EPITHELIAL PATHOLOGY FROM A TO Z and Systemic Considerations: What Every Clinician Should Know Theresa Sullivan Gonzales, DMD, MS Colonel, United States Army Director, Orofacial Pain Management Tripler Army Medical Center Honolulu, Hawaii 96859 Diplomate, Oral and Maxillofacial Pathology The 15 Most Common Oral Pathoses (Based on examination of 23,616 U.S. adults; excludes caries & periodontitis) Number of Lesions per 1,000 Adults Diagnosis Rank Males Females Both Leukoplakia 1 42.5 13.1 23.7 Torus palatinus 2 13.2 21.7 18.7 Irritation fibroma 3 13.0 11.4 11.9 Fordyce granules 4 17.7 5.2 9.7 Torus mandibularis 5 9.6 7.9 8.5 Leaf-shaped fibroma (under denture) 6 0.4 12.9 6.7 Hemangioma 7 8.4 4.1 5.6 Inflammatory ulcer 8 5.4 5.1 5.2 Inflammatory erythema 9 4.5 4.8 4.7 Papilloma 10 5.3 4.2 4.6 Epulis fissuratum 11 3.4 4.4 4.0 Lingual varicosities 12 3.5 3.4 3.5 Fissured tongue 13 3.5 3.1 3.3 Geographic tongue 14 3.4 3.0 3.1 Papillary hyperplasia of palate 15 1.7 3.8 3.0 References: Bouquot JE. J Am Dent Assoc 1986; 112:50-57; www.oralpath.com Differential DX Deferential DX Differential Diagnosis M – Metabolic I – Inflammatory N – Neoplastic D - Developmental Clefts Oral and Maxillofacial Pathology Fordyce Granules Categories Osteogenesis Imp. Developmental CleidocranialFissured Tongue Dysplasia Paget’sDentigerousHairy Disease Tongue Cyst Odontogenic CGCGOKC/KOTTori BFOLCOC Teeth/Pulpal/Perio OsteomaOdontoma Ameloblastoma Erosion/Abfraction/Abrasion Mucosal Osteosarcoma AOT Amelogenesis Imperfecta Chondrosarcoma CEOT Dentinogenesis Imperfecta Infections Ewing’s Sarcoma Myxoma Gemination/Fusion Salivary Pulpal/Periapical Dis. Periodontal Dis. Bone Allergy/Immunologic Rec. Apthous Stomatitis Others Sarcoidosis Manifes of PhysicalWegner’s Granulomatosis Heme Dermatologic Forensics LichenSystemic Planus Dis. ChemicalAngioedemaPemphigus Pemphigoid ContactErythema Stomatitis Multiforme Erythema Migrans Lupus Ectodermal Dysplasia Cowden Syndrome Oromaxillofacial Pathology Categories Developmental Odontogenic Teeth/pulpal perio Mucosal Infections Salivary Amyloidosis Vitamin Deficiency Diabetes Bone Hyperparathyroidism Inborn Errors of Metabolism Addison’s Disease Crohn’sAllergy/Immunologic Disease Iron Def. Anemia Others Manifes of Physical Heme Dermatologic Forensics Systemic Dis. Chemical Oral Mucosal Lesions Epithelial Soft Tissue Neoplastic Reactive Reactive Neoplastic Benign Malignant Benign SCC Papillary/ Malignant Verruciform VerrucousFibroma C. Spindle Cell C. Basaloid SCC3 P’s Pigmented EphelisAdenosquamosEpulis Fissuratum ActinicBCC LentigoIPH Leurkoplakia/ MelasmaNasopharyngeal Erythroplakia OralCarc Melanotic of Max. Macule Sin MelanoacanthomaMerkel Cell Smoker’sMelanoma Melanosis Nevi Oral Mucosal Lesions Epithelial Soft Tissue Neoplastic Reactive Reactive Neoplastic Benign Malignant Benign Frictional Hyperkeratosis Linea Alba Pre-malignant Malignant Morsicatio Buccarum Morsicatio Linguarum Cotton Roll Burn Aspirin Burn SDK Radiation Mucositis Oral Submuc. Fibrosis Physical/ Sanguinaria-ass. keratosis Nicotine Stomatitis? Chemical Pyrophosphate-ass. keratosis Solar Keratosis Hyperplastic Candidiasis Leukoplakia Actinic Cheilitis Keratoacanthoma? Infectious PVL Epithelial Dysplasia Diagnosis – “through knowledge” … A solid knowledge of the basic principles of the various disease processes is essential for obtaining a good history. As Goethe stated: "The eyes see what the mind knows." Consider Anatomical Location Biological Plausibility Patient History Taking the patient's history is traditionally the first step in virtually every clinical encounter. Other than that Mrs. Lincoln, how was the play? Popular Searches Viagra Cialis Levitra Lipitor Zoloft Hair Transplant Health Insurance Healthy Diet Prescription Drug Information for Consumers & Professionals Lose Weight Pain Relief Multiplicity of Presentation Systemic Disease Syndromic Presentation A Recurrent Aphthous Stomatitis “aphthous ulcerations” “canker sores” Prevalence in the general population 5% to 66% with a mean of 20% Mucosal destruction – T-cell mediated immunologic reaction Etiologic Factors Allergies Genetic predisposition Nutritional deficiencies – B12, B6, Fe ++ Hematological abnormalities Hormonal influences Infectious agents Trauma Stress Four Principal Categories Primary immunodysregulation Decrease of the mucosal barrier Increase in antigenic exposure Genetic predisposition / HLA-12, HLA - B51 and Cw7 Systemic Disorders Associated with Recurrent Aphthous Stomatitis Behcet’s syndrome Celiac disease Cyclic neutropenia Nutritional deficiencies IgA deficiency Immunoincompetence Inflammatory bowel disease Three Clinical Variations Minor Major – Sutton’s disease or PMNR (periadenitis mucosa necrotica