,or isometric.Passive
jawexercise allows the patient to manually (orwith a device such as Therabite
JawMotion Rehabilitation System,Atos Med-ical,Milwaukee,WI,USA) increase inter-
incisal opening (Figure 48-2).Passive jawexercise has received a great deal
ofatten-tion recently.Many authors report signifi-cant improvement in pain and
mobility inthe nonsurgical phase oftreatment forTMD as well as for the
postoperative TMDpatients.34�37Passive jaw exercise is alsovery effective for
patients experiencingmuscular trismus and myofascial pain dys-function (MPD).It may
be contraindicat-ed in patients with severely displaceddisks,due to the possibility
ofdamage tothe disk or retrodiskal tissues.Active exercise using the patient�s
jawmusculature may be incorporated into ahome therapy program.One regimenallows the
patient to activate,for example,their suprahyoid muscles
(geniohyoid,mylohyoid,digastric,and stylohyoid),thereby inactivating the elevators
ofthe jaw(medial pterygoid,masseter,temporalis).This may allow for relaxation
ofhyperac-tive muscles ofmastication and may assistin increasing maximal incisal
opening.Inthe active stretch phase patients are advisedto keep their mouth open for
several sec-onds and relax.They are instructed to openuntil they perceive pain and
then advised tohold for several seconds and repeat thisexercise several times a
day.An active later-al stretch permitting the contralateral later-al pterygoid to
be stretched may be accom-plished by visualizing themselves in amirror.In the
active protrusion,also per-formed in front ofthe mirror,the mandibleis protruded
forward stretching the lateralpterygoids bilaterally.All active excursionsare
maintained for several seconds andslowly released.Isometric exercises have been
recom-mended for patients with severe pain andtrismus.There is no movement during
thisexercise while the depressor muscles areactivated,allowing for relaxation
oftheopposing elevator musculature
(medialpterygoids,masseter,temporalis).Theseexercises are performed by holding
themandible stationary as the muscles areactivated isometrically.The lateral ptery-
goids may also be exercised in a similarisometric fashion.Mongini describes a
three-stageoffice technique ofmandibular manipu-lation for patients with
pain,decreasedmobility,and disk displacement withoutreduction.38Right and left
lateral move-ments are initiated by the patient.Thepatient continues the movement
whilethe clinician applies light pressure in thesame direction,and in the last
stage themandible is moved to the opposite sidewith patient assistance.38Kurita and
col-leagues described a technique ofplacingone thumb on the last molar on
theaffected side while the other hand sup-ports the head in the temporal
region.39The mandible is then moved downwardand forward.The patient is instructed
toprotrude and move their jaw laterally,and open their mouth while the
clinicianmanipulates the jaw.Following thismovement the mandible is pushed backso
that the condyle is positioned postero-superiorly in the glenoid fossa.Only
18%ofthe patients received significant bene-fit from the manipulation,and the
moreadvanced the displacement,the less thesuccess ofthe treatment.39Yuasa andKurita
suggested that physical therapyalong with administration ofNSAIDs(for a 4-week
period) is a more effectiveway to treat TMJ disk displacement with-out osseous
changes.40Nonetheless,thereis no shortage ofrecommended exercis-es,and care must be
taken to do no harm(Table 48-14).FIGURE48-2Patient usingpassive jaw exercise
deviceto improve interincisalopening and to break anyfibrous bands.(This Ther-aBite
picture is reproducedwith the courtesy and per-mission ofAtos
Medical,Milwaukee,WI,USA.)Table 48-14Manual TherapySoft tissue
techniqueMassage,relaxation,stimulation,breaking scars,decreasing
swelling,stretchingManipulative therapy�spine realignmentPassive,quick,high-
velocity,short-amplitude,thrust that forces the joint beyond its normal end
rangePatient has no control;pain reliefimme-diate but short lived
956Part 7: Temporomandibular Joint DiseaseThermal AgentsThermal agents areoften
incorporated in the management ofTMD.The use ofcold and heat can allevi-ate muscle
pain and play an equal roleduring stretching and strengthening exer-cises.41�43Heat
therapy has been reportedto reduce muscle pain by increasing nerveconduction
velocity and local vasodilata-tion.43Superficial heat therapy can beimplemented
with conductive (hot packs,paraffin,whirlpool) or radiant (infrared)agents.The most
common types used are amoist hot washcloth,heating pad,orhydrocollator,a pad filled
with clay andheated in a water bath to 70�to 88�C.It iswrapped in a towel and
placed on the sitefor 15 to 20 minutes,causing a transientrise in skin temperature
to about 42�C.The use ofmoist heating pads is an effec-tive modality oftreatment
for myofascialpain associated with TMD.44Cryotherapy is often used as an aid
instretching muscles in an attempt toincrease maximal incisor opening limitedby
pain.41The pain perception modeldescribed by Melzack and Wall explainswhy cold
therapy stimulates the large Adelta fibers (temperature) inhibiting pain,which is
stimulated by the small C fibers.43A physical therapist would place refriger-ants
on the skin in a sweeping motion fol-lowed by stretching ofthe musculature.Cold
therapy should be used with cautionbecause ofthe potential for increased
jointstiffness,contracture,and immobility.Cold can also have analgesic effects
after atherapeutic exercise regimen.Ice wrappedin a towel,fluoromethane
spray,andreusable ice packs can all be used to deliv-er cryotherapy to the
temporomandibularjoint and related muscles.The stretch andspray technique,initially
described byModell and Simons and later modified byTravell and colleagues,is still
a mainstay ofoffice physiotherapy.41,42The therapistholds the fluoromethane spray
about 30 to45 cm from the patient and sprays in asweeping motion multiple times,and
thisis then followed by stretching exercises.Possible side effects include
frostbite andthe potential for joint stiffness.Many ther-apists follow cryotherapy
with moist heatto prevent the muscles from contracting.Ultrasonograpy and
PhonophoresisDeep heat can be delivered by ultrasonog-raphy or phonophoresis.The
ultrasoundmachine operates above audible frequen-cy sound waves (0.75 to 1.0
MHz),whichconvert to heat while traveling throughsoft tissue.The ultrasound machine
isapplied to the skin along with an acousticconductive gel,then moved slowly
overthe affected area in small circular move-ments.The operator must be careful
notto keep the machine in one place for toolong as it may cause overheating
oftheconnective tissue,causing structural dam-age.The deep heat is intended to
increaseperfusion to the area,decreasing pain andincreasing mobility.45Reported
effects ofultrasound therapy include altered cellmembrane
permeability,intracellularfluid absorption,decreased collagen vis-
cosity,vasodilatation,and analgesia.Thebeneficial effects to joints are
reducedcapsular contracture,break up ofcalciumdeposits,and decreasing hyaluronic
acidviscosity.46Because ultrasonographydelivers heat to the deeper structures,itmay
have some advantage in treating ten-donitis,capsulitis,muscle spasm,andtight
ligaments.Phonophoresis is an application ofultrasound heat therapy that
incorporates apad filled with a steroid or anesthetic creamplaced over the affected
area.As the ultra-sound waves are applied,the medicationsperfuse into the
tissues.The most commonindication for phonophoresis is synovitisassociated with
painful jaw hypomobility.Contraindications for the use ofultra-sonography and
phonophoresis includeareas that may have a reduced circulation,fluid-filled
organs,eyes,radiation therapysites,and malignant tissue.Ultrasoundtherapy should be
used with extreme cau-tion over active bone growth centers.47Electrical
StimulationTranscutaneousElectrical Nerve StimulationTENS hasbecome a viable home
therapy in treatingTMD.The precise mechanism ofaction isunknown,but it has been
suggested thatthe gate control theory,counter-irritation,neurohumoral substance
release,andperipheral blockade are all involved.48TENS uses a low-voltage
electrical currentthat is designed for sensory counterstimu-lation in painful
disorders.It is used todecrease muscle pain and hyperactivityand for neuromuscular
re-education.49,50TENS units are small and portable.Elec-trodes are placed along
dermatomes orover acupuncture and trigger points.Thepatient can control the
settings with vari-able frequency,amplitude,waveform,width,and pulse mode.Treatment
can lastseveral hours.TENS emits an asymmetricbiphasic wave of100 to 500 ms
pulse.Theefficacy ofTENS for analgesia and musclerelaxation in myofascial pain has
beendocumented.51Electrode placement iscontraindicated over the carotid
sinus,transcranially,directly on the spine,on apregnant womb,or on patients
withdemand-type pacemakers.52High-Voltage StimulationHigh-voltagestimulation units
deliver currents ofposi-tive and negative polarity with voltagesgreater than 100
V,which are delivered in aconstant or intermittent pattern.The pos-itive polarity
produces vasoconstriction,whereas the negative polarity producesvasodilatation.The
positive polarityreduces nerve irritability,and negativepolarity enhances
it.Negative polaritysoftens the affected tissue thus decreasingmuscle
tension.Treatment with high-voltage stimulation has improved jawmobility and
relieved pain intensity in TMD patients.53It can be used for painrelief,reduction
ofedema,and neuromuscular stimulation.53IontophoresisIontophoresis transfersions
from a solution through intact skin by
Nonsurgical Management ofTemporomandibular Disorders957passing a direct current
between two elec-trodes.54Positive ions are transmitted at thecathode,and negative
ions are transmittedat the anode.Examples ofnegatively ioniz-ing drugs are
dexamethasone and methyl-prednisolone.Other drugs used in ion-tophoresis include
lidocaine and salicylates.Iontophoresis was introduced in treatingTMD and
postherpetic neuralgia in 1982.55It appears to be most effective
againstinflammation,muscle spasm,and calciumdeposits.The deep penetration ofthe
med-ication aids in the treatment ofsevere jointinflammation and pain (Table 48-
15).Trigger Points and Muscle InjectionsAtrigger point is an area
ofhyperirritabilityin a tissue that,when compressed,is local-ly
tender,hypersensitive,and gives rise toreferred pain and tenderness.56Triggerpoint
development may be due to trauma,sustained contraction,or acute strain.When a
needle penetrates this area it maycause a twitch response and
referredpain.56Injection oflocal anesthetic agentswithout epinephrine may cause a
tempo-rary anesthesia,which enables the clini-cian to stretch the muscles in the
affectedarea.A vasodilator effect ofthe local anes-thetic may improve perfusion to
the area,thus allowing harmful metabolites whichmay induce pain to be more
readilyremoved by the vasculature.Stress-Reduction Techniques Relaxation and
BiofeedbackRelaxationand stress-reduction techniques forpatients with TMD can be
very effectivetreatment modalities.Various techniquesexist,an example being
contracting andreleasing skeletal muscles,starting fromthe feet and moving toward
the head andneck region.Patients can also use audio-tapes that teach breathing and
specificrelaxation techniques.Biofeedback tech-niques incorporate the use
ofelectromyo-graphy (EMG) and skin temperature tomeasure the patient�s physiologic
func-tion.The information is then conveyedback to the patient by a meter or
sound.The patient can gauge their level ofrelax-ation and measure progress
accordingly.57The aim is to achieve pschycological self-regulation and to monitor
the relationshipbetween muscular tension and pain.In areview ofthe literature
Crider and Glarosreported 69% ofsubjects rated asimproved or symptom free
followingbiofeedback and relaxation treatments,whereas only 35% ofpatients
receivingplacebo intervention showed anyimprovement.58Furthermore,on follow-up
examination the patients showed nodecline from post-treatment levels.58Scottand
Gregg advocate that relaxation tech-niques and EMG feedback can yield
goodresults,especially in patients who are notdepressed and have
temporomandibularpain for a short period oftime.59The chiefhurdle is the difficulty
to motivate patientsin pain (Table 48-16).Acupressure and AcupunctureAcupres-sure
and acupuncture may be implement-ed along with other modalities duringnonsurgical
treatment.Acupuncture usesthe relationship between energy flowthrough
meridians,natural elements,andpositive and negative life forces.Fine nee-dles are
used to reestablish proper energyflow.There are several theories on themechanism
ofaction ofacupuncture andacupressure.The first is the gate controltheory,which
states that the needle pro-duces a painless stimulation,causing gatesto close and
preventing signal propagationto the spinal cord.60Other explanationsinclude release
ofendorphins from thepituitary gland which block pain sensa-tion,promotion ofalpha
waves (associat-ed with stress reduction and relaxation),and rebalancing the
electric ion flow pat-tern (when disrupted,it may elicit pain).60There are several
different acupressuretechniques including Jin Shin (two acu-pressure points held
for 30 s to 5 m),Shi-atsu (more rapid,held 3 to 10 s),reflexol-ogy (acupressure on
feet,hands,and earscorresponding to areas ofthe body),Do-In (self-acupressure and
breathing exercis-es),and G-Jo (acupressure for first aidpurposes).Some studies
have reportedfavorable results when these techniquesare combined with other
modalities(splint therapy),but overall data are limit-ed.61,62These pain therapies
can be offeredas an alternative to conventional therapy.PsychotherapyIn some cases
TMD maybe the somatic expression ofan underly-ing psychiatric or psychological
disordersuch as depression or conversion.63,64TheTable 48-15Electrical
StimulationTranscutaneous electrical nerve stimulationIontophoresis�direct current
to drive drugs into tissue (hydrocortisone,lidocaine,salicylates);good for muscle
spasm or inflammationHigh-volume stimulation (100 V) (pumping effects ofmuscle
contraction can increase circulation)Table 48-16Behavioral Therapy Components
ofBehavioral TherapyTraining the patient to recognize stress,anxiety,and
depressionRelaxation training programs BiofeedbackSelf-hypnosisMeditationCognitive
therapyTypes ofBehavioral TherapyPsychiatric therapyPain clinic treatment (last
resort)
958Part 7: Temporomandibular Joint Diseaseclinician should screen for personal
orfamilial history ofpsychiatric disease,physical or sexual abuse,and
substanceabuse.Anxiety disorders occur at greaterrates in patients with chronic
pain.65Once identified these patients should bereferred to a psychiatrist and/or
psychol-ogist for adjunctive treatment.Psycho-logical treatments include
behavioraltherapy,cognitive-behavioral therapy,and self-management/support
groups.Psychiatric treatments include medica-tions with behavioral therapy.Often as
alast resort TMD patients are referred topain clinics for treatment,whether a psy-
chological component exists or not,oftenout offrustration.Occlusal Appliance
TherapyAn occlusal appliance is a removabledevice,usually made ofhard
acrylic,whichis custom fit over the occlusal surfaces ofthe mandibular or maxillary
teeth.Thesplint is constructed so that there is evenocclusal contact with the teeth
oftheopposing arch in centric and anterior con-tact only,in lateral and protrusive
excur-sions ofthe mandible.The physiologicbasis oftreatment is not well
understoodbut the effectiveness ofthe occlusal splinthas been attributed to a
decreased loadingon the TMJs and reduction ofthe neuro-muscular reflex
activity.Alleviation ofbruxism and MPD may be due to thechange in vertical
dimension,altering theproprioception in the postural position ofthe
mandible.66�68There are generally twotypes ofappliances:stabilization (flatplane)
and anterior repositioning.Stabilization (Flat Plane) ApplianceAstabilization
appliance covers all the teeth inone arch and is indicated to relax the mus-cles
ofmastication,aid in joint stability,andprotect teeth from bruxism (Table 48-
17,Figures 48-3 and 48-4).68,69Additional indi-cations for stabilization appliances
mayinclude myalgia,inflammation,andretrodiscitis secondary to trauma.With
astabilization appliance the condyles areplaced in the most muscularly stable posi-
tion while the teeth are contacting evenlyand simultaneously.70There must be bilat-
eral equal posterior contacts so that an envi-ronment ofstable physiologic posture
ispossible.Canine guidance is created for pro-trusive and lateral excursions.As
thepatient�s symptoms improve,the splintshould be adjusted to maintain even con-
tacts bilaterally.The splint is usually fabri-cated on the maxillary arch because
it coversmore tissue,especially with Class II or ClassIII patients where
fabrication ofa mandibu-lar appliance can be difficult.On the otherhand major
advantages ofthe mandibularstabilization appliance include better speechand less
visibility,which may contribute tobetter patient compliance.70The applianceshould
be worn 24 hours a day and takenout at mealtimes.Stabilization appliancescan be
weaned post-TMJ arthroscopyand/or as the patient�s symptoms subside.Major and Nebbe
reported effectivereduction in headaches and muscle painusing stabilization
appliances,but occlusalstabilization appliances have limited valuein reducing joint
pain.71Lundh and col-leagues concurred with the fact that thestabilization splints
have little value inpainful disk displacement without reduc-tion.72Kai and
colleagues reported thatafter treatment with a stabilizationocclusal splint ofthe
maxillary arch,clini-cal signs and symptoms ofnonreducinganteriorly displaced disks
decreased butosteoarthritic findings increased.73Anterior Repositioning
ApplianceTheanterior repositioning splint is an interoc-clusal appliance that
permits the mandibleto assume a position more anterior thannormal (Table 48-
18,Figures 48-5 and 48-6).The purpose ofthese appliances is toalter the structural
condyle-disk-fossarelationship in an effort to decrease jointloading.74Indications
for this device areprimarily disk derangement disorders.Themaxillary appliance is
preferred and it isfabricated with a guide ramp that permitsthe anterior
repositioning ofthemandible.73Anterior repositioning appli-ances are used less
frequently becauserepositioning ofthe mandible over a peri-od oftime can result in
irreversibleTable 48-17Stabilization Applianceocclusal changes such as posterior
openStabilizes temporomandibular jointsRedistribution offorcesRelaxation
ofmasticatory muscle Hard acrylicMaxillary archWear 24 h (except during
meals)FIGURE48-3Stabilization appliance.Hardacrylic full-coverage occlusal splints
used fornonsurgical phase oftreatment.FIGURE48-4The stabilization appliance doesnot
change the anterior/posterior jaw position.Table 48-18Repositioning ApplianceIn
therapy it attempts to recapture the anterior displaced diskNeed for possible
occlusal equilibration and constant adjustment
Nonsurgical Management ofTemporomandibular Disorders959bites,which could require
extensive pros-thetic rehabilitation.Occlusal AdjustmentThere is a limitedrole for
occlusal adjustment or selectivegrinding in the treatment ofTMD.75Thepurpose
ofselectively grinding the teeth isto permanently position the dentition into
abetter occlusion.It is an irreversible processand is best suited for the acute TMD
symp-toms arising from overcontoured restora-tions or postorthognathic surgery.In
theseselect cases the occlusal equilibration allowsfor proper condylar positioning
and pre-vents muscular problems associated withimproper interferences.Causes
ofFailureAs a singular modality it is very difficult toassess the clinical success
or failures ofnonsurgical treatments over time.DeLeeuw and colleagues reported
long-lasting satisfactory results for patientstreated with nonsurgical therapy for
inter-nal derangements and osteoarthrosis witha 30-year follow-up.76Symptoms such
asjoint noises persisted,whereas pain anddiscomfort generally subsided.There are
several possibilities thatcould explain the cause offailure ofnon-surgical therapy
for TMDs:incorrect his-tory taking,improper diagnosis and treat-ment,lack ofpatient
compliance,emotionally debilitated patient,or coexist-ing morbidities.77When
significant symp-toms persist after 3 to 6 months ofnon-surgical
therapy,alternative therapiesand/or diagnoses should be considered,including
surgery.SummaryTMD is a complex disorder with com-mon presenting signs and
symptoms.Inthis chapter we have presented nonsurgi-cal strategies used to alleviate
the painand dysfunction associated with theTMJ.Since an exact correlation
betweendiagnosis and treatment is not alwayspossible,success or failure with
nonsur-gical modalities is not a reliable outcome,even though this therapy may aid
indiagnosis and be the first step for mostpatients.When surgery is indicated
orevidence-based,nonsurgical techniquesare a crucial adjunct perioperatively,ifnot
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1990;63:472�7.51.Gold N,Greene CS,Laskin DM.Transcuta-neous electrical nerve
stimulation therapyfor treatment ofmyofascial pain dysfunc-tion syndrome.J Dent Res
1983;62:244.52.Ersek RA.Transcutaneous electrical neurostim-ulation.Clin Orthop
1977;128:314�24.53.Eisen AG,Kaufman A,Green CS.Evaluation ofphysical therapy for
MPD syndrome.J DentRes 1984;63(special issue):344,abstract1561.54.Lark MR,Gangarosa
LP.Iontophoresis:aneffective modality for the treatment ofinflammatory disorders
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1990;8:108�19.55.Gangarosa LP,Mahan PE.Pharmacologicmanagement ofTMJ-MPDS.Ear
NoseThroat J 1982;61:670.56.Gerald MJ.Physical medicine modalities andtrigger point
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AS,Assael LA.Temporomandibulardisorders:diagnosis and treatment.Philadelphia
(PA):W.B.Saunders Compa-ny;1991.p.522�5.58.Crider AB,Glaros AG.A meta-analysis
ofEMGbiofeedback treatment oftemporo-mandibular disorders.J Orofac Pain
1999;13(1):29�37.
Nonsurgical Management ofTemporomandibular Disorders96159.Scott DS,Gregg
JM.Myofacial pain ofthe tem-poromandibular joint:a review ofthebehavioral-
relaxation therapies [review].Pain 1980;9(2):231�41.60.Matsumura WM.Use
ofacupressure techniquesand concepts for nonsurgical management ofTMJ disorders.J
Gen Orthod 1993;4:5�16.61.Matsumura TM,Ali NM.Evaluation ofacupuncture and occlusal
splint therapy inthe treatment oftemporomandibular jointdisorders.Egypt Dent J
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JT,Moody PM.A study ofthe use ofocclusion splints in the treatmentofacute and
chronic patients with cran-iomandibular disorders.J Prosthet
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splint therapy andrelaxation procedures in patients with TMJdisorders.J Am Dent
Assoc 1983;107:420�4.68.Clark GT.A critical evaluation oforthopedicinterocclusal
appliance therapy:design,theory and overall effectiveness.J Am DentAssoc
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al.Temporomandibular disk displacementwithout reduction:treatment with flatocclusal
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H,Tabata O,et al.Long-term out-comes ofnonsurgical treatment in nonre-ducing
anteriorly displaced disk ofthe tem-poromandibular joint.Oral Surg Oral MedOral
Pathol 1998;85:258�67.74.Moloney F,Howard JA.Internal derangementsofthe
temporomandibular joint.III.Ante-rior repositioning splint therapy.Aust DentJ
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management oftempor-mandibular joint disorders.J Cran-iomandib Pract
1997;15(1):94�5.
CHAPTER 49Temporomandibular Joint Arthrocentesis and Arthroscopy:Rationale and
TechniqueJeffrey J.Moses,DDSSince the seventh century BC,papyrusimages have
revealed attempts at tem-poromandibular disorder (TMD) man-agement through
relocation ofdisloca-tions.Over a long and arduous routeclinicians have sought to
relieve thepainful dysfunction ofthis structurethrough various
mechanical,anatomic,and biochemical evaluations and correc-tional means.Through the
relativelyrecent advances oftechnology,and partlybecause ofthe equivocal successes
ofhis-toric management outcomes,modernmaxillofacial surgeons now have theaccess to
micronized minimally invasivetechniques to assist in TMD management.From the
diagnostic evidence producedby the thin intra-articular arthroscopeand the
evaluation ofthe fluid effudatecomes new information turning this erainto a
valuable epoch ofdiscovery.Suc-cessful long-term outcomes from relative-ly
simplified therapeutics have led manysurgeons to decrease the incidence ofopen-
joint arthroplasties and their poten-tial negative complication sequelae.Whilethis
chapter focuses on the techniques ofarthroscopy and arthrocentesis,the cur-rent
stage ofthe evolution oftreatmentphilosophies and understanding ofthesetechniques
as applied to the pathophysiol-ogy ofthe discussed temporomandibularjoint (TMJ) for
successful outcome inpatient management are emphasized.History ofOrthopedic
DevelopmentThe development ofbiomechanical andoptical accesses for the examination
ofintra-articular structures in the earlytwentieth century was accomplished byKenji
Tagaki in 1918 by his use ofa 7.3 mm diameter pediatric cystoscopeallowing him to
examine a knee joint.1Hislater development ofa 3.5 mm diameterscope made this
procedure practical.Ofhistoric significance,in 1921,Bircher pub-lished an
independent report ofthe resultsofhis arthroscopic studies ofthe kneejoint using a
laparoscope with gaseous dis-tention ofthe joint space using oxygen orcarbon
dioxide.2Another report usingarthroscopy was published by Kreyscher
in1925,predicting that it would become the definitive diagnostic modality
forderangements ofthe knee.3Following Tagaki�s modification ofthecystoscope and
diameter reduction to 3.5 mm in the early 1930s and the use ofsaline for joint
distention,several otherpioneers went on to improve arthroscopedesign and used
these in a patient series,publishing their clinical experiences.4Unfortunately,due
to the technologicrestraints at the time oflack ofillumina-tion and having only
direct eyepiece visu-alization with electronic assistance,therewas limited
acceptance ofthis method as avaluable diagnostic modality.A major turning point in
the fieldcame in the early 1950s with the recogni-tion that the technologic
advances inelectronics and optical design could assistin endoscopic equipment
development.This was appreciated and used by one ofTagaki�s students,Masaki
Watanabe.Watanabe and colleagues�design oftheno.21 arthroscope with 100ofield
ofvision and a 6.5 mm diameter using tung-sten light illumination and
cameraattachments turned the direction ofthisfield ofinterest around.5The work
doneby Casscells as well as Jackson and Abebuilt on this foundation
clinically,whichwas credited to Watanabe�s performanceofthe first surgical
procedure on thehuman knee joint in 1955.6,7Enthused with the
potential,RichardO�Conner returned home from a trip toJapan in 1970 and
subsequently developed
964Part 7: Temporomandibular Joint Diseasean operative arthroscope in 1974.He
usedthis to perform a meniscal resection,theresults ofwhich he published in
1977.8Ageneralized instrumentation explosion,coupled with the development ofmotor-
ized equipment by Lanny Johnson thenensued,which led to further
techniquedevelopments in arthroscopic manage-ments ofintra-articular
pathology.9Real-izing that these techniques would be bestlearned in specifically
designed courseswith hands-on experience,in 1973,JohnJoyce III and Michael Hardy,an
anatomist,organized the first ofmany courses thatdeveloped.This greatly enhanced
thespread ofthis treatment modalitythroughout the orthopedic community.Many ofthese
early courses were personal-ly overseen by the pioneering experts,including
Dr.Watanabe himself.Development ofTemporomandibular Joint ArthroscopyA major
breakthrough for small jointendoscopic access occurred in 1970 withthe development
ofthe Watanabe no.24Selfoc arthroscope with a 1.7 mm diame-ter.10This was
introduced into the TMJ byMasatoshi Ohnishi using a fiberoptic lightsource and
arthroscopic device manufac-tured by Olympus in the early 1970s.Ohnishi published
both the puncturetechnique and the anatomic findings andlater went on to describe
the usefulness ofthis technique for clinical applications inthe treatment ofTMJ
disease in 1980,including photographic documentation ofnormal anatomy as well as
providing earlyinformation on traumatic pathology andjoint fibrosis.11�14In 1978 an
animal study on rabbitsby Hilsabech and Laskin demonstratedthat TMJ arthroscopy was
a safe tech-nique that revealed the appearance ofintra-articular structures.15In
1980Williams and Laskin went on to intro-duce pathologic conditions in the
rabbitjoint and concluded that these could bediagnosed by the arthroscope.16Holm-
lund and colleagues published similarresults in 1986.17In 1982 Ken-IschiroMurakami
and Kazumasa Hoshinoreported their procedural terminologyand arthroscopic
anatomy,excellentlyillustrating the human TMJ with colorphotography.18During a
visit to theUnited States in 1984 Dr.Murakamiintroduced this concept to Bruce
Sanderswho,along with Joseph McCain but onseparate US coastlines,began to
performthe procedures clinically for patientswith TMD.Drs.Ronald Kaminishi,Jef-frey
Moses,Christopher Davis,as well asothers were introduced to the punctureand
arthroscopic visualization oftheTMJ during this time.Wanting again todevelop the
training ofthis techniquealong the same lines as their orthopediccounterparts,the
maxillofacial surgeonssought to develop educational symposiaand hands-on
training.The first interna-tional hands-on course using freshcadaveric specimens
for technique devel-opment was initiated by J.J.Moses in late1985 and continued on
through thesponsorship ofThe Pacific ClinicalResearch Foundation.Many ofthe
initialsurgeons exposed to the modality inde-pendently went on to develop a variety
oftechniques and courses using the com-munal efforts ofthe international pio-neers
at these sessions.In 1985,with references to thearthroscopic
observations,Murakamiand Hoshino described histologic cellularcharacteristics ofthe
inner surfaces oftheTMJ.19Also in 1985 Holmlund and Hells-ing published their
landmark paper onthe concept ofreproducible puncturesites correlating measurements
along thetragal-canthal line.20These are recom-mended for surgeons�early
learningstages in technique development.21Continued efforts by Murakami andOno to
improve surgical techniques werepublished in 1986,and McCain presentedan abstract
at the 1985 Annual Meeting ofthe American Association ofOral andMaxillofacial
Surgeons (AAOMS) on hisinvestigations.22,23A pivotal work waspublished in 1987 by
Sanders in the treat-ment ofclosed lock condition with thesurgical application
ofarthroscopic lysisand lavage over a 2-year period.24In 1986 the first major
didactic sym-posium on arthroscopy ofthe TMJ wasguided by Drs.Kaminishi and Davis
andsponsored by the Southern CaliforniaSociety ofOral and Maxillofacial Sur-
geons.This started the movement towardacademic research and clinical investiga-
tions.Notably Dr.Ohnishi provided ademonstration ofhis puncture techniqueat this
symposium,where many ofthe pio-neers ofthis group began to prepare them-selves for
the 1986 meeting ofthe FirstAnnual Symposium on Arthroscopy oftheTemporomandibular
Joint led by Dr.McCain,hosted in New York,and spon-sored by the Hospital for Joint
Diseases.Itwas at this subsequent meeting that theInternational Study Group (ISG)
for theAdvancement ofTemporomandibularJoint Arthroscopy was formed.This pio-neering
group provided many ofthenational and international liaisons forfuture
collaborations and collective dis-semination ofinformation,as well asexpertise at
the didactic and hands-oncadaveric symposium to follow.An explosion ofpapers and
presenta-tions on multiple techniques,equipmentdevelopment,and clinical studies
ensued.Partly in an effort to curtail the potentialfor similar untoward sequelae as
has been-experienced in the field ofopen TMJsurgery in the past,the ISG worked
togeth-er for the development ofstandards in cre-dentialing,technique
workshops,andrecording ofclinical results and providedclarification criteria for
insurance cover-age.As a result ofmuch ofthis work theAAOMS formed an ad hoc
committee andissued an official statement regarding TMJarthroscopy,going on in 1988
to form anadjunctive insurance task force.
Temporomandibular Joint Arthrocentesis and Arthroscopy: Rationale and
Technique965Important research over the earlyyears contributed to knowledge
showingthat although disk position may be indica-tive ofpathologic history,its lack
ofmobility more closely correlated to patho-logic presence.25Also,the chronicity
ofthepatient�s TMD history seemed to lenditselfto the development
ofarticularremodeling in the absence ofpain andlimitation ofmotion in the
postoperativephases.26Studies aimed at the identifica-tion ofchemicophysiologic
markers andmediators were done through joint fluidanalysis.It was found that
arthroscopicsurgery was successful even in Wilkes stageIII and stage IV
diseases.Recently morework has been done on diskal reshaping pro-cedures as well as
arthroscopic functionaldiskectomy through superior-anterior cap-sular release
combined with physical therapyfor joint space enlargement.Technique enhancements
still on thehorizon include early intervention withinjectable joint lubricants like
sodiumhyaluronate (HA) following initial arthro-centesis or even the use ofmodified
HA asan operating medium or for use as anintra-articular bandage.Even though
arthroscopic surgery isnot the panacea for TMJ surgical care,ithas proven itselfas
one ofthe basic tech-niques to be mastered by modern oral andmaxillofacial surgeons
in their completemanagement armamentarium.Patient Selection and Evaluation Although
many patients present with painin and around the TMJ,relatively few areselected for
surgery.At the centers workingwith the Pacific Clinical Research Founda-tion,manned
by teams ofdentists,psy-chologists,physical therapists,and ancil-lary medical
managers,only 10 patients in400 evaluated actually have intracapsularjoint
derangements or pathology amenableto invasive procedures.I have found arthroscopic
manage-ment to be successful in 8 out ofthose 10patients,with only 2 out ofthe
original400 requiring open surgery.A key to suc-cessful outcomes in any surgical
care iscareful patient selection and perioperativeteam management.While patients
certainly present withpain originating outside ofthe joint itself(such as atypical
facial pain and neural-gias and some pains related to systemicdiseases such as
rheumatoid arthritis),for the purposes ofthis chapter we willlimit our discussions
to those with intra-capsular etiology.In general one has to screen thepatient for
the basic premise ofpain ori-gin.Is it from within the joint or from themuscles? As
always there are etiologic fac-tors affecting both possibilities that needto be
identified.The most valuable screen-ing technique comes through a valid histo-ry
and physical examination that can befairly succinct.HistoryFirst it is comforting
to the patient toaddress their primary chiefcomplaint.Thisis done even though it is
often secondary tothe interest ofthe surgeon who wants todiscover how it originated
and what sec-ondary damage has occurred so that cor-rections can be planned for the
patient�scondition and to prevent recurrence.Thisis done by asking the patient to
identify thelocation,onset,and frequency ofthe pain,in addition to asking what the
aggravatingfactors are and the maneuvers used torelieve the pain.Notice how the
patientresponds when answering the locationquestion,whether they use a finger
point-ed to the joint as opposed to a flat handpalm placed on the face.The pointed
loca-tion tends to lend credibility to capsular-intracapsular joint problems.The
charac-ter and history ofthe progression ofthejoint noise is also helpful,paying
closeattention to how clicks proceeded tocatching and locking,or crepitus.Also
askabout the nonsymptomatic side since fre-quently there may be a history ofthe
samesequence indicating the possibility ofmore advanced degenerative disease onthat
side,which will be evidenced on theradiograph and through the range ofmandibular
motion examination.Patients often report pain in theshoulders and
neck,headaches,earaches,and feelings offullness in the ears ordulled hearing.It is
important to inquireas to the patient�s generalized physical oremotional status
regarding recent preg-nancy,childbirth,or menopause as well astheir condition
socially with jobs or fami-ly.This frequently adds significant overlayand insight
to associated etiology andtreatment management.Positive answers to pointed
questionsregarding the history ofrecent or child-hood trauma,habits ofbruxism or
clench-ing,and medications used,such as thoseinitiating dyskinesia,should be
explored.Also,one should inquire into past gnatho-logic treatments such as prior
orthodonticcare for closure ofopen bites,retrognathictreatment with class II
elastics or position-ers,extensive crown-and-bridge prosthet-ics,and equilibration
for balancing con-tact occlusal interferences.Physical ExaminationThe examination
can likewise be fairlyconcise and takes a close second to thehistory in
importance.The generalizedphysical examination can follow thefocused joint and
facial structure exami-nation in order to let the patient knowthat their
chiefcomplaint has been heard,thus giving them more confidence andtrust.Clinicians
examine the location ofpain,skeletofacial form,and the TMJ firstfollowed by the
nerve function,muscles,and dentition/occlusion.Initially notingthe form ofthe
skeletofacial structures,look for open bites,retrognathism (withor without deep
bites),asymmetries ofthe jaw and facial bones,and pseudobiteswhere the habitual
position ofthemandible is offofthe skeletal position.Careful checking ofcapsular
tendernessas well as palpating and auscultating for
966Part 7: Temporomandibular Joint Diseasejoint sounds,such as reciprocal
clicks,pops,catching,and crepitus,all lendvaluable information.Be certain to
loadthe affected and nonaffected sides inocclusion to ascertain the effect on
thepain as well.Next generally check sensory nervefunction and muscle response to
cognitivemotor stimulus.The muscle examinationnaturally follows with observations
beingmade for hypertrophy,asymmetry,andtenderness to palpation.Frequently
withlongstanding symptoms a cascading ofprotective muscle splinting will lead
toneck and shoulder symptoms.The earsand eyes are checked with notations forlater
specialist referrals ifabnormalitiesare found or complaints are elicited.Finally
the teeth and occlusion areexamined,looking for masked asymmetricskeletal
characteristics secondary to ortho-dontic treatments applied during
growth,pseudobite secondary to class II elastics,wear facets and balancing
interferences,supraerupted teeth,or loss ofposteriorsupport.It is at this point
that themandibular range ofmotion is measuredand observed,and
deviations,limitations,or hypermobilities are noted.Presurgical Diagnostics and
TherapeuticsFollowing the history and physical exam-ination and screening panoramic
exami-nation,clinicians usually initiate presur-gical conservative therapy.The use
ofapresurgical orthotic appliance designedto deprogram the habitual occlusion
andskeletal positions,as well as provide reliefto the muscular splinting and
resultantmyositis,cannot be overemphasized.Thisnot only assists physical therapists
intheir assessment and therapeutic care butalso provides the surgeon with
valuableinformation as to whether true skeletalasymmetries or open bites are
preexist-ing,which may have been masked by neu-romuscular programming through
priorclinical care.Usually this is accomplishedwith a maxillary splint built with
cuspidguidance in order to prevent the dentalmovement and opening ofthe
interdentalspaces produced with clenching or brux-ism.Ifan open bite exists,which
wouldrequire a mandibular splint due to theundesirable excessive bulk ofacrylic on
amaxillary splint,the splint should also bedesigned for lateral disclusion using
thebicuspid instead ofthe cuspid teeth.The use ofthe orthotic splint appli-
ance,combined with physical therapy andnonsteroidal anti-inflammatory
drugs(NSAIDs),should allow most experiencedphysical therapists and surgeons to
deter-mine whether an intracapsular pathologywill be responsive to nonsurgical
therapywithin a matter of6 to 8 weeks.Occasionally the decision is made
fortherapeutic muscular trigger-point injec-tions or intracapsular superior joint
com-partment diagnostic blocks ofdilutedlocal anesthetic solution in order to
segre-gate pain etiologic foci before proceedingto either arthrocentesis or
combinedarthroscopic surgery.ImagingTraditionally the panographic view is thefirst
revealing image ofthe TMJ.Currentconcepts ofmanagement have beenexpanded through
visualization ofaxial-ly corrected sagittal tomography basedon the submental vertex
view with thealignment ofthe x-ray beam along themedial-lateral pole axis ofeach
ofthecondyles,taken in the open mouth andclosed occlusion positions.This is aug-
mented by the coronal views in the pro-truded occlusion position with theincisors
placed edge to edge in order tovisualize the medial,lateral,and superiorcondylar
anatomy in relation to thesuperior condyle�s proximity along thefunctional area
ofthe eminentia.Theseviews can reveal osteophytes,erosions,and remodeling
impingements thatwould otherwise be undetected fromother bone imaging
techniques.For the shape,position,mobility,andintrinsic structural integrity ofthe
diskitself,magnetic resonance imaging (MRI)has proven to be extremely
reliable.27Whereas studies have shown that historyand clinical examination are
reliable forpredicting similar MRI diagnosis foranterior disk displacements
withoutreduction,and arthroscopic examina-tions have been shown to be
statisticallyreliable for disk displacements as well,additional information ofdisk
immobili-ty with normal disk position and diskalstructure and integrity loss with
myxo-matous changes can be ascertained byMRI,proving its overall value and relia-
bility for additional soft tissue informa-tion compared with other techniquessuch
as arthrography.28,29For patients with conditions that aresuspect for partial bony
ankylosis,whichoccurs with the advanced disease processassociated with repetitive
surgery or with afibrous ankylosis,a computerized axialtomography scan will
sometimes providethe best possible information.Whetherone chooses to proceed with
arthroscopyon basic imaging techniques and the histo-ry and physical examination
alone or toadd more sophisticated imaging to thepresurgical diagnostic package is a
deci-sion to be made by each clinician who isinvolved with the individual
patient.Indications and ContraindicationsIndicationsEarly meetings ofthe
International StudyGroup for the Advancement ofTMJArthroscopy were convened to
formulateinternational consensus on the variousindications and contraindications
forTMJ arthroscopy.Resolutions were for-warded for acceptance to the AAOMS,which
finalized the position paper onTMJ arthroscopy in 1988.30This paperseparated
indications for diagnostic andoperative arthroscopy with generalized
Technique967examples given ofpatients in whom dis-orders were found that were
notexplained by other means and for which adiagnostic confirmation would affect
thepatient�s care and outcome.It also includ-ed indications for diagnostic
arthroscopyin order to enhance treatment decisions.Examples include the
following:�Biopsy ofsuspected lesions or disease�Confirmation ofother
diagnosticfindings that could warrant surgicalintervention�Unexplained persistent
TMJ pain thatis nonresponsive to medical therapyThe indications for surgical
arthroscopyare matched carefully with the diagnosisbefore application.Helpful
criteria ofdis-ease staging should be applied throughthe combined use ofthe Wilkes
stagingclassification for internal joint derange-ment (Table 49-1),which was based
onclinical,radiologic,and anatomic divi-sions,and the Bronstein and
Merrillarthroscopic staging ofinternal jointderangements (Table 49-2) correlated
atthe time ofarthroscopic surgery.Intraop-eratively,internal joint surface proce-
dures are applied individually to the sig-nificant finding.Internal joint
derangement (IJD) isknown to be a preoperative indicationfor surgical
arthroscopy.The AAOMSposition paper defines IJD as a disrup-tion ofthe internal
aspects ofthe TMJwith either diskal displacements or alter-ations in the normal
dynamic motions ofthe intracapsular elements.This wouldinclude adhesions or
impingements inthe face ofeven normal disk position.The paper goes on to describe
surgicalarthroscopy as indicated for joint condi-tions that constitute a disability
for thepatient and which are refractory to med-ical treatments and require
structuralmodification.30Whereas internal derangements asso-ciated with
hypomobility due to adhe-sions,disk immobility,and disk displace-ments with
blockade are likely candidatesfor structural modifications,those jointswith recent
trauma,degenerative disease,synovial disease,and even hypermobilityare included in
the conditions indicatedfor arthroscopic surgical
intervention.ContraindicationsEven though there are relatively fewabsolute
contraindications to jointarthroscopy,it is generally recognized thatunderlying
medical instabilities,overlyingskin infections,and risks associated withTable 49-
1Wilkes Staging Classification for Internal Derangement ofthe Temporomandibular
Joint I.Early StageA.Clinical:no significant mechanical symptoms other than early
opening reciprocalclicking;no pain or limitation ofmotionB.Radiologic:slight
forward displacement;good anatomic contour ofthe disk;negative
tomogramsC.Anatomic/pathologic:excellent anatomic form;slight anterior
displacement;passiveincoordination demonstrableII.Early/Intermediate
StageA.Clinical:one or more episodes ofpain;beginning major mechanical problems
consisting ofmid- to late-opening loud clicking,transient catching,and
lockingB.Radiologic:slight forward displacement;beginning disk deformity ofslight
thickeningofposterior edge;negative tomogramsC.Anatomic/pathologic:anterior disk
displacement;early anatomic disk deformity;good central articulating
areaIII.Intermediate StageA.Clinical:multiple episodes ofpain;major mechanical
symptoms consisting oflocking(intermittent or fully closed),restriction
ofmotion,and difficulty with functionB.Radiologic:anterior disk displacement with
significant deformity/prolapse ofdisk(increased thickening ofposterior
edge);negative tomogramsC.Anatomic/pathologic:marked anatomic disk deformity with
anterior displacement;no hard tissue changesIV.Intermediate/Late
StageA.Clinical:slight increase in severity over intermediate
stageB.Radiologic:increase in severity over intermediate stage;positive tomograms
showing early to moderate degenerative changes�flattening
ofeminence;deformedcondylar head;sclerosisC.Anatomic/pathologic:increase in
severity over intermediate stage;hard tissuedegenerative remodeling ofboth bearing
surfaces (osteophytosis);multiple adhesions in anterior and posterior recesses;no
perforation ofdisk or attachmentsV.Late
StageA.Clinical:crepitus;scraping,grating,grinding symptoms;episodic or
continuouspain;chronic restriction ofmotion;difficulty with
functionB.Radiologic:disk or attachment perforation;filling defects;gross anatomic
deformity ofdisk and hard tissues;positive tomograms with essentially degenerative
arthritic changesC.Anatomic/pathologic:gross degenerative changes ofdisk and hard
tissues;perforation ofposterior attachment;multiple
adhesions;osteophytosis;flattening ofcondyle and eminence;subcortical cystic
formationAdapted from Bronstein SL and Thomas M.79
968Part 7: Temporomandibular Joint Diseasemalignant tumor seeding represent rela-
tive contraindications.31Arthroscopic Instrumentationand Anesthesia
ConsiderationSurgeons performing arthroscopicsurgery should be familiar with not
onlythe surgical technique but the supportiveelectronics and operating room set-up
aswell.As a guide for the surgeon a recom-mended schematic ofroom set-up isshown in
Figure 49-1.Video Monitoring EquipmentEven though the interior surfaces ofthejoint
can be visualized directly via the eye-piece,most arthroscopists prefer to usevideo
electronic enhancement and docu-mentation equipment.A video monitorand recording
device are placed at the headofthe patient,easily orienting everyone inattendance
to the 12:00 (twelve o�clock)position ofthe joint with the video cameraattached to
the arthroscopic eyepiece.Avideo monitoring cart (Figure 49-2) con-tains the
monitor,light source,and record-ing units with the cumbersome cordsdraped on the
contralateral side ofthepatient�s head to the surgeon�s position.The clear imaging
ofthe joint allows allpeople involved with the case to clearly par-ticipate with
interest.This has the addition-al benefit ofallowing them to better antici-pate the
progress and needs ofthe surgeon.Irrigation SystemA constant flow ofirrigation
fluid isessential to providing a clear view ofthejoint surfaces through the
distention ofthe potential joint space,as well as forwashing blood and debris away
from thelens objective.The inflow is attached tothe arthroscopic cannula,and an
outflowneedle is placed elsewhere in the jointspace.The diameter ofthe outflow
portalshould be ofa lesser size than the inflowportal,which allows a slight
pressure dif-ferential in order to maintain sufficientjoint distention.For routine
arthroscopic proceduresa 11/2inch 18-gauge short-beveled needleis ideal.Iflaser
d�bridement is anticipat-ed a second arthroscopic cannula with astopcock and rubber
obturator should beplaced so that the outflow volume can beadjusted to the higher
flows ofirrigationfluid required for the prevention ofexcessive thermal synovial
damage that ispossible from the heat generated by thelaser
photovaporization.Additional ben-efits ofthe irrigation include those asso-ciated
with the therapeutic effects oflavage and arthrocentesis.32The components ofa
simplifiedapproach to an irrigation system includeseveral units ofextension tubing
withLuer-loc attachments,a 30 mL or 60 mLsyringe,a three-way stopcock,the arthro-
scopic cannula,and a 11/2inch 18-gaugeshort-beveled needle.For most cases
thedrainage may be collected in a small basinwith the end ofthe exit tubing taped
to thebasin�s edge,allowing the surgical techni-cian visible evidence that the
fluid pushedinto the point is equal to that coming backout to prevent extravasation
into the peri-articular tissues.Alternatively for the higher volumesnecessary in
cases requiring laser-assistedtechniques,a pneumatic-assisted com-pression unit may
be used instead ofthesyringes to provide constant pressure on a500 mL bag
ofirrigation solution.Thisprovides a consistent joint distention aswell as a
cooling flow ofsolution across thejoint surfaces.The outflow in these cases
isusually voluminous and is collected in anTable 49-2Bronstein and Merrill
Arthroscopic Staging ofInternal Joint Derangements Correlated with the Wilkes
StagingI.Early StageRoofing,80% (closed position) to 100% (open or protrusive
positions);incipient bilaminar zone elongation;normal disk flexure at junction
ofdiskal eminence and superior lamina;normal synovium;incipient loss ofarticular
surface smoothness;normal superior compartment recesses and
vascularityII.Early/IntermediateRoofing,50% (closed) to 100% (open or
protrusive);bilaminar elongation with de-creased flexure;early adhesive synovitis
with beginning adhesion formation;slight lateroanterior capsular
prolapseIII.IntermediateAdvanced bilaminar elongation with accordion-shaped
redundancy and loss offlexure;prominent synovitis;diminished lateral
recess;advanced adhesion formation;anterior pseudowall formation in substage
BSubstage A:Roofing,5% (closed) to < 15% (open or protrusive);chondromalacia grades
I�II (softening,blistering,or furrowing)Substage B:No roofing,more severe anterior
recess changes;chondromalacia gradesII�III
(blistering,furrowing,ulceration,fraying,fibrillation,surface
rupture)IV.Intermediate/LateIncrease over intermediate stage disease;hyalinization
ofposterior attachment;chondromalacia grades III�IV
(ulceration,fraying,furrowing,fibrillation,surface rupture,cratering,bone
exposure)V.Late StageProminent fibrillations on articular
surfaces;perforation;retrodiskal hyalinization;false-capsule formation
anteriorly;generalized adhesions;advanced synovitis;chondromalacia grade IV
(cratering,bone exposure)Adapted from Bronstein SL and Thomas M.79
Technique969orthopedic shoulder arthroscopy bag,which has a drainage portal at the
apex.ArthroscopeThe manufacturers use four basic tech-niques for arthroscope
construction.Theearly design,in 1966,ofthe rod-lensendoscope by H.H.Hopkins
improvedthe traditional achromatic lens system,which made arthroscopic
examinationpractical by reducing the diameter oftheinstrument.By placing at least
two differ-ent types ofglass into the system,sec-ondary advancements made color
correc-tion possible.This led to brighter imagesdue to a reduced separation
ofspacesbetween the rod lenses when comparedwith the achromatic focusing lens
system,and lessened the likelihood ofbreakage.5A third advance came with the devel-
opment ofa unique type ofglass with anonuniform refractive index called theSelfoc
lens.The characteristic ofthis gradient-index system is that curved sur-faces are
not required,and the spacingbetween the lenses could be eliminatedusing optional
cements which allowed athinner diameter with brighter images andan equivalent
breakage resistance.33Theglass structure itselfprovides the focusingpower ofthe
system (Figure 49-3).In the fourth alternative,optical lensesare placed at either
end ofa fiberopticrelay,focusing the image along the fiberrelay,which transmits the
image from theobjective to the output ocular lens or eye-piece.These are primarily
used in workrequiring extreme flexibility such as vascu-lar
exploration.However,there are newdisposable fiberscopes now available forneedle
access to the small joint.No matter whether a rod lens or Selfoclens is used in
arthroscopic surgery,anybending ofthe lens sheath will produce adark halo crescent
and heralds possiblelens damage or fracture.Visual Fields and AnglesThe angle
ofvision consists ofthe angleformed extending from the outermostmargin ofthe
objective lens to the sub-ject viewed.The field ofvision consists ofthethree-
dimensional circular area withinthose angles ofthe angle ofvision.The angle
ofinclination is commonlytermed the direction ofview,which can bealtered by the
lens construct itself.Usualangles ofinclination are 10o,30o,and 70o.Through the
careful use ofrotation oftheangled arthroscope in an arc-like fashion,a wider field
ofvision can be produced(Figure 49-4).Another valuable insight into the opti-cal
characteristics ofthe arthroscope is thefact that the field ofview will be dimmed
bymagnification without providing increasedresolution.Light transmission is
critical inorder to keep the image definition clear andis reduced by increasing the
angle ofincli-nation from 0oto 70oincrementally.A good general rule to remember
isthat as the diameter ofthe scope decreasesand the angle ofthe scope
increases,theapparent field ofview and brightness ofthe image decreases.There are
two ways to overcome theseobstacles:(1) through the use ofan inte-grated video
arthroscopic system withzoom camera couplers,and (2) throughthe enhancement
oflight.Even though aquartz-halogen light may be sufficient forVideo
monitorPatientSurgeon orsurgical assistantSurgical
technicianAnesthesiologistAnesthesiamachineInstrumenttableFIGURE49-1Position
ofsurgical team and equipment for arthroscopic surgery.The surgeon and sur-gical
assistant may change positions freely without disturbing the positions ofthe
equipment or otherpersons helping.FIGURE49-2Video monitoring cart.
970Part 7: Temporomandibular Joint Diseasedirect visualization in small
joints,videowork is greatly improved through the useofa xenon or mercury-xenon arc
lamplight source.The light transmission through thearthroscope is accomplished by
the lightfibers surrounding the lens system (seeFigure 49-3) and is connected at
the side ofthe arthroscope to a fiber light-cord cou-pler,which,in turn,attaches it
to the lightsource.This light source is usually fittedwith an automatic light level
adjustmentsystem connected to the camera�s consolefor a feedback loop (Figure 49-
5).Instruments: Cannula,Trocars,Obturators,ElevatorsThe cannula is a sheath through
whicheither the arthroscope or the instrumentsmay be passed into the joint space
repeat-edly.A Luer-loc attachment together withstopcock valve is used for inflow
where thecannula is housing the arthroscope andused for outflow when on a second
cannu-la that is used for instrumentation access.Excess outflow can be restricted
bypartly closing the valve and adding a rub-ber stopper with a small hole
throughwhich the instruments are passed during atriangulation procedure.These
cannulaeare passed into the joint space after intro-ducing the sharp trocar into
the cannula,which is used to puncture through the skinand joint capsule.The joint
capsule is dis-tended with irrigation solution during thismaneuver from a needle
injection (see sec-tion in this chapter �Functional Anatomyand Joint Entry
Techniques�).The bluntobturator then replaces the sharp trocarwithin the cannula as
further entry intothe joint is accomplished,in order to avoidscuffing ofthe
articular cartilage.In the superior joint space,after visualconfirmation ofjoint
space access has beenachieved,the blunt trocar can sometimesbe incorrectly used as
a release elevator.This can often lead to bending ofthe can-nula and,with
repetition,can lead to even-tual breakage.It is recommended to use ahardened metal
release elevator iffurtherprocedures are anticipated (Figure 49-6).A series
ofdilation cannulae are alsoavailable for enlarging the diameter oftheaccess tube
in order to facilitate the use ofgraspers to remove debris or
brokeninstruments.Specialized InstrumentsA variety ofhand and motorized instru-
mentation is available to the arthroscopicsurgeon.The most commonly used are
thehooked probe,grasping and biopsy or cut-ting forceps,scissors,and retrograde
(pull)knives.Again,sufficient cannulae diame-ters to incorporate the grasping
forcepsafter it holds the object are critical in pro-viding a safe and smooth
retrieval oftheobject without having to remove the can-nula along with the
grasper.This avoidsthe risk ofsubcutaneous loss ofthe objecton the way out ofthe
joint space.LasersThe use oflaser energy in arthroscopic surgeryhas fought a long
battle for acceptance.Thecarbon dioxide laser proved ineffective forpractical
reasons relating to the joint insuffla-tion with gasses.33,34The neodymium:yttri-
um-aluminum-garnet (Nd:YAG) laser wasabandoned because it was shown to result
inNarrow angleof visionObjective lensConvex lensAirOcularlensWider angleof
visionObjective lensConvex glass cylinderSmall air spaceOcularlensLight
transmittingfiberopticglass fibersOuter metal tubeLensFIGURE49-3A,Conventional
endoscopic lens systemshowing the narrow angle ofvision.B,Rod-lens systemshowing
the wider angle ofvision.C,Cross-sectionalrepresentation ofendoscope.ABC55�Angle of
visionField of vision0�Angle of inclination15�FIGURE49-4A,Angle ofvision.B,Field
ofvision.The zero degree angle ofinclination gives a straight-aheadview.C,Dark
crescent at the edge ofthe field ofvision caused by bending ofthe
arthroscope.D,Angle ofincli-nation (direction ofview).Rotation ofan arthroscope
with an oblique angle ofinclination around its axisincreases the field
ofvision.ABCD
Technique971excessive depth oftissue damage.35Howev-er,the holmium:YAG (HO:YAG)
laserseems to have won approval within theorthopedic community and has beenshown to
be effective for the TMJ reductionofsynovial and vascular hyperplasias,aswell as
d�bridement offibrous tissues.36Itcan be used for the release ofthe anteriorcapsule
and,in the defocused mode,usedfor reduction ofchondromalacia.Onceagain generalized
synovial damage must beavoided through the use ofcopious irriga-tion during the use
oflaser energy withinthe joint compartment.Anesthesia and Medication
ConsiderationsTMJ arthroscopy can be performed in theoutpatient or inpatient
setting.When localanesthesia alone is used auriculotemporaland intracapsular
anesthetic blocks areplaced.This technique is usually reservedfor fine-needle
diagnostic arthroscopy.Alternatively it can be performed com-bined with intravenous
sedation for lysisofadhesions as well as eminentia releasecapsular stretch
procedures.Whereas most surgeons tend to segre-gate the general anesthesia
requirementsfrom the surgical,modern oral and max-illofacial surgeons naturally
integrate thetwo for enhanced outcome.Initially led byrequests for controlled
hypotensionrequired for beneficial effects duringorthognathic
surgery,considerations fol-lowed that were specific to the arthroscop-ic surgical
arena.Requests are made for the anesthesiol-ogist to administer certain drugs at
theonset ofthe intravenous (IV) access,aswell as muscle relaxants,and even to per-
form deep extubations at the conclusion ofsurgery.Injection ofmethylprednisoloneat
125 mg for adults and 40 mg for chil-dren is given in order to help stabilize
themast cell membranes to help to inhibit therelease ofhistamines due to tissue
injuryand to reduce the postoperative edema.Even though postoperative infections
arerare,a cephalosporin antibiotic is usuallygiven as well for prophylaxis.With the
anesthesiologist located at theposition indicated on Figure 49-1,clearaccess is
given to the surgeons while stillaffording the anesthesiologist the patient�sarm or
hand for IV access as needed.Mus-cle relaxants are given with sufficientlength
ofduration for the entire case inorder to allow the surgical assistant betterease
ofjoint mobilization,yielding the sur-geon sufficient space for
instrumentation.Even in cases ofanticipated shortduration it is helpful to explain
therequirement for absolute muscular relax-ation to the anesthesiologist ahead
oftimeand to allow sufficient postsurgical timefor the chemical reversal agents to
workadequately for extubation.The surgeoncan use this time to organize
progressnotes or findings and procedural dicta-tion.Also for the more involved
cases,apreemergence extubation can help to pre-vent the Valsalva response to the
endotra-cheal tube and thus limit intra-articularbleeding and hematoma
formation.37Biomechanics ofArticularPathology and ArthroscopicManagementThe
etiology ofpain in the TMJ diagnosedwith IJD is unclear.Certain surgical anato-my
ofthe TMJ is important to understandas it relates to the biomechanics
ofthefunctioning joint in order to effectivelytreat the dysfunctional state ofthe
patient.Clinical observations and findings ofthe synovial lining ofthe TMJ and
correla-tion offindings ofdisk perforations,mobility,and blockade also
significantlyguide the arthroscopic surgeons in theirmanagement decisions.There are
many theories regardingTMJ dysfunction.However,the followingquestion arises in
almost every discussion:What are the causes ofthe pain,and whycan one joint with
disk displacement nothurt whereas another,perhaps with a lessserious
problem,severely tender?Part ofthe answer involves the histo-chemical
characteristics ofpain mediatorswithin the joint fluid,but the direct andindirect
results ofinflammation andresulting fibrosis on the capsule,associatedtissues,and
musculature also play a role inpain symptoms.38RecorderVideo monitorFocusing
couplerCameraLight cordScopeCamera consoleLight sourceFIGURE49-5Schematic
ofequipment hook-up sequence.FIGURE49-6Moses�release elevator,trocar,and switching
stick.
972Part 7: Temporomandibular Joint DiseaseA review ofstudies ofsimilar jointpain
and restricted mobility in the shoul-der with acromial impingement syn-drome shows
striking resemblances toobservations made on the TMJ (Figure49-7).39�45Additional
studies performedon the basic biomechanics ofthe TMJhave shown that with jaw
rotationalmechanics,the linear velocity ofrotation(V) will differ between the
medial andlateral poles as a consequence ofanorthopedic system with two joints
func-tioning simultaneously (Figure 49-8).46An understanding ofthe force on
theload-bearing surfaces with the structuralinherent rotational and
translationalforces and their combined effects on rota-tional
force,moments,torque,and shear,are essential in helping to understand thereasons
that lateral condylar pole,emi-nential,and capsular pathologies are pre-sent in
higher frequency than at themedial joint location.This has led to the investigation
ofthelateral TMJ articulation by coronal MRIand by axial-corrected
tomographiclaminograms,both taken in the antero-posterior (AP) protruded jaw
positionperformed on patients who had failednonsurgical efforts to correct TMJ dys-
function and yet did not exhibit classicdisk displacement.47These cases were fur-
ther investigated by direct arthroscopicexaminations from the AP view viaendaural
puncture access.It has becomeapparent that there is a process ofpathol-ogy
occurring which ranges from seem-ingly minor capsulitis with proliferativesynovial
changes to frank degenerativedisease with disk/capsular impingements(see Figure 49-
7).Disk displacement actually mayoccur late in the pathophysiology ofinternal joint
derangement (Table 49-3).Early inflammatory changes,initiated bymacrotrauma or
microtrauma,may leadto a loss ofthe lubricating nature oftheHA and chondroitin
sulfate within thesynovial fluid.Capsulitis itself,with thesynovium proliferating
in an attempt torepair or regenerate damaged intracapsu-lar structures,combines
with inflamma-tion and leads to the production ofhyaluronidase,which breaks down
theHA within the TMJ.A loss oflubricationensues,leading to increased
surface�stickiness,�resulting in capsular fibrosisand relative immobility ofthe
TMJ,espe-cially within the superior joint compart-ment,on attempted translatory
move-ments ofthe mandible.FIGURE49-7A,Arthroscopic photograph ofendaural view
ofdisk impingement under articu-lar tubercle.Reproduced with permission fromMoses
JJ.47B,Drawing oflocation ofthe endauralview seen inA.C,Drawing ofendaural photo-
graph seen inA.B and C adapted from Moses JJ.47ABCFm? L ? m? m ? LLmmL??FIGURE49-
8With jaw rotational mechanics,the linear velocity ofrotation(v) will differ
between the medi-al and lateral poles.Given a fixed measurable angular velocity
ofrotation(r),the velocity ofpointm (medi-al pole) will differ from pointL (lateral
pole).FM = rotational force movement.FM
Technique973Ifallowed to mature the adhesionsmay vascularize and become part
oftherestrictions (Figure 49-9).On attemptedopening,lateral adhesive components
cancause incoordination ofdisk/condyle/eminence dynamics.Strain is placed onthe
lateral disk attachments as thecondyle is forced to begin translationfrom within
the inferior joint compart-ment.The disk,while relatively immobilein its
relationship to the articular emi-nence,may or may not be displaced atthis time
(Figure 49-10).Over a period oftime,translation,solely in the inferior joint
compartment,may cause a gradually increasing laxity ofthe lateral disk
attachment,allowing theanatomic migration ofthe disk antero-medially.The patient
may also experi-ence a �closed lock,�depending on themorphologic changes within the
diskand its ability to form a mechanicalobstruction (Figure 49-11).As the disk
slowly migrates forwardand medially,movement within the supe-rior joint compartment
generally remainsminimal.The inferior joint compartmentbegins to act as the
translatory compart-ment for the �wide-open�mouth position.Anterior disk
displacement tradition-ally has been diagnosed via arthrographicstudies and now
with MRI.A sagittal viewmay reveal a well-placed disk;however,theMRI coronal view
allows diagnosis ofmedial or lateral disk displacement,asMRI correlative studies on
more than 100arthroscopic confirmations ofdisk dis-placement have shown that disks
thatappeared in normal anatomic position onsagittal views were actually rotated
ontheir condyles with medial displacement(Figure 49-12).Diagnosis ofdisk
pathologies basedon two-dimensional studies can be mis-leading.In some cases the
posterior bandalmost becomes longitudinally placedanteroposteriorly along the
lateral rim ofthe condyle.This may lead to a �bulging�out ofthe capsule on coronal
MRI (Figure49-13).In other cases images ofa diskmore medially displaced may have
a�sucked-in�appearance ofthe lateral cap-sule on coronal MRI,which is termed lat-
eral capsular prolapse (Figure 49-14).Lat-eral capsular prolapse may play a role
inthe development ofthe lateral impinge-ment phenomenon.As disk displacement
progressesanteromedially the lateral attachmentTable 49-3Progressive Stages
ofImpingement LesionsStageDiagnosisClinical CourseTreatmentI.InflammationAcute
capsulitis and synovitisReversibleNSAIDs,rest,physical therapy,OSA,intracapsular
irrigations,and lavageII.FibrosisChronic adhesive capsulitis,Recurrent pain with
Arthroscopic lysis ofadhesions,lateralproliferative
synovitis,diskalactivityeminencia release and capsular stretch,displacement or
immobility,lavage,physical therapy,OSAsynovial plicaeIII.Bony remodelingDiskal
displacement or immobility,Progressive disabilityLateral eminencia release,capsular
stretch,and attachmenthyperplastic eminencia tubercle,lateral eminencia
osteoplasty,physicalmigrationdegenerative joint diseasetherapy,OSANSAIDs =
nonsteroidal anti-inflammatory drugs;OSA = orthotic splint appliance.FIGURE49-
9A,Arthroscopic photograph ofendaural view ofarticular
eminence,demonstratinginflamed synovial proliferative tissue and early
adhesions.Reproduced with permission from MosesJJ.47 B,Drawing ofthe endaural view
seen inA.Location ofthis tissue is the same as that seen in A.Adapted from Moses
JJ.47AB
974Part 7: Temporomandibular Joint Diseasemigrates forward as a result ofthe grad-
ual and progressive pull ofthe condyle,which stretches it during
attemptedtranslation in the inferior joint space.46�48The attachment carries with
it the boneofthe condylar lateral pole,developingthe anterior beaking or
�lipping�com-monly seen in sagittal tomography (Fig-ure 49-15).�Beaking�represents
an adap-tation ofcondylar remodeling to forcesplaced on it rather than a true
osteophyte.Ifthe load is not redistributed,areasofperforation can occur,and
furtherdegenerative changes may develop alongwith adaptive remodeling ofboth
hardand soft tissues (Figure 49-16).49Theconcept ofload distribution is a funda-
mental biomechanical principle that iscrucial to the understanding ofjointstructure
and function.The entire physi-ologic function ofthe joint and its asso-ciated
structures is load distribution,anddamage occurs when factors inhibit
thisfunction.Dysfunction occurs whenmetaplasia and adaptive remodeling can-not
repair this damage by restructuringload distribution.A review ofarthroscopic cases
revealsthat the majority ofpathologic adhesionsand restricted motion lie within the
lateralthird ofthe joint.The soft tissues ofthe cap-sule become fibrotic and
constricted,withinactivity and/or inflammation restrictingmandibular movement.From
the endauralarthroscopic approach,viewing anteriorlyalong the lateral trough ofthe
superiorcompartment,inflamed synovial prolifera-tion and projection are seen,as
well as adhe-sions binding the disk to the eminence andcapsule,leading to
restricted mobility andpossible pain (see Figure 49-9).In the advanced stage,areas
oflateralcondylar resorption,best seen in APtomograms (Figure 49-17),correlate
withthe hypertrophic articular tubercles thatimpinge on the lateral third ofthe
disk(Figure 49-18A�C).Ifthe joint space hasdiminished with degenerative
changes,this becomes especially important as thecondyle will articulate more
heavily in thelateral area on protrusive and openingmovements (Figure 18D and E).In
myexperience disk perforation occurs mostfrequently in the lateral posterior
bilami-nar zone/disk junction correlating withthis lateral impingement.Pain
itselfis not a disease.�Painmerely halts the function to allow heal-ing.The gradual
increase in functionallows the programming ofmesenchymalcell differentiation.�50The
goals oftreat-ment should include decreasing func-tional load and increasing the
capacity ofcells to accomplish articular remodeling.Clinical studies using the
lateral emi-nence release and capsular stretch proce-dures,combined with routine
arthroscopiclysis ofadhesions and lavage,have relievedboth pain and restricted
mandibular mobil-ity in over 92% ofpatients (see Table 49-3).27Patients with
lateral tubercle impingementson the disk seem to require
additionaleminoplasty,which gains joint space andFIGURE49-10A,Drawing depicting
relative disk immobility after maturation and vascularizationofadhesions:
translation is forced to occur in the lower compartment.Arrowsindicate the
movementofthe condyle under the immobile disk.B,Eventually there is laxity ofthe
lateral disk attachmentsand increased translatory movements in the lower joint
compartment.Arrowindicates the location ofthe lateral diskal attachment,which is
strained and possibly painful.Adapted from Moses JJ.47ABFIGURE49-11Disk
migration(A)and changes in disk morphology(B)leading to �closed lock.�Superior
compartment adhesions restrict translatory movements.Adapted from Moses JJ.47AB
Technique975relieves load concentration from that area(Figure 49-19).51MRI analysis
study revealed a consis-tent result ofno change in disk positionin the closed-mouth
status,both be-fore and after arthroscopic surgery in 92 patients.52The study
revealed anincrease in mobility ofthe disk followingarthroscopic release that was
directlycorrelated with the clinical success ofpain reduction and restoration
ofnormalmandibular function.The mobilization oftissues within andaround the
joint,combined with reduc-tion ofload concentrations,enhancesmesenchymal cell
reprogramming,allow-ing potential formation ofpseudodiskarticulations and condylar
remodeling.Studies are in progress at the present timeto investigate whether
condylar remodel-ing occurs long-term following arthro-scopic procedures (Figure
49-20).In a study using standardized tomog-raphy,Moses in 1994 showed that disk
andcapsule mobilizations have effectivelyrestored function with pain
reduction,while correlation to chronicity seems todictate whether or not articular
remodel-ing occurs.26In certain cases,when the chronicity ofthe displacement has
led to anterior diskdisplacement,the morphology ofthe diskcan �ball�up and effect a
blockade to condy-lar anterior movements.This phenomenonis termed obstructive disk
blockade.The tra-ditional approach to this condition�s man-agement is either
through open or closedsurgical attempts to reshape and repositionthe disk or
complete disk extirpation.53�55An arthroscopic surgical alternative isthat
consisting ofan anterior capsularrelease performed with either the HO:YAGlaser or
pull-knife assistance under arthro-scopic guidance via triangulation
portalaccess.Care is taken not to violate the ptery-goid muscle during this
procedure,keepingthe dissection on top ofthis structure.Thisprocedure,termed
anterior capsular release,allows the opening ofthe anterior joint com-partment for
functional remodeling to occurduring the postoperative rehabilitationenlarging the
space for the disk to move.56Functional Anatomy and JointEntry TechniquesOver the
past 15 years arthroscopy oftheTMJ region has gained popularity as both adiagnostic
tool and as a therapeutic modefor procedures involving IJD and intracap-sular
dysfunctional pathology.Althoughthis popularity gave rise to many
proposedprocedures and techniques,which give thesurgeon many choices on which to
basetheir treatments,the fundamentals allremain the same.As the skill
ofsurgeonsadvances,desired access for visibility andinstrumentation has led to the
increased useofangled view and alternate entry portalscombined with triangulation
techniques.Sectional planeABCFIGURE49-12Disk that appears to be well placed on
sagittal imaging(A)actually may be rotatedon the condyle with medial
displacement(B)and in time may suffer increased laxity ofthe lateral col-lateral
disk attachments (C).Adapted from Moses JJ.47
976Part 7: Temporomandibular Joint DiseaseGeneral PrinciplesIn any arthroscopic
surgical procedureinvolving small joints it is important toadhere to some basic
technical points:1.The joint should remain fully distend-ed,allowing easier trocar
punctureand minimizing the risk ofiatrogenicintracapsular damage.2.The skin should
be punctured with asharp trocar.3.All intra-articular procedures shouldbe done with
care to prevent articularsurface damage.4.Attention should be given to preserveas
much healthy synovium as possiblein order to enhance its physiologiceffects on the
joint.5.The joint space should be keptexpanded during instrumentation bya slow
infusion irrigation system.FIGURE49-13A,Magnetic resonance image,coronal view,ofthe
temporomandibular joint,demonstrating lateral capsular bulge.Reproducedwith
permission from Moses JJ.47B,Drawing ofthe image shown inA.Adapted from Moses
JJ.47ABFIGURE49-14A,Magnetic resonance image,coronal view,demonstrating lateral
capsular concavity and medial diskal displacement.Repro-duced with permission from
Moses JJ.47B,Drawing ofthe image shown inA.Adapted from Moses JJ.47AB
Technique977Puncture Anatomy and Landmarks The anatomic landmarks relevant foropen
joint surgery also apply for arthro-scopic surgery.The frontal branch ofthe facial
nerveappears to be the most likely nerve struc-ture to be involved.Whereas Greene
andcolleagues reported a mean distance of22.5 mm from this branch as it crossed
thezygomatic arch to the posterior aspect ofthe tragus with a range of16 to 29
mm,AlKayat and Bramley reported the mean dis-tance of20 mm from its crossing
measuredto the anterior margin ofthe bony audito-ry meatus with a range of8 to 35
mm.57,58The tympanic plate was found byGreene and colleagues to be 7 mm anteriorto
the posterior tragus (range 6 to 9 mm)and perpendicular to the skin at a meandepth
of25.4 mm (range 19 to 32 mm).57Finally,even though the mean distanceofthe
superficial temporal vessels from theposterior aspect ofthe tragus has beenmeasured
at 12.8 mm,there is some vari-ance and this structure occasionally can bevulnerable
to puncture lacerations.57There have been reports ofcases ofarteriovenous fistulas
developing as a resultofpuncture through these structures,requiring subsequent
vessel ligations.59An important point to rememberduring the puncture procedure is
thevisualization ofthe directional axis ofthetrocar angle,which should be
anteriorSectional planeABCFIGURE49-15Drawing depicting progressive development
ofanterior �beaking�or �lipping�com-monly seen on sagittal tomograms.Adapted from
Moses JJ.47FIGURE49-16Further degeneration ofhard and soft tissues in response to
undistributed load.A,Diskal lateral ligamental and bony changes.B,Disk
perforation.Adapted from Moses JJ.47ABFIGURE49-17A,Coronal tomogram taken
inslightly protruded position showing bony lateralimpingement and prominent
articular remodel-ing oflateral one-third ofthe condyle.B,Sagittaltomogram ofthe
same temporomandibular joint.Reproduced with permission from Moses JJ.47AB
978 Part 7: Temporomandibular Joint DiseaseFIGURE49-18Drawings showing advanced
stagesofcondylar remodeling and/or resorption.Areas oflateral condylar resorption
correlate with hyper-trophic articular tubercles (A�C) in response to
diskdisplacement and loss ofjoint space.D,Sagittal viewofdegenerative joint closed
mouth view.E,Sagittalview ofdegenerative joint�protruded jaw position.The dashed
linesectional plane correlates with thecoronal view in C.Degenerative joint with
bonychanges evident.Adapted from Moses JJ.47ABCDEFIGURE49-19Drawing showing
arthroscopicosteoplasty ofhypertrophic articular tubercle.Adapted from Moses
JJ.47FIGURE49-20A,Preoperative sagittal tomogram ofa temporomandibular joint (TMJ)
with adhe-sions.B,One-year postoperative sagittal tomogram ofsame TMJ showing
adaptive remodeling fol-lowing lysis ofadhesions and joint lavage.Reproduced with
permission from Moses JJ47AB
Temporomandibular Joint Arthrocentesis and Arthroscopy: Rationale and Technique
979and superior just above the �finger-palpated�lip ofthe glenoid fossa and
notperpendicular or posteriorly directed inorder to avoid middle ear or vessel dam-
age.A frequently overlooked situation lead-ing to a loss ofperceived direction
isimproper head positioning.The headshould be turned away from the operatorand as
flat to the operating table as possible.Several authors have advocated mark-ing the
skin with points measured at 10 mm,15 mm,and 20 mm along the linedrawn from the
posterior aspect ofthemidtragus to the lateral canthus.Thesepositions can be
helpful for orientationearly in the learning curve for the arthro-scopist.After
time,however,the size andweight ofthe patient as well as their agecan lead to
variations ofthis.60Experiencehas shown the initial palpation with themandibular
mobilization by the surgicalassistant to be more relevant and valuablethan
measurements alone.The surgeon can often palpate thepulse ofthe superficial
temporal vesselsand the posterior aspect ofthe condylewhile putting the fingernail
side ofthe sur-geon�s digit along the inferior lip oftheglenoid fossa with the
mandible distracteddownward and forward by the assistant.Arthroscopic ApproachesThe
initial puncture ofthe TMJ is done witha needle and irrigation solution and
isadministered for joint distention ofthepotential space ofthe superior joint com-
partment.A detailed description ofthe ini-tial joint puncture and the superior
postero-lateral and endaural approaches will followthis overview ofthe various
approaches tothe joint compartments (Figure 49-21).Because many ofour radiology
imag-ing procedures cannot accurately visualizeearly lateral capsular synovial
proliferation(see Figure 49-9),capsular herniations(Figure 49-22),or diskal
impingements(see Figure 49-7),various approaches tocapsular access become important
to thearthroscopic surgeon in correctly diagnos-ing intra-articular pathologies for
theapplication oftreatment modalities.Superior Posterolateral Approach In this
technique the mandible is distract-ed downward and forward,producing atriangular
depression in the front ofthetragus.61This depression represents an areabordered
superiorly by the glenoid fossa,anteroinferiorly by the dorsal aspect ofthecondylar
head,and posteriorly by theexternal auditory canal.It is at the roofofthis
depression,above the gloved fingernailofthe surgeon�s digit outlining the
inferioraspect ofthe glenoid fossa,that the trocaris inserted.The trocar is
directed anterosu-periorly toward the posterior slope oftheeminentia.This provides
access to the pos-terosuperior joint space and allows visual-ization ofthe superior
joint space.Theareas that are difficult to visualize are thesuperoanterior synovial
pouch and themedial paradiskal synovial groove.Inferior Posterolateral ApproachThis
is a variation ofthe inferolateralapproach,in that the trocar is directedagainst
the lateral posterior surface ofthemandibular head.62The inferoposteriorsynovial
pouch and posterior condylarsurface can then be
examined.SuperioranterolateralSuperiorendauralSuperiorposterolateralFIGURE49-
21Arthroscopic approaches to the temporomandibular joint.Adapted from Moses
JJ.47FIGURE49-22Capsular herniations noted in themedial wall ofa right
temporomandibular joint.Reproduced with permission from Moses JJ.47
980Part 7: Temporomandibular Joint DiseaseSuperior Anterolateral Approach In this
technique the trocar is directedsuperiorly,posteriorly,and medially alongthe
inferior slope ofthe articular eminenceafter first locating the prominence
ofthelateral articular tubercle as a landmark.The mandibular condyle is distracted
infe-riorly and positioned posteriorly by thesurgical assistant.This approach
allowsanterosuperior joint compartment instru-mentation or visualization.Inferior
Anterolateral ApproachThis is a technically more difficultapproach than those
described above andallows observation ofthe lower anteriorsynovial pouch.In this
technique thecondylar head and articular tubercle arepalpated.62The trocar is then
inserted at apoint anterior to the lateral pole ofthecondylar head and immediately
below thearticular tubercle.This places the trocar inthe lower anterior synovial
pouch,adja-cent to the anterior aspect ofthe condylarhead.The technique allows
observation ofthe lower anterior synovial pouch.Endaural Approach This access is
initiated by a trocar enteringthe posterosuperior joint space from apoint 1 to 1.5
cm medial to the lateral edgeofthe tragus through the anterior wall ofthe external
auditory meatus.The trocar isdirected in an anterosuperior and slightlymedial
direction toward the posteriorslope ofthe eminentia.This approach pro-vides access
and visualization ofthe poste-rior superior joint space as well as themedial and
lateral paradiskal troughs.Itsdetailed technique will be covered in thischapter
under �Endaural ArthroscopicApproach:Rationale/Technique.�Joint Distention and
TrocarPuncture Technique The arthroscopic surgical procedures aretypically carried
out with the patientunder general anesthesia via nasal endo-tracheal intubation and
complete neuro-muscular relaxation throughout the pro-cedure (Figure 49-23).A
11/2inch 20-gaugeshort-beveled needle is introduced intothe posterior aspect ofthe
superior jointcompartment,testing the depth and direc-tion for subsequent
trocar/cannula place-ment.Iced heparinized lactated Ringer�ssolution (2000 IU
ofheparin/L Ringer�slactate) is administered via a syringe as ajoint distension
medium (Figure 49-24).To facilitate this maneuver the mandible isdistracted
downward and forward by thesurgical assistant.The mandibular condyle is then
reposi-tioned downward and backward,and ashort-beveled 18-gauge outflow needle
isattached to the catheter tubing and directedfrom an anterior lateral approach
into theanterior aspect ofthe superior joint com-partment (see Figure 49-24).By
slow injec-tion oficed heparinized Ringer�s lactatesolution,irrigation ofthe
superior jointcompartment should be noted as fluidemerges from the outflow
extension tubing.The 20-gauge needle is then removed.Distention ofthe capsule is
main-tained by the slow infusion ofthe Ringer�ssolution temporarily applied to the
out-flow portal 18-gauge needle prior to trocarpuncture.This procedure allows a
moredistinct feel ofthe puncture into the joint,which should be done with a sharp
trocar.Skin incisions are not required.Superoposterior LateralApproachThe sharp
trocar is placed into the cannulaand,with a fingerstop applied to the cannu-la grip
to prevent inadvertent excessivepuncture depth,the trocar is directed intothe point
above the palpating digit�s finger-nail location at the inferior aspect
oftheglenoid fossa.It is aimed anterosuperiorlytoward the posterior slope ofthe
eminence.The sharp trocar is then replaced withthe blunt obturator and further
entry intothe joint is executed.The syringe ofRinger�s solution is then removed
from theoutflow tubing and connected to the irri-gation tubing attached to the
arthroscopiccannula stopcock.Bubbles are displacedfrom the cannula by flushing with
irriga-tion fluid as the arthroscope is placed inthe sheath.Examination ofthe
superiorjoint compartment is then initiated,andsystematic examination ofthe joint
is per-formed prior to further instrumentation.Lateral Eminentia Release
andCapsular Stretch ProceduresEven though these procedures shouldtechnically be
listed under surgical instru-mentation,their importance is assignednot only to
therapeutic management butalso to the creation ofsoft tissue mobiliza-tion
necessary for further joint explo-ration into the anterosuperior compart-ment by
the endoscope.Errors in Entry Occasionally the arthroscopist will en-counter
difficulty in entry to the superiorjoint compartment.Most commonly this isdue to
insufficient joint distention by theirrigation solution.Ifsevere fibrous strandsare
encountered in a joint not suspected offibrous ankylosis,the inadvertent position-
ing ofthe scope cannula into theretrodiskal tissue is likely to be the cause.Inthis
case removal ofthe scope from thecannula is recommended,and a repeatprocess
ofstandardized puncture for supe-rior posterolateral approach with the
bluntFIGURE49-23Example ofhair taped on head-wrap and endotracheal tube stabilizer
pad.Reproduced with permission from Moses JJ.47
Technique981probe is done.Only after confirmation ofactual joint space access is
visually achievedthrough the camera image can furtherinstrumentation be
initiated.Endaural Arthroscopic Approach:Rationale/Technique Certain limitations
have become evidentusing the traditional posterolateral andanterolateral
arthroscopic approaches to theTMJ.This is especially true for visualizationofthe
lateral trough and anterolateral jointspace or where access for instrumentationto
the medial and lateral paradiskal groovesis required.Clear visualization
ofthoseareas is impeded using the currently avail-able 15�angled scopes and lateral
portals.63To solve these visualization and accessproblems the endaural entry portal
pro-vides clear visualization and enhancesinstrumentation to the medial and,espe-
cially,the lateral spaces (Figure 49-25).Thisnew approach also provides better
accessfor the retrieval ofloose bodies and brokeninstruments.Working with the
arthroscopein the endaural portals permits access toother portals for
instrumentation.In order to perform this technique a30�angled arthroscope is
recommended,which increases the panoramic visualiza-tion ofthe joint.The off-axis
viewing angu-lation changes as the scope is rotated andpermits a more comprehensive
examina-tion ofthe TMJ in areas difficult to exam-ine with conventional
15�arthroscopes.Inorder to visualize the lateral capsule andattachment areas it is
important to obtainan arthroscope that has the visual axis ori-ented toward the
light cord,preventing theimpediment ofhaving the light cord forcedagainst the
patient�s temporal area.Becausethis is a deviation from the usual manufac-turer�s
product it must be specificallyrequested during the ordering process.For the
surgeon inexperienced in thistechnique it is best initially to penetrate
thesuperior joint space from the standard supe-rior posterolateral approach.Once
this hasbeen accomplished the arthroscope is thenrotated and angled
superiorly,posteriorly,and laterally so that the light shines throughthe anterior
wall ofthe external auditorycanal (Figure 49-26).This spot is usuallylocated
approximately 1 to 1.5 cm medial tothe lateral edge ofthe tragus in the
externalauditory canal (Figure 49-27).While themandible is distracted downward and
for-ward,the anterior wall ofthe external audi-tory canal is perforated with the
sharp tro-car and 30�arthroscopic cannula.Thecannula and trocar are angled
anterosuperi-orly and slightly medially,perpendicular tothe posterior slope ofthe
articular emi-nence.Most important,these instrumentsenter into the joint above the
level ofthearthroscope in order to ensure superiorcompartment puncture (Figure 49-
28).Penetration should be carried to a depth ofno greater than 1.5 cm using the
cannulaFIGURE49-24Initial steps in endaural approach.A,Injection ofheparinized
Ringer�s lactate to dis-tend joint.B,Placement ofoutflow needle inanterolateral
aspect ofjoint.C,Arthroscopicexamination ofjoint via inferolateral
approach.Reproduced with permission from Moses JJ.47ABCFIGURE49-25Clinical view
ofan arthroscopein the temporomandibular joint that has beenplaced through the
endaural portal.The work-ing portal is now located in the superior postero-lateral
location.Reproduced with permissionfrom Moses JJ.47FIGURE49-26The arthroscope via
the infero-lateral portal is angled so that the light from thescope is
transilluminated through the tragal car-tilage,identifying the site for endaural
punctureinto the joint.Reproduced with permission fromMoses JJ.47
982Part 7: Temporomandibular Joint Diseasemarkings as a guide.Visual confirmation
ofthe penetration into the joint space can thenbe made using the arthroscope,which
hasbeen placed in the inferolateral portal.Addi-tional confirmation that the
endaural can-nula tip lies within the superior joint spacecan be ascertained when
removal ofthe tro-car results in an outflow ofirrigation fluidfrom the endaural
cannula.The arthro-scope,with the attached fiberoptic cable andinflow tubing,can
then be removed fromthe inferolateral cannula and connected tothe endaural
cannula.The inferolateral can-nula can then be sealed offwith a rubbercap to
prevent excessive outflow when theTMJ is being irrigated,and the cannula canbe used
as a working portal while visualiza-tion is accomplished via the endaural portal.By
rotating the arthroscope,the medi-al,lateral,and superior aspects ofthe TMJcan be
examined.This approach is espe-cially helpful in visualizing the anterolater-al
synovial space,which is difficult to dofrom either the superior posterolateral
oranterolateral portal (Figure 49-29).Thistechnique also allows the superior pos-
terolateral or anterolateral portal to beused for the instrumentation
ifnecessary(see Figures 49-28 and 49-30).As skill is acquired,direct
puncturethrough the anterior wall ofthe externalauditory canal into the TMJ can be
per-formed after initial joint distention,with-out the need for superior
posterolateralcannulation.Following the arthroscopicsurgical procedure the lateral
puncturesite receives pressure and round bandagedressings.No sutures are
necessary.Theendaural puncture is difficult to dress andis left as is.Usually
ifthere is minimalmanipulation through this portal,thecartilaginous elastic memory
ofthe canalserves to close the puncture site.A rou-tine otoscopic examination is
alwaysmade following arthroscopy to visualizethe external acoustic meatus and tym-
panic membrane in order to confirm thatno iatrogenic damage has been caused bythe
procedure.PerioperativePreoperative ManagementIn the preanesthesia holding room
severalpreparatory functions usually help in man-agement.First,the anesthesiologist
assessesthe interincisal opening ofthe patient todetermine the extent ofthe
physical block-age versus that ofpainful restriction.Then,the intravenous line for
early administra-tion ofthe corticosteroid,methylpred-nisolone,is initiated in
order to prepare thepatient�s mast cell membrane stabilitywhich assists in
prevention ofexcessive his-tamine release on surgical tissue insult.This steroid is
followed by an intramuscu-lar injection of80 mg methylprednisoloneacetate at the
termination ofthe case.Finally,the patient�s hair is bundledinto a pillowcase and
the case is taped to theforehead and nape ofthe neck with theexcess rolled into a
�bun�on top ofthe fore-head.This is used to help support thenasoendotracheal tube
after intubation(seeFigure 49�23).Paper tape is placed alongthe sideburn
hair,holding it up and out ofthe field.Paper tape with benzoin is used inorder to
help prevent the �lifting�offofthetape when the surgical prep is
applied.Postoperative ManagementCloth adhesive strips or the ends ofclothbandages
are applied to the skin punctures,FIGURE49-27Diagram indicating approxi-mate site
ofpuncture for the endauralapproach.Coronal section is positioned justanterior to
the cartilaginous meatus and tragus.Adapted from Moses
JJ.47SuperioranterolateralSuperiorposterolateralEndauralFIGURE49-28Diagram
ofpuncture into the temporomandibular joint.The trocar and cannulaaredirected
anterosuperiorly and medially,perpendicular to the posterior slope ofthe articular
eminenceand above the inferolateral cannula.The probes,located in either ofthe
working portals,may now beused for the lateral eminence release and the capsular
stretch(see arrow).Adapted from Moses JJ.47
Technique983and an injection ofdiluted 10 mg triamci-nolone acetate is made into
the superiorjoint compartment and another portiondirected into the tendon ofthe
deep bellyofthe masseter muscle as it inserts underthe root ofthe zygomatic arch
anterior tothe eminentia.Otoscopic examination ofthe externalauditory meatus is
done,confirming theremoval ofthe protective cottonoid packand the absence ofany
tympanic membranedamage.The orthotic splint is applied to thepatient�s teeth,while
still sedated ifpossible,in order for the neurologic reprogrammingto assist in the
patient�s adjustment to its fitas the joint edema resolves.The patientshould keep
the head slightly elevated forthe first 12 to 24 hours postoperatively andavoid any
increased abdominal pressure orValsalva�s maneuvers.Jaw closure compression
pressure isused over the TMJ puncture sites on extu-bation unless the patient is
extubated�deep�while still anesthetized in order tohelp prevent bleeding and
hematomaintra-articularly.The dressing is removed the nextmorning and the adhesive
strips areremoved.The skin punctures may bewashed gently with soapy water
andrinsed.They are then coated with a lightcoat ofantibiotic
ointment.MedialLateralPterygoidmuscleTemporo-Anteriormandibular fossaBilaminar
zoneDiskSuperior compartment
viewAnteriorPosteriorAIIIIIIIISuperiorcompartmentInferiorcompartmentDiskMedialAnter
iorLateralPterygoidmuscleAnteriorDiskBilaminar zoneHead of condyleInferior
compartment viewPosteriorBCIFIGURE49-29Visible fields with the various arthroscopic
approaches: oriented to the left temporo-mandibular joint (TMJ) with the roofofthe
TMJ folded upward.Areas depicted with diagonal linesare difficult to observe
arthroscopically.A,Superior compartment,orientation ofthe sectional planes:I is
superior anterolateral area,II is superior posterolateral view,III is inferior
anterolateral view.B,Superior and inferior compartment views.C,Inferior
compartment,orientation ofthe sectionalplanes: I is inferior anterolateral view,II
is inferior posterolateral view.Adapted from Moses JJ.47
984Part 7: Temporomandibular Joint DiseasePostoperative MedicationsRoutine NSAIDs
are given for the postop-erative month and muscle relaxants for thefirst week.Oral
cephalosporin followingthe intraoperative IV bolus of1 gcephalosporin antibiotics
are routinelygiven for the first week as well.Cortisporinotic suspension eardrops
are prescribedfor the first 7 to 10 days with 2 drops in theear canal ofthe
affected side.Narcotic painmedications are rarely,ifever,indicated.Physical
TherapyPreparatory physical therapy evaluationand management are imperative for a
pre-dictable outcome.The patterns for exer-cise and postoperative mobilization will
bewell understood and compliance estab-lished.Active exercises for the patient con-
sist ofopening the jaw,moving it to eachside,and protruding the jaw,with
eachmovement performed to the fullest extentten times and repeated ten times daily
for10 days minimum (Rule of10�s).Moreimportant,however,is the passive
jointmobilization applied to the patient by thephysical therapist.The joint
distractionand mobilization,along with adjunctivetherapies,will increase success
rates dra-matically.This therapy usually can be pre-scribed with visits three times
a week forthe first 3 weeks postoperatively,twice aweek for the next 2 weeks,and
once a weekfor the next month (Rule of3-2-1).Appliance TherapyAn occlusal splint
should have beenapplied postoperatively to deprogram themuscles from periodontal
membrane neu-romuscular feedback.Occasional skeleto-facial deformities ofasymmetry
ormandibular hypoplasia may be thusrevealed,especially in cases where ortho-dontic
elastics have been used duringgrowth and pseudobites have developed.Sometimes the
splint used preopera-tively for myositis reduction and other den-tal attempts for
TMJ management may notbe applicable for postoperative use follow-ing the release
ofintra-articular pathology.This is explained to the referring clinicianas well as
the patient,and the new orthoticsplint appliance is placed on the patient�steeth on
emergence from anesthesia.The routine use ofthe splint is dictatedby the presence
or absence ofskeletofacialdeformity,muscular symptoms,and theinability to wean
offofthe device withoutsymptoms.At first the splint is worn full-time (day and
night),noting that is is espe-cially needed during meals,explaining itssimilarity
to a crutch after knee surgery.Ifthe patient requires orthodontics in prepa-ration
for orthognathic surgery,it is usual-ly recommended to maintain the splint onthe
maxilla while the opposing arch isaligned and leveled and then switch over
ifnecessary to the other arch.Ifthere is no further concern for
eithermyositis/bruxism control or skeletofacialdeformity stabilization,then weaning
ofthesplint from full-time use is indicated.Onesplint usage routine (Rule of4�s)
proveneffective is for the patient to wear the splintfull-time,including during
meals,for 1 month postoperatively until symptomsand range ofmotion are
normalized.Thenweaning takes place over the next 5 months,allowing the patient to
reduce wear eachmonth by any selected 4 hours oftheirchoosing,with the exception
being thetimes worn during sleep.This routine yieldsthe final fifth month ofwear
for nocturnaluse only.Many patients wish to maintainthe use ofthe splint at night
and a decisioncan be made at the 6-month postoperativevisit,whether this is
indicated.ComplicationsOne might expect there to be a largeincrease in the
complication rate for TMJarthroscopy when compared with theorthopedic experiences
due to the closeproximity ofmany anatomic structures inthe head and neck region and
their relativecomplexity offunction.At first glance themulticenter retrospective
study in 1987 of2,225 cases showed a global complicationrate significantly larger
than that reportedin a prospective study from orthopedic lit-erature for
knees.64�66The differences inthese studies,however,must be measuredby the severe
limitations ofa retrospectivedesign and reliance on surgeon�s recall.One
significant conclusion to the mul-ticenter study was that the majority
ofthecomplications were perioperative innature and resolved relatively
quicklypostoperatively without long-term seque-lae.With the learning curve
ofarthroscop-ic advancements behind us in this area,thevarious individual reports
ofusual andunusual complications have led to a betterunderstanding ofprophylactic
measuresthat assist the current surgeon.67Extravasation Whether or not a mechanical
pump orhand-operated syringe is used,extravasa-tion is a continual risk for
arthroscopicprocedures.Complications include pha-ryngeal embarrassment ofairway
requir-ing overnight hospitalization,periorbitaland temporal edema,and transient
cranialnerve V and VII effects.68Techniques ofFIGURE49-30Diagram showing lateral
emi-nence release.Adapted from Moses JJ.47
Technique985constant inflow-outflow volume monitor-ing during the procedure with
the outflowtubing lifted by taping the end to the edgeofa basin help reduce the
likelihood ofextravasation.Limiting the number ofpunctures laterally and preventing
unnec-essary medial capsular wall punctures willkeep extravasation down as
well.Procedures should be kept to a mini-mum duration,and ifanterior release pro-
cedures are required,they should be doneat the end ofall the other procedures per-
formed within the joint to help keep thehydraulic distention present and avoid
earlyextravasation limiting operating time.Neurologic InjuryNerve injury comprises
one ofthe largestcategories ofcomplication reported in thelonger retrospective
studies.64,65By far themost common are those to the peripheralsource ofthe sensory
nerve V and its variousbranches.While the auriculotemporalbranch is most frequently
affected,it is com-monly transient in its hypoesthesia and usu-ally resolves within
6 months.69The othernerve that is at risk for damage is the inferi-or alveolar
branch which,while usually onlytransiently affected by extravasation,can
beiatrogenically damaged by mandibularangle clamps placed for jaw manipula-
tion.70,71Safer methods ofmanipulationhave been described that use the
assistant�shands and thumbs on the teeth for jointpositioning or mobilization.72The
motorcranial nerve VII (temporozygomatic andmasseteric branches) has been
reporteddamaged in arthroscopic procedures,withreporting rates ranging from 0.56%
to 4%.The damage typically resolved within 6months according to reports
reviewed.64,65,73,74Management ofinjury to these motorbranches is done
postoperatively in a similarfashion to that occurring after open surgery,with
artificial tears,eye patching,physicaltherapy,electrostimulation,and oculoplas-tic
consultation ifneeded.Finally one must constantly be awareofthe variation ofanatomy
present with-in the TMJ.Rare cases ofglenoid fossadefects can result in middle
cranial fossaeperforation,and more commonly giantcell erosion ofbone from
previousimplant surgery can lead to increasedrisks ofcerebrospinal fluid leakage
aswell.75Management includes identifica-tion,neurosurgical consultations,hospi-
talization,observation with elevatedhead and rest,and rarely application
ofsubarachnoid drain placement.Fortu-nately in most cases the dura seals andthe
leak resolves.VascularIntraoperative intra-articular hemorrhageas well as
retrodiskal hemorrhages canoccur with inadvertent medial wall punc-ture and
anterior capsular release.This cansometimes be stopped by the mildhydraulic
pressure produced by blockingthe outflow portal and allowing inflowpressure to
build.Ifthis fails,removal ofthe instruments and firm compression ofthe joint,both
by shutting the teethtogether and lateral compression withgauze overlying the joint
capsule,is war-ranted for a few minutes.Vasoconstrictorsmay be introduced into the
joint space toassist this maneuver.Another hemorrhagic complicationofarthroscopy
involves inadvertentpuncture or laceration ofthe overlyingvessels on entry.These
may include,butare not limited to,superficial temporalartery/vein (A/V),transverse
facial A/V,or even the masseteric artery.Very rarelywill this event cause such
vigorous bleed-ing as to require intraoperative ligation orsubsequent management
ofan arteriove-nous fistula,evidenced by later �whoosh-ing�sounds overlying the
joint preauric-ularly.59,65,76Usually this event can bemanaged by the application
ofpressurewith gauze overlying the vessel,with thepatient�s head turned to the
opposite sideand supported by the operating tableheadrest,thus allowing continuance
ofthe surgery after homeostasis is achieved.Intra-articularThe small size ofthe TMJ
and the fact thatany joint space is in fact only a potentialjoint space requires
constant hydraulic andmechanical distention in order to negotiateinstrumentation
safely and without causingunnecessary joint surface scuffing anddamage.Entry into
the joint space throughthe capsule may be made with a sharp tro-car initially,with
the irrigation fluid dis-tending the space,but a blunt trocar shouldthen be used to
explore the entry success inorder to minimize the possibility ofscuff-ing and
damage.Additionally a lateral emi-nence release and a capsular stretch shouldbe
employed early in the procedure to alloweasy movements ofinstruments from
theposterior to the anterior recess in order tominimize surface damage and
potentialinstrument breakage.Instrument BreakageDue to the minimally invasive
nature ofarthroscopy and size restraints on themechanical
instruments,metallurgicstrengths are sometimes exceeded evenwith the most careful
oftechniques.Instrument manufacturers have beenencouraged to produce �shear
points�within their instruments which,onbreakage,keep all ofthe metallic
piecestogether.These act as a �fuse�breaker,failing just before the functioning
edge oftheir instrument breaks offinto the jointspace.Not all manufacturers use
thisprinciple,however,and the surgeon mustbe prepared to retrieve broken instru-
mentation parts from the joint space,either arthroscopically or via
openarthrotomy,thus making it imperative toinclude this possibility on the
operationconsent form.Arthroscopic retrieval can be per-formed through the use
ofdilation can-nulas,which gradually enlarge the accessportal to a size sufficient
for the grasperor magnetic retriever to hold the brokenfragment and come back
through the
986Part 7: Temporomandibular Joint Diseasesheath intact without becoming
trapped.Ifrestriction occurs and the sheath has tobe removed with the fragment,then
thereis a strong possibility that the fragmentmay be lost into the soft tissue
betweenthe capsule and the skin.As in standardpractice,instrument breakage
shouldrequire incident reporting.OtologicOne ofthe earlier complications ofarthro-
scopic surgery reported was that ofinjury tothe tympanic membrane and the middle
earossicles and permanent hearing loss.73,77Inretrospect it is seen that the
anatomic courseofthe auditory meatus is anterior andmedial.This fact,combined with
a patient�shead position,in anything other than anear-horizontal ear-flat-to-the-
table posi-tion portends an increased risk oftrocarpuncture from the posterolateral
approach.One must keep constant vigilance to thedirection ofthe entry trocar
anteriorly andsuperiomedially combinedwith an aware-ness ofthe positioned direction
ofthepatient�s head at the onset ofsurgery.Other rare otologic events include lac-
eration ofthe external auditory canal.64,65Treatment usually involves
observation,antibiotic drops,or occasional hemostaticcontrol.More minor events
otologicallyinclude otitis externa and otitis media,aswell as tympanic membrane
perforationresulting from too vigorous canal prepa-ration.78Otitis can occur
spontaneouslypostsurgically or from an inadvertentcontaminant such as cotton pieces
left inthe canal.72It is therefore prudent for thesurgeon to use an otoscope
postoperative-ly to visualize and dry the canal prior tocase conclusion,as well as
to prescribemedication such as an antibiotic hydro-cortisone suspension for
eardrops postop-eratively.Patients with nonresolving oto-logic issues or tympanic
membranedamage are referred to an otolaryngologyspecialist for
consultation.InfectionThe low overall infection rate of1% fol-lowing arthroscopic
surgery ofthe TMJfollows that ofthe orthopedic litera-ture.64,66Even the relative
contraindicationofpuncturing through overlying skininfection has had modifications
to allowentry into suppurative arthritis with thera-peutic benefit and no adverse
postopera-tive dissemination ofinfection or celluli-tis.65,75Although infections
are rare,thestandard regimen at present for prophylax-is remains at a 1 g bolus
ofcephalosporinplus oral coverage ofcephalosporin 500 mgevery 6 hours for 5
days.27,68,70Prophylacticantibiotic corticosteroid eardrops are usedfor 5 days as
well.27,68BurnsVarious procedures using electrocauteryand laser have led to
concerns regardingadequate protection oftissues to preventadverse affects.The use
ofelectrocauterywithin the joint for reduction ofinflamma-tory or granulation
tissue can rarely lead toinadvertent contact ofthe active electrode�send with the
metal ofthe cannula.This canlead to accidental thermal
injury.79Additionally,without copious amountsofirrigating solution to flush and
cool thesynovial lining ofthe joint,HO:YAG laserd�bridements can cause thermal
damage tothese important cells,inhibiting their nat-ural physiologic function
ofphagocytosisand production ofjoint lubricants.Notonly should the modern
arthroscopist havemechanical hand-eye coordination but anawareness ofphysiologic
colateral effects ofsurgery as well.Subcutaneous Fat AtrophySubcutaneous fat
atrophy has been report-ed both in the literature and in the commu-nity
anecdotally.32Triamcinolone is fre-quently used within the superior joint
spacepostoperatively at the case conclusion andin subsequent visits for management
ofrecurrent fibrosis or ankylosis.Its use inboth the reduction ofdeep masseter ten-
donitis by injection and in reduction ofcapsulitis by iontophoresis is also
common.Even though subcutaneous fat atrophy israre in occurrence,low concentrations
andlimiting administrations oftriamcinolonecan be helpful in limiting
risk.Anesthetic ComplicationManipulation ofthe jaw has been shownto have occasional
effects on the carotidbody and thus to result in unexpectedbradycardia.Ifsuch an
event is notreversed by relaxing the jaw position,atropine may be
administered.Converselyoccasionally epinephrine (1:200,000) isadministered to
assist in hemostasis dur-ing arthroscopic surgery after the initialexamination is
complete,so as not to maskthe grading ofthe synovitis.This hemosta-tic
vasoconstrictor may occasionally causecardiac arrhythmias.Any persistent pre-mature
ventricular contractions or ven-tricular irritabilities may be treated
withintravenous lidocaine ifindicated.Outcomes and DiscussionOver the past decade
numerousresearchers have shown the effectiveness ofTMJ arthroscopy,both in the
diagnosisand the surgical management ofTMJarticulopathies.71,80�85Although numerous
techniques havebeen developed for both open and arthro-scopic surgical
management,it wouldappear that the more complex the proce-dure applied,the more
difficult the post-operative management is,with resultingdiminishment ofsuccess
rates.The over-riding factors ofsimilarity for all proce-dures seem to include the
following:1.Preoperative splint and physical thera-py management2.Release
ofcapsular restrictions,eitherthrough incision or blunt obturatorrelease and
stretch3.Release ofintra-articular fibrosis andrestrictions
Technique9874.Application ofpostoperative physicaltherapy joint mobilizationThe
disk position,with the exceptionofthe severely shredded or morphologi-cally
obstructed disk,does not appear toaffect the patient�s outcome ofcomfortwith jaw
movements and clinical suc-cess.25,86While techniques designed toalter the position
ofthe disk,restricthypermobility,and the like are certainlysometimes
indicated,caution must betaken to rein in the enthusiasm for addingyet more
complexity to a system thatresponds very well to simplicity and isadaptive in its
articular remodeling andfunctional response.Even disks that areperforated and
joints with Grades III andIV degeneration respond well to thearthroscopic
approach.75Further advancements in arthroscopictechniques and treatment modalities
arecertainly arising and each advance isweighed with these risk-benefit
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Maxillofac Surg.
CHAPTER 50Surgery for Internal Derangements ofthe Temporomandibular JointLeslie
B.Heffez,DMD,MSThe chapter on surgery for internalderangements ofthe
temporomandibularjoint (TMJ) written for the first edition,published in 1992,has
stood the test oftime.The surgical procedures described are stillbeing performed
today,which is indicativeoftheir acceptance within the surgical com-munity and
perhaps oftheir success.Thehistory ofTMJ surgery has paralleled therise and
subsequent all but disappearance ofthe western cowboy.New surgical tech-niques that
neglected to pay attention to thefundamental underlying symptoms and eti-ology have
been heralded as panaceas,onlyto rapidly fade into obscurity,leaving a
trailofiatrogenia.The new TMJ surgeon mustbe wary ofthis
past.However,prudenceshould not lead to avoidance ofsurgery as atreatment
modality.According to Annandale,Sir AstleyCooper was the first to suspect the
existenceofaltered condyle disk-fossa relations.1Later the term internal
derangementwasadopted to describe any pathologic entitythat interfered with the
smooth function ofthe TMJ.The term is currently used exclu-sively to describe
alterations in disk-fossarelations.Historically,clinicians have recog-nized that
surgery for internal derange-ments should be reserved for patients withpain or
dysfunction that is severe and dis-abling and is refractory to
nonsurgicalmanagement.These conditions still formthe basic indications for
surgery.Opensurgery ofthe TMJ for primary disease hasundergone a complete
metamorphosis as aresult ofthe research and clinical results ofsurgical
arthroscopy.At one time only ahandful ofsurgeons professed the viabilityoffunction
with a displaced disk andargued against surgical repositioning.Today the tables are
reversed,and themajority ofsurgeons recognize that aninternal derangement does not
imply anipso facto need for surgery.Furthermore,the presence ofpersistent symptoms
inlight ofan internal derangement does notimply that surgical correction is
necessaryor imminent.Only ifthe mechanicalobstruction is felt to be the primary
etiolo-gy behind the symptoms is surgery indicat-ed.This philosophy has resulted in
a dra-matic reduction in the number ofopensurgical procedures performed.This reduc-
tion has,in turn,resulted in dramaticallyfewer cases deemed to have an
iatrogenicpathology;we continue to grapple with the1980 to 1990 vestiges ofsuch
cases.The chapter begins with sections oncriteria for diagnosis and goals for
surgicalintervention.A briefdiscussion ofsurgicalanatomic considerations is
followed by adescription ofthe classic surgicalapproaches to the joint capsule and
capsu-lar incisions.A critical review ofthe histo-ry,indications,rationale for
performance,and techniques ofprimary operations ofthe TMJ is then
presented.Numerous ref-erences are made to those authors whohave fueled the
development ofsurgery forinternal derangements.In my discussions Ihave used the
term posterior attachmenttodescribe tissue that is an extension oftheretrodiskal
tissue and inserts onto the pos-terior aspect ofthe disk.When the adjec-tive
remodeled is used to qualify an intra-articular structure,as in remodeledposterior
attachment,the structure is con-sidered pathologic.Criteria for DiagnosisInternal
derangements are classically divid-ed into two groups:reducing disk displace-ments
and nonreducing disk displace-ments.Qualifying descriptors aresometimes
included,such as the directionofdisplacement,degree ofdisplacement,and presence ofa
perforation.Unfortu-nately,these large diagnostic rubrics fail toidentify the finer
stages ofthe disease
990Part 7: Temporomandibular Joint Diseaseprocess.Disk morphology and severity
ofdisplacement are only gross indicators ofthe disease process.Although more
compli-cated classifications such as the Wilkes clas-sification exist,the
treatments applied tothe diagnostic categories have been diverse,rendering specific
recommendations illadvised.It suffices to say that an astute clin-ician must be
armed with that rare com-modity ofcommon sense rather than arigid algorithm
oftreatment modalities.The research and clinical work emanatingfrom arthroscopic
trials will,in the future,establish more specific diagnostic criteriafor
establishing treatment protocols.In the surgical decision-makingprocess the
specific diagnosis is only onepiece ofinformation necessary to makethe decision to
perform surgery.Surgeryshould be considered when the dysfunc-tion or pain cannot be
corrected to a levelofpatient satisfaction by nonsurgicalmodalities.Cookbook
approaches to thediagnosis and surgical management ofinternal derangements should
not be used.It is important to consider that no dys-function is identical to
another when thesurgeon factors into the treatment equa-tion the patient�s
perception ofhis or herproblem,the effect on daily routine,andthe patient
psyche.The diagnosis ofaninternal derangement is achieved predom-inantly through
clinical skills.Imaging ofthe joint usually is most useful only in thelater
planning stages ofsurgery,ratherthan during the establishment ofa work-ing
diagnosis.There is the occasionalinstance in which a diagnostic dilemmaexists and
magnetic resonance imaging(MRI) is required to elucidate the case.For the sake
ofdiscussion,the condi-tion internal derangement can be identi-fied in three
different clinical settings.Thefirst is the occurrence ofa primarily func-tional
disturbance.In this condition thechiefcomplaint is functional.The patientsmay
describe a need to perform a specialmaneuver with the mandible to achieve awide
opening,or they may describe anannoying terminal jolting associated
withclosing.Joint pain is typically not chronicand appears to be related to the
instabilityofthe condyle-disk relations.Pain occurswith the sudden separation
ofjoint sur-faces during disk reduction or displace-ment.However,pain may not be a
feature.Most ofthese cases demonstrate a reduc-ing disk displacement,in which the
diskrepresents a mobile mechanical obstacleand the condyle is not
permanentlyrestricted in its range ofmotion.Reduc-tion refers to the ability ofthe
condyle tonegotiate around the disk.The disk�s recoilpotential is minimal in the
pathologiccondition.The inferior surface ofthe diskis typically bulged and
histologically is thesite ofincreased proteoglycan deposition.Ifpain and
dysfunction persist despitetreatment ofa coexistent parafunctionalhabit,surgery
should be considered.Thesepatients are best managed with opensurgery and reduction
ofthe obstructingportions ofthe articular disk.Diskoplasty,partial diskectomy,or
full diskectomy maybe performed,depending on the degree ofdisk atrophy and
deformation.Disk repo-sitioning should be considered only whenthe disk is minimally
deformed and ofnear-normal length.Clinical indicators forsurgical intervention
ofthis condition arerare.Some clinicians prefer to performarthroscopic disk-
stabilizing proceduresusing suturing or sclerosing techniques.The second clinical
setting in whichinternal derangements are identified is thecondition ofclosed
lock.Closed lockrefersto an acute or chronic limitation ofmove-ment ofthe condyle
owing to an intra-articular disturbance.Patients experienc-ing closed lock often
complain ofmuscledysfunction secondary to efforts to reach abaseline mouth
opening.The coexistence ofmuscle dysfunctionand an internal derangement does
notimply a relationship.A large segment ofthegeneral population have minimal signs
andsymptoms associated with internal derange-ments.Careful recording ofthe
chiefandancillary complaints is imperative,withattention being paid to the details
ofonsetand duration offacial pain and joint noise,timing ofsymptoms offacial
tightness,inability to open or close the mouth,anddistribution
ofheadaches.Concomitantsources ofpain need to be identified andconsultations with
neurology,otolaryngolo-gy,psychology,or general dentistry,asrequired,obtained.The
history ofprevioustreatment is equally important.There are usually a number
offactorsthat are considered in the etiology ofclosed lock,including intracapsular
andextracapsular inflammation and adhe-sions,muscle tension or spasm,disk dis-
placement,synovial fluid viscosity,andreduction in synovial lubrication.The closed
lock phenomenon mayresolve spontaneously or gradually over aperiod ofweeks to
months.Hence,it isimportant to evaluate the patient on severalvisits to effectively
note a response to non-steroidal anti-inflammatory agents andmuscle relaxants.In
the absence ofpain,many patients are able to tolerate the restric-tion in mouth
opening,which graduallyimproves over several months to years.MRI ofthe closed lock
condition usu-ally demonstrates a displaced disk,withvarious degrees
ofdeformation.In somepatients the disk appears in a normal posi-tion but is unable
to be displaced down theslope ofthe eminence.Although not thesubject ofthis
chapter,it suffices to saythat T1 and T2 (or gradient echo imaging)in sagittal
planes is required to delineateintra-articular fluid,interstitial inflamma-tion,and
disk morphology.Magnetic reso-nance images demonstrate that thecondyle is unable to
displace the disk ante-rior enough to reach the apex ofthe emi-nence or beyond.On
fast magnetic reso-nance or T2 images,inflammatory fluid orincreased vascularity
appears as a high sig-nal intensity (Figure 50-1).Adhesions associated with closed
lockcannot be definitively identified on anMRI scan.They are suspected when there
Surgery for Internal Derangements ofthe Temporomandibular Joint991is a confluence
ofthe low signal intensitiesofthe condyle and glenoid fossa withoutintervening
intermediate signal intensity.Arthrocentesis followed by arthroscopiclysis
ofsuperior joint space adhesions,lavage,and manipulation are the treat-ments
ofchoice for this condition.Opensurgical procedures are indicated whenarthroscopy
has failed to resolve therestriction in opening.The choice ofopenprocedure largely
depends on disk anato-my and position.The third clinical setting is the
internalderangement condition ofdisk displace-ment that reduces on opening and is
asso-ciated with persistent preauricular painrefractory to nonsurgical therapy.This
isthe most difficult ofthe three conditionsto treat and requires long-term
therapywith control ofparafunctional habits.Theclinician must ask whether the pain
isoccurring from hypermobility caused bycontralateral hypomobility,acute orchronic
separation ofdisk surfaces duringdisplacement and reduction,noncompli-ance with
diet restrictions,or persistentparafunctional or work-related habits.There are
indications for surgical inter-vention;however,it is this condition thatcarries the
greatest peril ofbeing renderedinto the painful operated ankylosed jointafter
several fruitless surgeries.Arthrocentesis has supplanted arthro-scopic surgery as
the most successful treat-ment modality.It should be attemptedbefore performing any
open surgical pro-cedure.The type ofopen procedure is gov-erned by the degree
ofdisk morphology.The key to arthroscopy is to remove thesource ofthe persistent
inflammationincluding the vascular retrodiskal tissueand hyperplastic inflamed
synovium.Goals ofSurgeryThe general goals ofany surgical interven-tion are to
return the patient to a regulardiet,with some limitations,and to establishan
adequate functional range ofmotion.Each patient�s complaints must be individ-ually
analyzed,and specific outcomes setfor the operation.Postoperatively the sur-geon
should evaluate the patient�s responseto therapy according to whether the
patientfeels there has been a total eradication,sig-nificant reduction,or minimal
reduction ofhis or her complaints,or no change orworsening ofthe condition.It is
unreason-able for the surgeon to evaluate the resultsofan operation on the basis
ofattainmentofa finite mouth opening.Many patientsare quite satisfied with
reductions in theirmouth opening as long as their facial pain isrelieved.The goals
for all surgical proce-dures should include preservation ofartic-ular tissue to
permit normalization andregeneration ofsynovium,and a restora-tion ofthe articular
relations to permit thejoint structures to adapt and functionthrough an adequate
range ofmotion.Theremodeled disk is only one element ofthedegenerative
process.Joint function may beasymptomatic and satisfactory in the pres-ence
ofvarious types ofinternal derange-ment.Thus,surgically returning a displaceddisk
to the ideal position found in a healthyjoint may not be appropriate for an indi-
vidual patient.To illustrate this point,onewould not reposition a disk in a joint
inwhich the articular tissue is so severelydamaged that it is incapable
ofhealing.Inthis situation removing the disk is recom-mended.Repositioning the disk
is recom-mended in the patient with minimalchanges in the joint structures,in
whomsymptoms have persisted despite nonsurgi-cal and arthroscopic intervention.As
indi-cated above,this condition is indeed rare.Additional magnetic resonance
andarthroscopic information about the struc-ture and function ofthe joint in
healthand disease is needed to establish reliableindicators and predictors
ofsurgical out-come.Surgical ApproachesThe classic surgical approaches to the
TMJmay be classified as preauricular,endaural,and postauricular.The choice
ofapproachis usually a matter ofsurgeon�s preferenceand is based on his or her
ability and expe-rience.Cosmetic considerations may alsoinfluence the choice
ofapproach.Surgical Anatomic ConsiderationsAnterior to the auricle,the
auricularisanterior and superior muscles overlie theFIGURE50-1A,T1-weighted
sagittal magnetic resonance image demonstrating a dislocated disk.Notethe low
signal intensity,which represents a portion ofthe deformed disk (arrow).B,Fast
imaging(GRASS [gradient recalled acquisition in steady state]) ofthe same section
demonstrates the presence ofextra-articular and intra-articular fluid or an
increase in vascularity in the anterior regions ofthe joint.These changes may be
partly responsible for the closed lock phenomenon.AB
992Part 7: Temporomandibular Joint Diseasesuperficial temporalis fascia and the
tem-poralis fascia.These muscles are incised inthe classic preauricular and
endauralapproaches.The fascia superficial to themuscles is thin and a dull
white.This layeris confluent with the galea aponeuroticaabove and the
parotideomasseteric fasciabelow.The temporalis fascia is a toughfibrous connective
tissue structure,substan-tially thicker than the overlying superficialfascia.It is
stark white and extends from thesuperior temporal line ofthe temporal boneto the
zygomatic arch.The deep surface fur-nishes one ofthe origins ofthe
temporalismuscle.Inferiorly,at a variable distance,thefascia splits into two well-
defined layers(Figure 50-2).The outer layer attaches to thelateral margin ofthe
superior border ofthezygomatic arch,and the inner layer to themedial margin.A small
quantity offat,thezygomatico-orbital branch ofthe temporalartery,and
zygomaticotemporal branch ofthe maxillary nerve are located between thefascial
layers.The splitting ofthe fascial lay-ers is most noticeable at the level
ofthezygomatic arch.Posteriorly,superior to theglenoid fossa,the separation is not
as well-defined (Figure 50-3).The superficial temporal vessels aretypically located
in the superficial fasciabelow the auricularis anterior muscle.The vessels are
often visible,invested inthe superficial fascia without incising themuscle.The
superficial temporal vein liesposterior to the artery and the auricu-lotemporal
nerve immediately behindthe vessels.The superficial temporal ves-sels and
auriculotemporal nerve appearto take on a horizontal course once theflap is fully
developed and reflectedanteroinferiorly.2Numerous authors have studied thefacial
nerve�s anatomic relations to deter-mine clinically applicable landmarks forits
main trunk,temporofacial division,and temporal branches.Al-Kayat andBramley noted
that the facial nervebifurcated into temporofacial and cervi-cofacial components
within 2.3 cm(range 1.5�2.8 cm) inferior to the lowestconcavity ofthe bony external
auditorycanal and within 3.0 cm (range 2.4�3.5 cm) in an inferoposterior
directionfrom the postglenoid tubercle.3The tem-poral nerve branches lie closest to
thejoint and are the most commonly injuredbranches during surgery.These nervesare
located in a condensation ofsuperfi-cial fascia,temporalis fascia,and perios-teum
as they cross the zygomatic arch.The most posterior temporal brancheslie anteriorly
to the postglenoid tubercle.Their location was measured by Al-Kayatand Bramley as
3.5 �0.8 cm from theanterior margin ofthe bony externalauditory canal (Figure 50-
4).3Thus,the two potential sources offacial nerve injury are dissection anteriorto
the posterior glenoid tubercle where thetemporal branches cross the
arch,andaggressive retraction at the inferior marginofthe flap where the main trunk
and tem-porofacial division are located.Preauricular ApproachHistorically,a myriad
ofpreauricular inci-sions have been proposed.Many oftheearlier designs afforded
good access butincreased the risk offacial nerve injuryand compromised
esthetics.The preauric-ular incisions used today are essentiallymodifications ofthe
Blair curvilinear orinverted-Lincision.4This approach hasbecome the favorite chosen
by oral andmaxillofacial surgeons.The technique isan incision commencing from
within thetemporal hairline and extending inferiorlyFIGURE50-2Coronal section at
the level ofthezygomatic arch.Two well-defined layers oftemporalis fascia are noted
(arrows).FIGURE50-3Coronal section at the level oftheglenoid fossa.The splitting
ofthe temporalis fas-cia is not as well-defined (broken line).
Surgery for Internal Derangements ofthe Temporomandibular Joint993into a
preauricular crease immediatelyanterior to the auricle.The exact lengthand decision
to incorporate an anteriortemporal extension are governed largelyby the nature
ofthe surgical procedure.For some surgeons,the approach fordiskectomy requires a
smaller incisionthan that for diskoplasty.The incision is approximately 3 to 4cm in
length and consists oftwo limbs:asmall superior curved limb (1�2 cm) andan inferior
vertical limb anterior to thetragus (variable distance approximately1�2 cm) (Figure
50-5).The junction ofthese limbs is the site ofattachment ofthesuperior aspect
ofthe helix to the tempo-ral tissue.The extent ofthe superior limbofthe
preauricular incision is dictated bythe amount ofaccess required,which maynot be
determined until the dissection hasreached the lateral TMJ ligament and cap-
sule.The incision is usually not extendedas inferiorly as the lobule ofthe ear.The
incision should be placed poste-riorly to the superficial temporal vesselsand
auriculotemporal nerve and within apreauricular crease.The skin and subcu-taneous
tissues are incised the length ofthe entire incision.The deeper dissectionis begun
in the temporal region bysharply dissecting progressively throughthe auricularis
anterior and superficialfascial layers to the stark white tempo-ralis fascia
(Figure 50-6).A retractor isplaced on the anterior flap,and tension isapplied in a
forward direction.The dis-section over the zygomatic arch isaddressed.The anatomic
layers in thisregion are usually not clearly defined.There is a condensation
oftissues con-sisting variably ofthe auricularis interi-or,superficial
fascia,temporalis fascia,periosteum,and occasionally cartilage.This tissue is
incised to the level offibrous connective tissue.A retractor isplaced in the
incision opposite the tra-gus,and forward traction is applied tothe flap.This
results in the definition ofacleft between the perichondrium andcartilage ofthe
external auditory canaland the parotideomasseteric fascia.Theperichondrium is
followed medially withsharp dissection (Figure 50-7).Careshould be exercised not to
proceed per-pendicularly to the skin surface,as theexternal auditory canal inclines
antero-medially at approximately 45�to the sur-face.The dissection is continued
alongthe outer surface ofthe external auditory4231FIGURE50-4Landmarks for the
location ofthe temporal branches and main trunk ofthe facialnerve: (1) the distance
between the anterior margin concavity ofthe meatus to the zygomatic arch (3.5 �0.8
cm); (2) the distance between the inferior margin ofthemeatus to the trunk (2.3
�0.28 cm); (3) the distance between the postglenoid tubercle to the main trunk (3.0
�0.31 cm); (4) the distance from the tragus to the facial nerve trunk is
variable.FIGURE50-5Preauricular incision.FIGURE50-6The preauricular incision has
been carriedsharply through the skin,subcutaneous tissue,superficialtemporal
fascia,auricularis anterior and superior,and outerlayers ofthe temporal fascia.The
flap is reflected anteroinfe-riorly,revealing the inner layer ofthe temporal
fascia.
994Part 7: Temporomandibular Joint Diseasecanal until the lateral TMJ ligament is
reached.When the condyle and its overlyingtemporomandibular ligament are
palpated,the flap is reflected inferiorly and anteri-orly forward with a
combination ofsharpand blunt dissections.Scissors may beused to cut some fascial
attachments tothe lateral TMJ ligament.The blades ofthe scissors are held parallel
to the liga-ment to ensure that the joint is not vio-lated.The flap is reflected as
far forwardas the midportion ofthe anterior tuber-cle.The surgeon can now see the
bulgingofthe lateral pole ofthe condyle undercover ofthe lateral ligament and
capsule.Gentle manipulation ofthe jaw to causemovement ofthe condyle helps to
orientthe surgeon.The deep surface ofthe flapand the tissues overlying the
zygomaticarch may be touched with a nerve stimu-lator to ascertain the location
ofthe facialnerve.Retraction is accomplished using aself-retaining retractor
(eg,cerebellarWeitlaner or a Dolwick-Reich) placedbetween the flap and the
perichondrium.A small right-angled retractor may beplaced at the inferior portion
ofthe flap(Figure 50-8).Endaural ApproachRongetti described a modification ofLem-
pert�s endaural approach to the mastoidprocess for surgical improvement ofoto-
sclerosis,for approaching the TMJ.5,6Theendaural incisions employed today
eitherincorporate the anterior wall ofthe exter-nal auditory canal,or the tragus,or
simplythe skin overlying the mental aspect ofthetragus (Figure 50-9).The incision
begins well within theexternal auditory meatus at the superiormental wall.At this
level the incision ismade down to the bone and extended in acurvilinear fashion
upward hugging theanterior helix (see Figure 50-9).Itbecomes less penetrating as it
approachesthe superior surface,ending at about thelevel ofthe inferior tragus.The
incision isdeepened to the level ofthe temporalis fas-cia.The incision is now
continued inferi-orly,with the knife in continuous contactwith the tympanic
plate,to make a semi-circular incision to the inferior point ofthe meatus.The
incision is then continuedFIGURE50-7The parotideomasseteric fascia issharply
dissected from the perichondrium oftheexternal auditory canal (broken
line).FIGURE50-8Retraction is accomplished byusing a self-retaining retractor
positionedbetween the external auditory canal and flapand a right-angle retractor
at the interior por-tion ofthe flap.The condyle (dotted line) isnoted under the
lateral TMJ ligament and/orsimply the lateral capsule depending on thedepth ofthe
reflection.FIGURE50-9A�C,Endaural approach accord-ing to J.R.Rongetti.Adapted from
Rongetti JR.5ABC
Surgery for Internal Derangements ofthe Temporomandibular Joint995anteroinferiorly
to fall into the incisuraintertragica,ending just before itapproaches the
surface.The application offorward traction on the inner aspect ofthetragus assists
the surgeon in completingthe incision.Sharp dissection is carrieddeeply for some
distance along the peri-chondrium.The flap is then reflected enmasse
anteroinferiorly offthe lateral cap-sule and ligament.The advantages ofthis
incision lie inits excellent access to the lateral and pos-terior aspects ofthe
joint,good exposureofthe anterior aspect,and its estheticvalue.The access afforded
through thisapproach is equal to that obtainedthrough the preauricular
approach.Dis-advantages lie in the potential for peri-chondritis and an esthetic
compromise iftragal projection is lost.Postauricular ApproachIn the postauricular
approach the incisionis made posterior to the ear and involvesthe sectioning ofthe
external auditorymeatus.7Excellent posterolateral exposureis afforded with this
technique.The flap,once reflected,contains the entire auricleand superficial lobe
ofthe parotid gland.Aperimeatal approach combining thepreauricular and
postauricular incisionshas also been described.8,9The incision in the
postauricularapproach begins near the superior aspectofthe external pinna and is
extended tothe tip ofthe mastoid process.The supe-rior portion may be extended
obliquelyinto the hairline for additional exposure.The incision is made 3 to 5 mm
paralleland posterior to the postauricular flexure(Figure 50-10).The dissection is
per-formed through the posterior auricularmuscle to the level ofthe mastoid
fascia,which is contiguous with the temporalisfascia.A combination ofblunt and
sharpdissections is used to isolate the cartilagi-nous portion ofthe external
auditorycanal.A blunt instrument is placed in theexternal auditory canal to assist
in thetranssection ofthe external auditorycanal.The transsection may be partial
orcomplete,depending on the need forexposure.The incision should leave 3 to4 mm
ofcartilage on the medial aspect topermit adequate reapproximation ofthecanal
(Figure 50-11).This techniquehelps to prevent meatal stenosis.Theincision is
carried through the outerlayer ofthe temporalis
fascia,continuinginferiorly,reflecting the parotideomasse-teric fascia offthe
zygomatic arch andlateral TMJ ligament (Figure 50-12).Aself-retaining retractor is
used to main-tain exposure.The advantages ofthepostauricular approach lie in the
pre-dictability ofthe anatomic exposure.Dissection to the joint is rapid with min-
imal bleeding.The approach offers analternative for a patient who has had pre-vious
procedures in this region.Thisapproach may not be desirable in thepatient
susceptible to keloid formation,owing to the potential for a keloid todevelop in
the meatus.Meatal atresia hasbeen reported with this technique.10Therisk offacial
nerve injury is not eliminat-ed.Paresthesia in the area ofthe posteri-or aspect
ofthe auricle usually occursand lasts 3 to 4 months.Capsular IncisionsHori\zontal
Incision Over the Lateral Rimofthe Glenoid FossaThe lateral liga-ment,capsule,and
periosteum are reflectedinferiorly en masse.Diskal or posteriorattachment
connections,or both,to the lat-eral capsule are dissected sharply with scis-sors to
the level ofthe condylar neck (Fig-ure 50-13A).Posterior dissection isperformed
diligently to avoid severing theretrodiskal tissue.This portion ofthe dis-section
exposes the superior joint space(Figure 50-13B).A Freer septum elevatorFIGURE50-
10Postauricular approach.Theincision is placed 3 to 5 mm parallel and posteri-or to
the postauricular flexure.FIGURE50-11The external auditory canal is sec-
tioned,leaving 3 to 4 mm ofcartilage on the medi-al aspect to assist
reapproximation ofthe canal.FIGURE50-12The external auditory canal hasbeen
sectioned and the flap retracted forward.
996Part 7: Temporomandibular Joint Diseasemay be used to define and explore
thespace.The posterior attachment and diskattachments are then severed sharply at
thelateral pole ofthe condyle from within thedeveloped flap.The Freer septum
elevatoris used to reflect the posterior attachmentand disk superiorly offthe head
ofthecondyle to expose the inferior joint space.Aperiosteal elevator may be used to
stretchthe capsule and lateral ligament flap out-ward to form a pocket (Figure 50-
13C).There is a risk ofreflecting the fibrousconnective tissue that lines the
glenoidfossa when this approach is used (Figure50-14A).The surgeon may form the
incor-rect assumption that he or she is strippingadhesions from the temporal bone
whiledefining the space.The result may be apartial or total synovectomy ofthe
superi-or joint space.Prearthrotomy arthroscopicexaminations have alerted
clinicians tothis error.The ability ofthe pathologicjoint to regenerate this
synovium andfibrous connective tissue layer has notbeen determined.Horizontal
Incision Below the LateralRim ofthe Glenoid FossaA no.11 blademay be used to
puncture into the superiorjoint space at the level ofthe lateral disko-capsular
sulcus (Figure 50-14B).Theopening is then lengthened anteriorly andposteriorly
using sharp-pointed scissors.Adissection technique,similar to thatdescribed in the
foregoing approach,isused to define the superior joint space.Adissection is then
carried inferiorly remov-ing the attachment ofthe capsule to thedisk and exposing
the inferior joint space.There is less risk ofinjury to theretrodiskal tissue with
this approach;therisk to the fibrocartilage is also reduced.This is the approach I
favor.Horizontal Incisions Above and Below theDisk The horizontal approach aboveand
below the disk (Figure 50-14C) leavessome ofthe capsule and ligament attachedto the
disk or remodeled retrodiskal tissue.L-Shaped IncisionA horizontal incisionis made
at or below the lateral rim oftheglenoid fossa.The horizontal incision isthen
joined by either an anterior (Figure50-14D) or posterior (Figure 50-14E) ver-tical
extension.The posterior vertical inci-sion carries the risk ofsevering
theretrodiskal tissue.The anterior verticalincision should not be placed farther
ante-riorly than the tubercle to avoid injury tothe facial nerve.The capsule and
ligamentare then reflected either anteroinferiorly orposteroinferiorly.T-Shaped
IncisionA horizontal incisionis joined by a vertical incision to create aT-shaped
incision over the midportion ofthe glenoid fossa (Figure 50-14F).Cross-Hair
IncisionDissection oftheposterior attachment ofthe lateral liga-ment and capsule
may be tedious with thecross-hair incision (Figure 50-14G).Open-Sky IncisionIn the
open-sky inci-sion two horizontal incisions are joined bya central vertical
incision (Figure 50-14H).Vertical IncisionAfter a vertical incision ismade,the
capsular flaps are reflected anteri-orly and posteriorly to expose the
posteriorattachment and disk (Figure 50-14I).Clo-sure ofthe capsule is often
difficult toattain following open surgical procedures.When diagnostic arthroscopy
precedes theFIGURE50-13A,Entry into the superiorjoint space following its
distention with fluid.A no.11 blade incises the lateral capsule andligament (broken
line).Care is maintainednot to prolong the incision posteriorly toavoid injuring
the retrodiskal tissues.B,Theincision is prolonged posteriorly using babymetzenbaum
scissors.C,The horizontal cap-sular and ligament flap is developed inferior-ly and
the diskal insertions sharply dissected(broken line).The inferior joint space
isdefined by incising along the superolateralaspect ofthe condyle.A Freer septum
eleva-tor is used to define the joint spaces.ABC
Surgery for Internal Derangements ofthe Temporomandibular Joint997arthrotomy,the
inflow and outflow portsviolate the capsule,making watertight closure extremely
difficult.Support for thelateral ligament can be obtained by raisinga temporalis
muscle and fascia flap,about 2 cm in length,pedicled inferiorly,androtated
inferiorly over the lateral rim oftheglenoid fossa and sutured to the
lateralcapsular tissue.The pedicle stabilizes theflap but has not been shown to
containnutrient vessels.Closure ofthe capsulemay not be critical to the success
ofthediskectomy procedure,and in some casesthe closure may restrict
mandibularmotion.11,12However,closure ofthe cap-sule and ligament after disk
repositioninglends stability to the diskorrhaphy.Operative ProceduresA concerted
comparative evaluation ofdifferent surgical techniques is difficultbecause for many
years there was no uni-form set ofcriteria for selection ofpatientsor compilation
and evaluation ofresults.Criteria and guidelines for disk surgerywere initially
developed in 1984 by theAmerican Association ofOral and Max-illofacial Surgeons
(AAOMS).13The crite-ria were established through a literaturereview and
consensus.In 1990 a standardsand criteria document was published bythe AAOMS.14The
document establishedindications for surgery,identified markersfor favorable and
unfavorable results,andoutlined risk factors.These publicationshave laid the
groundwork for peer review.FIGURE50-14Capsular incision designs: A,horizontal
incision over the lateral rim ofthe glenoid fossa; B,horizontal incision below the
lateral rim ofthe glenoid fossa; C,horizontal incisions above and below the disk; D
and E,L-shaped incision; F,T-shaped incision; G,cross-hair incision; H,open-sky
incision; I,vertical incision.The lateral pole ofthe condyle and lateral aspect
ofthe remodeled posterior attachment (broken lines) are illustrated.ABCDEFGHI
998Part 7: Temporomandibular Joint DiseaseDisk-Repositioning ProceduresThe goal
ofdisk-repositioning procedures isto relocate the disk so that its posterior
bandcan be returned to the normal condyle-disk-fossa relationship.Essentially,the
reposition-ing places the posterior band over the supe-rior or superoanterior
surface ofthecondyle.This retropositioning is accom-plished by one ofthree
procedures:plicationin which the remodeled posterior attach-ment is folded on
itselfand the lateral tissuesare approximated (Figure 50-15);full-thickness
excision in which a wedge-shapedportion ofthe posterior attachment isremoved and
the lateroposterior tissues areapproximated (Figure 50-16);or partial-thickness
excision in which the superior lam-ina ofthe retrodiskal tissue and
posteriorattachment are removed,without violation ofthe inferior joint space,and
the lateroposteri-or tissues are approximated (Figure 50-17).When the disk
displaces,the patholog-ic changes are not seen uniformly through-out the entire
lateromedial extent ofthejoint.Typically,the medially displaced diskmust be rotated
posterolaterally to achievea correct condyle-disk-fossa relation;therefore,a
greater amount oftissue is pli-cated or excised laterally rather than medi-
ally.Rarely,the disk may be displaced in thelateral direction,in which event the
reversewould be true.The technical improvements in TMJarthrography in the 1970s
stimulated inter-est in correcting disturbances in thecondyle-disk-fossa
relations,15and theconcept that disk repair procedures were aviable answer to many
cases ofTMJ dys-function was re-introduced.16Reports onthe outcome ofdisk repair
procedures haveindicated an 80% or greater successrate.17�19The latter assumes an
accuratediagnosis has been made.Surgeon diag-nostic acumen has evolved with
time.Although the results ofthe procedures mayhave been good in the 1980s,readers
mustbe cautious as the indications for perform-ing the procedure have changed and
hencethe outcomes may be misleading given thenew subset ofsurgical candidates.The
histologic basis for performingsurgery within vascular retrodiskal tissuewas
described in animals by Wallace andLaskin and by Zeitler and
colleagues.20,21Synoviocytes play an important role in thehealing
process.Stimulated by inflamma-tion,synoviocytes proliferate and migrateto fill the
surgically created gap in the tis-sues.22�24The synoviocytes produceground
substance and collagen fibers andphagocytose the debris.The degree oftis-sue
vascularity and the distance from cap-sular and synovial vasculature have alsobeen
described as important factors in thehealing process.25,26Extrapolations to the
clinical situationmust be made from these results as an ani-mal model for TMJ
pathology is lacking.In the human,variable decreases in thevascularity ofthe
remodeled posteriorattachment are believed to occur with anincreasing duration
ofdisplacement andload.The disk-repositioning techniquesthus involve a repair in
the pathologicremodeled retrodiskal tissue with a vari-able degree
ofvascularity.The primarysource ofnourishment to the repositionedFIGURE50-15Disk
repositioning achieved through plication ofthe posterior attachment.Retention
ofdiskposition is through sutures to the lateral capsule ligament.A,Preoperative
location.B,Postoperative location.ABFIGURE50-16Disk repositioning achieved through
a full-thickness excision ofthe posterior attach-ment.Retention ofdisk position is
through sutures placed on posterior and lateral margins.A,A clamphas been placed
over the posterior attachment.The arrowrepresents the direction ofpull ofthe
clampto complete the incision and reveal the condylar surface.B,View from above
demonstrating the wedge-shaped resection (arrowindicates the direction
ofclosure).DiskCondyleAB
Surgery for Internal Derangements ofthe Temporomandibular Joint999disk appears to
be through the synoviumon the medial aspect ofthe disk and pos-terior recesses
ofthe joint spaces.Thus,acritical aspect ofthe successful surgicalrepair in the
retrodiskal tissue appears tobe the rapid migration ofsynoviocytes tothe area ofthe
surgical repair.Smith andWalters followed up 12 patients for 1 yearand reported
success suturing tears in theavascular portion ofthe disk.27Others,however,have
reported that suturing any-thing but vascularized tissue results in fail-ure ofthe
repair.20,28With an increasing displacement ofthe disk,the retrodiskal tissue comes
intocontact with the condole and sustainsincreasing loading.The loading results
indecreased vascularity ofthe retrodiskal tis-sue.With the reduction in retrodiskal
tis-sue vascularity,this tissue becomes trans-formed into a pseudodisk.MRI
ofchronically displaced retrodiskal tissuesdemonstrates a signal intensity ofthe
tis-sue that resembles the disk.In fact,radiol-ogists may inaccurately describe a
diskfragmentation because only a portion ofthe displaced disk may display its
originalsignal intensity.The remainder,owing toalterations in the glycoprotein
distributionand hence the attraction ofwater,demon-strate a moderate signal
intensity.Withincreasing displacement ofthe disk,thesuperior joint space does not
accommo-date for the increase in length oftheretrodiskal tissue.Rather,the disk
under-goes atrophy,deformation (buckling),andabsorption into the anterior
capsule.These changes can make anatomic reposi-tioning ofthe disk impossible.Disk
repositioning without diskoplas-ty is indicated in the following instances:�There
is minimal disk displacement �The disk is ofnear-normal length�The disk structure
is near normal(bow-tie)The rationale behind repositioning isfounded on the
beliefthat the diseaseprocess is reversible or can be halted bynormalizing the
position ofthe disk.Inaddition,removal ofthe posterior attach-ment overlying the
condyle is intended toremove a source oflocalized inflamma-tion.The repositioned
disk facilitatesmovement ofthe condyle previouslyblocked by the displaced
disk,providesjoint stabilization,and improves articularcartilage nutrition and
lubrication.More-over,the rationale is that the workload ofthe masticatory muscles
is reduced whenthe obstructing disk is repositioned.Before performing disk-
repositioningprocedures in patients with satisfactorydisk morphology,adequate
trials ofnon-surgical therapy should be undertaken todetermine whether the patient
can bemade symptom free despite disk displace-ment.In 1989,reports were
publisheddemonstrating,by postarthroscopic MRI,persistent disk displacement despite
theresolution ofpain and increase inmandibular mobility.29,30These reports,and the
appearance ofanterior disk dis-placement in patients without any historyofTMJ
symptoms,support the executionofnonsurgical therapy prior to decidingwhether it is
necessary to perform disk-repositioning surgery.Deformation ofthe disk in all
planes isan important feature to recognize whenplanning a repositioning
procedure.Whena bulge-shaped disk is ofappropriatelength and can be repositioned,a
disko-plasty may be performed to minimize thechange in the occlusion.31It has
beenreported that during function,the fiberarrangement and proteoglycan distribu-
tion ofthe repositioned disk change tothose ofa normal disk and that diskoplas-ty
therefore would be unnecessary.32Moreevidence is still required to
substantiatethese changes.In general,the limiting factor to diskrepositioning is
the degree oflateral diskatrophy or resorption.Despite severe lat-eral atrophy,the
most medial aspect ofthedisk may have a normal length and shape(Figure 50-18).Disk
shortening may pre-clude disk repositioning without an exten-sive release ofthe
anterolateral disk attach-ments,calling into question the
procedureofrepositioning.Disk Repositioning and DiskoplastyArosette-shaped
disposable orthopedicmeniscus knife,typically used for orthope-dic arthroscopic
procedures,is used toeffect a release ofthe disk from its mostanterior and lateral
attachments (Figure50-19).This is accomplished by gentlyprodding the knife along
the insideperimeter ofthe capsule (Figure 50-20).Asthe dissection is performed
under cover ofthe capsule,there is no danger ofinjuringthe facial nerve.Disk
mobility is evaluatedby applying posterolateral traction with aforceps (Figure 50-
21).A DeBakey bulldogvascular clamp is inserted to the mediallimit ofthe posterior
attachment andguided posteriorly as far as possible in theglenoid fossa (see Figure
50-20B).TheFIGURE50-17Disk repositioning achievedthrough a partial-thickness
excision ofthe supe-rior lamina ofthe retrodiskal tissue.The inferiorjoint space is
not violated.A,Outline ofa par-tial-thickness excision ofthe superior
lamina.B,Excision is closed,resulting in posterior reposi-tioning ofthe disk.AB
1000Part 7: Temporomandibular Joint Diseaseclamp greatly assists in the control
ofhem-orrhage from the retrodiskal tissue,stabi-lization ofthe posterior attachment
dur-ing tissue excision,and stabilization oftheposterior attachment during
suturing.33The design ofthe instrument minimizestissue damage.A wedge ofremodeled
pos-terior attachment is excised,leaving a 1 mm margin anterior to the beaks
oftheclamp.This permits suturing ofthe disk tothe retrodiskal tissue without
removal ofthe clamp.Range ofmotion is then veri-fied.Tissue forceps are used to
stabilizeand slightly evert the disk so that the infe-rior surface may be sculpted
with menis-cus knives (Figure 50-22).The tissue isclosed with nonresorbable suture
on an S-2 spatula needle (Figure 50-23).Once thedisk has been sutured into its new
posi-tion,its lateral rim is sutured to the lateralcapsule ligament.Operative
difficulties with the reposi-tioning techniques include control ofhemorrhage from
the retrodiskal tissueand access to the medial aspect ofthefossa.Bleeding may be
controlled by usingthe DeBakey clamp before sectioning theposterior
attachment.Access to the medialaspect ofthe joint is greatly improvedwhen the
anterior attachment is released,permitting the surgeon to draw the diskoutward
posterolaterally while it remainspedicled to the medial attachment.Inter-
estingly,the problem ofaccess was one ofthe impetuses for combining disk reposi-
tioning with a condylar and/or eminentialarthroplasty.Disk Repositioning and
ArthroplastySeveral operators have advocated combin-ing an arthroplasty ofthe
condyle or emi-nence with disk repositioning.16,32,34�36Arthroplasty reduces the
amount ofpos-terolateral repositioning required andtherefore permits repositioning
ofanatrophic disk (Figure 50-24).The currenttrend,however,is to avoid removal
ofanynormal articular bone since the postoper-ative healing phase already involves
someloss ofbone substance,which may beadditive and result in occlusal distur-
bances.In addition,postoperative bleed-ing from cut bone surfaces into the jointcan
result in fibrous adhesions ofthe diskor fibrous/bony ankylosis ofthe joint.A 2 to
4 mm condylar-eminencearthroplasty procedure can be performedwith rotary or hand
instruments.Handinstruments such as fine chisels are prefer-able to avoid heat
generation (Figure 50-25).Bone files should be used judiciouslybecause,once the
compact bony layer isinterrupted,the trabeculae ofbone can beeasily and rapidly
removed.A periostealelevator may be used to burnish sharpedges.Care should be
exercised not toexaggerate the arthroplasty in the lateralcondylar regions while
accessing the medi-al condylar region.In some cases anarthroplasty ofthe eminence
is essentiallya lateral tuberculectomy for access anddecompression ofthe anterior
recess ofthe superior joint space (Figure 50-26).36,37Disk repositioning is then
performedthrough the plication or excision tech-nique.The capsule is closed in the
custom-ary fashion.Intermaxillary fixation ortraining elastics are used for 1 to 3
weeksto allow muscular adaptation and dentalcompensations to occur.Repair
ofPerforated Posterior AttachmentPerforations rarely occur within the diskproper
but rather within the lateral third ofthe remodeled posterior
attachment.38,39FIGURE50-18A series ofsagittal histologic sec-tions through a
joint,demonstrating partial diskdisplacement.Note the change in disk length
andmorphology as one moves from lateral (A) tomedial (C)(hematoxylin eosin stain;
macroscop-ic section).ABCFIGURE50-19Orthopedic arthroscopic knifes(blade handles
are not illustrated): A,rosette mini-meniscus curved; B,curved (right or left
avail-able); C,sickle; D,retrograde.DCBA
Surgery for Internal Derangements ofthe Temporomandibular Joint1001When the disk is
perforated,it may be sec-ondary to a developmental rather than apathologic
process.Condylar overgrowthoften occurs in the areas ofthe perfora-
tions;therefore,an arthroplasty is frequent-ly performed in conjunction with the
pro-cedure.The repaired remodeled retrodiskaltissue is intended to maintain the
shape ofthe articular surface and to prevent ankylo-sis.Repair ofa perforation
without reposi-tioning the disk is successful only ifthe diskis atrophied and is
not an obstruction tocondylar movement.This procedure is per-formed rarely and only
in those patientsrefractory to intra-articular steroid injec-tion,arthrocentesis,or
arthroscopy.Management ofSmall Perforations Whenprimary closure ofa small
perforation (1�3 mm) is planned,the atrophic displaceddisk is repositioned
posteriorly to only aminor degree.Ifthe disk is to be fully repo-sitioned,the
margins ofthe perforationshould be excised and the posterior attach-ment on the
posterior edge ofthe diskapproximated to the tympanic portion ofthe retrodiskal
tissue.Anterolateral release ofthe diskal attachments is usually necessary
tomobilize the disk posteriorly.The margins ofthe perforation are oversewn in a
straight-line fashion with a nonresorbable material.The repair procedure is often
performed inconjunction with an arthroplasty to reducesharp bony spurs that may be
present.Management ofLarge PerforationsLarge perforations are usually grafted
afterexcision ofthe edges.The disk is not repo-sitioned.In many cases this
procedure is apartial diskectomy (Figures 50-27 and 50-Retrodiskal tissueDiskBeaks
of clampFIGURE50-20A,View ofpartially reducing disk displacement from above and
slightly posterior.Note that when the medial portion ofthe disk is in the normal
position,that portion ofthe disk maybe preserved.Note the path ofincision ofthe
crescent-shaped mini-meniscus knife (broken line).B,Positioning ofthe beaks ofthe
DeBakey clamp on retrodiskal tissue.ABPosterior attachmentCapsule"Bunched up"
posterior attachmentFIGURE50-21Aand B,The pathologicposterior attachment is grasped
with a for-ceps,and posterior traction is applied(arrow)to check disk mobility and
thepotential for surgical repositioning.AB
1002Part 7: Temporomandibular Joint Disease28).The graft material is laid over the
per-foration and posterior attachment.Auto-grafts (dermal) and homografts have
beenused (Figure 50-29).The free edges ofthegraft are sutured to the underlying
poste-rior attachment and disk.Typically,medi-al sutures are difficult to place.A
suturingtechnique using an S-2 spatula or RD-1needle is recommended.Disk-Removal
ProceduresPartial DiskectomyThe partial diskecto-my procedure is used to correct
partialreducing disk displacement.12,40The goalofthe procedure is to excise the
patholog-ic posterior attachment and that portionofthe displaced atrophic/resorbed
diskthat represents an obstruction or is pre-sumed to be responsible for terminal
jolt-ing.The portion ofthe disk that is proper-ly positioned,usually the medial
aspect ofthe disk,is left in place.This procedurewas recently re-described under
the termdisk reshaping.41Kondoh and colleaguesreported a favorable 5-year outcome
intheir patients.41The absence ofportions ofthe TMJ disk may predispose the joint
toareas offibrous or bony ankylosis.Thepostoperative import ofankylosis
largelydepends on the efficacy ofphysical thera-py,the surface area affected,and
ability ofsynovium to regenerate.The rationale for electing to performa partial
diskectomy rather than a diskrepositioning is based on the beliefthatthose factors
responsible for the initialdisk displacement are often not ade-quately controlled
or identified and thuseventually cause redisplacement ofthedisk.Usually osseous
remodelingchanges have occurred to accommodatethe change in disk
position.Sprinzdescribed the histologic basis for the par-tial diskectomy
procedure.42Surgicallycreated defects within the rabbit menis-cus healed
uneventfully ifthe defectsRetrodiskal tissueUnderside of diskKnifeFIGURE50-
22Diskoplasty is performed follow-ing wedge resection ofthe pathologic
posteriorattachment.The disk is slightly evened,and anarthroscopic orthopedic knife
is used to sculpt theinferior surface ofthe bulge-shaped disk.TheDeBakey vascular
clamp is in place.Note theprotruding edge ofthe posterior attachment(arrow)used for
reapproximation to the diskand lateral capsule.12354FIGURE50-23Disk
reapproximation: A,simple posterior and lateral sutures; B,layered closure
ofthesuperior and inferior lamina; C,figure-of-8 closure; D,the order ofpassage
ofthe figure-of-8 suturelabeled 1 to 5.ABCD
Surgery for Internal Derangements ofthe Temporomandibular Joint1003were close to
the vascular periphery.Inthe rabbit knee meniscus subjected topartial
meniscectomy,the replacementtissue appeared to be derived from thesynovium ofthe
articular capsule.43Preoperative confirmation ofa partialreducing disk using MRI or
arthrotomo-graphic images is imperative in decidingwhether to perform this
procedure.Afterexposure ofthe joint spaces,the DeBakeyclamp is inserted to the
medial limit oftheposterior glenoid fossa.Retrodiskal tissueand displaced portions
ofthe disk are thenFIGURE50-24A�C,Disk repositioning with arthroplasty according to
Walker and Kalamchi.The disk is sutured to the condyle stump.Adapted from Walker RV
andKalamchi S.32ABCFIGURE50-25Condylar arthroplasty using an osteotome.An
osteophyte hasalready been excised.The direction ofthe osteotome (arrow)is
indicated in orderto skim the condylar surface.Self-retaining and right-angle
retractors are in place.Posterior attachmentFIGURE50-26Lateral tuberculectomy may
beperformed to acquire access to the anterior gle-noid and eminence regions (broken
line indi-cates bone to be excisedand arrowindicatesdirection ofosteotome).
1004Part 7: Temporomandibular Joint Diseaseremoved in a piecemeal fashion using
oto-logic basket forceps (see Figure 50-27).Thetissues are removed until the
properly posi-tioned disk is noted.The surgeon may thengraft the surgical site with
an autologousdermal graft.The graft is sutured to a cuffoftissue left at the
circumference ofthe sur-gically created perforation (see Figures 50-28 and 50-
29).In some cases the surgeonmay elect not to graft the artificially
createdperforation.Capsular and skin closures areaccomplished in the customary
fashion.Following extirpation ofthe disk portion inquestion,joint movement is
simulated toensure that there is smooth condylar move-ment in lateral and anterior
planes.Theprocedure can produce excellent immediategratification to the patient and
improvejoint function.However,complete smoothexcision ofthe inferior aspect ofthe
disk isrequired to prevent reoccurrence.A perfo-ration is sometimes intentionally
created toremove the obstacle.The displaced disk isessentially changed to a
displaced meniscus.The perforation is rarely problematic forthe patient as it is
created anterior to thecondyle.The perforation repair describedearlier is performed
over the head ofthecondyle;such perforations can lead tochronic pain refractory to
steroid injection.Total DiskectomyTotal diskectomy isthe procedure in which the
remodeledposterior attachment and entire disk areexcised.It is the most extensively
used andreported surgical procedure,having beenapplied from as early as the
1900s.Totaldiskectomy has been used to treat the fullgamut ofinternal
derangements,withoutconsideration for the degree ofdisplace-ment ofdisk
morphology,with generallygood to excellent results.44�50Despite the reported
successes withdiskectomy,51�53the more sophisticateddiskoplasty techniques
supplanted thediskectomy during the 1970s to mid-1980s.51�53In the 1980s
diskectomybecame popular once again following theintroduction ofimplantable
biomaterialsthat were used as disk replacements.Diskectomy is indicated in those
situ-ations for which disk repositioning is notfeasible because ofdisk
atrophy,deforma-tion,or severe degeneration.A joint withan atrophied,deformed,or
degenerateddisk cannot be rejuvenated because someofthe associated pathologic
changes�col-lagen fiber reorientation,increasedground substance,presence
ofelasticfibers in all disk zones,cartilaginousdeposits,and increased
vascularity�areirreversible.The goal ofsurgery is to assistthe host to adapt to the
pathology at handby removing the physical impediment tomovement and the pathologic
posteriorattachment.Bowman studied the results oftotaldiskectomy in 52 patients
followed over 3 months to 22 years.12Thirty ofhispatients were studied for 4 years
or more.Subsequently,in 1986,Eriksson and West-esson reported a follow-up (mean 29
yr)on 15 ofBowman�s patients.40Bowman�sobservations,which have been corroborat-ed
by others,10,54,55form the basis ofmuchofthe discussion that follows.Total
diskectomy deprives the joint ofthe posterior attachment and posterioraspect ofthe
remodeled disk.In the dis-eased state these tissues serve as the shockabsorbers for
the bony surfaces.The resid-ual �normal�synovium is responsible forthe lubrication
and nutrition ofthe articu-lar surfaces.The absence ofretrodiskal tis-sue may
interfere with the normal flow anddiffusion ofsynovial fluid.56With diskecto-my,the
surgeon probably transforms ajoint into what more appropriately wouldbe described
as two bones in close apposi-tion.As a result,several adaptive changesPosterior
attachment(partially removed)DiskFIGURE50-27Partial diskectomy.Midcondylar regionis
illustrated.Bulge portions ofthe disk are excised in apiecemeal fashion using
otologic basket forceps.Portionsofthe excised disk partially excised are hatched
exposingthe remodeled disk in cross-section.Remodeled retrodiskal tissueCondyleArea
of disk removedCapsuleFIGURE50-28For repair ofa large perforation,apartial
diskectomy is performed first.A portion ofthe disk and the retrodiskal tissuemay
beretained.CapsuleGraft overlaps retrodiskaltissue and disk remnantFIGURE50-29A
dermal graft covers the surgi-cally created perforation.The edges ofthe
graftoverlay the disk,retrodiskal tissue,and lateralcapsule to assist in suturing.
