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Mosbys
Review for the NBDE
Part Two
SECOND EDITION
edited by
FRANK DOWD, DDS, PhD
Professor Emeritus
Department of Pharmacology
School of Medicine
School of Dentistry
Creighton University
Omaha, Nebraska
3251 Riverport Lane
St. Louis, Missouri 63043
MOSBYS REVIEW FOR THE NBDE, PART II, SECOND EDITION ISBN: 978-0-323-22568-7
Copyright 2015 by Mosby, an imprint of Elsevier Inc.
Copyright 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means,
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Section Editors
Myron Allukian, Jr., DDS, MPH Sanjay Mallya, BDS, MDS, PhD
Oral Health Consultant Assistant Professor
Boston, Massachusetts Diagnostic and Surgical Sciences
School of Dentistry
Nikola Angelov, DDS, MS, PhD University of California
Professor and Chair Los Angeles, California
Department of Periodontics
School of Dentistry Karen Novak, DDS, MS, PhD
University of Texas Health Sciences Center Professor
Houston, Texas Department of Periodontics
School of Dentistry
Oscar Arevalo, DDS, SCD, MBA, MS University of Texas Health Sciences Center
Private Practice Houston, Texas
Miami Childrens Hospital
Pediatric Dentistry Alejandro Peregrina, DDS, MS
Doral, Florida Clinical Associate Professor
Restorative and Prosthetic Dentistry
Larry L. Cunningham, Jr., DDS, MD, FACS College of Dentistry
Professor and Chief The Ohio State University
Division of Oral and Maxillofacial Surgery Columbus, Ohio
University of Kentucky
Lexington, Kentucky Kenneth L. Reed, DMD, FADSA, NDBA
Private Practice
Frank Dowd, DDS, PhD Tucson, Arizona
Professor Emeritis
Department of Pharmacology Andr V. Ritter, DDS, MS
School of Medicine Professor and Graduate Program Director
School of Dentistry Department of Operative Dentistry
Creighton University School of Dentistry
Omaha, Nebraska University of North Carolina
Chapel Hill, North Carolina
Jarshen Lin, DDS
Director, Predoctoral Endodontics Jeffrey C.B. Stewart, DDS, MS
Department of Restorative Dentistry and Biomaterials Associate Professor
Science Department of Pathology and Radiology
Harvard School of Dental Medicine Oregon Health and Science University
Boston, Massachusetts Portland, Oregon
Steven J. Lindauer, DMD, MDSc Mark Taylor, DDS, FACD

Professor and Chair, Department of Orthodontics Chair, Department of Pediatric Dentistry
Virginia Commonwealth University School of Dentistry
School of Dentistry Creighton University
Richmond, Virginia Omaha, Nebraska
iii
This page intentionally left blank
Contributors
Marla W. Deibler, Psy.D. Catherine Frankl Sarkis, JD, MBA
Director, The Center for Emotional Health of Greater Assistant Professor, Department of Health Policy &
Philadelphia Health Services Research
Cherry Hill, New Jersey Boston University
Henry M. Goldman School of Dental Medicine
Florence Kwo, DMD Boston, Massachusetts
Section of Endodontics
Division of Associated Clinical Sciences Bhavna Shroff, DDS, MDentSc, MPA
School of Dentistry Professor, Department of Orthodontics
University of Southern California Virginia Commonwealth University
Los Angeles, California School of Dentistry
Richmond, Virginia
Philip Lin, DDS
Resident Eser Tufekci, DDS, MS, PhD
Division of Oral and Maxillofacial Surgery Associate Professor, Department of Orthodontics
University of Kentucky Virginia Commonwealth University
School of Dentistry
Tom C. Pagonis, DDS, MS Richmond, Virginia
Assistant Clinical Professor
Department of Restorative Dentistry and Biomaterials
Science
Harvard School of Dental Medicine
Boston, Massachusetts
v
Preface
each other questions; test yourself with flashcards or
How to Use This Text notes that are partially covered from view; or answer
This review book is the compiled work by experts in each questions from this text. In each case, be sure to check
of the relevant disciplines represented on the National your answer to find out whether you achieved the
Board Dental Exam (NBDE). This second edition includes correct answer. Each section of this review book has
recent updates and important changes from the first edition practice exam questions. There is also a sample exam
for each NBDE subject. This text is a tool to help prepare with questions from each discipline. This book also con-
students for taking the NBDE and to help identify strengths tains explanations as to why an answer is a correct
and weaknesses so students can better utilize their study answer and why the distracters are not. See if these
time. This text is not meant to replace years of professional explanations agree with the reasons for making your
training nor to simply provide questions so that students selections. The questions are written in the formats used
may pass the exams if they memorize the answers. Instead, on the National Boards including the new formats
this book will help direct students to the topic areas they of matching, ordering and multiple correct/multiple
may need to further review and will strengthen students responses.
knowledge and exam-taking skills. 5. Block off time for practice examinations, such as the
Dental schools generally do well in preparing their stu- review questions and sample exam in this text. Time
dents for practice and for board exams. Usually, there is a yourself and practice your test speed; then compare
good correlation between students who do well in their your time to the estimated time needed to complete
dental courses and those who score well on their board each section of the NBDE.
exams. Therefore to best prepare for board exams, students 6. If your school offers board reviews, we highly recom-
should focus on doing well in their course work. It is in the mend taking them. These may assist you with building
students best interest to focus more board exam study time your confidence with what material you have already
on the areas in which they have not performed as well in mastered and may help you focus on material that you
their dental coursework. Most students are aware of their need to spend more time studying.
areas of weakness and therefore will have the opportunity 7. Stay positive about the board exam. If you prepare well,
to focus more resources on these areas when studying you should do well on the exam. Besides, think of all the
for boards. people who have preceded you and have passed the
exam. What has been done can be done. Consider
Helpful Hints for Preparing to Take Your making a study group composed of people who will be
good study partners and who are able to help the other
Board Examinations members in the group review and build confidence in
1. Pace yourself and make a study schedule. As when taking the exam.
taking a course, it is always better to give yourself suf- 8. Exams are administered by the Joint National Commis-
ficient assimilation time rather than cramming over a sion on Dental Education (JNCDE) contracting with
short period of time, and if you start studying early Prometric, Inc. (Prometric.com) at various testing cen-
enough, you should not have to make major changes in ters. Exams are taken electronically. Students seeking to
your daily schedule. take the National Board Exam must be approved by
2. Study in a quiet environment similar to that in which their Dean, who recommends eligibility for the exam to
the test is given. Stick to your schedule and minimize JNCDE. More information on the exam is available at
distractions to avoid last minute panic and the urge the American Dental Association (ADA) website.
to cram.
3. Know your weaknesses and focus more of your resources Helpful Hints During the Taking
on strengthening these areas. Look back at your grades
from the courses that relate to the exam topics. These
of Examinations
will indicate areas that need more attention. Also, use 1. It is important to note that questions that are consid-
this book as a trial run to help point to content areas ered good questions by examination standards will
that may need more review. have incorrect choices in their answer bank that are
4. Many find practice exams useful. You can employ prac- very close to the correct answer. These wrong choices
tice exams in several ways: study with others by asking are called distracters: they are meant to determine
vii
viii Preface
those who have the best knowledge of the subject. The to the exam. Be sure to read these instructions in
present NBDE review questions should be used to help advance.
the test taker better discriminate similar choices, as an 10. Make sure that once you have completed the exam all
impetus to review a subject more intensively. (Distrac- questions are appropriately answered. Review before
tors in questions on the actual board exam help deter- you submit your answers electronically.
mine which students have the best knowledge of the 11. Before coming to the exam, read over the checklist
subject.) Most test takers do better by reading the ques- provided on the ADA website under National Boards.
tion and trying to determine the answer before look- Presently, the part II exam is constructed as follows:
ing at the answer bank. Therefore consider trying to
answer questions without looking at the answer bank. Day 1
2. Eliminate answers that are obviously wrong. This will Description # of Items Time
allow a better chance of picking the correct answer and
Optional Tutorial NA 15 minutes
reduce distraction from the wrong answers.
3. Only go back and change an answer if you are abso- Discipline-based, multiple-choice test ~200 3.5 hours
lutely certain you were wrong with your previous items
choice, or if a different question in the same exam Optional scheduled break NA One hour max.
provides you with the correct answer. Discipline-based, multiple-choice test ~200 3.5 hours
4. Read questions carefully. Note carefully any negative items
words in questions, such as except, not, and false.
If these words are missed when reading the question, Day 2
it is nearly impossible to get the correct answer; Description # of Items Time
noting these key words will make sure you do not
Optional tutorial NA 15 minutes
miss them.
5. If you are stuck on one question, consider treating the Patient case problems with 100 3.5 hours
answer bank like a series of true/false items relevant to multiple-choice questions
the question. Most people consider true/false ques- Optional Post-exam Survey NA 15 minutes
tions easier than multiple choice. At least if you can
eliminate a few choices, you will have a better chance Helpful Hints for the
at selecting the correct answer from whatever is left.
6. Never leave blanks, unless the specific exam has a
Post-Examination Period
penalty for wrong answers. It is better to choose incor- It may be a good idea to think about what you will be doing
rectly than leave an item blank. Check with those after the exam.
giving the examination to find out whether there are
penalties for marking the wrong answer. 1. Most people are exhausted after taking board exams.
7. Some people do better on exams by going through the Some reasons for this exhaustion may be the number of
exam and answering known questions first, and then hours, the mental focus, and the anxiety that exams
returning to the more difficult questions later. This cause some people. Be aware that you may be tired, so
helps to build confidence during the exam. This also avoid planning anything that one should not do when
helps the test taker avoid spending too much time on exhausted, such as driving across the country, operating
a few questions and running out of time on less diffi- heavy machinery or power tools, or studying for final
cult questions that may be at the end. In addition, you exams. Instead, plan a day or two to recuperate before
may find additional insight to the correct answer in you tackle any heavier physical or mental tasks.
other exam questions later in the exam. 2. Consider a debriefing or detoxification meeting with
8. Pace yourself during the exam. Determine ahead of your positive study partners after the exam. Talking
time how much time each question will take to answer. about the exam afterwards may help reduce stress.
Do not rush, but do not spend too much time on one However, remember that the feelings one has after an
question. Sometimes it is better to move to the next exam may not always match the exam score (e.g., stu-
question and come back to the difficult ones later, since dents who feel they did poorly may have done well, or
a fresh look is sometimes helpful. students who feel they did well may not have.)
9. Bring appropriate supplies to the exam, such as read- 3. Consider doing something nice for yourself. After all,
ing glasses, appropriate for a computer screen. If you you will have just completed a major exam. It is impor-
get distracted by noise, consider bringing ear plugs. It tant to celebrate this accomplishment.
is inevitable that someone will take the exam next to
the person in the squeaky chair, or the one with the We wish you the very best with taking your exams and
sniffling runny nose. Most exams will provide you trust that this text will provide you with an excellent train-
with instructions as to what you may or may not bring ing tool for your preparations.
Additional Resources
This review text is intended to aid the study and retention Management of Temporomandibular Disorders and
of dental sciences in preparation for the National Board Occlusion, Seventh Edition
Dental Examination. It is not intended to be a substitute Jeffrey P. Okeson
for a complete dental education curriculum. For a truly
Medical Emergencies in the Dental Office,
comprehensive understanding of the basic dental sciences,
Sixth Edition
please consult these supplemental texts.
Stanley F. Malamed
Biomechanics and Esthetic Strategies in Oral Radiology: Principles and Interpretation,
Clinical Orthodontics Seventh Edition
Ravindra Nanda Stuart C. White, Michael J. Pharoah
Carranzas Clinical Periodontology, Twelfth Edition Orthodontics: Current Principles & Techniques,
Michael G. Newman, Henry Takei, Perry R. Klokkevold, Fifth Edition
Fermin A. Carranza Thomas M. Graber, Robert L. Vanarsdall, Jr.,
Katherine W. L. Vig
Color Atlas of Dental Implant Surgery, Third Edition
Michael S. Block Cohens Pathways of the Pulp, Tenth Edition
Stephen Cohen, Kenneth M. Hargreaves
Contemporary Fixed Prosthodontics, Fifth Edition
Stephen F. Rosenstiel, Martin F. Land, Junhei Fujimoto Periodontics: Medicine, Surgery, and Implants
Louis F. Rose, Brian L. Mealey, Robert J. Genco,
Little and Falaces Dental Management of the Medically
Walter Cohen
Compromised Patient, Eighth Edition
James W. Little, Donald Falace, Craig Miller, Pharmacology and Therapeutics for Dentistry,
Nelson L. Rhodus Sixth Edition
John A. Yagiela, Frank J. Dowd, Barton S. Johnson,
Dentistry, Dental Practice, and the Community,
Angelo J. Mariotti, Enid A. Neidle
Sixth Edition
Brian A. Burt, Stephen A. Eklund Endodontics: Principles and Practice, Fifth Edition
Mahmoud Torabinejad, Richard E. Walton, Ashraf Fouad
Functional Occlusion: From TMJ to Smile Design
Peter E. Dawson Sturdevants Art & Science of Operative Dentistry,
Sixth Edition
Handbook of Local Anesthesia, Sixth Edition
Theodore M. Roberson, Harald O. Heymann,
Stanley F. Malamed
Edward J. Swift, Jr.
Jongs Community Dental Health, Fifth edition
Wongs Essentials of Pediatric Nursing, Ninth Edition
George M. Gluck, Warren M. Morganstein
Marilyn Hockenberry-Eaton
Management of Pain & Anxiety in the Dental Office,
Fifth Edition
Raymond A. Dionne, James C. Phero, Daniel E. Becker
A special thank you to Dr. Michael J. Hoover, Dr. W. Thomas Cavel, Dr. Steven
J. Hess, and the Creighton University School of Dentistry, Department of
Diagnostics Sciences, for their immeasurable help in preparing some of
the cases.
ix
Contents
SECTION 1 1.1 Introduction and Etiology 35
Endodontics 1 1.2 Pathogenesis and Diagnosis 38
1.3 Prevention 38
Jarshen Lin, Florence Kwo, Tom C. Pagonis 1.4 Treatment Overview 39
Outline of Review 1 1.5 Summary 40
1.0 Clinical Diagnosis, Case Selection, Treatment 2.0 Patient Assessment, Examination, Diagnosis,
Planning, and Patient Management 1 and Treatment Planning 40
1.1 Pulpal Diseases 2 2.1 Patient Assessment Considerations 40
1.2 Apical Diseases 3 2.2 Examination and Diagnosis 40
1.3 Endodontic Diagnosis 5 2.3 Treatment Planning 44
1.4 Endodontic Examination and Testing 6 2.4 Summary 47
1.5 Cracked Tooth Syndrome 10 3.0 Instrumentation for Operative Dentistry
1.6 Vertical Root Fracture 11 Procedures 47
1.7 Endodontic-Periodontal Relationships 11 3.1 Hand Instruments for Cutting 47
2.0 Basic Endodontic Treatment Procedures 12 3.2 Overview of Powered Cutting
2.1 Nonsurgical Endodontics 12 Instruments 49
2.2 Surgical Endodontics 13 3.3 Rotary Cutting Instruments 49
2.3 Endodontic Emergencies 15 3.4 Cutting Mechanisms 50
2.4 Sterilization and Asepsis 16 3.5 Hazards with Cutting Instruments 51
2.5 Radiographic Techniques 17 4.0 Preparation of Teeth 51
2.6 Microbiology of Endodontics 18 4.1 Introduction 52
3.0 Procedural Complications 18 4.2 Stages and Steps in Tooth Preparation 52
3.1 Ledge Formation 18 4.3 Moisture Control 55
3.2 Instrument Separation 19 4.4 Tooth Preparation for Amalgam
3.3 Perforation 20 Restorations 56
3.4 Vertical Root Fracture 21 4.5 Tooth Preparation for Composite
4.0 Traumatic Injuries 21 Restorations 59
4.1 Examinations of Traumatic Injuries to 5.0 Restoration of Teeth 61
Teeth 21 5.1 Sealers, Liners, and Bases 61
4.2 Types of Injuries 22 5.2 Amalgam Restorations 62
4.3 Avulsion 24 5.3 Enamel and Dentin Bonding 66
4.4 Biologic Consequences of Traumatic 5.4 Composite Restorations 69
Injuries 25 5.5 Gold Inlay and Onlay Restorations 72
4.5 Inflammatory Root Resorption versus Sample Questions 76
Replacement Root Resorption 28
5.0 Adjunctive Endodontic Treatment 28
5.1 Dentin-Pulp Complex 28 SECTION 3
5.2 Vital Pulp Therapy 28 Oral and Maxillofacial Surgery and Pain
5.3 Bleaching Discolored Teeth 30 Control 79
6.0 Posttreatment Evaluation 30
6.1 Restoration of Endodontically Treated Larry L. Cunningham, Jr., Philip Lin,
Teeth 30 Kenneth L. Reed
6.2 Success and Failure 31 1.0 Oral and Maxillofacial Surgery 79
Sample Questions 31 1.1 Principles of Surgery 79
1.2 Dentoalveolar Surgery 79
SECTION 2 1.3 Trauma Surgery 84
Operative Dentistry 35 1.4 Orthognathic Surgery 86
1.5 Facial Pain and Neuropathology and
Andr V. Ritter Osteonecrosis of the Jaw 87
1.0 Dental Caries 35 1.6 Temporomandibular Disorders 91
xi
xii Contents
1.7 Odontogenic Infections 94 2.9 Intraoral Radiographic Examinations 143

1.8 Bisphosphonate-Related Osteonecrosis of 2.10 Radiographic Anatomy 143
the Jaws 98 2.11 Radiographic Appearance of Caries 148
1.9 Biopsies 99 2.12 Radiographic Appearance of Periodontal
1.10 Surgical Management of Cysts and Disease 149
Tumors 100 2.13 Panoramic Imaging 150
2.0 Local Anesthesia 102 Sample Questions 152
2.1 Local Anesthetic Drug Overview 102
2.2 Local Anesthesia Techniques 104 SECTION 5
Sample Questions 106 Orthodontics and Pediatric
Dentistry 155
SECTION 4
Oral Diagnosis 109 Steven J. Lindauer, Bhavna Shroff,
Eser Tufekci, Mark Taylor
Jeffrey C.B. Stewart, Sanjay M. Mallya 1.0 Orthodontics 155
1.0 Oral Pathology and Diagnosis of Soft Tissue 1.1 Epidemiology of Malocclusion 155
Diseases 109 1.2 Growth and Development 156
1.1 Developmental Conditions 109 1.3 Development of Occlusion 159
1.2 Mucosal LesionsPhysical-Chemical 111 1.4 Orthodontic Diagnosis 161
1.3 Mucosal LesionsInfections 112 1.5 Treatment Planning 165
1.4 Mucosal LesionsImmunologic 1.6 Biology of Tooth Movement 165
Diseases 114 1.7 Mechanical Principles in Tooth
1.5 Mucosal LesionsPremalignant Movement 168
Conditions 117 1.8 Orthodontic Materials 172
1.6 Mucosal LesionsMalignancies 118 1.9 Orthodontic Appliances 173
1.7 Connective Tissue TumorsBenign 118 1.10 Early Treatment 177
1.8 Connective Tissue TumorsMalignant 120 1.11 Growth Modification 179
1.9 Salivary Gland DiseasesReactive 1.12 Comprehensive Treatment 180
Lesions 120 1.13 Retention 181
1.10 Salivary Gland DiseasesBenign 1.14 Adult Treatment and Interdisciplinary
Neoplasms 121 Treatment 181
1.11 Salivary Gland DiseasesMalignant 1.15 Combined Surgical and Orthodontic
Tumors 122 Treatment 182
1.12 Lymphoid Neoplasms 122 2.0 Pediatric Dentistry 184
1.13 Odontogenic LesionsOdontogenic 2.1 Development and Developmental
Cysts 124 Disturbances of the Teeth 185
1.14 Odontogenic LesionsOdontogenic 2.2 Management of Child Behavior in the Dental
Tumors 125 Setting 189
1.15 Bone (Nonodontogenic) Lesions 2.3 Local Anesthesia and Nitrous Oxide Sedation
Fibro-osseous Lesions 127 for Children 192
1.16 Bone (Nonodontogenic) LesionsGiant Cell 2.4 Restorative Dentistry for Children 195
Lesions 127 2.5 Pulp Treatment for Primary Teeth 196
1.17 Bone (Nonodontogenic) Lesions 2.6 Space Management in the Developing
Inflammatory Diseases 129 Dentition 199
1.18 Bone (Nonodontogenic) 2.7 Periodontal Problems in Children 204
LesionsMalignancies 130 2.8 Dental Trauma in Children 205
1.19 Hereditary Conditions 130 2.9 Miscellaneous Topics in Pediatric
2.0 Oral Radiology 132 Dentistry 207
2.1 Radiation Physics 132 Sample Questions 213
2.2 Radiation Biology 134
2.3 Health Physics 137 SECTION 6
2.4 X-Ray Film and Intensifying Screens 138 Patient Management 217
2.5 Projection Geometry 139
2.6 Processing X-Ray Film 140 Oscar Arevalo, Myron Allukian, Jr.,
2.7 Digital Imaging 141 Marla W. Deibler, Catherine Frankl Sarkis
2.8 Radiographic Quality Assurance and Infection 1.0 Epidemiology 217
Control 142 2.0 Prevention of Oral Diseases 219
Contents xiii
3.0 Evaluation of Dental Literature 223 Local Anesthetics 308

4.0 Infection Control 229 General Anesthetics 310
5.0 Materials and Equipment Safety 232 5.0 Analgesics and Antihistamines 313
6.0 Dental Care Delivery Systems 234 Opioids 313
7.0 Communication and Interpersonal Skills 236 Nonsteroidal Antiinflammatory Drugs
8.0 Health Behavior Change 239 Nonnarcotic Analgesics 314
9.0 Anxiety and Pain Control 242 Drugs for Migraine 316
10.0 Professional Responsibilities and Liabilities 244 Antihistamines 316
Sample Questions 247 6.0 Cardiovascular Pharmacology and Diuretics 317
Antiarrhythmic Drugs 317
SECTION 7 Drugs Used in Treating Heart Failure 319
Periodontics 251 Antihypertensive Drugs 319
Antianginal Drugs 321
Karen Novak, Nikola Angelov Diuretic Drugs 322
1.0 Diagnosis 251 Drugs Used for Blood Lipid Disorders 322
2.0 Etiology 255 Anticoagulants and Procoagulants 323
3.0 Pathogenesis 261 7.0 Gastrointestinal and Respiratory
4.0 Treatment Planning 268 Pharmacology 323
5.0 Prognosis 270 Drugs Used to Treat Gastrointestinal
6.0 Therapy 272 Disorders 323
7.0 Prevention and Maintenance 286 Drugs Used to Treat Asthma 324
Sample Questions 287 8.0 Endocrine Pharmacology 324
Thyroid Pharmacology 324
SECTION 8 Insulin and Oral Hypoglycemics 325
Pharmacology 290 Adrenal Corticosteroids 327
Drugs That Affect Calcium Metabolism 328
Frank Dowd Sex Hormones 329
Cues That Help in Remembering Drugs by 9.0 Antimicrobial Drugs 330
Classes 290 Antibacterial Drugs 330
1.0 Principles of Pharmacology 291 Antifungal Drugs 334
Targets of Drug Action 291 Antiviral Drugs 334
Dose-Response Relationships of Drugs 291 10.0 Antineoplastic Drugs 335
Pharmacokinetics 292 11.0 Toxicology 337
Drug-Drug Interactions 293 12.0 Prescription Writing 337
2.0 Autonomic Pharmacology 294 Sample Questions 339
Organization 295
SECTION 9
Abbreviations, Definitions, and Receptors 295
Dynamics of Neurotransmission 296 Prosthodontics 343
Tissues and Organs 296
Alejandro Peregrina
Adrenergic Agonists 296
1.0 General Considerations 343
Adrenergic Receptor Blockers 298
2.0 Complete Dentures 347
Dental Implications of and Blockers 299
3.0 Removable Partial Prosthodontics 353
Cholinergic Receptor Agonists 299
4.0 Fixed Prosthodontics 356
Anticholinesterases 299
Sample Questions 368
Autonomics and the Eye 300
Antimuscarinic Drugs 300 Sample Examination 371
Dental Implications of Antimuscarinic Drugs and Answer Key for Section 1 405
Cholinergic Drugs 300 Answer Key for Section 2 408
Skeletal Neuromuscular Blockers 301 Answer Key for Section 3 411
3.0 Central Nervous System Pharmacology 302 Answer Key for Section 4 413
Antipsychotic Drugs 302 Answer Key for Section 5 415
Antidepressant Drugs 302 Answer Key for Section 6 418
Antimania Drugs 303 Answer Key for Section 7 421
Sedative Hypnotics 304 Answer Key for Section 8 423
Antiepileptic Drugs 305 Answer Key for Section 9 426
Anti-Parkinson Drugs 307 Answer Key for Sample Examination 429
4.0 Anesthetics 308 Index 455
SECTION 1
Endodontics
JARSHEN LIN
FLORENCE KWO
TOM C. PAGONIS
OUTLINE
Outline of Review
1. Clinical Diagnosis, Case Selection, Treatment
Planning, and Patient Management
A practice analysis was conducted using the 63 Competen
2. Basic Endodontic Treatment Procedures cies of the New Dentist, developed by the American Dental
3. Procedural Complications Education Association. For NBDE Part II, the findings of
4. Traumatic Injuries the dental practice survey were used to make changes in
the content specifications. There are 31 endodontic ques-
5. Adjunctive Endodontic Therapy
tions on the examination, divided into the following six
6. Posttreatment Evaluation subjects:
1. Clinical diagnosis, case selection, treatment planning,

and patient management (19)
The word endodontic comes from two Greek words meaning 2. Basic endodontic treatment procedures (7)
inside and tooth. Endodontics is the science of diagnos- 3. Procedural complications (1)
ing and treating pulpal and apical disease. Endodontics is 4. Traumatic injuries (1)
the branch of dentistry that is concerned with the morphol- 5. Adjunctive endodontic therapy (1)
ogy, physiology, and pathology of the human dental pulp 6. Posttreatment evaluation (2)
and apical tissues. The study and practice of endodontics
encompass the basic and clinical sciences, including the The American Association of Endodontists Glossary
biology of the normal pulp and the etiology, diagnosis, of Endodontic Terms is used in reference to endodontic
prevention, and treatment of diseases and injuries of the pathoses. In 2013, the endodontics diagnostic terminology
pulp and associated apical conditions.* adopted by the American Association of Endodontists as
This review outline is similar to the outline of the text- described in the December 2009 issue of Journal of Endo
books Principles and Practice of Endodontics (4th edition, dontics (Volume 35, Number 12, p. 1634) was incorporated
2009), Problem Solving in Endodontics (5th edition, 2011), in the NBDE Part II.
and Pathways of the Pulp (10th edition, 2010). Some
contents in this review have been taken from these texts.
This review is not meant to be a comprehensive review of 1.0 Clinical Diagnosis, Case
endodontics but rather a guide to study in preparing for Selection, Treatment Planning,
the endodontic section of Part II of the National Board
Dental Examination (NBDE). Students are referred to
and Patient Management
other sources including the aforementioned texts for a
more complete discussion in each area of endodontics. This
Outline of Review
review is intended to help organize and integrate knowl- 1.1 Pulpal Diseases
edge of concepts and facts. It also can help students to 1.2 Apical Diseases
identify areas requiring more concentrated study. 1.3 Endodontic Diagnosis
1.4 Endodontic Examination and Testing
1.5 Cracked Tooth Syndrome
The section editors acknowledge Dr. Meghan T. Cooper, Dr. Doreen Toskos,
Dr. Louis Lin, Dr. Peggy Leong and Dr. Brooke Blicher for their contributions.
*Council on Dental Education and Licensure, American Dental Association. Council on Dental Education and Licensure, American Dental Association.
1
2 Section 1 Endodontics
1.6 Vertical Root Fracture f. When C fiber pain dominates, it signifies irrevers-
1.7 Endodontic-Periodontal Relationships ible local tissue damage.
g. With increasing inflammation of pulp tissues, C
fiber pain becomes the only pain feature.
1.1 Pulpal Diseases h. Hot liquids or foods can increase intrapulpal pres-
A. The pulp. sure to levels that excite C fibers.
1. The pulp contains nerves, blood vessels, and connec- i. The pain is diffuse and can be referred to a distant
tive tissue. site or to other teeth.
2. Several factors make it unique and alter its ability to j. The sustained inflammatory cycle is detrimental
respond to irritation. to pulpal recovery, finally terminating in tissue
a. The pulp is almost completely surrounded by hard necrosis.
tissue (dentin), which limits the available room for C. Clinical classification of pulpal diseases.
expansion and restricts the pulps ability to tolerate 1. Normal pulp.
edema. a. A normal pulp is asymptomatic.
b. The pulp lacks collateral circulation, which severely b. A normal pulp produces a mild to moderate tran-
limits its ability to cope with bacteria, necrotic sient response to thermal and electrical stimuli that
tissue, and inflammation. subsides almost immediately when the stimulus is
c. The pulp possesses unique, hard tissuesecreting removed.
cells, or odontoblasts, as well as mesenchymal cells c. The tooth does not cause a painful response when
that can differentiate into osteoblasts that form percussed or palpated.
more dentin in an attempt to protect the pulp from 2. Reversible pulpitis.
injury. a. In reversible pulpitis, thermal stimuli (usually
B. Physiology of pulpal pain. cold) cause a quick, sharp, hypersensitive response
1. The sensibility of the dental pulp is controlled by that subsides as soon as the stimulus is removed.
A-delta and C afferent nerve fibers. b. Any irritant that can affect the pulp may cause
2. Dentinal pain. reversible pulpitis.
a. A-delta fibers are large myelinated nerves that (1) Early caries or recurrent decay.
enter the root canal and divide into smaller (2) Periodontal scaling or root planing.
branches, coursing coronally through the pulp. (3) Deep restorations without a base.
b. A-delta fiber pain is immediately perceived as a c. Reversible pulpitis is not a disease; it is a symptom.
quick, sharp, momentary pain, which dissipates (1) If the irritant is removed, the pulp reverts to an
quickly on removal of the inciting stimulus (cold uninflamed state.
liquids or biting on an unyielding object). (2) If the irritant remains, the symptoms may lead
c. The intimate association of A-delta fibers with the to irreversible pulpitis.
odontoblastic cell layer and dentin is referred to as d. Reversible pulpitis can be clinically distinguished
the pulpodentinal complex. from a symptomatic irreversible pulpitis in two
3. Pulpitis pain. ways.
a. In pulpal inflammation, the response is exagger- (1) Reversible pulpitis causes a momentary painful
ated and disproportionate to the challenging stim- response to thermal change that subsides as
ulus (hyperalgesia). This response is induced by the soon as the stimulus (usually cold) is removed.
effects of inflammatory mediators that are released However, symptomatic irreversible pulpitis
in the inflamed pulp. causes a painful response to thermal change
b. Progression of pulpal inflammation can change the that lingers after the stimulus is removed.
quality of the pain response. As the exaggerated (2) Reversible pulpitis does not involve a com-
A-delta fiber pain subsides, pain seemingly remains plaint of spontaneous (unprovoked) pain.
and is perceived as a dull, throbbing ache. This e. Frank penetration of bacteria into the pulp fre-
second pain symptom is from C nerve fibers. quently is the crossover point to irreversible
c. C fibers are small, unmyelinated nerves that course pulpitis.
centrally in the pulp stroma. 3. Symptomatic irreversible pulpitis.
d. In contrast to A-delta fibers, C fibers are not a. By definition, the pulp has been damaged beyond
directly involved with the pulpodentinal complex repair, and even with removal of the irritant, it will
and are not easily provoked. not heal.
e. C fiber pain surfaces with tissue injury and is b. Microscopic findings.
mediated by inflammatory mediators, vascular (1) Microabscesses of the pulp begin as tiny zones
changes in blood volume and blood flow, and of necrosis within dense acute inflammatory
increases in tissue pressure. cells.
Section 1 Endodontics 3
(2) Histologically intact myelinated and unmy and manifests as tenderness to percussion and
elinated nerves may be observed in areas with chewing.
dense inflammation and cellular degeneration. e. Microscopic findings.
c. Following irreversible pulpitis, pulp death may (1) As inflammation progresses, tissue continues
occur quickly or may require years; it may be to disintegrate in the center to form an increas-
painful or, more frequently, asymptomatic. The ing region of liquefaction necrosis.
end result is necrosis of the pulp. (2) Because of the lack of collateral circulation and
d. Characterized by spontaneous, unprovoked, inter- the unyielding walls of dentin, there is insuffi-
mittent or continuous pain. cient drainage of inflammatory fluids.
e. Sudden temperature changes (often to cold) elicit (3) The result is localized increases in tissue
prolonged episodes of pain that linger after the pressure, causing the destruction to progress
thermal stimulus is removed. unchecked until the entire pulp is necrotic.
f. Occasionally, patients may report that a postural (4) Bacteria are able to penetrate and invade into
change, such as lying down or bending over, dentinal tubules. (It is necessary to remove the
induces pain. superficial layers of dentin during cleaning and
g. Radiographs are generally insufficient for diagnos- shaping.)
ing irreversible pulpitis. 6. Previously treated pulp.
(1) Radiographs can be helpful in identifying a. Clinical diagnostic category indicating that the
suspect teeth only. tooth has been endodontically treated and the
(2) Thickening of the apical portion of the peri- canals are obturated with various filling materials
odontal ligament (PDL) may become evident other than intracanal medicaments.
on radiographs in the advanced stage. 7. Previously initiated therapy.
h. Electrical pulp test is of little value in the diagnosis a. Clinical diagnostic category indicating that the
of symptomatic irreversible pulpitis. tooth has been previously treated by partial endo
4. Asymptomatic irreversible pulpitis. dontic therapy (e.g., pulpotomy, pulpectomy).
a. Microscopically similar to symptomatic irrevers- 8. Other.
ible pulpitis. a. Hyperplastic pulpitisreddish, cauliflower-like
(1) Microabscesses of the pulp begin as tiny zones growth of pulp tissue through and around a carious
of necrosis within dense acute inflammatory exposure. The proliferative nature of this type of
cells. pulp is attributed to low-grade, chronic irritation
(2) Histologically intact myelinated and unmy of the pulp and the generous vascular supply char-
elinated nerves may be observed in areas with acteristically found in young people.
dense inflammation and cellular degeneration. b. Internal resorption.
b. There are no clinical symptoms, but inflammation (1) Most commonly identified during routine
produced by caries, caries excavation, or trauma radiographic examination. If undetected, inter-
occurs. nal resorption eventually perforates the root.
5. Pulp necrosis. (2) Histologic appearance.
a. Death of the pulp, resulting from the following. (a) Chronic pulpitis.
(1) Untreated irreversible pulpitis. (i) Chronic inflammatory cells.
(2) Traumatic injury. (ii) Multinucleated giant cells adjacent to
(3) Any event that causes long-term interruption granulation tissue.
of the blood supply to the pulp. (iii) Necrotic pulp coronal to resorptive
b. Pulpal necrosis may be partial or total. defect.
(1) Partial necrosis may manifest with some of the (3) Only prompt endodontic therapy can stop the
symptoms associated with irreversible pulpitis. process and prevent further tooth destruction.
For example, a tooth with two canals could (4) Partial pulp vitality is necessary for active inter-
have an inflamed pulp in one canal and a nal resorption.
necrotic pulp in the other.
(2) Total necrosis is asymptomatic before it affects 1.2 Apical Diseases
the PDL, and there is no response to thermal A. Definition of apical disease.
or electrical pulp tests. 1. Apical lesions of pulpal origin are inflammatory
c. In anterior teeth, some crown discoloration may responses to irritants from the root canal system.
accompany pulp necrosis. 2. Patient symptoms may range from an asymptomatic
d. Protein breakdown products and bacteria and response to various symptoms.
their toxins eventually spread beyond the apical a. Slight sensitivity to chewing.
foramen; this leads to thickening of the PDL b. Sensation of tooth elongation.
c. Intense pain. d. Occasionally, there may be slight tenderness to

d. Swelling. percussion or palpation testing.
e. Fever. e. The diagnosis of asymptomatic apical periodontitis
f. Malaise. is confirmed by the following.
3. The sign most indicative of an apical inflammatory (1) General absence of symptoms.
lesion is radiographic bone resorption, but this is (2) Radiographic presence of an apical
unpredictable. Apical lesions are frequently not radiolucency.
visible on radiographs. (3) Confirmation of pulpal necrosis.
4. Apical lesions do not occur as individual entities; f. A totally necrotic pulp provides a safe harbor for
there are clinical and histologic crossovers in termi- the primarily anaerobic microorganismsif there
nology regarding apical lesions because the terminol- is no vascularity, there are no defense cells.
ogy is based both on clinical signs and symptoms and g. Asymptomatic apical periodontitis traditionally
on radiographic findings. There is no correlation has been classified histologically as apical granu-
between histologic findings and clinical signs, symp- loma or apical cyst. The only accurate way
toms, and duration of the lesion. The terms acute and to distinguish them is by histopathologic
chronic apply only to clinical symptoms. examination.
B. Classification of apical diseases. 3. Acute apical abscess.
1. Symptomatic apical periodontitis. a. An acute apical abscess is painful, with purulent
a. Symptomatic apical periodontitis refers to painful exudate around the apex.
inflammation around the apex (localized inflam- b. It is a result of exacerbation of symptomatic apical
mation of the PDL in the apical region). It can periodontitis from a necrotic pulp.
result from the following. c. The PDL may radiographically appear within
(1) Extension of pulpal disease into the apical normal limits or only slightly thickened.
tissue. d. The periapical radiograph reveals a relatively
(2) Canal overinstrumentation or overfill. normal or slightly thickened lamina dura (because
(3) Occlusal trauma such as bruxism. the infection has rapidly spread beyond the con-
b. Because symptomatic apical periodontitis may fines of the cortical plate before demineralization
occur around vital and nonvital teeth, conducting can be detected radiographically).
pulp tests is the on1y way to confirm the need for e. Only swelling is manifest.
endodontic treatment. f. Lesions can also result from infection and rapid
c. Even when present, the apical PDL may radio- tissue destruction arising from within asymptom-
graphically appear within normal limits or only atic apical periodontitis.
slightly widened. g. Histopathologic findings.
d. The tooth may be painful during percussion (1) Central area of liquefaction necrosis containing
tests. disintegrating neutrophils and other cellular
e. If the tooth is vital, a simple occlusal adjustment debris.
can often relieve the pain. If the pulp is necrotic (2) Surrounded by viable macrophages and occa-
and remains untreated, additional symptoms may sional lymphocytes and plasma cells.
appear as the disease advances to the next stage, (3) Bacteria are not always found in the apical
acute apical abscess. tissues or within the abscess cavity.
f. Because there is little room for expansion of the h. Presenting signs and symptoms of acute apical
PDL, increased pressure can also cause physical abscess.
pressure on the nerve endings, which subsequently (1) Rapid onset of swelling.
causes intense, throbbing apical pain. (2) Moderate to severe pain.
g. Histopathologic examination reveals a localized (3) Pain with percussion and palpation.
inflammatory infiltrate within the PDL. (4) Slight increase in tooth mobility.
2. Asymptomatic apical periodontitis. (5) Extent and distribution of swelling are deter-
a. Asymptomatic apical periodontitis is a long- mined by the location of the apex and the
standing, asymptomatic or mildly symptomatic muscle attachments and the thickness of the
lesion. cortical plate.
b. It is usually accompanied by radiographically (6) Usually the swelling remains localized. How-
visible apical bone resorption. ever, it also may become diffuse and spread
c. Bacteria and their endotoxins cascading out widely (cellulitis).
into the apical region from a necrotic pulp cause i. An acute apical abscess can be differentiated from
extensive demineralization of cancellous and cor lateral periodontal abscess with pulp vitality testing
tical bone. and sometimes with periodontal probing.
4. Chronic apical abscess. 2. Location.

a. Associated with either a continuously or an inter- a. The site or sites where symptoms are perceived.
mittently draining sinus tract without discomfort. b. Could you point to the tooth that hurts or
b. The exudate can also drain through the gingival swells?the patient is asked to indicate the loca-
sulcus, mimicking a periodontal lesion with a tion by pointing to it directly with one finger.
pocket. c. The accuracy of the patients description of pain
c. Pulp tests are negative because of the presence of depends on whether the inflammatory state is
necrotic pulp. limited to the pulp tissue only.
d. Radiographic examination shows the presence of (1) If the inflammation has not reached the PDL,
bone loss at the apical area. it may be difficult for the patient to localize the
e. Treatmentthese sinus tracts resolve spontane- pain because the pulp contains sensory fibers
ously with nonsurgical endodontic treatment. that transmit only pain, not location.
5. Condensing osteitis. (2) The PDL contains proprioceptive sensory
a. Excessive bone mineralization around the apex of fibers. When the inflammatory process extends
an asymptomatic vital tooth. beyond the apex, it is easier for the patient to
b. Radiopacity may be caused by low-grade pulp identify the source of the pain. (Percussion test
irritation. can be used.)
c. This process is asymptomatic and benign. It does d. Referred pain.
not require endodontic therapy. (1) Pain can also be referred to the adjacent teeth
or in the opposing quadrant.
1.3 Endodontic Diagnosis (2) It is rare for odontogenic pain to cross the
A. Triage of patient with pain. midline of the head.
1. Orofacial pain can be the clinical manifestation (3) Referred pain may also be ipsilaterally referred
of various diseases involving the head and neck to the preauricular area, down the neck, or up
region. to the temple, especially for the posterior teeth.
2. The cause must be differentiated between odonto- (4) In posterior molars, pain can often be referred
genic and nonodontogenic. to the opposing quadrant or to other teeth in
a. Numerous orofacial diseases mimic endodontic the same quadrant.
pain (may produce sensory misperception as a (5) Maxillary molars often refer pain to the zygo-
result of overlapping between the sensory fibers of matic, parietal, and occipital regions of the
the trigeminal nerve). head, whereas lower molars frequently refer
b. Characteristics of nonodontogenic involvement pain to the ear, angle of the jaw, or posterior
(not all apply to all cases). regions of the neck.
(1) Episodic pain with pain-free remissions. 3. Chronology.
(2) Trigger points. a. When did you first notice this?inception.
(3) Pain travels and crosses the midline of the b. The patient may be aware of the history of dental
face. procedures or trauma, clinical course, and tempo-
(4) Pain that surfaces with increasing mental ral pattern of the symptoms.
stress. (1) Modeis the onset of symptoms spontaneous
(5) Pain that is seasonal or cyclic. or provoked (i.e., sudden or gradual)? If symp-
(6) Paresthesia. toms can be stimulated, are they immediate or
B. Medical history (developing data). delayed?
1. Endodontic treatment is not contraindicated with (2) Periodicitydo the symptoms have a temporal
most medical conditions. The only systemic contra- pattern (i.e., sporadic or occasional)?
indications to endodontic therapy are uncontrolled (3) Frequencyhave the symptoms persisted since
diabetes or a recent myocardial infarction (MI) they began, or are they intermittent? How
(within the past 6 months). often does this pain occur?
2. The patients medical history enables the clinician to (4) Durationhow long do symptoms last when
determine the need for a medical consultation or they occur (i.e., momentary or lingering)?
premedication of the patient. 4. Quality of pain.
C. Dental history. a. How the patient describes the complaint.
1. Chief complaint. (1) Bony origindull, gnawing, or aching.
a. Can you tell me about your problem?as (2) Vascular response to tissue inflammation
expressed in the patients words. throbbing, pounding, or pulsating.
b. The dentist should paraphrase the patients (3) Pathosis of nerve root complexes, sensory
responses to verify them. ganglia, or peripheral innervation (irreversible
pulpitis or trigeminal neuralgia)sharp, elec- question to establish the patients normal range of
trical, recurrent, or stabbing. response.
(4) Pulpal and apical pathosesaching, pulsing, B. Palpation.
throbbing, dull, gnawing, radiating, flashing, 1. When apical inflammation develops after pulp necro-
stabbing, or jolting pain. sis, the inflammatory process may burrow its way
5. Intensity and severity of symptoms. through the facial cortical bone and begin to affect
a. Quantify pain by assigning the pain a degree of 0 the overlying mucoperiosteum.
(none) to 10 (most severe). 2. Before incipient swelling becomes clinically evident,
6. Affecting factorsstimulated or spontaneous. it may feel tender during shaving or applying
a. Does the pain ever occur without provocation? makeup.
b. Provoking factors. C. Percussion.
(1) Does heat, cold, biting, or chewing cause 1. Although the percussion test does not indicate the
pain? health of the pulp, the sensitivity of the propriocep-
(2) The dental pain may be exacerbated by lying tive fibers reveals inflammation of the apical PDL.
down or by bending over. This change increases 2. A positive response to percussion indicates not
blood pressure to the head, which increases only the presence of inflammation of the PDL but
pressure on the inflamed, confined pulp. also the extent of the inflammatory process. The
c. Attenuating factors. degree of response correlates with the degree of
(1) Does anything relieve the pain? inflammation.
(2) Does drinking warm or cold liquids relieve 3. Other factors may also inflame the PDL and yield a
pain? positive percussion test result.
(3) Does lying down or sitting up relieve pain? a. Rapid orthodontic movement of teeth.
7. Disposition. b. A recently placed restoration in hyperocclusion.
a. How has the pain changed since it startedworse, c. A lateral periodontal abscess.
dissipated, eliminated. 4. The first percussion test should be performed with
8. Supplemental history. the clinicians finger on a nonsuspect tooth. If the
a. Past facts and current symptoms characterizing the patient is unable to discern, the blunt handle of a
difficult diagnosis. mouth mirror should be used.
(1) It might be necessary to wait a while for vague 5. Having the patient chew on a cotton roll, a cotton
symptoms to localize. swab, or the reverse end of a low-speed suction straw
(2) This conservative approach is often necessary may help.
in pulpal pathosis confined to the root canal D. Thermal tests (see Tables 1-1 and 1-2)thermal testing
space, which can refer pain to other teeth or to is especially valuable when the patient describes the
nondental sites. pain as diffuse. Thermal testing of vital pulps often
helps to pinpoint the source. However, the sensory
response of the teeth is refractory to repeated thermal
1.4 Endodontic Examination and Testing
stimulation. To avoid misinterpretation of a response,
Extraoral Examination the dentist should wait an appropriate amount of time
A. Examination should begin while the clinician is taking for tested teeth to respond and recover.
the patients history. 1. Cold testcold testing can be done with cold water
B. Facial asymmetry might indicate swelling of odonto- baths, sticks of ice, ethyl chloride (5C), dichloro-
genic origin. difluoromethane (Endo-Ice) (30C, 21F), and
C. Occasionally, facial lesions (e.g., a sinus tract) can be carbon dioxide ice sticks (77.7C, 108F).
traced to a tooth as the source. All sinus tracts should a. In the ethyl chloride or Endo-Ice method, ethyl
be traced with a gutta-percha point by radiograph chloride is sprayed liberally onto a cotton pellet.
(Figure 1-1). b. The chilled pellet is applied immediately to the
middle third of the facial surface of the crown.
Intraoral Endodontic Examination c. The pellet is kept in contact for 5 seconds or until
A. Intraoral diagnostic tests (Tables 1-1 and 1-2). the patient begins to feel pain.
1. Help define the pain by evoking reproducible symp- 2. Heat testthese include warm sticks of temporary
toms that characterize the chief complaint. stopping, rotating a dry prophy cup to create fric-
2. Help provide an assessment of normal responses for tional heat, and a hot water bath. The hot water bath
comparison with abnormal responses. yields the most accurate patient response.
3. The dentist should include adequate controls for test 3. Responses to thermal teststhe sensory fibers of the
procedures. Several adjacent, opposing, and contra- pulp transmit only pain, whether the pulp has been
lateral teeth should be tested before the tooth in cooled or heated. There are four possible responses.
A B
Figure 1-1 A, To locate the source of an infection, the sinus tract can be traced by threading the stoma with a gutta-percha point.
B, Radiograph of the area shows an old root canal in tooth #4 and a questionable radiolucent area associated with tooth #5, with no
indication as to the etiology of the sinus tract. C, After tracing the sinus tract, gutta-percha is seen to be directed to the source of
pathosis, the apex of tooth #5. (From Cohen S, Hargreaves KM: Pathways of the Pulp, ed 10. St Louis, Mosby, 2011.)
Table 1-1
Pulpal Diagnosis
PULPAL DIAGNOSIS CHIEF COMPLAINT OR HISTORY RADIOGRAPHIC FINDINGS EPT THERMAL TESTING
Normal pulp Normal + +
Reversible pulpitis Cold sensitivity Normal or widened PDL + ++
Symptomatic Hot or cold sensitivity with lingering Normal, widened PDL, or PRL + ++ with lingering pain
irreversible pulpitis pain
Asymptomatic No clinical symptoms Widened PDL or PRL +
irreversible pulpitis
Pulp necrosis Variable Normal, widened PDL, or PRL
Previously treated Tooth has been endodontically Canals obturated
pulp treated and canals obturated
Previously initiated Tooth has been treated by partial Pulpotomy or pulpectomy
therapy endodontic therapy
EPT, Electrical pulp test; PDL, periodontal ligament; PRL, periradicular (apical) radiolucency.
Table 1-2
Apical Diagnosis
CHIEF COMPLAINT RADIOGRAPHIC THERMAL
APICAL DIAGNOSIS OR HISTORY FINDINGS EPT TESTING PERCUSSION
Normal apical tissues Normal
Symptomatic apical Biting sensitivity Normal or widened PDL +/ +/ +
periodontitis
Asymptomatic apical PRL
periodontitis
Acute apical abscess Pain with swelling Normal, widened PDL, +
or PRL
Chronic apical abscess Bump in the gum PRL
Condensing osteitis Asymptomatic (usually) Increased radiopacity +/ +/ /+
or variable pulpal (increased apical bone
symptoms density)
EPT, Electrical pulp test; PDL, periodontal ligament; PRL, periradicular (apical) radiolucency.
a. No responsea nonvital pulp is indicated; it can f. Thicker enamel yields a more delayed response;
also indicate a false-negative response because of thinner enamel of anterior teeth yields a quicker
excessive calcification or recent trauma. response.
b. Mild to moderate degree of awareness of slight g. If the patients medical history reveals that a cardiac
pain that subsides within 1 to 2 secondswithin pacemaker has been implanted, the use of an elec-
normal limits. trical pulp tester is contraindicated.
c. Strong, momentary painful response that subsides 6. Causes of false readings.
within 1 to 2 secondsreversible pulpitis. a. False-positive response.
d. Moderate to strong painful response that lingers (1) Electrode or conductor contact with a metal
for several seconds or longer after the stimulus has restoration or the gingiva.
been removedirreversible pulpitis. (2) Patient anxiety.
E. Electrical pulp tests (see Tables 1-1 and 1-2). (3) Liquefaction necrosis may conduct current to
1. Electrical pulp test does not suggest the health or the attachment apparatus.
integrity of the pulp; it simply indicates that there are (4) Failure to isolate and dry the teeth before
vital sensory fibers present within the pulp. testing.
2. Electrical pulp test does not provide any information b. False-negative response.
about the vascular supply to the pulp, which is the (1) The patient has been heavily premedicated with
true determinant of pulp vitality. analgesics, narcotics, alcohol, or tranquilizers.
3. Electrical pulp test readings do not correlate with (2) Inadequate contact between the electrode or
the relative histologic health or disease status of conductor and the enamel.
the pulp. (3) A recently traumatized tooth.
4. Several conditions can cause false responses to elec- (4) Excessive calcification of the canal.
trical pulp testingit is essential that thermal tests (5) Recently erupted tooth with an immature apex.
be performed before a final diagnosis is made. (6) Partial necrosis.
5. Electrical pulp testing technique. F. Periodontal examination.
a. The teeth must be isolated and dried. 1. If a significant isolated pocket is discovered in the
b. The electrode of the pulp tester should be coated absence of periodontal disease, it increases the prob-
with a viscous conductor (e.g., toothpaste). ability of a vertical root fracture.
c. The electrode should be applied to the dry enamel 2. To distinguish disease of periodontal origin from
on the middle third of the facial surface of the disease of pulpal origin, pulp vitality tests along with
crown. periodontal probing are essential.
d. The current flow should be adjusted to increase G. Mobility.
slowly. 1. Tooth mobility is directly proportional to the integ-
e. The electrode should not be applied to any restora- rity of the attachment apparatus or to the extent of
tions (false reading). inflammation of the PDL.
2. The clinician should use two mouth mirror handles

to apply alternating lateral forces in a faciolingual
direction.
3. The pressure exerted by the purulent exudate of an
acute apical abscess may cause transient mobility of
a tooth.
4. Other causes of tooth mobility. Radiation
source Film or
a. Horizontal root fracture in the coronal half of the A sensor
tooth.
b. Very recent trauma.
c. Chronic bruxism.
d. Overzealous orthodontic treatment.
H. Selective anesthesia testthis test can be used when the
clinician has not determined through prior testing Radiation
which tooth is the source of pain. Because diffusion of source
the local anesthetic is not limited to a single tooth, the
clinician cannot make a conclusive diagnosis on the
basis of pain relief.
I. Test cavitythis test is done only in cases where pulp
necrosis is strongly suspected and corroborated by Change
other tests and radiographic findings, but a definitive vertical Film or
test is required. B angulation sensor
J. Radiographic examination. Figure 1-2 Radiographic images are only two-dimensional, and
1. Findings on radiographic examination. it is often difficult to discriminate the relative location of overlap-
a. A radiolucency does not begin to manifest until ping objects. A, When the source of the radiation is directly
demineralization extends into the cortical plate of perpendicular to overlapping objects, the image is captured
the bone. Clinicians should not rely exclusively on without much separation of the objects. However, when the radia-
radiographs to arrive at a diagnosis. tion source is at an angle to offset the overlapping objects, the
b. Because a radiograph is a two-dimensional image image is captured with the objects being viewed as separated.
only, radiographic strategy should involve the B, The object that is closest to the film (or sensor) moves the least,
with the object closest to the radiation source appearing farthest
exposure of two films at the same vertical angula-
away. (From Cohen S, Hargreaves KM: Pathways of the Pulp,
tion but with a 10- to 15-degree change in horizon- ed 10. St Louis, Mosby, 2011.)
tal angulation (Figure 1-2).
c. The status of the health and integrity of the pulp movement of the tube head or cone when com-
cannot be determined by radiographic images pared with a second radiograph. Objects closest to
alone. the lingual surface appear to move in the same
2. Radiographic interpretation. direction of the cone.
a. A single root canal should appear tapering from b. Proper application of this technique allows the
crown to apex. dentist to do the following.
b. A sudden change in appearance of the canal from (1) Locate additional canals or roots.
dark to light indicates that the canal has bifurcated (2) Distinguish between superimposed objects.
or trifurcated. (3) Differentiate various types of resorption.
c. A necrotic pulp does not cause radiographic (4) Determine buccal-lingual positions of frac-
changes until demineralization of the cortical tures and perforative defects.
plate. Significant medullary bone destruction may (5) Locate foreign bodies.
occur before any radiographic signs start to appear. (6) Locate anatomic landmarks in relation to the
d. The attending dentist should be cautious in accept- root apex.
ing prior diagnostic radiographs from the patient 4. Radiographic differential diagnosis of apical
or another dentist, no matter how recently they radiolucencies.
were made. Prior iatrogenic mishaps such as ledge a. Vertical root fracture.
formation, perforation, or instrument separation (1) A long-standing vertical root fracture may be
are critical for a newly treating dentist to uncover. viewed as a variant of apical periodontitis.
3. Buccal object rule (SLOB rulesame lingual, oppo- b. Lateral periodontal cyst.
site buccal). (1) Tracing of the lamina dura and normal
a. Principlethe object closest to the buccal surface responses to pulp vitality testing establish the
appears to move in the direction opposite the diagnosis.
c. Osteomyelitis. (2) Maxillamaxillary sinus, incisive foramen,

(1) A highly variable radiographic appearance greater (major) palatine foramen, nasal cavity.
with sclerotic and osteolytic processes occurs (3) Both jawsmarrow spaces, nutrient canal.
sometimes in the same patient. 5. Cone-beam computed tomography (CBCT)
d. Developmental cysts. although valuable in endodontic diagnosis and treat-
(1) An incisive canal cyst (nasopalatine duct cyst) ment, current intraoral radiographs have limitations
may exhibit radiographic features similar to because they display a two-dimensional view, which
apical periodontitis. Tooth vitality responses could lead to diagnostic inaccuracies. CBCT acquires
become particularly important in differential three-dimensional views, and its increased use should
diagnosis. improve diagnostic capabilities.
e. Traumatic bone cyst.
(1) Cyst usually reveals a smoothly outlined radio- 1.5 Cracked Tooth Syndrome
lucent area of variable size sometimes with a A. Clinical features.
sclerotic border. 1. Sustained pain during biting pressures.
(2) Pulp vitality testing is within normal limits in 2. Pain only on release of biting pressures.
most cases. 3. Occasional, momentary, sharp, poorly localized
f. Ameloblastoma. pain during mastication that is very difficult to
(1) Occurs primarily in the fourth and fifth decade. reproduce.
(2) Aggressive lesions occur as multilocular 4. Sensitivity to thermal changes.
radiolucencies. 5. Sensitivity to mild stimuli, such as sweet or acidic
(3) Frequently causes extensive resorption of roots foods.
in the area. B. Radiographic evidencea mesiodistal crack is impos-
g. Cemental dysplasia. sible to demonstrate on radiographs because the line of
(1) Lesion varies in radiographic expression from fracture is not in the plane of the radiograph.
radiolucent initially to more radiopaque later. C. Incidenceprimarily mandibular molars, with a slight
(2) It is more commonly associated with vital man- preference for the first over the second molar.
dibular anterior teeth. D. Diagnosis.
h. Cementoblastoma. 1. Transillumination.
(1) Radiographically appears as a well- 2. Use of a tooth slooth or a cotton-tipped applicator.
circumscribed dense radiopaque mass often Noting which cusps occlude when the pain occurs
surrounded by a thin, uniform radiolucent aids in the location of the fracture site.
outline. 3. Stain.
(2) Severe hypercementosis or chronic focal scle- E. Treatment.
rosing osteomyelitis (condensing osteitis) has 1. Healthy pulp or reversible pulpitis.
similar radiographic appearance. a. Splint with an orthodontic band and observe
i. Central giant cell granuloma. or prepare for crown (place sound temporary
(1) Lesion produces a radiolucent area with either crown and observe before placing permanent
a relatively smooth or a ragged border showing crown).
faint trabeculae. 2. Irreversible pulpitis (symptomatic and asymptom-
(2) Associated teeth are usually vital. atic) or necrosis with acute apical periodontitis
j. Systemic disease. (symptomatic and asymptomatic).
(1) Giant cell lesion of primary hyperparathyroid a. Endodontic treatment.
ism gives rise to a generally radiolucent appear- (1) Minimizing the removal of tooth structure.
ance of bone and later may give rise to (2) Minimizing condensation force.
well-defined oval or round radiolucencies. b. Restoration.
k. Other nonanatomic radiolucency. (1) If sufficient tooth structure remains, place a
(1) Odontogenic lesionsdental papilla (apical), glass-ionomer or acid-etched, dentin-bonded
dentigerous cyst, odontogenic keratocyst, re- core without post and restore with permanent
sidual (apical) cyst, odontoma (early stage). crown. Core material can be placed 2 to 3mm
(2) Nonodontogenic lesionsfibro-osseous le- into the canal orifices.
sions, osteoblastoma, cementifying fibroma, (2) If insufficient tooth structure remains, con-
ossifying fibroma, malignant tumor, multiple sider a passively placed post along with an
myeloma. acid-etched, dentin-bonded core and perma-
l. Anatomic radiolucencies. nent crown with margins of 2mm or more of
(1) Mandiblemental foramen, mandibular canal, sound tooth structure. Crown lengthening or
submandibular fossa, mental fossa. extrusion or both may be necessary.
F. Prognosis.
1. Presence and extent of an isolated probingguarded 1.7 Endodontic-Periodontal Relationships
prognosis. A. Communication of the pulp and periodontium.
2. Extension of the crack to the floor of the pulp 1. By way of the following.
chamberguarded prognosis. a. Dentinal tubules.
3. Fracture traceable all the way from mesial to distal b. Lateral or accessory canals.
poor prognosis. c. Furcation canals.
d. Apical foramen.
1.6 Vertical Root Fracture 2. Endodontic pathosis can cause periodontal disease,
A. Clinical findings. but periodontal disease usually does not cause endo
1. Vertical root fracture starts apically and progresses dontic problems (unless periodontal disease involves
coronally. the apex of the tooth).
2. It is usually in the buccal-lingual plane of the root. 3. Periodontal treatment can affect pulpal health
3. There is an isolated probing defect at the site of the because periodontal treatment (i.e., root planing) can
fracture in most cases. result in bacterial penetration into exposed dentinal
4. Important diagnostic signs include a radiolucency tubules, which can cause thermal sensitivity and sub-
from the apical region to the middle of the root (J sequent pulpitis.
shape or teardrop shape) (Figure 1-3). B. Types of endodontic or periodontal lesions.
5. May mimic other entities such as periodontal disease 1. Primary endodontic lesions.
or failed root canal treatment. a. Clinical presentation.
B. Etiologiespredisposing factors are a weakening of the (1) Inflammatory processes may or may not be
root structure by the following. localized at the apexmay appear along the
1. Extensive enlargement of the canal. lateral aspects of the root or in the furcation or
2. Mechanical stress from obturation. may have a sinus tract along the PDL space
3. Unfavorable placement of posts. appearing like a narrow deep pocket.
C. Diagnosisa vertical root fracture is confirmed by (2) Tooth tests nonvital.
visualizing the fracture with an exploratory surgical b. Treatmentendodontic therapy only because the
flap. primary lesion is of endodontic origin that has
D. Treatmentgoal of treatment is to eliminate the frac- merely manifested through the PDL.
ture space. 2. Primary periodontal lesions.
1. Single-rooted teethextraction. a. Clinical presentation.
2. Multirooted teeth. (1) Periodontal disease is progressiveit starts in
a. Hemisection or root resection with removal of the sulcus and migrates to the apex as deposits
only the affected root. of plaque and calculus produce inflammation
b. Extraction. that cause loss of surrounding alveolar bone
E. Prognosishopeless prognosis. and soft tissues.
A B
Figure 1-3 A, J-shaped radiolucency possibly indicating root fracture. B, Exploratory surgery confirms the presence of a vertical root
fracture. (From Cohen S, Hargreaves KM: Pathways of the Pulp, ed 10. St Louis, Mosby, 2011.)
(2) Manifestation of a periodontal abscess during (2) Improved obturation.

acute phase of inflammation. (3) Decreased procedural errors, such as ledges or
(3) Broad-based pocket formation. perforations.
(4) Teeth are vital. (4) Requires adequate tooth structure removal.
b. Treatmentperiodontal therapy. b. Conservation of tooth structure.
3. Primary periodontal lesions with secondary endo (1) Minimal weakening of the tooth.
dontic involvement. (2) Prevention of accidents.
a. Clinical presentation. c. Unroofing of the chamber to expose orifices and
(1) Deep pocketing with history of extensive peri- pulp horns.
odontal disease. (1) Maximum visibility.
(2) Possibly past treatment history. (2) Prerequisite in locating orifices of canals.
b. Treatmentendodontic therapy followed by peri- (3) Improved straight-line access.
odontal treatment. (4) Exposure of pulp horns.
4. True combined lesions. C. Instruments for cleaning and shaping.
a. Clinical presentationwhen endodontic and peri- 1. Gates-Gliddonlong thin shaft with parallel walls
odontal lesions coalesce, they may be clinically and short cutting head, side cutting with safety
indistinguishable. tips.
b. Treatment. a. Used to preenlarge coronal canal areas; cut dentin
(1) Both the endodontic and the periodontal as they are withdrawn from canal.
problem require treatment. 2. K-filestwisted square or triangular metal blanks
(2) Prognosis depends on how much of the peri- along their long axis; partly horizontal cutting blades.
odontal component actually caused the a. Can be used with the watch winding or balanced
destruction. forces technique.
3. Hedstrom filesspiraling flutes cut into the shaft of
round, tapered, stainless steel wire; very positive rake
2.0 Basic Endodontic Treatment angle.
Procedures a. Cut in one direction onlyretraction.
4. Barbed broachessharp, coronally angulated barbs
Outline of Review in metal wire blanks.
2.1 Nonsurgical Endodontics a. Used to remove vital pulp from root canals, sever
2.2 Surgical Endodontics pulp at constriction level, and remove materials
2.3 Endodontic Emergencies from canals.
2.4 Sterilization and Asepsis 5. Nickel-titanium rotary instrumentsdesigns vary
2.5 Radiographic Techniques in tip sizing, taper, cross section, helix angle, and
2.6 Microbiology of Endodontics pitch.
a. Important propertiessuperelasticity and high
2.1 Nonsurgical Endodontics resistance to cyclic fatigue, which allow continu-
A. Objectives. ously rotating instruments to be used in curved
1. To alleviate and prevent future adverse clinical root canals.
symptoms. b. Nickel-titanium instruments have reduced inci-
2. To dbride and shape the root canal. dence of blocks, ledges, transportation, and perfo-
3. To create the radiographic appearance of a well- ration but are believed to fracture more easily than
obturated root canal system where the root canal hand instruments.
filling extends as closely as possible to the apical c. ExamplesEndoSequence, Lightspeed, ProFile,
constriction. ProTaper, EndoSequence.
4. To maintain health or promote healing and repair of D. Working length determination.
apical tissues. 1. Reference point selection.
B. Access preparation. a. Select a point that is stable and easily visualized.
1. Most important phase of the technical aspects of root 2. Techniques for determining working length.
canal treatment. a. Estimate working length with a diagnostic film
2. Proper access preparation maximizes cleaning, taken using a paralleling technique with a No. 10
shaping, and obturation. or 15K-file.
3. Objectives. b. If necessary, correct the working length by measur-
a. Straight-line access. ing the discrepancy between the radiographic apex
(1) Improved instrument control, with less zipping, and tip of file. Adjust to 1mm short of the radio-
transportation, or ledging. graphic apex.
c. Use an apex locatoran electronic instrument (2) Treatment.

used to assist in determining the root canal working (a) Long-lasting local anesthetic.
length or perforation; operates on the principles of (b) Encourage drainage.
resistance, frequency, or impedance. (c) Steroids.
d. Feel for the apical constriction; however, in many (d) Cold compresses.
instances, this may be unreliable. (e) Antibiotics.
E. Cleaning and shaping. (f) Analgesics.
1. Best indicator of clean walls is the level of smooth- (g) Daily follow-up.
ness obtained. 2. Ethylenediamine tetraacetic acid (EDTA).
2. In shaping, it is best to precurve inflexible files a. Principal ingredientaqueous solution of 17%
because essentially all canals are curved. EDTA.
3. Taper of canal permits dbridement of apical canal, b. Indications.
reduces overinstrumentation of the foramen, and (1) Removes inorganic material.
improves ability to obturate. (2) Removes smear layer.
4. Techniques. 3. Chlorhexidinesynthetic cationic hydrophobic and
a. Crown-downclinician passively inserts a large lipophilic molecule that interacts with phospholipids
instrument into the canal up to a depth that allows and lipopolysaccharides on the cell membrane of
easy progress. The next smaller instrument is used bacteria and enters the cell by changing osmotic
to progress deeper into the canal; the third instru- equilibrium and is effective at a concentration of 2%.
ment follows, and this continues until the apex is The combination of chlorhexidine and NaOCl forms
reached. Hand and rotary instruments may be an undesirable precipitate, para-chloroaniline, which
used in this technique. is believed to affect the seal of root canal filling.
b. Step-backworking lengths decrease in stepwise 4. Calcium hydroxide.
manner with increasing instrument size. a. Best intracanal medicament available.
c. Hybrid techniqueabove-listed basic techniques b. Its high pH causes an antibacterial effect (pH 12.5).
may be combined into a hybrid technique to c. It inactivates lipopolysaccharide.
achieve the best outcome. d. It has tissue-dissolving capacity.
F. Apical preparation. I. Obturation of the root canal.
1. Apical stops help confine instruments, materials, and 1. Obturation purposes.
chemicals to the canal space and create a barrier a. To eliminate all avenues of leakage from the oral
against which gutta-percha can be condensed. cavity or the apical tissues into the root canal
G. File dimensions. system.
1. D1file size at the tip of the file (e.g., 0.08mm for a b. To seal within the system any irritants that cannot
size 8 file; 0.15mm for a size 15 file). be fully removed during canal cleaning and shaping
2. The diameter of the file where the cutting flutes end procedures.
(16mm) is known as D2 or D16. 2. Gutta-percha.
a. It is the diameter at the tip plus 0.32mm (e.g., for a. Advantages.
0.02 taper No. 8 file, it is 0.08mm + [16mm (1) Plasticityadapts with compaction to
0.02] = 0.40mm). irregularities.
H. Irrigation and medicaments. (2) Easy to manage.
1. Sodium hypochlorite (NaOCl). (3) Little toxicity.
a. Indications. (4) Easy to remove.
(1) Disinfection of root canalshypochlorite an- (5) Self-sterilizing (does not support bacterial
ion (ClO). growth).
(2) Dissolving organic matterproteolytic mate- b. Disadvantages.
rial. (1) Gutta-percha without sealer does not seal.
(3) Does not remove smear layer. (2) Lack of adhesion to dentin.
(4) Concentrations vary from 0.5% to 6%. (3) Elasticity causes rebound to dentin.
b. NaOCl accident. (4) Shrinkage after cooling.
(1) Signs and symptoms.
(a) Instant extreme pain. 2.2 Surgical Endodontics
(b) Excessive bleeding from the tooth. A. Incision and drainage and trephination.
(c) Rapid swelling. 1. Objectives are to evacuate exudates and purulence
(d) Rapid spread of erythema. and toxic irritants. Removal speeds healing and
(e) Laterbruising and sensory and motor reduces discomfort from irritants and pressure. The
nerve deficits. best treatment for swelling from acute apical abscess
is to establish drainage and to clean and shape the 3. Procedure.

canal. a. Root end resection is the preparation of a flat
2. Indications for incision and drainage of soft tissues. surface by the excision of the apical portion of the
a. If a pathway is needed in soft tissue with localized root and any subsequent removal of attached soft
fluctuant swelling that can provide necessary tissues.
drainage. b. Flap design.
b. When pain is caused by accumulation of exudates (1) Submarginal curved flap (semilunar flap).
in tissues. (a) Disadvantages.
c. When necessary to obtain samples for bacterio- (i) Restricted access with limited visibility.
logic analysis. (ii) Leaving the incision directly over the
3. Indications for trephination of hard tissues. lesion.
a. If a pathway is needed from hard tissue to obtain (iii) Often healing with scarring.
necessary drainage. (2) Submarginal triangular and rectangular flaps.
b. When pain is caused by accumulation of exudate (3) Full mucoperiosteal flap.
within the alveolar bone. c. A mucoperiosteal flap is elevated, and, when nec-
c. To obtain samples for bacteriologic analysis. essary, bone is removed to allow direct visualiza-
4. Procedure. tion of and access to the affected area.
a. Incision and drainage is a surgical opening created d. Root end resection.
in soft tissue for the purpose of releasing exudates (1) Resect 3mm of diseased root tip.
or decompressing an area of swelling. (2) The traditional 45-degree bevel has been
b. Trephination refers to surgical perforation of the replaced with lesser bevel (0 to 10 degrees).
alveolar cortical bone to release accumulated tissue (3) Leave 3mm for root end cavity preparation
exudates. and root end filling.
c. Profound anesthesia is difficult to achieve in the (4) Prepare 3mm of the root end with ultrasonic
presence of infection because of the acidic pH of instrumentation.
the abscess and hyperalgesia. (5) Increasing the depth of root end filling signifi-
d. The incision should be made firmly through peri- cantly decreases apical leakage.
osteum to bone. Vertical incisions are parallel with (6) Increasing the bevel increases leakage.
major blood vessels and nerves and leave very little e. Root end filling (retrofilling).
scarring. (1) A biologically acceptable filling material, such
e. These procedures may include the placement and as mineral trioxide aggregate (MTA), is placed
subsequent timely removal of a drain. into the 3-mm root end preparation to seal the
f. Antibiotics may be indicated in patients root canal system.
with diffuse swelling (cellulitis), patients with f. Primary closure of the surgical site is desired.
systemic symptoms, or patients who are C. Hemisection.
immunocompromised. 1. Surgical division (in approximately equal halves) of a
B. Root end resection (apical surgery or apicoectomy). multirooted tooth (e.g., mandibular molars). A verti-
1. Indications. cal cut is made through the crown into the furcation.
a. Persistent or enlarging apical pathosis after non- The defective half of the tooth is extracted.
surgical endodontic treatment. 2. Indications.
b. Nonsurgical endodontics is not feasible. a. Class III or IV periodontal furcation defect.
(1) Marked overextension of obturating materials b. Infrabony defect of one root of a multirooted tooth
interfering with healing. that cannot be successfully treated periodontally.
(2) Biopsy is necessary. c. Coronal fracture extending into the furcation.
(3) Access for root-end preparation and root-end d. Vertical root fracture confined to the root to be
filling is necessary. separated and removed.
(4) The apical portion of the root canal system with e. Carious, resorptive root or perforation defects that
apical pathosis cannot be cleaned, shaped, and are inoperable or cannot be corrected without root
obturated. removal.
2. Contraindications. f. Persistent apical pathosis in which nonsurgical
a. Anatomic factorssuch as a thick external treatment or apical surgery is impossible and the
oblique ridge or proximity of the neurovascular problem is confined to one root.
bundle. 3. Procedure.
b. Medical or systemic complications. a. Often performed in mandibular molars.
c. Nonrestorability. b. Hemisection requires root canal treatment on all
d. Poor root/crown ratio. retained root segments.
c. When possible, it is preferable to complete the root 1. Indicated when a root fracture occurs in the apical
canal treatment and place a permanent restoration portion and pulpal necrosis results.
into the canal orifices before the hemisection. 2. The fractured segment may be removed surgically
D. Bicuspidization. after or in conjunction with nonsurgical root canal
1. A surgical division (as in hemisection, usually a man- treatment.
dibular molar), but the crown and root of both halves 3. Surgical removal of the apical segment of a fractured
are retained. root is indicated in the following clinical situations.
2. The procedure results in complete separation of the a. Root fracture in the apical portion of the root.
roots and creation of two separate crowns. b. Pulpal necrosis in the apical segment as indicated
E. Root resection (root amputation). by an apical lesion or clinical signs or symptoms.
1. Removal of one or more roots of a multirooted tooth. c. Coronal tooth segment is restorable and
2. Indications for root resection. functional.
a. Class III or IV periodontal furcation defect. 4. Procedure.
b. Infrabony defect of one root of a multirooted tooth a. A mucoperiosteal flap is surgically elevated, and,
that cannot be successfully treated periodontally. when necessary, bone is removed to allow direct
c. Existing fixed prosthesis. visualization and access to the affected site.
d. Vertical root fracture confined to the root to be b. The apical portion of the affected root and all of
resected. the targeted tissue are removed.
e. Carious, resorptive root or perforation defects that
are inoperable or cannot be corrected without root 2.3 Endodontic Emergencies
removal. A. Definition.
f. Persistent apical pathosis in which nonsurgical 1. Endodontic emergencies are usually associated with
root canal treatment or apical surgery is pain or swelling or both and require immediate diag-
impossible. nosis and treatment.
g. At least one root is structurally sound. 2. Emergencies are usually caused by pathoses in the
3. Procedure. pulp or periapical tissues.
a. Amputation is the surgical removal of an entire 3. Emergencies include luxation, avulsion, or fractures
root leaving the crown of the tooth intact. of the hard tissues.
b. Root resection requires root canal treatment on all B. Categories.
retained root segments. 1. Pretreatment.
c. When possible, it is preferable to complete root a. Patient usually presents with pain or swelling
canal treatment and place a permanent restoration or both.
into the canal orifices. b. Challenge in this case is the diagnosis and treat-
F. Intentional reimplantation. ment of the offending tooth.
1. Indications. 2. Emergencies occurring between appointments or
a. Persistent apical pathosis after endodontic after obturation.
treatment. a. Also referred to as flare-up.
b. Nonsurgical retreatment is impossible or has an b. Easier to manage because the offending tooth has
unfavorable prognosis. been identified and diagnosed.
c. Apical surgery is impossible or involves a high 3. Diagnosis.
degree of risk to anatomic structures. a. A rule of a true emergency is that only one tooth
d. The tooth presents a reasonable opportunity for is the source of pain, so avoid overtreatment.
removal without fracture. b. Obtain a complete medical and dental history.
e. The tooth has an acceptable periodontal status c. Obtain a subjective examination relating to the
before the reimplantation procedure. history, location, severity, duration, character, and
2. Procedure. eliciting stimuli of the pain.
a. Intentional reimplantation is the insertion of a d. Obtain an objective examination including extra-
tooth into its alveolus after the tooth has been oral and intraoral examinations.
extracted for the purpose of accomplishing a root (1) Observe for swelling, discolored crowns, recur-
end filling procedure. rent caries, and fractures.
b. Stabilization of the reimplanted tooth may or may (2) Apical tests include palpation, mobility, percus-
not be needed. sion, and biting tests.
c. When possible, root canal therapy is performed (3) Pulp vitality tests are most useful to reproduce
before the reimplantation. reported pain.
G. Surgical removal of the apical segment of a fractured (4) Probing examination helps differentiate endo
root. dontic from periodontal disease.
(5) Radiographic examination is helpful but has c. No relationship exists between flare-ups and treat-
limitations because periapical radiolucencies ment procedures (i.e., single or multiple visits).
may not be present in acute periapical d. Treatment generally involves complete cleaning
periodontitis. and shaping of canals, placement of intracanal
4. Treatment. medicament, and prescription of analgesic.
a. Reducing the irritant, through reduction of pres- (1) Antibiotics are generally not indicated except
sure or removal of the inflamed pulp or apical in the instance of systemic symptoms and
tissue, is the immediate goal. cellulitis.
b. Pressure release is more effective than pulp or
tissue removal in producing pain relief. 2.4 Sterilization and Asepsis
c. Obtaining profound anesthesia of the inflamed A. Rationale for sterilization.
area is a challenge. 1. Endodontic instruments are contaminated with
d. Management of painful irreversible pulpitis. blood, soft and hard tissue remnants, bacteria, and
(1) Complete cleaning and shaping of the root bacterial by-products.
canals is the preferred treatment. 2. Instruments must be cleaned often and disinfected
(2) Pulpectomy provides the greatest pain relief, during the procedure and sterilized afterward.
but pulpotomy is usually effective in the absence 3. Because instruments may be contaminated when
of percussion sensitivity. new, they must be sterilized before initial use.
(3) Chemical medicaments sealed in chambers do B. Types of sterilization.
not help control or prevent additional pain. 1. Glutaraldehyde.
(4) Antibiotics are generally not indicated. a. Cold or heat labile instruments such as rubber dam
(5) Reducing occlusion has been shown to aid in frames may be immersed for a sufficient period of
the relief of symptoms if symptomatic apical time in solutions such as glutaraldehyde.
periodontitis exists. b. Generally 24 hours are required to achieve cold
e. Management of pulpal necrosis with apical sterilization.
pathosis. c. Immersion may be effective for disinfection, but it
(1) Treatment is twofold. fails to kill all organisms.
(a) Remove or reduce pulpal irritants. d. Because this method is not presently verifiable
(b) Relieve apical fluid pressure when with biologic indicators, it is least desirable in the
possible. office and should be reserved for instruments that
(2) When no swelling exists, complete canal d- cannot withstand heat.
bridement is the treatment of choice. 2. Pressure sterilization.
(3) When localized swelling exists, the abscess has a. Instruments should be wrapped and autoclaved for
invaded soft tissues. 20 minutes at 121C and 15psi.
(a) Complete dbridement. b. All bacteria, spores, and viruses are killed.
(b) Drainage to relieve pressure and purulence c. Either steam or chemicals can be used.
drainage can occur through the tooth or (1) Pressure sterilizers using chemicals rather than
mucosa (via incision and drainage). water have the advantage of causing less rusting.
(c) Patients with localized swelling seldom d. Both steam and chemical autoclaving dull the
have elevated temperatures or systemic edges of all cutting instruments owing to expan-
signs, so systemic antibiotics are sion with heat and contraction with cooling, result-
unnecessary. ing in permanent edge deformation.
(4) When diffuse swelling exists, the swelling has 3. Dry heat sterilization.
dissected into fascial spaces. a. Dry heat is superior for sterilizing sharp-edged
(a) Most important is the removal of the irri- instruments such as scissors for best preservation
tant via canal dbridement or extraction of of cutting edges.
the offending tooth. b. The cycle time for dry heat sterilization is tempera-
(b) Swelling may be incised and drained fol- ture dependent.
lowed by drain insertion for 1 to 2 days. (1) After the temperature reaches 160C, the
(c) Systemic antibiotics are indicated for instruments should be left undisturbed for
diffuse, rapid swelling. 60 minutes.
5. Flare-ups. (2) If the temperature decreases to less than 161C,
a. This is a true emergency and is so severe that an the full 60-minute heat cycle must be repeated.
unscheduled visit and treatment is required. c. The disadvantage to this method is the substan-
b. A history of preoperative pain or swelling is the tial time required both for sterilization and for
best predictor of flare-up emergencies. cooling.
C. Disinfection. of the tube head or cone when compared with

1. Surface disinfection during canal dbridement is a second radiograph. Objects closest to the
accomplished by using a sponge soaked in 70% iso- lingual surface appear to move in the same
propyl alcohol or proprietary quaternary ammonium direction of the cone. The fulfillment of this
solutions. principle requires two radiographs: the original
2. Files can be thrust briskly in and out of this sponge image and the second shifted image.
to dislodge debris and contact the disinfectant. (2) Depending on the direction of curvature rela-
3. This procedure cleans but does not disinfect tive to the cone, it can be determined if the
instruments. curvature is facial or lingual.
e. Determination of faciolingual location.
2.5 Radiographic Techniques f. Identification of undiscovered canals.
A. Diagnostic radiographs. (1) An anatomic axiom is that if a root contains
1. Angulation. only a single canal, that canal will be positioned
a. Paralleling techniquethe most accurate radio- close to the center of the root.
graphs are made using a paralleling technique. g. Radiographs must be taken at either a mesial or a
(1) With paralleling, there is less distortion, more distal angulation to see if another canal is present.
clarity, and reproducibility of the film and cone h. If the instrument is skewed considerably off center,
placement with preliminary and subsequent another canal must be present.
radiographs. i. Location of calcified canals.
b. If a paralleling technique cannot be used because (1) A root always contains a canal, however tiny or
of low palatal vault, maxillary tori, or long roots, impossible to negotiate.
the next best choice is the modified paralleling (2) Canals are frequently not visible on
technique. The film is not parallel to the tooth, but radiographs.
the central beam is oriented at right angles to the j. While searching for an elusive canal, two working
film surface. radiographs must be made: one from a straight
c. The least accurate technique is the bisecting angle. view and the other from a mesial or distal view. The
B. Working films. direction of the bur is adjusted accordingly.
1. Working length image. 3. Disadvantages of cone-image shifting.
2. Master cone image. a. Decreased clarity.
3. Check image. (1) The clearest radiograph with the most defini-
a. Taken of the master cone with accessory cones, tion is the parallel projection.
before searing off the excess gutta-percha during b. Superimposition of structures.
cold lateral obturation. E. Endodontic radiographic anatomy (Fig. 1-4).
C. Exposure considerations. 1. Limitations.
1. Proper x-ray machine settings and careful film a. A considerable amount of bone must be resorbed
processing are important for maximal quality before a lesion becomes visible radiographically.
radiographs. b. Periapical lesions become more evident if cortical
a. The optimal setting for maximal contrast between bone is resorbed.
radiopaque and radiolucent structures is 70kV. 2. Differential diagnosis of endodontic pathosis.
D. Cone image shifting. a. Characteristics of radiolucent lesions.
1. The cone image shift reveals the third dimension of (1) Apical lamina dura is absent.
the structures. (2) Most often, radiolucency is seen to be circular
2. Indications and advantages. about the apex, but lesions may have various
a. Separation and identification of superimposed appearances.
canals. (3) The radiolucency stays at the apex regardless of
(1) This is necessary in all teeth that may contain cone angulation.
two canals in a faciolingual plane. (4) A cause of pulpal necrosis is usually evident.
b. Movement and identification of superimposed b. Characteristics of radiopaque lesions.
structures. (1) These lesions are better known as focal scleros-
(1) Occasionally, radiopaque structures may over- ing osteomyelitis (condensing osteitis).
lie a root, as in the case of the zygoma. (2) Such lesions have an opaque diffuse appearance.
c. Determination of working length. (3) Histologically, they represent an increase in
d. Determination of curvatures. trabecular bone.
(1) Buccal object rule (SLOB rule) appliesthe (4) The radiographic appearance is one of diffuse
object closest to the buccal surface appears to borders and a roughly concentric arrangement
move in the direction opposite the movement around the apex.
Pulp horn
Pulp chamber
Root canal orifice

Figure 1-4 Major anatomic components of the Root canal Furcation canal
root canal system. (From Cohen S, Hargreaves KM: system
Pathways of the Pulp, ed 10. St Louis, Mosby, 2011.) Lateral canal
Root canal
Accessory foramina
Apical foramen Apical delta
(5) Condensing osteitis and apical periodontitis b. When released from the cell wall, lipopolysaccha-
frequently manifest together. rides are known as endotoxins.
(6) The pulp is often vital and inflamed. (1) Endotoxin is capable of diffusing across
dentin.
2.6 Microbiology of Endodontics (2) A relationship has been established between
A. Portals of entry of bacteria into the pulp. the presence of endotoxins and apical
1. Caries. inflammation.
2. Permeable tubules. C. Antibiotics used in endodontics.
a. Cavity preparation. 1. Penicillin V or amoxicillin are the first choice.
b. Exposure of dentin. a. They are effective against the following.
c. Leaking restorations. (1) Most strict anaerobes (Prevotella, Porphyromo
d. Neither dentinal fluid nor odontoblastic processes nas, Peptostreptococcus, Fusobacterium, and
are present in necrotic pulps. Actinomyces).
3. Cracks or trauma. (2) Gram-positive facultative anaerobes (strepto-
4. Pulp exposure. cocci and enterococci) in polymicrobial end-
B. Nature and dynamics of root canal infection. odontic infections.
1. Polymicrobial. 2. Clindamycin is effective against many gram-negative
2. Positive correlation between the number of bacteria and gram-positive organisms, including strict and
in an infected root canal and the size of apical facultative anaerobes.
radiolucency. 3. Metronidazole is effective against strict anaerobes;
3. Difference between primary infection and unsuc- since it is ineffective against facultative anaerobes and
cessful root canal therapy. aerobes it must always be used in combination with
a. Primary endodontic infection. another antibiotic, such as amoxicillin.
(1) Strict anaerobes predominate.
(2) Gram-negative anaerobicblack pigmented
Bacteroides (e.g., Prevotella nigrescens, Por 3.0 Procedural Complications
phyromonas) most common in endodontic
infections. Outline of Review
(3) Gram-positive anaerobicActinomyces (root 3.1 Ledge Formation
caries). 3.2 Instrument Separation
b. Unsuccessful root canal therapy (retreatment 3.3 Perforation
needed because of persistent infection). 3.4 Vertical Root Fracture
(1) Enterococcus faecalis (rarely found in infected
but untreated root canal). 3.1 Ledge Formation
(2) High incidence of facultative anaerobes. A. Definition of a ledge.
4. Lipopolysaccharides. 1. Artificial irregularity created on the surface of the
a. Lipopolysaccharides are found on the surface of root canal wall that impedes the placement of instru-
gram-negative bacteria. ments to the apex.
2. Working length can no longer be ascertained. (1) If the true canal is located, use a reaming
3. Radiographic findings. motion and occasionally an up-and-down
a. Instrument or obturation material is short of movement to maintain the space and dbride
the apex. the canal.
b. Instrument or obturation material no longer c. Flaring the access may help improve access to the
follows the true curvature of the root canal. apical third of the canal.
B. Why ledges occur. 3. Despite all effort, correction of a ledge is difficult
1. Lack of straight line access. because instruments and obturating materials tend to
a. Can be caused by improper access preparation. be directed into the ledge.
b. Can compromise the negotiation of the apical third 4. If unable to bypass ledge, clean and shape at the
of a canal through improper coronal flaring. new working length.
2. Anatomy of canal. D. Prognosis of the ledge.
a. Length. 1. Successful treatment after ledge creation depends
(1) Longer canals have a greater potential for ledge on the extent of debris remaining in the region past
formation. the ledge.
(2) With longer canals, recapitulate to confirm a. The amount of debris depends on when the ledge
patency. formation occurred in the cleaning and shaping
b. Canal diameter. process.
(1) Smaller diameter canals have greater potential b. Short and cleaned apical ledges have better
for ledge formation. prognoses.
c. Degree of curvature. 2. Inform the patient of the prognosis, and instill the
(1) As degree of curvature of the root canal system importance of recall and the signs that would indi-
increases, the potential for ledge formation cate failure.
directly increases.
(2) Given buccal radiographic exposure, the degree 3.2 Instrument Separation
of the buccolingual curvature of the root canal A. Definition.
system may not be appreciated. 1. A separated instrument is the breakage of an instru-
3. Inadequate irrigation or lubrication. ment within the confines of a canal.
a. NaOCl is a good irrigant for disinfection and B. How instruments separate.
removal of debris, but an additional lubricant is 1. Separation occurs because of limited flexibility and
necessary. strength of the instrument.
b. Lubricants allow for ease of file insertion, decrease 2. Improper use.
of stress on instruments, and ease of debris removal. a. May be overuse.
4. Excessive enlargement of curved canal with files. b. May be excessive force.
a. Instruments used to negotiate the root canal sys- 3. Manufacturing defects of instruments causing break-
tem have the tendency to cut straight ahead and age are rare.
straighten out. C. How to avoid separating instruments.
(1) The files cut dentin toward the outside of the 1. Recognize the stress limitations of the instruments
curvature at the apical portion of the root, a being used.
process called transportation. 2. Continual lubrication of the instrument within the
b. The transported tip of the file may gouge into the canal.
dentin and create a ledge or perforation outside the a. Use irrigants.
original curvature of the canal. b. Use lubricants.
c. Each successive file size should be used before a 3. Examine the instruments to be placed into the canal.
greater sized file is attempted (i.e., do not jump a a. Before separation, steel instruments often exhibit
file size). fluting distortions, highlighting unwound or
d. Flexible files reduce ledge formation. twisted regions of the file (signs of file fatigue).
5. Obstruction or the packing of debris in the apical b. Nickel-titanium files do not show the same visual
portion of the canal. signs of fatigue. These should be discarded before
C. Correction of ledge formation. visual signs occur.
1. The canal first must be relocated and renegotiated. 4. Replace files often.
2. One technique is to use a precurved (1 to 2mm 5. Do not proceed to larger files until the smaller ones
apically) small file to reestablish correct working fit loosely within the canal.
length. D. Treating canals with separated instruments.
a. Use plenty of lubrication. 1. Bypass the instrument.
b. Use a picking motion. a. Use the same principles as bypassing a ledge.
2. Remove the instrumentthis approach is usually un- 4. Root perforations.

successful, and referral to endodontist is necessary. a. Apical perforation.
3. Prepare and obturate the canal to the point of instru- (1) Can be a result of canal transportation, result-
ment separation. ing in a perforated new canal.
a. Clean to the new working length, which corre- b. Midroot perforation.
sponds to the coronal-most aspect of the separated (1) Usually occurs after ledge formation, when
instrument. a file is misdirected and creates an artificial
E. Prognosis of separated instrument. canal.
1. Successful treatment depends on the extent of debris C. Recognition of a perforation.
remaining in the region below the separated 1. Hemorrhage.
instrument. a. Perforation into PDL or bone may cause immedi-
2. Prognosis improves if instrument separation occurred ate hemorrhage (bone, being relatively avascular,
during the later stages of cleaning and shaping, after may cause little hemorrhage).
much of the canal has been dbrided to working 2. Sudden pain.
length. a. Occurs usually during evaluation of the working
3. Prognosis is poor for teeth where smaller instru- length.
ments have been separated. Separating a No. 40 b. Usually the anesthetic used was adequate for access
file at the working length is better than a No. 15 but not working length determination.
file, presumably because dbridement to the work- c. Burning pain or bad taste with NaOCl use.
ing length would have been performed at least 3. Radiographic evidence.
partially. a. Files are malpositioned in reference to the
4. Must inform patient and document history of the canal.
separated instrument. b. Take multiple x-rays from different horizontal
5. Overall, as long as the instrument separation is angles to assess file.
managed properly, the prognosis is favorable. 4. Apex locator readingsreadings are far short of the
6. If the patient has residual symptoms, the tooth is best initial file entrys working length.
treated surgically (root end resection). 5. Deviation of a file from its previous course.
6. Unusually severe postoperative pain.
3.3 Perforation D. Prognosis of a perforation.
A. Definitioniatrogenic communication of the tooth 1. Perforation into the PDL results in a questionable
with the outside environment. prognosis, and the patient must be informed
B. Different kinds of perforations. of this.
1. Coronal perforation. 2. Location.
a. Causefailure to direct the bur toward the long a. If located at or above the alveolar bone, the prog-
axis of the tooth during access. nosis for repair is favorable.
b. During access preparation, visualize the long axis (1) Can be easily repaired with restorative materi-
of the tooth periodically. als (similar to a class V lesion).
(1) Magnificationuse of loupes or a microscope (2) May require flap surgery.
aids. b. If below the crestal bone or at the coronal third
(2) Transilluminationthe fiberoptic light illumi- of the root, the prognosis is poor.
nates the pulp chamber floor. The canal orifice (1) Attachment often recedes, usually to the
appears as a dark spot. extent of the defect.
(3) Radiographsuse radiographs from different (2) Permanent periodontal pocket forms.
angles to provide information about the size 3. Size of defect.
and extent of the pulp chamber. a. Smaller perforations (<1mm) are more amenable
c. In cases of rotated or tilted teeth, misoriented cast to repair.
cores, or calcified chambers, follow the long axis of b. Cause less tissue destruction when smaller.
the roots carefully. 4. Timing of perforation.
2. Furcal perforation. a. Perforations occurring later in treatment, after
a. Usually occurs during the search for canal complete or partial dbridement of the canal,
orifices. have a better prognosis.
b. Should be repaired immediately. 5. Timing of repair.
3. Strip perforations. a. The sooner the perforation is repaired, the better
a. Involves the furcation side of the coronal root the prognosis.
surface. b. Minimizes the damage to the periodontal tissues
b. Sequela of excessive flaring with instruments. by bacteria, files, and irrigants.
c. Immediate sealing of defect reduces periodontal

breakdown. 3.4 Vertical Root Fracture
6. Isolationif tooth was well isolated at the time of A. Vertical root fracture has a poor prognosis.
repair, the prognosis is more favorable. B. Definition of vertical root fracture (see Figure 1-3).
7. Accessibility of the repair. 1. Occurs along the long axis of the tooth.
8. Sealing ability of the restorative material. 2. Often associated with a severe periodontal pocket in
9. Patient oral hygiene. an otherwise periodontally sound dentition.
10. Capabilities of dentist performing the repair. 3. Can be associated with a sinus tract.
11. Treatment of perforations. 4. Can be associated with a lateral radiolucency extend-
a. Coronal perforationrefer case to an endodon- ing to the apical portion of the root fracture.
tist to locate the canals. 5. A fracture can be identified only with visualization,
b. Furcal perforation. and surgery is often necessary to confirm the
(1) Usually accessible and able to be repaired fracture.
nonsurgically. C. How vertical fractures occur.
(2) Usually good prognosis if repaired (sealed) 1. Can occur after the cementation of a post.
immediately. 2. Can be the sequela of excessive condensation forces
c. Strip perforation. during obturation of an underprepared or overpre-
(1) Rarely accessible. pared canal.
(2) Usual sequelae are inflammation followed by a. Prevent fracture via appropriate canal
periodontal pocket. preparation.
d. Root perforation. b. Prevent fracture via balanced pressure of conden-
(1) Prognosis depends on the size and shape of sation forces during obturation.
perforation. D. Treatment of vertical root fractures.
(2) An open apex is difficult to seal and allows for 1. Removal of the involved root in multirooted teeth or
extrusion of sealing materials. extraction.
(3) Surgical treatment may be necessary. 2. Results in extraction of single-rooted teeth.
12. Follow-up.
a. Perforations should be monitored.
(1) Assess symptoms. 4.0 Traumatic Injuries
(2) Evaluate radiographs.
(3) Periodontal probing to evaluate periodontal Outline of Review
status. 4.1 Examinations of Traumatic Injuries to Teeth
E. Treatmentthe ultimate goal is to clean, shape, and 4.2 Types of Injuries
obturate as much of canal as is accessible. Avoid using 4.3 Avulsion
high concentrations of NaOCl because it may inflame 4.4 Biologic Consequences of Traumatic Injuries to Teeth
the periodontal tissues. 4.5 Inflammatory Root Resorption versus Replacement Root
1. Surgical repair. Resorption
a. Try to position the apical portion of the defect
above the crestal bone.
(1) Orthodontic extrusion. 4.1 Examinations of Traumatic Injuries
(2) Flap surgery and crown lengtheningused to Teeth
when the esthetic result is not compromised or A. Apical injuries.
if adjacent teeth require periodontal therapy. 1. Injury may result in swelling and bleeding that
(3) Hemisection. involves the PDL.
(4) Root amputation. 2. Teeth are sensitive to percussion.
(5) Intentional reimplantationindicated when 3. Apical displacement with injury to vessels entering
the defect is inaccessible or when multiple the apical foramen may lead to pulp necrosis.
problems exist (as with perforation and sepa- B. Pulp vitality testing.
rated instrument). 1. Test vitality of all teeth in the area.
b. Prognosis is guarded because of increased techni- 2. Testing immediately after the injury frequently yields
cal difficulty of procedures. The remaining roots a false-negative response.
are often prone to caries, periodontal disease, and 3. These data serve as a baseline for future reference.
vertical root fracture. The test results may be unreliable for 6 to 12 months.
2. Nonsurgical internal repair with MTAstudies have 4. False-negative test results.
shown MTA is very biocompatible and promotes the a. All the current pulp testing methods detect only
deposition of cementumlike material. the responsiveness and not the vitality of the pulp.
The vitality of the pulp is determined by the integ- C. Root fracturelimited to fracture involving roots only
rity of its blood supply. In reality, sensitivity tests (cementum, dentin, and pulp). It could be horizontal,
for nerve function do not indicate the presence or which may show bleeding from the sulcus.
absence of blood circulation within the pulp. 1. Horizontal root fracture.
b. In traumatic injury, the neural response from the a. Biologic consequences.
pulpal sensory nerves may be disrupted, but the (1) When a root fractures horizontally, the coronal
vascular supply may be intact. segment is displaced, but generally the apical
5. These tests should be repeated at 3 weeks, 3 months, segment is not displaced.
6 months, and 12 months and yearly intervals there- (2) Pulp necrosis of the coronal segment (25%)
after. The purpose of the tests is to establish a trend may result from displacement.
as to the physiologic status of the pulps. (3) Because the apical pulp circulation is not dis-
rupted, pulpal necrosis in the apical segment
is rare.
4.2 Types of Injuries b. Diagnosis.
Fracture Injuries (1) Because root fractures are usually oblique
A. Uncomplicated fractures (without pulp involvement). (facial to palatal), one periapical radiograph
1. Infraction. may miss it.
a. Definitionincomplete crack of enamel without (2) Radiographic examination should include an
the loss of tooth structure. occlusal film and three periapical films (one at
2. Enamel fracture (Ellis class I). 0 degrees, then one each at + and 15 degrees
a. Definitioninvolves enamel only (enamel chip- from the vertical axis of the tooth).
ping and incomplete fractures or cracks). (3) Healing patternsAndreasen and Hjorting-
b. Treatmentgrinding and smoothing the rough Hansen described four types of healing. The
edges or restoring lost structure. first three types are considered successful. The
c. Prognosisgood. fourth is typical when the coronal segment
3. Crown fracture without pulp involvement (Ellis loses its vitality.
class II). (a) Healing with calcified tissue.
a. Definitionuncomplicated fracture involving (i) Ideal healing is calcific healing. A cal-
enamel and dentin only. cific callus is formed at the fracture site
b. Treatmentrestoration with a bonded resin on the root surface and inside the canal
technique. wall.
c. Prognosisgood unless accompanied by a luxa- (b) Healing with interproximal connective
tion injury. tissue.
B. Complicated fractures (Figure 1-5). (c) Healing with bone and connective tissue.
1. Crown fracture with pulp involvement (Ellis (d) Interproximal inflammatory tissue without
class III). healing.
a. Definitiona complicated fracture involving c. Treatment.
enamel, dentin, and exposure of the pulp. (1) With root fractures that have maintained the
b. Treatmentvital pulp therapy versus root canal vitality of the pulp, the main goal of treatment
therapy depends on the following factors. is to enhance the healing process. Prognosis
(1) Stage of development of the toothin an im- improves with quick treatment, close reduction
mature tooth, vital pulp therapy should always of the root segments, and splinting. Splint as
be attempted if feasible because of the tremen- soon as possible, depending on location of the
dous advantages of maintaining the vital pulp. fracture and mobility.
(2) Time between the accident and treatmentin (2) Coronal root fracture.
the 24 hours after a traumatic injury, the initial (a) Poor prognosisif the fracture occurs at
reaction of the pulp is proliferative with no the level of or coronal to the crest of the
more than 2mm pulp inflammation. After 24 alveolar bone, the prognosis is extremely
hours, chances of direct bacterial contamina- poor.
tion increase. (b) Stabilize coronal fragment with rigid splint
(3) Concomitant periodontal injurya periodon- for 6 to 12 weeks.
tal injury compromises the nutritional supply (c) If reattachment of the fractured fragments
of the pulp. is impossible, extraction of the coronal
(4) Restorative treatment planif a more complex segment is indicated. The apical segment
restoration is to be placed, root canal therapy may be carried out by orthodontic forced
is recommended. eruption or by periodontal surgery.
Figure 1-5 Complicated crown fracture. A, Complicated coronal fracture is deep into the dentin, and pulp is exposed. B, Clinical
view. C and D, Tooth is treated with complete pulpectomy and root canal filling. (From Gutmann JL, Lovdahl PE: Problem Solving in
Endodontics, ed 5. St Louis, Mosby, 2011.)
(3) Midroot fracture. c. Physiologic splint.

(a) Stabilize for 3 weeks. d. Endodontic treatment if necessary (or observe for
(b) Pulp necrosis occurs in 25% of root frac- revascularization for open apices).
tures. For the most part, the necrosis is 3. Pulp outcome.
limited to the coronal segment. The pulp a. Mature teeth with closed apices.
lumen is wide at the apical extent of the (1) Extrusive luxation65% rate of pulpal
coronal segment, so apexification may be necrosis.
indicated. (2) Lateral luxation80% rate of pulpal necrosis.
(c) In rare cases when both coronal and apical E. Intrusive luxation.
pulps are necrotic, endodontic treatment 1. Description and diagnosisapical displacement of
through the fracture is difficult. Necrotic the tooth.
apical segments can be removed surgically. 2. Treatment.
(4) Apical root fracturehorizontal fractures in a. Immature teeth with open apicesallow to reerupt.
the apical one third (portion of the root closest b. Mature teeth (close apices).
to the root tip) have the best prognosis. The (1) Orthodontic reposition.
pulp is mostly vital, and the tooth has little or (2) Surgical reposition.
no mobility. (3) Endodontic treatment.
d. Prognosis. 3. Pulp outcome96% rate of pulpal necrosis.
(1) Improves as fracture approaches apex.
(2) Horizontal is better than vertical. 4.3 Avulsion
(3) Nondisplaced is better than displaced. A. Avulsion (exarticulation)complete separation of a
(4) Oblique is better than transverse. tooth from its alveolus by traumatic injury (Ellis class
VI) (Figure 1-6).
Displacement Injuries
A. Luxationdislocation of a tooth from its alveolus
resulting from acute trauma (Ellis class V).
B. Concussion.
1. Description and diagnosisno displacement, normal
mobility, sensitive to percussion; generally responds
to pulp testing. Pulp blood supply is likely to recover.
2. Treatment.
a. Baseline vitality tests and radiographs.
b. Occlusal adjustment.
c. No immediate treatment is needed. Let the tooth
rest (avoid bite), then follow-up.
C. Subluxation.
1. Description and diagnosisThe tooth is loosened
but not displaced.
2. Treatment.
a. Baseline vitality tests and radiographs.
b. Occlusal adjustment.
c. Splint for 1 to 2 weeks if mobile. A
3. Pulpal outcome.
a. Pulpal necrosis rate of 6% with closed apices.
b. Pulpal outcome more favorable with open
apices.
D. Extrusive or lateral luxation.
1. Description and diagnosis.
a. Tooth is partially extruded from its socket.
b. Occasionally this is accompanied by alveolar
fracture.
c. Lateral extrusionusually the crown was dis-
B
placed palatally, and the root apex was displaced
labially. Figure 1-6 A and B, Two cases of tooth avulsion. Sometimes
2. Treatment. the damage to the surrounding tissues can be extensive. (From
a. Radiographs. Gutmann JL, Lovdahl PE: Problem Solving in Endodontics, ed 5.
b. Reposition teeth. St Louis, Mosby, 2011.)
B. Treatmentfirst priority is to protect the viability of c. Open apex with extraoral dry time less than 60
the PDL. minutes and tooth stored in a special storage
1. Reimplantation immediately if possible. medium, milk, or saliva.
a. Immediate reimplantation improve PDL healing (1) If contaminated, clean the root surface and
prevent root resorption. apical foramen with a stream of saline.
2. If on-site reimplantation not possible, extraalveolar (2) Place the tooth in doxycycline (1mg/20mL
dry time must be considered. saline).
a. Critical extraalveolar dry time, success rate. (3) Remove coagulum from socket with saline and
(1) Less than 15 minutes, 90%. examine alveolar socket.
(2) 30 minutes, 50%. (4) Reimplant tooth slowly with slight digital
(3) More than 60 minutes, less than 10%. pressure.
b. Storage media. (5) Stabilize with a semirigid (physiologic) splint
(1) Optimal storage environmentmaintain and for 7 to 10 days.
reconstitute metabolites. (6) Administer systemic antibiotic (penicillin 4
(a) Viaspan. per day for 7 days or doxycycline 2 per day for
(b) Hanks Balanced Salt Solution. 7 days at appropriate dose for patient age and
(2) Wetjust maintains viability. weight).
(a) Milk. (7) Refer to physician to evaluate need for tetanus
(b) Saline. booster.
(c) Saliva (hypotoniccell lysis). d. Open apex with extraoral dry time more than 60
(d) Waterleast desirable (hypotoniccell minutes.
lysis and inflammation). (1) Reimplantation usually is not indicated.
3. Management in the dental office. 4. Endodontic treatment7 to 10 days after
a. Closed apex with extraoral dry time less than 60 reimplantation.
minutes and tooth stored in a special storage a. Extraoral time less than 60 minutes.
medium, milk, or saliva. (1) Closed apex.
(1) Do not handle the root surface and do not (a) Endodontic treatment is initiated at 7 to 10
curette the socket. days.
(2) Remove coagulum from socket with saline and (b) If endodontic treatment is delayed or signs
examine alveolar socket. of resorption are present, long-term
(3) Reimplant tooth slowly with slight digital calcium hydroxide treatment is given before
pressure. root canal filling.
(4) Stabilize with a semirigid (physiologic) splint (2) Open apex.
for 7 to 10 days. (a) Endodontic treatment should be avoided,
(5) Administer systemic antibiotic (penicillin 4 and signs of revascularization should be
per day for 7 days or doxycycline 2 per day for checked.
7 days at appropriate dose for patient age and (b) At the first sign of an infected pulp, the
weight). apexification procedure is begun.
(6) Refer to physician to evaluate need for tetanus b. Extraoral time more than 60 minutes.
booster. (1) Close apex.
b. Closed apex with extraoral dry time more than (a) Same protocol as with dry time less than 60
60 minutes. minutes.
(1) Remove debris and necrotic PDL. (2) Open apex (if reimplanted).
(2) Remove coagulum from socket with saline and (a) If endodontic treatment was not performed
examine alveolar socket. out of the mouth, the apexification proce-
(3) Immerse tooth in a 2.4% sodium fluoride solu- dure is initiated.
tion with pH of 5.5 for 5 minutes.
(4) Reimplant tooth slowly with slight digital
pressure. 4.4 Biologic Consequences
(5) Stabilize with a semirigid (physiologic) splint of Traumatic Injuries
for 7 to 10 days. A. Attachment damage (Table 1-3)external resorption.
(6) Administer systemic antibiotic (penicillin 4 1. Surface resorption.
per day for 7 days or doxycycline 2 per day for a. Transient phenomenon that is extremely common,
7 days at appropriate dose for patient age and self-limiting, and reversible.
weight). b. As a result of mechanical damage to the cementum
(7) Refer to physician to evaluate need for tetanus surface, the root surface undergoes spontaneous
booster. destruction and repair.
Table 1-3
External Root Resorption
INFLAMMATORY ROOT RESORPTION REPLACEMENT ROOT RESORPTION
Radiographs Resorptive defect on root surface is separated from PDL separating bone and tooth surface is absent
bone by radiolucency
Cause Root canal bacteria and their by-products move Trauma to PDL
through the wide dentinal tubules to root surface
Pulp Necrosis No known relationship between pulp vitality and
replacement resorption
Progress Rapid, but can be arrested Can be delayed, but cannot be stopped
Treatment and Immediate root canal treatment is required. In the absence of adverse signs and symptoms, no
prognosis Removing infected pulp halts resorption pulpal treatment is indicated, but radiographic
follow-up is essential
PDL, Periodontal ligament.
c. Repair occurs within 14 days. This is not clinically c. Clinical evidence.

significant. (1) Crestal bony defect associated with the
2. Replacement resorption (ankylosis). lesion.
a. Cause. (2) Pink spot possible (owing to the granulation
(1) PDL damage (nonviable PDL). tissue in the cervical dentin undermining the
(2) Occurs in 61% of reimplanted teeth (Andrea- crown enamel).
son, 1995). (3) Pulp vitality testing is within normal limits.
b. Radiographic evidence. d. Location.
(1) Continuous replacement of lost root with bone, (1) At the attachment level of the tooth.
no radiolucency (loss of cementum, dentin, (2) Usually begins at cementoenamel junction.
and PDL with ingrowth and fusion of bone to e. Treatmentsurgical removal of granulation tissue
the root defect). and repair with restoration.
c. Clinical evidence. B. Apical neurovascular supply damage.
(1) Progressive submergence with growth (leading 1. Pulp canal obliterationcalcific metamorphosis.
to infraocclusion). a. 27% of complications after luxation.
(2) Irreversibledental treatment cannot stop b. Occurs with increased likelihood with immature
progression of ankylosis. teeth (open apices), intrusions, and severe crown
(3) Metallic sound on percussion. fractures.
3. Cervical resorption (extracanal invasive resorption, 2. Pulpal necrosis.
subepithelial external root resorption). a. Frequency of pulpal necrosis.
a. Causesulcular infection from the following. (1) Type of injuryconcussion (2%) < subluxation
(1) Physical injuries. (6%) < extrusion (65%) < lateral luxation (80%)
(a) Trauma. < intrusion (96%).
(b) Orthodontics. (2) Stages of root developmentincomplete (17%)
(c) Periodontal treatment. < complete (68%).
(2) Chemical injuriesnonvital bleaching. 3. Inflammatory resorption (Table 1-4; see Table 1-3).
(3) Idiopathic. a. Causepulp necrosis.
b. Radiographic evidence. (1) Bacteria and toxins enter into the dentinal
(1) Mesiodistalit mimics the appearance of cer- tubules.
vical caries adjacent to an infrabony defect. (2) pH is lowered, and inflammatory root resorp-
(2) Buccolingualit shows a radiolucency over the tion ensues.
well-defined outline of the canal. b. Radiographic evidence.
(3) Ragged, asymmetric, and irregular moth- (1) Bowl-shaped resorption involving cementum
eaten appearance. and dentin.
(4) Most misdiagnoses of resorptive defects are (2) Occurs 3 weeks after trauma.
made between internal root resorptions, cervi- c. Locationat apical one third of the root, some-
cal caries, and cervical resorption. times progresses to entire root.
Table 1-4
Internal Root Resorption versus External Root Resorption
INTERNAL ROOT RESORPTION EXTERNAL ROOT RESORPTION
Definition Destructive process initiated within root canal system Destructive process initiated in periodontium
Etiology Inflammation from: 1. IRR: necrotic pulp, bacteria and bacterial
1. Caries by-products initiate and follow ports of exit to
2. Attrition, abrasion, erosion affect periodontium
3. Cracked teeth 2. RR: trauma to periodontium
4. Trauma 3. CR: sulcular infection from:
5. Ca(OH)2 pulpotomy a. Physical injuries: trauma, orthodontic or
6. Crown preparation periodontal treatment
7. Idiopathic b. Chemical injuries: nonvital bleaching
c. Idiopathic
Location 1. Occurs at any location along the root canal 1. IRR: occurs at apical and lateral aspects of root
2. Rare in permanent teeth 2. RR: occurs at any location along root
3. CR: at attachment level of the tooth (usually
begins at cementoenamel junction)
Clinical 1. Generally asymptomatic (usually first recognized RR:
manifestations clinically through routine radiographs) 1. Characteristic high-pitched, metallic sound to
2. Pink spot possible (owing to granulation tissue in percussion
coronal dentin undermining crown enamel 2. Progressive submergence with growth
3. Most misdiagnoses of resorptive defects are made CR:
between internal root resorptions and subepithelial 1. Crestal bony defect associated with lesion
external resorption (CR) 2. Pink spot possible
Radiographic 1. Margins are sharp, smooth, and clearly defined IRR and CR:
appearance 2. Oval, walls of root canal appear to balloon out 1. Margins are less well defined, ragged, and
3. Usually symmetrical irregular
4. Uniform in density 2. Moth-eaten appearance
5. Unaltered canal or chamber cannot be followed 3. Usually asymmetrical
through the lesion: loss of canal anatomy (defect 4. Variations in density that may appear striated
appears as an expansion of pulp chamber or canal) 5. Unaltered canal configuration can be followed
6. Does not move with angled radiographs through the area of lesion (root canal outline can
be seen running through radiolucent defect)
6. Moves with angled radiographs
RR:
1. More radiopaque than radiolucent
2. Disappearance of PDL space followed by bone
replacement
Vitality testing 1. Usually a positive response (for internal resorption 1. IRR: negative (nonvital) response
to be active, at least part of the pulp must be vital) 2. RR: not related
2. Sometimes a negative response because: 3. CR: normal response
a. Coronal pulp is necrotic and active resorbing
cells are more apical in the canal
b. Pulp becomes nonvital after a period of active
resorption
Treatment Prompt endodontic therapy stops the process 1. IRR: nonsurgical endodontic treatment
2. RR: root canal therapy is of little value. No
reliable techniques or medicaments
3. CR: surgical removal of granulation tissue and
repair with restoration
CR, Cervical resorption; IRR, inflammatory root resorption; PDL, periodontal ligament; RR, replacement resorption.
2. MTA.
4.5 Inflammatory Root Resorption versus a. Portland cement derivative made of primarily fine
Replacement Root Resorption hydrophilic particles.
Inflammatory resorption and replacement resorption are b. Consists of calcium phosphate and calcium oxide.
most commonly associated with luxation injuries. c. Sets in presence of moisture.
d. Long setting time (approximately 2 hours, 45
minutes).
5.0 Adjunctive Endodontic Treatment e. Nonresorbable quality makes it a great sealing
agent.
Outline of Review f. MTA used as a filling material appears to be able
5.1 Dental-Pulp Complex to induce cementoblastic cells to produce hard
5.2 Vital Pulp Therapy tissue.
5.3 Bleaching Discolored Teeth B. Vital pulp therapyindirect pulp capping, direct
pulp capping, partial pulpotomy, pulpotomy, and
5.1 Dentin-Pulp Complex apexogenesis.
A. Pulp biology. 1. Indirect pulp cap.
1. Pulp consists of loose, fibrous connective tissue. a. Definition.
2. There is a lack of collateral circulation. (1) Procedure in which a material is placed on a
3. Pulp does not expand owing to rigidity of the dentin. thin partition of remaining carious dentin that,
4. Within the pulp are odontoblasts, fibroblasts, nerves, if removed, might expose the pulp in perma-
blood vessels, and lymphatics. nent immature teeth.
B. Reparative dentin. b. Indications.
1. After injury or irritation, primary odontoblasts (1) When teeth have deep carious lesions approxi-
may die. mating the pulp but no signs or symptoms of
2. Secondary odontoblasts can form and produce repar- pulpal degeneration or apical disease.
ative dentin as a defense. c. Clinical objective.
3. Odontoblasts form reparative dentin at the site of an (1) To arrest the carious process and allow
irritant. remineralization.
4. The pulp can defend itself against most nonmicrobial (2) Wait for 6 to 8 weeks to allow deposition of
irritants. reparative dentin (at the rate of 1.4m/day).
5. When the irritant is too great, deposition of repara- (3) Remove the remaining caries leaving healthy,
tive dentin may be insufficient, and pulp defenses dentin and permanently restore the tooth.
become overwhelmed. 2. Direct pulp cap.
6. When bacteria enter the pulp with sufficient quantity a. Definition.
or virulence, complete pulpal necrosis is imminent (1) Dental material placed directly on a mechani-
and irreversible. cal or traumatic vital pulp exposure.
C. Caries and microleakage. b. Indications.
1. Bacteria from dental caries are the main cause of (1) Pulp has been exposed less than 24 hours.
more serious pulpal injury and the main cause of (2) Healthy pulp exposures during an operative
pulpitis. procedure.
2. This can be initial caries or caries developing under (3) Asymptomatic.
defective restorations (recurrent decay). (4) Small exposure site.
3. Bacteria can penetrate beyond the more obvious c. During follow-up visits.
carious lesion through dentinal tubules. (1) Test for palpation, percussion, thermal pulp
testing, and periapical radiograph.
5.2 Vital Pulp Therapy (2) A hard tissue barrier may be visualized 6 weeks
A. Materials for vital pulp therapy dressingcan stimulate postoperatively.
dentinal bridge formation. d. Prognosissurvival of the pulp depends on the
1. Calcium hydroxide. following.
a. Used as a pulp capping material since the 1930s (1) Quality of the bacteria-tight seal provided by
and has a solid history of clinical documentation. the restoration.
b. Its inherent high pH of 12.5 cauterizes tissue and (2) Degree of bleeding.
causes superficial necrosis. (3) Disinfection of the superficial pulp and dentin
c. This material develops a sterile necrotic zone that or elimination of any inflamed zone of pulp.
encourages the pulp to induce hard tissue repair 3. Partial pulpotomy (also known as Cvek pulpotomy
with secondary odontoblasts. and shallow pulpotomy).
a. Definitionsurgical removal of a small portion (3) Nonsurgical endodontic therapy can be per-
of coronal pulp tissue to preserve the remaining formed more safely and effectively to treat the
coronal and radicular pulp tissues (described by pulpal disease.
Cvek in 1978). c. Indications.
b. Indications. (1) Immature tooth with incomplete root forma-
(1) Inflammation is greater than 2mm into the tion and with damaged coronal pulp and
pulp chamber but has not reached the root healthy radicular pulp.
orifices. d. Contraindications.
(2) Traumatic exposures longer than 24 hours or (1) Avulsed teeth.
mechanical exposures. (2) Unrestorable teeth.
(3) Immature permanent tooth or mature tooth (3) Teeth with severe horizontal fracture.
with simple restorative plan. (4) Necrotic teeth.
c. Follow-up. e. Prognosisgood when pulp capping or shallow
(1) Same as pulp capping. pulpotomy is done correctly; conventional pulp-
(2) Sensitivity test is unavailable because of loss of otomy is not as successful.
coronal pulp. f. Success rate depends on the following.
(3) Use radiograph to assess continuation of (1) Extent of pulpal damage.
root formation or development of periapical (2) Restorability of the tooth.
lesion. C. Pulpectomy.
d. Prognosisgood prognosis depends on the 1. Pulpectomy is not vital pulp therapy because the
following. tooth is pulpless.
(1) Adequate removal of inflamed pulp. 2. Definitionto remove coronal and radicular pulp
(2) Good disinfection of dentin and pulp. tissues.
(3) Ability to avoid blood clot formation after 3. Applications.
amputation. a. Temporary pain relief on teeth with irreversible
(4) Bacteria-tight seal of restoration. pulpitis until nonsurgical endodontic treatment
4. Pulpotomy. can be performed.
a. Definition. D. Apexification.
(1) Surgical removal of the coronal portion of a 1. Apexification is not vital pulp therapy because the
vital pulp to preserve the vitality of the remain- tooth is pulpless.
ing radicular pulp. 2. Definitionmethod to stimulate the formation of
(2) The level of pulp amputation is chosen arbi- calcified tissue at the open apex of pulpless teeth.
trarily but usually at the level of the root 3. Indicationinfected teeth with open apices in which
orifices. standard instrumentation techniques cannot create
b. Indications. an apical stop to facilitate effective obturation of the
(1) Vital pulp in immature teeth with carious, canal.
mechanical exposure or traumatic exposures 4. Techniquedisinfection of canal followed by induc-
after 72 hours. tion or placement of an acceptable apical barrier.
(2) No history of spontaneous pain. a. Calcium hydroxide and MTA have been used to
(3) No abscess, radiographic bone loss, or create an apical barrier.
mobility. (1) Calcium hydroxide may be used to induce
c. Potential problemsoperators cannot determine apical hard tissue formation. A thick paste of
whether all diseased tissue has been removed. calcium hydroxide must be placed in the canal
5. Apexogenesis. and replaced every 3 months until a hard tissue
a. Definitionmaintenance of pulp vitality to allow barrier forms, against which gutta-percha
continued development of the entire root. Apical may be placed to fill the canal. This traditional
closure occurs approximately 3 years after technique may require 1 year for hard tissue
eruption. formation.
b. Clinical objectives. (2) MTA can be packed into the apical 3mm of
(1) The key is to allow the body to make a stronger the canal, and the remainder of the canal
root. can be filled with gutta-percha at the same
(2) This procedure relates to teeth with retained appointment.
viable pulp tissue in which the pulp tissue is (3) MTA has established biologic outcomes in
protected, treated, or encouraged to permit the terms of healing and root-end closure at least
process of normal root lengthening, root wall comparable to teeth treated with calcium
thickening, and apical closure. hydroxide.
b. Advantages of MTA compared with calcium that increases with the duration of saliva
hydroxidetreatment can be completed in less exposure.
time, improved patient compliance, reduced cost 2. The temporary restoration does not provide complete
of clinical time. protection against occlusal forces. When an immedi-
ate restoration is impossible, a bonded temporary
5.3 Bleaching Discolored Teeth restoration at the canal orifice can be used.
A. Causes of discoloration. 3. Permanent restorations are best placed as soon as
1. Pulp necrosis (or remnants of pulp tissue)tissue possible after obturation to seal the internal aspect of
disintegration by-products are released and penetrate the tooth from contamination.
tubules. 4. When the root canal space has been grossly recon-
2. Intrapulpal hemorrhage. taminated, retreatment should be considered.
3. Calcific metamorphosisextensive formation of ter- B. Structural considerations.
tiary dentin gives tooth a yellow color. 1. Endodontically treated teeth do not become brittle.
4. Age. The moisture content of endodontically treated teeth
5. Fluorosisgives teeth a mottled white-to-gray is not reduced even after 10 years.
appearance. 2. Teeth are weakened by loss of tooth structure.
6. Systemic drugs. a. Loss of marginal ridges is a major contributor to
7. Defects in tooth formation. reduced cuspal strength.
8. Blood dyscrasias. b. The loss of structural integrity with access prepara-
9. Obturation materialsfrom zinc oxideeugenol, tion (rather than changes in dentin) leads to a
plastics, or metallic components of sealers. higher occurrence of fractures in endodontically
B. Intracoronal (nonvital or internal) bleaching treated teeth compared with vital teeth.
techniques. c. The most important part of the restored tooth is
1. Thermocatalytic technique. the tooth itself.
a. Place oxidizing agent (30% hydrogen peroxide d. No combination of restorative materials can sub-
[Superoxol]) in the chamber and apply heat. stitute for tooth structure.
b. Complicationsexternal cervical resorption 3. Ferrule.
because irritation diffuses through the dentinal a. When a crown is needed, the axial walls of the
tubules to cementum and PDL. Heat combined crown engage the axial walls of the prepared tooth,
with chemicals may cause necrosis of the cemen- forming the ferrule. The ferrule is a band that
tum and inflammation of the PDL. encircles the external dimension of the residual
2. Walking bleach. tooth, similar to the metal bands around a barrel.
a. Place mix of sodium perborate and water in the It is formed by the walls and margins of the crown.
chamber. Because Superoxol is not used, 2-mm b. A longer ferrule increases resistance to fracture.
protective cement barrier is unnecessary. (1) Fracture resistance (to cervical tensile strength)
b. Return in 2 to 6 weeks. increases significantly with an increasing
amount of sound tooth structure.
(2) A longer ferrule increases fracture resistance
6.0 Posttreatment Evaluation and resists lateral forces from posts and lever-
age from the crown in function.
Outline of Review (3) Crown preparations with 1-mm coronal exten-
6.1 Restoration of Endodontically Treated Teeth sion of dentin above the margin have double
6.2 Success and Failure the fracture resistance compared with when the
core terminates immediately above the margin.
c. The ferrule must encircle a vertical wall of sound
6.1 Restoration of Endodontically tooth structure above the margin and must not
Treated Teeth terminate on restorative core material.
A. Coronal leakage. d. Insufficient remaining tooth structure to construct
1. Major cause of endodontic failure. a ferrule should be evaluated for crown lengthen-
a. More endodontically treated teeth are lost because ing surgery or orthodontic extrusion to gain access
of restorative factors than because of failure of the to additional root surface.
root canal treatment itself. 4. Post preparation.
b. After root canal therapy, the internal chambers of a. The primary purpose of the post is to retain a core
the tooth may become reinfected if coronal leakage in a tooth with extensive loss of coronal structure.
occurs. Saliva contamination with bacteria and b. The need for a post is dictated by the amount of
endotoxins can cause endodontic failure, a risk remaining coronal tooth structure.
c. Posts do not reinforce the tooth but further weaken A. Percussion

it by additional removal of dentin and by creating B. Palpation
stress that predisposes to root fracture. C. Electrical pulp test
d. At least 5 to 7mm of remaining gutta-percha is D. Cold test
recommended. 2. Symptomatic irreversible pulpitis pain in which of
the following sites is most likely to radiate to the
6.2 Success and Failure ear?
A. Causes of endodontic failures. A. Maxillary premolar
1. Inadequate seal of the root canal system. B. Maxillary molar
a. Coronal seal is more important than apical seal C. Mandibular premolar
in long-term. D. Mandibular molar
b. Historically, obturation has been accorded the 3. Which of the following statements regarding external
role of the most critical step and the cause of most root resorption is not true?
treatment failures. However, the two events are A. It is a destructive process initiated in the
associated but not by cause and effect because periodontium.
poorly obturated canals are usually poorly B. There are three main types: inflammatory root
dbrided as well. resorption, replacement resorption, and cervical
2. Poor access cavity. resorption.
3. Inadequate dbridement. C. It can be located anywhere along the root canal.
4. Missed canals. D. The margins are sharp, smooth, and well defined.
5. Vertical fractures. 4. Which of the following statements most likely applies
6. Procedure errors (perforation, ledging, loss of to a cracked tooth?
length). A. The direction of the crack usually extends
7. Leaking temporary or permanent restoration. mesiodistally.
8. Periodontal involvement. B. The direction of the crack usually extends
9. Resorption. faciolingually.
10. Compromised host factors (systemic conditions). C. Radiographic examination is the best way to detect
11. Misdiagnosis. a cracked tooth.
B. Factors influencing success rate. D. Choices A and C only
1. Apical pathosis. E. Choices B and C only
a. The presence of an apical lesion before treatment 5. Which of the following statements regarding treatment
reduces the success rate of endodontic treatment of a tooth manifesting with a sinus tract is true?
by 10% to 20%. A. Treat with conventional (nonsurgical) endodontic
2. Bacterial status of the canal. therapy.
a. The presence of bacteria in the canal before obtura- B. Antibiotics are not needed.
tion results in a poorer prognosis. C. The sinus tract should heal in 2 to 4 weeks after
3. Quality of endodontic work. conventional root canal therapy.
4. Quality of coronal seal. D. If the sinus tract persists after root canal therapy,
C. Principles of successful endodontics (note: factors perform root end surgery with root end filling.
1 through 3 represent the traditional endodontic E. All of the above
triad). 6. The major objectives of access preparation include
1. Microbial disinfection. all of the following except one. Which one is the
2. Dbridementthe key to success. exception?
3. Obturation. A. Attainment of direct straight-line access to canal
4. Diagnosis. orifices
5. Treatment plan. B. Confirmation of clinical diagnosis
6. Knowledge of anatomy of morphology. C. Conservation of tooth structure
7. Restoration. D. Attainment of direct straight-line access to the
apical root
7. Which of the following is not a property of NaOCl?
Sample Questions A. Chelation
B. Tissue dissolution at higher concentrations
1. An 8-year-old girl presents to the office with an Ellis C. Microbicidal activity
class II fracture. In an effort to determine a pulpal D. Flotation of debris and lubrication
diagnosis, which of the following tests is the least 8. While performing nonsurgical endodontic therapy,
accurate? you detect a ledge. What should you do?
A. Use a smaller instrument and get by the ledge B. Teeth with cracks may have erratic pain on
B. Fill as far as you have reamed mastication.
C. Use a small round bur and remove the ledge C. Pain is associated with release of pressure rather
D. Continue working gently to remove the ledge than increased biting force.
9. Which perforation location has the best prognosis? D. Pain, especially in response to cold, is a telltale sign.
A. Coronal third of root E. Absence of pain rules out the presence of a crack.
B. Apical third of root 16. In a tooth with a primary periodontal lesion with
C. Chamber floor secondary endodontic involvement, proceed first
D. Middle third of root with ____.
10. A classic teardrop-shaped apical lesion on a radio- A. Periodontal treatment
graph can indicate a vertical root fracture. The prog- B. Nonsurgical endodontic treatment
nosis of a vertical root fracture is hopeless, and the C. Antibiotic treatment
tooth should be extracted. D. Incision and drainage
A. The first statement is true, and the second state- 17. A patient calls late Saturday night because of severe,
ment is false. throbbing pain in a mandibular premolar aggravated
B. The first statement is false, and the second state- by heat, biting, and touching. What procedure is
ment is true. recommended?
C. Both statements are true. A. Instruct the patient to apply ice intermittently, take
D. Both statements are false. aspirin, and call Monday for an appointment
11. A patient presents with a chief complaint of swelling B. See the patient at the office and initiate endodontic
in the mandibular left quadrant that started 2 days ago treatment
and developed quickly. The patient has a mild fever C. See the patient at the office, remove the carious
with malaise, and clinical examination revealed local- dentin, and place a sedative zinc oxideeugenol
ized fluctuant swelling in the buccal vestibule of teeth cement temporary restoration
#18 and #19. Tooth #19 is nonresponsive to thermal D. Prescribe an analgesic and refer the patient to an
testing and exhibits moderate pain to percussion. endodontist
Radiographic findings reveal a slight widened PDL E. Refer the patient to the hospital oral surgery
space. Based on these findings, the most likely apical department for extraction
diagnosis is ____. 18. In an emergency patient, symptomatic irreversible pul-
A. Acute apical abscess pitis and symptomatic apical periodontitis of tooth #12
B. Irreversible necrotic apical periodontitis is diagnosed. Which of the following is the best treat-
C. Asymptomatic irreversible pulpitis ment protocol for this patient?
D. Symptomatic apical periodontitis A. Anesthesia followed by incision and drainage
12. Prolonged, unprovoked night pain suggests which of B. Anesthesia followed by extraction
the following conditions of the pulp? C. Anesthesia followed by pulpectomy
A. Pulpal necrosis D. Prescribe antibiotic for 1 week and follow with
B. Mild hyperemia nonsurgical endodontic treatment
C. Reversible pulpitis 19. In which of the following conditions is elective root
D. Periodontal abscess canal therapy contraindicated?
13. The pathognomonic symptom of symptomatic apical A. AIDS
periodontitis is ____. B. Recent MI
A. Swelling C. Leukemia
B. Intermittent pain D. Radiotherapy
C. Tenderness to palpation E. Second trimester of pregnancy
D. Tenderness to percussion 20. What is the best timing for performing incision and
14. In differentiating between an endodontic abscess and drainage at an area of infection?
periodontal abscess, first test ____. A. When the swelling is hard and diffuse
A. Pulp vitality B. When the area is the most painful
B. Probing depths C. When the area is large
C. Percussion sensitivity D. When the swelling is localized and fluctuant
D. Degree of mobility 21. Endodontic infection usually is polymicrobial. What is
15. Which of the following statements is not consistent the predominate type of microorganism found in a
with cracked tooth syndrome? tooth that requires endodontic therapy?
A. Symptoms are often variable because of direction, A. Aerobic bacteria
location, and extent of the crack. B. Facultative bacteria
C. Obligate anaerobic bacteria C. Grinding a silver metal blank to a nontapered

D. Yeast microorganisms square or rhomboid cross section
22. The danger zone of mandibular molar for perfora- D. Both B and C
tions during canal instrumentation is ____. E. All of the above
A. The periphery at the level of the dentinocemental 28. Benefits of intracanal irrigation include all of the fol-
junction lowing except one. Which one is the exception?
B. Within 2mm of the apex A. Dissolves organic debris
C. The furcation area B. Disinfects complex anatomy that is not accessible
D. The periphery of the access at the level of the by instrumentation
cementoenamel junction C. Removes the smear layer
23. What is the treatment of choice for an 8-year-old D. Facilitates obturation
patient who has a 1-mm intrusion injury of tooth #8? 29. The bacterial flora of an infected previously treated
A. Extract the tooth endodontic tooth is best characterized as:
B. Perform pulpotomy immediately A. Gram negative strict anaerobes
C. Splint the tooth for 10 to 14 days immediately B. Gram positive facultative anaerobes
D. Allow the tooth to reerupt C. Gram negative facultative aerobes
24. On routine radiographic survey of a new patient, you D. Gram positive strict aerobes
notice a circle-shaped radiolucency midroot and over 30. Because of its mesial concavity the following tooth is
the pulpal outline of tooth #6. You take a second mesi- vulnerable to iatrogenic perforation:
ally angulated radiograph and confirm the radiolu- A. The mandibular first premolar
cency is part of the pulp canal outline. After a vital B. The mandibular second premolar
response to cold testing, your diagnosis and subse- C. The maxillary first premolar
quent treatment plan are ____. D. The maxillary second premolar
A. Internal resorption and completion of nonsurgical 31. Which of the following is not an accepted treatment
endodontic treatment protocol for a NaOCl accident?
B. Internal resorption and surgical repair of the defect A. Instructions to minimize swelling with the use of
C. External root resorption and forced orthodontic cold compresses within the first 24 hours
eruption to expose the defect B. Irrigation with hydrogen peroxide
D. External root resorption and extraction C. Analgesics for pain control
25. During a nonvital bleaching procedure, if a barrier D. Antibiotics for patients at increased risk of second-
material is not placed between the root canal filling ary infection
and bleaching material, the tooth can be subjected 32. Ethylenediaminetetraacitic acid or EDTA is best char-
to ____. acterized as a ____ with a primary mode of action best
A. External cervical resorption described as ____:
B. Demineralization of tooth structure A. Chelating agent; removing the inorganic portion of
C. Gingival inflammation the smear layer
D. Poor color improvement B. Emulsifying agent; removing the organic portion of
26. A healthy 32-year-old man presents with localized the smear layer
fluctuant swelling associated with a necrotic pulp and C. Chelating agent; removing the organic portion of
an apical diagnosis of acute apical abscess for tooth #5. the smear layer
The principal modality or modalities for treating a D. Emulsifying agent; removing the inorganic portion
localized fluctuant swelling include which of the of the smear layer
following? 33. Of the following clinical diagnostic tests which is
A. Administration of antibiotics the most accurate in determining the state of pulpal
B. Achievement of drainage health?
C. Removal of the source of infection A. Electric pulp test (EPT)
D. Both A and C B. Heat test
E. Both B and C C. Cold test
27. Which of the following statements most accurately D. Both b and c
describes the manufacturing process for a K-type hand 34. What constitutes the largest portion of gutta-percha
instrument? obturation material?
A. Grinding a stainless steel wire to a tapered square A. Gutta-percha
or rhomboid cross section B. Zinc oxide
B. Twisting a square or rhomboid (cross section) non- C. Waxes and resins
tapered silver metal blank D. Heavy metal salts
35. Which is the most likely to cause pulp necrosis? A. A nonvital pulp test.
A. Subluxation B. A history of recent restoration of the tooth in
B. Extrusion question.
C. Avulsion C. A radiolucent lesion which, in time, becomes
D. Concussion radiopaque.
36. Which of the following statement(s) is(are) true D. None of the choices is true.
regarding treatment of a tooth presenting with a sinus 38. Once the root canal is obturated, what usually happens
tract? to the organism that had previously entered perira-
A. Treat with conventional root canal therapy. dicular tissues from the canal?
B. Antibiotics are not needed. A. They persist and stimulate formulation of a
C. The sinus tract should heal in 2 to 4 weeks after granuloma.
conventional root canal therapy. B. They are eliminated by the natural defenses of the
D. If the tract persists post-root canal therapy, do body.
root-end surgery with root-end filling. C. They reenter and reinfect the sterile canal unless
E. All of the above choices are true. root-end surgery is performed.
37. Features of focal sclerosing osteomyelitis often D. They will have been eliminated by various medica-
include: ments that were used in the root canal.
SECTION 2
Operative Dentistry
ANDR V. RITTER*
OUTLINE process (caries management based on risk assessment)

(Figures 2-1 and 2-2).
1. Dental Caries
B. Definitiondental caries is a multifactorial, transmis-
2. Patient Assessment, Examination, Diagnosis, sible infectious oral disease caused primarily by the
and Treatment Planning complex interaction of cariogenic oral flora (biofilm)
3. Instrumentation for Operative Dentistry with fermentable dietary carbohydrates on the tooth
Procedures surface over time. However, dental caries onset and
4. Preparation of Teeth activity are much more complex than this three-way
interaction because not all people with teeth and biofilm
5. Restoration of Teeth
who consume carbohydrates have caries over time.
Several modifying risk and protective factors influence
the dental caries process (Figure 2-3).
Operative dentistry is the art and science of the diagnosis, C. The caries balanceat the tooth level, caries activity
treatment, and prognosis of defects of teeth that do not is characterized by localized demineralization and loss
require full coverage restorations for correction. Such treat- of tooth structure. Cariogenic bacteria in the biofilm
ment should result in the restoration of proper tooth form, metabolize refined carbohydrates for energy and
function, and esthetics, while maintaining the physiologic produce organic acid by-products. These organic acids,
integrity of the teeth in harmonious relationship with the if present in the biofilm ecosystem for extended periods
adjacent hard and soft tissues, all of which should enhance of time, can lower the pH in the biofilm to below a
the general health and welfare of the patient. critical level (5.5 for enamel, 6.2 for dentin). The low
pH drives calcium and phosphate from the tooth to
the biofilm in an attempt to reach equilibrium, resulting
1.0 Dental Caries in a net loss of minerals by the tooth, or demineraliza-
tion. When the pH in the biofilm is restored and the
Outline of Review concentration of soluble calcium and phosphate is
1.1. Introduction and Etiology supersaturated relative to that in the tooth, mineral can
1.2. Pathogenesis and Diagnosis be added back to partially demineralized enamel in a
1.3. Prevention process called remineralization. At the tooth surface
1.4. Treatment Overview and subsurface level, dental caries results from a
1.5. Summary dynamic process of attack (demineralization) and res-
titution (remineralization) of the tooth matter. These
events occur several times a day over the life of the
1.1 Introduction and Etiology tooth and are modulated by many factors, including
A. Objectiveto understand and manage dental caries number and type of microbial flora in the biofilm, diet,
not only at the tooth level but also at the total patient oral hygiene, genetics, dental anatomy, use of fluorides
level, diagnosing and treating the underlying caries and other chemotherapeutic agents, salivary flow and
buffering capacity, and inherent resistance of the tooth
*Adapted from Heymann HO, Swift EJ, Ritter AV: Sturdevants Art & Science structure and composition, all of which differ from
of Operative Dentistry, ed 6. St. Louis, Mosby, 2013. Original contents were person to person, tooth to tooth, and tooth surface to
created by authors of that edition. The author also acknowledges the contribu-
tions of Dr. Theodore Ted M. Roberson to the previous edition(s) of the tooth surface. The balance between demineralization
present chapter and the aforementioned textbook. and remineralization has been illustrated in terms of
35
36 Section 2 Operative Dentistry
1. S. mutans is believed to be the primary causative

a agent of initial caries.
dt a. S. mutans adheres to enamel. Its glucosyltransfer-
rd ase enzyme causes the formation of an extracellu-
b p lar polysaccharide, which allows it to stick to
rd dt
s smooth tooth surfaces. It converts sucrose into
c fructans and glucans, which extrude from the
A B C bacterium and stick to the tooth.
b. S. mutans produces and tolerates acid. It metabo-
Figure 2-1 A, Caries may originate at many distinct sites: pits lizes sucrose to an end product of lactic acid.
and fissures (a), smooth surface of crown (b), and root surface (c).
c. S. mutans thrives in a sucrose-rich environment
Proximal-surface lesion of crown is not illustrated here because it
is a special case of smooth-surface lesion. Histopathology and
secondary to converting sucrose for adherence and
progress of facial (or lingual) and proximal lesions are identical. acid production.
Dotted line indicates cut used to reveal cross sections illustrated d. S. mutans produces bacteriocins, which kill off
in B and C. B, In cross section, the three types of lesions show competing organisms.
different rates of progression and different morphology. Lesions F. Enamel cariesion transfer continuously occurs at the
illustrated here are intended to be representative of each type. No biofilm-enamel interface. The initial decalcification
particular association between the three lesions is implied. Pit- occurs at the subsurface. It may be 1 to 2 years before
and-fissure lesions have small sites of origin visible on the occlusal enough decalcification occurs to cause surface integrity
surface but have a wide base. The overall shape of a pit-and-fissure lossthat is, a cavity.
lesion is an inverted V. In contrast, a smooth-surface lesion is G. Dentinal cariesonce enamel cavitation has occurred,
V-shaped with a wide area of origin and apex of the V directed
the underlying dentin has already been affected by the
toward pulp (p). Root caries begins directly on dentin. Root-
surface lesions can progress rapidly because dentin is less resistant
progression of the destruction, and the Lactobacillus
to caries attack. C, Advanced caries lesions produce considerable organism becomes a primary agent for further destruc-
histologic change in enamel, dentin, and pulp. Bacterial invasion tion of the dentin.
of the lesion results in extensive demineralization and proteolysis H. Salivaif sugars are the key to success of cariogenic
of the dentin. Clinically, this necrotic dentin appears soft, wet, and bacteria (a major pathologic factor), saliva is a major
mushy. Deeper pulpally, dentin is demineralized, but it is not block barring those same bacteria (a major protective
invaded by bacteria, and it is structurally intact. This tissue factor).
appears to be dry and leathery in texture. Two types of pulp- I. Protective mechanisms of saliva.
dentin response are illustrated. Under pit-and-fissure lesions and 1. Bacterial clearance.
smooth-surface lesions, odontoblasts have died, leaving empty a. Glycoproteins (large carbohydrate-protein mole-
tubules called dead tracts (dt). New odontoblasts have been dif-
cules) in saliva cause some bacteria to agglutinate
ferentiated from pulp mesenchymal cells. These new odontoblasts
have produced reparative dentin (rd), which seals off dead tracts.
(clump together) and then be removed by swallow-
Another type of pulp-dentin reaction is sclerosis (s)occlusion ing the 1.5L of saliva formed each day.
of the tubules by peritubular dentin. This is illustrated under a 2. Buffering action.
root-caries lesion. (From Heymann HO, Swift EJ, Ritter AV: Stur- a. Saliva contains urea and other buffers that help to
devants Art and Science of Operative Dentistry, ed 6. St. Louis, dilute any plaque acids.
Mosby, 2013.) 3. Antimicrobial actions.
a. Various proteins, enzymes, and antibodies in saliva
pathologic factors (i.e., factors favoring demineraliza- discourage or even kill bacterial growth.
tion) and protective factors (i.e., factors favoring rem- b. Lysozymedestroys cell walls and causes mem-
ineralization). Individuals in whom the balance tilts brane permeability of bacteria.
predominantly toward protective factors (remineraliza- c. Lactoferrinactively binds iron, which is impor-
tion) are much less likely to develop dental caries than tant for bacterial enzyme production and function.
individuals in whom the balance is tilted toward the It may also destroy S. mutans.
pathologic factors (demineralization). Understanding d. Lactoperoxidaseinactivates some bacterial
the balance between demineralization and remineral- enzymes.
ization is key to caries management (Figure 2-4). e. Type A secretory immunoglobulinsantibodies
D. Specific plaque hypothesisnot all of the 300 species of secreted by saliva, which fight against S. mutans
bacteria in the oral cavity can cause caries. Bacteria that attacks.
generate plaque biofilm resulting in caries are consid- 4. Remineralization.
ered to be cariogenic organisms. All plaque biofilm is a. Calcium, phosphate, potassium, and varying con-
not cariogenic. centrations of fluoride ions in saliva are readily
E. Streptococcus mutansa nonmotile, gram-positive bac- available to assist with remineralization. Some
terium, S. mutans is a cariogenic bacterium. salivary proteins, such as statherin, cystatins,
Section 2 Operative Dentistry 37
A B C D
Figure 2-2 Longitudinal sections (see inset for A) showing initiation and progression of caries on interproximal sur-
faces. A, Initial demineralization (indicated by shading in the enamel) on the proximal surfaces is not detectable clinically or radio-
graphically. All proximal surfaces are demineralized to some degree, but most are remineralized and become immune to further attack.
The presence of small amounts of fluoride in the saliva virtually ensures that remineralization and immunity to further attack will occur.
B, When proximal caries first becomes detectable radiographically, the enamel surface is likely still to be intact. An intact surface is
essential for successful remineralization and arrest of the lesion. Demineralization of the dentin (indicated by shading in the dentin)
occurs before cavitation of the surface of the enamel. Treatment designed to promote remineralization can be effective up to this stage.
C, Cavitation of the enamel surface is a critical event in the caries process in proximal surfaces. Cavitation is an irreversible process and
requires restorative treatment and correction of the damaged tooth surface. Cavitation can be diagnosed only by clinical observation.
The use of a sharp explorer to detect cavitation is problematic because excessive force in application of the explorer tip during inspection
of the proximal surfaces can damage weakened enamel and accelerate the caries process by creating cavitation. Separation of the teeth
can be used to provide more direct visual inspection of suspect surfaces. Fiberoptic illumination and dye absorption also are promising
new evaluation procedures, but neither fiberoptic illumination nor dye absorption is specific for cavitation. D, Advanced cavitated lesions
require prompt restorative intervention to prevent pulpal disease, limit tooth structure loss, and remove the nidus of infection of
odontopathic organisms. (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis,
Mosby, 2013.)
Primary modifying factors: Secondary modifying factors:

Tooth anatomy Socioeconornic status
Saliva Education
Biofilm pH Life-style
Use of fluoride Environment
Diet specifics Age (?)
Oral hygiene host Ethnic group (?)
Immune system Occupation
Genetic factors
cariogenic time
biofilm CARIES*
fermentable
carbohydrates
*In the absence of protective factors

and if other risk factors are present
Figure 2-3 Modified Keyes-Jordan diagram. In simple terms, dental caries is a result of the interaction of cariogenic oral flora
(biofilm) with fermentable dietary carbohydrates on the tooth surface (host) over time. However, dental caries onset and activity are
much more complex because not all persons with teeth and biofilm who consume carbohydrates have caries over time. Modifying risk
factors and protective factors influence the dental caries process. (Modified from Keyes PH, Jordan HV: Factors influencing initiation,
transmission and inhibition of dental caries. In Harris RJ, editor: Mechanisms of Hard Tissue Destruction. New York, Academic Press, 1963.)
The Caries Balance Box 2-1

Clinical Risk Assignment for Caries
Pathological Factors Protective Factors
Acid-producing bacteria Saliva flow and components A patient is at high risk for the development of new
Sub-normal saliva flow Remineralization (fluoride, cavitated lesions if:
and/or function calcium, phosphate)
1. High S. mutans counts are found. Bacteriologic
Frequent eating/drinking of Antibacterials (fluoride,
fermentable carbohydrates chlorhexidine, xylitol) testing for S. mutans should be done if:
Poor oral hygiene Good oral hygiene Patient has one or more medical health history
risk factors.
Patient has undergone antimicrobial therapy.
Demineralization Remineralization Patient presents with new incipient lesions.
(Caries) (No caries) Patient is undergoing orthodontic care.
Patients treatment plan calls for extensive
restorative dental work.
Figure 2-4 The caries balance. The balance between demin-
2. Any two of the following factors are present:
eralization and remineralization is illustrated in terms of patho-
Two or more active carious lesions.
logic factors (i.e., factors favoring demineralization) and protective
factors (i.e., factors favoring remineralization). (Modified from Numerous restorations.
Featherstone JDB: Prevention and reversal of dental caries: role of Poor dietary habits.
low level fluoride. Community Dent Oral Epidemiol 27:31-40, Low salivary flow.
1999.) (From Roberson TM, Heymann HO, Swift EJ: Sturdevants Art &
Science of Operative Dentistry, ed 5. St. Louis, Mosby, 2006.)
histatins, and proline-rich proteins, promote

remineralization.
J. Reduced salivary flow problems. 1.3 Prevention
1. Prolonged pH depression (decreased buffering). A. Objectives.
2. Decreased antibacterial effects. 1. Improve biofilm conditions to favor remineralization
3. Decrease in ions available for remineralization. and hinder demineralization.
4. Decreased elimination of microorganisms. 2. Realize that the repair of a caries lesion does not cure
the disease caries.
1.2 Pathogenesis and Diagnosis B. Antimicrobial.
A. Objectives. 1. Intense application on a short-term basis.
1. Identify caries lesions that need surgical treatment. C. Fluoride.
2. Identify caries lesions that need nonsurgical 1. Beneficial effects of fluoride.
treatment. a. Bactericidal.
3. Identify patients who are at high risk for caries and b. Provides fluoride ion for remineralization forming
need special preventive treatment. fluorapatite (which is more resistant to acid attack
4. Emphasis must shift from detection only of cavita- than hydroxyapatite enamel).
tions to the detection of high caries risk and predic- 2. Types and sources.
tions of caries progression. a. Community fluoridated water systems.
B. Identification of high-risk patients. b. Rinses.
1. Definitionidentification of patients who have c. Gels.
factors that place them at increased risk to develop d. Varnishes.
dental caries. There is no exact mechanism to make e. Toothpastes.
this determination. D. Saliva.
2. Option for high-risk identification (Box 2-1). 1. Alter saliva-reducing medications if possible.
a. High S. mutans counts. 2. Use saliva stimulants.
b. Any two of the following. a. Sugar-free gums and lozenges.
(1) Two or more active caries lesions. b. Saliva substitutes.
(2) Large numbers of restorations. c. Encourage diet high in protein and vegetables.
(3) Poor dietary habits. d. Use pilocarpine hydrochloride or cevimeline
(4) Low salivary flow. hydrochloride if needed.
(5) Poor oral hygiene. E. Sucrose.
(6) Suboptimal fluoride exposure. 1. Must decrease frequencymore important than
(7) Unusual tooth morphology. decreasing quantity.
2. A single exposure to sucrose for a caries-active mouth 2. If many cavitated lesions are present, caries-control
can result in pH being reduced below the 5.5 level for restorations (with glass-ionomer) are required. These
a sustained period because of the rapid metabolism may eventually be replaced with permanent res
by S. mutans. torations (with composite, amalgam, or indirect
F. Xylitol (note: the evidence for xylitol as a caries preven- materials).
tive agent is controversial). 3. Restorations alone do not cure the disease caries.
1. Natural sugar from birch trees (five-carbon sugar). C. Sealantssealants should be applied to at-risk molars
2. Keeps sucrose molecule from binding with S. mutans. and premolars.
3. S. mutans cannot ferment xylitol. D. Intense, short-term use of agents.
G. Oral hygienedisrupts plaque biofilm formation. 1. Chlorhexidine (note: the evidence for chlorhexidine
H. Sealantsremove habitats for S. mutans. as a caries preventive agent is controversial).
I. Restorations. 2. Fluoride varnishes.
E. Continuous, long-term use of agents.
1.4 Treatment Overview 1. Xylitol products (e.g., xylitol lozenge).
A. Objectivesfirst remove nidi of infection by restoring 2. Calcium phosphate products (e.g., CPP-ACP paste
large caries lesions and placing sealants. Assess patients or rinse).
caries risk, and institute individualized preventive mea- F. Fluoride rinses (over-the-counter).
sures (Table 2-1). 1. Begin after chlorhexidine is finished.
B. Restorationswhen cavitated lesions are present, they 2. Use at different times than for brushing twice a day.
should be restored first, usually before any antimicro- 3. Increase remineralization.
bial agents are used. If antimicrobials are used first, they G. Recall (3 months after chlorhexidine or fluoride varnish
disrupt the normal flora and allow the virulent organ- application).
isms in the protected (cavitated) areas to flourish on 1. Identify S. mutans counts.
now-unprotected tooth surfaces. 2. Clinical examination.
1. Restorations remove large nidi of infectious organ- a. Check sealants (if they fail, they usually come off
isms, but, more importantly, they remove habitats for early) and caries control restorations, if used.
more bacterial adherence. b. 3-month recalls.
Table 2-1
Suggested Risk-Based Interventions for Adults*
CARIES RISK
CATEGORY OFFICE-BASED INTERVENTIONS HOME-BASED INTERVENTIONS
High 3-month recare examination and oral prophylaxis Brush with prescription fluoride dentifrice
(e.g., 1/1%/5000ppm NaF)
Fluoride varnish at each recare visit Use sugar substitutes (e.g., xylitol, sorbitol)
Individualized oral hygiene instructions and use of Apply calcium-phosphate compounds (e.g.,
specialized cleaning aids (e.g., powered toothbrush, MI Paste)
Waterpik)
Dietary counseling Use antimicrobial agents (e.g., xylitol gum or
lozenge, chlorhexidine rinse)
Bite-wing radiographs every 6-12 months If xerostomic, increase salivary function (e.g.,
xylitol gum, rinses, oral moisturizers)
Moderate 4-6 month recare examination and oral prophylaxis Brush with fluoride dentifrice (e.g., 1450ppm
fluoride)
Fluoride varnish at each recall OTC fluoride rinse (e.g., 0.05% NaF)
Reinforce proper oral hygiene
Dietary counseling
Low 9-12 month recare examination and oral prophylaxis Brush with fluoride dentifrice
Reinforce good oral hygiene
Modified from Shugars DA, Bader JD: MetLife Quality Resource Guide, ed 3. Bridgewater, NJ, Metropolitan Life Insurance, Co., 2009-2012, p 6.
NaF, Sodium fluoride; OTC, over-the-counter; ppm, parts per million.
*These are general guidelines and should be customized based on the specific needs of the patient and the weight of individual risk factors uncovered with a caries risk
assessment instrument.
Data from U.S. Department of Health and Human Services, Public Health Service, Food and Drug Administration; and American Dental Association, Council on
Dental Benefit Programs, Council on Scientific Affairs: The selection of patients for dental radiographic examinations. Rev. ed. 2004. Available at: www.ada.org/prof/
resources/topics/radiography.asp. Accessed January 20, 2012.
1.5 Summary
A. Caries is a bacterial infection.
B. Efforts must be made to identify the cause of the patients
caries problem.
C. Efforts must be made to identify patients at high risk
for caries.
D. Early diagnosis of caries is important.
E. Nonsurgical treatment of incipient lesions should
be used.
F. Understanding the balance between demineralization
and remineralization is key to caries management.
G. Restoring a tooth does not cure the disease caries.
Figure 2-5 An accurate clinical examination requires a

2.0 Patient Assessment, Examination, clean, dry, well-illuminated mouth. Cotton rolls are placed in
Diagnosis, and Treatment Planning the vestibular space and under the tongue to maintain dryness
and enhance visibility. (From Heymann HO, Swift EJ, Ritter AV:
Pretreatment considerations consisting of patient assess- Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis,
ment, examination and diagnosis, and treatment planning Mosby, 2013.)
are the foundation of sound dental care. These consider-
ations follow a systematic progression because the diagno- c. Cheeks, vestibules, mucosa, lips, lingual and facial
sis and treatment plan depend on thorough assessment and alveolar mucosa, palate, tonsillar areas, tongue,
examination of the patient. and floor of the mouth.
C. Examination of teeth and restorations (Figures 2-5
to 2-8).
Outline of Review 1. Clinical examination for caries.
2.1 Patient Assessment Considerations a. Traditionally, dental caries has been diagnosed by
2.2 Examination and Diagnosis one or all of the following.
2.3 Treatment Planning (1) Visual changes in tooth surface texture or color.
2.4 Summary (2) Tactile sensation when an explorer is used
judiciously.
2.1 Patient Assessment Considerations (3) Radiographs.
A. Infection control. (4) Transillumination.
B. Chief complaint. b. Over the past decade, several technologies have
C. Medical review. emerged that show promising results for the clini-
1. Communicable diseases. cal diagnosis of caries.
2. Allergies and medications. (1) Laser fluorescence (DIAGNOdent).
3. Systemic diseases and cardiac abnormalities. (2) Digital imaging fiberoptic transillumination
4. Physiologic changes associated with aging. (DIFOTI).
D. Sociologic and psychological review. (3) Quantitative light-induced fluorescence (QLF).
E. Dental history. (4) Electrical conductance or impedance
F. Risk assessment. measurement.
c. Because no test currently available is completely
2.2 Examination and Diagnosis accurate, the dentist cannot rely solely on one test
A. General considerations. to make a decision whether to treat surgically or
1. Charting and records, preferably electronic. chemically.
2. Tooth denotation system. d. Caries is most prevalent in the pits and fissures of
3. Preparation for clinical examination. the occlusal surfaces where the developmental
4. Interpretation and use of diagnostic tests. lobes of the posterior teeth failed to coalesce, par-
B. Examination of orofacial soft tissues. tially or completely. Use of an explorer to diagnose
1. As with the other aspects of the clinical examina- fissure caries is strongly discouraged because inju-
tion, soft tissue evaluation requires a systematic dicious use of an explorer may cause fracture of
approach. the surface enamel that has been weakened by sub-
a. Submandibular glands and cervical nodes. surface demineralization. An occlusal surface is
b. Masticatory muscles. examined visually and radiographically. The visual
A B
C D
E F
Figure 2-6 Caries can be diagnosed clinically by careful inspection. A, Carious pit on cusp tip. B, Loss of translucency and
change in color of occlusal enamel resulting from a carious fissure. C, White chalky appearance or shadow under marginal ridge.
D, Incipient smooth-surface caries lesion, or a white spot, has intact surface. E, Smooth-surface caries can appear white or dark, depend-
ing on the degree of extrinsic staining. F, Root-surface caries. (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and Science of
Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
Figure 2-7 Caries can be diagnosed

radiographically as translucencies in
the enamel or dentin. A and B, Proximal
caries tends to occur bilaterally (a) and on
adjacent surfaces (b). C, Occlusal caries (c). A B
D, Recurrent caries gingival to an existing
restoration (d). Same recurrent caries (d) also
is shown in B. (From Heymann HO, Swift EJ,
Ritter AV: Sturdevants Art and Science of
Operative Dentistry, ed 6. St. Louis, Mosby,
2013.)
C D
fissure or pit. Radiographic diagnosis should be

made from a bite-wing radiograph when radiolu-
cency is apparent beneath the occlusal enamel
surface emanating from the dental enamel junc-
tion. In contrast, a noncarious occlusal surface has
either grooves or fossae that have shallow, tight
fissures that exhibit superficial staining with no
radiographic evidence of caries.
e. Precarious or carious pits are occasionally present
on cusp tips, on the occlusal two thirds of the facial
or lingual surface of the posterior teeth, and on the
lingual surface of maxillary incisors. Typically,
these pits are the result of developmental enamel
defects.
f. Proximal-surface caries, one form of smooth-
surface caries, is usually diagnosed radiographi-
cally. However, it also may be detected by careful
visual examination either after tooth separation or
through fiberoptic transillumination.
g. Brown spots on intact, hard proximal-surface
enamel adjacent and usually gingival to the con-
Figure 2-8 Extensively restored teeth with weakened
tact area are often seen in older patients whose
and fractured cusps. Note the distal developmental fissure in
caries activity is low. These discolored areas are a
the second molar, which further predisposes the distal cusps to
fracture. (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art result of extrinsic staining during earlier caries
and Science of Operative Dentistry, ed 6. St. Louis, Mosby, 2013.) demineralization-remineralization cycles. Such a
spot is no longer carious and is usually more resis-
tant to caries as a result of fluorhydroxyapatite for-
mation. Restorative treatment is not indicated.
examination is conducted in a dry, well-illuminated These arrested lesions sometimes challenge the
field. Through direct vision and reflecting light diagnosis because of faint radiographic evidence
through the occlusal surface of the tooth, the of the remineralized lesion.
occlusal surface is diagnosed as carious if there is h. Proximal coefficient of thermal expansion surface
chalkiness or apparent softening or cavitation of caries in anterior teeth may be identified by radio-
tooth structure forming the fissure or pit or brown- graphic examination, visual inspection (transillu-
gray discoloration radiating peripherally from the mination optional), or probing with an explorer.
i. Smooth-surface caries occur on the facial and in the diagnosis of caries and for confirmation of
lingual surfaces of the teeth, particularly in gingi- radiographic evidence of the disease.
val areas that are less accessible for cleaning. The 2. Clinical examination of amalgam restorations.
earliest clinical evidence of incipient caries on a. Evaluation of all restorations must be done system-
these surfaces is a white spot that is visually differ- atically in a clean, dry, well-lighted field. Clinical
ent from the adjacent translucent enamel and, in evaluation of amalgam restorations requires visual
contrast to enamel hypocalcification white lesions, observation, application of tactile sense with the
partially or totally disappears from vision by explorer, use of dental floss, interpretation of
wetting. Both types of white spots are undetectable radiographs, and knowledge of the probabilities
tactilely because the surface is intact, smooth, and that a given condition is sound or at risk for further
hard. For the carious white spot, preventive treat- breakdown. At least 11 distinct conditions may be
ment should be instituted to promote remineral- encountered when amalgam restorations are eval-
ization of the lesion. uated, including amalgam blues, proximal over-
(1) The presence of several facial (or lingual) hangs, marginal ditching, voids, fracture lines,
smooth-surface caries lesions in the same lines indicating the interface between abutted res-
patient suggests a high caries rate. In a caries- torations, improper anatomic contours, marginal
susceptible patient, the gingival third of the ridge incompatibility, improper proximal contacts,
facial surfaces of maxillary posterior teeth and recurrent caries, and improper occlusal contacts.
the gingival third of the facial and lingual sur- b. Amalgam blues or discolored areas are often seen
faces of the mandibular posterior teeth should through the enamel in teeth that have amalgam
be evaluated carefully because these teeth are restorations. This bluish hue results either from the
at a greater risk for caries. Advanced smooth- leaching of corrosion products of amalgam into the
surface caries exhibits discoloration and dentinal tubules or from the color of underlying
demineralization and feels soft to penetration amalgam as seen through translucent enamel. The
by the explorer. The discoloration ranges from latter occurs when the enamel has no dentin
white to dark brown, with rapidly progressing support, such as in undermined cusps, marginal
caries usually being light in color. With slowly ridges, and regions adjacent to proximal margins.
progressing caries in a patient with low caries When other aspects of the restoration are sound,
activity, darkening occurs over time because amalgam blues are not indicative of caries, do not
of extrinsic staining, and remineralization of warrant classifying the restoration as defective, and
decalcified tooth structure occasionally may require no further treatment. However, replace-
harden the lesion. Such an arrested lesion may ment of the restoration may be considered for
sometimes be rough, although cleanable, and a esthetics or for areas under heavy functional stress
restoration may not be indicated except for that may require a cusp capping restoration to
esthetics. The dentin in an arrested remineral- prevent possible tooth fracture.
ized lesion is termed sclerotic. c. Proximal overhangs are diagnosed visually, tac-
j. Root-surface cariesearly in its development, tilely, and radiographically.
root caries appears as a well-defined discolored d. Marginal gap or ditchingshallow ditching less
area adjacent to the gingival margin, typically than 0.5mm deep usually is not a reason for res-
near the cementoenamel junction (CEJ). Root toration replacement because such a restoration
caries is found to be softer than the adjacent usually looks worse than it really is. The self-sealing
sound tissue, and lesions typically spread laterally property of amalgam allows the restoration to con-
around the CEJ. Active root caries is detected by tinue serving adequately if it can be satisfactorily
the presence of softening and cavitation. Although cleaned and maintained. However, if the ditch is
root-surface caries may be detected on radio- too deep to be cleaned or it jeopardizes the integ-
graphic examination, a careful, thorough clinical rity of the remaining restoration or tooth structure,
examination is critical. A difficult diagnostic chal- the restoration should be replaced.
lenge is a patient who has attachment loss with e. Voidsaccessible small voids in other marginal
no gingival recession, limiting accessibility for areas where the enamel is thicker may be cor-
clinical inspection. These rapidly progressing rected by recontouring or repairing with a small
lesions are best diagnosed using vertical bite-wing restoration.
radiographs. However, differentiation of a caries f. Fracture lines are detected by clinical
lesion from cervical burnout radiolucency is examination.
essential. g. Lines indicating the interface between abutted res-
k. Regardless of the location or type of caries lesions, torations are detected by clinical examination and
a careful, thorough clinical examination is critical are acceptable.
h. Improper anatomic contoursamalgam restora- support; dentist-patient compatibility; availability

tions should duplicate the normal anatomic con- of specialists; and functional, esthetic, and techni-
tours of the teeth. Restorations that have improper cal demands. Even when modification is necessary,
anatomic contours, are impinging on the soft the practitioner is ethically and professionally
tissue, present recurrent caries, have inadequate responsible for providing the best level of care
occlusal contacts, have inadequate embrasure form possible. A treatment plan is not a static list of
or proximal contact, or prevent the use of dental services. Rather, it is a multiphase and dynamic
floss should be classified as defective. series of events. Its success is determined by its
3. Clinical examination of composite and other tooth- suitableness to meet the patients initial and long-
colored restorationssimilar to amalgam except that term needs.
more emphasis is given to esthetics when examining 2. Treatment plan sequencinggenerally, the concept
anterior restorations. Corrective procedures include of greatest need guides the order in which treatment
recontouring, polishing, repairing, or replacing. is sequenced. This concept dictates that what the
4. Clinical examination of cast restorationssimilar to patient needs most is performed first.
amalgam and composite. a. Urgent phase.
5. Radiographic examination of teeth and restorations b. Control phase.
as a general rule, patients at higher risk for caries c. Reevaluation phase.
or periodontal disease should receive more frequent d. Definitive phase.
and more extensive radiographic surveys. e. Maintenance phase.
a. For diagnosis of proximal-surface caries, restora- 3. Interdisciplinary considerations in operative treat-
tion overhangs, or poorly contoured restorations, ment planning.
posterior bite-wing and anterior periapical radio- a. Endodontics.
graphs are most helpful. When interpreting the b. Periodontics.
radiographic presentation of proximal tooth sur- c. Orthodontics.
faces, it is necessary to know what the normal d. Oral surgery.
anatomy looks like in a radiograph before any e. Occlusion.
abnormalities can be diagnosed. In a radiograph, f. Fixed and removable prosthodontics.
proximal caries appears as a dark area or a radio- B. Indications for operative treatment (Tables 2-2 and 2-3).
lucency in the proximal enamel at or gingival to 1. Operative preventive treatmentthis preventive
the contact of the teeth. This radiolucency is typi- program should include altering the oral environ-
cally triangular and has its apex toward the denti- ment to encourage remineralization of incipient
noenamel junction (DEJ). smooth-surface lesions and treating caries-prone pits
and fissures with sealants. As bacterial habitats are
2.3 Treatment Planning disrupted daily, diet is improved, and fluoride is
A. Introduction. incorporated into the enamel, there is a decrease in
1. General considerations. the occurrence of new lesions, along with remineral-
a. A treatment plan is a carefully sequenced series of ization of incipient lesions. Also, extensive acute
services designed to eliminate or control etiologic caries should be immediately eradicated by either a
factors; repair existing damage; and create a func- definitive restoration or a caries-control restoration
tional, maintainable environment. A sound treat- to help suppress the infectious process.
ment plan depends on thorough patient evaluation, 2. Treatment of incipient lesionsincipient caries
dentist expertise, understanding of indications and lesions are contained entirely within enamel and have
contraindications, and a prediction of the patients not spread to the underlying dentin. Assuming that
response to treatment. an incipient lesion has been properly identified, there
b. The development of a dental treatment plan for a are two basic options available to the dentist.
patient consists of four steps. a. First and more preferred is targeted reminer
(1) Examination and problem identification. alization followed by regular monitoring. This
(2) Decision to recommend intervention. approach is based on the facts that incipient caries
(3) Identification of treatment alternatives. lesions usually do not progress rapidly, and chang-
(4) Selection of the treatment with the patients ing the oral environment combined with the appli-
involvement. cation of fluoride varnish and self-administered
c. Notes: treatment plans are influenced by patient fluoride can lead to remineralization of these
preferences, motivation, systemic health, emo- lesions.
tional status, and financial capabilities. A treat- b. The second strategy used to treat incipient lesions
ment plan also can be modified by the dentists is restoration. This option is the last resort for man-
knowledge, experience, and training; laboratory aging incipient lesions. Many new caries detection
Table 2-2
Pit-and-Fissure Caries Treatment Decision Making*
From Roberson TM, Heymann HO, Swift EJ: Sturdevants Art & Science of Operative Dentistry, ed 5. St. Louis, Mosby, 2006.
*If a cavitated lesion exists in a pit or fissure, it must be restored. If the pit or fissure is not cavitated but at risk, it should be sealed. The pits and fissures of molar teeth
in children should be sealed routinely as soon as possible after eruption. Pits and fissures in adults should be sealed if the adult is found to have multiple active lesions
or found to be at high risk.
Table 2-3
Proximal Caries Treatment Decision Making*
*Proximal surfaces are difficult to judge clinically. The critical event in the caries process is surface cavitation. A cavitated surface must be restored, whereas a
demineralized noncavitated surface can be treated only by antimicrobial and fluoride agents. Bite-wing radiographs can reveal a decrease in density, but radiolucencies
alone are not diagnostic of cavitation. Restoration of all radiolucent surfaces results in excessive, unnecessary restorative treatment.
devices have high rates of false-positive findings, 7. Treatment of root-surface cariescare must be exer-
which can lead to the misdiagnosis of otherwise cised to distinguish the active root-surface caries
healthy teeth as diseased and planned for restora- lesion from the root-surface lesion that previously
tion. When a restoration is indicated, the prepara- was active but has become inactive (arrested). The
tion should be done as conservatively as possible. latter lesion shows eburnated dentin (sclerotic dentin)
In other words, only enough tooth structure should that has darkened from extrinsic staining, is firm to
be removed to ensure that the lesion is eliminated the touch of an explorer, may be rough but is clean-
and that the resulting preparation retains the able, and is seen in patients (usually older) whose
chosen restoration. oral hygiene and diet in recent years are good. If
C. Criteria for restoring. it is determined that the lesion needs restoration,
1. Elevated caries risk (see Box 2-1). it can be restored with amalgam or tooth-colored
2. Low frequency of routine dental care because of lack materials.
of motivation. D. Treatment of root-surface hypersensitivity.
3. Lesion extends to DEJ. 1. The most accepted theory of the cause of root-surface
4. Esthetic treatmentthese treatments include esthetic hypersensitivity is the hydrodynamic theory, which
recontouring of the anterior teeth, vital and nonvital postulates that the pain results from indirect innerva-
tooth bleaching, microabrasion, diastema closures, tion caused by dentinal fluid movement in the tubules
and other composite additions by means other than that stimulates mechanoreceptors near the predentin.
extensive full-coverage restorations. Also, porcelain Some of the causes of such fluid shifts are tempera-
veneers are available for esthetically prominent ante- ture change, air-drying, and osmotic pressure. Any
rior teeth. treatment that can reduce these fluid shifts by partially
5. Treatment of abrasion, erosion, attrition, and or totally occluding the tubules may help reduce the
abfraction. sensitivity.
a. Abrasionmechanical wear secondary to abnor- 2. Numerous forms of treatment have been used
mal forces (toothbrushing). to provide relief, such as topical fluoride, fluoride
b. Erosionwear secondary to chemical presence. rinses, oxalate solutions, dentin bonding agents, seal-
c. Attritionnormal tooth wear. ants, iontophoresis, and desensitizing toothpastes.
d. Abfractionbiomechanical loading causing loss of Although all of these methods have met with varying
tooth structure in the cervical area. This is usually degrees of success, dentin-bonding agents provide
due to occlusal forces causing the tooth to bend, the best rate of success. When these conservative
making microfractures in the cervical thin enamel, methods fail to provide relief, restorative treatment is
which is removed even more rapidly as a result of indicated.
additional toothbrushing abrasion. A pattern of E. Repairing and resurfacing existing restorations
the lesion often is seen below an occlusal cusp tip resurfacing or repair of composites and amalgam and
wear pattern. repair of cast restorations have been shown to be effec-
6. Areas of significant attrition that are worn into dentin tive. If a restoration has an isolated defect, and it can be
and are sensitive or compromise esthetics or function confirmed when explored operatively that all carious
should be considered for restoration. However, before tooth structure has been removed, it is acceptable and
cast restorations are used, a complete occlusal analy- often preferable to repair or recontour.
sis and an in-depth interview with the patient regard- F. Replacement of existing restorationsindications for
ing the etiology should be conducted to reduce replacing restorations include the following.
contributing factors. Also, bite guard therapy should 1. The restoration has significant discrepancies.
be considered. Abraded or eroded areas should be 2. The tooth is at risk for caries or fracture.
considered for restoration only if one or more of the 3. The restoration is a negative etiologic factor to adja-
following exists. cent teeth or tissue.
a. The area has caries involvement. 4. A marginal void, especially in the gingival one third,
b. The defect is sufficiently deep to compromise the cannot be repaired.
structural integrity of the tooth. 5. Poor proximal contour or a gingival overhang that
c. Intolerable sensitivity exists and is unresponsive to contributes to periodontal breakdown is present.
conservative desensitizing measures. 6. A marginal ridge discrepancy contributes to food
d. The defect contributes to a periodontal problem. impaction.
e. The area is to be involved in the design of a remov- 7. Overcontour of a facial or lingual surface results in
able partial denture. plaque gingival to the height of contour and resul-
f. The depth of the defect is judged to be close to tant inflammation of gingiva overprotected from
the pulp. the rubbing-cleansing action of a food bolus or
g. The patient desires esthetic improvements. toothbrush.
8. Poor proximal contact is either open (resulting in required for the other types of indirectly fabricated
interproximal food impaction and inflammation of tooth-colored restorations.
impacted gingival papilla) or improper in location I. Indications for cast metal restorationsalthough indi-
or size. cations for intracoronal castings are few, a gold onlay
9. Recurrent caries cannot be adequately treated by a that caps all of the cusps and includes some of the axial
repair restoration. tooth line angles is an excellent restoration. Cast metal
10. Ditching deeper than 0.5mm of the occlusal restorations may be the treatment of choice for patients
amalgam margin is judged carious or caries-prone. undergoing occlusal rehabilitation. Also, teeth with
The presence of shallow ditching around an deep subgingival margins are well treated with cast res-
amalgam restoration by itself is not an indication for torations because they provide a better opportunity for
replacement. control of proximal contours and for restoration of the
11. Esthetics is unacceptable for tooth-colored restora- difficult subgingival margin compared with amalgam
tions. Restorations that have only light marginal and composite restorations.
staining and are judged noncarious can be cor-
rected by a shallow, narrow, marginal repair 2.4 Summary
restoration. A. Proper diagnosis and treatment planning play a critical
12. In many instances, recontouring or resurfacing the role in the quality of dental care. Each patient must be
existing restoration can delay replacement. evaluated individually in a thorough and systematic
G. Indications for direct composite and other tooth- fashion. After the patients condition is understood and
colored restorationsthe American Dental Association recorded, a treatment plan can be developed and
has both supported the use of composite for many class rendered.
I and II restorations and indicated that such restora- B. A successful treatment plan carefully integrates and
tions should have a clinical longevity similar to amalgam sequences all necessary procedures indicated for the
restorations. Direct composite restorations are appro- patient. There are few absolutes in treatment planning;
priately indicated for most clinical applications, anteri- the available information must be considered carefully
orly and posteriorly. and incorporated into a plan to fit the needs of the
H. Indications for indirect tooth-colored restorations individual. Patients should have an active role in the
tooth-colored restorations that are indirectly fabricated process; they should be made aware of the findings, be
out of the mouth may be indicated for class I and II advised of the risks and benefits of the proposed treat-
restorations because of esthetics, strength, and other ment, and be given the opportunity to help decide the
bonding benefits. However, they are usually more costly course of treatment.
than direct tooth-colored restorations. Indirect tooth- C. Examination, diagnosis, and treatment planning are
colored restorations include the following. extremely challenging and rewarding for both the
1. Processed compositealthough processed compos- patient and the dentist if done thoroughly and properly
ite restorations possess improved wear resistance with the patients best interest in mind.
over direct composites, they are indicated primarily
for conservative class I and II preparations in areas
with low to moderate stress. 3.0 Instrumentation for Operative
2. Feldspathic porcelainfeldspathic porcelain inlays Dentistry Procedures
and onlays for class I and II restorations are highly
esthetic but are associated with a relatively high inci- Outline of Review
dence of fracture, especially if subjected to heavy
3.1 Hand Instruments for Cutting
occlusal forces. Porcelain restorations also have the
3.2 Overview of Powered Cutting Instruments
potential to wear opposing tooth structure.
3.3 Rotary Cutting Instruments
3. Cast ceramiccast ceramic inlays and onlays for
3.4 Cutting Mechanisms
class I and II preparations offer excellent marginal fit,
3.5 Hazards with Cutting Instruments
low abrasion to opposing tooth structure, and supe-
rior strength compared with processed composite or
feldspathic porcelain. They offer an excellent esthetic 3.1 Hand Instruments for Cutting
alternative to cast metal restorations. Modern hand instruments, when properly used, produce
4. Computer-generated (computer-aided design beneficial results for both the operator and the patient.
[CAD]/computer-aided manufacturing [CAM]) Some of these results can be satisfactorily achieved only
inlays and onlaysonlays and inlays can be gener- with hand instruments and not with rotary instruments.
ated with CAD/CAM. Because these restorations are Preparation form dictates some circumstances in which
fabricated chairside, only one appointment is required hand instruments are to be used, whereas accessibility dic-
for placement compared with two appointments tates others.
1. Excavatorsfour subdivisions.
a. Ordinary hatchetsthe ordinary hatchet has the
cutting edge of the blade directed in the same plane
as that of the long axis of the handle and is bibev-
a b c b a eled; it is used primarily on anterior teeth for pre-
paring retentive areas.
Figure 2-9 Double-ended instrument illustrating three
b. Hoesthe hoe has the primary cutting edge of the
component parts of hand instruments: blade (a), shank
(b), and handle (c). (Modified from Boyd LRB: Dental Instru- blade perpendicular to the axis of the handle and
ments: A Pocket Guide, ed 4. St. Louis, Saunders, 2012.) is used for planing tooth preparation walls and
forming line angles.
c. Angle-formersthe angle-former is used primar-
A. Terminology and classification. ily for sharpening line angles and creating retentive
1. Instrument categories. features in dentin. It also may be used in placing a
a. Cutting (excavators, chisels, and others). bevel on enamel margins. It is a monangle instru-
b. Noncutting (amalgam condensers, mirrors, explor- ment and has the primary cutting edge at an angle
ers, probes, and others). (other than 90 degrees) to the blade. It may be
2. Instrument designmost hand instruments, regard- described as a combination of a chisel and gingival
less of use, are composed of three parts: handle, margin trimmer. It is available in pairs (right
shank, and blade (Figure 2-9). For many noncutting and left).
instruments, the part corresponding to the blade is d. Spoonsspoon excavators are used for removing
termed the nib. The end of the nib, or working caries. The blades are slightly curved, and the
surface, is known as the face. The blade or nib is the cutting edges are either circular or clawlike. The
working end of the instrument and is connected to circular edge is known as a discoid, whereas
the handle by the shank. Some instruments have a the clawlike blade is termed a cleoid. The shanks
blade on both ends of the handle and are known as may be binangled or triple-angled to facilitate
double-ended instruments. The blades are of many accessibility.
designs and sizes, depending on the function they are 2. Chiselschisels are intended primarily for cutting
to perform. enamel.
3. Operative cutting instrument formulascutting a. Straight, slightly curved, or binanglethe straight
instruments have formulas describing the dimen- chisel has a straight shank and blade, with the bevel
sions and angles of the working end. These are placed on only one side. Its primary edge is perpendicular
on the handle using a code of three or four numbers to the axis of the handle. It is similar in design to
separated by dashes or spaces (e.g., 10-8.5-8-14). a carpenters chisel. The shank and blade of the
The first number indicates the width of the blade chisel also may be slightly curved (Wedelstaedt
or primary cutting edge in tenths of a millimeter design) or may be binangled. The force used with
(0.1mm). The second number of a four-number all of these chisels is essentially a straight thrust.
code indicates the primary cutting edge angle, mea- b. Enamel hatchetsenamel hatchets are used for
sured from a line parallel to the long axis of cutting and planning enamel surfaces.
the instrument handle in clockwise centigrades. The c. Gingival margin trimmersthe gingival margin
angle is expressed as a percent of 360 degrees. The trimmer is designed to produce a proper bevel
instrument is positioned so that this number always on gingival enamel margins of proximo-occlusal
exceeds 50. If the edge is locally perpendicular to the preparations. It is similar in design to the enamel
blade, this number is normally omitted, resulting in hatchet except the blade is curved (similar to a
a three-number code. The third number (second spoon excavator), and the primary cutting edge is
number of a three-number code) indicates the blade at an angle (other than perpendicular) to the axis
length in millimeters. The fourth number (third of the blade. It is made as right and left types.
number of a three-number code) indicates the blade 3. Other cutting instrumentsother hand cutting
angle, relative to the long axis of the handle in clock- instruments, such as the knife, file, and discoid-cleoid
wise centigrade. For these measurements, the instru- instrument, are used for trimming and carving
ment is positioned so that this number is always 50 restorative material rather than for cutting tooth
or less. structure.
B. Cutting instrument applicationscutting instruments C. Hand instrument techniques.
are used to cut hard or soft tissues of the mouth. Exca- 1. Modified pen grasp.
vators are used for removal of caries and refinement of 2. Inverted pen grasp.
the internal parts of the preparation. Chisels are used 3. Palm-and-thumb grasp.
primarily for cutting enamel. 4. Modified palm-and-thumb grasp.
5. Rests. the present time, lasers are used primarily for either soft
6. Guards. tissue applications or hard tissue surface modification.
They generally are not used for tooth preparations
3.2 Overview of Powered because it is difficult to generate a defined margin or
Cutting Instruments tooth preparation surface.
A. Rotary speed ranges (Figure 2-10)the rotational C. Air-driven particle abrasion equipmentContem
speed of an instrument is measured in revolutions per porary air-driven particle abrasion equipment (com-
minute (rpm). Three speed ranges are generally recog- monly known simply as air abrasion) is helpful for stain
nized: low or slow speeds (<12,000rpm), medium or removal, dbriding pits and fissures before sealing, and
intermediate speeds (12,000 to 200,000rpm), and high micromechanical roughening of surfaces to be bonded
or ultrahigh speeds (>200,000rpm). Most useful instru- (enamel, cast metal alloys, or porcelain). This approach
ments are rotated at either low or high speed. The works well when organic material is being removed and
crucial factor for some purposes is the surface speed of when only a limited amount of enamel or dentin is
the instrument, which is the velocity at which the edges involved. Although promoted for caries excavation, air
of the cutting instrument pass across the surface being abrasion cannot produce well-defined preparation wall
cut. This is proportional to both the rotational speed and margin details that are possible with conventional
and the diameter of the instrument, with large instru- rotary cutting techniques.
ments having higher surface speeds at any given rate of
rotation. 3.3 Rotary Cutting Instruments
B. Laser equipmentlasers are increasingly used in den- A. Common design characteristicsdespite the great vari-
tistry. Current units are expensive and must be used ation among rotary cutting instruments, they share
frequently in a dental practice to justify the expense. At certain design features. Each instrument consists of
A B
C
Figure 2-10 A, Contrangle air-turbine handpiece connected to the air-water supply line. B, Ventral view of the handpiece showing
four port for air-water spray (S) onto bur at cutting site and epoxied end of fiberoptic bundle (l) to shine light at cutting site. C, Electri-
cal handpieces and unit. (C, courtesy of DENTSPLY International, York, PA.)
d. A straight fissure bur is an elongated cylinder.

Shank Neck Head
Some clinicians advocate this shape for amalgam
tooth preparation. Modified burs of this design
Figure 2-11 Normal designation of three parts of rotary with slightly curved tip angles are available.
cutting instruments. (From Heymann HO, Swift EJ, Ritter AV: e. A tapered fissure bur is a portion of a tapered cone
Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis, with the small end of the cone directed away from
Mosby, 2013.)
the bur shank. This shape is used for tooth prepara-
tions for indirect restorations for which freedom
from undercuts is essential for successful with-
drawal of patterns and final seating of the restora-
tions. Tapered fissure burs can have a flat end with
the tip corners slightly rounded.
C. Diamond abrasive instrumentsabrasive rotary dental
cutting instruments are based on small, angular parti-
cles of a hard substance held in a matrix of softer
material.
Round Inverted Pear- Straight Tapered 1. Terminologydiamond instruments consist of three
cone shaped fissure fissure parts: metal blank, powdered diamond abrasive, and
Figure 2-12 Basic bur head shapes. (From Finkbeiner BL, metallic bonding material that holds the diamond
Johnson CS: Mosbys Comprehensive Dental Assisting. St. Louis, powder onto the blank. The blank in many ways
Mosby, 1995.) resembles a bur without blades. It has the same essen-
tial parts: head, neck, and shank. Various shapes and
designs of diamond cutting instruments are available
three parts: shank, neck, and head. Each has its own (Figure 2-13).
function, influencing its design and the materials used 2. Diamond particle factorsthe clinical performance
for its construction. There is a difference in the meaning of diamond abrasive instruments depends on the
of the term shank as applied to rotary instruments and size, spacing, uniformity, exposure, and bonding
to hand instruments (Figure 2-11). of the diamond particles. Increased pressure causes
B. Dental bursthe term bur is applied to all rotary the particles to dig into the surface more deeply,
cutting instruments that have bladed cutting heads. leaving deeper scratches and removing more tooth
1. Bur classification systemsto facilitate the descrip- structure.
tion, selection, and manufacture of burs, it is highly a. Diamond particle size is commonly categorized as
desirable to have some agreed-on shorthand designa- coarse, medium, fine, and very fine for diamond
tion that represents all variables of a particular head preparation instruments. The clinical performance
design by some simple code (Figure 2-12). of diamond instruments is strongly affected by the
2. Shapesthe term bur shape refers to the contour or technique used to take advantage of the design
silhouette of the head. Although there are a variety factors for each instrument.
of different bur shapes and blade configurations, the b. Diamond finishing instruments use even finer dia-
basic head shapes are round, inverted cone, pear, monds to produce smooth surfaces for final finish-
straight fissure, and tapered fissure. ing. Clinically smooth surfaces can be routinely
a. A round bur is spherical and is customarily used attained by using a series of finer and finer polish-
for initial entry into the tooth, extension of the ing steps.
preparation, preparation of retention features, and
caries removal. 3.4 Cutting Mechanisms
b. An inverted cone bur is a portion of a short tapered Effective and efficient cutting requires a powered hand-
cone with the apex of the cone directed toward the piece, air-water spray for cooling, high operating speed
bur shank. Head length is approximately the same (>200,000rpm), light pressure, and a new carbide bur or
as the diameter. This shape is particularly suitable diamond instrument. Carbide burs are better for end-
for providing undercuts in tooth preparations. cutting, produce lower heat, and have more blade edges per
c. A pear-shaped bur is a portion of a tapered cone diameter for cutting. They are effectively used for punch
with the small end of the cone directed toward the cuts to enter tooth structure, intracoronal tooth prepara-
bur shank. The end of the head either is continu- tion, amalgam removal, small preparations, and secondary
ously curved or is flat with rounded corners where retention features. Diamond instruments have greater
the sides and flat end intersect. A long-length pear hardness, and coarse diamonds have very high cutting
bur (length three times the width) is advocated for effectiveness. Diamonds are more effective than burs for
tooth preparations. both intracoronal and extracoronal tooth preparations,
Round Football Barrel Flat-end Beveled-end Inverted Flat-end

cylinder cylinder cone taper
Round-end Flame Needle Interproximal Pear Donut Wheel

taper
Figure 2-13 Characteristic shapes and designs for a range of diamond cutting instruments. (From Heymann HO,
Swift EJ, Ritter AV: Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
beveling enamel margins on tooth preparations, and D. Ear precautionsan objectionable high-pitched whine
enameloplasty. is produced by some air-turbine handpieces at high
speeds. Aside from the annoying aspect of this noise,
3.5 Hazards with Cutting Instruments there is some possibility that hearing loss can result
Almost everything done in a dental office involves some from continued exposure.
risk to the patient, dentist, or auxiliary personnel. For the 1. Potential damage to hearing from noise depends on
patient, there are pulpal dangers from the tooth prepara- the intensity or loudness (decibels), frequency (Hz),
tion and restoration procedures. There are also soft tissue duration (time) of the noise, and susceptibility of the
dangers. Everyone is potentially susceptible to eye, ear, and individual.
inhalation dangers. However, careful adherence to stan- 2. Increased age, existing ear damage, disease, and
dard precautions can eliminate or minimize most risks medications are other factors that can accelerate
associated with cutting instrument use. hearing loss.
A. Pulpal precautionsthe use of cutting instruments can E. Inhalation precautionaerosols and vapors are a health
harm the pulp by exposure to mechanical vibration, hazard to all present and are created by cutting tooth
heat generation, desiccation and loss of dentinal tubule structure and restorative materials. The aerosols are fine
fluid, and transection of odontoblastic processes. As the dispersions in air of water, tooth debris, microorgan-
thickness of remaining dentin decreases, the pulpal isms, and restorative materials. Aerosols and vapors
insult (and response) from heat or desiccation increases. should be eliminated as much as possible by careful
B. Soft tissue precautionsthe lips, tongue, and cheeks of evacuation near the tooth being operated on.
the patient are the most frequent areas of soft tissue 1. A rubber dam protects the patient against oral inha-
injury. The handpiece should never be operated unless lation of aerosols or vapors, but nasal inhalation of
there is good access and vision to the cutting site. A vapor and finer aerosol may still occur.
rubber dam is very helpful in isolating the operating 2. Disposable masks worn by dental office personnel
site. When the dam is not used, the dentist and dental filter out bacteria and all but the finest particulate
assistant can retract the soft tissue with a mouth mirror, matter.
cotton roll, or saliva ejector.
C. Eye precautionsthe operator, assistant, and patient
should wear glasses with side shields to prevent eye 4.0 Preparation of Teeth
damage from airborne particles during operative pro-
cedures using rotary instrumentation. When using high Outline of Review
speeds, particles of old restorations, tooth structure, 4.1 Introduction
bacteria, and other debris are discharged at high speeds 4.2 Stages and Steps in Tooth Preparation
from the patients mouth. 4.3 Moisture Control
4.4 Tooth Preparation for Amalgam Restorations (3) Less trauma to pulp.
4.5 Tooth Preparation for Composite Restorations (4) Stronger remaining tooth structure.
(5) More easily retained material.
4.1 Introduction 3. Type of restorative material to be used.
A. Why teeth need to be restored. a. Gold, porcelain, amalgam, or compositeeach
1. Remove caries. require different preparation forms (Table 2-4).
2. Correct fracture. 4. Biologic considerations.
3. Correct erosive tooth wear. a. Pulpal effects of preparation.
4. Reduce risk of pulp damage. b. Fracture potential of undermined enamel.
5. Improve or correct esthetics. c. Tooth strength considerations.
6. Improve or correct contour or function. E. Considerations in tooth preparations (Box 2-2).
B. Definition of tooth preparation.
1. Mechanically altering a tooth to remove diseased or 4.2 Stages and Steps in Tooth Preparation
weakened tooth structure. A. Initial (primary) tooth preparationextension of the
2. Mechanically altering a tooth to receive the appropri- preparation walls to sound tooth structure in all direc-
ate restorative material (Figure 2-14). tions except pulpally.
a. For maximum strength. 1. Outline form and initial depth (Figure 2-15).
b. For maximum form, function, and esthetics. a. Definitionextension to sound tooth structure at
C. Objectives of tooth preparation. an initial depth of 0.2 to 0.75mm into dentin.
1. Remove all defects. b. Principles.
2. Protect the pulp. (1) Place margins where finishable.
3. Be as conservative as possible. (2) Remove unsupported, weakened tooth
4. Make tooth and restoration strong. structure.
5. Make restoration functional and esthetic. (3) Include all faults.
D. Factors affecting tooth preparation. c. Dictated by the following.
1. General factors. (1) Caries.
a. Diagnosis. (2) Old material.
b. Patient desires. (3) Size of defect.
c. Multitreatment needs. (4) Occlusion.
2. Emphasis on conservation of tooth structure. (5) Marginal configuration.
a. Examples. (6) Adjacent tooth or contour.
(1) Supragingival margins. d. Features.
(2) Minimal pulpal depth. (1) Preserve cuspal strength.
(3) Minimal faciolingual width. (2) Preserve marginal ridge strength.
(4) Rounded internal line angles. (3) Keep faciolingual width narrow.
b. Benefits of smaller preparations. (4) Connect two close (0.5mm) preparations.
(1) Less removal of tooth structure. (5) Restrict depth to 0.2 to 0.75mm into dentin.
(2) Better esthetics. (6) Use enameloplasty.
Box 2-2
tal
Considerations in Tooth Preparations
Dis
Pulpal
Facial Internal Extent of caries Pulp protection
External Ling walls Extent of old material Patient cooperation
walls
ual
Gin
Axial
giv
a
Occlusion Fracture lines
l
Extent of defect Bone support
Pulpal involvement Caries activity
Cementoenamel
Esthetic needs Economics
junction (CEJ) Tooth contours Patient desires
Patient age Material limitations
Floors (or seats) are the gingival Bur design Radiographic findings
and pulpal walls
Patients homecare Overall diagnosis
Figure 2-14 External and internal walls for an amalgam Gingival status Anesthesia
tooth preparation.
Table 2-4
Tooth Preparation: Amalgam versus Composite
AMALGAM COMPOSITE
Outline form Include fault Same
May extend to break proximal Same
Include adjacent suspicious area No
Seal these areas
Pulpal depth Uniform 1.5mm Remove fault; not usually uniform
Axial depth Uniform 0.2-0.5mm inside DEJ Remove fault; not usually uniform
Cavosurface margin Create 90-degree amalgam margin 90 degrees
Bevels None (except possibly gingival) Large preparation, esthetics, and seal
Texture of prepared walls Smoother Rough
Cutting instrument Burs Diamonds
Primary retention form Convergence occlusally None (roughness/bonding)
Secondary retention form Grooves, slots, locks, pins, bonding Bonding; grooves for very large or root-surface
preparation
Resistance form Flat floors, rounded angles, box-shaped floors, Same for large preparations; no special form for
perpendicular or occlusal forces (?) small-to-moderate size preparations
Base indications Provide ~2mm between pulp and amalgam Not needed
Liner indications Ca(OH)2 over direct or indirect pulp caps Same
Sealer Gluma desensitizer when not bonding Sealed by bonding system used
Ca(OH)2, Calcium hydroxide.
e. Occlusal preparations. (2) Gingival walls of class V. Outline is governed

(1) Extend margin to sound tooth structure. only by extent of lesion except pulpally.
(2) Extend to include all of the fissure that is not g. Enameloplastyremoval of a defect by recon-
eliminated by enameloplasty. touring or reshaping the enamel when the defect
(3) Restrict depth to 0.2mm into dentin. is no deeper than one quarter the thickness of
(4) Join two preparations if less than 0.5mm enamel. When the defect is greater than one third
remaining. the thickness of enamel, the wall must be
(5) Extend to provide access for preparing, insert- extended.
ing material, and finishing the restoration. 2. Primary resistance form.
f. Smooth-surface preparations. a. Definitionprevention of tooth or restoration
(1) Proximal surfaces. fracture from occlusal forces along the long axis of
(a) Extend until no friable enamel remains. the tooth.
(b) Do not stop margins on cusp heights or b. Factors affecting primary resistance form.
ridge crests. (1) Occlusal contacts.
(c) Get enough access. (2) Amount of remaining tooth structure.
(d) Axial wall depth restricted to 0.2mm inside (3) Type of restorative material.
DEJ to 0.75mm depth from external c. Features.
surface. (1) Flat floors, pulpal, and gingival.
(e) Extend gingival margin to get 0.5mm (2) Box shape.
clearance. (3) Preserve marginal ridges.
(f) Extend facial and lingual proximal walls to (4) Preserve cuspal strength.
clearance. If it is necessary to extend the (5) Remove weakened tooth structure.
facial and lingual walls 1mm or more to (6) Cap cusps as indicated (Figure 2-16).
break the contact arbitrarily, the proximal (7) Rounded internal line angles.
margin is left in the contact. (8) Adequate thickness of material.
0.75 mm
701 0.2 mm
DEJ
CEJ
0.5 mm B
DEJ
0.75-0.8 mm
0.2 mm
DEJ
245
DEJ
0.2 mm
C
Figure 2-15 Initial tooth preparation stage for conventional preparations. A-C, Extensions in all directions are to sound tooth
structure, while maintaining a specific limited pulpal or axial depth regardless whether the end (or side) of bur is in dentin, caries, old
restorative material, or air. Dentinoenamel junction (DEJ) and cementoenamel junction (CEJ) are indicated in B. In A, initial depth is
approximately two thirds of 3-mm bur head length, or 2mm, as related to prepared facial and lingual walls, but is half the No. 245 bur
head length, or 1.5mm, as related to central fissure location.
2/
3 1/ OK
2
1 2/
Primary /2 to 3 Consider capping
groove 2/ or
3 more Recommend capping
Cusp tip
2
/3
1/
2
Facial
Primary groove
Mandibular groove
molar Central
groove
Figure 2-16 Rule for cusp capping. If extension from a primary groove toward the cusp tip is no more than half the distance, no
cusp capping should be done. If this extension is one half to two thirds of the distance, consider cusp capping. If the extension is more
than two thirds of the distance, usually cusp capping is done.
3. Primary retention form. (2) Groove extensions (may be for any

a. Definitionprevention of dislodgment of the restoration).
material. (3) Skirts (primarily for cast restorations).
b. Features. (4) Beveled enamel margins (primarily for cast and
(1) Preparation wall configurationshape, height, composite restorations).
form. (5) Pins, slot, steps, amalgam pins (primarily for
4. Convenience form. amalgam restorations).
a. Alterations to improve access and visibility for pre- b. Bonding.
paring and restoring the cavity. c. Cement (for cast restorations).
B. Final tooth preparationcompleting the tooth 3. Finishing the external walls.
preparation. a. Definitionestablishing the design and smooth-
1. Removing remaining caries. ness of the cavosurface margin.
a. Objectiveremove all microorganisms (infected b. Objectives.
dentin). (1) Best seal between tooth and material.
(1) Initial preparation may remove all caries. (2) Smooth junction between tooth and material.
(2) Deep excavation, questionable dentin near (3) Maximum strength for tooth and material.
pulp (indication for indirect pulp cap). c. Features.
(a) Leave last bit of leathery carious dentin, (1) Bevels.
place reinforced glass-ionomer as caries- (2) Butt joints.
control restoration. d. Considerations.
(b) May or may not use calcium hydroxide (1) Direction of enamel rods.
liner. (2) Support of enamel rods.
(c) May or may not reenter to reexcavate (3) Type of material.
after 6 to 8 weeks (note: evidence is (4) Location of margin.
controversial). (5) Degree of smoothness desired.
(d) After follow-up period (approximately 4. Final procedurescleaning, inspecting, sealing, and
6 to 8 weeks), restore with definitive applying surface treatments.
restoration. a. Readying the preparation for the material.
(3) Pulpal communication (exposure)indica- b. Removing any debris.
tions for direct pulp cap. c. Sealing or bonding.
(a) Small mechanical (noncarious) exposure
(<1mm). 4.3 Moisture Control
(b) Asymptomatic tooth. A. Isolation of the operating fieldthe goals of operating
(c) Isolated area. field isolation are the following.
(d) Hemorrhage controlled. 1. Moisture controlmoisture control refers to exclud-
(e) Use calcium hydroxide for reparative ing sulcular fluid, saliva, and gingival bleeding from
dentin. the operating field. It also refers to preventing the
(f) Place resin-modified glass ionomer (RMGI) handpiece spray and restorative debris from being
base over liner. swallowed or aspirated by the patient. The rubber
(g) Remove coronal portion of exposed pulpal dam, suction devices, and absorbents have variable
tissue in pulp chamber, and place calcium effectiveness in moisture control.
hydroxide liner and RMGI base. 2. Retraction and accessthe rubber dam, high-volume
(4) Endodontic treatment (root canal) evacuator, absorbents, retraction cord, and mouth
indications. prop are used for retraction and access.
(a) Large and carious exposure (>1mm). 3. Harm preventionprevention from harm is pro-
(b) Symptomatic tooth. vided as much by the manner in which these devices
(c) Area contaminated (saliva, debris). are used as by the devices themselves.
(d) Purulent exudate. 4. Local anesthesialocal anesthetics play a role in
2. Secondary resistance and retention formssecondary eliminating the discomfort of dental treatment and
resistance and retention forms may be performed controlling moisture.
after placement of liners and bases (see Section 5.1, B. Rubber damthe rubber dam is used to define the
Sealers, Liners, and Bases). operating field by isolating one or more teeth from
a. Mechanical or preparation features. the oral environment. The dam eliminates saliva from
(1) Retentive locks, grooves, coves (primarily for the operating site and retracts the soft tissue. Also,
metallic restorations). there are fewer interruptions to replace cotton rolls to
maintain isolation. When excavating a deep carious (2) A preoperative assessment of the occlusion also
lesion and risking pulpal exposure, use of the rubber should be made. This step should occur before
dam is strongly recommended to prevent pulpal con- rubber dam placement and should identify not
tamination from oral fluids. only the occlusal contacts of the tooth to be
1. Advantages. restored but also the contacts on opposing and
a. Increased access and visibility. adjacent teeth. For smaller amalgam restora-
b. Isolates area. tions, the projected facial and lingual exten-
c. Keeps area dry. sions of a proximal box should be visualized
d. Protects patient and operator. before preparing the occlusal portion of the
e. Retracts soft tissue. tooth, reducing the chance of overpreparing
f. Preserves and protects materials. the cuspal area, while maintaining a butt joint
2. Disadvantages. form of the facial or lingual proximal margins.
a. Some patients object. d. Requirementsas noted previously, appropriate
b. Some situations do not work. tooth preparation (Figure 2-17) for an amalgam
c. Partially erupted teeth. restoration depends on both tooth and material
d. Extremely malpositioned teeth. factors.
C. Cotton roll isolation and cellulose wafers. (1) 90-degree or greater amalgam margin (butt
1. Absorbents, such as cotton rolls and cellulose wafers, joint form).
can also provide isolation. Absorbents are isolation (2) Adequate depth (thickness of amalgam).
alternatives when rubber dam application is not (3) Adequate mechanical retention form (under-
used and when absorbents can be as effective as cut form).
rubber dam isolation. In conjunction with profound e. Principles of tooth preparation.
anesthesia, absorbents provide acceptable moisture (1) Initial stage.
control for most clinical procedures. Using a saliva (a) Place the tooth preparation extension into
ejector in conjunction with absorbents may abate sound tooth structure at the marginal areas
salivary flow further. (not pulpally or axially).
D. Other isolation devices.
1. Numerous new and innovative isolation devices have
been introduced more recently, some of them incor-
porating illumination and suction capabilities to the
usual cheek or tongue retraction.
90-degree
4.4 Tooth Preparation for cavosurface
margins
Amalgam Restorations DEJ
A. Clinical technique.
1. Initial clinical proceduresa complete examination,
diagnosis, and treatment plan must be finalized
before the patient is scheduled for operative appoint- A
ments (emergencies are an exception). A brief review
of the chart (including medical factors), treatment Pulpal floor
plan, and radiographs should precede each restor-
ative procedure. At the beginning of each appoint-
ment, the dentist should also examine the operating
site carefully and assess the occlusion, particularly of
the tooth or teeth scheduled for treatment.
a. Local anesthesia (when needed).
b. Isolation of the operating siteisolation for
amalgam restorations can be accomplished with a
rubber dam or cotton rolls. Retention
c. Other preoperative considerations. B lock
(1) A wedge placed preoperatively in the gingival Figure 2-17 A and B, Diagrams of class II amalgam tooth
embrasure is useful when restoring a posterior preparations illustrating uniform pulpal and axial wall depths,
proximal surface. This step causes separation of 90-degree cavosurface margins, and convergence of walls or pre-
the operated tooth from the adjacent tooth and pared retention form or both. DEJ, Dentinoenamel junction.
may help protect the rubber dam and the inter- (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and
dental papilla. Science of Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
1.5 mm
3 mm
0.8 mm
A B C
Figure 2-18 Pulpal floor depth. A, Pulpal depth measured from central groove. B, No. 245 bur dimensions. C, Guides to proper
pulpal floor depth: (1) one half the length of the No. 245 bur, (2) 1.5mm, or (3) 0.2mm inside (internal to) dentinoenamel junction.
(From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
(b) Extend the depth (pulpally or axially or axial depths on the root surface should be 0.75 to
both) to a prescribed, uniform dimension. 1mm deep, providing room for a retention groove
(c) Provide an initial form that retains the or cove, while providing for adequate thickness of
amalgam in the tooth. the amalgam (Figure 2-18).
(d) Establish the tooth preparation margins in g. Outline formthe initial extension of the tooth
a form that results in a 90-degree amalgam preparation should be visualized preoperatively by
margin when the amalgam is inserted. estimating the extent of the defect, the preparation
(2) The final stage of tooth preparation removes form requirements of the amalgam, and the need
any remaining defect (caries or old restorative for adequate access to place the amalgam into the
material) and incorporates any additional tooth. Otherwise, the enamel is subject to fracture.
preparation features (slots, pins, steps, or For enamel strength, the marginal enamel rods
amalgam pins) to achieve appropriate retention should be supported by sound dentin.
and resistance form. (1) When making the preparation extensions,
f. Initial tooth preparation depthall initial depths every effort should be made to preserve the
of a tooth preparation for amalgam relate to the strength of cusps and marginal ridges. When
DEJ except when the occlusal enamel has been possible, the outline form should be extended
significantly worn thinner and when the prepara- around cusps and avoid undermining the den-
tion extends onto the root surface. The initial tinal support of the marginal ridge enamel.
depth pulpally is 0.2mm inside (internal to) the (2) When viewed from the occlusal, the facial and
DEJ or 1.5mm as measured from the depth of the lingual proximal cavosurface margins of a class
central groovewhichever results in the greatest II preparation should be 90 degrees (i.e., per-
thickness of amalgam. The initial depth of the axial pendicular to a tangent drawn through the
wall form is 0.2mm inside the DEJ when retention point of extension facially and lingually). In
locks are not used and 0.5mm inside the DEJ most instances, the facial and lingual proximal
when retention locks are used. The deeper exten- walls should be extended just into the facial or
sion allows placement of the retention locks lingual embrasure. This extension provides
without undermining marginal enamel. However, adequate access for performing the preparation
(3) Factors dictating outline form include caries,

old restorative material, inclusion of the entire
defect, proximal or occlusal contact relation-
ship, and need for convenience form.
h. Cavosurface marginif either enamel or amalgam
has marginal angles less than 90 degrees, they
are subject to fracture because both are brittle
structures.
A i. Primary retention formretention form prepara-
tion features lock or retain the restorative material
in the tooth. Amalgam retention form is provided
by the following.
(1) Mechanical locking of the inserted amalgam
into surface irregularities of the preparation
(even though the desired texture of the prepa-
ration walls is smooth) to allow good adapta-
tion of the amalgam to the tooth.
90 (2) Preparation of vertical walls (especially facial
and lingual walls) that converge occlusally.
(3) Special retention features, such as locks,
grooves, coves, slots, pins, steps, or amalgam
pins, that are placed during the final stage of
tooth preparationthe first two of these are
B considered primary retention form features
and are provided by the orientation and type of
the preparation instrument. The third is a sec-
ondary retention form feature and is discussed
in a subsequent section. An inverted cone
carbide bur (No. 245) provides the desired wall
shape and texture.
j. Primary resistance formresistance form prepa-
ration features help the restoration and tooth resist
90
fracturing as a result of occlusal forces.
Amalgam (1) Resistance features that assist in preventing the
tooth from fracturing.
(a) Maintaining as much unprepared tooth
structure as possible (preserving cusps and
marginal ridges).
C (b) Having pulpal and gingival walls prepared
Figure 2-19 Proximal cavosurface margins. A, Facial and perpendicular to occlusal forces, when
lingual proximal cavosurface margins prepared at 90-degree possible.
angles to a tangent drawn through the point on the external tooth (c) Having rounded internal preparation
surface. B, A 90-degree proximal cavosurface margin produces a angles.
90-degree amalgam margin. C, 90-degree amalgam margins. (d) Removing unsupported or weakened tooth
(From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and structure.
Science of Operative Dentistry, ed 6. St. Louis, Mosby, 2013.) (e) Placing pins into the tooth as part of the
final stage of tooth preparation (note: this
(with decreased potential to mar the adjacent strategy is considered a secondary resis-
tooth), easier placement of the matrix band, tance form feature).
and easier condensation and carving of the (2) Resistance form features that assist in prevent-
amalgam. Such extension provides clearance ing the amalgam from fracturing.
between the cavosurface margin and the adja- (a) Adequate thickness of amalgam (1.5 to
cent tooth. For the more experienced operator, 2mm in areas of occlusal contact and
extending the proximal margins beyond the 0.75mm in axial areas).
proximal contact into the respective embrasure (b) Marginal amalgam of 90 degrees or
is not always necessary (Figure 2-19). greater.
Retention
lock
b>a
a
DEJ b
Axial Pulpal
wall floor
A B A B
Figure 2-20 Axial wall depth. A, If no retention grooves
needed, axial depth 0.2mm inside (internal to) dentinoenamel
Retention
junction (DEJ). B, If retention grooves needed, axial depth 0.5mm lock
inside (internal to) DEJ. (From Heymann HO, Swift EJ, Ritter AV:
Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis,
Mosby, 2013.)
DEJ
(c) Boxlike preparation form, which provides

uniform amalgam thickness.
(d) Rounded axiopulpal line angles in class II C
tooth preparations. Figure 2-21 Typical amalgam tooth preparation retention
(3) Many of these resistance form features can be form features. A and B, Occlusal convergence of prepared walls
achieved using the No. 245 bur, which is an (primary retention form). C, Retention grooves in proximal box
inverted cone design with rounded corners. (secondary retention form). DEJ, Dentinoenamel junction. (From
k. Convenience formconvenience form prepara- Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and Science of
tion features are features that make the procedure Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
easier or the area more accessible. Convenience
form may include arbitrary extension of the outline
form so that marginal form can be established;
caries can be accessed for removal; matrix can be from all angles. Careful assessment should be per-
placed; or amalgam can be inserted, carved, and formed to ensure that all caries has been removed,
finished. Convenience form features also may depths are proper, margins provide for the correct
include extending the proximal margins to provide amalgam and tooth preparation angles, and the
clearance from the adjacent tooth and extension tooth is cleaned of any residual debris.
of other walls to provide greater access for caries
excavation. 4.5 Tooth Preparation for
l. Removal of remaining fault and pulp protection Composite Restorations
if caries or old restorative material remains after A. Clinical technique.
the initial preparation, it should be located only in 1. Preliminary considerations.
the axial or pulpal walls (the extension of the a. Occlusion assessment of both operated and adja-
peripheral preparation margins should have cent teeth.
already been to sound tooth structure). b. Clean tooth with flour of pumice (only if no tooth
m. Secondary resistance and retention formif it is preparation is done).
determined (based on clinical judgment) that in- c. Select shade (before teeth are dried).
sufficient retention or resistance forms are present (1) Shade tab.
in the tooth preparation, additional preparation is (2) Place composite on tooth surface, cure, and
indicated. Many features that enhance retention then remove.
form also enhance resistance form. Such features d. Area isolation (rubber dam or cotton roll-retraction
include the placement of grooves, locks, coves, cord).
pins, slots, or amalgam pins. Usually, the larger the 2. Tooth preparation.
tooth preparation, the greater the need for second- a. General considerations.
ary resistance and retention forms (Figures 2-20 (1) Include all faults.
and 2-21). (2) Remove most weakened tooth structure (friable
n. Final proceduresafter the previous steps are per- enamel).
formed, the tooth preparation should be viewed (3) Pulp protection (if needed).
(4) Minimal mechanical retention needed except (1) Maintain preparation form of restoration.
in the following cases. (2) Bevel or roughen enamel (coarse diamond).
(a) No enamel (root surface, need more (3) May need to place retention if on root ( 1 4 round
retention). bur used to make cove).
(b) Large restoration (need more retention). d. Modifiedinitial preparations (Figure 2-23).
(5) Roughen enamel (or place bevel, only on facial, (1) Fault dictates outline form.
visible margins). (2) Remove only fault, scooped out.
(a) Bevel, usually 0.5mm wide and at 45 (3) Roughen or bevel enamel.
degrees. (4) Etch enamel.
(b) Coarse diamond. (5) Etch and prime dentin.
(c) Increased surface area = increased e. Controversial or new approaches.
retention. (1) Box-only preparations.
(6) Floors prepared perpendicular to long axis of (2) Tunnel preparations (not recommended).
tooth when concerned about resistance form or (3) Sandwich technique.
have large preparation. (4) Bonding a weakened tooth.
b. Conventionalroot surface preparations. (a) Arbitrary extension of grooves or walls.
(1) Remove fault. (b) Arbitrarily leaving weakened tooth
(2) Roughen or bevel enamel (if available). structure.
(3) Nonenamel areas. (c) These features may help in increasing
(a) 90-degree margins. the strength of the remaining weakened
(b) Mechanical retention. tooth structure because of the microme-
c. Beveled conventionalreplacement preparations chanical bond of the material reinforcing
(Figure 2-22). the tooth.
A B C D
E F
Figure 2-22 Larger preparation designs for class III (A and B), class IV (C and D), and class V (E and F) restorations. (From Heymann
HO, Swift EJ, Ritter AV: Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
A B C D
E F
Figure 2-23 Preparation designs for class III (A and B), class IV (C and D), and class V (E and F) initial composite restorations
(primary caries). (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis, Mosby,
2013.)
5.0 Restoration of Teeth chlorhexidine, or other desensitizers. Historically,

copal varnish was used as a liner under amalgam
Outline of Review restorations.
5.1 Sealers, Liners, and Bases B. Liners.
5.2 Amalgam Restorations 1. Liners are thin layers of material used primarily to
5.3 Enamel and Dentin Bonding provide a barrier to protect the dentin from residual
5.4 Composite Restorations reactants diffusing out of a restoration, from oral
5.5 Gold Inlay and Onlay Restorations fluids, or from both, which may penetrate leaky
tooth-restoration interfaces.
5.1 Sealers, Liners, and Bases 2. Liners also contribute initial electrical insulation;
A. Sealers. generate some thermal protection; and, in some for-
1. Occlusion of the dentinal tubules limits the potential mulations, provide pulpal treatment.
for tubular fluid movement and resultant sensitivity. 3. Liners are used to cover a direct or near pulpal expo-
2. Sealers (also referred to as desensitizers) are effective sure and to line very deep areas of a tooth preparation
disinfectants, provide cross-linking of any exposed in vital teeth.
dentin matrix and occlude (plug) dentinal tubules 4. Calcium hydroxide and RMGI are examples of typical
by cross-linking tubular proteins. liners used with direct restorations.
3. Sealers are typically aqueous solutions. C. Bases.
4. Some sealers may contain glutaraldehyde, hydroxy- 1. Bases (cement bases, typically 1 to 2mm) are used to
ethylmethacrylate (HEMA), benzalkonium chloride, provide thermal protection for the pulp and to
supplement mechanical support for the restoration b. Use a thin (0.5 to 0.75mm) layer of calcium
by distributing local stresses from the restoration hydroxide liner placed on the suspected exposure
across the underlying dentin surface. site followed by RMGI base and the proper appli-
2. Additional bulk (from the base) affords mechanical cation of a bonding agent along with the composite
and thermal protection to the pulp under metal restorative material.
(amalgam or gold) restorations. c. The objective is to prevent bacterial infiltration,
3. RMGI or conventional glass-ionomer cement is rec- while avoiding dissolution of the liner.
ommended as a base to overlay any calcium hydrox- F. Use with indirect restorations (gold, ceramic, processed
ide liner that has been placed. composite).
4. RMGI or conventional glass-ionomer cement base 1. Shallow excavations.
provides additional strength to resist amalgam con- a. RDT judged to be 2mm or more.
densation pressure as well as protection of the liner b. No sealer, liner, or base is needed.
from dissolution during bonded procedures. c. RMGI cement or a resin-based cement may be
D. Use with amalgam restorations. used for cementation, providing excellent dentinal
1. Shallow excavations. sealing.
a. Remaining dentin thickness (RDT) is 2mm 2. Moderately deep excavations.
or more. a. RDT judged to be 0.5 to 2mm.
b. Use a dentin sealer/desensitizing agent such as b. RMGI or conventional glass-ionomer cement may
Gluma Desensitizer or G5. Sealers/desensitizers be used to restore axial or pulpal wall contour and
replace the traditional use of copal varnish. to ensure an adequate thermal barrier.
2. Moderately deep excavations. c. The objective is to provide approximately 2mm
a. RDT is judged to be 0.5 to 2mm. of insulation between the restorative material and
b. Use a light-cured RMGI base, followed by a dentin the pulp.
sealer/desensitizing agent. d. The shallower the excavation, the less thickness of
c. The objective of the base application is to provide RMGI base is required.
approximately 2mm of insulation between the e. RMGI or resin-based material is recommended for
restorative material and the pulp. The shallower cementation.
the excavation, the less thickness of RMGI base is 3. Deep excavations.
required. This replaces the traditional approach of a. Noncarious (mechanical) pulpal exposure less
using a zinc oxideeugenol base material followed than 1.0mm in diameter or excavations where
by a copal varnish. RDT is judged to be less than 0.5mm such that a
3. Deep excavations. microexposure of the pulp is suspected.
a. Noncarious (mechanical) pulpal exposure less b. Use thin (0.5 to 0.75mm) layer of calcium hydrox-
than 1.0mm in diameter or excavations where the ide liner on the suspected exposure site followed
RDT is judged to be less than 0.5mm such that a by RMGI base to restore axial or pulpal wall
microexposure of the pulp is suspected. contour, ensure an adequate thermal barrier, and
b. Use a thin (0.5 to 0.75mm) layer of calcium seal the exposure site.
hydroxide liner on the suspected exposure site fol- c. The objective is to prevent bacterial infiltration,
lowed by RMGI base to seal the immediate site of while avoiding the base from dissolution.
the exposure. d. In these cases, given the much higher cost of
c. The objectives are to prohibit bacterial infiltration the indirect restoration compared with a direct
and protect the liner from dissolution. amalgam or composite restoration and the risk of
d. A dentin sealer/desensitizing agent or, if the endodontic complications secondary to the pulp
operator chooses, an appropriate amalgam bond- exposure, strong consideration should be given to
ing agent is placed on the remaining dentin. performing endodontic therapy before completion
E. Use with composite restorations. of the indirect restoration.
1. Shallow to moderately deep excavations. e. Occasionally, it may be deemed more efficient sim-
a. RDT is judged to be 0.5mm or more. ply to block out the excavated area on the die dur-
b. No liner or base material is indicated. ing laboratory procedures, allowing the cement to
c. Only a dentin bonding system along with the com- fill in the area of excavation during cementation.
posite restorative material is needed.
2. Deep excavations. 5.2 Amalgam Restorations
a. Noncarious (mechanical) pulpal exposure less A. Introduction.
than 1.0mm in diameter or excavations where the 1. Types.
RDT is judged to be less than 0.5mm such that a a. Low coppergenerally inferior, seldom used.
microexposure of the pulp is suspected. b. High copper.
(1) Spherical. c. There is no evidence ensuring that alternative

(a) Greater leakage. materials pose a lesser health hazard.
(b) Greater postoperative sensitivity. d. True allergies to amalgam rarely have been reported
(2) Admix. (50 cases since 1900).
2. Properties. e. Estimate of human uptake of mercury vapor from
a. The linear coefficient of thermal expansion of amalgams is 5g/m3.
amalgam is greater than that of tooth structure. 9. Requirements for a successful amalgam restoration.
b. The compressive strength of high-copper amalgam a. Appropriately indicated clinical situation.
is similar to tooth structure. b. High-copper material.
c. The tensile strength of high-copper amalgam is c. Adequate tooth preparation.
lower than tooth structure. d. 90-degree cavosurface margins.
d. Amalgams are brittle and have low edge strength. e. Thickness of amalgam (1 to 2mm).
e. High-copper amalgams exhibit no clinically rele- f. Mechanical retention form.
vant creep or flow. g. Seal dentinal tubules.
f. Amalgam is a high thermal conductor. h. Good condensation (including lateral conden
3. Clinical performance. sation).
a. Marginal fracture. i. Appropriate development of contours and con-
b. Bulk fracture. tacts.
c. Secondary caries. B. Restorative techniqueafter the tooth preparation for
4. Handling. most amalgam restorations, a sealer is placed on the
a. Operator preference regarding using admix or prepared dentin before amalgam insertion to occlude
spherical alloys. the dentinal tubules. This step may occur before or after
b. Mercury hygienevery important as described the matrix application.
subsequently. 1. Matrix placementa matrix primarily is used when
5. Uses. a proximal surface is to be restored.
a. Nonesthetic cervical lesions. a. The objectives of a matrix are the following.
b. Large class I and II preparations where heavy (1) Provide proper contact.
occlusion would be on the material. (2) Provide proper contour.
c. Class I and II preparations where isolation prob- (3) Confine the restorative material.
lems exist for bonding. (4) Reduce the amount of excess material.
d. Temporary or caries-control restorations. b. For a matrix to be effective, it should have the fol-
e. Foundations. lowing characteristics.
f. Patient sensitivity to other materials. (1) Be easy to apply and remove.
g. Where cost is a factor. (2) Extend below the gingival margin.
h. Inability to do a good composite. (3) Extend above the marginal ridge height.
6. Advantages. (4) Resist deformation during material insertion.
a. Strength. c. The matrix should be stabilized with a wooden
b. Wear resistance. wedge to close any gaps that may develop between
c. Easy to use. the matrix band and the gingival margin of the
d. Less technique-sensitive. preparation and to provide stability to the matrix
e. Self-sealing margins over time. during the condensation and initial carving of the
f. History of use. restoration. Care should be exercised to place the
g. Lower fee. wedge securely apical to the gingival margin of
h. Long-term clinical longevity. the preparation, not to push the matrix band into
7. Disadvantages. the tooth preparation area resulting in undercon-
a. Not esthetic. tour of the restoration (Figure 2-24).
b. Conductivity. 2. Mixing (triturating) the amalgam materialthe
c. Tooth preparation more demanding, less manufacturers directions should be followed when
conservative. mixing the amalgam material. Both the speed and the
8. Mercury controversy. time of mix are factors in the setting reaction of the
a. There is a lack of scientific evidence that amalgam material; alterations in either may cause changes in
poses health risks to humans except for rare aller- the properties of the inserted amalgam.
gic reactions. 3. Inserting the amalgam.
b. Efforts are under way to reduce the environmental a. Proper condensation is very important to
mercury to which people are exposed to lessen ensure confluence of the amalgam with the
their total mercury exposure. margins.
Incorrect
A B
Figure 2-24 A, Correct wedge position. B, Incorrect wedge positions. (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and
Science of Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
instrument, the instrument is switched, and the

Discoid-cleoid discoid end is used to smooth out the anatomic
form. A small Hollenbeck carver also can be
used to carve amalgam restorations. The amal-
gam is not deeply carved; some semblance of
pits and grooves is necessary to provide appro-
Amalgam priate sluiceways for the escape of food from
the occlusal table.
(2) It may be beneficial to ensure that the mesial
and distal pits are carved to be inferior to the
marginal ridge height, helping prevent food
from being wedged into the occlusal embra-
sure. Having definite but rounded occlusal
anatomy also helps provide sluiceways for the
Figure 2-25 Carving occlusal margins. (From Heymann escape of food from the occlusal table. For large
HO, Swift EJ, Ritter AV: Sturdevants Art and Science of Operative class II or foundation restorations, the initial
Dentistry, ed 6. St. Louis, Mosby, 2013.) carving of the occlusal surface should be rapid,
concentrating primarily on the marginal ridge
height and occlusal embrasure areas. These
b. Spherical amalgam is more easily condensed than areas are developed with an explorer tip or
admixed (lathe-cut) amalgam. carving instrument by mimicking the adjacent
c. As a general rule, use smaller amalgam condensers tooth. The explorer tip is pulled along the
first. This allows the amalgam to be properly con- inside of the matrix band, creating the occlusal
densed into the internal line angles and secondary embrasure form. When viewed from the facial
retention features. Subsequently, larger condensers or lingual, the created embrasure form should
are used. be identical to that of the adjacent tooth,
d. Place amalgam to slight excess with condensers. assuming the adjacent tooth has appropriate
e. Precarve burnish with a large, egg-shaped bur- contour. Likewise, the height of the amalgam
nisher to finalize the condensation, remove excess marginal ridge should be the same as that of
mercury, and initiate the carving process. the adjacent tooth. If both of these areas are
4. Carving the amalgamwhen precarve burnishing developed properly, the potential for fracture of
has been done, the remainder of the accessible resto- the marginal ridge area of the restoration is
ration must be contoured to achieve proper form and significantly reduced.
function. (3) When the initial occlusal carving has occurred,
a. Occlusal areas. the matrix is removed to provide access to
(1) A discoid-cleoid instrument is used to carve the other areas of the restoration that require
the occlusal surface of an amalgam restoration. carving.
The rounded end (discoid) is positioned on the b. Facial and lingual areasmost facial and lingual
unprepared enamel adjacent to the amalgam areas are accessible and can be carved directly after
margin and pulled parallel to the margin the matrix band and wedge have been removed. A
(Figure 2-25). When the pit and groove Hollenbeck carver is useful in carving these areas.
anatomy is initiated with the cleoid end of the The base of the amalgam knife (scaler 34/35) is also
and exerting pressure on that tooth rather than

the restored tooth, while moving the floss
through the contact area. Once the floss is into
the gingival embrasure area, it is wrapped
Blade around the restored tooth and moved occlus-
ally and gingivally both to determine whether
Excess
excess exists and to smooth the proximal

amalgam material. If excess material is felt
along the gingival margin, the amalgam knife
should be used again until a smooth margin is
obtained.
5. Finishing the amalgam restorationwhen the carv-
Figure 2-26 Gingival excess may be removed with ing is completed, the restoration is visualized from all
amalgam knives. (From Heymann HO, Swift EJ, Ritter AV: Stur- angles, and an assessment of the thoroughness of the
devants Art and Science of Operative Dentistry, ed 6. St. Louis, carving is made. If spacing is seen between the adja-
Mosby, 2013.) cent teeth and their opposing teeth, the area of pre-
mature occlusal contact on the amalgam should be
appropriate. For cervical areas, it is important to identified and relieved. Articulating paper is used to
remove any excess and develop the proper contour adjust the contacts more precisely until the proper
of the restoration. Usually, the contour is convex; occlusal relationship is generated. After the occlusion
care in carving this area is necessary. The convexity is adjusted, the discoid-cleoid can be used to smooth
is developed by using both the occlusal and the the accessible areas of the amalgam. A lightly moist-
gingival unprepared tooth structure adjacent to the ened cotton pellet held in the operative pliers can be
preparation as guides for initiating the carving. used to smooth the accessible parts of the restoration.
The marginal areas are blended, resulting in the If the carving and smoothing are done properly, no
desired convexity and providing the physiologic subsequent polishing of the restoration is needed,
contour that promotes good gingival health. and good long-term clinical performance results.
c. Proximal embrasure areas. 6. Repairing an amalgam restorationif an amalgam
(1) The development of the occlusal embrasure restoration fractures during insertion, the defective
already has been described. The amalgam knife area must be prepared again as if it were a small
(or scaler) is an excellent instrument for remov- restoration. Appropriate depth and retention form
ing proximal excess and developing proximal must be generated, sometimes entirely within the
contours and embrasures (Figure 2-26). The existing amalgam restoration. If necessary, another
knife is positioned below the gingival margin, matrix must be placed. A new mix of amalgam can
and excess is carefully shaved away. The knife be condensed directly into the defect and adheres to
is drawn occlusally to refine the proximal the amalgam already present if no intermediary
contour (below the contact) and the gingival material has been placed between the two amalgams.
embrasure form. The sharp tip of the knife also The sealer material can be placed on any exposed
is beneficial in developing the facial and lingual dentin, but it should not be placed on the amalgam
embrasure forms. Care must be used to prevent preparation walls.
carving away any of the desired proximal C. Common problemscauses and potential solutions.
contact. If the amalgam is hardening, the 1. Following is a list of common problems associated
amalgam knife must be used to shave, rather with amalgam restorations. Subsequent technique
than cut, the excess away. If a cutting motion is chapters may refer back to these problems.
used, the possibility of breaking or chipping the a. Postoperative sensitivitycauses.
amalgam is increased. (1) Lack of adequate condensation, especially
(2) The proximal portion of the carved amalgam lateral condensation in the proximal boxes.
can be evaluated by visual assessment (reflect- (2) Lack of proper dentinal sealing with sealer or
ing light into the contact area to confirm a pulp protection.
proximal contact) and placement of dental floss b. Marginal voidscauses.
into the area. If dental floss is used, it must be (1) Inadequate condensation.
used judiciously, ensuring that the contact area (2) Material pulling away or breaking from the
is not inadvertently removed. A piece of floss marginal area when carving bonded amalgam.
can be inserted through the contact and c. Marginal ridge fracturescauses.
into the gingival embrasure area by initially (1) Axiopulpal line angle not rounded in class II
wrapping the floss around the adjacent tooth tooth preparations.
(2) Marginal ridge left too high. a. Less microleakage.

