Exam Flashcards
Heart attack (Cardiac Arrest)
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.
Angina
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.
Asthma
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.
Syncope
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.
Stroke
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.
Anaphylaxis
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.
Choking
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
Hypoglycemia
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.
Hyperventilation
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.
LA toxicity
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.
Hep B,C
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.
TB
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.
Herpes
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)
HIV/AIDS
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.
Syphilis
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
COVID 19
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)
Post op infections
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…
Emphysema
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
Swelling of Floor of mouth
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.
IAN damage/ other nerve damage
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
Nerve injury from implant classification
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
Paresthesia
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.
Hemorrhage
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
Dry socket
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.
Pain management
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.
Trismus
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.
OAC/OAF
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.
Osteomyelitis
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.
ONJ/MRONJ
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
MRONJ
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
Peri implant mucositis
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).
peri implantitis
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.
Lingual, mental, IAN , nasopalatine nerves anatomical limitations
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
Lingual, GP artery
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.
Maxillary sinus, nasal cavity, FOM
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.
Sublingual foramen
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.
Lingual accessory canal
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.
Anatomy on CBCT
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.
Macrophages
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.
Pro inflammatory mediators
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
Anti inflammatory mediators
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
RANKL inhibitor mechanism of action
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.
ILbeta
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
Page and Schroder
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.
Ecological plaque hypothesis
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.
Smoking
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.
Diabetes
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
Molar Incisor pattern- etiology, bacterial involved
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.
New classification (2017)
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+
Leukoedema
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
Frictional keratosis
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.
Acute psudomembranous candidiasis (Thrush)
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)
Chronic hyperplastic candidiasis (candidal leukoplakia)
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
Lichen Planus - Reticular and Plaque
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
Lichen Planus Erosive/Bollous
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,
Hairy leukoplakia
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
Smoking related leukoplakia
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.
Smokeless tobacco keratosis
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
Nicotonic stomatitis
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)
Actinic chelitis
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
Erythematous candida
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.
Angular chelitis
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.
Erythroplakia
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.
Stomatitis Areata Migrans (erythema migrans, benign migratory glossitis, geographic tongue)
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.
Mucosal allergy
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.
Atrophic glossitis
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.
Plasma cell gingivitis
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.
Median Rhomboid Glossitis (median papillary atrophy)
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