Surgery for Internal Derangements ofthe Temporomandibular Joint1005rapidly
occur.These changes are reflectedin the manner in which the joint functionsand how
it appears radiographically.Manyclinical examples ofsuch a bony arrange-ment
providing the patient with adequatepain-free function may be drawn from
thereconstructive literature.Clinicians often observe the loss orreduction
ofgliding motion in the jointwith nonreducing disk displacement.Inthis situation
the joint behaves principal-ly as a ginglymoid joint.Initially there islimited
translational capability.As heal-ing progresses and osseous remodelingoccurs,the
rotational (hinge) movementbecomes minimal and the gliding motionpredominates.The
patient must rapidlyregain mobility through prescribed phys-ical therapy to prevent
the developmentofankylosis.Adult cartilage derives its nutrientssolely from
synovial fluid.The prolongedcontact ofbony surfaces following menis-cectomy may
interfere with diffusion ofnutrients from the synovial fluid.Thedecreased diffusion
ofnutrients to carti-lage may result in the eventual resorptionofnoncalcified
cartilage.After a diskectomy some masticatorymuscle and joint tenderness can be
expect-ed for a variable period,extending fromseveral weeks to months.The patient
atfirst favors mastication on the operatedside.Later,when healing is advanced,mas-
tication is performed on the nonoperatedside.An opening deviation ofas much as 8 to
9 mm may occur toward the operatedside.The deviation appears to be a
normalcompensatory function secondary to theloss ofposterior attachment and synovi-
um,the change in the joint architecture,and areas offibrous ankylosis.Counter-
acting the lateral deviation actively or pas-sively causes pain in the operated
joint.Hypermobility ofthe nonoperatedjoint may develop or increase after diskec-
tomy.Limitation ofmandibular move-ment on the operated side appears to
beresponsible for the hypermobility.Thehypermobility may be responsible
forawakening symptoms ofa quiescent inter-nal derangement.Capsular
tighteningprocedures have been performed in con-junction with diskectomy to
reducecondylar hypermobility (Figure 50-30).57�59Physical therapy greatly assists
thecontrol ofthe ipsilateral deviation andhence contralateral hypermobility.Joint
crepitations or �snappings�oftenoccur postoperatively.The snappings havebeen
attributed to the condyle rubbing onresidual nonextirpated portions ofthedisk and
usually cease after severalmonths.Patients often report an alterationin their
bite,although rarely as a majorcomplaint.The thicker the retrodiskal tis-sue
removed,the greater is the anticipatedchange in occlusion.The sensation ofanaltered
bite usually resolves within a weekto several months,with resolution ofintra-
articular edema,clot retraction,anddental compensations.Occlusal equilibra-tion is
rarely indicated.There is considerable variation in theability ofeach patient and
joint to adapt tothe postdiskectomy state.Individual fac-tors,such as inclination
ofthe eminence,state ofpreoperative symptoms,loss ofmolar support,and amount
ofpostopera-tive remodeling,do not seem to play a sub-stantial role.Clinicians are
often alarmed by thedegree ofosseous remodeling observedafter a diskectomy.The
morphologic andradiologic changes observed in the TMJconcur with those observed in
experimen-tal diskectomy.41,60After approximately 1 year the morphologic appearance
ofthecondyle and temporal bone appear similarto those observed in a typical
arthrodialjoint,that is,there are planar (flat) articu-lar surfaces.This is
reflected by the mannerin which the joint is observed to function.Agerberg and
Lundberg described erosionofthe articular surfaces and interruptionsofthe cortical
outline on transcranial radi-ographs.61The osseous changes appearedprimarily in the
lateral and anterior aspectsofthe joint.The posterior aspects wereleast
affected.Remodeling changes haveeven been identified in the lateral third ofthe
contralateral (nonoperated) joint.62,63However,this was not confirmed by Bow-
man.12Agerberg and Lundberg concludedthat the remodeling process stabilized after2
years.61They used the term remodelingand not osteoarthrosis to describe the radi-
ographic changes because the osseouschanges occurred in the absence ofsymp-toms.The
bony changes appear similar tothose that are observed longitudinally withchronic
disk displacement,suggestive ofthe same mechanism.The rate ofremodel-ing,however,is
accelerated in the post-diskectomy state.A similar observation hasbeen made in the
postmeniscectomyhuman knee joint.64Articular diskOrigin of lateral fibers of
lateral temporomandibularligament FIGURE50-30Capsular tightening procedure as per
Mar-tin and colleagues.The lateral ligament is reflected from thezygomatic arch
(arrow)(A) and then sutured posterior to itsanatomic origin (B).Adapted from Martin
BC et al.59AB
1006Part 7: Temporomandibular Joint DiseaseDiskectomy without
ReplacementDiskextirpation is facilitated when the atrophicdisk is severed from its
anterior and lateralattachments and then retracted laterallyand posteriorly to
complete the incisions.This approach permits the surgeon to veri-fy the ability
ofthe disk to be repositionedposteriorly before excision.With severeatrophy ofthe
disk,substantial resistanceto posterolateral traction is noted.A hemo-static clamp
is positioned across the anteri-or attachment to serve as a guide plane forthe
knife,which is used to sever the attach-ment lateromedially (Figure 50-31).As
theposterior attachment demonstrates a vari-able degree ofvascularity
changes,theDeBakey bulldog vascular clamp orstraight mosquito clamp may be
appliedhere before severing the posterior attach-ment.Next,a hemostat is used to
applyoutward traction to the tissue to be extir-pated (Figure 50-32).A meniscus
knife isused to sever the medial attachments.When the remodeled posterior
attachmentand disk are extirpated,the retrodiskal tis-sue is electrocauterized to
control bleeding.Care is taken not to disrupt the fibrousconnective tissue lining
ofthe fossa andcondyle.The morphology ofthe condyleand glenoid fossa often prevent
excision inone piece.Incomplete excision ofthe pos-terior attachment over the
lateral pole ofthe condyle may account for some cases offailure with
diskectomy.After the disk andposterior attachment are excised,the sur-geon should
verify that there is not a sig-nificant diaphragm ofirregular posteriorattachment
tissue that remains laterallyaround the head ofthe condyle.With the disk and
posterior attach-ment removed,mandibular range ofmotion is simulated by
manipulating themandible in lateral and protrusive excur-sions.Joint
noises,characterized as snap-pings,may indicate a disk remnant.Diskremnants are
usually located on the medi-al aspect ofthe joint cavity.The surgeonshould remove
all disk remnants thatappear to impede movement.Disk
ReplacementsAutogenous,homologous,and alloplasticreplacements for the disk have
been usedfollowing diskectomy to prevent or reduceintra-articular adhesions,osseous
remodel-ing,and recurrent pain.In addition,theinterpositional material was believed
todecrease joint noises by dissipating loadingforces on the osseous surfaces.The
effective-ness ofinterpositional grafts in reducingadhesions,protecting the
articular surfaces,and diminishing pain and postdiskectomyjoint noise has not been
substantiated.Theuse ofthese materials is sporadic andaccording to operator
preference.The dermal graft may be harvestedfrom the buttock,upper lateral
thigh,groin,or the inner aspect ofthe upperextremity.When the thigh is selected as
thedonor site,a dermatome may be used toraise the skin (0.30�0.38 mm) and thenthe
dermis (0.46�0.51 mm).The der-matome width should be set to take thedermal graft 20
to 30% larger than isrequired to compensate for immediatecontraction ofthe
graft.Bleeding in thedonor site should then be thoroughly con-trolled to prevent
hematoma formationunder the skin,which is replaced over thedonor site.Adhesive
strips may be applied,or the skin edges may be sutured with 5-0nylon.The surgical
site is then dressedwith an occlusive dressing.Postoperativelythe donor site should
be checked for sero-ma formation during the first 48 hours.Alternatively,when size
requirementsare minimal,the graft may be harvestedfreehand.An elliptic wedge
ofepidermisand underlying dermis is harvested.Theunderlying surface ofthe dermis
must bedefatted before being implanted.Thedefatted graft is trimmed and sutured
tothe retrodiskal tissue and the anterior andlateral capsular attachments.The
dermal graft is believed to func-tion as a framework for the new disk.Vas-
cularization ofthe graft is probablyderived from the joint periphery.20,21,28,42The
vascular retrodiskal tissue providespluripotential cells and synoviocytes
toparticipate in the healing process.Dermalgrafts implanted in the primate TMJ
wereDiskEminenceOrthopediccrescent knifeFIGURE50-31Total diskectomy.A straight
clamp isinserted onto the anterior attachment.A meniscus knifeseparates the
anterior attachmentguided by the clamp.The arrowrepresents the direction ofthe
incision.FIGURE50-32An arthroscopic knife severs theposterior attachment (broken
line),guided bytheclamp.The clamp retracts the disk anterolat-erally for
visibility.
Surgery for Internal Derangements ofthe Temporomandibular Joint1007reported to be
viable at postoperative week36.65The collagen and elastic elements ofthe dermal
graft were reported to persist,whereas the dermal appendages atro-phied.66,67Chao
and colleagues reported,however,that the dermal grafts were com-pletely repaired by
fibrous tissue.68The temporalis muscle has been usedas an interpositional
material.The flapmay be pedicled in a variety ofways,someofwhich risk the blood
supply owing totorsion ofthe pedicle.Advantages ofthistechnique over a free graft
include its sta-bility,owing to its connection at the base(Figure 50-33),its
availability at the samesurgical site,and its lack ofmorbidity.Feinberg and Larsen
described a tech-nique that pedicled the posterior temporalismuscle fibers
anteriorly.69A 1 cm�widepaddle is developed above the posterior rootofthe zygomatic
arch.The paddle is elevat-ed and rotated anteriorly and inferiorlyaround the
posterior root ofthe zygomaticarch.The muscle is then sutured to theretrodiskal
tissues (Figure 50-34).Sanders and Buoncristiani describeda technique for using the
temporalismyofascial flap for interpositional tissue inTMJ reconstruction.70The
shape and sizeofthe flap is outlined by incising posteri-orly near the postglenoid
spine ofthe jointthrough temporalis fascia muscle andperiosteum.This incision is
extendedsuperiorly near the temporal line.Subpe-riosteal dissection elevates the
amount offlap needed from the temporal bone.Atransverse incision is made at the
superiorportion anteriorly to create a 3 cm�wideflap.The width should be greater
than theanteroposterior coverage desired in thejoint to allow flap contraction.An
anteriorincision is made parallel to the posteriorincision.The superior aspect
ofthe anteri-or incision is carried to bone in this thinarea ofthe
temporalis.Inferiorly,as thearch is approached,the muscle thickens;therefore,the
dissections are not carriedcompletely through muscle to bone.Bluntdissection is
carried inferiorly to a pointjust medial to the arch to permit adequatemobility
ofthe flap.Branches ofthe tem-poral artery found in this area are pre-served
ifpossible.The length ofthe flap isusually 5 cm.The flap is fully reflected offthe
bone,and resorbable interrupted sutures areplaced in several areas on the edge
oftheflap through fascia,muscle,and theperiosteum to keep the layers from sepa-
rating.Holes are drilled in the bone ofthelateral lip ofthe glenoid fossa
posteriorlyand anteriorly before placement ofthe flapinto the joint.One suture is
placedthrough bone anteriorly near the emi-nence,and a second posterior suture
isplaced near the postglenoid spine.Twoadditional sutures hold the medial edge
toanterior and posterior medial tissues.These medial sutures are sometimes diffi-
cult or impossible to secure,and thesutures through lateral bone are
usuallyadequate to hold the flap in place.A cos-metic temporal defect may result
depend-ing on the thickness oftissue harvested.Autogenous fascia
interpositionalgrafts were described in 1911 for use asinterpositional material in
gap arthroplas-ties for ankylosis.71,72The attractiveness ofthis material lies in
its resistance to resorp-tion,response to mechanical
stress,andbiocompatibility.73�75BoneTemporalismuscleFIGURE50-33Disk replacement
using tempo-ralis mucle/fascial graft (broken line)pedicledfrom above the glenoid
fossa and rotated inward(arrow).Lateral,anterior,and posterior sutureshold the
graft in place.FIGURE50-34Aand B,Disk replacement usingtemporalis muscle/fascial
graft pedicled anteri-orly and rotated anteriorly and inferiorly around(beneath)
the posterior root ofthe zygomaticarch (arrow).The graft is sutured to
theretrodiskal tissues.AB
1008Part 7: Temporomandibular Joint DiseaseAutogenous conchal cartilage was
firstused as a disk replacement by Perko,according to Witsenburg and
Freihofer.76Cartilage harvested from the cavum con-chae results in minimal esthetic
compro-mise.The graft can be tailored to fit thecondyle or glenoid
fossa.Notably,thequality and thickness ofthe aural cartilageis variable.In some
cases an iatrogenic tearin the cartilage may occur during the har-vesting
process.The procedure to obtain chondral car-tilage as interpositional material for
TMJreconstruction has been described by Halland Link.77A 3 to 4 cm postauricular
inci-sion is made on the ear a few millimeterslateral to the auriculocephalic
sulcus and iscarried through to the perichondrium.The middle division ofthe
posterior auric-ular artery may be encountered and ligat-ed or cauterized.A careful
supraperichon-dral dissection with a fine dissectingscissors exposes the surface
ofthe carti-lage.A scalpel is used to cut through thecartilage in the shape ofthe
desiredamount ofgraft,usually 1.5 by 2.5 cm.It isimportant not to extend to the rim
oftheantihelix to avoid permanent deformity ofthe ear.Subperichondral
dissectionbetween the skin ofthe bowl and cartilagepermits the cartilage to be
removed with-out tearing it or perforating the skin.Theear is packed with gauze or
other materialto maintain the shape ofthe bowl and toapply pressure to the skin.The
pressurepack is maintained for 48 hours.Timmel and Grundschober andBoyne and
Stringer reported the use oflyophilized dura in both the porcine andhuman
TMJ.78,79Foreign body reactionswere always associated with the material.There was
gradual replacement ofthematerial with fibrous connective tissue,although they
noted this was not completeby 120 to 130 days.There is increasingresistance among
surgeons toward usingfresh homologous materials owing to thepossibility
oftransmitting communicablediseases.Relatively recently Creutzfeldt-Jakob disease
has been transmitted to apatient who received lyophilized dura.80In the future
surgeons may be able touse tissue explants or biocompatible allo-geneic collagen
sheets as disk replacements.81Alloplastic MaterialsThe requirementsfor an ideal
alloplastic implant are that it bebiocompatible,easily secured,adaptable tothe
variable morphology ofthe recipientsite,and resistant to the compressive andshear
forces ofthe joint.Currently there isno alloplastic material or technique
thatfulfills all ofthese requirements.Computer-aided design using three-dimensional
com-puted tomography images ofthe TMJ maybring us closer to defining the ideal
charac-teristics and design ofthe various compo-nents ofthe TMJ.Silicone elastomer
is a rarely usedimplantable material.It is exclusively andrarely used in the TMJ
for temporary use,but even in this application it is not free ofproblems.Its sole
reputed advantage isthat the material does not incorporate intothe surrounding
tissues.In the past whenit was used as a permanent implant,thematerial�s properties
were responsible forits migration through stabilizing wires.Gallagher and Wolford
suggested that thislack ofstability resulted in the loss ofasmany as one-third
ofall implants placedfollowing condylectomy.82Continuedloading ofsilicone elastomer
interposi-tional implants by the condyle has led tofragmentation and foreign body
reactionsbecause ofits high coefficient offrictionand poor wear characteristics
under directfunction.83Recognition ofthe limitationofthis material led to the
abandonment ofthe permanent silicone implant elastomerand its subsequent rare use
as only a tem-porary implant replacement.Implants laminated with a
compositeofpolytetrafluoroethylene (PTFE) andaluminum oxide were used extensively
inthe early and mid-1980s.84,85The PTFEmaterial�s ultraporosity and
wetabilitypermitted rapid ingrowth offibrous con-nective tissue to facilitate
anchorage oftheprosthesis.The polytefsurface on whichthe condyle interfaced was
chosen to pro-vide a smooth surface resistant to shearand compressive forces.In the
mid-1980s reports ofproblemswith the PTFE implant began to surface.84Patients
reported pain,swelling,jointcrepitus,and limitation ofrange ofmotion resistant to
conservative manage-ment.In such TMJ reconstructions thePTFE implants that were
removed demon-strated perforations,shredding,and dis-placement.Severe osseous
remodelingchanges,particularly ofthe condyle,werereported.86Previous reports
indicated thatthe PTFE-carbon implants elicited a severehistiocytic foreign body
reaction,87similarto what was being reported as happeningin the human TMJ.Because
ofthe growingnumber offailures with PTFE,in 1990 theFood and Drug Administration
formallywithdrew the PTFE implant from the mar-ket and cautioned that patients
should beclosely followed up for progressive bonychanges using radiographic studies
at 6-month intervals.Temporary Implant InsertionTo dateonly the high-performance
polymeric sili-cone implant has been considered for tem-porary (retrievable)
implant insertion.Thepaddle-shaped implant is inserted with theneck ofthe paddle
rolled over the zygo-matic arch (Figure 50-35).Several tackingsutures are placed to
the temporalis fascia.Retrieval is planned for 2 to 6 months post-operatively.As
the polymeric siliconematerial is never incorporated into thehost,the implant is
easily removed at a sec-ond operation under local anesthesia.Thefibrous connective
tissue that encapsulatesthe implant is left in place to act theoreti-cally as the
permanent layer between thecondyle and the fossa.However,at the timeofretrieval
ofthe temporary implant,thefibrous connective tissue encapsulationmay be
incomplete.As a result,this proce-dure has dropped out offavor.
Surgery for Internal Derangements ofthe Temporomandibular Joint1009CondylectomyLow
condylectomy or simply condylectomyis the procedure that is defined as theremoval
ofthe entire condylar process.Theprocedure used to be performed to increasethe
joint space to alleviate pressure on nerveendings,48but it has largely been
abandonedin the surgical repertoire for treatment ofinternal derangements because
ofproblemsofreduced condylar mobility,mandibulardeviations,and open bite.High
condylectomy is the removal ofonly the articular surface ofthe condyle.The disk is
left intact to prevent ankylosisand to promote healing.This contrastedwith the
radical condylectomy in whichthe tendon ofthe lateral pterygoid musclewas
released.Only slight mandibular devi-ation was reported in patients after
highcondylectomy.88�94When the condylar or eminence artic-ular surfaces appear
intact,most cliniciansare reluctant to shave the osseous surfaces.Arthroplasty is
performed when the rateand distribution ofbone remodeling haveresulted in
mechanical interferences.CondylotomyThe condylotomy procedure is an osteoto-my
performed through the condylar neck.Campbell,one ofthe originators
ofthetechnique,made the observation thatsymptoms ofTM dysfunction disappearedafter
condylar fractures.95This led to hisapplication ofthe closed condylotomy topatients
with TMJ symptoms refractory tononsurgical therapy.The rationale behindits use in
treatment ofinternal derange-ments was to produce anteromedial dis-placement ofthe
condyle to change thecondyle-disk-fossa relation,increase jointspace,shorten the
lateral pterygoid mus-cle,and alter load forces.88,96�100Originators ofthe
technique per-formed a closed osteotomy with a Gigliwire saw with the intent
ofcreating ananteromedial fracture dislocation.Inter-maxillary fixation was
sometimes appliedin the immediate postoperative period.Today,when the procedure is
performed,the intraoral route used for the verticalmandibular ramus osteotomy is
employed.Postoperative ManagementSurgery should reduce painful symptomsto a level
that represents little or no con-cern to the patient.It is important toweigh the
contribution ofmasticatorymuscle myalgia to the patient�s chiefcom-plaint.Although
joint surgery can relievethe joint pain,in many cases it may beineffectual in
controlling muscle discom-fort.Nonsurgical management ofthemuscle disorders must
continue in manypatients after surgery for internal derange-ments.Joint surgery
does not restore thejoint to its prepathologic state.The patientshould understand
that biting force maybe reduced and jaw fatigue may becomeapparent with heavy meals
or long conver-sations.After primary surgery (ie,no pre-vious TMJ surgery),one
should strive forthe following passive range-of-motionparameters:maximum
interincisal open-ing of35 to 40 mm,lateral excursivemovements of4 to 6 mm,and
protrusiveexcursive movements of4 to 6 mm.How-ever,success should not be measured
bythe attainment ofa finite measurement.Apatient�s overall success should be mea-
sured by the eradication or diminution ofthe preoperative complaints.Surgery
israrely performed to correct purely func-tional complaints.Elimination
ofpainduring function is usually the predomi-nant concern for the patient,who is
will-ing to accept some compromise in degreeofopening and lateral excursions.Bite
appliances should be used tomaintain a stable occlusal relation in theimmediate
postoperative phase.This isparticularly important after disk reposi-tioning.The
appliance is frequentlyadjusted as the edema resolves and disktissues heal.The
patient should be able toreturn to a normal mechanical diet withminimal dietary
restrictions.Restrictedfoods include such items as French bread,toffee apples,and
popcorn.A stableacceptable occlusion should be main-tained.Joint sounds may develop
or per-sist,but the asymptomatic sounds shouldbe ofminimal concern to the
patient.Postoperative outcomes may be influ-enced by several factors,including con-
comitant facial pain from other sources,degenerative bony
changes,advancedmorphologic changes in the disk,perfora-tion ofthe posterior
attachment,poorlycontrolled parafunctional habits,maloc-clusion,psychological
overlay,previousTMJ surgery,history offacial nerve paral-ysis or orofacial
numbness,history ofinfection,or systemic diseases affecting themuscles,ligaments,or
bone.14Historically,clinicians emphasizedrestricted joint function after
jointsurgery.The clinician must balance hisdesire to rapidly and actively restore a
nor-mal range ofmotion with the capacity ofthe joint and facial muscles to
adapt.Somelatitude must be maintained on the part ofImplantFIGURE50-35Temporary
(retrievable) poly-meric silicone implant inserted.The paddleextension is sutured
to the temporalis fascia.AFreer elevator holds the implant in place (arrow)while
the sutures are secured.
1010Part 7: Temporomandibular Joint Diseasethe clinician in dealing with a
patient�srehabilitation schedule.Care should beexercised in the rehabilitative
process ofthe patient with bilateral joint diseasewhose operation was
unilateral.Dietrestrictions are important.Excessive later-al excursive movements to
the ipsilateralside may contribute to the exacerbation ofcontralateral
symptoms.There is no cook-book recipe to postoperative managementofthese
patients.Some patients,regardlessofthe procedure,achieve an acceptablerange
ofmotion within 7 to 14 days,withminimal effort on their part.Others needto follow
a strict physical therapy regimen.The help ofa physical therapist may some-times be
enlisted to regain joint mobility,especially when patient cooperation with ahome
exercise program is questionable.Ingeneral,some light passive opening andprotrusion
stretching exercises are pre-scribed four times a day beginning 5
dayspostoperatively.With disk repair proce-dures the physical therapy exercises
shouldbe more gradual.Patients should be maintained on afull-liquid to soft diet
for the first 2 post-operative weeks.Heat may be appliedbefore and after exercises
to improve com-fort.Splint therapy is routinely used whena large parafunctional
component is pre-sent.Some authors advocate using anteri-or repositioning devices
to permit healingofsuture sites following disk reposition-ing.Patients should be
encouraged tochew gum after 4 weeks to improve lateralexcursive
movements.ComplicationsComplications may arise immediately(intraoperatively or
within 24 hr) or bedelayed (> 24 hr).Transient neuropraxia ofthe temporalbranches
ofthe facial nerve occurs in asmany as 20 to 30% ofcases.Typically,theinjury is
oflittle significance to the patientand resolves within 3 to 6 months.Theincidence
increases when a separate skinflap is raised.101Rarely,the zygomaticbranches
and,even more rarely,the entiretemporofacial division may be injured.Injury to the
chorda tympani from aggres-sive condylar retraction in the medialaspect ofthe fossa
may occur rarely aswell.Neuropraxia ofthe inferior alveolarand,less commonly,the
lingual nervesmay result from clamp placement for
jointmanipulation.Auriculotemporal syn-drome (gustatory sweating,Frey�s syn-drome)
has been reported as a result ofthedissection ofthe joint.Hemorrhage from the
retrodiskal tis-sue may interfere with performance ofthedisk repair.Temporary
control may beobtained with seating ofthe condyle in theglenoid
fossa.Electrocautery,injection ofepinephrine,or application ofhemostaticagents
while maintaining the mandible inthe closed position may be necessary.Infections
rarely occur.Microorgan-isms cultured may originate from the skinor external
auditory meatus flora.Auri-culitis and external otitis are more likely tooccur with
the postauricular and endauralapproaches.To avoid contamination anear packing is
avoided as it frequentlybecomes dislodged during surgery.Inaddition,the ear is not
suctioned duringsurgery.When the wound is closed theexternal auditory canal is
irrigated gentlywith saline via an 18-gauge angiocatheter.Postoperatively,joint
sounds are a fre-quent occurrence,regardless ofthesurgery.The sounds following
diskectomymay be the loudest.In some patients thesounds may be obtrusive enough to
dis-turb them.The surgeon should delay re-intervention until the patient is
reevaluat-ed at 6 to 12 months,as some sounds maybecome inconsequential to the
patient.SummaryRemarkably good success has been reportedwith several surgical
procedures,which dif-fer in their fundamental approach to theproblem and their
aggressiveness.Most ofthese techniques share common denomina-tors:first,a lateral
approach to the capsuleand ligament;second,a severing ofthe pos-terior attachment-
disk attachments to thecapsule once the superior joint space isaccessed;and,third,a
blunt delineation ofthe joint spaces.Although the capsule andligament tissues are
approximated at theconclusion ofthe procedure,the patient isencouraged to function
on the operatedjoint.Long before arthroscopic surgery,Toller recognized the
importance ofmobi-lizing the condyle-disk-fossa relations toachieve a successful
result.102He devised thelateral capsular arrangement procedure.Itremains to be
determined whether diskrepositioning,posterior attachment repair,diskectomy,high
condylectomy,and evencondylotomy derive some or all oftheir ther-apeutic benefits
through a lateral capsuleand ligament release and mobilization ofthedisk
complex.Arthrocentesis and arthro-scopic surgical procedures for treatment ofthe
closed lock condition appear to be ther-apeutic through the same mechanism.103Open
surgical approaches to TMJinternal derangements are now relegated toa tertiary line
ofcare following nonsurgicaltherapy and arthrocentesis/arthroscopy formost
conditions.They do,however,have aclear indication for certain mechanicalconditions
directly attributed to a diskobstruction.Much ofwhat was written in the pre-vious
edition ofthis chapter has stood thetest oftime.As we increase our under-standing
ofthe pathology,open surgicalprocedures are being performed for spe-cific well-
defined conditions.However,thenew TMJ surgeon will never quite appreci-ate the
experience that comes with perfor-mance ofarthrotomy procedures.Arthroscopy
developed as a consequenceofthis experience.Now,as we regress
withprogress,arthrocentesis with and withoutsteroid injection,a procedure
performedby many surgeons years before the pathol-ogy ofthe joint was even
elucidated,hasbecome a mainstay for treatment.Thistreatment alone has significantly
reducedthe need to intervene via arthrotomy.
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CHAPTER 51Management ofthe Patient with End-Stage Temporomandibular Joint
DiseaseStephen B.Milam,DDS,PhDThe patient with end-stage temporo-mandibular joint
(TMJ) disease is typical-ly characterized by a protracted history ofmultiple
therapeutic interventions,oftenincluding multiple TMJ surgeries.Thepatient with
end-stage TMJ disease com-monly suffers from unrelenting pain andsevere limitation
ofjaw movement.Inaddition,some patients with end-stageTMJ disease may also endure
facial defor-mities,sensory or motor abnormalities,dysfunctional malocclusions,and
upperairway compromise.The suffering oftheseunfortunate individuals is often com-
pounded by their compromised positionin managed health care systems andmounting
personal debt.Understandably,virtually all patients with end-stage TMJdisease
exhibit signs and symptoms ofdepression,often straining relationshipswith
significant others.Several factors likely contribute to theevolution ofend-stage
TMJ disease.Theprogression ofsome TMJ disorders maybe influenced by variables such
as sex (ie,mediated by sex hormones such as estro-gen and prolactin),genetic
backdrop (eg,predisposition to rheumatoid arthritis isassociated with some estrogen
receptorpolymorphisms),nutritional status,age,and psychological stress (eg,plasma
levelsofnerve growth factor,an endogenouspeptide implicated in the genesis
ofsomemuscular and neurogenic pains,are elevat-ed in humans following
psychologicalstress).In addition,it is clear that manypatients with end-stage TMJ
disease alsosuffer from iatrogenic injury.Currently the prognosis for recoveryofthe
patient with end-stage TMJ diseaseis extremely poor.Clearly,the best strategyis
prevention.How can risks for develop-ing end-stage TMJ disease be reduced?Basic
Elements ofCareEffective management ofany TMJ disorderis primarily dependent on
three elementsofcare:an accurate diagnosis,carefulpatient selection,and effective
periopera-tive patient management (Table 51-1).An accurate assessment ofa
patient�scondition(s) is an absolute requirementfor the selection ofan effective
treatment.The experienced clinician recognizes thatmany painful conditions ofthe
head andneck region can mimic a TMJ disorder.For example,it is well known that
somemasticatory myalgias can produce pain ofvarious qualities (ie,ranging from
achingsensations to �stabbing�or �throbbing�pains) that may be felt in the area
ofone orboth TMJs.1Furthermore,some ofthesepainful conditions,such as the
masticato-ry myalgias,may also be associated withrestricted jaw movement and may be
exac-erbated by such movement.Similaritiesbetween many painful head and neck dis-
orders with respect to clinical presentationcan pose a significant challenge for
theclinician to derive an accurate diagnosis.Failure to do so can lead to the
initiation ofan ineffective and perhaps damaging treat-ment that may ultimately
contribute toclinical anomalies that characterize end-stage TMJ disease.Proper
patient selection is importantsince,although appropriate surgical objec-tives and
proper technique are obviouslysignificant determinants oftreatment out-come,a
patient�s commitment and abilityto perform critical perioperative tasks (eg,regular
exercises,nutritional maintenance,abstinence from unhealthy habits) may bethe
single most important determinant ofthe outcome ofsurgical treatment ofaTMJ
disorder.Therefore,the clinician mustaccurately assess the patient�s
willingnessTable 51-1Basic Elements ofSurgical Care Accurate diagnosisCareful
patient selectionEffective perioperative managementPain managementRestoration ofjaw
movement
1016Part 7: Temporomandibular Joint Diseaseand ability to comply with an often-
difficult perioperative regimen.Dependingon the condition,patients who are unwill-
ing or unable to comply with a demandingbut essential perioperative regimen maynot
be viable candidates for the indicatedsurgery.Failure to recognize this
limitationpreoperatively often leads to a significantlycompromised surgical
outcome.It is also important to delineate realis-tic objectives oftherapy,including
surgery,and to recognize the limitations ofeachapproach.Experienced surgeons
oftenreliably achieve TMJ surgical objectives,including excision ofneoplastic or
dis-eased tissues,reliefofphysical obstruc-tions to joint movement,and
restorationofimportant anatomic relationships.However,even the most experienced
sur-geon may not reliably achieve some treat-ment objectives such as
reliefofpain.Clinicians may sometimes recommendtreatment by default (eg,other
approacheshave failed to provide adequate pain relief)without clearly delineated
and reliablyachieved treatment objectives.Such anapproach has significant potential
forworsening the patient�s overall condition byiatrogenic injury.All recommended
treat-ments should be based on an accurate diag-nosis,and a plan based on well-
delineatedachievable treatment objectives.Perioperative Management Patients with
end-stage TMJ disease sufferprimarily from persistent pain andrestricted jaw
function.Recent evidencesuggests that some persistent pain mayresult from
neuroplastic changes evoked innociceptive pathways ofthe central ner-vous system
(CNS) by intense stimulationor nerve injury.There is also strong evi-dence that
these changes may be preventedor significantly obtunded by preemptivetechniques
that reduce or block CNSresponses to surgical stimulation (ie,pre-emptive
analgesia).Two primary goals ofperioperative management ofthe operatedTMJ patient
are pain control (ie,usingpreemptive analgesia techniques) andestablishment and
maintenance ofaccept-able joint movements (ie,mandibularrange ofmotion).These goals
are notexclusive.Patients who suffer from tem-poromandibular pain are often noncom-
pliant with recommended jaw exercisesthat must be performed to achieve andmaintain
physiologic joint movements.Pain-Control StrategiesWith few exceptions,pain is the
primarychiefcomplaint ofpatients with TMJ dis-ease and is often the principal
limiting fac-tor in the patient�s willingness to complywith physical therapy
designed to restorejaw movements.In addition,patients suf-fering from persistent
pain often exhibitclinical signs ofdepression.They are oftensocially withdrawn,and
interpersonalrelationships with significant others maybecome
compromised.Therefore,effectivepain control strategies must be
identified,preferably in the preoperative period,andimplemented aggressively to
ensure anoptimum surgical outcome and to sustainan acceptable quality oflife for
the patient(Table 51-2).Preemptive AnalgesiaEffective postsurgical pain control
beginsin the operating room.It is now recog-nized that methods that limit CNS neu-
ronal activation by surgical stimulationmay significantly reduce pain in the post-
surgical period and may also reduce theliability for the development ofsome per-
sistent pains.The term preemptive analge-siais used to describe methods that appar-
ently reduce postsurgical pain byprotecting the CNS from surgical stimula-tion.The
concept is based on recent obser-vations that collectively indicate that noci-
ceptive processing is highly dynamic.Nociception and subsequent pathway sen-
sitization likely involves de novo proteinsynthesis and even establishment
ofnovelconnections by neurons in the affectedpathway.2�4The old view that
nociceptivepathways are merely static conductors ofneural signals generated by
noxious stim-uli appears to be invalid.We now knowthat gene transcription is
induced in stim-ulated neuronal populations.5,6Some neu-ropeptides that are
translated from thesegenes may facilitate future neural activitiesby receptive
field expansion or by facilita-tion ofspecific interneuronal interactions.The term
neuroplasticityis often used torefer to the dynamic state ofstimulatedneural
pathways.These,and perhaps othermore ominous changes (ie,neuronal deathfrom
excessive stimulation),may be fun-damental to the development ofsomechronic pain
states.Fortunately,these CNSresponses may be significantly attenuatedby preemptive
analgesic techniques.3,7Table 51-2Pain ManagementPerioperativePreemptive analgesic
techniques�Regional anesthesia�Opioid-based general
anesthesia�Ketamine�KetorolacImmediate postsurgical period�Regional
anesthesia�Opioids (patient controlled analgesia or scheduled
regimens)�KetorolacLong termPharmacologic�Tricyclic antidepressant (eg,amitripty-
line)�Opioids (scheduled dosing)�GABAergics (eg,baclofen,gabapentin)�Nonopioid
analgesics (for pain associated with inflammation)Nonpharmacologic�Regular
exercise�Acupuncture�Biofeedback�Transcutaneous electrical nerve
stimulation�Heat/cold packsGABA = ?-aminobutyric acid.
Management ofthe Patient with End-Stage Temporomandibular Joint
Disease1017TechniquesFrom animal and clinicalstudies there is evidence that
protractedneural responses to painful stimuli can bemodified or prevented by the
following:(1) neural blockade with localanesthetics,8�10(2) administration ofopi-
oids,11�15(3) administration ofN-methyl-D-aspartate receptor antagonists
(eg,MK801,ketamine,dextrophan),16�18or(4) administration ofketorolac,a periph-
erally and centrally acting nonopioidanalgesic.19�21These agents must
beadministered prior to noxious stimula-tion to prevent CNS changes that may
berelated to the development ofpostsurgi-cal pain,and perhaps persistent pain.It
isinteresting to note that a general anes-thetic state does not prevent
neuroplasticchanges induced by surgical stimulation,unless the general anesthetic
techniqueemploys high-dose opioids or ketamine.Neural impulses from surgical
stimula-tion apparently reach the CNS evokingsensitization despite the fact that
overtsigns ofsurgical stimulation (ie,patientmovement,heart rate,systemic
bloodpressure) are blocked by general anesthe-sia.This stimulus-dependent neural
sen-sitization,characterized by receptive fieldexpansion and the �wind-up�phenome-
non,2,3has been attributed to postsurgicalhyperesthesia and pain.When regional
anesthesia is employedas an adjunct to general anesthesia,there isstrong evidence
that postoperative pain issignificantly reduced,consistent with cur-rent models
ofcentral sensitization andneuroplasticity.However,to ensure thatneural activities
induced by surgical stim-ulation are fully blocked,the surgeon mustadminister
regional anesthesia priortosurgical stimulation.Ifnecessary duringlong
procedures,the surgeon shouldreanesthetize the operative field and notrely solely
on a general anesthetic state forCNS protection.Jebeles and colleagues studied
theeffects ofpreemptive regional anesthesiaon postsurgical discomfort
associatedwith tonsillectomy and adenoidectomyperformed under general
anesthesia.22Twenty-two children were given eitherbupivacaine or saline
infiltrations in theperitonsillar regions prior to surgicalstimulation.For this
study postsurgicalanalgesics were standardized for all sub-jects and postsurgical
pain was assessedover a 10-day period by three dependentmeasures (ie,constant
pain,pain evokedby swallowing a standard volume ofwater,and the time required to
drink 100 mL ofwater based on the assumption that therate-limiting factor for this
activity isthroat pain).All three dependent mea-sures confirmed that subjects given
bupi-vacaine regional anesthesia with generalanesthesia experienced significantly
lesspain over a 10-day postsurgical periodcompared with the saline-
injectedgroup.22Other studies have provided sim-ilar evidence that regional
anesthesia,pro-vided prior to surgical stimulation,cansignificantly reduce pain
following cra-niotomy and bone harvesting from theiliac crest.23,24To date no
published papershave documented the efficacy ofpreemp-tive regional anesthesia on
postoperativepain,or on the subsequent developmentofchronic pain,in the operated
patientwith TMJ disease.Nevertheless,existingevidence strongly suggests that the
use ofregional anesthesia as an adjunct to gener-al anesthesia will significantly
reducepostsurgical pain in such a patient.Opioids administered priorto surgi-cal
stimulation may also reduce postsur-gical hyperesthesia believed to be due
tocentral sensitization.For example,isoflu-rane or isoflurane and nitrous
oxide,administered in a concentration suffi-cient to suppress cardiovascular
respons-es to surgical stimuli (ie,minimum alve-olar concentration that blocks
adrenergicresponses [MACBAR]),do not inhibitformalin-induced hyperesthesia.25For-
malin injected intradermally provides apotent noxious stimulus that results ini-
tially in a volley ofneural activity thatsensitizes central nociceptive neurons
inthe pathway.This observation reinforcesprevious studies indicating that
generalanesthesia alone does not offer protec-tion against central
sensitization.How-ever,morphine administered priorto for-malin injection
significantly reducespostinjection hyperesthesia in thismodel.25In fact,a
significant reductionin formalin-induced hyperesthesia wasalso observed even
ifmorphine wasreversed by naloxone shortly after theformalin injection was
administered,indicating that even a briefexposure toan opioid prior to noxious
stimulation issufficient to prevent or significantlyreduce stimulation-induced
hyper-esthesia.25Likewise,alfentanil reducescapsaicin-induced hyperalgesia in
humansubjects,but only ifthis agent is adminis-tered priorto capsaicin
administration.26Capsaicin is a vanilloid extracted frompeppers that is known to
selectively stim-ulate C-fiber neurons expressing thevanilloid receptor (VR-
1).Stimulation ofC-fiber neurons by capsaicin administra-tion produces receptive
field expansionand hyperesthesia by mechanisms thatinvolve central
sensitization.3Notably,alfentanil did not effectively reduce painscores,flare
response,or secondaryhyperalgesia when administered afteranintradermal injection
ofcapsaicin inthese human studies.26These studieshighlight the fact that,as is
apparent forregional anesthesia,opioids are onlyoptimally effective as modulators
ofcen-tral sensitization and subsequent hyper-algesia ifthey are administered prior
tosurgical stimulation.Ketorolac is a peripherally and centrallyacting nonopioid
analgesic that is also aneffective preemptive analgesic.19�21In a ran-domized
double-blind trial involving 48patients undergoing ankle fracture surgery,ketorolac
30 mg administered prior to sur-gical stimulation significantly reduced post-
surgical pain relative to the same amount ofketorolac administered after
stimulation.20
1018Part 7: Temporomandibular Joint DiseasePreemptive Analgesia and Persistent
PainSome preemptive analgesia techniquessignificantly reduce postsurgical
pain.There is also evidence that preemptiveanalgesia may provide some
protectionagainst the development ofsome chronicpain states.Bach and colleagues
reportedone ofthe few investigations designed toassess the impact ofpreemptive
analgesiaon the evolution ofa chronic pain state.27In this clinical study 25
elderly patientsscheduled for a below-the-knee amputa-tion received either
treatment withepidural bupivacaine and/or morphine toproduce a pain-free state for
3 days priorto surgery,or no pretreatment (controlgroup).All patients subsequently
under-went amputation under spinal anesthesia.After 6 months,none ofthe
patientsassigned to the presurgery analgesia groupexperienced phantom limb
pain.27How-ever,38% ofthe subjects who did notreceive the presurgical pain
treatment hadphantom limb pain at the 6-month post-amputation
period.Furthermore,27% ofthese subjects experienced persistentphantom limb pain at
the 1-year follow-up period.27RecommendationsIt is recommendedthat,when feasible,an
opioid-based oropioid-supplemented general anesthetictechnique be employed for TMJ
surgery.Also,regional anesthetic should beadministered to cover the entire
surgicalfield priorto surgical stimulation.Duringlong procedures,the surgical field
shouldbe reanesthetized periodically.Ifthere areno contraindications (eg,bleeding
con-cerns),some consideration can also begiven to ketorolac administration (ie,0.5
mg/kg or 30 mg IV) prior to surgicalstimulation.Finally,postoperative painshould
also be well controlled with a com-bination ofregional anesthesia and opioidor
ketorolac analgesia.These regimensmay significantly reduce postsurgical
painfacilitating a shortened convalescence,and may also protect the patient fromCNS
responses to surgical stimulationthat may be involved in the genesis ofsome chronic
pain states.Postsurgical Pain Managementand Pharmacologic ApproachesEffective pain
management permitsimmediate postsurgery physical therapyby improving patient
compliance,whichis crucial to the establishment and main-tenance ofan acceptable
mandibularrange ofmotion.Based on the studiescited above,it is reasonable to
assumethat a continuation ofeffective pain con-trol beyond the intraoperative
periodmay offer some additional benefits in theprevention ofsome protracted
(ie,chron-ic) pain states,although this remains asubject for future studies.The
most com-mon methods ofpostsurgical pain man-agement incorporate a combination
ofopioid and nonopioid analgesics.In someinstances other medications
(eg,tricyclicantidepressants [TCAs],?-aminobutyricacid [GABA]-ergics) may also
offer sig-nificant pain relieffor the patient withend-stage TMJ
disease.Finally,somepatients may benefit from nonpharmaco-logic approaches
(eg,walking 30 min/dfor 6d/wk,acupuncture,cold or hot
packapplications,hypnosis,meditation,pro-gressive relaxation,biofeedback).that
canbe used as a substitute for (eg,the med-ication-intolerant patient) or in
tandemwith pharmacologic approaches.Nonopioid AnalgesicsNonopioid anal-
gesics,including salicylates (eg,acetylsalicylicacid),p-aminophenols
(eg,acetaminophen),arylacetic acids (eg,indomethacin),arylpropi-onic acids
(eg,ibuprofen),and keto-enolicacids (eg,piroxicam),are commonly used tomanage pain
that is associated with inflamma-tion.Nonopioid analgesics block the
synthesisofprostaglandins (PGs) from arachidonic acidby the action
ofcyclooxygenases (COXs) (Fig-ure 51-1).Some PGs (eg,PGE2) are known tosensitize
peripheral nociceptors contributingto the development ofhyperalgesia.Two isoforms
ofCOX are known(COX-1 and COX-2).COX-1 is constantlyexpressed in most tissues to
provide asteady production ofPGs that are requiredfor many normal cellular
functions.28�30On the other hand,COX-2 is an inducibleCOX.It is not typically
expressed undernormal conditions,but,rather,it is synthe-sized in response to
injury accounting forthe increased production ofPGs associat-ed with
inflammation.28,31,32Studies indi-cate that some PGs (eg,PGE2) sensitizesensory
neurons to stimulation by otherbiochemicals,including bradykinin andhistamine.33It
is generally felt that PGsplay an important role in the genesis ofinflammatory pain
via this mechanism.PGs,specifically PGE2,have been detectedin lavage fluid or
synovial fluid samplesobtained from symptomatic human TMJsin concentrations ranging
from 0.1 to 3.5 ng/mL.34,35These concentrations areabove the dissociation constants
forprostanoid receptors (ie,the concentra-tion required for receptor binding) and
aretherefore physiologic.Nonopioid anal-gesics are believed to exert their
primaryeffects by inhibiting the synthesis ofPGsin peripheral tissues,including the
TMJ.Some nonopioid analgesics may pro-duce analgesia by central mechanisms,perhaps
by suppressing COX activity inCNS neurons or adjacent glial cells.Anintrathecal
administration ofacetylsalicy-late produced analgesia in humans suffer-ing from
late-stage cancer pain.36Further-more,central injections ofnonopioidanalgesics
produce antinociception in sev-eral animal models ofpain.37,38Therefore,it appears
that some nonopioid analgesicsmay relieve some types ofpain by bothcentral and
peripheral mechanisms.Side EffectsAs noted above,it is current-ly believed that
basal levels ofPGs are gen-erated under normal circumstances in tis-sues by the
action ofCOX-1.30PGsregulate important physiologic processesin several
tissues,including gastric
Disease1019mucosa,kidney,bone,and cartilage.39�44For example,in the stomach
nonopioidanalgesic suppression ofPG synthesisresults in an increase in gastric acid
secre-tion since PGs inhibit this process.39Also,the secretion ofgastric mucus that
pro-vides a protective coating ofthe stomachlining is inhibited by some
nonopioidanalgesics.These combined effects,in sus-ceptible individuals,can produce
gastroin-testinal irritation and bleeding.In fact,chronic users ofnonopioid
analgesics havea threefold greater risk ofserious gastroin-testinal complications
compared with therisk in nonusers.45Selective COX-2 InhibitorsRelativelyselective
COX-2 inhibitors have beenintroduced for clinical use in an attempt toreduce
systemic side effects associatedwith chronic nonopioid analgesic con-sumption.Four
relatively selective COX-2inhibitors are available in the United Statesat the
present time:celecoxib,meloxicam,rofecoxib,and valdecoxib.There has beena general
misperception that these agentsprovide superior analgesia relative to
thetraditional nonselective COX inhibitors.However,clinical trials have generally
notsupported this notion.For example,ibuprofen provides superior analgesia
tocelecoxib following third molar extractionwith a similar side-effect
profile.46There-fore,the primary indication for the use ofrelatively selective COX-
2 inhibitorsappears to be the control ofinflammatorypain in patients with
gastrointestinal orrenal disorders.However,it should benoted that these agents do
not preventserious gastrointestinal or renal sideeffects,although the incidence
oftheiroccurrence may be relatively low.Leukotrienes: a Target for Future Thera-
piesLeukotrienes are generated fromarachidonic acid by the action oflipoxy-
genases.Leukotrienes (LTs),particularlyLTB4,are proinflammatory molecules
thatpromote leukocyte chemotaxis,sensitizenociceptors,stimulate free radical pro-
duction,and promote bone and cartilagedestruction.LTB4has been detected inlavage
fluids obtained from symptomatichuman TMJs.34In addition to well-documentedeffects
on bone and cartilage catabolism,some lipoxygenase products may alsoplay an
important role in nociception;they appear to be endogenous analogs
ofcapsaicin.47,48As noted above,the pepperextract capsaicin selectively
stimulatesnociceptors.The tertiary structures of12-hydroxyeicosatetraenoic acid and
12-hydroperoxyeicosatetraenoic acid arevery similar to that ofcapsaicin.47Fur-
thermore,these lipoxygenase productsare capable ofstimulating nociceptors ina
concentration-dependent fashion.Thisevoked activity can be inhibited byantagonists
for the primary capsaicinreceptor VR-1.47These findings indicatethat some
lipoxygenase products arecapable ofdirectly stimulating nocicep-tors.By this
mechanism,these arachi-donic acid products could contribute toinflammatory
pain.Therefore,lipoxyge-nase inhibitors may have significantanalgesic properties,in
addition topotential inhibitory effects on LT-medi-ated bone and cartilage
catabolism.RecommendationsAt the present timethe efficacies ofnonopioid
analgesicsemployed to manage pain in the patientwith end-stage TMJ disease have not
beendetermined.Some nonopioid analgesics totreat arthritic pain are
effective.Therefore,one may expect to see beneficial responsesto nonopioid
analgesics when a significantinflammatory component underlyingreported TMJ pain is
suspected.Nonopioid analgesics vary consider-ably in relative potency.All
clinicallyavailable nonopioid analgesics suppressPG synthesis to a variable extent
(ie,theydiffer in relative potencies for COX-1 andCOX-2 inhibition) in either
peripheral orCNS tissues.Some nonopioid analgesicsalso block LT synthesis in the
recom-mended dose range.LTs,as noted in theprevious discussion,can promote poten-
tially detrimental effects in inflamed tis-sues,and some lipoxygenase
productsFIGURE51-1Proinflammatory molecules derived from arachidonic
acid.Proinflammatoryprostanoids and leukotrienes (LTs) are derived from arachidonic
acid liberated from cell membranephospholipids by phospholipases.Prostanoids are
generated by the actions ofcyclooxygenases (COX-1 and COX-2).COX-2 is an inducible
form that is synthesized by cells stimulated by molecules pro-duced after injury
(eg,interleukin-1�[IL-1�],tumor necrosis factor [TNF],IL-6).Leukotrienes
aregenerated by the actions oflipoxygenases.12-hydroxyeicosatetraenoic acid (12-
HETE) and 12-hydroperoxyeicosatetraenoic acid (12-HPETE) may be capable
ofstimulating nociceptors by directaction (ie,by binding vanilloid receptor 1; see
text).Selective COX-2 inhibitors (eg,rofecoxib,cele-coxib,meloxicam,and valdecoxib)
block the activity ofCOX-2,thereby reducing prostanoid synthe-sis under
inflammatory conditions.Nonselective COX inhibitors
(eg,indomethacin,piroxicam,andibuprofen) inhibit both COX-1 and COX-2 activities.At
higher doses these drugs may also inhibitlipoxygenases.
1020Part 7: Temporomandibular Joint Diseasemay be endogenous algesics.At the pre-
sent time specific LT inhibitors are notavailable for clinical use,although com-
pounds have been identified that holdfuture promise.49Therefore,nonopioidanalgesics
that inhibit both PG and LTpathways may be preferred.All nonopioid analgesics
achieve syn-ovial fluid concentrations that are abovetheir median effective dose
(ED50) follow-ing the administration oftheir recom-mended oral dose.Therefore,it is
difficultto favor one nonopioid analgesic overanother in this respect.Nonopioid
analgesics may be indicat-ed when an inflammatory component ofthe patient�s
condition is suspected (ie,joint effusion,acute localized pain,localswelling,or
acute posterior open bite).Clearly,nonopioid analgesics may offersignificant
benefits in the postsurgicalperiod,perhaps used in combination withopioids.Given
well-documented poten-tially serious side effects,nonopioid anal-gesics should be
discontinued ifa brieftrial fails to provide significant clinicalbenefit or ifthe
patient experiences sideeffects.Ifbenefits are not apparent after areasonable trial
period (ie,7�10 d) or ifside effects are observed,the drug shouldbe withdrawn.Ifthe
nonopioid is found tobe effective,it can be continued.However,patients receiving
nonopioid analgesicsshould be monitored on a regular basis fordrug side
effects.Furthermore,periodictapered withdrawal trials should be per-formed to
reassess the need for the drug.OpioidsOpioids elicit their physiologiceffects via
interactions with one or moresubclasses ofopioid receptors located inthe CNS and in
peripheral tissues.Threeclasses ofopioid receptor are known toexist,designated �-
opioid receptor(MOR),d-opioid receptor (DOR),and ?-opioid receptor (KOR).In
addition,atleast two subclasses ofMOR and DORreceptors and four subclasses ofthe
KORreceptor have been identified.50,51Opioidsaffect neurons and some non-neural
cellssuch as leukocytes by several mechanisms,including inhibition ofcyclic
adenosinemonophosphate (cAMP) formation,acti-vation ofGoor Gi/oproteins,or
alteredCa++ or K+translocation.52�54Increasingevidence suggests that analgesia may
beproduced by opioid effects in the CNS,spinal cord,or peripheral tissues.Sometypes
ofpain may be refractory to opioideffects.For example,it is generally believedthat
opioids are ineffective for the reliefofneurogenic pain,although there is
recentevidence to the contrary.55In animal models ofTMJ injury,acti-vation
ofneurons in multiple areas oftrigeminal nuclei can be demonstrated byexpression
ofFos.56Fos is a transcriptionfactor that regulates the expression ofspe-cific
genes in all cells including neurons.Inneurons Fos expression is used as a mea-
surement ofactivation and is typicallydetermined using standard immunohisto-
chemical approaches employing mono-specific antibodies directed against
Fos.Systemically administered morphine sig-nificantly reduces Fos expression in
thetrigeminal nucleus following acute TMJstimulation in the rat.56Peripheral
Mechanisms ofOpioid AnalgesiaFor many years clinicians have been awareofthe
analgesic effects ofperipherallyadministered opioids.Chase reported thatlocal
application ofsmall amounts ofmor-phine was effective in relieving tooth-
ache.57Hargreaves and colleagues haverecently validated this early observation.58In
this latter study endodontic patientsdiagnosed with acute dental infection
wereadministered morphine (0.4 mg),lido-caine,or saline by intraligamentous injec-
tion in a randomized double-blinded fash-ion.These investigators found that atone-
tenth the systemic dose required torelieve dental pain,morphine administeredlocally
(ie,by intraligamentous injection)produced significant pain relief.This sup-ports
the beliefthat opioids can producereliefofsome types ofpain by actions inperipheral
tissues.There is additional support for theconcept that opioids may provide
reliefofTMJ pain by peripheral action.In the ratTMJ MOR has been detected at nerve
ter-minals supplying both anterior and poste-rior synovial tissues,as well as other
celltypes,presumed to be resident macro-phages,mast cells,and endothelial
cells.59In other articular joints local injections ofopioids can suppress the
release ofneu-ropeptides from peripheral nerve termi-nals supplying the injected
joint.60Someneuropeptides,such as substance P andcalcitonin gene�related
peptide,are proin-flammatory and have been detected innerve terminals supplying the
TMJ and insynovial fluid samples recovered fromsymptomatic TMJs.61�64Released
oftheseneuropeptides into articular tissues cangenerate a variety
ofinflammatoryresponses that may underlie joint pain anddisease.The term neurogenic
inflammationis used to describe this phenomenon.It isspeculated that the intra-
articular admin-istration ofan opioid into the TMJ couldinhibit neurogenic
inflammation byblocking the release ofproinflammatoryneuropeptides from stimulated
nerve ter-minals located in the TMJ.Opioidsemployed in this fashion could be
effective�anti-inflammatory�agents ifthis modelis correct.Despite clinical and
animal studies thatsuggest that peripherally administered opi-oids produce
analgesic responses,studiesexamining the effects ofintra-articularmorphine on TMJ
pain remain equivo-cal.65�67In the largest ofthe three publishedstudies to date,53
patients diagnosed withunilateral TMJ arthralgia or osteoarthritiswere assigned to
one ofthree groups receiv-ing a single intra-articular injection of1 mgmorphine
sulfate,0.1 mg morphine sulfate,or saline.67The dependent measuresemployed in this
study included pain at rest,assessed by a standard visual analog scale,pain at
maximum opening,pressure pain
Disease1021threshold,and mandibular range ofmotion measurements (ie,maximum ver-
tical opening,lateral and protrusivemovements).Significant group differ-ences in
pain at maximum opening werenot observed until 4 days after the injec-tion in
subjects given the 0.1 mg mor-phine dose.Subjects reported less pain atmaximum
opening indicating that intra-articular morphine lessened mechanicalallodynia
(ie,pain with non-noxiousmechanical stimulation or movement).However,no dose
response was observed(ie,the higher dose ofmorphine did notproduce a similar or
greater effect),andpain at rest was not affected by intra-articular morphine.The
pressure painthreshold was significantly elevated (ie,more pressure required to
produce pain)at the 1-week follow-up period in patientsgiven the 0.1 mg dose
ofmorphine.Several factors may govern responsesto locally administered
opioids.Opioidsdo not produce measurable effects whenadministered into normal
peripheral tis-sues.68�70However,when injected intoinflamed peripheral
tissues,opioids mayreduce pain,58,71inhibit plasma extravasa-tion and
edema,72,73and alter leukocytefunction.74,75Animal studies havedemonstrated potent
effects ofopioidsinjected into inflamed tissues.76Forexample,PG-induced
hyperalgesia is sup-pressed by nanomolar concentrations ofopioids.76The primary
mechanism(s) bywhich opioids exert their influence ininflamed peripheral tissues is
unknown.From previous studies ofopioid receptordistribution in the TMJ,it appears
that avariety ofcells,including neurons,leuko-cytes,synoviocytes,and endothelial
cells,can respond to peripherally administeredopioids.59Therefore,it is likely that
opi-oids exert their effects on both neural andnon-neural cell populations in
inflamedtissue.It is also possible that someinflammatory molecules
(eg,bradykinin,PGs) may �sensitize�opioid receptors toopioid stimulation.Factors
Affecting Response to Peripheraland Central OpioidsResponses toperipherally
administered opioids may besex dependent.Cai and colleagues exam-ined jaw muscle
electromyographic activi-ty in the rat following an injection ofglu-tamate,an
algesic amino acid,into theTMJ.77Peripherally applied morphine sig-nificantly
reduced glutamate-evoked mus-cle activity in male Sprague-Dawley ratsbut not when
administered to female ani-mals.This observation is consistent withsex-based
differences in neural responsesfollowing systemically administered opi-
oids.Brainstem neural responses tointense noxious stimulation ofthe TMJare obtunded
by a prestimulation systemicadministration ofmorphine in male ratsto a much greater
extent than is observedin female animals.5Morphine is predomi-nantly a MOR
agonist.Interestingly,aKOR agonist was found to attenuatebrainstem responses to TMJ
stimulationin the female to a greater extent than in themale.5These observations
indicate that sexhormones may differentially regulate theexpression ofdifferent
opioid receptortypes,and that males and females maytherefore differ significantly
in responsesto different opioids (eg,MOR agonists vsKOR agonists).Further research
is clearlyneeded in this area to confirm sex-baseddifferences in opioid receptor
expressionin the CNS and in peripheral tissues suchas the TMJ.Another factor that
may governresponsiveness to opioids is the geneticbackdrop ofthe
patient.Polymorphismsofopioid receptor genes could account forsome ofthe
variability observed inresponse to opioids.Polymorphisms aresubtle gene mutations
that result in theproduction ofa protein,in this case anopioid receptor that
differs from nativeprotein with respect to structure and func-tion.Some gene
polymorphisms may per-turb function ofthe protein,whereas oth-ers may enhance
function.Studies areneeded to determine whether polymor-phisms ofopioid receptors
explain appar-ent individual differences in clinicalresponse to either peripherally
or systemi-cally administered opioids.Chronic Opioid TherapyDrug depen-dency or
addiction,reinforcing drug-seeking behavior,drug-induced depres-sion,drug
tolerance,and fear ofgovern-ment prosecution are frequently cited rea-sons for
avoiding opioids in managementprotocols for chronic pain patients.Untilrecently
each ofthese concerns was con-sidered a valid reason for avoiding
opioidtherapy.However,recent evidence suggeststhat the risk ofaddiction may be
extreme-ly low in chronic pain patients with noprior history ofsubstance
abuse.78Druguse alone does not appear to be the majordeterminant
ofaddiction.Rather,otherfactors such as social,psychological,andeconomic conditions
appear to contributemore to addictive behavior.79Psychiatricconsultation may be
valuable in the iden-tification ofindividuals with true addic-tive behavior.Despite
clinical impressions to thecontrary,studies have not validated con-cerns regarding
development ofopioidtolerance.These data indicate that theanalgesic potency
ofopioids seldomdeclines over time,unless there is a wors-ening ofthe patient�s
physical condi-tion.80�82Furthermore,cross-tolerance isoften incomplete in patients
who doexhibit signs ofopioid tolerance.83,84Inthese instances switching to another
nar-cotic can produce an analgesic response.Future studies are required to
determinethe true benefits and risks ofprotractedopioid therapy to manage
persistent painexperienced by the patient with end-stageTMJ disease.Indications for
Opioid TherapyOpioidsdo not appear to be effective for all typesofpain.It is often
difficult to determinewhether the apparent lack ofefficacyobserved in some patients
is due to this
1022Part 7: Temporomandibular Joint Diseasefact or ifthe dose administered is
simplyinadequate.However,a rational approachthat can be employed to confirm the
anal-gesic efficacy ofopioid therapy for a spe-cific patient is suggested in a
study con-ducted by Dellemijn and Vanneste.55Theseinvestigators used an active
placebo(diazepam) and an inactive placebo(saline) to demonstrate the analgesic
effi-cacy ofan opioid (fentanyl) in patientssuffering from neuropathic pain.In
thisparticular study diazepam was no moreeffective than saline as an analgesic.How-
ever,diazepam did produce a sedativeeffect similar to that produced by fentanyland
was therefore suitable for use as anactive placebo.Using this
experimentaldesign,the investigators demonstrated theanalgesic efficacy offentanyl
for control ofneuropathic pain.A similar approachcould be employed to determine
whetheropioid therapy would provide effectiveanalgesia for a particular patient
with end-stage TMJ disease.In this way,the cliniciancould provide a better estimate
ofthe benefit-to-risk ratio ofopioid therapy.As-needed dosing schedules for opi-
oids are avoided.It is preferable to doseopioids on a scheduled basis for
optimumcontrol ofpain.For example,ifthe patientindicates that pain is worse in the
latemorning and afternoon hours,then anadequate loading dose ofthe opioidshould be
administered 1 to 2 hours priorto the morning peak pain period with sup-plemental
dosings at 3- to 6-hour intervalsdepending on the drug.During the titra-tion period
patients may be asked to logtheir pain using a 0 to 10 intensity scale athourly
intervals.Dose adjustments canthen be made based on patient reports ofpain.Some
consideration should be givento the use oflong-acting opioids or alter-nate
delivery systems (eg,transdermal,implanted infusion pumps) in thoseinstances when
severe protracted pain iscontrolled by opioid therapy.Thisapproach may be more cost
effective andcan provide better long-term pain relief.TCAsImipramine was the first
TCAfound to possess analgesic properties.85,86Since that time numerous well-
controlledtrials have documented pain relievingeffects ofTCAs.87�90Mechanism
ofAntinociceptionTCAsproduce significant analgesia independentoftheir
antidepressant effects.For exam-ple,analgesic effects ofTCAs are observedin pain
patients with normal mood.91,92Furthermore,TCA-induced analgesia istypically
observed prior to antidepressanteffects and at doses that are generallybelieved to
be too low for any significantantidepressant effect.93�95Amitriptyline and
imipramine,antide-pressants with antinociceptive actions,arepotent inhibitors
ofserotonin reuptake.96Though these agents have no direct effecton norepinephrine
reuptake,their metabo-lites are also potent norepinephrine reup-take
inhibitors.96In vivo,these TCAs canbe viewed as mixed monoamine reuptakeinhibitors
(ie,they inhibit the reuptake ofboth serotonin and norepinephrine).TCAs enhance the
biologic activitiesofserotonin and norepinephrine by reup-take blockade.Monoamine
receptor occu-pancy is increased by reuptake inhibitors(ie,TCAs) resulting in an
antinociceptiveeffect.There is recent evidence thatmonoamines may be important
modula-tors oftemporomandibular pain.97This isstrongly suggested in studies
investigatingthe relative sensitivities ofpatients whoexpress different versions
ofthe catecholO-methyltransferase (COMT) gene (ie,polymorphisms) to painful
masseter mus-cle stimulation.COMT is an enzyme thatregulates noradrenergic
neurotransmis-sion by catecholamine metabolism.Thegene for COMT exists in a variety
offormscreated by subtle mutations (ie,polymor-phisms).A COMT gene
polymorphismexists at codon 158 (a codon is a three-nucleotide deoxyribonucleic
acidsequence that encodes a specific aminoacid ofthe encoded protein,in
thisinstance COMT),where a valine code issubstituted by a methionine
code.Thissubstitution results in a COMT variantthat is three to four times less
active thanthe native COMT.Individuals who arehomozygous for this COMT
variantreport significantly more pain following ahypertonic saline injection ofthe
massetermuscle relative to those individuals whoexpress the normal
variant.97Interestingly,these individuals also show a reduction inendogenous opioid
responses to this stim-ulation in discreet regions ofthe thalamusas assessed by
functional magnetic reso-nance imaging studies.Efficacy for ReliefofMuscular
PainAmitriptyline significantly reduces theduration and frequency but not the
inten-sity ofchronic tension-type headaches.89,98However,selective serotonin
reuptakeinhibitors do not appear to affect chronictension-type
headaches.89Appropriatelycontrolled clinical studies have also pro-vided evidence
that amitriptyline is effec-tive in relieving pain associated
withfibromyalgia.99�103However,sustainedclinical improvement occurs in a
relativelysmall percentage offibromyalgia patientsgiven this agent.Efficacy for
ReliefofNeuropathic PainAs appears to be the case for reliefofmuscular
pain,antidepressants withmixed serotonin and norepinephrinereuptake inhibition
(eg,amitriptyline)are more efficacious than relatively selec-tive reuptake blockers
(eg,predominantnorepinephrine reuptake inhibition bydesipramine;predominant
serotoninreuptake inhibition by paroxetine orcitalopram) with respect to
reliefofneu-ropathic pain.92,104�108The efficacy ofmixed serotonin and
norepinephrinereuptake inhibitors has been demonstrat-ed for various types
ofneuropathic pain.For example,53% ofpatients with neuro-pathic pain following
treatment ofbreastcancer had a > 50% reduction in pain at a
Management ofthe Patient with End-Stage Temporomandibular Joint Disease1023median
daily dose of50 mg ofamitripty-line.105Amitriptyline has also been shownto be more
effective than placebo forreliefofpain associated with
diabeticneuropathy,postherpetic neuropathy,and central lesions.92,104�108Some
multi-ply operated patients with end-stage TMJdisease may suffer from
neuropathicpains,typically described as �sharp�or�burning,�that likely result from
trau-matic injury to peripheral neurons dur-ing surgery.When this is
suspected,itmay be appropriate to consider a mixedserotonin and norepinephrine
reuptakeinhibitor (eg,amitriptyline).Dosing RecommendationsThere is atremendous
intersubject variability in thepharmacokinetics ofsome TCAs.This isbelieved to be
due,in part,to expressedpolymorphisms ofthe sparteine/debriso-quin oxygenase system
that governsmetabolism ofthe TCAs.109Given thewide intersubject variability in TCA
phar-macokinetics,standard-dose regimensmay be poorly tolerated or ineffective for
aparticular individual.Therefore,thesedrugs should be titrated to effect.It
shouldbe also remembered that only 50 to 70% ofpatients are responders
(ie,individualswho experience a desired effect),and oftenthe response to the drug
is modest.Although there is a general perception thatthe analgesic response to TCAs
is delayed,studies have actually documented a rela-tively rapid analgesic response
to theseagents.In fact,as previously mentioned,measurable antinociceptive effects
havebeen observed after a single dose.95There-fore,an analgesic response should
beexpected within 1 week ofthe administra-tion ofan effective TCA dose,but a maxi-
mum response may not be observed for 4to 6 weeks.For most patients amitriptyline is
theTCA ofchoice for pain management in thepatient with end-stage TMJ
disease.OtherTCAs (eg,desipramine) may be less effectivefor reliefofpain owing to
their relativeselectivities for monoamine reuptake inhi-bition.In most instances
amitriptyline maybe administered as a single dose given atbedtime.An initial dose
of10 to 25 mg istypical for this application.The dose may beincreased at 2-week
intervals to a range of10 to 75 mg/d based on subjective painreports by the patient
and drug tolerance.Itshould be recognized that a therapeuticwindow has been
observed for some TCAs,with maximum analgesic responses typical-ly observed at
lower doses.110,111For this rea-son a ceiling dose of75 mg (1 mg/kg)amitriptyline
for an adult is recommended.Ifsignificant pain reliefis not observed aftertrial
dosing up to this recommended ceiling,then the agent should be withdrawn by
atapering regimen.Ifsignificant pain reliefisobserved,then the agent should be
contin-ued at the effective dose.Periodic taperedwithdrawals ofthe agent are
recommendedto ascertain the need for continued dosing.TCAs can usually be
administeredwith few side effects observed at recom-mended doses.However,side
effectsincluding morning sluggishness,urinaryretention,weight gain from
enhancedappetite,sleep disturbances,and constipa-tion are reported by some
patients.Seriousside effects,such as cardiac dysrhyth-mias/myocardial
infarction,seizures,stroke,agranulocytosis,and thrombocy-topenia,are very rare with
low-dose regi-mens in patients who are not otherwisemedically compromised.TCAs
should beadministered cautiously in patients with ahistory ofcardiovascular
disease,seizuredisorders,or urinary retention or whoconcurrently take medications
that caninfluence monoamine activities (eg,anti-
depressants/antipsychotics,tramadol).Drug-Induced Bruxism and Jaw ClenchingPatients
with end-stage TMJ disease maybe subjected to drugs that can exacerbatetheir
condition by induction offocal dys-tonias leading to increased bruxism or
jawclenching.For example,bilateral mastica-tory myalgia with TMJ symptoms was ob-
served shortly after the administration ofsustained-release bupropion in a 44-year-
oldman for reliefofdepression secondary tochronic lower back pain and
tensionheadaches.112These temporomandibularsymptoms developed within 48 hours
ofadose adjustment from 150 mg/d ofsus-tained-release bupropion to 300
mg/d.Furthermore,these symptoms resolvedcompletely with withdrawal ofthe medica-
tion.Dystonic reactions to some antipsy-chotic and antidepressant medicationsmay
result from an acute reduction indopaminergic activity in the brain.113,114Ninety
percent ofthese reactions occurwithin 3 to 5 days ofdrug initiation or
doseadjustment.112Selective serotonin reuptakeinhibitors
(eg,fluoxetine,citalopram,paroxetine,and sertraline) may evoke
thisresponse.Ironically,some patients withend-stage TMJ disease are placed on
theseagents to manage the inevitable depressionthat occurs in this group
ofpatients.Insome ofthese patients,it is conceivablethat the antidepressant could
worsen theircondition by evoking focal dystonic reac-tions or bruxism affecting the
masticatoryand cervical musculature.Such a responsecould provoke additional muscle
pain andmay even aggravate a TMJ condition byincreasing mechanical loads.Opioid
addiction may be associatedwith exaggerated oromotor behavior andsigns and symptoms
oftemporomandibu-lar dysfunction.Winocur and colleaguesstudied 55 individuals who
were addictedto opioids and were receiving treatment ata methadone clinic.115A
sex-,age-,andsocioeconomic class�matched nonaddictgroup served as the control in
this study.The addicted group exhibited a higher fre-quency ofbruxism and jaw
clenching,aswell as morning headache,TMJ noises,andmasticatory muscle tenderness.It
isunclear from this study whether the appar-ent effects on the stomatognathic
systemwere a direct manifestation ofchronic opi-oid use or a mere reflection ofa
personali-ty disorder that led to an opioid addiction.
1024Part 7: Temporomandibular Joint DiseaseNevertheless,many patients with end-
stageTMJ disease undergo chronic opioid ther-apy for pain management.In
someinstances it is possible that induction offocal dystonias in patients with end-
stageTMJ disease by opioids could exacerbatetheir condition,resulting in an
escalationin pain that could be confused with opioidtolerance.Ifthis phenomenon is
suspected,then a tapered withdrawal ofthe opioidshould be initiated.Contrary to the
reac-tion expected with an opioid-tolerantpatient,opioid withdrawal in this
instancemay provide paradoxic pain relief.GABAergicsGABA is an inhibitory neu-
rotransmitter that has been implicated innociception modulation.116�118GABAeffects
are mediated via at least two differ-ent types ofGABA
receptors:GABAAandGABAB.119,120A third GABA receptor,GABAC,may also exist,but its
distributionappears to be exclusively restricted to theretina ofthe
eye.121GABABreceptors are inhibitory G-protein coupled receptors that
attenuateneural activities.120,122The classic agonistfor the GABABreceptor is
baclofen.Baclofen administered either systemicallyor intrathecally suppresses
allodynia andhyperalgesia in animal models ofpain.123,124In a clinical study
oflower backpain,30 to 80 mg/d baclofen was found tobe superior to placebo as an
analgesic.125Gabapentin has been used to reducepain associated with some
neuropathicstates including pain that is sympathetical-ly maintained.126Gabapentin
appears toelicit this effect by increasing the endoge-nous synthesis
ofGABA.Gabapentin�sanalgesic effects appear to be pain-typespecific.In acute pain
animal models,gabapentin does not produce analgesia.Based on available data,it may
be reasonable to consider a trial ofbaclofen(30�80 mg/d) or gabapentin (300�1800
mg/d) for patients with end-stageTMJ disease who may be suffering from aneuropathic
component ofpain.As previ-ously mentioned,this might result fromprevious injury to
neurons innervating tis-sues ofthe TMJ region.However,given thelimited data
demonstrating efficacy fortemporomandibular pain,particularly inthe patient with
end-stage TMJ disease,these agents should be reserved for useafter other approaches
have been tried.Sympathetically Maintained PainSympathetically maintained pain
(SMP),reflex sympathetic dystrophy,causalgia,and most recently complex regional
painsyndrome (CRPS) are terms often used byclinicians in reference to a
syndrome(s)characterized by continuous burning painbelieved to be associated with
abnormalnociception affected by activity in the sym-pathetic nervous system.CRPS
typicallyfollows traumatic injury to the affectedregion.Some multiply operated
patientswith end-stage TMJ disease with localizedtactile or mechanical allodynia
and burn-ing pain complaints may be suffering fromsympathetically driven
pain.However,theincidence ofCRPS in patients with end-stage TMJ disease is
unknown.Clinical PresentationSigns or symp-toms ofCRPS occurring with an inci-dence
of75% or greater include weakness(95%),pain (93%),altered skin tempera-ture
(92%),skin color change (92%),lim-ited range ofmotion (88%),and hyperes-thesia
(75%).127Less common findingsinclude edema,altered hair
growth,tremor,hyperhidrosis,muscle/skin atro-phy,and bone resorption.127The
mechanism(s) underlying thedevelopment ofCRPS is unknown.Howev-er,there is emerging
evidence that suggeststhat this condition may result from neuro-plastic changes
induced by peripheral sen-sory nerve injury.In animals the sproutingofsympathetic
neurons into sensory gan-glia (ie,dorsal root ganglia) has beenobserved after
injury to peripheral sensorynerves.This sprouting may be induced by aneurotrophic
substance,known as nervegrowth factor (NGF),that is released intoinjured
tissues.128�132A similar response isobserved in animals in which NGF isadministered
intrathecally.132These dataare consistent with the beliefthat CRPSresults from an
abnormal sympatheticinput to sensory ganglia following periph-eral sensory nerve
injury.This abnormalsympathetic input may be made possible bythe development
ofphysical connectionsbetween sympathetic neurons and primaryafferent sensory
neurons.Injury may elicitthis abnormal response via molecular inter-
mediates,specifically NGF.Clearly this phe-nomenon does not occur in all
individualswho sustain injuries to sensory peripheralnerves.Future research is
needed to con-firm this model and to determine risk fac-tors that govern an
individual�s susceptibil-ity to the development ofCRPS.TreatmentOver 25 treatments
for CRPShave been reported in the literature.133Themost common therapeutic approach
hasinvolved the interruption ofsympatheticactivity via a stellate ganglion
block.Aneffective stellate ganglion block may pro-duce protracted pain
relief(ie,lastinglonger than the duration ofanestheticblockade),although this
effect is usuallytransient.Other pharmacologic interven-tions
(eg,phentolamine,prazosin,bretyli-um,guanethidine,calcitonin,nifedipine,gabapentin)
and surgical sympathectomyhave also been employed with inconsistentresults.133With
new information concern-ing the molecular events that may underliethe development
ofCRPS,it is hoped thatmore effective therapies will be developedin the near
future.Physical TherapyA primary goal ofall therapies directed tothe management
ofthe patient with end-stage TMJ disease is to restore normaljoint function
(ie,joint movement).Patients with end-stage TMJ disease typi-cally exhibit severely
restricted jaw move-
Disease1025ments.Pain and intra-articular fibrosis orfibro-osseous ankylosis often
coexist torestrict jaw movement.For this reason,pain management must be effective
foroptimum patient compliance with pre-scribed physical therapy.Passive jaw
exercises are effective atimproving joint function ifthey are per-formed regularly
over an extended periodoftime.Two devices are currently com-mercially available
that facilitate passivemotion ofthe TMJ.Alternatively,passivemotion exercises can
be performed withsimple finger crossover maneuvers or withtongue depressor blades.A
simple but effective protocol incor-porating passive motion exercises toincrease
mandibular movements in thepatient with end-stage TMJ diseaseinvolves repetitive
(10�12 times daily) ver-tical opening exercises.For these exercisesthe patient is
given a number oftonguedepressor blades that,when insertedbetween the maxillary and
mandibularteeth,produce an opening ofthe jaws thatis barely tolerated by the
patient.Thepatient is instructed to apply these tonguedepressor blades hourly (8�10
times daily)for 2 to 3 minutes.On the first day ofeachweek,the patient is
instructed to increasethe total number oftongue depressorblades used by addition
ofone blade.Thisapproach permits tissues to graduallyadapt to advancing jaw
movements and isgenerally well tolerated by the majority ofpatients with end-stage
TMJ disease.Therapy for Periarticular Ectopic Bone FormationPeriarticular ectopic
bone formation isviewed as a significant postsurgical com-plication with a negative
impact on func-tional outcomes in some patients withend-stage TMJ disease.Ectopic
bone mayform in adjacent native periarticular tis-sues or proximate to alloplastic
materialsused to reconstruct the TMJ.In eitherinstance,periarticular ectopic bone
for-mation is viewed as pathologic since ittypically restricts normal joint
movementand may contribute to ongoing pain.The pathogenesis ofperiarticularectopic
bone formation is poorly under-stood.It has been suggested that displacedosteogenic
precursor cells are stimulatedto form ectopic bone by inflammatorymediators formed
in response to surgicalinsult.134Alternatively,osteoinductivemolecules (eg,bone
morphogenetic pro-teins) may be dispersed into periarticulartissues during
surgery,resulting in thestimulation ofresident pluripotent cellsand subsequent
ectopic bone synthesis.Inaddition,there may be other factors,suchas genetics,sex
hormones,systemic disease(eg,ankylosing spondylitis,Paget�s dis-ease),or other
local conditions,that couldalso contribute to the formation ofectopicbone in
periarticular tissues ofthe TMJ.Two strategies have been employed in an attempt to
prevent or minimize periarticular ectopic bone formation ineither orthopedic
surgery patients orthose with TMJ disease.These are low-dose radiation therapy,and
nonsteroidalanti-inflammatory drug (NSAID) therapy.Low-Dose Radiation TherapySome
clin-icians have advocated the use oflow-doseradiation to prevent or minimize
postsurgi-cal fibro-osseous ankylosis oftheTMJ.135�138This approach is based on
anearlier report indicating that low-dose radi-ation may be effective at preventing
the for-mation ofectopic bone following hiparthroplasty.139For prevention
ofperiartic-ular ectopic bone formation ofthe TMJ,fractionated total doses of10 to
20 Gy have been used.One study reportedthat 10 Gy dosing was as effective as
higher-dose regimens.136Timing appears to be critical for opti-mum results from
low-dose radiationtherapy.It is believed that low-dose radia-tion therapy elicits
its effect on ectopicbone formation by prohibiting the prolif-eration ofpluripotent
cells that are pre-cursors to osteoblasts.Therefore,it is rec-ommended that low-
dose radiation thera-py be initiated within 4 days ofsurgery toprovide optimum
suppression ofectopicbone formation.Although there is someconcern that early
postsurgical radiationmay have a detrimental impact on woundhealing,in a recent
study ofthe efficacy ofa single dose of600 cGy administeredbetween postsurgical
days 2 and 4 (mean3.2 d),radiation did not appear to signifi-cantly impact wound
healing after hiparthroplasty.140Radiation therapy was used to pre-vent ectopic
bone formation in the peri-articular region ofthe TMJ in a 53-year-old man.137This
individual sustainedmandible fractures in an automobileaccident and subsequently
underwentfive operations to correct a TMJ ankylosissuffered as a complication ofhis
injury.Over an 18-year period,the patient suf-fered from a significant limitation
ofjawmovement,with reported maximuminterincisal movements as low as 6 mm.Following
his final TMJ arthroplasty,thepatient underwent fractionated cobaltradiation
therapy consisting often ses-sions beginning on the first postoperativeday.The
patient received a total radiationdose of20 Gy in equal fractions.Heapparently
tolerated the procedure wellwithout significant complications.At the3-year follow-
up,the patient had sus-tained a maximum interincisal distanceof25.5 mm.137Schwartz
and Kagan provided a reportdescribing a similar beneficial effect offractionated
radiation (ie,20 Gy in 10fractions) in a 51-year old man who expe-rienced a
zygomatico-coronoid ankylosisfollowing a depressed fracture ofthe zygo-matic
arch.138This condition was surgical-ly treated with a 5 mm gap arthroplastywith
placement ofan intervening sheet ofsilicone rubber.Postsurgical radiation
wasinitiated 1 week after the operation.At a19-month follow-up,the patient
exhibiteda 40 mm maximum interincisal distance.Although the patient initially
complained
1026Part 7: Temporomandibular Joint Diseaseofxerostomia and had some loss
offacialhair,there were no reported lasting illeffects from this
treatment.Experiences with 10 patients sufferingfrom bony ankylosis ofthe TMJ
werereported by Durr and colleagues.136Fourmen and six women (median age 32.5
yr,range 14�59 yr) with a previous history ofTMJ ankylosis underwent TMJ arthro-
plasties and immediate postsurgical (ie,1�3 d) radiation therapy consisting of10 to
11.2 Gy in five fractions over a 5-dayperiod.The median follow-up for thisreported
case series was 19 months (range7�31 mo).Only three patients (ie,30%)were followed
up for > 2 years postopera-tively.Forty percent ofthe patients in thisseries
experienced some recurrence ofectopic bone formation as assessed radi-
ographically.A parotitis was identified in30% ofthe patients in this series.Howev-
er,the radiation therapy did not appear tointerfere with healing,and there were
noother reported complications.Reid and Cooke have reported thelargest case series
to date involving post-operative radiation therapy to manageectopic bone formation
ofthe TMJ in 14 patients with histories ofmultiple TMJsurgeries.135Each patient
underwent TMJarthroplasty with total joint reconstruc-tion using an alloplastic
prosthesis.Themajority ofthese patients received a frac-tionated 10 Gy radiation
dose beginningon the first postoperative day.However,some patients treated early in
the seriesreceived a fractionated 20 Gy radiationdose.Patients in this series were
followedup postoperatively with a mean follow-upof4.2 years (range 1�9.6 yr).The
recur-rence rate for ectopic bone formation atthe 1-year follow-up was
21%.However,long-term follow-up revealed ectopic boneformation in 75% ofthe
patients seen at 5 years and 100% (n = 2) ofpatientsexamined at the 9-year follow-
up (Figure51-2).Consistent with earlier reports,nosignificant persistent side
effects ofradia-tion therapy were noted.A major concern with the use oflow-dose
radiation for the treatment ofectopicbone formation in the TMJ area is thepotential
for induction ofneoplasias.Despite the fact that there have been noreported cases
ofmalignant transforma-tion associated with low-dose radiationtherapy used to
manage periarticularectopic bone formation in the TMJ area,this concern seems
justified based on areport by Ron and colleagues.141Theseinvestigators examined
10,834 patientswho had undergone low-dose radiationtherapy for the treatment
ofringworminfection ofthe scalp (ie,tinea capitis).Allirradiated subjects received
treatment(mean radiation dose 1.5 Gy) before theage of16 years.Controls included
10,834nonirradiated age- and sex-matched indi-viduals not related to the radiated
subjects,serving as a general population control,and 5,392 nonirradiated siblings
ofthesubjects.The subjects were monitored forup to 33 years for the development
ofbenign and malignant neural tumors.Tumors developed in 73 individuals,60among
irradiated subjects,8 in the generalpopulation control group,and 5 amongsiblings
ofirradiated subjects.Overall,there was a sevenfold increase in neo-plasms ofthe
nervous system in individu-als who had undergone low-dose radiationtherapy.Twenty-
four malignant neo-plasias were identified in this study,with18 occurring in
irradiated patients,4 inthe general population control group,and2 in siblings
ofirradiated subjects.Therewas a 4.5-fold increase in the incidence ofmalignant
neoplasias in patients whounderwent low-dose radiation therapy rel-ative to the
control groups.The cumula-tive risk ofdeveloping a neural tumor overa 33-year
period was significantly higherin the irradiated group (0.84 �0.16%)than in the
controls (0.09 �0.03%).Itshould be noted that there was a pro-longed latency
oftumor occurrence (mean17.6 yr after radiation exposure).Fromthis study it appears
that the risk ofradiation-associated tumors was highestbetween 15 and 24 years
postradiation.This has significance in light ofthe factthat the longest published
follow-up forany case series reporting the effects low-dose radiation therapy for
management ofectopic bone formation in the TMJ area is9 years (only two
patients).135It should benoted that patients receiving radiationFIGURE51-
2Recurrence ofectopic bone in patients treated with low-dose radiation.Dataadapted
from Reid R and Cooke H.135
Management ofthe Patient with End-Stage Temporomandibular Joint Disease1027therapy
for tinea capitis in this study weresignificantly younger (< 16 yr old) thanthe TMJ
patients reported in the seriescited above.It is possible that the risk
ofradiation-associated neoplasia may be agedependent.However,this assumption hasnot
yet been validated in appropriatelydesigned studies.In summary,the evidence
supportingthe use oflow-dose radiation therapy toprevent or minimize ectopic bone
forma-tion in periarticular regions ofthe TMJ issupplied by case summaries that
reportbeneficial effects with 10 to 20 Gy expo-sures in fractionated doses
initiatedwithin 4 days ofsurgery.However,itshould be recognized that
definitivestudies (ie,appropriately blinded andcontrolled) have not been reported
todate.In the absence ofthese studies,thetrue efficacy ofthis therapy
remainsobscure.Furthermore,there is evidencethat such therapy may pose
significantlong-term health risks.141NSAID TherapySeveral studies haveprovided
evidence that NSAIDs may beeffective retardants ofectopic bone forma-
tion.140,142�145The mechanism(s) by whichthese drugs elicit this effect is
currentlyunknown.However,the effect is believedto be secondary to the ability
ofthesedrugs to inhibit prostanoid,and perhapsLT,synthesis associated with
normalinflammatory responses to injury.Kienapfel and colleagues compared theeffects
ofindomethacin,a nonselectiveCOX inhibitor (also capable
ofinhibitinglipoxygenase),with those oflow-dose radi-ation therapy employed to
prevent ectopicbone formation after hip arthroplasty.140For this study 154 patients
scheduled forhip arthroplasty to treat various degenera-tive arthritides were
randomly assigned toone ofthree groups:(1) low-dose radiationtreatment (600 cGy
administered as a sin-gle dose between postoperative days 2 and4);(2) indomethacin
treatment (50 mgadministered orally twice a day beginningon postoperative day 1 and
continuinguntil postoperative day 42);or (3) control(no postoperative radiation or
NSAID).Patients assigned to the indomethacintreatment group who were either at risk
forNSAID-induced gastrointestinal disease orwho developed dyspepsia with the
therapywere given cimetidine 200 mg (H2receptorantagonist) concomitantly.All
subjects enrolled in the study wereassessed clinically and radiographically 18
months after surgery.140Ectopic boneformation was significantly inhibited byboth
treatment conditions relative to thecontrol.Furthermore,both treatmentswere found
to be equally effective.Surgicalwound secretions were more persistent inthe
radiated subjects postoperatively,butneither treatment group subsequentlyexhibited
signs ofpoor wound healingthat were significantly different from thecontrol.The
incidence ofdyspepsia washigher in the indomethacin-treated group,but
gastrointestinal bleeding was notdetected in this group.Other NSAIDs have been used
toprevent or minimize ectopic bone for-mation following hip arthroplasty,including
ibuprofen,ketorolac,anddiclofenac.142,143,145All ofthese agentsare nonselective COX
inhibitors (ie,theyblock by COX-1 and COX-2).At the pre-sent time it is not known
whether theselective COX-2 inhibitors are effectiveretardants ofectopic bone
formation.To date there have been no reportedstudies ofNSAID use for the
managementofectopic bone formation ofthe TMJ.Therefore,the efficacy ofthese agents
forthis specific application remains to bedemonstrated.However,based on
theorthopedic surgery literature,it may beprudent to consider NSAID therapy
forpatients who are at risk for ectopic boneformation following TMJ
surgery.Thepotential gastrointestinal and renal com-plications associated with this
approachshould not be underestimated.Patientsundergoing NSAID therapy to prevent
orminimize ectopic bone formation shouldbe properly monitored.Ifindicated,miso-
prostol or an H2receptor antagonistshould be administered concomitantly toreduce
the potential for serious gastroin-testinal complications.ConclusionsThe patient
with end-stage TMJ disease istypically afflicted by severe
unrelentingpain,restricted jaw function,facial defor-mity,depression,compromised
interper-sonal relationships,and financial hard-ships.Given the complexities
involved,these patients pose a significant challengefor the most experienced
clinicians.Acoordinated team ofspecialists best pro-vides optimum care.However,in
mostcommunities this level ofcare is not avail-able.The local oral and
maxillofacial sur-geon is often looked on as the specialistwho will manage these
complicated cases.For the multiply operated patient withend-stage TMJ disease,few
surgicaloptions are viable.In these instances med-ical management is advised with
primarytreatment objectives typically being painmanagement and improvement in
jawmovements.When surgery is contemplat-ed,it is imperative that the surgeon com-
plete an accurate assessment ofthepatient�s condition.The surgeon mustestablish
realistic surgical objectives basedon this assessment.Finally,the surgeonmust
exercise good judgment in the selec-tion ofpatients for surgery.Patients whoare
incapable or unwilling to comply withdemanding but essential postsurgery reha-
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Radiat Oncol Biol Phys 1993;27:863�9.137.Robinson M,Arnet G.Cobalt radiation to
preventreankylosis after repeated surgical failures:report ofcase.J Oral Surg
1977;35:850�4.138.Schwartz HC,Kagan AR.Zygomatico-coronoidankylosis secondary to
heterotopic boneformation:combined treatment by surgeryand radiation therapy�a case
report.JMaxillofac Surg 1979;7:158�61.139.Coventry MB,Scanlon PW.The use ofradia-
tion to discourage ectopic bone.A nine-year study about the hip.J Bone Joint
Surg1981;63:201�8.140.Kienapfel H,Koller M,Wust A,et al.Preven-tion ofheterotopic
bone formation aftertotal hip arthroplasty:a prospective ran-domised study
comparing postoperativeradiation therapy with indomethacin.ArchOrthop Trauma Surg
1999;119:296�302.141.Ron E,Modan B,Boice JD,et al.Tumors ofthebrain and nervous
system after radiothera-py in childhood.N Engl J Med 1988;319:1033�9.142.Elmstedt
E,Lindholm TS,Nilsson OS,et al.Effect ofibuprofen on heterotopic ossifica-tion
after hip replacement.Acta OrthopScand 1985;56:25�7.143.Pritchett JW.Ketorolac
prophylaxis againstheterotopic ossification after hip replace-ment.Clin Orthop
1995;314:162�5.144.Sodemann B,Persson PE,Nilsson OS.Preven-tion ofheterotopic
ossification by nonsteroidantiinflammatory drugs after total hiparthroplasty.Clin
Orthop 1988;237:158�63.145.Wahlstrom O,Risto O,Djerk K,et al.Hetero-topic bone
formation prevented bydiclofenac.Prospective study of100 hiparthroplasties.Acta
Orthop Scand 1991;62:419�21.
CHAPTER 52Hypomobility and Hypermobility Disorders oftheTemporomandibular
JointMeredith August,DMD,MDMaria J.Troulis,DDS,MScLeonard
B.Kaban,DMD,MDHypomobilityEtiologyThe etiology ofmandibular hypomobilityis
varied,and successful treatment requiresan understanding ofthe underlying disor-
der.Trauma is the most commonly identi-fied cause,followed by infection (odonto-
genic,otitis media,and mastoiditis).Various systemic disease states have
beenassociated with hypomobility,includingankylosing spondylitis,rheumatoid arthri-
tis,and other collagen vascular diseasessuch as scleroderma.Iatrogenic causeshave
also been identified and include thesequelae ofhigh-dose radiation involvingthe
muscles ofmastication,craniotomyprocedures,and,uncommonly,orthog-nathic
surgery.Internal temporomandibu-lar joint (TMJ) derangements may alsolead to
chronic hypomobility problems.Traumatic perinatal events and neuro-muscular
conditions can result in hypo-mobility in infancy.In general terms,con-genital
ankylosis is defined as limitedinterincisal opening noted at birth with noknown
causative factor.Table 52-1 lists theetiologic factors associated with mandibu-lar
hypomobility.ClassificationVarious classification schemes have beenproposed to
describe hypomobility.1�3Trismus is most commonly found inconjunction with spasm
ofthe muscles ofmastication.It can be secondary tomyofascial pain
dysfunction,infection,trauma,tumors,and various medicationsas well as psychiatric
and neurologic fac-tors.Ankylosis may be classified accord-ing to location (intra-
articular vs extra-articular),type oftissue involved (bony,fibrous,or mixed),and
the extent offusion (complete vs incomplete).Trueankylosis is caused by either
fibrous orbony fusion ofthe structures containedwithin the TMJ capsule and,in its
mostsevere state,is characterized by a bonyunion ofthe condyle to the glenoid
fossa.True ankylosis has been further classifiedinto subtypes depending on the
anatomicpositioning ofthe condyle and the extentofbridging bone.Topazian proposed
athree-stage classification to grade completeankylosis as follows:stage I,ankylotic
bonelimited to the condylar process;stage II,ankylotic bone extending to the
sigmoidnotch;and stage III,ankylotic boneextending to the coronoid
process.4Otherclassification schemes have also been pro-posed.5However,the utility
ofthese des-ignations in terms oftreatment planningis questionable.So-called false
ankylosis(pseudoankylosis),in contrast,describeslimited mobility based on extra-
articularfactors such as fibrosis,mechanicalobstruction (eg,zygomatic arch
fracture),muscle spasm,or other pathologies.Clinical PresentationPatients with
fibrous or bony ankylosispresent with restricted mandibularmotion and,depending on
the patient�sage and the condition�s etiology,may havean abnormality in mandibular
size andshape.Unilateral pathology in childrenmay result in significant problems
withlower facial symmetry.A shortened ramuson the affected side is usually accompa-
nied by a prominent antegonial notch
1034Part 7: Temporomandibular Joint Diseasenoted on radiographs.Such
unilateralmandibular growth disturbances have sec-ondary effects on the maxillary
occlusalplane and midfacial structures (pyriformrims and bony orbits).Ankylosis in
adults is characterizedby limited jaw opening and decreasedtranslation,but the
morphologic charac-teristics found in the growing patient arefrequently absent.Loss
ofcondylar struc-ture and mandibular angle prominence isseen in cases caused by
rheumatologicdisease,specifically scleroderma.An asso-ciated anterior open bite is
frequentlynoted with the loss oframus/condyleheight (Figure 52-1).Unilateral
caseswith a traumatic etiology may result inmalocclusion and ipsilateral dental
pre-maturities.A physical examination ishelpful in identifying whether the
processis bilateral or unilateral and may be sug-gestive ofthe etiology.Imaging
AssessmentIn addition to the clinical examination,radiographic assessment is
critical in eval-uating and treating patients with hypomo-bility disorders.Plain
radiographs are lim-ited in delineating the true extent ofthedeformity.What can be
identified withthese studies are the presence or absence ofa TMJ space,obvious bony
abnormalitiesin the region ofthe joint,and coronoidhyperplasia.Sanders and
colleagues havereported that conventional radiographsunderestimate the extent
ofbony ankylo-sis and give little information about theanatomy medial to the
condyle.6The useofcomputed tomography (CT) scans(including axial,coronal,and
sagittalviews with three-dimensional reconstruc-tion) is helpful in fully defining
the extentofankylosis as well as the relationship ofthe ankylotic mass to important
anatomicstructures,especially at the skull base(pterygoid plates,carotid
canal,jugularforamen,and foramen spinosum) (Figure52-2).7,8Often in post-traumatic
cases thedistance between the maxillary artery andthe medial pole ofthe condyle
isreduced�a contrast CT helps to deter-mine this distance.Fusion ofthe
ankyloticmass to the base ofthe skull can also beappreciated on CT scans.Since
adequatetreatment requires the removal ofthe massin toto,knowledge ofthis anatomy
preop-eratively is critical to surgical planning andlong-term success.Magnetic
resonance imaging (MRI)has had a great impact on TMJ evaluation,especially
regarding the delineation ofmeniscal position.Diagnosis offibrousankylosis is
possible with the use ofMRI,but the CT scan is superior in demonstrat-ing bony
pathology.9Post-traumatic HypomobilityTrauma is the most common cause ofbony and
fibrous ankylosis as reported bymultiple authors.10�12It is hypothesizedthat the
formation ofan intra-articularhematoma with subsequent scarring andnew bone
formation is the common pre-cipitant.Most often,a medially displacedfracture
dislocation ofthe condyle isfound.Subsequent hypomobility is ofpar-ticular concern
in growing children inwhom the development ofhypomobilitycan have significant
impact on facialTable 52-1Etiologic Factors Associated with Hypomobility ofthe
Mandible TrismusOdontogenic:myofascial pain,malocclusion,erupting
teethInfection:pterygomandibular,lateral pharyngeal,temporalTrauma:fracture ofthe
mandible,muscle contusionTumors:nasopharyngeal tumors,tumors that invade jaw
musclesPsychologic:hysteric
trismusPharmacologic:phenothiazinesNeurologic:tetanusPseudoankylosisDepressed
zygomatic arch fractureFracture dislocation ofthe condyleAdhesions ofthe coronoid
processHypertrophy ofthe coronoid processFibrosis ofthe temporalis muscleMyositis
ossificansScar contracture following thermal injuryTumor ofthe condyle or coronoid
processTrue ankylosisTrauma:intracapsular fracture (child),medial displaced
condylar fracture (adult),obstetric trauma,intracapsular fibrosisInfection:otitis
media,suppurative arthritisInflammation:rheumatoid arthritis,Still�s
disease,ankylosing spondylitis,Marie-Str�mpell disease,psoriatic
arthritisSurgical:postoperative complications oftemporomandibular joint or
orthognathic surgeryFIGURE52-1Patient with systemic sclerosis(scleroderma)
demonstrating a limitation in jawopening and skin changes characterized by peri-
oral furrows and telangiectasia.
Hypomobility and Hypermobility Disorders ofthe Temporomandibular Joint1035growth
(Figure 52-3).In addition,resul-tant hypomobility can lead to
speechimpairment,difficulty with chewing,poororal hygiene,limited access to dental
care,and possible airway compromise.In largereviews ofpediatric facial
fractures,thecondylar and subcondylar regions wereinvolved in > 40% ofcases.13,14In
manycases a direct blow to the chin with trans-mission ofthe impact force to the
condylesresulted in the fracture.Prolonged immo-bilization,secondary to treatment
withmaxillomandibular fixation,splinting,ormechanical obstruction can lead to
subse-quent ankylosis.Extra-articular ankylosis can alsooccur with coronoid
fractures and frac-tures ofthe zygomatic arch.In both casesthe resultant hematoma
may calcify,resulting in a fusion ofthe coronoidprocess to the zygomatic
arch.Myositis ossificans traumatica (MOT),or fibrodysplasia ossificans
circumscripta,is generally associated with a traumaticevent or repeated episodes
ofminor trau-ma and can result in mandibular hypomo-bility.15,16The precise
mechanism remainsto be elucidated but appears to involvefibrous metaplasia and
subsequent ossifi-cation ofboth soft tissues and muscle afterbleeding and
myonecrosis.Histologically,both mature and woven bone can be noted(sometimes in
distinct zones),and bothosteoblasts and osteocytes are abundant.MOT is
characterized by soft tissue ectopicossifications and is relatively uncommonin the
head and neck regions.Ofall report-ed cases involving the muscles ofmastica-
tion,the masseter is most commonlyaffected.MOT involving the medial ptery-goid
muscle and secondary to local anes-thesia injections has also been
reported.17Diagnosis is confirmed by identificationofcalcifications within the
muscles ofmastication on CT scans (Figure 52-4).Minimal response is found with
physicaltherapy and stretching exercises;conse-quently,surgical treatment is
oftenundertaken to remove the ectopic bone.Other treatment modalities include
aceticacid iontophoresis,magnesium therapy,and the use ofetidronate
sodium.18,19Since repeated relapses and refractorycases are common,the use
ofmultipletreatment modalities may be associatedwith the best
outcome.Postinfectious HypomobilityA TMJ infection resulting in hypomobilityis most
commonly the result ofcontiguousspread from an odontogenic infection,oti-tis
media,or mastoiditis.20,21In the era ofaggressive antibiotic treatment
ofinfection,FIGURE52-2Three-dimensional (A,B) and axial(C,D) computed tomography
scans ofa patientwith extensive bony ankylosis ofthe left temporo-mandibular
joint.Note the comparison with theunaffected right side (A,C).Coronoid
hyperplasiais also seen on the affected left side (B,D).FIGURE52-3AandB,Evident
mandibular growth disturbance is noted in this child who has hadbilateral condylar
fractures.Note the submental scar secondary to a laceration sustained at the
timeofthe bony injury.FIGURE52-4Computed tomography scan ofpatient with myositis
ossificans traumaticademonstrating a focus ofcalcification within themedial
pterygoid muscle on the left side.ABABCD
1036Part 7: Temporomandibular Joint Diseasesuch reported cases are now
relativelyuncommon.Hematogenous spread ofinfection has also been reported in
associa-tion with disease states such as tuberculosis,gonorrhea,and scarlet
fever.Various case series describe deep fas-cial space infections manifesting them-
selves as hypomobility and often beingmisdiagnosed at initial
presentation.22,23Odontogenic infection is commonly asso-ciated with trismus.In
such cases associat-ed symptoms (fever,dysphagia) are likelypresent,and CT scanning
is invaluable indetermining a diagnosis and in treatmentplanning.Medial pterygoid
abscess forma-tion or fibrosis secondary to hematomaorganization can be
precipitated by aninferior alveolar nerve block or posteriorsuperior alveolar
block.A history ofrecentdental treatment should suggest this possi-bility;the use
ofCT imaging can helpdelineate the anatomy ofthe masticatorand pharyngeal
spaces.Mass lesions (both benign and malig-nant) can also result in mandibular
hypo-mobility.Squamous cell carcinoma ofthetongue base or tonsillar pillar is
oftenaccompanied by trismus.Masses involvingthe mandibular condyle invariably
affectrange ofmotion and need to be included inthe differential diagnosis
ofhypomobility.Hypomobility following Radiation TherapyMandibular hypomobility is a
commonsequela ofthe treatment ofhead and neckmalignancies (Figure 52-5).The
resultantfibromyositis caused by radiation therapymay exacerbate the postsurgical
problemscaused by large ablative procedures.24Goldstein and colleagues reviewed
theeffects oftumoricidal radiation therapy onrestricted mandibular opening and
found alinear dose-related effect.25Mandibulardysfunction increased as the dose to
thepterygoid muscles increased.The authorsreported diminution in opening with
dosesas low as 15 Gy.Pow and colleagues report-ed that 30% ofpatients treated
fornasopharyngeal carcinoma with high-doseradiation therapy had significant
trismuscompared with age-matched nonradiatedcontrol subjects.26Radiation therapy
forprimary tumors ofthe retromolar trigonewas associated with a 12% incidence
oflong-term trismus.This association,com-pounded by resultant
xerostomia,severelycompromises the ability ofthese patientsto maintain oral
health.The efficacy ofearly interventionalphysical therapy has been
described.Buchbinder and colleagues compared theoutcome ofunassisted
exercise,mechani-cally assisted exercise with the use oftongue blades,and use ofthe
TherabiteSystem in radiated patients.27All patientspresented with an interincisal
opening of< 30 mm.The response to each therapywas recorded every 2 weeks over a 10-
weekperiod.All groups showed improvementover the first 4 weeks,but the group usinga
mechanical exercising device (ie,Ther-abite System) continued to demonstratean
improvement ofmaximal interincisalopening (MIO) over the full 10-week peri-od that
was significantly greater than thatofthe other two groups.Postcraniotomy
HypomobilityMandibular hypomobility after intracra-nial surgical procedures is an
uncommonyet reported phenomenon.28,29Mechanis-tically,this problem is secondary to
neuro-surgical procedures performed throughthe temporal bone requiring an incision
ofthe temporalis muscle.Subsequent fibrosisofthe muscle may then result in
limitedopening,which is best treated with coro-noid resection followed by vigorous
phys-ical therapy.The incidence ofthis problemis not known,but a review by
Kawaguchiand colleagues reported limited mouthopening in as many as 33%
ofpatientsundergoing frontotemporal craniotomyprocedures.30Although most are self-
limiting,persistent hypomobility canseverely compromise subsequent airwayand
anesthesia management in thesepatients and needs to be recognized.Themaximal
opening is not improved with theuse ofmuscle relaxants or local or
generalanesthesia.Patients who have undergoneskull base surgery may also manifest
severehypomobility postoperatively.Ifsuchsurgery requires the dissection ofthe tem-
poralis muscle inferior to the zygoma,pseudoankylosis ofthe mandible may
beencountered.Inflammatory and Rheumatologic CausesAnkylosing spondylitis
(Bekhterev�s dis-ease) is a chronic and progressive inflam-matory condition most
commonly affect-ing the sacroiliac joints and the spine.Themale-to-female ratio
ofincidence is report-ed to be 2.4:1,and the severity and exten-sion ofthe disease
in male patients is foundto be more severe.TMJ involvement inankylosing spondylitis
has been reported inbetween 1 and 22% ofaffected individualsand can include severe
bony deformationand ankylosis.31,32The most commonlyreported radiographic findings
in theFIGURE52-5Patient with a history ofhigh-dose radiation therapy and subsequent
reirradi-ation for recurrence ofnasopharyngeal carcino-ma.Note the severe temporal
atrophy and thelimitation in opening.
Hypomobility and Hypermobility Disorders ofthe Temporomandibular Joint1037condyle
and glenoid fossa region
includeflattening,erosions,sclerosis,osteophytes,subcortical cysts,and bony erosion
at theinsertion ofthe masseter (angle ofthe jaw)and temporalis muscles (coronoid
process).One large prospective study evaluating 50 patients with ankylosing
spondylitis didnot show any correlation between the bonyseverity noted in the
cervical spine and TMJabnormalities.33These authors reported a22% incidence ofTMJ
involvement,eitherclinical or radiographic.Because the major-ity ofpatients
reported no pain or limita-tion in function,the radiographic findingsincluded in
this study may well have repre-sented early changes in the disease process.TMJ
involvement in rheumatoidarthritis follows the same destructive pathas do other
joints.Generally,the severity ofjoint dysfunction is correlated with thestage
ofrheumatoid arthritis.Radiograph-ically,the most common findings in thecondylar
region are the following:sclerosis(75%),erosion (50%),and flattening(30%).34These
bony changes commonlyresult in progressive malocclusion sec-ondary to the loss
oframus/condyle heightand subsequent apertognathia.Juvenilerheumatoid arthritis is
chronic arthritisdiagnosed in childhood before the age of16 years.It is estimated
that > 60% ofpatients with juvenile rheumatoid arthritismanifest TMJ
involvement.35However,multiple authors point out that despiteradiographic and
morphologic changes inthe joint,a minority ofaffected children(generally < 25%)
report pain with func-tion.36,37Svensson and colleagues reportthat restricted mouth
opening was a morecommon finding.38The duration ofactivedisease and a history
ofpain with functioncorrelate positively with progressive TMJdysfunction.With
active disease in growingchildren,abnormalities in facial growth,mandibular
hypoplasia,and hypomobilityare common problems (Figure 52-6).Scleroderma
(progressive systemic scle-rosis) is a disorder ofunknown etiologyaffecting
multiple organ systems and char-acterized by abundant fibrosis ofthe skin,blood
vessels,and visceral organs.It isbelieved that abnormalities in small bloodvessels
result in the progressive thickeningand fibrotic changes noted in affected tis-
sues,particularly those ofthe gastrointesti-nal tract,heart,lung,and kidney as well
asdiffuse skin involvement.Mandibularmovement can become severely limited
inaffected individuals secondary to facial skinfibrosis and atrophy ofthe muscles
ofmas-tication (particularly the masseter andmedial pterygoid muscles).39Bony
changesin the mandible are also reported andinclude severe resorption ofthe
angles,condyles,and coronoid processes (osteoly-sis).40The bony lesions are
believed to be ofischemic origin but may be exacerbated bythe tightness ofthe
tissue in the region ofthe mandibular angles causing pressureresorption as well.In
addition to the severelimitation in jaw movement,the smallmouth orifice and
progressive malocclusionmake oral function and access to dental careproblematic for
these patients.Hypomobility following Orthognathic SurgeryHypomobility following
orthognathicsurgery has been reported by multipleauthors and appears to be most
commonlyassociated with the bilateral sagittal splitosteotomy.41,42This
postoperative limitedopening has been commonly attributed tomuscle atrophy and soft
tissue scar forma-tion.Atrophic muscular changes seem to beexacerbated by prolonged
use ofmaxillo-mandibular fixation,and the advent ofrigidinternal fixation appears
to have limited thisproblem.Intra-articular pathology (edema,hemorrhage) as well as
condylar torque mayalso result in hypomobility.In such casesrigid internal fixation
may predispose tothis problem.Van Sickels and colleagueshave hypothesized that
condylar torque atthe time ofthe bilateral sagittal splitosteotomy may cause
impingement ofthecondyle against the disk,causing a mechan-ical impediment to
opening.43Management ofhypomobility afterorthognathic surgery depends on
theunderlying cause.Trauma to the musclesofmastication is best managed postopera-
tively by vigorous physical therapy proto-cols.Those patients who fail to
improvewithin the first 3 months need to be care-fully evaluated for an intra-
articularsource ofthe problem.Edema,bleeding,and fibrosis within the joint space
can fre-quently be managed by arthrocentesis pro-cedures,especially when recognized
early.Ifa mechanical obstruction to opening issuspected,CT is a helpful diagnostic
aid.Condylar torque is best treated by reoper-ation with appropriate positioning
oftheproximal segment.44General Treatment ConsiderationsThe treatment goal for all
hypomobilitystates is the restoration ofnormal and com-fortable jaw motion and
prevention ofdis-ease progression.Reversible causes such asmuscular hyperactivity
or spasm,infectiousand inflammatory causes,and medication-induced limitations must
be identified andtreated.Restoration offunction in cases ofFIGURE52-6Adult patient
with a history ofjuve-nile rheumatoid arthritis affecting the temporo-mandibular
joints and resulting in a mandibulargrowth disturbance and hypomobility.
1038Part 7: Temporomandibular Joint Diseaseankylosis can be difficult.Proper
treatmentrequires excision ofthe involved structuresand immediate
reconstruction.Many oper-ative techniques have been described in theliterature,with
varying and often less thansatisfactory results.As mentioned above,understanding
the etiology and anatomy ofthe problem is critical and can be greatlyaided with
CT.The gap arthroplasty is a procedurethat creates a new area ofarticulation dis-
tal to the fused TMJ and ankylotic seg-ment.45,46Advocates ofthis proceduredescribe
its simplicity.However,the cre-ation ofa pseudoarticulation significantlyshortens
the ramus height,and the proce-dure is associated with a high degree ofreported
reankylosis.Development ofpostoperative malocclusion and adecreased range ofmotion
are the mostcommon problems associated with thisprocedure as reported by Rajgopal
andcolleagues.47Because ofthese limitations,the use ofthe gap arthroplasty to
treatankylosis has been largely abandoned.Temporomandibular ankylosis ismore
commonly treated with completeexcision ofthe ankylotic mass and,ifrequired,by
subsequent joint reconstruc-tion.Our protocol for the treatment ofankylosis follows
that documented byKaban and colleagues,a sequential proto-col for the treatment
ofTMJ ankylosis thatis based on aggressive resection oftheankylotic mass.48Wide
intraoperativeexposure is required,and special attentionis directed to the medial
aspect ofthe jointto ensure that bony,fibrous,and granula-tion tissue are
completely removed.Inaddition to this aggressive resection ofthebony and fibrous
mass,dissection andstripping ofthe temporalis,masseter,andmedial pterygoid muscles
followed by ipsi-lateral coronoidectomy are performed inall cases through the same
incision.Long-standing ankylosis frequently results inmuscle fibrosis and coronoid
hyperplasia.After this resection is completed,the MIOis measured.Ifit is found to
be < 35 mm,a contralateral coronoidectomy is per-formed via an intraoral approach
to attainthe desired level ofopening.Because com-plete resection ofthe ankylotic
mass fre-quently results in substantial loss oframusheight,subsequent
reconstruction mustaddress this fact and attempt to restoreocclusion as well as
function.Commonly,a temporalis fascia flap and costochondralgraft are employed to
both line the glenoidfossa and create ramus height.The patientis placed into
maxillomandibular fixationfollowing the reconstruction,and the teethare placed into
a prefabricated occlusalsplint.Fixation is maintained for approxi-mately 10 days
and after release a strictprotocol ofphysiotherapy is employed.Overall results have
been excellent withthis approach.After 1 year MIO was main-tained at > 35 mm in all
18 patientsincluded in the report.Furthermore,absence ofpain with function was
report-ed in all but two patients (Figure 52-7).48Recently,the Kaban protocol has
beenmodified to substitute ramus/condylereconstruction using distraction osteogen-
esis,when possible,instead ofcostochon-dral grafting.49This protocol has the
majoradvantage ofeliminating the donor siteoperation and allowing for immediate
vig-orous TMJ mobilization.The surgical pro-cedure for the release ofthe ankylosis
isidentical to that described above.After therelease the jaw is mobilized and the
glenoidfossa lined with a temporalis myofascialflap ifthe native disk is
unavailable.Theremaining mandibular stump is reshapedto create a narrow and rounded
top.A cor-ticotomy is created distally,leaving suffi-cient bone to serve as a
transport disk.Thedistraction device is secured,the corticoto-my completed,and the
mobility ofthe seg-ments tested.Distraction then proceeds at1 mm/d until the
desired length isachieved.The patient begins a program ofactive jaw motion
exercises immediatelypostoperatively (Figure 52-8).The use oftotal joint prostheses
has aninteresting history in the TMJ.Advocatesdescribe two major advantages over
autoge-nous reconstruction:(1) the absence ofadonor site and (2) the ability ofthe
patientto return to function more quickly.Howev-er,multiple complications have
beenreported�some with devastating conse-quences for patients.50�52Foreign
bodyreaction to any alloplast may occur.In itsmost severe form,extensive bony
erosion inthe area ofthe glenoid fossa has beenfound.Fragmentation ofalloplastic
materi-al secondary to function with a migrationofparticles into contiguous tissue
andregional lymph nodes has also been report-ed.Progressive wear may result in a
loosen-ing and fracture ofthe prosthesis.In addi-tion,the lack ofgrowth potential
precludesthe use ofthese joint-replacement systemsin young children.Recurrent
ankylosis afterprosthesis placement has also been report-ed,with periprosthetic
calcifications mostcommonly seen in younger patients.TMJ reconstruction with a
variety ofautogenous tissues has been described.When the extent ofbony resection
does notseverely shorten ramus height,autogenousinterpositional grafts may be
employed.These include skin,temporal muscle,carti-lage,and fascia.A recent review
byChossegros and colleagues has demonstrat-ed superior results (defined by the
authorsas an interincisal opening of30 mm orgreater over a follow-up period of3
yr)using full-thickness skin grafts and tempo-ralis muscle.53Various bone grafts
(costo-chondral,sternoclavicular,iliac crest,andmetatarsal head) have been used to
recon-struct ramus height after the resection ofankylosis.First described in the
1920s,thecostochondral graft for TMJ reconstructionwas popularized in later years
by Poswillo,and MacIntosh and Henny.54,55Autogenoustissue (particularly the
costochondral graft)has the advantage ofbeing biologicallyacceptable and possessing
growth andremodeling potentials that make it a partic-ularly attractive
reconstructive choice in thegrowing child.Potential problems with itsuse include
fracture,resorption,donor site
Hypomobility and Hypermobility Disorders ofthe Temporomandibular Joint1039FIGURE52-
7Three-year-old boy with bilateral bony ankylosis after a motor vehicle accident
that also produced bilater-al lacerations ofthe commissures.Frontal photograph
(A),frontal maximal incisal opening (B),and lateral photograph(C).Note the limited
opening.Right (D)and left (E)panoramic views ofthe ankylotic masses ofthe
temporomandibu-lar joints (TMJs).Right (F)and left (G)TMJs exposed after the
dissection was completed.H,Harvested costochondralgrafts with 1�2 mm cartilaginous
caps.(CONTINUEDONNEXTPAGE)ABCDEFGH
1040Part 7: Temporomandibular Joint Diseasemorbidity,recurrence ofankylosis,and
avariable growth behavior ofthe graft in situ.Complications Associated with
TreatmentVarious complications have been reportedsecondary to the treatment
ofankylosis.Dolwick and Armstrong caution that asevere limitation ofopening can
make thepalpation oflandmarks difficult andincreases the surgical risks.56The
aggressivebony removal and recontouring that is oftenrequired can increase the risk
ofdevelop-ment ofan aural-TMJ fistula ifthe tympan-ic plate is displaced
posteriorly.In addition,stenosis ofthe external auditory meatus andsubsequent
hearing impairment may followtympanic plate displacement.Recurrent ankylosis may
result frominadequate initial treatment.It most com-monly occurs on the medial
aspect ofthecondyle where surgical access is most diffi-cult.Such maneuvers as the
postoperativeuse ofnonsteroidal anti-inflammatorydrugs and vigorous physical
therapy limitproblems with recurrent hypomobility.57,58In pediatric patients
treated for anky-losis,the expected outcome may be lesssanguine.59The improvement
in interin-cisal opening,despite strict adherence tothe above treatment protocol
and compli-ance with physical therapy regimens,isoften significantly less than 35
mm.Posnikand Goldstein reviewed the outcome ofnine children and demonstrated a
meanMIO of24.8 mm in unilateral cases and17.5 mm in bilateral cases measured
anaverage of2 years postoperatively.60Theauthors caution that improvement
inbilateral congenital cases is particularlyproblematic and may be confounded bythe
associated neuromuscular and atroph-ic changes found in these patients.Peripheral
nerve injuries are possiblesequelae ofall TMJ operations,with theupper branches
ofthe facial nerve beingthe most vulnerable.Parotid gland injurywith subsequent
sialocele and fistula for-mation has also been reported.As previously described,the
costo-chondral graft is the most commonlyused autogenous material for TMJ recon-
struction.However,its growth patterncan be unpredictable.Linear overgrowthFIGURE52-
7 (CONTINUED)Frontal (I),frontal opening (J),and lateral (K) facial views ofthe
patient 11 years postoperatively.Note maintenance ofthenormal MIO.L,Intraoral
views.Right (M) and left (N) panoramic radiographs show remodeling ofthe
costochondral grafts.Reproduced with permissionfrom Kaban LB.Acquired
temporomandibular deformities.In: Kaban LB,Troulis MJ,editors.Pediatric oral and
maxillofacial surgery.St.Louis (MO):Elsevier; 2004.p.361�5.IJKLMN
Hypomobility and Hypermobility Disorders ofthe Temporomandibular
Joint1041SkinFatSuperficial temporal fasciaAreolar planeVII nerveTemporalis
fasciaTemporalis muscleFIGURE52-8Thirteen-year-old female with recurrent ankylosis
ofthe left temporo-mandibular joint (TMJ) secondary to trauma sustained in a motor
vehicle accident.Frontal (A),frontal at maximum incisal opening (MIO) (B),and
lateral facial pho-tos (C) ofa teenage female with recurrent ankylosis ofthe left
TMJ.D,Panoramicradiograph prior to the first operation demonstrates bony ankylosis
ofthe left TMJ.E,Panoramic radiograph after the patient developed re-ankylosis.She
had had acondylectomy and coronoidotomy at another institution.The TMJ was
reconstructedwith a costochondral graft.There was no soft tissue lining in the
joint.F,Lateralcephalogram documenting the mandibular retrognathism.G,Diagram
ofoperativeplan,the ankylosis release is carried out via a preauricular incision
(outlined indashed blue line).Excision ofthe ankylotic mass and coronoidectomy is
shown by theshaded area.H,Diagram ofthe layers ofthe scalp.
(CONTINUEDONNEXTPAGE)ABCDEFGH
1042Part 7: Temporomandibular Joint DiseaseTemporalis fasciaflap elevatedTemporalis
fasciawrapped aroundzygomatic arch FIGURE52-8 (CONTINUED)I,Intraoperative view
after dissectionwas completed.Note the bony ankylotic mass and the coronoidprocess
with obliteration ofthe sigmoid notch.J,Diagram ofthebone removed (shaded area) and
the proposed reconstructionusing a distraction device (Synthes
Maxillofacial,Paoli,PA)instead ofa costochondral graft.K,Temporalis flap is
outlined withmalachite green.The flap is dissected and rotated over the arch (L)and
sutured in place (M,N).O,Specimen: ankylotic mass andcoronoid process.
(CONTINUEDONNEXTPAGE) IJKLMON
Hypomobility and Hypermobility Disorders ofthe Temporomandibular Joint1043FIGURE52-
8 (CONTINUED)Frontal (P),frontal opening (Q),and lateral (R) photographs at end
distraction.The patient was mobilized and started on physicaltherapy immediately
postoperatively.She was comfortable because there was no donor site operation and
no period ofmaxillomandibular fixation.Lateral (S)and anterior-posterior (A-P) (T)
designated as cephalogram and panoramic radiograph (U) at the end ofdistraction
osteogenesis demonstrating the lengthenedmandibular ramus.Frontal (V),frontal
opening (W),and lateral (X) photographs 1 year after completion oftreatment.The
patient maintained her TMJ motionand will be beginning presurgical orthodontic
treatment to correct her preexisting malocclusion.Open (Y) and closed (Z) intraoral
views with the patient open-ing 39 mm at 1 year.(CONTINUEDONNEXTPAGE)PQRSTUVWXYZ
1044Part 7: Temporomandibular Joint Diseasewith the subsequent development
ofasymmetry and malocclusion has beenreported by multiple authors.61,62The fre-
quency is more common in the growingpatient.Munro and colleagues reported 2 of22
cases ofconsiderable linear over-growth with resultant chin deviation
anddevelopment ofa Class III malocclu-sion.61Perrott and colleagues reported 3 of26
cases oflateral bony overgrowth(tumor-like overgrowth),with an evidentpreauricular
fullness and subsequent lim-itation ofopening.However,no cases oflinear overgrowth
were found in thatseries ofpatients.62Postoperative Physical TherapyPatients with
hypomobility disordersrequire aggressive physical therapy pro-grams,often in
conjunction with surgicaltreatment,to maintain a functional MIO.Various
rehabilitation programs have beendescribed in the literature,and approachesinclude
unassisted exercise,tongue-bladeand finger-stretch exercises,manual exer-cisers,and
mechanically assisted mandibu-lar motion devices (Figure 52-9).Manipu-lation under
general anesthesia may also berequired in refractory or recurrent cases.Most
authors agree that the duration ofphysical therapy should be prolonged wellafter a
desired MIO is achieved to preventsubsequent
relapse.63HypermobilityClassificationMandibular subluxation occurs whenthere is a
momentary inability to closethe mouth from a maximally open posi-tion.It is defined
as a self-reducing par-tial dislocation ofthe TMJ,during whichthe condyle passes
anterior to the articu-lar eminence.In distinction,dislocationmay be considered a
long-lasting inabili-ty to close the mouth.Subluxation ofthecondyle may be an early
feature ofTMJpathology in a subset ofpatients.It isoften associated with an
abnormally wideopening while eating or yawning.Extend-ed periods ofmouth opening
(eg,duringdental treatment or endotracheal anes-thesia) may also precipitate
subluxation.Subluxation may occur secondary toacute trauma or following a seizure
and isalso associated with systemic diseasessuch as Ehlers-Danlos syndrome
andParkinson�s disease.EtiologyTMJ dislocation is defined as an internalderangement
characterized by a condylarposition anterior and superior to the artic-ular
eminence that is not self-reducing.Recurrent dislocation is a relatively unusu-al
problem.Much like subluxation,the eti-ology is varied.It is observed most fre-
quently in patients with neurologic andconnective tissue disorders,those withTMJ
dysfunction,and those being treatedwith phenothiazines and other neurolepticagents
(Table 52-2).Extrinsic trauma,especially that sus-tained while the mouth is
open,may resultin dislocation.Wide opening ofany typeas well as capsular laxity may
be etiologic.Muscular problems secondary to medica-tion use or neurologic disorders
may beassociated.The problem may be unilateralor bilateral,and patients generally
presentwith associated muscle spasm and pain.FIGURE52-8 (CONTINUED)A-P cephalogram
(AA) and panoramic radiograph (BB) at 1 year.The ramuslengthening is demonstrated
by the space between the retained footplates.A�F,I,K,M and O�BB repro-duced with
permission and G,H,J,L,N adapted from Kaban LB.Acquired temporomandibular deformi-
ties.In: Kaban LB,Troulis MJ,editors.Pediatric oral and maxillofacial
surgery.St.Louis (MO): Elsevier;2004.p.354�7.AABBFIGURE52-9Photograph demonstrating
a con-tinuous passive motion device used in the post-operative management
ofhypomobility.
Hypomobility and Hypermobility Disorders ofthe Temporomandibular Joint1045Treatment
ConsiderationsIn the absence ofpain,subluxationrequires no specific treatment since
it isself-reduced by the patient.When associ-ated with wide mouth
opening,consciousefforts to avoid this are usually successfulat preventing
recurrent subluxation.Patients are advised to modify their diets,and dental
treatment is done over multipleshorter appointments.The use ofbite-blocks during
procedures can also be help-ful.In cases in which extreme laxity in thejoint
results in continued problems,surgi-cal intervention may be warranted.Reduction
ofmandibular dislocationshould be done precipitously before mus-cle spasm becomes
severe and makes theprocedure more difficult.Reduction isaccomplished by pressing
the mandibledownward and then backward to relocatethe condyle within the glenoid
fossa (Fig-ure 52-10).In acute cases this can general-ly be accomplished without
the use ofanesthesia.In cases ofprolonged or chron-ic dislocation,the use ofmuscle
relaxantsand analgesics may be required.Ifreduc-tion cannot be thus
achieved,general anes-thesia may be required.After reduction themandible should be
immobilized for sever-al days to allow for capsular repair,musclerest,and
prevention ofrecurrence.64,65Chronic dislocation usually requires amore
interventional approach.The use ofvarious sclerosing agents has beendescribed in
the past.However,causticagents can result in progressive damage toother joint
structures,and multiple reportsofmisapplications and complications haveresulted in
the abandonment ofthis tech-nique.Surgical treatments ofvarious typesare
reported.Identification ofetiology isimportant when considering surgical cor-
rection.In cases ofextreme joint laxity,mechanical tightening may be
indicated.Plication procedures involve fastening thecondyle to a fixed structure to
maintain itsposition within the glenoid fossa.Certainauthors advocate the creation
ofa mechan-ical impediment to translation by alteringthe conformation ofthe
articular emi-nence.Procedures targeting a decrease inmuscle pull can also be
effective.Plication procedures are aimed atlimiting mandibular motion and may
beaccomplished in various ways.Removal ofredundant capsular tissue (Figure 52-11)is
a relatively simple method for address-ing laxity,and a review by
MacFarlanereported excellent long-term results.66Pli-cation ofthe condyle to the
temporalbone and ofthe coronoid process to thezygomatic arch have also been
described.Multiple materials have been used for pli-cation procedures,including
bothresorbable and nonresorbable sutures andwire.Miniplates and surgical
anchorshave also been used in both the lateralTable 52-2Causes
ofHypermobilityIntrinsic trauma:overextension injuryYawningVomitingWide
bitingSeizure disorderExtrinsic traumaTrauma:flexion-extension injury to
themandible,intubation with general anesthesia,endoscopy,dental
extractions,forceful hyperextensionConnective tissue disorders:hypermobility
syndromes,Ehlers-Danlos syndrome,Marfan syndromeMiscellaneous causes:internal
derangement,dyssynchronous muscle function,contralateral intra-articular
obstruction,lost vertical dimension,occlusal discrepanciesPsychogenic:habitual
dislocation,tardive dyskinesiaDrug induced:phenothiazinesFIGURE52-10Bimanual
mandibular manipu-lation in a downward-posterior direction to dis-engage the
condyle from its open-locked positionposterior to the articular
eminence.Adaptedfrom RotskoffKS.Management ofhypomobilityand hypermobility
disorders ofthe temporo-mandibular joint.In: Peterson LJ,Indresano AT,Marciani
RD,Roser SM.Principles oforal andmaxillofacial surgery.Vol.3.Philadelphia:
J.B.Lippincott Company; 1992: p.2009FIGURE52-11Capsular plication.The exposed
lateral capsule is incised (A) and sutured back on itself(B)to tighten and limit
capsular laxity.Adapted from RotskoffKS.Management ofhypomobility and hyper-
mobility disorders ofthe temporomandibular joint.In: Peterson LJ,Indresano
AT,Marciani RD,Roser SM.Principles oforal and maxillofacial
surgery.Vol.3.Philadelphia: J.B.Lippincott Company; 1992: p.2010AB
1046Part 7: Temporomandibular Joint Diseasepole ofthe condyle and the posterior
roofofthe zygomatic arch.Wolford and col-leagues have described the threading
ofheavy suture material between the eyeletsofthe surgical anchors,thereby prevent-
ing condylar dislocation.67Mechanical impediments to condylartranslation
effectively deepen the glenoidfossa.Bone and cartilage grafts
(cranial,iliaccrest,rib,tibial) have been used for this pur-pose.Nonautogenous
material has also beenonlayed to the articular eminence.In 1943LeClerc and Girald
described a procedure forinferior displacement ofthe zygomatic archto prevent
translation (Figure 52-12).68Access was gained through an extendedpreauricular
incision,and dissection ofthezygomatic arch was performed.An obliqueosteotomy
downward and forward thenallowed the arch to be moved inferiorly.Chossegros and
colleagues reported excellentsuccess using this technique in 36 patientswith
chronic and recurrent dislocation.53The eminectomy procedure was firstintroduced by
Myrhaug in 1951 as a treat-ment for chronic and habitual dislocationofthe
condyle.69In addition to the stan-dard open eminectomy,reports describingthe use
ofthe arthroscope for this purposehave recently appeared in the literature.70Both
procedures involve the removal ofaportion ofthe articular tubercle and emi-nence to
allow the condyle to move freely.Concerns regarding the use oftheeminectomy
procedure include the fol-lowing:hypermobility ofthe joint withfurther damage to
contiguous tissues;significant and often bothersome TMJnoise (clicking and
crepitation) withfunction;the potential for facial nerveinjury;recurrent
dislocation;and inad-vertent temporal lobe exposure (anatom-ic variant).71Reported
success rates ofsurgery totreat dislocation vary considerably.Recur-rent
dislocation following standard eminec-tomy procedures ranges from 7 to
33%.72�74Patients with significant ligamentous laxityor predisposing conditions
(eg,seizure dis-orders) are prone to recurrent problems.Arthroscopic
eminectomy,owing to techni-cal limitations,prevents the completeremoval ofthe
medial aspect ofthe emi-nence.The consequence ofthis in terms ofrecurrence remains
to be elucidated.72,73Ifmuscular hyperactivity is associatedwith chronic recurrent
dislocation,removalofthe insertion ofthe lateral pterygoid mus-cle (lateral
pterygoid myotomy) may be aneffective treatment.Bowman has reportedgood success
with this procedure,74but sub-sequent animal studies have shown lateralpterygoid
electromyographic activity return-ing to baseline several months after the pro-
cedure.75However,the long-term efficacyoften attributed to this procedure may be
sec-ondary to scarring anterior to the joint cap-sule,thereby limiting condylar
excursion.76The injection ofbotulinum toxin type Ainto the lateral pterygoid
muscles has alsobeen proposed as a treatment for chronicand recurrent dislocation
ofthe mandible.Ziegler and colleagues reviewed 21patients treated in this
fashion.Injectionswere given on a 3-month basis with only 2of21 patients suffering
further disloca-tions.No adverse side effects were report-ed in this
series.77Botulinum toxin type Ahas an associated latency of1 week,and itsduration
ofaction is between 2 and 3 months.Injections should not be donemore often than
every 12 weeks to avoidthe development ofantibodies.An injec-tion dose ofbetween 10
and 50 U into thetargeted muscle is usually sufficient.Clark reviewed the use
ofbotulinumtoxin for the treatment ofmandibularmotor disorders,as well as for the
treat-ment offacial spasm,and expanded on thepotential side effects ofsuch
treatment.78Although local side effects are unusual,thetwo most common problems
encounteredwere alterations in salivary consistencyand an inadvertent weakness
ofswallow-ing,speech,and facial muscles.Thesecomplications were more
commonlyreported with lateral pterygoid,soft palate,and tongue injections and were
found tobe dose dependent.SummaryThis chapter summarizes the spectrum ofmobility
problems that can affect the TMJand contiguous structures.The varied etio-logic
factors associated with hypo- andhypermobility have been reviewed;anunderstanding
ofthe etiology in each par-ticular case is imperative for appropriatetreatment to
be rendered.Fortunately,improved imaging techniques,includingthree-dimensional
CT,can be invaluableadjuncts to the history and physical exami-nation.In cases
ofankylosis,the extent andnature ofthe problem is best appreciatedwith these CT
images.Altered anatomy andFIGURE52-12LeClerc procedure.A,An oblique cut using a
fissure bur is created anterior to the artic-ular eminence to decrease the
frequency ofcondylar dislocation by obstructing the path ofcondylarmovement.B,The
osteotomized segments ofthe articular eminence are made to overlap one
another.Adapted from RotskoffKS.Management ofhypomobility and hypermobility
disorders ofthe tem-poromandibular joint.In: Peterson LJ,Indresano AT,Marciani
RD,Roser SM.Principles oforal andmaxillofacial surgery.Vol.3.Philadelphia:
J.B.Lippincott Company; 1992: p.2010AB
Hypomobility and Hypermobility Disorders ofthe Temporomandibular Joint1047the
extent ofbony bridging can be assessedpreoperatively.In addition to
operativeintervention,long-term success in the man-agement ofankylosis requires
aggressivephysical therapy programs and longitudi-nal follow-up.Hypermobility (both
subluxation anddislocation) is similarly reviewed.Again,understanding the causative
factors (liga-mentous laxity,shallow eminentia,muscu-lar hyperactivity) helps one
to focus thetreatment planning and to minimize prob-lems with
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LM,Pitta MC,Mehra P.Mitekanchors for treatment ofchronic mandibu-lar
dislocation.Oral Surg Oral Med OralPathol Oral Radiol Endod
2001;92:495�8.68.LeClerc G,Girald G.Un nouveau procede debutee dans le traitment
chirurgical de la lux-ation recidivante de la manchoire inferieure.Mem Acad Chir
(Paris) 1943;69:457�9.69.Myrhaug H.A new method ofoperation forhabitual dislocation
ofthe mandible�review offormer methods oftreatment.ActaOdontol Scand
1951;9:247�61.70.Sato J,Segami N,Nishimura M,et al.Clinicalevaluation
ofarthroscopic eminoplasty forhabitual dislocation ofthe temporo-mandibular
joint:comparative study withconventional open eminectomy.Oral SurgOral Med Oral
Pathol Oral Radiol Endod2003;95:390�5.71.Undt G,Kermer C,Rasse M.Treatment
ofrecurrent mandibular dislocation,part II:eminectomy.Int J Oral Maxillofac
Surg1997;26:98�102.72.Westwood RM,Fox GL,Tilson HB.Eminecto-my for the treatment
ofrecurrent temporo-mandibular joint dislocation.J Oral
Surg1975;33:774�9.73.Courtemanche AD,Son-Hing QR.Eminecto-my for chronic recurring
subluxation ofthetemporomandibular joint.Ann Plast Surg1979;3:22�5.74.Miller
GA,Murphy EJ.External pterygoidmyotomy for recurrent mandibular dislo-cation.Review
ofthe literature and reportofa case.Oral Surg Oral Med Oral
Pathol1976;42:705�16.75.Burke RH,McNamara JA Jr.Electromyographyafter lateral
pterygoid myotomy in mon-keys.J Oral Surg 1979;37:630�6.76.Sindet-Pedersen
S.Intraoral myotomy ofthe lat-eral pterygoid muscle for treatment ofrecur-rent
dislocation ofthe mandibular condyle.JOral Maxillofac Surg 1988;46:445�9.77.Ziegler
CM,Haag C,Muhling J.Treatment ofrecurrent temporomandibular joint dislo-cation with
intramuscular botulinum toxininjection.Clin Oral Investig 2003;7:52�5.78.Clark
GT.The management oforomandibularmotor disorders and facial spasms withinjections
ofbotulinum toxin.Phys MedRehabil Clin N Am 2003;14:727�48.
Part 8ORTHOGNATHICSURGERY
CHAPTER 53Craniofacial Growth and Development:Current Understandingand Clinical
ConsiderationsPeter M.Spalding,DDS,MS,MSThis chapter will provide a summary
ofthecurrent understanding ofprenatal andpostnatal craniofacial growth and its
rele-vance for clinical treatment.Although thereclearly is awareness ofthe
importance ofgenetic and environmental influences oncraniofacial growth and
development,thecontrol and precise biologic mechanismsare not well understood and
continue to befertile areas ofinvestigation.The chapterwill review human
morphogenesis,prena-tal and postnatal growth and development,the factors that
influence these phases ofgrowth and development,and the orthope-dic and orthodontic
clinical considerationsthat will determine whether surgical inter-vention will be
necessary to achieve opti-mum cosmetic and functional craniofacialtreatment
outcomes.Prenatal Craniofacial DevelopmentHuman prenatal development can be con-
veniently divided into the embryonic peri-od,from fertilization through the
eighthweek ofdevelopment,and the fetal period,continuing from the ninth to the
fortiethweek at birth.The embryonic period ischaracterized by new tissue
differentiationand organogenesis,whereas the fetal peri-od is distinguished by
growth and expan-sion ofthe basic structures already formed.During the first few
days following theformation ofthe single-cell zygote at con-ception,four mitotic
divisions occur toform the 16-cell morula.After entering theuterus the morula
develops into a 100-cellblastocyst consisting ofan outer (tro-phoblast) and inner
(embryoblast) cellmass.The trophoblast further differenti-ates to form the placenta
and otherperipheral embryonic structures,whereasthe embryoblast differentiates into
thefuture embryo.At the end ofthe first weekthe blastocyst adheres to the
uterineendometrium to begin implantation.Dur-ing the second week the
embryoblastforms a bilaminar disk composed oftwogerm layers:the ectoderm,forming
theamniotic cavity floor;and the endoderm,lying beneath and forming the yolk
sacfloor.Later the ectoderm will form a vari-ety ofepidermal structures including
den-tal enamel,oral mucosa and nasal epithe-lia.The endoderm will later form
thepharyngeal epithelium.By the end ofthesecond week the endoderm develops
athickened area called the prechordal plate,located at the cranial end ofthe
bilaminardisk,that prefaces the development ofthehead (Figure 53-1).Embryonic
PeriodGerm Layer FormationCraniofacialembryogenesis begins during the thirdweek
ofgestation,when gastrulation andneurulation occur.Gastrulation is theprocess
whereby the bilaminar disk is con-verted into a trilaminar one with theappearance
ofthe third germ layer,themesoderm,forming between the othertwo from ectodermal
cell proliferation anddifferentiation in the caudal area ofthedisk.The prominence
created from thisproliferation forms a craniocaudal mid-line furrow termed the
primitive streak.Cell proliferation and differentiation ofthe cranial end ofthe
primitive streakforms the notochord around which theaxial skeleton will form.Neural
Tube FormationNeurulation,occurring at the same time as gastrulationduring the
third week and continuingthrough the fourth week,is a process thatresults in the
formation ofthe neural tube,
1052Part 8: Orthognathic Surgerythe primordium ofthe central
nervoussystem.Neurulation is characterized bydevelopment ofthe neural plate from
theectoderm overlying the notochord.As theneural plate grows caudally toward
theprimitive streak,the lateral edges oftheneural plate rise up to create neural
folds,forming the neural groove between them.Mesoderm on either side ofthe
groovedevelops into paired blocks oftissue calledsomites (ultimately 48 somite
pairs willdevelop).In the fourth week the neuralfolds begin to fuse at the midline
in thecentral part ofthe embryo,at the level ofthe fourth to fifth somite,to form
theneural tube (Figure 53-2).The neural tubecontinues to form toward the cranial
andcaudal ends,completing caudal formationby the time about 20 somite pairs are
pre-sent.The anterior portion ofthe neuraltube develops into the forebrain,mid-
brain,and hindbrain.After neural tubeclosure is complete on day 28,the
twohemispheres ofthe brain begin develop-ment,increasing in size to eventually
coverthe roofofthe brain stem.The otic,optic,and olfactory placodes develop in
associa-tion with the forebrain neuroectoderm.Cell Population
Origin,Migration,andInteractionBy the end ofthe fourth weekmultipotential neural
crest cells arisingfrom the neural folds must translocate ormigrate from the dorsal
margins oftheclosing neural tube to specific locationsalong hyaluronate-rich
fibronectin-linedextracellular pathways.1The migration ofneural crest cells follows
a proper sequenceand distinct pathways over extensive dis-tances,but there is
evidence that the cellshave an ability to differentiate into a varietyofderivatives
(Figure 53-3).2There is grow-ing evidence that neural crest cell differen-tiation
is not predetermined but dependenton their epithelial-mesenchymal
cellularinteractions with tissues along the route totheir final
destinations.3Multiple genes,inparticular a class ofhomeobox-
containingtranscription factors,affect subpopulationsofneural crest cells that help
regulate theirmigration and determine the pattern andposition ofstructures within
the pharyn-geal arches.4All ofthe skeletal and connec-tive tissue ofthe face,with
the exception ofdental enamel,is derived from neural crestcells,whereas skeletal
and connective tissueofthe trunk is mesodermal in origin.Manycraniofacial
malformations are producedfrom faulty neural crest formation orNotochordal
processPrimitive knotPrimitive streak(ectoderm)Cloacal membraneAllantois Body
stalkEndodermYolk sac (endoderm)Amnion (ectoderm)Neural plate(ectoderm)Prechordal
plateExtraembryonicmesodermIntraembryonicmesodermNotochordNeural platePrimitive
knotPrimitive streakCloacalmembranePrechordal plateCut edge of amnionYolk sacBody
stalkFIGURE53-1Embryo 14 days old.A,Longitudinal section showing amnion (above) and
yolk sac(below).Adapted from Sperber G.Craniofacial development.Hamilton (ON): BC
Decker Inc; 2001.p.19.B,Dorsal surface view with the amnion cover removed,showing
the embryonic disk.Adaptedfrom Sperber G.Craniofacial development.Hamilton (ON): BC
Decker Inc; 2001.p.20.AB
Craniofacial Growth and Development: Current Understanding and Clinical
Considerations1053migration,loss ofneural crest cells,orflawed epithelial-
mesenchymal interactionduring this fourth week ofgestation.Development ofFacial
PrimordiaThepharyngeal arches,which give rise to mostofthe head and neck
structures,developduring the fourth week as a result ofneur-al crest migration
(Figures 53-3 and 53-4).They consist offour bilaterally paired arch-es on the
ventral external surface ofthehuman embryo.Facial development occursbetween the
fourth and eighth weeks ofgestation.Development ofthe face beginswith five
prominences or primordia sur-rounding the stomatodeum or primitivemouth cavity.The
primordia form fromthe first pair ofpharyngeal arches arisingfrom neural crest
ectomesenchyme andinclude the single median frontonasal pri-mordium,the paired
maxillary primordia,and the paired mandibular primordia.Recent studies indicate
that these facial pri-mordia may be initiated through differentmorphogenetic
mechanisms.They arecomposed ofdifferent neural crest cells,have their outgrowth
regulated by differentNeural grooveAmnion cut edgeSomitomerePharyngeal
archesOropharyngeal membraneCardiogenic regionYolk sacLateral plate(mesoderm)Body
stalkAmnioticcavityCaudal neuroporeLateral
plate(mesoderm)SomitesRostralneuroporeNeural fold(neural crest)FIGURE53-
2Longitudinal section ofamnion in a 23-day-old embryo illustrating the fusion
ofneur-al folds and the initial formation ofsomites.Adapted from Sperber
G.Craniofacial development.Hamilton (ON): BC Decker Inc;
2001.p.21.ForebrainMidbrainForebrainHeartRhombomeresPharyngealarchesPharyngealarche
s112345678IIIIIIIIIIIIIVIVVVI234567FIGURE53-3Illustration ofneural crest migration
pathways from rhombomeres 1 to 7 to pharyngeal arch-es I to VI,from dorsal
(left)and lateral (right)views.Adapted from Sperber GH.Pathogenesis and mor-
phogenesis ofcraniofacial developmental anomalies.Ann Acad Med Singapore
1999;28:708�13.StomodeumPericardial swellingNasal pitUpper limb budPharyngeal
arches I�IVand groovesBody stalk(umbilical cord)SomitesLower limb budOtic
placodeOptic placodeFIGURE53-4Lateral view ofa 31-day-oldembryo showing somites
along the back anddevelopment ofthe pharyngeal arches and limbbuds.Adapted from
Sperber G.Craniofacialdevelopment.Hamilton (ON): BC Decker Inc;2001.p.24.
1054Part 8: Orthognathic Surgerygenes,and have different responses to ter-atogenic
agents.5The facial primordiamerge when the epithelium between thembreaks
down,followed by invasion ofthemesenchyme and coalescence oftheadjoining
prominences (Figure 53-5).Ini-tially the mandibular primordia merge inthe midline
to form the chin and lower lip.At the same time nasal placodes form inthe inferior
and lateral portion ofthe fron-tonasal primordium.On either side ofthese nasal
placodes,medial and lateralnasal primordia develop.The medial nasalprimordia move
toward each other andmerge in the midline early in the sixthweek,forming the
central part ofthe upperlip and the primary palate,including themaxillary incisors
and their surroundingalveolar bone.There still is some contro-versy regarding the
origin ofthe centralpart ofthe upper lip,which some believe isoffrontonasal
primordial origin.6Themaxillary primordia move medially aswell,merging with the
lateral and medialnasal primordia during the sixth week,tocomplete formation ofthe
upper lip.Atthis same time the maxillary andmandibular primordia merge
laterally,determining the width ofthe mouth.Merging offacial primordia requires
dis-integration ofsurface epithelia in order topermit the underlying mesenchymal
cellsto unite (Figure 53-6).The groovebetween the primordia is gradually filledout
by proliferation ofthe mesenchyme sothat the primordia appear to
merge.Facialclefting is a result offailure ofepithelialdisintegration and lack
ofmerging.Facialprimordial growth and merging is depen-dent on ectodermal-
mesenchymal interac-tions that appear to be regulated by thesecreted protein sonic
hedgehog (SHH).5Mutations in SHH that prevent its signalingduring early neural
plate patterning causemidline defects that range fromhypotelorism and cleft
lip/palate to holo-prosencephaly and cyclopia.7There is alsoevidence that adequate
epidermal growthfactor receptor signaling is necessary forsufficient secretion
ofmatrix metallopro-teinases for normal facial development.8From 5 weeks�gestation
to the early part ofthe fetal period at 9 weeks,there is medialmigration ofthe
eyes,assisted by frontaland temporal lobe expansion and greaterproliferation ofthe
lateral facial regions rel-ative to the central face,resulting in facialexpansion
and interocular reduction.The nasal placodes that formed atabout 5 weeks each are
separated inferior-ly by a nasal groove.With continued pro-liferation
ofmesenchyme,the placodessubmerge to form the nasal pits,the pre-cursors to the
anterior nares.As the nasalpits continue to submerge with the prolif-erating
mesenchyme,they are eventuallyseparated from the stomatodeum by onlya thin oronasal
membrane.This mem-brane will rupture at the beginning oftheseventh week,forming a
continuous nasaland oral cavity.Frontonasal prominenceMaxillary
prominenceMandibular arch (pharyngeal arch I)Hyoid arch (pharyngeal arch II)Optic
placodeFirst pharyngealgrooveFirst pharyngeal archSecond pharyngeal archFirst
pharyngealgrooveCardiacswellingCardiacswellingMedial nasalprominenceEyeEyeExternal
earEyeDevelopingeyelidsDevelopingeyelidsGlobularprominenceGlobularMandibularpromine
nceprominenceNaso-opticfurrowNaso-opticfurrowStomodeum4 weeks5 weeks6 weeks7
weeksOral pitNasal pitNasal pitNasal pitNasal pitLateral nasalprominenceLateral
nasalprominenceThird pharyngeal archFIGURE53-5Frontal view ofdeveloping face in
4-,5-,6-,and 7-week-old embryos showing themerging offacial primordia
(prominences).Adapted from Sperber G.Craniofacial development.Hamilton (ON): BC
Decker Inc; 2001.p.32.
Considerations1055Formation ofNeurocranium and Viscero-craniumFormation ofthe
craniofacialbones begins with development ofthe car-tilaginous and membranous
precursors tothe neurocranium and viscerocraniumduring the latter part ofthe fifth
week ofgestation (Figure 53-7).The membranousneurocranium (desmocranium) that
willgive rise to the flat bones ofthe calvaria isconnective tissue derived from the
paraxialmesoderm and neural crest.The cartilagi-nous neurocranium
(chondrocranium)that will form the cranial base is cartilagefrom neural crest
origin.Cartilage matura-tion occurs in a caudal-rostral sequence.The membranous
viscerocranium that willgive rise to the maxilla,zygomatic bone,squamous temporal
bone,and mandible isderived from the neural crest.The carti-laginous viscerocranium
that will form themiddle ear ossicles,styloid process ofthetemporal bone,hyoid
bone,and laryngealcartilages is from neural crest ectoderm.Endochondral
ossification centers occur inthe cartilaginous components andintramembranous
ossification centersform in the membranous components ofthe neurocranium and
viscerocranium.Osteoblast differentiation with the onset ofmineralization results
from a rapid angio-genic process with vascular ingrowth close-ly surrounding the
center ofossification.The earliest ossification ofthe craniofacialbones begins in
the seventh and eighthweeks ofgestation.There are eventually110 ossification
centers,nearly all ofwhichappear between 6 and 12 weeks�gestation,that develop in
the embryo to form 45bones at birth,which ultimately form 22bones in the
adult.OssificationThe onset ofossificationgenerally follows the chronologic
sequenceofmandible,maxilla,palatine,cranialbase,and cranium,with
intermembranouscenters usually preceding endochondralcenters.9Ossification ofthe
mandiblebegins in the mental foramen region.Endochondral ossification ofMeckel�s
car-tilage occurs anteriorly to this area andintramembranous ossification occurs
pos-teriorly.The condylar cartilage forms atthe posterior end ofthis intramembra-
nous portion,independently ofMeckel�scartilage.Maxillary ossification begins inthe
area ofthe infraorbital foramen.Intramembranous ossification occursanteriorly and
posteriorly to this region.The vertical portion ofthe palatine bonethen begins
intramembranous ossificationin the region ofthe palatine nerve,fol-lowed by
ossification ofthe anterior,thenposterior borders ofthe incisive foramen,spreading
through the hard palate fromthe canine area.Following ossification ofthe main
portion ofthe mandible andmaxilla,during the sixth week ofgesta-tion,endochondral
ossification ofthe cra-nial base occurs in the midline from theforamen magnum to
the nasal bone,andintramembranous ossification occurs lat-erally.Finally
intramembranous ossifica-tion ofthe cranial bones follows.Final Tissue
DifferentiationInterac-tion between pharyngeal endoderm andneural crest
tissue,followed by oral ecto-derm proliferation,produces identifiableodontogenic
tissue by the end of4 weeks�gestation.There are four origin sites ofodontogenic
epithelium for both themaxillary and mandibular arches,appearing at the end of5
weeks�gesta-tion.The primary anterior and firstmolar tooth germs appear at 6
weeks�ges-tation,followed by development oftheprimary second molar germs at 7
weeks.Apposition ofbone on the alveolar mar-gins ofthe maxilla and mandible in
thepresence ofdeveloping tooth germs formthe initial alveolar processes.The latest
orofacial structure to reachcompletion at the end ofthe embryonicperiod is the
secondary palate,developingfrom the paired lateral palatine shelves ofFIGURE53-
6Scanning electron micrograph ofa 41-day-old human embryo.A,Craniofacial region.LNP
= right lateral nasal primordium; MNP = right medial nasal primordium; NP = right
nasal pit;MXP = right maxillary primordium; AH = right auricular hillock; EAM =
right external acousticmeatus; MDP = mandibular prominence; ST = left side
ofstomodeum.B,Enlarged view,showing theepithelial bridges between the merging right
maxillary primordium (MXP) and the right medialnasal primordium (MNP).Failure
ofthese primordia to merge together with the lateral nasal pri-mordium (LNP)
results in cleft ofthe lip.Reproduced with permission from Hinrichsen K.The
earlydevelopment ofmorphology and patterns ofthe face in the human embryo.In:
Advances in anatomy,embryology and cell biology.Vol.98.New York: Springer-Verlag;
1985.AB
1056Part 8: Orthognathic Surgerythe maxilla.These shelves are oriented ver-tically
with the tongue interposed,but thetongue and floor ofthe oral cavity descendas the
nasal chambers expand laterally andinferiorly (Figure 53-8).As this occurs
thepalatal shelves become elongated and ele-vate medially toward each other,begin-
ning fusion at the end ofthe eighth weekand completing in the ninth week ofgesta-
tion.There is evidence that transforminggrowth factor (TGF)-�3 is
intimatelyinvolved in regulating secondary palatalfusion by mediating the breakdown
ofthemidline epithelial seam prior to fusion.10Fetal PeriodThe fetal period begins
during the eighthweek,at 60 days�gestation,lasting untilbirth at 40 weeks,and
overall somaticgrowth follows a cephalocaudal growthgradient (Figure 53-9).There is
a prenatalgrowth spurt between 20 and 30 weeks�gestation with the peak growth
velocity at27 to 28 weeks being approximately 2.5 cmper week.The prenatal spurt in
weight isslightly later at 30 to 40 weeks�gestationwith a peak at 34 to 36
weeks.11The ratesteadily decreases during the last trimesterand continues to
decline after birth untiladulthood,with two exceptions.The firstis a small
�midgrowth�spurt that occurs inmany children at 6 to 8 years old that hasbeen
attributed to increased adrenal secre-tion ofandrogenic hormones.The secondis a
dramatic endocrine mediated �puber-tal growth�spurt during adolescence.Growth ofthe
craniofacial complex dur-ing the fetal period is characterized by aconstant rate
during the second trimester.The craniofacial skeletal componentsincrease more in
the anteroposteriordimension than in the vertical or trans-verse,with the exception
ofthe mandiblewhich increases more in the transversedimension in order to maintain
appropri-ate articulation.12During the fetal period the neurocra-nium undergoes
precocious developmentrelative to the viscerocranium with earlierbrain and
neurocranial bone vault growththan facial and masticatory portions oftheskull.This
results in an early proportionalpredominance ofthe neurocranium overthe face that
only reduces to an 8:1 pro-portion by birth.The brain nearly doublesin size from 4
months to birth,achievingabout 25% ofits adult dimension.The for-mation and
maintenance ofcranialsutures are regulated by tissue interactionswith the
underlying dura mater as thebrain develops.13A number ofgrowth fac-tors have been
identified that regulate cra-nial bone growth and suture fusion,including TGF-
�1,TGF-�2,and TGF-�3,bone morphogenetic protein (BMP)-2,BMP-7,fibroblast growth
factor (FGF)-4,insulin-like growth factor (IGF)-I,andSHH.14,15Transcription factors
MSX2 andTWIST also play a role in suture develop-ment,binding to target effector
genes todetermine their expression.16The eyeballsgrow concurrently with the early
braingrowth,increasing facial expansion andseparating the neural and facial
skeletonsto increase skull height.The cranial base growth parallels therapid growth
ofthe cranial vault duringthe fetal period.The anterior cranial basegrows sevenfold
while the posterior cranialbase increases fivefold.The intraethmoidaland
intrasphenoidal synchondroses closebefore birth.The ossification centers that begin
theformation ofthe facial bones late in theembryonic period enlarge during the
earlyfetal period until most ofthe bones havedeveloped into a definitive shape by
Parietal bone Frontal
boneCartilaginousneurocraniumMembranousneurocraniumCartilaginousviscerocraniumMembr
anousviscerocraniumNasal boneMaxillaZygomatic boneMandibleMalleus, incus,
stapesHyoid boneLaryngeal cartilagesEthmoid boneSphenoid bonePetrous partof
temporal boneOccipital boneSquamous portionof temporal boneStyloid processof
temporal boneFIGURE53-7Lateral view of20-week-old embryo illustrating initial
development ofthe cartilagi-nous and membranous neurocranium and
viscerocranium.Adapted from Moore KL,Persaud TVN.The developing human:clinically
oriented embryology.5th ed.Philadelphia (PA): W.B.Saunders;1993.p.361.
Considerations105714 weeks.At this time they begin toremodel as they continue to
grow byintramembranous and/or endochondralossification.The anterior aspects
ofthemaxilla,mandible,and zygoma ofthe fetaland early postnatal face undergo
deposi-tion.This early anterior deposition is nec-essary to permit adequate osseous
mass forthe developing tooth buds ofthe primaryand permanent dentitions.Although
thetooth germs start to develop as early as 6 weeks�gestation,the onset
ofdentalmineralization does not begin until ossifi-cation has occurred.The maxilla
demon-strates a rapid height increase associatedwith dental development.17Once the
pri-mary teeth have erupted,these same ante-rior areas undergo resorption rather
thandeposition to produce the descent ofthemaxilla with continued growth.Mean-while
the posterior,infraorbital,and lin-gual surfaces ofthe maxilla are depositoryin
both fetal and postnatal development.The fetal temporal bone grows faster inheight
than width while the lateral andinferior margins ofthe zygomatic bonegrow faster
than its orbital margin.17The paranasal sinuses,including
themaxillary,sphenoidal,frontal,and eth-moidal,begin developing at the
beginningofthe fetal period.Pneumatization beginsfirst with the maxillary
sinus,starting at 5 months�gestation.It is proposed that aseptomaxillary
ligament,attached to thesides and anteroinferior border ofthe nasalseptum and
inserted in the nasal spine,transmits septal growth,pulling the
maxilladownward.Between the tenth week ofges-tation and birth,the nasal septum
increasesits vertical height sevenfold.The nasal sep-tum growth,together with
neural growthand facial sutural growth,transposes themaxilla inferiorly and
anteriorly.The fron-tomaxillary,frontonasal,frontozygomatic,frontoethmoidal,and
ethmoidolmaxillarysutures grow predominantly in a verticaldirection.The
temporozygomatic and naso-maxillary sutures contribute most oftheanteroposterior
change.The intermaxillaryand zygomaticomaxillary sutures providemost ofthe
transverse expansion ofthe face.Overall the middle and lower thirds oftheface
develop primarily in a downward andslightly forward direction away from thecranial
base due to brain development,maxillary and palatine sutural growth,andpossibly
nasal septum growth.Lateral palatal shelf(bent vertically)Primary palate7
weeksNasal septumNasal capsuleTongueLateral palatalshelf in
verticalorientationNasal septumFIGURE53-8Frontal view offace,coronal section ofthe
stomodeum,and inferior view ofthe palatein 7- and 12-week-old embryos.A,Embryo at 7
weeks showing palatal shelves vertically oriented.Adapted from Sperber
G.Craniofacial development.Hamilton (ON): BC Decker Inc; 2001.p.41,114.
