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Patho Ndbe Iı Final 2017 Student-Nbde Part 2 2020 DISCLOSURE This lecture has been adapted from Dr. Michael A. Kahn from Tufts University Images are take from various sources, including: Dr. Kahn’s original lecture Lectures of Dr. Bruno Jham Oral and Maxillofacial Pathology by Neville and Damm Oral Radiology by White and Pharoah Mosby’s Review NBDE Part 2 Fordyce Granules Sebaceous glands that occur on the oral mucosa Yellow plaques/granules Most common on buccal mucosa and upper lip vermillion Leukoedema Intracellular edema of cells More often seen in African Americans Bilateral on buccal mucosa KEY: white area disappears on pulling or stretching the mucosa Normal variant; no treatment required Leukoedema Varices Located on lip and under the tongue (most common) Typically seen in elderly Sublingual varices seen in 2/3 of older people Dilated blue veins Lip varcies may thrombose and calcify Geographic Tongue (Erythma Migrans) Red and white Red = flat central area (atrophy of filiform papillae) White – serpentine border (keratin, cell debris) Moves around; periodically appears Usually asymptomatic, but may cause soreness or burning Geographic Tongue (Erythma Migrans) Usually no treatment Steroid rinse if symptomatic (dexamethasone) Most common on ventral tongue, but can be on other areas Torus Palatinus Exostosis in the midline of hard palate Torus Mandibularis Radiographic Findings: may be superimposed over periapical region as radiopaque areas Physiologic Pigmentation (Racial Pigmentation) More common in darker skinned individuals Present most of life, but darkens with time Series of splotchy brown macules Ankyloglossia Congenital abnormality – short lingual frenum “Tongue-tied” Cleft Lip and Cleft Palate Cleft Lip Unilateral (80%) or bilateral (20%) Defect between medial nasal process and maxillary process Cleft Palate Lack of fusion between palatal shelves Cleft Lip Cleft Palate Cleft Palate Morsicatio Chronic mucosa chewing Buccal mucosa = morsicatio buccarum Labial mucosa = morsicatio labiorum Tongue = morsicatio linguarum White, rough tissue Above and below occlusal planes White Sponge Nevus Autosomal dominant genetic mutation of keratin production Multifocal Extensive thick, white folds of tissue No eye involvement White Sponge Nevus Symmetrical, thickened, white, corrugated/velvety, diffuse plaques. Bilateral23 in buccal mucosa, but also in ventral tongue, labial/alveolar mucosa, soft palate, floor of mouth Linea Alba White linear thickening at the level of the occlusal plane 24 Oral Hairy Leukoplakia White rough plaque on lateral border of tongue Seen in immunocompromised (commonly HIV+) patients Caused by Epstein-Barr virus Oral Hairy Leukoplakia 26 Hairy Tongue Elongation of filiform papillae Treatment: scrape tongue 27 Lichen Planus Manifests on skin and/or oral mucosa Middle aged women most often Skin: purple, polygonal, pruritic papules Oral – 2 types Reticular: Wickam’s straie – white lacy pattern that does not rub off More common; usually asymptomatic Erosive Painful ulcerations all over the mouth May see remnants of Wickam’s straie Both types: lesions should be multifocal Lichen Planus Most patients middle-aged adults; 3:2 F:M Skin features sometimes present Planar Purple Pruritic Polygonal Plaque Papule 29 RETICULAR PATTERN More common form Multifocal lesions Wickham’s striae: interlacing white lines Wax and wane over weeks or months EROSIVE PATTERN Less common, but more significant (PAIN) Central erosion/pseudomembrane with erythema and possibly Wickham’s striae May present as desquamative gingivitis Lichen Planus Reticular Erosive Lichen Planus Management: Reticular: White lesions are asymptomatic and are not treated If burning occurs, treated with topical corticosteroids Erosive Topical corticosteroids Flare-ups require reapplication of drugs or prophylactic treatment Severe cases require systemic corticoid therapy 32 Nicotinic Stomatitis Reactive change of hard palate due to heat of smoking Most common with pipe smokers Red, inflamed minor salivary gland ducts with background leukoplakic change Not premalignant Nicotinic Stomatitis 34 Red areas are inflamed minor salivary glands CANDIDOSIS (CANDIDIASIS) Candida albicans: most common oral fungal infection in humans Opportunistic: seen in people who are immunocompromised, on antibiotics or corticosteroids 2 variations: “Classic” white patches: pseudomembranous candidiasis (thrush) Red variations: Acute erythematous candidosis Chronic erythematous candidosis Denture stomatitis Median rhomboid glossitis 35 Candidosis - White Pseudomembranous (thrush): “Classic” white patches that rub off leaving red base Painful Acute Erythematous Candidosis Generalized pain, burning and erythema Typically