ORAL SURGERY by Dr.

Sammy
10/05/11

 If the patient is taking warfarin (5 mg daily) for prosthetic valve replacement,

ask the patient about his present INR. Good range is around 3.2 – 3.3.
Arrange for antibiotic prophylaxis. Contra indicated drugs when pt taking
warfarin are metronidazole, macrolides (erythromycin), tetracyclins,
cephalosporins.

 For antibiotic prescription do not say 1 tablet or 2 tablets per day but say upto
600 mg or 300 mg etc. For analgesics, can say 2 or 3 tabs per day

 Muscles forming floor of the mouth – mylohyoid – forms

diaphragm(mylohyoid ridge of mandi-body of hyoid)
Geniohyoid(Genial tub.-BO Hyoid)
Supra hyoid
Ant belly of digastric(Intermediate tendon-medial surface of mandi.)

 Most common cyst is radicular cyst (peri apical cyst). In early stages
confused with peri apical cemental dysplasia (radiolucent in the earlier stage
and later presents with radio opaque foci (cementum). In the latter, the tooth is
vital, no caries, common in middle aged African women

 Alveolar osteitis(Dry Socket)

Causes: excessive mouth rinsing, infection, LA with vasoconst., female pt , smoking,
pregnancy, OCP, mandible post, excessive tissue manipulation during ext/trauma,
food debris.
Management: atraumatic ext, SRP before ext, no smoking after exo, NSAIDS, clean
socket with warm saline, remove any debris, bone pieces , dressing/iodoform
gause/eugenol , balsam of peru, chlorobutanol, benzocain.. dressing in first 24 hr
then alternate day and then every 3-4 days..(Alveogel: Butylamino benzoate
which work as LA, Euginol work as obtudent, iodoform work as anti bacterial)

 Extra coronal course of facial nerve, trigeminal nerve

 Medical emergencies
Causes of unconsciousness in dental chair and state 3 characteristics for each
cause. Outline emergency management
Follow DR ABCD for resuccitation

Epileptic patient: When having seizures, first step is make sure patient is safe and
flat , not hurt himself, remove anything from the mouth.Then - tonic phase, give
puff of 02. If seizures again, confused, sleepy, unconscious - status epilepticus,
then call 000
 (Unconscious patient positioning – supine
Conscious patient – his comfortable position)

Cardiac arrest: 3 signs to look for is Response, Breathing and Pulse

Asthma: Make sure patient has brought his medication. If asthmatic attack,
patient chooses his position, 4 puffs of inhaler, wait for 4 min and repeat 4 puffs. If mild
attack (speaks in sentences), treatment is like above, if severe attack (speak in words
only), call 000.

 Examiner looks for the dentist’s position, jaw support, teeth extraction
movements. Follow the steps – LA, Xn and guaze.

 Inf Alv Nerve Block (IAN block)

Injection in pterygomandibular space. Boundaries
Medial: Medial perygoid (arises from medial of lateral pterygoid plate)
Lateral: Mesial side of ramus of the mandible
Anterior: Buccinator muscle
Posterior: Pharynx

Pterygomandibular raphe is a tendon attaching superior constrictor of pharynx to

buccinator. Needle penetrates buccinator but should not penetrate sup constrictor
muscle(????)When buccinator is slightly pulled outside, triangle is formed, needle is
injected at the apex of the triangle

Inj: 1 cm above lower occlusal plane, from opposite premolar.Guide needle until hits the
bone, slightly retract (2/3rds of needle inside), aspirate and give 3/5 th of the catridge.
Withdraw half way and 1/5th of catridge for lingual nerve block and finally for long buccal
nerve block, give remaining 1/5th at buccal of 8(wisdom tooth)

Premature needle hit, donot completely remove the needle, but direct needle from more
mesial/ anterior to the previous position (move towards midline)

If repeated IAN Blocks fail, then Gow Gates Technique used.

Complications:
If hit maxillary artery, patient screams and develops blanching( blanching is due to arterio
spam caused by adrenaline in LA). If deliverd into pterygoid plexus, develops
haematoma, compresses on lateral pterygoid and therefore trismus. Infection from
plexus can spread to cavernous sinus.

Arteries collect blood and carries it to peripheral circulation (arteriospasm caused by

adrenaline causes peripheral blanching) where as veins carry blood to systemic
circulation (heart) (causing systemic toxicity) and then carried to peripheral
circulation??.
Systemic toxicity can occur, 2 reasons of toxicity being 1) excessive dose 2)Intra vascular
Injection. Once adr in blood is metabolised, symptoms regress.

 Never give block for maxilla, as there is is an easy diffusion due to porosity of
the bone. Both buccal and palatal. Barrel of the needle facing towards the
bone – less painful and no lump formation.

 Commonly used drugs in dentistry

LA, Antibiotics, Anlgesics and Emergency drugs

Emergency drugs: Adrenaline, GTN, Aspirin, Glucagon, short acting bronchi dilator,
glucose.

Glucagon: Glucagon is produced from alpha cells and insulin from beta cells of pancreas,
both having counteracting actions. In a hypoglycemic patient, when conscious, give
glucose water?? And then give long acting polysaccharides like sandwich. If
unconscious, then glucose powder or smear honey (both glucose and honey are
monosaccharides)on the buccal sulcus and administer 1 mg of glucagons IM.
Brain(cerebral tissue) is very sensitive to glucose levels, and when the levels fall,
glucagons breaks down to form glucose (glycogenolysis), pushed into blood and
increase blood glucose levels.

 Extraction position and movements:

Read chapter from contemporary oral and maxillofacial surgery- Never

choose rotation only.

Position: Always at the front of the patient except for the 4th quadrant which is at the right
side of the patient.
Movements:
Maxilla
Anteriors (incisors and canines): root cross section being round to oval- ROTATION with
apical force

4s and 5s: 4-buccal and palatal roots, 5-MD flattened and

Molars – BUCCO PALATAL+STEP DOWN: First movement to buccal and bring back to
normal position(palatal movement means this, but not going to palatal from normal
position).Step down is move to buccal and normal and then pull down and continue to
buccal and then to normal and pull

Mandible
1s and 2s: flattened MD – LABIO LINGUAL (same as for max 4s 5s, do not come to
lingual lingual)
3s: oval – ROTATION with apical force
4s 5s: round or oval – ROTATION
6s 7s: M and D roots – BUCCO LINGUAL: here move bucally, move back to normal and
then go LINGUALLY (unlike for max molars) and then FIGURE 8 MOTION. Figure 8
motion may cause sub luxaton of adjacent tooth.

 Most common problem after extraction is sub luxation of the adjacent

tooth.Therefore after Xn, compress socket, ask patient to bite hard, check
occlusion and then place the guaze on the socket. If unnoticed and patient
comes after 24 hrs complaining of no able to bite on that side/very painful, it is
very difficult to position the tooth back which is then need to do selective
grinding

 OPG landmarks
1) Head of the condyle
2) Glenoid fossa
3) Articular eminence/tubercle
4) Zygomatic arch: Muscle attached to its inferior border is masseter muscle
5) Posterior border of maxillary sinus
6) Outline of maxillary sinus
7) Pterygo maxillary fissure: t shaped space at the posterior border of max
sinus, posterior to fissure, radio opaque line is pterygoid plate
8) Zyg process of maxilla:Seen in max sinus as an arch
9) Infra orbital margin
10) Hard palate
11) Nasal septum
12) Anterior nasal spine
13) Inferior concha/turbinates
14) Naso pharynx – Large radiolucent area near condyle and below
15) Oro pharynx – space below naso pharynx
16) Hyoid bone: lateral on both the sides
17) Radioopacity in the mid line of OPG: superimposition of cervical spine
18) Styloid process: from temporal bone. Attachments include 3 muscles and
2 ligaments forming styloid apparatus
3 muscles: stylohyoid, styloglossus and stylophharyngeus
2 ligaments: stylomandibular and stylohyoid

When stylod apparatus gets calcified and elongated – EAGLES Syndrome - patient
presents with difficulty of swallowing, painful swallowing, pain on lateral excurtions and
sometimes pass out due to pressure on carotid body

19) Coronoid process: Temporalis muscle attachment

20) Ear lobe

 Muscle attachments:
Medial pterygoid – medial side of ramus
Masseter – Lateral side of ramus
Lateral pterygoid – Has inferior head and superior head (arising from infratemporal bone of
greater wing of sphenoid. Inf head attach to condyle and pterygoid fovea(???);Superior
head attach to disc and capsule

 Muscles for opening of jaw(depression): Lateral pterygoid, digastric (both ant

and post bellies) and mylohyoid and geniohyoid
Muscles for closing of jaw (elevation): Temporalis, medial pterygoid and masseter

 For small oro antral communication: Allow blood clot formation, suture it. Ask
patient not to blow, Whistle, no mouth instruments, sneezing (diff to ask him
not to sneeze, so tell him to open his mouth and sneeze). Never ask the
patient to blow to check if communication is suspected, but the diagnosis s by
looking at air bubbles while breathing (in the socket). Antibiotic cover for 5
days and nasal decongestants

 Alveogel:
Ingredients: Butyl amino benzoate – LA – to relieve pain
Iodoform – Antiseptic
Eugenol – obtundant

In pts allergic to iodine, alveogel C.I. Therefore, znoe paste included into socket along with
sterile cotton and Vaseline (facilitates easy removal)

Isolate buccal and lingual with cotton, irrigate with saline (not with chlorhex – why?? May
be bcos chlorhex is pungent and patient jumps off chair when used to irrigate the
socket), dry the socket gently with guaze. NEVER CURETTE – though no bacteria in
the socket, mouth containing loads of bacteria might gain access to the root and bone
by curettage. Place alveogel upto the socket and recall in 2-3 days.Analgesics can be
given. Repeat the process if still doesnot heal. The socket heals from below to above
through the formation of granulation tissue.

 L.A: 2%Lignocaine
;
Ingredients - Lidocaine. 2% means 20 mg lidocaine in 1 ml of solution. In 2.2 ml(catridge
volume available), 44 mg of lidocaine is present. Always available in combi with
adrenaline.
Adenaline: Vasoconstrictor – 12.5 microgm in 1 ml of solution, in 2.2 ml, 27.5
micro gm present. It reduces toxicity by retarding absorption, maintain clear operating
field , increasing efficiency of the treatment.
Sodium meta bi sulphite – prevent oxidation of adrenaline
Nacl – provides chloride to maintain isotonicity of the solution
NaoH – buffering action to maintain the pH.9Acidic – 3.0???) LA doesnot work
in acidic envi as dissociation doesnot occur which is necessary to release lipophilic free
base that penetrates through the lipid membrane of the nerve to block Na channel.
Water – all ingredients suspended in water
 Methyl paraben -NO MORE used.

Sitanest – 1.8ml catridge: 3% prilocaine + felypressin (0.031 IU/ml). No Na meta

bisulphate present in the catridge.
Used in pts where adrenaline is absolutely C/I – Uncontrolled hypertension
Thyrotoxicosis (have elevated B.P)
MAO inhibitors
Sitanest not used in pts with methaemoglobinaemia and pregnant women (felypressin
action like oxytocin – premature labor (usually not happen with this minute dose)
Sitanest is also available with adrenaline

Scandonest: Mepivacaine – no Adrenaline

Procaine: unpredictable duration of action
Septanest: Articaine: always with adrenaline. Amide group also has ester link. If patient
allergic to amide/liver problem, ester cant be given as well, as pseudocholinesterase
that is needed for metabolism of esters is produced from liver. Therefore GA considered
in such a case.

