ORAL SURGERY by Dr.Sammy

10/05/11If 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 mabdi.)

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 3/5th 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 sinusArteries 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 thers 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 dentistryLA, Antibiotics, Anlgesics and Emergency drugs

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

Position: Always at the front of the patient except for the 4th quadrant which is at the right side of the patient.Movements:MaxillaAnteriors (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

Mandible1s and 2s: flattened MD – LABIO LINGUAL (same as for max 4s 5s, do not come to lingual lingual)3s: oval – ROTATION with apical force4s 5s: round or oval – ROTATION6s 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 landmarks1) Head of the condyle2) Glenoid fossa3) Articular eminence/tubercle4) Zygomatic arch: Muscle attached to its inferior border is masseter

muscle5) Posterior border of maxillary sinus6) Outline of maxillary sinus7) 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 arch9) Infra orbital margin10) Hard palate11) Nasal septum12) Anterior nasal spine13) Inferior concha/turbinates14) Naso pharynx – Large radiolucent area near condyle and below15) Oro pharynx – space below naso pharynx16) Hyoid bone: lateral on both the sides17) Radioopacity in the mid line of OPG: superimposition of

cervical spine18) Styloid process: from temporal bone. Attachments include 3

muscles and 2 ligaments forming styloid apparatus3 muscles: stylohyoid, styloglossus and stylophharyngeus2 ligaments: stylomandibular and stylohyoidWhen 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 attachment20) Ear lobe

Muscle attachments:Medial pterygoid – medial side of ramusMasseter – Lateral side of ramusLateral 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 geniohyoidMuscles 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 – obtundantIn 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 waterMethyl 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 CI – Uncontrolled hypertension Thyrotoxicosis (have elevated B.P)

MAO inhibitorsSitanest 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 AdrenalineProcaine: unpredictable duration of actionSeptanest: 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 daysDexon – Longest time for tensile strength for 28 daysSilk – 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 RatioNormal prothrombin time – 11-14 sec. Laboratory takes normal prothrombin time of many normal patients, get an average=Mean of normal rangeTherefore 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 socketFlush with normal salineCompress the socketSurgicel/gelfoam – to prevent bleeding form the boneHorizontal 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. halothaneMajor 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 puffersAsthmatic effect on chair: If forgot to get their puffer: Patient chooses his own comfortable positionMild attack: He talks in sentences, wheeze present. 4 puffs, wait for 4 min, 4 puffs and wait for 4 minSevere attack: He talks in words, no wheeze Call ambulance 4 rule again Give oxygenTB: 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 painSmoking:

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:

HepatitisHep A is food relatedHep 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 profileClotting 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 doneLA 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 - CarrierFull 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:DegloveWash and dress your woundBlood testIf pt has no infection – both pt and dentist give blood testIf 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

CJD: Creutzfeld Jacob Disease

Transmissable Spongiform Encephelitis

Neuro degenerative diseaseRapidly progressive and invariably fatalInfected agent: Prions Proteins

Classification:Classical: Sporadic mutation Familial Iatrogenic. These 3 are transmitted through prions proteinsVariantClassical CJD: Incubation period is longCommon in older people (60 – 70 yrs), present with dementia, confusion, disorientation, walking problems

Prions are not present outside CNS, therefore not present in oral cavityEarlier days: for CJD patients, thorough sterilization, infection control, disposable instruments mandatoryNow 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 diseaseBovine 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 shortCommon in younger age groups (20 – 40 yrs), present with psychiatric symptomsCan affect lymphoid tissue, closest being tonsils??)

Q: DiabetesIt is a common endocrine disorder involving metabolism of carbohydrates, proteins and lipidsIV types:Type i: IDDMType ii: NIDDMGestationalSecondary: 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 itMaturity onset – middle ageFamilial and also should think of lifestyle like exercise, diet - obesity, hypertension are the major risk factorsTrt:Oral hypoglycemics : Diamicron?? Metformin (diformin)

Management of diabetic patient:Usually mid morning or earlyafternoon appointmentNormal 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 movementsManagement: Stop trt Give orange juice , revives the patient back to normal and then can give strong coffee with double sugar Continue trtPrevention: 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 letterDoctor: Ask him to eat, give him a shot of insulin Dentist: Then give sub mucosal injection??(topical), drain pus and antibiotic coverWhy 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:HyperglycemiaKetoacidosisVascular 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 siteVascular phenomenon: Diminished blood supply, so enough of nutrients or oxygen do not reach the infected area for healing.