(CONTINUEDONNEXTPAGE)A
1058Part 8: Orthognathic SurgeryAlthough the midsagittal part ofthemiddle face
entirely consists ofnasal septalcartilage during the fetal period,ossifica-tion
leaves only a small anterior part ofthis cartilage remaining postnatally.Cur-rently
there is controversy regarding therole ofthe nasal septum in postnatal
facialgrowth.Some believe it is limited to acompensatory and biomechanical role,and
others believe it serves a more exten-sive role,particularly in promoting
verticalmaxillary growth.Although the mandible is larger than themaxilla during the
embryonic period,themandible approximates the size ofthe max-illa within the first
month ofthe fetal period.The three secondary cartilages ofthemandible do not appear
until the tenth andfourteenth weeks ofgestation,forming onthe lateral and superior
aspects ofthe condy-lar processes.This secondary type ofcarti-lage differs
morphologically from epiphysealand synchondrosal cartilage.18Two ofthesesecondary
cartilages forming at the mentalprotuberance and the coronoid process ossi-fy
before birth,leaving only the cartilage onthe condylar head as a site
ofpostnatalmandibular endochondral growth.This car-tilage never undergoes complete
ossification,providing a means for absorbing functionalforces and retaining growth
potentialthroughout life.Between the thirteenth andtwentieth weeks ofgestation,the
mandiblelags behind the maxilla again while there is atransition from Meckel�s
cartilage to condy-lar cartilage as the primary growth site.Dur-ing the third
trimester there is a significantdeepening ofthe corpus in association withthe
developing dentition.The mandibularramus growth rate is greater than the growthrate
ofthe mandibular body during thistime.19At the time ofbirth the mandibleusually is
equal in size again to the maxilla,although it is often in a retrognathic
positionrelative to the maxilla.Development ofthe permanent toothgerms begins at 16
weeks�gestation,with thefirst permanent molar germs developingposteriorly from the
dental lamina followedby the permanent anterior tooth germsemerging from the
lingual side ofthe prima-ry enamel organs.At birth the primary toothcrowns are
still not completely calcified,asthe first permanent molars begin to
calcify.Postnatal Craniofacial DevelopmentSkeletal DevelopmentDevelopment and
completion ofcranio-facial growth follow the overall somaticSoft
palateUvulaPalatine raphe(site of fusion oflateral palatal shelves)Incisive
foramen12 weeksLateral palatal shelfNasal septumFIGURE53-8 (CONTINUED)B,Embryo at
12 weeks showing fusion following elevation ofpalatal shelves.Adapted from Sperber
G.Craniofacial development.Hamilton (ON): BC Decker Inc; 2001.p.41,116.B
Considerations1059cephalocaudal growth gradient through-out prenatal and postnatal
growth,withcranial vault growth completing before thecranial base,followed by the
nasomaxillaand finishing with the mandible.Duringpostnatal growth the neurocranium
con-tinues to develop ahead ofthe viscero-cranium (Figure 53-10).It increases
fromabout 30% ofits ultimate adult size at thetime ofbirth to 50% by 6 months
ofage,and 75% by 2 years ofage,and nearly 90%by 3 years ofage.By 5 years
ofage,theorbits have reached nearly 80% oftheiradult size.20This is why a child
ofthis ageappears to have a disproportionately largecranium and eyes.After birth
the neuro-cranium increases about five times in size,whereas the viscerocranium
increasesabout ten times in size.There is also a dif-ference in the amount
ofpostnatalincrease in the three dimensions,with thevertical increasing by about
200%,theanteroposterior by somewhat less,and thetransverse by the least at
approximately75%.By 10 years ofage the neurocranialgrowth is nearly 95%
complete,whilefacial growth is only about 60% complete.The craniofacial complex can
bedivided conveniently into four primaryunits:the cranial vault,the cranial
base,the nasomaxilla,and the mandible.Eachofthese units has its growth regulated
tosome extent by both intrinsic and extrinsiccontrols.Our understanding
ofpostnatalcraniofacial growth has developed in partfrom cross-sectional anatomic
and histo-logic studies ofhuman cadavers and skele-tal material.What has been
particularlyhelpful in supplementing this material is anumber ofNorth American
longitudinalcraniofacial growth records and longitudi-nal implant (used for stable
referencepoints) studies that were gathered fromthe 1940s to the mid-1960s before
radia-tion hygiene and human subject researchstandards became more
stringent.21Cranial VaultAt birth the cranial bonesare separated by sutures with
fontanelleswhere the corners ofthe bones meet,per-mitting compression ofthe skull
duringthe birthing process (Figure 53-11).Post-natal bone growth results in
narrowing ofthe sutures with all ofthe fontanelles clos-ing within the first 2
years.The pressuresexerted by the developing brain determinethe size and shape
ofthe cranium.As thebrain expands,the pressure creates tensionacross the sutures
and compressionagainst the cranial bones,resulting inintramembranous bone growth by
sutureand surface apposition.Remodeling ofthecranial bones to a flatter shape is
necessaryto adapt to the expanding surface ofthebrain.This occurs primarily
fromendocranial resorption and ectocranialapposition.Although suture
apposition121638Fertilization age in weeks 9FIGURE53-9Changing fetal body
proportions with all stages drawn to the same total height.At thestart ofthe fetal
period,the head is about halfthe length ofthe fetus,and by birth,it is one-
quarterthe length.Adapted from Moore KL,Persaud TVN.The developing human:
clinically oriented embry-ology.5th ed.Philadelphia (PA): W.B.Saunders;
1993.p.97.54321FIGURE53-10Changing proportions ofthe postnatal skull with all
stages enlarged to the same skullheight and oriented in the Frankfurt horizontal
plane with skull height divided into fifths.A,Neonate,showing the viscerocranium
representing one-fifth ofthe total height; B,3-year-old and C,adultshowing the
proportional increase in the height ofthe viscerocranium relative to the
neurocranium.Adapted from from Sarnat BG.Normal and abnormal craniofacial
growth.Some experimental andclinical considerations.Angle Orthod 1983;53:263.ABC
1060Part 8: Orthognathic Surgeryplays a larger role than surface appositionin
overall cranial vault capacity,the post-natal shape primarily is determined
byextrinsic factors.By 6 to 7 years ofage the inner table ofthe cranial bones
becomes stable due tothe cessation ofcerebral growth.However,the outer table
continues to remodel inresponse to extracranial muscular forces.The temporal
muscles tend to laterallycompress the cranium,forming temporalsulci and zygomatic
arches.The lateral andposterior cervical muscles insert primarilyon the squamous
part ofthe temporal andoccipital bones,influencing their shape.Even after
attainment ofthe adult form,the cranial bones continue to thicken dur-ing
adulthood.Cranial BaseCompared with the othercraniofacial units the shape ofthe
cranialbase is relatively stable during growth,duelikely to its greater intrinsic
growth poten-tial.Perhaps more than any other cranio-facial area,growth ofthe
cranial base isgenetically predetermined and influencedthe least by functional
matrices.22,23How-ever,prenatal brain growth may provide aminor extrinsic
influence,causing someflattening ofthe cranial base,since thisdoes not occur with
anencephaly.In addi-tion there is recent evidence that chondralgrowth ofthe cranial
base can be alteredwith mechanical forces.24The anterior cranial base matures ear-
lier than the posterior cranial base withthe posterior intraoccipital
synchondrosesclosing during the second and third yearspostnatally and the anterior
intraoccipitalsynchondroses closing at 3 to 4 years ofage (Figure 53-12).The
sphenoethmoidalsynchondrosis closes at about 6 years ofage.Although the spheno-
occipital syn-chondrosis is not a main growth sitebefore birth,it provides the
greatest con-tribution to cranial base growth postnatal-ly,delaying fusion until
adolescence.Theprolonged postnatal growth period ofthespheno-occipital
synchondrosis permitsposterior growth ofthe maxilla to provideadequate bone for the
developing posteri-or permanent teeth and adequate space forthe nasopharynx.In
addition to endo-chondral bone growth,intramembranousremodeling ofthe cranial base
occurs,including apposition on the basioccipitalbone and anterior margin ofthe
foramenmagnum,resulting in continued lengthen-ing ofthe posterior cranial base even
afteradolescence.Enlargement ofthe sella tur-cica continues postnatally,with the
anteri-or wall stabilizing at about 6 years ofageand the posterior wall continuing
toresorb until late adolescence.NasomaxillaThe prenatal precocity ofneurocranial
growth relative to the facebecomes less predominant postnatally.Nevertheless
considerable postnatal dis-placement ofthe nasomaxilla downwardand forward occurs
due to continuedgrowth ofthe brain and cranial base.ThisLateralCoronal
sutureFrontalAnterolateral fontanelleNasalLacrimalMaxillaMandibleZygomaticSphenoid
greater wingSquamous temporalPetrous
temporalOccipitalsPosterolateralfontanelleParietalSuperiorSagittal
sutureAnteriorfontanelleFrontalCoronal sutureFrontal sutureOccipitalLambdoid
suturePosteriorfontanelleParietalPosteriorSagittal sutureParietalFIGURE53-
11Fontanelles and sutures ofthe neonatal skull.Adapted from Sperber G.Craniofacial
development.Hamilton (ON): BC Decker Inc; 2001.p.84.
Considerations1061inferior and anterior maxillary transposi-tion is augmented by
the sutural growthbetween the cranial base and maxilla andgrowth ofthe nasal
septum.Followingbirth the vertical growth ofthe maxillacontinues with contributions
from thefrontomaxillary,frontonasal,frontozygo-matic,frontoethmoidal,and ethmoidal-
maxillary sutures and possibly the nasalseptum (Figure 53-13).The verticaldescent
ofthe maxilla is further increasedby remodeling with resorption on the
nasalsurfaces and the simultaneous appositionon the oral
surfaces.Anteroposteriorgrowth continues with temporozygomaticand nasomaxillary
sutural growth andtransverse growth from intermaxillary andzygomaticomaxillary
sutures.The resultingdownward and forward translation dis-places adjacent bones and
permits ade-quate space for the developing naso-pharnyx and growth at the posterior
aspectEthmoidPresphenoidBasisphenoidNasalFrontonasal
sutureFrontalFrontoethmoidalsuturePresphenoethmoidalsynchondrosisMidsphenoidalsynch
ondrosisSpheno-occipitalsynchondrosisBasioccipitalFIGURE53-12Midsagittal neonatal
cranial base showing sutures and synchondroses.Adapted fromMooney MP,Siegel
MI.51Frontozygomatic suturePredominant directionof growthFrontonasal
sutureFrontomaxillary sutureNasomaxillary sutureZygomaticomaxillary
sutureResorption at point AMidpalatal sutureBone deposition alongalveolar
marginsTemporozygomatic sutureBone depositionalong tuberositiesOverall downward and
forward transpositionof maxilla= vertical= anteroposterior= transverseFIGURE53-
13Nasomaxillary intra-membranous growth at various sites,resulting in an overall
downward andforward transposition ofthe maxillarelative to the cranial
base.Adaptedfrom Sperber G.Craniofacial devel-opment.Hamilton (ON): BC DeckerInc;
2001.p.107.
1062Part 8: Orthognathic Surgeryofthe maxilla and maxillary tuberosities toprovide
adequate space for the develop-ment and eruption ofthe maxillarymolars.Following
the postnatal growth ofthe facial sutures,they serve as sites offibrous union where
some remodeling stillcan take place.In fact a number ofcranialand facial sutures
are interdigitated but stillnot fused even beyond 50 years ofage.Growth
determinants for postnatalnasomaxillary growth are not well under-stood and include
a variety ofintrinsic andextrinsic factors.Passive displacement sec-ondary to brain
and cranial base growth,and perhaps nasal septal growth guidance,are the most
significant influences on thedownward and forward movements ofthemaxilla after
birth until about the seventhpostnatal year.From that age through ado-lescence
these influences dramaticallydecrease as sutural growth and surfaceintramembranous
growth predominate.Maxillary growth also depends to someextent on various
functional matrices.Theorbits�early response to eyeball growth andtheir functional
movement,the influenceofrespiration on the nasal cavity,the influ-ence oforal
function in determiningtuberosity,palatal and alveolar develop-ment,and the
surrounding facial soft tis-sues all contribute functional roles indetermining
growth and remodeling ofthenasomaxilla.25Significant remodeling must occur inorder
to maintain the general shape ofthemaxilla as it is displaced downward.Asmentioned
above,resorption ofthe nasalside ofthe maxilla,providing nasal
cavityenlargement,occurs concomitantly withapposition on the oral side,resulting
indescent ofthe maxilla.Although sec-ondary pneumatization ofthe maxillarysinus
begins prenatally,it does not occurfor the other paranasal sinuses until afterbirth
(first 2 years for ethmoidal andfrontal sinuses and 6 to 7 years for sphe-noidal
sinuses).The vertical growth ofthemaxillary alveolar process is rapid duringdental
eruption,surpassing the verticaldescent ofthe palate threefold.The alveo-lar
development contributes to the depthand width ofthe palate and vertical heightofthe
face.Considerable resorption oftheanterior surface ofthe maxilla minimizesthe
overall forward displacement ofthemaxilla and creates a deeper supra-
alveolarconcavity while increasing the relativeprominence ofthe anterior nasal
spine.Transverse growth occurs by lateral dis-placement ofthe maxillary bodies
bymeans ofthe midpalatal suture and boneresorption on the lateral borders
ofthenasal cavity.Transverse development ofthemaxillary alveolar process continues
withbuccal eruption ofthe posterior teeth.Growth ofthe midpalatal suture ends
afterthe first two postnatal years,but the sutureremains patent until late
adolescence,withfusion usually not being complete until thethird decade.MandibleThe
mandible has the mostdelayed growth and the most postnatalgrowth ofall the facial
bones.Althoughusually in a retrognathic position relativeto the maxilla at
birth,there is rapid post-natal growth that corrects this discrepan-cy.The right
and left bodies ofthemandible are still separate at birth,unitingat the midline
mental symphysis duringthe first year oflife.The primary sites ofmandibular
postnatal growth are theendochondral apposition occurring at thecondylar
cartilages,and the intramembra-nous apposition on the posterior aspectsofthe rami
and the alveolar ridges (Figure53-14).Remodeling in the form ofresorp-tion ofthe
anterior surface ofthe condyle,the anterior contours ofthe ramus,andthe inner
surface ofthe mandibular bodyare integrated with the posterior apposi-tion.The
growth ofthe condylar cartilagescontributes most ofthe total ramusheight,whereas
growth ofalveolar bonecontributes about 60% to the mandibularbody
height.26Proliferation ofcondylarcartilage results in superior and posteriorgrowth
ofthe condylar heads,displacingthe mandible downward and forward inconcert with the
maxilla.Condylar growthappears to involve the sequential involve-ment
oftranscription factor SOX9,expressed by chondrocytes,which regu-lates the
synthesis ofType II collagen,TypeX collagen secreted as matrix,and
vascularendothelial growth factor secreted to regu-late the neovascularization
ofthe carti-lage.27At birth the inclination ofthemandibular condyles is more
horizontal,resulting in a greater increase in lengththan height.During childhood
the inclina-tion becomes more vertical so that condy-lar growth results in a
greater increase inheight than length.However,there is greatvariability in this
inclination within thegeneral population,influencing the degreeto which the
mandibular growth isexpressed in a forward anteriorly rotating,as opposed to
downward posteriorly rotat-ing,direction.Simultaneous remodelingofthe inferior
mandibular border tends toreduce the effect ofthis rotation on
facialmorphology.Although minimal maxillarygrowth occurs after about 10 years
ofage,mandibular growth continues longer,toOverall downward and forward
transpositionof mandible relative to cranial baseBone resorptionBone
depositionUpward and backwarddirection of growthFIGURE53-14Mandibular
intramembranousand endochondral growth,resulting in an overalldownward and forward
transposition ofthemandible relative to the cranial base.An outline ofthe fetal
mandible is superimposed on the adultmandible for size and shape
comparison.Adaptedfrom Sperber G.Craniofacial development.Hamil-ton (ON): BC Decker
Inc; 2001.p.130.
Considerations1063the end ofadolescent growth.This differ-ential growth,typically
characterized by apeak in the rate ofmandibular growth atpuberty,usually results in
the final correc-tion ofthe mandibular position relative tothe maxilla.Ifthe
cranial base is the craniofacialskeletal unit whose growth is least deter-mined by
extrinsic factors,the mandible isthe opposite extreme with its growth high-ly
dependent on the postnatal functionaldemands placed on it.It has a great capac-ity
to adapt to mandibular displacementand accommodate to lingual and labialsoft tissue
and muscular function.Thecondylar inclination,dictating the type ofmandibular
rotation,is determined bythese secondary functional influences.Therelevant
functional matrices include thelateral pterygoid attached to the condylarneck,the
growth and function ofthetongue,the masticatory muscles attachedto the buccal and
lingual aspects and to thecoronoid process,and the facial soft tissueand
musculature,all influencing the ulti-mate size and shape ofthe mandible.Forthis
reason the mandible,more than anyother part ofthe craniofacial complex,may have a
low intrinsic growth potentialthat is significantly increased and regulat-ed in
response to functional demand.Dental DevelopmentThe alveolar processes contribute a
greatportion ofthe vertical height ofthe lowerface.Their development is entirely
depen-dent on the presence and eruption oftheprimary and permanent dentition.Just
asvertical appositional alveolar growthaccompanies vertical dental
eruption,transverse apposition complements trans-verse dental eruption.This minor
contri-bution to the transverse dimension ofthealveolar processes continues until
about 7 years ofage,with eruption ofthe perma-nent incisors.Further transverse
dento-alveolar growth is minimal,occurring witheruption ofthe premolars and
canines.Facial growth and the concomitantincrease in the size ofthe jaws occur pos-
teriorly,creating additional space for thedentition only in the molar
region.Eruption ofthe maxillary teethenhances the vertical dimension ofthemaxilla
with posterior development ofthemaxillary tuberosities to accommodate
thedevelopment and eruption ofthe maxil-lary posterior teeth.In the
mandible,resorption ofthe anterior ramal bordersprovides room for the development
anderuption ofthe mandibular posteriorteeth.Eruption ofthe mandibular teethenhances
the vertical growth ofthemandible and also contributes to theheight ofthe
face.However,compensatorycondylar growth must occur to prevent themandible from
rotating posteriorly as themaxilla grows downward and the denti-tion erupts.Dental
emergence into theoral cavity begins at approximately thesixth postnatal month,and
the primarydentition is established by 2.5 years ofage.The primary incisors begin
to exfoliate at6 to 7 years ofage,and the permanentdentition begins to emerge with
eruptionofthe mandibular incisors and firstmolars.The permanent dentition is estab-
lished by 12 to 14 years ofage except forthe eruption ofthe third molars,con-
tributing to the vertical dimension ofthelower face during adolescent growth.Facial
DevelopmentThe growth ofthe facial soft tissue followsthe underlying facial bones
but is notdirectly correlated with bone growth.Facial soft tissue is thicker
relative to theunderlying skeletal tissue in the youngchild due to subcutaneous
fat.This is oneofthe reasons it is more challenging toassess potential underlying
skeletal dis-crepancies in the young child based onlyon a clinical appraisal.The
thicker soft tis-sue envelope,together with the relativeretrognathic position ofthe
mandible,cre-ates a more convex profile in infancy andearly childhood.Lip thickness
increasesuntil it reaches a maximum at the end ofthe pubertal growth spurt,then
decreasingin late teens and adulthood.28,29These laterchanges,combined with
continued for-ward nasal growth as well as anteriormandibular and chin
projection,leave thelips with a more retrusive appearance andthe nose and chin with
a more prominentappearance.These changes usually create aflatter facial profile in
older adolescentsand adults.This tendency is even greateron average in males than
females,due tothe less common presence ofsubcuta-neous fat,combined with more
nasalgrowth and anterior mandibular and chinprojection in males.The facial soft
tissue also follows thecephalocaudal growth gradient,with thesoft tissue ofthe
lower face growing morein magnitude and duration than the upperface.The vertical
length ofthe upper lip isa smaller proportion oflower face heightin the
preadolescent,often resulting inlack ofresting lip apposition.During andfollowing
pubertal growth the upper lipproportion increases with greater verticallip growth
than the underlying verticalskeletal growth,creating a more likelychance ofresting
lip apposition in adults.30There is significant growth in thelength ofthe nose
during adolescence,influencing the facial balance between thenose,lips,and
chin.31In fact the verticalnasal growth is much greater than antero-posterior or
transverse nasal growth.Nasalgrowth during adolescence is primarilylimited to
cartilage and soft tissue since thenasal bones usually have completedgrowth
earlier.The nasal shape oftenchanges prior to adolescence with theupper nasal
dorsum developing superiorlyand anteriorly,with the lower nasal dor-sum more often
following the lower facialgrowth pattern.In other words,individu-als who have a
more anterior and superiorrotational pattern oflower face growthwill exhibit a
similar rotation ofthe lowernasal dorsum.There is some evidence thatskeletal Class
II jaw relationships usuallydemonstrate a more prominent nasal
1064Part 8: Orthognathic Surgerybridge and convex dorsum than balancedjaw
relationships.32The upper third ofthe face grows themost rapidly early in life due
to braingrowth and achieves its ultimate size earli-est,finishing most growth by 12
years ofage.Orbital height already reaches 55% ofits adult height at birth and 94%
by 7 yearsofage.33The middle and lower thirds ofthe face are less affected by brain
growth,growing more slowly and for a longertime.Most ofthe middle third growth
iscompleted later during puberty,with thelower third ofthe face continuing to
growbeyond puberty into adulthood.In addition to this vertical sequentialgrowth
gradient,craniofacial growth doesnot take place at an equal rate in the threeplanes
ofspace.The completion ofgrowthfollows a sequence where transverse growthfinishes
first,followed by anteroposteriorand finally vertical growth.The face reflectsthe
early transverse neural expansion ofthecranium,the early fusion ofthe
mandibularsymphysis,and the early growth cessation ofthe midpalatal suture during
the first fewyears oflife.This presents clinically as a dis-proportionately wide
face relative to theheight in the infant and young child.As themaxilla and mandible
displace and growdownward and forward,the anteroposteriorand vertical growth begin
to take propor-tionately greater roles.The growth rate ofthe maxilla slows down
after about 10 yearsofage,and together with anterior maxillaryresorption,reduces
the relative anterior pro-jection ofthe midface.The maxillary lengthreaches
maturity prior to the upper facialheight,which is followed by mandibularlength and
finally ramus height.34Thesomewhat retrognathic position ofthemandible at birth is
usually corrected earlyin postnatal life.The mandible grows for alonger duration
than the maxilla,typicallyundergoing a growth spurt at puberty.Anteroposterior
growth is accompaniedand then followed by vertical facial growth,often continuing
well beyond puberty,evenin to the third and fourth decades.There are gender
differences in facialgrowth,with males characteristically hav-ing volume changes
ofgreater magnitudethan females.Females have much less nasalgrowth on average,with
many not evenexhibiting a pubertal nasal growth spurt,incontrast to males who
characteristicallyhave a nasal growth spurt throughoutpuberty.Females have earlier
soft tissuegrowth that follows their earlier pubertyand they have greater lip
thickness at allages.The flattening ofthe facial profileduring adolescence is less
dramatic infemales,due in part to their fuller lips,butalso due to females having
less forwardmandibular growth projection and chingrowth.Females have on average
more latevertical maxillary growth than males.Ifmandibular growth is not matching
theselate maxillary changes,the mandible trans-lates downward and
backward,resulting ina more convex profile.Not only are malefacial volume changes
on average greater inmagnitude,but the duration ofthe changesis longer,and there is
more predominanceofvolume increase in the lower third oftheface.35Males are on
average more likely tohave late mandibular growth that may bebeneficial in
improving a maxillary protru-sion or mandibular retrusion,but is disad-vantageous
when a mandibular prog-nathism or maxillary retrusion is presentprior to late
growth.Growth and Facial Changes during AdulthoodThere has been awareness since the
latenineteenth century that human growthcontinues beyond adolescence,at least
untilthe fourth or fifth decade oflife.36Never-theless investigators in the mid-
twentiethcentury were surprised to find that facialgrowth continues into the sixth
decade oflife.37More recently it was found that thecraniofacial complex remodels
throughoutadulthood,with thickening ofthe frontalregion ofthe cranium and a
symmetricmodest increase in the size ofthe cranium,cranial base,maxilla,and
mandible.38,39During the past two decades there havebeen a number oflongitudinal
craniofacialgrowth studies that have examined changesduring
adulthood.40�44Evaluation oftheserial cephalometric radiographs revealedthat
craniofacial growth continues withincreases in both anteroposterior and verti-cal
dimensions at all age levels,similar tothe changes seen during adolescence,but ofa
much lesser magnitude and rate.Femalesgrow less and their craniofacial growth
isexpressed more vertically with posteriormandibular rotation,whereas males tend
togrow with anterior mandibular rotationduring adulthood,thereby straighteningtheir
profile (Figure 53-15).Typical lip changes during adulthoodinclude less prominence
with decreasedthickness and thinning ofthe vermilion,with male lips continuing to
appear moreretrusive with age.Female lips generally donot become more retrusive and
their lowerlip thickness tends to increase slightly.Thelips become positioned more
inferiorly,resulting in less vertical display ofmaxil-lary incisors and less lip
separation.45Thenose continues to increase in size in alldimensions,but more so in
males,with thenasal tip dropping inferiorly.46There isdeepening ofthe nasolabial
folds and theoral commissures tend to sag inferiorly.There is more prominence ofthe
pogo-nion due to continued soft tissue increase,but this is typically limited to
males.The biologic regulator mechanism forinitiating and directing
craniofacialgrowth and dental eruption timing,pat-tern,and rate remains a poorly
under-stood phenomenon.It is clear that it is acomplex mechanism,influenced by
anintricate interaction ofgenetic,epigenetic,and local environmental
factors.Factors Influencing Craniofacial GrowthCraniofacial growth is a complex
processinfluenced by both prenatal and postnatalgenetic and environmental
factors.Theprincipal influence on craniofacial growth
Considerations1065and morphogenesis is one ofmultifactori-al genetic
control.However,the interac-tion ofthis genetic control with environ-mental factors
is a complex one,and it isusually impossible to accurately differenti-ate between
these influences.Prenatal FactorsPrenatal defects ofcraniofacial develop-ment can
be classified conveniently intothree categories:(1) malformation�amorphologic
defect ofan organ,part ofanorgan,or larger region ofthe body result-ing from an
intrinsically abnormal devel-opmental process,which is intrinsicallydetermined due
to the genome or a terato-gen,and occurs during the embryonicperiod;(2)
deformation�an abnormalform,shape,or position ofa part ofthebody caused by
mechanical forces,which isinfluenced directly by the fetal environ-ment;and (3)
disruption�a morphologicdefect ofan organ,part ofan organ,or alarger region ofthe
body resulting from theextrinsic breakdown of,or an interferencewith,an originally
normal developmentalprocess,which also occurs during the fetalperiod and may result
from intrauterinepressure as well,but can be ofmetabolic,vascular,and/or
teratogenic origin.47GeneticCraniofacial malformationsarise from disturbance in
morphogenesisas early as the germ layer formation to thefinal formation oforgan
systems at theend ofthe embryonic period.The fourthto eighth weeks�gestation is a
particularlycritical time because this is the periodwhen neural crest migration is
at its mostactive,the facial primordia and dentallaminae are forming,and
neurovascularbundles are being generated prior to facialbone
ossification.Malformations arecaused from chromosome abnormalitiesor single gene
mutations,or are multifac-torial (genetic and/or teratogenic) in ori-gin.Growth
retardation,premature death,and mental retardation seem to be morefrequent in
autosomal recessive or X-linked syndromes.48Craniofacial malfor-mations range from
acephaly to mild facialdefects such as a microform cleft or notch-ing ofthe
lip.Cranial malformationsinclude premature or delayed fusion ofthecranial
sutures,due to mutations infibroblast growth factor receptors and thetranscription
factor MSX2,associatedwith syndromes such as trisomy 21 andcleidocraniodysostosis
or with simply adeformation craniosynostosis.49,50Cranialbase malformations usually
are related tomalformations that affect cartilage growthsuch as
achondroplasia.Apert,Crouzon,and Pfeiffer syndromes involve prematurefusion
ofmultiple facial and cranialsutures as well as cranial base synchon-droses.51Many
facial malformations origi-nate from a deficiency,incomplete migra-tion,or failure
in cytodifferentiation ofneural crest tissue during embryogene-sis.52The result is
a failure in normal for-mation ofthe skeletal and connective tis-sue portions ofthe
facial primordia.Nasomaxillary malformations includedeficiencies and/or absence
offacial bonesthat occur in ectodermal dysplasia ormandibulofacial dysostosis,as
well asfacial clefts that are associated with over250 syndromes.The most common
cran-iofacial malformation is unilateral cleft lip,FemaleMaleFIGURE53-15Composite
lateral cephalometric views offemale and male showing longitudinalgrowth changes
from young adult (broken line at mean age 17) to middle age adult (solid lineatmean
age 47 to 51).Note the continued downward and forward skeletal and soft tissue
growth withrelative flattening ofthe lips.Adapted from Behrents RG.40
1066Part 8: Orthognathic Surgeryaffecting 1 in 700 to 800 births.Malforma-tions
that affect the mandible range fromthe rare absence (agnathia),to variousforms
ofmicrognathia,associated with anumber ofsyndromes,such as mandibulo-facial
dysostosis (Treacher Collins syn-drome) or Turner syndrome,to macrog-
nathia,associated with hyperpituitarism orhemifacial hypertrophy.Two more common
chromosomaldisorders that result in growth retardationare Down syndrome and Turner
syn-drome,both ofwhich are characterized byshort stature and brachycephaly.The pro-
truding tongue typical ofDown syn-drome usually results in an anterior open-
bite,whereas a narrow high-arched palateoften is seen with Turner
syndrome.TheRussell-Silver syndrome is a chromosomaldisorder characterized by poor
fetal andpostnatal growth and small triangularfacies.Other syndromes associated
withprenatal growth retardation includeBloom syndrome,de Lange
syndrome,leprechaunism (mutations ofthe insulinreceptor gene),Ellis-van Creveld
syn-drome,Aarskog syndrome,Rubenstein-Taybi syndrome,Perheentupa syndrome,Dubowitz
syndrome,and Johanson Bliz-zard syndrome.53Single-gene disorders that result in
fetalovergrowth include Sotos syndrome,Weaversyndrome,and Beckwith-Wiedemann syn-
drome.Sotos syndrome includes craniofacialfeatures
ofmacrocephaly,dolichocephaly,aprominent forehead,hypertelorism,promi-nent
ears,high-arched palate,and mandibu-lar prognathism.The Beckwith-
Wiedemannsyndrome,another example ofuniparentaldisomy,is associated with excessive
somaticand specific organ growth (eg,macroglossia)apparently caused by excess IGF-
II.In spite ofthe overgrowth with these disorders thatextends from the fetal period
into early child-hood,both lead to early epiphyseal fusion,resulting in adult short
stature.Klinefeltersyndrome (XXY) is a chromosomal disorderthat leads to postnatal
extended growth frompubertal failure,resulting in tall adult stature.An example ofa
single-gene growthdisorder is achondroplasia,the most com-mon form ofhuman
dwarfism,which isautosomal dominant with complete pene-trance,involving mutations
in the FGFR3gene.Since the primary cartilage ofthecranial base synchondroses is
affected,and not the secondary cartilage ofthemandibular condyles,midfacial
hypopla-sia resulting in a Class III skeletal discrep-ancy is the usual facial
outcome.A single-gene disorder that leads to postnatalovergrowth resulting in tall
adult statureis Marfan syndrome.EnvironmentalPrenatal environmentalgrowth factors
are those not directly deter-mined by the genome,including cytoplas-mic and
extracellular contents in theembryo or fetus and the placenta,influ-enced by the
mother and her interactionwith the external environment.Some ofthese environmental
factors may be inter-nal (such as focal embryonic hemor-rhages) or external (from
maternal malnu-trition,metabolic factors,and disease,orexposure to
pollutants,chemicals,drugs,infectious agents,or radiation),and mayimpair normal
growth or act as teratogensduring either the embryonic or fetal peri-od ifthe
maternal exposure is large or fre-quent enough (Figure 53-16).Cytomegalovirus and
rubella areexamples ofpathogens that can causemicrocephaly,hydrocephaly,and
microph-thalmia.Glucocorticoids,phenytoin,ethylalcohol,tobacco
smoke,aspirin,andretinoic acid (a vitamin A metabolite) areexamples ofan ever-
increasing number ofsubstances that are being identified as ter-atogens,causing
cleft lip and palate as wellas other craniofacial anomalies.54Terato-gens have
distinct mechanisms ofactionand are selective to certain target cells,butthe
severity ofthe resulting malformationis variable.It is speculated that the range
ofphenotypic effects caused by a teratogen isdue to factors that include the
concentra-tion or method ofdelivery,the timing andduration ofexposure,variations in
suscep-tibility,and synergistic interactions amongteratogenic compounds.55Even in
theabsence ofany detectable malformations,serious long-term physical and
mentaldevelopment can result from drug intakeduring pregnancy.When the fetal period
begins,environ-mental factors can still have a profoundgrowth effect on the
developing fetus.Maternal malnutrition adversely affectsfetal growth.56Maternal
diet compositionis relevant,with a high-protein diet beingassociated with increased
linear fetalgrowth and a high-fat diet linked to anincreased birth weight.Maternal
con-sumption ofalcohol,recreational drugs,ortobacco all have an important
negativeinfluence on growth in utero as well asduring the first year
oflife.57�59Evenmaternal exposure to passive tobaccosmoke reduces fetal
growth.60Frequenthigh maternal noise exposure has beenshown to adversely affect
prenatal growth,perhaps related to the stress imposed.61Maternal pathology such as
rubella is par-ticularly detrimental ifit occurs in the firsttrimester,causing a
growth deficit with nolong-term recovery.62Intrauterine pressures can result
indeformations or disruptions.Intrauterinerestrictions can result in mild to
severedeformations that can present as mild facialor cranial asymmetry.Some
isolated formsofcraniosynostosis,causing cranial defor-mations such as
plagiocephaly,may becaused from intrauterine mechanical fac-tors.63These
deformations may resolveafter birth with catch-up growth but usual-ly require
orthopedic or surgical interven-tion during infancy.Another deformationis the Robin
sequence whereby retrognathiafrom posterior restraint ofthe mandibleforces the
developing tongue into a posteri-or position,often acting as a
mechanicalobstruction that prevents elevation ofthepalatal shelves,resulting in an
isolated cleftpalate.A disruption is a typically more seri-ous anomaly than a
deformation,from the
Considerations1067standpoint ofboth treatment and futuregrowth,because it presents
as a morpho-logic and functional defect that requiressurgical repair.An example ofa
disruptionis where a strand oftorn amnion or amni-otic band is swallowed by the
fetus,result-ing in a facial cleft that is not located at asite ofembryonic
fusion.The hormonal regulation offetalgrowth is not well understood.Fetalandrogens
appear to be growth promoters.At midgestation the level ofgonadotropinis similar to
pubertal levels.64Althoughthere is some evidence that estrogen pro-motes fetal bone
development,there arealso data that suggest that it inhibits fetalgrowth.65,66There
is a marked and pro-gressive increase in prolactin during lategestation.Before 12
weeks�gestation,maternal hypothyroidism can have long-term deleterious effects on
hearing andintelligence,but neither maternal nor fetalhypothyroidism has an
appreciable effecton fetal length or weight.However,whenboth conditions are
present,linear growthis still unaffected but there is
incompletepulmonary,cardiovascular,and skeletalmaturation.67Although poorly under-
stood,insulin appears to have an impor-tant role in regulation and promotion
offetal growth.Maternal diabetes increasesfetal length and weight,whereas
fetalinsulin deficiency results in decreasedlength and weight at birth.68Although
growth hormone (GH) isessential for postnatal growth,growth inutero and probably in
the first 2 years oflife is largely GH independent.69,70Never-theless IGF-I and -II
play important rolesin determining fetal growth,but the spe-cific nature ofthese
roles are not wellunderstood.IGF-II is important in sup-porting fetal growth during
early gestationwhereas IGF-I has a greater role duringlater gestation and
especially in postnatallife.71The fetal roles ofgrowth factors suchas
nerve,epidermal,and platelet-derivedgrowth factors also remain
unclear.Other123456789Central nervous systemHeartUpper limbsEyesLower
limbsTeethPalateExternal genitaliaEar1620�3638Period of dividingzygote,
implantation,and bilaminar embryoNot susceptibleto teratogensAge of embryo (in
weeks)Fetal period (in weeks)Full termPrenatal deathMajor congenital anomalies
(dark blue)Functional defects andminor congenital anomalies (light
blue)CentralnervoussystemLimbsHeartEarExternal genitaliaCommon site of teratogenic
actionHeartEyeHeartEyePalateBrainTeethBrainEarFIGURE53-16Susceptibility to
teratogens during periods in prenatal human development.During the first two
weeks�gestation,damage from the ter-atogen results in death ofthe conceptus,or
damages only a few cells,allowing recovery by the embryo to develop without birth
defects.Dark blue indicateshighly sensitive periods when major defects may be
produced (eg,amelia,absence oflimbs).Light blueindicates less sensitive periods
when minor defectsmay be produced (eg,hypoplastic thumbs).Adapted from Moore
KL,Persaud TVN.The developing human: clinically oriented embryology.5th
ed.Philadelphia (PA): W.B.Saunders Co.; 1973.p.156.
1068Part 8: Orthognathic Surgeryfetal growth factors include hematopoieticgrowth
factors,fibroblast growth factors,vascular endothelial growth factor,andmembers
ofthe TGF-�family.72The placenta functions as an addition-al endocrine
organ,providing a secondarysource ofhypothalamic,pituitary,adrenal,and gonadal
hormones and growth fac-tors.73Placental GH and lactogen can alterthe production
ofmaternal IGF-I.71Maternal IGF-I in turn affects placentalnutrient
transport,increasing fetalgrowth.74Lactogen regulates maternal glu-cose,amino
acid,and lipid metabolism,facilitating nutrient transport to the fetus.Disruption
ofplacental GH or lactogenproduction can occur from vascular dis-ease,infection,or
intrinsic placentalabnormalities,impairing fetal growth.75Postnatal FactorsThe size
ofinfants in the first months oflife is more related to the prenatal environ-ment
than parental height.Ifprenatal fac-tors caused only mild growth attenuationand it
occurred during the last trimester,then postnatal catch-up growth is feasible.An
area ofcraniofacial growth can bedifferentiated as a growth center or growthsite.A
growth center is where there is pri-marily intrinsic genetic growth controlwith a
minimal environmental or func-tional role.Although a growth site also iscontrolled
to some extent by genetic pro-gramming,it is more vulnerable to extrin-sic growth
control,being dependent moreon the functional influence ofthe sur-rounding
tissues.Cranial base synchon-droses,where endochondral ossification ofprimary
cartilage occurs,represent growthcenters.The role ofthe cartilaginous nasalseptum
as a growth center or site remainscontroversial.There is a clearer under-standing
that the endochondral growth ofthe secondary cartilage ofthe mandibularcondyles
acts as a growth site,being great-ly influenced by mandibular and soft tis-sue
function.Areas ofmembranous bonegrowth resulting from sutural or
periostealossification are primarily growth sites andrepresent the bulk ofthe
remaining cran-iofacial complex.There are exceptions,such as craniosynostosis,that
can be dueto an underlying genetic cause.Membra-nous ossification by sutural and
periostealremodeling is essentially the only type ofcraniofacial bone growth that
occurs afteradolescence throughout adulthood.GeneticHeritability appears to have
aneffect on somatic growth,from a greater tolesser extent in the following
order:skele-tal length,skeletal breadth,weight,cir-cumference,and skin folds.By the
sametoken skeletal tissues respond less tochanges in the nutritional
environmentthan soft tissues.76The timing and pace ofmaturation is also genetically
controlled toa large degree.The extent to which hered-ity is the cause ofpostnatal
growth thatresults in jaw discrepancies is controver-sial.It appears that the
genetic influence isparticularly important for excessivemandibular growth and
excessive verticalfacial growth.77,78It is speculated thatprobably no more than 50%
offacialskeletal variation is due to the geneticcomponent with the remaining
halformore due to environmental influence.79Functional forces have a crucial
influencein modifying craniofacial bone growth.Although genetic influence is
important,the membranous viscerocranium is deter-mined to a great extent by
functionalinfluences,with these extrinsic factorshaving the greatest control over
mandibu-lar growth.EnvironmentalThere is a multitude ofpostnatal environmental
factors thatinteract with genetic control mecha-nisms,including
functional,traumatic,endocrine,nutritional,pathologic,psy-chological,cultural,and
climatic,or sea-sonal factors.The functional environment is deter-mined by
neuromuscular behavior neces-sary for survival such as respiration,mas-
tication,deglutition,speech,and posture.However,it is clear that functional influ-
ences at rest (ie,postural activity or thepresence ofa pathologic mass) are
muchmore important than transient musclecontractions and mandibular movementin
influencing craniofacial growth.80Chronic pressure alters regional skeletalgrowth
and may be used to improve orcorrect some craniofacial deformities.81Habitual
behavior such as non-nutritivesucking and other oral or postural habitsalso may
have an impact on growth ifit ispresent with great enough frequency
andduration.82,83Mastication limited to oneside for sufficient duration can
causeasymmetric mandibular growth.84There issome evidence that diet consistency has
aneffect on mandibular morphology.85,86The extent ofmasticatory muscularand dental
development can modify themorphology ofskeletal superstructures,including the
temporal fossae and sagittalcrests,the zygomatic arches,the lateralpterygoid
plates,the angular and coro-noid processes and rami ofthe mandible,and parts ofthe
temporomandibularjoints.87The size and function ofmastica-tory muscles has been
correlated withfacial morphology.88�90Other studies havedemonstrated an atrophic
effect frommuscle denervation.91,92However,it alsois clear that external
craniofacial bonegrowth nevertheless can occur in theabsence ofany muscle
function.93,94Growth deficiency due to neuromus-cular deficits can occur in muscle
weak-ness conditions such as muscular dystro-phy.The difficulty in returning
function tothe area makes such conditions particular-ly resistant to
treatment.However,ifthemuscle is normal,it appears that the nor-mal force range
ofmasticatory muscularfunction in the general population doesnot significantly
affect facial growth.95Long-term impairment ofnasal breathinghistorically has been
viewed as a cause oflong face deformity,but this assumptioncontinues to be
controversial.96There is
Considerations1069less disagreement about a relationshipbetween nasal obstruction
and facialdeformity than there is with the extent andduration ofmouth breathing
necessary tocause a deformity.Postnatal surgery during infancy forcongenital
malformations such as cleft lipand palate introduces scarring that isresponsible
for some midfacial growthattenuation.Typical surgery to closepalatal clefts
requires that mucoperiostealflaps be raised and moved medially andposteriorly.This
results in denuded bonyareas that will heal with the formation ofscar tissue bands
ofvariable size and elas-ticity.This scar tissue usually connectsacross the maxilla
and includes the palatalbones and possibly the pterygoid plates.Itis thought that
the presence ofthis scartissue during postnatal growth compro-mises midfacial
growth.97The longerpostnatal surgery can be delayed,the lessgrowth is
affected.Perinatal or postnatal trauma to thecraniofacial complex can modify
growthifthere is limitation ofblood supply ormechanical constriction due to
scarring.Extensive midfacial trauma can causemidface growth deficiency as a result
ofthe loss ofintrinsic nasal septal growthor from a structural collapse that pre-
vents normal morphologic expression ofgrowth.98Untreated burns ofthe headand neck
can cause significant craniofa-cial dysmorphology.99Neurologic dam-age may lead to
muscle paralysis that canalter craniofacial form due to decreasedmuscle
function.There should be cau-tion when considering early craniofacialreconstructive
surgery,since the surgeryitselfmay produce additional scarringthat can exacerbate
the growth attenua-tion.There is no evidence that the use ofrigid plate fixation
for trauma recon-struction causes restrictive growth effectsin addition to the
trauma alone.100Withtrauma involving the mandible,mandibular function must be main-
tained,often requiring physical therapyand the use ofa functional appliance.Aslong
as mandibular ankylosis is prevent-ed,surgery should be avoided whentreating
condylar fractures in children.101Endocrine disturbances originatingfrom pathology
or the environment areamong the most potent regulators ofpost-natal growth.The
primary growth pro-moting hormone,GH,is secreted by thepituitary and regulated by
somatostatinand GH-releasing hormone release fromthe hypothalamus.Studies have
demon-strated increased GH secretion throughoutthe day and night in the
newborn.Howev-er,IGF-I levels are lower at birth and grad-ually increase during
childhood and intoadolescence,indicating an early immaturi-ty in the feedback
loop.Although thegrowth process in utero and in the firstmonths after birth is more
nutritionallydependent than GH dependent,thischanges during the first year
oflife,withfull GH dependence attained during thesecond year.70GH has been shown to
havea direct stimulatory effect on cartilagegrowth,whereas IGF-I acts as a
secondarystimulatory effector.102Most ofour present understanding ofthe endocrine
influence on craniofacialgrowth has developed from assessingchildren who have
diagnosed endocrinedisorders.GH-deficient children haveexcess subcutaneous fat and
overalldelayed facial and cranial base develop-ment,resulting in infantile,but
propor-tional,facies.Dental development isdelayed as well but to a much
lesserdegree than facial or somatic growth.Incontrast the craniofacial growth is
dis-proportionate in an autosomal recessivecondition known as Laron syndromewhere
there is IGF-I deficiency in spite ofincreased serum GH levels.103There is anormal
calvarium with small facialbones,resulting in the forehead appear-ing large and
prominent relative to thesmall recessed face.104This suggests thatsome areas ofthe
face are more directlyaffected by GH than IGF-I.GH excess,usually a consequence
ofapituitary adenoma,results in gigantism ifitoccurs prior to the end ofadolescence
andpresents with overall larger craniofacialdimensions.Acromegaly is the outcome
ifthe GH excess is produced following adolescence,characterized by
increasedperiosteal bone that includes cranial thick-ening,increased size ofthe
frontal sinuses,prominent supraorbital ridges,and nasalenlargement as well as
renewed mandibu-lar condylar cartilage growth,leading tomandibular
prognathism.Hypothyroidism will decrease GHrelease and results in delayed bone
anddental development.105The craniofacialoutcome ofthis deficiency differs fromGH
deficiency primarily by the smallercranium.Anabolic steroids increase cran-iofacial
growth but may lead to excessiveanterior maxillary growth in high
doses.106Testosterone,GH,and IGF-I accelerateendochondral and
intramembranouscraniofacial skeletal growth as well as stat-ural height.Estrogen
appears to decreaseendochondral growth.107,108Although glucocorticoid production
isnecessary for normal growth,glucocorti-coid therapy in the prepubertal child
mustbe carefully managed to avoid its inhibito-ry effect on GH and IGF-I
production,resulting in short stature.109Though thereare no clinical studies
indicating the effecton craniofacial growth,animal modelstudies have suggested a
retarding effect onmandibular condylar cartilage growth andacceleration in dental
eruption.110,111Poor nutrition,hygiene,and healthadversely affect
growth.Insufficient caloricand protein intake is the most commoncause ofgrowth
failure worldwide.112Growth deficiency from malnutrition is pro-portional to the
severity ofthe nutritionaldeficit.Malnutrition is associated withincreased GH but
decreased production ofIGF-I,reallocating calories from anabolic tosurvival
requirements.113It is estimated that55% ofthe morphologic variation ofthecranium is
due to nutritional factors.114
1070Part 8: Orthognathic SurgeryBecause ofthe early rapid growth ofthebrain,the
cranium is affected more byinfant malnutrition than the rest ofthecraniofacial
complex.The size ofthe neu-rocranium decreases in rats subjected
tomalnutrition.115A diet deficient in calciumand vitamin D resulted in cranial
dimen-sional changes in rats.116It is thought thatmaternal vitamin A deficiency
altersendocrine function that causes a distur-bance in chondrogenesis,reducing the
cra-nial base.117Nasomaxillary hypoplasia inhumans can be related to maternal
vitaminK deficiency induced in rats,causing limit-ed nasal septal cartilage
growth.118Proteinmalnutrition in rats decreases the length ofthe skull relative to
the width.119,120Volun-tary undernutrition has become morecommon during
adolescence,especiallywith females trying to decrease weight forathletics and those
with anxiety about obe-sity.This may develop into extreme eatingdisorders such as
anorexia or bulimia,which may result in impaired growth,delayed puberty,and
osteopenia.121Chronic disease such as congenitalheart disease,malabsorption
syndrome(eg,chronic inflammatory disease,cysticfibrosis,celiac disease),chronic
renal orliver disease,chronic anemia,inbornerrors ofmetabolism,chronic
infections(eg,tuberculosis,acquired immunodefi-ciency syndrome),severe
asthma,orother chronic pulmonary disease canadversely affect growth.122There are
avariety ofmechanisms causing thegrowth deficits from these conditions,including
reduced nutritional intake,metabolic disbalance,hypoxia,chronicmetabolic acidosis
protein loss,and oftenthe treatment for the pathology itself.123Medications that
limit potential growthinclude chronic adrenal steroid therapy(used for
asthma,nephritic syndrome,lupus,and other chronic diseases) andcytostatics (for
cancer treatment).Irradi-ation ofthe head and face for childhoodcancer can result
in severe hypoplasia ofsoft and hard tissues.124,125Ifcranial irra-diation is
required in cases ofleukemiaand tumors ofthe central nervous sys-tem,hypothalamic
function can be dam-aged,affecting the release ofhypothalam-ic and pituitary
hormones,notably GH.Chronic psychological trauma,emo-tional deprivation,or
psychosocial stresscan have a profound effect on somaticgrowth,causing a functional
andreversible GH deficiency,often mimickinggrowth disorders that are caused
fromendocrine or nutritional deficiencies.126Additional less important factors
havebeen shown to have a significant influenceon postnatal growth and
development.These include climate,altitude,exposureto environmental
pollutants,andnoise.127�130Future research will increaseour understanding ofthe
role that theseand other yet unidentified environmentalfactors play in altering
human geneticgrowth potential.Orthopedic and OrthodonticClinical
ConsiderationsOrthopedic Treatment forGrowth ModificationJust as our understanding
ofcraniofacialgrowth is continually evolving,the appli-cation ofthis knowledge to
clinical prac-tice is also in a constant state offlux.Thisapplication is
particularly important inorder to determine the appropriate use ofgrowth
modification for treatment ofcraniofacial skeletal discrepancies.A harmonious
esthetic facial appear-ance and balanced dentoskeletal segmentsfacilitating a
functional occlusion are bothgoals that orthodontists and oral maxillo-facial
surgeons work to achieve by meansoforthodontic treatment combined withorthognathic
surgery.However,before asurgical correction is contemplated in agrowing patient,a
determination shouldbe made ifthe patient is a candidate fororthopedic treatment
that may modifycraniofacial growth to improve the skeletalimbalance to a favorable
esthetic and func-tional outcome without the need fororthognathic surgery.It is
well known thatcraniofacial orthopedic devices can gener-ate forces that cause
stress in sutures capa-ble ofmodifying suture growth.131As indi-cated earlier in
the chapter,almost 50% ofthe total cumulative growth ofthe midfaceand mandible
remains between the ages of10 years and adulthood,making it possibleto have an
orthopedic treatment effect onthe jaws during this time.In spite ofover a century
ofclinicalexperience with orthopedic facial appli-ances,it remains controversial as
to whatextent growth can be predictably and per-manently modified by orthopedic
treat-ment.Although there is consensus thatthere is an important genetic influence
onthe outcome ofcraniofacial growth,there isa wide range ofviews regarding the
amountin which postnatal factors,particularlyorthopedic treatment,influence this
out-come.Views range from the beliefthatorthopedic alteration ofjaw relationships
ispredictable and stable,to the contrastingopinion that facial growth is
primarilydetermined genetically and cannot be sig-nificantly altered by orthopedic
treatment.The reality is likely to be somewherebetween these two extreme views.It
hasbeen proposed that the typical range ofskeletal malocclusions include
individualswith normal gene polymorphisms for sig-naling molecules and growth
factors thatattenuate the capacity oftissues and cells toreliably respond to
orthopedic treatment.132The efficacy ofcraniofacial growthmodification has been a
controversial sub-ject for more than a century.At the onset ofthe twentieth century
there was universalconfidence by the orthodontic professionthat forces applied
through the dentition tothe growing face could effectively treatcraniofacial
skeletal discrepancies.After the1920s there was a decline in this convictionby
North American orthodontists.With theinvention ofthe cephalostat,more
preciseskeletal assessment oftreatment outcomesbecame possible during the
1950s.This
Considerations1071resulted in renewed faith in growth modifi-cation,with the
demonstration ofskeletalchanges from the use ofextraoral forceapplied with a
cervical headgear.In Europe there was less controversyregarding craniofacial growth
modifica-tion efficacy throughout the first halfofthe twentieth century.European
ortho-dontists relied primarily on removable�functional�appliances,designed to pro-
vide forces from facial muscles and softtissue function,for facial orthopedic
treat-ment.The separate philosophical pathstaken by European and American ortho-
dontists united in the 1960s,resulting in amore global acceptance ofeither
extraoral(headgear) or intraoral (functional) appli-ances,or a combination ofboth
to facili-tate craniofacial orthopedic treatment.This acceptance gained support
andenthusiasm from results ofbasic researchconducted during the 1970s using
animalmodels.Although this enthusiasm reachedits peak in the 1980s,it was
considerablymoderated in the 1990s from clinical expe-riences and the results
ofretrospectiveclinical studies.There remains little argu-ment that some
craniofacial growth mod-ification is feasible,but there continues tobe controversy
over the nature and extentofthe skeletal change possible in individ-ual patients as
well as the optimal treat-ment timing and appliance type.In addi-tion a reliable
and accurate method ofpredicting the direction,timing,and mag-nitude ofcraniofacial
growth for an indi-vidual has not been devised.The aim ofcraniofacial growth modi-
fication is to alter the growth pattern bychanging the relationships ofthe
jaws.Ifthe skeletal unit is too large,the aim oftheorthopedic treatment is to
attenuate orredirect its growth to improve its relation-ship relative to the
opposing jaw.Ifthe jawis too small,the growth modification treat-ment is aimed at
enhancing or redirectingits growth relative to the larger skeletalunit.Virtually
all ofthe growth modifica-tion appliances to date have been �tooth-borne�to some
extent,so that the orthope-dic forces applied to the skeletal units alsocreate
stress to the teeth that results insome dental movement.Although the
goalofcraniofacial growth modification is tolimit the changes to the skeletal units
withminimal movement ofthe teeth,the realityis that the treatment is a combination
ofskeletal and dentoalveolar changes.There is growing evidence that thelong-term
success ofmany forms ofgrowth modification requires that thetreatment be continued
until facial growthis nearly complete,making early treatmenta less efficient way to
treat many jaw dis-crepancies.The following discussion willsummarize the facial
orthopedic optionswe have for clinical application ofour pre-sent understanding
ofcraniofacial growthin the three planes ofspace.Transverse Orthopedic
TreatmentSincetransverse growth reaches completion earlier than anteroposterior or
verticalcraniofacial growth,it follows that trans-verse skeletal problems should
beaddressed early.The most common trans-verse skeletal problem is maxillary con-
striction,which can be treated in thepreadolescent child,even as early as duringthe
primary dentition.The most recentfederal epidemiologic study,the NationalHealth and
Nutrition Estimates Survey(NHANES-III) conducted from 1989through 1994,indicates
the prevalence ofposterior crossbite is about 5% ofthe USpopulation.133Significant
facial ormandibular asymmetry represents about0.1% ofthe total
population.134Althoughmaxillary orthopedic expansion deviceshave been used since
1860,they fell out offavor for a few decades prior to the 1940sdue to
unsubstantiated concerns regardingtheir safety and effectiveness.135Orthope-dic
expansion ofthe maxilla can beachieved with a variety oftoothborneappliances
(Figure 53-17).These appli-ances apply moderate to high forces to theteeth that are
transmitted as stresses to themaxilla,primarily distracting the mid-palatal sutures
but also producing less pro-nounced stresses to the sphenoid andzygomatic bones and
other adjacent struc-tures.136Within days following initialexpansion,new bone
forms,eventuallydepositing both perpendicular and paral-lel to the edges ofthe
expanded sutures.137Although a large amount ofthe skeletalFIGURE53-17Types
ofmaxillary orthopedicexpansion appliances.A,Quad-helix: An effec-tive skeletal
expansion appliance in the primarydentition.B,Banded Hyrax: This
traditionaljackscrew also can be used as an activation com-ponent for an appliance
bonded to the maxillaryposterior teeth.C,Bonded Minne-expander:This spring-loaded
component also can be usedas an activation component for an appliancebanded to the
maxillary posterior teeth.ABC
1072Part 8: Orthognathic Surgeryexpansion relapses during retention,over-all
stability is good ifthe extent ofsuturalpatency and magnitude ofexpansion aregreat
enough.A potential additional bene-fit to improvement in interarch
transversecompatibility is an increase in archperimeter made possible by the
maxillaryorthopedic expansion.138Although complete fusion ofthe mid-palatal suture
usually does not occur untilthe third postnatal decade,the processleading to fusion
is a gradual one,charac-terized by progressive sutural interdigita-tion and
ossification.139For this reasonmore effective sutural separation,requiringless
force and concomitant dental expan-sion,is possible in the younger child,espe-
cially prior to puberty,during a �phase 1�treatment in the mixed or early
permanentdentition.Treatment prior to the pubertalgrowth velocity peak may result
in greaterlong-term skeletal craniofacial transversewidth.140Treatment may even be
indicatedas early as the primary dentition in thepresence ofa transverse functional
shift.This compensatory functional problemcan result in asymmetric condylar posi-
tioning that may lead to asymmetricmandibular growth and uneven remodel-ing ofthe
glenoid fossae,possibly resultingin permanent facial asymmetry,even
iftheconstricted maxillary arch is corrected at alater date.141Maxillary
constriction with-out a transverse functional shift does notcarry the same urgency
and is convenient-ly treated closer to the onset ofpubertyduring the early
permanent dentition.142Maxillary orthopedic expansion in lateadolescent or
postadolescent patientsshould be attempted with caution.Even ifskeletal expansion
is possible in these olderpatients,the extent ofcircum-maxillarysutural patency is
limited enough to com-promise stability ofthe treatment out-come.It is appropriate
to confirm inter-maxillary expansion with an occlusalradiograph in these
patients,since thedevelopment ofa midline diastema mayonly indicate bending
ofmaxillary bones.Ifthe expansion is limited to lateral tip-ping ofmaxillary
posterior teeth,buccalalveolar bone height reduction and gingi-val recession may
occur.It usually is moreprudent to consider surgically assistedpalatal expansion
for late adolescent orpostadolescent patients to avoid periodon-tal compromises and
instability.The expansion appliance can be band-ed or bonded to the maxillary
posteriorteeth with a spring-loaded or nonspring-loaded palatal jackscrew that
usually isactivated by the patient 0.5 mm per day,delivering from 2 to more than 10
poundsofforce (this may increase to cumulativeloads of20 pounds or more with
multipleactivations in the absence ofadequatesutural separation).The
conventionaldescription for the expansion inducedwith this appliance is �rapid
palatal expan-sion.�However,it is possible to affect slow-er expansion with less
frequent activa-tions,requiring more active treatmenttime,but less retention time
to ensure sta-bility.143It is possible to achieve skeletalexpansion with simpler
appliances such asa W-arch or Quad-helix,provided that thepatient is in the primary
or very earlymixed dentition,when the maxillarysutures are more patent or when a
cleft ofthe hard palate is present (Figure 53-18).Since all ofthese expansion
appliancesare toothborne,unwanted dentoalveolarexpansion is an inevitable conse-
quence.144,145An additional undesirableoutcome is the long-term loss ofabout30%
ofthe skeletal expansion achievedduring active treatment due to therebound
ofstretched palatal tissues.146Tocompensate for these effects,maxillaryexpansion
should be continued until ade-quate overexpansion is achieved,usually tothe extent
that the lingual cusps ofthemaxillary molars are opposing the buccalcusps ofthe
mandibular molars (Figure53-19).Once adequate expansion has beenaccomplished,at
least 3 to 6 months ofretention is necessary to permit new boneFIGURE53-18Intraoral
radiographs demonstrating maxillary skeletal expansion with a Quad-helixduring the
primary dentition.Note the distraction ofthe midpalatal suture.A,Before
expansion.B,After initial expansion.AB
Considerations1073to fill in the spaces created by maxillaryseparation and to
permit time for dissipa-tion ofreaction forces stored in the facialbones that
promote relapse.The over-expansion permits the orthodontist toupright the posterior
teeth in their alveolarhousing without compromising the trans-verse occlusal
correction following reten-tion.Osseointegrated attachments mayhold future promise
for a means ofexpanding the maxilla without buccallytipping posterior teeth (Figure
53-20).147A less common transverse skeletalproblem than maxillary constriction
isasymmetric mandibular deficiency,usuallycaused from a previous trauma
associatedwith unilateral mandibular condylar frac-ture or hemifacial microsomia,a
congenitalfacial asymmetry.In both ofthese condi-tions the affected side exhibits
growth defi-ciency relative to the unaffected or normalside,resulting in a
mandibular deviationtoward the affected side.Ifleft untreated ina growing
individual,the alveolar processescompensate with limited eruption ofthemaxillary
posterior teeth on the affectedside and excessive eruption ofthe maxillaryposterior
teeth on the unaffected side,resulting in an occlusal cant that is higheron the
affected side.It is best to start ortho-pedic treatment with these individualsprior
to the pubertal growth spurt,as earlyas patient compliance will permit.The goalis
to maximize the growth expression onthe deficient side and minimize dentoalve-olar
compensation.The orthopedic appli-ance ofchoice is an asymmetric �hybrid�functional
appliance that is constructed toposture the mandible forward on the affect-ed
side,bringing the chin to the midline.148Posterior dental eruption is attenuated
onthe unaffected side with a bite block anderuption is facilitated on the affected
sidewith a buccal shield and the absence ofinterocclusal acrylic (Figure 53-
21).Sinceuntreated mandibular asymmetries ofthisnature invariably worsen with
growth,orthopedic treatment is considered success-ful ifthe asymmetry remains
stable orimproves.Treatment should not continue ifprogressive asymmetry is apparent
in spiteofreliable appliance use by the patient.Anteroposterior Orthopedic
Treatment:Class IIA Class II skeletal relationshipcan be the result ofa retrusive
and/or defi-cient mandible,a protrusive or verticallyexcessive maxilla,or a
combination ofthese skeletal problems.The prevalence ofthis type ofmalocclusion is
about 15 to20% ofthe US population,with about 2%severe enough to be considered as
handi-capping.133,134Prospective clinical studieshave supported that early growth
modifi-cation therapy may lead to an improve-ment in the skeletal Class II
malocclu-sion.149�151It should be kept in mind thatregardless ofwhether orthopedic
treat-ment is attempted during active facialgrowth,approximately 10%
ofpatientsultimately require orthognathic surgery tofully correct the Class II
malocclusion.150The headgear has been used as ameans ofClass II orthopedic
treatment inNorth America since the late nineteenthcentury (Figure 53-22).An
orthopedicforce ranging from 16 to more than 32 ounces is delivered using elastic
tractionfrom the headgear to a cervical or cranialattachment for 12 to 14 hours per
day,usu-ally for 9 to 12 months.Theoretically theforce is transmitted in a
posterior andFIGURE53-19Maxillary overexpansion to com-pensate for dentoalveolar
expansion and skeletalrebound.Note that the lingual cusps ofthe maxil-lary
posterior teeth are occluding with the buccalcusps ofthe mandibular posterior
teeth.FIGURE53-20Palatal distraction appliance.Reproduced with permission from
Gerlach KL,Zahl C.Traversal palatal expansion using apalatal distractor.J Orofac
Orthop 2003; 64:444.FIGURE53-21Asymmetric �hybrid�functionalappliance: A,right
lateral view;B,frontal view.On the left,unaffected side,posterior dentaleruption is
restricted with an interocclusalacrylic block.On the right,affected
side,themandible is postured forward and posterior den-tal eruption is encouraged
with a buccal shieldand absence ofan interocclusal acrylic block.Reproduced with
permission from Proffit WR,Fields HW.Contemporary orthodontics.3rd ed.St.Louis
(MO): Mosby; 2000.p.370.BA
1074Part 8: Orthognathic Surgerysuperior direction via the teeth through themaxilla
to compress the circum-maxillarysutures,limiting or redirecting
maxillarygrowth.Since the introduction ofstan-dardized cephalometric
radiographs,manyclinical studies have demonstrated thatmaxillary growth can be
altered with theuse ofthe headgear.152�170These clinicaldata have been supported by
primate stud-ies demonstrating that extraoral orthope-dic force directed against
the maxilla atten-uates forward growth and alters boneapposition at the maxillary
sutures.171�179There are some studies that suggest thatmandibular growth may be
enhanced aswell.Since the headgear is a toothborneappliance,there is some maxillary
dentalretraction that accompanies the skeletalchange.Another dentoalveolar effect
is theattenuation ofmaxillary molar eruption,resulting in anterior and
superiormandibular rotation.There is some sup-port for this being the only
clinically rele-vant skeletal effect.180A significant treat-ment effect usually
requires that a headgearbe worn 12 to 16 hours per day with asuperior and posterior
force ofone poundor more per side.Human GH and otherendocrine factors that promote
growthand dental eruption are primarily releasedduring the evening and
night.181�183It isfortuitous that this is the only time ofdaythat one can reliably
expect an adolescentto wear a headgear.Since it is a removableappliance,few
adolescents after the peak ofthe pubertal growth spurt will reliably wearthe
appliance.The alternative orthopedic methodfor treating a Class II skeletal
relationshipis the Class II functional appliance,whichhas been used since the early
twentiethcentury in Europe and since the 1960s inNorth America.These appliances
includethe removable toothborne activator,bio-nator,and twin block,the removable
andprimarily tissueborne Fr�nkel (functionalregulator) appliance,or the fixed
tooth-borne Herbst appliance (Figure 53-23).All ofthese appliances position
themandibular condyles downward and for-ward away from the glenoid fossae.Theo-
retically the distracted condylar positionsreduce the normal compressive
jointpressure on the growing condylar carti-lage and the forward mandibular postur-
ing alters muscle tension on the condyles,stimulating or accelerating the endo-
chondral condylar growth more thanwould normally occur.184There is somesupport from
animal studies that a histo-logic increase in condylar growth can
beachieved.185�187However,clinical studieshave not confirmed that a greaterabsolute
growth is the long-term treat-ment outcome.149,150Some retrospectiveclinical
studies have supported the asser-tion that clinically significant lengtheningofthe
mandible can be achieved withfunctional appliances.188�198Others haverefuted this
assertion.158,199�217Much ofthe skeletal change demonstrated with afunctional
appliance may result fromforces against the maxilla,similar tothose applied with a
headgear,that arecreated from the stretched facial musclesand soft tissues
attempting to return thepostured mandible back to its posteriorand superior
position.158,202,203,208,218�222Because ofthe toothborne nature ofthis
appliance,dentoalveolar changesaccompany the skeletal changes,includ-ing maxillary
dental retraction andmandibular dental protrusion.Clinical studies have
demonstrated fewdifferences in treatment outcome whencomparing the skeletal
response betweenheadgear and functional appliance treat-
ment.168,193,223However,there appears to bemore ofa maxillary effect with head-
gears.150,158,161,168There is more ofamandibular effect with functional appli-
ances.149,150,168,192,205Most functional appli-ances need to be worn for the same
dailyduration as the headgear (exceptions arethe Fr�nkel and Herbst appliances
whichFIGURE53-22Headgear,past and present.An orthopedic force is directed
posteriorly and superiorlyto the maxilla,attenuating circum-maxillary sutural
growth.A,Headgear from the late nineteenthcentury.Reproducedfrom Angle EH.Treatment
ofmalocclusion ofthe teeth.Philadelphia (PA): S.S.White Dental Manufacturing Co;
1907.p.234.B,Contemporary headgear.The appliance is fabri-cated with more durable
materials and has additional calibration and safety features but the overalldesign
has changed little in over a century.Adapted from McNamara JA,Brudon
WL.Orthodonticsand dentofacial orthopedics.Ann Arbor (MI): Needham Press,Inc.;
2001.p.365.AB
Considerations1075are worn full-time) for a significant treat-ment effect.Much like
the headgear,dependable wear is more realistic duringthe evening and at night when
the mostactive facial growth and dental eruptionusually occur.However,like the
headgear,its removable nature prevents it from beingreliably worn by most
adolescents after thepeak oftheir pubertal growth spurt.In the late 1960s,when
European andAmerican facial orthopedic philosophieswere becoming more fully
integrated,amethod was introduced in Europe using aheadgear in combination with a
function-al appliance (Figure 53-24).204,224�227Thisapproach was intended to
provide greatercumulative skeletal growth effects than useofeither appliance
alone,but this has yetto be demonstrated by clinical studies.Although there is
greater generalacceptance that treatment with a headgearor functional appliance may
achieve animproved long-term treatment outcome,there continues to be controversy
over theoptimum treatment time in the growingchild.It has already been
demonstratedthat orthopedic Class II treatment in thevery young child,in the
primary or earlymixed dentition,results in substantialrelapse and recurrence ofthe
originalfacial skeletal pattern by late adoles-cence.228However,there is great
debateregarding the efficacy oforthopedic treat-ment during later mixed dentition
as thefirst phase ofa two-phase treatment ver-sus delaying orthopedic treatment
untildefinitive orthodontic treatment duringpuberty,after the eruption ofthe perma-
nent dentition.Many orthodontists his-torically have preferred the earlier
firstphase since there is substantial potentialgrowth remaining,compliance in
wearingthe orthopedic appliance often is greater,and the arch space for the
remainingerupting dentition may be improved.Theadvocates for a delayed one-phase
treat-ment have contended that comparableskeletal treatment effects can be
achievedduring definitive orthodontic treatment,without putting the patient through
anunnecessary initial phase.229,230Recentprospective randomized clinical trialshave
supported this position,demonstrat-ing that early skeletal improvementachieved from
these appliances seems torepresent accelerated growth and can beused just as
effectively later during puber-tal growth.149�151They also showed thatthere was
substantial individual growthvariability with no reliable predictors for afavorable
growth response identified,andearly treatment did not reduce the needfor dental
extraction or orthognathicFIGURE53-23Class II functional appliances.All ofthese
appliances position the mandible down-ward and forward,distracting the condyles
from the glenoid fossae.This simultaneously creates pos-terior and superior forces
to the maxilla from the facial muscles and soft tissues attempting to returnthe
mandible to its normal position.A,Activator.B,Bionator.C,Twin
block.D,Fr�nkel.E,FixedHerbst.An alternative is to utilize occlusal acrylic and
bond the maxillary portion ofthe appliancewith a removable acrylic splint for the
mandibular arch.A ,C,and D reproduced with permissionfrom Bishara SE.Textbook
oforthodontics.Philadelphia (PA): W.B.Saunders; 2001.p.345.B repro-duced with
permission from Graber TM,Vanarsdall RL.Orthodontics: current principles and tech-
niques,3rd ed.St.Louis (MO): Mosby; 2000.p.488.E reproduced with permission from
McNamaraJA,Brudon WL.Orthodontics and dentofacial orthopedics.Ann Arbor
(MI):Needham Press,Inc.;2001.p.287.ABEDC
1076Part 8: Orthognathic Surgerysurgery during the definitive phase.Thesestudies
indicate that there is no adequateadditional benefit in treatment outcometo justify
the greater burden to the patient,their parents,and the orthodontist,asrepresented
by an early phase that pre-cedes the definitive phase oforthodontictreatment.It can
be concluded from past retro-spective and more recent prospective clini-cal trials
that headgear treatment tends tohave more ofa maxillary restrictive effectwhereas
functional appliances have more ofa mandibular enhancing effect.Eitherapproach can
be satisfactory and should beselected on the basis ofpatient acceptance ofthe
appliance and dentoalveolar side effects(there is more maxillary dental
retrusionwith headgear and more mandibular pro-trusion with a functional
appliance).Itappears that orthopedic treatment duringthe mixed dentition can only
be justifiedwhere there is increased trauma risk (due toexcessive
overjet),sufficient esthetic concernby the patient,or a precocious adolescentgrowth
spurt that substantially precedesdental development.Treatment at an earlierage has
been further justified by the argu-ment that there is lack ofreliable means
ofpredicting mandibular growth and thatimproved cooperation usually is presentwith
the younger patient.231Although improvement in skeletaldiscrepancy is expected,the
Class II cor-rection usually is due to a combinedresponse ofboth the dentoalveolar
andskeletal segments.Both headgear andClass II functional appliance use can
beeffective in limiting downward and for-ward eruption ofthe maxillary
molars.However,the functional appliance tendsto promote upward and forward
eruptionofmandibular molars,which may com-plement the correction in deep
overbitecases but is counterproductive in patientswith a long face.Since Class II
orthopedicappliances are toothborne,there may besome unwanted dentoalveolar
change,including retraction ofmaxillary anteriorteeth and protraction
ofmandibularanterior teeth.This compensatory changemay be undesirable ifthe
skeletal discrep-ancy ultimately requires orthognathicsurgery for correction.With
the advent ofosseointegrated attachments there maybe the future possibility
ofpreventingunwanted dentoalveolar change byattaching a force system directly to
theseattachments rather than using tooth-borne attachments.Anteroposterior
Orthopedic Treatment:Class IIIA Class III skeletal relationshipcan be the result
ofa retrusive and/or defi-cient maxilla,a large and/or prognathicmandible,or most
often,a combination ofthese skeletal problems.The prevalence ofthis type
ofmalocclusion is about 3 to 5% ofthe US population,with about 0.3% severeenough to
be considered as handicap-ping.133,134Since the late nineteenth century,when
headgear was being used for Class IIskeletal problems,the chin cup was theappliance
used for orthopedic treatment ofskeletal Class III problems (Figure 53-
25).Theoretically an orthopedic force is trans-mitted to the mandibular
condyles,com-pressing the condylar cartilage and limitingendochondral growth in
order to decreasethe ultimate length ofthe mandible.232Pri-mate studies suggest
that mandibulargrowth can be limited with heavy full-timeforces directed against
the condyles.233Full-time wear is unrealistic with humans andmost clinical studies
have demonstrated thatmandibular growth is not restrained,butrather vertically
redirected from chin cupwear,resulting in decreased chin promi-nence at the expense
ofincreased faceheight.234�238Studies also have suggested thatthe long-term
stability ofthese changes ispoor.239,240Treatment with a chin cup maybe an
acceptable option for an individualwith mandibular excess associated withdecreased
facial height but is contraindicatedwhere there is a normal or excessive
facialheight,since the treatment outcome simplywould be trading one deformity for
another.Class III functional appliances alsohave been developed,limiting eruption
ofmandibular posterior teeth and promot-ing eruption ofmaxillary posterior
teeth.These functional appliances have fewadvocates due to their effectiveness
beinglimited to dentoalveolar changes and theirinability to promote forward
maxillarygrowth or attenuate mandibular growth.241FIGURE53-24Combination headgear
andremovable functional appliance.The inter-occlusal acrylic permits the orthopedic
force to betransmitted further anteriorly and superiorlythrough the center ofthe
maxilla.A,Intraoralpart ofappliance with headgear tubes embeddedin the
interocclusal acrylic.B,Extraoral part ofappliance.Reproduced with permission
fromBishara SE.Textbook oforthodontics.Philadel-phia (PA): W.B.Saunders;
2001.p.341.AB
Considerations1077Jean Delaire,a French dentist,wasresponsible for developing the
protractionheadgear or facemask,the most effectiveorthopedic appliance for skeletal
Class IIIproblems since its introduction in theearly 1970s (Figure 53-
26).242Delaire rec-ognized that the offending jaw in many ofthe skeletal Class III
problems was themaxilla,so he departed from the historicfocus on the mandible and
directed treat-ment at the retrusive or deficient maxilla.The appliance creates
tension in the circum-maxillary sutures with elasticsfrom the maxillary dental arch
to a framethat uses the forehead and chin to dissi-pate the force
anteriorly.Primate studieshave demonstrated adaptive responses ofthe sutures to the
stress from the distrac-tion forces produced by this appliance.137Depending on the
developmentalstage and size ofthe patient,a protractiveforce ranging from 2 to 4
pounds isapplied to the facemask in an anterior andslightly inferior direction
relative to theocclusal plane for 12 to 16 hours per day,usually for 6 to 9
months.Clinical studieshave demonstrated clinically relevantmaxillary skeletal
protraction downwardand forward on average with this appli-ance,with some
concomitant protractionofthe maxillary teeth due to the tooth-borne nature ofthe
intraoral part oftheappliance.243�-246However,as with otherforms ofcraniofacial
orthopedic treat-ment,there is substantial variability andan unpredictable patient
response to theappliance,ranging from no appreciableskeletal change to about 5 mm
anteriormaxillary movement.247It is important toachieve overcorrection ofthe
anteriorcrossbite and anterior overbite since thereis some relapse following
discontinuationoftreatment.248Additional effects ofmax-illary orthopedic
protraction often includerotation ofthe maxilla downward in theposterior and upward
in the anterior,downward and backward rotation ofthemandible,and retraction ofthe
mandibu-lar incisors due to the reactive posteriorforce dissipated on the
chin.These addi-tional orthopedic and dentoalveolarchanges that accompany maxillary
skeletalprotraction would be contraindicated for aClass III pattern with excessive
verticaldevelopment or where mandibular excessis the underlying cause ofthe
problem.249The timing offacemask therapy usu-ally is recommended for patients in
theprimary to early mixed dentition (ie,ages4 to 8),due to the increased patency
ofthemaxillary sutures and compliance withappliance wear at this age.250,251As
thepatient ages there is more interdigitationand ossification ofthe
sutures,resultingin less skeletal and more dental responseto the protraction
forces.Neverthelessmost clinical studies have found few dif-ferences between early
and late treatmentup until puberty.251�254The stability ofmaxillary
orthopedicprotraction with a facemask is variableand dependent on favorable facial
growthfollowing active treatment.However,it iscommon for the original facial
growthpattern to resume after treatment,oftenresulting in relapse ofthe skeletal
dis-crepency.The best overall success rate atthe end ofadolescent growth cannot
beexpected to be more than 50%.255Oneshould expect that about 20% ofthesepatients
will ultimately require orthog-nathic surgery to fully correct the Class
IIImalocclusion.248The patients who relapseusually have mandibular growth
duringlate adolescence that overwhelms the earli-er correction.Long-term efficacy
offace-mask treatment has not been fully studied.Class III orthopedic appliances,as
withClass II devices,result in dentoalveolarmovements that accompany the
skeletalchanges.Treatment with the facemaskcauses protraction ofmaxillary
anteriorteeth and retraction ofmandibular anteriorteeth.The development
ofosseointegratedattachments may make it possible to trans-mit the orthopedic
protraction force tointraoral skeletal attachments that preventundesirable
dentoalveolar changes.256Vertical Orthopedic TreatmentVerticalmaxillary excess
presents with a maxillathat is inferiorly positioned,resulting inexcessive vertical
display ofmaxillaryFIGURE53-25Class III chin cup appliance.A retractive orthopedic
force is directed against the chinposteriorly and superiorly toward the condylar
heads.A,Chin cup from the late nineteenth century.Reproducedfrom Angle EH.Treatment
ofmalocclusion ofthe teeth.Philadelphia (PA): S.S.WhiteDental Manufacturing Co;
1907.p.194.B,Contemporary chin cup,with minimal change in design,but fabricated
with more comfortable and durable materials.Reproduced with permission from Prof-
fit WR,Fields HW.Contemporary orthodontics.3rd ed.St.Louis (MO): Mosby;
2000.p.271.AB
1078Part 8: Orthognathic Surgeryincisors relative to the upper lip,anddownward and
backward rotation ofthemandible,resulting in an increasedmandibular plane angle and
lower faceheight.The prevalence ofvertical facialproblems is less than 5% ofthe US
popu-lation with about 0.3% considered ashandicapping.133,134The orthodontist
presently does nothave very effective nonsurgical options tomanage vertical
skeletal problems.Ortho-pedic treatment strategy is directed atrestraining vertical
maxillary growth andposterior dental eruption in order to pro-mote anterior and
superior mandibularrotation.A high-pull headgear is used toapply a superior
intrusive force of2 to 4 pounds to inhibit eruption ofmaxillaryposterior teeth and
compress circum-maxillary sutures to limit the downwarddevelopment ofthe
maxilla.With excep-tional daily (14 to 16 hours) and long-term (throughout
adolescent growth)wear,mandibular growth may be redirect-ed in a more anterior than
downwarddirection,improving a Class II skeletal dis-crepancy with vertical
maxillary excess.However,this is counterproductive whentreating vertical maxillary
excess with anormal or prognathic mandible,since anydecrease in vertical maxillary
developmentwould promote anterior mandibular rota-tion,thereby aggravating the
Class III mal-occlusion.An alternative to the use ofhigh-pull headgear is a
removable ortho-pedic appliance that incorporates interoc-clusal acrylic bite
blocks in order to stretchthe facial musculature and soft tissuebeyond the normal
resting vertical dimen-sion,creating a reactive intrusive forceagainst the
mandibular as well as maxil-lary teeth.257,258As with the high-pullheadgear
option,exceptional daily andlong-term wear is necessary to obtain anyappreciable
benefit.Repelling magnetshave been embedded in the opposingacrylic bite blocks to
accentuate the intru-sive force.259�261Most ofthe treatmentbenefit from this method
appears to belimitation ofposterior vertical dentoalve-olar development rather than
any appre-ciable skeletal effect.261�263A significant treatment effect byeither the
headgear or interocclusal biteblock is rare since it is dependent on thepatient
wearing the appliance at least 14 to 16 hours per day over a number ofyears.In fact
significant clinical benefitfrom the use ofinterocclusal acrylic alonemay require
closer to 16 to 24 hours perday.As with the Class II orthopedic meth-ods these two
methods have been com-bined into one appliance with the hopethat this approach may
provide greatercumulative skeletal growth effects thanuse ofeither appliance
alone.264In combi-nation with the interocclusal bite blockthe force transmitted by
the headgear canbe distributed over all ofthe teeth FIGURE53-26Class III
protraction headgear or facemask.A protractive orthopedic force is directed
downward and forward,with the force being dissi-pated on the forehead and
chin,distracting the circum-maxillary sutures to augment anterior maxillary
growth.A,Delaire design.Reproduced with per-mission from Proffit WR,Fields
HW.Contemporary orthodontics.3rd ed.St.Louis (MO): Mosby; 2000.p.516.B,Petit design
(frontal and lateral views).Adapted from McNamara JA,Brudon WL.Orthodontics and
dentofacial orthopedics.Ann Arbor (MI):Needham Press,Inc.; 2001.p.378.AB
Considerations1079contacting the acrylic,and the force vec-tor can be directed
further forward andmore vertically,closer to the maxillarycenter ofresistance (see
Figure 53-24).Use ofeither or both ofthese orthope-dic appliances to treat vertical
maxillaryexcess is particularly challenging since it isimpossible to direct the
force in a straightvertical manner.Both methods includesome posteriorly directed
force to themaxilla that is not appropriate unless themaxilla is protrusive as well
as inferiorlypositioned.It also is counterproductive ina patient with maxillary
vertical excesscombined with a Class III skeletal relation-ship.Just as the
protraction headgearshould not be used with this individual toaddress the
anteroposterior skeletal prob-lem,the high-pull headgear and/or inter-occlusal bite
block are contraindicated inthis same clinical situation to address thevertical
excess.No studies to date have been able todemonstrate long-term stability with
anynonsurgical orthopedic methods for cor-recting vertical maxillary excess,with
orwithout an anterior open bite.265Achiev-ing stability is particularly difficult
due tothe extended duration ofvertical facialgrowth,often continuing well
beyondadolescence.40For a successful outcomeorthopedic treatment may have to
beextended over a number ofyears,from thetime ofthe mixed dentition
throughdefinitive orthodontic treatment in thepermanent dentition,perhaps including
aremovable orthopedic appliance even dur-ing orthodontic retention.This
extendedtreatment makes the vertical plane ofspace the most difficult to
successfullymanage by the orthodontist attemptingfacial growth
modification.Osseointegrat-ed attachments hold promise as a means ofanchorage to
potentially permit moreeffective treatment ofskeletal verticalproblems in the
future.266ConclusionFacial orthopedic treatmentmay be effective in resolving mild
to mod-erate skeletal discrepancies in somepatients.An orthopedic phase should
beattempted with a specific treatment timeframe established in order to assess
treat-ment progress toward successful correc-tion.This time frame must be honored
inorder to prevent protracted treatment withexcessive dental compensations that
needto be reversed for surgical correction.Theorthodontist attempting growth
modifica-tion must be mindful ofthe duration andextent oftreatment to prevent
excessivelength and morbidity ofthe orthodontictreatment.Ifsignificant skeletal
improve-ment is not being achieved within 6 to 8 months ofstarting orthopedic
treatment,the case needs to be reevaluated and thegrowth modification treatment
likelyabandoned as a treatment choice.It has become clear that there is
greatvariability in individual treatment response,even when factoring out wear
complianceand duration oftreatment.It has not beenpossible to identify the
variables to explainwhy some patients respond well and somedo not demonstrate any
significant skeletalimprovement with treatment regardless oftheir facial morphology
or the severity oftheir skeletal discrepancy.It is anticipatedthat future research
will reveal the variablesthat will enable the clinician to predict treat-ment
response.It also is expected that research willprovide a greater understanding
ofthenature and extent offacial growth modifi-cation possible in individual
patients as wellas the type ofappliance and timing oftreat-ment to achieve the best
outcome.Thedevelopment ofintraoral osseointegratedattachments holds promise for a
futuremeans ofdissipating orthopedic forces toprevent unwanted dentoalveolar
changesthat presently occur with our toothborneappliances.Analogous attachments
arepresently undergoing clinical testing forsurgically assisted orthopedic
movementsassociated with distraction osteogene-sis.267,268Recent and future
advances indevelopmental biology and genomics holdgreat promise in increasing our
under-standing ofthe molecular and geneticmediators ofcraniofacial
growth.132Thisunderstanding will be crucial for us tomake constructive
modifications ofourtreatment methods to target these media-tors in order to prevent
or correct a cranio-facial anomaly or developmental deformity.Orthodontic
Camouflage: Orthopedic Consequence versusSurgical PreparationOrthodontic
camouflage,rather thanorthognathic surgery,may indeed be anappropriate treatment
choice for somemild and moderate skeletal malocclusionsin patients who are beyond
the pubertalgrowth spurt.The treatment goal,howev-er,must include a realistic
outcome char-acterized by an acceptable dental and facialesthetic appearance with
favorable dentalfunction and occlusion.Since estheticappearance is subjective in
nature,it isessential to have the patient and parentperceptions dictate whether
camouflage isa reasonable option.Most mild and some moderate skeletalClass II
malocclusions can be effectivelycamouflaged with extraction oftwo max-illary
premolars and retraction ofmaxil-lary anterior teeth,leaving the posteriorteeth in
a Class II occlusion.However,these cases should mainly be limited tothose that
present without significant den-tal crowding,some protrusion ofthe max-illary
incisors,and where there is not sig-nificant maxillary gingival display
onsmiling.Ifthe maxillary incisors are nor-mally or palatally inclined prior to
treat-ment,orthodontic retraction oftheseteeth may result in an even poorer
estheticresult than the original problem even iftheocclusion is acceptable.The
unestheticappearance includes not just the incisorinclination but often an
unattractiveretrusive upper lip and increased gingivalexposure during smiling as
well.This iswhy the recent introduction ofpalatalimplants as orthodontic
anchorage,which
1080Part 8: Orthognathic Surgeryprovide the opportunity for the orthodon-tist to
retract maxillary incisors even fur-ther than was previously possible,is amixed
blessing.It is more challenging to camouflageClass III than Class II skeletal
malocclusionssince considerable natural dentoalveolarcamouflage (proclined
maxillary incisors,lingually inclined mandibular incisors) isoften already present
prior to treatment.Additional maxillary incisor proclinationmay be unesthetic,and
further lingual incli-nation ofmandibular incisors usuallyaccentuates an already
prominent chin.Forthis reason extraction ofmandibular pre-molars to permit more
retraction ofmandibular incisors to obtain positive over-jet often compromises the
esthetic outcome.Ifinterarch tooth size compatibility can bemaintained,extraction
ofone mandibularincisor rather than two premolars may pro-vide an acceptable
compromise.Camouflage ofan anterior open bitethat is due to maxillary vertical
excess hasbeen notoriously unsuccessful in the past.Recently an orthodontic
technique for sta-bly extruding anterior teeth has beenintroduced.269Unfortunately
this onlyexacerbates the excessive vertical display ofmaxillary gingiva and
anterior teeth.SummaryThe surgeon�s understanding ofcraniofa-cial growth has an
important impact onclinical treatment decisions to alter cranio-facial
morphology.This understanding isrelevant to the appreciation ofthe role
oforthopedic treatment in the prepubertaland pubertal patient to limit or
precludethe need for corrective surgery at a later age.Clinically relevant
modification ofcranio-facial growth is possible,but substantialadvances will be
necessary to elucidate howgrowth modification can be accomplishedin a controlled
and predictable manner toachieve an efficacious outcome.Optimaltiming and stability
ofcraniofacial surgeryare dependent on a thorough appreciationofthe
sequence,timing,magnitude,anddifferential expression ofcraniofacialgrowth.The
recent dramatic advances indevelopmental genetics and molecularbiology,highlighted
by complete mappingofthe human genome,usher in a new mil-lenium that promises to
bring an explosiveincrease to our understanding ofthe com-plex interactions ofthe
genetic and envi-ronmental influences that determinehuman craniofacial
morphogenesis,prena-tal development,and postnatal growth.Athorough understanding
ofthese genomicand epigenetic factors will be necessary todetermine the best timing
and method ofclinical intervention to achieve the opti-mum treatment
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CHAPTER 54Database Acquisition and Treatment PlanningMarc B.Ackerman,DMD David
M.Sarver,DMD,MSUntil the turn ofthe twenty-first century,treatment planning in
orthognathicsurgery was based primarily on a system ofclinical observation,a static
set ofrecords(models,radiographs),with the majorthrust oftreatment being directed
towardsatisfying lateral cephalometric goals.These goals might include particular
mea-surements (sella-nasion�A point and A point�nasion�B point differences)
oranalytical norms (Steiner,Ricketts),oreven comparison oflateral head film trac-
ings ofpersons with craniofacial skeletaldysplasia1�3to templates having
averageskeletal proportions derived from longitu-dinal growth studies.4The most
signifi-cant shortcoming ofthis reliance on thelateral cephalogram as the primary
deter-minant oftreatment goal setting is that itdid not take into account the
resting anddynamic hard�soft tissue relationships,which are the most critical
aspects in treat-ment planning in both orthodontics andorthognathic
surgery.Furthermore,cephalometric analysis quantifies dento-skeletal relationships
in angular and linearmeasures,which are not entirely represen-tative ofthe
multidimensional interrela-tionship ofcraniofacial parts.That is tosay,the
integumental soft tissue drape maysometimes be inconsistent with the under-lying
skeletal framework in a given patient.Whereas the skeletal framework may
bereasonably stable post-adolescence,thesoft tissues are more subject to matura-
tional and age-related changes.Thecephalometric approach to treatmentplanning is
now considered �Procrustean,�after the story based on Greek mythology.As the story
goes,Procrustes was aninnkeeper with only one bed.Ifa travelerwas too tall for the
bed,Procrustes wouldcut offthe traveler�s feet so that he or shewould fit the bed.A
traveler who was tooshort would be stretched on a rack to like-wise fit the bed in
length.This charmingstory relates to this chapter in that byapplying the same hard
tissue cephalomet-ric analysis to all patients,all ofourpatients end up being
crammed into thesame bed! The contemporary approach to thesurgical orthodontic
treatment ofdentofa-cial deformity will illustrate the use ofdentofacial
proportionality in the place ofapplying absolute linear or angular normsto the
individual patient.Patient-specifictreatment planning will be the focus ofthis
chapter.Contemporary Orthognathic Treatment PlanningThe emphasis in this chapter on
orthog-nathic diagnosis and treatment planningis intended to lead us into a new era
andmethodology ofpatient analysis andtreatment goal setting.In modernorthognathic
surgery,treatment goals aredetermined through systematic clinicalexamination and
quantification ofthepatient�s dentofacial characteristics.Therefore,the purpose
ofthis chapterwill be to introduce the reader to amethod ofsystematic dentofacial
analy-sis in all three dimensions with emphasison both static and dynamic relation-
ships,as well as both functional andesthetic objectives.Problem-oriented treatment
plan-ning has served us very well in the pastseveral decades,by focusing on the
prob-lems in need ofcorrection,including theidentification ofsolutions for each
prob-lem.The natural progression ofproblem-orientedtreatment planning should
nowinclude the identification offavorableattributes as well as the
problems.Thereason for this next step is the realizationthat focusing solely on the
problems andtheir solutions may result in a treatmentplan which potentially has a
negativeeffect on the positive attributes in thatpatient.A classic orthodontic
example iswhere the extraction ofmaxillary premo-lars in the correction ofa
skeletal Class IImalocclusion,while satisfying functional
1088Part 8: Orthognathic Surgeryand occlusal issues,may result in profileflattening
and an unfortunate effect onfacial appearance.In the orthognathicarena,a good
example is the widening ofthe alar base secondary to maxillaryadvancement and/or
impaction.The goaloforthognathic treatment is the opti-mization ofnegative
attributes,while atthe same time preserving those attributesthat are deemed
favorable (Figure 54-1).This systematic approach to clinicalexamination ofthe
patient is essential forthe development ofan optimization-oriented database.All
clinically detectabledeviations from the optimal range fallinto the two broad
categories offunctionand esthetics.Function and Dentofacial DeformityPatients with
severe discrepancies in thesize and position oftheir jaws and theirteeth often have
difficulty in oral function.Certain foods may be difficult to incise andchew.Speech
may also be affected by jawdeformity.Ifthe patient cannot bring thetongue and lips
into the proper position,itmay not be possible to produce a specificsound
properly.Besides careful examina-tion ofthe patient,it is doubtful that diag-nostic
tests offunction that can be carriedout in the dental or surgical office are use-
ful.The relationship oftemporomandibu-lar (TM) joint problems to severe maloc-
clusion and dentofacial deformities iscomplex but important.Although there issome
evidence that patients with specifictypes ofmalocclusion are more susceptibleto TM
joint problems,the increased risk isrelatively small.5In general terms,patientswith
dentofacial deformity are similar topatients with normal facial proportions inthe
prevalence ofTM joint problems.6Appearance and DentofacialDeformityAppearance and
dentofacial esthetics canbe divided into three
subcategories:macroesthetics,miniesthetics,and microes-thetics (Figure 54-2).The
specific concernsofthe patient can be elucidated throughopen-ended doctor-patient
communica-tion and then integrated into the diagnosticdecision tree.The surgeon and
orthodon-tist should be sensitive to the patient�sesthetic desires,balancing them
against cul-tural and familial standards.The physicalburden oftreatment is borne by
the patientand must be weighed when determiningthe extent ofsurgical
intervention.Forexample,when deciding whether treatmentshould involve orthodontics
alone,ortho-dontics and orthognathic surgery,oracceptable orthodontic
camouflage,thepatient should understand the risk-benefitratio ofany given treatment
sequence.Data CollectionPrimary data collection begins at the clin-ical examination
and is supplementedwith static and dynamic recordings ofthepatient in three spatial
dimensions.Recordtaking should replicate the functional andesthetic presentation
ofthe patient.Find-ings from the clinical examination shouldeither be confirmed or
challenged by dataobtained from the records.The analysis ofthe clinical database
will generate a diag-nostic summary and optimized problemlist.An emerging soft-
tissue paradigm insurgical orthodontic treatment planninghas refocused analysis on
facial propor-tionality and balance versus reliance onnormative data derived from
cephalomet-rics.7The art ofsurgical orthodontics restsin the ability to envisage
the patient�sdesired three-dimensional soft tissue out-come and then retroengineer
the dentaland skeletal hard tissues to produce such achange.The concept
ofretroengineeringwill be explained later in this chapterunder technological
applications toorthognathic treatment planning.In today�s clinical environment
thereare three methods ofdata collection.Thefirst and most commonly used
methodincludes still photography,study models,and cephalometric radiographs.The
sec-ond is the use ofdatabasing programs todocument direct clinical measurement
ofthe patient�s resting and dynamic relation-ships.The third involves the use
ofdigitalvideo to record the dynamics offacialmovement.This methodology as it cur-
rently exists does not dynamically quantifymovement.Expect to see greater recogni-
tion ofthe value ofthis technology,whichshould lead to research into the
quantifica-tion ofdynamic facial movements.Conventional RecordsStandard orthodontic
records have notchanged significantly in many years,butcontemporary records in
surgical ortho-dontic treatment are changing rapidly.FIGURE54-1Contemporary
treatment plan-ning flow chart.After the clinical examinationand databasing ofthe
quantitative measure-ments,both problems and positive attributes
areidentified.Solutions for the problems are identi-fied and the dotted
arrowindicates that eachpotential solution can negatively impact a posi-tive
feature.Therefore,the advantage ofmea-suring both problems and positive features
per-mits the clinician to recognize the potentialnegative impact that any given
solution has onthe positive attributes.This �decision tree�leadsto correction ofthe
problems but also preserva-tion ofthe positive attributes.The clinician
thenassimilates all ofthis information for optimiza-tion oftreatment.Problem
listPositive featuresSystematic dentofacial
examinationSolutionsPreservationAssimilationOptimization
Database Acquisition and Treatment Planning1089Surgical orthodontics demands
treating alldimensions ofpatients.In clinical prac-tice,standard records include
film or digi-tal photographs,radiographs,and studymodels (whether plaster,mounted
orunmounted,or electronic models).Thefacial images,which are universally con-
sidered standard records,include frontal atrest,frontal smile,and profile at
restimages.Whereas these orientations doprovide an adequate amount
ofdiagnosticinformation,they do not contain all oftheinformation needed for three-
dimensionalvisualization and quantification.Orthog-nathic surgery requires
expansion ofthedatabase compared to conventional ortho-dontic treatment.The
suggested records can be dividedinto two groups�static and dynamic.Theaccepted
facial photographic recordingsshould include frontal smile close-up,oblique facial
smile,oblique smile close-up,and profile smile.8Direct Measurement as a Biometric
Tool The goal ofthe clinical examination is toquantitatively assess soft and hard
tissueattributes ofthe dentofacial complex,andrecord what elements are satisfactory
andwhich are in need ofoptimization.Clinicalexamination procedures vary
greatlyamong practitioners.Measurement shouldbe thorough,systematic,and
consistent,thus minimizing the chance that some-thing ofimportance will be
overlooked.We want to avoid the situation where theclinician performs a cursory
examination,jotting down briefnotes as to abnormali-ties that are observed without
recordingany other descriptive data.This practice isoften justified by the
assumption thatmost diagnostic decisions can be madefrom the records after the
patient leaves.This is a poor diagnostic technique forseveral reasons.First,static
records cannot reflect thedynamic relationships that are importantin the overall
functional assessment ofthepatient.For example,the simple idea ofthe relationship
ofthe upper incisor at restand on smile is not reflected on radi-ographs or models
and is poorly evaluatedin photographs.Second,information thatmay have not looked
important enough towrite down during a cursory examinationmay be important
later,and thus would beunavailable because it was not recorded.Third,a thorough and
comprehensiveexamination record that includes normalobservations is an accurate
medicolegaldocument.It is hard for an unhappypatient to charge negligence when it
isclear that the information was obtainedand used.The more thorough and
welldocumented the record is,the more valu-able it is ifproblems arise.Contemporary
clinical examinationuses a computer-databasing program tofacilitate data entry,and
these data arethen merged into reports and treatmentplanning screens or forms.9Each
clinicalcharacteristic in the examination has apop-up menu containing all ofthe
possi-ble descriptions for that particular trait(Figure 54-3).By using a computer
inter-face,the surgeon or orthodontist savesvaluable time in both the clinical
examina-tion and diagnostic and treatment plan-ning work-up.The information is
thenstored for recall and analysis,and can evenhave predefined parameters that
identifyproblematic measurements automatically.As an example ofhow this
interfacefacilitates the examination ofdynamichard�soft tissue relationships,we
suggestthat the following frontal measurementsbe performed systematically in
evalua-tion ofanterior dental display,both atrest and at smile:�Philtrum height:The
philtrum heightis measured in millimeters from sub-nasale (the base ofthe nose at
themidline) to the most inferior portionofthe upper lip on the vermilion tipbeneath
the philtral columns.Theabsolute linear measurement is notparticularly
important,but what issignificant is its relationship to theupper incisor,and the
commissures ofthe mouth.In the adolescent,it iscommon to find the philtrum heightto
be shorter than the commissureheight,and the difference can beexplained in the
differential in lipgrowth with maturation.MacroestheticsProfileVertical
proportionsLip fullnessChin projectionNasal projectionEar
sizeMiniestheticsMicroestheticsIncisor displayTransverse smileSmile
symmetryCrowdingSmile arcGingival heightsTriangular holesEmergence
profilesSpacingTooth shadeTooth shapeIncisor angulationsFIGURE54-2Recommended
subcategories ofappearance and esthetics.
1090Part 8: Orthognathic Surgery�Commissure height:The commissureheight is measured
from a line con-structed from the alar bases throughsubspinale,then from the
commis-sures perpendicular to this line.�Interlabial gap:The interlabial gap isthe
distance in millimeters betweenthe upper and lower lips,when lipincompetence is
present.�Amount ofincisor show at rest:Theamount ofupper incisor show at rest isa
critical esthetic parameter becauseone ofthe inevitable characteristics ofan aging
tooth-lip relationship isdiminished upper incisor show at restand on smile.For
example,an adultpatient who displays 3 mm ofgingivaldisplay on smile and 3 mm
ofupperincisor at rest should only carefullyconsider maxillary incisor intrusion
ormaxillary impaction to reduce gingivaldisplay,since reduction in gingival dis-
play also results in diminished incisorshow at rest and during conversation(a
characteristic ofthe aging face).�Amount ofincisor display on smile:On
smile,patients will either showtheir entire upper incisor,or only apercentage ofthe
incisor.Measure-ment ofthe percentage ofincisor dis-play,when combined with the
crownheight measured next,leads the clini-cian to decide how much tooth move-ment
is required to attain the appro-priate smile for that patient.�Crown height:The
vertical height ofthe maxillary central incisors in theadult is measured in
millimeters and isnormally between 9 and 12 mm,withan average of10.6 mm in males
and9.6 mm in females.The age ofthepatient is a factor in crown heightbecause ofthe
rate ofapical migrationin the adolescent.�Gingival display:There is variabilityin
what is esthetically acceptable forthe amount ofgingival display onsmile,but it is
important to alwaysremember the relationship betweengingival display and the amount
ofincisor shown at rest.In broad terms,it is better for a patient to be treatedless
aggressively in reducing smilegumminess when considering thatthe aging process will
result in a nat-ural diminishment ofthis character-istic.A gummy smile is often
moreesthetic than a smile with diminishedtooth display.�Smile arc:The smile arc
should bedefined as the relationship ofthe cur-vature ofthe incisal edges ofthe
max-illary incisors and canines to the cur-vature ofthe lower lip in the
posedsocial smile.10,11The ideal smile archasthe maxillary incisal edge curva-ture
parallel to the curvature ofthelower lip upon smile,and the termconsonantis used to
describe this par-allel relationship.A nonconsonantorflat smile arc is
characterized by theFIGURE54-3A computer-databasing program facilitates data
entry,and these data are then merged intoreports and treatment planning screens or
forms.Each clinical characteristic in the examination has a pop-up menu containing
all ofthe possible descriptions for that particular trait.
Database Acquisition and Treatment Planning1091maxillary incisal curvaturebeing
flat-ter than the curvature ofthe lower lipon smile.The smile arc relationship
isnot as quantitatively measurable as theother attributes,so the
qualitativeobservation ofconsonant,flat,orreverse smile arcs is generally cited.Is
it important to measure these above-described characteristics in orthognathiccases?
The following case illustrates thesignificance ofresting and dynamic softtissue
measurement,and how surgical ororthodontic treatment planning is deter-mined by
direct measurement as much asit is by cephalometric analysis.The role
ofcephalometrics will be discussed later inthis chapter,and the emphasis will be
lesson static comparisons to norms and moreon its coordination with the soft
tissueoverlay ofthe face and the use ofpredic-tive algorithms to arrive at
finalmacrotreatment decisions.The patient in Figure 54-4 was a 16-year-old male who
presented for anopinion relative to his chiefcomplaint ofexcessive gingival display
on smile,or a�gummy smile�(see Figure 54�4A).He hadfinished orthodontic treatment
about 1 yearearlier,and when his mother asked theorthodontist ifsomething could be
done,the orthodontist felt that the only way toimprove that smile characteristic
was toconsider surgical maxillary superior reposi-tioning via Le Fort I osteotomy.A
referral tothe oral and maxillofacial surgeon was rec-ommended,and maxillary
impaction wasrecommended,but the surgeon felt that hewanted to wait until the
patient had reachedfull physical maturity.The patient�s motherfelt further
investigation was warranted.The examination revealed a well-treated orthodontic
case with excellentocclusion,and the macrorelations werealso quite normal in terms
ofprofile andfacial proportion.The anterior tooth-liprelationships were as
follows:�Resting relationships (see Figure 54-4B)Philtrum height:25 mmCommissure
height:25 mmMaxillary incisor at rest:2 mm�Dynamic relationships (see Figure 54-
4C)Percentage ofmaxillary incisor display on smile:100% Maxillary incisor crown
height:8 mm Gingival display on smile:4 mmSmile arc:consonantIt is instructive to
outline the etiolo-gies ofexcessive gingival display on smileand characteristics
seen with each in orderto demonstrate the decision-makingprocess in problem-
oriented treatmentplanning with optimization.�Vertical maxillary excess:Character-
ized by a disproportionately longlower facial height,lip incompetence,excessive
incisor display at rest,andexcessive gingival display on smile�Short philtrum:The
philtrum heightshorter than the commissure,exces-sive incisor display at rest,and
areverse resting upper lip line�Excessive smile curtain:Excessive ani-mation ofthe
upper lip on smile,dis-playing more tooth and gingiva thandesired�Short crown
height:Ifthe anteriorincisor height is short,excessive gingi-val display may result
In this case,vertical maxillary excesswas ruled out because facial proportional-ity
was normal,no lip incompetence waspresent,and only 2 mm ofupper incisorshowed at
rest.The second possibility,ashort philtrum,was ruled out since thephiltrum and
commissure heights wereFIGURE54-4A�D,Case illustration ofdirect measurement oflip-
tooth-gingival relationships.ABCD
1092Part 8: Orthognathic Surgerythe same,and no reverse upper lip
restingcharacteristics were noted.The third pos-sibility,excessive curtain,was
eliminatedbecause the vermilion was adequate onsmile and the margins ofthe
commissureand philtrum even on posed smile.Thefourth possibility,short crown
height,wassignificant since the maxillary incisorsmeasured to be only 8 mm in
height.Therapeutic options to decrease gingi-val display included maxillary
impaction,orthodontic intrusion ofmaxillary incisors,or periodontal crown
lengthening.�Maxillary impaction:A 4 mm superi-or repositioning ofthe maxilla
woulddecrease the gumminess ofthe smile,but would result in a �2 mm upperincisor
show at rest,greatly hasteningthe aging characteristics ofthe faceand
smile.�Orthodontic intrusion ofthe maxil-lary anterior teeth:This would like-wise
result in reduction ofincisor dis-play at rest but would also flatten thealready
consonant smile arc.�Periodontal crown lengthening:Theincrease in anterior crown
heightdecreases the gumminess ofthe smile(appropriate because the teeth
areshort),and optimizes treatment by notdecreasing incisor display at rest and
bymaintaining the consonant smile arc.After discussing all these options withthe
family,the family decided to proceedwith the third and recommended optionofcrown
lengthening,with an excellentoutcome (see Figure 54-4D).In summary,this case
demonstrates thenew direction in dentofacial treatment plan-ning,even though the
final result was not anorthognathic treatment plan.This case wasselected to make
the point that throughcareful observation and measurement,theappropriate treatment
plan was delivered.Digital VideographyDynamic recording ofpatient�s facialmotion is
accomplished with the use ofdigital videography.12This technologymay be used to
document and evaluatesuch characteristics as range ofmandibu-lar motion on opening
and laterotrusivemovements,deviations on opening,smile,and speech.Digital video and
computertechnology have primarily been used torecord anterior tooth display
duringspeech and smiling.Digital videos can berecorded in a standardized fashion
withthe camera at a fixed distance from thesubject.We recommend that these imagesbe
taken in a standard format with empha-sis on natural head position,so that
futureanalysis and research possibilities may bemaximized.We also recommend
thatvideo be taken in the frontal,oblique,andlateral dimensions.Clinically,an
exampleofwhere this technology is most relevantis the patient with an asymmetric
smile.The question that arises is whether or notthe patient has a dental
asymmetry,skele-tal asymmetry,or asymmetric movementofthe lip curtain during
animation.Thesingle smile photograph cannot corrobo-rate the clinical impression
gained duringthe data collection process.The video clipmay be reviewed and
evaluated during allplanning phases oftreatment as well as forcomparison ofthe
orthognathic treatmenteffects (Figure 54-5).Systematic Clinical
ExaminationofDentofacial DeformityWe have previously discussed the impor-tance
ofclinical observation and directmeasurement ofthe interaction ofhardand soft
tissues in planning appropriatecombined orthodontic and orthognathictreatments
ofdentofacial deformity.In thissection,we will describe the components ofthe
examination from the macro-,mini-,and microperspectives.Macroesthetic
Examination:Frontal ViewThe facial areas for macroesthetic exami-nation,as
investigated from the frontalview,can be summarized as follows:�Vertical
proportionsFacial heights:Lower third�Transverse proportionsRule offifthsMiddle
fifthInner canthiAlar baseMedial two-fifthsOuter canthiGonial angles
ofmandibleOuter two-fifthsEar deformityEar projectionNasal anatomyAlar
baseColumellaNasal tipDorsum�Transverse symmetry Nasal tip to midsagittal
planeMaxillary dental midline to midsagittal planeMandibular dental midline to
symphysisMandibular asymmetry with or without functional shiftMaxillomandibular
asymmetryChin asymmetryThe starting point for the macroes-thetic examination is the
frontal perspec-tive.Transverse and vertical relationshipscomprise the major
components ofthefrontal examination and analysis.Asemphasized in our
introduction,the pro-portionalrelationship ofheight and widthis far more important
than absolute valuesin establishing overall facial type.Facescan be broadly
categorized as eithermesocephalic,brachycephalic,or dolicho-cephalic (Figure 54-
6).13The differentia-tion between these facial types has to dowith the general
proportionality offacialbreadth to facial height,with brachy-cephalic faces being
broader and shorter incomparison to the longer and more nar-row dolichocephalic
faces.Generally,themost attractive faces tend to have common
Database Acquisition and Treatment Planning1093proportions and relationships that
gener-ally differ from normative values.14Vertical Facial ProportionsThe idealface
is vertically divided into equal thirdsby horizontal lines adjacent to the
hairline,the nasal base,and menton (Figure 54-7A).Surgical orthodontic treatment is
in alarge part limited to the lower facial third.Measurement ofthe upper face is
oftenhindered by the variability in identifica-tion ofbroad landmarks such as the
loca-tion ofthe hairline and radix.We will begin our clinical examina-tion with the
evaluation oflower facialheight.In the ideal lower third oftheface,the upper lip
makes up the upperthird,and the lower lip and chin com-pose the lower two-thirds
(Figure 54-7B).Disproportion ofthe vertical facialthirds may be a result ofmany
dental andskeletal factors,and these proportionalrelationships may help us define
the con-tributing factors related to verticaldentofacial deformities.In the
following sections,we presentcase illustrations oforthognathic changesin vertical
proportionality.Short Vertical ProportionsThe patient inFigure 54-8 presented for
correction ofherClass II deep bite secondary to hermandibular deficiency.Her
anterior verti-cal relationships were characterized by ashort lower facial third
relative to herupper thirds (see Figure 54-8A and B).Inaddition,the lower third was
comprised ofa 45:55 vertical relation ofthe upper lip tolower lip and chin
height.Recalling thatthe ideal proportions ofthe lower face areone-third upper lip
and two-thirds lowerlip and chin,the treatment plan was clear-ly a result ofthe
direct clinical examinationrather than any cephalometric standard.Other important
clinical measurementsentered into the decision process.Differen-tial diagnosis for
a short lower facial heightincluded the following:FIGURE54-5The video clip may be
reviewed and evaluated during all planning phases oftreatment as well as for
comparison ofthe orthog-nathic treatment effects.
1094Part 8: Orthognathic Surgery�Vertical maxillary deficiencies,whichare then
characterized by the follow-ing characteristics:Short lower facial thirdDiminished
maxillary incisor display at restDiminished incisor display on smile�Diminished
chin height,ascertainedthrough the proportionality in thelower face rather than a
linear cephalo-metric value�Posterior dental collapse secondary tothe loss
ofposterior dental supportThe functional goal ofmandibularadvancement to correct
the Class II den-toskeletal relationship was obvious,but anesthetic adjunctive
consideration was a ver-tical genioplasty to optimize the macroes-thetics ofher
vertical facial thirds.The finaldiagnosis depended not only on the verticalfacial
proportionality but on the measure-ment ofthe resting tooth-lip relationshipsas
well in order to more clearly define theetiology ofthe lower facial height.In
thiscase,our patient displayed 3 mm ofmaxil-lary incisor at rest,and all ofher
maxillaryincisor on smile (see Figure 54-8C),whichwas inconsistent with vertical
maxillarydeficiency.Since the chin height was short,the final diagnosis was
mandibular defi-ciency with short chin height.Therefore,the recommended treatment
plan wasFIGURE54-6A,The mesocephalic facial type is characterized by equal vertical
facial thirds.B,The brachycephalic facial type appears square with a
diminishedlower third.C,The dolichocephalic facial type appears ovoid with an
increased lower third.ABCABFIGURE54-7A,The ideal face is vertically divided into
equal thirds by horizontal lines adjacent tothe hairline,the nasal base,and
menton.B,In the ideal lower third ofthe face,the upper lip makesup the upper
third,and the lower lip and chin compose the lower two-thirds.
Database Acquisition and Treatment Planning1095orthodontic preparation for
mandibularadvancement and vertical genioplasty (seeFigure 54-8D) to increase the
lower facialheight (see Figure 54-8E�G).Long Vertical ProportionsLong lowerfacial
height is due to one oftwo possibili-ties:(1) vertical maxillary excess (VME) or(2)
excessive chin height.The clinical keysthat may be associated with VME aregummy
smile,open bite,lip incompetence,and steep mandibular plane as evidencedby gonial
angle form.Excessive chin heightis measured from the lower vermilion tothe soft
tissue menton.The clinical keysthat may be associated with excessive chinheight are
lower facial third disproportion-ate from the one-third upper lip to two-thirds low
lip and chin ratio,and theabsence ofVME characteristics.The patient in Figure 54-9A
wasreferred for correction ofan anterior openbite and a gummy smile.Our
systematicexamination revealed the following prob-lem list and
characteristics:�Frontal proportions at rest1.Long lower facial
third2.Disproportion ofchin height withthe upper lip occupying 25% oftheFIGURE54-
8A,This patient was referred for correction ofher Class II deep bite secondary to
her mandibular deficiency.B,Evaluation ofher anterior verticalrelationships was
characterized by a short lower facial third relative to her upper thirds.The lower
third was comprised ofa 45:55 vertical relationship ofthe upperlip to lower lip and
chin height.The ideal proportions ofthe lower face are one-third upper lip and two-
thirds lower lip and chin; thus the treatment plan wasderived from the direct
clinical examination ofthis patient rather than any cephalometric standard.C,Our
patient displayed 3 mm ofmaxillary incisor at rest,and all ofher maxillary incisors
on smile,inconsistent with vertical maxillary deficiency.D,The treatment plan was
orthodontic preparation for mandibularadvancement and vertical genioplasty.E,The
post-treatment frontal view demonstrating balance ofthe vertical facial
thirds.F,The vertical incisor position atsmile was maintained,while the lower
facial third was vertically augmented.G,The profile view shows improved mandibular
projection relative to the upper face,improved chin-neck angle,and improved chin-
neck length.ABCDEFG
1096Part 8: Orthognathic Surgerylower facial third and the lower lipand chin
occupying 75% ofthelower third ofthe face3.Lip incompetence of5 mm4.8 mm
ofmaxillary incisor displayat rest5.Midsymphysis to right 3 mm withno functional
shift6.Lip strain on closure (Figure 54-9B)Clinical assessment ofthe frontal rest-
ing macroesthetic evaluation:Thispatient had most ofthe macrocharac-teristics
ofvertical maxillary excesswith a long lower facial height andexcessive incisor
display at rest.Exces-sive chin height was also a contributorto the lower facial
height dispropor-tion,as is evidenced by the upper lipand chin height clinical
proportions.�Frontal proportions on smile (Figure 54-9C)1.100% ofmaxillary incisor
displayedon smile2.Excessive gingival display on smilewith 3 mm gingival display at
theright cuspid and 5 mm at the leftwith a transverse cant to thepalatal
plane3.Transverse cant to the maxilla withthe left side down 2 mm more thanthe
leftClinical assessment ofthe frontaldynamic (smiling) macroesthetic eval-uation:A
gummy smile was presentbut with normal incisor crown height.This would exclude
cosmetic peri-odontal crown lengthening as the pri-mary therapeutic choice for
improve-ment ofthe gummy smile.Theasymmetry ofthe maxilla is in com-pensation for
the mandibular asym-metry,and results in a canted frontalocclusal plane and smile
line.�Oblique at-rest facial observation (Figure 54-9D)1.Excessive lower facial
height2.Lip strain and excessive chin height3.Flat labiomental sulcus4.Nasal form
judged to be quite adequateClinical assessment ofthe obliquemacroesthetic
evaluation:The flat-tened labiomental sulcus was sec-ondary to the excessive lower
facialheight,lip incompetence,and chindeficiency.�Oblique smiling facial
observation (Figure 54-9E)1.No noticeable anteroposterior cantto the maxillary
occlusal plane2.The smile arc was consonant3.The excessive gingival display wasalso
evident on the oblique smileClinical assessment from the obliquesmiling
macroesthetic evaluation:Since the smile arc was consonant,alteration ofthe palatal
plane wouldnot have been indicated eitherthrough surgery or orthodonticincisor
repositioning.�Profile evaluation (Figure 54-9F)1.Long lower facial third2.Long
chin height3.Flat labiomental sulcus4.Lip strain on closureClinical assessment
ofthe profilemacroesthetic evaluation:As would beexpected from the frontal and
obliquecharacteristics,the lateral profilereflected the overall skeletal and
dentalcharacteristics ofvertical maxillaryexcess,but the chin deficiency thatbecame
evident on the oblique viewwas clearly demonstrated on the pro-file view.The
functional problem ofthe anteri-or open bite in this nongrowing patientnecessitated
superior repositioning ofthemaxilla to correct the functional com-plaint (Figure
54-9G�K).The exact surgi-cal movements were directed by the clini-cal examination
and measurements.Because the patient had the clinical diag-nosis ofvertical
maxillary excess,maxil-lary impaction was indicated,but somediscretionary decisions
were needed forappropriate position ofthe maxilla fromthe esthetic standpoint.From
the frontaldimension,the left side ofthe maxilla wasimpacted 2 mm more than the
right inorder to level the smile line.The differen-tial degree ofimpaction
reflected thedegree ofthe maxillary compensation forthe mandibular
asymmetry.Transverse Facial ProportionsTheassessment ofthe transverse components
offacial width is best described by the rule offifths.9This method describes the
idealtransverse relationships ofthe face.The faceis divided sagittally into five
equal partsfrom helix to helix ofthe outer ears (Figure54-10).Each ofthe segments
should be oneeye distance in width.Each transverse fifthshould be individually
examined and thenassessed as a complete group.The middle fifth ofthe face is delin-
eated by the inner canthus ofthe eyes.Avertical line from the inner canthus
shouldbe coincident with the alar base ofthenose.Variation in this facial fifth
could bedue to transverse deficiencies or excessesin either the inner canthi or
alar base.Forexample,hypertelorism in craniofacialsyndromes can create
disproportionatetransverse facial esthetics.A vertical line from the outer
canthusofthe eyes frames the medial three-fifthsofthe face,which should be
coincidentwith the gonial angles ofthe mandible.Although disproportion may be very
sub-tle,it is worth noting since our treatmentscan positively change the shape or
relativeproportion ofthe gonial angles.The outer two-fifths ofthe face is mea-sured
from the lateral canthus to lateralhelix ofthe ear,which represents the widthofthe
ears.Unless this abnormality is partofthe chiefcomplaint,prominent ears areoften a
difficult feature to discuss with thepatient because laypeople only recognize
itseffect on the face in severe cases.However,
Database Acquisition and Treatment Planning1097FIGURE54-9A,This patient was
referred for correction ofan anterior open bite and a gummy smile.B,Lip strain on
closure.C,Frontal proportions on smilewith 100% ofmaxillary incisor displayed.There
was excessive gingival display on smile with 3 mm gingival display at the right
cuspid and 5 mm at the left witha transverse cant to the palatal plane.Transverse
cant to the maxilla with the left side down 2 mm more than the left.D,Oblique at-
rest facial observation withexcessive lower facial height,lip strain and excessive
chin height,and a flat labiomental sulcus.The nasal form was judged to be quite
adequate.E,Oblique smil-ing facial observationwith no noticeable anteroposterior
cant to the maxillary occlusal plane.The smile arc was consonant.The excessive
gingival display was alsoevident on the oblique smile.F,Profile evaluation with
emphasis on a long lower facial third,long chin height,a flat labiomental
sulcus,and lip strain on closure.G�K,The functional problem ofthe anterior open
bite in this nongrowing patient necessitated superior repositioning ofthe maxilla
to correct the functional com-plaint.The exact surgical movements were obtained
from the clinical examination and measurements (see text).ABCDEFHIJGK
1098Part 8: Orthognathic Surgerystudies clearly indicate that large ears arejudged
by laypeople to be one ofthe mostunesthetic features,particularly in
males.Otoplastic surgical procedures are relativelyatraumatic and can dramatically
improvefacial appearance.In orthognathic cases inwhich this disproportion is noted
by theclinician,we feel that failure to mention thisfeature violates informed
consent.There-fore,otoplasty should be presented as atreatment option,whether
received posi-tively or not.These procedures can be per-formed on adolescents and
adults as is illus-trated in Figure 54-11A and B.Another significant frontal
relation-ship is the midpupillary distance,whichshould be transversely aligned with
thecommissures ofthe mouth.15Althoughthis is considered the ideal transverse
facialproportionality,there is little that can bedone therapeutically to correct
this dispro-portion,except in craniofacial synostosissuch as Apert syndrome.Nasal
anatomy in the transverse planeshould also be assessed through propor-tionality.The
width ofthe alar base shouldbe approximately the same as the intercan-thal
distance,which should be the same asthe width ofan eye.Ifthe intercanthal dis-tance
is smaller than an eye width,it is bet-ter to keep the nose slightly wider than
theintercanthal distance.The width ofthealar base is heavily influenced by
inheritedethnic characteristics.Asymmetry ofthe face is a somewhatnatural
occurrence.Systematic examina-tion ofthe patient�s facial symmetryshould be
directly measured in the frontalplane.The following measures composethis portion
ofthe clinical examination.Nasal Tip to Midsagittal PlaneHaving thepatient elevate
the head slightly and thenvisualizing the nasal tip in relation to themidsagittal
plane provides the best view toevaluate the position ofthe nasal tip (Figure54-
12).Any deviation ofthe nasal tip shouldbe noted in relation to the maxillary
midline.The clinician should not make the mistake oftreating the maxillary midline
to a distortednose.An attempt to obtain the etiology ofnasal tip asymmetry is
recommended.TheFIGURE54-10The face is divided sagittally intofive equal parts from
helix to helix ofthe outer ears.The middle fifth ofthe face is delineated by
theinner canthus ofthe eyes,the inner corner ofthe eyecontaining the lacrimal
duct.A line from the innercanthus should be coincident with the ala ofthebase ofthe
nose.A vertical line from the outer can-thus ofthe eyes frames the medial two-
fifths oftheface,which should be coincident with the gonialangles ofthe
mandible.The outer two-fifths oftheface is measured from the lateral canthus to the
lat-eral helix,which represents the width ofthe ears.Another significant frontal
relationship is the mid-pupillary distance,which should be transverselyaligned with
the commissures ofthe mouth.FIGURE54-11A,An otoplastic surgical procedure was
recommended for this patient�s prominentears.B,The facial transverse fifths were
improved,resulting in a dramatic facial improvement.ABFIGURE54-12The �gull in
flight�contour ofthe base ofthe nose.
Database Acquisition and Treatment Planning1099patient should be questioned as to
any previ-ous history ofnasal trauma or nasal surgeryfor a deviated septum.Patients
may then beadvised appropriately as to whether this devi-ation is severe enough to
consider correction.Maxillary Dental Midline to MidsagittalPlaneThe maxillary
dental midlineshould be recorded relative to the mid-sagittal plane.A discrepancy
could bedue to either dental factors or skeletalmaxillary rotation.Maxillary
rotation isa rarely occurring clinical finding and isusually accompanied by
posterior dentalcrossbite.The dental features ofmaxil-lary midline discrepancies
will be dis-cussed in both the miniesthetic andmicroesthetic
perspectives.Mandibular Dental Midline to MidsymphysisThe mandibular dental midline
tomidsymphysis relationship is best visual-ized by standing behind the patient
andthen viewing the lower arch from above(Figure 54-13).The patient should openhis
or her mouth in order for the clinicianto view the lower arch and its
relationshipto the body ofthe mandible and symph-ysis.Lower dental midline
discrepanciesare usually due to tooth related issues suchas dental crowding with
shifted incisors,premature exfoliation ofprimary teethand subsequent space closure
in pre-adolescents,congenitally missing teeth,oran extracted unilateral tooth.Ifthe
lowerdental midline is not coincident with themidsymphysis,it usually indicates a
dentalshift.However,chin asymmetry shouldalso be considered.Mandibular Asymmetry
with or withoutFunctional ShiftMandibular asymmetryis suspected when the
midsymphysis is notcoincident with the midsagittal plane.Animportant diagnostic
factor is whether alateral functional shift is present sec-ondary to a functional
shift ofthemandible due to crossbite.When thepatient is manipulated into centric
rela-tion,a bilateral,end-to-end crossbite usu-ally is present,and as the patient
moves theteeth into full occlusion,the patient mustchoose a side to move his or her
mandibleinto maximum intercuspation.This lateralshift is indicative not oftrue
mandibularasymmetry but oftransverse maxillarydeficiency and a resultant functional
shiftofthe mandible.True mandibular asymmetry is sus-pected when,in closure into
centric rela-tion,no lateral functional shift occurs.Thetruly asymmetric mandible
may be due toan inherited asymmetric facial growthpattern or a result oflocalized
or systemicfactors.A thorough history oftraumaticinjuries and a review ofsystems
ofthepatient will help ascertain potential etiolo-gies oftrue mandibular
asymmetry.Chin AsymmetryFacial asymmetry insome cases may be limited to the
chinonly.Ifthe systematic evaluation offacialsymmetry has dental and skeletal mid-
lines and vertical relationships ofthemaxilla normal and lower facial asymme-try is
noted,then the asymmetry may beisolated to the chin.Measurement ofthemidsymphysis
to the midsagittal plane isa logical indicator ofchin asymmetry,butthe
parasymphyseal heights should alsobe measured when chin asymmetry issuspected
(Figure 54-14).The frontalview is recommended,but a view fromthe superior facial
aspect (much like theevaluation ofthe mandibular dental mid-line) with the mouth
closed also affordsthe clinician excellent visualization ofthechin to the body
ofthe mandible and themidsymphysis.Maxillomandibular AsymmetryMan-dibular asymmetry
is often accompanied bymaxillary compensation,which is reflectedclinically by a
transverse cant ofthe maxilla.This means that evaluation ofmandibulardeformity
should now include the possibili-ty ofmaxillomandibular deformity.Trans-verse
tilting ofthe maxilla may be detectablecephalometrically but is most evident dur-
ing the macroesthetic examination (Figure54-15).Clinically,one notes this,for exam-
ple,as right maxilla 4 mm more superiorthan left.The transverse cant ofthe
maxillaFIGURE54-13Ifthe lower dental midline is notcoincident with the
midsymphysis,it usually indi-cates a dental shift.However,chin asymmetryshould also
be considered.FIGURE54-14Measurement ofthe midsymph-ysis to the midsagittal plane
is a logical indicatorofchin asymmetry,but the parasymphysealheights should also be
measured when chinasymmetry is suspected.FIGURE54-15Transverse tilting ofthe
maxillamay be detectable cephalometrically but is mostevident during the
macroesthetic examination.
1100Part 8: Orthognathic Surgeryis often determined by the relative differencein
gingival show present at the level ofthecanine moving posterior at smile.Differen-
tiation between the macro- and miniesthet-ic factors that are related to the
transversecant ofthe maxilla will be discussed later.Macroesthetic Examination:
Oblique ViewThe facial areas for macroesthetic exami-nation,as investigated from
the obliqueview,can be summarized as follows:�MidfacialOrbital positionNasal
formCheek/zygomatic form�Lower facial Lip formPhiltrumVermilion Mandibular formChin
projectionThe oblique view (Figure 54-16A) inthe macroesthetic examination affords
thesurgeon and orthodontist another perspec-tive for evaluating the facial
thirds.Withregard to the upper face,the clinician mayview the relative projection
ofthe orbitalrim and malar eminence.Orbital and malarretrusion is often seen in
craniofacial syn-dromes.Cheek projection is evaluated inthe area ofthe zygomaticus
and malar scaf-fold.Skin laxity and atrophy ofthe malarfat pad in this area may
actually be a char-acteristic ofaging and therefore seen in theolder orthognathic
population.16This areacan be described as deficient,balanced,orprominent.Nasal
anatomy,which wasdescribed in the frontal examination,mayalso be characterized in
this dimension.Lip anatomy is also examined in theoblique and lateral views.The
philtral areaand vermilion ofthe maxillary lip should beclearly demarcated.The
height ofthephiltrum should be noted as short,balanced,or excessive.Vermilion
display should betermed as excessive,balanced,or thin.The relative projection ofthe
maxillaand mandible can be assessed in theoblique view.Midface deficiency can
resultin increased nasolabial folding,relaxedupper lip support,and altered
columellaand nasal tip support.One ofthe greatest values oftheoblique view is
visualization ofthe bodyand gonial angle ofthe mandible as wellas the cervicomental
area.The patient inFigure 54-16A illustrates a desirable defi-nition ofthe chin-
neck anatomy.Thepatient in Figure 54-16B has a dolichofa-cial skeletal pattern with
a steepermandibular plane,not as estheticallypleasing as the previous
illustration.Thepatient in Figure 54-16C demonstrates abrachyfacial pattern with an
obtuse cervi-comental angle secondary to submentalfat deposition.Mandibular
deficiencywith associated dental compensation mayproduce lower lip
eversion,excessive ver-milion display,and a pronounced labio-mental sulcus.A
characterization ofmandibular formis also very important.The oblique viewalso
demonstrates the effects ofanimationon the appearance oflip and chin projec-
tion.The patient in Figure 54-17A and Bshows a moderate anterior divergence
andfacial concavity at rest,but during thesmile,animation reveals an increased
chinprojection with excessive concavity.FIGURE54-16A,Desirable definition ofthe
chin-neck anatomy.B,A dolichofacial skeletal pattern with a steeper
mandibularplane,not as esthetic as the previous illustration.C,A brachyfacial
pattern with an obtuse cervicomental angle secondary to sub-mental fat
deposition.ABC
Database Acquisition and Treatment Planning1101Macroesthetic Examination:Profile
ViewThe facial areas for macroesthetic exami-nation,as investigated from the
profileview,can be summarized as follows:�Lower facialMaxillomandibular projection
or facial divergenceLip formSizeProjectionLabiomental sulcusChin projectionThe last
view in the macroestheticexamination is the profile perspective.Natural head
position is essential for accu-rate evaluation ofprofile characteristics.The
patient should be instructed to lookstraight ahead and,ifpossible,into his orher
own image in an appropriately placedmirror.The visual axis is what
determines�natural head position.�This axis veryoften,but not always,approximates
theFrankfort horizontal plane.The classicvertical facial thirds should also be
appliedin profile view.An assessment oflowerfacial deficiency or excess should be
noted.The nasolabial angle describes theinclination ofthe columella in relation
tothe upper lip.The nasolabial angle shouldbe in the range of90 to 120�(Figure 54-
18A).17The nasolabial angle is determinedby several factors:(1) the
anteroposteriorposition ofthe maxilla to some degree;(2)the anteroposterior
position ofthe maxil-lary incisors;(3) vertical position or rota-tion ofthe nasal
tip,which can result in amore obtuse or acute nasolabial angle;and(4) soft tissue
thickness ofthe maxillarylip that contributes the nasolabial angle,where a thin
upper lip favors a flatter angleand a thicker lip favors an acute angle.The
characterization ofthe lower facein profile (Figure 54-18B) is measured bythe
relative degree oflip projection,thelabiomental sulcus,the chin-neck length,and the
chin-neck angle.Maxillary andmandibular sagittal position can bedescribed by means
offacial divergence.The lower third ofthe face is evaluated inreference to the
anterior soft tissue pointat the glabella.Based on the position ofthemaxilla and
mandible relative to thispoint,a patient�s profile will be describedas
straight,convex,or concave,and eitheranteriorly or posteriorly divergent.Lip
projection is a function ofmaxillo-mandibular protrusion or
retrusion,dentalprotrusion or retrusion,and/or lip thick-ness.The description oflip
projectionFIGURE54-17A,The amount offacial concavity and chin projection at rest is
within acceptable limits.B,When this patient animates,an excessive amount ofchin
projection and facial concavity is revealed.ABRadixDorsumSupratipNasal
tipInfratipColumellaNasolabialangleLabiomentalsulcusReflexChin-neck lengthChin-neck
angleABFIGURE54-18A,The facial profile view.Superiorly,the radix ofthe nose is
characterized by an unbrokencurve that begins in the superior orbital ridge and
continues along the lateral nasal wall.The nasal dorsumis made up ofboth bony and
cartilaginous tissues.The nasal tip is described as the most anterior point
ofthenose,and the supratip is just cephalic to the tip.The columella is the portion
ofthe nose between the base ofthe nose (subspinale) and the nasal tip.B,The
characterization ofthe lower face in profile is measured by therelative degree
oflip projection,the labiomental sulcus,the chin-neck length,and the chin-neck
angle.
1102Part 8: Orthognathic Surgeryshould include pertinent informationfrom any ofthe
above sources.For exam-ple,a patient with lower lip protrusionmay be maxillary
(midface) deficient withdentoalveolar compensation includingflared incisors and a
thin maxillary vermil-ion display,or simply may have a thicklower lip that appears
protrusive.The labiomental sulcus is defined asthe fold ofsoft tissue between the
lower lipand the chin and may vary greatly in formand depth.The clinical variables
that canaffect the labiomental sulcus include (1)lower incisor position,where
uprightlower incisors tend to result in a shallowlabiomental sulcus because oflack
oflower lip projection,whereas excessivelower incisor proclination deepens
thelabiomental sulcus;and (2) vertical heightofthe lower facial third,which has a
directbearing on chin position and the labio-mental sulcus.Diminished lower
facialheight will usually result in a deeper labio-mental sulcus (just as in the
overclosed fulldenture patient),whereas a patient with along lower facial third has
a tendencytoward a flat labiomental sulcus.Chin projection is determined by
theamount ofanteroposterior bony projectionofthe anterior,inferior border
ofthemandible,and the amount ofsoft tissuethat overlays that bony
projection.Theamount ofprofile chin projection is mea-sured by the distance from
pogonion (orPg,the most anterior point on the bonychin) to soft tissue pogonion'
(or Pg',themost anterior point on the soft tissue pro-file ofthe chin) and is not
particularly alter-able by surgical means.In the adolescent,the amount ofchin is
directly correlated tothe amount ofmandibular growth thatoccurs because the chin
point itselfis borneon the mandible as it grows anteriorly.The angle between the
lower lip,chin,and Rpoint (the deepest point along thechin-neck contour) should be
approxi-mately 90�.An obtuse angle often indicates(1) chin deficiency,(2) lower lip
procum-bency,(3) excessive submental fat,(4),retropositioned mandible,and (5)
lowhyoid bone position.Another important measure in this areais the chin-neck
length and chin-neck angle.The angle,also termed the cervicomentalangle,has been
studied extensively in plasticsurgery and orthognathic literature.18Stud-ies report
that a wide range ofnormal neckmorphology exists,and that the cervico-mental angle
may vary between 105�and120�,with gender being a major considera-tion.Age ofthe
patient must be consideredwith regard to this area.Soft tissue �sag�dueto the loss
ofskin elasticity during aging is amajor cause ofchange in the
cervicomentalregion.Weight gain is another importantfactor in the morphology ofthis
area.Miniesthetic Examination:Frontal ViewThe facial areas for miniesthetic
examina-tion,as investigated from the frontal view,can be summarized as
follows:�Vertical characteristics ofthe smileLip-tooth-gingival
relationshipsGingival display on smileExcessive gingival display on smileVertical
maxillary excessShort philtrum heightExcessive curtainShort clinical crown
heightUpright maxillary incisorsInadequate gingival display on smileVertical
maxillary deficiencyDiminished curtainShort clinical crown heightFlared maxillary
incisors�Transverse characteristics ofthe smileArch formBuccal corridorCant ofthe
transverse occlusal planeVertical CharacteristicsLip-Tooth-Gin-gival RelationshipsA
key feature ofver-tical facial esthetic characteristics is therelationship between
the incisal edges ofthe maxillary incisors relative to the lowerlip as well as the
relationship between thegingival margins ofthe maxillary incisorsrelative to the
upper lip.The gingival mar-gins ofthe cuspids should be coincidentwith the upper
lip,and the lateral incisorspositioned slightly inferior to the adjacentteeth.It is
generally accepted that the gin-gival margins should be coincident withthe upper
lip in the social smile.However,this is very much a function ofthe age ofthe
patient,since children show moreteeth at rest and gingival display on smilethan do
adults.19Excessive Gingival Display on SmileThe vertical characteristics offacial
mini-esthetics impact the relative amount ofgingival display at rest and during
anima-tion.Gingival display is the amount of�gumminess�ofthe smile.Measuring
theamount ofgingival display on smile easi-ly quantitates a �gummy�smile.The deci-
sion as to whether the amount ofgingivaldisplay is an esthetic problem in
whichtreatment is desirable is a personalchoice.Orthodontists and oral and max-
illofacial surgeons tend to see the�gummy�smile as an unesthetic charac-
teristic,while laypersons attach impor-tance only in the more extreme cases.Theuse
ofcomputerized graphic simulationofthe frontal view ofthe smile is useful
incounseling a patient and showing poten-tial treatment changes.The individual
isthen able to guide the clinician andexpress opinions about what should andshould
not be corrected.Computer imag-ing not only provides the patient with avisual
template for treatment but it alsoprovides the clinician with a testingground for
treatment options.Thepatient in Figure 54-19A exhibits exces-sive gingival display
on smile,secondaryto vertical maxillary excess.The diagnosisofvertical maxillary
excess is confirmedby the facial characteristics ofa longlower facial third,lip
incompetence,
Database Acquisition and Treatment Planning1103excessive incisor display at
rest,andexcessive gingival display on smile.Supe-rior repositioning ofthe maxilla
was per-formed with excellent facial proportionsand smile esthetics (Figure 54-
19B).The patient in Figure 54-20A alsoexhibited excessive gingival display,but
hasnormal vertical facial proportions.Herincisor crown height,however,is only 8
mm.The etiology ofher �gummy�smile isnot an orthognathic problem or an ortho-dontic
problem but a cosmetic or periodon-tal problem.This diagnosis was confirmedand
further visualized through computer-ized image modification (Figure 54-20B
andC),simulating the crown-lengthening pro-cedure.Orthodontic intrusion
ofmaxillaryincisors would have reduced gingival displaybut would also have
adversely affected thesmile arc with concomitant flattening.Thiscase example
emphasizes differential diag-nosis ofgingival display issues and it alsoemphasizes
the optimization ofunestheticfacial traits while preserving those positivefacial
esthetic attributes.Transverse CharacteristicsThe threetransverse characteristics
offacial estheticsin the frontal dimension are (1) arch form,(2) buccal
corridor,and (3) the transversecant ofthe maxillary occlusal plane.Arch form plays
a pivotal role in thetransverse dimension.Recently,much atten-tion has been focused
on using broad squarearch forms in orthodontic treatment andorthognathic surgical
treatment.In cases inwhich the arch forms are narrow or col-lapsed,the smile may
also appear narrowand therefore present inadequate transversesmile
characteristics.An important consid-eration in widening a narrow arch
form,particularly in the adult,is the axial inclina-tion ofthe buccal
segments.Cases in whichthe posterior teeth are already flared lateral-ly are not
good candidates for dental expan-sion.Upright premolars and molars allowfor a more
bodily transverse expansion ofthe buccal segments in both adolescent andadult
patients,but are particularly impor-tant in the adult where sutural expansion
isless likely.Orthodontic expansion andwidening ofa collapsed arch form can dra-
matically improve the appearance offacialesthetics and smile by decreasing the size
ofthe buccal corridors and improving thetransverse smile dimension( Figure 54-
21Aand B).The transverse smile dimensionABFIGURE54-19A,This patient exhibits
excessive gingival display on smile,secondary to verticalmaxillary excess.B,The
actual post-treatment outcome.FIGURE54-20A,This patient exhibits excessive gingival
display,but has normal vertical facial propor-tions.Her incisor crown
height,however,is only 8 mm.The etiology ofher �gummy�smile is not an orthog-nathic
problem or an orthodontic problem but a cosmetic or periodontal problem.Band C,This
diagnosiswas confirmed and further visualized through computerized image
modification,simulating the crown-lengthening procedure.ABC
1104Part 8: Orthognathic Surgery(and the buccal corridor) is related to thelateral
projection ofthe premolars and themolars into the buccal corridors.The widerthe
arch form is in the premolar area,thegreater would be the portion ofthe
buccalcorridor filled.As alluded to in the previous casesabove,arch expansion can
have undesir-able effects.Expansion ofthe arch formmay fill out the transverse
dimension ofthe smile,but two undesirable side effectsmay result and careful
observation shouldbe made to avoid these side effects wherev-er possible.First,the
buccal corridor canbe obliterated and create a �denture�-likesmile.Second,when the
anterior sweep ofthe maxillary arch is broadened,the smilearc may be
flattened.Although it may notbe possible to avoid these undesirableaspects
ofexpansion,the clinician mustmake a judgment in concert with thepatient as to what
�trade-offs�are accept-able in the pursuit ofthe ideal facialesthetic outcome.The
last transverse characteristic offacial esthetics is the transverse cant
ofthemaxillary occlusal plane.Transverse cantofthe maxilla can be due to
differentialeruption and placement ofthe anteriorteeth,and skeletal asymmetry ofthe
skullbase and/or mandible resulting in a com-pensatory cant to the
maxilla.Intraoralimages or even mounted dental casts donot adequately reflect the
relationship ofthe maxilla to the smile.Only frontal smilevisualization permits the
orthodontist tovisualize any tooth-related asymmetrytransversely.Smile asymmetry
may also be due tosoft tissue considerations such as an asym-metric smile
curtain.In the asymmetricsmile curtain,there is a differential eleva-tion ofthe
upper lip during smile,whichgives the illusion oftransverse cant to themaxilla.This
smile characteristic empha-sizes the importance ofdirect clinicalexamination in
treatment planning thesmile,since this soft tissue animation isnot visible in a
frontal radiograph orreflected in study models.It is not welldocumented in static
photographicimages,and is documented best in digitalvideo clips.Miniesthetic
Examination:Oblique ViewMiniesthetic examination from theoblique view involves two
main areas:�Orientation ofthe palatal andocclusal planes�Smile arcThe oblique view
ofthe smile revealscharacteristics ofthe smile that are notobtainable on the
frontal view and certain-ly not obtainable through any cephalo-metric analysis.The
palatal plane may becanted anteroposteriorly in a number oforientations.In the most
desirable orien-tation,the occlusal plane is consonantwith the curvature ofthe
lower lip onsmile (see discussion ofsmile arcbelow).Deviations from this
orientation include adownward cant ofthe posterior maxilla,upward cant ofthe
anterior maxilla,orvariations ofboth.20In the initial exami-nation and diagnostic
phase oftreatment,it is important to visualize the occlusalplane in its
relationship to the lower lip.The smile arcshould be defined as therelationship
ofthe curvature ofthe incisaledges ofthe maxillary incisors,canines,premolars,and
molars to the curvature ofthe lower lip in the posed social smile.Theideal smile
arc hasthe maxillary incisaledge curvature parallel to the curvature ofthe lower
lip upon smile,and the termconsonantis used to describe this parallelrelationship.A
nonconsonantor flat smilearc is characterized by the maxillaryincisal
curvaturebeing flatter than thecurvature ofthe lower lip on smile.Earlydefinitions
ofthe smile arc were limited tothe curvature ofthe canines and theincisors to the
lower lip on smile becausesmile evaluation was made on directfrontal view.The
visualization ofthecomplete smile arc afforded by theoblique view expands the
definition ofthesmile arc to include the molars and thepremolars (Figure 54-
22).Miniesthetic Examination: Profile ViewThe facial areas for miniesthetic
examina-tion,as investigated from the profile view,can be summarized as
follows:�Overjet�Incisor angulationUpright maxillary incisorsFlared maxillary
incisorsRetroclined mandibular incisors The two miniesthetic
characteristicsvisualized in the sagittal dimension are over-jet and incisor
angulation (Figure 54-23).Excessively positive overjet is one ofthe mostABFIGURE54-
21A,The transverse smile dimension in this patient was characterized by narrow
archform and excessive buccal corridor.In this adult,the axial inclinations ofthe
molars and premolars werefavorable for orthodontic expansion.B,The transverse smile
dimension after orthodontic treatment.
Database Acquisition and Treatment Planning1105recognizable dental traits to the
layperson.Adolescents tend to label unflattering namessuch as �Andy Gump�and �Bucky
Beaver�onto children unfortunate enough to haveinherited this dentoskeletal
pattern.Howoverjet is orthodontically corrected involvesmacroelements such as jaw
patterns and softtissue elements such as nasal projection.Excessive positive
overjet is not as readilyperceived in the frontal dimension as it is inthe sagittal
dimension.Many Class II pat-terns have very esthetic smiles frontally,butnot when
the patient�s smile is observedfrom the side.In Class III patterns,the
samephenomenon may be true,in that the smilelooks esthetic on frontal smile,but on
theoblique or sagittal view,the overall appear-ance reflects the underlying
skeletal patternand dental compensation.The patient andparents have to decide with
the clinicianwhether this is an acceptable outcome.The amount ofanterior
maxillaryprojection also has great influence on thetransverse smile dimension in
the frontalview.When the maxilla is retrusive,thewider portion ofthe dental arch is
posi-tioned more posteriorly relative to theanterior oral commissure.This creates
theillusion ofgreater buccal corridor in thefrontal dimension.Overall,the
sagittalcant ofthe maxillary occlusal plane in nat-ural head position can influence
the smilearc in the frontal dimension,affecting ver-tical characteristics.A
negative cant ofthisplane will diminish the apposition oftheincisal edges ofthe
maxillary anteriorteeth to the superior vermilion border ofthe lower lip at
smile.Dental ExaminationThe dental component ofthe clinicalexamination is the
evaluation ofanystanding periodontal or cariogenic diseaseprocess and the
assessment ofthe patient�socclusion.The areas for dental examina-tion can be
summarized as follows:�AlignmentCrowding Spacing Missing or supernumerary
teeth�Anteroposterior Angle classificationOverjetCompensation�Bite depthAnterior
PosteriorCompensation�TransverseCompensation�Functional occlusal issuesMissing
teeth and sequelaeOcclusal interferences and para-functionIntra-arch and interarch
relationshipsare described in the categories ofdentalalignment,anteroposterior
occlusion,andbite depth.Clinically,the patient�s occlu-sion should be examined both
in a staticand dynamic sense.The maxillary and mandibular dentalarches are
described as either well aligned,crowded,or spaced.The extent ofcrowd-ing or
spacing is usually noted in millime-ters.Individual teeth are described byvirtue
oftheir spatial position and degreeofrotation.Therefore,an incisor could
bedescribed as severely rotated and in lin-guoversion.Any congenitally
missing,lost,or supernumerary teeth are noted.Adescription ofteeth that have been
severe-ly worn or damaged due to trauma shouldbe included.In terms ofthe static
occlusion,Angle�s classification ofthe patient shouldbe recorded.The Angle Class I
relationshipis such that the mesiobuccal cusp ofthemaxillary first molar should
rest in thebuccal groove ofthe mandibular firstmolar.The Angle Class II
relationshipexhibits a more anterior position ofthemesiobuccal cusp ofthe maxillary
firstmolar and the Angle Class III relationshipexhibits a more posterior position
ofthemesiobuccal cusp ofthe maxillary firstmolar.The degree ofincisor overjet
thataccompanies an anteroposterior discrep-ancy should also be noted.Concepts
ofIncisor CompensationIncisor compensation in the sagittal view isvery important in
planning the presurgicalFIGURE54-22The smile arc is best visualized inthe oblique
view,and should be defined as therelationship ofthe curvature ofthe incisal
edgesofthe maxillary incisors,canines,premolars,and molars to the curvature ofthe
lower lip inthe posed social smile.The 45�view permitsvisualization ofvermilion
display,lip fullness,and turgor not readily seen in another view.FIGURE54-23The two
miniesthetic character-istics visualized in the sagittal dimension areoverjet and
incisor angulation.
1106Part 8: Orthognathic Surgeryorthodontics,yet not fully recognized byboth
orthodontists and surgeons alike.Inmost cases ofskeletal dysplasia,whether inthe
range ofsurgical or nonsurgical treat-ment,dental compensation is a
commonfeature.The forms and expression ofthiscompensation are as complex as the
myri-ad ofdentoskeletal problems that exist,but there are common patterns
frequentlyencountered.In the diagnosis and propertreatment ofthese cases,the
primaryresponsibility ofthe orthodontist is to rec-ognize these compensations and
eliminateor decompensatethem.The range ofwhichcompensations are problematic is not
con-crete,so the surgeon and the orthodontistmust decide how much compensation
isacceptable and what is to be done fordecompensation.Although we tend tothink
ofthese compensations as ananteroposterior consideration (incisorangulation
problems),dental compensa-tion can occur in all planes ofspace.Class II and Class
III ProblemsTheclassic pattern ofcompensation in ClassII skeletal patterns is the
proclination ofthe mandibular incisors and retroclina-tion ofthe maxillary
incisors.Converse-ly,Class III skeletal dysplasias often fea-ture retroclination
ofthe mandibularincisors and proclination ofthe maxil-lary incisors.The
orthodontist must rec-ognize these compensations and decidewhat degree
ofcompensation is accept-able and what requires substantive treat-ment.For
example,iflower incisor flarein the Class II patient is only moderate,what is the
value ofremoving twomandibular premolars to upright theincisors? These
decompensation deci-sions affect the treatment outcome inthree basic ways:(1)
inadequate incisorpositioning can compromise buccalinterdigitation;(2) incisor
positioningcan substantially affect the esthetic out-come;and (3) in certain types
offunc-tional problems such as obstructive sleepapnea syndrome,esthetic
considerationshave a lower priority compared to cor-rection ofthe functional
problem.The effect ofincisor angulation onbuccal occlusal relationships wasadvanced
and best expressed byAndrews.21In presurgical preparation formandibular
advancement,maxillaryincisors that are not properly flared ormandibular incisors
that are left overlyflared may result in the following:(1)insufficient overjet to
provide for ade-quate advancement ofthe mandible fromthe esthetic standpoint,and
(2) theinability to achieve desired Class I buccalsegments because the advanced
nature ofthe lower incisor edge does not permitinterdigitation ofthe buccal
segments(Figure 54-24A and B).The appropriateamount ofincisor angulation can
bedetermined either through cephalomet-ric investigation or by simply holdingstudy
models in a simulated Class Imolar relationship.Vertical Characteristics and
Compensa-tionsBite DepthThe vertical compo-nent ofthe dental examination
describesbite depth.A patient�s anterior bite depthis the amount ofmaxillary
incisor overbiterelative to the mandibular incisors.There-fore,a patient can be
described as havingan anterior open bite,satisfactory bite (25to 50% overbite),or
an anterior deep bite.The posterior bite depth is usually charac-terized as being
open,satisfactory,or col-lapsed.The latter is seen when the patientis missing
unilateral or bilateral posteriordental units.FIGURE54-24A,Inadequate
decompensation in Class II correction makes Class I buccal segments not attainable
because the flared lower incisors do notpermit interdigitation ofthe posterior
segments.B,Inadequate decompensation in Class III correction makes Class I buccal
segments not attainable becausethe upright lower incisors or flared maxillary
incisors do not permit interdigitation ofthe posterior segments.AB
Database Acquisition and Treatment Planning1107Curve ofSpeeDental compensation
inthe vertical plane has to do with aberra-tions in the curve ofSpee.The curve
ofSpee is measured by the arc extending fromthe cusp tips ofthe incisors
posteriorly tothe cusp tips ofthe molars in a sagittalview.Clinically,the study
model can beplaced on a flat surface and the cusp tipsrelative to that flat plane
will give a roughestimate ofthe maxillary and mandibularcurve ofSpee.This is an
important diag-nostic feature ofmodel analysis in recog-nizing potential pitfalls
that may beencountered during orthodontic prepara-tion for orthognathic surgery.For
example,in a patient in whom the anterior segmentis significantly superior (greater
than 2 mm) to the posterior segment,failure torecognize this occlusal plane
differentialmay result in orthodontic flattening priorto surgery and postsurgical
relapse,result-ing in anterior open bite.22Transverse CompensationsThe Class
IIpatient often has narrowing ofthe maxillain response to the narrower portion
ofthemandible being placed in the broader por-tion ofthe maxillary arch.In the
Class IIIpatient,the maxillary posterior segmentsare often flared buccally in
compensationfor the wider portion ofthe mandiblebeing placed into the narrower
aspect ofthe maxilla.By holding the study modelsin a simulated Class I
relationship,thesecompensations can be easily recognized(Figure 54-25).Functional
Occlusal IssuesThe last por-tion ofthe dental examination relates todynamics
ofocclusal function.The clini-cian should ascertain whether the patientexhibits a
discrepancy between maximumintercuspal position and retruded contactposition in the
anteroposterior dimen-sion.In general,small differences exist inthe vast majority
ofpatients.Only largeslides should be recorded.Ifthe patient�sdentition is
mutilated the clinician shouldnote the resultant occlusal compensa-tions.Any
supererupted teeth will createlateral and anteroposterior interferences.A history
ofbruxism or other parafunc-tional habits will affect orthodontic appli-ances and
will impact on the type ofretention used post-treatment.Microesthetic
ExaminationThe microesthetic portion ofthe clinicalexamination focuses on the
morphologyoftooth-to-tooth contacts and the sur-rounding intraoral
tissues,summarizedas follows:�Dentogingival relationshipsTooth form/tooth
contact/gingival architectureAs a structural unit,the dentogingivalcomplex is
defined by the relationship ofthe teeth to the alveolar bone and sur-rounding
gingival and masticatory mucosa.The factors that influence the appearance ofthe
dentogingival complex are the patient�speriodontal status and past history ofdis-
ease,the proximal and occlusal contacts ofthe teeth,the shape ofthe individual
teeth,and the type ofgingival architecture.An assessment ofthe patient�s
currentperiodontal status is exceedingly impor-tant from an orthodontic and
surgicalpoint ofview.The clinician should take anaccurate dental history in order
to ascer-tain whether the patient has had any peri-odontal disease and related
treatment.Clinically,the teeth should be examinedfor plaque accumulation and
anysupragingival calculus.Patients who can-not maintain a satisfactory level
oforalhygiene are at risk for gingival inflamma-tion,attachment loss,and caries
duringpresurgical orthodontic treatment.Peri-apical radiographs combined with
apanoramic radiograph will reveal alveolararchitecture and any evidence ofhorizon-
tal or vertical bone loss.Suspected peri-odontal defects should be probed and
thedepths recorded.The extent ofattachmentloss and degree oftooth mobility
willinfluence tooth movement.Surgical treatment planning ofthesegmental Le Fort I
osteotomy shouldconsider gingival architecture in relationto maxillary
segmentation.Ifthe incisionsare made mesial to the maxillary canines,the patient
may lose the interdental papil-la in between this tooth and the maxillarylateral
incisor.By positioning the incisionsdistal to the maxillary canines,an obliter-ated
papilla can be more easily camou-flaged due to the convexity ofthe
canine.Computerized Cephalometric PredictionFor computer image prediction,a
digitalmodel ofthe cephalometric tracing must beentered into computer memory.It
isimportant that the radiograph be obtainedin natural head position,with the
teethlightly together and in retruded contactposition and the lips relaxed.The
details ofthe digital model vary among the severalcurrently available software
programs butthe similarities are more impressive thanthe differences.The more
points in the dig-ital model,the greater the anatomic fidelityofthat model.On the
other hand,the morepoints that are digitized,the more time ittakes to perform the
digitization process.A lateral image ofthe patient�s profile,matching the
cephalograms as closely asFIGURE54-25Transverse problems are firstdiagnosed by
holding the study models together ina simulated Class I relationship.The most com-
monly found transverse problem is that the max-illa is narrower than the mandible
in cases similarto that ofthis patient who was being evaluated forClass II
correction by mandibular advancement.