 Surgicel: Oxidised methyl cellulose – acidic – coagulates blood protein. Used

to prevent post operative bleeding. Acts as a meshwork or scaffold for platelet
 aggregation (primary clot)(Later fibrin forms firm clot). Plug into socket. Lower
3rd molar sockets and Lower PM sockets – no surgicel as being acidic can
cause nerve paresthesia (mand/lingual/mental nerves).

Gell foam: Meshwork. All sockets

 Sutures: To approximate and hold tissues together for which tensile strength
is needed.
Plain gut – Tensile strength for 5-7 days; chromic gut for 7-10 days (both from cattle gut)
Vicryl – 21 days
Dexon – Longest time for tensile strength for 28 days
Silk – non resorbable.

17/05/11

 MEDICAL HISTORY:
Good medical history is required to prevent complications

Q: Have u stayed in hospital, GA, operation?

Ex: If patient says that he has got open heart surgery done – it could be Coronary bypass
surgery. If in less than 6 months, then consider antibiotic prophylaxis; or – it could be
Valvular replacement, organize for antibiptic prophylaxis. The patient will be on warfarin
too. Look for INR. If <4 or up to 4, single tooth extraction can be carried out, but need a
lower level if need multiple extractions.

INR: International Normalised Ratio

Normal prothrombin time – 11-14 sec. Laboratory takes normal prothrombin time of many
normal patients, get an average=Mean of normal range
Therefore INR = Pateint’s prothrombin time/Mean of normal range. It is a ratio, so no units.
Obtain INR a day before or even on the day of surgery. Do not stop warfarin if INR is upto
4. If >4, then it takes atleast 3 days for change in INR to occur after reduction of
warfarin dose. Check for INR, If in normal range, continue treatment. Also organize for
antibiotic prophylaxis.

Warfarin:
An anticoagulant that interferes with the clotting factors ii,vii,ix and x factors all of which
are vit k dependent. Vit k injections given to reverse the action of warfarin.(other clotting
factor produced in liver other than above mentioned is factor v- not vit k dependent and
warfarin has no effect)

Management of patient after extraction:

Currette the socket
Flush with normal saline
Compress the socket
Surgicel/gelfoam – to prevent bleeding form the bone
Horizontal mattress suture is the best – compress gingival against alv bone, prevents
bleeding from gingival (suturing-starting from buccal, go to lingual and then from other
point on lingual to buccal and then knot on buccal.
4.8%tranexemic acid mouthwash – an anti fibrinolytic agent, protects fibrin clot. Very
crutial in the first 2 days after extraction. It is available as a tablet also(cyclokapron) –
Dissolve 1 tab in 10 ml of water

Q: Have u or an immediate family member had any reaction to GA? Eg. halothane
Major life threatening complication to GA is malignant hyperthermia. If even recorded in
immediate family member, then do not administer GA. Malig Hyperth is due to
hypermetabolism of skeletal muscles caused by certain constituents of GAnesthetic
(like ketamine, catecholamine:not sure).Patient has rigidity, hyper metabolism in
muscles, high temperature, acidosis, myoglobinuria due to increased metabolism.

If GA carried out and patient develops symptoms-management:

Immediately stop the procedure, Give IV cold fluids, ice blankets both to decrease the
temp. Muscle relaxant IV(life saver drug) – Dantrolene

Q:Any serious problems after dental surgery?

Usually patients complain of pain and swelling. Listen attentively to patient. Not very
significant

Q: Any heart disease, high blood pressure, heart murmer or rheumatic fever?

If no congenital heart disease and functional murmer – no need for antibiotic

prophylaxis.If uncorrected cong heart disease and murmer – then antibiotic
prophyaxis.If patient says had rheumatic fever when a child, no need for
prophylaxis.Only in Indigenous Australians prophylaxis considered (both for rheumatic
fever and Rheumatic heart disease) coz poor SocioEcoStatus and malnutrition.

History of angina: GTN (glyceryl trinitrate) is available as sublingual tablets or spray.

Description of pain: Retrosternal area, centre of chest. In 10 minutes after GTN, pain
should be relieved. If getting worse even after 10 min of administration of GTN, give
soluble aspirin straight away – as it is MI.

History of MI: Defer treatment for 6 months, unless until an absolute emergency, in which
case just relieve the pain. The procedure should be as short, painless as possible. No
adrenaline – so scandonest or citanest used. MI patient will also be on warfarin,
therefore should be stabilized.

Stroke: Most common cause being uncontrolled, untreated hypertension. Defer trt for 6
months, until absolute emergency. Patient will be on anti coagulants, therefore risk of
bleeding.Vasoconstirctors should be cautiously used, max of 1 catridge.
Hypertension: Normal BP : 120/80 mm Hg. If patient says he has BP, ask him if it is under
control. If uncontrolled BP >140/>90, defer trt until BP is controlled. If excessive pain,
BP further increases. Emergency pain relief under LA with no adrenaline, therefore
citanest used. If hypertensive patient in limits upto 130-140/80-90 mHg – treated as for
normal patient.

Q: Pacemaker?
No ultrasonic scalers or electric pulp testers. No need for prophylaxis

Q:Epilepsy?
When was the last seizure? If 1 seizure per day/week – refer to GP, if trt required, done
under GA. If 1 in few months, ask if on medications?
Patient usually knows if they are about to get the seizure (aura). If occurs, stop trt, make
sure patient do not hurt himself, remove any object from mouth, put him supine (NEVER
RESTRAIN THE PATIENT).Initially is rigid tonic phase, then clonic movements phase
and then gains consciousness. If turning blue – cyanotic – give oxygen. No trt after this
episode, temporize, ask him to call some one to escort him and take him to GP straight
away. No driving/operatory

Q:psychiatric treatment?
If properly medicated , no problem. If elaborative treatment need to be done – proceed
under G.A

Q:TB, Asthma, Lung disease?

Bronchial asthma is the commonest problem. Ask history: How often do you get? He could
say he had an attack when he was a child or gets attack – seasonal, exertion, nervous
or tensed.
Medication: Salbutamol (vantalin, bentamol??)
Seretide (Bronchodilator)
Ask the patient to get their inhalers or puffers
Asthmatic effect on chair: If forgot to get their puffer: Patient chooses his own comfortable
position
Mild attack: He talks in sentences, wheeze present.
4 puffs, wait for 4 min, 4 puffs and wait for 4 min
Severe attack: He talks in words, no wheeze
Call ambulance
4 rule again
Give oxygen

TB: Becoming common. Usually gets treatment under public health.

If had a history of TB, but treated – treatment as a normal patient
If have active TB, referred by doctor to the dentist as source of pain – toothache:
Last appointment in the day (as clinic to be closed after this patient for
infection control)
 Rubber dam mandatory
Only slow speed
No triplex. All three to avoid aerosols/droplets
Simple, practical and short period of treatment to relieve pain

Smoking:
Warn the patient of the consequences after extraction if smokes within 24 hours
of xn – example: Dry socket, which is even more painful than toothache.
Periodontal health is also usually poor

Q: Infectious diseases:

Hepatitis
Hep A is food related
Hep B and C: Should be immunized against Hep B. If not immunized against it, the chance
of infectivity after a needle prick injury against
Hep B is 30 – 35%
Hep C is 1 -2 %
HIV is 0.3%
Liver is compromised in Hep A,B and C and also in cirrhosis of liver (Fibrosis of liver
parenchyma, lung becomes nodular and firm – common in chronic alcoholics)

Hep B:
If full blown Hep B, he will be jaundiced, very very infectious. Liver is involved therefore
bleeding problem. LA drugs, which are metabolized in the liver are cautiously used.
If the patient already had Hep B infection ,Immunization against it does not help. He will a
Hep B carrier. Treatment can be carried out after performing liver function tests
INR Coagulation profile
Clotting problem suspected always with liver problem.

Hep C:
Common in IV drug users (infected, contaminated shared needles, blood transmission)
Perform liver function tests, coagulation profile

In chronic alcoholic – cirrhosis of liver

suspect bleeding problem.
Elaborative trt not done
LA cautiously given: LA remains in circulation as there is much reduced/no metabolism. If
given continuously, accumulates in circulation. Referred to hosp: Perform blood test to
see the levels in circulation and once drop down can give the next dose.

Mechanism of drug metabolism:

Cytochrome P45O system, in distal part of liver, contains enzymes that metabolise drugs.
Receives blood supply from hepatic artery. Once liver parenchyma fibrosed, blood
supply to distal part compromised, metabolism is also compromised – toxicity
Renal failure patient: on dialysis – antibiotic prophylaxis

HIV+ve:
Could be full blown disease – AIDS
Could be HIV carrier – treat as normal patient
Ask for recent blood test (platelet count should be acceptable)
If CD4 count <200 – AIDS
>200 - Carrier
Full blown AIDS – Might also have leucopenia (prone to infections)
Thrombocytopenia (prone to bleeding)
On immunosuppressants
Trt: Only relief of pain/symptoms
If require xn: Full course of antibiotics (prophy + course)
Platelet count (normal is 150 – 400) – up to 100 – can do
xn
< 80 – no xn; give platelet concentrate in the hospital

Sharp injury:
Deglove
Wash and dress your wound
Blood test
If pt has no infection – both pt and dentist give blood test
If pt does not agree – dentist alone gives blood test three times (soon after accident, 6
weeks after that and 6 months after 2nd test)
If needle stick injury from known Infectious pt: Call hospital, Prophylaxis –
immunoglobulins taken within 24 hours to boost immune system, fight against virus

Prion diseases

CJD: Creutzfeld Jacob Diseases

Transmissable Spongiform Encephelitis
Neuro degenerative disease
Rapidly progressive and invariably fatal
Infected agent: Prions Proteins

Classification:
Classical: Sporadic mutation
Familial
Iatrogenic. These 3 are transmitted through prions proteins
Variant
Classical CJD:
Incubation period is long
Common in older people (60 – 70 yrs), present with dementia, confusion, disorientation,
walking problems
Prions are not present outside CNS, therefore not present in oral cavity
Earlier days: for CJD patients, thorough sterilization, infection control, disposable
instruments mandatory
Now a days: CJD patients are treated like a normal patients, with standard precautions.
Only problem could be during Maxillo facial surgery involving trigeminal ganglion,
neurosurgery and posterior orbit surgery, special precautions needed.

Q:Why is 1972 – 1989 duramater grafts mentioned in the medical history:

During that time, instruments could not have been properly sterilized, and if used in
duramater graft procedures (neurosurgery), more likelihood of carrying a disease.
Iatrogenic CJD: If human pituitary hormones are donated from a donor (prior to 1986) who
could have been diseased – more likelihood of transmission of the disease.