ThyroidQ: Kidney problems

If kidneys removed or stones removed – no problem in treating the patientIf 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 adrenalineAdrenal cortex – produces corticosteroidsSteroid 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: ArthritisPatients with arthritis are on NSAIDS – Aspirin, an antiplatelet agent – cause bleedingRheumatoid arthritis: an autoimmune disorder of joints- take daily dose of steroids and weekly dose of methotrexate – both of which are immunosuppressants. Therefore need ABcoverJoint 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 fetus2nd 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 laborDrugs safe: Amox Paracetamol. No NSAIDS - cause bleeding Q: Bisphosphonates:Can be Nitrogen containing (N2) or Non-Nitrogen containingCan be given orally or IVGiven 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 chancesPrevention 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 bisphosphoPt should stop taking drugs for 3 monthsTrt the patientContinue to stop drugs for next one monthThen 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 gramsTest performed as soon as starting drug holiday and then after 3 months of drug holidayWhen performing Xn: We need a value of 200 ngm/ pgm (>170) to perform an Xn.Antibiotic prophylaxisSavcol mouthrinsesAlways suture (ONJ starts in alveolar bone)Routin post op instructionsABcover for 1 weekPost op review in 2 weeks Then in 8 weeks. If healed – no ONJ; if not healed – ONJIf 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:

31/05/11Q: 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 intentionReduce bleedingReduce formation of haematoma / odemaReduce risk of infection

Types of sutures:Resorbable / absorbable: Organic: catgut, plaingut, chromic gut, collagen sutures Synthetic: Vicryl (polyglactin) Dexon (polyglycolic acid) Polysorb – difficult to tieNon 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 activelyPlain gut: 5- 7 daysChromic gut: treated with chromic salt to increase strength 10 – 14 daysVicryl: 21 daysDexon: 28 days. Sometimes to be removed as they are present in the mouth even after a monthOrganic 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 reactionMulti 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 holderToothed tissue forcepsSuture scissorsCheek retractor/ flap retractorGood lighting

Types of suture techniques:Single interrupted: Single suturesHorizontal mattress: Bleeding sockets (especially posteriors)ContinuousVertical 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 diagnosisTypes:Incisional (FNAC, Punch biopsy included)ExcisionalCytology (Brush/exfoliative)Aspiration biopsy (for cystic lesions)

Autopsy (To establish the cause of death) - need not include here

Indications:To establish diagnosis of a suspicious lesionUlcer lasting > 2 weeksChronic infl lesion not responding after the removal of the cause, even after 2 weeksMucosal hyperkeratosis (white lesions)Bony lesionsLarge 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)

Cytology:Application: Candidial infection (smear or swab) ` Actinomycosis (sulphur granules)Aspiration biopsyApplication: cystic contentsInstruments 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 aspirationIt is Solitary bone cyst or traumatic bone cystTrt: 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 cystTrt: RCT or Xn???

Multilocular radiolucent cystic lesion, vital teeth, plenty of blood coming on aspirationIt 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 outIt is a solid tumor (ameloblastoma)

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 salineFill 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 laminaEarly invasive scc: Just penetrated lamina propriaTrue invasive scc: Epi, connec and all tissues (muscles, bone etc) involved

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 – incisionalLarge (>cm) nodular fixed lump – excisional

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 fluidClassification: with lining With out liningWith 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, ranulaEpithelial lining cyst: Odontogenic Non – odontogenicOdontogenic 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 cyst3) Epithelial rests of Malassez from PDL: Radicular syst

Residual cystCommon cysts in order: Radicular>Dentigerous>Nasopalatine>OKC

Non-odontogenic cyst: Nasopalatine Nasolabial

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 formationRadiographic features: Well defined radiolucency with a radioopaque border Loss of lamina duraAspiration: Straw colored / plain tea colored fluid, shiny cholesterol crystalsQ: PATHOGENESIS of radicular cyst:Non vital tooth – has bacteria and bacterial toxins in pulp chamber and root canalIrritate periapical tissues and epithelial rests of malassez in PDLRests proliferate in order to contain the infectionMass of granuloma formationSize grows and centrally placed cells devoid of nutrients, undergo necrosis, fluid formationHigh osmotic pressure and osmotic gradient develps leading to transudation of fluid from periphery into cystic cavityThis increase hydrostatic pressure in the cystic cavity exerting pressure on the peripheral boneCells continue to proliferate and break down and the process of gradient continues slowly and slowlyAlso the peripheral cells contain PGs which causes bone resorption leading to cyst expansionSource of cholesterol crystals: The cell membrane and nuclear membrane very rich in cholesterol (denti cyst also have cholesterol crystals)Residual cyst: left over residual cyst even after Xn or RCT. Grows in size