(3) Occlusal embrasure form incorrect. b. Less marginal staining.
(4) Improper removal of matrix. c. Less recurrent caries.
(5) Overzealous carving. d. Less pulpal sensitivity.
d. Amalgam scrap and mercury collection and dis- e. More conservative tooth preparation.
posal problemscauses. f. Improved retention.
(1) Careless handling. g. Reinforcement of remaining tooth structure.
(2) Inappropriate collection technique. h. Reduced sensitivity in noncarious cervical
2. Potential solutions. lesions.
a. Careful attention to proper collection and i. More conservative treatment of root-surface
disposal. carious lesions.
b. Following the Best Management Practices for 2. Uses of adhesive techniques.
Amalgam Waste as presented by the American a. Change shape and color of anterior teeth.
Dental Association (available at www.ada.org). b. Restore class I, II, III, IV, V, and VI lesions.
D. Controversial issuesbecause the practice of operative c. Improve retention for metallic or porcelain fused
dentistry is dynamic, constant changes are occurring. to metal crowns.
As new products and techniques are developed, their d. Bond ceramic restorations.
effectiveness cannot be assessed until appropriately e. Bond indirect composite restorations.
designed research protocols have tested their worth. f. Seal pits and fissures.
Many such developments are occurring at any time, g. Bond orthodontic brackets.
many of which do not have the necessary documenta- h. Bond periodontal splints.
tion to prove their effectiveness, even though they i. Bond conservative tooth-replacement restorations.
receive very positive publicity. Several examples of such j. Repair existing restorations (composite, amalgam,
controversies follow. ceramic, metal).
1. Amalgam restoration safetyamalgam restorations k. Provide foundations for crowns or onlays.
are safe. The U.S. Public Health Service has reported l. Desensitize exposed root surfaces.
the safety of amalgam restorations. Even recognizing m. Impregnate dentin and enamel to make them less
these assessments, the mercury contained in current susceptible to caries.
amalgam restorations still causes concerns, both n. Bond fragments of anterior teeth.
legitimate and otherwise. Proper handling of mercury o. Bond prefabricated and cast posts.
during mixing of the amalgam material, condensing p. Reinforce remaining enamel and dentin after tooth
and carving of the amalgam restoration, removal of preparation. Reinforcement of remaining tooth
old amalgam restorations, and amalgam scrap dis- structure by bonding is believed to be temporary.
posal is very important. 3. Status of bonding to tooth structure.
2. Spherical or admixed amalgamspherical materials a. Enamel bonding.
have advantages in providing higher earlier strength (1) 10- to 15-second acid etch (with 30% to 40%
and permitting the use of less pressure. Admixed phosphoric acid) is sufficient to etch enamel.
materials permit easier proximal contact develop- (2) Is fast, reliable, predictable, and strong.
ment because of higher condensation forces. (3) Microleakage is virtually nonexistent at etched
3. Bonded amalgam restorationsbonded amalgam enamel margins.
restorations are no longer recommended, even (4) Resists polymerization shrinkage forces of
though some operators may select them for large res- composite.
torations. If bonding an amalgam, the use of typical b. Dentin bonding.
secondary retention form preparation features (e.g., (1) Is accomplished with either etch-and-rinse
grooves, locks, pins, slots) is still required. Small to (simultaneous with enamel etch) or self-etch
moderate amalgam restorations should not be (with a self-etching primer or all-in-one adhe-
bonded. sive) techniques.
4. Proximal retention locksproximal retention locks (2) Is less reliable, less durable, and not as predict-
for large amalgam restorations may be beneficial, able as enamel bonding.
although their use for smaller restorations is not (3) May have some microleakage, especially after
deemed necessary. Correct placement of proximal aging of the restoration.
retention locks is difficult. (4) May have similar or higher bond strengths than
enamel.
5.3 Enamel and Dentin Bonding (5) May not resist polymerization shrinkage forces.
A. Introduction. 4. Factors that affect the ability to bond to dentin versus
1. Advantages of bonding to the tooth structure. enamel.
a. Microstructural features of enamel and dentin. a. Etch-and-rinse three-step systems, also known as
(1) Composition. multibottle or fourth-generation systems (etchant,
(a) Enamel90% mineral (hydroxyapatite). primer, adhesive)1990s.
(b) Dentinmuch less mineral, more organic (1) General considerationsthese remain the gold
(type I collagen), and more water. standard.
(2) Structural variations. (a) How the systems work.
(a) Enamel prisms and interprismatic areas (i) The tooth structure is etched with an
all etched and bondable. acid to demineralize enamel and dentin
(3) Dentin-tubulesperitubular, intratubular, and selectively, increase the surface area,
intertubular channels. and clean the surface of debris. Etched
(a) Tubules from pulp to DEJ. enamel appears chalky; dentin does not.
(b) Contain the odontoblastic extensions and Etched dentin exposes a layer of colla-
fluid. gen. The primer serves to increase the
(c) Much larger (2.4m) and numerous collagen, and the adhesive flows between
(45,000/mm2) near pulp than near DEJ the collagen and interlocks with it to
(0.6m, 20,000/mm2). form a sandwich or hybrid or resin-
(d) Fluid movement inside that is dictated by reinforced layer.
pulpal pressure. (b) Most bond strength is from the formation
(e) Sclerosisdentin that is aging, below a of the hybrid layer. The surface layer is only
caries lesion, or exposed to oral fluids a few microns thick, creating a demineral-
exhibits increased mineral content and is ized layer of dentin intermingled with resin.
much more resistant to acid-etching, and (c) Seals the dentindecreases postoperative
the penetration of dentin adhesive is sensitivity.
limited. (d) Good dentin bonding strengthssame or
(f) Smear layerthe debris left on the surface better than enamel bond (note: must have
after cutting and consists of hydroxyapatite bond strength of 17 to 21MPa to resist
and altered denatured collagen and fills polymerization contraction force of
the orifices of the tubules (forming smear composite).
plugs), decreasing dentin permeability by (2) Steps.
86%. Etching that removes the smear layer (a) Etch enamel and dentin for 10 to 15 seconds.
results in greater fluid flow onto the den- (i) Etches enamel.
tinal surface, which may interfere with (ii) Removes smear layer.
adhesion. (iii) Opens and widens dentin tubules.
(g) Linear coefficient of thermal expansion (iv) Demineralizes dentin surface.
for dentin, is altered four times less than (v) Etches out mineral (hydroxyapatite)
the composite material when subjected to but leaves collagen fibrils (these have
thermal changes. low surface energy).
b. Material factorscomposites shrink as they (b) Rinse well and leave moist or rewet (Aqua
polymerize, creating stresses up to 7 megapascals Prep or Gluma Desensitizer).
(1MPa = 150lb/in2). (c) Apply two to three layers of primer HEMA/
c. Preparation factorspreparations with multiple biphenyl dimethacrylate.
walls or boxlike shapes (configuration) have (i) Resin monomer wetting agent.
limited stress relief opportunity for the composite (ii) Dissolved in acetone, ethanol, and
material (polymerization shrinkage), and the high water.
configuration factor (C-factor) may result in inter- (iii) Bifunctionalwets dentin (increases
nal bond disruption and marginal gaps. the surface tension) and bonds to over-
(1) C-factor is determined by the ratio of prepared lying resin.
(bonded) versus unprepared (unbonded) walls (iv) Acts as a solvent.
within a tooth preparation. (d) Apply adhesive (bonding agent)bisphe-
(2) High C-factor may indicate increased chance nol A-glycidyl methacrylate or other
for postoperative sensitivity. methacrylate.
B. Current adhesive systems used for bonding. (i) May also contain HEMA or other
1. Etch-and-rinse, previously called total-etch (etch primer constituents to enhance
enamel and dentin)this concept advocated the bonding.
etching of dentin with acids along with the etching (ii) Penetrates primed intertubular dentin
of enamel. and tubules.
(iii) Provides a polymerized surface layer. (i) Most research and development are in
(iv) Bonds primer and composite. this area.
(e) Place composite. (ii) Does not remove smear layer.
b. Etch-and-rinse two-step systems, also known as (iii) Very simple to use.
one-bottle or fifth-generation systems (primer and (iv) Initial poor clinical research but getting
adhesive are combined but still need etchant). better.
(1) General considerations. (v) Not as good a bond to dentin (25MPa).
(a) Primer and adhesive combined. (2) Self-etch two-step (self-etch primer and then a
(b) Still require etchantsremove the smear bonding adhesive).
layer. (a) General considerations.
(c) Most require wet bonding. (i) Requires approximately five coats.
(d) Bond mechanism is the hybrid layer (ii) Does not remove smear layer.
formation. (iii) Fast and easy to use.
(e) Generally, bond strengths not as high as (iv) No rinsing; no worry about moisture.
multibottle systems, but this is likely not (v) Very low postoperative sensitivity.
clinically significant. (vi) Beginning to get good clinical results.
(f) Very technique-sensitivemust follow (vii) Does not bond well to uncut enamel
manufacturers directions exactly. 12MPa; must roughen enamel, and
(g) Must have dentin wettability just right. consider etching.
(h) Use primarily for direct procedures. c. Advantages of self-etch systems.
(i) Not faster than multibottle materials. (1) Easy to use.
(2) Steps. (2) Eliminates variables with wet bonding.
(a) Etch for 10 seconds. (3) Depth of etch is self-limiting.
(b) Rinse well and leave moist or rewet. (4) Sensitivity is reduced.
(c) Apply two to three layers of primer/ d. Disadvantages of self-etch systems.
adhesive, thin gently with air, and light-cure (1) Bond strengths to enamel and dentin generally
(surface should appear shiny). lower.
(d) Reapply adhesive, thin, and light-cure. (2) Some do not adequately etch uncut enamel.
(e) Place composite. (3) Bond strengths to autocuring composites are
2. Self-etching systemsetchant and primer or etchant, poor.
primer, and adhesive combined, the objective (4) Clinical performance not proven.
being to remove the operator variables (rinsing and (5) Bond durability questionable.
drying). C. Conclusions.
a. General considerations. 1. Technique suggestions.
(1) They do not completely remove the smear layer, a. Use microbrushes to apply primer/adhesive.
which is probably why they have less postop- b. Place bonding agent in a small well to minimize
erative sensitivity. evaporation.
(2) They need to be refrigerated owing to reactive c. Replace caps quickly and tightly.
components. d. Dispense only 1 to 2 drops for each tooth.
(3) Use carbide burs, not diamonds, because dia- 2. Technique factors for optimum bond.
monds leave a much thicker smear layer, which a. Must have proper isolation of the field.
makes bonding more difficult. b. Roughen sclerotic dentinincreases surface area
(4) These do not etch enamel as well as phosphoric and removes some of the sclerotic dentin.
acid. c. May still need mechanical retention.
(5) Enamel etching with phosphoric acid may be d. Bevel or roughen and etch enamel.
beneficial, but do not etch dentin because it e. Must have dentin moist (or rewet) for etch-and-
decreases dentin bond. rinse systems.
(6) Agitate the application, and place multiple f. Dispense adhesives just before use; otherwise, the
coats. solvent evaporates.
(7) Air dry at least 10 seconds because material g. Apply and dry primer adequately; otherwise, may
must have some water and needs to have a have gross leakage and postoperative sensitivity
longer drying time to remove the water. (gently dry with air syringe). Too much primer is
b. Types. better than too little.
(1) Self-etch one-step systems, also known as all- (1) Do not overthin the bonding agent (adhesive)
in-onemost risky category. too much; otherwise, may get an air-inhibited
(a) General considerations. layer only, and it does not bond as well.
(2) Fill incrementally and cure in appropriate d. Microhybrid composites.

thicknesses (1 to 2mm); may no longer be as (1) APS = 0.4 to 0.8m (500 to 800nm).
critical a factor with offsetting polymerizaton (2) Light-cured.
shrinkage. (3) Retain good properties of hybrids (strength),
(3) Follow directions. with improved handling.
3. Longevity of resin-dentin bonds. (4) Polishability almost equal to microfills.
a. Laboratory results show a loss of bond strength (5) Universal useanterior and posterior
over time. restorations.
(1) Perhaps from hydrolysis of the adhesive resin e. Nanofilled/nanohybrid composites.
or the collagen fibers or both. (1) Filler characteristicsvary with brand but
(2) The all-in-one types show the worst results. typically 20nm nanomers and 0.6 to 1.5m
(3) Bond durability is much greater when the nanoclusters.
peripheral margin is all in enamel. (2) Light-cured.
D. Summary. (3) Excellent handling.
1. Dentin and enamel bonding strengths are similar for (4) Highly polishable.
most etch-and-rinse systems. (5) Low shrinkage.
2. Most etch-and-rinse adhesive systems bond better to (6) Universal useanterior and posterior
moist dentin (i.e., leave dentin moist or remoisten restorations.
with water or a sealer/desensitizer). f. Flowable composites.
3. Self-etch systems are promising but not proven. (1) High matrix/filler ratio content.
4. One-bottle systems may be simpler but are not better; (2) Higher polymerization shrinkage.
three-step systems may still be best. g. Packable composites.
5. Dentin variability remains a problemsclerosis, (1) Increased viscosity.
tubule size, tubule location. (2) No documented benefits.
6. Proper clinical technique is critical to success. 2. Properties.
7. Enamel bonding is fast, strong, and long-lasting. a. High coefficient of thermal expansion = percola-
8. Dentin bonding may be strong but may not be tion, recurrent caries, stain.
long-lasting. b. High water absorption = deterioration of
material.
5.4 Composite Restorations c. All composites undergo polymerization
A. Introduction. shrinkage.
1. Types. d. Wear resistance has improved substantially with
a. Macrofilled composites. research and development.
(1) Average particle size (APS) = 10m. e. Surface texture is a function of filler size (smaller
(2) First-generation restorative composites. = smoother) and type.
(3) Paste-paste, chemical cure. 3. Clinical performance.
(4) Limited shade-matching capabilities. a. Marginal fracturemicrofilled composites.
(5) Poor physical and mechanical properties. b. Bulk fracturerare.
(6) Poor esthetics. c. Secondary caries.
b. Microfilled composites. d. Wearwhen used in heavy occlusal load areas.
(1) APS = 0.04m (40nm). e. Marginal leakage heavily dependent on bonding.
(2) Light-cured. 4. Handlingmethod of polymerization.
(3) Suboptimal fracture toughnessnot strong for a. Auto (chemical) curedno longer used.
occlusal bearing areas. b. Light-cured.
(4) Excellent esthetics and polishability. (1) Requires light source.
(5) Lower elastic modulusbetter in class V (2) Controlled insertion time.
situations. (3) Less finishing time required.
(6) Use primarily in anterior restorations. (4) Less porosity.
c. Hybrid (midifill, minifill) composites. c. Types of curing lights.
(1) APS = 1m (0.001mm). (1) Quartz/tungsten/halogen.
(2) Light-cured. (2) Light-emitting diode lights are more promising
(3) Good properties. light systems available today.
(4) Good esthetics but not as polishable as 5. Uses.
microfills. a. Class I, II, III, IV, V, and VI preparations.
(5) Universal useanterior and posterior b. Sealants.
restorations. c. Esthetic enhancements.
d. Hypocalcified areas. (1) Be easy to apply and remove.

e. Partial veneers. (2) Extend below the gingival margin.
f. Full veneers. (3) Extend above the marginal ridge height in pos-
g. Anatomic additions. terior restorations and the incisal edge in ante-
h. Resin-bonded bridges. rior restorations.
i. Luting agent. c. The matrix should be stabilized with a wooden
j. Diastema closure. wedge to close any gaps that may develop
k. Foundation. between the matrix and the gingival margin of
6. Advantages. the preparation and to provide stability to the
a. Esthetics. matrix during insertion of the composite. Care
b. Insulation. should be exercised to place the wedge securely
c. Bonding to tooth structure. apical to the gingival margin of the preparation,
d. Conservation of tooth structure. not to push the matrix band into the tooth prep-
e. Less mechanical retention form needed. aration area resulting in undercontour of the
f. Strengthening of remaining tooth structure restoration.
reinforcement of remaining tooth structure by 2. Placing adhesive system on enamel and dentin.
bonding is believed to be temporary. a. Follow manufacturers directions.
g. Minimal to no microleakagedecreased interfa- b. See previous section relative to adhesive systems.
cial staining, recurrent caries, or postoperative 3. Inserting the composite (Figure 2-27).
sensitivity. a. Apply matrix if not already applied.
7. Disadvantages. b. Proper incremental placement is important to
a. Wear potentialonly when all of occlusal contact ensure adaptation to tooth preparation and mar-
on composite. gins and to avoid voids or gaps in between
b. Very technique-sensitive; must have dry field; dif- increments.
ficult to do; takes more time. c. Insertion instruments.
c. Polymerization shrinkagemay cause contraction (1) Composite hand instruments (plastic or
gaps on root surfaces between composite and metal).
root. (2) Syringe.
d. C-factor may cause sensitivity, especially in class I d. Use incremental portions.
lesions. (1) Light cures only to 2- to 3-mm depth in most
8. Requirements for a successful composite restoration. composites and curing units.
a. Etched or primed enamel and dentin and adhesive (2) Large restorations require multiple increments.
placement. e. Cure each increment for the time prescribed by the
b. All occlusion should not be on composite. manufacturer (varies with composite type, shade,
c. Must not contaminate operating area. and opacity).
d. Adequate technical skill of operator. f. Use dentin and enamel shades in esthetic cases.
B. Restorative techniqueall composite restorations are g. Try to develop contour on last increment as close
bonded in with a dental adhesive. A liner or base or as possible to final anatomy of the tooth. Keep
both may be needed depending on the RDT, as dis- excess to a minimum.
cussed previously. When a matrix is used (class II, III, h. Remove matrix (if used).
and IV), typically the liner or base is placed before (1) Check for voids and undercontour, and repair
matrix placement, whereas the dental adhesive is placed (add composite) if needed.
after matrix placement. (2) Cure again from other angles.
1. Matrix placementa matrix primarily is used when 4. Contouring and finishing the restorationgood
a proximal surface is to be restored. For composites, insertion technique significantly reduces the amount
a thin Mylar strip matrix is used for most class III of finishing required. Usually only a slight excess of
and IV restorations, whereas a precontoured metal material is present that must be removed to provide
matrix (sectional or not) is used for most class II the final contour and smooth finish.
restorations. a. Use medium-coarse diamond instruments to
a. Objectives of a matrix. remove gross excess.
(1) Provide proper contact. b. Use fine diamond finishing instruments, 12-bladed
(2) Provide proper contour. carbide finishing burs, and abrasive finishing discs
(3) Confine the restorative material. to obtain proper contour.
(4) Reduce the amount of excess material. c. Select instrument that fits surface being contoured
b. For a matrix to be effective, it should have the fol- and finished, amount of contour needed, and
lowing characteristics. desired finish level.
A B
C D
E F
G H
Figure 2-27 Class I composite incremental insertion. A, Tooth preparation for class I direct composite restoration. B, After
resin-modified glass-ionomer base is placed, the first composite increment is inserted and light-activated. C-F, Composite is inserted
and light-activated incrementally, using cusp inclines as anatomic references to sculpt the composite before light activation. G, Com-
pleted restorations. H, At 5-year follow-up. (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and Science of Operative Dentistry,
ed 6. St. Louis, Mosby, 2013.)
Inlay
4 Tooth
271 8862
169L
A B 0.8 mm 0.5 mm
C x
Figure 2-28 A, Proposed outline form for disto-occlusal preparation. B, Dimensions and configuration of No. 271, No. 169L, and No.
8862 instruments. C, Conventional 4-degree divergence from line of draw (line xy). (From Heymann HO, Swift EJ, Ritter AV: Sturdevants
Art and Science of Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
d. Flexible abrasive discs and finishing strips are suit- 5. Requirements for a successful gold onlay.
able for convex and flat surfaces. a. Tooth preparation.
e. Finishing points and oval-shaped finishing burs (1) Draw/draft (divergence to the external surface
are more suitable for concave surfaces. of 2 to 5 degrees per prepared wall).
f. Finishing cups can be used in both convex and (2) Removal of weakened tooth structure.
concave surfaces. (3) Beveled finish lines.
g. Use medium speed with light intermittent brush (4) Pulpal protection.
strokes and air coolant for contouring and (5) Soft tissue management.
finishing. (a) Causes of inadequate tissue management.
h. Check occlusion after the rubber dam is removed, (i) Careless, traumatic preparation.
if one was used. (ii) Poor-fitting temporary restoration.
(iii) Temporary cement irritation.
5.5 Gold Inlay and Onlay Restorations (iv) Careless use of retraction cord.
A. Introduction (Figure 2-28). (b) Problems resulting from bleeding or
1. Definitionintracoronal cast metal restorations unhealthy tissues.
(inlay) that cap (cover) all cusps (onlay). (i) Access, vision impairment.
2. Advantages. (ii) Impression difficulty.
a. Excellent track record. (iii) Temporary fabrication difficulty.
b. Good fit. (iv) Cementation difficulty.
c. Excellent method to restore occlusal relationship. b. Laboratory fabrication.
d. Structurally sound material. (1) Accurate impression.
3. Disadvantages. (2) Appropriate waxing.
a. Nonesthetic. (3) Adherence to laboratory protocol.
b. Complicated tooth preparation. c. Cementation.
c. Complicated marginal finishing. (1) Adequate marginal finishing.
d. Need adequate laboratory support. (2) Proper manipulation of luting agent.
e. Cost. B. Clinical proceduretooth preparation.
4. Indications. 1. Introduction.
a. Large occlusal surface needs. a. Draw/draft.
b. Tooth contour needs. (1) 0.2 to 5 degrees per wall.
c. Fractures. (2) The longer the wall, the greater the amount of
d. Splinting. draw/draft.
e. Bracing for teeth with root canal treatment. (3) Must draw for casting to seat on tooth.
f. Bridge retainers. (4) More parallel = more retention.
g. Partial retainers. b. Retention.
(1) Primary retention. (b) Occlusal bevel.

(a) Draw/draft. (i) 0.5-mm width.
(b) Length of longitudinal (vertical) walls. (ii) Want 40-degree gold margin.
(2) Secondary retention. (iii) On occlusal surface.
(a) Retention grooves (proximally). (iv) May not need because angulation of
(b) Skirts. the facial and lingual cusps may provide
(c) Groove extensions. for the fabrication of a 40-degree gold
c. Objectives for beveled margins. margin without preparation.
(1) Good fit of gold to tooth. (c) Groove extension bevel.
(2) Strong tooth margin. (i) Lingual/facial groove extension.
(a) Usually strongest enamel margin. (ii) 0.5-mm width.
(3) Burnishable gold margin. (iii) Want 40-degree gold margin.
(a) Can bend a 30- to 50-degree gold margin. (d) Cusp counterbevel.
(b) Less than 30 degrees may be too thin and (i) 0.5- to 1.0-mm width.
may break. (ii) Want 30-degree gold margin.
(c) Greater than 50 degrees may be too thick (iii) For nonesthetic capped cusps.
and will not bend. (e) Stubbed margin.
d. Pulp protection. (i) 0.25- to 0.5-mm width.
(1) Caries removal. (ii) Perpendicular to long axis of crown.
(2) Liners, bases, and build-ups. (iii) For esthetic capped cusps.
(a) Must be retained in preparation for impres- (f) Secondary flare.
sion, temporary, try-in, cementation. (i) Extends facial and lingual proximal
2. Tooth preparation. margin into facial and lingual
a. Initial tooth preparation. embrasure.
(1) Occlusal extensions. (ii) Want 40-degree gold margin.
(a) Cap cusps as soon as possible. (iii) Diamond held perpendicular to long
(i) Use depth cuts. axis of preparation.
(ii) Removes weakened tooth structure. (iv) Occlusogingival width is not uniform.
(iii) Increases access. (g) Collar.
(iv) Increases visibility. (i) Beveled shoulder design around a
(b) Preserve noncapped cusps. capped cusp.
(c) Preserve noninvolved marginal ridges. (ii) Provides bracing.
(d) Smooth outline form. (iii) Shoulder prepared with No. 271 bur.
(2) Wall design. (iv) 0.5-mm bevel prepared with diamond.
(a) No. 271 bur. (h) Skirt.
(b) 2- to 5-degree taper per wall. (i) Extends casting around line angle.
(c) Increased wall height increases retention. (ii) Increases retention form.
(d) Increased draw decreases retention. (iii) Increases resistance form.
(3) Proximal box. (iv) Minicrown prep.
(a) Gingival extension (to include all faults and (v) Use diamond.
obtain clearance with adjacent tooth). (vi) Facial and lingual finish lines result in
(b) Draw (same 2 to 5 degrees). 40-degree gold margin.
(c) Facial and lingual extension (to include all (vii) Gingival finish line is a chamfer with
faults and obtain clearance with adjacent a minimum depth (not uniform) of
tooth). 0.5mm and extended into the gingival
(d) Cavosurface margin (30 to 40 degrees). one third of the crown.
(e) Blend with other bevels. (i) Gingival bevel.
b. Final tooth preparation. (i) 0.5- to 1-mm width.
(1) Removing remaining caries. (ii) Want 30-degree gold margin.
(2) Pulp protection, base, and build-up. (iii) All bevels must blend with each
(3) Secondary retention formretention grooves, other.
skirts, and groove extensions. c. View preparation from all angles (Figures 2-29 and
(4) Margination and bevels. 2-30).
(a) General rules. (1) Check draw.
(i) Use diamond (fine). (2) Check reduction.
(ii) Cut dry for final marginating for better (3) Check margin continuity.
vision. (4) Ensure all of fault removed.
A B C D
E F G H
I J K L
x z
M N O P z
Figure 2-29 A, Maxillary molar with caries on distofacial corner and mesial surface. B and C, Completed mesio-occlusal, distofacial,
and distolingual inlay for treating caries shown in A: facio-occlusal view (B) and distolinguo-occlusal view (C). D-H, Preparation for
treating caries illustrated in A: disto-occlusal view with diamond instrument being applied (D), occlusal view (E), distal view (F),
distolinguo-occlusal view (G), and mesio-occlusal view (H). I, Maxillary molar with deeper caries on distofacial corner and with mesial
caries. J, Preparation (minus bevels and flares) for mesio-occlusal, distofacial, and distolingual inlay to restore the carious molar shown
in I. No. 271 carbide bur is used to prepare the gingival shoulder and the vertical wall. K and L, Beveling margins. M and N, Completed
preparation for treating caries shown in I. Gingival and facial bevels blend at x, and y is the cement base. O and P, When the lingual
surface groove has not been prepared and when the facial wall of the proximal box is mostly or totally missing, forces directed to displace
the inlay facially can be opposed by lingual skirt extension (z). (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and Science of
Operative Dentistry, ed 6. St. Louis, Mosby, 2013.)
30
30
A B C
D E F
G H I
Figure 2-30 A, Caries has been removed, and the cement base has been inserted. B, Counterbeveling facial and lingual margins of
reduced cusps. C, Section of B. D, The fissure that extends slightly gingival to the normal position of the counterbevel may be included
by slightly deepening the counterbevel in the fissured area. E, Junctions between the counterbevels and the secondary flares are slightly
rounded. F, Axiopulpal line angle is lightly beveled. G, Improving the retention form by cutting proximal grooves. H, Completed mesio-
occlusodistal onlay preparation. I, Completed mesio-occlusodistofacial onlay preparation showing extension to include the facial surface
groove or fissure. (From Heymann HO, Swift EJ, Ritter AV: Sturdevants Art and Science of Operative Dentistry, ed 6. St. Louis, Mosby,
2013.)
Sample Questions the external tooth surface, they usually diverge

facially.
1. Which of the following statements regarding caries C. Using four corner coves instead of two full-length
risk assessment is true? grooves conserves dentin near the pulp and may
A. The presence of restorations is a good indicator of reduce the possibility of a mechanical pulp
current caries activity. exposure.
B. The presence of restorations is a good indicator of D. If the outline form approaches an existing proximal
past caries activity. restoration, it is better to leave a thin section of
C. The presence of plaque biofilm is a good indicator tooth structure between the two restorations
of current caries activity. (<1mm) than to join the restorations.
D. The presence of pit-and-fissure sealants is a good 8. In the conventional class I composite preparation,
indicator of current caries activity. retention is achieved by which of the following
2. Which of the following statements about indirect pulp features?
caps is false? 1. Occlusal convergence
A. Some leathery caries may be left in the 2. Occlusal bevel
preparation. 3. Bonding
B. A liner is generally recommended in the 4. Retention grooves
excavation. A. 2 and 4
C. The operator should wait at least 6 to 8 weeks B. 1 and 3
before reentry (if then). C. 1 and 4
D. The prognosis of indirect pulp cap treatment is D. 2 and 3
poorer than that of direct pulp caps. 9. Many factors affect tooth/cavity preparation. Which of
3. Smooth-surface caries refers to _____. the following would be the least important factor?
A. Facial and lingual surfaces A. Extent of the defect
B. Occlusal pits and grooves B. Size of the tooth
C. Mesial and distal surfaces C. Fracture lines
D. A and C D. Extent of the old material
4. The use of the rubber dam is best indicated for ______. 10. Which of the following statements about an amalgam
A. Adhesive procedures tooth/cavity preparation is true?
B. Quadrant dentistry A. The enamel cavosurface margin angle must be 90
C. Teeth with challenging preparations degrees.
D. Difficult patients B. The cavosurface margin should provide for a
E. All of the above 90-degree amalgam margin.
5. For a dental hand instrument with a formula of 10-8.5- C. All prepared walls should converge externally.
8-14, the number 10 refers to the ______. D. Retention form for class V preparations can be
A. Width of the blade in tenths of a millimeter placed at the DEJ.
B. Primary cutting edge angle in centigrades 11. Causes of postoperative sensitivity with amalgam res-
C. Blade length in millimeters torations include all of the following except one. Which
D. Blade angle in centigrades one is the exception?
6. When placement of proximal retention locks in class A. Lack of adequate condensation, especially lateral
II amalgam preparations is necessary, which of the condensation in the proximal boxes
following statements is not correct? B. Voids
A. One should not undermine the proximal enamel. C. Extension onto the root surface
B. One should not prepare locks entirely in the axial D. Lack of dentinal sealing
wall. 12. When carving a class I amalgam restoration, which of
C. Even if deeper than ideal, one should use the axial the following statements is false?
wall as a guide for proximal lock placement. A. Carving may be made easier by waiting 1 or 2
D. One should place locks 0.2mm inside the DEJ minutes after condensation before it is started.
to ensure that the proximal enamel is not B. The blade of the discoid carver should move paral-
undermined. lel to the margins resting totally on the partially set
7. Which of the following statements about class V amalgam.
amalgam restorations is not correct? C. Deep occlusal anatomy should not be carved.
A. The outline form is usually kidney-shaped or D. The carved amalgam outline should coincide with
crescent-shaped. the cavosurface margins.
B. Because the mesial, distal, gingival, and incisal 13. The setting reaction of dental amalgam proceeds pri-
walls of the tooth preparation are perpendicular to marily by _____.
A. Dissolution of the entire alloy particle into mercury 20. Triturating a dental amalgam _____.
B. Dissolution of the copper from the particles into A. Reduces the size of the alloy particles
mercury B. Coats the alloy particles with mercury
C. Precipitation of tin-mercury crystals C. Reduces the crystal sizes as they form
D. Mercury reaction with silver on or in the alloy D. Dissolves the alloy particles in mercury
particle 21. Which of the following materials has the highest linear
14. Restoration of an appropriate proximal contact results coefficient of thermal expansion?
in all of the following except one. Which one is the A. Amalgam
exception? B. Direct gold
A. Reduction or elimination of food impaction at the C. Tooth structure
interdental papilla D. Composite resin
B. Provides appropriate space for the interdental 22. A cervical lesion should be restored if it is _____.
papilla A. Carious
C. Provides increased retention form for the B. Very sensitive
restoration C. Causing gingival inflammation
D. Maintenance of the proper occlusal relationship D. All of the above
15. Major differences between etch-and-rinse (previously 23. Compared with amalgam restoration, composite res-
known as total-etch) and self-etching primer adhesive torations are _____.
systems include all of the following except one. Which A. Stronger
one is the exception? B. More technique-sensitive
A. Time necessary to apply the materials C. More resistant to occlusal forces
B. Amount of smear layer removed D. Not indicated for class II restorations
C. Bond strengths to enamel 24. The one constant contraindication for a composite res-
D. Need for wet bonding toration is _____.
16. A casting may fail to seat on the prepared tooth owing A. Occlusal factors
to all of the following factors except one. Which one is B. Inability to isolate the operating area
the exception? C. Extension onto the root surface
A. Temporary cement still on the prepared tooth after D. Class I restoration with a high C-factor
the temporary restoration has been removed 25. Which of the following statements regarding the choice
B. Proximal contacts of casting too heavy or too between doing a composite or amalgam restoration
tight is true?
C. Undercuts present in prepared tooth A. Establishing restored proximal contacts is easier
D. The occlusal of the prepared tooth was with composite.
underreduced B. The amalgam is more difficult and technique-
17. All of the following reasons are likely to indicate the sensitive.
need for restoration of a cervical notch except one. C. The composite generally uses a more conservative
Which one is the exception? tooth/cavity preparation.
A. Patient age D. Amalgam should be used for class II restorations.
B. Esthetic concern 26. Match each condition of tooth loss with the most
C. Tooth is symptomatic closely linked type of tooth loss.
D. Deeply notched axially
A. Mechanical wear secondary 1. Abfraction
18. All of the following statements about slot-retained
to abnormal forces (s.a.
complex amalgams are true except one. Which one is
toothbrushing) ___
the exception?
B. Normal tooth wear ___ 2. Attrition
A. Slots should be at least 1.5mm in depth.
C. Wear secondary to chemical 3. Erosion
B. Slots should be 1mm or more in length.
presence ___
C. Slots may be segmented or continuous.
D. Tooth loss in the cervical area 4. Abrasion
D. Slots should be placed at least 0.5mm inside
secondary to biomechanical
the DEJ.
loading ___
19. Which one of the following acids is generally recom-
mended for etching tooth structure? 27. From the following list, select the reasons to consider
A. Maleic acid the restoration of abraded or eroded (noncarious) cer-
B. Polyacrylic acid vical lesions. (Choose four.)
C. Phosphoric acid A. Caries develops in the lesion.
D. Tartaric acid B. The defect is shallow and does not compromise the
E. Ethylenediaminetetraacetic acid structural integrity of the tooth.
C. Intolerable sensitivity exists and is unresponsive to 30. Place the following steps for the application of an etch-
conservative desensitizing measures. and-rinse (total-etch) three-step dental adhesive in
D. The defect contributes to a phonetic problem. correct sequence.
E. The area is to be involved in the design of a remov- A. Apply adhesive ___
able partial denture. B. Rinse etchant and leave surface wet ___
F. Teeth are endodontically treated. C. Complete tooth preparation ___
G. The patient desires an esthetic improvement. D. Apply two to three layers of primer ___
28. From the following list, select the reasons associated E. Etch enamel and dentin with phosphoric acid for
with replacement of existing restorations. (Choose 10 to 15 seconds ___
four.) F. Light-cure ___
A. Marginal ridge discrepancy that contributes to 31. Place the following steps for a class II amalgam restora-
food impaction tion in correct sequence.
B. Existing restoration has significant discrepancies A. Check occlusion of restoration and adjust if neces-
and is a negative etiologic factor to adjacent teeth sary ___
or tissue B. Place matrix and wedge ___
C. Light marginal staining not compromising esthet- C. Carve amalgam material ___
ics and judged noncarious D. Mix amalgam material ___
D. Poor proximal contour or a gingival overhang that E. Complete tooth preparation ___
contributes to periodontal breakdown F. Condense amalgam material ___
E. Recurrent caries that can be adequately treated by 32. From the following list, select the functions of skirts in
a repair restoration gold onlay tooth preparations. (Choose two.)
F. Presence of shallow ditching around an amalgam A. Increase retention form
restoration B. Provide bracing
G. For tooth-colored restorations, unacceptable C. Increase resistance form
esthetics D. Enhance esthetics
29. Match each pulpal condition with the most closely E. Provide pulp protection
linked recommended pulp therapy. F. Improve draw
A. Mechanical pulp exposure, 1. Endodontic
noncarious (<1.0mm) ___ therapy
B. Remaining dentin 2. No pulp therapy
thickness greater than required
2.0mm over vital pulp ___
C. Carious pulp exposure 3. Direct pulp cap
(>1.0mm) with purulent
exudate ___
D. Residual questionable 4. Indirect pulp cap
dentin near pulp,
asymptomatic tooth ___
SECTION 3
Oral and Maxillofacial

Surgery and Pain Control
LARRY L. CUNNINGHAM, JR.
PHILIP LIN
KENNETH L. REED
OUTLINE B. Aseptic technique.

C. Incisions.
1. Oral and Maxillofacial Surgery
D. Flap design.
2. Local Anesthesia E. Tissue handling.
F. Hemostasis.
1.2 Dentoalveolar Surgery

There are many indications for the removal of teeth.
1.0 Oral and Maxillofacial Surgery
Although performing a dental extraction is most often a
Larry L. Cunningham, Jr., Philip Lin minor surgery, it is still a surgery. Any invasive procedure
This chapter reviews the basic aspects of oral and maxil- requires that the practitioner have complete knowledge of
lofacial surgery to help prepare dental students for the the patients history and perform a head and neck physical
National Board Dental Examination. As with the other examination. Thorough documentation of the history and
chapters in this text, this chapter is not meant to be all- physical examination, indications for the procedure, and
inclusive. This review is based on topics found in Contem- the patients informed consent is the standard of care.
porary Oral and Maxillofacial Surgery (see References). A. Indications for dental extractions.
Questions that arise from the use of this review should 1. Severe cariesteeth that cannot be restored.
be researched in that text and other, more in-depth 2. Pulpal necrosis and irreversible pulpitis when
references. endodontics is not an option.
3. Severe periodontal diseasewith irreversible bone
Outline of Review loss and tooth mobility.
1.1 Principles of Surgery 4. Orthodontic prescriptionscommonly extracted
1.2 Dentoalveolar Surgery teeth are the maxillary and mandibular first premo-
1.3 Trauma Surgery lars and third molars.
1.4 Orthognathic Surgery 5. Malposed teethteeth that cause mucosal trauma
1.5 Facial Pain and Neuropathology and Osteonecrosis of and cannot be repositioned with orthodontics; teeth
the Jaw in hyperocclusion that are unopposed and interfer-
1.6 Temporomandibular Disorders ing with other restorative care.
1.7 Odontogenic Infections 6. Cracked teeth.
1.8 Bisphosphonate-Related Osteonecrosis of the Jaws 7. Preprosthetic extractionswhen a patients treat-
1.9 Biopsies ment plan includes complete dentures or when
1.10 Surgical Management of Cysts and Tumors certain teeth interfere with planned prosthetic
treatment.
1.1 Principles of Surgery 8. Impacted teethteeth that will not erupt into
Many surgical techniques exist, as you have learned from proper occlusion.
your training, and these are reviewed here. All of these 9. Supernumerary teeth.
techniques should be used with specific principles in mind. 10. Teeth associated with pathology.
A. Visualizationrequirements for adequate visua 11. Radiation therapypatients needing radiation
lization. therapy for head and neck cancer should be evalu-
1. Assistance. ated for the health of the dentition. Questionable
2. Access. teeth should be extracted before radiation therapy.
79
80 Section 3 Oral and Maxillofacial Surgery and Pain Control
B. Contraindications. e. Hypercementosis or widely divergent roots.

1. Overviewthere are few true contraindications to f. Extensive decay or crown loss.
the extraction of teeth. Elective dentoalveolar surgery E. Surgical extractions and impactionsan impacted
in extremely ill patients should be carefully consid- tooth is one that fails to erupt into the dental arch
ered by the practitioner. In some instances, a patients within the expected time. The tooth becomes impacted
health may be so compromised that the patient because adjacent teeth, dense overlying bone, or exces-
cannot withstand a surgical procedure. sive soft tissue prevents eruption. Because impacted
2. Examples. teeth do not erupt, they are retained for the patients
a. Severe uncontrolled metabolic diseases (brittle lifetime unless surgically removed. The most commonly
diabetes). impacted teeth are the mandibular third molars, maxil-
b. End-stage renal disease. lary third molars, and maxillary canines. The term
c. Advanced cardiac conditions (unstable angina). unerupted includes both impacted teeth and teeth that
d. Leukemia and lymphomapatients with these are in the process of erupting. The term embedded
conditions should be treated before dental is occasionally used interchangeably with the term
extractions. impacted. Inadequate arch length is the primary reason
e. Hemophilia or platelet disorderspatients with that teeth fail to erupt. The most common teeth to
these conditions should be treated before dental become impacted are the third molars because they are
extractions. the last to erupt.
f. Head and neck radiationextractions in patients 1. All impacted teeth should be considered for removal
with a history of head and neck radiation can lead at the time of diagnosis for the following reasons.
to osteoradionecrosis. These patients commonly a. Prevention of periodontal disease in teeth adjacent
are treated with hyperbaric oxygen therapy before to impacted teeth.
dentoalveolar surgery. b. Prevention of dental caries.
g. Intravenous bisphosphonate treatmentpatients c. Prevention of pericoronitis.
treated with intravenous bisphosphonates (e.g., d. Prevention of root resorption of adjacent teeth.
for treatment of bone malignancies or severe e. Prevention of odontogenic cysts and tumors.
osteoporosis) are at increased risk of osteonecrosis f. Treatment of pain of unexplained origin.
of the jaw. g. Prevention of jaw fractures.
h. Pericoronitispericoronitis is an infection of the h. Facilitation of orthodontic treatment.
soft tissues (cellulitis) around a partially erupted 2. Contraindications to extraction of impacted teeth.
mandibular third molar. Generally, this infection a. Extremes of age (preteen or asymptomatic full
should be cleared before extracting the involved bony impaction in patients >35 years old).
tooth; antibiotics, irrigation, and removal of the b. Compromised medical status.
maxillary third molar should be considered as part c. Likely damage to adjacent structures.
of the treatment of pericoronitis. F. Classifications of impacted teeth.
3. Other relative contraindications to oral surgery 1. Angulationmesioangular (least difficult), horizon-
are acute infectious stomatitis and malignant tal, vertical, distoangular (most difficult).
disease. 2. Pell and Gregory classification.
C. Radiographic examination. a. Relationship to anterior border of ramus.
1. Relationship of associated vital structures. (1) Class 1normal position anterior to the
2. Configuration of roots. ramus.
3. Condition of surrounding bone. (2) Class 2one half of the crown is within the
4. Mechanical principles involved in tooth extraction. ramus.
D. Indications for surgical extractionsmore difficult (3) Class 3entire crown is embedded within the
extractions can often be predicted from the examina- ramus.
tion or from preoperative radiographs. Surgeons should b. Relationship to occlusal plane.
consider performing an elective surgical extraction (1) Class Atooth at the same plane as other
when they perceive a possible need for excessive force molars.
to extract a tooth. (2) Class Bocclusal plane of third molar is
1. Examples. between the occlusal plane and the cervical line
a. After initial attempts at forceps extraction have of the second molar.
failed. (3) Class Cthird molar is below the cervical line
b. When the patient has especially dense bone. of the second molar.
c. In older patients, owing to less elastic bone. 3. Factors relating to difficulty of extraction (Boxes 3-1
d. Short clinical crowns with severe attrition and 3-2).
(bruxism). G. Surgical principles.
Section 3 Oral and Maxillofacial Surgery and Pain Control 81
Box 3-1 Box 3-3

Factors That Make Impaction Surgery Prevention of Soft Tissue Injuries
Less Difficult
1. Pay strict attention to the soft tissues to prevent
1. Mesioangular position injuries.
2. Pell and Gregory class 1 ramus 2. Develop adequate-sized flaps.
3. Pell and Gregory class A depth 3. Use minimal force for retraction of soft tissue.
4. Roots one third to two thirds formed* Modified from Hupp JR, Tucker MR, Ellis E: Contemporary Oral and
5. Fused conical roots Maxillofacial Surgery, ed 4. St. Louis, Mosby, 2003.
6. Wide periodontal ligament*
7. Large follicle*
8. Elastic bone* 2. Bone removalremoval of bone is often needed for
9. Separated from second molar atraumatic extractions. It is better to remove some
10. Separated from inferior alveolar nerve* bone with a surgical bur than to fracture off an entire
11. Soft tissue impaction buccal cortex because of the use of too much force.
The amount of bone removed is usually much greater
From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and
Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013. for an impacted third molar than for a normal surgi-
*Present in young patients. cal extraction. A trough of bone on the buccal aspect
of the tooth down to the cervical line should be
removed initially. Additional bone removal may be
required depending on the tooth position and root
Box 3-2 morphology. Care should be taken not to injure the
Factors That Make Impaction Surgery lingual cortex of the mandible.
More Difficult 3. Tooth sectioningsectioning of tooth may also be
needed to avoid radical removal of mandibular bone
1. Distoangular or injury to other vital structures. The mandibular
2. Pell and Gregory class 2 or 3 ramus third molars frequently require sectioning of the
3. Pell and Gregory class B or C depth tooth, but other teeth may also need to be sectioned
4. Long, thin roots* to avoid fracture of the buccal alveolus. The tooth is
5. Divergent curved roots delivered in pieces after it is sectioned.
6. Narrow periodontal ligament* 4. Irrigation of the woundcopious irrigation is impor-
7. Thin follicle* tant to avoid the presence of fractured tooth or bone
8. Dense, inelastic bone* spicules below the soft tissue flap, which may lead to
9. Contact with second molar a subperiosteal abscess. Replacement of the soft
10. Close to inferior alveolar canal tissue flaps completes the procedure (Box 3-3).
11. Complete bony impaction 5. Complications.
From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and a. Tearing of the mucosal flap can be avoided by ini-
Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013. tially creating an appropriately sized incision. Any
*Present in older patients. significant mucosal tears should be repaired at the
end of the procedure.
b. Puncture wounds in the palate, tongue, or other
1. Exposurewhether removing third molars or other soft tissue areas are caused by the application of
difficult extractions, there are several important prin- excessive and uncontrolled force to the instru-
ciples for surgical extractions. The first is that the ments. These wounds are treated with pressure to
surgeon must have adequate visibility of the surgical stop any bleeding and are left open to heal by sec-
site. There must be exposure with an adequate-sized ondary intent. Consideration should be given to
flap. An envelope flap is most often used, but releas- antibiotic coverage, depending on the injury.
ing incisions are common. The base (vestibular) c. Oral-antral communications should be managed
portion of the flap should always be wider than the with a figure-of-eight suture over the socket, sinus
apex (crestal) portion of the flap to maintain ade- precautions, antibiotics, and a nasal spray to
quate blood supply to the released soft tissues. Care prevent infection and keep the ostium open.
should be taken in developing this flap for mandibu- d. Root fracture.
lar third molars. The mandible posterior to the third e. Tooth displacement.
molar thins and diverges laterally. An incision made (1) Maxillary molar root into the maxillary sinus.
too far medially could damage the lingual nerve, (2) Maxillary third molars into the infratemporal
causing numbness on that half of the tongue. fossa.
(3) Mandibular molar roots forced into the sub- primary denture-bearing area; the vestibular depth; the
mandibular space through the buccal cortical location of muscle attachments; the jaw relationships;
bone. and the presence of soft tissue or bony pathologic
(4) Tooth lost into the oropharynx. conditions. This examination should include the use
(a) May result in airway obstruction. of palpation, radiographs, and models of the patient.
(b) Patient should be transported to an emer- Alveoplasty can be minor and may include only the thin
gency department for chest and abdominal and sharp edges of the alveolus after tooth extraction,
radiographs. or it may be more aggressive and include removing
f. Injury to adjacent teeth. undercuts and sharp edges from areas such as the mylo-
(1) Fracture of teeth or restorations. hyoid ridge.
(2) Luxation of adjacent teeth. I. Tori removalexostoses and palatal tori are over-
g. Alveolar process fractures and fractures of maxil- growths of bone on the lateral surfaces of the alveolar
lary tuberosity can occur when excessive force is ridges or in the palate. Exostoses can grow to great sizes
used to remove teeth. but are considered a variation of normal and need to be
h. Trauma to the inferior alveolar nerve may occur removed only when there is a need for denture or
in the area of the roots of the mandibular third partial denture construction or because of repeated
molars, causing numbness to the lower lip and trauma to the area.
chin. The lingual nerve travels very near the lingual J. Soft tissue surgerysometimes the bone is well con-
cortex of the mandible adjacent to the mandibular toured for denture or partial denture construction, but
third molars and can be affected by cortical frac- the soft tissues limit the ability to achieve appropriate
ture during third molar removal. This injury would thickness of denture material or interfere with appro-
cause loss of sensation and taste on that side of the priate fit of the prosthesis. Areas for soft tissue surgery
tongue. Patients with numbness lasting more than may include the following.
4 weeks should be referred for microneurosurgical 1. Mandibular retromolar pad.
evaluation. 2. Maxillary tuberosity.
i. Bleeding is an uncommon complication of dental 3. Excessive alveolar ridge tissue.
extractions. Causes of excessive bleeding are injury 4. Inflammatory fibrous hyperplasia.
to the inferior alveolar artery during extraction of 5. Labial and lingual frenum.
a mandibular tooth (usually the third molar); a K. Reconstructive dentoalveolar surgery.
muscular arteriolar bleed from the elevation of a 1. Implant dentistry is currently the state of the art for
mucoperiosteal flap for third molar removal; or replacement of lost dentition. Implants are used for
bleeding related to the patients hemostasis. Exam- the replacement of one or multiple teeth and to retain
ples of patients with altered hemostasis are patients complete prostheses in an overdenture fashion.
who are taking warfarin or drugs for platelet inhi- Dental implants are made of titanium that osteointe-
bition, patients who have hemophilia or von Wil- grates with bone. Whether used as single tooth
lebrands disease, and patients who have chronic replacements or as an anchor for a denture, several
liver insufficiency. principles are important for success of the dental
j. Infections are uncommon in healthy patients. implant.
Whenever a mucoperiosteal flap is elevated for a a. Primary stability.
surgical extraction, there is the possibility for a b. Quantity and quality of bone.
subperiosteal abscess. All surgical flaps should be (1) Denser cortical bone (e.g., at the anterior man-
irrigated liberally before suturing. Treatment for a dible) has a higher implant success rate than
subperiosteal abscess is drainage of the abscess and loose cancellous bone and thin cortical bone
antibiotic treatment. (e.g., at the posterior maxilla).
k. Localized osteitis (dry socket) can occur in 3% (2) There are four types of bone quality (Figure
of mandibular third molar extractions but does 3-1). Regardless of implant height, types I
not require antibiotics; it heals with irrigation through III bones are associated with higher
of the socket and local treatment for pain implant success rates compared with type IV
control. bone, which is mostly marrow with thin corti-
H. Alveoplastyalveoplasty is indicated for the removal of cal bone.
any area that may cause difficulty in denture construc- c. Anatomic structures (Table 3-1).
tion or in the patients satisfaction with the prosthesis. (1) Sinus.
An intraoral and extraoral examination of the patient (2) Adjacent teeth.
should include an assessment of the existing tooth rela- (3) Inferior alveolar nerve and mental nerve.
tionships, if any remain; the amount and contour of 2. When teeth have been missing for an extended time,
remaining bone; the quality of soft tissue overlying the alveolar bone resorbs, leaving a flattened and, in
Figure 3-1 Bone types based on quan-

tity of cortical bone and density of can-
cellous marrow. (From Hupp JR, Tucker
MR, Ellis E: Contemporary Oral and Maxil-
lofacial Surgery, ed 6. St. Louis, Mosby, 2013.)
I II III IV
Table 3-1 is the requirement of a second surgical site

(i.e., the donor site).
Anatomic Limitations to Implant
(2) Allograftthis graft material is obtained from
Placement
cadaver bone that is processed to ensure steril-
MINIMUM REQUIRED ity and to decrease substances in the bone that
DISTANCE BETWEEN IMPLANT can trigger host immune response. However,
STRUCTURE AND INDICATED STRUCTURE
this process destroys the osteoinductive capa-
Buccal plate 1mm bility of the bone, whereas the osteoconductive
Lingual plate 1mm property of the graft remains. Although al-
Maxillary sinus 1mm lograft avoids the need for a second surgical
Nasal cavity 1mm site, a greater amount of the grafted material is
Incisive canal Avoid midline maxilla resorbed compared with autografts.
(3) Xenograftxenograft is acquired from a genet-
Interimplant distance 3mm between outer edge of
implants ically different species than the recipient.
Bovine bone is an example of xenograft. Xeno-
Inferior alveolar canal 2mm from superior aspect of
bony canal grafts and allografts have similar advantages
and disadvantages, including elimination of
Mental nerve 5mm from anterior or bony
foramen a donor site and significant resorption after
grafting.
Inferior border 1mm
(4) Bone morphogenetic protein (BMP)BMP
Adjacent natural tooth 1.5mm belongs to a family of proteins that can induce
Modified from Peterson LJ, etal: Contemporary Oral and Maxillofacial bone formation and enhance graft healing.
Surgery, ed 4. St. Louis, Mosby, 2003.
Recombinant human BMP (rhBMP-2) has
been used in maxillofacial skeleton reconstruc-
tion. To reconstruct a larger bony defect, BMP
is sometimes combined with allograft, using
some cases, depressed alveolar ridge that is inade- the osteoinductive and osteoconductive prop-
quate for denture retention. This bone resorption erties from both graft materials.
occurs commonly in the mandibular arch, where the b. Distraction osteogenesis (DO)DO is a biologic
surface area for prosthesis retention is comparatively process of new bone deposition and formation
smaller. Alveolar ridges can be augmented for pros- between osteotomized bone surfaces that are sepa-
thesis retention in different ways. rated by gradual traction. Because DO uses the
a. Grafting of the alveolusthis can be accomplished bodys innate ability to generate new bone, no
with various grafting materials. grafting materials are needed. This process is useful
(1) Autogenous bone. to provide height or length to bone but is less sat-
(a) Cortical bone can be obtained from numer- isfactory for providing width of bone.
ous areas for reconstruction of alveolar 3. Alveolar ridge preservation (i.e., socket preservation)
ridges, depending on the amount of bone maintains height and width of alveolar ridge after
needed. The most common graft sites for teeth removal. The success of alveolar ridge preserva-
this purpose include the following. tion depends on atraumatic extraction without com-
(i) Anterior cortex of the symphysis (when promising buccal and lingual bone. The extraction
the volume of bone needed is smaller). site is thoroughly cleaned to remove debris and gran-
(ii) Lateral cortex of the ramus and exter- ulation tissues. Grafting materials such as allograft or
nal oblique ridge. xenograft are placed in the socket covered by resorb-
(iii) Iliac crest. able collagen membrane. Resorbable sutures are
(iv) Rib. used to secure grafting material and membrane,
(b) Biocompatibility is the greatest advantage and primary closure at the surgical site is usually
of autograft. The disadvantage of autograft unnecessary.
Box 3-4
Classification of Dentoalveolar Injuries
Crown Craze or Crack (i.e., Infraction) Mobility (i.e., Subluxation or Looseness)
Crack or incomplete fracture of the enamel without a Injury to the tooth-supporting structure, resulting in
loss of tooth structure tooth mobility but without tooth displacement
Horizontal or Vertical Crown Fracture Tooth Displacement

Confined to enamel Intrusion (displacement of tooth into its socketusually
Enamel and dentin involved associated with compression fracture of socket)
Enamel, dentin, and exposed pulp involved Extrusion (partial displacement of tooth out of its
Horizontal or vertical socketpossibly no concomitant fracture of alveolar
Oblique (involving the mesioincisal or distoincisal angle) bone)
Labial displacement (alveolar wall fractures probable)
Crown-Root Fracture Lingual displacement (alveolar wall fractures probable)
No pulp involvement Lateral displacement (displacement of tooth in mesial
Pulp involvement or distal direction, usually into a missing tooth
spacealveolar wall fractures probable)
Horizontal Root Fracture
Involving apical third Avulsion
Involving middle third Complete displacement of tooth from its socket (may
Involving cervical third be associated with alveolar wall fractures)
Horizontal or vertical
Alveolar Process Fracture
Sensitivity (i.e., Concussion) Fracture of alveolar bone in the presence or absence of
Injury to the tooth-supporting structure, resulting in a tooth or teeth
sensitivity to touch or percussion but without
mobility or displacement of the tooth
From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.
1.3 Trauma Surgery Coronoid
A. Tooth fracturesclassifications of tooth fractures have

been well described (Box 3-4). When tooth fractures 1.3%
29.1%
involve the pulp chamber, treatment usually includes
Condylar Not specified: 2.2%
root canal therapy. Nonrestorable teeth should be
1.7%
extracted. See Section 1 on Endodontics for more
information. Ramus 3.1% Alveolar
B. Facial fracturesfacial fractures require a very thor- 24.5%
ough physical examination. Signs of a bone fracture are 16% 22%
Angle
pain, contour deformity, ecchymosis, laceration, abnor-
mal mobility of the bone, numbness, crepitation, and Body
hematoma. Fractures should always be considered and Symphysis
ruled out with a history of a motor vehicle collision, an
Figure 3-2 Anatomic distribution of mandibular frac-
altercation, a fall, or a sports accident.
tures. (From Hupp JR, Tucker MR, Ellis E: Contemporary Oral
C. Mandible fracturesmandible fractures can almost and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.)
always be identified on a panoramic radiograph. Sus-
pected fractures should always be visualized in at least tures can be classified as greenstick, simple, commi-
two radiographs, including panoramic view, Townes nuted, and compound (open) (Figures 3-2 and 3-3).
view, posterior-anterior skull view, or lateral oblique 2. Contemporary treatment for mandible fractures that
view. are displaced and mobile is with open reduction and
1. The most common sites for the mandible to fracture internal fixation using titanium bone plates and
are the condyle, the angle, and the symphysis. Frac- screws. If the patient has teeth, the occlusion is used
A B
C D
Figure 3-3 Types of mandible fractures classified according to extent of injury in the area of the fracture site.
A, Greenstick. B, Simple. C, Comminuted. D, Compound. Bone would be exposed through the mucosa near teeth. (From Hupp JR,
Tucker MR, Ellis E: Contemporary Oral and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.)
A B C
Figure 3-4 Le Fort midfacial fractures. A, Le Fort I fracture separating the inferior portion of the maxilla in a horizontal fashion,
extending from the piriform aperture of the nose to the pterygoid maxillary suture area. B, Le Fort II fracture involving separation of
the maxilla and nasal complex from the cranial base, zygomatic orbital rim area, and pterygoid maxillary suture area. C, Le Fort III
fracture (i.e., craniofacial separation), which is complete separation of the midface at the level of the naso-orbital-ethmoid complex and
zygomaticofrontal suture area. Fracture also extends through the orbits bilaterally. (From Hupp JR, Tucker MR, Ellis E: Contemporary
Oral and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.)
to guide the surgeon during the repair of the fracture. evaluation of fractures of the midface, which can involve
Other methods of repair include lingual splinting the maxilla, zygoma, nose, and orbits.
(pediatric patients) and intermaxillary fixation 1. Maxillary fractures have been described as Le Fort
(wiring the jaws closed). levels I, II, and III (Figure 3-4). As with mandible
D. Midface fracturesmidface fractures are best evaluated fractures, midface fractures are described by the bone
with computed tomography (CT) scans of the face. Two involved as simple (closed), compound (open), or
orientations (axial and coronal) are needed for full comminuted.
2. Maxillary Le Fort fractures, orbital fractures, and C. Imaginglateral cephalograms are the main images
zygomatic fractures usually require internal rigid used in treatment planning for orthognathic surgery,
fixation. Isolated zygomatic arch fractures can often although panoramic radiographs, anterior-posterior
be reduced with a minor surgical procedure and cephalograms, and periapical radiographs are taken as
without the use of bone plates and screws. Simple needed. Cephalometric analysis, when combined with
nasal fractures are repaired with internal and exter- facial evaluation, helps determine the jaw primarily
nal splints. involved in the deformity, direction of growth of the
jaws, and the most ideal procedure for the patients
1.4 Orthognathic Surgery diagnosis (Figure 3-6).
Evaluation of a patient with a dentofacial deformity is D. Diagnosisthe primary diagnoses in patients with
guided by the principle of balance and symmetry. Orthog- dentofacial deformity are maxillary hyperplasia or
nathic surgery is performed to correct severe skeletal dis- hypoplasia and mandibular hyperplasia or hypoplasia.
crepancies that prevent appropriate dental occlusion and Other common descriptive terms are apertognathic
most often is done in conjunction with orthodontics. (anterior open bite), vertical maxillary excess (when the
Dental health and oral hygiene are important consider- maxilla is too long, and the patient has an excessively
ations in these patients. gummy smile), horizontal transverse discrepancy
A. Patients are evaluated according to normal facial pro- (when the patient is in posterior crossbite), and macro-
portions (Figure 3-5). Vertically, the face is divided into genia or microgenia (when the chin is too big or too
relatively equal thirds. Horizontally, the face is divided small). Some patients may have a cant or a vertical
into relatively equal fifths. Patients can be described as asymmetry in addition to the other diagnoses.
having concave or convex profiles. E. Surgerysurgical treatment depends on the specific
B. Angle classifications of occlusion are used to describe diagnosis and the facial evaluation. Generally, when
the dental arch relationships as well as the facial profile. a diagnosis of a deficient or excessive jaw is made,
1. Angle class Inormal dental occlusion with a straight surgery is performed to correct the problem. Surgical
(orthognathic) profile. work-up typically includes radiographs and cephalo-
2. Angle class IImandibular first molars and canines metric analysis and a prediction tracing, model surgery,
are in a posterior position relative to the maxillary and construction of an acrylic splint to be used
counterparts, and the face appears posteriorly con- intraoperatively.
vergent (retrognathic). 1. Maxillary surgerymaxillary surgeries are referred
3. Angle class IIImandibular first molars and canines to as Le Fort I osteotomies. The maxilla can be moved
are in an anterior position relative to the maxillary forward and down more easily than it can be moved
counterparts, and the face appears to be anteriorly up or back. It can also be segmented into two or three
convergent (prognathic). pieces to position the occlusion better.
1/3
1/3
1/3
1/3
2/3
1 1/5 1 1 1/5
/5 /5 /5
A B
Figure 3-5 Normal facial proportions. A, Full-face view of proportional relationships. Relationships of medial intercanthal distance,
alar base width, and lip proportions to remainder of facial structures are demonstrated. B, Normal profile proportions demonstrate
relationships of upper, middle, and lower thirds of face and proportional relationships of lip and chin morphology within lower third
of face. (From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.)
HP
N-ANS
NF
1-NF
6-NF
MP
HP ANS-Me
MP-HP
angle 1-MP
A
B
Figure 3-6 A, Lateral cephalometric radiograph. B, Tracing of lateral cephalometric head film, with landmarks identified for evaluating
facial, skeletal, and dental abnormalities by using a system of cephalometrics for orthognathic surgery. (A, From Hupp JR, Tucker MR,
Ellis E: Contemporary Oral and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013. B, From Burstone CJ, etal: Cephalometrics for orthog-
nathic surgery. J Oral Surg 36:269, 1978.)
2. Mandibular surgerymandibular surgery is most

often done using one of two osteotomies: bilateral
sagittal split osteotomy (Figure 3-7) or vertical ramus
osteotomy (Figure 3-8). The mandible can be moved
anteriorly to correct retrognathia or posteriorly to
correct prognathism. In addition, the chin can be
moved using a genial osteotomy (genioplasty) to
correct macrogenia or microgenia.
3. DOwith DO, oral and maxillofacial surgeons have
much greater flexibility in treating difficult deformi-
ties of the facial skeleton. Patients with deformities
such as cleft lip and palate and hemifacial microso-
mia previously required difficult surgeries. DO
involves cutting an osteotomy to separate segments
of bone and the application of an appliance that facil-
itates the gradual and incremental separation of bone
segments (Figure 3-9).
Figure 3-7 Sagittal split osteotomy. Ramus of mandible is
1.5 Facial Pain and Neuropathology and divided by the creation of a horizontal osteotomy on the medial
Osteonecrosis of the Jaw aspect and a vertical osteotomy on the lateral aspect of the man-
A. Overview. dible. These are connected by an anterior ramus osteotomy. The
1. The differential diagnosis of facial pain includes lateral cortex of the mandible is separated from the medial aspect,
pathology of dental structures, muscles, joints, blood and the mandible is advanced or set back for correction of
vessels, salivary glands, sinuses, eyes, ears, and central mandibular deficiency or excess, respectively. (From Hupp JR,
Tucker MR, Ellis E: Contemporary Oral and Maxillofacial Surgery,
and peripheral nervous systems.
2. The perception of pain has physiologic and psycho-
logical aspects. For pain to be experienced from a
physiologic perspective, transduction (activation of
A-delta and C fibers to the spinal cord or brainstem),
A B
C D
E F
Figure 3-8 Case report of mandibular excess. A and B, Preoperative facial esthetics photos demonstrate typical features of class
III malocclusion resulting from mandibular excess. C and D, Presurgical occlusal photos. E and F, Diagrams of intraoral vertical ramus
osteotomy with posterior positioning of mandible and rigid fixation.
G H
I J
K L
Figure 3-8, contd G and H, Postoperative frontal and profile views of the patient (compare with A and B). I and J, Postoperative
occlusion (compare with C and D). K and L, Preoperative and postoperative radiographs. (From Hupp JR, Tucker MR, Ellis E: Contem-
porary Oral and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.)
Table 3-2
Classifications of Orofacial Pain
PAIN TYPE SOURCE
Somatic (increased Musculoskeletal (TMJ, periodontal,
stimulus yields muscles)
increase in pain) Visceral (salivary gland, dental pulp)
Neuropathic (pain Damage to pain pathways (TN,
independent of trauma, stroke)
stimulus intensity)
Psychogenic Intrapsychic disturbance (conversion
reaction, psychotic delusion,
A malingering)
Atypical Facial pain of unknown cause/
diagnosis pending
Data from Peterson LJ, etal: Contemporary Oral and Maxillofacial Surgery,
ed 4. St. Louis, Mosby, 2003.
TMJ, Temporomandibular joint; TN, trigeminal neuralgia.
than 50 years. Trigeminal neuralgia is treated med-

ically with anticonvulsant drugs (e.g., carbamaze-
pine, oxcarbazepine, gabapentin) and surgically
(microvascular decompression [Jannetta proce-
B dure], stereotactic radiosurgery, percutaneous
needle rhizotomy, entry zone balloon root
Figure 3-9 Distractor appliance used for mandibular compression).
advancement. A, Osteotomy of posterior mandibular body and b. Odontalgia secondary to deafferentation (atypical
ramus area with distractor in place. B, Distraction appliance fully
odontalgia) occurs as a result of trauma or surgery
expanded. Regenerated bone fills the intrabone gap during slow
incremental activation of distractor that slowly separates the seg-
(endodontic therapy or extraction). These proce-
ments. (From Hupp JR, Tucker MR, Ellis E: Contemporary Oral dures result in damage to the afferent pain trans-
and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.) mission system. Proposed mechanisms include
peripheral hyperactivity at the surgical site and
central nervous system hyperactivity secondary to
transmission (pain information in the central nervous changes in the second-order nerve in the trigemi-
system sent to the thalamus and cortical centers nal nucleus.
for processing of sensory and emotional aspects), c. Postherpetic neuralgia is a potential sequela of a
and modulation (limitation of rostral flow of pain herpes zoster infection. The pain is classically
information from the spinal cord and trigeminal described as burning, aching, or electric shock
nucleus to higher cortical centers) must occur. The like. It is treated medically with anticonvulsants,
human experience of pain is the sum total of these antidepressants, or sympathetic blocks. Ramsay
physiologic processes and the psychological factors Hunt syndrome is a herpes zoster infection of the
of higher thought and emotions (Figure 3-10). sensory and motor branches of cranial nerves VII
3. When pain lasts longer than 4 to 6 months, it is and VIII resulting in facial paralysis, vertigo, deaf-
defined as chronic, and the psychological aspects are ness, and cutaneous eruption of the external audi-
especially important in patient treatment and tory canal.
management. d. Neuromas may occur after nerve injury. The proxi-
B. Classifications of orofacial pain (Table 3-2). mal section of the transected nerve (if no connec-
1. Neuropathic pain. tion to the distal nerve fragment is present) forms
a. The prototypic neuropathic facial pain is trigemi- sprouts filled with Schwanns cells and other neural
nal neuralgia (tic douloureux). There is classically elements. This area (neuroma) can become very
a trigger point, and the pain typically manifests as sensitive to stimuli and can cause chronic neuro-
electrical, sharp, shooting, and episodic (seconds pathic pain.
to minutes in duration) followed by refractory e. Burning mouth syndrome is most commonly seen
periods. It is most commonly seen in patients older in postmenopausal women. Patients complain of
TRANSMISSION MODULATION
Frontal cortex
Reticulothalamic fibers Somatosensory

cortex
Hypothalamus
Trigeminothalamic tract
plus Periaqueductal
Midbrain Midbrain
spinothalamic tract gray
Main sensory Main sensory

trigeminal trigeminal
Pons
Facial pain
Pons
Trigeminal nucleus caudalis
Trigeminal nucleus
caudalis
Spinothalamic tract Spinal cord
Pain--spinal
innervated regions
Figure 3-10 Trigeminal and spinal pain transmission pathways (left) and trigeminal pain modulation system (right).
Dotted line indicates decreased pain transmission. (From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and Maxillofacial Surgery,
pain, dryness, and burning of the mouth and localized pain in the preauricular region, often
tongue. They may also complain of altered taste involving other muscles of mastication. Pain and
sensation. This syndrome is believed to be second- tenderness develop as a result of abnormal muscle
ary to a defect in pain modulation. In 50% of function and hyperactivity. A parafunctional habit
patients, the symptoms resolve without treatment (clenching, posturing, and bruxing) may be etiologi-
over a 2-year period. Hormonal therapy has not cally related to this clinical entity. It can also be the
been proven to be efficacious, and anticonvulsants result of disc displacement disorders and degenera-
and antidepressants have not yielded consistent tive arthritis. Wear facets may be seen in these
results. patients; in patients with a nocturnal parafunctional
f. Chronic headache is categorized as being migraine, habit, symptoms are often worse in the morning.
tension type, or cluster. 2. Disc displacement disorders are seen with and
g. The presenting symptoms of temporal arteritis without reduction (the return of the normal disc-to-
(giant cell arteritis) are often difficult to differenti- condyle relationship). When reduction is present,
ate from other causes of jaw and head pain, and a normal interincisal opening without deviation can be
delay in diagnosis often leads to blindness in the seen despite joint and muscle tenderness. The opening
affected side (Table 3-3). click corresponds to the condyle moving over the
posterior area of the anteriorly displaced disc, result-
1.6 Temporomandibular Disorders ing in reduction. The reciprocal click (closing click)
A. Overviewclassifications of temporomandibular dis- occurs when the jaw is closed and the disc fails to
orders include myofascial pain, disc displacement dis- maintain its normal reduced relationship to the
orders, degenerative joint disease (DJD), systemic condyle. Nonreduction disc displacement disorders
arthritic conditions, chronic recurrent dislocation, result in limited range of motion and resultant ipsi-
ankylosis, neoplasia, and infections. lateral deviation on opening (Figure 3-11).
B. Types. 3. Systemic arthritic conditions include rheumatoid
1. Myofascial pain disorder (MPD) is the most com- arthritis, systemic lupus erythematosus, and crystal-
mon cause of masticatory pain and compromised line arthropathies including calcium pyrophosphate
function. MPD is characterized by diffuse, poorly dihydrate deposition (pseudogout). There are usually
Table 3-3
Differential Diagnoses of Common Headaches
TEMPORAL ARTERITIS MIGRAINE CLUSTER TENSION
Onset Acute or chronic Acute Acute Chronic
Location Localized Unilateral (40%) Unilateral Global, unilateral
Associated Weight loss, polymyalgia, Nausea, vomiting, Rhinorrhea, lacrimation Multisomatic
symptoms rheumatic, fever, decreased photophobia, of ipsilateral side complaints
vision, jaw claudication phonophobia
Pain character Severe throbbing over Throbbing Sharp stabbing Aching
affected area
Duration Prolonged Prolonged 30min2hr Daily
Prior history + + +
Diagnostic test ESR (+) Nonehistory Nonehistory Nonehistory
PE Tender temporal arteries, Nausea, vomiting, Unilateral, rhinorrhea,
myalgias, fever photophobia, lacrimation, partial
phonophobia Horners syndrome
ESR, Erythrocyte sedimentation rate; PE, physical examination.
A B C
Figure 3-11 Anterior disc displacement without reduction. A, Disc that has been chronically anteriorly displaced now has an
amorphous shape rather than a distinct biconcave structure. B, When the condyle begins to translate forward, the disc remains anterior
to the condyle. C, In maximum open position, disc tissue continues to remain anterior to the condyle, with posterior attachment tissue
interposed between the condyle and the fossa. (From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and Maxillofacial Surgery, ed 6.
St. Louis, Mosby, 2013.)
other clinical systemic signs and symptoms with C. Nonsurgical therapy for TMJ dysfunction.
these conditions. 1. Overviewnonsurgical therapy classically includes
4. Chronic recurrent dislocation occurs when the man- patient education, physical therapy, pharmacother-
dibular condyle translates anterior to the articular apy, and occlusal considerations. Treatment objec-
eminence and requires mechanical manipulation to tives are to decrease pain symptoms and improve
achieve reduction. It is associated with pain and function. In cases of ankylosis and severe symptom-
muscle spasm. When the problem becomes chronic atic DJD, surgery may be the preferred initial treat-
(multiple recurrences), interventions include botuli- ment of choice. For most cases of DJD, MPD, and
num toxin A (Botox) injection of lateral pterygoids internal derangement (reducing and nonreducing),
or surgery. the nonsurgical approach is preferred for initial man-
5. Ankylosis can occur intracapsularly or extracapsu- agement (Figure 3-12).
larly and can be fibrous or bony. Bony ankylosis 2. Counselingparafunctional habits (e.g., nail biting)
results in more limitation of motion. Trauma is the can be associated with MPD, and the patient should
most common cause of ankylosis; however, surgery, be counseled concerning any such habits. Stress may
radiation therapy, and infection can also result in also be related to MPD and pain from internal
temporomandibular joint (TMJ) ankylosis. A patient derangement, and the patient should be counseled by
with ankylosis presents with severely restricted range an appropriately trained professional if indicated.
of motion that may be accompanied by pain. Patients 3. Medical therapymedications used for treatment of
are often able to demonstrate limited translation on TMJ disorders include nonsteroidal antiinflamma-
the affected side but nonetheless have severe limita- tory drugs, steroids, narcotic and nonnarcotic anal-
tion in interincisal opening. gesics, antidepressants, and muscle relaxants. The
modality is based on distention of the joint capsule,

release of adhesions, and potential for removal of
chemical mediators associated with joint pathology.
D. Surgical treatments.
1. Overviewsurgical treatments of the TMJ include
arthrocentesis, arthroscopy, disc repositioning, disc
repair or removal, condylotomy, and total joint
replacement.
2. Arthroscopy involves the placement of two cannulas
to allow access for intracapsular instrumentation
of the superior joint space. Disc manipulation, disc
release, posterior band cautery, and disc reposition-
ing and stabilization techniques all have been
Figure 3-12 Anteriorly displaced disc results in stress on described. Arthroscopy appears to be an effective
retrodiscal tissue. Subsequent fibrosis provides adaptation, modality in a select group of surgical patients and
producing a functional, although anatomically different, interpo-
offers a potentially less morbid access to the joint.
sitional disc. (From Hupp JR, Tucker MR, Ellis E: Contemporary
Oral and Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.)
3. Disc repositioning surgery (open arthroplasty) is
used in patients with painful, persistent clicking-
popping and closed lock. The disc is mobilized, and
choice of medication should be based on the diagno- a posterior wedge may be removed, with suturing
sis, cause of the symptoms, and medical comorbidi- used to reposition the disc into a more anatomically
ties associated with the individual patient. desirable position. Generally, good results are seen
4. Physical therapyphysical therapy modalities can initially, but 10% to 15% of patients report no benefit
be very helpful in the nonsurgical management or worsening symptoms postoperatively.
of patients with TMJ disorders. Biofeedback, ultra- 4. Disc repair or removal (discectomy) is indicated
sound, transcutaneous electrical nerve stimulation when the disc is severely damaged. There is wide
(TENS), massage, thermal treatment, exercise, and variation in the reported results with this procedure,
iontophoresis may be considered. Many of these ranging from excellent resolution to severe degenera-
modalities result in increased circulation to the tion and associated pain and dysfunction. When the
affected region, facilitating the removal of painful disc is removed, recommendations for replacement
metabolic by-products and delivering therapeutic have been made. Some prosthetic materials have
medications. It is believed that TENS may override proven to be problematic, so there is a tendency to
pain input or that it results in the release of endog- favor autogenous materials. Preferred tissues include
enous endorphins. temporalis muscle and fascia, fat, and auricular
5. Occlusionsplints usually can be classified as either cartilage.
autorepositioning or anterior repositioning. The 5. Condylotomy is accomplished by performing an
autorepositioning splint is used for muscle and joint intraoral vertical ramus osteotomy. The proximal
pain when no specific anatomically based pathologic segment is not fixated; this theoretically allows the
entity can be identified. It is hypothesized to work by soft tissues to reposition the condyle and disc pas-
reducing intraarticular pressure. It is designed to sively into a more functionally neutral position. This
have no working or balancing interferences with full technique has been described for treatment of inter-
arch contact. The anterior repositioning splint pro- nal derangement with and without reduction, DJD,
trudes the mandible into a forward position, hypo- and chronic dislocation.
thetically recapturing the normal disc-to-condyle 6. Total joint replacement is indicated for severely
relationship (this has not been shown to be a valid or pathologic joints, as is seen in rheumatoid arthritis,
reliably efficacious modality). Occlusal modification severe DJD, ankylosis, neoplasia, and posttraumatic
may be accomplished via equilibration, prosthetic destruction. Costochondral bone graft reconstruc-
restoration, orthodontics, and orthognathic surgery. tion is the most common autogenous material used.
The role of occlusion in temporomandibular disor- However, this material does not address fossa pathol-
ders is unclear. ogy, which may be significant and must be addressed
6. Arthrocentesis has been shown to be beneficial in in pathologic joints associated with the use of some
patients with internal derangement. One or two prosthetic materials. Total prosthetic joint recon-
needles are placed into the superior joint space. A few structions usually involve a prosthetic condyle and
milliliters of saline or lactated Ringers solution is fossa. Results with this technique have been variable
injected. Some surgeons advocate lavage at this time and may reflect the complexity and diversity of the
as well. It is hypothesized that the efficacy of the cases studied.
area of bone cortex and directly enter an anatomic

1.7 Odontogenic Infections space. The most common space involved is the vestibu-
A. Pathophysiologythe microbiology of odontogenic lar space. These often drain spontaneously and result in
infections represents the flora of the head and neck, an asymptomatic, chronic draining fistula.
mouth, teeth, and gingiva. These infections are polymi- D. Fascial spacesfascial spaces (Table 3-6) involved
crobial. The most common organisms are aerobic in odontogenic infections commonly include the ves-
gram-positive cocci, anaerobic gram-positive cocci, and tibular, buccal, canine, sublingual, submandibular, sub-
anaerobic gram-negative rods (Tables 3-4 and 3-5). mental, masticator (pterygomandibular, masseteric,
B. Organismsthe pathologic mechanism by which these superficial temporal, deep temporal), and lateral pha-
complex infections develop has been well described. ryngeal spaces. They are referred to as potential spaces
The highly virulent aerobic Streptococcus species initiate because under healthy conditions there is no space;
the infectious process after inoculation into deep abscess formation causes cavities along these anatomic
tissues. Cellulitis occurs, followed by proliferation of planes. These spaces are contiguous; as the abscess
anaerobic organisms. The aerobic organisms consume matures and spreads, more of these spaces become
oxygen, making the microenvironment favorable for involved, resulting in increased pain, trismus, dyspha-
the anaerobes. gia, and dysphonia. Canine space infections and deep
C. Progressionthe natural history of the progression of temporal space infections can result in cavernous sinus
odontogenic infections relates to their origin as either thrombosis via the ophthalmic veins. Lateral pharyn-
pulp necrosis and periapical abscess or periodontal geal infections can traverse the retropharyngeal and
infections. Once the infection is into deep tissues, it prevertebral spaces and spread into the mediastinum.
follows the path of least resistance. It may travel through All of these infections should be considered life-
the intramedullary space or perforate through a thin threatening medical emergencies (Figures 3-13 to 3-17).
E. Treatment principlestreatment of odontogenic infec-
Table 3-4 tions requires adherence to six principles.
1. Determine the severity of infection through history
Role of Anaerobic Bacteria
and physical examination. The history should specify
in Odontogenic Infection
%
Anaerobic only 50
Mixed anaerobic and aerobic 44
Aerobic only 6
Data from Brook I, Frazier EH, Gher ME: Aerobic and anaerobic microbiology
of periapical abscess. Oral Microbiol Immunol 6:123-125, 1991. IN Hupp JR,
Tucker MR, Ellis E: Contemporary Oral and Maxillofacial Surgery, ed 6.
St. Louis, Mosby, 2013.
Table 3-5 2
Major Pathogens in Odontogenic

3
Infections 1
Buccinator
PERCENT OF CASES muscle 1
SAKAMOTO HEIMDAHL
MICROORGANISM ETAL (1998) ETAL (1985) 4
2 Mylohyoid
Streptococcus milleri group 65 31 muscle
Peptostreptococcus species 65 31 5
Other anaerobic 9 38 Platysma
muscle
streptococci
Prevotella species (e.g., 74 35
P. oralis and P. buccae) Figure 3-13 As infection erodes through bone, it can
express itself in various places, depending on the thick-
Porphyromonas species 17
ness of overlying bone and the relationship of muscle
(e.g., P. gingivalis)
attachments to the site of perforation. Six possible locations
Fusobacterium species 52 45 are illustrated: vestibular abscess (1), buccal space (2), palatal
From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and Maxillofacial abscess (3), sublingual space (4), submandibular space (5), and
Surgery, ed 6. St. Louis, Mosby, 2013. maxillary sinus (6). (From Cummings CW, etal: Otolaryngology:
Head and Neck Surgery, ed 3, vol 4. St. Louis, Mosby, 2006.)
Table 3-6
Borders of the Deep Fascial Spaces of the Head and Neck
SUPERFICIAL DEEP OR
SPACE ANTERIOR POSTERIOR SUPERIOR INFERIOR OR MEDIAL* LATERAL
Buccal Corner of Masseter muscle Maxilla Mandible Subcutaneous Buccinator
mouth tissue and skin muscle
Pterygomandibular Infraorbital
space space
Infraorbital Nasal Buccal space Quadratus Oral mucosa Quadratus labii Levator anguli
cartilages labii superioris oris muscle
superioris muscle
muscle
Maxilla
Submandibular Anterior belly Posterior belly Inferior and Digastric Platysma muscle Mylohyoid
digastric digastric muscle medial tendon muscle
muscle surfaces of
mandible
Stylohyoid muscle Investing fascia Hyoglossal
muscle
Stylopharyngeus Superior
muscle constrictor
muscles
Submental Inferior Hyoid bone Mylohyoid Investing fascia Investing fascia Anterior
border of muscle bellies of
mandible digastric
muscles
Sublingual Lingual Submandibular Oral mucosa Mylohyoid Muscles of Lingual
surface of space muscle tongue* surface of
mandible mandible
Pterygomandibular Buccal space Parotid gland Lateral Inferior border Medial pterygoid Ascending
pterygoid of mandible muscle* ramus of
muscle mandible
Submasseteric Buccal space Parotid gland Zygomatic Inferior border Ascending ramus Masseter
arch of mandible of mandible* muscle
Lateral pharyngeal Superior and Carotid sheath and Skull base Hyoid bone Pharyngeal Medial
middle scalene fascia constrictors and pterygoid
pharyngeal retropharyngeal muscle
constrictors space*
Retropharyngeal Superior and Alar fascia Skull base Fusion of alar Carotid sheath
middle and and lateral
pharyngeal prevertebral pharyngeal
constrictor fasciae at space
muscles C6T4
Pretracheal Sternothyroid- Retropharyngeal Hyoid Superior Sternothyroid- Visceral fascia
thyrohyoid space cartilage mediastinum thyrohyoid over trachea
fascia fascia and thyroid
gland
From Flynn TR: Anatomy of oral and maxillofacial infections. IN Topazian RG, Goldberg MH, Hupp JR, editors: Oral and Maxillofacial Infections, ed. 4, Philadelphia,
2002, WB Saunders.
*Medial border.
Lateral border.
a chief complaint and determine time and circum- vital signs to determine evidence of sepsis, airway
stances of onset, duration of symptoms, speed of compromise, probable cause, and specific anatomic
progression, and critical systemic symptoms (e.g., space involvement.
dysphagia, dysphonia, trismus, fever, chills, malaise, 2. Evaluate the state of the patients host defense mecha-
numbness of face, headache, meningeal signs, altered nisms with a thorough history and physical examina-
vision). The physical examination should include tion. Certain metabolic diseases (e.g., diabetes),
Figure 3-14 A, Buccal space lies

between the buccinator muscle and the
overlying skin and superficial fascia.
This potential space may become
involved via maxillary or mandibular
molars (arrows). B, Typical buccal
space infection, extending from the
Buccal
level of the zygomatic arch to the infe- space
rior border of the mandible and from
the oral commissure to the anterior
border of the masseter muscle. (From
Flynn TR: The swollen face. Emerg Med
Clin North Am 15:481-519, 2000.)
B
A
Temporalis muscle
Superficial temporal space

Submandibular gland
Temporal
fascia Deep temporal space Mylohyoid muscle
Sphenoid bone Submandibular abscess
Zygomatic Infratemporal
space Platysma muscle
arch
Lateral Figure 3-16 The submandibular space lies between the mylo-
pterygoid hyoid muscle and anterior layer of the deep cervical fascia, just
muscle deep to the platysma muscle, and includes the lingual and inferior
Submasseteric surfaces of the mandible below the mylohyoid muscle attachment.
space Hamular (From Cummings CW, etal: Otolaryngology: Head and Neck Sur-
process
gery, ed 3, vol 4. St. Louis, Mosby, 2006.)
Masseter Medial
muscle pterygoid
muscle
malnutrition, obesity, and drug use may increase or
disguise the severity of these infections (Box 3-5).
Pterygomandibular
space 3. Determine whether the patient should be treated by
a general dentist or a specialist. Some odontogenic
Mandible
infections are life-threatening and require aggressive
medical and surgical intervention. However, most
Figure 3-15 The masticator space is bounded by the can be treated with minor surgical procedures and
fascia overlying the masseter muscle, the medial ptery- commonly used antibiotics (Box 3-6).
goid muscle, the temporalis muscle, and the skull. The
4. Treating the infection surgically is fundamental in
superficial and deep temporal spaces are separated from each
other by the temporalis muscle. The lateral pterygoid muscle
the management of odontogenic infections. Removal
divides the pterygomandibular space from the infratemporal of the source of infection and decompression and
portion of the deep temporal space, and the zygomatic arch drainage of purulence are the goals of surgery.
divides the submasseteric space from the superficial temporal a. Surgical interventions may vary in spectrum from
space. (Redrawn from Cummings CW, etal: Otolaryngology: Head pulpotomy to transfacial incision and drainage of
and Neck Surgery, ed 3, vol 4. St. Louis, Mosby, 2006.) multiple fascial spaces.
Scalene Fascia
Sternocleidomastoid m.
Parotid 4A
Gland Jugular V.
Sympathetic chain
Post. Facial v. I.C.A.
E.C.A.
Stylohyoid m. Post Digastric m.
Lateral P.F. V.F. Stylopharyngeal m.
Pharyngeal Space A.F.Tonsil
Styloglossus m. Aponeurosis
of Zuckerkandel
1 and Testut
Skin
Submandibular
Mandible Gland
P.F. - Internal Carotid artery I.C.A. - Internal Carotid artery

A.F. - Alar Fascia E.C.A. - External Carotid artery
V.F. - Visceral Fascia
Figure 3-17 The lateral pharyngeal space is located between the medial pterygoid muscle laterally and the superior
pharyngeal constrictor medially. The retropharyngeal and danger spaces lie between the pharyngeal constrictor muscles and the
prevertebral fascia. The retropharyngeal space lies between the superior constrictor muscle and the alar fascia. The danger space lies
between the alar layer and the prevertebral fascia. (From Flynn TR: Anatomy and surgery of deep fascial space infections. In Kelly JJ, editor:
Oral and Maxillofacial Surgery Knowledge Update 1994. Rosemont, IL: American Association of Oral and Maxillofacial Surgeons, 1994.)
Box 3-5 Box 3-6

Compromised Host Defenses Criteria for Referral to an
Oral-Maxillofacial Surgeon
Uncontrolled Metabolic Diseases
Poorly controlled diabetes Difficulty breathing
Alcoholism Difficulty swallowing
Malnutrition Dehydration
End-stage renal disease Moderate to severe trismus (interincisal opening
<20mm)
Immune SystemSuppressing Diseases Swelling extending beyond the alveolar process
HIV/AIDS Elevated temperature (>101F)
Lymphomas and leukemias Severe malaise and toxic appearance
Other malignancies Compromised host defenses
Congenital and acquired immunologic diseases Need for general anesthesia
Failed prior treatment
Immunosuppressive Therapies From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and
Cancer chemotherapy Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.
Corticosteroids
Organ transplantation
From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and d. Usually at least 2mL of purulent aspirate is ade-
Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013.
quate and can be obtained with the use of a 5- to
10-mL syringe and an 18-gauge needle. The site of
aspiration should be surgically prepared before
b. The goal is to obtain adequate drainage so that obtaining the sample.
the spread of infection can be brought under e. Depending on the microbiology laboratory policy,
control and the offending agent can be treated with the specimen either should be capped with a
either extraction or endodontic or periodontal rubber stopper after the removal of any evidence
management. of air in the specimen or should be immediately
c. Before incision and drainage, a specimen for placed into an anaerobic specimen tube and sent
culture and sensitivity should be obtained. Ideally, without delay to the laboratory for processing.
the specimen is obtained before the initiation of f. Gram stains also should be obtained to guide anti-
antibiotics. It can be done under local or general biotic management.
anesthesia, depending on the severity of the 5. Support the patient medically with adequate airway
infection. management, hydration and electrolytes, antibiotic
Box 3-7 Box 3-8

Indications for Culture and Antibiotic Bone Vascularity Factors
Sensitivity Testing
Radiation therapy
Infection spreading beyond the alveolar process Osteoporosis
Rapidly progressive infection Osteopetrosis
Previous therapy with multiple antibiotics Pagets disease of bone
Nonresponsive infection (after >48 hours) Fibrous dysplasia
Recurrent infection Bone malignancy
Compromised host defenses Bone necrosis (heavy metals, bisphosphonates)
From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and From Hupp JR, Tucker MR, Ellis E: Contemporary Oral and
Maxillofacial Surgery, ed 6. St. Louis, Mosby, 2013. Maxillofacial Surgery, ed 4. St. Louis, Mosby, 2003.
management, nutritional considerations, analgesics, common initiating causes are odontogenic infec-
and identification of medical comorbidities and their tions and trauma, and they follow a contiguous
possible role in the infection. path. The infection usually begins in the medullary
6. Choose and prescribe appropriate antibiotics. The space involving the cancellous bone. The cortical
use of antibiotics has benefits and risks. Conse- bone, periosteum, and soft adjacent tissues eventu-
quently, the determination that there is a need must ally become involved.
first be established. Generally, if there is evidence c. Occurrenceosteomyelitis is relatively rare and is
of bacterial invasion into underlying tissues that more commonly seen in the mandible than in the
is greater than host defenses can resist, antibiotics maxilla secondary to the difference in blood supply.
should be used. The clinical presentation of bacterial Hematogenous spread of infection to bone can also
invasion can vary substantially based on previously result in osteomyelitis; however, this mechanism is
mentioned host defense capacities. The following cri- rarely seen in the jaw. Patients with host defense
teria have been recommended as indications for anti- suppression are more likely to get osteomyelitis
biotic use (Box 3-7). (see Box 3-5).
7. Odontogenic infection. F. Microbiologythe causative bacteria in osteomyelitis
a. Bacterial targetsbecause the causative bacteria are similar to the bacteria that cause odontogenic infec-
seen in odontogenic infections are highly predict- tions (streptococci, anaerobic cocci, and gram-negative
able, routine empiric therapy is acceptable. The rods). Treatment of osteomyelitis is medical and surgi-
choice should be effective against streptococci and cal. Adequate dbridement, use of appropriate antibiot-
oral anaerobes. ics, and medical assessment to rule out and treat any
b. Antibioticspenicillin V is often the preferred host factors that may predispose the patient to develop-
drug. If the patient is penicillin-allergic, clinda ing osteomyelitis all play a part in the proper manage-
mycin and clarithromycin are good choices. ment of this complex infection.
Narrow-spectrum antibiotics are preferable over
broad-spectrum antibiotics because they are less
likely to alter the normal flora with associated 1.8 Bisphosphonate-Related
symptoms and impact on development of resistant Osteonecrosis of the Jaws
strains. The selected antibiotic should have the A. Overviewbisphosphonate medications inhibit osteo-
lowest incidence of toxicity and side effects; bac clast activities, resulting in decreased bone resorption.
tericidal agents are preferred to bacteriostatic They also affect osteoblast activities, which indirectly
(particularly in immunocompromised hosts), and influences osteoclasts. Because of their effectiveness,
responsible use must take into consideration the bisphosphonates have been used in treating bony
cost of the selected agent. diseases such as multiple myeloma, Pagets disease of
8. Osteomyelitis. bone, and metastatic diseases. However, increasing
a. Definitionosteomyelitis means inflammation of evidence has demonstrated postoperative complica-
the medullary portion of bone. tions associated with bisphosphonate use, including
b. Progressioninfection, inflammation, and isch- chronic bony exposure that does not heal and sponta-
emia are the mechanisms by which osteomyelitis neous exposure of alveolar bones. This process is known
spreads until surgical and medical interventions as bisphosphonate-related osteonecrosis of the jaws
can bring the process under control. The most (BRONJ).
Box 3-9
Stage-Specific BRONJ Treatment Recommendations
At risk category No surgical or medical treatment indicated
Patient education and routine dental care
Stage 1 Antibacterial mouth rinse
Clinical Follow-up on a quarterly basis
Patient education and review of indications for continues bisphosphonate therapy
Stage 2 Oral antibacterial mouth rinse
Symptomatic treatment with oral antibiotics and pain medication
Only superficial dbridements to relieve soft tissue irritation
Stage 3 Antibacterial mouth rinse
Antibiotic therapy and pain control
Surgical debridement or resection for longer term palliation of infection and pain
From Fonseca RJ: Oral and maxillofacial surgery, 2e, Saunders, St. Louis, 2009.
B. Diagnosisthe criteria for diagnosis of BRONJ include 2. Stage-dependent treatment recommendations for
nonhealing bony exposure in jaws for at least 8 weeks patients with BRONJBRONJ is separated into
and current or previous bisphosphonate use without stages, and treatments are modified based on the
history of radiation therapy to the jaws. severity of each stage (Box 3-9).
C. Oral versus intravenous bisphosphonatesoral
bisphosphonates have been used to manage milder 1.9 Biopsies
bony diseases such as osteoporosis, whereas intrave- A. Overviewfour types of biopsies are cytology, aspira-
nous bisphosphonates have been effective in treating tion, incisional, and excisional. The indications vary
bone metastases and hypercalcemia resulting from based on history, anatomy, differential diagnosis, and
malignancy. BRONJ has a greater association with morbidities in the specific clinical setting.
intravenous bisphosphonate use than with oral B. Biopsy techniques.
therapy. 1. Overviewsoft tissue biopsy techniques and prin-
D. Patient managementowing to insufficient scientific ciples conform to standard surgical principles. Block
data, current recommendations for BRONJ manage- anesthesia is preferable because injection into the
ment are based on expert opinions. Before initiating lesion from which the biopsy specimen will be taken
bisphosphonate therapy, patients should have a thor- can distort the architecture and sometimes make
ough dental evaluation and plan to extract teeth that are diagnosis difficult. Tissue stabilization is necessary so
nonrestorable or with guarded prognosis, to remove that accurate surgical incisions can be made. Hemo-
tori, and to perform alveoloplasty. The goal is to stasis is important so that high-volume suction is not
reduce factors that can initiate BRONJ. When possible, needed.
bisphosphonate therapy should be delayed to allow a. Suctiona gauze-wrapped suction tip on a low-
adequate healing time after oral surgery, usually about volume suction device has been recommended to
2 to 3 weeks. avoid the possibility of aspirating the biopsy speci-
1. Duration of bisphosphonate therapythe risk of men into the evacuation device.
BRONJ is increased as duration of bisphosphonate b. Incisionthe incision is preferably done with a
therapy exceeds 3 years. No treatment adjustments sharp scalpel because it is less damaging to the
are needed for patients who take oral bisphospho- specimen and adjacent soft tissue. With this tech-
nates less than 3 years and who have no comorbid nique, margins are most clearly defined, and the
risk factors. A 3-month drug holiday is recom- anatomic architecture of the lesion has the least
mended for patients taking oral bisphosphonates for chance of being altered.
longer than 3 years. To prevent dental problems that c. Lasera carbon dioxide laser in the super-pulsed
eventually require oral surgery, it is important to mode with a small, focused beam is acceptable
emphasize good oral hygiene with patients who have when concerns for homeostasis are significant;
a recent history of bisphosphonate use or who are however, a fine peripheral zone of necrosis does
currently receiving bisphosphonate therapy. If pos- occur.
sible, surgeries and dental implant placement should d. Handling and taggingthe tissue specimen must
be avoided, and endodontic treatments should be be handled with care to avoid mechanical trauma
considered before extractions. that can render the specimen nondiagnostic. A
traction suture can help with this issue. If a malig- area of the lesion, avoiding areas of necrosis, with
nancy is suspected, a tissue tag (identification of adequate depth to make a definitive histologic
surgical margin) should be used to help identify diagnosis.
the orientation of the specimen. If a margin is 5. Excisional biopsy is used on smaller lesions (<1cm)
found to be positive, further resection can be that appear benign and on small vascular and pig-
appropriately directed. Proper specimen care mented lesions. It entails the removal of the entire
requires that the tissue be placed in 10% formalin lesion and a perimeter of surrounding uninvolved
in a volume 20 times that of the specimen. tissue (margin).
e. Wound managementwound management re- 6. Hard tissue or intraosseous biopsy techniques and
quires either a primary closure (if possible) or principles.
placement of periodontal dressings in cases of gin- a. Originmost intraosseous lesions are of odonto-
gival or palatal biopsies in which secondary healing genic origin, usually inflammatory. When this is
would be necessary. not the case, biopsy is usually indicated unless the
f. Recordsa biopsy data sheet should be accurately history suggests otherwise.
filled out, including pertinent history and clinical b. Methoda good history and physical examination
findings. Margin markers should be noted, illustra- are imperative before treatment. Hard tissue biop-
tions used when needed, and radiographs or clini- sies follow the same surgical principles as soft
cal photos included when warranted. It is the tissue lesions; however, there are some special
dentists responsibility to understand the nature considerations secondary to anatomic issues. All
and implications of the diagnosis. If the histopath- radiolucent lesions that require biopsy should be
ologic diagnosis is inconsistent with the clinical aspirated first. Aspiration provides the dentist with
diagnosis, this must be reconciled before further valuable information regarding the nature of the
surgical intervention. Further discussion with lesion (i.e., solid, cystic, fluid-filled, air-filled, vas-
the pathologists, additional biopsy specimens, or cular). It helps determine whether further studies
second opinions from an expert in oral and maxil- are needed (e.g., arteriogram) or whether surgery
lofacial pathology may be required. should proceed (e.g., for a fluid-filled cyst).
2. Oral brush cytology. c. Flapsmucoperiosteal flaps are always used for
a. Usesdetecting cancerous and precancerous intraosseous lesions and should be full thickness,
lesions. It may be useful for monitoring or screen- over sound bone allowing 4- to 5-mm margins,
ing lesions in an adjunctive role to observation. and avoid major neurovascular structures.
b. Methodthe cytology brush is placed over the d. Osseous windows.
suspicious lesion and rotated 5 to 10 times to (1) Osseous windows may be necessary for central
obtain cells from all three epithelial layers. The lesions of the jaw and are determined by size of
collected cells are transferred to a glass slide where the lesion, cortical perforations, and proximity
a fixative is placed. When the specimen is dried, it to teeth and neurovascular structures.
is sent to a laboratory for computer and human (2) The bony structure should be identified for the
analysis. One of three categories is assigned to the pathologist and submitted for histopathologic
cellular specimen: negative, positive (definitive examination with the underlying specimen.
evidence of cellular atypia or carcinoma), or atypi- (3) Specimen removal depends on whether the
cal (abnormal epithelium). All positive and atypi- biopsy is excisional or incisional. In the case of
cal findings should undergo definitive scalpel excisional biopsy, care should be taken to
biopsy. remove the specimen thoroughly while paying
3. Aspiration biopsy or fine-needle aspiration. attention to the anatomy of adjacent teeth and
a. Methoda technique that uses a special syringe neurovascular structures.
and needle to collect cells from a clinically or (4) After the lesion is removed, 1mm of adjacent
radiographically identified mass. osseous tissue should be removed by curettage
b. Usesrelatively low morbidity and high diagnos- in all directions. In an incisional biopsy, the
tic accuracy for most lesions. Other uses of aspira- desired section of specimen is removed, and
tion techniques include simple aspiration of a hard the wound is closed after irrigation. Specimen
or soft tissue lesion to determine if the lesion is care is similar to care of soft tissue biopsy
solid, cystic, or vascular. This use of aspiration is specimens.
indicated in any intraosseous lesion before surgical
exploration. 1.10 Surgical Management of Cysts
4. Incisional biopsy is a technique used when a lesion and Tumors
is large (>1cm), polymorphic, suspicious for malig- A. Overviewgoals of surgical management are eradica-
nancy, or in an anatomic area with high morbidity. tion of the pathologic entity and esthetic functional
The specimen must be obtained in a representative rehabilitation. For this to occur, issues that affect final
reconstruction and return to function must be taken c. Cancer of the breast, prostate, lung, kidney, thyroid,
into consideration at the initiation of treatment. Things hematopoietic system, and colon can metastasize
to consider are patient expectations and physical and to the head and neck region.
emotional tolerances, methods and indications for d. When a primary cancer of the head and neck
grafting, soft tissue management, dental rehabilitation, is diagnosed, clinical staging should be per-
and strength and range-of-motion rehabilitation. Con- formed before definitive treatment. Staging may
siderations for nerve preservation are predicated on the include (in addition to a thorough history and
anatomy and cell type and biologic characteristics of the physical examination) CT scans, positron emis-
lesion. sion tomography scans, chest radiographs, and
B. Cysts and cystlike lesions can be classified as fissural or panendoscopies.
odontogenic. Odontogenic keratocysts tend to act more e. Combinations of surgery, radiation therapy, and
aggressively and have higher rates of recurrence than chemotherapy are used for treating this class of
fissural cysts and cysts of odontogenic inflammatory disease.
origin. Cysts of the jaw are treated by enucleation, f. Decisions for treatment of head and neck malig-
marsupialization, a staged combination of enucleation nancies are driven by histologic type, stage, loca-
and marsupialization, or enucleation and curettage tion, and whether it is a primary or metastatic
(Table 3-7). lesion. In addition, before any definitive treatment,
C. Tumors of the jaws. the patients wishes and medical comorbidities
1. Overviewjaw tumors vary in their natural history, must be taken into consideration.
origin, duration, and clinical behavior. Depending on 3. Reconstruction.
these factors, taking into consideration the anatomic a. The decision to reconstruct after jaw resection
location and size, enucleation and curettage or resec- is ideally made before definitive surgery as part
tion may be an option. Categories of resection are of a comprehensive treatment plan that takes
marginal, partial thickness, total, and composite. into account patient expectations, medical
Table 3-8 summarizes in general terms the primary comorbidities, prognosis, and the functional and
treatment modalities for tumors of the jaw based on esthetic considerations based on the anatomic
histologic criteria. deformity.
2. Malignant tumors. b. Treatment options range from no reconstruction
a. Most common are epidermoid carcinomas (squa- with wound management and secondary healing
mous cell). (possible removable prosthetic use) to complex
b. The salivary glands, blood vessels, lymphatics, microvascular osteocutaneous reconstruction with
muscle, bone, and other connective tissue can placement of endosseous implants.
also give rise to primary malignancies of the head c. The timing of the reconstruction varies among
and neck. medical centers.
Table 3-7
Treatment of Cysts of the Jaws
TECHNIQUE DESCRIPTION INDICATIONS PROS/CONS
Enucleations Shelling out without rupture Treatment of choice should be Often definitive treatment,
used when it can safely be done easier postoperative
without sacrificing adjacent wound care/may weaken
structures jaw, damage structure
Marsupialization Surgical window decompression When enucleation would damage Simple and may spare vital
evacuation adjacent structures. Morphology structure/difficult wound
of lesion makes enucleation care, pathologic tissue is
unlikely to be successful left
Staged enucleation and 1st-degree marsupialization/ See above if cyst is not totally See above
marsupialization 2nd-degree enucleation obliterated after
marsupialization heals
Enucleation and Shelling out without rupture, Odontogenic keratocysts. Any cyst May recur, more destructive
curettage followed by 1- to 2-mm that recurs after enucleation to adjacent structures
curettage of adjacent bone
Data from Peterson LJ, etal: Contemporary Oral and Maxillofacial Surgery, ed 4. St. Louis, Mosby, 2003.
Table 3-8
Types of Jaw Tumors and Primary Treatment Modalities
ENUCLEATION OR CURETTAGE MARGINAL OR PARTIAL
OR BOTH RESECTION COMPOSITE RESECTION*
Odontogenic Tumors
Odontoma Ameloblastoma Malignant ameloblastoma
Ameloblastic fibroma ameloblastic Calcifying epithelial odontogenic Ameloblastic fibrosarcoma
fibro-odontoma tumor
Ameloblastic odontosarcoma
Adenomatoid odontogenic tumor Myxoma Primary intraosseous carcinoma
Calcifying odontogenic cyst Ameloblastic odontoma
Cementoblastoma Squamous odontogenic tumor
Central cementifying fibroma
Fibro-osseous Lesions
Central ossifying fibroma Benign chondroblastoma Fibrosarcoma
Fibrous dysplasia (if necessary) Osteosarcoma
Cherubism (if necessary) Chondrosarcoma
Central giant cell granuloma Ewings sarcoma
Aneurysmal bone cyst
Osteoma
Osteoid osteoma
Osteoblastoma
Other Lesions
Hemangioma Hemangioma Lymphomas
Eosinophilic granuloma Intraosseous salivary gland malignancies
Neurilemoma
Neurofibroma Neurofibrosarcoma
Pigmented neuroectodermal tumor Carcinoma that has invaded jaw
Note: These are generalities. Treatment is individualized for each patient and each lesion.
*These lesions are malignancies and may be treated variably. For lesions totally within the jaw, partial resection may be performed without adjacent soft tissue and
lymph node dissections. Radiotherapy and chemotherapy may also play a role in overall therapy.
d. Cases involving reconstruction are complex and applied locally in a concentration without toxic
benefit from a multidisciplinary team approach effects. We are concerned with sensory nerves den-
from the time of definitive treatment through tally; however, local anesthetics also block motor
reconstruction. nerves if the concentration is sufficient.
B. Pharmacodynamics of local anesthetics (block sodium
channels).
2.0 Local Anesthesia 1. Differential nerve blockade (concept of critical
Kenneth L. Reed length).
a. In 1942, Takeuchi and Tasaki reported that com-
Outline of Review plete anesthesia occurs when three consecutive
2.1 Local Anesthetic Drug Overview nodes of Ranvier are blocked (assuming myelin-
2.2 Local Anesthesia Techniques ated nerves), and this finding continues to be
reported in dental textbooks today. This principle
of critical length also applies to unmyelinated
2.1 Local Anesthetic Drug Overview nerves.
A. Selected pharmacology of local anesthetics (see Section b. Studies have demonstrated that anesthetic block-
8 on Pharmacology for further details). ade can be cumulative along the axon length,
1. Definitiona local anesthetic is a drug that revers- resulting in a gradual reduction in conduction
ibly blocks the conduction of nerve impulses when velocity that eventually leads to a complete
blockade. Increasing the length of the nerve (2) Protects the vasoconstrictor from oxidation.
exposed to the local anesthetic may increase the (3) Present only in local anesthetic cartridges with
success of clinical anesthesia. This finding might a vasopressor (epinephrine or levonordefrin).
suggest that if an inferior alveolar nerve block fails, 3. Methemoglobinemia.
the clinician may wish to perform a second injec- a. Essentially unique to prilocaine when exceeding
tion via the Gow-Gates technique because this 600mg (for a 70-kg adult), but a lower dose applies
would lead to an increase in the length of inferior in a patient with hereditary methemoglobinemia.
alveolar nerve bathed in local anesthetic. The second most common local anesthetic to cause
c. All nerves are susceptible to blockade, regardless this is articaine.
of their function. E. Potency.
(1) Motor and sensory. 1. Potency and clinical efficacy are separate issues.
d. Sensations disappear and reappear in a definite a. When used for inferior alveolar nerve blocks, all
order. local anesthetics have been demonstrated to have
(1) Pain. equal efficacy; there is no one local anesthetic that
(2) Temperature. has been shown to be superior.
(3) Touch. b. All local anesthetic manufacturers have adjusted
(4) Pressure. the concentration of their drugs such that 1mL of
C. Pharmacokinetics of local anesthetics (see Section 8 on drug A is equivalent to 1mL of drug B with
Pharmacology). respect to potency (and toxicity).
1. Redistribution is affected by the following. c. For two drugs that reach the same therapeutic
a. Diffusion away from the site of action. effect per volume, a drug in 1mg/mL is more
b. Vascularity of the injection site. potent than a drug in 2mg/mL.
(1) Increased blood flowshorter duration of d. Bupivacaine is the most potent local anesthetic
action. packaged for dentistry, and prilocaine and artic-
c. Protein binding characteristics of the local anes- aine are the least potent.
thetic that are directly related to lipid solubility. F. Addition of vasoconstrictors (see Section 8 on
(1) Increased protein bindingincreased lipid Pharmacology).
solubility (increased duration of action). 1. Primary rationale.
2. Principles. a. Increase the duration of effect.
a. Duration of action of local anesthetics is directly 2. Secondary rationales.
proportional to protein binding and lipid a. Reduce systemic toxicity by decreasing the rate
solubility. of systemic absorption of a given dose of local
b. The lower the pKa of the drug (closer to physiologic anesthetic.
pH), the faster the onset of action. b. Reduce bleeding by decreasing blood flow into the
D. Systemic toxicities. operative area.
1. Initial clinical signs and symptoms. (1) This applies to infiltration into the local area
a. Mild to moderate toxicity. not epinephrine used in a nerve block (given
(1) Talkativeness, apprehension, excitability, distant from the site).
slurred speech, dizziness, and disorientation. 3. Drug interactions.
b. Severe toxicity. a. Antidepressantstricyclic (e.g., amitriptyline
(1) Seizures, respiratory depression, coma, death. [Elavil]) and newer atypical drugs (e.g., duloxetine
2. Allergic responses. [Cymbalta]).
a. Esters have a high incidence (approximately 5% of (1) Increased sensitivity to epinephrine.
the population). b. Nonspecific blockerspropranolol (Inderal).
b. Amides have a low incidence (<1% of the (1) Enhance peripheral 1-adrenergic effects with
population). 2 blockade (unopposed ).
c. Note: an allergy to a local anesthetic packaged in a (a) blockade decreases heart rate.
dental cartridge before 1985 may have been due to (b) Epinephrine increases blood pressure.
an allergy to methylparaben, not the local anes- (c) The net result is likely to be an increase in
thetic agent itself. For patients allergic to esters and blood pressure without tachycardia.
amides, diphenhydramine (Benadryl) may be an c. Normal, healthy (American Society of Anesthesi-
alternative choice; however, the package insert for ologists [ASA] 1) patient.
diphenhydramine specifically warns against this. (1) Maximum of 200g of epinephrine.
d. Metabisulfite. d. Patients with cardiovascular compromise or
(1) An antioxidant, not a preservative, with a low patients taking tricyclic or atypical antidepressants
incidence of allergenicity. or nonselective blockers.
(1) Limit epinephrine to no more than 40g per 2. Techniqueposition of the needle.
appointment. a. Distal to the malar process.
G. Pregnancy and lactation. b. At 45 degrees to the mesiodistal plane.
1. Pregnancy class C drugsarticaine, bupivacaine, c. At 45 degrees to the buccolingual plane.
mepivacaine, epinephrine. d. With a 15- to 16-mm depth of penetration.
2. Pregnancy class Blidocaine, prilocaine. e. Deposit 1.0mL of local anesthetic (cartridge
H. Pediatrics. volume = 1.8mL) slowly after aspiration.
1. If safety of a local anesthetic is based on the number C. True anterior superior alveolar nerve block.
of milliliters that may be administered to a pediatric 1. Area of anesthesiafrom the midline of the maxilla
patient of a given size, 2% lidocaine with 1:100,000 to the mesiobuccal aspect of the maxillary first
epinephrine is the safest local anesthetic for use in molar.
children. a. Anesthetizes the anterior superior alveolar, middle
2. Bupivacaine is not approved by the U.S. Food and superior alveolar, inferior palpebral, lateral nasal,
Drug Administration for use in children younger and superior labial nerves.
than 12 years. b. Does not anesthetize palatal tissue.
3. The maximum recommended doses of local anes- 2. The entrance to the infraorbital foramen is located
thetics for adults are as follows. just inferior to the infraorbital rim at the infraorbital
notch along an imaginary line from the pupil of the
Maximum Maximum
eye to the ipsilateral commissure of the lip.
Recommended Total Dose
a. Needle penetration is over the maxillary first
Drug pKa Dose (mg/kg)* (mg)*
premolar.
Articaine (4%) 7.7 7
b. Needle penetration is in the long axis of the tooth,
Bupivacaine (0.5%) 8.1 90
15mm deep and lateral to or at the height of the
Lidocaine (2%) 7.7 7 500
buccal vestibule.
Mepivacaine 7.6 6.6 400
c. The needle touches bone as an endpoint.
(2%, 3%)
d. After aspiration, 0.9mL ( 1 2 cartridge) of anesthetic
Prilocaine (4%) 7.8 8 600
is injected slowly.
*Lower of the two values. (1) Note: 2a-d describes the infraorbital nerve
Based on combination with 1:100,000 epinephrine. block, which guarantees only anesthesia of the
soft tissue. To convert the infraorbital nerve
block to the true anterior superior alveolar
2.2 Local Anesthesia Techniques nerve block that guarantees anesthesia of the
A. Needle dimensions. pulps of teeth, add the next step.
1. Lengthshort needles average 20mm and long e. Pressure applied for 2 minutes (by the clock).
needles average 32mm. D. Greater palatine.
2. Outside diameter. 1. Area of anesthesiaon the palate from the canine
a. 30-gauge averages 0.3mm. distally to the posterior aspect of the hard palate and
b. 27-gauge averages 0.4mm. from the gingival margin to the midline.
c. 25-gauge averages 0.5mm. 2. The greater palatine foramen is generally located
3. Needle gauge. roughly halfway between the gingival margin and
a. Positive aspiration is directly correlated to needle midline of the palate and approximately 5mm ante-
gauge. rior to the junction of hard and soft palate.
b. Larger gauge needles do not deflect as often. 3. Technique.
c. Larger gauge needles do not break as often. (There a. Topical anesthesia.
have been hundreds of lawsuits that have gone to b. Pressure anesthesia20 seconds minimum.
court concerning needle breakage. About 97% of c. Angulation of needle insertion is immaterial.
needle breaks have involved breakage of a 30-gauge d. Depth of penetration: to bone (generally about
needle.) 5mm).
d. Patients cannot tell the difference between e. Inject 0.5mL (approximately 1 3 cartridge) after
25-gauge, 27-gauge, and 30-gauge needles. aspiration.
B. Posterior superior alveolar nerve block. E. Nasopalatine.
1. Area of anesthesiafrom the maxillary third molar 1. Area of anesthesiapalatal soft tissue from canine to
anteriorly to the maxillary first molar with the pos- canine, bilaterally (the premaxilla).
sible exception of the mesiobuccal aspect of the max- 2. Technique.
illary first molar. This injection does not anesthetize a. Topical anesthesia.
palatal tissue. b. Pressure anesthesia20 seconds minimum.
c. Needle tip at a 45-degree angle to the palatal soft b. Anesthesia.

tissue; penetration is at the junction of the palate (1) Inferior alveolar.
and incisive papilla. (2) Lingual.
d. Endpointbone. (3) Long buccal.
e. Inject 0.5mL after aspiration. c. Useful for treating for the following.
F. Local anesthesiamandibular techniques. (1) Uncooperative children.
1. Mental or incisive. (2) Patients with trismus.
a. Area of anesthesia (mental nerve block)soft d. Technique.
tissue on the buccal of the premolars anteriorly to (1) A long needle is inserted parallel to the maxil-
the midline lip, chin, periosteum, and bone in the lary occlusal plane at the level of the maxillary
affected area. buccal vestibule.
b. Topical anesthesia. (a) Note: the original technique recommended
c. Insert needle in the depth of the buccal vestibule at the level of the maxillary mucogingival
opposite the mandibular premolars. junction.
d. 5-mm depth of insertion. (2) The depth of penetration is approximately one
e. Deposit 0.9mL ( 1 2 cartridge) local anesthetic. half the mesiodistal length of the ramus.
(1) Note: 1a-e describes the mental nerve block, (a) About 25mm in adults.
which guarantees only anesthesia of the soft (b) Proportionately less in children.
tissue. To convert the mental nerve block to the (3) This endpoint is just superior to the lingula.
incisive nerve block that guarantees anesthesia (4) The injection is performed blindly because no
of the pulps of teeth, add the next stay. bony endpoint exists.
f. Pressure for 2 minutes. (5) In adult patients, a rule of thumb is that at the
2. Inferior alveolar nerve block. depth of needle penetration, the hub of the
a. Area of anesthesiapulps and buccal soft tissues needle should be between the maxillary first
of the mandibular teeth (except the area inner- and second molars.
vated by the buccal nerve), lip, chin, periosteum, 4. Gow-Gates technique.
and bone in the affected area. a. First described in the literature in 1973.
b. Traditional (Halstead) block. b. Originally the technique involved only extraoral
c. Approach from the contralateral premolars. landmarks.
(1) 1.0cm above the mandibular occlusal plane c. Anesthesia.
and parallel to it. (1) Inferior alveolar.
(2) With a needle endpoint 50% of the mesiodistal (2) Lingual.
length of the ramus, distally. (3) Auriculotemporal.
d. Alternatively, higher mandibular block. (4) Mylohyoid nerve.
(1) Approach from the contralateral premolars. (5) Long buccal (75% of the time).
(a) 1.5cm above the mandibular occlusal plane d. Technique.
and parallel to it. (1) Have the patient open the mouth as widely as
(b) With a needle endpoint 60% of the mesio- possible to rotate and translate the condyle
distal length of the ramus, distally. forward.
e. With either block. (2) The condyle is palpated with the fingers of the
(1) Advance a 25-gauge long needle until you hit nondominant hand while the cheek is retracted
bone (required). with the thumb.
(a) Withdraw 1mm. (3) Beginning from the contralateral canine, the
(b) Aspirate. needle is positioned so that a puncture point
(c) Inject 1.5mL (approximately 3 4 of a is made approximately at the location of
cartridge) of local anesthetic over 2 the distobuccal cusp of the maxillary second
minutes. molar.
(d) Withdraw the needle halfway (approxi- (a) The needle is inserted slowly to a depth of
mately 10 to 15mm). 25 to 30mm until bone is contacted.
(e) Aspirate. (b) The injection must not be performed unless
(f) Slowly inject the lingual nerve. bone is contacted.
(g) Save a few drops of anesthetic for the buc- (c) The needle is withdrawn slightly, and the
cinator (long buccal) nerve if needed. entire cartridge of local anesthetic solution
3. Vazirani-Akinosi technique. is injected after aspiration.
a. First described in the literature in 1960 by Vazirani (d) This injection is unique among intraoral
and again by Akinosi in 1977. injections because the operator does not
attempt to get as close as possible to the 5. On evaluation of an immediate postoperative pan-

nerve to be anesthetized. oramic film of a dental implant replacing tooth #30,
(e) The needle tip should be approximately you measure a distance of 1.5mm from the apex of the
1.0cm directly superior to the nerve, in the implant to the inferior alveolar nerve canal. This is a
superior aspect of the pterygomandibular titanium implant in an otherwise healthy patient.
space. Which of the following actions is indicated?
A. Proceed with immediate loading of the implant
B. Continue but perform a two-stage procedure only
References C. Back the implant out approximately 0.5mm to
Hupp JR, Tucker MR, Ellis E: Contemporary Oral and Max- ensure a safe distance from the nerve
illofacial Surgery, ed 6. St. Louis, Mosby, 2013. D. Remove the implant and plan a repeat surgery after
Larsen P, Ghali GE, Waite P: Petersons Principles of Oral 4 months of healing
and Maxillofacial Surgery, ed 3. Shelton, CT: Peoples 6. Myofascial pain dysfunction may be described as
Medical Publishing House, 2012. _____.
Peterson LJ, et al: Contemporary Oral and Maxillofacial A. Masticatory pain and limited function
Surgery, ed 4. St. Louis, Mosby, 2003. B. Clicking and popping of the joint
C. An infectious process
D. Dislocation of the disc
Sample Questions 7. A 21-year-old man is referred for an orthognathic
surgery consultation. After routine examination and
1. Which of the following does not represent a fascial review of radiographs, you note the following problem
space for the spread of infection? list: class III skeletal facial deformity with a negative
A. Superficial temporal space overjet of 6mm and significant maxillary crowding,
B. Pterygomandibular space missing left mandibular first molar owing to dental
C. Masseteric space decay with multiple other early carious lesions, and
D. Rhinosoteric space calculus on the lingual surfaces of teeth #22 through
E. Submental space #27 with gingival inflammation. Which of the follow-
2. Which of the following classifications of impacted ing is the most appropriate order in which this patients
teeth must always involve both bone removal and sec- oral health needs should be sequenced?
tioning during the surgical procedure? A. Definitive crown and bridge therapy, orthodontics
A. Mesioangular impaction to relieve crowding and to coordinate arches, caries
B. Horizontal impaction management, surgery to correct the skeletal dis-
C. Vertical impaction crepancy, and periodontal therapy to control gin-
D. A and B only gival inflammation
E. A, B, and C B. Caries management, orthodontics to relieve crowd-
3. Which of the following does not represent a possible ing and to coordinate arches, definitive crown and
finding of severe infection? bridge therapy, periodontal therapy to control
A. Trismus gingival inflammation, and surgery to correct the
B. Drooling skeletal discrepancy
C. Difficult or painful swallowing C. Periodontal therapy to control gingival inflamma-
D. Swelling and induration with elevation of the tion, definitive crown and bridge therapy, ortho-
tongue dontics to relieve crowding and to coordinate
E. Temperature of 99F arches, surgery to correct the skeletal discrepancy,
4. You are performing a 5-year follow-up on a 43-year- and caries management
old patient with an implant. When comparing radio- D. Periodontal therapy to control gingival inflamma-
graphs, you estimate that there has been almost 0.1mm tion, caries management, orthodontics to relieve
loss of bone height around the implant since it was crowding and to coordinate arches, surgery to
placed. Which of the following is indicated? correct the skeletal discrepancy, and definitive
A. Removal of the implant and replacement with a crown and bridge therapy
larger size implant 8. Systemic effects of obstructive sleep apnea syndrome
B. Removal of the implant to allow healing before include all of the following except one. Which one is
another one can be placed 4 months later the exception?
C. Remaking the prosthetic crown because of tangen- A. Hypertension
tial forces on the implant B. Cor pulmonale
D. The implant is doing well; this amount of bone loss C. Aortic aneurysm
is considered acceptable D. Cardiac arrhythmia
9. Which of the following is not a vital part of the physical A. Soft tissue lesion is 0.5cm 1. Excisional biopsy
examination for patients with TMJ complaints? in size __ 2. Incisional biopsy
A. Soft tissue symmetry B. Osteomyelitis of the jaw __ 3. Aspiration or
B. Joint tenderness and sounds C. Soft tissue lesion is 4cm in fine-needle
C. Soft palate length size __ biopsy
D. Range of motion of the mandible D. Cystic or vascular soft 4. Hard or tissue or
E. Teeth tissue lesions deep to intraosseous
10. Which of the following is considered the highest and mucosa __ biopsy
most severe classification of maxillary fracture?
A. Le Fort I 16. Of the following anesthetics, which one is the least
B. Le Fort II appropriate and which one is the most appropriate
C. Le Fort III local anesthetic for use in children? (Choose two.)
D. Le Fort IV A. Articaine
11. Which of the following is not a relative contraindica- B. Bupivacaine
tion for routine elective oral surgery? C. Lidocaine
A. Unstable cardiac angina D. Mepivacaine
B. History of head and neck radiation E. Prilocaine
C. Chronic sinusitis 17. Most injectable local anesthetics used in dentistry
D. Hemophilia today are ______.
12. Which of the following statements regarding temporo- A. Esters
mandibular disorders is true? B. Amides
A. The primary treatment for most patients with facial C. Hybrids of both esters and amides
pain is TMJ surgery. D. None of the above
B. Disc displacement without reduction can cause a 18. Which of the following local anesthetics is marketed
decrease in interincisal opening. for dentistry in the United States in more than one
C. Myofascial pain is commonly related to para- concentration?
functional habits but not commonly related to A. Articaine
stress. B. Bupivacaine
D. Systemic arthritic conditions do not affect the TMJ C. Lidocaine
because it is not a weight-bearing joint. D. Mepivacaine
13. Select from the following list correct applications and 19. The major factor determining whether aspiration can
indications of antibiotic use in odontogenic infections. be reliably performed is the _____.
(Choose three.) A. Needle gauge
A. Antibiotic should cover Staphylococcus aureus and B. Needle length
aerobes C. Injection performed
B. -Lactam antibiotics (e.g., penicillin V) are D. Patient
preferred 20. The ______ injection is recommended for palatal soft
C. No antibiotic coverage is indicated for patients with tissue anesthesia from canine to canine bilaterally in
high-grade fever the maxilla.
D. Clindamycin can be used if a patient is allergic to A. Posterior superior alveolar
penicillin B. Inferior alveolar
E. Broad-spectrum instead of narrow-spectrum anti- C. Long buccal
biotic coverage is preferred D. Nasopalatine
F. Bactericidal agents are preferred to bacteriostatic 21. Which of the following local anesthetics has the lowest
agents in immunocompromised patients pKa?
14. Select from the following list factors that make surgical A. Lidocaine
removal of impacted third molars more difficult. B. Prilocaine
(Choose three.) C. Mepivacaine
A. Distoangular positioned third molar D. Bupivacaine
B. Mesioangular positioned third molar 22. Assuming a 1.8mL-cartridge, three cartridges of 2%
C. Narrow periodontal ligament lidocaine with 1:100,000 epinephrine contain _____
D. Tooth roots are one half to one third formed lidocaine.
E. Close proximity to inferior alveolar nerve A. 36mg
F. Fused conical roots B. 54mg
15. For each clinical condition listed, select the most C. 54g
appropriate biopsy methods from the list provided. D. 108mg
23. Which nerve block anesthetizes the distobuccal aspect C. Nasopalatine

of the mandibular first molar? D. Inferior alveolar
A. Posterior superior alveolar 27. Which of the following are possible reasons why some
B. Middle superior alveolar local anesthetic preparations have a longer duration of
C. Anterior superior alveolar action than others? (Choose all that apply.)
D. Inferior alveolar A. Presence of a vasoconstrictor
24. Which of the following is the longest acting local B. Percent protein binding
anesthetic? C. Degree of lipid solubility
A. Mepivacaine D. pKa of the drug
B. Lidocaine E. pH of the preparation
C. Prilocaine F. Concentration of the local anesthetic solution as
D. Bupivacaine marketed
25. For a patient with a history of very significant liver 28. Which of the following apply to articaine? (Choose all
disease, which of the following would be the safest that apply.)
local anesthetic? A. Has amide properties
A. Articaine B. Has ester properties
B. Prilocaine C. Is packaged in the lowest concentration of all local
C. Lidocaine anesthetics in dentistry
D. Bupivacaine D. Is packaged in the highest concentration of all local
26. Which of the following injections has the highest anesthetics in dentistry
degree of failure? E. Has hepatic biotransformation
A. Posterior superior alveolar F. Has extrahepatic biotransformation
B. Lingual
SECTION 4
Oral Diagnosis
JEFFREY C.B. STEWART
SANJAY M. MALLYA
OUTLINE 1.16 Bone (Nonodontogenic) LesionsGiant Cell Lesions

1.17 Bone (Nonodontogenic) LesionsInflammatory Diseases
1. Oral Pathology and Diagnosis 1.18 Bone (Nonodontogenic) LesionsMalignancies
2. Oral Radiology 1.19 Hereditary Conditions
1.1 Developmental Conditions

Developmental conditions are soft tissue or hard
1.0 Oral Pathology and Diagnosis tissue defects that occur during the development of the
Jeffery Stewart individual, either before or after birth. Most are easily
A working knowledge of oral pathology is fundamental recognizable.
to the recognition and diagnosis of oral and maxillofacial A. Oral-facial clefts.
diseases in patients. This outline and the test questions 1. Cleft lip.
that follow are intended to refresh and test the students a. Unilateral (80%) or bilateral (20%).
memory of clinical oral pathology. Some entities are simply b. Defect between medial nasal process and maxillary
listed, and some entities are not included because of their process.
rarity. If students detect any areas of weakness, they are c. Approximately 1 in 1000 births, but varies with
encouraged to consult a current textbook for detailed dis- race.
cussions of the entities and conditions that require addi- 2. Cleft palate.
tional study. a. Lack of fusion between palatal shelves; approxi-
mately 1 in 2000 births.
Outline of Review b. Cleft lip (25%), cleft palate (25%), cleft lip and
1.1 Developmental Conditions palate (50%).
1.2 Mucosal LesionsPhysical-Chemical B. Lip pits.
1.3 Mucosal LesionsInfections 1. Invaginations at the commissures or near the midline.
1.4 Mucosal LesionsImmunologic Diseases C. Fordyce granules.
1.5 Mucosal LesionsPremalignant Conditions 1. Ectopic sebaceous glands.
1.6 Mucosal LesionsMalignancies 2. Commonly seen in buccal mucosa or lip.
1.7 Connective Tissue TumorsBenign D. Leukoedema.
1.8 Connective Tissue TumorsMalignant 1. Bilateral opacification of the buccal mucosa.
1.9 Salivary Gland DiseasesReactive Lesions 2. Common; no significance.
1.10 Salivary Gland DiseasesBenign Neoplasms E. Macroglossia (Box 4-1).
1.11 Salivary Gland DiseasesMalignant Tumors F. Thyroid congenital abnormalities.
1.12 Lymphoid Neoplasms 1. Lingual thyroid.
1.13 Odontogenic LesionsOdontogenic Cysts a. Thyroid tissue mass, midline tongue base.
1.14 Odontogenic LesionsOdontogenic Tumors b. Caused by incomplete descent of thyroid anlage.
1.15 Bone (Nonodontogenic) LesionsFibro-osseous Lesions c. May be patients only thyroid.
2. Thyroglossal tract cyst.
The section editors acknowledge Drs. Joseph Regezi and Stuart C. White for a. Midline neck swelling secondary to cystic change
their contributions as authors and editors of the Oral Diagnosis section of the
first edition. Their outstanding efforts provided the foundation for this of remnants of thyroid tissue.
revision. b. Located along embryonic path of thyroid descent.
109
110 Section 4 Oral Diagnosis
Box 4-1
Causes of Macroglossia
Congenital hyperplasia/hypertrophy
Tumorslymphangioma, vascular malformation,
neurofibroma, multiple granular cell tumors, salivary
gland tumors
Endocrine abnormality
Acromegaly, cretinism
Infections obstructing lymphatics
Beckwith-Wiedemann syndrome
Macroglossia, exophthalmos, gigantism
Amyloidosis
Figure 4-2 Stafne bone cyst. (From Regezi JA, Scuibba JJ,
Jordan RCK: Oral Pathology: Clinical Pathologic Correlations,
ed 6. St. Louis, Saunders, 2012.)
2. Vascular malformation.
a. Persistent malformation of capillaries, veins, and
arteries.
b. Exhibits a thrill (palpate a pulse) and bruit (hear a
pulse).
c. Type of vascular malformation known as
Sturge-Weber syndrome (encephalotrigeminal
angiomatosis).
(1) Lesions involve skin along one of the branches
of the trigeminal nerve.
(2) The leptomeninges of the cerebral cortex may
be involved by the malformations, leading to
mental retardation and seizures.
Figure 4-1 Geographic tongue. (From Regezi JA, Scuibba JJ, J. Lymphangioma.
Jordan RCK: Oral Pathology: Clinical Pathologic Correlations, 1. Congenital focal proliferation of lymphatic channels.
ed 6. St. Louis, Saunders, 2012.) 2. When occurring in the neck, it is called hygroma colli.
K. Exostoses.
1. Excessive cortical bone growth of unknown cause.
G. Geographic tongue (benign migratory glossitis, ery- 2. Buccal exostoses, torus palatinus, torus mandibu-
thema migrans) (Figure 4-1). laris.
1. Common (2% of population) benign condition of the L. Developmental soft tissue cysts (including thyroglossal
tongue of unknown cause. tract cyst).
2. Appears as white annular lesions surrounding atro- 1. Dermoid cyst.
phic red central zones that migrate with time. a. Mass in midline floor of mouth if above mylohyoid
3. Occasionally symptomatic (mild pain or burning). muscle.
4. No treatment necessary. b. Mass in upper neck if below mylohyoid muscle.
H. Fissured tongue. 2. Branchial cyst.
1. Fissuring of tongue dorsum. a. Epithelial cyst within lymph node of the neck.
2. Common (3% of population) and usually 3. Oral lymphoepithelial cyst.
asymptomatic. a. Cyst within lymphoid tissue that is the counterpart
3. Component of Melkersson-Rosenthal syndrome. of branchial cyst of the neck.
a. Fissured tongue, granulomatous cheilitis, and b. Nodule commonly in soft palate, oral floor, or
facial paralysis. lateral tongue.
I. Hemangioma. M. Developmental jaw cysts and cystlike lesions
1. Congenital hemangioma. (pseudocysts).
a. Focal proliferation of capillaries. 1. Stafne (static) bone defect (Figure 4-2).
b. Most lesions undergo involution; persistent lesions a. Diagnostic radiolucency of the mandible second-
are excised. ary to invagination of the lingual surface of the jaw.
Section 4 Oral Diagnosis 111
Figure 4-3 Traumatic bone cyst. (From Regezi JA, Scuibba JJ, Figure 4-4 Nicotine stomatitis. (From Regezi JA, Scuibba JJ,
Jordan RCK: Oral Pathology: Clinical Pathologic Correlations, Jordan RCK: Oral Pathology: Clinical Pathologic Correlations,
ed 6. St. Louis, Saunders, 2012.) ed 6. St. Louis, Saunders, 2012.)
b. Located in the posterior mandible below the man- 1. Very common.

dibular canal. 2. Chronic ulcers mimic oral cancer and chronic infec-
2. Nasopalatine duct (canal) cyst. tious ulcers.
a. Lucency, often heart-shaped, in the nasopalatine D. Chemical burn.
canal. 1. Usually manifest as ulcers.
b. Caused by cystification of nasopalatine duct 2. May be caused by aspirin, hydrogen peroxide, silver
remnants. nitrate, phenol, or other agents.
3. Globulomaxillary lesion. E. Nicotine stomatitis (Figure 4-4).
a. Clinical term denoting any pathologic radiolu- 1. White change in palate caused by smoking.
cency between the maxillary cuspid and the lateral 2. Red dots in the lesion are inflamed salivary duct
incisor. orifices.
b. Histopathologic analysis is required for definitive 3. Not considered premalignant, unless related to
diagnosis because lesions in this location may rep- reverse smoking (lighted end in mouth).
resent a wide array of inflammatory lesions, odon- F. Amalgam tattoo.
togenic cysts and tumors, and nonodontogenic 1. Traumatic implantation of amalgam particles into
bone diseases. mucosa.
4. Traumatic (simple) bone cyst (Figure 4-3). 2. Most common oral pigmented lesion.
a. Radiolucent dead space (no epithelial lining) in the G. Smoking-associated melanosis.
mandible of teenagers. 1. Caused by a chemical in tobacco smoke that stimu-
b. Some (not all) associated with jaw trauma. lates melanin production.
5. Focal osteoporotic bone marrow defect. 2. Typically seen in the anterior gingival.
a. Lucency in the jaw that contains hematopoietic 3. Reversible if smoking is discontinued.
bone marrow; often in an extraction site. H. Melanotic macule.
1. Most common melanocytic lesion.
1.2 Mucosal Lesions 2. May be postinflammatory, syndrome-associated
Physical-Chemical (primarily Peutz-Jeghers syndrome [freckles and
Trauma and chemicals are frequent causes of oral lesions. benign intestinal polyps]), or idiopathic.
Some of these lesions have an iatrogenic cause (i.e., caused I. Drug-induced pigmentation.
by the dental practitioner). 1. Most common culprits: minocycline, chloroquine,
A. Focal (frictional) hyperkeratosis. cyclophosphamide, azidothymidine (zidovudine).
1. Common white lesion caused by chronic friction on J. Hairy tongue.
mucosa. 1. Elongation of filiform papillaeof cosmetic signifi-
2. Differentiated from idiopathic leukoplakia because cance only.
cause is known. 2. Several causes, including extended use of antibiotics,
B. Linea alba. corticosteroids, and hydrogen peroxide.
1. Type of frictional hyperkeratosis that appears as a K. Dentifrice-associated slough.
linear white line in buccal mucosa. 1. Superficial chemical burn of buccal mucosa caused
C. Traumatic ulcer. by some dentifrices.
f. Lesion on finger is called herpetic whitlow.

1.3 Mucosal LesionsInfections g. Intranuclear viral inclusions in epithelial cells are
Oral infections are viral, bacterial, or fungal in nature. The diagnostic when taken in clinical context.
most commonly encountered infections are viral, usually 2. Varicella (chickenpox).
herpes simplex virus (HSV) infections. Clinical presenta- a. Self-limiting childhood disease caused by varicella-
tion of viral infections depends on viral type: herpes causes zoster virus (VZV).
mucosal ulceration (preceded by vesicles), human papil- b. Oral lesions are uncommon.
lomavirus (HPV) typically induces a verruciform (warty) 3. Herpes zoster.
lesion, and Epstein-Barr virus (EBV) causes a white lesion a. This disease represents reactivation of latent VZV.
(hairy leukoplakia). Most bacterial and fungal infections b. The latent virus is believed to reside in the dorsal
manifest as chronic ulcers. The fungus Candida albicans root and trigeminal ganglia.
can cause either white or red lesions. 4. Coxsackievirus infections (hand-foot-and-mouth
A. Viral infections. disease, herpangina).
1. HSV infections (Figure 4-5 and Table 4-1). a. Both diseases are self-limiting childhood systemic
a. High frequency of occurrence of infections. infections, usually endemic.
b. Primary disease predominantly in children. b. Sites of lesions in hand-foot-mouth disease: hands,
c. Severe in immunocompromised patients. feet, and mouth.
d. Secondary disease is reactivation of latent virus in c. Sites of lesions in herpangina: posterior oral cavity.
the trigeminal ganglion. 5. Measles (rubeola).
e. Reactivation is triggered by sunlight, stress, or a. Self-limiting childhood systemic infection caused
immunosuppression. by measles virus.
b. Fever, malaise, skin rash.
c. Punctate buccal mucosa ulcers (Kopliks spots)
precede skin rash.
6. HPV infections.
a. Papillomas.
(1) Benign epithelial proliferations (pedunculated
or sessile) of little significance.
(2) Include verruca vulgaris (wart).
(a) Warts much more prevalent in HIV-positive
patients.
(3) Most, if not all, caused by HPV.
b. Condyloma acuminatum (genital warts).
(1) Caused by HPV 6 and 11.
(2) Oral lesions acquired by oral-genital contact.
(3) Broad-based verruciform lesion.
c. Focal epithelial hyperplasia (Hecks disease).
Figure 4-5 Secondary herpes simplex infection. (From (1) Most common in certain ethnic groups
Regezi JA, Scuibba JJ, Jordan RCK: Oral Pathology: Clinical Patho- Native Americans, Inuits, and Central
logic Correlations, ed 6. St. Louis, Saunders, 2012.) Americans.
Table 4-1
Common Herpes Infections
VIRUS LOCATION SIGNS SYMPTOMS TREATMENT
Primary herpes HSV 1 Perioral, oral, especially Vesicles, ulcers Fever, malaise, Acyclovir, symptomatic
simplex gingiva painful ulcers
Secondary herpes HSV 1 Lips, hard palate, and Vesicles, ulcers Painful ulcers Acyclovir, others
simplex gingiva
Varicella Varicella-zoster Trunk, head, and neck Vesicles, ulcers Fever, malaise, Symptomatic, acyclovir
virus painful ulcers
Herpes zoster Varicella-zoster Unilateral trunk, Vesicles, ulcers Painful ulcers Acyclovir, Zoster
virus unilateral oral vaccine
HSV, Herpes simplex virus.
(2) Multiple, small, dome-shaped warts on oral b. Associated malignanciesBurkitts lymphoma,

mucosa. nasopharyngeal carcinoma.
(3) Caused by HPV 13 and 32. (1) There is good evidence that EBV has an etio-
7. EBV infections (Box 4-2 and Figure 4-6). logic role in these two malignancies.
a. Hairy leukoplakia. B. Bacterial infections.
(1) Opportunistic infection resulting in white Acute bacterial infections are uncommon in oral
patch or patches of the lateral tongue. mucosa, presumably owing to the protective effects
(2) Almost all associated with HIV (may be a pre- (immunologic and physical) that saliva provides the
AIDS sign). stratified squamous epithelium lining the mouth. Acute
(3) Infrequently seen in patients with other immu- pustular staphylococcal infections occasionally may
nosuppressed states; very rare in normal appear after deep trauma or surgery. These infections
patients. are treated with appropriate antibiotics and surgical
(4) Diagnosis is made from biopsy specimen techniques (see Section 8 on Pharmacology and Sec-
showing intranuclear viral inclusions. tion 3 on Oral and Maxillofacial Surgery and Pain Con-
(5) Occurrence decreasing with use of new AIDS trol). Chronic bacterial infections are also uncommon
drugs. in oral mucosa, probably for the same reasons that
acute infections are not often seen. The chronic infec-
tions outlined subsequently are uncommon to rare but
are well known and distinctive.
Box 4-2 1. Syphilis.
Oral Complications of AIDS a. Caused by contact with patients infected with
Treponema pallidum.
Infections b. Primary lesion (chancre), secondary lesions (oral
Herpes simplex and herpes zoster mucous patches, condyloma latum, maculopapular
EBV-associated hairy leukoplakia rash), and tertiary lesions (gummas, central
Cytomegalovirus nervous system involvement, cardiovascular
HPV-associated warts involvement).
Tuberculosis c. Congenital syphilis is an in utero infection with
Histoplasmosis multiple stigmata, including Hutchinsons triad
Candidiasis (notched incisors, deafness, ocular keratitis).
Neoplasms 2. Tuberculosis.
Kaposis sarcoma (human herpesvirus 8) a. Caused by inhalation of Mycobacterium
High-grade lymphomas tuberculosis.
Severe aphthous ulcers b. Oral nonhealing chronic ulcers follow lung
Xerostomia infection.
Gingivitis and periodontal disease c. Incidence increasing secondary to overcrowding,
debilitation, and AIDS.
d. Caseating granulomas with multinucleated giant
cells (Langerhans giant cells).
e. Multidrug therapy (e.g., isoniazid, rifampin,
ethambutol).
3. Gonorrhea.
a. Sexually transmitted disease caused by Neisseria
gonorrhoeae.
b. Oral manifestation is oral pharyngitis but is rarely
seen.
4. Actinomycosis.
a. Opportunistic bacterium (Actinomyces israelii)
found in oral flora of many patients.
b. Chronic jaw infection may follow dental surgery.
c. Head and neck infections are called cervicofacial
actinomycosis.
d. Treated with long-term, high-dose penicillin.
Figure 4-6 Hairy leukoplakia. (From Regezi JA, Scuibba JJ, 5. Scarlet fever.
Jordan RCK: Oral Pathology: Clinical Pathologic Correlations, a. Systemic infection caused by some strains of group
ed 6. St. Louis, Saunders, 2012.) A streptococci.
b. In addition to the usual manifestation of strep (2) Patients who are medically debilitated or
throat (pharyngitis, fever, and malaise), children immunocompromised are at risk.
develop a skin rash caused by erythrogenic toxin. (3) In the head and neck, most lesions appear as
c. Strawberry tongue (white-coated tongue with red, destructive ulcerations in the paranasal sinuses
inflamed fungiform papillae). or nasal cavity.
d. Treated with penicillin to prevent complications of (4) Intense antifungal therapy is indicated, along
rheumatic fever. with controlling the contributing condition.
C. Fungal infections.
1. Deep fungi (histoplasmosis, coccidioidomycosis, 1.4 Mucosal LesionsImmunologic
blastomycosis, cryptococcosis). Diseases
a. Histoplasmosis is endemic to the U.S. Midwest, These conditions are related to autoimmune or hyperim-
and coccidioidomycosis (San Joaquin Valley fever) mune reactions to known or undetermined antigenic
is endemic to the U.S. West. stimuli. Clinical manifestations include vesicles or bullae,
b. Deep fungal infections of the lung may lead to oral ulcers, erythema, and white patches.
chronic granulomatous ulcers secondary to oral A. Aphthous ulcers (Figure 4-8, Box 4-4, and Table 4-2).
implantation of microorganisms. 1. Recurrent painful ulcers (not preceded by vesicles).
c. Oral lesions must be differentiated from oral 2. Unknown cause, but probably related to a focal
cancer and chronic traumatic ulcers. immune defect.
2. Opportunistic fungi.
a. Candidiasis (thrush, moniliasis) (Figure 4-7).
(1) Caused by C. albicans, part of the normal flora
in most patients. Box 4-3
(2) Predisposing factors exist for fungal over- Predisposing Factors for Candidiasis
growth (Box 4-3).
(3) Acute lesions are white, which represent the Immune deficiency
fungal colonies growing in mucosa; removal Endocrine abnormality
leaves raw, bleeding surface. Diabetes mellitus
(4) Chronic lesions are erythematous. Pregnancy
(5) Specific types of chronic candidiasisdenture Hypoparathyroidism
sore mouth, angular cheilitis, and median Hypoadrenalism
rhomboid glossitis. Stress
(6) Topical treatment: nystatin, clotrimazole. Prolonged antibiotic therapy
(7) Systemic treatment: fluconazole, itraconazole, Prolonged corticosteroid therapy
caspofungin. Chemotherapy for malignancies
b. Aspergillosis, mucormycosis, Rhizopus. Xerostomia
(1) These infections are caused by organisms that Poor oral hygiene
are found throughout the environment.
Figure 4-7 Acute candidiasis. (From Regezi JA, Scuibba JJ, Figure 4-8 Minor aphthous ulcer. (From Regezi JA, Scuibba
Jordan RCK: Oral Pathology: Clinical Pathologic Correlations, JJ, Jordan RCK: Oral Pathology: Clinical Pathologic Correlations,
ed 6. St. Louis, Saunders, 2012.) ed 6. St. Louis, Saunders, 2012.)
Box 4-4
Clinical Types of Aphthous Ulcers
Minor Aphthous Ulcers
One to several painful oval ulcers <0.5cm
Most common type
Duration of 7-10 days
Major Aphthous Ulcers

Up to 10 deep crateriform ulcers >0.5cm
Very painful and may be debilitating
May take several weeks to heal
Herpetiform Aphthous Ulcers

Figure 4-9 Lichen planus. (From Regezi JA, Scuibba JJ, Jordan
Recurrent crops of minor aphthae RCK: Oral Pathology: Clinical Pathologic Correlations, ed 6.
Painful, take 1-2 weeks to heal St. Louis, Saunders, 2012.)
May be found on any mucosal surface
Same cause as other aphthae (not viral)
2. Minor form associated with secondary herpes

Table 4-2 simplex hypersensitivity; major form (Stevens-
Systemic Diseases in Which Aphthous Johnson syndrome) often triggered by drugs.
Ulcers Are Seen D. Drug reactions and contact allergies.
1. Potentially caused by any drug or foreign protein.
SYSTEMIC ORAL 2. May be a hyperimmune response or nonimmuno-
CONDITION LESIONS
logic (overdose, toxicity, irritant).
Crohns disease Granulomatous Minor aphthae 3. Oral lesions include vesicular, ulcerative, erythema-
inflammation of
GI tract
tous, and lichenoid.
4. Acquired angioedema is a specific type of allergic
Behets Immune dysfunction Minor aphthae
syndrome featuring vasculitis
reaction.
a. Precipitated by drugs or food (shellfish, nuts).
Celiac sprue Gluten-sensitive Minor aphthae
enteropathy
b. Mediated by mast cell release of IgE.
c. Results in characteristic soft, diffuse swelling of
AIDS Immunodeficiency Major aphthae
lips, neck, or face.
GI, Gastrointestinal. d. Hereditary angioedema is a rare form that is an
autosomal dominant trait.
E. Wegeners granulomatosis.
3. Appear on wet (not vermilion) nonkeratinized oral 1. Destructive granulomatous lesions with necrotizing
mucosa (i.e., not hard palate or hard gingiva). vasculitis of unknown cause.
4. Three clinical typesminor, major, herpetiform. 2. Affects upper respiratory tract, lungs, and kidneys.
5. May be seen in association with some systemic 3. Diagnosis based on biopsy and demonstration of
diseases. antineutrophil cytoplasmic antibodies.
B. Behets syndrome. 4. Treatment is with cyclophosphamide and corticoste-
1. Multisystem disease believed to represent immune roids or rituximab; prognosis is good.
dysfunction in which vasculitis is a prominent F. Midline granuloma.
feature. 1. Destructive necrotizing midfacial phenomenon
2. Oral and genital aphthous-type ulcers, conjunctivitis, that clinically mimics lesions of Wegeners
uveitis (inflammation of the layers of the eye), arthri- granulomatosis.
tis, headache, and other central nervous system 2. Most cases represent peripheral T-cell lymphomas of
manifestations. the upper respiratory tract or mouth (perforation of
3. Treated with corticosteroids and other immunosup- the hard palate may be seen).
pressive drugs. 3. Good prognosis when treated early with radiation.
C. Erythema multiforme. G. Lichen planus (Figure 4-9 and Box 4-5).
1. Self-limiting hypersensitivity reaction that affects 1. Common mucocutaneous disease (1% to 2% of
skin or mucosa or both. adults affected).
Box 4-5
Clinical Features of Lichen Planus
Oral Lesions
Oral lesions typically bilateral in the buccal mucosa,
although tongue and gingival frequently affected
Lesions exhibit white (hyperkeratotic) lines
Clinical types
Reticular: lesions consist of interlacing lines
(Wickhams striae)
Erosive: ulceration also present
Erythematous or atrophic: lesions predominantly
red
Plaque: lesions predominantly plaquelike Figure 4-10 Mucous membrane pemphigoid. (From Regezi
JA, Scuibba JJ, Jordan RCK: Oral Pathology: Clinical Pathologic
Cutaneous Lesions Correlations, ed 6. St. Louis, Saunders, 2012.)
Cutaneous lesions characteristically purple pruritic
papules on lower legs and arms
Lesions respond to corticosteroids d. Serologic tests include antinuclear antibodies and
Erosive form may have slightly increased risk for lupus erythematosus cell test.
malignant change e. Treated with corticosteroids and other immuno-
suppressive drugs.
I. Scleroderma.
1. Autoimmune, multiorgan disease of adults, espe-
2. T lymphocytes target (destroy) basal keratinocytes; cially women.
the reason for this immunologically mediated phe- 2. Fibrosis of tissues eventually leads to organ
nomenon is unknown. dysfunction.
3. Microscopy. 3. May occur concomitantly with other autoimmune
a. Hyperkeratosis. diseases, such as lupus erythematosus, rheumatoid
b. Lymphocyte infiltrate at epithelial-connective arthritis, dermatomyositis, and Sjgrens syndrome.
tissue interface. 4. Cutaneous changes include induration and rigidity,
c. Basal zone vacuolation secondary to basal kerati- atrophy, and telangiectasias.
nocyte destruction. 5. Oral changes include restriction of orifice, uniform
d. Epithelium may exhibit a saw tooth pattern as it widening of periodontal membrane, and bony
remodels after basal cell damage. resorption of posterior margin of the mandibular
H. Lupus erythematosus. ramus (best seen on a panogram).
1. Autoimmune disease that occurs in either discoid or J. Pemphigus vulgaris.
systemic form. 1. Autoimmune, mucocutaneous disease in which anti-
2. Discoid (chronic) type. bodies are directed against desmosomal protein (des-
a. Affects skin (especially face and scalp) or oral moglein 3).
mucosa (buccal mucosa, gingival, vermilion). 2. Clinical features.
b. Usually affects middle-aged adults, especially a. Manifests as multiple, painful ulcers preceded by
women. bullae that form within the epithelium.
c. Lesions are erythematous; oral lesions mimic b. Positive Nikolskys sign may be present (formation
erosive lichen planus. of blister with rubbing or pressure).
d. No systemic signs or symptoms; rarely progresses c. Oral lesions precede skin lesions in about half of
to systemic form. cases.
e. Treated with corticosteroids and other drugs. d. Progressive clinical course; may be fatal if
3. Systemic (acute) type. untreated.
a. Multiple organ involvement (heart, kidney, joints, 3. Treated with systemic corticosteroids or other immu-
skin, oral). nosuppressive drugs.
b. Classic signbutterfly rash over bridge of the K. Mucous membrane pemphigoid (Figure 4-10).
nose. 1. Autoimmune disease of mucous membranes; anti-
c. Autoantibodies directed against nuclear and cyto- bodies directed against basement membrane anti-
plasmic antigens. gens (e.g., laminin 5, BP180).
2. Clinical features. 3. Biopsy is mandatory because diagnosis cannot be

a. Affects older adults (typically >50 years old). made clinically.
b. Manifests as multiple, painful ulcers preceded by 4. Transformation of benign lesions to squamous cell
bullae that form below the epithelium at the base- carcinoma is 5% to 15%.
ment membrane. 5. Treatmentexcision; recurrence common.
c. Oral lesions may be found in any region, especially B. Proliferative verrucous leukoplakia.
and sometimes exclusively in the attached gingival; 1. High-risk form of leukoplakia.
ocular lesions can lead to blindness if untreated. 2. Cause is unknown, although some are associated
d. Positive Nikolskys sign may be present. with HPV 16 and 18.
e. Persistent disease. 3. Lesions are recurrent or persistent and usually
3. Patients are managed with corticosteroids. multiple.
4. Lesions may start with a flat profile but progress to
1.5 Mucosal Lesions broad-based, wartlike (verruciform) lesions.
Premalignant Conditions 5. High risk of malignant transformation to verrucous
Patients with any of the following lesions are at risk for the carcinoma or squamous cell carcinoma.
development of squamous cell carcinoma. Some are caused C. Erythroplakia (erythroplasia) (Box 4-7).
by a known stimulus (especially tobacco), and some are 1. High-risk, idiopathic red patch of mucosa.
idiopathic. 2. Most represent dysplasia or malignancy.
A. Idiopathic leukoplakia (Figure 4-11 and Box 4-6). 3. Biopsy mandatory.
1. White or opaque oral mucosa lesions that do not rub D. Actinic (solar) cheilitis.
off and are not clinically diagnostic for any other 1. Causeultraviolet (UV) light, especially UVB, 2900
white lesion. to 3200nm.
2. Cause is unknown, although tobacco and alcohol 2. The lower lip shows epithelial atrophy and focal kera-
may be contributing factors. tosis. The upper lip is minimally affected because it
is more protected from UV light.
3. The junction of vermilion and skin becomes
indistinct.
4. May progress to squamous cell carcinoma.
E. Oral submucous fibrosis.
1. Irreversible mucosal change thought to be due to
hypersensitivity to dietary substances, especially
betel nut.
2. Mucosa becomes opaque secondary to submucosal
scarring.
3. May progress to squamous cell carcinoma.
F. Smokeless tobaccoassociated white lesion.
1. White mucosal change resulting from direct effects
of smokeless tobacco and additives.
2. By definition, not idiopathic leukoplakia because
Figure 4-11 Idiopathic leukoplakia. (From Regezi JA, Scuibba cause is known and lesion is clinically diagnostic
JJ, Jordan RCK: Oral Pathology: Clinical Pathologic Correlations, (however, it could be classified under a more generic
ed 6. St. Louis, Saunders, 2012.) designation of leukoplakia or white patch).
Box 4-6
Idiopathic Leukoplakia Box 4-7
Erythroplakia (Erythroplasia)
Cause unknown, tobacco and alcohol add risk
Usually occurs >40 years old Much less common than idiopathic leukoplakia
High-risk sites (for malignant transformation): floor of Cause unknown (idiopathic), some are tobacco related
mouth and tongue Usually occurs between 50 and 70 years old
Microscopy at time of first biopsy High-risk sites: floor of mouth, tongue, retromolar area
Hyperkeratosis (80%) Microscopy
Dysplasia (12%) Mild to moderate dysplasia (10%)
In situ carcinoma (3%) Severe dysplasia/carcinoma in situ (40%)
Squamous cell carcinoma (5%) Squamous cell carcinoma (50%)
Box 4-8
Clinical Features of Oral Squamous
Cell Carcinoma
Most manifest as indurated nonpainful, nonhealing
ulcer
Others manifest as white or red patch or mass
Males more frequently affected than females, 2:1
High-risk sites: posterior lateral tongue and floor of
mouth
Treatment
Surgical excision of primary
Neck dissection with positive nodes or large primary
Figure 4-12 Squamous cell carcinoma. (From Regezi JA,
lesion
Scuibba JJ, Jordan RCK: Oral Pathology: Clinical Pathologic Cor-
Radiotherapy
relations, ed 6. St. Louis, Saunders, 2012.)
Combination surgery and radiotherapy
Radiotherapy combined with chemotherapy
Overall 5-year survival 45%-50%
3. Seen in labial and buccal vestibules where tobacco is
held. Prognosis
4. May cause focal periodontal destruction, tooth abra- Good if lesion <2cm in greatest dimension (stage I)
sion, or hypertension. Malignant transformation Fair if lesion 2-4cm and no neck disease (stage II)
is rare. Poor if metastasis is found in neck (stages III and IV)
1.6 Mucosal LesionsMalignancies

The various types of carcinomas can manifest as nonheal-
ing ulcers, red patches, or irregular surface masses. b. Most commonly seen in posterior-lateral tongue
Melanomas manifest as abnormally pigmented surface and floor of mouth.
lesions that start at the junction of the epithelium and c. In regard to patient prognosis, clinical stage is
submucosa. more important than microscopic classification.
A. Verrucous carcinoma. 3. Treatmentexcision or radiation; prognosis depen-
1. Well-differentiated, slow-growing form of carcinoma dent mostly on stage.
that infrequently metastasizes. a. Overall 5-year survival is 45% to 50%; with neck
2. Tobacco and HPV 16 and 18 may have etiologic roles. metastasis, 25%.
3. Exhibits a broad-based verruciform architecture. C. Basal cell carcinoma.
4. Treated by surgical excision; good prognosis. 1. Common low-grade skin cancer that rarely
B. Squamous cell carcinoma (Figure 4-12 and Box 4-8). metastasizes.
1. Etiology. 2. Usually in sun-damaged skin; very rare in mucosa.
a. Caused by mutation, amplification, or inactivation 3. Usually manifests as nonhealing, indurated chronic
of oncogenes and tumor suppressor genes. ulcer.
b. Accumulation of genetic alterations results in loss 4. Treated with surgery; very good to excellent
of cell cycle control, abnormal signaling, increased prognosis.
cell survival, and cell motility. D. Oral melanoma (Figure 4-13).
c. Causes of genetic alterations include tobacco and 1. Malignancy of melanocytes.
heredity. 2. High-risk sites are palate and gingiva.
d. Increased incidence of oropharyngeal (including 3. Some lesions have prolonged in situ phase preceding
tonsillar) squamous cell carcinoma, many of which vertical (invasive) growth.
are associated with detection of oncogenic HPV 4. Occurs almost always in adults; rarely seen in
infection (HPV 16 and 18). children.
e. Increased risk of oral cancer in patients with 5. For oral mucosal lesions, 5-year survival is less than
Plummer-Vinson syndrome (mucosal atrophy, 20%; for skin lesions, greater than 65%.
dysphagia, iron-deficiency anemia).
2. Clinical features. 1.7 Connective Tissue TumorsBenign
a. May manifest as chronic, nonhealing ulcer, red or Connective tissue tumors manifest as masses (lumps or
white patch, or mass. bumps) within the submucosa. Overlying epithelium is
Figure 4-13 Melanoma. (From Regezi JA, Scuibba JJ, Jordan Figure 4-14 Granular cell tumor. (From Regezi JA, Scuibba JJ,
RCK: Oral Pathology: Clinical Pathologic Correlations, ed 6. Jordan RCK: Oral Pathology: Clinical Pathologic Correlations,
St. Louis, Saunders, 2012.) ed 6. St. Louis, Saunders, 2012.)
Box 4-9 (3) Papillary hyperplasia (palatal papillomatosis)

Systemic Modifying Factors of of the palate is another type of fibrous hyper-
Generalized Gingival Hyperplasia plasia associated with ill-fitting dentures.
(4) No malignant potential.
Drugs 2. Neuraltraumatic neuroma.
Phenytoin (Dilantin) a. Entangled submucosal mass of neural tissue
Cyclosporine and scar.
Nifedipine and other calcium channel blockers b. Caused by injury to nerve.
Hormonal changes associated with puberty and c. Most commonly seen at mental foramen in oral
pregnancy cavity.
Leukemic infiltrates 3. Vascularpyogenic granuloma.
Genetic factors a. Hyperplasia of capillaries and fibroblasts.
b. Caused by trauma or chronic irritation.
c. Common in gingiva but can be seen anywhere
generally intact, unless ulceration occurs because of trauma there is mucosal (or skin) trauma.
to the lesion. These tumors generally fall into one of two B. Neoplastic.
groups: reactive or neoplastic. 1. Fibrous.
A. Reactive. a. Nodular fasciitis.
1. Fibrous lesions. (1) Rare submucosal proliferation of fibroblasts.
a. Peripheral fibroma. (2) Reactive lesion that exhibits rapid growth.
(1) Fibrous hyperplasia of the gingiva. (3) Treated with surgical excision, rare
(2) Caused by trauma or chronic irritation. recurrence.
b. Generalized gingival hyperplasia. b. Fibromatosis.
(1) Fibrous hyperplasia caused by local factors and (1) Although benign, this troublesome fibroblastic
modified by systemic conditions. neoplasm is locally aggressive and infiltrative.
(2) Phenytoin (Dilantin) for seizures and calcium (2) Difficult to eradicate and often recurs.
channel blockers may contribute to gingival (3) Behavior similar to low-grade fibrosarcoma.
hyperplasia (Box 4-9). 2. Neural.
c. Focal fibrous hyperplasia. a. Granular cell tumor (Figure 4-14).
(1) Fibrous hyperplasia of oral mucosa. (1) Benign, nonrecurring submucosal neoplasm of
(2) Caused by chronic trauma or chronic Schwanns cells.
irritation. (2) Tumor cells have granular or grainy cytoplasm.
(3) Also known as traumatic fibroma, irritation (3) Overlying epithelium may exhibit pseudoepi-
fibroma, and hyperplastic scar. theliomatous hyperplasia (microscopically
d. Denture-induced fibrous hyperplasia. mimics carcinoma).
(1) Fibrous hyperplasia associated with ill-fitting (4) Most commonly seen in tongue.
dentures. (5) Infant counterpartcongenital granular cell
(2) Usually seen in anterior labial vestibules. tumor (congenital epulis).
(a) Occurs on gingiva only as pedunculated c. Most commonly seen as a complication of AIDS;
mass. incidence markedly reduced by new antiretroviral
(b) No pseudoepitheliomatous hyperplasia. therapies.
(c) Surgical excision, no recurrence. d. May also be seen as endemic African type or classic
b. Schwannoma (neurilemoma). Mediterranean type.
(1) Benign neoplasm of Schwanns cells. D. Muscle.
(2) Any site; tongue favored. 1. Leiomyosarcoma.
(3) Solitary; not syndrome-related. a. Rare sarcoma showing microscopic evidence of
c. Neurofibroma. smooth muscle differentiation.
(1) Benign neoplasm of Schwanns cells and peri- 2. Rhabdomyosarcoma.
neural fibroblasts. a. Rare sarcoma showing microscopic evidence of
(2) Any site, especially tongue and buccal mucosa. skeletal muscle differentiation.
(3) Solitary to multiple. E. Fatliposarcoma.
(4) Syndrome of neurofibromatosis 1. 1. Rare sarcoma showing microscopic evidence of fat
(a) Multiple neurofibromas. cell differentiation.
(b) Six or more caf au lait macules (each
>1.5cm diameter). 1.9 Salivary Gland Diseases
(c) Axillary freckling (Crowes sign) and iris Reactive Lesions
freckling (Lisch spots). Both major and minor salivary glands can be subject to
(d) Malignant transformation of neurofibro- numerous reactive influences. Causes of these changes
mas occurs in 5% to 15% of patients. include trauma, infection, metabolic changes, and immu-
d. Mucosal neuromas of multiple endocrine neopla- nologic dysfunction.
sia 2B. A. Mucous extravasation phenomenon.
(1) Autosomal dominant inheritance. 1. Recurring submucosal nodule of saliva (often bluish
(2) Syndrome components. in color) resulting from escape from duct of salivary
(a) Oral mucosal neuromas (hamartomas). gland.
(b) Medullary carcinoma of the thyroid. 2. Caused by traumatic severance of salivary excretory
(c) Pheochromocytoma of the adrenal gland. duct.
3. Muscle. 3. Common in lower lip (rare in upper lip) and buccal
a. Leiomyoma. mucosa.
(1) Rare, benign neoplasm of smooth muscle 4. Recurrence if contributing gland is not removed.
origin. B. Mucous retention cyst.
b. Rhabdomyoma. 1. Submucosal nodule (often bluish in color) resulting
(1) Very rare, benign neoplasm of skeletal muscle from blockage of salivary duct by a salivary stone
origin. (sialolith).
4. Fatlipoma. 2. Common in floor of mouth, palate, buccal mucosa,
a. Uncommon benign neoplasm of fat cell origin. and upper lip (rare in lower lip).
b. Buccal mucosa is characteristic site. 3. Known as ranula when occurring in floor of mouth
(Figure 4-15).
1.8 Connective Tissue TumorsMalignant
Connective tissue tumors are rare tumors that arise from
malignant conversion of connective tissue cells within the
submucosa. They manifest as masses or ulcerated masses.
A. Fibrousfibrosarcoma.
1. Rare sarcoma showing microscopic evidence of
fibroblast differentiation.
B. Neuralmalignant peripheral nerve sheath tumor
(neurosarcoma).
1. Rare sarcoma showing microscopic evidence of
neural differentiation.
2. May arise from preexisting neurofibroma or de novo
(no preexisting lesion).
C. Vascular.
1. Kaposis sarcoma. Figure 4-15 Ranula. (From Regezi JA, Scuibba JJ, Jordan RCK:
a. Malignant proliferation of endothelial cells. Oral Pathology: Clinical Pathologic Correlations, ed 6. St. Louis,
b. Human herpesvirus 8 has etiologic role. Saunders, 2012.)
Box 4-10
Metabolic Conditions Associated with
Bilateral Parotid Enlargement
Chronic alcoholism
Dietary deficiencies
Obesity
Diabetes mellitus
Hypertension
Hyperlipidemia
Sjgrens syndrome
Figure 4-16 Maxillary sinus retention cyst. (From Regezi JA, 3. Granulomas (macrophage infiltrates) cause organ
Scuibba JJ, Jordan RCK: Oral Pathology: Clinical Pathologic Cor-
nodularity and loss of parenchyma.
relations, ed 6. St. Louis, Saunders, 2012.)
4. Diagnosis is made by biopsy, radiographic studies,
and laboratory tests.
a. Serum chemistry for hypercalcemia and elevated
C. Necrotizing sialometaplasia. angiotensin-converting enzyme.
1. Chronic ulcer of the palate secondary to ischemic b. Chest films for pulmonary involvement.
necrosis of palatal salivary glands. c. Radiographs for bone involvement.
2. Believed to be triggered by trauma, surgery, or local 5. Treated with corticosteroids and other immunomod-
anesthesia. ulating drugs.
3. Heals in 6 to 10 weeks without treatment. G. Metabolic enlargement of major salivary glands
4. Mimics carcinoma clinically and microscopically (Box 4-10).
(squamous metaplasia of ducts). 1. Bilateral parotid enlargement is associated with
D. Maxillary sinus retention cyst or pseudocyst (Figure several systemic and metabolic conditions. The
4-16). parotids generally feel soft to palpation.
1. Common insignificant incidental finding in pan- H. Sjgrens syndrome.
oramic image. 1. Chronic lymphocyte-mediated autoimmune disease
2. May represent blockage of sinus salivary gland or affecting exocrine glands and other organ systems.
focal fluid accumulation of sinus mucosa. 2. Primary Sjgrens syndrome consists of keratocon-
3. Lesions are asymptomatic and require no treatment. junctivitis sicca (dry eyes) and xerostomia (dry
E. Infectious sialadenitis. mouth).
1. Infections of salivary glands may be acute or chronic, 3. Secondary Sjgrens syndrome consists of dry eyes
viral or bacterial. and mouth plus another autoimmune disease, usually
2. Viral infections. rheumatoid arthritis.
a. Mumps is an acute viral infection usually of the 4. Diagnosis.
parotid glands. a. Assessment of salivary function (usually labial sali-
b. Cytomegalovirus infections are chronic and may vary gland biopsy).
be seen in immunosuppressed patients or (rarely) b. Assessment of decrease in lacrimal function
in infants via transplacental infection. (Schirmer test).
3. Bacterial infections. c. Laboratory tests for autoantibodies (rheumatoid
a. Bacterial infections usually occur when salivary factor, antinuclear antibodies, Sjgrens syndrome
flow is reduced or impeded, especially in major A, Sjgrens syndrome B).
glands, allowing bacterial overgrowth. 5. Cause is unknown, and treatment is symptomatic.
b. Staphylococci and streptococci are the usual infect- 6. Patients are at risk for development of lymphoma.
ing agents. 7. Complication of cervical caries associated with dry
F. Sarcoidosis. mouth.
1. Chronic granulomatous disease of unknown cause,
although bacteria (possibly mycobacteria) are 1.10 Salivary Gland Diseases
suspected. Benign Neoplasms
2. This is predominantly a pulmonary disease, although Benign salivary gland neoplasms manifest as asymptomatic
many other organs may be affected, including sali- connective tissue masses. Overlying mucosa or skin is typi-
vary glands and mucosa. cally intact (Table 4-3).
Table 4-3
Most Common Minor Salivary Gland Tumors
USUAL SITE PRESENTATION MICROSCOPY PROGNOSIS
Mixed tumor Palate Submucosal mass Epithelial and mesenchymal cells Excellent
Monomorphic adenomas Palate, upper lip Submucosal mass Epithelial cells only Excellent
Mucoepidermoid Palate Mass and/or ulcer Mucous cells and epithelial cells Low-grade, excellent;
carcinoma high-grade, fair
Polymorphous low-grade Palate Mass and/or ulcer Polymorphous epithelial cell Good
adenocarcinoma patterns
Adenoid cystic Palate Mass and/or ulcer Cribriform (Swiss cheese) Poor
carcinoma epithelial cell patterns
1.11 Salivary Gland Diseases

Malignant Tumors
Malignancies of salivary gland origin have been classified
into numerous types based on microscopic appearance,
and not all are listed here. The behavior and prognosis
associated with these tumors range from low-grade behav-
ior with excellent prognosis to high-grade behavior with
poor prognosis (see Table 4-3).
A. Mucoepidermoid carcinoma.
1. Most common salivary malignancy in both minor
and major glands.
2. Palate is the most common intraoral site.
3. Composed of mucous and epithelial cells.
Figure 4-17 Mixed tumor. (From Regezi JA, Scuibba JJ, Jordan 4. Microscopic low-grade lesions rarely metastasize and
RCK: Oral Pathology: Clinical Pathologic Correlations, ed 6. have an excellent prognosis.
St. Louis, Saunders, 2012.) 5. Microscopic high-grade lesions frequently metasta-
size and have a fair prognosis.
A. Mixed tumor (pleomorphic adenoma) (Figure 4-17). B. Polymorphous low-grade adenocarcinoma.
1. Most common benign salivary gland tumor (major 1. Second most common minor salivary gland malig-
and minor glands). nancy (rare in major glands).
2. Mixture of more than one cell type (epithelial and 2. Palate most common site.
connective tissue elements) in many patterns 3. Polymorphous microscopic patterns.
(pleomorphic). 4. Low-grade malignancygood prognosis after surgi-
3. Palate is most common site for minor gland lesions. cal excision.
4. Occasional recurrences associated with incomplete C. Adenoid cystic carcinoma.
or poorly formed tumor capsule. 1. High-grade salivary malignancy.
B. Monomorphic adenomas. 2. Palate most common site.
1. Benign salivary tumors composed of a single cell 3. Cribriform or Swiss cheese microscopic pattern.
type. 4. Spreads through perineural spaces.
2. Includes basal cell adenomas, canalicular adenomas, 5. 5-year survival rate is 70%; 15-year survival rate
myoepitheliomas, and oncocytic tumors (oncocytes is 10%.
stain bright pink because of abundant mitochondrial
proteins). 1.12 Lymphoid Neoplasms
3. Treated with surgical excision with infrequent All lymphoid neoplasms are malignant. Hodgkins lym-
recurrences. phoma, characterized by Reed-Sternberg cells, is part of
C. Warthins tumor. this group but is very rare in the oral cavity. Most lymphoid
1. Warthins tumor is an oncocytic tumor that also con- neoplasms occur in lymph nodes, although they occasion-
tains lymphoid tissue. ally arise in extranodal tissues, such as mucosa-associated
2. Usually found in the parotid of older men. lymphoid tissue (MALT). Oral manifestations include
3. Occasionally bilateral. mass, ulcerated mass, and radiolucency.
Box 4-11
Lymphomas
Cause
Undetermined for most lymphomas
EBV is important causative factor in immunodeficiency
and in some Burkitts lymphomas
Chromosome translocations are factors in some
lymphomas, including Burkitts lymphoma
Classification
Microscopic criteria used to separate various types of
lymphoma
Important for predicting behavior and prescribing
Figure 4-18 Lymphoma. (From Regezi JA, Scuibba JJ, Jordan treatment
RCK: Oral Pathology: Clinical Pathologic Correlations, ed 6. Most are B-cell type; T-cell lymphomas are very rare
St. Louis, Saunders, 2012.) in the mouth
Staging
A. Non-Hodgkins lymphoma (Figure 4-18; Box 4-11).
Determination of clinical extent of disease
1. Malignancy of one of the cells making up lymphoid
Important factor for deciding type and intensity of
tissue.
therapy
2. Microscopic classification of the various types of
Helps determine prognosis
lymphomas currently follows the Revised European-
American Lymphoma classification. Clinical Features
B. Multiple myeloma or plasma cell myeloma.
Lymphoma behavior patterns range from indolent to
1. Represents a monoclonal neoplastic expansion of
highly aggressive
immunoglobulin-secreting B cells (plasma cells) in
Most head and neck tumors start in lymph nodes or
what could be termed a monoclonal gammopathy.
in mucosa-associated lymphoid tissues (MALT
2. Clinical features.
lymphomas)
a. Multiple punched-out bone lucencies (solitary
Tonsils and palate are most common intraoral sites
plasmacytoma invariably becomes multiple
Bone involvement, especially in Burkitts lymphoma,
myeloma) in patients older than 50 years.
often results in swelling, pain, tooth mobility, and
b. Abnormal immunoglobulin protein peak (M
lip paresthesia
protein) on serum electrophoresis.
AIDS-associated lymphomas are typically high-grade
c. Urinary monoclonal light chains (Bence-Jones
B-cell tumors
protein).
d. Pain, swelling, and numbness. Treatment
e. Anemia, bleeding, infection, and fracture associ-
Dependent on lymphoma classification and stage
ated with extensive marrow involvement.
Typically, radiation is used for localized disease, and
f. Treated with chemotherapy; poor prognosis.
chemotherapy is used for extensive disease;
3. A form of amyloidosis occurs in 10% of patients with
chemoradiotherapy is also used
multiple myeloma.
Some indolent low-grade lymphomas, known to
a. Amyloidosis in this context is due to formation of
respond poorly to therapeutic regimens, are not
complex proteins in which immunoglobulin light
treated
chains are precursors.
b. Amyloid protein is deposited in various organs and
can lead to organ dysfunction (especially kidney,
heart, gastrointestinal tract, liver, and spleen).
c. Microscopically, amyloid proteins react with arthritis, chronic osteomyelitis, and chronic
Congo red stain producing a green birefringence renal failure.
in polarized light. (2) Single organ or localized amyloidosis (may be
d. Other forms of amyloidosis (different precursor seen in the tongue).
proteins). C. Leukemias.
(1) Secondary amyloidosis developing in patients 1. Group of neoplasms of bone marrow (lymphocyte or
with chronic diseases such as rheumatoid myeloid precursors).
2. Malignant cells occupy and replace normal marrow 3. Rests of Malassez within a dental granuloma
cells, including megakaryocytes (platelet-forming epithelialize the lesion, resulting in formation of a
cells); malignant cells are also released into the cyst.
peripheral blood. 4. Treated by root canal filling, apicoectomy, or tooth
3. Causes. extraction with apical curettage.
a. Genetic factors, such as chromosome B. Dentigerous cyst (Figure 4-19).
translocations. 1. Manifests as a lucency around the crown of an
b. Environmental agents (e.g., benzene, radiation). impacted tooth.
c. Viruses (e.g., human T-lymphotropic virus 1). 2. Third molar and canines most often affected.
4. Classification is based on cell lineage (myeloid or 3. Called eruption cyst if lesion occurs over tooth that
lymphoid) and whether the disease is acute or has erupted into submucosa.
chronic. 4. Epithelial lining from reduced enamel epithelium has
5. Clinical features. potential to transform into ameloblastoma.
a. Bleeding (owing to reduced platelets), fatigue C. Lateral periodontal cyst.
(owing to anemia), and infection (owing to agran- 1. Unilocular or multilocular lucency in the lateral peri-
ulocytosis) are important clinical signs of odontal membrane of adults.
leukemias. 2. Most are found in the mandibular premolar region.
b. Infiltration of gingival tissues by leukemic cells is 3. Associated tooth is vital.
common in chronic monocytic leukemia. Gingiva 4. Gingival cyst in an adult is soft tissue counterpart of
is red, boggy, and hemorrhagic. this lesion.
c. Treatment with chemotherapy is quite successful
for acute leukemias but is less so for chronic
leukemias.
1.13 Odontogenic Lesions

Odontogenic Cysts
Odontogenic cysts are derived from cells that are associated
with tooth formation. Residual odontogenic epithelium
may undergo cystification any time after tooth formation.
Except for periapical cysts and some odontogenic kerato-
cysts (keratocystic odontogenic tumors), the stimulus for
cystic change is unknown (Table 4-4).
A. Periapical cyst (radicular cyst).
1. Most common odontogenic cyst; always associated
with nonvital tooth.
2. Necrotic pulp causes periapical inflammation.
a. If acute, a periapical abscess forms. Figure 4-19 Dentigerous cyst. (From Regezi JA, Scuibba JJ,
b. If chronic, a dental granuloma (granulation tissue Jordan RCK: Oral Pathology: Clinical Pathologic Correlations,
and chronic inflammatory cells) forms. ed 6. St. Louis, Saunders, 2012.)
Table 4-4
Comparison of Odontogenic Cysts
TOOTH RECURRENCE SYNDROME-
VITAL? EPITHELIAL SOURCE INCIDENCE POTENTIAL? ASSOCIATED?
Periapical cyst No Rests of Malassez Common No No
Dentigerous cyst Yes Reduced enamel epithelium Common No No
Lateral periodontal cyst Yes Rests of dental lamina (Seres) Uncommon No No
Gingival cyst Yes Rests of dental lamina (Seres) Adults, rare; No No
newborns,
common
Odontogenic keratocyst Yes Rests of dental lamina (Seres) Uncommon Yes Yes
Calcifying odontogenic cyst Yes Rests of dental lamina (Seres) Rare Yes No
Glandular odontogenic cyst Yes Rests of dental lamina (Seres) Rare Yes No
D. Gingival cysts of newborn. 2. Mutation of the patched (PTCH) tumor suppressor

1. Multiple small gingival nodules resulting from cysti- gene is evident in syndrome-related cysts and prob-
fication of rests of dental lamina. ably in many solitary cysts. A proposed change of
2. Also known as Bohns nodules; inclusion cysts in the diagnostic terminology to keratocystic odontogenic
palates of infants are known as Epsteins pearls. tumor reflects the concept that the lesion is a neo-
3. No treatment necessary. plasm with cystic architecture rather than a develop-
E. Odontogenic keratocyst (keratocystic odontogenic mental cyst.
tumor) (Figure 4-20 and Box 4-12). 3. Lining epithelium is thin and parakeratinized.
1. Lesions may be clinically aggressive, recurrent, or 4. Less common orthokeratinized odontogenic cyst has
associated with nevoid basal cell carcinoma (Gorlin) much lower recurrence rate and is not syndrome-
syndrome (multiple odontogenic keratocysts, numer- associated.
ous cutaneous basal cell carcinomas, skeletal abnor- F. Calcifying odontogenic cyst.
malities, calcified falx, and other stigmata). 1. Rare odontogenic cyst of unpredictable behavior.
2. Recurrence potential, especially for the solid variant.
Box 4-12 3. Ghost cell keratinization characterizes this cyst
Odontogenic Keratocysts (Keratocystic microscopically.
Odontogenic Tumors) a. Ghost cells may undergo calcification that may be
detected radiographically (lucency with opaque
Aggressive, recurrence risk, association with nevoid foci).
basal cell carcinoma syndrome 4. Cutaneous counterpart known as Malherbe calcifying
epithelioma or pilomatricoma.
Solitary Cysts G. Glandular odontogenic cyst (sialo-odontogenic cyst).
5%-15% of all odontogenic cysts 1. Rare odontogenic cyst that may be locally aggressive
10%-30% recurrence rate and exhibit recurrence potential.
2. Name derived from glandlike spaces and mucous
Multiple Cysts (No Syndrome) cells in epithelial lining.
5% of all keratocysts
Recurrence rate greater than for solitary cysts 1.14 Odontogenic Lesions
Odontogenic Tumors
Syndrome-Associated Multiple Cysts Odontogenic tumors are bone tumors that are unique to
5% of all keratocysts the jaws. These lesions are derived from epithelial or mes-
Recurrence rate greater than for multiple cysts (no enchymal cells involved in the formation of teeth. These
syndrome) lesions are almost always benign, although some may
exhibit aggressive behavior and may have significant recur-
rence potential (Table 4-5). Some rare odontogenic tumors
have not been included in this outline.
A. Ameloblastoma (Figure 4-21).
1. Benign but aggressive odontogenic tumor with sig-
nificant recurrence potential, especially if treated
conservatively.
Figure 4-20 Odontogenic keratocyst. (From Regezi JA, Figure 4-21 Ameloblastoma. (From Regezi JA, Scuibba JJ,
Scuibba JJ, Jordan RCK: Oral Pathology: Clinical Pathologic Cor- Jordan RCK: Oral Pathology: Clinical Pathologic Correlations,
relations, ed 6. St. Louis, Saunders, 2012.) ed 6. St. Louis, Saunders, 2012.)
Table 4-5
Characteristic Features of Odontogenic Tumors
AGE (MEAN) COMMON LOCATION RADIOGRAPHIC CHANGES BEHAVIOR
Ameloblastoma (solid Adults (40yr) Molarramus Unilocular or multilocular Benign, aggressive,
type) lucency recurrences
Calcifying epithelial Adults (40yr) Molarramus Unilocular or multilocular Benign, aggressive,
odontogenic tumor lucency; may have opaque foci may recur
Adenomatoid Teens Anterior jaws Lucency, may have opaque foci Benign, never
odontogenic tumor recurs
Odontogenic myxoma Adults (30yr) Either jaw Unilocular or multilocular Benign, aggressive,
lucency recurrences
Ameloblastic fibroma Children and Molarramus Unilocular or multilocular Benign, rarely
and fibro-odontoma teens (12yr) lucency recurs
Odontoma Children and Compound type, anterior; Opaque Benign, no
teens complex type, posterior recurrence
2. Cystic variant (cystic ameloblastoma) is less aggres-

sive and is less likely to recur.
3. Peripheral or gingival ameloblastoma exhibits banal
behavior.
4. Very rare malignant lesions are known as malignant
ameloblastoma and ameloblastic carcinoma.
5. Several microscopic subtypes, all of which mimic to
some degree the enamel organ, described for solid
ameloblastomas; no difference in behavior.
6. Treatment ranges from wide excision to resection.
B. Calcifying epithelial odontogenic tumor (Pindborg
tumor).
1. Rare odontogenic tumor with unusual microscopy
(sheets of large epithelioid cells with areas of amyloid,
some of which may become calcified). Figure 4-22 Cementoblastoma. (From Regezi JA, Scuibba JJ,
Jordan RCK: Oral Pathology: Clinical Pathologic Correlations,
2. Similar age distribution and location to ameloblas-
ed 6. St. Louis, Saunders, 2012.)
toma but less aggressive.
C. Adenomatoid odontogenic tumor.
1. Uncommon to rare odontogenic hamartoma that 2. Well-defined radiolucency in either jaw; often
contains epithelial ductlike spaces and calcified multilocular.
enameloid material. 3. Treated with surgical excision; few recurrences.
2. Two thirds in the maxilla, two thirds in females, two F. Cementifying fibroma.
thirds in the anterior jaws, and two thirds over crown 1. Can be considered similar or identical to ossifying
of impacted tooth. fibroma.
3. Does not recur after conservative treatment. 2. Well-circumscribed lucency.
D. Odontogenic myxoma (fibromyxoma). 3. Some lesions are lucent with opaque foci.
1. Uncommon to rare tumor of myxomatous connec- 4. Seen in adults and young adults, typically in the body
tive tissue (primitive-appearing connective tissue of mandible.
containing little collagen similar to dental pulp). 5. Treated with curettage or excision; recurrences rare.
2. Either jaw affected. G. Cementoblastoma (Figure 4-22).
3. Radiolucency, often with small loculations (honey- 1. Well-circumscribed radiopaque mass of cementum
comb pattern). and cementoblasts replacing root of a tooth.
4. Treated with surgical excision; moderate recurrence 2. Lesion is excised. The associated tooth is removed
potential owing to lack of encapsulation and tumor with lesion because of intimate association.
consistency. 3. No recurrence after excision.
E. Central odontogenic fibroma. H. Periapical cemento-osseous dysplasia (Figure 4-23).
1. Rare tumor of dense collagen with strands of 1. Reactive process of unknown cause that requires no
epithelium. treatment.
Box 4-13
Microscopic Differential Diagnosis for
Giant Cell Lesions of Bone
Central giant cell granuloma
Hyperparathyroidism
Aneurysmal bone cyst
Cherubism
2. Can be considered similar or identical to cementify-

ing fibroma, although some may reach considerable
size.
Figure 4-23 Periapical cemento-osseous dysplasia. 3. Clinical features.
(From Regezi JA, Scuibba JJ, Jordan RCK: Oral Pathology: Clinical a. Radiographically appears as either a well-
Pathologic Correlations, ed 6. St. Louis, Saunders, 2012.)
circumscribed lucency or a lucency with opaque
foci.
2. Clinical features. b. Seen in adults and young adults, typically in the
a. Commonly seen at the apices of one or more man- body of the mandible.
dibular anterior teeth. c. A variant known as juvenile ossifying fibroma
b. No symptoms; teeth vital. occurs in younger patients and may exhibit an
c. Most frequently seen in middle-aged women. aggressive course.
d. Starts as circumscribed lucency, which gradually 4. Microscopically composed of fibroblastic stroma in
becomes opaque. which new bony islands or trabeculae are formed.
e. An exuberant form that may involve the entire jaw 5. Treatmentcurettage or excision; recurrences rare.
is known as florid osseous dysplasia. B. Fibrous dysplasia.
I. Ameloblastic fibroma and ameloblastic fibro- 1. Uncommon to rare unencapsulated fibro-osseous
odontoma. lesion associated with mutations of the GNAS1 gene,
1. The only difference between these lesions is the addi- affecting proliferation and function of osteoblasts
tion of an odontoma to the latter; they are otherwise and fibroblasts.
the same lesion. 2. Clinical features.
2. Children and teens affected. a. Involves the entire half jaw; more common in the
3. Typically seen in mandibular molar region. maxilla.
4. Appears as a radiolucency (unilocular or multilocu- b. Affects children and typically stops growing after
lar) or as a radiolucency with an opacity (represent- puberty.
ing an odontoma). c. Radiographic pattern is diffuse opacity (ground-
5. Microscopically, an encapsulated myxomatous glass appearance).
connective tissue lesion containing strands of d. McCune-Albright syndrome consists of polyos-
epithelium. totic (more than one bone) fibrous dysplasia; cuta-
6. Treated with enucleation or excision; rarely recurs. neous caf au lait macules; and endocrine
J. Odontoma. abnormalities, especially precocious puberty.
1. Opaque lesion composed of dental hard tissues. 3. Treated with surgical recontouring for cosmetic
2. Compound type contains miniature teeth; complex appearance.
type composed of a conglomerate mass. C. Osteoblastoma.
3. Treated with curettage; no recurrence. 1. Circumscribed opaque mass of bone and
osteoblasts.
1.15 Bone (Nonodontogenic) Lesions 2. Young adults most commonly affected; 50% of
Fibro-osseous Lesions patients have associated pain.
Nonodontogenic lesions can occur in any bone of the skel- 3. Treated with surgical excision; few recurrences.
eton. Fibro-osseous lesions are benign tumors composed
of fibrous tissue in which new bony islands develop. These 1.16 Bone (Nonodontogenic) Lesions
lesions have similar microscopic features, making diagno- Giant Cell Lesions
sis dependent on clinicopathologic correlation. Microscopically, bone (nonodontogenic) lesions have mul-
A. Ossifying fibroma. tinucleated giant cells in common; this makes clinicopatho-
1. Common fibro-osseous lesion. logic correlation important for diagnosis (Box 4-13).
A. Peripheral giant cell granuloma.