1108Part 8: Orthognathic Surgerypossible in head position and lip posture,must be
captured and entered into thecomputer program (either directly via dig-ital
photography or by scanning a slide).Ideally,the radiograph and profile imagewould
be taken simultaneously,althoughthe hardware arrangement to do this doesnot yet
exist.The patient in Figure 54-26A present-ed for correction ofa severe Class II
dento-facial deformity.After clinical examinationand diagnostic records,digital
image inte-gration and algorithmic projections areused for consultation with the
patient.After the records are gathered,the nextstep in the treatment planning is to
super-impose the profile image and radiograph,with the hard and soft tissues
matched toeach other as closely as possible.Most pro-grams use the profile as the
major methodofimage coordination.Once the imagesare coordinated,any cephalometric
analy-sis can be displayed,although in contem-porary surgical planning,the goal
oftreat-ment is not what the analysis indicates.At that point,a �treatment
screen�(Fig-ure 54-26B) provides the clinician with�handles�(the blue squares) by
whichselected sections ofhard tissue can bemoved (eg,the mandible,the
maxilla,ormaxillary incisor segment);the proceduressimilar to the use oftemplates
and manualprediction.In this case illustration,surgicalmandibular advancement is
being contem-plated.Dental compensation is present inthe form offlared mandibular
incisors,anddecompensation is recommended todecompensate the dentition in order
toincrease the overjet,thus maximizing themagnitude ofmandibular
advancement.Simulation oflower first premolar extrac-tion and lower incisor
retraction is made onthe treatment screen;the software applies itsimbedded
algorithms for profile predictionand creates a new line drawing ofthe
profile(Figure 54-26C) reflecting the expected pro-file change after incisor
decompensation.The algorithms may be ratios based onregressive equations and
multiple correla-tions.They are not the same in all programs:the quality ofthe
algorithms is the majordeterminant ofhow well or poorly the pre-dicted profile
matches the actual changeproduced by the treatment.The quantitativetable on the
right ofFigure 54-26C providesto the clinician the measurements ofthemovements made
on screen calibrated toactual movements required clinically toachieve the projected
change.After decompensation movements aresimulated,the mandible is advanced on
thetreatment screen to ideal overjet,and thesoftware then �warps�the original
profileimage to fit the prediction line drawing,producing an image that conveys
muchmore visual information to the clinicianand patient than the line drawing
(Figure54-26D).As treatment is being planned,the amount ofchange is suggested
until,within the limits ofpossible surgicalchange,it looks best;it is advantageous
toinclude the patient in this process ofadjusting the amount ofchange to providean
optimal outcome.In this case,a com-parison image is generated so the patientmay
visualize the profile outcome expectedwith mandibular advancement (Figure 54-
26E).The profile was judged to beimproved but was still clearly chin defi-
cient.Simulation ofchin advancement isthen performed (Figure 54-26F),not byusing
any cephalometric norm or predeter-mined value,but by simply using the
facialoutline as a guide.In other words,the chinis moved horizontally and
vertically until itmeets the approval ofthe patient.The pro-jected final profile
image is depicted in Fig-ure 54-26G.The quantitative table reflectsthe exact
movements in millimeters so thatthe surgeon and orthodontist have a pre-cise plan
for the amount ofchange neededto produce the desired result seen in Figure54-
26H.Presurgical planning using thismethodology should eliminate �on-the-
table�estimates ofwhether or not thepatient needs �a bit more chin.�It is ludi-
crous to make esthetic treatment decisionswith the patient under general
anesthesia,horizontal,fully draped,paralyzed,andwith a nasal tube in place.An
important consideration is theaccuracy ofthe computer predictionprocess.Although it
is far from perfect(some computer programs are more accu-rate than others),it is
good enough to beclinically useful.23�27Chin predictions areusually quite accurate
and those oftheupper lip are reasonably good,whereas pre-dictions ofthe lower lip
can be problemat-ic.As the data on which algorithms arebased become more
extensive,as differentalgorithms are applied when vertical andanterior changes
occur,and as multipleregression equations replace simple ratios,accuracy can be
expected to improve.28It could be said that in this era ofinformed consent and
bioethical decision-making,the patient should be activelyinvolved in the process
ofcomputer predic-tion and treatment planning.Cultural andfamilial traits may be
important to thepatient.Surgeons and orthodontists tend towant to �optimize�all
patients to the pre-vailing esthetic norm,which diminishes anyethnic variation in
dentofacial appearance.Synthesis ofan OptimizedProblem ListThe data derived from
the systematic clini-cal examination and analysis ofpatientrecords are synthesized
into a diagnosticoptimized problem list.Essentially there aretwo branches in the
problem-solving tree:esthetics and function.Thus,the diagnosticproblem list should
be subdivided into thecategories ofmacroesthetic problems,mini-esthetic
problems,microesthetic problems,and functional problems.All recognizableproblems
that are relevant to the patient�schiefcomplaint should be rank-ordered.Lastly,each
problem should be evaluated interms ofits therapeutic modifiability.Conceptually
and operatively,the ortho-dontist and surgeon have to visualize thedesired solution
to the specific problem andthen assess whether the given solution willnegatively
impact some other dentofacial
Database Acquisition and Treatment Planning1109feature at the same time.The concept
offacial optimization involves the preserva-tion ofas many positive elements as
possi-ble,while harmonizing those elements thatfall short ofthe esthetic and
functionalneeds ofthe patient.The problems thatmight exceed the limitations
oftreatmentor perhaps have a poor therapeutic progno-sis should be
described.Informed consentand bioethical treatment ofthe surgicalpatient requires
that the clinician explainthe risk/benefit considerations ofthe pro-posed treatment
strategy.The goal ofthesystematized clinical examination and opti-mized problem-
oriented diagnosis is torecord and analyze the data in such a waythat the required
treatment becomesimplicit in the description ofthe problem.FIGURE54-26A,This
patient presented for correction ofa severe Class II dentofa-cial deformity.B,A
�treatment screen�provides the clinician with �handles�(theblue squares) by which
selected sections ofhard tissue can be moved (eg,themandible,the maxilla,or the
maxillary incisor segment); the procedures are similarto the use oftemplates and
manual prediction.C,Simulation oflower first premo-lar extraction and lower incisor
retraction is made on the treatment screen.The soft-ware applies its imbedded
algorithms for profile prediction and creates a new linedrawing ofthe profile
reflecting the expected profile change after incisor decompen-sation.D,After
decompensation movements are simulated,the mandible isadvanced on the treatment
screen to ideal overjet,and the software then �warps�theoriginal profile image to
fit the prediction line drawing,producing an image thatconveys much more visual
information to the clinician and patient than the linedrawing.E,In this case,a
comparison image is generated so that the patient mayvisualize the profile outcome
expected with mandibular advancement.F,Simulationofchin advancement is then
performed,not by using any cephalometric norms orpredetermined value,but by simply
using the facial outline as a guide.G,The pro-jected final profile image.H,The
actual treatment result.
A
B C
E F G
H
D
1110Part 8: Orthognathic SurgeryReferences1.Jacobson A.The proportionate template
as adiagnostic aid.Am J Orthod 1979;75:156�72.2.Jacobson A.Orthognathic diagnosis
using theproportionate template.Oral Surg1980;238:820.3.Jacobson
A,editor.Radiographic cephalometry:from basics to videoimaging.Carol
Stream(IL):Quintessence Publishing Co.;1995.4.Broadbent BH Sr,Broadbent BH
Jr,GoldenWH.Bolton standards ofdentofacial devel-opmental growth.St.Louis
(MO):C.V.Mosby Co.;1975.5.Sonnesen L,Bakke M,Solow B.Malocclusiontraits and
symptoms and signs oftemporo-mandibular disorders in children with
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andtemporomandibular disorders.Oral SurgOral Med Oral Pathol Oral Radiol
Endod1997;83:107�17.7.Sarver DM,Ackerman JL.About face � the re-emerging soft
tissue paradigm.Am J OrthodDentofacial Orthop 2000;117:575�6.8.Sarver DM,Ackerman
MB.Dynamic smilevisualization and quantification:part 1.Evolution ofthe concept and
dynamicrecords for smile capture.Am J OrthodDentofacial Orthop
2003:124;4�12.9.Sarver DM.Esthetic orthodontics and orthog-nathic surgery.St.Louis
(MO):C.V.MosbyCo.;1997.10.Sarver DM.The smile arc � the importance ofincisor
position in the dynamic smile.Am JOrthod Dentofacial Orthop
2001;120:98�111.11.Ackerman Jl,Ackerman MB,Brensinger CM,Landis JR.A morphometric
analysis oftheposed smile.Clin Orth Res 1998;1:1�11.12.Ackerman MB.Digital video as
a clinical toolin orthodontics:dynamic smile design indiagnosis and treatment
planning.29thAnnual Moyers Symposium on Informa-tion Technology and Orthodontic
Treat-ment.Vol 40.Ann Arbor (MI):UniversityofMichigan Press;2003.13.Farkas LG,Munro
JR.Anthropometric facialproportions in medicine.Springfield (IL):Charles C.Thomas
Publisher Ltd;1987.14.Peck H,Peck S.A concept offacial esthetics.Angle Orthod
1970;40:284�317.15.Mazur A,Mazur J,Keating C.Military rankattainment ofa West Point
class:effects ofcadets�physical features.Am J Soc1984;90:125�50.16.Pessa JA.The
potential role ofstereolithographyin the study offacial aging.Am J
OrthodDentofacial Orthop 2001;119:117�20.17.Krugman ME.Photo analysis ofthe
rhinoplas-ty patient.J Ear Nose Throat 1981;60:56�9.18.Sommerville JM,Sperry
TP,BeGole EA.Mor-phology ofthe submental and neck region.Int J Adult Orthod
1988;3:97�106.19.Zachrisson BU.Esthetic factors involved inanterior tooth display
and the smile:ver-tical dimension.J Clin Orthod 1998;32:432�45.20.Burstone
CJ,Marcotte MR.The treatmentocclusal plane.In:Problem solving inorthodontics:goal-
oriented treatmentstrategies.Chicago (IL):Quintessence Pub-lishing
Co.;2000.p.31�50.21.Andrews LF.Straight wire:the concept and theappliance.San Diego
(CA):L.A.Wells Inc.;1989.22.Lo FM,Shapiro PA.Effect ofpresurgicalincisor extension
on stability ofanterioropen bite malocclusion treated withorthognathic surgery.Int
J Adult OrthodOrthognath Surg 1998;13:23�34.23.Sinclair PM,Kilpelainen P,Phillips
C,et al.Theaccuracy ofvideo imaging in orthognathicsurgery.Am J Orthod Dentofacial
Orthop1995;107:177�85.24.Upton PM,Sadowsky PL,Sarver DM,HeavenTJ.Evaluation ofvideo
imaging predictionin combined maxillary and mandibularorthognathic surgery.Am J
Orthod Dento-facial Orthop 1997;112:656�65.25.Syliangco ST,Sameshima GT,Kaminishi
RM,Sinclair PM.Predicting soft tissue changesin mandibular advancement
surgery:acomparison oftwo video imaging systems.Angle Orthod
1997;67:337�46.26.Sameshima GT,Kawakami RK,Kaminishi RM,Sinclair PM.Predicting soft
tissue changesin maxillary impaction surgery:a compari-son oftwo video imaging
systems.AngleOrthod 1997;67:346�54.27.Kazandjian S,Sameshima GT,Champlin T,Sinclair
PM.Accuracy ofvideo imaging forpredicting the soft tissue profile aftermandibular
set-back surgery.Am J OrthodDentofacial Orthop 1999;115:382�89.28.Peters DG.Lower
lip changes in surgical cor-rection ofClass I malocclusion
[Master�sdissertation].Chapel Hill (NC):UniversityofNorth Carolina;2001.
CHAPTER 55Orthodontics for Orthognathic SurgeryLarry M.Wolford,DMDEber
L.L.Stevao,DDS,PhDC.Moody Alexander,DDS,MSJoao Roberto Goncalves,DDS,PhDModerate to
severe occlusal discrepanciesand dentofacial deformities in late adoles-cents and
adults usually require combinedorthodontic treatment and orthognathicsurgery to
obtain optimal,stable,func-tional,and esthetic results.The basic
goalsoforthodontics and orthognathic surgeryare to (1) satisfy the
patients�concerns,(2)establish optimal functional outcomes,and (3) provide good
esthetic results.Toaccomplish this the orthodontist and theoral and maxillofacial
(OMF) surgeonmust be able to correctly diagnose existingdental and skeletal
deformities,establishan appropriate treatment plan,and prop-erly execute the
recommended treatment.The orthodontist is limited,to a greatextent,by growth,and
although the ortho-dontist can move teeth and,to somedegree,the alveolar bone,he or
she doesnot have any appreciable effect on the basalbone ofthe jaws.The
orthodontist�s role isto align the teeth relative to the maxillaryand mandibular
jaws.The OMF surgeon isresponsible for surgically repositioning thejaw(s) and
associated structures.It is very important to listen to andunderstand the patients
concerns.Empa-thetic listening from the first appointmentand throughout the
treatment will buildtrust,improve communication,and helpprovide a quality end
result for all partiesinvolved.Comprehensive analysis ofthepatient and the complete
orthodonticrecords (cephalograms,pantomograms,photographs,dental models) are impor-
tant for diagnosis and development ofthepresurgical orthodontic
goals.Althoughdetailed analysis ofthe patient�s facial andjaw structures from a
clinical and radi-ographic perspective are vitally important,the focus ofthis
chapter will be the teethand orthodontic considerations in prepa-ration for
orthognathic surgery.Otherimportant factors in diagnosis,treatmentplanning,and
outcomes,such as patientconcerns,psychosocial factors,masticato-ry
dysfunction,airway problems,speechdifficulties,temporomandibular joint(TMJ)
pathologies,and comprehensiveorthognathic surgery work-up are dis-cussed elsewhere
in this book.The normal values provided in thischapter are not absolutes for every
patientbecause ofindividual size,morphologicvariances,and racial and ethnic differ-
ences.They are provided as a guide to helpthe clinician evaluate his or her
patient.Establishing an all-inclusive diagnosisis paramount to developing a
comprehen-sive treatment plan.The orthodontistmust determine the orthodontic
goalsbased on the pretreatment findings and onthe projected treatment
outcome.Thischapter will first present orthodontic diag-nostic information,followed
by orthodon-tic treatment considerations.Clinical and Dental Model DiagnosisFrom an
orthodontic standpoint,in eval-uating the occlusion and dental factors,the clinical
and dental model analyses cor-related with the cephalometric analysisprovide the
most information for diagno-sis and treatment planning.There are 12 basic
evaluations that are helpful forthese determinations.1.Arch length:This assessment
corre-lates the mesiodistal widths oftheteeth relative to the amount ofalveo-lar
bone available and aids in identify-ing the presence ofcrowding or
1112Part 8: Orthognathic Surgeryspacing.This helps determine ifteethneed to be
extracted or ifspaces needto be either created or closed (Figure 55-1).Clinical and
dentalmodel assessment correlated tocephalometric analysis will aid indetermining
arch length require-ments.Generally Class II patients willtend to have more
crowding in themandibular arch and less in the max-illary arch,whereas Class III
patientsmay have spacing in the mandibulararch but a tendency for crowding inthe
maxillary arch.2.Tooth-size analysis:This analysisrelates the mesiodistal width
ofthemaxillary teeth compared with themandibular teeth.A tooth-size dis-crepancy
(TSD) causes incompatibili-ty ofthe dental alignment and canoccur in the anterior
teeth,premolars,and molars.Approximately 40% ofpatients with dentofacial
deformitieswill have an anterior TSD affecting theanterior six teeth ofthe
maxillary andmandibular arches (the mandibulararch is commonly too large
comparedwith the maxillary arch),usually dueto small maxillary lateral
incisors.Insuch cases proper tooth alignmentwith all spaces closed often
precludesthe establishment ofa good Class Icuspid-molar relationship with treat-
ment.Instead,a Class II end-on cuspid-molar occlusal relationshipmay
result.Occasionally the maxillaryanterior six teeth may be too large forthe
mandibular anterior teeth,creat-ing an excessive anterior overjet whenin a Class I
cuspid relationship.Deter-mination ofa TSD pretreatment willprovide the opportunity
to correct theTSD during the presurgical orthodon-tic phase oftreatment.Explaining
tothe patient,before treatment,thatsmall maxillary lateral incisors mayneed
restorative bonding to maximizethe quality esthetic and functionaloutcome is
important,so that thepatient is aware from the onset ofthetime and financial
commitment nec-essary for treatment.The normalmesiodistal widths ofeach ofthe per-
manent teeth are recorded in Tables55-1 and 55-2.Variations from thenorm may create
difficulties in theteeth fitting properly.Bolton�s analysisis a method tocorrelate
the widths ofthe maxillaryand mandibular anterior six teeth.Needle-point calipers
can be used tomeasure each individual tooth,andsuccessive holes punched into a
tabletfor each ofthe anterior six teeth foreach arch.Then a measurement fromthe
first to last holes will give the sum-mation ofmesiodistal widths oftheanterior six
teeth for each arch (Fig-ures 55-2 and 55-3).The summationofthe mesiodistal widths
ofthe max-illary anterior six teeth measured atthe contact level,divided into
thecombined width ofthe mandibularanterior six teeth,yields a value calledFIGURE55-
1Arch length assessment correlatesthe mesiodistal widths ofthe teeth relative to
theamount ofalveolar bone available and aids inidentifying the presence ofcrowding
or spacing.The curved wire illustrates ideal cuspid andincisor tip position
relative to the basal bone.Table 55-1Maxillary Mesiodistal Teeth DiametersCentral
Lateral FirstSecondFirst Second
Incisor*Incisor*Cuspids*Bicuspids*Bicuspids*Molars*Molars*Males8.9 (0.59)6.9
(0.64)8.0 (0.42)6.8 (0.47)6.7 (0.37)10.6 (0.56)9.5 (0.71)Females8.7 (0.57)6.8
(0.64)7.5 (0.36)6.6 (0.46)6.5 (0.46)10.2 (0.58)8.8 (0.73)Adapted from Moyers RE et
al.2 *Measurements in mm (SD).Table 55-2Mandibular Mesiodistal Teeth
DiametersCentral Lateral FirstSecondFirst Second
Incisor*Incisor*Cuspids*Bicuspids*Bicuspids*Molars*Molars*Males5.5 (0.32)6.0
(0.37)7.0 (0.40)6.9 (0.63)7.2 (0.47)10.7 (0.60)10.0 (0.67)Females5.5 (0.34)5.9
(0.34)6.6 (0.34)6.8 (0.70)7.1 (0.46)10.3 (0.74)9.5 (0.59)Adapted from Moyers RE et
al.2 *Measurements in mm (SD).
Orthodontics for Orthognathic Surgery1113the intermaxillary (Bolton�s) index.The
average index (percentage) is 77.5�3.5.1 A simple conversion ofthis fac-tor would
be to measure the width ofthe mandibular anterior six teeth andthen multiply that
sum by 1.3.Thisresults in a calculated ideal maxillaryarch width.The difference
betweenthe calculated and the actual maxillaryarch width values determines the
TSD(see Figure 55-3).This evaluation isvery helpful in determining presurgi-cal
orthodontic and surgical goals.TSDs can also occur in the premolarand molar areas
(normally the samemaxillary and mandibular teeth aresimilar in size) where the
mandibularteeth may be significantly larger thanthe maxillary teeth.The Bolton�s
analysis is not perfectand functions only as a guide inassessing the tooth-size
compatibilityofthe anterior teeth because it doesnot take into consideration the
labi-olingual thickness ofthe incisors,theaxial inclination ofthe teeth,or
thethickness and prominence ofthe mar-ginal ridges.A thin labiolingualdimension
ofthe maxillary incisorsmay compensate for small TSDs,butthicker than normal
dimensions orprominent marginal ridges may pre-clude a Class I cuspid
relationshipeven though the Bolton�s index is nor-mal.An accurate dental model
ortho-dontic wax set-up may achieve a moreaccurate assessment.3.Incisor
angulation:This refers to theangulation ofthe maxillary andmandibular incisors
relative to theirrespective basal bones.The dentalmodels are correlated to the
cephalo-metric analysis and the ideal axialinclination ofthe incisors
determined(Figure 55-4).The incisor angulationanalysis contributes to the
determina-tion ofwhether extractions are neces-sary,spaces need to be created or
elim-inated,and what mechanics arerequired to align and level the archesor segments
ofthe arches.The key is toget the incisors in proper position andangulation over
basal bone.4.Arch width analysis:This refers to theevaluation ofthe intra-arch
transversewidths between the maxillary andmandibular arches.The average maxil-lary
and mandibular arch widths foradults are listed in Tables 55-3 and 55-4(data from
University ofMichigan Caucasian study).2These averages areonly guides and do not
account forFIGURE55-2Bolton�s analysis.Needle-pointcalipers are used to measure
each tooth at acontact-point level to aid in tooth-size analysis.FIGURE55-3Bolton�s
analysis.Successive holesare punched into a tablet for each ofthe anteriorsix teeth
for each arch.Then measuring from thefirst hole to the last hole will give the
summationofthe mesiodistal widths ofthe anterior six teethin each arch.Multiplying
the summation ofthemandibular anterior six teeth (LA) by 1.3 yieldsthe calculated
arch width for the maxillary ante-rior six teeth (UA).Subtracting the actual max-
illary anterior arch width from the calculatedwidth yields the tooth-size
discrepancy.88448202290FIGURE55-4Cephalometricanalysis.Normal maxillary depthangle
is 90�3�and mandibulardepth is 88�3�.Normal occlusalplane angulation is
8�4�.Normalmaxillary incisor angulation to thenasion point A (NA) line is 22�2�with
the labial surface ofthe incisorbeing 4 mm �2 mm anterior to theNA line.Normal
mandibularincisor angulation to the nasionpoint B (NB) line is 20�2�withthe labial
surface ofthe incisorbeing 4 mm �2 mm anterior to theNB line.
1114Part 8: Orthognathic Surgerypatient size,or racial or ethnic differ-
ences.However,from a practical stand-point a good way to analyze the archwidth is
to relate the models to theocclusal position that is to be achievedwith the
surgical correction and thenassess the transverse relationship.Forexample,ifa
patient has a Class IIocclusion,position the models in aClass I cuspid-molar
relation and eval-uate the transverse width relationship.Likewise,a patient with a
Class IIIocclusion is evaluated by positioningthe models into a Class I cuspid-
molarrelationship.When a Class II relation-ship is shifted to a Class I
relationship,the maxilla may be narrow and requireexpansion.In some cases it may be
indi-cated to evaluate the transverse rela-tionship by placing the models into
aClass II molar position to determine ifaClass I cuspid and Class II molar rela-
tionship (this would require maxillarybicuspid extractions) would be best forthat
particular patient;this may be ben-eficial when there is significant crowd-ing in
the maxillary arch and no crowd-ing in the mandibular arch.Transversediscrepancies
will influence the presur-gical orthodontics and dictate the surgi-cal procedures
required.5.Curve ofSpee:This evaluates the verti-cal position ofthe anterior teeth
com-pared with the posterior teeth.Thisassessment can be determined by plac-ing the
occlusion ofthe maxillary den-tal model on a flat plane;the incisorsshould be about
1 mm above the flatplane (Figure 55-5A).Placing theocclusion ofthe mandibular
dentalmodel on a flat plane should see themandibular incisors elevated 1 mmabove
the midbuccal teeth.A signifi-cant accentuated curve ofSpee in themaxilla is
usually associated with ananterior open bite and a reverse curveassociated with an
anterior deep bite.An accentuated curve ofSpee in themandible (Figure 55-5B) is
commonlyassociated with an anterior deep biteand a reverse curve associated with
anopen bite.Accentuated or reversecurves ofSpee will influence whetherthe curve in
each arch requires correc-tion,and ifso,whether the correctionwill be achieved by
orthodontics,withor without extractions,opening spaces,or by surgical
intervention.6.Cuspid-molar position:This identi-fies the angle classification and
den-tal interrelationships.It is usuallypreferable to have a Class I cuspid-molar
relationship as an outcomeresult;however,a Class II molar rela-tionship is
acceptable.A Class IIImolar relationship is less desirablebecause the mandibular
first molarfunctions against the maxillary sec-ond bicuspid,but it may be
indicatedin some cases.Table 55-3Maxillary Arch Width*Cuspids�First
Bicuspids�Second Bicuspids�First Molars�Second Molars�Males32.3 (1.7)36.7 (2.0)41.5
(2.5)47.1 (2.8)52.3 (3.4)Females31.2 (2.45)34.6 (3.2)39.3 (2.2)44.3 (2.3)49.3
(2.8)Adapted from Moyers RE et al.2*All measurements at centroid.�Measurements in
mm (SD).Table 55-4Mandibular Arch Width*Cuspids�First Bicuspids�Second
Bicuspids�First Molars�Second Molars�Males24.8 (1.3)32.8 (1.5)37.6 (2.3)43.0
(2.7)49.0 (2.3)Females23.1 (2.0)31.8 (1.4)36.8 (1.3)41.7 (2.3)47.2 (2.1)Adapted
from Moyers RE et al.2*All measurements at centroid.�Measurements in mm
(SD).FIGURE55-5A,This maxillary arch demon-strates an increased curve ofSpee.B,An
accen-tuated (increased) curve ofSpeeis seen in themandibular arch.AB
Orthodontics for Orthognathic Surgery11157.Tooth arch symmetry:This comparesthe
left to right side symmetry withineach arch.There may be a significantasymmetry
within the arch,such as acuspid on one side being more anteri-orly positioned in
the arch than thecuspid on the opposite side (Figure 55-6).This problem often
occurs with aunilateral missing tooth.Also,verticalasymmetries can occur with
individualteeth,sections ofthe dentoalveolus,orthe entire dental arches,creating a
cantin the transverse occlusal plane.Cor-recting these types ofconditions
mayrequire special orthodontic mechanics,unilateral extraction or opening-
upspace,asymmetric extractions,and/orsurgical procedures.8.Curve ofWilson (buccal
tooth tipping):This evaluates the mediolateral positionofthe occlusal surfaces
ofthe maxillary(Figure 55-7) and mandibular posteriorteeth.Ifthe occlusal surfaces
ofthe max-illary or mandibular posterior teeth aretipped too far buccally,it may be
diffi-cult to achieve a proper occlusal inter-digitation relationship.In the
presenceofa transverse maxillary deficiency withpreexisting increased curve
ofWilsonand posterior crossbites,it is very diffi-cult,ifnot impossible,to correct
theproblem orthodontically,orthopedical-ly,or even with surgically assisted
rapidpalatal expansion (SARPE).The curveofWilson will usually get much worsewith
these mechanics.In these types ofcases surgical expansion by multiplemaxillary
osteotomies may be indicatedto decrease the curve ofWilson.When the mandibular
posteriorteeth are tipped buccally,it is oftenrelated to macroglossia or
habitualtongue posturing.Orthodontic lingualtipping ofthe posterior teeth is
verydifficult when macroglossia is presentand will likely be unstable.A
reductionglossectomy may be indicated beforeorthodontics in order to permit a
morestable orthodontic result.9.Missing,broken down,or restoredteeth:These must be
identified sincethey may influence treatment design.Ifa tooth is nonrestorable and
requiresextraction,it must be determined iftheextraction space requires
orthodonticclosure or the space maintained forlater dental reconstruction.In
somecases it may be helpful to maintain thecondemned tooth to improve
stabilityduring surgical alignment ofthe jawsor segments thereof,with
removalpostsurgery.Crowns on previouslyrestored teeth may need to be redonepost-
orthodontics and -orthognathicsurgery,since the crown anatomy mayneed to be changed
for proper occlu-sion with the new dental relationships.Determination ofsalvageable
teeth andrestorative requirements are integralcomponents in the planning and treat-
ment ofpatients.10.Ankylosed teeth:Ifundiagnosed,ankylosed teeth can have
devastatingeffects on the presurgical orthodon-tics.Tooth ankylosis,the fusion
ofalveolar bone and cementum,resultsfrom damage to the periodontal liga-ment
(PDL).An ankylosed tooth may be identi-fied by failure to move with orthodon-tic
forces (Figure 55-8),failure ofatooth to erupt,submerged or incom-plete tooth
eruption (Figure 55-9),orlack oferuption ofa tooth comparedwith adjacent teeth and
alveolar bonegrowth.The most sensitive diagnostictest is percussion,where the
ankylosedtooth has a high,clear,solid metallicsound.A normal tooth has a
dullsound,being protected by the PDL.However,an erupted tooth with animpacted tooth
directly against it willalso have a solid sound to percussion.Normal multirooted
teeth present amore solid sound than single-rootedteeth.Therefore,percussion
testingshould be compared with similar teeth(ie,test bicuspids against
bicuspids,molars against molars,using both sidesofthe arch).An ankylosed tooth
lacksFIGURE55-6Tooth arch symmetry.This modeldemonstrates that the cuspid on one
side ofthearch is significantly more anteriorly positionedin the arch compared with
the cuspid on theopposite side.FIGURE55-7Curve ofWilson.This evaluatesthe
mediolateral position ofthe occlusal surfacesofthe maxillary and mandibular
posterior teeth.FIGURE55-8This dental model shows apalatally displaced
tooth,unresponsive to ortho-dontic mechanics,indicating probable ankylosis.
1116Part 8: Orthognathic Surgerymobility.Over 90% ofankylosed teethare
deciduous;most often the secondmolar followed by the first molar.3Ankylosed primary
teeth are not sus-ceptible to resorption by the follicle ofthe underlying permanent
tooth andmay result in its impaction.3Ankylosed teeth can cause signifi-cant
problems with jaw growth anddevelopment.Early ankylosis results innoneruption or
partial eruption,resulting in incomplete development ofthe alveolar
process.4Permanent teethmay be displaced from normal erup-tion pathways with
resulting loss ofalveolar bone height.The failure ofanankylosed tooth to erupt may
allowadjacent teeth to drift and permitsuper-eruption ofthe tooth in theopposing
arch.Ankylosed teeth do notrespond to orthodontic forces and cancreate significant
orthodontic prob-lems when malaligned and tied into theorthodontic arch wire
(Figure 55-10).5The ankylosed tooth functions as ananchor and in active
uncontrolledorthodontics,will move adjacent teethto align with its position,with
subse-quent development ofan occlusal andpossibly facial deformity.11.Periodontal
evaluation:This is veryimportant,since preexisting peri-odontal pathologies could
be exacer-bated during orthodontic and orthog-nathic surgical
treatments.6Factorsthat can adversely affect the health andoutcome ofthe
periodontal tissues aswell as the orthodontics and orthog-nathic surgery include
smoking,excessive consumption ofalcohol orcaffeine,habitual patterns such asbruxism
and clenching,preexistingconnective tissue/autoimmune dis-
eases,diabetes,malnutrition,andother diseases that could affect thelocal tissue
blood supply perfusion,and healing.Any pretreatment ofacute or chronic periodontal
diseaseshould be addressed prior to theorthodontics and surgery.The lack ofattached
gingiva around the teeth(most commonly seen in themandibular anterior arch) can
causegingival retraction,loss ofbone,andloosening ofteeth iforthodontics
isinitiated and the mandibular incisorsare tipped forward (Figure 55-11).Gingival
grafting may be indicatedprior to orthodontics to provideattached gingiva so as to
prevent theseproblems.Good communicationbetween the periodontist,orthodon-tist,and
OMF surgeon is ofutmostimportance.Orthodontics can help prepareinterdental
osteotomy sites by tippingthe roots ofthe adjacent teeth awayfrom each other to
increase theinterosseous space between the roots.There have been a number
ofstudiesdemonstrating that interdentalosteotomies have a minimal effect onthe
periodontium when they are prop-erly performed.7�11Having healthystable dental
tissues to work with dur-ing the orthodontics and surgery willmaximize the
periodontal outcome aswell as the overall outcome.The fail-ure to recognize
preexisting periodon-tal pathology,identify risk factors,poor performance
ofsurgery,and/orlack ofattention to detail could resultin significant periodontal
problems aswell as other problems that couldcompromise the final result.12.Tongue
assessment:An enlarged tongue(macroglossia) can cause dentoskeletalFIGURE55-9This
pantomogram demonstratesincomplete eruption ofa primary tooth withouta permanent
successor,indicating ankylosis.FIGURE55-10This illustration depicts a partially
submerged ankylosed maxillary cuspid (A).Iftiedinto an active straight arch wire
(B),the adjacent teeth will be orthodontically moved toward theankylosed
tooth,resulting in the development ofa significant malocclusion.AB
Orthodontics for Orthognathic Surgery1117deformities,instability oforthodonticand
orthognathic surgical treatments,and create masticatory,speech,and air-way
management problems.There are anumber ofcongenital and acquiredcauses oftrue
macroglossia,includingmuscular hypertrophy,glandularhyperplasia,hemangioma,lymphan-
gioma,Down syndrome,and Beckwith-Wiedemann syndrome.Acquired fac-tors include
acromegaly,myxedema,amyloidosis,tertiary syphilis,cysts ortumors,and neurologic
injury.12Thereare specific clinical and cephalometricfeatures that may help the
clinicianidentify the presence or absence ofmacroglossia,although not all
ofthesefeatures are always present.Specificclinical features include the
following(Figure 55-12):�Grossly enlarged,wide,broad,andflat tongue�Open bite
(anterior or posterior)�Mandibular prognathism�Class III malocclusion with or with-
out anterior and posterior crossbite�Chronic posturing ofthe tonguebetween the
teeth at rest (rule outhabitual posturing ofa normal-sized tongue)�Increased curve
ofWilson ofmax-illary posterior teeth�Reverse curve ofWilson ofmandibular posterior
teeth�Accentuated curve ofSpee in themaxillary arch�Reverse curve ofSpee in
themandibular arch�Increased transverse width ofmaxillary and mandibular
arches�Diastemata with increased incisorangulation in the mandibularand/or
maxillary arches�Crenations (scalloping) on thetongue�Glossitis (due to excessive
mouthbreathing)�Speech articulation disorders�Asymmetry in the maxillary
ormandibular arches associatedwith an asymmetric tongue�Difficulty eating and
swallowing(severe cases)�Instability in orthodontic mechan-ics or orthognathic
surgical proce-dures that in normal circumstanceswould be stable�Airway
difficulties,such as sleepapnea,secondary to oral ororopharyngeal
obstruction�Drooling Cephalometric radiographic featurescommonly seen with
macroglossia (Figure55-13) include the following:�Tongue filling the oral cavity
andextruding through an anterior open bite�Mandibular dentoalveolar protru-sion or
bimaxillary dentoalveolarprotrusionFIGURE55-11Periodontal concerns.Thispatient had
lack ofattached gingiva prior to initi-ation oforthodontics and was left
untreated,caus-ing severe gingival retraction and loss ofsupport-ing bone.Gingival
grafting should have beenperformed prior to initiation oforthodontics.FIGURE55-
12Macroglossia.Some ofthe clini-cal features associated with macroglossia
includeanterior open bite,diastemata between the teeth,accentuated curve ofSpee
maxillary arch,andreverse curve ofSpee mandibular arch.5143935842290FIGURE55-
13Macroglossia.Cephalo-metric analysis shows mandibular den-toalveolar protrusion
and overangula-tion ofthe mandibular anterior teeth.The tongue fills the oral
cavity (dottedline) and the oropharyngeal airway isdecreased (normal distance from
poste-rior aspect oftongue to posterior pha-ryngeal wall is 11 mm).
1118Part 8: Orthognathic Surgery�Overangulation ofthe maxillary andmandibular
anterior teeth�Disproportionately excessive mandibu-lar growth�Decreased
oropharyngeal airway�Increased gonial angle�Increased mandibular plane
angle�Increased mandibular occlusal planeangle Most open bite cases are not related
tomacroglossia.In fact it has been estab-lished that closing open bites with
orthog-nathic surgery will allow a normal tongue(which is a very adaptable organ)
to re-adjust to the altered volume ofthe oralcavity,with little tendency
towardrelapse.13,14However,iftrue macroglossiais present with the open bite,then
instabil-ity ofthe orthodontics and orthognathicsurgery will likely occur,with a
tendencyfor the open bite to return.Pseudo-macroglossia is a condition where
thetongue may be normal in size,but itappears large relative to its anatomic inter-
relationships.This can be created by (1)habitual posturing ofthe tongue;
(2)hypertrophied tonsils and adenoid tissuedisplacing the tongue forward;(3)
lowpalatal vault,decreasing the oral cavityvolume;(4) transverse,vertical,or
antero-posterior deficiency ofthe maxillaryand/or mandibular arches decreasing
oralcavity volume;and (5) tumors that dis-place the tongue.Pseudomacroglossiamust
be distinguished from truemacroglossia because the methods ofmanagement are
different.Diagnostic ListBefore a treatment plan can be properlydeveloped,a
diagnostic list ofthe existingproblems is established based on patientconcerns,and
clinical,radiographic,den-tal model,and other indicated evaluations.This will
include all findings relative tomusculoskeletal and dental imbalances,occlusal
problems,esthetic concerns,TMJand/or myofascial pain
problems,missingteeth,crowns,bridges,endodonticallytreated teeth (these teeth are
sometimesankylosed),periodontal problems,otherfunctional disorders,as well as any
othermedical factors that may affect treatmentoutcomes.The treatment plan is
formulat-ed from the diagnostic problem list.Presurgical Orthodontic GoalsThe basic
presurgical orthodontic goalsare as follows:�Align and position teeth over basal
bone�Avoid excessive intrusion or extrusionofteeth�Decompensate teeth�Avoid
unstable expansion ofthe den-tal arches�Avoid class II and class III
mechanics(unless required for dental decompen-sation correction in the
arches)�Perform stable and predictable ortho-donticsRelative to the position ofthe
maxillaryand mandibular incisors,the ideal presurgi-cal orthodontic goals are as
follows:1.Position the long axis ofthe maxillarycentral incisors approximately
22�tothe nasion point A (NA) line,with thelabial surface ofthe incisors 4 mm ante-
rior to the NA line relative to a normal-ly positioned maxilla and normalocclusal
plane angle (see Figure 55-4)2.Position the long axis ofthe mandibu-lar central
incisors 20�to the nasionpoint B (NB) line with the labial sur-face ofthe incisors
4 mm anterior tothat line relative to a normally posi-tioned mandible and normal
occlusalplane angle (see Figure 55-4)3.Satisfy arch length requirements(crowding or
spacing) We have found that using the idealposition ofthe maxillary and
mandibularincisors to the NA and NB lines,respec-tively (see Figure 55-4),is the
most conve-nient and practical method to establish thepresurgical orthodontic goals
for theincisors.However,these presurgical ortho-dontic goals may be different
iftheocclusal plane angle is to be altered surgi-cally.Removal ofdental
compensations ishelpful before surgery so that maximumskeletal correction can be
achieved.Anexact orthodontic treatment plan,includ-ing the specific mechanics and
anchoragerequirements necessary to position theteeth to satisfy the presurgical
orthodonticgoals,must be developed and executed.Initial Surgical Treatment
ObjectiveThe surgical treatment objective (STO),also known as a prediction
tracing,is atwo-dimensional visual projection ofthechanges in osseous,dental,and
soft tissuesas a result oforthodontics and orthog-nathic surgical correction ofthe
dentofa-cial and occlusal deformity.The purposeofthe STO is threefold:(1)
establishpresurgical orthodontic goals,(2) developan accurate surgical objective
that willachieve the best functional and estheticresult,and (3) create a facial
profile objec-tive which can be used as a visual aid inconsultation with the
patient and familymembers.A prediction tracing oftheanticipated presurgical
orthodontic dentalmovements is created by placing an acetatesheet on the original
cephalometric trac-ing and retracing the teeth into the posi-tion they will be
placed with the presurgi-cal orthodontics,based on the goals andavailable mechanics
(Figure 55-14A).Theinitial STO is then constructed with theteeth in their
presurgical orthodontic finalposition.The STO has significant importancein two
phases oftreatment planning:(1)the initial STO is prepared before treat-ment to
determine the orthodontic andsurgical goals;and (2) the final STO is pre-pared
after the presurgical orthodonticsare completed but prior to surgery todetermine
the exact vertical and antero-posterior skeletal and soft tissue move-ments to be
achieved (Figure 55-14B).The
Orthodontics for Orthognathic Surgery1119STO is invaluable to the orthodontist
andsurgeon in establishing treatment objec-tives and projected results,acting as
thetreatment plan blueprint.Definitive InterdisciplinaryTreatment PlanThe
definitive treatment plan is formulatedbased on the patient�s
concerns,clinicalevaluation,radiographic analysis,dentalmodel evaluation,initial
STO,and otherrelevant evaluations.The general sequenc-ing ofthe treatment that may
be involved isdescribed below.Dental and Periodontal TreatmentAny indicated
periodontal or generaldental care related to maintaining teethor improving dental
health should beperformed prior to orthodontics andsurgical intervention.The
objective is tomaintain as many teeth as possible andstabilize the
periodontium.Temporarycrowns and bridges should be placedwhere necessary for the
orthodontic andsurgical phases ofthe treatment.Perma-nent crowns,inlays,and bridges
shouldbe constructed and inserted after thesurgery and orthodontics have
beencompleted.This gives the restorativedentist the opportunity to
provideescapement grooves,cuspid protection,and incisal guidance for optimum func-
tion and esthetics.Initial periodontalmanagement may include scaling
andcurettage,eliminating pockets,as well asgingival grafting to provide
adequateattached gingiva.Occasionally,inpatients with several missing
teeth,osseointegrated implant placement priorto orthodontics and
orthognathicsurgery may provide anchorage fororthodontics and additional dental
unitsto help in repositioning the jaw struc-tures at surgery.Presurgical
OrthodonticsThe orthodontist is responsible for posi-tioning the teeth to the most
desirableposition over basal bone in preparation forsurgery.The development
ofprescriptionbrackets and straight wire orthodontictechniques has helped simplify
orthodon-tics.Most prescription bracket systems aredesigned to tip the cuspid roots
distally,creating some space between the roots ofthe lateral incisors and
cuspids.In casesrequiring segmentalization ofthe maxilla,this interdental space may
be adequatethrough which to perform interdentalosteotomies,but
ifinadequate,additionalroom can be created by tipping the lateralincisor roots
mesially and the cuspids moredistally.Bonded brackets are clean andeliminate
interdental spacing problems83313134FIGURE55-14A,Presurgical orthodontics.The
orthodontic movements are traced on the acetate paper overlying the original
lateral cephalometric trac-ing with the teeth in their predetermined,simulated
positions.The solid lines,are the original position ofthe teeth.The dashed linesare
the new posi-tion ofthe teeth following simulated extraction offour first bicuspids
and orthodontic closure ofthe spaces.B,Surgical treatment objective (STO).This isan
example ofa completed final STO which shows the predicted outcome ofthe presurgical
orthodontics and the anticipated surgical treatment.Thearrows andnumbers indicate
the direction and millimeters ofmovement.AB
1120Part 8: Orthognathic Surgerycreated by circumferential bands.Bondedbrackets
with the currently availableresins are quite adequate for orthognathicsurgery
procedures.However,inaccurateplacement ofthe brackets on the teeth canresult in
undesired rotations,vertical dis-crepancies between teeth,malalignmentofmarginal
ridges and labial surfaces ofadjacent teeth,and unfavorable root posi-tions.Careful
placement ofbrackets isparamount in helping to achieve high-quality results.Nickel-
titanium or similarly shapedmemory arch wires can be advantageousfor many
orthognathic cases to aid inpresurgical orthodontic dental
alignmentgoals.However,there are cases whereshape memory wires could be detrimen-
tal,such as in an anterior open bite withan accentuated maxillary curve ofSpee.The
use ofnickel-titanium wires or anytype ofstraight wire in these cases cancreate
unstable results such as extrusionofteeth and buccal tipping ofthe molarsas a
result ofreciprocal forces.Stainlesssteel wires with compensating bends(Figure 55-
15A) or sectional wires (Fig-ure 55-15B) may be a better-controlledmechanical force
in these types ofcases.The type ofarch wire and how long eachis left in place is
critical and must be care-fully monitored by the orthodontist.To follow are basic
presurgical ortho-dontic factors that commonly must beaddressed in preparing
patients for orthog-nathic surgery.It is important to avoid interarch classII
mechanics (ie,class II elastics,growthappliances,TMJ �disk
recapturing�splints,Herbst�s appliances) unless they are specif-ically required
during the presurgicalorthodontics (ie,to correct arch asymme-try,decompensate
mandibular arch withlingually inclined mandibular incisors).Long-term class II
mechanics positionsthe mandibular condyle downward andforward in the fossa and may
allow hyper-trophy (thickening) ofthe TMJ bilaminartissues (Figure 55-16).This same
situationcan occur in patients with a �Sunday�bite.In these situations,following
surgicalmandibular advancement,the bilaminartissue will slowly thin out over time
caus-ing a slow relapse ofthe mandible towarda Class II relationship.In addition
postur-ing the mandible forward for an extendedtime could result in foreshortening
oftheanterior articular disk attachments,increasing the risk ofTMJ articular
diskdisplacement postsurgery.Ifa patient has been treated with long-term class II
mechanics or has a �Sunday�bite,it may be an advantage to use light classIII
mechanics for a few months presurgeryto eliminate the hypertrophied bilaminartissue
and to decompensate for any unstableorthodontics that may have been created.Ifthe
TMJ articular disk does become dis-placed,it would be better to have that
occurbefore surgery because the articular disk canbe surgically repositioned and
stabilizedwith high predictability at the same time asthe orthognathic
surgery.15�18Attempts torecapture a TMJ displaced disk with splinttherapy prior to
surgery could be detrimen-tal to the patient relative to outcome stabili-ty and
pain.In most cases nonsurgical�recapturing�the disk procedures haveproved
clinically unsuccessful.Treatment Options for Specific Orthodontic Problems This
section presents specific dental mal-relationships and the orthodontic and sur-
gical treatment options for consideration.Comprehensive assessment ofthe patientand
developing treatment objectives willaid in selecting the appropriate
treatment.Adjustment for Tooth-Size DiscrepancyUsually TSDs occur because ofsmall
max-illary lateral incisors,making the combinedFIGURE55-15A,Compensating steps
(arrow)have been placed in the orthodontic arch wire so thatthe anterior teeth are
aligned at an elevated level compared with the posterior teeth to eliminate extru-
sion or intrusion ofteeth that may otherwise result in unstable orthodontic
movements.B,Sectioningthe arch wire (arrow)is another approach to aligning teeth at
separate independent levels to avoidextrusion or intrusion ofteeth as seen in this
maxilla.However,the use ofsectional wires may decreasepositional control ofthe
teeth adjacent to the ends ofthe cut wire.ABFIGURE55-16Use oflong-term class
IImechanics,anterior repositioning splints,growthdevices,or �Sunday�bite
relationships can causehypertrophy ofthe bilaminar tissue,positioningthe condyle
downward and forward in the fossa.Postsurgery,particularly with
mandibularadvancements,this tissue will slowly thin out,and the condyles will move
posteriorly in thefossa causing a shift ofthe mandible and occlu-sion toward a
Class II position.
Orthodontics for Orthognathic Surgery1121mesiodistal width ofthe maxillary anteri-
or six teeth too small to fit properlyaround the mandibular anterior six teeth,so
that when the teeth are properlyaligned,an end-on Class II cuspid rela-tionship
will result (Figure 55-17).IftheBolton�s analysis indicates a
significantTSD,presurgical orthodontic adjustmentscan usually correct the
discrepancy andaid in providing a solid Class I cuspidrelationship at surgery and
in the finaloutcome.TSDs can also occur in thebicuspids and molars,with the
maxillaryteeth usually being too small comparedwith the mandibular teeth.The
followingare treatment options that can be used tocorrect TSDs.Slenderizing Teeth
(Interproximal ToothSize Reduction)This technique reducesthe mesiodistal dimension
ofthe involvedteeth.Since most TSDs involve largermandibular anterior teeth
compared tothe maxillary anterior teeth,slenderizingthe mandibular anterior teeth
can addressthe issue (Figure 55-18).Approximately 10 to 12% ofthe mesiodistal width
can besafely removed from each tooth with 50%ofthe interproximal enamel
remaining.Up to 3 mm ofreduction can usually besafely achieved in the mandibular
anteriorsix teeth.Slenderizing the mandibularanterior teeth is an advantageous
proce-dure,where the maximum width oftheincisors is toward the incisor edge,partic-
ularly in the presence ofcrowding and/oroverangulation ofthe mandibularincisors.It
is not advantageous ifthemandibular anterior teeth are decreased inangulation
(lingual inclination),sinceclosing the resultant spaces will furtherdecrease the
incisor angulation and mayadversely affect esthetics and stability.Thistechnique is
not indicated when the con-tact points are positioned toward the gin-giva,as this
could result in tissue strangu-lation with loss ofpapilla and
interdentalbone,creating significant periodontalissues.In the rare case where the
maxillaryteeth are too large for the mandibularteeth,the maxillary teeth can be
slender-ized,but this is best used when the maxil-lary teeth are crowded and/or
overangulat-ed,and the individual crowns are widerthan normal (see Table 55-1).When
TSDs occurs in the bicuspidand/or molar area,slenderizing themandibular teeth will
usually correct theproblem,unless the slenderizing will causeexcessive retraction
ofthe mandibularanterior teeth.Ifthis appears to be apotential outcome,then careful
closure ofthe spacing by loosing (slipping) posterioranchorage (using mechanics
that willmove the posterior teeth forward insteadofthe anterior teeth backward) may
solvethe problem.This approach may includeclass II mechanics to provide
forwardforces on the posterior teeth or movingone tooth at a time on each
side.Dentalimplants placed adjacent to or posterior tothe molars could provide
stable anchorageto aid in applying the mechanics necessaryto push the posterior
teeth forward.Creating Space In the ArchThis canenlarge the circumference ofthe
involvedarch.Since TSDs are often related to smallmaxillary lateral
incisors,opening spacearound the maxillary lateral incisors maybe a logical
approach.A simple techniqueinvolves placement ofcoil springs betweenthe cuspids and
lateral incisors and ifneed-ed between the lateral incisors and centralincisors to
open spaces (Figure 55-19).Atthe end oftreatment the lateral incisors canbe built
up by bonding,veneers,or crowns.This technique can also be used in themandibular
arch when the mandibularanterior teeth are too small compared tothe maxillary
anterior teeth.In either archthis technique is most applicable when theteeth are
decreased in angulation,sinceopening space will increase the axial incli-nation
ofthe incisors.It may not be indi-cated when the maxillary or mandibularincisors
are overangulated or crowded,asFIGURE55-17This patient has well-alignedand leveled
teeth in each arch.Maxillary lateralincisors are small creating a tooth-size
discrep-ancy (TSD).Note that with the best possible fit,the patient has an end-on
Class II occlusal rela-tionship secondary to the TSD.FIGURE55-18Mandibular anterior
teeth can be slenderized using (A) diamond strip or (B) thincylindrical diamond bur
to reduce the width ofthe teeth at the contact level.Spacing generated canthen be
closed with orthodontics.AB
1122Part 8: Orthognathic Surgerythe resultant increased angulation may beunstable
and cause untoward periodontalchanges.However,ifthere is significantcrowding or
overangulation ofthe incisorsrequiring extraction ofbicuspids,duringclosure ofthe
bicuspid spacing by retrac-tion ofthe anterior teeth,space could becreated around
the lateral incisors.When maxillary incisors are alreadyoverangulated,it is not
feasible to openspaces during the presurgical orthodon-tics.In this situation
performing interden-tal osteotomies between the maxillary cus-pids and lateral
incisors will permitopening space at surgery and the incisorscan also be uprighted
to decrease theiraxial angulation.A maximum 3 mm ofspacing (1.5 mm on each side)
can usuallybe acquired with this approach.When the TSD occurs in the bicuspidor
molar area,space can be opened aroundthe maxillary bicuspids and/or molars
tocompensate for the tooth mass deficiency.Bonding,veneers,or crowns can then
beplaced to eliminate the created space.Altering Axial Inclination ofIncisorsThis
technique can affect the labial cir-cumference ofthe anterior teeth.Increased axial
inclination slightly increas-es the arch length,and decreased axialinclination
slightly decreases it.Applica-tion ofthis technique would result inincreasing the
maxillary incisors�angula-tion above normal and decreasing themandibular
incisors�angulation belownormal.This technique can accommodatesmall TSD
differences,but may place theteeth in a compromised position relativeto stability
and esthetics.Surgery can alter the axial inclinationofthe anterior teeth.In the
maxillary arch,interdental osteotomies between the later-al incisors and
cuspids,and in themandibular arch anterior subapicalosteotomies,will provide a
means to alteraxial inclination ofthe incisors.Altering Mesiodistal Angulation
ofMaxil-lary IncisorsTipping the roots ofthemaxillary central incisors distally
awayfrom each other alters the position ofthecontact points,making the
intercontactdistance on each tooth slightly wider.Thiscan only be used for small
differences.However,it then usually requires recon-touring ofthe distal aspect
ofthe incisoredges and could cause a soft tissue voidbetween the mesial contact
points and gin-gival tissues (�the black triangle�),creatingmuch concern for the
patient.This tech-nique is rarely recommended.Extraction ofMandibular
IncisorThistechnique should only be used for largeTSDs (5 mm or more) and only
ifthere issignificant crowding and/or significantoverangulation ofthe
mandibularincisors.Removing a mandibular incisorusually creates a significant space
(thewidth ofthe tooth),and closure ofthatspace may significantly decrease the
axialinclination ofthe mandibular incisors.Inaddition it may cause a decreased
trans-verse width between the cuspids result-ing in relative narrowing ofboth
maxil-lary and mandibular arches.Extractionofa mandibular incisor may produce
anincreased overjet.Ifthe patient has agood maxillary arch but mandibularcrowding
and overangulation,large TSD,and an end-on or slight Class III
anteriorocclusion,the single mandibular incisorextraction may be the treatment
ofchoice.An alternative in cases with largetooth-size discrepancies would be
toslenderize the mandibular anterior teethand create spacing around the
maxillarylateral incisors.A surgical alternative for a large TSD,when the teeth are
not crowded and havegood axial angulation,would be to extractthe mandibular incisor
and perform a verti-cal ostectomy through the mandible at theextraction site and
rotate the segmentstogether to eliminate the extraction space(Figure 55-20).This
would prevent furtherdecreased angulation ofthe incisors withsubsequent
orthodontics but may narrowthe anterior aspect ofthe mandible.Correct Overangulated
(Proclined) and/or CrowdedMaxillary Anterior TeethOverangulated and/or crowded
maxillaryanterior teeth are most commonly seen inpatients with maxillary
deficiency(hypoplasia).The following treatmentmethods can be used to correct this
typeofsituation.Slenderizing and RetractionThis tech-nique involves removal oftooth
structureat the contact points and is applicablewhen there is a rare reverse TSD
with themaxillary anterior teeth too large for themandibular anterior teeth.Usually
up to 3 mm oftooth structure can be safelyremoved from the contact area
ofthemaxillary anterior six teeth with a marginof50% ofenamel remaining at the con-
tact areas.However,this could make themaxillary incisors slightly smaller in
sizeunless they are significantly oversized tobegin with.Extraction and
RetractionFirst or sec-ond bicuspids can be extracted depend-ing on the amount
ofcrowding,theanchorage requirements,and the amountofretraction ofthe incisors
necessary.FIGURE55-19Placing coil springs between themaxillary cuspids and lateral
incisors as well as thelateral incisors and central incisors can open upspacing
around the lateral incisors to correct a tooth-size discrepancy.Post-treatment,the
lateral incisorscan be built up by bonding,veneers,or crowns.
Orthodontics for Orthognathic Surgery1123Every 1 mm ofincisor retraction
willrequire 1 mm ofspace on each side ofthearch.Therefore,ifthe orthodontic goal
isto retract the maxillary incisors by 3 mm,then 6 mm ofmaxillary arch space will
berequired to accomplish this.Extractingfirst bicuspids will result in
greaterincisor retraction,whereas six multiroot-ed posterior dental units (compared
tosix single-rooted anterior dental units)provide greater posterior
anchorage.Extracting second bicuspids will result inless incisor retraction,whereas
four pos-terior dental units (compared to eightanterior units) provide less
posterioranchorage so that the posterior teeth willmove forward a greater amount
com-pared with first bicuspid extractions.Theocclusal plane angle will also affect
theposterior anchorage.Low occlusal planeangle cases will have greater
posterioranchorage stability,even with secondbicuspid extraction,than will
highocclusal plane angle cases.High occlusalplane angle cases will have less
posterioranchorage stability,even with first bicus-pid extraction,than low occlusal
planeangle cases.These factors are probablyrelated to bite force
influences.Theamount ofcrowding may also influencewhich teeth to
extract.Distalizing Posterior TeethThis objectivecan be accomplished using
pendulum-typeappliances,headgear,class II mechanics,orosseointegrated implants
(ie,implants pos-terior to molars,zygomatic implants,palatal implants,or buccal
corteximplants).Distalizing maxillary posteriorteeth can be augmented with class
IImechanics but should only be used short-term and discontinued several monthsprior
to surgery to minimize postsurgicalskeletal relapse potential that can occurwith
the use oflong-term class II mechan-ics and the subsequent adverse effects onthe
TMJs.Another option is to distalize onetooth at a time on each side ofthe
arch,beginning with the second molars (2 teethmoved against 12 anchor
teeth).Anotherfeasible approach is to use osseointegratedanchors to distalize the
maxillary arch,withimplants placed in either the zygoma but-tress,posterior to
second molars,orattached to the buccal cortex.The implantscan be left submerged
after orthodontictreatment is completed,or could requireadditional surgery for
removal ifnotremoved during the orthognathic surgery.Anterior Maxillary Segmental
Osteoto-miesThis technique permits uprightingofthe anterior teeth but will cause
the api-cal base ofthe segment to shift forward rel-ative to the incisor edges
unless teeth areextracted to reposition the incisal edges ofthe anterior teeth
posteriorly.Carefulassessment ofthe profile esthetics is neces-sary to determine
ifthe patient can estheti-cally benefit from this change.The inter-dental
osteotomies should be done betweenthe lateral incisors and cuspids as this
offersthe best control in uprighting the segments(Figure 55-21) and also allows
opening ofspace between the lateral incisors (up to 3 mm with 1.5 mm per side) that
can beused for correction ofcrowding or TSD.Maxillary Expansion by
Orthodontics,Orthopedics (Rapid Palatal Expansion),and Surgically Assisted Rapid
PalatalExpansion These techniques will increasearch length and may allow retraction
oftheanterior teeth.However,they will alsoincrease the curve ofWilson as the trans-
verse width ofthe maxillary arch increasesbecause the teeth will expand three times
asmuch as the palate expands (Figure 55-22).In addition,with SARPE,the palate
movesinferiorly.The expanded arches may not beas orthodontically stable,requiring
long-term or permanent retention.Correct Overangulated (Proclined) and/or
CrowdedMandibular Anterior TeethOverangulated and/or crowded mandibu-lar teeth
occur most often with mandibu-lar deficiency (hypoplasia).The followingFIGURE55-
20In the case ofa tooth-size dis-crepancy (TSD) =5 mm,in the presence ofwell-
aligned teeth in proper angulation,the TSD canbe managed by removing a mandibular
centralincisor and performing a vertical midline ostec-tomy (A) with closure ofthat
space (B) and sta-bilization with a bone plate.ABFIGURE55-21An anterior maxillary
segmentalosteotomy can be used to upright the maxillaryincisors.However,the
dentoalveolus at the apicalbase will rotate anteriorly ifno teeth are extract-
ed.Since this may affect the position ofthe noseand upper lip,careful evaluation
offacial esthet-ics is necessary to determine ifthis approach isappropriate.Dashed
linerepresents the originalposition ofthe anterior maxilla,and the
solidlinerepresents the uprighted segment.
1124Part 8: Orthognathic Surgerytreatment options can be used to correctthese types
ofconditions.Slenderizing and RetractionThis tech-nique involves removal oftooth
structureat the contact points and is most applica-ble when there is a TSD with the
mandibu-lar anterior teeth being too large for themaxillary anterior teeth.Up to 3
mm oftooth structure can be safely removedfrom the contact areas ofthe
mandibularanterior six teeth with a margin of50% ofenamel remaining at the contact
areas.Subsequent retraction will decrease theaxial inclination ofthe incisors
providingthat no major crowding is present.Extraction and RetractionFirst or sec-
ond bicuspids can be extracted dependingon the degree ofangulation,amount
ofcrowding,the anchorage requirements,and the amount ofretraction oftheincisors
necessary.Every 1 mm ofincisorretraction will require 1 mm ofspace oneach side
ofthe arch.Therefore,iftheorthodontic goal is to retract the mandibu-lar incisors
by 3 mm,then 6 mm ofmandibular arch space will be required toaccomplish
this.Extracting first bicuspidswill result in greater incisor retraction,whereas
six multirooted posterior dentalunits (compared with six single-rootedanterior
dental units) provide greater pos-terior anchorage.Extracting the secondbicuspids
will result in less incisor retrac-tion,whereas four posterior dental
units(compared with eight anterior units) pro-vide less posterior anchorage,so that
theposterior teeth will move forward a greateramount compared with first
bicuspidextractions.The occlusal plane angle willalso affect the posterior
anchorage.Lowocclusal plane angle cases will have greaterposterior anchorage
stability,even withsecond bicuspid extraction,than will highocclusal plane angle
cases.High occlusalplane angle cases will have less posterioranchorage stability
even with first bicuspidextraction than low angle cases.These fac-tors are probably
related to bite force influ-ences.The amount ofcrowding may alsoinfluence which
teeth to extract.Ifthere isa large TSD (=5 mm),then extraction ofamandibular
incisor could be considered.Distalize Posterior TeethThe mechanicsto accomplish
this include intra-arch,inter-arch,extraoral,or implant mechanics.ClassIII
mechanics (ie,elastics,headgear) can beused to distalize the mandibular
teeth,butmay increase loading on the TMJs and couldinitiate TMJ problems.Another
option is todistalize one tooth at a time on each side ofthe arch,beginning with
the second molars (2 teeth moved against 12 anchor teeth).However,this technique
takes a lot oftime.The placement ofdental implants posterior tothe molar teeth or
in the posterior buccal cor-tex could facilitate retraction without appre-ciably
increasing the load to the TMJs.Anterior Mandibular Subapical OsteotomiesThis
technique permits uprighting oftheanterior teeth,but will cause the apical base
ofthe segment to shift forward relative to thechin (Figure 55-23),unless teeth are
extractedat the time ofsurgery to reposition the incisaledges ofthe anterior teeth
posteriorly.Bilateral Mandibular Body OsteotomiesThis technique will permit
uprighting oftheanterior teeth and forward rotation ofthechin (Figure 55-24),unless
teeth are extract-ed.Without extraction,bilateral body bonegrafting will be
required to provide bonycontinuity between the segments and facili-tate
healing.This technique would only beindicated ifthe chin is
anteroposteriorlydeficient before surgery.Mandibular Symphysis
DistractionOsteogenesisThis technique,usuallyperformed with a midline vertical
osteoto-my,will allow expansion ofthe dentoalve-olus and widening ofthe mandibular
arch,FIGURE55-22Maxillary expansion by orthodontics,orthopedics,or surgically
assisted rapid palatalexpansion (SARPE) will cause an increase ofthe curve
ofWilson.Even with SARPE,the occlusal sur-face will expand three times as much as
the palate will expand,thus increasing the curve ofWilson.The palate will also move
inferiorly.
Orthodontics for Orthognathic Surgery1125providing room to retract and/or align
theteeth.This is an excellent treatmentmethod to gain space for major archlength
discrepancies.However,it is doneas a prerequisite surgery to achieve theorthodontic
goals prior to the majororthognathic surgery.Orthodontic prepa-ration may be
necessary prior to perform-ing the midline vertical osteotomy.Theroots ofthe
central incisors (or the adja-cent teeth,wherever the osteotomy is to beperformed)
must be tipped away fromeach other to make room for the interden-tal osteotomy.This
can be accomplishedby placing the mesial aspect ofthe brackethigher than the distal
aspect on each ofthecentral incisors.Placing a short segmentstraight arch wire will
then tip the rootsdistally,creating space to safely performthe vertical interdental
osteotomy (Figure55-25).Ifa tooth-borne distraction deviceis used,orthodontic
treatment on anyother teeth should not be initiated untiladequate healing ofthe
distraction areahas occurred (approximately 4 monthsfrom initiation ofthe
distraction).Other-wise it may result in developing dentalmobility and orthodontic
instability,withthe teeth expanding more than the basalbone.This can result in
transverse dentalrelapse postdistraction with less expansionofthe dental arch than
desired.Bone-borne devices are not affected by predis-traction orthodontics.Correct
Underangulated (Retroclined) Maxillary IncisorsUnderangulated maxillary incisors
aremost commonly seen in Class II Division 2malocclusions or with missing teeth in
thearch.The following approaches can beused to correct this type
ofcondition.Correct CrowdingCrowding ofthemaxillary anterior teeth can
accompanyvertically inclined teeth.Therefore,cor-recting the crowding will increase
theincisor angulation.Open SpaceIn Class I and Class II patientsunderangulated
incisors may be presentbecause ofprevious extractions (ie,bicus-pids),congenitally
missing teeth,previoustrauma resulting in loss ofteeth,or smallmaxillary anterior
teeth (ie,small maxillarylateral incisors).Opening space in the bicus-pid
areas,ifthe problem exists there,can cor-rect this problem and provide
additionaldental units for a more complete occlusalresult.The use ofcoil springs
usually workswell for this situation.Ifthe problem is in thelateral incisor
area,opening space can helpcorrect the TSD as well as increase theincisor
angulation (Figure 55-26).Interarch MechanicsThe use ofclass IIImechanics
(ie,elastics) can increase max-illary incisor angulation.However,theclass III
mechanics can be detrimental byoverloading the TMJs.FIGURE55-23The anterior
mandibular sub-apical osteotomy can be used to upright themandibular anterior
teeth,causing the apicalbase ofthe segment to shift forward relative tothe
chin,ifteeth (bicuspids) are not extracted atthe time ofsurgery.This may or may not
be adesired outcome.A chin augmentation may berequired to achieve optimal
esthetics.FIGURE55-24Bilateral body osteotomies canbe used to upright the
mandibular anteriorteeth,but the chin will rotate forward unlessteeth are
extracted.A gap created in themandibular body area will require graftingunless
teeth are extracted (first bicuspids) toallow the mandibular anterior teeth to
moveposteriorly,thus decreasing the forward move-ment ofthe chin.FIGURE55-
25Mandibular symphysis distractionosteogenesis.A,Often the incisor roots are
veryclose together.B,Space must be created betweenthe roots ofteeth adjacent to the
intended verticalosteotomy.C,Placing brackets on only the centralincisors with the
mesial aspect ofthe brackets high-er than the distal aspect on each tooth and
placinga short straight wire segment,will tip the roots dis-tally away from each
other,creating space to per-form the vertical interdental osteotomy.BAC
1126Part 8: Orthognathic SurgeryInterdental OsteotomiesAn anteriormaxillary
subapical osteotomy or seg-mentalized Le Fort I osteotomy will per-mit rotation
ofthe anterior teeth toincrease their angulation.However,sig-nificant room must be
created betweenthe roots ofthe adjacent teeth (lateralincisors and cuspids) at the
osteotomyareas.Since bone removal between theteeth may be required,there is
anincreased risk ofdamage to the adjacentteeth.Ifthe maxilla requires
surgicalexpansion,then segmentalizationbetween the lateral incisors and cuspidswill
allow the anterior segment to rotateposteriorly between the expanded poste-rior
segments with fewer requirementsfor bone removal,ifrequired at all.Correct
Underangulated (Retroclined) MandibularIncisorsUnderangulated mandibular incisors
aremore commonly seen in patients withprognathic mandibles or with missingteeth.The
following treatment methodscan be used to correct this condition.Correct
CrowdingCrowding ofthemandibular anterior teeth often accompa-nies vertically
inclined teeth.Therefore,correcting the crowding will increase theincisor
angulation.Open SpaceIn Class I and Class IIpatients underangulated incisors may
bepresent because ofprevious extractions,congenitally missing teeth,previous trau-
ma resulting in loss ofteeth,or smallmandibular teeth.In Class III
patientsunderangulated incisors may be presentdue to an excessive amount
ofalveolarbone compared with the size ofthe teeth.Ifbicuspids are missing,opening
space inthe bicuspid areas can correct this prob-lem and provide additional dental
unitsfor a more complete occlusal result.Theuse ofcoil springs usually works well
forthis situation (see Figure 55-26).Occasionally a mandibular incisormay be
missing for various reasons.Viableoptions include opening appropriate spacearound
the remaining three incisors andbuilding up the crowns by bonding,veneers,or
crowns.This technique worksbest ifthere is a TSD that is less than thewidth ofthe
missing tooth.However,themaxillary dental midline will be in thecenter ofa
mandibular incisor.Anotheroption would be to open space in the areaofthe missing
tooth and then replace itwith a dental implant or bridge.This tech-nique may work
best when there is no TSDwith a full-size dental replacement.Interarch MechanicsThe
use ofclass IImechanics (ie,elastics,Herbst�s appliance)can increase mandibular
incisor angula-tion.However,long-term class II mechan-ics can be detrimental to
outcome stabilityand results,because ofthe potential unto-ward effects on the
TMJs.Interdental OsteotomiesAn anteriorsubapical osteotomy or bilateral
anteriorbody osteotomies will permit rotation ofthe anterior teeth to increase
their angula-tion.However,significant room must becreated between the roots ofthe
teethadjacent to the osteotomy areas.Sincebone removal between the teeth may
berequired,there is an increased risk ofdam-age to the adjacent teeth.Correct
Excess Curve ofSpee: Maxillary Arch This condition is most often seen withanterior
open-bite situations and highocclusal plane facial types.Careful assess-ment ofthe
curve ofSpee is importantbecause using only orthodontic mechanicsto correct this
condition may not be verystable.An increased curve ofSpee usuallymakes it difficult
to get the occlusion to fittogether.The condition can be addressedby the following
treatment options.Extruding Anterior TeethConventionalorthodontics with straight
wire techniqueswill tend to extrude the anterior teeth,andas a byproduct will tip
the molars buccal-ly,increasing the curve ofWilson.Thesedental changes may be
unstable andfraught with relapse potential.Intruding Midbuccal TeethThis is a
verydifficult technique,unless high-pull head-gear or osseointegrated implants are
usedto provide intrusive forces.This wouldFIGURE55-26Coil springs to open space.In
some cases,�retroclined�incisors are a result ofDivision
2malocclusion,crowding,missing dental units,or small teeth.Ifthere is no
significant crowding,spacingcan be created by the use ofcoil springs that will tip
the incisors forward.A,Small maxillary lateralincisors and missing mandibular
bicuspids.B,The use ofcoiled springs is demonstrated to open up inter-dental spaces
around the maxillary lateral incisor (to correct for an anterior tooth-size
discrepancy) andin the mandibular first bicuspid area (to replace a missing dental
unit and increase the angulation oftheanterior teeth).The spaces around the
maxillary lateral incisor can be eliminated by bonding,veneer,or crown.In the
mandibular arch,the space can be eliminated by surgical ostectomy versus
replacementofthe missing dental unit by crown-and-bridge or osseointegrated implant
and crown.AB
Orthodontics for Orthognathic Surgery1127require significant patient compliance
andis not a commonly applied procedure.Extraction and RetractionExtraction
ofmaxillary first or second bicuspids withretraction will usually decrease the
curve ofSpee,providing the incisors are overangu-lated to begin
with.Orthodontic,Orthopedic,or SurgicallyAssisted Rapid Palatal Expansion
withRetractionExpansion ofthe maxillaryarch by any ofthese techniques willincrease
the arch length and allow someretraction ofthe anterior teeth.In lateadolescence or
adulthood,SARPE mayprovide better stability than the other
twotechniques.However,note that the curveofWilson will increase because the expan-
sion at the occlusal level compared withthe palate will be a 3:1 ratio.19Surgical
CorrectionThe maxilla can beorthodontically aligned in segments byaligning the four
incisors at a differentlevel,compared with the posterior teeth,toavoid
extrusion,intrusion,and buccal tip-ping ofteeth.Placing compensating verti-cal
steps between the lateral incisors andcuspids (see Figure 55-15A) will accom-plish
alignment at different levels.Forsome cases the vertical positional differ-ence may
occur between the cuspids andbicuspids,or could occur asymmetricallyon one side
ofthe arch compared with theother side.The step in the arch would thenbe made
between the appropriate teeth.Another technique to use involves cuttingthe arch
wire into two or more segmentsand aligning groups ofteeth in individualunits (see
Figure 55-15B).However,itmay be more difficult to control rota-tions and root
position,particularly ofthe teeth adjacent to the ends ofthe seg-mented
wires,compared with using acontinuous wire with compensating ver-tical steps.The
arch can then be leveledsurgically with a three-piece maxilla per-forming
osteotomies between the lateralincisors and cuspids.The three-piece LeFort I
osteotomy,with interdentalosteotomies performed between the lat-eral incisors and
cuspids,will permitrepositioning ofthe anterior segmentindependent ofthe posterior
segments(Figure 55-27).The anterior segment canbe reoriented vertically and
anteroposte-riorly,and the axial inclination oftheincisors can be changed to
correct thecurve ofSpee and achieve the best inter-digitation ofthe
segments.Correct Accentuated Curve ofSpee: Mandibular ArchAn accentuated curve
ofSpee in themandibular arch most often occurs inanterior deep-bite
relationships.Intruding Mandibular Anterior TeethIntrusion mechanics can
predictably infe-riorly position mandibular anterior teethapproximately 2 mm.Beyond
2 mm thevertical relapse approaches 60%.Withaccentuated curves ofSpee the
contactarea ofthe teeth will be at a different levelwhere the teeth are more
narrow,belowthe normal contact level.Therefore,forevery 1 mm ofleveling ofthe
mandibulararch,the mandibular incisor edges willmove forward 0.6 mm to 1 mm as the
con-tact points align.Any crowding ofthe archwill further contribute to flaring
oftheincisors.Intruding teeth will decrease theanterior mandibular vertical height
andmust also be taken into consideration sothat the anterior mandibular height is
notexcessively shortened.Extruding Midbuccal TeethExtrusionofmidbuccal teeth may be
more stablethan intrusion ofanterior teeth.Howev-er,this technique is difficult to
performwithout special considerations.Ifthepatient�s malocclusion has the
bicuspidsand first molars in occlusion,extrusionwill be virtually
impossible.However,constructing a splint that will open thebite and engage only the
mandibularanterior teeth and second molars,withthe bicuspids and first molars out
ofcon-tact with the splint,will permit extrusionFIGURE55-27Surgery for correcting
an excessive curve ofSpee.A,Aligning the maxilla in seg-ments with the incisors at
an elevated level compared with the posterior teeth will permit inter-dental
osteotomies to be performed.B,Surgical leveling ofthe occlusal plane from a
predictabilityand stability standpoint is superior to orthodontic means
alone,particularly when no extractionsare performed.AB
1128Part 8: Orthognathic Surgeryofthe midbuccal teeth.Another alterna-tive would be
to correct the accentuatedcurve ofSpee after the mandible andocclusion are
surgically repositioned,placing the incisors and molars intoproper contact,and then
extrude themidbuccal teeth postsurgery.With thisapproach the molars may tip
distally andthe arch may widen somewhat.Interdental OsteotomiesAn anteriorsubapical
osteotomy (Figure 55-28) or bilat-eral anterior body osteotomies (Figure 55-29)
will permit downward repositioning ofthe anterior teeth,with very stable
resultswhen the surgery is properly performed.Ifthe anterior vertical height ofthe
mandibleis excessive,then the subapical osteotomywould be indicated since it will
shorten theanterior mandibular height by the amountthat the incisors are
lowered.Bilateral anteri-or body osteotomies would be indicatedwhen the vertical
height ofthe anteriormandible is normal or less,so that the ante-rior height
remains unaltered while thecurve ofSpee is corrected.Correct Reverse Curve ofSpee:
Maxillary ArchReverse curves ofSpee are more common-ly seen in Division 2
malocclusions and invertical maxillary deficiencies with ananterior deep bite.The
maxillary incisorsare commonly in a decreased axial inclina-tion.Crowding may or
may not be present.Correct Crowding or Division 2 RelationsEliminating crowding and
Division 2 den-tal positions will tip the incisors forward,increasing the incisor
axial angulation anddecreasing the reverse curve ofSpee.These movements will
usually fill out theupper lip,but may decrease the maxillarytooth-to-lip
relationship.Maxillaryincisors may become intruded with astraight wire
technique.Extruding Midbuccal TeethThis tech-nique is difficult ifthe midbuccal
teeth arein occlusion with mandibular teeth.How-ever,the bite can be opened with a
splintthat affords contact on only the maxillarysecond molars and anterior
teeth,with themaxillary midbuccal teeth out ofcontactwith the splint.The midbuccal
teeth(bicuspids and first molars) can then beextruded into position to improve
thecurve ofSpee.Open SpacesIfthe reverse curve ofSpee is related to missing teeth
or TSDs,then spaces can be opened to aid inincreasing the axial inclination
oftheincisors and decreasing the reverse curveofSpee.These spaces can then be
elimi-nated by bonding,crown and bridge,ordental implants and crowns.Interdental
OsteotomiesMultiple maxil-lary osteotomies can be performed so thatthe maxilla can
be repositioned in segments,enabling leveling ofthe arch.Presurgicalorthodontics
should be designed to alignthe teeth at different vertical levels to facili-tate
the surgery and minimize orthodonticrelapse potential.It is usually easiest andmost
applicable to make the osteotomiesbetween the lateral incisors and cuspids.This may
particularly be indicated when themaxilla must be repositioned anyway andmaxillary
expansion is also required.Per-forming a three-piece segmented maxillaryosteotomy
will then allow vertical alterationbetween the anterior and posterior seg-ments to
level the curve ofSpee.Correct Reverse Curve ofSpee: Mandibular ArchThis condition
is most commonly seen inpatients with macroglossia,habitualtongue posturing,or
tongue thrust,withan associated anterior open bite.The fol-lowing techniques can be
used to correctthis type ofcondition.Extruing Anterior TeethExtrusion ofanterior
teeth may not be very stable longFIGURE55-28Subapical osteotomy correctingan
accentuated curve ofSpee in the mandibulararch.A,This can be accomplished with a
sub-apical osteotomy composed oftwo interdentalosteotomies and a subapical
ostectomy to set theanterior teeth inferiorly.B,C,This is indicatedwhen the
anterior mandibular height is greaterthan normal,as this technique will shorten
theanterior mandibular height.This same basictechnique can be used to elevate the
segment toAcorrect a reverse curve ofSpee.BC
Orthodontics for Orthognathic Surgery1129term,and without permanent retention,could
result in re-intrusion and redevelop-ment ofan anterior open bite.Intrusion
ofMidbuccal TeethThis is adifficult technique but may be accom-plished with
osseointegrated implants asanchors.However,it is not known ifthiswould be stable
long term.Extract and RetractIfthe mandibularincisors are significantly
overangulated,with or without crowding,bicuspidextractions can be performed and
theincisors retracted,which will decrease thereverse curve ofSpee.Bonding the
Mandibular AnteriorsThistechnique can be used to level the arch bybuilding up the
incisors,increasing thecrown height.However,care must betaken not to exceed a safe
crown-root ratioand/or create an esthetic compromise.Interdental
OsteotomiesAnterior sub-apical (see Figure 55-28) or anterior bilat-eral mandibular
body osteotomies (seeFigure 55-29) can be used to elevate theanterior teeth.Ifthe
anterior mandibularheight is short,then the subapical osteoto-my can also be used
to increase the anteri-or height ofthe mandible.Ifthe anteriormandibular height is
normal,then thebilateral anterior body osteotomies willpermit elevation ofthe
anterior teethwhile maintaining the anterior height ofthe mandible.Anteroposterior
Arch Asymmetry (Maxilla or Mandible)Anteroposterior arch asymmetry,whenthe cuspid
on one side ofthe arch is ante-rior to the cuspid on the opposite side ofthe
arch,is fairly common in patients withdentofacial deformities.Arch asymmetriescan
be related to developmental abnor-malities,missing teeth,or ankylosed teeth.Dental
midlines may not align with thefacial midline.Extract UnilaterallyIn some cases
uni-lateral extraction and retraction will cor-rect the problem.The decision must
bemade as to which tooth to extract.Extrac-tion ofa first bicuspid will allow
greateranterior retraction compared withextracting a second bicuspid.This extrac-
tion would only be indicated ifthere weresignificant overangulation ofthe
incisors,crowding,and/or significant midlinedental shift.Open Space
UnilaterallyThis techniquewould be indicated ifa tooth is missing,there is
significant decreased angulation ofthe incisors,and/or the midline is signifi-
cantly deviated to one side.Interarch MechanicsThis technique canbe effectively
used by incorporating class IImechanics on one side and class IIImechanics on the
opposite side.Anteriorcross-arch elastics can also be helpful.Ifonly one arch is
involved,then maximiz-ing anchorage in the other arch is veryimportant so that an
asymmetry does notdevelop in the normal arch.Osseointe-grated implants can be used
as anchors tocorrect asymmetry in an arch withouthaving to use interarch
mechanics.OsteotomiesOsteotomies can be used inthe maxillary arch by
segmentalization ofthe maxilla and advancing one side morethan the other
side.Osteotomies in themandibular arch to correct arch asymme-try can become
somewhat complex.Ante-rior subapical osteotomies with removal ofa unilateral tooth
can correct some largediscrepancies (6 to 9 mm).However,thesubapical osteotomy may
need to be com-bined with ramus sagittal split osteotomiesand a unilateral or
bilateral body osteoto-my,with or without extraction,to shift theocclusion into a
symmetric position.These types ofmovements require a highdegree ofsurgical
skill,but can providehigh-quality outcomes.Divergence ofRoots Adjacent to
Interdental Surgical Sites When interdental osteotomies areplanned it may be
necessary for theorthodontist to tip the adjacent toothroots away from the area
ofthe plannedosteotomy to prevent damage to the teeth(Figure 55-30).Ifthe roots are
too closetogether,postsurgical periodontal prob-lems may develop with possible loss
ofinterdental bone and teeth.Creatinginterdental space between the roots sig-
nificantly improves the margin ofsafety.This can be easily achieved by
selectiveFIGURE55-29A,B,Bilateral mandibular body osteotomies will permit leveling
ofthe excessive curveofSpee without shortening the vertical height ofthe mandible
and are indicated when the mandibu-lar anterior dental height is normal or even
slightly short vertically.This basic technique can also beused to correct a reverse
curve ofSpee by elevating the anterior segment.AB
1130Part 8: Orthognathic Surgerybracket placement.For the tooth mesialto the
osteotomy,the bracket is slightlyrotated so that the mesial aspect ofthebracket is
positioned slightly more gingi-vally compared with the distal aspect ofthe bracket
(Figure 55-31).Converselythe distal tooth bracket is positioned sothat the distal
aspect ofthe bracket isplaced slightly more gingivally comparedwith the mesial
aspect ofthe bracket.With a straight wire technique the rootswill
diverge.Postsurgically,periapical radiographymay be necessary for the orthodontist
tocheck for rebonding the adjacent teethbrackets to ensure proper root angulationat
completion oftreatment.Extraction Versus NonextractionThe decision to extract or
not to extractcan sometimes be difficult.There are anumber offactors that may
contribute tothis determination.Overangulated Anterior TeethExcessiveover-angulated
anterior teeth may requireextraction to set the teeth over basal bone.However,ifthe
arch is to be expanded orteeth slenderized for TSD,for example,then extraction may
not be necessary.CrowdingThis is a common indicator,particularly with major
crowding oroverangulated teeth.However,ifcrowdingis mild to moderate,widening ofthe
archor teeth slenderizing for TSD may elimi-nate the need for extraction.Tooth-Size
DiscrepancyTSDs ofsignifi-cant magnitude may indicate the need
forextraction,particularly ifthe TSD oftheanterior mandibular teeth is 5 mm
orgreater and the mandibular incisors areoverangulated and/or crowded,in whichcase
a mandibular incisor extraction couldbe considered.Curve ofSpeeAccentuated curves
ofSpeein the maxillary arch usually have overangu-lated maxillary incisors,and
reverse curvesofSpee in the mandibular arch usually haveoverangulated mandibular
incisors.Extrac-tion ofbilateral first or second bicuspidsand retraction will
result in leveling ofthearches.However,arch expansion,whenindicated,may create
enough room so thatextractions are not necessary.Arch AsymmetriesWith
significantanteroposterior arch asymmetries,unilat-eral or bilateral asymmetric
extractions(ie,first bicuspid on one side and a sec-ond bicuspid on the opposite
side) maybe indicated when there is coexistingcrowding overangulated incisors,or
mid-line shift.Coordination ofMaxillary andMandibular Arch Widths In some cases
transverse arch width dis-crepancies can be corrected with stableand predictable
orthodontic movements,but in other cases orthodontic correctionmay be very unstable
and fraught withrelapse.It must be determined whetherto correct width problems by
orthodon-tics,orthopedics,SARPE,or surgicalexpansion.Even with SARPE using afixed
device,the palate only expandsapproximately one-third the amount ofthe expansion
that occurs at the occlusallevel,thus increasing the curve ofWil-son.19For
example,ifthe maxilla isexpanded with SARPE and the expansionat the occlusal level
is 6 mm,then theexpansion at the palatal level will only be2 mm (see Figure 55-
22).Patients withreverse curves ofWilson in the maxillaryarch may benefit more from
these tech-niques,but those with a pretreatmentaccentuated curve ofWilson may
haveunfavorable results,with subsequent dif-ficulty getting the buccal cuspids
tointerdigitate.The following predictablechanges will occur with maxillary
archexpansion by orthodontic,orthopedic,or SARPE procedures.FIGURE55-30Interdental
osteotomies.A,Pantomogram demonstrating inadequate room betweenthe roots ofthe
lateral incisors and cuspids.Performing osteotomies with roots in this position
couldresult in severe periodontal compromise and possible loss ofteeth.B,Adequate
spaces for interdentalosteotomies can be created by selective bracket placement on
the adjacent teeth.ABFIGURE55-31Selective bracket placementcancreate adequate
interdental space for osteotomies.On the tooth mesial to the
osteotomy,slightlyrotate the mesial aspect ofthe bracket gingivally,and on the
distal tooth,slightly rotate the distalaspect ofthe bracket gingivally.A straight
wirewill then diverge the roots.
Orthodontics for Orthognathic Surgery11311.The bite may open anteriorly,particu-
larly ifthe maxillary incisors have sig-nificant initial vertical inclination.Ifthe
maxillary incisors are overangulat-ed,then the bite may deepen anterior-ly as the
spacing is closed.2.Buccal tipping ofthe maxillary poste-rior teeth will increase
the curve ofWilson,because the lingual cusps willmove downward relative to the
buccalcusps.This may make it very difficultto properly interdigitate the
buccalcusps orthodontically.Therefore,these techniques are not recommend-
ed,especially when there is a preexist-ing accentuated curve ofWilson.3.Long-term
or perhaps permanentretention may be necessary to coun-terbalance the orthodontic
relapsepotential seen in a high percentage ofthese patients.4.In late adolescent
and adult patients,SARPE will likely be necessary toexpand the maxilla
orthopedically sincethe midpalatal suture is usually closed.Surgical expansion
ofthe maxilla atthe time ofthe Le Fort I procedure usingmultiple segmentation ofthe
maxilla,sta-bilization with bone plates and palatal orocclusal splints,and
hydroxyapatite syn-thetic bone grafting in the palate and lat-eral maxillary walls
can provide a goodoutcome.This technique when properlyperformed is very stable and
eliminates theorthodontic relapse potential inherentwith the other
techniques.Missing TeethTeeth can be missing from the arches fora number ofreasons
such as congenitalabsence,uneruption,previous orthodon-tic extractions,extractions
for periodon-tal or dental pathology,and trauma.Insome cases (ie,congenital absence
ofmaxillary lateral incisors,previous inap-propriate bicuspid extraction)
openingspace to accommodate replacement teethmay be indicated.This is most
applicablewhen the incisors are decreased in angu-lation without appreciable
crowding.Ifthe incisors are already overangulatedand/or crowding is present,then
openingspace orthodontically may be detrimentalto stability and periodontal
health.In thissituation with missing maxillary lateralincisors,the cuspids can be
used as later-al incisors,but may require considerablerecontouring to esthetically
and func-tionally conform to lateral incisor mor-phology.Although this cuspid
substitu-tion can work well for missing lateralincisors,it is done less frequently
nowthat dental implants are so predictableand successful,thereby allowing thecanine
to be placed in its normal andmore functional position.When conditions
permit,openingspace for replacement teeth can be accom-plished by appropriate
mechanics toachieve the required space.Surgery canalso be used to create spacing in
someareas.In the mandibular arch,distractionosteogenesis can be used to create
space.The missing teeth can then be replacedwith dental implants,bridges,or
partialdentures for example.Correction ofRotated TeethBracket placement and arch
wire adapta-tion are the primary keys to correctingrotated teeth and it is usually
best toachieve these corrections presurgery.However,ifthe malrotations do not
inter-fere with the establishment ofthe desireddentoskeletal relationship,then the
rota-tions can be corrected postsurgery.Severerotations may require supracrestal
fiberot-omy to prevent relapse and improve per-manent retention.This can often be
doneat the time oforthognathic surgery.Management ofAnkylosed TeethTreatment
ofankylosed teeth depends on(1) whether the tooth is primary or per-manent,(2) the
surrounding dentition,(3)the eruption status,(4) tooth position andorientation,(5)
the time ofonset anddiagnosis,(6) the age ofthe patient and,(7) the treatment
goals.Ankylosed Primary ToothThis canimpede the development and eruption ofthe
permanent successor.Ifa primarytooth has a permanent successor,treat-ment is
immediate extraction followed byspace maintenance until the permanenttooth
erupts.Ifno permanent successor ispresent and the primary tooth ankylosisoccurs at
an early stage in jaw growth anddevelopment with submergence ofthetooth
eminent,treatment includes extrac-tion and space maintenance.20Ifthe anky-losis
occurs late with no permanent suc-cessor,the occlusal and proximal contactscan be
reestablished with restorative den-tistry to provide esthetics and functionwith
perhaps many years ofservice.21It is important to diagnose and treatthe ankylosed
tooth before the adolescentgrowth phase.Retaining an ankylosedtooth during jaw
growth leads to arresteddevelopment ofthe alveolar ridge.Theseverity ofalveolar
growth loss depends onthe amount offacial growth left at the timethat the ankylosis
occurs.Timing theremoval ofan ankylosed tooth just at thestart ofthe pubertal phase
ofadolescentgrowth may achieve the treatment objec-tive ofmaintaining alveolar
ridge heightwhile allowing the tooth to remain longenough to act as a space
maintainer andesthetic temporary.22Ankylosed Permanent ToothAn unrec-ognized
ankylosed permanent tooth tiedinto the arch wire can result in a
significantmalocclusion (Figure 55-32).There are sev-eral ways oftreating the
permanent anky-losed tooth.Ifankylosis ofthe permanenttooth has an early onset
during eruption,thetooth should be luxated,allowing for furthereruption.2Ifrepeated
luxation proves inef-fective,the tooth should be extracted to pre-vent
submergence.Ifthe onset ofankylosisoccurs late in the normal eruption pattern,the
tooth should be luxated.Ifthe attempt is
1132Part 8: Orthognathic Surgeryunsuccessful and the tooth does not sub-merge,it
may be vertically restored ongrowth maturity.A composite build-up orcrown can be
added to a partially eruptedankylosed tooth to level and align the arch.21A deeply
unerupted ankylosed tooth,prima-ry or permanent,may be left undisturbedunless it is
infected,alters the alveolar bonegrowth potential,or constitutes an immedi-ate
threat to the occlusion or adjacent teeth,or would impede the placement
ofanosseointegrated implant.3Other treatment options includeextraction followed by
reimplantation,osseointegrated implant,or prostheticreplacement.23The patient�s
developmentalage is very important in considering replac-ing an ankylosed tooth
with an osseointe-grated implant.The implant will have thesame effect on growth
ofthe alveolar ridgeas the ankylosed tooth,and therefore shouldbe considered for
placement after alveolargrowth is essentially complete.24Proffit suggests surgical
luxation ofthe tooth with extraction forceps disrupt-ing the cementum-bone fusion
followedby immediate orthodontic traction tomove the tooth into
position.20Luxationinvolves breaking the bony bridge ofankylosis without damaging
the apicalnutrient vessels.This procedure formsfibrous inflammation tissue in the
repar-ative process.This tissue forms a falseperiodontal membrane,and tooth erup-
tion may resume.Orthodontic move-ment should begin immediately.Compli-cations
include possible crown,root,andalveolar fractures,loss ofviability andvitality,as
well as re-ankylosis.When anankylosed tooth is impacted,a similartechnique can
bring an impacted tooth(usually canines) into the arch.Exposureinvolves surgical
uncovering,applicationoforthodontic bonding,and tensionforces applied to direct the
tooth intoocclusion.However,ifthe tooth becomesre-ankylosed,the orthodontic forces
willintrude adjacent teeth.Orthodontics for Surgical Management ofAnkylosed
TeethPresurgical orthodon-tics may be indicated to create adequatespace (minimum
of2 to 3 mm) betweenthe roots ofthe adjacent teeth to safelyaccommodate interdental
osteotomiesaround the ankylosed tooth.Spacing isbest assessed with pantomographic
orperiapical radiographs.The ankylosedtooth is left out ofthe arch wire,and
allother teeth are properly aligned.Iforthog-nathic surgery is required to correct
adentofacial deformity,the orthodonticsare performed in the traditional manner,but
the ankylosed tooth must remain outofthe arch wire,unless it aligns well withone
ofthe dental segments.Followingsurgery,orthodontic mechanics can beinitiated
immediately to help get themobilized dental segment with the anky-losed tooth into
the best possible position.OsteotomyPerforming single-tooth os-teotomies or
sectional-arch osteotomieswith mobilization ofthe segment will per-mit immediate
repositioning ofthe anky-losed tooth (Figure 55-33),or facilitaterepositioning by
distraction osteogenesis.In select cases where an ankylosed pri-mary molar is
present,without a successor,a treatment option is to remove the anky-losed tooth
and eliminate the extractionspace by performing a vertical body ostec-tomy in
conjunction with a mandibularramus osteotomy and advance the posteri-or teeth and
mandibular body forward(Figure 55-34).This eliminates the needfor osseointegrated
implants and extensivedental reconstruction.Final Presurgical PreparationAs
presurgical orthodontic treatment pro-gresses,new diagnostic records
(lateralcephalograms,pantomograms,dentalmodels) are taken to determine the
feasibil-ity and timing ofsurgical procedures.Thiswill also aid the orthodontist in
identifyingspecific areas that may need to be addressedin completing the
presurgical orthodonticgoals (ie,sectional leveling ofthe arch FIGURE55-32An
ankylosed first molar tiedinto the arch wire has prevented development ofthe
alveolus and consequently created a signifi-cant posterior open bite.FIGURE55-
33Single-tooth osteotomies can beperformed as isolated cases or they can be per-
formed in combination with multiple maxillaryosteotomies to allow individual
movement ofthedental osseous segments or application ofimme-diate distraction
osteogenesis to reposition thetooth properly.The case illustrated had an anky-losed
maxillary right cuspid (see Figure 55-8)treated with segmental maxillary
osteotomiesincluding a single tooth segment containing theright cuspid (A,B)AB
Orthodontics for Orthognathic Surgery1133segments,marginal ridge alignment,verti-
cal dental alignment,buccal surface align-ment,additional TSD correction).During
surgery the jaws are usuallywired together once or twice,as each jaw
isindependently mobilized and stabilized withrigid fixation.To facilitate wiring
the jawstogether as well as providing a means ofusing postsurgical elastics
ifrequired,fix-tures attached to the brackets or arch wiresare usually
necessary.Fixtures attached tothe brackets are dependent on the manufac-turer but
may include ball hooks built ontothe brackets,Tpins,and Khooks,(Figure55-
35).Fixtures attached to the arch wireinclude crimped-on hooks and solderedpins
(Figure 55-36).Hooks built onto thebrackets are preferred,followed by the
otherhooks placed on the brackets (Tpins,Khooks).The least preferred are the hooks
onthe arch wire.The reason is that ifpost-surgery elastics are required for an
extendedtime,the elastics and hooks on the arch wirewill activate the arch
wire,possibly creatingunwanted orthodontic forces and move-ments (ie,tipping the
crowns lingually andthe roots buccally).This undesirabletorquing occurs to a much
lesser degreewhen the hooks are directly on the brackets.When the maxilla or
mandible are tobe segmentalized,it may be better for theorthodontist to section the
arch wire (seeFigure 55-15B) and bend the ends inwardat the predetermined osteotomy
areasimmediately prior to surgery,or the sur-geon can cut the wire at surgery.The
best type ofarch wire to placeprior to surgery is a rectangular stainlesssteel wire
that fills the bracket slot.Forexample,with an 18 slot,a 17 �25 gaugewire is
recommended,and for a 22 slot,a21 �25 gauge wire is indicated.This willhelp
stabilize the individual dental unitstogether as a whole arch or in segmentswhen
segmental surgery is required.Thefinal wire should be placed 2 to 3 monthsprior to
surgery.Postsurgical OrthodonticsIn preparation for the postsurgery ortho-dontic
phase oftreatment,the surgical sta-bilizing splint,ifused,is usually removed 4 to 6
weeks postsurgery.Ifthe palatalsplint design is used and a large maxillaryexpansion
has been performed,the splintcan remain for a longer period and thepostsurgical
orthodontics can be per-formed around it.The maintenance ofthesplint will enhance
the transverse stabilityand it can be left in for 2 to 3 months orlonger
ifnecessary.It can be made into aremovable appliance.Ifrigid skeletal fixation is
used,activeorthodontics involving changing the archwires can usually resume 4 to 6
weeks post-surgery,when patients are usually comfort-able enough to tolerate
changing their archwires.The orthodontist can be fairlyaggressive at finishing the
occlusionbecause the osseous segments can still bemoved slightly.The teeth move
much morerapidly for the first few months post-surgery because there is an
increased bonymetabolism as a result ofthe surgery.Theorthodontist can therefore
accomplish in 1 to 2 weeks what would normally take 4 to 6 weeks to
complete.Applying activemechanics at this early postsurgical ortho-dontic phase
oftreatment and booking thepatient for a routine orthodontic follow-up 4 to 6 weeks
later could result in uncon-trolled excessive orthodontic movements,resulting in an
unfavorable outcome.FIGURE55-34A,B,An ankylosed submergedprimary tooth without a
permanent successorcan be treated with extraction ofthe primarytooth as well as a
vertical body ostectomy in con-junction with a mandibular ramus sagittal
splitosteotomy to advance the posterior teeth forwardto eliminate the ankylosed
tooth and associatedspace.This eliminates the need for an osseointe-grated implant
or crown-and-bridge work.ABFIGURE55-35Orthodontic hooks.Ball hooksbuilt onto the
brackets (blue arrows)provide thebest stability.Other options include Tpins and
Khooks (white arrows) or other methods to pro-vide attachments directly on the
brackets.FIGURE55-36Soldered pins on the arch wire orcrimped hooks (white
arrows)onto the archwire can also be used but are not preferredbecause the use
ofpostsurgical elastics will acti-vate the arch wire,possibly creating
unwantedorthodontic movements.
1134Part 8: Orthognathic SurgeryFor most cases the orthodontistshould see the
patient once a week for thefirst month,then every 2 weeks for thenext 2 months for
adjustments so thatorthodontic changes can be closely moni-tored.At the initial
appointments rootpositions are checked,loose brackets andbracket positions are
evaluated and cor-rected,and new arch wires are placed ifindicated.Interarch
mechanics (ie,class IIor III elastics,vertical elastics,and/orcross-arch elastics)
can be applied as nec-essary to finalize the occlusion.Once theinitial healing
phase is completed (approx-imately 3 to 4 months postsurgery) andthe occlusion is
stable,the orthodonticappointment intervals can be extended tothe more traditional
time frame.The finalpositioning ofthe teeth usually takes from3 to 12 months
ofpostsurgical orthodon-tic treatment but could be longer depend-ing on the
postsurgical orthodonticrequirements.Although reasonable stabil-ity from surgical
healing occurs in approx-imately 3 to 4 months,the final postsurgi-cal healing
phase takes 9 to 12 months.References 1.Bolton WA.The clinical application ofa
tooth-size analysis.Am J Orthod 1962;48:504�29.2.Moyers RE,van der Linden
FPGM,Riolo ML,McNamara JA.Standards ofhumanocclusal development.The University
ofMichigan Ann Arbor (MI):The Center forHuman Growth and
Development;1976.p.53�94.3.Alling CC III,Helfrick JF,Alling
RD.Impactedteeth.Philadelphia (PA):WB Saunders Co.;1993.p.4.4.Biederman W.The
problem ofthe ankylosedtooth.In:Spengeman WG,editor.Dentalclinics ofNorth
America.Philadelphia(PA):WB Saunders Co.;1968.p.409�24.5.Jacobs SG.Ankylosis
ofpermanent teeth:a casereport and literature review.Aust Orthod
J1989;11(1):38�44.6.Schultes G,Gaggl A,Karcher H.Periodontaldisease associated with
interdentalosteotomies after orthognathic surgery.JOral Maxillofac Surg
1998;56:414�7.7.Wolford LM.Periodontal disease associatedwith interdental
osteotomies after orthog-nathic surgery.J Oral Maxillofac
Surg.1998;56:417�9.8.Dorfman HS,Turvey TA.Alterations inosseous crestal height
following interdentalosteotomies.Oral Surg Oral Med OralPathol
1979;48:120�5.9.Shepherd JP.Long-term effects ofsegmentalalveolar osteotomy.Int J
Oral Surg 1979;8:327�32.10.Kwon H,Philstrom B,Waite DE.Effects on theperiodontium
ofvertical bone cutting forsegmental osteotomy.J Oral MaxillofacSurg
1985;43:953�5.11.Fox ME,Stephens WF,Wolford LM,el Deeb M.Effects ofinterdental
osteotomies on theperiodontal and osseous supporting tissues.Int J Adult Orthod
Orthogn Surg 1991;6:39�46.12.Wolford LM,Cottrell DA.Diagnosis ofmacroglossia and
indications for reductionglossectomy.Am J Orthod DentofacOrthop
1996;110:170�7.13.Turvey TA,Journot V,Epker BN.Correction ofanterior open bite
deformity:a study oftongue function,speech changes,and sta-bility.J Maxillofac Surg
1976;4:93�101.14.Wickwire NA,White RP Jr,Proffit WR.Theeffect ofmandibular
osteotomy on tongueposition.J Oral Surg 1972;30:184�90.15.Wolford LM,Karras S,Mehra
P.Concomitanttemporomandibular joint and orthognath-ic surgery:a preliminary
report.J OralMaxillofac Surg 2002;60:356�62.16.Wolford LM,Mehra P,Reiche-Fischel
O,et al.Efficacy ofhigh condylectomy for manage-ment ofcondylar hyperplasia.Am J
OrthodDentofac Orthop 2002;121:136�51.17.Mehra P,Wolford LM.The Mitek mini
anchorfor TMJ disc repositioning:surgical tech-nique and results.Int J Oral
Maxillofac Surg2001;30:497�503.18.Wolford LM,Cardenas L.Idiopathic
condylarresorption:diagnosis,treatment protocol,and outcomes.Am J Orthod
DentofacOrthop 1999;116:667�76.19.Schwarz GM,Thrash WJ,Byrd DL,Jacobs
JD.Tomographic assessment ofnasal septalchanges following surgical-orthodonticrapid
maxillary expansion.Am J Orthod1985;87(1):39�45.20.Proffit WR.Contemporary
orthodontics.StLouis (MO):C.V.Mosby Co.;1986.p.191�2,352.21.Williams
HS,Zwemer,JD,Hoyt DJ.Treatingankylosed primary teeth in adult patients:acase
report.Quintessence Int 1995;26:161�6.22.Steiner DR.Timing ofextraction
ofankylosedteeth to maximize ridge development.JEndodont 1997;23:242�5.23.Geiger
AM,Bronsky MJ.Orthodontic manage-ment ofankylosed permanent posteriorteeth:a
clinical report ofthree cases.Am JOrthod Dentofac Orthop 1994;106:543�8.24.Oesterle
LJ.Implant consideration in the grow-ing child.In:Higuchi KW,editor.Ortho-dontic
applications ofosseointegratedimplants.Chicago (IL):Quintessence Pub-lishing
Co.;2000.p.133�59.
CHAPTER 56Principles ofMandibular Orthognathic SurgeryDale
S.Bloomquist,DDS,MSJessica J.Lee,DDSThe development ofmandibularosteotomies for
correction ofdentofacialdeformities closely parallels the advance-ment oforal and
maxillofacial surgery as aspecialty more than any other group ofsurgical
techniques.From Hullihen,who in1849 was the first to describe a
mandibularosteotomy,to Obwegeser,who developedthe sagittal osteotomy ofthe
verticalramus,there has been dramatic progress inthe techniques ofmandibular
osteotomies.After Obwegeser�s original paper in Ger-man,and especially since his
description oftechniques in the English literature,orthognathic surgery has seen
dramaticchanges in use as well as refinement oftheosteotomies.Although the
development ofosteotomy techniques is ongoing,it is thepurpose ofthis chapter not
only todescribe the most commonly used surgicalprocedures for the mandible but also
toemphasize the refinements in techniquethat have been the result ofthe most
recentclinical as well as basic research.HistoryHullihen corrected a patient with
anterioropen bite and mandibular dentoalveolarprotrusion with an intraoral
osteotomy,verysimilar to what we now describe as an ante-rior subapical osteotomy
(Figure 56-1).1Hisefforts did not seem to stimulate muchinterest,for it was almost
50 years laterwhen Angle described a body osteotomydone by V.P.Blair (Figure 56-2A)
for apatient with mandibular horizontalexcess.2,3This technique,with minor mod-
ifications,was advocated until the 1970s.Since then the only major modifications
inthe body osteotomy that have occurred area greater emphasis being placed on pre-
serving the inferior alveolar nerve and aswitch to an intraoral approach.The
horizontal osteotomy ofthe verti-cal ramus popularized by Blair (Figure 56-2B) was
accomplished through anextraoral route.4As with many ofthe earlymandibular
procedures a horizontal bonecut was made above the lingula and wasdescribed for
correcting both mandibularhorizontal deficiency and horizontalexcess.An intraoral
technique was notsuggested until Ernst discussed his proce-dure approximately 25
years later.5Thismethod ofcorrecting mandibular defor-mities was used for almost 60
years,butbecause ofits lack ofpostoperative stabili-ty,it has fallen into
disuse.The subcondylar osteotomy (Figure56-2C),a form ofwhich was first reportedby
Limberg as an extraoral technique,hasundergone relatively minor refinement tothe
intraoral vertical subcondylar osteoto-my that is popular today.6There has,how-
ever,been a substantial number ofosteotomy designs through the verticalramus that
begin in the sigmoid notch,which has led to some confusion in theFIGURE56-
1Hullihen�s mandibular subapicalosteotomy.Adapted from Bloomquist DS.Princi-ples
ofmandibular orthognathic surgery.In:Peterson LJ,Indresano AT,Marciani
RD,RoserSM.Principles oforal and maxillofacial surgery.Vol 3.Philadelphia (PA):
J.B.Lippincott Com-pany; 1992.p.1416.
1136Part 8: Orthognathic Surgerynomenclature ofwhat is a fairly closelyrelated
group ofosteotomies.The namesthat have been developed have generallybeen based on
the length and direction ofthe cuts made in the posterior portion ofthe vertical
ramus.The subcondylarosteotomy was used to describe the condy-lar neck osteotomies
ofKostecka and ofMoose.7,8Generally longer cuts thatextended to the posterior
border above theangle,such as described by Limberg,Thoma,and Robinson,were
described asoblique osteotomies.5�10Shira,however,coined the term oblique sliding
osteotomyfor this particular surgery.11Finally Cald-well and Letterman described a
verticalosteotomy ofthe mandibular ramus thatincluded a cut from the sigmoid notch
tothe inferior border in front ofthe angle ofthe mandible.12The cut was kept
behindthe foramen ofthe mandibular nerve,anda portion ofthe lateral cortex ofthe
distalfragment was decorticated to allow a larg-er area ofbone contact.Generally
theselatter two groups ofosteotomies are nowbeing called vertical osteotomies,but
somesemantic differences still persist.Specifi-cally the terms vertical
subcondylarosteotomies (VSOs) and vertical ramusosteotomies (VROs) are still used
inter-changeably in the literature.Primarily thistype ofosteotomy was designed for
correc-tion ofmandibular horizontal excess ofmandibular asymmetries,although Robin-
son described its use with a bone graft forhorizontal deficiencies.10The intraoral
approach to the sub-condylar osteotomies is relatively new,hav-ing first been
described by Moose in1964.13He approached the condylar neckmedially with a straight
bur.Winstanleysuggested a lateral approach in 1968,but itwas not until Hebert and
colleaguesdescribed the use ofa special oscillatingsaw that this approach became
popular.14,15A variation ofthe vertical subcondylarosteotomy was suggested by
Wassmund in1927 (Figure 56-3A),which is similar towhat is now called the inverted
Losteoto-my.16Pichler and Trauner later suggestedthe use ofbone grafts into the
defect leftby the advancement ofthe mandible.17Caldwell and colleagues further
modifiedthe inverted Lby adding a horizontal cutjust above the inferior border
ofthemandible to create what is now called theCosteotomy (Figure 56-3B).18The
statedadvantage ofthe Costeotomy was that thebone cut design made the use ofa
bonegraft unnecessary.This advantage was fur-ther enhanced by the modification sug-
gested by Hayes,with the splitting oftheinferior limb sagittally so that more
bonecontact can be achieved.19A further inter-esting approach to this group
ofverticalramus osteotomies done for horizontalmandibular deficiency is the
modified Losteotomy described by Fox and Tilson.20They deleted the superior
horizontal cut ofthe C osteotomy and instead extended thevertical cut to the
sigmoid notch.Then thecoronoid process was removed and addedas a free graft into
the defect resulting fromthe mandibular advancement.The greatest development
inosteotomies ofthe vertical ramus is thesagittal osteotomy,credited to
Obwegeserand Trauner,but generally now used in afashion modified from the original
tech-nique described in 1955.21Lane has beenmentioned as the developer ofa form
ofFIGURE56-2A,Blair�s body osteotomy.B,Blair�s ramus
osteotomy.C,Limberg�s�oblique�osteotomy ofthe ramus.Adapt-ed from Bloomquist
DS.Principles ofmandibular orthognathic surgery.In:Peterson LJ,Indresano
AT,Marciani RD,Roser SM.Principles oforal and maxillo-facial surgery.Vol
3.Philadelphia (PA):J.B.Lippincott Company; 1992.p.1416.ABC
Principles ofMandibular Orthognathic Surgery1137the sagittal osteotomy,with
parallel hori-zontal bone cuts made through the medialand lateral cortices ofthe
vertical ramus(Figure 56-4).22The medial cut was madejust above the lingula,with
the lateral cutmade just below it.This idea was expandedby Schuchardt before being
refined andpopularized by Obwegeser.23The majormodifications in the osteotomy
designwere first made by DalPont with his verti-cal cut through the lateral cortex
as well asthe suggestion that the medial horizontalcut be extended only to a point
above thelingula and not to the posterior border(Figure 56-5).24This latter
techniqueshortens the split posteriorly,and as wasfurther discussed by
Hunsuck,decreasesthe trauma to the overlying soft tissue.25Many clinicians have
offered suggestionsfor improving the sagittal osteotomy,butthe only other major
innovation to thistechnique has been the use ofinternal rigidfixation.Spiessl
suggested the use ofscrewsfor fixation ofthe fragments in the
sagittalosteotomy.26Although wire osseous fixa-tion is still used by some
surgeons,rigidinternal fixation in some form has becomethe standard technique for
the bilateralsagittal split osteotomy (BSSO).Osteotomies ofthe mandibular bodydo
not generally receive the same degree ofattention as osteotomies ofthe
verticalramus,but they have undergone refine-ments and variations from the
originalanterior alveolar osteotomies ofHullihenand the body osteotomies
ofBlair.The firstvariation ofHullihen�s procedure did notappear until 90 years
after the originaldescription,when Hofer demonstrated ananterior mandibular
alveolar osteotomy toadvance anterior teeth in correction ofamandibular
dentoalveolar retrusion (Fig-ure 56-6A).27Kole modified this procedureby suggesting
the use ofbone grafts fromthe mental region to the defect caused bythe rotation
ofthe anterior dentoalveolarsegment (Figure 56-6B).28Clinicians nowFIGURE56-
3A,Losteotomy.B,Costeotomy.Adapted from Bloomquist DS.Principles ofmandibular
orthognathic surgery.In: Peterson LJ,IndresanoAT,Marciani RD,Roser SM.Principles
oforal and maxillofacial surgery.Vol 3.Philadelphia (PA): J.B.Lippincott Company;
1992.p.1417.ABFIGURE56-4Lane�s osteotomy.Adapted fromBloomquist DS.Principles
ofmandibularorthognathic surgery.In: Peterson LJ,IndresanoAT,Marciani RD,Roser
SM.Principles oforaland maxillofacial surgery.Vol 3.Philadelphia(PA):
J.B.Lippincott Company; 1992.p.1417.FIGURE56-5DalPont�s modification ofthesagittal
osteotomy.Adapted from BloomquistDS.Principles ofmandibular orthognathicsurgery.In:
Peterson LJ,Indresano AT,MarcianiRD,Roser SM.Principles oforal and maxillofa-cial
surgery.Vol 3.Philadelphia (PA): J.B.Lip-pincott Company; 1992.p.1418.
1138Part 8: Orthognathic Surgeryemploying Hofer�s osteotomy generally usesome form
ofbone graft in the alveolardefect ifsignificant movement ofthe frag-ment is
planned.Mandibular alveolarosteotomies have expanded in primarilytwo ways from
Hofer�s original procedure.Kent and Hinds initially presented the useofthe single-
tooth osteotomies ofthemandible in 1971,and MacIntosh closelyfollowed with his
description ofthe totalmandibular alveolar osteotomy in1974.29,30This latter
procedure continuesto be popular,with minor variations beingadded by other
clinicians.Osteotomies ofthe body ofthemandible have been described in almostevery
conceivable form,with the mostdurable advancements being the
steposteotomy,initially described by VonEiselberg in 1906 (Figure 56-7A),and
thehorizontal osteotomy ofthe symphysisdescribed by Hofer in 1942 (Figure 56-
7B).31,32The step osteotomy was origi-nally described for treatment ofmandibu-lar
horizontal deficiency,but it has beenused in various forms for mandibular hor-
izontal excess as well as asymmetry.Thehorizontal osteotomy ofthe symphysis hasalso
developed a large degree ofversatility,with its use in various forms being sug-
gested for almost any skeletal deformity ofthe bony chin.Anatomic and Physiologic
Considerations ofMandibularSurgeriesVascular SupplyA major concern with surgery
ofthe facialskeleton is the vascular supply ofthe bonesegments.This was
dramatically demon-strated by the explosion oforthognathicFIGURE56-6A,Hofer�s
subapical osteotomy.B,Kole�s subapical osteotomy.Adapted from Bloomquist
AT,Marciani RD,Roser SM.Principles oforal and maxillofacial surgery.Vol
3.Philadelphia (PA): J.B.Lippincott Company; 1992.p.1418.ABFIGURE56-7A,Von
Eiselberg�s step osteotomy.B,Hofer�s horizontal osteotomy.Adapted from Bloomquist
AT,Marciani RD,Roser SM.Principles oforal and maxillofacial surgery.Vol
3.Philadelphia (PA): J.B.Lippincott Company; 1992.p.1419.AB
Principles ofMandibular Orthognathic Surgery1139surgery in the United States after
Bell andLevy�s studies ofvascular effects oftheosteotomies.33Although all ofthe
tech-niques they looked at had been previouslyused in patients,there had not been
anyexperimental evaluations ofthe physio-logic basis for many ofthe
procedures.Belland Levy�s work demonstrated that bloodflow through the mandibular
periosteumcould easily maintain a sufficient bloodsupply to the teeth ofa mobile
segment,even when the labial periosteum wasdegloved.Blood flow from the
periosteumwas termed centripetal,to distinguish itfrom the blood flowing from
endosteal ves-sels outward (centrifugal) that was associ-ated with long
bones.Previously cliniciansfelt that the inferior alveolar artery had aprimary role
in nourishing the mandible,but Bell and Levy demonstrated that thereis also a
sufficient blood supply from thesurrounding soft tissues,even ifthe inferi-or
alveolar artery was obstructed.Morerecent work in animals suggests that theblood
supply to the body ofthe mandibleunder normal conditions comes almostentirely from
the inferior alveolar artery.34However,when this source is obstructed,the
peripheral blood vessels quickly takeover for the anterior mandible.The poste-rior
mandibular dentoalveolus,however,does not benefit from this kind ofcollater-al
blood supply,which calls into questionthe safety ofposterior mandibular segmen-tal
alveolar osteotomies.Zisser and Gat-tinger showed pulpal necrosis in themolars
ofhorizontal osteotomies doneabove the inferior alveolar nerve in thebody ofthe
mandible ofdogs.35The safety ofcombined mandibularosteotomies,such as ramal
procedures andbody osteotomies,has been a concernbecause ofthe predominant role
oftheinferior alveolar artery.36The fragility ofthe vascular supply to the
mandibularalveolus engenders some concern over thecommon use ofsubapical
osteotomies.Although their relative safety has beendemonstrated by both animal
studies andsubstantial clinical experience,subapicalosteotomies need to be
carefully plannedto ensure as large a vascular pedicle as pos-
sible.33,37Complications,such as pulpalnecrosis,soft-tissue defects,and loss
ofteeth and bone,have demonstrated thedelicate nature ofthe blood supply,espe-
cially when attempts at moving small den-toalveolar fragments are made.The
effectofaging on the vascular supply to themandibular body is an area about
whichvery little information is known,particu-larly whether aging causes a switch
fromthe centrifugal to centripetal blood supply.Bradley has demonstrated an
apparentdecreasing capacity ofthe inferior alveolarvessels that occurs with
aging,but theimpact ofthis effect on mandibularosteotomies is unknown.38Osteotomy
designs ofthe verticalramus have profited by studies ofthe effectofsurgery on
vascular supply.The proxi-mal segment ofthe vertical subsigmoidosteotomy maintains
its blood supplythrough the temporomandibular jointcapsule and the attachment ofthe
lateralpterygoid muscle.However,the inferiortip ofthis fragment has undergone
vascu-lar necrosis in experimental studies.39Thisled to the suggestion that fewer
problemsmay occur ifthe cut was made above theangle ofthe mandible.39The importance
ofthe periostealblood supply as well as the endosteal sup-ply in the vertical ramus
has been exploredby animal research.40�43When the medialpterygoid and masseter
muscles arestripped,both blood flow and blood sup-ply studies have demonstrated the
possibil-ity ofavascular necrosis in the proximalsegment.Comparisons ofextensive
musclestripping ofthe vertical ramus againstpreservation ofthe masseter
attachmenthave demonstrated a significant differencein the vascularity ofthe
inferior portion ofthe proximal fragment.These studies ofblood supply ofthe
vertical ramus may beofvalue in predicting the vascular effects ofthe Cor
Losteotomies.However,resorp-tion ofthe proximal fragment has not beenreported in
these particular bone cuts pos-sibly because ofthe rarity oftheir use.However,given
the available research,it iswise to minimize the periosteal and muscleattachment
stripping on the medial surfaceofthe proximal fragment with either the Cor
Losteotomy or any oftheir variations.The last unanswered question con-cerning
vascular supply in mandibularorthognathic surgery is the determinationofa safe
distance away from the apex oftheteeth to make horizontal bone cuts.Manyofthe
references to this question are basedon research done in the maxilla.44Fromthese
early animal studies the pulpal bloodsupply ofa tooth should not be affected ifa
cut was made at least 5 mm away fromthe apex ofthe tooth.Zisser and
Gattinger,however,saw pulpal changes in dogs withsome horizontal cuts that were
made 10 mmaway from the apex.35Whether these dis-tances have any relevance to
humans is pre-sumptive.Clinically the incidence oftoothdevitalization from
horizontal subapicalosteotomies is extremely low and it can beassumed that,for the
most part,5 mm is agood guideline.A cut made 10 mm fromthe apices,although allowing
a greater safe-ty margin,is often impractical because ofother anatomic
limitations.The greaterdistance from the apices ofthe teeth notonly minimizes
direct pulpal injury butincreases the vascular pedicle to the mobilesegment as
well.NervesThe surgeon working around the facemust be constantly aware ofthe nerve
net-work that exists in this area.Fortunately,on approaching the mandible,these
con-cerns can be narrowed to essentially twomajor nerves:the marginal
mandibularbranch ofthe seventh cranial nerve andthe third division ofthe trigeminal
nerve,most frequently one ofits branches,theinferior alveolar nerve.The
marginalmandibular branch is usually only at riskduring extraoral
procedures.Although
1140Part 8: Orthognathic Surgerytrauma to this nerve has been reported tohave
occurred during intraoral approach,it is rare and for the mort part appears tobe
preventable.Avoiding damage to thisnerve during extraoral approaches to themandible
is a major surgical goal;in mostcases in orthognathic surgery it is achievedbecause
soft tissue anatomy in patientsundergoing the surgery has not been dis-turbed by
disease or trauma.The tech-niques ofthese approaches are coveredelsewhere in these
book volumes as well asare the methods for minimizing the risksofdamage to the
marginal mandibularbranch.Damage to the third division ofthe trigeminal
is,however,a much-discussed problem in mandibular surgery.The course ofthe inferior
alveolar nerveinto the vertical ramus and then throughthe body ofthe mandible makes
itextremely susceptible to damage fromalmost every mandibular surgical proce-
dure.In most cases the surgeon�s maingoal relative to this nerve is to minimizethe
trauma because its avoidance is almostimpossible.In the past surgeons stressedthe
importance oflooking for and some-times freeing up the nerve as it eitherentered or
left the mandible before makingosteotomies in the areas ofthe
foramina.However,there is a trend toward avoidingthis step,unless it is absolutely
necessary tomake the osteotomy as close to the nerveas possible.The simple act
ofexposing thenerve seems to increase the chance forpostoperative sensory
deficiency.Often the debates on whether onemandibular osteotomy is preferable
toanother are primarily based on the poten-tial ofdamaging the inferior alveolar
nerve.This has resulted in many clinicians trivial-izing the damage found following
a certaintechnique.Well-defined standards for bothlong- and short-term follow-up
ofnervedamage during mandibular procedureshave been discussed45;however,in
mostpapers these have not been used to evaluatesensory deficits.In addition very
few con-trolled studies have been published com-paring procedures;as a result not
muchcan be said in support ofany ofthe differ-ing attempts to minimize nerve
damage.Studies looking at the loss oftoothsensibility from horizontal
osteotomiesbelow the dental apices,however,havebeen quite consistent.Most authors
founda relatively high loss ofresponse to pulptesting immediately after
osteotomies,especially when teeth are close to a
verticalosteotomy.46�48However,this loss may notcorrelate with actual loss oftooth
vitalityand,thus,either tooth loss secondary to anosteotomy or the need for
endodontictherapy is very low.The MuscleOrthognathic surgery affects muscles
inprimarily two ways:it changes the lengthofa muscle or it changes the direction
ofmuscle function.Effects ofthese changesare still not understood,although
variousauthors have emphasized the importanceofcontrolling muscular
changes.Themuscles commonly discussed in ortho-gnathic surgery ofthe mandible have
beenthe muscles ofmastication and thesuprahyoid group ofmuscles.Recentinterest on
the soft tissue effects offacialskeletal surgery has expanded interest tothe other
facial muscles.This latter group,however,has generally not been discussedrelative
to mandibular osteotomies,withthe possible exception ofthe effect oftheanterior
mandibular osteotomies on theattachment ofthe mentalis muscle.Themuscles
ofmastication,however,havereceived considerable attention,datingback to the early
vertical ramus proce-dures.Research interest on the effects ofaltering these
muscles concentrated eitheron their effect on the skeletal changes,especially
relapse following mandibularosteotomies,or on the changes in functionofthese
muscles.Distraction ofthe superior fragmentofa horizontal osteotomy ofthe
verticalramus following surgery was noted earlyby surgeons who used this
technique.49Evaluation ofthis procedure followingcorrection ofprognathism found a
superi-or movement ofthe mandible in thegonial region as well as a downward
andbackward movement at the symphysis.This change,which was attributed to theforces
ofthe pterygomasseteric sling,hasreceived considerable attention,not onlyin
mandibular setbacks done withosteotomies through the vertical ramusbut also in
mandibular advancements.50�55The apparent shortening ofthe verticalramus has been
noted in a number ofstudies,and in some a correlation has beendemonstrated between
this change and theposterior movement ofthe symphysis.Theexact reason for the
change in the gonionhas not been clearly demonstrated.Kohndemonstrated the movement
ofthis pointinferoanteriorly in mandibular advance-ments by way ofa measurement he
termedthe gonial arc (Figure 56-8).54Most inves-tigators feel this represents
distraction ofthe condyle from the fossa,and thisFIGURE56-8Gonial arc used for
showingcondylar position change with a mandibularosteotomy.Adapted from Bloomquist
DS.Prin-ciples ofmandibular orthognathic surgery.In:Peterson LJ,Indresano
AT,Marciani RD,RoserSM.Principles oforal and maxillofacial surgery.Vol
3.Philadelphia (PA): J.B.Lippincott Com-pany; 1992.p.1422.
Principles ofMandibular Orthognathic Surgery1141hypothesis was further supported by
themigration ofthe gonion back during thepostoperative period.54,55The long-
termpostoperative decrease in gonial arc wasgenerally believed to be due to
remodel-ing,especially resorption that occurred atthe mandibular
angle.40,43Especially inearly studies,resorption could haveaccounted for this
change because ofthethen-accepted technique ofcompletelystripping muscle attachment
from theproximal segment.However,in morerecent studies in which minimal
musclestripping was done,a similar result hasbeen noted.56,57Will and colleagues
noteda condyle distraction followed by an �over-shoot�in the resettling ofthe
condyle inthe fossa.58This change in condylar posi-tion may be due to either
displacement ofthe disk within the joint or compression ofthe soft tissues ofthe
joint by increasedpressures secondary to the muscles ofthepterygomasseteric
sling.The rotational change in the proximalsegment ofa mandibular osteotomy hasbeen
implicated in relapse by multipleclinicians who believe that the muscles ofthe
pterygomasseteric sling reassert them-selves after the surgery.59,60Therefore,there
has been an emphasis on carefullyrepositioning the proximal segment closeto its
preoperative position.Unfortunatelya correlation between mandibular
ramuspositioning and relapse in the case ofmandibular advancements has never
beendemonstrated.There have been a few stud-ies that have shown a relation
betweenrelapse ofmandibular setback surgeriesand the position ofthe vertical
ramus.61Ithas been noted in these surgeries that thedegree ofclockwise rotation
ofthe proxi-mal fragment in a sagittal osteotomyseems to relate to the amount
offorwardrelapse ofthe distal segment.Franco andcolleagues theorized that a
stretching ofthe medial pterygoid muscle as well as theelongation ofthe anterior
fibers ofthemasseter and temporalis muscles from theclockwise rotation ofthe
proximal seg-ment both can contribute to relapse inlengthening the muscles ofthe
pterygo-masseteric sling.61This can result in achange in mandibular position as has
beendocumented by Yellich and colleagues.62The degree to which this is active
inorthognathic surgery remains unclear.The contribution ofthe suprahyoidmuscles to
relapse in mandibular advance-ment surgery is equivocal,with many clini-cians
claiming an existence ofthis relation-ship.Ellis and Carlson demonstrated inmonkeys
that relieving the suprahyoidmuscles from the symphysis ofthemandible decreased the
amount ofrelapsewhen the mandibles were advanced.63Clin-ical studies,however,have
failed to show arelation between suprahyoid myotomiesand relapse.64,65Animal
studies have alsodemonstrated that adaptive changes occurin the connective tissues
at the muscle-tendon and tendon-bone interfaces butonly with large
advancements.66The belief,however unsubstantiated,that muscle pull in some way does
affectthe stability ofmandibular osteotomieshas led to a variety
ofrecommendations.Historically the most common methodadvocated is the attempt at
minimizing thechange in muscle position and length.Thecutting ofmuscle
attachments,such as hasbeen recommended for the suprahyoidgroup,has the potential
for increasingmorbidity.Without significant evidencethat this is ofmuch value,this
additionalsurgery cannot be justified.However,therehas been recognition that
muscles andtheir attachments seem to adapt fairlyquickly ifthe bone is held rigidly
for a longenough time.66,67It is important to recog-nize that intermaxillary dental
fixationdoes not provide a completely stablemethod ofbone fixation,especially
iftheteeth have been under active orthodonticmovement.Additionally the
greatestamount ofrelapse ofmandibularosteotomies seems to occur in the first 3 to6
weeks after surgery.Whatever the causesofthe instability during this time therehave
been several techniques designed toprovide increased stability for this
initialperiod,to improve the stability ofmandibular osteotomies.Primarily
twotechniques have been attempted:externalsupporting mechanisms and internal
rigidfixation.The only external technique thathas been ofmuch value has been
thewiring technique that has been termedskeletal fixation.With this procedure
thebony skeletons are tied to one another,cir-cumventing the periodontal ligaments
ofthe teeth.This has been used with inter-maxillary fixation,keeping the
mandibleimmobilized for 6 to 8 weeks (Figure 56-9).58,67,68The alternative
procedures ofinternal rigid fixation techniques usingplates or screws will be
discussed in thesucceeding sections on the osteotomies.Osteotomy TechniquesVertical
Ramus OsteotomiesOsteotomies in the vertical ramus have beenthe preferred technique
for correctingdevelopmental deformities ofthe mandible.This preference has
increased with closercooperation between orthodontists and FIGURE56-9Skeletal
fixation used with maxillo-mandibular fixation or mandibular advancement.Adapted
from Bloomquist DS.Principles ofmandibular orthognathic surgery.In: Peterson
LJ,Indresano AT,Marciani RD,Roser SM.Principlesoforal and maxillofacial surgery.Vol
3.Philadel-phia (PA): J.B.Lippincott Company; 1992.p.1423.
1142Part 8: Orthognathic Surgerysurgeons in treating dentofacial deformities.Most
ofthe time the dental arch discrepan-cies can be orthodontically corrected,leav-ing
the surgeon the responsibility for mov-ing the coordinated dental arch into its
newposition,as dictated by functional andesthetic demands.Operations in the
verticalramus,therefore,have become almost auto-matically considered when the
dental archas a unit has to be moved.As previouslynoted there have been numerous
techniquessuggested for osteotomies ofthe ramus,butessentially three different
procedures,withminor variations,have been accepted by thesurgical
community.Vertical SubcondylarOsteotomiesOsteotomies extending from the
sigmoidnotch vertically behind the inferior alveolarnerve foramen to the inferior
border orangle have had several different names,butgenerally,the VSOs seem to
describe theprocedure best (Figure 56-10).Thisosteotomy was initially done through
anextraoral approach but with the develop-ment ofsmall oscillating blades with
along shaft,the intraoral route has becomepreferred.IndicationsThe VSOs have most
com-monly been limited to deformities requir-ing the mandible to be set back
formandibular horizontal excess or to berotated for mandibular asymmetry.Robinson
and Lytle have stated that thisosteotomy can be used for mandibularadvancement but
generally this recom-mendation was not taken seriouslybecause ofthe question
ofstability.69Halland McKenna revived this indication forminor (2 to 3 mm)
advancements.70TechniquesWhen preparing for an intra-oral VSO,one needs to closely
evaluate thepanoramic and lateral head films for theposition ofthe inferior
alveolar foramen rel-ative to the posterior border ofthemandible.The incision is
made in themucosa from midway up the anterior bor-der ofthe ramus to the first
molar area.Theperiosteum is reflected laterally to exposethe entire ramus,with the
exception ofthecondyle neck and coronoid tip.The posteri-or and inferior borders
can be cleared ofperiosteum;muscle attachments at theangle are generally difficult
to elevate andshould be left to ensure blood supply to thisarea.A special retractor
can be placed thatfits around the posterior border and,at thesame time,retracts
tissue laterally so that anoscillating saw can be used (Figure 56-11A).The saw
chosen should have a round-ed blade that is set at an obtuse angle tothe long shaft
to facilitate the cut.Theblade should be used first to score the pro-posed
osteotomy line on the lateral cortex.This line is then closely checked for
itsposition relative to the sigmoid notch,posterior border,and angle.The use
oftheso-called antilingula has been proposed asthe landmark for the mandibular
foramen,but has generally fallen into disfavor,bothbecause ofthe difficulties with
its identifi-cation and its lack ofpredictable relationto the foramen.12,71,72The
cut should bemade no more than 5 to 7 mm anterior tothe posterior border at the
anticipatedlevel ofthe foramen,using the retractor asa guide to the posterior
border.73The cut iscarried through the medial cortex,startingin the middle ofthe
ramus.It is carriedsuperiorly to the sigmoid notch and thenfinished at the inferior
border (Figure 56-11B).As the cut is completed,antero-lateral tension is kept on
the retractor sothat the proximal fragment will bebrought out laterally.A straight
clamp canFIGURE56-10Different lengths ofthe osteotomy in the vertical subcondylar
osteotomies.Adapted from Bloomquist DS.Principles ofmandibular orthog-nathic
surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal and
maxillofacial surgery.Vol 3.Philadelphia (PA): J.B.Lippin-cott Company;
1992.p.1423.ABC
Principles ofMandibular Orthognathic Surgery1143be used to rotate the segment
laterally afterthe cut is made and then to stabilize itwhile periosteum and muscle
are strippedfrom the medial cortex down to the angle(Figure 56-11C).Again a small
attachmentis left at the angle to ensure a blood supply.This proximal fragment can
be held for-ward and laterally by a small gauze packwhile the opposite side is
being completed.Ifthe proximal fragment is lost medially,itusually can be brought
into the field withthe help ofa small periosteal elevator thatis inserted
posteromedially at the level ofthe sigmoid notch while the distal frag-ment is
being pulled forward.Themandibular dentition is brought into itsnew position after
the completion ofbothosteotomies,as established by a preformedocclusal splint and
stabilized with maxillo-mandibular fixation.Attention is directed back into
thewound and toward the placement and stabilization ofthe proximal fragment.Wire
osseous fixation is generally not need-ed,although advocated by some surgeons.Most
important is the achievement ofasbroad a bone contact as possible,withoutdisplacing
or rotating the condyle.Adjust-ment ofthe lateral cortex ofthe distal frag-ment may
be performed with a straight fis-sure or small acrylic bur to permit theproximal
fragment to lie as flat as possibleagainst the vertical ramus.Care should betaken
to ensure that the long axis oftheproximal fragment does not differ appre-ciably
from its preoperative position.Aftera thorough irrigation ofthe wound themucosa is
closed with a running stitch,using a resorbable suture.No drains orexternal
dressings are placed,and thepatient is left in fixation for 6 to 8
weeks.Postsurgical radiographs should be taken assoon as possible to confirm that
thecondyles have not been displaced.A smallamount offorward and downward
positionofthe condyle is common,and this gener-ally resolves during the period
ofmaxillo-mandibular fixation (Figure 56-12).Submentovertex radiographs havebeen
suggested to identify divergence ofthe posterior border.It has been suggestedthat
an angle smaller than 130�producessuch a significant surgical problem thatthis type
ofpatient should be avoided andanother technique used.The use ofthisradiograph as a
criterion for choosing thistechnique has been questioned,but somestill feel that it
can be pursued to identifythe more difficult cases.73,74A large number ofvariations
oftheVSO have come in the osteotomy design.Oblique versions with the cut ending
abovethe angle have been described by manyclinicians,with the only apparent
benefitbeing the relative ease in the technique.Theoretically there should also be
lesschance ofdamaging the inferior alveolarnerve,but there has been no study to
con-firm this benefit.Interestingly the oneFIGURE56-11The intraoral vertical
subcondylar osteotomy.A,Exposure.B,Vertical ramus osteotomy.C,Proximal fragment
displaced laterally.Adapted fromBloomquist DS.Principles ofmandibular orthognathic
maxillofacial surgery.Vol 3.Philadelphia (PA): J.B.Lippincott Company;
1992.p.1424.ABC
1144Part 8: Orthognathic Surgerypotential drawback,that ofdecreasedskeletal
stability,appears not to bedemonstratable.75In contrast with thisshorter cut others
have recommendedthat a larger portion ofthe inferior borderbe left with the
proximal fragment,espe-cially in the larger mandibular setbacks.70This permits a
good attachment ofthemedial pterygoid muscle to be left at themandibular
angle,which has beenclaimed to help seat the condyle in thefossa as the patient
wakens from anesthe-sia.This variation,including the use of8 weeks offixation,is
claimed to decreaseone ofthe problems ofthe intraoral VSO,specifically that
ofcondylar sag and theresulting open bite that can occur on therelease
offixation.Unfortunately no clin-ical data have been reported that back
thisclaim.The use ofosseous wire fixation hasbeen advocated to ensure the seating
ofthe condyle.Again no study comparingwire osseous fixation with no fixation
hasshown any advantage for the use ofthewire.76�78This may be explicable in
theintraoral procedures by the technical dif-ficulties ofwire
placement.However,Ritzau and colleagues showed in an excel-lent prospective study
that even from anextraoral approach,the position oftheFIGURE56-12Patient who was
treated with an intraoral VSO for mandibular horizontal excess.A�D,Preoperative
pho-tographs and radiograph.E�H,Postoperative photographs and radiograph.Reproduced
with permission from BloomquistDS.Principles ofmandibular orthognathic surgery.In:
surgery.Vol 3.Philadelphia (PA): J.B.Lippincott Company; 1992.p.1426.ABDGEFHC
Principles ofMandibular Orthognathic Surgery1145condyle in the fossa is not
improved withthe use ofwire osseous fixation.77The effect ofthe temporalis on
relapsehas led to other recommendations thatinclude either stripping the
temporalisattachment completely offthe coronoid orcutting offthe coronoid.The use
ofthis lat-ter coronoidotomy has been recommendedby some clinicians for large
setbacks,with afew using this modification routinely.Theadvantage ofthe
coronoidotomy relative toprevention ofrelapse has not been studied,but the
stability ofthe intraoral verticalsubcondylar osteotomy (IVSO) with coro-
noidotomy,compared with the sagittal splitosteotomy ofthe vertical ramus
inmandibular setbacks,has been investigatedand the IVSO seemed to be more
stable.79The use ofthe inverted Losteotomy isanother way to neutralize the
temporalis.This modification ofthe IVSO requiresstripping ofthe medial periosteum
toidentify the lingula so that a horizontalcut can be made without increasing
therisk ofdamaging the inferior alveolarnerve.A further modification oftheinverted
Losteotomy has been the use ofrigid internal fixation.Although techni-cally a
difficult surgery it permits the earlyrelease from maxillomandibular
fixation.Unfortunately there are no long-termstudies on the stability ofany
oftheinverted Ltechniques.Alternative TechniquesThe major vari-ation ofthe
described technique is the useofan extraoral approach.The soft tissueincision is
similar to that commonly usedfor an external approach to a fracture ofthe
mandibular angle,with an approxi-mately 4 cm incision made 2 cm below theangle and
the inferior border ofthemandible (Figure 56-13A).A combinationofsharp and blunt
dissection is used to getto the inferior border ofthe mandible.Care is taken to
avoid damaging the mar-ginal mandibular branch ofthe facialnerve.After incising
through the perio-steum,the bone cuts are similar to thosethat have been described
(Figure 56-13B).The external approach has been advo-cated for large mandibular
setbacks ofgreater than 10 mm,difficult asymmetries,or large vertical moves in
patients withunusual facial structure.Except for the riskofthe scar,the risks
ofthis technique havebeen reported as being comparable withthe intraoral
technique.50,80ComplicationsStabilityPostoperativechange in skeletal and dental
position fol-lowing the use ofa VSO in the treatmentofmandibular horizontal excess
hasreceived much attention.Goldstein wasthe first to use serial cephalograms to
eval-uate the postoperative change ofthemandible after surgical correction
ofthemandibular prognathism.81He noted theanterior relapse that has now been
welldocumented.Poulton and colleagues rec-ommended overcorrecting the mandibu-lar
setback by 2 mm to provide for therelapse they noted.82This amount ofaver-age
relapse has surprisingly remained fair-ly consistent throughout the history
ofthistechnique,even though technical changesin procedures have been
made.80,83Stellaand colleagues noted that the variation inFIGURE56-13The extraoral
vertical subcondylar osteotomy.Adapted from Bloomquist DS.Principles
ofmandibularorthognathic surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM.Principles oforal and maxillofacial surgery.Vol 3.Philadelphia (PA):
J.B.Lippincott Company; 1992.p.1428.AB
1146Part 8: Orthognathic Surgerythe amount ofrelapse in mandibular set-backs was
large and attempts at identifyingcontrollable variables should be made.84They
suggested that the proximal frag-ment rotation affects the short-term pogo-nion
changes,although they did not pre-sent any corroborative research.Thefinding that
the pogonion tends to moveposteroinferiorly during intermaxillaryfixation has been
well documented.52Thismovement,later followed by the anterosu-perior �relapse�that
occurs after skeletalfixation wires,does seem to stabilize theinitial movement but
does not affect thelong-term relapse.50,51,56Vertical instability ofthe VSO
developssoon after the release ofintermaxillary fixa-tion in many patients.This
problem was ini-tially attributed to the �condylar sag�seenon x-ray films taken
soon after surgery.73Although condylar sag may be one cause ofrelapse,a major
contributor seems to beinsufficient time offixation.The VSO isgenerally not
considered an appropriatesurgery for correction ofanterior open bite.In
Scandinavian countries,however,thissurgical procedure has been successfullyused for
patients with mandibular horizon-tal excess and anterior open bite.85Neural
DamageThe chance ofdamag-ing the marginal mandibular branch ofthe facial nerve is
one ofthe reasons givenby several surgeons for avoiding the extra-oral approach to
the VSO.This concern,however,seems to be unsubstantiated,inthat almost all ofthe
clinicians reportingon the results ofthis approach have notedvery
little,ifany,motor nerve damage.Damage to the inferior alveolar nerve,however,is a
concern in using a VSO.Theincidence oftrauma to the inferior alveo-lar nerve at the
time ofsurgery has beenreported to vary from being �rare�tooccurring 36% ofthe
time.70Long-termsensory defects have also been reported tovary from none to
35%.45,86These appar-ent discrepancies can be explained by thedifferences in the
sensitivity ofthe mea-surement techniques;in addition there is awide variation in
the time after surgeryduring which the patients were tested.Other variables,such as
whether theosteotomy was approached intraorally orextraorally as well as variations
in thelength ofthe cut,theoretically could affectthe incidence ofsensory
problems,butcomparison studies have not been done.From studies that have been done
the inci-dence ofdamage to the inferior alveolarnerve is low with the VSO compared
withthe sagittal osteotomy.86,87The patient,however,should be warned that short-
term sensory loss is a definite risk,andpermanent neuropathy is
possible.Temporomandibular Joint DysfunctionThere has been interesting literature
pub-lished on changes in tempromandibularjoint function after a VSO.These
haveincluded a number ofradiographic stud-ies documenting positional change
ofthecondyle relative to the fossa.Radiograph-ically there is an initial downward
andforward movement ofthe condyle,with asubsequent tendency to return to its pre-
operative position.77,78,82Sometimes adouble contour ofthe condyle
appearsapproximately 6 months postoperatively,which has been attributed to
thecondyle�s remodeling after the surgery.88Remodeling ofthe glenoid fossa has
alsobeen documented.78In one early review of100 cases 6 patients were reported to
have temporo-mandibular joint problems at 1 year aftersurgery.89A form ofthe VSO
has beenused to treat patients with temporo-mandibular pain and
dysfunction.Itappears that the VSO does not put thetemporomandibular joint at any
signifi-cant risk,and it may in fact be salutary forpatients with temporomandibular
jointdysfunction.90�92Other ComplicationsAmong the otherreported complications
ofthe VSO,vas-cular necrosis ofthe proximal segmentseems to be the most potentially
devastat-ing.The maintenance ofsome muscleattachment to the angles makes this
possi-bility unlikely.InvertedL andC RamusOsteotomiesOsteotomy designs in the
vertical ramusthat include both the condyle and coro-noid in the same segment have
variedfrom Blair�s simple horizontal osteotomyto the modified Costeotomy
ofHayes.The horizontal osteotomy ofthe verticalramus has generally fallen into
disusebecause ofthe substantial relapse poten-tial,but many ofthe remaining
suggestedvariations continue to have treatmentvalue.The two procedures that seem to
bethe most popular are the inverted Landthe Costeotomites.Both are
generallyapproached extraorally,although intraoralvariants are possible.93Clinical
studies ofeither technique are rare,but those thatexist seem to demonstrate
reasonable suc-cess in correcting skeletal deformities withminimal
complications.IndicationsThe Costeotomy is generallyreserved for treatment
ofhorizontalmandibular deficiencies,with some authorssuggesting that it can be used
to close ante-rior open bite.The inverted L,however,hasbeen used for the correction
ofmost kindsofmandibular horizontal discrepancies,including anterior open
bite.Generallyadvancements ofthe distal segment witheither technique require bone
grafting toensure adequate bone union.TechniquesThe basic techniques for
anextraoral approach to do a Cand invertedLare the same,with the only
modificationbeing the inferior horizontal cut in the Costeotomy.For that reason the
inverted Lwill be described first,with various modi-fications ofthe Cdiscussed
later.Thepatient is prepared and draped,such thataccess to both the mouth and the
sub-mandibular incision area can occur with-
Principles ofMandibular Orthognathic Surgery1147out contamination ofthe skin wound
byoral organisms.This can be accomplishedin a variety ofways,but most surgeons usea
plastic drape with adhesive on one edgeto separate the two areas.The externaldrapes
should be arranged so that theyallow turning ofthe head for access to
thesubmandibular wounds as well as access tothe mouth.The submandibular incision is
made 2 cm below the angle and inferior borderofthe mandible.The posterior portion
iscurved superiorly to follow the cervicalskin line as well as to improve the
access tothe entire vertical ramus.Generally theincision is approximately 6 cm in
length.Sharp dissection is used down throughthe platysma,and then blunt dissection
isbegun to minimize risk to the marginalmandibular branch ofthe facial nerve.The
incision through the pterygo-mandibular sling and periosteum is madealong the
inferior border and is carriedaround the angle and up the posteriorborder about 2
cm.Periosteum andattachments for the masseter are com-pletely stripped offthe
lateral cortex ofthe vertical ramus up to the level ofthesigmoid notch.Very little
periosteum isstripped offthe medial side,especially atthe angle,to retain as much
blood supplyas possible to the proximal fragment.Theposterior vertical osteotomy is
made atleast 7 mm in front ofthe posterior bor-der and extends to a point ofthe
inferiorborder just in front ofthe angle.The hor-izontal cut is made above the
anticipatedposition ofthe inferior alveolar foramen(Figure 56-14A).As mentioned
abovewith the VSO it is wise to have a goodradiographic view ofthe ramus so that
theposition ofthis foramen can be moreaccurately located.The study by Reitzikand
colleagues ofthe position ofthe fora-men relative to the lateral landmarks
ishelpful to review to lessen trauma to theneurovascular bundle.72Once the cuts are
made the medialperiosteum may have to be elevated fromsome ofthe distal fragment to
allow itsadvancement.Moist gauze is placed in thewound,and a similar procedure is
done onthe opposite side.After completion ofthesecond side,drapes are pulled back
andshifted such that the oral cavity can beentered to place the mandibular teeth
intothe new occlusal position and secured withmaxillomandibular dental
fixation.Thesurgeons who are involved in the intraoralfixation should change gloves
and surgicalgowns before the drapes are replaced sothat the skin incisions can
again beapproached.The next step varies depend-ing on the type ofmandibular
movementthat occurred;however,the importance ofmaintaining the proximal fragment
closeto its preoperative position remains.Ifthedistal segment is set back,then the
proxi-mal segment has to be overlapped laterally(Figure 56-14B).As described with
theVSO some adjustments ofthe lateral cortexofthe distal segment may be necessary
topermit passive position ofthe proximalfragment as well as to provide a good
areaofbone contact.The use ofsome form ofABFIGURE56-14The extraoral inverted
Losteotomy.Adapted from Bloomquist DS.Principles ofmandibular orthognathic
maxillofacial surgery.Vol 3.Philadelphia (PA): J.B.Lippincott Company; 1992.p.1430.
