Exam

Question 1

Heart attack (Cardiac Arrest)

Answer 1

Prevention: Health history questionnaire, vital signs, Monitoring neck vein distension and ankle edema
Manifestations: Sudden onset of severe, anginal type pain usually without an obvious precipitating cause. Pressure or weight on your chest.
Management: Only emergency treatment within 6 months of MI. For acute MI nitroglycerine does not relieve pain. Discontinue dental treatment. Position conscious patients upright. Initiate BLS if needed. Supplemental O2 4-6L/min. Sublingual Nitroglycerin unless pt has taken viagra/cialis. Chew 325mg Aspirin. Activate EMS for definitive care.

Question 2

Angina

Answer 2

Prevention: evaluation for a history of unstable angina, a significant risk factor for MI
Dental considerations: Short appointments, consider supplemental O2, ensure adequate anesthesia, but limit to 0.04mg Epi.
Management: Discontinue dental treatment. Position the patient upright. BLS as needed. Administer O2, sublingual nitroglycerine (0.3-0.6mg) up to 3 doses in 15 minutes. Summon medical assistance if necessary.

Question 3

Asthma

Answer 3

Prevention: Screen patients for history of Asthma. Avoid opioids for cases of sedation, and caution with ibuprofen
Signs and symptoms: feeling of chest congestion, coughing, wheezing, Dyspnea
Management: Termination of dental procedure and remove all dental materials. Position the patient upright. Administer O2 and bronchodilator (press down inhaler, breathe in slowly for 5 seconds as deeply as possible, and hold your breath and count to ten. Wait 1 minute between puffs
Severe reactions: 0.3ml 1:1000 Epinephrine repeated every 30-60 minutes as needed. Can also administer 100-200mg hydrocortisone sodium succinate.

Question 4

Syncope

Answer 4

Clinical manifestations: a sudden drop in BP (systolic below 70mmHg), lightheadedness, can result in a loss of consciousness.
Management: Assess consciousness, activate office emergency. Place patient in supine position, monitor for BLS. Administer O2, monitor vitals. If the patient does not respond rapidly, then contact EMS. Discharge when Pt has recovered for sufficient time.

Question 5

Stroke

Answer 5

CLinical signs: headaches, dizziness/vertigo, drowsiness, sweating/chills, nausea and vomiting. Loss of consciousness and convulsions are less common but more serious signs. Weakness and paralysis in the extremities/face contralateral to the CVA also occur, along with speech alterations.
Management: Depends on how rapid the onset of symptoms are but BLS is usually indicated. Discontinue dental procedure, activate emergency team/EMS. Place Pt in a 45 degree position (slightly upright). BLS as needed, with vital sign monitoring. Establish IV access if available with lactated RIngers. Administer O2.

Question 6

Anaphylaxis

Answer 6

Signs: immediate or delayed reactions can occur. REdness in the skin can occur, as well as respiratory distress, lightheadedness/syncope can occur.
Management: Position based on patient comfort. Montor for BLS. Administer a histamine blocker if mild anaphylaxis (diphenhydramine, 50mg TID for 3 days) Medical consult required. For severe reaction administer O2 and Epi (0.3mg every 5-20 minutes up to 3 doses.) Activate EMS if Epi administered.

Question 7

Choking

Answer 7

Population at risk: Children, elderly, sedated patients
Prevention: Oral packing, using ligatures.
What to do if an object falls into the back of a patients throat: move patient into the Trendelenburg position (head facing down over the side of the chair), attempt to suction the object out or use Magill forceps. Do not allow patient to sit up
Management: Partial obstruction. Encourage coughing, do not touch Pt. Complete obstruction: Phase 1 (first 1-3 mins) if conscious Heimlich maneuver, call for help, 911. Phase 2 (2-5 minutes) loss of consciousness, call for help, 911, begin CPR, begin with airway opening and then compressions

Question 8

Hypoglycemia

Answer 8

Clinical manifestations: Usually when pt has not eaten for several hours. Signs may resemble alcohol intoxication. This is followed by sympathetic hyperactivity (sweating, tachycardia, piloerection, and anxiety.
Management: Terminate the procedure, seat in an upright position. BLS as indicated and EMS if unconscious. Administer oral carbohydrates (sugar drink/tablets if conscious, perinatal carbohydrates if unconscious, Glucagon 1mg IM/IV or 50mL 50% dextrose IV over 2-3 minutes. Monitor the patient until medical assistance arrives.

Question 9

Hyperventilation

Answer 9

Prevention: management of anxiety
Signs and symptoms: Initiated by fear. Hyperventilation causes a change in blood chemistry which causes lightheadedness/giddiness, which intensifies apprehension further, in extreme cases carpopedal tetany (muscle flexion in the wrist/hand)
Management: terminate dental procedure, position the patient upright. Calming the patient. Rebreathing their exhaled air in a bag or their hands (for increased CO2 concentrations). Can use benzos in extreme cases to reduce anxiety. Future visits should be done under sedation.

Question 10

LA toxicity

Answer 10

Signs: Confusion, Talkativeness, Apprehension, Excitement, elevated BY/HR/RR. Lightheadedness, dizziness, blurred vision, ringing in ears, disorientation. Severe reactions include tonic-clonic seizures, generalized nervous system depression, depressed BP, HR and RR, loss of consciousness
Management: In most cases the reaction is transitory and mild, so no specific treatment is needed. Aggressive IV management comes when simpler means fail to terminate the seizure. Terminate dental procedure, reassure pt and place in a comfortable position, BLS as needed, administer O2, and purposely hyperventilate, administer anticonvulsant if needed (Midazolam 1-2mg or Diazepam 2.5-5mg IV). Call EMS for severe reaction.

Question 11

Hep B,C

Answer 11

Hep B - Double shelled DNA virus. Acute phase begins incubation period of 30-150 (mean 75) days. Virus is generally undetectable during peak illness, and recovery happens several weeks to months after loss of HepB virus. Chronic infection is an infection that lasts longer, and is relatively rare. Transmissible through blood or sexual contact. Vaccination recommended for all newborns, and especially for healthcare workers that are exposed to blood. Post vaccination seropositive testing is recommended for healthcare workers. Post exposure prophylaxis with HBIG is recommended if percutaneous exposure. Antiretroviral therapy is recommended for Chronic Hep B patients, but not for acute infection. Patients should be monitored after to ensure that chronic infection does not occur (chronic infection occurs in 90% of newborns, 30% of infants, and less than 10% of adults, ~2-7%)
Hep C - Hep C becomes a chronic liver problem for 85% of people infected. Predominantly spread through parenteral route, so it is the most significant infection of concern for dental professionals. It is an RNA virus. THere are no vaccines or precautions to prevent HCV infection other than avoiding parental exposure.

Question 12

TB

Answer 12

Mycobacterial infection transmitted by droplets. M. tuberculosis, an acid-fast, nonmotile, intracellular rod, obligate aerobe, which is why it infects the lungs. 90% of patients will present with nothing more than a positive skin test and radiographic findings, and progression typically only progresses in those with underlying conditions. Treatment is directed against people with active TB or latent TB infection (chronic granulomatous inflammatory reaction with activated epithelioid macrophages and formation of granulomas) if considered a high risk of disease progression. Patients should be screened for close contact with disease, patients with infectious disease should be hospitalized, Dental offices are considered low risk for exposure to TB. Standard infection control protocol is necessary, and anyone with active TB positive sputum cultures should not be treated. A history of TB is not a contraindication. Often you will see a classic irregular ulcer in the dorsum of the tongue.

Question 13

Herpes

Answer 13

Elective dental treatment should be delayed until the lesion has resolved. THey are infectious during the papular, vesicular, and ulcerative stages through contact with the lesion or infected saliva. They affect both keratinized and non-keratinized surfaces with the lips and tongue the most frequently affected. The primary infection is the most severe, with sores throughout the lips and mouth, and flu-like symptoms. Recurrent lesions are milder and more localized. The lesions are usually self limiting within 10-12 days. If caught early though (1-3 days) they can be treated with antivirals (Valacyclovir (Valacyclovir 500mg, take 4 tablets at first sign of attack, and then 4 tablets 12 hours later) or topical Acyclovir (Acyclovir Ointment 5%, Disp 15g, apply to lesion 6-7 times per day for 7 days) Or palliative measures (Lidocaine 2% Viscous 100mL 15mL no more than every 3 hours to relive pain, not to exceed 8 doses/day)

Question 14

HIV/AIDS

Answer 14

RNA virus, treated with HAART protocol. Frequently transmitted through male to male sexual contact or injection drug use. HIV seeks out CD4 lymphocytes, which results in a reduction in the CD4 lymphocyte count. As the Cd4 cells approach 200 cells/microL is when the patient will become symptomatic (weight loss, diarrhea, night sweats). HIV+ patients with CD4 of 350/microL or more are generally ok for all treatment, however if they are under 200/microL they have increase susceptibility to opportunistics infections and may need premedication. Low viral load count is <1500 copies/mL. Standard precautions will prevent transmission in a dental setting, and a direct needlestick will only result in transmission in 0.3% of cases, but a practitioner would be recommended a post-exposure prophylaxis regimen. Other infections associated with HIV are HSV, CMV, EBV, Herpes zoster, aphthous ulcers, linear gingival erythema, MUP, TB, syphilis, HPV, candidiasis, hairy leukoplakia, Kaposi’s sarcoma. Kaposis ais related to HSV-8, hairy leukoplakia is EBV.

Question 15

Syphilis

Answer 15

Caused by Treponema Pallidum. Primary syphilis is usually a single cancre at the site of exposure that subsides in 3-6 weeks. Secondary is associated with hematogenous spread with systemic signs and symptoms (fever, malaise, headache lymphadenopathy, hair loss, and generalized eruption of the skin and mucous membranes. Symptoms do resolve but transforms into latent syphilis. Tertiary syphilis occurs in 10-40% of persons years later, and is divided into neurosyphilis, cardiovascular and gummatous disease. It is treated with Penicillin G IM one 2.4 million IU dosage. Any lesions are infections, the patient may remain infectious for a few months or longer than 1 year. Anyone who is still seropositive should be viewed as infectious. Elective dental treatment should be delayed until the oral lesions are treated using standard precautions. The oral chancres and mucous patches are usually painless unless secondarily infected. Typically solitary lesions that involve the lips, tongue, oropharynx, or other oral sites, from 1mm to more than 2cm. Palatal Gummas can invade the bone and perforate the nasal cavity or maxillary sinus. Congenital syphilis shows peg-shaped permanent central incisors with notching at the incisal edge (Hutchinson’s incisors) defective molars with multiple supernumerary cusps (mulberry molars) and a high, narrow palate and perioral rhagades

Question 16

COVID 19

Answer 16

Flu symptoms, with up to ⅓ of patients being asymptomatic. Test can be done against the viral nucleic acid. Transmission is through contaminated droplets/aerosols and airborne particles containing the virus. Current guidelines recommend masking in common areas, but are not mandated. Patients with flu like symptoms are recommended to delay treatment until the symptoms are resolved. Not a lot of current information on any additional precautions (leaving the room untouched after patient care, UV sanitization, air circulation, etc)

Question 17

Post op infections

Answer 17

Infection occurs 4-10% of times after surgery (and infection results in 66% of implants failing). Wound openings of <1 hour have an infection rate of 1.3% vs longer than 3 months is 4%, postulating that infection rate doubles for every hour of the procedure.
Factors associated with infection: Diabetes, smoking, long term corticosteroid use, immunocompromised systemic disorders, malnutrition/obesity, elderly, ASA ¾. Adding graft material, periodontal disease, tissue inflammation, odontogenic infections, incision line opening, inadequate hygiene also increases changes of infection. Longer surgery or wound contamination during surgery, or a foreign body (implant/graft/membrane) also increases changes of infection
Signs of infection: Fever (>38C), Pulse >100bpm, increased BP/RR. Signs of inflammation are PRISH (Pain, Redness, Immobility, Swelling, Heat). Severe inflammation can have trismus (reduced jaw opening), Lymphadenopathy, Dysphagia (difficulty chewing/swallowing), Dyspnea (difficulty breathing)
Forms of infection: Abscess (hard, well defined borders, fluctuant with pus). Cellulitis (larger, more widespread, diffuse borders, hard to palpation, no pus. Fistula, Edema.
Treatment: Incision and drainage (abscess or cellulitis) to decrease bacterial load and reduce hydrostatic pressure and prevent spread into deeper anatomic spaces. Usually includes the insertion of a drain to prevent closure. Consider culture and antibiotic sensitivity testing for infection spreading into fascial spaces, symptomatic and rapidly progressing, non-responsive to antibiotics after 48 hours, multiple doses of antibiotics, chronic, recurrent infection. Antibiotics. Amoxicillin, Metronidazole, Amoxicillin+Metronidazole, Amoxicillin+Clavulanic acid, Azythromycin, Clindamycin…

Question 18

Emphysema

Answer 18

Penetration of air into the subcutaneous tissues and fascial planes
Differential diagnosis: hypersensitivity reaction, hematoma, cellulitis, angioedema, subcutaneous facial emphysema
Caused by air penetration through the tissues, usually from an air syringe, a front venting handpiece, or airflow
Management: prescription of 500mg Amoxicillin TID for 7 days. Pain can be managed by Acetaminophen. Avoid activities that increase intraoral air pressure (blowing balloons, straws, sneezing. Complete resolution typically after 7-10 days

Question 19

Swelling of Floor of mouth

Answer 19

Masticatory spaces (Masseteric space between mandible, parotid, lateral pharyngeal, temporal)
Sublingual space: bound by mylohyoid muscle and geniohyoid and genioglossus muscles. Contains lingual artery and nerve, hypoglossal nerve, glossopharyngeal nerve. Infectious spread through a perforation in the lingual mandibular cortical plate. Can usually be treated with incision and drainage of the abscess through an intraoral approach.
Submental space: Bounded anteriorly by the symphysis of the mandible, laterally by the digastric muscles, superiorly by the mylohyoid muscle, and inferiorly by the platysma. No vital structures transverse. Odontogenic infections of the anterior mandible. Surgical access for drainage of infection is generally through extraoral incision below the chin
Submandibular space: from the hyoid bone to the mucosa of the floor of the mouth, anteriorly and laterally by the mandible and inferiorly by the superficial layer of the deep cervical fascia. Separated from the sublingual space by the mylohyoid muscle. Surgical access can be intraoral or extraoral. If the spread is bilateral it is one of the components of Ludwig’s angina. Surgical drainage of these situations is almost always multiple extraoral incisions.
Lateral pharyngeal space. An inverted cone with the boundary at the base of the skull and apex at the hyoid bone. Rotation of the neck away from the side of swelling causes severe pain. Spread into this space is high risk of airway impingement. Typically require extraoral drainage.

