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  • Lichen planus is an autoimmune inflammatory mucocutaneous condition affecting the skin, mucosal surfaces, scalp, or nails.

  • Evidence suggests that lichen planus is due to altered self-antigens on basal keratinocytes, a process that appears to be multifactorial.

  • Lichen planus has a multitude of clinical variants, including some actinic variants that occur in darker skin types.

  • Lichen nitidus is characterized by clusters of numerous, tiny, discrete, skin-colored, uniform, pinhead-sized papules.

  • Histology of lichen nitidus reveals a ‘ball and claw’ arrangement.

  • There is an actinic variant of lichen nitidus that occurs predominantly in people with more darkly pigmented skin.


Lichen planus (LP) is an autoimmune inflammatory mucocutaneous condition that can affect the skin, oral mucosa, scalp, or nails. LP is often idiopathic but at times may be linked to drugs (eg, penicillamine, gold, angiotensin-converting enzyme [ACE] inhibitors, antimalarials, or quinidine) or viral infections (especially hepatitis C virus [HCV] infection). Topical steroids are used to treat localized LP, whereas systemic steroids and other modalities are used to treat patients with generalized LP.1


LP affects from 0.22% to 1% of the adult population,2 whereas oral LP (OLP) affects 1% to 4%.3 There is no apparent racial predisposition. Worldwide incidence varies from 0.29% in those of African descent to 0.1% to 1% in East Indians.4 Two-thirds of patients develop the disease between the ages of 30 and 60 years.5 There is a slight predominance in women, although some authors report women being affected twice as often as men.1,4,5 Women tend to develop the disease later in life in comparison to men (sixth vs fourth decade).2 There may be a small genetic component to LP because 1% to 2% of cases are familial.6

OLP may be found in 50% to 75% of cases of cutaneous LP.7,8 Cutaneous LP is found in 10% to 20% of OLP cases. Of patients with LP of any form, 25% will have solely mucosal involvement.8


A growing body of evidence suggests that LP represents a T-cell–mediated autoimmune process directed against basal keratinocytes that express altered self-antigens on their surfaces.8 How these altered self-antigens arise appears to be multifactorial.

The role of viruses has been investigated to explain the origin of antigens in the generation of effector T-cells with cytotoxic potential. HCV is one of the suspected viruses. Several case-control studies have found that HCV is more prevalent in LP populations than in controls by 4% to 38%.6,9 Conversely, it has been reported that 5% of all HCV patients have LP.6 HCV is believed to be more commonly associated with OLP than cutaneous LP. Moreover, HCV RNA has been found in 93% of OLP lesions via the ...

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