Abstract
Oral lichen planus (OLP) is a chronic inflammatory oromucosal disease. The N-acylethanolamines (NAEs), are a family of endogenous biologically active lipid mediators, with palmitoylethanolamide (PEA) being of particular interest here due to its anti-inflammatory and analgesic properties. In this study using oral mucosa biopsies from OLP patients and healthy controls, we investigated whether NAE synthesis was mobilized in response to the inflammation associated with OLP. PTGS2 levels, coding for cyclooxygenase-2 (COX-2), were increased approximately 4-fold in OLP compared to controls and a significant increase in the ratio of PTGS2 to NAPEPLD, the latter coding for a key enzyme in NAE synthesis, was seen. This was matched by an increased ratio of COX-2-derived prostaglandins to PEA in a second patient cohort. We conclude that there is an imbalance between prostaglandins and PEA in OLP, opening up the possibility that PEA might be a useful treatment for this disorder.
Highlights
Oral lichen planus (OLP) is a common chronic inflammatory disease affecting the oral mucosa, where it forms lesions that are troublesome for those affected
In the PCR cohort pathology alone precludes an analysis of the different OLP subtypes, but we have indicated in Figure 1 samples that were analyzed, all but three cases showed atrophic pathology and all but four showed whether the cases have atrophic pathology and accompanying genital or skin lichen planus
Three weaknesses of this study should be stated: sizes are small given the heterogeneous nature of OLP; (2) the qPCR data give gene expression rather
Summary
Oral lichen planus (OLP) is a common chronic inflammatory disease affecting the oral mucosa, where it forms lesions that are troublesome for those affected. OLP is a subtype of lichen planus, a family of inflammatory diseases affecting the skin in various areas, commonly genitalia and mucosa [1]. The prevalence of OLP has been estimated to 1–2% worldwide, and women are predominantly affected over men [2]. The etiology of OLP, which has periods of improvement and relapses, is currently unknown, but involves, among other factors, activated cytotoxic CD8+. The expression of cyclooxygenase-2 (COX-2), responsible for production of prostaglandins (PGs) in inflammatory tissues, is upregulated in OLP [4,5,6,7] and has been suggested to be part of the proposed autoimmune character of the disease [6]. The first-in-line treatment option for OLP is topical (or sometimes systemic) steroids, their efficacy is variable and there is a clear need for novel treatment strategies
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