1. Reactive red-to-purple gingival mass believed to be
caused by local factors.
2. Found in gingiva, typically anterior to permanent
molar teeth.
3. Composed of fibroblasts and multinucleated giant
cells, similar to central counterpart.
4. Treated with excision that extends to periosteum or
periodontal ligament (PDL).
5. Occasional recurrences are seen.
B. Central giant cell granuloma.
1. Tumor that exhibits unpredictable clinical behavior;
some are aggressive and have recurrence potential,
whereas others have a bland course.
2. Radiolucency, sometimes loculated, in teenagers;
anterior mandible favored.
Figure 4-24 Cherubism. (From Regezi JA, Scuibba JJ, Jordan
3. Composed of fibroblasts and multinucleated giant
RCK: Oral Pathology: Clinical Pathologic Correlations, ed 6.
cells. St. Louis, Saunders, 2012.)
4. Treatment is excision, but occasional recurrences
are encountered. Medical management (calcitonin
or interferon) for large lesions is a possible
option.
C. Aneurysmal bone cyst.
1. Pseudocyst (cystlike spaces but no epithelial lining)
that is composed of blood-filled spaces lined by fibro-
blasts and multinucleated giant cells.
2. Multilocular lucency occurring typically in
teenagers.
3. Cause unknown; excision and occasional
recurrences.
D. Hyperparathyroidism (von Recklinghausens disease of Figure 4-25 Langerhans cell disease. (From Regezi JA,
bone). Scuibba JJ, Jordan RCK: Oral Pathology: Clinical Pathologic Cor-
1. Multiple bone lesions resulting from effects of exces- relations, ed 6. St. Louis, Saunders, 2012.)
sive levels of parathormone.
2. May be caused by functioning parathyroid tumor Box 4-14
or compensatory parathyroid hyperplasia secondary Classification of Langerhans Cell Disease
to renal failure, malabsorption, or vitamin D
deficiency. Eosinophilic granuloma (chronic localized form)
3. Clinical features. solitary or multiple bone lesions
a. Multiple radiolucent foci of fibroblasts and multi- Hand-Schller-Christian disease (chronic disseminated
nucleated giant cells as well as loss of lamina dura form)bone lesions, exophthalmos, and diabetes
around tooth roots. insipidus
b. Systemic signs include kidney stones, metastatic Letterer-Siwe disease (acute disseminated form)
calcification, osteoporosis, neurologic problems, bone, skin, and internal organ lesions
and arrhythmias (in addition to elevated parathor-
mone and alkaline phosphatase).
E. Cherubism (Figure 4-24). 3. Microscopically, this is another giant cell lesion. A
1. Autosomal dominant condition of the jaws in distinctive perivascular collagen condensation may
children. also be seen.
2. Clinical features. F. Langerhans cell disease (idiopathic histiocytosis, Lang-
a. Symmetrical (bilateral) swelling of one or both erhans granulomatosis) (Box 4-14 and Figure 4-25).
jaws. 1. All forms represent abnormal proliferation of Lang-
b. Stabilizes after puberty and requires no erhans cells.
treatment. 2. Clinical features.
c. Loculated radiolucencies described as having soap a. Radiographs show discrete punched-out lesions
bubble appearance. or lucencies around tooth roots (floating teeth).
b. Treatmentvariable, including excision, low-dose

radiation, and chemotherapy.
3. Microscopically, eosinophils are mixed with the
tumor Langerhans cells. Some Langerhans cells are
multinucleated.
4. Prognosis very good when disease is localized; acute
disseminated form is usually fatal.
G. Pagets disease.
1. Progressive metabolic disturbance of many bones
(usually spine, femur, cranium, pelvis, and sternum).
2. Cause is unknown, and treatment is generally
symptomatic.
3. Clinical features.
a. Adults older than 50 years affected.
b. Jaw involvement.
(1) Symmetrical enlargement.
(2) Dentures become too tight.
(3) Diastemas and hypercementosis may appear.
c. Bone pain, headache, altered vision and hearing Figure 4-26 Focal sclerosing osteomyelitis. (From Regezi
(canal sclerosis). JA, Scuibba JJ, Jordan RCK: Oral Pathology: Clinical Pathologic
d. Bleeding may complicate surgery because bone is Correlations, ed 6. St. Louis, Saunders, 2012.)
highly vascular in early stages.
e. Jaw fracture and osteomyelitis are late complica- b. Mild to moderate pain and possibly an exudate.
tions secondary to bone sclerosis. c. Lucent or mottled radiographic pattern.
4. Microscopically, osteoblasts and multinucleated d. Treated with antibiotics and sequestrectomy.
osteoclasts are found in abundance. As lesion 2. Chronic osteomyelitis with proliferative periosteitis
advances, dense bone with numerous reversal or (Garrs osteomyelitis).
growth lines is seen, giving the tissue a mosaic a. Form of chronic osteomyelitis that involves the
pattern. periosteum.
5. Treatment strategy is directed at suppression of bone b. Usually associated with carious molar in children.
resorption and deposition. Bisphosphonatesand to c. Lucent or mottled radiographic pattern plus con-
a lesser extent, calcitoninhave shown efficacy. centric periosteal layering.
d. Treated with tooth removal and antibiotics.
1.17 Bone (Nonodontogenic) Lesions 3. Focal sclerosing osteomyelitis (condensing osteitis)
Inflammatory Diseases (Figure 4-26).
Inflammation of bone (and bone marrow) or osteomyelitis a. Bone sclerosis (opacity) resulting from low-grade
is common in the jaws. Most lesions are associated with inflammation, usually secondary to chronic
extension of periodontal or periapical inflammation. pulpitis.
Others are associated with trauma to the jaws. b. Asymptomatic and found on routine examination.
A. Acute osteomyelitis. c. Treatment consists of determining and addressing
1. Acute inflammation of bone and bone marrow of the the cause, and possibly endodontics.
jaws. 4. Diffuse sclerosing osteomyelitis.
2. Causes include extension of periapical or periodontal a. Bone sclerosis (opacity) resulting from low-grade
disease, fracture, surgery, and bacteremia. inflammation, usually secondary to chronic pulpi-
3. Staphylococci and streptococci are most common tis or periodontal disease.
infectious agents. b. Low-grade pain, swelling, or drainage may be
4. Pain, paresthesia, and exudation are typically present. present.
5. Radiographic changes (diffuse lucency) appear only c. Jaw fracture and osteomyelitis are late complica-
after the inflammation has been present for an tions secondary to densely sclerotic bone.
extended period. d. Treatment consists of determining and addressing
6. Treatmentappropriate antibiotic and drainage of the cause and probable use of antibiotics.
the lesion. 5. Bisphosphonate-related osteonecrosis of the jaws.
B. Chronic osteomyelitis. a. Characterized by exposed bone in maxillofacial
1. Chronic osteomyelitis (chronic osteitis). region for longer than 8 weeks in a patient who has
a. Chronic inflammation of bone and bone marrow received a bisphosphonate medication.
of the jaws. b. Usual presenting symptom is jaw pain.
c. Tooth mobility, infection, sequestration, and Box 4-15

pathologic fracture are potential outcomes.
Malignancies Most Commonly Metastatic
d. Risk of development much greater with intrave-
to the Jaws
nous bisphosphonates as opposed to oral drugs,
and osteonecrosis is more likely to develop in areas Adenocarcinoma of the breast
of oral trauma. Carcinoma of the lung
e. Treatment includes conservative local measures Adenocarcinoma of the prostate
such as chlorhexidine rinses, antibiotic therapy, Adenocarcinoma of the colon
and conservative surgery. Carcinoma of the kidney (renal cell)
1.18 Bone (Nonodontogenic)

LesionsMalignancies
Malignancies manifesting in bone include sarcomas, lym- here, although many uncommon to rare hereditary syn-
phomas or leukemias, and metastatic carcinomas. Numb dromes are not included.
lip, representing neoplastic invasion of nerve, is a frequent A. White sponge nevus.
presenting symptom. 1. Autosomal dominant condition secondary to muta-
A. Osteosarcoma. tions of keratin 4 or 13.
1. Sarcoma in which new bone (osteoid) is formed. 2. Results in asymptomatic white, spongy-appearing
2. Cause is unknown, although an association with buccal mucosa bilaterally.
several specific genetic alterations has been detected. 3. Biopsy for diagnosis; no treatment necessary.
3. Clinical features. B. Epidermolysis bullosa.
a. Pain, swelling, and paresthesia are typically present; 1. The term epidermolysis bullosa encompasses several
PDL invasion results in uniform widening. genetic conditions and one acquired disease.
b. Mean age of patients is 35 years (range, 10 to 85 2. Hereditary patterns range from autosomal dominant
years). to autosomal recessive.
c. Mandible affected more commonly than maxilla. 3. Clinically common to all forms is the appearance of
4. Most jaw tumors are microscopically low-grade bullae from minor trauma (especially over elbows
lesions. and knees).
5. Treatment and prognosis. 4. Oral lesions (blisters, scarring, and hypoplastic teeth)
a. Treated with resection and usually neoadjuvant are characteristically seen in severe recessive form.
chemotherapy (preoperative) or adjuvant chemo- C. Hereditary hemorrhagic telangiectasia.
therapy (postoperative). 1. Rare autosomal dominant condition in which telan-
b. 5-year survival rate 25% to 40%. giectatic vessels are seen in mucosa, skin, and occa-
c. Prognosis better for mandibular tumors than for sionally viscera.
maxillary tumors. 2. Red macules or papules (telangiectasias) are an occa-
d. Initial radical surgery results in survival rate sional source of bleeding.
of 80%. 3. Epistaxis (nosebleed) is a frequent presenting sign;
B. Chondrosarcoma. oral bleeding may occur.
1. Rare sarcoma of the jaws in which cartilage is pro- D. Cleidocranial dysplasia.
duced by tumor cells. 1. This autosomal dominant condition is manifested by
2. Clinical features and treatment similar to many alterations, especially of teeth and bones.
osteosarcoma. 2. The most distinctive features include delayed tooth
C. Ewings sarcoma. eruption and supernumerary teeth, hypoplastic or
1. Rare round cell malignant radiolucency of aplastic clavicles, cranial bossing, and hypertelorism.
children. E. Hereditary ectodermal dysplasia (Figure 4-27).
2. Aggressive multimodality therapy; fair prognosis. 1. X-linked recessive condition that results in partial or
D. Burkitts lymphoma (see Box 4-11). complete anodontia.
E. Metastatic carcinoma (Box 4-15). 2. Patients also have hypoplasia of other ectodermal
1. Pain, swelling, and especially paresthesia may occur. structures, including hair, sweat glands, and nails.
2. Ill-defined lucent-to-opaque radiographic changes F. Gardners syndrome.
are noted. 1. Autosomal dominant disorder.
F. Multiple myeloma (see Box 4-11). 2. Consists of intestinal polyposis, osteomas, skin
lesions, impacted permanent and supernumerary
1.19 Hereditary Conditions teeth, and odontomas.
A genetic causation is known for many oral conditions. 3. Intestinal polyps have a very high rate of malignant
Some of these have already been outlined. Others are listed conversion to colorectal carcinoma.
Figure 4-27 Hereditary ectodermal dysplasia. (From Figure 4-29 Dentinogenesis imperfecta.
Regezi JA, Scuibba JJ, Jordan RCK: Oral Pathology: Clinical Patho-
logic Correlations, ed 6. St. Louis, Saunders, 2012.)
Figure 4-30 Dentin dysplasia.
Figure 4-28 Amelogenesis imperfecta.

I. Dentinogenesis imperfecta (Figure 4-29).
1. Autosomal dominant condition in which there is
G. Osteopetrosis (Albers-Schnberg disease, marble intrinsic alteration of dentin.
bone). 2. All teeth of both dentitions are affected.
1. Generalized bone condition that may be inherited as a. Teeth have yellow or opalescent color.
an autosomal dominant (less serious) or recessive b. Extreme occlusal wear secondary to enamel frac-
trait (more serious). ture (poor dentin support).
2. Lack of bone remodeling and resorption leads to c. Short roots, bell-shaped crowns, and obliterated
bone sclerosis. pulps.
3. Bone pain, blindness and deafness from sclerosis of d. May be seen with osteogenesis imperfecta.
ostia, anemia from sclerosis of marrow, and osteomy- e. Represents a cosmetic problem that is treated with
elitis secondary to diminished vascularity are seen. full crown coverage.
H. Amelogenesis imperfecta (Figure 4-28). J. Dentin dysplasia (Figure 4-30).
1. Rare group of hereditary conditions that affect 1. Autosomal dominant condition in which there is
enamel tissue intrinsically. intrinsic alteration of dentin.
2. All teeth of both dentitions are affected. 2. All teeth of both dentitions are affected.
a. Enamel is typically yellow in color, reduced in a. Teeth have normal color.
volume, and pitted. b. Pulps are obliterated but may have residual spaces
b. Dentin and pulps are normal. (chevrons).
c. Although teeth are soft, there is no increase in c. Roots are short and are surrounded by dental
caries rate. granulomas or cysts that may contribute to tooth
d. Represents a cosmetic problem that is treated with loss.
full crown coverage. d. Teeth are not good candidates for restoration.
K. Regional odontodysplasia. b. Nucleus.

1. Dental abnormality of unknown cause; genetics, (1) Proton: charge of +1 and mass 1836 times the
trauma, nutrition, and infection have been mass of the electron.
suggested. (2) Neutron: no charge and slightly heavier than
2. A quadrant of teeth exhibit short roots, open apices, the proton.
and enlarged pulp chambers. 2. Ionization.
3. The radiographic appearance of these teeth has sug- a. Occurs when an electrically neutral atom loses an
gested the term ghost teeth. electron and becomes a positive ion; the free elec-
4. Teeth are usually extracted because of the poor tron is a negative ion.
quality of enamel and dentin. B. Radiation.
1. Electromagnetic radiation.
a. Movement of energy through space as a combina-
tion of electrical and magnetic fields.
2.0 Oral Radiology b. Quantum theory considers electromagnetic radia-
Sanjay M. Mallya tion as small bundles of energy called photons that
The proper clinical use of ionizing radiation for optimal travel at the speed of light and contain a specific
application to patient care requires knowledge and integra- amount of energy. Electromagnetic radiations com-
tion of radiologic concepts. This review follows a standard prise a spectrum of radiations with varying energy.
sequence similar to the textbook Oral Radiology: Principles c. Wave theory considers these radiations to be prop-
and Interpretation, ed 7 (2013, Mosby, St. Louis) by White agated in the form of waves. Wavelength is inversely
and Pharoah. proportional to the photon energythe shorter
This review is not meant to be a comprehensive treat- the wavelength, the higher the energy.
ment of radiology, but rather a guide to study in preparing d. The spectrum of electromagnetic radiations in-
for the Radiology section of Part II of the National Board cludes gamma rays, x-rays, UV rays, visible light,
Dental Examination. Radiographic interpretation of oral infrared radiation (heat), microwaves, and radio
disease is covered in the Pathology section of this review waves, arranged in order of decreasing energies (or
book. Students are referred to other sources, including the increasing wavelength). Gamma rays, x-rays, and
text by White and Pharoah, for more complete discussions UV radiation have sufficient energy to ionize bio-
in each area of radiology. This review is intended to help logic molecules and are referred to as ionizing
organize and integrate knowledge of concepts and facts. It radiation.
also can help students identify areas requiring more con- 2. Particulate radiation.
centrated study. a. Atomic nuclei or subatomic particles moving at
high velocity.
b. Alpha and beta particles and electrons (cathode
Outline of Review rays) are examples.
2.1 Radiation Physics C. X-ray machines.
2.2 Radiation Biology 1. X-ray tube (Figure 4-31).
2.3 Health Physics a. Cathode.
2.4 X-Ray Film and Intensifying Screens (1) Tungsten filament is the source of electrons
2.5 Projection Geometry within an x-ray tube.
2.6 Processing X-Ray Film (2) Molybdenum focusing cup electrostatically
2.7 Digital Imaging focuses electrons emitted by the incandescent
2.8 Radiographic Quality Assurance and Infection Control filament into a narrow beam directed at a small
2.9 Intraoral Radiographic Examinations area on the anode (focal spot).
2.10 Radiographic Anatomy b. Anode.
2.11 Radiographic Appearance of Caries (1) Tungsten target.
2.12 Radiographic Appearance of Periodontal Disease (a) Converts kinetic energy of electrons gener-
2.13 Panoramic Imaging ated from the filament into x-ray photons.
(b) Focal spot is an area on the target onto
2.1 Radiation Physics which the focusing cup directs electrons.
A. Matter. (c) As the size of the focal spot decreases,
1. Generation, emission, and absorption of radiation the sharpness of the radiographic image
occur at the subatomic level. increases.
a. Electrons. (2) Copper stem.
(1) Exist in orbitals around the nucleus and carry (a) Dissipates heat and reduces risk of target
an electrical charge of 1. melting.
Focal spot on
tungsten target Glass envelope
Filament and
electron cloud Vacuum
Copper stem
Figure 4-31 X-ray tube with major compo-

nents labeled. (From White SC, Pharoah MJ: Oral
e + Radiology: Principles and Interpretation, ed 7. St.
Louis, Mosby, 2014.)
Electronic
focusing cup
Cathode (-) Tube Anode (+)

window Useful x-ray beam
kVp selector
Timer
X-ray tube
AC power kVp mA
supply
Figure 4-32 Dental x-ray machine circuitry
with major components labeled. (From White SC,
Pharoah MJ: Oral Radiology: Principles and Interpreta-
High-voltage tion, ed 7. St. Louis, Mosby, 2014.)
Filament
transformer
transformer
Autotransformer mA selector
2. Power supply (Figure 4-32). (2) The high-voltage transformer increases voltage
a. Heats x-ray tube filament. significantly and provides the high voltage
(1) Provides low-voltage current by use of a step- required by the x-ray tube to accelerate elec-
down transformer that reduces the voltage of trons from the cathode to the anode and to
the incoming alternating current. generate x-rays.
(2) Controlled by a milliamperage (mA) switch (3) Beam quality refers to the mean energy of an
that regulates the temperature of the filament x-ray beam, which increases with increasing
and the number of electrons emitted. kVp.
(3) Tube current. (4) The number of photons (beam intensity) also
(a) Flow of electrons through the tube from the increases with increasing kVp.
filament to the anode and back to the (5) Because line current is alternating (60 cycles/
filament. sec), the polarity of the x-ray tube alternates,
(b) The quantity of radiation produced by an and the x-ray beam is generated as a series of
x-ray tube is directly proportional to the pulses.
tube current (mA) and the exposure c. Time exposure (s).
time (s). (1) The timer controls the length of time high
(c) Controls the number of photons generated voltage is applied to the tube and the time
(intensity of the beam) but not the beam during which the tube current flows and x-rays
energy. are produced.
b. High-voltage transformer generates high potential 3. Producing x-rays.
difference between the anode and the cathode. a. High-energy electrons produced by the filament
(1) The kVp control selects voltage from different interact with the tungsten atoms at the target
levels on the autotransformer and applies it resulting in an energy loss, which is converted to
across the primary winding of the high-voltage heat and x-ray photons.
transformer. b. Bremsstrahlung radiation.
(1) Primary source of x-ray photons from the x-ray receptor to reduce further unnecessary patient
tube. exposure.
(2) Results from stopping or slowing of high-speed e. Inverse square law.
electrons at the target. (1) Intensity of the x-ray beam at a given point is
(a) An electron is attracted toward positively inversely proportional to the square of the dis-
charged nuclei and loses velocity. tance from the source.
(b) Lost kinetic energy is given off in the form (2) Changing the distance between the x-ray tube
of new bremsstrahlung x-ray photons. and the patient has a marked effect on beam
(c) Bremsstrahlung interactions generate x-ray intensity.
photons with a continuous spectrum of (3) This principle is also applied to operator pro-
energy. tection, where the operator stands at a distance
c. Characteristic radiation. of at least 6 feet from the x-ray source to mini-
(1) Results when electrons from the filament mize the intensity of the x-ray photons.
collide with and eject an inner orbital electron, D. Interactions of x-rays with matter.
which is replaced by an outer orbital electron 1. Coherent scattering.
and release of a photon of specific energy. a. Occurs when a low-energy photon passes near an
4. Factors controlling the x-ray beam. outer electron, the photon ceases to exist, and the
a. Kilovoltage. excited electron returns to ground state, generating
(1) kVp affects both the quality and the quantity of another photon with the same energy as in the
the x-ray photons. incident beam.
(2) When the kVp increases, the total number of b. Approximately 8% of interactions with photons in
photons produced increases, and mean energy a dental x-ray beam.
and maximum energy of the x-ray beam 2. Photoelectric absorption.
increase. a. Occurs when a photon collides with a bound elec-
b. Milliamperage and exposure time. tron, which is ejected from its orbital, and the inci-
(1) mA and s affect the quantity of the x-ray dent photon ceases to exist.
photons produced. Although they can be indi- b. Frequency of photoelectric interaction is directly
vidually varied, their product (mAs) is used as proportional to the third power of the atomic
the parameter to describe the x-ray beam. number of the absorber and contributes greatly to
(2) When the mAs increases, the total number the differences in radiographic density of enamel,
of photons increases, but the mean and dentin, bone, and soft tissue on radiographs.
maximum energies of the x-ray beam are c. About 30% of interactions with photons in a dental
unchanged. x-ray beam.
c. Filtration. 3. Compton scattering.
(1) Accomplished by placing an aluminum filter in a. Occurs when a photon interacts with an outer
the path of the beam. orbital electron, which recoils from the impact,
(2) Reduces patient dose by preferentially remov- and the incident photon is scattered in a new direc-
ing lower energy (less-penetrating) photons tion with lower energy.
from the beam. b. About 62% of interactions with photons in a dental
(3) After filtration, the total number of photons x-ray beam.
decreases. However, because lower energy E. Dosimetry (Table 4-6).
photons are preferentially removed, the mean 1. Exposure.
energy of the x-ray beam increases. a. Measure of radiation quantity; capacity of radia-
(4) Governmental regulations require total filtration to ionize air.
tion to be equal to the equivalent of 1.5mm of 2. Absorbed dose.
aluminum for up to 70kVp and 2.5mm of alu- a. Unit is gray (Gy), where 1 Gy equals 1 joule/kg.
minum for higher voltages. 3. Effective dose.
d. Collimation. a. Used to estimate risk in humans.
(1) A collimator is a metallic barrier with an aper- b. Unit of effective dose is sievert (Sv).
ture to reduce the size of the x-ray beam and 4. Radioactivity.
the volume of irradiated patient tissue. a. Decay rate of radioactive material.
(2) Dental x-ray beams are usually collimated to a b. Unit is becquerel (Bq); 1 Bq equals 1 disintegration/
circle 2.75 inches (7cm) in diameter with the sec.
collimator typically built into open-ended
aiming cylinders. 2.2 Radiation Biology
(3) Rectangular collimators further limit the size A. Radiation biology is the study of the effects of ionizing
of the beam to just larger than the image radiation on living systems.
Table 4-6
Summary of Units and Quantities
SYSTEME
INTERNATIONAL TRADITIONAL
QUANTITY DUNITES UNIT DEFINITION UNIT CONVERSION
Exposure Air kerma (Gy) Energy absorbed in air, 1 joule/kg Roentgen (R) 1Gy = 100rad
1rad = 0.01Gy (1cGy)
Absorbed dose Gray (Gy) Energy absorbed in tissue, 1 joule/kg Rad 1Gy = 100rad
1rad = 0.01Gy (1cGy)
Effective dose Sievert (Sv) Energy absorbed in tissue times
tissue weighting factors, 1 joule/kg
Radioactivity Becquerel (Bq) For radioactive isotopes, 1 Curie (Ci) 1Bq = 2.7 1011Ci
disintegration per second 1Ci = 3.7 1010Bq
Source: http://physics.nist.gov/cuu/units/units.html. Accessed Dec. 1, 2006.
1. Deterministic effects. (2) The sensitive site in the nucleus is DNA.

a. There is a threshold below which a response is not (3) Chromosome changes serve as useful markers
seen. for radiation injury.
b. Severity of response is proportional to dose. 2. Effects on cell kinetics.
c. Changes resulting from killing of many cells after a. Mitotic delay.
moderate to high doses of radiation. (1) Mitotic delay occurs after irradiation of divid-
d. Example: oral mucositis after radiation therapy. ing cells.
2. Stochastic effects. (2) Severity is dose-dependent.
a. There is no minimum threshold dose. b. Cell death.
b. Probability of response, rather than severity, is (1) Cell death is caused largely by damage to chro-
dose-dependent. mosomes, preventing successful mitosis.
c. Changes resulting from damage to DNA of single (2) Radiation also causes cell death by apoptosis.
cells. c. Recovery.
d. Examples: radiation-induced cancer and heritable (1) Cell recovery involves enzymatic repair of
effects. single-strand breaks of DNA.
B. Radiation chemistry. (2) Double-strand breaks (damage to both strands
1. Direct effect. of DNA at the same site) is usually lethal to
a. Direct alteration of biologic molecules (carbohy- a cell.
drates, lipids, proteins, DNA) by ionizing radiation. 3. Radiosensitivity and cell type.
b. Approximately one third of biologic effects of x-ray a. Cells that are mitotically active and undifferenti-
exposure result from direct effects. ated and have long mitotic futures (e.g., oral
2. Indirect effects. mucous membrane basal cells) are more radiosen-
a. Radiation effects mediated through water. sitive than cells that no longer divide (e.g., neurons
b. Ionizing radiation converts water to hydrogen and or striated muscle cells).
hydroxyl free radicals (radiolysis of water), which D. Radiation effects at the tissue and organ level.
alter biologic molecules. 1. Short-term effects.
c. About two thirds of radiation-induced biologic a. Rapidly proliferating tissues (bone marrow, oral
damage results from indirect effects. mucous membrane) are lost primarily by mitosis-
3. Changes in biologic molecules. linked death.
a. Nucleic acids. 2. Long-term effects.
(1) Damage to the DNA molecule is the primary a. Long-term deterministic effects depend primarily
mechanism for radiation-induced cell death, on mitotic activity of the parenchymal cells and the
mutation, and carcinogenesis. extent of damage to fine vasculature.
C. Cellular radiation effects. E. Radiation effects on oral cavity.
1. Intracellular structures. 1. Rationale of radiotherapy.
a. Nucleus. a. Irradiation often used to treat radiosensitive
(1) The nucleus is far more radiosensitive than oral malignant tumors, usually squamous cell
cytoplasm, especially in dividing cells. carcinomas.
b. Fractionation of total x-ray dose into multiple excellent oral hygiene, and topical applications
small doses provides greater tumor destruction of sodium fluoride.
than is possible with a large single dose. f. Bone.
2. Radiation effect on oral tissues. (1) Primary damage to mature bone results from
a. Oral mucous membrane. radiation-induced damage to the vasculature of
(1) Near the end of the second week of therapy, as the periosteum and cortical bone, which are
basal epithelial cells die, the mucous membrane normally already sparse.
begins to show areas of redness and inflamma- (2) After irradiation, normal marrow may be
tion (mucositis). replaced with fatty marrow and fibrous connec-
(2) As mucous membrane breaks down, it forms a tive tissue that becomes hypovascular, hypoxic,
white-to-yellow pseudomembrane (desqua- and hypocellular.
mated epithelial layer). (3) Endosteum becomes atrophic, showing a lack
(3) At the end of therapy, mucositis is most severe, of osteoblastic and osteoclastic activity, and
discomfort is at the maximum, and food intake some lacunae of compact bone are empty; this
is difficult. is an indication of necrosis.
(4) Secondary yeast infection by C. albicans is a (4) When these changes are so severe that bone
common complication and may require death results, the condition is termed osteora-
treatment. dionecrosis; this is the most serious clinical
(5) After radiation therapy is completed, mucosal complication that occurs in bone after
healing begins and is usually complete by about irradiation.
2 months. (5) The decreased vascularity of the mandible
(6) At later intervals (months to years), the mucous renders it easily infected by microorganisms
membrane becomes atrophic, thin, and rela- from the oral cavity.
tively avascular, which complicates denture (6) This infection may cause a nonhealing wound
wearing. in irradiated bone that is difficult to treat and
b. Taste buds. causes extensive bone loss.
(1) Radiation therapy causes extensive degenera- (7) Osteoradionecrosis is more common in the
tion of normal histologic architecture of taste mandible than in the maxilla because of richer
buds and loss of taste acuity during the second vascular supply to the maxilla and because the
or third week. mandible is more frequently irradiated.
c. Salivary glands. F. Effects of whole-body irradiation.
(1) Dose-dependent and progressive loss of sali- 1. When the whole body is exposed to low or moderate
vary secretion usually seen in the first few doses of radiation, characteristic changes (termed
weeks after initiation of radiotherapy. acute radiation syndrome) develop, which are quite
(2) Mouth becomes dry (xerostomia) and tender, different from changes seen when a relatively small
and swallowing becomes difficult and painful volume of tissue is exposed.
because residual saliva loses normal lubricating 2. Radiation effects on embryos and fetuses.
properties. a. Prenatal irradiation may lead to death or specific
(3) Reduced salivary flow that persists beyond 1 developmental abnormalities, depending on the
year is unlikely to show significant recovery. stage of development at the time of irradiation.
(4) Salivary changes have a profound influence on b. No effects on embryos or fetuses have been shown
oral microflora, often leading to radiation from low doses used in dental radiography.
caries. G. Late somatic effects seen in years after exposure.
d. Teeth. 1. Carcinogenesis.
(1) Irradiation of developing teeth with therapeu- a. Radiation-induced cancer is a stochastic effect;
tic doses severely retards tooth formation. that is, there is no threshold below which the effect
(2) Depending on the severity of the dose, aberrant does not occur.
formation or arrested root development may b. The risk of developing cancer increases with
occur. increasing dose.
e. Radiation caries. c. Radiation-induced cancers are not distinguishable
(1) Carious lesions result from changes in salivary from cancers produced by other causes.
glands and saliva, including reduced flow (re- d. Incidence of leukemia increases soon after expo-
sulting in xerostomia), decreased pH, reduced sure of bone marrow and returns nearly to baseline
buffering capacity, and increased viscosity. rates within 40 years.
(2) Best restorative results are achieved from a e. Radiation-induced solid cancers, including in the
combination of restorative dental procedures, thyroid, brain, and salivary glands, generally
Terrestial Internal
7% radionuclides
9%
Space Figure 4-33 Distribution of ubiquitous background (A) and man-

11% made (B) sources of radiation. The two sources contribute equally to the
Radon total average radiation exposure. Medical and dental diagnostic and therapeu-
73% tic radiation is the major source of exposure to man-made radiation. (From
White SC, Pharoah MJ: Oral Radiology: Principles and Interpretation, ed 7.
St. Louis, Mosby, 2014.)
Background
A 3.1 mSv/year
Consumer products
and other
Dental
4%
0.26% Conventional radiography
and fluroscopy
10%
Computed Interventional radiography
tomography (CT) and fluroscopy
47% 14%
Nuclear medicine
25%
Medical, consumer products and other

B 3.1 mSv/year
appear 10 or more years after exposure, and ele- radiation exposure of people living in the United
vated risk remains for the patients lifetime. States (Figure 4-33, B).
f. Persons younger than 20 years old are more at risk a. Radiation exposure from medical or dental diag-
for solid tumors and leukemias than adults. nostic and treatment procedures accounts for
approximately 96% of man-made sources.
2.3 Health Physics (1) Computed tomography (CT) scans are the
A. Dentists must be prepared to discuss with patients the major contributor to medical radiation
benefits and possible risks associated with x-rays and exposure, accounting for 47% of man-made
describe means to minimize these risks. sources.
B. Sources of radiation exposure (Figure 4-33). (2) Dental x-ray examinations are responsible for
1. The average annual exposure to individuals living in only 0.26% of man-made radiation exposure.
the United States is approximately 6.2mSv. This b. Consumer and industrial products and sources
includes exposure from ubiquitous background radi- 4%.
ation and man-made radiation sources. (1) Include smoking, domestic water supplies,
2. Ubiquitous background radiationcontributes to combustible fuels, dental porcelain, television
approximately 3.1mSv, accounting for 50% of radia- receivers, pocket watches, smoke alarms,
tion exposure of people living in the United States nuclear power, and airport inspection systems.
(Figure 4-33, A). C. Exposure and dose in radiography.
a. Radon is the major contributor (73%) to back- 1. The goal of health physics is to prevent occurrence
ground radiation exposure. Radon, a gas, is proof deterministic effects and reduce the likelihood of
duced by radioactive decay of uranium in the soil. stochastic effects by minimizing the exposure of
b. Other sources of background radiation exposure office personnel and patients during radiographic
include terrestrial, internal radionuclides, and examinations.
space radiation. 2. This goal is accomplished by the philosophy that
3. Man-made sources of radiationcontribute to exposure should be As Low As Reasonably Achiev-
approximately 3.1mSv, accounting for 50% of able (ALARA).
3. Dose limits. i. Operator protection.

a. Occupational exposure limit is 50mSv of whole- (1) The operatory should be arranged so that the
body radiation exposure in 1 year. operator can stand at least 6 feet from the
(1) Data from radiation monitoring services show patient and not in the path of the primary x-ray
that individuals occupationally exposed in beam during exposure.
operation of dental x-ray equipment typically (2) Ideally, the operator can leave the room or take
receive an annual average of 0.2mSv (0.4% of a position behind a suitable barrier or wall
allowable limit). during exposure.
b. There are no dose limits for patients exposed in the (3) The operator should never hold films in the
course of dental and medical treatment. patients mouth.
4. Estimates of risk. (4) Neither the operator nor the patient should
a. Primary risk from dental radiography is radiation- hold the radiographic tube housing during
induced cancer. exposure.
b. Organs at risk include the thyroid gland, red bone 3. Processing film.
marrow, and salivary glands. a. Perform film processing under manufacturer-
c. Although the risk involved with dental radiogra- recommended time and temperature conditions.
phy is extremely small, no basis exists to assume b. Use proper safelights.
that it is zero. 4. View film-based and digital radiographs in a semi-
D. Methods of exposure and dose reduction. darkened room to improve diagnosis.
1. Patient selection.
a. Dentists should exercise professional judgment to 2.4 X-Ray Film and Intensifying Screens
identify patients likely to benefit from diagnostic A. X-ray film.
exposure. The American Dental Association has 1. Composition.
developed guidelines to help dentists to select a. Emulsion.
patients for radiographic examination. (1) Silver halide grains (primarily silver bromide)
b. Diagnostic radiography should be used only after are sensitive to x-radiation and visible light;
clinical examination, consideration of the patients they are flat, tabular crystals in modern emul-
history, and dental and general health needs. sions and are attached to base with a collage-
2. Conduct of examination. nous vehicle.
a. Use E/F-speed films or digital imaging for periapi- (2) The smaller the crystals, the greater the image
cal and bite-wing examinations. resolution.
b. Use rare-earth intensifying screens for panoramic b. Base.
and cephalometric radiography. (1) A flexible plastic film base supports the
c. Use an extended (16-inch) source-patient distance emulsion.
(focal spot-to-film distance) to reduce patient 2. Intraoral x-ray film.
exposure and improve image clarity. a. Identification dota raised dot impression in the
d. Collimationbeam shape. corner of film used for film orientation.
(1) Rectangular collimation reduces patient expo- 3. Screen filmfilm sensitive to visible light and placed
sure by more than 50% compared with round between two intensifying screens when an exposure
collimation. is made.
e. Leaded aprons and collars. B. Intensifying screens.
(1) Leaded thyroid collars are recommended for 1. Intensifying screens are made of a base supporting
individuals younger than 30 years old. material and a phosphor layer (usually rare-earth ele-
(2) Leaded lap aprons are required in most ments lanthanum and gadolinium).
states. 2. Phosphors incorporated into intensifying screens
f. Receptor/film-holders that align the collimated fluoresce in proportion to the x-ray energy absorbed.
beam with the image receptor should be used. 3. Use of intensifying screens results in substantial
g. A kilovoltage range of 60 to 80kVp is most suitable reduction in patient dose but decreased image
for dental radiographs. resolution because of dispersion of light from
h. Exposure time. the phosphors.
(1) Set mA value to highest possible value if C. Image characteristics.
variable. 1. Radiographic densityoverall degree of darkening
(2) Adjust exposure time to achieve optimum of exposed film.
radiographic density. a. Measured as optical density of area of x-ray film.
(3) Adjust exposure time to account for patient
Io
size and anatomic location. (1) Optical density = log10 .
It
(2) Where Io is the intensity of incident light (e.g., c. Causes of increased radiographic blur.
from viewbox), and It is the intensity of light (1) Increased size or decreased number of silver
transmitted through the film. grains in film emulsion.
(3) In a well-exposed and processed radiograph, (2) Use of intensifying screens in extraoral
the optical density of enamel is about 0.4; of radiography.
dentin, about 1.0; and of soft tissue, about 2.0. (3) Movement of film, subject, or x-ray source
b. Increasing mA, kVp, or exposure time increases during exposure.
the number of photons reaching the film and (4) Large focal spot or short source-to-object
increases the density of the radiograph. distance.
c. Reducing the distance between the focal spot and
the film also increases the film density. 2.5 Projection Geometry
d. The thicker the subject or the greater its den- A. A radiograph is a two-dimensional representation of a
sity, the more the beam is attenuated, and the three-dimensional object and is subject to distortion.
lighter the resultant image. B. Image sharpness is improved by the following.
2. Radiographic contrastrange and number of densi- 1. Use of as small an effective focal spot as is practical.
ties on a radiograph. 2. Increasing the distance between the focal spot and
a. Subject contrast is the range of characteristics of the object by using a long, open-ended cylinder.
the subject that influences radiographic contrast. 3. Minimizing the distance between the object and the
b. Film contrast is the capacity of radiographic films receptor.
to display differences in subject contrast, that is, C. Image size distortion (magnification) is minimized by
variations in intensity of the remnant beam. the following.
c. Scattered radiation results from photons that have 1. Increasing focal spot-to-film distance.
interacted with the subject by Compton or coher- 2. Decreasing object-to-receptor distance.
ent interactions, cause emission of photons that D. Image shape distortion is minimized by the following.
travel in directions other than that of primary 1. Positioning the receptor parallel to the long axis of
beam, and cause an overall darkening of the image the object.
that results in loss of radiographic contrast. a. Foreshortening results from excessive vertical
3. Radiographic speedamount of radiation required angulation when the x-ray beam is perpendicular
to produce an image of a standard density. to the receptor but not the tooth.
a. The fastest dental film currently available has a b. Elongation results when the x-ray beam is oriented
speed rating of F (preferred). Only films with a D at right angles to the object but not to the
or faster speed rating are appropriate for intraoral receptor.
radiography. 2. Orienting the central ray perpendicular to the object
4. Film latitudemeasure of range of exposures that and the receptor.
can be recorded on film. E. Paralleling and bisecting-angle techniques.
a. A film optimized to display a wide latitude can 1. Bisecting-angle techniquethe receptor is placed as
record a subject with a wide range of subject close to the teeth as possible, and the central ray is
contrast. directed perpendicular to an imaginary plane that
b. A film optimized to display a narrow latitude can bisects the angle between the teeth and the receptor.
distinguish objects with similar subject contrasts. 2. Paralleling technique (preferred method for making
5. Radiographic noiseappearance of uneven density intraoral radiographs)the receptor is placed paral-
of a uniformly exposed radiographic film. lel with the long axis of the tooth, and the central ray
a. Radiographic mottle is uneven density resulting is directed perpendicular to the long axis of the teeth
from the physical structure of the film or the inten- and the receptor.
sifying screens. F. Object localization.
6. Radiographic artifactsdefects caused by errors in 1. Two projections taken at right angles to each other.
film handling (e.g., fingerprints or bends in the film), 2. Tube shift techniqueSLOB (Same Lingual, Oppo-
errors in film processing (e.g., splashing developer or site Buccal).
fixer on a film), or marks or scratches from rough a. If the tube is shifted and directed at a reference
handling. object (e.g., the apex of a tooth) from a more mesial
7. Radiographic blurring. angulation and the object in question also moves
a. Sharpness is the ability of a radiograph to define mesially with respect to the reference object, the
an edge precisely. object lies lingual to the reference object.
b. Resolution, or resolving power, is the ability of a b. Alternatively, if the tube is shifted mesially and the
radiograph to record separate structures that are object in question appears to move distally, it lies
close together. buccal to the reference object.
2.6 Processing X-Ray Film Table 4-7

A. When a beam of photons exposes an x-ray film, it Development Times by Temperature
chemically changes the photosensitive silver halide
DEVELOPMENT TIME
crystals in the film emulsion (a latent image). Exposed TEMPERATURE (F) (MINUTES)
areas become radiolucent, whereas nonexposed areas
68 5
become radiopaque.
B. The developing process converts a latent image into a 70 4.5
visible radiographic image. 72 4
C. Formation of latent image. 76 3
1. Silver halide crystals contain sensitivity sites that trap 80 2.5
electrons generated when the emulsion is irradiated
to produce crystals containing neutral silver atoms
(latent image).
D. Processing solutions. 4. Develop films for the indicated time.
1. Developer solution. 5. Rinse in running water for 30 seconds.
a. Converts exposed silver halide crystals (with 6. Fixplace hanger and film in fixer solution for 10
neutral silver atoms at each latent image site) into minutes.
metallic silver grains that are seen as dark on a 7. Wash and dryafter fixation of films is complete,
radiograph. place the hanger in running water for at least 10
b. Developers. minutes to remove residual processing solutions.
(1) Phenidone is as the first electron donor that F. Automatic film processing.
reduces silver ions to metallic silver at the latent 1. Most automatic processors have an in-line arrange-
image site. ment of rollers.
(2) Hydroquinone provides an electron to reduce 2. The primary function of rollers is to move the film
oxidized phenidone back to its original active through the developing solutions.
state so that it can continue to reduce silver 3. The chemical compositions of the developer and fixer
halide grains to metallic silver. are modified to operate at higher temperatures than
2. Rinsing. the temperatures used for manual processing and to
a. Dilutes the developer, slowing the development meet requirements of rapid development, fixing,
process. washing, and drying of automatic processing.
b. Removes the alkali activator, preventing neutral- 4. It is important to maintain constituents of the devel-
ization of the acid fixer. oper and fixer carefully to preserve optimal sensito-
3. Fixing solution. metric and physical properties of the film emulsion
a. Dissolves and removes undeveloped silver halide within the narrow limits imposed by the speed and
crystals (without latent image sites) from the temperature of automatic processing.
emulsion. 5. As with manual processing, 8oz. of fresh developer
b. Clearing agent. and fixer should be added per gallon of solution
(1) Aqueous solution of ammonium thiosulfate per day.
(hypo) that dissolves silver halide grains. G. Safelighting.
c. Hardener. 1. Use a Kodak GBX-2 safelight filter or equivalent with
(1) Aluminum sulfate complexes with gelatin in a 15-watt bulb at least 4 feet from the working surface.
the emulsion during fixing and prevents 2. An ML-2 filter should not be used because it fogs
damage to gelatin during subsequent panoramic film.
handling. 3. A penny test checks for proper safelighting by
4. Washing. determining whether an exposed film, covered with
a. After fixing, the processed film is washed in water a penny in the darkroom, shows an image of the
to ensure removal of all thiosulfate ions and silver penny after processing. If so, it implies film fogging
thiosulfate complexes that would stain the film and light leaks or improper safelighting.
if left. H. Common causes of faulty radiographs.
E. Manual processing procedures. 1. Box 4-16 lists common causes of faulty radiographs.
1. Replenish the developer and the fixer and stir the 2. Mounting radiographs.
solutions. a. The preferred method of positioning periapical
2. Mount films on hangers. and occlusal films in the film mount is to arrange
3. Set timertypically 5 minutes at 68F. Table 4-7 them with the dot (bump) facing the viewer so that
shows effect of temperature on development time. images of teeth are in anatomic position and have
Box 4-16
Common Problems in Film Exposure Development
Light Radiographs Overdevelopment
Processing Errors Contaminated solutions
Underdevelopment (temperature too low; time too Deteriorated film (stored at high temperature; stored at
short; thermometer inaccurate) high humidity; exposed to radiation; outdated)
Depleted developer solution
Dark Spots or Lines
Diluted or contaminated developer
Excessive fixation Fingerprint contamination
Black wrapping paper sticking to film surface
Underexposure Film in contact with tank or another film during fixation
Insufficient milliamperage Film contaminated with developer before processing
Insufficient peak kilovoltage Excessive bending of film
Insufficient time Static discharge to film before processing
Film-source distance too great Excessive roller pressure during automatic processing
Film packet reversed in mouth Dirty rollers in automatic processing
Dark Radiographs Light Spots

Processing Errors Film contaminated with fixer before processing
Overdevelopment (temperature too high; time too long) Film in contact with tank or another film during
Developer concentration too high development
Inadequate fixation Excessive bending of film
Accidental exposure to light before processing
Improper safelighting or light leaks Yellow or Brown Stains
Overexposure Depleted developer
Excessive milliamperage Depleted fixer
Excessive peak kilovoltage Insufficient washing
Excessive exposure time Contaminated solutions
Film-source distance too short
Blurring
Insufficient Contrast Movement of patient
Underdevelopment Movement of x-ray tube head
Underexposure Double exposure
Excessive peak kilovoltage
Partial Images
Excessive film fog
Top of film not immersed in developing solution
Film Fog Misalignment of x-ray tube head (cone cut)
Improper safelighting (improper filter; excessive bulb
Emulsion Peel
wattage; inadequate distance between safelight and
work surface; prolonged exposure to safelight) Abrasion of image during processing
Light leaks (cracked safelight filter; light from doors, Excessive time in wash water
vents, or other sources)
the same relationship to the viewer as when the available for panoramic and cephalometric imaging. Cone-
viewer faces the patient, that is, with the right beam CT imaging is exclusively digital.
quadrants in the left side of the film mount and the A. Analog versus digital.
left quadrants in the right side. 1. Analogcontinuous gray scale; a conventional film
image.
2.7 Digital Imaging 2. Digital.
Digital imaging is becoming increasingly important in a. Gray scale divided into discrete number of
dental radiography. It is estimated that about 15% to 25% values.
of dental offices use some form of digital imaging. It is b. Number of values is a power of 2; typically from 28
most frequently used for intraoral radiography but also is or 256 gray steps.
c. An 8-bit image has 256 gray levels, a 12-bit image Excessive image sharpening may also create arti-
(212) has 4096 gray levels. facts at the edges of radiopaque restorations, which
d. Images are composed of many pixels (picture ele- may be mistaken for recurrent caries.
ments), each having a discrete gray level. 2. Image analysis.
B. Digital detectors. a. Measurementusually used for endodontics. Ac-
1. Charge-coupled device (CCD) and complementary curacy depends on calibration with known object.
metal oxide semiconductors (CMOS).
a. Silicon sensor captures x-ray energy from exposure 2.8 Radiographic Quality Assurance
as a voltage potential. and Infection Control
b. Silicon chip reads out voltage of each pixel. A. Radiographic quality assurance.
c. Usually connected to computer by a wire but may 1. A quality assurance program in radiology is a series
be wireless. of procedures implemented to ensure optimal and
d. Rapid display of image on monitor after consistent operation of each component in the
exposure. imaging chain. When all components are functioning
e. Used for intraoral, panoramic, and cephalometric properly, the result is consistently high-quality radio-
imaging. graphs made with low exposure to patients and office
2. Photostimulable phosphor plates (PSP). personnel. When a problem is identified, it is impor-
a. Plates made of barium fluorohalide with traces of tant to determine the probable source and take cor-
europium. rective action.
b. Plates capture and store x-ray energy from dental 2. Daily tasks.
exposure. a. Compare radiographs with reference film to reveal
c. After exposure, the plates are placed into the reader problems before they interfere with diagnostic
where stored energy is released as fluorescence by quality of images.
laser. b. Record all errors in a retake log for films that must
d. Reader measures released light from plate and be reexposed.
forms image. c. Replenish processing solutions.
e. Time to image display after plate is placed in reader d. Check temperature of processing solutions.
varies from seconds to minutes. 3. Weekly tasks.
C. Digital detector characteristics. a. Replace the processing solutions, clean the pro-
1. Contrast resolution. cessing equipment and viewboxes, and review the
a. Ability to distinguish shades of gray. retake log.
b. Limited by bit-depth of image capturing receptor. 4. Monthly tasks.
c. Usually displayed as an 8- to 12-bit image (256 to a. Clean the intensifying screens and rotate the film
4096 gray levels). stock.
2. Spatial resolution. b. Examine photostimulable phosphor plates for
a. Ability to detect edges or separate two close points. scratches.
b. For intraoral systemsfilm better than CCD and c. Inspect lead aprons and thyroid collars for cracks
CMOS, both of which are better than PSP. or tears.
c. For panoramic and cephalometric systemsfilm, 5. Yearly task.
CCD, and PSP all equivalent. a. Have the x-ray machine calibrated by a health
3. Detector latitude. physicist.
a. Range of structures of varying density shown on b. Verify digital sensors with a quality assurance
image. phantom.
b. PSP better than CCD and CMOS, which are better B. Infection control.
than film. 1. The goal of an infection control program is to avoid
4. Detector sensitivity. cross-contamination among patients and between
a. Dose required to achieve standard gray level. patients and operators.
b. Doses for CCD and CMOS about half of F-speed 2. Apply universal precautions.
film. a. Universal precautions are infection control guide-
D. Digital image display. lines designed to protect workers from exposure to
1. Image adjustment. diseases spread by blood and certain body fluids.
a. Brightness and contrastusually beneficial but Under universal precautions, all human blood and
may introduce artifacts, particularly in images saliva are treated as if known to be infectious for
with narrow latitude. HIV and hepatitis B virus. The means employed to
b. Sharpening and smoothingsometimes useful, protect against cross-contamination are used uni-
but sharpening may introduce a grainy appear- versally, that is, for all individuals.
ance, and smoothing may give a blurring effect. b. Wear gloves during all radiographic procedures.
c. Disinfect and cover x-ray machine, working sur- Central axis of tooth
faces, chair, and apron.
d. Sterilize nondisposable instruments.
e. Use barrier-protected film (sensor) or a disposable
container.
f. Prevent contamination of processing equipment.
(1) Remove film from a packet without touching
(contaminating) it.
(2) Put on a clean pair of gloves, pick up the film
packet by its color-coded end, and pull the
tab upward and away from the packet to reveal A
the black paper tab wrapped over the end of
Central axis of tooth
the film.
(3) Holding the film over a clean towel, carefully Imaginary bisector
grasp the black paper tab that wraps the film
and pull the film from the packet.
(4) When the film is pulled from the packet, it falls
from the paper wrapping onto the towel.
(5) After opening all films, gather the contami-
nated packaging and container and discard
them along with the contaminated gloves.
2.9 Intraoral Radiographic Examinations

B
A. Criteria of quality.
1. Every radiographic examination should produce Figure 4-34 Intraoral radiographic techniques. (A) Paral-
radiographs of optimal diagnostic quality, incorpo- leling technique illustrates parallelism between the long axis of
rating the following features. the tooth and the receptor. The x-ray beam is directed perpen-
a. Complete areas of interest recorded on the dicular to each. (B) Bisecting angle technique illustrates that the
receptor is positioned at an angle to the long axis of the tooth. The
image.
x-ray beam is directed perpendicular to the bisector of this angle.
b. Least possible amount of distortion. (From White SC, Pharoah MJ: Oral Radiology: Principles and
c. Optimal density and contrast to facilitate Interpretation, ed 7. St. Louis, Mosby, 2014.)
interpretation.
2. It is unnecessary to retake a view that fails to open a D. Radiographic examination of children.
contact or show a periapical region if the missing 1. Concern about radiation protection is most impor-
information is available on another view. tant for children because of their greater sensitivity
B. Periapical radiography. to irradiation.
1. Paralleling technique (also called right-angle or long- 2. The best way to reduce unnecessary exposure is for
cone technique). the dentist to make the minimal number of films
a. Film is supported parallel to the long axis of the required for each patient and to use thyroid shields.
teeth (Figure 4-34, A). E. Pregnancy.
b. The central ray of the x-ray beam is directed at 1. No incidences have been reported of damage to a
right angles to the teeth and the film. fetus from dental radiography.
2. Bisecting-angle technique. 2. Prudence suggests that radiographic examinations be
a. Position the film as close as possible to the lingual kept to a minimum consistent with the mothers
surface of the teeth, resting in the palate or in the dental needs.
floor of the mouth (Figure 4-34, B). 3. With the low patient dose afforded by use of optimal
b. Direct the central ray of the x-ray beam at right radiation safety techniques, an intraoral or extraoral
angles to an imaginary plane that bisects the film examination should be performed whenever a rea-
plane and the long axis of the teeth. sonable diagnostic requirement exists.
3. Bite-wing examinations.
a. Direct the central ray slightly downward through 2.10 Radiographic Anatomy
the contacts and include crowns of the maxillary A. Teeth (Figure 4-35).
and mandibular teeth and the alveolar crests. 1. Enamel.
C. Occlusal radiography. a. The enamel cap characteristically appears more
1. Displays a large segment of a dental arch. radiopaque than other tissues because it is the
2. May include the palate or floor of the mouth and a most dense naturally occurring substance in
reasonable extent of contiguous lateral structures. the body.
Inferior concha
Nasal septum Nasal fossa
Cancellous bone
Tip of nose Anterior nasal spine
Lateral fossa
Incisive Intermaxillary suture
Figure 4-35 Periapical radiograph of the anterior foramen
Lamina dura
maxilla with anatomic features identified.
Periodontal Pulp
ligament
space Alveolar crest
Enamel
Dentin
Bite block
2. Dentin. layer) is derived from its radiographic

a. Dentin is about 75% mineralized, and because of appearance.
its lower mineral content, its radiographic appear- b. This layer is continuous with the shadow of cortical
ance is roughly comparable to that of bone. bone at the alveolar crest.
b. Dentin is smooth and homogeneous on radio- c. Developmentally, the lamina dura is an extension
graphs because of its uniform morphology. of the lining of the bony crypt that surrounds each
c. The junction between enamel and dentin appears tooth during development.
as a distinct interface that separates these two d. Small variations and disruptions in continuity of
structures. the lamina dura may represent superimpositions of
3. Cementum. trabecular pattern and small nutrient canals
a. The thin layer of cementum on the root surface has passing from mandibular bone to the PDL.
a mineral content of approximately 50%. e. The presence of an intact lamina dura around
b. Cementum is not usually apparent radiographi- the apex of a tooth strongly suggests a
cally because the contrast between it and dentin is vital pulp.
so low, and the cementum layer is so thin. 2. Alveolar crest.
4. Pulp. a. The level of the alveolar crest is considered normal
a. The pulp of normal teeth is composed of soft tissue when it is not more than 2mm from the cemen-
and consequently appears radiolucent. toenamel junction (CEJ) of adjacent teeth.
b. At the apex of a developing tooth, the root pulp 3. PDL space.
canal diverges, and the walls of the root rapidly a. The PDL appears as a radiolucent space between
taper to a knife-edge. When a tooth reaches matu- the tooth root and the lamina dura.
rity, pulpal walls in the apical region begin to con- b. The shape of a tooth creates the appearance of the
strict and finally come into close apposition. PDL space. When an x-ray beam is directed so that
c. In normal, fully formed teeth, the root canal is two convexities of a root surface appear on a film,
usually apparent, extending to the apex of the root; a double PDL space may be seen.
an apical foramen is usually recognizable. The 4. Cancellous bone.
canal sometimes may appear constricted in the a. Cancellous bone (also called trabecular bone or
region of the apex and not discernible in the last spongiosa) lies between the cortical plates in both
millimeter or so of its length. In this case, the canal jaws. The radiographic pattern of trabeculae nor-
may occasionally exit on the side of the tooth, just mally shows considerable intrapatient and interpa-
short of the radiographic apex. tient variability.
d. Aging or trauma to a tooth (e.g., caries, a blow, b. To evaluate the trabecular pattern in a specific area,
restorations, attrition, erosion) also may stimulate the practitioner should examine the trabecular dis-
dentin production, leading to a reduction in size of tribution, size, and density and compare them
the pulp chamber and canals. throughout both jaws.
B. Supporting structures. c. If trabeculae are apparently absent (suggesting
1. Lamina dura. the presence of disease), it is often helpful to
a. Tooth sockets are bounded by a thin radiopaque examine previous radiographs of the region in
layer of dense bone. The name lamina dura (hard question.
Nasal fossa Lateral wall

of nasal aperture
Anterior nasal
Curved nasal Floor of nasal
spine
septum fossa
Intermaxillary Lateral wall of Ala of nose
Cancellous suture nasopalatine Maxillary sinus
bone of lateral canal Anterior wall of
fossa Tip of nose maxillary sinus
Incisive Lateral fossa
foramen
Figure 4-36 Periapical radiograph of the anterior maxilla

with anatomic features identified.
Figure 4-37 Periapical radiograph of the anterior maxilla
with anatomic features identified.
d. If prior films are unavailable, it may be appropriate
to expose another radiograph at a later time to caused divergence of the roots of the central
monitor for evidence of changes. incisors.
5. Maxilla. (5) The lateral walls of the nasopalatine canal may
a. Intermaxillary suture (Figure 4-36 and see be visualized as a pair of radiopaque lines
Figure 4-35). running superiorly from the incisive foramen.
(1) The intermaxillary suture (also called the e. Lateral fossa (Figure 4-37 and see Figure 4-36).
median suture) appears on intraoral periapical (1) The lateral fossa (also called the incisive fossa)
radiographs as a thin radiolucent line in the is a gentle radiolucent depression in the maxilla
midline. near the apex of the lateral incisor.
b. Anterior nasal spine (see Figures 4-35 and 4-36). (2) The image is often misinterpreted as a patho-
(1) The anterior nasal spine is radiopaque and logic condition. However, the presence an
most frequently demonstrated on periapical intact lamina dura around the root of the lateral
radiographs of the maxillary central incisors in incisor should direct attention to the anatomic
between and slightly above the root apices of nature of this radiolucency.
the maxillary central incisors. f. Nose (see Figures 4-35 through 4-37).
c. Nasal fossa (see Figures 4-35 and 4-36). (1) The soft tissue of the tip of the nose is fre-
(1) On periapical radiographs of incisors, the infe- quently seen in projections of the maxillary
rior border of the fossa appears as a radiopaque central and lateral incisors, superimposed over
line extending bilaterally away from the base of the roots of these teeth.
the anterior nasal spine. g. Maxillary sinus (Figures 4-38 and 4-39 and see
d. Incisive foramen (see Figures 4-35 and 4-36). Figure 4-37).
(1) The incisive foramen (also called the nasopala- (1) The borders of the maxillary sinus appear on
tine or anterior palatine foramen) in the maxilla periapical radiographs as a thin, delicate, radi-
is the oral terminus of the nasopalatine canal. opaque line (actually a thin layer of cortical
(2) Its radiographic image is usually projected bone).
between the roots and in the region of the (2) In adults, the sinus is usually seen to extend
middle and apical thirds of the central from the distal aspect of the canine to the pos-
incisors. terior wall of the maxilla above the tuberosity.
(3) The foramen varies markedly in its radio- (3) Root apices may project anatomically into the
graphic shape, size, and sharpness. It may floor of the sinus, causing small elevations or
appear smoothly symmetrical or irregular, with prominences. The thin layer of bone covering
a well-demarcated or ill-defined border. the root is seen as a fusion of the lamina dura
(4) The presence of an incisive canal cyst is sus- and the floor of sinus. Rarely, defects may be
pected if the width of the foramen exceeds present in the bony covering of the root apices
1cm, if enlargement can be demonstrated on in the sinus floor, and a periapical radiograph
successive radiographs, or if it appears to have fails to show the lamina dura covering the apex.
Posterior border of zygomatic Anterior border of zygomatic

process of maxilla process of maxillary
Zygoma
Nutrient canal in maxillary sinus
Maxillary sinus
Floor of maxillary sinus
Figure 4-38 Periapical radiograph of the posterior maxilla with anatomic features identified.
Inferior border of zygomatic

process of maxilla
Junction of lateral wall
and floor of nasal fossa
Pterygoid plates
Septum in maxillary sinus
Coronoid process of mandible
Mucosa
Figure 4-39 Periapical radiograph of the posterior maxilla with anatomic features identified.
(4) Often, one or several radiopaque lines traverse j. Pterygoid plates (see Figure 4-39).
an image of the maxillary sinus. These septa (1) The medial and lateral pterygoid plates, when
represent folds of cortical bone projecting a few apparent, almost always cast a single radi-
millimeters away from the floor and wall of the opaque, homogeneous shadow without
antrum. evidence of trabeculation posterior to the
h. Zygomatic process of maxilla (see Figures 4-38 maxillary tuberosity.
and 4-39). (2) The hamular process extends inferiorly from
(1) On periapical radiographs, the zygomatic the medial pterygoid plate. It may exhibit
process of the maxilla appears as a U-shaped trabeculae.
radiopaque line with its open end directed 6. Mandible.
superiorly. The enclosed rounded end is pro- a. Genial tubercles (Figure 4-40).
jected in the apical region of the first and (1) The genial tubercles are located on the lingual
second molars. surface of the mandible slightly above the infe-
i. Zygoma (see Figure 4-38). rior border and in the midline.
(1) The inferior portion of the zygomatic bone may (2) They are well visualized on mandibular occlu-
be seen extending posteriorly from the inferior sal radiographs as one or more small
border of the zygomatic process of the maxilla. projections.
(2) The zygoma can be identified as a uniform gray (3) Their appearance on periapical radiographs of
or white radiopacity over the apices of the the mandibular incisor region is variable; often
molars. they appear as a radiopacity (3 to 4mm in
diameter) in the midline below the incisor (2) Its image is quite variable, and it may be identi-
roots. fied only about half of the time because the
(4) When genial tubercles are seen on periapical opening of the mental canal is directed superi-
radiographs, it is often possible to see the orly and posteriorly.
lingual foramen. (3) It may be round, oblong, or irregular and par-
b. Mental protuberance (see Figure 4-40). tially or completely corticated.
(1) On periapical radiographs of the mandibular (4) When the mental foramen is projected over
central incisors, the mental protuberance one of the premolar apices, it may mimic peri-
(ridge) may occasionally be seen as two thick apical disease. Look carefully for the presence
radiopaque lines extending bilaterally forward of an intact lamina dura to rule out periapical
and upward toward the midline. disease.
c. Mental fossa (see Figure 4-40). e. Mandibular canal (Figure 4-42).
(1) The mental fossa is a radiolucent depression on (1) The radiographic image of the mandibular
the labial aspect of the mandible extending lat- canal is a dark, linear shadow with thin, radi-
erally from the midline and above the mental opaque superior and inferior borders cast by
ridge. the layer of bone that bounds the canal.
d. Mental foramen (Figure 4-41). (2) Sometimes the borders are seen only partially
(1) The mental foramen is usually seen near the or not at all. This is more common in patients
apex of the second premolar. with osteopenia or osteoporosis.
f. Nutrient canals (see Figure 4-41).
(1) Nutrient canals carry a neurovascular bundle
and appear as radiolucent lines of fairly uniform
width. They are most often seen on mandibular
periapical radiographs running vertically from
the inferior dental canal directly to the apex of
a tooth or into the interdental space between
the mandibular incisors.
g. Mylohyoid ridge (see Figure 4-41).
(1) The mylohyoid ridge is a slightly irregular crest
Lingual foramen
of bone on the lingual surface of the mandibu-
Mental Genial tubercles
fossa lar body.
(2) Its radiographic image runs diagonally down-
Mental ward and forward from the area of third molars
protuberance to premolar region, at approximately the level
of the apices of the posterior teeth.
h. Submandibular gland fossa (see Figure 4-41).
Figure 4-40 Periapical radiograph of the anterior man- (1) On the lingual surface of the mandibular body,
dible with anatomic features identified. immediately below the mylohyoid ridge in the
Nutrient canal
Submandibular gland fossa

Mental foramen
Mylohyoid ridge
Figure 4-41 Periapical radiograph of the posterior mandible with anatomic features identified.
External oblique ridge
Inferior border of
mandibular canal
Mental foramen
Inferior border of mandible
Figure 4-42 Periapical radiograph of the posterior mandible with anatomic features identified.
molar area, there is frequently a depression in streptococci plays a central role in the demineralization.
the bone. This concavity accommodates the The demineralized tooth surface, called the carious lesion,
submandibular gland and often appears as a is not the disease but is a reflection of ongoing or past
radiolucent area with a sparse, trabecular microbial activity in the plaque.
pattern characteristic of the region. A. Use of intraoral radiographs.
(2) Although the image may appear strikingly 1. Caries appears as a radiolucent zone.
radiolucent (accentuated by the dense mylohy- 2. Radiography is a valuable supplement to a thorough
oid ridge and the inferior border of mandible), clinical examination of the teeth for detecting
awareness of its possible presence should pre- caries.
clude its being confused with a bony lesion. 3. Clinical access to proximal tooth surfaces in contact
i. External oblique ridge (see Figure 4-42). is quite limited.
(1) The external oblique ridge is a continuation of 4. A radiographic examination can reveal carious
the anterior border of the mandibular ramus. lesions in occlusal and proximal surfaces that would
(2) Characteristically, it is projected onto posterior otherwise remain undetected.
periapical radiographs superior to the mylohy- 5. Bite-wing radiographs are the most useful radio-
oid ridge, with which it runs an almost parallel graphic examination for detecting interproximal
course. caries.
(3) It appears as a radiopaque line of varying width, B. Proximal surfaces.
density, and length, blending at its anterior end 1. The shape of the early radiolucent lesion in the
with the shadow of the alveolar bone. enamel is classically a triangle with its broad base at
j. Inferior border of mandible (see Figure 4-42). the tooth surface.
(1) Occasionally, the inferior mandibular border 2. When the demineralizing front reaches the den-
is seen on periapical projections as a charac- tinoenamel junction, it spreads along the junc-
teristically dense, broad radiopaque band of tion, frequently forming the base of a second
bone. triangle with the apex directed toward the pulp
k. Coronoid process (see Figure 4-39). chamber.
(1) The image of the coronoid process of the 3. This triangle typically has a wider base than in the
mandible is frequently apparent on periapical enamel and progresses toward the pulp along the
radiographs of the maxillary molar region as a direction of the dentinal tubules.
triangular radiopacity, with its apex directed 4. A lesion in proximal surfaces most commonly is
superiorly and anteriorly, superimposed on the found just apical to the contact point.
region of the third molar. 5. Various dental anomalies such as hypoplastic pits and
concavities produced by wear can mimic the appear-
2.11 Radiographic Appearance of Caries ance of caries.
Caries requires the presence of bacteria and a diet con 6. Approximately half of all proximal lesions in enamel
taining fermentable carbohydrates. The mutans group of cannot be detected by radiography.
C. Occlusal surfaces. 8. A permanent record of the condition of the bone

1. Carious lesions in children and adolescents most throughout the course of the disease.
often occur on occlusal surfaces of posterior teeth. B. Limitations of radiographs.
2. The classic radiographic appearance of occlusal 1. Radiographs provide a two-dimensional view of a
caries extending into the dentin is a broad-based, three-dimensional situation.
radiolucent zone, often beneath a fissure, with little 2. Radiographs typically show less severe bone destruc-
or no apparent changes in the enamel. tion than is actually present.
D. Buccal and lingual surfaces. 3. Radiographs do not demonstrate soft tissue-to-hard
1. Small caries on the buccal and lingual surfaces of tissue relationships and provide no information
teeth are usually round. about the depth of soft tissue pockets.
2. As they enlarge, they become elliptic or semilunar. 4. Bone level is often measured from the CEJ; however,
3. They often demonstrate sharp, well-defined borders. this reference point is not valid in situations in which
E. Root surfaces. either overeruption or severe attrition with passive
1. Radiographs of proximal root surfaces may reveal eruption exists.
lesions that have gone undetected clinically. 5. For these reasons, although radiographs play
2. A pitfall in the detection of root lesions is that a an invaluable role in treatment planning, they
surface may appear to be carious as a result of the must be used to supplement a careful clinical
cervical burnout phenomenon. examination.
3. Caries may be distinguished from an intact surface C. Normal anatomy.
primarily by the absence of an image of the root edge 1. The normal alveolar bone crest lies at a level approxi-
and by the appearance of a diffuse rounded inner mately 0.5 to 2mm below the level of the CEJs of
border where the tooth substance has been lost. adjacent teeth.
F. Dental restorations. 2. In the absence of disease, this bony junction between
1. A carious lesion developing at the margin of an exist- the alveolar crest and lamina dura of posterior teeth
ing restoration may be termed secondary or recurrent forms a sharp angle next to the tooth root.
caries. 3. The PDL space is often slightly wider around the
2. A lesion next to a restoration may be obscured by the cervical portion of the tooth root, especially in ado-
radiopaque image of the restoration. lescents with erupting teeth.
3. Liners without radiopaque fillers appear radiolucent D. Mild periodontitis.
and may resemble recurrent or residual caries. 1. The early lesions of adult periodontitis appear as
areas of localized erosion of the interproximal alveo-
2.12 Radiographic Appearance lar bone crest.
of Periodontal Disease 2. The anterior regions show blunting of the alveolar
The most common disorders of the periodontium are gin- crests and slight loss of alveolar bone height.
givitis and periodontitis, which represent chronic infec- 3. The posterior regions may also show a loss of the
tious diseases. Essential components of these diseases are normally sharp angle between the lamina dura and
the presence of certain bacteria in plaque and the inflam- alveolar crest.
matory host response. Gingivitis is a soft tissue inflamma- E. Moderate periodontitis.
tion involving the gingiva surrounding teeth. Periodontitis 1. Horizontal bone loss.
entails the loss of soft tissue attachment and supporting a. Horizontal bone loss is a term used to describe the
bone of the involved teeth. radiographic appearance of loss in height of the
A. Radiographs are especially helpful in the evaluation of alveolar bone around multiple teeth; the crest is
the following points. still horizontal (i.e., parallel with the occlusal
1. Amount of bone present. plane) but is positioned apically more than a few
2. Condition of the alveolar crests. millimeters from the line of the CEJs.
3. Bone loss in the furcation areas. b. In horizontal bone loss, the crest of the buccal and
4. Width of the PDL space. lingual cortical plates and the intervening inter-
5. Local initiating factors that cause or intensify peri- dental bone have been resorbed.
odontal disease. 2. Vertical osseous defects.
a. Calculus. a. The term vertical (or angular) osseous defect
b. Poorly contoured or overextended restorations. describes the types of bony lesions that are most
6. Root length and morphology and crown-to-root commonly localized to one or two teeth.
ratio. b. With these defects, the crest of the remaining
7. Anatomic considerations. alveolar bone typically displays an oblique angula-
a. Position of the maxillary sinus in relation to a peri- tion to the line of the CEJs in the area of involved
odontal deformity. teeth.
F. Severe periodontitis. f. Panoramic images are most useful clinically for

1. In severe adult periodontitis, the bone loss is so diagnostic problems requiring broad coverage of
extensive that the remaining teeth show excessive the jaws.
mobility and drifting. 4. The main disadvantage of panoramic radiology is
2. Extensive horizontal or vertical osseous defects may that the image does not display the fine anatomic
be present. detail available on intraoral periapical radiographs.
3. As with moderate bone loss, the lesions seen during B. Principles of panoramic image formation.
surgery usually are more extensive than is suggested 1. Image layer.
by the radiographs alone. a. The image layer is a three-dimensional curved
G. Multirooted teeth. zone or focal trough where structures lying
1. Progressive periodontal disease and its associated within this layer are reasonably well defined on the
bone loss may extend into the furcations of multi- final panoramic image. The structures seen on a
rooted teeth. panoramic image are primarily structures located
2. Widening of the PDL space at the apex of the inter- within the image layer.
radicular bony crest of the furcation is strong evi- b. Objects outside the image layer are blurred, magni-
dence that the periodontal disease process involves fied, or reduced in size and are sometimes dis-
the furcation. torted to the extent of not being recognizable. The
3. The bony defect may involve either the buccal or the shape of the image layer varies with the brand of
lingual cortical plate and extend under the roof of the equipment used.
furcation. 2. Patient positioning and head alignment.
4. The most common route for furcation involvement a. Remove dental appliances, earrings, necklaces,
of the maxillary permanent first molar is from the hairpins, and any other metallic objects in the head
mesial side. and neck region.
H. Periodontal abscess. b. Align the occlusal plane so that it is lower anteri-
1. A periodontal abscess is a rapidly progressing, orly, angled 20 to 30 degrees below horizontal.
destructive lesion that usually originates in a deep c. Position patients with their backs and spines as
soft tissue pocket. erect as possible.
2. If the lesion persists, a radiolucent region appears, 3. Image receptors.
often superimposed over the root of a tooth. a. Intensifying screens are routinely used in pan-
I. Differential diagnosis. oramic radiography because they significantly
1. Most cases of bone loss around teeth are caused by reduce the amount of radiation required for prop-
periodontal diseases. erly exposing a radiograph.
2. Squamous cell carcinoma of the alveolar process b. Several manufacturers have developed digital
occasionally is treated as periodontal disease, result- acquisition panoramic machines. The receptor on
ing in a delay in diagnosis and treatment. such a machine is either an array of CCDs or a
3. Any lesion of bone destruction that has ill-defined film-sized PSP rather than film.
borders and a lack of peripheral bone response (scle- C. Interpreting the panoramic image.
rosis) should be viewed with suspicion. 1. Introduction.
a. View the image as if you were looking at a patient,
2.13 Panoramic Imaging with the structures on the patients right side posi-
A. Introduction and rationale. tioned on your left (Figures 4-43 and 4-44).
1. Panoramic imaging is a technique for producing a b. The image is presented to you in the same orienta-
single tomographic image of facial structures. tion as that of periapical and bite-wing images,
2. This is a curvilinear variant of conventional tomog- making interpretation more comfortable.
raphy based on the principle of reciprocal movement 2. Anatomic structures (see Figures 4-43 and 4-44).
of an x-ray source and an image receptor around a 3. Superimpositions and ghost images (see Figure 4-44).
central point or plane. a. Many radiopaque objects out of the image layer
3. Principal advantages of panoramic images. superimpose on the image of normal anatomic
a. Broad coverage of facial bones and teeth. structures. Such objects typically appear blurred
b. Low patient radiation dose. and project either over the midline structures (as
c. Convenience of examination for the patient. with cervical vertebrae) or onto the opposite side
d. Can be used in patients unable to open their of the radiograph in reversed configuration and
mouths. more cranially positioned than the real structure.
e. Patients readily understand panoramic images; These contralateral images are termed ghost
they are also a useful visual aid in patient education images, and they may obscure normal anatomy or
and case presentation. be mistaken for pathology.
1 10 7
6 18
2 8 9
14 15 16
4 20
11 12 17
5 13 22
3 21
19
23
29
24
28
30
25 25
27 30
26 L
1. Pterygomaxillary fissure 11. Floor of the nasal cavity 22. Coronoid process
2. Posterior border of maxilla 12. Anterior nasal spine 23. Posterior border of ramus
3. Maxillary tuberosity 13. Incisive foramen 24. Angle of mandible
4. Maxillary sinus 14. Hard palate/floor of the nasal cavity 25. Hyoid bone
5. Floor of the maxillary sinus 15. Zygomatic process of the maxilla 26. Inferior border of mandible
6. Medial border of maxillary sinus/ 16. Zygomatic arch 27. Mental foramen
lateral border of the nasal cavity 17. Articular eminence 28. Mandibular canal
7. Floor of the orbit 18. External auditory meatus 29. Cervical vertebrae
8. Infraorbital canal 19. Styloid process 30. Epiglottis
9. Nasal cavity 20. Mandibular condyle
10. Nasal septum 21. Sigmoid notch
Figure 4-43 Panoramic radiograph with anatomic features identified. (From White SC, Pharoah MJ: Oral Radiology: Principles
and Interpretation, ed 7. St. Louis, Mosby, 2014.)
A L
Middle turbinate
Nasal septum
Inferior turbinate
Tip of nose
Soft palate
Ear lobe
Tongue
B L
Nasal airway
Nasopharynx
Oral airway
Velopharynx
Oropharynx
C L
Figure 4-44 Panoramic radiograph (A) showing superimposed soft tissue structures (B) and airway space (C). (From
White SC, Pharoah MJ: Oral Radiology: Principles and Interpretation, ed 7. St. Louis, Mosby, 2014.)
Sample Questions D. Condyloma latum

E. Focal epithelial hyperplasia
1. Acantholysis, resulting from desmosome weakening 3. Intranuclear viral inclusions are seen in tissue speci-
by autoantibodies directed against the protein desmo- mens of which of the following?
glein, is the disease mechanism attributed to which of A. Solar cheilitis
the following? B. Minor aphthous ulcers
A. Epidermolysis bullosa C. Geographic tongue
B. Mucous membrane pemphigoid D. Hairy leukoplakia
C. Pemphigus vulgaris E. White sponge nevus
D. Herpes simplex infections 4. The odontogenic neoplasm, which is composed
E. Herpangina of loose, primitive-appearing connective tissue
2. HPV has been found in all of the following lesions that resembles dental pulp, microscopically is known
except one. Which one is the exception? as _____.
A. Oral papillomas A. Odontoma
B. Verruca vulgaris of the oral mucosa B. Ameloblastoma
C. Condyloma acuminatum C. Ameloblastic fibroma
D. Ameloblastic fibro-odontoma C. Varicella

E. Odontogenic myxoma D. Primary syphilis
5. A biopsy specimen of the lower lip salivary glands E. Actinomycosis
showed replacement of parenchymal tissue by lympho- 11. The idiopathic condition in which destructive inflam-
cytes. The patient also had xerostomia and keratocon- matory lesions featuring necrotizing vasculitis are seen
junctivitis sicca. These findings are indicative of which in the lung, kidney, and upper respiratory tract is
of the following? known as ______.
A. Lymphoma A. Epidermolysis bullosa
B. Crohns disease B. Stevens-Johnson syndrome
C. Mumps C. Sturge-Weber syndrome
D. Sjgrens syndrome D. Wegeners granulomatosis
E. Mucous extravasation phenomenon E. Secondary syphilis
6. A patient seeks help for recurrent palatal pain. She 12. From the following list, select the jaw lesions or dis-
presents with multiple punctate ulcers in the hard eases that are characterized microscopically by the
palate that were preceded by tiny blisters. Her lesions presence of conspicuous numbers of multinucleated
typically heal in about 2 weeks and reappear during giant cells. (Choose four.)
stressful times. She has ______. A. Central giant cell granuloma
A. Aphthous ulcers B. Ossifying fibroma
B. Recurrent primary herpes C. Hyperparathyroidism
C. Recurrent secondary herpes D. Calcifying epithelial odontogenic tumor
D. Erythema multiforme E. Aneurysmal bone cyst
E. Discoid lupus F. Calcifying odontogenic cyst
7. Conservative surgical excision would be appropriate G. Cherubism
treatment and probably curative for which of the 13. For each clinical feature listed, select the most closely
following? linked disease or lesion from the list provided.
A. Nodular fasciitis
A. Solitary, shallow, oval ulcer of 1. Granular cell
B. Fibromatosis
buccal mucosa tumor
C. Fibrosarcoma
B. Bilateral, reticular white lines 2. Leukemia
D. Rhabdomyosarcoma
of buccal mucosa
E. Adenoid cystic carcinoma
C. Generalized enlargement of 3. Amalgam
8. On a routine radiographic examination, a well-defined
erythematous gingival tissues tattoo
radiolucent lesion was seen in the body of the man-
D. Solitary nodular mass of the 4. Aphthous
dible of a 17-year-old boy. At the time of operation, it
dorsal tongue ulcer
proved to be an empty cavity. What is this lesion?
E. Darkly colored macule of 5. Mucous
A. Osteoporotic bone marrow
attached gingiva extravasation
B. Aneurysmal bone cyst
phenomenon
C. Odontogenic keratocyst
F. Fluctuant nodule of lower lip 6. Lichen planus
D. Static bone cyst
E. Traumatic bone cyst 14. From the following list, select the systemic diseases in
9. A 21-year-old woman went to her dentist because of which patients may develop aphthous ulcers. (Choose
facial asymmetry. This asymmetry had developed three.)
gradually over 3 years. The patient had no symptoms. A. Celiac sprue
A diffusely opaque lesion was found in her right B. Sarcoidosis
maxilla. All laboratory tests (complete blood count, C. Amyloidosis
alkaline phosphatase, calcium) were within normal D. Behets syndrome
limits. A biopsy specimen was interpreted as a fibro- E. Crohns disease
osseous lesion. This patient most likely has ______. F. Neurofibromatosis
A. Cementoblastoma 15. X-ray beam A is produced using 70kVp, 7mA, and
B. Fibrous dysplasia 0.1s. X-ray beam B is produced using 70kVp, 10mA,
C. Cherubism and 0.15s. Which of the following statements are
D. Osteosarcoma correct? (Choose two.)
E. Chronic osteomyelitis A. Beam A has higher mean energy.
10. A cutaneous maculopapulary rash of the head and B. Beam B has higher mean energy.
neck preceded by small ulcers in the buccal mucosa C. Beam B has a higher number of x-ray photons.
would suggest which of the following? D. The mean energies of the two beams are equal.
A. Primary herpes simplex infection E. The maximum energy of the x-ray photons is
B. Rubeola higher for beam B.
16. Which of the following items influence the mean view of the same region, made with the x-ray machine
energy of an x-ray beam? (Choose two.) oriented more from the mesial, reveals that the
A. Kilovoltage object has moved mesially with respect to the molar
B. Milliamperage roots on the first view. The location of the object
C. Exposure time is ______.
D. Amount of filtration A. Buccal to the roots
E. Collimation B. Lingual to the roots
F. Using a rotating anode C. In the same plane as the roots
17. The function of the filament is to ______. D. Unknown because information is insufficient to
A. Convert electrons into photons form an opinion
B. Convert photons into electrons 24. Cone-cutting results from _______.
C. Release photons A. Too great a target-film distance
D. Release electrons B. Not selecting the proper kVp
E. None of the above C. Not enough time exposure
18. The most radiosensitive of the following cells in terms D. The x-ray machine being improperly aimed
of cell killing is the _____. 25. If your film-based radiographs start coming out too
A. Cardiomyocyte light, it may be that the ______.
B. Basal epithelial cell A. Exposure time is too long
C. Endothelial cell B. Developer needs changing
D. Neuron C. Developer is too hot
E. Polymorphonuclear leukocyte D. Fixer needs changing
19. For each of the numbered radiation effects, indicate E. Films are not sufficiently washed
whether the effects are stochastic or deterministic. 26. If an unwrapped, nonprocessed x-ray film is exposed
A. Stochastic effect to normal light for just a second and then processed,
B. Deterministic effect it ______.
___ 1. Thyroid cancer A. May still be used but will be a little dark
___ 2. Xerostomia B. May still be used but will be a little light
___ 3. Cataract formation C. May still be used but will be brown
___ 4. Heritable effects D. Will be completely black
___ 5. Oral mucositis E. Will be completely clear
20. Photoelectric interactions are highest in _____. 27. To ensure high radiographic image quality, it is impor-
A. Enamel tant to ______ daily.
B. Dentin A. Check the temperature of the processing solutions
C. Cementum B. Clean the processing equipment
D. Pulp C. Clean the intensifying screens
21. The photosensitive component of an x-ray film D. Calibrate the mA linearity
is ______. 28. Radiographs of a pregnant patient ______.
A. Silver halide crystals A. Should never be made
B. Sodium thiosulfate crystals B. Should be made only in the third trimester of
C. Gelatin pregnancy
D. Rare earth elements C. Should be made only with triple leaded aprons on
22. The effective dose from a limited cone-beam CT scan the patients lap
of the anterior maxilla is 20Sv. The effective dose D. Should be made when there is a specific need
from a full-mouth radiographic examination (with 29. Radiographic examination plays an important role in
round collimation and thyroid collar) is 120Sv. Based assessing periodontal disease. Intraoral radiographs
on these data, which of the following statements is true permit assessment of several disease features related to
regarding radiation-induced cancer risk? periodontal disease. Which features from the follow-
A. Risk from the full-mouth radiographic examina- ing list cannot be assessed by radiographic examina-
tion is higher. tion? (Choose two.)
B. Risk from the CT scan is higher. A. Bone loss in the furcation areas
C. Risk from both examinations is the same. B. Amount of bone present
D. Risks cannot be compared because they are differ- C. Crown-to-root ratio
ent imaging modalities. D. Depth of the soft tissue pocket
23. You are unsure of the location of an opaque mass E. Assessment of the three-dimensional nature of the
seen over a molar root on a periapical view. A second vertical periodontal defect.
SECTION 5
Orthodontics and
Pediatric Dentistry
STEVEN J. LINDAUER, BHAVNA SHROFF,
ESER TUFEKCI, MARK TAYLOR
OUTLINE 1.1 Epidemiology of Malocclusion

1. Orthodontics
Malocclusion is not a disease but a variation from what is
2. Pediatric Dentistry considered ideal. It is difficult to estimate the prevalence
of malocclusion in the population. Studies have focused
instead on the prevalence of characteristics of malocclu
sion, such as the presence of incisor crowding, overjet
(usually accompanying Angle class II malocclusions),
1.0 Orthodontics reverse overjet or anterior crossbite (usually associated
with Angle class III malocclusions), midline diastema,
This review summarizes key concepts important to ortho deep or open bite, and posterior crossbite. Various charac
dontic diagnosis and treatment. It is organized in a manner teristics of malocclusion are seen more commonly at dif
similar to standard textbooks on the subject, including ferent ages and in different ethnic groups. It is important
Contemporary Orthodontics, ed 5, by Proffit etal, and Text- to note which characteristics are likely to change or
book of Orthodontics, ed 3, by Bishara (see References). This improve naturally over time and distinguish them from
review is not meant to be an in-depth examination of all of others that may require treatment or intervention during
the intricacies of orthodontics but rather to serve as a guide development.
for further study. It should help students pinpoint areas
where they require additional information, and the test Prevalence
questions that follow can help in this manner as well. Stu A. Crowding.
dents can consult other sources, such as the aforemen 1. Incisor crowding tends to increase in children as the
tioned textbooks, for more detailed explanations of the permanent teeth erupt because permanent incisors
material. require more space than their predecessors.
2. Lower incisor crowding continues to worsen into
adulthood.
Outline of Review 3. Nearly 15% of adolescents and adults have severely
1.1 Epidemiology of Malocclusion crowded incisors, suggesting that extraction of teeth
1.2 Growth and Development would be necessary to create enough space to align
1.3 Development of Occlusion them.
1.4 Orthodontic Diagnosis B. Angle classification (see 1.4, Orthodontic Diagnosis, for
1.5 Treatment Planning definitions).
1.6 Biology of Tooth Movement 1. Overjet of greater than 5mm, suggesting class II
1.7 Mechanical Principles in Tooth Movement malocclusion, occurs in 23% of children, 15% of ado
1.8 Orthodontic Materials lescents, and 13% of adults.
1.9 Orthodontic Appliances 2. Reverse overjet, suggesting class III malocclusion, is
1.10 Early Treatment much less frequent than class II malocclusion in the
1.11 Growth Modification U.S. population.
1.12 Comprehensive Treatment 3. Class II relationships are more common in whites of
1.13 Retention northern European descent.
1.14 Adult Treatment and Interdisciplinary Treatment 4. Class III relationships are more prevalent in Asian
1.15 Combined Surgical and Orthodontic Treatment populations (2% to 5%).
155
156 Section 5 Orthodontics and Pediatric Dentistry
5. Estimation of the percentage of the U.S. popula

tion that fall into Angles four major classification
groups. Ethmoid Frontal bone
a. Class I normal occlusion: 30%. Presphenoid
b. Class I malocclusion: 50% to 55%.
Spheno-
c. Class II malocclusion: 15%. ethmoid
d. Class III malocclusion: approximately 1%. Basis
sphenoid Intersphenoid
1.2 Growth and Development Spheno-occipital

Basis
Theories of Growth Control occipital
No single theory explains all of craniofacial growth Synchondroses
control. of the cranial base
A. Direct genetic controlbone, as all other tissues, is Figure 5-1 Diagrammatic representation of the synchon-
directly under the control of genetics. droses of the cranial base, showing the location of these
B. Epigenetic growth controlcartilage is the primary important growth sites. (From Proffit WR, Fields HW, Sarver
determinant of skeletal growth and indirectly controls DM: Contemporary Orthodontics, ed 5. St. Louis, Mosby, 2013.)
the growth of bone. Cartilage grows and is then replaced
by bone.
C. Environmental growth control: the functional matrix B. Cranial base.
theorygrowth of bone is influenced by adjacent soft 1. Ethmoid, sphenoid, and occipital bones (Figure 5-1)
tissues through environmental changes in forces exerted at the base of the skull are formed initially in cartilage
on the bones that stimulate their growth. and later transformed into bone by endochondral
ossification.
Endochondral versus Intramembranous 2. As ossification occurs, three bands of cartilage
Bone Formation remain, which are important growth centers called
A. Endochondral bone formationformed first in carti synchondroses: sphenoethmoid synchondrosis, in
lage, then transformed into bone. Bones formed in this tersphenoid synchondrosis, and sphenooccipital
way are probably less susceptible to environmental synchondrosis.
influences during growth and are under more direct 3. Each synchondrosis acts like a two-sided epiphyseal
genetic control. The bones of the cranial base are plate with growing cartilage in the middle and bands
endochondral. of maturing cartilage cells extending in both direc
B. Intramembranous bone formationformed by secretion tions that are eventually replaced by bone.
of bone matrix directly within connective tissues, 4. These synchondroses eventually become inactive: the
without intermediate formation of cartilage. Growth of intersphenoid probably around age 3, the sphenoeth
intramembranous bones is more influenced by the moid around age 7, and the sphenooccipital consid
environmental forces around them. The cranial vault, erably later.
maxilla, and mandible are examples of intramembra 5. Because they are endochondral bones, the bones
nous bones. making up the cranial base are minimally affected
directly by growth of the brain.
Sites of Growth in the Craniofacial Complex C. Maxilla.
A. Cranial vault. 1. Growth of the maxilla is intramembranous. Growth
1. Intramembranous bones that form without cartilagi occurs at the sutures posterior and superior to the
nous precursors. maxilla at its connections to the cranium and cranial
2. At birth, the bones are widely separated by loose con base and by surface remodeling.
nective tissues at the fontanelles. Apposition of bone 2. The maxilla migrates downward and forward away
along the edges of the fontanelles eliminates these from the cranial base (Figure 5-2) and undergoes
open spaces, but the bones remain separated by the significant surface remodeling (Figure 5-3).
cranial sutures. 3. Surface remodeling includes resorption of bone ante
3. As brain growth occurs, the cranial bones are pushed riorly and apposition of bone inferiorly.
apart, and apposition of new bone occurs at the 4. Much of the anterior movement of the maxilla is
sutures. negated by anterior resorption, and downward
4. Remodeling also occurs with new bone added on migration is augmented by inferior apposition of
the external surfaces and removed on the internal bone.
surfaces (periosteal apposition and endosteal 5. As with all bones, interstitial growth within the min
resorption). eralized mass of the maxilla is impossible; addition
Section 5 Orthodontics and Pediatric Dentistry 157
2. Cartilage covers the surface of the mandibular

condyle at the temporomandibular joint (TMJ).
However, this cartilage does not grow independently
similar to an epiphyseal plate or synchondrosis.
3. Cartilage is transformed into bone at the condyle as
the mandible grows downward and forward, away
+ ++
+ from the cranial base. Surface apposition and resorp
+ + tion occurs in other areas of the mandible.
++
+ + +
+
+ + 4. Most growth of the mandible occurs by new bone
++ forming at the condyle and by resorption of the ante
+
+ rior part of the ramus with apposition posteriorly.
Minor amounts of remodeling occur anteriorly and
inferiorly.
5. Embryonic development.
a. The mandible develops in the same area as the
cartilage of the first pharyngeal arch: Meckels
Figure 5-2 As growth of surrounding soft tissues trans- cartilage. However, development of the mandible
lates the maxilla downward and forward, opening up
itself proceeds just lateral to Meckels cartilage and
space at its superior and posterior sutural attachments,
is entirely intramembranous in nature.
new bone is added on both sides of the sutures. (Redrawn
from Enlow DH, Hans MG: Essentials of Facial Growth. Philadel- b. Meckels cartilage disintegrates, and its remnants
phia, Saunders, 1996.) are transformed into a portion of two of the small
bones of the middle ear (malleus and incus). Its
perichondrium persists as the sphenomandibular
ligament.
c. Condylar cartilage develops independently and is
initially separated by a gap from the body of the
intramembranous mandible. It later fuses with the
developing mandibular ramus.
6. As with the maxilla, interstitial growth within the
mineralized mass of the mandible is impossible.
Space for eruption of the posterior teeth occurs as the
anterior portion of the ramus resorbs extensively. In
a child with crowded teeth, it is unreasonable to
expect that interstitial growth of the mandible will
occur to create space within the body of the mandible
to alleviate the crowding.
7. Extensive surface apposition occurs on the posterior
surface of the ramus.
8. Mandibular growth rotation.
a. As growth at the condyle facilitates movement of
Figure 5-3 Remodeling of the palatal vault (which is also the mandible downward and forward, away from
the floor of the nose) moves it in the same direction as the cranial base, a gap is available between the
it is being translated; bone is removed from the floor of
maxilla and mandible in which the maxillary and
the nose and added to the roof of the mouth. On the
anterior surface, bone is removed, partially canceling the forward
mandibular teeth erupt.
translation. As the vault moves downward, the same process of b. Average closing rotationin most children, con
bone remodeling also widens it. (Redrawn from Enlow DH, Hans dylar growth exceeds molar eruption, and the
MG: Essentials of Facial Growth. Philadelphia, Saunders, 1996.) mandible rotates slightly closed over time. This
closing rotation, along with the downward and
forward growth of the mandible itself, helps
of new bone can occur only at the surfaces. Increased make the chin appear more prominent as children
space for the eruption of posterior teeth occurs by age. It also indicates that posterior face height
addition of bone posteriorly at the tuberosity as the increases more than anterior face height in most
maxilla migrates downward and forward. cases.
D. Mandible. c. Severe closing rotationin some children, condylar
1. Growth of the mandible is both endochondral and growth greatly exceeds molar eruption, and the
intramembranous. mandible rotates more substantially closed, leading
to development of a shorter face and a deeper ante 200

rior overbite tendency.
d. Opening rotationrarely, condylar growth is less
than molar eruption, and the mandible rotates Lymphoid
open during growth. In these children, a long
lower face and tendency for an anterior open bite
develop.
Percent of adult size

Timing of Growth
A. Cephalocaudal gradient of growth. Neural
100
1. In general, structures farther from the brain grow
more and later.
2. In the third month of fetal development, the head
takes up almost 50% of the total body length. By the
time of birth, the trunk and limbs have grown so that
General
the head is 30% of the body. In an adult, the head
represents about 12% of the total height.
3. The mandible is farther from the brain than the Genital
maxilla and grows more and later. 0
B. Scammons growth curves. Birth 10 Years 20 Years
1. Neural tissues, including the brain, continue to grow
Figure 5-4 Growth curves for the maxilla and mandible
rapidly after birth and reach near 100% adult size by
shown against the background of Scammons curves.
about age 6 or 7. Growth of the jaws is intermediate between the neural and general
2. Lymphoid tissues, including tonsils and adenoids, body curves, with the mandible following the general body curve
also grow quickly, reaching twice the adult size by more closely than the maxilla. The acceleration in general body
about age 10, and then involute during the pubertal growth at puberty, which affects the jaws, parallels the dramatic
growth spurt to reach adult size. increase in development of the sexual organs. Lymphoid involu
3. Genital or reproductive tissues do not grow much tion also occurs at this time. (From Scammon RD: The measure-
until puberty and then rapidly increase to adult size ment of the body in childhood. In: Harris JA, editor. The
corresponding to the time of the pubertal growth Measurement of Man. Minneapolis, University of Minnesota Press,
spurt. 1930.)
4. General body tissues, including muscle and bone,
grow rapidly after birth, then slow in growth during
childhood, and then accelerate again at the same time 2. There is considerable individual variation in the
as reproductive tissues proliferate. timing of growth relative to chronologic age; early-
5. Maxillary and mandibular growth (Figure 5-4). maturing boys may reach peak growth before late-
a. The maxilla, located closer to the brain than the maturing girls.
mandible, grows earlier and follows a pattern 3. Generally, the earlier the peak of growth, the shorter
closer to that of neural tissues. the duration of the growth spurt will be, and less
b. The mandible grows later and exhibits more char overall growth occurs.
acteristics of a growth spurt paralleling the puber 4. Girls generally start growth sooner, grow for a shorter
tal growth spurt in body height. amount of time, and grow less than boys.
C. Growth velocity curve (Figure 5-5). E. Predictors.
1. The velocity curve shows that growth in height is very 1. Chronologic age is not a perfect predictor of when
rapid after birth but decelerates quickly to a lower, peak growth will occur (correlation about 0.8).
more constant level in childhood. 2. Basing growth predictions on dental age is even less
2. Around puberty, growth accelerates again, reaching reliable (correlation about 0.7). In other words, chil
a pubertal growth peak before slowing and virtually dren whose teeth erupt early do not erupt early.
stopping at maturity. 3. Physical growth status correlates well with skeletal
3. Predicting the timing of this growth spurt may be age, which is determined by the relative level of mat
important for orthodontic treatment designed to take uration of the skeletal system.
maximal advantage of growth changes. a. A hand-wrist radiograph, revealing the ossification
D. Sex differences. of the bones of the hand and wrist, is the standard
1. Girls reach their growth peak about 2 years earlier on for assessing skeletal development.
average than boys. Average peak growth for girls is b. Another possibility is evaluating the develop
around age 12 and for boys is age 14. ment of the vertebral bones as visualized on a
cephalometric radiograph (cervical vertebral 4. Because sex hormones have a direct effect on endo
maturation). chondral bone growth, sexual development and
c. It is also possible to plot increases in body height growth in height are well correlated.
over time. F. Directions of growth.
d. Successive cephalometric radiographs can be 1. Growth in width of the jaws is generally completed
superimposed (usually using the stable cranial before the adolescent growth spurt begins.
base structures) to determine when a growth spurt 2. Growth in length of the jaws continues through the
or termination of significant growth is occurring growth spurt.
in an individual. 3. Vertical growth continues longer.
De Montebeillards son Cleft Lip and Palate and Other

1759-1777 Developmental Abnormalities
200 22
A. Incidence.
20
180 1. The most common craniofacial defect, second only
18 to clubfoot in congenital deformities, is clefting
Height gain (cm per year)

160 16 of the lip or palate or both, occurring in 1 in 700
births.
Height (cm)
140 14
B. Embryology.
12
120 1. Nearly all the tissues of the face and neck originate
10 from ectoderm.
100
8 2. There are principal stages in craniofacial develop
80 6 ment. Some abnormalities in facial form and jaw
relationships can be traced to malfunctions that
4
60 occur during specific stages (Table 5-1).
3. Cleft lip occurs when there is a failure of fusion
2 4 6 8 10 12 14 16 18
between the frontonasal (medial nasal) process and
Age (years)
the maxillary process. This fusion includes the lip
Figure 5-5 Growth can be plotted either in height or and alveolar ridge (the primary palate).
weight at any age or in the amount of change in any given 4. Closure of the secondary palate occurs about 2 weeks
interval. A curve such as the age line is called a distance curve, later, when the palatal shelves elevate and join
whereas the height line is a velocity curve. Plotting velocity rather together in a process that proceeds from anterior to
than distance makes it easier to see when accelerations and decel
posterior.
erations in the rate of growth occurred. These data are for the
growth of one individual, the son of a French aristocrat in the late 1.3 Development of Occlusion
eighteenth century, whose growth followed the typical pattern.
Note the acceleration of growth at adolescence, which occurred A. Stages of normal dental development.
for this individual at about age 14. (Data from Scammon Amer F 1. Gum pad stage.
Phys Anthrop, 1927. IN Proffit WR, Fields HW, Sarver DM: Con- a. Birth to about 6 to 7 months of age, ending with
temporary Orthodontics, ed 5, St Louis, Mosby, 2013.) the eruption of the first incisor.
Table 5-1
Stages of Embryonic Craniofacial Development
TIME (HUMANS,
STAGE POSTFERTILIZATION) RELATED SYNDROMES
Germ layer formation and initial Day 17 Fetal alcohol syndrome
organization of structures
Neural tube formation Days 18-23 Anencephaly
Origin, migration, and interaction Days 19-28 Hemifacial microsomia, mandibulofacial dysostosis
of cell populations (Treacher-Collins syndrome), limb abnormalities
Formation of organ systems
Primary palate Days 28-38 Cleft lip and/or palate, other facial clefts
Secondary palate Days 42-55 Cleft palate
Final differentiation of tissues Day 50birth Achondroplasia synostosis syndromes (Crouzons, Aperts)
From Proffit WR, Fields HW, Sarver DM: Contemporary Orthodontics, ed 4. St. Louis, Mosby, 2007.
b. The future position of the teeth can be observed by 3. Mixed dentition stage.
the elevations and grooves present on the alveolar a. Starts around age 6 with the eruption of the first
ridges. permanent tooth.
2. Primary dentition stage. b. As each permanent tooth erupts, it is expected that
a. Starts with the eruption of the primary teeth and its antimere (corresponding contralateral tooth)
lasts until about 6 years of age, when the first per will erupt within 6 months.
manent tooth erupts. c. Ugly duckling stageas the maxillary central
b. The maxillary anterior primary teeth are about incisors erupt, they move labially, and a temporary
75% of the size of their permanent successors. diastema is often present between them. This has
c. The mandibular anterior primary teeth are about been referred to as the ugly duckling stage of the
6mm narrower mesiodistally on average than mixed dentition. This is a normal stage of develop
their successors. ment but does not always occur. When the perma
d. Overbite, defined as the vertical overlap of the nent canines erupt, their mesial movement will
mandibular teeth by the maxillary teeth, develops likely close the diastema if one is present and if it
as teeth erupt. Overbite can be measured in is 2mm or less.
millimeters, but it is preferable to measure it d. The mandibular incisors erupt lingually to the
in percentages. Overbite normally varies from 10% primary incisors, and they move facially.
to 40%. e. A transient open bite may be observed as a result
e. Open bite is lack of overbite. Open bite or reduced of partial eruption of anterior teeth. Under normal
amount of overbite is not unusual in children conditions, the open bite resolves with further
during the primary dentition because of thumb- or tooth eruption.
finger-sucking habits. f. The molar relationship is described in the sagittal
f. Overjet is the horizontal distance between the plane according to the Angle classification. The
mandibular teeth and the maxillary teeth. Overjet Angle classification system was introduced by
normally ranges from 0 to 4mm. Digit sucking Angle in 1907 and is based on the anterior-posterior
habits also cause an increase in overjet. relationship of the first mandibular molar to the
g. Spacing. maxillary permanent first molar.
(1) Children in the primary dentition often have (1) Class I molar or normo-occlusion.
generalized spacing between their teeth. The (2) Class II molar or disto-occlusion.
extra space helps accommodate the larger sized (3) Class III molar or mesio-occlusion.
permanent teeth as they erupt. If a child lacks g. Predicting molar relationshipaccording to Bishara
spacing or has crowding in the primary denti (2001), during the transition period from the
tion, the permanent dentition will exhibit primary to the mixed dentition, flush terminal
crowding. plane develops into a class I in 56% of cases and
(2) Spacing is especially noticeable in two locations into a class II in 44% of cases. Mesial step can
called the primate spacesbetween the lateral transition into a class I or, much less commonly, a
incisor and canine in the maxilla and between class III molar occlusion according to the initial
the canine and first primary molar in the severity.
mandible. h. Normal characteristics of the mixed dentition
h. Crowding is uncommon in the primary dentition. molar and canine relationships are class I; leeway
i. Molar relationship. space is present; well-aligned incisors or up to
(1) Flush terminal planethe distal aspects of the moderate crowding of the incisors; proximal con
second deciduous maxillary and mandibular tacts are tight.
molars are at the same sagittal level. i. Leeway space.
(2) Mesial stepthe mandibular terminal plane is (1) The difference in mesiodistal size between the
mesial to the maxillary terminal plane. primary canine, primary first molar, and
(3) Distal stepthe mandibular terminal plane is primary second molar and their permanent
distal to the maxillary terminal plane. replacements. The leeway space is larger in the
(4) By the age of 5, about 90% of children have a mandibular arch, averaging 2.5mm per side. In
terminal plane relationship that is flush or with the maxillary arch, the leeway space measures
a 1-mm or greater mesial step. about 1.5mm per side.
(5) The first permanent molar is guided along the (2) The leeway space can affect the eventual clas
terminal plane during eruption. The terminal sification of the molar in the permanent denti
plane relationship determines the molar clas tion or may aid in resolution of crowding, or a
sification in the mixed dentition. combination of both.
4. Permanent dentition stage. b. Measured from the distal aspect of the second
a. Begins when the last primary tooth is lost. primary molar (mesial aspect of the first perma
b. The maxillary teeth should overlap the mandibular nent molar) on one side and around the arch to the
teeth vertically and buccolingually. distal aspect of the second primary molar on the
c. The arches have curvature in the sagittal plane other side.
(curve of Spee) and the frontal plane (curve of c. Mandibular arch circumference decreases signifi
Wilson). cantly in the mixed to permanent dentition because
d. Overbite is generally 10% to 20% but can vary up of the mesial shift of the permanent molars into the
to 50%. leeway space, the mesial drift tendency of the pos
e. Overjet should be 1 to 3mm. terior teeth in general, the slight amount of inter
f. The interarch relationship (also referred to as the proximal wear, and the lingual positioning of the
buccal occlusion) should be class I molar, premolar, incisors secondary to the differential growth of the
and canine. maxilla (less) compared with the mandible (more).
g. Permanent dentition relationships are fairly stable d. Maxillary arch circumference increases very
once established, with one notable exception: slightly.
during the second to fourth decades of life, there C. Sequence of eruption.
is a tendency for anterior crowding to develop or 1. Eruption is earlier by 5 months on average in females
worsen over time. compared with males.
B. Dimensional changes in the dental arches. 2. Primary dentition.
1. Width. a. Primary teeth begin calcification between the third
a. The maxillary intercanine width increases by and fourth month in utero.
approximately 6mm between the ages of 3 and 13. b. The mandibular teeth usually start the calcification
An additional increase of 1.7mm occurs until process before the maxillary teeth.
age 45. c. At birth, no teeth are present in the newborn
b. The maxillary intermolar width in the primary infant.
dentition increases 2mm between the ages of 3 d. Eruption of the first primary tooth starts at about
and 5. The permanent intermolar width increases 6 to 7 months of age, and new teeth continue to
by 2.2mm between the ages of 8 and 13 and erupt until age 2 to 3.
decreases about 1mm by age 45. e. The typical sequence of eruption is A-B-D-C-E: the
c. Part of the increase in width of the maxillary arch central incisor (A), the lateral incisor (B), the first
is because the alveolar bone is divergent, and the primary molar (D), the canine (C), and the second
width increases as growth and eruption occurs. primary molar (E).
d. The mandibular intercanine width increases by 3. Permanent dentition.
3.7mm from age 3 to 13. From age 13 to 45, the a. The permanent teeth begin calcification shortly
intercanine width decreases by 1.2mm. after birth.
e. The mandibular primary intermolar width b. The first permanent molar shows signs of calcifica
increases by 1.5mm between the ages of 3 and 5. tion the second postnatal month, and the third
The permanent molar width increases by 1mm permanent molar begins to calcify around age 8 to
from age 8 to 13 and decreases by 1mm by age 45. 9 years.
2. Length. c. Mandibular arch eruption sequence: first molar,
a. Arch length is measured at the midline from a central incisor, lateral incisor, canine, first pre
point midway between the central incisors to a molar, second premolar, second molar, and third
tangent touching the distal surfaces of the second molar.
primary molars or the mesial surfaces of the first d. Maxillary arch eruption sequence: first molar,
permanent molars. central incisor, lateral incisor, first premolar,
b. In the maxilla, there is a small decrease in arch second premolar, canine, second molar, and
length with age because the incisors become more third molar. In the maxillary arch, the eruption
upright. sequence in the posterior segments is frequently
c. In the mandibular arch, a similar decrease in arch asymmetrical.
length is observed in the mixed and permanent
dentition as a result of uprighting of the incisors 1.4 Orthodontic Diagnosis
and the loss of the leeway space. The first step in orthodontic treatment planning is gather
3. Circumference (perimeter). ing the data required to make a diagnosis. The information
a. A measure of the amount of space available for the comes from talking to the patient or parents or both, clini
dentition. cal examination, and diagnostic records.
A. Patient interview.
1. Chief complaintwhy treatment is desired.
2. Medical and dental history.
a. Although it is usually impossible to pinpoint
a cause of malocclusion, it may be possible in a
few cases when there is a history of early tooth
loss, trauma, family history of a certain type
of malocclusion, habits, or a developmental Overjet
malformation.
b. Medical problems that may affect orthodontic
treatment, including susceptibility to periodontal
disease, and medications that inhibit bone remod
eling (bisphosphonates). Figure 5-6 Overjet is defined as horizontal overlap of the
3. Growth history. incisors. Normally, the incisors are in contact, with the upper
4. Social and behavioral assessment. incisors ahead of the lower by only the thickness of the upper
a. Cooperation. edges (i.e., 2- to 3-mm overjet is the normal relationship). If the
b. Habits. lower incisors are in front of the upper incisors, the condition is
B. Clinical examination (oral and extraoral). called reverse overjet or anterior crossbite. (From Proffit WR,
1. Pathologyincluding caries and periodontal prob Fields HW, Sarver DM: Contemporary Orthodontics, ed 5. St.
lems, oral hygiene. Louis, Mosby, 2013.)
2. Functionmastication, jaw opening, TMJ, speech,
functional shifts, interferences.
3. Dental and occlusal characteristics.
a. Intraarch. 2. Division 2maxillary incisors
(1) Teeth present or missing. upright (laterals flared) and deep
(2) Arch shape, symmetry. overbite.
(3) Alignmentcrowding, spacing, rotations. (iv) Class IIImesiobuccal cusp of the
(a) Space analysis in the mixed dentition using maxillary first molar posterior to the
radiographs or proportionality tables or buccal groove of the mandibular first
both. molar.
(4) Tooth size analysistooth size discrepancies (b) Overjet.
(Bolton, 1958). (i) Excess overjet (usually with class II)
b. Interarch (in three dimensions)discrepancies (Figure 5-6).
may be dental or skeletal in origin. For example, a (ii) Reverse overjet (anterior crossbite
patient with a class II interarch relationship may usually with class III).
have a class I skeletal relationship (maxilla and (2) Vertical (overbite)normal (20% overbite),
mandible are in good relationship) or a class II deep (>50% overbite), or open.
skeletal relationship with the maxilla forward or (3) Width (transverse, posterior crossbite).
the mandible back or both. (a) Normalmaxillary lingual cusp in man
(1) Anterior-posterior. dibular fossa.
(a) Angle classification. (b) Crossbite or lingual crossbitemaxil
(i) Class I normal occlusionmesiobuccal lary buccal cusp in mandibular fossa
cusp of the maxillary first molar in the (Figure 5-7).
buccal groove of the mandibular first (c) Complete lingual crossbitewhole maxil
molar and intraarch relationships lary tooth lingual to mandibular tooth.
among teeth are correct. (d) Complete buccal crossbitewhole maxillary
(ii) Class I malocclusionmesiobuccal tooth buccal to mandibular tooth.
cusp of the maxillary first molar in the 4. Facial esthetics and proportions.
buccal groove of the mandibular first a. Frontal examination.
molar (but intraarch relationships are (1) Right-left symmetry and proportions (rule
abnormal). of 5s).
(iii) Class IImesiobuccal cusp of the (2) Vertical proportions (vertical facial thirds).
maxillary first molar anterior to the (3) Lip posture (lip competence)with the teeth
buccal groove of the mandibular first together and lips at rest, the lips should lightly
molar. touch or be slightly apart. A gap of more than
1. Division 1maxillary incisors flared. 3 to 4mm indicates lip incompetence because
of a long lower face, protruding incisors, large (5) Gingival show on smileup to 1 or 2mm is
overjet, or short lips. considered esthetically pleasing, with more
(4) Incisor show at rest (lip to tooth)amount of being excessive.
upper incisor below the upper lip; 2 to 4mm is b. Profile examination.
considered esthetically pleasing. (1) Facial convexity (Figure 5-8).
(a) Convex (more convex than average, class
Palatal width II), straight (average, class I), or concave
(prognathic, midface deficient, class III).
(2) Lip prominence, usually evaluated relative to
Ricketts esthetic line, which extends from
AB the tip of the nose to the chin. The lips
should be slightly behind this line for esthetics.
Incisor anterior-posterior position affects lip
prominence
(b) Full (procumbent, protrusive), average, or
flat (retrusive).
CD
(3) Nasolabial angleangle between the base of
Palatal width the nose and the upper lip; should be perpen
dicular or slightly obtuse.
(c) Acute (usually along with full lips), average,
AB or obtuse (usually along with flat lips).
5. Skeletal relationships (cephalometrics)cephalo
metric radiographs are standardized two-
dimensional films of the skull. Subsequent films can
be superimposed to evaluate growth or treatment
effects. Individual films can evaluate dentofacial
CD
proportions or help clarify the anatomic basis for a
malocclusion. This information should be used to
Figure 5-7 Posterior crossbite can be either dental, as
confirm information from the clinical examination.
in a patient with adequate palatal width (i.e., distance AB
approximately equals distance CD), or skeletal because Measures can be used to compare an individual with
of inadequate palatal width (i.e., distance CD is consider- population norms, taking into account that there is
ably larger than distance AB). (From Proffit WR, Fields HW, much normal variation in the population.
Sarver DM: Contemporary Orthodontics, ed 5. St. Louis, Mosby, a. Cephalometric landmarks (Figures 5-9 and 5-10).
2013.) b. Cephalometric reference planes (lines).
A Convex B Straight C Concave
Figure 5-8 A-C, Profile convexity or concavity results from a disproportion in the size of the jaws but does not by
itself indicate which jaw is at fault. A convex facial profile (A) indicates a class II jaw relationship, which can result from either a
maxilla that projects too far forward or a mandible too far back. A concave profile (C) indicates a class III relationship, which can result
from either a maxilla that is too far back or a mandible that protrudes forward. (From Proffit WR, Fields HW, Sarver DM: Contemporary
Orthodontics, ed 5. St. Louis, Mosby, 2013.)
6
5
4
8
1 3 7
2 9
Na 10
S
PNS 14
Ba ANS 11
A
12
13
Go
B
Figure 5-10 Definitions of cephalometric landmarks (as
Pog seen in a lateral cephalometric tracing). 1, Bo (Bolton
Me Gn point), The highest point in the upward curvature of the retro
condylar fossa of the occipital bone. 2, Ba (basion), The lowest
Figure 5-9 Definitions of cephalometric landmarks (as
point on the anterior margin of the foramen magnum, at the base
they would be seen in a dissected skull). A, The innermost
of the clivus. 3, Ar (articular), The point of intersection between
point on the contour of the premaxilla between the anterior nasal
the shadow of the zygomatic arch and the posterior border of the
spine and the incisor tooth. ANS (anterior nasal spine), The tip of
mandibular ramus. 4, Po (porion), The midpoint of the upper
the anterior nasal spine (sometimes modified as the point on the
contour of the external auditory canal (anatomic porion), or the
upper or lower contour of the spine where it is 3mm thick).
midpoint of the upper contour of the metal ear rod of the cepha
B, The innermost point on the contour of the mandible between
lometer (machine porion). 5, SO (sphenooccipital synchondro
the incisor tooth and the bony chin. Ba (basion), The lowest point
sis), The junction between the occipital and basisphenoid bones
on the anterior margin of foramen magnum, at the base of the
(if wide, the upper margin). 6, S (sella), The midpoint of the cavity
clivus. Gn (gnathion), The center of the inferior point on the
of sella turcica. 7, Ptm (pterygomaxillary fissure), The point at the
mandibular symphysis (i.e., the bottom of the chin). Na (nasion),
base of the fissure where the anterior and posterior walls meet. 8,
The anterior point of the intersection between the nasal and the
Or (orbitale), The lowest point on the inferior margin of the orbit.
frontal bones. PNS (posterior nasal spine), The tip of the posterior
9, ANS (anterior nasal spine), The tip of the anterior nasal spine
spine of the palatine bone, at the junction of the hard and soft
(sometimes modified as the point on the upper or lower contour
palates. Pog (pogonion), The most anterior point on the contour
of the spine where it is 3mm thick). 10, Point A, The innermost
of the chin. (From Proffit WR, Fields HW, Sarver DM: Contempo
point on the contour of the premaxilla between the anterior nasal
rary Orthodontics, ed 5. St. Louis, Mosby, 2013.)
spine and the incisor tooth. 11, Point B, The innermost point on
the contour of the mandible between the incisor tooth and the
bony chin. 12, Pog (pogonion), The most anterior point on the
(1) S-N: anterior cranial base. contour of the chin. 13, Me (menton), The most inferior point on
(2) FH: Frankfort horizontal (Po-Or). the mandibular symphysis (i.e., the bottom of the chin). 14, Go
(gonion), The midpoint of the contour connecting the ramus and
(3) OP: occlusal plane.
body of the mandible. (From Proffit WR, Fields HW, Sarver DM:
(4) MP: mandibular plane (Go-Me or Go-Gn). Contemporary Orthodontics, ed 5. St. Louis, Mosby, 2013.)
c. Cephalometric measures.
(1) SNA: anterior-posterior position of the maxilla
bigger means maxilla is more anterior. (5) Y-axis: S-N to S-Gnbigger indicates more
(2) SNB: anterior-posterior position of the vertical development, with long lower face and
mandiblebigger means mandible is more anterior open bite tendency.
anterior. (6) 1/-SN: upper incisor angulationbigger is more
(3) ANB: anterior-posterior difference between flared.
maxilla and mandiblemore positive indicates (7) /1-MP: lower incisor angulationbigger is
skeletal class II; more negative indicates skeletal more flared.
class III. (8) Interincisal angle.
(4) MP-SN: mandibular plane anglebigger is 6. Individual, racial, and ethnic variation.
steeper and indicates vertical growth pattern, a. There is a significant amount of variation in esthetic
with long lower face and anterior open bite appearance and proportions and cephalometric
tendency. values among individuals.
b. There is a significant difference in esthetics and 6. Growth potential and growth tendencies should also
cephalometric values among racial and ethnic be considered. (e.g., a class III growth tendency in
groups. someone who is already class III and with substantial
c. Cephalometric measures should be used to explain growth remaining would be considered a problem.)
or support a diagnosis based on occlusal and C. Development of treatment objectivestreatment objec
esthetic characteristics, to help differentiate the tives mirror problems and should be listed in priority
underlying cause of an observed malocclusion. order.
Individual cephalometric measures should not be D. Evaluation of possible solutionsfor each problem or
used by themselves to make a diagnosis. objective, the possible solutions should be examined,
7. Other radiographic information. and the appropriate option for a given patient should
a. Panoramic or full-mouth radiographs, or both, are be chosen.
necessary to evaluate locations and orientations of E. Compromises and other considerations.
teeth, root parallelism, bone heights. 1. The ideal is to achieve the best possible function,
b. Periapical radiographs, especially of incisors, are esthetics, and stability for each patient.
recommended to document and follow signs of 2. Often, the ideal goals cannot be met by a reasonable
root resorption that may be present or induced orthodontic plan. One goal may need to be sacrificed
during treatment. at the expense of achieving the best possible result for
c. Three-dimensional cone-beam computed tomog a given patient.
raphy may be performed to locate unerupted or 3. The relative risk/cost-benefit should be considered
impacted teeth more precisely, evaluate skeletal along with the patients preferences. Not all patients
asymmetry, assess craniofacial defects, or con want to incur the risks and costs of surgery to achieve
struct cephalometric or other radiographic the ideal result. Some patients may be at increased
images. caries or periodontal risk, and objectives can be mod
ified to decrease treatment time to reduce those risks.
1.5 Treatment Planning 4. Alternative treatment options should be presented
A. Development of a problem list. to patients who can help make a decision on the
1. Diseases or pathologic processes (systemic diseases, best treatment, given various circumstances. In
caries, periodontal concerns). formed consent to treatment is important. Patients
2. Factors contributing to or describing the malocclu need to know and understand the relative risks and
sion (e.g., dental crowding, anterior deep bite, class benefits.
II interarch relationship, mandibular deficiency, long
lower face, flat lips). 1.6 Biology of Tooth Movement
3. Cephalometric measures in themselves are usually A. Fundamental principlesbiology of tooth movement
not considered problems, but what they indicate may refers to the orthodontic movement of a tooth within
be (e.g., protrusive maxilla, small mandible, flared and through the alveolar bone. It results from the appli
maxillary incisors, vertical growth tendency). cation of a force system to the tooth and the transduc
B. Prioritization of the problem listlisting the problems tion of that mechanical signal into a biologic signal and
in order of priority is important because it helps when a response.
developing a systematic plan that addresses as many of 1. A force system is applied at the crown of a tooth, and
the patients problems as possible. The problems are not the mechanical signal is transmitted or transducted
always addressed in their priority sequence during to the supporting structures of the tooth (bone and
treatment. periodontal ligament [PDL]). For tooth movement,
1. Systemic diseases or pathology take top priority and the force need not be continuous, but it is critical that
usually need to be controlled before orthodontic the force be applied for a minimally acceptable period
treatment can begin. of time to elicit the biologic response necessary. The
2. Impacted teeth are usually a high priority. amount of force (heavy or light) determines the bio
3. Esthetic or occlusal problems may be next, depend logic pathway of tooth movement and the formation
ing on the severity, the patients chief complaint, or or lack of formation of a hyalinized zone with under
other concerns. mining resorption.
4. Within occlusal problems, interarch relationships 2. The PDL, a well-organized connective fibrous tissue,
usually take priority over intraarch relationships remodels significantly during orthodontic tooth
(class II interarch relationship takes priority over movement. Under physiologic conditions, the PDL is
mild anterior crowding). However, priority may vary rich in collagen fibers well organized to resist the
depending on severity (e.g., severe crowding might forces of mastication.
take priority over mild anterior overbite). 3. Pressure or compression sideside toward which the
5. Habits should also be considered. tooth is moving. This is where bone resorption is
taking place. Resorption of the alveolus is primarily equivalent signal of opposite direction
the result of osteoclastic activity. The osteoclast is a when the force is released.
giant, multinucleated cell with a ruffled border. The (b) The PDL is compressed, and fluid is
resorption lacunae created are called Howships expressed from the area of compression,
lacunae. resulting in instant movement of the tooth
4. Tension sideside opposite to the direction of the within the PDL in 1 to 2 seconds.
movement of the tooth. Apposition of bone occurs (c) As the fluids are expressed from the PDL,
on this side. Areas of resorption may also undergo pain is felt as a result of the pressure applied
appositional remodeling if the tooth movement within 5 seconds. The tooth is now com
changes direction and the pressure side of the alveo pressed against the bone surface, and no
lus undergoes tension. further tooth movement occurs until
5. Different types of tooth movement are characterized undermining resorption takes place.
by different patterns of stress distribution in the PDL (d) Undermining resorption occurs within the
and corresponding areas of bone resorption and alveolar bone (in the marrow spaces) and
bone apposition. moves toward the PDL area.
a. Intrusionwhen a tooth is intruded, the area of (i) Appearance of osteoclastic cells in the
compression of the PDL is concentrated at the apex bone marrow spaces is the first indica
of the tooth. tion of undermining resorption.
b. Tippingduring tipping, the crown and the apex (ii) Undermining resorption can last 2
move in opposite directions, creating two areas of weeks to a few weeks. No tooth move
compression: the cervical area on the side toward ment can occur until the undermining
which the tooth is tipping and the apical region on resorptive process is completed when
the side opposite from which the tooth crown is heavy orthodontic forces are applied.
moving. The tension areas are located on the oppo (iii) The compressed PDL undergoes sig
site sides of where compression occurs. nificant tissue changes. On the com
c. Translation or bodily movementduring bodily pression side, the hyalinized zone starts
movement or translation, one side of the PDL to develop (an area of the PDL that has
experiences compression (the side toward which lost all structural organization shows
the tooth is moving), and the other side experi signs of necrosis and a lack of cellular
ences tension. activity).
B. Biologic control of orthodontic tooth movement. (iv) Hyalinization of the PDL occurs within
1. During tooth movement, the tension and the com hours of the application of a heavy
pression occur in the PDL and at its two interfaces: force.
with the bone on the alveolar side and with the (v) Cells from the surrounding bone
cementum on the dental (tooth) side. Tension and marrow start to migrate into the area
compression also occur with physiologic tooth move from the bone marrow spaces within 3
ments during functions such as mastication. Forces to 5 days, and undermining resorption
ranging from 1 to 50kg (10 to 500 N) are experi simultaneously starts within the bone
enced by the PDL during mastication, and the sup marrow spaces.
porting apparatus of the tooth (alveolar bone and (2) Secondary period of tooth movement (after
PDL) undergoes bone bending and compression and undermining resorption).
tension of the PDL. (a) The hyalinized PDL is in the process of
2. When an orthodontic force is applied, two scenarios healing.
can develop depending on whether the force is heavy (b) Secondary tooth movement occurs after a
or light. lag period during which undermining
a. Heavy forcethe use of heavy orthodontic forces resorption takes place.
does not make tooth movement more efficient. It c. Light forcethe use of light forces causes smooth,
actually delays tooth movement by causing a lag continuous tooth movement without formation of
period after the initial movement of the tooth a significant hyalinized zone in the surrounding
within the PDL. PDL. As a result, teeth subjected to light orthodon
(1) Initial period of tooth movement. tic forces start to move earlier and in a more physi
(a) Bone bending and creation of a piezoelec ologic way than teeth subjected to heavy forces.
tric signal occurs in less than 1 second. The (1) Initial reaction includes partial compression of
piezoelectric signal is characterized by a the blood vessels and a distortion of the PDL
quick decay rate and the production of an fibers.
(2) Within minutes, blood flow is altered, the (3) The best way to decrease the pain during ortho
oxygen tension changes, and prostaglandins dontic tooth movement is to minimize the
and cytokines are released within the PDL. amount of force applied on the tooth.
(3) Metabolic changes, such as enzyme activity and (4) Patients should be given acetaminophen
chemical messengers that alter cellular activity, (Tylenol) rather than aspirin or ibuprofen. Evi
start to appear in this area of the PDL after a dence indicates that the analgesic mechanism
few hours. First messengers that have been of action of acetaminophen does not com
suggested in the literature include hormones pletely overlap that of aspirin and ibuprofen.
(parathyroid hormone and calcitonin), fibro Acetaminophen may also have a more favor
blast distortion, substance P, some neurotrans able adverse effect profile compared with
mitters, and prostaglandins. aspirin and ibuprofen.
(4) Within a few hours, as signal transduction c. Tissue inflammation.
starts in the PDL, the second messenger cyclic (1) Usually results from poor oral hygiene.
adenosine monophosphate levels increase. (2) A less likely cause is an allergic reaction to latex
(5) Cellular differentiation takes place in the PDL, or nickel. Nickel allergy occurs to some degree
and the coupling between osteoclast and osteo in about 20% of the general U.S. population,
blast activities results in frontal resorption of but its effects are not observed frequently in
the alveolus within a few days. orthodontics. The onset of an allergic reaction
(6) The process of frontal resorption as seen with primarily depends on the quality of the stain
light force application allows a faster and more less steel used to fabricate the orthodontic
efficient biologic response than heavy forces appliances. Better quality stainless steel does
and results in an earlier onset of tooth not leak nickel in the oral environment.
movement. d. Effect on the pulp.
(7) Even when light forces are applied to a tooth, (1) Symptoms ranging from mild pulpitis to loss of
because the PDL itself is nonuniform and vitality are rare.
stresses created in the PDL vary depending on (2) Loss of vitality is seen in teeth that have had a
the location observed, it is likely that some history of trauma or extensive restorations or
areas along the tooth will experience some in teeth that are moved with unusually heavy
undermining resorption. force or over long distances.
3. Deleterious effects of orthodontic forces. (3) If the apex of a tooth is moved out of the alveo
a. Mobility of teeth subjected to orthodontic forces. lar bone, the blood supply can be potentially
(1) Forces cause bone and PDL to undergo remod severed, and the tooth may lose vitality.
eling, and the PDL is temporarily widened. (4) Teeth that have been successfully endodonti
(2) Moderate mobility of the teeth occurs during cally treated can be moved orthodontically
tooth movement and resolves with the comple without specific concerns. Endodontically
tion of therapy as long as there is no active treated teeth do not appear to be more prone
periodontal disease. to root resorption than vital teeth.
(3) If the tooth is in traumatic occlusion or the e. Root resorption during orthodontic tooth
patient is grinding or clenching, the mobility is movement.
significantly increased, and there may be a (1) Root resorption is a potential side effect of
need to adjust the occlusion or at least monitor orthodontic therapy.
it until the tooth does not have an occlusal (2) As the PDL experiences hyalinization in spe
interference. cific stress areas of compression, the adjacent
b. Pain. cementum shows signs of resorption by clastic
(1) Heavy orthodontic forces applied to a tooth can cells.
cause pain as soon as the PDL is initially (3) Heavy continuous forces have more potential
compressed. to create root resorption than light forces.
(2) Typically, pain occurs within a few hours of the (4) The resorptive defect repairs, but its ability to
initiation of force application and lasts 2 to 4 do so is a function of its severity, size, and loca
days. The pain experienced after the applica tion on the root. Small defects repair easily to
tion of heavy forces is due to the development the initial contour of the root. Larger defects
of areas of ischemia or necrosis (hyalinization) and specifically defects located at the apex do
in the PDL. These areas undergo remodeling, not repair to the contour of the tooth. In those
and the pain decreases until the next appliance cases, the length of the root is irreversibly
activation. reduced, and the root/crown ratio is modified.
(5) Occurrence and severity of root resorption are (c) Taking periodic periapical radiographs
difficult to predict for a given individual. There to monitor the amount of resorption
are numerous risk factors for root resorption. occurring.
(a) Genetic factorsa patient with a family (d) Detailed informed consent and good com
history of root resorption is more likely to munication with the patient and parents
experience it during orthodontic tooth and any referring providers.
movement. Susceptibility to root resorption C. Rapid acceleratory phenomenon.
seems to be of multifactorial polygenic 1. It is possible to accelerate tooth movement by per
inheritance. forming a surgical procedure involving tissue reflec
(b) Heavier forces, certain types of tooth move tion and selective corticotomy cuts and perforations
ment, and more movement of a tooth around teeth to be moved. Bone grafting is also often
during treatment increase the potential for performed. This is followed by a period where tooth
root resorption. movement proceeds rapidlytermed the rapid accel-
(c) Single-rooted teeth such as maxillary lateral eratory phenomenon.
incisors have a higher incidence of root
resorption than multirooted teeth. 1.7 Mechanical Principles
(d) Teeth subjected to trauma, bruxism, and in Tooth Movement
heavy masticatory forces have a higher inci Physical laws of statics are applied to explain the force
dence of resorption. systems developed by orthodontic appliances. The biologic
(e) A tooth that had signs of root resorption reaction to force systems results in orthodontic tooth
before the initiation of treatment will likely movement.
to continue to resorb during orthodontic A. Forces.
therapy. 1. Forces are vectors and have direction and magnitude
(f) Movement of roots into the cortical plate of (e.g., a force directed mesially moves a tooth
the bone. mesially).
(g) Asians are less at risk for root resorption 2. Forces can act anywhere along their line of action (a
than Hispanics or whites. pulling force is the same as a pushing force).
(6) Teeth with substantial root resorption but 3. The point of force application also influences tooth
intact marginal peridontium do not experience movement.
any more mobility than unresorbed teeth. The 4. A force acting through the center of resistance of a
longevity of teeth experiencing root resorption tooth can cause pure translation of the tooth in the
is not compromised as long as the supporting direction of the force (Figure 5-11). Pure translation
periodontium is healthy. The current standard is movement of all points on the tooth in the same
of care for patients at risk for root resorption direction the same amount; there is no rotation. This
or presenting with root resorption at the onset is also called bodily movement.
of treatment includes the following. 5. For a free body floating in space, the center of
(a) Use of light forces. resistance is coincident with the center of mass or
(b) Building periods of rest into treatment gravity.
when wires are kept passive to allow for 6. For a tooth, the location of the center of resistance
repair to occur. depends on the size and shape of the tooth and the
F F
F
A B C
Figure 5-11 A-C, White circles indicate the center of resistance at the starting tooth position. Shaded circles show the
center of resistance moved in the direction of the force. A force through the center of resistance causes all points of the tooth to move
the same amount in the same direction. This type of movement is called translation or bodily movement. (From Bishara SE: Textbook
of Orthodontics, ed 3. Philadelphia, Saunders, 2001.)
d
MF
MF d d
F MF
F
A B MF = F d C
Figure 5-12 A-C, A force, applied at a bracket that does not act through the center of resistance, causes rotation of
a tooth. This tendency to rotate is measured in moments and is called the moment of the force (MF). The magnitude of MF is measured
as the magnitude of the force times the perpendicular distance from the line of force to the center of resistance (i.e., MF = F d). Rota
tions are shown in the first (A), second (B), and third (C) order. (From Bishara SE: Textbook of Orthodontics, ed 3. Philadelphia,
Saunders, 2001.)
Plus Equals
F F F
A B C
Figure 5-13 A-C, Rotational movement caused by a force not acting through the center of resistance is best visual-
ized as the simultaneous process of tooth translation. A, Moves the center of resistance in the direction of the force and tooth
rotation. B, Around the center of resistance. C, The result is a combination of translation and rotation around the center of resistance.
(From Bishara SE: Textbook of Orthodontics, ed 3. Philadelphia, Saunders, 2001.)
quality and level of the supporting structures (PDL

and alveolar bone).
7. In a healthy tooth, the center of resistance is pre Center of Rotation (CRot)
sumed to be about one half the distance from the
Center of Resistance (CRes)
alveolar crest to the root apex. This is about 10mm
from where an orthodontic bracket would be located
on the crown of a tooth. F
8. The center of resistance is more apical for a periodon
tally compromised tooth with loss of attachment.
B. Moments.
1. A moment is defined as a tendency to rotate and may Figure 5-14 The center of rotation is an arbitrary point
refer to rotation, tipping, or torque in orthodontics. about which a body appears to have rotated as deter-
a. Orders of tooth movement and rotation mined from its initial and final position. It is the result of the
(Figure 5-12). relative amounts of translation and rotation occurring during
(1) First order or rotation (in the occlusal view). tooth movement. (From Bishara SE: Textbook of Orthodontics,
ed 3. Philadelphia, Saunders, 2001.)
(2) Second order or tipping (viewed from the
buccal or lingual).
(3) Third order or torque (viewed from the mesial 3. The center of rotation is the mathematical point
or distal). about which the tooth appears to have rotated after
2. If a force is applied at any point other than the center movement is complete (Figure 5-14).
of resistance, in addition to moving the center of 4. Increasing the magnitude of the force or applying the
resistance in the direction of the force, a moment is same force even farther from the center of resistance
created (Figure 5-13). increases the tendency for rotation. The magnitude of
b. The center of rotation is at the center of

resistance.
d 2. Tipping (uncontrolled tipping).
a. When a force is applied at the bracket, the center
of resistance moves in the direction of the force,
F F
and the tooth crown tips in the direction of the
MC
force, whereas the apex moves in the opposite
MC direction.
b. The center of rotation is apical to the center of
MC
resistance.
c. This is the easiest and fastest tooth movement to
accomplish but often the least desirable.
d F F 3. Crown movement (controlled tipping).
F F a. A force is applied at the bracket; a small couple is
also applied to partially negate the tipping of the
d crown caused by the force.
b. The center of rotation is at the root apex.
c. This is a slightly more difficult type of tooth move
MC = F d ment and occurs more slowly.
Figure 5-15 Diagrammatic representation of couples in 4. Pure translation (bodily movement).
the first, second, and third order. The forces acting on the a. A force is applied at the bracket; a larger couple is
teeth are equal and opposite (straight arrows). The rotational ten also applied to exactly negate the tipping of the
dency (curved arrows) is called the moment of the couple (Mc). The crown caused by the force.
moment of the couple is measured as the magnitude of one of the b. The center of rotation is so far apical to the tooth
forces (F) of the couple times the perpendicular distance between (at infinity) that the tooth translates without
the two forces of the couple (d) (i.e., MC = F d). (From Bishara tipping.
SE: Textbook of Orthodontics, ed 3. Philadelphia, Saunders, 2001.)
c. This is a difficult and slow type of tooth
movement.
5. Root movement.
a moment (M) is equal to the magnitude of the a. A force is applied at the bracket, and an even larger
applied force (F) times the distance (d) of that force couple is applied to more than negate the tipping
from the center of resistance (M = Fd). of the crown caused by the force. Only the root
C. Couples. moves in the direction of the force.
1. A couple is two equal and opposite, noncollinear b. The center of rotation is at the crown of the tooth.
forces (Figure 5-15). c. This is the most difficult and slowest type of tooth
2. A couple applied to a tooth produces pure rotation movement.
without translation. F. Static equilibrium.
3. The tooth rotates about its center of resistance regard 1. All orthodontic appliances obey Newtons Third Law:
less of the point of application of the couple. for every action, there is an equal and opposite
4. The magnitude of the moment created by a couple reaction.
depends on the force magnitude and distance between 2. For each appliance, the sum of the forces and the sum
the forces (M = Fd). of the moments acting on it sum to zero.
5. Couples are usually applied by engaging a wire in an 3. It is impossible to design an appliance that defies this
edgewise bracket slot. law of physics.
D. Equivalent force systems. 4. Examples of types of appliances.
1. Determining how a tooth will move can be calculated a. Equal and opposite forces.
by expressing what the tooth will feel at the center (1) An elastic band or a coil spring stretched
of resistance secondary to force systems applied at between two brackets produces equal and
the bracket. For example, a force at the bracket would opposite forces (the sum of the forces equals
cause the tooth to feel a force at the center of resis zero).
tance plus a tendency to rotate, tip, or torque in the b. One-couple appliances.
direction of the force. (1) Inserted into a bracket at one end and tied as a
E. Types of tooth movement. point contact at the other end.
1. Pure rotation. (2) A couple is produced only at the engaged end.
a. When a couple is applied to a tooth, it rotates (3) Equal and opposite forces (in a direction
around its center of resistance. opposite to the couple at the engaged end)
are produced at the two attachment sites

(Figure 5-16).
(4) The sum of the forces (equal and opposite) is
zero. The sum of the moments (the couple
created by the wire plus the oppositely directed
couple produced by equal and opposite forces)
is zero.
c. Two-couple appliances.
(1) Inserted into a bracket at both ends.
(2) Both a couple and a force are produced at each
end.
(3) The magnitude of the couple is largest at the
end closer to the bend in the wire (Figure 5-17) F2 d2 F2
or at the bracket that is more severely angled in
the case of a straight wire. F1 d1 F1
(4) The sum of the forces (equal and opposite) is
zero. The sum of the moments (the couples Figure 5-16 Equilibrium in a one-couple system. The first
created by the wire at each end plus the couple circle (solid) shows a passive intrusion arch. It is activated by tying
produced by the equal and opposite forces) it down anteriorly at the level of the bracket. This causes an intru
is zero. sive force at the incisor and an extrusive force at the molar. This
circle shows the direction of the couple associated with this extru
G. Anchorageanchorage is defined as resistance to
sive and intrusive force. The second circle (dotted) shows a second
movement. Because forces applied to teeth are distrib
couple at the molar bracket (MC) that is equal and opposite in the
uted along the root surface to activate cells in the PDL, direction to the first couple. (From Bishara SE: Textbook of
the anchorage value of any tooth is roughly equivalent Orthodontics, ed 3. Philadelphia, Saunders, 2001.)
to its root surface area.
II III
B C
IV V
D E
Figure 5-17 V bend couple. A, A centered V bend, which produces an equal and opposite couple and equal and opposite equilibrium
forces that cancel each other out. B-E, The tooth with the greater MC (greater angle of entry) and direction of rotation is shown with
curved arrows. The associated equilibrium forces are shown with straight arrows. (From Bishara SE: Textbook of Orthodontics, ed 3.
Philadelphia, Saunders, 2001.)
1. Reciprocal tooth movementtwo equal anchorage Point of arbitrary clinical loading Failure
value teeth or groups of teeth (units) are moved Yield point
point
against each other and move the same amount toward Proportional limit
or away from each other.
2. Reinforced anchorageadding additional teeth to a
Force
unit to distribute the force over a greater area and
slowing the movement of the anchor unit. Another s
method for reinforcing anchorage would be extraoral es
fn
tif
force, such as with headgear, with interarch elastics, S
or by using an implant (see later).
3. Stationary anchoragethe term stationary is used,
although it is not an accurate name. Teeth meant to 0.1% Springback
Range
be the anchor are activated to undergo difficult,
Deflection
slow movements, such as bodily movement (transla
tion) or root movement, which distribute forces dis Figure 5-18 Typical force-deflection curve for an elastic
persed over large areas of the PDL, whereas the material such as an orthodontic archwire. The stiffness of
reactive units undergo tipping, which occurs faster the material is given by the slope of the linear portion of the curve.
and more easily as a result of concentrated forces in The range is the distance along the x-axis to the point at which
permanent deformation occurs (usually taken as the yield point,
the PDL.
at which 0.1% permanent deformation has occurred). Clinically
4. Cortical anchorageanchor teeth roots are moved useful springback occurs if the wire is deflected beyond the yield
into cortical bone, which resorbs more slowly than point (as to the point indicated here as arbitrary clinical loading),
medullary bone. This is a controversial concept but it no longer returns to its original shape. At the failure point,
because root resorption would likely be increased as the wire breaks. (From Proffit WR, Fields HW, Sarver DM: Con
roots are forced into cortical bone. temporary Orthodontics, ed 5. St. Louis, Mosby, 2013.)
5. Implants for anchorageimplants, including palatal
implants, miniscrews or temporary anchorage Ultimate tensile strength
devices, and bone plates, can serve as absolute Yield strength Failure point
anchorage for holding or moving teeth. A stable Yield point
implant does not move because it has no PDL. Proportional limit
Stress
1.8 Orthodontic Materials E Stiffness E

Orthodontic tooth movement is achieved by the forces that
Springiness 1/E
are exerted on the tooth by an archwire via brackets during
orthodontic treatment. The forces transmitted to a tooth
depend on the physical and mechanical properties of the
wires used and the relationship between the brackets in
which the wire is engaged. The faciolingual and occluso 0.1%
gingival dimensions of the edgewise bracket slot allow the Strain
use of wires with different cross-sectional shapes and sizes.
Figure 5-19 Stress and strain are internal characteristics
The two bracket slot sizes most commonly used are 0.018 that can be calculated from measurements of force and
inch 0.025 inch and 0.022 inch 0.028 inch. The magni deflection, so the general shapes of force-deflection and
tude of the forces generated in the faciolingual and occlu stress-strain curves are similar. Three different points on a
sogingival direction is partly dependent on the bracket stress-strain diagram can be taken as representing the strength.
slot size. The slope of the stress-strain curve, E, is the modulus of elasticity,
A. Wire material properties. to which stiffness and springiness are proportional. (From Proffit
1. Stress-strain relationshipthe mechanical behavior WR, Fields HW, Sarver DM: Contemporary Orthodontics, ed 5.
of a ductile orthodontic wire (e.g., stainless steel) in St. Louis, Mosby, 2013.)
tensile loading may be analyzed in a force-deflection
or stress-strain plot (Figures 5-18 and 5-19). Stress 2. Ideal characteristicsan ideal orthodontic wire
() is the internal response of a wire to the applica should have the following properties: high strength,
tion of external forces defined as force (load) (F) per low stiffness, high working range, and high form
cross-sectional area (A) ( = F/A). Strain () is the ability. These important characteristics of wires
deformation or deflection of the archwire as a conse depend on the alloy composition, the crystal struc
quence of the stress and is defined as the dimensional ture of the metal, and the manufacturing process.
change (d) divided by the original dimension (d) 3. Wire propertieseach of the major elastic properties
( = d/d). (strength, stiffness, and range) is affected by a change
in the length and cross section of a wire (see Figure

5-18). Doubling the length of a wire decreases its 1.9 Orthodontic Appliances
strength by half, makes it eight times less stiff (or A. Fixed appliances.
eight times springier), and gives it four times the In modern orthodontic treatment, the straightwire
range. Similarly, when the diameter of a wire is (preadjusted edgewise) systems are the commercially
doubled, it becomes 8 times stronger and 16 times available appliances most commonly used. In the origi
stiffer, and its working range is decreased by half. nal, standard edgewise appliance, the orientation of
4. Wire selectionfor large orthodontic movements the bracket slot was at right angles to the long axis of
(usually during initial stages of orthodontic treat the tooth, and the thickness of the bracket base was the
ment), wires with a low load/deflection rate are desir same for all teeth. During treatment, bends were placed
able because they are able to provide constant low to position each tooth individually in the buccolingual
forces as the tooth moves and the appliance is deac direction (in-out, first-order bends), to provide proper
tivated. However, for minimal tooth movements such angulation in the mesiodistal direction (second-order
as in maximum anchorage extraction cases or during bends) and in the buccolingual direction (torquing
finishing, a high load/deflection rate is desirable. or third-order bends). In the straightwire appliance
Several factors influence the load/deflection rate of system, this information is incorporated into the brack
an appliance. ets for each individual tooth, eliminating or reducing
a. Wire materialthe load/deflection rate is propor the need for first-order, second-order, and third-order
tional to the modulus of elasticity of the material. bends. These built-in adjustments (the bracket pre
Stainless steel exhibits the highest modulus of scription) in the bracket slots help to achieve the
elasticity. The most flexible wire (wire with the proper position of each individual tooth.
lowest load/deflection rate) is made of a nickel 1. Preadjusted edgewise appliances (brackets with pre
titanium alloy. scriptions) allow the following.
b. Wire cross sectionthe load/deflection rate varies a. Rotational controlby twin bracket wings or by the
directly with the fourth power of the diameter of a incorporation of rotational arms in a single-wing
round wire and with the third power of the width bracket system.
of a rectangular wire. b. Horizontal controlby varying the relative thick
c. Wire lengththe load/deflection rate varies ness of the bracket base for teeth of different
inversely with the third power of the length of a thickness.
wire segment. Increasing the interbracket distance c. Mesiodistal tip controlthe slot of the bracket is
by incorporating loops or helices into the archwire angulated relative to the base of the bracket to pro
decreases the load/deflection rate. vide the proper tipping movement for each tooth.
B. Orthodontic archwire materials. d. Torquethe slot is angulated labiolingually to
1. Nickel-titaniumthese wires offer two very impor provide the proper root and crown movements.
tant characteristics: a very low modulus of elasticity (1) Brackets.
and an extremely wide working range. (a) Metal bracketsthese brackets are made of
2. Beta titaniumthese wires are frequently known as stainless steel. Their disadvantage is the
TMA (titanium-molybdenum alloy) wires. They have unesthetic appearance of the metal color.
an intermediate modulus of elasticity (approximately (b) Ceramic bracketsthese brackets are made
half that of stainless steel and twice that of nickel of monocrystalline or polycrystalline ce
titanium). They exhibit excellent resilience, which ramics. Although highly esthetic, these
provides a wide working range. One drawback of brackets are prone to fracture during tor
these wires is their high coefficient of friction. They sional and tipping activations. They exhibit
have high formability, which allows the clinician to increased frictional resistance to sliding
bend the wires and incorporate stops or loops into mechanics. They may cause abrasion of op
them if desired. They can also be spot-welded. posing teeth.
3. Stainless steelstainless steel wires remain popular (c) Self-ligating bracketsa locking mechanism
because of their good mechanical properties, excel is incorporated into these bracket systems
lent corrosion resistance, and low cost. The typical to hold the archwire in the slot. This mecha
composition of stainless steel alloys used in ortho nism eliminates the need for a ligature
dontics is 18% chromium and 8% nickel (18-8). placement. It is purported that these systems
Chromium gives this wire its corrosion resistance. shorten treatment time by reducing friction
When compared with nickel-titanium and beta tita and because the wire is efficiently kept
nium archwires, these wires exhibit the highest elastic engaged in the bracket slot; however, these
modulus (stiffness) and lowest springback. They can claims are controversial and generally
be soldered and welded. unsubstantiated scientifically.
(2) Bandsin contemporary orthodontic treat mandibular growth is expected with restraint of the
ment, all of the teeth (including molars) may maxilla. Growth modification is most successful in pre
be bonded. However, banding the molar teeth adolescent children with good compliance and growth
is preferred by many clinicians. Before banding, potential.
separators are placed between the teeth to 1. Headgearheadgear is used to modify growth of the
create enough space to allow band fitting and maxilla, to distalize (retract) or protract maxillary
subsequent cementation. Elastomeric or metal teeth, or to reinforce anchorage. There are different
separators may be used. types of headgear that can be used to achieve a
(3) Bondingbrackets are attached to the enamel desired effect. The type of headgear and desired force
surfaces using bonding resins. Direct bonding levels should be selected according to the specific
is the direct attachment of orthodontic appli treatment objectives for a patient. Headgear should
ances to the etched teeth using either chemi be worn preferably 12 to 14 hours per day to achieve
cally cured or light-cured adhesives. Indirect the goals. For orthopedic changes, a force level of
bonding techniques involve first positioning 250g to 500g per side is recommended; for dental
the brackets on study casts with a water-soluble movements, 100g to 200g per side should be used.
adhesive and then transferring them to the The success of headgear treatment depends on patient
mouth with a custom tray for bonding to the compliance.
teeth. The principal mechanism of attachment a. High-pull headgearcommonly used in the treat
between the tooth surface and resin-bonding ment of preadolescent patients with class II maloc
systems is the mechanical interlocking of the clusions and increased vertical dimension, minimal
bonding agent onto the etched enamel. overbite, and increased gingival exposure on smile.
(a) Bonding procedure. It consists of a high-pull headstrap and a standard
(i) Enamel prophylaxis with pumicethis facebow inserting into the headgear tubes of
procedure removes the pellicle and the maxillary first permanent molar attachments.
enhances the wettability of the enamel The objectives are restriction of anterior and down
surface for subsequent acid application. ward maxillary growth and molar distal move
(ii) Enamel etchingthe most commonly ment, intrusion, and control of maxillary molar
used enamel etching agent is 37% eruption.
phosphoric acid. Conventional acid- b. Cervical-pull headgearused to correct class II
etching (two-step) creates a micropo malocclusions with deep bite. It consists of a cervi
rous enamel surface that increases the cal neckstrap and a standard facebow inserting
retention of the resin. The enamel sur into the headgear tubes of the maxillary first per
face is then conditioned with an appli manent molar attachments. The objectives are to
cation of a primer. restrict anterior growth of the maxilla and to dis
1. Self-etching primers (one-step) talize and erupt maxillary molars. Because of the
combine the conditioning and direction of the line of force, this appliance pro
priming steps into a single treatment duces an extrusive and distal force on the maxillary
step. The advantage of self-etching first molars.
primers is the reduced clinical chair c. J-hook headgearconsists of a high-pull headstrap
time. that attaches to two hooks on the anterior part of
(iii) Bracket positioningeach bracket is the maxillary archwire. This J-hook design delivers
placed in a position relative to teeth in intrusive and posteriorly directed extraoral forces
the same arch to ensure proper rela to the anterior maxilla. However, it is generally
tionships between the teeth at the com used to retract canines and incisors, rather than for
pletion of treatment. If a light-cured orthopedic purposes.
type of composite resin is used, once d. Protraction headgear (reverse-pull, facemask)
the bracket is positioned, the adhesive used in patients with class III malocclusions where
is cured using a light source such as there is a maxillary deficiency. It is adjustable and
halogen, plasma, or light-emitting consists of two pads that rest on the soft tissue in
diode (LED). the forehead and chin region that are connected by
B. Appliances to modify the growth of the maxilla and the a midline framework. A metal bar with hooks con
mandiblethese appliances allow differential growth of nected to the framework allows attachment of elas
the jaws. During adolescence, the mandible has more tics to exert a downward and forward pull on the
potential for growth than the maxilla. Whether an maxilla.
extraoral force (headgear) or a functional appliance is e. Chin cup (chin cap)used to correct class III mal
used to modify growth in class II patients, differential occlusions (resulting from excessive mandibular
growth) in young children by restraining or redi between the maxillary and mandibular parts
recting mandibular growth. It consists of a head controls how much the mandible is postured
strap and a cup that fits on the patients chin to forward and how much the maxilla and mandible
exert superior and posterior forces that usually also are separated in the vertical dimension. This appli
cause opening rotation of the mandible. ance is supposedly more easily tolerated by patients
2. Functional appliancesfunctional appliances hold because of its two-part design.
the mandible in a protrusive position and transmit e. Mandibular anterior repositioning appliance
the forces created by the resulting stretch of the (MARA; Allesee Orthodontic Appliances, Sturte
muscles and soft tissues to the dental and skeletal vant, Wisconsin)consists of oversized stainless
components to produce movement of teeth and steel crowns on the maxillary and mandibular
modification of growth, most commonly to achieve molars, elbows that insert into the tubes on the
correction of a class II malocclusion. Because most maxillary crowns, and arms that protrude from
functional appliances are removable, patient compli the mandibular crowns. Because of the design of
ance plays a major role in their success. Whether the appliance, the lower arms interfere when the
fixed or removable, these appliances restrain the patient attempts to bite down, forcing the mandible
maxilla and displace the mandible, while allowing to reposition forward into a class I relationship;
the normal amount of mandibular growth potential this results in anterior force to the mandibular arch
to express itself. and posterior force to the maxillary arch.
a. Herbst appliancea fixed (or sometimes remov C. Noncompliant appliances to correct class II malocclu
able) functional appliance that consists of a piston sionsbecause compliance is a major concern when
and tube device that places the mandible in a treating class II malocclusions, fixed appliances not
forward position as the patient closes the mouth. requiring patient cooperation have been developed.
It is usually cemented or bonded to the maxillary Their use is generally indicated in patients with full or
and mandibular dental arches. There is a tendency cusp-to-cusp (end-on) molar/canine relationships,
for the mandibular incisors to procline (flare) mild to moderate crowding (0 to 6mm), and a profile
because of the forces that are indirectly delivered or other characteristics that do not support an extrac
to these teeth. tion treatment plan.
b. Activatorthis was the first removable functional 1. Pendulum appliancethe cemented appliance con
appliance developed. The name activator was sists of an acrylic body to use the palate as anchorage
given because of the belief that mandibular growth with wire extensions to the maxillary premolars. Two
was activated to correct class II malocclusions. This springs extending from the posterior portion of the
term is generically used today to describe any appliance are inserted into lingual molar attachments
functional appliance that is used for this purpose. and are activated to distalize the molar teeth. If
It consists of an acrylic body that covers part of the expansion of the maxilla is also needed, an expansion
palate and the lingual aspect of the mandibular screw may be incorporated into the acrylic body in
alveolar ridge. A labial bow fits anterior to the the midpalatal region. In this case, the appliance is
maxillary incisors. On the acrylic adjacent to the called a Pendex.
maxillary posterior teeth, facets are cut to allow 2. Forsus Fatigue Resistant Device (3M Unitek Ortho
occlusal, distal, and buccal movement of these dontic Products, Monrovia, California)consists of
teeth. On the lingual aspect of the mandibular pos bypass rod, push rod, ball pin, and stainless steel
terior teeth, facets allow occlusal and mesial move spring module (force module) for each side. This
ment. In addition to their effects on the growth of interarch force delivery system has been shown to be
the mandible, these appliances can tip anterior efficient in treating class II malocclusions with
teeth and control eruption of teeth in the vertical minimal compliance and breakage problems. It deliv
dimension. ers forward, downward force to the anterior man
c. Bionatorthis removable appliance is less bulky dibular arch and backward, upward force to the
than the activator. It consists of lingual, horseshoe- posterior maxillary arch.
shaped acrylic with a wire in the palatal area. D. Alignersclear, removable aligners, such as Invisalign
Facets are introduced into the acrylic to guide the (Align Technology, San Jose, California), can be used to
maxillary and mandibular posterior teeth and hold align teeth. A series of trays are manufactured accord
the mandible forward in a postured relationship. A ing to a prescription developed by the provider to be
labial bow is present anterior to the maxillary inci worn by the patient. Additional attachments are usually
sors, extending distally, to eliminate the pressure required to aid in specific tooth movements and for
from the buccal musculature. aligner retention. Control of tooth movement is not as
d. Twin block appliancethis removable or cemented precise as with fixed appliances. Patient cooperation is
appliance has a two-part design. The interaction required for wearing the trays full-time.
E. Appliances to correct posterior crossbitesmaxillary the maxillary dental arch and for correcting rotated
or palatal expansion appliances are used to correct molars. Because of the tendency to cause buccal
transverse discrepancies by skeletal expansion of the tipping of teeth, they are suggested for use in cases
maxilla or by dental expansion. If expansion is carried where only a small amount of expansion is needed or
out at a rate of about 0.5mm/day, it is called rapid in young children for skeletal expansion before the
palatal expansion/rapid maxillary expansion. Slow sutures are well developed.
expansion is carried out at a much slower rate of 5. Transpalatal archfor dental movement, this appli
1mm/week. ance consists of heavy wire that extends from one
1. Hyrax appliance (banded type)for skeletal expan maxillary first molar along the contour of the palate
sion, this is the most commonly used type of rapid to the maxillary first molar on the opposite side. The
palatal expansion/rapid maxillary expansion appli arch is adapted to the contour of the palate approxi
ance. It consists of a metal framework with an expan mately 2 to 3mm away from the tissue. This appli
sion screw. Bands are cemented on the maxillary first ance is very versatile because it may be used for
premolars and molars that are connected to the expansion or constriction of the intermolar width,
expansion screw by rigid wires. The screw is activated for producing root movement of the first molars,
by at least 0.25mm (one quarter turn) daily and may for derotation of these teeth, and for anchorage
produce force levels of 100 N. The maxillary arch reinforcement.
width is increased by opening the midpalatal suture. F. Appliances used in the mixed dentition.
Expansion is usually continued until the lingual 1. Nance applianceused as a space maintainer or for
cusps of the maxillary posterior teeth come into anchorage purposes. It has a heavy wire soldered to
contact with the lingual inclines of the buccal cusps the palatal aspect of the maxillary first permanent
of the mandibular posterior teeth. A diastema usually molars and connected to an acrylic button located in
appears between the central incisors as the midpala the most superior and anterior part of the palatal
tal suture separates. In a few weeks, this space closes vault.
spontaneously as a result of the pull of the supra 2. Lower lingual archmade of heavy orthodontic wire
crestal fibers. When active expansion is completed, adapted to the lingual aspect of the mandibular inci
retention for 3 to 6 months is recommended with the sors. It may be fixed or removable. Two U loops in
appliance in place. The result is a combination of the wire mesial to the first molars make it possible to
skeletal and dental expansion. However, it is widely adjust this appliance. The lingual arch may be used
believed that the skeletal component is more signifi for anchorage reinforcement, as a holding arch for
cant than the dental component (minimal dental space maintenance, for expansion, and for increasing
tipping). dental arch length.
2. Haas appliancefor skeletal expansion, this appli 3. Lip bumperconsists of a heavy wire inserted into
ance consists of bands that are cemented on maxil the buccal tubes on the mandibular first permanent
lary first premolars and first molars. Two acrylic pads molars. The anterior portion lies about 2 to 3mm
with a midline jackscrew are connected to the rest of away from the alveolar process and the mandibular
the appliance. The acrylic pads are in contact with the incisors and usually carries a plastic or acrylic pad. It
palatal mucosa. It is believed that contact with the is used to control or increase the mandibular dental
palate allows forces from the appliance to be applied arch length, to upright mesially or lingually tipped
directly to the underlying hard and soft tissues, mini mandibular molars, and to prevent the interposition
mizing the amount of dental tipping and maximizing of the lower lip between the maxillary and mandibu
the skeletal effect. However, difficulty in maintaining lar incisors. By removing the pressure of the buccal
hygiene and possible inflammation of the palate are musculature on the teeth, it allows lateral and ante
considered disadvantages by some clinicians. rior dentoalveolar development. By transmitting the
3. Hawley-type removable appliance with a jackscrew force from the lip to the mandibular first molars, it
for skeletal or dental expansion, this appliance may causes distal movement and tipping of the mandibu
be used to correct mild posterior crossbites in chil lar first molars.
dren and young adolescents. Compliance and diffi G. Appliances used to control vertical incisor position.
culty retaining the appliance in the mouth are 1. Intrusion archthis is an archwire used for deep bite
potential disadvantages. correction in which extrusion at the molars and
4. Quad-helix and W-archgenerally for dental expan intrusion at the incisors takes place. This archwire is
sion, these appliances consist of heavy stainless steel activated for incisor intrusion by placing tip-back
wire with four (quad-helix) or three (W-arch) helices bends mesial to the molar tubes.
that are incorporated to increase the range and flex 2. Extrusion archthis is an archwire used for open bite
ibility. They may be fixed or removable. They may be correction in which intrusion at the molars and
used for symmetrical or asymmetrical expansion of extrusion at the incisors takes place.
H. Elasticselastomeric bands are used to produce forces 1. Space maintenance (in cases where primary teeth
for tooth movement. There are different types of elastics have been lost and space is otherwise adequate).
based on their purpose, location, and orientation. a. Band and loop.
1. Class I elastics (intramaxillary elastics)used for b. Distal shoe (before eruption of a permanent
traction between teeth and groups of teeth within the molar).
same arch. During canine retraction, they may be c. Lingual arch.
used to facilitate sliding mechanics. d. Nance appliance (maxillary arch).
2. Class II elastics (intermaxillary elastics)worn from 2. Space regaining (localized space loss)indicated
a tooth located in the anterior part of the maxilla when space loss is minor (<3mm).
(usually from the maxillary permanent canine) to a a. Removable appliance with finger springs to tip
tooth located in the posterior part of the mandible teeth distally.
(usually to the mandibular permanent first molar). b. Headgear (for the maxillary arch).
They are used to correct class II malocclusion, c. Activated lingual arch (for the mandibular arch).
to reduce overbite by extruding the molar, to d. Lip bumper (for the mandibular arch).
retract anterior maxillary teeth, and to minimize e. Limited fixed appliances.
anchorage loss in the maxilla during maxillary (1) Followed by placement of a space maintainer
incisor retraction. after space is regained.
3. Class III elastics (intermaxillary elastics)worn from 3. Moderate crowding (<4mm).
a tooth located in the posterior part of the maxilla a. Arch expansion (this is a controversial topic).
(usually from the maxillary permanent first molar) b. Extraction of primary canines.
to a tooth located in the anterior part of the mandible (1) Borrows space until permanent teeth erupt.
(usually to the mandibular permanent canine). They (2) Lingual arch necessary if mandibular primary
are used to aid in protraction of the maxillary poste canines are extracted because the permanent
rior teeth, to improve the overjet in an edge-to-edge incisors will upright lingually and space will
or anterior crossbite relationship, and to make use of be lost.
intermaxillary anchorage during mandibular incisor c. Flaring of incisors.
retraction. (1) Fixed appliances.
4. Crossbite elasticsthese are worn from the palatal of (2) Removable appliances.
one or more maxillary teeth to the buccal of one or 4. Severe crowding (>4mm).
more teeth in the mandible to help correct crossbites. a. Arch expansion (this is a controversial topic).
In addition to the desired forces, they cause extrusion b. Serial extraction.
of the teeth and should be used with caution in (1) Timed extraction of primary and ultimately
patients with an open bite tendency and a long lower permanent teeth.
anterior facial height. (2) Usually reserved for large space discrepancies
5. Anterior diagonal elastics (midline elastics)these (>10mm per arch).
elastics are run from one side of the maxillary (3) Sequence of extractions.
teeth to the other side of the mandibular teeth cross (a) Extraction of primary incisors, if necessary.
ing the midline. They are used in the correction (b) Extraction of primary canines to allow per
of noncoinciding maxillary and mandibular dental manent incisors to erupt and align.
midlines. (c) Extraction of primary first molars to
encourage eruption of the permanent first
1.10 Early Treatment premolar (ideally, before the permanent
Early treatment is designed to alleviate or prevent moder canine erupts).
ately severe orthodontic problems or potential problems (d) Extraction of permanent first premolars to
before the permanent dentition is completely erupted. allow the permanent canine to erupt and
Often, further comprehensive treatment is indicated when align.
the permanent dentition has erupted, unless the problem (4) Increased overbite usually results as the inci
is very minor and localized. Setting goals is very important sors tip lingually into any excess space.
in early treatment. The endpoint should be well defined to (5) Comprehensive treatment is almost always
avoid lengthy treatment that extends into the permanent required later to achieve ideal alignment, root
dentition. Retention is needed until the permanent teeth positioning, ideal overbite, and closure of
erupt, and such devices may interfere with eruption or lose excess space.
retention as primary teeth exfoliate. B. Anterior spacing.
A. Crowded and irregular teethcaused by lack of ade 1. Maxillary midline diastema less than 2mm.
quate space for alignment or interferences with normal a. Commonly present and self-correcting.
eruption. b. Ugly duckling stage.
c. Large space may indicate supernumerary tooth or 2. Maxillary lateral incisors.

mesiodens or missing lateral incisors. a. Substituting canine in lateral position is an
d. Treatment may be indicated if there is an esthetic option.
concern or central incisors are inhibiting eruption b. Retaining space for later replacement is an option.
of lateral incisors or canines. c. The best choice may depend on occlusion and
2. Large maxillary midline diastema greater than 2mm. esthetic demands.
a. Not likely to close spontaneously. E. Occlusal relationship problems.
b. Fixed appliances may be indicated. 1. Posterior crossbites.
c. Frenectomy after treatment if space reopens per a. Unilateral crossbites are usually due to a mandibu
sistently or bunching of tissue is unresolved after lar shift.
space is closed. b. If causing a shift, treatment should be initiated.
3. Generalized spacing. (1) Equilibration to eliminate shift.
a. Postpone treatment unless there is an esthetic (2) Maxillary expansion using fixed or removable
complaint. appliance.
b. If spacing of anterior teeth is accompanied by pro 2. Anterior crossbites.
trusion, fixed appliances are usually required to a. Differentiate skeletal from dental causes.
achieve bodily movement. b. Skeletal may be due to deficient maxillary or exces
C. Eruption problems. sive mandibular growth.
1. Overretained primary teeth. c. Dental is usually due to inadequate space. After
a. Remove primary tooth to encourage eruption of space is created, the teeth can be moved forward
permanent tooth. with fixed or removable appliances with or without
2. Ankylosed primary teeth. extraction of adjacent primary teeth.
a. Usually resorb on their own. 3. Maxillary dental protrusion with spacing.
b. Remove if they cause a delay in permanent tooth a. May be due to skeletal discrepancy.
eruption or if permanent tooth eruption path is b. May be due to finger or thumb sucking.
deflected. c. Treatment is indicated if esthetically objectionable
c. If the successor is missing, an ankylosed primary or in danger of trauma.
tooth should be removed to decrease chances of a d. A removable appliance can be used to upright
vertical alveolar defect. teeth.
3. Ectopic eruptioneruption of a tooth into an unex 4. Deep bites.
pected location or into an adjacent tooth. a. Biteplates can be used to open the bite posteriorly
a. Lateral incisors. and allow eruption of posterior teeth in patients
(1) May cause loss of adjacent primary canine. with short lower face heights.
(2) Usually indicates lack of sufficient space. b. In patients requiring overbite correction by intru
(3) If unilateral, may cause midline shift. sion, this should be deferred until later compre
(4) Treat by extracting primary canines or space hensive treatment because of inability to retain in
regaining. the mixed dentition.
b. Maxillary first molars. 5. Oral habits and open bites.
(1) May erupt into second primary molar. a. Pacifiers and finger sucking may cause increased
(2) Upright erupting molar. overjet, decreased overbite, and posterior
c. Maxillary canines. crossbite.
(1) May lead to canine impaction. b. If the habit stops before eruption of permanent
(2) May resorb adjacent lateral incisor. incisors, most of the negative changes resolve
(3) Extraction of primary canine is indicated. spontaneously.
D. Missing teethmost commonly missing permanent c. Most important is convincing a child that he or
teeth (excluding third molars). she wants to stop; otherwise, any treatment is
1. Mandibular second premolars. likely to fail.
a. Maintaining primary second molars may be an d. Any reminder is helpfulbandage on finger, habit
option. appliance.
b. Some reduction in width of the primary second e. Reward system.
molars may be necessary to attain good posterior f. If an appliance is used, it should remain in place
interdigitation. for about 6 months after the habit appears to have
c. Early extraction of primary second molars (at age ceased.
7 to 9) may be attempted to encourage closure g. Open bites that persist after the habit has ceased
of the space, but this is unpredictable, and later are likely to have a skeletal component and may
orthodontic treatment is likely to be needed. need more complex treatment.
2. Functional appliances allow eruption of upper and

1.11 Growth Modification
lower posterior teeth.
Treatment of Skeletal Problems C. Treatment of vertical excess (long face).
in Preadolescents 1. High-pull headgear to the molars inhibits eruption
Timing of Growth Modification of maxillary posterior teeth.
Successful growth modification can occur only during 2. Functional appliance with bite blocks to block poste
periods of growth. Early modification often requires rior eruption.
retreatment because unfavorable growth continues. Waiting D. Treatment of maxillary deficiency.
until the permanent dentition erupts may be too late to 1. Transverse deficiency can be treated with
modify growth, especially in girls (because they stop expansion.
growing earlier than boys). 2. Anterior-posterior deficiency (class III) can be
A. Treatment of mandibular deficiency (class II). treated with a facemask (protraction headgear,
1. Theoretically, headgear restrains maxillary growth reverse-pull headgear) (Figure 5-20).
forward, whereas functional appliances stimulate a. Anterior force is placed on the maxilla.
mandibular growth, but the distinction is less clear b. Encourages growth at the maxillary sutures.
in practice. c. Often used after rapid expansion to disrupt the
2. Timing should be when the mandible is growing sutures.
actively, before peak adolescent growth. d. Ideal timing is earlier (8- to 9-year-olds) to encour
3. Functional appliances. age maxillary growth (because the maxilla grows
a. Often accelerate or redirect mandibular growth, earlier than the mandible).
but a long-term increase in size does not seem to E. Treatment of mandibular excess.
occur. 1. Chin cup or chin cap therapy to restrain mandibular
b. Also put a restraining force on maxillary growth. growth.
c. Move the mandibular teeth anteriorly and the a. Generally redirects mandibular growth downward
maxillary teeth posteriorly. rather than deterring growth.
4. Headgear. b. Contraindicated in long-face individuals.
a. Puts a restraining force on maxillary growth and F. Treatment of facial asymmetry.
allows the mandible to grow normally to catch up. 1. Facial asymmetry may be due to a congenital anomaly
b. Puts posterior forces only on maxillary teeth, or an early condylar fracture.
usually the first molars. 2. Asymmetrical functional appliances may be
B. Treatment of vertical deficiency (short face). helpful.
1. Cervical headgear has an extrusive force on the max 3. Early surgery may be indicated when asymmetry is
illary molar, which erupts. progressively worsening.
Figure 5-20 Delaire-type face-

mask. A, The facemask contacts the
forehead and chin for anchorage and
should be adjusted several millimeters
away from the other soft tissues.
B, Adjustment of the wire framework
produces desired fit and direction of
pull on the maxilla (usually down
ward for increased vertical facial
development and patient comfort)
when the elastics are placed from the
mask to the splint. (From Proffit WR,
Fields HW, Sarver DM: Contemporary
Orthodontics, ed 5. St. Louis, Mosby,
2013.)
A B
a. Extrusion of posterior teeth may be favorable for

1.12 Comprehensive Treatment patients with short lower face heights but is con
A complete set of fixed appliances can be used when all traindicated in patients with long faces.
permanent teeth have erupted. b. Intrusion of anterior teeth, maxillary or mandibu
A. Extraction versus nonextraction decisions. lar depending on facial esthetics.
1. The need for extractions (usually first premolars) is c. Flaring of anterior teeth, especially in nonextrac
usually dictated by the amount of crowding present. tion treatment, may also decrease overbite.
When space is needed, the arches can be expanded 3. Correction of molar relationship.
and anterior teeth flared forward but only to a limited a. Growth modification.
degree because teeth require bony support. Expand b. Interarch elastics.
ing too much may be unstable and leave teeth in a c. Distal movement of upper molars.
periodontally compromised position. The alternative 4. Space closure.
is creating space by extracting teeth. a. If molars have been moved to achieve a class I
2. Another indication for extraction may be to camou relationship or if teeth have been extracted, space
flage a class II or class III malocclusion by extracting closure is necessary.
premolars in one arch only to achieve class I canines b. Depending on the amount of space that must be
and a normal overjet and overbite. Upper premolars closed in each arch, the anchorage requirements
would be extracted to camouflage a class II; lower may vary in each arch.
premolars would be extracted to camouflage a c. Interarch elastics, extraoral force (headgear), or
class III. use of temporary anchorage devices may help in
3. There may be esthetic considerations to remove or maintaining anchorage during space closure.
not remove teeth because anterior tooth position 5. Root correction.
affects lip fullness. a. Especially when spaces have been closed, the teeth
4. Removing premolars and uprighting incisors gener may have tipped into the extraction space, and
ally increases overbite, whereas aligning moderately roots need to be paralleled to improve stability and
crowded teeth without extractions flares incisors and periodontal health.
decreases overbite. b. The incisors may have uprighted during retrac
5. Often the decision is not clear-cut, and various indi tion, and the roots may need to be torqued
cations and contraindications should be considered. lingually.
6. Indications for extraction. 6. Detailing and finishing.
a. Large amount of dental crowding (arch length a. Intraarchfinal tooth positioning by rebracketing
deficiency). misbracketed teeth or by small bends in the
b. Minimal overbite or open bite present. wire to eliminate small discrepancies in all three
c. Flared incisors. dimensions: rotations, vertical relationships, and
d. Full (procumbent or protrusive) lips. torque.
e. Acute nasolabial angle. b. Interarchsettling of the occlusion into a solid
f. Anterior recession or minimal or thin attached relationship can be accomplished using light wires
gingiva. or vertical elastics or by having the patient wear a
g. Camouflage of class II or class III relationship. positioner (a rubber or plastic appliance made with
h. Other missing or severely compromised teeth. teeth reset into ideal position).
i. Asymmetrical occlusion (unilateral class II or 7. Special considerations.
class III). a. Tooth size discrepancies (Bolton discrepancy)
7. Indications to avoid extraction. smaller or larger teeth in one arch than the
a. Minimal crowding or spacing present. other can affect intercuspation and overjet present.
b. Deep overbite. Large teeth (most often mandibular second pre
c. Upright incisors. molars) may require interproximal reduction
d. Flat (recessive) lips. (IPR) to reduce width. Small teeth (most often
e. Obtuse nasolabial angle. maxillary lateral incisors) may require buildups to
B. Stages of comprehensive treatment. fill space, or the discrepancy can be masked by IPR
1. Alignmentgenerally with light, flexible wires at of lower incisors. Small discrepancies may be
first, followed by slightly stiffer wires. masked by tipping or torquing teeth to take up
2. Overbite correction (leveling)achieving overbite more space.
correction is necessary before molar correction and b. Unfavorable growthpatients with anticipated
space closure because a deep overbite would prevent unfavorable growth patterns, class II or class III,
retraction (posterior movement) of the incisors to a may be continued on headgear at night (e.g., to
normal overjet. control further growth).
c. Overtreatmentanticipated rebound of anterior- B. Removable retainers.

posterior discrepancies (class II or III), crossbites, 1. Hawley retainer.
or rotations may be overcorrected in treatment in a. Incorporates clasps for retention and an outer bow
anticipation that they will rebound afterward to with adjustment loops.
some degree. b. Acrylic on the palate can act as a potential biteplate
d. Supracrestal fiberotomysupracrestal gingival to control overbite.
fibers exert some elastic force that may move teeth c. The outer bow retains incisor position and
after treatment, especially rotations. Cutting these rotations.
fibers has been shown to reduce significantly, but d. Clasps or wires that cross the occlusion may wedge
not fully eliminate, this tendency. space open or prevent closure of spaces that remain
or develop.
1.13 Retention 2. Wraparound retainer.
A. Purpose of retention. a. Similar to a Hawley retainer but without wires that
1. Allow time for reorganization of the gingival and cross the occlusion.
periodontal fibers. 3. Positioner.
a. Significant reorganization of the PDL occurs in 3 a. May be used as a finishing device and then as a
to 4 months, and full-time retention is recom retainer.
mended for that time. b. Bulky and may not be tolerated well.
b. Part-time retention after 4 months to about 12 c. Maintains interarch and intraarch relationships.
months is recommended to allow more complete C. Fixed retainers.
reorganization of the PDL. Long-term retention is 1. Bonded flexible lingual wires attached to individual
often recommended. teeth or bonded rigid wires usually bonded to two
2. Prevent soft tissue pressures from altering posttreat teeth, especially between lower canines.
ment tooth position. 2. Maintain lower incisor position.
3. Hold the new position of teeth until growth is 3. Hold diastema closed.
completed. 4. Maintain space for a pontic or implant.
a. Retention after class II correctionrelapse may 5. Keep extraction spaces closed.
occur, especially in patients who have worn class D. Active retainers.
II elastics in treatment. There may also be unfavor 1. For realignment of irregular teeth.
able growth, and patients can wear a headgear or 2. Irregular teeth are reset on a model, and the retainer
functional appliance on a limited basis. is made to the new setup.
b. Retention after class III treatmentrelapse may 3. The retainer needs to have some flexibility to fit over
occur, especially because of continued mandibular the irregular teeth.
growth. 4. IPR may be required to allow space for teeth to rotate.
c. Retention after overbite correctiona retainer with
acrylic lingual to the upper incisors usually blocks 1.14 Adult Treatment and
deepening of the bite. Interdisciplinary Treatment
d. Retention after open bite correctioncontinuation Adult orthodontic treatment for the most part is identical
of a finger-sucking habit (or a tongue thrust, to treatment of children with some differences.
although this is controversial) may intrude incisors A. Psychological considerationsusually self-motivated
or cause separation of posterior teeth, allowing compared with children, whose motivation is often
them to erupt. In the absence of an obvious cause, their parents. Adults are generally more compliant
open bite relapse usually occurs because of poste and perform better oral hygiene. Appearance of the
rior tooth eruption rather than intrusion of appliances may be a concern, and adults are more
incisors. likely to request ceramic, lingual, or invisible braces
e. Retention after lower incisor alignmentwith or (aligners).
without growth, pressure from the lip may cause 1. Periodontal improvementmotivation may include a
crowding of the lower incisors. There is little evi need to improve tooth positions for periodontal
dence that pressure from third molars causes concerns.
incisor crowding. Late mandibular growth is a pos 2. Restorativemotivation may be to achieve a desired
sible contributor to incisor crowding, even in restoration or replacement of missing teeth.
patients who did not have orthodontic treatment. 3. TMJpatients may be referred for orthodontic treat
f. Permanent retention may be needed if the teeth ment to improve TMJ dysfunction. This is a highly
have been placed in inherently unstable positions. controversial topic; orthodontic treatment is not
Long-term retention is often recommended considered a primary method for treating TMJ
regardless. problems.
B. Periodontal aspects of adult treatment. b. Mandibular surgery.

