Vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) in oral lichen planus: An immunohistochemical study for the correlation between vascular and inflammatory reactions

Objectives: Oral lichen planus (OLP) is characterized by a subepithelial lymphocytic infiltration. To find the correlation between vascular and inflammatory reaction, the expressions of vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), CD34, and CD68 were investigated. Materials and methods: 30 cases of OLP and 20 normal oral tissues samples were subjected to immunohistochemistry for VEGF, iNOS, CD34 and CD68. CD34-positive (+) blood vessels (microvessel density, MVD), degree of lymphocytic infiltration, and CD68+ macrophages were correlated with the expression of VEGF and iNOS. OLP cases were histopathologically subdivided into active (non erosive and erosive/ulcerative) and non-active stages. Results: Expression of VEGF was observed in all epithelial layers of OLP while iNOS was in basal and parabasal layers. They were significantly higher (P < 0.001) than those in controls. The mean MVD (CD34+) was significantly increased in all cases of OLP (P < 0.05), especially in the active (erosive/ulcerative) stage (P < 0.01) compared with controls. The mean number of CD68+ cells was significantly increased (P < 0.01) in OLP, especially higher in the active (erosive/ulcerative) OLP (P < 0.001). The expressions of VEGF (P < 0.05) and iNOS (P < 0.01) were significantly correlated in OLP. There was significant positive correlations between the lymphocytic infiltration and the expressions of VEGF and iNOS (P < 0.05), MVD (P < 0.01), and CD68 counts (P < 0.001) in OLP. Conclusion: The present results indicated that the upregulation of VEGF and iNOS plays an important role in pathogenesis of OLP through activated angiogenesis and chronic inflammatory cell infiltrates. Novel strategies directed to inhibition of these markers could be developed for OLP treatment. (C) 2013 Asian AOMS, ASOMP, JSOP, JSOMS, JSOM, and JAMI. Published by Elsevier Ltd. All rights reserved.