Sections

Lichen Planus

Overview

Practice Essentials

Lichen planus (LP; see the image below) 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 sclerosus, and myasthenia gravis. A rare type of LP, familial bullous lichen planus, could be gene-related. LP may be triggered by diuretics and antimalarials, metal fillings (causing oral LP), stress, and infection. It has been found to be associated with hepatitis C virus (HCV) infection.

Close-up view of lichen planus.

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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 with oral LP or with large, annular, hypertrophic lesions and mucous membrane involvement

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

Mucous membranes
Genitalia
Nails
Scalp

The clinical presentation of LP has several variations, as follows:

Hypertrophic LP
Atrophic LP
Erosive/ulcerative LP
Follicular LP (lichen planopilaris)
Annular LP
Linear LP
Vesicular and bullous LP
Actinic LP
LP pigmentosus
LP pemphigoides

See Clinical Presentation for more detail.

Diagnosis

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 LP 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.

Management

LP is a self-limited disease that usually resolves over several months but can sometimes take years to do so. It recurs in about 20% of patients, and it may linger for years, particularly oral LP. LP commonly results in postinflammatory hyperpigmentation and occasionally leaves hypertrophic scars, which may be the result of scratching. 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. Classic idiopathic LP characteristically is highly sensitive to corticosteroid treatment.

Pharmacologic therapies include the following:

Cutaneous LP - Topical steroids, particularly class I or II ointments (first-line treatment); systemic steroids; various oral agents (eg, metronidazole, acitretin, sulfasalazine, apremilast)^{[1, 2, 3, 4, 5]}; and other treatments of unproven efficacy (eg, mycophenolate mofetil)
LP of the oral mucosa - Topical steroids; topical calcineurin inhibitors (eg, tacrolimus, pimecrolimus); oral or topical retinoids (with close monitoring of lipid levels^[6])

Patients with widespread LP may respond to the following:

Narrowband or broadband ultraviolet (UV)-B radiation^{[7, 1, 2]}
Psoralen with UV-A (PUVA) radiation^{[1, 2]}; 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.

Next: Background

Background

Lichen planus (LP) is a pruritic eruption that can be associated with hepatitis C. Lesions are characteristically papular, purple or violaceous in color, polygonal, and often peripherally located on the distal extremities. LP has various distinct subtypes and clinical presentations, including but not limited to those affecting the genitalia or mucous membranes. Although the pathophysiology is unclear, it is an immunologically mediated reaction.

Next: Background

Pathophysiology

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

Associations have been noted between LP and hepatitis C virus (HCV) infection,^{[8, 9, 10, 11, 12, 13]}chronic active hepatitis, and primary biliary cirrhosis.^[14]In one meta-analysis, 16% of patients with LP had hepatitis C infection.^[10]This association has been shown to exist in all regions of the world, including North America.^[11]A workup for hepatitis C should be considered in patients with widespread or unusual presentations of LP. Onset or exacerbation of LP has also been linked to stressful events.^[15]

Next: Background

Etiology

The exact cause of LP has not been established, though the condition is known to be 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 infiltrate, effacing the dermoepidermal junction.

Some patients with LP have a positive family history.^[16]It has been noted that affected families have an increased frequency of human leukocyte antigen (HLA)-B7. Others have found an association between idiopathic LP and HLA-DR1 and HLA-DR10; thus, LP may be influenced by a genetic predisposition.

Next: Background

Epidemiology

US and international statistics

In the United States, LP 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.

Internationally, no significant geographical variation in frequency exists for LP.

Age-, sex-, and race-related demographics

More than two thirds of LP patients are between the ages of 30 and 60 years; however, LP can occur at any age.^[17]

No significant differences in the incidence of LP are noted between male and female patients; however, in women, LP may present as desquamative inflammatory vaginitis.^[18]

No racial predispositions have been noted for LP.

Next: Background

Prognosis

The prognosis for LP is good, in that most cases regress within 18 months. Some cases recur. In LP, atrophy and scarring are seen in hypertrophic lesions and in lesions on the scalp. Cutaneous LP does not carry a risk of skin cancer, but ulcerative lesions in the mouth, particularly in men, do occasionally exhibit malignant transformation; however, the rate of malignant transformation for oral LP is low (< 2% in one report).^[19]Vulvar lesions in women may also be associated with squamous cell carcinoma.

Next: Background

Patient Education

Patients should be informed about the self-limiting nature of LP. Because LP is not common, no large randomized controlled clinical trials have been conducted for therapy. It may be necessary to try several different treatments. Patients should also be told about the small likelihood of recurrence and the potential adverse effects from the various treatments offered.

