Lichen planus is a recurrent, pruritic, inflammatory eruption characterized by small, discrete, polygonal, flat-topped, violaceous papules that may coalesce into rough scaly plaques, often accompanied by oral and/or genital lesions. Diagnosis is usually clinical and supported by skin biopsy. Treatment generally requires topical or intralesional corticosteroids. Severe cases may require phototherapy or systemic corticosteroids, retinoids, or immunosuppressants.
Lichen planus (LP) is thought to be caused by a T cell–mediated autoimmune reaction against basal epithelial keratinocytes in people with genetic predisposition. Drugs (especially beta-blockers, NSAIDs, ACE inhibitors, sulfonylureas, gold, antimalarial drugs, penicillamine, and thiazides) can cause LP; drug-induced LP (sometimes called lichenoid drug eruption) may be indistinguishable from nondrug-induced LP or may have a pattern that is more eczematous.
Typical lesions are pruritic, violaceous (purple), polygonal, flat-topped papules and plaques. Lesions initially are 2 to 4 mm in diameter, with angular borders and a distinct sheen in cross-lighting. They are usually symmetrically distributed, most commonly on the flexor surfaces of the wrists, legs, trunk, glans penis, and oral and vaginal mucosae but can be widespread. The face is rarely involved. Onset may be abrupt or gradual. Children are affected infrequently.
During the acute phase, new papules may appear at sites of minor skin injury (Koebner phenomenon), such as a superficial scratch. Lesions may coalesce or change over time, becoming hyperpigmented, atrophic, hyperkeratotic (hypertrophic LP), or vesiculobullous. Although pruritic, lesions are rarely excoriated or crusted. If the scalp is affected, patchy scarring alopecia (lichen planopilaris) may occur.
The oral mucosa is involved in about 50% of cases; oral lesions may occur without cutaneous lesions. Reticulated, lacy, bluish white, linear lesions (Wickham striae) are a hallmark of oral LP, especially on the buccal mucosae. Tongue margins and gingival mucosae in edentulous areas may also be affected. An erosive form of LP may occur in which the patient develops shallow, often painful, recurrent oral ulcers, which, if long-standing, rarely become cancerous. Chronic exacerbations and remissions are common.
Vulvar and vaginal mucosae are often involved. Up to 50% of women with oral mucosal findings have undiagnosed vulvar LP. In men, genital involvement is common, especially of the glans penis.
Nails are involved in up to 10% of cases. Findings vary in intensity with nail bed discoloration, longitudinal ridging and lateral thinning, and complete loss of the nail matrix and nail, with scarring of the proximal nail fold onto the nail bed (pterygium formation).
Although the diagnosis of lichen planus is suggested by appearance of the lesions, similar lesions may result from any of the papulosquamous disorders, lupus erythematosus, and secondary syphilis, among others. Oral or vaginal LP may resemble leukoplakia, and the oral lesions must also be distinguished from candidiasis, carcinoma, aphthous ulcers, pemphigus, mucous membrane (cicatricial) pemphigoid, and chronic erythema multiforme. Typically, biopsy is done.
If LP is diagnosed, laboratory testing for liver dysfunction, including hepatitis B and C infections, should be considered.
Many cases resolve without intervention, presumably because the inciting agent is no longer present. Recurrence after years may be due to reexposure to the trigger or some change in the triggering mechanism. Sometimes treatment of a previously occult infection, such as a dental abscess, results in resolution.
Vulvovaginal LP may be chronic and refractory to therapy, causing decreased quality of life and vaginal or vulvar scarring. Oral mucosal lesions usually persist for life.
Asymptomatic LP does not require treatment. Drugs suspected of triggering LP should be stopped; it can takes weeks to months after the offending drug has been stopped for the lesions to resolve.
Few controlled studies have evaluated treatments. Options differ by location and extent of disease. Most cases of LP on the trunk or extremities can be treated with topical treatments. Topical corticosteroids are first-line treatment for most cases of localized disease. High-potency ointments or creams (eg, clobetasol, fluocinonide) may be used on the thicker lesions on the extremities; lower-potency drugs (eg, hydrocortisone, desonide) may be used on the face, groin, and axillae. As always, courses should be limited to reduce risk of corticosteroid atrophy. Potency may be enhanced with use of polyethylene wrapping or flurandrenolide tape. Intralesional corticosteroids (triamcinolone acetonide solution diluted with saline to 5 to 10 mg/mL) can be used every 4 wk for hyperkeratotic plaques, scalp lesions, and lesions resistant to other therapies.
Local therapy is impractical for generalized LP; oral drugs or phototherapy is used. Oral corticosteroids (eg, prednisone 20 mg once/day for 2 to 6 wk followed by a taper) may be used for severe cases. The disease may rebound when therapy ceases; however, long-term systemic corticosteroids should not be used.
Oral retinoids (eg, acitretin 30 mg once/day for 8 wk) are indicated for otherwise recalcitrant cases. Griseofulvin 250 mg po bid given for 3 to 6 mo may be effective. Cyclosporine (1.25 to 2.5 mg/kg bid) can be used when corticosteroids or retinoids fail. Light therapy using psoralen plus ultraviolet A (PUVA) or narrowband ultraviolet B (NBUVB) is an alternative to oral therapies, especially if they have failed or are contraindicated.
Dapsone, hydroxychloroquine, azathioprine, systemic cyclosporine, and topical tretinoin may also be useful. As with any disease with so many therapies, individual drugs have not been uniformly successful.
Treatment of oral LP differs slightly. Viscous lidocaine may help relieve symptoms of erosive ulcers; because inflamed mucous membranes can absorb high amounts, dose should not exceed 200 mg (eg, 10 mL of a 2% solution) or 4 mg/kg (in children) qid. Tacrolimus 0.1% ointment applied twice daily may induce lasting remission, although it has not been fully evaluated.
Other treatment options include topical (in an adhesive base), intralesional, and systemic corticosteroids.
Erosive oral LP may respond to oral dapsone, hydroxychloroquine, or cyclosporine. Cyclosporine rinses also may be helpful.
Lichen planus (LP) is thought to be an autoimmune disorder in patients with a genetic predisposition but may be caused by drugs or be associated with disorders such as hepatitis C.
LP is characterized by recurrent, pruritic papules that are polygonal, flat-topped, and violaceous and can coalesce into plaques.
Oral and genital lesions can develop, become chronic, and cause morbidity.
Diagnose LP by clinical appearance and, if necessary, biopsy.
Treat localized LP with topical or injected corticosteroids.
Treat generalized LP with oral drugs or phototherapy.