Variant CJD:
Also called Mad Cow disease
Bovine in origin: Consumption of infected meat in UK between 1980 -1986, not accept
blood transfusions.
Catgut suture material, derived from cattle gut, was not used for sometime thinking that it
could carry infected material.
Incubation period is short
Common in younger age groups (20 – 40 yrs), present with psychiatric symptoms
Can affect lymphoid tissue, closest being tonsils??)

Q: Diabetes
It is a common endocrine disorder involving metabolism of carbohydrates, proteins and
lipids
IV types:
Type i: IDDM
Type ii: NIDDM
Gestational
Secondary: To some other causes – ex: removal of pancreas due to tumor leading to
diabetes.
(Diabetes insipidus – doesn’t come under classification of diabetes – it is due to lack of
ADH hormone)

Type i:
Autoimmune disorder of beta cells – not enough insulin produced.
Juvenile
(Familial)Strong family trait
>15%
Trt: Insulin injections

Type ii:
Enough insulin is produced but the tissues are insensitive to it
Maturity onset – middle age
Familial and also should think of lifestyle like exercise, diet - obesity, hypertension are the
major risk factors
Trt:
Oral hypoglycemics : Diamicron??
Metformin (diformin)

Management of diabetic patient:

Usually mid morning or earlyafternoon appointment

Normal medication and normal meal: If taken medication with out meal => Hypoglecemia.
Check if the patient has taken his medication and meal; if not send him to eat and wait
for atleast ½ hour before starting treatment
During elaborative trt, for ex: crown prep, impending hypoglycemia (patient beginning to
develop hypoglycemia) is shown by any unsual behaviour:
Patient becoming figity? – uncooperative
Sweating, disoriented, sudden jerky movements

Management: Stop trt

Give orange juice , revives the patient back to normal and then can give
strong coffee with double sugar
Continue trt
Prevention: not book longer appointments

Uncontrolled diabetes:
Infection sets in easily and very hard to heal (in a diabetic patient)
Different situations to deal with:
If new patient walks into clinic with severe pain, say around 3 pm and says he is a
diabetic: Ask him to eat, after ½ hr proceed with the trt and then antibiotic cover for 5
days.

If middle aged patient, type ii diabetes on medication presents with throbbing pain acute
alveolar abcess (huge):
Send him to doctor/hospital with a referral letter
Doctor: Ask him to eat, give him a shot of insulin

Dentist: Then give sub mucosal injection??(topical), drain pus and antibiotic cover

Why giving insulin to type ii diabetic patient: When infected, even type ii pt can develop
ketoacidosis (whch is common in type I pt), this is the reason to give insulin.

Three primary manifestations of diabetes:

Hyperglycemia
Ketoacidosis
Vascular phenomenon
Hyperglycemia: Interferes with function of PMNs
Favors growth of bacteria (Due to increased sugar levels)
Ketoacidosis: Interferes with migration of PMNs to the injury site
Vascular phenomenon: Diminished blood supply, so enough of nutrients or oxygen do not
reach the infected area for healing.

Q: Kidney problems
If kidneys removed or stones removed – no problem in treating the patient
If underwent dialysis, then yes it is a concern:
Do not treat the patient the same day of dialysis trt as the process itself would take
long time and also that heparin effects take atleast 6 hours to seize. Therefore treat the
pt the day after dialysis.
Antibiotic prophylaxis – to prevent the infection of the A-V shunt that is used for dialysis
Patient appears anemic as the haemopoisis (production of RBCs) is effected due to
lack of haemopoitin (which is produced in kidney)

Q: Adrenals:
When patients on steroid therapy (where adrenals removed or where synthetic steroid trt
given), adrenal cortex undergo atropy (suppression) after 3 weeks of >5mg of
prednisolone. (ACTH from pituitary gives feedback when the body needs steroids,
stimulating adrenal cortex to secrete coticosteorids. When patient on steroids, No
stimulation from Pituitory, therefore adrenal cortex has no function, therefore
suppression/atropy). It takes atleast 2 weeks for adrenals to revive back to produce
steroids after the dose is stopped.

Adrenal medulla – produces adrenaline

Adrenal cortex – produces corticosteroids

Steroid supplement is necessary for patients who are on long term steroid
treatment (for ex: in rheumatoid arthritis)

Management: Double the daily dose of the steroid on the day of the treatment.

Morning appointment – to avoid the risk of adrenal crisis: After 8 hours of

treatment, patient might feel sick, lethargic. Therefore if the trt is done in the morning ,
this phase would occur before night, which can be identified and be admitted to the
hospital. If trt is done in the afternoon, this phase could occur at night, which might be
mistaken to be falling asleep.

Antibiotic cover needed – as immunosupression due to longterm steroid

therapy
If post op pain expected, maintain double dose the next day; otherwise
patient can go back to normal dose the next day.

Situations:
If patient on long term steroid therapy – went off therapy < 2weeks ago, need steroid
supplement, the dose would be his last maintenance dose he used earlier – antibiotic
cover needed.
Went of therapy >2 weeks ago, no need for supplement/ antibiotic cover

Q: Thyroid:
Overactive thyroid – acute thyrotoxicosis – no trt
If trt to be done, absolute minimal trt under LA
WITHOUT adrenaline (as systolic BP is already too high)

Underactive thyroid – Hypothyroidism – If on medication, usually presents no problem.

Q: Arthritis
Patients with arthritis are on NSAIDS – Aspirin, an antiplatelet agent – cause bleeding

Rheumatoid arthritis: an autoimmune disorder of joints- take daily dose of steroids and
weekly dose of methotrexate – both of which are immunosuppressants. Therefore need
ABcover

Joint Replacement Surgery: If done <6 months with no infection – AB prophyaxis

If done >6 months with no infection – call orthopedic surgeon
if the pt needs – he would usually say 2gm cephalosporins
(99.5% joint replacements need AB prophylaxis)

AB prophy needed if joint is infected, If diabetic pt/ immunosuppressed (due to medication)

or immunocompromised (due to disease itself) pt/ rheumatoid arthritis, pt needs joint
replacement surgery.

Q:Antibiotics: If patient has type I hypersensitivity to pencillin, then more chances of

being allergic to cephalosporins as well.
If just rashes to penicillin, then can give cephalosporins

{ four types: type I, immediate hypersensitivity reactions, mediated by interaction of IgE

antibody and antigen and release of histamine and other mediators; type II,antibody-
mediated hypersensitivity reactions, due to antibody-antigen interactions on cell
surfaces; type III, immune complex, local or general inflammatory responses due to
formation of circulating immune complexes and their deposition in tissues; and type
IV cell-mediated hypersensitivity reactions, initiated by sensitized T lymphocytes either
by release of lymphokines or by T-cell–mediated cytotoxicity.}

Q: Pregnancy:
If pregnant and in first trimester : no trt as organs are forming, medications could affect
fetus and stress could lead to death of fetus
2nd trimester and first1/2 of 3rd trimester are safe periods to trt: usually short period
emergency trt.

If required to take an x-ray – use thyroid collar and lead apron.

LA for pregnant: 1 to 1.5 catridges – do not shoot too much of LA, as body pH of pregnant
woman is 7.4 and pH of fetus is 7.2 – LA can cross placental barrier – affects pH of
fetus – Ion Trapping – harming fetus.

Position of the patient: left lateral side – no compression on inferior vena cava . If put in
supine position – uterus can compress on diaphragm, therefore no compression on
venacava.

Late half of 3rd trimester: No trt as stress could lead to premature labor
Drugs safe: Amox
Paracetamol.
No NSAIDS - cause bleeding

Q: Bisphosphonates:
Can be Nitrogen containing (N2) or Non-Nitrogen containing
Can be given orally or IV
Given to treat bone diseases, bone metastasis

If patient on IV bisphospho, refer to specialist straight away – incidence of BRONJ (Bispho

Related OsteoradioNecrosis of Jaw) is 10%

After Xn, if socket doesn’t heal even after 8 weeks, BRONJ developed. Even if socket
heals after 8 weeks, if dentures given, can lead to ONJ. Never think of immediate
dentures after Xn; wait for atleast 4 – 6 months to give dentures, with special care given
to inner/lining surfaces.

Window period:
If patient on bisphospho for 2-3 years, less chances of ONJ
For >3 years, more chances

Prevention of ONJ: doctor should refer to dentist, dentist should do full mouth restoration.If
patient already on bisphospho, no trt; if have to treat and if has other problems (like
diabetes or radiotherapy to jaw) refer to surgeon

Drug holiday:Protocol to manage patient on bisphospho

Pt should stop taking drugs for 3 months
Trt the patient
Continue to stop drugs for next one month
Then start taking the drugs.
Before going for a drug holiday – Fasting CTX test (for serum telopeptide – which is
breakdown product of I collagen in the bone (beta cross lapps test??)performed:
This test tells us how suppressed the bone turnover rate is: Turn over rate= osteoblastic
+osteoclastic activity). If taking bisphospho= osteoclastic activity is suppressed)
For every 1 month stoppage of drug, 25% turn over rate is returned. Increase in value
means that bone turnover rate is returning.

Units in which it is measured is nano or pico grams

Test performed as soon as starting drug holiday and then after 3 months of drug holiday

When performing Xn:

We need a value of 200 ngm/ pgm (>170) to perform an Xn.
Antibiotic prophylaxis
Savcol mouthrinses
Always suture (ONJ starts in alveolar bone)
Routin post op instructions
ABcover for 1 week
Post op review in 2 weeks
Then in 8 weeks. If healed – no ONJ; if not healed – ONJ
If no ONJ – wait for another 2-3 months to construct dentures with special care to lining
surfaces of the denture.

Better no implants in these patients as there would be no osseointegration with the bone.

 IAN Block landmarks:

Push buccinator towards raphae – forms a prominent sulcus/line between the two – Give
injection at the apex of the sulcus from the opposite premolar region at 1 cm above from
the occlusal plane.

 Mental nerve block/MENTAL INFILTRATION:

Just inject in between two premolars, just in to sulcus (not until it hits the bone – damages
the nerve) and deposit the solution – leads to formation of bump, now slightly press with
index finger to deposit the solution into the foramen.
INSTRUMENTS:

31/05/11
Q: SUTURES:

Role of sutures:
Splinting – To return tissues to its original position or to a new preplanned position.
Haemostasis – By directly ligating vessels/ compress soft tissue (vessels) against alv
bone/ Hold the pack over the wound (in case of capillary bleeding)
Immobilisation is to promote rapid healing – healing by primary intention
Reduce bleeding
Reduce formation of haematoma / odema
Reduce risk of infection

Types of sutures:
Resorbable / absorbable:
Organic: catgut, plaingut, chromic gut, collagen sutures
Synthetic: Vicryl (polyglactin)
Dexon (polyglycolic acid)
Polysorb – difficult to tie
Non resorbable / Non absorbable:
Monofilament: Nylon, praline, ss suture, polyester
Multifilament: Black (braided) silk

Lifespan of sutures:
Tensile strength is the period for which sutures hold the tissues actively
Plain gut: 5- 7 days
Chromic gut: treated with chromic salt to increase strength 10 – 14 days
Vicryl: 21 days
Dexon: 28 days.
Sometimes to be removed as they are present in the mouth even after a month
Organic sutures undergo proteolytic resorption and synthetic undergo hydrolytic resorption
(so longer time to resorb)
Silk lasts for a year

Tissue reaction to sutures depend on the material. Organic >>reaction than synthetic
More size, more reaction
Multi filamental silk has got worst tissue reaction, so therefore waxed to reduce.