Question 20

IAN damage/ other nerve damage

Answer 20

The IAN is one of the most common nerves to damage from it’s location, usually during implant, bone grafting, or soft tissue grafting procedures in this location.
Prevention - mental foramen: Ensure all vertical incisions are far enough from the location of the mental foramen to avoid severing the nerve, and consider its location when doing any periosteal release.
Prevention - IAN: Removal or a 3rd molar or an implant can bruise, crush, or sharply injure the nerve or its canal. It can also be damaged by the needle during IAN, 20X more likely if using Articaine

Question 21

Nerve injury from implant classification

Answer 21

Partial intrusion into mandibular canal can cause mechanical IAN trauma
Full implant intrusion into mandibular canal can cause IAM transection
Implant too close to mandibular canal can cause IAN compression
Partial implant intrusion into mandibular canal can cause indirect trauma due to hematoma and secondary ischemia
Partial implant intrusion into mandibular canal can cause indirect trauma due to bone debris and secondary ischemia
Cracking of the root of the mandibular canal can cause compression and primary ischemia

Question 22

Paresthesia

Answer 22

Iatrogenic injury with sensory impairment to branches of the trigeminal nerve is a major concern. 73% of doctors who perform implants have encountered such postoperative complications, with 75% of cases resulting in permanent injury.
Infraorbital nerve emerges from the infraorbital foramen, and provides sensation to the skin of the nose, upper lip, and lower eyelid. Can be damaged by a minnesota retractor when working close to the orbital ridge.
Lingual nerve: Divides from the mandibular nerve (V3) inside the body of the mandible. It passes inferiorly to the superior constrictor and then to the lateral surface of the tongue, providing the sensory to the anterior ⅔ of the tongue. It also carries the fibers from CN7 via the Chorda Tympani which relays taste. Occasionally (~20%) the lingual nerve passes along the medial ridge of the retromolar triangle, where it passes anteriorly along the superior lingual alveolar crest, slightly lingual to the teeth. If the lingual plate is perforated during osteotomy the nerve can be damaged, but usually it is due to flap elevation over the retromolar pad.
Local Anesthesia can cause nerve damage. IT is reported that damage during IAN is 1:25,000 blocks, with most (85%) patients recovering fully in 8-10 weeks. This is usually caused by the needle (lingual nerve most common to be damaged by the needle). A hematoma can also cause nerve damage from the needle, which may lead to scar tissue formation. Anesthetic toxicity can cause damage due to the acidity of the injection with articaine 21X more likely to cause mandibular block injuries.
Direct or indirect trauma from the implant preparation. Either directly cutting the nerve, or encroaching the nerve which leads to overheating the bone or pressure during implant placement. Partial penetration will result in sensory deprivation equivalent to the damage to the nerve. Reversing the implant a few turns and monitoring is the treatment. Complete transection has the lowest probability of regeneration. If a known traction or compression of the nerve occurs, place Dexamethasone 1-2mL of 4mg/mL in the socket to reduce the neuronal inflammation and possibly enhance the neurosensory deficit. Do not place bone grafting or implant into the site.
Mandibular socket grafting can lead to chemical neuritis and possibly an irreversible neuropathy.

Question 23

Hemorrhage

Answer 23

Classifications: Arterial hemorrhage (bright red, spurting/pulsatile) Venous hemorrhage (dark red, continuous) and Capillary hemorrhage (bright red, continuous)
Onset: Primary (during surgery from incision, retraction, usually controlled with mechanical or hemostatic agents) and Reactionary hemorrhage (within hours of surgery, usually with patients on anticoagulant therapy or having postoperative trauma to the surgical area, or from arterial vasospasm after epi wears off. Secondary hemorrhage is 7-10 days after surgery, usually as a result of infection.
For patients on anticoagulants, we measure Prothrombin time (PT) or more accurately INR for Coumadin, Partial Thromboplastin time (PTT) for patients on heparin, bleeding time can be used too. Interruption of anticoagulant therapy has very limited evidence, and generally patients with INR of <3 will not alter medications, and the anti-platelet drugs we generally don’t alter.
Mechanical bleeding control - Apply pressure, sit patient upright to reduce arterial pressure (can reduce bleeding by 38%). Sutures used to ligate the vessels (enter 4mm from the vessel, 3m below the vessel) placed proximal to the bleeding tissue. Cna clamp the vessel with hemostat forceps for 2-3 minutes, ideally ligating the vessel before releasing the forceps.
Pharmacologic techniques: Epinephrine (topical 1:50k epi soaked gauze), however beware of rebound hyperemia postoperatively. 1:100k epi may have less rebound after. Tranexamic acid solution can be used as a mouthwash postoperatively to enhance clotting or placed topically during surgery.
Topical hemostatic agents: Collagen (collatape/oraplug) absorms many times its weight. Cellulose (surgicel) slightly antimicrobial, expands 3-4X its size and forms a gel, but it might for a foreign body reaction, and needs to be removed. Synthetic bone hemostatic agents (Bone wax) tamponades the osseous vascular spaces, it is insoluble, and must be removed or it will cause inflammation and a foreign body reaction. Kaolinite (K gauze) naturally occurring mineral activates factor XI and XII, must be placed directly onto the wound, and causes an exothermic reaction

Question 24

Dry socket

Answer 24

Delayed healing but not associated with an infection. Significant post operative pain but without fever, swelling or erythema.
Typically is noted on day 3-4 after tooth removal, almost always in lower molars. Visually the socket is almost empty with a partially or completely lost blood clot nad exposed bone, dull aching is moderate to severe
The cause is not clear, but appears to be caused by fibrinolytic activity resulting in lysis of the blood clot and subsequent exposure of bone, possibly from subclinical infections, inflammation of the marrow space, or other factors. About 2% of extractions, but about 20% of mandibular 3rd molars
Prevention: minimize trauma and bacterial contamination to the site, irrigate the wound with saline. Gelatine sponge can reduce dry socket (PRF??)
Treatment: The primary goal is reducing pain during healing, as treatment does not hasten healing time. Treatment is irrigation and placing of a medicated dressing. Do not curette the socket. Medicated dressing contains eugenol (pain relief) and a topical anesthetic such as benzocaine, and a carrying agent. This dressing is changed every other day for 3-5 days depending on the severity of pain. Once the pain is relieved the dressing should not be replaced as it will act like a foreign body.

Question 25

Pain management

Answer 25

Pain from oral surgery reaches its peak 12 hours after surgery. 50% of cases pain is inadequately treated in some studies Prevention: GOod surgical technique, postoperative long- acting anesthetics, adequate postoperative pain control and instructions, limitation of patient activities post-operatively Treatment: The most important principle is timing of medication. Administer analgesics before the LA subsides, as it will take more medication to dull pain after LA has worn off. Max dosage of Acetaminophen is 4g/day. Ibuprofen is 2.4g/day. Tramadol is a combination opioid and antidepressant that has an effect similar to codeine, and can be used in combination with acetaminophen.

Question 26

Trismus

Answer 26

This can be caused by many factors, but the most common is LA during an IAN block. Complicated surgeries with a full thickness flap resulting in edema can lead to trismus. Prevention: minimize excessive opening of the patient where spasm of the muscles will result. Treatment: Usually resolves with time, however maintain a soft diet and minimize overactivity. Additionally physiotherapy, split therapy, NSAIDS, muscle relaxants, and steroids.

Question 27

OAC/OAF

Answer 27

High risk if the sinus is pneumatized and there is minimal bone adjacent to the sinus. Risk factors: Chronic maxillary sinusitis, and chronic oroantral communication. Probability of these occurring is the size of the communication Treatment: if there is a small communication at time of surgery (<2mm) no treatment is needed other than measures to ensure a high quality blood clot and advise sinus precautions (reducing maxillary sinus pressure)For a moderate opening (2-6mm) additional measures should be taken, including a figure eight suture over the tooth socket, and possibly clot promoting substances such as gelatin sponge before suturing, and sinus precautions, plus antibiotics (amox). For a large opening (7mm+) you should aim for primary closure, preferably the day that opening occurs.

Question 28

Osteomyelitis

Answer 28

Acute and chronic condition, with chronic lasting for over 1 month. An inflammatory condition of the bone from an infection of the medullary space that extends to the cortical bone and periosteum that compromises blood supply. Treatment: usually surgical debridement, followed by long term antibiotic regimen. Radiographic changes show a poorly defined, radiolucent bone loss with intermixed radiopaque areas (only visible when the lesion si at least 1cm and compromises 30-50% of bone mineral content). T1 weighted MRI can show the results sooner.

Question 29

ONJ/MRONJ

Answer 29

Stage 0: no evidence of necrosis but non-specific pain. No tx indicated Stage 1: exposed necrotic bone/fistula but no pain. Systemic abx/pain management Stage 2: exposed necrotic bone/fistula with pain. Systemic antibiotics, oral CHX, possibly surgical debridement, pain control Stage 3: exposed necrotic bone/fistula extending to the inferior border of the mandible, maxillary sinus, zygoma in the maxilla, resulting in pathologic fracture. Systemic abx, oral CBX, surgical debridement/resection

Question 30

MRONJ

Answer 30

Patients treated with oral BPs risk is 0.02=0.05%. Post extraction risk is roughly 0.15% IV BP’s risk is 0.02% RANKL inhibitors risk is 0.3%. Post extraction risk is around 1%. For cancer patients the risk for MRONJ after tooth extraction is between 1.6-14.8%, clustering between 1-5%, similar to irradiated patients. MRONJ is more likely in mandible than maxilla, and more likely with dentures

Question 31

Peri implant mucositis

Answer 31

Definition: inflammation in the absence of bone loss. Clinical sign is BOP (other than point bleeds) although erythema, swelling and suppuration can also occur. PD progression or 6+mm also considered Reversibility: may take longer than 3 weeks to reverse, but resolution of the biomarkers can be seen at 21 days. More pronounced and larger inflammatory lesion than in gingivitis. Risk indicators/factors: Oral hygiene, compliance with SPT. materials and surface characteristics of implant components, design of implant supported prosthesis (accessibility for biofilm removal/cement, Dimensions of KT (not definitive).

Question 32

peri implantitis

Answer 32

Definition: Inflammation with associated bone loss. Progressive PD or 6+mm. Bone loss of 2mm from the first year, or greater than 2mm from the implant platform or progression of more than 0.2mm per year. Risk indicators/factors: Same as mucositis. History of periodontitis, poor plaque control. Currently no evidence for smoking or diabetes. Almost all peri-implantitis occurs in the presence of inflammation.

Question 33

Lingual, mental, IAN , nasopalatine nerves anatomical limitations

Answer 33

Lingual nerve: no distal extensions over the retromolar pad of lower 7’s, 8’s, have to orient buccally. Also no vertical incisions on the lingual, especially in the molar area, and consider any periosteal releases ensuring that you are staying shallow with them. By the premolars you can do vertical incisions if you want to, but only if absolutely needed Mental: Know where it is and avoid any vertical releases in between the premolars if you can’t see it radiographically. This will limit implant placement depth in the premolars and depth you can elevate when doing a GBR IAN: Digital planning your implant cases, leaving a 2mm margin of error minimum. Also be cautious with the heat produced by the drill. Nasopalatine: Not sure if it is much of a limitation, if your implant runs into it you might have to graft it. Enucleate it if it is greater than 6mm in diameter. Severing it doesn’t seem to impact patients at all IANB given- facial blanching why? - injecting the parotid gland

Question 34

Lingual, GP artery

Answer 34

Greater palatine: Limits the depth of harvest that can be done. Average measurement is 14.5mm from the seconde molar CEJ and 8.7mm from the CEJ of the canine. Feel for the greater palatine fossa before doing a harvest to avoid the artery. Lingual artery: courses medially to the greater horn of the hyoid bone then transverses deep to the digastric and stylohyoid muscles, and between the hyoglossus and genioglossus muscles. Of most significance is the lingual artery supplies the sublingual salivary gland, mylohyoid, and surrounding muscles, and the mucous membranes and gingiva of the mandible. A distal branch runs medially in the anterior lingual mandibular gingiva and anastomoses with the contralateral artery. An additional branch connects with the submental artery under the mylohyoid muscle. In dentate patients the risk of hemorrhage is high with vessels above the mylohyoid. In edentulous patients the mylohyoid line approaches the alveolar crest, leading to high risk of hemorrhage. The implant length should be carefully evaluated and avoid bicortical stabilization. THis can cause bleeding into the sublingual and submaxillary spaces which will cause elevation of the tongue and floor of the mouth.

Question 35

Maxillary sinus, nasal cavity, FOM

Answer 35

Sinus: Caution when extracting the roots if you are in close proximity to the sinus. Implants consider need for sinus augmentation protocols, and cautious drilling at depth. Can place an implant 1mm into the sinus with minimal concern, 2-3mm consider grafting with or without bone (for boards with), and more than 3mm consider direct sinus lift Nasal cavity: Can do bicortical stabilization if needed for implant placement, but try not to plan for it unless required. For extractions still be cautions with extraction technique when thin bone over the nasal cavity Floor of mouth: Caution with flap elevation as the distance to detach the mylohyoid is small. Once through the mylohyoid you have the lingual nerve and lingual artery that are easy to damage. Avoid vertical releases and extreme caution with periosteal releases.

Question 36

Sublingual foramen

Answer 36

A central foramen at the midline of the mandible, where the lingual artery enters into the mandible. If severed with osteotomy you will get profuse bleeding through the osteotomy. If this happens place the radiographic indicator pin into the site with firm pressure to stop the bleeding. Can use the implant to compress the site as well.

Question 37

Lingual accessory canal

Answer 37

Small nutrient canals that enter the jaw from the lingual aspect. Be aware of them and avoid placing osteotomy into them just in case. If they are disrupted, likely similar to the lingual foramen, place the radiographic indicator in with pressure until the bleeding subsides. If the osteotomy is complete the implant can also be placed which will compress the site.

Question 38

Anatomy on CBCT

Answer 38

There are approximately 3.2 incidental findings per CBCT, so consider rad report, using the smallest FOV possible to avoid unrecognized incidental findings. Mandibular canal will not show up on transaxial view in CBCT in about 40% of cases, so you have to be cautious in using different views to visualize it, beginning and the mandibular foramen or mental foramen. Evaluate maxillary sinus for ostium opening if visible (ideally 2mm+) sinus septum Anatomic variations to consider: Anterior loop of IAN (30-50% prevalence mean distance 1.16mm up to ~5mm). Accessory foramen 12.4% prevalence average diameter 1mm. Lingual concavity 4% prevalence. Incisive canal will extend to the midline in 18% of patients, and sometimes anastomosis with the other side. Calcified Carotid Artery.