follow broad-spectrum antibiotics (“antibiotic sore mouth”) www.hivdent.org www.washington.edu Chronic Erythematous Candidiasis Commonly seen in denture wearers, aka denture stomatitis Erythematous areas confined to denture-baring area May cause pain/burning or be asymptomatic Denture stomatitis may not be caused by other things (not candida): poorly fitting dentures, prolonged wearing of denture, poor hygiene Regezi et al., 2012 Regezi et al., 2012 ANGULAR CHEILITIS Typically occurs with reduced vertical dimension of occlusion, but does not have to be 20% C. albicans alone 60 % combined C. albicans and S. Aureus 20% S. aureus alone MEDIAN RHOMBOID GLOSSITIS Anterior to the circumvallate papilla “Kissing lesion” on palate may be present Regezi et al., 2012 Chemical/Physical Burn Does not represent keratosis; is coagulative necrosis of the surface White pseudomembrane that rubs off with difficulty Heat (pizza) or chemical (aspirin) Scarlet Fever Group A Streptococcus infection “Strawberry tongue” White strawberry tongue: early; white coating with protruding hyperplastic fungiform papillae Red strawberry tongue: 4-5 days later; white coating is lost Hemangioma Venous Malformation HEMANGIOMA - blanches Not present at birth Tumor of infancy that has rapid growth and endothelial cell proliferation Gradual involution VENUS MALFORMATION - blanches Present at birth and persist through life Anomalies of blood vessels without endothelial proliferation 43 Hemangioma Sturge Weber Antiomatosis Port wine stain (venous malformation) Meningeal angiomas Convulsive disorders Mental retardation www.dermatlas.me d.jhmi.edu Submuccosal Hemorrhage Bruise from minor trauma DO NOT BLANCH PETECHIAE = very small hemorrhages into skin, mucosa ECCHYMOSIS = blood accumulation greater than 2 cm HEMATOMA = accumulation produces a mass 46 Kaposi’s Sarcoma Malignancy seen in HIV+ patients Cause is HHV-8 (human herpes virus 8); not HIV, EBV, CMV, HPV Acquired Melanocytic Nevus (Mole; Nevus) Controlled proliferation of melanocytes Junctional type – nevus cells in at junction of epithelium and connective tissue Compound type – nevus cells in epithelium and connective tissue Intramucosal type – nevus cells in connective tissue Malignant Melanoma Can begin as blue-brown macule May become raised and difficult to distinguish from nevus Oral melanoma has extremely poor prognosis Heavy Metal Intoxication Lead Burton’s line: blue-gray line along gingival margin seen with lead Traumatic Ulcer Caused by simple mechanical trauma Other causes: factitious and iatrogenic Acute or chronic Any ulcer lasting for more than 2 weeks without a known cause should be biopsied Aphthous Stomatitis Cause: unknown, but not infectious NON-keratinized mucosa Minor, Major, Herpitiform Red halo surrounding central yellow/white area Treatment: Corticosteroids Herpes Simplex Oral herpes: human herpes virus–1, or 2 HHV-1 and HHV-2 aka herpes simplex (1 or 2) HHV-2 can also infect oral cavity, but HHV-1 more common US incidence estimate of herpes infection is 80-85% Often present as 1-3 mm vesicles that rupture and coalesce to form larger area of ulceration Specific triggers: Sunlight Tissue injury and inflammation Physical or emotional stress Herpes Simplex Primary herpes on ➢ Recurrent herpes on keratinized AND non- keratinized tissue only keratinized tissue ➢ Recurs in same location Usually have fever, ➢ No fever, malaise, malaise, lymphadenopathy lymphadenopathy ➢ Prodrome precedes lesions May be subclinical Herpes Treatment Primary Herpes (within first 3 days of symptoms) Acyclovir suspension Rinse and wallow 5 times daily Children: 15mg/kg; Adults: 200mg Recurrent Herpes RX: Valacyclovir 1 g tablets (Valtrex) Disp: 4 tablets Sig: 2 tablets at onset of symptoms, then 2 tablets 12 hours after first dose Herpes Zoster Recurrent Varicella (HHV-3) infection Unilateral distribution on skin and intraorally (follows dermatome) Herpes Zoster (Shingles) 58 Generalized Vesiculoerosive Lesions Long duration (months): Pemphigus Vulgaris Pemphigoid Erosive Lichen Planus Lupus Short duration (days): Erythema Multiforme Short or Long Drug-induced mucositis Nikolsky Sign Seen in pemphigus vulgaris and mucous membrane pemphigoid Induction of bullae by lateral pressure 60 or application of air Pemphigus Vulgaris Autoimmune disease attacking epithelial desmosomes Intraepithelial splitting Generalized ulcerations of skin and/or mucosa Nikolsky sign may be present Demonstrates immunoglobin fluorescence Mucous Membrane Pemphigoid Autoimmune disease attacking epithelial HEMI-desmosomes Subepithelial splitting Skin, mucosa and EYE involvement Symblepharon formation which may lead to blindness Must be seen by ophthamologist Nikolsky sign
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