1. Any periodontal conditions should be stabilized (1) Advancement (to correct a class II)bilateral
before beginning orthodontic treatment. sagittal split osteotomy (BSSO) of the ramus is
2. Good oral hygiene must be maintained because gin the most preferred procedure. Paresthesia is
givitis in adults may progress to periodontal disease; a common side effect, usually disappearing
this is rarely the case in children. in 2 to 6 months, but 20% to 25% of patients
3. Level and condition of attached gingiva must be continue to have long-term alterations in
monitored to prevent recession. sensation.
4. Patients with a history of periodontal disease must be (2) Setback (to correct a class III)BSSO can also
monitored and be on a frequent maintenance sched be used to move the mandible posteriorly.
ule (every 2 to 4 months). Airway reduction leading to possible sleep
5. Steel ligatures retain less plaque than elastomeric apnea may limit use of mandibular setback
ligatures. procedures, so class III correction is often done
6. Lower forces can be used on teeth with reduced by advancing the maxilla instead.
support because the PDL area is reduced. 2. Vertical corrections.
7. Closure of old extraction sites may be difficult a. Maxillary surgery.
because of remodeling and narrowing of the alveolar (1) Superior repositioning (to correct an open
bone. bite)Le Fort I is used to move the maxilla
8. Proper sequence for interdisciplinary treatment superiorly, allowing the mandible to autorotate
disease control (caries, periodontal disease); ortho closed to correct an open bite and shorten
dontic tooth movement; definitive treatment the face.
(periodontal bone recontouring, final restorations (2) Inferior repositioning (to correct a deep bite)
such as crowns, bridges, implant restorations). Positioning the maxilla downward would rotate
C. Lack of growth. the mandible open to reduce overbite and
1. Because adults do not have the benefit of mandibu lengthen the face. This is one of the least stable
lar growth during treatment, all interarch correc surgical procedures.
tions must be accomplished dentally or with b. Mandibular surgery.
surgery. (1) Surgical procedures in the mandible to rotate
2. Without growth to supplement dental changes, it closed (to correct an open bite) are not rec
overall treatment may proceed more slowly, although ommended because they cause downward
the tooth movement itself may proceed at the same rotation at the gonial angle and stretch the
rate. muscles of the pterygomandibular sling,
causing instability.
1.15 Combined Surgical and (2) Anterior and downward rotation of the man
Orthodontic Treatment dible (to correct a deep bite) can be accom
A. Indicationssurgery is indicated when a problem is too plished with BSSO for patients with a deep bite
severe for orthodontics alone (Figure 5-21). Growth and short lower face (tripoding).
modification in growing patients may allow some cor 3. Transverse correctionsfor correction of crossbites,
rections that cannot be achieved in adults. Other con the maxilla can be expanded or constricted during a
siderations include functional limitations and esthetic Le Fort I procedure. Changes in mandibular width
goals, which may be indications for surgery even if are more difficult.
orthodontic correction alone is possible. a. Maxillary expansioncan be accomplished surgi
B. Surgical proceduresany one or a combination of max cally with positioning of the lateral segments in
illary and mandibular procedures can be performed to ideal position or as a surgically assisted rapid
correct a malocclusion and achieve good skeletal func expansion where surgical cuts are made to free up
tional relationships with improved esthetics. the lateral segments. Expansion proceeds with a
1. Anterior-posterior corrections. jackscrew device, as in adolescents.
a. Maxillary surgery. b. Maxillary constrictioncan be accomplished sur
(1) Advancement (to correct a class III)Le Fort I gically with bone removed to allow for constriction
downfracture of the maxilla mobilizes it so that of the lateral segments.
it may be advanced. 4. Genioplastythe chin can be augmented to improve
(2) Setback (to correct a class II)it is difficult or esthetic outcome using an osteotomy or by adding
impossible to move the entire maxilla posteri implant material. The sliding osteotomy is the pre
orly; if desired, a premolar is usually extracted, ferred method and can be used to move the chin in
and the anterior segment is moved posteriorly all three dimensions. Reduction is generally the least
(segmental osteotomy). predictable for esthetic changes.
Figure 5-21 With the ideal position of the upper and lower incisors shown by the origin of the x-axis and y-axis, the
envelope of discrepancy shows the amount of change that could be produced by orthodontic tooth movement alone
(the inner envelope of each diagram), orthodontic tooth movement combined with growth modification (the middle
envelope), and orthognathic surgery (the outer envelope). The possibilities for each treatment are not symmetrical with regard
to the planes of space. There is more potential to retract than procline teeth and more potential for extrusion than intrusion. Because
growth of the maxilla cannot be modified independently of the mandible, the growth modification envelope for the two jaws is the
same. Surgery to move the lower jaw back has more potential than surgery to advance it. (From Proffit WR, Fields HW, Sarver DM:
Contemporary Orthodontics, ed 5. St. Louis, Mosby, 2013.)
C. Timing of surgery. Surgical-Orthodontic Treatment:

1. Surgery is rarely performed before the adolescent A Hierarchy of Stability
growth spurt except in cases with significant psycho
MORE Maxilla up VERY
logical impact of a facial deformity. In those cases, STABLE
Mandible forward*
the expectation is that the procedure may need to be Chin, any direction
redone later.
2. In cases with growth excess, such as a class III with Maxilla forward
excessive mandibular growth, surgery should be Maxilla, asymmetry STABLE
delayed until growth is complete. Otherwise, the STABLE
PREDICTABLE Mx up 1 Mn forward
mandible may continue to grow, and the class III STABLE
Mx forward 1 Mn back Rigid fix only
relationship will return. Mandible, asymmetry
3. In cases with growth deficiency, such as a class II
with a small mandible, surgery can be considered Mandible back
earlier. Maxilla down
4. Exceptions where early surgery is indicated include LESS Maxilla wider PROBLEMATIC
cases with congenital growth deficiencies or cases * Short or normal face height only
where growth is restricted because of mandibular
Figure 5-22 Hierarchy of stability. In this context, very
ankylosis. In these cases, correction is required stable means a greater than 90% chance of no significant post
because progressive worsening of the growth defi surgical change; stable means a greater than 80% chance of no
ciency occurs without it. change, and major relapse is quite unlikely; problematic means
D. Sequencing of combined surgical-orthodontic some degree of relapse is more likely, and major relapse is pos
treatment. sible. (From Proffit WR, Fields HW, Sarver DM: Contemporary
1. Pretreatment considerationsdisease control and, Orthodontics, ed 5. St. Louis, Mosby, 2013.)
especially, good gingival health and adequate attach
ment should be established before treatment begins.
Unerupted or impacted third molars usually need to E. Maximizing skeletal movements.
be removed well in advance (6 to 9 months) of 1. In surgery to correct a class II occlusion, extraction
surgery to allow good bone healing in the area. of mandibular premolars with closure of that space
2. Orthodontics is performed to align the teeth within would increase the overjet presurgically and allow a
each arch and remove compensations in the denti greater surgical movement of the jaws to correct the
tion that may mask the underlying skeletal discrep class II. This would be recommended for a patient
ancy. For example, in class III patients, the lower needing maximal esthetic change, usually to bring
incisors are often upright and the upper incisors are the lower jaw forward.
flared, giving the appearance of a minimal anterior 2. In surgery to correct a class III occlusion, if maxi
crossbite. By flaring the lower incisors and uprighting mizing skeletal movement were the goal to achieve
the upper incisors, the crossbite is made more severe, desired esthetics, upper premolars might be ex
allowing a more significant movement of the jaws to tracted to make the anterior crossbite more severe
correct the discrepancy. Before surgery, models are presurgically.
taken to ensure that the occlusion will fit when F. Stability of orthognathic surgical procedures
surgery is performed. (Figure 5-22).
3. Surgery is performed with the orthodontic appli
ances on. Rigid wires to stabilize the teeth are present
in the appliances. The jaws are repositioned accord
ing to the planned correction and are held in place
2.0 Pediatric Dentistry
using rigid internal fixation or (rarely) intermaxillary Mark Taylor
wire fixation. A soft diet is required for 6 to 8 weeks Because pediatric dentistry is multidisciplinary in nature,
after surgery. this review encompasses a wide range of dentistry. However,
4. The patient returns to continue orthodontics pediatric dentistry is not the same as dentistry for adults.
usually for about 6 months to detail the occlusion and Children present the practitioner with a set of challenges,
finish. treatment decisions, and treatment that can be quite differ
5. Surgery firstthis is a concept that encourages ent from that of adults.
surgery earlier in the combined orthodontic-surgical Given that pediatric dentistry involves all disciplines, it
treatment sequence to correct skeletal relationships is impossible in a format of this kind to cover all topics. The
early and take advantage of the rapid tooth move intent of this section is to prepare the candidate for the
ment (rapid acceleratory phenomenon) that occurs National Board Dental Examination; it is not meant to be
immediately after surgical intervention. an all-inclusive review of pediatric dentistry. For more
in-depth review, McDonald and Averys Dentistry for Chil-

dren and Adolescents, ed 9, by Dean, Avery, and McDonald,
and Pediatric Dentistry, Infancy Through Adolescence, ed 5,
by Casamassimo, Fields, McTigue, and Nowak, are excel
lent sources (see References).
Outline of Review
2.1 Development and Developmental Disturbances of the Teeth
2.2 Management of Child Behavior in the Dental Setting
2.3 Local Anesthesia and Nitrous Oxide Sedation for Children
2.4 Restorative Dentistry for Children
2.5 Pulp Treatment for Primary Teeth
2.6 Space Management in the Developing Dentition
2.7 Periodontal Problems in Children
2.8 Dental Trauma in Children
2.9 Miscellaneous Topics in Pediatric Dentistry
2.1 Development and Developmental

Disturbances of the Teeth
Development of the Tooth
A. Initiation (bud stage).
1. Week 6 of embryonic life.
2. All primary teeth and permanent molars arise from
the dental lamina.
3. Permanent incisors, canines, and premolars arise Figure 5-23 Supernumerary tooth obstructing eruption.
from the primary predecessor.
4. Failure of initiation results in congenitally missing
teeth.
5. Excessive budding results in supernumerary teeth
(Figure 5-23).
B. Proliferation (cap stage).
1. Peripheral cells of the cap form the inner and outer
enamel epithelium.
2. Failure in proliferation results in congenitally missing
teeth.
3. Excessive proliferation results in a cyst, odontoma, or
supernumerary tooth, depending on amount of cell
differentiation.
Figure 5-24 Peg maxillary lateral incisors.
C. Histodifferentiation and morphodifferentiation (bell
stage).
1. Cells of dental papilla differentiate into a primary incisor may disrupt enamel apposition and
odontoblasts. result in an area of enamel hypoplasia.
2. Cells of the inner enamel epithelium differentiate E. Calcification.
into ameloblasts. 1. Enamel is composed of 96% inorganic material and
3. Failure in histodifferentiation results in structural 4% organic material and water.
abnormalities of the enamel and dentin (amelogen 2. Calcification begins at cusp tips and incisal edges and
esis imperfecta, dentinogenesis imperfecta). proceeds cervically.
4. Failure in morphodifferentiation results in size and 3. Localized infection, trauma, and excessive systemic
shape abnormalities, such as peg lateral incisors and fluoride ingestion may cause hypocalcification.
macrodontia (Figure 5-24).
D. Apposition. Calcification and Eruption of the Dentition
1. Ameloblasts and odontoblasts deposit a layerlike A. Table 5-2 shows the approximate time calcification
matrix. begins for primary teeth. The sequence of calcification
2. Disturbances in apposition result in incomplete of primary teeth is A-D-B-C-E, and all primary teeth
tissue formation. For example, an intrusive injury to begin calcification in utero.
Table 5-2 Table 5-4

Approximate Calcification Start Times for Calcification Start Times for
Primary Teeth Permanent Teeth
TOOTH CALCIFICATION MAXILLA MANDIBLE
Central incisor (A) 14 weeks in utero First molar Birth Birth
First molar (D) 15 weeks in utero Central incisor 3-4 months 3-4 months
Lateral incisor (B) 16 weeks in utero Lateral incisor 10-12 months 3-4 months
Canine (C) 17 weeks in utero Canine 4-5 months 4-5 months
Second molar (E) 18 weeks in utero First premolar 1.5 years 1.75 years
Second premolar 2 years 2.25 years
Second molar 2.5 years 2.75 years
Table 5-3
Eruption Times for Primary Teeth
Table 5-5
MAXILLA MANDIBLE
Approximate Calcification Start Times for
Central incisor 10 months 8 months Permanent Teeth
Lateral incisor 11 months 13 months
TIME TEETH THAT BEGIN TO CALCIFY
Canine 19 months 20 months
Birth First molars
First premolar 16 months 16 months
6 months Anterior teeth except maxillary laterals
Second premolar 29 months 27 months
12 months Maxillary laterals
18 months First premolars
24 months Second premolars
B. Eruption of primary teeth. 30 months Second molars
1. Table 5-3 shows the approximate eruption times for
primary teeth.
2. Sequence is A-B-D-C-E.
3. Teeth B, C, and D tend to erupt earlier in the maxilla. Table 5-6
4. A 6-month variation in time of eruption is consid Eruption Times (Years) of Permanent Teeth
ered normal.
TOOTH MAXILLA MANDIBLE
C. Calcification of permanent teeth.
1. It is important to know the calcification times of per 1 7-8 6-7
manent teeth because if the practitioner sees a pattern 2 8-9 7-8
of hypoplasia or hypocalcification of the permanent 3 11-12 9-10
teeth, the approximate timing of the cause can be 4 10-11 10-12
determined. This information can aid the dentist in 5 10-12 11-12
counseling parents in regard to anticipated enamel
6 6-7 6-7
defects.
2. Table 5-4 shows the average times at which calcifica 7 12-13 11-13
tion begins for permanent teeth. 8 17-21 17-21
3. Because this table can be difficult to memorize, it is
helpful to remember that a different group of teeth
begin calcification every 6 months; this is only an enamel hypoplasia secondary to a systemic
approximation but is easier to remember (Table 5-5). disturbance.
4. Eruption of permanent teeth. (2) It takes approximately 10 years from start of
a. Average eruption times are listed in Table 5-6. calcification to root completion except for
b. Eruption begins when the crown has completed canines (13 years).
calcification. (3) Teeth typically erupt through the bone with
c. Average numbers to know for eruption of teeth. two thirds root formation.
(1) Typically, it takes 4 to 5 years for most crowns (4) Teeth typically erupt through the gingiva with
to complete formation except for first molars three fourths root formation.
(3 years) and cuspids (6 years). This knowledge (5) Interval between crown calcification and full
is important in determining the timing of interdigitation is about 5 years.
Figure 5-26 Fusion of primary lateral incisor and primary

canine. There are nine discrete tooth entities.
incisor position and then performing restor

Figure 5-25 Rudimentary supernumerary, conical form. ative lateralization of the permanent canines.
Alternatively, the canines may be placed in
their normal position and the lateral incisors
(6) Eruption to root completion is approximately replaced prosthetically.
3 years. B. Anomalies of size.
d. Sequence 6-1-2-4-5-3-7 is most common in the 1. Microdontia and macrodontia.
maxilla. a. Microdontia is seen in ectodermal dysplasia, chon
e. Sequence 6-1-2-3-4-5-7 is most common in the droectodermal dysplasia, hemifacial microsomia,
mandible. and Down syndrome. Another example of micro
dontia is a pegged lateral incisor.
Developmental Disturbances of the Teeth b. Macrodontia is seen in facial hemihypertrophy
A. Anomalies of number. and otodental syndrome.
1. Supernumerary teeth (Figure 5-25). 2. Fusion (Figure 5-26).
a. Male-to-female ratio is 2:1. a. Fusion is the union of two primary or permanent
b. Affect 3% of population. teeth.
c. Most common supernumerary teeth are mesiodens, b. More common in primary teeth.
most of which are palatal. c. Fused teeth have two pulp chambers and two pulp
d. Classified as supplemental (has typical anatomy) or canals.
rudimentary (are conical, tuberculate, or molar- d. Almost always in anterior teeth.
shaped). e. In addition to examining the root structure, the
e. Supernumerary teeth may block normal eruption key to determining fusion is to count erupted
of permanent teeth. In such cases, consideration teeth. Because fusion ordinarily occurs between
should be given to early removal to prevent impac two teeth, there is one less discrete tooth entity
tion of the permanent teeth. than normal. In other words, in a primary denti
2. Congenital absence (hypodontia). tion, children have 10 discrete tooth entities per
a. Incidence 1.5% to 10%, excluding third molars. arch; in a patient with fusion, there are only 9 dis
b. Most common congenitally missing tooth is the crete tooth entities.
mandibular second premolar, followed by the 3. Gemination (Figure 5-27).
lateral incisor, followed by the maxillary second a. Gemination is the division of a single tooth bud,
premolar. resulting in a bifid crown.
c. Treatment options with congenital absence. b. More common in primary teeth.
(1) Congenital absence of premolar is commonly c. Geminated teeth have a single pulp chamber.
treated orthodontically if the patient would (1) Because gemination occurs on a single tooth,
have normally required extraction treatment. there is the normal complement of tooth
In these cases, all spaces are closed. If the masses.
patient has excellent occlusion, normal over C. Anomalies of shape.
bite and overjet, and minimal or no crowding, 1. Dens evaginatus.
the congenital absence may be treated a. An extra cusp.
prosthetically. b. Called talon cusps in incisors (Figure 5-28).
(2) Congenital absence of lateral incisor may be c. Has enamel, dentin, and pulp; care must be taken
treated by placing the canine in the lateral with any operative procedure.
Figure 5-27 Gemination of a primary mandibular lateral

incisor. This patient has the appropriate number of discrete tooth
entities. There are three other primary incisors and a discrete
primary canine present.
Figure 5-29 Dens in dente in a permanent peg lateral

incisor. Also note the congenitally absent contralateral lateral
incisor.
Figure 5-28 Talon cusp, lateral incisor.
2. Dens invaginatus (dens in dente) (Figure 5-29).

a. Caused by invagination of the inner enamel
epithelium.
b. Has been termed tooth within a tooth. Figure 5-30 Taurodontism in the mandibular first primary
c. Most common in permanent maxillary lateral molar.
incisors.
d. If enamel and dentin are not formed correctly anterior teeth develop lingual to the primary pre
within the defect, a direct communication from decessor, injuries to the anterior primary teeth may
the oral environment with pulp tissue can occur. also displace or bend the developing permanent
e. Ideal treatment is preventive; a small restoration tooth.
or sealant may be placed to prevent pulpal b. Dilaceration is also a consistent finding in congeni
involvement. tal ichthyosis.
3. Taurodontism (Figure 5-30). D. Anomalies of structure.
a. Characterized by vertically long pulp chambers 1. Enamel hypoplasia.
and short roots. a. Hypoplasia refers to quantity deficiencies of
b. May be clinically significant if pulp therapy is enamel.
required or during the exfoliation process. b. May be due to environmental or genetic factors.
4. Dilaceration. (1) Environmental.
a. A dilacerated, or bent or twisted tooth, usually (a) Systemic diseases, especially fevers, may
occurs as the result of an intrusive or displacement cause disruption in the developmental
injury to a primary incisor. Because permanent process of the tooth.
(b) Fluorosisoccurs with excessive ingested (c) Short, pointed roots.

fluoride. (d) Absent pulp chambers and canals, primary
(c) Nutritional deficiencies, particularly and permanent teeth.
vitamins A, C, and D; calcium; and (e) Multiple periapical radiolucencies, primary
phosphorus. and permanent teeth.
(d) Neurologic defects, such as Sturge-Weber (2) Shields type 2.
syndrome and cerebral palsy. (a) Primary teeth appear similar to dentino
(e) Cleft lip and palate, radiotherapy and che genesis imperfecta.
motherapy, nephrotic syndrome, lead poi (b) Permanent teeth have normal color, pulp
soning, and rubella embryopathy all have stones, thistle tubeshaped pulp chambers
been linked to hypoplasia. with no periapical radiolucencies.
(f) Local infection, trauma. 6. Other conditions affecting dentin.
(2) Geneticamelogenesis imperfecta (see Ame a. Regional odontodysplasia.
logenesis imperfecta further on). b. Vitamin Dresistant rickets.
2. Enamel hypocalcification. c. Hypoparathyroidism.
a. Hypocalcification refers to quality deficiencies of d. Pseudohypoparathyroidism.
enamel.
b. May be due to environmental or genetic factors. 2.2 Management of Child Behavior
(1) Environmental factors are the same as for in the Dental Setting
hypoplasia. A. Classification of behavior.
(2) Genetic amelogenesis imperfecta, hypocalci 1. Cooperative.
fied typenormal thickness of enamel but is a. Children with minimal apprehension and are com
poorly calcified and fractures easily. municative, comprehending, and willing.
3. Amelogenesis imperfecta. b. These children respond well to behavior shaping.
a. Incidence of approximately 1 in 14,000. 2. Lacking cooperative ability.
b. The defect is related to the enamel only and is a. Children who are deficient in comprehension or
dependent on the developmental stage of the communication skills or both.
enamel. b. Examples are very young children (typically <3
c. Normal pulpal and root morphology. years old) and children with certain disabilities.
d. Treatment depends on type and severity. Severe 3. Potentially cooperative.
cases, especially in terms of quality of enamel, a. Children who are capable of appropriate behaviors
require full-coverage restorations. Veneers may be but are disruptive in the dental environment.
appropriate in some hypomaturation and hypo b. Types of potentially cooperative patients.
plastic types. (1) Uncontrolled.
4. Dentinogenesis imperfecta. (a) Typically 3 to 6 years old.
a. Incidence approximately 1 in 8000. (b) Characterized by a tantrum.
b. Occurs during histodifferentiation stage. (2) Defiant.
c. Predentin matrix is defective resulting in amor (a) Can be all ages.
phic, atubular dentin. (b) Characterized by an I dont want to atti
d. Primary and permanent teeth affected. tude in young children.
e. Teeth are reddish brown to gray opalescent color. (c) Characterized by passive resistance in
f. Roots are slender. adolescents.
g. Pulp chambers and canals appear small or absent. (3) Timid.
h. Enamel chips away easily. (a) Typically preschool and younger grade
i. Teeth can become severely abraded. schoolage children.
j. Treatment may include full-coverage crowns to (b) Characterized by shielding behavior and
prevent severe abrasion. Bonded veneers on ante hesitating behaviors. For example, children
rior teeth have proven successful in some cases that with shielding behavior may stand behind
are less severe. a parent in the reception area or may keep
5. Dentin dysplasia. their hands close to their face and mouth.
a. Primary and permanent teeth affected. (c) Timid children may deteriorate into uncon
b. Types. trolled behaviors, especially in the absence
(1) Shields type 1. of proficient management techniques.
(a) Normal crown anatomy. (4) Tense-cooperative.
(b) Color is closer to normal than in dentino (a) Typically older children (at least 7 years
genesis imperfecta. old).
(b) These children want to cooperate with the (2) If procedures prove to be stressful to these
dentist and try to behave in an adult manner children, they may revert to undesirable
but are very nervous. These patients have behaviors.
also been termed white knuckler patients (3) Proper familiarization techniques and behavior-
because they grip the arms of the dental shaping strategies are valuable tools to influ
chair so tightly. ence childrens behaviors positively in this age
(5) Whining. group.
(a) Whining behavior is usually continuous. 2. Maternal anxiety.
(b) Typically there is an absence of tears. a. There is a high correlation between maternal
(c) This behavior is difficult to overcome in one anxiety and a childs negative behavior in the dental
dental visit. office.
B. Frankl behavioral rating scale. b. This effect is greatest on children less than 4 years
1. Common behavioral scale used in pediatric dentistry. of age.
2. Ratings. 3. Past medical history.
a. Rating 1definitely negative refusal of treatment; a. Children who have had positive medical experi
forceful crying, fearfulness, or any other overt evi ences are more likely to have positive dental
dence of extreme negativism. experiences.
b. Rating 2negative reluctance to accept treatment; b. Children who have experienced pain during previ
uncooperativeness; some evidence of negative atti ous medical visits are more likely to exhibit nega
tude but not pronounced (sullen, withdrawn). tive behavior in the dental setting.
c. Rating 3positive acceptance of treatment; cau c. Previous surgery is correlated with negative behav
tious behavior at times; willingness to comply with ior at a first visit.
the dentist, at times with reservation, but patient 4. Patient awareness of problems.
follows the dentists directions cooperatively. a. If a child thinks he or she has a dental problem,
d. Rating 4definitely positive good rapport with the the child is more likely to exhibit negative
dentist; interest in the dental procedures; laughter behavior.
and enjoyment. D. Functional inquiry.
C. Variables influencing childrens behavior in the dental 1. Two goals of a functional inquiry.
environment. a. Learn patient and parent concerns.
1. Age. b. Estimate of cooperative ability.
a. Less than 2 years oldthese children are typically 2. Two methods.
lacking in cooperative ability. a. Written questionnaire.
b. 2 years old. b. Direct interview.
(1) There is a wide variance in ability to commu 3. Functional inquiry sample questions.
nicate in 2-year-olds. a. Reaction to past medical experiences?
(2) The dentist should use communication tech b. Parental anxiety level?
niques such as Tell-Show-Do (TSD) because c. Is the patient worried about the condition of his or
the child may have adequate communication her teeth?
skills and may be cooperative with a normal d. How do you think the patient will react to an
explanatory, friendly approach. examination?
(3) It can be helpful to have the parent present 4. Functional inquiry review of medical historythese
because the 2-year-old may be unable to over are questions on the medical history that can help
come anxiety resulting from separation from the practitioner understand a childs potential
the parent. behavior.
c. 3 to 7 years old. a. Attention-deficit/hyperactivity disorder (ADHD).
(1) Children in this age range are most often coop b. Learning disability.
erative and willing to comply with dental c. Mental health disorder.
procedures. d. Drug or alcohol abuse.
(2) Proper familiarization techniques and behavior- e. Is this the childs first visit to the dentist? Is the
shaping strategies are valuable tools to influ child extremely nervous about dentistry?
ence childrens behaviors positively in this age f. Any difficult visits to a physician or hospital?
group. g. Childs hobbies or sports.
d. 8 years old and older. h. Parent or legal guardian comments.
(1) As children get older, they normally try to i. Review patients medications.
control their apprehensions and anxieties to (1) Gives clues to potential behavior.
the best of their ability. (2) Review adverse reactions; may alter behavior.
E. Behavior management techniques and strategies. and communicate, it is crucial for the prac
1. Goal of treatment strategies. titioner to familiarize them with the various
a. Perform quality dental care for the patient. procedures.
b. Promote a positive patient attitude and confidence 4. Aversive conditioning.
in self in the dental environment. a. Definitiona psychological strategy that uses
2. Strategies before the appointment. some form of negative stimulus with the pur
a. Brochure or discussion with parent. pose of extinguishing or improving negative
b. DVD/video presentation. behavior.
c. Brochures, DVDs, information on the office b. Purpose.
website. (1) Establish better communication.
d. Modeling with siblings or parents. (2) Gain control of behavior.
3. Behavior shaping. (3) Protect the child from injury.
a. Definitiona procedure that slowly develops (4) Eventually make the dental experience a pleas
behavior by reinforcing successive approximations ant one.
to a desired goal. For example, if the goal is to have c. Indications.
a child patient open his or her mouth very wide, (1) Normal children who are momentarily uncon
the dentist positively reinforces each effort on the trolled or defiant.
part of the patient to open wide. If a child is asked (2) Usually 3 years old or older.
to open his mouth for examination of the teeth and d. Contraindications.
the child complies, but to a very limited degree, the (1) Patients who lack cooperative ability.
dentist should give the child positive reinforce (2) Younger than 3 years old.
ment. This response from the dentist is likely to (3) Timid children.
cause the patient to open wider, which is followed (4) Tense-cooperative children.
again by positive reinforcement. e. Historically, aversive conditioning has been applied
b. Reinforcement of desired behavior may be verbal in various forms. A disapproving look may be con
or nonverbal. Nonverbal reinforcement may strued as aversive conditioning. A method termed
consist of a pat on the shoulder, a smile, or a wink. voice control, in which the dentist speaks to the
Nonverbal reinforcers can be very effective. child in firm tones, is considered a higher level of
c. Reinforcement should be immediate and specific aversive conditioning. Hand-over-mouth exercise
to the desirable behavior. Nonspecific reinforce (HOME) is a technique in which the dentist places
ment such as You are a good boy does not help fingers or a hand over the patients mouth in an
shape the desired behaviors and becomes boring effort to gain the attention of an uncontrolled
and meaningless to the patient after several times. patient.
d. TSD technique. (1) Most pediatric dentistry graduate programs do
(1) This is a behavioral management technique in not teach HOME as an acceptable behavior
which the dentist explains a procedure or a part management technique.
of a procedure to the child patient using age- (2) Aversive conditioning should always be fol
appropriate terminology (Tell), familiarizes the lowed by positive reinforcement or praise for
patient with the instruments and procedures by improved behaviors.
gentle demonstration (Show), then performs (3) All pediatric dentistry programs teach that
the procedure (Do). appropriate pharmacologic techniques (nitrous
(2) Indications. oxide, conscious sedation, general anesthesia)
(a) Cooperative childrenthese children should are acceptable.
be introduced to dental procedures using (4) Communication with parents before and after
TSD to maintain cooperative behavior. aversive conditioning is a necessity.
(b) Children who are lacking cooperative (5) Using aversive conditioning can expose the
abilitysome patients who initially may dentist to liability. If the practitioner chooses to
not seem to have cooperative ability may use aversive conditioning, informed parental
understand more than what an initial consent should be obtained.
assessment reveals. 5. Miscellaneous.
(c) Timid, tense-cooperative, and whining a. Appointment lengthstudies are conflicting
childrenfamiliarization with the various regarding the effect of appointment length on chil
procedures can help children with initial drens behavior in the dental environment.
anxieties to relax. b. Appointment timesome dentists believe that
(d) Uncontrolled or defiant childrenwhen morning appointments are better for preschool
patients in these categories begin to listen children because the patient is rested. However,
other dentists hold that children may be less active Table 5-7
in the afternoon and more manageable. One study
Common Local Anesthetics and Maximum
demonstrated no difference between morning and
Recommended Doses
afternoon appointments.
c. There are two common methods for checking for MAXIMUM
cavities or trauma in a toddler. RECOMMENDED
DOSE OF
(1) The parent sits in the dental chair and ANESTHETIC DURATION ANESTHETIC
cradles the child in his or her arms and helps
2% lidocaine with Pulpal: 60min 4.4mg/kg
restrain the patients arms, if necessary. The 1:100,000 Soft tissue: 3-5hr
dentist examines the patient with hands on epinephrine
both sides of the patients head so head move 3% mepivacaine Pulpal: 20-40min 4.4mg/kg
ment can be sensed and restricted, if necessary. Soft tissue: 2-3hr
The dental assistant is positioned on the oppo 4% prilocaine Pulpal: 60-90min 4.4mg/kg
site side of the chair from the dentist and can with 1:200,000 Soft tissue: 3-8hr
restrain the legs, if necessary. epinephrine
(2) In the second method, the parent and the
dentist sit knee-to-knee. The patients head
rests on the dentists thighs. The parent restrains
the childs legs and the dental assistant can aid
in restraining the patients arms. 2.3 Local Anesthesia and Nitrous Oxide
d. ADHD. Sedation for Children
(1) Basic information. A. Common local anesthetics and dosages.
(a) ADHD involves two sets of symptoms: inat 1. The practitioner must know the maximum recom
tention and a combination of hyperactive mended dose of anesthetics used and then calculate,
and impulsive behaviors. based on the patients weight, the maximum number
(b) ADHD usually manifests between the of cartridges.
ages of 3 and 5, but manifestation varies 2. The possibility for adverse reactions increases with
widely. concomitant use of sedative agents.
(c) Worldwide, 2% to 9.5% of all school-age 3. Table 5-7 shows three common local anesthetic
children have ADHD. solutions.
(d) Researchers have identified ADHD in every 4. Calculation of maximum dose and cartridgesthe
nation and culture they have studied. ADA/PDR Guide to Dental Therapeutics indicates
(e) Can persist into adulthood. some cartridges contain 1.7 to 1.8mL and others
(2) Common medications and examples of adverse contain 1.8mL depending on the anesthetic.
reactions. Although many cartridges are labeled as 1.7mL, the
(a) Methylphenidate (Concerta, Ritalin, Meta following calculations are based on cartridges that
date): adverse effects include nausea, may contain up to 1.8mL.
hypertension. a. Obtain the patients weight in pounds and convert
(b) Atomoxetine (Strattera): adverse effects to kilograms by dividing by 2.2 (2.2lb = 1.0kg).
include hypertension, dry mouth, nausea. (1) Example: (44-lb child)/(2.2lb/kg) = 20kg.
(c) Amphetamine/dextroamphetamine (Ad- b. Multiply weight in kilograms by the maximum rec
derall): adverse effects include hyperten ommended dose of local anesthetic to obtain the
sion, headache, nausea, dry mouth. maximum milligram dosage.
(3) Treatment modifications. (1) Example: (20kg) (4.4mg/kg lidocaine) =
(a) Depends on age and severity. 88mg.
(b) Shorter appointments. c. Calculate the number of milligrams per cartridge
(c) Step-by-step verbal reinforcement. of anesthetic by multiplying the percent of local
e. Attire worn by the dental team. anesthetic times 10, then multiplying by the size of
(1) Verification is inconclusive regarding the effect the cartridge, typically 1.8mL.
of the color and style of clothing and uniforms (1) Example: (2%) (10) (1.8) = 36mg/cartridge.
worn by the dental team on childrens behavior. d. Divide the maximum milligram dosage (step 4b)
Other factors, such as parenting style and the by the number of milligrams per cartridge (step 4c)
ability of the dental team to communicate well to obtain the maximum allowable cartridges of
with children, are much more important in anesthetic.
determining the childs reaction to the dental (1) Example: (88mg maximum dose)/(36mg/
environment. cartridge) = 2.44 cartridges.
B. Topical anesthetic. of anterior teeth occurs from the opposite side

1. A good-tasting benzocaine topical anesthetic is across the midline, it is advisable to supplement
recommended by authors of major pediatric den a mandibular block with local infiltration
tistry texts. anesthesia.
a. Benzocaine has a rapid onset. 3. Maxillary primary molars.
b. The mucosa is dried with gauze, and the topical a. Innervationposterior superior alveolar nerve for
anesthetic is applied for a minimum of 30 seconds. permanent molars and the middle superior alveo
2. The usefulness of topical anesthetic in children is lar nerve for the mesiobuccal root of the first per
debated. Some authorities believe that placing topical manent molar and primary molars.
anesthetic may cause more anxiety because the child b. Infiltration.
has more time to anticipate the injection. In addition, (1) Local infiltration anesthesia is effective for first
the topical anesthetic can trigger a conditioned primary molars, owing to relatively thin overly
response because the injection always follows the ing bone.
topical application. However, most clinicians use a (2) Local infiltration used alone for second primary
topical anesthetic. molars is less effective because of the thickness
C. Local anesthesia techniques for children. of bone in the area.
1. Mandibular primary molars. c. Posterior superior alveolar nerve block.
a. Innervationinferior alveolar nerve. (1) This block is used for second primary
b. Inferior alveolar nerve block (mandibular block). molars in conjunction with local infiltration
(1) Indicated for deep caries, pulp therapy, and anesthesia.
extractions. (2) A posterior superior alveolar nerve block is
(2) In the primary dentition patient, the mandibu used for the maxillary first permanent molar
lar foramen is located lower than the plane of also, with a local infiltration applied for the
occlusion. Mandibular block injections for mesiobuccal root.
pediatric patients are made lower than what is 4. Maxillary primary anterior teeth.
done for adult patients. a. Innervationanterior-superior alveolar branch of
(3) About 1mL of solution is deposited in the area the maxillary nerve.
of the mandibular foramen. b. Infiltration.
(4) In the primary dentition, the syringe should (1) Local infiltration anesthesia is effective for
bisect the primary molars on the opposite side maxillary anterior teeth.
of the injection. (2) The solution should be deposited close to the
c. Lingual nerve block. apex of the teeth to be anesthetized.
(1) A small amount of anesthetic solution is 5. Palatal tissues.
deposited on insertion or withdrawal of the a. Innervationanterior palatine and nasal palatine
needle during administration of a mandibular nerves.
block. b. Anesthesia for most restorative procedures or
d. Long buccal block. minor extractions can be accomplished by
(1) A small amount of anesthetic solution is depos first depositing anesthetic via the free marginal
ited in the mucobuccal fold distal to the most gingiva. If needed, this can be supplemented by
posterior tooth. giving a palatal local infiltration injection in an
e. Infiltration. area already blanched by anesthetic given
(1) Some studies have shown that local infiltration previously.
anesthesia for primary molars is effective, espe c. Surgical procedures may require anterior or nasal
cially for restorative procedures. palatine nerve blocks. These injections are quite
(2) There is an increased probability for anesthesia painful and are to be avoided if possible.
failure using local infiltration for pulp therapy D. Complications of local anesthesia.
and extraction procedures. 1. Toxicity.
2. Mandibular primary anterior teeth. a. The maximum dose of anesthetic should be calcu
a. Innervationinferior alveolar nerve. lated (see under Common local anesthetics and
b. Infiltration. dosages, earlier).
(1) Infiltration used alone in primary anterior b. Overdosage may cause central nervous system
teeth is effective for small carious lesions or complications, such as dizziness, blurred vision,
extractions of mobile primary incisors. seizures, central nervous system depression, and
c. Inferior alveolar nerve block (mandibular block). death.
(1) A mandibular block is used in cases that require c. Cardiac complications may include myocardial
regional anesthesia. Because some innervation depression.
Table 5-8 3. Purpose of nitrous oxide sedation.

a. Reduce fear, apprehension, or anxiety.
Typical Pulse Rates, Blood Pressures, and
b. Raise pain reaction threshold.
Respiratory Rates in Children and Adults
c. Reduce fatigue.
(Normal Patients)
d. Enhance communication.
AGE 3 AGE 5 AGE 12 ADULT e. Increase tolerance for longer appointments.
Pulse (beats/min) 110 100 75 70 f. Help in care of developmentally or physically
Systolic BP 100 100 110 120 challenged
(mm Hg) g. Decrease the gagging reflex.
Diastolic BP 60 65 70 75 4. Minimum alveolar concentration.
(mm Hg) a. Minimum alveolar concentration is a measure of
Respiratory rate 25 20+ 20- 15 potency. It is the concentration required to
(breaths/min) produce immobility in 50% of patients.
b. Minimum alveolar concentration of nitrous oxide
BP, Blood pressure.
= 105%.
5. Four plateaus of stage I anesthesia (analgesia).
a. Paresthesiatingling of hands, feet.
2. Lip or cheek trauma. b. Vasomotorwarm sensations.
a. Because of the new sensation of being numb, some c. Drifteuphoria, pupils centrally fixed, sensation
children either scratch their cheek or chew the lip of floating.
or cheek area. Parents and patients should be d. Dreameyes closed but open in response to
warned of this possibility, and parents should questions, difficulty in speaking, jaw sags open.
supervise their children closely. 6. Preparation of patient.
b. Should the patient traumatize the cheek or lip, the a. Patient in reclined position.
parent should be reassured that these lesions b. Use TSD.
almost always heal without complication. In addi c. Describe sensations in advance.
tion, a description of the typical appearance (swell d. Adult-sized nasal hoods do not fit all children
ing, whitish yellow membrane) should be given to well. Smaller nasal hoods must be available for
the parent, and the child should be seen at soon as pediatric patients.
possible in the office. 7. Technique basics.
E. Nitrous oxide sedation for children. a. The bag is filled with oxygen, and the hood is
1. Physiologic differences between children and adults placed on the patients nose.
relative to nitrous oxide administration (Table 5-8). b. The total flow rate is 4 to 6L/min for most chil
a. Basal metabolic activity is greater in children. dren. The practitioner can check the bag and
b. Higher respiratory rate in children. make adjustments if necessary.
c. Higher risk of airway obstruction in children c. The percentage of nitrous oxide is increased in
because of narrower airway passages; large tonsils, 10% to 20% increments until the drift plateau is
adenoids, and tongue; and more oral secretions. achieved and the patient is staring at the ceiling.
d. Higher risk of desaturation in children because of The injection is given at this time.
less capability to expand on inspiration and less d. Maintenance dose during an operative procedure
oxygen reserve. is typically about 30%.
e. Heart rate is higher in children. e. Nausea with or without vomiting is the most
f. Blood pressure is lower in children. common complication with nitrous oxide use.
g. Heart rate has a greater effect on blood pressure This complication occurs with an excessive con
in children. For example, when there is a decrease centration of nitrous oxide or an excessively long
in heart rate, blood pressure decreases relatively procedure. Nitrous oxide levels should be reduced
more in a child. periodically during a procedure, especially after
h. Drug effects are more variable in children. 30 minutes duration.
2. The administration of nitrous oxide at levels less f. Patients must remain under observation while
than 50% (with no combination with other sedative/ using nitrous oxide. The childs color, respiratory
narcotic/depressant agents) is considered to be rate and rhythm, and responsiveness must be
minimal sedation. A minimally sedated patient may continually assessed.
have temporary cognitive and coordination impair 8. Signs of saturation.
ment, but heart and lung function is unimpaired. In a. Reminding child continuously to hold mouth
addition, minimally sedated patients are able to open.
communicate verbally. b. No response to questions.
c. Agitation. 3. Rounded line angles decrease internal stresses in the

d. Sweating. restorative material and help prevent breakage with
e. Nausea. the smaller primary teeth.
f. Unconsciousness. 4. Occlusal preparation extends into susceptible pits
9. Diffusion hypoxiawhen nitrous oxide is discontin and fissures.
ued, there is a high outpouring of nitrous oxide 5. Buccal and lingual extensions for a class II prepara
from the tissues into the lung. This can dilute avail tion minimally break contact.
able oxygen in the lungs. Although diffusion hypoxia 6. Buccal and lingual walls converge occlusally.
is very rare (especially in normal, healthy individu 7. Gingival seat contact is broken.
als), patients should be given 100% oxygen for 3 to 8. Isthmus width is one third the intercuspal
5 minutes after a nitrous oxide procedure. dimension.
10. Contraindications of nitrous oxide sedation. C. Restoring primary molar teeth with composite.
a. Patients with blocked eustachian tube, pneumo 1. Preparations may be more conservative than when
thorax, pneumoperitoneum, sinusitis. Any rigid, using amalgam.
noncompliant air space can lead to increased 2. Preparation of class I restorations may be limited to
pressure with nitrous oxide use. the carious lesion if sealant is used as part of the
b. Pregnancy. restoration.
c. Significant emotional disturbances. 3. Some authors advocate more conservative class II
d. Patients with drug dependencies. preparations in which access to the interproximal
e. Some upper respiratory infections. lesion is gained through the marginal ridge or from
f. Patients being treated with bleomycin sulfate. the facial if the pits and fissures are not susceptible.
g. Methylenetetrahydrofolate reductase deficiency. 4. Preparation for a class II composite is similar
h. A physician consultation should be obtained for to amalgam if caries exist occlusally and
patients with significant medical conditions, such interproximally.
as obstructive pulmonary disease, congestive 5. Composites are very technique-sensitive and are suc
heart failure, and sickle cell disease. Also, patients cessful only if a dry field is maintained.
with acute otitis media and tympanic membrane D. Posterior stainless steel crown preparation and
grafts should have a physician consultation before adaptation.
treatment. 1. Indications.
a. Teeth with extensive carious involvement.
2.4 Restorative Dentistry for Children b. Teeth with pulpectomy or pulpotomy treatment.
A. Anatomic differences in primary teeth compared with c. Malformed teeth.
permanent teeth. d. Teeth with rampant caries.
1. Primary teeth have thinner enamel. e. Mesial lesions on first primary molars.
2. The pulp chamber is relatively larger in primary f. Ankylosed primary molars.
teeth. g. Young permanent molars as a semipermanent
3. The pulp horns are closer to the surface of the tooth. restoration.
4. The enamel rods in the gingival third slope occlusally h. Fractured teeth.
instead of cervically as in permanent teeth. i. Teeth needed for abutments for appliances.
5. The crown is relatively shorter and has a greater con 2. Contraindications.
striction in the cervical region. a. If good esthetics are of primary importance.
6. The interproximal contacts are broader and flatter b. Teeth nearing exfoliation.
than permanent teeth. c. Excessive crown loss resulting in lack of mechani
7. Enamel and dentin shades are generally whiter than cal retention.
permanent teeth. d. Space loss; if a neighboring tooth has tipped into
8. The occlusal table is narrower on primary molars. the carious defect, adequate crown coverage may
B. Basic principles in restoring primary molar teeth with be impossible.
amalgam. e. Caries extending cervically so that coverage of the
1. Preparation depth is 0.5mm into dentin; on primary defect becomes an issue.
molars, the depth of preparation is approximately f. As a permanent restoration in the permanent
1.5mm. dentition.
2. No. 330 and No. 245 burs are common for prepara E. Restoration of anterior primary teeth.
tion of primary teeth. The No. 330 bur is 1.5mm in 1. Incisors.
length, and the No. 245 bur is 3.0mm in length. a. Small class III lesions may be restored with com
These burs can aid the practitioner in establishing the posite similarly to that of permanent incisors.
proper depth of the preparation. b. Compromised or involved incisal edge.
(a) An open-face stainless steel crown can be

created. The facial of the stainless steel
crown is removed and is replaced by
composite.
(b) Facings veneered to a stainless steel crown
are available commercially or from some
laboratories.
(c) Prefabricated zirconia anterior and poste
rior crowns are available. These crowns
must fit passively because they do not flex
the way stainless steel crowns do.
2. Primary canines.
Figure 5-31 Composite crowns preoperatively. a. The distal surface of primary canines is a common
site for caries in caries-prone patients.
b. It is often necessary to place lingual, or sometimes
labial, dovetails to aid in retention and placement
of restorative material.
2.5 Pulp Treatment for Primary Teeth

A. Treatment options. The dentist has four treatment
options if a primary tooth has pulp involvement. If the
indications and contraindications for each of these pro
cedures are known, the dentist may choose the treat
ment with the greatest efficacy.
1. Pulp capping.
2. Pulpotomy.
3. Pulpectomy.
4. Extraction.
B. General pulp therapy contraindications.
Figure 5-32 Composite crowns postoperatively. 1. Pulp therapy is generally contraindicated in children
who have serious illnesses. Extremely serious com
(1) Some authors recommend a preparation that plications secondary to acute infection can arise
includes proximal reduction and labial or should the pulp therapy fail.
lingual dovetails in the cervical third. 2. Situations in which pulp therapy is contraindicated.
(2) With significant incisal edge loss, a composite a. Patients susceptible to bacterial endocarditis.
resin crown is a good choice if there is adequate b. Patients with leukemia.
tooth remaining for bonding and if esthetics is c. Patients with nephritis.
of primary importance (Figures 5-31 and 5-32). d. Patients with cancer.
(a) Preparation includes caries removal, mesial e. Patients with depressed polymorphonuclear leu
and distal IPR, and placing an undercut kocyte and granulocyte counts.
area approximately 1mm incisal and fol C. Important clinical signs.
lowing the free marginal gingiva. Preserva 1. Mobilityindicates loss of vitality if mobility is due
tion of enamel is important. An alternative to bone destruction, root destruction, or both. Vital
preparation is to create a 1-mm cervical pulpotomy technique is inappropriate.
shoulder on the entire tooth. 2. Swelling or fistulaindicates necrotic pulp. Vital
(b) A celluloid crown form is trimmed and pulpotomy technique is inappropriate.
adapted to cover the cervical margins. At 3. Furcation radiolucencyindicates necrotic pulp.
least one vent hole is created on the incisal Vital pulpotomy technique is inappropriate. Pulpec
edge to allow escape of excess composite. tomy may be appropriate if the tooth does not dem
(c) The crown form is filled with composite and onstrate internal or external root resorption.
seated. 4. Percussion or palpation sensitivityindicates at least
(3) Primary incisors with extensive loss of tooth advanced pulpal inflammation. Pulpotomy may not
structure may require stainless steel crowns. be advisable.
Improved esthetics may be obtained in several 5. Spontaneous painindicates at least advanced pulpal
ways. inflammation. Other indicators should be used to
determine treatment of the tooth, but pulpotomy

may not be advisable.
D. Pulp capping.
1. Indirect pulp cap.
a. Indications.
(1) Symptom-free.
(2) No radiologic evidence of pathosis.
(3) Minimal caries in an area that, if caries were
removed, would result in a pulp exposure.
b. Procedure.
(1) Caries removal, leaving caries that would
expose the pulp.
(2) Calcium hydroxide layer or base cement, or
both.
(3) Restoration of tooth.
(4) Wait 6 to 8 weeks.
(5) Reenter and remove remainder of caries. Some Figure 5-33 The mandibular second primary molar has
clinicians avoid this step and proceed with the tipped mesially into the carious lesion of the first primary
molar. Obtaining a proper margin with a stainless steel crown
restoration.
would be very difficult.
2. Direct pulp cap.
a. Indications.
(1) Very small, pinpoint exposure only.
(2) Noncarious exposure only.
(3) Symptom-free.
(4) Some authors are hesitant to recommend direct
pulp caps on primary teeth because of a concern
of internal root resorption.
b. Procedure.
(1) Calcium hydroxide layer.
(2) Restoration of tooth.
E. Pulpotomy.
1. Definitioncoronal removal of vital pulp tissue.
2. Indications.
a. Vital primary tooth with carious or accidental
exposure.
b. Clinical signs of a normal pulp canal (e.g., no
swelling, no draining fistulas, no pathologic mobil Figure 5-34 The coronal pulp tissue has been removed,
ity, no history of spontaneous pain, no pathologic and the remaining tissue has been treated.
radiographic radiolucencies).
c. The tooth must be restorable. The dentist should 4. Evaluationa successful pulpotomy is free from
think of restorability in terms of extent of decay clinical and radiographic symptoms.
and in terms of drift of adjacent teeth. For example, a. Asymptomatic tooth.
occasionally an adjacent tooth may tip into a b. No mobility or fistulas.
carious defect, preventing an appropriate adapta c. No furcation radiolucency.
tion of a stainless steel crown (Figure 5-33). d. No internal or external root resorption.
3. Procedure (Figures 5-34 to 5-36). e. Success rate 70% to 97%.
a. Remove superficial and lateral decay. 5. Medicaments.
b. Remove roof of the chamber. a. Formocresol.
c. Extirpate coronal pulp, No. 4 round bur, slow (1) Buckleys formocresol is the most commonly
speed, light pressure. used medicament for pulpotomies on primary
d. Dry cotton pellets to arrest pulpal hemorrhage. teeth.
e. Formocresol application for 5 minutes; if hemor (2) 35% cresol, 19% formalin in aqueous
rhage cannot be controlled, consider pulpectomy glycerine.
or two-visit pulpotomy. (3) Acts by direct contact.
f. Zinc oxideeugenol (ZOE) buildup. (4) A 20% solution produces equivalent results as
g. Stainless steel crown coverage. full strength.
3. Contraindications.
a. Nonrestorable tooth.
b. Internal or external root resorption.
c. Teeth without accessible canals (commonly first
primary molars).
d. Significant bone loss.
4. Technique.
a. Remove coronal pulp as for pulpotomy.
b. Irrigate chamber gently with sodium hypochlorite
or with sterile saline, and dry with cotton pellet.
c. Carefully remove radicular pulp tissue with small
file or barbed broach.
d. Obtain test lengths 1 to 2mm short of apex.
e. Enlarge canal approximately three sizes.
f. Wash frequently and carefully with sodium hypo
chlorite or sterile saline.
Figure 5-35 The pulpotomy on the mandibular first g. Dry with paper points.
primary molar is failing. Note the furcation involvement and
h. Filling methods.
the external and internal root resorption. The failure may be
related to the inadequate crown coverage on the distal aspect of
(1) Pressure syringe.
the tooth. (a) Using a paper point or file, coat the walls of
the canals with a creamy mix of ZOE.
(b) Fill with creamy ZOE mix, starting 1 to
2mm from the apex.
(2) Condensation.
Stainless steel crown (a) Coat the walls of the canals with creamy
ZOE build up
mix of ZOE.
(b) Continue mixing ZOE to a condensable
thickness, roll into points, and condense
Fixation zone with small endodontic or amalgam
pluggers.
Coagulation 5. Evaluationa successful pulpectomy is free from
necrosis clinical and radiographic symptoms.
a. Asymptomatic tooth.
Vital tissue
b. No mobility or fistulas.
c. No furcation radiolucency.
Figure 5-36 Pulp tissue zones in a formocresol pulpot- d. No internal or external root resorption.
omy. ZOE, Zinc oxideeugenol
G. Decision-making treeit is helpful to illustrate the
decision-making process for pulp therapy in diagram
matic form (Figure 5-37).
(5) Other medicaments have been studied or advo 1. Furcation?
cated because of a concern regarding possible a. If there is no furcation involvement, the tooth is
toxic effects of formocresol. likely vital, and a vital pulpotomy is generally
b. Ferric sulfate. appropriate if the tooth is restorable.
(1) Success rates comparable to formocresol. 2. First primary molar?
(2) Ferric sulfate is less toxic than formocresol. a. If there is furcation involvement and the tooth is a
c. Mineral trioxide aggregate. first primary molar, an extraction should be
(1) Mineral trioxide aggregate pulpotomies gener strongly considered because of the difficulty of
ally show higher success rates than formocresol adequately removing diseased pulp tissue in this
pulpotomies. tooth.
F. Pulpectomy. 3. Restorable?
1. Definitioncomplete removal of all remaining pulp a. The tooth must be restorable. The dentist should
tissue. think of restorability in terms of extent of decay
2. Indications. and in terms of drift of adjacent teeth. For example,
a. Necrotic or chronically inflamed, strategically occasionally an adjacent tooth may tip into a
located tooth with accessible canals. carious defect, preventing an appropriate adapta
b. Essentially normal supporting bone. tion of a stainless steel crown (see Figure 5-35). If
EXT
Furcation? EXT
YES YES
Ist Primary Molar? Root Resorption?

NO YES
NO
NO
YES
PO Restorable?
PE
NO
EXT
Figure 5-37 Decision-making tree for pulp therapy on primary molars. EXT, Extraction; PE, pulpectomy; PO, pulpotomy.
the tooth is not adequately restorable, it should be c. Second primary molarsPHA unilateral and
extracted. bilateral.
4. Root resorption? B. Incisor loss.
a. Generally, if a tooth has internal or external root 1. Primary dentition.
resorption, it should be extracted. An exception to a. Loss of a primary incisor in the primary dentition
this rule is if the tooth is located strategically. For does not generally cause loss of overall arch cir
example, a second primary molar with mild to cumference, as defined as the distance from the
moderate root resorption on a 5-year-old patient distal of the second primary molar, around the
may be considered for pulp treatment. The purpose arch through the contact points, to the distal of
of this treatment would be to maintain space until the other second primary molar.
the first permanent molar erupts and then extract b. Loss of a primary incisor may result in localized
the primary molar and place a space maintainer. space loss, especially if there was no interdental
This strategy may avoid the need for a distal shoe primary spacing before the loss.
space maintainer, making another space main c. Replacement of lost primary incisors is considered
tainer when the first permanent molar erupts. more for esthetics and possibly development of
speech than for space maintenance. If the patient
2.6 Space Management in is not in the process of developing speech, placing
the Developing Dentition an appliance is unnecessary if there is not an
A. Basic rules. esthetic concern.
1. Eruption of anterior teeth should be reasonably d. Partial dentures (kiddie partials).
symmetrical. (1) Removable.
a. Extract contralateral primary tooth if there is a (a) Posterior Adams clasps, C clasps, or ball
significant exfoliation asymmetry. clasps are placed for retention.
b. Exfoliation usually occurs during eruption of per (b) The patient is usually at least 3 years old,
manent incisors. A permanent incisor erupting and it is determined after consultation with
may exfoliate the next, more distal primary tooth, parents that there is a reasonable expecta
which creates an asymmetry in exfoliation. This tion that the patient will tolerate wearing
asymmetry can lead to significant midline the appliance.
deviations. (2) Fixed (Figure 5-38).
2. Primary dentition. (a) Orthodontic bands on second primary
a. First primary molarsband-loop space main molars.
tainer (BLS) unilateral and bilateral loss. (b) 0.036-inch to 0.040-inch stainless steel wire
b. Second primary molarsdistal shoe or acrylic is used.
partial. (c) The replacement teeth are fixed to the wire.
c. Incisorsconsider esthetics and speech; use fixed (d) This appliance is intended mostly for
or removable appliance. patients younger than 3 years old or of
3. Mixed dentition. questionable compliance in wearing a
a. Primary mandibular canineslower lingual removable appliance.
holding arch (LLHA). e. Ectopic eruption.
b. First primary molarsBLS unilateral or palatal (1) Lingual eruption of permanent incisors
holding arch (PHA) bilateral. characterized by a double row of teeth.
Figure 5-40 Space loss in permanent incisor region.
Figure 5-38 Fixed kiddie partial.
Figure 5-41 Mandibular midline is shifted to the left

because of early loss of a primary canine.
of choice so as to minimize a midline

deviation.
2. Permanent dentition.
Figure 5-39 Ectopic eruption of mandibular permanent
a. Loss of a permanent incisor.
central incisors causing early exfoliation of a primary
lateral incisor.
(1) Localized space loss can occur very quickly
after loss of a permanent tooth (Figure 5-40).
An appliance should be constructed and in
(a) This is a very common problem in the early serted as soon as possible after the tooth loss.
mixed dentition. (2) If localized space loss occurs, it may be treated
(b) If the primary incisor is very loose, no treat with a removable appliance with finger springs
ment is necessary initially. Most of these or with fixed orthodontics.
teeth exfoliate within a reasonable amount C. Primary canine loss.
of time. 1. Unilateral loss usually causes the following.
(c) If the primary incisor is only moderately a. Lingual collapse of permanent incisors.
loose, extraction is usually the best option. b. Loss of arch length.
(d) Erupting lingual incisors almost always c. Increased overbiteafter lingual collapse, the
move labially until they contact another mandibular incisors erupt further, increasing
tooth. overbite.
(2) Lateral ectopic eruption of permanent incisors d. Increased overjet secondary to lingual collapse of
characterized by early exfoliation of a primary mandibular incisors.
lateral incisor (Figure 5-39). e. Midline deviation to the side of the canine loss
(a) Ectopic eruption of this type often results in (Figure 5-41).
a midline deviation. 2. Bilateral loss usually causes the following.
(b) With early detection, extraction of the a. Lingual collapse of permanent incisors.
remaining lateral incisor is the treatment b. Loss of arch length.
Figure 5-42 The holding arch was seated before erup-

tion of the permanent lateral incisor, which erupted
lingually. Figure 5-43 Nance holding arch features an acrylic
button to aid in preventing mesial movement of maxillary
posterior teeth.
c. Increased overbiteafter lingual collapse, the
mandibular incisors erupt further, increasing
overbite. (b) A 0.040-inch wire extends distally to the
d. Increased overjet secondary to lingual collapse of mesial of the unerupted first permanent
mandibular incisors. molar.
3. Appliances. (c) A V-shaped extension is soldered to the
a. Bilateral canine loss in a mixed dentition wire, which is inserted gingivally and posi
LLHA. tioned mesial to the permanent first molar.
b. Unilateral canine loss in a mixed dentition. (2) Acrylic partial denture.
(1) Extract contralateral primary canine and place (a) This option may be indicated in children
LLHA. with multiple missing teeth (lack of abut
(2) LLHA with a spur if a midline deviation has not ment teeth) or medical conditions that con
occurred. A spur is a soldered extension from traindicate an appliance such as a distal shoe
the main LLHA wire that engages the distal of (e.g., a blood dyscrasia, a congenital heart
the permanent lateral incisor, preventing distal defect, immunosuppression, diabetes).
drift. (b) The appliance is designed so that there is a
D. Primary first molar loss. mild amount of pressure applied by the
1. Primary dentition. acrylic on the alveolar ridge where the
a. Unilateral lossBLS maintainer. mesial of the unerupted first permanent
b. Bilateral lossBLS maintainer on both sides. molar would be. Often after extraction, the
c. Do not use LLHA until permanent incisors are acrylic can be positioned mesial to the soft
erupted. Permanent incisors commonly erupt tissue contour of the first permanent molar.
lingually and can be trapped by the appliance b. Mixed dentition.
(Figure 5-42). (1) Unilateral loss of a second primary molar in the
2. Mixed dentition. mixed dentition usually requires a bilateral
a. Unilateral lossBLS maintainer. holding arch.
b. Bilateral lossLLHA or PHA, or Nance appliance (2) If a band and loop space maintainer is placed,
(Figure 5-43). there is no abutment tooth when the first
E. Primary second molar loss. primary molar exfoliates.
1. Reasons for space loss. (3) It is always important to consider the eruption/
a. Space loss as a result of early extraction. exfoliation sequence in planning space
b. Space loss as a result of ectopically erupting first maintenance.
permanent molar. 3. Bilateral loss.
2. Unilateral loss. a. Appliance choices.
a. Primary dentition. (1) Lingual holding arch (Figure 5-44).
(1) Distal shoe space maintainer. (2) PHA.
(a) A stainless steel crown is adapted to the first (3) Nance holding arch.
primary molar. (4) Removable appliance.
Figure 5-44 This lingual holding arch prevents posterior

teeth from tipping mesially. The lingual holding arch can also
Figure 5-45 The first and second premolars erupted very
be used to prevent lingual movement of incisors following pre
early in this patient, who had extensive furcation involve-
mature primary canine loss.
ment of the primary molars. There is approximately one third
root development.
F. Factors to consider in planning for space

maintenance. c. The average tooth pierces the gingival tissue with
1. Amount of resorption of primary roots. three fourths root formation.
a. If more than one fourth of the root remains owing 4. Time elapsed since loss.
to normal resorption, space maintenance is likely a. Most space closure occurs within the first 6 months.
necessary. b. Closure can occur in days.
b. If less than one fourth of the root remains and if c. In the molar area, closure occurs essentially by
there is no bone left between the primary tooth tipping, not bodily movement of the tooth.
and permanent tooth, space maintenance is likely 5. Eruption of neighboring teeth.
unnecessary. a. Active eruption of a neighboring tooth tends to
2. Amount of bone covering the permanent tooth. increase amount of space loss. For example, if a
a. If there is no bone remaining between the primary second primary molar is removed during the erup
molar and permanent premolar and if the cusp tip tion of the first permanent molar, more space loss
of the permanent tooth is radiographically at the will likely result.
level of the furcation, no space maintenance is 6. Patients age.
necessary. a. Chronologic age and average times of eruption are
b. If bone is interposed between the primary molar not important factors in planning space mainte
and the permanent premolar, space maintenance is nance. The dentist should not use average times of
usually indicated. eruption in treatment decisions.
c. If there is bone destruction in the region of the b. Teeth normally erupt through the gingiva with
primary molar furcation, it is possible that the per three fourths root development.
manent tooth may erupt very early, with less than c. Rule of 7 for primary molars.
three fourths root completion (Figure 5-45). (1) Eruption is delayed if loss of the primary molar
d. If there is bone destruction in the region of the occurs before age 7.
primary molar furcation, it is also possible that (2) Eruption is accelerated if loss of the primary
bone will form again, covering the permanent molar occurs after age 7. This does not mean
tooth. that space maintenance is not needed after age
e. If the prediction of eruption of the permanent 7. It only means that if a primary molar is lost
tooth is difficult, the dentist should use a space after age 7, the permanent tooth on average
maintainer. Because space loss can occur very tends to erupt faster that it ordinarily would.
quickly, a space maintainer is often necessary, even 7. Delayed or deviant eruption.
if only for a few months duration. a. Ectopic permanent molars.
3. Amount of root development. (1) First permanent molars may become impacted
a. Eruptive movement begins on crown completion. under the distal aspect of the second primary
b. The average tooth pierces the bone with two thirds molar (Figure 5-46).
root formation. (2) More common in maxilla.
Figure 5-46 The maxillary first permanent molar is

ectopically erupting under the distal aspect of the second
primary molar. Figure 5-48 The maxillary first primary molars are anky-
losed. These should be extracted before they become further
submerged and are surgically more difficult. A space maintainer
should be fabricated.
(d) Space maintenance is necessary unless the

cusp tip of the premolar is at the level of the
floor of the pulp chamber of the primary
molar and if, on extraction, the permanent
tooth can be visualized.
(2) Buccal or lingual eruption.
(a) Buccal or lingual eruption of premolars is
very common.
(b) If the primary molar is not ready to exfoli
ate within a few weeks, extraction of the
primary molar is the treatment of choice.
(c) After extraction, the permanent premolar
tends to move to a more normal position as
long as there is adequate space for the tooth
Figure 5-47 Distal eruption of a second bicuspid. After
and the permanent tooth is only partially
extraction of the second primary molar, the bicuspid usually
uprights and erupts into a reasonably normal position.
erupted.
c. Ankylosed primary molars.
(1) Background.
(a) Common: 1% (African-Americans) to 4%
(3) Varies in severity; if mild, some self-correct, or (whites).
jump. (b) Familial pattern.
(4) Treatment options. (c) Higher prevalence with congenitally absent
(a) Orthodontic separator. premolars.
(b) Titanium clip separator. (d) Usually begins after root resorption begins.
(c) Brass ligature wire. (e) The change in occlusal height is due to the
(d) Humphrey appliance. teeth other than the ankylosed teeth con
(e) Nance appliance and open coil spring. tinuing normal eruption (Figure 5-48).
b. Ectopic premolars. (f) Ankylosis is progressive (i.e., the difference
(1) Distal eruption (Figure 5-47). in occlusal height becomes greater with
(a) This is most common in mandibular second time). The practitioner must monitor the
premolars. condition regularly.
(b) Resorbs the distal root of the second (2) Diagnosis.
primary molar but not the mesial root. (a) Appearanceout of occlusion.
(c) Often requires extraction of the primary (b) No mobility, even with advanced
molar. resorption.
(c) Hollow sound when tapped. 3. Treatment involves improvement in oral hygiene,
(d) Perhaps seen on radiographbreak in peri removal of local irritants, and nutrition counseling.
odontal membrane. C. Herpes simplex infection.
(3) Treatment. 1. Primary herpetic gingivostomatitis.
(a) Possibly, even probably, no treatment. a. Etiologyherpes simplex virus type 1.
(b) Observe for space loss and tipping of adja b. Usually affects children younger than 6 years.
cent teeth. c. No previous exposure.
(c) If ankylosed tooth is below the normal d. Most primary infections are subclinical.
height of contour of the interproximal 2. Acute herpetic gingivostomatitis.
surface of the adjacent tooth, extract and a. Symptoms.
consider space maintenance. (1) Liquid-filled yellow or white vesicles intra
(d) As a temporary treatment, a stainless steel orally and periorally that rupture.
crown or composite bonding has been used (2) Ruptured vesicles are 1 to 3mm in diameter
to extend the existence of the ankylosed with a pseudomembrane and have erythema
tooth. tous borders.
8. Congenitally absent teeth. (3) Locationmucous membrane, including
a. Incidence 1.5% to 10%, excluding third molars. tonsils, hard and soft palates, buccal mucosa,
b. If third molars are not included, the most common tongue, palate, gingiva.
congenitally missing tooth is the mandibular (4) Fever, malaise, lymphadenopathy.
second premolar, followed by the lateral incisor, (5) Duration of 10 to 14 days.
followed by the maxillary second premolar. b. Treatment.
c. Treatment options with congenital absence. (1) Topical anesthetics such as 0.5% dyclonine
(1) Congenital absence of bicuspid is commonly hydrochloride and viscous lidocaine.
treated orthodontically if the patient would (2) Coating solutions such as diphenhydramine
have normally required extraction treatment. elixir and kaolin-pectin compound.
In these cases, all spaces are closed. If the (3) Topical acyclovir or penciclovir.
patient has excellent occlusion, normal over (4) Analgesics such as acetaminophen and
bite and overjet, and minimal or no crowd ibuprofen.
ing, the congenital absence may be treated 3. Recurrent herpes simplex (cold sore or fever
prosthetically. blister).
(2) Congenital absence of lateral incisor may be a. Usually on the outside of the lips.
treated by placement of the canine in the lateral b. Recurrence is frequently associated with emotional
incisor position and restorative lateralization stress or local physical trauma.
of the permanent canines. Alternatively, the c. Treatmentsystemic or topical antiviral medi
canines may be placed in their normal position, cations.
and the lateral incisors may be replaced D. Recurrent aphthous ulcer.
prosthetically. 1. Etiology unknown.
2. Painful oval ulceration on unattached mucous
2.7 Periodontal Problems in Children membrane.
A. Gingivitis. 3. Minor aphthae heal in 7 to 10 days.
1. Very common in children. 4. Treatmenttopical antiinflammatory and analgesic
2. Treated with improved oral hygiene. agents.
3. Parental participation in oral hygiene is necessary in E. Minimal attached gingiva and recession.
children younger than 8 years old because of the 1. A labial eruption path is the most common cause of
childs lack of manual dexterity. inadequate attached gingiva.
4. Parental supervision is often necessary in older chil a. Sometimes orthodontic treatment may result in
dren because of the childs lack of interest or under some increase of attached gingiva.
standing of consequences. b. Common treatmentfree gingival graft.
5. Common conditions in children such as mouth 2. Other causes may be a high frenum attachment, high
breathing, crowded teeth, erupting teeth, and braces vestibule, self-inflicted injury, trauma, and use of
may further aggravate inflamed gingiva. smokeless tobacco.
B. Puberty gingivitis. F. Abnormal frenum attachment.
1. Prepubertal and pubertal period. 1. Maxillary frenum.
2. Characterized by enlarged, bulbous interproximal a. In the absence of recession, treatment of a heavy
gingival tissue on the labial aspects of the anterior maxillary frenum with diastema is delayed until
teeth. the permanent cuspids have erupted.
b. If the midline diastema has not closed, orthodontic

closure is accomplished first, and a frenectomy is 2.8 Dental Trauma in Children
performed afterward. A. Etiology.
2. Lingual frenum (tongue tie). 1. Boys more commonly affected (male-to-female ratio
a. A patient is considered to have restricted tongue 2:1).
movement if the tongue cannot touch the maxil 2. Maxillary anterior teeth most commonly affected.
lary alveolar process. 3. Children with increased overjet more commonly
b. With restricted tongue range of motion, children affected.
may be unable to develop proper speech sounds 4. Trauma to the primary dentition occurs in 30% of
and surgery may be indicated in conjunction with children.
speech therapy. 5. Trauma to the permanent dentition occurs in 22% of
c. Lingual frenum may also cause recession. children by age 14.
3. Mandibular anterior frenum. B. Possible reactions of a tooth to trauma/
a. A high mandibular anterior frenum may be associ 1. Pulpal hyperemiamay lead to infarction and necro
ated with gingival recession. sis as a result of increased intrapulpal pressure.
b. Frenectomy and gingival graft are common surgi 2. Internal hemorrhage.
cal treatments. a. Capillary rupture secondary to increased pressure.
G. Periodontal disease in children. b. Occurs within 2 to 3 weeks after trauma.
1. Aggressive periodontitis. c. May cause discoloration.
a. Localized aggressive periodontitis in the perma 3. Calcific metamorphosis (pulp canal obliteration).
nent dentitionpreviously known as localized a. Partial obliteration of the pulp chamber and
juvenile periodontitis. canal.
(1) Loss of attachment and bone on first perma b. These teeth normally remain vital.
nent molars and permanent incisors. c. Yellow, opaque appearance.
(2) Rapid loss of attachment. 4. Internal resorption.
(3) Increased bacterial counts of Aggregatibacter a. Caused by osteoclastic action.
(Actinobacillus) actinomycetemcomitans. b. Pink spot perforation may occur.
(4) Most common in African-American children. 5. Peripheral root resorption.
(5) Treatment includes surgical intervention and a. Caused by damage of periodontal structures.
antibiotics (metronidazole with or without b. Usually occurs in severe injuries with displacement
amoxicillin, tetracycline). of the tooth.
b. Generalized aggressive periodontitis. c. Types.
(1) Involvement of the entire dentition. (1) Surfacenormal PDL, small areas.
(2) Significantly increased amount of plaque and (2) Replacementankylosis.
calculus. (3) Inflammatorygranulation tissue, radiolu
(3) Treatment includes surgical intervention and cency.
antibiotics. 6. Pulpal necrosis.
c. Localized aggressive periodontitis in the primary a. Caused by severing of apical vessels or prolonged
dentitionpreviously known as localized prepu hyperemia and strangulation.
bertal periodontitis. b. May not occur for several months.
(1) Most common in the primary molar area. 7. Ankylosis.
(2) Most common in African-American children. a. Ankylosis can occur with PDL injury, which leads
(3) Treatment includes dbridement and anti to inflammation and osteoclastic activity. This may
biotics. cause fusion between bone and root surface.
H. Acute necrotizing ulcerative gingivitis. b. Clinically, occlusal or incisal surface of ankylosed
1. Characteristics. tooth is gingival to adjacent teeth.
a. Painful, bleeding gingival tissues. c. During growth, eruption of normal teeth contin
b. Blunting of interproximal papillae. ues, but because ankylosed teeth are osseointe
c. Pseudomembrane on the marginal gingiva. grated, these teeth appear to be sinking into the
d. Fetid breath. gingival tissue.
e. High fever. C. Consequences to permanent teeth with injury to the
2. Caused by fusiform bacilli (spirochetes) and other primary predecessor.
anaerobes. 1. Primary anterior teeth are positioned labial to their
3. Most common in teenagers and young adults. permanent successor. An injury that forces the root
4. Responds well to dbridement, oxidizing mouth of the primary tooth into the developing permanent
rinses, and antibiotics. tooth may result in one of the following.
a. Hypocalcification and hypoplasia. g. Typically, radiographs are indicated at 1-, 2-, and
b. Reparative dentin. 6-month intervals after a traumatic incident.
c. Dilaceration (or bending of the permanent 4. Diagnostic tests.
tooth). a. Electrical pulp tests and thermal tests may be unre
D. Patient assessmentcertain issues should be assessed liable in primary teeth.
for all trauma cases. b. If a tooth is incompletely erupted or is being
1. Medical history. orthodontically treated, the tooth may be normal
a. Pay particular attention to the following. even if there is little sensitivity to electrical pulp
(1) Drug sensitivities. testing.
(2) Congenital or acquired cardiac problems. 5. General initial assessment of hard tissue injury.
(3) Coagulation disorders. a. Check for crown fracture.
(4) Seizure disorders. b. Check for pulp exposures.
b. Determine tetanus coverage. c. Check for displaced or avulsed teeth.
(1) Uncovered childrenantitoxin (tetanus im d. Check for mobility.
mune human globulin). e. Examine adjacent and opposing teeth for injury.
(2) Children with previous but dated coverage 6. General follow-up assessment.
toxoid booster. a. Accomplished generally at 1, 2, and 6 months.
(3) Active immunization. b. Clinical examination.
(a) Three injections of diphtheria, pertussis, (1) Mobility.
and tetanus (DPT) vaccine during first (2) Percussion sensitivity.
year. (3) Discoloration and when discoloration began.
(b) Booster at 1.5 and 3 years. (4) History of spontaneous pain.
(c) Booster at 6 years and then every 4 to 5 (5) Swelling or fistula.
years. (6) Pulp testing.
c. Neurologic assessment. c. Radiologic examination.
(1) Obtain information regarding loss of (1) External root resorption.
consciousness. (2) Internal root resorption.
(a) Neck or head pain. (3) PDL space.
(b) Numbness. (4) Periapical radiolucencies.
(c) Amnesia. (5) Continued narrowing of pulp canal space.
(d) Nausea/vomiting. (a) Indicates vital pulp.
(e) Drowsiness. (b) May lead to calcific metamorphosis.
(f) Blurred vision. (6) Root fractures.
(2) If in doubt regarding neurologic status, refer to E. Treatment of traumatic injuriesall of the following
an emergency medical facility. require follow-up assessment as outlined under
2. Dental history questions. General follow-up assessment.
a. How did the trauma occur? 1. Concussion and subluxation.
b. When did the trauma occur? a. Concussion is defined as an injury to the tooth
c. Where did the accident occur (school, home, ath without displacement or mobility. The PDL is
letic field)? inflamed and tender to percussion.
d. Where in the craniofacial region did the trauma b. Subluxation is defined as an injury to the tooth
occur? without displacement, but mobility is exhibited.
e. Was there a previous injury to area? c. Primary and permanent teeth.
f. Was there previous treatment to area? (1) Usually no treatment is immediately
g. Did the patient experience unconsciousness, head necessary.
ache, amnesia, or nausea? (2) Recommend soft diet.
h. Is there a problem biting together in the normal (3) Reinforce need for good oral hygiene.
manner? (4) Some authors recommend 0.12% chlorhexi
3. Radiographs. dine gluconate oral rinse or 3% hydrogen per
a. X-ray injured tooth, adjacent teeth, and opposing oxide to aid healing.
teeth. (5) Teeth with open apices are more likely to
b. Evaluate proximity of fracture to pulp. remain vital.
c. Estimate root development. 2. Intrusion.
d. Look for root and alveolar fractures. a. Primary teeth.
e. Note any periapical pathology. (1) After an intrusive injury to an anterior primary
f. Note previous treatment. tooth, the root of the primary tooth is likely
positioned closely to the labial of the perma (1) Antibiotics after replantation.
nent incisor. (a) Not susceptible to tetracycline staining:
(2) Unless it can be determined that the primary doxycycline 4.4mg/kg/day q 12h on day 1,
tooth is impinging on the permanent successor, 2.2 to 4.4mg/kg/day for 7 days.
intruded primary teeth are left alone in the (b) Susceptible to tetracycline staining: penicil
hopes that they will spontaneously reerupt. lin V 25 to 50mg/kg/day in three to four
(3) These teeth should be reviewed, and radio divided doses for 7 to 10 days.
graphs should be obtained. (2) Endodontic treatment of replanted teeth (see
b. Permanent teeth (see Section 1, Endodontics). Section 1, Endodontics).
3. Extrusion. 8. Root fracture.
a. Primary teeth. a. Primary teeth.
(1) The greater the distance from a normal posi (1) Root fractures in primary teeth are rare, owing
tion, the greater the chance for severing of the to the bone surrounding the teeth at that age
apical vasculature and pulpal necrosis. If a being more malleable.
primary incisor is extruded greater than 3mm, (2) If the root fracture is in the apical half, splinting
the tooth should likely be extracted. may be unnecessary, especially if there is
(2) If the patient is seen before formation of a peri minimal mobility.
apical blood clot, the tooth may be repositioned (3) If the root fracture is in the coronal half with
carefully and splinted for 7 to 14 days. Endo increased mobility, either a rigid splint or
dontic treatment should be initiated. extraction is the treatment of choice.
b. Permanent teeth (see Section 1, Endodontics). b. Permanent teeth (see Section 1, Endodontics).
4. Fracture through enamel only (primary and perma 9. Splinting.
nent teeth). a. Nonrigid splint for reimplantation and displace
a. Smooth enamel. ments.
b. Check vitality at 1, 2, and 6 months because of (1) Bond 0.016-inch 0.022-inch stainless steel
possible concussion injury. orthodontic wire or 0.018-inch round stainless
5. Fracture through enamel and dentin (primary and steel wire or monofilament nylon (20- to 30-lb
permanent teeth). test).
a. Primary teeth. (2) 0.028-inch round stainless steel if three to four
(1) Smooth edges. teeth are mobile.
(2) Restore if necessary. (3) Titanium trauma splint.
(a) Dentin/enamel bonding. (4) The wire must be passive (not cause pressure
(b) Traditional strip crown for primary teeth. on the teeth).
(c) Incisal edge composite. (5) Use either composite or flowable composite.
6. Fracture through enamel, dentin, and pulp. (6) The splint should remain in place for 7 to
a. Primary teeth. 14 days.
(1) Pulpotomy for vital pulps. (7) Long-term rigid splinting of replanted teeth
(2) Pulpectomy for necrotic pulps, if there is increases risk of replacement root resorption
not significant internal or external root (ankylosis).
resorption.
(3) Extraction is the treatment of choice if the 2.9 Miscellaneous Topics
tooth has internal or external root resorption. in Pediatric Dentistry
b. Permanent teeth (see Section 1, Endodontics). A. Mouth guards.
7. Avulsion. 1. Mouth guards are helpful in preventing the frequency
a. Replanting primary teeth. and severity of dentoalveolar injuries.
(1) Poor prognosis. 2. Three main types of mouth guards.
(a) Replantation could be considered if within a. Stock.
30 minutes of avulsion. (1) Available at sporting goods stores.
(b) Splint if necessary. (2) Are not custom-adapted to the teeth.
(c) Soft diet. (3) Inexpensive.
(d) Antibiotic prescription. b. Mouth-formed.
(e) Follow with primary endodontics. (1) Available at sporting goods stores.
(2) Space maintainer if endodontic treatment is (2) Two types.
impossible. (a) The boil and bite-type mouth guard is
b. Replanting permanent teeth (see Section 1, softened in hot water, then adapted to the
Endodontics). teeth.
(b) The shell-type mouth guard has an outer Table 5-9

shell that is firm and an inner liner that is
Dental Procedures That May Cause
made from ethyl methacrylate.
Bacteremia
c. Custom-fabricated.
(1) Impression taken by the dentist. Endocarditis Prophylaxis RecommendedLikely
(2) Two types. Significant Bacteremia*
(a) Vacuum-formedmouth guard is adapted Dental extractions
Periodontal procedures including surgery, subgingival
by heating the mouth guard material in a placement of antibiotic fibers or strips, scaling and root
vacuum molding machine. planing, probing, recall maintenance
(b) Pressure-laminatedhas multiple layers of Dental implant placement and reimplantation of avulsed
material and is subject to less distortion. teeth
(3) Mouth guard is trimmed and smoothed. Endodontic (root canal) instrumentation or surgery only
beyond the apex
(4) Custom mouth guards generally fit better and Initial placement of orthodontic bands but not brackets
are worn more successfully by athletes. Intraligamentary local anesthetic injections
3. Mouth guards should be cleaned daily in cool water. Prophylactic cleaning of teeth or implants where bleeding is
4. Storage should be in plastic retainer cases. anticipated
B. Antibiotic prophylaxis for at-risk patients. Endocarditis Prophylaxis Not RecommendedUsually
1. A few cardiac conditions require antibiotic prophy Insignificant Bacteremia
laxis before rendering dental care that may cause a Restorative dentistry (operative and prosthodontic) with or
without retraction cord
bacteremia. Because of the diversity of circumstances
Local anesthetic injections (nonintraligamentary)
with each patient, it is recommended that the practi Intracanal endodontic treatment; postplacement and
tioner consult with the appropriate medical person buildup*
nel if the complete medical status of the patient is not Placement of rubber dam*
fully known. Postoperative suture removal
Placement of removable prosthodontic or orthodontic
2. Cardiac conditions (important factors).
appliances
a. Cardiac conditions that predispose to endocarditis. Oral impressions
b. Dental procedures that may cause bacteremia Fluoride treatments
(Table 5-9). Taking of oral radiographs
c. American Heart Association prophylaxis Orthodontic appliance adjustment
Shedding of primary teeth
recommendations.
In general, the presence of moderate to severe gingival
3. Compromised immunity. inflammation may elevate these procedures to a higher
a. Patients with compromised immunity may have risk of bacteremia
difficulty combating a bacteremia and require anti *Prophylaxis is recommended for patients with high and moderate cardiac
biotic prophylaxis. risk as well as high-risk prosthesis conditions.
b. Because of the diversity of circumstances with each This includes restoration of decayed teeth and replacement of missing teeth.
patient, it is recommended that the practitioner Clinical judgment may indicate antibiotic use in any circumstances that may
create significant bleeding.
consult with the appropriate medical personnel if
the complete medical status of the patient is not
fully known.
c. Partial list of conditions associated with compro
mised immunity. b. Examples.
(1) Any immunodeficiency or immunosuppres (1) Vascular catheters.
sion. (2) Ventriculoarterial and ventriculovenous shunts
(2) Diabetes. used in hydrocephalus.
(3) Organ transplantation. 5. Patients with prosthetic joints or other implanted
(4) Corticosteroid use. devices require consultation with the childs physi
(5) Sickle cell anemia. cian regarding antibiotic prophylaxis.
(6) Neutropenia. C. Systemic fluoride supplementation.
(7) Lupus erythematosus. 1. Systemic fluoride rule of 6.
(8) Splenectomy. a. If fluoride level is greater than 0.6ppm, no supple
(9) Cancers. mental systemic fluoride is indicated.
4. Shunts, indwelling vascular catheters, and other b. If the patient is less than 6 months old, no supple
medical devices. mental systemic fluoride is indicated.
a. Bacterial colonization may occur with various c. If the patient is more than 16 years old, no supple
medical devices following bacteremia. Antibiotic mental systemic fluoride is indicated.
premedication is indicated. 2. Fluoride table (Table 5-10).
Table 5-10
Fluoride Supplementation Schedule Based
on Fluoride Ion Level (ppm)
AGE <0.3 0.3-0.6 >0.6
Birth6 months None None None
6 months3 years 0.25mg None None
3-6 years 0.50mg 0.25mg None
6-16 years 1.0mg 0.50mg None
D. Candidiasis (thrush, moniliasis).

1. Caused by Candida albicans.
2. Common in newborns or young children after anti
biotic therapy.
E. Anticipatory guidance.
1. Counseling patients and parents regarding the childs
home oral health care that is age-appropriate and is
focused on prevention. Figure 5-49 Fixed digit-sucking appliance.
2. Subjects to discuss with parents.
a. Oral hygiene.
b. Oral development. (3) Bluegrass appliance, which is a fixed appli
c. Fluoride. ance that features a six-sided plastic roller in
d. Diet and nutrition. the anterior palate region.
e. Oral habits. G. Teething.
f. Trauma and injury prevention. 1. Symptoms that have been associated with teething
F. Digit-sucking habits. include increased temperature, drooling, diarrhea,
1. Very common up to age 3. dehydration, and loss of appetite.
2. Risk of malocclusion is a function of amount of time 2. Symptoms other than drooling and slight loss of
per day the habit is practiced, the duration of the appetite should be viewed with suspicion of a sys
habit in terms of weeks and months, and the intensity temic disturbance.
of the habit. 3. With any significant symptoms, the patient should be
3. Effects of digit-sucking. referred to a pediatrician. Serious complications can
a. Increased overjet, owing to proclination of maxil occur if the practitioner overlooks systemic distur
lary incisors and retroclination of mandibular bances by attributing them to teething.
incisors. 4. Teething symptoms may be reduced by using chilled
b. Open anterior bite, owing to supereruption of pos teething rings. Some authors recommend using
terior teeth. topical anesthetic and nonaspirin analgesics.
c. Posterior crossbite, owing to the tongue not being H. Natal and neonatal teeth.
positioned between the maxillary alveolar pro 1. Natal teeth are teeth that are present at birth.
cesses and cheek constriction. 2. Neonatal teeth are teeth that erupt in the first
d. Class II posterior occlusion with prolonged habits. 30 days.
4. Treatment. 3. Most natal and neonatal teeth are primary teeth
a. Traditionally, intervention by the dentist with (90%); very few are supernumerary teeth (10%).
appliance therapy is recommended at age 5 or 6 Most are mandibular incisors (85%).
if the child has not stopped the digit-sucking 4. Treatment.
habit. Some authors now recommend earlier a. Extract supernumeraries.
intervention. b. Extract primary teeth if extremely mobile and
b. Appliances. there is danger of aspiration.
(1) Removable maxillary retainer with rounded c. If the tooth is causing ulceration on the ventral side
stainless steel wire loops placed in the anterior of the tongue (Riga-Fede disease), the tooth may
palate region. be smoothed or extracted.
(2) Fixed reminder appliance in which a stainless d. If the tooth is causing nursing difficulties, a breast
steel crib is placed in the anterior palate region pump or smoothing or extraction may be
(Figure 5-49). recommended.
I. Early childhood caries (ECC). sizearch length deficiency in the permanent

1. ECC definition by the American Academy of Pediatric dentition.
Dentistry (AAPD)the presence of more than one 2. Moyers mixed dentition analysis.
decayed (noncavitated or cavitated), missing (owing a. Basics.
to decay), or filled tooth surface in any primary tooth (1) The combined mesiodistal widths of the man
in a child younger than 6. dibular permanent incisors are used to predict
2. Severe ECC. the combined mesiodistal widths of the patients
a. Younger than 3 yearsany sign of smooth surface buccal segment (cuspidfirst bicuspidsecond
decay. bicuspid).
b. Ages 3 to 5. (2) InstrumentsBoley gauge and study models.
(1) One or more cavitated, missing (owing to (3) Arch length is measured in segments.
caries), or filled smooth surface in primary (a) Anterior segmentchoose a midline point,
maxillary anterior teeth. measure from this point to the mesial of
(2) A decayed, missing, or filled surface (DMFS) each primary canine, and sum.
score of greater than 4 (age 3), greater than 5 (b) Posterior segmentsmeasure from the
(age 4), or greater than 6 (age 5). mesial of each primary canine to the mesial
3. Previously termed baby bottle syndrome or of the first permanent molar.
nursing bottle caries. (4) Measure mesiodistal diameter of the mandibu
4. Typical presentation of baby bottle syndrome. lar incisors and sum.
a. Caries are present on maxillary anterior teeth and (5) Predict permanent buccal segment tooth sizes
primary molars. by using the prediction chart.
b. The mandibular incisors are unaffected because of (6) Total the differences between arch lengths
the tongue covering these teeth during feeding. (space available) and tooth sizes to obtain
c. History often reveals that the child is consistently amount of tooth sizearch length discrepancy.
put to bed with a nursing bottle containing milk or (7) The same procedure is used in the maxillary
a sugar-containing drink. arch except that the predicted tooth sizes of the
5. AAPD recommendations. maxillary buccal segment are still calculated
a. Infants should not be put to sleep with a bottle. Ad from the mandibular incisor measurement.
libitum nocturnal breast-feeding should be avoided b. Incisor region.
after the first primary tooth begins to erupt. (1) Measure mesiodistal diameter of the mandibu
b. Parents should be encouraged to have infants drink lar incisors and sum.
from a cup as they approach their first birthday. (2) Measure the space available for mandibular
Infants should be weaned from the bottle at 12 to incisors.
18 months of age. (3) Subtract (1) from (2); a negative number indi
c. Repetitive consumption of any liquid containing cates crowding in the incisor region.
fermentable carbohydrates from a bottle or no-spill (4) In the example in Table 5-11, there is 3.2mm
training cup should be avoided. of crowding in the anterior region.
d. Oral hygiene measures should be implemented by c. Buccal segment region.
the time of eruption of the first primary tooth. (1) Measure space available for 3-4-5 on each side
e. An oral health consultation visit within 6 months of the arch.
of eruption of the first tooth and no later than 12 (2) Measure from the mesial of each primary
months of age is recommended to educate parents cuspid to the mesial of the first permanent
and provide anticipatory guidance for prevention molar.
of dental disease.
f. An attempt should be made to assess and decrease
the mothers or primary caregivers Streptococcus
mutans levels to decrease the transmission of car
Table 5-11
iogenic bacteria and lessen the infants or childs
risk of developing ECC. Incisor Measurements (mm) for Mixed
g. In children younger than 2 with moderate to high Dentition Analysis
caries risk, a smear of fluoridated toothpaste should LEFT INCISORS RIGHT
be used. All children age 2 to 5 should use a pea-
Space available 19.8
sized amount of fluoridated toothpaste.
J. Mixed dentition analysis. Tooth size 23.0
1. The purpose of this analysis is to predict, in the Difference 3.2
mixed dentition, the amount of crowding, or tooth
(3) In the example in Table 5-12, there is 20.1mm (b) This late mesial shift decreases available
of space available for the mandibular left buccal space because arch length is smaller.
segment and 19.5mm of space available for the (c) Traditionally, 1.7mm is added for each
mandibular right buccal segment. side that is in an end-to-end relationship.
(4) Calculate the size of teeth 3-4-5 from predic (d) In the example, if one side was in an end-
tion table (Table 5-13). to-end relationship, the total amount of
(a) Find the total size of the mandibular per crowding would be 9.7mm.
manent incisors in the top row. 3. Tanaka-Johnson analysis.
(b) The mandibular buccal segment (3-4-5) a. Measurements of space available (arch length) are
tooth size is 22.2mm. the same as for the Moyer analysis.
(c) This tooth size is estimated at the 75th per b. Measurements of the permanent mandibular inci
centile, which essentially means that the sors are the same as for the Moyer analysis.
teeth will be smaller than the predicted size c. Obtain the predicted tooth size for the mandibular
in 75% of patients. buccal segment.
(5) Calculate tooth sizearch length differences in (1) Divide the total tooth size of the mandibular
the buccal segments. incisors by 2.
(a) Subtract tooth size from space available (2) Add 10.5mm.
on the patients left and right buccal (3) For example, if the total mesiodistal widths
segments. of the mandibular permanent incisors were
(b) Negative numbers indicate crowding. 22.8mm, the predicted buccal segment tooth
(c) In the example in Table 5-14, there is size would be 21.9mm ([22.8mm/2] +
2.1mm of crowding in the mandibular left 10.5mm).
buccal segment and 2.7mm of crowding in d. Obtain the predicted tooth size for the maxillary
the mandibular right buccal segment. buccal segment.
(6) To obtain the total amount of predicted crowd (1) Divide the total tooth size of the mandibular
ing, add the three numbers in the difference incisors by 2.
row. In this example, there is 8.0mm of pre (2) Add 11.0mm.
dicted crowding in the mandibular arch. e. The remaining calculations are similar to those for
(7) Allowance for late mesial shift of mandibular the Moyer analysis.
first permanent molars. K. Child abuse and neglect.
(a) If the permanent molars are in an end-to- 1. Dentists are mandated by law to report suspected
end relationship, they must shift mesially to child abuse or neglect. Proof of abuse or neglect is
achieve a class I molar occlusion. unnecessary.
Table 5-12 Table 5-14

Incisor Measurements (mm) with Mixed Dentition Analysis Summary*
Available Spaces for Teeth 3-4-5
LEFT INCISORS RIGHT
for Mixed Dentition Analysis
Space available 20.1 19.8 19.5
LEFT INCISORS RIGHT
Tooth size 22.2 23.0 22.2
Space available 20.1 19.8 19.5
Difference 2.1 3.2 2.7
Tooth size 23.0
*Using data (in mm) from Tables 5-11 to 5-14 and minimum 75% tooth size
Difference 3.2 from Table 5-13.
Table 5-13
Prediction of Available Space for Teeth 3-4-5 (Rows 2 and 3) Based on Incisor Tooth Size
(Row 1)* (mm)
19.5 20.0 20.5 21.0 21.5 22.0 22.5 23.0 23.5 24.0
Maximum 75% 20.6 20.9 21.2 21.5 21.8 22.0 22.3 22.6 22.9 23.1
Minimum 75% 20.1 20.4 20.7 21.0 21.3 21.6 21.9 22.2 22.5 22.8
*Note tooth size = 23.0 from Tables 5-11 and 5-12, with predicted available space in bold.
2. Failure to report suspected child abuse may result in

significant legal ramifications for the dentist, includ
ing a fine, jail sentence, and civil liability.
3. Types.
a. Physical.
(1) Intentional, not accidental.
(2) Common injuries include bruises, welts, lac
erations, burns, and fractures.
(3) 50% of physical abuse is in the craniofacial
region.
(4) 25% of physical abuse is in the oral region.
b. Emotional.
(1) Difficult to identify a causal link between
parental behaviors and harm to the child.
(2) Examples of emotional abuse include denial Figure 5-50 Dry angle usage to maintain a moisture-free
of affection, isolation, extreme threats, and field.
corruption.
c. Sexual.
(1) Generally defined as activity of a sexual nature (c) Toothbrush with pumice or toothpaste.
that is inappropriate for a parent-child (d) 3% hydrogen peroxide.
relationship. (e) Enameloplasty.
(2) Examples of sexual abuse include any form of b. Isolation.
parent-child sexual activity, exhibitionism, and (1) Rubber dam.
pornography. (2) Cotton rolls or dry angles are used with high-
d. Neglect. volume evacuation (Figure 5-50).
(1) Generally defined as willful negligence to c. Acid etching.
provide for the basic needs of a child, such as (1) 35% to 40% phosphoric acid is the most
food, shelter, clothing, medical care, supervi common etchant.
sion, protection, and guidance. (2) 20-second etching time for permanent teeth.
(2) Definition from the AAPDwillful failure of (3) Etchant should not be rubbed into the tooth.
parent or guardian to seek and follow through (4) Some authors recommend longer etching
with treatment necessary to ensure a level of times for primary teeth (approximately 30
oral health essential for adequate function and seconds).
freedom from pain and infection. (5) Wash for 30 seconds.
L. Pit and fissure sealants. (6) Dry with compressed air for 15 seconds.
1. Selection. (7) If a frosty appearance is not achieved, repeat
a. Indications. etching, washing, and drying.
(1) Deep pits and fissures. d. Placement.
(2) Caries-free surface, although sealants placed (1) Some authors recommend a bonding agent
on undetected incipient caries do not result before sealant placement.
in progressive lesions if the sealant remains (2) Ensure that sealant is placed in all occlusal,
intact. buccal, and lingual grooves.
b. Contraindications. (3) Avoid excessive amount of sealant.
(1) Rampant caries. (4) Polymerize sealant according to manufacturers
(2) Interproximal caries. directions.
(3) Well-coalesced grooves. (5) Check occlusion with articulating paper and
(4) Inability to maintain a dry field. adjust occlusion, if necessary.
2. Technique. 3. Resin-based sealants are most common and have
a. Cleaning. superior retention compared with glass-ionomer
(1) It is agreed that it is necessary to have clean pits based sealants.
and fissures to have good retention; how this is 4. The tag formation in the enamel is about 40m.
accomplished varies among authors. 5. Fluoride-containing sealants have similar retention
(2) Methods. rates as conventional sealants and show a 60% reduc
(a) Pumice prophylaxis with rubber cup or tion of secondary caries.
bristle brush. 6. Any saliva contamination after isolation requires
(b) Air polishing device. repeating the wash, dry, etch, wash, dry cycle.
References C. Class I dental malocclusion

Bishara WA: Textbook of Orthodontics, ed 3. Philadelphia, D. Class II skeletal malocclusion
Saunders, 2001. 6. Which of the following reactions is least likely to be
Bolton WA: Disharmony in tooth size and its relation to observed during orthodontic treatment?
the analysis and treatment of malocclusion. Am J Orthod A. Root resorption
28:113-130, 1958. B. Devitalization of teeth that are moved
Casamassimo PS, et al: Pediatric Dentistry, Infancy Through C. Mobility of teeth that are moved
Adolescence, ed 5. St. Louis, Mosby, 2012. D. Development of occlusal interferences
Ciancio SG, et al: ADA Guide to Dental Therapeutics, ed 5. 7. Doubling the force applied at the bracket of a tooth
Chicago, ADA, 2009. would have what effect on the moment affecting tooth
Dean JA, Avery DR, McDonald RE: McDonald and Averys movement?
Dentistry for Children and Adolescents, ed 9. St. Louis, A. The moment would decrease by 50%
Mosby, 2010. B. The moment would not change
Proffit WR, et al: Contemporary Orthodontics, ed 5. St. C. The moment would double
Louis, Mosby, 2013. D. The moment would increase fourfold
8. Class II elastics are used by stretching an elastic
between which of the two following points?
A. From the posterior to the anterior within the max
Sample Questions illary arch
B. From the posterior to the anterior within the man
1. Which of the following statements regarding crowding dibular arch
of the dentition is true? C. From the posterior of the maxillary arch to the
A. Crowding of the primary dentition usually resolves anterior of the mandibular arch
as the permanent teeth erupt. D. From the posterior of the mandibular arch to the
B. Spacing in the primary dentition usually indicates anterior of the maxillary arch
spacing will be present in the adult dentition. 9. When class III elastics are used, the maxillary first
C. Approximately 15% of adolescents have crowding molars ______.
severe enough to consider extraction of permanent A. Move distally and intrude
teeth as part of treatment. B. Move mesially and extrude
D. Lower incisor crowding is more common C. Move mesially and intrude
in African-American individuals than white D. Move mesially only; there is no movement in the
individuals. vertical direction
2. Bones of the cranial base include which of the 10. What is the usual order of extraction of teeth if serial
following? extraction is chosen as the treatment to alleviate severe
A. Maxilla, mandible, and cranial vault crowding?
B. Ethmoid, sphenoid, and occipital A. Primary second molars, primary first molars, per
C. Palatal, nasal, and zygoma manent first premolars, primary canines
D. Frontal and parietal B. Primary canines, primary first molars, permanent
3. According to Scammons growth curves, which of the first premolars
following tissues has a growth increase that can be C. Primary first molars, primary second molars,
used to help predict timing of the adolescent growth primary canines
spurt? D. Primary canines, permanent canines, primary first
A. Neural tissues molars, permanent first premolars
B. Lymphoid tissues 11. A 7-year-old patient has a 4-mm maxillary midline
C. Reproductive tissues diastema. Which of the following should be done?
4. Children in the primary dentition most often present A. Brackets should be placed to close it.
with a (an) ______. B. A radiograph should be taken to rule out the pres
A. Increased overbite ence of a supernumerary tooth.
B. Decreased overbite C. Nothing should be done. It will close on its own.
C. Ideal overbite D. Nothing should be done. Treatment should be
D. Significant open bite deferred until the rest of the permanent dentition
5. An adult patient with a class II molar relationship and erupts.
a cephalometric ANB angle of 2 degrees has which 12. Reduction of overbite can be accomplished most
type of malocclusion? readily by which of the following tooth movements?
A. Class II dental malocclusion A. Intruding maxillary incisors
B. Class II skeletal malocclusion B. Uprighting maxillary and mandibular incisors
C. Using a high-pull headgear to the maxillary molars D. A significantly depressed level of consciousness in
D. Using a lip bumper which the patients ability to maintain an airway
13. Congenitally missing teeth are the result of failure in independently and continuously is retained
which stage of development? 16. The enamel rods in the gingival third of primary teeth
A. Initiation slope occlusally instead of cervically as in permanent
B. Morphodifferentiation teeth. The interproximal contacts of primary teeth are
C. Apposition broader and flatter than the interproximal contacts of
D. Calcification permanent teeth.
14. During an emergency dental visit in which a tooth is to A. The first statement is true, and the second state
be extracted because of extensive pulpal involvement, ment is true.
a moderately developmentally challenged 5-year-old B. The first statement is true, and the second state
child becomes physically combative. The parents are ment is false.
unable to calm the child. What should the dentist do? C. The first statement is false, and the second state
A. Discuss the situation with the parents. ment is true.
B. Force the nitrous oxide nosepiece over the childs D. The first statement is false, and the second state
mouth and nose. ment is false.
C. Use the hand over mouth exercise (HOME). 17. Formocresol has been shown to have a very good
D. Use a firm voice control. success rate when used as a medicament for pulpot
15. Which of the following is the definition of conscious omy procedures. Why is there continued interest to
sedation? find another medicament that performs as well as or
A. A minimally depressed level of consciousness that better than formocresol?
retains the patients ability to maintain an airway A. Application of formocresol is a clinically time-
independently and continuously and respond consuming procedure.
appropriately to physical stimulation or verbal B. Formocresol is toxic, and there is the possibility of
command blood-borne spread to vital organs.
B. A significantly depressed level of consciousness in C. It has been demonstrated that formocresol may
which the patients ability to maintain an airway cause spontaneous abortion.
independently and continuously and respond D. It has been demonstrated that formocresol may
appropriately to physical stimulation or verbal cause failure to develop adequate lung capacity in
command is retained children.
C. A minimally depressed level of consciousness in
which the patients ability to maintain an airway
independently and continuously is retained
18. The following teeth are erupted in an 8-year-old patient. What is the space maintenance of choice?
3 A B C 7 8 9 10 H I 14
30 T S R 26 25 24 23 M L K 19
A. Band-loop space maintainer
B. Lower lingual holding arch
C. Nance holding arch
D. Distal shoe space maintainer
19. The mother of a 5-year-old patient is concerned about 20. Which of the following statements regarding ortho
the childs thumb-sucking habit. On examination 6 dontic closure of a midline diastema in a patient with
months ago, the patient had a 5-mm overjet and a a heavy maxillary frenum is true?
3-mm anterior open bite. Today, the patient has a 10% A. Orthodontic closure is accomplished before frenum
overbite and a 3.5-mm overjet. The mother says that surgery.
the child only sucks his thumb every night when falling B. Orthodontic closure is accomplished after frenum
to sleep. Which of the following is the best advice? surgery.
A. Refer to a speech pathologist C. After orthodontic closure, frenum surgery is typi
B. Recommend tongue thrust therapy cally not indicated.
C. Recommend a thumb-sucking appliance D. After frenum surgery, orthodontic closure is typi
D. Counsel the parent regarding thumb sucking, and cally not indicated.
recall the patient in 3 months
21. In a 4-year-old patient, tooth E was traumatically 28. The nature of the bond between the enamel and the
intruded, and approximately 50% of the crown is resin used to attach an orthodontic bracket is ______.
visible clinically. What is the treatment of choice? A. Chemical
A. Reposition and splint B. Mechanical
B. Reposition, splint, and primary endodontics C. Dependent on whether the resin used is light-cured
C. Reposition, splint, and formocresol pulpotomy or chemically cured
D. None of the above D. Dependent on whether the surface preparation
22. In a 4-year-old patient, the maxillary right primary used is conventional etch or self-etch primer
central incisor was traumatically avulsed 60 minutes 29. In general, the width of the incisors in the primary
ago. What is the treatment of choice? dentition is smaller than the width of their successors
A. Replant, splint, and primary endodontics in the permanent dentition. This is called the leeway
B. Replant, splint, and formocresol pulpotomy space and provides room for eruption of the perma
C. Replant, no splint, and primary endodontics nent incisors.
D. None of the above A. Both statements are true.
23. A young permanent incisor with an open apex has a B. Both statements are false.
pinpoint exposure as a result of a traumatic injury that C. The first statement is true, and the second state
occurred 24 hours previously. Which of the following ment is false.
is the best treatment? D. The first statement is false, and the second state
A. Place calcium hydroxide on the pinpoint exposure ment is true.
B. Open the pulp chamber to find healthy pulp tissue 30. A wire with a low load/deflection rate is capable of
and perform a pulpotomy generating constant forces that do not depend much
C. Initiate a calcium hydroxide pulpectomy on the amount of activation. Bending loops into an
D. Initiate conventional root canal treatment with archwire reduces its load/deflection rate by increasing
gutta-percha wire length.
24. A permanent incisor with an open apex is extruded A. Both statements are true.
4mm following an injury 15 minutes ago. What is the B. Both statements are false.
treatment of choice? C. The first statement is true, and the second state
A. No immediate treatment; monitor closely for ment is false.
vitality D. The first statement is false, and the second state
B. Reposition, splint, and monitor closely for vitality ment is true.
C. Reposition, splint, and initiate calcium hydroxide 31. Which of the following statements best describes the
pulpotomy prognosis of a 12-year-old boy with moderate man
D. Reposition, splint, and initiate calcium hydroxide dibular anterior crowding whose permanent dentition
pulpectomy is fully erupted?
25. Which of the following is the most likely cause of A. Crowding is likely to improve as the arches expand
pulpal necrosis after trauma to a tooth? during the adolescent growth spurt.
A. Ankylosis B. Crowding is likely to improve as the mandible con
B. Calcific metamorphosis tinues to grow anteriorly during the adolescent
C. Pulpal hyperemia growth spurt.
D. Dilaceration C. Crowding is likely to improve as resorption of the
26. Order the sequence of events that occur when heavy anterior portion of the ramus occurs over time.
orthodontic forces are placed on teeth. D. Crowding is not likely to improve over time.
____ A. The PDL experiences compression on the 32. Match the exhibited behavior of a child dental patient
side toward which the tooth is moving with the classification of potentially cooperative
____ B. The alveolar bone experiences undermining patient.
resorption
Exhibited Behavior Classification
____ C. The PDL undergoes hyalinization
____ A. Gripping the arms of 1. Timid
____ D. Frontal resorption occurs at the surface of
the chair very tightly
the alveolus
____ B. Patient says I dont 2. Defiant
27. Which of the following orthodontic wire types would
want to and does
be the best choice for a patient with a known nickel
not open the mouth
allergy?
____ C. Temper tantrum 3. Tense-cooperative
A. Stainless steel
____ D. Shielding behavior 4. Uncontrolled
B. Nickel titanium
C. Beta titanium 33. Order the four plateaus of stage I anesthesia
D. Multistranded cobalt chromium (analgesia).
____ A. Drift 35. Which of the following are likely contraindications for
____ B. Paresthesia performing a pulpotomy on a primary molar? (Choose
____ C. Dream three.)
____ D. Vasomotor A. A patient requiring infective endocarditis antibi
34. Which of the following are characteristics of primary otic premedication
tooth anatomy? (Choose three.) B. A 3-year-old patient
A. Occlusal table is wider C. Swelling associated with the tooth
B. Enamel is thinner D. Furcation radiolucency
C. Greater constriction at the cementoenamel E. Marginal ridge breakdown owing to extensive
junction decay
D. Interproximal contacts are broader and flatter F. A patient with amelogenesis imperfecta
E. Enamel rods in gingival third slope cervically G. A 5-year-old patient with a pinpoint carious pulp
F. Pulp chamber is relatively smaller exposure
SECTION 6
Patient Management
OSCAR AREVALO, MYRON ALLUKIAN, JR.,
MARLA W. DEIBLER, CATHERINE FRANKL SARKIS
OUTLINE with the dental education of the public, with applied dental
research, and with the administration of group dental care
1. Epidemiology
programs as well as the prevention and control of dental
2. Prevention of Oral Diseases diseases on a community basis.
3. Evaluation of Dental Literature Material for this review is drawn from the texts Den-
4. Infection Control tistry, Dental Practice, and the Community, ed 6, by Burt
and Eklund; Management of Pain & Anxiety in the Dental
5. Materials and Equipment Safety
Office, ed 5, by Dionne etal; Jongs Community Dental
6. Dental Care Delivery Systems Health, ed 5, by Gluck and Morganstein; and Wongs Essen-
7. Communication and Interpersonal Skills tials of Pediatric Nursing, ed 7, by Wong etal. Please consult
8. Health Behavior Change these texts and the other references included at the end of
this review for more detailed information. All of the above-
9. Anxiety and Pain Control
mentioned texts are listed in full in the References.
10. Professional Responsibilities and Liabilities
1.0 Epidemiology
Charles-Edward Amory Winslows (1877-1957) definition
of public health is perhaps the most widely accepted and Epidemiology is the study of the distribution and determi-
quoted. Winslow defined public health as the science and nants of disease. In public health, groups of people are
art of preventing disease, prolonging life, and promoting studied to answer questions about etiology of diseases, pre-
physical health and efficiency through organized commu- vention, disease patterns, and allocation of resources.
nity efforts. A. Epidemiologic measures.
Today, a public health problem is defined as an issue that 1. DMFT/DMFSthe conventional method of defining
meets the following criteria: dental caries in a population is to measure either the
number of teeth or the number of tooth surfaces that
A condition or situation that is widespread and has an
are decayed, missing, or filled as a result of caries.
actual or potential cause of morbidity or mortality.
When this measure is applied to the permanent den-
There is a perception on the part of the public, govern-
tition, the acronyms DMFT and DMFS are used;
ment, or public health authorities that the condition is a
when this measure is applied to the primary denti-
public health problem.
tion, the acronyms deft and defs are used, with e
Dental public health has been defined by the American indicating a carious primary tooth that is indicated
Board of Dental Public Health as follows: The science and for extraction. Measuring caries by affected surfaces
art of preventing and controlling dental diseases and pro- (i.e., DMFS or DFS) is more precise than measuring
moting dental health through organized community efforts. caries by affected teeth.
It is that form of dental practice which serves the commu- a. Problems associated with caries indices.
nity as a patient rather than the individual. It is concerned (1) Not related to number of teeth at risk or age.
(2) Can be invalid in older adults.
(3) Preventive restorations.
The section editor acknowledges Bonnie Graham, JD, for her contributions as (4) Sealants.
author of the section on Professional Responsibilities and Liabilities in the first
edition of this book. Bonnie, who passed away in 2010, was a fabulous faculty, 2. Gingival index (GI)the GI of Le and Silness uses
mentor, and surrogate mother to dozens of dental students. six indicator teeth or all erupted teeth. Scoring is on
217
218 Section 6 Patient Management
a scale of 0 to 3, with 0 being normal and 3 being Examination Survey (NHANES), among children
ulcerated tissue with a tendency toward spontaneous 2 to 11 years old, this trend has reversed: a small
bleeding. The GI grades the gingiva on the mesial, but significant increase in primary decay was
distal, buccal, and lingual surfaces of the teeth. The found. This trend reversal was more severe in
GI has been used on selected teeth in the mouth as younger children.
well as on all erupted teeth. The GI assigns grades by b. Early childhood caries (ECC)previously called
applying a four-category qualitative assessment baby bottle tooth decay, ECC is caused by inap-
(normal, mild, moderate, or severe inflammation) to propriate feeding practices that result in pro
four sites on each examined tooth. These values can gressive dental caries on the buccal and lingual
be averaged to yield a score for the individual. surfaces of newly erupted primary maxillary ante-
3. Periodontal indicesseveral indices have been devel- rior teeth of infants and toddlers. The current best
oped in an attempt to provide a standardized method estimate of ECC prevalence in the United States is
of measuring periodontal disease among groups of approximately 5% nationwide. The U.S. Centers for
people in epidemiologic studies, most notably the Disease Control and Prevention (CDC) reported
periodontal index and the periodontal disease index. in 2005 that more than 28% of preschool age chil-
However, both of these indices have been criticized dren have experienced tooth decay. This figure
because they combine gingivitis and periodontitis suggests that more than 4 million children are
measures into a common score. For this reason, these affected nationwidean increase of more than
indices are not considered the best methods to 600,000 additional preschoolers over a decade.
measure periodontal disease. However, the literature indicates important ECC
a. The Community Periodontal Index of Treatment prevalence difference across children of different
Needs (CPITN), developed by the World Health race, ethnic, and socioeconomic backgrounds,
Organization to summarize treatment needs, com- with ethnic minority and lower socioeconomic
bines an assessment of gingival health, pocket status children being at greatest risk.
depth, and the presence of supragingival and sub- c. Coronal caries in adultsthe prevalence of coronal
gingival calculus. Proponents of the CPITN state caries has declined in recent decades among U.S.
that the CPITN allows for a rapid, simple, uniform adults. However, more than 90% of U.S. adults
method by which the average periodontal status older than 20 years of age have at least one decayed
and treatment needs of populations can be deter- or filled tooth. The prevalence of caries among
mined using minimal equipment. Critics of the dentate adults 20 years and older increases with age
CPITN, including the American Academy of Peri- until 59 years old, after which it plateaus at approx-
odontology, argue that combining gingival health, imately 30 decayed and filled surfaces. Data from
pocket depth, and presence of calculus into one U.S. national surveys of adults indicate that among
score is inconsistent with current approaches to dentate adults older than 20, the mean number of
describing periodontal disease and that failure of decayed and filled permanent teeth (DFT) was 8.0
the CPITN to measure gingival recession leads to and the mean decayed and filled permanent sur-
an inaccurate estimate of attachment loss. faces (DFS) was 20.9. Similarly, it has been deter-
4. Simplified Oral Hygiene Index (OHI-S)the OHI-S mined that whites have significantly higher coronal
sets forth a method of quantifying the amount of DFS compared with nonwhites. For instance,
plaque and calculus in its two components, the debris according to data from NHANES 1999-2002,
index and the calculus index. These components are whites had a mean coronal DFS twice as high as
added to obtain a single score. The OHI-S has been African-Americans (i.e., 23.1 surfaces in whites
widely used in surveys. It is quick and practical, versus 12.1 surfaces in African-Americans).
although its lack of sensitivity makes it less useful in d. Root surface cariesaccording to NHANES 1998-
the individual patient than in a group. 2002, approximately 18% of dentate adults older
B. Epidemiology of oral diseases. than 20 had root caries. Although the prevalence
1. Cariesa pathologic process of localized destruction has decreased compared with previous national
of tooth tissues by microorganisms. surveys, root surface caries is three times higher
a. Caries in childrenimportant changes have among adults 60 years and older compared with
occurred in the prevalence of dental caries in the adults younger than 40. This prevalence is lower
United States. The prevalence of caries in the for whites compared with other racial groups.
United States declined substantially from the early 2. Periodontal diseasesLoe defined periodontal
1970s until the mid-1990s as a result of fluorida- disease as a group of lesions affecting the tissues
tion, the use of fluorides, and other preventive surrounding and supporting the teeth in their
measures. From the mid-1990s until the most sockets. Most cases of periodontal disease can be
recent (1999-2004) National Health and Nutrition classified as either gingivitis or periodontitis.
Section 6 Patient Management 219
a. Gingivitisthe prevalence of gingivitis among Among African-Americans, the 5-year survival rates
school-age children has been reported to be 40% are 51.6% for women versus 42.9% for men. In 2010,
to 60%. National survey data suggest that the prev- approximately 275,193 individuals had a history of
alence of gingivitis declines from its highest preva- cancer of the oral cavity and pharynx181,084 men
lence during the second and third decades and and 94,109 women.
remains relatively constant after age 30. According
to NHANES III, among the U.S. population
20 years and older, the prevalence of gingivitis 2.0 Prevention of Oral Diseases
was 53%.
b. Chronic periodontitischronic periodontitis is the A. Introduction.
most common form of periodontitis. The preva- 1. Prevention is classified into three different levels.
lence, extent, and severity increase with age. A a. Primary preventionprevents the disease before
study that used NHANES 2009-2010 data indi- it occurs. This level includes health education, dis-
cated that the total prevalence of periodontitis in ease prevention, and health protection. Examples
adults 30 and older was 47.2%. This figure repre- include community water fluoridation and seal-
sents about 64.7 million adults 30 and older in the ants. Preventing a disease before it occurs is the
United States. According to the same study, peri- most effective way to improve health and control
odontitis ranged from 24.4% in adults 30 to 34 to costs.
70.1% in adults 65 and older. b. Secondary preventioneliminates or reduces dis-
3. Oral canceraccording to the National Cancer eases after they occur. Examples include amalgam
Institute, 41,380 (29,620 men and 11,760 women) and composite restorations. This level requires
new cases would be diagnosed and 7890 men and more resources than primary prevention and is
women would die of cancer of the oral cavity and more costly.
pharynx in 2013. Most of these are epidermoid car- c. Tertiary preventionlimits a disability from a
cinomas and squamous cell carcinomas. Surveil- disease or rehabilitates an individual in later stages
lance, Epidemiology, and End Results (SEER) data to restore tissues after the failure of secondary pre-
(2006-2010) indicate that the annual age-adjusted vention; this is the most costly type of prevention
incidence of oral and pharyngeal cancer in the for an individual. Examples include dentures,
United States is 10.8 new cases per 100,000. These crowns, and bridges.
rates vary substantially by gender, with men showing 2. Prevention may be on a community or population
an annual age-adjusted incidence rate of 16.2 per basis or individual basis. Table 6-1 provides an over-
100,000 compared with 6.2 per 100,000 for women. view of effective community and individual preven-
In the United States, oral cancer represents about 4% tive measures for dental caries prevention. Only
of all cancers and 2.2% of all cancer deaths. The inci- effective or evidence-based preventive measures
dence of oral and pharyngeal cancers increases with should be used.
age and alcohol or tobacco use and is uncommon a. On a community level, preventive measures may
before age 40. The overall rate of new cases of disease be implemented in a school, neighborhood, city,
has been stable in more recent years. However, there town, state, or nation. Prevention on a community
has been a more recent increase in cases of oro level is usually the most cost-effective and most
pharyngeal cancer linked to infection with human practical, because everyone in the target popula-
papillomavirus. tion benefits, such as in a school fluoride or sealant
Cancers of the lip and oral cavity account for prevention program or a fluoridated community.
approximately two thirds of all new oral and pharyn- b. On an individual basis, preventive measures may
geal cancers, with the tongue being the most common be implemented in a dental office or community
site of incident cancers of the oral cavity. According setting. On an individual level in a dental office,
to SEER, in 2006-2010, whites had a higher incidence the person needs to be motivated to seek out the
of oral and pharyngeal cancers compared with other service and have the ability to pay for the service.
racial groups. These requirements limit access to preventive ser-
From 2006-2010, the median age at diagnosis of vices for some individuals.
cancer of the oral cavity and pharynx was 62 years, B. Community-based and school-based prevention.
and the median age at death was 67. Overall, the 1. Community water fluoridationthe CDC has recog-
5-year survival rate for oral and pharyngeal cancers nized community water fluoridation as one of the
is approximately 63%. However, survival rates vary ten great public health achievements of the twentieth
considerably depending on gender and race. For century. Community water fluoridation refers to
instance, 5-year survival rates for white Americans is the adjustment of the concentration of fluoride of a
64.7% compared with 44.5% for African-Americans. community water supply for optimal oral health. The
Table 6-1
Effective Community and Individual Preventive Measures for Dental Caries Prevention
MEASURE METHOD OF APPLICATION TARGET PERIOD OF USE
Community Programs
Community water fluoridation Systemic Entire population Lifetime
School water fluoridation Systemic Schoolchildren School years
School fluoride tablet program Systemic Schoolchildren Age 5-16 yr
School fluoride rinse program Topical Schoolchildren Age 5-16 yr
School sealant program (professionally applied) Topical Schoolchildren Age 6-8 and 12-14 yr
Individual Approach
Prescribed fluoride tablets or drops Systemic Children Age 6 mo6 yr
Professionally applied fluoride treatment Topical Individual need High-risk populations
Over-the-counter treatments Topical Individual need High-risk populations
Fluoride toothpaste Topical Entire population Lifetime
Professionally applied dental sealants Topical Children Age 6-8 and 12-14 yr
From Gluck GM, Morganstein WM: Jongs Community Dental Health, ed 5. St. Louis, Mosby, 2002.
recommended level of fluoride for a community of many other fluoride-containing products now
water supply in the United States ranges from 0.7 to available, such as fluoride rinses, toothpastes, and
1.2 parts per million (ppm) of fluoride, depending on professionally applied treatments, in the United
the mean maximum daily air temperature over a States, the measurable effectiveness of community
5-year period. In the United States, most communi- water fluoridation in the United States is about 20%
ties are fluoridated at approximately 1ppm, which is to 40%. These fluoride products have an additive pre-
equivalent to 1.0mg of fluoride per liter of water. ventive benefit to fluoridation.
Based on epidemiologic studies of communities that All health care providers have a responsibility to
were naturally fluoridated, community water fluori- educate their patients about the safety and effective-
dation was first initiated as a clinical trial in 1945 in ness of community water fluoridation, whether or
Grand Rapids, Michigan, on a trial basis. not their community is fluoridated, in addition to
In 2012, there were more than 210 million Ameri- other preventive measures.
cans living in fluoridated communities, or about 74% 2. School water fluoridationschool water fluoridation
of the U.S. population living in areas with public was developed and tested in the United States in the
water supplies. In 2011, the U.S. Department of 1960s for use in rural schools with an independent
Health and Human Services (DHHS) proposed water supply. Fluoridation of water supplies of indi-
decreasing the recommended levels of fluoride to vidual schools is similar to community water flu
0.7ppm because more recent data have shown that oridation in that no direct action is required of
over time, water consumption is relatively the same beneficiaries other than direct consumption of or use
regardless of the air temperature of a community. As of the water in food preparation. The major differ-
of March 2014, this change has not been imple- ence is that the recommended concentration for
mented, but it is expected to be in the near future. school water fluoridation is 4.5 times the concentra-
At 0.7ppm or 1.0ppm, fluoridated water is safe, tion of fluoride recommended for community water
odorless, colorless, and tasteless. Of all the measures supplies in the respective geographic area. The higher
used to prevent dental caries in the United States, concentrations are recommended to compensate for
water fluoridation is the most economical and cost- part-time exposure because children spend only part
effective. of their time at school. Studies conducted on school
Fluoridation is considered the foundation for fluoridation have shown that a 20% to 30% reduction
better oral health for a community. The effectiveness in caries can be expected when children have con-
of fluoridation is well documented, and water fluori- sumed school water fluoridation for 12 years. The
dation prevents tooth decay for people of all ages. practicality of school water fluoridation is good when
Early studies demonstrated that fluoridation prevents a community does not have a central water supply. All
50% to 70% of caries in the permanent teeth of the children benefit with no individual effort required
children. However, because of the widespread use on the part of the recipient.
3. Salt fluoridationin countries that do not have a safe fluoride tablets on school days provides up to a
public water supply or where community water fluo- 30% reduction in new carious lesions.
ridation is not practical or feasible, community salt Because the daily compliance required for this
fluoridation may be used. Salt fluoridation is the con- regimen at home on an individual basis for 16
trolled addition of fluoride during the manufacturing years may be more than most parents can achieve,
of salt for use by humans. Fluoride is added to salt this preventive method often is used in schools on
products such as the salt used domestically, table salt, a classroom basis. The daily consumption of fluo-
bakers salt, and salt distributed in bulk quantities to ride tablets or lozenges in school settings is an
the food industry. The recommended fluoride con- excellent method to use in areas where the water
centration ranges from 200 to 350mg of fluoride per is fluoride-deficient.
1kg of salt, depending on the communitys or coun- See the Pedodontics section for fluoride supple-
trys circumstances. Community salt fluoridation has mentation chart.
benefits similar to water fluoridation and can prevent c. Fluoride mouth rinsefluoride mouth rinse has
dental caries by 33% to 66%. The combination of been used in schools in the United States for
both salt fluoridation and water fluoridation in a approximately 4 decades, and it is the most popular
community or country is not recommended. Salt school-based fluoride regimen in the United States.
fluoridation is not used in the United States. Fluoride rinse solutions are used to provide the
4. Fluoride supplementsfluoride supplements are tooth enamel surface with a constant supply of
available only by prescription and are intended for fluoride ions, which help remineralize initial
use by children at risk for dental caries who live in carious lesions. This method is recommended only
nonfluoridated areas. For optimal benefits, use of for children 6 years old or older because younger
fluoride supplements should begin when a child is 6 children may swallow the solution. For this reason,
months old and be continued daily until the child is fluoride rinse solutions are not appropriate for the
16 years old. The need for taking fluoride supple- treatment of infants with ECC. The rinsing is gen-
ments over an extended period of time makes dietary erally supervised in classrooms by teachers or adult
fluoride supplements less cost-effective than water volunteers. This procedure is usually not used in
fluoridation; fluoride supplements are considerably schools in communities that have been fluoridated
less practical as a widespread alternative to water for 3 or more years.
fluoridation as a public health measure. Numerous studies have demonstrated that
Before prescribing any fluoride supplement, an dental caries can be prevented by approximately
accurate assessment of all potential sources of fluo- 25% to 28% by rinsing daily or weekly in school
ride intake should be explored. Fluoridated water with dilute solutions of fluoride. Rinsing weekly
may be consumed from sources other than the home with a 0.2% neutral sodium fluoride (NaF) solution
water supply, such as the workplace, school or day requires fewer supplies and less time than daily
care, bottled water, filtered water, and from processed rinsing with a 0.05% NaF solution
beverages and foods prepared with fluoridated water. 5. Sealantsa fissure sealant is a plastic, professionally
If the daily intake of fluoride is insufficient, parents applied material used to occlude the pits and fissures
should be informed that small daily dosages are ben- of teeth. The objective is to provide a physical barrier
eficial to a childs teeth. to the impaction of substrate for cariogenic bacteria
a. Fluoride dropsfluoride supplementation can best in those crevices and to prevent caries from develop-
be accomplished initially by the use of fluoride ing. Sealants are recommended for the first and
drops. Around the age of 3, the drops can be second permanent molars for children at risk for
replaced by chewable fluoride tablets or lozenges. dental caries. Sealants also can halt the carious
For children in the first 3 years of life, studies show process after it has begun and can be used as a form
47% less caries experience in the primary teeth and of prevention or treatment for incipient caries in pits
43% less for 3- to 6-year-olds. and fissures.
b. Tablets and lozengesanother method for admin- The use of fluorides is the best approach to pre-
istering systemic fluoride is in school settings by venting caries. However, fluoride is believed to be
the daily use of dietary fluoride supplements in the least effective on the occlusal or chewing tooth sur-
form of chewable tablets or lozenges. Supervised, faces. Because most decay among school-age chil-
self-administered use of fluoride tablets is a well- dren occurs on the chewing surfaces, pit and fissure
established regimen that has been used in the sealants are needed to provide nearly total caries pre-
United States and abroad for more than 47 years. vention. The effectiveness of dental sealants on per-
Lozenges and chewable fluoride tablets provide manent first molars has been reported to be 71.3%
topical and systemic benefits. Studies conducted in for 5 years and 65% for 9 years after the initial appli-
the United States have shown that the daily use of cation of the sealant.
6. Topical fluoridethe application of topical fluoride to b. Health literacy is the capacity at which individuals
the teeth increases tooth resistance to caries, espe- obtain, process, and understand basic health infor-
cially on smooth surfaces. It is more effective for indi- mation and services. It is an important skill for
viduals at high risk for tooth decay. The fluoride can both patients and oral health professionals in pre-
be delivered either brushed as a varnish or in a tray as venting and managing diseases and for navigating
a gel. Topical fluoride applications are not usually the health care system to facilitate access.
cost-effective in community-based or school-based C. Office-based preventive measuresoffice-based mea-
prevention programs. Fluoride gels are discussed in sures include sealants, topical fluoride, fluoride supple-
the office-based preventive methods section. ments, and health education. Sealants, supplements,
a. Fluoride varnishesfluoride varnishes were ac- and health education were discussed previously. Only
cepted for use in the United States in 1994 and are topical fluoride gels and foams are discussed in this
used in place of topical fluoride solutions or gels section.
when they are easier to apply. Fluoride varnish is 1. Fluoride gels and foamsthe fluoride gel compounds
considered a vehicle for holding fluoride in close that dental professionals routinely use in tray applica-
contact with the tooth for a longer period of time, tions are highly concentrated. Careful attention is
but it is not a substitute for dental fissure sealants. required for the technique, the amounts used, and
A theoretical advantage of varnishes over other the 4-minute exposure time. Fluoride gels and foams
methods of professional fluoride application is that prevent tooth decay by about 26% on permanent
varnishes are adhesive and should maximize fluo- teeth of children living in nonfluoridated communi-
ride contact with the tooth surface. Varnishes are ties. Professional gel tray applications have long been
a way of using high fluoride concentrations in considered not to be cost-effective for public health
small amounts of material. programs, although they might be a reasonable
Tooth decay prevention by fluoride varnishes is approach for highly susceptible special groups in tar-
expected to be similar to other topical fluorides. In geted initiatives.
primary teeth, the range is 18% to 25%. Fluoride Since the early 1960s, acidulated phosphate fluo-
varnishes may be especially useful to prevent root ride (APF) has become the most widely used fluo-
surface caries among the growing number of older ride compound for professional application. APF
adults who have gingival recession. In addition, has a pH of about 3.0 and was developed after
fluoride varnishes may be especially practical for experimental work showed that the topical uptake of
use with very young children, elderly adults, indi- fluoride by enamel was greater in an acidic environ-
viduals with disabilities, and bed-bound patients ment. The agent has been tested in several concen-
who still have their own teeth. Fluoride varnishes trations, the most common being 1.23% fluoride,
are also used in programs to help prevent infant usually as NaF, in orthophosphoric acid. The mate-
caries or ECC in high-risk children. Most states rial is nonirritating and nonstaining, tolerates the
allow physicians to provide varnishes to at-risk addition of flavorings, and is well accepted by
children in their offices. patients.
7. Mouth guardsmouth guards may be made for ath- Procedures for the professional application of
letes as a community program in the schools or on fluoride agents were originally developed on the
an individual basis in the dental office. See Pedodon- assumption that the fluoride would form a fluorapa-
tics section. tite in the crystalline structure of the enamel. A
8. Health education and health literacy. prophylactic treatment was considered mandatory
a. Health education is necessary at all stages of before the application of the fluoride to maximize
designing, implementing, evaluating, and continu- this reaction. Subsequent research showed that high-
ing oral health programs. The scope of health edu- concentration fluoride, such as that in APF gels,
cation may include educational interventions for tends to form a calcium fluoridelike material on
children, parents, policy makers, or health care the enamel surface and serves as a reservoir of fluo-
providers. Education of all relevant groups is a ride that becomes available for remineralization
critical factor in the process to gain acceptance and when pH decreases. As a result of the formation of
use of preventive measures, although education this calcium fluoridelike material, a prophylaxis
alone cannot function as a method to prevent dis- before a professional fluoride application is unneces-
ease. Knowledge is a confidence-building element. sary because it is no more beneficial than tooth-
Lacking appropriate knowledge, individuals can brushing and flossing by the patient.
neither make nor be expected to make intelligent D. Home-based preventive methodshome-based meth-
decisions about their oral health or, in the case ods include brushing, interdental cleaning, diet,
of decision makers, for the oral health of their fluoride gels, and fluoride mouth rinses (discussed
constituents. previously).
1. Brushingdental plaque has been depicted as the base that does not contain an abrasive system. Rec-
root cause of both caries and periodontal disease. ommended use involves toothbrushing with gel
Brushing is an individual approach for mechanical (similar to using a dentifrice), allowing the gel to
plaque removal and aids in removing the source of remain in the oral cavity for 4 minutes, and then
tooth decay. expectorating thoroughly. Fluoride gels for home use
a. In terms of frequency of brushing to prevent peri- are an adjunct to the use of professional, topical fluo-
odontal disease, the limited existing information ride application and fluoride dentifrices as a collec-
indicates that a thorough oral cleansing should be tive means of achieving caries control in patients who
carried out at 24- to 48-hour intervals. Consider- are especially prone to caries formation.
ing the time needed for plaque to mature bacterio-
logically, brushing after every meal is unnecessary
to prevent gingivitis. But because toothbrushing 3.0 Evaluation of Dental Literature
with a fluoride toothpaste is also a major source of
fluoride exposure for caries prevention, it is best A. Types of studiesepidemiologic studies can be orga-
carried out at least twice per day using a pea-sized nized into three categories: descriptive, analytical, and
amount of fluoride toothpaste to maintain oral experimental.
health. Brushing in the morning and evening fits 1. Descriptive epidemiologydescriptive epidemiology
with most peoples daily routines and should be the is used to quantify disease status in the community.
basis for education of the public and dental patients. However, for disease quantification to be descriptive
For children younger than age 6, brushing with of a group, it must be seen in proportion to it. The
fluoridated toothpaste should be supervised by an major parameters of interest are prevalence and
adult to avoid unnecessary toothpaste ingestion. incidence.
2. Interdental cleaningthere is limited evidence that a. Prevalenceindicates what proportion of a given
interdental cleaning, by floss or interdental brushes, population is affected by a condition at a given
reduces interdental gingivitis and plaque more than point in time. It is expressed as percentage and
toothbrushing by itself. The rationale for supple- ranges from 0% to 100% (e.g., the prevalence of
menting toothbrushing with use of dental floss, inter- periodontal disease among 100,000 adolescents
dental brushes, or wood points to clean below the was 5%).
contact areas is that even assiduous use of the tooth-
brush usually cannot penetrate these areas efficiently.
Flossing does not prevent tooth decay but may be
helpful for gingival health. b. Incidenceindicates the number of new cases that
3. Dietthe precise cariogenicity of any food is not are expected to occur within a population over a
easily predicted. Controlling dental caries through period of time (e.g., the incidence of people dying
diet modification is complex and has been only mod- of oral cancer is 10% per year in men 55 to 59 in
erately successful. Adequate oral hygiene immedi- our community).
ately after the ingestion of cariogenic foods and
reducing the consumption of cariogenic food may be
helpful in reducing the incidence of dental caries.
When there is a general decline in the incidence of 2. Analytical epidemiologyalso called observational
caries, there is a weaker association between sugar epidemiology, analytical epidemiology is used to
consumption and the incidence of caries, especially determine the etiology of a disease. The researcher
when there is an optimal concentration of fluoride in tries to establish a causal relationship between the
the drinking water. In general, it is more important factors and disease. Three study designs are com-
to control the frequency of sugar consumption and monly used: cross-sectional study, case-control study,
whether it is consumed during daytime activity or and cohort study (prospective and retrospective).
immediately before bedtime and the length of time a. Cross-sectional studystudy in which the health
that residual food material, especially sticky sweets, conditions in a group of people who are, or are
remain in the mouth after eating. A diet that is gener- assumed to be, a sample of a particular population
ous in vegetables and fruits and is light in processed (a cross section) is assessed at one time. Consider
foods is recognized universally as compatible with the hypothesis that drinking alcohol increases the
general health and dental health. risk of developing oral cancer. If researchers chose
4. Fluoride gelsfluoride gels for home use are available to conduct a cross-sectional study to explore this
as additional measures to help achieve caries control. hypothesis, they might examine a group of men
These gels contain either stannous fluoride (0.4%) or who drink alcohol and compare the occurrence
NaF (1.0%) and are formulated in a nonaqueous gel of oral cancer among men who are not alcohol
drinkers. The researchers could then determine of prevention or therapy. There are two types: clinical
whether there is an association between the pres- trials and community trials.
ence of oral cancer and alcohol. Although this a. Clinical trialsClinical trials attempt to evaluate
study is relatively quick and inexpensive, its poten- the effects of a treatment. A clinical trial aims to
tial to contribute to a judgment of causation is isolate one factor (e.g., a new drug) and examine
limited because it cannot determine whether the its contribution to a patients health by holding all
outcome (in this case, oral cancer) occurred before other factors as constant as possible. Well-designed
the men started drinking or if it developed as a clinical trials use a double-blind design in which
result of some other cause (e.g., metastasis). neither the subject nor the investigator knows to
b. Case-control studypeople with a condition which group a subject belongs. This design helps
(cases) are compared with people without it prevent the potential for a biased interpretation of
(controls) but who are similar in other character- treatment effect (better or worse) that might occur
istics. Hypothesized causal exposures are sought in if either the investigator or the subject knew
the past medical records of the participants. If the to which treatment group (i.e., placebo or experi-
researchers had chosen to conduct a case-control mental agent) a subject belonged. Clinical trials
study to explore the same hypothesis, subjects compare the incidence of disease and side effects
would have been split into two groupssubjects between the groups in the study to draw inferences
with oral cancer and subjects without it, based on about the safety and efficacy of the treatment or
examinations. To search for an association with treatments under investigation.
alcohol drinking, a history before the occurrence b. Community trialsin a community trial, the group
of oral cancer would be sought (e.g., through past as a whole is studied rather than the individuals in
medical records). The case-control study could it. The more similar the communities, the more
establish a temporal relationship between the valid the results. A known example of a commu-
exposure and disease of interest, in this case, a nity trial was the 1945 Newburgh-Kingston water
history of alcohol drinking before the appearance fluoridation trial. In this study, NaF was added to
of oral cancer. the water of Newburgh, New York, and DMFT was
c. Cohort study. compared with Kingston, New York, which was
(1) Prospective cohort studya general population nonfluoridated.
is followed through time to see who develops B. Components of a scientific articlefollowing is the
the disease, and the various exposure factors standard format of most of the scientific research that
that affected the group are evaluated. In this appears in journals.
case, the investigators choose or define a sample 1. Titlethe title of the study briefly indicates the topic
of subjects who do not yet have the outcome of and the focus of the study. The text of the title should
interest, such as oral cancer. The investigators reflect or indicate the central question being posed.
measure risk factors in each subject (e.g., 2. Abstractthe purpose of the abstract is to allow the
habits) that may predict the subsequent reader to determine quickly whether the study is of
outcome. They follow these subjects with peri- interest. The abstract, which usually appears at the
odic surveys or examinations to detect the head of the article and is often reproduced in the
outcome or outcomes of interest. Following the literature database, summarizes the background and
group over a period of time, the investigators focus of the study, the population sampled or objects
describe the prevalence of outcomes (e.g., oral studied, and the experimental design. It also includes
cancer) in the cohort. They then compare the a brief statement of the findings and the conclusions.
prevalence of the disease in men who drink In addition, the abstract may include key words that
alcohol with the prevalence of men who do not allow the study to be indexed in the database.
drink. 3. Introduction, literature review, and hypothesisin the
(2) Retrospective cohort studyused to evaluate the introduction, the researcher attempts to educate the
effect that a specific exposure has had on a reader regarding the importance and the history of
population (e.g., occupational hazards). Inves- the problem. Past controversies are summarized, and
tigators choose or define a sample of subjects the question is clarified. In the literature review, the
who had the outcome of interest. They measure researcher provides a summary of the field to date. It
risk factors in each subject that may have pre- is the obligation of the researcher to make the reader
dicted the subsequent outcome. aware of the relevant past research and findings;
3. Experimental epidemiologyexperimental epidemi- to define the key issues, variables, and questions
ology is used primarily in intervention studies. When involved; and to create a context and rationale for the
etiology has been established, the researchers try to current study. The theory being tested is stated,
determine the effectiveness of a particular program and the rival hypotheses are reviewed. Finally, the
researcher clearly states the research question or the undertaken, additional observations, and related
hypotheses being tested. findings. This post hoc analysis may provide im-
4. Methodsthe methods section organizes the research portant cues for future studies and explorations of
article and allows the reader to assess the validity of the topic.
the study and the reliability of the measures. The 6. Discussionafter the results are presented, the exper-
reader should be provided with specific and detailed imenter interprets and explains the results obtained.
information regarding how the study was conducted. In this section, the researcher attempts to make
From this description, the reader should be able to sense of the findings. The first step in this discussion
replicate the study. This section, combined with the is to review the hypothesis and theory in the light of
results section, provides the reader an opportunity to the findings. When the study is concerned with prod-
develop an independent understanding of what this ucts or epidemiologic investigations, inferences are
research study has found and to evaluate the legiti- drawn about the material or the population, and an
macy of the conclusions offered by the author at the evaluation is made of the assumptions that led to the
conclusion of the report. Although the author may original study.
be tempted to interpret or extend the study findings Although such findings as statistical significance
in the discussion and conclusion sections, the reader may be reported, it is also interesting for the
should be able to develop an independent conclusion researcher to speculate on the effects of the method-
after reviewing the methods and results section. The ology, unanticipated characteristics of the subjects or
methods section usually includes four subsections: of the conditions, and possible limitations of the
a. Sampling strategyprovides a description of the theory. Although many readers rely on reports of
sampling strategy, the sample size, and the methods statistical significance to determine the value of a
for assigning samples to conditions. study, commentaries in statistical and research meth-
b. Measurement strategies and measurement instru- odology journals have criticized this approach in
mentshow the variables are measured deter- favor of an approach that emphasizes effect size and
mines exactly what is being studied. Although the variance analysis.
variables studied are discussed in the abstract, the Because research seldom genuinely proves or
introduction, and the conclusion, the actual defini- disproves a hypothesis, the discussion is likely to
tions of the variables are stated in the measurement focus on the level of statistical support for the theory
strategy. and the additional information provided by the sec-
c. Experimental designdescribes operationally the ondary, or post hoc, analysis of the data. Also, the lab
study design in a step-by-step sequence. The notebook (incidental and general observations) can
description should be sufficiently detailed so that be used to shed light on the research findings.
the reader is able to replicate the study. Perhaps the subjects did not comply with the experi-
d. Statistical analytical proceduresthe proposed mental protocol, or perhaps the subjects were influ-
strategy for quantifying, evaluating, and analyzing enced by external conditions. The discussion session
the results is presented along with the actual is an opportunity for the researcher to editorialize
statistical procedures proposed. In the discussion, and dialogue with the reader and to propose different
the experimenter describes how the appropriate ways to conceptualize the outcome data and to recon-
sample size was determined (level of power chosen ceptualize the theory.
and effect size criteria). The proposed statistical 7. Summary and conclusionsat the end of the article,
analytical procedures are specified, and the chosen the researcher provides a summary and interpreta-
statistical significance level is stated. tion of the study findings and attempts to draw con-
5. Resultsin the results section, the researcher de- clusions related to the original theory and study
scribes the specific findings and actual outcomes question. Often, the commentary editorializes and
of the project. The findings are reported clearly and goes beyond the actual findings to use the analysis as
descriptively but are not interpreted. Tables, charts, a basis for speculation and suggestions for future
and graphs, where appropriate, are used to support research. These speculations may go far beyond the
the narrative, which provides a qualitative and quan- actual findings of the study.
titative descriptive and inferential statistical review. 8. References and bibliographyaccurate primary refer-
Subject characteristics are described, and the out- ences are provided to the reader so that it is possible
comes from the measurements of the dependent vari- to pursue the problem further and to learn more.
able are reported. The experimenter provides, where Where established research design methodologies,
relevant, such statistics as statistical significance, cor- instruments, observation guidelines, and statistical
relation, risk ratio, and effect size. After reporting the techniques are used, their source in the literature
results of the test of the hypotheses, the experimenter should be provided so that the reader can verify and
also provides the results of any secondary analyses follow up what is asserted. Studies and formal reviews
should be documented so that the reader can draw

an independent conclusion as to their content and
findings.
C. Basic statisticsa basic understanding of general bio-
statistics principles provides the foundation for the
important skill of critically interpreting new informa-
tion as it becomes available in the scientific literature
and via presentations.
1. Statistics can be defined as the practice, study, or
result of the application of mathematical functions to
collections of data to summarize or extrapolate that
Figure 6-1 Normal distribution.
data. Biostatistics is the science of statistics applied to
the analysis of biologic or medical data. The subject
of statistics can be divided into descriptive statistics,
or describing data, and analytical statistics, or drawing
conclusions from data.
2. Frequency distributionsthe distribution of mea-
surements may take various different forms. Some
more common situations are described next. Let us
assume that each of these distributions represents the
times required by a group of 100 dental students to
complete a restorative dentistry final examination.
The time limit to complete the examination was
1 hour.
Figure 6-2 Positive skewed distribution.
a. Normal distributiona substantial number of nat-
urally occurring phenomena are approximately
distributed according to the symmetrical, bell-
shaped, or normal distribution as shown in Figure
6-1. For this particular group of students, there was
one clear average time. About as many finished
faster than average as finished slower than average,
and we have a bell-shaped distribution as a result.
b. Skewed distributionasymmetrical frequency dis-
tributions are skewed distributions. Positively
skewed (to the right) distributions and negatively
skewed (to the left) distributions can be identified
by the location of the tail of the curve (not by the Figure 6-3 Bimodal distribution.
location of the humpa very common error).
Positively skewed distributions have a relatively
large number of low scores and a small number of the following series of observations (21, 23, 29, 20,
very high scores (Figure 6-2), whereas negatively 18, 22, 14), the mean would be calculated as
skewed distributions have a large number of high follows.
scores and a relatively small number of low scores. (1) Add up the observations.
For this particular group of students, we ended up
21 + 23 + 29 + 20 + 18 + 22 + 14 = 147
with positively skewed (right-skewed) distribu-
tion. A relatively large number of students com- (2) Divide the result from (1) by the number of
pleted the examination in a short time, whereas a measurements.
small number of students completed the examina-
147/7 = 21
tion toward the end of the time.
c. Bimodal distributiona peak in a distribution is b. Medianthe median is the middle measurement
called a mode. When a distribution has two peaks in a set of data where half the data are above and
(Figure 6-3), it is called a bimodal distribution. half the data are below the number. To find the
3. Measures of central tendency. median, two steps must be followed:
a. Meanthe mean or average is the value obtained (1) Sort the observations in order of magnitude.
by adding all the measurements and dividing
by the number of measurements. For example, for 14, 18, 20, 21, 22, 23, 29
(2) Find the middle number. units. To overcome this, the square root of the vari-
ance is generally used as a measure of spread in
14, 18, 20, 21, 22, 23, 29
preference to variance itself.
c. Modethe mode is the most frequent measure- 5. Inferential statistics.
ment in a set of data. a. Statistical significancethe p value is the final
arithmetic answer that is calculated by a statistical
0, 1, 1, 2, 2, 3, 4 test of a hypothesis (H0, called the null hypothesis).
1, 2 Its magnitude informs the researcher as to the
validity of the H0, that is, whether to accept or
In this particular example, we have two mea- reject the H0 as worth keeping. The p value is
surements, 1 and 2, which are the most frequent. crucial for drawing the proper conclusions about a
We have two modes. set of data. What numerical value of p should be
4. Measures of dispersion. used as the dividing line for acceptance or rejection
a. Rangethe range is the simplest measure of vari- of the H0? Here is the decision rule for the observed
ability. It is the difference between the highest and value of p and the decision regarding the H0:
lowest values in the distribution. For example in
the distribution If p < .05, reject the H0.
5, 20, 21, 21, 22, 23, 29 If p > .05, accept the H0.
the range is If the observed probability is less than or equal

to .05 (5%), the null hypothesis is rejected (i.e., the
29 5 = 24
observed outcome is judged to be incompatible
b. Variance (s )the variance is a method of ascer-
2
with the notion of no difference or no effect),
taining the way individual values are located and the alternative hypothesis is adopted. In this
around the mean. The larger the variance, the more case, the results are said to be statistically signifi-
widely the data items are spread about the mean cant. If the observed probability is greater than
value. A variance of zero indicates no spread at all 0.05 (5%), the decision is to accept the null hypoth-
(i.e., all the scores have the same value). Mathemat- esis, and the results are called not statistically sig-
ically, it is defined as the sum of the squares of the nificant or simply NSthe notation often used in
deviations about the sample mean divided by one tables.
less than the total number of items. For instance, b. Correlation/correlation coefficient (r)the correla-
let us calculate the variance for the following series tion coefficient quantifies the relationship between
of observations. variables (x and y) (Figure 6-4). r takes on values
from 1 to +1 where
21, 23, 29, 20, 18, 22, 14
(1) Determine the mean, or 21, as calculated above. r = x and y increase in the same direction
(2) Subtract the mean from every item in the dis- r = x andy vary in opposite directions
tribution, square the difference, and add the
results. c. Multiple regressiona multiple regression pro-
vides a mathematical model of linear relationship
(21 21)2 + (23 21)2 + (29 21)2 + (20 21)2 +
(18 21)2 + (22 21)2 + (14 21)2 = 128
(3) Divide the result by the number of items in the Example of Correlation (r) = 0.87
distribution minus 1.
3
128/(7 1) = 21.33 y= 0.8963x - 0.038
2
R2 = 0.8062
The variance (s2) = 21.33. 1
c. Standard deviationthe standard deviation mea-
0
sures the typical or average deviation from the 4 2 0 2 4
Y
mean. Mathematically, the standard deviation is 1

equal to the square root of the variance (s2). Using 2
the same distribution as used in the previous 3
example, our standard deviation is equal to the
square root of 21.33, or 4.62. 4
The mean is measured in the same units as the X
data items, but variance is measured in squared Figure 6-4 Correlation coefficient.
various kinds. Any health care practitioner using a

diagnostic test wants to know how good the test is.
To evaluate the quality of a diagnostic test, it is neces-
sary, at a minimum, to know its validity, reliability,
sensitivity, and specificity.
a. Validitythe validity of a test is the extent to which
it actually tests what it claims to test (i.e., how
closely its results correspond to the real state of
affairs). The validity of a test is determined by its
ability to show which individuals have the disease
in question and which do not. Numerically, the
validity of a test is determined by comparison with
an accepted or gold standard that is known to be
totally correct. To be really valid, a test should be
Figure 6-5 Multiple regression. highly sensitive, specific, and unbiased.
b. Reliabilityreliability is equal to the repeatability
and reproducibility of a test (i.e., the level of agree-
Table 6-2 ment between repeated measurements of the same
Caries Status variable). A reliable test would produce very
similar results when used to measure a variable at
WATER CARIES- NOT CARIES- different times.
FLUORIDATED FREE FREE TOTAL
c. Sensitivitysensitivity is defined as the percent of
Yes 310 190 500 persons with the disease who are correctly classi-
No 200 300 500 fied as having the disease (those who have the
Total 510 490 1000 disease).
TP
Sensitivity = 100%
TP + FN
between a dependent (i.e., an outcome variable) (1) True positive (TP)those who have the disease.
and two or more independent or predictor vari- (2) False negative (FN)those who are incorrectly
ables (Figure 6-5). classified as not having the disease (i.e., missed
d. Chi-square (2) testthe chi-square test measures diagnosis).
the association between two categorical variables. (3) The sensitivity of a test is its ability to detect
It is used for the comparison of groups when the people who do have the disease; it is the per-
data are expressed as counts or proportions. For centage of the people with the disease who are
example, an investigator might wish to compare correctly detected or classified. A test that is
the proportion of caries-free children living in a always positive for individuals with disease
district whose water supply is fluoridated with the (identifying every individual with the disease)
proportion of caries-free children living in a non- has a sensitivity of 100%. A test that is insensi-
fluoridated district. In each district, the investiga- tive leads to missed diagnoses (false-negative
tor would count the number of caries-free and results), whereas a sensitive test produces few
noncaries-free children. The research question false-negative results.
involves two categorical variables: caries status of d. Specificityspecificity is defined as the percent of
the child (caries-free or not) and fluoridation persons without the disease who are correctly clas-
status of the district (yes or no) (Table 6-2). sified as not having the disease (those who do not
e. t-testthe t-test is used to analyze the statistical have the disease).
difference between two means. It provides the TN
researcher with the statistical difference between Specificity = 100%
TN + FP
treatment and control groups or groups receiving
treatment A versus treatment B. (1) True negative (TN)those who do not have
f. Analysis of variance (ANOVA) testthe ANOVA the disease.
test analyzes whether or not the means of several (2) False positive (FP)those who do not have
groups are equal and generalizes a t-test to more the disease but are identified by the test.
than two groups. (3) The specificity of a test is its ability to detect
6. Biostatistics in decision makingdecision making people who do not have the disease. A test
frequently involves using quantitative data or tests of that is always negative for healthy individuals
Table 6-3 (3) DiagnosisHBV is diagnosed based on a phys-

ical examination, medical history, and blood
Sensitivity and Specificity of Diagnostic
tests. HBV blood tests include hepatitis B anti-
Tests
gens and antibodies and hepatitis B viral DNA
TEST RESULT DISEASE NO DISEASE (HBV DNA), which detects genetic material
Positive True positives False positives (DNA) from the HBV.
Negative False negatives True negatives (4) Preventiona vaccine to immunize recipients
against HBV is available. Three doses are given
to confer immunity: an initial dose, a second
dose 1 month later, and a third dose 6 months
after the first. Because HBV is highly infectious,
(identifying every person without disease) has all dental personnel should be vaccinated
a specificity of 100%. A test that is low in speci- against HBV. The mainstay of postexposure
ficity leads to many false-positive diagnoses, prophylaxis is hepatitis B vaccine, but hepatitis
whereas a test that is highly specific produces B immune globulin is recommended in certain
few false-positive results (Table 6-3). circumstances in addition to vaccine for added
protection.
b. HCV.
4.0 Infection Control (1) Etiologythe disease is caused by HCV, a
single-stranded RNA virus that appears to have
A. Diseases and routes of transmissiondental profession- cytopathic activity.
als are at risk for any orally transmissible disease from (2) Risk of transmissionapproximately 1.8%
the blood or saliva of the patients they treat. The trans- (range, 0% to 10%) after a needle-stick or
missible diseases of greatest concern to the dental pro- sharps exposure.
fessional are hepatitis B virus (HBV), HIV, hepatitis C (3) DiagnosisHCV is diagnosed based on a thor-
virus (HCV), and tuberculosis. However, the list of ough medical history and physical examination
transmissible diseases is more widely encompassing. to determine the symptoms and the likelihood
Each of these diseases is discussed in terms of etiology, of exposure to HCV and blood tests. The HCV
diagnosis, risk of transmission, and recommendations test detects antibodies or genetic material
for prevention. (RNA) of the virus that causes hepatitis.
1. Routes of transmissionthe route of transmission is (4) Preventionno vaccine or postexposure pro-
the process by which a pathogen is transferred to a phylaxis is available; prevention is vital. Com-
susceptible host. pared with HBV, HCV is less transmissible after
a. Direct contacttransmits infection by person-to- a single exposure. The average risk of infection
person contact. after a needle-stick injury is approximately
b. Indirect contactthe spread of infection by an 1.8%. This figure falls between risk estimates of
inanimate object (i.e., by person object HBV and HIV transmission.
person). c. HIV.
c. Droplets or aerosolsthe spread of disease through (1) EtiologyHIV is caused by an RNA virus.
the air by droplets that contain pathogens. (2) Risk of transmission0.3% from percutaneous
d. Parenteral contactthe transmission of patho- exposures and 0.09% for mucous membrane
genic microorganisms by piercing the skin exposures (less for skin contacts).
(intravenously, subcutaneously, intramuscularly) (3) DiagnosisHIV is diagnosed when antibodies
through an accidental or intentional stick with a to HIV are detected in the blood. The two
needle or other sharp instrument that is contami- primary blood tests used to detect HIV anti-
nated with blood or other body fluid. bodies are enzyme-linked immunosorbent
2. Transmissible diseases. assay (ELISA) and Western blot assay, which is
a. HBV. used to confirm the results of a positive ELISA
(1) Etiologythe disease is produced by a highly test. HIV is diagnosed only after two or more
infective virus known as the Dane particle. This positive ELISA tests are confirmed by a positive
intact virus consists of an inner core antigen Western blot assay.
(hepatitis B core antigen) and an outer coat (4) Preventionno vaccine is available; use of stan-
surface antigen (hepatitis B surface antigen). dard infection control procedures is crucial.
(2) Risk of transmission30% after percutaneous Postexposure prophylaxis consists of antiviral
injury from an infected patient. The disease can drugs similar to drugs given to patients with
be transmitted by 1 108mL of blood. AIDS.
d. Mycobacterium tuberculosis. routinely at least once every hour and more often
(1) Etiologytuberculosis is caused by M. tubercu- in the presence of heavy aerosol contamination.
losis, a slow-growing bacterium that thrives in c. Protective glassesprotective glasses protect eyes
areas of the body that are rich in blood and from spatter, splash, or metal chips from crown/
oxygen, such as the lungs (although it may amalgam restoration that have the potential for
occur in almost any part of the body). creating projectiles. During dental procedures,
(2) Risk of transmissionthe most common mode large particles of debris and saliva can be ejected
of transmission of tuberculosis is inhalation of toward the providers face. These particles can
infected droplet nuclei. In some other parts of contain large concentrations of bacteria and can
the world, bovine tuberculosis, which is carried physically damage the eyes. Protective eyewear is
by unpasteurized milk and other dairy prod- indicated not only to prevent physical injury but
ucts from tuberculous cattle, is more prevalent. also to prevent infection. Protective glasses that
A rare mode of transmission is by infected give the best protection have both top and side
urine, especially for young children using the shields, and some models are made to fit over
same toilet facilities. regular corrective glasses.
(3) Diagnosispulmonary tuberculosis is diag- d. Gownsprotective clothing such as reusable or
nosed based on a medical history and physical disposable gowns, laboratory coats, or uniforms
examination. In addition, some tests include should be worn when clothing is likely to be soiled
sputum cultures, chest x-rays (if a person had with blood or other body fluids. Protective cloth-
a positive tuberculin skin test or an uncertain ing should be changed at least daily or as soon as
reaction to the tuberculin skin test because of it becomes visibly soiled. Protective garments
a weakened immune system). should be removed before oral health care provid-
(4) Preventionpatient medical histories should ers leave areas of the facility used for laboratory or
include questions on tuberculosis. Patients patient care activities.
with suggestive symptoms should be referred 2. Surface coversan effective cover must be imperme-
for medical evaluation. These individuals able to water. A material manufactured and adver-
should not remain in the dental office any tised as a surface barrier should be accompanied by
longer than is required for a referral, and evidence of the impermeable nature of the product.
they should wear masks and be instructed Impervious-backed paper, aluminum foil, or plastic
to cover their mouths and noses when cough- covers should be used to protect items and surfaces
ing or sneezing. Elective dental treatment that may become contaminated by blood or saliva
should be deferred until a physician confirms during use and that are difficult or impossible to
that the patient does not have infectious clean or disinfect. Between patients, the coverings
tuberculosis. If urgent care is required, such should be removed (with gloved hands), discarded,
care should be rendered in a facility that can and replaced with clean materials (after gloves are
provide tuberculosis isolation. Dental health removed and hands are washed).
care workers providing care in these circum- C. Occupational Safety and Health Administration
stances should use respiratory protection. (OSHA)OSHA is responsible for establishing stan-
Dental health care workers symptomatic for dards for safe and healthy working conditions for all
tuberculosis should be evaluated and should employees and regulating maintenance of these stan-
not return to the workplace until a diagnosis dards. These standards require all employers to provide
of tuberculosis has been excluded or until they to all employees a workplace that is free from recog-
are receiving therapy and determined to be nized hazards that are causing or likely to cause death
noninfectious. or serious physical harm. OSHA is concerned with
B. Barrier techniquesbarrier techniques provide a physi- regulated waste within the office.
cal barrier between the body and microorganisms. They 1. OSHA blood-borne pathogens standard.
prevent microorganisms from contaminating the body a. The OSHA blood-borne pathogens standard sets
and surfaces in the operatory and should be used wher- forth the specific requirements OSHA believes can
ever the potential exists for contacting blood, blood- prevent the transmission of blood-borne diseases
contaminated saliva, or mucous membranes. to employees. The blood-borne pathogens stan-
1. Personal protective equipment (PPE). dard is highly comprehensive and detailed. It
a. Glovesone must wear gloves whenever touching includes exposure determinations; an exposure
anything that is contaminated with potentially control plan; engineering and work practice con-
infectious body fluids. trols; and training of employees assisting or pro-
b. Masksit is recommended that a new mask be viding direct care as well as employees who clean
worn for each patient and that masks be changed operatories, instruments, and gowns.
b. The dental facility must have an exposure control D. Sterilizationsterilization is basically absence of all
plan designated to eliminate or minimize employ- life forms. The limiting requirement and basic crite-
ees exposure to blood-borne diseases. The plan rion for sterilization is the destruction of high
sets forth the offices policy and protocols to protect numbers of bacterial and mycotic spores because
employees from these diseases. Included in this these are the most heat-resistant microbial forms. A
plan are exposure determination, schedule of basic guideline of effective clinical infection control is:
implementation, methods of compliance, training do not disinfect when you can sterilize. Sterilization is
program, and use of PPE. the most important component of an infection control
(1) Exposure determinationevery employees program.
daily activities are evaluated to determine By custom, the term disinfection is reserved for
whether he or she is exposed during specific chemicals applied to inanimate surfaces, whereas anti-
duties. septic is used for antimicrobial agents that are applied
(2) Schedule of implementationthe dental facility to living tissues. A major distinction between high-level
must schedule in writing the various parts of disinfection and sterilization is the ability of steriliza-
the exposure control plan. tion to kill spores of spore-forming bacteria (Bacillus
(3) Methods of compliance. and Clostridium). Bacillus spores are the benchmark
(a) Standard infection control precautionsthe organisms for sterilization. If a process kills Bacillus
same infection control procedures are used spores, it will also kill easier-to-kill bacteria, fungi,
for all patients. viruses, and protozoa.
(b) Engineering controlsthis section of the 1. Sterilization process.
plan describes the devices, instruments, a. Autoclavingthe proper time and temperature for
and materials used to prevent blood-borne autoclaving is 250F (121C) for 15 to 20 minutes,
pathogen exposure. Some examples include which yields 15lb pressure of steam, or 270F
use of sharps containers and recappers. (134C) for a minimum of 3 minutes, which yields
(c) Practice controlspolicies and procedures, 30lb pressure of steam. Moist heat destroys bacte-
such handwashing for employees and when ria by denaturation of the high-protein-containing
to change gloves. bacteria. There are two methods to ensure that the
(4) Training programemployees in the dental sterilization process is being performed properly:
facility must be provided with initial training biologic monitors and process indicators.
and annual retraining. Records of the curricu- (1) Biologic monitorsalso referred to as spore
lum and attendance must be kept in the office. tests. The process consists of placing into the
The training must be at a level that is under- autoclave bacterial spores on strips or in enve-
standable by the employees and provided on lopes along with a normal instrument load. If
paid time at the dental office. the autoclave is working properly, the autoclave
(5) Use of PPEPPE must be provided by the reaches the temperature and pressure required
employer to all exposed employees (described to kill the spores. Spore testing must be con-
previously under Barrier Techniques). ducted weekly.
1. Immunization (hepatitis B vaccination)HBV (2) Process indicatorsindicators change color,
vaccine must be offered to all exposed dental workers. which shows that a normal load has reached a
The vaccine must be free to the worker. At the time given temperature. However, this method dem-
of employment, each person should be asked to onstrates only that certain physical conditions
provide documentation of previous immunizations. have been reached. This method does not show
A review of this documentation indicates which that the microorganisms have been eliminated.
immunizations are needed, saving valuable time and Although process indicators are helpful, they
emotional stresses in the event that exposure occurs do not replace biologic monitors.
on the job. b. Dry-heat sterilizationdry-heat sterilization re-
2. Exposure incident and follow-upan exposure inci- quires high heat for a specific period of time. This
dent a specific occupational incident involving the method requires a higher temperature (320F
eye, mouth, or other mucous membrane; nonintact [160C]) and longer time (1 to 2 hours) than steam
skin; or parenteral contact with blood or other poten- autoclaving. Because of the high temperatures,
tially infectious material, including saliva. The most only glass or metal objects can be sterilized by dry
common example is an injury from a contaminated heat.
sharp. After a report of an exposure incident, the c. Ethylene oxide (Chemiclave)ethylene oxide is a
employer must make immediately available, at no chemical widely used in the health care industry to
cost to the employee, a confidential medical evalua- sterilize medical devices. Ethylene oxide gas uses
tion and follow-up. relatively low temperatures for sterilization. Using
a heated unit, sterilization can be achieved in 2 to mercury or through the exposure to potential sources
3 hours at 120F (48.9C). However, a lengthy of mercury vapors.
aeration time must follow each cycle. 1. Recommendations by the American Dental Associa-
d. Chemical (cold) sterilizationchemical sterilization (ADA) Council on Scientific Affairs.
tion is used for instruments and other items that a. Train all personnel involved in the handling of
are heat-sensitive or when methods that require mercury and dental amalgam regarding the poten-
heat are unavailable. Items are sterilized by soaking tial hazards of mercury vapor and the need for
them in a particular chemical solution followed by good mercury hygiene practices.
rinsing them in sterile water. It takes 10 hours to b. Work in well-ventilated work areas, with fresh air
kill bacterial spores in an instrument placed in a exchanges and outside exhaust. Air-conditioning
2% solution of glutaraldehyde. filters should be replaced periodically if the work
(1) Just immersing dental instruments in cold dis- areas are air-conditioned.
infectants would not destroy spores or the c. Use proper work area design to facilitate spill con-
hepatitis viruses (they are resistant to physical tainment and cleanup. Floor coverings should be
and chemical agents). nonabsorbent, seamless, and easy to clean. The
2. Disinfectiondisinfection is a process in which an ADA Council on Scientific Affairs does not recom-
antimicrobial agent destroys (germicide) or avoids mend the use of carpeting in operatories.
the growth of (microbiostatic) pathogenic microor- d. Periodically check the operatorys atmosphere for
ganisms. Disinfectants should be able to kill M. mercury vapor. This may be done by using dosim-
tuberculosis; this is the benchmark organism for dis- eter badges or through the use of mercury vapor
infectants. Spores are not destroyed in this process. analyzers. The current OSHA standard for mercury
The term disinfectant is reserved for chemicals is 0.1mg per cubic meter of air averaged over an
applied to inanimate surfaces (e.g., laboratory tops, 8-hour work shift.
counter tops, headrests, light handles). e. Use high-volume evacuation systems (equipped
3. Antisepsisantiseptics are chemical agents similar to with traps or filters) when finishing or removing
disinfectants, but they may be applied safely to living amalgam.
tissue. Alcohol is the most commonly used antiseptic f. Small mercury spills can be cleaned up safely using
to reduce the number of pathogenic microorganisms commercially available mercury cleanup kits and
on the skin surface. by following your states recommendations (e.g., in
E. Disposal of contaminated wastewaste in the dental Michigan, the Michigan Department of Environ-
office must be disposed of according to state, local, and mental Qualitys table Management of Mercury
federal guidelines and requirements. The U.S. Environ- Spills). Cleanup of large mercury spills requires the
mental Protection Agency (EPA) regulates the trans- use of an experienced environmental contractor
portation of waste from the dental office (e.g., biohazard specialized in toxic spill cleanup.
waste, mercury, x-ray fixer). Following are the three B. Environmental contaminants.
general categories of waste produced in a dental office 1. Gaseshazardous gases or vapors (e.g., nitrous
and the general guidelines for disposal. oxide) should be vented directly to the outside air or
1. Sharpsinclude scalpel blades, syringes, injection should be collected from the air using scrubbing
needles, and burs. Most states require special collec- devices to protect individuals within the office and to
tion and storage of contaminated sharps. Treatment prevent contamination of other local air systems.
rooms must have sharps containers that must be col- 2. Airborne particlesrotary instrumentation is capable
lected by biohazard waste firms. of creating airborne contaminants from bacterial
2. Infectious wasteincludes materials contaminated residents in the water spray system and microbes
with blood or bloody saliva, such as extracted teeth, present in saliva, tissues, blood, and fine debris from
gauzes, gloves, and gowns. These materials must be teeth and plaque. These airborne contaminants could
collected separately and disposed of by licensed waste be present as spatter, mist, and aerosols. Spatter con-
firms. sists of large, visible particles (50m) that fall
3. Noninfectious wasteincludes elements such as within 3 feet of the patients mouth, coating the face
plastic covers and cups, patient bibs, and others. and outer garments of the dental provider. Spatter is
There are no guidelines for their disposal. considered a potential route of infection for dental
health care workers by blood-borne pathogens. Mist
consists of droplets that approach or exceed 50m.
5.0 Materials and Equipment Safety Mist tends to settle from the air after 10 to 15 minutes.
Mists produced by the cough of a patient with unrec-
A. Mercury hygienedental health care workers can be ognized active pulmonary or pharyngeal tuberculosis
exposed to mercury through direct skin contact with are likely to transmit the infection. Aerosols are
invisible particles that range in size from 5 to 50m Since 1995, owing to technologic improvements,
and can remain floating in the air for hours. Although water delivered to patients during nonsurgical dental
there is no scientific evidence that aerosols can trans- procedures consistently contained no more than 200
mit either HBV or HIV, it is acknowledged that aero- cfu/mL of aerobic mesophilic heterotrophic bacteria
sols may carry agents of respiratory infections borne at any point in time in the unfiltered output of the
by the patient. dental unit.
a. Use of PPE is required to prevent contamination In 2012, the ADA Council on Scientific Affairs
from airborne particles. In addition, to help reduce issued a new statement on dental unit waterlines.
exposure to airborne particles, adequate air circu- The specific recommendations are to employ one or
lation should be maintained and masks worn until more available commercial devices and procedures
personnel leave the operatory or air exchange has designed to treat, filter, and improve the quality of
occurred in the room. water. Commercially available options at the present
3. Mercurydental amalgam waste can be recycled to time include the use of independent water reservoirs,
help prevent the release of mercury to the environ- chemical treatment regimens, source water treatment
ment. Although the contribution of dental amalgam systems, daily draining and air purging regimens,
to overall mercury pollution is negligible, the ADA and point of use filters. Previous CDC recommenda-
has developed Best Management Practices for tions that dental waterlines be flushed at the begin-
Amalgam Waste. These practices include using pre- ning of the clinic day to reduce the microbial load is
capsulated alloys; recycling waste amalgam; using no longer recommended because studies have dem-
chair-side traps, vacuum pump filters, and amalgam onstrated that this practice does not affect biofilm in
separators; recycling extracted teeth that contain the waterlines or reliably improve the quality of water
amalgam; and using appropriate line cleaners. used during dental treatment.
C. Operatory equipment. D. Hazardous chemicalsthe OSHA hazard communica-
1. Noise controlsources of noise in the dental office tion standard requires employees to receive training
that can be potentially damaging to hearing are high- about the risks of using hazardous chemicals and the
speed and low-speed handpieces, high-speed suction, safety precautions required when handling them.
ultrasonic instruments and cleaners, vibrators and Employees must be trained in identification of hazard-
other mixing devices, and model trimmers. The ous chemicals and PPE to be used for each chemical.
degree of risk to the dental health care worker This training must occur within 30 days of employment
depends on different factors, including the intensity or before the employee uses any chemicals and annually
or loudness (decibels [dB]), frequency (cycles per thereafter. Just as with the blood-borne pathogen stan-
second [cps]), and duration (time) of the noise as dard, a written plan identifying employee training and
well as personal susceptibility. detailing specific control measures used in the work-
Noise-induced hearing loss develops slowly over place must be compiled for hazardous chemicals. Penal-
time and is caused by any exposure regularly exceed- ties can be imposed on the employer if the office is not
ing a daily average of 90 dB. Protective measures are in compliance.
recommended when the noise level reaches 85 dB 1. Material safety data sheets (MSDSs)each office
with frequency ranges from 300 to 4800 cps. Protec- must have a material safety data manual that is alpha-
tion is mandatory in areas where the level transiently betized, indexed, and available to all employees.
reaches 95 dB. These manuals can be in hard copy or on a computer.
2. Photopolymerization units and lasersdental person- The manual contains the MSDSs. These sheets come
nel and patients should be protected from high- from the material manufacturer. If MSDSs are
intensity visible light using colored plastic shields unavailable, the employer or a designated employee
(attached to the fiberoptic tip). Special precautions must request them from the manufacturer.
are required when using a laser. Laser light can be a. The National Fire Protection Association color and
inadvertently reflected from many surfaces in the number method is used to identify information
dental operatory. The operatory should be closed, about various hazardous chemicals easily on the
and appropriate signs are needed to indicate the pres- MSDSs and product labels. The color and number
ence of laser equipment. Eye protection is required method is used to signify a warning to employees
for the operator, assistant, and patient to protect using the chemicals.
against reflected laser light. (1) Blue identifies the health hazard.
3. Waterlinesthe CDC recommends that coolant (2) Red identifies the fire hazard.
water used in nonsurgical dental procedures meet (3) Yellow identifies the reactivity or stability of a
EPA regulatory standards for drinking water, which chemical.
is less than or equal to 500 colony-forming units (cfu) (4) White identifies the required PPE when using
of heterotrophic bacteria per milliliter (mL) of water. this chemical.
b. The level of risk for each category is indicated by payment, the dentist agrees to provide specified
the use of numbers 0 through 4. The higher the dental services for patients who present and who are
number, the greater the danger. assigned to the dentist by the capitation plan. The
dentist bears most of the financial risk for the treat-
ment promised under the plan. For the dentist, such
6.0 Dental Care Delivery Systems plans allow for predictable income for budgeting
purposes, an influx of new patients (with potential
In this section, we review third-party reimbursement, the referrals), and little processing of claims. The dentist
managed dental care concept, delivery models, quality can also control the type and frequency of services
assurance principles, and the relationship of government provided.
and public health. B. Dental managed caredental managed care is a com-
A. Third-party reimbursementthird-party reimburse- prehensive approach to the provision of quality oral
ment is a system in which a provider of coverage con- health care that combines clinical preventive, restor-
tracts to pay for some of the patients dental treatment. ative, and emergency dental services and administrative
Following are the major forms of third-party reim- procedures to provide timely access to primary dental
bursement currently in use. care and other medically necessary dental services in a
1. Usual, customary, and reasonable (UCR)under cost-effective manner.
UCR, reimbursement is based on the dentists usual 1. Dental health maintenance organization (D-HMO)
charge, unless the charge exceeds certain parameters. D-HMO is the type of plan most commonly associ-
For example, the plan pays the dentist fee unless the ated with dental managed care. This type of plan is
fee exceeds 80% of the charges for that service in a also called a capitation dental plan, which derives
given geographic area. To determine UCR fees, den- from the payment mechanism. Dentists are paid on
tists usually must become participating providers a per capita basis at a fixed (usually monthly) rate
with a plan and agree to file their fees periodically. for each individual or family. The dentist is paid
2. Table of allowancesin this type of reimbursement, regardless of the number or types of services pro-
the third-party payer generally determines what fees vided or the number of beneficiaries seen. Dentists
it is willing to pay for each procedure. Participating are individually at risk in D-HMOs: if the value of
dentists agree to charge plan members these prene- services exceeds payments, it is the dentists loss;
gotiated fees as payment in full, or the plan may allow however, if payment exceeds value, the dentist gains
the dentist to engage in balance billing. Balance financially.
billing involves charging the patient any difference 2. Dental preferred provider organization (D-PPO)D-
between what the plan agrees to pay and the dentists PPO is an arrangement between a plan and a panel
UCR fees. of providers whereby the providers agree to accept
3. Fee schedulesa fee schedule is a list of fees estab- certain payments (usually less than their usual fees)
lished or agreed to by a dentist for the delivery of in anticipation of a higher volume of patients. This
specific dental services. A fee schedule usually repre- higher volume of patients results from a benefit
sents payment in full, whereas a table of allowances structure that gives the subscriber a financial incen-
might not. With a fee schedule, the dentist must tive to use providers from the panel. These incentives
accept the listed amount as payment in full and not typically come in the form of reduced cost-sharing or
charge the patient anything. Fee schedules are some- richer benefits.
times established by public programs, such as Med- 3. Dental individual practice association (D-IPA)D-
icaid in many states. IPA is basically a hybrid D-HMO, a delivery system
4. Reduced fee for servicereduced fee for service is that combines the risk sharing of an HMO with fee-
most commonly associated with preferred provider for-service reimbursement. D-IPAs may be owned
organization (PPO) plans, which are discussed later. and operated by participating dentists who sign a
Under reduced fee for service, participating dentists contract agreeing to certain conditions, including
agree to provide care for fees usually lower than other quality assurance, utilization review, and risk sharing.
dentists in a particular geographic area. Although Dentists are collectively at risk, as opposed to in
PPO dental plans generally provide partial payment D-HMOs, where they are individually at risk. The
for care received from a nonparticipating dentist, dentist is paid on a fee-for-service basis and is at risk
the patient becomes responsible for the difference if payout exceeds premiums. If this occurs, either fees
between the dentists charge and the amount paid by may be reduced, or the dentist may not receive
the plan. payment for treatment beyond a certain amount.
5. Capitationunder capitation, the dentist is paid a D-IPAs usually have an open invitation to all dentists
fixed amount (usually on a monthly basis) directly in an area to join. It usually needs capitalization from
by the capitation plan. For this periodic per capita its member dentists, accounting for the risk sharing,
and may allow for dentist input in plan and benefit the economic and social well-being of families, chil-
design. dren, individuals, and communities and is responsi-
C. Delivery modelsdental managed care plans can be ble for the Head Start program, which provides
designed with different delivery models, which include educational, social, medical, dental, nutritional, and
the staff model, the network model, and the closed mental health services to preschool children from
model. low-income families.
1. Staff modelthe staff model usually has one or more 2. Centers for Medicare and Medicaid Services (CMS)
dental offices that use salaried staff dentists. This CMS administers the Medicare and Medicaid pro-
model is found in many of the capitation plans. It grams, which provide health care to about one in
may be a closed panel (offering services for its own every four Americans. Medicare provides health
beneficiaries) or a contracted dental office (providing insurance for more than 43 million elderly and dis-
services for one or more purchasers). abled Americans. Medicare does not cover dental
2. Network modelthe network model uses multiple care except when dental services are directly related
dental offices in various locations and is the most to the treatment of a medical condition (e.g., extrac-
common method of delivering dental benefits in tion of teeth before radiation therapy for cancer).
managed dental care. The administrator usually con- a. CMS is responsible for the oversight of the federal
tracts with private dental offices that are principally portion of the Medicaid program, a joint federal-
fee-for-service practices. These offices may be limited state program that provides health coverage for
to a specific geographic area or may be widespread approximately 55 million low-income Americans,
over several states. including parents and children, people with dis-
3. Closed modelin the closed model, also known as abilities, and elderly adults. Federal Medicaid laws
the exclusive provider organization, the beneficiaries mandate that states offer comprehensive dental
have a limited choice of offices where they can go to services to children under the Early Periodic
obtain dental care. If they go to offices not included Screening Diagnostic and Treatment (EPSDT)
in the panel, they receive no benefits. This model is program. States are required to provide dental
often used in a D-HMO or PPO plan. examinations to children no later than age 3
D. Quality assessment and quality assurancealthough and to treat comprehensively any oral problems
people use the terms quality assessment and quality identified. EPSDT also requires states to take
assurance as synonyms, they describe different action to ensure that children can truly access care.
concepts. These actions include provision of information,
1. Quality assessment measures the quality of care pro- transportation, and scheduling assistance. Medic-
vided in a particular setting, whereas quality as aid adult dental coverage is optional, and states
surance measures the quality of care and the vary widely in the dental benefits made available
implementation of any necessary changes either to to adults.
maintain or to improve the quality of care rendered. b. CMS also administers the Childrens Health Insur-
2. Quality assessment is limited to the assessment of ance Program (CHIP) through approved state
whether or not standards of quality have been met, plans (S-CHIP). S-CHIP provides health coverage
whereas quality assurance includes the additional to nearly 8 million children in families whose
dimension of action to take the necessary corrective incomes are too high to qualify for Medicaid but
steps to improve the situation in the future. Several who cannot afford private insurance. Dental cover-
concepts relate to quality assurance. age is not a requirement of the S-CHIP program.
a. Structurelayout and equipment of the facility. However, when it was created as part of the Bal-
b. Processactual services that the dentist and dental anced Budget Act of 1997, 49 of the 50 states chose
hygienist perform for the patient and how well to offer dental coverage as part of their S-CHIP
they perform. programs and to provide relatively comprehensive
c. Outcomethe change in health status that occurs benefits. Although not as broad as the Medicaid
as a result of the care delivered. EPSDT program, coverage under most S-CHIP
E. Role of the government in public healthThe DHHS is programs includes basic preventive, diagnostic,
the principal agency of the U.S. government for protect- and restorative services.
ing the health of all Americans and providing essential c. The Affordable Care Act (ACA), currently under
human services, especially for citizens who are least implementation, contains a variety of initiatives
able to help themselves. The following DHHS health that relate to oral health, including coverage and
agencies are involved with the delivery, funding, and access, prevention, oral health infrastructure and
research aspects of oral health. surveillance, and the dental health workforce. ACA
1. Administration for Children and Families (ACF)the expands Medicaid coverage to 133% of the federal
ACF is responsible for federal programs that promote poverty level with an enhanced federal matching
rate and extends CHIP until 2019. Oral health ser- 8. Agency for Healthcare Research and Quality (AHRQ)
vices were included as part of the pediatric essen- the AHRQ supports research on health care systems,
tial health benefits. health care quality and cost issues, access to health
3. Health Resources and Services Administration care, and effectiveness of medical treatments. It pro-
(HRSA)HRSA provides access to essential health vides evidence-based information on health care out-
care services for people who have low incomes, are comes and quality of care.
uninsured, or live in rural areas or urban neighbor-
hoods where health care is scarce. Through its differ-
ent bureaus, HRSA administers a variety of programs 7.0 Communication and
to improve oral health, including funding for preven- Interpersonal Skills
tion and fluoridation, and provides loan repayment
to health professionals who work in underserved A. Listening and nonverbal communication.
areas through the National Health Service Corps. 1. Listening is an active process that involves the recep-
HRSA also provides grants to migrant and commu- tion and selection of auditory information, the gen-
nity health centers to render comprehensive health eralization and interpretation of the information, and
care, including dental services, to the poor and the reconstruction of what was heard. Listening is
migrants. Through the Ryan White CARE Act, HRSA fundamental to quality clinician-patient communi-
funds dental care programs for people who are HIV- cation, with the goal of engaging, facilitating, and
positive or have AIDS. HRSA-funded dental pro- encouraging the patient to speak openly and feel
grams provided care to more than 4 million patients comfortable with the health care provider. Strong
in fiscal year 2010. listening skills also contribute to accuracy in diagno-
4. CDCthe CDC provides a system of health surveil- sis, collaborative treatment planning, and patient
lance to monitor and prevent disease outbreaks satisfaction.
(including bioterrorism), to implement disease pre- a. Listening techniques.
vention strategies, and to maintain national health (1) Preparationpreparing to listen by setting
statistics. The Division of Oral Health has the respon- aside appropriate time for discussion, free
sibility for supporting state and local oral disease from distraction. This preparation serves to
prevention programs, promoting oral health nation- build rapport, increase ones ability to antici-
ally, and fostering applied research to enhance oral pate the patients actions and responses accu-
disease prevention. Among the oral healthrelated rately, and improve patient adherence and
activities of the CDC are dental infection control, satisfaction.
community water fluoridation, oral health surveil- (2) Paraphrasingrepeating, in ones own words,
lance, oral and pharyngeal cancer and tobacco- what someone has said. Paraphrasing serves to
related issues, and support for state oral health confirm ones understanding, validate a patients
programs. feelings, convey interest in the patients experi-
5. U.S. Food and Drug Administration (FDA)the FDA ence (building rapport), and highlight impor-
is responsible for protecting the health of the nation tant points.
against impure and unsafe foods, drugs, cosmetics, (3) Reflectionhearing the patients verbal mes-
and other potential hazards. sage, interpreting the meaning of this com
6. Indian Health Service (IHS)the IHS focuses on the munication, and conveying this interpreted
goal of raising the health status of American Indians meaning to the patient in an effort to ensure
and Alaska Natives. The IHS supports a comprehen- understanding.
sive health services delivery system of hospitals, (4) Acknowledgingcontinually conveying atten-
health centers, school health centers, health stations, tiveness and interest through verbal and non-
and urban Indian health centers to provide services verbal means, including leaning forward,
to nearly 2.1 million American Indians and Alaska maintaining good eye contact, facing the
Natives of 566 federally recognized tribes. In 2013, patient, asking questions, summarizing points
more than 3.7 million dental services were delivered and concerns, nodding, smiling, and maintain-
through IHS programs. ing close proximity.
7. National Institutes of Health (NIH)the NIH is the (5) Interpretationidentifying the underlying
worlds premier medical research organization, sup- reason for a communication. Interpretation
porting more than 44,000 research and training grant serves to build rapport, increase patient trust
projects nationwide. Among its institutes and centers and comfort with disclosure, and raise issues
is the National Institute of Dental and Craniofacial for discussion that may be important but with
Research (NIDCR), which supports and conducts which the patient may be uncomfortable in ini-
basic, clinical, and epidemiologic research. tiating dialogue.
2. Nonverbal communicationinvolves the expression disclose important information fully and accu-
or reception of meaning through nonverbal means rately, feel confident in and adhere to the providers
(e.g., facial expressions, gestures, eye contact, inter- treatment recommendations, and feel satisfied
personal distance, dress, touch, vocal tone, rate and with the care provided.
rhythm of speech). 5. To facilitate good communication, care must be
a. Nonverbal communication may take the place of, taken in verbal communication.
modify, or regulate the flow of a verbal message a. Using the following techniques requires caution in
and express emotion and interest. carefully constructing the verbal message.
b. Characteristics of nonverbal communication. (1) Presumingassuming a patients thoughts or
(1) Continuousone can continually monitor a feelings may undermine rapport; alternatively,
patients nonverbal communication, even when ask rather than presume.
not engaged in verbal exchange. One also can (2) Overassertive communicationverbal commu-
convey empathy and other messages to patients nication often is driven by strong emotion or
through nonverbal means. the belief that ones perspective is the correct
(2) Automaticit often occurs on a semiconscious or only perspective; alternatively, clearly ex-
or precognitive level, allowing for additional plain your impressions and recommendations,
insight into a patients emotional experience; respecting any concerns or differing views a
attention to a patients nonverbal communica- patient may have and taking the time to evalu-
tion is important to understanding their expe- ate and discuss differing views or treatment
rience and identifying and addressing concerns options.
or discomfort. (3) Reliance on technical jargon and abstract or
(3) Informativethe reception of nonverbal infor- vague communicationthese may cause confu-
mation can contribute to an understanding of sion and undermine rapport; alternatively, be
patient emotions when a patient lacks the simple, specific, and direct.
awareness of or ability to describe them, adding (4) Giving advicecan interfere with patient ad-
to a rich, multidimensional perspective of a herence and patient decision-making responsi-
patients experience. bility; alternatively, provide information and
3. Rapport is a mutual sense of trust and openness education to the patient so that he or she may
between individuals that, if neglected, compromises make an informed decision.
communication. (5) Providing reassuranceproviding inappropri-
a. Rapport is reciprocal; patients are more likely to ate reassurance (e.g., telling a patient every-
respect a clinicians beliefs and opinions if the clini- thing will be fine) can backfire and result in
cians is willing to listen to and respect theirs. compromised rapport and trust; alternatively,
b. Strategies for building rapport include greeting provide accurate information, discuss any
each patient by name; maintaining good eye patient concerns or questions fully, and offer
contact; smiling; asking about a patients interests support.
(e.g., work or school, family); and disclosing some 6. Professionalism is an essential component of the
personal information, as appropriate. clinician-patient relationship.
4. Empathy is the active interest in and effort to under- a. Professionalism is characterized by confidence;
stand anothers perspective. care; warmth; and appropriate ethical, professional
a. Characteristics of empathy. behavior.
(1) Understanding the patients situation: for b. Professionalism in communication may be con-
example, How would I feel if I were he?. veyed in numerous ways, including leaning for-
(2) Reflecting that understanding back to the ward, maintaining eye contact, using facilitative
patient: for example, What can I say to him nonverbal communication (e.g., smiling, nod-
to let him know that I understand how he ding), maintaining a relaxed posture, exhibiting
must feel?. appropriate facial expressions, conveying respect
b. A clinician who effectively conveys empathy builds and interest, and practicing ethically.
rapport and trust, elicits and addresses the patients B. Clinical interviewing.
feelings that have the potential to interfere with 1. Clinical interviewing is an art of communication that
treatment, assists the patient in assuming respon- serves many functions.
sibility for his or her feelings, accepts the patients a. It allows a clinician to collect vital health history
feelings as real and important, and remains objec- information.
tive and nonjudgmental. b. It serves to establish ground rules regarding com-
c. Empathy is of the utmost importance because a munication (e.g., the level of formality or informal-
patient who feels understood is more likely to ity, how a patient may express emotion, how a
clinician is likely to respond, what is acceptable and that it feels as though it is irritating your upper
self-disclosure and what is not). gum.).
c. It provides insight into a patients response style h. Transitioningacknowledging the importance of a
and attitudes regarding their understanding of patients communication and shifting to a new
dental health and hygiene and toward illness and topic of discussion.
other health problems. i. Silencethe use of a silent pause in communica-
d. It assesses the patients perceived needs (e.g., their tion encourages the patient to speak.
presenting problem). j. Verbal and nonverbal facilitationthese facilitative
e. It assess the patients values, what is important to gestures and brief comments convey interest
the patient (e.g., a bright smile, straight teeth). and warmth in addition to encouraging further
2. Numerous interviewing techniques are useful in elic- comment (e.g., head nodding, or I see.).
iting important health information and facilitating k. Empathysee earlier discussion of empathy under
communication. Listening and nonverbal communication.
a. Open-ended questionsthe use of open-ended l. Observationcommenting on a patients behavior,
questions invites a patient to express what he or she especially that which is inconsistent with the
feels is important, strengthening rapport (e.g., patients verbal communication, may encourage
What brings you in today?). the patient to discuss a topic with which he or she
(1) In general, it is preferable to begin an interview may be uncomfortable but that may be important
in an unstructured manner and progress to a to treatment (e.g., You seem uncomfortable when
more structured format. This approach pro- I mention the use of local anesthetic.).
vides patients with an opportunity to express C. Treatment planning.
what is important to them in seeking the clini- 1. Treatment planning is a joint agreement between the
cians services. clinician and patient regarding shared decision
b. Closed questionsdirect questions may be used to making and collaboration.
provide more guidance for a response or to elicit a. If a treatment plan is not acceptable to both the
specific information (e.g., Have you ever required patient and the clinician, it is likely to fail, even if
premedication for a dental examination?). the treatment selected is the treatment of choice for
(1) Too many closed questions in succession can a particular presenting problem.
lead to patient disengagement. 2. Treatment plans involve many elements.
c. Closed questions with optionsopen questions that a. Presentation of diagnosis.
restrict potential answers by providing options (1) It is important to be clear, use language free of
(e.g., So, what are you hoping to accomplish technical jargon, and use illustrative methods
reduce the need for future intervention or find a (e.g., radiographs, pictures, drawings) to ensure
quick and inexpensive option?). that the patient fully understands the nature
d. Leading questionsleading questions direct the and origins of the presenting problem.
patient to respond in specific way (e.g., That didnt (2) A clinician should be sensitive when relaying
hurt, did it?). information that may be difficult to hear and
(1) Leading questions are not recommended with which to cope (e.g., presenting indications
because they may easily undermine trust and of oral cancer).
rapport. b. Proposal of treatment approach.
e. Probingprobing allows a clinician to gather addi- (1) The clinician presents treatment alternatives to
tional information regarding a particular topic the patient in descending order of desirability
without leading the patient toward a particular (e.g., treatment of choice, option 2, option 3, no
response (e.g., Tell me more about the discomfort treatment, referral).
youve been experiencing in your left lower teeth.). (2) Be sure to present only options that are consis-
f. Laundry list questionsthese questions ask a tent with your standard of care and that would
patient to respond from a list of given choices (e.g., be acceptable to you.
Is the pain sharp, dull, constant, or throbbing?). c. Presentation of potential treatment benefits,
g. Summarizingchaining together a set of reflec- hazards, and patient responsibilities.
tions. The clinician hears the patients communica- (1) Provide a comprehensive review of potential
tion, interprets its meaning, and conveys a brief benefits and hazards and patient responsibili-
summary of ones understanding of what was said. ties in language that may be easily understood
Summarizing a patients communication conveys by the patient.
understanding and concern in addition to encour- d. Verify patient comprehension.
aging further comment (e.g., I understand that (1) To verify patient understanding, ask the patient
your denture has been quite uncomfortable for you what his or her understanding is of the
treatment options. The clinician listens to the 2. The behavioral change process occurs in several
patient convey his or her understanding in his stages.
or her own words and corrects or clarifies any a. Precontemplationan individual is not consider-
information as needed. ing a behavior change.
e. Discussion. b. Contemplationan individual begins to consider
(1) It is important to provide an opportunity for a behavior change.
patients to ask questions about the treatment c. Preparationpreparing to take steps to change
alternatives and to allow sufficient time for (often expresses a desire to change a behavior).
discussion. As comprehension and comfort d. Actionan individual is engaged in taking action
increase, satisfaction and adherence increase toward behavior change (often requires support for
as well. his or her efforts).
f. Treatment decision. e. Maintenancean individual attempts to maintain
(1) Although a clinician may have a preferred a changed behavior.
treatment approach, the decision is ultimately D. Behavior change theory.
the patients. 1. Social cognitive theory.
(2) Use caution in giving advice. When a patient a. Behavioral motivation is influenced by cognitive
takes responsibility for choosing his or her factors and the social environment. Important
treatment, adherence, follow-up care, and sat- tenets of this model are the following.
isfaction are improved. (1) The notion of self-efficacy (ones perception of
(3) Support the patient in his or her decision by himself or herself as being effective).
providing encouragement. (2) Behavioral modeling (learning a behavior from
g. Document. models in the environment).
(1) It is important to document the completion of (3) Social reinforcement (positive social conse-
each step of the treatment planning process. quences).
3. Patient education is an important component of b. This model is often used to illustrate the effective-
treatment planning as well as throughout treatment. ness of oral health care education. For example,
a. A patient who is well informed is more likely to demonstrating good oral health care (e.g., tooth-
adhere to treatment and follow-up and report sat- brushing) for a patient; allowing the patient to
isfaction with services. practice the skill, supervised or unsupervised (pro-
viding confidence-building mastery experiences);
and praising the patient for good work tend to lead
8.0 Health Behavior Change to improved oral self-care.
2. Health belief model (Rosenstock, 1966).
A. Health behavior change is an intrinsically motivated a. Behavioral motivation (i.e., the likelihood one will
change that happens outside of the dental office in the engage in a particular behavior, such as preventive
everyday settings of patients lives. oral hygiene) is influenced by several factors.
B. Clinicians may approach the topic of health behavior (1) Perceived susceptibility (to disease or problem).
change in ways that may serve to facilitate the desired (2) Severity of the consequences.
behavior. (3) Perceived costs and benefits (of engaging in the
1. The clinical environment is important to how influ- behavior).
ential information is received. (4) Cues to action (external or internal stimuli that
2. The ability to convey empathy is critical in influenc- serve as prompts to engage or not engage in the
ing health behavior change. behavior).
3. Clinicians may facilitate the consideration of b. This model is often used to predict the likelihood
health behavior change by eliciting a rationale for of a behavior or behavior change and to assess the
change from the patient through thoughtful ques- need for behavioral intervention to assist in the
tioning regarding how or why the patient might change process.
change. c. For example, this model asserts that a person is
4. Patient ambivalence is a normal part of the process more likely to engage in good preventive oral
of behavior change. health care if the patient believes he or she is sus-
5. It is important to have a flexible approach to com- ceptible to oral health problems; the consequences
municating throughout the process. of not performing these health behaviors could be
C. Stages of change modeltranstheoretical model significant; as a result, taking the time to care for
(Prochaska & DiClemente, 1986). ones teeth to have healthy teeth is preferable to a
1. People change their behavior when they are ready to lack of care leading to oral health problems; and
change. there are cues in the environment to encourage the
behavior (e.g., the individual owns a toothbrush, occurs many times, eventually the presence of a
floss). dentist alone (CS), without the presence of an
3. Theory of planned behavior. injection (US), can elicit some degree of anxiety
a. The best predictor of patient behavior is the indi- and feeling upset (CR).
viduals intention to perform the behavior which is b. If such an associative learning response occurs
influenced by several factors. (CR), it can be extinguished through a process
(1) Attitudes regarding the behavior. known as classical extinction, in which the response
(2) Perceived social norms regarding the is not reinforced.
behavior. (1) For example, if on many occasions the anxiety-
(3) Degree to which the individual perceived the provoking dentist gives injections that are not
behavior to be within his or her control. painful, the response, anxiety and feeling upset,
4. Self-determination theory. may no longer occur (may be suppressed) in
a. Theory regarding origin of motivation consisting response to the mere presence of the dentist.
of four assumptions about intrinsic motivation 4. Operant conditioninga behavior is followed by a
that must be met. particular consequence (reinforcement or punish-
(1) Competenceperceived ability to achieve ment), and the frequency of the behavior increases
desired outcome. or decreases as a result.
(2) Autonomyperception of oneself as being re- a. Positive reinforcementa positive consequence
sponsible for or in control of behavior change. that increases a desired behavior (e.g., receiving
(3) Relatednessindividual seeks interactions verbal praise or a tangible reward may increase the
with others. frequency of toothbrushing).
(4) If the first three assumptions are not met, b. Negative reinforcementthe removal of a negative
there will be decreased motivation and other stimulus that increases a desired behavior (e.g., the
difficulties. repair of a cavity should relieve a patients tooth-
5. Cultural factorsin our increasingly diverse commu- ache, which may increase the frequency of
nities, it is important to consider cultural factors in toothbrushing).
health care (e.g., access to and use of care, preventive c. Positive punishmenta negative consequence that
care, diagnosis, treatment planning, clinician-patient decreases an undesirable behavior (e.g., giving a
communication). child an extra chore to do in response to his or her
E. Foundations for behavior change. failure to brush his or her teeth may decrease the
1. Health behavior can be understood in terms of cogni- frequency of toothbrushing neglect). This is also
tive behavioral theoryas a complex interaction known as aversive conditioning.
between ones thoughts, ones feelings, and ones d. Negative punishmentthe removal of a positive
behavior. Each interacts with and influences the stimulus to decrease an undesirable behavior (e.g.,
other, resulting in behavior and behavioral patterns. decreasing a childs weekly allowance from $3 to
2. Behavior theory (ABC model)the occurrence of a $1 may decrease the frequency of toothbrushing
particular behavior can be understood as a complex neglect).
interaction between an antecedent (A), a facilitating (1) Research supports the greater efficacy of rein-
factor to a behavior; a behavior itself (B); and the forcement over punishment because the use of
consequences of a behavior (C). This is referred to as punishment has several disadvantages: it often
behavior theory or the ABC model. results in the avoidance of the punisher; it can
a. For example, when an individual experiences dis- elicit negative emotions; and it fails to teach an
comfort because of particulate lodged between two alternative, more desirable behavior.
teeth (A), the individual may choose to floss (B) e. Operant extinctionthe removal of reinforcers to
and, as a result, experience a sense of relief (C). decrease a behavior.
3. Classical conditioning (also known as respondent or (1) For example, a young patient learns that if she
pavlovian conditioning)a neutral stimulus (one that cries at the dentists office, her mother gives her
is not associated with a particular response) is paired much-needed attention and terminates the
with an unconditioned stimulus (US), one that natu- dental appointment. Asking the mother to
rally elicits a particular response (UR). After many refrain from providing this attention and allow-
pairings, the conditioned stimulus (CS) elicits a con- ing the dentist to continue communicating
ditioned response (CR), which is essentially a weaker with the child for the remainder of the sched-
form of the UR, without the presence of the US. uled appointment is likely over time to decrease
a. For example, a dentist gives a painful injection the crying behavior. However, the behavior
(US), and the patient experiences anxiety and may first appear to increase (extinction burst)
becomes upset (UR). Given that this scenario before it decreases.
5. Observational learning (modeling) (Bandura, 1962) is immediately improving without interven-

the acquisition and performance of a skill through tion, this effect is often short-lived, and the
observation of another engaging in the task. This is behavior returns to baseline within weeks.
most effective when the model is an individual the g. As the intervention is implemented, continually
person views as similar (e.g., age, gender). This tech- reassess the behavior to monitor for progress,
nique may be particularly useful if used in the context provide reinforcement for behavior change, and
of asking an anxious or uncooperative child to determine whether the intervention is successful
observe his or her cooperative sibling. or whether it requires alteration.
C. Strategies for behavior change. (1) Consider using charts to monitor progress
1. OARS in communicationopen questions, affir- because they provide visual positive reinforce-
mations, reflective listening, summarizing (see ment for behavior change.
Section 7.0, Communication and Interpersonal (2) Be sure to create reachable goals.
Skills). 3. Behavioral strategiesall behavioral strategies may
2. Assessmentto create and implement an effective be conceptualized using the ABC model. Behavior
strategy for behavior change, one must first assess the change (B) can be successfully accomplished by alter-
behavior. Behavior assessment should include the ing either an immediate antecedent (A) or an imme-
following. diate consequence (C). By altering A or B, a learning
a. Identify the problemdefine the problem and experience is created that shapes behavior. (For addi-
determine its origin. tional behavioral strategies, see Section 9.0, Anxiety
b. Consider motivation. and Pain Control.)
c. Consider readinessa patient may be willing to a. Altering antecedents and stimulus control
change a behavior, but the present time may not be changing ones routine by placing a behavior cue
the ideal time to commit to such an endeavor (e.g., can increase the frequency of a behavior (e.g.,
current life circumstances causing increased stress, keeping dental floss on the nightstand may serve
sleep deprivation, decreased time to devote to such as a daily reminder to floss). The removal of a
a task). behavior cue, in the case of a goal to decrease a
d. Consider willingness to change. behavior, can also be a useful strategy (e.g.,
e. Consider ability to changeconsider existing self- someone who always smokes a cigarette in his or
management skills, social support, current life her favorite chair on the porch may remove the
stressors, and locus of control. chair from the porch, making it less likely that
(1) Internal locus of controla tendency to attri- person will engage in the behavior).
bute events to internal forces (internally moti- b. Shaping (stimulus-response theory)recognition
vated; e.g., I failed my exam because I didnt and reinforcement of successive approximations of
study as much as I should have.). These indi- a behavior; in other words, creating small, doable
viduals tend to be more motivated and success- steps, followed by praise for successfully com
ful at behavior change. pleting these steps, toward achieving a target
(2) External locus of controla tendency to attri- behavior.
bute events to external forces (externally moti- (1) This is a useful technique because the most
vated; e.g., I failed my examination because common reason for failure in behavior change
the test was unfair.). is setting unrealistic goals and expectations,
f. Collect baseline dataanswer the question, What leading to failure and decreased motivation.
is the target behavior frequency currently? This (2) When using shaping, begin slowly, with an
allows you to establish a starting point for com- easily accomplished task, and use positive rein-
parison later to determine whether the interven- forcement at each step.
tion is successful. c. The Premack principlemaking a behavior that has
(1) Event and time samplingask the patient to a higher probability of being performed contingent
record each time the behavior occurs over a on (used as reinforcement) the performance of a
predetermined period of time. Charts or coun- less frequent behavior may increase the perfor-
ters may be helpful in counting and recording mance of the less frequent behavior (e.g., making
the data. reading a childs evening bedtime story contingent
(2) In the case of a child, ask a parent to observe on toothbrushing).
and record the behavior of the child. d. Altering consequencesaltering the immediate
(3) Be aware of the potential for a self-monitoring consequences, such as in the use of a reward system
bias, in which the target behavior tends to (providing positive reinforcement) following a
improve simply as a result of self-monitoring. behavior, may alter future performance of the
Although it may appear as though the behavior behavior (see point e).
e. Providing feedbackproviding praise regarding (b) Sustain talkpatients communication

work toward a specific goal. Visual aids (e.g., the favors remaining in current behavior
use of charts, diagrams, records, logs) can be very pattern.
useful in demonstrating success. (c) Change talkpatients communication
f. Extinctionidentifying the positive consequences favors change or movement toward change.
or reinforcements that maintain a behavior and (d) Commitment talkpatients communica-
ceasing or withholding these reinforcements or tion expresses a readiness, ability, and will-
consequences (e.g., requiring a patient who regu- ingness to change behavior.
larly presents 20 minutes late to appointments to
reschedule for another time, rather than see the
patient when he or she arrives late each visit). 9.0 Anxiety and Pain Control
g. Incompatible behavior and stimulus controlthe
use of an incompatible behavior to decrease the A. Stress and dental anxiety.
frequency of an undesirable behavior (e.g., instruct- 1. Anxietya subjective experience involving cogni-
ing an individual to put on a pair of gloves each tion, emotion, behavior, and physiologic arousal.
time the individual feels compelled to bite his or Stress is a perceived threat to ones well-being. It is
her fingernails). subjective in that each individual appraises each
h. Observational learningsee Section 9.0, Anxiety potentially stressful event in terms of its familiarity,
and Pain Control. predictability, controllability, and imminence and
4. Cognitive strategiesinfluencing ones behavior (and arrives at a conclusion regarding how anxiety-
emotional response) through the use of reasoning or provoking he or she believes the situation to be.
thought-provoking strategies. (For additional cogni- 2. Clinicians should be familiar with presenting symp-
tive strategies, see Section 9.0, Anxiety and Pain toms of anxiety so that they may adequately recog-
Control.) nize any potential anxiety response before it occurs.
a. Establishing rapport. 3. It is essential that dental professionals be familiar
b. Maintaining good communication. with some brief interventions and management strate-
c. Motivational interviewing (Miller & Rollnick, gies for the treatment of anxiety to facilitate best a
2012)a person-centered counseling style to assist successful dental experience for an anxious patient.
in the resolution of ambivalence and help move Effectively using these skills is likely to result in
toward behavior change. The spirit of motiva- increased treatment compliance and patient follow-
tional interviewing is a compassionate, accepting, up, better quality of care, and better current and
collaborative process in which there is shared deci- future dental experiences for both the patient and the
sion making and in which the patients autonomy clinician.
is honored in using a patients strengths to elicit a. Provide the patient with a sense of control.
motivation to change. The process involves con- (1) Provide informationlet patients know what
necting behavioral goals to a patients beliefs, to expect. Research indicates that negatively
values, and concerns. Motivational interviewing anticipated events are less stressful when they
involves four processes. are predictable (e.g., tell patients what they will
(1) Engagingforming a relationship with the likely feel, see, smell, and taste; inform them of
patient. procedure length and keep them informed of
(2) Focusingexploring the patients motivation to progress; use the Tell-Show-Do method, par-
change behavior as well as the patients values ticularly with children; offer patients mirrors
and goals in treatment and the meaning of for them to observe; offer patients choices
these values and goals in his or her life. when appropriate).
(3) Evokingeliciting from the client his or her (2) Use hand signalsagree on a way in which the
own motivation to move toward change. patient can express anxiety (e.g., raising a
(a) Strategies include discussing disadvantages hand), which will serve as a signal for the clini-
of remaining in current behavior pattern, cian to break temporarily to allow the patient
discussing advantages of change, exploring to regain coping.
personal strengths that may contribute (3) Time structuringusing a timing mechanism
to change, and exploring intention to (e.g., an egg timer, a clock, counting to a certain
change. number, singing a certain song) to encourage a
(4) Planningexploring how one might move behavior by increasing ones sense of control
toward change. and expectations. This technique is particularly
(a) Ambivalence is a normal part of the change useful with children, who do not yet have
process. a well-developed time sense, or an anxious
patient who cannot easily tolerate parts of a all) to 10 (the highest he or she had ever experienced)
procedure (e.g., drilling). (e.g., How anxious are you feeling now?).
b. Acknowledge the patients experience. Demonstrate 5. Although most of the procedures listed previously
an understanding of how anxious or uncomfort- may be used with children (with adaptation for
able the patient feels and how important the developmental level), there are special considerations
patients comfort is to you, the clinician. in pediatric anxiety.
c. Use brief cognitive-behavioral interventions, based a. Additional anxiety management strategies for
on cognitive-behavioral therapy, which posits that children.
thoughts, feelings, and behaviors are interrelated (1) Structure choicesfor example, plain or fruit-
and influence one another; intervening in one of flavored dental floss.
these areas can produce change in the remaining (2) Tell-Show-Doexplain, demonstrate, and
two areas. allow the child to learn and understand what
(1) Diaphragmatic (paced) breathing and relax- will be happening before proceeding.
ationeducate the patient regarding the relax- (3) Use specific direction and specific feedback (e.g.,
ing benefits of deep breathing. Demonstrate I need you to open your mouth as widely as
this technique. Practice four to five breaths you can. Thats good the way youre opening
with the patient. Remind the patient to use your mouth for me. Keep up the good work.).
these skills during the visit and to practice the (4) Teach simple coping strategies (e.g., deep breath-
skill at home. ing, counting to a specified number).
(2) Progressive muscle relaxationa technique that (5) Use praise.
involves systematically tensing and relaxing (6) Reward good behavior.
certain muscle groups, directing the patient to (7) Use hand signals.
attend to the differences in sensation between (8) Consider inviting a parent into the room for
tension and relaxation. support.
(3) Guided imagerya procedure in which a (9) Provide positive experiences by choosing to do
patient uses diaphragmatic breathing skills simple, less anxiety-provoking procedures first.
while imagining a pleasant scene of his or her B. Dental pain (Milgrom, 2001; Milgrom etal, 1995).
choosing, evoking all senses. 1. Gate-control theorya dorsal spinal gating mecha-
(4) Hypnosisa technique involving attentional nism can control (by opening or closing, or partially
focus, paced breathing, and relaxation. closing) the flow of signals from noxious stimuli (i.e.,
(5) Behavioral rehearsalsproviding a patient with stimuli that cause pain) from the periphery to the
the opportunity to practice coping strategies brain. The flow is varied according to what signals are
(e.g., diaphragmatic breathing) while experi- received from the brain and may be influenced by
encing a simulated procedure or part of a inhibitory agents, competitive stimuli, or signals
procedure. (e.g., cold, hot, emotions, expectations, memories,
(6) Systematic desensitizationexposing a patient cultural attitudes).
to items from a collaboratively constructed a. This theory does not account for cognitive or emo-
hierarchy of slowly increasing anxiety- tional factors.
provoking stimuli (related to the target fear) 2. Pain is a complex phenomenon involving cognition,
while using relaxation skills. emotions, beliefs, expectations, and past experiences.
(7) Cognitive coping (reframing)assisting patients Fear and anxiety and pain are interrelated. A fear
in changing their thinking about something to response to a stressor initially causes a release of
a more adaptive or realistic thinking style (e.g., endorphins from the pituitary, resulting in an anal-
helping the patient to change his or her thought gesic effect. However, ultimately, pain thresholds are
from I cant do this to This may be difficult reduced, and anxious patients are more likely to
for me, but I can manage this. I did okay last report pain or discomfort for many reasons (e.g.,
time.). hypervigilance, muscle tension, cognitive misattribu-
(8) Use praisedemonstrate progress; set realistic tion of danger, conditioning, catastrophic thinking,
expectations. Ask patients to practice coping perceived lack of control). In addressing patient pain,
skills at home and when in the office. clinicians must attend to both pain and anxiety.
(9) Distractiongiving the patient a competitive 3. As with anxiety, a goal of minimizing pain and
attentional focus can be useful (e.g., listening to increasing the patients coping skills is essential as
music, watching a video). well as ongoing pain assessment.
4. Continually assess level of anxiety throughout treat- a. Clinicians may inquire about pain level through
ment using a subjective unit of distress scale, asking the use of the subjective units of distress scale (see
patients to rate their level of anxiety from 0 (none at following text) and pulp vitality testers.
4. The behavioral (nonpharmacologic) management of

patient pain may be useful in the control of mild to 10.0 Professional Responsibilities
moderate pain and an effective supplement to phar- and Liabilities
macologic strategies.
5. Although most of the procedures listed previously A. Ethical principlesthe principles of ethics guide the den-
may be used with children (with adaptation for tists decision making in practice. Five fundamental
developmental level), there are special considerations principles form the foundation of the ADA Principles
in pediatric pain. of Ethics and Code of Professional Conduct: patient
a. Research indicates that dentists consistently under- autonomy, nonmaleficence, beneficence, justice, and
estimate the pain experiences of children. veracity.
b. Factors influencing pediatric dental pain include 1. Section 1. Principle: Patient Autonomy (self-
age (behavior, level of understanding, and self- governance). The dentist has a duty to respect
report differ according to developmental level), the patients rights to self-determination and
perceived level of control, past experiences, confidentiality.
expectations, and family or cultural norms and 2. Section 2. Principle: Nonmaleficence (do no harm).
beliefs. The dentist has a duty to refrain from harming the
c. Ongoing assessmentin addition to the subjective patient.
units of distress scale and pulp vitality testers, use 3. Section 3. Principle: Beneficence (do good). The
of the Wong-Baker Faces Pain Rating Scale may be dentist has a duty to promote the patients welfare.
particularly useful with children. Because children 4. Section 4. Principle: Justice (fairness). The dentist
do not have the cognitive and emotional maturity has a duty to treat people fairly.
and verbal ability of adults, it is especially impor- 5. Section 5. Principle: Veracity (truthfulness). The
tant to use observation skills in assessing a childs dentist has a duty to communicate truthfully.
pain (facial expressions, verbal responses, behavior B. Informed consentconsent and informed consent are
or motor responses, physiologic arousal). two separate and distinct legal theories. Except where
d. Additional pain management strategies for chil- the patients condition (e.g., an emergency) justifies the
dren (in addition to those used with adults, when performance of a procedure or the rendering of a
developmentally appropriate and in addition to service, the patients consent to treatment is required,
anxiety management strategies; see Stress and even if the unauthorized procedure is skillfully per-
Dental Anxiety, earlier). formed and is beneficial to the patient.
(1) When possible, use short and simple proce- 1. Backgroundthe doctrine of informed consent
dures. If multiple procedures are indicated, emerged during the 1950s. It is based on the ethical
choose the simplest and least invasive proce- principle of patient autonomy, and it requires that the
dure first. patient be informed of any information that would
(2) When possible, use procedures that do not affect a reasonable persons decision making, includ-
involve injections or handpieces. ing the nature of a procedure explained in under-
(3) Foster an environment of support and standable terms, potential benefits and risks of the
learning. procedure or service, and costs of the procedure.
(4) Introduce patients to tools, procedures, and Failure to do so invalidates the consent.
sensations in a systematic manner. Some courts have determined that in a situation
(5) Use Tell-Show-Do, graded exposure, and in which a patient is mentally and physically able to
explanation. consult about his or her condition, in the absence of
(6) Use age-appropriate language. an emergency, the patients informed consent is a
(7) Structure time. prerequisite to tests, treatment, intrusive procedures,
(8) Give choices when possible and appropriate. or surgery. If a procedure is done without an informed
(9) Use hand signals, and immediately respond to consent, the dentist may be held accountable for
signal of discomfort. assault and battery, which may not be covered by
(10) Use distraction when appropriate (e.g., story- professional liability insurance. A technical assault
telling, imagery, hypnosis, breathing exer- and battery makes the dentist liable for any resulting
cises). Distraction is less effective and not injuries, regardless of whether the treatment was
ideal for children who are extremely anxious appropriate and not negligently administered. The
and hypervigilant. duty to apprise a patient of the nature of the proce-
(11) Provide information and offer hand mirrors dure is limited to the doctor performing the proce-
to observe. dure for which consent is being obtained.
Refer to Section 5, Orthodontics and Pediatric Den- 2. Informed consent consists of the information that a
tistry, for additional discussion of this topic. doctor is required to share with the patient and the
consent that the doctor is required to obtain from the the emergency must be carefully recorded by the
patient. doctor in the patients chart. Before treatment, docu-
a. Required informational elements for informed mented efforts should be made to contact the appro-
consent. priate consenting party.
(1) Explanation of the procedure in understand- C. Risk management and risk avoidancerisk manage-
able terms. ment is a concept derived from industry wherein one
(2) Reasons for the procedure and the benefits identifies areas possibly exposing one to liability; weighs
and risks of the procedure and anticipated the risks against the benefits; and controls that exposure
outcome. by monitoring, insuring, or eliminating the dangerous
(3) Any alternatives and their risks and benefits, activity. It is basically a two-pronged attack where one
including no treatment at all. is alerted to possible dangers and then handles inci-
(4) The costs of the procedure and the alternatives. dents by immediate action. This heightened awareness
b. Required elements for consent. and early warning system allow the practitioner to be
(1) Consent must be voluntary and not coerced. prepared if and when a lawsuit is filed. It also provides
(2) Information and consent must be given in a a sound basis for determining whether to defend or
language that the patient understands. settle the lawsuit. In addition to learning to identify
(3) The patient must be given an opportunity to potential exposures to liability, the second part of risk
ask questions, and the doctor must be available management is knowing what to do when something
to answer any patient questions. bad happens.
(4) Only the patient or the patients legal guardian 1. Documentation is an essential part of risk manage-
can authorize treatment decisions. ment. In the eyes of many courts, If it is not written
(5) Make sure to check state regulations, which down, it did not happen, meaning that significant
often outline who must obtain consent from events should be written down and that the courts
the patient and whether it must be in writing will not rely on memory, several years after the fact,
or signed. particularly in cases of medical malpractice. Medical
3. Any doubt as to the necessity of obtaining consent records must be thorough, consistent, and complete.
should be resolved in favor of procuring the consent. They should include not only actual visits but also
4. Emancipated minorsin negligence law, a sliding missed visits and other evidence of noncompliance.
scale is in effect. From ages 1 through 7, a child is 2. To reduce liability for the physical facility, regular
considered an infant and is not responsible for his logs that detail inspections, maintenance, and phone
actions (i.e., cannot be contributorily or compara- calls reporting problems can provide evidence that
tively negligent, cannot assume a risk). From ages 8 things are being handled properly.
through 14, the child is judged on a sliding scale of 3. Another type of documentation is an incident report,
competence, depending on the sophistication of the which is completed when something happens. An
child and the activity he or she is involved in (e.g., a incident report should be objective; this is no time to
12-year-old driving a boat would be considered more point fingers, as in As usual, Tom did not bother to
responsible for his actions than an 8-year-old on a turn on the lights.
bicycle). Finally, from age 15 on, minors are consid- 4. All documentation is discoverable; that is, the counsel
ered totally responsible for their own actions (e.g., a for an injured party is entitled to all writings con-
16-year-old driving a car is held to the same standard cerning the problem, including any handwritten
as all drivers, regardless of experience). Minors notes.
younger than 18 can give implied consent but not 5. Objectivity also requires that you do not create facts.
actual consent (i.e., they can get on the ride at the Write down what you actually saw, not what some-
amusement park, but they cannot sign a release). The body tells you. For example, Patient found on floor
exception is the case of emancipated minors. is an objective statement. Patient slipped on spilled
A conscious, mentally competent patient younger Coke is not, unless you actually saw it. The problem
than 18 may give consent to his or her own medical is that if you state, Patient slipped on spilled Coke,
treatment, counseling, or testing if he or she is eman- you may have created a liability situation.
cipated, married, a parent, pregnant, or in an emer- a. If possible, physically view the accident scene and
gency situation. An emancipated minor can also document what you foundspilled Coke or water,
consent to treatment of his or her child. or a clean, dry floor? Pools of slush or a clean,
5. Exceptionsin an emergency situation where imme- sanded sidewalk? Did you actually see the injured
diate treatment is required to preserve life or limb or party or just hear about it? What happened to the
alleviate severe pain, and the patient or legally injured party? Did an ambulance come, did a
responsible party is not unable to give consent, the friend provide a ride, was he ambulatory, was he
doctor may proceed without it. The factual basis of seen by a doctor, and so forth.
b. Your writings are discoverable; do not write any- b. If you realize the error at a later time, write an
thing you do not want read aloud in court. For addendum after the last note that was written in
example, do not characterize the patient using the chart. This is important because anyone sub-
insulting remarks; instead, detail the behavior, as sequently reviewing the chart may already have
in Patient was loud and aggressive, argumentative, read the existing note and will be unaware that
refused to listen to office staff. the content of the note changed unless you refer-
6. When an incident occurs, your insurance company ence this in an addendum.
should be put on notice. If you wait until you are (1) Never erase, white-out, or otherwise obliterate
actually sued, and you had prior notice, the insurance anything that was written in the chart. A
company may refuse to provide coverage. plaintiff s attorney can say the obliterated
7. Once you have written something, do not go back material says anything he or she wishes.
and change it when a lawsuit is filed. If you have (2) Never change so much as a comma once a
second thoughts, provide an addendum. Never lawsuit has been filed; the plaintiff probably
change anything you wrote. If you make a legitimate already has a copy of the chart, and your alter-
mistake, draw a single line through the error (so it ations can be enough to lose the suit. Tamper-
can still be read), mark error, and initial and date it. ing or changing the record with self-serving
D. Documentationthe primary weapon against a possi- intent can be disastrous.
ble lawsuit is appropriate and adequate documentation. 7. Never make or sign an entry for someone else or have
If you have been sued, it is your only defense. As stated another make or sign an entry for you.
earlier, according to some judges, if it is not written 8. Countersign carefully. Never countersign an entry
down, it did not happen. without reading it and, if necessary, checking the
1. Be specific. Write facts only, not opinions; describe accuracy. You become as responsible as the person
observations, findings, and assessments. General- who originally signed.
izations are confusing, as in Patient doing well 9. Do not complain, belittle, criticize, or blame others in
(compared with Patient no longer experiencing your documentation. It can provide the plaintiff with
pain on tooth No. 3). What is your evidence? What ammunition.
have you observed? 10. Document informed consent in your progress notes,
2. Be objective. Avoid personal characterizations in addition to having the patient sign an informed
(Patient uncooperative). Instead, state specific consent form. Document discussion, evidencing
behavior, such as Refuses to eat, take medication, patients understanding.
stop smoking, which implies noncompliance. Do 11. Your chart may be read in court. Avoid derogatory,
not create facts; do not state, Fractured mandible; insulting, or unprofessional remarks that you would
patient punched by husband, unless you saw it. be embarrassed to explain in front of judge and jury.
Instead, state, Patient presents with fractured man- E. Statute of limitationsthe statute of limitations varies
dible; states husband hit her. If your information from state to state, and there are two basic rules that
comes from the patient, always preface it with states follow: the occurrence rule and the discovery
Patient states: Otherwise, you have created a rule. The occurrence rule allows for the statute of limi-
fact that you cannot back up if you are called to tations to start to run when the possible injury or mal-
testify. practice occurred. The discovery rule allows for the
3. Be complete. Take special care in documenting statute of limitations to run when the patient discovers
patient education and home care. or should have discovered the injury or malpractice.
4. Be timely. Make all entries promptly. The type of rule followed by the state affects the
5. Be readable. Write legibly; you may have to rely on minimum time required for patient record retention.
your notes years later, and both you and your attor- Ethically, you should advise a patient when you have
ney must be able to read them. Make continuous done something wrong because it is the right thing to
entries in the chart; avoid gaps in time or treatment. do; legally, you should advise a patient because that will
Stay with traditional forms and abbreviations. document the time of discovery and the statute will
Make certain entries are consistent and avoid begin to run. In cases of minors, parents can sue imme-
contradictions. diately; however, the minor may have additional time
6. The integrity of the chart is your top priority and after the age of 18 to bring suit on his or her own behalf;
must be preserved. Make corrections or alterations if you have a pediatric practice, you may have to retain
according to approved procedures: your records longer.
a. If you realize your mistake at the time you are F. Confidentialitythe original record is your custodial
writing the note, draw a single line through the property and, by law, must be retained by you. Copies
error so it is still readable. Write the correction of charts and x-rays may be provided to patient or attor-
and indicate the date, time, and your initials. ney with signed authorization by the patient (and you
can charge copying fees). The chart is confidential and Gluck GM, Morganstein WM: Jongs Community Dental
should not be discussed with anyone without authoriza- Health, ed 5. St. Louis, Mosby, 2003.
tion from the patient. Mayes DS: Dental Benefits: A Guide to Dental PPOs, HMOs
G. Witnesses. and Other Managed Plans. Brookfield, WI, International
1. Expert testimonyto prove an allegation of malprac- Foundation of Employee Benefit Plans, 2002.
tice, the plaintiff must produce an expert who will Milgrom P, Weinstein P, Getz T: Treating Fearful Dental
testify to the existing standard of care in the profes- Patients: A Patient Management Handbook. Seattle,
sion and how it was breached by the defendant. The University of Washington, 1995.
expert must be qualified by virtue of training, experi- Miller WR, Healher N, editors: Treating Addictive Behav-
ence, and credentials, and the defense has the right iors. New York, Plenum Press, 1986.
to provide its own expert to rebut the plaintiff s Miller WR, Rollnick S: Motivational Interviewing: Prepar-
expert. The expert can have general expertise in the ing People for Change, ed 2. New York, Guilford Press,
field, such as a general dentist, or have special exper- 2002.
tise, such as an oral surgeon or orthodontist. An Miller WR, Rollnick S: Motivational Interviewing: Helping
expert witness appears voluntarily and attests to the People Change, ed 3. New York, Guilford Press, 2012.
experts best medical judgment and opinion to a Ost L, Skarat E: Cognitive Behaviour Therapy for Dental
reasonable medical certainty. Usually experts charge Phobia and Anxiety. New York, Wiley-Blackwell, 2013.
an hourly rate, including record review and prepara- Prochaska JO, DiClemente CO: Toward a comprehensive
tion time. In some states, there is no limit on expert model of change. In: Miller WR, Heather N, editors:
witness fees except that such fees should be reason- Addictive Behaviors: Processes of Change. New York,
able. As a witness, your fee arrangement cannot be Plenum Press, 1986, pp 3-7.
contingent on the outcome of the litigation. When Ramseier C, Suvan J: Health Behavior Change in the Dental
the expert witness is asked about compensation, he Practice. New York, Wiley-Blackwell, 2010.
or she should not be flustered. The proper response Rosenstock IM: Why people use health services, Milbank
is, I am being paid for my expertise, training, experi- Memorial Fund Q 44:94, 1966.
ence, and time. Selye H: The general adaptation syndrome and the diseases
2. Fact witnessesa fact witness is someone with first- of adaptation. J Clin Endocrinol 6:117, 1946.
hand knowledge of the facts of the case. He or she Weinstein P, Getz T, Milgrom P: Oral Self-Care: Strategies
can testify only about first-hand knowledge and is for Preventative Dentistry. Seattle, University of
not allowed to offer an opinion about treatment pro- Washington, 1991.
vided. A fact witness is usually subpoenaed and must Weintraub JA, Douglas CW, Gillings DB: Biostats Data
appear; the individual cannot charge for his or her Analysis for Dental Health Care Professionals. Chapel
services; rather, the witness receives a statutory sum Hill, NC, CAVCO Publications, 1985.
depending on the jurisdiction where he or she is Wong DL, et al: Wongs Essentials of Pediatric Nursing,
appearing. ed 7. St. Louis, Mosby, 2005.
a. Some courts have held that a fact witness who has
treated a patient cannot testify against that patients
interests; that is, he or she may not give an opinion Sample Questions
detrimental to the patients case and must testify
only to the facts in an objective fashion. 1. Which of the following is not a process in motivational
interviewing?
Bibliography A. Focusing
ADA Council on Scientific Affairs: Dental mercury hygiene B. Analyzing
recommendations. J Am Dent Assoc 134:1498, 2003. C. Evoking
American Dental Association: ADA Principles of Ethics and D. Engaging
Code of Professional Conduct. Chicago, ADA, 2005. E. Planning
American Dental Association: ADA Principles of Ethics and 2. Which behavior change theory emphasizes the impor-
Code of Professional Conduct. Chicago, ADA, 2013. tance of self-efficacy and behavioral modeling and
Bandura A: Social Learning Through Imitation. Lincoln, reinforcement?
NE, University of Nebraska Press, 1962. A. Cognitive behavioral theory
Burt BA, Eklund SA: Dentistry, Dental Practice, and the B. Self-determination theory
Community, ed 6. St. Louis, Mosby, 2005. C. Social cognitive theory
Chambers DW, Abrams RG: Dental Communication. D. Classical conditioning
Sonoma, CA, Ohana Group, 1992. E. Motivational interviewing
Dionne RA, et al: Management of Pain & Anxiety in the 3. A patient is conflicted about wearing a night guard,
Dental Office, ed 5. St. Louis, Mosby, 2002. despite your recommendations to prevent further
damage from bruxism. The patient states, I have so with it, and near the end of the procedure you feel
much going on right now that I just dont think Im much better. Which concept does this scenario best
going to be able to wear it consistently like I should. exemplify?
This is an example of: A. Covert conditioning
A. Resistance B. Systematic desensitization
B. Sustain talk C. Habituation
C. Commitment talk D. Cognitive restructuring
D. Back talk E. Psychoeducation
E. Change talk 10. During a previous dental visit, you assisted a patient
4. Informed consent requires that the patient be advised by generating his statement, Even if there is some
of all of the following except one. Which one is the pain, it will be brief. I have ways to cope and Ive
exception? done well using them. The patient will remind him-
A. Benefits of the procedure self of this during future dental procedures. This
B. Risks of the procedure patients statement exemplifies which of the following
C. Description of the procedure using technical strategies?
terms A. Rational response
D. Cost of the procedure B. Self-efficacy induction
5. From the following list, select the ethical principles C. Relaxation statement
found in the ADA Principles of Ethics and Code of D. Imagery
Professional Conduct. (Choose all that apply.) E. Systematic desensitization
A. Tolerance 11. In clinical practice, you frequently encounter young
B. Compassion patients who are nervous about seeing the dentist.
C. Beneficence Knowing which factors are important influences
D. Integrity on young patients comfort, consider which of
E. Veracity the following will help your patients to feel more
F. Competence comfortable?
6. From the following list, select the elements required A. Inviting a parent into the operatory for support
for a patient to give consent to treatment. (Choose all B. Placing toys and childrens books in the waiting
that apply.) room
A. Patient must be able to pay. C. Hanging child-friendly dcor in the operatory
B. Patient must voluntarily agree to treatment. D. Talking to the child about his or her interests before
C. Patient must be given the opportunity to ask beginning your work
questions. E. All of the above
D. Patient must be a minor. 12. Dental intervention studies suggest that educating
E. Patient must be experiencing an emergency. patients regarding dental care (patient education) is
F. Patients family must agree. more effective than behavioral modification (behav-
7. Risk management includes all of the following except ioral intervention) in increasing compliance.
one. Which one is the exception? A. True
A. Weighing the risks and benefits in practice B. False
B. Monitoring risky activity C. Sometimes
C. Exposing oneself to liability D. Both are equally effective
D. Eliminating dangerous activity. E. Cannot be determined
8. From the following list, select the items that support 13. Which technique is typically not useful in treating an
appropriate and adequate documentation of the patient anxious patient?
record. (Choose all that apply.) A. Using less structure in establishing rapport
A. Include specific facts B. Reassuring the patient by telling the patient not to
B. Include personal characterizations worry
C. Include criticism of patients behavior C. Providing reasons before asking for sensitive
D. Include complete documentation of contact with information
patient D. Using empathy
E. Include abbreviations E. Making expectations clear
F. Include timely entries and avoid gaps in time 14. The most common site for cancers in the oral cavity
9. The first time you perform a complicated dental pro- is _____.
cedure, you feel uncomfortable and nervous. At one A. Lip
point, you even think for a moment that you will be B. Soft palate
unable to complete the procedure. However, you stay C. Hard palate
D. Tongue A. Antisepsis
E. Tonsils B. Microbacterial control
15. The most effective method to prevent caries on the C. Sterilization
occlusal surfaces among school-age children is ______. D. Disinfection
A. Sealants E. Asepsis
B. Community water fluoridation 22. Which of the following biologic tests is used to check
C. School dietary fluoride the effectiveness of the sterilization process?
D. School fluoride mouth rinse A. Spore test
E. School fluoridation B. Total bacterial count test
16. Neither the subject nor the investigator knows to C. Aseptic test
which group a subject belongs in which type of study D. EPA test
design? E. Disinfection test
A. Matching studies 23. Which of the following guidelines are for disinfectants
B. Randomized used in dental practice?
C. Double-blind A. Have an EPA registration number
D. Single-blind B. Kill Mycobacterium tuberculosis
E. None of the above C. Have an ADA seal of approval
17. The _____ of a scientific article provides the reader D. Must be used according to guidelines
with detailed information regarding the study design. E. All of the above
A. Introduction 24. Which of the following statements about MSDSs is
B. Background correct?
C. Literature review A. Employees have the right to know about on-the-job
D. Methods hazards.
E. Abstract B. MSDSs help to protect employees.
18. The variance for data set A is 25 and for data set B is C. MSDSs contain information on hazardous materi-
9. We can conclude _____. als, substance, and wastes.
A. There are more items in data set A than data set B D. MSDSs describe chemical hazards and how to work
B. The mean of data set B is smaller than the mean of with chemicals safely.
data set A E. All of the above
C. The items in data set A are more widely spread 25. Some dental plans allow the dentist to charge the
about the mean value than the items in data patient any difference between what the plan agrees to
set B pay and the dentists UCR (usual, customary, reason-
D. The standard deviation for data set B is larger than able) fees. This arrangement is called _____.
the standard deviation for data set A A. Payment differential
E. None of the above B. Balance billing
19. What route of transmission of infectious disease is a C. Prospective reimbursement
needle-stick injury? D. Managed care
A. Direct contact E. None of the above
B. Indirect contact 26. Which of the following is true for the fluoride in fluo-
C. Accidental contact ridated water?
D. Parenteral contact A. It is odorless
E. Droplets B. It is colorless
20. Which of the following statements regarding recom- C. It is tasteless
mendations for the use of masks is true? D. A and B
A. Masks should be used whenever aerosols or spatter E. All of the above
may be generated. 27. Approximately how many people in United States live
B. A new mask should be worn for each patient. in a fluoridated community?
C. Masks should be changed at least once every A. 80 million
hour. B. 124 million
D. Masks should be changed more frequently in the C. 180 million
presence of heavy aerosol contamination. D. 204 million
E. All of the above E. 262 million
21. _____ refers specifically to the process in which an 28. What percentage of the U.S. population on public
antimicrobial agent destroys (germicide) or inhibits water supplies lives in a fluoridated community?
the growth of (microbiostatic) pathogenic microor- A. 26%
ganisms on inanimate surfaces. B. 37%
C. 55% D. Community water fluoridation

