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Oral Lichen Planus

  • Author: Philip B Sugerman, MDS, PhD; Chief Editor: William D James, MD  more...
 
Updated: Sep 21, 2015
 

Background

Oral lichen planus (OLP) is a chronic inflammatory disease that causes bilateral white striations, papules, or plaques on the buccal mucosa, tongue, and gingivae. Erythema, erosions, and blisters may or may not be present. Note the images below.

Plaquelike oral lichen planus on the buccal mucosa Plaquelike oral lichen planus on the buccal mucosa on the left side.
Reticular oral lichen planus on the buccal mucosa Reticular oral lichen planus on the buccal mucosa on the left side.
Ulcerative oral lichen planus on the dorsum of the Ulcerative oral lichen planus on the dorsum of the tongue.
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Pathophysiology

Current data suggest that oral lichen planus is a T-cell–mediated autoimmune disease in which autocytotoxic CD8+ T cells trigger apoptosis of oral epithelial cells.[1, 2, 3]

The dense sub-epithelial mononuclear infiltrate in oral lichen planus is composed of T cells and macrophages, and there are increased numbers of intra-epithelial T cells. Most T cells in the epithelium and adjacent to the damaged basal keratinocytes are activated CD8+ lymphocytes. Therefore, early in the formation of oral lichen planus lesions, CD8+ T cells may recognize an antigen associated with the major histocompatibility complex (MHC) class I on keratinocytes. After antigen recognition and activation, CD8+ cytotoxic T cells may trigger keratinocyte apoptosis. Activated CD8+ T cells (and possibly keratinocytes) may release cytokines that attract additional lymphocytes into the developing lesion.[2]

Oral lichen planus lesions contain increased levels of the cytokine tumor necrosis factor (TNF)–alpha.[4, 5] Basal keratinocytes and T cells in the subepithelial infiltrate express TNF in situ.[6, 7] Keratinocytes and lymphocytes in cutaneous lichen planus express elevated levels of the p55 TNF receptor, TNF-RI.[8] T cells in oral lichen planus contain mRNA for TNF and secrete TNF in vitro.[9] Serum and salivary TNF levels are elevated in oral lichen planus patients.[10, 11, 12, 13] TNF polymorphisms have been identified in patients with oral lichen planus, and they may contribute to the development of additional cutaneous lesions.[14] Oral lichen planus has been treated successfully with thalidomide,[15, 16] , while thalidomide is known to suppress TNF production.[17, 18] Together, these data implicate TNF in the pathogenesis of oral lichen planus.

The lichen planus antigen is unknown, although it may be a self-peptide (or altered self-peptide), in which case lichen planus would be a true autoimmune disease. The role of autoimmunity in the pathogenesis is supported by many autoimmune features of oral lichen planus, including its chronicity, onset in adults, predilection for females, association with other autoimmune diseases, occasional tissue-type associations, depressed immune suppressor activity in patients with oral lichen planus, and the presence of autocytotoxic T-cell clones in lichen planus lesions. The expression or unmasking of the lichen planus antigen may be induced by drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), viral infection, or other unidentified agents.[19, 20, 21]

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Epidemiology

Frequency

United States

The prevalence of oral lichen planus in the United States is unknown.

International

Oral lichen planus affects approximately 1-2% of the general adult population, although the prevalence of the disease is unknown in many areas.[22] Oral lichen planus is a common noninfectious oral mucosal disorder among adult patients who attend oral pathology and oral medicine clinics.

Race

Oral lichen planus affects all racial groups.

Sex

The female-to-male ratio for oral lichen planus is 1.4:1.

Age

Oral lichen planus predominantly occurs in adults older than 40 years, although younger adults and children can be affected.

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Contributor Information and Disclosures
Author

Philip B Sugerman, MDS, PhD Senior Clinical Science Manager, Abbott Immunology, Abbott Laboratories

Philip B Sugerman, MDS, PhD is a member of the following medical societies: American Academy of Oral and Maxillofacial Pathology, International Association for Dental Research

Disclosure: Nothing to disclose.

Coauthor(s)

Stephen R Porter, MD, PhD FDS RCS, FDS RSE, Professor of Oral Medicine, University College London; Academic Head, Director of Research Strategy, Oral Medicine/Special Needs Unit, Division of Maxillofacial Diagnostic, Medical and Surgical Sciences, Eastman Dental Institute for Oral Health Sciences

Stephen R Porter, MD, PhD is a member of the following medical societies: British Association of Oral and Maxillofacial Surgeons, Royal College of Surgeons of England, Royal Society of Medicine, Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, 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, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Gregory J Raugi, MD, PhD Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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Plaquelike oral lichen planus on the buccal mucosa on the left side.
Reticular oral lichen planus on the buccal mucosa on the left side.
Ulcerative oral lichen planus on the dorsum of the tongue.
 
 
 
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