Question 39

Macrophages

Answer 39

Macrophages are crucial cellular components of the innate immune system, and contribute to the inflammation and restoration of tissue homeostasis in response to peridontitis associated bacterial communities, through pattern recognition receptor-induced signaling cascades. Some macrophages appear to be pro-inflammatory (M1) and others are anti-inflammatory (M2). These are usually derived from tissue resident macrophages, or can be derived from circulating macrophages. M1 are primed in response to LPS or T helper cytokines such as IFNgamma. M1 produces IL-6 and TNFalpha. M2 are polarized by IL-4 and IL-13, and produce IL-10, TGF Specifically targeting M2 macrophage differentiation may be a periodontitis treatment in the future.

Question 40

Pro inflammatory mediators

Answer 40

IFNgamma - Activates M1 macrophages to promote periodontal bone loss IL-6 - Promotes periodontal tissue damage RANKL - Promotes periodontal bone loss TNFalpha - promotes periodontal bone loss MMP-9 - Promotes extracellular matrix degradation and alveolar bone resorption MMP-13 - Promotes periodontal bone loss CCL-2 - recruits macrophages to the site of infection and induces alveolar bone loss and epithelial lesions IL-1beta - Promotes periodontal bone loss

Question 41

Anti inflammatory mediators

Answer 41

IL-4 - activates M2 macrophages to regulate inflammation IL-10 - inhibits osteoclastogenesis and stimulates osteoblastic differentiation TGFbeta - enhances the production and deposition of ECM and suppresses the expression of pro-inflammatory cytokines CystatinC - promotes bone regeneration by regulating osteoblasts and osteoclasts

Question 42

RANKL inhibitor mechanism of action

Answer 42

RANKL inhibition blocks osteoclast maturation, function, ans survival, reducing bone resorption This is in contrast with bisphosphonates which bind bone material, where the absorbed by mature osteoclasts, including osteoclast apoptosis and suppression resorption.

Question 43

ILbeta

Answer 43

Cytokine produced by activated macrophages, monocytes, and dendritic cells. Involved in cellular activities including cell proliferation ,differentiation and apoptosis Increased presence of IL1beta is found in patients with a number of chronic autoinflammatory syndromes. Intestinal dysbiosis has been shown to induce osteomyelitis through alterations in IL1beta

Question 44

Page and Schroder

Answer 44

Initial Lesion: 2-4 days. These features merely reflect an enhanced level fo activity of mechanisms of normal host defense. Leukocytes may be observed migrating towards the gingival sulcus into the JE. itis localized to the region of the gingival sulcus, affecting a portion of the JE and the most coronal part of CT. Vessels become engorged and dilated. A portion of perivascular collagen disappears with space occupied by fluid proteins, and inflammatory cells. This phase may not be visible at all in clinical situations, but be a chronic situation in an otherwise healthy gingival tissue, and may show signs of gingivitis sooner than normal healthy tissue. Early lesion: 4-7 days. Significant numbers of immunoblasts appear throughout the reaction site, while the plasma cells reside only at the later and apical periphery of the infiltrate. Collagen loss may reach 60-70% and the fibroblasts appear altered in the site, with ruptured membranes and 3X larger than others. Gingival fluid flow and sulcular leukocytes reach their maximum and level off between 6-12 days. THe JE has an increased number of migrating neutrophilic granulocytes and infiltrating mononuclear cells (especially lymphocytes) Established lesion: begins at 2-3 weeks. The distinguishing feature is the presence of a predomination of plasmas cells within the affected connective tissue prior to bone loss. (this happens more rapidly in adolescents with braces). Plasma cells are not confined to the reaction site, and also appear in clusters along the blood vessels and between collagen fiber bundles deep in the CT. Fibrosis and scarring can occur. It is not known if this lesion is reversible, or what causes it to advance further at this time, but most do not progress for long periods of time Advanced lesion: Frank and overt periodontitis (pocket formation, surface ulceration and suppuration, fibrosis of the gingiva,destruction of alveolar bone and PDL, tooth mobility and drifting). THe lesion is no longer localized, extending apically and laterally. The size of the band depends on the extent of disease. The marrow spaces are opened by the bone destruction, and the marrow is hypercellular, undergoes fibrosis and transforms into a scar like CT. The fiber bundles of the marginal gingival lose their characteristic orientation and architecture completely, but the transseptal fiber bundles continuously regenerate as the lesion processes apically. Frank tissue necrosis is generally not observed.

Question 45

Ecological plaque hypothesis

Answer 45

The evolution of the non-specific plaque hypothesis (theory that it is the total amount of plaque that determines disease), to the specific plaque hypothesis (that is trying to determine the individual bacterial strains that are causing disease). The ecological plaque hypothesis is that disease is caused by an imbalance between the different biofilm ecologies that allows the pathologic microflora to thrive. This preceded the keystone pathogen hypothesis, which stated that certain species initiate the host inflammatory response and are essential to the progression of disease. The all encompassing ecologic hypothesis that explains disease progression is still lacking.

Question 46

Smoking

Answer 46

Tobacco is one of the modifiable risk factors that has enormous influence on the progress development and treatment of periodontal disease Smoking is an independent risk factor in the initiation, extent, and severity of periodontal disease, and affects treatment outcomes as well. Cross sectional and longitudinal data shows that smoking increases CAL and bone loss. It changes the microflora, human immune response, and this leads to the destruction. The symptoms are often masked so it takes years to notice for the patient. Differences in AL for smokers to non smokers was 0.37mm in 35 year olds, and up to 1.33mm in 75 year olds. Never smokers had a root percent in bone of 83% vs smokers at 77%. Smokers are 2-6X more likely to have periodontal destruction than non-smokers depending on the definition. There is a strong correlation with mean bone loss and pack years of smoking. There is less Attachment gain in smokers to surgical and nonsurgical therapy. Implant success rates have been reported at 89% in 6 years for smokers vs 96% for non-smokers. Impairment in phagocytosis of neutrophils has been seen in smokers.

Question 47

Diabetes

Answer 47

Diabetes is a risk factor for gingivitis, periodontitis, and level of glycemic control. One study found that Type 1 diabetic children had higher rates of periodontitis than their non-diabetic siblings (13% rate between age 13-18 and 39% at 19-32 years, compared to controls at <3% for both age groups) In the PIMA indians diabetic patients had a 2.8-3.4 fold increase odds ratio of having periodontitis. Poor diabetic control usually shows a higher OR of periodontal disease than well controlled, with well controlled showing limited difference in periodontitis risk to healthy subjects. Periodontal disease treatment has been shown to decrease HbA1c levels by about 0.5 Immune cell function is inhibited in diabetics, with neutrophil chemotaxis and phagocytosis is affected, which results in a prolonged inflammatory response to Pg. IL1beta levels in GRF are almost double when HbA1c is 8+ vs below 8 AGEs associated with periodontal disease form on collagen increase collagen cross linking and increasing formation of stable collagen molecules, which accumulate in tissues and increase their resistance to normal enzymatic degradation. These can form in blood vessels, resulting in thickening of the vessel and thinning of the lumen. AGEs activate the receptor knows as RAGE on the surface of smooth muscle cells, endothelial cells, neurons, and monocytes/macrophages, which causes vascular permeability and thrombus formation. The chronic inflammatory state of periodontitis is likely the link between effects of periodontal disease on diabetes control

Question 48

Molar Incisor pattern- etiology, bacterial involved

Answer 48

Molar incisor pattern (classified as Grade C) is typically aggressive in nature Bacteria involved is most commonly Aa, specifically The JP2 strain, along with the red complex (T forsythia, P gingivalis, T denticola). Systemic antibiotics are typically used in initial therapy as a supportive treatment. RX of 500mg TID/7 days amox, 400-500mg TID for 7 days for metronidazole (250mg has been shown to be no more effective than placebo) or a combination of 500mg amox and 400-500mg metro (again 250 did not show significant differences) can also be used. Azithromycin 500mg for 6 days Familial aggregation of molar incisor pattern tends to occur, indicating that there is a significant genetic component to the disease.

Question 49

New classification (2017)

Answer 49

Stage 1: 1-2mm CAL, RBL 15% or less, no tooth loss, max PD 4mm, no vertical defects Stage 2: 3-4mm CAL, RBL 15-30%, no tooth loss, max PD of 5mm, no vertical defects Stage 3: CAL 5+mm RBL to the middle ⅓, up to 4 teeth lost due to periodontitis, PD of 6+mm, 3mm deep vertical defects, class II or III furcations, moderate ridge defects Stage 4: All criteria of Stage III, plus 5 or more teeth lost due to periodontitis, or multiple complexity factors (masticatory dysfunction, secondary occlusal trauma (tooth mobility 2+), severe ridge defects, bite collapse, drifting, flaring, <20 occluding teeth) Grade A: no bone loss over 5 years or <0.25 ratio of %BL/age. Heavy biofilm deposits with low levels of destruction, non-smoker, no diabetes Grade B: <2mm bone loss over 5 years or 0.25-1 ratio of %BL/age, destruction commensurate with biofilm deposits, <10 cigarettes/day, HbA1c<7 Grade C: >2mm bone loss over 5 years or >1 ratio of %BL/age, destructions exceeds expectations due to biofilm, indicating rapid progression, 10+cigarettes/day, HbA1c 7+

Question 50

Leukoedema

Answer 50

Etiology: thickening of the epithelium and accumulation of edema fluid within individual epithelial cells Findings: bilateral, stretching the mucosa causes the white appearance to diminish, painless, persistent. More apparent in darker skin individuals. Differential diagnosis: frictional keratosis, plaque type lichen planus, smokeless tobacco keratosis. Diagnostic steps: does not rub off, stretching causes appearance and surface corrugations to diminish Treatment: none required; follow up regularly to ensure no other mucosal changes with overlying leukoedema

Question 51

Frictional keratosis

Answer 51

Etiology: Chronic irritation of low intensity stimulates thickening of the epithelium with the production of excess keratin (broken tooth, restoration, cheek/lip chewing, vigorous toothbrushing, hyperocclusion, ill fitting denture. Common sites: lateral border of tongue, buccal mucosa, attached gingiva, RMP, denture bearing mucosa Differential diagnosis: plaque type lichen planus, chronic hyperplastic candidiasis, hairy leukoplakia, smoking related leukoplakia, smokeless tobacco leukoplakia Diagnosis: Identify and remove source of irritation is possible Re-evaluate in 2 weeks If no resolution; cytology brush biopsy to see if abnormal epithelial cells are present Conventional biopsy may be necessary to assess biologic potential of lesion. If tobacco related- view with high suspicion Treatment: remove source of irritation is possible, biopsy results may require removal of entire lesion, palliative treatment with: Benzocaine, Triamcinolone.

Question 52

Acute psudomembranous candidiasis (Thrush)

Answer 52

Etiology: infection of oral mucosa caused by fungus (C. albicans); fungal organisms grow primarily on the epithelial surface Findings: multiple, non adherent white plaque on epithelium, removal reveals erythematous mucosal surfaces, often on buccal mucosa, tongue, palate. Acute onset, may complain of dry mouth and bad taste Differential diagnosis: Diagnostics: cytology smear; fungal organisms forming hyphae by using periodic acid Shiff PAS stain. Treatment: Antifungal agenets for oral candidiasis:Clotrimazole oral troches, Nystatin oral suspension, Nystatin ointment, Nystatin pastilles, Ketoconazole cream 2%, Amphoteracin B ointment 3%. Systemic antifungal agents for chronic candidiasis: ketoconazole, fluconazole, itraconazole. Follow up: after 2-4 weeks if lesions return, when discontinues antifungal, then underlying systemic disease such as diabetes, HIV, other immunocompromised states may be considered. Persistent and recurrent episodes of acute pseudomembranous candidiasis may indicate that the patients immune status is compromised Also associated with antibiotic therapy, topical/ systemic corticosteroid therapy, dentures, chronic dry mouth, endocrine disease, immunosupression (recurrence likely associated with compromised immunity)

Question 53

Chronic hyperplastic candidiasis (candidal leukoplakia)

Answer 53

Etiology: Infection caused by fungus (C.albicans). Infected epithelium becomes hyperplastic with formation of excess surface keratin. Findings: does not rub off. Common sites: buccal mucosa adjacent to commissure, and may involved lateral borders of tongue. Painless, persistent, more common in adults. Differential diagnosis: frictional keratosis, smoking related leukoplakia, hairy leukoplakia, plaque type lichen planus. Diagnostics: cytology smear can be done but may not reveal fungal organisms. Incisional biopsy stained with periodic acid-Schiff PAS stain may be necessary to confirm the presence of fungal organisms. Treatment: Antifungal agents for oral candidiasis treatment: clomitrazole oral troches, Nystatnin oral suspension, Amphoteracin B oral suspension 100mg/ml, Nystatin ointment, Nystatin pastilles, Ketoconazole cream 2%, Amphoteracin B ointment 3% Systemic antifungal agents to chronic candidiasis: Ketoconazole, Fluconazole, Itraconazole capsules 100mg Follow up: after 2-4 weeks of treatment, if lesions return, discontinue antifungal and consider underlying systemic disease such as diabetes, HIV and immunosupression Clinical significance: chronic hyperplastic candidiasis may show evidence of epithelia dysplasia on microscopic examination suggesting lesions are premalignant. Smokers= increased suspicion

Question 54

Lichen Planus - Reticular and Plaque

Answer 54

Etiology: defect in cell mediated immunity resulting in damage to the basal cells of the oral epithelium Findings: painless, and more common in females Reticular: adherent, interlacing, white striations (Wickhams striae), most frequently occurs on buccal mucosa Plaque: adherent, circumscribed, white plaques, most often occurs on dorsal tongue Differential diagnosis: frictional keratosis, hairy leukoplakia, hyperplastic candidiasis, leukoedema, smoking related leukoplakia, smokeless tobacco keratosis. Diagnostics: clinical appearance, in the absence of striations, microscopic examination may be necessary to confirm the diagnosis Treatment: Reticular and plaque type treated based on symptoms, and these are usually symptomless. Mild steroid application: Triamcinolone, Fluocinonide Higher potency steroid: Dexamethasone, Clobetasol ; usually not used but can be if symptoms increase. Clinical significance: lichenoid reactions look clinically identical to lichen planus