Size of sutures:
Number is in o (oh). The higher the number, the finer is the suture. 3-o and 4-o are
commonly used in oral surgery

Needles:
Swaged needles (needle directly attached to suture)
3/8th circle needle (which is less than half circle)
Reverse cutting needles (not round body needles): Triangular in cross section, Reverse
has cutting edge on the outer convex surface of the needle so that it does not damage/
tear the wound tissue while penetrating through it.

Instruments used for suturing:

Needle holder
Toothed tissue forceps
Suture scissors
Cheek retractor/ flap retractor
Good lighting

Types of suture techniques:

Single interrupted: Single sutures
Horizontal mattress: Bleeding sockets (especially posteriors)
Continuous
Vertical mattress (not in oral surgery, but used for suturing skin)
Figure 8: To hold a pack on the wound

Knots: 2 in clockwise and 1 in anti clockwise

 BIOPSY:
Removal of a representative sample of the pathological lesion to establish a definitive
diagnosis
Types:
1. Incisional (FNAC, Punch biopsy included)
2. Excisional
3. Cytology (Brush/exfoliative)
4. Aspiration biopsy (for cystic lesions)
5. Autopsy (To establish the cause of death) - need not include here

Indications:
To establish diagnosis of a suspicious lesion
Ulcer lasting > 2 weeks
Chronic infl lesion not responding after the removal of the cause, even after 2 weeks
Mucosal hyperkeratosis (white lesions)
Bony lesions
Large cystic lesions of the jaw

Refer to an oral surgeon:

In case of medically compromised pt, Lesion in the posterior most area where
inaccessible, increase tendency of bleeding, Very suspicious (seeding of cancer cells).
 1. Incisional biopsy:

A thin, deep, narrow wedge of tissue, expecting to be big/cancerous is sent to lab to

establish diagnosis. (deep tissue needed to see if infiltration has occurred). Suture the
tissue edges.
Store the sample in specimen bottle containing 10% formalin saline
Fill details of the patient (name, age, identification etc??) and the site where the tissue
taken from and clinical notes (ex: indurated lesion on right buccal mucosa 2 cm * 3 cm)
and provisional diagnosis (ex: scc)
If two similar lesions at two different sites, biopsy taken and stored in 2 separate specimen
bottles (to differentiate the diagnosis/differentiate which diagnosis from which specimen)
Immune test no formalin immediate to lab for freezing or Michel solution.

Pathology report:
Carcinoma insitu: It is a dysplasia involving all layers of epithelium but not penetrated
basal lamina
Early invasive scc: Just penetrated lamina propria
True invasive scc: Epi, connec and all tissues (muscles, bone etc) involved

2. Excisonal biopsy:
Swipe the entire tissue and send it to lab. Usually done for benign lesions/very suspicious
small cancerous lesion

Small (<cm) nodular movable lump – incisional

Large (>cm) nodular fixed lump – excisional

3. Cytology:
Application: Candidial infection (smear or swab)
` Actinomycosis (sulphur granules)

4. Aspiration biopsy
Application: cystic contents
Instruments used: LA, syringe, 17/18 guage needle, blade, periosteal elevator,
osteotome/drill (if lesion in bone), suturing

 Examples of Cysts:
 Scalloped radiolucent lesion around teeth in the body of the mandible. Teeth
vital. No bony expansion, Intact lamina dura, AIR on aspiration
It is Solitary bone cyst or traumatic bone cyst
Trt: Open it, curette it, induce bleeding, healing in 6 months

 Swelling on buccal side, non vital tooth, straw colored (plain tea colored) fluid,
when held against light has shimmery shiny nature (cholesterol crystals)
It is radicular cyst or residual cyst
Trt: RCT or Xn???
  Multilocular radiolucent cystic lesion, vital teeth, plenty of blood coming on
aspiration
It is aneurismal bone cyst or it is haemangioma or could have entered a blood vessel

 Unilocular or multilocular radiolucent lesion. On aspiration – white cheesy

material. Confirmed by smear biopsy showing keratinized epithelial
squams(??)
It is OKC

 Unilocular or multilocular radiolucency, during aspiration, needle cannot be

pulled out
It is a solid tumor (ameloblastoma)

** Bone biopsy: For suspicious bony lesion ex: monoostotic fibrous dysplasia- have
ground glass appearance on x ray
Raise flap, remove chunk of bone by drill (preferable)/osteotome, suture.

 CYSTIC LESIONS OF JAWS:

Cyst: a cavity containing fluid

Classification: with lining
: With out lining

With lining could be : Epithelial

: Non epithelial/connective tissue

Non-epithelial/connective tissue lining cyst: Aneurysmal bone cyst

Solitary bone cyst
Stafne’s idiopathic bone cyst (present below
inf alv canal at the inferior border of the mandible)

Soft tissue cysts: Mucocoele, ranula

Epithelial lining cyst: Odontogenic
Non – odontogenic

Odontogenic cyst: derived from 3 sources of odontogenic epithelium

1) Remnants of dental lamina (glands of serres): OKC
Lateral periodontal cyst (LPC)
Gingival cyst
2) Reduced enamel epithelium (epithelium has undergone all stages of
differentiation and covers the developing crown): Dentigerous cyst
Eruption cyst
3) Epithelial rests of Malassez from PDL: Radicular cyst
 Residual cyst
Common cysts in order: Radicular>Dentigerous>Nasopalatine>OKC

Non-odontogenic cyst: Nasopalatine

Nasolabial

1. Radicular cyst:

Clinical features: Non vital tooth

Swelling on buccal (could be palatal in case of lateral incisor, where root
apex inclined palatally)
Can be of diff sizes (small to big), can be firm, but once perofrates bone,
presents as fluctuant swelling. Sometimes erodes bone and when palpated bone gets
depressed
Can get infected from infected non vital tooth leading to pus formation

Radiographic features: Well defined radiolucency with a radioopaque border

Loss of lamina dura
Aspiration: Straw colored / plain tea colored fluid, shiny cholesterol crystals

Q: PATHOGENESIS of radicular cyst:

Non vital tooth – has bacteria and bacterial toxins in pulp chamber and root canal
Irritate periapical tissues and epithelial rests of malassez in PDL
Rests proliferate in order to contain the infection
Mass of granuloma formation
Size grows and centrally placed cells devoid of nutrients, undergo necrosis, fluid formation
High osmotic pressure and osmotic gradient develps leading to transudation of fluid from
periphery into cystic cavity
This increase hydrostatic pressure in the cystic cavity exerting pressure on the peripheral
bone
Cells continue to proliferate and break down and the process of gradient continues slowly
and slowly
Also the peripheral cells contain PGs which causes bone resorption leading to cyst
expansion
Source of cholesterol crystals: The cell membrane and nuclear membrane very rich in
cholesterol (denti cyst also have cholesterol crystals)

2. Dentigerous cyst:
Associated with unerupted tooth, envelops the crown
Usually in posterior mandible (3rd molars) also in max 3rd molars, max canines, mand
premolars
Increases in size involving ramus of the mandible

Eruption cyst: Bluish translucent swelling, prevent eruption of permanent tooth.

Trt: take baby tooth out, give linear incision, allow eruption
 3. OKC:
It is thought to be replacing missing tooth/supernumerary tooth
40% associated with unerupted teeth – dentigerous origin OKC
Uni radiolucency
Well defined sclerotic border
Grows in the medullary space of the mandible in antero posterior direction
Invoves bony erosion (cortex involvenment) at a later stage

DD: Denti cyst

Uni ameloblastoma
60% arise from remnants of dental lamina (glands of serrus) – primordial origin OKC
Multilocular
Recurrence very very high in primordial origin as the epithelium has potential for
proliferation if remnants are left after surgical removal

Trt: Conservative approach: Enucleation, curettage and long term follow up

Syndrome associated – Gorlin Goltz:
Multiple OKCs
Multiple BCC
Calcified flax cerebri, bifid ribs

4. Residual cyst:
left over residual cyst even after Xn or RCT. Grows in size

5. Nasopalatine cyst (Incisive canal cyst):

Swelling along the midline of the palate near central incisors
can cause displacement of central incisors and can cause non vitality/discolration if grows
in size .
painful and salty discharge
Well defined radioluceny >6 mm – suspect this cyst

6. Nasolabial cyst:
Soft tissues cyst in nasolabial fold obliterating it.

Management of these cysts:

Enucleation: Removal of entire lesion
Marsupialisation: Remove the lid, to de pressurize the cyst, keep the opening patent.
Performed when the lesion is big and has potential for fracture if attempted to remove
the entire lesion
  DD for unilocular lesion

Ameloblastoma
OKC
Denti cyst
CGC Granuloma
DD for multilocualr lesion
Ameloblastoma
OKC
CGC Granuloma
Odontogenic myxoma
Central ossifying fibroma
Botryoid odontogenic cyst (Multilocular variety of LPC)
Haemangioma

 DD for multilocular bone lesion

Osteomyelitis
Aneurismal bone cyst
Tumors

7/6/11

 Surgical Removal of Teeth:

Indications: When conventional removal of tooth fails
When customary force fails to produce luxation (movement) of the tooth
Partially erupted tooth
Supernumeraries; any malposed tooth
Extremely decayed tooth/ root till the level of gingiva
Need a very good radiograph
Whether to do a surgical or not is dictated by THREE things :
ONE: Root
Root pattern and associated pathology
Dilacerated root
Locked tooth/ ankylosed (especially deciduous tooth – Locks bone and
sometimes permanent tooth. If perman removed during removal of deci – put the perm
tooth back and suture it
Widely divergent roots
Hypercementosed roots
TWO: Crown
Grossly broken down tooth
Extremely restored tooth – ex: post and core
RCT treated tooth – due to loss of most of tooth structure rendering tooth
brittle
Long standing maxillary molar – look at root and bone also
 If conical roots and enough surrounding bone – conventional method
used
If divergent and pneumatisation?? – then alv bone is
resorbed/atrophied – surgical removal
If ankylosis – Surgical removal

THREE: Bone
Mandible: If surrounding bone is thick, compact, cortical type (very opaque)
If tooth in multiple exostoses (Tori mandibularis – premolars Xn)
Atropied mandible
Maxilla: If max sinus undergoing pnematisation dipping between roots of
molars
Lone standing molar and hollowed out maxillary tuberosity
Habitual dislocation:
People move and reduce their joints by themselves. Such patients feel
pain on one side while undergoing Xn on the other side. Therfore ask them to bite on
bite block for support.

Procedure: Need good access to the surgical area.