D. 74% E. School sealant programs
E. 85% 34. Fluoride supplementation for a 2-year-old child who
29. Fluoridation prevents tooth decay for what age group? lives in a nonfluoridated community can best be
A. 1 to 12 years accomplished by initially prescribing _____.
B. 13 to 20 years A. Fluoride tablets
C. 1 to 20 years B. Fluoride lozenges
D. All ages C. Fluoride drops
E. None of the above D. Fluoride mouth rinses
30. Which one of the following is an effective community E. Fluoride toothpaste
prevention program? 35. An amalgam restoration is considered _____.
A. Brushing twice a day A. Primary prevention
B. Flossing once a day B. Secondary prevention
C. A and B C. Tertiary prevention
D. School sealant programs D. Both primary and secondary prevention
E. Regular dental checkups E. Both primary and tertiary prevention
31. Which of the following is not an effective community 36. Who is responsible for educating the public on
prevention program? the safety and effectiveness of community water
A. School fluoride rinse programs fluoridation?
B. School sealant programs A. Hygienists
C. School fluoridation B. Nurses
D. Community water fluoridation C. Physicians
E. Flossing daily D. Dentists
32. What is the recommended level of fluoride for com- E. All of the above
munity water fluoridation? 37. Which one of the following statements is true?
A. 1.2 to 2.2 ppm A. Fluoride mouth rinses have been used in schools
B. 0.7 to 1.2 ppm in the United States for about a decade.
C. 0.2 to 2.2 ppm B. Fluoride varnish is a method of administering sys-
D. 2 to 4 ppm temic fluoride.
E. 7 to 12 ppm C. Sealants can halt the carious process after it has
33. What is the most cost-effective and practical measure begun.
to prevent tooth decay? D. Sealants are recommended for the first and second
A. School fluoride mouth rinse programs premolars.
B. School fluoride tablet programs E. The use of sealants is the best approach for prevent-
C. Brushing and flossing daily ing dental caries.
SECTION 7
Periodontics
KAREN NOVAK
NIKOLA ANGELOV
OUTLINE The following sections help the reader review the process
of diagnosis, treatment, and prevention while understand-
1. Diagnosis
ing the etiology and pathogenesis of the various perio
2. Etiology dontal conditions and how this may impact the ultimate
3. Pathogenesis prognosis for the patient. This review covers the topics
4. Treatment Planning outlined in the 2013 Specifications for the National Board
Dental Examination, Part II. The information in this review
5. Prognosis
is from Carranzas Clinical Periodontology, ed 10 and 11 (St.
6. Therapy Louis, Saunders, 2006, 2012), by Newman etal, and from
7. Prevention and Maintenance published literature.
1.0 Diagnosis
Periodontal disease describes a group of inflammatory
conditions that affect the supporting structures of the teeth A. Components of an accurate diagnosis of the extent and
or periodontium. The initiation, development, diagnosis, severity of periodontal disease.
and subsequent treatment of periodontal disease follow a 1. Medical history, including any serious familial condi-
well-documented sequence (Figure 7-1). Microbial plaque tions of parents or siblings such as diabetes or car-
is generally considered to be the initiating factor in peri- diovascular disease, and history of tobacco use.
odontal disease. When plaque accumulates on tooth and 2. Dental history, including current and prior family
gingival surfaces, it instigates the development of an inflam- history of periodontal disease.
matory response in the periodontal tissues. The nature and 3. Full-mouth series of periapical radiographs for
duration of the inflammatory response are critical to the assessment of alveolar bone levels.
clinical outcome. If the inflammatory response is sufficient 4. Examination of the head, neck, oral cavity, and lymph
to control the challenge from plaque without destruction nodes for any pathology.
of periodontal ligament (PDL) or alveolar bone, the clinical 5. Oral and radiographic examination of the peri
condition is termed gingivitis. If there is destruction of PDL odontal structures for the presence of plaque and
and alveolar bone, the condition is termed periodontitis. calculus (assessment of the patients level of home
The fundamental diagnosis of gingivitis or periodontitis care); inflammation (redness, swelling, bleeding
affects treatment. With gingivitis, there is no destruction of on probing); and destruction of the periodontal
the periodontium, and treatment should be focused on tissues (probing pocket depths, clinical attachment
removing plaque and controlling inflammation. In peri- levels, alveolar bone loss, tooth mobility, furcation
odontitis, the removal of plaque and control of inflamma- involvement).
tion may be supplemented with attempts to repair or 6. Notes should be made of areas of suppuration, abscess
regenerate the lost periodontal tissues and correct any ana- formation, minimal width of attached gingival (sub-
tomic deformities that may have resulted from the disease tract pocket depth from width of gingiva), obvious
process. recession, and areas of trauma from occlusion.
7. Examination of the teeth for dental caries, develop-
mental defects, anomalies of tooth form, wasting,
The section editors acknowledge Dr. M. John Novak for his previous contribu- areas of hypersensitivity, and proximal contact
tions as author and editor of this section. relationships.
251
252 Section 7 Periodontics
Genetic risk factors
Antibody Cytokines
PMNs
Antigens Host Prostanoids Connective

immune- tissue and Clinical
Microbial
inflammatory bone signs of
challenge LPS
response metabolism disease
MMPs
Other
virulence
factors
Environmental and acquired

risk factors
Tissue breakdown products and ecological changes
Figure 7-1 Schematic illustration of the pathogenesis of periodontitis. The microbial challenge presented by subgingival
plaque bacteria results in an upregulated host immune-inflammatory response in the periodontal tissues that is characterized by the
dysregulated and increased production of inflammatory cytokines (e.g., interleukins and tumor necrosis factor-); prostanoids (e.g.,
prostaglandin E2); and enzymes, including the matrix metalloproteinases (MMPs). These upregulated proinflammatory mediators are
responsible for most periodontal tissue breakdown that occurs, including alveolar bone resorption via activation of osteoclasts. Over
time, these changes result in the clinical signs of periodontal disease developing. The process is modified by environmental factors, such
as smoking, and by genetic susceptibility. LPS, Lipopolysaccharide; PMNs, polymorphonuclear leukocytes. (Modified from Page RC,
Kornman KS: The pathogenesis of human periodontitis: an introduction. Periodontol 2000 14:9, 1997.)
a. Erosion (sometimes called corrosion)usually in

the cervical area of facial surface of tooth; may be
caused by acid beverages or citrus fruits.
b. Abrasionloss of tooth substance by mechanical
wear. Horizontal toothbrushing (scrubbing) with
an abrasive dentifrice is the most common cause.
c. Attritionocclusal wear resulting from functional
contacts with opposing teeth; results in wear facets
on the occlusal surfaces of teeth; may be due to
functional or parafunctional habits.
d. Abfractionocclusal loading resulting in tooth
flexure, mechanical microfractures, and tooth sub-
stance loss in the cervical area; may appear similar
to erosion. A B C
e. Hypersensitivityas a result of exposure of den- Figure 7-2 Different types of periodontal pockets. A, Gin-
tinal tubules in root surfaces to thermal changes gival pocket. There is no destruction of the supporting periodon-
following recession and removal of cementum by tal tissues. B, Suprabony pocket. The base of the pocket is coronal
toothbrushing, dietary acids, root decay, or profes- to the level of the underlying bone. Bone loss is horizontal.
sional treatment such as scaling and root planing. C, Intrabony pocket. The base of the pocket is apical to the level
B. Periodontal examination. of the adjacent bone. Bone loss is vertical. (From Newman
1. Probing pocket depth (distance from the gingival MG, etal: Carranzas Clinical Periodontology, ed 12. St. Louis,
margin to the base of the pocket detected with the Saunders, 2015.)
periodontal probe, which can be classified as gingi-
val, suprabony, and intrabony) (Figure 7-2); clinical are the most objective periodontal measures and
attachment loss (distance from the cementoenamel enable the clinician to differentiate between health,
junction [CEJ] to the base of the pocket detected gingivitis, and periodontitis.
with a periodontal probe); and bleeding on probing 2. Additional measures include gingival recession (expo-
(measure of inflammation in the periodontal tissues) sure of the root surface because of an apical shift in
Section 7 Periodontics 253
the position of the gingival margin). Recession is b. Factors involvedfactors that can predispose a
measured from the CEJ to the crest of the gingival tooth to furcation involvement include short root
margin and is associated with attachment loss. Reces- trunk length, short roots, and narrow interradicu-
sion may be enhanced by trauma from toothbrush- lar dimension. The presence of cervical enamel
ing, teeth that are positioned or have been moved projections into the furcation also can be a predis-
buccally with orthodontics, or teeth that are large posing factor.
compared with the width of the periodontal support- c. Probingfurcations in mandibular molars are
ing tissues. probed from the buccal/facial and from the lingual.
3. Alveolar bone loss is frequently used as a measure of Furcations in maxillary molars are probed from
periodontal disease from examination of x-rays. This the mesial (mesial furcation between mesiobuccal
is not a reliable measure of periodontal disease and palatal roots), buccal (buccal furcation between
because there is considerable variability in the normal the two buccal roots), and distal (distal furcation
height of the alveolar bone. Bone loss on x-rays between distobuccal and palatal roots).
should be evaluated in combination with probing C. Radiographic assessment.
pocket depth and clinical attachment loss to provide 1. Bone loss on traditional x-raysthe average distance
an accurate measure of a patients periodontal status. from the CEJ to the crest of the alveolar bone in
Bone loss may be described as horizontal or vertical. health is approximately 2mm. The normal angula-
Vertical defects can be classified by the number of tion of the crest of the alveolar bone is parallel to a
bony walls they have remaining. line joining the CEJs of adjacent teeth. A horizontal
4. Suppuration is an important measure of the inflam- pattern of bone loss occurs parallel to this line.
matory response to periodontal infection because it Angular bone loss is usually created when bone is lost
is due to the presence of large numbers of neutrophils on one tooth surface at a greater rate and greater
in the periodontal pocket. Suppuration from the extent than on an adjacent tooth surface. A full-
pocket may be seen during periodontal probing or by mouth series of periapical radiographs is recom-
palpation of the pocket wall. These areas should be mended to visualize all proximal root surfaces and
aggressively treated to reduce the microbial chal- bone levels.
lenge. Suppuration may be seen frequently in patients 2. Digital and subtraction radiographydigital radiog-
with severe disease or patients who have a systemic raphy allows for computerized images to be stored
condition that alters the ability of the host to deal and corrected for exposure. Digital radiography may
with infection. reduce exposure to radiation compared with tradi-
5. Mobility assessmentincreases in tooth mobility may tional x-rays. Using serial x-rays of teeth and bone
be due to a loss of periodontal support, excessive taken at the same location and angulation, changes
occlusal forces, or a combination of both. Mobility is in bone density can be observed using a computer-
usually measured by placing an instrument on the ized technique known as subtraction radiography.
buccal surface and an instrument on the lingual/ Changes in bone density may be associated with
palatal surface and moving the tooth buccolingually. disease progression.
Mobility can be measured in many ways but is 3. Cone beam computed tomography (CBCT)CBCT
assessed based on the ease and extent of tooth provides an accurate three-dimensional image of
movement. teeth and supporting structures, including bony
a. Grade Islightly more than normal. defects. CBCT is an advanced imaging technique that
b. Grade IImoderately more than normal. is currently used primarily for patients requiring
c. Grade IIIsevere mobility faciolingually or mesio- implant therapy.
distally (or both), combined with vertical displace- D. Summarizing clinical findingsusing the information
ment (the tooth can be depressed in the socket). described previously, the clinician can now diagnose
6. Furcation assessmentthe complex anatomy of the one of the following conditions (Box 7-1).
furcation makes this a difficult area to treat and 1. Periodontal healthno inflammation and no loss of
maintain. clinical attachment and alveolar bone.
a. Classification of furcation involvements. 2. Gingival diseasegingival inflammation with no loss
(1) Grade Iincipient. of clinical attachment and alveolar bone.
(2) Grade IIcul-de-sac with definite horizontal 3. Periodontitisperiodontal inflammation that has
component. extended into the PDL and alveolar bone, resulting
(3) Grade IIIcomplete bone loss in the in loss of clinical attachment and alveolar bone;
furcation. usually accompanied by increased probing pocket
(4) Grade IVcomplete bone loss in the furcation depths, although deep pockets may not be present if
and recession of the gingival tissues resulting recession of the gingival margin occurs at the same
in a furcation opening that is clinically visible. rate as attachment loss.
Box 7-1
Classification of Periodontal Diseases and Conditions
Gingival Diseases Abscesses of the Periodontium
Plaque-induced gingival diseases* Gingival abscess
Nonplaque-induced gingival lesions Periodontal abscess
Pericoronal abscess
Chronic Periodontitis Periodontitis Associated with Endodontic Lesions
Localized Endodontic-periodontal lesion
Generalized Periodontal-endodontic lesion
Combined lesion
Aggressive Periodontitis
Localized Developmental or Acquired Deformities
Generalized and Conditions
Localized tooth-related factors that predispose to
Periodontitis as a Manifestation plaque-induced gingival diseases or periodontitis
of Systemic Diseases Mucogingival deformities and conditions around teeth
Necrotizing Periodontal Diseases Mucogingival deformities and conditions on edentulous
Necrotizing ulcerative gingivitis ridges
Necrotizing ulcerative periodontitis Occlusal trauma
Data from Armitage GC: Development of a classification system for periodontal diseases and conditions. Ann Periodontol 4:1, 1999.
*These diseases may occur on a periodontium with no attachment loss or on a periodontium with attachment loss that is stable and not progressing.
Chronic periodontitis can be further classified based on extent and severity. As a general guide, extent can be characterized as localized (<30%
of sites involved) or generalized (>30% of sites involved). Severity can be characterized based on the amount of clinical attachment loss (CAL) as
follows: slight = 1 or 2mm CAL; moderate = 3 or 4mm CAL; and severe 5mm CAL.
4. Necrotizing ulcerative gingivitis or periodontitis plaque bacteria and the tissues and inflammatory
usually accompanied by necrotic ulceration of the cells of the host. The severity and duration of the
marginal gingival tissues, bleeding, pain, and fetid response can be altered by local and systemic factors
breath; may sometimes be accompanied by fever, that can affect plaque formation and retention and
malaise, and lymphadenopathy. the host response.
5. Periodontal abscesses. a. Gingival diseases modified by systemic factors
6. Periodontitis associated with endodontic lesions. systemic factors that alter the magnitude or dura-
E. Clinical features of gingivitis. tion of the host response affect the clinical
1. Overviewgingivitis is frequently associated with appearance of gingivitis. Examples include endo-
changes in color, contour, and consistency that are due crine changes during puberty, pregnancy, and dia-
to changes in the levels of inflammation. Color betes. Blood dyscrasias (e.g., leukemia) may affect
changes are due to increases in blood flow; contour the immune response through their effects on
changes are due to increases in inflammatory exu- white blood cells.
dates or edema within the gingival tissues; and con- b. Gingival diseases modified by medications
sistency changes are due to levels of inflammation or examples of medications that can cause gingival
fibrosis that frequently occurs when gingivitis is enlargement are phenytoin; immunosuppressive
long-standing and chronic. Gingival bleeding is also drugs such as cyclosporine; calcium channel block-
a characteristic of gingivitis and can occur spontane- ers such as nifedipine, verapamil, and diltiazem;
ously, during mastication, during toothbrushing, or sodium valproate; and oral contraceptives.
during periodontal probing. Gingivitis is usually c. Gingival diseases modified by malnutritionexcept
characterized as gingival inflammation in the absence for the effects of vitamin C deficiency (scurvy),
of clinical attachment loss. More recently, gingivitis there is little information on the effects of
also has been described in cases of gingival inflam- malnutrition.
mation around teeth that have been successfully 3. Nonplaque-induced gingival conditions.
treated for periodontitis but have developed gingival a. Gingival conditions, although uncommon, can
inflammation with no additional attachment loss as occur in response to specific infections, including
a result of poor home care. sexually transmitted infections (Neisseria gonor-
2. Plaque-induced gingivitisthe most common form rhoeae, Treponema pallidum), viral infections (her-
of gingivitis is the result of an interaction between pesviruses), and fungal infections (Candida).
b. Gingival conditions may also be hereditary (hered-

itary gingival fibromatosis) or the result of allergies
to common foods, restorative materials, tooth-
pastes or mouth rinses, and chewing gum.
c. Traumatic lesions can be factitious (unintention- A B
ally produced), iatrogenic (trauma-induced by a
dentist or health professional), or accidental
(damage through burns from hot foods and
drinks).
d. Foreign body reactions can also occur to restor-
ative materials, such as amalgam and polishing
paste, when introduced into the gingival tissues.
F. Clinical features of periodontitisperiodontitis is
defined as an inflammatory disease of the supporting
tissues of the teeth caused by specific microorganisms
or groups of specific microorganisms resulting in
progressive destruction of the PDL and alveolar
bone with pocket formation, recession, or both. The
clinical feature that distinguishes periodontitis from
gingivitis is the presence of clinically detectable attach- C D E
ment loss. The most common forms of periodontitis
and their distinguishing characteristics are listed in Figure 7-3 Diagrammatic representation of different
types of endoperiodontal problems. A, Originally an end-
Box 7-2.
odontic problem, with fistulization from the apex and along the
1. Necrotizing periodontal diseasesthe clinical appear- root to the gingiva. Pulpal infection can also spread through
ance of necrotizing diseases is unique among accessory canals to the gingiva or the furcation. B, Long-standing
periodontal diseases because of the characteristic periapical lesion draining through the PDL can become second-
ulceration and necrosis of the marginal gingiva. The arily complicated, leading to a retrograde periodontitis. C, Peri-
gingiva may be covered by a yellowish white or odontal pocket can deepen to the apex and secondarily involve
grayish slough or pseudomembrane and have blunt- the pulp. D, Periodontal pocket can infect the pulp through a
ing of the papillae, bleeding on provocation or spon- lateral canal, which can result in a periapical lesion. E, Two inde-
taneous bleeding, pain, and fetid breath. The disease pendent lesions, periapical and marginal, can coexist and eventu-
may manifest as necrotizing ulcerative gingivitis (no ally fuse with each other. (Redrawn and modified from Simon JH,
attachment loss) or necrotizing ulcerative periodonti- Glick DH, Frank AL: The relationship of endodontic-periodontic
lesions. J Periodontol 43:202, 1972.)
tis (with attachment and bone loss). Predisposing
factors may be stress, smoking, and immunosuppres-
sion such as seen with HIV infection.
2. Abscesses of the periodontiuma localized purulent 2.0 Etiology
infection defined by its tissue of origin, gingival
abscess or periodontal abscess. Frequent causes are A. Periodontal microbiologydental plaque is considered
impaction of food, such as fish bones or popcorn, the initiator of the periodontal disease process through
into the periodontal tissues. An abscess may also its ability to promote an inflammatory response in
be caused by suppuration from a periodontal the periodontal tissues, which may lead to destruction
pocket being unable to discharge through the pocket of those same tissues. Dental plaque is a complex
into the mouth and draining into the periodontal biofilm that, if left intact, is resistant to antimicrobial
supporting tissues, causing swelling and possible agents such as antibiotics. Mechanical dbridement is
pain. necessary to disrupt the biofilm. The composition of
3. Periodontitis associated with endodontic lesions plaque is considered important in the inflammatory
these may be endodontic-periodontal lesions (pulpal process, and specific microorganisms have been more
necrosis leading to periodontal problems as pus frequently associated with this disease process than
drains through the PDL), periodontal-endodontic others.
lesions (bacterial infection from a periodontal pocket 1. Dental plaque composition.
spreads to the pulp causing pulpal necrosis), or a a. Supragingival.
combined lesion (pulpal and periodontal necrosis (1) Tooth associatedgram-positive cocci and
occurring together) (Figure 7-3). If there is evidence short rods.
of pulpal disease and periodontal involvement, the (2) Mature outer surface of plaquegram-
endodontic treatment should be completed first. negative rods and filaments and spirochetes.
Box 7-2
Periodontitis
The disease periodontitis can be subclassified into the Hyperresponsive macrophages, producing increased
following three major types based on clinical, radio- PGE2 and IL-1.
graphic, historical, and laboratory characteristics. In some cases, self-arresting disease progression.
Aggressive periodontitis may be further classified into
Chronic Periodontitis localized and generalized forms based on the common
The following characteristics are common to patients features described above and the following specific
with chronic periodontitis: features:
Prevalent in adults but can occur in children. Localized Form

Amount of destruction consistent with local factors. Circumpubertal onset of disease.
Associated with a variable microbial pattern. Localized first molar or incisor disease with proximal
Subgingival calculus frequently found. attachment loss on at least two permanent teeth,
Slow to moderate rate of progression with possible one of which is a first molar.
periods of rapid progression. Robust serum antibody response to infecting agents.
Possibly modified by or associated with the
Generalized Form
following:
Usually affecting persons <30 years old (but may be
Systemic diseases such as diabetes mellitus and
older).
HIV infection.
Generalized proximal attachment loss affecting at
Local factors predisposing to periodontitis.
least three teeth other than first molars and incisors.
Environmental factors such as cigarette smoking
Pronounced episodic nature of periodontal
and emotional stress.
destruction.
Chronic periodontitis may be further subclassified Poor serum antibody response to infecting agents.
into localized and generalized forms and characterized
as slight, moderate, or severe based on the common Periodontitis as a Manifestation
features described above and the following specific of Systemic Diseases
features: Periodontitis may be observed as a manifestation of the
Localized form: <30% of sites involved. following systemic diseases:
Generalized form: >30% of sites involved. 1. Hematologic disorders
Slight: 1 to 2mm CAL. a. Acquired neutropenia
Moderate: 3 to 4mm CAL. b. Leukemias
Severe: 5mm CAL. c. Other
2. Genetic disorders
Aggressive Periodontitis a. Familial and cyclic neutropenia
The following characteristics are common to patients b. Down syndrome
with aggressive periodontitis: c. Leukocyte adhesion deficiency syndromes
d. Papillon-Lefvre syndrome
Otherwise clinically healthy patient.
e. Chdiak-Higashi syndrome
Rapid attachment loss and bone destruction.
f. Histiocytosis syndromes
Amount of microbial deposits inconsistent with
g. Glycogen storage disease
disease severity.
h. Infantile genetic agranulocytosis
Familial aggregation of diseased individuals.
i. Cohen syndrome
The following characteristics are common but not j. Ehlers-Danlos syndrome (types IV and VIII
universal: autosomal dominant)
Diseased sites infected with Aggregatibacter k. Hypophosphatasia
(formerly Actinobacillus) actinomycetemcomitans. l. Other
Abnormalities in phagocyte function. 3. Not otherwise specified
Data from Flemmig TF: Periodontitis. Ann Periodontol 4:32, 1999; Kinane DF: Periodontitis modified by systemic factors. Ann Periodontol 4:54, 1999;
and Tonetti MS, Mombelli A: Early-onset periodontitis. Ann Periodontol 4:39, 1999.
CAL, Clinical attachment loss; IL-1, interleukin-1; PGE2, prostaglandin E2.
b. Subgingival. ability to coaggregate (cell-to-cell recognition of

(1) Cervical region. genetically distinct partner cell types) with both
(a) Tooth associatedgram-positive rods and early colonizers and other secondary colonizers.
cocci. C. Dental plaque as a complex bacterial biofilm.
(b) Tissue associatedgram-negative rods 1. Overviewdental plaque is a biofilm composed of
and cocci, filaments, flagellated rods and microcolonies encased in a polysaccharide matrix.
spirochetes. Fluid-filled channels run through the plaque mass,
(2) Deeper in sulcus or pocket. permitting the passage of nutrients. Bacteria growing
(a) Tooth associatedgram-negative rods. in a biofilm are more resistant to antimicrobials than
(b) Tissue associatedgram-negative rods bacteria grown in a planktonic, or free-swimming,
and cocci, filaments, flagellated rods and form. Bacteria grown in biofilms communicate with
spirochetes. each other through quorum sensing. Quorum sensing
c. The major organic constituents of the plaque is important in the regulation of expression of spe-
biofilm are polysaccharides, proteins, glycopro- cific genes and in controlling the microbial species in
teins, and lipids. The major inorganic constituents the biofilm (encouraging the growth of species of
are calcium and phosphorus with trace amounts of benefit to the biofilm and discouraging the growth of
sodium, potassium, and fluoride. Saliva is the main competitors).
source of inorganic components in supragingival 2. Maturationas the biofilm matures, there is a
plaque, whereas components in subgingival plaque shift from a predominance of facultative, gram-
are derived primarily from the gingival crevicular positive microorganisms to gram-negative, anaerobic
fluid. microorganisms.
B. Dental plaque formationplaque formation can be 3. Complexesresults of DNA-DNA hybridization
divided into three phases. studies (checkerboard analyses) have led to the
1. The first phase is formation of the pellicle, which identification of complexes of periodontal microor-
occurs within seconds after the tooth surface is ganisms that were given color designations.
cleaned. The pellicle consists of glycoproteins a. The so-called red complex (P. gingivalis, Tannerella
(mucins), proline-rich proteins, phosphoproteins forsythia, and Treponema denticola) is associated
(e.g., statherin), histidine-rich proteins, enzymes with bleeding on probing and deeper pockets.
(e.g., amylase), and other molecules that serve as b. The presence of so-called orange complex mi
attachment sites for bacteria. croorganisms (Fusobacterium species, Prevotella
2. The second phase is the initial adhesion and attach- species, and Campylobacter species) precedes
ment of bacteria. The initial adhesion is reversible and the presence of the red complex, supporting
is mediated through van der Waals and electrostatic the sequential nature of plaque formation and
forces. After initial adhesion, a firm attachment is maturation.
established that is dependent on specific bacterial c. The existence of complexes of species in plaque
adhesin molecules and host pellicle receptor also is a reflection of bacterial interdependency
interactions. within the biofilm.
3. The third phase is colonization and plaque matura- D. Factors influencing dental plaque biofilm formation
tion. This occurs when the firmly attached, primary factors that can influence the rate of dental plaque
colonizing bacteria provide new receptors for attach- biofilm formation between individuals include clinical
ment of other bacteria (coadhesion). The aggre- wettability of the tooth surface, saliva-induced aggrega-
gated bacteria start growing, resulting in the tion of oral bacteria, salivary flow conditions, diet,
formation of microcolonies and the development of chewing fibrous food, smoking, tongue and palate
a mature biofilm. brushing, stability of bacteria in the saliva, chemical
4. Phases of specific bacteriathere is a sequential composition of the pellicle, and retention depth of the
nature to the deposition of bacteria on the tooth dentogingival area. Plaque formation also varies by area
surface. of the mouth, tooth surface, and presence or absence of
a. Streptococcus and Actinomyces species are early or inflammation.
primary colonizers. E. Characteristics of bacteria found in the dental plaque
b. Late (secondary) colonizers include Prevotella biofilmgram-positive early colonizers use sugars as
intermedia, Prevotella loescheii, Capnocytophaga an energy source and saliva as a carbon source. Anaero-
species, Campylobacter species, Porphyromonas bic microorganisms that predominate in mature plaque
gingivalis, Treponema species, and Aggregatibacter are asaccharolytic and use amino acids and small pep-
actinomycetemcomitans. tides as energy sources. Bacterial enzymes that degrade
c. Fusobacterium nucleatum serves as an important host proteins may be important in the acquisition of
middle or bridging microorganism because of its these amino acids and small peptides. Endotoxin is a
constituent of gram-negative microorganisms that is an rods and filaments appear, followed by spirochetal
important initiator of the inflammatory host response. and motile microorganisms.
F. Plaque hypotheses in the initiation of periodontal 3. Chronic periodontitisthe microflora of chronic
disease. periodontitis is composed predominantly of gram-
1. The nonspecific plaque hypothesis states that peri- negative, anaerobic species. The species often include
odontal disease results from the elaboration of P. gingivalis, T. forsythia, P. intermedia, Campylo-
noxious products by the plaque biomass, indicating bacter rectus, Eikenella corrodens, F. nucleatum, A.
that the quantity of plaque is of most importance in actinomycetemcomitans, Peptostreptococcus micros,
the initiation of disease. This hypothesis is contra- Treponema species, and Eubacterium species. There
dicted by the finding that some patients with little also is evidence that the herpesvirus microorgan-
plaque have severe periodontitis. isms, Epstein-Barr virus 1 and human cytomegalovi-
2. The specific plaque hypothesis states that the patho- rus, are associated with chronic periodontitis and the
genic potential of plaque depends on the presence of, presence of P. gingivalis, T. forsythia, P. intermedia,
or increasing numbers of, specific microorganisms. and T. denticola.
As a result, many years have been spent trying 4. Aggressive periodontitisA. actinomycetemcomitans
to identify the specific pathogens associated with is generally accepted as the primary etiologic agent
disease. of localized aggressive periodontitis. Other associ-
3. The ecologic plaque hypothesis states that putative ated microorganisms include P. gingivalis, E. cor-
periodontal pathogens are present in both healthy rodens, C. rectus, F. nucleatum, B. capillus, Eubacterium
and diseased sites. A change in the pocket environ- brachy, Capnocytophaga species, and spirochetes.
ment (e.g., a change in the nutrient status) is the Generalized aggressive periodontitis is primarily
primary cause for the overgrowth of the putative associated with P. gingivalis, P. intermedia, T. for-
pathogens (Figure 7-4). sythia, and Treponema species.
G. Microbiology of specific periodontal diseases. 5. Necrotizing diseaseshigh levels of P. intermedia, spi-
1. Periodontal healththe microflora associated with rochetes, and Fusobacterium species are found in
periodontal health is primarily composed of gram- necrotizing periodontal diseases.
positive facultative cocci and rods. These microor- 6. Periodontal abscessesmicroorganisms associated
ganisms are primarily of the genera Streptococcus and with abscesses of the periodontium include F. nuclea-
Actinomyces. tum, P. intermedia, P. gingivalis, P. micros, and T.
2. Gingivitisthe microflora associated with gingivitis forsythia.
was assessed in a classic model system referred to as 7. Dental implantshealthy sulci around dental
experimental gingivitis. In this model, periodontal implants are characterized by a predominance of
health is established by professional cleaning and coccoid, aerobic species with a low number of gram-
personal oral hygiene measures. This is followed by a negative anaerobic species. In contrast, the pockets
21-day period of abstinence from all oral hygiene associated with periimplantitis are colonized by high
measures. The initial microbiota is composed of proportions of anaerobic gram-negative rods, motile
gram-positive rods and cocci and gram-negative microorganisms, and spirochetes. They also may be
cocci. In the transition to gingivitis, gram-negative colonized by other species such as Pseudomonas
Predominantly
gram +ve micobiota,
Plaque Reduced Low GCF flow many facultative anaerobes,
reduction inflammation higher Eh gingival health
Inflammatory Environmental
Ecological shift
response change
Plaque Increased High GCF flow Predominantly

accumulation inflammation lower Eh gram -ve micobiota,
many obligate anaerobes,
peridontal disease
Figure 7-4 Ecologic plaque hypothesis in relation to periodontal diseases: gingivitis and periodontitis. Accumulation
of plaque causes inflammation of adjacent tissues (gingivitis) and other environmental changes that favor the growth of gram-negative
anaerobes and proteolytic species, including periodontopathogens. The increased proportions of such species results in destruction of
periodontal tissues (i.e., periodontitis). Eh, Redox-potential; GCF, gingival crevicular fluid; gram +ve, gram-positive; gram ve, gram-
negative. (Adapted from Marsh PD: Microbial ecology of dental plaque and its significance in health and disease. Adv Dent Res 8:263,
1994.)
aeruginosa, Candida albicans, and Staphylococcus pregnancy gingivitis and necrotizing periodontal
species. diseases.
H. Virulence factors of periodontopathogensvirulence 5. C. rectus is a motile, gram-negative rod that has a
factors (molecules that contribute to disease) of peri- polar flagellum. It grows anaerobically and grows as
odontal microorganisms can be classified into factors a pigmented colony when sulfide is added to the
that promote colonization (fimbriae or pili); factors that medium.
promote host tissue destruction (extracellular proteo- 6. F. nucleatum is a nonmotile, gram-negative bacillus
lytic enzymes, specifically P. gingivalis gingipains and A. that has pointed ends. It grows anaerobically. Specific
actinomycetemcomitans collagenase); factors that help virulence properties include induction of apoptotic
the bacterium to evade the host immune response cell death in mononuclear and polymorphonuclear
(extracellular capsule); molecules that degrade host cells and release of tissue-damaging substances from
immune cells (e.g., the A. actinomycetemcomitans leu- leukocytes. F. nucleatum can be found in both healthy
kotoxin); molecules that bind or degrade complement and diseased patients. F. nucleatum is considered to
components; and molecules that promote invasion of be an important bridging microorganism between
host cells. Characteristics and select virulence factors of early and late colonizers of dental plaque.
specific periodontal pathogens include the following. 7. Spirochetes are motile, gram-negative spiral microor-
1. A. actinomycetemcomitans is a nonmotile, gram- ganisms. The spirochetes most often associated with
negative straight or curved rod. There are five sero- periodontal diseases include T. denticola, T. vincentii,
types based on polysaccharide composition. It grows and T. socranskii. They are difficult to grow and
as smooth, white, nonhemolytic colonies on blood require strict anaerobic conditions. Specific patho-
agar plates. It is capnophilic, meaning it grows well genic properties include penetration of epithelium
in a carbon dioxide environment (5% to 10%). It is and connective tissue and production of proteolytic
most closely associated with localized aggressive enzymes that can degrade collagen and destroy
periodontitis. Specific virulence factors include the immunoglobulins and complement factors. Oral
following. treponemes are closely associated with necrotizing
a. A leukotoxin that kills human neutrophils, mono- periodontal diseases. T. denticola is a red complex
cytes, and some lymphocytes. bacterium.
b. Lipopolysaccharide. 8. P. micros and Eubacterium species are both gram-
c. Collagenase. positive, anaerobic microorganisms. P. micros is a
d. A protease that cleaves IgG. coccus; Eubacterium species are small, pleomorphic
2. T. forsythia is a nonmotile, gram-negative pleomor- rods.
phic rod. It grows slowly only under anaerobic condi- I. Local factors that may promote the accumulation and
tions and requires specific growth factors such as retention of plaque microorganisms and lead to peri-
N-acetylmuramic acid. Specific virulence factors odontal diseasealthough bacterial plaque is the
include proteolytic enzymes that cleave immuno- primary etiologic factor for the initiation of periodontal
globulins and complement components. It is a disease, other factors that may contribute to gingival
member of the red complex of bacteria. inflammation include calculus, malocclusion, faulty
3. Porphyromonas gingivalis is a nonmotile, gram- restorations, complications associated with orthodontic
negative pleomorphic rod. It grows anaerobically and therapy, self-inflicted injuries, use of tobacco, and radi-
becomes darkly pigmented on blood agar plates. It ation therapy.
also can invade epithelial and endothelial cells. It is 1. Calculus is mineralized bacterial plaque. It forms on
most closely associated with chronic periodontitis natural teeth and on prosthetic devices. Precipita-
and is a member of the red complex of bacteria. Spe- tion of mineral salts into soft plaque usually starts
cific virulence factors include the following. within 1 to 14 days of plaque formation. The initia-
a. Fimbriae important in adherence. tion of calcification and rate of calculus formation
b. Presence of a capsule. vary among individuals, within an individual, and
c. Proteases that cleave immunoglobulins and com- for individual teeth. Calculus can be classified as
plement components. supragingival and subgingival.
d. Proteases that cleave other tissue-associated host a. Supragingival calculus is often white in color,
proteins (gingipains). unless stained by food and tobacco products.
e. Collagenase. Inorganic components, calcium phosphate (75%),
f. A hemolysin. calcium carbonate (3%), and traces of magnesium
4. P. intermedia and Prevotella nigrescens are nonmotile, phosphate and other metals, account for 70%
gram-negative, rods. They grow anaerobically and to 90% of supragingival calculus. Most of the
become darkly pigmented when grown on blood agar inorganic component of calculus is crystalline
plates. P. intermedia is most closely associated with in structure. The main crystal forms are
hydroxyapatite (58%), magnesium whitlockite cells, and leukocytes that is less adherent than dental
(21%), octacalcium phosphate (12%), and brush- plaque. Materia alba generally can be easily dis-
ite (9%). Saliva is the primary source of sub- placed with water spray or irrigation. The presence
stances important in the mineralization of of bacteria may lead to materia alba serving as an
supragingival calculus. Because of the proximity irritant to gingival tissues.
of Whartons, Bartholins, and Stensens ducts, 3. Stains on the teeth do not contribute to gingival
supragingival calculus commonly forms on the inflammation and are primarily an esthetic concern.
lingual surfaces of mandibular anterior teeth and 4. Malocclusion, manifest as irregular alignment of the
buccal surfaces of maxillary molars. teeth, may create plaque retentive areas and make
b. Subgingival calculus is often dark as a result of plaque removal more difficult. Roots of teeth that
exposure to gingival crevicular fluid. The com are prominent in the arch or that are associated with
position is similar to supragingival calculus. frenum attachments often exhibit gingival reces-
However, the components important in mineral- sion. Mesial drift or extrusion associated with failure
ization are derived from the gingival crevicular to replace missing teeth may result in occlusal prob-
fluid rather than saliva. lems that contribute to food impaction and plaque
c. The organic component of calculus is composed retention.
of a mixture of protein-polysaccharide com- 5. Faulty restorations, manifest by overhanging mar-
plexes, desquamated epithelial cells, leukocytes, gins, rough surfaces, open margins, open contacts,
and microorganisms. and overcontoured crowns, may create an environ-
d. Calculus attachment occurs through four ment conducive to plaque retention. This is espe-
mechanisms. cially detrimental when the faulty restoration is
(1) Attachment via organic pellicle on enamel. located subgingivally, where a niche is created for
(2) Mechanical locking into surface irregularities. the growth of disease-associated microorganisms
(3) Close adaptation of calculus undersurface and plaque removal is difficult.
depressions to cementum. 6. Subgingival margins, even when not faulty, are
(4) Penetration into cementum. associated with plaque accumulation, gingival
e. Plaque becomes mineralized by two proposed inflammation, and deeper pockets. Well-contoured
mechanisms. supragingival margins have little detrimental effect
(1) A local increase in the degree of saturation of on the periodontium.
calcium and phosphate ions, potentially sec- 7. Removable partial dentures may result in increased
ondary to an increase in pH of saliva and mobility of abutment teeth and increased plaque
binding of calcium and phosphate ions into accumulation.
colloidal proteins in saliva, which ultimately 8. Orthodontic therapy has been shown to increase
leads to a precipitation of calcium phosphate plaque retention and to result in increases in the
salts. numbers of Prevotella melaninogenica, P. interme-
(2) The induction of small foci of calcification dia, and Actinomyces odontolyticus. It also can lead
secondary to the presence of seeding agents to direct damage of gingival tissues and the creation
such as the intercellular matrix of plaque. of excessive forces on the periodontium. These
This second mechanism is known as the factors may be most important in adult patients
epitactic concept or heterogeneous nucleation. undergoing orthodontic therapy. In all cases, peri-
Mineralization starts extracellularly around odontal health should be established before initiat-
both gram-positive and gram-negative mi ing orthodontic therapy.
croorganisms, although Bacterionema and 9. Self-inflicted injuries, such as improper toothbrush-
Veillonella species can form intracellular hy- ing, improper use of toothpicks, application of
droxyapatite crystals. fingernail pressure against gingival tissues, and
f. Calculus deposits can be detected visually or with application of caustic agents against the gingival
an explorer. Drying calculus with air improves the tissues (e.g., aspirin) can damage gingival tissues.
ability to see it visually. Calculus located on inter- 10. Wearing oral jewelry in the tongue or lip also
proximal surfaces (supragingival and subgingi- can result in recession, pocket formation, and
val) frequently can be seen radiographically. bone loss.
g. Although calculus does not serve as a mechanical 11. An aggressive horizontal brushing technique can
irritant to the gingival tissues, it is always covered cause abrasions of the gingiva and tooth structure.
with a layer of bacterial plaque. This bacterial This damage is enhanced if the patient also uses an
plaque serves as the primary irritant. abrasive dentifrice or uses an electronic toothbrush
2. Materia alba is a concentration of microorganisms, improperly. Gingival recession and root surface
salivary proteins and lipids, desquamated epithelial exposure can be sequelae of these habits.
3.0 Pathogenesis in an increase in the extent and severity of periodon-

tal tissue damage.
The pathogenesis (genesis of pathologic change; the cellular 3. A combination of these factors.
events and reactions and other pathologic mechanisms D. Characteristics of the host response in periodontal
occurring in the development of disease) of periodontal disease.
diseases is the result of a complex interaction between 1. Cells of the host response.
plaque microorganisms and the host response to the pres- a. Overviewneutrophils, monocytes/macrophages,
ence of microorganisms on tooth and gingival tissues. As mast cells, and dendritic cells are considered to be
outlined in Figure 7-1, microbial plaque is considered to be cells of the innate immune response that is with
the initiator of the disease process because it serves as a us and protects us from birth. Lymphocytes are
challenge to the host and host tissues (periodontal tissues). considered part of the specific immune response,
How the host responds to the plaque challenge determines and these cells develop antigen-specific responses
the severity and extent of the tissue damage associated with throughout life. T cells, B cells, and plasma cells are
that response. the major cells of the specific response.
A. Periodontal healthin periodontal health, there is b. Polymorphonuclear neutrophils (PMNs; polymor-
insufficient plaque challenge to elicit an inflammatory phonuclear leukocytes)PMNs migrate from the
response that is clinically visible as a change in color, blood vessels of the subepithelial vascular plexus
contour, or consistency of the gingival tissues. When into the periodontal pocket where they interact
clinically healthy periodontal tissues are viewed by his- with plaque microorganisms (Figure 7-5). The
tology, there is usually some degree of gingival inflam- primary role of PMNs is to protect the body from
mation as evidenced by the presence of neutrophils. infection through phagocytosis and bacterial
Perfect periodontal health is nearly impossible to killing. However, they are also considered to be an
achieve because of the inability to remove plaque com- important cell in the destruction of the periodontal
pletely from tooth and gingival surfaces. The lack of tissues through the release of destructive mole-
plaque challenge can be due to several reasons. cules, such as matrix metalloproteinases (MMPs),
1. Minimal amounts of plaque present because of excel- lysosomal enzymes, cytokines, and reactive oxygen
lent oral hygiene. species (ROS). PMNs move from blood vessels
2. A plaque that is made up primarily of gram-positive toward sites of infection by a process of directed
bacteria that do not promote a discernible host locomotion (chemotaxis) along a gradient of pow-
response. erful chemotaxins such as C5a, IL-8, LtB4, and the
3. A combination of both characteristics. bacterial protein N-fMLP. PMNs are capable of
B. Gingivitispathologic changes observed in gingivitis internalizing microorganisms by a process of
are characterized by changes in color, contour, and con- phagocytosis and, once internalized, they can kill
sistency of the gingival tissues that are frequently asso- and digest the microorganisms using a powerful
ciated with increased redness, swelling, and bleeding on mixture of oxygen radicals (H2O2, O2) and granule
probing. These clinical and histologic changes are due enzymes (myeloperoxidase) that form the biologic
to the presence of an increased inflammatory response equivalent of commercial bleach. Abnormalities in
that extends into and destroys cells and matrices of the neutrophil function (Chdiak-Higashi syndrome,
gingival tissues but does not result in destruction of Papillon-Lefvre syndrome, leukocyte adhesion
PDL and bone. The pathology associated with gingivitis deficiency) and numbers (neutropenia, agranulo-
is completely reversible with the removal of plaque and cytosis) make the host more susceptible to infec-
the resolution of the inflammation. tion (Table 7-1).
C. Periodontitispathologic changes in periodontitis are c. Monocytes/macrophagesmonocytes are also part
the same as changes that occur in gingivitis except of the leukocyte family but live much longer in the
that the inflammation and tissue destruction extend tissues than neutrophils. They are responsible for
from the gingival tissues into the PDL and alveolar ingesting antigens (e.g., bacteria) and presenting
bone, resulting in an irreversible destruction of peri- them to the cells of the specific immune response.
odontal tissues. The extent and severity of periodontal They are also very important in regulating the
destruction reflects the extent and severity of the immune response through the release of chemical
inflammatory process. The extent and severity of the signals called cytokines. Fixed macrophages and
inflammatory response can be influenced by several histiocytes are present in the gingival connective
factors. tissue as part of the reticuloendothelial system.
1. The failure to remove plaque from tooth and gingival d. Mast cells are important in immediate inflamma-
surfaces, resulting in a chronic challenge to the host. tion and are responsible for creating vascular per-
2. Environmental or genetic factors that may enhance meability and dilation. They are important cells in
the host response to the plaque challenge, resulting anaphylaxis and allergic responses.
A. Chemotaxis e. Dendritic cells are distributed throughout the

tissues and are important in antigen processing
Bacterial
pathogen and presentation to cells of the specific immune
response. Dendritic cells and macrophages express
C5a pattern recognition receptors that interact with
microbe-associated molecular patterns on micro-
organisms to initiate immune responses. These
types of innate immune responses provide imme-
B. Initiate Phagocytosis diate protection from microbial infection. Signal-
ing pathways activated by pattern recognition
receptors generally upregulate cytokine secretion
iC3b
CR3 and lead to enhanced signaling of the adaptive
immune response.
f. Lymphocytesthe predominant lymphocytes are B
cells and T cells. B cells differentiate into plasma
C. Oxygen Reduction cells and are responsible for the production of anti-
bodies. T cells (derived from the thymus) fall into
NADPH oxidase
O2 + e- O2- + H+ HO2 two major groups: T helper cells (CD4 cells), which
iC3b O2- + HO2 + H+ H2O2
CR3 help in the production of antigen-specific antibod-
ies by B cells and plasma cells, and T cytotoxic cells
(CD8 cells), which are important in controlling
intracellular antigens such as bacteria, fungi, and
D. Killing viruses. Natural killer (NK) cells are T cells that
H2O2 + Cl- HOCl can recognize and kill tumor and virally infected
Myeloperoxidase cells.
iC3b
CR3 2. Controlling the bacterial challengeneutrophils
(PMNs) are the most important cells involved in con-
trolling the bacterial challenge. They migrate from
Phagolysosome
blood vessels under the gingival epithelium (subepi-
Defensins, neutral serine proteases, thelial vascular plexus), into the periodontal pocket,
bactericidal/permeability increasing
protein, LL37, lysozyme where they form a barrier to protect the body from
periodontal bacteria. They phagocytose and kill bac-
Figure 7-5 After neutrophils exit the blood, they must kill teria and release large quantities of oxygen radicals
the offending pathogens. This process consists of overlapping and enzymes (myeloperoxidase, lysozyme, collage-
steps, as illustrated in this diagram. A, Chemotaxis refers to nase) into the extracellular environment where they
directed motility that enables the leukocyte to locate its target. can damage host tissues.
C5a is a chemotaxin, which may be generated by any target that 3. Tissue destruction in periodontal diseaseperiodontal
activates complement. B, Phagocytosis also requires the interac- cells and tissues are destroyed by cells and proteins
tion of receptors with a few ligands. The diagram illustrates the
of the immune response. MMPs are considered the
important interaction between the opsonin iC3b, which coats
most important proteinases involved in the destruc-
an offending particle or cell, and the opsonic receptor CR3.
C, Oxygen reduction requires the presence of oxygen and a certain tion of periodontal tissues. They are produced by
oxidation-reduction (redox) potential, both of which can vary in most cells of the periodontal tissues, but PMNs
the gingival crevice. The formation of several oxygen metabolites produce large quantities of MMP-8 (collagenase)
can kill some bacteria. D, Killing involves several processes. First, that is responsible for destroying collagen of the
phagocytosis traps the microorganism in the stringent environ- periodontal connective tissues and PDL (Table 7-2).
ment of the phagosome. Second, the phagosome and lysosomes MMPs are inhibited by tetracycline class antibiotics.
(granules) fuse to form the phagolysosome. In this step, all the Subantimicrobial formulations of doxycycline exploit
toxic compounds of the lysosome (e.g., defensins, neutral serine this property, and doxycycline has been licensed as a
proteases) are dumped into the phagolysosome. Third, myeloper- systemic adjunctive drug for treating periodontitis.
oxidase in the phagolysosome can convert hydrogen peroxide
Oxygen radicals (superoxide and hydrogen perox-
(H2O2) to hypochlorous acid (HOCl). (From Newman MG, etal:
ide) produced by inflammatory cells (PMNs and
Carranzas Clinical Periodontology, ed 12, St. Louis, Saunders,
2015.) macrophages) are also toxic to cells of the periodon-
tium having a direct effect on cell functions and
DNA.
4. Cytokines are important signaling molecules released
from cells. The cytokine IL-1 is important in bone
Table 7-1
Systemic Neutrophil Abnormalities Associated with Aggressive Periodontitis
CONDITION NEUTROPHIL ABNORMALITY PERIODONTAL MANIFESTATIONS
Neutropenia, Decreased number of neutrophils Severe aggressive periodontitis
agranulocytosis
Chdiak-Higashi Decreased neutrophil chemotaxis and secretion Aggressive periodontitis and oral ulceration
syndrome
Neutrophil granules fuse to form characteristic Syndrome caused by mutation in the vesicle trafficking
giant granules called megabodies regulator gene, LYST
Papillon-Lefvre Multiple functional neutrophil defects, Severe aggressive periodontal destruction at an early
syndrome including myeloperoxidase deficiency, age, which may involve primary and permanent
defective chemotaxis, and phagocytosis dentition
Recently associated with mutation in cathepsin C gene
Leukocyte adhesion Defects in leukocyte function caused by lack of Aggressive periodontitis at an early age and affecting
deficiency type 1 integrin-2 subunit (CD18) primary and permanent dentition, in individuals
(LAD-1) who are homozygous for defective gene
Neutrophil defects include impaired migration
and phagocytosis
Histologically, almost no extravascular
neutrophils are evident in periodontal lesions
Leukocyte adhesion Neutrophils fail to express the ligand (CD15) Aggressive periodontitis at a young age
deficiency type 2 for P- and E-selectins, resulting in impaired
(LAD-2) transendothelial migration in response to
inflammation
From Newman MG, etal: Carranzas Clinical Periodontology, ed 12. St. Louis, Saunders, 2015.
resorption; IL-8 is important in attracting inflamma- 7. Pathogenesis of periodontitisthere are few dif
tory cells (chemotactic); and tumor necrosis factor ferences between stage 3 of gingivitis and the de-
(TNF) is important in activating macrophages. structive lesion of periodontitis except that the
5. Prostaglandins are produced from arachidonic acid of inflammatory lesion becomes bigger and moves into
cell membranes in response to cyclooxygenases the PDL and bone. The severity and extent of peri-
(COX-1 and COX-2). They have widespread proin- odontal destruction is determined by the magnitude
flammatory effects but can be inhibited by nonsteroi- and duration of the inflammatory response. With in-
dal antiinflammatory drugs (NSAIDs) (e.g., aspirin). creased severity of the response, there is an increase
However, the negative side effects of these drugs have in the release of the tissue destructive MMPs and
limited their use as adjuncts in treating periodontal proinflammatory cytokines listed earlier. Risk factors
disease. such as smoking, diabetes, and genetic susceptibility
6. Pathogenesis of gingivitisthe development of gingi- to an enhanced or diminished host response may
vitis from healthy tissues is characterized in three affect the extent and severity of the host response
stages (Box 7-3). (Figure 7-6).
a. Stage 1, initial lesion2 to 4 days with vascular 8. Environmental and systemic factors that may influ-
dilation, infiltration of PMNs, perivascular colla- ence the progression of periodontal disease
gen loss, and increased gingival crevicular fluid although bacterial plaque is the primary etiologic
flow. factor for periodontal disease, how the host responds
b. Stage 2, early lesion4 to 7 days with increase in to this bacterial challenge is critical in the pathogenic
vasculature, lymphocyte infiltration, increased col- process. The host response varies among individuals
lagen loss, and redness and bleeding on probing. and may explain much of the difference in disease
c. Stage 3, established lesion14 to 21 days with severity seen in periodontal disease. Either an insuf-
increased vasculature; mature plasma cells in the ficient response or an exaggerated host response can
tissues; collagen loss; and clinical changes in color, lead to more severe forms of disease. Various envi-
contour, and consistency. ronmental and systemic influences can have an effect
d. A fourth stage has been described as the advanced on the periodontium. The magnitude of the inflam-
stage, which is the stage where characteristics of matory response can be altered by environmental
stage 3 move into the PDL and bone to create (smoking/tobacco use), systemic (endocrine disor-
periodontitis. ders and hormonal changes, hematologic disorders,
Table 7-2 Box 7-3

Biologic Activities of Selected Matrix Key Features of Histologic Stages of
Metalloproteinases Relevant to Gingivitis and Periodontitis
Periodontal Disease
Initial LesionCorresponds to Clinically Healthy
MMP TYPE ENZYME BIOLOGIC ACTIVITY Gingival Tissues
Collagenases All Degrade interstitial Slightly elevated vascular permeability and
collagen (type I, II, III)
vasodilation.
Digest ECM and non-ECM
molecules GCF flows out of the sulcus.
MMP-1 Keratinocyte migration Migration of leukocytes, primarily neutrophils, in
and reepithelialization relatively small numbers through the gingival
Platelet aggregation connective tissue, across the junctional epithelium,
MMP-13 Osteoclast activation
and into the sulcus.
Gelatinases All Degrade denatured
collagens and gelatin Early LesionCorresponds to Early Gingivitis
MMP-2 Differentiation of That Is Evident Clinically
mesenchymal cells with
inflammatory phenotype Increased vascular permeability, vasodilation, and
Epithelial cell migration GCF flow.
Increased bioavailability of Large numbers of infiltrating leukocytes (mainly
MMP-9
neutrophils and lymphocytes)
Stromelysins All Digest ECM molecules Degeneration of fibroblasts.
MMP-3 Activates pro-MMPs
Collagen destruction, resulting in collagen-depleted
Disrupted cell aggregation
Increased cell invasion areas of the connective tissue.
Proliferation of the junctional and sulcular
Matrilysins MMP-7 Disrupted cell aggregation
Increased cell invasion epithelium into collagen-depleted areas.
Membrane- All Digest ECM molecules Established LesionCorresponds to
type MMPs Activate pro-MMP-2
(except MT4-MMP)
Established, Chronic Gingivitis
MT1-MMP Epithelial cell migration Dense inflammatory cell infiltrate (plasma cells,
Degrade collagen types I, lymphocytes, neutrophils).
II and III Accumulation of inflammatory cells in the
Adapted from Hannas AR, Pereira JC, Granjeiro JM, etal: The role of matrix connective tissues.
metalloproteinases in the oral environment. Acta Odontol Scand 65:1, 2007.
Elevated release of MMPs and lysosomal contents
ECM, Extracellular matrix; MMPs, matrix metalloproteinases; MT, membrane
type. from neutrophils.
Significant collagen depletion and proliferation of
epithelium.
Formation of pocket epithelium containing large
numbers of neutrophils.
immune deficiencies, stress, and psychosomatic dis-
orders), and genetic (polymorphisms in inflamma- Advanced LesionMarks Transition from
tory genes) influences (see Figure 7-1). Gingivitis to Periodontitis
a. Cigarette smoking is a risk factor for periodontal
Predominance of neutrophils in the pocket
disease. Cigarette smokers have more periodontal
epithelium and in the pocket.
disease than nonsmokers and exhibit increased
Dense inflammatory cell infiltrate in the connective
attachment and bone loss, an increased number of
tissues (primarily plasma cells).
deep pockets, and an increased amount of calculus
Apical migration of junctional epithelium to
formation. There is a dose response with increased
preserve intact epithelial barrier.
risk for disease in individuals who smoke more
Continued collagen breakdown resulting in large
cigarettes (Tables 7-3 and 7-4).
areas of collagen-depleted connective tissue.
(1) The number of years of tobacco use, calculated
Osteoclastic resorption of alveolar bone.
in pack-years, is a significant factor in tooth
Adapted from Page RC, Schroeder HE: Pathogenesis of inflammatory
loss and periodontal disease. The prevalence
periodontal disease. A summary of current work. Lab Invest
and severity of periodontal disease in individu- 34:235-249, 1976.
als who stop smoking is between that found in GCF, Gingival crevicular fluid; MMPs, matrix metalloproteinases.
current smokers and nonsmokers. Both former
smokers and nonsmokers respond better to
Risk factors (e.g., genetics Reduction of

smoking, diabetes) risk factors
Overproduction of proinflammatory or Expression of host-derived antiinflammatory

destructive mediators and enzymes (e.g., or protective mediators
IL-1, IL-6, PGE2, TNF-, MMPs) (e.g., IL-4, IL-10, IL-1ra, TIMPs)
Underactivity or overactivity Host modulatory Resolution of

of aspects of host response therapy Inflammation
Poor compliance Subgingival OHI, SRP, surgery, antiseptics, antibiotics

Poor plaque control bioburden to reduce bacterial challenge
DISEASE HEALTH
Figure 7-6 The periodontal balance. The balance between periodontal breakdown (disease) and periodontal stability (health)
is tipped toward disease by risk factors; excessive production of inflammatory cytokines and enzymes (e.g., interleukin-1 and interleukin-6
[IL-1 and IL-6], prostaglandin E2 [PGE2], tumor necrosis factor- [TNF-], matrix metalloproteinases [MMPs]); and underactivity or
overactivity of aspects of the immune-inflammatory host response, poor compliance, and a pathogenic microflora. The balance can be
tipped toward health by risk factor modification; upregulation; and restoration of balance between naturally occurring inhibitors of
inflammation (e.g., interleukin-4 and interleukin-10 [IL-4 and IL-10], interleukin-1 receptor antagonist [IL-1ra], tissue inhibitors of
metalloproteinases [TIMPs] and host modulatory therapy (HMT) as well as antibacterial treatments such as oral hygiene instructions
(OHI), scaling and root planing (SRP), surgery, antiseptics, and antibiotics. (From Newman MG, etal: Carranzas Clinical Periodontol-
ogy, ed 12, St. Louis, Saunders, 2015.)
Table 7-3 Table 7-4

Effects of Smoking on the Etiology and Effects of Smoking on Prevalence and
Pathogenesis of Periodontal Disease Severity of Periodontal Disease
ETIOLOGIC PERIODONTAL
FACTOR IMPACT OF SMOKING DISEASE IMPACT OF SMOKING
Microbiology No effect on rate of plaque accumulation Gingivitis Gingival inflammation and bleeding
Colonization of shallow periodontal on probing
pockets by periodontal pathogens Periodontitis Prevalence and severity of periodontal
Levels of periodontal pathogens in destruction
deep periodontal pockets Pocket depth, attachment loss, bone
Immune- Altered neutrophil chemotaxis, loss
inflammatory phagocytosis, and oxidative burst Rate of periodontal destruction
response TNF- and PGE2 in GCF Prevalence of severe periodontitis
Neutrophil collagenase and elastase in Tooth loss
GCF Prevalence with increased number of
Production of PGE2 by monocytes in cigarettes smoked per day
response to LPS Prevalence and severity with smoking
Physiology Gingival blood vessels with cessation
inflammation From Newman MG, etal: Carranzas Clinical Periodontology, ed 12. St. Louis,
GCF flow and bleeding on probing Saunders, 2015.
with inflammation , Decreased; , increased.
Subgingival temperature
Time needed to recover from local
anesthesia
From Newman MG, etal: Carranzas Clinical Periodontology, ed 12. St. Louis,
Saunders, 2015.
GCF, Gingival crevicular fluid; LPS, lipopolysaccharide; PGE2, prostaglandin
E2; TNF-, tumor necrosis factor-; , decreased; , increased.
periodontal therapy (nonsurgical and surgical) hyperglycemia may play a role in the progres-
than current smokers. sion of periodontal disease.
(2) There are no differences in rates of plaque for- e. Hormonal changes associated with puberty, men-
mation in smokers versus nonsmokers. This struation, pregnancy, use of oral contraceptives,
finding suggests qualitative rather than quanti- and menopause can affect the periodontium.
tative differences in the microflora may be These changes may manifest as an exaggerated
involved in the disease process. Results of inflammatory response of the gingival tissues
checkerboard DNA-DNA hybridization dem- to local factors. The hormonal change itself does
onstrated that the orange and red microbial not cause gingivitis. Rather, it has an impact on
complexes were significantly more prevalent in how the host responds to the microbial plaque
current smokers than in former smokers and challenge.
nonsmokers. There also is evidence that T. for- (1) Puberty and related conditionsincreases in
sythia levels are higher in smokers than in gonadotropic hormones during puberty may
nonsmokers. lead to increased levels of P. intermedia and
(3) Smoking exerts a significant negative effect on Capnocytophaga species in the bacterial plaque.
the protective elements of the immune system. These increases have been associated with the
These may include functional alterations in increased gingival bleeding often seen during
neutrophils (decreased chemotaxis, decreased puberty. Hyperplastic responses of the gingival
oxidative burst), reduced levels of IgG2, ele- tissues also have been noted.
vated levels of TNF-, PGE2, neutrophil elas- (2) Menstruationincreased gingival bleeding is
tase, and MMP-8. These findings suggest that often seen during menstruation.
smoking not only dampens the response of (3) Pregnancypregnancy gingivitis increases in
host defense cells such as neutrophils but also severity beginning in the second or third
leads to increased release of tissue-destructive month. It is manifest as enlarged, edematous
enzymes. gingival tissues that demonstrate increased
(4) There appear to be alterations in the gingival ease of bleeding when the patient performs oral
microvasculature in smokers, resulting in hygiene procedures. These changes appear to
decreased blood flow and decreased clinical be associated primarily with increased levels of
signs of inflammation. progesterone, which causes dilation of the gin-
b. Smokeless tobacco use can lead to localized attach- gival microvasculature, circulatory stasis, and
ment loss and recession at the site of tobacco increased susceptibility to mechanical irritants.
product placement. In some cases, the gingival tissues become
c. Radiation therapy to oral tissues can result in enlarged to the point that they appear as large
increased periodontal attachment loss and tooth masses, which are referred to as pregnancy
loss on the irradiated side. Periodontal health tumors (pyogenic granulomas). These gingival
should be established before beginning radiation changes seen during pregnancy are usually
therapy reversible postpartum, provided that the local
d. Diabetespatients with diabetes have a higher etiologic factors have been removed.
prevalence and severity of periodontal disease than (a) Increased levels of P. intermedia have been
individuals without diabetes. Diabetes does not found during pregnancy. This increase
cause periodontal disease, but there is evidence appears to be associated with the elevation
that it alters the response of the periodontal tissues of systemic levels of estradiol and proges-
to bacterial plaque. terone, which are proposed to substitute for
(1) Patients with poorly controlled diabetes often menadione, a required growth factor for P.
have enlarged gingival, polyploid gingival pro- intermedia.
liferations, abscess formation, and loosened (b) Immune suppression during pregnancy
teeth. Patients with poorly controlled diabetes may contribute to the increased susceptibil-
often have PMNs that demonstrate impaired ity to gingival inflammation seen in many
chemotaxis, defective phagocytosis, or impaired women.
adherence. (c) Hormonal changes during pregnancy can
(2) The hyperglycemia that characterizes diabetes have an impact on cellular proliferation,
leads to nonenzymatic glycosylation of pro- differentiation, and keratinization (estrogen
teins and matrix molecules. These glycated effects) and on permeability of the vascula-
molecules accumulate in various sites and are ture, the rate and pattern of collagen turn-
called advanced glycosylation end-products over, and metabolic breakdown of folate
(AGEs). The increase in AGEs as a sequela of (progesterone).
(d) Periodontal treatment during pregnancy tissue. Patients with pernicious anemia, iron
should include plaque control through oral deficiency anemia, and sickle cell anemia may
hygiene instruction and scaling and root have a marked pallor to their gingiva. Peri-
planing. These procedures can be per- odontal manifestations in thrombocytopenia
formed any time during the pregnancy, but purpura may include swollen, soft, friable
elective treatment is best performed during gingiva that bleeds easily on probing. Severe
the second trimester. Although the safety periodontal disease may be seen in individuals
of performing dental radiographs during with neutropenia, agranulocytosis, Chdiak-
pregnancy is well documented, it is recom- Higashi syndrome, lazy leukocyte syndrome,
mended that no radiographs be taken leukocyte adhesion deficiency, Down syn-
during the first trimester. If radiographs are drome, and Papillon-Lefvre syndrome.
necessary for diagnosis, a protective lead (5) Down syndrome and other syndromes
apron must be used. increased numbers of P. intermedia have been
(e) Medications should be limited during preg- reported in patients with Down syndrome.
nancy. Some local anesthetics (mepiva- Hypophosphatasia, congenital heart disease,
caine, bupivacaine, procaine) and analgesics tetralogy of Fallot, and Eisenmengers syn-
(aspirin, ibuprofen, codeine, hydrocodone, drome all are disorders that may be associated
oxycodone) commonly used in dental prac- with increased severity of periodontal disease.
tice must be used with caution. Propoxy- (6) Stresschronic or long-term stress appears to
phene, commonly used in the past in have effects on the periodontium. People with
dentistry, has been withdrawn from the less stable lifestyles and more negative life
market because of a high risk-to-benefit events have more periodontal disease than
ratio (see Section 8, Pharmacology). Tetra- people with more stable lifestyles and fewer
cycline should not be given during preg- negative life events. For example, long-term
nancy because this drug can lead to financial stress in patients with poor coping
depressed bone growth, enamel hypoplasia, skills may exacerbate periodontal destruction.
tooth discoloration, and hepatic damage. Stress not only may induce changes in an indi-
Ciprofloxacin, metronidazole, gentamicin, viduals behavior, but it also influences the
vancomycin, and clarithromycin either immune system. Stress increases cortisol pro-
should be used with caution or should be duction, which can subsequently suppress the
avoided. Penicillin, erythromycin, and immune response. In the presence of the
cephalosporins can be used. microbial challenge that is the primary etio-
(f) Oral contraceptivesoral contraceptives logic factor for periodontal disease, immune
may contribute to gingival changes similar suppression may increase the potential for
to those seen in pregnancy. these pathogens to induce disease.
(g) Menopausesome postmenopausal women (7) Nutritionthe impact of nutrition on peri-
present with gingivostomatitis, manifest as odontal disease is unclear. Although there are
dry, shiny oral mucosa that bleeds easily. no known nutritional deficiencies that alone
There also may be thinning of the mucosa. cause periodontal disease, deficiencies can
Use of toothbrushes with soft bristles, affect the barrier function of epithelial cells
dentifrices with minimal abrasiveness, and (vitamin A), contribute to osteoporosis of alve-
rinses with low alcohol content may be olar bone in dogs (vitamin D), contribute to
advised. Osteopenia and osteoporosis have gingivitis (B complex), and increase the sever-
been associated with menopause. There is ity of gingivitis in the presence of bacterial
evidence for a probable association between plaque, leading to severe bleeding, swollen gin-
osteoporosis and alveolar bone loss. gival, and loosened teeth (vitamin C). Protein
(4) Blood dyscrasiaspatients with leukemia may deficiency may lead to altered integrity of the
present with proliferative gingival enlarge- periodontal tissues, resulting in the patient
ments that appear bluish red and cyanotic with having tissues that are more susceptible to
spongelike consistency. The enlargements are destruction precipitated by bacterial plaque.
often found in the interdental gingival. As with (8) Heavy metalsingestion of metals such as
other gingival alterations, bacterial plaque is bismuth, lead, and mercury can lead to altera-
the initiating factor. Gingival bleeding, caused tions in the periodontium. Bismuth intoxica-
by thrombocytopenia, also is often found in tion can lead to discoloration of the gingival
leukemic patients. In addition, these patients margin in areas affected by inflammation; lead
often have discrete ulcerations in the gingival intoxication can lead to gingival pigmentation
and ulceration; mercury intoxication also can conditions that cause gingival inflammation. Periodontal
lead to gingival pigmentation and ulceration. treatment also is designed to eliminate pain, arrest soft
(9) Medicationsbisphosphonates inhibit osteo- and hard tissue destruction (loss of attachment), establish
clast activity and are used primarily to treat occlusal stability and function, reduce tooth loss, and
cancer (intravenous administration) and osteo- prevent disease recurrence (long-term goals). It is not
porosis (usually oral administration). Bisphos- designed to save all teeth. The periodontal treatment
phonates are rapidly absorbed in bone, giving plan takes into consideration the diagnosis, risk factors,
them a long half-life. Osteonecrosis of the and the desires of the patient. Treatment plans should be
jaw after dental procedures has been associ- presented to patients in terms they can understand. They
ated with bisphosphonates (bisphosphonate- should be informed of the diagnosis, prognosis, and
induced osteonecrosis of the jaw). Dental options for treatment. The linkages between periodontal
health care providers should evaluate patients and restorative phases of therapy should be explained to
carefully before providing surgical interven- the patient.
tions in patients with a history of bisphospho- A. Phases of periodontal therapy (Box 7-4).
nate use, particularly at higher doses used in 1. Preliminary or emergencyhopeless teeth may be
treating cancer. extracted in this phase.
2. Nonsurgical (phase I therapy)the objective of this
phase is to alter or eliminate the microbial etiology
4.0 Treatment Planning and contributing factors to periodontal diseases,
leading to reduction in inflammation. This objective
The treatment plan is the outline of therapy designed to is achieved by caries control in patients with rampant
establish and maintain oral health. A good treatment plan caries (including patient education in diet control),
coordinates therapy across disciplines. Other than manag- removal of local factors (plaque and calculus) through
ing emergencies, treatment should not be initiated until prophylaxis or scaling and root planing, correction
the treatment plan is established. The primary (short- of defective restorations, treatment of carious lesions,
term) goal of the periodontal treatment plan is elimination and institution of oral hygiene practices. It also may
of gingival inflammation through the correction of the include local or systemic antimicrobial therapy,
Box 7-4
Phases of Periodontal Therapy
Preliminary Phase Evaluation of Response to Nonsurgical Phase
Treatment of Emergencies Rechecking
Dental or periapical Pocket depth and gingival inflammation
Periodontal Plaque and calculus, caries
Otherextraction of hopeless teeth and provisional
replacement if needed (may be postponed to a more Surgical Phase (Phase II Therapy)
convenient time) Periodontal therapy, including placement of implants
Endodontic therapy
Nonsurgical Phase (Phase I Therapy)
Plaque Control and Patient Education Restorative Phase (Phase III Therapy)
Diet control (in patients with rampant caries) Final restorations
Removal of calculus and root planing Fixed and removable prosthodontic appliances
Correction of restorative and prosthetic irritational Evaluation of response to restorative procedures
factors Periodontal examination
Excavation of caries and restoration (temporary or
final, depending on whether a definitive prognosis Maintenance Phase (Phase IV Therapy)
for the tooth has been determined and the location Periodic Rechecking
of caries) Plaque and calculus
Antimicrobial therapy (local or systemic) Gingival condition (pockets, inflammation)
Occlusal therapy Occlusion, tooth mobility
Minor orthodontic movement Other pathologic changes
Provisional splinting and prosthesis
minor orthodontic tooth movement, occlusal therapy, Box 7-5

and provisional splinting and prostheses. The evalu-
Categories of Risk Elements for
ation phase is designed to determine the effectiveness
Periodontal Disease
of treatment provided during phase I therapy through
rechecking pocket depths and the presence of inflam- Risk Factors
mation as well as an evaluation for remaining plaque,
Tobacco smoking
calculus, and dental caries. It should occur approxi-
Diabetes
mately 4 to 8 weeks after the completion of phase I
Pathogenic bacteria
therapy; this permits time for epithelial and connec-
Microbial tooth deposits
tive tissue healing by the formation of a long junc-
tional epithelium. Risk Determinants and Background
3. Surgical (phase II therapy)this phase includes all Characteristics
periodontal surgical therapy, including placement of
Genetic factors
implants and endodontic therapy.
Age
4. Restorative (phase III therapy)this phase includes
Gender
placement of final restorations and fixed and remov-
Socioeconomic status
able prosthetic appliances, evaluation of the response
Stress
to these restorations, and periodontal examination.
5. Maintenance (phase IV therapy)periodontal proce- Risk Indicators
dures during the maintenance phase include evalua-
HIV/AIDS
tion of oral hygiene status, presence or absence of
Osteoporosis
local factors, condition of the periodontium (pocket
Infrequent dental visits
depths, attachment levels, mobility, furcation involve-
ments, mucogingival issues and occlusion) and other Risk Markers and Predictors
pathologic changes. This phase should begin after the
Previous history of periodontal disease
completion of phase II therapy. This phase may also
Bleeding on probing
be called supportive periodontal therapy.
B. Risk factors, determinants, indicators, and markers for
periodontal diseaserisk factors that must be consid-
ered when establishing a treatment plan include tobacco c. There is evidence that the risk for aggressive
smoking, diabetes, and pathogenic bacteria and micro- periodontitis may be heritable. Segregation analy-
bial tooth deposits as well as anatomic factors that favor ses support the role of a major gene in the etiol-
plaque accumulation (see Section 2.0, Etiology). Other ogy of these diseases. Genetic and inherited
risk determinants, risk indicators, and risk markers that disorders associated with aggressive periodontitis
should be considered when developing a periodontal include leukocyte adhesion deficiency types I
treatment plan include genetic factors, age, gender, and II, acatalasia, chronic and cyclic neutropenia,
socioeconomic status, immune status, osteoporosis, Chdiak-Higashi syndrome, Ehler-Danlos syn-
history of previous periodontal disease, and bleeding drome, Papillon-Lefvre syndrome, hypophos-
on probing (Box 7-5). When an at-risk patient is identi- phatasia, trisomy 21, prepubertal periodontitis,
fied, the treatment plan may be modified based on the and Kindler syndrome.
identified risk factors and the impact they may have on d. Alterations in neutrophil and monocyte functions,
the predicted outcome of treatment. in the receptor for IgG2, and in IgG2 titers are
1. Genetic factors. under genetic regulation. Each of these alterations
a. Studies conducted in twins have shown that genetic has been shown to have an impact on periodontal
factors influence periodontal status. Results from disease.
these studies have demonstrated that there is a 2. Age.
heritable component to chronic periodontitis. a. Changes in the periodontium associated with
b. Some studies have shown that polymorphisms in aging include thinning and decreased keratiniza-
both the interleukin IL-1 and IL-1 genes have tion of the epithelium, coarser and denser gingival
been associated with increased IL-1 production connective tissues, decreases in fibroblasts and
and severe chronic periodontitis in nonsmoking organic matrix production in the PDL, increased
subjects. However, other studies have demon- width of cementum, and more irregular periodon-
strated limited association of these gene alterations tal surface of bone and less regular insertion of
with periodontitis. The presence of these polymor- collagen fibers.
phisms may be only one of several factors related b. Evidence that age has an impact on the microbial
to the risk for periodontal disease. flora is equivocal.
c. The prevalence and severity of periodontal disease and root planing, lavage, and oral hygiene instruc-
increase with age; however, this is most likely due tion. The lesions may be painful, leading to the
to prolonged exposure to etiologic factors associ- need for local anesthesia. Antimicrobial agents
ated with the disease rather than with degenerative such as chlorhexidine may be administered. Resolu-
changes related to aging. Older adults with peri- tion of any underlying systemic factor may be neces-
odontal disease generally present with chronic sary to treat necrotizing ulcerative periodontitis
periodontitis. Medical and mental conditions, successfully.
medications, functional status, lifestyle behaviors, 6. Osteoporosisalthough there are conflicting studies,
manual dexterity, and disease severity must be the reduced bone mass seen in patients with osteo-
considered when developing a treatment plan for porosis may have an impact on progression of peri-
these patients. Although some age-related changes odontal disease.
occur in the host response, these changes do not 7. Previous history of periodontal diseasepatients
appear to be correlated with periodontitis. The risk with the most severe prior loss of attachment are at
of dental caries from the exposure of root surfaces greatest risk for future loss of attachment.
through nonsurgical and surgical treatment must 8. Bleeding on probingbleeding on probing is the best
be considered as well. clinical indicator of gingival inflammation.
d. Young people with periodontal disease may present 9. Stressemotional stress may interfere with normal
with aggressive periodontitis. Although the treat- immunologic function, and the incidence of necro-
ment plan for these patients typically consists of tizing ulcerative gingivitis increases during periods
conventional periodontal therapy (patient educa- of stress; both of these suggest a potential relation-
tion, scaling and root planing, frequent mainte- ship between stress and periodontal disease.
nance appointments), adjunctive antimicrobial
therapy (systemic antibiotics) and host-modifying
drugs (systemic subantimicrobial dose doxycy- 5.0 Prognosis
cline [SDD]) often are necessary to obtain a posi-
tive response. In the localized form of disease, The prognosis is a prediction of the outcome of a disease.
several studies support the adjunctive administra- It takes into consideration the presence of risk factors for
tion of systemic tetracycline or doxycycline. A the disease. The prognosis for individual teeth must be
combination of metronidazole and amoxicillin considered in the context of the prognosis for the entire
also has been shown to enhance the response in dentition. Teeth that will serve as abutments for prosthetic
patients with aggressive periodontitis. Decisions devices must have a periodontal prognosis consistent with
regarding the prognosis for retention of individual their long-term maintenance. Attempts to retain teeth with
teeth and plans for replacing teeth that must be severe periodontal disease are not advisable if retention
extracted also are important components of the jeopardizes adjacent healthy or less affected teeth. The
treatment plan for patients with aggressive disease. prognosis should be reassessed after the completion of
After stabilization of the periodontium, frequent phase I therapy (Box 7-6).
maintenance visits are important in these patients A. Clinical factors that affect the prognosis include the
to allow for early detection and treatment of sites patients age, disease severity, level of plaque control,
that begin to lose attachment. and patient compliance. Younger patients with evidence
3. Gendermales generally have more local factors and of periodontitis generally have a poorer prognosis than
more loss of attachment than females. This difference older patients with comparable levels of disease. Clini-
is most likely attributable to preventive habits and cal attachment level is more important than pocket
practices rather than to physiologic differences. depth in determining prognosis. The amount of bone
4. Socioeconomic statusdecreased dental awareness loss also is important, especially when prosthetic care
and frequency of dental visits and the presence of is part of the treatment plan. The type of bony defect
other risk factors such as smoking are likely contribu- must be considered. Teeth with vertical defects may
tors to the increased incidence of periodontal disease have a better prognosis than teeth with comparable
found in individuals of lower socioeconomic status. levels of horizontal bone loss owing to the potential for
5. Immune status (HIV infection and other systemic treating the vertical defect with regenerative therapy.
factors that influence the immune system)necro- The success of this regenerative procedure is affected by
tizing ulcerative periodontitis is often diagnosed in the contour of the vertical defect and the number of
immunocompromised individuals. Dentists should remaining walls. Patients with poor plaque control and
treat a patient presenting with this form of disease in noncompliant or uncooperative patients also have a
conjunction with the patients physician to establish poorer prognosis than patients with good oral hygiene
potential systemic factors contributing to the disease. practices and demonstrated compliance with recom-
Treatment includes local dbridement with scaling mended treatment.
Box 7-6 serve as contraindications to recommended surgical

periodontal therapy (e.g., uncontrolled diabetes melli-
Factors to Consider When Determining
tus) are associated with a poorer prognosis. Genetic
a Prognosis
factors that influence the host response to a microbial
Overall Clinical Factors challenge also can have an impact on the prognosis.
Chronic stress and poor coping mechanisms may also
Patient age
contribute to a poor prognosis.
Disease severity
C. Local factors that affect prognosis include plaque or cal-
Plaque control
culus, subgingival restorations, anatomic factors, and
Patient compliance
tooth mobility. Bacterial plaque is the primary etiologic
Systemic and Environmental Factors agent for periodontal disease. Subgingival restorations
may contribute to plaque retention, leading to a poorer
Smoking
prognosis. Teeth with short, tapered roots and large
Systemic disease or condition
crowns have a poor prognosis because of the dispro
Genetic factors
portionate root/crown ratio and reduced root surface
Stress
available for periodontal support. Cervical enamel pro-
Local Factors jections extending into furcations and enamel pearls
serve as plaque retentive areas and interfere with the
Plaque and calculus
attachment apparatus. Root concavities, developmental
Subgingival restorations
grooves, root proximity, and furcation involvements all
Anatomic Factors create situations that make the tooth difficult to clean
and have an impact on the prognosis. In the presence
Short, tapered roots
of bacterial plaque, mobile teeth do not respond as well
Cervical enamel projections
to therapy as nonmobile teeth.
Enamel pearls
D. Prognosisthe prognosis is usually classified as excel-
Bifurcation ridges
lent, good, fair, poor, questionable, or hopeless. Char-
Root concavities
acteristics of each classification listed include one or
Developmental grooves
more of the following.
Root proximity
1. Excellentno bone loss, gingival health, good patient
Furcation involvement
cooperation, no secondary systemic or environmen-
Tooth mobility
tal factors.
Prosthetic and Restorative Factors 2. Goodadequate alveolar bone support, potential to
control etiologic factors and establish maintainable
Abutment selection
situation, good patient cooperation, no environ
Caries
mental factors, either no systemic factors or well-
Nonvital teeth
controlled systemic factors.
Root resorption
3. Fairinadequate alveolar bone, mobility, grade I fur-
From Newman MG, etal: Carranzas Clinical Periodontology, ed 12.
cation involvement, potential to establish maintain-
St. Louis, Saunders, 2015.
able situation, adequate patient cooperation, limited
environmental or systemic factors.
4. Poormoderate to advanced alveolar bone loss,
B. Systemic factors that affect the prognosis include ciga- mobility, grade I and II furcation involvement, ques-
rette smoking, systemic diseases and conditions, genetic tionable patient cooperation, difficult areas to main-
factors, and stress. Cigarette smokers not only have a tain, presence of systemic or environmental factors.
higher prevalence and severity of periodontal disease 5. Questionableadvanced bone loss, grade II and III
but also have a decreased healing response to both non- furcation involvements, mobility, inaccessible areas,
surgical and surgical therapy. Current cigarette smokers presence of environmental or systemic factors.
with periodontal disease have a poorer prognosis than 6. Hopelessadvanced bone loss, inability to establish
patients who have never smoked. However, smokers maintainable situation, extraction indicated, uncon-
who successfully complete a cessation program have a trolled environmental or systemic factors.
better prognosis than current smokers. Patients with E. The prognosis varies with the periodontal diagnosis.
poorly controlled diabetes mellitus have a poorer prog- 1. Patients with a diagnosis of gingivitis associated with
nosis than patients with well-controlled diabetes mel- dental plaque, which is a completely reversible
litus or healthy patients with no history of diabetes disease, have a good prognosis if the local initiating
mellitus. Diseases that compromise the patients ability factors (usually plaque and calculus) can be reduced
to perform oral hygiene (e.g., Parkinsons disease) or or eliminated. The prognosis for patients with
plaque-induced gingival diseases modified by sys-

temic factors and plaque-induced gingival diseases
modified by medications is also dependent on elimi-
nation of the secondary factors involved. The prog-
nosis for patients with nonplaque-associated Reduction of Risk factor
gingivitis (e.g., lichen planus, pemphigoid, lupus ery- bacterial modification:
burden: smoking cessation
thematosus) depends on management of the associ-
SRP, topical therapy, diabetes
ated dermatologic disorder. antimicrobials, control
Best chance
2. Patients with aggressive periodontitis usually have a surgical pocket for clinical
poorer prognosis than patients with chronic peri- reduction improvement
odontitis. However, in patients with localized aggres-
sive periodontitis that is diagnosed early, conservative
therapy is effective, and the prognosis is good.
3. The prognosis of patients with periodontitis associ-
ated with systemic diseases depends on the severity Host response modulation:
subantimicrobial dose doxycycline
of the systemic disease.
for inhibition of MMPs
4. The prognosis for patients with necrotizing peri-
odontal diseases is variable, depending on the extent
and severity of environmental and systemic factors.
Figure 7-7 Complementary treatment strategies in peri-

6.0 Therapy odontitis. The best chance for clinical improvement may come
from implementing complementary treatment strategies that
A. Rationaleperiodontal therapy is performed to elimi- target different aspects of the periodontal balance. Reduction of
nate pain, eliminate gingival bleeding, reduce inflam- the bacterial burden by scaling and root planing (SRP) is the
mation, reduce periodontal pockets, arrest destruction cornerstone of treatment and can be augmented by the use of
of soft tissue and bone, reduce mobility, reduce tooth topical antimicrobials and surgical pocket therapy. In addition to
this antibacterial treatment approach, the host response can be
loss, and prevent the recurrence of disease. The phases
treated by the use of host modulatory therapy, such as sub
of periodontal therapy are outlined in Box 7-4 and
antimicrobial dose doxycycline, for the inhibition of matrix
Figure 7-7. metalloproteinases (MMPs). Risk factor assessment and modifica-
1. The removal of bacterial plaque and of factors that tion must form a key part of any periodontal treatment strategy,
favor its accumulation is the primary consideration including smoking cessation counseling. These different but com-
in local therapy. plementary treatment strategies can be used as part of a compre-
2. Systemic administration of antibiotics or host- hensive management approach. (From Newman MG, etal:
modifying drugs or both may be used as an adjunct Carranzas Clinical Periodontology, ed 12. St. Louis, Saunders,
to local therapy. 2015.)
B. Nonsurgical phase (phase I therapy).
1. Plaque control (see Section 7.0, Prevention and
Maintenance). d. Sickle scalers are used to remove supragingival cal-
2. Scaling and root planing. culus. They have two cutting edges and a pointed
a. Instrumentation reduces the numbers of subgingi- tip. They have a triangular shape in cross section.
val microorganisms and results in a shift in the e. Ultrasonic scalers, hoe, chisel, and file scalers are
microflora from disease-associated, gram-negative used for removal of tenacious calculus.
anaerobes to health-associated, gram-positive, fac- f. Curettes are the instrument of choice for subgingi-
ultative microorganisms. val scaling and for root planing. They have a
b. The best evidence for the success of instrumenta- spoon-shaped blade and rounded toe and back and
tion is the response of the tissue. Response should are shaped like a semicircle in cross section.
be assessed no sooner than 2 weeks after comple- (1) Universal curettes have two cutting edges and
tion of instrumentation. can be used in any area of the mouth. The face
c. Scaling is the removal of both supragingival and of the blade is at a 90-degree angle to the lower
subgingival plaque and calculus. Root planing is shank when seen in cross section from the tip.
the removal of embedded calculus and areas of The blade is curved in one direction.
cementum to produce a clean, hard, smooth (2) Area-specific curettes (Gracey curettes) are
surface. The primary objective of scaling and root designed to adapt to specific tooth surfaces.
planing is to restore gingival health by removing They provide the best access and adaptation to
these etiologic factors. the root surface. The blade is angled 60 to 70
degrees from the lower shank, providing an kept in contact with the tooth. This usually means
offset blade. When the lower shank is parallel that 1 to 2mm of the working end of the instru-
to the long axis of the tooth, the blade is prop- ment is adapted to the tooth.
erly adapted to the root surface. The blade is c. When initially inserting an instrument into the
curved from head to toe and along the side of pocket, the angulation between the blade and the
the cutting edge, providing only one cutting tooth should be 0 degrees. During scaling and root
edge that can be accurately adapted to the root planing, this angulation is changed to 45 to 90
surface. When using these instruments, the degrees.
lower shank must be parallel to the surface d. The types of strokes used during instrumentation
being instrumented. Examples of Gracey are exploratory (a light feeling stroke used with
curettes and the teeth they are designed to probes and explorers), scaling (a short, strong pull
adapt to follow. stroke used with bladed instruments for the
(a) Gracey 1-2 and 3-4anterior. removal of calculus), and root planing (a moderate
(b) Gracey 5-6anterior and premolars. to light pull stroke used for final smoothing and
(c) Gracey 7-8 and 9-10posterior teeth, facial planing of the root surface).
and lingual. e. Plastic instruments or special metal curettes are
(d) Gracey 11-12posterior teeth mesial sur- available for removing deposits from implant
faces only. surfaces.
(e) Gracey 13-14posterior teeth distal sur- 5. Ultrasonic instruments.
faces only. a. Overviewultrasonic instruments are used for
(3) Gracey curvettes are curettes with shorter, removing plaque, calculus, and stain from tooth
more curved miniblades designed to adapt surfaces. The vibrations at the tip of these instru-
more closely to the root surface. ments range from 20,000 to 45,000 cycles/sec.
(4) Extended-shank curettes have a longer termi- Ultrasonic instrumentation is accomplished by
nal shank, a thinned blade, and a large-diameter using light, intermittent strokes with the tip paral-
terminal shank. They are available in finishing lel to the tooth and in constant motion. A contra-
or rigid designs and are used for light scaling indication to the use of ultrasonic instruments
or removal of tenacious deposits, respectively. includes presence of older cardiac pacemakers.
(5) Mini-bladed curettes have shorter blades than Contraindications to the use of ultrasonic and
conventional curettes for better adaptation into sonic instruments include patients with communi-
furcations; developmental grooves; line angles; cable diseases that can be spread by aerosol,
and tight, deep pockets. They also are available patients at risk for respiratory disease (patients
in finishing or rigid designs. with immunosuppression or patients with chronic
(6) Langer and mini-Langer curettes combine the pulmonary diseases), and patients with titanium
shank design of Gracey curettes with the uni- implants (unless plastic ultrasonic or sonic tips are
versal blade design (90-degree angle of the face used).
and lower shank). b. Characteristics.
(7) Schwartz periotrievers are magnetized instru- (1) In magnetostrictive ultrasonic instruments, the
ments designed to retrieve broken instrument tip vibrates in an elliptic pattern, meaning that
tips from periodontal pockets. all sides of the tip are active.
3. Instrument sharpeningperiodontal instruments (2) In piezoelectric ultrasonic instruments, the tip
must have thin, fine cutting edges to be effective and vibrates in a linear (or back-and-forth) pattern,
efficient. The objective of sharpening is to restore this meaning that two sides are more active.
cutting edge after use of the instrument. Instruments (3) Tips in both units operate in a wet field with a
can be sharpened using mounted or unmounted water spray. There are small vacuum bubbles
stones. within the spray that collapse, releasing energy
4. Holding and activating hand instruments. in a process termed cavitation. This cavitation
a. Hand instruments are held in the modified pen spray helps flush debris out of the pocket.
grasp. A finger rest is established to stabilize the 6. Sonic instrumentssonic instruments have a hand-
hand and instrument. It provides a firm fulcrum. piece that attaches to a compressed air line. Vibra-
The fourth finger usually serves as the finger rest. tions range from 2000 to 6000 cycles/sec.
Finger rests may be intraoral or extraoral. 7. Other instruments.
b. Adaptation of the instrument to the tooth surface a. A dental endoscope has been designed that con-
is important to prevent trauma to soft tissues and sists of a reusable fiberoptic endoscope covered
the root surface. The lower third of the working with a disposable sterile sheath. It fits onto spe-
end of the instrument (closest to the toe) must be cially designed periodontal probes and ultrasonic
instruments. It should enable the operator to view margin (apically displaced flap), 1 to 2mm
subgingival deposits and should aid in their from the free gingival margin (modified
removal. Widman flap), or just coronal to the base of the
b. The enhanced visual assessment system uses a pocket (undisplaced flap). It also is known as
series of motor-driven diamond files mounted the reverse bevel incision. This incision removes
on a special handpiece to correct overhanging the pocket lining, conserves the outer dimen-
restorations. sion of the gingiva, and produces a thin sharp
c. Rubber cups and bristle brushes are used to remove flap margin that can be adapted to the bone-
plaque and stains from the teeth. tooth junction.
d. The prophy-jet delivers a slurry of water and (2) The second is the crevicular incisionmade
sodium bicarbonate to remove extrinsic stains and from the base of the pocket to the crest of the
soft deposits. It can damage cementum and dentin alveolar bone. The combination of the internal
as well as restorations when used improperly. Its bevel and crevicular incisions creates a collar of
use is contraindicated in patients with respiratory tissue around the teeth.
illnesses, hypertension, electrolyte imbalance, and (3) The third is the interdental incisionthis inci-
infectious diseases and patients on hemodialysis. sion separates the collar of gingiva from the
C. Surgery (phase II therapy)phase II surgical therapy is tooth. Reflection of the flap after placement of
performed to reduce or eliminate periodontal pockets, these three incisions allows for visualization of
correct soft and hard tissue anatomic or morphologic the alveolar bone.
defects, regenerate periodontal tissues, or place h. Vertical incisions for full-thickness flapsif the flap
implants. The need for surgery is assessed after the is to be positioned apically in a pocket reduction/
completion and evaluation of the success of phase I elimination procedure, vertical releasing incisions
therapy. Procedures performed at this reevaluation that extend beyond the mucogingival junction can
phase include assessment of oral hygiene, clinical be made. These incisions should not be made in
attachment levels, and pocket depths. Patients with the center of the papilla or over the radicular
residual deep pockets, osseous defects, and persistent surface of a tooth. Vertical incisions should be
mucogingival problems who have demonstrated the avoided on the lingual and in the palate.
ability to maintain adequate oral hygiene are candidates i. The modified Widman flap uses the three horizon-
for periodontal surgery, provided that there are no tal incisions described previously but is not
medical or psychological contraindications. reflected beyond the mucogingival line. This flap
1. Flap design and management are important compo- design allows for removal of the pocket lining
nents of periodontal surgery. There are several basic and exposure of the tooth roots and alveolar bone
principles of flap design. but does not allow for apical repositioning of
a. The base of the flap should be wider than the free the flap.
margin. j. Periodontal packsmost surgical sites are covered
b. The lines of the incision should not be placed over with a periodontal pack. Packs are placed to protect
any defect in the bone. the surgical wound, minimize patient discomfort,
c. Incisions should not be made over a bony maintain tissue placement, and help prevent post-
eminence. operative bleeding. Packs usually do not enhance
d. Corners of the flaps should be rounded. the healing rate of the tissues. Packs usually contain
e. Flaps can be classified as either full thickness zinc oxide and may be either eugenol-containing
(mucoperiosteal) or partial thickness (mucosal). In or noneugenol-containing. Antibiotics have been
full-thickness flaps, all soft tissue and periosteum incorporated into some packs. Packs are retained
are reflected to expose the alveolar bone. In partial- mechanically by interlocking into interdental
thickness flaps, only the epithelium and the under- spaces.
lying connective tissue are reflected. k. Chlorhexidinein the first postoperative week,
f. Depending on how the interdental papilla is the patient should rinse with 0.12% chlorhexidine
managed, flaps can either split the papilla (conven- twice daily until normal oral hygiene procedures
tional flap) or preserve it (papilla preservation can be resumed, which is usually during the second
flap). postoperative week.
g. Horizontal incisions for full-thickness flapsthree D. Gingival surgery.
horizontal incisions are usually associated with a 1. Gingivectomy is an excision of the gingiva. Surgical
full-thickness flap design. gingivectomy is performed to eliminate suprabony
(1) The first is the internal bevel incision pockets, gingival enlargements, or suprabony peri-
depending on the goal, this incision can be odontal abscesses. A gingivectomy should not be
made 0.5 to 1mm from the free gingival performed if osseous recontouring is needed, if the
bottom of the pocket is apical to the mucogingival displaced flap, the subepithelial connective tissue
junction, if there is inadequate attached gingiva, or if graft, and guided tissue regeneration techniques.
there is an esthetic concern. The procedure can be When planning a laterally positioned (displaced)
performed with scalpels, electrodes, or lasers. A flap, the donor site should have adequate facial bone
beveled incision is made apical to the pocket depth. and adequate thickness and width of attached gingiva.
The tissue is removed, the area is dbrided, and a 5. The Miller classification system for recession is an
surgical pack is placed. Healing is by secondary important consideration when root coverage proce-
intention with the formation of a protective clot, epi- dures are planned, when there is severe bone and soft
thelial migration, and connective tissue repair. tissue loss interdentally or severe tooth malposition.
2. Gingivoplasty is performed to reshape the tissues The prognosis for root coverage for classes I and II is
where there are deformities, such as gingival clefts or good to excellent; only partial coverage can be
craters, gingival enlargements, and shelflike inter- expected for class III. Class IV has a very poor prog-
dental papillae. It is not performed to reduce or elim- nosis for coverage.
inate periodontal pockets. It can be accomplished a. Class Imarginal tissue recession does not extend
with a periodontal knife, scalpel, rotary diamond to the mucogingival junction. There is no loss of
stone, or electrodes. bone or soft tissue in the interdental area.
E. Mucogingival surgerymucogingival surgical proce- b. Class IImarginal tissue recession extends to or
dures are performed to correct relationships between beyond the mucogingival junction. There is no loss
the gingival and the oral mucous membranes. They of bone or soft tissue in the interdental area.
include widening of attached gingiva, deepening of c. Class IIImarginal tissue recession extends to or
shallow vestibules, and resection of aberrant frena. beyond the mucogingival junction. There is bone
1. No minimum width of attached gingiva has been and soft tissue loss interdentally or malpositioned
established as a standard necessary for gingival teeth.
health. Persons with excellent oral hygiene may d. Class IVmarginal tissue recession extends to or
maintain health with almost no attached gingiva. beyond the mucogingival junction. There is severe
Persons with suboptimal oral hygiene can be helped bone and soft tissue loss interdentally or severe
by the presence of keratinized tissue and vestibular tooth malposition.
depth. 6. A frenum is a problem if the attachment is too close
a. Widening the attached gingiva can be performed. to the marginal gingiva. Tension from the frenum
(1) To enhance plaque removal around the gingival may pull the gingival margin away from the tooth,
margin. creating a situation conducive to plaque retention. A
(2) To improve esthetics by covering denuded root frenectomy is complete removal of the frenum; a fre-
surfaces. notomy is incision of the frenum. Both may be used
(3) To reduce inflammation around restored teeth to correct frenum attachment problems, but the fre-
by creating a wider zone of attached gingiva notomy is usually adequate for relocating the attach-
around teeth that serve as abutments for fixed ment to create a zone of attached gingiva between the
and removable partial dentures and in ridge gingival margin and the frenum.
areas related to dentures. 7. Deepening the vestibule can be accomplished by the
2. Techniques to increase the width of attached gingiva use of free gingival autogenous graft techniques.
include free gingival autograft, free connective tissue 8. For all mucogingival procedures, blood supply is the
autograft, and the displaced (apically or laterally) most significant concern. The surgical site also should
positioned flap. be free of plaque, calculus, and inflammation. Grafts
3. The palate is the most common donor site for the free must be stabilized on the recipient site, and there
gingival autograft and the connective tissue auto- should be minimal trauma to the surgical site. There
graft. The ideal thickness for the free gingival graft is must be adequate tissue present at the donor site.
1 to 1.5mm. The success of the graft depends on F. Osseous surgeryaccess to the alveolar bone is accom-
survival of the connective tissue. In connective tissue plished through full-thickness flap reflection. Visualiza-
autografts, only connective tissue is used from the tion of the bony architecture allows the clinician to
undersurface of the palatal flap, which is sutured determine the types of bony defects that are present and
back in primary closure. This results in less discom- the extent of those defects.
fort postoperatively. 1. Osseous craterthis is an osseous, two-walled con-
4. Techniques used for widening the attached gingiva cavity in the crest of the interdental bone confined
apical to an area of recession can also be used for root within the facial and lingual walls (Figure 7-8). This
coverage. These include the free gingival and connec- defect is best corrected by recontouring the facial
tive tissue autograft. Other techniques include the and lingual walls to restore normal interdental
laterally positioned (displaced) flap, the coronally architecture.
2. Vertical or angular defectsthe base of the bone should be performed only on teeth with moderate
defect is located apical to the surrounding bone. bone loss.
These defects can have one, two, or three walls (Figure 4. Interproximal bonein normal alveolar bone mor-
7-9) or any combination (Figure 7-10). These defects phology, the interproximal bone is more coronal than
may be corrected by resective osseous surgery or by the facial or lingual/palatal bone (positive architec-
periodontal regeneration (for details, see Resective ture). Deviations from this include negative architec-
osseous surgery and Periodontal regeneration ture (interproximal bone is apical to the facial or
further on). lingual bone) and flat architecture (interproximal
3. Recontouringit is believed that discrepancies in bone and radicular bone are at the same height). The
bony contour predispose the patient to recurrence of embrasure space dictates the interproximal form, and
deep pockets after soft tissue surgery. Resective the position of the bony margins follows the contours
osseous surgery is the recontouring and removal of the cementoenamel junction.
of alveolar bone to correct these discrepancies 5. Resective osseous surgery.
restoring the alveolar bone to the contour that was a. Resective osseous surgery can be accomplished
present before periodontal destruction. It is usually through ostectomy (removal of tooth supporting
performed in combination with apical repositioning bone) or osteoplasty (removal of nonsupporting
of the gingival flap for pocket reduction or elimina- alveolar bone).
tion. Because osseous resective surgery is performed b. After ostectomy, peaks of bone often remain at the
at the expense of bony tissue and attachment level, it line angles. These are called widows peaks. If left,
they predispose the patient to recurrence of peri-
odontal pockets in these areas.
2
1
1/
2
Figure 7-8 Diagrammatic representation of an osseous Figure 7-10 Combined type of osseous defect. Because
crater in a faciolingual section between two lower molars. the facial wall is half the height of the distal (1) and lingual (2)
Left, Normal bone contour. Right, Osseous crater. (From Newman walls, this is an osseous defect with three walls in the apical half
MG, etal: Carranzas Clinical Periodontology, ed 12. St. Louis, and two walls in the occlusal half. (From Newman MG, etal: Car-
Saunders, 2015.) ranzas Clinical Periodontology, ed 12. St. Louis, Saunders, 2015.)
A B C
2 2
1 1 1
Figure 7-9 One-, two-, and three-walled vertical defects on right lateral incisor. A, Three bony walls: distal (1), lingual (2),
and facial (3). B, Two-wall defect: distal (1) and lingual (2). C, One-wall defect: distal wall only (1). (From Newman MG, etal: Carranzas
Clinical Periodontology, ed 12. St. Louis, Saunders, 2015.)
c. Resective osseous surgery is most successful in a. Autogenous grafts can be obtained from intraoral
interproximal bony craters, early furcation involve- sites. Osseous coagulum (a mixture of bone dust
ments, and cases with thick alveolar bone. It should and blood obtained from cortical bone), bone
not be performed in areas where there is an esthetic blend (bone obtained from a predetermined site
concern. that is triturated in an autoclaved plastic capsule
6. Mechanisms of healing after periodontal treatment. and pestle), and cancellous bone marrow trans-
a. Regenerationgrowth and differentiation of the plants (obtained from the maxillary tuberosity,
same type of tissue (bone, cementum, and PDL) edentulous areas, and healing sockets) are exam-
that was damaged through periodontal disease. ples of autogenous grafts. Autogenous bone also
b. Repairhealing by scar. can be obtained from extraoral sites, such as iliac
c. New attachmentembedding of new PDL fibers cancellous marrow bone.
into new cementum and attachment of gingival b. Allograft materials include undecalcified, freeze-
epithelium to a previously diseased root surface. dried bone allograft (osteoconductive material)
G. Periodontal regenerationperiodontal regeneration and decalcified, freeze-dried bone allograft (osteo-
(reconstruction) is the formation of new bone, cemen- genic material owing to the presence of bone mor-
tum, and PDL. Various techniques have been developed phogenetic proteins that are exposed during the
to enhance the likelihood of achieving the goal of demineralization process).
regeneration of the periodontium. c. Bio-Oss is a xenograft material (an anorganic,
1. Guided tissue regeneration (GTR) is a method for bovine-derived bone that is an osteoconductive,
preventing epithelial migration along the cemental porous bone mineral matrix).
side of a pocket during wound healing after peri- d. Nonbone graft materials include bioactive glass
odontal flap reflection. GTR uses various barrier (PerioGlas, Biogran) and coral-derived materials.
membranes to cover the bone and PDL before flap e. Regeneration can be attained without the use of
replacement in an attempt to exclude the epithelium bone grafts in three-walled osseous defects that are
and connective tissue from the root surface during meticulously dbrided and in periodontal and
the healing phase. These barriers also may serve to endodontic abscesses.
protect the clot that is formed, allowing for connec- f. Regeneration through the placement of bone graft
tive tissue attachment during the early phases of material is most successful in three-walled bony
wound healing. defects. It is least successful in through-and-
2. The root surface can be treated with agents designed through (class III) furcation defects.
to enhance new attachment of gingival tissues after H. Oral implantology.
surgical excision. These include citric acid, which is 1. Titanium-tissue interactiontitanium is the material
often used in conjunction with free gingival grafts, that offers the best biologic attachment to bone and
fibronectin, tetracycline, and various growth factors. gingival tissue.
Enamel matrix proteins (e.g., Emdogain) have also a. Titanium implants have a layer of titanium oxide
been used to enhance new attachment. on their surface that is responsible for osseointe-
3. Numerous hard tissue graft materials have been gration. The oxide content of titanium oxide is
used for restoring periodontal osseous defects, essential for the nucleation process that forms
including autografts (material to be grafted obtained calcium phosphate precipitates, which lead to min-
from the same individual), allografts (material to be eralized bone formation.
grafted obtained from a different individual of the b. The placement of a titanium implant into a pre-
same species), and xenografts (material to be grafted pared hole in bone leads to bone apposition on the
obtained from a different species). Bone graft mate- implant surface by mechanisms that are similar to
rials are evaluated based on their osteogenic poten- fractured bone healing. The process leading to suc-
tial (ability to induce the formation of new bone by cessful bone apposition on implant surfaces after
cells contained in the graft), osteoinductive potential surgical implant placement is outlined in Figure
(ability of molecules contained in the graft to convert 7-11. The main goal of implant treatment is to
neighboring cells into osteoblasts), and osteocon- achieve and maintain a stable bone-to-implant
ductive potential (ability of the graft material to connection, also called osseointegration. Implants
serve as a scaffold that favors outside cells to pene- are frequently loaded after 2 to 3 months, when
trate the graft and form new bone). Three-wall woven bone is still present.
defects are most predictable to respond with bone c. The attachment of gingival tissue to a titanium
grafting as opposed to two-wall defects because implant is outlined in Figure 7-12, and the blood
of better blood supply and cell source proximity. supply to this area is shown in Figure 7-13.
One-wall defects should not be treated with bone The vascular supply of the periimplant gingival
grafting. tissue or alveolar mucosa is more limited than the
A B
Figure 7-11 A, Three-dimensional diagram of the tissue and titanium interrelationship showing an overall view of the intact interfacial
zone around the osseointegrated implant. B, Physiologic evolution of the biology of the interface over time. (From Newman MG, etal:
Carranzas Clinical Periodontology, ed 12. St. Louis, Saunders, 2015.)
T/I I
c a b
b
T/I 3 MR
D c
Ab
HD 2 aAE
HD A/I
4
a LD
5
Im
EA
BC LL Bo
LBI
LBE
A B C
Figure 7-12 A, Histologic scheme of epithelial attachment (EA) (identical for tooth and implant). BC, Basal complex; LBE, lamina
basalis externa (only location where cell divisions occur); LBI, lamina basalis interna; T/I, titanium implant; a, long junctional epithelial
attachment zone; b, sulcular epithelial zone; c, oral epithelial zone. B, At electron microscopic level, basal complex at epithelial attach-
ment (three most apical cells) and connection with stroma. C, Cuticle; D, desmosome; HD, hemidesmosomes; LD, lamina densa;
LL, lamina lucida. C, Implant, abutment (Ab), and crown within alveolar bone and soft tissues. aAE, Apical (point) of attached epithe-
lium; A/I, abutment/implant junction; Bo, marginal bone level; Im, endosseous part of implant; MR, margin of gingiva/alveolar mucosa;
1, implant crown; 2, vertical alveolar gingival connective tissue fibers; 3, circular gingival connective tissue fibers; 4, circular gingival
connective tissue fibers; 5, periosteal-gingival connective tissue fibers; a, junctional epithelium; b, sulcular epithelium; c, oral epithelium.
(From Newman MG, etal: Carranzas Clinical Periodontology, ed 12. St. Louis, Saunders, 2015.)
Epithelial attachment
Abutment
Connective tissue cuff
Implant Figure 7-13 Schematic illustration shows the
shoulder blood supply in the connective tissue cuff sur-
Gingival epithelium
rounding the implant/abutment is scarcer than in
the gingival complex around teeth because none
Cortex
originates from a PDL. (From Newman MG, etal:
Cancellous Carranzas Clinical Periodontology, ed 12. St. Louis,
bone Saunders, 2015.)
Mucogingival
junction
vascular supply around teeth. Because there is no 4. Risk factors and contraindications for implantsrisk
PDL around an implant, the vascular supply may factors and contraindications for implant therapy are
often be missing. listed in Table 7-5.
2. Comparison of tissues surrounding natural dentition 5. Posttreatment evaluation and management of
and osseointegrated implants. implantsimplant stability is the most important
a. There is no PDL around implants. measure of success. It has low sensitivity (cannot
b. There is no supracrestal connective tissue inserting accurately determine levels of bone loss) but high
into the implant as in teeth. specificity (if the implant is mobile, it has probably
c. When probing around implants, the probe tip may failed). Intraoral radiographs should be taken at the
penetrate to the level of bone; on natural teeth, the time of placement, at the time of abutment connec-
probe tip stops in the junctional epithelium in tion, and regularly thereafter to assess bone levels.
health or in the supracrestal connective tissue in Traditional oral hygiene measures should be used,
disease. but ultrasonic instruments should be avoided. Plastic
d. A lack of a PDL means that implants should not be instruments or specifically designed curettes should
used in growing individuals because implants do be used for cleaning of implants.
not continue to erupt like normal teeth. 6. Types and prevalence of implant complications.
3. Clinical applications and evaluation of the patient a. The most common complication reported for
with implants. single crowns was abutment or prosthesis screw
a. Greater than 90% to 95% success rates can be loosening (2% to 45%).
expected for endosseous titanium implants in b. Loosening rates are higher in posterior than
healthy patients with good bone and normal anterior.
healing capacity. c. Implant fracture is less than 1% of cases.
b. Implants can be placed in edentulous and partially d. Technical complications are higher for implants
edentulous patients. used with overdentures than for implants support-
c. Fully edentulous patients seem to benefit the most ing fixed prostheses.
from implants. e. Implant failures for biologic reasons (periimplan-
d. Implant-supported removable or fixed prostheses titis, soft tissue lesions)7% to 8%.
can be used. f. Failure rates in totally edentulous patients are twice
e. Clinical evaluation requires evaluation of chief that seen in partially edentulous patients.
complaint; medical history (for risk factors); dental g. Failure rates are three times higher in edentulous
history (for infections, plaque control, previous maxilla compared with edentulous mandible.
surgical procedures); intraoral examination (for h. No differences for partially edentulous between
dental and periodontal health, oral hygiene, jaw maxilla and mandible.
relationships, temporomandibular joint [TMJ] 7. Biologic complications.
conditions); articulated diagnostic study models; a. Periimplantitisinflammatory process affecting
hard tissue evaluation (for bone levels); radio- the tissues around an osseointegrated implant
graphic examination (quantity, quality, and loca- in function, resulting in loss of supporting
tion of bone; can use periapical x-rays, panoramic bone.
x-rays, and tomographic imaging); and soft tissue b. Dehiscence and recession of periimplant soft tissues
evaluation (extent of keratinized versus nonkera- occurs when support for those tissues is lacking or
tinized mucosa; quality and quantity of tissue). has been lost.
Table 7-5
Risk Factors and Contraindications for Implant Therapy
RISK FACTOR CONTRAINDICATION
Medical and Systemic Health-Related Issues
Diabetes (poorly controlled) ??Possibly Relative
Bone metabolic disease (e.g., osteoporosis) ??Probably Relative
Radiation therapy (head and neck) Yes Relative/absolute
Bisphosphonate therapy (intravenous) ??Probably Relative/absolute
Bisphosphonate therapy (oral) ??Possibly Relative
Immunosuppressive medication ??Probably Relative
Immunocompromising disease (e.g., HIV, AIDS) ??Possibly Relative
Psychological and Mental Conditions
Psychiatric syndromes (e.g., schizophrenia, paranoia) No Absolute
Mental instability (e.g., neurotic, hysteric) No Absolute
Mentally impaired; uncooperative No Absolute
Irrational fears; phobias No Absolute
Unrealistic expectations No Absolute
Habits and Behavioral Considerations
Smoking; tobacco use Yes Relative
Parafunctional habits Yes Relative
Substance abuse (e.g., alcohol, drugs) ??Possibly Absolute
Intraoral Examination Findings
Atrophic maxilla Yes Relative
Current infection (e.g., endodontic) Yes Relative
Periodontal disease ??Possibly Relative
I. Effects of smoking on periodontal therapycurrent the three pharmacologic agents (NSAIDs, bisphos-
smokers do not respond as well to periodontal therapy phonates, and SDD), only SDD is approved by the
as nonsmokers or former smokers. U.S. Food and Drug Administration (FDA) and
J. Pharmacologic therapy. indicated as an adjunct to scaling and root planing
1. Host modulationthe host immune and inflamma- in the treatment of chronic periodontitis. SDD is
tory responses to bacterial plaque are primarily administered in a 20-mg dose (a typical antimicro-
responsible for the destruction of the periodontium. bial dose of doxycycline is 100mg), twice daily for
Pharmacologic agents that can modify these 3 to 9 months. The 20-mg dose inhibits MMPs but
responses can be used as adjuncts to conventional has no antibacterial activity. SDD should not be
mechanical therapy in the prevention and treatment given to patients with a history of allergy or hyper-
of periodontitis (Figure 7-14). sensitivity to tetracyclines, pregnant or lactating
a. Systemically administered NSAIDs (e.g., ibupro- women, or children younger than 12 years. Doxy-
fen, flurbiprofen, naproxen)inhibit the forma- cycline concentrates in the skin, and there is an
tion of prostaglandins (PGE2). increased risk for sensitivity to sunlight. SDD
b. Bisphosphonatesinhibit bone resorption by should be prescribed to coincide with the initiation
osteoclasts; reports of bisphosphonate-related of scaling and root planing. It should be used only
osteonecrosis of the jaw have raised concerns as an adjunct to mechanical therapy. SDD can also
about the use of bisphosphonates to treat be combined with the local delivery of antibiotics
periodontitis. to address both the host and the bacterial sides
c. SDD (Periostat)inhibits MMP destruction of of the disease process. Chemically modified tetra-
collagen. SDD inhibits MMP-8 and MMP-13. Of cyclines are a newer group of host-modulating
Bisphosphonates
NSAIDs Periostat
Periostat
Antimicrobials Osteoclasts
Pockets
Prostaglandins and
Bone
CAL
Bacterial Host Cytokines resorption
products cells (IL-1, IL-6, TNF)
Connective
MMPs Tooth
tissue
mobility
breakdown
and
loss
Periostat
Bacterial + Host response component = Clinical

component sequelae
Figure 7-14 Potential adjunctive therapeutic approaches. Possible adjunctive therapies and points of intervention in the treat-
ment of periodontitis are presented related to the pathologic cascade of events. CAL, Clinical attachment loss; IL-1, interleukin-1; IL-6,
interleukin-6; NSAIDs, nonsteroidal antiinflammatory drugs; TNF, tumor necrosis factor. (From Newman MG, etal: Carranzas Clinical
Periodontology, ed 12. St. Louis, Saunders, 2015.)
drugs in which all antibiotic properties have been the growth of A. actinomycetemcomitans, and
removed with retention of the host-modifying, exert an anticollagenolytic effect. Tetracy-
anticollagenolytic properties. clines are bacteriostatic, are more effective
d. Locally administered host-modifying agents in- against gram-positive than gram-negative
clude topical NSAIDs and numerous agents used bacteria, and concentrate in the gingival cre-
as adjuncts to surgical therapy, including enamel vicular fluid at levels effective against many
matrix proteins (Emdogain), bone morphogenetic periodontal pathogens. Minocycline and dox-
proteins (BMP-2, BMP-7), growth factors (platelet- ycycline are commonly used tetracyclines.
derived growth factor, insulinlike growth factor), Both are effective in reducing periodontal
and tetracyclines. Of these agents, only Emdogain pathogens. Advantages include decreased
and platelet-derived growth factor (GEM 21S) dosing (tetracycline, four times/day; mino
have been approved by the FDA for adjunctive use cycline, two times/day; doxycycline, one
during surgery. time/day), which may improve patient
2. Antiinfective agents act by reducing the number of compliance.
bacteria present. Antibiotics are one type of antiinfec- (4) Metronidazole is bactericidal to anaerobic
tive agents. Antiseptics are chemical antimicrobial organisms. It disrupts bacterial DNA. It has
agents that can be applied topically to destroy micro- been used in conjunction with amoxicillin.
organisms. Disinfectants are applied to inanimate There can be a disulfiram (Antabuse) effect
objects to destroy microorganisms. (severe cramps, nausea, and vomiting) when
a. Antibiotics. alcohol is ingested during metronidazole
(1) Because the primary initiating agent of peri- treatment.
odontal disease is bacterial plaque, systemic (5) Amoxicillin is a bactericidal, semisynthetic
antibiotics can be used as adjuncts to mechan- penicillin that is effective against both gram-
ical dbridement to decrease the number of positive and gram-negative microorganisms.
bacteria in the periodontal pocket. They It is susceptible to penicillinase (-lactamase).
should not be used as a monotherapy in the Amoxicillin combined with clavulanate po
absence of mechanical dbridement. tassium (Augmentin) is resistant to many
(2) No single antibiotic inhibits all putative peri- penicillinases.
odontal pathogens. A combination of antibi- (6) Cephalosporins are in the -lactam family
otics may be necessary for significant reduction and are similar to penicillins. They are not
of the number of bacteria in the periodontal often used to treat oral infections.
pocket. (7) The spectrum of clindamycin includes anaer-
(3) Tetracyclines are often used in the treatment obic bacteria, and it can be used when the
of localized aggressive periodontitis. They can patient is sensitive to penicillin. It has been
concentrate in the periodontal tissues, inhibit associated with pseudomembranous colitis.
(8) Ciprofloxacin is a quinolone that is active occlusion is present when periodontal tissue injury
against facultative and some anaerobic peri- has occurred secondary to occlusal forces. Occlu-
odontal pathogens. sal therapy should be integrated into periodontal
(9) Erythromycin is not effective against most therapy after completion of home care instruction
periodontal pathogens. However, azithromy- and phase I therapy (scaling and root planing). The
cin is effective against anaerobes and gram- exception to this guideline occurs when occlusal
negative bacilli. It appears to concentrate in forces are contributing to pain or dysfunction.
gingival tissues. Teeth that remain mobile after phase I therapy
(10) Bacteriostatic and bactericidal drugs usu- should be evaluated for occlusal trauma and treated
ally should not be given at the same time. with either interocclusal appliance therapy (a bite
However, they may be given serially. For guard) or occlusal adjustment. The purpose of
example, metronidazole-amoxicillin and either therapy should be to establish a functional
metronidazole-amoxicillin/clavulanate have occlusion that is favorable to periodontal health.
been used effectively in cases that did not Occlusal stability is present when there is maxi-
respond to tetracyclines. mum intercuspation, smooth excursive move-
(11) Antibiotics also can be delivered locally. Two ments without interferences, and no trauma from
formulations available in the United States are occlusion.
10% doxycycline (Atridox) and 2% minocy- b. Each patient should receive a temporomandibular
cline (Arestin). These agents are used as disorder (TMD) screening evaluation that includes
adjuncts to mechanical dbridement. examination for maximal interincisal opening,
(12) Chlorhexidine (2.5mg) is available in a opening and closing pathway, auscultation for TMJ
resorbable delivery system (PerioChip). This sounds, palpation for TMJ tenderness, and palpa-
agent is used as an adjunct to mechanical tion for muscle tenderness. An intraoral examina-
dbridement. tion should include identification of occlusal
K. Wound healing, repair, and regeneration. contacts in maximum intercuspation, guidance in
1. Immediately after suturing to close a periodontal excursive movements, initial contact in centric-
flap, a clot forms that connects the flap to the tooth relation closure, tooth mobility, and attrition.
and alveolar bone. Epithelial cells begin to migrate 2. Signs and symptoms of a nonphysiologic occlusion
over the border of the flap 1 to 3 days after surgery. include damaged teeth and restorations, abnormal
An epithelial attachment is in place 1 week after mobility, fremitus, widened PDL, and possibly pain.
surgery, consisting of hemidesmosomes and a basal 3. Bruxism is defined as a parafunctional activity that
lamina. The clot is replaced by granulation tissue. can include clenching, grinding, gnashing, and
Collagen fibers appear 2 weeks after surgery. Within bracing of the teeth. Bruxism may contribute to wear
1 month, the gingival crevice is lined with epithe- and damage to the teeth and restorations, mobility,
lium, and an epithelial attachment is present. and muscle pain.
2. Reflection of a full-thickness flap results in bone 4. Tissue injury occurs when occlusal forces exceed the
necrosis at 1 to 3 days and osteoclastic resorption that adaptive capacity of the periodontium. This injury is
peaks at 4 to 6 days. Resulting bone loss is approxi- called trauma from occlusion or occlusal trauma. The
mately 1mm. occlusion that causes this damage is termed trau-
3. Healing of a free gingival graft begins with diffusion matic occlusion. Trauma from occlusion can be
of fluids from the recipient bed, adjacent gingiva, and caused by alterations in occlusal forces, reduced
alveolar mucosa. Revascularization starts by the capacity of the periodontium to withstand occlusal
second or third day. Capillaries from the recipient forces, or a combination of both. When trauma from
bed proliferate into the graft to form a network of occlusion is the result of occlusal alterations, it is
new capillaries. The epithelium undergoes degenera- called primary trauma from occlusion. An example
tion and sloughing. It is replaced with new epithe- would be excessive occlusal force, such as a high res-
lium from the borders of the recipient site. The toration, on a tooth with a healthy periodontium.
genetic predetermination for the specific character of When it results from reduced ability of the tissues to
the epithelium depends on the nature of the connec- resist occlusal forces, it is called secondary occlusal
tive tissue bed. trauma. An example would be a normal occlusal
L. Splinting and occlusal correction. force on a tooth with loss of attachment (reduced
1. Overview. periodontium).
a. Occlusion is a dynamic relationship that involves 5. Occlusal therapy should be delayed until inflamma-
the teeth, TMJs, and muscles of mastication. A tion is resolved through completion of nonsurgical
physiologic occlusion is defined as having no signs therapy and implementation of home care. Persistent
of dysfunction or disease. In contrast, traumatic mobility can be assessed and managed through
occlusal adjustment or treatment with appliance should be instructed to avoid alcohol and tobacco,
therapy. These appliances are designed to provide a rinse with chlorhexidine, get adequate rest, remove
reversible means of redistributing occlusal forces to bacterial plaque gently, and take an analgesic as
minimize excessive force on specific teeth. needed for pain. Patients should return in 1 to 2
a. Occlusal adjustment or coronoplasty is the selective days for reevaluation and further dbridement.
reshaping of occlusal surfaces with the goal of Patient should be seen again approximately 5 days
establishing a stable, nontraumatic occlusion. This later for reevaluation; further counseling regarding
is an irreversible intervention. It should not be diet, rest, and tobacco use; reinforcement of
used as a primary means of either preventing or oral hygiene instruction (including chlorhexidine
treating TMD. There is evidence that when patients rinses); and periodontal evaluation.
with a defined need for occlusal adjustment receive b. Acute pericoronitis is treated by gently flushing the
that treatment, their response to periodontal area to remove debris and swabbing with antisep-
therapy may be more favorable. However, as with tic. Occlusion should be evaluated to ensure the
other forms of occlusal therapy, coronoplasty opposing tooth is not in contact with the inflamed
should be deferred until inflammation is resolved. tissue. If there is contact, the tissue may need to be
If significant occlusal adjustment is deemed neces- excised. Drainage should be obtained if there is
sary, it should be performed with restorative needs evidence that the inflamed tissue is fluctuant; anti-
of the patient in mind. biotics should be prescribed if there is evidence of
b. Interocclusal appliance therapy is used to redistrib- systemic involvement. When the acute condition
ute occlusal forces and to minimize excessive force subsides, the associated tooth should be evaluated
on individual teeth. for extraction.
6. Splintingthe most common reason for splinting is c. Acute herpetic gingivostomatitis diagnosed early
to improve patient comfort and function by immo- (within 3 days of onset) is treated immediately with
bilizing excessively mobile teeth. If splinting is being antiviral therapy (acyclovir, 15mg/kg five times
performed because of mobility, the cause of the daily for 7 days). All patients should receive pallia-
mobility should be determined first. If the cause is tive care, including plaque removal, systemic
occlusal trauma, occlusal adjustment should be per- NSAIDs, and topical anesthetics. Proper nutrition
formed in conjunction with resolution of inflamma- should be maintained. Patients should be made
tory periodontal disease before splinting the teeth. aware of the contagious nature of this disease when
a. Splinting should be considered in the following vesicles are present.
situations. d. Aggressive periodontitis.
(1) Increasing mobility of teeth. (1) Patients with a diagnosis of aggressive peri-
(2) Mobility that impairs a patients function. odontitis do not typically respond as predict-
(3) Migration of teeth. ably to conventional therapy as patients with
(4) Prosthetics where multiple abutments are less aggressive forms of disease, such as chronic
necessary. periodontitis. An important aspect of manag-
b. Splinting materialsteeth may be splinted with ing patients with this form of disease is patient
bonded external materials or appliances, intracor- education about the disease in terms of causes
onal appliances, or cast restorations. Regardless of and risk factors. Patients should be educated
the method used, the splint should be designed concerning their role in managing the disease.
such that it does not impinge on the gingival tissues (2) Resective surgical therapy is often difficult in
and it allows room for the patient to perform ade- patients with localized aggressive periodontitis
quate oral hygiene procedures. because teeth adjacent to the teeth affected with
M. Special therapeutic problems. disease may be completely unaffected. Regen-
1. Acute gingival diseasesacute gingival diseases erative surgical therapy may be effective in
include acute necrotizing ulcerative gingivitis), acute these cases, especially in patients with localized
pericoronitis, and acute herpetic gingivostomatitis. two-wall or three-wall bony defects.
a. Treatment of acute necrotizing ulcerative gingivitis (3) Various systemic antibiotics have been used as
includes evaluation of the medical history, appli adjuncts to mechanical dbridement in the
cation of topical anesthetic followed by gently treatment of aggressive periodontitis, including
swabbing the necrotic lesions to remove the pseu- tetracycline; doxycycline; clindamycin; cipro-
domembrane, and removal of local factors such as floxacin; metronidazole; and combinations
calculus (often with ultrasonic instruments unless of amoxicillin-clavulanate, metronidazole-
contraindicated by the medical history). Systemic amoxicillin, and metronidazole-ciprofloxacin.
antibiotics should be prescribed only if there is (4) In patients with aggressive periodontitis,
evidence of lymphadenopathy or fever. The patient severely compromised teeth should be extracted
early. The restorative treatment plan should (usually 1 to 2 days). The area is then treated
include plans to accommodate future tooth with scaling and root planing and evaluated
loss. The use of dental implants should be con- for possible surgical therapy. Antibiotic
sidered when designing the overall treatment therapy is indicated when treating peri-
plan for these patients. odontal abscesses if there is evidence of
(5) Frequent maintenance visits are an important cellulitis, a deep inaccessible pocket, fever,
component of treating patients with aggressive or lymphadenopathy or when treating an
periodontitis. immunocompromised patient.
(6) Patients who do not respond to therapy may be g. Pulpal disease.
classified as refractory. These patients may (1) Dental caries is the most common cause of
benefit from selective antibiotic therapy in con- pulpal disease. Other causes are direct trauma
junction with the use of host-modifying drugs (e.g., tooth fracture); progressive dental caries;
such as SDD. or instrumentation during periodontal, restor-
e. Necrotizing ulcerative periodontitis. Necrotizing ative, or prosthetic procedures.
ulcerative periodontitis may be associated with (2) Pulpal infection is polymicrobial, primarily
immunosuppression. A patient with this diagnosis comprising gram-negative anaerobic bacteria.
must be treated in consultation with his or her Combined endodontic-periodontal lesions can
physician. Resolution or treatment of the systemic originate from pulpal necrosis spreading to the
condition may be necessary for the periodontal periodontium via the apex or accessory canals
condition to resolve. Treatment of the oral lesions (primary endodontic lesion/secondary peri-
consists of local dbridement, lavage, and oral odontal lesion), or progressive loss of attach-
hygiene instruction that may include daily use of ment that reaches accessory canals or the
antimicrobial agents such as chlorhexidine. These apex (retrograde pulpitis; primary periodontal
lesions are often painful, leading to the need for lesion/secondary endodontic lesion). The
local anesthetic during dbridement. second mechanism is relatively rare. In true
f. Abscesses. combined lesions (development and extension
(1) Gingival abscesses are localized to the gingival of an endodontic lesion into an existing peri-
tissues, whereas periodontal abscesses involve odontal pocket), loss of pulpal vitality should
the deeper supporting structures of the teeth. be treated first, followed by periodontal therapy,
Gingival abscesses are attributed to plaque, for resolution to occur.
trauma, or foreign body impaction and are (3) Both pulpal and periodontal disease can result
treated by dbridement and drainage. in abscess formation. Periodontal abscesses are
(2) Periodontal abscesses can be classified as acute usually not painful; acute endodontic abscesses
or chronic. Acute abscesses can be characterized usually are painful.
by mild to severe discomfort, localized swell- h. Oral malodorgingivitis, periodontitis, and
ing, presence of a periodontal pocket, mobility, tongue coating are the predominant causes of oral
extrusion of tooth in the socket, percussion or malodor. Acute pharyngitis, purulent sinusitis, and
biting sensitivity, presence of exudate, elevated postnasal drip also can contribute to the problem.
temperature, and lymphadenopathy. Chronic The unpleasant odor originates from volatile sulfur
abscesses usually are not painful, have slight compounds, which include hydrogen sulfide,
extrusion, have intermittent exudation, are methylmercaptan, dimethyl sulfide, putrescine,
associated with a fistulous tract and deep cadaverine, indole, skatole, and butyric or propi-
pocket, and have little systemic involvement. onic acid. Most of these compounds are formed
(a) Causesperiodontal abscesses can be by oral microorganisms (primarily gram-negative
attributed to various factors, including anaerobes) that degrade peptides from various
untreated moderate to deep periodontal intraoral sources. Treatment strategies include
pockets, incomplete calculus removal in tongue cleaning with either a toothbrush or a
periodontal pockets, tooth perforation or tongue scraper, interdental cleaning and tooth-
fracture, and foreign body impaction. brushing, and professional treatment of periodon-
(b) Periodontal abscesses are treated by first tal disease. Chewing gums, mouth rinses, and
resolving the acute lesion by the establish- toothpastes may be used as adjuncts.
ment of drainage either through the pocket i. Root sensitivityroot sensitivity is often a problem
or through an external excision. Patients after periodontal therapy. Adequate plaque control
should be instructed to rinse with warm salt is essential to reducing or eliminating root sensitiv-
water and to apply chlorhexidine to the ity. Desensitizing agents used by the patient in-
area until the signs and symptoms subside clude dentifrices that contain strontium chloride,
potassium nitrate, and sodium citrate. These agents is placed 2mm away from the alveolar bone) can
act through the precipitation of crystalline salts lead to inflammation and localized bone loss (Figures
that block dentinal tubules. Agents that can be 7-15 and 7-16). Because of individual variations in
professionally applied include cavity varnishes, the biologic width, probing to the bone level (sound-
zinc chloridepotassium ferrocyanide, formalin, ing to bone) is recommended to determine the
calcium hydroxide, dibasic calcium phosphate, definitive diagnosis of biologic width violation.
sodium fluoride, stannous fluoride, strontium 2. The location of the interproximal contact can have
chloride, and potassium oxalate. an impact on the gingival embrasure. Restorations
j. Gingival enlargementsgingival enlargements are should be designed to allow adequate space for the
usually caused by inflammation (acute and chronic) interproximal papillae. Contacts located too high
or are drug-associated. Enlargements associated
with acute inflammation are usually treated with
scaling and root planing. Chronic enlargements
may require surgical removal, either through a gin-
givectomy procedure or through a flap procedure.
Drug-associated gingival enlargement is usually
attributable to phenytoin; calcium channel block-
ers; or cyclosporine, an immunosuppressant. There
are both inflammatory and chronic components to
these enlargements, so treatment must include
Biologic Connective tissue 1.0 mm
removal of plaque and calculus. Surgical therapy width
may be recommended, but the patient should be 2.0 mm Junctional epithelium 1.0 mm
aware that the enlargement may recur if he or she
continues taking the medication. A discussion Sulcus 1.0 mm
with the patients physician regarding possible dis-
continuation or substitution of the medication
should be part of the treatment plan.
(1) Gingival enlargements associated with blood
dyscrasias (e.g., leukemia) should be treated
with phase I therapy (scaling and root planing). Figure 7-15 Average human biologic width. Connective
Adjunctive antibiotic therapy to prevent infec- tissue attachment 1mm in height; junctional epithelial attach-
ment 1mm in height; sulcus depth of approximately 1mm. The
tion may be indicated.
combined connective tissue attachment and junctional epithelial
(2) Gingival enlargements associated with preg- attachment, or biologic width, equals 2mm. (From Newman
nancy should initially be treated by scaling MG, etal: Carranzas Clinical Periodontology, ed 12. St. Louis,
and root planing and oral hygiene instruction. Saunders, 2015.)
Surgical excision may be indicated if the
enlargement creates problems with occluding
the teeth.
N. Periodontal restorative considerationsperiodontal
therapy, including nonsurgical and surgical treatment,
should precede extensive restorative care. Periodontal
therapy allows for better assessment of margin location;
ensures adequate tooth length for retention, optimal
tooth stability, and resolution of mucogingival prob- Bone loss
lems; and allow for alveolar ridge reconstruction.
Inflammation
1. Restorative margin placement can be supragingival
(least impact on the periodontium), at the marginal
gingival crest, or subgingival (greatest impact on the
periodontium). Subgingival margins should not
Figure 7-16 Ramifications of a biologic width violation if
impinge on the attachment apparatus. The space for
a restorative margin is placed within the zone of the
soft tissue above the alveolar bone is termed the bio- attachment. On the mesial surface of the left central incisor,
logic width. The average human biologic width has bone has not been lost, but gingival inflammation occurs. On the
been defined as 2mm; this includes an average width distal surface of the left central incisor, bone loss has occurred,
of 0.97mm for the junctional epithelium and and a normal biologic width has been reestablished. (From
1.07mm for the connective tissue attachment. Bio- Newman MG, etal: Carranzas Clinical Periodontology, ed 12.
logic width violation (i.e., when a restorative margin St. Louis, Saunders, 2015.)
coronally can cause an open gingival embrasure. The supragingival plaque control can affect the growth
high coronal contact can be due to diverging root and composition of subgingival plaque. Complete
angulation or an excessively tapered tooth. When plaque removal must be accomplished at least every
restoring excessively tapered crowns with an open 48 hours. However, patients with periodontal dis-
embrasure space, the margins of interproximal resto- ease should remove plaque every 24 hours because
rations should be placed 1 to 1.5mm subgingival. of enhanced susceptibility to disease.
This placement successfully moves the contact in an 2. Toothbrushing.
apical direction, closing the embrasure space and a. The use of hard bristle toothbrushes, vigorous
allowing for the maintenance of gingival health. horizontal brushing, and extremely abrasive tooth-
3. Access for oral hygiene procedures is an important pastes may lead to cervical abrasions and gingival
aspect of pontic design. The ovate pontic is created recession. Soft nylon bristle brushes do not tend
by forming a flat or concave receptor site in the alveo- to traumatize the gingival tissues. Toothbrushes
lar ridge with a diamond bur or electrosurgery. The should be replaced approximately every 3 months.
alveolar bone must be a minimum of 2mm from the b. Powered toothbrushes typically use the mechani-
most apical portion of the pontic. This pontic design cal contact of the bristles on the tooth to remove
has a convex undersurface, which makes it easy to plaque. However, the addition of low-frequency
clean. The sanitary pontic also has this design but acoustic energy to generate dynamic fluid move-
does not contact the soft tissue and is a less esthetic ment can provide cleaning without direct contact
restoration. of the bristles. Studies have shown that although
4. Teeth with periodontal involvement that are treated powered brushes can remove more plaque, they do
by root resection should be restored in a manner that not improve measures of gingival inflammation
allows for hygiene access. The remaining tooth struc- beyond those found with manual brushes. Powered
ture should be reshaped such that, facially and lin- brushes can be beneficial in patients who are poor
gually, the contours are a straight line from the brushers, patients with dexterity problems, chil-
margin coronally, whereas the interproximal con- dren, and caregivers of individuals who cannot
tours emerge from the margin as either a straight line clean their own teeth.
or slightly convex. c. In Bass brushing, the toothbrush bristles are placed
at the gingival margin at a 45-degree angle to the
tooth. The bristles extend into the gingival sulcus
7.0 Prevention and Maintenance when pressure is applied to the brush in a horizon-
tal direction (Figure 7-17).
A. Prevention. d. Interproximal cleaningbecause periodontal
1. Overvieweffective plaque control is key to effec- disease usually begins in interdental areas, tooth-
tive phase I nonsurgical therapy and is an im brushing must be augmented with interproximal
portant component of preventive therapy. Good cleaning.
A
45
B
Figure 7-17 Bass method. A, Proper position of the brush in the mouth aims the bristle tips toward the gingival margin. B, Diagram
shows the ideal placement, which permits slight subgingival penetration of the bristle tips. (From Newman MG, etal: Carranzas Clinical
Periodontology, ed 12. St. Louis, Saunders, 2015.)
B. Maintenance. 3. The distance from the CEJ to the base of the pocket is
1. Overviewthe maintenance phase is initiated after a measure of _____.
the completion of phase I therapy and reevaluation. A. Clinical attachment level
It is performed in a continuum with phase II (surgi- B. Gingival recession
cal) therapy and phase III (restorative) therapy. It is C. Probing pocket depth
essential to long-term preservation of the remaining D. Alveolar bone loss
teeth. The primary rationale for maintenance ther- 4. Your examination reveals a probing pocket depth of
apy is continued disruption of bacterial plaque 6mm on the facial of tooth #30. The free gingival
through professional subgingival instrumentation. margin is 2mm apical to the CEJ (there is 2-mm reces-
After completion of phase I therapy, the maintenance sion on the facial). How much attachment loss has
interval for the first year should typically be every 3 occurred on the facial of this tooth?
months. This recommended interval is based on lon- A. 6mm
gitudinal clinical studies that evaluated the time B. 2mm
required for recolonization of periodontal pockets by C. 8mm
proposed pathogens after subgingival dbridement. D. 4mm
The maintenance interval may be altered after the 5. The key feature that differentiates periodontitis from
first year, based on the response of the individual gingivitis is _____.
patient to therapy. Factors that can affect the mainte- A. Loss of clinical attachment
nance interval include oral hygiene status, rate of B. Periodontal pockets greater than 3mm
calculus formation, presence and severity of second- C. Gingival recession
ary systemic or environmental factors, presence of D. Bleeding on probing
remaining pockets, complicated prosthetic therapy, 6. In general, what microorganisms are predominant in
recurrent caries, occlusal problems, ongoing orth- supragingival tooth-associated attached plaque?
odontic therapy, and amount of attachment and A. Gram-negative rods and cocci
alveolar bone loss. B. Gram-negative filaments
2. Procedures performed at each maintenance. C. Gram-positive filaments
a. Examinationreview of medical history; oral D. Gram-positive rods and cocci
pathology examination; evaluation of oral hygiene 7. The inorganic component of subgingival plaque is
status; clinical measures to assess for changes in the derived from _____.
gingiva, pocket depths, mobility, attachment levels, A. Bacteria
furcations, and occlusion; caries evaluation; restor- B. Saliva
ative evaluation; and radiographic evaluation when C. Gingival crevicular fluid
indicated. D. Neutrophils
b. Treatmentoral hygiene reinforcement, scaling, 8. What are the characteristics of the primary (initial)
polishing, chemical irrigation if indicated. bacterial colonizers of the tooth in dental plaque
c. Establish what is necessary for the next visitthe formation?
next maintenance visit, further periodontal treat- A. Gram-negative facultative
ment, or referral for restorative or prosthetic B. Gram-positive facultative
treatment. C. Gram-negative anaerobic
D. Gram-positive anaerobic
9. Which of the following is an important constituent of
Sample Questions gram-negative microorganisms that contributes to ini-
tiation of the host inflammatory response?
1. What is dental wear caused by tooth-to-tooth contact A. Exotoxin
called? B. Lipoteichoic acid
A. Abrasion C. Endotoxin
B. Attrition D. Peptidoglycan
C. Erosion 10. Calculus is detrimental to the gingival tissues because
D. Abfraction it is _____.
2. Occlusal loading resulting in tooth flexure, mechanical A. A mechanical irritant
microfractures, and loss of tooth substance in the cer- B. Covered with bacterial plaque
vical area is _____. C. Composed of calcium and phosphorus
A. Abrasion D. Locked into surface irregularities
B. Attrition 11. Restoration margins are plaque-retentive and pro-
C. Erosion duce the most inflammation when they are located
D. Abfraction _____.
A. Supragingival D. The first statement is false, and the second state-

B. Subgingival ment is true.
C. At the level of the gingival margin 19. Which of the following is most important in determin-
D. On buccal surfaces of teeth ing the prognosis for a tooth?
12. Select from the following list cell types that are part of A. Probing pocket depth
the innate immune system. (Choose four.) B. Bleeding on probing
A. T cells C. Clinical attachment level
B. B cells D. Level of alveolar bone
C. Neutrophils 20. When treating diabetic patients, the most common
D. Dendritic cells problems in the dental chair are usually associated
E. Plasma cells with _____.
F. Monocytes/macrophages A. Hyperglycemia
G. Mast cells B. Hypoglycemia
13. Which of the following are antigen-presenting cells? C. Insulin deficiency
A. Neutrophils D. Insulin resistance
B. T lymphocytes 21. Offset angulation is a characteristic feature of _____.
C. Macrophages A. Sickle scalers
D. Plasma cells B. Universal curettes
14. Which of the following are the most important pro- C. Area-specific curettes
teinases involved in destruction of the periodontal D. Chisels
tissues? 22. Patients with which of the following should not be
A. Hyaluronidase treated with ultrasonic instruments?
B. Matrix metalloproteinases A. Deep periodontal pockets
C. Glucuronidase B. Edematous tissue
D. Serine proteinases C. Infectious diseases
15. The predominant inflammatory cells in the periodon- D. Controlled diabetes
tal pocket are _____. 23. Order the following types of cells by their ability to
A. Lymphocytes populate a wound area during the healing process
B. Plasma cells from fastest to slowest.
C. Neutrophils 1. PDL cells
D. Macrophages 2. Epithelial cells
16. Which of the following are part of preliminary phase 3. Gingival connective tissue cells
therapy? 4. Bone marrow cells
1. Treatment of emergencies A. 1, 2, 4, and 3
2. Extraction of hopeless teeth B. 2, 3, 1, and 4
3. Plaque control C. 3, 2, 1, and 4
4. Removal of calculus D. 1, 3, 4, and 2
A. 1, 2, and 3 24. What is the most important procedure to perform
B. 2, 3, and 4 during the initial postoperative visits after periodontal
C. 1 and 2 only surgery?
D. 2 and 4 only A. Plaque removal
17. Polymorphisms in which of the following genes have B. Visual assessment of the soft tissue
been associated with severe chronic periodontitis? C. Periodontal probing
A. IL-6 D. Bleeding index
B. IL-1 25. When performing a laterally repositioned flap, which
C. TNF of the following must be considered relative to the
D. PGE2 donor site?
18. Given the same amount of attachment loss and same A. Presence of bone on the facial
pocket depth, a single-rooted tooth and a multirooted B. Width of attached gingiva
tooth have the same prognosis. The closer the base of C. Thickness of attached gingiva
the pocket is to the apex of the tooth, the worse the D. All of the above
prognosis. 26. During preparation of implant osteotomy (drilling
A. Both statements are true. for an implant), the critical temperature that should not
B. Both statements are false. be exceeded is _____ at an exposure time of 1 minute.
C. The first statement is true, and the second state- A. 37C
ment is false. B. 47C
C. 57C C. Tooth mobility

D. 67C D. Tooth attrition
27. Which class of bony defect responds best to regenera- 30. For most patients affected with periodontitis, what
tive therapy? is the recommended interval for maintenance
A. One-walled appointments?
B. Two-walled A. 1 month
C. Three-walled B. 3 months
D. Shallow crater C. 6 months
28. Guided tissue regeneration is a method for preventing D. 1 year
_____ in a healing surgical site. 31. The minimal mesiodistal space required for the place-
A. Plaque accumulation ment of two standard-diameter implants (4.0mm
B. Cementum deposition diameter) between teeth is _____ mm.
C. Epithelial migration A. 4
D. Clot formation B. 10
29. The most common clinical sign of occlusal trauma is C. 14
_____. D. 18
A. Tooth migration
B. Tooth abrasion
SECTION 8
Pharmacology
FRANK DOWD
OUTLINE
Cues That Help in Remembering Drugs
1. Principles of Pharmacology
by Classes
2. Autonomic Pharmacology
3. Central Nervous System Pharmacology The suffixes of the following generic drug names listed are
4. Anesthetics indicative of the corresponding drug classes:
5. Analgesics and Antihistamines
caine = local anesthetic (e.g., lidocaine)
6. Cardiovascular Pharmacology and Diuretics coxib = cyclooxygenase (COX)-2 inhibitors (e.g.,
7. Gastrointestinal and Respiratory Pharmacology celecoxib)
8. Endocrine Pharmacology dipine = dihydropyridine calcium channel blockers
(e.g., nifedipine)
9. Antimicrobial Drugs
dronate = bisphosphonate (e.g., alendronate)
10. Antineoplastic Drugs fungin = glucan synthesis inhibitor, antifungal (e.g.,
11. Toxicology caspofungin)
12. Prescription Writing gliptin = dipeptidyl peptidase-4 inhibitor drug for type
2 diabetes (e.g., sitagliptin)
glitazone = peroxisome proliferator activated receptor
gamma (PPAR) activator for type 2 diabetes (e.g.,
pioglitazone)
grel = P2Y12 adenosine diphosphate (ADP) receptor
Pharmacology is a science that bridges basic science and inhibitor in platelets (e.g., clopidogrel)
clinical dentistry and medicine. This chapter reviews both olol = -adrenergic receptor blockers (e.g., pro
aspects. The proper clinical use of drugs requires knowl- pranolol)
edge and integration of pharmacologic concepts and ilol or alol = -adrenergic receptor blocker that also
drugs. This review follows a standard sequence similar to blocks 1-adrenergic receptors (e.g., carvedilol)
the textbook Pharmacology and Therapeutics for Dentistry, mab = monoclonal antibodies (e.g., infliximab)
ed 6 (St. Louis, Mosby, 2011), by Yagiela etal. Several onium or urium = quaternary ammonium com-
figures and tables in this review have been taken from pounds, usually competitive, peripherally acting skeletal
that text. muscle relaxers (e.g., pancuronium)
This review is not meant to be a comprehensive treat- osin = 1-adrenergic receptor blockers (e.g., prazosin)
ment of pharmacology but rather a guide to study in pre- oxacin = fluoroquinolone antibacterial (e.g., moxi
paring for the pharmacology section of Part II of the floxacin)
National Board Dental Examination. Students are referred parin = heparin or low-molecular-weight heparin (e.g.,
to other sources, including the above-mentioned text, for tinzaparin)
more complete discussions in each area of pharmacology. prazole = proton pump inhibitor (e.g., esomeprazole)
(See also References at the end of this chapter.) This review penem = carbapenem -lactam antibacterial (e.g.,
can help students organize and integrate knowledge of con- ertapenem)
cepts and facts. It can also help students to identify areas pril or prilat = angiotensin-converting enzyme (ACE)
requiring more concentrated study. inhibitors (e.g., captopril)
290
Section 8 Pharmacology 291
sartan = angiotensin II receptor blockers (e.g., 7. Intrinsic activity is the maximal effect of a drug
losartan) (Figure 8-1).
statin = 3-hydroxy-3-methylglutaryl coenzyme A 8. Efficacy is the effect of a drug as a function of level
(HMG-CoA) reductase inhibitor antilipid drugs (e.g., of binding to its receptor.
lovastatin) 9. Affinity is a term that refers to the attractiveness of
teplase = tissue plasminogen activator drug (e.g., a drug to its receptor. Affinity is usually measured
alteplase) by the dissociation constant (Kd). The lower the Kd,
triptan = serotonin 5-HT1B/1D agonist antimigraine the higher the affinity.
drugs (e.g., sumatriptan) 10. Potency is the response to a drug over a given range
of concentrations (usually measured by the effective
concentration of the drug leading to its half maximal
1.0 Principles of Pharmacology effect [EC50]) (see Figure 8-1).
11. Graded dose-response curves are also helpful in dis-
Drugs are the agents studied in pharmacology. These playing the effect of antagonists. In Figure 8-2, the
chemicals have their effects through numerous targets tracings in Figure 8-1 have been used to show the
in the body. Targets refer to the types of sites at which effect of antagonists on the response of an agonist.
drugs act. In this case, tracing A slows the effect of an agonist
alone compared with the effect of an agonist in the
Targets of Drug Action presence of a competitive antagonist (tracing B) and
A. Receptors are proteins on or in cells that mediate the in the presence of a noncompetitive antagonist
effect of drugs and to which drugs bind with affinity (tracing C). The pure antagonist has no intrinsic
and selectivity. There are five classes of drug receptors. activity.
1. G proteinlinked (seven plasma membrane domain)
receptors.
Intrinsic activity (Emax)
2. Ion channel receptors.
3. Transmembrane receptors with cytosolic enzyme 100%
domains. A
B
4. Intracellular nuclear receptors that alter gene
expression.
EC50
5. Cell surface adhesion receptors. 50% C
B. Enzymes (free or associated with cells) are also subject Graded
to inhibition (or stimulation) by certain drugs. response
C. Drugs may also act as chemical or physical agents with
low selectivity, such as antacids, or high selectivity, such
as monoclonal antibodies. 0%
Log dose of the drug
Dose-Response Relationships of Drugs
Potency
A fundamental principle in pharmacology is that the effects
of drugs are dose-dependent. These effects can be shown Figure 8-1 Graded dose-response curves of three
on two types of dose-response curves. agonists.
A. Type Igraded dose-response curves are useful for de-
termining characteristics of agonists and antagonists.
100%
1. Agonists have intrinsic activity. A
2. Antagonists (pure antagonists) have no intrinsic B
activity.
3. If a full agonist has an intrinsic activity of 1 and an EC50
C
50%
antagonist has an intrinsic activity of 0, a partial
Graded
agonist has an intrinsic activity of more than 0 but
response
less than 1.
Antagonist alone
4. D + R DR effect, where D = drug concentra-
tion, R = receptor concentration, and DR = concen- 0%
tration of drug bound to receptor. Log dose of the drug
5. By examining DR, we can investigate the drug
Potency
binding characteristics to the receptor.
6. By examining the effect, we investigate the tissue, Figure 8-2 Graded dose-response curves showing the
organ, or organisms response to a drug. effect of antagonists.
292 Section 8 Pharmacology
All = 100%
Percentage of animals responding

(desired response or lethal effect)
Therapeutic 100 mg
Half = 50% = = 10
Figure 8-3 Quantal dose-response index 10 mg
curves.
LD50
ED50
None = 0%
0.1 1 10 100 1000 10,000
Dose of drug (log scale)
B. Type II Quantal dose-response curvesquantal dose- Stomach pH = 1.4 Plasma pH = 7.4

response curves look very similar to graded dose-
response curves, but the two are quite different. Aspirin
A HA HA A
Although both curves determine a response based on (pKa = 3.4) 0.01 1.0 1.0 10,000
dose or concentration of the drug (using a log scale), (Total drug = 1.01) (Total drug = 10,001)
the y-axis (ordinate) of the quantal dose-response curve
indicates the number of subjects responding to a drug.
BH B B BH
The response is a specific quantitative response (e.g., a Codeine 3.16 3 106 1.0 1.0 3.16
30-mm increase in blood pressure). LD50/ED50 = thera- (pKa = 7.9)
peutic index (TI). The TI is an estimate of the margin (Total drug = 3.16 3 106) (Total drug = 4.16)
of safety for the drug (Figure 8-3).
Figure 8-4 Unequal distribution of two drugs across a
Pharmacokinetics semipermeable membrane because of the pH of each
Pharmacokinetics is the study of what the body does to the compartment and the pKa values of the two drugs. The
drug. It involves absorption, distribution, metabolism, and pH and pKa of the drug determine the concentration of weak acids
excretion. and weak bases in various body fluids and are important in deter-
A. Acid-base. mining the rate of absorption and rate of excretion. (Modified
The acid or base properties of a drug and the pH of from Yagiela JA, etal: Pharmacology and Therapeutics for Den-
various body fluids are important considerations for tistry, ed 6. St. Louis, Mosby, 2011.)
drug distribution (Figure 8-4). Many drugs are either
weak acids or weak bases.
1. Weak acids tend to concentrate in compartments of cytoplasm or that enhance drug excretion (notably
high pH, where they are more charged. anion and cation transporters).
2. Weak bases tend to concentrate in compartments of 5. Metabolism is important because it usually leads to
low pH, where they are more charged. inactivation of the drug as well as making the drug
B. Absorption, distribution, metabolism, and excretion. more water-soluble. If a drug is made active by
1. The kidney is a good example of pH affecting excre- metabolism, it is called a prodrug.
tion of weak acids and weak bases. Weak acids are 6. Types of reactions involved in drug metabolism.
excreted more rapidly at higher urinary pH because a. Phase I reactions involve reactions such as oxida-
weak acids are concentrated in the lumen of the tion, reduction, and hydrolysis.
kidney tubule. b. Phase II reactions involve conjugation, in which
2. Most drugs are administered by mouth. This a chemical substituent is added to the drug. The
involves the portal system of the liver. most common type of conjugation reaction is
3. Some compartments in the body have added barri- glucuronide conjugation.
ers against drugs gaining access to the compart- 7. Most metabolism of drugs occurs in the liver.
ment. The best example of such a barrier is the a. In the liver, metabolism can be microsomal
blood-brain barrier. (includes cytochrome P-450 enzymes).
4. Many cells contain transport systems (mainly b. Alternatively, metabolism in the liver can be
P-glycoproteins) that remove drugs from the nonmicrosomal.
8. Excretion usually occurs in the kidney, especially used to determine Cp0 (plasma concentration at
for more soluble drugs. Processes involved include zero time) and t1/2. The equations can then be used
the following. to determine Vd, ke, and Cl.
a. Glomerular filtration. 11. Zero-order elimination kinetics refers to the elimi-
b. Active tubular secretion. nation of a constant amount of drug eliminated
c. Passive tubular transfer of the drug either from regardless of dose, as opposed to first-order kinet-
blood to lumen or from lumen to blood ics, the most common type (see previously), in
(reabsorption). which a constant percentage of remaining drug is
9. Most mathematical calculations that involve phar- eliminated.
macokinetics apply to elimination kinetics. The fol- 12. Although accumulation of drug in the body can
lowing are among the more important equations. occur with repeated doses, both in first-order and
(The following assume first-order kinetics.) in zero-order elimination, the risk of accumulation
a. ke t1/2 = 0.693, where k = first-order rate constant is usually greater for zero-order kinetics.
and t1/2 = half-time.
b. D = Cp0 Vd, where D is the drug dose (single Drug-Drug Interactions
dose), Cp0 is the plasma concentration at zero Drugs may interact by acting at the same receptor or signal
time, and Vd is the apparent volume of transduction pathway, or, more commonly, a drug may
distribution. affect the pharmacokinetics of another drug. The most
c. Cl = ke Vd, where ke is the first-order rate con- common form of drug-drug interaction is one drug affect-
stant of elimination, Cl is the clearance, and Vd is ing the metabolism of another drug. Drug-drug interac-
the apparent volume of distribution. tions based on metabolism involve either induction or
d. t1/2 = 0.693 Vd/Cl (this equation is derived from inhibition.
two of the previous equations). A. Induction of metabolism is a reaction to certain drugs
10. In Figure 8-5, plotting plasma concentrations shown in which the number of liver cytochrome enzymes
(on a log scale) versus time (linear scale) results in increases, resulting in a reduction in the effect of the
a straight line if the drug is eliminated by first-order other drug. Some drugs that induce liver enzyme can
kinetics. The phase usually refers to the linear also induce P-glycoprotein transporters.
section of the tracing after redistribution and equili- B. Inhibition of metabolism is a process by which one drug
bration have occurred. This straight-line plot can be either competes for metabolism of another or directly
inhibits drug-metabolizing enzymes. Some drugs that
inhibit liver enzyme can also inhibit P-glycoprotein
transporters.
1000 C. Most drug-drug interactions involving metabolism
occur in the liver. Induction and inhibition usually
involve microsomal enzymes.
D. Genetics and pharmacologyenzyme characteristics are
Cpo = 200 g/mL
important in determining the response to a drug; this
is especially true for drug-metabolizing enzymes. The
93 g/mL
Plasma concentration (g/mL)
100
rate of drug metabolism can vary greatly, depending on
44 g/mL the cytochrome P-450 isozyme profile of the patient.
See also idiosyncratic reaction, following.
21 g/mL
E. Examples of drug-drug interactions in dentistry are
presented in Table 8-1.
10 g/mL
Adverse Drug Reactions
10 A. Toxicity results when the dose of the drug is excessive
4.9 g/mL
for the particular patient. It is due to a similar mecha-
2.3 g/mL nism of action as the therapeutic effect (extension
effect).
B. Side effectan adverse effect that occurs within the
therapeutic dose range of the drug.
C. Drug allergyan adverse effect secondary to an immune
1
reaction to a drug.
0 1 2 3 4 5 6 7 D. Idiosyncratic reactionan adverse drug reaction that is
Hour due to a genetic change usually involving a change in
Figure 8-5 Drug plasma concentration on a semilog plot. enzyme activity (Table 8-2).
Table 8-1
Examples of Drug-Drug Interactions Important in Dentistry
DENTAL DRUG INTERACTING DRUG COMMENTS
Diazepam or Itraconazole, clarithromycin, or other Increased sedation owing to reduced metabolism of benzodiazepine
triazolam cytochrome P-450 3A inhibitor
Tetracyclines Oral antacids Reduced absorption of tetracyclines
Aspirin Anticoagulants Increased bleeding tendency
Aspirin Probenecid Decreased effect of probenecid
Aspirin Methotrexate Increased methotrexate toxicity
Acetaminophen Alcohol Increased risk of liver toxicity in chronic alcoholics
Local anesthetics Cholinesterase inhibitors Antagonism of cholinesterase inhibitorreduced effectiveness of
the cholinesterase inhibitor in the patient with myasthenia gravis
Table 8-2
Idiosyncratic Reactions to Drugs Used in Dentistry
IDIOSYNCRATIC
GENETIC ABNORMALITY DRUGS INVOLVED RESPONSE
NADH-methemoglobin reductase deficiency Benzocaine, prilocaine Methemoglobinemia
Glucose-6-phosphate dehydrogenase deficiency Aspirin, primaquine, sulfonamides Hemolytic anemia
Abnormal heme synthesis Barbiturates, sulfonamides Porphyria
Low plasma cholinesterase activity Procaine and other ester local anesthetics Local anesthetic toxicity
Altered muscle calcium homeostasis Volatile inhalation anesthetics, succinylcholine Malignant hyperthermia
Prolonged QT interval Some antipsychotics and antiarrhythmics Torsades de pointes
Modified from Yagiela JA, etal: Pharmacology and Therapeutics for Dentistry, ed 6. St. Louis, Mosby, 2011.
NADH, Reduced nicotinamide adenine dinucleotide.
Miscellaneous Principles Table 8-3

A. Clinical testing of drugs. Drug Testing Phases
After preclinical testing of drugs in animals, clinical
testing is conducted in four phases (Table 8-3). After a PHASE REMARKS
successful phase III, the drug company submits to the I Uses normal volunteers. Safety and
U.S. Food and Drug Administration (FDA) a New Drug pharmacokinetics are assessed.
Application (NDA) to market the drug. II Uses patients who could benefit from the drug.
B. Drugs and pregnancythe relative risks of certain drugs Clinical efficacy, pharmacokinetics, and safety
are assessed.
in pregnancy is categorized into risk categories A, B, C,
D, and X, with A being considered the safest (adequate III Uses larger number of patients, often involving
several medical centers. Safety and clinical
and well-controlled studies have failed to demonstrate efficacy are assessed.
a risk to the fetus in the first trimester of pregnancy, and
IV Postmarketing surveillance. Safety, patterns of
there is no evidence of risk in later trimesters). The use, and new indications are assessed.
other extreme is the X category (studies in animals and
human beings have demonstrated fetal abnormalities,
or there is positive evidence of human fetal risk based
on adverse reaction data from investigational or mar-
keting experience, or both, and the potential risk of the 2.0 Autonomic Pharmacology
drug in pregnant women clearly outweighs the poten-
tial benefit). This section addresses drugs that affect the autonomic
C. Drug legislationTable 8-4 lists seven drug laws as rep- nervous system. Because of similarities with the nerves
resentative of drug legislation since 1906. to skeletal muscles (somatic nervous system) and some
Table 8-4
Major Drug Legislative Acts
YEAR LAW COMMENTS
1906 Pure Food and Drug Act Forbade the adulteration and mislabeling of drugs
1914 Harrison Narcotic Act Regulated opiates and cocaine
1938 Food, Drug, and Cosmetic Act Mandated the safety of drugs and the role of FDA in enforcing safety
1952 Durham-Humphrey Act Used restrictions for certain drugs by prescription only
1983 Orphan Drug Amendment Provided incentives for developing drugs for rare diseases
1997 FDA Modernization Act Replaced legend with label Rx only; allowed manufacturer to discuss off-label
uses of drugs with practitioners; revised accelerated track approval for drugs
that treat life-threatening disorders; made provisions for pediatric drug
research; revised interaction of agency with individuals doing clinical trials
2005 Combat Methamphetamine Established new regulations for sale of ephedrine, pseudoephedrine, and
Epidemic Act phenylpropanolamine
FDA, U.S. Food and Drug Administration.
Somatic nervous system

CNS
Striated
ACh*
muscle
Autonomic nervous system
Sympathetic division
Heart
ACh* NE Smooth muscle
Glands
Sweat glands
ACh* ACh Some blood vessels
Adrenal E
ACh*
medulla NE
Parasympathetic division
Heart
ACh* ACh Smooth muscle
Glands
*Nicotinic site
Muscarinic site
Figure 8-6 Autonomic nerves and somatic nerves to skeletal muscle: synapses and junctions. (From Yagiela JA, etal:
Pharmacology and Therapeutics for Dentistry, ed 6. St. Louis, Mosby, 2011.)
overlap of drug actions, the nerves to skeletal muscle and Abbreviations, Definitions, and Receptors
the receptors associated with these nerves are also reviewed ACh: acetylcholine
with the autonomic nervous system. E: epinephrine
NE: norepinephrine
Organization Cholinergic: pertaining to ACh as in a cholinergic drug,
A. Organization of the autonomic nervous system. cholinergic nerve, or cholinergic receptor
1. Most tissues and organs receive innervation from Adrenergic: pertaining to adrenaline (E) or NE
both sympathetic and parasympathetic nervous
systems. A. Synapses and junctions.
2. All nerve pathways originate from the central nervous 1. The synapses (nerve-nerve) and junctions (nerve-
system (CNS)the sympathetics from thoracolum- effectors) for the autonomic nervous system and
bar outflow and the parasympathetics from cranial- somatic nerves to the skeletal muscles are shown in
sacral outflow. Figure 8-6.
2. The neurotransmitter at each site is identified. Table 8-5

3. It is important to distinguish muscarinic cholinergic
Adrenergic Receptors, Locations,
sites from nicotinic cholinergic sites.
and Signal Transduction
a. Muscarinic sites.
(1) At neuroeffector sites for all postganglionic RECEPTOR SIGNALING
cholinergic neurons (this is characteristic of all TYPE LOCATION PATHWAY
parasympathetic postganglionic nerves). 1* Blood vessels, radial Gq, PLC, Ca2+
(2) At neuroeffector sites of postganglionic sympa- muscle of eye, sphincter
and trigone muscle of
thetic nerves to the sweat glands and a very few
bladder, sphincter
blood vessels (these postganglionic nerves are muscle of GI tract
also cholinergic).
2* Blood vessels, Gi, cAMP
b. Nicotinic sites. prejunctional sites that
(1) At the skeletal neuromuscular junction (involv- act as autoreceptors
ing the somatic nerves). 1 Heart, GI tract, salivary Gs, cAMP
(2) At ganglionic sites (note: the same type of glands, adipose tissue
nicotinic receptor is present in sympathetic (lipolysis), kidney
ganglia, parasympathetic ganglia, and the juxtaglomerular cells
adrenal medulla). 2 Bronchi, blood vessels, Gs, cAMP
4. The two nicotinic receptors are distinct and different heart
receptor types. There are drugs that can distinguish 3 Adipose tissue (lipolysis) Gs, cAMP
one from the other. cAMP, Cyclic AMP; GI, gastrointestinal; PLC, phospholipase C.
5. The adrenal medulla secretes the hormones E and *1 and 2 receptors (postjunctional) are associated with vasoconstriction.
NE. There is no ganglion here, but the ACh receptors 2 autoreceptors (prejunctional), when stimulated by agonists, mediate a
are ganglionic nicotinic in type. reduction in release of neurotransmitters.
6. Muscarinic receptors are divided further into M1, 2 receptors are associated with vasodilation.
M2, M3, M4, and M5 receptors; however, most anti-
muscarinic drugs are unable to distinguish between
the various muscarinic receptors. The roles of the M4
and M5 receptors are unknown. D. The neurotransmitters ACh, NE, and dopamine are
7. Muscarinic receptors (M1 and M3) are linked to stored in vesicles or granules.
Gq, phospholipase C, and Ca2+, whereas M2 recep- E. Termination of transmission by ACh occurs primarily
tors are linked to Gi and a decrease in cyclic adenos- by metabolism by acetylcholinesterase located on post-
ine monophosphate (cAMP). synaptic or postjunctional membranes.
8. Adrenergic receptors are important clinically. Several F. Termination of transmission by NE occurs primarily by
clinically useful adrenergic drugs are selective for a reuptake of NE into prejunctional nerves and second-
receptor type (Table 8-5). arily into other cells. Monoamine oxidase (MAO) and
catechol O-methyltransferase (COMT) play a role in
Dynamics of Neurotransmission metabolizing NE.
A. Biosynthetic pathway for ACh.
Step 1: choline (taken up into nerve via action of Tissues and Organs
permease). A. Another important part of autonomic pharmacology is
Step 2: choline acetyltransferase catalyzes the synthesis linking specific receptors and autonomic pathways to
of ACh from acetyl CoA and choline. given tissue responses (Table 8-6).
B. Biosynthesis of NE and E. B. Knowing the receptor preference for a drug, the recep-
Step 1: tyrosine to DOPA (enzyme is tyrosine tors located in a given tissue, and the response to the
hydroxylase). receptor, one can predict the response to a drug.
Step 2: DOPA to dopamine (enzyme is aromatic L-
amino acid decarboxylase). Adrenergic Agonists
Step 3: dopamine to NE (enzyme is dopamine beta- The receptor preferences for some adrenergic agonists are
hydroxylase). shown in Table 8-7.
Step 4 (mostly in adrenal medulla): NE to E (enzyme is A. Figure 8-7 shows the response to three catecholamines.
phenylethanolamine N-methyltransferase). To determine all of the effects of these drugs, one must
(Some flow charts show synthesis beginning with remember that, especially for heart rate, the reflex effect
phenylalanine.) mediated by baroreceptors must be taken into account.
C. Tyrosine hydroxylase catalyzes the rate-limiting step in Notice the role of each receptor and baroreceptor reflex
the synthesis. This enzyme is inhibited by metyrosine. in the various phases of the responses in Figure 8-7.
Table 8-6
Some Important Tissue Receptors and Responses
SYMPATHETIC ADRENERGIC PARASYMPATHETIC
EFFECTOR SYMPATHETIC RESPONSE RECEPTOR* RESPONSE
Eye
Radial muscle of the iris Contraction (mydriasis) 1
Sphincter of the iris Contraction (miosis)
Heart
SA node Increase in rate 1, 2 Decrease in rate
AV node Increase in automaticity and 1, 2 Decrease in conduction velocity
conduction velocity
Ventricles Increased contractility, conduction 1, 2
velocity, and automaticity
Blood vessels Constriction (), dilation () 1, 2, 2
Lungs
Bronchial smooth muscle Relaxation 2 Contraction
GI tract
Smooth muscle Decreased motility and tone 1, 2 1, 2 Increased motility and tone
Sphincters Contraction 1 Relaxation
Salivary glands Viscous secretion, amylase secretion 1, 1, 2 Profuse, watery secretion
Urinary bladder
Detrusor Relaxation 2 Contraction
Trigone and sphincter Contraction 1 Relaxation
AV, Atrioventricular; GI, gastrointestinal; SA, sinoatrial.
*Receptors in bold type have the greatest effect.
1 1 and
Heart rate (beats/min)
100 reflex
70
40
Reflex
200 Figure 8-7 Cardiovascular effects of three adren-

ergic agonists. Some important receptors are linked
to responses.
Arterial blood pressure (mm Hg)
160 Systolic
120
Diastolic
80
40 Norepinephrine Epinephrine Isoproterenol

B. Indirectly acting sympathomimetic (sympathetic-type) addition to blocking 1 and 2 receptors (not shown in
drugs act by releasing NE. Examples include amphet- Table 8-8).
amines and ephedrine (the latter has both direct and B. -Adrenergic receptor blockers.
indirect action). These drugs demonstrate tolerance 1. Phentolamine and phenoxybenzamine are proto-
and are orally active, in contrast to E and NE. types of nonselective -adrenergic receptor blockers
(1 and 2) and are rarely used in medicine because
Adrenergic Receptor Blockers of their nonselectivity. However, phentolamine is
A. Table 8-8 shows adrenergic receptor blockers and their used in dentistry to reverse soft tissue anesthesia
adrenergic receptor preferences. Every drug in each more quickly after procedures involving a local anes-
column is an antagonist at that receptor. Almost all thetic with a vasoconstrictor.
blockers end in olol. Exceptions include carvedilol 2. Prazosin.
and labetalol, which block 1-adrenergic receptors in a. Example of a selective 1 blocker.
b. 1 blockers are used to treat hypertension, heart
Table 8-7 failure, and benign prostate hypertrophy (1 block-
Some Adrenergic Agonists, Their Receptor ers cause vasodilation, reduce afterload and preload
Preferences, and Main Uses of the heart, reduce contraction of smooth muscle
in the sphincter and trigone muscles of the bladder,
RECEPTOR
DRUG USE PREFERENCE and reduce contraction of the prostate).
c. Adverse effects of 1 blockershypotension (espe-
Epinephrine Reverse 1, 2, 1, 2, 3
anaphylaxis, cially first-dose effect), fluid retention, dry mouth,
vasoconstriction, nasal stuffiness.
bronchodilation 3. Epinephrine reversalthe vasoconstrictor effect of
Norepinephrine Vasoconstriction 1, 2, 1 epinephrine is converted into a vasodilator effect in
Isoproterenol Bronchodilation,
the presence of an blocker. The 2 vasodilator
1, 2, 3
reverse heart response becomes the major vascular response to
block epinephrine because receptors are blocked by the
Phenylephrine Nasal 1, 2 blocker. This reversal is more complete with non-
vasoconstriction selective blockers.
Naphazoline Nasal 2 C. -Adrenergic receptor blockers ( blockers).
vasoconstriction 1. Used more often than blockers.
Clonidine Antihypertensive 2 2. Some are partial agonists (have intrinsic sympatho-
mimetic activity).
Methyldopa Antihypertensive 2
3. Propranolol is the prototype of nonselective block-
Dexmedetomidine IV sedation 2 ers, but most are selective 1 receptor blockers.
Albuterol Bronchodilation 2 4. blocker effectsdecrease blood pressure, reduce
Terbutaline Bronchodilation 2 angina, reduce risk after myocardial infarction,
Salmeterol Bronchodilation 2 reduce heart rate and force, have antiarrhythmic
effect, cause hypoglycemia in diabetics, decrease
Dobutamine Cardiac 1, 1
stimulation intraocular pressure.
5. Carvedilolnonselective blocker that also blocks
Methylphenidate CNS stimulation (Indirect action)
1 receptors; used for heart failure.
Amphetamine CNS stimulation (Indirect action) D. Adrenergic neuron blockers.
CNS, Central nervous system; IV, intravenous. 1. Metyrosineinhibits tyrosine hydroxylase; used to
treat pheochromocytoma.
Table 8-8
Adrenergic Receptor Blockers
RECEPTOR TYPE BLOCKED 1 AND 2 1 SELECTIVE 1 AND 2 1 SELECTIVE
Drugs Phentolamine Prazosin Propranolol Metoprolol
Phenoxybenzamine Terazosin Pindolol Atenolol
Doxazosin Nadolol Acebutolol
Tamsulosin Timolol Esmolol
Table 8-9
Cholinergic Receptor Agonists
STRUCTURALLY SIMILAR
DRUG RECEPTOR AFFINITY TO ACETYLCHOLINE USE
Acetylcholine MN Ophthalmic
Bethanechol MN Yes To increase GI and urinary tract motility
Methacholine MN Yes To test reactivity of airway
Carbachol N>M Yes To treat glaucoma
Pilocarpine MN No, occurs in nature To treat glaucoma, stimulate salivary flow
Cevimeline MN No To stimulate salivary flow
Nicotine* NM No, occurs in nature For smoking cessation
Varenicline NM No For smoking cessation
GI, Gastrointestinal; M, muscarinic; N, nicotinic.
*Nicotine acts at both types of nicotinic receptors. It also causes desensitization of nicotinic receptors, leading to receptor blockade in a time-dependent manner.
2. Reserpinedepletes granules containing NE in nerve B. These drugs are longer lasting than ACh because they
endings, releases NE (rarely used). are not subject to rapid metabolism similar to ACh
3. Guanethidine and guanadrelblock adrenergic nerve (Table 8-9). ACh is metabolized by acetylcholinesterase,
endings by a series of actions; used rarely for located near receptors for ACh. In the plasma and other
hypertension. sites, ACh and many other esters are metabolized by
4. MAO inhibitors, such as pargyline and tranylcypro- pseudocholinesterase. The other cholinergic agonists
mine, indirectly reduce granule content of NE but used as drugs are metabolized slowly or not at all by
increase it in the cytoplasmic pool of adrenergic these enzymes.
neurons. MAO inhibitors should not be used with C. ACh given in low doses stimulates mostly muscarinic
indirectly acting drugs, such as amphetamines, receptors; in very high doses, more nicotinic effects
ephedrine, and tyramine (in many foods and bever- occur (see Table 8-9).
ages). Newer MAO-A and MAO-B selective inhibi- D. The muscarinic effects of cholinergic agonists include
tors are available for clinical use. salivation, miosis, bradycardia, bronchoconstriction,
increase in gastrointestinal (GI) motility, increased
Dental Implications of and Blockers urination, and sweating. (Postganglionic sympathetic
A. Phentolamine (OraVerse) is used in dentistry to reverse nerves to sweat glands release ACh, which stimulates
soft tissue anesthesia more quickly after procedures muscarinic receptors.) Vasodilation, another effect of
involving a local anesthetic with a vasoconstrictor. muscarinic receptor agonists, is not as obvious. The
B. The disorders for which these drugs are used often vasculature is almost exclusively innervated by the
affect dental treatment. sympathetic system. Why do we get vasodilation from
C. blockers increase the vasoconstrictor response to E injected muscarinic receptor agonists? Because the
but reduce the tachycardia resulting from E. blood vessels have muscarinic receptors on their endo-
D. blockers inhibit the vasoconstrictor response to E and thelial cells. These receptors are linked to synthesis and
levonordefrin. release of nitric oxide, which causes vasodilation.
E. MAO inhibitors should not be used with indirectly E. Adverse effects of muscarinic receptor agonists are
acting sympathetic drugs and with several other drugs extensions of the effects listed previously.
such as opioids, especially meperidine. F. Nicotinic receptor agonists include nicotine itself and
F. E and levonordefrin have exaggerated effects when varenicline, a partial agonist at the 42 type nicotinic
given with depleting drugs, such as reserpine, guanethi- receptor. Each is used in smoking cessation.
dine, and guanadrel.
Anticholinesterases
Cholinergic Receptor Agonists A. These drugs act as indirect agonists at both muscarinic
A. Most drugs in this group are used for their muscarinic and nicotinic sites.
effects. They mimic the effects of postganglionic cholin- B. They inhibit acetylcholinesterase located near both
ergic nerves. nicotinic and muscarinic receptors.
Table 8-10
Cholinesterase Inhibitors
TYPE OF DURATION INHIBITORY EFFECT ON
DRUG INHIBITION OF ACTION PSEUDOCHOLINESTERASE USES
Edrophonium* Reversible Very short Little To reverse curare-type drugs, diagnosis
Neostigmine* Reversible Extended Little To reverse curare-type drugs, to treat
myasthenia gravis
Physostigmine Reversible Short Little For glaucoma, antidote for atropine
Pyridostigmine* Reversible Extended Little To treat myasthenia gravis
Tacrine Reversible Extended Little To treat Alzheimers disease
Donepezil Reversible Extended Little To treat Alzheimers disease
Galantamine Reversible Extended Little To treat Alzheimers disease
Rivastigmine Pseudoirreversible Extended Little To treat Alzheimers disease
Malathion Irreversible Long Substantial Insecticide
Echothiophate Irreversible Long Substantial For glaucoma
Sarin Irreversible Long Substantial Nerve gas
Soman Irreversible Long Substantial Nerve gas
*Does not enter the central nervous system.
Table 8-11 ciliary muscles also accounts for some removal of intra-
ocular fluid.
Effects of Anticholinesterases*
B. 1-Adrenergic receptor agonists stimulate the radial
MUSCARINIC NICOTINIC muscle of the eye to contract, increasing the size of the
Miosis, salivation, pupil (mydriasis) and in some cases slowing the removal
Muscle twitching and
sweating, bradycardia, weakness, tachycardia, of fluid from the eye.
bronchoconstriction, increase in blood pressure C. Adrenergic agonists and antagonists and certain pros-
increased GI motility, taglandins reduce formation of intraocular fluid and
urination
reduce intraocular pressure.
GI, Gastrointestinal.
*Central nervous system effects of anticholinesterases include restlessness, Antimuscarinic Drugs
ataxia, and respiratory depression.
A. Block the effect of ACh and all drugs that stimulate
muscarinic receptors.
B. Atropine and scopolamine are prototypes.
C. Effects are shown in Table 8-12.
C. The characteristics of cholinesterase inhibitors vary D. Indications are shown in Table 8-13. (A limited number
(Tables 8-10 and 8-11). of muscarinic receptor subtypeselective drugs are
D. Drugs that are metabolized by pseudocholinesterase are available.)
synergized by pseudocholinesterase inhibitors.
E. Pralidoxime is used to reactivate acetylcholinesterase Dental Implications of Antimuscarinic
after irreversible inhibition by an organophosphate Drugs and Cholinergic Drugs
(e.g., echothiophate, isoflurophate, sarin, soman). A. Atropineoral administration is 0.5mg (adult dose)
for reducing salivary flow.
Autonomics and the Eye B. Contraindications for using antimuscarinic drugs.
A. Muscarinic receptor agonists stimulate the circular 1. Narrow-angle glaucoma.
muscle of the eye to contract, decreasing the size of the 2. Prostate hypertrophy.
pupil (miosis). They also cause contraction of the ciliary 3. Paralytic ileus.
muscle, leading to focusing for near vision. Contraction 4. Tachycardia.
of these muscles also leads to enhanced removal of C. Reduced salivary flow leads to increased risk of caries.
intraocular fluid through the canal of Schlemm and the D. Pilocarpine and cevimeline are used to stimulate sali-
trabecular network. Uveoscleral drainage through the vary flow.

Effects of Antimuscarinic Drugs Curare-Type Neuromuscular Junction
Blockers
ORGAN EFFECT
Eye Mydriasis, cycloplegia (fixation SOME
for distant vision) CHARACTERISTICS
OTHER THAN
Salivary glands Reduced secretion HISTAMINE MUSCLE
Lacrimal glands Reduced secretion DRUG RELEASE RELAXATION
D-tubocurarine ++ Ganglionic blockade
Heart Tachycardia (moderate and larger
doses) Pancuronium Steroid, has some
Bronchi Bronchodilation, reduce secretion antimuscarinic effects
GI tract Reduced peristalsis, reduced Atracurium + Metabolized by esterase
secretion and Hoffman
degradation
Bladder Urinary retention
Vecuronium Antimuscarinic, steroid
Sweat glands Reduced secretion
Pipecuronium Steroid
CNS
Basal ganglia Antitremor activity Rocuronium Steroid
Vestibular apparatus Antimotion sickness Doxacurium Slightly more delayed
Higher centers Drowsiness or stimulation, onset
depending on drug and dose
Mivacurium + Metabolized by esterase
CNS, Central nervous system; GI, gastrointestinal.
Skeletal Neuromuscular Blockers

A. Types.
Table 8-13 1. Depolarizing noncompetitive blockers (succinyl
Antimuscarinic Drugs and Uses choline).
2. Nondepolarizing competitive blockers of ACh
DRUG USES
(curare-type drugs).
Atropine Prototype, to reduce salivary B. These drugs are used during surgery for relaxing skel-
flow, for antivagal effect
during surgery, antidote for etal muscle, for endotracheal intubation, for treatment
physostigmine of tetanus, and for a few other purposes.
Scopolamine Prototype, for motion sickness C. They have permanent positive charges and do not enter
the CNS, and they are not absorbed after oral
Propantheline For overactive bladder
administration.
Tolterodine For overactive bladder D. The effects of competitive skeletal neuromuscular
Trospium For overactive bladder blockers can be antagonized by cholinesterase
Glycopyrrolate To reduce stomach acid, to inhibitors.
reduce bradycardia during E. The contrasting properties of curarelike drugs are pre-
surgery sented in Table 8-14.
Homatropine To cause mydriasis F. Dantrolene.
Cyclopentolate To cause mydriasis 1. A drug that relaxes skeletal muscle without blocking
Tropicamide To cause mydriasis nicotinic receptors.
Benztropine To reduce parkinsonian
2. Prevents release of Ca2+ from the sarcoplasmic
symptoms reticulum.
Trihexyphenidyl To reduce parkinsonian
3. Used for prophylaxis against malignant hyperther-
symptoms, to treat some mia and to overcome muscle contraction and damage
dystonias secondary to malignant hyperthermia.
Oxybutynin For overactive bladder 4. Used also for upper motor neuron disorders (e.g.,
Ipratropium To treat asthma
cerebral palsy).
G. Botulinum toxin A (Botox).
Pirenzepine (M1 selective) To treat peptic ulcers
1. Prevents release of ACh from neurons.
Darifenacin (M3 selective) For overactive bladder 2. Used in ophthalmology to relax extraocular muscles.
Solifenacin (M3 selective) For overactive bladder 3. Used for muscle dystonias.
4. Used to remove wrinkles.
3.0 Central Nervous System Table 8-15

Pharmacology Dopaminergic Cell Groups and Related
Effects of Antipsychotics
Antipsychotic Drugs
CELL GROUP ACTION
A. Indications.
Mesolimbic and mesocortical Antipsychotic effect
1. Schizophrenia and other types of psychosis.
2. Tourettes syndrome. Nigrostriatal Motor side effects
3. Huntingtons chorea. Tuberoinfundibular Stimulation of prolactin
4. Other disorders, such as obsessive-compulsive release, galactorrhea
disorders. Chemoreceptor trigger zone Antiemetic effect
B. Drugs. Medullary-periventricular Increased appetite
1. Phenothiazines.
a. Aliphatic derivatives.
(1) Chlorpromazine.
b. Piperidine derivatives. 5. Malignant syndrome.
(1) Thioridazine. 6. Tardive dyskinesia (a more permanent effect that is
(2) Mesoridazine. difficult to reverse).
c. Piperazine derivatives. 7. Many motor-adverse (extrapyramidal) effects can be
(1) Fluphenazine. relieved by antimuscarinic drugs that are able to
(2) Perphenazine. gain access to the brain because acetylcholine and
(3) Prochlorperazine. dopamine oppose each other in the basal ganglia.
(4) Trifluoperazine. Blocking muscarinic receptors tends to correct the
2. Haloperidol resembles piperazine phenothiazines. imbalance of blocking dopamine receptors by anti-
3. Thiothixene resembles piperazine phenothiazines. psychotic drugs.
4. Others (e.g., loxapine, pimozide). F. Other adverse effects of antipsychotic drugs.
5. Newer and more atypical antipsychotic drugs. 1. Antimuscarinic effects.
a. Clozapine. 2. Orthostatic hypotension.
b. Olanzapine. 3. Convulsions.
c. Quetiapine. 4. Photosensitivity.
d. Risperidone. 5. Cardiac arrhythmias (long QT syndrome).
e. Ziprasidone.
f. Aripiprazole. Antidepressant Drugs
g. Paliperidone. Drug treatment of depression is based on increasing sero-
C. Mechanism of actiontreatment of psychosis has been tonin (5-HT) or NE (or both) at synapses in selective tracts
largely based on the dopamine hypothesis. Drugs in the in the brain; this can be accomplished by different mecha-
phenothiazine class (as well as haloperidol, thiothixene, nisms. Treatment takes several weeks to reach full clinical
and others such as loxapine and pimozide) block dopa- efficacy.
mine receptors in the mesolimbic and mesocortical A. Drugs.
pathways. The D2 receptor is the key antipsychotic 1. Tricyclic antidepressants.
receptor. Blocking dopamine receptors is important not a. Amitriptyline.
only for antipsychotic action but also for other effects, b. Desipramine.
including adverse effects of antipsychotic drugs. Newer c. Doxepin.
and more atypical drugs differ as follows. d. Imipramine.
1. They may preferentially inhibit selective dopamine e. Protriptyline.
receptors. 2. Selective serotonin reuptake inhibitors (SSRIs).
2. They also inhibit serotonin (5-hydroxytryptamine a. Fluoxetine.
[5-HT]) receptors of the 5-HT2 type, accounting for b. Paroxetine.
part of their antipsychotic action. c. Sertraline.
D. Effects of antipsychotic drugs are shown in Table 8-15. d. Fluvoxamine.
E. Adverse motor effects of antipsychotic drugs. e. Citalopram.
1. Acute dystonias. 3. Serotonin norepinephrine reuptake inhibitors
2. Akathisia. (SNRIs).
3. Parkinsonism. a. Venlafaxine.
4. Perioral tremor. b. Duloxetine.
4. MAO inhibitors. 4. MAO inhibitors (nonselective) inhibit the metabo-

a. Tranylcypromine. lism of NE, dopamine, and 5-HT in nerve endings.
b. Phenelzine. 5. Mirtazapine increases the release of NE and 5-HT
c. Selegiline (MAO-B selective). from nerve endings.
5. Miscellaneous antidepressants. 6. Bupropion increases the release of NE and dopa-
a. Bupropion. mine. Increasing dopamine in the synapses may con-
b. Maprotiline. tribute to its action, especially in its use in smoking
c. Mirtazapine. cessation.
d. Trazodone. 7. Trazodone blocks 5-HT2A and 1 adrenergic
e. St. Johns wort. receptors.
B. Contrasting mechanisms of action of antidepressants. 8. St. Johns wort reduces the membrane potential of
1. Tricyclic antidepressants inhibit reuptake of NE and nerves and may indirectly reduce uptake of NE and
5-HT. The inhibition of reuptake leads to a sequence 5-HT.
of events that eventually results in an antidepressive C. Pharmacokineticsmost of these drugs are lipid-
effect. Box 8-1 shows this progression. soluble, have long half-lives, and are metabolized.
2. SSRIs inhibit reuptake only of 5-HT. D. Adverse effects are listed in Table 8-16.
3. SNRIs inhibit reuptake of NE and 5-HT to varying 1. Tricyclic antidepressants are very likely to cause xero-
degrees based on concentration. stomia. Amitriptyline is especially potent in this
regard.
2. MAO inhibitors should not be used with agents that
release catecholamines and serotonin (see Section
Box 8-1 2.0, Autonomic Pharmacology). MAO inhibitors
Action of Many Antidepressants should not be used with other antidepressants.
Inhibition of reuptake of norepinephrine, serotonin, or Antimania Drugs

both Antimania drugs are used to treat manic-depressive illness.
A. Drugs.
Increase in synaptic concentrations of 1. Lithium.
neurotransmitter 2. Carbamazepine.
3. Valproic acid.
Desensitization of nerve terminal autoreceptors 4. Lamotrigine.
B. Mechanisms of action.
Increase of neuronal release of neurotransmitters 1. Lithium works inside the cell to block conversion of
inositol phosphate to inositol.
Selective changes in postsynaptic receptors 2. Carbamazepine blocks sodium channels (see section
on antiepileptic drugs).
Table 8-16
Comparison of Adverse Effects of Antidepressants
NAUSEA,
CARDIAC VOMITING, ANTIMUSCARINIC
DRUG SEDATION SEIZURES HYPOTENSION EFFECTS DIARRHEA EFFECTS
Tricyclic antidepressants +++ + +++ ++ + ++++
Selective serotonin 0 0 0 0 ++++ 0
reuptake inhibitors
Monoamine oxidase 0 + ++++ 0 + 0
inhibitors
Miscellaneous agents
Trazodone ++++ + ++ 0 + 0
Bupropion 0 ++ + 0 0 0
Duloxetine + 0 + + 0 0
0, No effect; +, ++, +++, ++++, indicate degree of effect.
3. Valproic acid blocks sodium and calcium channels GABA

(see section on antiepileptic drugs).
4. Lamotrigine blocks sodium channels.
C. Lithium toxicity.
1. Nausea, diarrhea, convulsions, coma, hyperreflexia, Picrotoxin
cardiac arrhythmias, hypotension.
2. Thyroid enlargement; increases thyroid-stimulating
hormone secretion; may cause hypothyroidism.
3. Polydipsia, polyuria (lithium inhibits the effect of Chloride
channel
antidiuretic hormone on the kidney).
D. Clinical applications concerning lithium.
1. Patients must be warned against sodium-restricted
diets because sodium restriction leads to greater
Barbiturate
retention of lithium by the kidney.
2. Patients must have regular (e.g., monthly) blood
checks because the margin of safety is narrow.
E. Drug-drug interactions of lithium.
Benzodiazepine
1. Diuretics and newer nonsteroidal antiinflammatory
drugs (NSAIDs) reduce lithium excretion and may Figure 8-8 Chloride channel with GABA and three drugs.
cause lithium toxicity. (Adapted from Sieghart W: GABAA receptors: ligand-gated Cl ion
channels modulated by multiple drug-binding sites, Trends Phar-
Sedative Hypnotics macol Sci 13:446-450, 1992. IN Yagiela JA, Dowd FJ, Johnson BS,
Mariotti AJ, Neidle EA: Pharmacology and Therapeutics for
Sedative hypnotics work by numerous mechanisms. Most
Dentistry, ed 6, St Louis, Mosby, 2011.)
of the drugs enhance chloride channel activity (i.e., increase
chloride conductance in the brain). These drugs are used
for various purposes depending on the drug, dose, and conductance. (Other aforementioned drugs do not
route of administration. bind to the GABAB receptor.)
A. Drugs and their actions. 8. Antihistamines (e.g., diphenhydramine)block H1
1. Benzodiazepinesenhance the effect of - histamine-1 (H1) receptors. Doing so in the CNS
aminobutyric acid (GABA) at GABAA receptors on leads to sedation.
chloride channels; this increases chloride channel 9. Ethyl alcoholactions include a likely effect on the
conductance in the brain (GABAA receptors are ion chloride channel.
channel receptors). 10. Flumazenilblocks benzodiazepine receptors
2. Barbituratesenhance the effect of GABA on the (both BZ1 and BZ2) and reverses the excessive seda-
chloride channel but also increase chloride channel tion of sedatives acting at these receptors.
conductance independently of GABA, especially B. Chloride channel.
at high doses, giving barbiturates greater sedative Figure 8-8 shows the chloride channel. It is com-
and hypnotic effects than benzodiazepines. Barbi posed of subunits and has several binding domains that
turates also decrease activation of glutamate - include binding domains for GABA, benzodiazepines,
amino-3-hydroxy-5-methylisoxazole-4-propionic and barbiturates. There are two benzodiazepine recep-
acid (AMPA) receptors. tors, BZ1 (also called omega-1) and BZ2 (also called
3. Zolpidem and zaleplonwork in a similar manner omega-2), on the chloride channels, reflecting different
to benzodiazepines but do so only at the benzodi- subunit structures of the channels.
azepine1 (BZ1) receptor type. (Both BZ1 and BZ2 are C. Benzodiazepines.
located on chloride channels.) 1. All benzodiazepines are metabolized, most with
4. Chloral hydrateprobably similar action to active metabolites. Glucuronidation terminates the
barbiturates. sedative action. Elimination half-lives vary a great
5. Buspironepartial agonist at a specific serotonin deal from drug to drug.
receptor (5-HT1A). a. Triazolam (1 to 2 hours).
6. Other sedatives (e.g., mephenesin, meprobamate, b. Midazolam (2 to 5 hours).
methocarbamol, carisoprodol, cyclobenzaprine) c. Oxazepam (5 to 15 hours).
mechanisms not well described. Several mecha- d. Alprazolam (12 to 15 hours).
nisms may be involved. e. Lorazepam (10 to 18 hours).
7. Baclofenstimulates GABAB receptors that are f. Chlordiazepoxide (5 to 30 hours).
linked to the G protein, Gi, resulting in an in- g. Diazepam (30 to 60 hours).
crease in K+ conductance and a decrease in Ca2+ h. Flurazepam (50 to 100 hours).
2. -Hydroxylation is a rapid route of metabolism that 2. Used for insomnia.

is unique to triazolam, midazolam, and alprazolam; 3. Selective action at BZ1 receptorreduces risk of tol-
this accounts for the very rapid metabolism and short erance and dependence.
sedative actions of these drugs. 4. Do not have anticonvulsant action.
3. Pharmacologic effects of benzodiazepines. 5. Do not greatly affect sleep patterns.
a. Antianxiety. F. Chloral hydrate.
b. Sedation. 1. Short-acting sleep inducerless risk of hangover
c. Anticonvulsant (including drug-induced convul- effect the next day.
sions). 2. Little effect on REM sleep.
d. Amnesia, especially drugs such as triazolam. 3. Metabolized to trichloroethanol, an active metabo-
e. Relax skeletal muscle (act on CNS polysynaptic lite; further metabolism inactivates the drug.
pathways). 4. Used for conscious sedation in dentistry. Repetitive
4. Indications. doses should not be used.
a. Intravenous sedation (e.g., midazolam, diazepam, 5. Can result in serious toxicity if dose is not
lorazepam). controlled.
b. Antianxiety. G. Buspirone.
c. Sleep induction. 1. Short half-life (2 to 4 hours).
d. Anticonvulsant (e.g., diazepam, clonazepam). 2. Relieves anxiety.
e. Panic disorders. 3. Does not act as an anticonvulsant.
f. Muscle relaxation. 4. Is not a good muscle relaxant.
5. Adverse effects. 5. Minimum abuse potential.
a. Ataxia, confusion. H. Other sedativescarisoprodol, cyclobenzaprine, and
b. Excessive sedation. methocarbamol are used for muscle relaxation.
c. Amnesia (not a desired effect with daytime I. Baclofen.
sedation). 1. Used in spasticity states to relax skeletal muscle.
d. Altered sleep patterns (increase stage 2 and 2. Occasionally used in trigeminal neuralgia.
decrease stage 4 sleep). J. Antihistamines (first-generation H1 receptor blockers).
D. Barbiturates. 1. Used for sedation (e.g., diphenhydramine).
1. Long-actingphenobarbital is used to treat certain K. Ethyl alcohola sedative hypnotic, but not used clini-
types of seizures (see section on antiepileptic drugs). cally as a sedative. Its main impact is chronic abuse,
2. Intermediate-actingamobarbital, pentobarbital (oc- which can cause significant damage to the liver, brain,
casionally used for sleep), secobarbital. and other organs. Disulfiram inhibits aldehyde dehy-
3. Short-actinghexobarbital, methohexital, thiopental drogenase, which when given with ethyl alcohol results
rarely used as intravenous anesthetics. in the accumulation of acetaldehyde, leading to adverse
4. Pharmacologic effects of barbiturates. effects.
a. Similar to benzodiazepines except for the impor-
tant differences shown in Table 8-17.
b. Induce an increased synthesis of porphyrins and Antiepileptic Drugs
are contraindicated in certain types of porphyria. Seizures are caused by inappropriate and excessive activity
E. Zolpidem and zaleplon. of motor neurons in the CNS. Seizure activity is either
1. Short half-lives (zolpidem 2 hours; zaleplon partial or generalized, depending on the extent of hyperac-
1 hour). tivity. Partial seizures usually involve one side of the brain
Table 8-17
Comparison of Benzodiazepines with Barbiturates
CHARACTERISTIC BENZODIAZEPINES BARBITURATES
Dose-response profile Less steep, reaches a plateau at higher doses Steep, no plateau
Therapeutic index High Low
Inducer of liver enzymes Weak Strong
Respiratory depression Lower potential High potential
Shortens REM sleep resulting in REM rebound Somewhat To a significant degree
Potential for abuse Significant Higher
Table 8-18
Antiepileptic Mechanisms of Drugs
BLOCKS SODIUM BLOCKS T-TYPE BINDS TO THE CHLORIDE CHANNEL INCREASES
DRUG CHANNELS CALCIUM CHANNELS AND INCREASES ITS CONDUCTANCE GABA
Phenytoin Yes
Phenobarbital Yes
Primidone Yes
Carbamazepine Yes
Gabapentin* Yes
Pregabalin* Yes
Tiagabine Yes
Topiramate Yes Yes
Lamotrigine Yes
Vigabatrin Yes
Valproic acid Yes Yes
Ethosuximide Yes
Clonazepam Yes
Diazepam Yes
Zonisamide Yes Yes
GABA, -aminobutyric acid.
, No major or known effect.
*Binds to the 2-1 protein subunit of high voltageactivated calcium channels.
May increase synthesis and release of GABA owing to effect on high voltageactivated calcium channels.
Inhibits GABA reuptake.
at the onset, whereas generalized seizures involve both 2. Pharmacokinetics.

sides at the onset. Although seizure disorders exist in a. Slow absorption with oral use.
several forms, it is convenient to divide them into partial b. Antacids may decrease absorption.
and generalized, with two subdivisions of the latter, for c. Highly bound to plasma protein.
purposes of determining drug therapy. d. Often eliminated by zero-order kinetics.
A. Types of seizures (brief summary). e. Metabolized in liverthis can be a basis for drug-
1. Partial seizures. drug interactions.
2. Generalized seizures. 3. Adverse effects.
a. Tonic-clonic (grand mal). a. Gingival hyperplasia, caused by an increase in
b. Absence (petit mal). fibroblast growth and an increase in connective
B. Mechanisms of action of antiepileptic drugs (Table tissue. A similar effect can occur in the face.
8-18)antiepileptic drugs act through one or more b. CNSnystagmus, ataxia, vertigo, diplopia.
mechanisms. c. Hyperglycemia.
1. Inhibition of sodium channels. d. Lymphadenopathy.
2. Inhibition of T-type calcium channels. e. Osteomalacia secondary to effects on vitamin D
3. Binding to 2-1 subunits of high voltageactivated and on calcium absorption.
calcium channels, which reduces activity of these f. Hirsutism.
channels. g. Deficiency of folate and megaloblastic anemia.
4. Increasing conductance at chloride channels. h. Congenital defects secondary to in utero effects.
5. Inhibition of AMPA or N-methyl-d-aspartate D. Carbamazepine.
(NMDA) glutamate receptorsas a result of these 1. Nonseizure indications.
mechanisms, the seizure focus (foci) or spread of a. Trigeminal neuralgia.
excitation or both are reduced. b. Manic-depressive illness.
C. Phenytoin. 2. Pharmacokinetics.
1. Nonseizure indicationsoccasionally for trigeminal a. Metabolized in the liver.
neuralgia. b. Inducer of liver enzymes.
3. Adverse effects. Table 8-19

a. GI upset.
Some Indications of Antiepileptic Drugs
b. Dizziness, diplopia, blurred vision.
c. Visual disturbances. TONIC- PARTIAL
d. Peripheral neuritis. DRUG CLONIC (FOCAL)* ABSENCE
e. Rashes. Phenytoin 3 3 1
f. Aplastic anemia (rare). Phenobarbital 2 2 0
g. Agranulocytosis (rare). Primidone 1 1 0
h. Jaundice secondary to liver effects.
Carbamazepine 3 3 1
E. Phenobarbital.
1. Adverse effects. Valproic acid 3 1 3
a. Induces liver enzymes (can be an adverse effect). Ethosuximide 0 0 3
b. Sedation. Clonazepam 0 0 2
c. Neurologic and behavioral effects. Lamotrigine 1 2 2
d. Hepatic toxicity. Gabapentin 1 2 0
e. Hypersensitivity leading to hematologic side
Pregabalin ? 2 ?
effects.
f. Osteomalacia. Tiagabine 1 2 0
g. Respiratory depression. Topiramate 2 2 0
F. Primidone. Rufinamide ? 3 ?
Acute systemic and CNS toxicity tend to limit use of Higher numbers indicate greater effectiveness or desirability. Negative
primidone. Common side effects include sedation, numbers indicate worsening of the condition by the drug. Zero indicates a
lack of effect.
vertigo, nausea, vomiting, ataxia, diplopia, nystagmus,
*Simple and complex.
and hepatic and hematologic toxicity. Useful for certain types of neuropathic pain.
G. Gabapentin.
1. Nonseizure indicationneuropathic pain.
2. Adverse effects. A. Strategies for therapy.
a. Sedation. 1. Increase dopaminergic receptor stimulation in basal
b. Ataxia. ganglia.
H. Valproic acid. 2. Block muscarinic receptors in the basal ganglia
1. Nonseizure indicationmanic depressive illness. because cholinergic function opposes the action of
2. Adverse effects. dopamine in the basal ganglia.
a. Hair loss. 3. Block NMDA glutamate receptors.
b. GI upset. B. Drugs.
c. Hyperglycemia. 1. Levodopa plus carbidopa (Sinemet).
d. Hyperuricemia. 2. Bromocriptine, pergolide, pramipexole, ropinirole,
e. Weight gain. apomorphine.
f. Hepatic toxicity (especially in patients <2 years old 3. Benztropine, trihexyphenidyl, biperiden, procy
and patients receiving other medications). clidine.
g. Thrombocytopenia. 4. Diphenhydramine.
h. Teratogenicmay cause spina bifida. 5. Amantadine.
I. Ethosuximide. 6. Tolcapone and entacapone.
1. Adverse effects. 7. Selegiline, rasagiline.
a. GI irritation. C. Mechanisms of action of three drugs affecting DOPA
b. CNS depression. are shown in Figure 8-9.
c. Hematologic side effects (uncommon). 1. Levodopa plus carbidopalevodopa is able to pen-
d. Lupus (rare). etrate the blood-brain barrier and is then converted
J. Rufinamide blocks sodium channels. into dopamine. Carbidopa inhibits dopa decarboxyl-
K. Seizure indications are shown in Table 8-19. ase, which catalyzes the formation of dopamine. Car-
bidopa does not penetrate the blood-brain barrier; it
prevents the conversion of levodopa to dopamine
Anti-Parkinson Drugs outside the CNS but allows the conversion of
Parkinsons disease involves degeneration of dopaminergic levodopa to dopamine inside the CNS.
neurons in the nigrostriatal pathway in the basal ganglia. 2. Bromocriptine, pergolide, pramipexole, ropinirole,
The cause is usually unknown. Sometimes it is associated and apomorphine are direct dopamine receptor
with hypoxia, toxic chemicals, or cerebral infections. agonists.
3-O-MD
Carbidopa
7. Selegiline and rasagiline.
a. Nausea.
Tolcapone b. Dry mouth.
Dopa decarboxylase c. Dizziness.
L-dopa dopamine d. Insomnia and anxiety (mostly selegiline).
e. Although selegiline and rasagiline are selective for
MAO-B, they can still cause excessive toxicity in
Selegiline MAO COMT the presence of tricyclic antidepressants, SSRIs,
and meperidine.
F. Indications.
DOPAC 3MT
Parkinsons disease is the obvious major use of
Figure 8-9 Sites of action of carbidopa, MAO inhibitors, the drugs described previously. Parkinson-like symp-
and COMT inhibitors. DOPAC, Dihydroxyphenylacetic acid; toms can occur with many antipsychotic drugs. These
3-O-MD, 3-O-methyldopa; 3MT, 3 methyltyrosine. symptoms are often treated with antimuscarinic drugs
or diphenhydramine.
G. Dental implications of anti-Parkinson drugs.
3. Benztropine, trihexyphenidyl, biperiden, and procy- 1. Dyskinesia caused by drugs can present a challenge
clidine are antimuscarinic drugs. for dental treatment.
4. Diphenhydramine is an antihistamine that has anti- 2. Orthostatic hypotension poses a risk when changing
muscarinic action. from a reclining to a standing position.
5. Amantadine releases dopamine and inhibits NMDA 3. The dentist should schedule appointments at a
receptors. time of day at which the best control of the disease
6. Selegiline is an irreversible inhibitor of MAO-B, occurs.
which metabolizes dopamine. Selegiline increases 4. Dry mouth occurs with several of these drugs.
the level of dopamine.
7. Tolcapone and entacapone are inhibitors of COMT,
another enzyme that metabolizes dopamine. 4.0 Anesthetics
D. Dopamine and acetylcholineloss of dopaminergic
neurons in parkinsonism leads to unopposed action by Local Anesthetics
cholinergic neurons. Inhibiting muscarinic receptors The use of local anesthetics dates back at least to the dis-
can help alleviate symptoms of parkinsonism. covery of cocaine, present in the coca plant, followed by the
E. Adverse effects. development of benzocaine in the late 19th century. Pro-
1. Levodopa. caine was developed in 1906, and drugs such as lidocaine
a. Therapeutic effects of the drug decrease with were developed later in the 20th century.
time. A. Drugs.
b. Oscillating levels of clinical efficacy of the drug 1. Esters.
(on-off effect). a. Procaine (Novocain).
c. Mental changespsychosis. b. Propoxycaine.
d. Tachycardia and orthostatic hypotension. c. Tetracaine (Pontocaine).
e. Nausea. d. Benzocaine (topical only).
f. Abnormal muscle movements (dyskinesias). e. Cocaine.
2. Tolcapone, entacapone (similar to levodopa)hepa- 2. Amides.
totoxicity with tolcapone. a. Lidocaine (Xylocaine).
3. Direct dopamine receptor agonists (similar to b. Mepivacaine (Carbocaine).
levodopa)apomorphine causes more nausea and c. Prilocaine (Citanest).
vomiting. d. Bupivacaine (Marcaine).
4. Antimuscarinic drugs. e. Etidocaine (Duranest).
a. Typical antimuscarinic adverse effects such as dry f. Dibucaine.
mouth. g. Articaine (Ultracaine).
b. Sedation. h. Ropivacaine (Naropin).
5. Diphenhydramine (see antimuscarinic drugs). i. Levobupivacaine (Chirocaine).
6. Amantadine. 3. Ketone typedyclonine (used as a lozenge).
a. Nausea. 4. Other chemicals that act like local anesthetics.
b. Dizziness. a. H1 antihistamines such as diphenhydramine.
c. Edema. b. Saxitoxin.
d. Sweating. c. Tetrodotoxin.
Aromatic ring Connecting chain Amino terminus
CH3
C2H5
NHCOCH2 N (can become
charged)
C2H5
CH3
Lidocaine
Figure 8-10 Lidocaine.
Table 8-20
Properties of Some Local Anesthetics
RELATIVE LIPID RELATIVE ANESTHETIC RELATIVE DURATION
DRUG SOLUBILITY POTENCY OF ANESTHESIA pKa RATE OF ONSET
Procaine + + + 8.9 Slower
Mepivacaine ++ ++ ++ 7.7 Fast
Prilocaine ++ ++ ++ 7.8 Fast
Lidocaine +++ +++ +++ 7.8 Fast
Bupivacaine ++++ ++++ ++++ 8.1 Moderate
Adapted from Yagiela JA, etal: Pharmacology and Therapeutics for Dentistry, ed 6. St. Louis, Mosby, 2011.
The greater the number of + signs, the greater the relative lipid solubility, potency, and duration of anesthesia.
B. Chemistry. Table 8-21

The components of the structure of lidocaine, an
Some Systemic Effects of Vasoconstrictors
example of an amide drug, are shown in Figure 8-10.
Note that local anesthetics become more charged as the ADRENERGIC
pH is lowered. RECEPTOR
DRUG PREFERENCE EFFECT
C. Mechanism of action of local anesthetics.
1. Block sodium channels in the nerve membrane. Epinephrine 1, 2, 1, 2 heart rate
blood pressure
2. Prevent depolarization of the nerve.
D. Pharmacokinetics and action of local anesthetics. Levonordefrin 1, 2 blood pressure
1. For better solubility, local anesthetics are marketed as
the salts of strong acids, such as hydrocloric acid. The
pH of the solution in the cartridge is acidic.
2. Injection of the drug places the drug in a solution of G. Metabolismmetabolism of esters occurs primarily in
higher pH because of the buffers in the body. A the plasma, whereas amides such as lidocaine are
higher percentage of the drug becomes noncharged metabolized in the liver by three types of reactions.
and can more readily penetrate through lipid barriers 1. Dealkylation of the amino terminus.
and into nerves. The higher the lipid solubility, the 2. Hydrolysis of the amide bond.
more potent and long-lasting the drug. The lower the 3. Hydroxylation of the aromatic ring.
pKa, the faster the onset of action of the drug. At low 4. The most abundant urinary metabolite of lidocaine
pH in tissues, anesthesia becomes more difficult to is 4-hydroxyxylidine. Metabolism of lidocaine is
attain because of the presence of a higher percentage rapid (terminal half-life 2 hours).
of the charged form of the drug (Table 8-20). H. Nerve sensitivity to local anestheticsnerves that
E. Vasoconstrictors are used with local anesthetics. conduct pain sensation (C and A) are smaller and
1. To increase depth and duration of anesthesia. conduct slowly compared with most other nerves.
2. To reduce systemic absorption of local anesthetics. Smaller diameter nerves are more sensitive to local
F. Cardiovascular effects and receptor preferences of two anesthetics (Box 8-2).
common vasoconstrictors used in dentistry are shown I. Effects of local anesthetics at sites other than peripheral
in Table 8-21. nerves leading to adverse effects.
Box 8-2 mixing the two drugs, and this is useful for oral
topical anesthesia.
Relative Sensitivity of Nerve Fibers
13. Articaine is an amide, but it also has a side chain
to Local Anesthetics
that is an ester that is required for most of its anes-
(Arranged in decreasing order of sensitivity) thetic effect. Rapid metabolism of this ester bond
Pain Temperature Touch Pressure Motor gives it a short half-life.
14. Pregnancy categorieslidocaine, prilocaine (B);
mepivacaine, bupivacaine, articaine (C).
1. CNS effects. K. Drug-drug interactions.
a. Lightheadedness. 1. Procaine, which is metabolized to para-aminobenzoic
b. Dizziness. acid, may inhibit the antimicrobial effect of
c. Muscle twitching. sulfonamides.
d. Convulsions. 2. The systemic effects of esters are increased in the
e. Respiratory arrest. presence of plasma esterase inhibitors.
2. Cardiac effectssome cardiac depression but also 3. -Adrenergic receptor blockers increase the effect of
specific antiarrhythmic effects. amides owing to lower hepatic blood flow resulting
J. Characteristics of local anesthetics unique to specific from blockers.
drugs or drug classes. 4. Basic drugs may compete with lidocaine and other
1. Benzocaine does not have an amino terminus and amides at plasma 1-acid glycoprotein binding sites.
does not become charged. It is poorly soluble in 5. Enzyme inducers decrease the plasma half-life of
water, even at low pH. lidocaine and other amides.
2. Esters are metabolized primarily in the plasma; 6. Opioids can increase the systemic toxicity of local
amides are metabolized in the liver. anesthetics.
3. Esters are more allergenic than amides. 7. Cimetidine increases plasma levels of lidocaine
4. Cocaine is an ester whose metabolism is more (reduced metabolism secondary to cimetidine).
complex than other esters. 8. Local anesthetics may antagonize the beneficial effect
5. Cocaine also has sympathetic effects because it of acetylcholinesterase inhibitors in patients with
inhibits the reuptake of E and NE. myasthenia gravis.
6. Cocaine also has addictive properties and a euphoric L. Calculation of amounts of anesthetic and vasoconstric-
effect most likely secondary to its blockade of reup- tor used in one anesthetic cartridge, assuming lidocaine
take of dopamine in the brain. 2% with epinephrine 1:100,000 and a cartridge volume
7. All local anesthetics except cocaine are vasodilators of 1.8mL.
at the concentrations used for local anesthesia. 1. Calculation of the amount of anesthetic used in one
However, mepivacaine has less of a vasodilator cartridge (1.8mL):
effect compared with the others and is the drug
usually chosen when a vasoconstrictor is not used Lidocaine 2% = 2 g/100 mL
with the local anesthetic. Lidocaine 2% = 0.02 g/mL
8. Esters show greater apparent toxicity in patients
with a hereditary deficiency in plasma esterases. Lidocaine 2% = 0.036 g/1.8 mL
9. Prilocaine forms o-toluidine on metabolism; this Lidocaine 2% = 36 mg/1.8 mL
may cause methemoglobinemia.
10. Allergies are more likely with esters, and they 2. Calculation of the amount of vasoconstrictor used in
display cross-allergenicity. Amides are much less one cartridge (1.8mL):
likely to cause allergies, and cross-allergenicity is
Epinephrine 1 : 100, 000
apparently less common with the amides. Methyl-
paraben, which was used as a preservative, can also 1 : 1 = 1 g/mL
cause allergies. Sulfites, also used as preservatives,
1 : 1000 = 1 mg/mL
can cause intolerance and perhaps should be avoided
in steroid-dependent asthmatics. 1 : 100, 000 = 0.01 mg/mL
11. Bupivacaine is more selective for sensory nerves
1 : 100, 000 = 0.018 mg/1.8 mL
compared with etidocaine, another long-acting
drug. 1 : 100, 000 = 18 g/1.8 mL
12. EMLA is a eutectic mixture of local anesthetics
such as lidocaine 2.5% plus prilocaine 2.5%. When General Anesthetics
formulated together, there is an increased solubility General anesthetics reduce pain and consciousness. They
of both drugs. Greater penetration is attained by were developed in the 19th century when nitrous oxide
(N2O) and diethyl ether were developed. Halothane, a pro- 1. Stage 1: analgesiaamnesia is common. N2O falls in
totypical halogenated inhalation anesthetic, was developed this category when it is used for conscious sedation.
in the 1950s, followed by others in that class. Injectable 2. Stage 2: deliriumexcitement phase. This stage
anesthetics have been used for some time, with some im- begins with unconsciousness.
portant more recent additions to this type of anesthetic. 3. Stage 3: surgical anesthesiaprogressive loss of
A. Drugs. reflexes and muscle control.
1. Inhaled anesthetics. 4. Stage 4: respiratory paralysis.
a. N2O. D. Terms applied to the properties of general anesthesia.
b. Halogen-containing anesthetics. 1. Blood:gas solubility coefficientthe lower the
(1) Halothane. blood:gas solubility coefficient, the faster the onset
(2) Enflurane. and termination of anesthesia. The effect of the
(3) Isoflurane. blood:gas solubility coefficient on onset of anesthe-
(4) Sevoflurane. sia is illustrated in Figure 8-11, showing how N2O
(5) Desflurane. (which has a very low blood:gas solubility coeffi-
2. Injectable anesthetics. cient) approaches plasma steady-state levels fastest.
a. Propofol. 2. Minimum alveolar concentration (MAC)the mini-
b. Thiopental. mum concentration of anesthetic in the alveolus that
c. Ketamine. is sufficient to give no response from a surgical stim-
d. Etomidate. ulus in 50% of patients.
B. Mechanism of action of general anesthetics. E. N2O.
1. The traditional explanation has been based on the 1. Characteristics.
Meyer-Overton hypothesis (i.e., anesthesia occurs a. Mechanism includes inhibition of nicotinic cho-
when a chemical reaches a certain concentration in linergic and NMDA receptors.
the nerve membrane, disrupting its function). b. Used in conscious sedation (stage 1 anesthesia).
2. It has been shown more recently that general anes- c. 20% N2O80% O2 to start. Concentrations of N2O
thetics act by various mechanisms. They likely modu- are often increased from there.
late ion channels, such as stimulation of GABA d. Compressed in cylinders at 750 psi (in a liquid
receptors and inhibition of nicotinic cholinergic and state).
NMDA glutamate receptors. e. Nonflammable and nonexplosive but support
3. Sites within the CNS most sensitive to the effect of combustion.
general anesthetics. f. Inert gas (no chemical changes or combinations
a. Dorsal lamina of spinal cord. in the body are known to occur).
b. Reticular activating system. g. Rapid onset and termination, colorless, tasteless.
c. Relay circuits between the thalamus and cortex. h. Nonirritating, pleasant.
d. Hippocampus. i. 1.5 times heavier than air.
C. Stages of general anesthesia based on depth of j. Blood:gas solubility coefficient = 0.47; induction
anesthesia. is fast.
100
Arterial gas tension (as % of inspired gas)
80 Nitrous oxide
Isoflurane
Halothane
60 Diethyl ether
Figure 8-11 Effect of anesthetics on

40 arterial gas tension.
20
0
0 5 10 15 20 25 30 35
Time (min)
k. Not a respiratory depressant (a weak anesthetic). Table 8-22

l. Minimal depressant effects on myocardial con-
Properties of Anesthetics
tractibility and cardiovascular system.
m. Low incidence of nausea. ANESTHETIC PARTITION COEFFICIENT
n. No skeletal muscle relaxant properties. AGENT MAC (%) AT 37 C BLOOD:GAS
o. Inhibits vitamin B12dependent methionine syn- Halothane 0.75 2.3
thase by oxidizing the cobalt in cyanocobalamin. Isoflurane 1.2 1.4
p. Prolonged exposure (e.g., >24 hours) causes bone Enflurane 1.6 1.8
marrow suppression.
Sevoflurane 2.0 0.65
q. Can cause diffusion hypoxia at end of administra-
Desflurane 6.0 0.45
tion if N2O is not washed out with oxygen.
r. Diffuses into closed air spaces in the body; this is Nitrous oxide 105.0 0.47
especially noticeable in the bowel. Modified from Yagiela JA, etal: Pharmacology and Therapeutics for Dentistry,
s. Very useful anesthetic agent because of its analge- ed 6. St. Louis, Mosby, 2011.
sic properties. MAC, Minimum alveolar concentration.
2. Adverse effects.
a. Decreased mental performance.
b. Decreased audiovisual ability.
c. Decreased manual dexterity. 2. Table 8-22 compares MAC values and blood:gas
d. Adverse reproductive effectsreduced fertility solubility coefficients for halogens and N2O. Notice
with longer and higher exposure. the range of partition coefficients and MAC values.
e. Reports of spontaneous abortion with higher 3. Unique qualities of certain halogenated anesthetics.
exposure. a. Halothane.
f. Reports of neurologic and kidney disease with (1) Poses a risk with epinephrine.
higher exposure. (2) Associated with hepatitis.
g. Bone marrow suppression with longer exposure (3) Poor skeletal muscle relaxation.
secondary to vitamin B12 effect. b. Enflurane.
3. Some contraindications to the use of N2O. (1) Good skeletal muscle relaxation.
a. Head injury. (2) Less risk with epinephrine.
b. Chest trauma (pneumothorax). (3) Not associated with hepatitis.
c. Bowel obstruction, undiagnosed abdominal pain, c. Isoflurane, desflurane, sevoflurane.
or marked abdominal distention. (1) Fast-acting.
d. Vitreoretinal surgery with intraocular gas (avoid (2) Similar to enflurane.
N2O for at least 3 months). G. Injectable anesthetics.
e. Hypotensionshock. 1. Propofol.
f. Inability of patient to communicate or follow a. Agonist at GABAA receptors.
commands. b. Given intravenously.
g. Chronic obstructive pulmonary disease. c. Rapid onset and termination.
4. Some recommendations to reduce risk of exposure d. Vasodilator.
to N2O. 2. Thiopental.
a. Monitor airborne N2O (badge) and do leak testing. a. Barbiturate.
b. Maintenance and work practices to reduce b. Fast-acting.
exposure. 3. Ketamine.
c. Worker education. a. Blocks NMDA glutamate receptors.
d. Protective gear. b. May cause hallucinations on emergence (given
e. Scavenging system. with diazepam to avoid this).
F. Halogen-containing anesthetics that are inhaled. c. Increases blood pressure.
1. Characteristics. 4. Midazolam, a benzodiazepine.
a. Mechanism includes ion channel modulation. 5. Neuroleptanesthesia (droperidol plus fentanyl plus
b. Widely used clinically. nitrous oxide).
c. Many advantages over earlier drugs such as diethyl H. Antihistamines used for conscious sedation.
ether (nonexplosive, well tolerated, lower blood:gas 1. Promethazine.
solubility coefficient). 2. Hydroxyzine.
d. Dose-dependent decreases in cardiac output and I. Balanced anesthesiathis term refers to the use of
blood pressure. several drugs from the following list to obtain the
e. Not analgesic. desired anesthetic effect.
1. Inhaled drugs (N2O plus a halogen-containing Table 8-23

anesthetic).
Receptor Targets of Opioid Agonists
2. Peripheral skeletal muscle relaxant.
and Antagonists
3. Sedative such as a benzodiazepine.
4. Opioid. COMPOUND MU () DELTA () KAPPA ()
5. Others such as scopolamine. Morphine ++ +
Fentanyl +++
5.0 Analgesics and Antihistamines Pentazocine P ++
Buprenorphine P
Opioids Met-enkephalin ++ +++
Opioids are also called narcotic analgesics. However, mor- -Endorphin +++ +++
phine is also used for pulmonary edema, codeine is also
Naloxone
used for cough, and loperamide and diphenoxylate are
used exclusively for diarrhea. Opium, from the opium Naltrexone
poppy, yields morphine, codeine, and other alkaloids. Data from Brunton LL, Chabner BA, Knollman BJ: Goodman & Gilmans
Pharmacological Basis of Therapeutics, ed 12. New York, McGraw-Hill, 2011.
Newer members of the opioid group of drugs include semi-
+, Agonist; , antagonist; P, partial agonist.
synthetic opium derivatives and synthetic drugs. They act
The number of + signs indicates relative potency.
as agonists at one or more of the opioid receptors. A sepa-
rate group of synthetic drugs has mixed opioid action (i.e.,
they may antagonize one opioid receptor and stimulate
another). In addition, there are endogenous peptides that
have opioid-type actions. Naloxone and naltrexone are
antagonists at opioid receptors. D. Effects of morphine and other opioids.
A. Mechanism of action of opioids. 1. CNSanalgesia, drowsiness, respiratory depression,
1. Opioids are agonists at opioid receptors, which are in euphoria, physical dependence, miosis. Head injury
the plasma membranes of neurons, located both pre- is a contraindication.
synaptically and postsynaptically. 2. GIdecreased peristalsis.
2. Stimulation of opioid receptors leads to activation of 3. Othershistamine release, orthostatic hypotension.
the G protein, Gi, resulting in a decrease in calcium E. Signs and symptoms of acute overdose of morphine and
conductance, which accounts for a decrease in the many other opioids.
presynaptic release of neurotransmitters. Gi activa- 1. Coma.
tion by opioids also increases potassium conductance 2. Pinpoint pupil.
resulting in an increase in the postsynaptic potential 3. Respiratory depression.
and reduced neuronal conduction. F. Pharmacokinetics of morphine.
B. Opioid receptors. 1. Significant liver metabolism after oral doses.
1. Mu () 2. The metabolite, morphine-6-glucuronide, is an active
2. Delta () metabolite.
3. Kappa () 3. t1/2 ~ 3 hours.
4. Each receptor mediates analgesia; however, the G. Other opioids.
receptor is also largely responsible for mediating 1. Codeine.
euphoria, reduced GI motility, physical dependence, a. Well-absorbed orally.
and respiratory depression. Note the different b. t1/2 ~ 3 hours.
combinations for drugs and receptors. Morphine c. Less potent than morphine.
and fentanyl are similar in receptor preference to d. Converted to morphine by cytochrome P-450
the natural, semisynthetic, and most synthetic 2D6. Patient responses to codeine are variable.
opioids. 2. Hydrocodonesimilar to codeine.
5. Opioid receptor preferences of some drugs 3. Dihydrocodeinesimilar to codeine.
(Table 8-23). 4. Meperidine.
C. Sites of analgesic action of opioid analgesics. a. Can be used orally.
1. Descending pathway in the CNS (modulation of pain b. More potent than codeine but less potent than
sensation) including the spinal cord. morphine.
2. Ascending pathway in the CNS (includes pain pro- c. A metabolite, normeperidine, is a CNS stimulant.
cessing and appreciation, or motivational-affective d. Not recommended for long-term pain relief.
component of pain). e. Contraindicated with MAO inhibitors.
3. Peripheral nerve endings. f. t1/2 ~ 3 hours.
5. Methadone. treatment of pain. GI and kidney toxicity are typical adverse

a. Used orally. effects of NSAIDs, particularly in elderly patients.
b. Used in maintenance for treating opioid addic- A. Drugs.
tion as well as for pain. 1. NSAIDs.
c. t1/2 ~ 15 to 40 hours. a. Aspirin and other salicylates.
6. Oxycodone. b. Ibuprofen and similar drugs.
a. Orally useful. c. Piroxicam.
b. t1/2 ~ 3 hours. d. Other NSAIDs, such as ketorolac, sulindac, and
c. More potent than codeine. etodolac.
d. OxyContin is controlled-release oxycodone. e. COX-2 inhibitors.
7. Heroin. f. Nabumetone.
a. Diacetylmorphine. g. Indomethacin.
b. Drug of abuse. 2. Acetaminophen.
8. Fentanylmore potent than morphine. B. Mechanism of action.
9. Fentanyl congeners (e.g., sufentanil, alfentanil, 1. NSAIDs inhibit COX, inhibiting production of pros-
remifentanil). taglandins and other prostanoids (Figure 8-12).
10. Propoxyphene has been withdrawn from the market 2. Most NSAIDs inhibit both forms of COX (COX-1
because of high risk/benefit ratio. Risks include and COX-2). COX-2 is usually the therapeutic target.
cardiac toxicity. NSAIDs have several adverse effects resulting largely
11. Pentazocine. from inhibition of COX-1 (Figure 8-13).
a. Mixed-action agonist.
b. Increases blood pressure.
c. Orally useful. Phospholipids
d. Given with naloxone (Talwin NX) to prevent
Phospholipase A2
injecting pentazocine.
12. Buprenorphine (see Table 8-23). Arachidonic acid
13. Opioid antagonists. COX Lipoxygenase
a. Naloxoneshort t1/2.
b. Naltrexonelonger t1/2. Prostaglandins Leukotrienes
c. Alvimopan and methylnaltrexonedo not enter
Thromboxanes
CNS; used in special cases to treat constipation
Prostacyclin
secondary to opioids. Causes pain,
14. Tramadol. inflammation,
a. Weak receptor agonist. and fever Helps in blood clotting
b. Also blocks reuptake of norepinephrine and
Figure 8-12 Pathway affected by COX and lipoxygenase
serotoninleads to analgesia. enzymes.
15. Diphenoxylate.
a. Antidiarrheal drug.
b. Acts directly on opioid receptors in GI tract.
16. Loperamide. Arachidonic acid
a. Antidiarrheal drug. COX-2
b. Does not cross blood-brain barrier. COX-1
17. Dextromethorphan.
a. Weak NMDA receptor antagonist.
b. Used as a cough suppressant but does not act Prostaglandins Prostaglandins PGI2
through opioid receptors.
Thromboxanes
c. Also has weak analgesic properties.
Nonsteroidal Antiinflammatory Inflammation

plain
DrugsNonnarcotic Analgesics fever
GI protection
NSAIDs are used to treat pain, fever, inflammation, and renal function Platelet
some other conditions. NSAIDs are, by definition, antiin- aggregation
flammatory and are analgesics; acetaminophen is an anal-
gesic but has very little antiinflammatory effect and is not Cardiovascular
protection
an NSAID. Certain NSAIDs (as well as acetaminophen)
are also commonly used with opioid analgesics for the Figure 8-13 Pathways from arachidonic acid.
3. COX-2-selective drugs affect mainly the right arm 7. Aspirincontraindications.

in Figure 8-13 and are generally less irritating to the a. Disorders involving excessive bleeding, recent
GI tract. surgery, use of anticoagulants.
4. Acetaminophenthe mechanism is still obscure, but b. Ulcers.
it appears to inhibit COX-1 and COX-2 in the CNS c. Use of a drug that interacts with aspirin.
and may activate the CB1 cannabinoid receptor as d. Recent viral infection in children and teens (Reyes
well as the TRPV1 cation channel (vanilloid or cap- syndrome may result).
saicin) receptor. e. Asthma.
C. Salicylates. 8. OtherNSAIDs that are nonselective COX
1. Aspirin is most often used. inhibitors.
2. Indications for aspirin use. a. Propionic acid derivatives.
a. Pain. (1) Ibuprofen.
b. Fever. (2) Naproxen (t1/2 14 hours).
c. Inflammation. (3) Ketoprofen.
d. Antiplatelet effect. (4) Oxaprozin (t1/2 50 hours).
3. Mechanism of actionirreversible inhibition of (5) These drugs have half-lives of 2 to 4 hours
COX accomplished by acetylation of the enzyme. except as noted.
This irreversible inhibition is unique to aspirin, even b. Others (less use in dentistry).
among other salicylates. (1) Etodolac.
a. Inhibits both COX-1 and COX-2. (2) Sulindac.
b. Doses vary depending on desired effect (e.g., pain (3) Ketorolac (oral use is indicated only as con-
versus inflammation). tinuation of intravenous or intramuscular
c. The antiplatelet effect lasts beyond the presence of administration of ketorolac).
aspirin in the body. (4) Piroxicam (t1/2 50 hours).
4. Aspirin metabolismsalicylate levels can increase (5) Nabumetone (more effect on COX-2 than
significantly with aspirin overdose. Note the slower COX-1).
rate of metabolism from salicylate to inactive metab- 9. Selective COX-2 inhibitor.
olites (Figure 8-14). a. Rationale for its useantiinflammatory effect
5. Acute aspirin toxicity. without as much GI toxicity as occurs with tradi-
a. Acid-base problems (with increasing doses). tional NSAIDs.
(1) Initially increases respiration, leading to respi- b. Celecoxib (Celebrex).
ratory alkalosis. c. This drug is associated with added cardiovascular
(2) Medullary suppression can follow, leading to risks in some patients.
respiratory acidosis. D. Acetaminophen and its effects (not an NSAID).
(3) Eventually can cause metabolic acidosis. 1. Analgesic.
b. Carbohydrate metabolism causes release of epi- 2. Low effect on peripheral COX.
nephrine and glucocorticoids (leads to hyperglyce- 3. Few drug-drug interactions.
mia and depletion of glycogen). 4. Not antiinflammatory.
c. Fever, dehydration, hypokalemia. 5. Analgesic ceiling is comparable to most NSAIDs.
6. Chronic aspirin toxicity. 6. Liver toxicity with higher doses.
a. Salicylism. 7. Acetaminophen metabolism (Figure 8-15).
b. CNS effects. 8. Acute acetaminophen toxicityhepatic necrosis
c. Bleeding. results from toxic metabolites that are produced
d. GI disturbances. when, at higher doses, the nontoxic metabolic path-
e. Kidney toxicity. ways are saturated (see Figure 8-15). The toxic
metabolites deplete glutathione in the liver.
Aspirin
(Rapid)
Acetaminophen
Salicylate
(Conjugation) (Oxidation)
(Slower)
Non-toxic Toxic
Metabolites In urine metabolites metabolites
Figure 8-14 Aspirin metabolism. Figure 8-15 Metabolic pathways of acetaminophen.

