Noushin Jalayer Naderi
Abstract
Dear Editor, Cigarette smoking has destructive effect on periodontal tissue. The rates of loss of periodontal attachment and recession of gingival are higher in smokers than non-smokers (1-2). Previous studies on the inflammatory immune responses in smokers’ periodontitis have mainly focused on ...
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Dear Editor, Cigarette smoking has destructive effect on periodontal tissue. The rates of loss of periodontal attachment and recession of gingival are higher in smokers than non-smokers (1-2). Previous studies on the inflammatory immune responses in smokers’ periodontitis have mainly focused on the role of neutrophils. Tumor necrosis factor–α, prostaglandin E2 and matrix metalloproteinase-8 have been shown to rise in smokers with periodontitis (3-4). Different functions of mast cells and eosinophils in inflammatory immune responses make them distinctive cells in disease pathogenesis (5-6). In an investigation, our team examined the effect of smoking on mast cells density in chronic periodontitis. The study showed that the mean number of mast cells in smokers was significantly lower compared to the non-smokers. Based on the literature, no research was found regarding the effect of cigarette smoking on eosinophil cells in human periodontitis. Eosinophils and mast cells regulate the hypersensitivity reactions by affecting each other function (5). Thus, in the next study, we examined this issue on the same samples. The results revealed that the number of eosinophil count in smokers was significantly lower than non-smokers. Considering the findings of both studies on decreased number of mast cells and eosinophils in the same samples, it seems that cigarette smoke had an apoptotic function on extra-vascular immune inflammatory related cells in human periodontitis. According to our opinion, with the death of mast cells and eosinophils, a cascade of different events occurs in the microenvironment of gingiva which causes more tissue damage in the smokers. The apoptotic effect of cigarette smoke on gingival connective tissue must be studied in the enzymatic level.The Heme Oxygenase-1 (HO-1)/Carbon Monoxide (CO) system demand to explain the pathogenesis of diseases by using the basic metabolism and enzymatic activities. HO-1 has a regulatory action on inflammatory signaling programs. CO is an end-product of HO-1. CO affects the apoptosis and cellular inflammation by modulating the inflammatory related cytokines. Modulating the HO-1 and application of CO-releasing molecules are new therapeutic strategies in inflammatory diseases (7). Based on our previous findings, we suggest that further study on HO-1/CO can probably determine the effect of cigarette smoke on inflammatory immune cells in human chronic periodontitis. The system can be potentially considered as a therapeutic target in inflammatory disease of periodontium in cigarette smokers. Conflict of Interest The authors declared no conflict of interest regarding the publication of this article.
Oral Pathology
Noushin Jalayer naderi; Hasan Semyari; Reza Hemmati
Abstract
Background and objective:Gingival bleeding reduction in smokers has been associated with decreased blood vessel density. The mechanism of suppressive effect of cigarette smoking on blood vessel density is not precisely defined. The aim of this study was to evaluate the impact of smoking on angiogenesis ...
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Background and objective:Gingival bleeding reduction in smokers has been associated with decreased blood vessel density. The mechanism of suppressive effect of cigarette smoking on blood vessel density is not precisely defined. The aim of this study was to evaluate the impact of smoking on angiogenesis by assessing mast cells density and VEGF expression in chronic periodontitis. Materials& Methods: 52 paraffin embedded block of gingiva tissues with periodontitis obtained from 30 nonsmokers and 22 smokers undergoing flap surgery were examined immunohistochemically for VEGF expression. Mast cell counts was completed on toluidine blue stained slides. Exposure to cigarette smoking was calculated by the number of packs × year. Patients were classified into 4 groups based on the number of smoked cigarettes. The correlation between VEGF expression and mast cell counts was evaluated and compared in nonsmokers and smokers. Results: The mean number of mast cells (p=0.004) and average value of VEGF expression (p = 0.000) in nonsmokers was significantly higher than smokers. No correlation was noted between VEGF expression / mast cell counts and number of smoked cigarettes in four groups of smokers (p=0.29,0.12 , 0.20 and 0.11, respectively). Conclusion: Mast cells and VEGF expression may account for suppressive effect of cigarette smoking on blood vessels in periodontitis.