1148Part 8: Orthognathic Surgeryfixation is generally recommended,although the use
ofno interosseous fixa-tion has been suggested.93The type ofosseous fixation varies
widely;however,rigid internal fixation with metal plates ormesh secured with screws
has becomemore popular (Figure 56-15).93After irri-gation the wound is closed in
layers bywhatever suturing method and materialFIGURE56-15Patient who was treated
with an extraoral inverted Losteotomy (for mandibular horizontal
deficiency).A�D,Preoperative photographs and radi-ograph.E�I,Postoperative
photographs and radiograph.Reproduced with permission from Bloomquist DS.Principles
ofmandibular orthognathic surgery.In: Peter-son LJ,Indresano AT,Marciani RD,Roser
J.B.Lippincott Company; 1992.p.1432�3.ABCEFHIGD
Principles ofMandibular Orthognathic Surgery1149the surgeon prefers.Care should be
takento ensure hemostasis as the wound isclosed.Ifthere is any concern
abouthematoma formation a small drain shouldbe placed.External pressure dressings
aremaintained for 24 to 48 hours.When thebone has been stabilized with wire
fixation,maxillomandibular fixation is kept in placefor at least 6 weeks and
preferably 8 weeks.Alternative TechniquesThe most com-monly used variation ofthe
previouslymentioned technique is the Costeotomy.This technique was first described
jointlyby Caldwell and colleagues in an articlereviewing their experiences with
what theycalled a vertical Losteotomy.18Theydescribed a variation oftheir basic
verticalLwith the addition ofa horizontal cut thatextended forward from the
vertical cutbelow the inferior alveolar canal (Figure56-16A).This permitted a
larger amountofbone contact when the mandible wasadvanced.They also realized the
problemscaused by advancing the coronoid processand recommended either cutting the
coro-noid loose (coronoidotomy) or includingit with the proximal segment (Costeo-
tomy).Arcing the inferior cut was suggest-ed to permit increased bone contact as
thedistal segment was advanced (Figure 56-16B).95Unfortunately the proposed
arccannot always be made since the positionofthe neurovascular bundle may
interfere.Sagittal splitting ofthe inferior limb oftheCosteotomy was proposed both
toincrease the bone contact area when themandible was advanced and to decreasethe
problem of�notching�ofthe inferiorborder (Figure 56-16C).19This latter prob-
lem,which is noticeable in some patients,is caused by the defect along the
inferiorborder resulting from the advanced distalsegment ofthe mandible.A further
varia-tion used to improve bone healingincludes a bone graft taken from the later-
al cortex ofthe distal segment and trans-ferred back into the gap ofthe
midramusarea (Figure 56-16D).The coronoidprocess has also been recommended as afree
graft in to this defect.20A further major modification ofthedescribed techniques is
the use ofrigidinternal fixation.94,96,97The use ofvitaliummesh with two screws in
each fragmenthas been demonstrated as being effective,but any rigid plate with
screws can be usedto permit the early release ofmaxillo-mandibular dental
fixation.ComplicationsThe skeletal stability ofthe inverted Land its
modifications,unlike the VSO,seems to be technique-sensitive to the type offixation
used.Likestability studies for almost all aspects oforthognathic surgery,controlled
clinicalstudies are nonexistent,and the compari-son oftechniques by a single
institution,ifreported,lacks sufficient numbers ofpatients to make valid
conclusions.Farrelland Kent looked at inverted Land Costeotomies and reported
skeletal relapsesimilar to what had been reported for theBSSO.93However,because
there were dif-ferent criteria for the use ofthese twoFIGURE56-16Different forms
ofthe Costeotomy.Adapted from Bloomquist DS.Principles ofmandibular orthognathic
surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principlesoforal and
1992.p.1434.ABCD
1150Part 8: Orthognathic Surgerytypes ofosteotomies,comparisonsbetween them are
questionable.Greebeand Tuinzing compared the stability ofmandibular advancement by
way ofaninverted Lor a BSSO.98With only a fewpatients they did not show any
differencebetween the groups,but they did claimthat skeletal relapse was dependent
on theratio ofposterior facial height to anteriorfacial height.The largest studies
ofthe sta-bility ofthe inverted Lincluded the use ofrigid internal fixation in
patients who hadthe mandible advanced.These seem todemonstrate that the use ofrigid
fixationfor this type ofprocedure is more stablethan simple maxillomandibular fixa-
tion.96,97However,statements relative tostability ofmandibular setbacks or the clo-
sure ofopen bites cannot be made,although a few authors seem to advocatethese
skeletal deformities as indicationsfor the use ofthe inverted Losteotomy.96,99The
incidence offacial nerve damagehas not been mentioned in any review ofthese
techniques,although it can beinferred to be quite low,given the reportsfor the
external approach to the VSO.Theincidence ofdamage to the inferior alveo-lar nerve
should be higher than the extra-oral VSO because ofthe horizontal por-tions ofthe
osteotomy,but Reitzik andcolleagues reported only a 6% incidence ofpermanent
anesthesia with inverted Losteotomies.96The incidence ofunsightlyscars,which many
clinicians claim detersthem from using this approach,isunknown with this group
ofosteotomies.Bilateral Sagittal Split Osteotomy ofthe Vertical RamusThe BSSO ofthe
vertical ramus has in arelatively short time become the predomi-nant orthognathic
procedure ofthemandible.Schuchardt is generally givencredit for the use ofan
intraoral approachto what some call the �step�osteotomy ofthe vertical
ramus.23Specifically hedescribed parallel horizontal cuts throughthe cortex ofthe
vertical ramus,the medialcut being placed above the lingula and alateral cut being
made about 1 cm belowthat.A split was then made between thesetwo cortices,and the
distal segment couldthen be advanced or set back.Lane evi-dently described a very
similar procedureearlier,but it probably was done extraoral-ly (see Figure 56-
4).22The singular creditfor improving on this osteotomy,as well asbeing its
strongest advocate,belongs toObwegeser,who together with Trauner in1955 described a
sagittal split ofthe verti-cal ramus.21This intraoral techniqueincluded the medial
horizontal cut abovethe lingula,but the lateral horizontal cutwas lower than
Schuchardt�s and extendedto a point just above the angle,at least 25 mm below the
lingual cortical cut (Fig-ure 56-17A).A wide-splitting osteotomewas then used to
obtain a split between thecortices,with care taken to preserve theinferior alveolar
nerve and vascular bun-dle.This procedure was later slightly mod-ified by Obwegeser
by angling the lateralcut more toward the inferior border ofthemandible (Figure 56-
17B).The majormodifications still in use today were sug-gested by DalPont.24The
change common-ly attributed to DalPont is the vertical cutthrough the lateral
cortex behind the sec-ond molar.But he also suggested the use ofa medial cut that
extends just past the lin-gula so that the posterior split would occurin the
mylohyoid groove instead ofback atthe inferior border.Multiple other modifi-cations
have been suggested,but surpris-ingly the present-day osteotomy remainsvery similar
to that initially described byObwegeser and DalPont.IndicationsThe BSSO has been
advocat-ed for almost every possible move thatincludes the entire horizontal ramus
ofthemandible.TechniqueThis osteotomy has had mul-tiple variations suggested,as
would beexpected for such a popular procedure,but many ofthem are based on a
surgeon�sindividual preference,and their effect onthe outcome ofthe osteotomy is
question-able.Therefore,only the basic proceduresto be followed will be outlined,as
well asthe significant modifications that havebeen shown to affect the outcome or
seemto have a good theoretical basis.The incision is started on the anteriorportion
ofthe vertical ramus,midwaybetween the occlusal planes.It is carrieddownward
through the middle ofthe retro-molar fossa to a point about 5 mm behindthe second
(or in some cases third) molar.FIGURE56-17Obwegeser�s osteotomies ofthe
ramus.A,Original cortical cuts.B,Later lateral cortexcuts.Adapted from Bloomquist
DS.Principles ofmandibular orthognathic surgery.In: Peterson LJ,Indresano
AT,Marciani RD,Roser SM.Principles oforal and maxillofacial surgery.Vol 3.Philadel-
phia (PA): J.B.Lippincott Company; 1992.p.1435.AB
Principles ofMandibular Orthognathic Surgery1151Then the incisions wind laterally
and for-ward to a point distal ofthe first molar (Fig-ure 56-18A).The incision
should be keptlateral enough to allow easy closure ofthewound with the teeth in
fixation.Theperiosteum is reflected to expose the lateralcortex to the mandible
down to the inferiorborder.The exposure should be limited pos-teriorly to maximize
the blood supply to theproximal fragment;this usually means theexposure ends at
about the antegonialnotch.A lateral channel retractor can beplaced at this time to
assist in retraction asthe periosteum is elevated from the retro-molar area up the
anterior border ofthevertical ramus.Special periosteal strippershave been developed
to assist this portion ofthe surgery.The attachment ofthe tempo-ralis muscle can be
tenacious,but it has tobe removed to at least the level ofthe sig-moid notch to
ensure adequate access forthe medial cut.Most times this means strip-ping about a
centimeter ofthe temporalisattachment offthe anterior border ofthecoronoid.The
periosteum is then elevatedfrom the medial surface ofthe verticalramus,starting at
about the level ofthe sig-moid notch and extending back to themedial flare at the
start ofthe condylar neck.Inferiorly the medial cortex is exposed tothe
lingula,with care being used to mini-mize trauma to the inferior alveolar nerve
asit exits behind and below this point.Theperiosteal elevation can be
extendedinferoanteriorly along the internal obliqueline to the distal ofthe second
molar toallow better exposure ofthe osteotomy site.A variety ofretractors are
available for theprotection ofthe medial soft tissue andnerve,but it is wise to
choose one that per-mits as much visualization as possible whileat the same time
protecting the soft tissue(Figure 56-18B).Excessive medial retractionshould not be
done in order to minimizeneural damage.It should be noted that noattempt is made to
carry the exposure to theposterior border ofthe vertical ramus.The osteotomy is
started by making ahorizontal bone cut through the medialcortex ofthe vertical
ramus that extendsfrom a point just posterior to and abovethe lingula to the
anterior border.Anteri-orly the cut is made about halfwaythrough the ramus,but in
the concavityabove and behind the lingula it should beshallow to allow the
posterior medial splitto initiate in the mylohyoid groove (Figure56-18C).Sometimes
it is helpful to use alarge round or acrylic bur to remove bonefrom the internal
oblique ridge so that thedepth ofthis concavity can be visualized.Occasionally at
the level ofthis horizontalcut there is no significant cancellous boneto delineate
the cortices.Here the use ofahalfthickness ofthe ramus is the mostpractical
guideline for judging the depthofthis cut.The vertical cut through the buccalcortex
is generally made just distal to thesecond molar and extends from the inferi-or
border superiorly to the externaloblique ridge.Sometimes the mandible isthin and
the external oblique ridge ends atthe distal buccal aspect ofthe secondmolar.In
this case the superior aspect ofthe vertical cut should be posterolateralenough so
that the roots ofthe secondmolar are not placed at risk.The cutshould be as close
to perpendicular to theinferior border as possible and extendedjust into cancellous
bone.Caution must beused such that the cut is not taken anydeeper because the
inferior alveolar nervecan be just medial to the cortex.The vertical and horizontal
corticalcuts are connected,starting superiorly atthe anterior border ofvertical
ramus andcontinuing down just inside the externaloblique ridge to the vertical cut
(Figure56-18D).Again the cut is made into can-cellous bone,when at all
possible,with thesuperior part ofthis connection being asdeep as
possible,especially ifthere is nocancellous bone present.This will mini-mize the
chance ofan inadvertent fractureofthe medial cortex.Difficulty is encoun-tered
often ifa third molar is present andhas been scheduled to be removed at thetime
ofsurgery.It is generally wise to planfor the mandibular third molars to beremoved
well in advance ofthe sagittalosteotomy since they can make the surgerymore
difficult.Experienced surgeons canremove the tooth and obtain a successfulsplit,but
almost all try to avoid this situa-tion because it may increase the risk
ofanunplanned buccal or lingual cortical platefracture and can make rigid fixation
withthe use ofscrews more difficult.Techniques vary widely in how thesplit is
accomplished.The method to bedescribed is an attempt to be as universalas
possible.First,steps are taken to ensurethat the limits ofthe split occur as
definedby the horizontal and vertical bone cuts.Anarrow (4 mm) thin osteotome is
drivenalong the horizontal cut and directed sothat it cuts through the medial
cortexabove and behind the lingula.It is alsoused to ensure that the split at the
base ofthe vertical cut is started through the mid-point ofthe inferior border.Many
sur-geons also use this type ofthin osteotometo �step�along the connecting cut to
helpensure that the split stays close to the lat-eral bone cortex.Traditionally
wide-wedging osteotomes have been used toslowly complete the split.More oftentoday
a special spreading instrument isused along with a smaller osteotome toallow more
control ofthe split.Generallythe movement is initiated along the verti-cal cut and
carefully extended posteriorly.The fine osteotome can be used to keepthe split
close to the lateral cortex.Ifthenerve is encountered it is carefully sepa-rated
from the proximal fragment.Thesplit along the inferior border can be dif-ficult to
control,and the judicious use ofathin osteotome will assist in this area.Finally as
the posterior split through themedial cortex is made care should be usedto prevent
the split from continuingbehind the mylohyoid fossa and startingup the neck ofthe
condyle.The speed ofthe split often varies,depending on theelasticity ofthe bone.In
older patients,in
1152Part 8: Orthognathic Surgerywhom the bone is not as elastic,the splitcan occur
very suddenly.Preventing inap-propriate fractures is dependent on thecare used not
only in making the corticalbone cuts but also in ensuring that thesplits occur as
planned at the posterioraspect ofthe horizontal cut and along theinferior
border.Periosteum ofthe muscle attachmentofthe medial pterygoid is stripped
offtheproximal fragment to permit freedom ofmovement between the two
fragments.Ifthe mandibular teeth are scheduled to bemoved posteriorly,either on one
side whencorrecting an asymmetry or bilaterally forcorrection ofhorizontal
mandibularexcess,an appropriate amount ofbone isremoved at this time from the
anterioredge ofthe proximal fragment.Theamount ofremoval can be based on
modelsurgery or on the prediction tracings.Onlarge setbacks,bone will need to be
removedfrom the anterior edge ofthe vertical ramusto prevent this area from
interfering withFIGURE56-18The bilateral sagittal split osteotomy.A,Incision.B
andC,Medial exposure and horizontal cut.D,Vertical cut.E,Bone removeal for
setback.F,Bone removal for large adjustments.Adapted from Bloomquist DS.Principles
ofmandibular orthognathic surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser
J.B.Lippincott Company; 1992.p.1436�7.ABCDEF
Principles ofMandibular Orthognathic Surgery1153the patient�s ability to clean the
mandibularsecond molars (Figure 56-18E).Converselyin large advancements,bone
sometimeshas to be removed from the remaining por-tion ofthe anterior border ofthe
verticalramus ofthe distal segment just anterior tothe lingula,to prevent
encroachment ofthesegment against the tuberosity (Figure 56-18F).After the opposite
side is split themandible is moved into its new positionand stabilized by
maxillomandibular fixa-tion.It is preferable that an occlusal splintbe used to
ensure accurate position ofthemandible relative to the maxilla,based onthe
presurgical model surgery.It is rare thatteeth occlude well enough that a splint
isnot needed.The placement ofosseous fixation ismade at this point.As multiple
techniquesare possible,different options will bedescribed in the following section
�Alterna-tive Techniques.�After placement ofosseousfixation,ifrigid fixation is
used,the maxil-lomandibular fixation is released,allowingthe occlusion to be
checked.The woundsare thoroughly irrigated and closed with theuse ofa resorbable
running suture.Nodrains or external dressings are generallynecessary (Figure 56-
19).Alternative TechniquesThere are manyvariations to the foregoing
technique.Inthis section only the major ones will bediscussed.The design ofthe
osteotomyitselfis an area that has received muchattention,with each ofthese
variationsgenerally representing an attempt todecrease the incidence ofone or
morecomplications.There is very little support-ive research for any ofthe
modifications.Obwegeser was responsible for two varia-tions,the first being his
original design,inwhich the buccal cut was horizontal andparallel to the lingual
cut through the cor-tex ofthe vertical ramus (see Figure 56-17A).This original
technique wasmodified by making the lateral cortical cutat an angle to the medial
cut so that theposterior portion ofthe osteotomy endedjust above the angle (see
Figure 56-17B).100A popular modification ofDalPont�svertical osteotomy is the
continuation ofthis cut completely through the inferiorborder,which,according to
its advocates,made the split easier.59This technique,however,makes the use ofrigid
fixationwith screws difficult.101A few modifica-tions have been suggested for the
connect-ing cut,with the primary goal ofallowingbetter control ofthe proximal
fragment.These modifications appear to be primar-ily personal preferences as there
is no evi-dence that these changes improve the suc-cess ofthe procedure.A major
area ofvariation for the sagit-tal split osteotomy ofthe vertical ramusoccurs in
the use,or nonuse,ofosseous fix-ation.21,25,102,103The original Obwegesertechnique
used wire through the superiorlateral and medial cortices.104This tech-nique,with
minor variation,became thestandard for the sagittal osteotomy untilscrew fixation
became popular.59The use ofcircumandibular wire and inferior borderwires have also
been suggested as possiblybetter ways ofcontrolling the proximalfragment.105No
evidence exists that any ofthese wire techniques have an advantage forminimizing
complications.26Spiessl introduced the concept ofusingscrews for the �rigid
internal fixation�ofthesagittal osteotomy.26Following its introduc-tion in 1974
there was a slow acceptance ofthis method ofosseous fixation.Currentlythere is
little debate on the advantages ofusing rigid internal fixation.However,thereexists
a wide variety ofmethods and materi-als used.Initially the use ofthree 2.7
mmABCEDFIGURE56-19Patient who was treated with bilateral sagittal split osteotomies
(for mandibular horizontal deficiency).A�E,Preoperative photographs and
headradiograph.(CONTINUEDONNEXTPAGE)
1154Part 8: Orthognathic Surgery�lag�screws on each side was advocated.Alag screw
is placed by drilling a �guiding�hole with a larger drill through the
lateralcortex,followed by a smaller hole throughthe medial cortex that is threaded
with theuse ofa tap.Lag screws are then used to fixthe proximal fragment tightly to
the distalfragment.Compression across the osteo-tomy site is felt to be important
to speed thehealing ofthe osteotomy as well as to ensurethe stability ofthe
mandible.Concern existsthat compression may cause increased nervedamage and
displacement ofthe condyles,with subsequent temporomandibular
jointdysfunction.106,107An alternative technique,the position screw or bicortical
screw,inwhich both cortices are tapped,has beenadvocated for stabilizing osteotomy
seg-ments.100This technique permits mainte-nance ofthe gaps that may occur
betweenthe proximal and distal fragments,with noeffort being made to compress the
two seg-ments together.Standardization oftech-niques does not exist in rigid
fixation ofthesagittal osteotomy as there are differences inscrew sizes,number
ofscrews,materialsused,and whether plates are used across theosteotomy sites.Most
ofthe research in theUnited States has centered on the use ofthree screws that are
2 mm in diameter.Direct comparisons ofdiffering rigid fixa-tion techniques are rare
and do not demon-strate that any one technique is an advan-tage.108�110One
exception was noted byFujioka and colleagues,who found thatthere was more rotation
through theosteotomy sites in patients with mono-cortical plate and screw
fixation.111The use ofresorbable screws has beena recent addition to fixation
techniques.First attempted in Finland,the screws aremade from polyglycolic acid
using differ-ent manufacturing techniques and formu-las.Development ofthese self-
reinforcedpolylactic/polyglycolic polymers that havereliable strength to withstand
forces ofmastication have made their use possible inorthognathic surgery.The
obvious advan-tage ofresorbable fixation is to obviate theneed for future hardware
removal,whichhas become important with patient con-cerns over the potential risks
ofany kind ofpermanent implants.The key features thatare crucial in its application
in orthognathicsurgery are the material�s rigidity andstrength with an ability to
resorb in a time-ly fashion.A few small studies have shownFIGURE56-19
(CONTINUED)F,Pre-surgery head radiograph.G�L,Postop-erative photographs and
radiographs.(Courtesy ofDr.S.Lake.)GHIJKFL
Principles ofMandibular Orthognathic Surgery1155apparent stability ofthese
resorbableimplants comparable to the metallic fixa-tion;however,some inherent
problemswith material handling and early fixationfailures have been
reported.112�114Suuro-nen and colleagues reported on the use ofpoly-L-lactic acid
(PLLA) screws for fixa-tion in BSSO,with no apparent malocclu-sion or skeletal
relapse.112Harada andEnomoto and later Ferretti and Reynekecompared titanium and
resorbable screwsand noted no difference in healing betweentwo groups and no
statistically significantdifference in skeletal relapse.113,114Howev-er,Harada and
Enomoto�s patients wereplaced in maxillomandibular fixation for aperiod ranging
from 9 to 14 days followingsurgery.112Kallela and colleagues used self-reinforced
PLLA (SR-PLLA) screws formandibular osteotomies and no maxillo-mandibular fixation
was used postopera-tively.115Mean advancement was 4.57 mm at B point,and the mean
relapsewas 17%.In their 2-year follow-up study in1999,the authors reported
osteolyticchanges seen around the resorbable screwsin 27% ofcases,and the screw
canalsremained as radiolucent shadows withoutbony filling.Turvey and colleagues
report-ed their experience with resorbable fixa-tion for 194 osteotomies ofthe
maxillaand/or mandible.116Forty-three ofthepatients had a sagittal osteotomy with 2
mm screws placed on each side for fixa-tion.They reported only one infection at
asagittal osteotomy site and one patient whoexhibited abnormal masticatory
pressuresthat resulted in loosening ofthe fixation.Acceptance ofthe routine use
ofresorbablefixation with the sagittal split is going torequire long-term
evaluations with well-designed studies comparing these materi-als to the metal
hardware.The majorpotential risk ofpermanent metal fixationis the possibility
ofbone remodeling,caus-ing the hardware to become noticeable andpossibly irritating
to the patient.Althoughnot reported in the literature oral andmaxillofacial
surgeons have had experiencewith patients returning to have plates andscrews
removed simply because theseimplants have become noticeable.Thisproblem has to be
weighed against the stillunexplored or unknown side effects oftheresorbable
materials.A good example ofthese unknowns is the precise time neededfor total
resorption and degradation ofPLLA in human tissues,which is reportedto range
anywhere from 90 days to 5 years.Surgeons are going to have to closely followthe
literature to determine the practicalityofthese new materials.An interesting
suggested modificationin the BSSO technique is the purposefulchanging ofthe
rotational position oftheproximal fragment to control the directionofmandibular
growth.It has generallybeen recommended that the proximal seg-ment be maintained as
close as possible toits preoperative position.O�Ryan andEpker have further
suggested that rotatingthe proximal fragment in a growingpatient can change the
vector ofcondylargrowth and,thereby,influence the finalmandibular
position.117Studies have failedto support this contention.118Also there isconcern
in using a sagittal osteotomy ingrowing children,especially those requir-ing long
advancement.Huang and Rossdemonstrated what they felt to be a stop-page in
mandibular growth and condylarresorption in growing patients in whomsagittal
osteotomies were performed.119Whether this was a problem ofthe tech-niques used or
a problem with performingsurgery in such a young group ofpatientsis unknown,but
this effect has not beennoted in any further literature.A final modification ofthe
BSSO is theconcomitant use ofa midsymphysealosteotomy to allow for correction
ofwidthdiscrepancies in the dental arch.Althoughthis procedure could be used with
any oftheramal osteotomies,it has only beendescribed with the sagittal
osteotomies.Firstmentioned by Bell,it has become morepractical with the use ofrigid
internal fixa-tion.120A single four-hole plate across thebone cut,along with an
intact orthodonticarch wire,provides sufficient stability.121Concerns ofadverse
effects on the temporo-mandibular joint and the periodontiumwere also shown to be
insignificant.122ComplicationsStabilityThe stabilityofthe sagittal osteotomy ofthe
verticalramus is the most studied complication inorthognathic surgery.Since the
relapsepatterns differ between mandibularadvancements and setbacks,their particu-
lar causes most likely differ;however,many ofthe principles in preventingrelapse
may be the same.Whereas much ofthe research on mandibular advancementhas been done
in the United States,mandibular prognathism has generallyreceived the greatest
interest in the Scandi-navian countries and the Far East.Thishighlights one ofthe
major problems forsurgeons attempting to decide on whichtechniques to use to
minimize postopera-tive skeletal change.There are large varia-tions in research
techniques as well as sur-gical approaches that exist not onlybetween surgical
centers in different coun-tries but also within the same country.Fortunately there
is enough corroborationin the literature that some general state-ments can be
made.One ofthe most important findingsmade in the stability ofmandibularosteotomies
was that intermaxillary fixa-tion does not prevent postoperative skele-tal
change.Although this is true ofanytype ofmandibular osteotomy,it was
firstrecognized in the evaluation ofmandibu-lar sagittal osteotomies.It is
generally feltthat soft tissue pressures and muscle pullare the major factors
influencing relapse,especially in mandibular advance-ment.52,53,122However,early
attempts atminimizing these effects,such as suprahy-oid myotomies and external
supportivedevices,have not been shown to be effec-tive.64Internal support
techniques,howev-er,have been shown to be effective.Beforerigid fixation screws and
plates were used,
1156Part 8: Orthognathic Surgerya type ofinternal support called skeletalfixation
was shown to be effective indecreasing the down and back relapse pat-tern
ofmandibular advancements.64Thisfixation was usually used in addition
tomaxillomandibular fixation and consistsofwires running from the piriform rim
tocircumandibular wires placed in the cus-pid or molar areas (see Figure 56-
9).Inter-estingly,Van Sickles noted a decrease inrelapse in patients with large
advance-ments when skeletal fixation was com-bined with rigid internal screw
fixation.123Other possible causes ofrelapse thathave been implicated are patient�s
age,pre-operative mandibular plane steepness,rota-tional position ofthe proximal
fragment,amount ofdistal segment advancement,and the displacement ofcondyle from
thefossa.The effect ofmandibular plane steep-ness is somewhat controversial because
ofvariable results reported in the literature,most ofwhich looked at patients who
hadwire osseous fixation with intermaxillaryfixation.Mobarak and colleagues did
clear-ly find decreased stability in patients withsteep mandibular plane angles
when rigidinternal fixation was used.124Oftheremaining variables only the last
twoappear to be definitively supported by clin-ical studies as being important.In
theirmulticenter study,Schendel and Epkerfound that displacement ofthe condylefrom
the fossa was a significant predictor ofrelapse.64This was further confirmed byLake
and colleagues,who also showed therelation between the amount ofadvance-ment and
the amount ofrelapse.55The final area that has been consid-ered as possibly
affecting relapse in bothmandibular advancement and setback isthe rigidity ofthe
fixation across theosteotomy site.Early investigators felt thatfixation across the
osteotomy site may hin-der the normal repositioning ofthecondyle in the fossa that
occurs duringmaxillomandibular fixation.103Later stud-ies showed that wire
osteosynthesis wassuperior to no osseous fixation in frag-ment position,and the
incidence ofrelapse was less.102However,the search fora superior osseous wiring
technique thatwould decrease relapse has not been suc-cessful,with most studies
that looked atosseous wiring techniques being very con-sistent in finding a mean
relapse ofapproximately 30%.The large range ofindividual relapses that does exist
has ledmany surgeons to believe that there aremultiple factors that influence
relapse.The use ofrigid internal fixation tech-niques has become the preferred
methodfor minimizing skeletal relapse in theBSSO.Spiessl together with Schmoker
andcolleagues first discussed the advantages oflag screws in mandibular sagittal
splitosteotomies.Their initial study ofskeletalstability looked at mandibular
setbacks,comparing the use ofthree 2.7 mm screwsagainst wire fixation and one or
twoscrews.125It was not until 1985 that VanSickels and Flanary showed evidence that
asimilar rigid fixation technique providedincreased stability in mandibular
advance-ments.126Furthermore larger and longerstudies have clearly shown the
stability ofusing three bicortical screws for fixation ofthe sagittal
osteotomy.127�130These studieshave reported a mean relapse rate ofbetween 0 and
8%.The majority ofstudiescomparing rigid internal fixation tech-niques against the
use ofwire osseous fixa-tion have also confirmed a significant dif-ference in
stability between thetechniques.131�135Interestingly the onlyclinical study that
evaluated the stability ofosseous wire fixation versus rigid screw fix-ation on
patients treated at the same centerseemed to show a comparable long-
termstability.136This study,however,reportedan unusually high stability ofthe
wireosseous fixation group and did nothing todispute the stability ofthe screw
fixation.The number ofscrews may very well influ-ence the stability,although only
Spiessl�soriginal study demonstrated a difference.Another common method for
rigidinternal fixation ofthe BSSO is the use ofminiplates with monocortical
screws.Generally 2 mm systems are used with twoscrews placed on either side ofthe
osteoto-my.137�140Questions remain over the min-imum number ofscrews necessary to
pre-vent relapse and whether more or largerscrews will improve stability in
longeradvancements.It has been shown that asingle 2 mm screw does not seem
toincrease mandibular stability over wireosseous fixation,and thus it could
beargued,in light ofthe previously reviewedresearch,that an increase in number
orsize ofscrews can result in more osseousstability.130,141Nerve DamageThe
possibility ofdamageto the inferior alveolar nerve during thesagittal osteotomy has
been well knownsince the technique was first described,butsurprisingly the problem
was minimized byearly surgeons.Kole first mentioned a highincidence ofsensory
problems immediatelyafter surgery for patients with sagittalosteotomies,but most
clinicians claimed avery low incidence oflong-term prob-lems.142,143Walter and
Gregg,during anobjective study ofsensory problems,noteda large incidence oflong-
term problems.45Since this first definitive study there hascontinued to be a
variety ofreportedinstances ofboth immediate postsurgical aswell as chronic sensory
disturbances.Westermark and colleagues evaluated496 sagittal osteotomies for
possible corre-lations between neurosensory dysfunctionand other variables,such as
the age ofthepatient,mandibular movement,type ofsplit technique and fixation,degree
ofintraoperative nerve encounter,and surgi-cal skill.144Nerve dysfunction developed
in40% ofthe cases.The patient�s age had asignificant influence on the recovery
oftheneurosensory function as well as the sever-ity ofneurosensory
disturbance.Intra-operative nerve encounter and nervemanipulation as well as
surgical experi-ence were also reported to have an effecton nerve dysfunction.Other
variables had
Principles ofMandibular Orthognathic Surgery1157no significant effects on the
incidence ofneurosensory dysfunction.Ylikontiola andcolleagues also found a
statistically signifi-cant positive correlation between subjec-tive neurosensory
loss and the patient�s ageand,in addition,magnitude ofmandibu-lar movement and
degree ofmanipulationofthe nerve.145A number ofother clinical researchershave noted
a significant relation betweenthe patient�s age and nerve recovery.Thisfinding was
noted early on by MacIntosh,who emphasized that he does not use thisosteotomy for
patients over age 40 years.146The only other interesting correlation wasmade by Van
Sickels and colleagues whoreported that patients with a concurrentgenioplasty had a
greater loss ofsensationinitially.147Unfortunately the wide variationin measurement
protocols makes compar-isons ofthese various reports difficult.Thisalso makes
difficult the evaluation oftech-niques that have been suggested to decreasethe
incidence ofnerve damage.White and colleagues pointed out thatdamage to the
inferior alveolar nerve mostlikely occurs either during the medialretraction ofthe
soft tissues and the nerveas it enters the canal or during the verticalbone
cut.148Guernsey and DeChamplainfelt that damage occurred during the split-ting
ofthe mandible and reported theproblem ofparts ofthe nerve staying in theproximal
fragment after the split.149Thishas led some surgeons to recommend theuse ofa small
flat (spatula) osteotome dur-ing the split,instead ofthe wide-
splittingosteotome.150The fine osteotome is mallet-ed carefully along the lateral
cortex andcancellous bone junction.The nerve isexposed less often during the split
by thistechnique,and consequently it has beenassumed that this results in less
sensory dis-turbances.151,152Unfortunately this tech-nique has not been directly
compared withany other,and the comparison oftheoccurrence ofsensory disturbance
betweenreports is impossible.Yoshida and col-leagues and later Yamamoto and
colleagues,found that nerves that were close to the lat-eral cortex,as determined
by radiographs,were more likely to have severe sensoryalteration after
surgery.152,153The deficitswere also more likely to be present 1 yearafter surgery
when the marrow spacebetween the mandibular canal and theexternal cortical bone was
0.8 mm or less.Some authors feel that by making the verti-cal cut in the lateral
cortex more posterior,a lower incidence ofsensory problemsoccurs.152,154This has
not been substantiat-ed in comparison studies.Another possible cause ofsensory
lossto the nerve may be due to the sharp boneirregularities ofthe proximal fragment
orto compression ofthe nerve when theproximal fragment is positioned
andfixed.155,156A round or acrylic bur can beused to remove any bone spicules as
well asto widen and deepen the canal in the prox-imal fragment to prevent this
effect.Caremust be taken when working around thenerve so that instruments used
during theosteotomy do not themselves cause directdamage.This concern was
heightenedwith the use ofscrew fixation.Paulis andSteinhauser noted slightly higher
inci-dences oflong-term sensory loss inpatients with rigid screw fixation com-pared
with simple osseous fixation but sta-tistics were not used and the
significanceoftheir numbers is highly suspect.157Nishioka and colleagues did a
comprehen-sive study involving sensory loss after theuse ofscrew fixation and found
the inci-dence ofinferior alveolar sensory loss tobe high but well within the range
ofsenso-ry loss reported by other well-designedobjective studies.158Subsequently
theeffect oftype offixation on the neurosen-sory functional outcome was
extensivelystudied by a number ofauthors using dif-ferent methods ofclinical
testing.159�162Brush stroke detection was diminished toa greater extent in the
rigid fixation groupcompared with the wire fixation groupfrom 8 weeks through 2
years postopera-tively;however,monofilament detectiondid not show significant
differencebetween types offixation throughout the2-year follow-up.159Despite a
great num-ber ofstudies on neurosensory distur-bance following orthognathic
surgery,theseverity ofinferior alveolar nerve injury isdifficult to compare across
different stud-ies since there is lack ofstandardization asto which neurosensory
tests were used,ways the tests were performed,and howthe results were
interpreted.Certainneurosensory tests are more sensitive indetecting sensory nerve
deficit than oth-ers.Tests that evaluate patients�abilities todiscriminate
direction have been shown tobe more sensitive indicators oftrigeminalneurosensory
impairment than other testssuch as light touch detection.Westermarkand colleagues
used visual analog scale,light touch perception,and temperaturetesting and
concluded that there is a goodpositive correlation with nerve dysfunc-
tion.160Alternatively,Chen and colleaguescompared three methods ofassessing neu-
rosensory disturbance following BSSO:two-point discrimination,pressure-
painthresholds,and perceived sensationchanges in specific facial regions.161Thetwo-
point discrimination test was consis-tent with patients�self-ratings ofneuro-
sensory problems using facial maps,butthe pressure-pain test was the least sensi-
tive to neurosensory changes.The frequen-cy ofthe inferior alveolar nerve distur-
bance ranged from 10 to 94% dependingon the test method and the test site used.In a
well-controlled study by Nakagawaand colleagues,the occurrence ofa long-lasting
postoperative trigeminal sensoryhypoesthesia was found to be dependenton the nerve
involvement at the bone splitinterface,the manner offixation,or theintraoperative
handling ofthe tissue sur-rounding the nerve.162Although the neurosensory
functionofthe inferior alveolar nerve followingsagittal split osteotomy has
received a greatdeal ofattention,very few studies havedocumented the incidence
oflingual nerve
1158Part 8: Orthognathic Surgerydysfunction.Jacks and colleagues retro-spectively
reviewed the patient-reportedincidence,duration,and perceived deficitassociated
with lingual nerve function.163In the BSSO patients 19% reported lingualnerve
sensory changes ofwhom 69%reported a resolution ofsymptoms withina year and 88%
reported altered dailyactivities.When compared with the inferi-or alveolar
nerve,lingual nerve sensorychanges occurred much less frequentlyand resolved more
frequently and sooner,but they were associated with greater per-ceived deficits in
patients�daily activities.Zuniga and colleagues were the first toreport on studies
performed to assess theeffect oflingual nerve injury and repair onhuman taste
perception.164Gent and col-leagues later examined perceived tasteintensity and
taste quality identificationon localized regions ofthe tongue afterorthognathic
surgery.165Lingual nervefunction in taste perception was dimin-ished at 1 to 2
months after surgery,likelydue to impared chorda tympani nervefunction,but it
improved by 6 to 9 monthsafter surgery.Temporomandibular Joint DysfunctionThe
incidence oftemporomandibularjoint dysfunction will be considered in
twoways:first,the incidence oftemporo-mandibular joint symptoms that are pre-sent
after surgery compared with preoper-ative findings;and second,the change
inmandibular range ofmotion.The lattermay obviously not be related to temporo-
mandibular joint dysfunction;on theother hand it has to be considered ifeval-uating
the effects ofthe surgery on thetemporomandibular joint.Unfortunatelyvery few
authors related these two areaswhen they reported on the effect ofthesagittal
osteotomy.Another factor thatmust be taken into account in evaluatingthe effects on
the temporomandibular jointin any recent orthognathic surgery is thepossible
contribution ofthe orthodonticsas provided in conjunction with thesurgery.There is
still debate on how muchorthodontics itselfmay help or cause tem-poromandibular
joint dysfunction.Similar to sensory loss the potential ofthe sagittal osteotomy
causing temporo-mandibular joint dysfunction was recog-nized early in its
use.24Reporting oftheincidence oftemporomandibular jointproblems,however,has been
highly vari-able,with most authors recording only thepostoperative complaint
without any ref-erence to the preoperative condition.Some ofthe first reviews that
did look atpre- and postoperative temporomandibu-lar joint symptoms seemed to imply
anincrease in joint noises,but not in pain,following the sagittal
osteotomy.56,166,167The use ofrigid screw fixation was felt bysome to cause an
increase in temporo-mandibular joint problems.168This con-cern was highlighted by
radiographic find-ings ofcondylar changes that occurredwith rigid screw
fixation.Kundert andHadjianghelou demonstrated that thistendency occurred with both
wires andscrews but was greater with rigid fixationthan with a wire osseous
fixation tech-nique.106In neither study was there a dis-cussion ofwhether these
changes had anyclinical consequences.Hackney and col-leagues found in their study
ofpatients,inwhom bicortical screw fixation withmandibular sagittal split was used
formandibular advancements,that littlechange in condylar position occurred,andthere
was no significant effect ofthesurgery on temporomandibular jointsymptoms.169Paulis
and Steinhauser com-pared preoperative and postoperative tem-poromandibular joint
symptoms in twolarge groups who had either rigid screwfixation or wire osseous
fixation ofsagittalosteotomies.157They could find no differ-ence in postoperative
incidence betweenthe two groups and in fact found a notabledecrease in
temporomandibular joint painin both groups.The possibility that thesagittal
osteotomy may benefit manypatients with temporomandibular jointsymptoms was
suggested by Martis andKarabouta.170,171He reported that only11% ofthe patients who
had temporo-mandibular joint symptoms before surgeryhad any symptoms after,whereas
about 4%ofthe asymptomatic patients had prob-lems after surgery.These results were
betterthan but consistent with a study ofall typesoforthognathic surgery
patients,whichshowed an improvement in a large per-centage ofpatients,with
relatively smallrisk for the asymptomatic patient.172There is,surprisingly,a body
ofevi-dence in the literature that sagittal splitosteotomy may have a beneficial
effect onpreexisting temporomandibular joint dys-function.It is generally believed
that tem-poromandibular joint dysfunction is foundat a higher incidence in Class II
patientscompared with patients with Class I and IIImalocclusions.The use ofthe
sagittal splitosteotomy as an alternative to themandibular condylotomy to treat
patientswith painful temporomandibular joint dys-function has been proposed by
someauthors.173They suggest repositioning theproximal segment and increasing the
jointspace,both ofwhich are thought to have anunloading effect on the highly
innervatedretrodiskal tissues.However,this is contro-versial and there has not been
adequateresearch to confirm this impression.Debate on rigid versus wire
fixationrelative to their effects on the temporo-mandibular joint has led to a
number ofstudies.Most have shown that there is nosignificant difference in the
incidence oftemporomandibular joint symptomsbetween patients who have received
rigidfixation versus wire osteosynthesis duringsagittal split
osteotomies.174Feinermanand Piecuch compared the temporo-mandibular joint outcomes
ofthe mini-plate with monocortical screw group ver-sus the superior border wire
fixation withmaxillomandibular fixation group.175They found no demonstrable long-
termdifferences between the two groups withrespect to mandibular vertical opening,
Principles ofMandibular Orthognathic Surgery1159crepitance,and temporomandibular
jointpain.In fact masticatory muscle pain andtemporomandibular joint clicking im-
proved with rigid fixation and worsenedwith nonrigid fixation.The only negative
report on the effectsofBSSOs on the temporomandibular jointwas submitted by Wolford
and colleagues.176They evaluated changes in temporo-mandibular joint dysfunction in
patientswith presurgical temporomandibular jointinternal derangement as well as the
long-term stability ofpatients who underwentorthognathic surgery.Unlike other
clini-cians they observed the appearance ofnewor an aggravation ofexisting temporo-
mandibular joint symptoms in a group ofpatients who were an average of14
monthspostsurgery.Therefore,the authors recom-mended that surgical correction
ofpreexist-ing temporomandibular joint pathology beconsidered,either preceding or
simultane-ous with the orthognathic surgery.In sum-mary it appears that there is a
low risk ofworsening temporomandibular joint symp-toms in patients who do have some
form oftemporomandibular joint dysfunctionwhen using the BSSO.Conversely
thisosteotomy may result in improved symp-toms in a greater number
ofpatients.Unfortunately methods ofpredicting thisoutcome in individual patients
have notbeen developed.Mechanical displacement ofthecondyle out ofits correct
position hasbeen implicated as a significant factor inpostsurgical skeletal relapse
after sagittalsplit osteotomy.For this reason,as well asin an attempt to minimize
temporo-mandibular joint problems,a great deal ofinterest has been focused by early
investi-gators on the issues ofcondylar positionafter sagittal split
osteotomy.177There havebeen a myriad oftechnical notes on howto maintain the
preoperative condylarposition and use ofdifferent condylarrepositioning
devices,based on anecdotalreports ofindividual surgeon�s experi-ences.Harris and
colleagues examined fac-tors influencing condylar position aftersagittal split
osteotomy fixed with rigidfixation.178The amount ofadvancementdid not correlate
with condylar displace-ment.Condyle angulation and superior-inferior movement did
correlate some-what with the amount ofadvancement.Inaddition Van Sickels and
colleagues foundthat the condylar position was slightly dif-ferent with rigid
fixation versus wireosteosynthesis beyond 8 weeks postopera-tively,but the ultimate
position ofthecondyle was not different.179They found,as have many others,that the
final condy-lar position was posterior and superiorafter a mandibular
advancement.Renziand colleagues specifically examined ClassIII patients without
preoperative tem-poromandibular joint dysfunction;halfofthe patient population was
treated with acondylar positioning device whereas theother halfofpatients was
treated withmanual control ofcondylar position.180The condylar repositioning device
did notprevent the changes in condyle positionsin all cases.Neither group had any
skeletalor occlusal relapse or postsurgical tem-poromandibular joint
dysfunction.How-ever,the incidence ofnew onset oftem-poromandibular joint
dysfunction inhealthy individuals following orthognath-ic surgery is known to be
low as previous-ly mentioned,and this study only includedpatients without
preoperative temporo-mandibular joint symptoms.Therefore,itis not surprising that
the patients did notdevelop any postsurgical temporo-mandibular joint
dysfunction.The clinicalimplication ofcondylar position in thehealthy versus the
preexisting temporo-mandibular joint dysfunction groups maybe
different;therefore,the true clinical sig-nificance ofcondylar position in
exacerba-tion oftemporomandibular joint symp-toms remains an enigma.Computed
tomography (CT) hasenabled clinicians to assess and quantifycondylar position
changes in three planesofspace.Alder and colleagues reportedthat changes in
condylar position occurredin all planes ofspace,but the most com-mon postoperative
condyle position wasmore lateral with increased condyle angle,the coronoid process
was higher,and thecondyle was again reported to be moresuperior and posterior in
the fossa.181Rebellato and colleagues found in theirstudy group that there was
increased supe-rior postsurgical movement ofthecondyles with increasing magnitudes
ofsurgical advancement ofthe mandible.182Magnetic resonance imaging (MRI)has
revolutionized the examination ofthetemporomandibular joint,in that it allowsnot
only the evaluation ofcondylar posi-tion but also provides information on
thedisk.Gaggl and colleagues reported clinicaland MRI findings ofthe
temporomandibu-lar joint in Class II patients,preoperativelyand 3 months
postoperatively.183Clinicallypatients had improvements in joint painand abnormal
joint sounds such as clicking.The MRI showed displacement ofthe diskin 38 ofthe 50
joints preoperatively and in28 postoperatively.No correlation wasmade between the
change in disk positionand improvement in temporomandibularjoint symptoms,which is
consistent withother MRI studies.Ueki and colleaguesmade interesting comparisons
ofthecondylar and disk positions after BSSO andintraoral vertical ramus osteotomy
(IVRO)and correlated these findings with tem-poromandibular joint symptoms
postoper-atively.184Fewer or no temporomandibularjoint symptoms were reported by
88% ofthe patients who underwent IVRO and by66% ofpatients who underwent BSSO.MRI
study showed no change in anteriordisk displacement after BSSO;however,improvement
was seen in 44% ofpatientswho underwent IVRO,at least in the earlypostsurgical
period.The effect ofthe sagittal osteotomy ofthe vertical ramus on mandibular range
ofmotion has been extensively studied.Whereas Stacy found that patients
whounderwent mandibular setbacks with
1160Part 8: Orthognathic Surgerymaxillomandibular fixation generallyreturned to
presurgical limits within 9 months following surgery without anyphysical
therapy,other authors have foundvery different results.185Storum and Bellfound that
without active physical therapyafter the release ofmaxillomandibular fix-ation
there was a decrease in the patient�sability to achieve preoperative openingwhen
compared with patients who had anactive rehabilitation program.186This lat-ter
study is consistent with most clinicians�experience,and some form ofactive phys-
ical therapy is recommended after releasefrom maxillomandibular fixation.Howev-
er,there is some evidence that rigid inter-nal fixation that permits
mandibularmovement soon after surgery may result ina more rapid return to
preoperativemandibular movement.187Nishimura andcolleagues found that final
postoperativemouth opening was not significantlyinfluenced by the type
offixation.188A final poorly understood temporo-mandibular joint complication is
sponta-neous resorption ofcondyles followingsagittal osteotomies.189This is a
processthat may be different from standardrelapse with the abnormal resorptionbeing
seen primarily in a specific group ofpatients�young females who have had ahistory
oftemporomandibular joint dys-function before surgery and have under-gone a
mandibular advancement.Remod-eling ofthe condyles is now accepted tooccur after
sagittal osteotomies,but fortu-nately only rarely has this condylar resorp-tion
resulted in significant clinicalchanges.Cutbirth and colleagues evaluat-ed long-
term condylar resorption aftermandibular advancement stabilized withbicortical
screws.190Large advancementand preoperative temporomandibularjoint symptoms
significantly correlatedwith long-term postoperative condylarresorption at the mean
follow-up of3 years.The amount ofvertical resorptiondid not directly correlate with
the amountofrelapse seen between 6 to 8 weeks andlong term.Surprisingly there was
animprovement in temporomandibular jointsymptoms for the group as a whole andeven
among the group who developedcondylar resorption.It should be noted,however,that it
is often difficult to draw aline between normal condylar remodelingand condylar
resorption.In the Cutbirthstudy,the authors arbitrarily established aparameter
ofless than 10% loss ofheightofthe condyle to be considered as
�normalremodeling.�190Attempts to delineate thenormal versus pathologic process are
diffi-cult,and may lead to an underestimationofthe number ofcondylar
resorptionsthat may occur.Hoppenreijs and colleagues evaluatedthe long-term
treatment results of26 patients (23 women and 3 men) whodeveloped progressive
condylar resorptionfollowing orthognathic surgery.191Thepreoperative condylar
configuration wasnoted in patients with deep bites to havemore resorption on the
superior aspect ofthe condyle,whereas patients with anteri-or open bites had
resorption on the supe-rior and anterior surfaces ofthe condyle.Thirteen patients
were managed withoutsurgery after the diagnosis ofcondylarresorption,and only 3
patients had Class Iocclusion at the end oftreatment.Thir-teen patients underwent a
second surgicalcorrection,with 7 patients having satisfac-tory occlusal
results.Four ofthe patientshad relapse with a stable occlusion notrequiring further
treatment,and 2 patientshad complete relapse requiring a third sur-gical
procedure.It was suggested thatwithout surgical intervention after condy-lar
resorption,further resorption ceasedafter approximately 2 years.The
authorsspeculated that either the mechanicalloading during or after BSSO and/or
theimpediment ofblood flow to the condylarsegment and the temporomandibularjoint
capsule may play a role in the condy-lar resorption.However,the etiology forthis
process is still unclear,but it doesseem to be self-limiting and the
resultingdental skeletal deformity can usually besuccessfully treated with further
mandibu-lar surgery.Miscellaneous ComplicationsA widevariety ofother complications
have beenreported following the sagittal splitosteotomy ofthe mandibular
ramus.Earlyreviews ofcomplications from this proce-dure noted some trouble with
excess bloodloss,postoperative airway compromise,large aseptic bone loss,and facial
nervedamage.Greater experience and betterinstrumentation seem to have dramatical-ly
decreased the incidence ofthese prob-lems.Bleeding is generally easily managedby
direct or indirect pressure over thebleeding soft tissue and vessels.Laniganand
colleagues,reporting on a question-naire sent to a large number oforal
andmaxillofacial surgeons,found only 21cases ofsignificant bleeding
followingmandibular osteotomies.192Suspectedsources ofbleeding included the
inferioralveolar artery,facial artery,maxillaryartery,and retromandibular
vein.Manage-ment primarily included direct pressurepacking or ligation ofthe vessel
via theopen wound.Extraoral approaches to gainaccess to the facial or external
carotidartery can be ineffective due to the collat-eral circulation.Angiography
withembolization is considered appropriate incases ofacute persistent
postoperativearterial bleeding.One group ofproblems that seems topersist is the
inappropriate fracture in theproximal segment or the posterior lingualaspect ofthe
distal segment.Good surgicaltechnique minimizes these problems,andcare used during
the split is worth theeffort,as correcting a �bad�split can be dif-
ficult.Fortunately the use ofscrews andplates does improve the chance ofobtain-ing
a satisfactory result,in light ofan unex-pected fracture,with minimum
furthermorbidity to the patient.193It has been feltthat one ofthe major risk
factors predis-posing to buccal cortex fracture is the pres-
Principles ofMandibular Orthognathic Surgery1161ence ofimpacted third
molars.Preciousand colleagues retrospectively reviewed twogroups ofpatients:one
group with retainedimpacted third molars removed duringBSSO and the other group
with thirdmolars having been removed at least 6months before BSSO.194There was a
1.9%incidence ofunfavorable fractures,and themajority offractures occurred with
thegroup who had the third molars removed atleast 6 months before the BSSO.Mehra
andcolleagues reported 2.2% unfavorable frac-tures in 500 procedures.195They noted
alarger percentage ofunfavorable fracturesin the patients with retained third
molars(3.2% vs 1.2%).This finding is consistentwith that ofReyneke and colleagues
whofound that the presence ofunerupted thirdmolars increased the degree
ofdifficulty ofBSSO,and all 4 (out of139 patients) unfa-vorable fractures occurred
in those patientswith unerupted third molars present at thetime
ofsurgery.196Ideally third molarsshould be extracted at least 6 (preferably
9)months prior to the mandibular osteotomy,both to minimize unfavorable fractures
andto allow optimal bony healing,especiallywhen using internal rigid
fixation.Airway patency has become an area ofconcern to some clinicians,especially
inthe cases where the mandible is set back.Riley and colleagues reported two
patientswho were surgically treated for prog-nathism and later developed
sleepapnea.197Kawamata and colleagues stud-ied patients with mandibular
prognathismwho were treated with either sagittal splitosteotomy or IVRO for
mandibular set-back.198Using three-dimensional CTimages they quantified the airway
spaceafter surgery and found that the lateraland frontal widths ofthe pharyngeal
air-way had decreased by 23% and 11%,respectively.This reduction in airwaydimension
did not resolve at 1 year aftersurgery.However,in the longer postopera-tive
period,a visible recovery ofpharyn-geal width was seen in some cases.Thesefindings
ofthe decreased airways sec-ondary to mandibular setback have beenconfirmed by
other investigators.Note-worthy,however,is that only one oftheseclinical studies
had a reported incidence ofa patient developing sleep apnea followingorthognathic
surgery.Therefore oneshould be cognizant ofany physiologicand medical etiologic
factors that mayhave contributed to the emergence ofsleepapnea symptoms,rather than
simply usingthe measurement ofthe posterior airwayspace following mandibular
osteotomiesas the sole means ofpredicting a new onsetofsleep apnea disorders.In
general,the risk ofinfection seemsto be low with the BSSO.In their clinicalreview
of700 consecutive cases ofmandibular osteotomies,Bouwman andcolleagues reported
that screw removaldue to infection was performed in 2.8% ofcases.199Screw loosening
occurred in thefirst postoperative week,which resulted inan occlusal discrepancy in
four patients.Fifteen sides required one or more screwsto be removed as a result
ofinfection.In alarge study ofcomplications in ortho-gnathic surgery,Acebal-Bianco
and col-leagues reported 36 infections out of802 mandibular osteotomies
(0.05%),butonly 5 patients had hardware removeddue to infections.200Horizontal
Ramus OsteotomiesSince Blair�s first description ofhisosteotomy ofthe horizontal
ramus,therehave been a variety ofosteotomy designsdocumented.Initially the surgeons
usedextraoral,or a combination ofextraoraland intraoral techniques,but since
theearly 1950s the advocated approacheshave primarily been intraoral.It is diffi-
cult to choose a representative techniquefor the body osteotomies because ofthewide
variations described as well as therelative infrequency ofthese techniques.Ofthe
described procedures,the steposteotomy will be reviewed because ofitsversatility
and its apparent common usein some centers.IndicationsThe largest limitation ofbody
osteotomies is that the osteotomyhas to be made through the dental
alveolusand,thus,edentulous spaces are usuallyrequired.Because these osteotomies
aremade in front ofthe pterygomassetericsling,some surgeons feel that the
resultsare more stable and,therefore,prefer bodyosteotomies in the treatment
ofprog-nathism when there are already edentu-lous spaces.Other unusual
mandibularabnormalities,such as asymmetries,mayalso be treated more appropriately
withone ofthese forms ofosteotomy.With the step osteotomy the surgeonhas to be
concerned about the horizontalcomponent ofthe �step,�which often hasto be made
between the inferior alveolarnerve and the apices ofthe teeth.Sufficientroom should
therefore be available for thiscut,unless the surgeon plans to externalizepart
ofthe inferior alveolar nerve so thatthe cut can be made at the level oforbelow the
canal.TechniqueAn incision is made 4 to 5 mm below the level ofthe attached gin-
giva (enough tissue is left superiorly topermit later suturing) and is carried for-
ward at this level until the cuspid,where itcan be dropped down 5 mm and
extendedforward to the midline (Figure 56-20A).The periosteum is elevated
inferiorly untilthe mental foramen is located and then theremainder ofthe
periosteum is stripped toexpose the area ofthe osteotomy.Theattached gingiva is
also carefully elevatedin the area ofthe dental alveolar cut so thatit can be
protected during the osteotomy.The vertical cut through the alveolus ismade with
either a saw or bur.A fingershould be kept on the lingula to prevent thepower
instrument from penetrating themucosa.When the surgical plan includes amandibular
setback,a block ofbone needsto be removed to permit this movement.The distance
between the parallel cuts nec-essary to remove the bone should be asclose as
possible to the planned setback,as
1162Part 8: Orthognathic Surgerydetermined by the model surgery.The ver-tical cuts
are taken inferiorly to the level ofthe planned horizontal cut,which would beat
least 5 mm below the dental apices.Theinferior vertical cuts are then
made,againusing parallel cuts as necessary for a setbackofthe distal
fragment.Finally the horizon-tal cut is made,preferably by a saw,to min-imize bone
removal and endangerment ofthe apices or the inferior alveolar nerve(Figure 56-
20B).The distal segment is related to theproximal segment with an occlusal
splintand fixed with maxillomandibular fixation.Ifthe mandible is set back any
distance awedge ofattached tissue over the alveolarvertical osteotomy needs to be
removed topermit the setback.This wedge should benarrower than the planned movement
toallow tight mucosal contact.This eliminatesthe need for suturing in this
area,which isoften difficult,ifnot impossible.Osseouswire fixation can be placed at
the inferiorborder or,ifa rigid fixation technique isdesired,straight four-holed
plates withmonocortical screws can be placed aboveand below the nerve.With a rigid
fixationtechnique the maxillomandibular wires canbe cut and the segment�s stability
and posi-tion are checked before closure ofthewound.The surgical sites are
thoroughlyirrigated and the mucosa is then closedwith a resorbable
suture.Maxillomandibu-lar fixation,ifused,is maintained for 6 to 8 weeks (Figure
56-21).Alternative TechniquesThere are mul-tiple variations ofbody
osteotomies.Generally the mucosal approaches aresimilar,although some surgeons
preferto make a cervical incision posterior tothe mental foramen and then carry
itbelow the attached tissue in the anteriorsymphyseal region.This approach unfor-
tunately presents some difficulty inwound closure,especially ifmaxillo-mandibidar
fixation is chosen.One ofthe most difficult variations inthe surgical approach
occurs when there isa need for visualization or exteriorizationofthe inferior
alveolar nerve,ifanosteotomy is planned through the canal.The easiest method for
this is similar tothat described by Epker.201After the lateral surface ofthe
mandibleis exposed in the area ofthe plannedosteotomies,parallel horizontal
corticalcuts are made on either side ofthe antici-pated route ofthe nerve.These
cuts areextended beyond either side ofthe plannedosteotomy,sufficient to permit
adequateapproach to the nerve,as well as to permitenough freedom ofthe nerve
duringstretching or compression that will occurwith the planned segment
movements.Per-pendicular cuts are made just through thecortex at about 1 cm
intervals (Figure 56-22).Starting with the forward cuts a thinsharp 4 mm osteotome
is carefully used tostart a cleavage line through the cancellousbone,preferably
just below the cortex.Aseach individual section is broken away themedial aspect
ofthe fragment needs to bechecked to ensure that a nerve is not stillattached to
it.After all the small lateral cor-FIGURE56-20The step osteotomy.Adapted from
Bloomquist DS.Principles ofmandibular orthognathic surgery.In: Peterson
LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal and maxillofacial
surgery.Vol 3.Philadelphia (PA): J.B.Lippincott Com-pany; 1992.p.1444.AB
Principles ofMandibular Orthognathic Surgery1163ABEFHIGDCFIGURE56-21Patient who was
treated with a step osteotomy for mandibular horizontal excess.A�D,Preoperative
photographs and radi-ograph.E�I,Postoperative photographs and
radiographs.Reproduced with permission from Bloomquist DS.Principles
ofmandibularorthognathic surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM.Principles oforal and maxillofacial surgery.Vol 3.Philadel-phia (PA):
J.B.Lippincott Company; 1992.p.1446�7.
1164Part 8: Orthognathic Surgerytical segments have been removed,often thenerve has
been exposed and judicious use ofa small surgical curette is all that is neededto
remove any bone spicules over the nerveas well as carefully lift the nerve out
ofitscanal.Ifcancellous bone is still coveringthe nerve,then a medium-sized round
burcan be used to carefully remove the over-lying bone.A small periosteal elevator
or asurgical curette can be positioned in thelateral aspect ofthe canal when the
nerveis exposed and the thin bur used to removethe remaining overlying
bone.Followingthe visualization or exteriorization ofthenerve the osteotomies can
proceed asplanned.Although primarily used for distal frag-ment setback,the step
osteotomy can beused for advancement.To accomplish that,a horizontal incision has
to be made on thelingual side ofthe alveolus,posterior to thevertical alveolar bone
cut.The mucoperios-teum below this cut can then be elevated toallow it to be
stretched with the advance-ment.The lateral incision is designed topermit the
labial tissue to be pulled lingual-ly,without tension,so that soft tissue closure
can be done.Bone grafts are gener-ally used in the gaps created by the advance-
ments,especially in the alveolar area,whereprostheses may later be placed.Sagittal
osteotomies ofthe horizontalramus have been described with either anextraoral or
intraoral approach possi-ble.202,203In the intraoral approach the lin-gual exposure
has to be increased to makethe vertical cortical cut.This generallyrequires that
the incision on the lingualside ofthe teeth be brought forward,closeto the
midline,so that retraction mayoccur without endangering the surround-ing soft
tissue.The advantage ofthis typeofosteotomy is that it allows the use ofrigid
internal fixation with bicorticalscrews,and generally a bone graft is notneeded
ifthe distal segment is advanced.ComplicationsReports ofbody osteoto-mies in the
literature include mostly casehistories;hence,there are few series report-ing an
incidence ofcomplications.The widevariety oftechniques makes it impossible tomake
any definitive statements about bodyosteotomies.Therefore,this section will
beprimarily limited to the listing ofthe report-ed complications,many ofwhich can
beanticipated simply from the knowledge ofthe anatomy ofthe area.StabilityOne ofthe
primary reasonsgiven by surgeons for using a body proce-dure is the stability ofthe
technique.San-dor and colleagues looked at relapse ofthestep osteotomy and found it
to be verystable.204Most other authors have notstrictly analyzed the results but
claim agood long-term stability with their partic-ular technique.205,206Neural
ComplicationsThose studiesthat include reports ofthe incidence orduration
ofneurosensory damage report ahigh recovery ratio.205,206Unfortunatelythese studies
are ofquestionable valuebecause ofthe inadequate testing method.It can be
expected,however,that immedi-ate postoperative sensory loss will be pre-sent after
any ofthe body osteotomies,especially those that require visualizationor
exteriorization ofthe nerve.The inci-dence ofdevitalization ofteeth on eitherside
ofthe osteotomy,or ofthose teethabove the horizontal cut ofthe steposteotomy,is
unknown,although it isprobably similar to those reported withmandibular subapical
osteotomies.The increased potential ofnonunionin body osteotomies has been
discussed,but the incidence is unknown.The possi-bility ofthis occurring is
probably verylow if,as has been suggested,care is usedin osteotomy design to ensure
sufficientbone contact as well as in the provision ofadequate fixation.The
possibility ofperiodontal defectsdoes exist for osteotomies made close tothe teeth
where the surrounding soft tissuepedicle may be injured.As has been notedearlier
the possibility ofthis occurring inmidline osteotomies is low,but whetherthis can
be related to other parts ofthedental alveolus is doubtful.207Subapical
OsteotomiesThere are essentially three types ofmandibular subapical
osteotomies:theanterior subapical,the posterior subapical,and the total alveolar
osteotomy.Each hasa place in orthognathic surgery and,there-fore,the indications
and techniques ofeach shall be described individually.Theircomplications are
similar;accordingly theywill be discussed together in one section.Anterior
Subapical OsteotomyIndica-tionsThe subapical osteotomy has histor-ically been
popular because ofits versatility,and it has been used to move the
anteriormandibular teeth and alveolus in almostevery conceivable direction.The
biggestconcern ofsurgeons in this procedure is thepotential ofdamaging teeth
and,therefore,FIGURE56-22Decortication for exposure oftheinferior alveolar nerve
and vessels.Adapted fromBloomquist DS.Principles ofmandibularorthognathic
surgery.In: Peterson LJ,IndresanoAT,Marciani RD,Roser SM.Principles oforaland
maxillofacial surgery.Vol 3.Philadelphia(PA): J.B.Lippincott Company; 1992.p.1448.
Principles ofMandibular Orthognathic Surgery1165space must be present or made to
permit asafe vertical cut in the dental alveolus.ProcedureIfnecessary,teeth
areremoved to permit the osteotomies or toprovide space for the planned
alveolarmovement.The incision is started about 1 cm behind the planned vertical
osteoto-my and is carried forward about 4 to 5 mmbelow the attached tissue until
reachingthe cuspid,at which time it can bedropped down and carried to the midlineto
connect with an opposing incision.Periosteum is elevated,exposing the later-al
cortex ofthe mandible,with care beingused around the mental foramen as well assome
attachments being left at the inferiorborder to ensure stability ofthe soft
tissuechin.The attached tissue at the plannedvertical osteotomy site needs to be
elevat-ed,and ifposterior movement ofthe seg-ment is anticipated,some ofthis
tissuemay have to be removed.As mentionedwith the step osteotomy the width
ofthetissue removed should be less than theplanned posterior movement to
ensureadequate soft tissue contact.The vertical osteotomies are madeusing parallel
cuts when the posteriormovement ofthe segment is planned.Good preoperative
radiologic evaluationand planning will minimize the chance ofdamage to the inferior
alveolar nerve.Most anterior subapical osteotomies aredesigned to include the
cuspids and theincisors,which generally place the verticalcuts anterior to the
mental foramen.Dif-ficulties arise ifthe planned osteotomyincludes extraction ofthe
first bicuspid orifthe cut is planned behind this point.The importance ofbeing able
to make thehorizontal cut at least 5 mm below theteeth apices cannot be
overemphasized.Not only the vitality ofthe teeth but thewhole segment is affected
by the level ofthe horizontal cut.Ifparallel horizontalcuts are planned to move the
anterior seg-ment apically,the superior cut is madefirst.The inferior cut is then
made,andthe segment ofbone is removed withoutoverly manipulating the dental
alveolarsegment and increasing the likelihood ofinjuring the soft tissue pedicle
(Figure 56-23A).Beveling ofthe cut from anteri-or to posteroinferior will minimize
theamount ofbone to be removed andincrease the size ofthe lingual
pedicle.Usually,on trying to position the mobiledental alveolar segment to the rest
ofthemandible,further bone interferences arefound.These exist primarily on the lin-
gual cortex ofthe vertical cuts and caremust be used in the rotation ofthe
mobilesegment to access this cortex.Ifpossible aretractor should be placed between
thebone and the thin lingual mucosa to min-imize the soft tissue trauma.After
ensuring a good fit in the surgi-cal splint the segment is stabilized byeither
wiring the splint to the teeth indi-vidually (Figure 56-23B) or by circumfer-ential
mandibular wires that can be com-bined with intermaxillary fixation.Osseous wires
or plates with monocorticalscrews are rarely needed for stability butcan be used
ifdesired.Bone gaps causedby movement ofthe segment,especially byvertical movement
necessary for the clo-sure ofan anterior open bite,should begrafted.The use
ofcortical bone from thesymphysis,as advocated by Kole,has beenpopular because many
patients with ananterior open bite have the long anteriorface which can be improved
by removal ofthe bone (Figure 56-23C).28The surgicalsite is then irrigated
thoroughly and closedwith resorbable sutures.Posterior Subapical OsteotomyIndica-
tionsThe posterior subapical osteotomyhas few indications,especially ifortho-
dontics are available to the patient.Pri-marily it can be used as a correction
ofsupereruption ofposterior mandibularteeth or ankylosis ofone or more posteri-or
teeth.Abnormal buccal or lingual posi-FIGURE56-23The anterior subapical
osteotomy.A,Osteotomy.B,Occlusal splint.C,Bone graft from chin for correction
ofanterior open bite (Kole).Adapted from Bloomquist DS.Principles ofmandibular
orthognathic surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principles
oforaland maxillofacial surgery.Vol 3.Philadelphia (PA): J.B.Lippincott Company;
1992.p.1450.ABC
1166Part 8: Orthognathic Surgerytion ofthese teeth can also be improved onwhen
orthodontics is not feasible.208TechniqueThe following technique isthat
ofPeterson,who first described thisosteotomy.208This procedure can be doneunder
local anesthesia with sedation aswell as with general anesthesia.An incisionis
started 3 to 4 mm laterally to theattached gingiva,beginning at the anteriorborder
ofthe vertical ramus.This incisionis made down into the bone and is carriedforward
to the cuspid.Periosteum isstripped superiorly and inferiorly suffi-ciently to
expose the lateral cortex for theplanned osteotomies (Figure 56-24).Theosteotomy is
outlined with a bur,based onthe preoperative radiographic analysis ofthe length
ofthe roots and the position ofthe nerve.The vertical cuts are made firstthrough
both cortices with a fineosteotome or thin saws.The horizontal cutis carried only
through the buccal cortex,and a thick splitting osteotome is used tocomplete the
osteotomy.Care is taken toensure that the nerve is not caught in themobile segment
and that appropriate boneadjustments are made to permit theplanned movement.The
segment is posi-tioned and stabilized with an acrylic splintand wire.Grafting is
used ifa bone gapremains.The mucosa is closed with a run-ning resorbable
suture.Alternative TechniquesMajor modifi-cation ofthe foregoing technique wouldbe
appropriate ifinsufficient distance laybetween the dental apices and the inferi-or
alveolar nerve.In that situation thenerve can be externalized,as
describedpreviously,and a horizontal cut madethrough the canal.Periapical
radiographstaken intraoperatively after the buccalhorizontal cut will ensure that
theosteotomies lie safely away from the teethand nerve.This latter technique has
beenfound to be useful,as a good visual angleis difficult with the posterior
teeth.Also,with either ofthese techniques,the hori-zontal cut can be taken safely
throughthe lingual cortex,which does away withthe unpredictability ofthe lingual
corti-cal fracture.Total Alveolar OsteotomyIndicationsThe total mandibular alve-
olar osteotomy,first described by MacIn-tosh and Carlotti,has limited
applicationbut can prove valuable in mandibulardental alveolar protrusion or
retrusion.209It has also been advocated for the closureofanterior open bite when
used with abone graft.TechniqueAn incision is started on theexternal oblique ridge
ofthe base ofthevertical ramus.The incision is carrieddown to bone and extends
forward 4 to 5 mm below the attached gingiva.Theincision can drop lower as the
canine ispassed and meets the contralateral inci-sion at the midline.The periosteum
is ele-vated to expose the lateral cortex,with careused around the mental nerve,as
well asleaving some attachment at the inferiorborder ofthe symphysis for the soft
tissuechin.The vertical cut posterior to the lastmolar is made first and is taken
down tothe level ofthe planned horizontalosteotomy.As with the step osteotomiesthe
horizontal cut needs to be well placed,based on periapical radiographs.Ifthis
cutcannot be made safely between the dentalapices and the inferior alveolar
nerve,thenthe nerve needs to be exteriorized or thecut placed below the nerve
(Figure 56-25A).The horizontal cut can then beplaced low enough to be away from
dentalapices as well as allowing a good vascularpedicle to the dental alveolus.The
angle ofthe horizontal cut can be made to facilitatethe segment movement;for
instance,a flatcut permits the straight advancement ofthe segment without changing
mandibu-lar height,at the same time maintaining alarge area ofbone contact.The
mobile segment is related to themaxilla with an acrylic occlusal splint
andintermaxillary fixation.Osseous fixation isachieved,with the lateral cortical
wiresbeing placed in the first bicuspid area.Aswith correction ofan anterior open
biteany bone gaps created are filled with graftmaterial.The wound is thoroughly
irrigat-ed and closed with resorbable suture.Technique VariationsBooth and col-
leagues suggested a variation ofthe totalmandibular subapical osteotomy
thatcombines the sagittal split osteotomy ofthe vertical ramus with the total
mandibu-lar alveolar osteotomy (Figure 56-25B).210This modification has a number
ofadvan-tages over the original technique.First theosteotomy is made below the
inferior alve-olar nerve,thereby decreasing the risk ofdamaging the inferior
alveolar nerve andthe apices ofthe teeth,at the same timepreserving much ofthe
vascular supply tothe mobile segment.Also the sagittal partofthe osteotomy allows a
larger bone con-tact area to assist in healing.FIGURE56-24The posterior subapical
osteotomy.Adapt-ed from Bloomquist DS.Principles ofmandibularorthognathic
maxillo-facial surgery.Vol 3.Philadelphia (PA): J.B.LippincottCompany; 1992.p.1451.
Principles ofMandibular Orthognathic Surgery1167The total mandibular alveolar
osteoto-my can also be divided into interdentalsegments to correct axial
inclination ofteeth or to close the edentulous area.Thesemodifications are not
easily done withBooth�s osteotomy but can be valuable as avariation ofthe original
procedure.ComplicationsThe complications ofallmandibular alveolar osteotomies will
beconsidered together because oftheir simi-larities.Stability is often mentioned as
oneofthe advantages ofany ofthe alveolarosteotomies because ofthe minimal
softtissue forces generally placed on theseareas.Unfortunately there have been
veryfew studies to document this claim.Thosethat have been done question the
stabilityofthese segmental osteotomies.Theisenand Guernsey evaluated six patients
whohad anterior subapical osteotomies.211At 1 year after surgery,an average of1 mm
ofmovement ofincisors was noted on lateralcephalograms.In contrast
Kloostermanevaluated a much larger group and founda 30% recurrence ofopen bite
after anteri-or maxillary osteotomies.48Unlike segment stability,neurologic
andvascular complications have received a lot ofattention.Most ofthis evaluation
has beendirected at pulpal changes and not at periph-eral inferior alveolar sensory
loss or avascu-lar bone loss.Both ofthese latter problemsare recognized
complications ofmandibularsubapical osteotomies,but there are no clin-ical studies
noting their incidence.28,36Manyauthors report some incidence ofsensorychange ofthe
lip but claim there have beenno permanent problems;normal sensationreturns in about
3 months.209,211,212Clinical and animal studies oftheeffect ofmandibular
osteotomies on thepulp are numerous.35,37,39,40An early ani-mal study did not note
many vascularchanges when a lingual vascular pediclewas maintained.33However,all
subsequentstudies have noted a significant decrease inblood flow,especially to the
dental pulp.213Histologic studies ofdental pulp after sub-apical osteotomies reveal
some pulpalnecrosis in most teeth.35,214Whether this isofclinical importance is
questionable,asthere were relatively few teeth in clinicalseries that required
endodontics or thatneeded to be extracted.47,48It is likely thatsome pulpal
necrosis occurs in greaternumbers ofteeth than are clinically obvi-ous.215The only
way the pulpal changeshave been assessed clinically is with �vital-ity testing.�A
change in pulpal nerve sen-sation obviously may not be related to adecrease in
pulpal vascularity.However,the rate ofrecovery ofsensory loss seemsto give some
measure ofthe trauma to theteeth.Early clinical studies seem to showthat teeth in
mandibular alveolarosteotomies fare better than their maxil-lary
counterparts.216More recent and larg-er studies,however,have demonstrated
thereverse.47,48One report found that approx-imately 40% ofthe teeth in the reposi-
tioned segment remain unreactive at 1 year.47This high incidence ofpulpaltrauma was
attributed to technical errorsduring surgeries.The incidence ofteethrequiring
endodontics range from 1.5 to10%.The teeth at greatest risk for damageare those in
the mobile segment next to avertical osteotomy.The teeth immediatelyposterior to
the vertical cut are approxi-mately equal in risk to the teeth in the cen-ter ofthe
mobile segment.Periodontal problems have been brieflymentioned by authors reviewing
mandibu-lar alveolar osteotomies.48,211The incidenceand quantitative evaluations
ofsoft andhard tissue loss have not been done,FIGURE56-25A andB,Variations ofthe
total mandibular alveolar osteotomy.Adapted from BloomquistDS.Principles
ofmandibular orthognathic surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser
J.B.Lippincott Company; 1992.p.1451.AB
1168Part 8: Orthognathic Surgeryalthough individual cases ofsignificantinterdental
bone loss have been noted.Periodontal problems are seen less frequent-ly when the
vertical cuts are made in extrac-tion sites than when the cuts are attemptedbetween
teeth without extraction.48Horizontal Osteotomy oftheSymphysisThe horizontal
osteotomy ofthe symphy-sis differs very little from that originallydescribed by
Hofer,except that the proce-dure is done intraorally.32The versatility ofthis
procedure for skeletal deformities ofthe chin is impressive.IndicationsThis
osteotomy with minorvariations can be used to improve almostevery conceivable
skeletal abnormality ofthe chin.The technique is primarily usedonly for esthetic
reasons.Therefore,its usedepends on the patient�s concern aboutappearance ofthis
area ofthe face.Often thesurgeon has to bring to the patient�s atten-tion the need
for a genioplasty when otherfacial osteotomies are planned because ofthe impact
that these osteotomies will haveon chin prominence.The indications,there-fore,are
often made apparent by compre-hensive treatment planning by the
surgeon.TechniqueThe horizontal osteotomy ofthe symphysis is often done in
conjunctionwith other major osteotomies and,thus,isfrequently accomplished under a
generalanesthetic.However,it can be performedas a separate procedure on an
outpatientbasis under sedation and local anesthesia.The mucosal incision is made on
thelabial side ofthe vestibule at about 1 cmabove its depth and extends posteriorly
tothe first bicuspids.This incision is carriedjust below the mucosa to the depth
ofthevestibule and then angled directly to thelabial cortex through the mentalis
muscle(Figure 56-26A).Periosteum is elevatedinferiorly to a point just below the
intendedlevel ofosteotomy.Laterally the periosteumis elevated to the mental foramen
and thenextended posteroinferiorly to the inferiormandibular border.The extent
ofthe pos-terior cortical exposure is generally deter-mined by the position ofthe
mental fora-men and the vertical height ofthe mandiblein this area.In many cases
this means that itwill end in about the first molar area.No attempt is generally
made to exposethe mental nerve by releasing the soft tissuearound it,primarily
because the nerve canbe small and friable,making inadvertentsevering possible.The
periosteal elevationbehind the foramen is minimized to justthat needed for
placement ofa narrowretractor and the saw blade or bur.It is helpful at this point
to inscribe avertical mark (or marks) into the boneacross the planned osteotomy
site so thatthe transverse position ofthe inferior frag-ment can be more easily
oriented after theosteotomy.The osteotomy cut is thenmade with a reciprocating saw
(Figure 56-26B).The length and angle ofthe hori-zontal cut can have profound
effects onpostsurgical results.Further osteotomies orosteoplasties are made after
mobilizationofthe lower segment.The stabilization ofthe segment in its new position
can bemade with cortical wires,circumandibularwires,or plates and screws.The wound
isirrigated and closed in two layers (muscleand mucosa) with resorbable
suture.Tapeplaced across the lip and chin is main-tained for 24 to 48 hours to
minimizehematoma formation as well as to helpsupport the suture lines.Patients
should beinstructed not to pull their lip to minimizedehiscence ofthe
wound.Alternative TechniquesThe primarytechnique differences for the
horizontalosteotomy center on the osteotomy design,and these design differences
depend on thesymphyseal deformity that is being correct-ed.Obwegeser concentrated
on correctionofhorizontal deficiency ofthe chin when hedescribed the basic
procedure (Figure 56-27A).100He suggested that a midsagittalosteotomy ofthe
inferior fragment may behelpful in preventing the prominence oftheposterior ends
ofthe fragment,relative tothe body ofthe mandible,as the fragment isadvanced
(Figure 56-27B).A narrower chinpoint can also be obtained by taking awedge ofbone
out from the lingual aspectofthis cut (Figure 56-27C).The length ofABFIGURE56-26The
surgical approach for the horizontal osteotomy.A,Soft tissue
approach.B,Ostetomy.Adapted from Bloomquist DS.Principles ofmandibular orthognathic
maxillofacial surgery.Vol 3.Philadelphia (PA): J.B.Lippin-cott Company;
1992.p.1453.
Principles ofMandibular Orthognathic Surgery1169the cut posteriorly has important
estheticconsequences.Most notably larger advance-ments require a larger cut to the
first or sec-ond molar region.This permits a smootherline to the inferior border
ofthe mandible.Overlapping an advanced inferior fragmenton the lateral cortex ofthe
symphysis allowsboth an increase in horizontal prominence aswell as a decrease in
the anterior mandibularvertical height (Figure 56-27D).217Largeradvancements ofthe
inferior fragment canbe obtained by double or triple osteotomies,rotation ofthe
fragment combined with agraft at the posterior gap,and bone graftbetween the
symphysis and the fragment(Figure 56-27E�G).218,219Horizontal chin excess is
traditionallytreated by moving the inferior fragmentposteriorly.220Depending on the
angle ofthe cut this will also increase facial height.Sometimes when this is done
it is necessaryto remove the posterior ends ofthe inferiorfragment to prevent
unsightly protrusionsfrom the inferior border ofthe mandible(Figure 56-27H).When
the patient hasnormal facial height,the plane oftheosteotomy should parallelthe
FrankfortFIGURE56-27A�G,Various forms ofthe horizontal osteotomy.
(CONTINUEDONNEXTPAGE)ABCDEFG
1170Part 8: Orthognathic Surgeryhorizontal or natural head position,ifatall
possible.The anterior chin projectioncan be reduced by using parallel or V-shaped
osteotomies cut in a more verti-cal plane,with the middle segmentremoved (Figure
56-27I).Vertical symphyseal excess can bereduced by removing the middle seg-ment
ofbone when the plane oftwo par-allel osteotomies is more horizontal(Figure 56-
27J).These cuts,however,donot always need to be parallel and in factshould be
designed to fit the particularstructural problem.This design also per-mits the
correction ofa mild horizontaldeficiency that is combined with a mildvertical
excess (Figure 56-27K).Thisskeletal problem can also be corrected bymaking a single
osteotomy more verticaland moving the segment anteriorly andforward (Figure 56-
27L).Vertical sym-physeal deficiency can be handled onlyby some type
ofinterpositional material,with either bone grafts or implants (Fig-ure 56-
27M).Even the use ofplatesalone to hold the fragment in a lowerposition has been
suggested (Figures 56-28 and 56-29).The use ofwires,screws,or plate andscrews for
the fixation ofthe inferior frag-FIGURE56-27 (CONTINUED)H�M,Various forms ofthe
horizontal osteotomy.Adapted from Bloomquist DS.Principles ofmandibularorthognathic
1992.p.1454�5.IJKLMH
Principles ofMandibular Orthognathic Surgery1171FIGURE56-28Patient who was treated
with a horizontal osteotomy for hori-zontal chin excess.A�C,Preoperative
photographs and radiograph.D�G,Post-operative photographs and
radiographs.Reproduced with permission fromBloomquist DS.Principles ofmandibular
orthognathic surgery.In: PetersonLJ,Indresano AT,Marciani RD,Roser SM.Principles
oforal and maxillofacialsurgery.Vol 3.Philadelphia (PA): J.B.Lippincott Company;
1992.p.1456.ABCDEFG
1172Part 8: Orthognathic SurgeryFIGURE56-29Patient was treated with a horizontal
osteotomy for horizontalchin deficiency.A�C,Preoperative photographs and
radiograph.D�G,Postop-erative photographs and radiographs.Reproduced with
permission fromBloomquist DS.Principles ofmandibular orthognathic surgery.In:
PetersonLJ,Indresano AT,Marciani RD,Roser SM.Principles oforal and
maxillofacialsurgery.Vol 3.Philadelphia (PA): J.B.Lippincott Company;
1992.p.1457.ABCDEFG
Principles ofMandibular Orthognathic Surgery1173ment is still common.Precious and
col-leagues evaluated the changes that occur asthe bone remodels following a
horizontalosteotomy.221They recommended that thefixation take into account these
changes,especially the positioning ofrigid fixationsuch as plates.Plates along the
superiorborder ofthe inferior fragment maybecome noticeable to the patient as
thebone remodels.ComplicationsThe incidence ofpost-operative problems after a
horizontalosteotomy ofthe symphysis is rarelymentioned.This may be because genio-
plasties are frequently done in conjunc-tion with other osteotomies,whichmakes the
attribution ofvarious compli-cations difficult.Most ofthe literatureconcerning
genioplasties concentrates onthe soft tissue response to the
skeletalmovement.Reports ofrelapse after genioplastiesare sparse and
conflicting.Some cliniciansreport that there is essentially no relapseafter a
genioplasty,with a rounding ofthesharp corners ofthe advanced segmentoccurring with
time.222�225These studies,however,follow patients for only up to 1 year.Two other
studies with follow-up ofat least 1 year do seem to show some insta-bility ofthe
skeletal advancement.226,227Themean relapse with a genial advancementvaries widely
(2.6 to 30%).The one seem-ingly consistent finding is that much oftheskeletal
relapse occurs within the first year.As with stability studies ofotherosteotomies
there exists a large variation inindividual relapse,and no attempt has beenmade to
identify the causes.However,thereare probably many factors involved,includ-ing the
magnitude ofadvancement.Therehave been no studies in the stability ofthissurgery in
correction ofother symphysealdeformities.Martinez and colleagues foundthat
regeneration ofthe cortical thicknessofthe symphysis was significantly better
inpatients younger than 15 years ofage.224They suggested that this may be
beneficial iffurther surgical advancement ofthe chin isto be considered.The
predictable possibility ofsensoryloss from this procedure has not been ade-quately
evaluated.In one study it was notedthat postsurgical sensory loss was found inall
patients but was temporary,with normalsensation returning within 12
months.228Another study reported a 3.5% long-termincidence ofsensory deficits
followinggenioplasties.Other complications such asbone loss and infections have
been reported,but small samples preclude any definitivestatements on
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consecutivecases.Br J Oral Maxillofac Surg 1995;33:231.200.Acebal-Bianco
F,Vuylsteke PL,MommaertsMY,De Clercq CA.Perioperative complica-tions in corrective
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surgical correction.St Louis (MO):C.V.Mosby;1986.202.Beke AL,Yahner VB.Surgical
correction ofoverbite and overjet with sagittal osteotomyofthe mandibular
horizontal ramus:reportofcase.J Oral Surg 1969;27:358.
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ofmalunitededentulous mandibular fractures.J Max-illofac Surg 1982;10:18.204.Sandor
GK,Stoelinga PJ,Tideman H.Reap-praisal ofthe mandibular step osteotomy.JOral
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mandibular bodyfor correction ofprognathism.J Oral Surg1978;36:361.207.Kavanaugh
SH.Maxillary midline split surgery[dissertation].Department ofOrthodon-
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segmentalalveolar osteotomy.J Oral Surg 1978;36:454.209.MacIntosh RB,Carlotti
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ofclass III malocclusion by combined sagittalramus and subapical body
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sequelaeafter anterior segmental osteotomies.OralSurg Oral Med Oral Pathol
1976;41:139.212.Pangrazio-Kulbersh V,MacIntosh RB.Totalmandibular alveolar
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in a primate model.J Maxillofac Surg 1977;5:39.215.Scheideman GB,Kawamura H,Finn
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after subapical osteotomy.J OralSurg 1969;27:256.217.Converse JM,Wood-Smith
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(genioplasty).Oral Surg1975;39:522.220.Hinds EC,Kent JN.Genioplasty:the
versatilityofhorizontal osteotomy.JOral Surg1969;27:690.221.Precious DS,Armstrong
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WR.Osseousremodeling after inferior border osteotomyfor chin augmentation:an
indication for earlysurgery.J Oral Maxillofac Surg 1999;57:1175.225.Talebzadeh
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with reference toresorption and the hinge sliding osteotomy.Int J Oral Surg
1974;3:247.227.McDonnell JP,McNeill RW,West RA.Advance-ment genioplasty:a
retrospective cephalo-metric analysis ofosseous and soft tissuechanges.J Oral Surg
1977;35:640.228.Hohl TH,Epker BN.Microgenia:a study oftreatment results,with
surgical recommen-dations.Oral Surg Oral Med Oral Pathol1976;41:545.229.Nishioka
GJ,Mason M,Van Sickels JE.Neu-rosensory disturbance associated with theanterior
mandibular horizontal osteotomy.J Oral Maxillofac Surg 1988;46:107.1178Part 8:
Orthognathic Surgery
CHAPTER 57Maxillary Orthognathic SurgeryVincent J.Perciaccante,DDS Robert
A.Bays,DDSHistoryOrthognathic surgery ofthe maxilla wasfirst described in 1859 by
von Langenbeckfor the removal ofnasopharyngealpolyps.1The first American report
ofamaxillary osteotomy was by Cheever in1867 for the treatment ofcomplete
nasalobstruction secondary to recurrent epis-taxis for which a right
hemimaxillarydown-fracture was used.2Over the next 70 years numerous authors
describedosteotomy techniques that mobilized theentire maxilla for the treatment
ofpatho-logic processes.In 1901 Le Fort published his classicdescription ofthe
natural planes ofmaxil-lary fracture.3In 1927 Wassmund firstdescribed the Le Fort I
osteotomy for thecorrection ofmidface deformities.4How-ever,total mobilization
ofthe maxilla withimmediate repositioning was not per-formed until 1934 by
Axhausen.5Separa-tion ofthe pterygomaxillary junction wasadvocated by Schuchardt in
1942.6Mooreand Ward in 1949 recommended horizon-tal transection ofthe pterygoid
plates foradvancement.7Willmar reported on over40 cases treated this way and
ofseverebleeding in most,thereby abandoning thisprocedure in favor ofseparation at
thepterygomaxillary junction.8Most ofthesetechniques simply mobilized the maxillato
one degree or another,and then placedorthopedic forces on it to achieve thedesired
repositioning�a sort ofuninten-tional distraction osteogenesis.Thesemethods were
associated with high levelsofrelapse.In 1965 Obwegeser suggested com-plete
mobilization ofthe maxilla so thatrepositioning could be accomplishedwithout
tension.9This proved to be amajor advance in stabilization,as docu-mented by
Hogemann and Willmar,deHaller,and Perko,respectively.10�12Anterior segmentalization
ofthe max-illa was also addressed in the early descrip-tions,including those by
Wassmund,byCohn-Stock,and by Spanier.4,13,14Again,complete mobilization ofthe
maxilla withvascular compromise was avoided,andmultiple segments contributed to
poorstability.Cupar,Kole,and Wunderer,respectively,reported more direct
surgicalaccess to these procedures with improvedmobilization and maintenance
ofbloodsupply.15�18Posterior segmentalization ofthe maxilla was used by Schuchardt
but ithad limited stability also owing to incom-plete mobilization.19Kufner
improved onthis technique by completely mobilizingthe osteotomized segment prior to
reposi-tioning.20Logically,anterior and posteriorsegmental osteotomies were
combined toaccomplish total maxillary alveolarosteotomy for repositioning and
segmen-tal manipulation simultaneously.21,22Sev-eral forms oftotal maxillary
osteotomieswere described by Cupar,Converse andShapiro,and
Kole,respectively.15,23,24Will-mar further established the stability oftheLe Fort I
osteotomy,and Bell and col-leagues documented the overall superiori-ty ofthe total
down-fracture Le Fort Iosteotomy for segmental and one-piecemaxillary
osteotomy.8,25Bone grafting toenhance stabilization was advocated byCupar,Gillies
and Rowe,and Obwegeser,respectively,who first advocated graftingin the
pterygomaxillary fissure.15,16,26,27Interestingly,Willmar did not find a dif-
ference in stability with and without bonegrafting in nonclefted cases.8Early
descriptions ofthe rigid fixationofmaxillary osteotomies were published byMichelet
and colleagues in 1973,Horster in1980,Drommer and Luhr in 1981,andLuyk and Ward-
Booth in 1985.28�31Sincethat time,many methods have been advo-cated for the rigid
fixation ofmaxillaryosteotomies.These have included boneplates,metallic
mesh,pins,the rigid ad-justable pin (RAP) system,and resorbablefixation.32�34Since
these landmark papers,volumes have been written regarding awide variety oftechnical
factors,many ofwhich reflect operator preference.Basic PrinciplesMaxillary
deformities may manifest in anyofthe three planes ofspace:sagittal,axial,and
coronal.Patients displaying abnormal
1180Part 8: Orthognathic Surgeryfacial anatomy often exhibit elements ofmaxillary
and mandibular deformities.Therefore,the clinician must recognizeand be prepared to
treat maxillary andmidface deformities.Subjectively,patientswith maxillary
deformities often describetheir problem in terms ofthe relativemandibular
appearance.Patient expecta-tions clearly demonstrate the importanceofthe chin in
patient satisfaction.35Thisperceptual preoccupation with apparentmandibular excess
or deficiency in theabsence ofa significant absolute mandibu-lar abnormality may
necessitate extensiveconsultation and guidance from the sur-geon to assist the
patient in recognition ofthe contribution made by the midface andmaxilla to overall
facial appearance.Simi-larly the patient may relate the importanceofnasal
prominence or deficiency indescribing his or her chiefcomplaint.Scrutiny ofphysical
characteristics,model surgery,and cephalometric analysiswith prediction tracings
will assist inobtaining a satisfactory treatment plan.These important diagnostic
and treatmentplanning modalities are discussed exten-sively elsewhere in the
text;however,model surgery is the most valuable tool inpreparing for orthognathic
correction ofskeletal facial deformities.While modelsurgery is essential for
immediate preoper-ative surgical simulation and splint con-struction,it may be even
more importantin early treatment planning.Prior to anyorthodontic or surgical
treatment,modelsurgery is the best method to determinethe postoperative position
ofthe mandibleas well as the maxilla.No cephalometricprediction (computer generated
or handdrawn) or photographic manipulation canreveal all ofthe three-dimensional
andocclusal information gleaned from accu-rate model surgery.In the
pretreatmentstate the teeth may not fit together perfect-ly during this preliminary
model surgery,but orthodontics can be simulated to per-mit an accurate projection
ofthe specificmovements required ofthe maxilla andmandible to achieve the desired
results.The model measurements made at thetime ofthis exercise should be exactly
thesame as those used for the actual preoper-ative model surgery (see
below).Pretreat-ment model surgery is essential when con-templating maxillary
surgery alone andvery useful when planning two-jawsurgery.Pretreatment model
surgery per-mits the three-dimensionalevaluation ofthe maxilla and the
mandible,whether themandible is autorotated without surgeryor also
osteotomized.Model Surgery,ReferenceMarks,and Intraoperative PositioningThe
purposes ofpreoperative modelsurgery are to (1) mark the models tofacilitate three-
dimensional measurementofthe pre- and postoperative positioning;(2) place the jaw
models into the desiredpositions based on all ofthe databaseincluding three-
dimensional clinicalassessment (the most important),radi-ographic analysis,model
studies andpatient desires;(3) evaluate the feasibilityofthe planned surgical moves
using themeasurements and make necessary adjust-ments;(4) determine the vertical
changethat will be achieved at the time ofsurgeryin such a way that it can be
accuratelyduplicated intraoperatively;and (5) con-struct the surgical splint(s).The
following method has been usedsuccessfully for over 20 years by the seniorauthor
(RAB).The technique is based onthree simple principles:1.A measurement is made from
a pointabove the osteotomy to a point belowit at model surgery and intraopera-
tively.After the maxilla is moved thesame superior point is used but thepoint on
the maxilla has been movedalong a predetermined plane.This cre-ates a triangle
defined by one superiorpoint and two inferior points (pre-and postoperatively).This
triangle canbe measured accurately on modelsand on the patient at surgery.2.Central
incisor vertical measurementscan be made directly on the models.3.Ifthe
measurements made on themodels and at surgery have the samepre- and postoperative
differences,theincisor vertical will be correct.Centric relation mounted models
aremarked to record all possible surgicalmovements anteriorly and
posteriorly(Figure 57-1).For the purpose ofillustra-tion Figure 57-1A and B
demonstrate themeasurements that are necessary for intra-operative control ofthe
vertical positionofthe maxilla.The vertical measurementsat the maxillary canines
and first molarsare the critical ones for use intraoperative-ly (see Figure 57-
1C).The bilateral verticalmeasurements must be made from stablepoints on the top
ofthe mounting ring,not just anywhere along the mountingring (points A and P) to
cusp tips.Gingi-val cuffs will be used intraoperatively (Fig-ure 57-2) on the
canines (point B) andfirst molars (point C).The maxillarymodel is then moved to the
desired posi-tion,including vertical.The measurementofthe vertical position ofthe
incisor ismade by placing the Boley gauge flat onthe top ofthe mounting ring
(parallel tothe Frankfort horizontal) to the tip oftheincisor (see Figure 57-
1D).This verticalmeasurement ofthe maxillary centralincisor is constantly
controlled while themaxilla is positioned in all other planes ofspace (see Figure
57-2A).After the maxil-lary model has been fixed in the properposition,an imaginary
triangle is createdby points A,B,and B'and by points P,C,and C'.The lines A�B and
P�C are the pre-operative vertical values and the lines A�B'and P�C'are the
hypotenuses ofthe trian-gles and the postoperative vertical values(see Figure 57-
2B).The differencesbetween lines A�B and A�B'and lines P�Cand P�C'are the important
values.Theabsolute numbers are not.
Maxillary Orthognathic Surgery1181Intraoperatively marks are madeabove the proposed
osteotomy sites in thepiriform rims and the first molar/buttressareas (points A and
P) (see Figure 57-2C).Measurements are made from point A tothe gingival cuffofthe
canine (point B)and from point P to the first molar (pointC).The gingival cuffs are
used because thecusps will be hidden under the splint andthe brackets may come
loose duringsurgery.During maxillary positioning,lines A�B'and P�C'can be measured
untilthe difference between lines A�B and A�B'and lines P�C and P�C'are as
predicted bythe models (see Figures 57-2D and E).When this is accomplished the
anteriorvertical changes ofthe central incisors willbe as they were on the
models,so that nodirect measurement ofincisors is neces-sary.Usually the maxilla is
repositionedanteroposteriorly and sometimes medio-laterally as it is moving
vertically.Thismethod ofmeasurement is especiallyimportant when large
anteroposterior ormediolateral moves are included.Our experience and that ofothers
hasshown that external reference marks addnothing to the accuracy ofvertical maxil-
lary positioning ifthe internal referencemethod is as outlined above.36,37Surgical
AnatomyOsseous StructuresThe body ofthe maxilla contains themaxillary sinus in its
entirety,exceptrarely when the apex extends into thezygomatic bone.38The anterior
surface ofthe maxilla is the anterolateral wall ofthesinus.The infraorbital foramen
is locatedat variable distances below the inferiororbital rim.Continuing inferiorly
is theFIGURE57-1A,Mounted models marked for orthognathic surgery with vertical
preoperative values recorded.B,Frontal view shows mid-line markings that can be
seen on either side ofthe pin when it is placed.C,Straight-line measurements are
made from pointsA toB andpointsP to Con each side.D,Maxillary central incisor is
measured perpendicular to the Frankfort horizontal,which is from the top
ofthemounting ring.(Note: This is not a straight point-to-point measurement,but a
perpendicular to Frankfort one.)ABCD
1182Part 8: Orthognathic Surgerycanine fossa lateral to the canine tooth.The
anterior alveolar process ofeachmaxilla surrounds the piriform aperture,and they
unite in the midline to form theanterior nasal spine.This bony spine isthe most
anterior and inferior attach-ment for the mobile anterior cartilagi-nous nasal
septum.An elevated sharpcrest at the junction ofthe anterior andnasal surfaces
ofthe maxilla,whichforms the nasal floor,inclines this struc-ture superiorly at the
aperture.The bodyofthe maxilla and its frontal processform the superolateral
boundary ofthepiriform aperture as a thin edge ofbone(Figure 57-3).In the midline
the nasal crest ofthemaxilla articulates with the septal or quad-rangular cartilage
and vomer.39,40The septalcartilage rests in a central groove,whichextends posterior
to the anterior nasal spine.This articulation is flexible but strengthenedby the
perichondrium-periosteum continu-ity and interposed connective tissue.In themidline
at the junction ofthe maxilla andthe premaxilla is the incisive
fossa,whichtypically presents the openings offourcanals through which the
nasopalatinearteries and nerves are conducted.The palate is formed by the
palatineprocess ofthe two maxillas and the hori-zontal lamina ofthe palatine
bones.41Thetransverse suture between the maxilla andpalatine bones lies roughly 1
cm anteriorto the posterior margin ofthe hard palate.At its lateral extent the
suture widens intothe greater palatine foramen,which isapproximately 1 cm
posteromedial to thesecond molar (Figure 57-4).PACBLine P�CLine A�BLine P�C'Line
A�B'FIGURE57-2A,Maxillary model has been moved into desired position including
vertical.Maxillary incisor is again measured perpendicular to the
Frankforthorizontal (ie,from the top ofthe mounting ring).B,Straight line
measurements are made from points A to B'and P to C'bilaterally.C,At surgery,slots
are madein the piriform rim and holes in the buttress to simulate pointsA andP
bilaterally.The gingival cuffs ofthe canines and first molars represent points B
and C.D,Following mobilization ofthe maxilla it is placed so that the
differencesbetween lines A�B and A�B'are the same as they were on the models.Lines
P�C andP�C'can be used similarly.Note: Ifthis is done precisely,the vertical change
at the central incisors will be the same as it was on the models so that there is
no needto make a direct measurement ofthe centrals.E,Illustration ofmeasurement
method at surgery.ABCDE
Maxillary Orthognathic Surgery1183The greater palatine canal is formedsimilarly
between the perpendicular lami-nae ofthe palatine and maxillary bones,which form
the inferior lateral nasal wall.The inferior nasal concha also articulateswith the
maxillary and palatine compo-nents ofthe lateral nasal wall.Posterolaterally the
maxillary tuberos-ity is behind the third molar.Above thistuberosity the posterior
superior alveolarforamina may be observed through whichthe nerves and vessels
emerge.The pyra-midal process ofthe palatine bone unitesthe two pterygoid plates
ofthe sphenoidbone with each other and to the maxilla.The pterygomaxillary
junction,formed bythe palatine bone,ends superiorly in thepterygomaxillary fissure
leading into thepterygopalatine fossa.42,43The foramenrotundum enters the posterior
wall ofthepterygopalatine fossa and the pterygoid orvidian canal.Medially the
sphenopalatineforamen leads to the lateral nasal cavityposterior to the middle
nasal concha oftheethmoid bone.Anteriorly the infraorbitaland zygomatic nerves and
infraorbital ves-sels run in the infraorbital canal,and infe-riorly the descending
palatine artery andgreater palatine nerves course within thegreater palatine
canal.Vascular StructuresAlthough numerous texts describe theanatomy ofthe intact
maxilla,severalaspects ofmaxillary blood flow remain indoubt following maxillary
osteotomy.The Le Fort I maxillary osteotomy hadbeen performed for over 100 years
beforeBell first identified the exact nature ofblood vessels in the osteotomized
max-illa,which provided information regard-ing the viability to the pedicled maxil-
la.44,45It was obvious that even thoughthe direct blood supply to the
maxillaryteeth and periodontium was interrupted,collateral circulation existed to
perfusethe dental pulp and surrounding struc-tures (Figures 57-5 and 57-6).This
samecirculation was also responsible for thesurvival ofthe rest ofthe
maxilla;howev-er,the exact nature ofthe various factorsaffecting maxillary
perfusion is still notwell documented or understood.Bell�sstudies revealed that
saving the descend-ing palatine arteries made little differ-ence,indicating that a
collateral vas-culature existed,probably from the softpalate,which was adequate for
maxillaryperfusion.The down-fractured maxillahas a rich blood supply via the
ascendingpharyngeal artery and the ascendingpalatine branch ofthe facial
artery.46Bell also verified the revascularizationofanterior maxillary osteotomies
usingthe microangiographic technique.45Brusati and Bottoli performed revascular-
ization studies similar to those ofBell andfound quite different results.47They
foundthe tunneling technique to be superior inmaintaining the blood
supply,especially tothe pulpal tissues,when compared withthe labial pedicled
anterior maxillary pro-cedures.17,18This was just the oppositefrom the findings
ofBell.45A possibleexplanation for this discrepancy is thatBell used monkeys
whereas Brusati andBottoli used dogs,which they claimed pos-sess a more similar
maxillary vasculatureto that ofthe human.48The clinical signif-icance ofthese
differences is not clear tothis day.Revascularization does not necessarilyrepresent
blood flow,and therefore Nelsonand colleagues used a radioactive micro-sphere
technique to evaluate maxillaryblood flow.49Unfortunately several vari-ables were
present in this study that makeinterpretation difficult.In none oftheabove-
mentioned studies were the maxillasmoved to a new position,which may rep-resent the
largest insult to the blood supplyat the time ofactual maxillary
osteotomy.Additionally,in Nelson�s study,severance ofthe descending palatine
vessels was inadver-tent and no ligation was performed.49Thisallowed bleeding to
occur through the lacer-ated vessels and prevented a pressure
headInferiorturbinateAnterior superioralveolarvesselsIncisivecanal
withnasopalatinevesselsFIGURE57-3Cross-sectional anatomy ofthemaxilla at the
piriform rim.Infraorbital
nervePterygopalatinenervesSphenopalatinearteryPterygopalatineganglionVomerDescendin
gpalatine arteryHorizontal plateof palatine bonePterygoid platesFIGURE57-4Cross-
sectional anatomy at thepterygomaxillary junction.Note the position ofthegreater
palatine foramen and perpendicular plateofthe palatine
bone.NasopalantinearteryDescendingpalantine artery Lesser palantineartery Greater
palantineartery Maxillary artery Ascendingpharyngeal artery Ascendingpalatine
artery Facial artery External carotidartery FIGURE57-5Pathway ofthe ascending pala-
tine,ascending pharyngeal,and descendingpalatine arteries as they continue into the
greaterpalatine arteries.
1184Part 8: Orthognathic Surgeryfrom developing to maintain distal flow tothe
anterior maxilla.Also there were largedifferences in the preoperative
microspherevalues between animals such that postoper-ative comparisons were
impossible.In otherstudies involving anterior maxillaryosteotomies,Nelson and
colleagues foundno significant differences among three dif-ferent techniques that
were similar to theones described by Brusati and Bottoli,plus athird procedure
using only a palatal pedi-cle.47,50Although no statistical differencewas seen,the
palatal flap seemed to beslightly superior to the others.Again thesame problems
existed with this study asbefore,rendering conclusions impossible.Soft Tissue
Envelope ofthe MaxillaThe midfacial superficial fascia or subcu-taneous tissue
contains a variable amountofadipose tissue with the muscles offacialexpression in
its deep layer.This is tightlybound to bone except adjacent to the buc-cal fat pad
and in the lower eyelids.Hollinshead divided the mimetic or facialmuscles into five
chiefgroups concerningthe mouth,nose,orbit,ear,and scalp.42Ofconcern to the present
discussion are themuscles ofthe mouth and nose,which areinnervated at their
posterior inferioraspect by the facial nerve.They insert intothe skin and most
arise from periosteumofthe facial skeleton.The upper oral group ofmuscles radi-ates
from their insertions near the cornerofthe labial commissure.From a horizon-tal to
vertical orientation and inferior tosuperior the risorius,zygomaticus majorand
minor,and the levators (levator labiisuperioris alaeque nasi) insert and blendwith
the skin and orbicularis oris.Therisorius does not arise from bone but orig-inates
from the superficial fascia over theparotid gland.The risorius,zygomaticusmajor,and
zygomaticus minor elevate andretract the corner ofthe mouth and
upperliplaterally.The superficial levator mus-cles and a third deeper one,the
levatoranguli oris,elevate the lateral upper lip.Inaddition the levator labii
superiorisalaeque nasi attaches to the skin andgreater alar cartilage ofthe
nose,thus lift-ing the ala and widening the naris.The orbicularis oris is composed
ofmany multidirectional fiber groups thatblend with other surrounding facial mus-
cles,encircle the mouth,originate fromperiosteum covering the roots ofthecanine
teeth,insert laterally at the cornerofthe mouth,and pass at right angles tothe
encircling sphincter fillers connectingskin to labial mucosa.This diverse
muscledraws the lips together,purses the lips,presses the lips against the
teeth,and pullsthe corners ofthe lips inward.The buccinator arises from themandible
and maxilla and the pterygo-mandibular raphe,by which it is separatedfrom the
superior pharyngeal constrictor.The fibers pass forward and slightly inferi-orly to
blend with the orbicularis oris andattach to the mucosa and skin ofthe
labialregion.The buccinator flattens the cheekagainst the teeth.Both Lightoller and
Nairn placeemphasis on the modiolus,which is thepoint at the lateral aspect and
just superi-or to the corner ofthe mouth where mus-cles ofthe oral group ofthe
mimetic mus-cles converge.51,52The orbicularis oris andbuccinator joined at the
modiolus form acontinuous muscular sheet on either sideofthe midline.The
zygomaticus major,levator anguli oris,and depressor angulioris (as a group referred
to as �modiolarstays�) immobilize the modiolus in anyposition.Additionally the
marginal andperipheral parts ofthe orbicularis orismuscle are distinguished.The
peripheralaspect ofthe muscle lies parallel with theinner labial mucosal
surface,and the mar-ginal part curls outward following the ver-milion surface.As
tension is expressed inthe orbicularis oris,the marginal aspect ofthe muscle is
thought to straighten anddecrease vermilion exposure,therebypulling the upper and
lower lips towardeach other and against the dentition.The nasal group offacial
musclesdilates and compresses the nares.Thenasalis arises from the maxilla lateral
andinferior to the ala.The transverse portionunites with the contralateral muscle
overthe dorsum ofthe nose.The alar partinserts into the greater alar
cartilage.Thus,the two parts compress and dilate the nasalapertures
respectively.The depressor septimuscle lies beneath the orbicularis oris
andattaches to the base ofthe columella andposterior ala.Its action narrows the
naris.The posterior and anterior dilator musclesare intrinsic muscles ofthe nose
thatcourse from the alar cartilages to the mar-gin ofthe pads.The nasal
mucoperiosteumis firmly fixed to the elevated piriform rimabove the floor ofthe
nose,to the lateralmargin ofthe nasal aperture and the ante-rior nasal spine.The
premaxillary wingsthat flare laterally from the anterior mid-line nasal crest
provide an irregular attach-ment ofthe mucoperiosteum along theinferoanterior nasal
floor.The palate is covered by mucosa firm-ly adherent to the periosteum and
contain-ing mucous minor salivary glands.Themucosa is thin in the central palate
andFIGURE57-6Soft palatal,ascending pharyngeal,and ascending palatal vessels
anastomose with thegreater palatine artery.Major vessels have beensectioned and
tied.The arrows signify direction ofblood flow.
Maxillary Orthognathic Surgery1185thickens toward the alveolar process.Thepalatine
crest is a transverse elevation atthe posterior border ofthe horizontal plateofthe
palatine bone that gives attachmentto the tensor veli palatini muscle.The larg-er
lateral pterygoid plate is the origin oftheinferior head ofthe lateral and the
medialpterygoid muscles.A small part ofthemedial pterygoid also arises from the
max-illary tuberosity.The tensor veli palatinimuscle curves around the
hamulus,whichis the inferior end ofthe medial pterygoidplate.From the hamulus the
tensor muscleofthe palate enters the soft palatal tissues.The tensor aponeurosis is
an adherent con-nective tissue sheath continuous with theperiosteum,which covers
the posteriorhard palate attaching laterally to the sub-mucosal layer ofthe pharynx
and the ten-sor veli palatini tendon.Surgical TechniquesSoft Tissue Incision and
Surgical Exposure ofthe Maxilla Exposure ofthe anterior,lateral,andpterygomaxillary
regions is most com-monly achieved by incising horizontallythrough the buccolabial
mucoperiosteumabove the attached gingival margin at thelevel ofthe maxillary teeth
apices (Figure57-7A).The vestibular incision coursesfrom the first molar to the
contralateralfirst molar (Figure 57-7B).The parotidpapilla is identified and
retracted supero-laterally during completion ofthe incisionposteriorly.The incision
can be made withelectrocautery or steel as there have beenno studies performed that
show a differ-ence between the two.After initial pene-tration ofthe mucosa the
natural tenden-cy to cut more superiorly with deeperpenetration must be
avoided.This is par-ticularly important in the incisor area,asthis would carry one
into the nasal cavity.The superior tissues are reflected sub-periosteally,first at
the piriform aperturemargins (Figure 57-7C).Progressivelymore superior exposure
lateral to the nasalaperture will expose the infraorbital nerveexiting from its
foramen.Posterior reflec-tion proceeding from the delineated infra-orbital foramen
reveals the zygomatico-maxillary suture,zygomatic buttress,andthe most anterior
aspect ofthe zygomaticarch.Inferiorly,with subperiosteal tunnel-ing,the lateral
aspect ofthe maxillarytuberosity and its junction with palatinebone and pterygoid
plates ofthe sphenoidbone are identified.Care should be takento direct this
subperiosteal dissection infe-riorly,toward the mucogingival junction,as it is
carried back toward the pterygo-maxillary fissure,to avoid vascular struc-
tures.Meticulous maintenance ofthe sub-periosteal plane ofdissection will
preventtroublesome exposure ofbuccal fat padtissue,which impairs visualization
andretraction ofsoft tissue during subsequentosseous surgery.A retractor with a
curvi-linear end is placed in the pterygomaxil-lary junction to facilitate
exposure.Atten-tion should be paid to the placement ofthis retractor,as it too can
be responsiblefor periosteal rents and exposure ofthebuccal fat.Tissues inferior to
the horizontal inci-sion are elevated minimally.In areas ofinterdental osteotomies
for segmentaliza-tion ofthe maxillary arch the inferiorattached gingiva and
periosteum are elevat-ed conservatively,with a Woodson elevator,while retraction
laterally is provided by skinhooks (Figure 57-8A).Since the alveolarosteotomy will
be accomplished with thinosteotomes,osseous exposure requirementsat the alveolar
crest level are minimal.When intersegmental movement willbe great and may result in
tearing ofthegingival papilla,an alternative approach tothe interdental region may
be used.Addi-tionally a wider exposure ofalveolar boneis frequently needed when an
osteotomy isto be performed in an edentulous orextraction space.In these situations
a ver-tical mucosal incision at the line angle,one-tooth distant from the ostectomy
site(Figure 57-8B),will facilitate wider expo-sure for osseous procedures.This
incisionshould be used only when an anterior labi-al pedicle is maintained to
maximize thelabial vascular pedicle during multiseg-mental
osteotomy.HighLowFIGURE57-7A,The soft tissue incision formaxillary surgery.B,The
circumvestibular in-cision extends from thearea ofthe first molar tothe same
location on the opposite side.C,Thenasal mucosa is elevated beginning on
theAsuperolateral surface ofthe piriform rim.BC
1186Part 8: Orthognathic SurgeryFor one-,two-,and most routinethree-piece maxillary
osteotomies,a cir-cumvestibular incision with minimalinterdental exposure is
preferred.Forthree-piece maxillary osteotomies thatinvolve exceptionally wide
expansion orextreme changes at the interdental site,four-piece maxillary
osteotomies,andosteotomies in some ex-cleft patients,softtissue incisions can be
modified from sec-ond molar to first premolar to maintain ananterior labial pedicle
(Figure 57-9).Amidline vertical incision is placed to gainaccess to the midline
ofthe maxilla.Once the labial incisions are complet-ed the nasal mucoperiosteum is
elevated tocomplete soft tissue exposure oftheosseous surgical site (see Figure 57-
7C).Initial establishment ofa subperiostealdissection plane is imperative for
comple-tion ofnasal tissue dissection without dis-ruption ofmucoperiosteal
integrity.Because the nasal cavity is more volumi-nous inside the piriform rim than
at thepiriform aperture,the elevator should beheld at an oblique angle to the
surround-ing maxillary bone adjacent to the nasalaperture.While maintaining the
elevatortip against bone,the mucoperiosteum isreflected from the nasal
floor,lateral nasalwall,and nasal crest ofthe maxilla.Thedissection should continue
superiorly for acentimeter up the vertical nasal walls toprevent tearing during
osteotomy ordown-fracture ofthe maxilla,particularlyat the superior reflections
ofthe nasalfloor medially and laterally.Theanteroposterior depth ofthis soft
tissuedissection is approximately 15 to 20 mm.The remaining posterior soft tissue
isreflected more precisely after initial down-fracture ofthe maxilla.Osseous
SurgeryAfter recording the reference measure-ments as outlined earlier (see Figure
57-2),the osteotomy is performed.The design ofthe osteotomy will depend on the
maxil-lary movement desired.Regardless ofthedesign ofthe osteotomy the
measurementmarks are used as illustrated in Figure 57-2.Initially the basic
horizontal osteotomywill be discussed and then alterations willbe described for
specific situations.Seg-mentalizationofthe maxilla may be neces-sary in certain
cases.Specifics ofthis pro-cedure will be discussed at the end ofthebasic
horizontal technique.The lateralmaxillary osteotomy (Figure 57-10) isstarted at the
greatest convexity ofthezygomatic buttress because that is the eas-iest starting
surface for the reciprocatingsaw.It is advanced anteriorly through thelateral
piriform rim below the inferiorturbinate while the nasal mucoperiosteumis retracted
and protected using aperiosteal elevator.For the basic maxillaryosteotomy this
horizontal osteotomy isparallel to the maxillary arch wire approx-imately
coincident with the cut performedpreviously during model surgery.After theanterior
osteotomy is completed,it is con-tinued posteriorly by tapering inferiorlytoward
the pterygomaxillary junction.Athin reciprocating saw blade and copiousirrigation
are used for this osseous cut.The most posterior centimeter or so ofthelateral wall
can be cut with the same saw,but from inside out (Figure 57-11).Next a nasal septal
osteotome isdirected slightly downward and posterior(Figure 57-12) beginning just
above theanterior nasal spine while the anteriornasal mucoperiosteum is
retracted.Pro-ceeding posteriorly the osteotome is care-fully maintained in the
midline.The ten-dency toward superior deviation whileseparating the cartilaginous
and vomerineseptum from the nasal crest ofthe maxillaFIGURE57-8Ifsegmentalization
is necessary,itis best to perform interdental osteotomies beforehorizontal
osteotomies and down-fracture.A,Minimal exposure technique for
interdentalosteotomies.B,Vertical incision for interdentalosteotomies.ABFIGURE57-
9Bilateral vestibular incisions aremade from the first premolar to the secondmolar;
shown with a midline vertical incision.
Maxillary Orthognathic Surgery1187necessitates maintenance ofa slightdownward
inclination ofthe septalosteotome.The lateral nasal wall is sev-ered using a thin
osteotome directed pos-teriorly while medial retraction ofthenasal mucoperiosteum
is accomplishedwith a periosteal elevator.The osteotomeis gently malleted
posteriorly for a dis-tance ofapproximately 20 mm to avoidpremature injury to the
descending pala-tine neurovascular bundle that resides inthe lateral posterior
nasal wall.After the above osteotomies havebeen performed,the pterygoid plates
areseparated from the maxillary tuberosity(Figure 57-13) using a small sharpcurved
osteotome.This instrument ispreferred over the traditional thickpterygomaxillary
osteotome because thethin cutting edge limits fracture and pro-motes precise
division ofthis bony junc-tion.53The tip ofthe osteotome is di-rected as
anteriorly,inferiorly,andmedially as the tunneled buccal soft tis-sue allows.A
finger placed palatal andposterior to the maxillary tuberosity willfacilitate early
verification ofthe com-plete separation ofbone while avoidingtrauma to the palatal
vascular pedicle.The authors prefer to have this instru-ment sharpened before each
case.Downward pressure is placed on theanterior maxilla using the sharp hooks
ofaSenn retractor to facilitate initial down-fracture ofthe maxilla (Figure 57-
14).Ifmoderate pressure does not result inmobilization ofthe inferior
segment,thecompleteness ofthe above osteotomiesmust be suspect.The cement
spatulaosteotome is used to ensure completebony severance ofthe anterior lateral
nasalwall and zygomaticomaxillary portions ofthe osteotomy.The curved osteotome
isagain placed into the pterygomaxillaryjunction,malleted gently,and thentorqued to
mobilize the maxilla.Ifno sig-nificant movement is detected,then theosteotome may
be stepped slightly superi-orly,directed anteriorly,and malleted untilthe
separation is complete.When mobility occurs the nasalmucoperiosteum is elevated
progressivelymore posteriorly until the posterior edgeofthe hard palate is
encountered (see Fig-ure 57-14).Portions ofthe pterygoidplates or perpendicular
process ofthepalatine bone that resist fracture may becompletely separated from the
maxillausing an osteotome under direct visualiza-tion (Figure 57-15).The descending
pala-tine neurovascular bundle is isolated,lig-ated,and divided.Significant
movement ofthe posteriormaxilla can cause tensile forces on thedescending palatine
neurovascular compo-nents.Superior repositioning ofthe maxillamay also compress the
exposed vessels andnerve between the inferior and superiorosseous segments.Severe
postoperativebleeding after Le Fort I maxillary osteotomyhas been
reported.54�57Attempts to preservethe neurovascular bundle may increase
thispossibility.Ligation and division ofthisstructure has been shown to have no
delete-rious influence on perfusion or neuro-sensory function.58,59The bone ofthe
per-pendicular plate ofthe palatine bonesurrounding the neurovascular bundle
isFIGURE57-10Lateral wall osteotomy is begunat greatest convexity ofthe buttress
and broughtforward to the piriform rim with a periosteal ele-vator protecting the
nasal mucosa and the endo-tracheal tube.FIGURE57-11The saw is then turned insideout
and the osteotomy from the buttress to thepterygomaxillary junction is made
anglingdownward as it goes posteriorly.FIGURE57-12Separation ofthe nasal septumfrom
the septal crest ofthe maxilla with a specialosteotome.FIGURE57-13Pterygomaxillary
separation witha small sharp curved osteotome directed medially.
1188Part 8: Orthognathic Surgerycarefully removed using a Woodson eleva-
tor,burs,and rongeurs,and the neurovascu-lar bundle is ligated and divided (see
Figure57-15).After down-fracture,completemobilization ofthe maxilla is the
nextobjective.A Jstripper normally used forperiosteal elevation in sagittal
osteotomiesengages the posterior border ofthe midlinenasal floor at the posterior
nasal spine (Fig-ure 57-16),and anterolateral pressure isexerted to progressively
increase mobility ofthe maxilla.The goal ofthese maneuvers isto move the maxilla
into the approximatefinal position with only gentle digital pres-sure.After
mobilization from the cranialbase is completed,a reassessment ofthe sur-gical move
is considered.Based on themovement planned any possible bony inter-ferences
posterior to the second molar mustbe removed before application ofmaxillo-
mandibular fixation (MMF).When all pos-sible interferences posterior to the
secondmolar have been removed,the maxilla iswired to the mandible with the
occlusalsplint interposed.We prefer to have the patient com-pletely paralyzed
during the period ofmaxillary positioning.Condylar position-ing while rotating the
maxilla andmandible is paramount to success.Thephysiologic position ofthe condyles
isthought to be a superoanterior orienta-tion relative to the glenoid fossae
againstthe posterior slopes ofthe articular emi-nences,with the disk interposed
betweenthe condyle and the fossa.The surgeonmust position the condyles ofthe
maxillo-mandibular complex in this upward andforward direction prior to
autorotation(Figure 57-17).The importance ofthisstage ofthe surgery cannot be
overesti-mated.The most likely points ofunrecog-nized bony interferences are in the
areasofthe pterygoid plates,the maxillarytuberosities,and the perpendicular
plateofthe palatine bone.It is quite possible torotate the maxillomandibular
complexinappropriately while being unaware ofapremature pivot point in these
posteriorbony areas (Figure 57-18A).This willresult in Class II open bite
discrepancyonce the patient is released from MMF.Ifa significant period ofMMF or
trainingelastics is used postoperatively,this dis-crepancy may not become apparent
forweeks or months (Figure 57-18B).Oncethese posterior interferences have
beenremoved,the surgeon continues to rotatethe entire complex around the tem-
poromandibular joints until the appro-priate vertical relationship is achieved
asdescribed above.The cartilaginous sep-FIGURE57-14Down-fracture is
accomplishedwith a sharp-toothed Senn retractor,with simul-taneous elevation
ofnasal mucoperiosteum.FIGURE57-16Mobilization ofthe maxilla witha J
stripper.FIGURE57-17Manual positioning ofthe maxil-lomandibular complex with
condyles seated.Notethe posterior pivot point that must be removed.FIGURE57-
15Complete removal ofbonearound the perpendicular plate ofpalatine bone.The
descending palatine artery is isolated,ligat-ed,and divided.
Maxillary Orthognathic Surgery1189tum and vomer as well as the nasal crestofthe
maxilla are reduced in heightequal to the planned movement ofthemaxilla.This may
entail a submucousresection ofthe cartilaginous nasal sep-tum to prevent buckling
ofthe septumfrom pressure as the maxilla is reposi-tioned.A groove can be fashioned
in themidline ofthe nasal floor to accommo-date the recontoured septum.A portion
ofthe inferior edge ofthecartilaginous septum should be removed.The tendency is to
remove too littlebecause ofthe irregular inferior contactbetween septum and
maxilla.Even ifthemaxilla is inferiorly positioned,bucklingofthe septum may occur
because the car-tilaginous septum extends anterior andinferior to the anterior
nasal spine andtherefore can be buckled as the maxillamoves forward even ifthere is
somedownward movement (Figure 57-19).Allofthe maxillary positioning has been pre-
determined by the model surgery andsplint construction,except for the vertical.As
the maxilla is rotated upward aroundthe condyles,bone is only removed at thepoint
ofcontact,not a full wedge (Figure57-20).This facilitates ideal bone-to-bonecontact
and avoids large gaps in between.Once the desired vertical relationship hasbeen
achieved based on the measurementsdescribed above,the maxilla should befixed in
position with internal rigid fixa-tion.Sequentially eliminating only inter-fering
osseous structures ensures optimalbone contact.This method is preferredover a wedge
ostectomy.60Maxillo-mandibular fixation is removed and themandible is rotated into
the splint whileheld to the maxilla.Ifthe occlusion is cor-rect,the splint is
removed and not left inplace postoperatively.Variations in the above basic osteoto-
my design may enhance osseous contact,facilitate bone graft placement,or aid fixa-
tion device application,and result inimproved stability ofthe superiorly,inferi-
orly,or anteriorly repositioned maxilla.These variations will be described below
asthey apply to specific maxillary move-ments.To prevent septal deviation
despiteadequate bone and cartilage removal,it isoften desirable to suture the nasal
septumto the anterior nasal spine.This is done bydrilling a hole through the
anterior nasalspine and passing a 1-0 polyglycolic acidFIGURE57-18A,Inappropriate
position-ing ofthe condyles around posterior pivotpoints will result in (B)open
bite afterrelease from maxillomandibular fixation.ABFIGURE57-19A,Anterior aspect
ofthe cartilaginousnasal septum extends anteroinferiorly to the anteriornasal
spine.B,Pure horizontal advancement ofthe max-illa will buckle the septum unless
adequate bony and car-Atilaginous reliefis provided.B
1190Part 8: Orthognathic Surgerysuture through the hole and then throughthe
cartilaginous septum (Figure 57-21).This will also prevent postoperative dis-
placement ofthe septum during extuba-tion or in the Post-anesthesia Care
Unit.SegmentalizationA wide range ofpermutations may beundertaken
ifsegmentalization is needed.Three-piece maxillary osteotomy is perhapsthe most
common.The decisions regardingwhich ofthe many options will be used aremade by
pretreatment and preoperativemodel surgery.The need for extractions isalso
determined at this stage.Ifno extrac-tions are necessary,interdental osteotomiescan
be safely made between parallel roots ofthe canines and laterals or canines and
pre-molars.Ifextractions are decided on by thecoordinated efforts oforthodontist
and sur-geon,they may be done early in treatment orduring the osteotomy.A complete
discussionofthe indications and considerations thatinfluence these decisions is
covered else-where in this book.However,ifthere are nospecific orthodontic reasons
to extract teeth,it has been our experience that it is rarelynecessary to extract
just for the purpose ofsurgery.The most common need for seg-mentalization is to
widen the maxilla andadjust the angulations ofthe posterior max-illary
segments.Ifthe anterior six maxillaryteeth fit well with the lower anterior
teeth,the interdental osteotomy is performedbetween the canine and premolar
teeth.Thisplaces the potential for a periodontal defectat the interdental osteotomy
site more poste-riorly in the mouth.But ifthe canines needto be widened along with
the posterior seg-ments,the interdental osteotomy is placedbetween canine and
lateral incisor teeth.Weprefer to make this osteotomy with a thincement spatula
osteotome while palpatingpalatally.The standard circumvestibularincision can be
made with conservative tun-neling from the incision inferiorly to thealveolar crest
on the buccal surface ofthemaxilla.The osteotome is malleted throughuntil palpated
under the palatal mucosa (seeFigure 57-8A).With care the osteotomy canbe carried
superiorly to the level ofthe hori-zontal maxillary osteotomy and medially tothe
horizontal surface ofthe palate.Thisshould be done before any ofthe other max-
illary osteotomies are done because the max-illa must be stable at the time
ofmalleting.Ifteeth are to be extracted at the time ofosteotomy,an alternative to
tunneling is tolay a flap into the gingival sulcus for betteraccess (see Figure 57-
8B).However,ifthis is done,it is recommended that an anteriorpedicle be retained
for blood supply (seeFigure 57-9).Segmentalization using this or any othertechnique
is more difficult when significant-ly altered osteotomy designs are used,suchas
high Le Fort I,II,or III.When the Zosteotomies (see below) are used,inter-dental
segmentalization between caninesand laterals is feasible,but more difficult
ifattempted between canines and premolars.FIGURE57-20Removal ofbony wallsand
slotting ofthe contact points.FIGURE57-21A andB,To avoid septal devia-tion the
cartilaginous septum should be sutured toAthe anterior nasal spine.B
Maxillary Orthognathic Surgery1191Following the down-fracture and fullmobilization
ofthe maxilla,the remain-der ofthe segmentalization can be per-formed.The palatal
soft tissue is verythin in the midline and the bone is verythick,but the opposite
is true 6 to 8 mmlateral to the midline.For that reasontwo parasagittal osteotomies
are madealong the floor ofthe nose using a burwith a rounded tip,such as a Steiger
bur(Figure 57-22).The parasagittal cuts arejoined with the interdental ones to
freethe three dentoalveolar segments.Ifanysignificant torquing ofthe anterior seg-
ment is to be done,the two parasagittalcuts must be joined across the midline
sothat there are three dentoalveolar seg-ments and one midpalatal bony frag-ment.In
two-piece osteotomies the twoparasagittal cuts are joined with theinterdental cut
between the centralincisors at the incisive canal.The orthodontic arch wire is cut
atthe interdental osteotomy sites,and thesegments are mobilized appropriately.The
segments are wired to the preformedsurgical splint.Ifbone grafting is neededon the
palate it must be done before themaxilla is positioned and stabilized verti-
cally.Interdental and buccal bone graft-ing can be done just before closure
ofthesoft tissue wounds.Following splint fixa-tion the orthodontic arch wire can
beluted back together with quick curingacrylic ifnecessary.This avoids the time-
consuming practice oftying in a pre-formed surgical arch wire.Iftwo-piece maxillary
osteotomy is tobe performed in the midline,we still pre-fer to use two parasagittal
osteotomies thatare brought together at the incisive canal.The interdental
osteotomy is also per-formed with a cement spatula osteotomebefore the other
osteotomies.Four-piecemaxillary osteotomy is practically neverindicated with a
competent orthodonticset-up.Ifit is attempted,a tunneling tech-nique is recommended
in which an anteri-or pedicle ofmucoperiosteum is retainedto assist in the
perfusion ofthe anteriorsegments.The length oftime that the splint is leftin place
depends on the amount and type ofmovements made by the various segments.The range
oftime the splint is left in placewould be 3 weeks for smaller movementsand up to 8
weeks for greater expansion.The patient is returned to the orthodontistimmediately
after removal ofthe splint forfabrication ofthe appropriate retention andresumption
oforthodontic treatment.Finally iflarge interdental boneremoval is necessary to
close largeextraction spaces,access may be neededon the palate,especially in the
midline.In this case we prefer to retain an anteri-or labial mucoperiosteal pedicle
with asmall midline vertical incision to accessthe anterior nasal spine (Figures
57-23and 57-24).This allows for a midlinepalatal incision and conservative cir-
cumdental incisions to access the palatalbone removal.FIGURE57-22Following down-
fracture themaxilla is segmentalized with a rounded endcutting bur such as a
Steiger bur by making twoparasagittal cuts that join across the midline andconnect
with the interdental osteotomies.FIGURE57-23The traditional method ofgaining access
for total maxillary alveo-lar osteotomy was to make vertical incisions
bilaterally.This technique can be usedfor other segmental osteotomies.FIGURE57-
24The traditional total maxillaryalveolar osteotomy midline palatal incision with
aYat the anterior aspect can be used with caution.
1192Part 8: Orthognathic SurgerySuperior RepositioningLateral maxillary wedge
ostectomy priorto maxillary repositioning often leaveslarge gaps between the bony
interfaces asthe maxilla is moved superiorly.60Shift-ing,tilting,or advancing the
maxilla mayreduce bone-to-bone contact.Sequentialremoval ofosseous contacts avoids
thisneedless loss ofbone and provides moresecure contact between the maxilla andthe
cranial base (see Figure 57-20).Therefore,only one horizontal osteotomyis made and
no bone is removed untilMMF is established and vertical reposi-tioning is
begun.With MMF in place the maxilla andmandible are moved through the arc
ofrotation as dictated by the seatedmandibular condyle (see Figures 57-17and 57-
18).The areas ofbone contact cannow be seen as the maxilla is
positionedsuperiorly.Just enough bone is removed atthe contact points to permit the
superiorrepositioning planned.In many cases thiswillresult in the formation ofslots
orgrooves in the zygomatic buttress wall orelsewhere along the maxillary wall (see
Figure 57-20).One must be carefulthat the grooves do not inhibit the free
rotational movement ofthe maxillo-mandibular complex.This technique isparticularly
valuable when the maxilla isbeing shifted laterally or torqued in atransverse
direction,which makes predic-tion ofan ostectomy difficult.The maxillais rigidly
fixed and the MMF removed,themandible autorotated into occlusion,andcorrect
maxillary position confirmed.Anterior RepositioningThe traditional Le Fort I
osteotomy isinclined inferiorly from anterior to poste-rior in order to avoid the
relatively largemaxillary cuspid tooth root and place-ment ofthe cut inferior to
the lateralextent ofthe zygomatic buttress.Theresultant inclined plane may be
problem-atic ifthis does not coincide with thedesired movements.A variety
ofstraight,stepped,and Zosteotomies can be designed to accom-modate the planned
moves (Figures 57-25�57-28).61�65Ifgrafting (Figure 57-29) isdesirable,the steps or
Zosteotomies pro-vide much better grafting sites than thepterygomaxillary
fissure.Inferior RepositioningInferior repositioning ofthe maxilla offersa special
challenge in orthognathic surgerybecause there is a great relapse tenden-
cy.66�69Various mechanisms have beenadvocated for stabilization and fixation ofthe
maxilla after inferior repositioning.There have been a variety oftechniquesused to
stabilize the inferior positionedmaxilla,including suspension wires,interosseous
wires,bone plates,Steinmannpins,Wessberg pins,and RAPs.33,62,65,70�72Stabilization
ofthe inferiorly reposi-tioned maxilla may not require bone graft-ing from a
distant site ifa series ofslantedZor step osteotomies are used (see Figure57-
25).61,65The angulations oftheosteotomies are planned so that the maxil-la will
slide down the incline plane ofthecuts,maintaining bone contact as it
isrepositioned anteriorly and inferiorly.Depending on the inclination ofthe ante-
rior versus posterior osteotomies,the max-illa may be positioned more anteriorly
ormore inferiorly (see Figures 57-26�57-28).Most surgeons prefer to use bonegrafts
and rigid fixation to stabilize themaxilla that has been inferiorly re-positioned
and has no bone-to-bone con-tact.Grafts can be secured with bonescrews or plates
ifsufficient bone is avail-able or with wire (see Figure 57-29).Can-didates for
inferior maxillary reposition-ing often have paper-thin maxillary bone.Internal
rigid fixation with interosseousmetal plates is the stabilization method
ofchoice;however,occasionally insufficientbone is available adjacent to the
osteotomysites.In these cases the RAP system can bea crucial alternative (Figure
57-30).Theapplication ofthis system has beendescribed elsewhere.65Posterior
RepositioningPosteriorly repositioning the maxillamust be approached cautiously due
toresultant loss ofupper labial andparanasal osseous support for the overly-ing
soft tissue.Ifthe osteotomy is carriedthrough the pterygomaxillary junction,bone
must be removed either from thepterygoid plates (with great caution) or
themaxillary tuberosity.An alternative is todirect the osteotomy through the
maxillaryFIGURE57-25A,A Z-shaped osteotomy can be designed in the lateral walls
ofthe pirifom rims and thebuttresses so that the maxilla may be moved downward and
forward(B)without loss ofall bony contact.AB
Maxillary Orthognathic Surgery1193tuberosity just posterior to the
secondmolar.73,74This will leave tuberosity boneattached to the pterygoid
plates,whichcan be more safely removed.Dangers ofthe technique include damage to
thegreater palatine artery distal to its anasta-mosis with the lesser
palatine.Maxillary horizontal excess may alsobe addressed by anterior
maxillaryosteotomy when extractions are indicatedor edentulous sites are
present.Thesetechniques are discussed in detail later inthis chapter.Stable
Fixation for MaxillaryOsteotomiesRigid internal fixation with bone platesand screws
has become the standard formaxillary stabilization.Although thistechnique has
eliminated many oftheearly postoperative stability concerns,thetechnique is less
forgiving than wire fixa-tion.Therefore,intraoperative position-ing is even more
important.A wide vari-ety ofplating systems and sizes areavailable.Each surgeon
will discover hisor her preference,but 2.0 mm four-holeplates are used in most
cases (Figure 57-31).These will require a little more effortfor adaptation than
lighter ones,but withpractice can be used just as accurately andwith more
stability.When used,theseplates virtually eliminate postoperativeplate fracture or
mobility.Specific ProceduresTotal Maxillary AlveolarOsteotomyThe total maxillary
alveolar osteotomy wasdesigned to avoid some ofthe problemsseen with the Le Fort I
down-fracturetechnique;however,it did not fare any bet-ter.75Purported advantages
includingimproved nasal airway,improved stabilitydue to better bony
contact,improved abil-ity to widen the maxilla,and better maxil-lary perfusion have
not been realized.75�81In several thousand maxillary osteotomiesover the past 20
years,we have not found aneed for this procedure.Anterior Maxillary
OsteotomyNumerous techniques have been used toaccomplish the anterior maxillary
osteoto-my.The three major techniques involve theuse ofone ofthree vascular
pedicles:labial(Figure 57-32),palatal (Figure 57-33),and acombination ofthese with
vertical incisionsin both (Figure 57-34).All ofthese can besuccessful,and when done
properly havefew complications;however,what scant lit-erature exists would indicate
that the palatalpedicle provides the best vascularity.50Anterior maxillary
osteotomies aregenerally used to treat horizontal maxil-lary excess when the
posterior occlusionis correct or correctable by mandibularsurgery.Commonly,anterior
maxillaryosteotomy with premolar extractions isused for bimaxillary protrusion in
whichboth the anterior maxilla and the anteri-or mandible are to be retracted
(FigureFIGURE57-26A,A Zosteotomy with the posterior cut steeper than the anterior
one to increase pos-terior facial height and to(B)rotate the maxilla downward and
forward with adjustment to theocclusal plane.ABFIGURE57-27A,A Zosteotomy with the
posterior cut shallower than the anterior one to increaseanterior facial height and
to(B)rotate the maxilla down in the front and adjust the occlusal plane toa steeper
angle.AB
1194Part 8: Orthognathic Surgery57-35).These procedures are also usedfor correction
ofanterior open bite.Occasionally anterior maxillary osteoto-my may be coupled with
mandibularadvancement and anterior mandibularsegmental surgery in patients with
asevere curve ofSpee.Sequencing the work-up when bothjaws are involved requires
imagination,because the surgical procedures need to bedone systematically so that
the surgeonnever loses orientation.There are two pos-sible scenarios:(1) the
posterior occlusionis not going to be changed because the pos-terior maxillary and
mandibular teethneed not be moved,or (2) mandibularsurgery will be performed
thereby correct-ing the posterior occlusion.This a crucialdifference because ifthe
posterior occlu-sion is notgoing to be changed by surgery,then the models must be
mounted in cen-tric occlusion,not centric relation.Iftheposterior occlusion will be
altered bymandibular surgery,then a new centricrelation will be established by the
surgeryand model surgery can be done as usual.Inthe first case the maxillary
anterior modelis cut and repositioned to the best relation-ship against the uncut
mandible in centricocclusion and the remaining maxillarydentition,and then a splint
is constructed.Ifmandibular surgery is to be done,two mandibular models are
mounted,onemandibular model is cut,and the other isleft intact to preserve the
intermediatephase.The anterior maxilla and themandible are cut and repositioned
togeth-er to the final position and a final splint ismade.The cut maxilla can then
be articu-lated with the uncut mandible to establishthe intermediate position and a
second(intermediate) splint is made.The finalsplint will be wired to the maxilla
for apostoperative period so there must be aseparate intermediate splint that
articu-lates with the final splint and themandibular teeth.Particularly in
segmental surgery themodel surgery should simulate the actualsurgery to provide a
clear understandingofthe three-dimensional movements nec-essary to the proper
performance ofthesurgical procedure.Measurement marksshould be made at the level
ofthe inter-proximal spaces and the root tips.Marksshould also be made on the
palate at theroot tips and the maxillary midline.Ifwidening is to
occur,transpalatal marksshould also be used.The use ofintermedi-ate splints in
segmental cases is a little dif-ferent from their use in total arch cases.Since the
posterior maxilla is not mobi-lized,the anterior maxillary positioning ismore
difficult and can be deceiving.Forexample,the anterior maxilla can fit intothe
splint and appear ideal until themandible is rotated into occlusion.Ifthemandible
does not arc into the ideal occlu-sion,it is possible that the anterior maxil-la is
tipped superiorly or inferiorly andmust be adjusted.For this reason themandible
should not be wired into MMFbut left free to rotate into the
maxilla.Atsurgery,ifthe mandible is held into inter-maxillary fixation during the
fixationprocess for the anterior maxilla,it is possi-ble to pull the condyles out
ofthe fossaeFIGURE57-28An alternative method for advancement is to create a step
(A)in the buttress and placea bone graft(B)in the step after
repositioning.ABFIGURE57-29A,A single hole is placed in the middle ofthe bone graft
and a loop of28-gauge stainlesssteel wire is placed through the hole from inside
out.The two ends are divided,with one placed throughthe superior cranial base wall
and the other through the inferior maxillary segment.Finally one end ispassed
through the loop and twisted to the other,much like an Ivy loop.B,Bone graft shown
in place.AB
Maxillary Orthognathic Surgery1195with a resultant malocclusion.Therefore,the
splint must be ligated to the posteriormaxilla first,and the anterior maxilla
isthen brought into the splint and ligated.Ifthe mandible rotates into the desired
oc-clusion,then the maxilla can be consid-ered to be in the correct place and
fixedaccordingly.Ifmandibular surgery isrequired,it can be initiated at this
time.The choice ofsurgical technique ismade on the basis ofaccess and the areasthat
will be most difficult to visualizeintraoperatively.For example,in cases ofopen
bite in which no teeth are to beextracted,the anterior segment will berotated
clockwise downward after inter-dental osteotomies.Access to the interden-tal
area,the midline ofthe palate,and theanterior nasal spine is not as critical as it
iswith other surgical movements.This pro-cedure can be done with a circumvestibu-
lar incision or with bilateral horizontalincisions in the canine-molar regions anda
vertical incision in the midline betweenthe central incisors.On the other
hand,iffirst premolars are to be extracted or havealready been,and the anterior
maxilla is tobe retracted several millimeters,access tothe midpalatal area is
essential.The Wun-derer technique,in which the palatal softtissue is elevated
posteriorly,gives greataccess to the palatal bony tissue,but caremust be taken to
preserve the labial softtissue pedicle.18However,ifsuperior repo-sitioning is
required,the access to thejunction ofthe anterior nasal spine andthe nasal septum
is poor.A vertical inci-sion can be made over the anterior nasalspine,but since
this labial flap representsthe total blood supply to the anterior max-illa,it is
not recommended.Our choice ofprocedures for mostanterior maxillary osteotomies is a
hybrid(see Figure 57-34).The labial incisions aremade laterally as per Wunderer
with a ver-tical midline incision to permit access tothe anterior nasal spine�nasal
septum.However,in place ofa full palatal flap,cir-cumdental incisions are made
around thenecks ofthe teeth on either side oftheinterdental osteotomies and a
midline inci-sion is made over the midpalatal suturewith a small anterior
Yifnecessary.The Yshould be anterior to the interdental bonecut and be as
conservative as possible.Fixation ofanterior maxillaryosteotomies is as varied as
the surgicaltechniques.82Orthodontic arch wires andcast splints represent two ofthe
extremesFIGURE57-30A,Rigid adjustable pin system.A 0.045 inch orthodontic wire is
fabricated on askull preoperatively and adapted to the newlypositioned maxilla
intraoperatively so that thewire lies passively,close to the orthodontic appli-
ances or arch bars.B,The acrylic cements thejunction ofthe wire and the orthodontic
appli-ances; the end ofthe wire is also covered.ABFIGURE57-31Bone plating
encompasses awide variety ofplates and screws,ranging fromvery rigid to very
malleable.Generally 2.0 mmplates are used in the piriform rims and either2.0 or 1.5
mm plates in the buttresses.OsteotomylineFull-thicknesspalatal flapFIGURE57-
32Labial pedicle for anterior max-illary osteotomy; the palate is flapped
open.FIGURE57-33Palatal pedicle for anterior max-illary osteotomy is created with a
horizontallabial incision.
1196Part 8: Orthognathic Surgeryin techniques used for fixation.Orthodon-tic
appliances,ifthey are in place,are thehandiest to use at least for part ofthe fixa-
tion.However,supplemental fixation maybe desirable.An occlusal splint,with skele-
tal wire in the anterior nasal spine,is help-ful in such cases,especially iftension
onthe free segment is expected.Small platesand screws can be carefully used to
fixatethe segment.Arch bars have been used andin certain cases may be
appropriate,but alower level ofprecision can be expected.The most important
guideline is that,at the time ofsurgery,the anterior maxillamust be mobile enough
so that it does notrequire any significant pressure to move itinto the desired
position.Fixation canthen be instituted by one ofthe manymethods that will hold the
segment in theproper position throughout the healingperiod.Maxillomandibular
fixation isalmost never required.Posterior Maxillary OsteotomyThe posterior
maxillary osteotomy and itsmodifications are rarely
indicatedtoday.19,22,83�88Ifopen bite or transverseexpansion is needed,the Le Fort
I down-fracture is much easier,quicker,and morepredictable.Posterior maxillary
osteotomyis usually indicated as a preprosthetic pro-cedure to correct
hypereruption ofa pos-terior maxillary dentoalveolar segment.Meticulous model
surgery is essential tovisualizing the three-dimensional move-ments and in
anticipating osseous inter-ference ofthe segment.Periapical radi-ographs are useful
for evaluating plannedinterdental and supra-apical osteotomysites.Once again the
models should bemounted in centric occlusion,not centricrelation,unless the
mandible is also goingto be operated on.Outpatient anesthesia can be used
forisolated posterior segmental procedures.Ahigh palatal vault permits palatal
osteoto-my transantrally beneath the nasal floor.The soft tissue incision is made
horizon-tally in the maxillary buccal vestibule fromthe anticipated anterior
interdentalosteotomy site to the second molar (Figure57-36).Mucoperiosteal
dissection beneaththe superior aspect ofthe incision exposesthe lateral maxilla.The
pterygomaxillaryregion is exposed and soft tissue retractedin a tunneling
dissection.At the anteriorinterdental osteotomy site,conservativetunneling ofthe
periosteum exposes thefull vertical extent ofthe dentoalveolus.After retraction
ofthe soft tissue with skinhooks and right-angle retractors,the buc-cal interdental
osteotomy can be outlinedwith a small fissure bur in a rotary hand-piece or can be
directly completed with athin cement spatula osteotome.A horizontal osteotomy is
madeapproximately 5 mm above the roots oftheteeth and connected with the
anteriorinterdental cut (see Figure 57-36).The ver-tical interdental osteotomy
should be com-pleted first so that the segment is notmobile while using interdental
osteotomes.The palatal osteotomy is accomplishedwith a small sharp curved
osteotomedirected at the juncture ofthe vertical alve-olus and horizontal palatal
shelf.The sur-geon places a finger in the palatal mucosato detect complete osseous
sectioningwhile minimizing palatal mucosal trauma(Figure 57-37A and B).In cases
with highpalatal vaults the transantral cut is com-pleted along the entire
anteroposteriorextent ofthe planned palatal osteotomy(see Figure 57-37B),except in
the area ofthe descending palatal neurovascular bun-dle.Next the pterygomaxillary
junction isseparated with a chisel using a techniquesimilar to that for a total
maxillary osteoto-my.Patients with low flat palatal vaults aremore easily
osteotomized through thenasal floor (Figure 57-37C).The posterior dentoalveolar
segmentis down-fractured using digital pressure.Anticipated osseous interference
may beFIGURE57-34A combination oflabial andpalatal pedicles can be used for an
anterior max-illary osteotomy without extractions.FIGURE57-35Anterior maxillary
osteotomy withfirst premolars extracted corrects maxillary excess,bimaxillary
protrusion,and anterior open bite.FIGURE57-36Posterior maxillary
osteotomy.Horizontal vestibular incision with tunnelingaccess to the interdental
papilla.The dashed linemarks horizontal and interdental osteotomies.
Maxillary Orthognathic Surgery1197removed using a bur or rongeur.Previ-ously
inaccessible medial and posteriorwalls ofthe mobile segment are addressedfollowing
mobilization and displacementofthe posterior segment.Bone removalat the
perpendicular plate ofthe palatinebone and mobilization should continueuntil the
segment can be repositionedwith minimal digital force (Figure 57-38).Final
contouring is accomplished whileholding the splint on the stable portionofthe
maxilla.The mandible is rotatedinto its dictated occluding position toensure that
no distortion ofthe splinthas occurred.A slightly thicker splintand transpalatal
acrylic or wire rein-forcement will add rigidity to preventinadvertent distortion
ofthe posteriorextension ofthe splint.The segment isligated to the splint.The
repositioned posterior maxillarysegment may be fixated with
interosseouswire,suspension wire,stable pin fixation,or bone plates.Osseous grafts
are rarelyrequired but may be obtained from localregional sites.Additional
stability isattained by luting the orthodontic archwire back together with quick
curingacrylic or by placing a rectangular archwire across the interdental osteotomy
site.Intermaxillary fixation is not required.Ifthe posterior segment is to be repo-
sitioned laterally or medially to any extent,added access is necessary.A
midlinepalatal incision may be made and thepalatal tissue reflected laterally
(Figure 57-39).Careful dissection ensures theintegrity ofthe greater palatine
vascula-ture.This approach gives access to thesinus and nasal cavity.Ifthe palatal
vault ishigh,the osteotomy is usually carriedthrough the sinus (see Figure 57-
37B).Ifthe alveolus is short and the palatal vaultshallow,the osteotomy usually
crosses themedial sinus wall and passes through thefloor ofthe nose (see Figure 57-
37C).Surgically Assisted Rapid Palatal Expansion: HistoryThe concept ofcorrecting
maxillarytransverse width discrepancies originat-ed in the United States in 1860 by
Angell,who reported it in Dental Cosmos.Angelldescribed a widening ofthe
maxillarydental arch by opening the midpalatalsuture.89The concept fell into disuse
byAmerican practitioners by the early1900s.Haas re-introduced the concept in1961
with rapid palatal expansion (RPE,also referred to as rapid maxillary expan-
sion),appliances that effectively correct-ed arch width discrepancies.90In
growingchildren nonsurgical RPE results inopening ofthe midpalatal
suture,butstability has been questioned.Timmsand Moss,Haas,and Isaacson andIngram
have shown orthodontic RPE toresult in alveolar bending,periodontalmembrane
compression,lateral toothdisplacement,and tooth extrusion.91�93For those reasons
Haas believed thatoverexpansion was very important.EvenFIGURE57-37A,Transantral
osteotomy is made at the junction ofthe horizontal palate and vertical alveolar
process.B,Approach for deep vaultedpalates.C,Approach for flat shallow
palates.ABCFIGURE57-38Bone is removed at the perpen-dicular plate ofthepalatine
bone using atransantral approach.
1198Part 8: Orthognathic Surgerywith 50% overexpansion,nonsurgicalRPE has been
associated with relapse andsubsequent failure in adults,but has beenrelatively
successful in children and adolescents.91�93Although historically the
midpalatalsuture was thought to be the area ofresistance to expansion,Isaacson
andIngram have shown that the major site ofresistance is not the midpalatal
suturebut the remaining maxillary articula-tions.93Lines as well as Bell and
Epkerdemonstrated that increased facial skele-tal resistance to expansion was at
thezygomaticotemporal,zygomaticofrontal,and zygomaticomaxillary sutures.94,95Wertz
theorized that the resistance wasdue to the zygomatic arches.96Identifica-tion
ofthese areas ofresistance in thecraniofacial skeleton stimulated thedevelopment
ofvarious maxillaryosteotomies to expand the maxilla inconjunction with orthodontic
appli-ances.96Published surgical techniquesreport the removal ofthe bony
resistanceofthe maxilla in order to symmetricallyexpand the hemimaxillas with
short-term orthopedic forces.94,95,97�101Lehmanand colleagues have also
demonstratedexpansion with an RPE appliance.97Kennedy and colleagues reported a
sig-nificant increase in the amount oflateralmovement in animals that
hadosteotomies prior to orthodontic RPE.98Reported results varywith technique
andthe timing ofplacement ofan activeorthopedic expansion device,but all notethe
expansion to be more stable thanorthodontic RPE alone.The role ofsurgery with RPE
is torelease the areas ofresistance in the maxil-las before RPE.Whether RPE will be
donealone or in conjunction with surgery willdepend on the patient�s age and the
condi-tion ofthe midpalatal suture,but not themaxillomandibular relation.Lines
foundsurgically assisted rapid palatal expansion(SARPE) to be extremely valuable in
youngpatients (growing children) exhibitingmaxillary collapse,maxillary
retrusion,and pseudo-Class III malocclusions.94SARPE is distraction osteogenesis
ofthe maxilla in a transverse plane.The ben-efits ofits use are gradual callous
distrac-tion that allows the soft tissues to accom-modate,and greater long-term
stability.When maxillary expansion and totalmaxillary osteotomy are
needed,twotreatment regimens are possible:SARPE asa first stage followed by a one-
piece maxil-lary osteotomy at a later date or multiple-piece maxillary osteotomy in
the normalorthognathic sequence.The four factorsthat must be considered when
determin-ing which method is preferred are archlength discrepancy,arch
morphology,ver-tical dimension,and ectopic eruption ofposterior teeth.Arch Length
DiscrepancyIn cases ofarch length deficiency,a SARPE increasesarch circumference
sufficiently,especiallyin the anterior,to permit alignment ofcrowded teeth and
avoid extraction ofpremolars or excessive tipping ofincisors.SARPE is also
beneficial when minimalchanges in the sagittal dimension are nec-essary because
ofthe nasolabial angle andlip-to-tooth considerations.Arch MorphologyThe majority
ofcasesoftransverse deficiency characteristicallyexhibit a narrow tapering arch
form withthe discrepancy pronounced in the canineregion.To achieve a functional
occlusion,the intercanine width must be increased andthe anterior segment flattened
for a normalelliptical arch morphology.Ifnonextractionorthodontic therapy is
desired,a SARPE isthe treatment ofchoice.A three- or four-piece segmental maxillary
surgical proce-dure may be less ideal,particularly becauseofpotential periodontal
problems and pos-sible vascular compromise.Ifthe discrepancy is minimal
andextraction ofthe first premolars is desired,a three-piece segmental maxillary
proce-dure is indicated,but only after the ca-nines are orthodontically moved
posteri-orly to provide an increased width.Theinherent problem is relapse ofthe
buccallydisplaced canines.This procedure is in-dicated ifthere is no transverse
discrepan-cy in the canine region but significant con-striction in the premolar-
molar region.Vertical DimensionThe vertical dimen-sion is ofparticular concern in
patientswho exhibit anterior open bites.Segmentalorthodontics is suggested,with no
attemptto level the arch,using a three- or four-piece maxillary procedure to level
the archand at the same time correct the bilateralabsolute transverse maxillary
deficiency.Ectopic Eruption ofOne or Two PosteriorTeethIfectopic eruption is
seriousenough that it cannot be treated withorthodontic therapy,a segmental
osteoto-my with expansion may be done.The stability ofSARPE has
beenreported.99,102In one reported study onlong-term stability ofSARPE,the
surgicalresults remained stable with only 6.4 to7.5% relapse in the
canine,premolar,andmolar regions.99This stability exceeds thatofmultiple-piece Le
Fort osteotomies.100,102Surgically Assisted Rapid PalatalExpansion: Surgical
TechniqueBilateral mucoperiosteal incisions aremade from the piriform rims to
zygomaticFIGURE57-39A midline palatal incision givesaccess for the removal ofbone
as the posteriormaxillary segment is moved medially.
Maxillary Orthognathic Surgery1199buttresses (Figure 57-40A).Bilateralosteotomies
are then made from the piri-form rims to low in the pterygomaxillaryjunction (see
Figure 57-40A).A simpleanteroposterior osteotomy from the piri-form rim to the
pterygomaxillary junctionis suggested for SARPE.More complicateddesigns appear to
be advantageous in two-dimensional drawings,but in fact aremeaningless when applied
to three-dimensional geometric structures such asthe maxilla.103The theory put
forth byBetts and colleagues shows a sloped cutfrom the piriform to the
buttress.103Thesupposition is that as the maxilla isexpanded,it will �ride
down�this slope.This concept appears valid in a two-dimensional
drawing;however,three-dimensionally,ifthe osteotomy is madeflat from lateral to
medial,as expansionoccurs,then the bone at the piriform slideslaterally over the
flat surface lateral to itand the bone ofthe buttress slides lateral-ly over the
flat surface lateral to it.There-fore,ifthe lateral maxillary wall saw cutsare made
straight in perpendicular to themidsagittal plane from lateral to medial,then the
angulation ofthe cut from anteri-or to posterior does not affect the
verticalposition ofthe segments as they areexpanded.This can be easily
demonstratedon a dry skull.Osteotomies are made ofthe anterior1.5 cm ofthe lateral
nasal wall because thisis the thickest portion ofthe anterior nasalwall.Separation
ofthe hemimaxillas isperformed by driving a spatula osteotomebetween the central
incisors parallel to thepalate for approximately 1 to 1.5 cm (Fig-ure 57-40B�D).The
expansion device isturned until separation is noted betweenthe central incisor
teeth (Figure 57-41).Both segments are mobilized by pryinguntil equal mobility is
seen bilaterally.Mobilization is continued until approxi-mately 1.5 to 2.0 mm is
opened betweencentral incisors.Some authors recommend a subtotalLe Fort I osteotomy
with a horizontalosteotomy,vertical midline osteotomy,and pterygoid and septal
separation.103Shetty and colleagues demonstrated,with a photoelastic model,that the
mid-palatal and pterygomaxillary articula-tions were the primary anatomic sites
ofresistance to expansion forces.104Thearticle by Shetty and colleagues in
1994report performing only incomplete cutsofthe lateral maxillary wall,from
secondbicuspid to second molar.It is unclearwhether these findings would be as sig-
nificant with complete cuts from the pir-iform to the pterygomaxillary fissure.Need
for separation ofthe pterygomaxil-lary junction is therefore a point
ofdebate.However,since our results haveOsteotomyPiriformrimFIGURE57-40Surgically
assisted rapid palatal expansion.A,Bilateral horizontal mucoperiostealincisions are
made,followed by bilateral osteotomies from the piriform rims to pterygomaxillary
junc-tions.B�D,Division ofhemimaxillae is accomplished by inserting an osteotome in
the midline.ACDBSpace betweenthe central incisorsFIGURE57-41Surgically assisted
rapid palatalexpansion.Expansion device is turned to sepa-rate hemimaxillas.
1200Part 8: Orthognathic Surgeryshown minimal relapse without pterygo-maxillary
disjunction,we do not performthis maneuver in most cases.99Iftwo sources
ofpotential hemor-rhage (manipulation ofthe pterygomaxil-lary junction and
separation ofthe nasalseptum from the nasal crest ofthe maxilla)are avoided,this
procedure can be done asan office-based procedure,on an outpa-tient basis,and under
intravenous seda-tion.Steroids are routinely used butantibiotics are not
necessary.A 5-day post-operative rest period is observed,afterwhich the expansion
appliance is turnedaccording to specific instructions until thedesired expansion is
achieved.Unilateral SARPE can be achieved bycompleting a vertical interdental
osteoto-my between the appropriate teeth andconnecting that with a horizontal
osteot-omy extending posteriorly to the pterygo-maxillary junction.Ifthe entire
hemimax-illa is to be mobilized,it is performed inthe same way as described for a
bilateralcase,only unilaterally.Ifa widening ofonly the posterior part ofthe
hemimaxillais desired,the interdental osteotomy mustbe completed all the way to the
midlinesuture (Figure 57-42).The segment ismobilized (Figure 57-43A) and expandedin
the same manner as the bilateral proce-dure (Figure 57-43B).Zygomatic OsteotomyIn
patients with severe midface deficiency itmay be favorable to enhance the
prominenceFIGURE57-44Zygomatic osteotomy.A,Parasagittal vertical osteotomy cuts
through the root ofthezygoma.B,With out-fracturing and placement ofgraft material
for transverse augmentation ofthemalar eminence.C,Mushroom-shaped graft placement
for anteroposterior and transverse augmen-tation ofthe malar eminence.ACBFIGURE57-
43Unilateral surgically assistedrapid palatal expansion.A,Segment is mobi-
lized.B,Expander is activated until the desiredexpansion is achieved.ABOutline of
osteotomyFIGURE57-42Unilateral surgically assistedrapid palatal
expansion.A,Osteotomy is driven tomidpalatal suture.B,Horizontal osteotomy
iscompleted in the same manner as bilateralosteotomy.BA
Maxillary Orthognathic Surgery1201ofthe zygomas.Also,esthetically,highcheekbones
have always been popular,andwith a growing public awareness ofsurgi-cal
capabilities an increasing demand hassurfaced for procedures to enhance
thisarea.Numerous methods have been devel-oped to augment the malar eminences,most
involving grafts or implants.Autolo-gous grafts are disappointing because
ofresorption and the need for a donor site.Allogeneic transplants such as
lyophilizedcartilage have been used with some successbut are prone to
migration.Presently ourchoice for malar augmentation is with allo-plastic implants
(porous polyethylene).However,when alloplasts are con-traindicated,the zygomatic
osteotomy maybe useful.The zygomatic osteotomy isapproached through an intraoral
incision.Areciprocating saw is used to make aparasagittal osteotomy through the
zygomajust adjacent to the root ofthe structure(Figure 57-44A and B).This is done
as closeto the lateral orbital rim as possible.Thezygoma is out-fractured gently so
that an in-terpositional material can be placed to holdit in position.The
interpositional materialcan be stabilized in any traditional method,since it is not
difficult to fixate this area.Thistechnique does not give anterior projectionunless
the interpositional material is fash-ioned to project forward (Figure 57-
44C).Modified Le Fort OsteotomiesOsteotomies that extend the traditional LeFort I
have been called by many namesincluding modified Le Fort I,II,III;high LeFort I;and
pyramidal,middle,intermediary,quadrangular,and maxillary-malar-infraor-bital
osteotomies (Figure 57-45A�C).Wehave used them all and have described
thempreviously.105This group ofosteotomies isseverely limited regarding
expansion,androtational and torquing movements.There-fore,with the success ofporous
polyethyl-ene implants to the malar,infraorbital,later-al orbital,and paranasal
regions,we rarelysee a need for these more invasive osteo-tomies (Figure 57-
46A�C).FIGURE57-45Modified Le Fort I osteotomy.A,High Le Fort I below the
infraorbital rims.B,Quadrangular Le Fort I extending into theorbital
floor.C,Quadrangular Le Fort I includ-ing the lateral orbital rim and
zygoma.ABCFIGURE57-46Porous polyethelene implants.A,Infraorbital augmentation with
the zygoma.B,Infraorbital augmentation with the zygomaand lateral orbital
rim.C,Zygoma augmentation.ABC
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localization and emboliza-tion.J Laryngol Otol 1988;102:260�3.57.Newhouse RF,Schow
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steposteotomy and Steinmann pin stabilization.J Oral Maxillofac Surg
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Surg 1975;33:842�51.76.Hooley J,West R.Vertical repositioning oftotalmaxillary
alveolus to compensate for �shortupper lip.�Second Congress ofthe EuropeAssociation
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effect ofLe Fort I maxillary impaction on nasal airwayresistance.Am J Orthod
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1204Part 8: Orthognathic SurgeryStability ofsurgical maxillary expansion.Int J
Adult Orthod Orthognath Surg 1992;7(3):139�46.101.Stephens C.An examination ofthe
long-termstability ofsurgical-orthodontic maxillaryexpansion
[dissertation].Columbus (OH):Ohio State University;1986.102.Pogrel MA,Kaban
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adults.Int J Adult Orthod Orthog-nath Surg 1992;7(1):37�41.103.Betts NJ,Vanarsdall
RL,Barber HD,et al.Diag-nosis and treatment oftransverse maxillarydeficiency.Int J
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AA,Chaconas SJ.Bio-mechanical rationale for surgical-orthodonticexpansion ofthe
adult maxilla.J Oral MaxillofacSurg 1994;52(7):742-9;discussion 750�1.105.Bays
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(PA):J.B.Lippincott;1992.p.1349�414.
CHAPTER 58Management ofFacial AsymmetryPeter D.Waite,MPH,DDS,MDScott
D.Urban,DMD,MDIn the 1960s surgical treatment oforthog-nathic deformities developed
when satis-factory results were unobtainable byorthodontics alone.Mild cases
ofjawdeformities and malocclusion can some-times be camouflaged by dental
treatmentand growth modification.1Severe maloc-clusion is often beyond the envelope
oforthodontic treatment;therefore,surgicalprocedures ofthe maxilla and mandiblehave
been developed.Just as some maloc-clusions are beyond orthodontics alone,some
orthognathic deformities are beyondsurgery directed at a single jaw,that
is,themaxilla or the mandible.Although a singleosteotomy might improve function
andesthetics,bimaxillary surgery or double-jaw surgery is often indicated for
largeanteroposterior discrepancies,open bite,and most asymmetries.2�5As
orthognathicsurgery has been refined,it has becomeevident that some problems are
beyondtreatment ofa single jaw.The novicemight assume that single-jaw surgery
isbetter�simple and less complicated�butthe final outcome is often a compromiseand
unstable.Bimaxillary surgery allows amuch greater degree offlexibility withregard
to three-dimensional treatment.In the 1960s and 1970s surgeonsattempted to limit
orthognathic surgery toone jaw,usually the mandible.Ramusosteotomies with maxillary
osteotomieswere complex,technically difficult,timeconsuming,unstable,and associated
withhigher morbidity.6It is impossible to cor-rect a canted maxilla without
adjusting themandibular plane ofocclusion.Even sim-ple midline discrepancies
resulting fromunilateral tooth loss can be quicklyimproved by mild rotational
changes inthe facial skeleton.This chapter focuses on the uniquenature ofasymmetric
orthognathic defor-mities as an indication for bimaxillarysurgery,which is really
nothing more thana combination oftwo procedures.Themost important aspect
ofbimaxillarysurgery is not the ability to do simultane-ous maxillary and
mandibular procedures,but to understand the indications andtreatment plan and how
to maintain a sta-ble reference during surgery.Little has been written on
orthognath-ic asymmetries as an indication for bimax-illary surgery.Poor treatment
planningand poor surgical reference are commonmistakes.Asymmetries require three-
dimensional changes and complex skeletalmovements with adjunctive soft
tissuesymmetry.The current discussionincludes etiology amenable to orthognath-ic
procedures,diagnostic imaging,treat-ment planning,and surgery.Facial symmetry has a
high correlationwith attractiveness.Even a slight asymme-try is quickly noticed by
the human eye.Greater degrees ofasymmetry are correlat-ed with clinical
depression,neurosis,infe-riority complex,poor self-esteem,and gen-eral poor-
quality-of-life health problems.7Mandibular asymmetry is a significantdysfunction
and difficult to correct.Etiology There are multiple causes ofmandibularand facial
asymmetry,but the differentialcan be separated into three classes:con-
genital,developmental,and acquired.8,9Congenital anomaliesare conditionsacquired
during in utero developmentand can be further subdivided into mal-
formations,deformities,and disruptions.Malformations are the result ofan intrin-
sically abnormal developmental processin embryogenesis.Unilateral cleft lip is
anexample ofa malformation.9Deformitiesare an abnormal form or position ofapart
ofthe body caused by a nondisrup-tive mechanical force during the
fetalperiod.9Mandibular deformation mayresult from a prolonged sharply
laterallyflexed position ofthe head with theshoulder pressed against the
mandibleduring late intrauterine growth.Disrup-tions are morphologic defects
resultingfrom a breakdown ofan otherwise nor-mal developmental process.9Rare
facialclefting and limb amputation from anamniotic band are good examples ofdis-
ruption.9Developmental anomalies areconditions arising during postuterinegrowth
through adulthood.Acquiredanomalies are conditions arising fromeither trauma or
pathology.
1206Part 8: Orthognathic SurgeryCongenital AnomaliesHemifacial MicrosomiaHemifacial
microsomia (HFM) is a cranio-facial malformation ofthe first and secondbranchial
arches presenting with asymmet-ric unilateral or bilateral hypoplasia
oftheorbit(s),maxilla,mandible,ear,cranialnerves,and soft tissue (Figure 58-
1).10Cur-rent evidence supports the theory thathemifacial microsomia results from
adefect in the proliferation and migration ofembryonic neural crest
cells.11,12Other the-ories have included hemorrhage ofthestapedial artery during
fetal development,which ultimately leads to impaired unilat-eral facial
growth.13,14However,the trueetiologic factors still remain unknown.Two important
factors need to beconsidered in the treatment planning ofHFM:(1) the facial growth
potentialand/or restriction and its effect on sur-rounding structures and (2) the
degree ofhypoplasia involving the glenoid fossa,mandibular condyle,and ramus
unit.15,16Classifying the extent ofthe HFM defor-mity can provideclarity in
determiningideal reconstruction and accurate progno-sis.The Pruzansky HFM
classification,17modified by Kaban and colleagues,18cur-rently provides a
clinically useful frame-work to help guide the treatment planbased on the presence
or absence ofcriti-cal structures.18,19HFM type I deformity can be summa-rized as a
generalized mild hypoplasticstate involving the muscles ofmastication,the glenoid
fossa,and the mandibularcondyle and ramus unit.The temporo-mandibular joint (TMJ)
functions withnormal rotation and restricted translation.Patients present with mild
mandibular ret-rognathia and facial asymmetry.Becausethere is satisfactory TMJ
occlusal functionand mild dysmorphology,surgical therapyis usually not
indicated.HFM type IIA deformity involves ahypoplastic cone-shaped condylar
head.The condyle is located medial and anteri-or to a hypoplastic glenoid
fossa.TMJfunction is often satisfactory.Again,sur-gical intervention ofthe TMJ is
usuallynot indicated.HFM type IIB deformity involves amoderate to severe hypoplasia
ofthe gle-noid fossa,condyle,and mandibularramus.Unlike the type IIA
deformity,these patients have no articulationbetween the temporal bone and a
condyle.However,manual manipulation reveals aposterior �stop�ofthe condyle
contactingthe glenoid fossa.20A patient with HFM type III has acomplete absence
ofthe mandibularramus and condyle.No manual condylarseating or posterior stop is
present.Thesepatients present with severe mandibulardysmorphology and often require
TMJsurgical reconstruction (Figure 58-2).20The treatment ofHFM is controver-
sial.The treatment philosophy ofintercep-tive orthodontics and surgical treatmentin
growing children is based upon the the-ory that HFM is a progressive
deformity.15Conversely,a treatment protocol based onthe theory that HFM is not
progressive innature is well described by Posnick.16Cleft Lip and Cleft
PalatePatients with a cleft lip and cleft palateoften present with a bilateral or
unilater-al midface deficiency resulting in aug-mentation and involving the
paranasal,nasal,infraorbital,and zygomatic regionsas well as the occlusal
level.21However,the degree and location ofmaxillofacialgrowth deficiency in
children with cleftsis largely dependent on the location andtype ofcleft lip/cleft
palate repair and theage ofthe child at the time ofrepair.22�24Most studies show
that children with arepaired cleft lip/cleft palate havedecreased vertical and
horizontal maxil-lary growth and decreased verticalgrowth ofthe ramus and steep
mandi-bular plane angle.25�27Ross has shownthat approximately 25% ofpatients witha
repaired cleft lip or cleft palate have amidface deficiency and class III malocclu-
sion that require skeletal surgery.28PlagiocephalyPlagiocephaly is derived from the
Greekword plagios,which refers to the twistedshape ofthe skull when viewed
cranially-caudally.The etiology is often a unilater-al synostosis ofthe coronal or
lambdoidFIGURE58-1A 16-year-old female with mildhemifacial microsomia type I.Note
the cantedmaxilla,dental deviation,and facial asymmetry.FIGURE58-2A 14-year-old
female with severehemifacial microsomia type III,which is associatedwith facial
clefting and a total absence ofcondyle.
