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Clinical Updates

Oral Lichen Planus

Tuesday, September 23, 2008

Oral lichen planus (OLP) is as common as psoriasis and affects approximately 1-2% of the population.1 The disease develops in women more than twice as often as in men and most commonly occurs in the fifth to sixth decade of life; although, the disease can sometimes affect children.2, 3 In patients with OLP, cutaneous disease develops in approximately 15% and vulvar and/or vaginal involvement in 25%. However, scalp, nail, esophageal and ocular involvement are uncommon.4 cutaneous lesions of lichen planus (LP) are self-limiting and pruritic,5 whereas oral lesions are chronic, rarely undergo spontaneous remission, potentially premalignant, and are often a source of morbidity and difficult to palliate.

OLP may manifest in one of three clinical forms: 1) reticular, including raised hyperkeratotic papules and plaques; 2) erythematosus, including atrophic lesions; and 3) erosive, including ulcerated and bullous lesions. Reticular lesions, the most recognized form of OLP, often occur as isolated lesions and may be the only clinical manifestation of the disease. Erythematous lesions are accompanied by reticular lesions and erosive lesions are accompanied by reticular and erythematous lesions in almost all cases. This feature helps clinically differentiate OLP from other diseases such as pemphigus and pemphigoid, which are characterized by isolated areas of erythema and/or erosions. Erythematous and erosive lesions result in varying degrees of pain as well as burning, swelling, irritation, and bleeding with brushing.

The diagnosis of OLP can be made from the clinical features if they are sufficiently characteristic, particularly if typical skin lesions are also present, but biopsy is recommended to confirm the diagnosis.

OLP develops most frequently on the posterior buccal mucosa followed by the tongue, gingiva, labial mucosa, and vermilion of the lower lip. Lesions on the palate, floor of the mouth, and upper lip are uncommonly observed. Approximately 10% of patients with OLP have the disease confined to the gingiva and present as raised white lacy lesions or more commonly as desquamative gingivitis, typically with atrophic and erosive lesions. Direct immunofluorescence is an effective method of excluding other causes of desquamative gingivitis that share similar clinical features with OLP, including pemphigus, pemphigoid, linear IgA disease and foreign body gingivitis.6

Oral lichenoid reactions, eruptions in the oral cavity that have an identifiable etiology and that clinically and histologically resemble OLP, are well recognized. An allergy or toxic reaction should be suspected when OLP lesions are confined to areas of the oral mucosa in close contact with amalgam restorations, especially fillings that are worn and cracked. When identified, such lesions show considerable improvement after replacement of the filling. Although uncommon, drug-induced oral lichenoid reactions are reversible upon withdrawal of the implicated drug. Therefore, a thorough medication history, with emphasis on non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors, is warranted. Many drugs implicated in cutaneous lichenoid reactions have not been associated with oral lesions.

An association between hepatitis C virus (HCV) infection and OLP has been investigated, but studies have been inconsistent. While many reports have demonstrated a significant association of the two diseases in Southern Europe and in Asia, studies from Northern Europe and North America failed to demonstrate any link.7 These conflicting results may be related to genetic factors however, with further prospective studies warranted.

The development of squamous cell carcinoma is controversial but is the most feared complication of OLP. Studies of the malignant potential of OLP have been fraught with inconsistencies in the diagnostic criteria of OLP and the criteria adopted to identify a true case of malignant transformation. The reported frequency of malignant transformation varies between 0.4% to over 5% over periods of observation from 0.5 to over 20 years, with almost all carcinomas developing in patients with atrophic and/or erosive lesions.8 Given the uncertainty of the premalignant nature of OLP and the fact that early detection of oral cancer results in improved survival, it seems prudent to monitor all patients with OLP carefully and long term.

Topical corticosteroids are the mainstay of treatment of OLP with 65% to 100% responding at least partially.9 Generally, higher potency preparations appear to be most effective, achieving a rapid response; one should lower the strength of the steroid as soon as erosions heal and erythematous lesions become asymptomatic. Once the disease becomes inactive with only white reticular lesions present, therapy may be temporarily discontinued.