9. The antidote for liver toxicity secondary to acet- 3. Have considerable vascular toxicity, especially
aminophen is N-acetylcysteine. ergotamine.
10. Acetaminophen is preferred over aspirin when an 4. Used for abortive treatment of migraine.
analgesic or antipyretic drug is indicated and when C. Other drugs used for abortive treatment of migraine.
a condition such as one or more of the following is 1. NSAIDs.
present. 2. Tramadol.
a. Patient is asthmatic. 3. Isometheptene, a vasoconstrictor.
b. Patient is at added risk of an ulcer. D. Methysergide.
c. Patient is experiencing bleeding. 1. Blocks 5-HT2 receptors.
d. Patient is taking anticoagulants. 2. Used for prophylaxis against migraine.
e. Patient is sensitive or allergic to aspirin. E. Other drugs used for prophylaxis against migraine
f. Patient is taking drugs such as probenecid or blockers, valproic acid, topiramate, tricyclic antidepres-
methotrexate. sants, calcium channel blockers, ACE inhibitors, angio-
g. Acetaminophen would also be preferable to tensin II receptor blockers.
NSAIDs other than aspirin in most of the above-
listed cases as long as an antiinflammatory effect Antihistamines
is not the goal. Antihistamines are drugs that block histamine receptors.
11. Aspirin, acetaminophen, and ibuprofen (commonly Clinically relevant drugs block either H1 or histamine-2
used) are often combined with an opioid such as (H2) receptors. Traditionally, the term antihistamine is
codeine, hydrocodone, oxycodone, or pentazocine limited to H1 blockers.
for analgesic use. A. Histamine.
12. Other drugs. 1. Receptors and effects (Table 8-24).
a. Ziconotide inhibits N-type calcium channels and 2. Classification of histamine receptor blockers
is used intrathecally for severe pain. (Figure 8-16).
b. Misoprostol, a prostaglandin E1 analogue, is used 3. H1 antihistamine drugs.
to prevent peptic ulcers resulting from NSAIDs a. H1 receptor blockers (antihistamines) (first-
(see Figure 8-23). generation).
Drugs for Migraine

Three antimigraine drug classes indicate the importance of
serotonin and its receptors in migraine and its alleviation.
Histamine receptor
Vasodilation and inflammation are important functional
blockers
components of migraine. The dura vessels in the brain and
their nerves as well as pain pathways in the brainstem are
important targets for these drugs. There are three classes of
antimigraine drugs.
H1 blockers H2 blockers
A. Triptans.
1. Examplesumatriptan.
2. Are agonists at serotonin 5-HT1B/1D receptors.
3. Used for abortive treatment of migraine. First generation Second generation
B. Ergot alkaloids. (Sedating (Non-sedating
antihistamines) antihistamines)
1. Ergotamine and dihydroergotamine.
2. Act similarly to triptans. Figure 8-16 Histamine receptor blockers.
Table 8-24
Histamine Receptor Mechanisms and Effects
RECEPTOR SIGNALING PATHWAY LOCATION EFFECT OF HISTAMINES
H1 Inositol 1,4,5-triphosphate and Bronchi, blood vessels, Bronchoconstriction, vasodilation,
diacylglycerol, leading to in cell calcium mucous glands, nerves secretion, pain, itch
H2 Stimulation of adenylyl cyclase leading to Stomach parietal cells, Acid secretion, vasodilation, increase
in cAMP blood vessels, heart in force and rate of heart
cAMP, Cyclic adenosine monophosphate.
(1) Diphenhydramine. 10. Adverse effects of H2 receptor blockers.

(2) Dimenhydrinate (salt of diphenhydramine) a. Cimetidine (but not other H2 blockers) has an
(Dramamine). antiandrogen effectcan lead to impotence, loss
(3) Pyrilamine. of libido, and gynecomastia.
(4) Hydroxyzine. b. Inhibition of liver metabolism occurs with cimeti-
(5) Chlorpheniramine. dine and, to a lesser degree, with ranitidine. This
(6) Promethazine. inhibition of liver metabolism can lead to an
b. H1 receptor blockers (nonsedating antihista- increase in activity of other drugs such as warfa-
mines) (second-generation). rin and carbamazepine.
(1) Fexofenadine (Allegra).
(2) Loratadine (Claritin).
(3) Desloratadine (Clarinex).
6.0 Cardiovascular Pharmacology
(4) Cetirizine (Zyrtec). and Diuretics
(5) Acrivastine (in Semprex-D).
4. Comparison of first-generation and second- Antiarrhythmic Drugs
generation histamine receptor blockers. A. Arrhythmias of the heart.
a. Second-generation drugs do not cross the blood- 1. Impulse generation.
brain barrier. 2. Impulse conduction.
b. Second-generation drugs do not cause the B. Anatomic sites (Figure 8-17).
drowsiness that occurs with first-generation 1. Sinoatrial (SA) node.
drugs. 2. Atrial myocardium.
c. Second-generation drugs do not have the 3. Atrioventricular (AV) node.
antimuscarinic activity that first-generation 4. His-Purkinje system.
drugs do. 5. Ventricular myocardium.
d. Duration of action3 to 6 hours for most first- C. Antiarrhythmic actionsantiarrhythmic drugs do one
generation drugs; 12 to 24 hours for second- or more of the following; the electrocardiogram (ECG)
generation drugs. changes reflect these effects of drugs.
5. Actions of H1 antihistamines. 1. Reduce automaticity of SA nodereduce automaticity
a. Block pain and itch from histamine. at phase 4 of the action potential, reducing impulse
b. Block vasodilation from histamine. generation; reduce heart rate and increase the PP
c. Block bronchoconstriction from histamine. interval on the ECG, reducing abnormal rapid
d. Useful in mild allergies and colds. rhythms in the atria.
e. Local anesthetic effect (first-generation drugs 2. Reduce conduction velocity in the atria and ventricle
only). reduce arrhythmias owing to rapid conduction; effect
f. Reduce motion sickness (first-generation drugs on the ventricle is widening of QRS complex.
only). 3. Reduce AV nodal conduction rateslow rate of im-
g. Promote sleep (first-generation drugs only). pulses from the atria into the ventricles, resulting in
6. Characteristics of H1 nonsedating antihistamines an increase in PR interval.
(second-generation drugs). 4. Increase refractory periodin the ventricle this leads
a. Long half-lives (12 to 24 hours). to an increase in the QT interval.
b. Do not readily cross blood-brain barrier. 5. Reduce His-Purkinje automaticityreduce the gen-
c. Little or no sedation. eration of abnormally rapid and ectopic ventricular
d. Higher risk of cardiac arrhythmias (long QT arrhythmias.
syndrome). D. Antiarrhythmic drug classes and how they act.
7. H2 receptor blockers. 1. Class I.
a. Cimetidine. a. Block sodium channels.
b. Ranitidine. b. Three divisions (IA, IB, IC) based on how they
c. Famotidine. block sodium channels.
d. Nizatidine. 2. Class IIblock -adrenergic receptors.
8. H2 histamine receptor blockers inhibit the action of 3. Class IIIblock potassium channels.
histamine on the parietal cells of the stomach. 4. Class IVblock calcium channels.
9. Indications for H2 receptor blockers. 5. Miscellaneousadenosine stimulates adenosine re-
a. Dyspepsia. ceptors in the heart; this leads to increased potassium
b. Peptic ulcer. conductance and decreased calcium conductance.
c. Duodenal ulcer. E. Drugs and their principal actions (actions refer to anti-
d. Gastroesophageal reflux disease (GERD). arrhythmic actions described earlier).
SA node
0 3
50mv
4
SA Node
AV node MDP
Atrium
Atria
AV Node 1
2
0
3
4
Purkinje Fiber
Ventricle
Ventricle
Purkinje
(ECG) P Q T
fibers R
A S
0.2 sec.
Figure 8-17 Cardiac electrophysiology. A and B, Drugs affect each site by affecting ion channels. As a result, they affect the action
potentials that depend on activity of ion channels. The action potentials are from cells of five regions of the heart. The dotted vertical
lines indicate the occurrences of the P wave, QRS complex, and T wave on the electrocardiogram compared with the occurrences of the
action potentials. AV, Atrioventricular; SA, sinoatrial; MDP, maximum diastolic potential. (From Yagiela JA, etal: Pharmacology and
Therapeutics for Dentistry, ed 6. St. Louis, Mosby, 2011.)
1. Class IAquinidine and procainamide. Table 8-25

a. Reduce automaticity.
Antiarrhythmic Drugs Indicated for
b. Decrease conduction velocity.
Arrhythmias*
c. Increase refractory period.
2. Class IBlidocaine; reduces automaticity at abnor- CLASS
mal pacemakers in His-Purkinje system and ven- (EXAMPLE) SUPRAVENTRICULAR VENTRICULAR
tricular myocardium. IA (quinidine) Yes Yes
3. Class ICflecainide, propafenone. IB (lidocaine) No Yes
a. Reduce automaticity. IC (flecainide) Yes Yes
b. Decrease conduction velocity. II (propranolol) Yes Yes
4. Class IIpropranolol, esmolol.
III (amiodarone) Yes Yes
b. Decrease conduction velocity in AV node. IV (verapamil) Yes No
5. Class IIIamiodarone, dronedarone, sotalol. Adenosine Yes No
a. Reduce automaticity. *There are many types of arrhythmias in these two general categories.
b. Increase refractory period.
6. Class IVverapamil, diltiazem.
b. Decrease conduction velocity in AV node. 3. Lidocaineconvulsions.
7. Adenosine. 4. Flecainideconvulsions, cardiac risk with recent
a. Reduces automaticity. myocardial infarction.
b. Decreases conduction velocity in AV node. 5. Propranololbronchoconstriction, heart block.
F. General uses of antiarrhythmic drugs (based on sites of 6. Amiodaronepulmonary fibrosis, thyroid abnor-
action) (Table 8-25). malities, skin discoloration, cornea deposits, periph-
G. Adverse effects (common, or typical). eral neuropathy. Dronedarone is chemically related
1. Quinidinecinchonism, hypotension, torsades de to amiodarone but has fewer adverse effects than
pointes. amiodarone.
2. Procainamidemental changes, torsades de pointes, 7. Calcium channel blockersflushing, AV node con-
lupus. duction defects, reduced contractility of the heart.
Table 8-26 Increased

Digitalis Na+, K+-ATPase intracellular
Elimination Half-Lives of Antiarrhythmic Ca++
Drugs Figure 8-18 Action of digitalis.
DRUG HALF-TIME
Quinidine 4-10hr b. Adverse effects of digitalis.
Lidocaine 1.5-2hr (1) Heart block.
(2) Ventricular arrhythmias.
Flecainide 12-27hr
(3) Nausea, vomiting.
Esmolol 0.2hr (4) Visual and mental disturbances.
Amiodarone 25-100 days c. Drug-drug interactions involving digitalis.
Dronedarone 13-19hr (1) Drugs that lower plasma potassium levels (e.g.,
Adenosine <10sec thiazide and loop diuretics) increase digitalis
toxicity.
(2) Some antibiotics may reduce metabolism of
8. Adenosineflushing, asthma, dyspnea, SA nodal digoxin in the gut and increase its absorption.
arrest, AV nodal block. (3) Quinidine and some other drugs increase the
H. Half-lives of some antiarrhythmic drugs are compared plasma levels of digitalis drugs.
in Table 8-26. (4) Epinephrine may increase the risk of ventricu-
lar arrhythmias in the presence of digitalis.
Drugs Used in Treating Heart Failure C. Drugs used in acute treatment of heart failure.
Drugs used for treating heart failure are aimed at reducing 1. Dobutaminecatecholamine.
vascular resistance, reducing fluid volume, or increasing 2. Dopaminecatecholamine.
the force of contraction of the heart. 3. Inamrinone, milrinone, vesnarinoneinhibit phos-
A. Drugs for chronic heart failure. phodiesterase III.
1. Thiazide and loop diuretics. 4. Nesiritideatrial natriuretic peptide.
2. ACE inhibitors. 5. Tolvaptanvasopressin receptor antagonist.
3. Angiotensin II receptor blockers.
4. Aldosterone antagonistsspironolactone, eplere- Antihypertensive Drugs
none. A. Drug treatment for hypertension is aimed at one or
5. -Adrenergic receptor blockers. more of the following.
6. Digitalis. 1. Reducing cardiac output.
7. Vasodilatorsnitrates, hydralazine. 2. Reducing plasma volume.
B. Mechanisms of action. 3. Reducing peripheral resistance.
1. Diuretics reduce fluid load. 4. Figure 8-19 shows specific potential targets for anti-
2. ACE inhibitors, angiotensin II receptor blockers, and hypertensive drugs. Some, such as ganglionic sites,
-adrenergic receptor blockers reduce the vasocon- are rarely used in therapy.
strictor response and aldosterone-releasing effect of B. Major antihypertensive drugs.
the angiotensin pathway. 1. Diuretics.
3. Aldosterone antagonists block the effects of aldoste- 2. ACE inhibitors.
rone. Aldosterone has several deleterious effects in 3. Angiotensin II receptor antagonists.
heart failure. 4. -Adrenoceptor blockers.
4. -Adrenergic receptor blockers, in addition to inhib- 5. 1-Adrenoceptor blockers.
iting renin release, reduce downregulation of 6. Calcium channel blockers.
receptors and have an antiarrhythmic effect. Carve- 7. Direct renin inhibitor (aliskiren).
dilol is a blocker used to treat heart failure that also C. Minor antihypertensive drugsused only in combi
blocks 1-adrenergic receptors and has an antioxi- nation.
dant effect. 1. Centrally acting antihypertensive drugs.
5. Digitalisdigoxin is the most important drug in this 2. Hydralazine.
group. It increases the force of contraction of the 3. Minoxidil.
heart by inhibiting Na+,K+-ATPase and indirectly 4. Guanethidine.
increasing intracellular calcium (Figure 8-18). D. Diuretics.
a. Other actions of digitalis. 1. Include thiazide and loop diuretics (see section on
(1) Vagal effect on heart. diuretic drugs further on).
(2) Slows AV nodal conduction. 2. Cause enhanced Na+ and water excretion and reduced
(3) Increases automaticity in His-Purkinje system. fluid volume.
Central nervous system
Centrally acting drugs
Blood
vessel Ganglionic blockers
Heart
Autonomic ganglia
-Adrenoceptor antagonists
Endothelial Drugs reducing

cells adrenergic transmission
Angiotensin II receptor antagonists -Adrenoceptor

antagonists
Smooth ACE inhibitors

muscle
cells
ACE Angiotensinogen
ANG I
ANG II Renin
Calcium channel blockers

Other directly acting vasodilators Renin
inhibitors
Kidney
1. Tubules:
Diuretics
2. JG cells:
-Adrenoceptor antagonists
Figure 8-19 Sites of antihypertensive drug action. ANG, Angiotensin. (Modified from Yagiela JA, etal: Pharmacology and
Therapeutics for Dentistry, ed 6. St. Louis, Mosby, 2011.)
3. Mechanisminhibit Na/Cl cotransport (thiazides); ACE

inhibit Na+/K+/2Cl cotransport (loop diuretics).
4. More effective in volume expanded hypertension. Forms Degrades
E. Summary of drugs affecting the renin-angiotensin angiotensin bradykinin
system (none should be used in pregnancy).
Figure 8-20 Dual function of ACE.
1. ACE inhibitors.
2. Angiotensin II receptor antagonists.
3. blockers inhibit renin release. 2. Lower angiotensin II leads to less vasoconstriction.
4. ACE is nonspecific and catalyzes the breakdown of 3. Lower angiotensin II leads to less aldosterone secre-
bradykinin (Figure 8-20). tion and less sodium and water retention.
5. Direct renin inhibitors bind to and inhibit the 4. Lower angiotensin leads to less cell proliferation and
enzyme, renin. remodeling. This leads to a long-term benefit for the
F. ACE inhibitors. heart and blood vessels.
1. Mechanism of actioninhibition of angiotensin II 5. Drugs (names end in pril or prilat)examples
formation. are captopril, enalapril, lisinopril, fosinopril.
6. ACE inhibitors are especially useful for patients with e. Pose a risk of adverse cardiac events if the drug is
concomitant congestive heart failure, cardiac arrhyth- short-acting.
mias, or diabetes mellitus. f. Verapamil and diltiazem are more cardioselective
7. Adverse effects. than the dihydropyridines.
a. Cough (common). K. Other antihypertensive drugsdilate blood vessels.
b. Hyperkalemia if used with K+-sparing drugs. 1. Directly acting vascular smooth muscle relaxants.
c. Angioneurotic edemarare but serious. a. Hydralazine.
d. Increased bradykinin may play a role in cough and b. Minoxidil (also used to increase growth of hair).
angioneurotic edema. c. Diazoxide.
G. Angiotensin II receptor antagonists. d. Nitroprusside.
1. Drug examples (names end in sartan). 2. Centrally acting sympatholytics (2-adrenoceptor
a. Losartan agonists).
b. Valsartan a. -Methyldopa.
c. Candesartan b. Clonidine.
2. Angiotensin II blockers are used for similar indica- c. Guanabenz.
tions as ACE inhibitors; however, fewer adverse d. Guanfacine.
effects are associated with angiotensin II blockers 3. Drugs used in hypertensive emergencies.
because they do not increase bradykinin. a. Nitroglycerin.
3. Adverse effects. b. Nitroprusside.
a. Dizziness. c. Fenoldopam (a D1-dopamine receptor agonist).
b. Diarrhea. d. Labetalol.
c. Myalgia. e. Diazoxide.
H. -Adrenergic receptor blockers (names end in olol, f. Hydralazine.
ilol, or alol). L. Drugs for pulmonary hypertension.
1. Lower blood pressure because of the following. a. Epoprostenol (prostacyclin).
a. Reduction of cardiac output. b. Endothelin receptor antagonists (bosentan, am-
b. Reduction of renin release. brisentan).
c. CNSreduction of sympathetic outflow. c. Phosphodiesterase type 5 inhibitors (sildenafil,
2. Carvedilol, the ilol drug, also blocks 1- tadalafil).
adrenoceptors. M. Dental implications of antihypertensive drugs.
I. -Adrenergic receptor blockers. 1. Centrally acting drugs cause sedation.
1. Nonselective (1 and 2) phentolamine and 2. Vasoconstrictors in local anesthetics can be used
phenoxybenzaminerarely used in medicine; how- in these patients, but dose restrictions are recom-
ever, phentolamine is used in dentistry to reverse soft mended.
tissue anesthesia more quickly after a procedure 3. NSAIDs can inhibit the antihypertensive effect of
involving local anesthesia with a vasoconstrictor. ACE inhibitors, blockers, and diuretics.
2. Selective (1) (names end in osin). 4. Orthostatic hypotension can result from centrally
a. Examplesprazosin, terazosin. acting drugs, blockers, and direct vasodilators.
3. Adverse effects. 5. Xerostomia is likely from centrally acting drugs and
a. First-dose effecthypotension, syncope. occasionally occurs with other drugs.
b. Tachycardia. 6. ACE inhibitors can alter the sense of taste.
c. Nasal congestion. 7. ACE inhibitors can cause angioneurotic edema in a
d. Dry mouth. few cases.
J. Calcium channel blockers. 8. ACE inhibitors cause cough in approximately 10% of
1. Types. patients.
a. Nifedipine and other dihydropyridines. 9. Detection of hypertension is important.
b. Diltiazem.
c. Verapamil.
2. The names of the dihydropyridines end in dipine. Antianginal Drugs
3. Calcium channel blockers block the l-type calcium Antianginal drugs work by reducing cardiac rate and force,
channel, reducing vasomotor tone. reducing peripheral vascular resistance, or dilating coro-
4. Adverse effects. nary blood vessels.
a. Flushing. A. Drugs.
b. Headache. 1. Nitrates and nitrites (dilate mostly veins).
c. Hypotension. 2. Calcium channel blockers (dilate peripheral and cor-
d. Gingival hyperplasia. onary blood vessels).
3. -Adrenergic receptor blockers (reduce cardiac rate Proximal Tubule Distal Convoluted Tubule
Osmotic Diuretics
and force). Carbonic Anhydrase Inhibitors
Thiazides
Cortical
4. Antiplatelet drugs (reduce platelet aggregation). Collecting Duct
Na+ Channel Blockers
5. Ranolazine improves contractile dysfunction. Spironolactone
6. Lipid-lowering drugs.
B. Nitrates and nitrites (e.g., nitroglycerin, amyl nitrite).
Glomerular
1. Mechanismdonate nitric oxide, which causes Filtration Thick Ascending
vasodilation.
Limb of Henle
2. Adverse effects. Loop Diuretics
a. Headache.
b. Syncope. Thin Descending
c. Tachycardia. Limb of Henle
d. Tolerance. Osmotic Diuretics
e. Methemoglobinemia.
C. See previous discussions of blockers and calcium
channel blockers. Figure 8-21 Sites of actions of diuretics. (From Yagiela JA,
D. Other drugs used to reduce the risk of myocardial etal: Pharmacology and Therapeutics for Dentistry, ed 6. St.
infarction. Louis, Mosby, 2011.)
1. Aspirin.
2. Clopidogrel, prasugrelinhibit the effect of ADP on
platelets. They block P2Y12 ADP receptors and reduce C. Loop diuretics.
platelet aggregation. 1. Examplesfurosemide, bumetanide, torsemide.
3. GPIIb-IIIa glycoprotein receptor inhibitorsthese 2. Have a high ceiling or high maximal effect.
bind to GPIIb-IIIa on platelets and reduce 3. Can cause hyperuricemia.
aggregation. 4. Can increase excretion of Ca2+.
a. Examplesabciximab (a Fab fragment of a mono- 5. Can cause tinnitus and hearing loss.
clonal antibody), eptifibatide, and tirofiban. 6. Can cause hyponatremia and excessive fluid loss.
4. Ranolazineinhibits late sodium current and D. Amiloride and triamterene.
reduces sodium overload in cardiac cells, improving 1. K+-sparing diureticsreduce the driving force for K+
ischemia-induced contractile dysfunction. movement into the lumen.
5. Lipid-lowering drugs (see Drugs Used for Blood 2. Used with other diuretics to reduce the risk of
Lipid Disorders further on). hypokalemia.
E. Dental implications. 3. There is a risk of hyperkalemia.
1. Stress reduction is important. E. Spironolactone and eplerenone.
2. Gingival hyperplasia may occur with calcium channel 1. True antagonists of aldosterone.
blockers. 2. Similar in effects to amiloride and triamterene.
Diuretic Drugs Drugs Used for Blood Lipid Disorders

Diuretic drugs act on the kidney to cause excretion of Drugs are used to reduce abnormally high blood lipid
sodium and water. These drugs are used in edema states, levels. The two major lipoproteins that are targeted are
hypertension, and heart failure. Figure 8-21 indicates where very-low-density lipoproteins (VLDLs) and low-density
in the kidney they act. lipoproteins (LDLs). The primary lipids of VLDLs are the
A. Major drugs and their mechanism of action (see triglycerides, and the primary lipids of LDLs are cholesteryl
Figure 8-21). esters. Higher levels of LDL increase the risk of cardiovas-
1. Thiazidesdecrease Na+ and Cl cotransport. cular disease, whereas higher levels of VLDL increase the
2. Loop diureticsdecrease Na+/K+/2Cl cotransport. risk of pancreatitis. Hypercholesterolemia (high LDL) is a
3. Amiloride, triamterenedecrease Na+ reabsorption very common abnormality.
by blocking Na+ channels. A. Drugs and their actions.
4. Spironolactoneblocks aldosterone receptor. 1. Fibric acid derivativesfenofibrate, gemfibrozil.
B. Thiazidesbenzothiadiazides, such as hydrochloro- These agents activate PPAR nuclear receptor,
thiazide and related chlorthalidone. increase extrahepatic lipoprotein lipase, increase
1. Can cause hypokalemia. hepatic oxidation of fatty acids, and produce other
2. Reduce Ca2+ excretion. effects that reduce VLDL and LDL.
3. Can cause hyponatremia. 2. HMG-CoA reductase inhibitors (statins)atorvas-
4. May increase plasma uric acid. tatin, lovastatin, pravastatin, simvastatin. Inhibition
5. Sometimes used for nephrogenic diabetes insipidus. of this enzyme leads to reduction in cholesterol
synthesis and an increase in LDL receptors in the 2. The effect of warfarin takes several days to reach full
liver; this reduces LDL. effect.
3. Nicotinic acidreduces fat cell lipolysis and lowers 3. Antidotevitamin K (phytonadione).
VLDL. B. Heparin.
4. Bile acid sequestrantscholestyramine, colesevelam, 1. Heparin blocks the action of factors Xa (activated)
colestipol. These agents bind bile acids in the gut, and IIa (thrombin) by stimulating antithrombin III
leading to conversion of more cholesterol to bile (see Figure 8-22).
acids, lowering LDL. 2. Heparin acts immediately to reduce blood
5. Inhibitors of cholesterol absorption from the intestine coagulation.
ezetimibe. These agents prevent cholesterol absorp- 3. Antidoteprotamine.
tion at the brush border and lower LDL. C. Low-molecular-weight heparins (enoxaparin, daltepa-
B. Adverse effects of drugs used for blood lipid disorders rin, tinzaparin) activate antithrombin III, mostly inhib-
(Table 8-27). iting factor Xa (not factor IIa). Protamine partially
antagonizes these agents.
Anticoagulants and Procoagulants D. Fondaparinuxinhibits factor Xa by binding to anti-
Various drugs are used either to prevent blood coagulation thrombin III. Protamine is inactive as an antagonist.
or to dissolve clots. Drugs are sometimes used to enhance E. Direct thrombin inhibitorslepirudin, bivalirudin,
clotting in bleeding disorders. argatroban, dabigatran, rivaroxaban. Protamine is inac-
A. Warfarin. tive as an antagonist.
1. Warfarin inhibits the vitamin Kdependent synthesis F. Antiplatelet drugsaspirin, dipyridamole (inhibits
of factors II (prothrombin), VII (proconvertin), IX phosphodiesterase). See also platelet inhibitors under
(Christmas factor), and X (Stuart-Prower factor) Antianginal Drugs.
(Figure 8-22). G. Dental implications.
1. The effect of warfarin is measured by the interna-
Table 8-27 tional normalized ratio (INR). Normal INR is 0.8 to
1.2. The typical target INR range for low-intensity
Adverse Effects of Antilipid Drugs anticoagulant therapy is 2.0 to 3.0 and for high inten-
DRUG OR DRUG sity therapy is 2.5 to 3.5.
CLASS ADVERSE EFFECTS 2. Risks from bleeding depend on extent of the surgical
Fibric acid derivatives Increases the action of warfarin, procedure and INR; the higher the INR, the greater
GI effects, gallstones the risk.
HMG-CoA reductase Myalgia, GI effects, impotence 3. Restoration of normal INR after warfarin withdrawal
inhibitors takes several days because of the need to resynthesize
Nicotinic acid Flushing, itching clotting factors.
Bile acid sequestrants Hyperchloremic acidosis, GI effects H. Plasminogen activatorsused to break down clots by
promoting fibrinolysis.
Probucol GI effects, cardiac arrhythmias
1. Tissue plasminogen activatoralteplase.
Ezetimibe GI effects, back pain 2. Tissue plasminogen activator variantstenecteplase,
GI, Gastrointestinal; HMG-CoA, 3-hydroxy-3-methylglutaryl coenzyme A. reteplase.
3. Streptokinase.
4. Urokinase.
VII + TF
I. Plasminogen inhibitoraminocaproic acid; used to
VIIa-TF
inhibit fibrinolysis.
Heparin
IX IXa
inhibits
7.0 Gastrointestinal and Respiratory
X Xa Pharmacology
VIIIa Heparin
inhibits
Drugs Used to Treat Gastrointestinal
Warfarin ll lla Disorders
inhibits Va Drugs are used for various indications related to the GI
synthesis tract, including to reduce the risk of ulcers and GERD, to
alleviate diarrhea, to alleviate constipation, and to promote
Fibrinogen Fibrin
emesis. Drugs used for increasing or decreasing salivation
Figure 8-22 Sites of action of heparin and the oral anti- are discussed in the sections on cholinergic receptor ago-
coagulants represented by warfarin. nists and antimuscarinic drugs.
Antacids Bulk-forming Stimulant (irritant)

Alginic acid (magnesium, examples: examples:
forms a floating calcium, aluminum psyllium bisacodyl
protectant vs.GERD. methylcellulose senna
salts) raise pH.
Stimulates
enteric
Sucralfate nerves
Bismuth subsalicylate binds to and H2O
has an antimicrobial protects the
and antidiarrheal ulcer.
H2O Swells and
effectused vs. distends colon H2O
ulcers and
H2O
traveler's Misopostol
diarrhea. Increases Moistens to
(PGE2)
Stomach fluid volume ease passage
protects
Saline (osmotic) Wetting agents
vs ulcers examples: examples:
from magnesium hydroxide docusate
NSAIDs. lactulose mineral oil
H2 histamine Figure 8-24 Mechanisms of the major laxatives. (From

receptor Yagiela JA, etal: Pharmacology and Therapeutics for Dentistry,
Antibiotics antagonists
(metronidazole, ed 6. St. Louis, Mosby, 2011.)
Proton pump inhibit H+
tetracycline, release by
amoxicillin, inhibitors
(e.g., esomeprazole, parietal cells.
clarithromycin)
Iansoprazole)
2. Oral glucocorticoids can be given in resistant cases
inhibit H. pylori, (see Section 8.0, Endocrine Pharmacology). Inhaled
which can reduce H+ release
cause ulcers. from parietal corticosteroids, such as beclomethasone and flutica-
cells. sone, are commonly used.
Figure 8-23 Mechanisms of action of antiulcer and anti- 3. Antimuscarinic anticholinergic drugsipratropium,
GERD drugs. tiotropium. Both of these drugs are quaternary
ammonium drugs that are not systemically absorbed
A. Drugs used to treat ulcers and GERD (Figure 8-23). after inhalation.
B. Emeticsyrup of ipecac stimulates the chemoreceptor 4. Cromolyn, nedocromilinhibit mast cell degranu
trigger zone and the stomach. lation.
C. Antiemeticsusually drugs that control activity in the 5. Leukotriene pathway modifiersleukotrienes play a
chemoreceptor trigger zone. key role in asthma treatment.
1. Antihistaminespromethazine, cyclizine. a. 5-Lipoxygenase inhibitorzileuton; blocks the
2. Droperidoldopamine receptor antagonist. synthesis of cysteinyl leukotrienes.
3. Metoclopramidedopamine and serotonin 5-HT3 b. Cysteinyl leukotriene receptor inhibitorsmonte-
receptor antagonist. lukast, zafirlukast.
4. Dexamethasonethe mechanism of the antiemetic 6. Omalizumaba monoclonal antibody; given subcu-
effect in cancer has not been definitely determined. taneously, binds to IgE and prevents its action at the
5. Ondansetroninhibits 5-HT3 receptors. IgE receptor.
6. Dronabinola cannabinoid. 7. Theophylline has a low therapeutic index. Its metab-
7. Aprepitantneurokinin (NK1) receptor antagonist. olism is affected by several other drugs, leading to
D. Major laxatives (Figure 8-24). potential problems with theophylline. Theophylline
E. Antidiarrheal drugs. inhibits phosphodiesterase leading to an increase in
1. Magnesium aluminum silicate plus pectin absorbs cAMP. It also stimulates histone deacetylase, reduc-
water and irritants in GI tract. ing inflammatory gene expression. Both mechanisms
2. Diphenoxylate and loperamide stimulate opioid appear to have benefit in asthma.
receptors in GI tract.
Drugs Used to Treat Asthma 8.0 Endocrine Pharmacology

A. Several different classes of drugs are used to treat
asthma (Table 8-28). Thyroid Pharmacology
B. Other notes. Drugs are used to treat both hypothyroidism and
1. Epinephrine is used to treat anaphylactic shock. hyperthyroidism.
It stimulates 1-adrenergic, 2-adrenergic, 1- A. Thyroid hormones.
adrenergic, and 2-adrenergic receptors. 2 receptor 1. Bind to intracellular receptors in target cells and acti-
stimulation aids in relieving bronchospasms. vate transcription in the nucleus.
Table 8-28
Antiasthma Drugs
DRUG CLASS DRUG EXAMPLES ACTION COMMENTS
2-Adrenergic agonists Albuterol Stimulate 2 receptors, relax smooth Used by inhalation for rapid action
Metaproterenol muscle in the lung (salmeterol is slow-acting); can
Salmeterol lead to tachycardia and tremor
Inhaled glucocorticoids Beclomethasone Increase lipomodulin, which inhibits Reduce inflammation in airway;
Budesonide phospholipase A2, other mechanisms can lead to oral candidiasis
Flunisolide
Fluticasone
Antimuscarinic drug Ipratropium Block muscarinic receptors in bronchi, Used by inhalation; can lead to
Tiotropium leading to bronchodilation xerostomia
Methylxanthine Theophylline Blocks adenosine receptors, blocks Taken orally; watch toxicity
phosphodiesterase leading to an (nausea, vomiting, arrhythmias,
increase in cAMP, causes CNS toxicity)
bronchodilation
Leukotriene synthesis Zileuton Inhibits synthesis of leukotrienes by Taken orally; reduces
inhibitor inhibiting 5-lipoxygenase inflammation
Leukotriene receptor Montelukast Block leukotriene (Cys-LT1) receptors Taken orally; long-acting
antagonists Zafirlukast
Inhibitors of mast cell Cromolyn Block degranulation of mast cells Given by inhalation
degranulation Nedocromil
Anti-IgE monoclonal Omalizumab Binds to IgE, preventing its effect at Given subcutaneously
antibody the IgE receptor
cAMP, Cyclic adenosine monophosphate; CNS, central nervous system.
2. Used to treat hypothyroidismT4 (levothyroxine), f. Adverse effectsGI irritation, parotid gland pain,
T3 (liothyronine), and T3 plus T4 (liotrix) are available headache, cough.
for therapy. 3. Radioactive iodide (131I) destroys thyroid cells.
3. T4 has a longer half-life.
4. They are usually used orally. Insulin and Oral Hypoglycemics
5. Adverse effects of thyroid hormones. Insulin is used to treat both type 1 and type 2 diabetes.
a. Nervousness. It is required for type 1 diabetes because the cells of
b. Tachycardia, angina, risk with epinephrine. the pancreas are devoid of insulin. In type 2 diabetes,
c. Nausea, diarrhea. drugs other than insulin can often be used because the
d. Tremor, weight loss, heat intolerance. cells are able to secrete insulin, albeit in a more sluggish
B. If iodine deficiency causes hypothyroidism, this condi- manner.
tion is treated with iodide. A. Insulin.
C. Antithyroid drugsused to treat hyperthyroidism 1. Mechanism of action.
(Figure 8-25). a. Reduces blood glucose by increasing its uptake and
1. Thioamide drugsmethimazole, propylthiouracil. increasing conversion to glycogen and lipid.
a. Inhibit thyroid peroxidase, inhibiting oxidation of b. Reduces lipolysis.
iodide and iodination. c. Increases protein synthesis and cell growth.
b. Adverse effectsrash, nausea, agranulocytosis. d. Figure 8-26 shows major insulin pathways by
2. Iodides (mostly potassium iodide). which the aforementioned mechanisms are
a. Inhibit release of thyroid hormone and several accomplished.
steps in synthesis. 2. Effects of insulin.
b. High doses are used. a. Corrects hyperglycemia of diabetes.
c. Concentrate in thyroid. b. Reduces long-term adverse effects of diabetes.
d. Decrease vascularity of thyroidused before 3. Drug preparations (Table 8-29).
surgery. B. Sulfonylurea oral hypoglycemic drugsinsulin secreta-
e. Have a short-term effect. gogues.
Thyroid Gland
Transport (Oxidation) (Organification) (Coupling)

into thyroid Peroxidase Peroxidase Peroxidase
I I I*
MIT and DIT in T3 and T4
thyroglobulin in thyroglobulin
SCN
ClO4
inhibit
Thioamides
inhibit
Proteolysis of
thyroglobulin
Iodides
inhibit
*= Iodine in hypoiodate form Free T3 and T4

released
Figure 8-25 Synthesis of thyroid hormones and sites of action of antithyroid drugs. DIT, Diiodotyrosine; MIT, monoiodotyrosine.
(From Yagiela JA, etal: Pharmacology and Therapeutics for Dentistry, ed 6. St. Louis, Mosby, 2011.)
Table 8-29 e. Glibenclamide.

f. Glipizide.
Insulin Preparations
g. Glimepiride.
TYPE ONSET* DURATION* 2. Mechanism of action.
Short-Acting a. Close ATP-sensitive potassium channels in cell
Regular 30-60min 4-6hr membranes of cells.
b. Stimulate release of insulin from pancreas.
Lispro 15min 3-5hr
c. Increase sensitivity of target organs to insulin.
Aspart 15min 3-5hr 3. Adverse effects.
Glulisine 15min 3-5hr a. Hypoglycemia.
Long-Acting b. GI upset.
NPH 1-4hr 12-18hr c. Vertigo.
d. Edema, sodium retention.
Glargine 1-4hr 20-24hr
4. Indications for sulfonylurea drugstype 2 diabetes.
Detemir 1-4hr 20-24hr C. Other oral hypoglycemic drugs.
Data from Golan DE, etal: Principles of Pharmacology, The Pathologic Basis 1. Meglitidesrepaglinide and nateglinide; insulin
of Drug Therapy, ed 3. Philadelphia, Lippincott Williams & Williams, 2012;
and Brunton LL, Chabner BA, Knollman BJ: Goodman & Gilmans secretagogues.
Pharmacological Basis of Therapeutics, ed 12. New York, McGraw-Hill, 2011. a. Mechanismsimilar to sulfonylureas.
All of the above-listed preparations incorporate small but important changes b. Used orally.
in the amino acid sequence of insulin except for regular and NPH insulin.
c. Act like the sulfonylureas.
*After subcutaneous injection.
d. Adverse effecthypoglycemia.
e. Used for type 2 diabetes.
2. Metformininhibitor of liver glucose production.
1. Examples. a. Activates AMP kinase, which regulates energy
a. Tolbutamide. production.
b. Acetohexamide. b. Used orally.
c. Tolazamide. c. Reduces gluconeogenesis and lipogenesis in the
d. Chlorpropamide. liver.
Insulin e. Adverse effectsGI problems and malabsorption.

Glucose f. Used for type 2 diabetes.
Insulin receptor
4. Pioglitazone and rosiglitazoneinsulin sensitizers.
a. Activate transcription factor PPAR leading to
increased insulin sensitivity of muscle, liver, and
GLUT-4 fat cells.
P P b. Adverse effectsGI problems, headache, dizziness,
liver toxicity.
P IRS-1 P CBL P c. Used for type 2 diabetes.
P IRS-2 P d. Used orally.
P Shc 5. Pramlintideamylin analogue.
P IRS-3 P
a. Amylin analogue that stimulates CNS amylin
P IRS-4 P GLUT-4 receptors.
P GAB-1 P
vesicle b. Reduces gastric emptying.
c. Reduces glucagon release and glucose levels.
d. Given subcutaneously.
MEK/ERK PI=3K e. Used in type 1 and type 2 diabetes.
6. Exenatide and liraglutideis a glucagonlike peptide-1
(GLP-1) analogue.
MAP kinase
AKT
a. Analogues of GLP-1 (an incretin).
pathway b. By stimulating GLP-1, these agents cause insulin
secretion, block glucagon release, and reduce food
intake.
Increased glycogen/lipid/protein synthesis
Decreased lipolysis c. Given subcutaneously.
Cell growth and differentiation 7. Sitagliptin and saxagliptinincrease GLP-1 indi-
rectly.
a. Inhibit dipeptidyl peptidase-4, which inactivates
Figure 8-26 Mechanism of action of insulin. Signaling
GLP-1.
pathways for insulin are shown leading to increases in synthesis,
b. Actions are due to an increase in GLP-1.
growth, and differentiation. The action of insulin on its receptor
leads to phosphorylation (P) of the receptor and key proteins in c. Used orally.
the signaling pathways. Effects of insulin are realized through d. Used in type 2 diabetes.
numerous mechanisms, including enhancing gene transcription
and protein synthesis. The translocation of the glucose trans- Adrenal Corticosteroids
porter (Glut-4) to the plasma membrane, which is stimulated by Adrenal corticosteroids are composed of mineralocorti-
insulin, is integral to glucose uptake and subsequent glucose use coids (e.g., aldosterone) and glucocorticoids (e.g., hydro-
in cells of key target tissues. AKT, Protein kinase B; CBL, calci- cortisone). Mineralocorticoids are used as replacement
neurin Blike protein; ERK, extracellular signalregulated therapy, such as in Addisons disease. Glucocorticoids,
kinases; IRS, insulin receptor substrates; MAP, mitogen-activated although useful in replacement therapy, are most often
protein; MEK, mitogen-activated protein kinase; PI-3K, phospha-
used as antiinflammatory drugs and antiimmune drugs.
tidylinositol 3-kinase; Shc, Src homology 2 domain-containing.
Adrenal steroids are used much more often for glucocorti-
(Modified from Robbins SL, etal: The endocrine system. In
Robbins and Cotran Pathologic Basis of Disease. St. Louis, coid effects than for a mineralocorticoid effect.
Saunders, 2010.) A. Drugs and their relative potencies as mineralo
corticoids and glucocorticoids (as measured by
sodium retention and glycogen deposition, respec-
tively) (Table 8-30).
d. Increases sensitivity to insulin in muscle, liver, and B. Actions of glucocorticoidsall steroid hormones bind
fat cells. to receptors inside the cell, stimulating mRNA synthesis
e. Adverse effectsGI problems, lactic acidosis. and protein synthesis, resulting in many metabolic
f. Used for type 2 diabetes. effects.
3. Acarbose, miglitol, and voglibosedelayers of carbo- 1. Decrease cell uptake of glucose.
hydrate digestion. 2. Stimulate gluconeogenesis.
a. Inhibit -glucosidase. 3. Stimulate lipolysis.
b. Used orally. 4. Reduce immune and inflammatory responses, partly
c. Reduce digestion of carbohydrates in gut. by inhibiting the nuclear factor, NF-B.
d. Decrease glucose absorption. 5. Inhibit action of macrophages.
Table 8-30 7 dehydrocholesterol UV light on skin

Comparison of Steroids
Vitamin D3
Liver
POTENCY AS AN
ANTIINFLAMMATORY SODIUM
DRUG DRUG RETENTION
Aldosterone 0.1 3000
Fludrocortisone 10 3000
Cortisone 0.8 0.8 PTH stimulates 25 OHD3
Hydrocortisone 1 1 1-hydroxylation
Prednisone 4 0.8
Prednisolone 4 0.8 OH
Kidney
Triamcinolone 5 0
CH2
Dexamethasone 25 0
Betamethasone 25 0 OH OH
Modified from Yagiela JA, etal: Pharmacology and Therapeutics for Dentistry,
ed 6. St Louis, Mosby, 2011. 1,25-Dihydroxycholecalciferol
(1,25-dihydroxyvitamin D)
Hydrocortisone is assigned an arbitrary number of 1 for comparison
purposes. The higher the number, the greater the relative effect of the drug.
Figure 8-27 Synthesis and activation of vitamin D3.
6. Inhibit phospholipase A2 by stimulating the produc- A. Vitamin D.

tion of lipomodulin. 1. Binds to intracellular receptors in target cells and
C. Uses of glucocorticoids. activates transcription in the nucleus.
1. Asthma. 2. Derived from dietary sources and from the effect of
2. Inflammatory disease. ultraviolet light on skin.
3. Collagen diseases. 3. Increases calcium absorption from the GI tract.
4. Some lymphomas and leukemias. 4. 1,25-Dihydroxyvitamin D3 is the active form (also
5. Cerebral edema. known as 1,25-dihydroxycholecalciferol). Ergocalcif-
6. Rheumatic diseases erol (D2) is from plant origins.
7. Acute attacks of multiple sclerosis. 5. Synthesis and activation (Figure 8-27).
D. Adverse effects of glucocorticoids. 6. Action on GI tract.
1. Insomnia, agitation. a. Acts on intracellular receptor to increase mRNA
2. Infections. and protein synthesis.
3. Hypertension, atherosclerosis. b. Increases calcium-binding protein in the gut.
4. Skin and mucosal atrophy. c. Increases calcium absorption.
5. Negative calcium balance, osteoporosis. d. In higher doses, vitamin D has additional effects
6. Muscle wasting. resembling PTH.
7. Obesity, glucose intolerance. 7. Indications.
8. Peptic ulcers. a. Vitamin supplementation for optimum health.
9. Cataracts. b. Nutritional lack.
E. Dental applications. c. Hypoparathyroidism.
1. Glucocorticoids are used to reduce inflammation. d. Osteoporosis.
Topical application is common. Oral administration e. Psoriasis.
is used in more serious cases. Oral glucocorticoids B. PTH.
are used in some cases of acute allergies. 1. Secreted by parathyroid cells when plasma calcium
2. Long-term treatment leads to several adverse effects, decreases.
including risk of infection. 2. Increases cAMP in target cells (bone and kidney).
3. Simulates osteoclast activity under most conditions.
Drugs That Affect Calcium Metabolism 4. Stimulates production of active vitamin D in kidney
Three major hormones, vitamin D, parathyroid hormone (see Figure 8-27).
(PTH), and calcitonin, have profound effects on calcium 5. Decreases calcium excretion in the kidney.
balance, affecting the bones, kidneys, and GI tract. In addi- 6. Increases plasma calcium.
tion, several other drugs affect calcium metabolism, espe- 7. Used in the short molecular form (1-24) (teripara-
cially affecting bone. tide) once a day for postmenopausal osteoporosis
PTH 1-34 Estrogens Calcitonin, 5. Denosumab.

(Intermittent) Bisphosphonates a. Monoclonal antibody that binds and inhibits
receptor activator of nuclear factor kappa-B ligand
(RANKL) (see Figure 8-28).
Denosumab b. Inhibits formation and activation of osteoclasts.
RANKL (-) c. Used subcutaneously for osteoporosis.
Osteoblast
(osteocyte)
(+) OPG 6. Estrogens (see Sex Hormones, next, and Figure
(-)
RANKL Osteoclast 8-28).
(-) RANK precursor
RANKL
(-)
(-) Sex Hormones
IL-1 IL-6 Estrogens, progesteronelike compounds (progestins), and
Figure 8-28 Action of several drugs on bone cells. Estro- androgens are used for various clinical indications. They
gens act both directly and indirectly to inhibit osteoclast forma- are steroid hormones with effects on numerous systems of
tion and action. Indirect effects include a decrease () in the the body. Their action involves binding to intracellular
release of cytokines such as interleukin (IL)-1 and IL-6 and recep- receptors in target cells and activating transcription in the
tor activator of nuclear factor kappa-B ligand (RANKL) by osteo- nucleus.
blasts. (Stimulation by several cytokines and stimulation of RANK A. Estrogens.
lead to increases in numbers of osteoclasts resulting in bone 1. Estradiol is the most potent human estrogenic
breakdown.) Estrogens also increase (+) the synthesis and secre- hormone.
tion of osteoprotegerin (OPG). OPG binds to RANKL, preventing
2. Estrogens have important supportive effects on preg-
its binding to receptor activator of nuclear factor kappa-B (RANK)
nancy and secondary sex characteristics.
receptors on osteoclast precursors. Denosumab is a monoclonal
antibody drug that binds to RANKL and prevents its action at 3. Support bonestimulate osteoblasts but also reduce
RANK. Many of the effects of intermittent parathyroid hormone RANKL and cytokine gene expression in osteoblasts,
1-34 (PTH 1-34) on osteoblasts are similar to estrogens. Calcito- ultimately decreasing the number and action of
nin and bisphosphonates act directly on osteoclasts and osteoclast osteoclasts (see Figure 8-28); also inhibit osteoclasts
precursors to inhibit their activity. directly.
4. Reduce LDL and increase high-density lipoprotein.
5. Indications.
(Figure 8-28). There is a clear difference in the effect a. Oral contraception.
on bone between PTH (1-24) given once a day and b. Replacement therapy.
the hormonal effect of endogenous release of PTH. c. Prevention of osteoporosis.
C. Calcitonin. d. Reduce symptoms of menopause.
1. Secreted by parafollicular C cells. 6. Drugs used.
2. Increases cAMP in osteoclasts, reducing their a. Estradiol.
activity. b. Ethinyl estradiol.
3. Increases calcium excretion in the kidney. c. Mestranol.
4. IndicationsPagets disease, hypercalcemia, osteopo- d. Conjugated estrogens.
rosis. B. Selective estrogen receptor modulators.
D. Other drugs affecting bone (see Figure 8-28). 1. Raloxifene is a major drug.
1. Bisphosphonates. 2. Estrogen receptor agonist in bone but antagonist in
a. Examplesalendronate, pamidronate, tiludronate. the endometrium and breast.
b. Reduce turnover rate of hydroxyapatite (inhibit 3. Used to treat postmenopausal osteoporosis.
osteoclasts by inhibiting prenylation of key C. Progestins.
proteins). 1. Progesterone is the natural compound.
c. Used in Pagets disease, osteoporosis, hypercalce- 2. Important for sexual development and in pregnancy.
mia, and bone metastasis. 3. Indications for progestins (progesteronelike com-
d. Adverse effectsGI symptoms; esophageal ero- pounds).
sions; osteonecrosis of the jaw, especially in high a. Oral contraception.
doses. b. Endometriosis.
2. Fluoride ion. c. Postmenopausal hormone replacement.
a. Increases osteoblast activity. d. Dysfunctional uterine bleeding.
b. Used for dental applications. 4. Prevent proliferative effects (and endometrial cancer)
3. A summary of these and other drugs is given in from estrogen therapy.
Figure 8-28. 5. Drugs used.
4. PTH 1-34 (teriparatide) is the shortened form of a. Norethindrone.
PTH. b. Norethynodrel.
Table 8-31 O S CH3

Composition of Some Oral Contraceptives R C NH CH CH C
CH3
C N CH
ESTROGEN PROGESTIN
O COOH
Desogen, 28-pack Ethinyl estradiol Desogestrel
Figure 8-29 Penicillin nucleus.
Necon 1/50, 28-pack Mestranol Norethindrone
Ortho-Novum 1/35, Ethinyl estradiol Norethindrone
28-pack cidal drugs kill bacteria, whereas static drugs prevent
growth of bacteria. These descriptions are applied to the
Yaz Ethinyl estradiol Drospirenone
concentrations of each drug that can reliably be attained
Camila, 28-pack Norethindrone in vivo. The spectrum of any antimicrobial drug refers to
Seasonale* Ethinyl estradiol Levonorgestrel the extent (broad, extended, or narrow) of the organisms
Plan B Levonorgestrel affected by the drug and the specific organisms affected.
ella Ulipristal acetate Extended therapy with a specific drug almost always leads
to some resistance of certain organisms to that drug.
Combination oral contraceptives are either monophasic or multiphasic, the
latter containing varying doses of one or both hormones during the pill cycle. Superinfection, defined as a growth of resistant organ-
*Extended (91-day) cycle. isms owing to therapy targeting sensitive organisms, is
Emergency contraceptives. usually more likely to occur with broad-spectrum or
extended-spectrum drugs compared with narrow-spectrum
drugs. The potency of antibacterial drugs is often estimated
c. Medroxyprogesterone. using measures such as the minimum inhibitory concen-
d. Levonorgestrel. tration (MIC).
D. Oral contraceptives. A. Mechanisms of action of antibacterial drug classes
1. Types. (Table 8-32).
a. Combination estrogen and progestin. B. Cell wall inhibitors inhibit one of the steps in peptido-
b. Minipill (progestin only, e.g., Camila). glycan synthesis, important in the cell wall.
c. Emergency (progestin). C. Many antibiotics inhibit ribosomal protein synthesis.
2. Major action of combination and minipillinhibition D. Penicillins.
of ovulation. 1. Chemistrythe -lactam ring gives the name
3. Examples of oral contraceptives (Table 8-31). -lactam to this group of drugs, which includes peni-
4. Some adverse effects of combination estrogen and cillins (Figure 8-29), cephalosporins, and atypical
progestin. -lactams.
a. Hypertension. 2. Penicillinase is a type of -lactamase, formed by bac-
b. Thrombophlebitis. teria, that renders them resistant to many penicillins.
c. Gallbladder disease. 3. Penicillin G and penicillin V are narrow-spectrum
d. Nausea. penicillins (Table 8-33).
E. Fertility drugs. a. Penicillin G and V are very similar except that
1. Antiestrogenclomiphene. penicillin V is more acid-stable and has a higher
2. Human menopausal gonadotropins (menotropins). bioavailability when given orally.
3. Human chorionic gonadotropin (hCG). b. Penicillin V is often used to treat oral infections
4. Gonadotropin-releasing hormone analogue caused by a wide variety of sensitive oral bacteria.
gonadorelin (pulsatile use). c. Organisms susceptible to penicillin G and V
5. Follicle-stimulating hormone (FSH)follitropin and viridans streptococci, Streptococcus pyogenes,
urofollitropin. Streptococcus pneumoniae (gram-positive), Neisse-
6. Antiestrogens and gonadorelin stimulate gonadotro- ria gonorrhoeae, Neisseria meningitidis, oral Bacte-
pin release from the pituitary; menotropins, hCG, roides, oral Fusobacterium, Leptotrichia buccalis
and FSH stimulate the ovary directly. (gram-negative), Treponema pallidum, Actinomy-
ces israelii.
d. Gram-negative cocci are sensitive.
9.0 Antimicrobial Drugs e. Penicillins, similar to all cell wall inhibitors, are
bactericidal against susceptible organisms.
Antibacterial Drugs f. The elimination half-life of penicillins is short. The
Antibiotics are chemicals produced by microorganisms that t1/2 for penicillin G and V is about 0.5 hour because
inhibit other microorganisms. By this definition, most anti- of rapid excretion by the kidney, 90% of which
bacterial drugs discussed here are antibiotics. Antibacterial is by tubular secretion. Very little drug gets
drugs are classified as either bactericidal or bacteriostatic; metabolized.
Table 8-32
Mechanisms of Action and Characteristic Adverse Effects of Antibacterial Drugs
DRUG MECHANISM OF ACTION, WHAT IS INHIBITED ADVERSE EFFECTS
Penicillins Transpeptidase, stage 3 in cell wall synthesis Allergies, neurotoxicity in high doses
Cephalosporins Transpeptidase, stage 3 in cell wall synthesis Allergies, neurotoxicity in high doses, renal toxicity
Macrolides Translocation step of ribosomal protein synthesis GI upset, especially with erythromycin, inhibition
of drug metabolism, QT prolongation*
Clindamycin Peptide bond formation in ribosomes Diarrhea, pseudomembranous colitis
Tetracyclines Binding of aminoacyl-tRNA to ribosome and Tooth staining, liver toxicity in pregnancy,
protein synthesis photosensitivity, Fanconis syndrome with
outdated drug
Sulfonamides Dihydropteroate synthase step in folic acid synthesis Crystalluria (some drugs), allergies, psychosis
Streptogramins Peptide bond formation in ribosomes Phlebitis, myalgia, arthralgia
Linezolid tRNA binding to ribosome and initiation of protein Myelosuppression, GI effects, peripheral
synthesis neuropathies
Trimethoprim Dihydrofolate reductase step in folic acid synthesis Megaloblastic anemia
Leukopenia
Fluoroquinolones DNA gyrase and topoisomerase IV, transcription GI upset, CNS toxicity, photosensitivity (some)
Aminoglycosides Initiation complex of protein synthesis, cause Renal toxicity, ototoxicity, neuromuscular blockade
misreading in protein synthesis
Vancomycin Transglycosylase in cell wall synthesis Renal toxicity, ototoxicity, red man syndrome
Metronidazole Damages DNA after being reduced by GI effects, metallic taste, oral candidiasis
nitroreductase
Chloramphenicol Peptide bond formation in ribosomes Bone marrow hypoplasia, aplastic anemia, gray
baby syndrome
Bacitracin Inhibits bactoprenol in cell wall synthesis Rare adverse effects, used topically
CNS, Central nervous system; GI, gastrointestinal.
*Azithromycin given for 5 days has been shown to increase the risk of cardiovascular death in individuals with preexisting cardiovascular risk factors.1 Azithromycin
increases the QT interval, which is a likely contributor to the increased risk.
From Ray WA, et al: Azithromycin and the risk of cardiovascular death, N Eng J Med 366:1881-90, 2012.
Table 8-33
Comparison of Penicillin Drugs
DRUG CLASS AND/OR RESISTANT TO UNIQUE ADVERSE
DRUGS SPECTRUM PENICILLINASE? INDICATIONS EFFECTS
Penicillin G and V Narrow No Oral infections, many
infections caused by
sensitive bacteria
Methicillin, oxacillin, Narrow Yes Staphylococcus aureus
cloxacillin, dicloxacillin, infections
nafcillin
Aminopenicillins Extended (includes No Mixed infections, Rash in people who have
(ampicillin, amoxicillin, many gram- infections owing to mononucleosis or who
bacampicillin) negative rods) gram-negative rods take allopurinol
Anti-Pseudomonas Extended No Effective against
penicillins (ticarcillin, Pseudomonas,
piperacillin) Enterobacter, and
indole-positive Proteus
Procaine penicillin G Narrow No IM injection to achieve a
(combined with more sustained effect
benzathine penicillin) of penicillin
Benzathine penicillin G Narrow No Long-term, low-level
penicillin effect
IM, Intramuscular.
4. Amoxicillin (see Table 8-33). H. Macrolide antibiotics.

a. Oral extended-spectrum penicillin is used for oral 1. Drugserythromycin, clarithromycin, azithromy-
infections and in dental prophylaxis. cin, dirithromycin (Table 8-35).
b. Prophylaxis protocol (see Table 8-36). 2. Sensitive organisms.
E. -Lactamase inhibitors. a. Legionella pneumophila.
1. Clavulanic acid, sulbactam, and tazobactam. b. Mycoplasma pneumoniae.
2. Used with amoxicillin, ticarcillin, ampicillin, and c. Chlamydia pneumoniae.
piperacillin to reduce the effect of plasmid-mediated d. Streptococci and some other gram-positive cocci
-lactamases. and some gram-negative cocci.
F. Cephalosporins (Table 8-34). e. Clarithromycin and azithromycin are more potent
1. Broad-spectrum drugs. than erythromycin and are more effective against
2. Characteristics of five generations of cephalosporins Helicobacter pylori and Mycobacterium avium.
(see Table 8-34). I. Tetracyclines.
3. Cephalosporins as options in dental prophylaxis 1. Broad spectrum.
three cephalosporins are indicated (see Table 8-36). a. Various Rickettsia species.
4. About 10% cross-allergenicity with penicillinsthe b. M. pneumoniae.
risk is greater with patients who have a history of c. C. pneumoniae.
acute or immediate types of allergies. d. H. pylori.
G. Atypical -lactams. e. Borrelia burgdorferi (Lyme disease).
1. Imipenem. f. Escherichia coli.
a. Used with cilastatin, which inhibits imipenem g. Bacteria associated with refractory and localized
metabolism in the kidney. aggressive periodontitis.
b. Used against Pseudomonas aeruginosa and several h. Bacteria associated with acne.
other gram-negative rods as well as some 2. Representative drugs.
streptococci. a. Tetracycline.
2. Ertapenem, meropenem, doripenem, aztreonam b. Doxycycline.
similar indications as imipenem. c. Minocyclinerisk of vestibular toxicity.
Table 8-34
Cephalosporin Generations and Sensitive Organisms
GENERATION EXAMPLES SENSITIVE ORGANISMS
1 Cefazolin Escherichia coli, Staphylococcus aureus (methicillin sensitive), various streptococci
Cephalexin
Cefadroxil
2 a. Cefoxitin a. Oral Bacteroides
b. Cefaclor b. Haemophilus influenzae
3 a. Cefotaxime, ceftriaxone a. Neisseria gonorrhoeae, Neisseria meningitides, E. coli, H. influenzae
b. Ceftazidime b. Pseudomonas aeruginosa
4 Cefepime P. aeruginosa
5 Ceftaroline Multidrug-resistant S. aureus, Streptococcus pneumoniae, H. influenzae
Table 8-35
Comparison of Macrolides and Adverse Effects
DRUG-DRUG CHOLESTATIC USED IN DENTAL
DRUG GI UPSET INTERACTIONS JAUNDICE PROPHYLAXIS
Erythromycin Significant, owing to stimulation More Usually seen only with No
of motilin receptor estolate form
Clarithromycin Less Less No Yes
Azithromycin Less Much less No Yes
Dirithromycin Less Much less No No
GI, Gastrointestinal.
J. Clindamycin. 2. Sensitive organisms and indications.

1. Narrow-spectrum. a. S. aureus, including methicillin-resistant staphylo-
2. Sensitive organisms. cocci.
a. S. pneumoniae. b. Streptococci, enterococci, C. difficile.
b. Viridans streptococci. 3. Administrationgiven intravenously.
c. S. pyogenes. M. Aminoglycosides.
d. Staphylococcus aureus (not methicillin-resistant 1. Examplesstreptomycin, gentamicin, amikacin,
staphylococci). neomycin.
e. Oral Bacteroides and some other oral anaerobes. 2. Spectrum limited to aerobes, mostly gram-negative
3. Uses. rods.
a. Infections caused by several anaerobic rods and 3. Sensitive organisms and indications.
cocci. a. E. coli.
b. Some streptococcal and a few staphylococcal b. Enterobacteriaceae.
infections. c. Klebsiella pneumoniae.
c. Oral infections. d. P. aeruginosa.
d. Osteomyelitis. 4. Use of streptomycin is largely limited to tuberculosis.
e. Dental prophylaxis (Table 8-36). 5. Use of neomycin is topical.
K. Metronidazole. N. Sulfonamides (and trimethoprim).
1. Antimicrobial spectrum. 1. Examplessulfamethoxazole, sulfisoxazole, silver
a. Bacterialimited to anaerobes. sulfadiazine, sulfacetamide (topical).
b. Parasitic infections. 2. Spectrum broadened with the addition of
2. Sensitive organisms and indications. trimethoprimsulfamethoxazole-trimethoprim
a. Bacteroides. combination is commonly used.
b. Fusobacterium. 3. Organisms sensitive to sulfamethoxazole-
c. Clostridium difficile. trimethoprim combination.
3. Contraindications. a. K. pneumoniae.
a. Pregnancy. b. E. coli.
b. Alcohol use. c. Salmonella species.
c. Disulfiram use. d. Shigella species.
L. Vancomycin. e. Pneumocystis jiroveci (formerly Pneumocystis
1. Narrow-spectrum (gram-positive aerobes and anaer- carinii).
obes). f. Haemophilus influenzae.
Table 8-36
Antibiotic Prophylaxis Guidelines for the Prevention of Bacterial Endocarditis*
DOSAGE FOR ADULTS DOSAGE FOR CHILDREN
Standard regimen (oral)
Amoxicillin 2g 50mg/kg
Penicillin allergy (oral)
Clindamycin or 600mg 20mg/kg
Cephalexin or 2g 50mg/kg
Clarithromycin or azithromycin 500mg 15mg/kg
Unable to take oral medications
Ampicillin or 2g IM or IV 50mg/kg IM or IV
Cefazolin or ceftriaxone 1g IM or IV 50mg/kg IM or IV
Penicillin allergy and unable to take oral medications
Clindamycin 600mg IM or IV 20mg/kg IM or IV
Cefazolin or ceftriaxone 1g IM or IV 50mg/kg IM or IV
Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocarditis: Guidelines from the American Heart Association. A guideline from the American Heart
Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical
Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. JADA
2008;139(1):3S-23S, American Dental Association, 2007.
IM, Intramuscularly; IV, intravenously.
*Single dose 30 to 60 minutes before procedure.
Total dose for children should not exceed adult dose.
Cephalosporins should not be used in patients with a history of immediate allergic reactions (urticaria, angioedema, anaphylaxis) to penicillin.
Table 8-37
Comparison of Antifungal Drugs
CLASS EXAMPLES MECHANISM OF ACTION ADVERSE EFFECTS
Polyenes a. Amphotericin B Combine with ergosterol to form a. Renal toxicity, hemolytic anemia,
b. Nystatin membrane pores hypokalemia
Pyrimidine Flucytosine Converted to 5-fluorouracil in fungal Liver toxicity, alopecia, bone marrow
cell and inhibits thymidylate synthase suppression
Azoles a. Ketoconazole Inhibit ergosterol synthesis (inhibit Hormone imbalance (especially
14--demethylase) ketoconazole), inhibit drug metabolism
(especially ketoconazole), liver toxicity
a. Imidazoles a. Clotrimazole
b. Triazoles a. Miconazole
b. Fluconazole
B. Itraconazole
Allylamines Terbinafine Inhibit ergosterol synthesis (inhibit Liver toxicity (only terbinafine is used
Benzylamines Naftifine squalene monooxygenase) systemically)
Butenafine Same as for allylamines Topical only
Echinocandins Caspofungin Inhibit glucan synthesis Release histamine
Micafungin
Anidulafungin
Other Griseofulvin Inhibits mitosis Photosensitivity, induces liver
metabolism, liver toxicity
O. Fluoroquinolones. a. Macrolides.
1. Examplesciprofloxacin, moxifloxacin, norfloxacin, b. Clindamycin.
levofloxacin, sparfloxacin. c. Tetracyclines (special periodontal applications).
2. Spectrum (mostly aerobes) depends to a certain d. Metronidazole (oral anaerobes).
degree on the individual drug. e. Others, based on culture and sensitivity tests.
3. Sensitive organisms and indications.
a. E. coli. Antifungal Drugs
b. H. influenzae. A. Antifungal drugs (Table 8-37).
c. K. pneumoniae. B. Comments on specific drugs.
d. N. gonorrhoeae. 1. Amphotericin B.
e. M. pneumoniae. a. Used systemically.
f. L. pneumophila. b. Very toxic.
g. Moxifloxacin is also useful against anaerobes. c. Given intravenously (in detergent or lipid
P. Bacitracintopical peptide antibiotic with a spectrum medium).
similar to penicillin. 2. Nystatin.
Q. Antituberculosis drugs (first-line)combination ther- a. Used topically.
apy is used for active disease. b. Often used against oral candidiasis.
1. Isoniazidinhibits mycolic acid synthesis. C. Indications (Table 8-38).
2. Rifampininhibits DNA-dependent RNA poly- D. Dental applicationsoptions for treating oral
merase. candidiasis.
3. Ethambutolinhibits synthesis of arabinogalactan. 1. Clotrimazole oral troches.
4. Pyrazinamideinhibits mycolic acid synthesis. 2. Nystatin oral pastilles or rinse.
5. Rifabutininhibits DNA-dependent RNA poly- 3. For more extensive disease.
merase. a. Fluconazole (oral).
R. Dental prophylaxis against bacterial endocarditis from b. Itraconazole (oral).
a dental procedure (see Table 8-36). c. Caspofungin (intravenous).
S. Oral infections.
1. Among the antibacterial drugs, penicillins are most Antiviral Drugs
commonly used for oral infections. Antiviral drugs attack the mechanisms used by the viruses
2. Other antibiotics used for active oral infections. to replicate and infect. The mechanism of action of most of
Table 8-38 these drugs is to inhibit DNA or RNA synthesis and func-
tion. To the extent that this mechanism of action is selective
Indications for Antifungal Drugs
for the virus, human toxicity of the drug is usually lessened.
DRUG INDICATIONS Table 8-39 shows the indications for the antiviral drugs.
Amphotericin B Most systemic fungal infections Table 8-40 shows the mechanism of action of antiviral
Nystatin Used primarily to treat Candida albicans drugs.
Clotrimazole, Used topically to treat candidiasis
miconazole
Fluconazole, Used systemically to treat various fungal
10.0 Antineoplastic Drugs
itraconazole, infections
posaconazole, Antineoplastic drugs are used to inhibit various steps in
voriconazole cancer cell growth. However, these targets are also found
Flucytosine Used systemically to treat a limited in normal cells, and anticancer drugs lead to significant
number of fungal infections (e.g., toxicity and have low margins of safety. Combination
fungal meningitis) therapy is often used to enhance the anticancer effect. This
Caspofungin, Used systemically to treat a limited approach is more desirable if the drugs have little overlap-
micafungin, number of fungal infections, ping toxicity. If possible, it is desirable to target cell
anidulafungin including Candida species components (e.g., enzymes) that are overexpressed in the
Terbinafine Used orally for dermatophytes cancer cell.
Naftifine Used topically for dermatophytes A. Mechanisms of antineoplastic drugs. Figure 8-30 shows
Butenafine Used topically for dermatophytes the sites of action of several anticancer drugs. Figure
8-31 shows the action of anticancer drugs at cell cycle
sites. Enzymes that are targets of anticancer drugs are
listed in Table 8-41. Adverse effects are an important
issue with anticancer drugs. These are presented in
Tables 8-42 and 8-43.
B. Dental applications of cancer chemotherapy (Table
8-44).
Table 8-39
Indications for Antiviral Drugs
DRUG INFLUENZA A INFLUENZA B HSV VZV CMV HIV RSV HBV, HCV, HPV
Amantadine, rimantadine +
Oseltamivir, zanamivir + +
Idoxuridine +
Vidarabine, trifluridine +
Acyclovir, valacyclovir + +
Famciclovir, penciclovir + +
Foscarnet + + +
Ganciclovir, valganciclovir +
Ribavirin +
Reverse transcriptase inhibitors* +
Integrase inhibitor (raltegravir) +
Protease inhibitors +
Interferon and 2b +
CMV, Cytomegalovirus; HBV, hepatitis B virus; HCV, hepatitis C virus; HIV, human immunodeficiency virus; HPV, human papillomavirus; HSV, herpes simplex virus;
RSV, respiratory syncytial virus; VZV, varicella-zoster virus.
*Includes both nucleoside (e.g., zidovudine, didanosine, stavudine, zalcitabine, abacavir) and nonnucleoside (e.g., nevirapine, delavirdine) inhibitors.
Includes saquinavir, indinavir, fosamprenavir, lopinavir, nelfinavir, and ritonavir.

Mechanism of Action of Antiviral Drugs Known Enzyme Targets of Antineoplastic
Drugs*
DRUG ANTIVIRAL MECHANISM
Amantadine Blocks uncoating of virus and TARGET DRUG
blocks replication Dihydrofolate reductase Methotrexate
Oseltamivir Inhibits neuraminidase DNA polymerase Cytarabine, fludarabine
Vidarabine Incorporated into DNA/inhibits Thymidylate synthase 5-Fluorouracil, capecitabine
DNA polymerase
Topoisomerase Mitoxantrone, etoposide,
Acyclovir Inhibits viral DNA polymerase after teniposide, topotecan,
undergoing phosphorylation doxorubicin, daunorubicin
Famciclovir, Inhibit viral DNA polymerase after Ribonucleoside diphosphate Hydroxyurea
penciclovir undergoing phosphorylation reductase
Ganciclovir Inhibits viral DNA polymerase after Caspases Arsenic trioxide
undergoing phosphorylation
Tyrosine kinases Imatinib, gefitinib
Foscarnet Inhibits viral DNA polymerase
Aromatase Anastrozole, letrozole
Ribavirin Inhibits several enzymes involved
in RNA synthesis Histone deacetylase Vorinostat
Reverse transcriptase Inhibit viral RNA-dependent DNA *All listed targets are inhibited by the corresponding drugs except for
caspases, which are stimulated by arsenic trioxide.
inhibitors polymerase
Protease inhibitors Inhibit HIV protease and inhibit
assembly of infectious virions
Bleomycin Actinomycin
Etoposide Daunorubicin
Teniposide Doxorubicin
Cytarabine Idarubicin
Daunorubicin
Doxorubicin
CMP Strand Idarubicin
breaks Intercalation
dCMP
Cisplatin
Fluorouracil Free radical Cyclophosphamide
Replication DNA Dacarbazine
formation
TMP Mechlorethamine
Alkylation Melphalan
Transcription Nitrosoureas
FH2 Procarbazine
Purines
FH4
dUMP Mercaptopurine Fluorouracil
Thioguanine
Methotrexate
RNA
De novo Salvage
Translation
synthesis pathway
Asparaginase
PROTEIN
Tubulin
Drug inhibits this step
Paclitaxel
Drug is incorporated into Vinblastine
macromolecule Vincristine
Figure 8-30 Metabolic steps inhibited by anticancer drugs. Inhibition of tubulin results in inhibition of mitosis. CMP, Cytidine
monophosphate; FH2, dihydrofolate; FH4, tetrahydrofolate; TMP, thymidine monophosphate; UMP, uridine monophosphate. (From
Yagiela JA, etal: Pharmacology and Therapeutics for Dentistry, ed 6. St. Louis, Mosby, 2011.)
Differentiation
M (0.5-1 hr)
G0 Nitrosoureas
Docetaxel
Paclitaxel Vinblastine
Vincristine
Bleomycin
Etoposide Recruitment
G2
Teniposide
(2-10 hr)
Figure 8-31 Cell cycle sites
G1 of anticancer drugs. DNA syn-
(18-30 hr) Non-phase specific thesis occurs during the S phase;
Asparaginase Busulfan
Steroids M is mitosis and G0 is the resting
Carboplatin phase. (From Yagiela JA, etal:
Carmustine
Cytarabine Chlorambucil Pharmacology and Therapeutics
Floxuridine Cisplatin for Dentistry, ed 6. St. Louis,
Fludarabine Cyclophosphamide Mosby, 2011.)
Fluorouracil Dacarbazine
Mercaptopurine Dactinomycin
Methotrexate Daunorubicin
Thioguanine (16-20 hr) Doxorubicin
Hydroxyurea
S Idarubicin
Interferon Ifosfamide
Mechlorethamine
Melphalan
Mitomycin
Mitoxantrone
Procarbazine

Typical Adverse Effects of Most Adverse Effects That Are More Unique to
Antineoplastic Drugs Certain Anticancer Drugs
Myelosuppression Alopecia ADVERSE EFFECT DRUGS
GI toxicity Dermatotoxicity Cystitis Cyclophosphamide
Oral mucositis Ifosfamide
GI, Gastrointestinal. Neurotoxicity Mechlorethamine
Methotrexate
Vinblastine
11.0 Toxicology Cisplatin
Fluorouracil
Paclitaxel
Heavy metals are often toxic. Other compounds, such as Docetaxel
gases and organic chemicals, may be toxic. It is important Teniposide
to know antidotes to the extent they have been identified Pulmonary toxicity, fibrosis Chlorambucil
as well as symptoms of more common toxins. Melphalan
A. Common toxins and therapy (Table 8-45). Carmustine
Lomustine
Bleomycin
Mitomycin
12.0 Prescription Writing
Cardiac toxicity Daunorubicin
Doxorubicin
Prescriptions are written for a variety of drugs used in Epirubicin
dentistry. The use of abbreviations and Latin terms is gen- Idarubicin
erally discouraged. Nevertheless, dentists should know the Arsenic trioxide
more common abbreviations used in prescriptions. More Radiation recall Daunorubicin
importantly, the dentist should know what is required in Doxorubicin
writing an unambiguous prescription.
A. Prescription
A sample prescription is shown in Figure 8-32, with
the terms referring to the various parts of the
prescription. Comments are made about various parts Table 8-46

of the prescription. In almost every case, the use of
Examples of Controlled (Scheduled)
generic drug names is preferred. Some states require the
Substances
dispensing of generic drugs.
A prescription is required for all so-called legend SCHEDULE EXAMPLES
drugs (those labeled by the FDA as Rx only). Pre- I Heroin, 3,4-met
scriptions can also be used to prescribe over-the- hylenedioxymethamphetamine (Ecstasy)
counter drugs. (Schedule I drugs may not be prescribed)
B. Prescription example (see Figure 8-32). II Morphine, cocaine, oxycodone, fentanyl
C. Tables 8-46 and 8-47 provide useful information related III Codeine* plus acetaminophen tablets
to prescriptions. IV Phenobarbital, diazepam
V Codeine cough syrups
*<90mg codeine per dose unit.
2mg/mL codeine.
Table 8-44
Adverse Oral Effects of Many
Antineoplastic Drugs
EFFECT TREATMENT
Stomatitis (including Palliative (rinses, protective agents,
mucositis) analgesics) Table 8-47
Salivary gland Saliva substitutes, pilocarpine, Common Latin Abbreviations and Two
dysfunction* cevimeline Common Weight and Volume Equivalents
Decreased resistance More aggressive chemotherapy
to infection against bacterial, fungal, and viral b.i.d., t.i.d., q.i.d. 2, 3, 4 times a day
infections q4h Every 4hr
Neutropenia, Possible antibiotic prophylaxis for p.r.n. As needed
thrombocytopenia oral procedures, postpone elective Sig Label
surgery, reduce risk of bleeding
1 grain = 65mg
*Destruction of salivary gland tissue and resulting xerostomia has been more
closely linked to radiotherapy to the head and neck. 1 ounce = 30g or 30mL
Table 8-45
Some Toxins, Toxic Symptoms, and Therapy
TYPE TOXIN SYMPTOMS THERAPY*
Heavy metal Mercury Dyspnea, weakness, GI symptoms, gingivitis, a. Chelation (dimercaprol or
a. Elemental tremor, salivation, kidney dysfunction, penicillamine or succimer)
b. Inorganic neurologic and visual disturbances b. Chelation (penicillamine, succimer,
c. Organic polythiol resins)
c. Chelation (penicillamine, polythiol
resin in GI tract, succimer)
Heavy metal Lead Metallic taste, hemolysis, renal damage, colic, Chelation (EDTA, dimercaprol,
palsy, mental deterioration, anemia penicillamine, succimer)
Heavy metal Copper Anemia, proteinuria, swelling of liver, Chelation (penicillamine)
osteomalacia
Heavy metal Iron Abdominal pain, vomiting, acidosis, Chelation (deferoxamine)
cardiovascular collapse
Inorganic anion Cyanide Ashen gray appearance, coma, respiratory arrest Sodium nitrite, sodium thiosulfate
Gas Carbon monoxide Mental confusion, tachycardia, coma Oxygen
EDTA, Ethylenediaminetetraacetic acid; GI, gastrointestinal.
*In addition to supportive care.
John R. Smith, DDS

242 Broadway Street
Your Town, NY
Phone: (000) 000-0000
For: Age:
Date:
Rx (Symbol)
Amoxicillin
(Medication)
500 mg
Dispense 4 capsules (Directions to pharmacist)
Label: Take 4 capsules with water 1 hour before dental appointment. (Patient
directions)
Substitution: permitted
not permitted
Refill 0 1 2 3 (Signature)
(Required for all scheduled drugs) DEA#
Figure 8-32 A prescription with various parts identified. In this case, the direction to the pharmacist is in three sections. Notice
when the Drug Enforcement Administration (DEA) number is required. Notice the striking out of the unwanted refill numbers.
Bibliography A. Maximal effect

Ciancio SG, editor: ADA/PDR Guide to Dental Therapeu- B. Potency
tics, ed 5. Chicago, American Dental Association, 2009. C. Receptor affinity
Hersh EV, et al: Reversal of soft tissue anesthesia with phen- D. Therapeutic index
tolamine mesylate in adolescents and adults. J Am Dent E. Aqueous solubility
Assoc 139:1080, 2009. 3. What receptor or signaling pathway is linked most
Malamed SF: Medical Emergencies in the Dental Office, directly to 2-adrenoceptor stimulation?
ed 6. St. Louis, Mosby, 2007. A. Gi and a reduction in cAMP
Malamed SF: Handbook of Local Anesthesia, ed 6. St. Louis, B. Gs and an increase in cAMP
Mosby, 2012. C. Gq and calcium
Tavares M, et al. Reversal of soft tissue anesthesia with D. Sodium ion channel
phentolamine mesylate in pediatric patients. J Am Dent E. Membrane receptor containing tyrosine kinase
Assoc 139:1095, 2009. 4. What tissue or organ has many muscarinic receptors
Yagiela JA, et al: Pharmacology and Therapeutics for Den- but lacks innervation to those receptors?
tistry, ed 6. St. Louis, Mosby, 2011. A. Heart
B. Parotid gland
C. Blood vessels
Sample Questions D. Sweat glands
E. Urinary bladder
1. Which drugs tend to concentrate in body compart- 5. Which of the following drugs used in the therapy for
ments with a high pH? parkinsonism does not cross the blood-brain barrier?
A. Permanently charged drugs A. Amantadine
B. Drugs that are not charged B. Carbidopa
C. Weak organic acids C. Levodopa
D. Weak organic bases D. Selegiline
E. Inorganic ions E. Tolcapone
2. Drug agonists having the same intrinsic activity also 6. After an injection, which of the following drugs would
have the same ______. be expected to have the longest duration of action?
(Assume no vasoconstrictor was injected with the local 12. What is the clinical setting for the use of ketorolac by
anesthetic.) the oral route?
A. Bupivacaine A. For severe pain
B. Lidocaine B. For initial treatment of pain
C. Mepivacaine C. To continue therapy after an intravenous or intra-
D. Prilocaine muscular dose of ketorolac
E. Procaine D. Only in combination with an opioid
7. A very low blood:gas solubility coefficient (partition E. Only in combination with an NSAID
coefficient = 0.47), analgesic effect, and ability to in- 13. At what cell type is the use of H2 histamine receptor
hibit methionine synthase best describes which drug? blockers most clinically useful?
A. Ketamine A. Beta cells of the pancreas
B. Nitrous oxide B. Basophils
C. Halothane C. Mast cells
D. Isoflurane D. Juxtaglomerular cells
E. Propofol E. Parietal cells
8. Levonordefrin is added to certain cartridges contain- 14. Which class of antihypertensive drug most effectively
ing mepivacaine. The desired effect of levonordefrin is reduces the release of renin from the kidney?
due to what pharmacologic effect? A. -Adrenergic receptor blockers
A. Inhibition of nicotinic cholinergic receptors B. ACE inhibitors
B. Inhibition of muscarinic cholinergic receptors C. -Adrenergic receptor blockers
C. Stimulation of -adrenergic receptors D. Calcium channel blockers
D. Stimulation of -adrenergic receptors E. Angiotensin II receptor blockers
E. Stimulation of dopamine receptors 15. The administration of ______ results in epinephrine
9. Match each drug with its mechanism of action at the reversal (decrease in blood pressure from epineph-
nerve terminal. rine) if given before administration of epinephrine.
A. Guanethidine
A. Amphetamine 1. Blocks the release of a B. Propranolol
_____ neurotransmitter. C. Phentolamine
B. Fluoxetine 2. Inhibits an enzyme that D. Tyramine
_____ metabolizes a 16. What is the mechanism of action of enoxaparin?
C. Botulinum toxin neurotransmitter inside A. Inhibition of synthesis of clotting factors II, VII, IX,
_____ the nerve. and X
D. Tranylcypromine 3. Stimulates the release of B. Activation of antithrombin III with resulting inhi-
_____ a neurotransmitter from bition of clotting factor Xa
E. Physostigmine the cytoplasmic pool. C. Indirect activation of tissue plasminogen activator
_____ 4. Inhibits the metabolism D. Direct inhibition of plasminogen with resulting
of a neurotransmitter at degradation of fibrin
the postjunctional or E. Dilation of coronary blood vessels
postsynaptic site. 17. Oropharyngeal candidiasis is an adverse effect most
5. Prevents the reuptake of likely to occur with ______.
a neurotransmitter. A. Inhaled salmeterol
B. Inhaled ipratropium
10. Naloxone antagonizes the therapeutic and toxic effects C. Inhaled nedocromil
of which drug? D. Inhaled beclomethasone
A. Acetaminophen E. Inhaled methacholine
B. Aspirin 18. Oral antacids are most likely to reduce the absorption
C. Carbamazepine of which of the following drugs when given orally?
D. Fentanyl A. Clarithromycin
E. Ibuprofen B. Clindamycin
11. What is the mechanism of the analgesic action of C. Metronidazole
aspirin? D. Penicillin V
A. Stimulates opioid receptors E. Tetracycline
B. Blocks histamine H2 receptors 19. A decrease in glycogenolysis in the liver would be
C. Inhibits COX expected from which of the following drugs?
D. Inhibits lipoxygenase A. Albuterol
E. Blocks sodium channels in nerves B. Epinephrine
C. Glucagon _____ D. Movement of GLUT-4 to the plasma

D. Insulin membrane
E. PTH _____ E. Stimulation of insulin receptor
20. What effect does nitroglycerin have on blood vessel 27. What events would occur after a submucosal injection
smooth muscle? of phentolamine in the oral cavity? (Choose three.)
A. Increase in level of intracellular calcium A. Blockade of -adrenergic receptors
B. Increase in level of cyclic guanosine monophos- B. Blockade of -adrenergic receptors
phate (cGMP) C. Inhibition of sodium channels
C. Antagonism at 1-adrenergic receptors D. Blockade of the vasoconstrictor effect of norepi-
D. Antagonism at -adrenergic receptors nephrine released from neurons
E. Inhibition of L-type calcium channels E. Inhibition of protein synthesis in oral bacteria
21. Clavulanic acid offers an advantage therapeutically F. Antagonism of the vasoconstrictor effect of a
because ______. subsequent injection of epinephrine in the same
A. It inhibits streptococci at a low MIC area of the oral cavity during the same dental
B. It inhibits transpeptidase appointment
C. It inhibits penicillinase 28. Match the proper description with the drug.
D. It inhibits anaerobes at a low MIC
_____ A. This is an 1. Quetiapine
E. It inhibits DNA gyrase
antimuscarinic 2. Gabapentin
22. Inhibition of which of the following enzymes is most
drug used to treat 3. Solifenacin
responsible for the cell wall synthesis inhibitory effect
overactive bladder. 4. Codeine
of penicillin G?
_____ B. This is an 2- 5. Dexmedetomidine
A. -Lactamase
adrenergic receptor 6. Pilocarpine
B. DNA gyrase
agonist used for 7. Zaleplon
C. Nitro reductase
intravenous 8. Carbamazepine
D. Transglycosylase
sedation.
E. Transpeptidase
_____ C. This drug blocks
23. Which of the following drugs is often combined with
serotonin 5-HT2
sulfamethoxazole for the treatment of respiratory tract
and dopamine D2
and urinary tract infections?
receptors and is
A. Amoxicillin
used for
B. Ciprofloxacin
schizophrenia.
C. Clindamycin
_____ D. This sedative
D. Metronidazole
selectively inhibits
E. Trimethoprim
a benzodiazepine
24. Which of the following organisms is usually sensitive
receptor subtype.
to clindamycin?
_____ E. This antiepileptic
A. Candida albicans
drug binds to the
B. Klebsiella pneumoniae
2-1 subunit of
C. Methicillin-resistant Staphylococcus aureus
the high-voltage
D. Viridans streptococci
calcium channel
E. Pseudomonas aeruginosa
and blocks this
25. Which anticancer drug inhibits the enzyme dihydro-
channel.
folate reductase?
A. Bleomycin 29. Match the enzyme with the drug that inhibits it.
B. Cisplatin
C. Doxorubicin _____ A. Acetylcholinesterase 1. Sitagliptin
D. 5-Fluorouracil _____ B. ACE 2. Terbinafine
E. Methotrexate _____ C. Dipeptidyl peptidase-4 3. Aliskiren
26. A patient has been prescribed glipizide for type 2 dia- _____ D. DNA-dependent RNA 4. Fluconazole
betes. Arrange the following events, leading to a reduc- polymerase 5. Neostigmine
tion in plasma glucose, in their order of occurrence as _____ E. 14 -demethylase 6. Ciprofloxacin
a result of this drug. _____ F. DOPA decarboxylase 7. Lisinopril
_____ A. Insulin release from beta cells _____ G. MAO B 8. Lithium
_____ B. Increase in glucose uptake in target cell 9. Carbidopa
_____ C. Closing of ATP-sensitive potassium 10. Selegiline
channels 11. Rifampin
30. Select the drugs that antagonize the effect of pilocar- _____ A. Osteonecrosis of 1. Terazosin
pine on salivary flow rate. (Choose three.) the jaw especially 2. Acetaminophen
A. Rivastigmine at high doses 3. Pamidronate
B. Benztropine _____ B. Cough in 10% of 4. Prilocaine
C. Metoprolol patients taking the 5. Lidocaine
D. Tolterodine drug 6. Diphenhydramine
E. Oxybutynin _____ C. First dose 7. Aspirin
F. Epinephrine hypotensive effect 8. Clopidogrel
31. Identify which drugs are commonly used in the treat- _____ D. Sedation 9. Fosinopril
ment of herpes simplex viral infections. (Choose two.) _____ E. Reyes syndrome
A. Ganciclovir in young patients
B. Indinavir with recent viral
C. Acyclovir infection
D. Ribavirin _____ F. Methemoglobinemia
E. Penciclovir
F. Zidovudine
32. Match each adverse effect with the drug it is more typi-
cally associated with compared with the other drugs
listed.
SECTION 9
Prosthodontics
ALEJANDRO PEREGRINA
OUTLINE expectations and objectives set forth. Partially edentu-

lous patients can be restored with a fixed dental pros-
1. General Considerations
thesis (FDP), removable dental prosthesis (RDP), and
2. Complete Dentures implant-supported FDP.
3. Removable Partial Prosthodontics 1. Considerations when replacing missing teeth.
4. Fixed Prosthodontics a. FDP.
(1) FDP abutments with half or less of bone
support and loss of attachment have a poor
prognosis.
This review with test questions is intended to serve as a (2) Rigid fixed retainers should be at each end of
study guide in preparing for the prosthodontic section of the pontic except in a cantilever FDP.
Part II of the National Board Dental Examination in the (3) A single retainer cantilever FDP has a poor
areas of fixed, complete, and removable partial prosth- prognosis.
odontics and implant-supported prostheses. This review (4) Splinting teeth is generally done to distribute
has been compiled and organized, for the most part, using occlusal forces; this is recommended where
the following textbooks: Rosenstiel SF, etal: Contemporary the periodontal surface of the abutment tooth
Fixed Prosthodontics, ed 4 (St. Louis, Mosby, 2006); Carr does not provide the needed support for a
AB, etal: McCrackens Removable Partial Prosthodontics, prosthesis (FDP or RDP).
ed 11 (St. Louis, Mosby, 2005); Zarb GA, etal: Prosthodon- (5) Multiple-splinted abutment teeth, nonrigid
tic Treatment for the Edentulous Patient, ed 12 (St. Louis, connectors, or intermediate abutments can
Mosby, 2004); Powers JM and Sakaguchi RL: Craigs Restor- compromise the long-term prognosis.
ative Dental Materials, ed 12 (St. Louis, Mosby, 2006); (6) When replacing the maxillary or mandibular
Anusavice KJ: Phillips Science of Dental Materials, ed 11 canine, the central and lateral should be
(Philadelphia, Saunders, 2003); and Okeson JP: Manage- splinted to prevent lateral drifting of the
ment of Temporomandibular Disorders and Occlusion, ed 5 FDP.
(St. Louis, Mosby, 2003). The student is encouraged to (7) Compromised endodontically treated teeth
consult these or other current textbooks for additional should not be used as retainers.
information. (8) Abutment teeth must align to a common path
of insertion.
(9) Occlusal forces that may cause drift or tooth
1.0 General Considerations mobility should be avoided.
(10) Teeth with a short root/crown ratio (<1:2)
A. Diagnosis and treatment planning. with conical roots should be avoided as
Treatment planning in prosthodontics should be abutments.
based on the individual patients needs. According to (11) Diverging multirooted, curved, and broad
Rosenstiel etal. (2006), treatment should accomplish labiolingual roots are preferred over fused,
the following: correct existing disease, arrest decay, single, conical, and round circumferential
prevent future disease, restore function, and improve roots.
appearance and oral hygiene. (12) Teeth with a large root surface area (e.g.,
The sequence, materials, and techniques chosen canines and molars) are better abutments
to treat a patient should take into consideration the than central incisors and premolars.
343
344 Section 9 Prosthodontics
(13) The supportive surface area (periodontium) occlusal corrections are necessary before any
of the abutment teeth should be equal to, but definitive prosthodontic treatment or where MI
not less than, that of the teeth to be replaced. is impossible to maintain (e.g., multiple teeth to
(14) Natural teeth exert more force than an RDP restore; complete dentures).
or complete denture when opposing an FDP. c. Accurate CR interocclusal records require precise
b. Indications for RDP. manipulation of the mandible by the dentist. The
(1) Where teeth are missing and there are no pos- bimanual manipulation technique described by
terior abutment teeth to support an FDP (distal Dawson (2007) is recommended.
extension). d. The use of anterior deprogramming devices such as
(2) Where the span of teeth to be replaced is a leaf gauge or acrylic resin jig (known as a Lucia
beyond the load that the existing teeth can bear jig) keep the teeth apart and, when left for a deter-
with an FDP. mined period of time, can deprogram the existing
(3) Where there is bone loss with a questionable proprioceptive reflexes and aid to manipulate the
prognosis if restored with an FDP. mandible into CR.
(4) Where the cost of an FDP or implants is e. Most common materials used for interocclusal
prohibitive. records are wax (Aluwax) and fast-setting elasto-
c. Complete denture. meric materials such as polyvinyl siloxane and
(1) Used when all teeth are missing and when an polyether.
implant-supported prosthesis cannot be used f. Casts mounted with an interocclusal record are
instead. Complete dentures are contraindicated mounted more accurately if the material used is
when only the mandibular anterior teeth are selected according to the accuracy of the casts
present because severe damage to the opposing being articulated (casts produced with irreversible
premaxilla occurs (combination syndrome). hydrocolloid are more accurately mounted with
d. Implant-supported prosthesis. wax records, and casts obtained with elastomeric
(1) Used for replacing single or multiple teeth materials are more accurately mounted with
instead of conventional FDP, RDP, and com- elastomeric registration materials or zinc oxide
plete dentures. eugenol paste).
(2) Use is dependent on available bone width and 3. Anterior guidance must be preserved, especially when
length, type of bone, bone volume, placement restorative procedures change the surfaces of anterior
away from significant anatomic structures or posterior teeth that guide the mandible in excur-
(nerves, adjacent teeth), interocclusal space, sive (lateral, protrusive) movements.
and osseointegration. a. The mechanical anterior guide table provides
(3) Used in edentulous patients to support and limited adjustments that give insufficient informa-
improve the retention of complete dentures via tion to reproduce the lingual contours of maxillary
attachments directly or indirectly retained by anterior natural teeth. Their use has been mainly
the implants. for the fabrication of complete dentures and occlu-
B. Maxillomandibular relationships, interocclusal records, sal appliances.
and anterior guidancethere are two maxillomandibu- b. Custom incisal guide tables are generally made of
lar relationships in which the mandibular teeth can be acrylic resin and are made to reproduce the sur-
oriented to the maxillary. faces of teeth (usually the lingual concavity and
1. Centric relation (CR) is considered a terminal hinge incisal edges of anterior teeth) that have a direct
position and is defined as the maxillomandibular influence in guiding the mandible through all
relationship in which the condyles articulate with excursive movements.
the thinnest avascular portion of their respective C. Diagnostic impressions and casts.
discs with the condyle-disc complex in the 1. Irreversible hydrocolloid or alginate is the material of
anterior-superior position against the shapes of the choice to produce diagnostic casts. Composition is
articular eminences (The glossary of prosthodontic mainly sodium or potassium salts of alginic acid.
terms, 2005). The salts react chemically with calcium sulfate to
2. Maximal intercuspal position, maximum intercus produce insoluble calcium alginate. Diatomaceous
pation (MI), or centric occlusion is defined as the earth is added for strength, and trisodium phos-
complete intercuspation of the opposing teeth inde- phate and other compounds are added to control
pendent of condylar position (The glossary of the setting rate.
prosthodontic terms, 2005). 2. Most types of trays are suitable to produce accept-
a. In 90% of people, CR and MI do not coincide. able, accurate impressions.
b. Casts are often mounted in CR primarily to 3. Tray adhesive should always be used to prevent dis-
perform an occlusal analysis to determine whether tortion at the time of removal.
Section 9 Prosthodontics 345
4. The greater the bulk that irreversible hydrocolloid values (e.g., the use of the external auditory
has, the more favorable the surface area/volume meatus to stabilize the bow).
ratio and the lower the susceptibility to water loss (2) Some semiadjustable articulators allow the use
or gain and unwanted dimensional change. of kinematic facebows, allowing more accuracy
5. The tray should be removed 2 to 3 minutes after when mounting casts than with the use of
gelation. arbitrary facebows. The kinematic facebow is
6. The impression should be rinsed and disinfected placed on the hinge axis (the horizontal axis
with glutaraldehyde or iodophor and should be around which the mandible purely rotates
poured within 15 minutes from the time the impres- when opening and closing), the location of
sion was removed from the mouth. which has been previously determined. Using
7. Pouring with American Dental Association type IV the hinge axis is especially necessary when the
or V stone is recommended. vertical dimension is altered in the articulator
8. Poured impressions should be allowed to set undis- or when an interocclusal record was made at a
turbed for the recommended time, which usually vertical dimension of occlusion different from
ranges from 30 to 60 minutes depending on the type the one to be used.
of stone used. (3) Most semiadjustable articulators permit some
9. To achieve less distortion of the irreversible hydro- adjustments in the condylar inclination, lateral
colloid and maximum strength and surface detail of translation, Bennett angle (side shift), anterior
the cast, the poured impression can be stored for 45 guidance, and intercondylar distance.
minutes in a humidor. 4. Fully adjustable articulatorsthese are capable of
10. Casts should be evaluated for inaccuracies such as duplicating a wide range of mandibular movements
voids and nodules that might interfere with proper but are generally set to follow the patients border
articulation. movements. The terminal hinge axis is located, and a
D. Articulators. pantograph is used to record the mandibular move-
1. Hand-held casts provide limited information with ments. These mandibular movement tracings or
respect to the individual arches and tooth recordings are used to set the articulator. The infor-
alignment. mation provided is useful to treat cases in which
2. Nonadjustable articulator. complex mandibular movements exist that require
a. Does not reproduce the full range of mandibular extensive occlusal mouth rehabilitation. The fully
movement. adjustable articulators use a kinematic facebow record
b. The arc of closure is not the same as the patients to orient and articulate the maxillary cast. These
arc of closure because the distance between the articulators can be adjusted to repeat precisely the
hinge and the teeth is significantly shorter than condylar inclination, Bennett angle (side shift),
in the patient. This difference may affect the immediate side shift, rotating condylar movement,
construction of restorations, resulting in prema- and intercondylar distance.
ture contacts and incorrect ridge and groove E. Restorative implantology.*
direction. Implants allow patients with single or multiple
3. Semiadjustable articulatorsthere are two types of missing teeth to benefit from implant-supported pros-
articulators. theses with a high degree of success. Implants can be
a. Arcon, in which the condyles are attached to the divided in three major groups: subperiosteal, transos-
lower member of the articulator, and the fossae are teal, and endosteal. Endosteal implants (root or cylin-
attached to the upper member. The mechanical der, blades form implants) are the most common
fossae are fixed relative to the occlusal plane of the implants used today. Most implants are made of tita-
maxillary cast. This makes them more accurate for nium or titanium alloy with or without hydroxyapatite
fabricating fixed restorations, especially when an coating. These materials have the highest biofunctional-
interocclusal record is used to mount the man- ity. Threaded and nonthreaded designs are available.
dibular cast. Many titanium implants today are grit-blasted or acid-
b. Nonarcon, which has the upper and lower members etched to roughen the surface to increase the surface
rigidly attached. The occlusal plane is relatively area contacting bone.
fixed to the occlusal plane of the mandibular cast. 1. Treatment planning.
These articulators provide easier control in setting a. Indications for implants in partially edentulous
teeth for complete and partial dentures. patients.
(1) Semiadjustable articulators generally use an (1) Where there is inability to wear an RDP or
arbitrary facebow record; this orients the cast in complete denture.
the anterior-posterior and mediolateral posi-
tion in the articulator to anatomic average *Compiled from Rosenstiel etal. (Ch. 13) and McGlumphy (Ch. 2).
(2) Where multiple teeth are missing and a long-

span FDP is contraindicated. Implants should be
placed at least 3 mm
(3) Unfavorable number and location of potential apart and 1 mm from
natural tooth abutments. adjacent teeth.
(4) Single tooth replacement that would necessi-
tate preparation of unrestored or minimally
restored teeth for an FDP. 1 4 3 4 1
b. Contraindications.
(1) Acute illness.
(2) Terminal illness.
(3) Pregnancy.
(4) Uncontrolled metabolic disease.
(5) Unrealistic patient expectation.
(6) Improper patient motivation.
(7) Lack of operator experience.
(8) Inability to restore with prosthesis.
c. Clinical and radiographic evaluation.
(1) Detection of flabby excess tissue.
(2) Bony ridges.
(3) Sharp underlying osseous formations. Figure 9-1 Recommended minimum distances (in milli-
(4) Undercuts that would limit implant insertion. meters) between implants and between implants and
(5) Posterior maxillary and mandibular bone natural teeth. (From Rosenstiel SF, Land MF, Fujimoto J: Con-
width is visually determined. temporary Fixed Prosthodontics, ed 4. St. Louis, Mosby, 2006.)
(6) Panoramic radiograph is best for initial view
to determine approximate bone height and in the mandible and four in the maxilla (Carr
lingual nerve location. etal. [Ch. 29]).
(7) Cephalometric radiographs are used to deter- (7) For additional considerations regarding place-
mine anterior maxillary and mandibular ment in the maxilla and the mandible, refer to
widths. Rosenstiel etal. (Ch. 13).
(8) Computed tomography scans give more b. Implant-supported restorations.
accurate information of anatomic landmarks, (1) Implants support screw-retained or cement-
but higher radiation and expense may limit retained restorations.
their use. (2) Implant bodies can be a one-stage restoration,
d. Preimplantation preparation. in which the implant bodies project through
(1) Diagnostic casts to determine the following. the soft tissue with a cover screw after surgical
(a) Maxillomandibular relationships. placement, or a two-stage restoration, in which,
(b) Interocclusal space. after placement, a cover screw is placed and
(c) Existing dentition. covered with soft tissue, to be uncovered in a
(d) Implant site placement with the aid of diag- second operation.
nostic wax-up. (3) Abutment placements are screwed directly into
(e) Construction of surgical templates. the implant.
2. Implant placement. (4) Adequate healing time before impression
a. Principles for implant placement. making is 2 weeks in noncritical esthetic areas
(1) Should be placed entirely in bone. and 3 to 5 weeks in esthetic areas.
(2) Must be placed away from significant struc- (5) Abutment size and angulation selection depend
tures such as inferior alveolar nerve canal, on the interocclusal space available, the implant
sinus, and incisive foramen. long axis position and the orientation of
(3) Ideally, should be placed engaging two cortical multiple implants to be restored, and type of
plates of bone. implant-supported prosthesis to use.
(4) When placing several implants, they should be (6) Fixed, detachable prostheses (acrylic resin and
at least 3mm apart and 1mm away from an metal framework) are indicated where soft
adjacent tooth (Figure 9-1). tissue and teeth are being replaced with a pros-
(5) Restorative needs should dictate possible thesis supported by implants (a minimum of
implant selection. five in the mandible and six in the maxilla are
(6) In an elderly edentulous patient, a reduction in recommended) instead of a conventional com-
the number of implants is recommended: two plete denture (Box 9-1).
Box 9-1
Advantages of Osseointegrated Implants
1. Surgical
a. Documented success rate
b. In-office procedure
c. Adaptable to multiple intraoral locations
d. Precise implant site preparation
e. Reversibility in the event of implant failure
2. Prosthetic
a. Multiple restorative options
b. Versatility of second-stage components
(1) Angle correction
(2) Esthetics
(3) Crown contours
(4) Screw-retained or cement-retained options
c. Retrievability in the event of prosthodontic failure
Figure 9-2 When a single implant is attached to a natural
From Rosenstiel SF, Land MF, Fujimoto J: Contemporary Fixed tooth, biting forces on the natural tooth and pontic cause
Prosthodontics, ed 4. St. Louis, Mosby, 2006. stress to be concentrated at the superior portion of the
implant. (From Rosenstiel SF, Land MF, Fujimoto J: Contempo-
rary Fixed Prosthodontics, ed 4. St. Louis, Mosby, 2006.)
c. Guidelines when placing an implant-supported

prosthesis. (3) Access hole is through the occlusal table of pos-
(1) Attaching implants to natural teeth is not terior teeth or lingual of anterior.
recommended. (4) Main disadvantage is that the screw may loosen
(2) Two implants can support a three-unit FDP during function because of excessive lateral
when the crown/implant ratio is favorable. forces, excessive cantilever force, or improperly
(3) If implants are short and crowns are long, one screwed crowns.
implant to replace each missing tooth is highly 3. Occlusionsimilar occlusion principles apply to
recommended. natural teeth and to implants.
(4) When heavier occlusal load is expected, addi- a. Occlusal forces should be directed in the long axis
tional implants are recommended to support of the implant.
multiple units or a long edentulous span. b. Lateral forces in the posterior part of the mouth
(5) If retaining the prosthesis by implants and are greater and more destructive than lateral forces
natural teeth, protecting the teeth with tele- in the anterior part of the mouth.
scopic copings (six) is recommended. A single c. When unable to eliminate lateral forces, the occlu-
implant attached to a natural tooth causes con- sion should be balanced so that the stress is distrib-
centration of stress at the superior portion of uted over as many teeth as possible (Figure 9-3).
the implant (Figure 9-2).
d. Cement-retained implant crown.
(1) More economical (in some systems). 2.0 Complete Dentures
(2) Allows minor angle corrections to compensate
for discrepancies between the implant inclina- A. Examination.
tion and the facial crown contour. 1. Clinical examinationone of the purposes of the
(3) Easier to use in small teeth than screw-retained clinical examination is to detect (recognize) prob-
implant crown. lems in the supporting structures of the denture that
(4) Requires more chair time and has the same might compromise the success of the prosthesis. It
propensity to loosen. includes examination and diagnosis of supporting
e. Screw-retained implant crown. structures, tongue, floor of mouth, temporomandib-
(1) Retrievability allows for crown removal, facili- ular joint, and any existing prosthesis. Critical areas
tating maintenance (e.g., soft tissue evaluation, that are frequently missed are tuberosity, retromolar
calculus removal). pad, buccal undercuts of tuberosities, and mandibu-
(2) Future modification capability. lar tori.
(3) Pathologic conditions.

A carefully designed (4) Hypermobile ridgeif inflamed, treat with a
occlusion is critical to
implant success. tissue conditioner.
(a) Change one to two times weekly to main-
tain resiliency of conditioner and healing
effect. If effective (2 to 3 weeks), may
proceed with impression; in hypermobile
tissue, use large relief in the tray or perfo-
rate a custom tray.
(b) If tissue conditioner is ineffective, use elec-
trosurgery or laser surgery to eliminate
tissue.
(c) Caution: this procedure might also elimi-
nate the vestibule and risk making it even
more difficult to attain a seal. Immediately
after surgery, a soft liner must be placed to
prevent epulis fissurata from forming.
Figure 9-3 Sharper cusp inclines and wider occlusal
(5) Epulis fissuratahyperplastic tissue reaction
tables increase the resultant force on implant compo- caused by an ill-fitting or overextended flange
nents. (From Rosenstiel SF, Land MF, Fujimoto J: Contemporary in a denture.
Fixed Prosthodontics, ed 4. St. Louis, Mosby, 2006.) (a) Treatmentadjust denture border and use
tissue conditioner; surgery is indicated if
inadequate response.
(6) Fibrous maxillary tuberositycommon when
2. Radiographic examination. large maxillary tuberosities contact mandibular
a. Residual root tips. retromolar pads. Radiographs can aid in deter-
(1) General ruleroot tips with no radiolucency mining whether soft tissue reduction alone
and cortical margin of bone intact may remain; would suffice. Soft relining immediately pre-
however, the patient should be informed of vents further problems secondary to an ill-
their presence and risk and of the need to have fitting denture.
them removed in the future. They should be (7) Combination syndromebelieved to be a spe-
removed if the cortical plate is perforated or the cific pattern of bone resorption in the anterior
periodontal ligament or radiolucent area is portion of edentulous maxillae, caused by
enlarging. wearing a complete denture opposing anterior
b. Radiolucencies and radiopacities. teeth (partial dentate).
(1) Assess if normal (e.g., salivary gland (8) Benign soft tissue lesionsexcisional biopsy,
depression). then reline denture.
B. Conditions that compromise the optimal function of (9) Unknown lesions.
complete dentures. (a) Excisional biopsy.
1. Preprosthetic treatment. (b) Incisional biopsy.
a. Soft tissue surgery. (c) Brush biopsy.
(1) Frenectomycommon for labial, less for buccal, b. Nonsurgical pathologic conditions.
rare for lingual. (1) Papillary hyperplasiafound in the palatal
(a) Labialattachment close to ridge crest vault. Multiple papillary projections of the epi-
interferes with good seal and possibly thelium caused by local irritation, poor-fitting
esthetics. denture, poor oral hygiene, and leaving den-
(b) Lingualhigh attachment is rare; familial; tures in all day and night. Candidiasis is the
usually causes speech problem and is noted primary cause.
in children. Historically, lingual frenecto- (a) Treatmenteducate patient in oral hygiene;
mies were performed in children for this advise patient to leave denture out at night;
condition. Today, speech therapy is gener- soak dentures for 30 minutes in a 1%
ally recommended instead. solution of sodium hypochlorite and rinse
(c) SurgeryZ-plasty must include fibrous thoroughly; use tissue conditioner (see
attachment to bone. hypermobile ridge earlier). Patient should
(2) Free gingival graftnecessary for some over- brush irritated area lightly with a soft
denture teeth. brush.
(2) Candida albicansCandida is characterized by (2) Reposition neurovascular bundle (i.e., mental
pinpoint hemorrhage or white patches or both. nerve).
A cytologic smear should be performed to f. Augmentation.
confirm infection. (1) Bone graftssources include anterior iliac crest
(a) Treatmentuse nystatin or clotrimazole of hip and rib. Resorption is unpredictable;
pastilles (note: both contain sugar and often lose greater than 75%.
should be avoided in diabetic patients) or (2) Hydroxyapatitebiocompatible bone substi-
clotrimazole or nystatin powder in oral sus- tute; available as resorbable, nonresorbable,
pension. Laser surgery and electrosurgery solid, and particulate.
are difficult and painful on the palatal (3) Freeze-dried bone.
tissue; because it is easy to go through tissue (4) Connective tissue.
to bone, it is preferable to try local treat- g. Implants.
ment first. C. Occlusion.
(3) Pagets disease of bonebone disease character- 1. The CR record of an edentulous patient provides
ized by bone resorption followed by attempts at the ability to increase or decrease the vertical dimen-
bone repair, leading to bone deformities. The sion of occlusion more accurately in the articulator
etiology is unknown, and it occasionally by establishing a radius of the mandibles arc of
involves the maxilla and mandible. A denture closure.
or RDP in a patient with this disorder may have 2. A protrusive record registers the anterior-inferior
to be remade periodically because of bone condyle path at one particular point in the transla-
expansion. tory movement of the condyles. Some clinicians use
c. Hard tissue surgery to eliminate interferences to this type of record to determine the amount of space
prosthesis placement. between maxillary and mandibular teeth or occlusal
(1) Alveoloplastythe improvement of the alveolar rims to maintain balanced occlusion throughout the
bone by surgical reshaping or removal. mandibular functional range of movement when
(2) Pendulous tuberosities can occur unilaterally or articulating teeth.
bilaterally and can interfere with denture con- a. Christensens phenomenon refers to the distal
struction by limiting interarch space. Surgical space created between the maxillary and mandibu-
excision of fibrous tissue, which can be accom- lar occlusal surfaces of the occlusion rims of den-
panied by bone, is indicated. tures when the mandible is protruded. It is caused
(3) Sharp, spiny, or extremely irregular ridges. by the downward and forward movement of the
d. Exostoses and tori removal. condyles.
(1) Palatal torus is removed in the following 3. Vertical dimension of rest or physiologic rest position
situations. of the mandible is the position when the elevator and
(a) It is so large that it fills the vault and pre- depressor muscles are in a state of equilibrium or
vents the formation of an adequate denture balance. This position most commonly results in a
base when it is undercut. separation of the maxillary and mandibular teeth of
(b) It extends too far in the posterior direction about 3mm at the first premolar region. This separa-
and interferes with placement of the poste- tion is called the interocclusal space.
rior palatal seal. a. Effects of excessive vertical dimension of
(c) It disturbs the patient psychologically occlusion.
(cancer phobia). (1) Excessive display of mandibular teeth.
e. Soft tissue surgery (to increase denture base area). (2) Complaint of fatigue of muscles of mastication.
(1) Vestibuloplastythis technique increases the (3) Clicking of the posterior teeth when speaking.
relative height of the alveolar process by api- (4) Strained appearance of the lips.
cally repositioning the alveolar mucosa and the (5) Patient unable to wear dentures.
buccinator, mentalis, and mylohyoid muscles (6) Discomfort.
as they insert into the mandible. After the (7) Excessive trauma to the supporting tissues.
vestibuloplasty, the periosteum is uncovered. (8) Gagging.
Usually a mucosal graft (from cheek or palate) b. Effects of insufficient vertical dimension.
is placed over the periosteum. If necessary, the (1) Aging appearance of the lower third of the face
use of customized acrylic resin templates or the because of thin lips, wrinkles, chin too near the
patients modified dentures can be used to nose, overlapping corners of the mouth.
support the vestibuloplasty in the mandible. (2) Diminished occlusal force.
(a) Lingual vestibuloplasty is more traumatic (3) Angular cheilitis (occurs in conjunction with
and is rarely indicated. candidiasis).
4. Plane of occlusionthe plane of orientation for separation should be 1 to 1.5mm. This is

complete denture construction is established in the known as the closest speaking space.
anterior-posterior direction with the maxillary occlu- d. The b, p, and m sounds are made by contact of the
sal wax rim parallel to Campers line, which is an lips. Insufficient lip support by the teeth or the
imaginary line traced from the ala of the nose to the labial flange can affect the production of these
tragus of the ear, and with the interpupillary line in sounds.
the transverse plane, which is an imaginary line E. Anatomic considerations in complete denture
drawn between the pupils of the eyes. fabrication.
5. Balanced occlusion. 1. The limiting structures of the maxillary denture.
a. Balanced occlusion requires that the maxillary a. In the anterior regionthe labial vestibule, which
lingual cusps of the posterior teeth on the non- extends from the right buccal frenum to the left;
working side contact the lingual incline of facial laterally, from the right and left buccal vestibules
cusps of mandibular posterior teeth in conjunction extending in the posterior aspect on each side to
with balanced contact of teeth in the working side. the right and left hamular notches, respectively.
b. As the condylar inclination increases, the compen- b. The posterior limit extends to junctions of movable
sating curve must increase to keep a balanced and immovable tissue; this coincides with the line
occlusion. drawn through the hamular notches and approxi-
c. Anterior guidance in complete denture occlusion mately 2mm anterior to the foveae palatina
should be avoided to prevent dislodgment of the (vibrating line).
denture bases. c. Support for a maxillary complete denture is pro-
D. Phonetic considerations in the patient with complete vided by the maxillary and palatine bones.
dentures. 2. Limiting structures of the mandibular denture.
1. Speech sounds. a. The mandibular anterior labial area extends from
a. Fricatives or labiodental sounds f, v, ph (e.g., 51, the labial frenum to the right and left buccal
52) are made between the maxillary incisors con- frenums. The action of the mentalis muscle and the
tacting the wet/dry lip line of the mandibular lip mucolabial fold determines the extension of the
(labiolingual center to the posterior third of the denture flange in this area. The mentalis elevates
mandibular lip). These sounds help determine the the lower dentures unless this border is established
position of the incisal edges of the maxillary ante- by accurate border molding.
rior teeth. b. The mandibular labial frenum is a band of fibrous
b. Linguoalveolar sounds or sibilants (sharp sounds: s, connective tissue that helps attach the orbicularis
z, sh, ch, and j, with ch and j being africatives) are oris muscle. A wide opening stretches and creates
made with the tip of the tongue and the most ante- a narrow sulcus that limits the extension of the
rior part of the palate or lingual surface of the denture border and the thickness of the denture
teeth. These sounds help determine the vertical base and affects the position of the mandibular
length and overlap of the anterior teeth. The teeth. If the teeth are set too far labial, stability is
tongues anterior dorsum forms a narrow opening adversely affected.
near the midline. When there is a small opening, c. The buccal vestibule extends posteriorly from the
the result is a whistling sound. If the space is large, buccal frenum to the lateral posterior corner of the
the s sound will be developed as an sh sound, like retromolar pad. The buccal vestibule is influenced
a lisp. A whistling sound with dentures is indica- by the buccinator muscle, which extends from
tive of having a posterior dental arch form that is the modiolus anteriorly to the pterygomandibular
too narrow (sounds like 61, 62, church). raphe posteriorly and has its lower fibers attached
c. Linguodental sounds (tip of the tongue slightly to the buccal shelf and the external oblique ridge.
between the maxillary and mandibular teeth, such Proper extension in this area provides the best
as this, that, those) help determine the labio- support for the lower denture. The buccinator
lingual position of the anterior teeth. The way th muscle fibers run in an oblique fashion and have
sounds are made provides information regarding little displacing action. This area is referred to as
the labiolingual position of the anterior teeth. If the the buccal shelf. Proper extension is necessary to
tip of the tongue is not visible, the teeth most likely distribute the load of mastication more widely.
are too far anterior (except in class II malocclusion d. In the masseter area, the denture is limited in a
or where there is excessive vertical overlap). The lateral direction by the action of this muscle. When
opposite occurs where the tongue extends too far the patient occludes with force, a medial force
outthe teeth are most likely too far lingual. is exerted against this area of the denture base. If
(1) Vertical dimensionevaluate during pronun- this border is overextended, extreme soreness can
ciation of the s sound; the interincisal result.
e. The retromolar pad marks the distal termination (2) Cohesion (attraction of molecules for each
of edentulous ridge. This structure needs to be other) depends on the following.
covered for support and retention. The integrity of (a) Area covered.
bone in this area is maintained and allows for (b) Type of saliva (thick, ropyunfavorable;
support. thin, waterygreater retention).
f. In the lingual frenum area, the borders must be (3) Atmospheric pressure.
established with movements of the tongue. The (a) Proportionate to area covered.
denture should not be overextended; excessive (b) Depends on peripheral seal.
reduction can result in almost total loss of denture (c) Effective only when dislodging forces
retention. The genioglossus muscle influences the applied.
length of this flange during normal movements of (4) Mechanicalridge size, shape (undercuts), and
the tongue. interridge distance.
g. The sublingual gland areamaximum extension G. Management of abused tissues.
desired without overextension. The tongue may 1. Treatment plan for tissue recovery.
rest on this area, helping to retain the denture. a. Removal of dentures.
h. The mylohyoid areathe flange in this area must (1) Abnormal mucoperiosteum beneath the den-
accommodate the movement of the muscle in tures is best treated by complete removal of the
deglutition. In most instances, the flange extends dentures until the tissues return to a normal
below the mylohyoid ridge. Initially, the extent of size, shape, color, consistency, and texture.
this flange is determined by the elevation of the Even the most healthy mouth should receive a
floor of the mouth when the patient wets the lips 24-hour rest period.
with the tip of tongue. It is then modified to accom- b. Dentures should be kept clean after meals by
modate this muscle for deglutition. rinsing them and brushing them (soft brush with
i. The retromylohyoid areaperhaps the most diffi- no abrasives) at least once a day to remove plaque
cult region to manage. This area is limited posteri- buildup. They should be soaked for at least 30
orly by the action of the palatoglossus muscle and minutes in a denture disinfectant solution, which
inferiorly by the lingual slip of the superior con- is commercially available.
strictor muscle. These muscles are activated on c. If the patient has dry mouth (xerostomia), a saliva
swallowing and if impinged on, a sore throat substitute or continuous sips of water may be
develops. needed.
3. Maxillary and mandibular lip support in a patient d. C. albicans is normal in the oral cavity, but under
with complete dentures is provided by the facial sur- trauma or antibiotic usage it may cause generalized
faces of teeth and the denture base. inflammation (candidiasis). It may involve the
F. Retention and stability related to final impression and corners of the mouth (angular cheilitis), which
occlusion. is common in patients with diminished vertical
1. Denture support refers to resistance to vertical seating dimension.
forces. e. Therapy.
2. Denture stability is necessary to resist dislodgment of (1) Nystatin oral rinse four times a day: hold in the
a denture in the horizontal direction. mouth for 2 minutes, then expectorate.
3. Denture retention is the ability of the denture to with- (a) Nystatin oral suspension (contains sugar
stand dislodging forces exerted in the vertical plane. caution with diabetic patients).
a. Surfaces of a denture that play a part in retention. (b) Dispensed: 60mL of 100,000 units/mL.
(1) Intimate contact of the denture base and its (c) Instructions: 4mL three times daily. After
basal seat. each meal, rinse mouth for 2 minutes.
(2) Teethno occlusal prematurities to break (2) Nystatin (with triamcinolone acetonide)
retention. creamused for angular cheilitis.
(3) Design of the labial, buccal, and lingual (a) Dispensed: 15-g tube.
polished surfacesconfiguration harmonious (b) Instructions: apply to affected area a small
with forces generated by the tongue and amount four times daily (after meals and
musculature. bedtime) for 14 days.
b. Factors that influence denture impression surface. (3) See Section 8, Pharmacology, for more options.
(1) Adhesionsaliva to denture and to tissues: f. Resilient liners for denturesif the tissues are
primary retentive force. abused, the use of soft acrylic resin liners for
(a) Proportionate to area covered. several days may be needed for complete recovery.
(b) Close adaptationtissue thickness, tissue These are placed inside the patients old dentures
health, tissue displacement. to provide an even, cushioned bearing against the
mucoperiosteum and aid recovery during periods teeth that will be extracted on the day of the
when the patient must wear dentures. denture delivery.
H. Immediate dentures. d. For a detailed description of the technique, review
1. Advantages. Zarb and Bolender (2004).
a. The patient avoids the embarrassing period of I. Overdentures.
being without teeth. 1. The advantage is the retention of roots, which
b. Immediate dentures produce the least possible decreases bone resorption, while maintaining the
change in the patients facial appearance because proprioceptive fibers within the periodontal
it enables one to place the individual artificial ligament.
teeth in the exact positions that the natural teeth 2. Selection of maxillary teeth as overdenture abut-
occupied. ments (Table 9-1).
2. Disadvantages. J. Insertion and postinsertion.
a. Wax try-in may not be possible, depending on how 1. Insertion.
many teeth remain before the delivery day. The a. Check intaglio surface of denture with finger for
remaining teeth are extracted at the same time that nodules or sharp places.
the denture is scheduled to be delivered. b. Check contour of polished surface.
b. More time is required for construction and c. Check extension of peripheries with pressure-
adjustment. indicating paste. Reduce lingual flanges in molar
c. Greater cooperation from the patient is necessary. area to actual floor of mouth with tongue in oppo-
d. Earlier need for rebasing. site cheek.
3. Technique. d. Check thickness of flanges and any possible inter-
a. Most procedures are similar to the construction of ference of the coronoid process against buccal
conventional complete dentures. The main differ- flange of maxillary denture.
ence is in the impression, which can be challenging e. Check freedom of frenal and muscle attachments.
because of severe tooth and ridge undercuts. Tray f. Check for pressure areas on impression surface of
modifications and impression material selection dentures with pressure-indicating paste. Use digital
are important to deal with this problem. pressure only, one denture at a time. Special atten-
b. The denture teeth are placed by removing the teeth tion is given to hard palate and mylohyoid ridge
from the cast and placing them in a similar posi- areas.
tion the natural teeth occupied when the teeth g. Complete final maxillomandibular relation proce-
were in an acceptable vertical and horizontal dures and correction of occlusion. At the time of
position. placement of complete dentures, small occlusal
c. A second problem is that an esthetic tooth try-in discrepancies are often noted, even though a
generally is not possible because of the presence of laboratory remount has been done to correct
Table 9-1
Considerations in Selection of Maxillary Teeth as Overdenture Abutments
MAXILLARY
TEETH ADVANTAGES DISADVANTAGES
Central incisors Ideal location; provide protection of the Proximity and alveolar prominence may complicate use
premaxilla
Lateral incisors Widely separated, facilitating plaque control Diminished root surface area
Tissue undercuts do not pose a problem
Path of placement/removal is not compromised
Ability to create a flange/peripheral seal
Canines Longest root of anterior teeth Diverging facial tissue undercuts
Overcontoured flanges
Excessive lip support
Potentially uncomfortable placement/removal of
prosthesis
Complicates placement of prosthetic teeth
Internal relief to accommodate canines may weaken,
create a food trap, compromise peripheral seal
From Zarb GA, Bolender CL: Prosthodontic Treatment for Edentulous Patients, ed 12. St. Louis, Mosby, 2004.
laboratory errors. If this is the case, use articulating 3.0 Removable Partial Prosthodontics
paper (preferably horseshoe-shaped) to determine
premature contacts in CR and in excursions after A. Kennedy classification system (Figure 9-4).
CR is corrected. 1. Class Ibilateral edentulous areas located posterior
2. Postinsertion. to the remaining natural teeth.
a. If major occlusal discrepancies are present, a new 2. Class IIunilateral edentulous area located posterior
interocclusal record is made with Aluwax or with to the remaining natural teeth.
an elastic registration material. 3. Class IIIunilateral edentulous area with natural
b. Occlusal adjustment is checked most accurately in teeth remaining both anterior and posterior to it.
an articulator with accurately remounted dentures 4. Class IVsingle, but bilateral (crossing the midline),
with an interocclusal record. edentulous area located anterior to the remaining
c. Cheek biting is due to insufficient horizontal overlap teeth.
between maxillary and mandibular teeth. It occurs B. Applegates rules governing the application of Kennedy
between the facial surface of mandibular teeth and classification system.
the central aspect of the maxillary teeth. Reducing 1. Rule 1classifications should follow rather than
the facial of mandibular posterior teeth in question precede any extractions of teeth that might alter the
can solve the problem. original classification.
d. Overextension usually causes dislodgment of the 2. Rule 2if a third molar is missing and not to be
denture. replaced, it is not considered in the classification.
Figure 9-4 Representative examples of partially edentulous arches classified by the Kennedy, Bailyn, and Skinner
methods. (From Carr AB, McGivney GP, Brown, DT: McCrackens Removable Partial Prosthodontics, ed 11. St. Louis, Mosby, 2005.)
3. Rule 3if a third molar is present and is to be used more rigid designs cannot be used. It is com-
as an abutment, it is considered in the classification. monly used when a large, inoperable palatal
4. Rule 4if a second molar is missing and is not to be torus exists or when anterior teeth need
replaced, it is not considered in the classification. replacement.
5. Rule 5the most posterior edentulous area always (5) Single palatal bara palatal bar, by definition,
determines the classification. is less than 8mm in width because the strap
6. Rule 6edentulous areas other than those determin- width is greater than 8mm. The bar must be
ing the classification are referred to as modifications centrally located in the framework and needs
and are designated by their number. bulk to be rigid to provide the needed cross-
7. Rule 7the extent of the modification is not consid- arch support.
ered, only the number of additional edentulous areas. (6) Anterior-posterior palatal barssimilar to the
8. Rule 8there can be no modification areas in class single bar and are configured similarly to the
IV arches. anterior-posterior palatal strap. The main dis-
C. Components of an RDP and their use. advantage is the bars needed bulk.
1. Major connectors. b. Mandibular arch.
a. The function of the major connector is to connect (1) Lingual barshaped like a half-pear tapered
all the RDP components of one side of the arch toward the tissue in the superior border and
with the opposite side to unite them. has its greater bulk at the inferior border. For
b. Provides stability to resist displacement while in a lingual bar, the depth of the vestibule should
function. exceed 7 to 8mm. This is the simplest and
c. Major connector should be rigid and not be most commonly used major connector.
placed on movable tissue. (2) Lingual platethis major connector may be
d. Undercut areas and soft and bony prominences used when the depth of the lingual vestibule
(e.g., tori, median palatal suture) should be is less than 7mm, when additional loss of
avoided, removed, or relieved, depending on the teeth is anticipated, when lingual tori are
severity. present, and when all posterior teeth are to be
e. Relief should be provided to prevent tissue replaced bilaterally.
impingement secondary to distal extension (3) Labial bar (swinglock)a hinged continuous
denture rotation. labial bar located buccal and distal to the
2. Types of major connectors. remaining dentition. It has a latching mecha-
a. Maxillary arch. nism opposite to the hinge. It is indicated
(1) Anterior-posterior palatal strapthe most when there is a missing canine (e.g., teeth #22,
rigid major connector for the amount of tissue #23, #24, #25, #26), where there are unfavor-
covered; used in almost any Kennedy class of able tooth or soft tissue contours, and when
partial design, especially class II and IV. All there are teeth with questionable periodontal
major connectors should cross the midline at prognosis.
a right angle rather than on a diagonal. 3. A minor connector is a rigid component that con-
(2) Single palatal strapindicated in tooth-borne nects the major connector or base with other com-
RDP (Kennedy class III) with bilateral, short- ponents of the partial denture such as rests, indirect
span edentulous areas. The palatal strap retainers, and clasps.
should be wide and thin for strength and 4. Beading is the procedure of scribing a rounded
comfort. The anterior border should be pos- groove (0.05mm) outlining the anterior and poste-
terior to the rugae. rior borders of a maxillary major connector. Beading
(3) Palatal platecan be designed as a wide an RDP adds strength to the major connector and
palatal strap short of the rugae area for distal maintains tissue contact to prevent food impaction.
extension RDP where more than the anterior 5. Direct retainerthe purpose of a clasp is to retain
teeth are present. A complete palatal plate is the RDP by means of the abutments. Clasps need
the most rigid of all major connectors and is adequate encirclement (greater than one half the
indicated when all posterior teeth are missing tooth circumference), retention (retentive arm), sta-
bilaterally; in a Kennedy class I, modification bility (minor connector and rest), support (rest),
1 RDP; and for periodontally compromised and passivity when seated (engaging the undercut
teeth, shallow vault, small mouth, or flat or when a dislodging force is applied) (Table 9-2). To
flabby ridges. Various design configurations prevent horizontal movement of the clasp, this
exist, combined with acrylic resin coverage should encircle the tooth more than 180 degrees or
(see Carr etal., pp. 49-51). one half the circumference of the tooth.
(4) U-shaped palatal (horseshoe)the least rigid a. Retentive clasps should become active only when
maxillary connector; used only when other, dislodging forces are applied to them.
Table 9-2 c. Clasp selection guidelines.

(1) RPI (rest, proximal plate, I bar) and RPC or
Function and Position of Clasp
RPA (rest, proximal plate, and a cast circum-
Assembly Parts
ferential clasp or an Akers clasp) designs are
COMPONENT generally used in Kennedy class I and II arch
PART FUNCTION LOCATION forms.
Rest Support Occlusal, lingual, (2) Reduction in the torqueing force on abutment
incisal teeth is achieved with the use of a wrought
Minor Stabilization Proximal surfaces wire clasp system; indicated for periodontally
connector extending from a weakened teeth or endodontically treated
prepared marginal
teeth.
ridge to the
junction of the (3) A wrought wire direct retainer is indicated if
middle and retention is placed on the opposite side of the
gingival one third fulcrum line from the edentulous ridge.
of abutment crown (4) Kennedy class III arch forms use the circum-
Clasp arms Stabilization Middle one third of ferential design. The occlusal rest seats are
(reciprocation) crown located adjacent to the edentulous spaces.
Retention Gingival one third of
(5) In a distal extension situation, the order of
crown in measured
undercut preference of use of clasp assembly is RPI,
RPC, and wrought wire.
From Carr AB, McGivney GP, Brown DT: McCrackens Removable Partial
Prosthodontics, ed 11. St. Louis, Mosby, 2005. 6. A reciprocal clasp or stabilizing clasp arm originates
from the minor connector and rest. The reciprocal
clasp should contact the tooth on or above the
height of contour of the tooth, allowing for insertion
and removal with passive force. Generally, they are
b. There are two types of direct retainers. placed on the lingual side.
(1) Intracoronal retainercomposed of a prefab- 7. The indirect retainer is the component of an RDP
ricated machined key and keyway (precision located on the opposite side of the fulcrum line to
attachment). They are more esthetic than the the extension base. It assists the direct retainer to
extracoronal retainer because they eliminate prevent displacement of denture base in an occlusal
clasps, and the vertical rest directs the forces direction. It consists of one or more rests, their
through the horizontal axes of the abutment minor connectors, and proximal plates adjacent to
teeth. the edentulous areas. The indirect retainer should
(2) Extracoronal retainerthese are the most always be placed as far as possible from the distal
common. extension base.
(a) Suprabulge (originate above the survey 8. Rests are critical for the health of the soft tissues
line). underlying the denture resin basis and the minor
(i) Circumferential clasp. and major connectors. It should prevent tilting
(ii) Ring clasp. action and should direct forces through the long
(iii) Combination clasp. axis of the abutment tooth.
(iv) Embrasure clasp. a. Types of rests.
(v) Manufactured attachments with inter- (1) Occlusal rest.
locking devices (Dalbo attachments) (a) Has a rounded (semicircular) outline
or the use of spring-loaded devices form.
that engage a tooth contour to resist (b) One third facial lingual width.
occlusal displacement. These devices (c) One half width between cusps.
have manufactured attachments with (d) 1.5mm deep for base metal.
flexible clips or rings that engage a (e) Floor inclines apically toward center.
rigid cast or attached component to (f) The angle formed with the vertical minor
the external surface of an abutment connector is less than 90 degrees.
crown. (2) Cingulum rest.
(b) Infrabulge (originate below the survey (a) Inverted V or U shape.
line). (b) Mesiodistal length 2.5 to 3mm.
(i) I bar. (c) Labiolingual width 2mm.
(ii) T bar. (d) Incisoapical depth 1.5mm.
(iii) Bar type. (e) Generally contraindicated for mandibular
(iv) Y type. central and lateral incisors.
(3) Incisal rest. 2. Cobalt-chromium RDPs fracture when the physical

(a) Rounded notch at an incisal angle. properties of an alloy are altered by the following.
(b) 2.5mm wide; 1.5mm deep. a. Cold-workingreduces the percentage elongation.
(c) Used as an indirect retainer. This causes an increase in hardness, which makes
(d) Less favorable leverage than lingual rest. the alloy more susceptible to fracture. Chronic
(e) Seldom used because of esthetic com flexure of the clasp assembly as an RDP is seated
promise. and dislodged as well as during function has the
9. Proximal platea metal plate that contacts the prox- effect of work hardening.
imal surface or guide plane of an abutment tooth. b. These alloys are known to shrink approximately
10. Guide planestwo or more parallel surfaces in the 2.3%. This shrinkage is irregular because of irregu-
abutment teeth that provide a path of insertion and larities in framework design, and the result is
removal and can contribute to the retention of an porosity. Sprues used in the thicker sections can
RDP. Guiding planes are parallel to the path of reduce shrinkage.
placement of the RDP, preferably to the long axes of c. A low percent elongation is directly related to
the abutment teeth. They should be about one third greater brittleness. Carbon is present and reacts
of the buccolingual width of the tooth and extend 2 with other constituents to form carbides. These last
to 3mm vertically from the marginal ridge in the during casting and appear in the grain boundaries,
cervical direction. which embrittle the alloy.
D. Type of support for RDPs. d. Cobalt-chromium alloys are more rigid compared
1. Tooth-borne RDPs should have the rests located next with gold and palladium alloys.
to the edentulous area, providing less opportunity for
the framework to flex, and assist in proper placement
together with the guide planes. 4.0 Fixed Prosthodontics
2. Distal extension RDPs rotate when a force is directed
on the denture base because of displacement of the A. Tooth preparation for cast fixed prostheses (see
soft tissue of the residual ridge and the ligament of Rosenstiel etal.).
the abutment teeth. The altered cast technique records 1. Conservation of tooth structure by partial coverage
the form of the edentulous segment by means of the instead of complete coverage whenever possible is
metal RDP framework, which holds the custom tray preferred.
material. 2. Minimal taper between axial walls conserves tooth
E. Insertion and postinsertion. structure, prevents undercuts, enhances resistance,
Just as in the FDP, the tooth-supported RDP should and enhances retention (6-degree taper between
provide direct resistance to functional forces. Changes walls is recommended).
in tissue support need to be evaluated with time in 3. Remove tooth structure evenly, considering the
the tooth tissuesupported RDP to maintain proper morphology of the pulp.
stability. 4. Tooth preparation should allow sufficient space for
F. Material science. developing contours and occlusal morphology that
1. Acrylic resinsthe mechanical properties of acrylic is biologically, technically, and esthetically func-
resin denture bases are affected by several factors. tional (see buccolingual dimension later under Con-
a. The molecular weight of the polymer is indicative siderations for restoring teeth in a biological,
of how well the polymethyl methacrylate was mechanical, and esthetic form). The labial reduc-
cured. The greater the molecular weight, the better tion should be in two planes to avoid overtapering
the polymerization and the harder the resin. or lack of occlusal clearance or insufficient space for
b. The degree of cross-linking within the final poly porcelain.
mer is directly proportional to the degree of 5. Prepare margins that are readable and compatible
polymerization. with the materials selected and the design of the
c. A polymer with a greater molecular weight is final restoration.
formed if more cross-linking occurs. 6. Margins ideally should be placed supragingivally or
d. Shrinkage of an acrylic resin occurs but is increased at the gingival crest whenever possible, for mainte-
when excessive monomer is incorporated to the nance care, ease of preparation, and impression.
polymer during the mixture. The volumetric 7. Well-executed finish lines that are smooth and even
monomer/polymer ratio is 1:3. facilitate tissue displacement, impression making,
e. Porosity on an acrylic resin denture base is caused die fabrication, waxing, and finishing procedures.
by underpacking with resin at the time of process- 8. Foundation restorations or cores should be built to
ing or a thick denture base heated too rapidly. restore missing tooth structure before preparing
f. Chemical composition of denture base resins. teeth for crowns.
9. Surgical crown lengthening can improve the outcome and II gold alloys are used for intracoronal cast
of a short clinical crown or when the placement of restorations. Type III and IV gold alloys or an alter-
a margin impinges on the normal soft tissue attach- native to gold alloy are used for crowns and FDPs.
ment. It is important to maintain the biologic width g. A minimum metal thickness of 1.5mm over centric
(the combined width of the connective tissue attach- or occlusal bearing cusps and 1.0mm over non-
ment and the junctional epithelium, which averages bearing or noncentric cusps is needed to withstand
approximately 2mm). occlusal forces when metal alone is used and
10. Factors that affect retention are magnitude of the 2.0mm when porcelain is used.
dislodging forces (e.g., sticky food), geometry of the h. Sufficient space for metal (0.5mm) at the margin
tooth preparation, roughness of the fitting surface is required to prevent distortion during function
of the restoration, the materials being cemented, and construction of the restoration (casting, por-
and the film thickness of the luting agent. celain firing).
11. Cements act by increasing the frictional resistance i. Adequate porcelain thickness (1.5mm minimum)
between tooth and restoration. The cement grains is needed to obtain good esthetic results.
prevent two surfaces from sliding, although they do j. The appropriate retainer for a tooth with a short
not prevent one surface from being lifted from clinical crown is a complete crown.
another. k. Partial veneer crowns include three quarter and
12. Grooves should be included for additional retention seven eighths crowns. Their advantages include
and resistance in short clinical crowns or when conservation of tooth structure, margins being
retention is compromised. accessible for finishing procedures and inspection,
13. Grooves or boxes added to a preparation with good and margins being accessible for hygiene.
retention do not increase retention significantly, but 2. A pontic design can be classified in two categories:
where a groove limits the path of withdrawal, reten- mucosal contact and nonmucosal contact pontics
tion is improved. (Table 9-3).
14. Teeth with a large surface area are more retentive a. Mucosal ponticsridge lap, modified ridge lap,
(e.g., long axial walls versus short; molars versus ovate, conical, or bullet shape. All of these pontics
premolars). should be concave and passively contact the ridge.
15. Root canaltreated teeth restored with core build- b. Nonmucosal ponticssanitary (hygienic) and
ups or post and cores can serve as abutments. modified sanitary (hygienic). These are generally
Teeth with short roots or little remaining coronal used in nonesthetic areas.
structure are not recommended because failures c. A saddle pontic design covers the ridge labiolin-
can occur. gually, forming a concave area that is not cleansable
B. Considerations for restoring teeth in a biologic, and for that reason is not used.
mechanical, and esthetic form. 3. Connectors for FDP.
1. The following are considerations when restoring a. Rigid connectors.
teeth. (1) Cast (one-piece casting).
a. Axial contours should correspond to the emergence (2) Soldered (see later under Dental Materials).
profile (usually flat or concave) of the tooth to b. Nonrigid connectorindicated when it is impossi-
prevent plaque accumulation, gingival inflamma- ble to obtain a common path of insertion between
tion, and bone loss. FDP abutments.
b. The buccolingual dimension of a cast restoration is C. Tissue management for making impressions.
usually determined by the occlusal morphology of 1. Fluid controlsaliva can be controlled by the
the opposing tooth. following.
c. Occlusal point contacts between opposing teeth a. Mechanical means (saliva ejectors, cotton rolls,
are preferred to broad, flat occlusal contacts to paper wafers).
prevent wear. b. Medications such as atropine, propantheline, and
d. Two occlusal schemes are recognized: cusp hyoscyamine act as antisialogogues (reduce sali-
marginal ridge and cusp-fossa. Class I occlusion vary secretions) and should be used with caution.
(in general) and unworn teeth have a cusp (1) Anticholinergic drugs should not be prescribed
marginal ridge scheme. A cusp-fossa arrangement for patients with glaucoma, especially narrow-
is generally found in class II malocclusion. angle glaucoma. In the latter case, these drugs
e. Supragingival margins are preferred over subgingi- can lead to a rapid increase in intraocular
val (see previously under Tooth preparation for pressure and blindness. Anticholinergic drugs
cast fixed prostheses). should be used with caution in patients with
f. The material used must provide sufficient strength heart disease and patients with urinary
to prevent deformation during function. Type I retention.
Table 9-3
Pontic Designs
PONTIC RECOMMENDED
DESIGN APPEARANCE LOCATION ADVANTAGES DISADVANTAGES INDICATIONS CONTRAINDICATIONS MATERIALS
Sanitary/ Posterior mandible Good access for Poor esthetics Nonesthetic zones Where esthetics is All-metal
hygienic oral hygiene important
2 mm Impaired oral Minimal vertical

hygiene dimension
Saddle- Not recommended Esthetic Not amenable to Not recommended Not recommended Not applicable
ridge-lap oral hygiene
Conical Molars without esthetic Good access for Poor esthetics Posterior areas Poor oral hygiene All-metal
requirements oral hygiene where esthetics Metal-ceramic
is of minimal All-resin
concern
Modified High esthetic requirement Good esthetics Moderately easy to Most areas with Where minimal esthetic Metal-ceramic
ridge-lap (e.g., anterior teeth and clean esthetic concern concern exists All-resin
premolars, some All-ceramic
maxillary molars)
Ovate Very high esthetic Superior Requires surgical Desire for optimal Unwillingness for surgery Metal-ceramic
requirement esthetics preparation esthetics All-resin
Maxillary incisors, Negligible food Not for residual High smile line Residual ridge defects All-ceramic
canines, and premolars entrapment ridge defects
Ease of cleaning
From Rosenstiel SF, Land MF, Fujimoto J: Contemporary Fixed Prosthodontics, ed 4. St. Louis, Mosby, 2006.
(2) Glycopyrrolate is an anticholinergic agent used silicone. Advantages, disadvantages, and recommended
as an adjunct in treatment of peptic ulcer that uses are summarized in Table 9-4. Their composition is
also reduces secretions. as follows:
2. Modes to achieve tissue displacementtissue dis- 1. Reversible hydrocolloidsThese are agar hydrocol-
placement is necessary to expose a prepared tooth loids that, when heated, change from gel to sol
finish line. This can be achieved by mechanical, a between 71C and 99C; on cooling, they return to
combination of mechanical and chemical, and surgi- the gel state at 30C. To heat and temper the mate-
cal means. rial, special equipment is needed. Special trays with
a. Mechanical modes. internal tubing that connect to a water line are used
(1) Cordsstretch the circumferential periodontal to cool the material.
fibers by placing them in the gingival sulcus. 2. Polysulfide polymerthe base paste main component
They can be twisted, braided, or knitted and be is a polysulfide polymer, a filler to add strength (tita-
preimpregnated or be impregnated with a nium dioxide), a plasticizer (dibutyl phthalate), and
chemical solution. They are supplied in differ- an accelerator (sulfur). The reactor (catalyst) contains
ent size ranges with different diameters, which lead dioxide and the same filler found in the base, a
are selected according to the size of the sulcus retarder to control the setting reaction (oleic or steric
to be displaced. acid). On polymerizing, water is released as a
b. Mechanical/chemicalimpregnated cords provide by-product causing dimensional contraction. The
better sulcus displacement. Chemicals that contain cast must be poured within 45 minutes.
aluminum or iron salts cause transient ischemia 3. Condensation siliconethe main component in the
and shrinkage of the gingival tissue and absorb base is polydimethylsiloxane with fillers such as
seepage of gingival fluid. Among these are alumi- calcium carbonate or silica. The accelerator may be
num chloride, aluminum sulfate, ferric sulfate, and stannous octate suspension and alkyl silicate. Similar
ferric chloride. Cords preimpregnated with epi- to polysulfides, the condensation silicones release
nephrine should be avoided because they can cause alcohol as a by-product reaction of their polymeriza-
tachycardia. tion, causing dimensional contraction.
c. Surgical. 4. Polyetherthe base paste contains a polyether
(1) Electrosurgerywhen a cord by itself might not polymer, colloidal silica as filler, triglycerides, and
achieve the desired tissue displacement, elec- nonphthalate plasticizer. The accelerator paste con-
trosurgery is indicated. To remove minor tains an alkyl-aromatic sulfonate, filler, and a plasti-
tissue, the electrosurgery unit is set to a fully cizer. This material has excellent dimensional stability
rectified electrical current (unmodulated alter- owing to the fact that no volatile by-products are
nating current) and a small electrode. formed. It is very susceptible to change by water
(2) Considerations when using electrosurgery. absorption. The material is very stable, but it is rec-
(a) It is contraindicated in patients using ommended that the cast be poured promptly for
medical devices such as cardiac pacemak- greater accuracy.
ers, a transcutaneous electrical nerve stim- 5. Addition silicone (vinyl polysiloxane)the addition
ulation unit, or an insulin pump and in reaction polymer is terminated with a vinyl group
patients with delayed healing. and cross-linked with hydride groups activated by
(b) Not recommended for thin attached a platinum salt catalyst. No reaction by-products
gingiva. are developed, but hydrogen gas release may occur
(c) Use plastic instruments (e.g., mirror, saliva if a reaction between moisture and residual hydrides
evacuators) instead of metal to prevent of the base polymer occurs. The result is a cast
burning and tissue destruction of the with small voids if the impression is poured soon
surface contacted. after removal from the mouth. Platinum or palla-
(d) Rapid, single, light stroke made with the dium is added by the manufacturer to act as a scav-
electrode. enger for the hydrogen gas. Another option is to
(e) When cutting, 5-second intervals should wait an hour before pouring to allow the release
be used. of gas.
(f) The electrode should not contact metallic E. Metal-ceramic restorations.
restorations or tooth structure because this 1. Classifications of alloys for metal-ceramic resto
may cause irreversible pulp damage. rations.
D. Impression materials. a. Noble metals are gold (Au), platinum (Pt), and pal-
Elastic impression materials for final impressions for ladium (Pd). (Silver [Ag] is not considered noble;
fixed restorations include reversible hydrocolloid, poly- it is reactive and improves castability but can cause
sulfide, condensation silicone, polyether, and additional porcelain greening.)
Table 9-4
Available Elastic Impression Materials
RECOMMENDED
ADVANTAGES DISADVANTAGES USES PRECAUTIONS
Irreversible Rapid set Poor accuracy and Diagnostic casts Pour immediately
hydrocolloid Straightforward surface detail Not suitable for
technique definitive casts
Low cost
Reversible Hydrophilic Low tear resistance Multiple preparations Pour immediately
hydrocolloid Long working time Low stability Problems with moisture Use only with stone
Low material cost Equipment needed
No custom tray required
Polysulfide High tear strength Messy Most impressions Pour within 1hr; allow
polymer Easier to pour than Unpleasant odor 10min to set
other elastomers Long setting time
Stability only fair
Condensation Pleasant to use Hydrophobic Most impressions Pour immediately
silicone Short setting time Poor wetting Take care to avoid bubbles
Low stability when pouring
Addition silicone Dimensional stability Hydrophobic Most impressions Delay pouring of some
Pleasant to use Poor wetting materials
Short setting time Some materials release H2 Take care to avoid bubbles
Automix available Hydrophilic formulations when pouring
imbibe moisture
Polyether Dimensional stability Set material very stiff Most impressions Take care not to break
Accuracy Imbibition teeth when separating
Short setting time Short working time cast
Automix available
b. High noble alloys (old term was precious metal) (4) Biologic compatibilitycan be a problem with
have a noble metal content of 60 wt% or greater Ni and Be in base metal alloys (allergies), and
and a gold content of 40% or greater. Be dust and vapors are carcinogens.
c. Noble alloys (old term was semiprecious metal) (5) Corrosion resistance.
have a noble metal content of 25% or greater. (6) The metal coefficient of thermal expansion
(Palladium-copper [Pd-Cu], palladium-silver [Pd- should be higher than the porcelain to leave the
Ag], and palladium-cobalt [Pd-Co] alloys have no porcelain in compression in a stronger state.
stipulation for gold.) b. Metal composition.
d. Base metal alloys (old term was nonprecious metal) (1) Colorwhite, silver, yellow, or gold, depending
contain less than 25% noble metals (nickel- on its alloy composition (percent of Au, Ag, Pd,
chromuim [Ni-Cr], nickel-chromium-beryllium and Pt).
[Ni-Cr-Be], cobalt-chromium [Co-Cr], titanium (2) Densitybase metals are least dense; consider
[Ti], and Ti alloys). the weight of long-span FDPs.
2. Desirable properties of alloys for metal-ceramic (3) Oxidative elementsmust be present for porce-
restorations. lain to bond to the alloy (tin, indium, and
a. Mechanical properties. gallium).
(1) High yield strengthminimizes permanent 3. Bonding of porcelain to metal.
deformation under occlusal force and porcelain a. The tooth preparation reduction for metal-ceramic
fracture secondary to framework deformation. restorations (1.5 to 2.0mm) must provide space
(2) High modulus of elasticity (stiffness)minimizes for metal (0.5mm) and porcelain (1.0 to 1.5mm).
flexure of long-span FDPs and porcelain frac- b. A metal substructure provides support and
ture secondary to framework deformation. increases the strength of the porcelain.
(3) Casting accuracybase metal alloys are less c. All internal angles where porcelain is veneered
accurate than gold. should be rounded to prevent stress concentration.
d. The metal-porcelain junction should be at a right when exposed to ultraviolet light emits reflected
angle to avoid porcelain fracture. light).
e. Occlusal contacts at least 1.5mm away from f. Opalescence is the light effect of a translucent
porcelain-metal junction. material (incisal edge of some teeth) appearing
f. Metal oxide formation is necessary for metal- blue in reflected light and red-orange in transmit-
ceramic bond (oxidation of a metal is accomplished ted light.
by heating the metal structure in a furnace before g. The Vitapan 3D-Master Shade Guide (Vita, Bad
the application of porcelain). Sackingen, German) is arranged in five lightness
g. The coefficient of thermal expansion of the porce- levels and a level for bleached teeth. Each lightness
lain must be slightly lower than that of the metal level has sufficient variations in chroma and hue to
to place the porcelain in slight compression when cover the natural tooth color space.
cooled. 6. Characterizationthe art of reproducing natural
h. Porcelain is stronger under compressive forces defects; this can be particularly successful in making
than it is under tensile forces. a crown blend with the adjacent natural teeth.
4. Metal-ceramic restorationporcelain is composed a. Chroma and hue adjustment.
primarily of feldspar (main constituent), quartz (to (1) The addition of yellow stain increases the
strengthen), kaolin (binder), and metallic oxides chroma of a basically yellow shade. Addition
(give opacity and color). Three layers of porcelain are of orange has the same effect on a crown as a
used to build a ceramic restoration. yellow-red hue. Too high a chroma is impos-
a. Opaque porcelain must mask the dark oxide color sible to decrease in hue or increase in value.
and provide the porcelain-metal bond. Bond (2) Hue adjustmentspink-purple moves yellow
strength depends on good wetting of the metal toward yellow-red, whereas yellow decreases
surface. Masking must be accomplished with the the red content of a yellow-red shade. These are
minimum thickness of opaqueabout 0.1mm the only two modifications that should be nec-
leaving maximum space to develop a natural essary because the hue of a natural tooth always
appearance with body and incisal porcelains. lies in the yellow-red to yellow range.
b. Body or dentin porcelain contains most of the color b. Value adjustmentsadding a complementary color
or shade and is used generally to build most of can reduce value. Violet is used on yellow restora-
the crown. tions, which has the added effect of mimicking
c. Incisal porcelain is the most translucent layer of translucency. Gray is not encouraged because it
porcelain. produces a semitranslucent effect and makes the
5. Shade selection and color. surface cloudy.
a. Hue refers to shade or color (red, green, yellow). In c. Staining can cause a loss of fluorescence in the
the Vita Lumin Vacuum Shade Guide (now called finished restoration and an increase in the meta-
Vita Classical Shade Guide; Vita, Bad Sackingen, meric effect (a mismatch under some lighting con-
Germany), A1, A2, A3, A3.5, and A4 are hues ditions). It usually results in decrease of value.
similar to the B, C, and D shades. The hue should d. Glazingthe degree of gloss or surface luster of a
be selected first. porcelain restoration depends on the autoglazing
b. Chroma is the saturation or intensity of the color procedure. Both time and temperature must be
or shade. Once the hue is selected (e.g., A, B, C), carefully controlled. During glazing, the surface
the saturation of that hue is selected (e.g., if the B layers of porcelain melt slightly, coalescing the par-
hue was selected, the saturation would be B1, B2). ticles and filling in surface defects. Glazing must
It is always better to choose a shade with a lower be performed without vacuum.
chroma, which is easier to alter with surface colo- 7. Metal-ceramic failures.
rant modifiers. a. Modes of failure in metal-ceramic restorations.
c. Value is the relative lightness or darkness of a (1) Adhesive failure modes.
color. Shade guides can be arranged in order of (a) Porcelain-metal interfaceoxide was not
increasing lightness to determine whether the formed.
value of a tooth is within the range of the shade (b) Oxide-metal interfacecontamination of
guide. metal.
d. Metamerism is the phenomenon where a color (c) Porcelain-oxide interfacecontamination
match under a lighting condition appears different of oxide surface.
under a different lighting condition. (2) Cohesive failure modes.
e. Fluorescence is the physical property where an (a) Porcelain-porcelaininclusions or voids;
object emits visible light when exposed to preferred type of failure.
ultraviolet light (e.g., the dentinal layer of a tooth (b) Oxide-oxideoxide layer too thick.
Table 9-5
Comparison of Available All-Ceramic Systems
BRAND
Ceramco IPS IPS Empress In-Ceram
Captek 3 Cerinate Empress Empress 2 Cosmo Finesse In-Ceram Spinell
Manufacturer Precious Dentsply Den-Mat Ivoclar Ivoclar Ivoclar Dentsply Vident Vident
Chemicals
Crystalline Leucite Leucite Leucite Leucite Lithium Lithium Leucite Alumina Alumina,
phase disilicate phosphate spinel
Recommended Crowns Inlays, Inlays, Inlays, Anterior Endodontic Inlays, Crowns, Crowns,
usage onlays, onlays, onlays, 3-unit foundation onlays, veneers veneers
veneers crowns, crowns, FDPs, crowns,
veneers veneers crowns veneers
Fabrication Sintered Sintered Sintered Heat- Heat- Heat-pressed Heat- Slip-cast Slip-cast
on pressed pressed pressed and and
metal sintered sintered
foil
Strength Low Low Medium/ Medium/ High Medium Medium/ High High
low low low
Fracture Medium/ Medium/ Medium/ Medium/ High Medium Medium/ High High
toughness low low low low low
Translucency Opaque Medium Medium Medium Medium Medium Medium Opaque Medium
Enamel Medium Medium High Medium Low * Medium High High
abrasiveness
Marginal fit Good Fair Fair Fair Fair * * Fair Fair
CAD/CAM, Computer-aided design/computer-aided manufacturer (or computer-assisted machining); FDP, fixed dental prosthesis.
*Not tested.
(c) Metal-metalnot clinically relevant; never 4. All-ceramic crowns with no glass content (zirconia
happens. and alumina) are luted to the tooth with conventional
(d) Fracture of a porcelain fused to metal res- or resin cements.
toration can usually be attributed to inad- 5. Machine grinding of ceramics can induce surface
equate framework design. cracks.
b. Long-span metal-ceramic FDPs may be subjected 6. Repeated loading (chewing) can cause extension of a
to bending and may cause cracking or fracture of preexisting defect or crack, reducing the longevity of
the porcelain because of its low ductility. the restoration.
F. All-ceramic restorations. G. Provisional restorations.
All-ceramic restorations are increasingly being used 1. Requirementsprotection, maintain periodontal
today on anterior and posterior teeth. The main health, occlusal stability, maintain tooth position,
purpose for their use is esthetics. The crystalline phase biocompatible, color match.
found on ceramics influences the mechanical and 2. Materials used for provisional restorations
optical properties of the material. For a summary of (Table 9-6).
the properties and use of all-ceramic systems, see a. Poly ethyl methacrylate.
Table 9-5. b. Polymethyl methacrylate.
1. All-ceramic restorations are more prone to fracture c. Microfilled composite.
if the preparation line angles are not rounded. d. Light-cured.
2. Ceramic inlays and onlays have better abrasion resis- 3. Types of materials to produce provisional
tance than composite resins. restorations.
3. All-ceramic crowns that are glass infiltrated (feld- a. Preformed crowns.
spathic, leucite, lithium disilicate) are etched with (1) Cellulose acetate tooth form.
diluted hydrofluoric acid and treated with a silane- (2) Polycarbonate crown form.
coupling agent and bonded to the tooth. (3) Aluminum crown form.
BRAND
In-Ceram YZ blocs Cercon Procera Procera Metal-
Zirconia Mark II ProCAD (inVizion) Zirconia Lava Alumina Zirconia ceramic
Manufacturer Vident Vident Ivoclar Vident Dentsply 3M ESPE Nobel Nobel Various
Biocare Biocare
Crystalline Zirconia- Feldspar Leucite Zirconia Zirconia Zirconia Alumina Zirconia Leucite
phase alumina
Recommended 3-unit Inlays, Inlays, Crowns, Crowns, Crowns, Crowns, Crowns, Crowns,
usage FDPs onlays, onlays, FDPs FDPs FDPs FDPs FDPs FDPs
crowns crowns
Fabrication Slip-cast CAD/ CAD/ CAD/ CAD/ CAD/ CAD/ CAD/ Cast
and CAM CAM CAM CAM CAM CAM CAM framework,
sintered and and and and and sintered
sintered sintered sintered sintered sintered porcelain
Strength Very high Medium/ Medium/ Very high Very high Very high High Very high Very high
low low
Fracture Very high Medium/ Medium/ Very high Very high Very high Very high Very high Medium
toughness low low
Translucency Opaque Medium Medium Opaque Opaque Opaque Opaque Opaque Opaque
Enamel High Medium * * * * * * Medium
abrasiveness
Marginal fit Fair Fair * * * * * Good
Table 9-6
Ranked Characteristics of Representative Provisional Restoration Resins
MATERIAL/CHARACTERISTIC A B C D E F G H I J K L M N
Jet (PMMA) 2* 2 3 1 1 3 1 2 1 1 2|| 1 3 1
Duralay (PMMA) 1 3 1 2 1 1 1 3 1
Trim (PRMA) 2 1 2 3 3 2 3 1 1 3 1 2 1
Snap (PRMA) 2 2 2 2 2 3 1 1 1 2 1
Protemp Garant (bis-GMA composition) 1* 1 1 2 2 1 2 3 2 2 1|| 2 1 2
Unifast LC (light-cured, PRMA) 2* 2 3 2** 2 1 3 1 2 3 2
Triad (light-cured, urethane DMA composition) 2 3 1 1 1 1 3 1 3 3 3 1 3
From Rosenstiel SF, Land MF, Fujimoto J: Contemporary Fixed Prosthodontics, ed 4, St. Louis, Mosby, 2006.
Column heads: A, marginal adaptation (indirect); B, temperature release during reaction; C, toxicity/allergenicity; D, strength (fracture toughness); E, repair strength
(% original); F, color stability (ultraviolet light); G, ease of trimming and contouring; H, working time; I, setting time; J, flowability for mold filling; K, contaminated
by free eugenol; L, special equipment needed; M, odor; N, unit volume cost.
Numbers in table: 1, most desirable; 2, less desirable; 3, least desirable.
PMMA, Polymethyl methacrylate; PRMA, poly(R methacrylate) (the R represents an alkyl group larger than methyl [e.g., ethyl or isobutyl]); Bis-GMA comp,
microfilled composite; Ureth. DMA comp., urethane dimethacrylate composite.
*Tjan AHL, etal: Marginal fidelity of crowns fabricated from six proprietary provisional materials. J Prosthet Dent 77:482, 1997.
Wang RL, etal: A comparison of resins for fabricating provisional fixed restorations. Int J Prosthodont 2:173, 1989.
Gegauff AG, Pryor HG: Fracture toughness of provisional resins for fixed prosthodontics. J Prosthet Dent 58:23, 1987.
Koumjian JH, Holmes JB: Marginal accuracy of provisional restorative materials. J Prosthet Dent 63:639, 1990.
|| Gegauff AG, Rosenstiel SF: Effect of provisional luting agents on provisional resin additions. Quintessence Int 18:841, 1987.
Castelnuovo J, Tjan AH: Temperature rise in pulpal chamber during fabrication of provisional resinous crowns. J Prosthet Dent 78:441, 1997.
**Doray PG, etal: Accelerated aging affects color stability of provisional restorative materials. J Prosthodont 6:183, 1997.
(4) Tin-silver crown form. (2) Zinc polycarboxylate cement is more viscous
(5) Nickel-chromium crown form. when mixed and has a shorter working time
b. Custom-made. than zinc phosphate cement. It adheres to tooth
(1) Impressions are made before preparing teeth structure owing to chelation to calcium.
with irreversible hydrocolloid or silicones. (3) Glass-ionomer cement adheres to enamel and
(2) Preformed thermoplastic sheets (cellulose dentin and releases fluoride. Its mechanical
acetate or polypropylene) adapted to a cast. properties are superior to zinc phosphate and
4. Types of provisional restorations. polycarboxylate cements (see Table 9-7).
a. Direct procedurethe material used (e.g., acrylic (4) Resin-modified glass-ionomer luting agents have
resin) is directly formed intraorally with the aid of properties similar to glass-ionomer cements
a material that has a predetermined tooth form but have higher strength and low solubility.
(e.g., a polycarbonate crown). They should not be used with all-ceramic res-
(1) Disadvantages. torations because of reports of ceramic frac-
(a) Potential tissue trauma from polymerizing ture, most likely the result of expansion from
resin. water absorption.
(b) Poorer marginal fit than indirect method. (5) Resin luting agents are unfilled resins that bond
b. Indirect procedurean unprepared cast is used to to dentin, which is achieved with organophos-
produce a template (e.g., a thermoplastic sheet). phonates (2-hydroxyethyl methacrylate or 4-
The tooth is prepared, and an impression is made methacryloyloxyethyl trimellitate anhydride).
of the prepared tooth. The template and the pre- These luting agents are less biocompatible than
pared cast are used to produce the provisional res- glass-ionomers if not well polymerized and
toration with the material of choice (e.g., acrylic they provide a greater film thickness than other
resin). cements. They are most effective when bonded
(1) Advantages. to tooth structure.
(a) No tissue trauma. I. Important points about occlusion.
(b) Good marginal adaptation. 1. Horizontal forces on teeth are the most destructive to
H. Delivery of cast restorations. the periodontium.
1. Sequence for crowns and FDPs. 2. A nonworking condyle moves down, forward, and
a. Internal surface fit. medially.
b. Adjustments of proximal contacts and pontic- 3. Nonworking interferences generally occur on inner
ridge contact relationship. aspects of the facial cusps of mandibular teeth.
c. Marginal integrity. 4. In selective grinding or occlusal equilibration, cusp
d. FDP stability. tips should not be reduced; they can be narrowed,
e. Axial contours. or the opposing fossa or marginal ridge can be
f. Occlusion (centric and eccentric contacts). adjusted.
2. Luting agents (cements)the thickness of the cement 5. Terminal hinge position is when the condyles are in
film at the margins should be minimized to reduce the articular fossae and the mandible is capable of
dissolution of the luting agent. Through careful tech- pure rotary opening. In CR, the mandible can
nique, a marginal adaptation less than 30m can be rotate around the horizontal axis 20 to 25 mm. It
obtained consistently. is measured between the maxillary and mandibular
a. Factors that increase the cement space for crowns. incisal edges of the teeth. The horizontal axis
(1) Use of die spacers. around which the hinge movement occurs is referred
(2) Increased expansion of the investment mold. as the hinge axis.
b. Comparison, indications, and contraindications 6. Translation is the motion of a body in which all of its
for luting agent types (Tables 9-7 and 9-8). points move in the same direction at the same time.
c. Properties and manipulation. When the condyle is said to translate, the condyle
(1) Zinc phosphate cement should be mixed by and the disc translate together during jaw opening
incremental additions every 15 to 20 seconds. beyond the point where motion is purely rotational.
Ensuring saturation of the powder with the Translation occurs within the superior cavity of the
liquid adds strength to the cement. A frozen joint between the disc-condyle complex and the
slab technique or decreasing the rate of articulator fossa. The lateral pterygoid is responsible
addition of powder to liquid retards the for condylar translation.
setting cement. The cement film thickness is 7. Canine protected occlusion is a form of mutually pro-
about 25m. Phosphoric acid is very acidic tected occlusion in which the canine teeth disocclude
(pH = 3.5). or aid in separating the posterior teeth in excursive
Table 9-7
Comparison of Available Luting Agents
IDEAL ZINC POLY- GLASS- RESIN COMPOSITE ADHESIVE
PROPERTY MATERIAL PHOSPHATE CARBOXYLATE IONOMER IONOMER RESIN RESIN
Film thickness Low 25 <25 <25 >25 >25 >25
(m)*
Working time Long 1.5-5 1.75-2.5 2.3-5 2-4 3-10 0.5-5
(min)
Setting time Short 5-14 6-9 6-9 2 3-7 1-15
(min)
Compressive High 62-101 67-91 122-162 40-141 194-200 179-255
strength (MPa)
Elastic modules Dentin = 13.2 Not tested 11.2 Not tested 17 4.5-9.8
(GPa) 13.7
Enamel =
84-130
Pulp irritation Low Moderate Low High High High High
Solubility Very low High High Low Very low High to very Very low to
high low
Microleakage Very low High High to very Low to very Very low High to very Very low to
high low high low
Removal of Easy Easy Medium Medium Medium Medium Difficult
excess
Retention High Moderate Low/moderate Moderate High Moderate High
to high
From Rosenstiel SF, Land MF, Fujimoto J: Contemporary Fixed Prosthodontics, ed 4, St. Louis, Mosby, 2006.
*White SN, Yu Z: Film thickness of new adhesive luting agents. J Prosthet Dent 67:782, 1992; see also Figure 31-2 in Rosenstiel etal (2006).
Rosenstiel SF, etal: Strength of dental ceramics with adhesive cement coatings. J Dent Res 71:320, 1992.
OBrien WJ: Dental Materials and Their Selection, ed 2. Chicago, Quintessence Publishing, 1997, p 351.
Cheylan JM, etal: In vitro push-out strength of seven luting agents to dentin. Int J Prosthodont 15:365, 2002.
movements of the mandible. When preparing maxil- line, orbitale, or incisal pin notch. This precise
lary or mandibular anterior teeth, a mechanical or positioning does the following.
custom anterior guide table is used to preserve a (a) Allows the teeth to be within a close radius
record of the degree of disocclusion given by the of the correct arc of closure when the artic-
linguoincisal concavity on maxillary teeth and the ulator is used in hinge movement.
buccoincisal contour of the mandibular teeth. (b) Allows the teeth to reproduce more accu-
8. Group function occlusion is seen when the maxillary rately the lateral arc during excursions.
and mandibular teeth of multiple posterior teeth (c) Minimizes occlusal discrepancies caused by
contact in lateral excursive movements on the changes in vertical dimension (e.g., mount-
working side. This type of occlusion is seen in some ing cast with interocclusal records).
natural dentitions and is used in restoring some den- (i) In complete denture construction, the
titions with the idea of distributing the occlusal facebow transfer record can be pre-
forces. served by means of a plaster index of
9. A facebow transfer positions the maxillary cast in the occlusal surfaces of the maxillary
three dimensions. denture before removing the denture
a. Relating the maxillary cast to the condylar ele- from the articulator and cast after pro-
ments anteroposteriorly. cessing and occlusal adjustment is
b. Relating the maxillary cast vertically with some completed.
third point of reference. J. Dental materials.
(1) Relating the maxillary cast with a tentative 1. Common materials used in prosthodontics and their
occlusal plane, which is parallel to the alatragus application (Table 9-9).
Table 9-8
Indications and Contraindications for Luting Agent Types
RESTORATION INDICATION CONTRAINDICATION
Cast crown, metal-ceramic crown, partial FDP 1, 2, 3, 4, 5, 6, 7
Crown or partial FDP with poor retention 1 2, 3, 4, 5, 6, 7
MCC with porcelain margin 1, 2, 3, 4, 5, 6, 7
Casting on patient with history of posttreatment sensitivity Consider 4 or 7 2
Pressed, high-leucite, ceramic crown 1, 2 3, 4, 5, 6, 7
Slip-cast alumina crown 1, 2, 3, 4, 6, 7 5
Ceramic inlay 1, 2 3, 4, 5, 6, 7
Ceramic veneer 1, 2 3, 4, 5, 6, 7
Resin-retained partial FDP 1, 2 3, 4, 5, 6, 7
Cast post-and-core 1, 2, 3, 5, 6 4, 7
KEY:
LUTING AGENT TYPE CHIEF ADVANTAGES CHIEF CONCERNS PRECAUTIONS
1. Adhesive resin Adhesive, low solubility Film thickness, history of use Moisture control
2. Composite resin Low solubility Film thickness, irritation Use bonding resin, moisture
control
3. Glass-ionomer Translucency Solubility, leakage Avoid early moisture exposure
4. Reinforced ZOE Biocompatible Low strength Only for very retentive
restorations
5. Resin ionomer Low solubility, low Water sorption, history of use Avoid with ceramic restorations
microleakage
6. Zinc phosphate History of use Solubility, leakage Use for traditional cast
restorations
7. Zinc polycarboxylate Biocompatible Low strength, solubility Do not reduce powder/liquid
ratio
FDP, Fixed dental prosthesis; MCC, metal-ceramic crown; ZOE, zinc oxideeugenol.
2. Gypsum. nuclei of crystallization per unit volume and

a. The setting expansion of any gypsum product is increases the amount of space between crystalliz-
a function of calcium sulfate dihydrate crystal ing nuclei, increasing porosity when drying. This
growth. Some is the result of thermal expansion. causes a decrease in the interaction of dihydrate
b. Dental gypsum classification. crystals and diminishes any outward thrust of the
(1) Type Iplaster, impression plaster. mass. Consequently, setting expansion is decreased.
(2) Type IImodel plaster. f. Potassium sulfate and sodium chloride accelerate
(3) Type IIIdental stone. setting of gypsum, whereas sodium citrate and
(4) Type IVdental stone, high strength (die borax retard setting.
stone). g. Manipulationwhen hand spatulating, powder is
(5) Type Vhigh strength. added and allowed to settle into the water for about
c. The particle size shape of dental gypsum products 30 seconds. This minimizes the amount of air
differs, requiring different water/powder ratios. incorporated into the mix during initial spatula-
Type I and II plasters require a higher water/ tion. Spatulation to wet and mix the powder uni-
powder ratio than type III and IV stones. formly with the water requires about 1 minute at 2
d. A thinner mix of a gypsum base product decreases revolutions per second. A power-driven mechanical
the degree of exothermia, decreasing setting spatulator requires that the powder initially be wet
expansion. by the water, as with hand mixing. The mix is spat-
e. Increasing the water/powder ratio increases the ulated for 20 seconds on the low-speed drive of the
setting time and decreases strength. The increase mixer. Vacuuming during mixing reduces the air
in water/powder ratio decreases the number of entrapped in the mix.
Table 9-9
Common Materials Used in Prosthodontics and Their Application
Amalgam Commonly used for conservative restorations where esthetics is not a concern. It is underused
as a core buildup material for crowns. Mechanical properties are inferior to cast metal and
ceramic restorations.
Composite Commonly used for conservative restorations where esthetics are desired. Also used as a core
buildup material with some inferior physical properties (moisture and thermal expansion)
compared with amalgam.
Cast metal Extracoronal restorations or crowns are used to replace tooth structure damaged secondary to
caries or trauma, as retainers for FDP, and as retainers for RDP. Strengthens and protects a
tooth.
Intracoronal restorations or inlay (gold) are used for conservative restorations with better physical
properties than amalgam. They require removal of more tooth structure than amalgam.
Metal-ceramic Similar to cast metal restorations but used where esthetics are a consideration because porcelain
is bonded to the metal.
Complete ceramic Crowns, inlays, and laminate veneers made with dental porcelain are used instead of the above
materials where good esthetics are desired.
Drawbacks include fracture potential and in some ceramic materials marginal fit.
FDP, Fixed partial prosthesis; RDP, removable dental prosthesis.
h. The poured cast should be allowed to set for 45 change in the phase structure of the alloy, making
to 60 minutes before separating it from the it more malleable for finishing procedures.
impression. c. Sprues should always be larger in diameter than the
i. Casts can be disinfected by immersion in a 1:10 cross-section area of the pattern where they are
dilution of sodium hypochlorite for 30 minutes or attached.
with iodophor spray. d. Crucibles should always be used with only one type
3. Investments and casting. of alloy to prevent contamination, regardless of the
a. Investments expand during setting, when heated type of casting being performed.
(thermal). When additional expansion is desired, 4. Solderingprocedure to join metal components by
use a hydroscopic technique by placing the in- heating a piece of metal (solder) that melts at a tem-
vested ring in water while setting. Investment ex- perature slightly lower than the metals to be joined
pansion provides a larger mold for the metal together.
being cast, which compensates for the contrac- a. The recommended gap or distance between the
tion that the metal experiences when it solidifies. parts to be joined should be 0.25mm (the thick-
Investments commonly used in dentistry are as ness of a typical business card) for accuracy.
follows. b. Soldering flux dissolves surface oxides and allows
(1) Gypsum-bonded investments are used for the melted solder to wet and flow onto the adjoin-
casting alloys containing 65% to 75% gold at ing alloy surfaces. Flux is composed of borax,
temperatures near 1100C. They have a gypsum potassium fluoride (some fluxes), and boric acid.
binder. c. Antiflux restricts the flow of solder away from
(2) Phosphate-bonded investments are used for undesired surfaces and is applied on areas such as
casting metal-ceramic alloys because of their occlusal grooves and margins. Graphite and iron
capability to withstand high temperatures oxide (rouge) are antifluxes.
(1100C). They have a metallic oxide and
phosphate binder. Gas and oxygen torches are Bibliography
used for melting metal-ceramic alloys. The glossary of prosthodontic terms. J Prosthet Dent 94:
(3) Silica-bonded investments are used for casting 10, 2005.
base metal alloys for frameworks for dental Anusavice KJ: Phillips Science of Dental Materials, ed 11.
prostheses. They have a silica gel binder. Philadelphia, Saunders, 2003.
b. Quenching is the procedure performed on a metal Beuer F, Schweiger J, Edelhoff D: Digital dentistry: an over-
when it is brought to an elevated temperature and view of recent developments for CAD/CAM generated
is cooled rapidly. It is usually performed when a restorations. Br Dent J 204:505, 2008.
complete gold crown is cast and immediately Carr AB, McGivney GP, Brown T: McCrackens Removable
quenched in water. This softens the alloy owing to Partial Prosthodontics, ed 11. St. Louis, Mosby, 2005.
Dawson PE: Evaluation, Diagnosis, and Treatment of Occlu- A. Widening of the periodontal ligament
sal Problems, ed 2, St. Louis, Mosby, 1989. B. Soft tissue sore area around the tooth
Okeson JP: Management of Temporomandibular Disorders C. Bone loss
and Occlusion, ed 5. St. Louis, Mosby, 2003. D. All of the above
Powers JM, Sakaguchi RL: Craigs Restorative Dental Mate- 8. Which of the following is true of an occlusal rest for
rials, ed 12. St. Louis, Mosby, 2006. an RDP?
Rosenstiel SF, Land MF, Fujimoto J: Contemporary Fixed 1. One third facial lingual width of the tooth
Prosthodontics, ed 4. St. Louis, Mosby, 2006. 2. 1.5mm deep for base metal
Zarb GA, et al: Prosthodontic Treatment for the Edentulous 3. 2.0mm labiolingual width of the tooth
Patient, ed 12. St. Louis, Mosby, 2004. 4. Floor inclines apically toward the center of the
tooth
A. All of the above
Sample Questions B. 1, 3, and 4
C. 1, 2, and 4
1. The impression material that is mainly composed of D. 3 and 4
sodium or potassium salts of alginic acid is ____. 9. A patient is unhappy with the esthetics of an anterior
A. Polyether metal-ceramic crown, complaining that it looks too
B. Irreversible hydrocolloid opaque in the incisal third. The reason for this is most
C. Polyvinyl siloxane likely ____.
D. Polysulfide A. Using the incorrect opaque porcelain shade
2. A patient with complete dentures presents with angular B. Inadequate vacuum during porcelain firing
cheilitis. A review of recent medical history revealed C. Not masking the metal well enough with the
that vitamin deficiency is not a factor. A possible pre- opaque
disposing factor is ____. D. The tooth was prepared in a single facial plane
A. Excessive vertical dimension of occlusion 10. An endodontically treated tooth was restored with a
B. A closed or insufficient vertical dimension of cast post-and-core and a metal-ceramic crown. The
occlusion patient complains of pain, especially on biting, 3
C. Improper balance of the occlusion months later. Radiographic findings and tooth mobil-
D. Poor contour of the denture base ity tests are normal. The most probable cause of pain
3. All of the following are a feature of papillary hyperpla- is ____.
sia except one. Which one is the exception? A. A loose crown
A. It is a proliferative bone disease B. Psychosomatic
B. It can be caused by wearing dentures at night C. A vertical root fracture
C. It can be caused by poor oral hygiene D. A premature eccentric contact
D. It can be caused by an ill-fitting denture 11. For an occlusal appliance used for muscle relaxation to
4. For optimal esthetics when setting maxillary denture be effective, the condyles must be located in their most
teeth, the incisal edges of the maxillary incisors should stable position from a musculoskeletal perspective.
follow the ____. This is ____.
A. Lower lips during smiling A. Centric occlusion
B. Upper lips during smiling B. At the vertical dimension of rest
C. Lower lips when relaxed C. Centric relation
D. Upper lips when relaxed D. Maximum intercuspal position
5. Excessive monomer added to acrylic resin results 12. A diagnostic wax-up is indicated when ____.
in ____. A. Reestablishing anterior guidance
A. Increased expansion B. A provisional fixed prosthesis is to be fabricated
B. Increased heat generation C. Uncertainty exists regarding esthetics
C. Increased shrinkage D. All of the above
D. Increased strength 13. Which of the following is the most important predictor
6. What is the purpose of adjusting the occlusion in of clinical success of a cast post and core?
dentures? A. Amount of remaining coronal tooth structure
A. To obtain balanced occlusion B. Post length
B. To stabilize dentures C. Post diameter
C. To obtain even occlusal contacts D. Positive horizontal stop
D. All of the above 14. Factors associated with bone loss include ____.
7. Which of the following may be a consequence of occlu- A. Initial implant instability
sal trauma on implants? B. Excessive occlusal force
C. Inadequate hygiene A. It is rigid and provides unification of the arch

D. Inadequate prosthesis fit stability
E. All of the above B. It does not substantially alter the natural contour
15. Which of the following statements is true concerning of the lingual surface of the mandibular alveolar
the evaluation of the occlusion on a cast restoration? ridge or the palatal vault
A. The restoration is in proper occlusion if it holds C. It contributes to the support of the prosthesis
shim stock. D. All of the above
B. The restoration is in proper occlusion if the adja- E. Only A and B
cent teeth hold shim stock. 22. When does an FDP that was cast in one piece need to
C. The restoration is in proper occlusion when articu- be sectioned?
lating paper marks multiple points of contact on A. When a cantilever pontic is used
the restoration. B. When the fit cannot be achieved or verified with a
D. A, B, and C. one-piece cast
E. None of the above. C. When single crowns are adjacent to the FDP
16. In a Kennedy class I arch in which all molars and the D. Always to achieve a good fit
first premolar are missing and the rest of the teeth have 23. When soldering an FDP, what is the effect of flux when
good periodontal support, the preferred choice of heated on the area to be soldered?
treatment is ____. A. To remove oxides from the metal surface
A. RDP replacing all missing teeth B. To displace metal ions from the area
B. FDP replacing the missing premolar and RDP C. To change the composition of the alloy
replacing the molars D. To reduce the surface tension of the metal
C. Implant-supported crowns replacing the first pre- 24. Which component of an RDP is spoon-shaped and
molars and RDP replacing the molars slightly inclined apically from the marginal ridge of
D. A and B are preferred over C a tooth?
E. B and C are preferred over A A. Indirect retainer
17. The surveyor is used to ____. B. Minor connector
A. Aid in the placement of an intracoronal retainer C. Rest
B. Block out a master cast D. Lingual bar
C. Measure a specific depth of an undercut 25. Metamerism invariably involves ____.
D. All of the above A. A color difference between two objects under one
E. A and B or more illuminants
18. A dentist is preparing all maxillary anterior teeth for B. One object having a lower chroma than another
metal-ceramic crowns. Which of the following proce- C. One object having a lower lightness than another
dures is necessary to preserve and restore anterior D. A significant color change of one object as it moves
guidance? from one illuminant to another
A. Protrusive record 26. A patient has generalized severe alveolar bone loss
B. Template for provisional restorations with resulting teeth mobility for the maxillary and
C. Custom incisal guide table mandibular anterior and posterior teeth. All remaining
D. Interocclusal record in centric relation teeth need to be extracted. The patient has opted to
19. A radiolucency near the apex of tooth #28 is seen have immediate maxillary and mandibular complete
radiographically. The tooth is asymptomatic and does dentures. The patient does not want to wait for healing
not have caries or periodontal problems. What is the after all the teeth are extracted before dentures can be
most likely cause of the radiolucency? constructed mainly because of esthetic concerns. What
A. Submandibular fossa is the best esthetic option for the patient that would
B. Periapical granuloma minimize drastic changes in the supporting tissue the
C. Complex compound odontoma day of the delivery of the immediate denture?
D. Mental foramen A. Extract all the anterior teeth, leave the posterior
20. The minor connector for a mandibular distal extension teeth to maintain the vertical dimension, construct
base should extend posteriorly about ____. an immediate denture, and extract the posterior
A. Two thirds the length of the edentulous ridge teeth the day of delivery of the immediate denture
B. Half the length of the edentulous ridge B. Extract the posterior teeth, leave the anterior teeth,
C. One third the length of the edentulous ridge wait a month for healing, construct the dentures,
D. As long as possible and extract the anterior teeth the day of delivery of
21. The characteristics of a major connector that contrib- the immediate dentures
ute to health and well-being include which of the C. Extract all the teeth because it is very difficult to
following? predict the esthetic outcome of immediate dentures
when most of the posterior and anterior teeth are C. The tooth has a crack and requires a crown
present D. None of the above
D. Extract only the worst posterior and anterior teeth, 29. The preparation of a tooth for a Zirconia crown can be
and construct the immediate complete dentures; the same as for ____.
extract the remaining teeth the day of the delivery A. Metal-ceramic crown
of the dentures B. Full metal crown
27. In the scenario for question 26, if constructing an C. All-ceramic crown
immediate denture, which of the following constitutes D. All of the above
the most difficult procedure? 30. You are evaluating an FDP replacing tooth #4 because
A. Border molding before the final impression with the margins are open secondary to probable distortion
existing teeth during the manufacture of the prosthesis. Which (if
B. Sequencing the treatment plan any) of the following should you do first before decid-
C. Delivery of the complete dentures ing to section between one of the retainers and the
D. All are equally difficult pontic to see if the fit improves and to obtain a solder
28. A 55-year-old patient presents with a DO amalgam in relationship for the prosthesis?
tooth #14 and a cervical abfraction on the buccal 1. Assessment and adjustment of occlusal
surface. The patient complains of pain when chewing relationships
and sensitivity to cold liquids but only while drinking 2. Assessment and adjustment of proximal
the cold liquids. The clinical examination and radio- contacts
graphs reveal no apparent abnormalities except for 3. Assessment and adjustment of axial contours
mild discoloration of the lingual distal cusp. An ice test 4. Assessment of marginal integrity
is positive immediately, and there is pain when occlud- A. All are correct
ing with a tooth sleuth. What is the most likely cause B. 1, 2 and 3 are correct
of the pain, and what treatment does the tooth require? C. 2, 3 and 4 are correct
A. The tooth has an occlusal prematurity and needs an D. 2 and 4 are correct
occlusal adjustment E. 1 and 4 are correct
B. The abfraction causes the sensitivity, and a cervical
restoration is needed
Sample Examination 371
Sample Examination
Endodontics C. Smaller myelinated nerve fibers with slower con-
duction velocities
1. A patient complains of recent severe pain to percus- D. Smaller unmyelinated nerve fibers with faster con-
sion of a tooth. The most likely cause is ____. duction velocities
A. Acute periradicular periodontitis 8. When compared with the bisecting-angle technique,
B. Chronic periradicular periodontitis the advantages of the paralleling technique in end-
C. Reversible pulpitis odontic radiology include all of the following except
D. Irreversible pulpitis one. Which one is the exception?
2. Which of the following statements regarding post A. Significant decrease in patient radiation
preparation is not correct? B. More accurate image of the tooths dimensions
A. The primary purpose of the post is to retain a core C. Easier to reproduce radiographs at similar angles
in a tooth with extensive loss of coronal structure. to assess healing after treatment
B. The need for a post is dictated by the amount of D. Most accurate image of all dimensions of the tooth
remaining coronal tooth structure. and its relationship to surrounding anatomic
C. Posts reinforce the tooth and help to prevent verti- structures
cal fractures. 9. The primary reason for designing a surgical flap with
D. At least 4 to 5mm of remaining gutta-percha after a wide flap base is to ____.
post space preparation is recommended. A. Avoid incising over a bony protuberance
3. Prolonged, unstimulated night pain suggests which of B. Obtain maximum access to the surgical site
the following conditions of the pulp? C. Maintain an adequate blood supply to the reflected
A. Pulpal necrosis tissue
B. Mild hyperemia D. Aid in complete reflection
C. Reversible pulpitis 10. The apical portion of the maxillary lateral incisor
D. Periodontal abscess usually curves to the ____.
4. A nasopalatine duct cyst is located between ____. A. Facial
A. Two maxillary central incisors B. Palatal
B. Maxillary central and lateral incisors C. Mesial
C. Maxillary lateral and canine D. Distal
D. Maxillary canine and first premolar 11. Aqueous ethylenediamine tetraacetic acid (EDTA) is
5. The severity of the course of a periradicular infection primarily used to ____.
depends on the ____. A. Dissolve organic matter
A. Resistance of the host B. Dissolve inorganic matter
B. Virulence of the organisms C. Kill bacteria
C. Number of organisms present D. Prevent sealer from extruding out of the canal
D. Both A and B only space
E. All of the above 12. A noncarious tooth with deep periodontal pockets that
6. Informed consent requires that the patient be advised do not involve the apical third of the root has devel-
of all of the following except one. Which one is the oped an acute pulpitis. There is no history of trauma
exception? other than a mild prematurity in lateral excursion.
A. Benefits of endodontic treatment What is the most likely explanation for the pulpitis?
B. Cost of endodontic treatment A. Normal mastication and toothbrushing have driven
C. Risks of endodontic treatment microorganisms deep into tissues with subsequent
7. Which of the following statements best describes pulp involvement at the apex.
pulpal A-delta fibers compared with C fibers? B. During a general bacteremia, bacteria settled in
A. Larger unmyelinated nerve fibers with slower con- this aggravated pulp and produced an acute
duction velocities pulpitis.
B. Larger myelinated nerve fibers with faster conduc- C. Repeated thermal shock from air and fluids getting
tion velocities into the deep pockets caused the pulpitis.
371
372 Sample Examination
D. An accessory pulp canal in the gingival or the 19. Which of the following is the best radiographic tech-
middle third of the root was in contact with the nique to identify a suspected horizontal root fracture
pockets. in a maxillary anterior central incisor?
13. On a radiograph, the facial root of a maxillary first A. Multiple Waters projections
premolar would appear distal to the lingual root if B. Multiple angulated periapical radiographs in addi-
the ____. tion to a normal, parallel-angulated, periapical
A. Vertical angle of the cone was increased radiograph
B. Vertical angle of the cone was decreased C. Panoramic radiograph
C. X-ray head was angled from a distal position rela- D. Reverse Townes projection
tive to the premolar 20. An 8-year-old boy sustained a traumatic injury to a
D. X-ray head was angled from a mesial position rela- maxillary central incisor. Electrical and thermal vital-
tive to the premolar ity tests performed 1 day later failed to elicit a response
14. If a canal is ledged during instrumentation, the best from the tooth. This finding dictates ____.
way to handle the problem is to ____. A. Pulpectomy
A. Continue instrumenting at the ledge; although it B. Apexification
may take some time, you will eventually bore your C. Calcium hydroxide pulpotomy
way to patency in the periodontal ligament space D. Delay for the purpose of reevaluation
B. Stop immediately and fill to where the ledge begins 21. Twisting a triangular wire best describes the manufac-
C. Bind your irrigating needle in the canal and use turing process of a ____.
short bursts of irrigant to loosen any debris block- A. Reamer
ing the canal; this will reopen the natural canal B. Barbed broach
D. Prebend the tip of a small file, lubricate, and try to C. Hedstrm file
negotiate around the ledge D. K-Flex file
E. Place citric acid or ethylenediamine tetraacetic acid 22. Direct pulp cap is recommended for teeth with ____.
in the canal to soften the dentin; a small Gates A. Carious exposures
Glidden or other rotary can be used to bypass the B. Mechanical exposures
ledge C. Calcification in the pulp chambers
15. Which of the following factors affects long-term prog- D. Closed apices more than teeth with open apices
nosis of teeth after perforation repair? 23. Which of the following is the treatment of choice for
A. Size of the defect a 7-year-old child with a nonvital tooth #30 with buccal
B. Location of the defect sinus tract?
C. Time elapsed between the perforation and its A. Gutta-percha filling
repair B. Gutta-percha filling followed by root-end surgery
D. All of the above C. Extraction
16. Which of the following statements best describes treat- D. Apexogenesis
ment options for a separated instrument (e.g., finger E. Apexification
spreader) at the filling stage of treatment? 24. Which of the following is the main side effect of
A. Immediately attempt to remove the instrument. bleaching an endodontically treated tooth?
B. Do not attempt removal, and proceed to A. External cervical resorption
obturation. B. Demineralization of tooth structure
C. Attempt to bypass the obstructed instrument. C. Gingival inflammation
D. Both A and C are options. 25. What is the safest recommended intracoronal bleach-
17. Endodontically treated posterior teeth are more sus- ing chemical?
ceptible to fracture than untreated posterior teeth. The A. Hydrogen peroxide
best explanation for this is ____. B. Sodium perborate
A. Moisture loss C. Sodium hypochlorite
B. Loss of root vitality D. Carbamide peroxide
C. Plastic deformation of dentin 26. Pulp capping and pulpotomy can be more successful
D. Destruction of the coronal architecture in newly erupted teeth than in adult teeth because
18. There is a horizontal root fracture in the middle third ____.
of the root of tooth #10 in an 11-year-old patient. The A. A greater number of odontoblasts are present
tooth is mobile and vital. How should this be treated? B. Of incomplete development of nerve endings
A. Extract C. An open apex allows for greater circulation
B. Immediate pulpectomy and splint D. The root is shorter
C. Splint and observe 27. Zinc oxide eugenol is a good temporary restoration
D. Do nothing and follow-up in 10 to 14 days because ____.
A. It is less irritating 35. The danger zone of mandibular molars for perfora-
B. It has increased strength over other restorations tions during canal instrumentation is ____.
C. It provides a good seal A. The periphery at the level of the dentinocemental
D. It is inexpensive junction
28. During a routine 6-month endodontic treatment recall B. Within 2mm of the apex
evaluation, you note a marked decrease in the radio- C. The furcation area
graphic size of the periradicular radiolucency. Which D. The periphery of the access at the level of the
of the following is the most appropriate treatment cementoenamel junction
plan? 36. What is the treatment of choice for an 8-year-old
A. Extraction patient who has a 1-mm intrusion injury of tooth #8?
B. Nonsurgical endodontic retreatment A. Extract the tooth
C. Recall the patient in another 6 months B. Perform pulpotomy immediately
D. Surgical endodontic retreatment C. Immediately splint the tooth for 10 to 14 days
29. What is the radiographic sign of successful pulpotomy D. Allow the tooth to reerupt
in a permanent tooth? 37. On routine radiographic survey of a new patient, you
A. Open apex notice a circle-shaped radiolucency at the midroot and
B. Apex has formed over the pulpal outline of tooth #6. You take a second
C. Loss of periradicular lucency mesially angulated radiograph and confirm the radio-
D. No internal resorption lucency is part of the pulp canal outline. After a vital
30. Which of the following statements is false regarding response to cold testing, your diagnosis and subse-
internal root resorption? quent treatment plan are ____.
A. It happens rarely in permanent teeth. A. Internal resorption and completion of nonsurgical
B. It appears as an asymmetrical moth-eaten lesion endodontic treatment
in radiographs. B. Internal resorption and surgical repair of the defect
C. Chronic pulpal inflammation is the primary C. External root resorption and forced orthodontic
cause. eruption to expose the defect
D. Prompt endodontic therapy stops the process. D. External root resorption and extraction
31. An emergency patient is diagnosed with symptomatic 38. During a nonvital bleaching procedure, if a barrier
irreversible pulpitis and symptomatic apical periodon- material is not placed between the root canal filling
titis of tooth #12. Which of the following is the best and bleaching material, the tooth can be subjected
treatment protocol for this patient? to ____.
A. Anesthesia followed by incision and drainage A. External cervical resorption
B. Anesthesia followed by extraction B. Demineralization of tooth structure
C. Anesthesia followed by pulpectomy C. Gingival inflammation
D. Prescribe antibiotic for 1 week and follow with D. Poor color improvement
nonsurgical endodontic treatment 39. A healthy 32-year-old man presents with localized fluc-
32. In which of the following conditions is elective root tuant swelling associated with a necrotic pulp and an
canal therapy contraindicated? apical diagnosis of acute apical abscess for tooth #5. The
A. AIDS principal modality or modalities for treating a localized
B. Recent myocardial infarction (MI) fluctuant swelling include which of the following?
C. Leukemia A. Administration of antibiotics
D. Radiotherapy B. Achievement of drainage
E. Second trimester of pregnancy C. Removal of the source of infection
33. What is the best timing for performing incision and D. Both A and C
drainage at an area of infection? E. Both B and C
A. When the swelling is hard and diffuse 40. Which of the following statements most accurately
B. When the area is the most painful describes the manufacturing process for a K-type hand
C. When the area is large instrument?
D. When the swelling is localized and fluctuant A. Grinding a stainless steel wire to a tapered square
34. Endodontic infection usually is polymicrobial. What is or triangular cross section
the predominate type of microorganism found in a B. Twisting a square or rhomboid (cross section) non-
tooth that requires endodontic therapy? tapered silver metal blank
A. Aerobic bacteria C. Grinding a silver metal blank to a nontapered
B. Facultative bacteria square or rhomboid cross section
C. Obligate anaerobic bacteria D. Both B and C
D. Yeast microorganisms E. All of the above
Operative Dentistry C. Provide a complete seal around the teeth

D. All of the above
1. A good preventive and treatment strategy for dental 9. For a dental hand instrument with a formula of 10-8.5-
caries includes ____. 8, the number 10 refers to ____.
A. Limiting cariogenic substrate A. The width of the blade, in tenths of a millimeter
B. Controlling cariogenic flora B. The primary cutting-edge angle, in centigrades
C. Elevating host resistance C. The blade length, in millimeters
D. All of the above D. The blade angle, in centigrades
2. Which of the following statements regarding caries 10. The tooth preparation technique for a class I amalgam
risk assessment is correct? on a mandibular first molar does not include which of
A. The presence of restorations is a good indicator of the following?
current caries activity. A. Maintaining a narrow isthmus width
B. The presence of restorations is a good indicator of B. Initial punch cut placed in the most carious pit
past caries activity. C. Establishment of pulpal depth of 1.5 to 2mm
C. The presence of dental plaque is a good indicator D. Orientation of bur parallel to the long axis of the
of current caries activity. tooth
D. The presence of pit-and-fissure sealants is a good 11. When placement of proximal retention locks in class
indicator of current caries activity. II amalgam preparations is necessary, which of the
3. Which of the following is considered a reversible following is not correct?
carious lesion? A. One should not undermine the proximal enamel.
A. The lesion surface is cavitated. B. One should not prepare locks entirely in the
B. The lesion has advanced to the dentin axial wall.
radiographically. C. Even if deeper than ideal, one should use the axial
C. A white spot is detected on drying. wall as a guide for proximal lock placement.
D. The lesion surface is rough or chalky. D. One should place locks 0.2mm inside the denti-
4. Which of the following statements about indirect pulp noenamel junction (DEJ) to ensure that the proxi-
caps is false? mal enamel is not undermined.
A. Some leathery caries may be left in the 12. When the gingival margin is gingival to the cementoe-
preparation. namel junction (CEJ) in a class II amalgam prepara-
B. A liner is generally recommended in the tion, the axial depth of the axiogingival line angle
excavation. should be ____.
C. The operator should wait at least 6 to 8 weeks A. 0.2mm into sound dentin
before reentry (if then). B. Twice the diameter of a No. 245 carbide bur
D. The prognosis of indirect pulp cap treatment is C. 0.75 to 0.80mm
poorer than the prognosis of direct pulp caps. D. The width of the cutting edge of a gingival marginal
5. Smooth surface caries refers to ____. trimmer
A. Facial and lingual surfaces 13. Which of the following statements about class V
B. Occlusal pits and grooves amalgam restorations is not correct?
C. Mesial and distal surfaces A. The outline form is usually kidney-shaped or
D. Both A and C crescent-shaped.
6. How many blades does a finishing bur have compared B. Because the mesial, distal, gingival, and incisal walls
with a cutting bur? of the tooth preparation are perpendicular to the
A. Fewer blades external tooth surface, they usually diverge facially.
B. Same number of blades C. Using four corner coves instead of two full-length
C. More blades grooves conserves dentin near the pulp and
D. Number of blades is unrelated to the bur type may reduce the possibility of a mechanical pulp
7. The use of the rubber dam is best indicated for ____. exposure.
A. Adhesive procedures D. If the outline form approaches an existing proximal
B. Quadrant dentistry restoration, it is better to leave a thin section of
C. Teeth with challenging preparations tooth structure between the two restorations
D. Difficult patients (<1mm) than to join the restorations.
E. All of the above 14. When preparing a class III or IV composite tooth
8. A rubber dam is inverted to ____. preparation, which of the following statements regard-
A. Prevent the dam from tearing ing placement of retention form is false?
B. Prevent the underlying gingiva from accidental A. Placement of retention form often involves gingival
trauma and incisal retention.
B. Placement of retention form is placed at the axio- C. Extension onto the root surface
gingival line angle regardless of the depth of the D. Lack of dentinal sealing
axial wall. 21. Factors that affect the success of dentin bonding
C. Placement of retention form may be needed in include all of the following except one. Which one is
large preparations. the exception?
D. Placement of retention form is usually prepared A. Dentin factors such as sclerosis, tubule morphol-
with a No. 1 4 round bur. ogy, and smear layer
15. In the conventional class I composite preparation, B. Tooth factors such as attrition, abrasion, and
retention is achieved by which of the following abfraction
features? C. Material factors such as compressive and tensile
1. Occlusal convergence strengths
2. Occlusal bevel D. C-factor considerations
3. Bonding 22. Which of the following statements regarding carving a
4. Retention grooves class I amalgam restoration is false?
A. 2 and 4 A. Carving may be made easier by waiting 1 or 2
B. 1 and 3 minutes after condensation before it is started.
C. 1 and 4 B. The blade of the discoid carver should move parallel
D. 2 and 3 to the margins resting on the partially set amalgam.
16. The success of an amalgam restoration depends on all C. Deep occlusal anatomy should not be carved.
of the following features of tooth and cavity prepara- D. The carved amalgam outline should coincide with
tion except one. Which one is the exception? the cavosurface margins.
A. Butt-joint cavosurface margin that results in a 23. The generally accepted maximum thickness of a com-
90-degree margin for the amalgam posite increment that allows for proper cure is ____.
B. Adequate tooth removal for appropriate strength of A. 1 to 2mm
the amalgam B. 2 to 4mm
C. Divergent (externally) preparation walls C. 4 to 6mm
D. Adequate retention form features to lock the D. There is no maximum thickness restriction.
amalgam mechanically in the preparation 24. The setting reaction of dental amalgam proceeds pri-
17. Many factors affect tooth/cavity preparation. Which of marily by ____.
the following would be the least important factor? A. Dissolution of the entire alloy particle into mercury
A. Extent of the defect B. Dissolution of the copper from the particles into
B. Size of the tooth mercury
C. Fracture lines C. Precipitation of tin-mercury crystals
D. Extent of the old material D. Mercury reaction with silver on or in the alloy
18. Which of the following statements about an amalgam particle
tooth/cavity preparation is true? 25. What is the half-life of mercury in the human body?
A. The enamel cavosurface margin angle must be 90 A. 5 days
degrees. B. 25 days
B. The cavosurface margin should provide for a C. 55 days
90-degree amalgam margin. D. 85 days
C. All prepared walls should converge externally. E. 128 days
D. Retention form for class V amalgam preparations 26. Restoration of an appropriate proximal contact results
can be placed at the dentinoenamel junction in all of the following except one. Which one is the
(DEJ). exception?
19. A skirt feature for a gold onlay preparation ____. A. Reduces or eliminates food impaction at the inter-
A. Has a shoulder gingival margin design dental papilla
B. Is prepared by a diamond held perpendicular to the B. Provides appropriate space for the interdental
long axis of the crown papilla
C. Is used only for esthetic areas of a tooth C. Provides increased retention form for the
D. Increases both retention and resistance forms restoration
20. Causes of postoperative sensitivity with amalgam res- D. Maintains the proper occlusal relationship
torations include all of the following except one. Which 27. The best way to carve amalgam back to occlusal cavo-
one is the exception? surface margin is to ____.
A. Lack of adequate condensation, especially lateral A. Use visual magnification
condensation in the proximal boxes B. Use a discoid-cleoid instrument guided by the
B. Voids adjacent unprepared enamel
C. Make deep pits and grooves A. Slots should be 1.5mm in depth.