Dentigerous cyst:

Associated with unerupted tooth, envelops the crownUsually in posterior mandible (3rd molars) also in max 3rd molars, max canines, mand premolarsIncreases 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

OKC:

It is thought to be replacing missing tooth/supernumerary tooth40% 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 stageDD: Denti cyst Uni ameloblastoma60% 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 removalTrt: Conservative approach: Enucleation, curettage and long term follow upSyndrome associated – Gorlin Goltz: Multiple OKCs Multiple BCC Calcified flax cerebri, bifid ribs

Nasopalatine cyst (Incisive canal cyst):Swelling along the midline of the palate near central incisorscan cause displacement of central incisors and can cause non vitality/discolration if grows in sizepainful and salty dischargeWell defined radioluceny >6 mm – suspect this cyst

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

Management of these cysts:Enucleation: Removal of entire lesionMarsupialisation: 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 lesionAmeloblastomaOKCDenti cyst

CGC GranulomaDD for multilocualr lesionAmeloblastomaOKCCGC GranulomaOdontogenic myxomaCentral ossifying fibromaBotryoid odontogenic cyst (Multilocular variety of LPC)Haemangioma

DD for multilocular bone lesionOsteomyelitisAneurismal bone cystTumors

7/6/11Surgical 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 gingivaNeed a very good radiographWhether to do a surgical or not is dictated by THREE 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 rootsTWO: 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 tuberosityHabitual 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 procedureTypes 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:

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.

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 wellSubmerged tooth – deciduous ankylosed toothOrder 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 removalAdvanced caries with or without periapical pathologyPeriodontitisCystic changes associated with unerupted teeth (dentigerous cyst)Resorption or decay of adjacent toothOrthodontic and orthognathic reasonsMandibular fracture involving unerupted tooth/ partially erupted tooth- otherwise the area gets infectedProphylactic 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 => XnIf all 4 wisdom teeth present inside bone; unerupted; no pathology; no symptomsIf high risk to inferior alveolar nerve – confirmed from x raysSeverely medically compromised pt – uncontrolled diabetes; clotting disorders+ on medicationsIf 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 spacePDL space clearly outlined (ankylosed)Roots incompletely formed Completely formedInf alv canal far away from root Very close; more chances of damageExcellent blood supply PoorMore 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 tuberosityMandible: 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 2nd 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 recoveryAxonotmesis: Damage to nerve but peri and endoneurium are intact; neuropraxia, anesthesia present;chances of recovery but slowNeurotmesis: 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:LAFlap design and retractionBone removal (as minimal as possible)Section the tooth (as any pieces as possible)Wound debridementSutureAntibiotics: if infection, repeated pericoronititsAnalgesics: Panadene forte (paracetamol + codeine (30 – 60 mg ??) especially for 3rd molar surgery Ibuprofen – has both analgesic + anti inflammatory effects (panadene also has paracet + codeine (10 mg)

Common post op complications:PainSwellingTrismusBleedingDrysocket (smoking , OCP related)Infected woundHaematomaNerve injuries (parasthesia , anaesthesia)Fracture of jaw

Q: Skull and foramen

From base of skullHypoglossal 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

Q: Mandible:Mandibular foramenMental nerve – between roots of lower 4 &5Mylohyoid groove – caused by mylohyoid nerve; on the medial surface of the body

Muscles: Lateral pterygoid: Opening of mouth Lateral excursions (One muscle), proteusion 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

Q:OPGOn OPG, a radiopaque mass seen on the posterior aspect of mandible, just extending beyond the inferior border of the mandible (Superimposed by soft tissue mass)DD: Calcified sialolith Calcified lymphnodeOcclusal x ray is the specific one for this caseClinically, on palpation can be symptomatic if in duct but asymptomatic if in intraglandular??If radioopaque mass seen completely within the mandible, includeDD : focal sclerosis (osteoma) along with the above two.

