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Oral lichen planus (OLP) is a relatively common chronic inflammatory mucocutaneous autoimmune disease that primarily affects the skin and mucosal surfaces including the oral cavity with a variety of clinical manifestations including reticular, papular, hyperkeratotic, atrophic, erosive, and bullous forms 1,2. The erosive, atrophic, and bullous type lesions are usually accompanied with pain or burning sensation that affects the patient's quality of life3. Intraorally, the buccal mucosa, dorsum of the tongue and the gingiva are commonly affected 4 .OLP has most often been reported in middle aged patients3. Women account for 60% to 75% of patients with OLP 5.

OLP is estimated to affect1% to 2.0% of the general population. Around 40% of lesions occur on both oral and cutaneous surfaces, 35% occurs on cutaneous surfaces alone, and 25% occur on oral mucosa alone 6,7.

Several predisposing factors might be involved in the pathogenesis of OLP. Earlier studies have implicated stress, anxiety and depression as possible factors. Familial cases of OLP have been reported and the role of genetic predisposition was considered8.

The exact etiology of OLP is still unknown, but cell-mediated immune dysfunction is implicated in the complex etio-pathogenesis of this disease. Large amounts of cytokines that are released by affected keratinocytes and the associated inflammatory elements play a key role in the selective recruitment of cytotoxic CD8+ T cells trigger apoptosis of the basal cells of the oral epithelium. T-cell dominated infiltrate in the sub epithelial region, which characterizes OLP, induces further release of cytokines9.

Cytokines may be produced by nearly every cell, but mostly act locally on cell receptors and have high potency10. Their production gives rise to an inflammatory cascade. One of the most important elements in this cascade is overexpression of tumor necrosis factor-alpha (TNF- α). TNF- α causes tissue destruction and overproduction of other cytokines, especially interleukin (IL)-6 which, in turn, leads to further inflammation and tissue degradation 11. Production of cytokines can in turn stimulate production of Reactive Oxygen Species (ROS) and cause oxidative damage to the tissues 12 .