D. Use a round finishing bur after the amalgam B. Slots should be 1mm or more in length.
has set C. Slots may be segmented or continuous.
28. Major differences between total-etch and self-etching D. Slots should be placed at least 0.5mm inside the
primer dentin bonding systems include all of the fol- dentinoenamel junction (DEJ).
lowing except one. Which one is the exception? 35. Bonding of resins to dentin is best described as involv-
A. The time necessary to apply the material ing ____.
B. The amount of smear layer removed A. Mechanical interlocking
C. The bond strengths to enamel B. Ionic bonding
D. The need for wet bonding C. Covalent bonding
29. Which of the following statements is not true regard- D. van der Waals forces
ing bonding systems? 36. Which one of the following acids is generally recom-
A. Although dentin bonding occurs slowly, it results mended for etching tooth structure?
in a stronger bond than to enamel. A. Maleic acid
B. Enamel bonding occurs quickly, is strong, and is B. Polyacrylic acid
long-lasting. C. Phosphoric acid
C. One-bottle dentin bonding systems may be simpler D. Tartaric acid
but are not always better. E. Ethylenediamine tetraacetic acid
D. Dentin bonding is still variable because of factors 37. The principal goals of bonding are ____.
such as sclerosis, tubule size, and tubule location. A. Sealing and thermal insulation
30. A casting may fail to seat on the prepared tooth because B. Strengthening teeth and esthetics
of all of the following factors except one. Which one is C. Esthetics and reduction of postoperative
the exception? sensitivity
A. Temporary cement still on the prepared tooth after D. Sealing and retention
the temporary restoration has been removed E. Retention and reduction of tooth flexure
B. Proximal contacts of casting are too heavy or too 38. Triturating a dental amalgam ____.
tight A. Reduces the size of the alloy particles
C. Undercuts present in prepared tooth B. Coats the alloy particles with mercury
D. The occlusal of the prepared tooth was C. Reduces the crystal sizes as they form
underreduced D. Dissolves the alloy particles in mercury
31. For a gold casting alloy, which of the following is added 39. Which of the following is a primary contraindication
primarily to act as a scavenger for oxygen during the for the use of a composite restoration?
casting process? A. Occlusal factors
A. Copper B. Inability to isolate the operating area
B. Palladium C. Nonesthetic areas
C. Silver D. Extension onto the root surface
D. Zinc 40. Which of the following materials has the highest linear
32. All of the following are likely to indicate the need for coefficient of expansion?
restoration of a cervical notch except one. Which one A. Amalgam
is the exception? B. Direct gold
A. Patient age C. Tooth structure
B. Esthetic concern D. Composite resin
C. Tooth is symptomatic 41. Which of the following is the most common pin used
D. Tooth is deeply notched axially in restorative procedures?
33. When comparing pin retention with slot retention for A. Friction-locked pin
a complex amalgam restoration, which of the following B. Cemented pin
statements is false? C. Amalgam pin
A. Slots are used where vertical walls allow opposing D. Self-threaded pin
retention locks. 42. A cervical lesion should be restored if it is ____.
B. Slots provide stronger retention than pins. A. Carious
C. Slots and grooves can be used interchangeably. B. Very sensitive
D. Pin retention is used primarily where there are few C. Causing gingival inflammation
or no vertical walls. D. All of the above
34. All of the following statements about slot-retained 43. With regard to the mercury controversy related to the
complex amalgams are true except one. Which one is use of amalgam restorations, which of the following
the exception? statements is not correct?
A. Scientific evidence is lacking that amalgam poses A. Skirt

health risks to humans except for rare allergic B. Stubbed margin
reactions. C. Secondary flare
B. Alternative amalgamlike materials with low or no D. Groove extension bevel
mercury content have promise. E. Collar
C. True allergies to amalgam rarely have been 51. After completing the tooth preparation for the applica-
reported. tion of an etch-and-rinse (total-etch) three-step dental
D. Efforts are under way to reduce the environmental adhesive, what is the next step?
mercury to which people are exposed to lessen A. Apply adhesive
their total mercury exposure. B. Rinse etchant and leave surface wet
44. Compared with amalgam restorations, composite res- C. Apply two to three layers of primer
torations are ____. D. Etch enamel and dentin with phosphoric acid for
A. Stronger 10 to 15 seconds
B. More technique-sensitive E. Light-cure
C. More resistant to occlusal forces
D. Not indicated for class II restorations
45. Which of the following statements regarding the choice Oral and Maxillofacial Surgery
between doing a composite or amalgam restoration and Pain Control
is true?
A. Establishing restored proximal contacts is easier 1. You have placed a dental implant for replacement of
with composite. tooth #9. Preoperatively, you obtained a panoramic
B. The amalgam is more difficult and technique- and a periapical film. During the surgery, you used a
sensitive. crestal incision, series of drills, and paralleling pins as
C. The composite generally uses a more conservative necessary. On restoration of the crown, obtaining ideal
tooth/cavity preparation. esthetics is difficult because the implant is placed too
D. Only amalgam should be used for class II close to the labial cortex, causing the restoration to
restorations. appear overcontoured. Which of the following tech-
46. Eburnated dentin has which of the following charac- niques could most adequately have prevented this
teristics? (Choose all that apply.) problem?
A. Is sclerotic dentin A. Using an anterior surgical template
B. Indicates recent poor hygiene B. Obtaining preoperative tomograms of the
C. Usually appears as a white patch alveolus
D. Is firm to the touch of an explorer C. Using a tissue punch technique
E. Is usually seen in older patients D. Using a smaller size of implant
47. Rounding internal cavity preparation angles is part of 2. The third molar impaction most difficult to remove is
what form in cavity preparation? the ____.
A. Resistance form A. Vertical
B. Retention form B. Mesioangular
C. Convenience form C. Distoangular
D. Outline form D. Horizontal
48. Which of the following terms refers to tooth structure 3. On a panoramic radiograph of a 13-year-old patient,
loss in the cervical area secondary to biomechanical there is evidence of crown formation of the third
loading? molars but no root formation yet. These teeth fall into
A. Abfraction the category of impacted teeth.
B. Abrasion A. True
C. Attrition B. False
D. Erosion 4. Which of the following is not appropriate treatment
49. For a mechanical pulp exposure that is noncarious and for an odontogenic abscess?
the exposure is less than 1.0mm, what is usually the A. Placing the patient on antibiotics and having him
most appropriate treatment? or her return when the swelling resolves
A. No pulp treatment B. Surgical removal of the source of the infection as
B. Direct pulp cap early as possible
C. Indirect pulp cap C. Drainage of the abscess with placement of surgical
D. Endodontic therapy drains
50. A beveled shoulder design around a capped cusp of a D. Close observance of the patient during resolution
gold onlay preparation is termed a ____. of the infection
E. Medical management of the patient to correct any A. Le Fort I osteotomy

compromised states that might exist B. Segmental maxillary osteotomy
5. Before the exploration of any intrabony pathologic C. Bilateral sagittal split osteotomy
lesion, which type of biopsy must always be done? D. Intraoral vertical ramus osteotomy
A. Cytologic smear 12. Obstructive sleep apnea syndrome (OSAS) often re-
B. Incisional biopsy sults in all of the following except one. Which one is
C. Excisional biopsy the exception?
D. Aspiration biopsy A. Excessive daytime sleepiness
6. You are performing a 5-year follow-up examination B. Aggressive behavior
on a 43-year-old patient with an implant. When com- C. Personality changes
paring radiographs, you estimate that there has been D. Depression
almost 0.1mm of lost bone height around the implant 13. Which of the following procedures would be consid-
since it was placed. Which of the following is ered the least invasive surgical treatment for temporo-
indicated? mandibular joint complaints?
A. Removal of the implant and replacement with a A. Splint therapy
larger size implant B. Arthrocentesis
B. Removal of the implant to allow healing before C. Arthroscopy
another one can be placed 4 months later D. Disc removal
C. Remaking the prosthetic crown because of tangen- E. Total joint replacement
tial forces on the implant 14. A 23-year-old college student is suspected to have sus-
D. The implant is doing well; this amount of bone loss tained a mandible fracture during an altercation.
is considered acceptable Which of the following statements is false?
7. The major mechanisms for the destruction of osseoin- A. At least two x-rays should be obtained.
tegration of implants are ____. B. The most common x-ray obtained is a panoramic
A. Related to surgical technique radiograph.
B. Similar to those of natural teeth C. The most likely area for this patients mandi-
C. Related to implant material ble to be fractured is the mandibular dental
D. Related to nutrition alveolus.
8. After completing your postoperative instructions for D. Point tenderness, changes in occlusion, step defor-
dental implant placement for replacement of tooth mities, and gingival lacerations all should be noted
#14, your patient asks you how long it will be before on physical examination.
she can get her new tooth. Which of the following is 15. Which of the following is not a classification of man-
most correct to allow complete osseointegration? dible fractures?
A. 3 weeks A. Anatomic location
B. 6 weeks B. Description of the condition of the bone fragments
C. 3 months at the fracture site
D. 6 months C. Angulation of the fracture and muscle pull
9. The imaging evaluation of the temporomandibular D. Le Fort level
joint (TMJ) is most likely to include any of the follow- 16. Although the state-of-the-art treatment for facial frac-
ing except one. Which one is the exception? tures is internal rigid fixation using bone plates and
A. Panoramic radiographs screws, a proper occlusal relationship must be estab-
B. TMJ tomograms lished before fixation of the bony segments if the
C. Xeroradiography reduction is to be satisfactory.
D. Magnetic resonance imaging A. True
10. When is distraction osteogenesis preferred over a tra- B. False
ditional osteotomy? 17. Which of the following statements regarding possible
A. When a large advancement is needed complications resulting from dental extractions is
B. When a small advancement is needed true?
C. When exacted interdigitation of the occlusion is A. Patients with numbness lasting more than 4
needed weeks should be referred for microneurosurgical
D. When the treatment needs to be done in a very evaluation.
short period of time B. Infections are common, even in healthy patients.
E. Distraction osteogenesis is always preferred over a C. Dry socket occurs in 10% of patients with third
traditional osteotomy molar extractions.
11. The most common mandibular surgical osteotomy to D. Teeth lost into the oropharynx are usually swal-
advance the mandible is ____. lowed and do not require further intervention.
18. Which of the following statements regarding the pos- B. Increased rate of needle breakage for 25-gauge
sibilities for reconstruction of an atrophic edentulous needles
ridge before denture construction is true? C. Aspiration of blood is easier and more reliable
A. Dental implants are used only as a last resort after through a larger lumen
bone grafting attempts have failed. D. There is no difference in pain of insertion
B. Distraction osteogenesis is too new a technique to 25. A 1.0-mL volume of a 2% solution contains ____.
be applied to ridge augmentation. A. 18mg
C. Potential bone graft harvest sites for ridge recon- B. 20mg
struction include rib, hip, and chin. C. 36mg
D. The need for ridge augmentation is more common D. 54mg
in the maxilla than in the mandible. 26. During local anesthetic administration, the patient
19. You are evaluating a patient 5 days after extraction should be placed in a ____ position.
of tooth #17. The patient complains of a severe throb- A. Trendelenburg
bing pain that started yesterday, 4 days after extraction. B. Supine
The patient most likely has which of the following C. Reclined
conditions? D. Semisupine
A. Dry socket 27. According to Malamed, slow injection is defined as the
B. Subperiosteal abscess deposition of 1mL of local anesthetic solution in not
C. Periapical periodontitis in tooth #18 less than ____.
D. Neuropathic pain A. 15 seconds
20. Which of the following patients would not be expected B. 30 seconds
to experience delayed healing of an extraction site? C. 60 seconds
A. A patient older than 60 years of age D. 2 minutes
B. A patient younger than 10 years of age 28. The ____ nerve block is recommended for manage-
C. A patient with diabetes ment of several maxillary molar teeth in one
D. A patient with a heavy smoking habit quadrant.
21. All of the following are desirable properties of an A. Posterior superior alveolar
ideal local anesthetic except one. Which one is the B. Inferior alveolar
exception? C. Long buccal
A. It should have sufficient potency to give complete D. Nasopalatine
anesthesia even if harmful results occur at thera- 29. In an adult of normal size, penetration to a depth of
peutic doses ____ mm places the needle tip in the immediate vicin-
B. It should be relatively free from producing allergic ity of the foramina, through which the posterior supe-
reactions rior alveolar nerves enter the posterior surface of the
C. It should be stable in solution and readily undergo maxilla.
biotransformation in the body A. 10
D. It should be either sterile or capable of being steril- B. 16
ized by heat without deterioration C. 20
22. What is the direct effect of local anesthetics on blood D. 30
vessels in the area of injection? 30. The ____ nerve block is useful for dental procedures
A. Constriction involving the palatal soft tissues distal to the canine.
B. Dilation A. Nasopalatine
C. Sclerosis B. Greater palatine
D. Thrombosis C. Long buccal
23. All of the following describe lidocaine as packaged D. Inferior alveolar
in dental cartridges except one. What one is the 31. At about what threshold does elevation of cardiovas-
exception? cular signs occur with epinephrine that is injected in
A. Provided in a 2% solution a local anesthetic solution in a patient with cardiovas-
B. Provided with or without epinephrine cular compromise?
C. Has a pKa = 8.1 A. 40 g
D. Has a rapid onset B. 100 g
24. All of the following are reasons that 25-gauge needles C. 200 g
are preferred to smaller diameter needles except one. D. 1000 g
Which one is the exception? 32. According to Malamed, the maximum local anesthetic
A. Greater accuracy in needle insertion for 25-gauge dose of lidocaine (with or without vasoconstrictor)
needles is ____.
A. 1.5mg/kg C. Bupivacaine
B. 2.0mg/kg D. Procaine
C. 4.4mg/kg 41. A portion of which cranial nerve is anesthetized when
D. 7.0mg/kg performing an infraorbital nerve block?
33. Which of the following injections, when properly per- A. VII
formed, does not lead to pulpal anesthesia? B. V
A. Inferior alveolar C. III
B. Lingual D. II
C. Posterior superior alveolar 42. Which of the following local anesthetics has the short-
D. Infraorbital (true anterior superior alveolar nerve est half-life?
block) A. Lidocaine
34. The optimal volume of local anesthetic solution deliv- B. Prilocaine
ered for a true anterior superior alveolar nerve block C. Bupivacaine
is usually about ____. D. Articaine
A. 0.5mL 43. In odontogenic infections such as abscesses, which
B. 1.0mL groups of organisms should be the usual targets of
C. 1.5mL empiric therapy with antibiotics?
D. 1.8mL A. Fungi and enveloped viruses
35. The local anesthetic agent that is most appropriate for B. Methicillin-resistant Staphylococcus aureus
use in most children is ____. C. Methicillin-sensitive S. aureus and aerobes
A. 3% mepivacaine D. Streptococcal species and anaerobes
B. 2% mepivacaine with 1:20,000 levonordefrin 44. Which of the following are reasons for removing an
C. 2% lidocaine with 1:100,000 epinephrine impacted tooth? (Choose all that apply.)
D. 0.5% bupivacaine with 1:200,000 epinephrine A. Prevention of pericoronitis
36. Which of the following local anesthetics causes the B. Asymptomatic full bony impaction in a 65-year-
least amount of vasodilation? old patient
A. Lidocaine C. Prevention of periodontal disease in a tooth adja-
B. Mepivacaine cent to the impacted tooth
C. Bupivacaine D. Prevention of odontogenic cysts and tumors
D. Articaine 45. Which biopsy procedure should be used initially for a
37. According to Malamed, how many cartridges of 2% soft tissue lesion deep to the oral mucosa?
lidocaine can be safely administered to a child weigh- A. Incisional
ing 40lb? B. Excisional
A. Three cartridges C. Aspiration
B. One cartridge D. Hard tissue
C. Nine cartridges E. Mucoperiosteal flap
D. Two cartridges 46. The pKa of a local anesthetic is most likely to determine
38. If a local anesthetic has a low pKa, it usually has a ____. which of its characteristics?
A. Greater potency A. Potency
B. Higher degree of protein binding B. Duration of action
C. Faster onset of action C. Risk of allergy
D. Greater vasodilating potential D. Compatibility with a vasoconstrictor
39. What areas are anesthetized with correct administra- E. Rate of onset of anesthesia
tion of the (long) buccal injection? 47. Which nerve block results in anesthesia of palatal soft
A. Soft tissues and periosteum buccal to the mandibu- tissue from canine to canine?
lar molar teeth A. Nasopalatine
B. Soft tissues and periosteum lingual to the man- B. Greater palatine
dibular molar teeth C. Mental
C. Soft tissues and periosteum lingual to the man- D. Anterior superior alveolar
dibular premolar teeth E. Posterior superior alveolar
D. Soft tissues and periosteum buccal to the mandibu-
lar premolar teeth
40. Which local anesthetic is most hydrophobic and has Oral Diagnosis
the highest degree of protein binding?
A. Mepivacaine 1. Which of the following is a potential sequela of an
B. Lidocaine acute periapical abscess?
A. Central giant cell granuloma D. Fibrous dysplasia

B. Peripheral giant cell granuloma E. Langerhans cell disease
C. Osteosarcoma 8. A 15-year-old patient has a numb lower lip and pain
D. Periapical granuloma in her right posterior mandible. A radiograph shows
E. Periapical cemento-osseous dysplasia uniform thickening of the periodontal membrane
2. Which of the following odontogenic cysts occurs as a space of tooth #30. The tooth shows abnormally
result of stimulation and proliferation of the reduced increased mobility. Which one of the following diag-
enamel epithelium? noses should be seriously considered?
A. Dentigerous cyst A. Periapical cyst
B. Lateral root cyst B. Periapical granuloma
C. Radicular cyst C. Traumatic bone cyst
D. Odontogenic keratocyst D. Ameloblastoma
E. Gingival cyst E. Malignancy
3. Two cystic radiolucencies in the mandible of a 16-year- 9. Which of the following signs or symptoms suggests a
old boy were lined by thin, parakeratinized epithelium chronic benign process?
showing palisading of basal cells. All teeth were vital, A. Paresthesia
and the patient had no symptoms. This patient most B. Pain
likely has which of the following? C. Vertical tooth mobility
A. Odontogenic keratocysts D. Uniformly widened periodontal membrane space
B. Periapical granulomas E. Sclerotic bony margins
C. Periapical cysts 10. Which of the following features are shared by central
D. Traumatic bone cysts and peripheral giant cell granulomas?
E. Ossifying fibromas A. Microscopic appearance
4. When a diagnosis of odontogenic keratocyst is made, B. Clinical behavior
the patient should be advised regarding the ____. C. Recurrence rate
A. Need for full-mouth extractions D. Similar forms of treatment
B. Association with colonic polyps E. Radiographic appearance
C. Associated recurrence rate 11. Diffuse soft swelling of the lips and neck after
D. Likelihood of malignant transformation the ingestion of drugs, shellfish, or nuts is known
E. Need for additional laboratory studies as ____.
5. A painless, well-circumscribed 1cm 3cm radiolu- A. Fixed drug reaction
cent lesion with radiopaque focus was found in the B. Anaphylaxis
posterior mandible of an 11-year-old boy. Which of C. Urticaria
the following should be included in a differential D. Acquired angioedema
diagnosis? E. Contact allergy
A. Ameloblastic fibro-odontoma 12. A 7-year-old patient presents with a quadrant of teeth
B. Pagets disease showing abnormal formation of both enamel and
C. Dentigerous cyst dentin. All of his other teeth appear clinically normal.
D. Ameloblastoma Radiographically, the affected teeth can be described
E. Langerhans cell disease as ghost teeth. The patient has ____.
6. Herpes simplex virus is the cause of which of the A. Regional odontodysplasia
following? B. Dens evaginatus
A. Minor aphthous ulcers C. Dentin dysplasia
B. Herpetiform aphthae D. Ectodermal dysplasia
C. Herpetic whitlow E. Cleidocranial dysplasia
D. Herpangina 13. An adult patient presents with a 0.5cm 0.5cm sub-
E. Herpes zoster mucosal mass in the posterior lateral tongue. A biopsy
7. A 12-year-old patient presents with premature loss of specimen shows a neoplasm composed of glandlike
primary teeth. On radiographic examination, a sharply elements and connective tissue elements. It is covered
marginated lucency is seen in the area of tooth loss. A by normal-appearing epithelium. This could be which
biopsy specimen shows a round cell infiltrate with of the following?
numerous eosinophils. Which of the following diagno- A. Oral wart
ses is suggested? B. Pleomorphic adenoma (mixed tumor)
A. Cherubism C. Granular cell tumor
B. Gardners syndrome D. Idiopathic leukoplakia
C. Pagets disease E. Peripheral giant cell granuloma
14. Oral squamous cell carcinomas manifest typically in 21. Nevoid basal cell carcinoma syndrome includes
which of the following ways? multiple basal cell carcinomas, bone abnormalities,
A. Vesicular eruption and ____.
B. Pigmented patch A. Osteomas
C. Inflamed pustule B. Caf au lait macules
D. Submucosal swelling C. Odontogenic keratocysts
E. Indurated nonhealing ulcer D. Hypoplastic teeth
15. A clinical differential diagnosis of an asymptomatic E. Lymphoma
submucosal lump or nodule in the tongue would 22. All of the following lesions characteristically manifest
include all of the following except one. Which one is in individuals younger than age 20 years except one.
the exception? Which one is the exception?
A. Traumatic fibroma A. Traumatic bone cyst
B. Neurofibroma B. Adenomatoid odontogenic tumor
C. Granular cell tumor C. Ameloblastic fibroma
D. Salivary gland tumor D. Compound odontoma
E. Dermoid cyst E. Ameloblastoma
16. Ectopic lymphoid tissue would most likely be found in 23. Oral and genital lesions are seen in patients with ____.
which of the following sites? A. Behets syndrome
A. Hard gingiva B. Peutz-Jeghers syndrome
B. Soft gingiva C. Herpangina
C. Floor of mouth D. Wegeners granulomatosis
D. Dorsum of tongue E. Hairy leukoplakia
E. Vermilion of the lip 24. A 32-year-old man presented with a 1cm 2cm mac-
17. Schwanns cell is the cell of origin for which of the fol- ular red-blue lesion in the hard palate. The lesion was
lowing tumors? asymptomatic and had been present for an unknown
A. Odontogenic myxoma duration. He had no dental abnormalities and no sig-
B. Rhabdomyoma nificant periodontal disease. This lesion could be all of
C. Neurofibroma the following except one. Which one is the exception?
D. Mixed tumor A. Vascular malformation
E. Leiomyoma B. Nicotine stomatitis
18. A 43-year-old man presents with an asymptomatic C. Ecchymosis
anterior palatal swelling. A radiograph shows a 1cm D. Kaposis sarcoma
1cm lucency and divergence of tooth roots #8 and E. Erythroplasia
#9. All teeth in the area are vital. What lesion does this 25. Bremsstrahlung radiation results from ____.
most likely represent? A. X-rays interacting with electrons
A. Periapical granuloma B. Electrons interacting with electrons
B. Aneurysmal bone cyst C. Electrons interacting with nuclei
C. Nasopalatine duct cyst D. L shell electrons falling into the K shell
D. Globulomaxillary lesion E. Photons interacting with nuclei
E. Dermoid cyst F. Photons converting into electrons
19. The globulomaxillary lesion of bone ____. 26. X-rays are produced in most conventional dental x-ray
A. Is associated with the crown of an unerupted machines ____.
tooth A. Continuously during operation
B. Occurs between maxillary lateral and canine teeth B. When there is a large space charge
C. Typically causes pain C. Half the time during operation
D. Typically manifests as a mixed lucent-opaque D. When the anode carries a negative charge
lesion with ill-defined margins E. Only when the beam is collimated
E. Is always associated with a nonvital tooth F. Only during the first half of each second
20. A generalized red, atrophic tongue would suggest 27. Deterministic effects ____.
all of the following except one. Which one is the A. Show a severity of response proportional to dose
exception? B. Are seen only in the oral cavity
A. Vitamin B deficiency C. Are found after exposure to low levels of
B. Pernicious anemia radiation
C. Chronic candidiasis D. Result from particulate radiation such as alpha and
D. Iron deficiency anemia beta particles but not x-rays
E. Peripheral giant cell granuloma E. None of the above
28. In the radiolysis of water, ____. A. Density

A. Free radicals are formed, which are nonreactive B. Contrast
B. The presence of dissolved oxygen reduces the C. Resolution
number of free radicals D. Magnification
C. The formation of free radicals is the direct effect E. Both C and D
D. The resultant free radicals may alter biologic 37. The primary function of developer is to ____.
molecules A. Reduce crystals of silver halide to solid silver grains
E. Two of the above B. Reduce solid silver grains to specks of silver halide
F. None of the above C. Remove unexposed silver halide crystals
29. The radiosensitivity of cells depends on ____. D. Remove exposed silver halide crystals
A. Mitotic future 38. If an exposed radiograph is too dark after proper
B. Mitotic activity development, you should ____.
C. Degree of differentiation A. Place it back in the fixer
D. All of the above B. Place it back in the developer
E. None of the above C. Decrease development time
30. Rectangular collimation is recommended because D. Increase milliamperage
it ____. E. Decrease exposure time
A. Deflects scatter radiation F. Decrease development temperature
B. Decreases patient dose 39. The radiolucent portions of the images on a processed
C. Increases film density dental x-ray film are made up of ____.
D. Increases film contrast A. Microscopic grains of silver halide
31. It is acceptable for the operator to hold the film in a B. Microscopic grains of metallic silver
patients mouth ____. C. A gelatin on a cellulose acetate base
A. If the patient is a child D. Unexposed silver bromide
B. If the patient or parent grants permission 40. The purpose of the penny test is to check ____.
C. If the patient has a handicap A. Developer action
D. If no film holder is available B. Fixer action
E. Never C. For proper development temperature
32. Comparing screen film/intensifying screen combina- D. For proper safelighting conditions
tions with direct-exposure films reveals that screen 41. Proper radiographic infection control includes all of
film/intensifying screen combinations ____. the following except one. Which one is the exception?
A. Render less resolution A. Wearing gloves while making radiographs
B. Require more exposure B. Disinfecting x-ray machine surface
C. Require special processing chemistry C. Covering working surfaces with barriers
D. Are preferred for intraoral radiography D. Sterilizing nondisposable instruments
33. It is important that the film base be ____. E. Sterilizing film packets
A. Opaque 42. Occlusal radiographs are useful for all of the following
B. Very rigid except one. Which one is the exception?
C. Flexible A. For views of the temporomandibular joint (TMJ)
D. Completely clear B. For displaying large segments of the mandibular
E. Sensitive to x-rays arch
34. Excessive vertical angulation causes ____. C. When the patient has limited opening
A. Overlapping D. When there are sialoliths in the floor of the mouth
B. Foreshortening E. When there is buccal-lingual expansion of the
C. Elongation mandible
D. Cone-cutting 43. From the following list, select the systemic diseases
35. Which of the following statements about obtaining that involve a defect in the immune system. (Choose
the most geometrically accurate image is false? all that apply.)
A. The film should be parallel to the object. A. Celiac sprue
B. The central ray should be parallel to the object. B. Sarcoidosis
C. The central ray should be perpendicular to the C. Amyloidosis
film. D. Behets syndrome
D. The object-to-film distance should be short. E. Crohns disease
E. The object-to-anode distance should be long. F. Neurofibromatosis
36. The size of the x-ray tube focal spot influences radio- 44. Sjgrens syndrome is characterized by which of the
graphic ____. following conditions? (Choose all that apply.)
A. Xerostomia A. Anterior aspect

B. Aphthous ulcers B. Middle aspect
C. Hairy leukoplakia C. Posterior aspect
D. Keratoconjunctivitis sicca D. Right aspect
E. Lymphocyte infiltration in minor salivary glands 5. Children in the primary dentition most often present
45. Which of the following apply to filtration of an x-ray with ____.
beam in a modern x-ray unit? (Choose all that apply.) A. An increased overbite
A. Decreases the mean energy of the x-ray beam B. A decreased overbite
B. Reduces patient exposure by removing lower C. An ideal overbite
energy photons D. A significant open bite
C. Provided by an aluminum filter 6. During the mixed dentition, a 1-mm diastema devel-
D. Required to be 1.5mm thick for 70kVp ops between the maxillary incisors. Which of the fol-
46. On a radiograph, you observe a radiolucency extend- lowing is most likely to happen?
ing from the distal aspect of the maxillary canine to A. The diastema will need orthodontic intervention to
the posterior wall of the maxilla above the tuberosity. be closed
The most likely cause of this radiolucency is ____. B. The diastema will resolve once the canines erupt
A. Dentigerous cyst C. The diastema will resolve only when all of the per-
B. Ameloblastoma manent teeth erupt
C. Zygomatic process of the maxilla D. The diastema will continue to widen as permanent
D. Maxillary sinus teeth erupt
47. Discoid lupus erythematosus has all of the follow- 7. A patient with the maxillary first permanent molar
ing characteristics except one. Which one is the mesiobuccal cusp sitting distal to the buccal groove
exception? of the mandibular first molar has which type of
A. Produces oral lesions that resemble erosive lichen malocclusion?
planus A. Class I
B. Predominately affects middle-aged women B. Class II, division 1
C. Involves damage to the heart and kidney C. Class II, division 2
D. Affects the skin of the face and scalp D. Class III
8. An adult patient with a class II molar relationship and
a cephalometric ANB angle of 2 degrees has which
Orthodontics and Pediatric Dentistry type of malocclusion?
A. Class II dental malocclusion
1. Which of the following types of malocclusions is most B. Class II skeletal malocclusion
common? C. Class I dental malocclusion
A. Class I malocclusion D. Class II skeletal malocclusion
B. Class II malocclusion 9. Which of the following would be the preferred method
C. Class III malocclusion of overbite correction in a patient who displays exces-
D. Open bite malocclusion sive maxillary incisor at rest, has an excessive lower
2. According to Scammons growth curves, which of the face height, and has a deep overbite?
following tissues has a growth increase that can be A. Eruption of posterior teeth to rotate the mandible
used to help predict timing of the adolescent growth open
spurt? B. Intrusion of maxillary incisors
A. Neural tissues C. Intrusion of mandibular incisors
B. Lymphoid tissues D. Flaring of maxillary and mandibular incisors
C. Reproductive tissues 10. In tooth movement, the formation of a hyalinized zone
3. Which of the following is the least reliable way to on the pressure side is due to ____.
predict the timing of the peak of the adolescent growth A. Application of light, continuous forces
spurt for an individual? B. Application of heavy forces
A. Plotting changes in height over time on a growth C. Normal forces of mastication
curve D. Abnormal swallowing patterns
B. Following eruption timing of the dentition 11. Which of the following reactions is least likely to be
C. Taking a hand-wrist radiograph to assess skeletal observed during orthodontic treatment?
development A. Root resorption
D. Observing changes in secondary sex characteristics B. Devitalization of teeth that are moved
4. In a patient with incomplete cleft palate, which of the C. Mobility of teeth that are moved
following aspects is most likely to remain open? D. Development of occlusal interferences
12. Root resorption is correlated to the pattern of stress C. Bend to provide correct angulation of a tooth in
distribution in the periodontal ligament (PDL) and labiolingual direction (torque)
type of tooth movement. D. Bend to rotate a tooth
A. True 20. When class III elastics are used, the maxillary first
B. False molars ____.
13. Putting a force through which of the following points A. Move distally and intrude
would cause pure translation of a tooth without rota- B. Move mesially and extrude
tion, tipping, or torque? C. Move mesially and intrude
A. Center of rotation D. Move only mesially; there is no movement in the
B. Center of resistance vertical direction
C. Center of the bracket 21. An adolescent patient presents to your office with a
D. Apex of the root skeletal and dental class II malocclusion and a deep
14. Doubling the force applied at the bracket of a tooth bite. Which of the following would be a proper treat-
would have what effect on the moment affecting tooth ment plan for this patient?
movement? A. Reverse-pull headgear, extrusion arch, and full
A. Moment would decrease by 50% fixed appliances
B. Moment would not change B. Reverse-pull headgear, intrusion arch, and full
C. Moment would double fixed appliances
D. Moment would increase fourfold C. Extraction of maxillary first premolars, extrusion
15. Two equal and opposite forces that are not collinear arch, and full fixed appliances
applied to a tooth are called ____. D. Extraction of maxillary first premolars, intrusion
A. The center of resistance arch, and full fixed appliances
B. The center of rotation 22. When using a cervical-pull headgear, the forces gener-
C. Root movement ated on the maxillary first molar cause this tooth to
D. A couple move in which of the following ways?
16. A wire extending from the molars to the incisors is A. Mesially and to extrude
activated to intrude the incisors. What is the side effect B. Distally and to extrude
on the molars? C. Mesially and to intrude
A. Molars tip forward and intrude D. Distally and to intrude
B. Molars rotate mesiobuccally 23. Which of the following depicts the usual order of
C. Molars tip distally and extrude extraction of teeth if serial extraction is chosen as the
D. Molars rotate distobuccally treatment to alleviate severe crowding?
17. Class II elastics are used by stretching an elastic A. Primary second molars, primary first molars, per-
between which of the two following points? manent first premolars, primary canines
A. From the posterior to the anterior within the max- B. Primary canines, primary first molars, permanent
illary arch first premolars
B. From the posterior to the anterior within the man- C. Primary first molars, primary second molars,
dibular arch primary canines
C. From the posterior of the maxillary arch to the D. Primary canines, permanent canines, primary first
anterior of the mandibular arch molars, permanent first premolars
D. From the posterior of the mandibular arch to the 24. Closure of a 2-mm maxillary midline diastema should
anterior of the maxillary arch be accomplished orthodontically in an 8-year-old child
18. What makes it possible for nickel-titanium archwires in which of the following circumstances?
to exhibit superelastic behavior? A. If the lateral incisors are missing
A. This behavior is based on a reversible transforma- B. If the space creates an esthetic concern and the
tion within the austenitic phase. child is being teased about it
B. This behavior is based on a reversible transforma- C. If there is also deep overbite present
tion between the austenitic and martensitic phases. D. If mild crowding is also present
C. This behavior is based on a reversible transforma- 25. In a patient with missing permanent maxillary lateral
tion within the martensitic phase. incisors, the decision of whether to substitute canines
D. This behavior is based on an irreversible transfor- in the lateral spaces depends on all of the following
mation within the martensitic phase. except one. Which one is the exception?
19. What is a second-order bend? A. Amount of crowding in the maxillary arch
A. Bend to position a tooth buccolingually B. Interarch relationship between the maxillary and
B. Bend to provide angulation of a tooth in mesiodis- mandibular dentition
tal direction (tip) C. Esthetic appearance of the permanent canines
D. Type of orthodontic appliance used to align the D. The implants will appear to submerge as the child
teeth gets older.
26. All of the following may be indications to consider 33. On the health history form, the mother of a 6-year-old
extraction of permanent teeth in an orthodontic new patient notes that the child is moderately mentally
patient except one. Which one is the exception? challenged. The dentist should ____.
A. Excessive crowding A. Refer to a pediatric dentist
B. Class II interarch relationship B. Use a Tell-Show-Do technique of behavior
C. Flat lip profile management
D. Anterior open bite C. Use conscious sedation
27. Which of the following is an advantage of fixed wire D. Use restraints after obtaining informed consent
retention compared with a removable Hawley-type 34. The functional inquiry questionnaire reveals that a
retainer? mother has had negative dental experiences and
A. Does not require the patient to remember to remains very nervous regarding her dental care. How
wear it would this most likely influence her 3-year-old childs
B. Is easier to clean reaction to dentistry?
C. Design can be altered to achieve minor tooth A. Increase the likelihood of a negative behavior
movements B. Increase the likelihood of a positive response to
D. Can incorporate an acrylic bite plate to avoid dentistry
relapse of overbite correction C. Cause an initial positive reaction, which changes to
28. The preferred surgical procedure to correct a class a negative reaction with the slightest stress.
II malocclusion owing to a deficient mandible D. Maternal anxiety has little effect on a childs behav-
is ____. ior in a dental setting.
A. Maxillary impaction 35. Which of the following local anesthetic techniques is
B. Maxillary setback recommended for anesthetizing a primary mandibular
C. Mandibular setback second molar that is to be extracted?
D. Mandibular advancement A. Buccal and lingual infiltration adjacent to the
29. Which of the following is considered to be the least second primary molar
stable orthognathic surgical movement? B. Inferior alveolar nerve block
A. Advancement of the mandible C. Inferior alveolar nerve block and lingual nerve
B. Advancement of the maxilla block
C. Superior movement (impaction) of the maxilla D. Inferior alveolar, lingual, and buccal nerve block
D. Inferior movement of the maxilla 36. In the primary dentition, the mandibular foramen is
30. Your patient exhibits enamel hypoplasia near the located where in relation to the plane of occlusion?
incisal edges of all permanent incisors and cuspids A. Higher than the plane of occlusion
except for the maxillary lateral incisors, which appear B. Much higher than the plane of occlusion
normal. At what age would you suspect some kind of C. Lower than the plane of occlusion
systemic problem? D. The same level as the plane of occlusion
A. Before birth 37. What is the minimum alveolar concentration of nitrous
B. From birth to 1 year of age oxide (vol %)?
C. From 1 to 2 years of age A. 50
D. From 2 to 3 years of age B. 75
31. Fluorosis is the result of excessive systemic fluoride C. 95
during which stage of tooth development? D. 105
A. Initiation 38. After administration of a local anesthetic, most patients
B. Morphodifferentiation can be maintained in conscious sedation at ____.
C. Apposition A. 20% to 40% nitrous oxide
D. Calcification B. 20% to 40% oxygen
32. Why are implants not generally performed on a C. 50% nitrous oxide
12-year-old patient with congenitally missing lateral D. 10% nitrous oxide
incisors? 39. In a 9-year-old patient, the mandibular left first
A. The patient likely would be unable to tolerate the primary molar has a large, carious lesion on the
surgical procedure. distal and on the occlusal, and the tooth has greater
B. Waiting for the crowns is too much of an esthetic mobility than what you would normally expect. You
issue with most children that age. should ____.
C. The gingival tissue will recede as the child gets A. Take a radiograph of the area
older. B. Perform a pulpotomy
C. Perform a pulpectomy 46. If the fluoride level in the drinking water is greater
D. Extract the tooth and consider space maintenance than 0.6ppm at any age, no supplemental systemic
40. Why are rounded internal line angles desirable in fluoride is indicated. If the patient is younger than 12
the preparation of amalgam restorations in primary months old, no supplemental systemic fluoride is indi-
teeth? cated, whatever the water fluoride level.
A. They increase retention A. The first statement is true, and the second state-
B. They conserve tooth structure ment is true.
C. They increase resistance B. The first statement is true, and the second state-
D. They decrease internal stresses in the restorative ment is false.
material C. The first statement is false, and the second state-
41. A 7-year-old patient has a very large, carious lesion on ment is true.
tooth T. What radiologic factors should be used to D. The first statement is false, and the second state-
determine the best treatment of choice between pulp- ment is false.
otomy and primary endodontics? 47. A 1-year-old patient has his first dental examination.
A. Furcation involvement The dentist reviews with the parent when to expect the
B. External root resorption next teeth to erupt, teething, and oral hygiene tips for
C. Internal root resorption toddlers and discusses fluoride issues with bottled
D. Two of the above water and toothpaste. The term that describes this pro-
E. All of the above active approach to dental care is ____.
42. Which pulpotomy medicament demonstrates better A. Risk assessment
success rates than formocresol? B. Probability counseling
A. Mineral trioxide aggregate C. Anticipatory guidance
B. Calcium hydroxide D. Preventive support counseling
C. Resin-modified glass ionomer cement 48. Most natal and neonatal teeth are primary teeth. They
D. Fifth-generation bonding agents should be extracted.
43. The pulp tissue of primary teeth ____. A. The first statement is true, and the second state-
1. In general is smaller proportionately than per- ment is true.
manent pulps in relation to tooth crown size B. The first statement is true, and the second state-
2. Is closer to the outer surface of the tooth than the ment is false.
permanent teeth C. The first statement is false, and the second state-
3. Follows the general surface contour of the ment is true.
crown D. The first statement is false, and the second state-
4. Has the mesial pulp horn closer to the surface ment is false.
than the distal pulp horn 49. The willful failure of parent or guardian to seek and
A. 1, 2, and 4 are correct follow-through with treatment necessary to ensure
B. 2, 3, and 4 are correct a level of oral health essential for adequate function
C. 1, 3, and 4 are correct and freedom from pain and infection is a definition
D. 1, 2, 3, and 4 are correct. of ____.
44. The following teeth are erupted in an 8-year-old A. Munchausen syndrome by proxy
patient. What is the space maintenance of choice? B. Emotional abuse
C. Parental corruption
3 A B C 7 8 9 10 H I 14
D. Neglect
30 T S R 26 25 24 23 M L K 19
50. Where do lesions commonly occur in the primary
A. Band-loop space maintainer form of acute herpetic gingivostomatitis?
B. Lower lingual holding arch A. Buccal mucosa
C. Nance holding arch B. Tonsils and hard and soft palate
D. Distal shoe space maintainer C. Tongue
45. The following teeth are erupted in a 4-year-old patient. D. Gingiva
What is the space maintenance of choice? E. All of the above
51. Localized aggressive periodontitis in the primary den-
A B C D E F G H I J
tition is seen most commonly in the primary molar
S R Q P O N M L K
area. It is most common in Asian children.
A. Band-loop space maintainer A. The first statement is true, and the second state-
B. Lower lingual holding arch ment is true.
C. Nance holding arch B. The first statement is true, and the second state-
D. Distal shoe space maintainer ment is false.
C. The first statement is false, and the second state- used to help predict timing of the adolescent growth
ment is true. spurt?
D. The first statement is false, and the second state- A. Neural tissues
ment is false. B. Lymphoid tissues
52. In an 8-year-old patient, tooth #8 was avulsed and was C. Reproductive tissues
replanted within 30 minutes. What is the best splint 59. Which of the following features characterize the
to use? primary dentition? (Choose two.)
A. Rigid fixation for 7 days A. Spacing between the teeth
B. Rigid fixation for 2 months B. Crowding of the teeth
C. Nonrigid fixation for 7 days C. Increased overbite
D. Nonrigid fixation for 2 months D. Decreased overbite
53. In an 8-year-old patient, teeth #8 and #9 have approxi- E. Ideal overbite
mately 50% of their crowns erupted. The patient fell F. Anterior crossbite
from a skateboard 1 month ago and hit teeth #8 and 60. An adult patient with a class II molar relationship and
#9 on the sidewalk. The radiograph today shows open a cephalometric ANB angle of 2 degrees has which
apices of these teeth, normal periodontal ligament, and type of malocclusion?
no apparent periapical radiolucency. The patient has A. Class II dental malocclusion
no reaction to electrical pulp tests. What is your treat- B. Class II skeletal malocclusion
ment of choice? C. Class I dental malocclusion
A. Calcium hydroxide pulpotomy D. Class II skeletal malocclusion
B. Formocresol apexification technique 61. Which of the following reactions is least likely to be
C. Calcium hydroxide apexification technique observed during orthodontic treatment?
D. Repeat examination and radiographs in 6 weeks A. Root resorption
54. A permanent incisor with a closed apex is traumati- B. Devitalization of teeth that are moved
cally intruded. What is the treatment of choice? C. Mobility of teeth that are moved
A. Gradual orthodontic repositioning and calcium D. Development of occlusal interferences
hydroxide pulpectomy 62. Doubling the force applied at the bracket of a tooth
B. Surgical repositioning and calcium hydroxide would have what effect on the rotational tendency
pulpectomy during tooth movement?
C. Gradual orthodontic repositioning and conven- A. The moment would decrease by 50%.
tional endodontic therapy B. The moment would not change.
D. Surgical repositioning and conventional endodon- C. The moment would double.
tic therapy D. The moment would increase fourfold.
55. Which of the following is the most likely cause of 63. Which of the following statements describe accurately
pulpal necrosis after trauma to a tooth? the ugly duckling stage of occlusal development?
A. Ankylosis (Choose three.)
B. Calcific metamorphosis A. This is considered to be a normal stage of occlusal
C. Pulpal hyperemia development.
D. Dilaceration B. It requires treatment whenever it is observed.
56. What is the sequence of treatment when orthodontic C. It occurs in the primary dentition.
therapy is involved as part of an interdisciplinary D. It occurs in the mixed dentition.
plan? E. The crowding that occurs in the maxillary incisors
A. Orthodontic alignment is likely to continue to worsen over time as the
B. Caries control permanent canines erupt.
C. Periodontal surgery including bone recontouring F. The small diastema created between the maxillary
D. Placement of full coverage crown central incisors is likely to close as the permanent
57. From the following, select the bones that grow primar- canines erupt.
ily by endochondral bone formation. (Choose three.) 64. When class III elastics are used, the maxillary first
A. Maxilla molars ______.
B. Mandible A. Move distally and intrude
C. Ethmoid B. Move mesially and extrude
D. Frontal C. Move mesially and intrude
E. Occipital D. Move only mesially; there is no movement in the
F. Sphenoid vertical direction
58. According to Scammons growth curves, which of the 65. Order the sequence of steps when performing serial
following tissues has a growth increase that can be extraction treatment.
A. A decision is made that the patient definitely needs medication youre giving me isnt strong enough?
extraction of permanent teeth to provide room for Choose the most appropriate response.
alignment in the future A. Did she make you feel worried about that?
B. Extraction of the permanent first premolars B. It sounds like youre worried that you might not
C. Extraction of the primary canines have enough pain relief when youre home.
D. Extraction of the primary first molars C. I understand your concern.
66. A 7-year-old patient has a 4-mm maxillary midline D. Dont worry. Ill give you plenty of pain medicine.
diastema. Which of the following should be done? E. It sounds like your sister had a unusually bad
A. Brackets should be placed to close it. experience. Dont believe what others tell you, and
B. A radiograph should be taken to rule out the pres- certainly dont let that worry you. Youll be fine.
ence of a supernumerary tooth. 2. During admission, a patient interrupts you on numer-
C. Nothing should be done. It will close on its own. ous occasions with stories about past dental experi-
D. Nothing should be done. Treatment should be ences while you are attempting to take a complete
deferred until the rest of the permanent dentition medical history. Your best response would be ____.
erupts. A. Say nothing, listen to the patient, and finish your
67. Reduction of overbite can be accomplished most intake as best you can.
readily by which of the following treatment B. Say, Id like to focus on your present experience
strategies? and right now I need to know your medical history.
A. Intruding maxillary incisors C. Say, It seems like youve had some important expe-
B. Uprighting maxillary and mandibular incisors riences and I would like to hear more about them,
C. Using a high-pull headgear to the maxillary molars but first, lets discuss this health questionnaire
D. Using a lip bumper before we address them, okay?
68. Match the stage of tooth development with the D. Say, I dont need to know the details of your dental
anomaly. history. Please inform me of the experiences asked
about in the questionnaire.
A. Initiation ____ 1. Excessive systemic
E. Say, We have about 30 minutes to complete this
B. Histodifferentiation fluoride ingestion
questionnaire and get started in your examination,
____ 2. Peg permanent
so lets focus on that.
C. Morphodifferentiation lateral incisor
3. A 7-year-old child has a history of recurrent pain and
____ 3. Dentinogenesis
discomfort in a second molar, which has a necrotic
D. Calcification ____ imperfecta
pulp. You present the treatment options to the parents.
4. Congenitally missing
There are several ways in which we can treat this
tooth
problem. We could do a pulpectomy in which we .
69. Which of the following are consistent with dentino- We could do something called a pulpotomy, which
genesis imperfecta? (Choose three.) involves . We could apply a pulp cap, which is .
A. Internal root resorption We could remove the tooth. Or we could leave the
B. Primary and permanent teeth affected tooth untreated for now and see how things go. You
C. Pitted enamel have phrased the options so that they are in what you
D. Enamel chips easily believe to be the order of descending desirability, and
E. Small or absent pulp chambers or canals you have indicated that to the patient. Which option
F. Normal tooth color is most likely to be chosen by the parents?
70. Order the process of tooth formation. Match each A. Pulpectomy
letter with its proper sequence number. B. Pulpotomy
1. ____ A. Apposition C. Pulp cap
2. ____ B. Histodifferentiation D. Extraction
3. ____ C. Calcification E. No treatment
4. ____ D. Initiation 4. Which of the following statements regarding motiva-
5. ____ E. Proliferation tion is false?
A. Motivation is strengthened when a person suc-
ceeds and is weakened when a person fails to
Patient Management achieve his or her goals.
B. Motivation is increased when the person focuses
1. A patient is sitting in the chair immediately after an on long-term goals.
extraction. She says, Thank you. That wasnt as bad as C. Motivating a person can be achieved by generating
I expected, but my sister told me that the first night interest, showing your concern, and providing
after having a tooth pulled is very painful. What if the information.
D. Encourage a sense of personal acceptance in the 9. Which of the following statements regarding the rela-
face of the inevitable difficulties involved in break- tionship between pain and fear is false?
ing old habits and establishing new ones. A. Fear initially inhibits pain owing to a release of
E. Help a patient cope with relapses by emphasizing endorphins from the pituitary, resulting in an anal-
the knowledge gained. gesic effect.
5. Which of the following statements about behavioral B. Although muscle tension contributes to the experi-
contracts is false? ence of anxiety, it does not contribute to the per-
A. It is a legal and binding agreement between health ception of pain.
care professional and patient. C. Any autonomic activation causes one to have a
B. It helps solidify an agreement with a patient. lower pain threshold.
C. It should always be open to modification. D. Catastrophic thinking and a perceived lack of
D. It helps clarify agreements. control are common factors that influence pain
E. The clinician should give a copy to the patient and perceptions.
keep one for himself or herself. E. Misattribution occurs when patients identify an
6. A 6-year-old patient likes to tell you stories about event as painful because they can identify a fearful
school. Each time he begins a story, you stop working stimulus.
to listen. After three long sessions, you realize that the 10. Which of the following is an example of a cognitive
child is attempting to avoid or delay the dental work strategy that may be useful in pain management?
by telling stories. You decide that from this point on A. Address expectations by providing information
you are going to continue working while engaged in and addressing any questions or concerns
conversation with the patient. At first, the child tells B. Suggest to patients that they learn to identify, eval-
you more stories about school and tries other strategies uate, and eliminate maladaptive thinking
to get your attention and stop your work. He eventually C. Encourage patient efforts to address their anxiety
settles down and allows you to work, whether or not and pain management
you are engaged in conversation. This is an example D. Suggest to patients that they learn to generate,
of ____. evaluate, and apply more realistic thinking
A. Shaping E. All of the above
B. Extinction 11. Which of the following scenarios is an example of
C. Modeling classical conditioning?
D. Stimulus control A. You teach an anxious patient diaphragmatic breath-
E. Power ing (unconditional stimulus [US]), which naturally
7. Which of the following is not a factor in the appraisal induces the physiologic relaxation response (un-
of stress? conditional response [UR]). You seat the anxious
A. Familiarityhow familiar the situation is; the less patient in the dental chair for an examination (con-
familiar, the more stressful it may seem ditional stimulus [CS]) and ask the patient to use
B. Predictabilityhow predictable the situation is; diaphragmatic breathing during the examination
the less predictable, the more stressful it may (US). While using the breathing skills, the patient
seem feels more relaxed (conditional response [CR]).
C. Controllabilityhow controllable the situation B. You teach an anxious patient diaphragmatic breath-
seems to be; the less controllable, the more stressful ing (US), which naturally induces the physiologic
it may seem relaxation response (UR). You ask the patient to
D. Imminencethe more imminent the situation is, practice that technique at home (CS) and use it
the more stressful it may seem during procedures to reduce the subjective experi-
E. Positive or negative valencewhether the situation ence of anxiety (CR).
is positive or negative; positive situations (e.g., a C. You teach an anxious patient diaphragmatic breath-
wedding) are typically experienced as less stressful ing (US), which naturally induces the physiologic
than negative situations (e.g., a divorce) relaxation response (UR). You seat the anxious
8. The substitution of a relaxation response for an anxiety patient in the dental chair for an examination (CS)
response (using a relaxation strategy such as diaphrag- and ask the patient to use diaphragmatic breathing
matic breathing) when one is exposed to a hierarchy during the examination (US). The focus on breath-
of feared stimuli is called ____. ing serves as a distraction (US) from what the
A. Progressive muscle relaxation patient feels is threatening and fearful (CR), and
B. Habituation the patient reports less anxiety (CR).
C. Flooding D. You teach an anxious patient diaphragmatic breath-
D. Systematic desensitization ing (US), which naturally induces the physiologic
E. Biofeedback relaxation response (UR). You seat the anxious
patient in the dental chair for an examination (CS) B. If you praise your 5-year-old patient and reward
and ask the patient to use diaphragmatic breathing him for keeping his legs still while you are drilling,
during the examination (US). After a number of this will increase the likelihood that he will remain
these experiences, the patient feels relaxed during still in similar situations in the future.
the examination while using the breathing tech- C. If you make the dental environment a child-
nique (UR) and without using it at all (CR). friendly place, your young patient will be more
E. None of the above comfortable.
12. The best strategy for addressing dental fear that is D. If you pair the dental chair with having a
based on distrust of the dentist is to ____. parent present, the child will be less likely to be
A. Use distraction techniques anxious.
B. Use cognitive coping strategies E. None of the above.
C. Enhance informational and behavioral control 17. According to research on anxiety disorders, it has been
D. Teach diaphragmatic breathing suggested that ____ is the most important component
E. Reassure the patient that he or she can trust you of systematic desensitization.
13. What behavior can you typically expect from an A. Cognitive restructuring
anxious patient in the dental chair? B. Progressive muscle relaxation
A. He or she is more likely to sit still, hands clasped C. Diaphragmatic breathing
together. D. Exposure
B. He or she is more likely to sit casually, legs crossed, E. Psychoeducation
reading a magazine. 18. Sarah S. is a young child who consistently presents as
C. He or she is more likely to keep to himself or herself anxious, hypervigilant, and upset during dental visits.
and not speak unless spoken to. Sarah is often accompanied by her parent, who appears
D. He or she is more likely to fidget in the chair, to be very concerned about the child and wants to be
moving his or her hands and feet. involved at all times in her evaluation and treatment.
E. Both A and C. During this visit, Sarahs treatment requires an injec-
14. With no other intervention or instruction, which of tion and a rubber dam application, which you antici-
the following is most likely to trigger a physiologic pate may lead to increased anxiety. Which strategy
relaxation response? would be the least effective in completing the rubber
A. Observing ones own physiologic responses (e.g., dam application?
heart rate, blood pressure) A. Tell-Show-Do
B. Muscle tensing B. Distraction
C. Reassurance C. Ask the child to be a helper
D. Thought stopping D. Structure time
E. Diaphragmatic breathing E. Rehearsals
15. A 32-year-old man is fearful of receiving injections. 19. Which of the following factors are involved in the cog-
You decide to use a cognitive-behavioral strategy with nitive appraisal of a threat?
him to help him through an injection. You have A. Interference, adaptability, longevity, and reactance
already instructed him in diaphragmatic breathing B. Adaptability, preventability, inevitability, and
and ask him to practice this skill throughout the constancy
procedure. First, you show him the syringe. You C. Controllability, familiarity, predictability, and
talk about the characteristics of the needle. Next, imminence
you place the needle in his mouth with the cap on. D. Validity, reliability, adaptability, and predictability
You simulate the procedure with the cap on. You then E. Accountability, reliability, validity, and familiarity
simulate the procedure with the cap off. Eventually, 20. A patient has difficulty inhibiting the gag reflex during
you proceed with the injection. What does this pro x-ray procedures. You suggest that the patient take
cedure exemplify? several x-ray packets home and practice holding the
A. Habituation packets in his or her mouth for increasingly longer
B. Cognitive control periods of time. Which of the following techniques
C. Flooding does this best exemplify?
D. Systematic desensitization A. Reinforcement
E. Behavior modification B. Graded exposure
16. Principles of operant conditioning teach us that ____. C. Modeling
A. If you praise your 5-year-old patient and reward D. Behavioral control
him for keeping his legs still while you are drilling, E. Systematic desensitization
this will make the child happy and more likely to 21. When faced with a frightened child patient, which
like you and less likely to resist your requests. would be the most appropriate or effective response?
A. Ask the child about his or her fears 28. The supplemental fluoride daily dosage schedule for a
B. Reschedule the appointment for a later date 5-year-old child who lives in a community where the
C. Reassure the child concentration of fluoride in the drinking water is less
D. Tell the child that dentistry should not be than 0.3ppm is ____.
frightening A. 0mg
E. Chastise the child B. 0.10mg
22. Research suggests that life events and perceived stress C. 0.25mg
or distress ____ predictors of self-reported health D. 0.50mg
concerns. E. 1mg
A. Are 29. What type of epidemiology is primarily used in inter-
B. Are not vention studies?
C. Are sometimes A. Descriptive
D. Have little to do with B. Analytical
E. None of the above C. Observational
23. Patients experiencing stress and anxiety typically D. Experimental
require ____ interpersonal distance for comfortable E. None of the above
interaction. 30. A researcher follows a group of individuals in a popu-
A. Greater lation over 10 years to determine who develops cancer
B. Less and then evaluates the factors that affected the group.
C. The same as patients who are not experiencing What type of study is this?
stress and anxiety A. Cross-sectional
D. Individualized B. Case-control
E. Behaviorally controlled C. Randomized
24. Which of the following statements about the use of D. Prospective cohort
silence as an interviewing technique is true? E. Retrospective cohort
A. It permits and encourages patient participation. 31. A group of researchers undertook a study to assess the
B. It is a nonverbal technique for showing interest in relationship between squamous cell carcinoma and
the patient. chewing tobacco. The researchers determined past
C. It is a nonverbal technique for encouraging the exposure records among subjects who had been diag-
patient to speak. nosed with the disease. This type of study was a ____.
D. It is done by silently attending to the patient, while A. Clinical trial
maintaining eye contact. B. Community trial
E. All of the above C. Retrospective cohort study
25. How do people typically respond to stress? D. Case-control study
A. Physiologically (fight-or-flight response, i.e., auto- E. Randomized clinical trial
nomic arousal) 32. Which part of a scientific article summarizes the
B. Cognitively (beliefs of self-efficacy, stress background and focus of the study; the population
appraisal) sampled; and the experimental design, findings, and
C. Behaviorally (e.g., disturbed sleep or appetite, conclusion?
impaired attention, acting out) A. Introduction
D. Emotionally (e.g., anxiety, anger, fear) B. Background
E. All of the above C. Literature review
26. Which of the following indices is not reversible? D. Methods
A. DMFT E. Abstract
B. GI 33. In what section of a scientific article does the researcher
C. PI interpret and explain the results obtained?
D. OHI-S A. Summary and conclusion
E. None of the above B. Results
27. The recommended level of fluoride for community C. Discussion
water supply systems in the United States ranges D. Abstract
from ____. E. None of the above
A. 0.2 to 0.5ppm 34. The following were the scores for six dental students
B. 0.7 to 1.2mL in their Restorative Dentistry examination: 56, 64, 68,
C. 1.2 to 1.5ppm 46, 82, 86. The median is ____.
D. 0.2 to 0.5mL A. 68
E. 0.7 to 1.2ppm B. 64
C. 67 A. Antisepsis
D. 40 B. Microbacterial control
E. 66 C. Sterilization
35. A correlation analysis shows that as the income of the D. Disinfection
population increases, the number of decayed teeth E. Asepsis
decreases. An expected value for this correlation coef- 41. Which of the following is the most common method
ficient (r) would be ____. of sterilization?
A. 0 A. Dry heat
B. 1 B. Ethylene oxide
C. 1 C. Glutaraldehyde at 2%
D. 2 D. Autoclave
E. 2 E. Chemiclave
36. A test result that erroneously excludes an individual 42. A set of precautions designed to prevent transmission
from a specific diagnostic or reference group is of HIV, hepatitis B virus (HBV), and other bloodborne
called ____. pathogens when providing first aid or health care is
A. Erroneous known as ____.
B. False positive A. Asepsis
C. False negative B. Infection control
D. Mistaken C. Sterilization
E. None of the above D. Disinfection
37. Which of the following statements about transmissible E. Standard infection control procedures
diseases is false? 43. Which of the following chemical agents is not a
A. The risk of transmission after percutaneous injury disinfectant?
is higher for hepatitis B virus (HBV) than for HIV. A. Iodophors
B. Hepatitis C virus (HCV) and HIV are both caused B. Sodium hypochlorite
by an RNA virus. C. Synthetic phenol
C. A vaccine to immunize against HBV is available. D. Isopropyl alcohol
D. The average risk of infection for HBV after a E. Glutaraldehyde
needle-stick injury falls between that for HCV 44. Which of the following recommendations must be
and HIV. followed when handling mercury?
E. All of the above A. Train personnel involved in the handling of
38. In HIV diagnosis, the Western blot assay is used to mercury
confirm the results of a positive enzyme-linked immu- B. Work in properly ventilated areas
nosorbent assay test. We can say that the Western blot C. Use high-volume evacuation systems when finish-
test would confirm a ____. ing or removing amalgams
A. True-positive result D. Avoid direct skin contact with the metal
B. True-negative result E. All of the above
C. False-positive result 45. According to the U.S. Centers for Disease Control and
D. False-negative result Prevention (CDC), the acceptable water quality in a
E. None of the above dental office should be ____.
39. Which of the following statements about the hepatitis A. Less than 125CFU/mL
B virus (HBV) vaccination is true? B. Less than 250CFU/mL
A. The HBV vaccine must be offered to all potentially C. Less than 500CFU/mL
exposed dental workers. D. Less than 750CFU/mL
B. The HBV vaccine must be free to all potentially E. Less than 1000CFU/mL
exposed dental workers. 46. Which of the following American Dental Association
C. At the time of employment, each person should Principles of Ethics states that a dentist has a duty to
be asked to provide documentation of previous respect the patients right to self-determination and
immunizations. confidentiality?
D. Three doses of HBV vaccine are given to confer A. Patient autonomy
immunity. B. Nonmaleficence
E. All of the above C. Beneficence
40. Which of the following terms refers specifically to the D. Justice
process where an antimicrobial agent destroys (germi- E. Veracity
cide) or avoids the growth (microbiostatic) of patho- 47. Which of the following are characteristics of proper
genic microorganisms on inanimate surfaces? documentation in a dental record?
A. Specific C. Mean of a set of data

B. Objective D. Middle measurement in a set of data
C. Complete 54. Which statistical test is used to analyze whether or not
D. Timely the means of several groups are equal and generalizes
E. All of the above a t test to more than two groups?
48. Which of the following is an arrangement between a A. Analysis of variance (ANOVA)
plan and a group of dentists whereby the providers B. 2 test
agree to accept certain payments (usually less than C. Correlation coefficient
their usual fees) in anticipation of a higher volume of D. Multiple regression
patients? 55. Which characteristic does not apply to community
A. PPO water fluoridation?
B. Capitation A. Prevents tooth decay in all age groups
C. HMO B. Water fluoridation usually requires supplemental
D. IPA systemic fluoride treatment in children younger
E. None of the above than 12 years of age
49. Which of the following agencies monitors and pre- C. Approximately 75% of the U.S. population have
vents disease outbreaks, implements disease pre proper water fluoridation
vention strategies, and maintains national health D. The optimal fluoride level in the water supply is 0.7
statistics? to 1.2ppm
A. CDC 56. For which of the following infectious diseases is there
B. FDA an effective immunization?
C. DEA A. Hepatitis A virus (HAV)
D. IHS B. Hepatitis B virus (HBV)
E. None of the above C. HIV/AIDS
50. Which of the following federal agencies is the principal D. Tuberculosis
agency of the U.S. government for protecting the E. Hepatitis C virus (HCV)
health of all Americans and providing essential human 57. The National Fire Protection Association color and
services? number method is used to identify easily information
A. DHHS about various hazardous chemicals on the material
B. NIH safety data sheets and product labels. Which color
C. HRSA identifies the reactivity or stability of a chemical?
D. AHRQ A. Blue
E. None of the above B. Red
51. Which of the following statements pertain to a case- C. Yellow
control study? (Choose all that apply.) D. White
A. Patients with a specific condition or disorder are 58. Which of the following are required informational
compared with controls. elements for informed consent? (Choose all that
B. A general population is followed through time to apply.)
see who develops a disease. A. Explanation of the procedure in understandable
C. Investigators seek an association with or cause for terms
(e.g., lifestyle or dietary habits) a condition. B. Reasons for the procedure and the benefits and
D. Investigators seek to establish a temporal relation- risks of the procedure and anticipated outcome
ship between a cause and a condition. C. Any alternatives and their risks and benefits,
52. Which of the following are common subsections of including no treatment at all
the methods section of a scientific article? (Choose all D. The costs of the procedure and the alternatives
that apply.)
A. Sampling strategy
B. Measurement strategies and measurement Periodontics
instruments
C. Experimental design 1. Loss of tooth substance by mechanical wear is ____.
D. Commentary on the results A. Abrasion
E. Statistical analytical procedures B. Attrition
53. In a measurement of a set of data, the median is defined C. Erosion
as the ____. D. Abfraction
A. Average of the set of data 2. The width of keratinized gingiva is measured as the
B. Most frequent measurement in a set of data distance from the ____.
A. Free gingival margin to the mucogingival junction A. Porphyromonas gingivalis

B. Cementoenamel junction to the mucogingival B. Streptococcus gordonii
junction C. Haemophilus parainfluenzae
C. Free gingival groove to the mucogingival junction D. Fusobacterium nucleatum
D. Free gingival margin to the base of the pocket 10. What features best characterize the predominant
3. Which of the following best distinguishes periodontitis microflora associated with periodontal health?
from gingivitis? A. Gram-positive, anaerobic cocci and rods
A. Probing pocket depth B. Gram-negative, anaerobic cocci and rods
B. Bleeding on probing C. Gram-positive, facultative cocci and rods
C. Clinical attachment loss D. Gram-negative, facultative cocci and rods
D. Presence of suppuration 11. Which of the following microorganisms is frequently
4. A 22-year-old college student presents with oral pain, associated with localized aggressive periodontitis?
erythematous gingival tissues with blunt papillae A. Porphyromonas gingivalis
covered with a pseudomembrane, spontaneous gingi- B. Actinobacillus actinomycetemcomitans
val bleeding, and halitosis. There is no evidence of C. Actinomyces viscosus
clinical attachment loss. What form of periodontal D. Streptococcus mutans
disease does this patient most likely have? 12. Which of the following is the primary etiologic factor
A. Gingivitis associated with dental plaque associated with periodontal disease?
B. Localized aggressive periodontitis A. Age
C. Generalized chronic periodontitis B. Gender
D. Necrotizing ulcerative gingivitis C. Nutrition
5. Which of the following methods of radiographic D. Bacterial plaque
assessment are best for identifying small volumetric 13. Inadequate margins of restorations should be cor-
changes in alveolar bone density? rected primarily because they ____.
A. Bitewing A. Cause occlusal disharmony
B. Periapical B. Interfere with plaque removal
C. Subtraction C. Create mechanical irritation
D. Panoramic D. Release toxic substances
6. What tooth surfaces should be evaluated for furcation 14. Light smokers are likely to have less severe periodon-
involvement on maxillary molars? titis than heavy smokers. Former smokers are likely to
A. Palatal, facial, and distal have more severe periodontitis than current smokers.
B. Mesial, distal, and palatal A. Both statements are true.
C. Facial, palatal, and mesial B. Both statements are false.
D. Facial, mesial, and distal C. The first statement is true, and the second state-
7. What bacterial species are found in increased numbers ment is false.
in the apical portion of tooth-associated attached D. The first statement is false, and the second state-
plaque? ment is true.
A. Gram-negative rods 15. Well-controlled diabetics have more periodontal
B. Gram-positive rods disease than nondiabetics. Well-controlled diabetics
C. Gram-positive cocci generally can be treated successfully with conventional
D. Gram-negative cocci periodontal therapy.
8. What are the major organic constituents of bacterial A. Both statements are true.
plaque? B. Both statements are false.
1. Calcium and phosphorus C. The first statement is true, and the second state-
2. Sodium and potassium ment is false.
3. Polysaccharides and proteins D. The first statement is false, and the second state-
4. Glycoproteins and lipids ment is true.
A. 1 and 2 16. Oral contraceptives can cause gingivitis. Oral contra-
B. 2 and 3 ceptives can accentuate the gingival response to bacte-
C. 3 and 4 rial plaque.
D. 2 and 4 A. Both statements are true.
9. Although many plaque bacteria coaggregate, which of B. Both statements are false.
the following bacteria is believed to be an important C. The first statement is true, and the second state-
bridge between early colonizers and late colonizers ment is false.
as plaque matures and becomes more microbiologi- D. The first statement is false, and the second state-
cally complex? ment is true.
17. Which of the following cells produce antibodies? 25. Scalers are used to remove supragingival deposits.
A. Neutrophils Curettes are used to remove either supragingival or
B. T lymphocytes subgingival deposits.
C. Macrophages A. Both statements are true.
D. Plasma cells B. Both statements are false.
18. Defects in which inflammatory cell have most fre- C. The first statement is true, and the second state-
quently been associated with periodontal disease? ment is false.
A. T lymphocyte D. The first statement is false, and the second state-
B. Mast cell ment is true.
C. Plasma cell 26. Which of the following is not a characteristic of sickle
D. Neutrophil scalers?
19. What is the major clinical difference between the A. Two cutting edges
established lesion of gingivitis and the advanced lesion B. Rounded back
of periodontitis? C. Cutting edges meet in a point
A. Gingival color, contour, and consistency D. Triangular in cross section
B. Bleeding on probing E. Used for removal of supragingival deposits
C. Loss of crestal lamina dura 27. The modified Widman flap uses three separate
D. Attachment and bone loss incisions. It is reflected beyond the mucogingival
E. Suppuration junction.
20. Which interleukin (IL) is important in the activation A. Both statements are true.
of osteoclasts and the stimulation of bone loss seen in B. Both statements are false.
periodontal disease? C. The first statement is true, and the second state-
A. IL-1 ment is false.
B. IL-2 D. The first statement is false, and the second state-
C. IL-8 ment is true.
D. IL-10 28. The free gingival graft technique can be used
21. Scaling and root planing are used in which phases of to increase the width of attached gingival tissue. Api-
periodontal therapy? cally displaced full-thickness or partial-thickness flaps
1. Initial (hygienic) can also be used to increase the width of attached
2. Surgical (corrective) gingiva.
3. Supportive (maintenance) A. Both statements are true.
A. 1 only B. Both statements are false.
B. 1 and 2 only C. The first statement is true, and the second state-
C. 2 and 3 only ment is false.
D. 1 and 3 only D. The first statement is false, and the second state-
E. 1, 2, and 3 ment is true.
22. What is the most objective clinical indicator of 29. Miller class I recession defects can be distinguished
inflammation? from class II defects by assessing the ____.
A. Gingival color A. Location of interproximal alveolar bone
B. Gingival consistency B. Width of keratinized gingiva
C. Gingival bleeding C. Involvement of the mucogingival junction
D. Gingival stippling D. Involvement of the free gingival margin
23. A 25-year-old patient presenting with generalized 30. The reshaping or recontouring of nonsupportive alveo-
marginal gingivitis without any systemic problems or lar bone is called ____.
medications should be classified with which periodon- A. Ostectomy
tal prognosis? B. Osteoplasty
A. Good C. Osteography
B. Fair D. All of the above
C. Poor 31. How many walls does an interdental crater have?
D. Questionable A. One
24. Instrumentation of the teeth to remove plaque, calcu- B. Two
lus, and stains is defined as ____. C. Three
A. Coronal polishing D. Four
B. Scaling 32. During the healing of a surgically treated intrabony
C. Gingival curettage (infrabony) pocket, regeneration of a new periodontal
D. Root planing ligament, cementum, and alveolar bone occurs only
when cells repopulate the wound from which of the C. For patient comfort
following sources? D. As a preventive measure
A. Gingival epithelium 41. In the treatment of an acute periodontal abscess, the
B. Connective tissue most important first step is to ____.
C. Alveolar bone A. Prescribe systemic antibiotics
D. Periodontal ligament B. Reflect a periodontal flap surgery
33. Which of the following is least likely to be successfully C. Obtain drainage
treated with a bone graft procedure? D. Prescribe hot salt mouth washes
A. One-walled defect 42. Which of the following medications often result in
B. Two-walled defect overgrowth of gingival tissues?
C. Three-walled defect A. Penicillin, calcium channel blockers, phenytoin
D. Class III furcation defect B. Calcium channel blockers, phenytoin, and
34. When osseointegration occurs, which of the following cyclosporine
best describes the implant-bone interface at the level of C. Cyclosporine, penicillin, and cephalosporins
light microscopy after osseointegration? D. Ampicillin, tetracycline, and erythromycin
A. Epithelial attachment 43. Which of the following is the most important pre
B. Direct contact ventive and therapeutic procedure in periodontal
C. Connective tissue insertion therapy?
D. Cellular attachment A. Professional instrumentation
35. The most effective topical antimicrobial agent currently B. Subgingival irrigation with chlorhexidine
available is ____. C. Patient-administered plaque control
A. Chlorhexidine D. Surgical intervention
B. Stannous fluoride 44. How many hours after brushing does it usually take for
C. Phenolic compounds a mature dental plaque to reform?
D. Sanguinarine A. 1 to 2
36. What is the active ingredient in PerioChip? B. 5 to 10
A. Doxycycline C. 12 to 24
B. Tetracycline D. 24 to 48
C. Metronidazole 45. Placing the toothbrush bristles at a 45-degree angle
D. Chlorhexidine on the tooth and pointing apically so that the bristles
37. How many days does it usually take for surface epithe- enter the gingival sulcus describes which brushing
lialization to be complete after a gingivectomy? technique?
A. 3 to 7 A. Charter
B. 5 to 14 B. Stillman
C. 14 to 18 C. Bass
D. 20 to 27 D. Roll
38. The most obvious clinical sign of trauma from occlu- 46. Systemically administered subantimicrobial doses of
sion is increased tooth mobility. The most obvious doxycycline are sometimes used to treat chronic peri-
radiographic sign of trauma from occlusion is an odontitis because the doxycycline inhibits which
increase in the width of the periodontal ligament enzyme?
space. A. Amylase
A. Both statements are true. B. -Lactamases
B. Both statements are false. C. Metalloproteinases
C. The first statement is true, and the second state- D. Cyclooxygenases
ment is false. E. 5-Lipoxygenase
D. The first statement is false, and the second state- 47. Place in their order of sequence (earliest first), the
ment is true. events that normally take place after suturing is done
39. Trauma from occlusion refers to the ____. to close a periodontal flap.
A. Occlusal force A. Collagen fibers appear
B. Damage to the tooth B. Epithelial cells begin to migrate
C. Injury to the tissues of the periodontium C. Clot formation
D. Widened periodontal ligament D. An epithelial attachment is in place
40. Which of the following is the primary reason for 48. For which conditions (occurring either alone or to-
splinting teeth? gether) are systemic antibiotics indicated for treatment
A. For esthetics of acute necrotizing ulcerative gingivitis? (Choose
B. To improve hygiene two.)
A. Foul oral smell A. One

B. Pain B. Two
C. Lymphadenopathy C. Three
D. Fever D. Four
E. Presence of a pseudomembrane 5. In what situation is the postganglionic nerve of the
49. Regarding furcation involvement of a periodontal sympathetic system a cholinergic nerve?
pocket, what grade of involvement would include cul- A. The nerves to the eye
de-sac formation with a definite horizontal component B. The nerves to the heart
but without complete bone loss in the furcation? C. Most nerves to blood vessels
A. I D. Most nerves to sweat glands
B. II E. Most nerves to salivary glands
C. III 6. Which of the following is a nicotinic receptor?
D. IV A. Receptor for the neurotransmitter at the skeletal-
50. In plaque formation, which two organisms are the ear- neuromuscular junction
liest colonizers? B. Receptor for the neurotransmitter at the junction
A. Prevotella species and Capnocytophaga species between the postganglionic sympathetic nerve and
B. Porphyromonas gingivalis and Aggregatibacter sweat glands
actinomycetemcomitans C. Receptor for the neurotransmitter at the junction
C. Streptococcus species and Actinomyces species between the postganglionic parasympathetic nerve
D. Campylobacter species and Fusobacterium and the parotid gland
nucleatum. D. Receptor for the neurotransmitter at the junction
between the postganglionic sympathetic nerve and
blood vessels
Pharmacology E. Receptor for the neurotransmitter at the junction
between the postganglionic parasympathetic nerve
1. Tight capillary cell junctions resulting in an added and the heart
barrier to the entry of drugs is most characteristic of 7. Which of the following effects is a typical effect of an
which organ or tissue? antimuscarinic drug?
A. Adrenal gland A. Bronchoconstriction
B. Brain B. Lacrimation
C. Heart C. Miosis
D. Liver D. Sweating
E. Lung E. Urinary retention
2. A prescription for which of the following drugs 8. The administration of which compound would provide
requires a valid Drug Enforcement Administration epinephrine reversal (decrease in blood pressure
(DEA) number on the prescription? from epinephrine) if given before administration of
A. Amoxicillin epinephrine?
B. Carbamazepine A. Atropine
C. Dexamethasone B. Guanethidine
D. Diphenhydramine C. Propranolol
E. Oxycodone D. Phenoxybenzamine
3. What would be the effect of prior administration of a E. Tyramine
competitive drug antagonist on the concentration- 9. Motor adverse effects from phenothiazine antipsy-
response profile of a drug agonist on a graded chotic drugs are due to drug effects in what region of
concentration-response curve? (Assume that both the brain?
drugs act at the same receptor.) A. Chemoreceptor trigger zone
A. The agonist curve would shift to the left. B. Cerebrum
B. The agonist curve would shift to the right. C. Cerebellum
C. The agonist curve would not change. D. Nigrostriatal pathway
D. The agonist curve would not shift but would reach E. Mesolimbic pathway
a lower maximal effect than the curve with agonist 10. A patient is administered haloperidol. Along with the
alone. haloperidol, the patient also receives benztropine.
E. The agonist curve would both shift to the left and What is the most likely reason for administering the
have a lower maximal effect. benztropine?
4. How many human drug testing phases are carried out A. To reduce the effects of histamine release
before a drug is marketed? B. To aid in the therapeutic response to haloperidol
C. To reduce the motor adverse effects of D. Ibuprofen, naproxen

haloperidol E. Aspirin, ibuprofen
D. To overcome a decrease in salivary flow resulting 18. Your patient takes a small daily dose of aspirin (82mg)
from haloperidol prescribed by the patients physician. The object of this
E. To reduce the rate of kidney excretion of therapy is most likely what mechanism?
haloperidol A. To mimic the effect of endogenous endorphins
11. The benzodiazepine receptors BZ1 and BZ2 are located B. To inhibit the production of prostaglandin E1
on which ion channel? C. To inhibit the production of thromboxane A2
A. Calcium D. To inhibit the production of arachidonic acid
B. Chloride E. To inhibit the production of leukotrienes
C. Magnesium 19. Your patient indicates that he is taking medication for
D. Potassium atrial fibrillation. He reports that a blood test has indi-
E. Sodium cated that he has an international normalized ratio
12. Methemoglobinemia is an adverse effect associated (INR) value of 4.0. An emergency dental extraction is
with which local anesthetic as a result of its metabo- now required. Which postoperative medication would
lism to o-toluidine? pose the greatest risk for an adverse effect in this
A. Lidocaine patient?
B. Mepivacaine A. Acetaminophen
C. Prilocaine B. Amoxicillin
D. Bupivacaine C. Aspirin
E. Benzocaine D. Codeine
13. Which of the following drugs poses the greatest risk of E. Ibuprofen
a cardiac arrhythmia when administered at the same 20. Which drug blocks H1 histamine receptors but is least
time as epinephrine? likely to cause sedation?
A. Desflurane A. Diphenhydramine
B. Halothane B. Hydroxyzine
C. Isoflurane C. Fexofenadine
D. Propofol D. Albuterol
E. Sevoflurane E. Famotidine
14. Local anesthetics act on what type of receptor? 21. The use of selective cyclooxygenase-2 inhibitors has
A. Ion channel receptor been restricted or discontinued more recently because
B. Nuclear receptor of what type of adverse effects?
C. Seven-membrane domain receptor linked to Gs A. Carcinogenesis
D. Seven-membrane domain receptor linked to Gq B. Cardiovascular disorders
E. Membrane receptor with tyrosine kinase activity C. Convulsive disorders
15. Which of the following drugs lacks the amine terminus D. Striated muscle disorders
that other anesthetics have and is used only topically? E. Skeletal disorders
A. Procaine 22. Sodium reabsorption in the thick ascending limb of
B. Mepivacaine the loop of Henle is inhibited by which drug?
C. Lidocaine A. Bumetanide
D. Benzocaine B. Chlorthalidone
E. Prilocaine C. Hydrochlorothiazide
16. Injecting a local anesthetic into an area of inflamma- D. Spironolactone
tion would ____. E. Triamterene
A. Increase the rate of onset of anesthesia 23. Torsades de pointes, or polymorphic ventricular tachy-
B. Decrease the rate of metabolism of the anesthetic cardia, is linked most closely to what characteristic of
C. Reduce the net anesthetic effect of the drug the electrocardiogram (ECG)?
D. Reduce the vasodilator effect of the local A. Inverted T wave
anesthetic B. Shorter PR interval
E. Reduce the need for a vasoconstrictor with the C. Shorter PP interval
local anesthetic D. Longer QT interval
17. Which two drugs have mechanisms of analgesic action E. Normal ECG
that are most similar? 24. Which antihypertensive drug also increases bradyki-
A. Fentanyl, ibuprofen nin levels?
B. Aspirin, codeine A. Candesartan
C. Oxycodone, acetaminophen B. Furosemide
C. Lisinopril C. Mycoplasma pneumoniae

D. Metoprolol D. Streptococcus pneumoniae
E. Nifedipine E. Streptococcus pyogenes
25. Which one of the following drugs enters the target cell 33. What is the approximate elimination half-time for
and acts on a nuclear receptor? penicillin V?
A. Diazepam A. 0.5 hour
B. Epinephrine B. 2 hours
C. Insulin C. 4 hours
D. Prednisone D. 8 hours
E. Heparin E. 12 hours
26. Inhibiting -glucosidase and reducing glucose absorp- 34. ____ has an antibacterial spectrum that is limited to
tion from the gastrointestinal tract is the mechanism anaerobes.
of action of ____. A. Amoxicillin
A. Acarbose B. Clarithromycin
B. Acetohexamide C. Clindamycin
C. Glyburide D. Gentamicin
D. Metformin E. Metronidazole
E. Pioglitazone 35. Which drugs are very susceptible to metabolism by
27. Which of the following drugs blocks the aldosterone serum cholinesterases? (Choose two.)
receptor? A. Carbachol
A. Amiloride B. Articaine
B. Triamterene C. Bethanechol
C. Losartan D. Acetylcholine
D. Spironolactone E. Pilocarpine
E. Furosemide 36. Match the antidiabetic drug with its mechanism of
28. Which of the following drugs is most selective as a action.
glucocorticosteroid?
A. Glibenclamide ____ 1. Inhibits -glucosidase
A. Aldosterone
B. Metformin ____ and delays carbohydrate
B. Dexamethasone
C. Rosiglitazone ____ digestion in the gut
C. Fludrocortisone
D. Sitagliptin ____ 2. Activates transcription
D. Hydrocortisone
E. Miglitol ____ factor PPAR, leading
29. Stimulation of gluconeogenesis and lipolysis are most
to increased insulin
characteristic of which hormone?
sensitivity in tissues
A. Calcitonin
3. Inhibits dipeptidyl
B. Cortisol
peptidase-4, increasing
C. Insulin
the level of glucagonlike
D. Parathyroid hormone
peptide
E. Progesterone
4. Increases the release of
30. Fanconis syndrome resulting from outdated tetracy-
insulin
clines affects predominantly which organ?
5. Activates adenosine
A. Brain
monophosphate (AMP)
B. Heart
kinase, reducing liver
C. Kidney
glucose production,
D. Pancreas
gluconeogenesis, and
E. Stomach
lipogenesis
31. Methicillin-resistant staphylococci are most likely to be
inhibited by which drug? 37. Which antiepileptic drugs bind to the 2/-1 protein
A. Amoxicillin subunit of high-voltageactivated calcium channels
B. Clarithromycin and inhibit these channels? (Choose two.)
C. Clindamycin A. Gabapentin
D. Vancomycin B. Phenobarbital
E. Penicillin V C. Carbamazepine
32. Which of the following organisms is usually clinically D. Ethosuximide
sensitive to clarithromycin but not to penicillin V? E. Pregabalin
A. Viridans streptococcus 38. Which of the following benzodiazepines have the
B. Leptotrichia buccalis shortest half-lives? (Choose two.)
A. Chlordiazepoxide C. Structural metal defects

B. Diazepam D. Occluding against the antagonist tooth
C. Lorazepam 5. The primary purpose of a maxillary denture occlusal
D. Midazolam index is to ____.
E. Triazolam A. Maintain the patients vertical dimension
39. Which of the following reactions are not involved in B. Maintain both correct centric and vertical relation
the metabolism of lidocaine? (Choose two.) records
A. Hydroxylation of the aromatic ring C. Maintain the patients centric relation
B. Cleavage of the aromatic ring D. Preserve the face-bow record
C. Dealkylation of the amino terminus 6. An edentulous patient with a diminished vertical
D. Hydrolysis of the amide bond dimension of occlusion is predisposed to have which
E. Hydrolysis of an ester bond of the following conditions?
40. Flumazenil blocks the receptors stimulated by which A. Epulis fissurata
of the following drugs? (Choose all that apply.) B. Pemphigus vulgaris
A. Baclofen C. Papillary hyperplasia
B. Buspirone D. Angular cheilosis
C. Diazepam 7. When performing a diagnostic occlusal adjustment
D. Zolpidem on diagnostic casts, the mandibular cast should be
E. Zaleplon mounted to the maxillary cast in an articulator using
which of the following?
A. Centric relation interocclusal record
B. Hinge articulator
Prosthodontics C. Maximum intercuspation wax record
D. Face-bow transfer
1. The incisive papilla provides a guide for the anterior- 8. When border molding a mandibular complete denture,
posterior placement of maxillary anterior denture the extension of the lingual right and left flanges are
teeth. The labial surfaces of natural teeth are generally best molded by having the patient ____.
8 to 10mm anterior to this structure. A. Purse the lips
A. Both statements are true. B. Wet the lips with the tongue
B. The first statement is true, and the second state- C. Open wide
ment is false. D. Swallow
C. The first statement is false, and the second state- E. Count from 50 to 55
ment is true. 9. The main function of the direct retainer of a removable
D. Both statements are false. partial denture is ____.
2. Which of the following statements is true concerning A. Stabilization
vertical dimension of rest (VDR)? B. Retention
A. VDR is a physiologic rest position. C. Support
B. VDR is a position of the mandible when opening D. Add strength to the major connector
and closing muscles are at rest. 10. Lack of reciprocation of a removable partial denture
C. VDR is a postural relationship of the mandible to (RPD) clasp is likely to cause ____.
maxilla. A. Tissue recession because of displacement of the
D. VDR is the amount of jaw separation controlled by RPD
jaw muscles when they are in a relaxed state. B. Insufficient resistance to displacement
E. All of the above C. Fracture of the retentive clasp
3. All of the following are characteristics of a postpalatal D. Abutment tooth displacement during removal and
seal of complete dentures except one. Which one is the insertion
exception? 11. Centric relation is the maxillomandibular relationship
A. Compensates for shrinkage of the acrylic resin in which the condyles are in their most ____.
caused by its processing A. Posterior position with the disc interposed at its
B. May reduce the gag reflex thickest avascular location
C. Improves the stability of the maxillary denture B. Posterior position with the disc interposed at its
D. It is most shallow in the midpalatal suture area thinnest locale
4. Which of the following is the most likely cause of an C. Superior position with the disc in its most anterior
occlusal rest fracture? position
A. Inadequate rest-seat preparation D. Superior-anterior position with the disc interposed
B. Improper rest location at its thinnest location
12. The denture base of a mandibular distal extension 20. You are planning to replace a maxillary central incisor
removable partial denture (RPD) should cover ____. with a fixed prosthetic device. The edentulous space is
A. The retromolar pads slightly wider than the contralateral tooth. To achieve
B. All undercut areas and engage them for retention acceptable esthetics, you should ensure that ____.
C. The hamular notch A. The line angles of the pontic are placed in the same
D. The pterygomandibular raphe relationship as the contralateral tooth
13. A good landmark for anterior-posterior positioning B. The pontic is made smoother than the contralateral
of the anterior maxillary teeth in a complete denture tooth
is the ____. C. The pontic has a higher value than the contralateral
A. Residual ridge tooth
B. Incisive papilla D. The line angles are shaped to converge incisally on
C. Incisal foramen the pontic
D. Mandibular wax rim 21. Polycarboxylate cement achieves a chemical bond
14. Which one of the following is a purpose or character- to tooth structure. The mechanism for this bond
istic of the postpalatal seal? is ____.
A. Provides a seal against air being forced under the A. Ionic bond to phosphate
denture B. Covalent bond to the collagen
B. Usually should extend posterior to the foveae C. Chelation to calcium
palatinae D. These cements do not form a chemical bond
C. Improves the stability of the maxillary denture 22. Which of the following properties of a gold alloy
D. Is carved deeper in the midpalatal suture area exceeds a base metal alloy in numerical value?
15. The ____ is used as a guide to verify the occlusal plane. A. Hardness
A. Ala-tragus line B. Specific gravity
B. Interpupillary line C. Casting shrinkage
C. Campers line or plane D. Fusion temperature
D. All of the above 23. Which of the following impression materials has the
16. Balanced occlusion is less important during chewing highest tear strength?
than during nonchewing events. This difference occurs A. Polyether
because the time teeth are in contact during nonchew- B. Polysulfide
ing events is much greater than the time teeth are in C. Addition silicone
contact during chewing. D. Condensation silicone
A. Both statements are true. 24. Chroma is the aspect of color that indicates ____.
B. The first statement is true, and the second state- A. The degree of translucency
ment is false. B. The degree of saturation of the hue
C. The second statement is true, and the first state- C. Combined effect of hue and value
ment is false. D. How dark or light a shade is
D. Both statements are false. 25. For an alloy to be considered noble metal, it should
17. Which of the following conditions can be caused in an ____.
edentulous patient by an ill-fitting denture flange? A. Contain at least 25% silver
A. Papillary hyperplasia B. Contain at least 25% platinum or palladium
B. Epulis fissurata C. Contain 40% gold
C. Candidiasis D. Contain at least 80% gold
D. Fibrous tuberosity 26. The purpose of fabricating a provisional restoration
18. Inadequate rest-seat preparation for a removable with correct contours and marginal integrity is ____.
partial prosthesis can cause ____. A. For protection
A. Tooth mobility B. To supervise the patients dental hygiene and give
B. Ligament widening the patient feedback during this stage
C. Occlusal rest fracture C. To preserve periodontal health
D. Occlusal rest distortion D. All of the above
19. Which of the following is the main disadvantage of 27. A compomer cement ____.
resin-modified glass ionomer compared with conven- 1. Is indicated for cementation of metal-ceramic
tional glass ionomer? crowns
A. Reduced fluoride release 2. Is indicated for cementation of all-ceramic
B. Increased expansion restorations
C. Reduced adhesion 3. Is indicated for some all-ceramic crowns, inlays,
D. Cost and veneers with some contraindications
4. Has low solubility and sustained release of C. Should conform to the interdental embrasure
fluoride D. All of the above
A. All are correct. E. A and C only
B. 1, 2, and 3 are correct. 34. The design of a restored occlusal surface depends on
C. 1, 3, and 4 are correct. the ____.
D. 2, 3, and 4 are correct. 1. Contour of the articular eminence
28. Heating the metal structure in a furnace before opaque 2. Position of the tooth in the arch
application in a metal-ceramic crown is necessary 3. Amount of lateral shift in the rotating condyle
to ____. 4. Amount of vertical overlap of anterior teeth
1. Harden the metal A. 1 and 3
2. Oxidize trace elements in the metal B. 2, 3, and 4
3. Eliminate oxidation C. 2 and 4 only
A. 1 only D. 3 and 4 only
B. 1 and 2 E. All of the above
C. 1 and 3 35. Which of the following is a main function of a guide
D. 2 only plane surface contacted by a minor connector of a
E. 3 only removable partial denture (RPD)?
29. Which of the following are probably not clinically sig- A. Provides a positive path of placement and removal
nificant in terms of influencing the retention of a for the RPD
cemented restoration? B. Can provide additional retention
1. Tooth preparation C. Aids in preventing cervical movement
2. Surface texture D. All of the above
3. Casting alloy E. Only A and B
4. Tooth taper 36. Which of the following components of a removable
5. Luting agent partial denture (RPD) must be rigid?
A. 1, 3, and 4 A. Major connector, minor connector, and retentive
B. 1, 2, 3 clasp
C. 1, 2, 3, 5 B. Wrought wire clasp, rests, and minor connector
D. 3 and 5 C. Minor connector, rest, and major connector
30. Which articulator is capable of duplicating the border 37. Which type of clasp is generally used on a tooth-
mandibular movements of a patient? supported removable denture?
A. Nonadjustable A. Circumferential cast clasp
B. Arcon B. Combination clasp
C. Non-arcon C. Wrought wire clasp
D. Fully adjustable 38. Which of the following disinfectants can be used with
31. Tooth #30 is endodontically treated after a conser alginate impressions?
vative access cavity was made through a typical A. Alcohol
MO amalgam restoration. The restoration of choice B. Iodophor
is a ____. C. Glutaraldehyde
A. Chamber-retained amalgam foundation D. All of the above
B. Custom cast post and core E. B and C only
C. Wire post and core 39. A dentist replaces an amalgam on tooth #5 and notices
D. Parallel-sided prefabricated post with cast core a small pulpal exposure. The dentist elects to perform
32. Potential problems in connecting implants to natural a direct pulp cap procedure. Which of the following
teeth include all of the following except one. Which best predicts success of the procedure?
one is the exception? A. Size of the lesion
A. Stress is concentrated at the superior portion of the B. Isolation of the lesion
implant C. Use of calcium hydroxide
B. Breakdown of osseointegration D. Age of the patient
C. Cement failure on the natural abutment 40. In a tooth-supported removable partial denture (RPD)
D. Screw or abutment loosening with a circumferential cast clasp assembly, there
E. Fracture in the connector area of the prosthesis is ____.
33. A minor connector of a removable partial denture A. More than 180 degrees of encirclement in the
____. greatest circumference of the tooth
A. Should be thin so as not to interfere with the tongue B. A distal rest on the tooth anterior to the edentulous
B. Should be located on a convex embrasure surface area
C. A mesial rest on the tooth posterior to the edentu- C. Create the main color for the restoration
lous area D. A and B are correct
D. Only B and C E. A, B, and C are correct
E. All of the above 46. The light effect of a translucent material (e.g., incisal
41. What is a nonrigid connector? edge of some teeth) appearing blue in reflected light
A. An appliance composed of a key and keyway that and red-orange in transmitted light is called ____.
is used to connect one piece of a prosthesis to A. Metamerism
another B. Opalescence
B. An appliance that is used to connect two crowns C. Value
rigidly fixed D. Chroma
C. A bar appliance that is used to maintain a space for E. Fluorescence
a tooth that has not erupted 47. Which of the following are considered noble elements?
D. None of the above (Choose all that apply.)
42. The distance between the major connector on a maxil- A. Silver
lary removable partial denture framework and the gin- B. Gold
gival margins should be at least ____. C. Platinum
A. 3mm D. Palladium
B. 2mm E. Chromium
C. 6mm 48. Reversible hydrocolloid is composed of ____.
D. 15mm A. Polysulfide polymer
43. The ____ is the component that is responsible for con- B. Agar
necting the major connector with the rest and clamp C. Polyether polymer
assembly. D. Polydimethylsiloxane
A. Bar 49. Electrosurgery is contraindicated under what condi-
B. Minor connector tions? (Choose all that apply.)
C. Proximal plate A. Patient with a transcutaneous electrical nerve stim-
D. Guide plane ulation (TENS) unit
44. The three dimensions of the Munsell Color Order B. Patients with a cardiac pacemaker
System, the basis for shade guides such as Vita Lumin, C. Patients with an insulin pump
are ____. D. Patients with delayed healing
A. Absorption, scattering, and translucency 50. Regarding extracoronal retainers in a removal dental
B. Color, translucency, and gloss prosthesis, which ones originate above the survey line?
C. Size, shape, and interactions with light (Choose all that apply.)
D. Hue, value, and chroma A. Circumferential clasp
45. The purpose of applying a layer of opaque porcelain in B. I bar
a metal-ceramic restoration is to ____. C. T bar
A. Create a bond between the metal and porcelain D. Ring clasp
B. Mask the metal oxide layer and provide a porce-
lain-metal bond
Answer Key Endodontics 405
Answer Key for Section 1

1. C. Until apical closure occurs, teeth do not respond accessory canals that are inaccessible. However,
normally to electrical pulp testing. In addition, a if left untreated, it may become covered with an
traumatic injury may temporarily alter the conduc- epithelial lining and become a true periodontal
tion capability of nerve endings or sensory recep- pocket.
tors, or both, in the pulp. A patient with a vital 6. B. Confirmation of clinical diagnosis should be made
pulp may not experience any sensation right after before treatment is rendered. Access is the first and
trauma. arguably most important phase of nonsurgical root
2. D. The perception of pain in one part of the body that canal therapy. The objectives are (1) to achieve
is distant from the actual source of the pain is straight-line access to the apical foramen or curva-
known as referred pain. Teeth may refer pain to ture of the canal, (2) to locate all root canal orifices,
other areas of the head and neck. Referred pain is and (3) to conserve sound tooth structure.
usually provoked by stimulation of pulpal C-fibers, 7. A. NaOCl is the most widely used irrigant and has
the slow conducting nerves that when stimulated effectively aided canal preparation for years. NaOCl
cause an intense, dull, slow pain. The pain always is a good tissue solvent as well as having an anti-
radiates to the ipsilateral side. Posterior teeth may microbial effect. It acts as a lubricant for root canal
refer pain to the opposite arch or periauricular instrumentation. It is toxic to vital tissue, so a
area. Mandibular posterior teeth tend to transmit rubber dam should always be used. The antibacte-
referred pain to the periauricular area more often rial action of NaOCl is based on its effects on the
than maxillary posterior teeth. bacterial cell wall. When the cell wall is disrupted,
3. D. External root resorption is a process that is initi- the vital contents of the bacteria are released. The
ated in the periodontium, in contrast to internal bacterial membrane and intracellular associated
root resorption, which begins within the root canal functions cease. NaOCl is an effective necrotic
system. There are three main types: inflammatory tissue solvent. Because it fulfills all these require-
root resorption, replacement resorption, and cervi- ments, NaOCl remains the main irrigating solution
cal resorption. Although some types are located of choice in endodontic treatment.
only along the apical and lateral end, replacement 8. A. Ledges can sometimes be bypassed; the canal
resorption can be located anywhere along the coronal to the ledge must be sufficiently straight-
root. However, external root resorption is charac- ened to allow a file to operate effectively. This
terized radiographically by margins that are less straightening may be achieved by anticurvature
well defined, ragged, and irregular. filing (file away from the curve). Precurve the file
4. A. Cracks extend deep into the dentin and are usually severely at the tip and use it to probe gently past
propagated mesiodistally in posterior teeth, often the ledge. Otherwise, clean to the ledge and fill
in the region of the marginal ridge. Dyes and trans- it, but you must warn the patient of poorer
illumination are very helpful in the visualization of prognosis.
cracks. However, it is often impossible to deter- 9. B. Apical perforations occur through the apical fora-
mine how extensive a crack is until the tooth is men or the body of the root (a perforated new
extracted. canal). Generally, the more subcrestally located the
5. E. In chronic apical abscess, a continuously or inter- lesion, the better the prognosis. However, all per-
mittently draining sinus tract usually drains into forations have an inherently worsened prognosis.
the oral mucosa. The exudate can also drain 10. C. Often the radiographic interpretation of a vertical
through the gingival sulcus of the involved tooth, root fracture is the pattern of bone loss occurring
mimicking a periodontal lesion with a pocket. in a teardrop shape.
However, this is not a true periodontal pocket 11. A. Periodontal abscess occurs with preexisting peri-
because there is not a complete detachment of con- odontitis and is characterized by localized purulent
nective tissue from the root surface. Treatment is inflammation of the periodontal tissues. It is also
with conventional root canal therapy. Antibiotics known as lateral periodontal abscess or parietal
are not needed because the infection is localized abscess. This acute infection occurs in the walls
and draining. If the tract does not heal within a few of periodontal pockets as a result of the invasion
weeks, root end surgery may be required to treat of bacteria into the periodontal tissues. Although
405
406 Answer Key Endodontics
abscesses usually occur spontaneously in patients 17. B. The patient is displaying characteristic signs of
with untreated periodontitis, they are more com- irreversible pulpitis. The treatment of choice is to
mon in patients with periodontitis and a systemic remove the source of pulpitic infection by initiating
disease such as diabetes, in which there is a reduced endodontic therapy. The scenario in the question
ability to combat infections. In some cases, an is considered an endodontic emergency, and treat-
abscess can occur a few days after dental cleaning ment should be rendered to relieve the patients
as a result of mechanical disruption of junctional pain.
epithelium, allowing the bacteria to gain entrance 18. C. The best treatment of symptomatic irreversible pul-
into the tissues. This is not the same as acute pitis with a corresponding bony lesion is removal
apical abscess because the involved tooth usually of the source of infection via pulpectomy.
is vital. Abscesses tend to worsen as time goes 19. B. The current recommendation for patients with a
on. Symptoms include tenderness or pain and recent MI is to postpone dental or surgical treat-
the site of the abscess being warm to the touch. ment for at least 6 months. Risk for a second MI in
Symptoms of discomfort or pain depend mainly patients with recent MI if given a general anes-
on the site of the abscess, although larger ones thetic is as follows: 0 to 3 months after MI, 31% risk
because they are a source of infection within of reinfarction; 3 to 6 months after MI, 15% risk of
the bodycan cause fever, chills, sweating, and reinfarction; more than 6 months after MI, 5% risk
malaise. of reinfarction. It is recommended to defer elective
12. A. Lingering spontaneous pain is evidence of C-fiber care for at least 6 months after MI.
stimulation. Even in degenerating pulps, C fibers 20. D. Incision and drainage techniques work best for
may respond to stimulation. The excitability of C fluctuant abscesses, so as to release purulent
fibers is less affected by disruption of blood flow exudate. Local anesthesia should be obtained first.
compared with A-delta fibers. C fibers are often An incision should be placed at the most depen-
able to function in hypoxic conditions (e.g., at the dent part of the swelling. The incision should be
early stage of pulpal necrosis.) wide enough to facilitate drainage and allow blunt
13. D. Symptomatic apical periodontitis is characterized dissection. After irrigation, a drain may be placed
by pain, commonly triggered by chewing or per- to maintain patency of the wound.
cussion. It is usually caused by localized inflamma- 21. C. Many studies have shown definitively the predomi-
tion of the periodontal ligament in the periradicular nant role of gram-negative obligate anaerobic bac-
region. Symptomatic apical periodontitis alone is teria in endodontic periapical infections. Earlier
not indicative of irreversible pulpitis. Tenderness to studies generally implicated facultative organisms,
percussion is a pathognomonic symptom of symp- but improved culturing techniques established the
tomatic apical periodontitis. predominance of obligate anaerobes.
14. A. In a periodontal abscess, the pulp vitality test 22. C. Danger zone refers to the distal area in the mesial
would be within normal limits. root in mandibular molars. Usually a straight layer
15. E. Patients with cracked teeth may experience pain in of dentin, it becomes a preferable site for strip per-
the tooth on biting or chewing. However, the dis- foration during instrumentation. Safety zone is
comfort is not constant, as with a decay-induced described as the mesial area of the root, with a
toothache or abscess. Often the pain is mimicked thicker layer of dentin, slightly touched by the end-
only when a patient bites a certain way. The tooth odontic instruments.
may be more sensitive to cold temperatures. If 23. D. In an intrusive dental injury, the patient may com-
the crack worsens, the tooth may become loose. plain of pain. The patients tooth is misaligned, or
Many people with cracked tooth syndrome have there is no sense of tooth mobility. This type of
symptoms for months, but it is often difficult for displacement has the worst prognosis. For intruded
them to explain what is wrong because the symp- primary teeth, allow teeth to reerupt before possi-
toms are not consistent. Some patients present ble repositioning. For intruded adult teeth, allow
with asymptomatic cracks that are only clinically reeruption and then stabilize.
evident. 24. A. Internal resorption begins on the internal dentin
16. B. True-combined lesions are treated initially as surface and spreads laterally. It may or may not
primary endodontic lesions with secondary peri- reach the external tooth structure. The process is
odontal involvement. Periodontal surgical proce- often asymptomatic and becomes identifiable only
dures are almost always indicated. The prognosis after it has progressed enough to be detectable
of a true-combined periodontal-endodontic lesion radiographically. The etiology is unknown. Trauma
is often poor or even hopeless, especially when is often, but not always, implicated. Resorption that
periodontal lesions are chronic with extensive loss occurs in inflamed pulps is characterized histo
of attachment. logically by dentinoclasts, which are specialized,
Answer Key Endodontics 407
multinucleated giant cells similar to osteoclasts. 33. D. In comparing accuracy among the three pulp diag-
Treatment is prompt endodontic therapy. However, nostic tests, a cold test or heat test exhibits the
when external perforation has caused a periodon- highest sensitivity or the ability to identity teeth
tal defect, the tooth is often lost. with pulpal disease and highest specificity or the
25. A. Internal bleaching alone causes 3.9% of external ability to identify teeth without pulpal disease.
cervical root resorption (also referred to as periph- 34. B. Composition of gutta-percha for clinical endo
eral inflammatory root resorption). The presence of dontic use is: gutta-percha (19%-22%), zinc oxide
a barrier (base material) between the root filling (59%-79%), heavy metal salts (1%-17%), waxes or
material and the internal bleaching material should resins (1%-4%).
be approximately 4mm to prevent this resorption. 35. C. Avulsion. To have pulp space infection, the pulp
26. E. Emergency treatment of localized swelling associ- must first become necrotic. This will occur in a
ated with an endodontic infection is to achieve fairly serious injury in which displacement of the
drainage either through the root canal or by inci- tooth results in severing of the apical blood vessels.
sion and drainage and to remove the source of 36. E. All of the choices are true. Suppurative apical peri-
infection. Administration of antibiotics is consid- odontitis: continuously or intermittently draining
ered with the concomitant presentation of fever sinus tract, usually drains into the oral mucosa. The
and malaise and for diffuse swelling (cellulitis). exudate can also drain through the gingival sulcus
27. A. The manufacturing process of a K-type instrument of the involved tooth, mimicking a periodontal
(K-file or K-reamer) is grinding a stainless steel lesion with a pocket. However, this is not a true
wire to a tapered square or triangular cross- periodontal pocket because there is not a complete
section. detachment of connective tissue from the root
28. D. Irrigation of the root canal system is a critical com- surface. It should be treated with conventional root
ponent in nonsurgical endodontic treatment. Ben- canal therapy. Antibiotics are not needed, since the
efits of irrigation include dissolution of organic infection is localized and draining. If the tract does
debris, disinfection of complex anatomy that is not not heal within a few weeks, root-end surgery may
accessible by instrumentation, destruction of end- be required. If left untreated, however, it may
odontic pathogens, and removal of the smear layer. become covered with an epithelial lining and
Additionally, irrigation acts as an intracanal wetting become a true periodontal pocket.
medium. 37. B. A history of recent restoration of the tooth in ques-
29. B. In a primary infection gram-negative bacteria are tion. Focal sclerosing osteomyelitis (FSO) consists of
the most common pathogens. In post-treatment a localized, usually uniform zone of increased radi-
disease most (but not all) gram-negative bacteria opacity adjacent to the apex of a tooth that exhibits
are eliminated. Bacteria persisting after chemome- a thickened periodontal ligament space or an apical
chanical debridement are typically gram-positive inflammatory lesion. The size of the lesions usually
facultative anaerobes exhibiting the ability to measure less than 1 cm in diameter. There is no
adapt to antimicrobial treatment. Samples typically radiolucent halo surrounding this type of lesion.
include Pseudoamibacter micra, Actinomyces The osteitis microscopically appears as a mass of
species, Propionibacterium species, Parvimonas dense sclerotic bone.
alactolyticus, lactobacilli, and Enterococcus faecalis. FSO is most often found in patients younger
30. C. The maxillary first premolar has a pronounced than 20 years of age, around the apices of man-
mesial crown concavity making this tooth vulner- dibular teeth (most commonly molars) with large
able to mesial perforation after access opening carious lesions and chronically inflamed pulps or
particularly when the tooth is restored with a with recent restorations. Most sources agree that
full crown. the associated tooth may or may not be vital.
31. B. Irrigation with saline and not hydrogen peroxide is Gender is not a predisposing factor. FSO can be
advocated for treating a NaOCl accident. Addi- asymptomatic or the patient can experience mild
tional treatment includes cold compresses within pain, depending on the cause. FSO is usually dis-
the first 24 hours and warm compresses after to covered upon radiographic analysis. It represents a
control swelling, analgesics for pain control and chronic, low-grade inflammation.
antibiotics for patients at increased risk for second- 38. B. They are eliminated by the natural defenses of the
ary infection. body. Obturation prevents coronal leakage and
32. A. EDTA is a decalcifying chelating agent used in bacterial contamination and seals the remaining
buffered solution in concentrations between 15 irritants in the canal. After root canal obturation,
and 17%. Ethylenediaminetetraacitic acid acts as a the remaining bacteria should have lost their
chelator and typically targets calcium ions and source of nutrition, becoming susceptible to the
removes the smear layer from root canal walls. bodys immune system.
408 Answer Key Operative Dentistry
1. B. A restored or sealed tooth indicates potential past kidney-shaped or crescent-shaped, and the exten-
carious activity but not current activity. The pres- sions are to the line angles, resulting in the mesial
ence of plaque biofilm does not indicate caries and distal walls diverging externally. The convexity
presence. Sealants are used for preventive pur- of the tooth in the gingival one third results in the
poses, not caries treatment. occlusal and gingival walls diverging externally.
2. D. When doing an indirect pulp cap, some caries Several retention groove designs are appropriate,
may be left; a liner (usually calcium hydroxide) is including four corner coves, occlusal and gingival
usually placed over the excavated area, and the area line angle grooves, or circumferential grooves.
may be assessed 6 to 8 weeks later. Regardless, the However, as with any restoration, if there is only a
prognosis for an indirect pulp cap is better than the small amount of tooth structure (<1mm) between
prognosis for a direct pulp cap. the new and existing restoration, it is best to join
3. D. Smooth-surface caries occurs on any of the axial the two restorations together and prevent the pos-
(facial, lingual, mesial, and distal) tooth surfaces sibility of fracture of the small amount of remain-
but not the occlusal. ing tooth structure.
4. E. The advantages and benefits of rubber dam usage 8. B. Typically, the class I composite preparation has
are reflected in all of the items listed. The rubber occlusally converging walls that provide primary
dam isolation increases access and visibility. retention form. The actual bonding also provides
5. A. The first number is the width of the blade or retention form. However, an occlusal bevel is not
primary cutting edge in tenths of a millimeter indicated on class I preparations, and retention
(0.1mm). The second number of a four-number grooves are not used.
code indicates the primary cutting edge angle, 9. B. A tooth preparation is dictated by the extent of the
measured from a line parallel to the long axis carious lesion or old restorative material, the cre-
of the instrument handle in clockwise centigrades. ation of appropriate convenience form for access
The angle is expressed as a percent of 360 degrees. and vision, and the anticipated extensions neces-
The instrument is positioned so that this number sary to provide an appropriate proximal contact
always exceeds 50. If the edge is locally perpen- relationship. Fracture lines present should nor-
dicular to the blade, this number is normally mally be included in the restoration. However, it is
omitted, resulting in a three-number code. The rare that the size of the tooth affects the design of
third number (second number of a three-number the tooth preparation.
code) indicates the blade length in millimeters. The 10. B. Although the amalgam margin must be 90 degrees,
fourth number (third number of a three-number the enamel margin may not be 90 degrees, espe-
code) indicates the blade angle, relative to the long cially on the occlusal surface. Most walls converge
axis of the handle in clockwise centigrades. occlusally, but many class V amalgam preparations
6. C. Retention locks, when needed in class II amalgam have walls that diverge externally. No retention
preparations, should be placed entirely in dentin, form should be placed at the DEJ; otherwise, the
not undermining the adjacent enamel. They are adjacent enamel would be undermined and subject
placed 0.2mm internal to the DEJ, are deeper gin- to fracture.
givally (0.4mm) than occlusally (i.e., they fade out 11. C. The primary causes of postoperative sensitivity for
as they extend occlusally and translate parallel to amalgam restorations are voids (especially at the
the DEJ). If the axial wall is deeper than normal, margins), poor condensation (that may result in a
the retention lock is not placed at the axiofacial or void), or inadequate dentinal sealing. Extension
axiolingual line angles but rather is positioned onto the root surface does not result in increased
0.2mm internal to the DEJ. If placed at the deeper sensitivity.
location, it may result in pulp exposure, depending 12. B. Amalgam carving should result in coincidence
on the location of the axial wall depth. with the cavosurface margin and should not result
7. D. Because of the typical shape of a carious lesion in deep occlusal anatomy because such form may
in the cervical area, the resulting restoration is create acute amalgam angles that are subject to
408
Answer Key Operative Dentistry 409
fracture. Depending on the condensation rate of than the other choices. Direct gold is slightly higher
the amalgam used, waiting a couple of minutes than tooth structure, and amalgam is about twice
before initiating carving may allow the amalgam to as high as tooth structure.
harden enough that the carving is easier and over- 22. D. All of these factors indicate that a cervical lesion
carving is minimized. When carving the occlusal should be restored. In addition, if the lesion is large
cavosurface margin, the discoid carver should rest and the pulpal or gingival tissues are in jeopardy,
on the adjacent unprepared enamel, which will it should be considered for restoration.
serve as a guide for proper removal of amalgam 23. B. Composite restorations are more technique-
back to the margin. sensitive than amalgam restorations because the
13. D. The trituration process mixes the amalgam com bonding process is very specific (requiring exact,
ponents, and the reaction results in the alloy par- correct usage of the various materials and an iso-
ticle being coated by mercury and a product being lated, noncontaminated field), and the insertion
formed. and contouring of composites are more demanding
14. C. Proper proximal contacts reduce the potential for and time-consuming. Composites are not stronger
food impaction, preserving the health of the under- than amalgam and have similar wear resistance
lying soft tissue. A missing proximal contact may compared with amalgams. Composites are indi-
result in tooth movement that has an adverse effect cated for class II restorations.
on the occlusal relationship of the tooth. Having a 24. B. The constant contraindication for using a compos-
correct contact does not enhance the retentive ite restoration is the inability to isolate the operat-
properties of the restorative material. ing area properly. Occlusal wear of composite is
15. A. Self-etch adhesive systems differ from etch-and- similar to that of amalgam. Extension onto the root
rinse (total-etch) adhesive systems by removing surface may result in gap formation with compos-
less of the smear layer (they use a less potent acid), ite but also results in initial leakage with amalgam,
creating a weaker bond to enamel (especially non- indicating that there is no ideal material for root-
prepared enamel), and not requiring wet bonding surface extended restorations. A high C-factor
that may be necessary for most etch-and-rinse (class I) can be largely overcome by using (1) a liner
systems. Although fewer actual materials may be under the composite, (2) a filled adhesive, and (3)
needed with some self-etch systems, they need to incremental insertion of the composite.
be applied in multiple coats, and the time necessary 25. C. The restoration of a proximal contact is easier with
to apply the materials is similar for both systems. amalgam than composite. Amalgam is easier to
16. D. Occlusal reduction would not affect the ability to use and is less technique-sensitive. Either material
seat a casting. However, temporary cement, heavy can be used for class II restorations. Because an
proximal contacts, or tooth undercuts could keep amalgam restoration requires a tooth preparation
the casting from seating completely. that has (1) a specified depth (for strength of the
17. A. If a patient has a notched cervical area that is very amalgam), (2) cavosurface marginal configurations
sensitive or esthetically objectionable, restoration that result in 90-degree amalgam margins, and (3)
is usually indicated. If the notched area is very undercut form to its walls or secondary retention
deep, adverse pulpal or gingival responses may form features, they require more tooth structure
occur. Although more notched areas are encoun- removal than composite tooth preparations. Com-
tered in older patients, a patients age is not a factor posite tooth preparations require (1) removal of
in the need for restoration. the fault, defect, or old material; (2) removal of
18. A. The longer a slot, the better. They should be inside friable tooth structure; and (3) no specific depths
the DEJ and prepared with an inverted cone bur to they are more conservative.
a depth of 1mm. 26. A4; B2; C3; D1.
19. C. Although some self-etch bonding systems use 27. A, C, E, G. Abraded or eroded noncarious lesions are
milder acid, the primary acid system used for restored when the area is cariously involved (A),
etching tooth structure is phosphoric acid. when there is intolerable sensitivity unresponsive
20. B. Triturating (mixing) the amalgam particle with the to conservative desensitizing measures (C), when
mercury is intended to result in coating the parti- the area is to be involved in the design of a remov-
cles with a surface of mercury and creating the able partial denture (E), and the patient desires an
desirable phases in the set amalgam. All of the alloy esthetic improvement (G). The restoration of these
particle is not dissolved in the mercury, and the lesions has no impact on phonetics, restoration is
size is not significantly reduced. not needed when the defect is shallow and it does
21. D. Composite materials exhibit more dimensional not compromise the structural integrity of the
change (2.5 times greater than tooth structure) tooth, and restoration is unnecessary because the
when subjected to extreme changes in temperature tooth is treated endodontically.
410 Answer Key Operative Dentistry
28. A, B, D, G. Light marginal staining not compromising 30. A5; B3; C1; D4; E2; F6.
esthetics, recurrent caries that can be adequately 31. A6; B2; C5; D3; E1; F4.
treated by a repair restoration, and shallow ditch- 32. A, C. Skirts increase retention and resistance forms.
ing around an amalgam restoration are not reasons They do not provide bracing (collars do), enhance
to replace an existing restoration. esthetics, provide pulp protection, or improve
29. A3; B2; C1; D4. draw.
Answer Key Oral and Maxillofacial Surgery and Pain Control 411
1. D. The superficial temporal, pterygomandibular, mas- snoring, patients being sedated, or patients needing
seteric, and submental spaces are potentially incomplete denture construction, it does not contrib-
volved in odontogenic infection. There is no ute directly to TMJ dysfunction.
rhinosoteric space. 10. C. Maxillary fractures may be classified as Le Fort I,
2. B. Depending on the ramus relationship, mesioangu- II, or III. Le Fort III is the highest and most severe
lar and vertical impactions may not require removal classification.
of bone or sectioning of the tooth. Horizontal 11. C. Chronic sinusitis is not a relative contraindication
impaction always requires removal of bone and to most elective oral surgical procedures. Unstable
sectioning. chest pain should be evaluated by an internist or
3. E. A patient with severe infection and systemic cardiologist before any dental treatment. Radiation
involvement, unless immunocompromised, is ex- to the jaws and a history of clotting disorders both
pected to present in a febrile state, or a temperature would require further investigation of the health
of greater than 100F. All the other items refer history and likely alter the patients treatment plan
to symptoms that indicate potential airway to lessen the likelihood of osteoradionecrosis or of
emergency. bleeding complications.
4. D. Criteria for implant success include mean vertical 12. B. Disc displacement without reduction can result in
bone loss of less than 0.02mm annually after the decreased range of motion because the condyle
first year of service. In this question, no further becomes restricted by the anteriorly displaced disc,
treatment is necessary at this time. limiting translation.
5. C. Implants should be placed a minimum of 2mm 13. B, D, F. Choice A is incorrect because antibiotics used
from the inferior alveolar canal. to treat odontogenic infections should be effective
6. A. In myofascial pain dysfunction, the source of the against streptococci and oral anaerobes. S. aureus
pain and dysfunction is muscular. Dysfunction is commonly seen on respiratory tract and skin,
is associated with decreased opening or inability not on oral mucosa. Choice C is incorrect because
to chew. high-grade fever resulting from infection suggests
7. D. Periodontal management is the first step in the systemic involvement, and antibiotic therapy
management of this patient. If the patient is unwill- should be initiated. Choice E is incorrect because
ing, or unable, to maintain adequate hygiene before narrow-spectrum antibiotics are preferred over
placement of orthodontic appliances, their subse- broad-spectrum antibiotics because of less likeli-
quent placement would make the periodontal situ- hood in altering the normal flora and less impact
ation more difficult. For the same reasons, dental on the development of resistant strains.
decay should be treated before beginning orth- 14. A, C, E. Mesioangular impacted third molars are the
odontic treatment. The final prosthetic manage- least difficult to remove because the withdrawal
ment should not be completed before the underlying path does not run into the mandibular ramus as
skeletal anomaly is addressed because the occlu- distoangular impacted third molars do. It is easier
sion would be constructed to the bestand final to remove a tooth with roots that are one half to
anatomic location. one third formed because such length prevents the
8. C. Systemic sequelae of obstructive sleep apnea syn- tooth from spinning in place compared with
drome include hypertension, cor pulmonale, and teeth with less formed roots. Finally, teeth with
cardiac arrhythmia. fused conical roots are less difficult to extract
9. C. Tissue symmetry, tenderness, joint noises, dental because there are no undercuts compared with
health, and occlusion and range of motion all are diverged or dilacerated roots.
critical components of the physical examination in 15. A1, B4, C2, D3. Incisional biopsy is often
the patient with TMJ complaints. Although the used in lesions larger than 1cm in size, as opposed
length of the soft palate is important in the evalu- to excisional biopsy, which is often used in lesions
ation of patients with sleep apnea, patients with less than 1cm. Osteomyelitis is an infection and
411
412 Answer Key Oral and Maxillofacial Surgery and Pain Control
inflammation of the bone. A hard tissue bone 24. D. The degree of hydrophobicity and protein binding
biopsy is required to reach a definitive diagnosis of are the most important factors in determining
osteomyelitis. Aspiration or fine-needle biopsy on duration of action of a local anesthetic. Bupiva-
a soft tissue lesion deep to mucosa should be done caine is highly hydrophobic (lipophilic) and is 95%
first to confirm if the entity is truly cystic, vascular, bound to protein. The other listed agents are less
or solid. Otherwise, an attempt to obtain a biopsy hydrophobic and are 55% to 75% bound to protein.
specimen of a soft tissue lesion that is vascular in 25. A. All amide local anesthetics are biotransformed in
origin, such as an arteriovenous malformation, can the liver. One available local anesthetic also has an
result in hemorrhagic complications. ester side chain, which means it has some degree
16. B, C. Bupivacaine is not approved by the Food and of extrahepatic biotransformation (outside the
Drug Administration for use in children younger liver). This drug is articaine and is the most appro-
than 12 years. In children, the most significant priate drug for patients with liver disease.
safety issue with respect to local anesthetics is 26. D. The inferior alveolar nerve block has a stated
related to overdose. Overdose is most often directly success rate of 85%, the lowest of any intraoral
related the volume of the drug injected. Lidocaine injection. Lingual and nasopalatine injections are
allows the greatest volume to be injected safely. close to 100% successful, and the posterior supe-
17. B. Most local anesthetics packaged in dental car- rior alveolar nerve block is also much more than
tridges are tertiary amines. At the present time, the 85% effective.
only local anesthetic packaged in dental cartridges 27. A, B, C. Vasocontrictors prolong the duration of
that has an ester bond is articaine, but the bond in action of local anesthetic preparations by keeping
the connecting chain in the drug molecule is an the drug at the site of action longer. Agents with
amide. greater protein binding have a greater attraction for
18. D. Bupivacaine is packaged in dental cartridges only receptor sites and remain within sodium channels
as a 0.5% solution. Likewise, lidocaine is always a for a longer time, which prolongs the duration of
2% solution (in the United States), and articaine is action of the drug. Although lipid solubility is pri-
always a 4% solution. Mepivacaine is packaged in marily related to potency, it is secondarily related
both 2% and 3% solutions in the United States. to duration of action because lipid solubility is
19. A. The larger the lumen of the needle, the easier it is directly related to protein binding. The pKa deter-
to determine whether the needle is actually in a mines the onset of the local anesthetic, not the
vessel. The needle length is irrelevant, as is the duration. The pH and concentration of the local
patient. The injection performed is relevant in anesthetic have no relationship to the duration of
regard to the frequency of obtaining a positive action.
aspiration but not the reliability of the aspiration 28. A, B, D, E, F. See chemical structure of articaine, dem-
per se. onstrating both an amide and an ester linkage.
20. D. The palatal tissue from canine to canine bilaterally Articaine is packaged as a 4% drug, in the highest
is the premaxilla. The nasopalatine injection anes- concentration of all local anesthetics in dentistry.
thetizes this area. The amide component of articaine is biotrans-
21. C. The pKa for lidocaine or prilocaine is 7.8, for mepi- formed in the liver where the ester component of
vacaine is 7.7, and for bupivacaine is 8.1. articaine is biotransformed in the plasma (an
22. D. By definition, a 2% solution of any drug contains extrahepatic site).
20mg/mL. A dental cartridge of local anesthesia
has a fluid volume of 1.8mL. 20mg 1.8 = 36mg O
S
of lidocaine per cartridge. Three cartridges of
OCH3
2% lidocaine with 1:100,000 epinephrine contain
108mg. NH
23. D. All mandibular molars are anesthetized by the O
inferior alveolar nerve block. The other three NH
answer choices are maxillary injections.
Answer Key Oral Diagnosis 413

1. C. In pemphigus vulgaris, autoantibodies attach to 12. A, C, E, G. Central giant cell granulomas, jaw lesions
antigens (desmoglein) found in desmosomes that in patients with hyperparathyroidism (so-called
keep keratinocytes linked to each other. Cells even- brown tumors), and jaw lesions in cherubism all
tually separate from each other (acantholysis), re- microscopically demonstrate significant numbers
sulting in short-lived intraepithelial vesicles or of osteoclastlike, multinucleated giant cells distrib-
bullae. uted within a fibrovascular matrix. Aneurysmal
2. D. Condyloma latum is one of the lesions that may be bone cysts contain similar types of tissues and cells,
seen in secondary syphilis, which is caused by including multinucleated giant cells, but also dem-
Treponema pallidum. All the other lesions listed onstrate a prominent pseudocystic architecture.
may be associated with HPV. 13. A4, B6, C2, D1, E3, F5. For choice A,
3. D. Hairy leukoplakia is viral in origin and shows minor aphthous stomatitis is the most common
intranuclear inclusions in infected epithelial cells. form of this disorder and is usually characterized
Hairy leukoplakia is caused by EBV, a herpesvirus. by the development of a single, superficial ulcer of
Intranuclear epithelial inclusions are also seen nonkeratinized mucosal areas such as buccal
other herpesvirus infections (e.g., HSV infections). mucosa. For choice B, the reticular form of lichen
4. E. Odontogenic myxomas are connective tissue neo- planus often manifests with asymptomatic, inter-
plasms that contain little collagen; this gives them lacing white lines in a bilateral distribution. Buccal
an embryonic look microscopically. mucosa is a common site for these lesions, although
5. D. This triad of signs defines primary Sjgrens syn- tongue and gingiva are also affected often. For
drome. The patient has secondary Sjgrens syn- choice C, infiltration of gingival tissues by leuke-
drome if rheumatoid arthritis or other autoimmune mic cells may occur in some patients, most com-
disease is present. monly patients with chronic monocytic leukemia.
6. C. Recurrent intraoral herpes infections occur only The gingival appears enlarged because of malig-
in the hard palate and hard gingiva except in nant cell infiltration, and the tissue is often red,
patients with AIDS. A history of blister (vesicle) boggy, and hemorrhagic. For choice D, the tongue
formation and recurrence are also supportive of is the most common site in the body for the devel-
this diagnosis. opment of a granular tumor. This is a benign pro-
7. A. Nodular fasciitis is a rapidly developing reactive liferation or aggregation of cells with features
lesion that typically does not recur after excision. similar to Schwanns cells that results in a firm,
Fibromatosis is an aggressive nonencapsulated often yellow nodule in the substance of the tongue.
lesion that is associated with a significant potential For choice E, amalgam tattoo is the most common
for recurrence. The other lesions listed are malig- pigmented lesion in the oral cavity. For choice F,
nancies and require more than simple excision to mucous extravasation phenomenon is a pool of
prevent recurrence. extraductal mucin that collects after traumatic sev-
8. E. Traumatic bone cysts characteristically occur in erance of the minor salivary gland duct. The lower
the body of the mandible of teenagers. They are lip is the most common location for this reactive
pseudocysts because they have no epithelial lining. lesion.
They are empty cavities. 14. A, D, E. Aphthous or aphthouslike ulcers may develop
9. C. Cherubism is a fibro-osseous lesion that occurs in in patients with celiac sprue, Behets syndrome, or
teenagers. Characteristically, it manifests with ill- Crohns disease, all examples of diseases in which
defined margins and a ground-glass appearance immune system dysfunction is an important factor
radiographically. The other features described also in the pathogenesis. Although oral manifestations
support this diagnosis. may be variable, lesions in patients with sarcoid-
10. B. The maculopapular rash of rubeola (measles) is osis, amyloidosis, and neurofibromatosis typically
preceded by the herald sign of Koplics spots (punc- manifest as submucosal nodules and masses.
tate ulcers of the buccal mucosa). 15. C, D. X-ray beam B was produced with a higher mA
11. D. Destructive inflammation in the three sites noted and higher exposure time (s). Both these factors
is characteristic of Wegeners granulomatosis. increase the total number of photons produced.
413
414 Answer Key Oral Diagnosis
However, the peak or mean energies of the x-ray doses from different examinations can be directly
beam do not change. compared. The higher the effective dose, the higher
16. A, D. The mean energy of an x-ray beam is influenced the estimated risk.
by the kilovoltage setting on the machine. As the 23. B. Use the rule of SLOB: Same Lingual, Opposite
kilovoltage setting is increased, the mean energy of Buccal.
the beam increases. The amount of built-in filtra- 24. D. Cone-cutting results from misalignment of the
tion that preferentially absorbs low-energy photons x-ray tube. Use a film-holding device with an exter-
also results in an increase in the mean energy of nal guide.
the beam. 25. B. If proper processing procedures are followed, the
17. D. When heated, the filament releases electrons developer will become depleted with age and need
(thermionic emission). changing.
18. B. Basal epithelial cells are the most mitotically 26. D. Visible light exposes all the silver bromide crystals,
active of the cells on the list and are the most and the film is black after processing.
radiosensitive. 27. A. Daily check of the processing solution temperature,
19. A1, 4; B2, 3, 5. Thyroid cancer and heritable whether using automatic processing or manual
effects are stochastic effects. Xerostomia, cataract tanks, and comparison with the manufacturers
formation, and oral mucositis are deterministic recommended values improves image quality. The
effects. other procedures are useful but can be performed
20. A. The probability of photoelectric interactions is less frequently.
directly proportional to the cube of the atomic 28. D. Prudence suggests that radiographic examinations
number. Enamel has the highest effective atomic of a pregnant patient should be kept to a minimum
number. consistent with the patients dental needs.
21. A. Silver halide in an x-ray film is sensitive to x-rays 29. D, E. Radiographs demonstrate calcified structures
and visible light. Sodium thiosulfate is a compo- such as bone and teeth. Radiographic examination
nent of the fixer. Gelatin is used to suspend the does not permit evaluation of the depth of the soft
silver halide crystals, but is not radiosensitive. Rare tissue pocket. Additionally, intraoral radiographs
earth elements are used in intensifying screens. are two-dimensional images; they are unable to
22. A. The effective dose considers the dose absorbed by characterize loss of specific bony walls of a peri-
each tissue and weighs the dose depending on odontal defect and do not depict three-dimensional
the type of tissue exposed. The numerical effective anatomy.
Answer Key Orthodontics and Pediatric Dentistry 415

1. C. According to available data, approximately 15% 11. B. When a large diastema greater than 2mm is
of adolescents have severe crowding that would present, it likely will not close on its own. Diagnos-
require major expansions or numerous extractions tic tests, such as a radiograph, should be performed
to resolve. The other statements are false. Crowd- to rule out the presence of a supernumerary tooth,
ing in the primary dentition is very rare and would usually a mesiodens.
indicate crowding will occur in the permanent 12. A. Intruding incisors would decrease overbite while
dentition; spacing in the primary dentition is uprighting teeth, and using a high-pull headgear
normal; and African-Americans generally have less could make overbite correction more difficult.
crowding than whites. A lip bumper would likely have little effect on
2. B. The cranial base includes, from anterior to poste- overbite.
rior, the ethmoid, sphenoid, and occipital bones. 13. A. Initiation and proliferation are the only possibili-
3. C. Reproductive tissues grow at the same time as the ties for congenitally absent teeth, the bud and cap
adolescent growth spurt, and the appearance of stages, respectively. In the histodifferentiation
secondary sexual characteristics can be used to stage, the teeth are present; failure in this stage
help predict the timing of growth. results in structural abnormalities of the enamel
4. B. Young children often present with minimal over- and dentin. Failure in the morphodifferentiation
bite or anterior edge-to-edge relationship. Habits stage results in size and shape abnormalities.
such as thumb sucking increase the likelihood that 14. A. For any child patient, it is imperative to discuss
less overbite will be present. any kind of physical restraint with the parent to
5. A. The molars are class II, but the skeletal relationship obtain an informed consent. An informed consent
described by a normal ANB measurement is includes recommended treatment, reasonable
normal, so the malocclusion is dental in origin. alternatives to that treatment, and the risk of no
6. B. Root resorption is common during orthodontic treatment. If the dentist wants to use a firm voice
treatment, although lesions often resolve on the control, it is recommended that a discussion take
root surface. Mobility of teeth is also common as place beforehand as well.
the PDL reorganizes and widens during tooth 15. A. Conscious sedation is defined as a minimally
movement. It is uncommon for teeth to become depressed level of consciousness as opposed to
devitalized as a result of orthodontic movement, deep sedation or general anesthesia. There are four
unless they have also been substantially compro- stages of anesthesia (analgesia delirium sur-
mised by injury or infection. gical anesthesia respiratory paralysis), and the
7. C. Because M = Fd, doubling the force would double patient is conscious only in the first stage (analge-
the moment, or tendency to rotate, tip, or torque. sia). The patient should be able to maintain an
8. D. Class II elastics work in the direction that would airway and respond to stimulation and command.
be used to correct a class II malocclusion, to pull 16. A. Both of these statements are true. As a result of
the mandibular teeth forward and the maxillary these differences, there are modifications in prepa-
teeth distally. ration design for class II amalgams. Beveling the
9. B. Class III elastics are worn from the maxillary first gingival seat of class II amalgams is not recom-
molars to the mandibular canines. The force system mended. There is a greater convergence from cervi-
created by class III elastics produces mesial move- cal to occlusal of the buccal and lingual walls of
ment and extrusion of the maxillary first molars. class II amalgam preparations because of the broad
10. B. Primary canines are extracted to encourage align- and flat contact areas.
ment of the crowded incisors. However, the inci- 17. B. There have been concerns regarding the blood-
sors align and upright, borrowing space otherwise borne spread of formocresol at least since 1983,
needed for eruption of the permanent canine. when a study was published describing the tissue
Primary first molars are extracted to encourage changes induced by the absorption of formocresol
eruption of the first premolar so that it may be from pulpotomy sites in dogs. Ferric sulfate and
extracted to make room for the permanent canine mineral trioxide aggregate have been demonstrated
to erupt. to be reasonable alternatives to formocresol.
415
416 Answer Key Orthodontics and Pediatric Dentistry
18. A. A band-loop space maintainer would work well in anesthetized, and, under sterile conditions, the cli-
this case because the maxillary first bicuspid nor- nician should open the pulp chamber to search for
mally erupts before the loss of either the second healthy pulp tissue. It is likely that vital tissue will
primary molar or the primary cuspid. be present within 24 hours of the injury.
19. D. The patients overbite and overjet improved from 24. B. An extruded permanent incisor with an open apex
the previous examination, and so it is likely that the should be repositioned, splinted, and monitored
patients thumb-sucking habit had decreased sig- closely for loss of vitality. Because of the open apex,
nificantly. The mother stated that the patient sucks the tooth may remain vital and continue to develop;
his thumb only while falling asleep. When thumb immediate pulp treatment is contraindicated.
sucking occurs for a limited time per day, not only 25. C. The other three answer choices may occur as the
is tooth movement normally associated with thumb result of trauma but do not cause loss of vitality.
sucking unlikely, but also it is possible for teeth Pulpal hyperemia causes increased intrapulpal
to return to a more normalized position. The risk pressure and swelling, which may result in an inter-
of malocclusion as related to habitual activity is a ruption of the pulps blood supply. Without an
function of amount of time per day the habit is adequate blood supply, the pulp becomes necrotic.
practiced, the duration of the habit in terms of This process can take time, and symptoms (either
weeks and months, and the intensity of the habit. radiographic or clinical) may not manifest for
Because the occlusion seems to be improving and weeks or months. Typically, follow-up examination
because the habit has significantly decreased, the and radiographs are indicated at 1-, 2-, and
best treatment is to counsel the parent regarding 6-month intervals after a traumatic incident.
thumb sucking and recall the patient in 3 months. 26. A1, B3, C2, D4. When heavy forces are
20. A. Orthodontic closure of a midline diastema is applied during orthodontic treatment, the tooth is
accomplished before the periodontal surgery. If a moved in the direction in which the force is
frenectomy is performed before orthodontic treat- pushing, compressing the PDL on the side toward
ment, it is possible that scar tissue could form in which the tooth is moving. The area of the com-
the area, which may impede orthodontic tooth pressed PDL becomes necrotic or hyalinized. Cell
movement. migration occurs from surrounding bone marrow
21. D. Unless it can be determined that the primary tooth spaces, and undermining resorption occurs. As the
is impinging on the permanent successor, intruded force dissipates over time and repair occurs, frontal
primary teeth are left alone in the hopes that they resorption can begin to occur.
will spontaneously reerupt. Intruded permanent 27. C. Beta titanium is a titanium and molybdenum alloy
teeth have a poorer prognosis. If there is an open that does not contain nickel. Stainless steel used in
apex, an intruded permanent tooth should be orthodontic wires is generally 8% nickel and 18%
closely monitored for spontaneous eruption. An chromium. Cobalt chromium has a small amount
intruded permanent tooth with a closed apex of nickel in its composition. Nickel titanium is the
should be repositioned orthodontically, and a wrong answer because it has nickel in its name.
calcium hydroxide pulpectomy should be per- 28. B. Acid etching of the enamel performed during the
formed 2 weeks after the injury. orthodontic bonding procedure causes micropo-
22. D. Replanting primary teeth has a poor prognosis rosities in enamel, which are filled with bonding
but could be considered if performed within 30 primer and resin to achieve a mechanical inter-
minutes. A primary tooth that is replanted is locking between the tooth and composite resin
likely to require splinting. The patient should be material. The composite itself can be chemically
placed on antibiotics, be restricted to a soft diet, cured or light-cured. However, the bond between
and undergo a primary endodontic procedure the tooth and resin is mechanical, not chemical.
accomplished. 29. C. The width of the permanent incisors is greater
23. B. Because the exposure site is likely significantly con- than the deciduous or primary incisors, so it is
taminated from the injury that occurred 24 hours normal and desirable for there to be spacing
previously, direct pulp capping with calcium between primary incisors so that the permanent
hydroxide is contraindicated. A calcium hydroxide successors have adequate space to erupt. However,
pulpectomy should not be the automatic procedure this extra space is not the leeway space. The term
performed because continued root elongation and leeway space refers to the extra width of the
closure of the pulp canal will likely not occur. A primary canine, primary first molar, and primary
calcium hydroxide pulpotomy is preferable for a second molar (combined) compared with their
traumatized tooth with an open apex with either a permanent successors (permanent canine and first
large exposure or a small exposure of several hours and second premolars). This extra leeway space
or days postinjury. Clinically, the tooth should be becomes available when these posterior teeth
Answer Key Orthodontics and Pediatric Dentistry 417
exfoliate, and the permanent teeth, which are typi- 34. B, C, D. The enamel is thinner and the pulp chambers
cally smaller, erupt. are relatively larger; therefore, restorative prepara-
30. A. Low/load deflection means that a low amount of tions must be shallower than typical permanent
force is required to create a particular amount of teeth. The greater constriction at the cement-
deflection of a wire. That means that the wire is enamel junction allows for a retentive area for
very flexible compared with a high load/deflection stainless steel crowns; however, this feature also
wire (a stiffer wire), which would require a greater may cause a problem in attaining a gingival seat
amount of force to deflect it the same amount. If when a class II preparation is prepared too cervi-
the amount of force change per unit of deflection cally. Interproximal contacts are broader and flatter
is small, the amount of force delivered does not in primary teeth and therefore, preparations for
change much as the wire is activated more and primary teeth are altered by preparing relatively
more. Increasing the length of a wire (by adding wider gingival seats with increased convergence to
loops or helices to its design) makes it more springy the occlusal, thereby removing more lateral inter-
(less stiff), reducing its load/deflection. proximal decay while maintaining a conservative
31. D. When the permanent dentition is fully erupted, occlusal outline form.
there is little or no likelihood that crowding will 35. A, C, D. Choice A: Pulp therapy is generally contra-
resolve on its own without intervention. Widening indicated in children who have serious illnesses.
of the dental arches during occlusal development Extremely serious complications secondary to
continues to occur naturally to a small degree acute infection can arise should the pulp therapy
during growth until the permanent canines are fail. Choice B: A patients chronologic age has little
erupted. There is some increase in space available to do with decisions regarding pulp therapy. The
for the dentition as the permanent premolars erupt clinician instead should be cognizant of the dental
to replace the primary molars owing to the leeway age of the patient, stage of development and posi-
space. However, there is no increase in the length tion of the permanent successor, and other factors
of the mandible that occurs within the dental in the decision-making process. Choices C and D:
arches during growth. The mandible grows by Teeth with caries involvement that are mobile, have
addition of bone at the condyle and deposition of swelling, furcation radiolucency, pain to percus-
bone at the posterior ramus. Resorption of bone at sion, and spontaneous pain likely either have
the anterior border of the ramus provides room for advanced inflammation or are necrotic. The pulp-
the posterior teeth (first molar, second molar and, otomy procedure is reserved for vital teeth only.
perhaps later, third molar) to erupt but does not Choice E: Marginal ridge breakdown is a common
provide room for anterior dental crowding to issue with severely decayed teeth. This condition
resolve. alone does not rule out a pulpotomy procedure
32. A3, B2, C4, D1. It is important to observe unless the caries is very extensive and renders the
the behavior of the child to better treat the tooth nonrestorable either by extending cervically
patient. excessively or by interproximal space loss second-
33. A3, B1, C4, D2. It is important to know ary to the carious process. Choice F: Amelogenesis
these stages in order to effectively manage the imperfecta is not a contraindication to a pulpot-
expectations of the patient and to prevent deeper omy procedure. Choice G: Carious exposures with
stages that may lead to nausea, vomiting, and other normal pulp tissue are typically treated with a
adverse outcomes. pulpotomy procedure.
418 Answer Key Patient Management

1. B. The four processes of motivational interviewing are completely the patient visits and contacts, make
engaging, focusing, evoking, and planning. timely entries, and avoid gaps in time. Never make
2. C. Important tenets of social cognitive theory are the personal characterizations that criticize patient
notion of self-efficacy, behavioral modeling, and behavior; instead, be objective and factual in docu-
social reinforcement. mentation. Entries must be readable, and use of
3. B. Sustain talk is communication that conveys a desire abbreviations and shorthand should be avoided.
to maintain the current behavior. 9. C. Habituation is the decrease in response that occurs
4. C. Informed consent requires that the patient be as a result of repeated or prolonged exposure to a
advised of reasons for the procedure and the ben- conditioned stimulus.
efits and risks of the procedure and anticipated 10. A. A rational response is a cognitive therapy tech-
outcome, any alternatives and their risks and nique in which the patient develops (with or
benefits including no treatment at all, and the without assistance) a more adaptive thought or
costs of the procedure and the alternatives and be statement as a means of coping.
given an explanation of the procedure in under- 11. E. Creating a child-oriented environment (e.g., having
standable terms for a layperson (not technical toys and books in the waiting room, hanging pic-
terms). tures on the wall or ceiling that a child would find
5. C, E. The ethical principles listed in the question that interesting), conveying interest in the child by
are found in the ADA Principles of Ethics and Code asking about their interests, and having the parent
of Professional Conduct include beneficence (do present in the operatory all are variables that may
good) and veracity (truthfulness). The remain- put child patients more at ease.
ing ethical principles found in the ADA Principles 12. B. Research has demonstrated that behavioral inter-
of Ethics and Code of Professional Conduct include vention is typically more effective than patient
patient autonomy (self-governance), nonmalefi- education. A combination of the two is considered
cence (do no harm), and justice (fairness). the most effective approach to increasing patient
6. B, C. The required elements for a patient to give compliance.
consent include the patient must voluntarily 13. B. Clinicians should use caution in providing prema-
agree to treatment and the patient must have the ture reassurance because trust and rapport may be
opportunity to ask questions. Additional elements compromised if the outcomes are inconsistent with
required for a patient to give consent include the what the clinician asserted.
following: information and consent must be given 14. D. The tongue is the most common place for incident
in a language that the patient understands; the cancers in the oral cavity.
doctor must be available to answer any patient 15. A. Community water fluoridation is the most cost-
questions; only the patient or the patients legal effective and economical method to prevent dental
guardian can authorize treatment decisions; and all caries. However, fluoride is believed to be the least
state regulations that outline who must obtain effective on the occlusal surface. Most decay among
consent from the patient and whether it must be in school-age children occurs on the pits and fissures
writing or signed are met. of the chewing surfaces.
7. C. Risk management is a concept derived from indus- 16. C. Double-blind designs help prevent the potential for
try wherein one identifies areas possibly exposing a biased interpretation of a treatment effect that
one to liability; weighs the risks against the bene- might occur if either the investigator or the subject
fits; and controls that exposure by monitoring, knows to which group the latter belongs.
ensuring, or eliminating the dangerous activity. 17. D. The methods section of a scientific article allows
Risk management does not include intentionally the reader to assess the validity of the study and the
and knowingly exposing oneself to liability. reliability of the measures. This section provides
8. A, D, F. A very important weapon against a possible the reader with specific and detailed information
lawsuit is appropriate and adequate documentation regarding how the study was conducted. Based
of patient contacts. When making entries in patient on this information, the reader should be able to
records, be sure to include specific facts, document replicate the study.
418
Answer Key Patient Management 419
18. C. The variance determines the way individual values of the MSDS should be maintained with each
are located around the mean. The larger the vari- chemical.
ance, the more widely the data items are spread 25. B. Prospective reimbursement is a mechanism in
about the mean value. Variance is measured in which the dentist is compensated before treatment
squared units (s2). The standard deviation is the is provided (i.e., in capitation systems). Managed
square root of the variance. The mean is expressed care is an arrangement in which a third party
in the same units as the data items, but the variance mediates between providers and patients negotiat-
is expressed in squared units. The standard devia- ing reimbursement for certain services and over-
tion measures the average deviation from the mean seeing the treatments delivered.
in the same units as the mean. 26. E. Fluoridated water is odorless, colorless, and taste-
19. D. Parenteral contact is defined as the transmission of less at the recommended level of fluoride for a
pathogenic microorganisms by piercing the skin or community water supply, which ranges from 0.7 to
mucous membrane (e.g., intravenous, subcutane- 1.2 parts per million (ppm) of fluoride. At this
ous, intramuscular) by an accidental or intentional dosage, it is imperceptible to the human senses.
stick with a needle or other sharp instrument that 27. D. According to the U.S. Centers for Disease Control,
is contaminated with blood or other body fluid. in 2012, more than 210 million people in the
20. E. Masks that cover the mouth and nose reduce inha- United States lived in fluoridated communities.
lation of potentially infectious aerosol particles. 28. D. According to the CDC, in 2010, about 74% of the
They also protect the mucous membranes of the U.S. population on a public water supply lived in
mouth and nose from direct contamination. Masks fluoridated communities.
should be worn whenever aerosols or spatter may 29. D. Studies shows that fluoridation prevents tooth
be generated. If a mask is worn longer than 20 decay for people of all ages. It has both a topical
minutes in an aerosol environment, the outside and a systemic effect.
surface of the mask becomes a nidus of pathogenic 30. D. The best response is school sealant programs
bacteria rather than a barrier. It is recommended because it is the only choice that is a community-
that a new mask be worn for each patient and that level or population-level prevention program.
masks be changed routinely at least once every Choices A, B, and E are individual prevention
hour and more often in the presence of heavy measures.
aerosol contamination. 31. E. Flossing daily is the only choice that is an individ-
21. D. Disinfection refers only to the inhibition or destruc- ual prevention measure, not a community preven-
tion of pathogens. Spores are not killed during tion program. Flossing does not prevent tooth
disinfection procedures. By custom, the term dis- decay.
infection is reserved for chemicals applied to inani- 32. B. According to the CDC, the recommended level of
mate surfaces, and the term antiseptic is used for fluoride for a community water supply is 0.7 to
antimicrobial agents that are applied to living 1.2ppm of fluoride depending on the mean annual
tissues. temperature over 5 years. In 2011, the U.S. Depart-
22. A. The spore test is a biologic monitor. The process ment of Health and Human Services proposed
consists of placing into the autoclave bacterial decreasing this to 0.7ppm, but as of July 2013, it
spores on strips or in envelopes along with a had not been implemented. The rationale is that
normal instrument load. If the autoclave is working fluid intake of people is the same regardless of
properly, the autoclave reaches the temperature yearly air temperature of a community.
and pressure to kill the spores. Spore testing must 33. D. Community water fluoridation is the most cost-
be conducted weekly. effective and the most practical preventive measure
23. E. A disinfectant should be able to kill M. tuberculosis. to prevent tooth decay. Everyone in the community
This is the benchmark organism for disinfectants. benefits with no individual or group effort needed,
It is much harder to kill than most bacteria, viruses, at a minimal cost to society and at no cost to an
fungi, and protozoa. This resistance is partially due individual. All the other prevention programs
to the waxy cell wall of Mycobacterium. listed require staff or individual effort for
24. E. MSDSs are an easy reference for information on everyone.
hazardous substances. MSDSs must be readily 34. C. For a child who lives in a nonfluoridated commu-
accessible to workers exposed to hazardous sub- nity it is recommended, depending on existing
stances. MSDSs provide information on hazardous water fluoride levels, to start fluoride dietary sup-
materials, substances, and wastes. Chemical manu- plements from 6 months until 16 years old. For
facturers develop and provide an MSDS for each children 3 years old or younger, it is much easier
hazardous product. The distributor is responsible to use fluoride drops because children at that age
for getting MSDSs to employers. At least one copy have difficulty swallowing or chewing tablets.
420 Answer Key Patient Management
35. B. Secondary prevention is the elimination or reduc- 37. C. Sealants seal in and block the caries process before
tion of a disease after it occurs. An amalgam resto- or after it has begun. Sealants prevent incipient
ration is considered secondary prevention because caries in pits and fissures from progressing. Seal-
tooth decay is removed and a restoration is placed. ants are primarily recommended for first and
36. E. All health care providersdentists, hygienists, second permanent molars. Sealants are not the best
nurses, and physiciansare responsible for educat- preventive measure for large populations; fluorida-
ing the public on the safety and effectiveness of a tion is. Sealants are primarily for children at risk
public health measure that benefits everyone such for dental caries. Fluoride mouth rinses have been
as community water fluoridation. used in U.S. schools for more than 4 decades.
Answer Key Periodontics 421

1. B. Wasting diseases of the teeth include erosion 8. B. Streptococcus and Actinomyces species are initial
(corrosion; may be caused by acidic beverages), colonizers of dental plaque. They are gram-
abrasion (caused by mechanical wear as with positive, facultative microorganisms.
toothbrushing with abrasive dentifrice), attrition 9. C. Endotoxin or lipopolysaccharide is an important
(caused by functional contact with opposing teeth), constituent of the gram-negative outer membrane
and abfraction (flexure secondary to occlusal that contributes to initiation of the host inflamma-
loading). tory response.
2. D. Wasting diseases of the teeth include erosion 10. B. Calculus is calcified dental plaque. It is always
(corrosion; may be caused by acidic beverages), covered by a layer of uncalcified plaque, which is
abrasion (caused by mechanical wear as with detrimental to the gingival tissues.
toothbrushing with abrasive dentifrice), attrition 11. B. Supragingival margins are least detrimental to the
(caused by functional contact with opposing teeth), gingival tissues; subgingival margins are the most
and abfraction (flexure secondary to occlusal detrimental because of the accumulation of dental
loading). plaque.
3. A. The periodontal examination includes probing 12. C, D, F, G. T cells, B cells, and plasma cells are cells
pocket depth (distance from the gingival margin to of the acquired immune system. The acquired
the base of the pocket) and clinical attachment immune system must see a foreign substance to
level (distance from the CEJ to the base of the attack it effectively and can confer long-term
pocket). Both of these measures are made using a immunity to the host. Cells of the innate immune
periodontal probe. Gingival recession can be mea- system defend the host in a nonspecific manner
sured as the distance from the CEJ to the free gin- by responding to foreign substances in a generic
gival margin. Alveolar bone loss is measured way. These cells include neutrophils (polymorpho-
radiographically. nuclear leukocytes), dendritic cells, monocytes/
4. C. When the free gingival margin is apical to the CEJ, macrophages, and mast cells.
recession has occurred. Attachment loss is the 13. C. Neutrophils are one of the primary defense cells
measure from the CEJ to the base of the periodon- of the innate immune system. T lymphocytes are
tal pocket. With the free gingival margin 2mm important activators of the specific (adaptive)
apical to the CEJ and the probing pocket depth immune system. Macrophages are antigen-
measurement 6mm, there has been 8mm loss of presenting cells. Plasma cells produce antibodies.
attachment. 14. B. Matrix metalloproteinases are the most important
5. A. Loss of clinical attachment is the hallmark that dis- proteinases involved in the destruction of peri-
tinguishes periodontitis from gingivitis. In both odontal tissues.
diseases, patients may present with periodontal 15. C. Neutrophils are the predominant inflammatory
pocket depths greater than 3mm. In gingivitis, cells in the periodontal pocket and have migrated
these are often referred to as pseudopockets. Gin- across the pocket epithelium from the subgingival
gival recession can occur in a healthy periodon- vascular plexus.
tium as a result of factors such as aggressive 16. C. Preliminary phase therapy is used to treat emer-
toothbrushing or orthodontic tooth movement. gencies and remove hopeless teeth.
Bleeding on probing is a hallmark sign of inflam- 17. B. Polymorphisms in the IL-1 genes have been associ-
mation in the periodontal tissues and can occur in ated with severe chronic periodontitis.
both diseases. 18. D. Single-rooted teeth have a poorer prognosis than
6. D. Supragingival plaque is either tooth-associated or multirooted teeth with comparable loss of attach-
outer layer. Tooth-associated plaque is composed ment. Loss of attachment that extends to the apex
primarily of gram-positive cocci and short rods. of the root alters the root/crown ratio and makes
7. C. Saliva is the source of inorganic components the prognosis worse.
(calcium, phosphorus) for supragingival plaque. 19. C. The amount of clinical attachment loss is most
Gingival crevicular fluid is the source of inorganic important in determining the prognosis. Deep
components of subgingival plaque. pocket depths and bleeding on probing can
421
422 Answer Key Periodontics
be found in both gingivitis and periodontitis. 25. D. Laterally positioned flaps should be performed
Although the level of alveolar bone is usually con- only when there is adequate bone and adequate
sistent with the amount of clinical attachment loss, width and thickness of attached gingiva on the
there are circumstances under which these two facial of the donor site.
measures are not comparable. 26. B. If the bone is overheated (>47C) for prolonged
20. B. Diabetic patients may experience hyperglycemia, periods (>1 minute) during the preparation of the
which is greater than normal amounts of glucose osteotomy, it leads to necrosis of the bone cells and
in the blood. However, this is not the most common bone tissue, causing bone sequestration or creation
problem for diabetic patients undergoing dental of nonmineralized soft scar tissue at the osteotomy
treatment. They are more likely to experience site. This type of aberrant bone healing leads to
hypoglycemia, or low blood glucose concentra- prevention or disruption of the normal process
tions, as a result of inadequate carbohydrate inges- of osseointegration around the dental implant,
tion. Insulin resistance is a physiologic condition causing implant failure. During the osteotomy
in which cells do not respond normally to the phase, it is critical to use profuse irrigation
actions of insulin. Insulin deficiency is when the (cooling), along with gentle moderate-speed
pancreas does not produce enough insulin. drilling and sharp drills, to prevent overheating
21. C. Sickle scalers and universal curettes do not have of the site.
offset angulation of the blade. The working ends of 27. C. Three-walled defects respond best to regenerative
area-specific curettes are offset at a 60-degree angle therapy.
relative to the terminal shank. The working ends of 28. C. The primary goal of guided tissue regeneration is
sickle scalers and universal curettes are not offset to prevent the migration of epithelial cells into
they are at a 90-degree angle relative to the termi- the healing surgical site. When those cells are
nal shank. present on the root surface, healing is by estab-
22. C. Patients with active infectious diseases should not lishment of a long junctional epithelium. By
be treated with ultrasonic instruments because of excluding these cells, the membrane allows for
the aerosol that is created when using this type of stabilization of the clot and regeneration of the
instrument. periodontiumthe deposition of cementum on
23. B. During the course of periodontal treatment, a the root surface and regeneration of alveolar bone
wound (space) is created that becomes an area and the PDL. Plaque accumulation does occur on
where cells from multiple tissue types are present the surface of the membrane during this healing
in close proximity. Because of their diverse charac- process.
teristics, different cell types have dissimilar prolif- 29. C. Although tooth migration can be a sign of occlusal
erative and migratory capabilities that affect the trauma, tooth mobility is the most common clini-
speed and order of healing. Epithelial cells are typical sign.
cally fastest in their response and migratory capa- 30. B. Most patients who have been treated for periodon-
bilities and engage in this process first, resulting in titis should be seen at 3-month intervals for sup-
what is often called healing by long junctional portive periodontal therapy (maintenance).
epithelium. Connective tissue cells from the gin- 31. C. The minimal space needed between an implant and
gival tissue and the PDL cells follow in their migra- a natural tooth or between two implants in mesio-
tory abilities, with bone cells being the slowest in distal direction is 2mm of bone. This dimension
these capabilities. Although this process is depen- provides at least 1 to 1.5mm of adjacent bone
dent on the physiologic capabilities of the different present to allow for proper healing and prevent
cell types in general, it can be influenced by other bone loss around or between implants. If two
systemic or local factors. During periodontal treat- implants (4mm each; 8mm total) are used, 6mm
ment, the ultimate goal is the creation of new (2 + 2 + 2) is needed to allow a sufficient amount
attachment, which can be achieved only if the PDL of mesiodistal bone between tooth #1/implant #1,
cells repopulate the area of lost attachment. implant #1/implant #2, and implant #2/tooth #1.
24. A. Plaque removal during the initial postoperative The minimum dimensions of the total mesiodistal
visits after periodontal surgery is essential to space needed for placement of two 4-mm implants
healing of the periodontal tissues. is 14mm.
Answer Key Pharmacology 423

1. C. Only weak acids and weak bases are greatly concentration of catecholamines and serotonin in
affected in their distribution by changes in pH. the cytoplasmic pool of nerves but indirectly
Weak organic acids dissociate more from protons reduces the level of neurotransmitter in the secre-
at higher pH, making a higher percentage of tory granule. Amphetamine is well known for its
their molecules charged; this traps them in that sympathetic effect because of release of catechol-
compartment. amines. Physostigmine inhibits acetylcholinester-
2. A. Drug agonists have an intrinsic activity of greater ase, which metabolizes acetylcholine. The enzyme
than 0 and less than or equal to 1. Intrinsic activity is primarily located on the postjunctional and post-
refers to the maximal effect attainable by the drug. synaptic membranes. Fluoxetine is an antidepres-
Potency and receptor affinity are not directly sant that inhibits the reuptake of serotonin.
related to intrinsic activity. The therapeutic index 10. D. Naloxone is a competitive antagonist at opioid
requires a quantal dose-response curve, in contrast receptors.
to the other characteristics listed, which require 11. C. COX is a key enzyme in the synthesis of prosta-
graded concentration-response curves. Drugs with glandins. Prostaglandins, including PGE2 and
the same intrinsic activity may vary a great deal in PGF2, are important mediators for functions such
their aqueous solubility. as pain and are a product of COX. Aspirin inhibits
3. A. Inhibition of adenylyl cyclase through Gi, resulting both COX-1 and COX-2.
from stimulation of 2-adrenergic receptor, leads 12. C. Oral ketorolac (an NSAID) is used only to continue
to a reduction in intracellular cAMP. therapy after a parenteral dose.
4. C. Circulating muscarinic cholinergic receptor ago- 13. E. Basophils and mast cells release histamine.
nists stimulate these receptors on endothelial cells, However, the cell that responds to histamine stim-
leading to release of nitric oxide and vasodilation. ulation at the H2 receptor is the parietal cell of the
5. B. Carbidopa is used to inhibit dopa decarboxylase. stomach. Stimulation of this receptor leads to
Its usefulness is based on reducing conversion of proton release and a decrease in the pH of the
levodopa to dopamine outside the CNS. Carbidopa stomach lumen. H2 histamine receptor blockers are
does not penetrate the blood-brain barrier and used to reduce stomach acid.
does not interfere with the beneficial effect of 14. A. Renin release from the kidney is enhanced by stim-
levodopa in the brain, but it prevents the adverse ulation of the 1-adrenergic receptors in the juxta-
effects of dopamine in the periphery. glomerular cells. Among the answer choices, only
6. A. Bupivacaine has the highest lipid solubility of the blockers reduce renin release. Although ACE
drugs listed. Lipid solubility is the major chemical inhibitors and angiotensin II receptor blockers act
characteristic of the local anesthetic that deter- on the renin-angiotensin system, they do not
mines duration of action. Procaine is the only ester inhibit renin release. These agents tend to increase
given as a choice and is rarely used. plasma renin.
7. B. Nitrous oxide oxidizes the cobalt in vitamin B12, 15. C. -Adrenoceptor blockers, such as phentolamine,
resulting in the inhibition of methionine synthase. inhibit the vasoconstrictor effect of epinephrine
Nitrous oxide has greater analgesic potency than but not the vasodilator effect of epinephrine. The
other inhaled anesthetics (e.g., halothane, isoflu- administration of blockers results in epinephrine
rane). Ketamine is not inhaled; rather, it is injected. reversal. Propranolol would block only the vasodi-
It also does not inhibit methionine synthase. The lator effect of epinephrine. Guanethidine and tyra-
same is true for propofol. mine act largely at prejunctional sites and do not
8. C. -Adrenergic receptor stimulation accounts for the block adrenergic receptors.
vasoconstrictor effect of levonordefrin. 16. B. Enoxaparin is a low-molecular-weight heparin. It
9. A3, B5, C1, D2, E4. Botulinum toxin pre- activates antithrombin III and inhibits factor Xa.
vents fusion of the secretory vesicles with the 17. D. The effect of glucocorticosteroids remaining in the
plasma membrane in cholinergic nerves, prevent- mouth after inhalation is to make the oral cavity
ing the release of acetylcholine. Tranylcypromine more susceptible to fungal infection. The mouth
is a nonselective MAO inhibitor. It increases the should be rinsed with water after inhalation use.
423
424 Answer Key Pharmacology
Inhaled methacholine, in contrast to the other 27. A, D, F. Phentolamine blocks both 1-adrenergic and
drugs listed, is not used therapeutically, but rather 2-adrenergic receptors. It blocks the vasoconstric-
is used to diagnose hyperactive airway. tor effects of norepinephrine and epinephrine,
18. E. Divalent and trivalent cations, such as those found both of which cause vasoconstriction by stimulat-
in oral antacids, chelate tetracyclines and prevent ing -adrenergic receptors. The effect of phen
their absorption. tolamine would last long enough to block the
19. D. A decrease in glycogen breakdown is a classic vasoconstrictor effect of a subsequent injection
effect of insulin. Epinephrine (by acting as an of epinephrine. Phentolamine does not block
agonist at 1-adrenergic and 2-adrenergic recep- -adrenergic receptors or sodium channels. It does
tors), albuterol (by acting as an agonist at 2- not block protein synthesis in bacteria and does
adrenergic receptors), and glucagon (by acting at not have an antimicrobial effect. Phentolamine is
glucagon receptors) all tend to increase glycoge- used in dentistry to reverse soft tissue anesthesia
nolysis. Parathyroid hormone has little effect on more quickly after local anesthesia.
glycogenolysis. 28. A3, B5, C1, D7, E2. Several drugs are
20. B. Nitroglycerin is a nitrovasodilator. It produces approved for the treatment of overactive bladder.
nitric oxide, which activates guanylyl cyclase which These are typically antimuscarinic drugs that block
catalyzes the production of cGMP. the effect of acetylcholine on the detrusor muscle
21. C. Clavulanic acid has very little antimicrobial activ- of the bladder. Solifenacin is a newer drug that
ity. Its value in combination with certain penicillins happens to be a selective antagonist at the M3
is due to its ability to inhibit certain penicillinases. muscarinic receptor. Stimulation of 2-adrenergic
This inhibition protects the penicillin from bacte- receptors in the brain and spinal cord reduces sym-
rial enzyme attack. Transpeptidase is inhibited by pathetic outflow and leads to sedation, analgesia,
-lactams, such as penicillin. DNA gyrase is inhib- and reduced blood pressure. As a result of this
ited by fluoroquinolones, such as ciprofloxacin. mechanism, dexmedetomidine is a useful intrave-
22. E. Transpeptidase is the enzyme that catalyzes nous sedative. Quetiapine is a newer antipsychotic
the peptide cross-linking of peptidoglycan. drug that is able to block both the dopamine D2
Transpeptidase is inhibited by penicillins and and the 5-HT2 receptors, resulting in fewer adverse
cephalosporins. effects compared with older antipsychotic drugs.
23. E. Trimethoprim, by virtue of its inhibition of bacte- Zaleplon blocks the BZ1 receptor selectively,
rial dihydrofolate reductase, acts synergistically whereas a benzodiazepine, such as diazepam,
with the sulfonamides. blocks both the BZ1 and the BZ2 receptors. Both are
24. D. Clindamycin is useful for some oral infections, located on chloride channels. Gabapentin binds
including infections involving viridans strepto- selectively to the 2-1 subunits of the high-voltage
cocci. K. pneumoniae and P. aeruginosa are gram- calcium channel. Pregabalin has a similar mecha-
negative rods and not subject to clinical inhibition nism. These drugs are useful for certain partial
by clindamycin. Methicillin-resistant staphylo- seizures and for neuropathic pain and, at least for
cocci are insensitive to clindamycin and most tra- pregabalin, for fibromyalgia. Codeine is an opioid
ditional antistaphylococcal drugs. C. albicans is a receptor agonist that has analgesic and antitussive
yeastlike fungus and is not inhibited by antibacte- properties. Pilocarpine is a muscarinic receptor
rial drugs such as clindamycin. agonist that does not act at any of the receptors
25. E. The mammalian enzyme form of dihydrofolate mentioned and would have an effect on the bladder
reductase is the target for methotrexate. Bleomycin opposite to that desired for overactive bladder.
produces strand breaks in DNA. Cisplatin is an Carbamazepine is a sodium channel blocker, which
alkylating agent. Doxorubicin intercalates with is used as an antiepileptic drug and for neuropathic
DNA and inhibits topoisomerase. 5-Fluorouracil, pain such as trigeminal neuralgia.
after undergoing activation, inhibits thymidylate 29. A5, B7, C1, D11, E4, F9, G10.
synthase. The effect of neostigmine on acetylcholinesterase
26. 1C, 2A, 3E, 4D, 5B. Glipizide is an oral makes it a useful drug for myasthenia gravis.
hypoglycemic drug that causes the release of ACE inhibitors end in pril (generic names) and
insulin from the beta cells of the pancreas by are useful for various cardiovascular indications.
closing the ATP-dependent potassium channels. By inhibiting dipeptidyl peptidase-4, sitagliptin
The effect of insulin is mediated by binding to its reduces the breakdown of the incretin, GLP-1. The
receptor, followed by several events including the resulting increase in GLP-1 reduces glucose uptake
movement of the glucose transporter, GLUT-4, to from the gut, inhibits glucagon release, increases
the plasma membrane, resulting in an increase of insulin release, and normalizes insulin levels. This
glucose uptake into the cell. mechanism makes sitagliptin a useful drug for type
Answer Key Pharmacology 425
2 diabetes. Rifampin inhibits DNA-dependent by host enzymes results in the inhibition of viral
RNA polymerase, making it effective in certain DNA polymerase. The drugs are selective for the
bacterial infections. It is useful in treating tubercu- virus because they are poorly phosphorylated by
losis in combination with other drugs. The enzyme, thymidine kinase in mammalian cells. Their toxic-
14 -demethylase, is important in the synthesis of ity is low despite their effectiveness against the
ergosterol and for membrane integrity of many virus. Ganciclovir is also activated in a similar way;
fungi. Inhibition of this enzyme is the antifungal however, its selectivity is lower, and its toxicity pre-
mechanism of the azoles, including fluconazole. cludes its use for herpes simplex virus, although
DOPA decarboxylase catalyzes the conversion of the risk/benefit ratio is acceptable in treating
DOPA to dopamine. By inhibiting this enzyme, cytomegalovirus. Indinavir is an inhibitor of HIV
carbidopa reduces the conversion of DOPA to aspartyl protease and is targeted to HIV. Zidovu-
dopamine. The reason this inhibition is useful is dine is a nucleotide derivative that inhibits HIV
because it allows more DOPA to enter the CNS reverse transcriptase, restricting its use to retrovi-
where it can be converted to dopamine. Neither ruses. Ribavirin inhibits RNA synthesis and is used
dopamine nor carbidopa enters the CNS, so pre- to treat respiratory syncytial virus.
serving DOPA for CNS conversion to dopamine is 32. A3, B9, C1, D6, E7, F4. Bisphospho-
effective in treating parkinsonism, and the use of nates, especially at doses used to treat neoplasms
carbidopa means that the dose of DOPA does not of the bone, have been linked to osteonecrosis of
have to be large, and the side effects of dopamine the jaw. Pamidronate is a member of this class of
are minimized. MAO-B is selective for the metabo- drugs. ACE inhibitors are known commonly to
lism of dopamine. Selegiline increases the level of cause a nonproductive cough. This cough is likely
dopamine in the CNS, making the drug useful for due to the increase in bradykinin resulting from
parkinsonism and without as many adverse effects inhibition of bradykinin breakdown by ACE. The
as nonselective MAO inhibitors. Terbinafine inhib- generic names of ACE inhibitors end in pril (e.g.,
its squalene epoxidase (squalene monooxygenase), fosinopril). The -adrenergic receptor blockers,
making it useful for dermatophyte fungal infec- including 1-selective blockers such as terazosin,
tions. Aliskiren is a direct inhibitor of renin. This are associated with a risk of first dose hypotension
drug is useful in treating hypertension. Ciprofloxa- because of the high degree of sensitivity to these
cin inhibits DNA gyrase and topoisomerase IV, drugs until the body adapts to them. Diphenhydr-
making it useful as an antibacterial drug. Lithium amine is an H1 histamine receptor blocker. It also
inhibits inositol monophosphate phosphatase. This passes through the blood-brain barrier. These two
and other mechanisms mediate an antimanic effect characteristics predict a high probability of seda-
from the drug. tion when given. The drug is used for its antihista-
30. B, D, E. The drugs that most effectively antagonize minic effects, but it is also used to produce sedation.
pilocarpine are agents that block muscarinic recep- The use of aspirin, and by extension other salicy-
tors because pilocarpine is a muscarinic receptor lates, in individuals younger than 20 years old with
agonist. Tolterodine and oxybutynin are used to concurrent or recent viral infections has been
treat overactive bladder, whereas benztropine linked to Reyes syndrome. This syndrome is char-
is used principally to overcome Parkinson-like acterized by encephalopathy and liver damage and
(extrapyramidal) adverse effects from antipsy- is often fatal. It has not been implicated with use
chotic drugs. All three drugs are antimuscarinic of acetaminophen. Although there have been
agents. Rivastigmine increases salivary flow rate some anecdotal reports of methemoglobinemia
because of its inhibition of acetylcholinesterase with acetaminophen or lidocaine, these cases are
with resultant muscarinic effects in the salivary extremely rare. There is a more direct connection
glands. Metoprolol is a selective 1-adrenergic with the use of prilocaine because it is metabolized
receptor blocker and does not directly affect the to o-toluidine, which can lead to oxidation of
secretory flow rate increase from pilocarpine. Epi- hemoglobin. Neither acetaminophen nor lidocaine
nephrine stimulates -adrenergic and -adrenergic is metabolized to o-toluidine. Clopidogrel blocks
receptors and does not directly affect the secretory the P2Y12 receptor for ADP in platelets and reduces
flow rate increase from pilocarpine. platelet aggregation. It is not linked to any of the
31. C, E. Acyclovir and penciclovir both become initially descriptions given here. Bleeding is its most impor-
phosphorylated by thymidine kinase in the herpes tant adverse effect.
simplex virus. The eventual activation of the drugs
426 Answer Key Prosthodontics