14/06/11Drugs used in dentistry:

LAAnalgesicsAntibioticsEmergency 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 molarA: 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 sideFrom upper molarFrom Maxillary nerve => Trigeminal ganglion and so on as above

Sensory innervation of oral cavity:MaxillaHard palate: Nasopalatine - from canine to canine Greater palatine – from 1st premolar to posterior maxillaSoft palate: Lesser palatineMaxillary teeth: Posterior Superior Alveolar nerve – molars xcept MB root of 1st 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 nerveMandible:All teeth – Inf alv nerveFloor of mouth – lingual nerveTongue – 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 + adrenalineCitanest: Prilocaine + felypressinScandonest: Plain MepivacaineSeptanest: 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 AdrenalineNacl – To maintain isotonicity of LANaoH – 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 adultChildren 3 to 6 yrs: 1.8mlChildren 6 to 14 yrs: 2.7ml

Q: Classification of LA:Amides: Aromatic ring + amide group + amide linkEsters: Same as above but with ester link (not amide link). It has unpredictable duration of action and also mostly allergicArticaine 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 equilibriumIt 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 inFor 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 potentProtein binding: Determines duration of action of LA – long binding time , then more duration of action Q: Basic injection techniquePrecautions to be taken: Need to have emergency (resuscitation) setup (equipment): O2 and Adrenaline are first line defense drugsSlow 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 cautiouslyLook 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 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 LAIn liverIn 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 increasesAt higher limit of the high dose – cardiac output decreases and circulatory collapseMethaemoglobinemia: 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 injectionBest way of avoiding toxicity – Know maximum dosages Frequent aspirationsWhen 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).Lignocaine4.4 mg/kg upto a max of 300 mg = 6/7 cartridges (absolute maximum) (no other calculations with lignocaine as plain lignocaine is not manufactured)Prilocaine6 mg/kg upto a max of 400 mg. therefore 1.8 ml cartridge contains 54 mg of prilocaine, 400/54 = --- catridges MepivacaineSame as lignocaineArticaine7 mg/kg upto max of 500 mg. 4% of 2.2 ml cartridge contains 88 mg = approx 5/6 cartridgesBupivacaine (marcaine??) effects of LA lasts for 8 – 10 hrs. Q: Why LA fails?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 mandibleLook 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)) premolarPenetrate needle till it hits bone, withdraw so that 2/3rds of needle is inside, aspirate and give 3/5th of solution for IAN nerve blockPull needle half way out, aspirate, give 1/5th of solution for lingual blockWithdraw 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 2nd molar, till it hits condyle. Ask patient to gradually close his mouth.Advantage: Blocks all three nerves in one injectionAkinosii ?? 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 prophylaxisIntrapulpal inj: Warn the patient before itself that it stings.

Patient dependent causes of failure:Anatomical variations: If mandibular foramen is too high – aim high Too low – normal aim will deliver solutionAccessory 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 mylohyoidLingual nerve – all lower teethGreater palatine nerve – Palatal root of upper molarAnatomical 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 mediumPsychological 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.

21/6/11Q: 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

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 analgesicsNarcotic analgesics

Non Narcotic Analgesics: Include NSAIDS (pronounced as nasaids) ParacetamolNSAIDS: Has anti inflammatory + analgesic actions Commonly used NSAIDS: Aspirin IbuprofenMechanism of action: Inhibit cox (cyclooxygenase), thus inhibiting PGS from arachidonic and thromboxanes?? Which play key role in inflammation.Ibuprofen (200 mg) = NeurofenIbuprofen (200 mg) + Codeine (12.5 mg) = Neurofen plusIbuprofen (200 mg) + Paracetamol (500 mg) = Panafene

Dosage:Ibuprofen:Available as 200 mg tablet/ capsuleMax daily dose: 2400 mg Per dose: 200 – 400. mg (i.e., 2 tablets) 6 hourly, is very responsiveSmall doses of combined drugs are more effective than large single drug dose.Ex: Neurofen plus PanafeneChildren: 5 to 10 mg/kg orally, 6-8 hrly (max 2400mg/24 hrs)

Adverse effects of NSAIDS:GI tract irritationPost 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 actionMechanism 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 tabletMax daily dose: 4 gmPer dose: 500 - 1000 mg (2 tablets) 6 hourlyChildren: 15 mg/ kg body wt pral and rectal Rectal suppositories also available: 20 mg/kg body wt 5 ml syrup formula availableIt is rapidly absorbed in GI tract, peak volumes reach in 30 min. No toxicity at therapeutic levelsNo tolerance or dependenceNo 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 analgesicPain transmission is prevented by inhibiting/ preventing neuronal activity at multiple areas of neuron)Adverse effects:Habitual addictionRespiratory depressionCNS depressionConstipationBradycardia, hypotensionUrinary retentionChest wall rigiditySweating, flushing, urticaria, pruritus