Question 55

Lichen Planus Erosive/Bollous

Answer 55

Etiology Defect in cell mediated immunity resulting in damage to the basal cells of oral epithelium. Causes epithelial sloughing in erosive lichen planus and subepithelial blister formation in bullous lichen planus Findings: Erosive: mucosal erosions that can slough fro form superficial ulcerations Bullous: blisters that quickly rupture to form superficial ulcerations Both of the types above most often occurs on the posterior buccal mucosa and adjacent mandibular buccal vestibule. Lesions may involve tongue, gingiva, labial mucosa, gingival lesions produce desquamative gingivitis More common in middle age women Local discomfort ranging from burning to severe pain Diagnostics: incisional biopsy, direct immunofluorescent studies to differentiate between erosive/bullous LP and mucous membrane pemphigoid and pemphigus vulgaris Treatment: Triamcinolone, Fluocinonide, higher potency (dexamethasone, clobetasol), benzocaine. Periodic biopsy may be required to evaluate malignant changes. Clinical significance: erosive/bullous LP sometimes can be infected with Candida albicans,

Question 56

Hairy leukoplakia

Answer 56

Etiology: hyperplasia of oral epithelium with production of excess keratin caused by Epstein Barr virus infection. Surface of lesion infected with Candida albicans. Most commonly occurs in immunocompromised such as HIV. Findings: most often occurs on lateral tongue, appearance usually corrugated/shaggy. Bilatera. Usually painless, persistent, and in young males. Differential diagnosis: frictional keratosis, plaque type lichen planus, chronic hyperplastic candidiasis, smoking related leukoplakia Diagnostics: microscopic examination to confirm non specific viral changes, Epstein Barr can be identified using DNA probe. Treatment: Acyclovir high dose; lesions may reccur if treatment stopped

Question 57

Smoking related leukoplakia

Answer 57

Etiology:chronic exposure to chemical carcinogen generated by tobacco Findings: circumbscribed, adherent white plaques, vary in size, thickness and surface configuration. Most common site: lower lip, buccal mucosa, gingiva (lesions on the ventral tongue and floor or mouth are more likely to show microscopic evidence of premalignancy or malignancy). Painless, persistent, history of smoking Differential diagnosis: frictional keratosis, hyperplastic candidiasis, plaque type lichen planus Diagnostics: exfoliative cytology or brush biopsy to determine if abnormal cells are present. Conventional biopsy is indicated if abnormal epithelial cells are identified if the lesions persists. Treatment: smoking cessation advice, if lesion regresses, patient should be re-evaluated, if lesion does not regress, it should be excised for microscopic examination.

Question 58

Smokeless tobacco keratosis

Answer 58

Etiology: chronic exposure of chemical carcinogen from smokeless tobacco Findings: circumscribed adherent white plaque varying thickness with corrugated surfaces. Mandibular labial or buccal vestibule. Often associated with recession of labial gingiva. Painless, persistent, history of smokeless tobacco use Differential diagnosis: frictional keratosis, hyperplastic candidiasis, leukoedema, plaque type lichen planus Diagnostics: exfoliate cytology/brush biopsy, conventional biopsy if lesion persists. Treatment: cease smokeless tobacco use, if lesions regress in a few weeks, periodic revelation is indicated. Patient should be re-evaluated at regular intervals for mucosal changes. Clinical significance: lesions can develop into verrucous carcinoma

Question 59

Nicotonic stomatitis

Answer 59

Etiology: chronic exposure to heat liberated from burning tobacco Findings: diffuse, white, thickening of palatal mucosa with interspersed elevated white papules each with a red central depression (white papules with a red center and inflamed openings of minor salivary glands). Often painless, persistent, history of smoking. Differential diagnosis: due to location and characteristics, infrequently confused with other lesions Treatment: smoking cessation advice, once smoking stopped, lesions usually regress, evaluate patient at regular intervals (minimal risk of malignant transformation)

Question 60

Actinic chelitis

Answer 60

Etiology: chronic exposure to UV radiation Findings: irregular, diffuse, adherent, white thickening of the involved epithelium. Occurs on vermillion border. Persistent, painless, more common in males, more common in light complexion. Differential diagnosis: frictional keratosis, smoking related leukoplakia, plaque type lichen planus. Diagnostics: conventional biopsy Treatment: use sunscreen, if persistent biopsy indicated Squamous cell carcinoma persists in 10% of cases

Question 61

Erythematous candida

Answer 61

Etiology: Fungus (C. Albicans), broad spectrum antibiotics, ill fitting dentures, immunosupression (chemothearpy, radiotherapy), dry mouth Findings: mucosal erythema, frequently affects dorsal tongue and palate. Commonly affects denture bearing mucosa. Usually associated with localized burning discomfort. Differential diagnosis: atrophic glossitis, erythroplakia, stomatitis areata migrans, mucosal allergy Diagnostics:cytologic smear with periodic acid Schiff stain. Treatment: Reline denture if denture related Antifungal agents for oral candidiasis treatment Clotrimazole oral troches Nystatin oral suspension Amphoteracin B oral suspension Nystatin ointment Nystatin pastilles Ketoconazole cream 2% Amphoteracin B ointment 3% Systemic antifungals for chronic candidiasis Ketoconozole 200mg Fluconazole 100mg Itraconazole 100mg Follow up: 2-4 weeks of treatment, if lesion returns, patient discontinues antifungal, then underlying systemic diseases such as diabetes, HIV, and other immunocompromised states must be reconsidered.

Question 62

Angular chelitis

Answer 62

Etiology: infection of mucosa at corners of mouth caused by fungus (C. albicans). Other contributing factors: loss of VDO(usually associated with ill fitting dentures), bacterial infection (Staph A), nutritional deficiency (Vit B complex and iron), chronic irritation from habitual licking corners of lips. Findings: exaggerated creases at corners of mouth with erythematous fissuring. Edentulous and wear ill fitting dentures. Pts may describe burning sensation at corners of mouth Differential diagnosis: clinical appearance is characteristic Diagnostics: cytology smear with acid Schiff PAS stain to identify fungal organisms. Culture to see if staph infection is present Treatment: antifungal/anti inflammatory therapy. New denture is loss of VDO, treat bacterial infection is present, treat nutritional deficiency if present.

Question 63

Erythroplakia

Answer 63

Etiology: chronic exposure to carcinogenic component of tobacco is a significant risk factors for erythroplakia. Findings: erythematous plaques varying in sizes, thickness and surface configuration, frequently occurs on floor of mouth, ventral tongue and soft palate. Painless, persistent, more common in male adults, tobacco exposure. Differential diagnosis: erythematous candidiasis, mucosal allergy Diagnostics: cytology or brush biopsy, conventional biopsy Treatment: smoking cessation advice, if premalignancy or malignancy more extensive tx required. Re-eval at regular intervals Clinical significance: occurs less frequently than leukoplakia, but is more likely to exhibit evidence of dysplasia, premalignancy or malignancy. Many erythroplakia represent carcinoma in situ.

Question 64

Stomatitis Areata Migrans (erythema migrans, benign migratory glossitis, geographic tongue)

Answer 64

Etiology: uknown, hypersensitivity, hormonal imbalance and emotional stress may predispose to stomaitis areata migrans in some patients. Findings: circumscribed erythematous patches, may be encircled with elevated hyperkeratotic margins. Occurs on dorsal, ventral surface tongue, may be associated with fissured tongue. Occasional burning sensation Differential diagnosis: erythematous candiasis, erythroplakia. Diagnostics: definitive diagnosis made on basis of clinical presentation. Incisional biopsy Treatment: mostly asymptomatic, requires no treatment. Symptomatic lesions can be treated with topical anti inflammatory agent such as Triamcinolone or Flucinonide. If fungal involvement, anti fungal therapy as in erythematous candidiasis. Clinical significance: increased incidence in diabetics.

Question 65

Mucosal allergy

Answer 65

Etiology: allergies to doof, falvouring agents, toothpastes, mouthwashes, dental materials. Findings: circumscribed ertyhematous patches on the site of contact with allergen Differential diagnosis: atrohic glossitis, erythematous candidiasis,erythroplakia, stomatitis areata migrans. Treatment: removal of suspected allergens, treatment with antihistamines and topical corticosteroids such as Tramcinolone.

Question 66

Atrophic glossitis

Answer 66

Etiology: associated with a dietary deficiency or poor absorption or nutritional components (iron, vit B12- needed of oral maturation), chronic dry mouth may contribute to atrophic glossitis Findings: loss of papilla- focal or generalized on dorsal tongue with mucosal redness, possible burning sensation Differential diagnosis: erythema candidiasis, stomatitis areata migrans, mucosal allergy, median rhomboid glossitis. Diagnostics: refer to physician for hematology, other indicators of chronic dry mouth should be considered (generalized mucosal dryness, decreased flow of parotid saliva, decreased pooled saliva in the floor of mouth, presence of thick saliva, increased cervical caries, and fissured tongue) Treatment: therapy for dietary deficiency or absorption, palliation for glossitis until normal mucosa is restored.

Question 67

Plasma cell gingivitis

Answer 67

Etiology: allergic (hypersensativity) reaction to chewing gum, toothpaste, or peppers Findings: generalized enlargement of maxillary and mandibular attached gingiva, bright red, angular chelitis, fissured tongue. May have burning lips, tongue, allergen contact. Differential diagnosis: atrophic glossitis, angular chelitis, stomatitis areata migrans, mucosal allergy Diagnostics: clinical presentation, biopsy necessary to confirm diagnosis Treatment: remove allergens, corticosteroids(Triamcinolone) is usually not necessary. Stop chewing gum.

Question 68

Median Rhomboid Glossitis (median papillary atrophy)

Answer 68

Etiology: developmental defect of dorsal tongue, now considered to be a clinical manifestation of chronic erythematous candidiasis. Findings: rhomboid shaped area of papillary atrophy of midline dorsal tongue, intermittent burning discomfort occasionally, persistent. Differential diagnosis: atrophic glossitis, erythematous candidiasis, stomatitis areata migrans, mucosal allergy Diagnostics: infrequently confused, microscopic examination, staining of biopsy with acid Schiff PAS, confirm fungal organisms. Clinical significance: can be confused to SCC, but SCC rarely occurs on dorsal tongue

Question 69

Submucosal Hemorrhages

Answer 69

Etiology:petechiae and ecchymosis are commonly caused by suction from dentures , sore throat (mononucleosis) and sexual activity (fellatio). Hematomas are caused by more severe trauma to oral mucosa. Findings: Petechiae- multiple, small, red spots Ecchymoses- larger, more diffuse, red macules with irregular margins Petechiae and ecchymoses most often occur in the palate Hematomas present as circumscribed, compressible red nodules. Hematomas occur most often on labial and buccal mucosa Differential diagnosis: Petichiae-characteristic clinical apperance; infrequently confused with other red lesions Ecchymoses- confused with macules such as chronic erythematous candidiasis and mucosal allergy Hematomas- may be confused with hemangiomas Treatment: counseling regarding cause, periodic re-evaluation. Clinical significance: more extensive hemmorhage, involving gingiva, thrombocytopenia, leukemic, bleeding disorders such as hemophilia

Question 70

Traumatic ulcer

Answer 70

Etiology: mechanical injury: biting, sharp foods, tooth brushing, ill fitting dentures, iatrogenic, fictious trauma Findings: superficial ulcer with a erythematous margin, surface covered with yellow pseudomembrane. Commonly occurs on tongue, lips and buccal mucosa, hard palate, gingiva, vestibular mucosa. Most often occurs on lateral tongue. Usually painful, history of trauma, superficial traumatic ulcers heal in 2 weeks. Some traumatic ulcerated granulomas may persist for a month or longer. Differential diagnosis: apthous ulcers, reccurent intraoral herpes, herpes zoster, herpangia, ulcers associated with systemic disease Diagnostics: determine history of trauma, remove suspected etiology, treat with palliation, if lesion not resolved, then microscopic exam to confirm diagnosis. Treatment: remove etiology, self limiting, palliation- Triamcinolone

Question 71

Apthous ulcers

Answer 71

Etiology: immunologic defect, humoral and cellular immune mechanisms damage affected oral mucosa. Physical and emotional stress appears to be a precipitating factor in many patients. Findings: superifical ulcer with erythematous border and white-yellow psudeomembrane. Rarely occurs in keratinzed mucosa, more common in young adults, severe local discomfort, multiple recurrence is common. Minor <0.5cm Major >0.5cm - may heal with scarring Herpetiform clusters of small ulcers (resembles recurrent intraoral herpes) Differential diagnosis: primary herpetic gingivostomatitis, recurrent intraoral herpes, herpes zoster, herpangina, erythema multiforme traumatic ulcers, ulcers associated with systemic diseases. Diagnostics: clinical presentation, cytology smear, stained with papanicolaou stain to rule out virology Treatment: Amlexanox, Triamcinolone, Flucinoide, Higher potency steroid ( dexamethasone, clobetasol) Clinical significance: recurrent apthous ulcers can be a component of Bechets syndrome (oral, mucosa, and conjunctival).

Question 72

Primary Herpetic gingivostomatitis

Answer 72

Etiology: acute infection with herpes simplex, virus spread by direct contact with contaminated saliva Findings: multiple vesicles rupture forming small superficial ulcers, small ulcers merge to large ulcers, any oral mucosal site can be involved. Gingiva is diffusely enlarged and erythematous, often occurs in children, painful, lymaphadenopathy may precede presentation, severe, difficulty eating, irritability malaise. Differential Diagnosis: aphtous ulcers, recurrent intraoral herpes, herpes zoster, herpangia, erythema multiforme, Diagnostics:clinical presentation, cytology smear stained with papanicolaou stain to demonstrate the presence of virus Treatment:Acyclovir 200mg 5x/day or Acyclovir ointment, self limiting 7-14d, antibiotics if secondary bacterial infection- Pen V 500mg Clinical significance: majority are asymptomatic; after primary infectionn, remains latent in trigeminal gangilion and can be reactivated to cause recurrent lesions. Both vesciular and ulcerated stages if infection are contagious

Question 73

Recurrent herpes

Answer 73

Etiology: reactivation of herpes simplex virus. Can be triggered by aging, exposure to sunlight, local trauma, physical and emotional stress and immunosupression Findings: clusters of small blisters which quickly rupture, small ulcers merge to form larger ulcers, involvement of lower lip most common manifestation recurrent herpes, often covered with hemorrhagic crust, intraoral lesions are less common then recurrent herpes labialis and tend to occur on keratinized mucosa. Can be preceded by prodrome of itching, burning or tingling, local discomfort. Differential diagnosis: apthous ulcers, herpes zoster, herpangina, erythema multiforme, necrotizing ulcerative gingivitis, ulcers associated with systemic disease. Diagnostics: clinical presentations, cytologic smear Treatment: Acyclovir 200mg 5x/day, acyclovir ointment Clinical significance: heal within 7-10 days, recurrence greater in immunocompromised individuals. Recurrent herpes can trigger erythema multiforme.

