Lichen Planus

Etiology • Unknown • Autoimmune T cell–mediated disease targeting basal ker-
atinocytes (antigen unknown) • Lichenoid changes associated with galvanism, graft-versus-host
disease (GVHD), certain drugs, contact allergens
Clinical Presentation • Up to 3 to 4% of population have oral lichen planus • 0.5 to 1% of population have cutaneous lichen planus; 50%
also have oral lesions (25% with oral lesions have concomitant skin lesions)

• White females (60%) • Occurs in fourth to eighth decades • Variants: reticular (most common oral form); erosive (painful);
atrophic, papular, plaque types; bullous (rare) • Bilateral and often symmetric distribution • Oral site frequency: buccal mucosa (most frequent), then
tongue, then gingiva, then lips (least frequent) • Skin sites: forearm, shin, scalp, genitalia
Microscopic Findings • Hyperkeratosis • Basal keratinocyte necrosis • Lymphocytes at epithelial-connective tissue interface
Diagnosis • Examination of oral mucosa, skin, genitalia • Negative ocular mucosa history; no history of blistering • Use of drugs, galvanism, GVHD to be ruled out • Biopsy • Direct immunofluorescence–fibrinogen and cytoid bodies at
interface help confirm
Differential Diagnosis • Lichenoid drug eruptions • Erythema multiforme • Lupus erythematosus • Contact stomatitis • Mucous membrane pemphigoid
Treatment of Oral Lichen Planus • Mild to moderate: topical corticosteroids • Severe: systemic immunosuppression, chiefly with prednisone • Corticosteroid-sparing drugs with prednisone • Topical tacrolimus ointment
Prognosis • Control, not cure, can be expected. • Good prognosis; rare malignant transformation (0.5–3%) • May be cyclic; may last for years/decades • Tends to be chronic