The Effect of Smoking on Clinical Presentation and Expression of TLR-2 and CD34 in Oral Lichen Planus Patients

Clinical and Immunohistochemical Study

Nermine Raouf Amin; Nermin Yussif; Enji Ahmed


BMC Oral Health. 2020;20(129) 

In This Article


Lichen planus is a common disorder in which auto-cytotoxic T-lymphocytes trigger apoptosis of epithelial cells leading to chronic inflammation.[1] It is considered to be a precancerous condition.[2] Chronic inflammation in OLP induces the expression of various cytokines which impacts cell migration, proliferation and differentiation, hence leading to cancer development.[3] Inflammation has been established by previous studies as a strong risk factor for cancer development.[4,5]

Toll-like receptors (TLRs) are members in the pattern-recognition receptors (PRRs) which recognize microbial antigens to which oral mucosa is continuously exposed. TLRs are triggered, not only by microbial structures, but also during tissue or cell damage[6] and enhance the inflammatory response.[7]

Ohno et al.[8] found that TLR-2 was highly expressed in OLP tissues and may affect its pathogenesis. Moreover, Ng et al.[9] illustrated the role of TLR-2 in epithelial dysplasia.

Angiogenesis has an attentive role in the pathogenesis of chronic inflammatory diseases.[10] Alterations to angiogenesis using the endothelial cell marker CD34, have been implicated in the pathogenesis of OLP.[11] Moreover, CD 34 overexpression is considered a useful marker preceding oral cancer development as it increases from normal mucosa to dysplasia to carcinoma.[12]

Smoking is associated with potentially malignant disorders of the oral mucosa.[13] According to the authors' analysis, tobacco smoking increases the risk of OLP malignant transformation[14] as cigarette smoke contains substances that induce chronic inflammation at mucosal surfaces.[15]

The purpose of this study was to evaluate the effect of smoking on clinical presentation and expression of TLR-2 and CD34 in OLP as markers of inflammation.