Question 74

Herpangia

Answer 74

Etiology: various strains of Coxsackie A, transmitted from contaminated saliva Findings: multiple small blisters, affected mucosa erythematous, typically located on soft palate and tonsillar fauces, occurs most often in children, painful, fever, sore throat, difficulty eating and malaise. Differential diagnosis: apthous ulcers, primary herpetic gingivostomatiits, recurrent intraoral herpes, herpes zoster. Diagnostics: clinical presentation, small ulcers on palate and tonsillar fauces Treatment: self limiting, and supportive care only . heal in 7-10d, immunity develops and won't recur by that strain

Question 75

Herpes zoster (shingles)

Answer 75

Etiology : recurrent infection caused by varicella zoster. Initial infection is varicella zoster (chicken pox) then virus remains in sensory ganglia- trigeminal ganglion which cause intraoral lesions. Reactivation triggered by local trauma, immunosupression and malignancy. Findings:clusters of small blisters rupture fro form small superficial ulcers, occurs on keratinized and non keratinzed mucosa, usually extends to midline but does not cross it. Differential diagnosis: apthous ulcers, primary herpetic gingivostomatisi, recurrent intraoral herpes, herpangina, erythema multiforme Diagnostics: clinical presentation, cytologic smear Treatment : supportive care only, inimmunocompromised patients consider Acyclovir Clinical significance: post herpetic neuralgia may persist for months after lesions resolve. Recurrent episodes may be associated with undiagnosed malignancy.

Question 76

Primary syphilis

Answer 76

Etiology: initial infection with spirochetes (Treponema pallidum), usually via sexual transmission, oromucosal transmission via urogenital contact Findings: indurated, deep seated ulcers with elevated margins, most often occurs on lips and tongue,develops a few weeks after inoculation, painless, cervical lymphadenopathy appears one week after chancre appears. Differential diagnosis: TB, deep seated fungal infection, large traumatic ulcer, SCC. Diagnostics: serologic test for antibodies to Treponema pallidum usually positive within the first few weeks of infection. Microscopic examination to confirm the diagnosis Treatment: By physician, high dose Penicillin Clinical significance: chancre will heal spontaneously within several weeks without treatment, some are at risk of secondary syphillis. Chanres are cnotagious.

Question 77

Secondary syphilis

Answer 77

Etiology: secondary infection with the spirochetes Treponema palliddum Findings: multiple superficial ulcers covered with white to yellow pseudomembrane , often occurs on tongue, lip, buccal mucosa and soft palate. Sore throat, weight loss, fever, malaise Differential diagnosis: pseudomembranous candidiasis, plaque type lichen planus Diagnostics: serological tests positive for Treponema pallidum. Smear for immunofluroscent antibodies. Treatment: physician- high dose penicillin. Clinical significance: mucous patches that heal spontaneously. Risk of developing tertiary syphilis years later, mucous patches are contagious

Question 78

TB

Answer 78

Etiology: Mycobacterium tuberculosis, oral mucosal lesions secondary to pulmonary tuberculosis, occasionally spreads through blood vesses to oral tissues. Findings: ulcerated granulomatous mass, tongue and palate most common, may involve recent extraction site. Persistent painful ulceration, chronic cough Differential diagnosis: primary syphilis, deep seated fungal infection, traumatic ulcerative granuloma, SCC Diagnostics: TB skin test, chest radiograph, microscopic examination ( granulomous with caseous necrosis and multinucleated giant cell) Acid bacillus test for infective organism Treatment: physician, isoniazid, rifampin, streptomycin Clinical significance: contagious, relapse following treatment indicated possible immune problem.

Question 79

Fungal infection ( deep fungal infection/histoplasmosis)

Answer 79

Etiology: infection by inhalation of fungal spores. Oral lesions secondary to pulmonary infection. Pre-existing wound inoculation with infected sputum. Findings: ulcerated granulomatous mass, tongue, palate, gingiva, may involve recent exo site. Persistent painful ulceration, chronic cough, low grade fever, night sweat, malaise, weight loss. Differential diagnsois: primary syphilis,tuberculosis, traumatic ulcerative granuloma, SCC Diagnostics: serology, chest radiograph, microscopic examination (biopsy reveals granulomatous proliferation with multinucleated giant cells, staining periodic acid Schiff (PAS) stain Treatment: physician , Amphoteracin B, Ketoconazole Clinical significance: contagious

Question 80

Necrotizing sialometaplasia

Answer 80

Etiology: loss of blood supply to minor salivary glands resulting in ischemic necrosis Findings: deep seated ulcer, preceded by erythematous swelling, typically located in hard palate, more common in adults, pain, parasthesia. Differential diagnosis: primary syphilis, TB, deep seated fungal infection, SCC, salivary gland carcinoma Diagnostics: microscopic examination Treatment: once diagnosis is confirmed, no treatment required. Lesion heals in 2 months Clinical significance: can mimic malignancy

Question 81

Squamous cell carcinoma

Answer 81

Etiology: squmaous epithelial origin, precise etiology unknown. Risk factors: tobacco, alcohol, solar radiation, genetic, nutritional deficiency (iron anemia in Plummer Vinson syndrom), immunosuperssion, infections (candidal leukoplakia and HPV) Findings: Deep seated ulcerated mass (extending into adjacent tissues), fungated ulcerative mass, margins elevated, adjacent tissues firm on palpation (indurated), may be residual leukoplakia and or erythroplakia. Continuous enlargement, more common in adults, local pan, referred pain and parasthesia. Differential diagnosis: primary syphillis, TB, deep funal infection, traumatic ulcerated granuloma Diagnostics: cytological smear, brush biopsy Treatment: smoking cessation, combination therapy: surgery, radiation, chemothearpy, periodic re-evaluation Clinical significance: lymph node metastasis. Patient who had one oral cancer are at a greater risk of having a second oral cancer.

Question 82

Salivary gland carcinoma

Answer 82

Etiology: adenocarcinomas of minor salivary gland origin, precise etiology unknown Findings: deep seated ulcerated mass, lesions surface exhibits telangiectatic blood vessels, occurs most commonly in the hard palate off the midline. Continuous enlargement, more common adults, local discomfort, may have evidence of bone destruction on radiographs. Differential diagnosis: primary syphillis, TB, deep seated fugal infection, benign salivary gland neoplasm, necrotizing sialometaplasia Diagnostics: microscopic examination Treatment: surgery and radiation, re-evaluation Clinical significance: half of these are malignant, local recurrence is common following treatment, metastasize often to lungs and bone.

Question 83

Mucous Membrane Pemphigoid

Answer 83

Etiology: defect in cell mediated immunity resulting in damage to the epithelial basement membrane. This causes the epithelium to separate from the underlying connective tissue (subepithelial blister formation) Findings: blisters rupture to cause desquamation and ulceration. Can involve any oral mucosal site, however, gingiva is the most common location. When on gingiva plaque related gingivitis may also be present because it is often too painful for the patients to brush effectively. Associate with severe pain, often in middle aged women. Differential diagnosis: Erosive/bullous lichen planus, pemphigus vulgaris, erythema multiforme, lupus erythematosus. Diagnostics: incisional biopsy placed in formalin for histology, and Michels solution for direct immunoflurescence. Direct immunofluorescence reveals deposits of IgG and complement C3 along the epithelial basement membrane zone. (direct immunoflurescence is necessary to differentiate between MMP, LP and PV) Treatment: Mild steroids (triamcinolone or fluocinonide), higher potency steroid ( Dexamethasone, Clobetasol), systemic steroids ( prednisone or methylprednisone) Clinical significance: conjunctiva- can cause blindness.

Question 84

Pemphigus Vulgaris

Answer 84

Etiology :immunological defect causes the production of autoantibodies against desmosomes which hold adjacent epithelial cells together. Destruction of desmosomes causes adjacent epithelial cells to separate (acanthokysis) producing an intraepithelial blister Findings: blisters will rupture to form erosions and ulcerations, any oral mucosal site can be involved, gingival lesions produce desquamative gingivitis, when on gingiva, plaque related gingivitis may also be present because it is often too painful for the patient to brush effectively. More common in Jewish descent. Equal frequency in male and female, severe discomfort, positive Nikolsky sign (formation of blister on apparently normal skin after slight mechanical pressure) Differential diagnosis: erosive/bullous lichen planus, MMP, erythema multiform, lupus erythematosus Diagnostics: incisional biopsy, palace half in formalin for histology and half in michels solution for direct immunoflurescence. Autoantibodies can be demonstrated in patients serum by indirect immunoflurescence Treatment: seldom treated in isolation from systemic diseases, steroids ( prednisone), topical corticosteroids. Clinical significance: life threatening, 50% of patients with PV present with oral mucosal lesions before the onset of skin lesions. Lesions resembling PV can occur in pts with leukemia and lymphoma.

Question 85

Erythema multiforme

Answer 85

Etiology: unknown, or immunologic defect ( allergic/hypersensativity reaction), hypersensitivity reaction can be triggered by a preceding infection or by exposure to various medications Findings: multiple blisters, erosions and ulcerations affecting virtually any oral mucosal sites, hemorrhagic cresting at the vermillion oof the lips is a characteristics feature. Acute onset, erythematous skin lesions Differential diagnosis: primary herpetic gingivostomatitis, major aphthous ulcers, erosive bullous LP, MMP, PV. Diagnostics: usually clinical presentation especially if acute onset and characteristics lesions (hemmorhagic crusting of the vermillion of lips and target lesions on skin), cytology, biopsy Treatment: systemic steroids in combination physician, acyclovir Clinical significance: Steven Johnson syndrome is a more severe manifestation of erythema multiforme characterized by oral mucosal leisons, skin lesions and conjunctival lesions and genital lesions.

Question 86

Lupus Erythematosus

Answer 86

Etiology:an autoimmune disease involving defects in both the humoral and cellular immune system. Circulating and tissue bound autoantibodies have been identified. Genetic defect or viral infection may trigger the autoimmune reaction Findings: erythema, erosion, superficial ulceration frequently associated with keratosis striations. Most common sites: buccal mucosa, gingiva and lip. Scaly erythematous patches, localized to sun exposed skin (butterfly rash involving the malar areas and bridge of the nose) Differential diagnosis: erosive LP, MMP, PV, erythema multiforme, mucosal allergy Diagnostics: incisional biopsy, half in formalin for histology and half in Micheals solution for direct immunoflurescence. In direct immunoflurescnce, it reveals shaggy deposits of IgM, IgG and compliment C3 along the epithelial basement membrane zone. Treatment: topical steroids (Flucinonide), systemic steroids, mild steroid application (Triamcinolon), higher potency steroid application (dexamethasone) Clinical significance: potentially life threatening involvement of kidney and heart can occur in systemic lupus erythematosus.

Question 87

Physiologic pigmentation

Answer 87

Etiology: pigmentation caused by normal amounts of melanin in basal cells of oral epithelium Findings: diffuse pigmentation, located most often on attached gingiva, painless, persistent, individuals with dark skin Differential diagnosis: clinically characteristic Diagnostics: clinical presentation only Treatment: none required

Question 88

Amalgam tattoo

Answer 88

Etiology: contamination of pre existing oral mucosal wound with amalgam particles Findings: circumscribed, darkly pigmented macule, overlying mucosa is intact, often on gingiva and adjacent mucosa, painless, persistent, history of previous dental treatment involving the use of amalgam, amalgam particules occasionally visible on radiographs Differential diagnosis: melanotic macule, melanocytic nevus, malignant melanoma. Diagnostics: clinical evidence of previous amalgam restoration, clinical presentation, microscopic examination is indicated if diagnosis can not be made on clinical presentation alone. Treatment: none necessary if diagnosis is confirmed. Clinical significance: if any doubt, carry out biopsy

Question 89

Black hairy tongue

Answer 89

Etiology: formation of excess keratin causes elongation of filiform papillae on the dorsal of tongue . Keratin becomes pigmented by pigment producing bacteria and or components in tobacco, beverages and foods. May be infected with C. albicans. Findings: elongation of filiform papillae, brown to black pigmentation, posterior dorsal tongue. Patients have poor OH, bad taste. Differential diagnosis: clinical presentation, infrequently confused with other pigmented lesions. Diagnostics: clinical presentation, cytology smear with PAS to rule out fungal involvement. Treatment: elimination of predisposing factors, clean dorsal tongue with soft toothbrush, treat candida if present Clinical significance:should not be confused with HIV related lesion hair leukoplakia

Question 90

Melanotic macule

Answer 90

Etiology: solar radiation on lower lip, unknown Findings: circumscribed tan to brown macule covered with intact mucosa, usually less than 0.5cm in diameter, most common on lower lip, then gingiva, palate, and buccal mucosa. Painless, persistent Differential diagnosis: amalgam tatoo, melanocytic nevus, malignant melanoma Diagnostics: microscopic examination to confirm the diagnosis and exclude malignant melanoma ( excisional biopsy) Treatment: no treatment necessary if diagnosis is confirmed Clinical significance: multiple labial oral melanotic macules can be a component of Peutz Jeghers syndrome and Addison's disease (primary adrenal cortical insufficiency)

Question 91

Smokers melanosis

Answer 91

Etiology : irritated in tobacco smoke stimulate melanocytes to synthesize excess melanin, female sex hormones, oral contraceptives, are predisposing factors) Findings: diffuse, irregular, dark brown macules, covered with intact mucosa, anterior labial mucosa, buccal mucosa and palate, more often in women who smoke and use oral contraceptives. Differential diagnosis: multiple oral melanotic macules, physiologic pigmentation Diagnostics: documentation of smoking history and oral contraceptive use in women, usually diagnosis can be made on basis of clinical presentation Treatment : smoking cessation advice

Question 92

Melanocytic nevus

Answer 92

Etiology : benign neoplasm of melanin producing cells (melanocytes), can be congenital or acquired Findings: circumscribed, tan to brown, papular lesion, usually less than 0.5cm in diameter, covered with intact mucosa, located most often on the hard palate. Painless, persistent, more common in women Differential diagnosis : amalgam tattoo, melanotic macule, malignant melanoma Diagnostics: microscopic examination necessary to confirm diagnosis and exclude malignant melanoma Treatment: no treatment necessary once diagnosis confirmed Clinical significance: Nevi with microscopic evidence of junctional activity may develop into malignant melanoma.

