Lichen planus is a common inflammatory skin disease. It is unique in that it can affect the skin, the mucous membranes, the nails, and the epithelium of the hair follicles. Lichen planus most commonly affects the skin, but the other areas can be involved either solely or in conjunction with one another. Lichen planus that involves the skin has a tendency to spontaneously remit within 1 to 2 years after onset, whereas the oral version is almost always chronic in nature.
Clinical Findings: Lichen planus can affect people at any age, but it is much more common in adulthood. It has no gender or racial predilection. The rash classically has been described as flat-topped, polygonal, pruritic, purple papules. Frequently, a whitish, lacy scale, referred to as Wickham’s striae, overlies the papules. Lichen planus is unusual in that the pruritus causes the patient to rub the area, rather than scratch. Lichen planus exhibits the Koebner phenomenon, and often areas of linear arrangement are seen secondary to trauma or rubbing. This is helpful when clinically examining a patient, because scratch marks and excoriations are rarely seen, whereas lichenification from repeated rubbing of the lesions is frequently seen. The rash has a tendency to be more prominent on flexural surfaces, especially of the wrists. The glans penis is another distinctive location in which lichen planus commonly occurs.
Many clinical variations of lichen planus have been described. An afflicted individual may have more than one morphology. Hypertrophic lichen planus has the appearance of thickened, scaly plaques with a rough or verrucal surface. There may be areas on the periphery that appear more classic in nature. This variant can be difficult to diagnosis clinically, and often a biopsy is required. It also can be difficult to treat effectively, and it runs a chronic course. Rarely, hypertrophic lichen planus has been reported to transform into malignant squamous cell carcinoma. Bullous lichen planus is an extremely uncommon variant that usually occurs on the lower extremities. The vesicle or bulla typically forms within the center of the lichen planus lesion.
Lichen planopilaris is the term given to describe lichen planus affecting the terminal hair follicles. This is most common on the scalp and leads to a scarring alopecia. The typical findings are small, erythematous patches surrounding each hair follicle. As the disease progresses, loss of hair follicles is observed, signifying that scarring is taking place. The central crown is the area most often affected. It is uncommon for the entire scalp to be affected. Once scarring has occurred, the hair loss is permanent. Lichen planopilaris runs a chronic waxing and waning clinical course.
Lichen planus may affect the mucous membranes of the oral cavity, the genital region, and the conjunctiva. These areas appear as glistening patches with lacy, white reticulations on the surface. Mucous membrane lichen planus has a higher tendency to ulcerate than the cutaneous form does. There have been reports of malignant transformation to squamous cell carcinoma. For this reason, long-term follow-up is required. Lichen planus may also affect the nail matrix and nail bed, leading to dystrophy and nail abnormalities. The most frequently seen nail abnormality is longitudinal ridging, but the most characteristic nail finding is pterygium formation.
Pathogenesis: Lichen planus appears to be mediated by an abnormal T-cell immune response. The T cells act locally on the keratinocytes to induce the clinical findings. The exact pathomechanism has yet to be described.
Histology: The lesions show characteristic findings that include a dense lichenoid lymphocytic infiltrate along the dermal-epidermal border. Necrotic keratinocytes are frequently encountered within the hyperplastic epidermis and have been named Civatte bodies. Hypergranulosis is a prominent feature as is the “saw- tooth” pattern of epidermal hyperplasia. The presence of eosinophils should lead one to consider the diagnosis of a lichen planus–like drug eruption or lichenoid contact dermatitis.
Treatment: Isolated lesions can be treated with topical corticosteroids. Up to two thirds of skin lesions resolve spontaneously. Patients with widespread disease present a therapeutic challenge. Ultraviolet phototherapy, oral corticosteroids, and oral retin ids such as acitretin and isotretinoin have been used.