Abstract
BackgroundOral lichen planus is a chronic inflammatory disease which is considered as a potential precancerous condition. Numerous studies have confirmed that inflammation is a strong risk factor for cancer development. Smoking is associated with potentially malignant disorders of the oral and oropharyngeal mucosa. The adverse consequences of smoking in various pathologies are mediated by its effects on the immune-inflammatory system. Little is known about the influence of cigarette smoke content on the course of OLP and inflammatory response.MethodsTwenty oral lichen planus smoker patients, 20 oral lichen planus non-smoker patients and 20 control patients were included in this work. Pain and clinical scores were calculated for each patient. Image analysis to calculate area percent for TLR-2 and CD34 immuno-expression was performed. Data was tabulated and statistically analyzed.ResultsThe present study showed no statistically significant difference in clinical and pain scores between the smoker and non-smoker groups. However, there was a significant difference in area percent values for TLR-2 and CD34 immuno-expression between the smoker and the non-smoker groups.ConclusionSmoking enhanced TLR-2 and CD34 expression in OLP which are considered as inflammatory mediators and are contributing factors in the pathogenesis of oral lichen planus.
Highlights
Oral lichen planus is a chronic inflammatory disease which is considered as a potential precancerous condition
Microscopic examination of immunostained sections Toll-like receptor (TLR)-2 Cytoplasmic TLR-2 immunoexpression was seen in basal and suprabasal cells of stratified squamous epithelium of the control group. (Fig. 1a)
In this work, clinical examination revealed that both groups whether smokers or non-smokers showed the classical presentation of Oral lichen planus (OLP) and this was confirmed by calculating the mean clinical score values which showed no significant difference between both groups
Summary
Oral lichen planus is a chronic inflammatory disease which is considered as a potential precancerous condition. Numerous studies have confirmed that inflammation is a strong risk factor for cancer development. Smoking is associated with potentially malignant disorders of the oral and oropharyngeal mucosa. Lichen planus is a common disorder in which autocytotoxic T-lymphocytes trigger apoptosis of epithelial cells leading to chronic inflammation [1]. Chronic inflammation in OLP induces the expression of various cytokines which impacts cell migration, proliferation and differentiation, leading to cancer development [3]. Inflammation has been established by previous studies as a strong risk factor for cancer development [4, 5]. TLRs are triggered, by microbial structures, and during tissue or cell damage [6] and enhance the inflammatory response [7]
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