- Lichen planus (LP) is a pruritic eruption that may be self-limited or chronic, and may affect skin, mucosa (including the esophagus), and hair.
- The classic morphology of lichen planus is violaceous-to-purple, flat-topped polygonal papules, often with a white-to-lavender reticulate overlying scale (Wickham’s striae). They may occur in areas of prior trauma or injury (koebnerization).
- The prevalence of hepatitis C viral (HCV) infection-not hepatitis B-is higher in patients with lichen planus; viral screening should be considered for patients with lichen planus, especially if potential HCV risk factors are present.
- Different variants of lichen planus exist: oral, follicular, erosive, actinic lichen planus, lichen planus pigmentosum, annular, atrophic, bullous, and hypertrophic.
- Erosive forms of lichen planus, especially of the oral mucosa, genitalia, and rarely of the skin, may be complicated by the development of squamous cell carcinoma.
- Lichen planus may be triggered by or found in association with exogenous factors, such as medications or contact allergens; a treatable cause should always be sought. Nearly 40% of patients with oral lichen planus may have a contact hypersensitivity to metallic dental prosthetics (containing mercury, copper, or gold).
- Treatment of lichen planus may involve high-potency topical corticosteroids but may require systemic immunosuppression in severe cases.
Lichen planus may be self-limited or chronic and presents as localized or generalized disease, usually with mild to severe pruritus. It affects 0.5-2% of the population, with women more commonly affected than men (3:1 female to male ratio in one study), presenting typically between the fourth and sixth decade of life. Lesions of lichen planus may present across a wide clinical spectrum and distribution. Occasionally, patients have ulcerative, painful lesions; such erosive lesions of lichen planus may be complicated by the development of squamous cell carcinoma. Patients with lichen planus are now recognized to have a higher prevalence of HCV infection (odds ratio of 4.85, 95% CI, 3.58-6.56) than in individuals who do not have lichen planus (see references Lodi et al., 2010 and Birkenfeld et al., 2011); there is no known association between lichen planus and hepatitis B viral infection. Screening for HCV should be strongly considered for patients with lichen planus, especially if potential HCV risk factors are present.
The pathogenesis of lichen planus is poorly understood. It may be incited by trauma or infection (such as hepatitis C) and is likely mediated by CD8+ T lymphocytes. Furthermore, genetic polymorphisms in the interferon-gamma gene promoter may increase susceptibility to oral lichen planus.
The aim of therapy is to control symptoms and therefore must be appropriate to the extent and severity of the disease. Given that the disease is often chronic in nature, a judicious approach to controlling inflammation is advised. Localized forms can often be managed with topical or intralesional therapy; in rare severe cases, or in cases where scarring or alopecia can result, systemic immunosuppression should be considered. Generalized forms often require systemic treatment, such as immunosuppression or phototherapy. Specific variants, such as erosive disease, require additional monitoring for evolution of squamous cell carcinoma, a rare clinical complication of the disease in which the true incidence is controversial.
Lesions of lichen planus are marked by violaceous-to-purple flat-topped papules, often with a white-to-lavender reticulate overlying scale (Wickham’s striae). Patients report intense pruritus and sometimes koebnerization (development of lesions at areas of trauma/ injury). Presentation is almost always bilateral and symmetric. Oral mucosa is commonly affected (15% of cases), and buccal mucosal disease is present in 90% of cases of oral lichen planus. When oral involvement is present, patients may subjectively complain of discomfort, stinging, or pain due to hot foods and drinks. Lesions may be found less frequently around the anus and on the genitalia. When the palms and soles are affected, the lesions may be firm and rough with a yellowish hue.