Question 93

Kaposi’s sarcoma

Answer 93

Etiology:malignancy of blood vessels.cytomegalovirus has been implicated as a possible cause. Loss of immunologic surveillance increases the risk for Kaposi sarcoma Findings: bluish purple macule, plaque or nodule, surface is usually intact, located most often on hard palate and gingiva, usually painless, continuous enlargement, patient has a history of HIV, skin lesions may be present Differential diagnosis: Hematoma, Hemangioma, Pyogenic granuloma, malignant melanoma Diagnostics:microscopic examination necessary to confirm Treatment: appropriate surgery and chemotherapy, determined by symptoms, cosmetic concerns and staging based on tumour bulk CD4 count and B symptoms. Local: radiotherapy- intralesional vinblastine, surgical excision, cryotherapy or laser ablation Systemic: cytotoxic chemotherapy Clinical significance: most common malignancy with AIDS, more than 50% of patients Kaposi sarcoma have oral mucosal lesions, also may be first manifestation of AIDs

Question 94

Malignant melanoma

Answer 94

Etiology:melanin producing cells (melanocyte), may rise directly from melanocytes in area of or form pre existing nevus, chronic exposure to solar radiation and a fair complexion increases the risk for skin lesions Findings: larger than 0.5cm diameter, irregular margins, irregular pigmentation, any change in pigmentation, ulceration of overlying mucosa, macular or elevated, often on gingiva or palate. Usually painless, rapidly enlarging Differential diagnosis: amalgam tatoo, melanotic macule, melanocytic nevus Diagnostics: microscopic examination Treatment : appropriate surgery and chemotherapy- refer to physician Clinical significance : malignant melanoma- aggressive cancer, patients with oral mucosal lesions generally have a poor prognosis.

Question 95

Squamous papilloma

Answer 95

Etiology: local trauma, HPV Findings: usually solitary, white, papillary lesion attached with a narrow pedunculated based.occurs most often on the soft palate and ventral tongue. Painless, persistent Differential diagnosis: verruca vulgaris, focal epithelial hyperplasia, condyloma acuminatum. Diagnostics: microscopic examination necessary to establish definitive diagnosis Treatment: local excision Follow up: recurrence is common, often due to inadequate excision or viral etiology

Question 96

Verruca vulgaris (common wart)

Answer 96

Etiology: an infection casued by HPV-2, HPV-4, HPV 40 Findings: usually solitary, white, papillary lesion attached with narrow (pedunculated or broad (Sessile) base. Occurs most often on labial mucosa. Painless, persistent. Differential diagnosis: squamous papilloma, focal epithelial hyperplasia, condyloma acuminatum Diagnostics: microscopic examination Treatment: local excision Clinical significance: lesions may recur following conservative surgical therapy

Question 97

Condyloma acuminatum

Answer 97

Etiology: infection casued by HPV 6, HPV 11, HPV16, HPV 18 , STD Findings: multiple, pink, slightly papillary nodules attached with broad bases . commonly arranged clusters, occurs on lips, tongue, and soft palate. Painless, persistent, anogenital lesions may be present. Differential diagnosis: squamous papilloma, verruca vulgaris, focal epithelial hyperplasia Diagnostics: microscopic examination necessary, identification of virus by immunohistochemcial studies or in situ DNA hybridization Treatment: local excision, laser ablation/stripping is commonly used although there is some concern over vaporization or viral particles. Clinical significance: lesions commonly recur following surgical excision. Reinoculation among sexual partners is common

Question 98

Focal epithelial hyperplasia

Answer 98

Etiology: an infection caused by HPV 13 Findings: multiple, pink, slightly papillary nodules attached with broad sessile bases. Commonly arranged in clusters, occurs most often on lips, buccal mucosa and tongue. Painless, persistent, more common in children and young adults, may be present in multiple family members. Differential diagnosis: squamous papilloma, verruca vulgaris, condyloma acuminatum Diagnostics: microscopic examination. Identification of virus by immunohistochemical studies or in situ DNA hybridization Treatment: local excision, lesions often regress spontaneously.

Question 99

Inflammatory papillary hyperplasia

Answer 99

Etiology: chronic mechanical irritation from an ill fitting maxillary denture. Often infected with C. albicans Findings: multiple, erythematous, sessile nodules, most often lcoated on the mucosa of the palatal vault, occasionally on alveolar ridge. Painless, persistent, more common in older individual who wear a complete or partial maxillary denture, patients often wear dentures continuously Differential diagnosis: characteristics clinical appearance,inflammatory papillary hyperplasia is infrequently confused with other papillary lesions Diagnostics: clinical features are characteristics, cytology smear for fungal consideration Treatment: reline and remake denture, treat candidiasis is present. Nystatin, Clotrimazole, systemic antifungals ( ketoconazole, fluconazole). Remove lesions if they persist Clinical significance: inflammatory papillary hyperplasia often associated with chronic erythematous candidiasis (denture stomatitis)

Question 100

Proliferative verrucous leukoplakia

Answer 100

Etiology: precise etiology unknown, often associated with tobacco exposure Findings: diffuse, white, papillary, corrugated thickenings, commonly involve the tongue and floor of mouth, painless, persistent Differential diagnosis: verrucous carcinoma Diagnostics: microscopic examination Treatment: surgical excision, laser ablation, periodic re-evaluation Clinical significance: can eventually develop into verrucous carcinoma or conventional SCC

Question 101

Verrucous carcinoma (snuff dippers cancer)

Answer 101

Etiology: unknown, smokeless tobacco, HPV 16,18 has been identified in some lesions Findings: diffuse, white, papillary or corrugated thickening, commonly occurs on mandibular buccal vestibule and gingiva, painless, continuous enlargement Differential diagnosis: proliferative verrucous leukoplakia Diagnostics: microscopic examination Treatment: smoking cessation, complete surgical ablation, periodic re-evaluation Clinical significance: rarely metastizie, complete surgical ablation, periodic re-evaluaiton

Question 102

Pyogenic granuloma (pregnancy tumour, pregnancy gingivitis)

Answer 102

Etiology: a reactive hyperplasia of vascularized granulation tissue that develops in response to local irritating factors (bacterial plaque/ calculus) Findings: solitary, circumscribed, red nodule attached with a broad sessile or narrow pedunculated base. Surface is lobulated and commonly ulcerated. The lesion may bleed spontaneously or on gentle manipulation. More than 75% occur on gingiva (less frequently on labial mucosa, tongue or buccal mucosa). Firm to palpation, painless, persistent, more common in women, commonly associated with pregnancy, gingival lesions associated with poor OH, patients report an episode of trauma Differential diagnosis: peripheral giant cell granuloma, peripheral ossifying fibroma, metastatic carcinoma. Diagnostics: microscopic examination to confirm the diagnosis and rule out metastatic carcinoma Treatment: local surgical excision, treat local factors (remove bacterial plaque and or calculus) Clinical significance: lesions occasionally recur, metastatic carcinoma can mimic pyogenic granuloma

Question 103

Peripheral giant cell granuloma (giant cell epulis)

Answer 103

Etiology: reactive hyperplasia containing osteoclast like multi nucleated giant cells that develops in response to local irritating factors (bacterial plaque and or calculus) Findings: solitary circumscribed red nodule, with broad sessile or narrow pedunculated base. The surface is commonly ulcerated, occurs exclusively on gingiva, dental radiographs may show erosion of adjacent alveolar bone. Firm to palpation, painless, persistent, more common in women, often associated with poor OH Differential diagnosis: pyogenic granuloma, peripheral ossifying fibroma, metastatic carcinoma Diagnostics: microscopic examination necessary to confirm diagnosis and rule out metastatic carcinoma. Treatment: local surgical excision, treat local factors (remove bacterial plaque and or calculus) Clinical significance: recurrence of approx 10%, can occasionally mimic a brown tumour or hyperparathyroidism, metastatic carcinoma can also mimic peripheral giant cell granuloma.

Question 104

Peripheral ossifying fibroma (peripheral fibroma with calcifications)

Answer 104

Etiology: reactive hyperplasia similar to a pyogenic granuloma with focal calcifications. Findings: solitary circumscribed red to pink nodule with a broad sessile or narrow pedunculated based, the surface is smooth or ulcerated, occurs exclusively on gingiva (most often the incisor cuspid area.) firm to palpation, painless, persistent chronic, more common in women, more common in adults Differential diagnosis: pyogenic granuloma, peripheral giant cell granuloma, fibroma, metastatic carcinoma Diagnostics: microscopic examination necessary to rule of metastatic carcinoma Treatment : local surgical excision, treat local factors (remove bacterial plaque and or calculus) Clinical significance : recurrence of 15%, metastatic carcinoma can mimic peripheral ossifying fibroma, metastatic carcinoma can mimic peripheral ossifying fibroma

Question 105

Fibroma( irritation fibroma, traumatic fibroma)

Answer 105

Etiology: reactive hyperplasia or fibrous connective tissue in response to trauma or local irritation. Gingival lesions may represent fibrosis of a pre-existing pyogenic granuloma Findings: solitary, circumscribed pink nodule with broad sessile base, covered with smooth mucosa unless secondarily traumatized (then calloused or ulcerated), occurs most often on buccal mucosa, labial mucosa, tongue and gingiva. Firm to palpation, painless, persistent, history of trauma, gingival lesions may be associated with bacterial plaque or calculus, patient may report a pre-existing pyogenic granuloma Differential diagnosis: lesion on buccal mucosa or tongue can mimic a benign neoplasm such as a nueroma or nuerofibroma. A lesion on labial mucosa can mimic a mucocele. Diagnostics: microscopic examination Treatment : local surgical excision Clinical significance : recurrence unlikely if adequate excision, multiple oral fibromas can be a component of multiple hamartoma and tuberous sclerosis, Cowdens syndromes include skin tumours and breast cancer.

Question 106

Epulis fissuratum (denture epulis)

Answer 106

Etiology: reactive hyperplasia of fibrous connective tissue caused by chronic irritation from denture flange Findings: circumscribed, pink nodule, with broad sessile based, nodule often creased by trough produced by the denture flange. The surface is smooth unless secondarily traumatized then calloused or ulcerated. Occurs most often on the labial surface of the maxillary alvoealr ridge or the lingual surface of the mandibular alveolar ridge. Firm to palpation, painless, persistent, patient has usually worn the same denture for many years. (bone resorption allows denture flange to impinge on adjacent soft tissues) Differential diagnosis: due to clinical presentation, confused with other soft tissue swelling, when ulcerated lesions can mimic SCC Diagnostics: microscopic examination Treatment: local surgical excision, reline existing denture or fabricate a new denture. Clinical significance: often associated with denture stomatitis, and or inflammatory papillary hyperplasia, persistent lesions thought to be denture related should be viewed with suspicion in the mouths of individuals at risk for oral cancer.

Question 107

Mucocele

Answer 107

Etiology: local trauma damaged the excretory duct of a minor salivary gland, saliva escaped into the adjacent connective tissue causing chronic inflammatory reactions. Findings: solitary circumscribed nodule with a broad sessile base, superficial lesions are typically blue in colour, while deeper lesions are pink. The surface is usually smooth unless secondarily traumatized, occurs most often on the lower lip. Soft to palpation, painless, persistent, occasionally fluctuant in size, history of trauma. Differential diagnosis: fibroma, neuroma, neurofibroma, hemangioma. Diagnostics: microscopic examination Treatment: local surgical excision, remove minor salivary glands at site to reduce likelihood of recurrence. Clinical significance: recurrence likely if minor salivary glands at the wound edges are not removed.

Question 108

Ranula:

Answer 108

Etiology: usually caused by a sialolith (salivary duct stone) or local trauma to the duct of the submandibular salivary gland (whartons duct) Findings: circumscribed, blue, sessile nodule usually covered with smooth mucosa. Occurs in the floor of mouth away from midline. May occasionally extend below the mylohyoid muscle to produce a swelling int he upper neck (plunigng ranula), soft to palpation, painless, persistent, patient may report a history a local trauma. Differential diagnosis: hemangioma, lymphangioma, salivary gland neoplasms Diagnostics: microscopic examination is necessary to confirm the diagnosis Treatment recommendations: marsupialization, removal of submandibular glandular tissue may be necessary

Question 109

Parulis

Answer 109

Etiology: a soft tissue, extension of an abscess originating from the apex of a tooth root or periapical abscess or periodontal abscess origin Findings: circumscribed, erythematous, gingival mass, fistula with purulent discharge may be present, usually located on the buccal gingiva, acute pain associated with the tooth or inflamed gingival tissue, exacerbated by percussion Differential diagnosis: actinomycosis, pyogenic granuloma Diagnostic steps: PA radiograph, if lesion is present at apex of tooth or alveolar bone loss is present. EPT, microscopic examination Treatment: endodontic therapy, apical surgery, Antibitoics, periodontal therapy

Question 110

Actinomycosis

Answer 110

Etiology: soft tissue swelling caused by an infection with the bacteria (Actinomyces israelii). Most common infection is cervicofacial. The initial site of infection is an area of soft tissue injury a periodontal pocket, a periapical abscess, or an extraction site. Findings: cutaneous swelling with fistula formation, yellow colonies or organisms called sulfur granules exude from the fistula. Swelling occurs most often at the inferior border of the mandible. Can also be present as a gingival swelling. Dental radiographs may show PA raiolucency associated with a non vital tooth. Persistent, pain of odontodgenic or periodontal origin. Differential diagnosis: clinical presentation characteristics, infrequently confused with other soft tissue swellings, gingival lesions can mimic parulis. Diagnostics: bacterial culture (less than 50% positive), microscopic examination Treatment: treat infected tooth( endo, apical surgery, exo), antibiotics, may require drainage and debridement

Question 111

Lipoma:

Answer 111

Etiology: benign neoplasm of fat, may also represent a reaction of fat to local trauma Findings: solitary circumscribed nodule with a broad (sessile) base. Usually covered with smooth mucosa, superficial lesions are typically yellow in colour, while deeper lesions are pink Occurs most often on the buccal mucosa, ventral tongue and floor or mouth Findings: soft to palpation, painless, persistent Differential diagnosis: fibroma, neuroma, neurofibroma, salivary gland neoplasms Diagnostics: microscopic examination Treatment: local surgical excision Clinical significant: recurrence unlikely

Question 112

Hemangioma

Answer 112

Etiology: neoplasm of endothelial cells that form blood vessles, can be present at birth (congenital) or acquired later in life. Findings: circumscribed red to blue nodule with broad sessile base. Covered with smooth mucosa, solitary or multiple, digital pressure may cause the lesion to blanch, occurs most often on the tongue, lips and buccal mucosa. Soft to palpation, painless, congenital lesions may regress with time. Acquired lesions tend to be persistent. DIfferential diagnosis: mucocele, hematoma, pyogenic granuloma, lymphangioma. Diagnostics: microscopic examination necessary to confirm the diagnosis Treatment: local surgical excision, laser therapy, and embolization Clinical significance: multiple hemangionas are a component of encephalotrigeminal angiomatosis .Other components of the syndrome include hemangiomas involving skin of the face and brain