For intractable erosive OLP lesions, intralesional triamcinolone (10-20 mg/ml) injections can be highly effective and repeated every several weeks.

Potent topical immunosuppressants such as cyclosporine, tacrolimus, and pimecrolimus are beneficial for OLP.10-12 The high cost of cyclosporine precludes its routine use although utilizing a small quantity of drug reduces the cost. In small controlled studies, both pimecrolimus and tacrolimus reduced the symptoms and signs of OLP. Burning was the most common side effect of each. Tacrolimus may be at least as equally effective or more effective than potent topical steroids. However, relapses of OLP after cessation of therapy is expected with calcineurin inhibitors. When I use one of these agents, I do so in conjunction with a topical steroid using both twice daily. Given the Food and Drugs Administration (FDA) warning about calcineurin inhibitors and the potential association with an increased risk of cancer, the long-term use of these drugs for this chronic disease may be limited.

A number of systemic immunosuppressive agents have been anecdotally reported to be beneficial in the treatment of OLP.13  Based upon my personal experience of treating over two thousand patients, I have found that methotrexate (12.5-20 mg/week), azathioprine (100-150 mg/day), mycophenolate mofetil (1-2 g/day), and hydroxychloroquine (400 mg/day) are the most useful systemic agents. We and others have also been using thalidomide and tumor necrosis factor (TNF)-alpha inhibitors for refractory cases. Although none of these agents provide long-term remission, significant clinical benefits are achieved and maintained with long term administration. It is unclear whether reducing inflammation by aggressive therapy influences the malignant transformation of the disease.

Finally, it is important to minimize or eliminate exacerbating factors such as heat and irritation from tobacco products, friction from sharp cusps, rough dental restorations and poorly fitting dental prostheses, and oral habits including lip and cheek chewing. OLP lesions will then either revert to the less severe forms of the disease or resolve completely.


  1. Scully C, Beyli M, Ferreiro MC, et al. Update on oral lichen planus; etiopathogenesis and management. Crit Rev Oral Biol Med. 1998;9:86-122.
  2. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol. 2002;46:207-214.
  3. Nanda A, Al-Ajmi HS, Al-Sabah H, et al. Childhood lichen planus: a report of 23 cases.Pediatr Dermatol. 2001;18:1-4.
  4. Eisen D. The evaluation of cutaneous, genital, scalp, nail, esophageal, and ocular involvement in patients with oral lichen planus. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999;88:431-436.
  5. Boyd As, Neldner KH. Lichen planus. J Am Acad Dermatol. 1991;25:593-619.
  6. Helander, SD, Rogers RS 3rd. The sensitivity and specificity of direct immunofluorescence testing in disorders of mucous membranes. J Am Acad Dermatol. 1994;30:65-75.
  7. Carrozzo M, Brancatello F, Dametto E, et al. Hepatitis C virus-associated oral lichen planus: is the geographical heterogeneity related to HLA-DR6? J Oral Pathol Med. 2005;34:204-208.
  8. Gonzalez-Moles MA, Scully C, Gil-Montoya JA. Oral lichen planus: controversies surrounding malignant transformation. Oral Dis. 2008;14:229-243.
  9. Eisen D. The clinical manifestations and treatment of oral lichen planus. Dermatol Clin.  2003;21:79-89.
  10. Passeron T, Lacour JP, Fontas E, et al. Treatment of oral erosive lichen planus with 1% pimecrolimus cream: a double-blind, randomized, prospective trial with measurement of pimecrolimus levels in the blood. Arch Dermatol. 2007;143:472-476.
  11. Eisen D, Ellis CN, Duell EA, et al. Effect of topical cyclosporine rinse on oral lichen planus. A double-blind analysis. N Engl J Med. 1990;323:290-4.
  12. Corrocher G, Di Lorenzo G, Martinelli N, et al. Comparative effect of tacrolimus 0.1% ointment and clobetasol 0.05% ointment in patients with oral lichen planus. J Clin Periodontol. 2008;35:244-249.
  13. Scully C, Eisen D, Carrozzo M. Management of Oral Lichen Planus. Am J Clin Dermatol.2 000;5:287-306.