Abstract

OBJECTIVE: Oral lichen planus (OLP) is chronic inflammatory disease of the oral mucosa, presenting in various clinical forms. The etiology of OLP is still unknown but mounting evidence points to the immunologic basis of this disorder. AIM: Our study was undertaken to quantify the salivary levels of pro-inflammatory tumor necrosis factor-alpha (TNF-alpha) in the reticular and the erosive/atrophic forms of OLP, compared with age-matched healthy control volunteers. SUBJECTS AND METHODS: Whole saliva from 40 patients with active lesions of OLP, as well as from 20 healthy persons, was investigated for the presence of TNF-alpha by enzyme immunoassay. RESULTS: Salivary TNF-alpha levels were significantly increased in patients with OLP in comparison with healthy subjects. The presence of TNF-alpha showed positive correlation to clinical forms of OLP, being significantly higher in the erosive/atrophic type than in the reticular type of disease. CONCLUSION: Saliva provides an ideal medium for the detection of pro-inflammatory markers of the oral cavity. In patients with OLP, TNF-alpha levels in saliva are elevated, correlating with the severity of illness. Salivary TNF-alpha analysis may be a useful diagnostic tool and a potential prognostic marker in OLP.

Highlights

  • Oral lichen planus (OLP) is a relatively common mucocutaneous disease of unknown etiology.[1]

  • In this report we present data characterizing the pattern of tumor necrosis factor-alpha (TNF-a) production in whole saliva of patients with OLP

  • Salivary levels of tumor necrosis factor (TNF)-a were elevated in all patients presenting symptomatic OLP

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Summary

Introduction

Oral lichen planus (OLP) is a relatively common mucocutaneous disease of unknown etiology.[1]. The cause of OLP is still not known, but cell-mediated immune dysfunction is implicated in the complex ethiopathogenesis of this disease. The large amount of cytokines released by affected keratinocytes and the associated inflammatory elements plays a key role in the selective recruitment of the T lymphocytes. T-celldominated infiltrate in the subepithelial region, which characterizes OLP, induces further release of chemokines and cytokines belonging to either the Th1 or Th2 groups.[2] Such a mixed cytokine profile has been demonstrated by Simark-Mattsson et al, who found elevated concentrations of interleukin (IL)-2, IL-6 and IL-10, as well as tumor necrosis factor (TNF)-a and transforming growth factor-b within the subepithelial infiltrate in OLP patients.[3]

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