recurrens) Herpetiform Minor Aphthous Ulcerations Non-keratinized mucosa Prodromal symptoms – burning, itching, stinging Erythematous macule – fibrinopurulent membrane with a erythematous halo * except in immunocompromised Major Aphthous Ulcerations Larger - 1 to 3 cm Deeper Clinically persistent Develop post pubertal Recurrences for up to 20 years or more Herpetiform Aphthous Ulcerations Greatest number of lesions Increased frequency of occurrence Superficial resemblance to herpes simplex viral infection Any mucosal surface may be involved Behcet’s Syndrome “the silk route” Behcet’s Syndrome 1937 – Turkish dermatologist –Hulusi Behcet described this condition Ocular Inflammation Orogenital Inflammation Multisystem Disorder Behcet’s Disease Highest Prevalence – Middle East and Japan Oral Involvement – primary manifestation in 25% to 75% of the cases All three forms of aphthous stomatitis may be seen Behcet’s Disease Genital lesions are clinically similar to oral lesions 75% of the patients demonstrate the genital lesions Genital lesions are generally more symptomatic in males Behcet’s Disease Criteria for the Diagnosis of Behcet’s Disease (International Study Group) Recurrent oral ulceration Plus two of the following: Recurrent genital ulcerations Eye lesions –anterior/posterior uveitis Skin lesions + pathergy – read by 24-48 hours Behcet’s Disease Treament Topical or intralesional corticosteriods Oral colchicine Thalidomide Low-dose methotrexate Systemic corticosteriods Cyclosporine Interferon alpha2A Treatment Triamcinolone 0.1% in Orabase (Kenalog in Orabase) Apply to dried ulcer two to four times daily until healed Randomized, controlled studies show decreased pain Dexamethasone elixir, 0.5 mg per 5 ml Swish and spit with 5 mL every 6 hours As above B Burning Mouth Syndrome About 1.3 million American adults, mostly postmenopausal women, are afflicted with Burning Mouth Syndrome, a chronic often debilitating condition whose cause remains a medical mystery. Burning Mouth Syndrome The main symptom of burning mouth syndrome is a burning sensation involving the tongue, lips, gums, palate, throat or widespread areas of the whole mouth. People with the syndrome may describe the sensation in the affected areas as hot or scalded, as if they had been burned with a hot liquid. Burning Mouth Syndrome Dry mouth Sore mouth A tingling or numb sensation in your mouth or on the tip of your tongue A bitter or metallic taste Causes Dry mouth (xerostomia). Nutritional deficiencies Allergies. Psychological factors. Nerve disturbance or damage (neuropathy). Treatments Potentially efficacious medicines include: * tricyclic antidepressants (like amitriptyline - brand name, Elavil) * benzodiazepines (like clonazepam - brand name, Klonopin; or *chlordiazepoxide brand name - Librium) * even anticonvulsants have proven effective in some cases. BMS: Treatment Tricyclic antidepressants Amitriptyline (Elavil)10 to 150 mg per day 10 mg at bedtime; increase dosage by 10 mg every 4 to 7 days until oral burning is relieved or side effects occur BMS: Treatment Benzodiazepines Clonazepam (Klonopin)0.25 to 2 mg per day0.25 mg at bedtime; increase dosage by 0.25 mg every 4 to 7 days until oral burning is relieved or side effects occur; as dosage increases, medication is taken as full dose or in three divided doses BMS: Treatment Anticonvulsants Gabapentin (Neurontin) 300 to 1,600 mg per day100 mg at bedtime; increase dosage by 100 mg every 4 to 7 days until oral burning is relieved or side effects occur; as dosage increases, medication is taken in three divided doses C Candidiasis Oral thrush and other Candida infections occur when your immune system is weakened by disease or drugs such as prednisone, or when antibiotics disturb the natural balance of microorganisms in the body. Predisposing factors for infection Infancy or old age Serious underlying disease, such as cancer or infection with HIV Dry mouth due to disease of the salivary glands or medications e.g. antihistamines, diuretics Dentures (especially if they are not regularly cleaned or fit badly) Predisposing factors for infection Smoking Injury to the mouth Nutritional deficiency e.g. iron &/or B-vitamin deficiency Inhaled corticosteroids used to treat asthma e.g. beclometasone, budesonide, fluticasone. Drink water after inhalation to reduce this complication Clinical features Acute pseudomembranous candidiasis. There are white patches on gums, tongue & inside the mouth that can be peeled off leaving a raw area. Acute atrophic candidiasis. There are smooth red shiny patches on the tongue. The mouth is very sore. Chronic atrophic candidiasis. This is common in those with dentures. The underlying mucosa is red and swollen. Clinical features Angular