In the hypertrophic form of the disease, papules coalesce to form thick plaques or nodules that are often found on the lower extremities. Pruritus may be severe, particularly in the generalized or hypertrophic forms of the disease. Common sites of involvement are the flexor surfaces of the wrists, the sacrum, the mucous membranes of the mouth, the medial thighs, and the genitalia. A follicular form known as lichen planopilaris may result in scarring alopecia. Variants of lichen planus with distinct morphologic features include actinic, annular, bullous, hypertrophic, linear, ulcerative, and zosteriform forms.
Skin biopsy confirms the clinical diagnosis.
Characteristically, the epidermis shows hyperkeratosis, a prominent granular layer, liquefaction degeneration of the basal cell layer, and an intense upper dermal inflammatory infiltrate. Immunoperoxidase studies using monoclonal antibodies to cell surface antigens have shown that the majority of cells in the infiltrate are of the helper-inducer T cell subset. Colloid bodies coated with immunoglobulin are frequently seen in the dermal papillae. On ultrastructural examination, numerous Langerhans cells can be observed at the dermoepidermal junction. The etiology of lichen planus is unknown.