Question 113

Lymphangioma

Answer 113

Etiology: benign neoplasm of the endothelial cells that from lymphatic vessels. Can be present at birth or acquired later. Findings: circumscribed, sessile, blue, nodule with the broad sessile base, covered in smooth mucosa, occasionally the lesions are more diffuse and exhibit a pebbly multinodular surface. The tongue is the most common site of involvement. Soft to palpation, painless Differential diagnosis: mucocele, hemangioma Diagnostics: microscopic examination Treatment: local surgical excision Clinical significance: common cause in children

Question 114

Neuroma

Answer 114

Etiology: caused by traumatic injury to nerve bundle, nerve bundle proliferated to produce a mass in response to the trauma, precipitating injury is often secondary to tooth extraction. Findings: solitary circumscribed, pink nodule with broad sessile base, covered in smooth mucosa, occurs often on mucosa over the mental foramen area (caused by injury to mental nerve during exo of tooth in the area). Occasionally involves dorsal tongue. Pain, history of trauma Differential diagnosis: fibroma, neurofibroma Diagnostics: microscopic examination Treatment: local surgical excision Clinical significance: multiple oral mucosal neuromas are components of multiple endocrine neoplasia syndrome (MEN) type III. Other components of MEN type III are pheochromocytoma ( a benign neoplasm of the adrenal gland) and meduallry carcinoma of the thyroid gland

Question 115

Neurofibroma

Answer 115

Etiology: benign neoplasma of neurofibroblasts ( the cells that form the supporting structure for nerves) Findings: solitary circumscribed, pink nodule with broad sessile base, usually covered with smooth mucosa, occurs most often on tongue and buccal mucosa. Firm to palpation, painless Differential diagnosis: fibroma, neuroma Diagnostics: microscopic examination Treatment: local surgical excision Clinical significance: multiple mucosal neurofibromas are a component of neurofibromatitis (von recklingh disease of the skin). Other components of syndrome include multiple cutaneous neurofibromas and pigmented skin lesions called cafe au lait macules. As many as 15% of patients with the syndrome will develop neurofibrosarcomas

Question 116

Benign salivary gland neoplasms

Answer 116

Etiology: benign neoplasm one or more component of salivary gland tissue Findings: solitary circumscribed, pink mass with broad sessile base. Usually covered with smooth mucosa. Occurs most often on the hard palate away from the midline. Painless, persistent. Differential diagnosis: benign connective tissue neoplasms, malignant salivary gland neoplasms Diagnostics: microscopic examination Treatment: local surgical excision Clinical significance: some benign salivary gland neoplasms have the potential to become malignant.

Question 117

DIGO:

Answer 117

Etiology: gingival enlargement caused by variety of drugs including phenytoin, calcium channel blockers and cyclosporine Findings: generalized, pink, nodular enlargement of attached gingiva, anterior facial gingiva, may completely obscure the teeth, in the presence of significant local factors (bacterial plaque and calculus) the involved gingiva is red and bleeds easily. Firm to palpation, painless, persistent, phenytoin- hyperplasia more common in children and young adults. Hyperplasia secondary to calcium channel blockers and cyclosporin more common in adults. Differential diagnosis: pregnancy gingivitis, leukemic gingivitis. Diagnostics: medical history will often reveals that the patient uses one of the offending drugs. Microscopic examination Treatment: substitute drug, removal local factors, gingivectomy to remove excessive tissue.

Question 118

Leukemic gingival infiltrate

Answer 118

Etiology: gingival involvement caused by proliferation of malignant white blood cells (monocytes, myelocytes, or lymphocytes). Occurs most often in acute monocytic leukemia Findings: spontaneous bleeding from gingival sulcus. Firm to palpation, may present with gingival ulcerations, candidiasis, and recurrent intraoral herpes. Dental radiographs may reveal alveolar bone loss and involved teeth may be mobile, may have fever, weight loss, fatigue. Differential diagnosis: pregnancy gingivitis, DIGO Diagnostics: microscopic examination Treatment: physician- chemotherapy ; patient may develop oral mucositis

Question 119

Metastatic carcinoma

Answer 119

Etiology: caused by hematogenous (vascular) spread of a distant malignant, most common primary sites: breast, lung, colon and prostate Findings: solitary circumscribed, red to pink nodule usually with a broad sessile base, surface often ulcerated, occurs frequently on gingiva, firm to palpation, continuous enlargement, discomfort Differential diagnosis: pyogenic granuloma, peripheral giant cell granuloma, peripheral ossifying fibroma Diagnostics: microscopic examination Treatment: therapy for cancer Clinical significance: may be first indication of disease, associated with poor prognosis.

Question 120

Ameloblastoma

Answer 120

Etiology: benign odontogenic neoplasm that can develop from remnants of the dental lamina (rests of serres), hertwigs root sheath (rests of malassez), reduced enamel epithelium lining and dental follicle or basal cells of surface epithelium Findings: circumscribed unilocular or multilocular radiolucent lesions, may be associated with erosion or divergence of the roots of adjacent teeth. More common in mandible, teeth adjacent to lesions are asymptomatic and vital, may exhibit cortical expansion. Differential diagnosis: periapical granuloma, periapical cyst, simple bone cyst, central giant cell granuloma, calcifying odontogenic cyst. Diagnostics steps: percuss teeth, test the teeth for vitality, microscopic examination Treatment: surgical excision Clinical significance: locally aggressive lesions and have a high rate recurrent. Occasionally metastasize.

Question 121

Odontogenic Keratocyst

Answer 121

Etiology: originated from embryologic remnants of dental lamina, may develop from lining of dentigerous cyst. Findings: circumscribed, unilocular or multilocular radiolucent lesions with corticated margins. The lesion develops most often around an unerupted mandibular molar. Commonly displaces the unerupted tooth around which it develops. Often causes cortical expansion. Differential diagnosis: dentigerous cyst, ameloblastoma, ameloblastic fibroma, adenomatoid odontogenic tumour, calcifying odontogenic cyst. Diagnostics: microscopic examination Treatment: enucleation for smaller lesions, more extensive surgical resection is necessary for larger lesions. Because of recurrent potential of the lesion, close follow up required. Clinical significance: behaves like a benign neoplasm than a developmental cyst, (30% recurrence). Multiple OKCs are a feature of nevoid basal cell carcinoma syndrome (bifid ribs, basal cell carcinomas)

Question 122

Osteoradionecrosis

Answer 122

Etiology: patient treated with radiation therapy Findings: no specific clinic signs, numbness or parasthesia of lip may be an early indicators. Non healing necrotic bone which may or may not be exposed. Differential diagnosis: MRONJ, osteomylitis Diagnostics:based on pt history, clinical symptoms, radiographic fingings Treatment: Prior to radiation therapy to prevent osteoradionecrosis All extractions should be done 3-6 weeks prior to initiation of radiation therapy to allow for adequate healing. Perform adequate alveoloplasty after dental extractions to eliminate sharp bony projections. Do not overstretch the mucosa and achieve primary closure. If dental extraction was done because of severe periapical infection, prescribe antibiotics e.g., penicillin V potassium 500mg (dispense 28 tablets, take 1 tablet 4times/day) or Amoxicillin 500 mg (dispense 28 tablets, take 1 tablets 4 times/day to reduce risk of infection

Question 123

Dental treatment after radiation therapy to prevent osteoradionecrosis

Answer 123

Due to the risk of osteoradionecrosis, avoid invasive surgical procedures, involving exposure of irradiated bone for at least 6-12 months after radiation treatment. If tooth extraction is unavoidable, exercise extreme caution while extracting the tooth. Conservative surgical technique and antibiotic coverage should be given to assure complete healing.

Question 124

Osteoradionecrosis treatment

Answer 124

Perform minor debridement, eliminating sharp bone edges, sharp tooth surfaces. Advise patient to maintain local hygiene of the area of exposed bone with topical antibacterial agents, such as chlorhexidine gluconate 0.12% (dispense 1 bottle rinse with 20 ml for 30 seconds 3 times/day). To control secondary bacterial infections: Prescribe Penicillin V potassium 500mg (dispense 28 tablets, take 1 tablet 4 times/day). Alternatively, prescribe Amoxicillin 500 mg (dispense 28 tablets, take 1 tablets 4 times/day) or Clindamycin 150mg or 300 mg (dispense 150 to 300 mg (dispense 28 capsules, take 1 capsule every 6 hours). For pain control: prescribe acetaminophen 325 mg, taken every 4 hours. Conservative bone sequestromy may be required in extensive cases in consultation with an oral surgeon. Surgical removal of large areas of necrotic bone may be required in consultation with an oral surgeon.

Question 125

Sinus Pathologies

Answer 125

Mucocele- complete opacification of the sinus with expansion of its wells Destructive lesions Inverted papilloma- can see extensive bone destruction despite being considered benign. Can undergo malignant transformation Wegners Granulomatosis - rare, non caseating poly systemic lesion. Positive for anti neutrophil cytoplasmic antibodies, septal erosion, mucosal thickening, bone changes. Malignancies SCC Non Hodgkins Lymphoma Odontogenic neoplasms Ameloblastoma KCOT Odontogenic myxoma Osteosarcoma- intraoral mass, largely soft tissue, sunburst striae at the periphery of the lesion Polyp- sac of inflammatory exudate under the sinus mucosa. Dome shaped arising from sinus floor, multiple can frequently be present. Mucosal Antral Pseudo Cyst (MAC)- accumulation of fluid within the antral mucosa, but without epithelial lining, and may be referred to as a pseudocyst. Likely to be present singularity Fibrous dysplasia-origin from alveolus or within the base of the skull. Generally radiodensity of ground glass. Silhouette Effect-soft tissue structures, visible on conventional radiographs due to this effect, surface contours visible by contrasting against air filled spaces, occasionally soft tissues may have a radiopaque periphery. Silent sinus syndrome- downwards displacement of the eyes into the sinus and facial deformities. Sinusitis Inflammation of sinus mucosa, as a result of an upper respiratory tract infection or via infection from a subjacent tooth Carious exposure of the dental pulp resulting in periapical, infection and oroantral fistulas Ridge height and tx options for implants

Question 126

Techniques for sinus lifts

Answer 126

Crestal window approach - useful to prevent a large perforation in a clinical situations in which the oral mucosa and the schneiderian membrane are fused at the level of the alveolar crest which may have resulted from inadequate healing after complicated / traumatic extraction or because of previous history of sinus pathosis. Technically more demanding. Can be used to avoid the PSA artery. Delayed implant placement is advised with this technique. Palatal window approach -viable option in extreme bone atrophy. Should only be considered in very specific cases when no other alternatives are feasible Transalveolar approach- aka indirect sinus lift: the technique is initiated by a small osteotomy, creating a pathway for the insertion of osteotomes of increasing diameter to both compact the surrounding alveolar bone and elevate sinus membrane. Disadvantages is that there could be inadvertent perforation of the sinus membrane. The sinus floor may be elevated by 5mm without perforating the membrane. Lateral window approach - aka direct sinus lift.

Question 127

Residual bone height and recommended protocol:

Answer 127

RBH >9mm: standard implant (length >8mm) RBH >5 to <9: transalveolar approach and simultaneous standard implant placement or short implant (length <8mm) placement with no bone augmentation. RBH >3 to <5mm: lateral window approach and simultaneous implant placement RBH <3mm: lateral window approach and delayed implant placement

Question 128

Maxillary Sinus Blood supply

Answer 128

Branches of the maxillary artery Posterior superior alveolar or alveolar antral artery Infraorbital artery Posterior lateral nasal artery *** PSA + infraorbital artery form an anastomoses Greater palatine artery Anterior ethmoidal artery Superior labial arteries

Question 129

Maxillary Sinus Venous drainage

Answer 129

Goes into sphenopalatine vein and pterygomaxillary plexus

Question 130

Maxillary Sinus Innervation

Answer 130

Anterior, middle and posterior superior alveolar branches of maxillary nerve (2nd division of the 5th cranial pair- trigeminal nerve) as well as branches of the infraorbital nerve and the greater palatine nerve.

Question 131

Sinus Septa

Answer 131

Primary- developmental Secondary- functional or pathological adaptation

Question 132

Sinus Shape and boundaries

Answer 132

Base- medial wall Apex- laterally towards zygomatic arch Anterior wall- from orbital rim to apex of canine Posterior wall- separated sinus cavity from temporal fossa (pterygomaxillary region) Superior wall- orbital floor Inferior wall- determined by apices of posterior maxillary teeth and patterns of bone remodelling after tooth loss

Question 133

Location of ostium

Answer 133

28.5mm

Question 134

Location and height of anastomosis

Answer 134

16-19mm in dentate and 11.25 in edenulous

Question 135

Prognosis McGuire and Nunn

Answer 135

Good prognosis - Etiologic factors can be controlled. Adequate periodontal support. Teeth can be adequately maintained by the professional and patient. Systemic factors controlled Fair prognosis - Up to 25% attachment loss (clinical and radiographic). Grade I furcation with access. limited systemic factors Poor prognosis - Up to 50% attachment loss. Grade II furcation. Greater than class I mobility. Poor crown to root ratio. lack of compliance, systemic factors. Questionable prognosis - Greater than 50% attachment loss. Grade II or III furcation that is inaccessible to maintenance. Endodontically involved tooth that must be resolved before periodontal treatment. Teeth not easily maintained by patient. Hopeless prognosis - Inadequate attachment to support the tooth. Grade III or IV furcation. Miller Class III mobility. Tooth or teeth cannot be maintained by the professional/patient

Question 136

Kwok and Caton

Answer 136

Hopeless - The tooth must be extracted Unfavorable - The periodontal status of the tooth is influenced by local and systemic factors that cannot be controlled Questionable - the periodontal status of the tooth is influenced by local and/or systemic factors that may not be controlled Favorable - the periodontal status of the tooth can be stabilized with comprehensive periodontal treatment and professional maintenence

Question 137

Hypoxemia classification

Answer 137

SpO2 numbers None (95+) Mild (90-94%) Moderate (85-90%) Severe (<85%) Cerebral anoxia (70%) Cyanosis (65%) Consider reversal if below 95 if it is a respiratory depression issue

Question 138

Midazolam characteristics

Answer 138

Half life 2.8-6 hours Contraindications: MAO inhibitors, Prozac, Narrow angle glaucoma, myasthenia gravis, bronchospasm

Question 139

Reversal agents

Answer 139

Benzos - Flumazenil 0.2mg/ml. Administer one mL every 3-5 minutes (most need 0.6-1mg). Half life is 20-80 minutes. Max dose 3mg. Opiods - Naloxone 1mg.mL given at 0.1-0.2mg every 2-3 minutes IV. Max dose 10mg. Half life is 1-1.5 hours After reversal need to monitor the patient for 2 hours.

