Lichen planus is a subacute or chronic inflammatory skin disease of complex etiology that occurs on the skin and mucous membranes. Approximately 2/3 of cases develop between the ages of 30-60 years, and a higher incidence of the disease has been reported in winter and spring.
Etiology and pathogenesis: The disease is a T cell-mediated autoimmune inflammatory disease in which autoantigens are antigens that have been altered on the surface of basal keratin-forming cells and cause damage to these cells. There is an association between the development of the disease and exposure to some exogenous antigens (e.g., viruses, drugs, contact allergens). Antigen-presenting cells in the skin present key components of exogenous antigens, induce the production of potentially cytotoxic effector T cells, produce a variety of inflammatory cytokines, and subsequently trigger a process of inflammatory response in the body.
Clinical manifestations: Typical lesions are purple-red or purple-blue polygonal flat papules with clear boundaries and waxy luster, positive Wickham’s striae; 50% of patients may have mucosal damage, manifesting as reticular white or gray-white keratotic plaques or plaques, or as vesicular or maculopapular lesions; some patients have nail damage, manifesting as nail plate thinning, longitudinal ridges, distal nail plate splitting, nail lysis, hyperkeratosis, etc. Some patients have nail damage, including thinning of the nail plate, longitudinal ridges, splitting of the distal nail plate, nail lysis and hyperkeratosis under the nail. Depending on the onset of the disease and the morphology and arrangement of the lesions, there are various clinical manifestations or subtypes: annular lichen planus, linear lichen planus, hypertrophic lichen planus, atrophic lichen planus, herpetic lichen planus, vesicular/ulcerative lichen planus, follicular lichen planus, solar lichen planus, etc. Sometimes lichen planus occurs together with lupus erythematosus and is called lichen planus-lupus erythematosus overlap syndrome. A few patients who develop ulcers may develop squamous cell carcinoma.
Histopathology: hyperkeratosis of the epidermis, thickening of the granular layer often wedge-shaped, irregular thickening of the spiny layer, jagged epidermal protrusions, liquefaction and deformation of basal cells at the epidermal-dermal junction, occasionally some of the following epidermis, dyskeratotic cells in the epidermis or dermal papillae, band-like infiltration of dense lymphocytes in the upper dermis; red-stained gelatinous vesicles and melanophages in the epidermal papillae.
Treatment: It is difficult to evaluate the efficacy of different treatments for lichen planus because most treatment reports are small samples or case reports. Currently, it is believed that well-established treatment regimens for lichen planus include topical, intralesional injections and systemic systemic application of glucocorticoids, retinoid preparations, immunosuppressants, immunomodulators, antihistamines, hydroxychloroquine, and topical application of calcium phosphatase inhibitors.