After LA, raise a full thickness mucoperiosteal flap
Remove very little bone
Division of tooth/ roots
Removal of fragments
Wound debridement: Smoothen sharp bone edges with bone file
Pick up bone fragments
Curette if periapical granuloma (i.e., infection)
Flush with normal saline
Approximate flap and suture

Flap:
Flap design: Very important in healing of wound
The base of the flap should be wider than the distal part – to ensure good blood
supply
Good adequate size of the flap – for access and visibility
Small sized flap - more tension on suturing – delayed healing
Good sized flap – Less tension – Easy healing
Should not damage adjacent anatomical structures
ex: Mental nerve – never incise between lower 4 & 5, flap should be incised
either before or behind the mental foramen
Blade should be sharp and used at right angle – only tip hits the bone
Do not split interdental papilla
Rest flap on sound bone at the end of the procedure
Types of flap:
Buccal envelope flap – only one vertical incision – commonly used
Trapezoidal flap – 2 vertical incisions – also used
Triangular flap
 Semilunar flap – in anterior segments where aesthetics is a problem – to
access apical area (especially when PJC (porcelain jacket crowns) present.

Once flap raised by periosteal elevator, keep flap retracted by minnessota retractor (or
with rake retractor or ostim???)
Bone removal should be as conservative as possible – as now a days there is an option of
replacement of missing teeth by implants – which requires as much bone as possible)

Different situations and teeth:

1. Xn of grossly broken down 46 with divergent roots:

Raise envelope flap: it could be a vertical incision at distal of 46 and continue till diatal
of 44 or it could be a vertical incision at distal of 44 and continue till distal of 47
Removal by 2 methods:
1: With fissure bur cut the crown horizontally – remove the crown; Divide 2 roots with
fissure bur till furcation – remove one by one
2: Remove buccal bone; with fissure bur severe one root bucco lingually( root to be
severed is the one that is on the caried side of the crown (if mesial crown has gross
caries – cut mesial root); The rest of the tooth with one root can easily be removed,
even with luxator; Remove the other root.

2. Esthetic zone: Mid apical 3rd root fracture of mandibular canine or

premolar – pt wants implants
Raise an envelope flap (look for mental foramen in case of lower premolar xn)
For canine – flap extension till distal of 5
With probe into the socket, measure the depth at which the remaining root is placed
Remove a window of bone below that point
With cryers, using point of application (/ purchase point) flick the root fragment in an
upward direction.
Maxillary anteriors: After Xn, if apical 3rd of root fragment remained, but no
periapical infection – later develops infection with draining sinus, confirmed by the x ray
that root fragment present:
No conventional envelope flap (especially teeth with PJC crowns – more chances of
recession; therefore semilunar flap elevated well above lip line and bone removed over
the retained root fragment.

 Impacted teeth:
Any tooth that is completely or partially erupted; positioned against bone/ adjacent tooth/
soft tissue.
Supernumeraries are impacted as well
Submerged tooth – deciduous ankylosed tooth
Order of impaction:
Max/mand 3rd molar> max canine> mand premolar (erupt lingually)> mand canine

Indications of impacted teeth removal:

Pericoronitis – usually occurs with partially erupted teeth – commonest indication of
removal
Advanced caries with or without periapical pathology
Periodontitis
Cystic changes associated with unerupted teeth (dentigerous cyst)
Resorption or decay of adjacent tooth
Orthodontic and orthognathic reasons
Mandibular fracture involving unerupted tooth/ partially erupted tooth- otherwise the area
gets infected
Prophylactic removal to avoid trouble incase of patients with risk of endocarditis (no more
called SABE anymore)
Preprosthetic surgery (when tooth erupts due to bone resorption)

Contraindications:
If patient doesnot give consent for Xn
If active infection present: ex:Pericoronitis – abcess=> Drain abcess and antibiotics +
trismus=> limited access. Conservative trt only as infection can spread to bone if tried to
elevate infected flap and drill the bone. After active infection subsides => Xn
If all 4 wisdom teeth present inside bone; unerupted; no pathology; no symptoms
If high risk to inferior alveolar nerve – confirmed from x rays
Severely medically compromised pt – uncontrolled diabetes; clotting disorders+ on
medications
If fully erupted and can be used as an abutment

Age changes in relation to teeth and bone:

Young pts (18-20 yrs) Old pts (60 yrs)
2mm pericoronal space around unerupted tooth No pericoronal or PDL space
PDL space clearly outlined (ankylosed)
Roots incompletely formed Completely formed
Inf alv canal far away from root Very close; more chances of damage
Excellent blood supply Poor
More elastic bone More dense

Risk factors associated with 3rd molar surgery:

Maxilla:
If in high position – can be displaced into infratemporal fossa
Even in normal postion – chances to be displaced into max sinus
Divergent curved roots
Mesiopalatal presentation
Pt’s age: Elderly pt- more chances of fracture of max tuberosity
Mandible:
Proximity of tooth to inf alv nerve or lingual nerve – possibility to traumatize nerve
Labial parasthesia (numb lip)
Lingual parasthesia (numb tongue)
Long curved divergent roots
Distoangular impactions (very very difficult)
 Deep impactions even associated with pathology – experience of surgeon
Displacement of tooth into submandibular space

Types of impaction:
Vertical
Mesio angular
Disto angular (very difficult – roots are also very close to the 2 nd molar roots)
Horizontal
Buccolingual (on x rays seen as round opaque mass)
Aberrant

Q: From OPG how can we tell that tooth or root is close to inf alv nerve?
Deflection of roots or canal
Dumbell narrowing of canal
Superimposition of canal running over the roots
Radiolucent shadow of canals behind the roots
If no bone separating root and canal (inf alv canal is a cortical bone)

Q: Structures at risk with lower 3rd molar surgery?

Contents of Inf alv canal: Inf alv nerve + artery + vein
Nerve trauma => labial paresthesia (lower lip numbness)
Artey and vein damage => bleeding; management: compress
bone with artery forceps followed by haemostasis (gel foam + suture)
Lingual nerve damage: Paresthesia – numb tongue
Damage to mand 2nd molar (therefore to disimpact 3rd molar??)
Soft tissue damage: Flap, lips, cheek, tongue
Remote possibility: Mand fracture (angle fracture along the line of weakness (for ex
unerupted tooth)
Damage to nerve and degree of damage:
Paresthesia – altered sensation
Anestheisa – no sensation
Dysesthesia – Painful sensation to normal sensation

Neuropraxia: mildest degree of damage; no damage to nerve but conduction deficit due to
compression of nerve by post op odema; rapid full recovery
Axonotmesis: Damage to nerve but peri and endoneurium are intact; neuropraxia,
anesthesia present;chances of recovery but slow
Neurotmesis: Complete destruction of nerve, end up with amputation neuroma; no
recovery – only way to recovery is to perform microvascular surgery within 3 months
following destruction.

Duty of the dentist: to sit with the patient and discuss with him the details of surgery, its
procedure and complications and get his consent (both verbal and written)

Procedure:
LA
Flap design and retraction
Bone removal (as minimal as possible)
Section the tooth (as any pieces as possible)
Wound debridement
Suture
Antibiotics: if infection, repeated pericoronitits
Analgesics: Panadene forte (paracetamol + codeine (30 – 60 mg ??) especially for 3 rd
molar surgery
Ibuprofen – has both analgesic + anti inflammatory effects
(panadene also has paracet + codeine (10 mg)

Common post op complications:

Pain
Swelling
Trismus
Bleeding
Drysocket (smoking , OCP related)
Infected wound
Haematoma
Nerve injuries (parasthesia , anaesthesia)
Fracture of jaw

 Skull and foramen

From base of skull

Hypoglossal canal: Hypoglossal nerve: Motor supply to all intrinsic and extrinsic muscles
of tongue (except palatoglossus muscle of tongue - by??)
(Sensory supply to anterior 2/3rd of tongue – by lingual nerve
Posterior 1/3rd of tongue by glossopharyngeal nerve

Jugular foramen: Inferior petrosal sinus becomes internal jugular vein after passing
through this foramen. Ix, x, xi nerves

Carotid canal: Internal carotid artery (has no branches in neck; only ext carotid artery has
branches) , Carotid Nerve plexus

Foramen ovale : Mandibular division of Trigeminal nerve, accessory menengial artery

Foramen spinosum: Middle meningeal artery and meningeal branch of mand nerve

Foramen lacerum: Only seen in cadavers, not in living persons (Dense connective tissue
cartilage and periosteum of adjacent bone ??) deep petrosal nerve, some manengial
artery branches

Stylomastoid foramen: Facial nerve vii

From inside of skull:
Internal auditory meatus: VI and VIII nerves

Foramen rotundum (round ): Maxillary nerve

Optic foramen: Optic nerve II, opthelmic arteries

Q: Extracranial course of facial nerve:

After passing through stylomastoid foramen, gives 2 small branches posteriorly
One supplies post auricular muscles
Another supplies posterior belly of digastric (attached to mastoid)
Main trunk enters parotid gland, where it divides into 5 branches: supplies all muscles of
facial expression
Temporal
Suprazygomatic
Buccal
Mandibular
Cervical

Mandible:
Mandibular foramen
Mental nerve – between roots of lower 4 &5
Mylohyoid groove – caused by mylohyoid nerve; on the medial surface of the body
Muscles:
Lateral pterygoid: Opening of mouth
Lateral excursions (One muscle), protrusion with med
pterygoid.
Superior head origin: Infratemporal surface of the greater wing of sphenoid
Insertion: Articular disc and capsule
Inferior head origin: lateral side of lateral pterygoid plate
Insertion: Pterygoid fossa/fovea (antero medial part of neck of
condyle)

Medial pterygoid: Closing of mouth

Superior head origin: Medial side of lateral pterygoid plate
Inferior head origin: Tiny head – from maxillary tuberosity
Insertion: both heads into mesial surface at the angle of the mandible

Temporalis: Closing of mouth

Origin: bone of temporal fossa and temporal facia
Insertion: coronoid process

Massetor: Closing of mouth

Origin: Inferior surface of the zygomatic arch
Insertion: Lateral side (surface) of ramus of the mandible
  OPG
Scenario : On OPG is shown with a radiopaque mass seen on the posterior aspect of
mandible, just extending beyond the inferior border of the mandible (Superimposed by
soft tissue mass)
D/D: Calcified sialolith
Calcified lymphnode
Occlusal x ray is the specific one for this case
Clinically, on palpation can be symptomatic if in duct but asymptomatic if in
intraglandular??

If radioopaque mass seen completely within the mandible, include

DD : focal sclerosis (osteoma) along with the above two.

