Lichen Planus

Updated: Feb 24, 2020
  • Author: Tsu-Yi Chuang, MD, MPH, FAAD; Chief Editor: William D James, MD  more...
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Practice Essentials

Lichen planus is a cell-mediated immune response of unknown origin. It may be found with other diseases of altered immunity, such as ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis. A rare type of lichen planus, familial bullous lichen planus, could be gene-related. It may be triggered by diuretics and antimalarials, metal fillings (causing oral lichen planus), stress, and infection. Lichen planus (see the image below) has been found to be associated with hepatitis C virus infection. [1, 2, 3, 4, 5, 6]

Close-up view of lichen planus. Close-up view of lichen planus.

Signs and symptoms

The following may be noted in the patient history:

  • Lesions initially developing on flexural surfaces of the limbs, with a generalized eruption developing after a week or more and maximal spreading within 2-16 weeks

  • Pruritus of varying severity, depending on the type of lesion and the extent of involvement

  • Oral lesions that may be asymptomatic, burning, or even painful

  • In cutaneous disease, lesions typically resolve within 6 months (>50%) to 18 months (85%); chronic disease is more likely oral lichen planus or with large, annular, hypertrophic lesions and mucous membrane involvement

In addition to the widespread cutaneous eruption, lichen planus can involve the following structures:

  • Mucous membranes

  • Genitalia

  • Nails

  • Scalp

The clinical presentation of lichen planus has several variations, as follows:

  • Hypertrophic lichen planus

  • Atrophic lichen planus

  • Erosive/ulcerative lichen planus

  • Follicular lichen planus (lichen planopilaris)

  • Annular lichen planus

  • Linear lichen planus

  • Vesicular and bullous lichen planus

  • Actinic lichen planus

  • Lichen planus pigmentosus

  • Lichen planus pemphigoides

See Clinical Presentation for more detail.


Direct immunofluorescence study reveals globular deposits of immunoglobulin M (IgM) and complement mixed with apoptotic keratinocytes. No imaging studies are necessary.

Distinguishing histopathologic features of lichen planus include the following:

  • Hyperkeratotic epidermis with irregular acanthosis and focal thickening in the granular layer

  • Degenerative keratinocytes (colloid or Civatte bodies) in the lower epidermis; in addition to apoptotic keratinocytes, colloid bodies are composed of globular deposits of IgM (occasionally immunoglobulin G [IgG] or immunoglobulin A [IgA]) and complement

  • Linear or shaggy deposits of fibrin and fibrinogen in the basement membrane zone

  • In the upper dermis, a bandlike infiltrate of lymphocytic (primarily helper T) and histiocytic cells with many Langerhans cells

See Workup for more detail.


Lichen planus is a self-limited disease that usually resolves within 12-18 months. It recurs often, in about 20% of patients, and it may linger for years, particularly oral lichen planus. Lichen planus usually leaves hypertrophic scars and dark brown postinflammatory hyperpigmentation. Mild cases can be treated with fluorinated topical steroids. More severe cases, especially those with scalp, nail, and mucous membrane involvement, may necessitate more intensive therapy.

Pharmacologic therapies include the following:

  • Cutaneous lichen planus: Topical steroids, particularly class I or II ointments (first-line treatment); systemic steroids; oral regimens like metronidazole, acitretin, methotrexate, hydroxychloroquine, griseofulvin, and sulfasalazine [7, 8, 9, 10] ; and other treatments with unproven efficacy (eg, mycophenolate mofetil)

  • Lichen planus of the oral mucosa: Topical steroids; topical calcineurin inhibitors (eg, tacrolimus, pimecrolimus); oral or topical retinoids (with close monitoring of lipid levels [11] )

Patients with widespread lichen planus may respond to the following:

  • Narrow-band or broadband UV-B radiation [12, 7, 8]

  • Psoralen with UV-A (PUVA) radiation; [7, 8] use of topical ointment at the time of UV-A treatment may decrease the effectiveness of PUVA; precautions should be taken for persons with a history of skin cancers or hepatic insufficiency

See Treatment and Medication for more detail.



Lichen planus (LP) is a pruritic eruption commonly associated with hepatitis C. Lesions are characteristically papular, purple (violaceous color), polygonal, and peripherally located (eg. on the distal extremities). LP may also affect the genitalia or mucous membranes. It is most likely an immunologically mediated reaction, though the pathophysiology in unclear. See Oral Lichen Planus for more information on this variant of lichen planus.



Lichen planus is a cell-mediated immune response of unknown origin. It may be found with other diseases of altered immunity; these conditions include ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis.

An association is noted between lichen planus and hepatitis C virus infection, [2, 3, 4, 5, 6] chronic active hepatitis, and primary biliary cirrhosis. [13] In one meta-analysis, 16% of patients with LP had hepatitis C infection. [3] This association has been shown to exist in all regions of the world, including North America. [4] A workup for hepatitis C should be considered in patients with widespread or unusual presentations of lichen planus. Onset or exacerbation of lichen planus has also been linked to stressful events. [14]



The exact cause of lichen planus is not known, although it is immunologically mediated. The initiating antigen is unclear; however, Langerhans cells process the antigen to T lymphocytes, resulting in an epidermotropic infiltrate. Histologically, the inflammation is described as a lichenoid infiltrated, effacing the dermo-epidermal junction.

Some patients with lichen planus have a positive family history. It has been noted that affected families have an increased frequency of human leukocyte antigen B7 (HLA-B7). Others have found an association between idiopathic lichen planus and human leukocyte antigen DR1 (HLA-DR1) and human leukocyte antigen DR10 (HLA-DR10); thus, lichen planus may be influenced by a genetic predisposition.




United States

Lichen planus is reported in approximately 1% of all new patients seen at health care clinics. Some areas have reported a higher incidence in December and January.


No significant geographical variation in frequency exists for lichen planus.


No racial predispositions have been noted for lichen planus.


No significant differences in incidence for lichen planus are noted between male and female patients, but in women, lichen planus may present as desquamative inflammatory vaginitis. [15]


More than two thirds of lichen planus patients are aged 30-60 years; however, lichen planus can occur at any age. [16]



The prognosis for lichen planus is good, as most cases regress within 18 months. Some cases recur. In lichen planus, atrophy and scarring are seen in hypertrophic lesions and in lesions on the scalp. Cutaneous lichen planus does not carry a risk of skin cancer, but ulcerative lesions in the mouth, particularly in men, do have a low rate of malignant transformation. However, the malignant transformation rate of oral lichen planus is low (< 2% in one report). [17] Vulvar lesions in women may also be associated with squamous cell carcinoma.


Patient Education

Patients should be told about the self-limiting nature of lichen planus. Because lichen planus is not common, no large, randomized, controlled clinical trials have been conducted for therapy. Several treatments may need to be tried.

Patients should be told about the small likelihood of recurrence and the potential adverse effects from the various treatments offered.