Management ofFacial Asymmetry1207suture.Unilateral synostosis ofthe coro-nal suture
results in an asymmetric par-allelogram-shaped forehead and brow.The affected side
is flattened,and thecontralateral side may show compen-satory bulging or bossing.In
addition,synostosis ofthe coronal suture oftenindirectly affects the lower facial
mor-phology.The root ofthe nose is deviatedto the involved side,and the chin is
oftendeviated to the side opposite ofthe flat-tened forehead.The mandible is
normal-ly developed but may exhibit secondarydysmorphology.29,30Congenital
Hemifacial HyperplasiaCongenital hemifacial hyperplasia is arare unilateral
enlargement ofthe cranio-facial soft and/or bony tissues.Althoughthe term
hemihypertrophyhas commonlybeen used,it is inappropriate because thecondition
refers to hemihyperplasia.31Pollock and colleagues have hypothesizedthat the reason
for the asymmetric facialdevelopment is abnormal neural crestmigration.32Yoshimoto
and colleagueshave found increased proliferative activi-ty ofosteoblasts in a
patient with congen-ital hemifacial hyperplasia and havehypothesized that
fibroblast growth fac-tor and its receptor signal transductionaxis in osteoblasts
may be selectivelyinvolved,lending to the progression ofhemifacial
overgrowth.33Developmental AnomaliesIntrinsic Jaw-Growth DeformitiesFacial
HemiatrophyFacial hemiatro-phy (Parry-Romberg syndrome) is char-acterized by a
progressive unilateralfacial loss ofskin,soft tissues,cartilage,and bony tissue
(Figure 58-3).Usually,the left side is affected rather than theright.Associated
abnormalities includejacksonian epilepsy,cutaneous dyspig-mentations,and
ipsilateral alopecia.31The syndrome usually starts during thefirst two decades
oflife and completesprogression within 2 to 15 years.34�36The etiology offacial
hemiatrophyremains largely unknown,but associa-tions with Lyme disease,ablation
ofthesuperior cervical sympathetic ganglia,localized scleroderma,Rasmussen en-
cephalitis,and systemic lupus erythe-matosus have been found.37�41Alter-ations in
the peripheral trophicsympathetic system is one ofthe moreemphasized
theories.31Treatments haveincluded silicone injections,alloplasticimplants,microfat
injections,andmicrovascular free tissue transfer.42�44Hemimandibular
Hyperplasia/Elonga-tionAnother condition resulting infacial asymmetry is
hemimandibularhyperplasia.Hemimandibular hyperpla-sia is characterized by a diffuse
enlarge-ment ofthe condyle,the condylar neck,and the mandibular ramus and
body.45In1986 Obwegeser and Makek describedthe deformity as hemimandibular hyper-
plasia or hemimandibular elongation.46In 1996 Chen and colleagues proposedthat all
cases ofhemimandibular hyper-plasia and hemimandibular elongationactually represent
variations ofcondylarovergrowth.47They proposed that ifcondylar overgrowth is not
arrested,itcan progress into hemimandibularhyperplasia and hemimandibular elon-
gation.In spite ofthe differences innomenclature,no etiologic factor hasbeen
established.Condylar growth pat-terns can be evaluated by serial
clinicalcomparisons,cephalometric tracings,and bone scanning with technetium
99mphosphate.However,no ideal methodhas been found to assess whether condy-lar
overgrowth is �inactive.�Therapy isguided by the patient�s age and condylargrowth
activity.Treatment modalitieshave ranged from condylectomy toorthopedic maxillary
management.However,strong consideration should begiven to refraining from surgery
untilgrowth activity has ceased.45Secondary Growth DeformitiesSternocleidomastoid
torticollis is a condi-tion thought to result from a birth trauma�induced hematoma
ofthe sterno-cleidomastoid muscle that fibroses overtime and leads to muscular
contraction.However,the precise etiologic factors arestill considered unknown.Ifthe
condi-tion is not corrected with proper physio-therapy for the
neck/sternocleidomastoidmuscle or surgical therapy,malformedfacial development may
occur ipsilateralto the side affected by the torticollis.48,49Duchenne�s muscular
dystrophy andcerebral palsy often result in areas ofdecreased muscle tone,which can
affectthe development offacial morphology bylimiting the amount ofbone formationat
sites ofmuscle attachment and func-tion.Consequently,facial asymmetry/dysmorphology
can be a finding withDuchenne�s muscular dystrophy andcerebral palsy.50FIGURE58-
3Right facial hemiatrophy (Parry-Romberg syndrome).At the time this photo-graph was
taken,the patient had undergoneskin and bone grafting.
1208Part 8: Orthognathic SurgeryAcquired Facial AsymmetriesCondylar TraumaA
frequent cause offacial asymmetry inthe growing child is trauma to themandibular
condyle (Figures 58-4 and 58-5).51Trauma-induced injury to thecondyle can lead to a
hemarthrosis,whichcan result in scarring and restricted trans-lation ofthe
condyle.Proffit and Turveydescribed this as a functional ankylosis orsoft tissue
extracapsular ankylosis.52Bonyankylosis ofthe condyle to the skull basecan also
occur from an intracapsularhemarthrosis.Consequently,traumatic-inducedscarring or
bony ankylosis ofthe TMJ canresult in relative degrees ofrestrictedskeletal
growth.In other words,the greaterthe degree oftranslational restriction,thegreater
the facial deformity.Thus,a fre-quently entertained question is whetheropen
reduction and internal fixation ofthe condylar fracture are required to stabi-lize
the condylar cartilaginous growth cen-ter.Studies in immature primates andchildren
have revealed that the displacedcondylar segment undergoes resorptionand that a new
condyle and the overlyingcartilage are regenerated.Thus,there isnothing
intrinsically important about thecondylar head tissue as a mandibulargrowth
center.Because the condylar headin children is generated spontaneously,thenecessity
ofopen reduction and internalfixation ofthe displaced condylar segmentis
eliminated.Moreover,the resulting scarand possible soft tissue and hard
tissuerestriction from open reduction couldoutweigh the benefits ofsurgical
andanatomic condylar alignment.Thus,openreduction ofcondylar fractures in
childrenshould be avoided.52�54Juvenile Idiopathic Arthritis Facial asymmetry can
be a finding inpatients affected with juvenile idiopathicarthritis (JIA) ofthe
TMJ.55JIA is a dis-ease characterized by chronic inflamma-tion ofone or more joints
affecting chil-dren up to the age of18 years.The TMJ isfrequently involved and can
lead to facialgrowth disturbance including facial asym-metry.55TMJ involvement can
be asym-metrical or asymptomatic and may not beevident
clinically.56,57However,sympto-matic TMJ involvement may not be asso-ciated with
facial growth disturbances,and,conversely,facial growth disturbancemay be present
without TMJ symptoms.56Both polyarticular- and pauciarticular-onset JIA have been
found to have a nega-tive impact on the form,function,andesthetics ofthe
face;however,the effectsare more pronounced with
polyarticularJIA.58,59Characteristic facial features ofpatients with JIA include a
small mandible,Class II malocclusion,and anterior openbite.Patients with
polyarticular JIA withTMJ involvement tend to have small shortfaces with
underdeveloped mandibles.60Currently there is no effective thera-peutic means to
eliminate the progressionofthe disease and its effect on facial devel-
opment;however,methotrexate therapyhas been shown to minimize TMJ destruc-tion and
craniofacial dysmorphology inpatients affected with polyarticular
JIA.61Corticosteroids have been used in thetreatment ofJIA,but their
therapeuticvalue is still controversial.Degenerative Joint DiseaseDegenerative
joint disease (DJD) is con-sidered an end-stage result ofprogressiveinternal
derangement ofthe TMJ.Usual-ly,patients have bilateral involvement ofthe
TMJ;however,unilateral involvementin not uncommon.The �wear and tear�effect ofDJD
on the TMJ results incondylar-glenoid erosion and decreasedcondylar ramus
height.Clinically,patients often present with increasingpreauricular crepitus,a
limited mandibu-lar range ofmotion,pain,and an anteri-or open bite.62Clinical
AssessmentPrinciples The method ofevaluating the patient witha dental facial
condition begins with ascer-taining the patient�s chiefcomplaint.Then,as the
medical history ofthe presentillness unfolds,the answers to pertinentquestions
regarding a history offacialtrauma,arthritis,and congenital malfor-mations,for
example,are obtained.A physical examination ofthe headand neck should include the
following63:1.Visual inspection ofthe entire faceincluding facial subunits for
symmetry2.Palpation ofthe face to differentiatebetween soft and hard tissue defects
FIGURE58-4This adult male sustained a frac-ture ofthe condyle as a teenager
resulting inabnormal growth.FIGURE58-5Panoramic radiograph ofthepatient in Figure
58-4 demonstrates condylarasymmetry.
Management ofFacial Asymmetry12093.Comparison ofdental and facial mid-lines with
each other and with the cen-tral facial axis4.Inspection for gonial angle
symmetryand differences in antegonial notching5.Analysis ofthe relationship
betweenthe upper lip and the maxillary centralincisors6.Inspection for
malocclusion,occlusalcanting,inclination ofanterior teeth,dental crowning,open
bites,maximalinterincisal opening,and mandibulardeviation with opening7.Examination
ofthe TMJ functionAfter the patient�s chiefcomplaint,history ofpresent illness,past
medical his-tory,physical examination,radiographsand articulator mounted diagnostic
castshave been obtained and evaluated,a prob-lem list and corresponding treatment
plancan then be constructed.Radiography Panoramic RadiographsThe
panoramicradiograph can provide informationregarding the relative height
ofthemandibular condyle and ramus.Degenera-tive changes or asymmetric morphologycan
be identified with a comparative verti-cal measurement ofthe condylar head apexto
the sigmoid notch base,and the sigmoidnotch base to the mandibular
angle.63Posteroanterior Cephalometric Radio-graphsThe posteroanterior cephalo-
metric radiograph enables one to under-stand the extent ofthe deformity relativeto
the cranial base.By tracing soft andhard tissue features and then placing atrue
vertical and horizontal midline axis,one can visualize deviations ofthe dentaland
skeletal midline,occlusal cants,andvertical asymmetries.63Lateral Cephalometric
RadiographsAlateral cephalometric radiograph can pro-vide clues ofvertical
differences by thelack ofsuperimposition (eg,two separateradiographic mandibular
inferior bor-ders).However,to determine the relativesignificance ofthe differences
in dentofa-cial superimposition,one must knowwhether the external auditory canals
arelevel with the patient�s natural head posi-tion.Only a single cephalometric ear
rodshould be used ifthe patient�s auditorycanals are not level.63Computed
TomographyComputed tomography (CT) can providetwo-dimensional localized views
ofthefacial skeleton,or it can be developed fur-ther into three-dimensional views
that canprovide excellent detail necessary for theproper diagnosis and treatment
ofa com-plex facial dysmorphology (Figure 58-6).Stereolithographic ModelingThree-
dimensional CT scans can provideinformation to allow the fabrication ofan actual
three-dimensional skeletalmodel.These models can help one makesurgical
predictions;however,because oftheir expense,these models are mainlyused for complex
dentofacial and cranio-facial deformities.64Technetium 99m PhosphateBone
ScansRadionuclide skeletal scintigraphy hasbeen shown to be a sensitive technique
foridentifying mandibular overgrowth in thepatient with a facial
deformity.However,scan findings are nonspecific and may bethe result ofa variety
ofbone and soft tis-sue abnormalities,including soft and hardtissue
carcinomas,sarcomas,metastaticdisease,hematologic disease,infections,inflammatory
states,metabolic diseases,and trauma.65In patients with facialasymmetry mandibular
overgrowth,nucleotide uptake is not symmetric bilat-erally.In these cases,patients
present withan increased nucleotide activity on theaffected side.However,caution
must betaken when evaluating an area ofincreased uptake not to mistake
condylarovergrowth for other conditions (ie,arthritis,TMJ disorders,trauma) that
canmimic nucleotide uptake activity.66Addi-tional techniques offusing single-
photonemission CT images to high-resolutionstructural CT images have been shown
toprovide a further precise anatomic delin-eation ofbone activity.67Surgical
TreatmentAsymmetry may not always be obvious tothe patient and family.Correct
treatmentbegins with proper diagnosis.One shouldevaluate the face in all
dimensions,careful-ly analyzing vertical and horizontal dimen-sions corresponding
to facial subunits.Failure ofthe surgeon to recognize asym-metry until after
surgery is often viewed bythe patient as an excuse for poor treatment.In
general,treatment planning offacialasymmetry is much the same as for
anyorthognathic case,except that moreemphasis is placed on the frontal
view.Cephalometrics may be grossly inac-curate owing to ear rod positioning.Pos-
teroanterior cephalometric radiographsare good simple screening tools but,stan-dard
computerized CT scans are muchmore accurate.CT data can be convertedby computer-
aided design/computer-aided manufacturing (CAD/CAM) imag-ing into an actual acrylic
model.ThisFIGURE58-6Three-dimensional computedtomographic scan ofasymmetric skull.
1210Part 8: Orthognathic Surgerymodel can be used for model surgery,implant
fabrication,and distraction osteo-genesis design.Ultimately,the clinical
examination isthe most important diagnostic tool.Bodyposture,mannerisms,and
hairstyle hidefacial asymmetry and may mislead thetreatment plan.In a University
ofNorth Carolinastudy of495 patients with facial asymme-try,the mandible was most
often affected.Upper facial asymmetry was found only in5%,but a chin deviation was
present in75% ofall cases.Chin deviation is mostoften to the left,indicating a
tendency forincreased right-sided growth.68Peoplenotice chin deviation.Delayed
TreatmentTreatment ofasymmetry in preadolescentchildren is extremely complex,and
theresults are not always predictable.Studiesofgrowth modification with
functionalappliance have been problematic becauseofa various treatment designs with
poortreatment group composition,poor con-trol group composition,and
difficultieswith randomization.The topic is often dis-cussed in orthodontic
pediatric textbooks.Although noninvasive techniques do notharm the patient,most
craniofacial asym-metry syndromes,condylar deformities,and traumatic injuries at an
early age dorequire surgery.Bite-block therapy can behelpful in controlling the
plane ofocclu-sion but rarely prevents surgery.Bite-blocktherapy is mainly directed
as an interven-tion for secondary growth deformities.Maintenance ofTMJ FunctionMild
asymmetry in a growing patient withfunctional condyles should receive
earlyinterceptive orthodontics,and the patientshould be allowed to finish growing
beforesurgery is performed.Jaw movement isimportant following condylar
fracture.Physical therapy and rehabilitation stimu-lates condylar and mandibular
growth.Poor function results in a more asymmet-ric mandible and secondary skull
base.Asymmetry ofthe skull base correlateswith maxillary midface asymmetry.Post-
traumatic mandibular hyper-plasia is less frequently seen than
growthretardation.Mandibular hyperplasia isusually apparent after adolescent
growth,whereas delayed growth is often presentearly in life.Regardless ofthe true
etiolo-gy,it is important to establish a surgicaltreatment plan with the most
esthetic,functional,and stable result.Orthognath-ic asymmetries should be treated
aftergrowth is complete,and often requirecombined maxillary and
mandibularsurgery.Orthodontic ConsiderationsHuman facial symmetry has long been
acritical factor for attractiveness.It is alsowell documented that true symmetry
isnot normal.69,70For the average orthodontic patient,minor asymmetries become a
concernonly as an esthetic issue.Severe asymme-tries often result in
crossbite,malocclu-sion,cheek biting,poor mastication,condylar
dysfunction,myositis,ten-donitis,and chronic pain.From a diag-nostic
standpoint,patients with asymme-tries differ from the typical orthodonticpatient in
several ways.The clinical exam-ination and records should generateenough
information to accurately diag-nose and formulate the best possibletreatment
plan.This includes multiplephotographs,lateral and posteroanteriorcephalometric
radiographs,and face-bow-mounted dental models.62�71Facial structures may be
evaluatedagainst a grid formed by the midsagittalplane and several perpendicular
lines,according to the area being evaluated
(eg,interpupillary,subnasal,stomion).Atongue blade or Fox plane can be used
todetermine whether a cant is present in theocclusal plane.Unilateral vertical
maxillaryexcess and mandibular asymmetries areusually associated with an occlusal
planecant.63This is why most asymmetries can-not be treated with single-jaw
surgery.Typical orthodontic diagnosticrecords rely heavily on a profile
view.Thelateral approach comes from the tradi-tional diagnosis based on
cephalometricradiographs;however,patients are moreaware oftheir esthetic
presentation fromthe frontal view.Additional diagnosticrecords may include a
posteroanteriorcephalometric radiograph,a submen-tovertex radiograph,and an
accurate face-bow transfer with casts mounted on asemiadjustable
articulator.65�73The orthodontic management ofpatients with asymmetries does not
differa great deal from that for a typical orthog-nathic patient.Good communication
anda team approach during all phases oftreat-ment are essential.Once the diagnosis
andtreatment plan are established,the presur-gical orthodontic phase is
initiated.Basicprinciples ofpresurgical orthodonticsmust be observed.All tooth
movementsthat may compromise stability must beavoided,especially ifthe intended
move-ment may be more easily accomplishedwith the movement ofa bony segmentduring
surgery,that is,transverse expan-sion.Dentoalveolar decompensation inthe upper arch
must take into account thepostsurgical position ofthe upper incisor.Maxillary
anteroposterior movements aswell as posterior impactions have thegreatest effect on
the upper incisors withregard to anteroposterior positioning
andtorque,respectively.Dentoalveolar decom-pensations in the lower arch must
observethe anatomic limits ofthe symphysis.Onemust observe that the morphogenetic
pat-tern ofpatients with maxillomandibulardiscrepancies results in specific
abnormalbony architectures.It is for this reason thatcephalometric norms should not
be used.There should be no compromise in thepresurgical orthodontic treatment plan
asit would severely limit the overall out-come.Do not hesitate to extract teeth
ifnecessary.Impressions and early model
Management ofFacial Asymmetry1211surgery are helpful and confirm that
thepresurgical goals are correct and/or havebeen achieved.Common problemsinclude
improper buccal root torque in theupper arch,improper arch coordination(especially
when anteroposterior move-ments are planned),and a lack ofoverjet(which would
hinder placement ofbuccalsegments in an ideal Class I occlusion).The decision to
extract teeth is oftendifficult.The first question that must beasked is whether
there is severe crowding.The answer is based primarily on theplanned position for
the upper and lowerincisors well positioned in basal bone.Theupper
incisors�relationships to the sella-nasion (SN) (104�),palatal plane (104�),and
nasion-A point (NA) line (4 mm and22�) are good indicators ofwhether theseteeth
need to be decompensated.It mustbe kept in mind that posterior impactionofthe
maxilla decreases the torque oftheupper incisors.In addition,large unilater-al
vertical changes such as impactiondowngrafting on one side also swing androtate the
midlines ofthe maxillary teeth.However,when this is anticipated,theupper incisors
should be maintainedslightly proclined.As a surgical objective,the position ofthe
upper incisor and thatofa point relative to the nasion perpendic-ularly can be used
as reasonable cephalo-metric references.Therefore,dentalcrowding and the desired
position for theupper incisors within basal bone ofthemaxilla ultimately determine
the need forextractions.Upper second bicuspids arethe teeth ofchoice for extraction
whenminimal incisor decompensation isrequired.Maxillary first bicuspids
areextracted when the upper incisors requiregreater degrees ofdecompensation,suchas
in Class III malocclusions.Ifmild crowding is present (up to 4 mm) and no
dentoalveolar decompensa-tion is needed,a nonextraction approachis acceptable,and
some interproximalreduction may be required.Ifdecompen-sation ofthe incisors is
required,thecephalometric correction must be factoredinto the crowding
assessment.For every 3�ofchange in the angle between the lowerincisor and the
mandibular plane,onemust add or subtract 2.5 mm to the mea-sured clinical
crowding.In patients withClass II malocclusion,cephalometric cor-rection most often
adds to the clinicalcrowding since the lower incisor typicallyrequires more upright
positioning.Inpatients with Class III malocclusion,cephalometric correction usually
alleviatescrowding.In other words,cephalometriccorrection takes into account the
goals forthe lower incisor in the crowding assess-ment;moreover,it helps one decide
whichteeth should be extracted.When the mea-sured crowding in the lower arch is
mod-erate (5�9 mm),second bicuspids shouldbe extracted.The result is the
alignmentand complete closure ofthe extractionsites.This should be achieved with
thelower incisor in the ideal position.Whencrowding is severe (> 10 mm)
aftercephalometric correction,first bicuspidsshould be extracted to allow
alignmentand proper positioning ofthe lowerincisor.The rationale is as
follows:Whentwo bicuspids are extracted,an average of14 mm ofspace is created.Ifthe
totalcrowding is 10 mm including cephalomet-ric correction,then 4 mm ofspace are
left.These 4 mm are used by forward move-ment ofthe posterior teeth as lost anchor-
age during the alignment and retraction ofthe lower anterior tooth.Maximum
decompensation is oftenrequired with minimal clinical crowding,therefore requiring
that the first bicuspidbe extracted.Ifcrowding exceeds 14 mm,extractions alone are
not sufficient to alle-viate crowding and achieve an ideal posi-tion for the lower
incisors.Interproximalreduction may help to create another 3 to4 mm
ofspace.Patients with hyperdivergent faceswith an asymmetry require
differentialmaxillary impaction.Such cases need aflattening ofthe curve ofSpee on
botharches prior to surgery.The curve ofSpeeis often different from left to
right.Flatten-ing this curve allows for maximum inter-cuspation to be achieved
between the ante-rior teeth and bicuspids,with minimumposterior open bites.Ifthe
posterior max-illa is intentionally overimpacted whenrelapse is expected,the result
is a posterioropen bite,and no vertical elastics areplaced distal to the bicuspids
for the first 8 weeks after surgery.Intercuspationshould be accomplished.In the
patientwith facial asymmetry,one side may bemore open than the other.It is usually
thehypoplastic side that remains slightly open,and teeth can be extruded
postsurgically.An open bite of2 mm is acceptable andsometimes desirable as settling
and somerelapse occur after surgery.After surgeryno orthodontic forces should be in
thedirection ofthe potential surgical relapse.Patients with hypodivergent asym-
metric faces typically require mandibularadvancement and an increase ofthe
loweranterior facial height.The original maloc-clusion is often characterized by an
exces-sive overbite,overjet,and curve ofSpee.The upper curve ofSpee should be flat-
tened and the ideal position ofthe upperincisors achieved.The degree ofcurve ofSpee
may be different from side to side.Noattempt should be made to level the lowercurve
ofSpee because forward movementofthe mandible to an ideal overbite andoverjet
automatically increases the lowerfacial height.Ifthe lower mandibularplane angle
has been maintained duringadvancement,this may result in a posteri-or open bite at
the bicuspid or molars.Theinterocclusal space leads to leveling ofthemandibular
curve ofSpee with minimaleffort after surgery.A flexible braided wireis used in the
lower arch as vertical inter-cuspation elastics are applied to extrudethe lower
posterior teeth.A class II or classIII vector may be incorporated to achieveoptimal
occlusion.The upper arch shouldbe stabilized by a heavy rectangular
wire.Postsurgical orthodontic procedures
1212Part 8: Orthognathic Surgeryusually are completed within 6 to 8 months
ofsurgery ifall other phases oftreatment are successful.Vertical elasticsmay be
directed by the orthodontistdepending on the occlusion and theunique differences
ofthe hyperplastic orhypoplastic side ofthe face.Severe orthog-nathic asymmetries
are often difficultfrom an orthodontic standpoint owing tothe presence ofunilateral
differences ofahyperplastic presentation and a contralat-eral hypoplastic dental
compensation.Surgical Approach and TechniquesIn rare cases asymmetries may be
treatedin a single jaw.Generally,asymmetricgrowth causes compensation in the
teeth,alveolus,and other jaw.Furthermore,thiscompensation is different from side to
sideand requires slightly different orthodonticmechanics.Facial asymmetry may
beimproved esthetically by an inferior bor-der ostectomy,augmentation,and genio-
plasty.The esthetic impact ofasymmetryinvolves both hard and soft tissue.Thezygoma
and periorbital and nasal struc-tures may be asymmetric.Even adjacentsoft
tissues,such as the salivary glands,muscles,and adipose tissue,can be differ-ent in
quantity from side to side.Thepatient should be well informed regardingthe
limitations and surgical expectations.Rarely can asymmetric deformities be cor-
rected completely.Most patients notice horizontal ortransverse discrepancies more
often thanvertical asymmetries.Maxillary dentalmidline,chin,and nasal deviations
areobvious clinically.Facial length is lessapparent.In severe cases,such as hemifa-
cial microsomia or other syndromes,softtissue augmentation and even free vascu-
larized tissue may be necessary.The oral and maxillofacial surgeonshould make a
note ofminor anatomicasymmetry.Orbital,nasal,and upper lipposition;maxillary
midline;smile arch;amount ofgingival show per side;cheekmass;dimples;mandibular
dental mid-lines;mandibular deviations on opening;TMJ
articulation;translation;gonialangles;and cervical anatomy should bedocumented.The
surgical procedureshould be selected based on the etiologyand a concern for
stability.For example,when correcting a maxillary cant,verticalimpaction is more
stable than is verticaldowngrafting.Often the discrepancy canbe corrected by a
combination ofbothimpaction and downgrafting.Severe asym-metries with a short ramus
height mayrequire an extraoral inverted L osteotomywith bone grafting.This
technique releasesthe mandibular sling and provides goodaccess to the hypotrophic
ramus,excellentbone grafting access,and accurate rigid fix-ation.Vertical changes
of< 6 to 8 mm maybe treated by intraoral sagittal splitosteotomies.Rotational
movements ofthemandible produce proximal segment flar-ing on the advancing side and
ramus col-lapse on the other.Proximal segment flar-ing may require modification
(see Chapter56,�Principles ofMandibular Orthognath-ic Surgery.�).Some surgeons
prefer a verti-cal oblique ramus osteotomy combinedwith a unilateral sagittal split
ramusosteotomy.This combination surgery usu-ally requires intermaxillary
fixation,whichmay be beneficial in asymmetric cases.With current
techniques,monocorticalplate fixation can be achieved with a verti-cal ramus
osteotomy.On the other hand,intermaxillary fixation is often necessaryand even
beneficial because alignment ofthe segments with rigid fixation is notalways
possible and the soft tissue pullsback to the original asymmetric
position.Atreatment plan should be established withan accurate clinical
examination,cephalo-metric analysis,and model surgery.Thesurgical procedure should
be executed effi-ciently,deftly,and with minimal morbidi-ty.The aforementioned
issues ofrelapse,stability,and mode offixation should beestablished prior to
surgery and discussedwith the patient.The first,and perhaps most impor-
tant,treatment plan decision the surgeonencounters involves the upper
incisorposition.The choice ofmaxillary incisorposition is key and essentially
determinesthe three-dimensional position ofevery-thing else.The surgeon must
correct max-illary incisor midlines,proclination,occlusal plane,smile
arch,dental/gingivalshow,and lip support.An intermediatesplint can be valuable in
positioning themaxilla,assuming an accurate face-bowtransfer and model surgery have
been per-formed.One should not be a slave to anintermediate splint for it is only
onemethod ofaligning the asymmetry.Surgi-cal experience and appreciation
ofestheticsymmetry are often more valuable.The maxilla must be placed in theproper
and most symmetric position.Consider the occlusion in relation to theunsplit
mandible and ask yourself,Doesthat look reasonable according to thetreatment plan?
The maxillary positioncan best be measured using a combinationofan external pin,Fox
plane,lip position,and internal reference marks.The inter-mediate splint helps one
place and holdthe maxilla in the correct position duringrigid fixation.The concept
ofan interme-diate splint is based on proper condylarposition.Functional condylar
position inan awake upright person is not the same asit is in a supine paralyzed
patient.Further-more,asymmetric problems often origi-nate from abnormal condylar
(TMJ) dis-orders.Many patients with facialasymmetry do not have symmetric condy-lar
rotation and therefore exhibit a greatdeal ofmuscular compensation with pos-
turing.Ifan intermediate splint does notseem to position the maxilla properly in
allthree dimensions,the surgeon should con-sider other references for facial
symmetry.Nothing can replace surgical experience.The mandible is usually cut first
but is notsplit until after maxillary surgery and fixa-tion.This prevents excessive
force on thenew maxillary position and seems to
Management ofFacial Asymmetry1213expedite the process.Some surgeons com-plete and
fixate the mandibular osteotomybefore maxillary surgery.This requires
apredetermination ofboth mandibular andmaxillary positions.Mandibular ramus surgery
is oftendifficult in cases ofasymmetry because theramus and body ofthe mandible
aredeformed and hypoplastic and the rangeofmotion limited.Limited surgical
accessand a smaller soft tissue envelope create adifficult challenge.Ifthe mandible
is cutfirst but not split,the osteotomies aremade and a moist sponge is placed
whilethe maxillary surgery is completed.Themandible is later split and moved to
theproper position with the maxilla and heldin the proper occlusion by an
occlusalwafer or splint with intermaxillary fixa-tion.Rigid fixation ofthe mandible
can beachieved with either bicortical positionscrews or monocortical
plates,assumingthe condylar position is correct.In largehorizontal rotations ofthe
mandible,bicortical screws cannot be placed as truecompression screws (lag screws)
withouttorquing the condyle.Modifications ofthelingual cortical plate and selective
grindingofthe bone can be helpful in increasingthe bony apposition.In most cases
mono-cortical plates seem to provide adequatestability without compression ofthe
nerveor torquing ofthe condyle.Surgical mobilization is a key point inbimaxillary
surgery.The mandible andmaxilla should be free enough to be posi-tioned passively
without pulling the softtissue.This is a significant point to be con-sidered
because the positioning can createa tight masseteric sling and limitedperiosteal
tissue.Ifthe segments are�stretched�into position,one cannotexpect long-term
stability.A balancebetween an excessive stripping ofthe vas-cularity and a
restricted connective tissueenvelope must be achieved.Therefore,incases ofsevere
hypoplastic asymmetrywith only rudimentary condyle,oneshould consider condylar
reconstructionor extraoral procedures ofthe ramus.Insome situations distraction
osteogenesismay even be helpful in growing more boneand essentially expanding
tissue.Adjunctive simultaneous soft tissueprocedures can be considered after suc-
cessful positioning ofthe maxillo-mandibular dental component by securerigid
fixation.Alignment ofthe chin,nose,and malar complex should be performedafter the
functional anatomy ofthe maxil-la and mandible is established.Simultane-ous surgery
has multiple advantages,butmay not always be feasible.The following case is an
example ofapatient with facial asymmetry resulting fromtrauma who required
combination maxil-lary and mandibular surgery (Figure 58-7).She was a 20-year-old
female with a chiefcomplaint ofdifficulty eating and chewing;she had chronic
myofascial pain and masti-catory dysfunction.She had sustained a jawfracture as a
young child and had notreceived treatment.The young lady experi-enced gradual
facial asymmetry and soughtorthodontic treatment.Such a case cannotbe treated
properly with orthodontics alone;neither can it be corrected in a single jaw.Her
physical examination revealed ahealthy young woman in no acute dis-tress but with
an obvious facial deformi-ty.The basal view often better demon-strates the
deformity,as does having thepatient bite on a tongue blade (Figure58-8).She was
normocephalic (althoughshe had a short face),asymmetric,andhad deviation ofthe jaw
to her right(Figure 58-9).The TMJ articulated andtranslated well without clicking
or pop-ping.The maximum incisal opening was56 mm,with a deviation to the
right.Themandibular midline was 7 mm to theright,the overjet was 5 mm,the
overbitewas 2 mm,and there was excessive lowerdental show.She had a right
buccalcrossbite,an anterior crossbite,maxillaryhypoplasia,a canted maxilla,and a
shortmandibular condyle (Figure 58-10).The presurgical work-up included athree-
dimensional CT scan,cephalomet-ric and panoramic radiography,and face-bow mounting
for an accurate intermedi-ate splint and model surgery (Figures58-11�58-13).The
Erickson table wasused to measure the vertical change and tofabricate an
intermediate splint to assist inpositioning the maxilla from the stablemandible
(Figures 58-14 and 58-15).Thesurgical plan was a Le Fort I advancementof3 to 4 mm
and a downgrafting of4 to 5 mm on the right side (Figure 58-16).The osteotomy gap
was bone grafted withFIGURE58-7A,Frontal view with a full smile.B,Later profile
shows a midface deficiency and rel-ative mandibular prognathism in spite ofthe old
mandible fracture.AB
1214Part 8: Orthognathic Surgerybanked tibial bone that was mortised
andfixated.This was determined with amodel surgery to level the cant ofthemaxilla.A
Steinmann pin was placed atthe nasal bone for an external vertical ref-erence.This
technique is valuable inestablishing the correct facial dimension.In addition,a Fox
occlusal plane was usedto evaluate the leveling ofthe maxilla inrelation to the
infraorbital rims duringsurgery (Figure 58-17).Multiple methodsofevaluating
symmetry are helpful inachieving a good
result.Intermediatesplints,internal/external reference marks,and careful clinical
inspection from dif-ferent perspectives are all valuable surgicalskills in
simultaneous jaw surgery for thepatient with facial asymmetry.The unsplitmandible
is also a key reference for deter-mining the change in maxillary position.In this
case,after the maxilla was correct-ly positioned and leveled,the mandiblewas split
and set to the plane ofocclusion.A bilateral sagittal split osteotomy ofthemandible
was cut prior to the Le Fort Iprocedure but was not split.This seems tobe a common
sequence for most sur-geons.Consideration was given to a verti-cal oblique
osteotomy on the left,but therotation seemed favorable and the fixa-tion more
stable.Most patients with facialasymmetry are hypoplastic and needlower facial
advancement not reduction.Ahorizontal geniotomy was performed toadvance the chin
point 4 mm and level thedeviation.After the orthognathic phase ofsurgery,the tube
was switched to themouth by the transpharyngeal route.Thistechnique is efficient
and is commonlyused for simultaneous rhinoplasty.A stan-dard internal rhinoplasty
was performedto narrow the nose,refine the tip,andreduce the dorsum.Often facial
asymme-try affects multiple facial subunits.Thenose may appear asymmetric or
deviatedin relation to the mouth and chin.GreatFIGURE58-9Cephalometric view showing
ashort right facial height.FIGURE58-10Clinical analysis ofthe teeth demon-strates
an asymmetry and midline discrepancy.FIGURE58-11This three-dimensional comput-ed
tomogram clearly identifies the asymmetry.FIGURE58-12Lateral cephalometric
viewappears to show a prognathic jaw even thoughthere is a history ofa condylar
fracture.FIGURE58-8A,Basal view shows facial asymmetry and a chin deviation to the
right.B,Clinicalphotograph ofa tongue blade demonstrating the canted occlusal plane
in relation to the orbital rim.AB
Management ofFacial Asymmetry1215attention must be given to creating mid-dle face
symmetry.At 3 months the postoperative resultswere satisfactory and the patient was
veryhappy (Figure 58-18).The occlusion waswell aligned and finishing
orthodonticswere completed without difficulty.Thiscase demonstrates well the
principles dis-cussed above.An example ofmild developmentalasymmetry is
demonstrated in the follow-ing case.Such a case can be challenging forthe
orthodontist/surgical team because theorthodontic preparation may be differentfor
right and left sides;the asymmetry ismild and it is tempting to undertreat
theproblem with single-jaw surgery.Thispatient was a 17-year-old female with anopen
bite and right laterognathia.She hadposterior vertical maxillary excess
mildcrowding,Class III molar relation,dento-facial asymmetry,and a pseudomandibu-
lar prognathism (Figures 58�19 58�22).She complained oflip incompetence,diffi-culty
chewing and biting food,nasalobstruction,and xerostomia.Her fatherhad a history
ofmandibular prognathismand orthognathic surgery.This patient denied previous
traumato her facial bones.The orbital rims weresymmetric,but the right ear was
slightlylower.The TMJs articulated well,andthere was no myofascial
pain.Themandibular midline was 4 mm to theright,as was the chin.She had 4 to 5
mmofgingival show with a high smile.Therewas no overjet and 4 mm ofopen bite.Shehad
a mild transverse deficiency oftheposterior maxilla.The treatment plan began with
anextraction ofteeth no.1,16,17,18,32,4,13,21,and 28 prior to presurgical ortho-
dontics.Orthodontics was performed tolevel alignment and to decompensate
inpreparation for a two-piece Le Fort Iosteotomy,bilateral sagittal
osteotomy,genioplasty,and rhinoplasty.Presurgicalrecords included surgical mounted
mod-els,a face-bow transfer,and detailed radi-ographs.A CT scan was not obtained.A
sagittal split osteotomy was cut butnot split until after the maxilla was posi-
tioned.The maxilla was impacted 4 mmposteriorly and widened by a segmentalosteotomy
between the central incisors.An intermediate splint was used to FIGURE58-13A face-
bow transfer is valuablebut sometimes difficult in cases ofsevere asym-metry owing
to an abnormal external audito-ry canal.FIGURE58-14Mounted dental models on
anErickson platform with reference marks help onedetermine the amount ofchange and
fabricationofan intermediate splint.Note the amount ofmidline discrepancy.FIGURE58-
15Lateral view ofmounted models.FIGURE58-16Intraoperative measurementconfirms the
treatment plan and correct posi-tioning as determined by the intermediate
splint.FIGURE58-17A prosthetic Fox plane can be usedas a final reference to
evaluate the leveling ofthemaxilla in reference to the infraorbital rim.
1216Part 8: Orthognathic Surgeryposition the maxilla.The maxilla wasrigidly fixated
with a resorbable mesh.Internal and external references were usedto properly
position the maxilla,as werethe predetermined intermediate splintand model
surgery.The mandible wasthen completed and rotated slightly by thesagittal split
osteotomy.The chin pointwas moved to the left and advanced with ahorizontal
genioplasty.The endotrachealtube was changed to the oral route,andrhinoplasty
performed to improve facialharmony and symmetry.The surgery wasperformed without
complications.The postoperative course was withoutcomplications.At 1 month the
splint wasremoved and the occlusion was satisfacto-ry (Figures 58-23 and 58-24).At
1 year thepatient�s occlusion was good,the open bitestable,and facial symmetry
excellent (Fig-ures 58-25�58-28).SummaryCorrection oforthognathic deformitiesoften
requires surgery ofboth the maxillaand the mandible.Combining osteotomiesofthe
maxilla and the mandible is morecomplicated than single-jaw surgery and isperhaps
associated with increased morbidi-ty,but the surgical options and results
arebetter.Double-jaw surgery does notresultin twice the morbidity ofsingle-
jawsurgery.The indications for bimaxillarysurgery are severe deformities
untreatablein one jaw,deformities ofboth jaws,unfa-vorable movement prone to
relapse,andcomplex three-dimensional movements forwhich single-jaw surgery would be
a func-tional/cosmetic compromise.Dentofacialasymmetry may develop from a
primarycause but presents with secondary compen-sation in the hard and soft tissues
oftheface.Such asymmetry is a good indicationfor bimaxillary surgery.FIGURE58-
18A,Postoperative lateral view with animation.B,Postoperative frontal view with
animation.FIGURE58-19A,Initial lateral profile.B,Initial frontal view with
smile.ABABFIGURE58-20The frontal view ofdentitiondemonstrates an open bite and
midline asymmetry.FIGURE58-21Initial cephalometric radiograph.FIGURE58-22Initial
panoramic radiograph.
Management ofFacial Asymmetry1217Current surgical techniques havereduced the
morbidity and length ofstayin the hospital and have improved the out-come.This
chapter presented combinedmaxillary and mandibular osteotomieswith a special
emphasis on asymmetries asan indication.The concept ofcomprehen-sive facial
analysis and treatment was rep-resented in the cases demonstrated.Ifcor-rection
ofmild asymmetries is attemptedwith single-jaw surgery,the results aresuboptimal
and disappointing.AcknowledgmentWe would like to thank Dr.Andre Ferreirafor
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CHAPTER 59Soft Tissue Changes Associatedwith Orthognathic SurgeryNorman
J.Betts,DDS,MSSean P.Edwards,DDS,MDWhile few patients and clinicians questionthe
functional benefits oforthognathicsurgery,the esthetic results that accompa-ny
surgery ofthe bony foundation oftheface are equally powerful,ifnot more so.Itis
therefore incumbent upon the surgeonto include a component ofsoft tissuechanges in
the surgical treatment planwhile working to achieve a stable,func-tional
dentoskeletal unit.Fundamental to such treatment plan-ning is a sound knowledge
ofthe behaviorofthe soft tissues ofthe face in response toboth orthodontic and
surgical changes.Close collaboration between surgeon andorthodontist is essential
for this to occur.The soft tissue response to orthog-nathic surgery will be
discussed in thischapter.In addition,the surgical proce-dures and techniques used
to control thesoft tissue changes will be presented andevaluated in order to help
the surgeonunderstand,control,and maximize thebeneficial aspects ofthe facial soft
tissueresponse to surgery.Historical PerspectiveThe orthodontic literature contains
theorigins ofpredicting changes in the softtissues ofthe face following the
treatmentofdentofacial deformities.Orthognathicsurgery initially was used to
correctskeletofacial deformities and the resultantfunctional problems,often at the
expenseofthe facial soft tissue esthetics.In time,agreater concern for the esthetic
aspects ofsurgery developed,such that facial soft tis-sue prediction became an
integral part ofpreoperative planning and postoperativeoutcome assessment.Early
studies produced average ratios,which related designated hard and soft tis-sue
landmarks.The ratios were ofuse forpredicting the response ofthe soft tissuesto
various skeletal and dental changes.These ratios are
averages,however,andinvestigators realized that individual vari-ability was
significant.It was surmised thatfacial soft tissue response to orthodonticsand
surgery was multifactorial in nature.As a result,more elaborate statisticalanalyses
were employed,with varyingdegrees ofsuccess,to elucidate the factorsgoverning the
soft tissue response tosurgery.Consequently,prediction equa-tions were developed
that would help inpreoperative surgical planning and post-operative outcome
assessment.Recently,much emphasis has beenplaced on developing procedures that
assistthe surgeon in controlling the soft tissueresponse to surgery.By using
proceduressuch as the alar cinch suture and V-Yclo-sure,the surgeon can minimize or
elimi-nate unesthetic soft tissue changes and mayoptimize positive esthetic
changes.Facial Esthetics in SocietyPhysical appearance is critically importantin
our society.1�3Perception ofoneselfandthe perceptions ofothers are both essentialto
self-esteem.The most significant aspectofone�s self-image is facial appearance.Asa
result,dentofacial and skeletofacialdeformities have a significant psychologi-cal
and social impact on those afflicted.Further,the correction ofthese deformi-ties
can have an equally significant impacton self-esteem and personality.General
ConsiderationsMuch has been written about soft tissuechanges associated with
orthognathicsurgery,and each paper has its strengthsand weaknesses.Variation in
design,het-erogeneity ofstudy design,surgical tech-nique,and patient populations do
notallow for direct comparison.To makesome objective comparisons
betweenmethodologically different studies,weidentified a set ofcharacteristics for
thetheoretically ideal study ofthe soft tissuechanges associated with orthognathic
1222Part 8: Orthognathic Surgerysurgery (Table 59-1).These criteria shouldhelp the
reader to evaluate individualinvestigations.This technique for assessingthe
previous literature is helpful andshould be considered for use in other
areasofscientific investigation.4Most ofthe studies dealing with thissubject
provide ratios ofsoft to hard tissuemovement.Ratios are averages.Averagesapply well
to groups but often fail toaccount for individual variation within
thegroup.Further,these ratios only describethe relationship oftwo specific
points.It ishighly improbable that consistently accu-rate predictions ofsoft tissue
change canbe accomplished with only simple correla-tions.The complex behavior ofthe
facialsoft tissue drape is much more realisticallydescribed by the interaction
ofseveral fac-tors within the skeletal framework.Thismay explain some ofthe extreme
variabil-ity that many authors have encountered.5�9At best,ratios serve to give a
generalappreciation ofthe expected outcome.9Some authors have stated that ratios
arejust as efficacious in predicting the soft tis-sue response to osseous surgery
as mul-tiple regression and stepwise regressionanalysis.6,9This may be a result
ofseveralfactors such as lack ofinclusion ofimpor-tant variables (eg,the method
ofsoft tissueclosure and osseous contouring) into theirdatabase;a mixed sample
population(race,age,or sex);small numbers ofpatients;or inability to limit the
sample tospecific vectors ofosseous movement.4,6,8,9Recent investigations have
shownimproved predictive ability when patientswere grouped by vector-specific move-
ments ofthe osseous segments.4,10Orthodontic ConsiderationsTooth position and
alveolar morphologyresult from the sum ofapplied forces dur-ing their
development.These applied forcesderive from the cheeks,lips,and tongue
andparafunctional habits.Obviously,skeletalimbalances are accompanied by soft
tissueimbalances.The result is dental compensa-tion for skeletal
malocclusions.Orthodon-tic correction ofthese compensatorychanges will often result
in a worsening ofthe malocclusion preoperatively,and thejaw-to-jaw discrepancy will
appear clinical-ly more severe.11,12Thus,initial treatmentplanning should consider
these changes,and final surgical treatment plans should bebased on records obtained
as close tosurgery as possible.When evaluating ratiostudies,it becomes apparent
that the posi-tion ofthe incisor teeth does not alwaysaccurately reflect the
osseous movement.This is because ofpostoperative orthodon-tic tooth movement.The
molar teeth orbony landmarks such as the anterior nasalspine (ANS) undergo less
postoperativechange and may more accurately describethe osseous surgical
movement.Therefore,these landmarks should produce a moreaccurate ratio or
prediction.9Cephalometric ConsiderationsThe use ofa standardized
cephalometrictechnique is essential to the study ofthissubject.The components ofa
standard-ized cephalometric technique are usingthe same cephalometer,with the
samesource-object and object-film distances,and positioning the patient in a
naturalhead position with the teeth in centricrelation and soft tissues in
repose.Thecephalogram obtained from the standard-ized cephalometric technique must
allowvisualization ofthe complete soft tissueprofile.Relaxation ofthe soft tissues
maybe difficult to produce and reproduce.Relaxed lip posture is especially
difficultto achieve in patients with excessive inter-labial gap.Straining to close
the gap bycontracting the mentalis muscles flattensTable 59-1Theoretical Ideal
Characteristics ofa Study to Investigate the Soft TissueChanges Associated with
Orthognathic Surgery1.Prospective2.Adequate sample size3.Randomized treatments
(iftreatments differ within the sample)4.Nongrowing patients5.No previous trauma to
the osseous structures ofthe face6.Exclusion ofpatients with congenital defects or
syndromes (eg,cleft patients)7.Elimination ofthe confounding effects ofpre- and
postoperative orthodontic tooth movement8.Constant presence or absence
oforthodontic appliances9.Same cephalostat used for all cephalograms with identical
source-subject and subject-film distances10.Soft tissues in repose for all
cephalograms11.Superimposition ofcephalograms on the nearest osseous structure not
affected by surgery or on a stable reference line12.Use ofa tracing template to
assist in landmark identification13.Evaluation ofboth profile and full facial soft
tissue changes,or 3-D analysis14.No concomitant or prior soft tissue
surgery15.Exclusion ofsegmental surgical procedures16.One vector ofmovement (or
grouped in study)17.No concomitant osseous surgery on another portion ofthe facial
skeleton18.Homogeneity ofthe soft tissue incisions and closure techniques19.No hard
tissue contouring (eg,recontouring ofANS)20.Use ofrigid osseous fixation21.Uniform
follow-up intervals22.Follow-up time ofat least 6 months (1 year is
preferable)23.Error analysis ofmeasurement and landmark identificationANS =
anterior nasal spine.Adapted from Betts et al.4
Soft Tissue Changes Associated with Orthognathic Surgery1223the labiomentalfold and
distorts the over-all contour ofthe chin.It is important thatpatients be instructed
to keep their lips inrepose for the cephalogram.13To minimize measurement error
dur-ing cephalometric analysis,landmarks orplanes approximating the structuresbeing
evaluated must be superimposed.This superimposition should be on land-marks not
modified or changed duringthe surgical procedure.9,14Another con-tributing factor
to measurement error isorthodontic tooth movement betweenthe times
ofcomparison.Orthodonticchanges can be minimized by obtainingthe preoperative
cephalogram within amonth ofthe planned surgical proce-dure,6,9and performing
minimal post-operative orthodontics.9Also,the pres-ence,or
absence,oforthodonticappliances must be constant during thestudy period.The
presence oforthodon-tic appliances influences lip posture,andtheir placement or
removal will changethe soft tissue drape.4Landmark identification is simplifiedand
becomes more accurate when tem-plates are used.9,10,14This is especiallyvalid for
soft tissue landmarks.11Soft tis-sue landmarks are often arbitrary andlocated on
gently curving contours.Theselandmarks can therefore move verticallyover the
surface ofthe tissue after surgi-cally induced change.8,12Iftracing tem-plates are
used,these points can be moreaccurately located.Soft Tissue ConsiderationsThe
ability to predict the hard and soft tis-sue changes prior to an orthognathic sur-
gical procedure is critical to the treatmentplanning process.With the refinement
ofsurgical procedures and the advent ofrigidfixation techniques,the surgeon is able
toaccurately reposition and retain theosseous components in a planned posi-
tion.However,the change in soft tissuemorphology after combined orthodonticand
surgical therapy depends on severalfactors.These include surgical proce-
dure,6,15�19method ofwound clo-sure,6,9,15,16,18,19the new spatial arrange-ment
ofthe skeletal and dental elements,19the adaptive qualities ofthe soft
tissues,19growth,17,20orthodontic vectors oftoothmovement,17,19lip
thickness,5,6,17,21�23liptonus,9lip area,lip contact (competence),lip
strength,interlabial gap,amount ofoverjet,amount offatty tissue and muscu-
lature,and postoperative edema.17Because ofswelling,tissue redistribu-tion,and
functional adaptation,long-termfollow-up is needed to assess soft tissuechanges
after surgical procedures.Mostauthors suggest that the soft tissues stabilizeafter
6 months.15,17,19,21,22Others suggestthat at least 12 months are required.11,24Hack
and colleagues found evidence ofcon-tinued soft tissue settling several years
aftersurgery.25Surgical technique and method ofwound closure have been shown to
affectsoft tissue relationships.6,9,15,16,18,19,26�28Forexample,the horizontal
incision in theupper labial vestibule commonly used togain access to the maxilla
for the Le Fort Iosteotomy causes shortening ofthe lip withloss ofvermilion and a
decrease in lip thick-ness,16whereas vertical incisions with a tun-neling approach
and palatal flap for thesame surgical procedure show minimalpostoperative lip
changes.19Betts and col-leagues,investigating the soft tissueresponse to maxillary
surgery,noted thatsoft tissue changes may be more affected bythe type and position
ofthe soft tissue inci-sion and methods used in closure than bythe surgically
induced hard tissue change.4Changes in facial esthetics and occlu-sion following
orthognathic surgerydepend highly on the stability achievedfollowing surgery.Simply
put,the soft tis-sue will mirror changes in the bony foun-dation should skeletal
relapse occur.Many authors have shown that thinlips move more predictably than
thicklips.5,6,10,17,22,23Two theories have beenadvanced to explain this
discovery.First,the actual bulk ofa thick lip may have atendency to absorb a large
amount ofbonyadvancement without a perceptiblechange in soft tissue
contour.Second,�dead space�under the lip may absorb thefirst portion ofa bony
advancementbefore the soft tissue is affected (eg,withsevere maxillary
retrognathia).5,6,10,17,22,23The general trend noted in the litera-ture is that the
horizontal changes in thesoft tissues are often predictable,whereasthe vertical
changes are unpredictable.This may be because ofsmaller move-ments in the vertical
plane and the use ofsoft and hard tissue landmarks better suit-ed for horizontal
assessment.Also,hardtissue change is less predictable and lessstable in the
vertical dimension.The cephalometric landmarks shown inFigure 59-1 will be used to
describe the rela-tionships between the soft and hard tissuechanges presented in
the rest ofthis chapter.Orthodontic Incisor RetractionMost orthodontic changes will
be reflectedin changes in the position and posture ofthe lips.Early studies in the
orthodontic lit-erature stressed that the soft tissue profilewas closely related to
skeletal and dentalstructures.29More recent work has demon-strated that a direct
relationship betweenhard and soft tissue changes may not alwaysexist.20,30Simply
put,the position ofthe lipsis not solely determined by tooth position.The effects
ofgrowth and development,large ANB angle (angle formed by A point,nasion,and B
point),positional relation-ship ofthe upper incisor on the lower lip(overbite and
overjet),and adipose tissueare other factors that confuse the issue andmay
contribute to the great individual vari-ability observed.14,31The changes in the
soft tissues associ-ated with orthodontic incisor movementsare seen in Table 59-
2.Review ofthe literature indicates thatwith incisor retraction,the upper
liprotates backward around subnasale,18withan associated reduction in the
prominenceofthe lips relative to their adjacent sulci.32
1224Part 8: Orthognathic SurgeryAlso,upper lip thickness increases withmaxillary
incisor retraction (1 mm with 3 mm ofincisor retraction,331 mm with1.5 mm ofincisor
retraction34).Correla-tion analysis discloses that upper lipresponse is related not
only to the upperincisor retraction,but also to lower incisormovement,mandibular
rotation,and theposition ofthe lower lip.The lower lip moves less predictablywith
retraction ofthe incisors than doesthe upper lip.32Several theories have
beenadvanced to explain this phenomenon.Hershey has theorized that this is
becausethe lower lip is much more self-supportingand not as dependent upon
underlyingincisor support.32Other investigators feelthat this is explained by
combined upperand lower incisor effects on the lower-lippositioning (note the �1:1
effect ofupperincisor retraction to lower-lip retrac-tion).35They feel that the
upper teeth,notthe lower,establish the curve ofthe lowerlip.Therefore,ifthe upper
incisor isretracted more than the lower incisor,thelower lip may displace more
posteriorlythan the lower incisor (�1.56:1,35�1.22:132).Another theory is that
manyfactors contribute to the final position ofthe lower lip.This theory is
supported bycorrelation analysis,which indicates thatmandibular rotation had a
greater influ-ence on lower lip response than did incisormovement.Stepwise
regression analysislends further support to this theory byrevealing a complex
interaction betweendental movement,mandibular rotation,and the perioral soft
tissues,as well as acomplex relationship within the soft tis-sues
themselves.Maxillary Surgical ProceduresMost soft tissue change after Le Fort
Isurgery is manifested in the nasal andlabial structures.36�38Nasal
StructuresMovement ofthe maxilla affects thelower aspect ofthe nasal
dorsum.5,6,21,36�39The general trend is a widening ofthealar base in all patients
regardless ofthevector ofmaxillary movement.An associ-ated shortening ofthe
columellar height,alar height and nasal tip projection hasbeen observed,and the
nasolabial angledecreases or remains constant in mostcases (Figure 59-
2 ).4Different movements ofthe maxillahave distinct effects on the nasal andlabial
morphology (Table 59-3).Superiorrepositioning ofthe maxilla causes eleva-tion ofthe
nasal tip,40,41widening ofthealar bases,4,41and a decrease in thenasolabial
angle.40Inferior maxillaryrepositioning produces loss ofnasal tipsupport,downward
movement ofthecolumella and alar bases,thinning ofthelip,and an increase in the
nasolabialangle.Anterior repositioning ofthe max-illa has a profound effect on the
nose andupper lip,resulting in advancement ofthe upper lip,subnasale and
pronasale,thinning ofthe lip,16widening ofthe alarbases,and an increase in the
supratipbreak ifthe ANS is left intact.8,36�38Thenasal tip advances approximately
one-halfthe distance ofsubnasale.21This maybe a result ofwidening at the alar
base,which reduces nasal tip protrusion.4Soft tissue mentonPronasaleA
pointSubnasaleSuperior labial sulcusProsthionIncisor A pointLabrale superiusStomion
superiusIncisionsuperiusStomion inferiusIncision inferiusLabrale inferiusIncisor B
pointInferior labial sulcusB pointPogonionSoft tissue pogonionGnathionSoft tissue
gnathionMentonAnterior nasal spinePosterior nasalspineFIGURE59-1The hard and soft
tissue cephalometric landmarks used for the evaluation ofthe hard and softtissue
changes associated with orthognathic surgical procedures.These landmarks are
referenced in Table 59-2.Adapted from Betts NJ et al.4
Soft Tissue Changes Associated with Orthognathic Surgery1225Preoperative alar-base
width ofthenose is important in final postsurgicaloutcome.Narrow noses were
observed towiden more at the alar base than didbroad noses.4,26Important nasal
changeshave been documented as a result ofrota-tion ofthe maxilla.9,42A
counterclockwiserotation ofthe occlusal plane raises thenasal tip,while a clockwise
rotation oftheocclusal plane decreases the superiormovement ofnasal tip.6,42Labial
StructureMaxillary surgery has a significant impacton upper lip morphology and
position.The upper lip is attached to the nose andthis prevents a 1:1 soft tissue
change.43Theupper lip widens and lengthens at thephiltral columns after maxillary
surgery.4Shortening ofthe upper lip with a loss ofexposed vermilion can occur ifa
V-Yclo-sure technique is not employed at the timeofsurgery.16,28Anterior Segmental
RepositioningThe soft tissue changes associated with themaxillary segmental setback
osteotomyinclude an increase in the nasolabial anglebecause ofposterior lip
rotation aroundsubnasale,43�46lengthening ofthe upper lip,decrease in interlabial
gap,46and uncurlingand retraction ofthe lower lip with associat-ed decrease in the
depth ofthe inferior labi-al sulcus (Table 59-4).45Table 59-2Soft Tissue Changes
Associated with Orthodontic Tooth MovementAnatomic StructureRatioOrthodontic
MovementAuthorSuperior sulcus (H)�0.89:1Upper incisor retractionUpper lip
(H)�0.87:1Upper incisor retractionLower sulcus (H)�0.87:1Lower incisor
retractionLower lip (H)�0.93:1Lower incisor retractionLower lip (H)�0.82:1Upper
incisor retractionBloom*14Upper lip (H)�0.34:1Upper incisor retractionLower lip
(H)�1.56:1Lower incisor retractionLower lip (H)�1:1Upper incisor
retractionRudee*35Upper,lower�0.75�0.9:1Incisor protrusion or Robinson et al*61lips
(H)retractionUpper lip (H)�0.5:1Ls:Ia Upper incisor retractionLower lip
(H)�1.22:1Li:Ib Lower incisor retractionHershey ,Smith7Upper lip
(H),�0.5:1Maxillary incisor retractionProffit,Epker18increased nasolabial angle,no
nasal changeUpper lip (H)�0.63:1Ls:Upper incisor
retractionRains,Nanda101Attarzadeh,Adenwalla31Upper lip (H)�0.4:1Ls:Upper incisor
retractionLower lip (H)�0.7:1Li:Upper incisor retractionYogosawa102Upper lip
(H)�0.44:1Ls:Upper incisor retractionLower lip (H)�1.2:1Li:Lower incisor
retractionKasai103*Includes growing patients.H = horizontal;Ia = incisor A point;Ib
= incisor B point;Li = labrale inferius;Ls = labrale superius.FIGURE59-2The general
trends ofpostsurgicalchanges in the nasal and labial soft tissuesexpressed in a
nonvector format (the arrows arenot specific for length,but are specific for direc-
tion).Generally,the alar base ofthe nosewidened and the nasal tip decreased in
height inrelation to the adjacent soft tissues.The philtralcolumns ofthe lip
widened and became longer,and the nasolabial angle decreased.Adaptedfrom Betts
NJ.Changes in the nasal and labialsoft tissues after surgical repositioning
ofthemaxilla.[master�s thesis] Ann Arbor (MI): Uni-versity ofMichigan; 1990.Table
59-3Nasal Effects ofMaxillary SurgeryDirection Maxillary MovementAlar BasesNasal
TipSupratip DepressionDorsal HumpNasolabial
AngleSuperiorIncreaseIncreaseIncreaseDecreaseDecreaseAnteriorIncrease*Increase*Incr
ease*DecreaseDecreaseInferiorInferiorDecreaseDecreaseIncreaseIncreasePosteriorNoneD
ecreaseDecreaseIncreaseIncrease*Indicates a greater magnitude ofchange.Adapted from
O�Ryan F,Schendel S.Nasal anatomy and maxillary surgery.III.Surgical techniques for
correction ofnasal deformities in patients undergoing maxillary surgery.Int J
AdultOrthodon Orthognath Surg 1989;4:157.
1226Part 8: Orthognathic SurgeryAnterior RepositioningMaxillary anterior
repositioning has thegreatest effect on the nose and upper lip.This movement
precipitates advancementofthe upper lip,subnasale,and nose,6,36�38slight shortening
ofthe upper lip,thinningofthe lip (approximately 2 mm),10,36�38,47widening ofthe
alar bases,36�38and a deep-ening ofthe supratip depression iftheANS is left
intact.21,23,36�38,48A progressiveincrease in the horizontal soft tissue dis-
placement is seen from the tip ofthe noseto the free end ofthe upper lip.37A con-
comitant decrease in nasolabial angle isobserved with only slight changes in
thelower lip.5,18Leaving the ANS intact has afavorable effect on the forward
displace-ment ofthe upper lip and especially thebase ofthe nose (subnasale).24The
ratiosderived from previous investigations canbe found in Table 59-5.A significant
difference between theratio ofhorizontal change ofupper incisorto vermilion border
ofthe upper lip in pre-vious studies (0.6:1)6,21,22compared with theratio reported
by Carlotti and colleagues(0.9:1)48is a result ofthe use ofthe alarcinch suture and
V-Yclosure during thesurgical procedure.The ratio reduces withlarger advancements
because ofsoft tissuestretching.48Ifthe ANS is left intact,thenasolabial angle may
remain relativelyunchanged.The nasal tip rises slightly sosubnasale migrates
forward along with theupper lip.15Superior RepositioningSuperior repositioning
ofthe maxilla caus-es elevation ofthe nasal tip,21,36�38wideningofthe alar bases
(2�4 mm),23,26,36�38and adecrease in the nasolabial angle (Table 59-6).36�38These
nasal changes occur withoutchange in angulation ofthe upper lip.6,8The upper lip
closely follows the move-ment ofthe maxillary incisor in the hori-zontal plane.The
lip follows superiorlyapproximately 40% ofthe vertical maxil-lary change.This lip
shortening is accentu-ated with combined anterior and superiormaxillary
movements.23The amount ofvertical soft tissue change increases pro-gressively from
the nasal tip to stomionsuperius,with loss ofvermilion ifa V-Yclosure is not
used.6,8However,Phillipsfound that the vermilion border oftheupper and lower lips
decreased slightly inthe lateral portion ofthe lip,even with aV-
Yclosure.26Interestingly,when super-imposition is done on maxillary land-marks,the
soft tissues ofthe lip migratedownward in relation to the maxilla.Thismay be
because ofthe connection oftheupper lip to the nose.6,8Inferior
RepositioningMaxillary inferior repositioning producesloss ofnasal tip
support,downward reposi-tioning ofthe columella and alar bases,thinning ofthe
lip,and an increase in thenasolabial angle.36�38Lengthening and thin-ning ofthe
upper lip is also observed.18Posterior RepositioningMaxillary setback procedures
result in lossofnasal tip support because ofposteriormovement ofthe ANS and the
bony sup-port area around the piriform aperture.37The lip rotates posteriorly and
superiorlyabout subnasale with increasing nasolabialangle8,49and thickens slightly
(Table 59-7).49Multidirectional MaxillaryMovementsMost maxillary movements are
multidi-rectional (anterior and superior,anteriorand inferior,posterior and
superior,poste-rior and inferior,etc).The expected softtissue changes would be a
combination ofthe expected changes from the pure vec-tors ofmovement (Figures 59-
3�59-5).Mandibular Surgical ProceduresGenerally the soft tissues ofthe
mandiblefollow the hard tissues closely.The exceptionis the lower lip.Because ofits
contact withthe upper incisor and upper lip,its move-ment is often variable and
unpredictable.Anterior Segmental PosteriorRepositioningThe lower lip follows the
lower incisorposteriorly,which causes a flattening ofthe labiomental fold.There is
less posteri-or displacement ofthe soft tissues as thechin is approached.No
effective change isobserved at the chin (Table 59-8).43Anterior RepositioningThe
soft tissue changes associated withmandibular advancement surgery are lim-ited to
the structures below the superiorlabial sulcus.There is little change in theupper
lip43,50�52and none above theANS.53The lower lip advancement is vari-able,and the
lip often lengthens.53Thelower labial sulcus and chin adhere to thebony structure
ofthe mandible.Conse-quently,they follow the underlyingosseous tissues
closely,advancing morethan the lower lip does (Figure 59-6).Thisleads to an opening
ofthe labiomentalTable 59-4Soft Tissue Changes Associated with Anterior Segmental
Setback OsteotomyAnatomic StructureRatioLandmarksAuthor(s)Increased nasolabial
angleUpper lip (H)�0.68:1Ls:IaBell,Dann69Upper lip
(H)�0.5:1Ls:IsLines,Steinhauser43Upper lip (H),�0.67:1increased nasolabial
angleLower lip (H)�0.3:1Proffit,Epker18Upper lip (H)�0.43:1Ls:IsNasolabial angle
12.2�IncreaseLew,et al46H = horizontal;Ia = incisor A point;Is = incision
superius;Ls = labrale superius.
Soft Tissue Changes Associated with Orthognathic Surgery1227fold.As with maxillary
and genial surg-eries,the vertical changes are variable.A correlation between the
verticalchange in menton and the angle and depthofthe labiomental fold has been
elucidat-ed.As menton moves caudally,the angleopens and the depth
decreases.50Facial height is also affected bymandibular advancement.In low-
angle,Angle Class II cases,facial height increasesslightly with advancement,but in
high-angle,Angle Class II cases,a large increasein facial height occurs with
advancement.Further,soft tissue changes may be morepronounced with advancements in
low-angle cases (Table 59-9).54The position ofthe lower lip is affectedby the upper
incisor,the lower incisor,andits contact with the upper lip.The anterosu-perior
position ofthe upper one-halfofthelower lip touches the upper incisor in AngleClass
II,non-open-bite cases and is usuallyfolded forward.As the mandible is advanced,the
chin and lower labial sulcus come for-ward,but the superior portion ofthe lowerlip
does not,since it was already folded for-ward by its contact with the upper
incisor.This causes an opening ofthe labiomentalfold and may explain why the ratio
ofadvancement at labrale inferius to theincisor inferius is reduced.18,43,53Conse-
quently during treatment planning,thelower lip must be righted to a relatively nor-
mal position before it is advanced in order toapproximate its true postsurgical
position.Dolce and colleagues,with 2 years offollow-up,suggest that these changes
aremore stable when rigid fixation techniquesare employed.55Long-term,more hori-
zontal relapse can be expected at the levelofthe lip and the lower labial sulcus
thanat the level ofpogonion.56As Johnston57and Mobarak54point out,the lack ofcor-
relation between surgical hard tissuemovements and the soft tissue changeslong-term
make prediction oflastingchanges difficult to predict.Posterior
RepositioningMandibular setback surgery has no effects onsubnasale or the tissues
superior to sub-nasale.However,a slight posterior displace-ment ofthe upper
lip,with lengthening,18,58,59and a slight increase in the nasolabial angle
isobserved.60The soft tissues follow themandible posteriorly,with the chin
followingmost closely,followed by the inferior labialsulcus and the lower lip.The
lower lip short-ens,becomes more protrusive by curling out,and the labiomental fold
deepens andbecomes more acute (Figure 59-7).7,58�60Ver-tical changes ofthe soft
tissues ofthe lips arerelated to hard tissue vertical changes.DuringTable 59-5Soft
Tissue Changes Associated with Maxillary AdvancementAnatomic
StructureRatioLandmarksAuthor(s)Upper lip (H)0.67:1Ls:Is Cleft
pts.Lines,Steinhauser 43removed ANSUpper lip (H)0.5:1Ls:IsUpper lip
(V)0.3:1Ls:IsNasolabial angle�1.2�:1Nasolabial angle:IsNasal tip
(H)0.28:1Pn:IsDann,et al 5Nasal base (H)0.57:1Sn:A pt.Upper lip (H)0.56:1Ls:Is
cleft ptsFreihofer 22Nasal base (H)0.57:1Sn:A pt.Nasal tip (H)0.28:1Pn:A pt.cleft
ptsFreihofer 21Upper lip (H)0.5:1Proffit,Epker 18Nasal tip (H)0.17:1Pn:IaUpper lip
(H)0.5:1Ls:IsRadney,Jacobs 8Nasal tip (H)0.17:1Pn:IaNasal base (H)0.24:1Sn:IaUpper
labial sulcus (H)0.52:1SLS:IaUpper lip (H)0.62:1Ls:IaMansour,et al 6Upper lip
(H)0.5:1Ss:A pt.Upper lip (V)-0.3:1Ss:A pt.Bundgaard,et al 42Upper labial sulcus
(H)0.8:1SLS:A pt.,alar cinch,V-YclosureUpper lip (H)0.9:1Ls:IsCarlotti,et al
48Upper lip (H)0.82:1Ls:IsUpper lip (V)�0.32:1Ss:IsNasal base (H)0.51:1Sn:A
pt.Rosen 23Nasal base (H)0.3:1Sn:A pt.(thick lip)Nasal base (H)0.46:1Sn:A pt.(thin
lip)Stella,et al 10Upper lip (middle) (H)1:13-D analysisMcChance,et al 104,105Nasal
base1.25:13-D analysisSubnasale0.63:1Sn:A pt.cleft ptsEwing,Ross 78Upper lip
(H)0.66:1SLS:IsNasal tip0.36:1Pn:IsUpper lip (H)0.91:1SLS:IsUpper labial sulcus
(H)0.38:1SLS:A ptNasal base (H)0.60:1Sn:ANSHack et al 25Upper Lip (H)0.74Ls:IsUpper
labial sulcus (H)0.76:1SLS:A ptLin,Kerr 106Upper lip (H)0.65:1Ls:IsRosenberg,et al
27A pt.= A point;ANS = anterior nasal spine;H = horizontal;Ia = incisor A point;Is
= incision superius;Ls = labrale Pn = pronasale;SLS = superior labial sulcus;Sn =
subnasale;Ss = stomion superius;V = vertical.
1228Part 8: Orthognathic Surgerysuperior mandibular repositioning,the lowerlip
becomes shorter,protrusive,and smallerin area.In contrast,with inferior
mandibularrepositioning,the lower lip becomes longerwith increased area.61The
vertical soft tissuechanges correlate poorly with hard tissuemovements (Table 59-
10).61 As withmandibular advancements,long-term softtissue changes have been found
to correlaterelatively poorly with the initial surgical bonychanges,though in the
short term they dochange predictably.62AutorotationDuring autorotation ofthe
mandible,thesoft tissues follow the osseous landmarkson approximately a 1:1
basis,6,8exceptthe lower lip,which falls slightly lingualto the arc
ofrotation.6,8,15A slightincrease in the labiomental angle is oftenobserved,6as is
a slight thickening ofthelips as the vertical facial height decreases(Table 59-
11).43Table 59-6Soft Tissue Changes Associated with Maxillary ImpactionAnatomic
StructureRatioLandmarksAuthor(s)Upper lip (V)�0.38:1Ls:Is vertical maxillary
excessUpper lip (V)�0.51:1Ls:Is Schendel,et al 49bimaxillary protrusionUpper lip
(V)�0.4:1Ss:IsUpper lip (V)�0.3:1Ls:IsUpper labial sulcus (V)�0.25:1SLS:IsNose
(V)�0.2:1Sn:IsNose (V)�0.16:1Pn:Is (ANS removed)Radney,Jacobs 8Upper labial sulcus
(H)0.76:1SLS:IaUpper lip (H)0.89:1Ls:IaNose (V)�0.15:1Pn:PrNasal base
(V)�0.28:1Sn:PrUpper lip (V)�0.31:1Ls:PrUpper lip (V)�0.42:1SLS:IsMansour,et al
6Upper labial sulcus (V)0.12:1SLS:ANSUpper lip (V)�0.06:1Ls:ANSUpper lip
(V)�0.41:1Ss:ANSSakima,Sachdeva9Upper lip (V)1.33:1Ss:A pt (V-Yclosure)Rosenberg,et
al 27Full face evaluationGreatest alar widthAverage = 3.4mmFull facial
photographsAlar base widthAverage = 2.7mmDecreased vermilionAverage l mmV-
YclosurePhillips,et al 26more lateralUpper lip (middle) (H)1:13-D
analysisMcChance,et al 104,105Alar Base (H)1.25:13-D analysisNasal base
(V)0.29:1Sn:ANSHack,et al 25Upper labial sulcus (V)0.54:1SLS:A ptUpper lip
(V)0.72:1SLS:IsA pt.= A point;ANS = anterior nasal spine;H = horizontal;Ia =
incisor A point;Is = incision superius;Ls = labrale superius;Me = menton;Pn =
pronasale;Pr = prosthion;SLS = superior labial sulcus;Sn = subnasale;Ss = stomion
superius;V=vertical.Table 59-7Soft Tissue Changes Associated with Maxillary
SetbackAnatomic StructureRatioLandmarksAuthor(s)Upper lip (H)�0.76:1Ls:Incisor
vertical maxillary excessUpper lip (H)�0.66:1Ls:Incisor Schendel et al49bimaxillary
protrusionUpper lip (H)�0.67:1Ls:IsUpper labial sulcus (H)�0.33:1SLS:IsNose
(H)�0.33:1Sn:IsNasolabial angleIncreaseRadney,Jacobs8H = horizontal;Is = incision
superius;LS = labrale superius;SLS = superior labial sulcus;Sn =
subnasale.FIGURE59-3The average hard and soft tissuechanges ofthe
advancement,impaction group invector format (arrows depict mean direction andmean
amount ofchange).Note that the nasal tipelevates slightly,but subnasale advances
more,effectively decreasing nasal tip protrusion.Adapted from Betts NJ.Changes in
the nasal andlabial soft tissues after surgical repositioning ofthe maxilla
[master�s thesis].University ofMichigan; 1990.
Soft Tissue Changes Associated with Orthognathic Surgery1229Genial Segment Surgical
ProceduresThe symphysis has been exposed bothintraorally and extraorally for
osteotomyofthe inferior border ofthe mandible
toadvance,retract,widen,narrow,lengthen,or shorten the chin.45The majority ofchange
seen after genioplasty is in the softtissue ofthe chin,and less effect is seen
inthe labial sulcus and lower lip.63Early stud-ies describing the soft tissue
changes asso-ciated with genial surgery had severalproblems.They included few
cases,relatedshort-term results,and superimposed thecephalograms on the cranial
base.Super-imposition ofthe cephalograms shouldoccur on the areas ofthe mandible
notchanged with surgery,13,64,65because con-comitant maxillary and
mandibularsurgery may invalidate chin measurementscalculated from superimpositions
on thecranial base.66�68Anterior Repositioning: BonyEarly attempts at advancement
genioplastyused nonpedicled free grafts or onlay bonegrafts.However,these
procedures were laterabandoned because ofexcessive resorptionand poor
predictability.Consequently,thesurgical emphasis shifted to the horizontalosteotomy
ofthe anterior mandible.At first a degloving incision was usedto expose the
anterior mandible.67,69,70However,several investigators demon-strated that minimal
soft tissue strippinggave a more predictable hard and soft tis-sue response because
ofless bone resorp-tion ofthe advanced segment.13,45,65,66,71,72No bony remodeling
ofgnathion or men-ton was observed.However,bone resorp-tion could be demonstrated
near theosteotomy (the anterosuperior and pos-teroinferior aspects ofthe advanced
genialsegment).66,67,69,70,72�74Bony appositionoccurred at B point and the inferior
bor-der osteotomy (Figure 59-8).67These samestudies demonstrated that when the
tech-nique ofminimal soft tissue stripping wasused,the soft tissues followed the
hard tis-sues closely without chin droop.13,45,65,66,68There was also a small but
negligible effecton the labiomental sulcus,66,68an increasein submental length,an
improved rela-tionship oflower lip to tooth,66less softtissue thinning,68and an
improved neck-chin angle.The soft tissue changes following hori-zontal advancement
genioplasty depend onthe magnitude and direction ofthe posi-tional change ofthe
genial segment,thedesign ofthe mucosal and osseous inci-sions,the amount ofsoft
tissue stripping,and other concomitant jaw movements(Table 59-
12).13,66,67,69,70FIGURE59-4The average hard and soft tissuechanges ofthe
advancement,downgraft group invector format (arrows depict mean directionand mean
amount ofchange).Note that thenasal tip elevates slightly,but subnasale
advancesmore,effectively decreasing the nasal tip protru-sion.Adapted from Betts
NJ.Changes in thenasal and labial soft tissues after surgical reposi-tioning ofthe
maxilla [master�s thesis].AnnArbor (MI): University ofMichigan; 1990.Average
advancementDowngraftImpactionFIGURE59-5Overlay ofaverage hard and softtissue
changes ofadvancement,impaction andadvancement,downgraft in vector format.Aver-age
advancement (see legend above) as definedby the mean direction and mean amount
ofchange,is indicated by arrows (downgraft)andlines with dots (impaction).Note that
subnasalemoves in the direction ofthe anterior nasal spineand A point.Adapted from
Betts NJ.Changes inthe nasal and labial soft tissues after surgicalrepositioning
ofthe maxilla [master�s thesis]Ann Arbor (MI): University ofMichigan; 1990.Table
59-8Soft Tissue Changes Associated with Mandibular Anterior
SegmentalOsteotomyAnatomic StructureRatioLandmarksAuthor(s)Lower lip
(H)�0.75:1Li:IiLines and Steinhauser43Lower lip (H)�0.67:1Chin (H)No
changeProffit,Epker18Lower lip (H)�0.71:1Li:IiLew et al46H = horizontal;Ii =
incision inferius;Li = labrale inferius.
1230Part 8: Orthognathic SurgeryThe advantages ofosseous genialsurgery are
preservation ofthe normal chincontour,75improved predictability ofthesoft tissue
response,45stability,45,68versatili-ty,45and preservation ofblood supply
toosteotomized segments.75Those patients who had both verticalreduction and
advancement genioplastiesshowed slightly larger soft tissue advance-ment than those
who had advancementgenioplasty only (0.93:1 vs 0.81:1).Thismay be explained by
bunching ofthe softtissues.When the soft tissues are bunched(vertical reduction
more than advance-ment),the soft tissues advance more thanwhen the soft tissues are
stretched(advancement only).66,76Tulasne suggested that the overlappingbone flap
genioplasty gives a more naturalcontour to the lower face and a better
balancebetween the lower lip,chin,and submentalregion than does the sliding
genioplasty asso-ciated with a wedge ostectomy.77However,itis associated with a
large amount ofbonyresorption,especially in adolescent patients.Predictions oflower
and genial softtissue changes when a genioplasty is addedto a mandibular
advancement are notori-ously variable.78However,the use ofrigidinternal fixation
for the mandibularadvancement makes the soft tissuechanges in the chin and lip more
durablein the long term.55Table 59-9Soft Tissue Changes Associated with Mandibular
AdvancementAnatomic StructureRatioLandmarksAuthor(s)Lower lip (H)0.62:1Li:IiChin
(H)1:1Pgs:GnLines,Steinhauser43Lower lip (H)0.85:1Li:IiLower labial
sulcus1.01:1ILS:B pt.Chin (H)1.04:1Pgs:PgTalbott51Lower lip (H)0.75:1Chin
(H)1:1Proffit,Epker18Lower lip (H)0.38:1Li:IiLower labial sulcus (H)0.97:1ILS:B
pt.Chin (H)0.97:1Pgs:PgChin (H)0.97:1Gns:GnChin (H)0.87:1Mes:MeQuast,et al11Lower
lip (H)0.56:1Li:IiLower labial sulcus1.06:1ILS:B pt.Chin (H)1.03:1Pgs:PgChin
(V)0.93:1Mes:MeMommaerts,Marxer50Upper lip (H)�0.02:1Ls:IiLower lip
(H)0.43:1Li:IiLower labial sulcus (H)0.93:1ILS:B pt.Chin (H)0.94:1Pgs:PgChin
(H)0.95:1Gns:GnChin (H)0.97:1Mes:MeHernandez-Orsini et al113Lower lip
(H)0.26:1Li:IiLower labial sulcus (H)1.19:1ILS:B pt.Chin (H)1.1:1Pgs:PgDermaut,De
Smit53Lower lip (H)1.25:13-D analysisChin (H)1.25:13-D analysisMcChance104,105Lower
lip (H)0.66:1Li:IiLower labial sulcus (H)0.88:1ILS:B ptChin (H)1:1Pgs:PgThuer,et
al52Lower lip (H)0.88:1ILS:B ptChin (H)1:1Pgs:PgKeeling,et al56Lower lip
(H)0.8:1Li:IiLower labial sulcus (H)1:1ILS:B pt.Chin (H)1:1Pgs:PgEwing,Ross78Lower
lip (H)0.6:1Li:Ii (all faces)Lower labial sulcus (H)0.86-0.95:1ILS:B pt.Chin (H)1-
1.1:1Pgs:PgMenton0.92-1.04:1Mes:MeMobarak,et al62B pt.= B point;Gn = gnathion;Gns =
soft tissue gnathion;H = horizontal;Ii = incision inferius;ILS = inferior labial
sulcus;Li = labrale inferius;Ls = Labrale superius;Me = menton;Mes = soft tissue
menton Pg = pogonion;Pgs = soft tissuepogonion;V = vertical.3 mm636666FIGURE59-
6Overlay ofaverage hard and softtissue changes ofmandibular advancement invector
format.Generally the soft tissues followthe bony movements in a 1:1 ratio.Adapted
fromBetts NJ,Dowd KF.Soft tissue changes associat-ed with orthognathic
surgery.Atlas Oral Max-illofac Surg Clin North Am 2000;8:13�38.
Soft Tissue Changes Associated with Orthognathic Surgery1231Anterior Repositioning:
AlloplasticEarly attempts at advancement genioplastyincluded the use ofalloplastic
implants.Unfortunately,long-term follow-up revealedseveral unforeseen
complications.For thisreason,advancement genioplasty with allo-plastic implants has
fallen out offavor.Thedisadvantages ofalloplastic materials includeresorption or
deformation ofthe underlyingsymphyseal bone with possible devitalizationofthe
mandibular anterior teeth,12,18,47,79�81migration ofthe implant,45,69,79extrusion
ofthe implant,79infection (especially with Pro-plast),45,69and a less predictable
soft tissue tohard tissue ratio.45,69In addition,alloplasticmaterials do not
address excessive or reducedchin height.69Newer materials have beendeveloped that
reduce the incidence ofthese1 mm4665.565.51FIGURE59-7Overlay ofaverage hard and
softtissue changes ofmandibular setback in vectorformat.The soft tissues ofpogonion
and B pointmove more predictably than labrale inferius.Adapted from Betts NJ,Dowd
KF.Soft tissuechanges associated with orthognathic surgery.Atlas Oral Maxillofac
Surg Clin North Am2000;8:13�38.Table 59-10Soft Tissue Changes Associated with
Mandibular SetbackAnatomic StructureRatioLandmarksAuthor(s)Lower lip
(H)�0.69:1Li:PgLower labial sulcus (H)�0.93:1ILS:PgAaronson60Lower labial sulcus
(H)approx.�1:1ILS:B pt.Chin (H)approx.�1:1Pgs:PgRobinson et al61Upper lip
(H)�0.2:1Ls:IiLower lip (H)�0.75:1Li:IiChin (H)�1:1Pgs:GnLines,Steinhauser43Upper
lip (H)�0.2:1Ls:PgLower lip (H)�0.6:1Li:PgChin (H)�0.9:1Pgs:PgHershey,Smith7Upper
lip (H)�0.2:1Lower lip (H)�0.75�0.8:1Chin (H)�1:1Proffit,Epker18Lower lip
(H)�0.93:1Li:IiLower labial sulcus (H)�.03:1ILS:B ptChin
(H)�.91:1Pgs:PgGjorup,Athanasiou110Lower Lip (H)�1:13-D analysisMcChance et
al104,105Chin (H)�1:13-D analysisUpper lip (H)�0.32:1Ls:PgLower lip
(H)�0.80:1Li:PgChin (H)�0.83:1Pgs:PgGaggl et al111Lower lip (H)�0.5:1Li:PgEnacar et
al112Lower lip (H)�1.02:1Li:IiLower labial sulcus (H)�1.09:1ILS:B pt.Chin
(H)�1.04:1Pgs:PgMobarak et al62B pt.= B point;Gn = gnathion;H = horizontal;Ii =
incision inferius;ILS = inferior labial sulcus;Li = labrale inferius;Ls = labrale
superius;Pg = pogonion;Pgs = soft tissue pogonion.Table 59-11Soft Tissue Changes
Associated with Mandibular AutorotationAnatomic
StructureRatioLandmarksAuthor(s)Chin (V)�0.8:1Pgs:GnLines,Steinhauser43Chin
(H)1:1Lower labial sulcus1:1ILS:B pt.Chin (H)1:1Pgs:PgRadney,Jacobs8Lower lip
(H)0.75:1Li:IiLower labial sulcus (H)0.9:1ILS:B pt.Chin (H)0.86:1Pgs:PgLower lip
(V)�0.93:1Si:IsChin (V)�1.2:1Mes:MeMansour et al6Lower lip (V)�1.03:1Si:MeLower lip
(V)�1.48:1*Li:MeInferior labial sulcus (V)�1.05:1ILS:MeInferior labial sulcus
(H)0.61:1ILS:MeChin (H)0.79:1Pgs:MeChin (V)�0.98:1Pgs:MeSakima Sachdeva9*May
represent uprighting ofthe lower lip due to a loss ofcontact with the upper
incisor.B pt.= B point;H = horizontal;ILS = inferior labial sulcus;Ii = incision
inferius;Li = labrale inferius;Gn = gnathion;Me = menton;Mes = soft tissue menton
Pg = pogonion;Pgs = soft tissue pogonion;Si = stomion inferius;V = vertical.
1232Part 8: Orthognathic Surgerycomplications,making alloplastic augmenta-tion a
more viable option.Ifalloplastic implants are used theyshould be placed
subperiostealy,low onthe inferior border below the mentalismuscle,and over dense
cortical bone.SeeTable 59-13 for soft tissue changes withalloplastic chin
implants.Alloplasticimplants should not be used in the cor-rection ofsevere
deformities but can beused in patients with a mild to moderatedeformity.13,47,80A
periodic radiographicexamination ofthe implant is recom-mended to monitor bony
resorption.47,81Posterior RepositioningEarly attempts at reducing horizontalexcess
ofthe genial segment ofthemandible by bony recontouring causedvery little
improvement ofthe soft tissueprofile.64This technique has been aban-doned.The soft
tissue changes associatedwith setback genioplasty are less well cor-related with
the hard tissue movementsthan during advancement genioplasty(Table 59-14).Reduction
genioplasty is contraindicat-ed in a patient with minimal or no labio-mental
fold.Flattening ofthe chin andelimination ofthe labiomental fold
willResorptionAppositionFIGURE59-8Osseous resorption at pogonion anddeposition at
menton.Adapted from Polido WD,Bell WH.Long-term osseous and soft tissuechanges
after large chin advancements.J Cranio-maxillofac Surg 1993;21:54�9.Table 59-12Soft
Tissue Changes Associated with Advancement GenioplastyAnatomic
StructureRatioLandmarksAuthor(s)Chin (H)0.57:1Pgs:Pg Ant.Sliding Bell,Dann69Chin
(H)0.75:lPgs:Pg H McDonnel et al67(some Multistep)Chin (H)0.67:1Proffit,Epker18Chin
(H)approx.1:1H with broad Bell14soft tissue pedicle IVRO setbackLip (H)0.44:1Li:Pg
HBusquets,Sassouni63Chin (H)0.83:1Pgs:Pg (some with ostectomy)Chin (H)0.97:1Pgs:Pg
H with broad pedicle (IVRO setback)Scheideman68Chin (H)0.85:1H with broad
Bell,Gallagher45pedicleChin (H)0.81:1Pgs:Pg Advancement only,H sliding with broad
pedicleChin (H)0.93:1Pgs:Pg Advancement and Gallagher et al66vertical reduction,H
sliding with broad pedicle,maxillary impactionChin (H)0.7:1HEpker,Fish107Chin
(H)0.73:1Pgs:Pg Overlapping,bone flapTulasne75Chin (H)0.97:1Pgs:Pg H with broad
pediclePark et al65Chin (H)1:1Pgs:PgKrekmanov,Kahnberg72Chin
(H)1.1:1Pgs:Pg,BSSO+GPEwing,Ross78Chin (H)0.83:1Pgs:Pg,H with Polido,Bell108broad
pedicle and large advancementsBSSO + GP = bilateral sagittal split osteotomy +
genioplasty;H = horizontal;IVRO = intraoral vertical ramus osteotomy;Li = labrale
inferius;Pg = pogonion;Pgs = soft tissue pogonion.Table 59-13Soft Tissue Changes
Associated with Alloplastic Chin ImplantsAnatomic
StructureRatioLandmarksAuthor(s)Chin (H)0.6:1Pgs:Pg Silicone Bell,Dann69(unstable
and causeresorption)Chin (H)0.9:1Pgs:Pg Proplast Dann,Epker79(resorption)Chin
(H)1:1Proffit,Epker18H = horizontal;Pg = pogonion;Pgs = soft tissue pogonion.
Soft Tissue Changes Associated with Orthognathic Surgery1233result.82It is also
important to realize thatsetback genioplasty will make undesirablechanges in the
neck-chin proportion.In apatient with a poor neck-chin proportion,this procedure is
contraindicated.Vertical Repositioning: Superior and InferiorThe soft tissues
follow the hard tissues veryclosely in augmentation genioplasty.How-ever,this is
not the case for vertical reduc-tion (inferior border ostectomy or
sandwichostectomy) genioplasty (Table 59-15).Special CircumstancesDistraction
OsteogenesisSince its first use in the human mandibleby McCarthy and
colleagues,this surgicaltechnique has exploded in popularity.83Itsuse does not lend
itselfwell to soft tissuepredictions ofthe sort used for orthog-nathic surgery for
various reasons,and fewefforts have been made in this regard.Dif-ficulties derive
from the fact that mostpatients are still growing when subjectedto the
technique,that the principle ofgradual distraction ofa bone is probablyaccompanied
by a component ofsoft tis-sue growth,so-called distraction histogen-esis,and that
very little is known about thedimensional stability ofthese bonychanges.Efforts in
this regard have exam-ined soft tissue profile changes associatedwith maxillary
distraction.84,85However,the technique allows forreal-time adjustment ofthe change
withinthe context ofdesired occlusion for mostapplications,thereby not requiring
precisepredictions as for conventional orthog-nathic surgery.The topic will be
ofgreatinterest,and the stability ofthe changesonly more so as its use for the
treatment ofobstructive sleep apnea in adults becomesmore prevalent.Overall,the
changes observed arecomparable to those for maxillaryadvancement via the Le Fort I
osteotomywith a decrease in midfacial concavity,increases in nasal tip
projection,advance-ment ofthe lip,and closing ofthenasolabial angle (Table 59-
16).84,85Bimaxillary AdvancementSurgery for Obstructive Sleep ApneaThe 5-year
incidence ofobstructive sleepapnea (OSA) in adult populations in theUnited States
has been estimated to be7.5% for moderately severe cases and 16%for less severe
cases.86While orthognathicsurgery has traditionally been applied tocorrect
stomatognathic deformities anddysfunction,it also has been shown to be apowerful
tool in correcting obstructivesleep apnea.87,88Little work has been done to
describethe facial changes associated with thissurgery,which differs from
traditionalorthognathic surgery in several ways.Patients presenting for
maxillomandibularadvancement surgery for OSA tend to beolder,in their fourth and
fifth decades oflife.89They tend to be obese and have athicker,laxer soft tissue
envelope withwhich to �absorb�these bony changes.Theywill often present without
skeletal imbal-ances that we traditionally seek to correct.Further,advancements
ofthis sort are gen-erally larger than those seen in the typicalorthognathic
surgery population,usuallyranging from 10 to 12 mm.The goals ofthissurgery are very
different.Here we seek tomaximize the skeletal advancement to thebenefit ofthe
airway but often to the detri-ment ofthe soft tissue profile.Treatmentplanning then
aims to minimize any unto-ward changes to the profile.Most patientsseem to approve
or be neutral with respectto their facial changes.90Prognathicpatients are more
likely to disapprove ofTable 59-14Soft Tissue Changes Associated with Setback
GenioplastyAnatomic StructureRatioLandmarksAuthor(s)Chin (H)�0.33:1Pgs:Pg
ant.recontouring Hohl,Epker67degloving dissectionChin
(H)�0.75:1InterpositionalWessberg et al109Chin (H)�0.58:1Pgs:Pg H with Bell13broad
pedicleChin (H)�0.50:1Pgs:PgKrekmanov,Kahnberg72H = horizontal;sulcus;PG =
pogonion;Pg ant.= pogonion anterior;Pgs = soft tissue pogonion.Table 59-15Soft
Tissue Changes Associated with Vertical Augmentation or
ReductionGenioplastyAnatomic StructureRatioLandmarksAuthor(s)AugmentationChin
(V)1:1InterpositionalWessberg et al109ReductionChin (V)�0.25:1Mes:Me,Inferior
border,Hohl,Epker64osteotomy,degloving dissectionChin (V)�0.26:1Pgs:Pg H with Park
et al65broad pedicleChin (V)�0.35:1Mes:MeKrekmanov,Kahnberg72Chin
(V)�0.40:1Mes:MeEwing,Ross78H = horizontal;Me = menton;Mes = soft tissue menton;Pg
= pogonion;Pgs = soft tissue pogonion;V = vertical.
1234Part 8: Orthognathic Surgerytheir new profile.90Adjunctive measuressuch as ANS
reshaping may help minimizeupper lip and nasal tip rotation,but littlecan be done
to minimize the effects ofsurgery at the chin (Table 59-17).In terms ofratios
ofchange in thispopulation,only one study has beenreported to date.91This overall
lack ofdatadoes not permit a comparison to tradi-tional orthognathic changes.Poor
Surgical Esthetic Resultsand Techniques ofSoft TissueControlMaxilla The secondary
soft tissue changes found withmaxillary surgery include widening ofthealar
bases,36�38,48,92upturning ofthe nasal tip,flattening and thinning ofthe
upperlip,19,36�38,48,92downturning ofthe commis-sures ofthe mouth,36�38,48,92and
opening ofthe nasolabial angle.These changes are simi-lar to those found in the
aging face and aregenerally perceived as unesthetic.36�38Otherpotentially
unesthetic changes include loss ofnormal lip pout and a decrease in visible ver-
milion.19,48,92Several investigators have suggestedthat the etiology ofthese soft
tissuechanges is attributable to three factors:(1) elevation ofthe periosteum and
mus-cle attachments adjacent to the nose with-out adequate replacement,(2)
postsurgicaledema,and (3) increased bony support inadvancement cases.24,41The
importance ofmuscle reposition-ing following superior repositioning ofthemaxilla
was stressed by many investiga-tors.24,48,92,93They state that the musclesdetached
during stripping ofthe perios-teum required for maxillary surgery short-en and
retract laterally.The muscles reat-tach in this position ifthey are
notreapproximated at the time ofsurgery.Thelateral movement ofthe muscles and sub-
cutaneous tissues causes the alar base toflare and the upper lip to thin.The loss
ofvisible vermilion may be aresult ofother causes.These include arolling under
ofthe vermilion ofthe upperlip secondary to an incision made high inthe vestibule
with associated scarring andretraction24,48,92and inclusion oflargeamounts oftissue
during closure.24Thisloss ofvermilion is especially unattractivein those
individuals with already thin lips40and is more pronounced with posteriorand
superior repositioning ofthe maxilla.Postsurgical widening ofthe alarbase after the
maxillary Le Fort I proce-dure may be a favorable outcome in apatient with vertical
maxillary hyperpla-sia and thin slit-like nares.15However,ifa wide preoperative
alar base is present,these same changes become undesir-able,24,41especially with
anterior orsuperior repositioning ofthe maxilla94(Figure 59-9A�D).Before techniques
tocontrol nasal width were developed,Belland Proffit suggested that at the time
ofpreoperative assessment,patients with awide nose be warned that a rhinoplastymay
be indicated.40Techniques to Control the Soft TissuesTo control the soft tissue
changes associat-ed with maxillary surgery,the surgeonmust first be aware ofany
preexistingdeformity,the anticipated soft tissue adap-tation to the surgical
procedure beingplanned,and the importance ofthe effectsoforofacial muscles on
form,function,and esthetics.Once this has occurred thesoft tissues can be
manipulated to advan-tage by the surgeon.4,93Several surgical techniques have
beensuggested to help control the detrimentalsoft tissue changes associated with
maxil-lary surgery.They include the V-Yclosure,the alar cinch suture,a combination
ofthealar cinch suture and the V-Yclosure,con-touring ofthe ANS,septum
reduction,and the double V-Yclosure.Table 59-17Soft Tissue Changes Associated with
Maxillomandibular Advancement for OSAAnatomic StructureRatioLandmarksAuthor(s)Nasal
tip (H)0.16:1Pn:IsSuperior labial sulcus (H)0.39:1Sn:IsUpper lip
(H)0.80:1SLS:IsNasal tip (V)0.16:1Pn:IsSuperior labial sulcus (V)0.16:1Sn:IsUpper
lip (V)0.16:1SLS:IsLouis et al91H = horizontal;Is = incision superius;Pn =
pronasale;SLS = superior labial sulcus;Sn = subnasale;V = vertical.Table 59-16Soft
Tissue Changes Associated with Maxillary Distraction Osteogenesis*Anatomic
StructureRatioLandmarksAuthor(s)Nasal tip 0.53:1Pn:ANSSuperior labial sulcus
(H)0.96:1SLS:A pt.Upper lip (H)0.8:1Ls:IsKo et al85Nasal
advancement0.57:1Pn:ANSSuperior labial sulcus (H)0.83:1Sn:ANSUpper
lip0.71:1Ls:ANSHarada et al84*All cleft patients.A pt.= A point;ANS = anterior
nasal spine;H = horizontal;Is = incision superius;Ls = labrale superius;Pn=
pronasale;SLS = superior labial sulcus;Sn = subnasale.
Soft Tissue Changes Associated with Orthognathic Surgery1235V-YClosureThere is
always an antero-posterior thinning ofthe upper lip (espe-cially with maxillary
advancement) and aloss ofvermilion (especially with maxil-lary impaction) unless a
V-Yclosure isused (Figure 59-10A�C).The upper lip,when closed in a V-Yfash-
ion,follows the hard tissues forward at morenearly a 1:1 ratio,with prevention
ofupperlip thinning and loss ofthe vermilion.10,15,48,93The V-Yclosure is
accomplished duringclosure ofthe maxillary vestibular incision.The mid portion
ofthe incision is identifiedand retracted anteriorly with a single skinhook.One
centimeter ofthe incision is closedin an anteroposterior direction.Using a sepa-
rate suture mucosa,periosteum and inter-posed muscular tissue is engaged by the
needleFIGURE59-9Unesthetic widening ofthe alar base and downturning ofthe corners
ofthe mouth in a patient with an already wide nose.This patient was treat-ed with a
maxillary procedure without an alar cinch or V-Yclosure.A,Preoperative full facial
view.B,Postoperative full facial view.C,Preoperative smiling fullfacial
view.D,Postoperative smiling full facial view.Reproduced with permission from Betts
NJ,Fonseca RJ.Soft tissue changes associated with orthognathicsurgery.In: Bell
WH,editor.Modern practice in orthognathic and reconstructive surgery.Vol
3.Philadelphia (PA): W.B.Saunders; 1992.p.2197.ABCDFIGURE59-10Unfavorable change in
the vermilion ofthe upper lip following maxillary impaction surgery in a
patientwith a preexisting thin vermilion.A,Preoperative state.Note preexisting
minimal vermilion exposure.B,Postoperativestate.C,Close-up view ofthe postoperative
state.Note that the loss ofvermilion is more pronounced in the lateral por-tions
ofthe lip than in the medial portion.Reproduced with permission from Betts
NJ,Fonseca RJ.Soft tissue changesassociated with orthognathic surgery.In: Bell
WH,editor.Modern practice in orthognathic and reconstructive
surgery.Vol3.Philadelphia (PA): W.B.Saunders; 1992.p.2198.ABC
1236Part 8: Orthognathic Surgeryon either side ofthe incision and sutured in
acontinuous fashion.The superior aspect ofthe incision is gradually advanced toward
themidline by taking smaller bites oftissue in theupper margin ofthe incision and
larger bitesin the lower margin (Figure 59-11A and B).Both sides ofthe incision are
closed in a sim-ilar fashion to the midline suture.Often,fol-lowing this type
ofclosure,the lip will lookrather full and short in the midline.Withinthe next
several days,the lip will lengthen andbecome more normal in appearance.93Alar
CinchCollins and Epker identifiedpatients who may develop undesirablenasal esthetic
changes as those who havenormal or wide frontonasal esthetics priorto surgery and
will undergo a superior oranterior surgical repositioning ofthemaxilla.94These
observations led to thedevelopment oftechniques designed tocontrol the alar base
width after maxillarysurgery.Bell and Proffit described adjunc-tive techniques to
ensure an estheticreconstruction ofthe alar base in maxil-lary impaction
cases.40These included (1) reduction ofthe anterior extent ofthepiriform rim,(2)
reduction ofthe ANS,and (3) trimming ofthe height oftheanterior nasal floor.A
different techniquefor correcting the flat and flaring nose wasdescribed by
Millard.95This served as amodel for the later development ofthealar cinch
techniques.94The original cinchsuture was passed from the fibroadiposetissue on one
side ofthe alar base to theother and was tied to a predeterminedwidth (Figure 59-
12A�E).This technique was then modified to afigure-eight suture that was passed
from lat-eral to medial,catching the fibroadipose tis-sue ofthe alar base (Figure
59-12F�H).24,41Schendel and Delarre suggest that the sutureshould be passed not
through the fibroadi-pose tissue but through the transversenasalis muscles ofthe
nose.92Past observations have suggested thatthe alar cinch suture does not control
thealar base width4,96and may even cause fur-ther widening ofthe alar
base.Subsequent-ly,another technique ofalar cinch suturingwas suggested.In this
technique,a hole isplaced in the ANS and the suture is passedthrough the soft
tissues at the base ofthenose and back to the ANS bilaterally andindividually tied
(Figure 59-12I�L).15A measurement ofthe greatest alarwidth must be taken on the
patient andrecorded in the chart preoperatively.Thisnumber should be available
during surgeryso that reference to it can be made at thetime ofnasolabial muscle
reconstruction.Combination ofAlar Cinch and V-Y ClosureSeveral investigators
indicatedthat the best control ofthe alar base inpatients having maxillary superior
or ante-rior repositioning could be achieved byusing the V-Yclosure and the alar
cinchsuture together.15,36�38,41,92,93Their objectivewas to quantify the alar base
width changeswith and without the alar base cinchsuture.All patients had a V-
Yclosure.TheyFIGURE59-11A,The V-Yclosure is accomplished during closure ofthe
maxillary vestibular incision.The midportion ofthe incision is identified and
retracted anteriorly with a single skin hook.One cen-timeter ofthe incision is
closed in an anteroposterior direction.B,Using a separate suture mucosa,periosteum
and interposed muscular tissue are engaged by the needle on either side ofthe
incision andsutured in a continuous fashion.The superior aspect ofthe incision is
gradually advanced toward themidline by taking smaller bites oftissue in the upper
margin ofthe incision and larger bites in the lowermargin.Both sides ofthe incision
are closed in similar fashion to the midline suture.Photographs repro-duced with
permission and illustrations adapted from Milles M,Betts NJ.Techniques to preserve
ormodify lip form during orthognathic surgery.Atlas Oral Maxillofac Surg Clin North
Am 2000;8:71�9.AB
Soft Tissue Changes Associated with Orthognathic Surgery1237FIGURE59-12A,Alar base
cinch suture.The upper lip is grasped between the forefinger and thumb,with the
forefinger placed directly on the junction ofthe ala with the face.B,The lip is
inverted and the tissue lying over the forefinger is grasped with a forceps.The lip
is released and the tissue grasped in theforceps is manipulated to ensure that the
alar base moves properly.Ifappropriate movement is not observed,the process must be
repeated until correct nee-dle placement is ensured.C�E,A nonresorbable suture
(ie,2-0 Prolene) is passed from the fibroadipose tissue (or transverse nasalis
muscle) on one side ofthe alar base to the other and is tied to a predetermined
width.(CONTINUEDONNEXTPAGE)ABCDE
1238Part 8: Orthognathic Surgeryfound that the alar bases widened in allpatients
and widening was lessened whenthe alar cinch suture was used.The alarbase widened
an average of2.9% with thealar cinch suture and 10.8% without it.41The effects
ofsimultaneous placementofan alar cinch suture and a V-Yclosureare successfully
repositioning the lip mus-cles in a predictable manner,93preventingshortening ofthe
lip in impactioncases,41,93maintaining the normal lippout,93preventing loss
ofvermilion,41,48,93maintaining the anteroposterior thicknessofthe lip,41decreasing
the widening ofthealar base,41,48,93and preventing droopingofthe corners ofthe
mouth93(Figure 59-13A�E).The ability ofthe figure ofeight alar cinch suture
combined with a V-Yadvancement closure to reconstruct thepatient to their
preoperative soft tissuestate was recently demonstrated in aprospective
investigation with long-termfollow-up.This study was performed in asurgical model
(surgically assisted maxil-lary expansion) that stressed the soft tissueclosure
technique and did not confoundthe soft tissue changes with vertical
oranteroposterior vectors ofmaxillarymovement.A figure-eight alar cinchsuture
combined with a V-Yadvancementclosure predictably reconstructed thepatient�s
preoperative soft tissue state.Suturing the alar bases independently tothe nasal
septum (combined with a V-Yclosure) was less effective but stillsuperior to a V-
Yclosure alone.97Contouring the ANSReduction oftheANS is indicated in patients
undergoinglarge advancements or impactions ofthemaxilla who already have good nasal
tipprojection (Figure 59-14).21The hard tissuechanges in the position ofthe ANS
affectprimarily the soft tissue landmarks sub-nasale and pronasale.4This technique
should not be used inpatients who have poor preoperative nasal tipprojection.The
nasal tip will rise ifthe ANS isleft intact when advancing or impacting
themaxilla.ANS reduction is also contraindicat-ed in patients who are having a
maxillary set-back procedure.The result could lead to a�polybeak�deformity or
drooping ofthe col-umella (Figure 59-15A�D).SeptoplastyThe cartilaginous nasal sep-
tum should be reduced during maxillaryimpactions ofgreater than 3 mm to pre-vent
postoperative deviation or bucklingofthe septum.40,46This is done by reflect-ing
the septal perichondrium and remov-ing the appropriate amount ofcartilagefrom the
inferior aspect ofthe nasal sep-tum with a scissor or scalpel blade (Figure59-16A
and B).The same amount ofsep-tum should be removed as the maxilla isimpacted.This
technique can be com-bined with reduction ofthe maxillarynasal crest.Prudence must
be exercised asoverreduction ofthe septum can result ineither a saddle nose
deformity or a poly-beak deformity depending on the locationofthe excessive
cartilage resection.15FIGURE59-12 (CONTINUED)F�H,The figure-eight alar cinch suture
technique.Following the initialsteps described above,the suture is passed in a
lateral to medial direction through the fibroadipose tis-sue on one side,and in the
identical fashion (lateral to medial direction) on the other side ofthe nose.It is
then tied in the midline to a predetermined width.(CONTINUEDONNEXTPAGE)FGH
Soft Tissue Changes Associated with Orthognathic Surgery1239DoubleV-YClosureThe
double V-Yclosure was first proposed by Lassus forthickening ofthe thin lip (Figure
59-17Aand B).98Hackney and colleagues com-pared muscle reorientation using an
alarcinch suture in conjunction with a simpleclosure technique,a single V-
Yclosuretechnique,and a double V-Yclosure tech-nique.99They observed that all
threemethods ofclosure yielded a significantincrease in alar base width,and the
dou-ble V-Yclosure preserved the vermilionFIGURE59-12 (CONTINUED)I�K,The dual-
suture alar cinch technique.Before identifying the appropriate tissues described
above,a hole is drilled in theANS.Individual sutures are placed through the
fibroadipose tissues,then through the hole below ANS and tied to a predetermined
width for each nostril.L,Modification ofthis technique.Instead ofthe sutures being
placed through the ANS,the individual sutures are passed through the anterior
caudal sep-tum.Adapted from Betts NJ.Techniques to control nasal features.Atlas
Oral Maxillofac Surg Clin North Am 2000;8:53�69.LJIK
1240Part 8: Orthognathic Surgery12/15/80 3.5 months preoperativeAge 15 years 4
months9/8/81 5 months postoperativeAge 16 years 1 monthFIGURE59-13Favorable soft
tissue changes after maxillary impaction surgeryand mandibular autorotation in a
patient with an already wide alar base byuse ofan alar cinch suture and a V-
Yclosure.A,Data from pre- and postoper-ative cephalograms.Patient 3.5 months
preoperation at age 15 years,4 months(solid line); patient at age 16 years,1 month
postoperation (dotted line).B,Pre- and C,postoperative full facial views.D,Pre- and
E,postoperative smilingfull facial views.F,Pre- and G,postoperative three-quarter
views.H,Pre- andI,postoperative profiles.A adapted from and B�I reproduced with
permissionfrom Betts NJ,Fonseca RJ.Soft tissue changes associated with
orthognathicsurgery.In: Bell WH,editor.Modern practice in orthognathic and
reconstruc-tive surgery.Vol 3.Philadelphia (PA): W.B.Saunders;
1992.p.2171�2209.ABDFHCEGI
Soft Tissue Changes Associated with Orthognathic Surgery1241(especially in the
lateral portion ofthelip) with less variability than with theother two techniques
ofclosure.The trueindication for this procedure is thepatient who preoperatively
has a thin lat-eral vermilion.100MandibleWhen contemplating a mandibular
setbackosteotomy the surgeon must carefully assessthe patient�s submentocervical
morphology.Ifa patient has a short submental length andpoor submentocervical
proportion,man-dibular setback may worsen this,resulting ina �double chin.�Ifthis
complication is a pos-sibility,the surgeon may elect to combine themandibular
setback procedure with anadvancement genioplasty or submentocervi-cal liposuction
(ifadipose tissue is present).ChinIncorrect planning,vestibular scarring,excessive
detachment ofsoft tissue from thechin,suprahyoid myotomy,improper clo-sure ofthe
soft tissue incision,hematomaformation,genial remodeling,and excessivebone
resorption may compromise theresults ofchin surgery.66Bone resorption is related to
the amountofsoft tissue dissection and therefore is morepronounced in nonpedicled
genioplasties.69Adolescent patients also have more boneresorption after genioplasty
procedures.77FIGURE59-14Reduction ofthe anterior nasal spine during a maxillary
osteotomy.This procedure isindicated in patients undergoing large advancements or
impactions ofthe maxilla who already havegood nasal tip projection.This procedure
is contraindicated in patients who have poor preoperativenasal tip projection or
are having a maxillary setback procedure.Adapted from Betts NJ.Techniquesto control
nasal features.Atlas Oral Maxillofac Surg Clin North Am 2000;8:53�69.FIGURE59-
15Poor esthetic outcome in a patient who had overzealous reduction ofanterior nasal
spine (ANS) after a maxillary advancement procedure.A,Pre-operative full facial
view.B,Postoperative full facial view.C,Preoperative profile view.D,Postoperative
profile view.Reproduced with permission from Betts NJ,Fonseca RJ.Soft tissue
changes associated with orthognathic surgery.In: Bell WH,editor.Modern practice in
orthognathic and reconstructive surgery.Vol 3.Philadelphia (PA): W.B.Saunders;
1992.p 2201.ABCD
1242Part 8: Orthognathic SurgeryChin ptosis or �witch�s chin�(Figure59-18A�C) is an
unesthetic complicationsecondary to the degloving dissection ofthe chin or to lack
ofreattachment ofthementalis muscle at the time ofsurgery.This may lead to an
inferior tissue slidecausing excess interlabial incompetenceand exposure ofthe
lower teeth secondaryto lower lip ptosis and redundant tissue inthe submental
area.45,68,70Several investigators have demonstrat-ed that using a procedure that
minimizessoft tissue stripping may produce a morepredictable hard and soft tissue
responsein the osteotomized segment.44,45,65,66,68,71Therefore,the surgeon should
attempt tomaintain as much soft tissue pedicle onthe labial and lingual aspects
ofthemandible as possible.In addition to a pre-dictable soft to hard tissue
ratio,preserva-tion ofthe soft tissue pedicle ensures agreater blood supply to the
osteotomizedsegment,less bony resorption,and adecreased risk
ofinfection.64,71During closure,the mentalis musclesmust be reapproximated to
prevent ptosisofthe chin.An incision out into the unat-tached tissues ofthe lip can
help preventpostoperative wound dehiscence and facil-itate muscle
reapproximation.FIGURE59-16A,Septal reduction during maxillary impaction
osteotomy.The cartilaginousnasal septum should be reduced during maxillary
impactions ofgreater than 3 mm to preventpostoperative deviation or buckling ofthe
septum.This is done by incising the nasal mucosaand reflecting the septal
perichondrium and removing the appropriate amount ofcartilagewith a scissor or
scalpel blade.The same amount ofseptum should be removed as the maxil-la is
impacted.This technique can be combined with reduction ofthe maxillary nasal
crest.B,Clinical example.A adapted from and B reproduced with permission from Betts
NJ.Tech-Aniques to control nasal features.Atlas Oral Maxillofac Surg Clin North Am
2000;8:53�69.BFIGURE59-17A,Double V-Yadvancement closure showing initial retraction
and closure ofanterior components ofvestibular incision.B,Clo-sure
completed.Adapted from Milles M,Betts NJ.Techniques to preserve or modify lip form
during orthognathic surgery.Atlas Oral MaxillofacSurg Clin North Am 2000;8:71�9.AB
Soft Tissue Changes Associated with Orthognathic Surgery1243A chin dressing
fabricated from elastictape should be placed at the end ofthesurgical procedure to
stabilize the soft tis-sues and prevent hematoma formation.These dressings are
typically worn for 5 to7 days postoperatively.Secondary Revision ofPoor Surgical
ResultsThe best method oftreatment for a poorsoft tissue outcome is
prevention.Thedeformity should be recognized,the softtissue effects ofthe surgical
procedureshould be anticipated,and the correctinterceptive procedures
instituted.How-ever,ifa secondary procedure is required,the same techniques
described in the pre-ceding sections can be used.Revisionsurgery is more difficult
than control ofthe soft tissues at the time the originalsurgery because ofscarring
and change innormal anatomic relationships.24,45Rosensuggests that these secondary
proceduresbe attempted only after the final soft tis-sue drape has been established
and theresidual defect has been identified.23Other procedures for revising a
poorsurgical outcome are submental lipecto-my,nasal wedge resection (Weir
excisions)(Figure 59-19),23and rhinoplasty.References1.Dion KE,Berscheid E,Walster
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1989;4:209�18
CHAPTER 60Prevention and Management ofComplications in Orthognathic SurgeryJoseph
E.Van Sickels,DDSComplications oforthognathic surgerycan be divided into several
broad andoverlapping categories.Whether surgeryofthe maxilla or mandible is
done,re-gional anatomy,amount ofmovement,number ofsegments needed,and type
offixation employed all influence the typesofproblems
observed.Difficultiesencountered can fall into one or more ofthe following
areas:vascular,neural,infec-tious,fracture management,occlusalchanges,joint
dysfunction,dental,andmiscellaneous complications.The approach to complications
usedin this chapter is divided into two areas:prevention and
management.Preventioncan be summarized as preoperative evalu-ation and treatment
planning.Many oftheless than desired results can be traced toerrors in preoperative
clinical examina-tion,models,or records.Patients withunusual anatomy may dictate
departurefrom established treatment modalities,buttheir care should be planned in
advance.Vascular ComplicationsHemorrhage in the MaxillaAcute InjuriesSevere
hemorrhage hasbeen documented with maxillary andmandibular surgery and can have
bothimmediate and secondary effects.1�7Mas-sive hemorrhage is rare whether acutely
orin the postoperative period,but is possiblewith maxillary surgery.The vessels
most atrisk ofinjury during maxillary surgery arethe internal maxillary artery,the
posteriorsuperior alveolar artery,and the greaterpalatine artery.Massive blood loss
can occur sec-ondary to injury to the internal carotidartery and the internal
jugular vein.Whenfracturing the pterygoid plates it is pos-sible to fracture the
base ofthe skull byvigorously manipulating chisels or direct-ing chisels against
the plates.8,9This canresult in direct or indirect damage tomajor vessels in the
neck or skull.Whenapproaching maxillary surgery one shouldremember that vessels may
be directlyinjured during osteotome placement orindirectly through shattering the
ptery-goid plates.Efforts should be made toproperly direct osteotomes in the ptery-
goid plates and to down-fracture the max-illa without excessive force.Ifthe
maxillais extremely difficult to mobilize,the pos-terior cut may be directed into
thetuberosity and away from the pterygoidplates (Figure 60-1).10Patients who
areundergoing a maxillary osteotomy to cor-rect malposition oftheir maxilla
followingtrauma may present special considera-tions.The previous midface trauma
mayhave resulted in fractures at the base oftheskull.Manipulations to mobilize the
max-illa may result in the osteotomy followingthe previous fracture lines.Generally
when brisk bleeding isencountered during surgery,the oste-otomy should be
completed,the maxilladown-fractured,and the site assessed forthe bleeding
source.Alternatively,theregion may need to be packed to controlblood loss,and then
the osteotomy com-pleted.The best opportunity to identify aFIGURE60-1The posterior
cut is directed intothe tuberosity behind the second molar when themaxilla is
difficult to mobilize.Adapted fromVan Sickels JE,Tucker MR.Prevention andmanagement
ofcomplications in orthognathicsurgery.In: Peterson LJ,Indresano
AT,MarcianiRD,Roser SM.Principles oforal and maxillofa-cial
surgery.Vol.3.Philadelphia (PA): JB Lip-pincott Company; 1992.p.1466.
1248Part 8: Orthognathic Surgerybleeding vessel is when it is first cut.Liga-ture
clips are applied or electrocautery isused ifthe vessel is easily seen.When hem-
orrhage obscures the field,packing fol-lowed by attempts to directly occlude
thevessel should be attempted.The lastoption is to pack resorbable materials inthe
region under pressure,with tampon-ade ofthe bleeding source.The carotid artery may
be susceptibleto both direct and indirect insult duringthe operation.Thrombosis
ofthe inter-nal carotid artery after orthognathicsurgery may occur because
ofexcessiveextension ofthe head and neck.11Mor-tality associated with thrombosis
oftheinternal carotid has been estimated at40%,with an additional 52% ofthepatients
being left with a serious neuro-logic deficit.Extension ofthe head andneck serves
to stretch and partially fix thecarotid artery against the cervical verte-brae,and
contralateral rotation ofthehead results in further stretch oftheartery.Positioning
the patient in thismanner places the internal carotid at riskfor direct or indirect
trauma.Delayed HemorrhageDelayed hemor-rhage following a Le Fort I
maxillaryosteotomy may occur as early as the nightofsurgery to as late as 9 days
post-operatively.The vessels most frequentlyinvolved are the greater palatine
artery,theinternal maxillary,and the pterygoidvenous plexus ofveins.6Suggestions to
reduce this type ofinjury include careful placement and ori-entation ofthe
pterygomaxillaryosteotome in the suture and angling theosteotomy inferior from the
zygomatico-maxillary crest toward the pterygoidplates.12The mean distance from the
mostinferior junction ofthe maxilla and thepterygoid plates to the internal
maxillaryartery in the pterygopalatine fossa is 25mm.With an average length
ofanosteotome of15 mm,assuming normalanatomy,the margin ofsafety to separatethe
entire pterygomaxillary junction is 10mm.However,patients with dentofacialand
craniofacial anomalies can haveanatomic variation from these normativedata.The
internal maxillary artery and itsbranches are most vulnerable to damagein their
course through the pterygopala-tine fossa and fissure when the maxillarytuberosity
is separated from the pterygoidplates with an osteotome.The posterior superior
alveolar and thegreater palatine arteries may be severedduring the Le Fort I
procedure becausethey lie in the bony walls,although the pos-terior superior
alveolar artery is notthought to present a significant problemfor bleeding.It is
generally recommendedthat the greater palatine arteries be pre-served by gently
removing bone that sur-rounds the vessels (Figure 60-2).However,ifbleeding is
encountered,the vesselshould be ligated rather than letting itretract and
bleed.Preserving the vesselsmaximizes the blood supply to segmentedmaxilla and
minimizes neural deficits tothe palate.There are several treatment optionsfor the
patient with postoperative hemor-rhage after maxillary surgery,and theyvary with
the degree and severity ofthebleeding.The most obvious sign ofthistype ofproblem is
hemorrhage comingfrom both nares.3When a patient is initial-ly seen with
postoperative bleeding,inter-maxillary fixation (IMF),ifpresent,should be
removed.The patient�s generalphysical status should be assessed andappropriate
bleeding and coagulationstudies ordered.Abnormal parameterswarrant correction and
possible consulta-tions.With a good light source present,thenose should be
suctioned to revealwhether a bleeding site is arterial orvenous in
nature.Ifadequate assessment isnot possible,the nose should be anes-thetized and
decongested with a localanesthetic and a vasoconstrictor.Localanesthetic injections
in the nose andFIGURE60-2Using a bur,a groove ismade both medially and laterally up
tothe greater palatine artery.A chisel isused to gently fracture the bone.Adapt-ed
from Van Sickels JE,Tucker MR.Prevention and management ofcom-plications in
orthognathic surgery.In:Peterson LJ,Indresano AT,MarcianiRD,Roser SM.Principles
oforal andmaxillofacial surgery.Vol.3.Philadel-phia (PA): JB Lippincott
Company;1992.p.1466.
Prevention and Management ofComplications in Orthognathic Surgery1249around the
greater palatine foramen arehelpful in stopping or slowing postopera-tive
hemorrhage.Ifthe bleeding is minor in nature,itmay be possible to treat the patient
withbed rest.Anterior and posterior packingfor 3 to 5 days combined with bed rest
canbe used for recurrent bleeding or for apatient not responding to initial
therapy.For a patient who does not respond tothese therapies or in whom the
bleeding issevere or persistent,exploration ofthesurgical site and direct ligation
or packingofproblematic regions is suggested.Anangiogram may be
necessary.Additionaloperative techniques may be employeddepending on clinical
examination or an-giographic findings.These include pack-ing ofthe maxillary sinus
and angio-graphic embolization ofthe specificvessel.Ligation ofthe external
carotidartery might be considered in extremeemergencies;however,with collateral
cir-culation,bleeding may still occur afterthis vessel is ligated.Hemorrhage in the
MandibleVascular InjuryAs with maxillarysurgery,major vessels can be injured
withmandibular procedures.Occlusion oftheinternal carotid has been described
follow-ing a sagittal split osteotomy.13Major cen-tral nervous system morbidity can
occurfollowing this injury.Vascular injuries are due to indirecttrauma either
through forceful placementofa retractor placed on the lingual surfaceofthe ramus
ofthe mandible or the use ofa mallet and chisel on the medial aspect ofthe
mandible.Medical and surgicalmanagement ofcarotid artery thrombosisis beyond the
scope ofthis text.Preventionis relatively easy.Placement ofretractorsand chisels on
the medial posterior aspectofthe mandible should be used with cau-tion.It is
preferable to limit dissection andsubsequent chisel placement just distal tothe
lingula.Hemorrhage with Sagittal Split Osteot-omyEarly reports noted numerous inci-
dences ofexcessive bleeding with the sagit-tal split osteotomy.14Vessels injured
werethe internal maxillary artery,the facialartery,and the inferior alveolar
artery.These injuries were attributed to inexperi-ence,excessive tissue
stripping,and lack ofsophisticated instrumentation.Excessivehemorrhage remains a
problem with thesagittal split osteotomy although to amuch lesser degree.In a
series of256 sag-ittal osteotomies the incidence ofhemor-rhage was 1.2% (3
cases).15This included 2cases ofinjury to the inferior alveolarartery and 1 to the
anterior facial artery.Hemorrhage occurring secondary tovascular injury on the
medial or lateralaspects ofthe mandible with a sagittalsplit osteotomy can be
controlled in anumber ofways.The simplest involvespacking,clamping,or injecting
epineph-rine (1:100,000) into vessel walls.Cau-tion should be used when applying
elec-trocautery in close proximity to theinferior alveolar nerve.When
necessary,bipolar cautery is suggested.Extraoraldissections to control bleeding
sourcesare seldom necessary.Hemorrhage with Other Ramal Proce-duresIn a study ofthe
intraoral verticalsubcondylar osteotomies there was a lowincidence ofdamage to the
maxillaryartery.16The masseteric artery may be in-jured by carrying a saw cut too
far into thesigmoid notch.The inferior alveolar arterymay also be injured with a
vertical sub-condylar osteotomy,which is usuallycaused by bringing the vertical cut
oftheramus too far anteriorly to the posteriorborder ofthe mandible.Access to the
bleeding vessel is diffi-cult given the approach.Fortunately inmost
instances,intraoperative bleedingalong the ramal cut or in the sigmoidnotch can be
controlled by tamponade.Late sequelae such as an aneurysm mayrequire
embolization.Loss ofVascularitySegmental ProceduresThe results ofvascular
compromise vary between maxil-lary and mandibular procedures.Compli-cations,ranging
from fibrosis ofpulpal tis-sues and periodontal defects to loss ofsegments,tend to
increase with the num-ber ofsegments.The most frequent causeofcomplications
associated with the max-illa is interruption ofthe blood supply.17Additional causes
may include lack ofseg-ment stabilization,patient factors,inade-quate preoperative
evaluations,poor follow-up,and multiple segments.17 Patientswho are heavy smokers
or who have othersystemic reasons for small vessel disease maymandate an altered
treatment plan.Several suggestions have been pro-posed to avoid vascular
complicationswith segmental procedures.Preoperativeplanning to ensure adequate
spacebetween teeth,model surgery that mini-mizes the amount ofbone
removed,andcareful examination ofperiapical radi-ographs prior to surgery are part
oftheplanning that goes on prior to arriving inthe operating room.Intraoperative
man-agement includes careful cutting betweensegments and the use ofchisels and
irri-gated burs to complete cuts.These stepswill minimize the amount ofheat
generat-ed and decrease the chance ofcreatingbone or tooth defects.Release ofsoft
tissueadjacent to osteotomy sites and gentlemobilization ofsegments to avoid
tearingand cutting offlaps is essential.Splintswith palatal bars used for
stabilizationshould not impinge on the palatal pediclethat serves as the major
blood supply tomaxillary segments.Special considerationsmust be given to the
patient who has hadprevious palatal surgery or multiple seg-mental procedures or is
a cleft palatepatient.In these instances standard flapdesigns may not be
adequate.Complications such as periodontaldefects,pulpal necrosis,and delayed union
1250Part 8: Orthognathic Surgeryare more commonly seen in the anteriorregion ofthe
mandible but may be as-sociated with any segmental operation.Mandibular segmental
procedures requiredetailed planning ofsoft tissue incisionsand careful elevation
ofsoft tissue pedi-cles.In order to minimize intraoperativecomplications,the
vascular supply toinvolved segments must be optimized bydesigning as large a flap
as possible to theinvolved segment,maintaining maximalsoft tissue attachment to the
segment to bemobilized,avoiding stripping the lingualmucoperiosteal pedicle,and
making thebony cut as apical as possible to include asmuch muscle as
possible.Aseptic NecrosisMajor loss ofsoft andhard tissue ofthe maxilla is rare and
is mostoften due to a compromised blood supply.This can be caused by a kinked
pedicle inthe palate or tearing offlaps.Isolated casesofloss ofthe entire maxilla
or segmentshave been reported (Figure 60-3).17Moresubtle complications secondary to
vascularcompromise range from flattening ofthepapilla and loss ofthe gingiva to
periodon-tal defects in areas ofosteotomy cuts.Aseptic vascular necrosis ofthe
proxi-mal segment with a sagittal split osteotomyhas been attributed to excessive
strippingofthe segments.18Loss ofbone secondaryto aseptic necrosis has resulted in
disfigure-ment ofpatients.As early as 1974 Gram-mer and colleagues noted in animals
thedeath oflarge areas ofbone in the proximalfragment secondary to elevation
ofthemucoperiosteal pedicle.19They proposedthat devitalized bone usually
revascular-ized.However,when revascularizationdoes not occur,a substantial loss
ofbonefrom the mandibular ramus can occur,especially in the gonial angle
region.In1977 Epkerpresented modifications ofthesagittal split and discussed a
technique inwhich the amount ofdissection ofthemasseter was greatly
decreased.20Adoptionofthis technique has greatly minimized theincidence ofavascular
necrosis after asagittal split osteotomy.Rigid fixation ofsegments,which allows
early revasculariza-tion,has also minimized the incidence ofaseptic necrosis.Early
publications suggested that anadvancement genioplasty could be donesuccessfully by
repositioning the lowerborder ofthe mandible as a free graft.However,when this is
done,resorption ofthe advanced segment occurs to varyingdegrees and results in
slight to almostcomplete loss ofthe genial segment.Leav-ing the lingual and the
buccal pediclesintact minimizes resorption and gives amore predictable chin
contour.Therefore,efforts should be made to preserve thelargest pedicle
possible.Large genialadvancements may mandate more releaseoflingual soft tissue to
achieve the desiredresults.However,with an adequate labialpedicle and rigid
fixation,bone lossshould not be appreciable.The intraoral vertical
subcondylarosteotomy is the mandibular procedurewhere the proximal segment is at
most riskdue to release ofperiosteal attachments.One study reported 2 out of42
patientswith necrosis ofthe distal tip ofthe proxi-mal segment.21The surgical
techniqueinvolved stripping the entire lateral andmedial surfaces ofthe mandible up
to themandibular neck.With more recent mod-ifications ofthe technique where a
pedicleofmedial pterygoid muscle attached to theposterior and medial aspect ofthe
proxi-mal segment is maintained,necrosis oftheproximal tip has not been a
problem.22Nonunion or Delayed Union ofthe MaxillaNonunion ofthe maxilla may be due
toboth local and systemic factors.The bloodsupply may be compromised by poor sur-
gical planning or may be questionablebecause ofprevious surgery,as in cleftpalate
patients.Scarring in large advance-ments may make it difficult to
passivelyreposition a maxilla.Patients may haveparafunctional activity or excessive
biteforces.In those patients in whom the max-illa has been moved superior and
posteri-or,there may be insufficient bone interfaceto allow healing.Patients with
systemicconditions that interfere with healing,such as diabetes and
smoking,requireindividual case planning to minimizecomplications.When an unstable
maxilla is anticipat-ed,bone plates may be combined with aux-iliary forms
ofstabilization.In most casesthis includes skeletal wires and a period ofIMF from 1
to 6 weeks.With inferior posi-tioning ofthe maxilla,bone plates andbone grafts can
be combined withadjustable pins (Figure 60-4).When theseare used the patient is not
kept in IMF formore than 1 week.Bone gaps greater than5 mm should be grafted.Ifthe
maxilla hasgood bone contacts in multiple regions,isolated defects may be filled
with alloplas-tic material.Large bone gaps in multipleregions require autogenous
grafts.After surgery the major sign ofa prob-lem is mobility ofthe maxilla when
theFIGURE60-3Necrosis ofthe soft and hard tis-sues has occurred in the left
lateral/cuspid regionafter a Le Fort I osteotomy.Adapted from VanSickels JE,Tucker
MR.Prevention and manage-ment ofcomplications in orthognathic surgery.In: Peterson
LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal and
maxillofacialsurgery.Vol.3.Philadelphia (PA): JB LippincottCompany; 1992.p.1468.
Prevention and Management ofComplications in Orthognathic Surgery1251patient
occludes.Treatment ofa mobilemaxilla may be divided into early and
latemanagement.The use ofIMF is controver-sial.Ifthe patient is not in fixation a
shortperiod offixation may help.On the otherhand,ifthe patient is in IMF,removing
itmay allow consolidation.This is particu-larly important in the patient who
hasparafunctional activities.Additionally,flatplane splints may be used to
distributeocclusal force more evenly.For minorproblems selective occlusal
equilibrationmay resolve premature contacts,con-tributing to movement ofthe
maxilla.Patients should be placed on a soft diet.Heavy elastics should be
discontinued,because with function they put intermit-tent strong forces on the
maxilla.Forpatients with posterior relapse,light shortclass III elastics can help
prevent furthermovement and may allow osseous consol-idation.However,all elastics
must be usedjudiciously as they may aggravate a prob-lem.Ifa patient ends up with a
minorClass III malocclusion,it is usually easierto manage than a nonunion
maxilla.Late management involves returningthe patient to surgery for autogenous
bonegrafting and very rigid stabilization ofthemaxilla.This would include large
boneplates,bone grafts,auxiliary techniques,and possibly alloplastic
materials.Reoper-ation should be approached aggressivelyby completely mobilizing
the maxilla andremoving fibrous tissue.Nonunion or Delayed Union ofthe
MandibleNonunion or delayed union ofthemandible may be due to avascular
necrosis,insufficient bone contact,instability ofthefixation appliances,or
instability ofbonefragments.It has been seen with sagittalsplit and vertical
subcondylar osteotomies.Vertical ramal osteotomies have specialconsiderations,not
only because a great dealoftissue may be stripped from the segmentsbut also because
the fragments may not liein close apposition or be stabilized.Anylarge
parafunctional movement ofthe jawsor trauma in the early phases after surgerymay
lead to nonunion (Figure 60-5).Large advancements are ofa greaterconcern than small
advancements.Foradvancements ofgreater than 7 mm,addi-tional plates may be needed
to maintainstability (Figure 60-6).Alternatively,skele-tal wires and a briefperiod
ofIMF havebeen shown to give increased stability.23Delayed union ofa sagittal
splitosteotomy can be treated by a period ofIMF.Alternatively,the patient may need
asecond operation and additional plates orscrews.Nonunion mandible following
avertical subcondylar osteotomy may bemore ofa problem with edentulouspatients or
when a very short vertical cut isused (Figure 60-7).A second operation,approaching
the fragment from an extrao-ral approach to align and rigidly fix it,maybe
necessary.Dental and Periodontal InjuriesDental and periodontal injuries can be
sec-ondary to both vascular and nonvascularFIGURE60-4The maxilla is inferiorly
posi-tioned using bone grafts,plates,and adjustablepins.Adapted from Van Sickels
JE,Tucker MR.Prevention and management ofcomplications inorthognathic surgery.In:
Peterson LJ,IndresanoAT,Marciani RD,Roser SM.Principles oforaland maxillofacial
surgery.Vol.3.Philadelphia(PA): JB Lippincott Company; 1992.p.1469.FIGURE60-5Aand
B,Patient whose platesgave way 2 weeks after surgery when vigorousmanipulation
ofher jaw was attempted.ABFIGURE60-6Large advancement ofthemandible with
monocortical plates and bi-cortical screws.
1252Part 8: Orthognathic Surgerycauses and are most frequently related toplanning
or technical errors made at thetime ofsurgery (Figure 60-8).Segmentalprocedures in
the maxilla and mandiblemay cause a number ofproblems,includingcut teeth,loss
ofteeth,need for postopera-tive root canals,and periodontal defects.Preoperative
orthodontic mechanicscan be used to maximize a space betweenroot apices in a
planned osteotomy site.Periapical radiographs should be studiedto note the
direction ofthe root apices.Aminimum space of3 mm is advocatedwhen placing
osteotomy cuts betweenteeth,and 5 mm is recommended abovethe apices to avoid injury
to pulp.24Precisemodel surgery can greatly reduce the fre-quency ofdentoalveolar
injury.Surgeryshould be planned so that a minimalamount ofbone is removed between
seg-ments.Manipulation and prying ofseg-ments should be done toward the apices
ofthe teeth rather than at the gingival mar-gin to minimize tears in the mucosa
andsubsequent periodontal defects.Segmentsshould be tipped apart whenever
possible.Copious irrigation offine fissure bursshould be used when cutting through
theouter cortex in the maxilla.This is fol-lowed by gentle and progressive
chiselplacement in the region to separate thesegments.When a bony palatal island
isused,release oftissue should occur underthe island rather than from the
alveolarsegments.After segments are gently sepa-rated,small amounts ofbone may be
judi-ciously removed.When larger wedges ofbone are planned for removal,alwaysremove
less bone than was planned.Whensegments do not fit together,they can begently
trimmed.Defects seen followingexcessive removal ofbone usually fill withscar
tissue.In the mandible it is necessary to cutboth the buccal and lingual
plates,leavingonly a small amount oflingual corticalplate near the cervical portion
ofteeth tobe separated by a chisel.Use ofsaws is rec-ommended to cut through the
mandible,with careful palpation on the lingual sur-face.Owing to the dense lingual
cortex,chisels are much more dangerous in themandible than in the maxilla where
theycould shatter the lingual cortex or tear thelingual pedicle region.For these
reasonschisels should be used cautiously follow-ing a saw cut,and segments should
bepried apart with minimal tapping throughto the lingual
surface.FistulasPostoperative fistulas in the oronasal andoroantral regions
generally result from softtissue injury at the time ofsurgery.Fistulashave been
reported with isolated segmentalas well as total maxillary osteotomies.25This may
occur as a result ofrotary instru-ments,saws,or osteotomies that perforatethe
palatal mucosa at the time the segmen-tal osteotomies are completed.Impinge-ment
ofsoft tissue in the segmentalosteotomy site during segment reposition-ing and
fixation may also result in tissuenecrosis and fistula formation.Tearing ofpalatal
mucosa at the time ofattempted tis-sue stretching may also result in non-healing
defects.This is most commonwhen a bony osteotomy is made in themidline ofthe
maxilla while attempting tostretch the midpalatal tissue (Figure 60-9).FIGURE60-
7Severe condylar rotation is com-mon with a short subcondylar osteotomy.Adapt-ed
from Van Sickels JE,Tucker MR.Preventionand management ofcomplications in ortho-
gnathic Surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal
andmaxillofacial surgery.Vol.3.Philadelphia (PA):JB Lippincott Company;
1992.p.1470.FIGURE60-8Injured root surface adjacent toan interdental cut.FIGURE60-
9A,Oronasal communication hasbeen created during a Le Fort I osteotomy withpalatal
sectioning.B,Sutures placed at the timeofsurgery,with good oral hygiene,resulted
inspontaneous closure at 8 weeks.AB
Prevention and Management ofComplications in Orthognathic Surgery1253Careful soft
tissue manipulation at thetime ofsurgery in an attempt to preventtissue perforation
is the best method forprevention offistula formation.Whenexpansion is needed,the
palatal mucosacan be incised with two parallel incisionsjust medial to the greater
palatine fora-men;bony separation then occurs in themidpalatal area.25The tissue
can stretchand expand in an area well away from thebony separation.An alternative
techniqueinvolves making parasagittal cuts in thenasal floor immediately adjacent
to the lat-eral nasal wall.The osteotomy can thus bemade over tissue that is
thicker and some-what more elastic.26Ifa small tear is notedfollowing a bony
cut,care should be takento release the palatal tissue from aboveprior to expansion
ofsegments.When a fistula is noted postoperatively,several measures can be pursued
that mayallow the fistula to close spontaneously.Preventing sinus or nasal
infections isessential.This includes antibiotic therapy,decongestants,and nasal
drainage.Con-struction ofan appliance that will obturatethe fistula without placing
pressure on theoverlying tissue will generally help in clo-sure by reducing food
contamination.Careful attention must be given to theconstruction ofany appliance
used to obtu-rate a fistula in the immediate postopera-tive period.Excess pressure
on the palatalmucosa may result in decreased vascularity,resulting in further loss
ofsoft tissue andassociated bone.Iflocal measures,appro-priate medical therapy,and
fistula obtura-tion have been unsuccessful,surgical clo-sure ofthe fistula will be
required.When considering closure ofa fistula,it is important to ensure that at
least 6months have elapsed to allow for revascu-larization ofthe maxillary
segment.Care-fully managed fistulas will continue toclose for 8 to 12 weeks.Ifthis
therapy isnot successful,a soft tissue flap should beraised from an area farthest
from segmentswith the least potential for decreased vas-cularity.Timing varies,but
the maxillashould be revascularized by 6 months.Ifalarge segment ofthe maxilla was
involvedin the initial hypovascular state,distantflaps should be
considered.Choicesinclude a buccal fat pad or a tongue flap,among others.Management
ofTissue after Vascular CompromiseDoppler flowmetry ofthe maxillary gin-giva can be
used to detect subtle decreas-es in the maxillary gingival blood flowfollowing a Le
Fort I osteotomy.27How-ever,its use is limited to clinical studiesat the present
time.Clinically,blanchedfollowed by cyanotic attached gingivaand adjacent free
mucosa are early indi-cations ofvascular compromise follow-ing orthognathic
surgery.28The overlyingtissue can be an indicator ofbonyinvolvement.Three scenarios
are possi-ble:loss ofvascularity to the soft tissue,whereupon the bone is
perfused;loss ofvascularity to the bone,whereupon softtissue is perfused;and loss
ofvascularityto both the bone and soft tissue.Ifcya-nosis is noted in the immediate
postop-erative period (hours to days aftersurgery),IMF,ifpresent,should bereleased
and the mouth inspected forkinked or constricted tissue.Splints mustbe carefully
evaluated to identify areas ofpressure on soft tissue by the appliance.Ifremoval
ofIMF and reliefor removalofsplints is not helpful or the tissue isalready
necrotic,then supportive care isnecessary to attempt to minimize theamount ofbone
loss.Loss ofthe soft tis-sue and exposure ofthe underlying boneis often what
occurs.In severe cases thisshould be treated as an intraoral freegraft.Meticulous
irrigation should beperformed several times a day with orwithout packing ofthe
wound.Like allgraft tissues it must be absolutely secure.Stability will allow some
degree ofrevas-cularization.Hyperbaric oxygen therapymay be helpful to minimize
bone losswhile promoting neovascularization.Reconstruction will vary and depend
onthe size ofthe resultant defect.Nerve InjurySensory Injuries in the
MaxillaSensory injuries in the maxilla have notbeen as thoroughly studied as those
seenwith mandibular surgery.With a carefullyplaced circumvestibular incision
combinedwith gentle retraction,nerve injury isinconsequential and limited to the
terminalbranches ofthe infraorbital nerve.Recoveryofsensation to the lip,cheeks,and
noseusually occurs within 2 to 8 weeks.Paresthesias secondary to damage ofthe
sensory nerve supply to the teeth andmucosa are more common.Decreasedsensation to
the mucosa is transient andnormal sensation commonly returns with-in 6 to 12
months.Although this is usuallythe case,patients will occasionally havepermanent
numbness intraorally on thepalate and buccal gingiva.This is annoy-ing,particularly
ifon the palate,as it canbe burned by hot food.To preserve sensa-tion to the
palate,some authors feel thatthe greater palatine neurovascular bundleshould be
preserved.28Failure ofthe teeth to respond to stim-ulation may also be
temporary.However,permanent loss ofresponse to electrical,hot,or cold stimulation
is not unusual,and does not necessarily represent a tooththat needs endodontic
therapy.The clini-cian must differentiate a nonvital toothfrom one that does not
respond to stimu-lation but has an intact blood supply.Atooth that shows periapical
radiolucencyon radiographs or a fistula upon examina-tion is a candidate for root
canal therapy.Sensory Injuries in the MandibleSagittal Split Osteotomy Transections
ofthe inferior alveolar nerve can occur dur-ing a sagittal split osteotomy.29The
mostlikely time for this to occur is during thesplitting process.When the segments
are
1254Part 8: Orthognathic Surgerybeing separated,care should be taken tovisualize
the nerve.Ifthe nerve is in thedistal segment or encased in cortical
bone,appropriate steps should be taken torelease it.This may be as simple as
releas-ing the nerve with an elevator from amedullar bone,or it may require
addition-al bone cuts to release it from cortical bone.One study suggested that low
body heightofthe patient and inferior position ofthenerve may increase the risk for
injury.29Repair ofthe nerve with one or moresutures placed in the epineurium has
beenrecommended.30However,one large serieshad a 3.5% incidence oftransection
oftheinferior alveolar nerve,which was anteriorto or in the third molar region in
allinstances.15Nerve endings were approxi-mated in 9 patients by positioning the
seg-ments but not suturing them.The length offollow-up for these patients was 2 to
5 years,and all ofthe patients had somereturn ofsensation to the normal
inferioralveolar nerve distribution.Whether thisrepresented regeneration or new
growthfrom the cervical plexus is unknown.Ifthe transection occurs at the verti-cal
bony cut,immediate repair may be dif-ficult.To expose more ofthe nerve in thedistal
segment a second cut anterior to thefirst is necessary.When excessive tensionis
present,the nerve may have to beexposed distally to the mental foramen toallow a
tension-free repair.The need forsuch an extensive procedure needs to beweighed
against other goals to be achievedwith the surgery.Injury to the inferior alveolar
nerve inthe absence ofa transection is frequentlyassociated with sagittal splitting
ofthemandibular ramus.Risk factors for anincreased amount ofneurosensory distur-
bance include the age ofthe patient,whether they have a genioplasty,and theamount
ofadvancement.31,32Multipletechniques have been suggested to preventthese
injuries,including osteotomy design,chisel placement,dissection
technique,decompression ofthe lateral fragment,and steroid use.Vigorous medial
retrac-tion may cause the inferior alveolar nerveto be compressed against the
lingula anddecrease intraoperative nerve conduc-tion.29,33Retraction on the medial
aspectofthe mandible should be done carefullyto avoid compression nerve
injuries.Thebest place to make the lateral (vertical) cutis in the first and second
molar regionwhere the cortex is the thickest,themandible is the thickest,and the
nerve isfurthermost from the lateral cortex.15,34Other suggestions have been made
to pre-vent nerve injuries based on clinical expe-rience,but no controlled studies
have beendone to prove whether one way is prefer-able to another.Injury to the
lingual nerve during asagittal split osteotomy can occur but it isunusual.35,36The
course ofthe lingualnerve near the medial surface ofthe man-dible
varies;therefore,any dissection onthe lingual aspect ofthe mandible in thethird
molar region may temporarily orpermanently injure this nerve.37As withinferior
alveolar nerve injuries,lingualnerve injuries should be carefully followedand
documented.Ifthe nerve is visualizedand has been transected,it should berepaired at
the time ofsurgery.Other Ramal ProceduresAlthough ver-tical or oblique ramal
osteotomies are fre-quently suggested as alternatives to a sagit-tal split
osteotomy for horizontalmandibular excess,these procedures mayalso cause permanent
injury to the inferi-or alveolar nerve.The incidence ofperma-nent paresthesia
following an intraoralvertical subcondylar osteotomy has rangedfrom 9 to
11%.38,39Endoscopic approach-es to the ramus may have a different inci-dence
ofnerve injury,but experience withthese techniques is limited.40The
precisemechanism ofinjury to the inferior alveo-lar nerve is unclear and steps to
preventthis complication require further study.The saw blade should follow the
posteriorborder ofthe ramus until it reaches a pointwell above the antelingual
bulge on the lat-eral aspect ofthe mandible.Postoperativeanesthesia should be
carefully followed.Motor Nerve InjuryInjury to the facial nerve is much morecommon
with extraoral approaches thanwith intraoral surgery.However,therehave been
multiple reports offacial nerveinjuries with sagittal split and vertical sub-
condylar osteotomies.41�44In one seriesthat studied 1,747 cases ofsagittal
splits,the incidence was 0.26%.43The degree ofinjury varies from partial to total
paralysisand is often seen following a setback ofthemandible,but has been seen with
amandibular advancement.42The possiblecauses ofinjury are impingement ofthenerve
when the distal segment was movedback,fracture ofthe styloid process andsubsequent
displacement,and introduc-tion ofretractors behind the ascendingramus with
impingement ofthe nerve.Most ofthe reported cases occurred withmandibular setbacks
without use oftheHunsuck modification.45The most likelycause ofnerve injury is
pressure on thenerve trunk,either by the distal segmentor byretractors placed
behind themandible (Figure 60-10).To prevent thisproblem a medial/ lingual split
should bejust distal to the inferior alveolar nervewhen a sagittal split is used to
set back themandible.Ifa medial split extends to theposterior border,bone should be
removedproximal to the lingula.Unfortunately themagnitude ofsetbacks causing this
prob-lem is unknown and probably varies withindividuals.Care should be taken
whenretractors are placed behind the mandibleon all ramus osteotomies.When a facial
paralysis occurs aftersurgery,there are a number ofelectricaltests that can be used
to determine thedepth ofinjury and subsequent therapy.Electroneurography,a study
ofperipher-al nerve conduction,or electromyogra-phy,which is the detection and
evalua-tion ofelectrical potentials from muscles,
Prevention and Management ofComplications in Orthognathic Surgery1255can be
used.46,47It is important to distin-guish between an injury that causes seg-mental
demyelination and one that caus-es wallerian degeneration.With axonalinterruption
the ability to transmit animpulse is lost over a period of5 to 7days.When axonal
degeneration occurs,the prognosis for complete recovery ispoor.When this is
noted,surgical explo-ration should be considered to rule out alaceration ofthe
nerve.As long as theaxon remains intact at the site ofblock-age,the nerve will
continue to respond tostimulation distal to the blockage eventhough paralysis is
present.Evokedeletromyography (EEMG),a test in whichthe degree ofmuscle twitch
elicited isrecorded,has been used as a prognostictest.48Ifthe response to EEMG
remainsgreater than 25% at 5 days,the injury ismild and the prognosis is
good.48Clinical management ofthe patientduring the paralysis can vary dependingon
the nerve branches and the type ofnerve injury involved.When the patienthas
difficulty achieving eyelid closure,aneye patch and methylcellulose eye dropsmay be
useful.Physical therapy such asheat,facial massage,and facial exerciseperformed
twice a day have been suggest-ed.Facial cream should be massaged intothe skin
around the eyes and mouth andover the midface,ideally using an
electricvibrator.Exercises may consist ofhavingthe patient stand in front ofa
mirror towatch his or her face while raising the eye-brows,blowing the cheeks,and
grinning.Even though no facial movement may benoted,intact nerve fibers will be
activatedand the exercise will help to maintainmuscle tone.Electrical and
mechanicalstimulation may maintain muscle tone.Steroids had been given
orally,intra-muscularly,and intravenously for facialnerve paralysis.Nasal and Sinus
ConsiderationsAlterations in Nasal Form: SeptumRepositioning ofthe maxilla
requiresmanipulation ofnasal components andthe maxillary sinus.As a result
ofthesemanipulations,alterations can occur withthe internal nasal anatomy
includingposition ofthe turbinates,nasal septum,and nasal valve.Adverse effects
ofmaxil-lary osteotomies on the alar bases,nasaltip,supratip depression,and upper
lipmay result in an unesthetic postoperativefacial appearance.49�51The maxillary
septum may be deviat-ed prior to surgery,at the time ofsurgery,or during
extubation.Hence the septumshould be inspected prior to surgery andat the time
ofsurgery.During a Le Fort Imaxillary surgery it is possible to alignthe septum at
its inferior anterior caudalend.At surgery the septum is disarticulat-ed from the
entire maxilla.In particular,with impaction,the maxilla will encroachon the
presurgical dimension ofthe nasalseptum.Because ofthis movement,atten-tion must be
given to the positioning ofthe septum at the time ofsurgery.Failureto do so may
result in septal deviationand obstruction,or in abnormal posi-tioning ofthe
columella and nasal tip.50There are several techniques for
superiorrepositioning,including resection ofanappropriate portion ofthe inferior
aspectofthe nasal septum or creating a groovein the superior aspect ofthe
maxilla.Insegmental osteotomies,creating a bonyisland with parasagittal palatal
cuts mayeliminate posterior superior pressure.However,it will not eliminate
pressurefrom the anterior portion ofthe maxillaon the septum.When septal deviation
is recognizedpostoperatively,three choices for manage-ment should be considered
(Figure 60-11).These include immediate manipulation,reoperation,or septoplasty at a
later time.Ifappropriate management ofthe nasalseptum was accomplished at the time
ofsurgery but the nasal septum appears to beasymmetric,manipulation with an instru-
ment placed within the nose on each sideofthe base ofthe nasal septum may allowfor
repositioning in the midline position(see Figure 60-11B and C).Ifrigid fixationhas
been used and the patient has no air-way difficulties,short-term packing may
beconsidered.Ifseptal deviation is due tointraoperative management or ifpostoper-
ative manipulation poses difficulty,imme-diate reoperation with further
septalsurgery may be indicated.Ifnone oftheprevious approaches seems
acceptable,andthe patient does not have significant airwaydifficulty,the deviation
can be reevaluatedat a later date with consideration for a sep-toplasty through
standard techniques.FIGURE60-10Two possible causes offacialnerve injury with a
sagittal split osteotomy.A,Retraction on the medial behind the ramus.B,Extension
ofthe distal segment beyond the prox-imal segment.Adapted from Van Sickels
JE,Tucker MR.Prevention and management ofcomplications in orthognathic surgery.In:
Peter-son LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal and maxillofacial
surgery.Vol.3.Philadelphia (PA): JB Lippincott Company;1992.p.1473.AB
1256Part 8: Orthognathic SurgeryAlterations in Nasal Form: Nasal ValveAn area
ofconcern in maxillary surgery isalteration in internal nasal anatomy,nasalairway
resistance,and breathing patternsas a result ofmaxillary surgery.Expansionofthe
maxilla with surgery has shown lit-tle change in the nasal airway.Somepatients
remain obligatory mouthbreathers even after expansion.52Ofgreater concern is the
possibility that supe-riorly repositioning the maxilla maydecrease the nasal
airway.Several studieshave documented that the reverse istrue.53�55Superior
maxillary repositioningappears to increase nasal cross-sectionalarea,decrease nasal
airway resistance,andincrease nasal breathing.The explanationfor this decrease in
nasal airway resistanceis most likely related to alteration inconfiguration ofthe
nasal valve area.53�55The nasal valve is formed by the nasal sep-tum,the floor
ofthe nose,the soft tissueon the lateral aspect ofthe nose,and thecaudal end ofthe
upper lateral nasal carti-lage.The increase in alar base width thatresults from
elevating the soft tissues toexpose the maxilla causes a slight widen-ing ofthe
nasal valve and thus reducesnasal airway resistance.Because this valveis at the
smallest cross-sectional area ofthenose,alterations in this area are likely tohave
a significant effect on nasal breathingwhereas changes in much larger
intranasalareas have little effect.This same phenom-enon has been demonstrated in
patientswith cleft palates.56Alterations in Nasal Form: Alar BaseIn addition to the
internal nasal changes,there are facial esthetic changes that mayresult from
maxillary surgery.Failure toproperly manage the nasal septum,para-nasal
musculature,and labial mucosa mayresult in undesirable facial esthetic
results.Adverse changes in nasal and perioral con-figuration following maxillary
surgery mayinclude excessive alar base widening,in-creased prominence ofthe alar
groove,upturning ofthe nasal tip (with an obtusenasolabial angle),flattening and
thinning ofthe upper lip,and downturning ofthe labi-al commissures.50These
complications mayalso be compounded by internal deviationofthe nasal septum or
asymmetric posi-tioning ofthe columella and nasal tip dueto septal deviation.These
types ofproblemsare difficult to manage and are best treatedby prevention.The need
to control alar basewidth and the necessity ofreconstructionofparanasal and
perioral musculature havebeen previously described.49Postoperative Sinus
SymptomsPostoperative complications related to themaxillary sinuses are primarily
limited toinfection,inadequate drainage,and openfistulas.Although many patients
experi-ence drainage and some sinus symptomsin the immediate postoperative
period,true perioperative infections ofthe sinusarea and long-term sinusitis are
rare.57,58Between 2 and 6 months after surgerythere will be normalization ofthe
bonyand soft tissue structures in over 55% ofthe patients.58However,at 6
months,30%ofthe patients will show some latentmucosal borderline swelling.58Despite
the rarity ofinfections thereare several potential causes ofinfections inthe
maxillary sinus area.The formationand retention oflarge blood clots in thesinus
cavity is an obvious source ofinfec-FIGURE60-11A,Deviated septum initially after
surgery.B,Manipulation.C,After manipulation..Reproduced with permission from Van
Sickels JE,Tucker MR.Prevention and management ofcomplications in orthognathic
maxillofa-cial surgery.Vol.3.Philadelphia (PA): JB Lippincott Company;
1992.p.1475.ABC
Prevention and Management ofComplications in Orthognathic
Surgery1257tion.Preoperative antibiotic prophylaxiswith subsequent antibiotic
levels present inthe clot will help reduce infections fromthis source.Other
potential causes ofinfec-tion in the sinus are preexisting disease,dental infection
secondary to trauma to theteeth,soft tissue ischemia and avascularity,and debris
within the sinus.Foreign ob-jects such as wires,bone plates,or screwsare
rarely,ifever,the isolated cause ofasinus infection and do not appear to causea
significant increase in the incidence ofinfection after maxillary
surgery.57Preoperative assessment ofpatientspresenting for maxillary surgery
shouldinclude a history and clinical examination,with careful attention to symptoms
ofanyexisting maxillary sinus infection.Evalua-tion ofpreoperative radiographs may
pro-vide some information regarding sinuspathology.Postoperative management ofsinus
infections should include appropri-ate antibiotic therapy verified by cultureand
sensitivity,decongestants,intranasalvasoconstrictors,and irrigation
ofpatentfistulas ifpresent.Generally sinus drainagecan be managed within 10 to 14
days withthese techniques.When a sinus infection isrefractory to medical
treatment,sinu-soscopy should be considered.Thesepatients should be managed in a
mannersimilar to treatment for patients who havenot had surgery.Unanticipated
MandibularOsteotomy FracturesFragment ManagementFragment management,or more appro-
priately intraoperative management ofunusual fragments,is a problem seenmore
frequently with mandibular proce-dures,especially sagittal split
osteotomy.Additional segments may occur oneither the proximal or distal
fragments.The incidence ofunfavorable fractureswith a bilateral sagittal split is
1.9 to2.2% with a slightly higher incidencewhen the third molars are
present.59,60These fractures may be in either theproximal or distal
segment.Intraoperative management ofaninadequate split is that separation
oftheproximal and distal segments must first becompleted.Intraoral management is
therule.A small or large fragment may havebeen fractured.Management will
varydepending on the size and location ofthefragment.It must first be
determinedwhere the fracture deviated from thedesired split.Often it is necessary
toremove the free segment to get access to theremaining mandible.Using a saw or a
burthe intact mandible or segments aregrooved so that a sagittal split can
occuralong the original planned lines.Chisels areused to complete the desired
split.The keyto management is to orient oneselfto whatis left.Once the split is
successfully com-pleted,the distal segment is advanced to itsdesired position.The
position and size ofthe remaining fragments may make posi-tioning ofthe condyle
difficult.Segmentsare sequentially stabilized to the remainingfragments.An
extraoral approach may bean option,but is usually not necessary.Thefollowing
examples will illustrate manage-ment ofvarious fractures.Proximal
Segment,MandibleIntactThe difficulty in managing segmentsdepends on the location
and size ofthefractured pieces.A fragment may shear offthe lateral aspect ofthe
mandible,leavingthe mandible intact.Whenever a buccalfragment shears off,the usual
cause is aninadequate bone cut on the inferior borderon the lateral vertical
cut.The split mustthen be completed.This can be done bymaking a deep groove on the
inferior bor-der and connecting it with the previousgroove coming down the external
obliqueridge.By gently prying and,when neces-sary,cutting bone,the segments will
beseparated as originally planned.Placing thedistal segment in occlusion,the free
frag-ment should be stabilized with screws andplates.In Figure 60-12 a buccal
fragmenthas been fractured.The main portion ofthe mandible was intact before
completionofthe split.The segment is stabilized witha plate and screw
osteosynthesis,as shownin Figure 60-13.Condylar position is notdifficult to
establish when a proximal seg-ment is large enough to be positioned andoverlapped
with the distal segment in itsnew position.Bicortical screws can be usedbetween the
areas ofcontact ofthe two seg-ments.With a small free fragment (asdepicted) it is
frequently easier to place aplate on it out ofthe mouth and then reat-tach it to
the proximal segment.Proximal Segment Split CompleteWhen the fragment occurs more
superior-ly,or there is a large advancement,suchthat there is no contact between
the proxi-mal and distal segments when placed intoocclusion (Figure 60-14),a
differentapproach must be taken.The condyle andcoronoid are in one piece,simulating
ahorizontal osteotomy ofthe mandible,BuccalfractureFIGURE60-12Buccal
segment,fractured off.Adaptedfrom Van Sickels JE,Tucker MR.Prevention and man-
agement ofcomplications in orthognathic surgery.In: Peterson LJ,Indresano
AT,Marciani RD,RoserSM.Principles oforal and maxillofacial
surgery.Vol.3.Philadelphia (PA): JB Lippincott Company; 1992.p.1477.
