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    You have a patient on a Friday night with irreversible pulpitis. She cannot tolerate rubber dam. You
    are the only dental practice for 300km. She has a wedding to attend on Sunday. she asks to
    immediately do something about the pain
    What can you do for her as a dentist?
    A. Do pulp therapy without rubber dam and use cotton roll as an isolation B. Extract the tooth
    C. Refer to endodontist
    D. GIve her topical analgesic
    E. Give her systemic analgesic to control the pain


    The most important factor in stainless steel crown retention in a primary tooth is the
    A. preservation of the coronal bulge.
    B. maintenance of parallelism.
    C. placement of accessory grooves.
    D. insertion of retentive pins


    • 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 3/5th 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.

    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.
    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

    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.


    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.

    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

    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

    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:

    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

    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
    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:
    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.

    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
    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.



    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

    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)
    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
    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

    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 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.


    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

    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
    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

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

    • DD for multilocular bone lesion
    Aneurismal bone cyst


    • 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 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
    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)

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

    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)

    Flap design and retraction
    Bone removal (as minimal as possible)
    Section the tooth (as any pieces as possible)
    Wound debridement
    Antibiotics: if infection, repeated pericoronitits
    Analgesics: 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:
    Drysocket (smoking , OCP related)
    Infected wound
    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

    Mandibular foramen
    Mental nerve – between roots of lower 4 &5
    Mylohyoid groove – caused by mylohyoid nerve; on the medial surface of the body
    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.


    • Drugs used in dentistry:
    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:
    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 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 nerve
    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

     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
    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.

    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.

    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

    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).

    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)

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

    Same as lignocaine

    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 1/5th 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 2nd 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.

    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:
    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

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

    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)

    Has anti inflammatory + analgesic actions
    Commonly used NSAIDS: Aspirin
    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

    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
    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

    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.

    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
    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.

    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
    Bradycardia, hypotension
    Urinary retention
    Chest wall rigidity
    Sweating, flushing, urticaria, pruritus

    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

    Dexamethasone – 4 mg tablet thrice daily. Especially after 3rd 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


    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
    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??
    Penicillin/ Amoxicillin are the safest drugs that can be used in pts on warfarin.


    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
    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.


    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
    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


    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.

    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:
    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.

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


    It is the commonest of head and neck infections.

    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??)
    Anatomical factors play a key role in the presentation of the infection

    Spaces involved are:
    Sub lingual
    Submassetric (between masseter muscle and ramus)
    Pterygomandibular (between medial pterygoid and medial surface of the ramus)

    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

    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.

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

    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:
    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.

    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

    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
    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.

    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
    Signs and symptoms:
    Neglected oral hygiene
    Multiple carious teeth
    Multiple discharging sinuses (extraorally and intraorally)
    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)

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

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

    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

    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
    Non healing socket with mass of granulation tissue formation
    Multiple discharging sinuses
    Numbness of lip if involves regional nerve area.

    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)


    In periodontitis maximum destruction is present in
    A. Lateral wall of pocket
    B. Root surface
    C. Junctional epithelium
    D. None


    Under normal conditions, the most definitive test to confirm the loss of pulp vitality is
    A. applying warm gutta percha to the crown.
    B. cutting into the dentin without anaesthetic.
    C. applying ethyl chloride to the crown.
    D. performing a radiographic examination of the tooth.
    E. performing an electric pulp test.


    When should pour polyether impression material?
    A. Within 24 hours after taking impression.
    B. Within 30 minutes after taking impression.
    C. Should be stored dry and then poured.
    D. Should be stored in humid place.


    The first molars are extracted in both arches:
    A. The bone resorption will be the same for both arches.
    B. Resorption is more on the palatal side of maxillary molars.
    C. Resorption is more on lingual side of mandibular molars.
    D. The ridge height resorbs more in maxilla than mandible


    Which one of the following is not an advantage of an enamel bonding agent over dentin bonding agent?
    A) decreased marginal leakage
    ? better colour stability
    C) increased bond strength
    D) easier to apply
    E) decreased moisture sensitivity


    All of the folollowing are clinical features of insulin-dependent DM, except:
    a. Age of onset usually less than 40 years.
    b. Normal or low body weight
    c. Positive family history of DM.
    d. Presence of Ketonuria.


    The pulpal floor of the Class II cavity for a mandibular first premolar should be:**

    A.​Parallel to occlusal plane
    B.​Perpendicular to long axis
    C.​Tilted lingually


    A gingivally extended chrome cobalt cast clasp
    A. Can extend 0.5 under the surveyor line
    B. Can extend 0.25 under the surveyor line
    C. Will resist deforming forces better compared to cast gold

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