1. B. Irreversible hydrocolloid or alginate is the material vertical minor connector should be less than 90
of choice to produce diagnostic casts. Its composi- degrees.
tion is mainly sodium or potassium salts of alginic 9. D. This is the best answer because generally it is the
acid. The salts react chemically with calcium sulfate dentists fault and not the technicians. Incorrect
to produce insoluble calcium alginate. opaque may influence the resultant shade. Inade-
2. B. A closed or insufficient vertical dimension of occlu- quate vacuum affects the esthetics. If the opaque
sion is thought to be one predisposing condition does not mask well, the metal result is a gray
for angular cheilitis, which usually is associated appearance or lower value in the restoration.
with Candida albicans. Improperly balanced occlu- 10. C. Usually, vertical fractures refer pain when biting.
sion and poor contour of the denture base are not In this case, the patient had recent endodontic
predisposing conditions for angular cheilitis. treatment, but there is no periapical lesion to
3. A. Pagets disease of bone is a bone disease character- indicate the pain is due to inadequate root canal
ized by bone resorption followed by attempts therapy. There is no sign that the crown is loose,
at bone repair involving proliferation leading to no premature contact, and no mobility.
bone deformities. Its etiology is unknown, and it 11. C. The condyles should be in centric relation, which
occasionally involves the maxilla and mandible. is defined as the maxillomandibular relationship
Papillary hyperplasia is characterized by multiple in which the condyles articulate with the thinnest
papillary projections of the epithelium caused avascular portion of their respective disks with
by local irritation, poor-fitting denture, poor oral the condyle-disk complex in the anterior-superior
hygiene, and leaving dentures in all day and position against the shapes of the articular emi-
night. nences (The glossary of prosthodontic terms.
4. A. Maxillary teeth should contact the wet dry lip line J Prosthetic Dent 94:21-22, 2005).
when fricative sounds f, v, and ph are made. These 12. D. Any time there is a question regarding the treat-
sounds help to determine the position of the incisal ment outcome involving a prosthetic device or
edges of the maxillary anterior teeth. the need to produce templates for provisional res-
5. C. Using more monomer than needed causes in- torations that reproduce a desired form of teeth,
creased shrinkage. The more monomer used, the it is recommended that a diagnostic wax-up be
less expansion, less heat, and reduced strength generated.
produced. 13. A. The length, canal enlargement, and a finish line for
6. D. Occlusal adjustment of dentures should be done the post are unimportant if there is no sound
with the premise of obtaining even occlusal con- remaining coronal tooth structure to get a ferrule
tacts with balanced occlusion to stabilize the den- of the final restoration.
tures during function. 14. E. Bone resorption around dental implants can be
7. C. Bone loss is usually seen on the most coronal caused by inadequate oral hygiene, premature
aspect of the implant in the form of a wedge. There loading, and repeated overloading. If an implant-
is no periodontal ligament on implants, so there is supported framework does not fit passively, the
no feeling of soreness. implant is placed under constant force. If signifi-
8. C. Rests are critical for the health of the soft tissues cant compressive forces are placed on the interfa-
underlying the denture resin basis and the minor cial bone, these can lead to implant failure.
and major connectors. Rests should prevent tilting 15. D. When checking the occlusion of a cast restoration,
action and should direct forces through the long mylar paper or shim stock is a very accurate
axis of the abutment tooth. To function as speci- method for testing occlusal contacts. The proce-
fied, an occlusal rest should have a rounded (semi- dure is to check with the mylar paper before placing
circular) outline form and be one third the facial the restoration in the teeth adjacent to the tooth to
lingual width of the tooth, one half the width be restored and the opposing side. The dentist
between cusps, and at least 1.5mm deep for base places the restoration and checks whether the same
metal. The rest floor inclines apically toward the occlusal contacts are maintained on the tested
center of the tooth, and the angle formed with the teeth. When all teeth, including the one being
426
Answer Key Prosthodontics 427
restored, hold the mylar paper on occluding and 25. A. Metamerism is the phenomenon where a color
even, articulating markings are present, occlusion match under a lighting condition appears different
contacts are correct. under a different lighting condition.
16. E. An FDP replacing the first bicuspids improves the 26. B. The patients main concern is not to lose the
prognosis of the second bicuspids when placing an anterior teeth and lose esthetics. Maintaining the
RDP. Implants would also improve the prognosis vertical dimension is not the main concern when
by not leaving the second bicuspid standing alone fabricating complete dentures because vertical
and acting as a cantilever when in function with dimension can be accurately reproduced. Extract-
the removable prosthesis. ing the posterior teeth and maintaining the ante-
17. D. The surveyor is used for surveying a diagnostic cast rior teeth until the day of delivery of the dentures
and to measure a specific depth of undercut. It also is the preferred method when placing immediate
helps to determine the most desirable path of dentures because the posterior teeth can be set
placement for an RDP. It identifies bony areas that (teeth placed in a wax setup). The vertical dimen-
may need to be surgically removed because they sion and the maxillomandibular relationship
interfere during insertion of the RDP. It is also used (centric relation) can be determined. The anterior
to survey crowns, place intracoronal retainers, teeth are set by means of removing the teeth from
machine or mill cast restorations, and survey and the cast and replacing them with the denture teeth
block out a master cast before constructing an RDP. in a position that is similar to that of the teeth in
18. C. Anterior guidance must be preserved by means of the cast or in a improved position if necessary,
construction of a custom incisal guide table, espe- being careful not to make very drastic changes.
cially when restorative procedures change the sur- Also, extracting the posterior teeth beforehand and
faces of anterior teeth that guide the mandible in allowing a period of about 1 month helps to reduce
excursive (lateral, protrusive) movements. major changes in the anatomic configuration of the
19. D. The tooth does not exhibit any pathology to indi- ridges, which provides stable ridges posteriorly for
cate that the radiolucency is derived from the the dentures at the time of delivery. It is better to
tooth. The mental foramen can appear on the apex, extract all the teeth and allow healing and con-
depending on the direction of the x-ray beam. struct the dentures. However, in this scenario, the
20. A. The minor connector for the mandibular distal patient would lose all the teeth, and this presents
extension base should extend posteriorly about an esthetic issue, which is the main concern of the
two thirds the length of the edentulous ridge; this patient (and generally this is the case with most
adds strength to the denture base. patients). Esthetics is the main concern, so the
21. D. Rigidity is provided by cross-arch stability through anterior teeth should be maintained. In some situ-
the principle of broad distribution of stress. The ations, the anterior teeth might not be worth
major connector should not alter dramatically the retaining even for a short time, such as if they have
contours of the supporting structures, and it should severe mobility or are broken down. In the case
contribute to the support of the prosthesis. presented, there is no indication that the anterior
22. B. Common reasons for an FDP not to fit in one piece teeth are severely mobile or broken down.
are lack of parallelism between the abutments and 27. A. Border molding can be challenging with teeth
distortion of the wax pattern during removal from present because there can be tissue undercuts, and
the dies. In any of these cases, the framework may it is more difficult to border mold areas with teeth.
not fit in the prepared abutment teeth and must be The area around anterior teeth is usually a difficult
sectioned between one of the connectors between area because of anatomic form. Sequencing the
the pontic and retainer to fit the two pieces indi- treatment is not the most difficult step because
vidually, and a solder record must be made to generally the steps are similar whether construct-
solder the pieces. ing a conventional denture or immediate denture.
23. A. The soldering flux used with gold alloys is usually Delivery is performed in the same manner as most
borax glass (Na2B4O7) because of its affinity for dentures.
copper oxides. Flux is applied to a metal surface to 28. C. A tooth with an occlusal prematurity is often sore
remove or prevent oxide formation. With an oxide- when occluding, and patients usually complain
free surface, the solder wets the surface freely and that the tooth occludes before the others. An area
spreads over the metal surface. of abfraction is generally sensitive to passing an
24. C. The rest should be spoon-shaped and is slightly explorer over it and sensitive to concentrating a
inclined apically from the marginal ridge of the puff of air on the abfraction. A cracked tooth is
abutment tooth. It should restore the occlusal mor- difficult to diagnose because often the crack is
phology of the tooth and not interfere with the invisible. Pain generally can be elicited by chewing
normal existing occlusion. something hard and during the release of the force
428 Answer Key Prosthodontics
applied to a tooth sleuth. The tooth is sensitive to 30. D. Assessment and adjustment of occlusal relation-
cold liquids. In some cases, there is discoloration ships and axial contours does not have any effect
of a cusp if the crack passes through the cusp. on marginal integrity or how the fixed prosthesis
29. D. Zirconia crowns can be placed on a preparation fits between the retainer teeth. Proximal contact is
with the same reduction required as for a full metal the first step when trying any fixed restoration
crown. A full metal crown requires less reduction because a tight proximal contact does not allow the
than a metal-ceramic crown. A Zirconia crown can prosthesis to seat completely on the tooth and
also be used on a tooth that has additional reduc- obtain marginal integrity.
tion needed for a metal-ceramic crown or an all-
ceramic crown, such as lithium disilicate crowns.
Answer Key for Sample Answer Key Sample Examination 429
Examination
Endodontics knowledge and understanding of the risks and
benefits to treatment. This principle is the basis
1. A. Acute apical (periradicular) periodontitis is char- for the practice of informed consent in the
acterized by pain, commonly triggered by chewing physician-patient transaction regarding health
or percussion. Acute periradicular periodontitis care.
alone is not indicative of irreversible pulpitis. It 7. B. The pulp contains two types of sensory nerve fibers:
indicates that apical tissues are irritated, which myelinated (A fibers) and unmyelinated (C fibers).
may be associated with an otherwise vital pulp. A fibers include A-beta and A-delta, of which
2. C. The most important part of the restored tooth is A-delta are the majority. A-delta fibers are princi-
the tooth itself. No combination of restorative pally located in the region of the pulp-dentin junc-
materials can substitute for tooth structure. Posts tion, are associated with a sharp pain, and respond
do not reinforce the tooth, but rather weaken it to relatively low-threshold stimuli. C fibers are dis-
further by additional removal of dentin and by tributed throughout the pulp, are associated with a
creating stress that predisposes to root fracture. throbbing pain sensation, and respond to relatively
3. A. Lingering spontaneous pain is evidence of C-fiber high-threshold stimuli.
stimulation. Even in degenerating pulps, C fibers 8. A. The paralleling, not right-angle, technique is best
may respond to stimulation. The excitability of C for endodontics. The film is placed parallel to the
fibers is less affected by disruption of blood flow long axis of the tooth, and the beam is placed at a
compared with A fibers. C fibers are often able to right angle to the film. The technique allows for the
function in hypoxic conditions (e.g., at the early most accurate and reproducible representation of
stage of pulpal necrosis). tooth size.
4. A. Nasopalatine duct cyst is a circular radiolucent 9. C. The principles of flap design are as follows: (1) flap
area seen as a marked swelling in the region of the design should ensure adequate blood supply, and
palatine papilla. It is situated mesial to the roots of the base of the flap should be wider than the apex;
the central incisors, at the site of the incisive (2) reflection of the flap should adequately expose
foramen. The pulps of the anterior teeth test vital the operative field; and (3) flap design should
(whereas a periapical cyst tests nonvital). This is permit atraumatic closure of the wound.
the most common type of maxillary developmental 10. D. Studies have shown that 50% of the roots of maxil-
cyst. They often remain limited in size and are lary lateral teeth were distally dilacerated. Over-
asymptomatic; they may become infected and sight of the distal direction of root dilaceration
show a tendency to grow extensively. of upper lateral incisors can be a contributing
5. E. A patients immune response to a periradicular factor in the failure of endodontic treatment of
infection varies according to the individual. The these teeth.
size and volume of the pulp, the number and 11. B. EDTA is the chelating solution customarily used in
quality of the nerves, and the pulpal vascularity endodontic treatment. Chelators remove inorganic
and cellularity all are unique to the individual components, leaving the organic tissue elements
patient. The different virulence of organisms intact.
causing the infection may cause differences in pain 12. D. Periodontal disease can have an effect on the
experienced and differences in the amount of pulp through dentinal tubules, lateral canals, or
orthoclastic activity. Sheer numbers of organisms both. Primary periodontal lesions with second-
can influence their virulence. ary endodontic involvement differ from primary
6. B. Any notion of moral decision making assumes that endodontic lesions with secondary periodontic
rational agents are involved in making informed involvement in their temporal sequence. Primary
and voluntary decisions. In health care decisions, periodontal problems have a history of extensive
respect for the autonomy of the patient would, in periodontal disease.
common parlance, mean that the patient has the 13. D. The buccal object rule (Clarks rule or SLOB rule
capacity to act intentionally, with understanding, [Same Lingual, Opposite Buccal]) is used to iden-
and without controlling influences that would mit- tify the buccal or lingual location of objects in
igate against a free and voluntary act. It implies relation to a reference object. If the image of the
429
430 Answer Key Sample Examination
object moves mesially when the x-ray tube is splinting period is completed, follow-up is as with
moved mesially, the object is located on the lingual. all dental traumatic injuries, at 3, 6, and 12 months
If the image of the object moves distally when the and yearly thereafter.
x-ray tube moves mesially, the object is located on 19. B. Radiographic examination for root fractures is
the buccal (facial). extremely important. Because a root fracture is
14. D. Ledges can sometimes be bypassed; the canal typically oblique (facial to palatal), one periapical
coronal to the ledge must be sufficiently straight- radiograph may easily miss its presence. It is
ened to allow a file to operate effectively. This imperative to take at least three angled radiographs
straightening may be achieved by anticurvature (45, 90, and 110 degrees) so that in at least one
filing (file away from the curve). The dentist pre- angulation the radiographic beam passes directly
curves the file severely at the tip and uses it to through the fracture line and makes it visible on
probe gently past the ledge. Otherwise, the dentist the radiograph.
cleans to the ledge and fills; the patient is warned 20. D. For decades, controversy has surrounded the valid-
of the poorer prognosis. ity of thermal and electrical tests on traumatized
15. D. Factors affecting the long-term prognosis of teeth teeth. Only generalized impressions may be gained
after perforation repair include the location of from these tests after a traumatic injury. They
the defect in relation to the crestal bone, the length are sensitivity tests for nerve function and do
of the root trunk, the accessibility for repair, not indicate the presence or absence of blood cir-
the size of the defect, the presence or absence of a culation within the pulp. It is assumed that after
periodontal communication to the defect, the traumatic injury, the conduction capability of the
time lapse between perforation and repair, the nerve endings or sensory receptors is sufficiently
sealing ability of the restorative material, and tech- deranged to inhibit the nerve impulse from an
nical skill. Early recognition and repair improve electrical or thermal stimulus; this makes the trau-
the prognosis. Smaller perforations (<1mm) matized tooth vulnerable to false-negative readings
cause less destruction. Subcrestal lesions, espe- from these tests. Teeth that give a positive response
cially lesions closer to the apex, have a better at the initial examination cannot be assumed to be
prognosis. healthy or that they will continue to give a positive
16. B. If an instrument is broken at the filling stage, it is response over time. Teeth that yield a negative
not necessary to remove or bypass the instrument response or no response cannot be assumed to
because the canal has already been cleaned and have necrotic pulps because they may give a posi-
shaped. Prognosis depends largely on the extent of tive response at later follow-up visits. It may take 9
undbrided material remaining within the canal. months for normal blood flow to return to the
The dentist should attempt to obturate as much of coronal pulp of a traumatized, fully formed tooth.
the canal as possible. As circulation is restored, responsiveness to pulp
17. D. Teeth that have been endodontically treated have tests returns.
lost much of their coronal dentin in the access 21. A. The K-file and K-reamer are the oldest instruments
formation, regardless of the caries state before end- for cutting and machining dentin. They are made
odontic treatment. This loss of dentin compro- from a steel wire that is ground to a tapered square
mises the internal architecture of the tooth. Less or triangular cross section and then twisted to
internal tooth structure, combined with the absorp- create either a file or a reamer. A file has more flutes
tion of external forces (usually occlusal) may per unit length than a reamer. The K-Flex file is a
exceed the strength of dentin and result in fracture. modification of the shape of the K-file, with a non-
Endodontic treatment and loss of pulp vitality are cutting tip design.
no longer thought to desiccate the tooth to the 22. B. The indications for a direct pulp cap for a tooth
point of increasing risk of fracture. are (1) asymptomatic tooth, (2) with little or no
18. C. When a root fractures horizontally, the coronal hemorrhaging, (3) small (<1mm), and (4) well-
segment is displaced to a varying degree, but gen- isolated traumatic pulp exposure. A direct pulp cap
erally the apical segment is not displaced. Because acts to stimulate the formation of a reparative
the apical pulpal circulation is not disrupted, pulp dentin bridge over the exposure site and to preserve
necrosis in the apical segment is extremely rare. the underlying pulpal tissue. It is especially suc-
Pulp necrosis in the coronal segment results cessful in immature teeth. Failure of direct pulp
because of its displacement; this occurs in only capping is indicated by (1) symptoms of pulpitis at
about 25% of cases. Because 75% do not lose vital- any time and (2) lack of vital pulp response after
ity, emergency treatment involves repositioning several weeks. Failures result in pulpal necrosis
the segments in as close proximity as possible (continual pulpal insult), calcification of the pulp,
and splinting the teeth for 2 to 4 weeks. After the or (rarely) internal resorption. Direct pulp capping
Answer Key Sample Examination 431
is primarily used on permanent teeth. It is not used cells adjacent to granulation tissue, and necrotic
often in primary teeth because of the alkaline pH pulp coronal to resorptive defect. Only prompt
of calcium hydroxide. It can cause either mild or endodontic therapy can stop the process and
(often) severe pulp irritation. With severe irrita- prevent further tooth destruction.
tion, the risk of internal resorption is increased. 31. C. The best treatment of symptomatic irreversible pul-
With primary teeth, severe resorption is more pitis with a corresponding bony lesion is removal
common; in permanent teeth, formation of repara- of the source of infection via pulpectomy.
tive dentin occurs more often. 32. B. The current recommendation for patients with a
23. E. If an immature tooth is nonvital, the diseased tissue recent MI is to postpone dental or surgical treat-
must be removed via pulpectomy. Apexification is ment for at least 6 months. Risk for a second MI in
the treatment of choice. patients with recent MI if given a general anes-
24. A. Internal bleaching alone causes 3.9% of external thetic is as follows: 0 to 3 months after MI, 31%
cervical root resorption (also referred to as periph- risk of reinfarction; 3 to 6 months after MI, 15%
eral inflammatory root resorption). A barrier (base risk of reinfarction; more than 6 months after MI,
material) of approximately 4mm between the root 5% risk of reinfarction.* defer elective care for at
filling material and the internal bleaching material least 6 months after MI.
should be present to prevent this resorption. 33. D. Incision and drainage techniques work best for
25. B. Sodium perborate is more easily controlled and fluctuant abscesses, so as to release purulent
safer than concentrated hydrogen peroxide solu- exudate. Local anesthesia should be obtained first.
tions and should be the material of choice for inter- An incision should be placed at the most depen-
nal bleaching. dent part of the swelling. The incision should be
26. C. In newly erupted teeth, the apical root end has not wide enough to facilitate drainage and allow blunt
fully formed, allowing for greater blood supply to dissection. After irrigation, a drain may be placed
the tooth. Subsequent pulpal regeneration leads to to maintain patency of the wound.
greater long-term success. 34. C. Many studies have shown definitively the predomi-
27. C. The physical and chemical properties of zinc oxide nant role of gram-negative obligate anaerobic bac-
eugenol are beneficial in preventing pulpal injury teria in endodontic periapical infections. Earlier
and in reducing postoperative tooth sensitivity. studies generally implicated facultative organisms,
Zinc oxide eugenol provides a good biologic but improved culturing techniques established the
seal; also, its antimicrobial properties enable it predominance of obligate anaerobes.
to suppress bacterial growth, reducing formation 35. C. Danger zone refers to the distal area in the mesial
of toxic metabolites that might result in pulpal root in mandibular molars. Usually a straight layer
inflammation. of dentin, it becomes a preferable site for strip per-
28. C. When endodontic treatment is done properly, foration during instrumentation. Safety zone is
healing of the periapical lesion usually occurs with described as the mesial area of the root, with a
osseous regeneration, which is characterized by thicker layer of dentin, slightly touched by the
gradual reduction and resolution of the radiolu- endodontic instruments.
cency on follow-up radiographs. The rate of bone 36. D. In an intrusive dental injury, the patient may com-
formation is slow, and complete resolution may plain of pain. The patients tooth is misaligned, or
take longer than the standard 6-month follow-up, there is no sense of tooth mobility. This type of
especially with elderly patients. As long as the displacement has the worst prognosis. For intruded
radiolucency appears to be resolving as opposed to primary teeth, teeth should be allowed to reerupt
enlarging, an extended reevaluation is in order. before possible repositioning. For intruded adult
29. B. Pulpotomy is normally not recommended in per- teeth, treatment is allow reeruption and then
manent teeth unless root development is incom- stabilize.
plete. If incomplete, calcium hydroxide pulpotomy 37. A. Internal resorption begins on the internal dentin
is recommended. This procedure is performed in surface and spreads laterally. It may or may not
permanent teeth with immature root development reach the external tooth structure. The process is
and with healthy pulp tissue. The success is indi- often asymptomatic and becomes identifiable only
cated when the root apex, if not completely formed, after it has progressed enough to be detectable
completes its full development. This procedure is radiographically. The etiology is unknown. Trauma
done only on teeth free of symptoms. is often, but not always, implicated. Resorption
30. B. Internal resorption is most commonly identified that occurs in inflamed pulps is characterized his-
during routine radiographic examination. Histo- tologically by dentinoclasts, which are specialized,
logically, it appears with chronic pulpitis, including multinucleated giant cells similar to osteoclasts.
chronic inflammatory cells, multinucleated giant Treatment is prompt endodontic therapy. However,
once external perforation has caused a periodontal 9. A. The first number is the width of the blade or primary
defect, the tooth is often lost. cutting edge in tenths of a millimeter (0.1mm).
38. A. Internal bleaching alone causes 3.9% of external The second number of a 4-number code indicates
cervical root resorption (also referred to as periph- the primary cutting edge angle, measured from a
eral inflammatory root resorption). The presence of line parallel to the long axis of the instrument
a barrier (base material) between the root filling handle in clockwise centigrades. The angle is
material and the internal bleaching material should expressed as a percent of 360 degrees. The instru-
be approximately 4mm to prevent this resorption. ment is positioned so that this number always
39. E. Emergency treatment of localized swelling associ- exceeds 50. If the edge is locally perpendicular to
ated with an endodontic infection is to achieve the blade, this number is normally omitted, result-
drainage either through the root canal or by inci- ing in a 3-number code. The third number (second
sion and drainage and to remove the source number of a 3-number code) indicates the blade
of infection. Administration of antibiotics should length in millimeters. The fourth number (third
be considered with the concomitant presentation number of a 3-number code) indicates the blade
of fever and malaise and for diffuse swelling angle, relative to the long axis of the handle in
(cellulitis). clockwise centigrade.
40. A. The manufacturing process of a K-type instrument 10. D. A tooth preparation for a mandibular molar should
(K-file or K-reamer) is grinding a stainless steel have a narrow isthmus, should be initiated in the
wire to a tapered square or triangular cross section. most carious (or distal) pit, and should establish
the initial pulpal floor depth of 1.5 to 2mm.
However, it should be oriented parallel to the long
Operative Dentistry axis of the crown, which tilts to the lingual. If pre-
pared in the long axis of the tooth, there is greater
1. D. Altering the organism, its nutrients, and its envi- potential of weakening the lingual cusps.
ronment enhances prevention and treatment 11. C. Retention locks, when needed in class II amalgam
objectives. preparations, should be placed entirely in dentin,
2. B. A restored tooth indicates potential past carious not undermining the adjacent enamel. They are
activity but not current activity. Plaque presence placed 0.2mm internal to the DEJ, are deeper gin-
does not indicate caries presence. Sealants are used givally (0.4mm) than occlusally (i.e., they fade out
for preventive purposes, not caries treatment. as they extend occlusally), and translate parallel
3. C. When an alteration (a break in continuity) occurs to the DEJ. If the axial wall is deeper than normal,
to the tooth surface from a carious attack, restora- the retention lock is not placed at the axiofacial or
tion is usually necessary. When a lesion is evident axiolingual line angles, but rather is positioned
in the dentin with an x-ray, the lesion usually needs 0.2mm internal to the DEJ. If placed at the deeper
a restoration. location, it may result in pulp exposure, depending
4. D. When doing an indirect pulp cap, some caries may on the location of the axial wall depth.
be left, a liner (probably calcium hydroxide) is 12. C. The guide for axial wall depth for a typical class II
usually placed over the excavated area, and the area preparation that has a gingival margin occlusal to
may be assessed 6 to 8 weeks later. Regardless, the the CEJ is 0.2 to 0.5mm internal to the dentinoe-
prognosis for indirect pulp caps is better than the namel junctionthe greater depth is necessary
prognosis for direct pulp caps. when placing retention locks. However, when there
5. D. Smooth surface caries occurs on any of the axial is no enamel proximally, the axial wall needs to be
(facial, lingual, mesial, distal) tooth surfaces but deep enough internally to provide for adequate
not the occlusal surface. strength of the amalgam material as well as to have
6. C. A finishing bur is designed to provide a smoother room to place retention locks if needed. This depth
surface and has more blades than a cutting bur. The is approximately 0.75mm.
increased number of blades results in a smoother 13. D. Because of the typical shape of a carious lesion
cut surface. in the cervical area, the resulting restoration is
7. E. The advantages and benefits of rubber dam usage kidney-shaped or crescent-shaped, and the exten-
are reflected in all of the items listed. The rubber sions are to the line angles, resulting in the mesial
dam isolation increases access and visibility. and distal walls diverging externally. The convexity
8. C. When the rubber dam edge around the tooth is of the tooth in the gingival one third results in the
turned gingivally (inverted), it significantly reduces occlusal and gingival walls diverging externally.
the leakage of moisture occlusally, sealing around There are several retention groove designs that
the tooth better and resulting in a better isolated are appropriate, including four corner coves,
operating area. occlusal and gingival line angle grooves, and
circumferential grooves. However, as with any res- 19. D. A skirt is a minicrown preparation around a line
toration, if there is only a small amount of tooth angle. It should be prepared by a diamond instru-
structure (<1mm) between the new and existing ment in the long axis of the tooth crown, extended
restoration, it is best to join the two restorations to the gingival one third, and result in an appropri-
together and prevent the possibility of fracture of ate amount of tooth removal. It is placed to increase
the small amount of remaining tooth structure. both retention form (having opposing skirt verti-
14. B. When needed for large restorations, retention form cal walls retentive with each other) and resistance
usually consists of a gingival groove and incisal form (enveloping the line angles similar to a barrel
cove prepared with a small round bur (No. 1 4). The hoop around a barrel). It extends the outline form
placement of the groove or cove is dependent on and so may be least appropriate for highly esthetic
the dentinoenamel junction (DEJ), placing the areas in the mouth.
retention 0.2mm internal to the DEJ entirely in 20. C. The primary causes of postoperative sensitivity for
dentin. It is not placed at the axiogingival or axio- amalgam restorations are voids (especially at the
incisal line angles if those line angles are deeper margins), poor condensation (that may result in
than ideal; otherwise, the retention form may be void), or inadequate dentinal sealing. Extension
too deep or cause a pulpal exposure. onto the root surface does not result in increased
15. B. Typically, the class I composite preparation has sensitivity.
occlusally converging walls that provide primary 21. C. Tensile and compressive strengths may have rele-
retention form. The actual bonding also provides vance for composite materials but not for dentin
retention form. However, an occlusal bevel is not bonding systems. The success of bonding depends
indicated on class I preparations, and retention on the various dentin structural factors, tooth
grooves are not used. factors, polymerization shrinkage, C-factor con-
16. C. A successful amalgam restoration requires 90- siderations, and technique sensitivity.
degree amalgam margins. Amalgam margins less 22. B. Amalgam carving should result in coincidence
than 90 degrees result in increased potential for with the cavosurface margin and should not result
fracture of the amalgam. Greater than 90-degree in deep occlusal anatomy because such form may
amalgam margins are good for the amalgam, but create acute amalgam angles that are subject to
the corresponding enamel margin is less than 90 fracture. Depending on the condensation rate of
degrees and potentially undermined and prone to the amalgam used, waiting a couple of minutes
fracture. Because the amalgam is not bonded to the before initiating carving may allow the amalgam
tooth, it must be retained in the tooth with under- to harden enough so that the carving is easier
cuts, in either the primary or the secondary prepa- and overcarving is minimized. When carving the
ration. An amalgam restoration needs a minimum occlusal cavosurface margin, the discoid carver
1-mm thickness in nonstress areas and 1.5- to should rest on the adjacent unprepared enamel,
2-mm thickness in areas that may be under load. which serves as a guide for proper removal of
The preparation must provide this dimension. amalgam back to the margin.
Except for class V amalgams, the prepared walls 23. A. Generally, composite can be properly polymerized
generally converge to the exterior. The prepared in 1- to 2-mm increments.
walls may diverge or converge externally. 24. D. The trituration process mixes the amalgam compo-
17. B. A tooth preparation is dictated by the extent of the nents, and the reaction results in the alloy particle
carious lesion or old restorative material, the cre- being coated by mercury and a product being
ation of appropriate convenience form for access formed.
and vision, and the anticipated extensions neces- 25. C. The half-life of mercury in the body is 55 days.
sary to provide an appropriate proximal contact 26. C. Proper proximal contacts reduce the potential
relationship. Fracture lines present should nor- for food impaction, preserving the health of the
mally be included the restoration. However, it is underlying soft tissue. A missing proximal contact
rare that the size of the tooth affects the design of may result in tooth movement, which would have
the tooth preparation. an adverse effect on the occlusal relationship of
18. B. Although the amalgam margin must be 90 degrees, the tooth. Having a correct contact does not
the enamel margin might not be 90 degrees, espe- enhance the retentive properties of the restorative
cially on the occlusal surface. Most walls converge material.
occlusally, but many class V amalgam preparations 27. B. Using the adjacent unprepared enamel at the cavo-
have walls that diverge externally. No retention surface margin to guide the discoid carving instru-
form should be placed at the DEJ because the adja- ment when carving away excess amalgam at the
cent enamel is undermined and becomes subject to occlusal margin is the best way to develop the junc-
fracture. tion correctly.
28. A. Self-etch dentin bonding systems differ from total- 36. C. Although some self-etch bonding systems use
etch dentin bonding systems by removing less of milder acid, the primary acid system used for
the smear layer (they use a less potent acid); creat- etching tooth structure is phosphoric acid.
ing a weaker bond to enamel, especially nonpre- 37. D. Bonding is primarily for sealing the dentin and
pared enamel; and not requiring wet bonding, enhancing the retention of the restorative material
which may be necessary for some total-etch in the preparation. Esthetic benefits are a welcome
systems. Although fewer actual materials may be side benefit when using a composite restoration.
needed with some self-etch systems, they need to Thermal insulation is provided by the use of com-
be applied in multiple coats, and the time neces- posite compared with amalgam but is not a benefit
sary to apply the materials is similar for both of the bonding. Bonding does not alter tooth
systems. flexure under normal load but may help bond the
29. A. Dentin bonding in laboratory studies may create unprepared tooth structure together better.
bond strengths similar to or greater than bond 38. B. Triturating (mixing) the amalgam particle with
strengths to enamel. However, clinical studies mercury is intended to result in coating the parti-
cannot corroborate that the dentin bond is stron- cles with a surface of mercury and creating the
ger, and the bond may deteriorate over time. Avail- desirable phases in the set amalgam. All of the alloy
able information is insufficient to predict accurately particle is not dissolved in the mercury, and the
the bond potential to dentin in every application. size is not significantly reduced.
However, bonding to enamel is predictable and 39. B. The only constant contraindication for the use of
good. The attempt to simplify the bonding mecha- composite is when the operating area cannot be
nism has resulted in fewer materials being involved properly isolated, decreasing the potential success
and less decision making on the part of the opera- of the bond.
torboth in an effort to get more predictable 40. D. Direct gold and tooth structure have similar linear
results. However, the newer bonding systems have coefficients of expansion. Amalgam exhibits twice
not yet been proven to be better. that expansion, whereas composite expansion
30. D. Occlusal reduction would not affect the ability to would be even greater (2.5 times greater than tooth
seat a casting. However, temporary cement, heavy structure).
proximal contacts, or tooth undercuts could keep 41. D. Self-threaded pins are used by most operators,
the casting from seating completely. when pin use is indicated.
31. D. Zinc is added to act as a scavenger for oxygen 42. D. All of these factors indicate a cervical lesion should
during the casting process. Copper and palladium be restored. In addition, if the lesion is large and
increase the hardness and affect the color. Silver the pulpal or gingival tissues are in jeopardy, res-
has an effect on the color as well. toration should be considered.
32. A. If a patient has a notched cervical area that is very 43. B. No known alternative low-mercury or no-mercury
sensitive or esthetically objectionable, restoration systems have been developed that provide the same
is usually indicated. If the notched area is very properties or clinical performance as amalgam.
deep, adverse pulpal or gingival responses may The other statements are true.
occur. Although more notched areas are encoun- 44. B. Composite restorations are more technique-
tered in older patients, a patients age is not a factor sensitive than amalgam restorations because the
in the need for restoration. bonding process is very specific (requiring exact,
33. B. Slots and pins may be used interchangeably. They correct usage of the various materials and an iso-
both provide good secondary retention form. Slots lated, noncontaminated field), and the insertion
are usually better when box forms or vertical walls and contouring of composites are more demanding
exist in the preparation, and pins are usually better and time-consuming. Composites are not stronger
when there are few or no vertical walls. The reten- than amalgams and have similar wear resistance
tion is similar for both. compared with amalgams. Composites are indi-
34. A. The longer a slot, the better. They should be inside cated for class II restorations.
the DEJ and prepared with an inverted cone bur to 45. C. The restoration of a proximal contact is easier with
a depth of 1mm. amalgam than with composite. Amalgam is easier
35. A. The bond of adhesives to dentin (and enamel) is to use and is less technique-sensitive. Either mate-
primarily a mechanical interlocking of the material rial can be used for class II restorations. Because
within the dentin (or enamel). The etching causes amalgam restorations require a tooth preparation
some removal of the surface, creating irregularities that has (1) a specified depth (for strength of the
or spaced collagen fibrils into which the adhesive amalgam), (2) cavosurface marginal configurations
enters. When polymerized, the adhesive is mechan- that result in 90-degree amalgam margins, and
ically locked into the surface. (3) an undercut form to its walls or secondary
retention form features, they require more tooth This procedure may yield material for biopsy and
structure removal than composite tooth pre would rule out a vascular lesion (e.g., arteriove-
parations. Composite tooth preparations require nous malformation), which could be dangerous to
(1) removal of the fault, defect, or old material; enter without prior diagnosis.
(2) removal of friable tooth structure; and (3) no 6. D. Criteria for implant success include mean vertical
specific depthsthey are more conservative. bone loss of less than 0.02mm annually after the
46. A, D, E. Eburnated dentin is also known as sclerotic first year of service. In this question, no further
dentin and has darkened from extrinsic staining. It treatment is necessary at this time.
is firm to the touch of an explorer and may be 7. B. The major causes for loss of osseointegrated im-
rough but is cleanable. It is seen in patients (usually plants are similar to the causes for loss of natural
older) whose oral hygiene and diet in recent years teeth: poor hygiene, occlusal load, and the resultant
are good. inflammatory processes that occur.
47. A. Resistance form preparation features help the res- 8. D. Traditionally, 6 months has been the recommended
toration and tooth resist fracturing as a result of period for integration and subsequent loading
occlusal forces. Resistance features that assist in of posterior maxillary implants. Today, because
preventing the tooth from fracturing include of technologic advancements in specified cases,
rounded internal preparation angles. earlier loading may be possible.
48. A. Abfraction is tooth loss in the cervical area caused 9. C. Imaging tools used in the evaluation of TMJ
by biomechanical loading. Abrasion is mechanical pathology include panoramic radiographs, tradi-
wear resulting from abnormal forces (e.g., tooth- tional and computer-generated tomograms, mag-
brushing). Attrition is normal tooth wear. Erosion netic resonance imaging, nuclear imaging, and
is wear secondary to chemical presence. arthrography.
49. B. A direct pulp cap is recommended for a mechanical 10. A. Distraction osteogenesis is preferred over tradi-
pulp exposure that is noncarious (<1.0mm). No tional osteotomies when large skeletal movements
pulp therapy is required when the remaining are required and the associated soft tissue cannot
dentin thickness is greater than 2.0mm over vital adapt to the acute changes and stretching that
pulp. Endodontic therapy is recommended for a results. Larger movements may be at increased risk
carious pulp exposure (>1.0mm) with purulent of some relapse; this is particularly true in a patient
exudate. An indirect pulp cap is recommended with a cleft palate, where there is significant soft
when there is residual questionable dentin near tissue scarring from previous surgeries.
pulp in an asymptomatic tooth. 11. C. Bilateral sagittal split osteotomy is the most
50. E. Collars provide bracing. commonly used osteotomy for mandibular
51. D. The correct order is D, B, C, A, E. advancement.
12. B. OSAS may result in mood disorders, daytime
fatigue, and personality changes. Aggressive behav-
Oral and Maxillofacial Surgery ior is not considered a sequela of OSAS.
and Pain Control 13. C. Although less invasive, arthrocentesis and splint
therapy are not considered surgical interventions.
1. A. The surgical guide template is a critical factor for 14. C. The mandibular condyle is the most common loca-
the placement of implant in the esthetic area. tion of mandibular fractures. The alveolus, ramus,
2. C. The most difficult impaction to remove is the dis- and coronoid are the least common sites.
toangular tooth because the withdrawal pathway 15. D. Le Fort level fractures are associated with maxillary
runs into the ramus of the mandible and requires injuries. Mandibular fractures are classified accord-
greater surgical intervention. ing to anatomic location, condition of the bone and
3. B. An impacted tooth is one that fails to erupt into the soft tissue, and muscle pull on the segments.
dental arch within the expected time. Conse- 16. A. A proper occlusal relationship is a prerequisite for
quently, the third molar in a 13-year-old patient satisfactory bony reduction. This is most com-
would be classified as unerupted or in the process monly accomplished by the use of intermaxillary
of erupting. fixation, or wiring the jaws closed, during surgery.
4. A. The primary principle of management of odonto- 17. A. Most nerve injuries are transient; however, in an
genic infections is to perform surgical drainage injury that lasts greater than 4 weeks, a surgical
and removal of the cause. Abscesses do not resolve evaluation is indicated.
on antibiotics alone and may progress even if the 18. C. Sites commonly used for reconstruction of the
patient is on antibiotics. atrophic mandibular ridge are dictated by the defi-
5. D. Any radiolucent lesion that requires biopsy should ciency and include chin, hip, ribs, prosthetic mate-
undergo aspiration before surgical exploration. rials, and donor bone (human and bovine). Dental
implants are commonly used, not just as a last palate and from the gingival margin to the midline
resort. The use of distraction of ridge augmenta- of the palate.
tion has been reported and is useful in certain 31. A. Jastak and Yagiela published data demonstrating
applications. The mandibular alveolar ridge is that patients with cardiovascular compromise who
more problematic in terms of resorption and are well monitored begin to show elevation of vital
denture retention, which more commonly neces- signs when more than about 40g (0.04mg) of
sitates reconstructive measures. epinephrine is administered in a local anesthetic
19. A. A dry socket (alveolar osteitis) occurs on day 3 to solution.
4 after extraction and, except for pain, does not 32. C. Malamed recommended that a maximum of
have the classic signs of infection. 4.4mg/kg (2.0mg/lb) of lidocaine be administered
20. B. Older age, diabetes, and smoking are risk factors regardless of whether vasoconstrictor is in the for-
for delayed healing. mulation. The package insert for lidocaine allows
21. A. Ideally, a local anesthetic should be relatively free up to 7mg/kg when lidocaine is packaged with
from producing allergic reactions, and it should be vasoconstrictor.
stable in solution and readily undergo biotransfor- 33. B. Inferior alveolar, posterior superior alveolar, and
mation in the body. It is an absolute requirement infraorbital injections all lead to pulpal anesthesia
that it should be either sterile or capable of being when performed properly. The lingual injection
sterilized by heat without deterioration. If proper leads to soft tissue anesthesia only.
doses are used and are properly injected, there is a 34. B. A true anterior superior alveolar nerve block, also
high success rate of obtaining anesthesia, while called infraorbital nerve block, requires a volume
being able to minimize adverse effects. of one half cartridge of local anesthetic solution, or
22. B. All local anesthetics are vasodilators to some about 1.0mL.
degree. 35. C. The local anesthetic drug of choice for administra-
23. C. The pKa of lidocaine is 7.9. It is packaged as a 2% tion in children is 2% lidocaine with 1:100,000
solution both with and without epinephrine and epinephrine because it allows the greatest volume
has a rapid onset of action. to be administered safely. Mepivacaine in either 2%
24. B. Of needles commonly used in dentistry, 25-gauge or 3% allows less volume to be safely administered,
needles have a much lower incidence of breakage and bupivacaine is not approved by the U.S. Food
versus any other needle size, whereas 30-gauge and Drug Administration for use in children.
needles have the highest incidence of breakage. 36. B. All local anesthetics cause some amount of vasodi-
25. B. A 2% solution is 20mg/mL; 1.0mL of a 20mg/mL lation. Agents packaged as plain drugs (i.e., without
solution is 20mg. vasoconstrictor) cause less vasodilation than agents
26. B. The supine position is correct. This position pre- that must be packaged with vasoconstrictor to have
vents fainting during or immediately after the efficacy. Of the listed drugs, mepivacaine is the
injection of local anesthetic. Reclined or semisu- only one packaged in dental cartridges without
pine is not back far enough, and Trendelenburg is vasoconstrictor.
too far back. 37. D. The formulation 2% lidocaine contains 36mg of
27. B. Malamed recommended that one cartridge of local lidocaine per cartridge. Because 80mg is the
anesthetic be delivered over not less than 1 minute; amount of lidocaine that can safely be adminis-
1mL (one half cartridge) should be delivered over tered to this child, the number of cartridges that
not less than 1 2 minute (30 seconds). can be administered is 80mg divided by 36mg per
28. A. Posterior superior alveolar nerve block is the only cartridge, which is roughly two cartridges.
injection listed that leads to pulpal anesthesia in 38. C. By definition, a low pKa means a fast onset of
the maxilla. Nasopalatine nerve block is a maxil- action. Hydrophobicity and protein binding
lary injection that leads to soft tissue anesthesia of directly affect duration of action and potency.
the premaxilla only. Inferior alveolar and long 39. A. The (long) buccal injection anesthetizes the soft
buccal nerve blocks are mandibular injections. tissues and periosteum buccal to the mandibular
29. B. The proper depth of penetration for the posterior molar teeth.
superior alveolar nerve is half the length (16mm) 40. C. Lipid solubility (hydrophobicity) and protein
of a long needle or three fourths the length (15mm) binding are the most important factors in deter-
of a short dental needle. Penetration beyond mining duration of action of a local anesthetic.
16mm has a significantly higher incidence of posi- Bupivacaine has the longest duration of action of
tive aspiration and hematoma formation. the local anesthetics listed and has the highest
30. B. The greater palatine injection provides soft tissue hydrophobicity; it is bound 95% to protein. The
anesthesia of the hard palate from the junction of other agents have lower hydrophobic qualities and
the premaxilla to the junction of the hard and soft are bound 75% or less to protein.
41. B. With all intraoral injections of local anesthesia, the Oral Diagnosis
intent is to anesthetize a portion of cranial nerve
(CN) V. With an improperly placed needle in a 1. D. An acute exudate (pus) at the apex of a tooth
mandibular block, it is possible to anesthetize a follows the path of least resistance (e.g., into sur-
portion of CN VII inadvertently, and it is possible rounding bone, gingiva, or skin). If the offending
to anesthetize CN VI inadvertently with certain tooth is not treated and the abscess becomes
second-division nerve blocks. chronic, a periapical granuloma may result.
42. D. Articaine has an ester bond and an amide bond. 2. A. Reduced enamel epithelium that overlies the crown
Because esters are biotransformed much more of an unerupted tooth may give rise to a cyst
rapidly than amides, articaine has a much shorter occurring in the same positionby definition, a
half-life than the other local anesthetics. dentigerous cyst. The stimulus for cystic epithelial
43 D. Antibiotics used to treat odontogenic infections proliferation is unknown.
should be effective against streptococci and oral 3. A. The key to this question is the description of the
anaerobes, which are common pathogens in the cystic lining of thin, parakeratinized epithelium
oral cavity. S. aureus is commonly seen in the respi- with basal cell palisading, which is typical of odon-
ratory tract and on the skin, not on oral mucosa, togenic keratocyst. Tooth vitality, lack of symp-
so choices B and C are incorrect. Most oral infec- toms, and more than one lesion also support the
tions such as abscesses are not primarily due to diagnosis.
fungal or viral organisms. 4. C. Odontogenic keratocysts are notable because of
44. A, C, D. An asymptomatic full bony impaction in their recurrence rate, their aggressive clinical
someone older than 35 years of age is usually behavior, and their occasional multiplicity. When
not surgically removed, if no pathology exists. All multiple, they may be part of the nevoid basal cell
the other choices are reasons to remove the carcinoma syndrome.
impaction. 5. A. Ameloblastic fibro-odontoma is the only lesion
45. C. Aspiration biopsy or fine-needle biopsy on a soft listed that is lucent with opaque foci. The patients
tissue lesion deep to mucosa should be done first age is also characteristic for this lesion. Pagets
to confirm if the entity is truly cystic, vascular, or disease may show a mixed opaque and lucent
solid. However, an attempt to obtain a biopsy spec- pattern, but it occurs only in patients older than
imen of a soft tissue lesion that is vascular in origin 50 years.
(e.g., arteriovenous malformation) can result in 6. C. Herpetic whitlow is a term used for secondary
hemorrhagic complication. Hard tissue biopsies herpes simplex infections that occur around the
and full-thickness flaps apply to bone lesions. Inci- nail bed. The cause of aphthous ulcers is unknown.
sional and excisional biopsies are used for surface Herpangina is caused by coxsackievirus, and
soft tissue lesions. herpes zoster is caused by varicella-zoster virus.
46. E. The pKa determines the degree to which a drug is 7. E. Premature tooth loss is seen in several conditions,
charged. A low pKa for a local anesthetic favors especially malignancies and Langerhans cell dis-
more of the noncharged species of a drug; this ease because of cellular invasion of the periodontal
increases the ability of the drug to penetrate to ligament. Sharply marginated bone lesions are
the nerve and increases the rate of onset of characteristic of Langerhans cell disease (and
anesthesia. Pagets disease affecting elderly patients). The
47. A. The nasopalatine nerve block leads to anesthesia of eosinophils in a round cell infiltrate suggest
palatal soft tissue from canine to canine, bilaterally Langerhans cell disease (the round cells would be
(the premaxilla). The mental nerve block is in the Langerhans cells).
mandible. The greater palatine nerve block leads to 8. E. Numb lip is malignancy of the jaw until proved
anesthesia in the palate from the canine distally to otherwise. About half of patients with numb lip
the posterior aspect of the hard palate and from the have associated malignancies. The other 50% of
gingival margin to the midline. The anterior supe- patients have acute bone infections or neurologic
rior alveolar nerve block anesthetizes from the problems.
midline of the maxilla to the mesiobuccal aspect of 9. E. Sclerotic bone margins indicate a long-term, low-
the maxillary first molar but does not anesthetize grade process because it takes a considerable
palatal tissue. The posterior superior nerve block amount of time for bone to become radiodense.
anesthetizes from the maxillary third molar ante- The signs and symptoms listed in choices A through
riorly to the maxillary first molar with the possible D are associated with malignancies.
exception of the mesiobuccal aspect of the maxil- 10. A. Peripheral and central giant cell granulomas have
lary first molar. This injection does not anesthetize very different clinical presentations and behaviors
palatal tissue. but identical light microscopic features.
11. D. Acquired angioedema is a rapidly developing aller- 25. C. X-ray photons (Bremsstrahlung radiation) results
gic reaction that results in characteristic nonery- from the interaction of high-speed electrons with
thematous swelling of lips, face, and neck. tungsten nuclei in the target.
12. A. Regional odontodysplasia is often referred to as 26. C. X-rays are produced in most dental x-ray machines
ghost teeth because of the thin layers of dentin half the time (i.e., in bursts at the rate of 60 per
and enamel produced. One quadrant of teeth is second, each lasting 1120 second) owing to the alter-
affected, and the teeth are nonfunctional. nating current supplied to the tube.
13. B. Salivary gland tumors manifest as submucosal 27. A. Deterministic effects are effects with dose thresh-
masses. The combination of epithelial and connec- olds, requiring at least moderate levels of exposure,
tive tissue elements is indicative of pleomorphic where the severity of response is proportional
adenomas, also termed mixed tumors. Oral warts to dose.
and leukoplakias are surface or epithelial lesions. 28. E. Direct effect refers to production of free radicals
Peripheral giant cell granulomas are exclusively from the ionization of water (choice C). These free
gingival lesions, and granular cell tumors are com- radicals formed in the radiolysis of water are highly
posed exclusively of cells with grainy or granular reactive and may alter biologic molecules (choice
cytoplasm. D). The presence of oxygen increases the number
14. E. Oral cancers (squamous cell carcinomas) manifest of free radicals.
typically as indurated nonhealing ulcers. They can 29. D. The radiosensitivity of cells depends on mitotic
also manifest as white patches, red patches, or future, mitotic activity, and degree of
irregular masses. differentiation.
15. E. Dermoid cyst occurs in the midline floor of the 30. B. Using a rectangular collimator restricts the area of
mouth when above the mylohyoid and geniohyoid the patients face exposed to the size of the receptor,
muscles and in the neck when below the mylohy- reducing the patient exposure by more than half.
oid and geniohyoid muscles. 31. E. If someone must hold a film and the patient cannot,
16. C. Ectopic (normal tissue, abnormal site) lymphoid it should be a family member or friend of the
tissue is commonly seen in the floor of the mouth patient, not an x-ray operator in the dental office.
as well as in the posterior lateral tongue, soft palate, 32. A. The dispersion of visible light from the crystals in
and tonsillar pillar. It appears as one or more small, the phosphor layer of the intensifying screen
dome-shaped yellow nodules. reduces image resolution compared with direct-
17. C. Schwanns cell is of neural origin and gives rise to exposure film.
several neoplasms, including neurofibroma and 33. C. The base needs to be flexible to go through auto-
schwannoma. matic processors and be put into film mounts.
18. C. Nasopalatine duct cysts are anterior midmaxil- Usually, the base is not completely clear, and it is
lary lesions that occur in the nasopalatine canal. the emulsion that is sensitive to x-rays.
The associated lucency is often heart-shaped be- 34. B. The film should be parallel to the long axis of the
cause of the superimposition of the nasal spine tooth, and the central ray of the beam should be
over the lesion. These cysts do not devitalize perpendicular to both the film and the tooth.
teeth. Increasing the vertical angulation foreshortens the
19. B. Globulomaxillary lesion is a clinical term used to image of the tooth.
designate any lucency that occurs between the 35. B. The central ray should be perpendicular to the
maxillary lateral incisor and canine. object.
20. E. Peripheral giant cell granuloma is the exception. 36. C. The smaller the focal spot size, the greater the reso-
Although it is red, it occurs only in the gingiva. lution. Other factors remaining equal, density, con-
Choices A through D are differential diagnoses for trast, and magnification are unchanged.
red atrophic tongue. 37. A. Developer reduces silver bromide to solid silver
21. C. Multiple odontogenic keratocysts are part of nevoid grains.
basal cell carcinoma syndrome. 38. E. Exposure time should be reduced. Development
22. E. The mean age for ameloblastoma is 40 years. All parameters should not be changed if they are
other lesions listed occur in children and correct.
teenagers. 39. B. Silver halide in the emulsion of an exposed film is
23. A. Behets syndrome includes lesions in the mouth, converted into grains of metallic silver in the
eye, and genitals. The other diseases do not affect developer.
the genitalia. 40. D. The penny test is a test of darkroom safelighting.
24. B. Nicotine stomatitis appears as opacification of the A penny is placed on an exposed film (after remov-
palate, with red dots representing inflamed salivary ing the film from its cover) for 2 minutes, and the
ducts. film is processed. If the processed film shows a
lighter area on the film corresponding to the penny, 3. B. Although developmental indicators generally cor-
the safelighting is too bright and is fogging the film. relate well with each other, using dental age to
41. E. Film packets need not be sterilized because the predict timing of growth is the least reliable of the
goal is to prevent cross-contamination, not ensure methods offered.
that everything that goes into a patients mouth is 4. C. Fusion of the palate proceeds from anterior to pos-
sterile. terior, so any disturbance that occurs during that
42. A. The TMJ is much too far from the occlusal plane time stops fusion at that point, leading to an
(the location of occlusal film) to be imaged with opening posteriorly.
this technique. The other choices all are proper 5. B. Young children often present with minimal over-
indications for using occlusal film. bite or anterior edge-to-edge relationship. Habits
43. A, D, E. Celiac sprue, Behets disease, and Crohns such as thumb-sucking increase the likelihood that
disease all are examples of diseases in which less overbite will be present.
immune system dysfunction is an important factor 6. B. Small diastemas between the maxillary incisors of
in their pathogenesis. Aphthous or aphthouslike 2mm or less generally close on their own as more
ulcers may develop in patients with these diseases, permanent teeth, specifically the canines, erupt.
but there is no clear link to a dysfunction of the The presence of a midline diastema before canine
immune system for aphthous ulcers or for the eruption is referred to as the ugly duckling stage.
other disorders. Although oral manifestations may 7. D. If the mandibular molar buccal groove is mesial to
be variable, lesions in patients with sarcoidosis, the mesiobuccal cusp of the maxillary molar, the
amyloidosis, and neurofibromatosis typically man- relationship is described as Angle Class III.
ifest as submucosal nodules and masses. 8. A. The molars are class II, but the skeletal relationship
44. A, D, E. These three signs clearly point to primary described by the ANB (the anterior-posterior
Sjgrens syndrome. Hairy leukoplakia is associ- angular difference between the maxilla and man-
ated with Epstein-Barr virus. Aphthous ulcers may dible) measurement is normal, so the malocclusion
be associated with other disorders. is dental in origin.
45. B, C, D. Filtration increases the mean energy of the 9. B. All of the choices are possible solutions to correct
x-ray beam because it filters out the low-energy a deep overbite. Erupting posterior teeth would
radiation, leaving the higher energy radiation. increase the already excessively long lower face
The filtration reduces low-energy radiation to the height, whereas intrusion of maxillary incisors
patient. would improve the excessive maxillary incisor
46. D. This anatomic position is the usual extent of show at rest.
the maxillary sinus. The zygomatic process of the 10. B. Heavy forces cause compression of the periodontal
maxilla usually appears as a U-shaped radiopaque ligament with hyalinization.
line with the open end pointing upward. A dentig- 11. B. Root resorption is common during orthodontic
erous cyst is associated with a tooth such as an treatment, although lesions often repair on the
impacted third molar. An ameloblastoma usually root surface. Mobility of teeth is also common as
occurs in the molar ramus. Neither a dentigerous the periodontal ligament reorganizes and widens
cyst nor an ameloblastoma would be expected nor- during tooth movement. It is uncommon for teeth
mally to duplicate the typical location of the maxil- to become devitalized as a result of orthodontic
lary sinus. movement unless they have also been substantially
47. C. Discoid (chronic type) lupus erythematosus does compromised by injury or infection.
not involve systemic disorders and rarely pro- 12. A. Although controversial, it is believed that types of
gresses to the systemic form. Systemic lupus ery- tooth movements that concentrate force in small
thematosus often affects the kidney, heart, and areas of the PDL are more likely to result in root
joints as well as skin and the oral cavity. resorption during orthodontic treatment.
13. B. The center of resistance is defined as the point at
which force application causes pure translation of
Orthodontics and Pediatric Dentistry a tooth.
14. C. Because M = Fd, doubling the force would double
1. A. Class I is the most common malocclusion, affecting the moment, or tendency to rotate, tip, or torque.
about 50% of the U.S. population, compared with 15. D. This is the definition of a couple. A couple results
class II (15%) and class III (about 1%). in a rotational tendency or pure moment.
2. C. Reproductive tissues grow at the same time as the 16. C. The sum of the forces and moments on an
adolescent growth spurt, and the appearance of appliance must equal zero. If the incisors intrude,
secondary sexual characteristics can be used to the molars extrude. These two forces form a
help predict the timing of growth. couple with a moment in one direction. The molars
experience a couple in the opposite direction, understand that there are some risks of performing
which causes them to tip distally. orthodontic treatment.
17. D. Class II elastics work in the direction that would 25. D. Excessive crowding may influence the decision
be used to correct a class II malocclusion, to pull in favor of canine substitution. However, esthetic
the mandibular teeth forward and the maxillary concerns may deter a decision to substitute ca-
teeth distally. nines for lateral incisors. Patients with a class II
18. B. Nickel-titanium archwires can exist in more than interarch relationship requiring maxillary extrac-
one phase: austenitic and martensitic phases. tions anyway may be better served to substitute
Superelastic behavior of these wires is attributed to canines for laterals rather than extracting healthy
the reversible transformation between these two first premolars.
phases. 26. C. Excessive crowding may necessitate extractions.
19. B. A second-order bend is placed to provide angula- Also, extraction of maxillary premolars may be
tion of a tooth in the mesiodistal direction, also indicated to camouflage a class II molar relation-
called tip. A first-order bend is placed in an arch- ship. Anterior open bites may be improved by
wire to position a tooth in the labiolingual direc- uprighting anterior teeth to increase overbite. Flat
tion (in-out bend) or to rotate a tooth as seen in lips would not be improved by extraction of per-
the occlusal plane. A bend to provide angulation in manent teeth, but other considerations may neces-
the labiolingual direction is called a third-order sitate extraction even in those patients.
bend (torquing bend). 27. A. Fixed retention requires no patient cooperation to
20. B. Class III elastics are worn from the maxillary first achieve retention. However, fixed retainers are
molars to the mandibular canines. The force system more difficult to clean and cannot be modified to
created by class III elastics produces mesial move- move teeth or control overbite relapse.
ment and extrusion of the maxillary first molars. 28. D. Class II correction by surgery requires moving the
21. D. This patient, if still growing, may be treated with a mandible forward or the maxilla back. In a patient
growth modification approach using headgear with a deficient mandible, it is preferable to move
(either cervical or high-pull, not reverse-pull) to the mandible forward. Moving the maxilla back
correct the class II malocclusion. Because deep significantly is difficult or impossible.
overbite is present, a cervical headgear should be 29. D. Inferior movement of the maxilla, especially
used because this type of headgear extrudes the without bone grafting and rigid fixation, has been
molars, which aids in reducing overbite; however, shown to relapse over time because of vertical
this was not one of the choices. If the patient is occlusal forces generated by the masticatory
finished growing, the second approach to treat musculature.
class II malocclusion is class II camouflage, which 30. B. All anterior permanent teeth begin calcification
includes extraction of maxillary first premolars to during the first 6 months except for maxillary
correct the malocclusion. An intrusion arch along lateral incisors. The maxillary lateral incisor may
with full fixed appliances should be used to correct be used as a key to timing; if this tooth is affected,
the deep bite. the causative event is likely to have occurred at 1
22. B. The line of force generated by a cervical headgear year of age or older.
causes the maxillary first molar to move distally, 31. D. Localized infection, trauma, and excessive sys-
usually also tip distally, and to extrude. A high-pull temic fluoride ingestion may cause hypocal
headgear would cause the molar to move distally cification. Disturbances in apposition result in
and intrude. incomplete tissue formation. For example, an
23. B. Primary canines are extracted to encourage align- intrusive injury to a primary incisor may disrupt
ment of the crowded incisors. However, the inci- enamel apposition and result in an area of enamel
sors align and upright, borrowing space otherwise hypoplasia.
needed for eruption of the permanent canine. 32. D. Implants are osseointegrated and behave as anky-
Primary first molars are extracted to encourage losed teeth. As teeth erupt and alveolar bond for-
eruption of the first premolar so that it may be mation occurs, an osseointegrated implant appears
extracted to make room for the permanent canine to submerge.
to erupt. 33. B. Many mentally challenged individuals can be
24. B. There is a high likelihood that a small diastema of mainstreamed and treated as any other patient.
2mm or less will close on its own over time as the Because a moderately challenged 6-year-old may
permanent teeth erupt. However, if a child experi- function as a preschool child, the normal manage-
ences psychological trauma because of esthetic ment techniques are likely applicable. The correct
concerns, the diastema can be closed. Parents answer for such a question would include some
should be informed of the reason for treatment and kind of normalization response.
34. A. Studies show that there is a high correlation progression to a nonvital pulp. If furcation involve-
between maternal anxiety and a childs negative ment is present, a pulpectomy would be the treat-
behavior in the dental office. This effect is greatest ment of choice in the absence of external or internal
for children younger than 4 years old. root resorption.
35. D. Inferior alveolar, lingual, and buccal nerve blocks 42. A. Mineral trioxide aggregate pulpotomies are very
are required to anesthetize this area adequately promising and generally show higher success rates
when performing deep restorations, pulp ther- than formocresol pulpotomies. However, mineral
apy, and extractions. Some studies have shown trioxide aggregate is very expensive at the present
that local infiltration anesthesia for primary time and is not used as often as formocresol or
molars is effective, but this is primarily reserved ferric sulfate.
for restorative procedures because there is an in- 43. B. The pulp chambers of primary teeth are propor-
creased probability for anesthesia failure using tionately larger compared with the size of the
local infiltration for pulp therapy and extraction crown; this is significant because there is a higher
procedures. risk of accidental pulp exposures on primary teeth.
36. C. In patients with primary dentition, the mandibular In particular, the mesiobuccal pulp horn of the first
foramen is located lower than the plane of occlu- primary molar is close to the external surface of the
sion. Mandibular block injections for these patients tooth.
are lower than for adult patients. 44. C. Tooth I typically exfoliates before the eruption of
37. D. Minimum alveolar concentration is a measure of tooth #13. One of the abutments of the space
potency. It is the concentration required to produce maintainer would be lost and render the space
immobility in 50vol % of patients responding to maintainer ineffective. A palatal holding arch and
surgical incision. A minimum alveolar concentra- a Nance holding arch, although bilateral holding
tion of 105vol % indicates that nitrous oxide alone arches, would be good options. However, there
does not produce profound surgical anesthesia at a may be situations where tooth #13 would have an
normal atmospheric pressure. accelerated eruption because of bone loss in the
38. A. The total flow rate is 4 to 6L/min for most chil- area and where the band-loop space maintainer
dren. The practitioner can check the bag and make would be appropriate.
adjustments if necessary. The maintenance dose of 45. D. The only possibility among these choices is the
nitrous oxide during an operative procedure is distal shoe space maintainer. Some clinicians find
typically about 30%. In other words, a standard that a removable kiddie acrylic partial can also
maintenance dose would usually be 4L of oxygen be successful. These kiddie partials extend dis-
and 2L of nitrous oxide. After a lengthy adminis- tally to the point where the mesial of the first per-
tration, it is wise to reduce the concentration manent molar would be. Some clinicians advocate
because of tissue saturation and nausea. placing a 1-mm-deep labial-lingual groove in the
39. A. It is difficult to know which treatment is indicated cast on the alveolar ridge on the mesial of the first
without more information than is presented in the permanent molar. This groove results in extra
question. The tooth could be mobile because of acrylic at the tissue-acrylic interface that causes
furcation involvement, internal or external root pressure; this may aid in keeping the unerupted
resorption, exfoliation, or a combination of all of first permanent molar in position.
these. A radiograph needs to be taken to obtain 46. B. The systemic fluoride rule of 6s states the follow-
more clinical information before any further treating: (a) If fluoride level is greater than 0.6ppm,
ment is rendered. no supplemental systemic fluoride is indicated.
40. D. Because of the small size of primary molars and (b) If the patient is younger than 6 months old, no
small restorations, it is helpful to reduce stresses supplemental systemic fluoride is indicated. (c) If
within the restorative material. It has been demon- the patient is older than 16 years old, no supple-
strated that rounded internal line angles aid in mental systemic fluoride is indicated. The state-
reducing stress compared with sharp internal line ment, If the patient is less than 12 months old,
angles. Many of the burs recommended for use in no supplemental systemic fluoride is indicated is
primary molars have a rounded end to help achieve false.
softened internal line angles. 47. C. Anticipatory guidance is counseling patients and
41. A. The treatment decision in this case should be made parents regarding the childs home oral health
based on the presence or absence of furcation care that is age appropriate and is focused on pre-
involvement. Absence of furcation involvement vention. Subjects to discuss with parents include
generally indicates a vital pulp. It is necessary oral hygiene, oral development, fluoride, diet and
to have vital tissue to perform a pulpotomy. Pres- nutrition, oral habits, and trauma and injury
ence of furcation involvement generally indicates prevention.
48. B. Most natal and neonatal teeth are primary teeth orthodontically (2 to 3 weeks), (b) stabilization
(90%); very few are supernumerary teeth (10%). for 2 to 4 weeks, and (c) calcium hydroxide pulp-
Most are mandibular incisors (85%). Extraction of ectomy 2 weeks after injury.
primary teeth should be accomplished only if they 55. C. The other three conditions listed may occur as the
are extremely mobile and there is danger of aspira- result of trauma but do not cause loss of vitality.
tion. Most commonly, natal and neonatal teeth are Pulpal hyperemia causes increased intrapulpal
left in position. pressure and swelling, which may result in an
49. D. Munchausen syndrome by proxy is a condition in interruption of the pulps blood supply. Without an
which a person, usually a parent, presents facti- adequate blood supply, the pulp becomes necrotic.
tious symptoms and illnesses in a child, which may This process can take time, and symptoms (either
result in extensive testing and hospitalizations. radiographic or clinical) may not manifest for
Examples of emotional abuse include denial of weeks or months. Typically, follow-up examination
affection, isolation, extreme threats, and corrup- and radiographs are indicated at 1-, 2-, and
tion. A parent who knowingly and willingly does 6-month intervals following a traumatic incident.
not seek care for a child who has pain, infection, 56. B, A, C, D. In any comprehensive treatment plan, the
or inadequate function is guilty of neglect. most urgent consideration is control of disease
50. E. The location of lesions of primary herpetic gingi- processes. In this case, caries control is the most
vostomatitis is on mucous membrane, including urgent need. Orthodontic movement should be
tonsils, hard and soft palates, buccal mucosa, second because alignment of teeth changes bony
tongue, palate, and gingiva. Children with this contours and modifies the occlusion. Final bone
disease can become very sick and require close recontouring can be performed if orthodontic
supervision and support. They typically have a sig- treatment did not correct previous defects. Defini-
nificant fever and can become dehydrated, and the tive prosthetic treatment should be done last so
disease can last 2 weeks. Treatment may consist of that restorations can be fabricated to fit the final
(a) topical anesthetics such as 0.5% dyclonine occlusion.
hydrochloride and viscous lidocaine, (b) coating 57. C, E, F. Most bones of the craniofacial complex form
solutions such as diphenhydramine elixir and by intramembranous ossification. The bones of the
kaolin-pectin compound, (c) antivirals such as cranial base are endochondral bones separated by
acyclovir, and (d) analgesics such as acetamino- synchondroses during development. The three
phen and ibuprofen. bones of the cranial base are the occipital, sphe-
51. B. Localized aggressive periodontitis in the primary noid, and ethmoid bones.
dentition, previously known as localized prepuber- 58. C. The adolescent growth spurt occurs during puberty
tal periodontitis, is most common in the primary and is characterized by an increase in body height.
molar area and occurs most commonly in African- Also, because puberty is the process of sexual mat-
American children. Treatment includes dbride- uration, reproductive tissues increase in size during
ment and antibiotic therapy. adolescence. In contrast, neural development,
52. C. The appropriate splint for an avulsed tooth is a characterized primarily by growth of the brain,
nonrigid splint, which is left in place for about 7 to occurs rapidly in young children and is mostly
14 days. A 0.016 0.022 stainless steel orthodontic complete by age 7. Lymphoid tissue, important
wire, a 0.018 round stainless steel wire, and a for development of immunity, increases until
monofilament nylon (20- to 30-lb test) line are puberty, and then these tissues shrink in size until
considered nonrigid. Long-term rigid splinting of adulthood.
replanted teeth increases risk of replacement root 59. A, D. Although any of the features listed are possible,
resorption (ankylosis). Rigid splinting is indicated the most common presentation of the occlusion in
for root fractures and remains in place for 2 to 3 the primary dentition is spacing and decreased
months. A 0.032 to 0.036 stainless steel wire is overbite. Spacing is an important and desirable
considered a rigid splint. characteristic because the permanent incisors and
53. D. If a tooth is incompletely erupted or is being canines will be much larger than their deciduous
orthodontically treated, the tooth may be normal predecessors. Decreased overbite is common
even if there is little sensitivity to electrical pulp because of sucking habits.
tests. In the absence of other symptoms, treatment 60. A. Angles classification of malocclusion is based on
is contraindicated. the anterior-posterior position of the buccal groove
54. A. Rapid root resorption, pulp necrosis, and anky of the mandibular first molar relative to the mesio-
losis are common sequelae to intruded per buccal cusp of the maxillary first molar. If the man-
manent teeth with mature apices. Treatment dibular first molar is distal to this position, the
includes the following: (a) gradual repositioning Angle classification is class II. An ANB angle of 2
degrees is the average (or normal) adult skeletal 67. A. Intruding maxillary incisors directly reduce the
relationship, so the origin of the class II relation- amount of overbite, and this is the best answer.
ship must be dental and not skeletal. Uprighting incisors would result in an increase of
61. B. The other choices all are common or even expected overbite as the teeth become more vertically over-
during orthodontic treatment. Root resorption, to lapping. High-pull headgear would intrude maxil-
some degree, is likely to occur in most patients as lary molars and encourage rotation of the mandible
a result of orthodontic treatment but usually closed, increasing overbite. Using a lip bumper is
has no clinical significance. Mobility of teeth and a distractor choice that is unrelated to controlling
transient occlusal interferences are expected dur- overbite. However, it is possible that use of a lip
ing tooth movement. Devitalization of teeth as a bumper would encourage flaring of lower incisors
result of orthodontics rarely occurs unless the teeth that would indirectly cause a reduction of overbite
have been previously traumatized or otherwise eventually.
compromised. 68. A4, B3, C2, D1.
62. C. The rotational tendency or moment is equal to 69. B, D, E.
the magnitude of the force applied times the per- 70. 1D, 2E, 3B, 4A, 5C.
pendicular distance of the line of action of the force
away from the center of resistance of the tooth (M
= Fd). Doubling the force would double the tooths Patient Management
tendency to rotate.
63. A, D, F. The ugly duckling stage occurs during the 1. B. Of the options given, the best response would be to
process of eruption of the maxillary canines. As the interpret what the patient is trying to communicate
maxillary canines migrate mesially before they and reflect the communication back to her. This
erupt, their crowns put pressure on the roots of the approach gently encourages the patient to express
erupted permanent lateral incisors, causing the openly and discuss the concern with the clinician.
crowns to tip distally and spaces to appear between It also serves to establish an environment of open-
the incisor crowns. This is called the ugly duck- ness and acceptance.
ling stage, and although it does not occur in 2. C. Of the options given, it is best to acknowledge that
everyone, it is considered a normal stage of devel- the patient is trying to convey information that is
opment during the mixed dentition. As the canines important to him or her and establish that there
erupt, their crowns compress the crowns of the will be a time to talk about those issues, while
incisors together, and any spacing that was present gently redirecting him or her to the task at hand.
is expected to close without treatment. 3. A. When a number of alternatives are presented and
64. B. Class III elastics are used to correct a class III rela- the first on the list is more desirable, there is a
tionship and are stretched from the maxillary first tendency for individuals to select the first option
molar region to the mandibular canine region. The and view the successive options as less desirable.
maxillary first molar would be expected to move 4. B. Focusing on long-term goals is not only a poor
mesially and extrude. motivator, but also it is often a pitfall in the effort
65. A, C, D, B. Serial extraction is a process that is used to change behavior because patients are less moti-
only when the decision is made early in dental vated when goals seem too big, impossible, or far
development that there will be a future need to from their current circumstances.
extract permanent premolars to create space for 5. A. Although the behavioral contract is not a legal
tooth alignment owing to a severe arch length document, it can be a useful approach in solidify-
deficiency (severe crowding). When the decision ing behavioral strategies and goals.
is made to proceed, the primary canines are 6. B. Extinction is the process of identifying all positive
extracted to allow the permanent incisors, which reinforcements (in this case, the dentist ceasing
are usually crowded and rotated in these patients, work on the childs teeth) that maintain a behavior
to align on their own. The primary first molar is and ceasing or withholding these.
extracted to encourage early eruption of the per- 7. E. Both positive and negative events or situations are
manent first premolar so that it may be extracted experienced as stress.
atraumatically. 8. D. Systematic desensitization is the process of system-
66. B. A midline diastema greater than 2mm is uncom- atically pairing a relaxation response with a hierar-
mon during normal development, and it is unlikely chy of feared stimuli.
to close on its own. The possible presence of a 9. B. Muscle tension is associated with the experience of
supernumerary tooth (mesiodens) should be ruled anxiety. Heightened anxiety contributes to lower
out radiographically before any attempt to close the pain thresholds, or sensitivity to the perception of
space orthodontically is made. pain.
10. E. All of the strategies listed may be considered questions. This approach also serves to alleviate
appropriate cognitive interventions in pain anxiety, provide an opportunity to correct any
management. misperceptions regarding dentistry, and establish
11. D. Classical conditioning (also known as respondent or maintain trust and rapport further.
or Pavlovian conditioning) occurs when a neutral 22. A. Perceived stress and distress in ones life has
stimulus, one that is not associated with a par been demonstrated to be a significant predictor
ticular response, is paired with an unconditioned (positively correlated) with self-reported health
stimulus (US), a stimulus that naturally elicits a concerns.
particular response (UR). After numerous pair- 23. A. Patients who are experiencing stress and anxiety
ings, the neutral stimulus (CS) elicits a conditioned typically feel more comfortable in having greater
response (CR), which is essentially a weaker form interpersonal space than they normally would
of the UR without the presence of the US. when not experiencing stress and anxiety.
12. C. Providing the patient with information and control 24. E. The use of silence can be a useful technique to
over his or her environment is likely to contribute encourage patient comment following a statement
to increased trust over time. Avoiding the issue of or question posed to the patient.
trust or providing reassurance that the patient can 25. E. Individuals respond to stress physiologically, be-
trust you without evidence is likely to maintain haviorally, cognitively, and emotionally.
poor trust. 26. A. Periodontal disease, measured by the PI, and gin-
13. E. Contrary to their behavior in the waiting room, gival disease, measured by the GI, are reversible
anxious patients are typically more likely to sit very processes. The amount of the debris and calculus,
still, often holding onto the arms of the dental measured by the OHI-S, can decrease as well.
chair, and engage in minimal verbal communica- Caries is not a reversible process.
tion unless encouraged by the clinician. 27. E. The recommended level of fluoride for a commu-
14. E. Diaphragmatic breathing naturally activates the nity water supply in the United States ranges from
parasympathetic nervous system, producing a 0.7 to 1.2ppm of fluoride, depending on the mean
relaxation response. maximum daily air temperature over a 5-year
15. D. Systematic desensitization is the systematic process period. The fluoride level would be lower in a
of exposing the patient to a hierarchy of increas- warm climate and would be higher in a cold
ingly anxiety-provoking stimuli while the patient climate. In the United States, most communities
uses relaxation skills such as diaphragmatic breath- are fluoridated at approximately 1ppm, which is
ing exercises. equivalent to 1.0mg of fluoride per 1L of water.
16. B. Operant conditioning posits that behavior is largely 28. D. Physicians and dentists can help prevent fluorosis
influenced by the consequences associated with the by prescribing dietary fluoride supplements ac-
particular behavior. cording to the Supplemental Fluoride Dosage
17. D. Research suggests that the most integral compo- Schedule recommended by the American Dental
nent of the treatment of anxiety is exposure to the Association Council on Scientific Affairs.
feared stimulus. 29. D. Experimental epidemiology is used primarily in
18. B. Of the choices, distraction would most likely be the intervention studies. When an etiology for a par-
least effective approachthe attention of a very ticular disease has been determined, the research-
anxious individual cannot typically be easily di- ers try to establish the effectiveness of a particular
verted. In such cases, distraction can have detri- program of prevention or therapy. Descriptive epi-
mental effects, such as compromising rapport or demiology is used to quantify disease status in a
increasing anxiety by failing to provide a positive community. Analytical epidemiology, also called
coping experience. Providing education and cop- observational epidemiology, is used to determine
ing strategiesincreasing predictability, familiar- the etiology of a disease.
ity, and controllabilityare typically more effective 30. D. In this case, the investigator chooses or defines a
strategies in working with anxious patients. sample of subjects who do not yet have the outcome
19. C. Controllability, familiarity, predictability, and im- of interest (in this case, cancer). The investigator
minence are significant factors that influence the measures risk factors in each subject (e.g., habits
cognitive appraisal of stress. that may predict the subsequent outcome) and
20. B. Graded exposure is the systematic process of ex- follows these subjects with periodic surveys or
posing the patient to a hierarchy of increasingly examinations to detect the outcomes of interest.
anxiety-provoking stimuli. 31. C. In a retrospective cohort study, the investigator
21. A. Asking the child about his or her fears creates an chooses a sample of individuals who have the
environment in which the child is encouraged outcome of interest (in this case, squamous cell
to discuss any worries or concerns and to ask carcinoma) and looks into the past for possible
variables that may have caused the disease (e.g., pressure of steam. Moist heat destroys bacteria
chewing tobacco). denaturation of the high-proteincontaining
32. E. The abstract allows the reader to determine whether bacteria.
the study is of interest. The abstract usually appears 42. E. A thorough medical history, physical examination,
at the head of the article and is reproduced in the and laboratory tests do not always detect patients
literature database. who are carriers of infectious diseases. You must
33. C. In the results section, the researcher describes assume that all patients are infected with HIV,
the specific findings and actual outcomes of the HBV, or other bloodborne pathogens. Similar
project but does not interpret them. The interpreta- infection control procedures must be used for all
tion and analysis of the results are part of the dis- patients, regardless of their medical history or the
cussion, where the researcher attempts to explain type of treatment to be performed.
the results. 43. D. Alcohol is not an accepted disinfectant. Alcohol
34. E. The median is the middle of a distribution: half the evaporates too quickly to be an effective disinfec-
scores are above the median, and half are below the tant. The term disinfection is reserved for chemicals
median. The median is less sensitive to extreme applied to inanimate surfaces, and the term anti-
scores than the mean, making it a better measure septic is used for antimicrobial agents (e.g., alcohol)
than the mean for highly skewed distributions. For that are applied to living tissues.
instance, the median income of a population is 44. E. Mercury can be absorbed through the skin as well
usually more informative than the mean income. as absorbed by inhalation. Safe handling, resulting
When there is an even number of numbers, the in part from proper training, helps reduce the risk
median is the mean of the two middle numbers. In of exposure.
this case, the median is (64 + 68)/2 = 66. 45. C. The CDC recommends, at a minimum to meet na-
35. C. The correlation coefficient (r) quantifies the rela- tionally recognized drinking water standards, less
tionship between variables (x and y). A positive than 500CFU/mL of heterotrophic bacteria. In
correlation coefficient indicates that the variables 1995, the American Dental Association addressed
increase in the same direction; a negative correla- the dental water concern by asking manufacturers
tion coefficient indicates that the variables vary in to provide equipment with the ability to deliver
opposite directions. The correlation coefficient treatment water with less than 200CFU/mL of un-
ranges from 1 to +1. filtered output from waterlines.
36. C. A false-positive test is a test result that erroneously 46. A. There are five principles in the ADA Principles of
assigns an individual to a specific diagnostic or Ethics:
reference group. 1. Patient autonomy (self-governance). The
37. D. The average risk of infection for HBV after a dentist has a duty to respect the patients rights
needle-stick injury does not fall between HCV and to self-determination and confidentiality.
HIV. For HBV, the risk of transmission after per- 2. Nonmaleficence (do no harm). The dentist has
cutaneous injury is 30%; this figure is 1.8% for a duty to refrain from harming the patient.
HCV and 0.3% for HIV. 3. Beneficence (do good). The dentist has a duty
38. A. Very specific tests are appropriate for confirming to promote the patients welfare.
the existence of a disease. If the result of a highly 4. Justice (fairness). The dentist has a duty to
specific test is positive, the disease is almost certain. treat people fairly.
High specificity is required in situations where 5. Veracity (truthfulness). The dentist has a duty
the consequences of a false-positive diagnosis are to communicate truthfully.
serious or unduly alarming (e.g., HIV positivity). 47. E. Being specific helps to avoid misinterpretation of
39. E. All of these measures help ensure the safety of reports. Being objective provides the basis for
dental personnel. accuracy in describing events. Being complete
40. D. Disinfection refers only to the inhibition or destruc- provides the basis for a thorough review of the
tion of pathogens. Spores are not killed during facts when reviewing the report. Being timely
disinfection procedures. By custom, the term dis- ensures the best opportunity to recall all relevant
infection is reserved for chemicals applied to inani- events.
mate surfaces, and the term antiseptic is used for 48. A. A preferred provider organization (PPO) is an
antimicrobial agents that are applied to living arrangement between a plan and a group of den-
tissues. tists whereby the providers agree to accept certain
41. D. The proper time and temperature for autoclaving payments (usually less than their usual fees) in
is 250F (121C) for 15 to 20 minutes, which yields anticipation of a higher volume of patients. Capita-
15 pounds pressure of steam, or 270F (134C) for tion is a payment mechanism whereby the dentist
a minimum of 3 minutes, which yields 30 pounds is paid a fixed amount regardless of the number of
patients seen or services provided. Health mainte- sequence. Statistical analytical procedures explain
nance organizations (HMOs) are also called capita- the proposed strategy for quantifying, evaluating,
tion plans because of the payment mechanism they and analyzing the results and is presented along
use. An individual practice association (IPA) is a with the actual statistical procedures proposed.
type of plan that combines the risk of capitation The commentary on the results is placed in the
with fee-for-service reimbursement. discussion section and the summary and conclu-
49. A. The Centers for Disease Control and Prevention sion section.
(CDC) monitors and prevents disease outbreaks, 53. D. The mean or average is the value obtained by
implements disease prevention strategies, and adding all the measurements and dividing by the
maintains national health statistics. The U.S. Food number of measurements. Choice A is equal to
and Drug Administration (FDA) is responsible for choice C. The most frequent measurement in a set
protecting the health of the nation against impure of data is termed the mode. The median is deter-
and unsafe foods, drugs, cosmetics, and other mined by sorting the observations in order of mag-
potential hazards. The Drug Enforcement Admin- nitude and finding the middle number.
istration (DEA) determines the levels of controlled 54. A. The 2 test measures the association between two
substances that have abuse potential. The Indian categorical variables. The correlation coefficient
Health Services (IHS) focuses on the goal of raising quantifies the relationship between variables (e.g.,
the health status of Native Americans and Native x and y). If the r value is +1, there is a perfect
Alaskans. correlation, with both values increasing in the
50. A. The Department of Health and Human Services same direction. A multiple regression analysis pro-
(DHHS) is the principal agency of the U.S. govern- vides a mathematical model of linear relationship
ment for protecting the health of all Americans between a dependent (i.e., an outcome variable)
and providing essential human services. DHHS and two or more independent or predictor
includes 11 agencies and more than 300 programs. variables.
The other agencies listed are part of the DHHS. The 55. B. Supplemental fluoride in addition to proper water
National Institutes of Health (NIH) is the worlds fluoridation could lead to fluorosis. Fluoride has
premier medical research organization. The Health both a topical and a systemic effect. The U.S.
Resources and Services Administration (HRSA) Centers for Disease Control and Prevention (CDC)
provides access to essential health care services for directive on the level of fluoride in the water is
people with low income, people with no health still in effect even though suggestions have been
insurance, and people who live in rural areas or made to reduce it to 0.7ppm. The CDC reported
urban neighborhoods where health care is scarce. in 2010 that 74% of the U.S. population have water
The Agency for Healthcare Research and Quality fluoridation.
(AHRQ) supports research on health care systems, 56. B. Three doses are given to confer immunity: an initial
health care quality and cost issues, access to health dose, followed by a second dose at 1 month, and a
care, and effectiveness of medical treatments. third dose 6 months after the first. Because HBV is
51. A, C, D. In a case-control study, people with a condi- highly infectious, all dental personnel should be
tion (cases) are compared with people without vaccinated against HBV. The mainstay of postex-
the condition (controls) but who are similar in posure prophylaxis is hepatitis B vaccine, but in
other characteristics. Hypothesized causal expo- certain circumstances hepatitis B immune globulin
sures are sought in the past medical records of the is recommended in addition to HBV vaccine for
participants. The case-control study could establish added protection.
a temporal relationship between the exposure and 57. C. Blue identifies the health hazard. Red identifies the
disease of interest, such as a history of alcohol fire hazard. Yellow identifies the reactivity or stabil-
drinking before the appearance of oral cancer. ity of a chemical. White identifies the required per-
Choice B applies to a prospective cohort study. sonal protective equipment (PPE) when using this
52. A, B, C, E. Sampling strategy provides a description chemical. The level of risk for each category is indi-
of the sampling strategy, the sample size, and the cated by the use of numbers 0 through 4, the higher
methods for assigning samples to conditions. Mea- the number, the greater the danger.
surement strategies and measurement instruments 58. A, B, C, D.
indicate how the variables are measured. Although
the variables studied are discussed in the abstract,
the introduction, and the conclusion, the actual Periodontics
definitions of the variables are stated in the mea-
surement strategy. Experimental design describes 1. A. Wasting diseases of the teeth include erosion
operationally the study design in a step-by-step (corrosion; may be caused by acidic beverages),
abrasion (caused by mechanical wear as with of the bacterial plaque biofilm is the primary initia-
toothbrushing with abrasive dentifrice), attrition tor of the disease.
(secondary to functional contact with opposing 13. B. Inadequate or overhanging margins serve as a
teeth), and abfraction (flexure secondary to occlu- nidus for dental plaque accumulation and make
sal loading). plaque removal difficult.
2. A. Keratinized gingiva extends from the free gingival 14. C. Individuals who smoke cigarettes are more likely
margin to the mucogingival junction. The attached to have periodontal disease than nonsmokers. The
gingiva extends from the free gingival groove to the number of cigarettes smoked and the number of
mucogingival junction. years of smoking affect the severity of disease.
3. C. Gingivitis is characterized by inflammation of the Former smokers usually have less disease than
gingival tissues with no loss of clinical attachment. current smokers.
Periodontitis is characterized by inflammation 15. D. The extent and severity of periodontal disease in a
with loss of clinical attachment. patient with well-controlled diabetes are usually no
4. D. Because there is no loss of attachment, the diag- more than the extent and severity of disease in
nosis would not be periodontitis. The clinical patients without diabetes. Patients with well-con-
description of pain, erythema, blunt papillae, trolled diabetes can usually be treated with conven-
pseudomembrane, and halitosis is consistent with tional periodontal therapy.
necrotizing ulcerative gingivitis. 16. D. Oral contraceptives can exacerbate the impact of
5. C. Radiographs must be taken in a standardized bacterial plaque on the gingival tissues. However,
format at repeated visits to be assessed for small oral contraceptives cannot cause gingivitis.
changes in bone density over time, using subtrac- 17. D. Neutrophils are one of the primary defense cells
tion radiography. Radiographs are usually stan- of the innate immune system. T lymphocytes are
dardized by using a bite registration block to important activators of the adaptive immune
relocate the x-ray at the same place and angulation system. Macrophages are antigen-presenting cells.
each time. Plasma cells produce antibodies.
6. D. Maxillary molars usually have three roots (mesio- 18. D. Although defects in any of the host defense cells
buccal, distobuccal, and palatal). Furcation in- could affect periodontal disease susceptibility,
volvement can be assessed on these teeth from the defects in neutrophils have been most frequently
facial (bifurcation between the mesiobuccal and described.
distobuccal roots), mesial (bifurcation between 19. D. The initial, early, and established lesions of gingi-
the mesiobuccal and palatal roots), and distal (bi- vitis do not have attachment loss associated with
furcation between the distobuccal and palatal them.
roots). 20. A. IL-1 is important in the activation of osteoclasts
7. A. Subgingival plaque can be in the cervical area or and stimulation of bone loss.
more apical. In both areas, it can be either 21. E. Scaling and root planing are used in all phases of
tooth-associated or tissue-associated. The apical periodontal therapy where there has been loss of
tooth-associated plaque is composed primarily of attachment through periodontitis.
gram-negative rods. 22. C. Although changes in gingival color and consis-
8. C. Calcium, phosphorus, sodium, and potassium are tency and loss of gingival stippling can be indica-
inorganic components of dental plaque. Polysac- tors of gingival inflammation, bleeding on probing
charides, proteins, glycoproteins, and lipids are is the most objective clinical indicator.
organic components of dental plaque. 23. A. Marginal gingivitis not complicated by systemic
9. D. F. nucleatum can be found in health and disease. problems or medications usually can be treated
This bacterium is an important bridge between successfully with phase 1 therapy, and a pa-
early and late colonizers of the dental plaque tient with this diagnosis would have a good
biofilm. prognosis.
10. C. Periodontal health is characterized by a microflora 24. B. Polishing is used to remove plaque and stains from
dominated by gram-positive, facultative cocci the teeth. Gingival curettage is used to remove the
and rods. epithelial lining of a periodontal pocket. Root
11. B. P. gingivalis has been associated with chronic peri- planing is used to create a smooth root surface
odontitis. A. viscosus is usually associated with through the removal of calculus and rough cemen-
health or gingivitis. S. mutans is associated with tum. Scaling is used to remove plaque, calculus,
dental caries. A. actinomycetemcomitans has been and stains from the tooth.
associated with localized aggressive periodontitis. 25. A. Scalers, with their pointed ends and back, are
12. D. Although age, gender, and nutrition may have an designed for supragingival instrumentation; cu-
impact on periodontal disease, the accumulation rettes, with their rounded ends and back, can be
used for both supragingival and subgingival 40. C. Teeth are usually splinted to improve patient
instrumentation. comfort during mastication.
26. B. Scalers have a pointed back; curettes have a 41. C. Establishment of drainage is the first step in treat-
rounded back, making them suitable for subgingi- ing an acute periodontal abscess. The patient may
val instrumentation. then use self-applied mouth rinses and be pre-
27. C. Three incisions are made in the modified Widman scribed antibiotics if there is evidence of systemic
flapinternal bevel, crevicular, and interdental. involvement (e.g., fever, lymphadenopathy). A flap
The flap is designed to provide exposure of the would be reflected in a subsequent appointment if
tooth roots and alveolar bone. However, the flap is the abscess did not resolve and became a chronic
not reflected beyond the mucogingival junction. problem.
28. A. Surgical techniques designed to increase the width 42. B. Calcium channel blockers, cyclosporine, and phe-
of attached gingiva include free gingival grafts and nytoin often result in overgrowth of gingival
apically repositioned flaps. tissues.
29. C. The Miller classification system for mucogingival 43. C. Patient cooperation and effectiveness in removing
defects takes into consideration the degree of bacterial plaque is of primary importance in main-
recession (whether or not it extends to the muco- taining a healthy periodontium.
gingival junction) and presence or absence of bone 44. D. Mature dental plaque usually reforms on the
loss in the interdental area. Both class I and class teeth within 24 to 48 hours after effective plaque
II defects are characterized by no loss of bone in removal.
the interproximal areas. In class I defects, the mar- 45. C. The Bass technique of brushing is designed to
ginal tissue recession does not extend to the muco- direct the bristles of the brush toward the gingival
gingival junction. In class II defects, recession sulcus.
extends to or beyond the mucogingival junction. 46. C. Under these conditions, doxycycline inhibits
30. B. Ostectomy is the removal of supporting alveolar metalloproteinases. By inhibiting matrix metallo-
bone. Osteoplasty is the reshaping or recontouring proteinase (MMP)-8 and MMP-13, collagen break-
of nonsupporting alveolar bone. down is reduced. Amylase is a normal constituent
31. B. An interdental crater has two bony walls remain- of saliva. -Lactamases break down -lactam anti-
ing. These walls are usually the facial and lingual biotics such as penicillins. Cyclooxygenases are
walls. inhibited by nonsteroidal antiinflammatory drugs.
32. D. Cells from the periodontal ligament are proposed 5-Lipoxygenase is important for the formation of
to allow for regeneration of the periodontal leukotrienes. None of the last four mentioned
tissues. enzymes is significantly affected by doxycycline.
33. D. Through-and-through (class III) furcation defects 47. C, B, D, A. Immediately after suturing to close a peri-
are least likely to be treated with bone graft odontal flap, a clot forms that connects the flap to
procedures. the tooth and alveolar bone. Epithelial cells begin
34. B. When evaluated by light microscopy, there appears to migrate over the border of the flap 1 to 3 days
to be direct contact at the bone-implant interface. after surgery. An epithelial attachment consisting
35. A. Chlorhexidine is the most effective antimicrobial of hemidesmosomes and a basal lamina is in place
agent currently available. 1 week after surgery. The clot is replaced by granu-
36. D. PerioChip is a biodegradable local delivery agent lation tissue. Collagen fibers appear 2 weeks after
for chlorhexidine. surgery. Within 1 month, the gingival crevice is
37. B. Epithelial cells migrate approximately 0.5mm/day. lined with epithelium.
It takes 5 to 14 days after a gingivectomy for surface 48. C, D. Only lymphadenopathy and fever indicate a
epithelialization to be complete. spreading infection.
38. A. Increased tooth mobility is the most common 49. B. Furcation involvement can be classified as follows:
clinical sign of trauma from occlusion. Increased grade I, incipient; grade II, cul-de-sac with definite
periodontal ligament width is the most common horizontal component; grade III, complete bone
radiographic sign. loss in the furcation; grade IV, complete bone loss
39. C. The term trauma from occlusion refers to the tissue in the furcation and recession of the gingival tissues
injury that occurs when occlusal forces exceed the resulting in a furcation opening that is clinically
adaptive capacity of the tissues. An occlusion that visible.
produces such an injury is called a traumatic occlu- 50. C. Streptococcus and Actinomyces species are early or
sion. The tooth may become damaged as a result primary colonizers. P. gingivalis and A. actinomy-
of excessive occlusal forces. The periodontal liga- cetemcomitans are late (secondary) colonizers, as
ment also may become widened as a result of the are Campylobacter species. F. nucleatum serves as
force. a middle or bridging microorganism.
Pharmacology of ion channel receptors. Ion channel receptors

contain several subunits arranged in a barrel shape.
1. B. The brain has especially tight capillary junctions as Drugs that bind to the channel can alter conduc-
well as glial cells that result in a blood-brain barrier. tance to the ion associated with that channel.
2. E. Oxycodone is a scheduled drug, requiring DEA 15. D. Benzocaine lacks the terminus group that pro-
registration on the part of the prescriber. caine, mepivacaine, prilocaine, and lidocaine have.
3. B. The characteristic response to a competitive antag- This amine group can become protonated, making
onist is a parallel shift to the right of the agonist these drugs more water-soluble and facilitating an
curve, with the two curves reaching the same injectable form. Benzocaine must be provided in a
maximal effect. cream-based or oil-based preparation allowing just
4. C. The fourth phase constitutes postmarketing a topical form. Procaine and mepivacaine have
surveillance. poor topical anesthetic properties.
5. D. This situation for sweat glands is atypical for the 16. C. An area of inflammation is an area of low pH. The
sympathetic nervous system. acid environment would convert more of the drug
6. A. Nicotinic receptors are located at the skeletal-neu- into the charged form, making it less able to diffuse
romuscular junction, in the ganglia, at the junction to the nerve cells. This would reduce the rate of
of the sympathetic nerve to the adrenal gland and onset and the net anesthetic effect of the drug.
the adrenal chromaffin cells, and in the central 17. D. All of the choices are combinations of an opioid
nervous system. and an inhibitor of cyclooxygenase (COX), except
7. E. All other choices are typical of muscarinic cholin- two: ibuprofen, naproxen and aspirin, ibuprofen.
ergic receptor agonists. Ibuprofen and naproxen are both reversible inhibi-
8. D. -Adrenoceptor blockers such as phenoxybenza- tors of COX and are propionic acid derivatives.
mine inhibit the vasoconstrictor effect of epineph- Aspirin is a salicylate and is an irreversible
rine but not the vasodilator effect of epinephrine. inhibitor.
The administration of blockers results in epi- 18. C. Thromboxane A2 increases platelet aggregation. Its
nephrine reversal. Atropine would have little effect inhibition is the target of low-dose aspirin, which
because it does not act at adrenergic receptors. Pro- inhibits cyclooxygenase. Inhibition of this enzyme
pranolol would block only the vasodilator effect of leads to a reduction in important downstream
epinephrine and the effect of epinephrine on the products, including thromboxane A2.
heart. Guanethidine and tyramine act largely at 19. C. The INR value indicates that the patient has
prejunctional sites and do not block adrenergic received anticoagulant therapy for atrial fibrilla-
receptors. tion. Aspirin increases the risk of postsurgical
9. D. The nigrostriatal pathway contains dopaminergic bleeding. The combination of increase in pro-
neurons, which are important in muscle control. thrombin time, surgery, and the antiplatelet effect
Many antipsychotic drugs block these, leading to of aspirin makes aspirin contraindicated in this
the motor adverse effects. situation. The effect of ibuprofen on the platelet is
10. C. The antimuscarinic action of benztropine tends to reversible, whereas the effect of aspirin on the
reduce the Parkinson-like symptoms and some platelet is irreversible. Aspirin poses a greater risk
other motor symptoms caused by haloperidol, a than ibuprofen in this situation.
dopamine receptor blocker. Benztropine does not 20. C. The first three choices are all H1 histamine receptor
improve the antipsychotic effect of haloperidol. blockers. However, fexofenadine is largely excluded
Histamine release appears to play little role in this from the central nervous system, in contrast to
interaction. Benztropine reduces salivary flow, and diphenhydramine and hydroxyzine. Albuterol is a
xerostomia can easily result from its administra- 2-adrenergic receptor agonist. Famotidine is a H2
tion. Benztropine has little effect on renal clear- histamine receptor antagonist.
ance of haloperidol. 21. B. The cardiovascular risks may be associated with
11. B. The two benzodiazepine receptor subtypes (targets adverse hematologic effects, but the exact mecha-
for drugs such as diazepam) are located on the nism is not yet known.
same chloride channel as the -aminobutyric acid 22. A. All the drugs listed are diuretics. However, only
A receptor. bumetanide acts on the ascending limb of the loop
12. C. Only prilocaine is metabolized to o-toluidine. of Henle. It is called a loop and high-ceiling
13. B. Halothane sensitizes the heart to epinephrine and diuretic because of its site of action in the nephron
other catecholamines. and maximal effect, respectively.
14. A. Inhibiting sodium channels leads to the inhibition 23. D. The long QT interval observed as a result of
of the nerve action potential and inhibition of certain drugs or as a hereditary condition makes
nerve conduction. Sodium channels are examples the patient more susceptible to this condition.
24. C. Lisinopril, by virtue of the fact that it inhibits 35. B, D. Nonspecific esterase in the plasma can metabo-
angiotensin-converting enzyme (also called pep- lize various esters. Articaine and acetylcholine
tidyl dipeptidase), inhibits the breakdown of have ester bonds that are susceptible to these
bradykinin. enzymes. Bethanechol and carbachol are designed
25. D. Diazepam, epinephrine, and insulin act at ion to be resistant to hydrolysis by acetylcholinesterase
channel receptors, G-proteinlinked receptors, and plasma esterases. Pilocarpine is an alkaloid
and tyrosine kinaselinked receptors, respectively. that is not significantly affected by these enzymes.
These three receptor types are cell surface recep- 36. A4; B5; C2; D3; E1. Glibenclamide is a
tors. Thyroid hormone and steroid hormones or newer sulfonylurea-type drug that increases insulin
drugs, such as prednisone, act on nuclear recep- secretion by closing adenosine triphosphatesensi-
tors, accounting for much of their action. The tive potassium channels in the cell membranes of
action of heparin is to stimulate antithrombin III cells. Activating AMP kinase has an effect of
in the plasma. Its action is extracellular. regulating energy production, leading to the effects
26. A. All of the choices are oral hypoglycemic agents. indicated above. An increase in glucagonlike
Only acarbose inhibits -glucosidase. peptide leads to stimulation of insulin release, inhi-
27. D. Spironolactone, a potassium-sparing diuretic use- bition of glucagon release, and reduced food intake.
ful in treating edema and heart failure, is a com- 37. A, E. Inhibitors of the 2/-1 protein subunit of
petitive antagonist at the aldosterone receptor. high-voltageactivated calcium channels have
28. B. Aldosterone and fludrocortisone are selective min- selective antiepileptic effects and have been
eralocorticosteroids. Hydrocortisone has signifi- found to be useful in treating neuropathic pain.
cant mineralocorticoid and glucocorticoid activity. Phenobarbital enhances chloride channel activity.
Dexamethasone has very little mineralocorticoid Carbamazepine is a sodium channel blocker,
activity. and ethosuximide is an inhibitor of T-type
29. B. Glucocorticoids characteristically stimulate gluco- calcium channels.
neogenesis and lipolysis. Insulin has the opposite 38. D, E. The half-lives are as follows: chlordiazepoxide, 5
effects. The other hormones listed have minor or to 30 hours; diazepam, 30 to 60 hours; lorazepam,
negligible effects. 10 to 18 hours; midazolam, 2 to 5 hours; triazolam,
30. C. Renal tubular acidosis, aminoaciduria, and hyper- 1 to 2 hours.
phosphaturia are some of the manifestations of 39. B, E. Cleavage of the aromatic ring rarely, if ever,
proximal tubule damage in Fanconis syndrome. occurs in the metabolism of local anesthetics.
31. D. Of the choices given, only vancomycin is effective Lidocaine does not possess an ester bond to be
against many methicillin-resistant staphylococci. metabolized.
Various penicillins, macrolides, and clindamycin 40. C, D, E. Flumazenil blocks both types of benzodiaz-
are ineffective. epine receptors associated with -aminobutyric
32. C. Because it lacks a cell wall, M. pneumoniae is not acid A (GABAA) channels, blocking the effects of
sensitive to cell wall inhibitors such as penicillin diazepam, zaleplon, and zolpidem, the latter
V. The macrolides (e.g., clarithromycin) are ri two being selective for the Bz1 receptor. Baclofen
bosomal protein synthesis inhibitors that are stimulates GABAB receptors, and buspirone is a
effective against M. pneumoniae. Viridans strepto- partial agonist at serotonin 5-hydroxytryptamine
coccus, S. pneumoniae, and S. pyogenes are gram- 1A receptors.
positive cocci. L. buccalis is a gram-negative oral
bacillus.
33. A. The short elimination half-time for penicillin V is Prosthodontics
due to rapid excretion of penicillin in the urine.
About 90% of this renal excretion is a result of 1. A. The incisive papilla provides a guide for the ante-
active tubular transport, a rapid and efficient rior-posterior position of the maxillary anterior
process. (Very little metabolism of penicillin teeth. The labial surfaces of the central incisors are
occurs.) usually 8 to 10mm in front of the papilla. This
34. E. Amoxicillin, clarithromycin, and clindamycin are distance varies depending of the amount of resorp-
effective against some anaerobes, but their spec- tion of the residual ridge, the size of the teeth, and
trum is not limited to anaerobic bacteria. Amino- the labiolingual thickness of the alveolar process.
glycosides are effective only against aerobes. The 2. E. All of the statements are correct. VDR is a physi-
action of metronidazole requires a reduced envi- ologic rest position; it is the position of the man-
ronment. Its antibacterial spectrum is limited to dible when the muscles are in their minimum state
anaerobes. Metronidazole is also effective against of tonicity, which occurs when a patient is relaxed
many parasites. with the trunk upright and the head unsupported.
In this position, the interocclusal distance is reciprocating clasp should contact the tooth on or
usually 2 to 4mm when observed at the first above the height of contour of the tooth, allowing
premolar area. for insertion and removal with passive force. Dis-
3. C. Stability is resistance to movement toward the placement of the RPD toward the tissue, causing
residual ridge. The function of the posterior palatal tissue recession, is a function of the lack of occlusal
seal is to improve retention, not stability. Stability rests.
is determined by the size, height, or shape of the 11. D. This meets the definition of centric relation and the
ridge. normal anatomic relationships of the temporo-
4. A. Failure of an occlusal rest rarely results from a mandibular discs to the condyles. Centric relation
structural defect in the metal and rarely if ever is is a clinically repeatable mandibular position pri-
caused by distortion. Therefore the blame for such marily defined by the temporomandibular joints,
failure must often be assumed by the dentist for not not the teeth.
having provided sufficient space for the rest during 12. A. The retromolar pad should always be covered for
mouth preparations (Carr AB, et al: McCrackens support of the mandibular denture base. The ret-
Removable Partial Prosthodontics, ed 11. St Louis, romolar pads and the buccal shelf are considered
Mosby, 2005). primary areas of support for a mandibular distal
5. D. To preserve the mounting relationship in the artic- extension RPD or complete denture.
ulator of the maxillary cast (face-bow record) after 13. B. Anatomic landmarks to be used as guides in ar-
processing a denture, an occlusal index of the max- ranging the anterior teeth are the incisive papilla,
illary denture is made after occlusal adjustments midsagittal suture, and ala of the nose (canine
and before decasting the denture. This procedure lines). The incisive papilla is a good guide for the
has nothing to do with the mandibles relationship anterior-posterior positioning of the maxillary an-
to the maxilla. terior teeth. The labial surfaces of the central inci-
6. D. Angular cheilosis is described as inflamed and sors are usually 8 to 10mm in front of the papillae.
cracked corners of the mouth that can become This distance varies depending on the size of the
infected with bacterial and fungal organisms. It is teeth and the labiolingual thickness of the alveolar
commonly seen in patients with dentures with process, so it is not an absolute relationship.
diminished vertical dimension of occlusion. It is 14. A. The vibrating line is located by finding the ptery-
best treated with antifungal creams and correcting gomaxillary (hamular) notches and continues to
the vertical dimension of occlusion. the median line of the anterior part of the soft
7. A. When performing an occlusal adjustment, the goal palate slightly anterior to the foveae palatinae. A
is to make centric relation and maximum intercus- V-shaped groove 1 to 1.5mm deep and 1.5mm
pation to coincide. None of the other choices broad at its base is carved into the cast at the vibrat-
allows one to mount the casts reliably in centric ing line. The narrow and sharp bead sinks easily
relation or allows one to perform this procedure into the soft tissue to provide a seal against air
accurately. being forced under the denture. Stability is resis-
8. B. The main purpose is to capture the influence of the tance to movement toward the residual ridge. The
mylohyoid muscle. The extent of this flange is post dam improves retention, not stability. It is
determined by the elevation of the floor of the carved shallow in the midpalatal suture area. Sta-
mouth when the patient wets the lips with the tip bility is determined by the size, height, or shape of
of tongue. Pursing the lips forms the extension of the ridge.
the buccal vestibule. The buccal vestibule is influ- 15. D. The ala-tragus line posteriorly and the interpupil-
enced by the buccinator muscle, which extends lary line anteriorly are used as guides to align the
from the modiolus anteriorly to the pterygoman- occlusal plane for complete dentures. The Campers
dibular raphe posteriorly and has its lower fibers line is also known as the ala-tragus line.
attached to the buccal shelf and the external oblique 16. A. Teeth come together every time a patient swallows.
ridge. This can dislodge dentures secondary to breaking
9. B. The function of the direct retainer is to retain the the denture seal.
removable partial denture by means of the abut- 17. B. Epulis fissurata is a reactive growth to an overex-
ments. Stabilization is provided by the minor con- tended or ill-fitting denture flange. It is best
nector. Support is provided by the rest. The indirect removed surgically. Papillary hyperplasia is found
retainers improve the efficiency of the direct retain- in the palatal vault. It is caused by local irritation,
ers. Direct retainers do not add strength to the poor-fitting dentures, poor oral hygiene, or leaving
major connector. dentures in 24 hours a day. Candidiasis is associ-
10. D. Tooth mobility is prevented or diminished ated with papillary hyperplasia. Fibrous tuberosity
during function by the reciprocating clasp. The is commonly seen with large tuberosities.
18. C. Failure of an occlusal rest rarely results from a 28. D. An important factor that affects the metal-ceramic
structural defect in the metal and rarely if ever is bond is the surface treatment of the alloy before
caused by accidental distortion. Therefore the firing porcelain. Air-abrasion of the cast alloy is
blame for such failure must often be assumed by typically performed before the oxidation step to
the dentist for not having provided sufficient space help remove surface contaminants that remain
for the rest during mouth preparations (Carr AB, from devesting and to help clean the casting and
et al: McCrackens Removable Partial Prosthodon- provide microscopic surface irregularities for
tics, ed 11. St Louis, Mosby, 2005). mechanical retention of the ceramic. The oxidation
19. B. Resin-modified glass ionomers combine some of step for the alloy can be performed in air or by
the advantages of glass-ionomer cements, such as using the reduced atmospheric pressure (approxi-
fluoride release and adhesion, but provide higher mately 0.1atm) available in dental porcelain
strength and low solubility. These materials are furnaces.
less susceptible to early moisture exposure than 29. D. The casting alloy and luting agent have been shown
glass-ionomer cements, but they exhibit increased to have a minimal effect on the retention of a
thermal expansion because of the addition of resin. crown. The geometry of the preparation, parallel-
20. A. The width of an anterior tooth is usually identified ism between the walls (taper), and surface texture
by the mesiofacial and distofacial position of of the preparation have an effect on the retention
the line angles, the shape of the surface contour, of a crown.
and light reflection between these line angles. The 30. B. The arcon articulator is capable of duplicating a
contralateral tooth features should be duplicated wide range of mandibular movements but is gener-
closely in the pontic, and the space discrepancy can ally set to follow the patients border movements.
be compensated by modifying the shape of the The terminal hinge axis is located, and a panto-
proximal areas. graph is used to record the mandibular move-
21. C. The carboxylate groups in the polymer molecule ments. These mandibular movement tracings or
chelate to calcium. recordings are used to set the articulator.
22. B. Gold alloys are heavier for a given volume. Gold 31. A. If there is an existing pulp chamber and remaining
alloys are softer. Base metals are cast at higher tem- sound tooth structure, there is no need to place a
peratures, leading to greater shrinkage. post. Placement of a post tends to require taking
23. B. Polysulfide has the highest tear strength of all elas- additional tooth structure, which weakens a tooth.
tomeric impression materials. 32. E. A tooth moves within the limits of its periodontal
24. B. Chroma is the saturation or intensity of the color ligament during function. The relative immobility
or shade. Value is the relative lightness or darkness of the osseointegrated implant compared with the
of a color. Opalescence is the light effect of a trans- functional mobility of a natural tooth can create
lucent material. stresses at the neck of the implant up to two times
25. B. Noble metals are gold, platinum, and palladium. the implied load on the prosthesis. Potential prob-
Silver is not considered noble; it is reactive but lems when connecting an implant with a tooth
improves castability. Noble alloys (old term was include (1) breakdown of the osseointegration, (2)
semiprecious metal) have a noble metal content cement failure on the natural abutment, (3) screw
greater than or equal to 25%. To be classified as or abutment loosening, and (4) failure of the
noble, palladium-copper, palladium-gold, and implant prosthetic component. Fracture in the
palladium-cobalt alloys have no stipulation for connector area is rarely seen in this situation.
gold. High noble alloys have a high content of 33. C. The minor connector must have sufficient bulk to
gold (>60%). be rigid so that it transfers functional stresses effec-
26. D. All these reasons are correct. The provisional is tively to the abutment or supporting teeth and
placed to protect the tooth and preserve healthy tissues. It should be located in the interdental
tissues if proper contours and marginal integrity embrasure where it does not disturb the tongue
are present. This is an excellent time to evaluate and should be thickest in the lingual surface, taper-
and give feedback to the patient on how well he or ing toward the contact area but not located on a
she is brushing and flossing. convex surface.
27. C. Compomer cements (also known as resin-modified 34. E. The posterior and anterior factors, position in the
glass ionomer cements) have low solubility, low mouth, and side shift influence the occlusal
adhesion, and low microleakage. They are not rec- anatomy of a restoration.
ommended to be used with all-ceramic restora- 35. E. The contact of the framework with parallel tooth
tions because they have been associated with surfaces acting as guide planes provides a positive
fracture, which is probably due to water absorption path of placement and removal for the RPD. In
and expansion. addition, guide planes can provide retention by
limiting the movement of the framework. The 43. B. The minor connectors are the components that
rest on the RPD prevents vertical or cervical serve as the part of the removable partial denture
movement. that connect the major connector and other com-
36. C. The clasps are meant to be flexible to engage in ponents, such as the clasp assembly, indirect retain-
undercut. The rest of the components of the RPD ers, occlusal rests, or cingulum rests.
should be rigid. 44. D. The Munsell Color System, which is the basis of
37. A. Circumferential cast clasps are more rigid than shade guides such as Vita Lumin, is divided into
combination clasps or wrought wire clasps. Because three dimensions: hue is the shade or color of an
there is good stability of the prosthesis when the object, chroma is the saturation or intensity of the
tooth is supported, there is no need for the added color or shade, and value is the relative lightness or
flexibility in a normal situation. darkness of a color.
38. E. The impression should be rinsed and disinfected 45. D. Opaque porcelain is used for masking the oxide
with glutaraldehyde or iodophor and should be layer of the metal and provides the porcelain-metal
poured within 15 minutes from the time the bond. The minimum thickness of the opaque is
impression was removed from the mouth. about 0.1mm.
39. B. Isolation is the most important factor because it 46. B. Chroma is the saturation or intensity of the color
prevents bacterial contamination, increasing the or shade. Value is the relative lightness or darkness
success of the pulp cap procedure. of a color. Metamerism is the phenomenon in
40. E. On a tooth-supported RPD with a circumferential which a color match under a lighting condition
cast clasp assembly, there should be more than 180 appears different under a different lighting condi-
degrees of encirclement by the clasp in the greatest tion. Fluorescence is the physical property in which
circumference of the tooth (that passes from di an object emits visible light when exposed to ultra-
verging axial surfaces to converging axial surfaces). violet light.
Mesial and distal rests anterior and posterior to the 47. B, C, D. Silver is not considered noble. It is reactive.
edentulous areas, respectively, are generally used. It improves castability but can cause porcelain
41. A. Nonrigid connectors are used when it is not pos- greening.
sible to prepare two abutments for a fixed partial 48. B. The base paste in polyether impression material
denture (FPD) with a common path of placement contains a polyether polymer. Polydimethylsilox-
or to segment a large or complex FPD into shorter ane is the main base component of condensation
components. Nonrigid connectors can be prefabri- silicone. Polysulfide polymer is found in polysul-
cated plastic patterns (female or keyway portion fide impression material. None of these is a revers-
and male or key portion) that are embedded in the ible impression material.
waxed crown and pontic patterns or custom-milled 49. A, B, C, D. Electrosurgery is contraindicated under all
in the cast crown. The second part is custom-fitted of the conditions listed.
to the milled retainer and cast. 50. A, D. Retentive clasps need to be occlusal to the
42. C. The recommended space or distance between the survey line because they approach the tooth from
border of the framework and the marginal gingiva the occlusal. The I bar and T bar engage the under-
should be at least 6mm. cuts of teeth by way of a gingival approach.
Index
Page numbers followed by f indicate figures, t indicate tables, and b indicate boxes.
A Adrenal corticosteroids, 327-328 Amalgam restorations, 62-66

ABC model, 240 Adrenal medulla, hormone secretion, 296 cavosurface margin, 58
Abfraction, 260 Adrenergic agonists, 296-298 clinical examination, 43-44
treatment, 46 cardiovascular effects, 297f convenience form, 59
Abrasion, 252 uses, 298t finishing, 65
treatment, 46 Adrenergic neuron blockers, 298-299 outline form, 57-58
Abscesses, 284 Adrenergic receptor blockers, 298-299, 298t primary resistance form, 58-59
Absorption (drugs), 292-293 Adults primary retention form, 58
Abstract/vague communication, usage, 237 children, physiologic differences, 194 repair, 65
Abused tissues, management, 351-352 coronal caries, 218 requirements, 63
Abutment teeth psychological considerations, 181 resistance form, 58-59
alignment, 343 risk-based interventions, 39t restorative technique, 63-65
torqueing force, reduction, 355 treatment, 181-182 safety, 66
Acarbose, 327 periodontal aspects, 182 tooth preparation, 56-59
Accelerator, type, 359 Adverse reactions, examples, 192 usage, 62
Accidental traumatic lesions, 255 Aerosols, usage, 229 Amalgam tooth preparation
Acetaminophen, 315 Affordable Care Act (ACA), 235-236 external/internal walls, 52f
effects, 315-316 Agency for Healthcare Research and Quality retention, 59f
metabolic pathways, 315f (AHRQ), 236 Amantadine, 308
preference, 316 Aggregatibacter actinomycetemcomitans, 257, Ameloblastic carcinoma, 126
Acetylcholine (ACh), biosynthetic pathway, 259 Ameloblastic fibroma, 127
296 Aggressive horizontal brushing technique, Ameloblastic fibro-odontoma, 127
Acid-base drug properties, 292 260 Ameloblastoma, 10, 125-126, 125f
Acid etching, 212 Aggressive periodontitis, 205, 256, 258, Amelogenesis imperfecta, 131, 131f, 189
Acknowledging, usage, 236 283-284 Amides, 308
Acquired immunodeficiency syndrome systemic neutrophil abnormalities, bond, hydrolysis, 309
(AIDS), oral complications, 113b association, 263t Amiloride, 322
Acrylic partial denture, 201 Agonists, graded dose-response curves, 291f Aminoglycosides, 333
Acrylic resins, 356 Airborne particles, environmental Amino terminus, dealkylation, 309
porosity, 356 contaminants, 232-233 Amiodarone, 318
shrinkage, 356 Air-driven particle abrasion equipment, 49 Amoxicillin, 281, 332
usage, 344 Akers clasp, 355 Amphetamine/dextroamphetamine, 192
Actinic cheilitis (solar cheilitis), 117 Albers-Schnberg disease (osteopetrosis), 131 Amylin analogue, 327
Actinomyces odontolyticus, 260 Aligners, 175 Amyloidosis, occurrence, 123
Actinomycosis, 113 All-ceramic crowns, 362 Anaerobic bacteria, role, 94t
Activating hand instruments, 273 All-ceramic restorations, 362 Analgesics, 313-317
Activator, 175 All-ceramic systems, comparison, 362t Analysis of variance (ANOVA) test, 228
Active retainers, 181 Allograft, 83, 277 Analytical epidemiology, 223-224
Acute acetaminophen toxicity, 315 materials, 277 Analytical statistics, 226
Acute apical abscess, 4 Alpha-adrenergic receptor blockers (alpha Anatomic contours, problems, 44
differentiation, 4 blockers), 298, 321 Anatomic radiolucencies, 10
presenting signs/symptoms, 4 adverse effects, 298 Anchorage, 171-172
Acute aspirin toxicity, 315 dental implications, 299 cortical anchorage, 172
Acute candidiasis, 114f Alpha-hydroxylation, 305 implants, 172
Acute gingival diseases, 283-285 Alpha particles, 132 reinforced anchorage, 172
Acute herpetic gingivostomatitis, 204, 283 Aluminum chloride/aluminum sulfate, 359 stationary anchorage, 172
Acute necrotizing ulcerative gingivitis, 205 Aluwax, 344 Anesthetics, 308-313
treatment, 283 Alveolar bone, periodontal disease measure amounts, calculation, 310
Acute osteomyelitis, 129 usage, 253 properties, 294t
Acute pericoronitis, 283 Alveolar concentration, minimum, 194 Aneurysmal bone cyst, 128
Acute radiation syndrome, 136 Alveolar crest, radiographic anatomy, 144 Angiotensin-converting enzyme (ACE)
Addition silicone (vinyl polysiloxane), 359 Alveolar process fractures, 82 inhibitors, 290, 322
A-delta fibers, 2 Alveolar ridge preservation, 83 adverse effects, 321
Adenoid cystic carcinoma, 122 Alveoloplasty, 349 dual function, 320f
Adenomatoid odontogenic tumor, 126 Alveolus, grafting, 83 usefulness, 321
Adenosine, 319 Alveoplasty, 82 Angiotensin II receptor antagonists, 321
Adenosine diphosphate (ADP) receptor, 290 Amalgam Angle classification, 155-156, 160
Adhesive techniques, uses, 66 blues, 43 Angle class III malocclusions, 155
Adjunctive endodontic treatment, 28-30 carving, 64-65 Angle class II malocclusions, 155
Adjunctive therapeutic approaches, 281f insertion, 63-64 Angle-formers, 48
Administration for Children and Families knives, usage, 65f Angular cheilitis, 351
(ACF), 235 scrap, collection/disposal problems, 66 Angular defects, 276
Admixed amalgam, 66 tattoo, 111 Angular osseous defect, 149
455
456 Index
Ankylosed primary molars, 203-204 Antihypertensive drugs (Continued) Area-specific curettes (Gracey curettes),
Ankylosis, 205 minor types, 319 272-273
occurrence, 92 types, 319 Aromatic ring, hydroxylation, 309
Anode, 132 Antiinfective agents, impact, 281-282 Arrhythmias, antiarrhythmic drugs
Antagonists Antilipid drugs, adverse effects, 323t (indication), 318t
graded dose-response curves, 291f Antimania drugs, 303-304 Arterial gas tension, anesthetics (effects), 311f
receptor targets, 313t action, mechanisms, 303-304 Arthroscopy, 93
Antecedents, alteration, 241 clinical applications, 304 Articaine, usage, 310
Anterior crossbites, 178 lithium toxicity, 304 Articulators, 345
Anterior deprogramming devices, usage, 344 types, 303 As Low As Reasonably Achievable (ALARA),
Anterior diagnoal elastics, 177 Antimicrobial actions, 36 137
Anterior disc displacement, reduction Antimicrobial drugs, 330-335 Aspergillosis, 114
(absence), 92f Antimuscarinic anticholinergic drugs, 324 Aspiration biopsy, 100
Anterior guidance, 344 Antimuscarinic drugs, 300, 308 Aspirin
preservation, 344 dental implications, 300 contraindications, 315
Anterior mandible, periapical radiograph, effects, 301t metabolism, 315, 315f
147f usage, contraindications, 300 preference, 316
Anterior maxilla, periapical radiograph, 144f uses, 301t toxicity, 315
Anterior nasal spine, 145 Antineoplastic drugs, 335 Asthma (treatment), drugs (usage), 324
Anterior palatine foramen, 145 adverse effects, 337t Asymptomatic apical periodontitis, 4
Anterior-posterior corrections, 182 adverse oral effects, 338t Asymptomatic irreversible pulpitis, 3
Anterior-posterior palatal bars, 354 enzyme targets, 336t Atomoxetine, 192
Anterior-posterior palatal strap, 354 mechanisms, 335 Atria, conduction velocity (reduction), 317
Anterior primary teeth, restoration, 195-196 Anti-Parkinson drugs, 307-308 Atrioventricular (AV) nodal conduction rate,
Anterior segment, 210 action, mechanisms, 307-308 reduction, 317
Anterior spacing, 177-178 adverse effects, 308 At-risk patients, antibiotic prophylaxis, 208
Anterior teeth, eruption (symmetry), 199 dental implications, 308 Atropine, 300
Antianginal drugs, 321-322 indications, 308 Attention-Deficit Hypersensitivity Disorder
nitrates/nitrites, 322 therapy, strategies, 307 (ADHD), 192
types, 321-322 types, 307 Attrition, 252
Antiarrhythmic actions, 317 Antiplatelet drugs, 323 treatment, 46
Antiarrhythmic drugs, 317-319 Antipsychotic drugs, 302 Atypical beta-lactams, 332
adverse effects, 318-319 action, mechanism, 302 Autoclaving, 231
classes/actions, 317 adverse effects, 302 Autogenous grafts, obtaining, 277
elimination half-lives, 319t adverse motor effects, 302 Autograft, 277
general uses, 318 drugs, 302 biocompatibility, 83
Antiasthma drugs, 325t effects, 302, 302t Autonomic nerves, 295f
Antibacterial drugs, 330-334 indications, 302 Autonomic pharmacology, 294-301
action, mechanisms, 331t Antisepsis, 232 Autonomics, 300
adverse effects, 331t Antiseptics, 281-282 Average closing rotation, 157
Antibiotic prophylaxis, 208 Antituberculosis drugs, 334 Averse conditioning, 191
Antibiotics, 281-282 Antiulcer drugs, action (mechanisms), Avulsion, 24-25
local delivery, 282 324f endodontic treatment, 25
Antibiotic sensitivity testing, indications, 98b Antiviral drugs, 334-335 exarticulation, 24-25
Anticancer drugs action, mechanism, 336t management, 25
adverse effects, 337t indications, 335t reimplantation, 25
cell cycle sites, 337f Anxiety, 242 treatment, 25
impact, 336f control, 242-244 Axial walls
Anticholinergic drugs, 357 Apexification, 29-30 depth, 59f
Anticholinesterases, 299-300 Apex locator readings (perforation symptom), taper, minimum, 356
effects, 300t 20 Aztreonam, 332
Anticipatory guidance, 209 Aphthous ulcers, 114-115
Anticoagulants, 323 clinical types, 115b B
Antidepressant drugs, 302-303 minor aphthous ulcer, 114f Baby bottle syndrome, 210
action, 303b systemic diseases, 115t Baby bottle tooth decay, 218
contrasting mechanisms, 303 Apical diagnosis, 8t Bacitracin, 334
adverse effects, comparison, 303t Apical diseases, 3-5 Baclofen, 304-305
types, 302-303 classification, 4-5 Bacteremia, dental procedures (impact),
Antiemetics, 324 definition, 3-5 208t
Antiepileptic drugs, 305-307 Apical injuries, 21-22 Bacteria
action, mechanisms, 306 Apical lesions, occurrence (absence), 4 adhesion/attachment, 257
adverse effects, 306 Apically displaced flap, 274 characteristics, 257-258
carbamazepine, 306-307 Apical neurovascular supply damage, 26 phases, 257
indications, 307t Apical pathosis, 31 Bacterial challenge, control, 262
pharmacokinetics, 306 impact, 16 Bacterial clearance, 36
Antiflux, 367 Apical radiolucencies, radiographic Bacterial colonization, occurrence, 208
Antifungal drugs, 334 differential diagnosis, 9-10 Bacterial endocarditis, prevention (antibiotic
comparison, 334t Apical root fracture, 24 prophylaxis guidelines), 333t
indications, 335t Apical surgery, 14 Bacterial infections, 113-114
Anti-GERD drugs, action (mechanisms), 324f Apicoectomy, 14 Bacterial plaque, removal, 272
Antihistamines, 304-305, 313-317 Apomorphine, 307 Bactericidal drugs, 282
usage, 312 Appliances, types, 170-171 Bacteriostatic drugs, 282
Antihypertensive drugs, 319-321 Apposition, 185 Balanced anesthesia, 312-313
action, sites, 320f Arachidonic acid, pathways, 314f Balanced Budget Act of 1997, 235
dental implications, 321 Arbitrary facebow, 345 Balanced occlusion, 350
Index 457
Ball clasps, 199 Bisphosphonate-related osteonecrosis of the Burs, 50

Band-loop space (BLS) maintainer, 199 jaws (BRONJ), 98-99, 129-130 classification systems, 50
Bands, 174 diagnosis, 99 shape, 50
Barbed broaches, 12 oral bisphosphonates, intravenous Buspirone, 304-305
Barbiturates, 304-305 bisphosphonates (differences), 99
benzodiazepines, comparison, 305t overview, 98-99 C
Barrier techniques, 230 patient management, 99 Calcification, 185-187
Basal cell carcinoma, 118 treatment recommendations, 99b small foci, induction, 260
Baseline data, collection, 241 Bisphosphonates, 329 Calcific metamorphosis (pulp canal
Base metal alloys, 360 Blastomycosis, 114 obliteration), 26, 205
Bases, 61-62 Blood Calcified canals, location, 17
Basic statistics, 226-229 dyscrasias, 267 Calcifying epithelial odontogenic tumor
Bass brushing, 286 gingival enlargements, association, 285 (Pindborg tumor), 126
method, 286f lipid disorders, drug Calcitonin, 328-329
Beading, 354 actions, 322-323 Calcium channel blockers, 318, 321
Behavior usage, 322-323 Calcium hydroxide, 13
change theory, 239-240 neutrophil exit, 262f usage, 29
incompatibility, 242 Blood-borne pathogens, OSHA standard, Calcium metabolism, drugs (impact),
management techniques/strategies, 230-231 328-329
191-192 Blood:gas solubility coefficient, 311 Calculus
reinforcement, 191 Blood vessels, dilation, 321 attachment, occurrence, 260
shaping, 191 Bodily movement, 166, 168 deposits, detection, 260
theory (ABC model), 240 pure translation, 170 mineralized bacterial plaque, 259-260
Behavior, change Body porcelain, 361 Campers line, 350
ability, consideration, 241 Bohns nodules, 125 Campylobacter rectus, 259
foundations, 240-241 Bolton discrepancy (tooth size discrepancies), Campylobacter species, 257
strategies, 241-242 180 Canal
Behavioral strategies, 241-242 Bonded amalgam restorations, 66 anatomy, 19
Behets syndrome, 115 Bonding, 174 bacterial status, 31
Benign connective tissue tumors, 118-120 adhesive systems, 67-68 treatment, separated instruments (usage),
Benign neoplasms, salivary gland diseases, procedure, 174 19-20
121-122 Bone Canal (nasopalatine) duct cyst, 111
Benign soft tissue lesions, 348 cells, drugs (impact), 329f Cancellous bone, radiographic anatomy,
Benzalkonium chloride, 61 grafts, 349 144-145
Benzocaine infection erosion, impact, 94f Cancellous marrow, density, 83f
amino terminus, absence, 310 loss, x-ray appearance, 253 Candida albicans, 349
topical anesthetic, 193 marble bone, 131 Candida albicans, 351
Benzodiazepines, 304-305 Pagets disease, 349 Candidiasis (thrush) (moniliasis), 114, 208,
adverse effects, 305 radiation effects, 136 351
barbiturates, comparison, 305t remodeling, absence, 131 predisposing factors, 114b
indications, 305 removal, 81 Canine protected occlusion, 364-365
pharmacologic effects, 305 types, 83f Capitation, 234
Benzotropine, 308 vascularity factors, 98b Capnocytophaga species, 257
Beta-adrenergic receptor blockers (beta von Recklinghausens disease, 128 Carbamazepine, 306-307
blockers), 298, 319, 321 Bone lesions (nonodontogenic lesions) Carbide burs, usage, 68
dental implications, 299 fibro-osseous lesions, 127 Carbidopa
Beta-lactamase inhibitors, 332 giant cell lesions, 127-129 action, sites, 308f
Beta particles, 132 inflammatory disease, 129-130 levodopa, combination, 307
Beta titanium archwire materials, 173 malignancies, 130 Carcinogenesis, 136-137
Beveled margins, objectives, 73 Bone morphogenetic protein (BMP), 83 Cardiac electrophysiology, 318f
Bicuspidization, 15 Botulinum toxin A (Botox), 301 Cardiovascular pharmacology, 317-323
Bilateral sagittal split osteotomy (BSSO), Brackets, 173 Caries, 28
182 positioning, 174 adults, risk-based interventions, 39t
Bile acid sequestrants, 323 Branchial cyst, 110 balance, 35-36, 38f
Bimanual manipulation technique, 344 Bremsstrahlung radiation, 133-134 cement base, insertion, 75f
Bimodal distribution, 226, 226f Brief interventions, 242-243 clinical diagnosis, 41f
Biogran, 277 Bristle brushes, usage, 274 clinical examination, 40-43
Biologic compatibility, 360 Broad-spectrum antibiotics, 98 clinical risk assignment, 38b
Biologic monitors, 231 Bromocriptine, 307 dental caries, 35-40
Biologic width, 285 Brown spots, 42 epidemiology, 218
violation, ramifications, 285f Brushing, usage, 223 high-risk patients, identification, 38
Bionator, 175 Bruxism, 282 initiation/progression, longitudinal
Bio-Oss, usage, 277 BSSO. See Bilateral sagittal split osteotomy sections, 37f
Biopsies, 99-100 Buccal eruption, 203 lesions, clinical examination, 43
overview, 99-100 Buccal object rule, 9, 17 objectives, 38-39
techniques, 99-100 Buccal shelf, 350 pathogenesis/diagnosis, 38
Biostatistics Buccal space, 96f prevention, 38-39
decision making, 228-229 Buccal vestibule, 350 radiographic appearance, 148-149
reliability, 228 Buccolingual dimensions, 356-357 radiographic caries, 42f
sensitivity, 228 Buckleys formocresol, 197 removal, 75f
specificity, 228-229 Buffering action, 36 sites, origination, 36f
test, sensitivity, 228 Buprenorphine, 314 status, 228t
validity, 228 Bur head shapes, 50f treatment overview, 39
Biperiden, 308 Burkitts lymphoma, 130 Carious lesions, impact, 136
Bisecting-angle techniques, 139 Burning mouth syndrome, 90-91 Carious pits, 42
458 Index
Carved amalgam, proximal portion Child behavior Class IV initial composite restorations,
(evaluation), 65 classification, 189-192 preparation designs, 61f
Carvedilol, 298 functional inquiry, 190 Class IV restorations, preparation designs, 60f
Carving occlusal margins, 64f management, dental setting, 189-192 Class V initial composite restorations,
Case-control study, 224 variables, 190 preparation designs, 61f
Case selection, 1-12 Children Class V restorations, preparation designs, 60f
Cast ceramic, 47 abuse/neglect, 211-212 Cleft lip developmental abnormality, 159
Casting, accuracy, 360 types, 212 Cleidocranial dysplasia, 130
Cast metal restorations, indications, 47 acute necrotizing ulcerative gingivitis, 205 Clindamycin, 333
Cast restorations adults, physiologic differences, 194 spectrum, 281
clinical examination, 44 blood pressures, 194t Clinical attachment loss, 252
delivery, 364 caries, epidemiology, 218 Clinical diagnosis, 1-12
Casts dental trauma, 205-207 Clinical examination, requirements, 40f
evaluation, 345 dosages, 192-195 Clinical factors, 270
mounting, 344 Frankl behavioral rating scale, 190 Clinical findings, summarizing, 253-254
Cathode, 132 frenum attachment, abnormality, 204-205 Clinical interviewing, 237-238
Cavitated lesions, restorations, 39 gingivitis, 204-205 Clinical trials, 224
Cavitation, process, 37f herpes simplex infection, 204 Closed model, 235
Cavities, checking (methods), 192 local anesthesia, 192-195 Closed questions, 238
Cavosurface margin, 58 techniques, 193 options, inclusion, 238
CBCT. See Cone-beam computed tomography minimal attached gingiva/recession, 204 Closing rotation, 157-158
C clasps, 199 nitrous oxide sedation, 194-195 Cobalt-chromium RDPs, fracture, 356
Cell kinetics, radiation (impact), 136 periodontal disease, 205 Cocaine, usage, 310
Cell surface adhesion receptors, 291 periodontal problems, 204-205 Coccidioidomycosis, 114
Cellular differentiation, occurrence, 167 puberty gingivitis, 204 Cognitive-behavioral interventions, usage, 243
Cellular radiation effects, 135 pulse rates, 194t Cognitive coping (reframing), 243
Cellulose wafers, 56 recurrent aphthous ulcer, 204 Coherent scattering, 134
Cemental dysplasia, 10 respiratory rates, 194t Cohort study, 224
Cement base, insertion, 75f restorative dentistry, 195-196 Cold test, 6
Cementifying fibroma, 126 Childrens Health Insurance Program (CHIP), Cold-working, 356
Cementoblastoma, 10, 126, 126f 235 Collar, 73
Cement-retained implant crown, 347 Chin cup (chin cap), 174-175, 179 usage, 138
Cements, action, 357 Chisels, intention, 48 Collimation, 134, 138
Cementum Chi-square (2) test, 228 Colonization, 257
radiographic anatomy, 144 Chloral hydrate, 304-305 Combination syndrome, 348
Centers for Disease Control and Prevention Chlorhexidine, 13, 61 Combined lesions, 255
(CDC), 236 availability, 282 Commitment talk, 242
Centers for Medicare and Medicaid Services Chloride channel, 304 Communication
(CMS), 235-236 GABA, usage, 304f listening techniques, 236
Central giant cell granuloma, 10, 128 Cholesterol absorption, inhibitors, 323 skills, 236-239
Central nervous system (CNS) pharmacology, Cholinergic agonists, muscarinic effects, 299 Community Periodontal Index of Treatment
302-308 Cholinergic drugs, dental implications, 300 Needs (CPITN), 218
Central odontogenic fibroma, 126 Cholinergic receptor agonists, 299, 299t Community trials, 224
Central tendency, measures, 226-227 Cholinesterase inhibitors, 300t Community water fluoridation, 219-220
Centric bearing cusps, metal thickness, 357 Chondrosarcoma, 130 Complementary metal oxide semiconductor
Centric occlusion, 344 Christensens phenomenon, 349 (CMOS), 142
Centric relation (CR), 344 Chronic aspirin toxicity, 315 Complementary treatment strategies, 272f
record, 349 Chronic heart failure, drugs (usage), 319 Complete buccal crossbite, 162
Cephalometrics (skeletal relationships), Chronic osteomyelitis, 129-130 Complete dentures, 344, 347-353
163-164 proliferative periosteitis, combination, 129 clinical examination, 347
landmarks, definitions, 164f Chronic periodontitis, 219, 256, 258 examination, 347-353
measures, 164-165 Chronic recurrent dislocation, occurrence, 92 fabrication, anatomic considerations,
radiographs, usage, 346 Cigarette smoking, risk factor, 264-266 350-351
Cephalosporins, 281, 332 Cingulum rest, 355 insertion/postinsertion, 352-353
generations, 332t Ciproflaxin, 282 optimal function, 348-349
Ceramic brackets, 173 Clasps phonetic considerations, 350
Cervical headgear, 179 assembly parts, function/position, 355t preprosthetic treatment, 348-349
Cervical-pull headgear, 174 selection guidelines, 355 radiographic examination, 348
Cervical resorption, 26 Classical conditioning, 240 Complete final maxillomandibular relation
Cevimeline, usage, 300 Class I composite incremental insertion, 71f procedures, 352-353
C fiber pain, 2 Class I elastics, 177 Complete lingual crossbite, 162
Chancre (primary lesion), 113 Class II amalgam tooth preparations, Complicated crown fractures, 23f
Change model, stages, 239 diagrams, 56f Complicated fractures, 22
Change talk, 242 Class II correction, impact, 181 Composite restorations, 69-72
Charge-coupled device (CCD), 142 Class II elastics, 177 clinical examination, 44
Charts, copies (provision), 246-247 Class III elastics, 177 clinical technique, 59-60
Checkerboard analyses, 257 Class III initial composite restorations, insertion, 70
Chdiak-Higashi syndrome, 261 preparation designs, 61f tooth preparation, 59-60
Cheek biting, 353 Class III malocclusion, 162 types, 69
Cheek trauma, 194 Class III restorations, preparation designs, usage, 62
Chemical burn, 111 60f Comprehensive treatment, 180-181
Chemical (cold) sterilization, 232 Class III treatment, impact, 181 stages, 180-181
Chemotaxins, 261 Class II malocclusion, 162 Compression side, 165-166
Chemotaxis, 262f Class I malocclusion, 162 Compromised host defenses, 97b
Cherubism, 128, 128f Class I normal occlusion, 162 Compton scattering, 134
Index 459
Computer-aided design/computer-aided Crowding, 177 Dental facility (Continued)

manufacturing (CAD/CAM), 47 obtaining, 211 infection control precautions, 231
Computer-generated onlays/inlays, 47 Crown fracture, 22 practice controls, 231
Concussion, 24 Crown movement, 170 Dental gypsum
Condensation silicone, 359 Crucibles, 367 classification, 366
Condensing osteitis (focal sclerosing Cryptococcosis, 114 products, particle size, 366
osteomyelitis), 129 Cultural factors, 240 Dental health maintenance organization
Condylar cartilage, development, 157 Culture sensitivity testing, indications, 98b (D-HMO), 234
Condyloma acuminatum (genital warts), 112 Curare-type drugs, 301 Dental history, 5-6, 251
Condylotomy, 93 Curare-type neuromuscular junction blockers, questions, 206
Cone-beam computed tomography (CBCT), 301t Dental implants, 258-259
10, 253 Curettes, usage, 272-273 Dental literature
Cone image shifting, 17 Curved canal, enlargement (excess), 19 descriptive epidemiology, 223
Confidentiality, 246-247 Cusp capping, rule, 54f evaluation, 223-229
Congenital absence (hypodontia), 187 Cusp counterbevel, 73 studies, types, 223-229
Congenitally absent teeth, 204 Cusp inclines, sharpness, 348f Dental managed care, 234-235
Congenital syphilis, 113 Custom-fabricated mouth guards, 208 Dental materials, 365-367
Connective tissue Custom incisal guide tables, 344 Dental pain, 243-244
cuff, blood supply (schematic illustration), Cutting Dental plaque
279f hand instruments, 47-49 bacterial biofilm, 257
tumors, types, 118-120 mechanisms, 50-51 biofilm formation, factors, 257
Conscious sedation, antihistamines (usage), Cutting instruments composition, 255-257
312 applications, 48 formation, phases, 257
Consent hazards, 51 Dental preferred provider organization
elements, 245 powered cutting instruments, 49 (D-PPO), 234
exceptions, 245 rotary cutting instruments, 49-50 Dental team, attire, 192
Consequences, alteration, 241 Cvek pulpotomy, 28-29 Dental trauma (children), 205-207
Contact allergies, 115 Cyclooxygenase (COX) etiology, 205-207
Contaminated waste, disposal, 232 COX-2 selective drugs, impact, 315 injury, 205-206
Contrangle air-turbine handpiece, air-water inhibition, 314 patient assessment, 206
supply line connection, 49f pathway, 314f reactions, 205
Control, internal locus, 241 Cystic ameloblastoma, 126 treatment, 206-207
Controlled (scheduled) substances, examples, Cysts Dental treatment plan, development, 44
338t classification, 101 Dental x-ray machine circuitry, components,
Controlled tipping, 170 surgical management, 100-102 133f
Cooperative patients, types, 189-190 Cytokines, 262-263 Dentigerous cyst, 124, 124f
Copper stem, 132 Dentin
Cores D bonding, 66-69
buildups, 357 Dantrolene, 301 demineralization, 37f
construction, 356 Decayed/Missing/Filled Surface (DMFS), 217 dysplasia, 131f, 189
Coronal caries (adults), 218 Decayed/Missing/Filled Teeth (DMFT), 217 fracture, 207
Coronal leakage, 30-31 Decision making, biostatistics, 228-229 microstructural features, 67
Coronal perforation, 20 Deep excavation, 55, 62 porcelain, 361
Coronal pulp tissue, removal, 197f Deep fascial spaces, borders, 95t radiographic anatomy, 144
Coronal root fracture, 22 Deep fungi, 114 Dentinal caries, 36
Coronoplasty, 283 Delaire-type facemask, 179f Dentinal pain, 2
Correlation coefficient, 227f Delivery models, 235 Dentinoenamel junction (DEJ), 44, 57
Correlation/correlation coefficient (r), 227 Demineralization, 35-36 lesions, 46
Corrosion, 252 Dendritic cells, 262 Dentinogenesis imperfecta, 131f, 189
resistance, 360 Denosumab, 329 Dentin-pulp complex, 28
Cortical anchorage, 172 Dens evaginatus, 187 Dentition
Cortical bone, quantity, 83f Dens invaginatus, 188 development, space management, 199-204
Cotton roll isolation, 56 Dental arches, dimensional changes, 161 mixed dentition, 199
Couples, 170 Dental burs, 50 primary dentition, 199
diagrammatic representation, 170f Dental care delivery systems, 234-236 Dentition, calcification/eruption, 185-187
Coxsackievirus infections, 112 Dental caries, 35-40 Dentoalveolar injuries, classification, 84b
CR. See Centric relation balance, 35-36 Dentoalveolar surgery, 79-83
Cracked tooth syndrome, 10-11 definition, 35 alveoplasty, 82
clinical features, 10-11 etiology, 35-38 contraindications, 80
diagnosis, 10 objective, 35-38 impacted teeth, classifications, 80
incidence, 10 plaque hypothesis, 36 radiographic examination, 80
prognosis, 10 prevention, community/preventive surgical extractions, 80
radiographic evidence, 10 measures, 220t indications, 80
treatment, 10 Streptococcus mutans (impact), 36 surgical impactions, 80
Cranial base, 156 teeth, examination, 251-252 surgical principles, 80-82
synchrondroses, diagrammatic Dental development, 159-161 Dentrifice-associated slough, 111
representation, 156f Dental extractions Dentures
Cranial vault, 156-158 bleeding complication, 82 base resins, chemical composition, 356
Craniofacial complex, growth sites, 156-158 indications, 79 impression surface, factors, 351
Crevicular incision, 274 Dental facility removal, 351
Cromolyn, 324 compliance, methods, 231 resilient liners, 351-352
Crossbite, 162 engineering controls, 231 retention, 351
elastics, 177 exposure control plan, 231 support, 351
Cross-linking, degree, 356 exposure determination, 231 Deoxyribonucleic acid (DNA), DNA-DNA
Cross-sectional studies, 223-224 implementation schedule, 231 hybridization, 257
460 Index
Department of Health and Human Services Distress scale, subjective unit, 243 Embryonic craniofacial development, stages,
(DHHS), 235-236 Distribution 159t
Depolarizing noncompetitive blockers, 301 bimodal distribution, 226 Emergence profile, 357
Dermoid cyst, 110 drugs, 292-293 Emotional abuse/neglect, 212
Descriptive epidemiology, 223 frequency distribution, 226 Empathy, 237-238
Descriptive statistics, 226 normal distribution, 226 Enamel
Desflurane, 312 skewed distribution, 226 bonding, 66-69
Detailing, 180 Diuretics, 317-323 caries, 36
Developing dentition, space management, actions, sites, 322f etching, 68, 174
199-204 loop diuretics, 322 fracture, 22, 207
Developmental abnormalities, 159 Documentation, 246 hatchets, 48
Developmental cysts, 10 Dopamine, 308 hypocalcification, 189
Developmental defects, 251-252 Dopaminergic cell groups, 302t hypoplasia, 188-189
Developmental jaw cysts, 110-111 Doripenem, 332 microstructural features, 67
Developmental soft tissue cysts, 110 Doses, recommendations, 192t prophylaxis, pumice (usage), 174
Dextromethorphan, 314 Dosimetry, 134 radiographic anatomy, 143
Diabetes, 266 Double-ended instruments, 48 Endochondral bone formation, 156
DIAGNOdent (laser fluorescence), 40 example, 48f intramembranous bone formation,
Diagnosis, 40-47, 251-255 Down syndrome, 267 differences, 156
treatment planning, 343-347 Drainage, 13-15 Endocrine pharmacology, 324-330
Diagnostic impressions/casts, 344-345 indications, 14 Endodontically treated teeth
Diagnostic radiographs, 17-18 Droplets, usage, 229 coronal leakage, 30-31
Diagnostic tests, sensitivity/specificity, 229t Drug-drug interactions, 293-294 ferrule, 30
Diamond abrasive instruments, 50 examples, 294t restoration, 30-31
terminology, 50 genetics/pharmacology, 293 structural considerations, 30-31
Diamond cutting instruments, shapes/designs, Drugs Endodontic diagnosis, 5-6
51f abbreviations/definitions/receptors, dental history, 5-6
Diamond particle factors, 50 295-296 medical history (developing data), 5
Diaphragmatic (paced) breathing/relaxation, actions, targets, 291 patient, triage, 5-6
usage, 243 adverse reactions, 293 Endodontic emergencies, 15-16
Diet, impact, 225 allergy, 293 categories, 15-16
Differential diagnosis, 150 antiepileptic mechanisms, 306t definition, 15-16
Differential nerve blockade, 102-103 classes, mnemonics, 290-291 treatment, 16
Diffuse sclerosing osteomyelitis, 129 clinical testing, 294 Endodontic examination/testing, 6-10
Diffusion hypoxia, 195 dose-response relationships, 291-292 Endodontic failure, 31
Digital detectors, 142 idiosyncratic reaction, 293, 294t causes, 32
characteristics, 142 legislation, 294 Endodontic lesions
Digital image display, 142 legislative acts, 295t periodontitis, association, 255
Digital imaging, 141-142 metabolism, 292-293 types, 11-12
analog imaging, differences, 141-142 occurrence, 292 Endodontic pain, orofacial diseases
Digital imaging fiberoptic transillumination reactions, types, 292 (mimicry), 5
(DIFOTI), 40 plasma concentration, semilog plot, 293f Endodontic pathosis, differential diagnosis,
Digitalis, 319 pregnancy, relationship, 294 17-18
action, 319f side effect, 293 Endodontic-periodontal lesions, 255
adverse effects, 319 testing phases, 294t Endodontic-periodontal relationships, 11-12
Digit-sucking habits, 209 toxicity, 293 Endodontic radiographic anatomy, 17-18
Dilaceration, 188 unequal distribution, 292f Endodontics
Diphenhydramine, 308 Dry heat sterilization, 16 microbiology, 18
Diphenoxylate, 314 Dry-heat sterilization, 231 success, principles, 31
Direct composite restorations, indications, 47 Endodontic success, 31
Direct contact, 229 E rate, factors, 31
Direct dopamine receptor agonists, 308 Early childhood caries (ECC), 210, 218 Endodontic term, usage, 1
Direct genetic control, 156 AAPD definition, 210 Endodontic treatment, 55
Direct pulp cap, 28, 197 definition, 210 procedures, 12-18
Direct retainer, 354-355 Early Periodic Screening Diagnostic and Endoperiodontal problems, types
types, 355 Treatment (EPSDT), 235 (diagrammatic representation), 255f
Direct thrombin inhibitors, 323 Ears, precautions, 51 Endorcine pharmacology, 324-330
Disc displacement disorders, 91 Ecologic plaque hypothesis, 258 Endosteal implant, 345-347
Discoloration, causes, 30 periodontal diseases, relationship, 258f Enflurane, 312
Discolored teeth, bleaching, 30 Ectopic eruption, 178, 199-200 Engaging (motivational learning), 242
Disc repair/removal (discectomy), 93 mandibular permanent central incisors, Entacapone, 308
Disc repositioning surgery (open 200f Environmental contaminants, 232-233
arthroplasty), 93 Ectopic permanent molars, eruption, 202-203 Environmental growth control, 156
Diseases, 229-232 Ectopic premolars, 203 Enzyme-linked immunosorbent assay
Disinfectants, 281-282 EDTA. See Ethylenediamine tetraacetic acid (ELISA), 229
Disinfection, 17, 232 Elastic impression materials, 360t Epidemiology, 217-219
Dispersion, measures, 227 Elasticity, high modulus, 360 measures, 217-218
Displacement injuries, 24 Elastics, 177 Epidermolysis bullosa, 130
Distal extension RDPs, 356 Electrical conductance, 40 Epigenetic growth control, 156
Distal step, 160 Electrical pulp tests, 8 Epinephrine reversal, 298
Disto-occlusal preparation, proposed outline, technique, 8 Epinephrine usage, 324
72f Electromagnetic radiation, 132 Epitactic concept, 260
Distraction, 243 Electrosurgery, 359 Epithelial attachment, histologic scheme, 278f
Distraction osteogenesis (DO), 83, 87 Emancipated minors, sliding scale, 245 Epstein-Barr virus (EBV), 112-114
Distractor appliance, usage, 90f Embedded, term (usage), 80 infections, 113
Index 461
Epulis fissurata, 348 Fluoroquinolones, 334

Equipment, safety, 232-234 F Flush terminal plaque, 160
ADA Council on Scientific Affairs Facebow transfer, 365 Focal epithelial hyperplasia (Hecks disease),
recommendations, 232 Facial asymmetry, treatment, 179 112-113
Equivalent force systems, 170 Facial convexity, 163 Focal fibrous hyperplasia, 119
Ergot alkaloids, 316 Facial esthetics/proportions, 155 Focal (frictional) hyperkeratosis, 111
Erosion, 252 Facial fractures, 84 Focal sclerosing osteomyelitis (condensing
treatment, 46 Facial pain, 87-91 osteitis), 129
Ertapenem, 332 differential diagnosis, 87 Focal trough, 150
Eruption Facial proportions, 86f Focusing (motivational interviewing), 242
cyst, 124 Facial (lingual) smooth-surface caries, Fondaparinux, 323
obstruction, supernumerary tooth (impact), presence, 43 Force-deflection curve, 172f
185f Factitious traumatic lesions, 255 Force system, 165
problems, 178 Fact witnesses, usage, 247 equivalent force systems, 170
sequence, 161 False negative (FN), 228 Fordyce granules, 109
Erythema multiforme, 115 False readings, causes, 8 Foreign body reactions, occurrence, 255
Erythromycin, 282 Fascial spaces, 94 Formocresol pulpotomy, pulp tissue zones,
Erythroplakia (erythroplasia), 117, 117b Fat, liposarcoma, 120 198f
Esters FDP. See Fixed dental prosthesis Forsus Fatigue Resistant Device, 175
allergies, 310 Feedback, provision, 242 Foundation restorations, 356
metabolism, 310 Fee schedules, 234 Fourth-generation systems, 67-68
Estrogens, 329 Feldspathic porcelain, 47 Fracture
Etch-and-rinse three-step systems Fentanyl, 314 injuries, 22-24
(multibottle/fourth-generation systems), congeners, 314 lines, detection, 43
67-68 Ferric sulfate/ferric chloride, 359 resistance (increase), ferrule (impact), 30
Etch-and-rinse two systems (one-bottle/ Ferrule, 30 Frankl behavioral rating scale, 190
fifth-generation systems), 68 Fertility drugs, 330 Free gingival graft, 348
Ethical principles, 246 Fibric acid derivatives, 322 Frenectomy, 348
Ethmoid bones, 156 Fibromatosis, 119 Frenum attachment
Ethosuximide, 307 Fibromyxoma (odontogenic myxoma), 126 abnormality, 204-205
Ethyl alcohol, 304-305 Fibro-osseous lesions, 127 problem, 275
Ethylenediamine tetraacetic acid (EDTA), Fibrous dysplasia, 127 Frequency distribution, 226
13 Fibrous lesions, 119 Fricatives, 350
Ethylene oxide (Chemiclave), 231-232 Fibrous maxillary tuberosity, 348 Frictional (focal) hyperkeratosis, 111
Etiology, 255-260 Fifth-generation systems, 68 Full-mouth radiographs, 165
Eubacterium species, 259 Filtration, 134 Full-thickness flap
Eutectic mixture of local anesthetics (EMLA), Fine-needle aspiration, 100 horizontal incisions, 274
310 Finishing, 180 reflection, 282
Event sampling, 241 Finish lines, smoothness, 356 vertical incisions, 274
Evoking (motivational interviewing), 242 First-generation histamine receptor blockers, Fully adjustable articulators, 345
Ewings sarcoma, 130 comparison, 317 Functional appliances, 175
Examination, 40-47 First premolars, eruption, 202f Functional inquiry, 190
Exarticulation (avulsion), 24-25 Fissured tongue, 110 Functional matrix theory, 156
Excavations, 62 Fissure sealants, 212 Fungal infections, 114
Excavators, subdivisions, 48 Fistula, 196 Furcal perforation, 20
Excisional biopsy, 100 Fixed appliances, 173-177 Furcation
Excretion (drugs), 292-293 completion, 180-181 assessment, 253
occurrence, 293 Fixed dental prosthesis (FDP), 343-347 involvements, classification, 253
Exenatide, 327 connectors, 357 radiolucency, 196
Exfoliation, occurrence, 199 nonrigid connector, 357 Fusobacterium nucleatum, 259
Exostoses, 110 rigid connectors, 357 impact, 257
Exothermia, 366 Fixed digit sucking appliance, 209f
Experimental design, 225 Fixed kiddie partial, 200f G
Experimental epidemiology, 224 Fixed prosthodontics, 356-367 Gabapentin, 307
Expert testimony, usage, 247 Fixed retainers, 181 Gamma-aminobutyric acid (GAB), effect
Exploratory strokes, 273 Flaps, 100 (enhancement), 304
Exposure classification, 274 Gardners syndrome, 130
incident/follow-up, 231 design, 14, 274 Garrs osteomyelitis, 129
time, 134 Flare-ups, 16 Gases, environmental contaminants, 232
Extended-shank curettes, 273 Flecainide, 318 Gastrointestinal disorders (treatment), drugs
External oblique ridge, 148 Florid osseous dysplasia, 127 (usage), 323-324
External root resorption, 26t Fluid control, 357-359 Gastrointestinal pharmacology, 323-324
internal root resorption, differences, 27t Flumazenil, 304 Gate-control theory, 243
External walls, finishing, 55 Fluorescence, 361 Gates-Gliddon instrument, 12
Extinction, 242 Fluoride General anesthetics, 310-313
Extracoronal retainer, 355 drops, 221 action, mechanism, 311
Extraction, 196 foams, 222 drugs, 311
indications, 180 gels, 222-223 properties, terms (application), 311
Extraoral examination, 6 mouth rinse, 221 stages, 311
Extrusion (primary teeth), 207 rinses, 39 Generalized aggressive periodontitis, 205
Extrusion arch, 176 supplements, 221 Generalized gingival hyperplasia, 119
Extrusive luxation, 24 usage, 38 systemic modifying factors, 119b
Eyes varnishes, 222 Generalized spacing, 178
autonomics, 300 Fluoride supplementation schedule, basis, Genial tubercles, 146-147
precautions, 51 209t Genioplasty, 182
462 Index
Genital warts (condyloma acuminatum), 112 Growth (Continued) Hepatitis B virus (HBV), 229
Geographic tongue, 110, 110f predictions, basis, 158 diagnosis, 229
Germination, 187 predictors, 158-159 etiology, 229
primary mandibular lateral incisor, 188f Scammons curves, 158 prevention, 229
Ghost images, 150 sex differences, 158 transmission, risk, 229
Giant cell arteritis (temporal arteritis), timing, 158-159 Hepatitis C virus (HCV), 229
presenting symptoms, 91 velocity curve, 158 diagnosis, 229
Giant cell lesions, 127-129 Guanethidine/guanadrel, 299 etiology, 229
Gingiva attachment, width (increase), 275 Guided imagery, 243 prevention, 229
Gingival abscesses, 284 Guided tissue regeneration (GTR), 277 transmission risk, 229
Gingival ameloblastoma, 126 Guide planes, 356 Herbst appliance, 175
Gingival bevel, 73 Gum pad stage, 159-160 Hereditary conditions, 130-132
Gingival cysts (newborns), 125 Gutta-percha, 13 Hereditary ectodermal dysplasia, 130, 131f
Gingival disease, 253 Gypsum, 366-367 Hereditary hemorrhagic telangiectasia, 130
malnutrition, impact, 254 setting expansion, 366 Heroin, 314
modification Gypsum-bonded investments, usage, 367 Herpangina, 112
medications, impact, 254 Herpes infections, 112t
systemic factors, impact, 254 H Herpes simplex infection, 204
Gingival enlargements, 285 Haas appliance, 176 Herpes simplex virus (HSV), 112-114
blood dyscrasias, association, 285 Hairy leukoplakia, 113, 113f Herpes zoster, 112
Gingival excess (removal), amalgam knives Hairy tongue, 111 Heterogenous nucleation, 260
(usage), 65f Halogen-containing anesthetics, 312 High-energy electrons, production, 133
Gingival graft, healing, 282 Halothane, 312 High noble alloys, 360
Gingival index (GI), 217-218 Hand-foot-and-mouth disease, 112 High-pull headgear, 174
Gingival margin trimmers, 48 Hand-held casts, 345 High-voltage transformer, potential difference
Gingival recession, 252-253 Hand instruments, 47-49 generation, 133
Gingival show on smile, 163 techniques, 48-49 High-volume evacuation systems, 232
Gingival surgery, 274-275 Hand signals, usage, 243 His-Purkinje automaticity, reduction, 317
Gingival tissues, attachment, 277-279 Hangover, risk, 305 Histamine, 316-317
Gingiva/recession, attached (minimum), 204 Hard bristle toothbrushes, usage, 286 H1 receptor blockers, 317
Gingivectomy, 274-275 Hard tissues H2 receptor blockers, 317
Gingivitis, 204-205, 219, 261 biopsy techniques, 100 receptor
clinical features, 254-255 graft materials, usage, 277 blockers, 316f
histologic stages, 264b injury, initial assessment, 206 mechanisms/effects, 316t
pathogenesis, 263 surgery, 349 Histoplasmosis, 114
Gingivoplasty, 275 trephination, indications, 14 HMG-CoA reductase inhibitors (statins),
Glass-ionomer cement, adherence, 364 Hawley retainer, 181 322-323
Glazing, 361 Hawley-type removable appliance, jackscrew Hoes, 48
Globulomaxillary lesion, 111 (usage), 176 Holding instruments, 273
Gloves, usage, 230 Hazardous chemicals, 233-234 Horizontal bone loss, 149
Glucocorticoids Head Horizontal control, 173
actions, 327-328 alignment, 150 Horizontal root fracture, 22-24
adverse effects, 328 deep fascial spaces, borders, 95t biologic consequences, 22
dental applications, 328 Headaches, differential diagnoses, 92t diagnosis, 22
potencies, 327 Headgear, 174-175, 179 treatment, 22-24
uses, 328 Health behavior Host modulation, 280-281
Glutaraldehyde, 61 change, 239-242 Host response cells, 261-262
Glycopyrrolate, 359 understanding, 240 Howships lacunae, 165-166
Gold inlay restorations, 72-73 Health belief model, 239-240 Hue, 361
clinical procedure, 72-73 Health physics, 137-138 Human biologic width, 285f
definition, 72 Health Resources and Services Administration Human immunodeficiency virus (HIV), 229
requirements, 72 (HRSA), 236 diagnosis, 229
tooth preparation, 73 Heart etiology, 229
Gonorrhea, 113 anatomic sites, 317 prevention, 229
Gow-Gates technique, 105-106 arrhythmias, 317-319 transmission risk, 229
Gowns, usage, 230 failure (acute treatment), drugs (usage), Human papillomavirus (HPV) infections,
G protein-linked receptors, 291 319 112-114
Gracey curettes (area-specific curettes), failure (treatment), drugs Hybrid composites, 69
272-273 action, mechanisms, 319 Hydroxyapatite, 349
Granular cell tumor, 119-120, 119f usage, 319 Hydroxyethylmethacrylate (HEMA), 61
Greater palatine, 104 Heat test, 6 application, 67
Grooves Heavy force, 166 Hyperalgesia, 2
boxes, addition, 357 Heavy metals, 267-268 Hyperglycemia, impact, 266
extension bevel, 73 Hecks disease (focal epithelial hyperplasia), Hypermobile ridge, 348
usage, 357 112-113 Hyperparathyroidism (bone, von
Group function occlusion, 365 Hedstrom files, 12 Recklinghausens disease), 128
Growth, 156-159 Hemangioma, 110 Hyperplastic pulpitis, 3
absence, 182 Hemisection, 14-15 Hyperplastic scar, 119
cephalocaudal gradient, 158-159 indications, 14 Hypersensitivity, 252
cephalometric radiographs, 159 procedure, 14-15 Hypertension, drug treatment, 319-321
control, theories, 156 surgical division, 14 Hypodontia (congenital absence), 187
directions, 159 Hemorrhage (perforation symptom), 20 Hypothyroidism
modification, 179 Heparin, 323 cause, iodine deficiency (impact), 325
timing, 179 action sites, 323f treatment, drugs (usage), 325
plotting, 159f Hepatitis B vaccination, 231 Hyrax appliance (banded type), 176
Index 463
Injectable anesthetics, 312 Irreversible pulpitis, management, 16

I Injuries Irrigation, 13
Iatrogenic traumatic lesions, 255 displacement injuries, 24 Irritation fibroma, 119
Idiopathic leukoplakia, 117, 117b fracture injuries, 22-24 Isoflurane, 312
Image layer, three-dimensional curved zone, types, 22-24 Isolation devices, 56
150 Instruments, sharpening, 273
Image receptors, 150 Instrument separation, 19-20 J
Image shape distortion, minimization, 139 avoidance, 19 Jackscrew, usage, 176
Image size distortion, minimization, 139 definition, 19-20 Jaws
Immediate dentures, 352 process, 19 bisphosphonate-related osteonecrosis, 98-99
Immunity, compromise, 208 Insulin, 325-327 cysts, treatment, 101t
Immunization, 231 action, mechanism, 327f metastatic malignancies, 130b
Impacted teeth effects, 325 neuropathology/osteonecrosis, 87-91
angulation, 80 preparations, 326t profile convexity/concavity, 163f
classifications, 80 Intensifying screens, 138-139 tumors, 101-102
Pell and Gregory classification, 80 Intentional reimplantation, 15 primary treatment modalities, 102t
Impaction surgery Interarch, 180 types, 102t
difficulty, factors, 81b discrepancies, 162 J-hook headgear, 174
factors, 81b Intercuspal position, maximum, 344
Impedance measurement, 40 Interdental cleaning, 223 K
Implants Interdental incision, 274 Kaposis sarcoma, 120
attachment, 347f Interdisciplinary treatment, 181-182 Kennedy classification system, 353-356
biologic complications, 279 sequence, 182 application, Applegates rules (impact),
clinical applications/evaluations, 279 Intermaxillary elastics, 177 353-354
complications, types/prevalence, 279 Intermaxillary suture, 145 Kennedy class III arch forms, 355
contraindications, 279 Internal bleaching techniques, 30 Ketamine, 312
implant-supported prosthesis, 344 Internal hemorrhage, 205 K-files, 12
placement, guidelines, 347 Internal resorption, 3 Kidneys
minimum distances, 346f Internal root resorption, external root diuretic drugs, impact, 322
placement, 346-347 resorption (differences), 27t excretion, occurrence, 293
anatomic limitations, 83t International normalized ratio (INR), 323 Killing, processes, 262f
posttreatment evaluation/management, 279 Interocclusal appliance therapy, 283 Kilovoltage, 134
risk factors, 279 Interocclusal records, 344 Kinematic facebows, 345
therapy, risk factors/contraindications, 280t Interpersonal skills, 236-239
types, 345-347 Interpretation, usage, 236 L
Impression materials, 359 Interproximal bone, 276 Labial bar (swinglock), 354
Incidence, 223 Interproximal cleaning, 286 Labiodental sounds, 350
Incident report, 245 Interproximal contact, location, 285-286 Lactation, local anesthetics (impact), 104
Incipient lesions, treatment, 44-46 Interproximal reduction (IPR), 180 Lamina dura, radiographic anatomy, 144
Incisal porcelain, 361 Interpupillary line, 350 Langer curettes, 273
Incisal rest, 356 Interviewing Langerhans cell disease, 128-129, 128f
Incisional biopsy, 100 motivational interviewing, 242 classification, 128b
Incisions, 13-15 techniques, 238 Laser equipment, 49
indications, 14 Intestinal polyps, 130 Laser fluorescence (DIAGNOdent), 40
Incisive foramen, 145 Intestine, cholesterol absorption (inhibitors), Lateral cephalometric radiograph, 87f
Incisors 323 Lateral fossa, 145
loss, 199-200 Intraarch, 180 Lateral luxation, 24
measurements, 211t Intracellular nuclear receptors, 291 Lateral periodontal cyst, 9, 124
restoration, 195-196 Intracellular structures, radiation (impact), Lateral pharyngeal space, location, 97f
Incisor show at rest, 163 135 Latin abbreviations, 338t
Indian Health Service (IHS), 236 Intracoronal bleaching techniques, 30 Laundry list questions, usage, 238
Indirect contact, 229 Intracoronal retainer, 355 Laxatives, mechanisms, 324f
Indirect pulp cap, 28, 197 Intramaxillary elastics, 177 Leaded aprons, usage, 138
Indirect retainer, 355 Intramembranous bone formation, 156 Leading questions, 238
Indirect tooth-colored restorations, endochondral bone formation, differences, Leaf gauge, usage, 344
indications, 47 156 Ledge
Indwelling vascular catheters, 208 Intraoral diagnostic tests, 6-10 definition, 18-19
Infection control, 142-143, 229-232 Intraoral endodontic examination, 6-10 formation, 18-19
precautions, 231 Intraoral radiographic examinations, 143 correction, 19
Infection source, location, 7f quality, criteria, 143 occurrence, reasons, 19
Infectious sialadenitis, 121 Intraoral radiographic techniques, 143f prognosis, 19
Infectious waste, disposal, 232 Intraoral radiographs, usage, 148 Leeway space, 160
Inferential statistics, 227-228 Intraoral x-ray film, 138 Le Fort midfacial fractures, 85f
Inferior alveolar nerve Intraosseous biopsy techniques, 100 Leiomyosarcoma, 120
block (mandibular block), 105, 193 Intrusion, 166, 206-207 Leukemias, 123-124
trauma, occurrence, 82 arch, 176 incidence, increase, 136
Inferior repositioning, 182 Intrusive luxation, 24 Leukocyte adhesion deficiency, 261
Inflammation, resolution, 261 Inverse square law, 134 Leukoedema, 109
Inflammatory diseases, 129-130 Inverted cone bur, 50 Leukotriene pathway modifiers, 324
Inflammatory resorption, 26 Investments, expansion, 367 Leveling (overbite correction), 180
Inflammatory root resorption, replacement Iodides, 325 Levodopa, 308
root resorption (differences), 28 Ion channel receptors, 291 carbidopa, combination, 307
Informed consent, 244-245 Ionization, 132 Lichen planus, 115-116, 115f
Infrabulge, 355 Ionizing radiation, 132 Lidocaine, 309f, 318
Inhalation precaution, 51 Irreversible hydrocolloid/alginate, 344 urinary metabolite, 309
464 Index
Light force, 166-167 Lower incisor angulation, 164 Mandibular growth, 158
Linea alba, 111 Lower incisors rotation, 157-158
Liners, 61-62 alignment, 181 Mandibular intercanine width, increase, 161
Lingual bar, 354 position, 183f Mandibular labial frenum, 350
Lingual crossbite, 162 Lower lingual arch, 176 Mandibular midline, shift, 200f
Lingual eruption, 203 Lower lingual holding arch (LLHA), 199, 201 Mandibular permanent central incisors,
Lingual frenum (tongue tie), 205 Low-molecular-weight heparins, 323 ectopic eruption, 200f
area, 351 Lupus erythematosus, 116 Mandibular plane angle, 164
Lingual holding arch Luting agents (cements) Mandibular primary anterior teeth, 193
impact, 202f comparison, 365t Mandibular primary intermolar width,
usage, 202f types, indications/contraindications, 366t increase, 161
Lingual nerve block, 193 usage, 364 Mandibular second primary molar, mesial
Lingual plate, 354 Luxation, 24 tipping, 197f
Lingual (facial) smooth-surface caries, Lymphangioma, 110 Mandibular surgery, 87
presence, 43 Lymphocytes, 262 MARA. See Mandibular anterior repositioning
Lingual thyroid, 109 Lymphoid neoplasms, 122-124 appliance
Lingual vestibuloplasty, 349 Lymphomas, 123b, 123f Marble bone, 131
Linguoalveolar sounds, 350 Non-Hodgkins lymphoma, 123 Marginal gap/ditching, 43
Linguodental sounds, 350 Marginal ridge fractures, causes, 65-66
Lipoxygenase enzymes, 314f M Marginal voids, 65
Lips MAC. See Minimum alveolar concentration Margins, preparation, 356
bumper, 176 Macrodontia, 187 Masks, usage, 230
pits, 109 Macrofilled composites, 69 Masseter area, 350
posture/competence, 162-163 Macroglossia, 109 Mast cells, 261
prominence, 163 causes, 110b Masticator space, boundaries, 96f
trauma, 194 Macrolide antibiotics, 332 Materia alba, concentration, 260
Liraglutide, 327 Macrolides, comparison/adverse effects, 332t Materials, safety, 232-234
Listening Macrophages, 261 ADA Council on Scientific Affairs,
communication, 236-239 Magnetostrictive ultrasonic instruments, 273 recommendations, 232
techniques, 236 Maintenance, 286-287 Material safety data sheets (MSDSs), 233-234
Liver, drug metabolism (occurrence), 292 Major salivary glands, metabolic enlargement, Maternal anxiety, 190
Local anesthesia/anesthetics, 102-106, 192t, 121 Matrix metalloproteinases (MMPs), 252f, 261
308-310 Malignant ameloblastoma, 126 Matrix placement, 63, 70
action, mechanism, 309 Malignant connective tissue tumors, 120 Matrix stabilization, 63, 70
cardiovascular effects/receptor preferences, Malignant peripheral nerve sheath tumor Matter, x-rays (interactions), 134
309 (neurosarcoma), 120 Maxilla, 156-157
chemistry, 309 Malignant tumors, 101 anterior-posterior position, 164
complications, 193-194 salivary gland diseases, 122 growth curves, 158f
drug-drug interactions, 310 Malnutrition, impact, 254 radiographic anatomy, 145-146
drugs, 308 Malocclusion, 260 zygomatic process, 146
overview, 102-104 crowding, 155-156 Maxillary anterior primary teeth, size, 160
effects, 309-310 epidemiology, 155-156 Maxillary arch eruption sequence, 161
greater palatine, 104 prevalence, 155-156 Maxillary cast, relationship, 365
mandibular techniques, 105-106 Management strategies, 242-243 Maxillary complete denture, support, 350
metabolism, 309 Mandible, 146-148, 157-158 Maxillary constriction, 182
needles, dimensions, 104-106 anterior-posterior position, 164 Maxillary deficiency, treatment, 179
nerve fibers, relative sensitivity, 310b diagnostic radiolucency, 110 Maxillary denture, limiting structures, 350
nerve sensitivity, 309 fractures, 84-85 Maxillary expansion, 182
pediatrics, 104 treatment, 84-85 Maxillary first permanent molar, ectopic
pharmacodynamics, 102-103 types, classification, 85f eruption, 203f
pharmacokinetics, 103, 309 growth curves, 158f Maxillary first primary molars, ankylosis, 203f
pharmacology, 102-104 physiologic rest position, 349 Maxillary fractures, description, 85
potency, 103 Mandible ramus, division, 87f Maxillary growth, 158
pregnancy/lactation, 104 Mandibular advancement, distractor Maxillary intercanine width, increase, 161
properties, 309t appliance, 90f Maxillary intermolar width, increase, 161
systemic toxicities, 103 Mandibular anterior frenum, 205 Maxillary Le Fort fractures, requirements, 86
techniques, 104-106 Mandibular anterior labial area, extension, Maxillary midline diastema, 177-178
toxicity, 193 350 Maxillary molar, caries, 74f
true anterior superior alveolar nerve block, Mandibular anterior primary teeth, size, 160 Maxillary primary molars, 193
104 Mandibular anterior repositioning appliance Maxillary sinus, 145-146
vasoconstrictors (MARA), 175 retention cyst, 121, 121f
addition, 103-104 Mandibular arch, 354 Maxillary surgery, 86, 182
usage, 309 eruption sequence, 161 Maxillary tuberosity, fractures, 82
Local anesthesia/anesthetics Mandibular canal, 147 Maxillofacial surgery, 84
characteristics, 310 Mandibular deficiency, treatment, 179 Maxillomandibular relationships, 344
Local factors, 271 Mandibular denture, limiting structures, Maximal intercuspal position, 344
Localized aggressive periodontitis, 205 350-351 Maximum intercuspation (MI), 344
Localized amyloidosis, 123 Mandibular excess McCune-Albright syndrome, 127
Locally administered host-modifying agents, case report, 88f-89f Mean, determination, 227
281 treatment, 179 Measles (rubeola), 112
Long buccal block, 193 Mandibular first primary molar Measurement strategies/instruments, 225
Long-span metal-ceramic FDPs, 362 pulpotomy, 198f Mechanical anterior guide table, 344
Loop diuretics, 322 taurodontism, 188f Mechanical modes, 359
Loperamide, 314 Mandibular fractures, anatomic distribution, Meckels cartilage, disintegration, 157
Low-density lipoproteins (LDLs), 322-323 84f Median, 226-227
Index 465
Median suture, 145 Minor salivary gland tumors, 122t Mycobacterium tuberculosis, 230
Medical history, 251 Misoprostol, 316 diagnosis, 230
developing data, 5 Mixed dentition, 199, 201 etiology, 230
functional inquiry review, 190 analysis, 210-211 prevention, 230
Medicaments, 13 incisor measurements, 210t transmission risk, 230
Medications, impact, 268 summary, 211t Mylohyoid area, 351
Meglitides, 326 analysis (Moyer), 210-211 Mylohyoid ridge, 147
Melanoma, 119f appliances, usage, 176 Myocardial infarction, risk (reduction), 322
oral melanoma, 118 characteristics, 160 Myofascial pain disorder (MPD), 91
Melanotic macule, 111 stage, 160
Melkersson-Rosenthal syndrome, component, Mixed tumor, 122f N
110 pleomorphic adenoma, 122 Nance appliance, 176
Menopause, 267 Mobility, 8-9, 196 Nanofilled/nanohybrid composites, 69
Menstruation, 266 assessment, 253 Narrow-spectrum antibiotics, 98
Mental foramen, 147 Mode, 227 Nasal fossa, 145
Mental fossa, 147 Moderate crowding, 177 Nasiolabial angle, 163
Mental nerve block, 105 Moderate periodontitis, 149 Nasopalatine, local anesthetics (usage),
Mental protuberance, 147 Modified Keyes-Jordan diagram, 37f 104-105
Mercury Modified Widman flap, 274 Nasopalatine duct (canal) cyst, 111
collection/disposal problems, 66 Moisture control, 55-56 Natal teeth, 209
controversy, 63 cellulose wafers, 56 National Fire Protection Association, color/
environmental contaminants, 233 cotton roll isolation, 56 number method, 233
hygiene, 232-234 isolation devices, 56 National Institutes of Health (NIH), 236
spills, cleanup, 232 operating field, isolation, 55-56 Natural teeth, implant attachment, 347f
Meropenem, 332 rubber dam, 55-56 Neck, deep fascial spaces, borders, 95t
Mesial step, 160 Moisture-free field (maintenance), dry angle Necrotizing diseases, 258
Mesiodistal tip control, 173 (usage), 212f Necrotizing periodontal diseases, 255
Metabolic changes, impact, 167 Molar relationship Necrotizing sialometaplasia, 121
Metabolism correction, 180 Necrotizing ulcerative gingivitis, 254
drugs, 292-293 description, 160 Necrotizing ulcerative periodontitis, 284
importance, 292 prediction, 160 Nedocromil, 324
induction, 293 Moments, 169-170 Negative punishment, 240
inhibition, 293 Moniliasis, 114, 209 Negative reinforcement, 240
Metal Monoamine oxidase (MAO) inhibitors, 299, Neglect, 211-212
oxidation, 361 302 Neonatal teeth, 209
porcelain, bonding, 360-361 Monocytes, 261 Neoplastic connective tissue tumors,
Metal brackets, 173 Monomorphic adenomas, 122 119-120
Metal-ceramic failures, 361-362 Morphine Network model, 235
Metal-ceramic restorations, 359-362 acute overdose, signs/symptoms, 313 Neurilemoma (Schwannoma), 120
alloys, properties, 360 effects, 313 Neurofibroma, 120
Metamerism, 361 pharmacokinetics, 313 Neuromas, occurrence, 90
Metastatic carcinoma, 130 Motivation, consideration, 241 Neurosarcoma (malignant peripheral nerve
Metformin, 326-327 Motivational interviewing, 242 sheath tumor), 120
Methadone, 314 Mouth-formed mouth guards, 207-208 Neurotransmission, dynamics, 296
Methemoglobinemia, 103 Mouth guards, 207-212, 222 Neutrophils, exit, 262f
Methylphenidate, 192 types, 207-208 Newborns, gingival cysts, 125
Methysergide, 316 Moyers mixed dentition analysis, 210-211 Nickel-titanium archwire materials, 173
Metronidazole, 281, 333 Mucoepidermoid carcinoma, 122 Nickel-titanium rotary instruments, 12
Metyrosine, 298 Mucogingival surgery, 275 Nicotine stomatitis, 111, 111f
Microdontia, 187 Mucormycosis, 114 Nicotinic acid, 323
Microfilled composites, 69 Mucosa-associated lymphoid tissue (MALT), Nicotinic receptors
Microhybrid composites, 69 122-124 agonists, 299
Microleakage, 28 Mucosal lesions, 111 distinction, 296
Midazolam, 312 contact allergies, 115 Nicotinic sites, 296
Midface fractures, 85-86 drug reactions, 115 Nitrates/nitrites, 322
Midline elastics, 177 immunologic diseases, 114-117 Nitrous oxide (N2O), 311-312
Midline granuloma, 115 infections, 112-114 adverse effects, 312
Midroot fracture, 24 malignancies, 118 exposure, risk (reduction), 312
Miglitol, 327 premalignant conditions, 117-118 use, contraindications, 312
Migraine, drugs (usage), 316 Mucosal pontics, 357 Nitrous oxide (N2O), sedation, 194-195
Mild periodontitis, 149 Mucous extravasation phenomenon, 120 contraindications, 195
Milliamperage, 134 Mucous membrane pemphigoid, 116-117, purpose, 194
Mineralocorticoids, potencies, 327 116f saturation, signs, 194-195
Mineral trioxide aggregate (MTA), 28 Mucous retention cyst, 120 Noble alloys, 360
advantages, 30 Multibottle systems, 67-68 Noble metals, 359
placement, 14 Multiple endocrine neoplasia type 3 (mucosal Nodular fascitis, 119
usage, 21 neuromas), 120 Noise control, 233
Mini-bladed curettes, 273 Multiple myeloma, 123, 130 Nonanatomic radiolucencies, 10
Mini-Langer curettes, 273 Multiple regression, 227-228, 228f Nonarcon, 345
Minimum alveolar concentration (MAC), Multirooted teeth, 150 Noncompliant appliances, 175
311 Muscarinic receptors Non-Hodgkins lymphoma, 123
Minimum inhibitory concentration (MIC), adverse effects, 299 Noninfectious waste, disposal, 232
330-334 agonists, stimulation, 300 Nonmucosal contact pontics, 357
Minor aphthous ulcer, 114f divisions, 296 Nonmucosal pontics, 357
Minor connector, 354 Muscarinic sites, 296 Nonnarcotic analgesics, 314-316
466 Index
Nonodontogenic lesions (bone lesions) Odontogenic infections (Continued) Oral implantology, 277-279
fibro-osseous lesions, 127 microbiology, 98 Oral infections, types, 112-114
giant cell lesions, 127-129 organisms, 94 Oral jewelry, wearing (impact), 260
inflammatory diseases, 129-130 pathogens, 94t Oral lymphoepithelial cyst, 110
malignancies, 130 pathophysiology, 94-98 Oral malodor, 284
occurrence, 127 progression, 94 Oral-maxillofacial surgeon, referral (criteria),
Nonphysiologic occlusion, signs/symptoms, treatment principles, 94-98 97b
282 Odontogenic keratocyst (keratocystic Oral melanoma, 118
Non-plaque-induced gingival conditions, odontogenic tumor), 125, 125b, 125f Oral mucous membrane, radiation (effects),
254-255 Odontogenic lesions, 124-127 136
Nonspecific plaque hypothesis, 258 Odontogenic myxoma (fibromyxoma), 126 Oral radiology, 132-150
Nonsteroidal antiinflammatory drugs Odontogenic tumors, 125-127 radiation physics, 132-134
(NSAIDs), 314-316 characteristics, 126t Oral squamous cell carcinoma, clinical
nonselective COX inhibitors, 315 Odontoma, 127 features, 118b
Nonsurgical endodontics, 12-13 Office-based preventive measures, 222 Oral submucous fibrosis, 117
access preparation, 12 Omalizumab, 324 Oral surgery, 79-102
apical preparation, 13 One-bottle systems, 68 Oral tissues, radiation effect, 136
cleaning/shaping, 13 One-couple appliances, 170-171 Orbital fractures, requirements, 86
instruments, 12 One-couple system, equilibrium, 171f Ordinary hatchets, 48
file dimensions, 13 One-walled vertical defects, 276f Organ level, radiation effects, 135
irrigation/medicaments, 13 Ongoing pain assessment, 243 Organs, 296
objectives, 12-13 Onlay restorations, 72-73 Orofacial pain, classifications, 90-91, 90t
working length determination, 12-13 clinical procedure, 72-73 Orofacial soft tissues, examination, 40
Nonverbal communication, 236-239 definition, 72 Orthodontic appliances, 173-177
characteristics, 237 tooth preparation, 73 Orthodontic archwire, 172f
Nonverbal facilitation, 238 Opalescence, 361 materials, 173
Nonvital bleaching techniques, 30 Opaque porcelain, 361 Orthodontic diagnosis, 161-165
Nonworking condyle, 364 Open bites, 160, 178 Orthodontic forces, deleterious effects,
Nonworking interferences, 364 correction, impact, 181 167-168
Normal distribution, 226, 226f Open-ended questions, 238 Orthodontic materials, 172-173
Nose, 145 Opening rotation, 158 Orthodontics, 155-184
Null hypothesis, 227 Open questions, affirmations, Reflective growth/development, 156-159
Nursing bottle caries, 210 listening, Summarizing (OARS), 241 performing, 184
Nutrient canals, 147 Operant conditioning, 240 treatment planning, 165
Nutrition, 267 Operating field, isolation, 55-56 Orthodontic therapy, 260
Nystatin oral rinse, 351 Operative cutting instrument formulas, 48 Orthodontic tooth movement, 168-172
Operative dentistry biologic control, 166-168
O patient assessment/examination/diagnosis/ Orthodontic treatment, surgical treatment
OARS. See Open questions, affirmations, treatment planning, 40-47 (combination), 182-184
Reflective listening, Summarizing procedures Orthognathic surgery, 86-87
Objectivity, impact, 245-246 instrumentation, 47-51 diagnosis, 86
Object localization, 139 terminology/classification, 48 imaging, 86
Observation, 238 Operative preventive treatment, 44 patient evaluation, 86
Observational epidemiology, 223-224 Operative treatment surgery, 86-87
Observational learning (modeling), 241-242 indications, 44-46 Orthognathic surgical procedures, stability,
Obturation, 13 planning, interdisciplinary considerations, 184
Occipital bones, 156 44 Osseointegrated implants, advantages, 347b
Occlusal adjustment, 283 Operator equipment, 233 Osseous crater, 275
Occlusal bearing cusps, metal thickness, 357 Opioids, 313-314 diagrammatic representation, 276f
Occlusal bevel, 73 action, mechanism, 313 Osseous defect, combined type, 276f
Occlusal correction, 282-283 agonists, receptor targets, 313t Osseous surgery, 275-277
Occlusal equilibration, 364 effects, 313 resective osseous surgery, 276-277
Occlusal point contacts, 357 receptors, 313 Osseous windows, 100
Occlusal radiography, 143 signs/symptoms, 313 Ossification, occurrence, 156
Occlusal relationship, problems, 178 Opportunistic fungi, 114 Ossifying fibroma, 127
Occlusal rest, 355 Oral-antral communications, management, 81 Ostectomy, 276
Occlusal schemes, 357 Oral bisphosphonates, intravenous Osteoblastoma, 127
Occlusal surfaces, 149 bisphosphonates (differences), 99 Osteomyelitis, 10, 98
Occlusal tables, impact, 348f Oral brush cytology, 100 Osteopetrosis (Albers-Schnberg disease), 131
Occlusal therapy, 282-283 Oral cancer, 219 Osteoplasty, 276
Occlusion, 347 Oral cavity, radiation effects, 135-136 Osteoporosis, 270
angle classifications, 86 Oral contraceptives, 267, 330 Osteosarcoma, 130
development, 159-161 composition, 309t Overassertive communication, 237
factors, 364-365 Oral diseases Overbite
impact, 282 community-based prevention, 219-222 absence, 160
plane, 350 diet, impact, 223 correction (leveling), 180
Occupational Safety and Health epidemiology, 218-219 correction, impact, 181
Administration (OSHA), 230-231 health education/literacy, 222 defining, 160
blood borne-pathogens standard, 230-231 home-based preventive methods, 222-223 Overdentures, 352
Odontalgia, 90 prevention, 219-223 abutments, maxillary teeth (selection), 352t
Odontogenic cysts, 124-125 school-based prevention, 219-222 Overextension, 353
comparison, 124t Oral-facial clefts, 109 Overjet, 155
Odontogenic infections, 94-98 Oral glucocorticoids, usage, 324 defining, 162f
anaerobic bacteria, role, 94t Oral hygiene procedures, access, 286 Overtreatment, 181
fascial spaces, 94 Oral hypoglycemics, 325-327 Oxidative elements, presence, 360
Index 467
Oxide-metal interface, 361 Pemphigus vulgaris, 116 Periodontal therapy

Oxycodone, 314 Pendulous tuberosities, occurrence, 349 maintenance (phase IV) therapy, 269
Oxygen reduction, 262f Pendulum appliance, 175 nonsurgical (phase I) therapy, 268-269
Penicillin G/Penicillin V, narrow-spectrum phases, 268-269, 268b
P penicillin, 330 restorative (phase III) therapy, 269
Pagets disease, 129, 349 Penicillins, 330-332 smoking, effects, 280
Pain, 167 drugs, comparison, 331t surgical (phase II) therapy, 269
chronology, 5 nucleus, 330f Periodontal treatment, healing mechanisms,
complexity, 243 Pentazocine, 314 277
control, 242-244 Percussion, 6 Periodontitis, 149-150, 253, 261
location, 5 sensitivity, 196 clinical features, 255
management strategies, 244 Perforation, 20-21 complementary treatment strategies, 272f
minimization, 243 definition, 19 endodontic lesions, association, 255
occurrence, 167 follow-up, 21 histologic stages, 264b
perception, physiologic/psychological kinds, 20 pathogenesis, 263
aspects, 87-90 nonsurgical internal repair, MTA (usage), schematic illustration, 252f
quality, 5-6 21 systemic disease manifestation, 256
referred pain, 5 prognosis, 20-21 types, 256b
spontaneous pain, 196-197 recognition, 20 Periodontium
suddenness (perforation symptom), 20 radiographic evidence, 20 abscesses, 255
triage, 5-6 repair, timing, 20-21 communication, 11-12
Palatal holding arch (PHA), 199 surgical repair, 21 Periodontopathogens, virulence factors, 259
Palatal plate, 354 timing, 20 PerioGlas, 277
Palatal tissues, 193 treatment, 21 Peripheral ameloblastoma, 126
Palatal vault, remodeling, 157f Pergolide, 307 Peripheral giant cell granuloma, 128
Palate, abnormalities, 159 Periapical cemento-osseous dysplasia, Peripheral root resorption, 205
Palpation, 6 126-127, 127f Permanent dentition, 161, 200
sensitivity, 196 Periapical cyst (radicular cyst), 124 stage, 161
Panoramic image Periapical radiographs, 165 Permanent incisors
advantages, 150 full-mouth series, 251 lateral ectopic eruption, 200
formation, principles, 150 Periapical radiography, 143 lingual eruption, 199-200
interpretation, 150 Periimplantitis, 279 region, space loss, 200f
Panoramic imaging, 150 Periimplant soft tissues, dehiscence/recession, Permanent retention, 181
Panoramic radiographs, 165 279 Permanent teeth
Panoramic radiology, disadvantage, 150 Periodontal abscesses, 150, 255, 258, 284 calcification, 186-187
Papillary hyperplasia, 348 Periodontal balance, 265f start times, 186t
Papillomas, 112 Periodontal conditions, classification, 254b covering, bone (usage), 202
Papillon-Lefvre syndrome, 261 Periodontal diagnosis, prognosis variation, eruption, 186-187
Paralleling techniques, 139 271-272 times, 186t
Paraphrasing, usage, 236 Periodontal disease, 218-219 primary teeth, anatomic differences,
Parathyroid hormone (PTH), 328-329 cigarette smoking, risk factor, 264-266 195-196
Parenteral contact, 229 classification, 254b replantation, 207
Partial dentures ecologic plaque hypothesis, relationship, Personal protective equipment (PPE), 230
kiddie partials, 199 258f usage, 231, 233
fixed kiddie partial, 200f etiology/pathogenesis, smoking (effects), Phagocytosis, 262f
removal, 260 265t Pharmacokinetics, 292-293
Partially edentulous arches, examples, 353f host response, characteristics, 261-268 mathematical calculations, 293
Partial pulpotomy, 28-29 matrix metalloproteinases, biologic Pharmacology, principles, 291-294
Partial veneer crowns, 357 activities, 264t Phenobarbital, 307
Particulate radiation, 132 microbiology, 258-259 Phenytoin, 306
Patched (PTCH) tumor suppressor gene, prevalence/severity, smoking (effects), 265t Phosphate-bonded investments, usage, 367
mutation, 125 radiographic appearance, 149-150 Photoelectric absorption, 134
Pathogenesis, 261-268 risk elements, categories, 269b Photopolymerization units/lasers, 233
Patients tissue destruction, 262 Photostimulable phosphor plates (PSP), 142
assessment, 40-47 Periodontal-endodontic lesions, 255 Physical abuse/neglect, 212
considerations, 40 Periodontal examination, 8, 252-253 Physical-chemical mucosal lesions, 111
comprehension, verification, 238-239 Periodontal health, 253, 258, 261 Physical facility, liability (reduction), 245
experience, acknowledgement, 243 Periodontal improvement, 181 Piezoelectric ultrasonic instruments, 273
implants, clinical applications/evaluations, Periodontal indices, 218 Pilocarpine, usage, 300
279 Periodontal lesions, type, 11-12 Pindborg tumor (calcifying epithelial
information, provision, 242 Periodontal ligament (PDL) odontogenic tumor), 126
management, 1-12 apical portion, thickening, 3 Pink spot perforation, occurrence, 205
objectivity, 246 compression, 166 Pioglitazone, 327
pain, behavioral/nonpharmacologic inflammation, 4 Pit-and-fissure caries treatment decision
management, 244 invasion, 130 making, 45t
positioning, 150 perforation, 20 Pit sealants, 212
refractory patients, 284 reorganization, occurrence, 181 Planned behavior, theory, 240
treatment decision, 239 space, radiographic anatomy, 144 Planning (motivational interviewing), 242
Pavlovian conditioning, 240 Periodontal microbiology, 255-260 Plaque
Pear-shaped bur, 50 Periodontal packs, 274 biofilm, organic constituents, 257
Pediatric dentistry, 184-212 Periodontal pockets, types, 252f control, 272
topics, 207-212 Periodontal restoration, considerations, hypothesis (hypotheses), 36, 258
Peg lateral incisor, dens in dente, 188f 285-286 maturation, 257
Peg maxillary lateral incisors, 185f Periodontal structures, oral/radiographic plaque-induced gingivitis, 254
Pellicle, formation, 257 examination, 251 Plasma cell myeloma, 123
468 Index
Plasma concentrations, 293 Prevotella melaninogenica, 260 Propoxyphene, withdrawal, 314

Plasminogen activators, 323 Prevotella nigrescens, 259 Propranolol, 298, 318
Plasminogen inhibitor, 323 Primary canines Prospective cohort study, 224
Pleomorphic adenoma (mixed tumor), 122 bilateral loss, 200-201 Prostaglandins, 263
Pocket depth, probing, 252 loss, 200-201 formation, inhibition, 280
Polyether, 359 Primary dentition, 199-200 Prosthodontics, materials (usage), 367t
Polymer, molecular weight, 356 localized aggressive periodontitis, 205 Protective glasses, usage, 230
Polymorphonuclear leukocytes, 261 loss, 201 Protraction headgear (reverse-pull)
Polymorphonuclear neutrophils (PMNs), 261 stage, 160 (facemask), 174
Polymorphous low-grade adenocarcinoma, Primary endodontic lesions, 11 Protrusive record, 349
122 Primary first molar loss, 201 Provisional restorations, 362-364
Polysulfide polymer, 359 Primary herpetic gingivostomatitis, 204 direct procedure, 364
Pontic design, 358f Primary hyperparathyroidism, giant cell indirect procedure, 364
classification, 357 lesion, 10 production, material types (usage), 362-364
Porcelain Primary incisors, loss, 196, 199 resins, characteristics, 363t
composition, 361 replacement, 199 types, 364
thickness, requirement, 357 Primary lateral incisor/primary canine, Proximal box, 73
Porcelain-metal interface, 361 fusion, 187f Proximal caries treatment decision making,
Porcelain-oxide interface, 361 Primary lesion (chancre), 113 45t
Porphyromonas gingivalis, 257, 259 Primary mandibular lateral incisor, Proximal cavosurface margins, 58f
Positioner, 181 germination, 188f Proximal embrasure areas, 65
Positive punishment, 240 Primary molar teeth Proximal overhangs, diagnosis, 43
Positive reinforcement, 240 pulp therapy, decision-making tree, 199f Proximal plate, 356
Positive skewed distribution, 226f restoration Proximal-surface caries, 42
Post and cores, service, 357 amalgam, usage, 195 Proximal surfaces, 148
Posterior Adams clasps, 199 composite, usage, 195 Pseudocysts, 110-111, 121
Posterior crossbite Rule of 7, 202 Pterygoid plates, 146
correction, appliances (usage), 176 Primary periodontic lesions, 11-12 Puberty, 266
types, 163f secondary endodontic involvement, 12 gingivitis, 204
Posterior crossbites, 178 Primary second molar loss, 201 hormonal changes, 266-268
Posterior mandible, periapical radiograph, bilateral loss, 201 Public health, government role, 235-236
147f-148f unilateral loss, 201 Pulmonary hypertension, drugs (usage), 321
Posterior maxilla, periapical radiograph, 146f Primary teeth Pulp, 2-3
Posterior segments, 210 calcification start times, 186t bacteria, entry portals, 18
Posterior stainless steel crown preparation/ eruption, 186 biology, 28
adaptation, 195 times, 186t canal obliteration (calcific metamorphosis),
Posterior superior alveolar nerve block, 104, extrusion, 207 26, 205
193 intrusion, 206-207 capping, 196-197
Posterior teeth (mesial tipping prevention), options, 196-199 communication, 11-12
lingual holding arch (usage), 202f permanent teeth, anatomic differences, death, 3
Postherpetic neuralgia, 90 195-196 effects, 167
Postoperative sensitivity, 65 pulp treatment, 196-199 fracture, 207
Posttreatment evaluation, 30-31 clinical signs, 196-197 necrosis, 3
Power-driven mechanical spatulator, 366 replantation, 207 previous treatment, 3
Powered cutting instruments, 49 Primary trauma, occlusion (impact), 282 protection, 73
Powered toothbrushes, usage, 286 Primidone, 307 radiographic anatomy, 144
Praise, usage, 243 Probing, 253 therapy
Pramipexole, 307 bleeding, occurrence, 252 contraindications, 196
Pramlintide, 327 usage, 238 decision-making tree, 198-199, 199f
Prazosin, 298 Problem list previous initiation, 3
Preadjusted edgewise appliances, 173-174 development, 165 treatment, 196-199
Preadolescents, skeletal problems (treatment), prioritization, 165 vitality testers, 243
179 Procagulants, 323 vitality testing, 21-22
Precarious pits, 42 Procainamide, 318 Pulpal communication, 55
Pregnancy, 266-267 Procedural complications, 18-21 Pulpal diagnosis, 7t
drugs, relationship, 294 Processed composite, 47 Pulpal diseases, 2-3, 284
gingival enlargements, association, 285 Process indicators, 231 classification, 2-3
hormonal changes, 266 Procyclidine, 308 Pulpal floor depth, 57f
immune suppression, 266 Professionalism, impact, 237 Pulpal hyperemia, 205
local anesthetics, impact, 104 Professional responsibilities/liabilities, Pulpal inflammation, progression, 2
medications, limitations, 267 244-247 Pulpal necrosis, 3, 26, 205
periodontal treatment, 267 Profile convexity/concavity, 163f management, apical pathosis (impact), 16
Preimplantation preparation, 346 Progestins, 329-330 Pulpal pain, physiology, 2
Premack principle, 241 Prognosis, 270-272 Pulpal precautions, 51
Prenatal irradiation, impact, 136 clinical factors, 270 Pulpectomy, 29, 196, 198
Preparation, 236 determination, factors, 271b Pulpitis pain, 2
Prescription writing, 337-338 local factors, 271 Pulpodentinal complex, 2
parts, identification, 339f systemic factors, 271 Pulpotomy, 29, 196-198
Pressure side, 165-166 variation, 271-272 Pumice, usage, 174
Pressure sterilization, 16 Progressive muscle relaxation, 243 Pure rotation, 170
Presuming, usage, 237 Projection geometry, 139 Pure translation (bodily movement), 170
Pretreatment considerations, 40 Proliferative verrucous leukoplakia, 117
Prevention, 286-287 Prophy-jet, water delivery, 274 Q
Prevotella intermedia, 257, 259-260 Propionic acid derivatives, 315 Quad-helix, 176
Prevotella loescheii, 257 Propofol, 312 Quality assessment, 235
Index 469
Quality assurance, 235 Recession, Miller classification, 275 Retrodiscal tissue (stress), anteriorly displaced
Quantal dose-response curves, 292, 292f Reciprocal clasp, 355 disc (impact), 93f
Quantitative light-induced fluorescence Reciprocal tooth movement, 172 Retromolar pad, 351
(QLF), 40 Recombinant human BMP 2 (rhBMP-2), 83 Retromylohyoid area, 351
Quantum theory, 132 Reconstructive dentoalveolar surgery, 82-83 Retrospective cohort study, 224
Quenching, 367 Recontouring, 276 Reverse bevel incision, 274
Quinidine, 318 Recurrent aphthous ulcer, 204 Reverse overjet, 155
Quorum sensing, 257 Recurrent caries, 149 Reverse pulpitis, 2
Recurrent herpes simplex (cold sore) (fever Reverse smoking, 111
R blister), 204 Reversible hydrocolloids, 359
Radiation, 132 Red complex, 257 Rhabdomyosarcoma, 120
biology, 134-137 Referred pain, 5 Right lateral incisor, vertical defects, 276f
caries, 136 Reflection, usage, 236 Risk management/avoidance, 245-246
characteristic radiation, 134 Refractory patients, 284 documentation, 245
chemistry, 135 Refractory period, increase, 317 Root canal
direct effect, 135 Reframing (cognitive coping), 243 infection, nature/dynamics, 18
electromagnetic radiation, 132 Regional odontodysplasia, 132 obturation, 13
exposure, sources, 137 Reinforced anchorage, 172 system, anatomic components, 18f
health physics, 137-138 Relaxation, usage, 243 Root correction, 180
indirect effects, 135 Remineralization, 36-38 Root development, amount, 202
late somatic effects, 136-137 Removable dental prosthesis (RDP), 343-347 Root end resection (apical surgery)
manmade sources, 137 components, 354-356 (apicoectomy), 14
distribution, 137f indications, 344 Root fracture, 22-24, 207
stochastic effects, 135 support, type, 356 J-shaped radiolucency, 11f
therapy, 266 Removable partial prosthodontics, 353-356 Root movement, 170
ubiquitous background, 137 Removable retainers, 181 Root perforations, 20
distribution, 137f Renin-angiotensin system, drugs (impact), Root planing, 272-273
units/quantities, 135t 320 Root resection, 15
Radiation-induced cancers, 136 Reparative dentin, 28 Root resorption, 167-168, 199
Radiation-induced solid cancers, 136-137 Replacement resorption (ankylosis), 26 occurrence/severity, 168
Radiation physics, 132-134 Replacement root resorption, inflammatory Root sensitivity, 284-285
matter, 132-134 root resorption (differences), 28 Root surface
X-ray machines, 132-134 Resective osseous surgery, 276-277 caries, 218
Radicular cyst (periapical cyst), 124 Resective surgical therapy, difficulty, 283 treatment, 277
Radiographic anatomy, 143-148 Reserpine, 299 Root-surface caries, 43
Radiographic artifacts, 139 Residual root tips, 348 Root-surface hypersensitivity, treatment, 46
Radiographic assessment, 253 Resin-based sealants, 212 Root surface preparations, 60
Radiographic blur, increase (causes), 139 Resin-dentin bonds, longevity, 69 Root surfaces, 149
Radiographic blurring, 139 Resin luting agents, bonding, 364 Ropinirole, 307
Radiographic contrast, 139 Resin-modified glass ionomer (RMGI) Rosiglitazone, 327
Radiographic examination, 9-10 base, 62 Rotary cutting instruments, 49-50
findings, 9 luting agents, 364 parts, designation, 50f
Radiographic images, two-dimensionality, 9f placement, 55 Rotary speed ranges, 49
Radiographic interpretation, 9 recommendation, 62 Rotational control, 173
Radiographic noise, 139 Respiratory pharmacology, 323-324 Rotational movement, causes, 169f
Radiographic quality assurance, 142-143 Respondent conditioning, 240 Rotation center, 169f
Radiographic speed, 139 Rest, proximal plate, cast circumferential clasp Round bur, 50
Radiographic techniques, 17-18 (RPC), 355 Rubber cups, usage, 274
exposure considerations, 17 Rest, proximal plate, I bar (RPI), 355 Rubber dam, 55-56, 212
Radiographs Rest, vertical dimension, 349 Rubeola (measles), 112
helpfulness, 149 Restorations Rudimentary supernumerary, conical form,
limitations, 149 contouring/finishing, 70-72 187f
problems, causes, 140-141 criteria, 46 Rufinamide, 307
Radiography examination, 40-44 Rule of 7, 202
dose problem, 260 Ryan White CARE Act, 236
limits, 138 radiographic examination, 44
reduction, 138 repair/resurface, 46 S
exposure replacement, 46-47 Saddle pontic design, 357
dose, 137-138 Restorative implantology, 345-347 Sagittal split osteotomy, 87f
methods, 138 treatment planning, 345-346 Salicylates, 315
risk, estimates, 138 Restorative margin placement, 285 Saliva, 36, 38
Radiopaque lesions, characteristics, 17-18 Rests protective mechanisms, 36-38
Radiosensitivity, 135 importance, 355-356 Salivary flow, reduction, 300
Ramsay Hunt syndrome, 90 types, 355-356 Salivary gland diseases
Range, 227 Retainers, usage, 357 benign neoplasms, 121-122
Ranula, 120f Retention, 181 malignant tumors, 122
Rapid acceleratory phenomenon, 168 class II correction, impact, 181 reactive lesions, 120-121
Rapport, usage, 237 class III treatment, impact, 181 Salivary glands, radiation effects, 136
Reactive connective tissue tumors, 119 factors, 357 Same lingual opposite buccal (SLOB), 9, 17,
Reactive lesions, salivary gland diseases, lower incisor alignment, impact, 181 139
120-121 open bite correction, impact, 181 Sampling strategy, 225
Reactive oxygen species (ROS), 261 overbite correction, impact, 181 Sarcoidosis, 121
Reassurance, providing, 237 permanent retention, 181 Saxagliptin, 327
Receptors, 291, 296t purpose, 181 Scaling, 272-273
preferences, uses, 298t Retentive clasps, 354 Scammons growth curves, 158
470 Index
Scarlet fever, 113-114 Single organ amyloidosis, 123 Statistical significance, 227
School water fluoridation, 220 Single palatal bar, 354 Statistics, 226
Schwannoma (neurilemoma), 120 Single palatal strap, 354 basic statistics, 226-229
Schwartz periotrievers, 273 Single-rooted teeth, root resorption, 168 inferential statistics, 227-228
Scientific article Sinoatrial (SA) node, automaticity Statute of limitations, 246
abstract, 224 (reduction), 317 Sterilization, 16-17, 231-232
components, 224-226 Sinus tract, tracing, 7f chemical (cold) sterilization, 232
discussion, 225 Sitagliptin, 327 dry heat sterilization, 16
introduction/literature review/hypothesis, Sjgrens syndrome, 121 dry-heat sterilization, 231
224-225 Skeletal movements, maximization, 184 pressure sterilization, 16
methods, 225 Skeletal muscle, autonomic nerves/somatic process, 231-232
references/bibliography, 225-226 nerves, 295f rationale, 16-17
results, 225 Skeletal neuromuscular blockers, 291-294 type, 16
summary/conclusions, 225 types, 301 Steroids, comparison, 328t
title, 224 Skeletal problems, treatment, 179 Stimulus control
Scleroderma, 116 Skeletal relationships (cephalometrics), alteration, 241
Sclerosis, 67 163-164 incompatibility, 242
Screw-retained implant crown, 347 Skewed distribution, 226, 226f Stimulus-response theory (shaping), 241
SDD. See Sub-antimicrobial dose doxycycline Skirt, 73 Stock mouth guards, 207
Sealants, 221 SLOB. See Same lingual opposite buccal Strain, internal characteristics, 172f
usage, 39 Smear layer, 67 Streptococcus mutans
Sealers, 61-62 Smokeless tobacco-associated white lesion, impact, 36
Secondary amyloidosis, 123 117-118 levels, 210
Secondary caries, 149 Smokeless tobacco use, impact, 266 Stress, 267
Secondary flare, 73 Smoking-associated melanosis, 111 internal characteristics, 172f
Secondary occlusal trauma, 282 Smooth-surface caries, occurrence, 43 Stress-strain relationship, 172
Second bicuspid, distal eruption, 203f S-Nto-S-Gn, 164 Strip perforations, 20
Second-generation histamine receptor Social cognitive theory, 239 Stubbed margin, 73
blockers, comparison, 317 Socket preservation, 83 Sub-antimicrobial dose doxycycline (SDD),
Second premolars, eruption, 202f Sodium hypochlorite, 13 usage, 270, 280-281
Sedative hypnotics, 304-305 Soft tissue diseases Subgingival calculus, 260
actions, 304 developmental conditions, 109-111 Subgingival margins, 260
Seizures oral pathology/diagnosis, 109-132 Sublingual gland area, 351
indications, 307 Soft tissues Subluxation, 24
types, 306 benign soft tissue lesions, 348 Submandibular gland fossa, 147-148
Selective anesthesia test, 9 growth, 157f Submandibular space, location, 96f
Selective estrogen receptor modulators, 329 incision/drainage, indications, 14 Submucosal nodule, 120
Selective grinding, 364 injuries, prevention, 81b Subperiosteal implant, 345-347
Selective serotonin reuptake inhibitors precautions, 51 Succinylcholine, 301
(SSRIs), 302 surgery, 82, 348-349 Sucrose, 38-39
Selegiline, 308 Solar cheilitis (actinic cheilitis), 117 Sulfonamides, 333
Self-determination theory, 240 Somatic nerves, 295f Sulfoylurea oral hypoglycemic drugs, 325-326
Self-etching primers, 174 Sonic instruments, 273 Summarizing, 238
Self-etching systems, 68 Space Superinfection, 330-334
Self-etch one-step systems (all-in-one), 68 closure, 180 Superior repositioning, 182
Self-etch two-step (self-etch primer), 68 maintenance, 177 Supernumerary teeth, 187
Self-inflicted injuries, 260 planning factors, 202-204 eruption obstruction, 185f
Self-ligating brackets, 173 Specific plaque hypothesis, 258 Supporting structures, radiographic anatomy,
Self-monitoring bias, 241 Sphenoid bones, 156 144-148
Semiadjustable articulators, 345 Spherical amalgam, 66 Supportive periodontal therapy, 269
usage, 345 Spinal pain transmission pathways, 91f Suppuration, 253
Separated instruments Splinting, 207, 282-283 Suprabulge, 355
prognosis, 20 materials, 283 Supracrestal fiberotomy, 181
Separated instruments, usage, 19-20 Spongiosa, 144 Supragingival calculus, 259-260
Sepsis, 16-17 Spontaneous pain, 196-197 Supragingival margins, 357
Serotonin norepinephrine reuptake inhibitors Spoons, usage, 48 Surface apposition, occurrence, 157
(SNRIs), 302 Sprues, 367 Surface covers, usage, 230
Severe closing rotation, 157-158 Squamous cell carcinoma, 118 Surface resorption, 25-26
Severe crowding, 177 oral squamous cell carcinoma, clinical Surgery
Severe periodontitis, 150 features, 118b principles, 79
Sevoflurane, 312 Stability, hierarchy, 184f timing, 184
Sex hormones, 329-330 Stabilizing clasp, 355 Surgical crown lengthening, 357
Sexual abuse/neglect, 212 Staff model, 235 Surgical endodontics, 13-15
Shallow excavations, 62 Stafne bone cyst, 110f incision/drainage/trephination, 13-15
Shallow pulpotomy, 28-29 Stage I anesthesia (analgesia), plateaus, 194 Surgical extractions, 80
Shank, term (usage), 51 Staining, 361 indications, 80
Shaping (stimulus-response theory), 241 Stainless steel archwire materials, 173 Surgical impactions, 80
Sharps, disposal, 232 Stains, 260 Surgical treatment, orthodontic treatment
Shunts, 208 Standard deviation, 227 (combination), 182-184
Sibilants, 350 State Childrens Health Insurance Program sequencing, 184
Sickle scalers, usage, 272 (S-CHIP), 235 Surveillance, Epidemiology, and End Results
Signal transduction, 293f Static equilibrium, 170-171 (SEER) data, 219
Silence, usage, 238 Statins, 322-323 Sustain talk, 242
Silica-bonded investments, usage, 367 Stationary anchorage, 172 Swelling, 196
Simplified Oral Hygiene Index (OHI-S), 218 Statistical analytical procedures, 225 Symptomatic apical periodontitis, 4
Index 471
Symptomatic irreversible pulpitis, 2-3 Temporomandibular joint (TMJ) dysfunction, Topical anesthetic, usage, 193
Symptoms, intensity/severity, 6 181 Topical fluoride, 222
Synapses/junctions, 295-296 nonsurgical therapy, 92-93 Tori removal, 82
Synchondroses, 156 Tension side, 166 Torque, 173-174
Syphilis, 109 Terminal hinge position, 364 Total joint replacement, indication, 93
Systematic desensitization, 243 Test cavity, 9 Total necrosis, symptoms (absence), 3
Systemic antibiotics, usage, 283 Tetracyclines, 332 Toxicology, 337
Systemic arthritic conditions, 91-92 usage, 281 Toxic symptoms/therapy, 338t
Systemic disease, 10 Theophylline, 324 Toxins, 338t
aphthous ulcers, presence, 115t Theory of planned behavior, 240 Trabecular bone, 144
Systemic factors, 271 Therapy, 272-286 Training program, 231
impact, 254 Thermal expansion Tramadol, 314
Systemic fluoride supplementation, 208 linear coefficient, 67 Transcutaneous electrical nerve stimulation
tablets/lozenges, usage, 221 surface caries, proximal coefficient, 42 (TENS), 93
Systemic toxicities, 103 Thermal tests, 6-8 Transitioning, usage, 238
responses, 6-8 Translation, 166, 364
T Thiazides, 322 Transmissible diseases, 229-230
Table of allowances, 234 Thioamide drugs, 325 Transmission
Talk, type, 242 Thiopental, 312 direct contact, 229
Talon cusp, lateral incisor, 188f Third-party reimbursement, 234 droplets/aerosols, usage, 229
Tanaka-Johnson analysis, 211 Three-dimensional cone-beam computed indirect contact, 229
Tannerella forsythia, 257, 259, 266 tomography, usage, 165 parenteral contact, 229
Taste buds, radiation (impact), 136 Three-walled vertical defects, 276f routes, 229-230
Taurodontism, 188 Thrush, 114, 209 Transosteal implant, 345-347
Technical jargon, reliance, 237 Thyroglossal tract cyst, 109-110 Transpalatal arch, 176
Teeth Thyroid congenital abnormalities, 109 Transportation, 19
absence, 178 Thyroid hormones, 324-325 Transtheoretical model, 239
avulsion, cases, 24f synthesis, 326f Transverse corrections, 182
development, 185-189 Thyroid pharmacology, 324-325 Transverse deficiency, treatment, 179
developmental disturbances, 185-189 Time sampling, 241 Trauma, occlusion/occlusal trauma (impact),
examination, 40-44 Time structuring, 242-243 282
form, anomalies, 251-252 Tipping, 166, 170 Trauma surgery, 84-86
fractures, 84-86 controlled tipping, 170 Traumatic bone cyst, 10, 111f
histodifferentiation/morphodifferentiation uncontrolled tipping, 170 Traumatic (simple) bone cyst, 111
(bell stage), 185 Tissues, 296 Traumatic fibroma, 119
horizontal forces, 364 comparison, 279 Traumatic injuries, 21-28
initiation (bud stage), 185 displacement (achievement), modes apical neurovascular supply damage, 26
large surface area, 357 (usage), 359 attachment damage, 25-26
mobility, 8-9 inflammation, 167 biologic consequences, 25-26
number, anomalies, 187-189 level, radiation effects, 135 examinations, 21-22
position, resistance center (indication), 168f management, usage, 357-359 treatment, 206-207
proliferation (cap stage), 185 receptors, 297t Traumatic lesions, types, 255
radiation effects, 136 responses, 297t Traumatic ulcer, 111
radiographic anatomy, 143-148 Titanium implants Treatment objectives, development, 165
radiographic examination, 44 gingival tissue, attachment, 277-279 Treatment planning, 1-12, 40-47, 238-239,
restorations, 42f, 61-73 placement, 277 268-270
considerations, 357 Titanium-tissue interaction, 277-279 age, 269-270
reasons, 52 three-dimensional diagram, 278f considerations, 44
root resorption, 168 Tolcapone, 308 diagnosis, 343-347
rotation, resistance center, 169f Tooth-borne RDPs, rest location, 356 genetic factors, 269
sectioning, 81 Toothbrushing, 286 joint agreement, 238
shape, anomalies, 187-188 Tooth-colored restorations Treatment plans, elements, 238-239
size clinical examinations, 44 Treatment plan sequencing, 44
analysis, 162 indications, 47 Trephination, 13-15
anomalies, 187 Tooth movement indications, 14
calculation, 211 biology, 165-168 Treponema denticola, 257
discrepancies (Bolton discrepancy), 180 mechanical principles, 168-172 Treponema species, 257
space. availability (prediction), 211t types, 166, 170 Triamterene, 322
splinting, 343 Tooth preparation, 59-60 Tricyclic antidepressants, 302
structure amalgam/composite, differences, 53t Trigeminal pain modulation system, 91f
anomalies, 188-189 considerations, 52b Trigeminal pain transmission pathways,
bonding, status, 66 contour space, 356 91f
conservation, 52 definition, 52 Trihexyphenidyl, 308
traumatic injuries, examinations, 21-22 depth, 57 Tripoding, 182
Teething, 209 factors, 52 Triptans, 316
Telangiectasias, 130 final tooth preparation, 55 True anterior superior alveolar nerve block,
Tell-Show-Do (TSD), 190, 243 objectives, 52 104
technique, 191 occlusal preparations, 53 True combined lesions, 12
Temporal arteritis (giant cell arteritis), principles, 56-57 True positive (TP), 228
presenting symptoms, 91 smooth-surface preparations, 53 t-test, 228
Temporomandibular disorders (TMDs), 91-93 stages, 52-55, 54f Tuberculosis, 113
screening evaluation, 282 steps, 52-55 Tumors, surgical management, 100-102
surgical treatments, 93 Tooth size-arch length differences, calculation, Tungsten target, 132
TMJ dysfunction, nonsurgical therapy, 211 Twin block appliance, 175
92-93 Tooth slooth, usage, 10 Two-couple appliances, 171
472 Index
Two-walled vertical defects, 276f Vertical incisor position (control), appliances Wound
Type I dose-response curves, 291 (usage), 176 healing/repair/regeneration, 282
Tyrosine hydroxylase, catalysis, 296 Vertical osseous defect, 149 irrigation, 81
Vertical overbite, 162 Wraparound retainer, 181
U Vertical root fracture, 9, 11, 21
Ultrasonic instruments, 273 clinical findings, 11 X
Ultrasonic scalers, 272 definition, 21 Xenograft, 83, 277
Uncomplicated fractures, 22-24 diagnosis, 11 material, 277
Uncontrolled tipping, 170 etiologies, 11 Xerostomia, 351
Undermining resorption, occurrence, 166 prognosis, 11 X-linked recessive condition, 130
Undisplaced flap, 274 treatment, 11, 21 X-ray beam, factors, 134
Unerupted, term (usage), 80 Very-low-density lipoproteins (VLDLs), X-ray film, 138-139
Universal curettes, 272 322-323 automatic film processing, 140
Upper incisors Vestibuloplasty, 349 development times, temperature
angulation, 164 Vinyl polysiloxane (addition silicone), (relationship), 140t
position, 183f 359 exposure development, problems, 141b
U.S. Food and Drug Administration (FDA), Viral infections, 112-113 fixing solution, 140
236 Vital pulp therapy, 28-30 image characteristics, 138-139
U-shaped palatal (horseshoe), 354 apexification, 29-30 latent image, formation, 140
Usual, customary, and reasonable (UCR), materials, 28-30 latitude, 139
234 methods, 28-29 penny test, 140
pulpectomy, 29 processing, 140-141
V Vita Lumin Vacuum Shade Guide, 361 solutions, 140
Valproic acid, 307 Vitamin D, 328-329 rinsing, 140
Value Vitamin D3, synthesis/activation, 328f safelighting, 140
adjustments, 361 Vitapan 3D-Master Shade Guide, 361 X-ray machines, 132-134
lightness/darkness, 361 Voglibose, 327 anode, 132
Vancomycin, 333 Voids, 43 cathode, 132
Variance (s2), 227 Volume equivalents, 338t high-voltage transformer, potential
Varicella (chickenpox), 112 von Recklinghausens disease, 128 difference generation, 133
Varicella-zoster virus (VZV), 112 power supply, 133
Vasoconstrictors W X-rays
addition, 103-104 W-arch, 176 copies, provision, 246-247
amounts, calculation, 310 Warfarin, oral anticoagulants, 323f deterministic effects, 135
systemic effects, 309t Warthins tumor, 122 dose, fractionation, 136
usage, 309 Waterlines, 233 health physics, 137-138
Vazirani-Akinosi technique, 105 Water/powder ratio, increase, 366 intensifying screens, 138-139
V bend couple, 171f Wave theory, 132 matter, interactions, 134
Ventricle, conduction velocity (reduction), Wedge positions, 64f production, 133-134
317 Wegeners granulomatosis, 115 X-ray tube, components, 133f
Verbal communication, care, 237 Weight equivalents, 338t Xylitol, 39
Verbal facilitation, 238 White sponge nevus, 130
Verrucous carcinoma, 118 Whole-body irradiation, effects, 136 Z
Vertical corrections, 182 Willful negligence, 212 Zero-order elimination kinetics, 293
Vertical defects, 276 Wire cross section, 173 Ziconotide, 316
Vertical deficiency, treatment, 179 Wire length, 173 Zinc phosphate cement, mixture, 364
Vertical dimension, 350 Wire material, 173 Zinc polycarboxylate cement, viscosity, 364
insufficiency, effects, 349 properties, 172-173 Zolpidem/zaleplon, 304-305
Vertical excess, treatment, 179 Wire selection, 173 Z-plasty, 348
Vertical fractures, occurrence (process), Witnesses, 247 Zygoma, 146
21 Working films, 17 Zygomatic fractures, requirements, 86

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International Standard Book Number: 978-0-323-22568-7

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Printed in the United States

Last digit is the print number: 9 8 7 6 5 4 3 2 1

Steven J. Lindauer, DMD, MDSc Mark Taylor, DDS, FACD

1.7 Odontogenic Infections 94 2.9 Intraoral Radiographic Examinations 143

3.0 Evaluation of Dental Literature 223 Local Anesthetics 308

1. Clinical diagnosis, case selection, treatment planning,

c. Intense pain. d. Occasionally, there may be slight tenderness to

4. Chronic apical abscess. 2. Location.

2. The clinician should use two mouth mirror handles

c. Osteomyelitis. (2) Maxillamaxillary sinus, incisive foramen,

(2) Manifestation of a periodontal abscess during (2) Improved obturation.

c. Use an apex locatoran electronic instrument (2) Treatment.

is to establish drainage and to clean and shape the 3. Procedure.

C. Disinfection. of the tube head or cone when compared with

Root canal orifice

2. Remove the instrumentthis approach is usually un- 4. Root perforations.

c. Immediate sealing of defect reduces periodontal

(3) Midroot fracture. c. Physiologic splint.

c. Repair occurs within 14 days. This is not clinically c. Clinical evidence.

c. Posts do not reinforce the tooth but further weaken A. Percussion

C. Obligate anaerobic bacteria C. Grinding a silver metal blank to a nontapered

OUTLINE process (caries management based on risk assessment)

1. S. mutans is believed to be the primary causative

Primary modifying factors: Secondary modifying factors:

*In the absence of protective factors

The Caries Balance Box 2-1

histatins, and proline-rich proteins, promote

Figure 2-5 An accurate clinical examination requires a

Figure 2-7 Caries can be diagnosed

fissure or pit. Radiographic diagnosis should be

h. Improper anatomic contoursamalgam restora- support; dentist-patient compatibility; availability

d. A straight fissure bur is an elongated cylinder.

Round Football Barrel Flat-end Beveled-end Inverted Flat-end

Round-end Flame Needle Interproximal Pear Donut Wheel

e. Occlusal preparations. (2) Gingival walls of class V. Outline is governed

3. Primary retention form. (2) Groove extensions (may be for any

(3) Factors dictating outline form include caries,

(c) Boxlike preparation form, which provides

5.0 Restoration of Teeth chlorhexidine, or other desensitizers. Historically,

(1) Spherical. c. There is no evidence ensuring that alternative

instrument, the instrument is switched, and the

and exerting pressure on that tooth rather than

excess exists and to smooth the proximal

(2) Marginal ridge left too high. a. Less microleakage.

(2) Fill incrementally and cure in appropriate d. Microhybrid composites.

d. Hypocalcified areas. (1) Be easy to apply and remove.

(1) Primary retention. (b) Occlusal bevel.

Sample Questions the external tooth surface, they usually diverge

Oral and Maxillofacial

OUTLINE B. Aseptic technique.

1.2 Dentoalveolar Surgery

B. Contraindications. e. Hypercementosis or widely divergent roots.

Box 3-1 Box 3-3

Figure 3-1 Bone types based on quan-

Table 3-1 is the requirement of a second surgical site

Horizontal or Vertical Crown Fracture Tooth Displacement

1.3 Trauma Surgery Coronoid

A. Tooth fracturesclassifications of tooth fractures have