14/06/11

 Drugs used in dentistry:

LA
Analgesics
Antibiotics
Emergency drugs

 LA:
Local anesthetic: A drug or an agent that reversibly blocks nerve conduction or
transmission

Q: Trace pain pathway from sore tooth (Ex:) from lower molar
A: Pain impulses from tooth => inf alv nerve => Mandibular branch => Trigeminal ganglion
=> sensory/spinal nucleus of Trig nerve situated in medulla oblongata (Extends to C2
vertebra) => thalamus and then => sensory cortex of contra lateral side
From upper molar
From Maxillary nerve => Trigeminal ganglion and so on as above

Sensory innervation of oral cavity:

Maxilla
Hard palate: Nasopalatine - from canine to canine
Greater palatine – from 1st premolar to posterior maxilla
Soft palate: Lesser palatine
Maxillary teeth: Posterior Superior Alveolar nerve – molars xcept MB root of 1 st molar
Mid Sup Alv Nerve – present only in 10% of people (MB root)
Ant Sup Alv Nerve – All other teeth (anteriors +pms)
PSA + ASA nerve form superior plexus??
Alveolar mucosa: Posterior alv mucosa – from gingival branch of PSA nerve
 Labial gingiva (5 – 5) – from Infraorbital nerve
Mandible:
All teeth – Inf alv nerve
Floor of mouth – lingual nerve
Tongue – Ant 2/3rd by lingual nerve, post 1/3rd glossopharyngeal nerve
Labial mucosa: Posterior teeth – Long buccal nerve
From 5-5 – Mental nerve

Q: Physiology of peripheral nerve (Ex: when we prick a person, what changes take
place?
Nerve membrane has a resting potential of around – 60 to -90??. When nerve is
stimulated, the membrane becomes permeable, so influx of Na+ ions (ion exchange)
into the membrane takes place altering resting potential. Inside of membrane (within the
nerve) becomes more +ve when compared to outside of the membrane. When it
reaches to Firing potential (around -50??), impulse Produced.
LA given prevents this physiology of nerve

Q: Popular LA s used

Lignospan: Lignocaine/xylocaine + adrenaline

Citanest: Prilocaine + felypressin
Scandonest: Plain Mepivacaine
Septanest: Articaine + Adrenaline

Composition:
 Lignocaine (7 mg/kg)
2.2ml (2.2 cc) catridge of 2% Lignocaine means
2.2 ml of LA solutions has 44 mg of Lignocaine (20 mg in 1 ml => 44 mg in 2.2ml)
27.5 microgm of adrenaline ( 12.5 microgm in 1 ml)
Na or K meta bisulphate – preservative for adrenaline – prevents oxidation of Adrenaline
Nacl – To maintain isotonicity of LA
NaoH – To maintain pH of the solution (buffering action)
Water – All components are dissolved in water

pH of LA is around 3.5 – 5.5. LA doesnot work in acidic medium as free base (which is
lipophilic) cannot be produced.

 Citanest: (9 mg/kg)
1.8ml (1.8cc) catridge of 3% LA contains
54 mg of prilocaine
0.03 IU Felypressin (some citanest can also come with adrenaline)
Same composition as of lignocaine, except for Na meta bisulphate

 Scandonest:
 Plain mepivacaine – 3%
pH – about 6
max 3 cartridge (2.2 ml) for adult
Children 3 to 6 yrs: 1.8ml
Children 6 to 14 yrs: 2.7ml

Q: Classification of LA:
Amides: Aromatic ring + amide group + amide link
Esters: Same as above but with ester link (not amide link). It has unpredictable duration of
action and also mostly allergic
Articaine has both amide and ester links.

Q: Mechanism of action / Mode of action:

LA exists in both ionized and unionized forms
Ionised form (component) Unionised component

BH+ B + H+
Water soluble Lipid soluble
More % Less %
BH+ <-------> B + H+
In equilibrium

It is lipid soluble B that crosses the nerve membrane which then forms BH+. It is this BH+
that acts on the Na+ channels on the membrane by binding onto the specific protein
receptors of Na+ channels => blockade of nerve conduction/induction. Therefore the
action of La is from inside the membrane.

pKa – Dissociation constant

Determines onset of action of LA (How fast does LA acts)
Determines how much proportions are the 2 components of LA are in
For ex: In case pKa = pH of the body (which is 7.4), then both components will be in 50 %
proportions.

BH+ <-------> B + H+
50% 50%
When B (50%) from outside the membrane goes inside the membrane , it then converts
into BH+ which would only make up to 25% from 50% B - therefore not very effective

Lipid solubility: Determines potency of LA – more soluble, then more potent

Protein binding: Determines duration of action of LA – long binding time , then more
duration of action

Q: Basic injection technique

Precautions to be taken:
 Need to have emergency (resuscitation) setup (equipment): O2 and Adrenaline are first
line defense drugs
Slow injection ( block atleast for a minute)with frequent aspirations (atleast 2)
Need to know anatomical landmarks
Warn child/ child’s parent to take care not to chew on lip as it will be numb (after inf alv
nerve block)
No adrenaline in cases of Uncontrolled hypertension
Thyrotoxicosis
MAO inhibitors.
In these cases LA used cautiously :
Look for patients with malignant hyperthermia – injections given carefully(even amide can
trigger)
In asthmatic pt: sulphite component of LA can trigger an attack

Infiltration with LA containing vasoconstrictors are more painful than one without
vasoconstrictors b’cos vasconstrictors causes constriction of blood vessels, LA stays
in a localized place. This is the same reason behind increased duration of action (as LA
is contained) and decreased toxicity (as LA slowly enters into circulation)
Never leave the patient alone after giving LA
Never tell the patient that you are giving injection or show the needle: tell that you are
putting tooth to sleep/ anesthesizing tooth and keep talking to the patient (doing well, it’s
almost done, u r fine)

Q: Metabolism of LA
In liver
In patients with liver disease, articaine is better (septanest), as only 20% of it is
metabolized in liver but rest of 80% is metabolized by carboxyesterase (not produced
by liver)

Q: Adverse effects of LA:

A: Apprehensive pt – No matter what LA is given, it would not work??
Damage to nerve – Paresthesia
Muscle – trismus
Blood vessel – bleeding or haematoma
Injection into parotid gland – facial paralysis
Needle breakage
Painful injections –Usually happens with LA consisting of adrenaline as adrenaline
causes arteriospasm (vasoconstriction). After block, patient screaming and blanching of
skin are due to arteriospasm, which is reversible. Arteriospasm can also occur when
infiltrating maxillary anterior teeth.
When needle hits periosteum

Systemic effects of LA:

These effects are more common in elderly people than in younger people as the elderly
(65 yrs) have 40% less blood flow when compared to the younger people (25 yrs) –
altered physiological response. Also they are usually have chronic diseases and are on
multiple medications.

CNS:
In small dose – involuntary muscle activity – excitation
In high dose – depressive action (can lead to unconsciousness, respiratory arrest).
Can be fatal, therefore do not exceed max limit.

CVS:
Has depressant action on heart (therefore also used in arrythmias for ex: ventricular
fibrillation).
At lower limit of the high dose – cardiac output increases
At higher limit of the high dose – cardiac output decreases and circulatory collapse

Methaemoglobinemia:
Seen in patients, especially when maximum dose of citanest is given. This
methaemoglobin cannot carry oxygen anymore. IV methylene blue given to reverse this
effect.

Toxicity due to LA could be of two reasons: Exceeding maximum limit dose

Intravascular injection
Best way of avoiding toxicity – Know maximum dosages
Frequent aspirations

When 2 lignocaine injections are given intravasularly- can cause cardiovascular arrest in
an adult patient.
Even a normal dose or half the maximum dose given in patients with liver disease can
cause toxicity

Systemic effects of Adrenaline:

Functions of Adrenaline (vasoconstriction): To prolong working time
To produce clean operating field
Slow absorption – decrease toxicity

When LA given, patient complains of increased heart rate. Patient becomes shaky when
given into intravascular (as intravascular adr stimulates production of more of
endogenous catecholamines from adrenal medulla which further increase heart rate)
Adrenaline not given in patients taking MAO inhibitors – as MAO is the enzyme that
metabolises adrenaline.

Toxicity of felypressin (octapressin/oxytocin) is much lesser than adrenaline. The former in

big doses can cause coronary artery constriction.
Q: Maximum dosages of LA:
In children, lignocaine is the LA of choice. We calculate the max dose based on the wt (in
kg).

Lignocaine
4.4 mg/kg upto a max of 300 mg = 6/7 cartridges (absolute maximum) (no other
calculations with lignocaine as plain lignocaine is not manufactured)

Prilocaine
6 mg/kg upto a max of 400 mg. therefore 1.8 ml cartridge contains 54 mg of prilocaine,
400/54 = --- catridges

Mepivacaine
Same as lignocaine

Articaine
7 mg/kg upto max of 500 mg. 4% of 2.2 ml cartridge contains 88 mg = approx 5/6
cartridges

Bupivacaine (marcaine??) effects of LA lasts for 8 – 10 hrs.

Q: Why LA fails?
1. Operator dependent causes:
Wrong choice of solution
Poor technique – not knowing landmarks, IV injection, inj into inflamed area
Insufficient solution

Correct IAN Block:

Ask patient to open the mouth
Feel anterior border of ramus of the mandible
Look at raphae + buccintor and the triangle (groove) formed by pushing bucci against
raphae.
At the deepest portion (apex), lateral to raphae, penetrating buccinator
1 cm above occlusal plane
From opposite side (contralateral)) premolar
Penetrate needle till it hits bone, withdraw so that 2/3rds of needle is inside, aspirate and
give 3/5th of solution for IAN nerve block
Pull needle half way out, aspirate, give 1/5 th of solution for lingual block
Withdraw needle and on distobuccal aspect of lower third molar region, give remaining
1/5th of solution for long buccal nerve infiltration.

Alternative techniques for IAN block:

Gow Gates technique: Wide open mouth technique
Penetrate needle into condyle taking guidance from contralateral
side canine and same side mesiopalatal cusp of upper 2 nd molar, till it hits condyle. Ask
patient to gradually close his mouth.
Advantage: Blocks all three nerves in one injection

Akinosii ?? technique: Closed moth technique

There is no bony landmark. Guidance by the hub of 35 mm long
needle that lies next to distal to upper 2nd molar with barrel of the needle lying parallel to
mucogingival floor
Patient in sitting position with Frankfort horizontal plane parallel to
the floor.
Aspirate and deposit solution.
May need additional inj for long buccal nerve infiltration.

In some patients, intraligamentary (intraosseus) inj needs AB prophylaxis

Intrapulpal inj: Warn the patient before itself that it stings.

2. Patient dependent causes of failure:

Anatomical variations:
If mandibular foramen is too high – aim high
Too low – normal aim will deliver solution
Accessory nerve supply:
Patient can experience pain when sectioning the tooth even after IAN block, due to
accessory supply from C2 – C3 (cervical plexus) (supplies mand teeth)
Lower molar accessory supply: long buccal nerve
Nerve to mylohyoid
Lingual nerve – all lower teeth
Greater palatine nerve – Palatal root of upper molar
Anatomical barrier:
Very thick zygomatic buttress – may not anesthesize first molar. Therefore give
infiltration from mesial or distal of buttress.

Pathological causes:
Trismus/ pericoronitis/ sub mand space infections – patient cannot open mouth
Inflammation / infection – LA does not work in acidic medium

Psychological causes:
Psychogenic causes .
Endodontists prefer articaine (septanest)

Success of IAN block: 70 – 85%. Failure rate: 15 – 30%

When one cartridge of articaine injected (infiltrated) into buccal sulcus, then success rate
come upto 92%. Very good bone and soft tissue diffusion. Can be used in case of molar
teeth extractions. (Articaine is not used for block due to risk of lingual nerve
paresthesia)

Q: ORN (osteoradionecrosis) and BRONJ (bisphospho related osteonecrosis of

jaw):
After radiotherapy, the more the time elapsed after radiation exposure, more chances of
development of ORN.
Damage is localized to the irradiated jaw. Post radiotherapy: damage to blood vessesls=>
endarteritis obliterans. Takes atleast 6 months to get back to normal??. Therefore in
case of infection, cannot fight against it=> necrosis.
In BRONJ, the effect is generalized to entire skeleton (takes atleast 10 years to get back to
normal bone turn over rate)
For ORN: Hyperbarric oxygen given:
Causes angiogenesis (formation of new blood vessels)
Causes opening of blood vessels (increased blood supply)
If teeth to be extracted:
Give 20 dives (doses) of Hyperbarric oxygen before xn,

extract the tooth, put on AB cover and send the patient again to hyperbaric department for
10 dives of oxygen.
Do it before the start of radiotherapy. Can also be done during the procedure of
radiotherapy.
If to be extracted after radiotherapy – be careful not to elevate the flap as there would be
only periosteal blood supply to bone (endosteal supply is lost after radiation) which
would be jeopardized.

