Title: Salivary cytokine levels of oral erosive lichen planus patients compared with the healthy subjects
Authors: Dr Aastha Chawla, Dr R.D. Mehta, Dr B.C. Ghiya, Dr Prasoon Soni
DOI: https://dx.doi.org/10.18535/jmscr/v7i6.44
Abstract
Introduction
Lichen planus is a chronic inflammatory disease of the skin which may involve the mucosa1. Oral lichen planus is an immune-mediated disorder and an interface stomatitis characterized by T-cell destruction2 of the basal cells of the epithelium, mediated by Th1 cytokines. T cells release pro-inflammatory cytokines, interleukins (IL) namely IL-6 and IL-8. The serum and saliva levels of the interleukins serve as a reliable indicator to assess the response to treatment on a molecular basis.
TNF-α enhances the activation of nuclear factor-κB in the subepithelial T cells and as a consequence leads to the increased expression of other proinflammatory cytokines3,4 including IL-6.IL-6 has been shown to be associated with multidrug resistance protein (MRP) expression by the keratinocytes9. These complex factors together have also been demonstrated to play a role in the pathogenesis of oral squamous cell carcinoma.
Cytokines are mediators that play a central role in both innate and adaptive immunity. Aberrant production of cytokines is central to the causation of immune deficiency, allergy or autoimmunity, which are involved in the pathogenesis of various immunemediated inflammatory diseases. Although a great progression has been achieved on the research of cytokines in OLP pathogenesis, there are still many unexplained aspects in this field. Cytokines do not work individually but in the complex immunomodulation pathways. It is very likely that disturbance in cytokine networks determine the progression of OLP. However, most published data are limited to the expressions of single or several cytokines in OLP, thus are not enough to explain the complexities of the cytokine network in the pathogenesis. In addition, knowledge about the intrinsic mechanisms by which the cytokine networks contribute to the chronic inflammatory environment of OLP is still lacking. Further investigation on the aberration of the cytokine network and their regulatory roles in the onset and development of OLP will deepen our understanding of the pathogenesis and lead to the identification of novel and better therapeutic approaches of this disease.
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