Question 140

Screw retained vs cement retained

Answer 140

Screw retained - advantages - retrievable, accessibility, facilitating replacement and maintenance of reconstruction, easier to shape emergence profile Provisionals and transfer to master cast Disadvantages: more expensive, screw loosening, screw fractures, screw access hole may impede occlusal morphology Cement retained - Advantage - Cheaper, accommodates better for suboptimal implant position, no screw access channel, superior esthetics, optimal occlusal morphology Disadvantages - difficulty removing cement, higher risk of peri-implant disease, complex retrievability, possible crown loosening due to loss of retention

Question 141

What is required to make a diagnosis of periodontal disease

Answer 141

Periodontal probing, CAL, recession, KT, mobility, furcation, plaque index, fremitus, radiographs, clinical exam including CC, medical history, dental history, intra/extra oral exam, occlusal exam, social history (smoking)

Question 142

When to graft prior to ortho

Answer 142

Adult patients with thin tissue phenotype (<1mm gingival thickness) and thin bony plate, where >10 degrees of proclination is planned.

Question 143

Why gingival swelling during ortho?

Answer 143

metal allergy Poor OH

Question 144

When to start ortho after perio surgery

Answer 144

Regen - 3-6 months non-surgical - after re-evaluation pending findings. End point no PD of 6+mm and no PD of 4+mm with BOP Perio surgery - after re-eval too?

Question 145

Ortho extrusion

Answer 145

To bring attachment about 1mm/month No attachment 1mm/week with gingival fibrotomy weekly. Retention of no less than 1 month for every mm

Question 146

Frenal pull classification

Answer 146

Mucosal= frenal fibers attached up to MGJ Gingival= fibers inserted within attached gingiva Papillary= fibers extend into interdental papilla Papillary penetrating= frenal fibers cross alveolar process and into palatine papilla

Question 147

GBR techniques

Answer 147

self-containing defect (bone substitute, collagen membrane without fixation) Form-stable devices (ti-PTFE membrane, Ti-PTFE mesh, Ti-mesh, Magnesium membrane) Fixing the membrane (sausage technique, vertical periosteal sutures, suspending the sutures by screws) Tenting (tenting screws, osteosynthesis plates, titanium frames) Blocks (onlay, inlay and distraction osteogenesis, shell technique, in situ shell technique, bone ring technique, allo and xenograft variants)

Question 148

Success of GBR

Answer 148

Graft resorptions is the main factor leading to bone volume reduction Micromotion can influence the volume of augmented bone Defect configuration (# walls) Type of graft (particulate vs block) PASS principle

Question 149

Treatment of peri-implant mucositis

Answer 149

Assess modifiable risk factors/indicators: smoking, periodontitis, uncontrolled diabetes Assess implant supported prosthesis OH and self performed biofilm removal Professional mechanical debridement Air polishing- as effective as hand instrumentation Adjunctive local antimicrobials (chx)- reduces BoP Adjunctive probiotics - no additional benefits Adjunctive laser irradiation - no additional benefits Adjunctive antimicrobial photodynamic therapy (aPDT)- limited benefits Adjunctive systemic antimicrobials- not recommended- no additional benefits

Question 150

Treatment of peri-implantitis

Answer 150

Professional mechanical debridement Laser irradiation Er YAG- no additional benefits vs mechanical debridement alone Air polishing-reduction in BoP Adjunctive antimicrobial photodynamic therapy (aPDT)- no additional benefits Adjunctive systemic antimicrobials- not supported Surgical treatment - Implant surface decontamination: Ti brush, scalers, air abrasives, lasers, implantoplasty Pocket elimination/reduction or reconstructive procedures:

Question 151

Peri-implantitis classification system

Answer 151

Class 1 - Intraosseous defect Class 2 - Horizontal defect Class 3 - Combined intraosseous and horizontal defect Class A - Buccal defect Class B - 2/3 wall defect Class C - circumferential defect

Question 152

How to describe a lesion

Answer 152

Location Distribution and definition - single, localized, well circumscribed Size- in millimeters Shape: eg. round, macule, vesicle, pustule, papule, nodule, plaque, sessile, pedunculated, ulcers or erosions Colour- single colour or mixed Consistency: soft, hard, fluctuant Texture: smooth, rough (papillary, corrugated, fissured, crusted) History: when?, pain? Lesions before? trauma? Medical changes/hx?

Question 153

Baceria involved in NPD

Answer 153

Selenomas, P intermedia, Treponema, Fusobacterium

Question 154

Which factor leads to an increase in RANKL

Answer 154

IL1, TNFalpha (also IL6, 7, 8, 17, IFNgamma)

Question 155

Factors to consider when determining prognosis:

Answer 155

Local factors: Biofilm and calculus Anatomic factors Short, tapered roots Cervical enamel projections: flat, ectopic extension of CEJ beyond the normal contours of CEJ; 28% of mandibular teeth, 17% of maxillary molars; mostly likely on buccal of mandibular 2nd molars Enamel Pearls: larger, round deposits of enamel in furcations or other areas on the root surface; less frequent (1.1-5.7% of molars); most prevalent in maxillary 3rd molars Bifurcation Ridges: 73% of mandibular molars Root concavities: more marked on upper 4s, the MB root of upper 6s, and lower incisors; create areas that are hard to clean both for the clinician and the patient; both in M and D roots of lower 6s → they are deeper on the mesial root (0.7 vs 0.5 mm) Developmental Grooves: palatogingival grooves → upper 2s (5.6%) or lower incisors; 3.4% in uppers 1s Root Proximity Furcation invasion: upper 4s→ 7-8 mm apical to CEJ (most unfavorable prognosis when involved); root trunk length of upper and lower molars → appx. 2.5-5 mm → AL over 3 mm can be a sign of furcation involvement Tooth mobility: Principle causes: BL, inflammatory changes in the perio, occlusal trauma Pockets in clinically mobile teeth does not respond as well, especially in regeneration; splinting can be helpful prior to surgery → but it can cause increased plaque accumulation Caries Tooth vitality Root resorption Overall Clinical factors: age, disease severity, biofilm control, patient compliance Systemic and environmental factors: smoking, systemic disease or condition, genetic factors, stress Prosthetic and restorative factors: subgingival restoration, tooth-supported prostheses, abutment selection

Question 156

Keystone pathogens

Answer 156

certain periodontal pathogens are able to evade host response and mediate the conversion of the whole microbial community into dysbiosis. P.gingivalis has been identified as a main keystone pathogen

Question 157

Adjunctive use of systemic AB to SRP

Answer 157

some additional benefit over SRP alone in terms of CAL reduction, especially in younger patients and in patients with severe/aggressive/active disease and/or specific microbiological profiles → neither of the two systematic reviews could assign superiority to any particular antibiotic

Question 158

ABX options for aggressive periodontitis

Answer 158

MTZ: bactericidal antimicrobial for anaerobic infections; a prodrug that requires metabolic activation by anaerobic organisms; selective efficacy against obligate anaerobes (such as red complex) makes it particularly appealing for the tx of periodontitis; AMX: semisynthetic penicillin; cephalosporins and penicillins are the main classes of beta-lactam antibiotics (bactericidal agents that kill bacteria by inhibiting the synthesis of the bacterial peptidoglycan cell wall); penicillin → narrow spectrum; AMX → broad-spectrum; the most important mechanism of resistance→ beta-lactamase-mediated hydrolysis of the beta-lactam ring; not established as the drug of choice for the tx of periodontitis MTZ + AMX: a potent tool in the tx of periodontitis, especially in patients harboring A.a; benefits in aggressive periodontitis, severe periodontitis, young patients with localized disease, smokers, and diabetics; AZI: a relatively new macrolide; a semisynthetic, bacteriostatic, wide-spectrum AB, rapidly absorbed by cells such as leukocytes and fibroblasts → helps to quickly bring the drug to the site of inflammation and to maintain its concentrations 10-100 times higher in tissues than in serum; slowly-released to the tissues → increased half-time; only once a day (500 mg) for short periods of time (3-6 days); facilitates patient adherence; heterogenous results

Question 159

Systemic antibiotic protocol/dosage with SRP

Answer 159

Dose and duration: AZI (500mg /daily for 3-5 days); MTZ (variation between studies); MTZ + AMX (250+500mg, three times a day); duration is different between studies, usually 7 days, in some studies 14 days Timing: ABs should be administered during the active phase of treatment (not at re-evaluation) and right after disruption of the subgingival biofilm

Question 160

Excessive gingival display

Answer 160

>2 mm of gingival display upon smiling APE, Coslet classification 1: adequate amount of AG; 2: inadequate amount of AG A: osseous crest apical to CEJ; B: osseous crest at CEJ 1A: gingivectomy; 1B: gingivectomy and osseous surgery; 2A: APF; 2B: APF + osseous surgery Dento-alveolar extrusion: orthodontic intrusion, and segmental osteotomy? Maxillary vertical excess: if severe → orthognathic surgery; if mild → may be camouflaged by Botox? short/hypermobile lip: Botox; what length is considered short? Average lip length in females: 20-22; males: 22-24 mm Lip mobility = normal is 6-8 mm

Question 161

Phases of periodontal treatment

Answer 161

Systemic phase including smoking cessation → to eliminate/decrease the influence of systemic conditions on the outcomes of therapy and to protect the patient and the dental care providers against infectious hazards Initial (or hygienic) phase, that is, cause-related therapy → to achieve clean and infection-free conditions in the oral cavity through complete removal of all soft and hard deposits and their retentive factors + motivating patient to perform optimal biofilm control + may include caries excavation and provisional root canal medication + concluded by re-evaluation and planning of both additional and supportive therapies Corrective phase, that is, additional measures such as periodontal surgery, and/or endodontic therapy, implant surgery, restorative, orthodontic, and/or prosthetic treatment → addresses the sequelae of the opportunistic infection Maintenance phase (care), that is, SPT → prevention of re-infection and disease recurrence: 1) assessment of deepened sites with BOP, 2) instrumentation of such sites, 3) fluoride application for the prevention of caries

Question 162

Treatment goals of periodontal therapy

Answer 162

reduction/resolution of gingivitis (BOP): FMBS ≤10% Reduction in PPD: no residual pockets with PPD >5 mm Elimination of open furcations: furcation involvement should not be >2-3 mm in horizontal direction Absence of pain Individually satisfactory esthetics and function

Question 163

Who needs periodontal therapy

Answer 163

First step of therapy: should be implemented in all perio patients, irrespective of the stage + should be re-evaluated frequently supragingival dental biofilm control, interventions to improve the effectiveness of OH (motivation and OHI), adjunctive therapies for gingival inflammation, professional mechanical plaque removal (PMPR) (interventions to remove supra-gingival plaque and calculus + plaque-retentive factors), risk factor control (smoking cessation, improved metabolic control of DM, and perhaps physical exercise, dietary counseling and weight loss) Second step of therapy (cause-related therapy): aimed at controlling (reducing/eliminating) the subgingival biofilm and calculus (subgingival instrumentation) → in all perio patients, irrespective of the stage ONLY in teeth with AL and/or pocket formation. In specific clinical situations, such as in the presence of deep pockets → simultaneous first and second step could be delivered simultaneously (for preventing perio abscess development) Third step of therapy: aimed at treating non-responding areas (PDs ≥4mm with BOP or deep PDs ≥6mm) Repeated subgingival instrumentation with or without adjunctive therapies Access flap periodontal surgery Resective periodontal surgery Regenerative periodontal surgery Supportive periodontal care

Question 164

Prognostic factors of an endo-perio lesion

Answer 164

1) presence/absence of root damage; 2) presence of periodontitis; 3) anatomic problems (grooves); 4) severity and extent of the periodontal defect on the affected tooth (including furcation involvement)

Question 165

Reasons to keep or extract a tooth with Endo-perio lesion

Answer 165

Presence/history of periodontitis Severity of periodontal destruction around the affected tooth if the tooth needs to be involved in an oral rehabilitation treatment

Question 166

Management of Necrotizing periodontla diseases

Answer 166

control of the acute condition → treatment of pre-existing condition → corrective tx of the disease sequelae → supportive or maintenance phase Clear systemic involvement (fever or malaise): Metronidazole 250 mg every 8 hours; locally delivered antimicrobials are not recommended Management of pre-existing gingivitis or periodontitis + control of the systemic predisposing factors (smoking, inadequate sleep, psychological stress, relevant systemic conditions) Gingivectomy/Gingivoplasty for superficial craters, or periodontal flap or regenerative surgery for deep craters

Question 167

Periodontal abscess differential diagnosis

Answer 167

Lateral periapical cyst, periapical abscess, vertical root fracture, endo-perio lesion, tumor lesion, pyogenic granuloma, osteomyelitis, OKC, self inflicted gingival injury

Question 168

periodontal abscess classificaiton

Answer 168

in periodontitis patient (in a pre-existing periodontal pocket) Acute exacerbation: untreated periodontitis; non-responsive to therapy periodontitis; SPT After treatment: post-scaling; post-surgery; post medication (systemic AB, and other drugs such as nifedipine) In non-periodontitis patient (not mandatory to have a pre-existing periodontal pocket) Impaction (dental floss, orthodontic elastic, toothpick, rubber dam, or popcorn hulls) Harmful habits (wire or nail biting and clenching) Orthodontic factors (ortho forces or crossbite) Gingival overgrowth Alteration of root surface Severe anatomic alterations (invaginated tooth, dens evaginatus, or odontodysplasia) Minor anatomic alterations (cemental tears, enamel pearls, or developmental grooves) Iatrogenic conditions (perforations) Severe root damage (fissure or fracture, cracked tooth syndrome) ERR

Question 169

Periodontal Abscess management

Answer 169

control of the acute condition + re-evaluation of treatment outcomes (24-48 hours after) + management of the pre-existing and/or residual lesion First line of treatment → drainage and debridement Alternative approaches: Extraction if hopeless; systemic AB as initial therapy when there is lack of access, or the abscess is not well-localized, or there is a need to premedicate the patient, and when possible→ drainage and debridement; adjunctive systemic AB when immune system is affected, or in cases of severe systemic involvement; periodontal surgery if solid evidence of foreign body impaction AB of choice: metronidazole 200-250mg TID for 2-3 days Subgingival mechanical instrumentation must be avoided in the first stage of tx (should only be performed once the acute lesion is controlled)