21/6/11
Q: Haemophilia A:
Deficiency of factor viii.
Haemophilia B: Christmas disease
Bleeding is the problem
Xn not indicated unless factors are corrected. Patient referred to haematologist..
For Haemophilia A: Cryoprecipitate or frozen plasma given
For Christmas disease: Frozen plasma given
(my reminder: add from not BT CT etc )

Q: Herpes Zoster:
Shingles
Does not cross the midline
During acute phase: No dental trt carried out (as increased viral load)
Corticosteroids are contra indicated if many ulcers are present – potential of ulcers
getting infected (as steroids cause immuno suppression)
Refer pt to physician – due to risk of post herpetic neuralgia

 ANALGESICS:
The primary factor patient comes to see a dentist is Pain – usually due to Inflammation.
3D principle: Diagnosis
Definitive dental treatment
Drugs

Ex: Patient comes with swelling of his face

Diagnose the condition: Acute alveolar abcess
Cause: Carious tooth
Definitive trt: Xn or Endo (if the tooth is restorable)
Drugs: Only conjunct to definitive trt (not first line of trt)

Pain management:
Non narcotic analgesics
Narcotic analgesics

Non Narcotic Analgesics: Include

NSAIDS (pronounced as nasaids)
Paracetamol

NSAIDS:
Has anti inflammatory + analgesic actions
Commonly used NSAIDS: Aspirin
Ibuprofen
Mechanism of action:
Inhibit cox (cyclooxygenase), thus inhibiting PGS from arachidonic and
thromboxanes?? Which play key role in inflammation.
Ibuprofen (200 mg) = Neurofen
Ibuprofen (200 mg) + Codeine (12.5 mg) = Neurofen plus
Ibuprofen (200 mg) + Paracetamol (500 mg) = Panafene
Dosage:
Ibuprofen:
Available as 200 mg tablet/ capsule
Max daily dose: 2400 mg
Per dose: 200 – 400. mg (i.e., 2 tablets) 6 hourly, is very responsive
Small doses of combined drugs are more effective than large single drug dose.
Ex: Neurofen plus
Panafene
Children: 5 to 10 mg/kg orally, 6-8 hrly (max 2400mg/24 hrs)

Adverse effects of NSAIDS:

GI tract irritation
Post operative bleeding (especially with aspirin)
Long term use can cause renal problems – End Stage Renal Disease

Paracetamol:
Has antipyretic + analgesic but very little anti inflammatory action
Mechanism of action:
Primary action in CNS: Readily cross CSF, acts on hypothalamus - inhibit spinal PGs.
At this therapeutic dose, peripherally, does not inhibit cox – therefore no anti
inflammatory effect.

Dosage:
Paracetamol:
Available as 500 mg tablet
Max daily dose: 4 gm
Per dose: 500 - 1000 mg (2 tablets) 6 hourly
Children: 15 mg/ kg body wt pral and rectal
Rectal suppositories also available: 20 mg/kg body wt
5 ml syrup formula available
It is rapidly absorbed in GI tract, peak volumes reach in 30 min.
No toxicity at therapeutic levels
No tolerance or dependence
No Gastric irritation

Adverse effects:
Paracetamol is metabolized in liver and excreted by kidney.
It is an over the counter drug – easily abused
Overdose: 100 mg/ kg body wt
In 70 kg adult- 100*70 = 7 gm or 14 tablets = acute toxicity (very
common in Australia). This overdose leads to Hepatotoxicity
Hypoglycemia
Acute renal tubular necrosis.
Overdose is a medical emergency – hospital
Drug combinations:
Panadene: Paracetamol (500 mg) + Codeine (8 mg)
Panadene forte: Paracet + Codeine (30 mg)
Mersyndol: Paracet (500mg) + Codeine (9.75mg) + Doxylamine (antihistamine) (5mg)
Mersyndol forte: Paracet + Codeine (30 mg) + Doxyl

NSAIDS are first line of choice of analgesics, unless gastric ulcers present or NSAIDS do
not work; in which case Opiods are given.

NARCOTICS/ OPIODS:
These are powerful analgesics, reserved for much stronger pain situations.
Mechanism of action:
Stimulates/ activates opiod receptors
There are 3 opiod receptors:
Mu receptors – activated by all narcotics
Kapa receptors – by Pantazocine (Fotryl injections) and by buphrenorphine-
used for drug addicts
Delta receptors – no known analgesic
Pain transmission is prevented by inhibiting/ preventing neuronal activity at multiple areas
of neuron)

Adverse effects:
Habitual addiction
Respiratory depression
CNS depression
Constipation
Bradycardia, hypotension
Urinary retention
Chest wall rigidity
Sweating, flushing, urticaria, pruritus

 CORTICOSTEROIDS:
Has anti inflammatory action
Used in case of inflammation of oral cavity when no signs of infection are developing
(Corticosteroids cause immunosupression – if infection present, then secondary
infection develops??)

Use of corticosteroids:
Adrenal crisis
Anaphylaxis, allergic reactions
Bronchial asthma (pumicot?? Inhaler)
Oral mucosal disease(pemphigus)
Oral ulcerations (Sometimes apthous ulcers)
Sever post operative swelling
TMJ – muscle inflammation
Endo – intra canal medicament (Kenalog: Orabase plus triamcinolone acetonide )

Glucocorticosteroids produced from Adrenal cortex are the one responsible for inhibiting
immune response and inflammation.
Inhibition of immune response – by inhibiting cytokine synthesis
Inhibition of inflammation – by inhibiting cells and factors responsible for infl
Anti infl effect >>NSAIDS

Drug:
Dexamethasone – 4 mg tablet thrice daily. Especially after 3 rd molar surgery – to bring
down inflammation., systemic use by sp. only

Adverse effects:
Decrease immune response
Cannot be used in presence of infections
Uncontrolled diabetes
Ulcerative colitis
GI tract ulcerations
Occular Herpes – can go blind
Properly monitor dental patient who is on corticosteroids

 ANTIBIOTICS:

General Principles: MIND ME: Microbiology, Indication, Narrow spec., Dosage, Minimim
duration, Ensure Monotherapy

a) Principles:
1- Use when scientifically proven (systemic signs and symptoms present)
2- Narrowest spectrum
3- Monotherapy, unless combined drug therapy proved to prevent emergence of resistant
organisms
4- Dose large enough to knock off bacteria, but prevent emergence of resistant organisms
5- Dose low enough to avoid toxicity

b) Therapy:
1- Emperical – therapy based on known pathogens likely causing the disease
2- Directed- therapy based on culture and sensitivity tests
3- Duration- Therapy for not more than 7 days (5-7)

Antibiotic prophylaxis:
Single large dose of antibiotic used in a compromised patient
- Prosthetic heart valves- surgically constructed shunts/ conduits
- Congenital heart defects- Repaired defects in first 6 months
Repaired defects with residual defect
Unrepaired defects (always)
- History of endocarditis
- RHD in indigenous Australians: Rheumatic fever is a disease of children.
Not all Australian children with rheumatic fever are prone to RHD, but indigenous
children with rheumatic fever are at the risk of developing RHD – Due to their low
immune status and also poor nutritional status.
Read about procedures that require AB prophylaxis and dosage from dental therapeutics

Antibiotics used in dentistry:

Penicillin V
Amoxicillin
Amoxiclav = augmentin= amox + Clavulonic acid. Beta lactamase produced by certain
bacteria destroys beta lactam antibiotics like penicillin, cephalosporins and ???
Clavulonic acid is a beta lactamase inhibitor that inhibits beta lactamase.
Metronidzole (flagyl) – Especially in perio cases (anaerobic bacteria)

Q: Patient on warfarin: The list of drugs are CI/ cautiously used??

Metronidazole
Erythromycin
Tetracyclins
Cephalosporins
Aspirin
Antifungals
Penicillin/ Amoxicillin are the safest drugs that can be used in pts on warfarin.
 MAXILLARY SINUS:
There are 4 pairs of paranasal sinuses: Frontal, maxillary, ethmoidal( ant, middle,
posterior) and sphenoid. The largest pair of sinuses in close relation to dental and
headache are maxillary sinuses.

The site of drainage and ventilation for paranasal sinuses is nose. Therefore in nasal
congestion, sinuses cannot drain, pt complains of headache, congestion.
Pansinusitis is inflammation of all paranasal sinuses and failure of drainage.

Frontal, maxillary, ant&middle ethmoid – drain into middle meatus of wall of nose

Post ethmoidal and sphenoid – drain into superior meatus.

(nasolacrimal duct opens into inferior meatus)

Shape of Max sinus: Pyramidal – apex, base and 4 walls

Base – lateral wall of nose.
Bones forming lateral wall –
Frontal process of maxilla
Perpendicular plate of palatine bone
Medial pterygoid plate
Apex – Zygomatic process of maxilla
4 walls:
Ant wall – anterior wall of maxilla
Post wall – Post wall of maxilla
Roof – Floor of orbit
Floor – Alveolar process of maxilla ((floor of nose is formed by hard palate))
Lining epithelium – pseudo stratified ciliated columnar epithelium (respiratory epithelium)

3 months IU life – Max sinus starts development

At birth – narrow slit like opening
As growth and development occurs – sinus increases in size by pneumatisation

Nasal floor and Max sinus floor:

At around 12 years, both at same level. Therefore very rare chances of development of
OAC (oro antral communication) in children.
Later (16-18 yrs), max floor 1 ½ cm below nasal floor. Therefore it is difficult to drain
infection from max sinus (becomes easier when lie down)

Teeth in close relation to max sinus:

7>6>8 or 6>7>8
5>4
3 is just anterior to sinus.

Q:How to differentiate sinusitis pain from dental pain:

Take history: Ask if the pat had a history of sinusitis?
Ask about pain: All posterior teeth will be tender to percussion – Unique Sign
(if dental pain, then that carious tooth alone will be tender.)
Infraorbital margin tender to palpation
Pt unable to bend head down
X ray: radiopacity of sinus.

ORO ANTRAL COMMUNICATION:

Ex: If after Xn of upper 6, OAC created, what is the management?

