Abstract
Lichen planus (LP) is a T cell-mediated disease affecting the stratified squamous epithelia of the skin and/or mucus membrane. Histologically, the disease is characterized by a lichenoid inflammatory infiltrate and vacuolar degeneration of the basal layer of the epidermis. LP has three major subtypes: Cutaneous, mucosal and appendageal LP. Rarely, it may affect the nails in the absence of skin and/or mucosal changes. LP may also be induced by several drugs, typically anti-hypertensive medication or be associated with infections, particularly viral hepatitis. The diagnosis is based on the clinical presentation and characteristic histological findings. Although the disease is often self-limiting, the intractable pruritus and painful mucosal erosions result in significant morbidity. The current first-line treatment are topical and/or systemic corticosteroids. In addition, immunosuppressants may be used as corticosteroid-sparing agents. These, however are often not sufficient to control disease. Janus kinase inhibitors and biologics (anti-IL-12/23, anti-IL17) have emerged as novel future treatment options. Thus, one may expect a dramatic change of the treatment landscape of LP in the near future.
Highlights
The term lichen planus (LP) stems from the Greek word “leichen,” which means “tree moss,” and the Latin word “planus,” which means “flat,” which aptly describes the surface of the cutaneous lesion [1]
LP is perceived as a T cell-mediated autoimmune disease, in which cytotoxic CD8+ Tcells are recruited into the skin and subsequently lead to an interface dermatitis [2,3,4,5,6,7,8]
Contact allergies may mimic lichen planus: Oral lichenoid lesions may be associated to type-IV-sensitization to mercury or dental amalgam [111, 112]; lichenoid skin lesions usually result from contact with rubber, chemicals used in clothing dyes or chemicals in wine industries [113]
Summary
Lichen planus (LP) is a T cell-mediated disease affecting the stratified squamous epithelia of the skin and/or mucus membrane. The disease is characterized by a lichenoid inflammatory infiltrate and vacuolar degeneration of the basal layer of the epidermis. LP has three major subtypes: Cutaneous, mucosal and appendageal LP. It may affect the nails in the absence of skin and/or mucosal changes. The disease is often self-limiting, the intractable pruritus and painful mucosal erosions result in significant morbidity. The current first-line treatment are topical and/or systemic corticosteroids. Janus kinase inhibitors and biologics (anti-IL-12/23, anti-IL17) have emerged as novel future treatment options. One may expect a dramatic change of the treatment landscape of LP in the near future
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