Clinical Presentation

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Chuang TY, Stitle L, Brashear R, Lewis C. Hepatitis C virus and lichen planus: A case-control study of 340 patients. J Am Acad Dermatol. 1999 Nov. 41 (5 Pt 1):787-9. [QxMD MEDLINE Link].
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Bigby M. The relationship between lichen planus and hepatitis C clarified. Arch Dermatol. 2009 Sep. 145 (9):1048-50. [QxMD MEDLINE Link].
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Georgescu SR, Tampa M, Mitran MI, Mitran CI, Sarbu MI, Nicolae I, et al. Potential pathogenic mechanisms involved in the association between lichen planus and hepatitis C virus infection. Exp Ther Med. 2019 Feb. 17 (2):1045-1051. [QxMD MEDLINE Link].
Korkij W, Chuang TY, Soltani K. Liver abnormalities in patients with lichen planus. A retrospective case-control study. J Am Acad Dermatol. 1984 Oct. 11 (4 Pt 1):609-15. [QxMD MEDLINE Link].
Manolache L, Seceleanu-Petrescu D, Benea V. Lichen planus patients and stressful events. J Eur Acad Dermatol Venereol. 2008 Apr. 22 (4):437-41. [QxMD MEDLINE Link].
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Balasubramaniam P, Ogboli M, Moss C. Lichen planus in children: review of 26 cases. Clin Exp Dermatol. 2008 Jul. 33 (4):457-9. [QxMD MEDLINE Link].
Murphy R, Edwards L. Desquamative inflammatory vaginitis: what is it?. J Reprod Med. 2008 Feb. 53 (2):124-8. [QxMD MEDLINE Link].
Ingafou M, Leao JC, Porter SR, Scully C. Oral lichen planus: a retrospective study of 690 British patients. Oral Dis. 2006 Sep. 12 (5):463-8. [QxMD MEDLINE Link].
Belfiore P, Di Fede O, Cabibi D, Campisi G, Amarù GS, De Cantis S, et al. Prevalence of vulval lichen planus in a cohort of women with oral lichen planus: an interdisciplinary study. Br J Dermatol. 2006 Nov. 155 (5):994-8. [QxMD MEDLINE Link].
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Media Gallery

Lichen planus on flexor part of wrist.
Close-up view of lichen planus.
Lichen planus shows Wickham striae (white, fine, reticular lines).
Lichen planus on oral mucosa with ulceration in center of lesion appears with whitish papules and plaques in periphery.
Lichen planus lesion. Image from Syed Wali Peeran, with no alterations, Wikimedia Commons (https://commons.wikimedia.org/wiki/File:Lichen_planus-Skin_lesion.jpg).
Intraoral lichen planus lesion. Image from Syed Wali Peeran, with no alterations, Wikimedia Commons (https://commons.wikimedia.org/wiki/File:Lichen_planus-intra_oral_lesion.jpg).
Bandlike infiltrate of lymphocytes obscures dermoepidermal junction. Eosinophilic apoptotic keratinocytes (colloid bodies) are visible. Image from Clay Cockerell, MD, Cockerell Dermatopathology, Dallas, TX.
Higher-power view. Wedge-shaped hypergranulosis and individual degenerated keratinocytes are visible in addition to hyperkeratosis. Vacuolar degeneration is visible. Image from Clay Cockerell, MD, Cockerell Dermatopathology, Dallas, TX.

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#author-disclosures{display:block}#author-disclosures.modal-layer{position:relative}#author-disclosures .modal-content{max-height:none}#author-disclosures .close-modal{display:none}

Author

Lauren Abigail Hoffpauir Doctor of Osteopathy Candidate, Texas College of Osteopathic Medicine

Lauren Abigail Hoffpauir is a member of the following medical societies: American College of Osteopathic Surgeons, American College of Surgeons, American Society of Plastic Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Edward J Zabawski, Jr, DO Medical and Surgical Dermatology

Edward J Zabawski, Jr, DO is a member of the following medical societies: American Osteopathic Association, New England Dermatological Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Warren R Heymann, MD Head, Division of Dermatology, Professor, Department of Internal Medicine, Rutgers New Jersey Medical School

Warren R Heymann, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Emeritus Professor, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, American Contact Dermatitis Society, Association of Military Dermatologists, Association of Professors of Dermatology, American Dermatological Association, Women's Dermatologic Society, Medical Dermatology Society, Dermatology Foundation, Society for Investigative Dermatology, Washington DC Dermatological Society, Atlantic Dermatologic Society, Philadelphia Dermatological Society, Pennsylvania Academy of Dermatology, College of Physicians of Philadelphia

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier<br/>Served as a speaker for various universities, dermatology societies, and dermatology departments.

Additional Contributors

Laura Stitle, MD Staff Physician, Department of Dermatology, Indiana University Medical Center

Laura Stitle, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Tsu-Yi Chuang, MD, MPH, FAAD Clinical Professor, Department of Dermatology, Keck School of Medicine of the University of Southern California; Dermatologist, HealthCare Partners

Tsu-Yi Chuang, MD, MPH, FAAD is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, International Society of Dermatology

Disclosure: Nothing to disclose.

Joshua A Zeichner, MD Assistant Professor, Director of Cosmetic and Clinical Research, Mount Sinai School of Medicine; Chief of Dermatology, Institute for Family Health at North General

Joshua A Zeichner, MD is a member of the following medical societies: American Academy of Dermatology, National Psoriasis Foundation

Disclosure: Received consulting fee from Valeant for consulting; Received grant/research funds from Medicis for other; Received consulting fee from Galderma for consulting; Received consulting fee from Promius for consulting; Received consulting fee from Pharmaderm for consulting; Received consulting fee from Onset for consulting.