After xn (extraction) of upper posteriors, always check for OAC. Ask patient to breathe
through nose, visualize for air bubbles from mirror. If OAC created, usually due to
palatal root, and is 2-3mm in diameter,
Induce clot formation,
Pack surgicel/alveogel,
Suture the socket.
Post operative instructions:
Antibiotics – as max sinus which is a sterile area is infected after communication with
oral cavity
Nasal congestants
Analgesics
No smoking, no sucking through straw, no blowing through nose,
Sneeze with mouth open (to reduce pressure)
Review after a couple of weeks

Ex: Solitary tooth with conical root xted, big OAC of 6 mm created, what is the
management?
Same management as above+ refer to oral surgeon for repair of OAC (with buccal sliding
flap)

Ex: While trying to dig the broken root (say MB root), it disappears. Step by step
procedure:
PA taken - to see if the root is lying sub mucosal or escaped into sinus.
 If sub mucosal, the root can be dug out/ or can be sucked out with fine sucker.
No further trt is necessary
If into max. sinus, Same management as above+ refer to oral surgeon (Cadwell
luc operation: In the ant wall of max sinus, canine fossa is the thinnest part of sinus.
After raising the flap, even with a hand instrument ,can perforate the sinus to remove
the foreign body from it)

Ex: Small OAC which is left to heal is developed into an OAFistula: If fistula is large, then
sinus drains through it. If fistula is small, then sinus flares up, antral mucosa gets
inflamed, which appears as polyp in the socket. Remove the polyp and refer the pt to an
oral surgeon (for ??)

Ex: Solitary (lone standing) upper molar tooth:

Do not just jump into xn as there are more chances of antral floor fracture in the
tuberosity area.
Look for relation of sinus to roots
Root pattern – if divergent, then surgical xn, refer to oral surgeon (If examiner
asks what if you are in a regional area, then tell the examiner that I will inform the
patient that it has to be surgically removed and there are these complications
associated with xn. If patient is in pain do access opening and extirpate the pulp give
ladermix dressing, analgesics and refer.
If conical, then conventional xn
If tuberosity fracture occurs with out OAC, no need for antibiotics.

Maxillary Tuberosity Fracture:

Ex: When xtng an upper max tooth, when‘cracking sound’ heard and whole segment
moving (instead of just the tooth), suspect tuberosity fracture.
Management: Replace it back to its exact position, suture it and secure the
fractured/loose fragment to maxilla for stabilization.(Stabilisation can also be achieved
by arch wire splinting)
Check for occlusion If high bite, reduce upper tooth from occlusion. Healing
usually occurs uneventfully.
Inform the patient that it was a diificult extraction, there was a small fracture
which has been replaced and reduced with sutures. It will take about 4-5 weeks to heal.
I will refer you to an oral surgeon now and once the healing occurs, he will perform a
surgical xn.

Ex: Sometimes in an old patient, bone is brittle. Heavy levering on upper 7 to take 6 out
can lead to a piece of bone broken and attached to the xted tooth. If the broken loose
fragment of bone has intact periosteum, suture the bone back; if periosteum connection
is lost, then the piece of the bone should be removed (if left – necrosis and
sequestration). If OAC created after removing the loose fragment, repair it.
Max sinus is also involved in the following:
Lefort II and III fractures
Isolated zygomatic fracture
Tumors – radiopacity of max sinus, outline is poorly defined – straight away referral.
Mucocoele, cysts, polyps – radiopacity of max sinus, outline is well circumscribed.
Tumors in max sinus grow into a large size (as sinus is a hollow area), and when
reaches full size, bursts
Through ant wall – presents through cheek, presents with
numbness of cheek.
Through post wall – presents trismus
When numbness of post max teeth (PSA nerve involved) and of buccal gingiva
present, be cautious and vary – suspect tumor.
Through roof – Effects infraorbital nerve; numbness of that side of
cheek, nose area. When tumor increases in size, leads to proptosis.
Through floor – presents bucally or palatally; teeth becomes loose

 PRINCIPLES OF ELEVATORS:

Elevators are used to elevate tooth or root

Parts of an elevator: Handle- shank/shaft- blade
Elevators takes use of “mechanical advantage” – Ratio of output force: input force. Use
small input force to achieve great output force.

Principles:
Wheel and axle (screw driver action): Force applied around long axis of the elevator??
(into bone) for rotation. Ex: Luxating tooth
Wedge: Force applied along long axis of the elevator?? Ex: broken root in a socket
Lever (crow bar action): Buccal bone acts as a fulcrum. Cryers work on this principle

Guiding principles:
1. Never use excessive force
2. Always support the tooth/root to be extracted
3. Force applied in the direction away from major structures (like sinus, mental foramen,
inf alv canal)
4. Never use an elevator blindly
5. Never use an adjacent tooth as s fulcrum
6.Use sharp instruments
7.Create point of application on the tooth/ root; sometimes bone should be removed to
create the point
8.Complete debridement of socket and suture it.
9.Should not be used:
Blindly
Very close proximity to sinus (infected root – try to get it out by apical pick)
 In Lower 3 rd molar area: Lingual plate is thinner, root can be forced into sub mand
space
In Edentulous jaw : angle of mand can fracture
Do no use elevator when xray not taken.

Grips:
Full grip (like we apply for wedge principle) and Thumb and index finger grip

 ODONTOGENIC INFECTIONS:
It is the commonest of head and neck infections.

Cause:
Pulpal death, secondary to dental decay
Pericoronal tissues
Periodontal tissues
Microbial origin:
Severity depends on the virulence and quantity of the organism
Polymicrobial in origin: 28% are mixed aerobes
72% are anaerobes
Most common aerobe: Streptococcus virulens
Anaerobes: Peptostreptococcus(dento??)
Fusobacterium
Anatomical factors play a key role in the presentation of the infection

Spaces involved are:

Buccal
Sub lingual
Submassetric (between masseter muscle and ramus)
Pterygomandibular (between medial pterygoid and medial surface of the ramus)
Submandibular
Parapharyngeal
Infratemporal

Spread of infections:
Follow the path of least resistance
Upper lateral incisor – to palatal (as root tip is inclined palatally??)
Other upper teeth – to buccal (as buccal bone is thin)

Host resistance:
If old age
If immunosuppressed
If immunocompromised: ex: diabetes, HIV, neoplasms etc.
Principle of management of odontogenic infections:
Remove infection: either by
Xn and drainage
In esthetic zone: RCT and drainage
If fluctuant swelling in buccal sulcus: Incision and drainage by Hiltons
method – Incise the mucosa, introduce small sinus forceps to drain the pus
If swelling is not fluctuant or if it is generalized: then do open drainage
(??)

Ex: Lower decayed tooth – Massive swelling (non fluctuant) – difficulty in

swallowing
A: If pt can open the mouth, IAN block and Xn
If pt cannot open the mouth (trismus) – call air ambulance

PERICORONITIS:
Inflammation of the pericoronal tissue associated with a partially erupted tooth (usually
wisdom tooth)
Initial attack is simple and can be treated with antibiotics
Subsequent attacks are much more severe than the previous attack.
If spread laterally – involve submassetric
Medially – parapharyngeal
Pterygomandibular -> then to infratemporal
Downwards – submandibular space
Trt: Assess the situation: If pericoronal abcess is present, drain it (how)
If operculum is swollen and upper 8 hitting on it, xn of upper 8 to relieve the
operculum from trauma.
Definitive trt: Xn of lower 8 at a later stage.

ACUTE PERIODONTAL INFECTION:

In a young patient, if present, he should be medically compromised (ex HIV-AIDS)
ANUG (Trench mouth):
Truncated (??) ulcers in interdental papilla
Foeta oris
Pain
Management: Local debridement, scaling
Oral hygiene
Oxygenated mouthwash (dilute H202)
Penicillin, Metronidazole
Analgesics

DENTOALVEOLAR ABCESS:
Acute: symptomatic, localized swelling
Chronic: Asymptomatic, till it undergoes acute exacerbation
Associated with hopeless carious tooth
Tender to percussion (periostitic??)
Radiolucent lesion periapically
Signs and symptoms:
Pain
Swelling
Discharge
Trismus
Dysphagia (sign of respiratory compromise)
Increase in temperature
Stomach upset

Cavernous sinus:
In anterior part of maxilla, infection can spread to cavernous sinus.
2 routes of spread: anterior route – by inferior ophthalmic vein (valveless)
Posterior route – by pterygoid plexus
Cavernous sinus thrombosis is fatal and pt presents with medial squint(partially closed eye
as looking in sunlight) (as lateral rectus muscle supplied by VI (abducent) cranial nerve
is affected).
Cranial nerves associated with cavernous sinus: III, IV,V(1) AND VI. Muscles innervated by
these nerves are affected at a later stage.

LUDWIGS ANGINA:
Bilateral spreading cellulitis involving 3 spaces
Sub mand + sub mental + sub lingual
Difficult to drain
Respiratory distress
Raise of tongue
Principle of trt:
Maintain/ secure airway
Massive IV antibiotics

ERYSIPELAS (?)
Acute onset of cellulitis, involve superficial layers of skin
Organism: Streptococcus; produces hyaluronidase that breaks down the barriers causing
spread of infection.
Regional lymph nodes are involved
DD:
If carious tooth, with swelling: Amox is given (even if swelling is because of erysipelas,
amox works as causative org is streptococcus)
 If no carious tooth, but sudden onset of swelling present, even then amox works.

OSTEOMYELITIS:
Inflammation of bone of infective origin secondary to dental decay (infection is from tooth)
Infection starts in medullary spaces, runs along nutrient canals, cause ischemic event
leading to necrosis of that part of the bone (sequestrum). Body tries to wall it off by
forming Involucrum

Causative organism: Staphyococcus

Presentation:
Signs and symptoms:
Neglected oral hygiene
Multiple carious teeth
Multiple discharging sinuses (extraorally and intraorally)
Pain
Swelling
Glands (??)may be involved
Almost always involve mandible (in babies, maxilla can be affected)
Numbness of lip (when asked the patient about sensation) – IAN paresthesia. After trt,
numbness is corrected (sensation returns)

Xray:
Patches of radio opaque and radiolucent patches (areas of destruction) – Moth Eaten
Appearance

Management:
Remove sequestrum – sequestrectomy
Remove the causative tooth
Refer to hospital
Long term antibiotics (penicillin) for 4-6 months
Assess progress: by return of sensation

Types:
Acute and Chronic forms
Suppurative and non suppurative forms
If acute osteomyelitis not well treated then results in chronic suppurative osteomyelitis.

Garry’s Osteomyelitis:
It is a chronic non suppurative osteomyelitis that occurs in Children, almost always
involving lower 6s (with gross carious lesion)
It is low grade infection leading to stimulation of periosteum to deposit bone (in children
periosteum of bone has more osteogenic potential) – bony hard swelling of the body of
the mandible
X ray: Laminated appearance or onion peel appearance
Trt: No antibiotics (low grade infection and no pus)
 Bone undergoes remodeling when cause removed

ACTINOMYCOSIS:
Cause: Actinomyces israelii. It is an oral commensal, (gram-positive rod-shaped
bacteria) becomes pathogenic once gets deeply inoculated into the tissues

Ideal situations: After Xn, actinomyces embedded into the socket

After compounded mandibular fracture
Presentation:
Non healing socket with mass of granulation tissue formation
Multiple discharging sinuses
Numbness of lip if involves regional nerve area.

Trt:
Curette the socket that has colonies of fungi – sulphur granules – and send this specimen
for culture
Irrigate the socket with saline
Long term antibiotics (6weeks)