1258Part 8: Orthognathic Surgerywith or without the angle as a
separatefragment.Control ofthe condylar positionis much more difficult.The large
fragmentthat was sheared offshould have a plateplaced on it outside the mouth.It
shouldbe re-inserted and connected to the proxi-mal segment (Figure 60-15).This
usuallyrequires two percutaneous incisions.Hav-ing done this the proximal segment
is easi-er to manage and it can be united with thedistal segment in its new
position.This canbe done with a series ofplates or bicorticalscrews.Control
ofcondylar position maybe established by posterior,superior,andvertical pressure on
the reunited proximalsegment,followed by clamp placementprior to placement
ofbicortical screws,orby the use ofa clamp on the coronoidprocess to stabilize the
proximal fragmentbefore screw placement.The last case scenario is a fracture ofthe
condyle with the coronoid and angle ina separate fragment.Here one must platethe
condyle to the advanced reunited dis-tal segment and use screws in other partswhere
there is overlap (Figure 60-16).Cor-rect condylar positioning is extremely dif-
ficult to achieve in this environment.Through percutaneous incisions a plate
isplaced on the condyle.Using the plate as ahandle,holes are drilled in the distal
frag-ment and screws placed.Lingual Segment FractureFortunately,fractures ofthe
lingual frag-ment occur less frequently than fracturesofthe buccal fragment.The
underlyingcause is frequently an impacted thirdmolar or it may be secondary to
wedgingtoo high on the medial aspect ofthemandible (Figure 60-17).To prevent
thistype offracture it is wise to have thirdmolars removed at least 9 months prior
tosurgery.When an unwanted fractureoccurs,the split must be completed alongthe
original planned osteotomy lines.Asthe free segment is not in the way when thesplit
is completed,it is frequently possibleFIGURE60-13A four-hole or larger plate is
used tostabilize the free fragment to the proximal segment.Additional bicortical
screws are placed to ensure sta-bility ofthe complex.Adapted from Van Sickels
JE,Tucker MR.Prevention and management ofcompli-cations in orthognathic surgery.In:
surgery.Vol.3.Philadelphia(PA): JB Lippincott Company;
1992.p.1478.FracturedramusFIGURE60-14The proximal fragment has a highor horizontal
fracture.Adapted from Van SickelsJE,Tucker MR.Prevention and management
ofcomplications in orthognathic surgery.In: PetersonLJ,Indresano AT,Marciani
RD,Roser SM.Princi-ples oforal and maxillofacial surgery.Vol.3.Philadelphia (PA):
JB Lippincott Company; 1992.p.1478.FIGURE60-15A plate has been placed on
theascending ramus with additional bicortical screwsplaced between the proximal and
distal segments.Adapted from Van Sickels JE,Tucker MR.Preventionand management
ofcomplications in orthognathicsurgery.In: Peterson LJ,Indresano AT,Marciani
RD,Roser SM.Principles oforal and maxillofacialsurgery.Vol.3.Philadelphia (PA): JB
LippincottCompany; 1992.p.1478.FIGURE60-16A plate is used on the condylar seg-ment
with additional screws placed to stabilize thefree fragment to the distal
segment.Adapted fromVan Sickels JE,Tucker MR.Prevention and man-agement
ofcomplications in orthognathic surgery.In: Peterson LJ,Indresano AT,Marciani
RD,RoserSM.Principles oforal and maxillofacial surgery.Vol.3.Philadelphia (PA): JB
Lippincott Company;1992.p.1479.
Prevention and Management ofComplications in Orthognathic Surgery1259to leave
substantial vascular pedicleattached to it.The distal segment is placedinto
occlusion.The free fragment ismanipulated to an anterior position and isfixed to
the proximal segment by one ormore bicortical screws.One or more platesor titanium
mesh may be placed across theosteotomy site (Figure 60-18).Excessive Lateral
DisplacementExcessive lateral displacement can occurduring a vertical subcondylar
osteotomy.Depending on the geometry ofthe move,the proximal fragment or condylar
seg-ment may be displaced laterally or medial-ly.The usual position is lateral to
the mainbody ofthe mandible.Even with moderateflaring there is considerable
remodelingpossible and this is usually not a problem.Occasionally the proximal
segment will beflared excessively.This can be remediedintraoperatively by removing
a secondwedge at the sigmoid notch region (Figure60-19).Care must be taken in this
regionbecause the masseteric branch or the max-illary artery itselfcan be
injured.Ifexcessive flaring is noted postopera-tively,the segment may be manually
repo-sitioned,but ifthis does not succeed,reop-eration is necessary.Medial
DisplacementIn some cases ofasymmetry the rotationmay be such that the condylar
fragmentmay be placed medially.Whether this willincrease the incidence ofnerve
injury isunknown.Medial displacement rarelycauses problems.A conceivable
patientcomplaint is irritation ofthe pharynx.Ifthis happens the medial fragment
needs tobe contoured or removed.Proximal Segment RotationLack ofcontrol ofthe
proximal segmentwith a sagittal split osteotomy can haveseveral effects that are
both esthetic andfunctional.Postoperation muscular pull issuch that the proximal
segment is pulledanterior and superior while the distal frag-ment is pulled
posterior and inferior (Fig-ure 60-20).Anterior superior rotation ofthe proximal
segment may result in an un-pleasant cosmetic result by flattening ofthe gonial
angle and notching the inferiorborder ofthe mandible anterior to theangle.This
causes a bulge in the cheek sec-ondary to the position ofthe proximalfragment.The
type ofosteosynthesis usedhas been shown to affect the position ofthe fragment
during surgery and in theinitial postoperative period.61Ideal management ofa
rotated proxi-mal segment is prevention.Several posi-tioning appliances have been
presented tocontrol the proximal segment duringsurgery.62�64Rigid fixation used
withoutpositioning appliances has shown minimalrotation ofthe proximal segment
withsurgery.61However,there is a tendency toFIGURE60-17A lingual split (distal
segment)has occurred in the third molar region.Adapt-ed from Van Sickels JE,Tucker
MR.Preventionand management ofcomplications in ortho-gnathic surgery.In: Peterson
LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal andmaxillofacial
surgery.Vol.3.Philadelphia (PA):JB Lippincott Company; 1992.p.1479.FIGURE60-18Two
bicortical screws are used tostabilize the free segment to the proximal seg-ment.A
plate can be used to stabilize the proxi-mal segment to the distal
fragment.Adaptedfrom Van Sickels JE,Tucker MR.Prevention andmanagement
ofcomplications in orthognathicsurgery.In: Peterson LJ,Indresano
AT,MarcianiRD,Roser SM.Principles oforal and maxillofa-cial
surgery.Vol.3.Philadelphia (PA): JB Lip-pincott Company; 1992.p.1480.FIGURE60-
19Excessive flaring caused by bonecontact at the sigmoid notch.This can be
resolvedby removing a wedge from the distal segment.Adapted from Van Sickels
JE,Tucker MR.Pre-vention and management ofcomplications inorthognathic surgery.In:
Peterson LJ,IndresanoAT,Marciani RD,Roser SM.Principles oforaland maxillofacial
surgery.Vol.3.Philadelphia(PA): JB Lippincott Company; 1992.p.1481.
1260Part 8: Orthognathic Surgeryrotate the proximal segment medially andsuperiorly
with large advancements.65Thiscan result in an unesthetic effect for
thepatient,especially ifthere was any discrep-ancy in the height ofthe ramus prior
tosurgery (Figure 60-21).To date,theamount ofrotation that will cause clinical-ly
significant decreases in muscle efficiencyand unesthetic facial changes is
unknown.Excessive rotation ofthe proximal seg-ment should be evaluated as to
whetherthere are functional (decreased bite force,hypomobility) or esthetic (loss
ofthegonial angle) problems,or both.Anesthetic problem seen in a patient
withacceptable occlusal results may be treatedby the use ofan alloplastic
implant.Ifthepatient has an occlusal problem withesthetic considerations,the
sagittal splitcan be redone (Figure 60-22).When theseare combined with decrease in
bite forceand hypomobility,then reoperation mustbe combined with a vigorous
postopera-tive physiotherapy program.Most patients demonstrate
decreasedmaxillomandibular opening comparedwith their preoperative state.The most
dra-matic decreases are seen after bilateral sagit-tal split
osteotomies.62Temporomandibularmobility must be restored by
postoperativephysiotherapy.Ellis examined the range ofmandibular motion after a
sagittaladvancement osteotomy in monkeys,wheneither IMF or rigid osseous fixation
wasused.66Animals that did not undergo IMFmaintained a greater range ofmotion in
theearly postsurgical period and obtained pre-operative mobility by 12 weeks
postopera-tively.Animals that underwent 6 weeks ofIMF showed significant decreases
in rangeofmotion when compared to the rigid fix-ation group at each time period
post-surgery.Several clinical studies have shownthat whether IMF or rigid fixation
is used,with postoperative physiotherapy,a normalor near-normal range ofmotion will
returnby 2 years after surgery.61,67There are several potential causes
ofhypomobility in patients undergoingorthognathic surgery.Scar tissue inducedby the
surgery plays a major role.However,immobilization can compound the
effectsofsurgical dissection and have adverseeffects on the muscles,joints,and
connec-tive tissues.Immobilization by itselfinduces atrophy with a marked decrease
inmuscle fiber diameter.This problem maybe compounded ifthe muscle is immobi-lized
in a shortened position.In addition,following IMF,a series ofdegenerativechanges
occur in articular cartilage andsynovial membranes.Techniques that eliminate or
min-imize immobilization will probablydecrease postsurgical hypomobility.Despite
this it is strongly suggested that allpatients have routine presurgical evalua-tion
ofmuscle and joint function and asystematic rehabilitation regimen as partoftheir
postsurgical program.Mandibularramal procedures are potentially the mostharmful to
the surrounding tissue ofthejaws.Mandibular advancements,in partic-ular,are
susceptible to postoperativehypomobility.Ifrigid fixation is used,mild self-
directed physiotherapy begin-ning 1 to 2 weeks after surgery may suffice,consisting
ofinstructions on active andpassive exercises.When a patient�sprogress is limited
or when surgery hasbeen associated with longer periods ofIMF,then more vigorous
physical therapyis needed.Ifthis is unsuccessful,intra-articular pathology may be
responsible forthe problem and additional steps mayneed to be taken to restore a
normal rangeofmotion.68Temporomandibular Joint DysfunctionShort-Term DisordersJoint
dysfunction in patients undergoingorthognathic surgery deserves careful pre-
operative examination.A number ofpatients presenting for orthognathic sur-gery will
have muscular temporo-mandibular dysfunction.69�71Although asmall percentage
ofpatients will developFIGURE60-20Pull ofthe muscles ofmastica-tion on the proximal
and distal segments.Adapt-ed from Van Sickels JE,Tucker MR.Preventionand management
ofcomplications in ortho-gnathic surgery.In: Peterson LJ,Indresano AT,Marciani
RD,Roser SM.Principles oforal andmaxillofacial surgery.Vol.3.Philadelphia (PA):JB
Lippincott Company; 1992.p.1481.FIGURE60-21Radiograph ofshort ramus.FIGURE60-
22Occlusal discrepancy.
Prevention and Management ofComplications in Orthognathic Surgery1261symptoms with
surgery,the large majori-ty will improve.Achieving a better func-tional
relationship can help temporo-mandibular symptoms,but orthognathicsurgery should
not be offered as a cure forthese problems.After surgery patientsmay have acute or
gradual increases intemporomandibular symptoms.Acuteexacerbations may be treated
with anti-inflammatory medications and physicaltherapy.Gradual increases or
chronicmanifestations oftemporomandibularproblems are managed with standard pro-
tocols for these patients.Concern existsthat with rigid fixation there will be
ahigher incidence oftemporomandibulardysfunction compared with the use ofwire
osteosynthesis.Studies that havecompared these two populations have notborne out
these assumptions.67,70Long-Term DisordersCondylar resorption has been noted
withand without orthognathic surgery.Thecause ofdelayed relapse may be secondaryto
a number offactors including preexist-ing internal derangements.The role
thatsurgery may play in these unusual cases isunknown.The incidence
ofcondylarresorption or progressive condylar resorp-tion ranges from 5 to 10% ofthe
patientswho undergo orthognathic surgery.72�77Patients who need large advancement
ofthe mandible and who have preoperativetemporomandibular symptoms are morelikely
to have this problem than those whohave smaller advancements and no symp-
toms.72,74Condylar resorption has beennoted 12 to 17 months after
surgery.76Management includes splint therapy,witha possible role for
medications.76,77Sec-ondary surgery is unpredictable,withadditional resorption
possible in as manyas 50% ofcases.76 Unanticipated Maxillary FracturesWhereas
several reports have discussedmanagement ofadditional fragments withmandibular
osteotomies,little attentionhas been directed to maxillary surgery.With modified
cuts ofthe maxilla,thebone leading to the zygomatic buttress(wing) may be thin and
fractured (Figure60-23).Management can be accomplishedby using a plate to span the
gap and thenre-inserting the fragment (Figure 60-24).Over- or underimpaction ofthe
max-illa can occur at the time ofsurgery.Thiscan be avoided with an external
reference.One choice is to place a pin at nasion at thebeginning
ofsurgery.Intraoperative mea-surements will ensure that the maxilla is atthe
appropriate position at the end ofsurgery.78When the maxilla is underimpacted,very
few options exist.Plates,ifpresent,may be removed and an attemptmade to impact the
maxilla with suspen-sion wires in an outpatient environment.However,it is unlikely
that this procedurewill achieve the desired results.When themaxilla is
overimpacted,it can rarely besuccessfully treated by multiple verticalelastics used
in the early postoperativeperiod.Ifunsuccessful,then a reoperationshould be
considered.Postoperative Occlusal DiscrepanciesOcclusal abnormalities may be
related to anumber offactors either in the preopera-tive,intraoperative,or
postoperative phaseofpatient management.A review ofcasesofmaxillary surgery
suggests that themajority ofdiscrepancies between whatwas desired and what was
obtained can betraced to inaccurate preoperative records.79Open BitesSurgical
Causes Anterior open bites after surgery may bedue to the technical difficulties
seen withboth the maxilla and mandible at the timeofsurgery.With the maxilla these
includeposterior interferences that are not recog-nized when the patient is in
IMF.Ifthemaxilla is fixed with condyles that are dis-located out ofthe glenoid
fossa,when theFIGURE60-23�Wing�ofthe maxilla fractured off.Adapted from Van Sickels
JE,Tucker MR.Preven-tion and management ofcomplications in orthog-nathic
surgery.In: Peterson LJ,Indresano AT,Mar-ciani RD,Roser SM.Principles oforal
andmaxillofacial surgery.Vol.3.Philadelphia (PA): JBLippincott Company;
1992.p.1483.FIGURE60-24Plate spans the gap; bone segmentlies under the
plate.Adapted from Van Sickels JE,Tucker MR.Prevention and management ofcom-
plications in orthognathic surgery.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM.Principlesoforal and maxillofacial surgery.Vol.3.Philadel-phia (PA): JB
Lippincott Company; 1992.p.1483.
1262Part 8: Orthognathic Surgerypatient is taken out offixation,the
occlusaldiscrepancy is usually recognized.Occa-sionally,however,it is not
recognized untilthe next day.Depending on the severity ofan open bite,the patient
may have to betaken back to the operating room.Open bites that occur after
orthodon-tic appliances have been removed may bedue to relapse ofsurgically or
orthodonti-cally treated transverse discrepancies.Sur-gical and orthodontic
correction ofseveretransverse discrepancies have been notedto be unstable.80When
relapse ofthetransverse discrepancy occurs,it is usuallymanifested by an anterior
open bite.Man-agement oflate discrepancy will dependon its severity.Dental or
Orthopedic CausesOpen bites have been noted to recur yearsafter treatment with both
orthodonticsand surgery.80,81Stability oforthodontictherapy varies depending on the
ortho-dontic techniques used to treat an openbite.82Rotation ofincisors that are
flaredwith closure ofan open bite may be nomore problematic than for other
toothmovements.When extrusion ofteeth hasoccurred with orthodontic
mechanics,theresults are less predictable.Why thisoccurs is somewhat
controversial.Extru-sion may have increased sensitivity toexternal factors,such as
the tongue andcircumoral musculature.Lack ofstabilityor recurrence ofthe open bite
is thereforefelt to be secondary to the continued pres-ence ofetiologic factors and
failure ofbio-logic adaptation.Measures taken to cor-rect these problems may
includeorthodontic cribs or surgical techniquessuch as partial
glossectomies.Relapse ofthe MandibleRelapse ofthe mandible following a bilat-eral
sagittal split has been well document-ed in the literature,especially with
largeradvancements.83�86However,occlusal dis-crepancies can occur secondary to
severalreasons.Many ofthese occlusal discrepan-cies can be traced to the technical
aspectsofrigid fixation.Occlusal changes seenwith rigid fixation may be secondary
tocondylar torque,condylar sag,or incorrectplacement ofthe fragments at the time
ofsurgery.This may result in anterior or pos-terior open bites or lateral
shifts.Severediscrepancies may need to have a secondoperation.Minor discrepancies
can betreated by early aggressive orthodontics.Posterior open bites ofless than 3
mm canbe treated with vertical elastics or ortho-dontic mechanics.Larger posterior
openbites may have to be reoperated,withremoval ofthe screws and replacementwith
either screws or wires.Anterior openbites represent failure to properly place
thecondyle or instability at the osteotomy site.IMF with anterior elastic traction
mayprevent reoperation when the cause isinstability at the osteotomy site.The
preferred time to initiate therapyis as soon after surgery as the discrepancyis
noted.Removal ofthe screws or plates inan outpatient environment at 3 weeks,coupled
with elastic therapy,can some-times correct some postoperative maloc-
clusions.Failure to place the condyle in thefossa,either unilaterally or
bilaterally,needs evaluation as to whether orthodon-tic therapy can correct the
problem or ifthe surgery needs to be repeated.A lateralshift ofthe occlusion where
the midline isoffto one side is usually due to condylartorque at the time
ofsurgery.When plac-ing a clamp between the proximal and dis-tal segments,the
proximal segment shouldbe observed for shifts or torque ofthe seg-ment.Ifseen the
fragments may need to becontoured or the clamp repositioned.After surgery a shift
in the midlines sec-ondary to torque ofthe segments may betreated by orthodontics
or by reoperation.Small shifts of1 mm or less can be man-aged by orthodontic
mechanics.Largerones may need a second surgery.Relapse ofa skeletal Class III
occlusalcondition upon release ofIMF has beennoted.87�89Several authors believe
this canbe caused by pushing the proximal frag-ment back during surgery.With the
releaseofIMF the mandible rotates forward.Toprevent this problem it has been
suggestedthat the inferior border ofthe proximaland distal segments be aligned and
thatthe medial sling be released.88Others dis-agree and feel that clockwise
rotation ofthe proximal segment is not responsiblefor the
relapse.89Additionally,the use ofamonocortical plate on the proximal seg-ment may
provide a more stable resultthan that seen with bicortical screws (Fig-ure 60-
25).When this occlusal discrepan-cy is seen after surgery,short class III elas-tics
can correct the problem ifit is small.Ifthe discrepancy is greater than 3 to 4 mm,a
second operation is necessary.Anterior Open BiteAs discussed above,an anterior open
bitemay be seen after a bilateral sagittal splitosteotomy (Figure 60-26).This is
usuallydue to a failure ofthe screws and/or platesplaced at the time offixation,or
technicaldifficulties incurred at the time ofsplittingthe segments with resulting
edema in thejoints which resolves with time.However,an anterior open bite is much
more com-monly seen in patients following an intra-oral vertical ramus osteotomy
uponFIGURE60-25Monocortical plate on the buccalsurface ofthe proximal and distal
segments.
Prevention and Management ofComplications in Orthognathic Surgery1263release
ofIMF.90,91Suggestions to preventthis problem from occurring includeremoving the
coronoid process,placingskeletal wires,or using modified cuts ofthe ramus and 8
weeks ofIMF.91Postoper-ative elastics have been used for 2 to 6 weeks when open
bites have been noted.Miscellaneous OccurrencesEndotracheal tubes have occasionally
beencut during maxillary surgery.In someinstances patients needed to be reintubat-
ed;in others packing around the endotra-cheal tube is sufficient.Alar rim injuries
are due to pressureon the rim from the nasotracheal tube.Care should be taken when
wrapping thehead so that there is no pressure on the tipofthe nose or the forehead
or ears.Emphysema in the cervical and facialregions has been noted after a variety
ofprocedures that are unrelated to orthog-nathic surgery.However,there are
severalreports ofair in the soft tissues ofthehead,neck,and chest following Le Fort
Iosteotomies.92Subcutaneous emphysemaofthe cheeks is probably due to
forcefulblowing ofthe nose,which allows air intothe surrounding tissues through the
max-illary sinus.Forceful coughing can allowair to pass into the retropharyngeal
spaceand into the mediastinum.Alternatively,rupture ofa perivascular bleb or
traumat-ic introduction ofair through the cervicalfascia is possible.Subcutaneous
emphyse-ma can be managed by observation,heat,and antibiotics.Therapy for pneumo-
mediastinum consists ofclose observa-tion,cardiac monitoring,intravenous flu-
ids,and antibiotics.Chest tubes ordrainage ofthe mediastinum may
benecessary.Supplemental oxygen as well aspulmonary physiotherapy should be
used.EpiphoraEpiphora may be seen following a maxil-lary osteotomy and is
frequently due toswelling ofthe nasal mucosa.Alternatively,the nasolacrimal duct
may be injuredwhen a concomitant turbinectomy is per-formed with an osteotomy.This
is espe-cially true ifthe bone cut along the medialwall ofthe sinus is high.Such
tearing isinfrequent and transient.Careful dissec-tion and osteotomies around the
medialaspect ofthe piriform aperture maydecrease the incidence ofthis finding.Per-
sistent tearing that does not decrease after3 weeks may need to be addressed by
adacryocystorhinostomy.Auriculotemporal SyndromeThe auriculotemporal
syndrome,gustatorysweating,or Frey�s syndrome is an unusualcomplication mainly
ofparotid surgery.After an injury to the auriculotemporalnerve,the symptoms are
believed to becaused by a misdirected regeneration ofparasympathetic fibers to
denervated sweatglands.A number ofauthors have reportedit occurring after extraoral
vertical ramusosteotomies and bilateral sagittal
splitosteotomies.93�96Patients�symptomsoccurred 3 months to 3 years after
surgery.Mild cases in which the patient mayonly have symptoms with spicy
foodsshould be observed,because the symptomsmay decrease with time.A variety
oftreat-ments have been suggested for more severesymptoms,including topical
scopolamineand insertion offascia lata or acellularhuman dermis matrix under the
skin.97Topical scopolamine has a series ofundesir-able side effects.Recently there
have beenreports ofthe use ofbotulinum toxin as asuccessful treatment for this
problem.98,99Facial ScarsAlthough attempts are made to camou-flage extraoral site
incisions,unattractivefacial scarring occasionally occurs.Egyediand colleagues
noted 6 undesirable scarsin a group of100 patients with extraoralincisions.100The
criteria they used todetermine what was attractive or unattrac-tive are
unknown.Percutaneous incisionsof2 to 4 mm seldom leave significantscars.More
problematic is when the skinsticks to the underlying muscles.Scar revi-sions are
usually able to improve on anexisting scar.Intraoral management withthe right
instruments may obviate theneed for most skin incisions.Salivary InjuriesInjuries
to the parotid gland can occurwith extraoral procedures.Painlessswelling,parotid
sialoceles,and fistulashave been seen in the first week aftersurgery.101The
treatment ofsialoceles orsalivary fistulas may include antisialo-gogues,pressure
dressings,and aspira-tion from a nondependent point.Sialog-raphy is not recommended
in the acutephases ofthese injuries,because it mayFIGURE60-26Open bite following a
bilateralsagittal split.A,At 24 hours.B,After 1 week.AB
1264Part 8: Orthognathic Surgerycreate a fistula or increase its size.Reso-lution
ofa sialocele should be seen with-in 1 month with nonsurgical therapies.Failure
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1266Part 8: Orthognathic SurgeryRigid versus wire fixation for
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CHAPTER 61Orthognathic Surgery in thePatient with Cleft PalateTimothy
A.Turvey,DDSRamon L.Ruiz,DMD,MDKatherine W.L.Vig,BDS,MS,D OrthBernard
J.Costello,DMD,MDThe estimated incidence oforofacial cleftsinvolving the lip and
palate in the UnitedStates is approximately 1 to 2 per 1,000births or approximately
1 in 700 live births.1The average cost ofrehabilitation ofa childborn with an oral
cleft is estimated atapproximately $100,000 (US).The occur-rence rate ofinfants
born with a cleft lipand/or palate is influenced by race and gen-der,and the cost
varies by the number ofprocedures and interventions performed.Care for an infant
born with an orofa-cial cleft begins with primary surgicalrepair ofthe lip followed
by the palate andcontinues in defined and appropriatestages to late adolescence,at
which pointpublic funding is usually discontinued.The burden ofcare assumed by the
patientand family in the indirect costs oftime offfrom work/school and
transportation bythe caregiver is not to be underestimated,and it is often
inadequately equated withthe financial or direct costs oftreatment.The
interdisciplinary approach to themanagement ofpatients with a cleft lipand/or
palate and other craniofacialanomalies requires careful coordinationand
communication;a cleft palate teamestablishes a patient-centered approachthat
follows critical pathways.2�5The tim-ing and sequencing ofcare is criticalbecause
ofthe interaction offacial growthwith the development ofthe dentition.Clefts ofthe
maxilla,especially the unilat-eral cleft lip and palate,are associated witha
skeletal maxillary deficiency in the trans-verse,anteroposterior,and vertical
dimen-sions.The dysmorphology in all threedimensions has been attributed to scar
tis-sue following the primary repair ofthe lipduring the first 6 months oflife and
thepalatal repair,which is performed typical-ly at 12 to 18 months.Clefts ofthe
maxil-la,both unilateral and bilateral,have beenconsidered to have an intrinsic
growthdeficiency ofskeletal,soft tissue,and den-tal components.However,in those
chil-dren who have unrepaired clefts early inchildhood,relatively normal occlusal
rela-tionships are established compared withthose relationships in children who
aresurgically repaired in the first 2 years oflife.This latter group is
characterized byanterior and posterior dental crossbites,midface sagittal
deficiency,and associatedvertical overclosure.6Because the cleftinvolves the
dentoalveolus and occursowing to the lack offusion ofthe primarypalate during
embryogenesis,the dentallamina may also be involved,with conse-quences ofextra
teeth such as supernu-merary teeth,malformed and misplacedteeth,or an absence
ofteeth in the cleftsite.Normal biologic variation is the resultofphenotypic
variation,which allows oneindividual to be distinguished from anoth-er by facial
appearance.Therefore,dentalmalocclusions may occur on all skeletalpatterns,but in
the population with a cleftlip and palate,the pathogenesis ofcleftingis
superimposed on the individuals�inher-ited facial pattern.Additionally,facialclefts
are associated with over 300 syn-dromic conditions,7,8so a patient mayhave
syndromic or nonsyndromic facialcleft;this distinction and diagnosis is con-firmed
by the geneticist on the team.Asymmetry is a typical facial charac-teristic and is
one ofthe stigmas associat-ed with unilateral orofacial clefts.Cleftpatients
typically express concerns abouttheir facial appearance,but they alsohave problems
with communicationbecause their speech is affected.This ispartially because the
velopharyngealmechanism is inadequate to close offthe oropharynx from the
nasopharynx,
1268Part 8: Orthognathic Surgeryresulting in hypernasality and a lack
ofintelligibility ofthe phonetic components.The severity ofthe skeletal aspect
ofthe malocclusion and facial asymmetrydetermines the
surgical/orthodonticapproach.Mild discrepancies may be cam-ouflaged by the
orthodontic dentoalveolarcompensation.However,during adoles-cence the compensation
for the skeletaldiscrepancy may be outgrown;orthog-nathic surgery is the treatment
ofchoicefor patients in their late teens.Becausegrowth prediction is not an exact
science,an anterior crossbite corrected in themixed dentition frequently
reestablishesfollowing the pubertal growth spurt andadolescent growth.The purpose
ofthis chapter is to dis-cuss the surgical and orthodontic correc-tion ofthe cleft
in dysmorphic faces.Thefocus is on patients with cleft lip andpalate who would
benefit from bone graftsin the early mixed dentition,and maxillaryadvancement with
contour bone graftingin adolescence when growth ofthe naso-maxillary complex has
stabilized.The suc-cessful correction ofthese secondaryskeletal deformities
frequently requirestreatment protocols that include orthog-nathic surgery in
conjunction with thefinal phase oforthodontic treatment.Patients with a cleft lip
and palate benefitfrom staged and coordinated proceduresto achieve optimal
results.These includebone-graft construction ofthe cleft maxil-la and palate in the
mixed dentition phaseofdevelopment,and orthognathic surgeryto correct the midface
deficiency in ado-lescence.These procedures are designed tobe only stages in the
process ofreconstruc-tion and rehabilitation.Timing and Sequencing ofBone Grafting
the Cleft Maxillaand PalateAn understanding ofcraniofacial growthand development is
critical in timing bothsurgical and orthodontic interventions.Inbone
grafting,dental development is moreimportant than is the chronologic age ofthe
patient.The decision for determiningorthodontic expansion to detect the
dentalcrossbite,as a presurgical phase ofortho-dontics,depends on the root
developmentofthe unerupted canine.Ifthe lateralincisor is developing on the
posterior sideofthe cleft,a bone graft needs to be per-formed early to allow
eruption to the cleftsite.Seminal papers defined the age forsecondary alveolar bone
grafting,which isnow a well-accepted procedure after pri-mary lip and palate
repair.9,10They divid-ed the timing into early,2 to 5 years ofage;intermediate,6 to
15 years ofage;and late,16 years to adult.A retrospective interdis-ciplinary study
reported the outcome ofbone grafts to the cleft maxilla relative toradiographic and
periodontal parameters;as well,it stated that the closure offistulasand the
eruption ofthe canine through thebone-graft site suggested high success inage-
appropriate patients.11A longitudinalretrospective study provided evidence forthe
timing and sequencing ofthe surgicaland orthodontic treatment,using cancel-lous
bone harvested from the iliac crestand the stage ofdevelopment oftheunerupted
canine,typically between 9 and11 years ofage.12Contemporary opinionconsiders this
intermediate time frame tohave the greatest benefits and the least riskin
compromising midface skeletal anddental growth and development.Benefits ofbone
grafting include thefollowing:�Bone is provided into which theunerupted teeth
adjacent to the cleftmay erupt or be moved orthodontical-ly.The timing and
sequencing ofthebone graft is determined by the posi-tion ofthe teeth adjacent to
the cleft,their root development,and theirstage oferuption,rather than
thechronologic age ofthe patient.�Supernumerary or malformed teethmay be removed at
the time ofthesurgical placement ofthe bone graftinto the cleft site.Patent
oronasal fis-tulas either in the palate or thenasolabial vestibule are
closed.Fistulaclosure is achieved by using a three-layered closure technique with
thegrafted bone sandwiched between thetwo soft tissue planes.�The grafted bone
provides supportand elevation ofthe alar base in thedefect and improves nasal and
lipsymmetry.�Because there is continuity ofthemaxilla,the restorative dentist has
theopportunity to provide a more esthet-ic and hygienic prosthetic replace-
ment,even ifteeth are missing.Theplacement ofimplants into bonegrafts is successful
and is a contempo-rary alternative to a bridge or remov-able appliance.�In repaired
bilateral clefts ofthe lipand palate,the placement ofbonegrafts bilaterally in the
cleft sites stabi-lizes the premaxilla while providingbone into which the adjacent
unerupt-ed teeth may erupt.Through efforts to determine the optimaltiming
oftreatment,several controversieshave arisen related to the age ofthepatient,the
type ofbone graft,the sitefrom which the graft is harvested,and theoptimal timing
oforthodontic expansionofthe maxilla in relation to the surgicalplacement ofthe
bone graft.12The surgical technique for bone graft-ing the cleft maxilla and palate
involves athree-layered closure with autogenouscancellous bone graft sandwiched
betweenthe nasal floor and the oral mucosa.Anincision is made around the cleft to
pre-serve the fixed gingiva to circumscribe thefistula (Figure 61-1).The tissue is
then ele-vated from the bone on both sides ofthecleft in the subperiosteal plane to
the levelofthe anterior nasal spine and the lateralpiriform rim.The tissue is
elevated,invert-ed,and sutured to form a reconstructednasal floor (Figure 61-
2).Fresh cancellous
Orthognathic Surgery in the Patient with Cleft Palate1269bone is then condensed in
the cleft defectand over the hypoplastic bone edges ofthecleft (Figure 61-3).Oral
tissue is eitherrotated or advanced to close over the bonegrafts (Figures 61-4�61-
6).Timing ofMidface AdvancementSurgery in AdolescentsBiologic and psychosocial
concerns governthe decision for the timing ofsurgicalmaxillary advancement.It is
always pru-dent to delay surgery ofthe nasomaxillarycomplex until growth has
stabilized andthe peak velocity ofsomatic growth haspassed.This improves the
predictabilityand long-term stability oftreatment andreduces the risk that
surgical-orthodonticcorrection will be outgrown.The optimaltime for surgical
correction ofthe skeletaldiscrepancy is when the patient is physi-cally and
psychologically prepared.Patients need to appreciate the relevanceoffacial growth
and development and theconsequences ifsurgical correction isundertaken prior to
maturation.Anotherbiologic consideration regarding the tim-ing ofsurgery is the
eruption ofthe per-manent dentition.Delaying surgery untilthe canine and second
molars have erupt-ed minimizes the risk ofendodonticrequirements and displacement
ofthe sec-ond molars.Third molars can usually beremoved at the time ofmaxillary
surgery,and their presence should not be a majorconcern.Patients,parents,and
treatingdoctors participate in the decision regard-ing when to proceed with
surgery;theapproach should be patient centered andevidence based with regard to the
risks,costs,and benefits.Patient autonomy inthe decision should be given the
highestpriority in orthognathic surgery.Thisrequires that patients be in late
adoles-cence to understand the consequences ofthe decision and be able to
rationalize theexpectations for the outcome.Adolescents are under enormouspressures
to conform to their peers.At noother time in life is an individual exposedto
concerns about their self-image andphysical attractiveness with such addi-tional
pressure ofpeer criticism ofappearance differences.Many adolescentpatients with
clefts are subjected toridicule about their facial appearance,andthis is
accompanied by low self-esteemand impaired socialization.Social with-drawal is
another issue resulting from thepressures felt by adolescents,especiallythose with
facial disfigurement.Althoughcounseling can help,the patient must stillFIGURE61-
1Outline ofthe incision to pre-pare the cleft site for bone grafting.The
fixedgingival tissues are preserved and suturedback.Adapted from Turvey TA,Vig
KWL,Fonseca RJ.Surgical management.In:Facial clefts and craniosynostosis:
principlesand management.Philadelphia (PA): W.B.Saunders Company;
1996.p.412.FIGURE61-2A,The tissues lining the cleft are elevated to the nasal
cavity to construct a floor.B,Closure ofthe nasal lining is accomplished with a
horizontal mattress suture to evert theedges toward the nasal side.Adapted from
Turvey TA,Vig KWL,Fonseca RJ.Surgical man-agement.In: Facial clefts and
craniosynostosis: principles and management.Philadelphia(PA): W.B.Saunders Company;
1996.p.413.FIGURE61-3Cancellous bone particles packed intothe defect must extend
from the nasal rim to the alve-olar crest.Adapted from Turvey TA,Vig KWL,Fon-seca
RJ.Surgical management.In: Facial clefts andcraniosynostosis: principles and
management.Philadelphia: W.B.Saunders Company; 1996.p.415.AB
1270Part 8: Orthognathic Surgerycope with the disfigurement;however,thismay be
improved with surgery.Improving facial appearance byaddressing the skeletal
disproportion oftenresults in dramatic and complementarychanges.Patients typically
perceive thesechanges positively�the changes send aclear message that someone cares
aboutthem and is sensitive to their concerns.Animprovement in self-concept and
image inpatients with a cleft lip and/or palate usu-ally follows surgical
correction ofthe mid-face deficiency and skeletal disproportion.Patients�perception
oftheir quality oflifeis an important consideration and shouldnot be overlooked in
the timing ofsurgery.However,care should be taken in the psy-chosocial assessment
to identify unrealis-tic expectations and to recognize thosepatients who use the
stigmas as an excusefor dependency.Identification oftheseindividuals prior to
surgery is not easy;interdisciplinary management shouldinclude the involvement ofa
psychologiston the cleft palate team.The decision to proceed with surgeryprior to
maturation may result in addi-tional surgery being needed once growth
iscomplete.This need is tempered by thereduced morbidity ofrepeat surgeries
incontemporary settings.The postoperativecourse for facial skeletal surgery
hasbecome more comfortable and convenientfor the patient since the
technologicadvancements ofbone plates and screwshave essentially replaced the need
forintermaxillary fixation.The contemporaryuse ofsteroids and antibiotics has con-
trolled swelling and infection,and alterna-tives to homologous blood
transfusion(autologous blood banking and the use ofrecombinant erythropoietin) are
effective-ly employed.Impatient surgeons or ortho-dontists should not rationalize
early skele-tal surgery prior to maturation for theirown convenience.Final
decisions regard-ing the timing ofsurgery should recognizethe wishes ofpatients and
parents,and theorthodontists and surgeons should pro-vide the information needed to
make aninformed decision.Presurgical CounselingPatients born with a congenital
facial mal-formation are psychologically differentfrom those patients with acquired
dento-facial deformities,who tend to be moreprone to neuroticism.13Patients with a
clefthave had their problem since birth andhave adapted to multiple changes
fromtheir previous surgical procedures.Manypatients with orofacial clefts have
experi-enced the disappointment ofprevious FIGURE61-4A buccal mucosal flap is
elevated,maintaining a wide and thick anterior base.Theflap is then rotated to
cover the defect.Adaptedfrom Turvey TA,Vig KWL,Fonseca RJ.Surgicalmanagement.In:
Facial clefts and craniosynostosis:principles and management.Philadelphia
(PA):W.B.Saunders Company; 1996.p.417.FIGURE61-5A,The rotated flap is de-
epithelialized in the areas where the fixed flaps will lie.B,Thefixed gingiva is
then secured to the flap and around the margins ofthe teeth.Adapted from
TurveyTA,Vig KWL,Fonseca RJ.Surgical management.In: Facial clefts and
craniosynostosis: principlesand management.Philadelphia (PA): W.B.Saunders Company;
1996.p.417.ABFIGURE61-6A sliding buccal gingival flap iselevated from around the
teeth andadvanced forward,leaving the posteriordefect to granulate.Adapted from
TurveyTA,Vig KWL,Fonseca RJ.Surgical manage-ment.In: Facial clefts and
craniosynostosis:principles and management.Philadelphia(PA): W.B.Saunders Company;
1996.p.419.
Orthognathic Surgery in the Patient with Cleft Palate1271surgical soft tissue
revisions that wereexpected to erase the scar on the lip andcorrect the nasal
asymmetry.However,unrealistic expectations ofskeletal surgeryshould be identified
before the surgicalintervention,and the patient should bereferred for
counseling.Skeletal surgery does not erase the lipscar,but it does provide an
opportunity toimprove the skeletal support for the soft tis-sue drape.It can help
improve the symme-try ofthe lip and nasal base and also sup-port the nasal
tip.Skeletal support mayreduce the stigmas ofmidface deficiencyassociated with the
cleft defect so that softtissue revisions may not be needed ordesired.The scar
commonly falls on a flatunsupported position ofthe lip andbecomes
obvious.Often,appropriate skele-tal support moves the scar to an area ofgreater
curvature,which reflects light dif-ferently and results in a less
conspicuousscar.Therefore,patients should be coun-seled that the skeletal surgery
sets the stagefor future definitive lip and nasal revisions.Orthognathic Surgery
for theCleft PatientIn contemporary cleft team settings,mostpatients with clefts
ofthe maxilla undergobone grafting at a developmentally appro-priated time in the
mixed dentition stage.When midface advancement surgery isplanned later in
adolescence,it is a relative-ly straightforward procedure.For thosepatients who
have not benefited from pre-vious bone grafts,the situation is morecomplex.In both
circumstances the gener-al principles offlap design for
maxillaryadvancement,ensuring adequate perfusionto the mobilized maxilla,are
ofparamountimportance.A cleft maxilla differs becauseofthe absence oftissues,and
multiple sur-gical procedures are needed to repair andclose defects.Perfusion ofthe
mobilizedmaxilla is dependent on vessels comingfrom the overlying soft
tissues,predomi-nantly the palatal tissues.In cleft patientsthis tissue is commonly
scarred and fibrot-ic;therefore,care must be exercised whendesigning the incision
to perform theosteotomy.With few exceptions,almost allpatients can be treated with
a Le Fort Iosteotomy via the circumvestibular inci-sion and a down-fracture
approach.Forthose with severe palatal scarring,whohave previously undergone an
islandpalatal repair,and those with bilateral cleftsofthe maxilla,an anterior
buccal pedicleshould be left on the mobilized maxilla tomaintain adequate
perfusion.Technically,this is a more challenging operation.The circumvestibular
incision is madefrom the zygomaticomaxillary buttress tothe opposite side,high in
the mucobuccalfold (Figure 61-7).Subperiosteal dissec-tion exposes the entire
lateral wall ofthemaxilla from the nose to the pterygoidplate and from the
alveolus,above theroots ofthe teeth,to the inferior orbitalrim.The broad exposure
permits excellentvisualization ofall osteotomies.At thetime ofmobilization,this
incision permitsthe maxilla to be down-fractured andentirely pedicled to the
palatal tissues andthe remaining buccal tissues below theincision.Good
visualization and ease ofmobilization are the major advantages ofthis
approach.Hemorrhage control is per-formed with direct visualization,usuallyby the
ligation ofvessels.When an anterior buccal pedicleremains,the operation is
technically moredifficult (Figure 61-8).Visualization isreduced,and mobilization by
down-fracturing is not possible.Mobilization ofthe midface is achieved by in-
fracturing,combined with anterior traction.For mostpatients with a cleft palate,the
area ofgreatest resistance to mobilization ofthemaxilla is the vertical portion
ofthe pala-tine bone,located in the posteromedialaspect ofthe maxillary sinus.The
bone isthick and access is limited,especially whendown-fracturing is not
possible.Com-pounding this is the presence ofthegreater palatine vessels,which
descendfrom the sphenopalatine fossa to the pos-terior maxilla (Figure 61-9).The
vessels,which run through the canal in this bone,are prone to rupture during
mobilization.Hemorrhage control is limited�packingand the use ofa vasoconstrictor
(epineph-rine 1:100,000) are usually effective.The surgical technique employed
forboth ofthese approaches has been describedin detail previously,and interested
readersare referred to more detailed sources.14Residual oronasal fistulas are
commonin patients whose maxillas have not beenbone grafted previously.An
incisiondesign should permit simultaneous clo-sure oforonasal fistulas.Ofkey impor-
tance is the construction ofa nasal floor,which is created by using the tissues
liningthe fistulas (Figures 61-10�61-12).FIGURE61-7A circumvestibular incision
isused when a Le Fort I down-fracture is per-formed.The incision is made high on
thezygomaticomaxillary buttress to ensure ade-quate perfusion to the anterior
maxilla.Note that the attached gingiva around theteeth on both sides ofthe cleft is
reflected andpreserved.The remaining tissue lining thecleft walls is later incised
and reflectedpalatally or buccally,depending on where itis needed for closure (see
Figure 61-11B).Adapted from Turvey TA et al.15
1272Part 8: Orthognathic SurgeryCreativity and care are the importantelements in
surgery to correct midface defi-ciency in patients with clefts.Since theskeleton is
always asymmetric in cleftpatients,it is crucial that the osteotomy isdesigned for
maximum improvement ofesthetics (Figure 61-13).Ifan adequateimprovement cannot be
obtained by anosteotomy alone,onlay bone grafting toenhance skeletal support and
shape shouldbe considered.Sometimes even subtle dif-ferences between osteotomy
designs on thecleft side reflect positive soft tissue changes.Adequate mobilization
is a key factorfor success when performing midfaceosteotomies in the presence ofa
cleft.Thescarring and thickness ofbone (particularlyin the vertical part ofthe
palatine bone) aretwo major obstacles.The posteromedialaspect ofthe maxillary sinus
is unusuallythick in cleft patients,and it must be cut orfractured to permit
adequate mobilization.This is usually accomplished with a smallosteotomy tapped
along the lateral nasalwalls (see Figure 61-9).Failure to weakenthese structures
prior to mobilization mayresult in an unfavorable fracture extendingto the skull
base or orbit.Blindness has beenreported following Le Fort I osteotomies incleft
patients,and an inadvertent fracture inthis area is the suspected
cause.15Ifexcessiveforces are required to mobilize the maxilla,repeated use ofthe
osteotomy to furtherweaken the structure is advisable prior tobeginning
mobilization.It is often tempting to segment themaxilla ofpatients with a cleft to
improveocclusal relationships.However,segment-ing the maxilla in this population
shouldbe undertaken with caution,consideringthe compromised vascularity and
scarringofthe tissues.Accepting posterior cross-bites and other occlusal
compromises maybe judicious,rather than risking necrosisofa segmental osteotomy.A
contempo-rary goal ofcleft care is to eliminate and/orreduce the need for
prosthetic manage-ment.Closing dental spaces with segmen-tal osteotomies is an
effective way toachieve this goal.Additionally,thismaneuver results in more soft
tissue avail-ability to create an intact nasal lining.Although opening the space
with segmen-tal osteotomies is possible,it requires bonegrafts and a rotation
ofsoft tissues to closethe defects.Except in extreme salvage cir-cumstances,dental
space opening shouldbe avoided (Figures 61-14 and 61-15).Bone Grafting with
Maxillary AdvancementThere are three important reasons to usebone grafts in
patients with a cleft whenperforming midface advancement.First,Pharyngeal
portFIGURE61-8A andB,A catheter passed nasally through the velopharyngeal ports
serves to guidethe nasoendotracheal tube past the pharyngeal flap.Adapted from
Turvey TA et al.15ABGreater palatineneurovascular bundleFIGURE61-9A small osteotome
is tappedthrough the lateral nasal wall posteriorlytoward the perpendicular part
ofthe palatalbone.At this point the resistance increasesbecause this part ofthe
lateral nasal wallthickens.The greater palatine neurovascularbundle descends
through this region and isat risk.Adapted from Turvey TA et al.15FIGURE61-10The
mucosa lining the cleftalveolar region is elevated from the nasalside and pushed
orally,where it is sutured onboth the palatal and buccal sides.The boneedges ofthe
cleft must be adequately exposedfor successful reconstruction.The nasalmucosa is
also closed primarily.Adaptedfrom Turvey TA et al.15
Orthognathic Surgery in the Patient with Cleft Palate1273the bone graft can be
wedged into thedefects in the lateral maxillary walls;thishelps to maintain the
position ofthe max-illa during healing.Second,the bone graftalso encourages bone
healing and reducesthe risks offibrous union.The third rea-son to use bone grafts
in midface advance-ment is to contour the middle face.Inpatients with a cleft,the
midface is not justretruded,it is also malformed.Thus,alter-ing the skeletal
morphology is importantfor esthetic enhancement.Augmentationofthe cheek
projection,infraorbitalregions,paranasal regions,nasal bridge,orchin is commonly
employed at the time ofmidface advancement.These maneuversare helpful and easily
performed at thetime ofsurgery,and their importanceshould not be underestimated.The
choice ofbone-graft material foruse in cleft surgery is always fresh autoge-nous
bone.Cancellous bone or cortico-cancellous blocks are generally reservedfor filling
defects in the alveolus or lateralmaxillary walls.The authors�preferencefor bone
grafts to contour the middle faceis split-thickness calvaria.For the chin apedicled
bone graft from the inferior bor-der ofthe mandible is always employed.Bone
Grafting ofthe Cleft Maxilla and PalateCancellous grafts can generally be con-
densed into cleft defects and are self-retained.Block grafts or onlay graftsshould
always be secured with a screw topromote healing,reduce resorption,andthe risk
ofinfection.There are multiple bone donor sources,including the
ilium,cranium,tibia,mandible,and ribs.Although harvestingbone requires more
surgical time and hasassociated morbidity,the predictability ofthe result easily
justifies its use.There is noautogenous bone substitute that has thesame success in
patients with a cleft as doesfresh autogenous bone.The morbidity ofNasal
mucosaPalatal mucosaFixed gingivaBone graftABFIGURE61-11A,Buccal view
demonstratingthe tissues lining the cleft elevated,pushedorally,and sutured on the
oral side.B,Deep-er view into the cleft demonstrating the clo-sure ofthe oral and
nasal tissues and thepocket for the bone graft.Adapted from Tur-vey TA et
al.15Fixed gingival flapPremaxillaFloor of noseFIGURE61-12The nasal floor is
constructedwith tissues lining the cleft that are mobi-lized superiorly and
sutured.Adapted fromTurvey TA et al.15FIGURE61-13The design ofthe lateral max-
illary osteotomy is determined by thepatient�s esthetic needs.A,The classic low-
level cut.B,A higher-level cut approachingthe infraorbital rims.C,A
modificationused when enhancement ofthe cheek promi-nence is desired.When the
options shown inFigures B and C are used,there is risk offracturing these
buttresses because the boneis thin.Repair is possible with microplates.Adapted from
Turvey TA et al.15ABC
1274Part 8: Orthognathic Surgerybone harvest can be reduced with a goodsurgical
technique and should not be anexcuse for using bone alternatives.Stabilizing the
Operated MaxillaThe development ofmore rigid fixationdevices permits improvement
ofresults ofcleft skeletal surgery.Originally,stainlesssteel plates and screws
and,later,titaniumsystems were used instead ofthe tradition-al stainless steel
wires to secure the posi-tion ofthe maxilla.The many benefits ofusing more rigid
fixation include areduced time for intermaxillary fixationand better assurance
ofthe position ofthemidface during healing.A single disadvan-tage ofthe use
ofmetallic bone plates andscrews is a reduced ability to manipulatetooth-bearing
segments with elastic trac-tion during the postoperative period tocorrect the
occlusal result.Velopharyngeal ConsiderationsOne ofthe complexities ofthe cleft
mal-formation involves the function ofthevelopharyngeal sphincter.Under
normalcircumstances,sealing the nasal cavityfrom the oral cavity occurs by a
simultane-ous elevation ofthe soft palate and con-traction ofthe lateral pharyngeal
walls toproduce closure ofthe nasopharynx fromthe oral cavity.In many patients with
arepaired cleft palate,the velopharyngealmechanism is fragile and the patient
haslearned to overcome a short or scarredimmobile palate by compensating
andrecruiting adjacent structures.Passavant�sbar (a hypertrophy oftissue in the
posteri-or pharyngeal wall) is a result ofa com-pensatory effort that many patients
with acleft develop to overcome the deficit andinadequacy ofvelar movement.Forward
displacement ofthe maxilla inpatients without a cleft is well tolerated,andthese
patients have adequate compensatoryreserve to overcome the change in positionofsoft
palate.A minority ofpatients with acleft are not able to tolerate even smalldegrees
ofmaxillary displacement,and thevelopharyngeal function may deteriorate,affecting
the patient�s speech and communi-cation ability.16This potential risk should
beevaluated before maxillary-advancementsurgery,and patients should be appropriate-
ly counseled.In patients with a cleft,theoccurrence ofvelopharyngeal
inadequacyfollowing midface advancement is infre-quent and additional surgical
proceduresare usually unnecessary.Almost all patientswith a cleft experience
hypernasality imme-diately following surgery.Fortunately,thisgradually resolves
with time,and mostpatients return to their baseline speech by 6 months after
surgery.It is prudent to delaysubsequent surgery to reduce nasality for atleast 6
months following maxillary advance-ment.This allows natural compensation tooccur
and permits bone healing to proceedwithout introducing more scarring,whichmay
contribute to relapse.17An interesting observation in somepatients with pharyngeal
flaps who donot have velopharyngeal adequacy priorto midface advancement is an
improve-ment ofnasal speech after surgery.Although sibilant distortions secondaryto
malocclusion are expected to improve,reduction ofhypernasality after
maxillaryadvancement is paradoxic.The explana-tion ofthis occurrence is the
altereddynamics ofthe sphincter that result afterBone graftsFIGURE61-14Onlay bone
grafts are positioned andsecured with screws.Wires are occasionally necessaryto
prevent displacement ofthe inlaid bone grafts intothe sinus.Adapted from Turvey TA
et al.15Onlay bonegraftsInterpositionalbone graftsCancellousbone chipsSuture
purchase softtissue at base of ala......and is passedthrough bur holein nasal
spineFIGURE61-15A andB,The premaxilla is secured with bone grafts,which are used to
construct theinferior piriform rim.These grafts are tunneled under the buccal flaps
and screwed to the nasal spineanteriorly and to the lateral maxilla
posteriorly.Adapted from Turvey TA et al.15AB
Orthognathic Surgery in the Patient with Cleft
Palate1275surgery.Apparently,stretching the flapand its positional change improve
thedynamics ofthe velopharyngeal mecha-nism so that improved speech occurs insome
patients.This observation is notpredictable,and patients must be cau-tioned
appropriately.When a pharyngeal flap is in place andmaxillary advancement is
undertaken,theflap should be removed only ifit does notpermit adequate mobilization
ofthe max-illa.When the flap is in place,nasal intu-bation can be difficult;the
anesthesiologistmust be prepared to use endoscopic assis-tance with endotracheal
tube insertion(see Figure 61-8).References1.Murray JC,Daack-Hirsh S,Buetow KH,et
al.Clinical and epidemiological studies ofthecleft lip and palate in the
Philippines.CleftPalate Craniofac J 1997;34:7�10.2.Christensen K.Methodological
issues in epi-demiological studies in oral clefts.In:Wyszynski D,editor.Cleft lip
and palate.Oxford:Oxford University Press;2002.3.Lidral AC,Vig KWL.The role ofthe
orthodon-tist in the management ofcleft lip and palate.In:Wyszynski D,editor.Cleft
lip and palate.Oxford:Oxford University Press;2002.4.Washington Department
ofHealth.Cleft lip andpalate:critical elements ofcare:Washington:Washington
Department ofHealth;1997.5.American Cleft Palate�Craniofacial Associa-
tion.Parameters for the evaluation oftreat-ment ofpatients with cleft lip/palate
orother craniofacial anomalies.Cleft PalateCraniofac J 1993;30 Suppl:4.6.Mars
M,Houston WJB.A preliminary study offacial growth and morphology in unoperat-ed
male unilateral cleft lip and palate sub-jects over 13 years ofage.Cleft Palate
J1990;27:7�10.7.Cohen MM Jr.Syndromes with cleft lip andpalate.Cleft Palate J
1978;15:306�28.8.Cohen MM Jr,Bankier A.Syndrome delin-eation involving orofacial
clefting.CleftPalate J 1991;28:119�20.9.Boyne PJ,Sands NR.Secondary bone
graftingofalveolar and palatal clefts.J Oral Surg1972;30:87.10.Boyne PJ,Sands
NR.Combined orthodontic-surgical interaction in the management ofresidual palato-
alveolar cleft defects.Am JOrthod 1976;70:21.11.Turvey TA,Vig KWL,Moriarty J,Hoke
J.Delayed bone grafting in the cleft maxillaand palate:a retrospective
multidisciplinaryanalysis.Am J Orthod 1984;86:244�56.12.Bergland O,Semb G,Abyholm
FE.Eliminationofthe residual alveolar cleft by secondarybone grafting and
subsequent orthodontictreatment.Cleft Palate J 1986;23:175.13.Phillips C,Proffit
WR.Psychosocial aspects ofdentofacial deformity and its treatment.In:Proffit
WR,White RP,Sarver DM.Contem-porary treatment ofdentofacial deformity.St.Louis
(MO):Mosby;2003.p.70�91.14.Vig KWL,Turvey TA,Fonseca RJ.Orthodonticand surgical
considerations in bone grafting inthe cleft maxilla and palate.In:Facial clefts
andcraniosynostosis:principles and management.Philadelphia
(PA):W.B.Saunders;1996.15.Turvey TA,Vig KWL,Fonseca RJ.Maxillaryadvancement and
contouring in the pres-ence ofcleft lip and palate.In:Facialclefts and
craniosynostosis:principlesand management.Philadelphia (PA):W.B.Saunders;1996.16.Lo
LJ,Huen KF,Chen YR.Blindness as a com-plication ofLeFort I osteotomy for maxil-lary
disimpaction.Plast Reconstr Surg2002;109:688�98.17.Mason RA,Turvey TA,Warren
DW.Speechconsiderations with maxillary advancementprocedures.J Oral Surg
1980;38:752.
CHAPTER 62Distraction OsteogenesisSuzanne U.Stucki-McCormick,MS,DDSDistraction
osteogenesis (DO),a usefultechnique to generate bone and soft tissue,can be applied
to craniofacial reconstruc-tion,including orthognathic surgery,cleftlip and palate
reconstruction,a newmandibular condyle regeneration,a den-toalveolar unit
reconstruction for dentalimplants and transport DO for disconti-nuity
defects.Regardless ofthe surgical site,adher-ence to the following basic Ilizarov
princi-ples is the key to surgical success1:1.Osteotomy ofthe bone site with min-
imal periosteal stripping2.Latency period:3,5,or 7 days,depending on the surgical
site 3.Distraction rate:1.0 mm per day(0.5�2.0 mm)4.Distraction rhythm:continuous
forceapplication is best,yet device activa-tion bid is more practical and allowsfor
better patient compliance5.Consolidation:until a cortical outlinecan be seen
radiographically acrossthe distraction gap,usually 6 weeksThe distraction technique
involves cre-ating an osteotomy in an area adjacent toan area ofbone
deficiency.Applying slowtension forces separates the bony edges,which creates a
regenerate chamber fromwhich the new bone and soft tissues areformed (Figure 62-
1).This regeneratechamber may be large and wide,withabundant blood supply from the
overlyingmuscle and skin,as in mandibular distrac-tion.Conversely,the distraction
gap maybe small,with thin mucosal coverage,as indentoalveolar distraction for
dentalimplants.The local periosteal blood supplyand the size ofthe distraction
segmentinfluence the treatment plan decisions;infact,for small bone segment
distraction,the rate ofdistraction may need to decreaseto 0.5 to 0.7 mm per
day.However,forsagittal distraction ofthe mandible where-by the bone segments
overlap,the distrac-tion rate should increase to 2.0 mm perday.I recommend
modifying the Ilizarovprinciples in each individual,based on thesize ofthe
distraction bone segment andthe regional blood supply (Table 62-1).Initially,the
regenerate chamber isfilled with a fibrous matrix that ossifiesfrom the periphery
centrally.2The distrac-tion gap shape and the resultant new DObone are influenced
by the vector ofdis-traction and the rate ofdistraction.Alter-ing the vector
ofdistraction during activeDO will correspondingly alter the three-dimensional
shape ofthe regeneratechamber and the resultant new DO bone(Figure 62-2).Ifthe
distraction rate is toorapid,then the regenerate chamber will behourglass
shaped,and the new DO bonewill be thinned centrally.The osteotomy location can
affect theshape ofthe regenerate chamber and thefinal new bone.Ifthe osteotomy is
createdin an area ofthin bone stock,then theregenerate chamber will thin and
assumethe shape ofthe native bone.In treatmentplanning and during surgery,it may
benecessary to adjust the osteotomy site,placing the bone cut in an area ofmaxi-mum
bone thickness to create a large androbust regenerate chamber (Figure 62-3).Until
the distraction gap ossifies com-pletely,the regenerate chamber is influ-enced by
the local muscle pull.As distrac-tion proceeds,the regenerate chamberbecomes
enlarged and is filled initiallywith a weak fibrous matrix.Simultane-ously,the
local muscles that are attachedto the DO site are stretched.The stretchedFIGURE62-
1During the distraction process thebony edges ofthe osteotomy (A) are
separatedslowly over time to create an initial radiolucentregenerate chamber
(B),which has the size andshape ofthe native bone.AB
1278Part 8: Orthognathic Surgerymuscles tend to return to their originalsarcomeric
length,pulling on the regener-ate chamber and on the interveningimmature bone
matrix,causing an alter-ation ofthe vector ofDO and displace-ment ofthe distraction
segment in thedirection ofthe muscle (Figure 62-4).This effect is most noticeable
by theaction ofthe temporalis and the mylohy-oid musculature.Vector control maneu-
vers,including the use ofsurgical guides,orthodontic appliances,and interim par-
tial dentures with a portal for DO deviceaccess,help to maintain and adjust
thevector ofdistraction.3 Clinicians may use the fibrous matrixnature ofthe
regenerate chamber to theiradvantage to mold the regenerate into theproper
orientation and location,includingdistraction ofa segment outside the nor-mal
anatomic periosteal plane.Specifical-ly,clinicians may mold the regenerate atany
time in the distraction process�dur-ing active DO and at the end ofDO.During active
distraction,the regener-ate is molded by altering the vector ofthedistractor.Some
DO devices have mechan-ical hinges that allow the clinician to adjustthe vector
ofdistraction.This is done easi-ly in an office setting,often using
localanesthesia,ifnecessary.Ifperforming a sig-nificant (=3mm) molding move or
vectorchange,then I recommend that a short (1 to 3 days) latency is observed prior
tocommencing with the distraction protocol.This allows for healing ofthe
disruptedmicrovasculature and osteoid matrix with-in the regenerate chamber that
the vectorchange produced.A longer latency (2 to 4 days) is recommended ifthe bone
seg-ment is small,as in dentoalveolar distrac-tion for dental implants.Perform
regenerate molding at theend ofactive distraction to help guide thebone segment
into its final position.4Afteronly 3 weeks ofconsolidation,remove thedistractor
prematurely,and reposition thesegment to its final position.Use tractionorthodontic
elastics to guide the segmentto its final position and to hold the seg-ment in this
position until final ossifica-tion occurs.At the time ofdevice removal,however,the
segment may be repositionedTable 62-1Distraction ProtocolDistractionLatency (d)Rate
(total)
(mm/d)RhythmMandible51.0bidMaxilla51.0bidAlveolus/implant5�70.5�0.7�1.0bidTransport
5�71.0bidCondyle:transport5�71.0tid,qidMandible:children3�51.0�2.0bidMandible:sagit
tal5�72.0bidTransport:neck dissection7�100.5�1.0bidTransport:XRT7�100.5bidbid =
twice a day;qid = four times a day;tid = three times a day;XRT = external beam
radiation therapy.FIGURE62-2Initially the distraction vector islinear (A).Once 5 mm
ofregenerate chamberhas been created,the distractor can be adjusted,altering the
vector ofdistraction,which corre-spondingly alters the three-dimensional shape
ofthe new bone (B).ABFIGURE62-3For transport distraction to create a new mandible
(A,B),the osteotomy should beplaced in an area ofmaximal bone stock (C,D) to create
a robust regenerate chamber.ABCD
Distraction Osteogenesis1279manually and held in place with rigid fix-ation plates
and screws.Perform �dancing�ofthe distractionsegment ifa discrepancy occurs
inplanned distraction amounts,such asbilateral mandibular advancement
forasymmetries.5Initially,both segments areadvanced at the planned distraction
rate.When the larger,less asymmetric sidereaches its final position,the
segmentbecomes the dancing side,advancing theDO segment in the morning then
turningit back the same amount in the evening.In the meantime,the lesser more asym-
metric segment continues to be advancedat the planned rate until it catches upwith
the contralateral side.Carry out anyfinal adjustments to the mandibular posi-
tioning when the asymmetry has beencorrected by advancing or dancing thetwo sides
as needed (Figure 62-5).As with orthognathic surgery,treat-ment planning for
distraction osteogenesisincludes predicting the amount and tra-jectory ofthe
planned bone movement.Although the DO device may be activated1.0 mm per day,this
does not translate to1.0 mm ofbone advancement per day.Theamount ofactual bone
movement isalways less than the distance that is indi-cated on the distraction
device,thereforethe clinician monitors the patient�sprogress closely,including
radiographs.The surgical approach and techniqueare similar to orthognathic
surgery.Whenlocating and positioning the bone cut,alsoconsider the placement and
orientation ofthe distraction device.Mark the plannedosteotomy.Then,create a
corticotomy,verifying the ability to place the distractorin the proper
orientation.Make the screwfixation holes for the distraction device,and remove the
device.The corticotomy is then converted atraumatically to anosteotomy,and the
distraction device isfixated into place.The device is activatedto ensure impedance-
free advancement ofthe distraction segments.6Remove anybony interferences,and
return the deviceto its closed neutral position.Prior to ini-tial device
orientation and placement,activate the distractor 1.0 to 2.0 mm.Thus,after the
osteotomy and the device aresecured into place,the DO device can be�closed�1.0 to
2.0 mm,reducing and min-imizing the initial distraction gap createdby the bone
cut.Mandibular DistractionFor patients with craniofacial microsomia,mandibular
distraction ofthe affected sideis a useful technique for generating bothbone and
soft tissue.The surgical approachis similar to a sagittal osteotomy.Create abone
cut in the ramus ofthe mandible onthe affected side above the lingua along theramus
to the posterior border ofthemandible above the gonial angle.Positionthe
distractor,and convert the corticotomyto an osteotomy,after which the distrac-tion
device is secured.Intraoral distractorsare preferred to external devices todecrease
scarring.Compared with a com-pletely submerged device,DO devices inwhich the
distraction mechanism is intrao-ral yet extramucosal allow the clinician tomonitor
the distractor directly without theneed for radiographs.In addition,removalofthe
device is facilitated ifthe distractionmechanism is extramucosal.The vector
ofdistraction is calculated based on the tra-jectory ofthe bone segment and on
thelocal anatomy,including bone stock,toothbuds and/or roots,and position ofthe
infe-rior alveolar nerve.Achieve chin point cor-rection by vertical distraction
ofthe ramus(Figure 62-6).7FIGURE62-4During the final stages ofdistrac-tion
osteogenesis,the weak regenerate chamber isunder the influence oflocal muscle
pull.A,Herethe mylohyoid created an open bite,which wascounteracted by orthodontic
elastics.B,Usingcallous manipulation with orthodontic elastics,the open bite was
closed.ABFIGURE62-5To correct asymmetry the devicesare initially distracted by the
same amount (A),then using �disk dancing,�the regenerate cham-ber can be advanced
or returned to bring the seg-ment into proper position (B).AB
1280Part 8: Orthognathic SurgeryThe distraction process continues 1.0 mm per day
until the mandibularasymmetry is corrected.I recommend age-dependant overcorrection
to compensatefor the decreased growth potential ofthegenetically affected
side.8Remove the dis-tractor when a cortical outline can be seenradiographically
(Figure 62-7).Performmandibular distraction for all Pruzansky-Mulliken
classifications ofcraniofacialmicrosomia (Figure 62-8).9Mandibular distraction
plays a uniquerole for infants with airway compromise,asa consequence
ofmicrognathia.10,11Earlydistraction ofthe body ofthe mandiblebilaterally has shown
promise for improv-ing airway volume and in decreasing air-way resistance,leading
to early decannula-tion or avoidance ofa tracheotomy.12,13For large mandibular
advancements orfor patients with a history oftemporo-mandibular joint disorders,DO
is a usefultreatment alternative.Use a modification ofthe classic sagittal split
technique for suchcases.5As the proximal and distal segmentsoverlap,the distraction
rate is increased to2.0 mm per day (0.5 mm qid [4 times aday]).Further,create a
groove in the superi-or aspect ofthe horizontal bone cut abovethe lingual to allow
for impedance-free rota-tion ofthe proximal segment during DO(Figure 62-
9).Ideally,the distractors areplaced parallel to the midsagital plane
ofthemandible,although this is not alwaysachieved.14,15Class II orthodontic
elasticsare placed to �unload�the temporo-mandibular joint.At the time
ofsurgery,place a maxillary occlusal surgical guide thatextends to one-halfofthe
occlusal surface ofthe maxillary second molar,with the finalocclusion indexed.As
distraction proceeds,guide the mandible into the proper occlu-sion using light
elastics.Sagittal distractionofthe mandible appears to provide condylaraxis
stability and has minimal deleteriouseffects on the temporomandibular
joint.5Mandibular WideningDO,a useful tool to create space forsevere mandibular
crowding,is oftencombined with maxillary transversewidening and surgically assisted
palatalexpansion (Figure 62-10).16For themandible,make a vestibular incision
similarto a genioplasty,approach the mandible,and score the planned osteotomy
site.Cre-ate the osteotomy in the corpus ofthemandible with a bur or a saw.Perform
theinterdental osteotomy with fine chisels in atunneling technique,reducing the
periostealstripping,being careful to avoid encroach-ing on or injuring the
periodontal ligamentofthe teeth in the osteotomy line.The tissuetype in the
osteotomy site is the template forDO.Consequently,ifthe osteotomy is posi-tioned
completely in the bone,bone will becreated.Ifthe osteotomy encroaches onperiodontal
ligament tissues,the distractiongap fills with bone and moderate
amountsofperiodontal ligament-like tissues,leadingto a pseudo-union.17For the
central incisorsthat are extremely crowded,carry out theinterdental osteotomy
laterally between lesscrowded teeth;namely,the lateral incisorand the cuspid.Create
a horizontal step 5 mm below the roots ofthe incisor teeth,and make the main
osteotomy ofcorpus ofmental region vertically in the midline.FIGURE62-6To correct
chin point deviation from congenital malformations,suchas craniofacial microsomia
(A�C),the distraction device is placed vertically to cor-rect the deficient ramus
(D).Here the open bite (E) and chin point deviation werecorrected (F�H).ABCDGHEF
Distraction Osteogenesis1281The distractor ofchoice is placed.Most distractors are
tooth and boneborne.Distractors that are solely boneborne tend to produce a V-
shaped regen-erate chamber,with more widening at thelevel ofthe alveolus and less
widening atthe level ofthe inferior border.After a 5- to 7-day
latency,distractionproceeds at 1.0 mm per day.Be sure toapply slow incremental
distraction forces;DO forces generated during mandibularwidening may translate to
the mandibu-lar condyle.18Minimal in nature,theseforces cause mild adaptive bony
changesthat are well tolerated.Nevertheless,monitor patients closely for any com-
plaints ofpreauricular pain or limitationofmotion,which would indicate alteringthe
1.0 mm per day DO protocol from 0.5 mm twice daily to 0.25 mm four timesdaily
device activation.After DO,the surgeon may place aplastic pontic tooth in the gap
between thecentral incisors to stabilize the teeth and toprevent their central
migration.19To pre-vent migration ofthe teeth into the DOgap,include these teeth in
the orthodonticarc wire,with the possible placement ofalight spring.Remove the
distractor once acortical outline can be seen on the radi-ograph.Place a lingual
arch to help stabi-lize the new transverse dimension.Simultaneous Maxillary and
Mandibular DistractionPatients who have craniofacial microso-mia often have
maxillary hypoplasia and aconcomitant occlusal cant toward theaffected side.Using
mandibular DO dur-ing the primary or mixed dentition phaseoften autocorrects the
maxillary occlusalcant (Figure 62-11).Ifthe maxillary molarteeth are present in
full occlusion or ifthepatient is in permanent dentition,then aconcomitant
maxillary distraction,alongwith the mandibular distraction,may beindicated.20,21The
surgeon performs a cor-ticotomy at the Le Fort I level,includingpterygoid
disjunction,taking care to avoidthe unerrupted tooth buds or roots duringthe bone
cut.The maxilla is loosened butnot down-fractured.Orthodontic elastics(8 oz) are
then applied bilaterally,withincreased elastic traction on the affectedside to
guide the maxilla to its proper ori-entation during the DO process (Figure62-
12).Elastic traction that results in max-FIGURE62-7The distractor is advanced until
the deformity is corrected (A�C).Initially,osteotomy (D) produces a radi-olucent
regenerate chamber (A) that ossifies with time (E), at which point the distractor
is removed (F).ABCDEF
1282Part 8: Orthognathic Surgeryillomandibular fixation (MMF) is notrequired to
guide the maxilla along withthe mandible during DO.22Maxillary Distraction
Likewise,use DO for maxillary advance-ment.This technique is especially usefulfor
patients with large advancements orin patients postpalatoplasty for cleft lipand
palate whose scarring causes inade-quate tissue or difficulty in moving
themaxilla.23,24The surgical approach is sim-ilar to conventional orthognathic
surgery,with the osteotomy at the Le Fort I level.The maxilla is freed butnot
completely down-fractured.Ifthemaxilla is inadvertently completelydown-
fractured,then loosely place a sus-pension suture (2-0 polydioxanonesuture) in the
bone across the bone gap atthe level ofthe first molar tooth and thezygomatic
buttress to help stabilize andprevent inferior tipping ofthe posteriormaxilla.The
distractors are pre-bent tofacilitate device placement.The zygomat-ic buttress
region is a good point fordevice fixation.Ideal trajectory wouldlocate the two
distractors that are parallelto each other and the midsagittal plane.Achieving this
congruity is much moredifficult in the maxilla owing to localanatomy,device
design,and location ofthe osteotomy,limiting device placementand orientation.Ensure
that the resultantmoment arm ofthe two distractors willnot cancel each other as the
distractorsFIGURE62-8This patient with grade III craniofacialmicrosomia (A�C)
successfully underwent ramal distrac-tion (D�F) to correct his deformity
(G,H).ABCEFGHD
Distraction Osteogenesis1283FIGURE62-9A�D,Classic sagittal split osteotomy
technique can be modified to allow for mandibular advancement.E,F,The horizontal
bone cut is modified toallow for impedance-free advancement during distraction
osteogenesis.(Courtesy ofDr.J.J.Moses.)ABCDEFFIGURE62-10A,B,Patients with narrow
arch forms and dental crowding are aided using mandibular widening as well as
surgically assisted maxillary expansion.C,D,Bone-borne devices can be placed into
the vestibule.E,F,The resultant increase in transverse dimension can be stabilized
with a lingual orthodontic appliance.ABCDEF
1284Part 8: Orthognathic Surgeryreach their maximal length.Use anteriortraction
elastics to guide the maxilla to itsproper position.Put an intravenous tub-ing that
is cut to size over the two ends ofthe distraction device activation rods toprevent
lip ulcers (Figure 62-13).Expanding the soft tissue envelope is often the rate-
limiting step in large maxillary advancements.In these patients (> 8 to 10 mm
advancement) or for thosewho have palatal scarring,the use ofanexternal halo frame
is indicated.Although abit cumbersome and unsightly,the externalframe can produce
significant and dramat-ic maxillary advancements (Figure 62-14).The surgery is
similar to conventionalorthognathic surgery.Perform a high Le Fort or stepped
osteotomy,ifindicated.Secure the device below the height ofcon-tour ofthe
skull;otherwise,the halo maydislodge vertically.Active DO requires careful
observation,as the center ofrotation ofthe maxilla is atthe level ofthe roots ofthe
maxillary firstmolar.25Left unchecked,the maxilla will bedistracted anteriorly and
superiorly,creat-ing an open-bite malocclusion.Using theexternal halo frame,adjust
the arms verti-cally to allow the maxilla to advance in adownward and forward
vector.Similarly,toallow for correction ofa maxillary asymme-try,the arms ofthe
halo device can be dif-ferentially activated (ie,0.5 mm on one sideand 1.0 mm per
day on the other (see Figure62-14).Once the ossification ofthe distrac-tion site is
complete (ie,until the maxilla isstable to palpation,usually in 5 to 6 weeks orwhen
radiographic evidence ofa corticaloutline is seen),the halo device is removedin the
office without the need for rigid fixa-tion ofthe maxilla.Occasionally,prior
tocomplete ossification ofthe site,the patientmay request to have the halo
removed.Thedevice is removed with concomitant place-ment ofrigid fixation
plates.Maxillary Segmental DistractionIn patients who have a wide alveolar
cleft,perform a segmental osteotomy in thelesser segment,advancing it via
distractionto close the alveolar defect.26The bone cutis usually located between
the bicuspidand the molar teeth ofthe lesser segment(Figure 62-15).In the same
way,place thebone cut in the greater segment betweenthe incisor and the cuspid
teeth to distractthe gap closed from either one or twodirections.Use oforthodontic
appliancesand the arch wire allows the distractionsegment to follow the curvature
ofthemaxillary arch.During post-distraction,place an orthodontic spring on the
archwire,paralleling the regenerate chamber toFIGURE62-11This patient in mixed
dentition with significant occlusal cant (A) underwent mandibular distraction using
a submerged device (B) to correct thedeformity (C).The neomandible (D) mimics the
native mandible (E) in size and form.The mandible was overcorrected with the dental
midline distracted one-halftooth toward the contralteral side (F).The maxillary
occlusal cant was autocorrected as the mandible was placed in the proper position
and with the erup-tion ofthe permanent teeth (G).ABCDEFG
Distraction Osteogenesis1285help hold the segment in proper orienta-tion.In 1 to 2
weeks after distraction ossi-fication,move the bicuspid and cuspidteeth
orthodontically back to their correctposition into the ossified DO bone,leav-ing
the anterior dentoalveolar unit forimplant reconstruction or for final perios-
teoplasty and smaller bone graft,ifindi-cated.This segmental distraction is a
formoftransport DO.For patients who have congenital age-nesis ofthe premaxilla or
who experiencetraumatic loss ofthe dentoalveolar unit,anterior maxillary segmental
distractionis indicated (Figure 62-16).Use tunnelingtechniques to perform the
anteriorosteotomy,making the horizontal bonecut parallel to the occlusal plane to
facili-tate segment advancement along a hori-zontal vector (Figure 62-
17).Bilateraldistractors are placed,and distractionproceeds after a 5-day latency
at a rate of1.0 mm per day.Anterior traction elasticsaid in the forward thrust
ofthe segment.The distractors are removed once a bonyoutline can be seen
radiographically andEFGHIFIGURE62-13An intravenous tubing can beplaced over the
free end ofmaxillary distractors toavoid lip ulcers.The tubing is removed to
activatethe device then reapplied.FIGURE62-12For adults in permanent dentition
(A),the occlusal cant involves not only the dentoalveolar unit but alsothe piriform
rim and affected paranasal areas (B�D).As this patient had a previously placed
costochondral graft,whichwas the site ofthe distraction,the neomandible has the
same size and shape ofthe original bony template ofthe costo-chondral graft
(E),rather than the contralteral side (F).The chin point deviation and occlusal
cant to the level ofthezygoma are best seen in the frontal and submentovertex views
(D,G).Postdistraction,the mandibular chin point isbrought to the midline.A
concomitant Le Fort I osteotomy is performed at the time ofdistraction osteogenesis
surgeryand the maxilla is brought down with the mandible using orthodontic
elastics.Note the correction ofthe occlusal cantand piriform rim and zygomatic
buttress regions (H).This is reflected in the soft tissue changes (I).ABCD
1286Part 8: Orthognathic Surgeryonce the segment is stable.The distrac-tors can be
removed prior to completeossification (3 to 4 weeks) to mold theregenerate or at
the patient�s request.Position rigid fixation plates at the timeofdevice
removal.Resorbable rigid fixa-tion plates are useful for this purpose;thesite will
ultimately undergo dentalimplant reconstruction.Transport Distraction
OsteogenesisThe power ofDO is that both bone and softtissues are
regenerated.Transport distractioninvolves creating a transport disk in the
bonestump,adjacent to a discontinuity defect or aresection site.The transport disk
is thenadvanced 1.0 mm per day as the distractiongap increases in size to span the
discontinu-ity defect (Figure 62-18).27The resultantregenerate chamber will have
the same sizeand shape ofthe transport disk.Carefultreatment planning is necessary
to plan thesite ofthe osteotomy,thus determining theshape oftransport disk and
regenerate (Fig-ure 62-19).Occasionally,a tooth may needto be sacrificed to allow
for osteotomy place-ment in an optimal position.Both external and submerged
deviceshave been used for transport DO.Threepoints offixation are required for
trans-port DO:(1) in the proximal stump,(2) inthe distal site,and (3) in the
transportdisk.Use a rigid fixation plate as a substi-tute for the three points
offixation alongwith a conventional distractor.The rigidfixation plate also acts as
a guide for thetransport disk during distraction (see Fig-ure 62-18).Once the
transport disk reach-es the docking site,the segment is held in neutral fixation
until a cortical outlineis seen in the regenerate.At the time ofFIGURE62-
14A,B,Patients withsevere maxillary hypoplasia are goodcandidates for maxillary
distractionusing an external halo frame.C�I,The frame is well tolerated and canbe
adjusted differentially to allow forforward as well as downward move-ment ofthe
maxilla during distrac-tion osteogenesis.ABCDEFGHI
Distraction Osteogenesis1287FIGURE62-15Segmental distraction can be performed for
focal bone and soft tissue deficiencies such as alveolar cleft defects.A�C,The bone
cut is made betweenthe molar and bicuspid teeth and the orthodontic wire acts as a
guide during distraction osteogenesis.D�F,A new dentoalveolar unit is formed and
the cuspid andbicuspid teeth can be moved back into proper position orthodontically
post-distraction osteogenesis.ABCDEFFIGURE62-16Patients with anterior maxillary
congenital deformities including anodontia (A,B) are treated with anterior
segmental maxillary distractionosteogenesis (DO) and concomitant posterior
mandibular DO widening (C,D).FIGURE62-17A,Patients with traumatic avulsion ofthe
premaxillary segment can be treated with segmental anteriordistraction
osteogenesis.B,The bone cutis made parallel to the occlusal plane and the
distractors placed via a tunneling technique (Courtesy ofKLS Martin
L.P.,Jacksonville,FL).C,D,A flat planeocclusal splint is inserted to allow for
impedance-free maxillary advancement.ABCDABCD
1288Part 8: Orthognathic Surgerydistractor removal,the surgeon may needto position
a small bone graft between thetransport disk and the docking sitebecause the
transport disk becomesrounded and encased with a fibrocarti-lagenous cap.Obtaining
osseous unionnecessitates removal ofthis interveningfibrocartilagenous cap.During
active DO,monitor the patientclosely to rule out soft tissue
dehiscence.Occasionally the leading edge ofthe trans-port disk can migrate through
the soft tis-sue.The suggested local wound-care mea-sures include antibiotics and
antimicrobialmouth rinses.A blood supply that is com-promised (eg,a patient status
post-radiationtherapy) indicates disk dancing until thedehiscence site
closes.Symphyseal reconstruction can be dif-ficult because the regenerate
chambertends to assume a straight line,rather thanfollow and maintain the
curvilinearshape.28Use molding devices,including anintraoral surgical guide,to
facilitate andmaintain the shape ofthe regeneratechamber (see Figure 62-
19).29Viewedfrom above,the dentoalveolar unitassumes an arcuate form.Viewed
frombelow,the mandible assumes five lines:two body regions,two
parsymphysealregions,and one symphyseal region.Thus,plan for five linear
distraction vectors toreconstruct the mandible (Figure 62-20).One alternative
treatment plan callsfor the creation ofa large transport disk(1.5 to 3.0 cm)
advanced in a linear fash-ion until the junction ofthe next linearsegment.28The
disk is held in neutral fix-ation for a few days or weeks until earlyossification
occurs.Subsequently,the diskis divided into two segments,with one-halfofthe
original transport disk held inplace to the reconstruction plate.Theother one-
halfbecomes a new transportdisk reoriented in the proper vector,which,after a 3- to
5-day latency,isadvanced by distraction in the new trajec-tory (see Figure 62-
20).Transport distraction has been usedsuccessfully either in primary reconstruc-
tion at the time ofbone resection or insecondary reconstruction.For
primaryreconstruction,the devices are placed atthe time ofresection.Ifa
concomitantneck dissection is done,then the latencyperiod should be increased to 7
days.Forsecondary reconstruction,limited surgicaldissection is advocated.As the
soft tissuebed may be heavily scarred,the distractionrhythm may need to be altered
to fourtimes a day rather than twice a day to allowincremental stretching ofthe
overlyingsoft tissues.Tension within the overlyingsoft tissue may cause daily
�relapse�byFIGURE62-18Transport distraction osteogenesis brings bone and soft
tissue into a defect by creating atransport disk (A),which is distracted to span
the gap creating new bone that is similar in shape to thenative mandible
(B,C).D,All tissues are created,including mucosa.E,The technique can be
combinedwith a submerged device and a rigid fixation plate to stabilize the
discontinuity defect.F,The hemi-mandible can be successfully
reconstructed.ABCDEFFIGURE62-19Surgical guides can be fabricated tohelp maintain
the curvilinear shape ofthe regener-ate during transport distraction osteogenesis.
Distraction Osteogenesis1289exerting a counterforce on the transportdisk.Transport
DO has been used to suc-cessfully create a neomandible in patientswho have had
post-resection radiationtherapy.30,31Although predistractionhyperbaric oxygen
therapy is appropriate,it is not mandatory.During active distrac-
tion,neovascularization has occurred.32Use transport DO to reconstruct a neo-
mandible without hyperbaric oxygen ther-apy.The distraction rate is reduced to 0.5
mm per day,and the overlying soft tis-sues are carefully monitored.DO can be used
in conjunction withconventional reconstructive techniques(eg,microvascular
flaps).One concern,however,is that the donor bone,such as afibula,may not have the
ideal form post-mandibular reconstruction for implantplacement and prosthetic
reconstruction.Use distraction as a secondary techniqueto obtain ideal height and
width forimplant reconstruction.33The technique issimilar to that for DO ofan
atrophicmandible for dental implants.Transport Distraction to Generate a
NeocondyleDuring transport DO,the transport diskbecomes rounded and covered by a
fibro-cartilagenous cap.This cap is removed toensure osseous continuity in
mandibularreconstruction.Use this fibrocartilagenouscap to reconstruct a
neocondyle.34�36Cre-ate a reverse Losteotomy in the ramus ofthe mandible from the
sigmoid notchbehind the lingua to 1.0 to 1.5 cm abovethe inferior border ofthe
mandible (Fig-ure 62-21).The distractor is oriented ver-tically,almost parallel to
the posterior bor-der ofthe ramus,to guide the transportdisk into the
fossa,creating a neocondyle.In the same way,the segment can be over-distracted to
increase posterior verticalramal height and to reestablish the gonialangle.For
bilateral cases,a coranoidecto-my prevents rotation ofthe proximal seg-ment from
temporalis muscle pull duringthe DO process.In patients who have bony
ankylosis,carry out a gap arthroplasty concomitantlywith the distraction surgery
(Figure 62-22).As the neocondyle assumes the form ofthefossa,it is important to
surgically shape thenew fossa well in all three planes ofspaceduring the gap
arthroplasty portion oftheprocedure.Distraction is initiated after a 5-day latency
period and proceeds until thetransport disk reaches the glenoid fossa.FIGURE62-
20During transport distraction osteo-genesis (DO),the mandible can be divided into
fivelinear segments.Transport DO can be performedsequentially (A�C).Sectioning the
transport diskto advance the segments (D�G).(Courtesy ofDr.J.J.Moses.)ABCDFGE
1290Part 8: Orthognathic SurgeryThe patient will remark that they can feelpressure
as the articulation ofthe condyleand fossa is reestablished.This is
confirmedradiographically.The DO device is held inneutral fixation until a cortical
outline isviewed in the regenerate chamber near theangle ofthe mandible.Patients
with condylar resorption(idiopathic,degenerative,and rheuma-toid arthritis)
experience a loss ofposte-rior vertical height and an anterior openbite as a
consequence ofthe resorptiveprocess ofthe condyle.The slow applica-tion offorce
over time via DO to generatenew bone is ideally suited to patientsrequiring
mandibular advancement whohave a history oftemporomandibularjoint involvement.Using
the sameosteotomy,the ramus is over distracted,creating an edge-to-edge Class III
profile(Figure 62-23).Remove the distractorsafter 3 weeks ofosseous
consolidation,and mold the regenerate using orthodon-tic elastics to rotate the
mandible counterclockwise and to close the open bite.Elas-tic maxillomandibular
fixation is notrequired to mold the regenerate.Insert amaxillary splint to decrease
the load onthe temporomandibular joints.Likewise,instruct patients to wear the
moldingelastics in intervals,allowing other timeintervals for free mandibular
movement(ie,4 hours in elastics and 3 hours off).Monitor patients closely,and
ifthepatient complains ofpreauricular dis-comfort or limitation ofmotion,adjustthe
regenerate molding protocol.Regardless ofthe etiology,all patientsundergoing
condylar transport DO are inactive physical therapy during the entire DOprocess and
are also instructed about at-home physical therapy exercises.Success ofthe
transport DO technique to create a neo-condyle depends on mandibular
motion.Alveolar Distraction Osteogenesisfor Dental ImplantsBone grafting techniques
for alveolar ridgereconstruction prior to dental implantreconstruction are well
established.Forcases requiring greater than 4 to 5 mm,apply vertical height
augmentation,or ifthe overlying soft tissue may not supportosseous
augmentation,alveolar DO is auseful treatment alternative.37�39Carry out a
vestibular incision toapproach the site.Minimal periosteal strip-ping is advocated
as the transport disk issmall.Carefully create the bone cut,using asaw or bur for
the horizontal cut,and usechisels at the alveolar crest,sparing the lin-gual or
palatal periosteum.The distractoris adapted to the site.Apply the distractorto the
outer cortical surface ofthe regener-ate chamber or place with a central activa-
tion pin extending transosseously (Figure62-24).Once placed,activate the
distractorFIGURE62-21A reverseLosteotomy is per-formed in the ramus ofthe mandible
for condy-lar transport distraction osteogenesis.FIGURE62-22A,B,A gap arthroplasty
is per-formed to release the ankylosis,without placementofintervening
materials.C,The distractor is ori-ented vertically,parallel to the posterior border
ofthe mandible.D,E,The transport segment is dis-tracted into the fossa to create a
neocondyle.ABDEC
Distraction Osteogenesis1291FIGURE62-23Patients with idiopathic condylar resorption
and anterior open bite (A,B) undergobilateral ramal distraction osteogenesis (C,D)
to correct the vertical height loss.Initially the mandibleis distracted into Class
II occlusion (E,F),the distractor is removed after 3 weeks
ofconsolidation,andelastics are used to guide the mandible into proper occlusion
(G,H).ABCDEFGHFIGURE62-24Alveolar distractors are interosseous (A) or extraosseous
(B).C,After device application the distractor is activated to ensure impedance-free
moment ofthe segment.The transport disk is then returned to the closed position.ABC
1292Part 8: Orthognathic Surgeryto check for impedance-free movement ofthe
distraction segment.Remove any bonyinterferences.The wound is closed andafter a 3-
to 5-day latency,the distractor isactivated up to 0.7 to 1.0 mm per
day.Thedistraction disk is small;thus,a rate of0.5to 0.7 mm per day is advocated
ifthe bloodsupply to the segment is compromised.Distraction proceeds until the
desiredamount ofbone is obtained.Often the seg-ment is overdistracted to a position
abovethe alveolar crest ofthe adjacent teeth.During implant placement,the excess
cre-stal bone can be sculpted and contouredusing a periodontal bur that produces
anesthetic implant site.The segment is heldin place to allow for
ossification.Someauthors recommend 8 weeks ofossifica-tion,whereas others recommend
12 weeksprior to implant placement.37,39Initially,the regenerate chamber is
radiolucent.Thisdecreases with time,but the generatechamber will continue to be
less radio-dense for up to 1 year post-distraction.Applying platelet rich plasma
(PRP) intothe distraction gap at the time ofinitial dis-traction surgery may
increase DO boneossification.40Both interosseous and extraosseousdistraction
devices work well;however,they have some drawbacks.Devices placedon the outer
cortical surface may causeslight buccal resorption ofthe outer cor-tex,requiring a
�patch graft�at the time ofdevice removal.Placing a guided boneregeneration (GBR)
membrane next to thebone below the distraction device will alsoact to decrease this
buccal resorption.41Devices that are placed transosseouslyresult in fibrous tissue
in-growth aroundthe central distraction pin.This tissue isremoved at the time ofthe
device removalbut can limit immediate implant place-ment.Dental implants may be
placed atthe time ofdistractor removal or at 1 month later.Second-stage implant
place-ment allows the soft tissues to mature andfacilitates treatment planning for
idealimplant placement.Place implants to spanthe regenerate chamber,including a
por-tion ofthe distal osteotomy site.Vector control is paramount withsmall-segment
distraction,such as DO fordental implants.The small bone segmentsare under local
muscle pull,especially themylohyoid.Vector control devices,includ-ing orthodontic
appliances and interimtreatment partials with an access hole forthe DO device
activation rod,are useful tohelp guide the distractor into place (Figure62-
25).Callus manipulation as previouslydescribed may be performed under
localanesthesia to re-direct the proper path ofdistraction.New alveolar DO devices
thatincorporate hinges allow the clinician toredirect the vector during active
distrac-tion (Figure 62-26).42,43Local osseous anatomy can influencedistraction
device placement.The fixationplates ofan extraosseous device mayrequire bending to
make the distractionpin more vertical and to optimize theideal vector.Placing the
device flushdirectly on the bone surface can direct thebone segment in an
inappropriate direc-tion,as is the case with the atrophic ante-rior maxilla and
mandible (Figure 62-27).Similarly,to ensure proper device trajec-tory,the central
pin hole ofan intra-osseous device may require angling morebuccally than along the
central axis ofthealveolus.The fixation plates may needaltering that takes into
account the localanatomy,including the mental nerve andpiriform rim regions.In
fact,place theextraosseous device in a cantilever fashionwith the central portion
ofthe device off-set (Figure 62-28).Knife-edge ridges can be a
difficultproblem.Distracting the alveolus in astraight vertical direction will
produce anincrease in height but a narrow bone stock.Perform differential
distraction by perform-ing the lingual cut incompletely,allowingthe lingual site to
act as a �hinge.�44,45TheFIGURE62-25Vector control devices include:orthodontic
devices (A),treatment partials withaccess holes (B),and occlusal splints with
ponticteeth (C�E).BDECA
Distraction Osteogenesis1293device is placed,and distraction proceeds asusual.The
hinge motion allows the buccalwall to be initially distracted differentiallymore
than the lingual;specifically,the buc-cal site �opens�to create a flat crestal
surfacesuitable for implants (Figure 62-29).Posterior saddle deformities
ofthemandible are also problematic.The curveofSpee dictates that straight vertical
dis-traction results in generating more bone inthe retromolar region.To alleviate
thisproblem,make an L-shaped bone cut adja-cent to the remaining teeth,and use
amonocortical miniplate to fixate the poste-rior-most portion on the bone cut
(Figure62-30).45,46Distraction proceeds with theanterior portion ofthe distraction
segmentrotating and hinging around the distal fix-ation plate to differentially
increase theanterior region.Use distraction to reconstruct atrophicedentulous
maxillas and mandibles.Thetechnique is the same.One device is placedin the
midline,and the vector is adjusted todistract the bone segment up and buccally.To
avoid fracture ofthe atrophic mandible,modify the bone cut to a trapezoidal
shape.Rounding the internal corners oftheosteotomy eliminates local inherent
stresses,which have been associated with mandibu-lar fractures.47For severely
atrophic cases,place a reconstruction plate,in conjunctionwith the distraction
devices,at the time ofthe osteotomy.48ComplicationsMost complications associated
with thedistraction technique are iatrogenic andFIGURE62-26Aand B,Alveolar
distraction devices with internal hinges allow for vector adjustmentduring active
distraction osteogenesis.(Courtesy ofDr.M.Robinoy.)ABFIGURE62-27Placing the
extraosseous distrac-tor flush on the native bone will produce a poortrajectory to
the vector.FIGURE62-28A,Distraction osteogenesis(DO) was performed prior to
extraction ofthismalpositioned,ankylosed,previously hopelesslyavulsed tooth.B,DO
prior to extraction facili-tated proper crestal bone and gingival height.C,D,The DO
device is placed lateral to the trans-port disk in a cantilever fashion to optimize
bonestock for device placement.BACD
1294Part 8: Orthognathic Surgeryeasily managed.49,50Inaccurate planningmay lead to
poor vector trajectory ofthebone segments.Molding the regeneratecan alleviate this
problem.Careful follow-up is mandatory during the entire distrac-tion
process,including the time ofpost-distraction ossification.During this lattertime
period,the regenerate chamber isfully extended and is most under the influ-ence
oflocal muscle pull.Also,the periodofpost-distraction ossification is the besttime
to easily mold the regenerate.Wound dehiscence problems canoccur.Local wound
care,including antibi-otics and antimicrobial mouth rinses,alle-viates this
problem.Disk dancing can beperformed to allow the local wound site toheal after
which DO can begin.Occasion-ally,however,the distractor fixation screwheads become
visible,but this is not a con-cern.Overdistracting the segment cancompensate for
potential crestal bone lossfrom screw-head exposure.References1.Ilizarov GA.The
principles ofthe Ilizarovmethod.Bull Hosp Joint Dis 1988;48:1�16.2.Karp NS,McCarthy
JG,Schreiber JS,et al.Membranous bone lengthening:a serialhistologic study.Ann Plas
Surg 1992;29:2.3.Herford A,Audia F,Stucki-McCormick SU.Alveolar distraction
osteogenesis and vectorcontrol�a preliminary report.In:ArnaudE,Diner
PA,editors.Proceedings 3rd Inter-national Meeting on Craniofacial DO;2001Jun
14�16;Paris,France.Bologna (IT):Monduzzi;2001.4.Hoffmeister B,Marcks
CH,WolffKP.Thefloating bone concept in intraoral distrac-tion.J Craniomaxillofac
Surg 1998;26Suppl 1:76�81.5.Moses JJ.Sagittal distraction ofthe mandible:atechnique
for nerve preservation andcondylar axis stability.Proceedings 4thInternational
Congress ofOsteogenesis ofthe Facial Skeleton;2003 Jul 2�5;Paris,France.Bologna
(IT):Monduzzi;2003.6.Watzinger F,Wanschitz F,Rasse M,et al.Computer-aided surgery
in distractionosteogenesis ofthe maxilla and mandible.Int J Oral Maxillofac Surg
1999;28:171�5.7.McCarthy JG,Stelnicki EJ,Grayson BH.Dis-traction osteogenesis ofthe
mandible:a ten-year experience.Semin Orthod 1999;1:3�8.8.Grayson BH,Stucki-
McCormick SU,SantiagoPE.Vector ofdevice placement and trajec-tory ofmandibular
distraction.J CraniofacSurg 1998;8:473�80.9.Stucki-McCormick SU,Fox R,Mizrahi
R.Dis-traction osteogenesis for congenitalmandibular deformities.Atlas Oral
Maxillo-fac Surg Clin North Am 1999;7:85�110.10.Perlyn CA,Schmelzer RE,Sutera SP,et
al.Effect ofdistraction osteogenesis oftheFIGURE62-29A,Differential osteotomy
ofknife-edge ridges allows the flat buccal surface to becomethe crest ofthe ridge
after distraction osteogenesis.B,The distractor is placed with the vector
orientedvertically and slightly lingually.C�E,The bone cutis incomplete on the
lingual site and acts as a hinge.(Courtesy ofDr.M.Robiony.)ABCDEFIGURE62-30For
posterior mandibular sad-dle deformities,anL-shaped osteotomy is per-formed in the
alveolus with a monocorticalminiplate placed at the distal tip acting as ahinge.
(Courtesy ofDr.G.Milessi.)
Distraction Osteogenesis1295mandible on upper airway volume andresistance in
children with micrognathia.Plast Reconstr Surg 2002;109:1809�18.11.Denny
A,Kalantarian B.Mandibular distractionin neonates:a strategy to avoid tracheosto-
my.Plast Reconstr Surg 2002;109:896�904.12.Woodson BT,Hanson PR,Melugin
MB,GamaAA.Sequential upper airway changes dur-ing mandibular distraction for
obstructivesleep apnea.Otolaryngol Head Neck Surg2003;128:142�4.13.Smith
KS.Pediatric sleep apnea and treatmentwith distraction osteogenesis.Ann R Aus-
tralas Coll Dent Surg 2000;15:163�7.14.Cope JB,Yamashita J,Healy S,et al.Force
leveland strain patterns during bilateralmandibular osteodistraction.J Oral Max-
illofac Surg 2000;58:171�89.15.Cope JB,Samchukov ML,Cherkashin AM,etal.Biomechanics
ofmandibular distractororientation:an animal model analysis.JOral Maxillofac Surg
1999;57:952�64.16.Contasti G,Guerrero C,Rodriguez AM,LeganHL.Mandibular widening by
distractionosteogenesis.J Clin Orthod 2001;35:165�73.17.Bell WH,Gonzalez
M,Samchukov ML,Guer-rero CA.Intraoral widening and lengthen-ing ofthe mandible in
baboons by distrac-tion osteogenesis.J Oral Maxillofac Surg1999;57:548�63.18.Kewitt
GF,Van Sickels JE.Long-term effect ofmandibular midline distraction osteogene-sis
on the status ofthe temporomandibularjoint,teeth,periodontal
structures,andneurosensory function.J Oral MaxillofacSurg
1999;57:1419�26.19.Guerrero CA,Bell WH,Contasti GI,RodriguezAM.Intraoral mandibular
distractionosteogenesis.Semin Orthod 1999;5:35�40.20.Molina F.Combined maxillary
and mandibu-lar distraction osteogenesis.Semin Orthod1999;5:41�5.21.Padwa BL,Kearns
GJ,Todd R,et al.Simultane-ous maxillary and mandibular distractionosteogenesis with
a semiburied device.Int JOral Maxillofac Surg 1999;28:2�8.22.Moses JJ,Vega
L.Sagittal distraction ofthemandible.In:Arnaud E,Diner PA,editors.Proceedings 3rd
International Meeting onCraniofacial DO;2001 Jun 14�16;ParisFrance.Italy.Bologna
(IT):Monduzzi;2001.23.Polley JW,Figueroa AA.Rigid external distrac-tion:its
application in cleft maxillary defor-mities.Plast Reconstr Surg
1998;102:1360�74.24.Cohen SR.Midface distraction.Semin Orthod1999;5:52�8.25.Ahn
JG,Figueroa AA,Braun S,Polley JW.Biome-chanical considerations in distraction
oftheosteotomized dentomaxillary complex.Am JOrthod Dentofacial Orthop
1999;116:264�70.26.Liou EJ,Chen PK,Huang CS,Chen YR.Inter-dental distraction
osteogenesis and rapidorthodontic tooth movement:a novelapproach to approximate a
wide alveolarcleft or bony defect.Plast Reconstr Surg2000;105:1262�72.27.Costantino
PD,Buchbinder D.Mandibular dis-traction
osteogenesis:types,applications,andindications.J Craniofac Surg
1996;7:404�7.28.Guerrero CA,Gonzalez M.Intraoral bonetransport by distraction
osteogenesis inmandibular reconstruction.In:Arnaud E,Diner PA,editors.Proceedings
4th Interna-tional Congress ofOsteogenesis oftheFacial Skeleton;2003 Jul
2�5;Paris,France.Bologna (IT):Monduzzi;2003.29.Herford AS.Use ofa plate guided
distractiondevice for transport distraction osteogene-sis ofthe mandible.In:Arnaud
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Facial Skeleton;2003 Jul 2�5;Paris,France.Bologna (IT):Monduzzi;2003.30.Stucki-
McCormick SU,Fox R,Mizrahi R,Erickson M.Transport distraction:mandibular
reconstruction.Atlas Oral Max-illofac Surg Clin North Am 1999;7:65�84.31.Gantous
A,Phillips JH,Catton P,Holmberg D.Distraction osteogenesis in the irradiatedcanine
mandible.Plast Reconstr Surg1994;93:164�8.32.Aronson J.Temporal and special
increases inblood flow during distraction osteogenesis.Clin Orthop Rel Res
1994;301:124�31.33.Klesper B,Lazar F,Siessegger M,et al.Verticaldistraction
osteogenesis offibula trans-plants for mandibular reconstruction � apreliminary
study.J Craniomaxillofac Surg2002;30:280�5.34.McCarthy JG,Stelnicki EJ,Mehrara
BJ,Lon-gaker MT.Distraction osteogenesis ofthecraniofacial skeleton.Plast Reconstr
Surg2001;107:1812�27.35.Stucki-McCormick SU,Fox RM,Mizrahi RD.Reconstruction ofa
neocondyle usingtransport distraction osteogenesis.SeminOrthod
1999;5:59�63.36.Piero C,Alessandro A,Giorgio S,et al.Com-bined surgical therapy
oftemporo-mandibular joint ankylosis and secondarydeformity using intraoral
distraction.JCraniofac Surg 2002;13:401�10.37.Chin M.Distraction osteogenesis for
dentalimplants.Atlas Oral Maxillofac Surg ClinNorth Am 1999;7:41�63.38.Jensen
OT,Cockrell R,Kuhike L,Reed C.Ante-rior maxillary alveolar distraction osteoge-
nesis:a prospective 5-year clinical study.IntJ Oral Maxillofac Implants
2002;17:52�68.39.Block MS,Gardiner D,Almerico B,Neal C.Loaded hydroxylapatite-
coated implantsand uncoated titanium-threaded implantsin distracted dog alveolar
ridges.Oral SurgOral Med Oral Pathol Oral Radiol Endod2000;89:676�85.40.Robiony
M,Polini F,Costa F,Politi M.Osteo-genesis distraction and platelet-rich plasmafor
bone restoration ofthe severely atroph-ic mandible:preliminary results.J
OralMaxillofac Surg 2002;60:630�5.41.Millisi W,Millisi-Schobel G.Alveolar distrac-
tion osteogenesis ofthe mandible.In:Arnaud E,Diner PA,editors.Proceedings4th
International Congress ofOsteogenesisofthe Facial Skeleton;2003 Jul
2�5;Paris,France.Bologna (IT):Monduzzi;2003.42.Zechner W,Bernhart T,Zauza K,et
al.Multi-dimensional osteodistraction for correc-tion ofimplant malposition in
edentuloussegments.Clin Oral Implants Res 2001;12:531�8.43.Stucki-McCormick
SU,Moses JJ,Robinson R,et al.Alveolar distraction devices.In:Jensen,editor.Alveolar
distraction osteoge-nesis.Carol Stream (IL):Quintessence Pub-lishing
Co.Inc;2002.p.41�58.44.Chin M.Alveolar distraction osteogenesis withendosseous
devices in 175 cases.In:ArnaudE,Diner PA,editors.Proceedings 3rd Inter-national
Meeting on Craniofacial DO;2001Jun 14�16;Paris,France.Bologna
(IT):Monduzzi;2001.45.Stucki-McCormick SU,Moses JJ.Vertical alve-olar distraction
ofthe posterior mandible.In:Jensen,editor.Alveolar distractionosteogenesis.Carol
Stream (IL):Quintes-sence Publishing Co.;2002.p.89�94.46.Millesi G,Klug C,Millesi
W,et al.Vertical dis-traction osteogenesis in the mandible com-bined with L-shaped
osteotomy and guidedbone regeneration.Cranio-maxillo-facialdistraction.Graz
(AU):University ofGraz;2002.47.Hidding J,Lazar F,Zoller JE.The Cologne con-cept on
vertical distraction osteogenesis.In:Arnaud E,Diner PA,editors.Proceedings3rd
International Meeting on CraniofacialDO;2001 Jun
14�16;Paris,France.Bologna(IT):Monduzzi;2001.48.Hidding J,Lazar F,Zoller JE.Initial
outcome ofvertical distraction osteogenesis oftheatrophic alveolar ridge.Mund
KieferGesichtschir 1999;3 Suppl 1:79�83.49.Garcia AG,Martin MS,Vila PG,Maceiras
JL.Minor complications arising in alveolar dis-traction osteogenesis.J Oral
MaxillofacSurg 2002;60:496�501.50.Grayson BH,Santiago PE.Treatment planningand
biomechanics ofdistraction osteogene-sis from an orthodontic
perspective.SeminOrthod 1999;5:9�24.
CHAPTER 63Surgical and Nonsurgical ManagementofObstructive Sleep
ApneaB.D.Tiner,DDS,MDPeter D.Waite,MPH,DDS,MDSleep and dreaming have been sources
ofmystery and fascination since biblicaltimes.Sleep consists ofinevitably recur-
ring episodes ofreadily reversible relativedisengagement from sensory and
motorinteraction with the environment.1 Thefunction ofsleep remains a
mystery,andonly in recent years has there beenresearch into specific symptom
complexesand causes ofsleep disorders.In 1979 theAssociation ofSleep Disorders
Center andthe Association for the Psychophysiologi-cal Study ofSleep published the
first clas-sification ofsleep and arousal disorders.2 Modern sleep research became
possiblein 1924 when Hans Berger,a German psy-chiatrist,described the recording
ofhumanelectroencephalography.3Loomis and col-leagues in 1935 published a
quantitativedescription ofthe four levels ofsleep basedon electroencephalogram
(EEG) character-istics.4,5The historic discovery ofa cyclicphase ofsleep
characterized by rapid conju-gate eye movements was made by Aserinskyand Kleitman
in 1953.6Subsequent studiesconfirmed this to be a very active phase ofsleep that
correlated closely with dreaming.7Normal Sleep StagesNormal sleep architecture
includes bothquiet sleep (nonrapid eye movement [non-REM] sleep) and active sleep
(rapid eyemovement [REM] sleep).Non-REM sleepconsists offour stages which are based
large-ly on the original criteria ofLoomis and col-leagues.4,5Stage 2 predominates
and com-prises 45 to 50% oftotal sleep time.Thefour stages ofnon-REM sleep
representprogressively deeper sleep marked by theincreasing appearance ofhigh-
amplitudeslow waves in stages 3 and 4,which are col-lectively known as delta
sleep.Non-REMsleep is characterized by a general slowing ofall levels
ofactivity.Progression through allfour stages ofnon-REM sleep usually occursrapidly
after sleep onset.REM sleep occursafter non-REM sleep has been established,and the
first REM period normally occursafter 70 to 90 minutes ofnon-REM sleep.The average
duration ofa period ofREMsleep is about 20 minutes.The initial REMperiod ofthe
night is usually very brief,butsubsequent REM periods become longer.During an
average night ofREM/non-REMcycle progression,4 to 6 REM periods nor-mally occur at
intervals of60 to 90 minutes.REM sleep occupies about 20 to 25% oftotal sleep time
in a healthy young adult.REM sleep EEG patterns look very similarto those seen
during the wakeful state.Gen-eralized skeletal muscle atonia (except forthe ocular
muscles) and absence ofreflexiveactivity are other features unique to
REMsleep.Marked physiologic changes alsooccur during REM sleep.Temperature,blood
flow,and oxygen use in the brain areincreased.Heart rate,blood
pressure,andrespiration show dramatic fluctuations andincrease in average
rate.During sleep the control ofrespirationis influenced by two systems:the
metabol-ic control system and the behavioral con-trol system.8The influences
ofhypoxia andhypercarbia on ventilation are the predom-inant components ofthe
metabolic controlsystem ofrespiration.This system predom-inantly controls
respiration during non-REM sleep.The behavioral control systemgoverns respiration
during voluntary activ-ities,such as swallowing or speaking,andmay suppress the
ventilatory response tometabolic stimuli.During REM sleep,theeffects ofhypoxia and
hypercarbia on ven-tilation are much less than during non-REM sleep,and the
behavioral control sys-tem may predominate.With a bluntedresponse to hypoxia and
hypercarbia,irregular respirations,and decreased skele-tal muscle tone ofthe upper
airway mus-cles during REM sleep,an episode ofpar-tial or complete airway
obstruction withapnea or hypopnea may occur.Sleep Apnea SyndromeThe sleep apnea
syndrome is a disordercharacterized by abnormal breathing in
1298Part 8: Orthognathic Surgerysleep and sleep fragmentation.At least 30episodes
ofapnea occur during 7 hours ofnocturnal sleep in these patients.Apnea isdefined as
the cessation ofairflow fromthe nostrils and mouth for at least 10 sec-onds.These
apneic episodes can result inhypoxemia,hypercarbia,systemic and pul-monary
hypertension,polycythemia,corpulmonale,bradycardia,and cardiac dys-rhythmias.Sudden
death has occurred inpatients with sleep apnea.Throughout thenight the alternating
episodes ofapneaand arousal from sleep may occur as fre-quently as 400 to 600
times,with each typ-ical apnea episode lasting 15 to 60 seconds.These episodes can
amount to as much as50% ofa night�s sleep.The frequent dis-ruption results in
symptoms similar tosleep deprivation.These include excessivedaytime
sleepiness,fatigue,depression,personality changes,and impotence.Thesedysfunctional
symptoms are common pri-mary complaints and are often the reasonpeople seek
treatment.Epidemiologic data suggest that sleepapnea syndrome may be quite
common,particularly in its milder forms.In fact,obstructive sleep apnea is the
second mostcommon sleep disorder,insomnia beingthe most common.A 1993 Sleep Commis-
sion Report estimated that 20 millionAmericans have sleep apnea,with themajority
being undiagnosed and untreat-ed.9 The exact prevalence is unknown,butsleep apnea
syndrome may affect up to 2to 3% ofadult males.8In certain popula-tions the
prevalence may be as high at10%.Most patients are diagnosed after age40,but sleep
apnea can occur at any age.There is a strong male predilection,withmen outnumbering
women by up to 8 to 1until menopause.This implies a hormonalinfluence.The cost for
diagnosis and treat-ment ofthis sleep disorder accounts forover $50 million (US) in
hospital bills eachyear.Overall,sleep disorders and sleepi-ness cost the United
States economy aminimum of$15.9 billion (US) in directcosts each
year.10ClassificationCentral sleep apnea,obstructive sleepapnea,and mixed sleep
apnea are the varia-tions ofapnea that occur in the syndrome.In central sleep
apnea,respiratory muscleactivity ceases simultaneously with airflowat the mouth and
nostrils.11This disorder isfound in patients with central nervous sys-tem (CNS)
insufficiency that affects the out-flow ofneural output from the respiratorycenter
to the diaphragm and other musclesofrespiration.CNS disorders associatedwith
central sleep apnea include brainstemneoplasms,brainstem
infarctions,bulbarencephalitis,bulbar poliomyelitis,spinalsurgery,cervical
cordotomy,and primaryidiopathic hypoventilation.Patients with central sleep apnea
havebeen treated with some success by usingrespiratory-stimulating drugs such
astheophylline,progesterone,and acetazo-lamide.In severe central
apnea,modalitiesoftreatment have included phrenic nervepacemaker implantation to
ensure regularrespiration during sleep and nocturnalmechanical ventilation with a
negativepressure ventilator for more severe cases.There are no simple and
convenient meth-ods oftreatment for mild central apnea.The most common type
ofsleepapnea by far is obstructive.This is charac-terized by sleep-induced
obstruction ofthe upper airway that results in cessationofairflow with preservation
ofrespiratoryeffort,respiratory center drive,anddiaphragmatic contraction.11Mixed
sleep apnea is a combination ofcentral and obstructive apnea.This patternbegins
with an episode ofcentral apneawith no airflow detectable at the mouthand nostrils
and no respiratory muscleactivity.The pattern ends with an episodeofobstructive
apnea with only cessation ofairflow at the mouth and nostrils.11Differential
DiagnosisProfound hypersomnolence is a character-istic feature ofboth sleep apnea
and nar-colepsy;hence,they are often confused.However,unlike sleep
apnea,narcolepsyaffects both sexes equally,with mostpatients experiencing the onset
ofsymp-toms around or shortly before puberty.12The first symptom to appear with
narcolep-sy is usually excessive daytime somnolence(EDS).The sleep attacks can
range frommild to severe and are characterized by thesudden onset ofoverwhelming
sleepinessthat lasts 30 seconds to 20 minutes.Follow-ing briefnaps,the narcoleptic
usually feelsrefreshed and relatively free from disturb-ing symptoms for up to 2
hours.Seriousaccidents,marital discord,and the inabilityto hold jobs frequently
result from thesesleep attacks.Another feature ofnarcolepsyis the abrupt loss
ofmuscle control (cata-plexy).Attacks can be particularly dis-abling,because they
are characteristicallyprecipitated by emotional experiences suchas
laughter,anger,or excitement.Addition-al associated symptoms ofnarcolepsyinclude
sleep paralysis and hypnagogic hal-lucinations.Sleep paralysis is the
skeletalmuscle atonia ofREM sleep persisting intothe awake state.Hypnagogic
hallucinationsare REM sleep imagery occurring whilefalling asleep.Patients are
sometimes mis-diagnosed as schizophrenic ifhypnagogichallucinations are
prominent.Diagnosis ofnarcolepsy is made by doc-umenting sleep-onset REM periods
duringa nocturnal polysomnography.12In normalsleep REM sleep is usually not seen
untilabout 70 to 90 minutes into sleep.The clin-ical features ofnarcolepsy probably
repre-sent abnormal manifestations ofREM sleep.Treatment modalities for
narcolepsyinclude behavioral therapies,CNS stimu-lants,tricyclic antidepressants,or
mono-amine oxidase inhibitors (only in resistantcases) and L-tryptophan.13Other
disorders that may be confusedwith sleep apnea syndrome include sleep-related
abnormal swallowing syndrome,gastroesophageal reflux,depression,alco-hol or drug
dependence,and sleep-relatednocturnal myoclonus.
Surgical and Nonsurgical Management ofObstructive Sleep Apnea1299History
ofObstructive Sleep Apnea SyndromeObstructive sleep apnea has a remarkablyshort
history considering the incidenceand disabling symptoms ofthe syn-drome.Burwell and
colleagues publishedthe first description ofthe syndrome in1956.14Their report
compared an obese,somnolent,polycythemic patient with thesleepy red-faced
boy,Joe,in the CharlesDickens novel The Posthumous Papers ofthe Pickwick
Club(1837).However,Bur-well and colleagues did not link theirpatient�s excessive
daytime sleepiness tonocturnal sleep fragmentation.In 1966,Gastaut and colleagues
were the firstinvestigators to demonstrate repeatedapneas in pickwickian patients
duringsleep.15They correctly attributed theexcessive daytime somnolence in
thesepatients to nocturnal sleep fragmentationcaused by repeated apneas.The
misdiagnosis ofnarcolepsy inpatients with sleep apnea and the generalskepticism
ofexcessive daytime somno-lence as a valid clinical sign are the twomain reasons
sleep apnea syndrome wasoverlooked for so long.Clinical ManifestationsSleep apnea
patients present with a vari-ety ofsymptoms and clinical manifesta-tions.Patients
with obstructive sleepapnea most often complain ofEDS.Thepatients may experience
serious social,economic,and emotional problems fromthe EDS associated with this
disorder.The uncontrollable desire to sleep maypredispose the patients to
occupationalor automobile accidents.Almost all patients or their bed part-ners give
a history ofheavy,loud snoringwhich has usually been present for sever-al years
before the EDS was noted.Thesnoring is produced from the passage ofair through the
oropharynx causingvibrations ofthe soft palate.Typically thesnoring is interrupted
periodically byapneic episodes that last 30 to 90 seconds.Bed partners usually
describe an episodein which the snoring stops and thepatient seems to stop
breathing for a peri-od oftime.A loud snort followed by ahyperventilation usually
signals an end tothe apneic episode.Other common presenting complaintsare morning
headaches and nausea thatresult from the hypercarbia which developswith the
hypoventilatory episodes.Depres-sion,personality changes,and
intellectualdeterioration may also develop.The systemic hypertension that is
acommon finding in obstructive sleepapnea may be related to the
catecholaminerelease triggered by the systemic hypox-emia.In more advanced severe
cases,pul-monary hypertension,polycythemia,andcor pulmonale may develop and
becomelife threatening.However,most patientsdo not manifest these
disturbancesbecause their ventilation during wakefulperiods is sufficient to
prevent these com-plications ofchronic hypoxia.A prominent sinus dysrhythmia
iscommonly associated with the apneicepisodes.The extent ofbradycardia isdirectly
proportional to the severity oftheoxygen desaturation.The greatest degreeofcardiac
slowing occurs in obstructiveapneas in which a M�ller maneuver is per-
formed.Increased vagal efferent tonemediates the bradycardia.The development
ofsevere and life-threatening medical complications fromthe apneic events clearly
depends on thefrequency,duration,and degree ofhypox-emia and associated
hypertensive response.Physical FindingsA major feature ofobstructive sleep apneais
obesity.The increased body weight cor-relates with increased frequency ofapneaand
the severity ofhypoxemia.However,the morbidly obese,somnolent,hyperven-tilating
patient with cor pulmonale repre-sents only a small number ofsleep
apneapatients.Lower BMI (body mass index)patients with obstructive sleep apnea
oftenhave more abnormal cephalometrics thanobese people.16,17Obstruction can occur
at a number ofpoints in the airway.Physical examina-tion ofthese patients may
reveal hyper-trophy ofthe tonsils or adenoids,retrog-
nathia,micrognathia,macroglossia,deviation ofthe nasal septum,a thickshort neck,or
tumors in the nasopharynxor hypopharynx.Both primary and sec-ondary medical
conditions are associatedwith obstructive sleep apnea,owing totheir effects on the
upper airway anato-my.These may include temporo-mandibular joint
disorders,myxedema,goiter,acromegaly,and lymphoma.Most patients with classic
obstructivesleep apnea have no identifiable craniofa-cial anomaly.However,there
does appearto be a significant subpopulation ofsleepapnea patients with
craniofacial anom-alies.18,19Lowe and colleagues found sever-al alterations in
craniofacial form in sub-jects with obstructive sleep apnea that mayreduce the
dimensions ofthe upper airwayand subsequently impair stability oftheupper
airway.20A sample of25 adult malepatients with moderate to severe obstruc-tive
sleep apnea showed a posteriorly posi-tioned maxilla and mandible,a steepocclusal
plane,overerupted maxillary andmandibular teeth,proclined incisors,asteep
mandibular plane,a large gonialangle,increased upper and lower facialheights,a
posteriorly placed pharyngealwall,and an anterior open bite in associa-tion with a
long tongue.20Bacon and col-leagues evaluated 32 patients with sleepapnea by
cephalometry and demonstratedan anteroposterior shortening ofthe cra-nial base,a
posterior facial compressionwith narrowing ofthe pharyngeal airway,and an increased
lower facial height.18Rivlin and colleagues reported on nineobstructive sleep apnea
patients with pos-terior displacement ofthe mandible.21Thenumber ofapneas
correlated with the totalposterior displacement.21
1300Part 8: Orthognathic SurgeryDiagnosisPhysical ExaminationA diagnostic
evaluation includes a thor-ough history and physical examination,fiberoptic
endoscopy,radiologic evalua-tion,and polysomnography.Little addi-tional information
can be gained fromroutine laboratory tests.Except in severecases,pulmonary function
tests,electro-cardiogram (ECG),arterial blood gases,and chest radiographs are often
normalduring wakefulness in sleep apnea patients.Other diagnostic tests that may
aid inevaluating sleep apnea patients include acomplete blood count (CBC),serum
elec-trolytes,and thyroid function tests.Sec-ondary polycythemia may be revealed by
aCBC,and nocturnal carbon dioxide reten-tion may be reflected by increased bicar-
bonate levels.Hypothyroidism,a con-tributing cause ofsleep apnea,may beidentified
from thyroid function studies.After a complete history is obtainedfrom the patient
and his or her bed part-ner,a complete clinical examination
ofthemouth,nasal,pharyngeal,and laryngealareas is performed.The emphasis
oftheclinical examination should be the identi-fication ofanatomic abnormalities
thatmay contribute to or produce obstructionduring sleep.The nose is examined for
adeviated nasal septum and enlargement ofthe turbinates.Micrognathia,retrog-
nathia,and macroglossia may be noted inexamination ofthe oral cavity.Occasional-ly
masses or tumors in the nasopharynx orhypopharynx may be noted.In the phar-
ynx,adenotonsillary hypertrophy,a longsoft palate,a large base ofthe
tongue,andexcess pharyngeal mucosa are potentialcauses ofobstruction.The larynx is
exam-ined for vocal cord webs and paralysis ofthe vocal cords.Obstructive sleep
apneapatients may present with any combina-tion ofthese anatomic
abnormalities.After topically anesthetizing the nasalcavity and pharynx,a
fiberoptic endo-scope is introduced through the nose.Insequential fashion the
nasopharynx,oropharynx,hypopharynx,and larynx areexamined.The appearance and
position ofthe soft palate,base oftongue,and lateralpharyngeal walls are
evaluated.Changes inthe position ofthe base ofthe tongue suchas forward movement
with protrusion ofthe mandible are noted.The appearance ofthe pharyngeal airway and
degree ofpha-ryngeal wall collapse is noted while thepatient performs a modified
M�llermaneuver.To accomplish this maneuverthe patient attempts to inspire with
themouth and nose closed.Increased negativepressure in the pharynx will
demonstratethe point ofcollapse.Cephalometric ExaminationA lateral cephalogram is
routinely obtainedin the radiologic evaluation ofsleep apneapatients (Figure 63-
1).Cephalometricanalysis is performed to identify any skele-tal and soft tissue
abnormalities that mayexist.The advantages ofcephalometry areits easy access,low
cost,and minimal radia-tion exposure.However,it should be recog-nized that there
are obvious limitations ofevaluating a three-dimensional area with atwo-dimensional
lateral cephalometry.Mandibular or maxillary position canbe evaluated by a number
ofmethodsincluding the SNA and SNB angles.Patientswith skeletal deficiencies are
more likely tohave obstruction at the base ofthe tongueor at the level ofthe soft
palate.Riley andcolleagues determined that obstructivesleep apnea patients had an
inferiorly posi-tioned hyoid bone,a longer-than-normalsoft palate,and a narrowing
at the base ofthe tongue.22,23The position ofthe hyoidbone is determined by drawing
a perpen-dicular line from the mandibular plane(MP) through the hyoid bone
(H).Themean MP-H distance for normal subjects is15.4 �3 mm (see Figure 63-1).The
posi-tion ofthe hyoid bone is important becauseit serves as a central anchor for
the musclesofthe tongue and thereby partly deter-mines tongue position.Soft palate
length ismeasured from a line drawn from posteriornasal spine (PNS) to the tip
ofthe softpalate shadow (P).The mean PNS-P dis-tance in normal subjects is 37 �3
mm.Pos-terior airway space is determined by a linedrawn from point B through the
gonion(Go) intersecting the base ofthe tongueand the posterior pharyngeal
wall.Figure63-2 demonstrates change in posterior air-way spaces following
maxillomandibularadvancement.Mean posterior airway spacein normal subjects was
determined to be 11�1 mm.Lower face height is measuredfrom the anterior nasal spine
(ANS) to thementon (Me).There is no absolute valuefor this measurement in
obstructive sleepapnea patients.However,some studies haveSNBaPNSPHPASGoMPGnSNA
82SNB 80PAS 11PNS-P 37MP-H 15BaS N 129BAANSFIGURE63-1Cephalometric screening used
forinitial evaluation ofpatients with obstructive sleepapnea syndrome.A = A point;
ANS = anteriornasal spine; B = B point; Ba = basion; Gn =gnathion; Go = gonion; H =
hyoid; MP =mandibular plane; N = nasion; P = palate; PAS =posterior airway space;
PNS = posterior nasalspine; S = sella; SNA = sella-nasion�A point; SNB= sella-
nasion�B point.Adapted from Tiner BD,Waite,PD.Surgical and nonsurgical manage-ment
ofobstructive sleep apnea.In: Peterson LJ,Indresano AT,Marciani RD,Roser
SM.Principlesoforal and maxillofacial surgery.Vol.3.Philadel-phia (PA):
J.B.Lippincott Company; 1992.p.1535.
Surgical and Nonsurgical Management ofObstructive Sleep Apnea1301shown an increased
lower face height and ashortened cranial base with obstructivesleep apnea
patients.18Computed TomographyComputed tomography (CT) is an alterna-tive to
cephalometry and has been used toprovide a quantitative assessment oftheupper
airway at various levels.With three-dimensional CT reconstructions,Lowe
andcolleagues found obstructive sleep apneapatients with larger tongue surface
areas andsmaller airway surface areas.24Haponik andcolleagues found significantly
decreasedcross-sectional areas ofthe nasopharynx,oropharynx,and hypopharynx in
obstruc-tive sleep apnea patients when comparedwith control subjects by using CT
scan-ning.25Some authorities feel that the airwaycan only be assessed by a CT
scan.However,Riley and colleagues compared patients whohad three-dimensional CT
scans and founda statistically significant correlation betweenthe posterior airway
space (PAS) measuredon the lateral cephalogram and the volumeofthe pharyngeal
airway measured on CTscans.23,26Waite and Villos demonstrated byhelical CT analysis
that maxillomandibularadvancement increases both anteroposteri-or and lateral
dimension ofthe airway at alllevels from nasopharynx to hyoid.27Manystudies are
currently being done to deter-mine the effects ofpatient position andchanges in
airway.A cephalogram and a CTscan are static evaluations at a fixed time ofa
dynamic system and they should beviewed as only part ofthe overall evaluationofthe
patient.PolysomnographyNocturnal polysomnography remains thegold standard for
establishing the diagno-sis ofsleep apnea,quantitating its severity,and determining
the success oftreatmentmodalities.The study is performed in asleep laboratory and
the patient�s sleep ismonitored overnight.At least 4 hours oftotal sleep time must
be recorded for adiagnostic study.The components ofthepolysomnogram include the
EEG,electro-oculogram (EOG),electromyogram(EMG),and electrocardiogram
(ECG,leadV2).Sleep staging and architecture aredetermined by the EEG,EOG,and
EMGtracings.Potentially lethal cardiac dys-rhythmias are detected by the ECG.Oxy-
gen saturation is measured by ear oxime-try.A 5% or greater decrease in
arterialoxygen saturation from baseline is signifi-cant during episodes ofapnea or
hypop-nea.Respiratory effort and breathing pat-tern are measured using
respiratoryinductive plethysmography or by measur-ing intrathoracic pressure
changes with anesophageal balloon catheter.The distinc-tion between an episode
ofcentral apneaand obstructive apnea is made by correlat-ing airflow at the nose
and mouth withmovement ofthe abdominal and thoracicrespiratory muscles.Central
apnea occursifboth airflow and respiratory musclemovement stop
simultaneously.Anepisode ofobstructive apnea occurs whenairflow at the mouth and
nose ceases butrespiratory muscles in the abdomen andthorax continue to move
dysfunctionally.Ofparticular interest are the numberofrespiratory events (apneas
and hypop-neas),the number ofoxygen desaturationsbelow 90%,and the lowest oxygen
desatu-ration.The respiratory disturbance index(RDI) can be calculated from these
data:RDI = Apneas + Hypopneas � 60Total sleep timeAn RDI greater than 5 is
consideredabnormal and an RDI greater than 20 isconsidered clinically
significant,becauseEDS usually does not occur below thislevel.Obstructive sleep
apnea alsobecomes clinically significant when oxy-gen desaturation events fall
below 85%.Site ofObstructionFollowing a complete presurgical evalua-tion,each
patient is grouped according tothe site ofobstruction:type I,oropharynx;type
II,oropharynx and hypopharynx;type III,hypopharynx.In a review of40obstructive
sleep apnea patients,Riley andcolleagues found the majority ofpatientshad a type II
obstruction (soft palate andbase oftongue).28The mandible,base oftongue,hyoid,and
pharyngeal wall are intimately relatedby their muscular and ligamentous attach-
ments.The mandible is related to the baseofthe tongue by the genioglossus
muscle.The tongue,through multiple muscularand connective tissue attachments,is
relat-ed to the hyoid bone and to the mandible insuch a way that retraction ofthe
mandibleresults in a narrowing ofthe airway andposterior movement ofthe tongue.Com-
pensatory mechanisms exist in non-sleepapneic patients to prevent occlusion
oftheairway.However,in sleep apneic patients,these mechanisms do not exist or
areunable to compensate adequately.SConNAAPogPreoperativePostoperativeA10
mmFIGURE63-2Change in posterior airwayspace following maxillary and
mandibularadvancement.A = A point; AA = anterior edgeofatlas; Con = condylion; N =
nasion; Pog =Pogonion; S = sella.Adapted from Tiner BD,Waite,PD.Surgical and
nonsurgical manage-ment ofobstructive sleep apnea.In: Peterson LJ,Indresano
AT,Marciani RD,Roser SM.Principlesoforal and maxillofacial surgery.Vol.3.Philadel-
phia (PA): J.B.Lippincott Company; 1992.p.1536.
1302Part 8: Orthognathic SurgeryObstruction ofthe upper airway isprimarily
prevented by the action ofthepharyngeal dilating muscles contracting inphase with
respiration.Reduced muscletone is normal and prominent duringREM
sleep.However,obstructive sleepapnea patients may have a significantreduction in
muscle activity during non-REM sleep so that the pharynx becomesnarrower and airway
resistance increases.In patients with abnormal skeletal devel-opment the reduction
in size ofthe restingairway may predispose them to upper air-way obstruction during
sleep.The patency ofthe upper airway isdetermined by a balance between the pha-
ryngeal musculature and the negativeoropharyngeal pressures that are generat-ed
from resistance to airflow in thenasopharynx.Because the airway ofobstructive sleep
apnea patients is unsta-ble even at rest,any structural narrowingofthe airway will
eventually hinder themuscular component ofthe balance.Col-lapse ofthe airway in
obstructive sleepapnea is primarily a result ofhigh intralu-minal negative
pressures associated withhypotonic pharyngeal wall musculatureand disproportionate
anatomy in eitherthe oropharynx or hypopharynx or both.Disproportionate anatomy
includes anycombination oflarge base oftongue,longsoft palate,narrow mandibular
arch,shal-low palatal arch,or retrognathic mandible.Medical TreatmentOnce the
diagnosis has been confirmed,the treatment approach for sleep apnea isdetermined by
the severity ofthe physio-logic derangements and the predominanttype
ofapnea.Regardless ofthe predomi-nant type ofapnea present,all patientsshould be
cautioned that certain drugsmay precipitate or exacerbate obstructivesleep
apnea.Alcohol and other centralnervous system depressants have beenshown to
aggravate sleep apnea and evento precipitate apnea and oxygen desatura-tions in
normal persons.29Weight loss and nasal continuouspositive airway pressure are the
initialmodes oftherapy that should be initiatedin obese patients with moderate
obstruc-tive sleep apnea.A study of16 patientswho lost an average of20 kg showed
fewerapneas,reduced oxygen desaturations,and less daytime sleepiness than a
controlgroup ofpatients who did not loseweight.30Many patients can relate
weightgain in preceding years to an increase inseverity oftheir obstructive sleep
apneasymptoms.Unfortunately weight loss bydietary measures is seldom
sustained,andobstructive sleep apnea symptoms recurwith weight gain.Riley and
colleaguesfound that 47 of50 obstructive sleepapnea patients who were between 20
and100% overweight at the time ofdiagnosishad regained all the weight they had ini-
tially lost 5 to 7 years later.31The role ofoxygen therapy in the treat-ment
ofsleep apnea is controversial.In astudy by Motta and
Guilleminault,theadministration ofoxygen increased theduration ofapneic episodes
and led toworsening ofacidosis and hypercarbiaduring both REM and non-REM sleep.32
Itis unknown how many oftheir patientshad chronic obstructive lung disease.Other
studies have shown that supplemen-tal oxygen therapy consistently reduced
theseverity ofoxygen desaturation anddecreased the frequency ofapnea.33,34The
combined experience ofthesereports suggests that oxygen therapy lim-ited to a flow
rate of2 L/min can be usedsafely in most obstructive sleep apneapatients and will
produce beneficialeffects on respiration.The dangers ofprofound hypoxemia are
greater than theconcerns ofprolonged apnea,acidosis,and hypercarbia.The effects
ofoxygentherapy on a patient with severe airwayobstruction or chronic respiratory
acido-sis should be monitored with oximetryor polysomnography.Several drugs have
been used in thetreatment ofobstructive sleep apnea syn-drome with variable
results.The carbonicanhydrase inhibitor acetazolamide stimu-lates respiration by
producing a metabolicacidosis.This drug reduced the number ofapneas and decreased
the severity ofoxygendesaturations in a group ofpatients withcentral sleep
apnea.35However,in severalcases,acetazolamide given to patients withmild
obstructive sleep apnea producedmore frequent obstructive apneas
oflongerduration.36Therefore,acetazolamide isprobably not indicated in the
managementofobstructive sleep apnea syndrome.Some patients with obstructive
sleepapnea benefit from the respiratory stimu-lant effect ofprogesterone,especially
thosewith the obesity-hypoventilation syn-drome.37�40Progesterone increases alveo-
lar ventilation and improves oxygenation,but its effect on frequency ofapnea is
lim-ited.Major side effects that limit its long-term use include decreased
libido,alope-cia,and impotence.The tricyclic antidepressant protripty-line is the
most effective and best studieddrug for the treatment ofobstructive sleepapnea.41In
a study of12 patients,Smithand colleagues showed a reduction inapnea frequency and
oxygen desaturationduring non-REM sleep,in addition to adecrease in REM
sleep.42Protriptyline pro-duces its beneficial effect by a preferentialstimulation
ofupper airway muscle toneand by decreasing the percentage oftimespent in REM
sleep,thereby reducing themore severe REM-related apneas.Anti-cholinergic side
effects such as dry mouth,constipation,urinary retention,and impo-tence are
frequent and limit its use.Oral AppliancesThe use ofa variety ofprosthetic devices
isanother approach to treatment.Thenasopharynx and the posterior tongue arethe two
anatomic areas ofconcern.Inser-tion ofa nasopharyngeal airway has beenused to
prevent upper airway occlusion atthe level ofthe soft palate.43The AmericanSleep
Disorders Association recommends
Surgical and Nonsurgical Management ofObstructive Sleep Apnea1303that oral
appliances may be used in patientswith primary snoring,mild obstructivesleep
apnea,or in patients with moderate tosevere obstructive sleep apnea who refuseor
are intolerant ofnasal continuous posi-tive airway pressure.The Food and
DrugAdministration has granted market clear-ance for 32 oral appliances for snoring
butonly 14 ofthese have received market clear-ance for treatment ofsnoring and
obstruc-tive sleep apnea (Table 63-1).44 Commonside effects oforal appliance
therapyinclude excessive salivation,xerostomia,soft tissue irritations,transient
discomfortofthe teeth and temporomandibular joint(TMJ),and temporary minor
occlusalchanges.Uncommon,more serious com-plications include permanent
occlusalchanges and significant TMJ discomfort.Removable anterior
repositioningsplints have been used somewhat success-fully to temporarily advance
the mandiblewhile passively bringing the tongue for-ward with it.44�46The optimal
amount offorward movement is between 50 and 75%ofthe patient�s maximum protrusive
dis-tance.An important design feature ofthese devices is that the appliance
mustmaintain the mandible in the forwardposition while the patient is
asleep.Bearand Priest used a mandibular anteriorrepositioning splint to determine
whethersurgical advancement ofthe mandiblewould have any lasting and positive
effecton a patient�s obstructive sleep apnea.47A tongue-retaining device (TRD)
thatpulls the tongue forward without movingthe mandible forward has also been
usedsuccessfully in some patients with mild tomoderate obstructive sleep
apnea.48,49TheTRD functions by placing the tongue intoa cup or bubble positioned
between theanterior teeth.Surface adhesion holds thetongue in place and the
appliance requiresthat the patient�s jaw remains partiallyopen.One disadvantage
ofthe TRD is thatthe tongue is not always held forwardbecause surface tension ofthe
tongue inthe bubble is lost after a time.The TRDand mandibular anterior
repositioningsplints both force nasal breathing,whichcan be difficult for patients
with inade-quate nasal airways.Arguably,the most researched oralappliance is the
Klearway titratable appli-ance developed by Alan Lowe,DMD,PhD,atthe University
ofBritish Columbia,Canada.It features a maxillary and mandibular com-ponent
connected with an adjustable screwmechanism (Figure 63-3).The componentsare made
ofa thermoactive acrylic resin thatis slightly soft at body temperatures andvery
compliant at high temperatures.Thisproperty decreases major tooth discomfortand
considerably increases retention inthose patients who have lost a significantnumber
ofteeth.A unique feature oftheKlearway appliance is that it permits bothlateral (1
to 3 mm) and vertical (1 to 5 mm)jaw movement during sleep which reducesthe risk
ofTMJ and jaw muscle discomfort.This movement also facilitates oral breath-ing in
patients with nasal airway obstruc-tion.The screw mechanism ofthe appli-ance allows
for an 11 mm anteriormovement ofthe mandible with a total of44 incremental steps
of0.25 mm.In a studyof38 patients with moderate to severeobstructive sleep apnea by
Lowe and col-leagues,the Klearway appliance reduced theRDI to less than 15 per hour
in 80% ofthemoderate group and in 61% ofthe severegroup.50The Klearway appliance is
market-ed worldwide by Great Lakes OrthodonticLtd.,Tonawanda,NY,USA.Another
commonly used and effectiveoral appliance is the Herbst appliance,which is an
anterior mandibular position-ing device.It consists oftwo full-coverageclear
acrylic components snapped ontothe maxillary and mandibular teeth con-nected with
two rod and tube attachmentsthat allow vertical opening,protrusion,limited lateral
movement,and no retrusivemovement.It is used only at night andadvances the mandible
5 to 7 mm or atleast 75% ofthe patient�s maximum pro-trusive distance.A study by
Clark and col-leagues on 24 patients with mild to severeobstructive sleep apnea
patients using theHerbst appliance showed a significantimprovement in the RDI after
4 months ofappliance use in 58% ofthe subjects on thepost-appliance
polysomnogram.51Another disadvantage oforal appli-ances is the need to wear them
nightly.Aswith any device,compliance has beenshown to be a problem with oral appli-
ances.Ifappliance therapy is successful,Table 63-1Food and Drug Administration
Approved Oral Appliances for the TreatmentofObstructive Sleep
ApneaAppliancesManufacturerAdjustable PM PositionerJonathan A.Parker,DDSElastic
Mandibular Advancement,Triation (EMA-T)Frantz Design,Inc.Elastic Mandibular
AdvancementFrantz Design,Inc.Elastomeric Sleep ApplianceVillage Park
OrthodonticsEqualizer Airway DeviceSleep Renewal Inc.HerbstOrthodontics,SUNY at
BuffaloKlearwayGreat Lakes Orthodontics,Ltd.NAPAGreat Lakes
Orthodontics,Ltd.OSAPSnorefree,Inc.PM PositionerJonathan A.Parker,DDSSilencerSilent
Knights Ventures,Inc.Sleep-In Bone Screw SystemInfluence Inc.SNOAR Open Airway
ApplianceKent J.Toone,DDSThornton Oral ApplianceW.Keith Thornton,DDS
1304Part 8: Orthognathic Surgeryfurther treatment options may includemandibular
advancement surgery toachieve the same forward tongue positionon a permanent
basis.Continuous Positive AirwayPressure Continuous positive airway pressure(CPAP)
through the nose has been shown tobe quite successful in treating a broad
rangeofobstructive sleep apnea patients and ispresently the most successful
nonsurgicaltreatment.52�54The nasal CPAP is adminis-tered while the patient is
asleep by means ofa tight-fitting mask that is connected to acompressor.A CPAP of7
to 15 cm ofwateracts as a pneumatic splint ofthe upper air-way and prevents passive
collapse ofsoft tis-sues during respiration.Stimulation ofmechanoreceptors ofthe
genioglossus mus-cle leading to increased airway tone has alsobeen suggested as a
mechanism ofaction.Sullivan and colleagues were the first toreport the successful
treatment ofsleepapnea with nasal CPAP in 1981.55In mostcases this therapy is
effective in eliminatingapneas and hypopneas,improving arterialoxygen
saturations,reducing or eliminatingexcessive daytime sleepiness,and eliminat-ing
sleep disruption and fragmentation.CPAP may be combined with surgery andweight
loss,or it may be used as a sole formoftherapy.Although initially recommendedfor
short-term reliefofsleep apnea,the useofnasal CPAP for long-term care ofpatientshas
increased over the past few years.Inrecent years bilevel positive airway
pressure(Bi-PAP) systems that allow independentregulation ofinspiratory and
expiratorypressures and the newest modification inCPAP systems,Auto-CPAP,have been
usedto more effectively treat obstructive sleepapnea and increase tolerance and
compli-ance.56,57Auto-CPAP units adjust the CPAPthroughout the night rather than
deliveringone fixed pressure.Optimal CPAP is deliv-ered to the patient adjusting
for positionalchanges,alcohol or sedative effects,sleep�state-dependent changes
(REM vsnon-REM),and the effects ofupper airwayinfections or congestion.Bi-PAP
($2,500)and Auto-CPAP ($1,600) systems are moreexpensive than traditional CPAP
($600 to$800) systems.Despite the uniform success ofthistherapy,patient compliance
remains aproblem.Compliance rates at 12 monthshave been reported as low as
54%.58Theaverage nightly use ofCPAP is 4.8 hoursand the rate ofuse is usually
determined inthe first week ofuse.Overall approximatelyone-third ofpatients love
CPAP,one-thirdstruggle with CPAP but eventually tolerateit,and one-third hate CPAP
and never useit.Patient dissatisfaction results from nasaldryness and
congestion,sore throat,dry-ness ofthe skin and eyes,claustrophobia,and the
inability to tolerate the noise,dis-comfort,or mask.Careful patient selectionand
follow-up are essential ifnasal CPAP isselected as a treatment modality.Surgical
TreatmentSurgery has been the primary form oftherapy for obstructive sleep apnea.To
besuccessful the surgical procedure musteither bypass the obstructive area or pre-
vent collapse ofthe soft tissues in theupper airway at the obstruction.Manypatients
and surgeons tend to view surgi-cal treatment ofobstructive sleep apnea asa quick
and permanent cure.However,aclear definition ofwhat constitutes a cureis lacking in
the literature.This problemoften makes a determination ofthe effica-cy ofindividual
surgical procedures diffi-cult.Only objective data obtained from apostoperative
polysomnogram can beaccepted as proofofefficacy for surgicalprocedures.Currently
the proceduresused in the surgical treatment ofobstruc-tive sleep apnea include
tracheostomy,nasal surgery,uvulopalatopharyngoplasty,and several orthognathic
surgical proce-dures.Selection ofthe individual proce-dure is determined by the
severity ofthesleep apnea,the presence ofa maxillofa-cial skeletal deficiency,the
site oftheobstructive segment,and the presence ofmorbid
obesity.TracheostomyTracheostomy was the first efficacious surgi-cal procedure for
treating obstructive sleepapnea,performed by Kuhlo and colleaguesin 1969.59It is
almost 100% curative inrelieving the signs and symptoms ofobstructive sleep apnea
because it bypassesall the potential obstructive sites in theupper airway.After
tracheostomy there is arapid and striking reduction in daytimesomnolence and a
marked improvement insleep architecture due to a major reductionin the frequency
ofarousals.Sinus dysrhyth-mias,bradycardia,pulmonary hyperten-sion,hypoxemia,and
apnea all improve dra-matically with the procedure.TracheostomyFIGURE63-3Klearway
oral appliance.
Surgical and Nonsurgical Management ofObstructive Sleep Apnea1305clearly is an
effective surgical treatment forpatients with obstructive apnea.The disadvantages
ofa permanent tra-cheostomy can have a devastating effect onsleep apnea
patients.Almost all patientsexperience psychological depression fromthe social and
medical problems associatedwith a lifelong tracheostomy.The tra-cheostomy leaves
the patient estheticallydisfigured and exposes the patient to com-mon local
complications such as bleeding,infection,pain,and granulation tissue for-
mation.Patients are also at increased risk forthe more serious complications
oftrachealstenosis or erosion into an adjacent bloodvessel.Because ofthese
disadvantages andcomplications,a permanent tracheostomyshould be reserved for
severe cases ofobstructive sleep apnea with significant car-diovascular
symptoms.Simmons and col-leagues have suggested that tracheostomyshould be the
primary therapy for allpatients who spend substantial time insevere oxygen
desaturations below 50% andfor those who have life-threatening cardiacdysrhythmias
during sleep apnea.60Tra-cheostomy may also be used as an interimtreatment until
adjunctive procedures toreconstruct the upper airway are completed.Nasal
SurgerySignificant obstruction in the nasal cavityhas been shown to cause excessive
daytimesleepiness,sleep fragmentation,hypop-neas,and periodic breathing
duringsleep.61In most patients with moderate tosevere obstructive sleep
apnea,nasalobstruction is not the major contributingfactor.The obstruction may be
due to adeviated nasal septum,nasal polyps,orenlargement ofthe turbinates.In
thesepatients septoplasty,nasal polypectomy,orturbinectomies are usually helpful
only asadjunctive surgical procedures in thetreatment ofobstructive sleep
apnea.Unless the obstruction in the nasal cavityis severe,surgical correction
usually willnot yield any significant improvement ona repeat
polysomnography.UvulopalatopharyngoplastyThe oropharynx and soft palate can
causesignificant airway obstruction duringsleep.At least 10% ofpersons over the
ageof40 years snore regularly and signifi-cantly.Loud and intermittent snoring
isfound in almost all patients with obstruc-tive sleep apnea.In many cases
habitualsnoring is present for many years beforesleep apnea is diagnosed.Ikematsu
fol-lowed a large number ofhabitual snorersover several years and found that 91%
ofthese patients had decreased oropharyn-geal dimensions and longer soft palatesand
uvulas than normal subjects.62 Hewas able to eliminate their snoring bysurgically
excising the excessive soft tissuein the palatal folds and partially excisingthe
uvula.With minor modifications,Simmonsand colleagues and Fujita and
colleaguespopularized the uvulopalatopharyngoplasty(UPPP) for the treatment
ofobstructivesleep apnea.60,63The procedure wasdesigned to eliminate
oropharyngealobstruction by performing a tonsillectomyand adenoidectomy,excising
the uvula,removing redundant lateral pharyngeal wallmucosa,and resecting 8 to 15 mm
along theposterior margin ofthe soft palate.The surgical technique ofUPPPvaries to
some degree by patient and sur-geon,but the basic goal is to shorten thepalate and
widen the posterior airwayspace (Figure 63-4).A mucosal incisionis created with
electocautery on the ante-rior surface ofthe soft palate.The dissec-tion is
frequently carried laterally toinclude the palatine tonsil.The tonsillarbed is
coagulated and hemostasisachieved.Palatal muscle is excised andmucosa from the
nasopharynx is pulledforward for primary closure.Multipleinterrupted resorbable
sutures areplaced.Ifthe tonsil is removed,themucosa ofthe anterior fauces pillar
isclosed to the posterior fauces pillar.Thisattempt to remove redundant
pharyngealTonsils removedFIGURE63-4A�C,Uvulopalatopharyngoplasty.Tonsilsand uvula
are removed and the anterior pillar is closed tothe posterior pillar.Adapted from
Tiner BD,Waite,PD.Surgical and nonsurgical management ofobstructive sleepapnea.In:
Peterson LJ,Indresano AT,Marciani RD,RoserSM.Principles oforal and maxillofacial
surgery.Vol.3.Philadelphia (PA): J.B.Lippincott Company; 1992.p.1540.ABC
1306Part 8: Orthognathic Surgerytissue and stretch or tighten the posteri-or
pharyngeal wall results in constric-tion.In addition,frequently by shorten-ing the
soft palate,the width ofthe softpalate is thickened,as
demonstratedcephalometrically.Lymphoid tissue fromthe tonsillar fossa can be
removed sepa-rately or in conjunction with the uvula(Figure 63-5).The amount
ofvelum tobe excised is determined by the locationofpalatal competence and closure
ofthenasopharynx.These can be estimated oridentified during
nasopharyngoscopy.Palatal incompetence can occur but usu-ally is ofminimal concern
ifthe patientswallows carefully.Pain with swallowingusually lasts for several
weeks.UPPP results in symptomatic improve-ment in the patient and eliminates
habitualsnoring in almost all cases.However,reports show that significant
objectiveimprovement on the postoperativepolysomnogram ranges only from 41
to66%.58,60,64,65This procedure only elimi-nates the obstruction at the level ofthe
softpalate and does not address obstructionsoccurring in the hypopharyngeal and
baseoftongue areas.Many patients have morethan one site ofobstruction.IfUPPP is
per-formed when the presurgical evaluationdemonstrates obstruction localized to
thesoft palate�tonsil area,then the success rateofthe surgical procedure approaches
90%treating obstructive sleep apnea.23,26Complications from UPPP are relatedto
changes in palatal function.Permanentvelopharyngeal incompetence occurs
inapproximately 5% ofpatients and is morecommon during the first 2 months post-
operatively.Patients experience occasionalreflux ofliquids into the nose and
mildnasal air escape during speech.However,hypernasal speech and changes in
thequality ofthe patient�s speech are usuallynot seen.Simmons and colleagues
report-ed a 5 to 10% rate ofminor wound infec-tions that resolved with
antibiotics.64Palatal stenosis is definitely a risk with thisoperation and occurs
in about 1% ofpatients.It occurs more frequently withexcessive resections ofthe
posterior tonsil-lar pillars and injudicious use ofelectro-cautery.Postoperative
pain after UPPP issignificant,and narcotic analgesia shouldbe used with caution to
prevent sedation-induced exacerbation ofobstructive sleepapnea.Postsurgical deaths
have resultedfrom the combination ofpharyngealedema and narcotic use.Laser-Assisted
UvulopalatoplastyIn the late 1980s Dr.Yves-Victor Kamami(Paris,France) designed a
procedure toreshape and recontour the soft palateunder local anesthesia with a
CO2laser totreat snoring and selected patients withobstructive sleep apnea
syndrome.66Heoriginally named the procedure �laserresection ofthe palatopharynx�or
LRPP.Initially the procedure was accomplishedin four or five sessions spaced at
monthlyintervals.Over time the procedure evolvedinto a one-stage technique for
mostpatients.It consisted oftwo paramedianvertical incisions placed lateral to the
uvulaextending up toward the junction ofthehard and soft palates for 2 to 3 cm.A
sec-ond horizontal incision was placed justunder the roofofthe uvula leaving a
smalluvula to prevent centripetal scar forma-tion.Over a 5-year period,Kamami
treated63 obstructive sleep apnea patients withthis technique.The RDI was reduced
bymore than 50% in 55 patients that wereclassified as successful responders.The
RDIimproved from 41.5 to 16.9 for the averageresponder,and for the entire group
theaverage RDI improved from 41.3 to 20.3.In the early 1990s in the United
States,Dr.YosefKrespi modified the procedureand renamed it �laser-assisted
uvulopalato-plasty�or LAUP.He initially used the pro-cedure to treat loud habitual
snoring.In astudy of280 patients treated in the officeunder local anesthesia,84%
were curedwith an average of2.7 sessions.67Overallresults for obstructive sleep
apnea patientstreated with LAUP are far less encouraging,with an average successful
surgical responseof52.2%.68Based on these findings the cur-rent main indications
for LAUP includeloud habitual snoring,upper airway resis-tance syndrome,and mild
obstructive sleepapnea (apnea index < 20).All snoringpatients who elect to undergo
LAUP shouldbe evaluated for obstructive sleep apneapreoperatively and again
postoperatively ifobstructive sleep apnea was previouslydiagnosed.Ifnot,then the
patient and sur-geon may be lulled into a false sense ofsecurity by eliminating the
snoring withouteliminating the undiagnosed obstructivesleep apnea,potentially
increasing patientmorbidity and mortality.69The most common complication fol-lowing
LAUP is a moderate to severe sorethroat.Patients experience pain 8 to 10 days after
surgery and reach their peakpain intensity on the fourth or fifth post-operative
day.Pain control is achieved withoral analgesics and anesthetic gels.The riskfor
velopharyngeal insufficiency is lowsince the procedure is frequently done instages
and the surgeon has the opportunityto evaluate speech and soft palate
functionFIGURE63-5Surgical specimen oftonsils anduvula.Reproduced with permission
from TinerBD,Waite,PD.Surgical and nonsurgical manage-ment ofobstructive sleep
apnea.In: Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principlesoforal and
maxillofacial surgery.Vol.3.Philadel-phia (PA): J.B.Lippincott Company;
1992.p.1541.
