Expression of endocan and vascular endothelial growth factor in recurrent minor aphthous ulcers.

Ea Mahmoud,Og Shaker,Dm Ghalwash,Wa Moneim

doi:10.4317/jced.55695

Abstract

BackgroundRecurrent aphthous ulcers (RAU) are common painful inflammatory lesions of the mucous lining of the mouth. Endocan, previously identified as endothelial cell specific molecule-1, is implicated as a vital player in the regulation of several inflammatory processes. A number of inflammatory cytokines and pro-angiogenic growth factors including VEGF upregulate endothelial cells synthesis and expression of endocan.Material and MethodsClinical scores of pain and ulcer size as well as level of endocan and VEGF were determined in swaps from aphthous ulcer and contra lateral normal mucosa in 30 patients (nine males and twenty one females) with age ranging from 18 to 45 years and mean age is 31.5 years.ResultsIn the early days of ulcer development, ulcer showed statistically significantly higher mean endocan (8.2 ±5.3) and VEGF levels (1220.7 ±294.6) than control healthy mucosal site (1.1 ±0.5) and (518.6 ± 61.7) respectively. An increase in endocan is associated with an increase in pain score and vice versa. A statistically significant positive correlation were also found between endocan and VEGF levels.ConclusionsEndocan and VEGF are strongly associated with the destructive phase of minor aphthous ulcers especially Endocan which was positively correlated with pain severity. Key words:Endocan, ESM-1, VEGF, Recurrent Apthous Ulcer.

Highlights

Recurrent aphthous ulcers (RAU) is the most communal inflammatory ulcer affecting the oral mucosa [1] with the prevalence of 5 - 25 % in the overall population
The most accepted theory regarding the aetiology of RAU is that these predisposing factors or unknown antigenic stimulation triggers oral mucosal keratinocytes to transform into a target of the uncontrolled action of lymphocytes, neutrophils and monocytes resulting in liberation of acute inflammatory mediators, damage of oral mucosal cells, the appearance of an aphthous ulcer [8,9]
The acute inflammatory mediators liberated during the initiation of the ulcerative process that included cytokines for instance TNF-α, IFN-Υ, IL-2 and IL-2, along with the migration of other lymphocytes, langerhans cells and neutrophils causes an over expression of Vascular Cell Adhesion Molecules (VCAM), Intercellular Adhesion Molecules (ICAM-1) and Selectine E leading to more lymphocytic accumulation and invasion of the epithelium locally [10]

Summary

Introduction

Recurrent aphthous ulcers (RAU) is the most communal inflammatory ulcer affecting the oral mucosa [1] with the prevalence of 5 - 25 % in the overall population. Vascular endothelial growth factor (VEGF) is a powerful endothelium-specific cytokine that effectively stimulates angiogenesis, inflammation, endothelium-dependent vasodilatation and amplified microvascular permeability [11]. It is principally produced by vascular endothelial cells, macrophages and neutrophils. In the present study, we aimed to investigate the expression levels of Endocan and VEGF in minor aphthous ulcer lesions during both the active and the healing stages. A number of inflammatory cytokines and pro-angiogenic growth factors including VEGF upregulate endothelial cells synthesis and expression of endocan. Conclusions: Endocan and VEGF are strongly associated with the destructive phase of minor aphthous ulcers especially Endocan which was positively correlated with pain severity

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