The aim is to investigate the influence of oral lichen planus on periodontal status of systemically healthy individuals.

Lichen planus, a chronic immune-mediated inflammatory disease affects the skin and mucous membranes. Oral lichen planus is the mucosal counterpart of cutaneous lichen planus. It was reported first described in 1866 as white papular eruptions in the oral cavity. The prevalence of OLP varies from 0.1% to 4%. OLP mostly occurs in middle aged and elderly patients, with female to male ratio of 3:2. OLP is characterized by lesions consisting of radiating white, grey, velvety, thread-like papules in a linear, annular and retiform arrangement forming typical lacy, reticular patches, rings and streaks. The lesions are most common on buccal mucosa, tongue, lips, gingiva, floor of mouth, palate. Clinically OLP has six clinical presentations namely reticular, erosive, atrophic, plaque-like, papular, bullous.

Reticular form, the most common clinical form presents as fine, asymptomatic intertwined lace-like pattern called "Wickham striae" in a bilateral symmetrical form. It mainly involves the posterior mucosa of the cheek. Erosive OLP represents symptomatic lesions. Atrophic lesions may resemble the combination of two clinical forms, such as the presence of white striae characteristic of the reticular type surrounded by an erythematous area. Plaque-like form mainly found on dorsum of the tongue and the mucosa of the cheek reveals whitish homogeneous irregularities similar to leukoplakia. Papular form presents with small white papules with fine striae in its periphery. Bullous form is the most unusual clinical form, exhibiting blisters that increase in size and tend to rupture, leaving the surface ulcerated and painful.

The pathogenesis of the disease is characterized by cytotoxic CD8+ T lymphocytes migration to the epithelium inducing apoptosis of basal keratinocytes. A number of etiological factors in OLP have been proposed such as local and systemic inducers of cell-mediated hypersensitivity, drugs, dental materials, infectious agents, and stress. The existence of a local cell-mediated immune disorder has been postulated as a factor underlying development of the lesions specifically, a delayed cellular hypersensitivity response probably triggered by some exogenous agent. Periodontal diseases are the most prevalent oral microbial infections that lead to chronic inflammation of the supporting tissues of teeth. Periodontal disease has a complex pathogenesis involving host microbiome interactions. It has an impact on both local and systemic health. The pathogenesis of periodontal disease involves a local inflammatory reaction and the activation. Thus, it is possible to speculate that some interference could exist and that the potential effect arising from these shared mechanisms⁄ mediators could be localized to sites where OLP lesions are present and alteration of host immune response in OLP may have an impact on periodontal health. With this consideration, the present study is aimed to assess periodontal status in systemically healthy individuals with and without oral lichen planus.

Inclusion Criteria:

Individuals aged 40-50 yrs. Clinically diagnosed and histo-pathologically confirmed cases of oral Lichen Planus

Exclusion Criteria:

History of periodontal therapy in last one year. Drug-induced lichenoid reaction or any other red or white lesions in the oral cavity.

The presence of any tooth restoration near the lesions. Smokers or patients with history of smoking. systemic diseases or conditions that are reported to be associated with periodontal diseases, including diabetes mellitus, osteoporosis, rheumatoid arthritis Pregnant and lactating women. Patients with history of systemic treatment for oral Lichen Planus Patients with cutaneous lichen planus

systemically healthy individuals with and without oral lichen planus

study protocol