Surgical and Nonsurgical Management ofObstructive Sleep Apnea1307after each
session.Patients are also at lowrisk for bleeding and infection.The greatmajority
ofpatients can eat,drink,andspeak almost immediately and can resumefull activities
the following day.Orthognathic Surgery ProceduresVarious orthognathic surgical
procedureshave been described for the treatment ofobstructive sleep apnea.The
majority ofpatients have airway obstruction at thelevel ofthe soft palate and at
the base ofthetongue (type II obstruction).Orthognath-ic surgical procedures can
change the sizeofthe airway in several regions.Mandibu-lar advancement and genial
advancementprobably work by changing the position ofthe mandible and hyoid bone
with subse-quent effects on the genioglossus and hyo-glossus muscles.Obstructive
sleep apneapatients with identifiable craniofacialanomalies can clearly benefit
from a vari-ety ofthese procedures.Mandibular AdvancementTotal mandibu-lar
advancement was the first orthognathicsurgical procedure used in the treatment
ofobstructive sleep apnea.Kuo and colleaguesin 1979 and Bear and Priest in 1980
reportedcomplete reversal ofsleep apnea symptomsin patients with horizontal
mandibular defi-ciency treated by mandibular advance-ment.47,70More recently
Alvarez and col-leagues reported the successful treatment ofan edentulous patient
with sleep apnea bymandibular and genial advancement.71A bilateral sagittal ramus
osteotomyis usually the procedure ofchoice fortotal mandibular
advancement.Theamount ofadvancement is determinedpreoperatively from the
orthognathicsurgery database.Adjunctive orthodontictreatment is frequently
necessary toobtain the desired occlusion and to elim-inate dental compensations
that wouldotherwise limit the amount ofadvance-ment.After advancement with the
stan-dard surgical technique,the fragmentsare rigidly fixed with screws or
boneplates.For large advancements of7 mmor more,long-term stability is enhancedwith
a 5- to 7-day course ofmaxillo-mandibular fixation and skeletal suspen-sion
wires.In advancements of6 mm orless,maxillomandibular fixation is usual-ly not
necessary.The exact reason for how mandibularadvancement improves obstructive
sleepapnea is not clearly known,but the suspect-ed effect is the pulling ofthe
tongue forwardoffthe pharyngeal wall.This effect is creat-ed by anteriorly moving
the insertion ofthegenioglossus and geniohyoid muscles.Ifthiswere the only
factor,then anterior chin pro-cedures would be equally effective as totalmandibular
procedures.Variations ofgeniotomies have been designed to maxi-mally pull the
tongue muscles forward.Genial AdvancementA rectangularosteotomy apical to the teeth
but main-taining the inferior border ofthe mandibleallows the genial tubercles with
their mus-cular attachments to be maximallyadvanced with minimal cosmetic
change(Figure 63-6).A modified vestibularmucosal incision is made in the
anteriormandible.Periosteum is reflected down tothe inferior border.An oscillating
saw isused to make parallel horizontal cuts thatinclude the genial tubercle.The
osteotomyis designed in a shape similar to a drawerso that it can be pulled outward
with thegenial muscles.The bone must be broadenough cuspid tocuspid to be rotated
90�and set on top ofthe buccal cortex.Theouter cortical and cancellous bone
oftherectangle can then be removed and theinner cortex rigidly fixed with
bonescrews.Any hemorrhage from the cancel-lous bone should be controlled.This
procedure does not change theesthetic chin or advance the anterior belly ofthe
digastric muscle,which may be helpfulin suspending the hyoid.In contrast to
thisprocedure a horizontal sliding geniotomydoes advance the genial tubercles and
theanterior belly ofthe digastric muscle.Genial Advancement with Hyoid Myoto-my and
SuspensionIn 1984 Riley andcolleagues described an alternative tech-nique in which
an inferior mandibularosteotomy and an associated hyoidmyotomy and suspension were
used inthe treatment ofobstructive sleep apnea(Figure 63-7).72This technique is
similarto a horizontal mandibular osteotomy,which is commonly used for advance-ment
genioplasty.The osteotomy isdesigned to include the genial tubercle onthe inner
cortex ofthe anterior mandiblewhere the genioglossus muscle attaches.Repositioning
the anteroinferior segmentofthe mandible forward with theattached genioglossus
muscle theoretical-ly pulls the tongue forward and improvesthe hypopharyngeal
airway.In conjunc-tion with the osteotomy,the body andgreater cornu ofthe hyoid are
isolatedFIGURE63-6Genial tubercle advancement.The outertable ofsymphysis is removed
and the inner table issecured with 2 mm screws.Adapted from Tiner
BD,Waite,PD.Surgical and nonsurgical management ofobstructive sleep apnea.In:
Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principles oforal and maxillo-facial
surgery.Vol.3.Philadelphia (PA): J.B.LippincottCompany; 1992.p.1542.
1308Part 8: Orthognathic Surgerythrough a submental incision.Theinfrahyoid muscles
are transected,takingcare to remain on the hyoid bone at alltimes to avoid injury
to the superiorlaryngeal nerves (see Figure 63-7A).Thisallows the hyoid bone to be
pulled anteri-orly and superiorly.Strips offascia ornonresorbable suture are passed
aroundthe body ofthe hyoid and attached to theintact portion ofthe anterior
mandible tocomplete the hyoid suspension.In 1989 Riley and colleagues publisheda
review of55 patients with obstructivesleep apnea who were treated with
inferiormandibular osteotomy and hyoid suspen-sion.73 Forty-two patients had
obstructionat both the oropharynx and hypopharynxand received concomitant UPPP and
inferi-or mandibular osteotomy with hyoidmyotomy and suspension.The remaining 6
patients were determined to have obstruc-tion localized to the base ofthe tongue
andunderwent the osteotomy and hyoid sus-pension only.All patients were reevaluated
6 months following surgery by poly-somnography.Thirty-seven patients (67%)were
considered to be responders to surgerybased on the polysomnogram
results.Genioglossus advancement ranged from 8to 18 mm with a mean of13
mm.Allresponders to surgery showed significantimprovement in their RDI and
oxygendesaturation events.Eighteen patients(33%) were considered nonresponders
andfailed to show significant improvement bypolysomnography.The presence ofpreex-
isting chronic obstructive pulmonary dis-ease was found to be a determining factor
inincreasing the risk offailure.In 1994 Riley and colleagues reportedon a new
modified technique for hyoidsuspension that fixed the hyoid to the thy-roid
cartilage instead ofthe anterior mar-gin ofthe mandible.74When this
modifiedtechnique was performed with inferiormandibular osteotomy,in lieu ofthe
orig-inal hyoid suspension technique,the sur-gical response rate (with or
withoutUPPP) was raised to 79.2%.The 5 nonre-sponders in this study of24
patientsachieved postoperative RDI values close tolevels at which they would have
been con-sidered surgical responders.Long-term follow-up ofthese patientshas shown
that the indication for this pro-cedure is limited.Patients with normalpulmonary
function,normal skeletalmandibular development,the absence ofobesity,and moderate
obstructive sleepapnea are candidates for treatment withinferior mandibular
osteotomy with hyoidmyotomy and suspension.The most serious reported complica-tion
from a hyoid suspension has beensevere aspiration in one patient,in whichthe
thyrohyoid membrane was totally sec-tioned.28 Other complications have includ-ed
wound infections,transient sensorydisturbances ofthe mental nerve,andmandibular
fracture.An advantage tohyoid suspension is that it circumvents theneed for
maxillomandibular fixation anddoes not affect the occlusion.Maxillomandibular
AdvancementCom-bined advancement ofthe maxilla andmandible with or without hyoid
suspen-sion is the most recent and efficacious sur-gical procedure for the
treatment ofobstructive sleep apnea.The surgical tech-nique includes a standard Le
Fort Iosteotomy in combination with amandibular sagittal split osteotomy
foradvancement ofthe maxilla and mandible.A concomitant inferior
mandibularosteotomy with or without hyoid myotomyand suspension,as previously
described,isalso performed.This surgery may result ina significant facial
change,which is mostoften favorable (Figures 63-8 and 63-9).Several authors have
described the use ofmaxillomandibular advancement (MMA)in treating large series
ofobstructive sleepapnea patients.75-80 In a series of23patients,Waite and
colleagues performed ahigh sliding horizontal geniotomy withoutthe hyoid myotomy
and suspension.75Allpatients were reevaluated by polysomnog-raphy at 6 weeks
postoperatively.The sur-gical success with MMA was 65% based ona postsurgical RDI
ofless than 10.Rileyand colleagues reported the largest series ofobstructive sleep
apnea patients treatedwith MMA in which 98% (89 of91) weresuccessfully treated
based on a postopera-tive RDI ofless than 20 with at least a 50%reduction in the
RDI compared to the pre-operative study.76It should be noted that67 ofthe 91
patients (74%) did not receivephase 1 therapy based on their two-phaseprotocol for
reconstruction ofthe upperFIGURE63-7Inferior mandibular osteotomyand hyoid
myotomy.A,Omohyoid,sternohy-oid,and thyrohyoid muscles released (see Fig-ure 63-8
for more detail on muscular relation-ships).B,Inferior segment is
advancedanteriorly and locked on the anterior mandible.Adapted from Tiner
BD,Waite,PD.Surgical andnonsurgical management ofobstructive sleepapnea.In:
Peterson LJ,Indresano AT,MarcianiRD,Roser SM.Principles oforal and maxillofa-cial
surgery.Vol.3.Philadelphia (PA): J.B.Lip-pincott Company; 1992.p.1543.AB
Surgical and Nonsurgical Management ofObstructive Sleep Apnea1309airway.Despite
this,the MMA was labeleda phase 2 procedure.In 1997,Hochban andcolleagues reported
a 98% success rate on38 obstructive sleep apnea patients consec-utively treated
with a 10 mm MMA as theprimary surgery,without any adjunctiveprocedures.77 Their
criteria for success werebased on the more rigid postoperative RDIofless than
10.Patient selection for MMAwas based on subjective symptoms ofexcessive daytime
sleepiness,an RDI ofgreater than 20,and specific craniofacialcharacteristics
determined cephalometri-cally.Only 2 patients who were morbidlyobese were treated
surgically.Based ontheir excellent results the authors conclud-ed that a stepwise
algorithm ofstaged sur-gical procedures was not justified.In aseries of50
obstructive sleep apneapatients consecutively treated with MMA,Prinsell reported a
100% success rate basedon a postoperative RDI ofless than 15,anapnea index (AI)
ofless than 5,or a reduc-tion in the RDI and AI ofgreater than60%.78In this series
occasional concomi-tant nonpharyngeal procedures and ananterior interior mandibular
osteotomywere accomplished with the MMA as a sin-gle-stage operation.In 1999 Lee
and col-leagues proposed a three-stage protocol forthe surgical treatment
ofobstructive sleepapnea patients.79 All 35 patients in theirseries had type II
obstruction with collapseat the oropharyngeal and hypopharyngealareas.Stage 1
reconstruction consisted ofaUPPP and inferior sagittal osteotomy withgenioglossus
muscle advancement,or ananterior mandibular osteotomy.Ifstage 1was
unsuccessful,then patients advancedto stage 2,which consisted ofMMA withrigid
fixation.A hyoid myotomy and sus-pension was the sole component ofstage
3reconstruction.Based on postoperativepolysomnography,69% (24 of35) wereconsidered
surgical respondents based onan RDI ofless than 20.Ofthe 11 stage 1failures,3
elected to proceed to stage 2reconstruction with MMA.All patientswho underwent MMA
had a postoperativeRDI ofless than 10,indicating a 100%response rate.No patient
required stage 3reconstruction.Bettega and colleaguestreated 51 consecutive
obstructive sleepapnea patients according to the Stanfordtwo-step surgical
procedure.80Forty-fourpatients had phase 1 surgery with a successrate of22.7% (10
of44).Twenty patientsunderwent MMA as part ofphase 2 in theprotocol.Ofthese,75% (15
of20) wereconsidered to be surgical responders basedon a postoperative RDI ofless
than 15 andat least a 50% reduction in the RDI.Ofthe5 failures,3 had postoperative
RDIs oflessthan 20.Stylohyoid musclePosterior digastric muscleMylohyoid
muscleGeniohyoid muscleThyrohyoid muscleOmohyoid muscleSternohyoid muscleAnterior
digastricmuscleFIGURE63-8Schematic drawings ofpreoperative (A)and postoperative
(B)two-jaw advancement,genial advancement,and hyoid suspension.Adapted from Tiner
BD,Waite,PD.Surgical and nonsurgi-cal management ofobstructive sleep apnea.In:
Peterson LJ,Indresano AT,Marciani RD,Roser SM.Prin-ciples oforal and maxillofacial
surgery.Vol.3.Philadelphia (PA): J.B.Lippincott Company; 1992.p.1544.ABFIGURE63-
9Preoperative (A) and postopera-tive (B)photographs ofa patient with obstruc-tive
sleep apnea syndrome who underwent two-jaw surgery with a genial
advancement.Reproduced with permission from Tiner BD,Waite,PD.Surgical and
nonsurgical manage-ment ofobstructive sleep apnea.In: Peterson LJ,Indresano
AT,Marciani RD,Roser SM.Principlesoforal and maxillofacial surgery.Vol.3.Philadel-
phia (PA): J.B.Lippincott Company; 1992.p.1545.AB
1310Part 8: Orthognathic SurgeryThe PAS consistently increases
withmaxillomandibular advancement.Howev-er,there is no direct relationship
betweenthe gain in PAS and the remission ofsleepapnea.MMA is effective for patients
whohave obstruction at the base ofthe tongue.This surgical treatment is the most
efficacious procedure for expanding thepharyngeal airway and improving or elimi-
nating obstructive sleep apnea.It remainsthe best current alternative to
tracheosto-my.81 Indications for this procedure includesevere mandibular deficiency
(SNB < 74�),morbid obesity,severe obstructive sleepapnea (RDI > 50,oxygen
desaturations < 70%),hypopharyngeal narrowing,andfailure ofother forms
oftreatment.82Thesuccess rate ofMMA appears to increasewhen adjunctive procedures
such as UPPP,partial glossectomy,septoplasty,or tur-binectomies are included in the
treatmentplan.This lends support to the theory thatmost obstructive sleep apnea
patients havemultiple levels ofobstruction.Adjunctive orthodontic therapy is usu-
ally indicated in patients selected for MMA.Presurgical orthodontics improves
thepostoperative occlusion and eliminates pre-existing dental compensations that
wouldotherwise limit the amount ofadvance-ment.Maximum advancement ofthe
facialskeleton and maintenance ofa functionalocclusion and acceptable esthetics are
thegoals ofsurgical-orthodontic correction.The osteotomies are rigidly fixedwith
miniplates and bicortical screws(Figure 63-10).With large advancements(> 7
mm),skeleton suspension wires anda short course ofmaxillomandibular fix-ation (1
wk) can be used to reduce surgi-cal relapse.Potential complications ofMMA include
surgical relapse,non-union,bleeding,malocclusion,infection,unfavorable changes in
facial appear-ance,and permanent or temporary sen-sory disturbances ofthe inferior
alveolarand infraorbital nerves.The long-term skeletal stability ofMMA has been
shown to be quite good.Louis and colleagues showed a meanrelapse of0.9 �1.8 mm
among 20 maxil-lary advancement patients who under-went MMA for obstructive sleep
apnea.83The mean follow-up period was 18.5months (range 6 to 29 mo).When
thepatients were divided into three groupsreflecting small (6 mm or less),medium(7
to 9 mm),and large (10 mm or more)advancements,there was no statisticaldifference
in the measured relapse amongthe groups.Rigid fixation was achievedwith four
miniplates and no bone graftswere used in any ofthe maxillaryadvancements.Nimkarn
and colleaguesreported on 19 obstructive sleep apneapatients who underwent MMA
withsimultaneous genioplasty and found rela-tively stable long-term (> 12 mo)
surgicalstability ofthe maxilla and mandible.84Maxillary and mandibular
advancementwas stable over the long term in both thevertical and horizontal
planes.With theexception ofgonion in the vertical plane,there was no statistically
significant cor-relation between the amount ofsurgicaladvancement and the amount
ofpostsur-gical instability.Mandibular SetbacksIn a small numberofpatients,a
mandibular setback proce-dure can be the initiating factor in thedevelopment
ofobstructive sleep apnea.Riley and associates reported on twowomen who developed
obstructive sleepapnea syndrome after mandibularosteotomies for correction ofClass
III mal-occlusion and skeletal prognathism.85Nei-ther patient had any symptoms
ofsleepapnea prior to surgery.Postoperatively bothpatients began to snore
loudly.Evaluationby polysomnography confirmed the pres-ence ofobstructive sleep
apnea syndrome.A comparative examination ofthe preoper-ative and postoperative
lateral cephalo-grams ofeach patient showed a more infe-riorly positioned hyoid
bone and anarrowing ofthe pharyngeal airway as aresult ofthe mandibular setback
procedure.In an attempt to identify thosepatients potentially at risk for
obstructivesleep apnea,all patients who are plannedfor mandibular setback
procedures shouldbe questioned preoperatively and postop-eratively about the
presence or absence ofsnoring,excessive daytime sleepiness,orobserved apneas during
sleep.Althoughthe vast majority ofpatients who undergoFIGURE63-10Preoperative (A)
and postopera-tive (B) radiographs ofa two-jaw surgery andgenial tubercle
advancement for sleep apnea.Reproduced with permission from Tiner
BD,Waite,PD.Surgical and nonsurgical manage-ment ofobstructive sleep apnea.In:
Peterson LJ,Indresano AT,Marciani RD,Roser SM.Principlesoforal and maxillofacial
surgery.Vol.3.Philadel-phia (PA): J.B.Lippincott Company; 1992.p.1546.BA
Surgical and Nonsurgical Management ofObstructive Sleep Apnea1311mandibular
setbacks are able to adapt tothe changes in the skeletal and
muscularapparatus,there is a subset ofpatients whomay be at risk for developing
overt signs ofobstructive sleep apnea followingmandibular setbacks.SummaryBecause
the obstructive sleep apnea syn-drome is a complex disorder,the type oftreatment
selected should be tailored tothe individual patient based on the relativerisks and
benefits ofthe therapy and theseverity ofthe disease.Although a subsetofthe
patients who present with obstruc-tive sleep apnea have an identifiable cran-
iofacial anomaly,care must be used inchoosing a simple mechanistic therapy.The
success ofthe chosen therapy shouldbe evaluated both subjectively and objec-
tively.There is no clear agreement on whatconstitutes a cure ofsleep
apnea.Mostauthors use the RDI in assessing severity ofdisease and success
oftreatment.However,all agree that the potentially significantphysiologic
consequences that can be lifethreatening result from hypoxemia.Insome cases
patients after treatment haveno oxygen desaturations below 90%,butin terms ofRDI
they are considered notcured and are deemed treatment failures.A more reasonable
approach would beto define the concept ofsuccess in terms ofexcellent,good,fair,and
poor and to avoidusing the term �cured�in assessing treat-ment outcomes.These terms
could bequantitatively approached assigning low-est oxygen desaturation and RDI
parame-ters to each one.In Table 63-2 the resultsof71 patients treated by
maxillomandibu-lar advancement are assessed by these cri-teria.In managing patients
with severesleep apnea,a �cure�is seldom achievedwith a single surgical or medical
treatment(tracheostomies excluded).However,maxillomandibular advancement may sig-
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ofobstructive sleepapnea:comparison ofvarious treatmentmodalities.Laryngoscope
1988;98:304.59.Kuhlo W,Doll E,Franck MD.Erfolgreichebehandlung eines pickwick-
syndromsddurch eine dauertrachealkanuele.DtschMed Wochenschr
1969;94:1286.60.Simmons FB,Guilleminault C,Silvestri R.Snoring,and some obstructive
sleep apnea,can be cured by oropharyngeal surgery.Arch Otolaryngol
1983;109:503.61.Heimer D,ScharfS,Lieberman A,et al.Sleepapnea syndrome treated by
repair ofdeviat-ed nasal septum.Chest 1983;84:184.62.Ikematsu T.Study ofsnoring,4th
report:ther-apy.J Jap Otorhinolaryngol 1964;64:434.63.Fujita S,Conway W,Zorick F,et
al.Surgicalcorrection ofanatomic abnormalities inobstructive sleep apnea
syndrome:uvu-lopalatopharyngoplasty.Otolaryngol HeadNeck Surg
1981;89:923.64.Simmons FB,Guilleminault C,Miles LE.Thepalataopharyngoplasty
operation for snor-ing and sleep apnea:an interim report.Otolaryngol Head Neck Surg
1984;92:375.65.Guilleminault C,Hayes B,Smith L,et al.Palatopharyngoplasty in
obstructive sleepapnea syndrome.Bull Eur Physiopathol Res1983;19:595.66.Kamami
YV.Outpatient treatment ofsleep apneasyndrome with CO2laser:laser-assistedUPPP.J
Otolaryngol 1994;23:395�8.67.Krespi YP,Pearlman SJ,Keidar A.Laser-assisteduvula-
palatoplasty for snoring.J Otolaryn-gol 1994;23:328�34.68.Terris DJ,Wang MZ.Laser-
assisted uvu-lopalatoplasty in mild obstructive sleepapnea.Arch Otolaryngol Head
Neck Surg1998;124:718�20.69.Sher AE.Update on upper airway surgery forobstructive
sleep apnea.Curr Opin PulmMed 1995;1:504�11.70.Kuo PC,West RA,Bloomquist DS,et
al.Theeffect ofmandibular osteotomy in threepatients with hypersomnia sleep
apnea.Oral Surg 1979;48:385.71.Alvarez CM,Lessin ME,Gross PD.Mandibularadvancement
combined with horizontal
Surgical and Nonsurgical Management ofObstructive Sleep Apnea1313advancement
genioplasty for the treatmentofobstructive sleep apnea in an edentulouspatient.Oral
Surg 1987;64:402.72.Riley R,Guilleminault C,Powell N,et al.Mandibular osteotomy and
hyoid boneadvancement for obstructive sleep apnea:acase report.Sleep
1984;7:79.73.Riley RW,Powell NB,Guilleminault C.Inferiormandibular osteotomy and
hyoid myotomysuspension for obstructive sleep apnea:areview of55 patients.J Oral
MaxillofacSurg 1989;47:159.74.Riley RW,Powell NB,Guilleminault C.Obstructive sleep
apnea and the hyoid:arevised surgical procedure.OtolaryngolHead Neck Surg
1994;111:717�21.75.Waite PD,Wooten V,Lachner J,et al.Maxil-lomandibular advancement
surgery in 23patients with obstructive sleep apnea syn-drome.J Oral Maxillofac Surg
1989;47:1256.76.Riley RW,Powell NB,Guilleminault C.Obstruc-tive sleep apnea
syndrome:a review of306consecutively treated surgical patients.Oto-laryngol Head
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maxillofacial treatment ofobstruc-tive sleep apnea.Plast Reconstr
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specific treatment approachfor obstructive sleep apnea in 50
consecutivepatients.Chest 1999;116:1519�29.79.Lee NR,Givens CD,Wilson J,Robins
RB.Staged surgical treatment ofobstructivesleep apnea syndrome:a review
of35patients.J Oral Maxillofac Surg 1999;57:382�5.80.Bettega G,Pepin JL,Veale D,et
al.Obstructivesleep apnea syndrome fifty-one consecutivepatients treated by
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NB,Guilleminault C.Obstructive sleep apnea syndrome:a surgi-cal protocol for
dynamic upper airwayreconstruction.J Oral Maxillofac Surg1993;51:742�7.82.Prinsell
JR.Maxillomandibular advancementsurgery for obstructive sleep apnea syn-drome.J Am
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advancement surgery inobstructive sleep apnea syndrome patients:long-term surgical
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NB,Guilleminault C,Ware W.Obstructive sleep apnea syndrome follow-ing surgery for
mandibular prognathism.JOral Maxillofac Surg 1987;45:450�2.
Part 9FACIALESTHETICSURGERY
CHAPTER 64BlepharoplastyHeidi L.Jarecki,MDMark J.Lucarelli,MDBradley
N.Lemke,MDCurrent blepharoplasty techniques were atleast two thousand years in the
making.Reports from as early as AD25 to 35,suchas De Re Medicaby Roman
encyclopedistand philosopher Aulus Cornelius,demon-strated appreciation ofupper
eyelid skinexcision in the treatment ofupper eyeliddisorders.1Early descriptions
ofsurgeryinvolving eyelid reconstruction by CarlFerdinand von Graefe,often regarded
asthe founder ofmodern plastic surgery,in1818,and Johann Karl George
Fricke,astudent ofvon Graefe�s,in 1829,representthe first reported uses ofthe term
ble-pharoplasty.1,2A.W.Sichel first accuratelydescribed �herniated orbital fat�in
1844.1Sidney Fox originated the term dermacha-lasis in 1952 to describe age-
associatedexcess in eyelid skin.2Cosmetic surgery was not embraceduntil the early
twentieth century whenCharles Conrad Miller penned the firstbook dedicated to
cosmetic surgery in1907 entitled Cosmetic Surgery: The Cor-rection ofFeatural
Imperfections.1Shortlythereafter Frederick Kolle published a texton plastic and
cosmetic surgery in whichhe detailed the value ofpreoperative eyelidskin marking to
determine the properamount to excise during surgery.2Thevalue ofpreoperative and
postoperativephotography was introduced in 1926 byParisian A.Suzanne No�l,one ofthe
firstfemale pioneers in cosmetic surgery.2These landmark contributions
spawnedcurrent blepharoplasty techniques,whichcontinue to be further refined and
opti-mized to achieve superior functional andcosmetic results.Blepharoplasty is
frequently per-formed either as an adjunctive procedureor as a freestanding
operation.A 2002American Academy ofCosmetic Surgery(AACS) survey reported 27,503
blepharo-plasty surgeries performed by AACS mem-bers,making blepharoplasty the
tenthmost frequently performed cosmetic pro-cedure in the United States
(K.Rybarczyk,personal communication,January 2003).Common indications for
blepharoplastyare dermatochalasis,blepharochalasis,orbital septum weakness with
resultant fatpad herniation,hypertrophic orbicularisoculi muscle,eyelid laxity with
malposi-tion,and other adnexal abnormalities (ie,herniated lacrimal
gland,varicoseveins,eyelid skin lesions).Dermatochalasisis simply an excess
ofeyelid skin,often theresult ofage- or ultraviolet (UV)-associateddecreases in
collagen and changes in elas-ticity and composition ofthe dermis
andepidermis.3Recurrent angioedema oftheeyelid results in characteristic
laxity,full-ness,and episodic edema known as ble-pharochalasis.Acquired
blepharoptosisindicates a drooping eyelid that usuallyresults from disinsertion
ofthe aponeurot-ic insertion ofthe levator palpebrae superi-oris into the upper
eyelid.Blepharoptosismay be present in the setting ofderma-tochalasis or
blepharochalasis.Orbital sep-tal weakness is evident when �bulges,�which represent
herniation oforbital fat,are present in the eyelids.A hypertrophicorbicularis oculi
muscle presents as a hori-zontal prominence ofthe lower eyelidimmediately beneath
the palpebral margin.Eyelid laxity may manifest as ectropion,canthal angle
alterations,and epiphora.The ensuing chapter is intended as asurvey ofimportant
information for theblepharoplasty surgeon to consider.Oncompletion ofthe chapter
the surgeonshould understand pertinent anatomy,beable to identify good
blepharoplasty can-didates,be capable ofdeveloping a surgi-cal plan,and understand
the major com-plications and how to avoid them.Thisinformation should serve as a
spring-board to direct the surgeon in routes ofappropriate inquiry.AnatomyA
thorough understanding ofthe topogra-phy ofthe upper two-thirds ofthe face
isrequisite for successful eyelid surgery.Eye-lids should not be viewed in
isolation butrather in context ofthe relationship to theeyebrow above and midface
below.
1318Part 9: Facial Esthetic SurgeryForehead and Eyebrow Understanding the normal or
idealizedbrow position is important during evalua-tion for blepharoplasty.4,5In
general mentend to have lower flatter brows at the levelofthe superior orbital
rim.The typicalfemale brow rests 1 cm above the superiororbital rim and peaks
between the lateralcorneal limbus and lateral commissure,creating a higher and
gently arched appear-ance.Figures 64-1 and 64-2 demonstratethe typical position
ofthe female and malebrow,respectively,in youth.Women fre-quently alter eyebrow
position and shapeby epilating eyebrow hair so as to approxi-mate the more
idealized arched brow.The eyebrow provides vertical supportto the upper
eyelid,contributing to thearchitecture ofthe eyelid.Eyebrow posi-tion is
significantly influenced by the ele-vators and depressors ofthe brow as wellas
underlying connective tissue attach-ments.The frontalis muscle,which origi-nates
within the galea aponeurotica,is themain elevator ofthe eyebrow.The corru-gator
supercilii,depressor supercilii,pro-cerus,and orbicularis oculi depress themedial
brow,whereas the orbicularis mus-cle is the main lateral brow depressor.Cor-rugator
contraction compresses the medi-al eyebrows toward the midline with
slightdepression,forming vertical or obliqueglabellar furrows.Contraction ofthe
pro-cerus depresses the glabella,creating hori-zontal rhytids across the dorsum
ofthenose.Depressor supercilii contractioncauses medial eyebrow depression and for-
mation ofoblique glabellar furrows.At itsinsertion point into the eyebrow
thefrontalis muscle interdigitates with theorbicularis oculi muscle.Beneath the
frontalis lies the eyebrowfat pad,a structure composed ofloosefibrous septae with
fat-filled interseptatespaces.The eyebrow fat pad is continuousinferiorly with the
filmy areolar posteriororbicularis fascia on the undersurface ofthe orbicularis
muscle.6On the undersideofthe eyebrow fat pad,dense connectivetissue attachments
fasten the superficialmuscle plane to the supraorbital ridge,thereby supporting the
medial one-halftotwo-thirds ofthe eyebrow.6Similar attach-ments for the lateral
third ofthe brow arelacking,thus explaining the preferentialptosis ofthe temporal
brow with aging.6Inaddition the elevating frontalis muscledoes not extend to the
lateral-most por-tion ofthe eyebrow,further contributingto temporal brow ptosis.The
eyebrow provides vertical supportto the anterior upper eyelid
structuresbelow,therefore ptosis ofthe eyebrowincreases the amount ofapparent
uppereyelid tissue.Failure to appreciate the con-tribution ofeyebrow ptosis to
upper eyeliddermatochalasis may result in excessiveeyelid skin removal,further
exacerbationofinferior brow displacement,and aninability to close the eyelids.With
mildtemporal brow ptosis as the only browposition abnormality,more eyelid skin
canbe removed laterally during blepharoplas-ty to provide a satisfactory
result.Withmore severe eyebrow and forehead ptosis,consideration ofeyebrow and
foreheadlifting is important.MidfaceComprising the area from the inferiororbital
rim to the mouth,the midface pos-sesses structures and landmarks importantto the
planning ofa successful lower lidblepharoplasty.Nasojugal and malar foldsseparate
the thin lower eyelid skin fromthe thicker skin ofthe cheek.The superfi-cial
musculoaponeurotic system (SMAS)is a fibrous fascial network interconnect-ing the
muscles offacial expression,whichacts as a force distributor offacial
musclecontractions to the skin to allow for facialexpression.7The SMAS divides the
subcu-taneous fat into two layers and possessesfibrous septae connecting to the
dermis.The orbitomalar and zygomatic ligamentsprovide connections between the
perios-teum and dermis.8,9In youth the eyelid cheek contour is asmooth single
convexity from the tarsusinferiorly to the cheek.With age numeroussoft tissue and
skeletal changes occur inthe eyelid and midface.The orbital septumweakens
permitting orbital fat prolapse,orbital rim exposure,and a prominence ofthe
cheek.Inferolateral aging-associateddescent ofthe orbicularis oculi muscle canalso
disrupt the eyelid cheek contour.10Descent ofthe malar fat pad
contributessubstantially to midfacial ptosis.11,12Anatomic studies demonstrate
attenua-tion or abnormal inferior displacement ofthe subcutaneous insertions ofthe
orbito-malar,masseteric cutaneous,and zygo-matic ligaments in the setting
ofmidfacialFIGURE64-1Typical female brow position.Notethe relationship ofthe brow
relative to the superi-or orbital rim.FIGURE64-2Typical male brow position.Notethat
relative to the female brow the male browposition is lower and flatter.
Blepharoplasty1319ptosis.12,13Important changes ofthe max-illa,as described by
Pessa and colleagues,also contribute to midfacial aging.14,15Ocular AdnexaThe
eyelid margin is traditionally dividedinto anterior and posterior
lamellae.Theanterior lamella is composed ofthe skin,orbicularis oculi muscle,muscle
ofRiolan,and glands ofZeis and Moll,whereas theposterior lamella is composed ofthe
palpe-bral conjunctiva,tarsal plates,and associat-ed meibomian glands.A cross-
section oftheupper and lower eyelid structures demon-strates the composition ofthe
anterior andposterior lamellae (Figure 64-3).The anteri-or and posterior lamellae
are divided by theorbital septum,a structure occasionallyreferred to as the middle
lamella.Eyelid SkinThicknessEyelid skin pos-sesses a minimal subcutaneous fibroadi-
pose layer and an attenuated dermis,con-tributing to its status as the thinnest
skin inthe body.Subcutaneous fat is completelyabsent in the pretarsal area.An
abrupt tran-sition to thicker skin with a corresponding-ly more dense fibroadipose
layer is encoun-tered near the orbital rim.Care must betaken to minimize surgical
incisions lateral-ly beyond the thin eyelid skin as scarappearance may markedly
differ.The eyelidskin ofAsians tends to be slightly thickerthan that ofCaucasians
primarily due to athicker dermis and subcutaneous fat.16Aging Skin ChangesAging
skin changes,such as pigmentary aberrations (dyschro-mia) and wrinkling
(rhytids),result from acombination ofUV-induced photodam-age,mechanical forces from
gravity,andfacial muscle contraction and alteredchemical environment.3Decreases in
thesynthesis ofType I collagen have beendemonstrated in aged human eyelid
skin.17Eyelid TopographyFissure Heights,Upper Eyelid CreaseThe adult
verticalinterpalpebral fissure measures 9 to 12 mm,whereas the horizontal
interpalpebral fis-sure is 28 to 30 mm.With age the horizon-tal fissure shortens by
approximately10%.18The lateral canthal angle lies 1 to 2 mm superior to the medial
canthal angle,giving the youthful eye a subtle lateral incli-nation.The apex ofthe
upper eyelid mar-gin rests slightly nasal to the pupil at thelevel oflimbus in
children and 1.0 to 2.0 mm below the limbus in adults,yieldingEyebrow fat
padFrontalis musclePretarsal orbicularismusclePreseptal orbicularismuscleLevator
muscleWhitnall's ligamentOrbital septumM�ller's muscleGlands of KrauseGlands of
WolfringLevator aponeurosisSuperior
rectusmuscleTarsusConjunctivaTarsusCapsulopalpebralfasciaCapsulopalpebralheadTenon'
s capsuleInferior tarsal muscleInferior rectusmuscleInferior orbitalseptumInferior
obliquemuscleMalar fat padPreseptal orbicularismuscleLockwood's ligamentFIGURE64-
3Cross-sectional view ofthe structures composing the upper and lower eyelid.Adapted
fromKikkawa DO and Lemke BN.41
1320Part 9: Facial Esthetic Surgerya margin reflex distance of4 to 5 mm.Thelower
eyelid margin peaks inferiorly direct-ly beneath the pupil.Figure 64-4 demon-
strates the normal upper and lower eyelidposition.As depicted in Figure 64-5
dermaland conjoined fascia attachments ofthelevator palpebrae superioris
aponeurosisform the upper eyelid crease,an importantanatomic and surgical landmark
often usedas an incision site.6,19,20Position oftheupper eyelid crease varies with
age,gender,and,to some degree,ethnicity.21The youth-ful eyelid crease is
approximately one-thirdofthe distance from the eyelid margin tothe lower edge ofthe
brow.22Elevation ofthe upper eyelid crease may signify disin-sertion or attenuation
ofthe levator muscleattachments due to age-related lipid infil-tration.Concomitant
upper lid blepharop-tosis is commonly present in the setting ofan elevated upper
lid crease.In generalupper eyelid creases in Caucasian femalesare 9 to 10 mm above
the upper lid margin,whereas in Caucasian males they are 7 to 8 mm above the upper
lid border.A cross-sectional study demonstrated upper lidcrease heights lower than
traditionally pur-ported values,although small sample sizeand variation in
measuring technique mayaccount for the inconsistency.21Upper eye-lid crease
position in African Americans hasnot been documented extensively in the lit-
erature,although clinical experience sug-gests a position similar to that found
inCaucasians.Asian Upper EyelidIn individuals ofAsian ethnicity three main
variations ofupper eyelid crease anatomy exist:singleeyelid,low eyelid crease
(inside-foldtype ofcrease),and double eyelid withlid crease parallel to lid margin
(Figure64-6).16,23�25In patients with a singleeyelid or low eyelid crease the
levatoraponeurosis fuses with the orbital sep-tum near the eyelid margin below
thesupratarsal border,creating an essential-ly absent or low upper lid crease.16In
theAsian double eyelid the level offusion ofthe orbital septum with the
levatoraponeurosis is higher than in the Asiansingle eyelid.16Aside from the
orbitalseptum fusion site,thicker fat layers anda lower primary insertion ofthe
levatoraponeurosis to the upper eyelid skincontribute to the characteristic
topogra-phy ofthe Asian eyelid.Lower Eyelid CreaseThe lower eyelidcrease,formed by
connective tissue fibersextending anteriorly from the capsu-lopalpebral fascia into
the subcutaneoustissues,is less prominent than its uppereyelid counterpart and is
often mostnoticeable in children.26The lower lidcrease begins medially 4 to 5 mm
inferiorto the lower lid margin and slopes inferi-orly as it proceeds
laterally.FIGURE64-4Normal position ofthe upper andlower eyelids.Whitnall's
ligamentM�ller's muscleLevator muscleLateral rectus muscleInferior tarsal
muscleInferior oblique muscleInferior orbicularis muscleConjunctivaLevator
aponeurosisSuperior septumInferior septumCapsulopalpebral fasciaOrbital fatOrbital
fatLockwood's ligamentTenon's capsuleFibrous attachment to skinfrom levator
aponeurosisConjunctivaInferior and superior tarsusFIGURE64-5Cross-sectional view
ofthe dermal and conjoined fascial attachments ofthe levatoraponeurosis responsible
for lid crease formation.Adapted from Lemke BN and Lucarelli MJ.111
Blepharoplasty1321Eyelid Connective TissueOrbital SeptumThe orbital septum,an
anatomic boundarybetween the eyelids and orbit,is a multil-amellar layer ofdense
connective tissue aris-ing from the arcus marginalis,a thickenedwhite fibrous line
on the periosteum ofthebony orbital margin.27The orbital septumforms the anterior
boundary ofthe orbit.Medially the septum splits to cover the pos-terior aspect
ofHorner�s muscle and adhereto the lacrimal fascia,inserting on the poste-rior
lacrimal crest and anterior lacrimalcrest,respectively.Laterally the septuminserts
anteriorly on the lateral canthal liga-ment and posteriorly on Whitnall�s
tubercleofthe lateral orbital rim.In the upper eyelidthe orbital septum joins the
levator aponeu-rosis 2 to 5 mm above the superior tarsalborder.27In the lower lid
the septum fuseswith the inferior tarsal border after joiningthe lower lid
retractors 4 to 5 mm inferior tothe tarsus.26A cadaver demonstration withartist�s
depiction ofthe orbital septum isshown in Figure 64-7.Orbital septalstrength varies
among individuals and withage.Attenuation ofthe septum allows foranterior orbital
fat prolapse.TarsusComposed ofdense fibrous tis-sue the tarsal plates contribute
structuralintegrity to the eyelids.Approximately 1.0to 1.5 mm thick the tarsal
plates measureapproximately 25 mm in length andrange from 10 to 12 mm in height in
theupper lid and 3 to 5 mm in the lower lid,with no difference noted between gen-
ders.28The tarsal plates taper convexlymedially and laterally to conform to
theglobe (Figure 64-8).Within the tarsalplastes are the meibomian glands,holocrine
sebaceous glands responsiblefor the lipid layer ofthe tear film.Themeibomian glands
are branched acinarglands with long central ducts opening atthe eyelid margin just
posterior to thegray line.There are approximately 25glands in the upper eyelid and
20 in thelower eyelid.Medial and Lateral Canthal LigamentsThe medial and lateral
tarsal borders arefirmly attached to the orbital rims via thefibrous medial and
lateral canthal liga-ments,respectively (see Figure 64-8).The medial canthal
ligament is morecomplex anatomically due to its oftentripartite attachment as well
as its rela-tionship with the lacrimal system.Theanterior arm inserts onto the
maxillarybone,anterosuperior to the lacrimalcrest.The posterior arm attaches to
theposterior lacrimal crest in a fanlike fash-ion and may partially fuse with the
pos-terior surface ofthe lacrimal sac.Thesuperior arm inserts onto the
orbitalprocess ofthe frontal bone,contributingto the formation ofthe lacrimal sac
fossaroof.29The lateral canthal ligamentinserts on the zygomatic bone at Whit-
nall�s tubercle 1.5 mm inside the lateralFIGURE64-6Artist depiction
demonstratingthree common variations ofthe upper eyelidcrease in Asians.A,Single
eyelid with absence ofcrease.B,Low eyelid crease with inside fold
typeofcrease.C,Double eyelid with parallel crease.Adapted from Chen WP.24Deep
orbicularis removedTag of deep galeaSeptum inserting on eyelid retractorsArcus
marginalisSeptum inserting onlevator aponeurosisFIGURE64-7A and B,Cadaver
demonstration ofthe orbital septum after removal ofthe forehead and eyelid
musculature.A adapted from and Breproduced with permission from Lemke BN and Della
Rocca RC.112ABABC
1322Part 9: Facial Esthetic Surgeryorbital rim and serves as both a stabilizerofthe
lids and a mobilizer ofthe lateralcanthal angle via attachments to the lat-eral
rectus check ligaments.30,31Whit-nall�s tubercle is a key surgical landmarkas it is
the site oflateral lid attachmentwhen performing a canthopexy.Approx-imately 2 mm
oftemporal movement ofthe lateral canthal angle is afforded onlateral gaze due to
the fusion ofthe later-al rectus check ligaments with the lateralcanthal
ligament.30Whitnall�s Superior Transverse LigamentThe junction ofthe levator muscle
andlevator aponeurosis is encircled by a trans-verse fibrous condensation known
asWhitnall�s superior transverse ligament,asupporter ofthe superior anterior
eyelid.Although originally thought to serve as acheck ligament for the
levator,Whitnall�sligament has also been postulated to func-tion as a suspender
providing vertical sup-port for the orbit (Figure 64-9).32,33Whit-nall�s ligament
inserts superomediallywithin the orbit on the frontal bonebehind the trochlea and
superolaterallynear the frontozygomatic suture afterattaching to the posterior
fibers ofthelacrimal gland capsule.34During ptosissurgery Whitnall�s ligament is a
key land-mark,often corresponding to the transi-tion from levator muscle to
aponeurosis.Lockwood�s LigamentThe lower lidcounterpart to Whitnall�s ligament
isLockwood�s ligament,a product oftheconjoined fascia ofthe inferior rectus
andinferior oblique.Inserting on the medialand lateral canthal ligaments as well
asthe bony orbital rim,Lockwood�s liga-ment serves as a suspensory sling for
theinferior anterior orbit.Lockwood�s liga-ment is strongest anterior to the
inferioroblique muscle.26Eyelid MusculatureOrbicularis OculiPart ofthe anterior
lamella ofthe uppereyelid,the orbicularis oculi is a ring-shaped superficial
sphincter muscle thatcan be thought ofin three concentric por-
tions:pretarsal,preseptal,and orbital.Fig-ure 64-10 demonstrates the
orbicularisoculi muscle in the setting ofthe superfi-cial facial muscles.Adherent
to the tarsusthe pretarsal orbicularis requires sharpdissection for
isolation.Posterior to thepreseptal orbicularis,a thin fibrofatty infe-rior
extension ofthe eyebrow fat pad,thepostorbicularis fascia facilitates
dissectionofthe preseptal orbicularis from theorbital septum.The peripheral-
mostorbital orbicularis covers the orbital rims.Together the pretarsal and
preseptal orbic-ularis comprise the palpebral orbicularis,responsible for reflexive
eyelid closure.The clinical implication ofthe palpebralorbicularis�function is
evident in the post-operative period when the reflexive blinkresponse is
temporarily decreased as aresult ofpreseptal orbicularis removal inthe
blepharoplasty skin muscle flap.Thepatient must be reminded to blink fullyand
frequently during postoperative heal-ing to adequately moisten the cornea.Orbital
orbicularis contraction producesforceful voluntary eyelid closure.Theorbicularis
has firm attachments to under-Nasal fat padMedial canthal ligamentNasal fat
padInferior oblique muscleTrochleaPreaponeurotic fat pad Temporal fat padLateral
canthalligamentLacrimal glandArcuate expansionof inferior obliquemuscleCentral fat
padFIGURE64-8Skeletonized anterior view oftarsus,canthal ligaments,and fat pads.The
medial can-thal ligament possesses a complex tripartite attachment.Adapted from
Kikkawa DO and Lemke BN.41Lower lid retractorsLevator muscleLevator
aponeurosisWhitnall's ligament(superior transverse ligament)FIGURE64-9Whitnall�s
ligament ofthe eyelid,levator palpebrae superioris,and the lower
eyelidretractors.Adapted from Nerad JA.76
Blepharoplasty1323lying structures at the lateral palpebralraphe,medial canthal
region,and upperand lower eyelid retractor insertions.Themuscle ofRiolan,a small
portion oftheorbicularis separated from the pretarsalorbicularis fibers by the
cilia,creates thegray line ofthe lid margin.The lacrimal(Horner-Duverney)
muscle,formed bythe deep pretarsal head ofthe orbicularisas it inserts on the
posterior lacrimal crestand lacrimal fascia,is thought to play arole in lacrimal
outflow,although theexact nature ofits function is controver-sial.35Contraction
ofthe lacrimal muscleresults in medial and posterior movementofthe lower eyelid
with the blink.Levator Palpebrae SuperiorisThe leva-tor palpebrae superioris,the
main retrac-tor ofthe upper eyelid,arises from thelesser wing ofthe sphenoid deep
in thebony orbit,coursing anteriorly above thesuperior rectus muscle and forming
anaponeurosis with several important bony,dermal,and tarsal attachments.As men-
tioned above,the dermal and conjoinedfascial attachments ofthe levator aponeu-rosis
are responsible for the superior lidcrease location (see Figure 64-9).19,20M�ller�s
MuscleM�ller�s muscle,a sym-pathetically innervated minor retractor ofthe upper lid
arising from the undersur-face ofthe levator palpebrae superiorismuscle,inserts
into the superior tarsalborder.Shortening ofthis muscle from theposterior aspect
may be performed as anadjunct ptosis repair during blepharoplas-
ty.36�38Approximately 2 mm ofupper lidlift are provided by contraction
ofM�ller�smuscle,practically evidenced by the mildupper lid lift experienced with a
rush ofsympathetic excitation (ie,during thefight-or-flight response).Lower Eyelid
RetractorsThe lower lidcounterparts ofthe levator and M�ller�smuscles are the
capsulopalpebral fasciaand the inferior tarsal muscle,the retrac-tors ofthe lower
lid (see Figure 64-9).Theterminal fibers ofthe inferior rectus mus-cle give rise to
a fibrous extension knownas the capsulopalpebral head ofthe inferi-or rectus which
splits to encompass theinferior oblique muscle,forming the infe-rior tarsal muscle
and the capsulopalpe-bral fascia.26These layers fuse anterior tothe inferior
oblique muscle,forming Lock-wood�s suspensory ligament,the analog toWhitnall�s
ligament ofthe upper lid.Con-tinuing anteriorly the lower lid retractorsinsert on
Tenon�s fascia,the inferior tarsalborder,and the orbital septum at a level 4 to 5
mm below the tarsal border.Eyelid Fat PadsOrbital RelationsInthe anterior
orbit,distinct fat compart-ments can be identified,although themajority ofthe
anterior orbital fat padsremain continuous with posterior orbitalfat (Figure 64-
11).39This continuityprompted concern that excessive tractionon orbital fat was
responsible for orbitalhemorrhage complicating blepharoplastywith fat
removal.40Most surgeons impli-cate faulty hemostasis offat pads,ratherthan
traction,as the cause ofpostble-pharoplasty orbital hemorrhage.Carefulhemostasis is
essential when performingeyelid fat removal.Peak of browForehead furrowsCorrugator
muscleFrontalis muscleOrbicularis oculi muscleProcerus muscleLevator
labiisuperioris muscleZygomaticus major muscleZygomaticus minor muscleOrbicularis
oris muscleUpper lid skin creaseMedial canthusPeak of upper lidLateral canthusLower
lid skin creaseMalar foldNasojugal foldNasolabial foldFIGURE64-10Selected
musculature ofthe eyelid.Orbicularis oculi in the setting ofthe superficial
facialmuscles.Adapted from Nerad JA.76TrochleaPreaponeurotic fatMedial fat
padOrigin of inferior obliqueLateral fat padFIGURE64-11Artist rendition ofthe
eyelid fat pad.Adapted from LemkeBN and Della Rocca RC.112
1324Part 9: Facial Esthetic SurgeryAging ChangesIn the youthful face,orbital fat is
held in check by a hearty orbitalseptum.Weakening ofthe septum associat-ed with
aging,chronic allergic swelling,ormedical problems resulting in fluid reten-tion
(ie,hypo- or hyperthyroidism) maypermit anterior prolapse oforbital fat,resulting
in steatoblepharon.Aging may alsocause atrophy ofeyelid fat,creating a supe-rior
sulcus deformity.Dietary deficiencyalone,however,has not been shown toresult in
orbital fat loss.41Upper Eyelid Fat PadsThe upper eyelidcontains central and medial
fat pocketsanterior to the levator muscle and aponeu-rosis.Immediately posterior to
the orbitalseptum lies the yellow central orpreaponeurotic fat,which is not
continu-ous with posterior orbital fat.Mediallyand inferior to the trochlea is the
firmerand more pale fibrous medial fat pad.39Manipulation ofthe medial fat pad
oftenrequires placement ofadditional anesthe-sia into the fat pad itself,as more
superfi-cial anesthesia will not adequately infil-trate this structure.Laterally
the superioranterior orbit houses the lacrimal gland.Orbital fat does not herniate
in the lateralupper eyelid.Care must be taken to avoidremoval oflacrimal tissue
when fat padexcision is intended.Inspecting for colordifference between the pink
lacrimal glandand yellow fat is helpful in differentiation.Note that lacrimal gland
prolapse mayoccur as an involutional change or in asso-ciation with thyroid
orbitopathy,makingthe position ofthe gland more anteriorthan usual.Lower Eyelid Fat
PadsThe lower lid con-tains medial,central,and lateral fat pads,which may prolapse
separately.Betweenthe medial and central compartmentsresides the arcuate expansion
ofthe inferi-or oblique muscle.Care must be taken toavoid damage to the inferior
oblique mus-cle during lower lid blepharoplasty as ver-tical or torsional diplopia
will result.Eyelid VasculatureArteriesThe eyelidvascular supply is rich,allowing
for excel-lent healing and infection resistance,whilemandating the surgeon to be
cognizant ofvascular relationships to avoid excessivebleeding.Both internal and
externalcarotid arteries contribute to eyelid bloodsupply via the ophthalmic artery
and thefacial and infraorbital arteries,respectively(Figure 64-12).The facial
artery becomesthe angular artery in the medial canthalregion and then perforates
the orbital sep-tum to anastomose with branches oftheophthalmic artery medial and
anterior tothe lacrimal sac.Arising from the maxil-lary artery the infraorbital
artery travelswithin the infraorbital sulcus and canal toemerge from the
infraorbital foramen andaid in arterial supply ofthe lower lid.Theophthalmic artery
terminates in thelacrimal,frontal,supraorbital,supra-trochlear,and nasal
arteries.Several anastomotic networks,knownas arcades,exist in the eyelids.The
periph-eral arcade ofthe upper lid lies superior tothe tarsus and directly anterior
to M�ller�smuscle,supplying the superior aspect ofthe upper lid and superior
conjunctivalfornix.The marginal arcades oftheupper and lower lids lie 2 to 4 mm
fromthe eyelid margin,directly anterior to thetarsi.A peripheral arcade may be
presentin the lower lid,although it is less welldeveloped.41VeinsThe eyelid venous
supply possess-es deep and superficial anastomoses.Thefacial vein,the principal
vein ofthe eye-lids,forms a deep anastomosis with thesuperior ophthalmic vein via
the supraor-bital vein and a second deep anastomosiswith the deep pterygoid plexus
via thedeep facial vein.Both anastomoses arepotential routes for cavernous sinus
spreadofsuperficial infection.LymphaticsRecent anatomic studiesdemonstrate the
lymphatic system oftheupper and lower eyelids to consist ofsuperficial subcutaneous
and deep pre-tarsal plexuses.42Using lymphoscintigra-phy to characterize drainage
pathways,parotid lymph node drainage from theupper eyelid,medial canthus,and
laterallower eyelid was shown.43Similar studiesdemonstrated medial and central
lowerOphthalmic arterySuperficial temporal arteryMiddle meningeal arteryForamen
spinosumMaxillary arteryInternal carotid arteryExternal carotid arteryFrontal
arteryLacrimal arteryInfraorbital arteryZygomaticofacial arterySupraorbital
arteryInfratrochlear arterySupratrochlear arterySuperior peripheral arcadeSuperior
marginal arcadeInferior marginal arcadeFacial arteryFIGURE64-12Orbital arterial
blood is supplied from both internal and external carotid arteries.Adapted from
Kikkawa DO and Lemke BN.41
Blepharoplasty1325eyelid drainage to the submandibularlymph nodes and a dual
drainage ofthecentral upper eyelid to both submandibu-lar and parotid
nodes.43InnervationMotorCranial nerve VII,the facial nerve,supplies motor
innervationfor all the facial muscles (Figure 64-13).The facial nerve arises from
the pons,even-tually dividing into temporal,zygomatic,buccal,mandibular,and
cervical branches.The temporal branch innervates bothfrontalis and orbicularis
oculi,whereas thezygomatic and buccal divisions also con-tribute in an overlapping
fashion to inner-vation ofthe orbicularis oculi.44The levator palpebrae
superiorisreceives motor innervation from the ter-minal branches ofthe superior
division ofcranial nerve III,the oculomotor nerve,which travels within the muscle
cone andenters the superior rectus inferiorly 15 mm from the orbital apex and
subse-quently enters the levator.M�ller�s muscleis sympathetically innervated by
postgan-glionic fibers that arise in the superior cer-vical ganglion,enters the
cavernous sinussurrounding the internal carotid artery,and subsequently joins nerve
branches toenter the orbit.SensorySensory innervation ofthe eye-lids is via the
ophthalmic and maxillarydivisions ofthe trigeminal nerve (cranialnerve V),which
give rise to the lacrimal,frontal,and nasociliary nerves,and
theinfraorbital,zygomatic,sphenopalatine,and posterosuperior alveolar
nerves,respectively (Figure 64-14).The lacrimalnerve courses superotemporally to
supplythe lacrimal gland,conjunctiva,and lateralupper lid and send an anastomotic
branchto the zygomaticotemporal nerve.Thefrontal nerve divides into supraorbital
andsupratrochlear branches near the orbitalrim.The supraorbital nerve exits the
orbitvia a notch or foramen in the superiororbital rim to provide sensation for
themajority ofthe forehead and scalp.Thesupratrochlear nerve,exiting the orbit lat-
eral to the corrugator muscle,conveys sen-sory input from the bridge ofthe nose
andmedial aspect ofthe upper eyelid and fore-head.45,46The nasociliary nerve gives
rise tothe anterior and posterior ethmoidalTemporal branch of thefacial
nerveFrontalis muscleMedial head of orbicularis oculi Superior procerus
musclesZygomatic branch of thefacial nerveZygomaticus major muscleDepressor
supercilii musclesCorrugator superciliiSuperior orbicularis oculiFIGURE64-13Anatomy
ofcranial nerve VII,the source ofmotor innervation for the face.Adapted fromKnize
DM.113Nasociliary nerve Supraorbital nerve Frontal nerve Supratrochlear nerve
Infratrochlear nerve Lacrimal nerve External nasal nerve Infraorbital nerve
Auriculotemporal nerve Zygomaticofacial nerve Anterior superioralveolar nerve
Foramen ovaleZygomaticotemporalnerve Optic nerveIntracranial viewCranial nerve
VOphthalmic division V1Gasserian ganglionMaxillary division V2Foramen
rotundumMandibular division V3Foramen ovaleFIGURE64-14Cranial nerves V1and V2supply
sensory innervation to the periorbital region.Adapted fromKikkawa DO and Lemke
BN.41
1326Part 9: Facial Esthetic Surgerynerves,the long ciliary nerves to theglobe,and a
sensory root to the ciliaryganglion and terminates as the sensoryroot to the
infratrochlear nerve.41Emerg-ing from the infraorbital foramen theinfraorbital
nerve supplies the skin andconjunctiva ofthe lower eyelid,nasal skinand septum,and
upper lip skin andmucosa via the inferior palpebral,lateralnasal,and superior
labial nerve terminalbranches,respectively.The zygomaticnerve divides into the
zygomaticofacialand zygomaticotemporal nerves.The for-mer travels along the
inferolateral orbit,traversing the zygomaticofacial foramenbefore innervating the
cheek skin,where-as the latter exits the orbit to the temporalfossa and supplies
the lateral forehead.Lacrimal System and Tear Film Compo-sitionLacrimal GlandsThe
lacrimalgland,incompletely divided by the later-al horn ofthe levator into orbital
andpalpebral lobes,lies in a shallow depres-sion ofthe superotemporal frontal
bone.In the superior and inferior conjunctivalfornices are the accessory lacrimal
glandsofKrause and Wolfring.Lacrimal Drainage SystemThe lacrimaldrainage system is
diagrammed in Figure64-15.The upper and lower lid puncta lie 8 and 10 mm lateral to
the tear sac,respec-tively,and are normally well apposed to theglobe.Initially
vertical for 2 mm the canali-culi make a 90� turn and travel 8 mm with-in the
orbicularis muscle just beneath thelid margin to join,forming the
commoncanaliculus.The common canaliculus thenjoins the lacrimal sac,which is found
with-in the bony lacrimal fossa.Ten percent ofthe population lacks a common
canalicu-lus,and the canaliculi simply lead to thelacrimal sac.The nasolacrimal
duct drainsbeneath the inferior turbinate into theinferior meatus.Tear Film
CompositionThe precornealtear film is comprised ofthree layers:mucin,aqueous,and
lipid.The innermucin layer,produced by conjunctivalgoblet cells,stabilizes the tear
film whilelubricating the corneal surface.Accessoryand main lacrimal glands account
for themiddle aqueous layer,the thickest por-tion ofthe tear film.The most
superficiallipid layer,secreted by the meibomianglands and glands ofZeis and
Moll,fur-ther stabilizes the tear film and preventsevaporation.Reflex tearing
prompted byemotion or an ocular irritant is producedby the main lacrimal
gland.Deficiency ofany component ofthe tear film leads todry eye symptoms.The tear
layer must be regularly redis-tributed by the eyelid blink mechanism tomaintain
ocular surface comfort andintegrity.Postoperative lessening ofthemagnitude and
frequency ofthe blink maytemporarily elicit dry eye symptoms inpredisposed
individuals.Blepharitis,con-junctivitis,and corneal irritation symp-toms are also
amplified by this temporarypostblepharoplasty eyelid dyskinesia.Patient
Evaluation:HistoryEliciting the ChiefConcernWhether primarily cosmetic or
functional,patient selection for blepharoplastyrequires careful consideration
ofhistoryelements,physical features,and patientexpectations as well as
investigation intopotential clinical pitfalls.The blepharo-plasty surgeon must
thoroughly explorethe goals ofthe patient.Patients needing afunctional
blepharoplasty owing to severedermatochalasis often describe frontalheadache or
fatigue from frontalis contrac-tion,impairment ofsuperior visual field,or a need to
raise the chin or use manualelevation ofthe brow or lids to enhancevision.Symptoms
are frequently exacer-bated by fatigue and are generally worse inthe evening
(ie,while reading in downgazePunctaTarsusAmpullaLateral nasal wall mucosa,middle
meatusCanaliculi of lacrimal sacLacrimal sacLacrimal ductMaxillary sinusInferior
turbinateFIGURE64-15The lacrimal system ofthe eyelid.Adapted from Lemke BN and
Lucarelli MJ.111
Blepharoplasty1327before bedtime).Patients may relate need-ing to raise their lid
skin to see better.Patients seeking cosmetic blepharoplastymay lament they �look
tired all the time�ordescribe a sagging change in their lid andeyebrow position
compared with the lidand brow position oftheir youth.Docu-mentation oflid effect on
patient quality oflife is valuable.Information on the impacton
occupation,hobbies,driving,and otheractivities ofdaily living is essential both
forbetter understanding ofthe patient�s goalsand for third party reimbursement.The
patient is encouraged to demon-strate the problem areas while looking at ahandheld
mirror.Patients are also asked tobring old photographs that reveal eyebrowposition
at an earlier age.Asian blepharo-plasty candidates are encouraged to pre-sent
photographs demonstrating thedesired upper eyelid crease type.Somesurgeons use
computer modeling pro-grams to illustrate possible results topatients.An immediate
demonstration ofthe effect ofeyebrow elevation or theimpact ofaging can be achieved
throughuse ofdigital photography ofthe patientwith comparison to prior
photographs.In functional and cosmetic patients,especially in the latter
group,expectationsmust be well defined.Ideal cosmetic candi-dates can describe
which physical parame-ters they find problematic.It is helpful tohave the patient
point out,either in a mir-ror or a photograph,the objectionable fea-tures.Vague
complaints or withdrawalfrom the decision-making process oftenpredict inadequate
understanding andunrealistic expectations.The issues underdiscussion should be
those ofthe surgicalcandidate,not issues generated by others.An open patient-
physician relationshipand thorough dialogue remain key build-ing blocks to a
successful surgical outcome.Important History ElementsHistoric questions on the
initial evaluationare designed to clarify the patient�s issueswhile identifying
factors that can altertreatment or contraindicate blepharoplas-ty.A complete past
ocular history,includ-ing documentation ofcontact lens use orintolerance,tearing
abnormalities,dry eyehistory,and previous surgery,as well as athorough past medical
history are neces-sary.Any history ofdry eye symptoms,such as ocular
scratchiness,blurred vision,foreign body sensation,or pain,should beinvestigated,as
blepharoplasty may aggra-vate these symptoms.Ophthalmologyconsultation should be
considered.Epiphora,ocular irritation with ambientwind,or current use ofartificial
tears allraise the possibility ofpostoperative dryeye symptoms.Keratoconjunctivitis
siccaor cicatricial conjunctival disease shouldmake the surgeon wary ofproceeding
withblepharoplasty.Prior facial,and especially lid andbrow,surgeries should be
discussed.Ifupper eyelid blepharoplasty has been pre-viously performed and the
patient com-plains ofa persistent skin fold,evaluate theeyebrow position to rule
out forehead pto-sis.Similarly the appearance ofmedial fatpad fullness can be
mimicked by medialeyebrow ptosis.A descended eyebrow fatpad or a prolapsed lacrimal
gland may alsobe mistaken by the patient as �residualupper eyelid fat�for which a
secondaryupper lid procedure is sought.The patientis shown their upper eyelid
appearancewith the forehead supported in the normalposition.Ifa significant effect
is noted thepatient must compromise on the final ble-pharoplasty result or accept
concomitantforehead lifting.Previously performedlower blepharoplasty may leave the
patientdesiring more fat removal,treatment ofanaccentuated nasojugal fold,skin
laxity ordeformity,eyelid malposition,or a lateralcanthal deformity.A surgeon
performing atranscutaneous lower blepharoplasty reen-ters the muscle later with an
increased riskofpostoperative lid retraction.Although rare with blepharoplastygiven
the thin nature ofthe eyelid skin,thepossibility ofhypertrophic scar
formationshould be discussed,especially with higherFitzpatrick skin types.47The
possibility ofpigmentary change ofthe surgical woundshould also be addressed.Any
history ofperiocular trauma should be explored asto the timing and nature ofthe
injury.Clinical course and physiologic stabil-ity should be documented in patients
withthyroid eye disease,as eyelid retractionassociated with thyroid
ophthalmopathymay worsen after poorly executed ble-pharoplasty.Eyelid
retraction,eyelidedema,and any herniated fat measure-ments in patients with thyroid
diseaseshould be stable for at least 6 months priorto consideration
ofsurgery.48Excessiveproptosis in patients with thyroid eye dis-ease is generally
treated with orbitaldecompression prior to any eyelid surgery.Patients with thyroid
orbitopathy oftenexhibit persistent eyelid fat herniation,eyebrow fat pad
hypertrophy,and a glabel-lar grimace (Figure 64-16).A full medication history
should bedocumented,especially the use ofaspirin,nonsteroidal anti-inflammatory
medica-tions,anticoagulants,homeopathic herbalFIGURE64-16Patient displaying
features char-acteristic ofthyroid orbitopathy.
1328Part 9: Facial Esthetic Surgerypreparations,and vitamin E,as patientswill need
to discontinue these medicinespreoperatively for 1 to 2 weeks.Warfarin isgenerally
held for 4 days preoperatively.Inquiry regarding cigarette,alcohol,andillicit drug
use should be made as the for-mer may influence skin quality and healingand the
latter two may affect the patient�sability to complete postoperative care.Physical
Examination The preoperative physical examination ofa patient requesting
blepharoplasty focus-es on eyelid function (ocular protection,tear film
distribution,and clearance ofthevisual axis) as well as structure and region-al
anatomy that may necessitate adjunctiveprocedures for a superior result.The
EyebrowExamination ofthe fore-head and eyebrow seeks to define browposition as a
contributor to apparentupper lid skin redundancy.Findings maybe demonstrated to the
patient with amirror.Eyebrow position below thesupraorbital rim yields a T-type
configu-ration to the nasal-eyebrow angle,where-as the youthful female brow
position cre-ates a Y-type nasal-eyebrow angleconfiguration.46Measuring the
distancefrom the central inferior eyebrow to theinferior corneal limbus while the
patientis in primary gaze can aid in identificationofpatients with brow ptosis.A
value lessthan 22 mm,especially in women,maywarrant consideration ofbrow
elevationas an adjunctive procedure.48Quantitativegrading ofbrow ptosis can be
obtained byplacing a millimeter ruler vertically overthe eyebrow and measuring the
differencein millimeters between current locationand ideal position when the
eyebrow iselevated by the clinician�s finger.Perform-ing the measurement over the
medial,central,and lateral brow is beneficial toquantify brow ptosis,which is often
seg-mental.Adjunctive brow elevation mustbe considered ifmore than mild browptosis
is present.Upper EyelidThe skin quantity,quality,and resilience are important in
determin-ing the amount ofskin to excise and use ofadjunctive procedures.With the
patient�seyes closed and gentle elevation ofthebrow to smooth out the upper eyelid
skin,an objective measurement ofthe amountofeyelid skin can be obtained.Generally
18 to 21 mm ofeyelid skin is retained dur-ing upper lid blepharoplasty.4Eyelid
skinshould be examined for
dermatopathology(ie,eczema),inflammation,pigmentaryinconsistencies,and prior
surgical scars.Any suspicious skin lesions suggestive ofneoplasia should be
documented and dealtwith prior to surgery.Rhytids should beassessed.Orbital fat
herniation,manifestedas lid fullness,can be appreciated in themedial and central
upper lid by palpation.Fullness in the lateral upper lid may signifylacrimal gland
prolapse,which may neces-sitate repositioning during blepharoplasty.The upper
eyelid crease is identified bygently lifting the eyebrow and asking thepatient to
look down,then slightly up,andthen down again while inspecting upperlid skin for a
dynamic crease that retractswith slight upgaze.Static eyelid skin creas-es may or
may not reflect this dynamicinfolding produced by levator muscleactivity.The
distance from the centralupper lid crease to the upper lid margin isnormally 9 to
11 mm in women and 7 to 8 mm in men,except for the aforemen-tioned variation in
Asian eyelid creaselocation.Greater values than expectedmay indicate levator
aponeurosis disinser-tion and possible blepharoptosis.Lesservalues may indicate
preaponeurotic fatpad incursion into the pretarsal space.Lidcrease reformation may
be consideredwhen desired.It is critical that the upper eyelid posi-tion,evaluated
with the forehead relaxed,be assessed preoperatively in the blepharo-plasty
candidate and that the measure-ments be recorded in the chart.The mar-gin reflex
distance (MRD),the distancefrom the middle ofthe pupil to the upperlid margin,is
determined by shining apenlight in the patient�s eyes to obtain apupillary light
reflex while the patient is inprimary gaze.Should the patient�s upperlid ptosis
preclude visualization ofthelight reflex,the lid should be raised untilthe reflex
is seen and the number ofmil-limeters oflift needed is recorded as a neg-ative
value.A normal MRD is 4 to 4.5 mm(Figure 64-17).Care must be taken to dis-tinguish
between genuine lid ptosis andsevere dermatochalasis wherein thedraped skin
obscures the light reflex.AnMRD greater than 5.5 mm and superiorscleral show are
indicative ofupper lidretraction.Investigation ofpossible thy-roid disease should
be considered.Uppereyelid position with the eyelids gentlyclosed should be
inspected for lagophthal-mos (incomplete lid closure),which mayherald dry eye
symptoms ifgreater than 2 mm.Special attention to lagophthalmosis warranted in
patients who have under-gone prior blepharoplasty.Levator palpebrae superioris
functionis key to upper lid position and should beobjectively measured.While
holding a ver-tical millimeter ruler lateral to the greatestdiameter ofthe
palpebral fissure,the upperlid margin is measured in extremedowngaze and extreme
upgaze.Care mustbe taken to immobilize the brow so as toavoid the influence
offrontalis recruit-ment.Repeating the measurement severaltimes is useful to obtain
an average,whichis recorded.Lid lag,evidenced by lack of4 mmFIGURE64-17The margin
reflex distance mea-sures the distance between the center ofthe pupiland the margin
ofthe upper eyelid.Adaptedfrom Putterman AM.48
Blepharoplasty1329smooth pursuit ofthe upper lid marginwith the superior corneal
limbus while thepatient moves from upgaze to downgaze,can alert the examiner to
possible thyroiddisease.The presence ofexcessive upper lidlaxity,upper lash
ptosis,and papillary con-junctivitis in a patient with ocular irrita-tion and
injection suggests floppy eyelidsyndrome.Lash ptosis is an altered trajec-tory
ofthe lashes whereby cilia projectinferiorly rather than anterosuperiorly.Iffloppy
eyelid syndrome is suspected,exam-ination findings will confirm abnormallyeasy
distraction ofthe upper lid offtheocular surface.Horizontal tightening oftheupper
eyelids,performed by lateral short-ening and re-insertion ofa tarsal stripwithin
the orbital rim,may be indicated.The eyelid margin should be inspect-ed.Evidence
ofblepharitis,such as col-larettes along the lashes,thickened lidmargins,and
plugged meibomian glands,should be noted and lid hygiene (ie,warmwashcloth soaks
with gentle baby sham-poo eyelid cleansing) prescribed to resolvethe blepharitis
prior to surgery.Lower EyelidCareful skin examinationis equally as important in the
lower eyelidarea as in the upper lid.Rhytids,especially�crow�s feet,�should be
noted,as promi-nence may necessitate adjunctive topicalretinoic acid,chemical
peels,laser resur-facing,and botulinum toxin A injections.Assessing for extra lower
lid skin is bestperformed in upgaze.The pinch test usesan angled forceps,such as a
Brown-Adson,to grasp a redundant fold oflower lid skinwithout altering lid position
while thepatient is in upgaze with his or her mouthopen (to allow for maximal
necessaryexcursion oflower lid skin).The amountofskin grasped approximates the
amountto excise.Orbital fat prolapse is noted inthe medial,central,and lateral
lower lid.Facile differentiation oforbital fat fromedema is achieved by gentle
ballottementofthe upper eyelid;fat herniation willresult in distinct anterior
movement ofthefullness whereas edema will not.Hyper-trophied orbicularis muscle is
mostprominent when the patient smiles.Lower lid position can be quicklyassessed by
examining the lower eyelidmargin position relative to the inferiorcorneoscleral
limbus.Any inferior scleralshow in primary gaze is objectively mea-sured from the
inferior corneoscleral lim-bus to the lower eyelid margin,or usingthe margin reflex
distance-2 (MRD2),thedistance from the pupillary light reflex tothe lower lid
margin in primary gaze.Together the MRD and MRD2composethe palpebral fissure
height.Normally thelower lid rests at or slightly above the infe-rior corneal
limbus.An increased MRD2raises concern oflower lid retraction fromthyroid
ophthalmopathy,lower lid laxity,mechanical forces,or cicatricial
causes.Ahypoplastic maxilla causing decreasedprominence ofthe inferior orbital
rimmay contribute to postoperative suscepti-bility to lower lid retraction and
ectropion.Abnormal lower lid position androunding ofthe lateral canthal angle
oftenresult from lower lid laxity.Laxity isassessed by distraction and the snap-
backtest.By gently grasping the lower lid cen-trally,the lid is distracted offthe
globeanteriorly.Normal distraction is less than6 mm.Greater distraction suggests
laxity.To perform the snap-back test the lowerlid is pulled inferiorly and released
whilethe patient refrains from blinking.A nor-mal lid returns to the globe quickly
withone or fewer blinks.A lax lid requires sev-eral blinks to resume its former
positionand may remain inferiorly displaced andeverted,indicating ectropion.Laxity
ofthelateral canthal tendon is the most com-mon cause oflower lid laxity.The
abilityto displace the punctum greater than 2 mm laterally indicates laxity ofthe
medi-al canthal tendon.49Lower lid horizontaltightening procedures should be per-
formed at the time ofblepharoplastysurgery for the lax lower lid to
preventpostoperative ectropion and recreate theyouthful,slightly elevated,well-
definedlateral canthal angle.Midface ArchitectureMidfacial ptosis,festoons,and
malar mounds are impor-tant aspects to note on evaluation,as sep-arate procedures
are necessary to addressthese concerns.Midfacial ptosis encom-passes a host
ofchanges caused by attenu-ation ofthe subcutaneous portions
oftheorbitomalar,masseteric cutaneous,andzygomatic ligaments,including soft
tissueinferior migration ofthe lower eyelidstructures,cheek,and midface,as well
asconcomitant prominence ofthe nasolabi-al fold (Figure 64-18).12When
attenuationofthe lower lid orbicularis oculi and laxi-ty oforbicularis attachments
to deep fas-cia develop,the orbicularis may sag orform redundant folds known as
fes-toons.50Several levels offestoons havebeen described including pretarsal,pre-
septal,orbital,and malar,and composi-tion varies to include one or more
ofthefollowing:skin,muscle,suborbicularis fat,FIGURE64-18Profile ofa patient with
descentofthe cheek prominence characteristic ofmid-facial ptosis.
1330Part 9: Facial Esthetic Surgeryand herniated orbital
fat.50Malarmounds,projections ofskin and fat in thearea ofthe malar eminence,are
areas ofaltered inferior orbital orbicularis fibersthat allow abnormal
communicationbetween subdermal and suborbicularisfat.50Malar mounds often prove
challeng-ing to resolve.Lacrimal Secretion and Ocular SurfaceEvaluationDry eye
symptoms are fre-quent following blepharoplasty,and pre-operative evaluation ofthe
lacrimal sys-tem may direct surgical intervention andpatient education,thereby
avoiding sig-nificant morbidity.The tear meniscus,tear break-up time,Schirmer
testing,and/ or fluorescein corneal staining areoften used.The tear meniscus may
bemeasured using a thin cross-sectionalbeam oflight ofa slit lamp biomicro-scope
focused on the patient�s lower lid.The beam height is changed to match theheight
ofthe tear meniscus on the lowerlid.Normal values are approximately 0.2 to0.3
mm.The tear break-up time testrequires instillation of2% fluorescein dyeon the
cornea and examination with acobalt blue light.The patient is asked toblink once
and then refrain from blink-ing.Any loss ofthe tear film continuity(evidenced as a
streaky dry spot and colorchange from green to blue) in less than 10 seconds is
considered abnormal.Thetear break-up test measures tear stability,which is largely
due to the lipid compo-nent ofthe tear film.The Schirmer tests,the gold standards
for lacrimal testing,quantify the aqueous tear secretory com-ponent.After blotting
the inferior cul desac and palpebral conjunctiva,a bent fil-ter paper strip (ie,a
Schirmer strip),isplaced in the lateral third ofthe lowereyelid with the strip
notch at the eyelidmargin such that the strip proceeds ante-riorly.The room lights
are dimmed toavoid reflex tearing.The strip is removedafter 5 minutes and the
amount ofstripwetting measured.Topical anesthesia isgenerally used in the basic
secretion test,which indicates basal tear secretion.Thenormal value is
approximately 15 mm.Tear hyposecretion is indicated with 5 to10 mm ofwetting and
less than 5 mmsuggests dry eye.Interpalpebral cornealand conjunctival staining with
fluores-cein (Figure 64-19) is characteristic ofkeratitis sicca,while inferior
cornealstaining suggests exposure keratopathy orblepharitis.51,52The extent
ofevaluationfor dry eye varies among surgeons andoften from patient to patient with
thesame surgeon.53There is controversy inthe literature regarding the most appro-
priate evaluation,although the generalconsensus is that historic and
physicalexamination elements suggestive ofdryeye warrant more thorough
evaluationand an especially conservative blepharo-plasty.54�56Patient education
shouldstress the role ofocular lubrication.One ofthe important ocular
surfaceprotective mechanisms is the Bell�s phe-nomenon,or the normal �rolling
back�ofthe eyes with lid closure.This may be testedby asking the patient to tightly
close theireyes while the examiner manually opensthe lids to assess corneal
position.A poorBell�s phenomenon indicates a risk ofpost-operative corneal exposure
and irritation.Corneal sensation is another keyaspect ofocular surface
protection.It maybe tested by touching a wisp ofcotton tothe peripheral cornea
while the patient is inupgaze.A blink response is normal.Patients who wear contact
lenses or whohave undergone refractive surgery mayhave decreased corneal
sensation.57�59Indi-viduals seeking cosmetic corneal surgeryoften seek cosmetic
blepharoplasty.Ocular Motility EvaluationDiplopiamay result spontaneously after
blepharo-plasty or be due to iatrogenic injury ofthesuperior or inferior oblique
muscles.Abaseline evaluation ofextraocular motilityis therefore warranted.Using a
musclelight or the examiner�s finger,the patient isdirected to look in the nine
positions ofgaze:superotemporal,superior,supero-
nasal,lateral,medial,inferotemporal,infe-rior,inferonasal,and straight
ahead.Anyocular motility deviations should be eval-uated prior to surgery.Patients
with thy-roid ophthalmopathy having impairedocular motility are generally
recommend-ed to have their strabismus surgery priorto any eyelid surgery.Visual
AcuityA vital sign ofocular func-tion,the best-corrected visual acuity ofboth
eyes,should be documented prior tosurgery.Ifvisual acuity is subnormal,oph-
thalmologic evaluation is especiallyimportant.In addition postoperative visu-al
complaints can be more accuratelyassessed when the baseline visual acuityhas been
recorded.Visual decline postop-eratively may be wrongly attributed to ble-
pharoplasty ifpreoperative visual acuityhas not been documented.Ancillary
StudiesBoth visual field testing and photographyaid in demonstrating preoperative
changesin visual function and appearance.Visualfield testing is necessary for
patients wish-ing to determine insurance benefits forsurgery.Visual Field
EvaluationPeripheral visu-al field testing is performed to documentvisual field
loss,usually ofthe superiorfield,due to upper eyelid dermatochalasisFIGURE64-
19Punctate staining ofthe corneatypical ofkeratitis sicca.
Blepharoplasty1331or blepharoptosis.Several differentperimeters may be used,such as
the auto-mated Humphrey or manually operatedGoldmann perimeter or tangent
screen.Perimetry is performed with the patient�seyelid unaltered and repeated with
theeyelid skin or ptotic lid elevated.Photographic DocumentationPreoper-ative
photography is key when performingeyelid surgery.Documentation ofpreop-erative
appearance serves as a benchmarkfrom which postoperative change can bedetermined
and is a valuable referencewhen initially unforeseen postoperativecomplications
arise.Minimum pho-tographs recommended include frontalprimary,upgaze and
downgaze,and later-al views.Discussion ofphotographicspecifics is beyond the scope
ofthis chap-ter and the reader is referred to alternatetexts for a more complete
discourse.60Anesthesia The majority ofblepharoplasty surgery isperformed in an
outpatient surgical envi-ronment or an office procedure room,under local
anesthesia,with or withoutintravenous sedation.Oral anxiolyticssuch as diazepam are
often employedwhen intravenous sedation is not used.Adjunctive procedures performed
at thetime ofblepharoplasty may warrant gen-eral endotracheal anesthesia,and the
anes-thesia and sedation needs may vary on anindividual basis.The blepharoplasty
surgeon should befamiliar with topical and local infiltrativeanesthesia
options.Commonly used topi-cal ocular anesthetics include the ester-type
compounds,proparacaine (0.5%)and tetracaine (0.5%).Commonly usedlocal infiltrative
anesthesia choices are allamides and include lidocaine (0.5 to2.0%),mepivacaine (1
to 2%),and bupi-vacaine (0.25 to 0.75%).Lidocaine andmepivacaine have an onset
ofaction from3 to 6 minutes and a comparable durationofaction (120 minutes) when
epinephrineis mixed with lidocaine.Bupivacaine has aslower onset ofaction (10
minutes) and alonger duration ofaction (8 to 12 hours).Epinephrine is added to
promote hemo-stasis through vasoconstriction and slowabsorption,thereby prolonging
durationofthe anesthetic and increasing the maxi-mum safe anesthetic dosage.No
addition-al therapeutic benefit is gained by addingconcentrations ofepinephrine
greaterthan 1:100,000.A mixture of2% lidocainewith 1:100,000 epinephrine and
0.5%bupivacaine with epinephrine allows forrapid onset ofprolonged anesthesia.Over-
dose toxicity ofthe amide-type anestheticsmanifests as mild hypertension and tachy-
cardia,lightheadedness,mild agitation,and confusion.Severe toxicity is markedby
seizures,coma,respiratory depression,bradycardia,ventricular dysrhythmias,and
asystole.Maximal doses based on mil-ligram per kilogram and total daily doseare 7
mg/kg and 500 mg for lidocaine withepinephrine,4.5 mg/kg and 300 mg forlidocaine
without epinephrine,and 7 mg/kg and 1,000 mg for mepivacaine.Bupivacaine daily dose
should not exceed175 mg and maximal daily dose with epi-nephrine is 225
mg.Hyaluronidase,an enzyme thatdegrades the polysaccharide hyaluronicacid,may be
added to local anesthetics toaid in anesthetic diffusion and tissue per-
meability.Duration ofanesthetic action isdecreased when hyaluronidase is
usedconcomitantly.Sodium bicarbonate has been advo-cated as a local anesthetic
adjunct toreduce the discomfort associated withanesthetic infiltration.61A
base,sodiumbicarbonate,partially neutralizes theacidic nature oflocal anesthetics
with epi-nephrine,thereby decreasing the irritationthat the acidic anesthetic pH
induces.Anesthesia injection is performedfrom the temporal aspect with the
needlebevel up.Keeping the needle as parallel aspossible to the eyelid skin and
carefullystabilizing the patient�s head during injec-tion guard against inadvertent
globe pene-tration.Injection sites are placed withinthe skin area to be
excised,thereby allow-ing removal ofthe occasionally producedmicrohematomas.Milking
the injectedfluid medially aids in minimizing thenumber ofsites injected.Injection
depth isat the level ofthe orbicularis muscle.Upper Eyelid Blepharoplasty
Preoperative ConcernsOn the day ofsurgery,review ofthe surgi-cal plan and
examination ofthe patient inan upright position are helpful.Once in the operating
room,skin inci-sion lines are marked with a methyleneblue surgical marking pen
prior to skinpreparation or immediately thereafter.The former has the advantage
ofallowingfull view ofthe patient�s face during themarking process and providing
severalminutes ofanesthesia infiltration whilethe surgeon is scrubbing for the
surgeryand the patient is being draped.Injectionprior to surgical marking is not
recom-mended unless the surgeon waits for theinjected volume to diffuse as the
injectedvolume may influence placement ofsurgi-cal marks.The patient�s periocular
areashould be thoroughly prepared with a 5% povidone-iodine or pHisoHex solu-
tion.Care should be taken to not allowpHisoHex solution to contact the cornealor
conjunctival surfaces.Irrigate the ocu-lar surface well ifcontact occurs.Caremust
be taken to avoid removing the sur-gical marking during preparation ifmark-ing is
performed prior to the prep.Topicalocular anesthesia drops (ie,proparacaineor
tetracaine) are instilled onto the ocularsurface and a protective corneal
contactmay be inserted.Surgical marking requires that thepatient be supine with the
surgeon inter-mittently elevating the brow manually so asto flatten any redundant
upper eyelid skin.Ifthe brow is not elevated,erroneously highsurgical marking may
result.Special care is
1332Part 9: Facial Esthetic Surgerytaken to provide vertical traction on
thepretarsal skin to remove any redundancy asthe inferior incision is designed.The
initialsurgical mark extends from the punctum tothe lateral canthus and lies along
the uppereyelid crease or where the intended lidcrease will be.The location ofthe
uppereyelid crease should be measured withcalipers to confirm proper placement
oftheinferior aspect ofthe incision.In womenthe initial surgical mark is generally
8.5 to10 mm above the superior lid margin cen-trally.The corresponding value in men
is 7 to 8 mm.The crease may be designed 0.5 mm lower than ultimately desired
asvertical traction will stretch the skin some-what and provide desired lash
eversion.Surgical marking in the Asian patient variesfrom these values and will be
discussedbelow.The superior surgical mark is placednext.Approximately 18 to 21 mm
ofuppereyelid skin should be left after the intendedskin is removed.Care should be
taken toavoid confusing epilated inferior eyebrowskin for true eyelid
skin.Excessive skinremoval will result in difficulty with eyelidclosure and impair
ocular surface protec-tion.Excessive skin removal might also pre-clude future
correction ofeyebrow or fore-head ptosis.The upper and lower surgicalmarks are
connected in a curvilinear man-ner (Figure 64-20).To test the adequacy oflid skin
remaining,the upper and lowermarks should be approximated using apinching technique
with forceps.The for-ceps should grasp all excessive skin withoutaltering the
closed eyelid margin.Slight ele-vation ofthe eyelashes with the pinch maybe
desired.Any opening ofthe lids duringmedial,central,and lateral pinch assess-ment
should warrant modification ofintended incision lines.Local anesthesia is next
injected sub-cutaneously into the skin intended forremoval.Gentle pressure may be
used todiffuse the injected fluid.Excision ofthe Skin-Muscle FlapAftersufficient
anesthesia infiltration hasoccurred and a corneal protector has beenplaced on the
operative eye ifdesired,theeyelid skin is held taut for the incision.Careful
traction perpendicular to the inci-sion site can be provided by the
surgicalassistant.A no.15 Bard-Parker blade,straight iris scissors,carbon dioxide
(CO2)laser,electrosurgical microdissection nee-dle,or radiosurgical unit is used to
incisethe skin and orbicularis muscle along thepreviously placed surgical marks.The
skin-muscle flap is next dissectedoffthe orbital septum by elevating the lat-eral
aspect ofthe flap superiorly with for-ceps while the assistant provides perpen-
dicular traction at the superior andinferior margins ofthe flap.A gentlepainting
motion is used,with care to avoidviolating the orbital septum.The edges ofthe flap
should be angled at approximate-ly 45�to avoid a bulky muscular ridgewhen the edges
are reapproximated duringclosure.Angulation ofthe edge is especial-ly important
temporally where the musclelayer is thicker.Hemostasis should beachieved with
cautery after flap dissectionand,ifno fat excision is planned,the skincan be closed
at this point.Fat DebulkingUpward traction is usedto lift the orbital septum prior
to openingthe septum in the superomedial aspectwith Westcott
scissors,electrosurgicalmicrodissection needle,or CO2laser.Theseptal opening is
extended laterally to com-prise the full width ofthe flap.The herni-ated orbital
fat pads should be evidentmedially and centrally.Color as well aslocation can be
helpful in differentiation,as the medial fat pad is a more pale lemoncolor as
opposed to the brighter yellowcentral fat pad.The connective tissue cap-sule
overlying the medial fat pad is opened.Gentle ballottement ofthe globe throughthe
upper lid aids in herniating the fatthrough the incised capsule.The medial fatpad
may require additional anestheticinjection to facilitate comfort
duringmanipulation.The fat is gently graspedwith straight forceps and teased
out,thenclamped at the base exiting the capsule.Cautery is used to separate the fat
from theclamp.Care should be taken to achieveexcellent fat pad hemostasis as
postopera-tive bleeding may contribute to the rare butvision-threatening
complication oforbitalhemorrhage.Herniation ofthe central orpreaponeurotic fat pad
is addressed in asimilar fashion by incising the overlyingcapsule,teasing out the
fat,and clampingand cauterizing the herniated fat.Over the last decade emphasis has
beenplaced on removing less fat during bothupper and lower blepharoplasty.In
maleblepharoplasty patients,fat excision shouldbe especially judicious as the
superior sul-cus in men is generally more full than inwomen and excessive fat
excision may fem-inize appearance by creating an unnatural-ly hollow-appearing
superior sulcus.With abilateral upper eyelid blepharoplasty,atten-tion should be
directed toward leavingrather than resecting symmetric amountsoffat.Alternatively
fat may be thermallysculpted to improve the eyelid contour.Lacrimal Gland ProlapseA
fullness tothe lateral upper eyelid may suggest pro-lapse ofthe orbital lobe ofthe
lacrimalgland,which is seen as a pink to tan firmlobulated structure
intraoperatively afterthe septum is opened.Care should betaken not to resect
lacrimal gland tissue aspostoperative dry eye may result.Reposit-ing the prolapsed
lacrimal gland in thelacrimal gland fossa should be easilyachieved.Difficulty in
repositing maysuggest a neoplastic or infiltrative processand warrant a biopsy.A
double-armed 5-0 polypropylene suture may be used torefixate the prolapsed gland to
the orbitalroofperiosteum.62,63Eyelid Crease Reformation and Skin Clo-
sureReformation ofthe upper eyelidcrease seeks to establish a connectionbetween the
levator aponeurosis and theorbicularis oculi muscle.In most instances
Blepharoplasty1333the inferior tissues are sufficiently adherentposteriorly such
that a lid reformationsuture may not be required.Prior to eyelidcrease
reformation,meticulous hemostasisshould again be checked.Reformation isperformed
using buried interrupted sutureswith an intermediate duration absorbablesuture
(ie,polyglactin) passed through bothupper and lower orbicularis edges and
thelevator aponeurosis at the level ofthe top ofthe tarsus.Care should be taken to
achievesymmetric upper lid creases bilaterally.The orbicularis is next
approximatedwith several buried interrupted sutures of7-0 polyglactin or a similar
suture material.Placement ofthese interrupted suturesshould allow facile reunion
ofthe upper eye-lid skin edges with a smooth contour.Redundant skin causing
cutaneous standingdefects should be excised using Burow�s tri-angle technique.The
skin is closed using 6-0 fast-absorbing gut suture in a runningfashion,beginning
medially and progressinglaterally.Alternative suture options for skinclosure
include nylon,polypropylene,or silk,although sutures that are not absorbablerequire
removal approximately 5 to 7 daysFIGURE64-20A,Upper eyelid transcutaneous
blepharoplasty.Surgical marking.B,Pinching technique to assess adequacy ofamount
ofremaining lid skin.C,Dissection ofthe skin-muscle flap.D,Completion ofskin-muscle
flap dissection showing intact orbital septum.E,Opening ofthe orbital septum.F,Fat
paddebulking.G,Closure ofthe orbicularis.H,Closure ofthe skin.I,Completed
result.ABCDEFGHI
1334Part 9: Facial Esthetic Surgerypostoperatively.Greater duration
ofsutureretention is required ifCO2laser resurfacingis performed concomitantly with
blepharo-plasty.Skin closure sutures should have onlyminimal tension.Recent
evidence suggeststhe tissue adhesive octyl-2-cyanoacrylate is aviable alternative
to sutures.64Several keysteps oftranscutaneous upper eyelid ble-pharoplasty are
shown in Figure 64-20.Transconjunctival Upper Lid Blepharo-plastyReserved for
patients with isolat-ed medial fat pad herniation and minimalor no wrinkling ofthe
upper eyelid skin isthe transconjunctival approach,which isrelatively new.65,66The
transconjunctivalapproach is a valuable one for patients inwhom a noticeable scar
would be unavoid-able with the transdermal approach (ie,young patients),patients
who have resid-ual medial fat pad prominence after tradi-tional upper lid
blepharoplasty,or as anadjunct to a brow lift and periorbital laserfor periorbital
rhytids.Patients with severeblepharoptosis,dermatochalasis or promi-nent upper lid
asymmetry are not candi-dates for this approach.65After instilling tetracaine on
the cornerofthe operative eye a corneal protectivelens is inserted.Local anesthesia
is nextinjected into the medial aspect ofthe upperfornix.A Desmarres retractor is
used toexpose the upper lid palpebral conjunctiva.An incision is made 3 to 4 mm
above theupper tarsal margin,and medial dissectiontoward the contralateral parietal
bone iscarried out using angled scissors.Once theconnective tissue ofthe medial fat
pad isopened the fat protrudes outward.The fatis next gently grasped,clamped,and
cau-terized at the excision base.When fat exci-sion is complete the lid is released
withoutclosure ofthe incision site.65,67Asian Upper Eyelid BlepharoplastyOriginally
described in 1896 by the Japan-ese physician M.Mikamo,the double eye-lid procedure
creates a superior palpebralcrease in Asian patients with single eye-lids.68This
frequently performed cosmeticprocedure seeks to create a defined creaseparallel to
the eyelid margin or an arcingcrease that begins at the medial canthalarea and
gradually fans away from the lidmargin laterally.69Consideration ofthepatient�s
facial features should guide surgi-cal planning ofthe lid crease.70Because
lidcrease asymmetry is the most frequentcomplication,careful surgical planningand
marking are critical to ensure propercrease placement.71The patient is prepared in
the man-ner described for a transcutaneous ble-pharoplasty.The lower surgical
mark,which indicates the final desired creaselocation,should be 5 to 8 mm from
theciliary margin,thereby approximating thesuperior tarsal margin.24Vertical
tarsalheight can be ascertained by lid eversion.The lower surgical mark shape
dependson whether a parallel or arcing crease isplanned.24The amount ofskin
excised,asdetermined by the superior surgicalmark,should be conservative.The skin-
muscle flap is next dissected.A suborbic-ularis fat pad may be encountered,whichcan
be carefully excised to reveal theorbital septum.16The orbital septum isnext gently
opened to allow for any nec-essary preaponeurotic fat pad treatmentand to access
the levator aponeurosis.Two options are frequently employed forlid crease
creation,which requires anadhesion between the skin and levatoraponeurosis.Direct
suturing ofthe pre-tarsal orbicularis to the levator aponeuro-sis is accomplished
via multiple smallinterrupted sutures that incorporate bitesofthe levator
aponeurosis and the pre-tarsal orbicularis in the area ofthedesired final lid
crease.A running suturewould then be used to close the skin.Alternatively the skin
edges can be direct-ly sutured to the levator aponeurosis bypicking up the lower
skin edge,incorpo-rating a small bite oflevator aponeurosisin the desired crease
location,and finish-ing by passing through the upper skinedge.Placing several such
sutures can fixthe crease location and the remainder ofthe skin incision can be
closed usingsutures performed in a running fashion.24Figure 64-21 depicts the
latter variationin Asian eyelid crease reformation.Lower Eyelid Blepharoplasty
Selection ofApproachBlepharoplasty ofthe lower eyelid can be approached via
ananterior transcutaneous or a posteriortransconjunctival approach depending onthe
abnormalities to be addressed.The tra-ditional transcutaneous route
providesexcellent visualization oflower lid fat padsand allows for excision
ofexcessive skin,hypertrophic orbicularis muscle,and her-niating fat.The risk
oflower lid malposi-tion,however,is not insignificant using anFIGURE64-21Asian lid
crease reformation.A,Direct suturing ofthe orbicularis to the lev-ator
aponeurosis.B,A continuous suture isused to approximate wound edges.Adaptedfrom
Chen WP.24AB
Blepharoplasty1335anterior approach.The transconjunctivalapproach carries a
significantly lower riskofpostoperative lower lid malposition anddoes not create an
external scar.Thetransconjunctival approach is ideal in thesetting ofisolated fat
herniation with mini-mal skin redundancy.The darkly pigment-ed patient predisposed
to altered pigmenta-tion or scar formation may also be a goodtransconjunctival
blepharoplasty candi-date.Patients with thyroid eye disease,whoare prone to lower
eyelid retraction,arepotential posterior blepharoplasty candi-dates provided enough
lid laxity is presentto allow conjunctival access.Adjunctiveprocedures such as
chemical peels,CO2laser skin resurfacing,or pinch skin exci-sion are commonly
performed in associa-tion with transconjunctival lower lid ble-pharoplasty.These
adjunctive procedureshave expanded the lower lid pathologiessuccessfully treated by
the transconjuncti-val approach to include most patients.72Presence oflower eyelid
laxity calls foran adjunctive horizontal lower lid tighten-ing procedure at the
time oflower eyelidblepharoplasty.Failure to perform such aprocedure heightens the
risk oflower lidretraction,lateral canthal abnormalities,and inferior scleral
show.Transcutaneous ApproachAn infracil-iary surgical mark is drawn
approximately1.5 mm beneath and parallel to the lowerlash line extending from the
punctum tothe lateral canthus.Temporal to the lateralcanthus the mark is continued
laterallywithin a preexisting �laugh line�forapproximately 5 mm.Care should be
takento avoid an inferiorly sloping terminationofthe incision as an unnatural
surgical scarwill result.Subcutaneous anesthesia is nextinjected and the patient is
prepared forsurgery in a similar manner to thatdescribed for upper eyelid
blepharoplasty.A no.15 Bard-Parker blade,CO2laser,microdissection needle,or
otherincising instrument is used to make theskin incision.A 4-0 silk traction
suturemay be placed through the skin,orbicu-laris,and superficial tarsus to aid
inupward displacement ofthe lower eyelid.Subcutaneous dissection is carried
outtaking care to minimize trauma to thepretarsal orbicularis.Next the
orbicularisis incised below the inferior tarsal borderwith Westcott scissors or
other appropri-ate instrument for the full length oftheincision.A skin and muscle
flap is dis-sected inferiorly toward the orbital rim.Excellent hemostasis should be
obtainedwith judicious use ofcautery.The orbitalseptum is next opened with Westcott
scis-sors where it overlies the lower eyelid fatpads.The fat pad capsules are
subse-quently incised beginning with the lateralfat pad,which is the more difficult
com-partment to visualize.Gentle ballotte-ment ofthe globe is used to aid in fat
pro-lapse.The herniated fat is grasped,clamped,and excised.Meticulous hemo-stasis
offat is essential to avoid retrobul-bar hemorrhage.Conservative fat resec-tion is
recommended,as over-resectionresults in a hollow appearance ratherthan a youthful
one.The central andmedial fat pads are debulked as needed ina similar fashion.Fat
removal is com-pared bilaterally for symmetry.A horizontal tightening procedure
isindicated in nearly all cases ofanteriorapproach lower lid
blepharoplasty.Thelateral tarsal strip procedure is a securetime-honored method
ofresuspendingthe lower eyelid but requires opening ofthe lateral
commissure.73Alternative pro-cedures addressing lower lid laxity includesuspension
ofthe lateral retinaculum andcanthal-sparing lateral canthopexy.74,75The skin and
muscle flap are drapedover the edge ofthe lid margin while the lidis not held in
traction and the patient islooking upward and opening his or hermouth.These latter
maneuvers simulatethe lower eyelid�s maximally extendedposition and aid in
preventing excessiveskin removal.72The redundant skin andmuscle flap is drawn
superolaterally,marked with a surgical marking pen,andsubsequently excised.A
conservativeapproach to skin and muscle excision iscrucial to prevent postoperative
lower lidmalposition.Rarely should more than 2 to3 mm ofthe skin muscle flap be
excised intotal.72Special care should be taken toavoid creating lateral canthal
rounding bynot removing excessive skin laterally.Suturing the muscle flap to the
zygomaticperiosteum prior to excision ofexcess skinand orbicularis muscle may
provide betterappreciation offinal tissue location andpermit modifications prior to
permanenttissue alteration.Ifhypertrophic orbicu-laris was earlier noted,a strip
oforbicularismuscle should be excised in the affectedarea prior to closure ofthe
skin.The mus-cle is later closed with interrupted buriedabsorbable suture (ie,7-0
polyglactin).Alternatively,should greater support bedesired,the muscle may be
anchored to thezygomatic periosteum,ifnot already per-formed.The skin is closed
with a running6-0 fast-absorbing gut suture proceedingfrom the medial to lateral
aspect.Figure64-22 demonstrates several ofthe impor-tant aspects oftranscutaneous
lower eyelidblepharoplasty.Transconjunctival ApproachFormalmarking is not performed
for transcon-junctival lower eyelid blepharoplasty,although marking the herniating
fat padsmay be ofbenefit.76Topical anesthesia isinstilled onto the ocular surface
and acorneal protective contact is inserted.Local anesthesia is injected
subcutaneous-ly in the central lower lid just beneath thelashes and into each fat
pad.The skin isnext prepared with 5% povidone-iodineor pHisoHex as in the
previouslydescribed fashion.The inferior palpebral conjunctiva isexposed using a
Desmarres retractor or a4-0 silk traction suture placed throughthe
skin,orbicularis,and superficial tar-sus in the central lower eyelid.The trac-tion
suture may be placed through the
1336Part 9: Facial Esthetic SurgeryFIGURE64-22Transcutaneous lower eyelid
blepharoplasty.A,Surgical marking.B,Skin incision along previously placed surgical
marks.C,Subcutaneous dis-section.D,Orbicularis incision beneath the inferior tarsal
border.E,Extension oforbicularis incision to achieve full length ofskin
incision.F,Gentle globe ballot-tement to expose herniated fat after orbital septal
incision.G,Herniated fat treatment after incision ofoverlying fat pad
capsule.H,Determination ofredundantskin and orbicularis.I,Excision ofredundant
tissue.J,Skin closure after orbicularis fixation and orbicularis closure.Adapted
from Putterman AM.48ABCDEFGHIJ
Blepharoplasty1337inferior conjunctiva and lower lid retrac-tors and fixed
superiorly to aid in expo-sure.An incision through the conjunctivaand the lower
eyelid retractors is madeapproximately halfway from the inferiorborder oftarsus and
the inferior fornix.The incision is extended mediallybeneath the punctum and
laterally nearlyto the lateral canthus.The lower lid isnext retracted anteriorly
and inferiorly tofacilitate isolation ofthe three fat pads,which are further
defined by blunt dissec-tion through the capsulopalpebral fascia.The inferior
oblique muscle should beidentified between the central and medialfat pads.Care
should be taken to avoidaggressive or sharp dissection that mayinduce injury to the
muscle.Fat removalor sculpting is next performed beginningwith the lateral fat
pad.As describedabove gentle ballottement ofthe globeaids in orbital fat
prolapse.The herniat-ing fat is carefully grasped and excised.Some surgeons favor
clamping the fatduring excision.Meticulous hemostasis isessential during fat pad
excision.After fatpad debulking the anterior border ofthefat pads should be flush
with the inferiororbital rim.Overzealous fat pad excisionrisks a postoperative
hollow appearance.The superior traction suture isremoved prior to closing the
conjunctiva.Complete hemostasis should be confirmedbefore closure is attempted.The
conjunc-tiva and lower eyelid retractors are reap-proximated with two or three
buried inter-rupted sutures of6-0 or 7-0 polyglactin orother suture.Several
important aspects oftransconjunctival lower eyelid blepharo-plasty are demonstrated
in Figure 64-23.Skin Pinch ExcisionTransconjunctivallower lid blepharoplasty does
not addressexcess lower lid skin,making skin pinchexcision a useful adjunct for
smallamounts ofexcess lower lid skin.Signifi-cant excessive lower lid skin is
identifiedusing the aforementioned pinch test.Localanesthesia is next injected and
the pinchtest is performed again,taking care toplace the tine ofthe forceps within
a pre-existing skin fold and create a pinched offridge oftissue to be removed.The
redun-dant skin is then excised using curved scis-sors.The skin is closed using 6-0
fast-absorbing gut suture in a running fashion.Lateral CanthopexyA time-
honoredprocedure for lateral canthopexy is the lat-eral strip procedure,which
entails deter-mining the amount ofhorizontal excess oflower eyelid (part ofwhich is
used as thetarsal strip),dividing the lower lid ofthestrip at the gray line,and
removing theanterior lamella,conjunctiva,cilia,and lidmargin�associated
glands.73Desired lowerlid position is determined and a suture ona semicircular
needle is used to fasten thetarsal strip to the periosteum inside the lat-eral
orbital rim at a level to yield the opti-mal postoperative lower lid location
andapposition oflower eyelid to the globe.Acanthal reformation suture is
passedthrough the gray line ofthe upper eyelidand the tarsal strip to recreate the
lateralcanthal angle.The orbicularis is closedusing buried interrupted
absorbablesuture.Fast-absorbing gut suture is used toclose the skin.Midfacial
RejuvenationStandardlower eyelid blepharoplasty does notaddress midfacial aging
changes oftenpresent in the blepharoplasty patient.Hamra proposed an arcus
marginalisrelease procedure to recreate the contourofthe youthful lower lid and
cheek.77The procedure entails creating a skin-muscle flap,incision ofthe arcus mar-
ginalis at the orbital rim,and removal ofa portion ofthe inferior orbital
septum,with subsequent reposition and fixationofthe orbital fat over the orbital
rim.77Atransconjunctival approach to the arcusmarginalis with similar transposition
oforbital fat has recently been advocated.78Elevation ofthe soft tissue ofthe mid-
face by suture plication using transcuta-neous,subperiosteal,transconjunctival,and
supraperiosteal routes has also beendescribed.79,80Steinsapir recently reported the
use ofa hand-carved expanded polytetrafluo-roethylene orbital rim as both a site
forresuspension ofthe midfacial soft tissuesand a mechanism to compensate for
lostmidface volume.81Postoperative ManagementPostoperative instructions seek to
limitedema and ecchymosis and prevent post-operative bleeding.Ice-cold compresses
are placed overthe operative site immediately on arrival inthe postoperative
recovery area.Thesecompresses should be used continuouslyfor 36 to 48 hours after
the procedure withcessation only for dining and bathroombreaks.After 48 hours warm
compressesmay be used for comfort and to hasten res-olution ofedema.Up to 4 weeks
should beallowed for resolution ofbruising,although the majority ofpatients note
lim-ited discoloration beyond 1 week.Com-plete resolution ofedema may require sev-
eral weeks.During the first 48 to 72 hours mini-mal physical activity is
recommended.Patients should remain supine withapproximately 30 degrees ofhead
elevationprovided by pillows or a recliner.Walkingand low impact activities can be
resumedafter postoperative days 2 to 3,althoughrefraining from strenuous physical
activityfor the first week postoperatively is strong-ly recommended.During weeks 2
and 3,activity may gradually be increased.In gen-eral most patients require 1 to 2
weeks offfrom work including the operative day.Forpatients with physically intense
occupa-tions,longer time away is required.Application ofa combination antibiot-ic
and steroid ointment to any dermal inci-sion site is recommended.Keeping
theabsorbable sutures moist allows for theirtimely dissolution.A typical
scheduleincludes three times per day application for
1338Part 9: Facial Esthetic Surgerythe first week,with taper to twice
dailyapplication in the second week and applica-tion four times daily in the third
week.Transconjunctival incision sites should belubricated with an antibiotic
ointment in asimilar schedule.Application ofmakeup tothe incision sites should be
deferred 1 week.Postoperative pain is usually not a sig-nificant
concern.Nonetheless a prescrip-tion for several tablets ofa low potencyopioid and
acetaminophen combinationanalgesic may be provided.Aceta-minophen should be
sufficient for themajority ofpatients.Routine aspirin andnonsteroidal anti-
inflammatory drug useFIGURE64-23Transconjunctival lower
eyelidblepharoplasty.A,Incision through conjunctiva.B,Incision through lower eyelid
retractors.C,Placement ofa superior traction suture.D,Treatment ofherniating
orbital fat.E,Reap-proximation ofthe conjunctiva after reapproxi-mation ofthe lower
eyelid retractors.Adaptedfrom Putterman AM.48ABCDE
Blepharoplasty1339can be resumed several days postoperative-ly.Warfarin may be
restarted on the dayafter surgery.Excessive postoperative dis-comfort should be
investigated as it mayherald an orbital hemorrhage or othercomplications.The
patient is advised to trim shortloose absorbable skin sutures.Care shouldbe taken
to avoid rubbing the incisions orvertically stressing the incisions with digi-tal
traction when attempting to open theeyes.The buried absorbable sutures
mayoccasionally be palpated postoperatively assmall nodules along the incision for
as longas 5 to 6 weeks.Occasionally these buriedsutures may surface and require
trimming.Follow-up evaluation 1 week postop-eratively is typical,with additional
visitsscheduled as needed.Postoperative pho-tography is typically obtained approxi-
mately 4 months after the procedure.Management ofComplicationsComplications
following blepharoplasty areeither cosmetic,functional,or vision-threatening.The
majority ofcomplicationscan be readily prevented by clear preopera-tive
communication,careful preoperativeand intraoperative measurements,andmeticulous
surgical technique.Prior to pur-suing surgery all the major possible compli-cations
should be discussed with the patient.Complications ofUpper Eyelid
BlepharoplastyInadequate Skin ExcisionA commonpostoperative cosmetic concern,inade-
quate skin excision manifests as a secondfold superior to the upper eyelid
crease.Previously unrecognized eyebrow ptosismay contribute to the appearance
ofexcessskin,especially laterally,and should there-fore be assessed.When a true
excess ofupper lid skin is present,careful addition-al resection ofskin and
orbicularis is indi-cated.In general revision blepharoplastyshould be delayed for
several months toallow resolution ofedema.Excessive Skin ExcisionOverzealousremoval
ofupper eyelid skin may result incosmetic as well as functional concerns.Patients
may describe a tight sensation intheir lids,demonstrate lagophthalmos,ordisplay
symptoms and signs ofexposurekeratitis.Like most complications,exces-sive skin
excision is best prevented as sub-sequent management is
challenging.Lidmassage,consisting ofvigorous down-ward massage on the anterior
tarsal sur-face,instituted 1 to 2 weeks postoperative-ly,can resolve mild cases.The
patient isadvised to blink fully and use artificialtears during the day and
ophthalmic ointment at night.More significant over-resection ofskin may require
full-thickness skin grafting,commonly per-formed after 6 months to allow for
morecomplete wound healing.Retroauricularskin is frequently used as a graft site
foreyelid reconstruction.Care must be takento properly thin the graft.Ifpossible
thegraft placement should be superior to thelid incision to lessen cosmetic
impact.Lid Crease AsymmetryRaising an infe-rior lid crease is easier than lowering
anexcessively high crease;therefore,unlessthe higher crease;is abnormally
elevated,the lower crease should be raised toachieve symmetry.Removing a crescent
ofskin and muscle above the low crease,withcare to make the inferior edge (the
newlocation ofthe lid crease) symmetric withthe opposite crease,lysing any
attachmentsinferior to the new crease location,andclosing the ellipse by
incorporating severalstitches through the levator aponeurosisrecreates the new lid
crease.48High Lid CreasesSuccessfully loweringan excessively high lid crease is
difficult.The adhesions forming the current lidcrease must be interrupted and an
incisionmade for the new crease closed by suturebites through the levator
aponeurosis andthe new incision wound edges.In somecases orbicularis muscle
transpositionfrom above can prevent the original skincrease adherence to the
underlying fibroustissue.A fat graft between the orbital sep-tum and levator
aponeurosis may berequired to prevent adhesions.82Excessive Fat RemovalA deep
medialconcavity or superior sulcus results fromaggressive medial fat
removal.Injection ofautogenous fat or dermal fat grafting hasbeen attempted to
augment an excessivelyhollow superior sulcus.Careful conserva-tive fat excision is
warranted to avoidsuperior sulcus syndrome,especially inmales,as creation ofa deep
sulcus femi-nizes the eyelid.Wound DehiscenceWound dehiscence isbest handled by
resuturing the eyelid ifthearea ofdehiscence is greater than severalmillimeters in
length.Small areas ofdehis-cence can be allowed to granulate ifgranu-lation does
not impair final scar cosmesis.Ifre-approximation is performed the woundbed should
be scraped free ofgranulationtissue and the edges trimmed to exposefresh tissue
prior to the second closure.Sur-gical closure should include adequate mus-cular
closure to minimize this complication.Suture MiliaSuture milia are small cys-tic
epithelial inclusions occurring at sutureentrance points into the skin.Commonand
temporary,suture milia appearapproximately 1 week postoperatively anddisappear over
the ensuing months.Hotcompresses may hasten milia resolution.Alternatively a large
bore needle or scissorscan be used to create an opening in thecyst to aid in
healing.Postoperative PtosisInjury to the levatoraponeurosis through direct
intraoperativetrauma or from stretching by postoperativehematoma may result in
postoperativeptosis.83Recent anatomic dissections evi-dencing terminal branches
ofthe superiordivision ofthe oculomotor nerve far ante-rior in the levator
palpebrae superioris
1340Part 9: Facial Esthetic Surgerymuscle prompted speculation that infil-trating
local anesthetics affecting these endbranches may induce transient ptosis.84Mild
postoperative ptosis (2 mm or less)from eyelid edema can be observed forspontaneous
resolution.Poor levator func-tion or severe ptosis warrants timely surgi-cal
exploration,as the fibrotic phase ofhealing will complicate repair.Surgical cor-
rection ofprolonged ptosis can be accom-plished with a conjunctival M�llerectomy,or
external levator repair in mild cases,andlevator aponeurosis advancement in
moreextensive cases.Dry Eye SymptomsDry eye symptomsare a frequent complication
ofblepharo-plasty due to altered lid function anddecreased spontaneous blink rate
andmagnitude.Topical artificial teardrops andlubricating ointment are often
sufficientfor symptom control,although punctalocclusion may be warranted in the
settingofmore severe dry eye symptoms.Punctalocclusion at the time ofblepharoplasty
inpatients with dry eye syndrome may be ofsome benefit in decreasing
postoperativeexacerbation ofsymptoms.85DiplopiaInjury to the superior obliquetendon
or trochlea,although uncommon,has been described following upper ble-pharoplasty
with medial fat excision.86,87Poor visualization during cautery or dissec-tion was
implicated during reportedcases.86,87Recent anatomic dissections con-firm a
consistent relationship between thetrochlea and superior orbital foramen andthe
superior oblique tendon and the fron-tozygomatic suture.88Direct
visualizationduring cautery and dissection coupled withfamiliarity ofassociated
anatomy decreasesthe risk oftendon or trochlear damage.BleedingIntraoperative and
postopera-tive bleeding can be vision-threateningcomplications.Patients should
beinstructed to discontinue aspirin,nons-teroidal anti-inflammatory drugs,andother
platelet-impairing medications 1 to2 weeks preoperatively.Warfarin is gener-ally
withheld 4 days preoperatively.Intra-operative bleeding often results from
theorbicularis muscle.Recent evidence sug-gests a prominent arterial
branch,whichpierces the orbital septum and levatoraponeurosis at the upper aspect
ofthe tar-sus,may account for excessive bleeding ifdamaged when the septum is
opened forfat excision.89Aside from causing significant ecchy-mosis,insufficient
hemostasis can result inretrobulbar hemorrhage or hematomaand concomitant loss
ofvision.90,91Manypatients will describe a small degree ofbruising and swelling
postoperatively,often beginning after a sneeze,cough,or inthe setting
ofhypertension.Significantpain,proptosis,marked upper lid swelling,restricted
extraocular motions,and/or anydecrease in vision raises suspicion for aretrobulbar
hemorrhage,a true emergencyrequiring immediate bedside woundrelease with or without
a lateral canthoto-my and cantholysis,hyperosmotic agents,and systemic
corticosteroids.Hematoma presents with severeecchymosis and eyelid edema.Visual
com-promise may be present ifthe lids aretense.Since compression ofthe globe
andoptic nerve is ofconcern,intraocular pres-sure (IOP) should be measured.Ifno
visu-al deterioration or increase in IOP isfound,conservative management with ice-
cold compresses can be used.Visual com-promise or increased IOP may necessitatea
return to the operating room to reopenthe incision site,evacuate any
clots,andaddress the source ofbleeding.Vision LossMost cases ofvision lossafter
blepharoplasty are due to hemor-rhage or hematoma formation with resul-tant optic
nerve damage or central retinalartery occlusion.90,92Angle-closure glau-coma
following blepharoplasty has alsobeen reported.93Instructing patients tomonitor
their vision and promptlyresponding to all patient reports ofexces-sive pain best
detect these complications.Complications ofLower Eyelid BlepharoplastyLower Eyelid
RetractionEyelid malposi-tion after lower lid blepharoplasty has sev-eral
etiologies:excessive anterior lamellaremoval,scarring ofthe orbital
septum,inadequate treatment oflower eyelid laxi-ty,or hematoma-associated
fibrosis.Delayed lower eyelid retraction resultingfrom scarring ofthe orbital
septum islargely associated with the anteriorapproach to lower eyelid
blepharoplasty.Aposterior approach avoiding incision ofthe orbital septum has been
demonstratedto minimize lower eyelid retraction.94Lower eyelid retraction is a more
frequentcomplication in patients with shalloworbits and prominent eyes.Initial
treatment oflower eyelidretraction varies with extent and durationofaltered lid
position.Early identificationofretraction warrants conservative treat-ment such as
vigorous upward massage,placement oftemporary traction sutures,or a temporary
tarsorrhaphy suture.95Postoperative edema may contribute toearly postoperative
retraction,emphasiz-ing the importance ofa period ofwatchfulwaiting and
conservative therapy.Persistant retraction resistant to con-servative measures can
be treated withseptal scar tissue lysis and lateral can-thopexy.Scar lysis is
accomplished by dis-section between the orbicularis and sep-tum via an incision
associated with alateral canthotomy.96Lateral canthopexy isusually performed using
the lateral tarsalstrip approach as described previously.73Temporary suspension
ofthe lower eyelidto the brow has been proposed to providefurther upward
traction.96Severe lower eyelid retraction maynecessitate posterior lamella
extensionwith a hard palate mucosal or ear cartilagegraft,often with a horizontal
tightening
Blepharoplasty1341procedure.96�99The palpebral conjunctivaand lower eyelid
retractors are incised andrecessed.Through a palpebral conjuncti-val incision
inferior to the lower tarsalborder,the orbicularis is exposed and thegraft sutured
inferior to the tarsus in therecipient bed.Lower Eyelid EctropionOften sympto-matic
due to drying ofthe exposed con-junctiva,lower lid ectropion may exist aloneor in
combination with lower lid retraction.Ifpreviously unappreciated lid laxity is pre-
sent,horizontal tightening is performed aspreviously described.A deficit
ofanteriorlamella is addressed using a full-thicknessskin graft harvested from the
upper eyelidor retroauricular area.Grafts must be sizedlarger than the ideal final
size to accommo-date postoperative contracture.Inadequate Fat RemovalFurther exci-
sion oflower eyelid fat should beaddressed through a posterior approach toavoid
excessive cutaneous scar formationand lower lid malposition.Often the later-al
lower eyelid fat pad is implicated.Excessive Fat RemovalA tear troughdeformity,the
lower lid analog to theupper lid superior sulcus syndrome,describes a prominent
inferior orbitalrim and nasojugal fold that may resultfrom aggressive lower lid fat
removal.Injection ofautologous fat into thedeformity,particularly directed at
theunderlying musculature,has beenattempted to address the tear
troughdeformity.100,101Eyelid fibrosis withdecreased mobility is associated
withexcessive fat removal and multiple surgi-cal interventions.DiplopiaDiplopia may
result after bothtranscutaneous and transconjunctivallower lid blepharoplasty due
to direct andindirect injury ofthe inferior oblique andinferior
rectus.87,102Inferior obliqueinjury should be suspected in patientscomplaining
ofvertical diplopia increas-ing in gaze contralateral to the operatedeye.Recent
anatomic dissections demon-strate a consistent relationship betweenthe inferior
oblique muscle and the infe-rior orbital rim,infraorbital foramen,and supraorbital
notch.103Preciseanatomic knowledge coupled with avoid-ance ofan excessively
inferior conjuncti-val incision and care when treating pro-lapsed fat are
recommended to avoidextraocular muscle injury.BleedingAs previously discussed
withcomplications ofupper lid blepharoplasty,hemostasis is critical in
blepharoplasty toavoid postoperative retrobulbar hemor-rhage and hematoma
formation.Vision LossCauses ofvision loss afterlower eyelid blepharoplasty are
similar to those described with upper eyelid blepharoplasty.Adjunctive Procedures
Chemical PeelingChemical peeling,or chemexfoliation,involves using a chemical agent
to woundthe epidermis and dermis,thereby evokingan inflammatory healing response
that actsto improve skin texture.The level ofthepeel is dictated by the depth
ofpenetration,nature ofdestruction,and inflammatoryresponse.A variety ofagents may
beemployed,most commonly trichloroaceticacid (TCA),glycolic acid,or phenol,andthe
concentration ofthe chemical agentvaries depending on the depth ofpeeldesired.104In
general more severe rhytidsor skin texture problems require a deeperpeel to achieve
the desired effect.Medium-depth TCA chemexfoliation in conjunc-tion with
transconjunctival lower eyelidblepharoplasty has been demonstrated toachieve
excellent results in improvinglower eyelid skin appearance.105Evaluating a
blepharoplasty patientfor chemexfoliation requires additionalappreciation ofskin
pigmentation,oftenusing the Fitzpatrick skin pigment typeclassification,inquiry
into history ofher-pes simplex infection,and knowledge ofthe patient�s need to
return to social activ-ities.47Previous herpes infections mayrequire prophylaxis
with antiviral agents.Patients with higher Fitzpatrick skin types,extensive sun
exposure,or diffuse freck-ling may have unacceptable scarring,hypopigmentation,or
noticeable demar-cation borders oftreated skin and henceshould be considered with
caution.106Chemexfoliation relies on even appli-cation ofthe peeling agent to the
intendedtreatment area.Pretreatment ofthe treat-ment area with retinoic acid can be
per-formed to enhance uptake.Any skin oil orgreases will impair even chemical
treat-ment,making careful soap and water skincleansing and acetone degreasing
crucial toa successful peel.Chemical peeling shouldfollow completion
ofblepharoplastysurgery.The peel is applied to the skinusing sturdy cotton-tipped
applicators,with care taken to achieve symmetric appli-cation,avoid inadvertent
corneal applica-tion,and treat more lightly those areas withthe thinnest skin
(ie,medial canthal andpretarsal skin).Initially a white frostbecomes apparent after
chemical applica-tion,which gives way to deep erythema.Cold compresses to the
treated area afterthe skin has dried may decrease discomfort.A bland lubricating
ointment should beapplied to treated skin prior to the patientleaving the
postoperative recovery area.Postoperative care for patients undergoingchemical peel
requires twice to four timesdaily mild soap cleansing,gentle patting todry,and
ointment re-application until alltreated skin has reepithelialized.Sun expo-
sure,which may cause skin burning andhyperpigmentation,should be
avoidedmeticulously by wearing a hat and darksunglasses during the first
month.Carefulsunscreen application is advised thereafter.Complications
ofchemexfoliationinclude pigmentary change,scarring or
1342Part 9: Facial Esthetic Surgeryother textural changes,corneal
damage,lidposition abnormalities,infection,pro-longed erythema,acne,and cold
sensitivity.Laser Skin ResurfacingLaser skin resurfacing employs a CO2orerbium
laser to thermally remove adefined layer ofdermal tissue and
shrinkcollagen,prompting improved skinappearance through collagen contraction,new
collagen formation,and remodelingand epidermal growth.The number ofpasses taken
determines the depth oftreat-ment.Laser resurfacing is ideal for patientswith
minimally pigmented skin who seekimprovement ofskin with photodamageor acne
scarring.107Adjunctive CO2laserresurfacing ofthe lower eyelid in conjunc-tion with
transconjunctival lower lid ble-pharoplasty has been demonstrated tosuccessfully
address lower eyelid wrinklingthat may result from transconjunctivalblepharoplasty
alone.108When comparedto a phenol chemical peel,CO2laser resur-facing was found to
be equally as effica-cious in diminishing rhytids in thin-skinned facial areas and
more effective atimproving texture in thicker glandularfacial areas.109The
erbium:yttrium-aluminum-garnet (YAG) laser has beenrecently introduced as an
alternativemethod oflaser skin resurfacing.History and physical elements to
beexplored are similar to those describedfor patients being evaluated for chemex-
foliation.Additionally past use ofisotretinoin (accutane) should beobtained,as the
drug-induced elimina-tion ofglandular architecture contraindi-cates laser
resurfacing for the subsequent1 to 2 years following drug discontinua-tion.110Prior
to undergoing laser resur-facing,patients predisposed to hyperpig-mentation are
typically treated for severalweeks with a skin bleaching agent.Pro-phylactic
antivirals and antibiotics arealso commonly employed.Surgical marking plays a
critical role insuccessful laser resurfacing by providing aroadmap to direct
treatment application.After carefully marking all significantrhytids,general
anesthesia or monitoredsedation coupled with proper local orregional nerve block
anesthesia is achieved.Resurfacing is performed using laser set-tings determined by
the area ofinterest.Resurfacing is carried out methodically,taking care to wipe the
ablated tissue awayprior to re-treatment to avoid excessive heatabsorbance in any
given location.Generallyone or two passes with lower power are per-formed on
periocular skin.110Color changeindicates depth oftreatment,progressingfrom pink to
orange to yellow-orange toyellow-white as more passes are made ormore energy is
used per pass.Excessivetreatment risks hypertrophic scarring.Afterprocedure
completion the skin is irrigated,gently patted dry,and a dry occlusive or
wetdressing is applied.Many surgeons haveabandoned occlusive dressings in favor
ofsimply keeping the face well lubricated witha bland lubricant such as petroleum
jelly.Dilute vinegar and water soaks are favoredby many for cleansing.Dressings
arechanged daily with additional lubricationointment applied until
reepithelializationoccurs,generally after 10 to 14 days.Antibi-otic ointment is
occasionally used;however,the risk ofinducing allergies to the appliedantibiotic
has lessened the frequency ofthispractice.Ice packs are used postoperativelyto
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CHAPTER 65Basic Principles ofRhinoplastyJames Koehler,DDS,MDPeter
D.Waite,MPH,DDS,MDFor many cosmetic surgeons rhinoplasty isone ofthe most
challenging surgical proce-dures.A clear understanding ofnasal anato-my is critical
in order to provide an estheticresult that does not compromise nasal func-
tion.Developing a pattern ofanalysis ofthenose is vital for proper diagnosis and
fordetermining the most appropriate treat-ment plan.Numerous rhinoplastic tech-
niques have been described.Some surgeonsfavor an endonasal approach whereas
othersbelieve that an external approach is moredesirable.Each surgeon must become
famil-iar with all technique options in order toaddress the wide variety
ofchallenges ofrhinoplasty surgery.The goal ofthis chapter is to give abroad
overview ofthe diagnosis and treat-ment ofnasal deformities.It is by no
meansexhaustive since multiple textbook volumeshave been written on this
subject.The read-er should gain an understanding ofnasalanatomy and determine how
to systemati-cally analyze the nose.Both endonasal andexternal rhinoplasty will be
described.Nasal AnatomyA clear understanding ofnasal anatomy isimportant to
successfully perform nasalprocedures and decrease the incidence
ofcomplications.Surface AnatomyThe terms used to describe the surfaceanatomy ofthe
nose are important innasal form analysis and for treatment planformulation (Table
65-1).For descriptivepurposes the spatial relationships aredescribed as
cephalic,caudal,dorsal,basal,anterior,posterior,superior,and inferior(Figure 65-
1).Skin and Soft TissueThe soft tissue that overlies the bone andcartilage may
influence the final result ofrhinoplasty.The thickness ofthe skinwill determine how
it will re-drape afterperforming a rhinoplasty.The skinthickness varies along the
dorsum ofthenose.The skin is fairly thick and mobilein the region ofthe nasion.It
quicklythins over the nasal dorsum and is gen-erally thinnest and most mobile in
themid-dorsal region (rhinion).In the dis-tal third ofthe nose the skin tends to
bemore thick and adherent and has anincreased sebaceous content.A patient with thin
skin will show dra-matic changes with alteration oftheunderlying bone and
cartilage,and thislimits room for error since little is camou-flaged by the
thickness ofthe skin.Con-versely for thick-skinned individuals moreTable 65-
1Surface Anatomy ofthe NoseGlabella:the most forward projecting point ofthe
forehead in the midline at the level ofthesupraorbital ridgesRadix:the junction
between the frontal bone and the dorsum ofthe noseRhinion:the anterior tip at the
end ofthe suture ofthe nasal bonesDorsum:the anterior surface ofthe nose formed by
the nasal bones and the upper lateral cartilagesSupratip break:the slight
depression in the nasal profile at the point where the nasal dorsumjoins the lobule
ofthe nasal tipInfratip lobule:the portion ofthe tip lobule that is found between
the tip-defining points and the columellar-lobular angleTip-defining points:there
are four tip defining points,which include the supratip break,the columellar-
lobular angle,and the most projected area on each side ofthe nasal tip formedby the
lower lateral cartilagesAlar sidewall:the rounded eminence forming the lateral
nostril wallAlar-facial junction:the depressed groove formed on the face where the
ala joins the faceColumella:the skin that separates the nostrils at the base ofthe
nose
1346Part 9: Facial Esthetic Surgeryaggressive sculpturing ofthe nasal skele-ton
must be performed in order to effectsignificant changes.Although thick skinmay mask
imperfections it does not re-drape as well and can result in underlyingfibrosis and
formation ofa polybeakdeformity (supratip scarring).Betterresults are possible with
thin-skinnedpatients,however the margin for error issmaller.The surgeon must
sometimesmodify the technique depending on thetype ofskin ofthe patient.Superficial
MusculoaponeuroticSystem and Nasal MusculatureThe muscles ofthe nose are encased in
thenasal superficial musculoaponeurotic sys-tem (SMAS).This is a fibromuscular
layerthat separates the skin and subcutaneoustissue from the nasal cartilage and
bone.The SMAS ofthe nose is in continuitywith the SMAS ofthe face.During rhino-
plastic surgery the dissection is performedbeneath the SMAS.Violating the SMASwill
often result in increased bleeding,scarring,and postoperative edema.The muscles
ofthe nose can be divid-ed into four categories:the elevators,thedepressors,the
compressors,and the dila-tors (Figure 65-2).The muscles ofsignifi-cance are the
paired depressor septi nasi.These muscles can result in drooping ofthenasal tip
during smiling.This added ten-sion on the nasal tip must be
recognizedpreoperatively and addressed by resectionin order to achieve a cosmetic
result.1Blood SupplyThere is a rich blood supply to the sub-dermal vascular plexus
ofthe nose thatarises from branches ofboth the internaland external carotid
arteries.The bloodsupply from the internal carotid arterythat supplies the external
nose includesthe dorsal nasal artery and the externalnasal artery.The dorsal nasal
artery is abranch ofthe ophthalmic artery.Theexternal nasal artery is a branch
oftheanterior ethmoid artery.The external nose is also supplied bybranches ofthe
facial artery and the inter-nal maxillary artery,which originate fromthe external
carotid artery.The facial arterybranches include the angular artery,lateralnasal
artery,alar artery,septal artery,andsuperior labial artery (Figure 65-3).The
internal nose is supplied by theinternal and external carotid branches.The
ophthalmic artery,a branch oftheinternal carotid,branches into the anteriorand
posterior ethmoidal arteries.Theanterior ethmoidal artery supplies
theanterosuperior part ofthe septum and thelateral nasal wall.The posterior
ethmoidartery supplies the septum,lateral nasalwall,and the superior turbinate.2The
internal maxillary artery branchesinclude the sphenopalatine artery and thegreater
palatine artery.The sphenopalatineartery supplies most ofthe posterior partofthe
nasal septum,lateral wall
oftheSuperiorPosteriorAnteriorCaudalCranial/cephalicInferiorBasal Dorsal FIGURE65-
1Spatial descriptors.In describingthe relationship ofone anatomic unit to
anothermany terms are used.The standard relationshipsare
anterior,posterior,superior,and inferior.Thenose is also described in terms
ofdorsal,basal,caudal,and cranial (or cephalic) positions.Adapt-ed from Austermann
K.Rhinoplasty: planningtechniques and complications.In: Booth PW,Hausamen
JE,editors.Maxillofacial surgery.New York: Churchill Livingstone;
1999.p.1378.Procerus muscleTransversenasalis muscleDilator narisanterior
muscleCompressornarium minor muscleOrbicularisoris muscle Depressor septi
nasimuscle Levator labii superiorisalaeque nasi muscleAlar nasalis muscleFIGURE65-
2Nasal musculature.The muscles ofthe nose are grouped into the elevators(light
blue),the depressors (dark blue),the compressors (light gray),and the dilators
(dark gray).Adapted fromJewett B.Anatomic considerations.In: Baker
SR,editor.Principles ofnasal reconstruction.St.Louis(MO):Mosby; 2002.p.17.
Basic Principles ofRhinoplasty1347nose,roof,and part ofthe nasal floor.Thegreater
palatine artery supplies a portion ofthe anterior and inferior portion ofthenasal
septum (Figure 65-4).2The surgically significant area forinternal nasal bleeding is
known as Kiessel-bach�s plexus (also termed Little�s area).This is the area in the
anteroinferior part ofthe nasal septum which is a common site ofexpistaxis.It is
where the sphenopalatine,greater palatine,superior labial artery,andanterior
ethmoid arteries anastamose (Fig-ure 65-5).2The venous drainage ofthenose is
primarily from the facial and oph-thalmic veins.One concern during nasal surgery
isthe possibility ofcompromised bloodflow to the nasal tip ifthe surgeon per-forms
an external rhinoplasty.The bloodsupply to the nasal tip has been analyzedby
lymphoscintigraphic studies,cadaverdissections,and histologic
sections.3,4Theconclusion is that the primary blood sup-ply to the nasal tip comes
from the bilat-eral lateral nasal arteries that course in aplane superficial to the
alar cartilages inthe subdermal plexus approximately 2 to3 mm above the alar
groove.Thus a col-umellar incision does not compromise tipblood supply.Also there
are no significantveins and minimal lymphatics in the col-umellar region.3,4Some
surgeons believethat external rhinoplasty remains moreedematous for longer
postoperative peri-ods than an endonasal rhinoplasty.Bone and CartilageThe
structure ofthe nose consists ofthepaired nasal bones as well as the frontalprocess
ofthe maxilla.The bone is thick-est near the junction with the frontalbone and
tapers as it joins with the upperlateral cartilages.The upper lateral cartilages
are in inti-mate contact with the nasal bones andunderlie the nasal bones for
approximately 6 to 8 mm.The connection between theSupraorbital arteryInfraorbital
arteryAngular arterySuperior labial arterySupratrochleararteryDorsal nasal
arteryExternal nasal branchof anterior ethmoidalarteryLateral nasal
arteryColumellar branchSeptal branchFacial arteryFIGURE65-3Arteries ofthe external
nose.The arterial supply ofthe external nose comes frombranches ofthe external
carotid artery(dark blue) and the internal carotid artery(light blue).Adapt-ed from
Jewett B.Anatomic considerations.In: Baker SR,editor.Principles ofnasal
reconstruction.St.Louis (MO): Mosby; 2002.p.18.Lateral internal nasal branch of
anterior ethmoidal arteryLateral branch of posterior ethmoidal arteryExternal nasal
branch of anterior ethmoidal arteryBranch of angular
arterySphenopalatinearteryDescendingpalatine arteryLesserpalatine
arteryGreaterpalatine arteryFIGURE65-4Arteries ofthe lateral nasal wall.The
arterial supply ofthe lateral nasal wall arises frombranches ofthe external carotid
artery(black) and the internal carotid artery(blue).Adapted fromJewett B.Anatomic
considerations.In: Baker SR,editor.Principles ofnasal reconstruction.St.Louis(MO):
Mosby; 2002.p.23.
1348Part 9: Facial Esthetic Surgerynasal bones and upper lateral cartilagesshould
not be violated since this may disruptthe internal nasal valve causing
nasalobstruction and asymmetry.The internalnasal valve is formed by the junction
oftheupper lateral cartilages and the nasal septum.The lower lateral cartilages
comprisethe lower third ofthe nose and connect tothe upper lateral cartilages in a
uniondescribed as the scroll.There are variousconfigurations ofthe scroll.5,6The
scroll isdescribed as interlocked (52%),overlap-ping (20%),end to end (17%),or
opposed(11%) (Figure 65-6).The scroll providessignificant support to the nasal
tip.Whenperforming an endonasal rhinoplasty thisarea is violated by the
intercartilaginousincision (Figures 65-7�65-9).The lowerlateral cartilage is
divided into medial andlateral crura.The medial crura are in inti-mate contact with
the nasal septum andprovide tip support.The lateral cruraextend superiorly and form
densefibroareolar tissue attachments with thepyriform aperture.The intermediate
crusis the diverging ofthe medial crus beforeturning to become the lateral crus
proper.The highest point ofthe intermediate crusis an important surgical landmark
knownas the tip-defining point (Figure 65-10).The nasal septum is formed by
bothbone and cartilage.The ethmoid andvomer provide bony support posteriorly.The
quadrangular cartilage provides sup-port anteriorly (Figure 65-11).Support for the
nasal tip is classi-fied into major and minor divisions.The major tip support comes
from thesize,shape,and strength ofthe lowerlateral cartilages,the attachment
ofthemedial crura ofthe lower lateral carti-lage to the caudal septum,and
thefibrous attachment ofthe lower lateralcartilage to the upper lateral
cartilage.The minor tip support comes from thenasal spine,the membranous septum,the
cartilaginous dorsum,the sesamoidcomplexes,the interdomal ligaments,and the alar
attachments to the skin(Table 65-2).5NervesThe sensory nerve supply to the skin
ofthe external nose is supplied by the oph-thalmic and maxillary divisions
ofthePosterior septal branch ofsphenopalatine arteryNasal septalcartilageSeptal
branch ofposterior ethmoidal arteryMedial internal nasal branchof anterior
ethmoidal arteryKiesselbach's plexusSeptal branch ofsuperior labial arteryFIGURE65-
5Arteries ofthe nasal septum.The arterial supply ofthe nasal septum arises
frombranches ofthe external carotid artery(black) and the internal carotid
artery(blue).Kiesselbach�splexus is formed by the sphenopalatine artery,greater
palatine artery,superior labial artery,and ante-rior ethmoid arteries.It is a
common site ofepistaxis.Adapted from Jewett B.Anatomic considera-tions.In: Baker
SR,editor.Principles ofnasal reconstruction.St.Louis (MO): Mosby; 2002.p.23.Various
configurations of the scroll20%17%11%52%FIGURE65-6Configurations ofthe
scroll.Therelationship ofthe upper lateral and lower later-al cartilages is termed
the scroll.Anatomic stud-ies have identified four common configurations:interlocked
(52%),overlapping (20%),end toend (17%),and opposed (11%).Adapted fromLam SM and
Williams EF III.5FIGURE65-7Partial transfixion.The partialtransfixion incision
through the membranousseptum and short ofthe medial crural foot pads.
Basic Principles ofRhinoplasty1349trigeminal nerve.Branches ofthe supra-trochlear
and infratrochlear nerves sup-ply the skin in the region ofthe radix andrhinion.The
lower halfofthe nose issupplied by the infraorbital nerve andthe external nasal
branch ofthe anteriorethmoidal nerve (a branch ofthenasociliary nerve that arises
from theophthalmic branch ofthe trigeminalnerve) (Figure 65-12).The main sensory
nerve supply to thenasal septum comes from the internal nasalnerve (a branch ofthe
anterior ethmoidalnerve) and the nasopalatine nerve (Figure65-13).The lateral nasal
wall sensation issupplied by the anterior ethmoidal nerve,branches ofthe
pterygopalatine ganglion,branches ofthe greater palatine nerve,theinfraorbital
nerve,and the anterior superi-or alveolar nerve.FIGURE65-8Intercartilaginous
incision.Theintercartilaginous incision,between the upperand lower cartilage,allows
access to the nasaldorsum.Note the incision does not violate thenasal
valve.FIGURE65-9Connecting intercartilaginousand partial transfixion incisions.The
intercarti-laginous incision extends along the upper edge ofthe lateral crus to
connect with the transfixionincision.This will provide access for a septoplas-ty
during internal rhinoplasty.Lateral crusMedial crus Intermediate crus:lobular
segmentdomal segmentLateral crusMedial crus Lateral crus Intermediate crus:domal
segmentlobular segmentMedial crus(columellar segment)Intermediate crus Medial
crus(footplate segment)ABCFIGURE65-10A�C,Anatomy ofthe lower lateral cartilages.The
lower lateral cartilages are often described as having a lateral crus,medial
crus,and an intermediatecrus.The intermediate crus is the most projected portion
ofthe lower lateral cartilages and these form two ofthe tip-defining points seen on
nasal tip analysis.Adaptedfrom Jewett B.Anatomic considerations.In: Baker
SR,editor.Principles ofnasal reconstruction.St.Louis (MO):Mosby; 2002.p.21.ABCAlar
cartilageUpper lateral cartilageSeptal cartilageNasal boneCribriform
platePerpendicular plate of ethmoid boneNasal crest of maxillaVomerFIGURE65-
11Anatomy ofthe nasal septum.The nasal septum is composed ofthe perpendicular
plateofthe ethmoid,the vomer,and the quadrangular cartilage.Adapted from Jewett
B.Anatomic consider-ations.In: Baker SR,editor.Principles ofnasal
reconstruction.St.Louis (MO): Mosby; 2002.p.22.
1350Part 9: Facial Esthetic SurgeryParasympathetic innervation is derivedfrom
branches ofthe pterygopalatine gan-glion which are derived from cranial
nerveVII.Some sympathetic branches reach thenasal cavity via the nasociliary
nerve.2,7Nasal ValveThe airflow through the nose is regulatedby the internal and
external nasal valves.The external nasal valve is comprised ofthe lower lateral
cartilage and the nasalseptum and floor.Collapse ofthe externalnasal valve can
sometimes be noted whenthe nares become occluded on even gentleinspiration.This
problem is seen inpatients with narrow nostrils,a projectingnasal tip,and thin alar
sidewalls.Externalnasal valve collapse is usually seen inpatients who have had
previous rhino-plasty surgery and excessive trimming ofthe cephalic portion ofthe
lower lateralcartilages.It is also seen with increasedage and in facial nerve
paralysis.Theexternal nasal valve collapse can be cor-rected by deprojecting the
overprojectednose,realigning the lateral crura into amore caudal orientation,and
placing alarbatten grafts to provide structural supportand prevent collapse.8The
internal nasal valve is formed bythe junction ofthe septum with the upperlateral
cartilages.The angle formed shouldbe a minimum of10�to 15�to
maintainpatency.Deviation ofthe nasal septum orseparation ofthe upper lateral
cartilagesfrom the nasal bones can lead to obstruc-tion.This problem is also seen
after rhino-plasty ifthe patient has had weakening ofthe upper and lower lateral
cartilages.These patients often have a pinchedappearance in the supra-alar
region.TheCottle test is used to evaluate obstructionat the internal valve by using
a finger to dis-tract the check and lateral wall ofthe nosethereby opening the
valve.Ifnasal airflowis dramatically improved,then the internalvalve may require
correction.Thesepatients often have symptomatic reliefbythe use ofexternal taping
devices.Surgicalcorrection involves the placement ofspreader grafts between the
septum andupper lateral cartilages to increase theangle at this
junction.8�10Cosmetic EvaluationThe cosmetic evaluation begins in thesame way as
with any examination,by elic-iting the chiefcomplaint ofthe patient.The patient
should be given a mirror andcotton-tipped applicator to point out specif-ic
cosmetic concerns.Following this a thor-ough medical history should be
obtained.Specific attention should be directed towardTable 65-2Tip Support
MechanismsThe three major tip support mechanisms include1.The size,shape,and
strength ofthe lower lateral cartilages2.The attachment ofthe medial crura to the
caudal septum3.The attachment ofthe lower lateral cartilages to the upper lateral
cartilagesThe minor tip support mechanisms include1.The interdomal ligament2.The
sesamoid complex extending the support ofthe lateral crura to the
piriformaperture3.The attachment ofthe alar cartilages to the overlying
skin4.Cartilaginous septal dorsum5.Nasal spine6.The membranous
septumSupratrochlearnerveInfratrochlear nerveSupraorbital nerveInfraorbital
nerveExternal nasal branchof anterior ethmoidal nerveFIGURE65-12Sensory nerves
ofthe external nose.The sensory innervation ofthe nose is derivedfrom the
V1(ophthalmic: colored black) and from V2(maxillary:colored blue) divisions
ofthetrigeminal nerve.Adapted from Jewett B.Anatomic considerations.In: Baker
SR,editor.Principles ofnasal reconstruction.St.Louis (MO): Mosby; 2002.p.19.
Basic Principles ofRhinoplasty1351obtaining a history ofnasal
trauma,nasalobstruction,previous nasal surgery,andmedications (including over-the-
counterand herbal medications).Psychiatric StabilityIn addition to analyzing the
nose the sur-geon needs to assess ifthe patient is psycho-logically prepared for a
cosmetic procedure.Patients should have realistic expectationsand motivations.A
patient who is internallymotivated (eg,wishes to improve their self-esteem) to have
the procedure is a bettercandidate than one who desires the proce-dure for external
reasons (eg,spouse wantsthem to have it done).11,12The surgeon should beware
ofpatientswho are indecisive,rude,uncooperative,depressed,have unrealistic
expectations,orhave significant personality disordersbecause they may never be
satisfied.Otherwarning signs ofpoor patients are thosewho overly flatter,are
talkative,considerthemselves to be a very important patient,have minimal or no
deformity,are surgeonshoppers,price hagglers,or involved in liti-gation.Most
importantly,do not operate ona patient that you do not like.11�14General Facial
AnalysisPrior to performing a specific analysis ofthe nose,a global assessment
ofthe faceand its proportions should be done.Referto Chapter 54,�Database
Acquisition andTreatment Planning,�for additional infor-mation on facial analysis
in orthognathicsurgery.Nasal AnalysisThe nasal examination should be per-formed in
a systematic manner so that theproper diagnosis is attained (Figures 65-14and 65-
15).General AssessmentSkinThe skin should be assessed for its thick-
ness,mobility,and sebaceous gland con-tent.Any pigmentations or scars shouldalso be
noted.Thick skin does not re-drape well after rhinoplasty.SymmetryAny gross
asymmetries in all views shouldbe noted.Lateral ViewNasofrontal AngleThenasofrontal
angle is defined as the angleformed from lines that are tangential tothe glabella
and the nasal dorsum andintersect through the radix as seen on aprofile view.The
normal angle is between125�and 135�(Figure 65-16).Internal
nasal(anteriorethmoidal)NasopalatineMedial posteriorsuperiorFIGURE65-13Sensory
nerves ofthenasal septum.The main sensorynerve supply comes from the internalnasal
nerve (a branch ofthe anteriorethmoidal nerve V1(black) and thenasopalatine nerve
V2(blue).Adapt-ed from Jewett B.Anatomic consider-ations.In: Baker
SR,editor.Princi-ples ofnasal reconstruction.St.Louis(MO): Mosby;
2002.p.19.FIGURE65-14Preoperative rhinoplasty.A,Preoperative frontal view shows the
width ofthe nose and alar base.B,Preoperative lateral view shows the nasal pro-file
and dorsum in relation to the nasofrontal angle and nasolabial angle.C,Preoperative
three-quarter,or oblique view,is most natural and often revealing forharmony ofthe
orbital rims and gull wings that flow into the nasal dorsum.D,Preoperative basal
view is either taken from above or below the patient and is agood view oftip and
base morphology.ABCD
1352Part 9: Facial Esthetic SurgeryThe postion ofthe radix should thenbe assessed
in terms ofits anteroposteriorand vertical positions from a profile view.The radix
should lie in a vertical planesomewhere between the lash line and thesupratarsal
folds.In addition it should be 4 to 9 mm anterior to the corneal plane(see Figure
65-16).Nasal DorsumIn women the nasal dor-sum should lie approximately 2 mm poste-
rior to a line drawn from the radix to thenasal tip.In males the nasal dorsumshould
lie on this line or slightly in front ofit (see Figure 65-16).The length ofthe nose
(radix to tip)can be measured clinically or on pho-tographs taken during the
initial examina-tion.The ideal nasal length should approx-imate the distance from
stomion tomenton ifthe lower facial height is pro-portionate to the middle facial
height(glabella to subnasale).Ifthe lower faceheight is not proportionate it is
best toestimate the nasal length as 0.67 times themiddle facial height.Nasal Tip
DefinitionThe nose shouldhave four tip defining points which whendrawn on the nose
in the frontal viewappear as two equilateral triangles (Figure65-17).These points
include the supratipbreak,the columellar-lobular angle,andthe two tip-defining
points (the most pro-jected portion ofthe nasal tip)Nasal Tip ProjectionNasal tip
projec-tion can be defined as the distance thatthe tip (pronasale) projects
anterior inthe facial plane.15Perception ofnasal tipprojection can be influenced by
may fac-tors:upper lip length,nasolabial angle,nasofrontal angle,dorsal
hump,andFIGURE65-15Postoperative rhinoplasty.A,Postoperative frontal view shows the
change in the width ofthe nose.This is the patient�s most critical
analysis.B,Postoperative lateral view shows the change in dorsal reduction and tip
position.C,Postoperative three-quarter,or oblique view,demonstrates the symmetry
andgraceful balance ofthe nose with the face.D,Postoperative basal view shows the
width ofthe nose and any tip deviation from the dorsal midline.ABCD4�9 mmNasal
tipRadix125�135�FIGURE65-16Position ofthe nasal dorsum and radix.The nasal dorsum
is typically 2 mm behind a line drawnfrom the radix to nasal tip in women.In men
the nasaldorsum typically lies on this line.The radix should liebetween the upper
eyelid margin and the supratarsal foldsin a vertical plane and approximately 4 to 9
mm anteriorto the corneal plane.Adapted from Austermann,K.,Rhinoplasty: planning
techniques and complications.In:Booth PW,Hausamen JE,editors.Maxillofacial
surgery.New York: Churchill Livingstone; 1999.p.1380.FIGURE65-17Nasal tip-defining
points.A noseshould have four tip-defining points.These aredefined by the
supratip,columellar-lobularangle,and the tip-defining points ofeach inter-mediate
crus ofthe lower lateral cartilages.
Basic Principles ofRhinoplasty1353chin projection.There are several meth-ods to
determine ifthe nasal tip projec-tion is adequate.Most cosmetic rhino-plasty
procedures are designed topreserve tip projection.The simplest method to remember
isSimons�method,which states that the lip-to-tip ratio is 1:1.Essentially the
length oftheupper lip (from subnasale to labrale superi-oris) should equal the
nasal projection(measured from subnasale to pronasale).This method may be invalid
because ofthewide variation in lip lengths.16The Goode method is another way
ofdetermining nasal projection.Using theGoode method a line is drawn from theradix
to the nasal tip.A second line is drawnfrom the radix to the alar columellar junc-
tion.A third line is drawn perpendicular tothis and passes through the nasal
tip.Goode�s analysis states that ifthe nasofacialangle is between 36�and 40�,then
the lengthofthe perpendicular line passing throughthe nasal tip should be 0.55 to
0.6 ofthelength ofthe nasal dorsum (Figure 65-18).16Rohrich describes another
techniqueofassessing nasal tip projection.Ifthenasal dorsal length is
appropriate,the tipprojection should be 0.67 times the idealnasal length.The ideal
nasal length shouldbe equal to the distance from stomion tomenton or 1.6 times the
distance from thenasal tip to stomion.The tip projection ismeasured from the alar
facial junction tothe nasal tip.17This method is subject to agreat deal offacial
variation.Additionally a vertical line drawnfrom the most projected portion
oftheupper lip should divide the nose in twoequal halves between the alar facial
grooveand the nasal tip.Ifthe anterior portion isgreater than 60%,then the nose is
likely tobe overprojected (Figure 65-19).17Nasal tip RotationThe nasal tip
rotationis evaluated by the nasolabial angle and thecolumellar-lobular
angle.Nasolabial angle isdefined as the angle formed by lines that aretangential to
the columella ofthe nose and the philtrum ofthe lip and intersect atthe
subnasale.In women this should beapproximately 95�to 110�,whereas in men this
should be 90�to 95�.Lip positionmay be dependent on tooth position.Thecolumellar-
lobular angle is defined as theangle formed by the intersection ofa linetangential
to the columella and a line tan-gential to the infratip lobule.This angle
isnormally between 30�and 45�.Tip SupportThe strength ofthe cartilagein the tip
ofthe nose is apparent when onepresses on the tip.A nose with poor sup-port may
require cartilaginous struts tocounteract the inherently weakened tipfrom the
rhinoplasty.The effect offacialanimation should also be noted.Somepatients have
overactive depressor septinasi muscles,which result in a droopingnasal tip on
smiling.The columella showon a lateral view should be 3 to 4 mmbelow the inferior
alar rim.13Frontal ViewWidth ofNasal DorsumThe width ofthe nasal body and tipshould
be approximately 80% ofthe alarbase width.This is assuming that the alarbase is in
proper anatomic proportions.The alar base width should approximatethe intercanthal
distance.Ifthe width ofthe nasal dorsum is significantly greaterthan 80%,then
lateral nasal osteotomiesshould be considered.The eyebrowsshould gracefully flow
into the nasal dor-sum analogous to a gull wing in flight.The alar rims and
columella shouldalso be a gently curving line that appearsas a bird in flight.Alar
WidthThe alar base width shouldapproximate the intercanthal distance.Sel-dom is the
nasal width less than the inter-canthal dimension.Basal ViewFrom a basal view the
columella-to-lobule ratio should be 2:1.Nostril size and shape should also
benoted.An esthetic nostril is teardropNasal tipx(0.55�0.6)xRadix36�40�FIGURE65-
18Goode method ofnasal projec-tion.This method is sometimes used to deter-mine
adequacy ofnasal projection.Ifthenasofrontal angle is between 36�to 40�,then
thelength ofa perpendicular line through the nasaltip should be 0.55 to 0.6 the
length ofthe nasaldorsum.x = nasal length.Adapted from Auster-mann,K.,Rhinoplasty:
planning techniques andcomplications.In: Booth PW,Hausamen JE,edi-
tors.Maxillofacial surgery.New York: ChurchillLivingstone;
1999.p.1380.50%50%FIGURE65-19Nasal projection.A vertical linethrough the most
projected part ofthe upper lipshould divide the nose into two equal
parts.Ifthenasal tip comprises > 60%,then the nose may beoverprojected.
1354Part 9: Facial Esthetic Surgeryshaped,but there is a great amount ofeth-nic
variation (Figure 65-20).Oblique ViewThe oblique view is mostnatural and sometimes
more revealing thanstandard photographs.It demonstrates theflow ofsubunits and
facial harmony.Thethree-quarters view is how we usually seeeach other in routine
interaction.Functional ConsiderationsAlthough the patient desires cosmetic cor-
rection oftheir nose,the functional signifi-cance ofthe nose should be closely
consid-ered.Nasal airflow through both theinternal and external nasal valves should
beevaluated.The septum should be evaluatedfor deviation and perforations.The
septumis often a good site for harvesting autoge-nous cartilage for grafting.The
turbinatesshould be evaluated for hypertrophy.Rhinoscopy with a nasal speculum can
beperformed both before and after theadministration ofa topical
decongestant.PhotographsThe examination is not complete withoutstandardized facial
photographs.Thestandard facial photographs shouldinclude frontal,right,and left
lateralviews;right and left oblique views;and ahigh and low basal view.Close-up
viewsare taken ifwarranted.The photographsare beneficial from a medicolegal stand-
point,and they also allow the surgeon tostudy the nose in more detail and todevelop
a surgical plan.AnesthesiaProper anesthesia ofthe nose is importantto ensure
minimal distortion ofthe tissuesas well as to provide adequate hemostasis.Prior to
injecting the nose,cottonoids orcotton-tipped applicators soaked in 4%cocaine or
oxymetazoline are placed ineach nostril to constrict the mucous mem-branes ofthe
turbinates.Ifthe rhinoplastyis to be performed under sedation,thencocaine is
preferred because ofits anes-thetic properties.Ifthe procedure is per-formed under
general anesthesia,thenoxymetazoline is sufficient.Three cottonoids are placed in
eachnostril:one along the middle turbinate,one along the superior nasal
vault,andone along the inferomedial septum.Local anesthesia is achieved with
2%lidocaine with 1:100,000 epinephrine.Inan endonasal rhinoplasty the
followingareas are injected:�0.5 cc deposited at the junction ofeach upper and
lower lateral cartilage(intercartilaginous area)�0.5 cc deposited in the region
ofeachmarginal incision�3 cc along the nasal dorsum and later-al nasal bones
(hugging periosteum)�1 cc along the nasal septum�0.5 cc at each alar base�1 cc at
each infraorbital nerve�1 cc at the nasal tipFor external rhinoplasty the
followingadditional area is injected:�1 cc to the
columellaIncisions/SequencingThere are multiple incision techniquesused to gain
access to the cartilage andbone support ofthe nose.Complete TransfixionThis
incision provides access to the caudalseptum,medial crura,and nasal spine.The
incision is made with a no.15 blade,beginning just caudal to the superior cau-dal
end ofthe nasal septum.The incisionextends inferiorly through the membra-nous
septum,following the cephalic mar-gin ofthe medial crura (see Figures 65-7and 65-
21A).It results in ptosis anddeprojection ofthe nose.Partial TransfixionThis
incision is similar to the completetransfixion incision except that it stops atthe
level ofthe medial footpads ofthelower lateral cartilages.The advantage ofthis
incision is that the attachments ofthemedial footpads ofthe lower lateral carti-
lages to the caudal septum are not dis-rupted (see Figures 65-7 and 65-
21B).HemitransfixionThis incision is a complete transfixion inci-sion that is
performed on only one side ofthe membranous septum.It does not tra-verse both
mucosal surfaces and thereforesome attachments ofthe medial crura tothe caudal
septum are maintained.Accessto the nasal septum is good with this inci-
sion;however,delivery ofthe lower lateralcartilage on the side opposite to the
incisionis difficult (see Figures 65-7 and 65�21C).Killian IncisionThis incision is
seldom used in rhinoplasty.It is a useful incision to gain access to thenasal
septum ifonly a septoplasty is to beperformed.The incision is made
severalmillimeters cephalad to the caudal edge ofthe septum.It can be extended onto
thenasal floor ifneeded.Intercartilaginous IncisionThis incision is made at the
junction oftheupper and lower lateral cartilages.Thenare is elevated superiorly
with a doubleskin hook.A no.15 blade should passbelow the lower lateral cartilage
and abovethe upper lateral cartilages.This incision istypically made after a
transfixion incision.The intercartilaginous incision is thenNasal tipNasal
base1/32/3FIGURE65-20Columella-to-lobule ratio.Thecolumella-to-lobule ratio should
be 2:1.
Basic Principles ofRhinoplasty1355connected to the transfixion incision (seeFigures
65-8,65-9,and 65-22).Intracartilaginous IncisionThis incision is made through both
thevestibular nasal mucosa and a portion ofthe lower lateral cartilages.This
incision issimilar to the intercartilaginous incisionexcept that it is made 3 to 5
mm posteriorto the junction ofthe upper and lower lat-eral cartilages.This incision
in effect per-forms a complete cephalic strip ofthelower lateral cartilages without
the needfor delivering the cartilage.The disadvan-tage is that the lower lateral
cartilage is notdirectly visualized and it may therefore bedifficul to achieve
symmetry between theright and left sides.Rim/Marginal IncisionThis incision
parallels the caudal edges ofthe lower lateral cartilages.The incision isused in
combination with an intercarti-laginous incision in an endonasal rhino-plasty.The
two incisions allow the lowerlateral cartilage to be delivered and visual-ized.This
allows the surgeon to moreaccurately trim the cartilage ifneeded.Inan open
rhinoplasty this incision is com-bined with a transcolumellar incision inorder to
gain access to the lower lateralcartilage and nasal dorsum (Figure 65-
23).Transcolumellar IncisionThis incision is made through the thinnestportion ofthe
columella at a level justsuperior to the flaring ofthe medial crura.The incision
can be made with a notchedV in the center ofthe columella or as a�stair step.�This
will break up the scar

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