CORTICOSTEROIDS: Has anti inflammatory actionUsed 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 crisisAnaphylaxis, allergic reactionsBronchial asthma (pumicot?? Inhaler)Oral mucosal disease(pemphigus)Oral ulcerations (Sometimes apthous ulcers)Sever post operative swellingTMJ – muscle inflammationEndo – 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 synthesisInhibition of inflammation – by inhibiting cells and factors responsible for inflAnti infl effect >>NSAIDS

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

Adverse effects:Decrease immune responseCannot be used in presence of infections Uncontrolled diabetes Ulcerative colitis GI tract ulcerations Occular Herpes – can go blindProperly 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 organisms4- Dose large enough to knock off bacteria, but prevent emergence of resistant organisms5- Dose low enough to avoid toxicityb) Therapy:1- Emperical – therapy based on known pathogens likely causing the disease2- Directed- therapy based on culture and sensitivity tests3- 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 VAmoxicillinAmoxiclav = 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 AntifungalsPenicillin/ 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 nosePost ethmoidal and sphenoid – drain into superior meatus.(nasolacrimal duct opens into inferior meatus)

Shape of Max sinus: Pyramidal – apex, base and 4 wallsBase – 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 developmentAt birth – narrow slit like openingAs 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>85>43 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 downX ray: radiopacity of sinus.ORO ANTRAL COMMUNICATION:Ex: If after Xn of upper 6, OAC created, what is the management?After xn 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 xnIf 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 fracturesIsolated zygomatic fractureTumors – 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 rootParts of an elevator: Handle- shank/shaft- bladeElevators 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 toothWedge: Force applied along long axis of the elevator?? Ex: broken root in a socketLever (crow bar action): Buccal bone acts as a fulcrum. Cryers work on this principle

Guiding principles: Never use excessive force Always support the tooth/root to be xted Force applied in the direction away from major structures (like sinus, mental foramen, inf alv canal) Never use an elevator blindly Never use an adjacent tooth as s fulcrum Use sharp instruments Create point of application on the tooth/ root; sometimes bone should be removed to create the point

Complete debridement of socket and suture itShould not be used: Blindly Very close proximity to sinus (infected root – try to get it out by apical pick) Lower 3 rd molar area: Lingual plate is thinner, root can be forced into sub mand space Edentulous jaw : angle of mand can fracture Do no use elevator when xray not taken.

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

ODONTOGENIC INFECTIONS:It is the commonest of head and neck infectionsCause:Pulpal death, secondary to dental decayPericoronal tissuesPeriodontal tissuesMicrobial origin: Severity depends on the virulence and quantity of the organism Polymicrobial in origin: 28% are mixed aerobes 72% are anaerobes Most common aerobe: Strptococcus virulensAnaerobes: Peptostreptococcus(dento??) FusobacteriumAnatomical 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 antibioticsSubsequent attacks are much more severe than the previous attack.If spread laterally – involve submassetric Medially – parapharyngeal Pterygomandibular -> then to infratemporal Downwards – submandibular spaceTrt: 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 an 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 ,localised swellingChronic: Asymptomatic, till it undergoes acute exacerbation Associated with hopeless carious tooth Tender to percussion (periostitic??) Radiolucent lesion periapicallySigns 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 plexusCavernous 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 cellutis involving 3 spaces

Sub mand + sub mental + sub lingualDifficult to drainResp distressRaise of tonguePrinciple of trt: Maintain/ secure airway Massive IV antibiotics

ERYSIPELAS (?)Acute onset of cellulites, involve superficial layers of skinOrganism: Streptococcus; produces hyaluronidase that breaks down the barriers causing spread of infection.Regional lymph nodes are involvedDD: 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 formsIf acute osteomyelitis not well treated then results in chronic suppu 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 deposite 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, becomes pathogenic once gets deeply inoculated into the tissues. Ideal situations: After Xn, actinomyces embedded into the socket After compounded mandibular fracturePresentation:Non healing socket with mass of granulation tissue formation Multiple discharging sinusesNumbness of lip if involves regional nerve area.

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