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Oral Lichen Planus
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- 2. Oral Lichen Planus Commonmucocutaneous disease with varying clinical presentation Premalignant condition Involvement of oral mucosa is frequent along with or preceded by lesions on skin and genital mucous membrane
- 3. Definition OLP isa rather common chronic mucocutaneous disease which probably arises due to abnormal immunological reaction and the disease have some tendency to undergo malignant transformation
- 4. Lichenoid reactions Exhibitsclinical and histological similarity Distinguished from OLP on the basis of 1. Association with administration of drug, contact with a metal, use of food flavors or systemic diseases 2. Resolution when the cause is eliminated or when disease is treated
- 5. Epidemiology Very common-1% of population In asians 1.5%(average) 3.7% mixed oral habits 0.3% non users of tobacco Risk more among who smoke and chew tobacco cutaneous lesion alone 35% mucosal lesion alone 25% both together 40%
- 6. Etiology Specific etiologyis unknown Psychological stress No evident genetic base or no uniform etiologic factors Abnormal recognition and expression of basal keratinocytes of epithelium as foreign antigens by langerhans cells
- 7. Pathogenesis CD8 + Tcells trigger the apoptosis of oral epithelial cells They recognize an antigen which is similar to an antigen associated with major histocompatability complex class 1 on keratinocytes They release cytokines that attract additional lymphocytes which accumulate in sub basilar connective tissue Liquefaction degeneration of basal keratinocytes
- 8. Clinical Features Middleaged or elderly people mean age of onset- 5th decade of life rarely in young adults and children More in females ( 1.4:1 ) Site- Both skin lesions and mucosal lesions are present
- 9. Skin Lesions Purple,pruritic and polygonal papules May be discreet or gradually coalesce into plaques each covered by fine glistering scale Bilaterally symmetrical Increase in size if subjected to any irritation Usually self limiting unlike the oral lesions lasting only one year or less
- 10. Skin Lesions Initiallyred > purple or violaceous hue > a dirty brownish color Periods of regression and recurrence “Koebner’s phenomenon”- skin lesions extend along the areas of injury or irritation Most often on wrist, forearms, knees, thighs and trunk Face remains uninvolved
- 11. Mucosal Lesions Normallyasymptomatic Bilaterally symmetrical Sometimes simultaneously have OSF, leukoplakia,etc. Clinical types 1.reticular 2.atrophic 3.erosive 4.bullous 5. other types
- 12. Reticular type Mostcommon and most readily recognized form Slightly elevated fine whitish lines (Wickham’s striae) in lace like or annular pattern Lines are wavy and parallel A tiny elevated dot like structure at the point of intersection of lines Commonly on buccal mucosa and buccal vestibule
- 14. Atrophic type Keratoticchanges combined with mucosal erythema smooth, poorly defined erythematus areas with or without peripheral striae Usually associated with desquamative gingivitis Pain and burning sensation
- 15. Erosive type Pseudomembrane covered ulcerations with keratosis and erythema Severe form with extensive degeneration and separation of epithelium from connective tissue Pain, burning sensation, bleeding, desquamative gingivitis Commonly on buccal mucosa and vestibule More dysplasia and malignant transformation
- 16. Bullous type Vesciculobullouspresentation combined with reticular or erosive pattern Rare form characterized by large vesicles or bullae (4mm to 2cm) Lesions usually develop within an erythematus base, rupture immediately leaving painful ulcers Usually have peripheral radiating striae and seen on posterior part of buccal mucosa
- 17. Other types Plaquetype: flattened white areas -dorsal surface of tongue -often resemble leukoplakia Hypertrophic type: well circumscribed, elevated white lesion resembling leukoplakia -biopsy needed for diagnosis Pigmented type: rarely erosive type can be associated with diffused erythema -usually on buccal mucosa and vestibule -reticulated white patches with or without a red erosive component flanked brown macular foci
- 19. Histopathology Hyper orthokeratinisationor hyper parakeratinisation Thickening of granular layer Acanthosis of spinous layer Intercellular oedema in spinous layer “Saw-tooth” rete pegs Liquefaction necrosis of basal layer Civatte ( hyaline or cytoid) bodies Juxta epithelial band of inflammatory cells
- 21. Immunofluorescent Studies Bandof fibrinogen in the basement membrane zone Multiple IgM staining cytoid bodies in dermal papilla or peribasalar area Highly suggestive of lichen planus if present in clusters
- 22. Differential Diagnosis Lichenoidreactions Leukoplakia Candidiasis Pemphigus Cicatricial pemphigoid Erythema multiforme Syphilis Recurrent aphthae Lupus erythematosus Squamous cell carcinoma
- 23. Malignant transformation Controversy Increased risk of oral squamous cell carcinoma Frequency of transformation is low, between 0.3% and 3% Erosive and atrophic forms commonly undergo transformation
- 25. Treatment No cure Management of symptoms Principal aims: resolution of painful symptoms, resolution of mucosal lesions, reduction of risk of cancer & maintenance of good oral hygiene Corticosteroids: both systemic & topical Topical: 0.05% fluocinonide ( Lidex) 0.05% clobetasol ( Temovate) as pastes or gels Candida overgrowth