Abstract
Aim:The purpose of this study was to compare IL-1β and IL-12 gene expression in the gingival tissue of smokers and non-smokers either with healthy periodontium or with chronic periodontitis.Materials and Methods:41 individuals consisting of 21 healthy controls (11 non-smokers and 10 smokers) and 20 chronic periodontitis patients (10 non-smokers and 10 smokers) participated in this study. Samples were collected from papillary regions of targeted areas and cytokines were analyzed using Real Time PCR. Shapiro-Wilk, Mann-Witney and Independent T tests were employed for statistical analysis.Results:IL-1β gene expression in gingival tissue of non-smoker group with chronic periodontitis was significantly higher than non-smoker-healthy group (p=0.011). Smoker-chronic periodontitis group showed lower IL-1β gene expression than non-smoker-chronic periodontitis group (p=0.003). IL-12 gene expression was not significantly different between analyzed groups.Conclusion:IL-1β gene expression increases in gingival tissue of non-smoker-chronic periodontitis patients due to inflammatory processes but smoking reduces the expression of this cytokine in diseased periodontal tissues. On the other hand periodontal condition and smoking habits do not seem to affect IL-12 gene expressions in gingival tissues. Authors concluded that reduced levels of IL1 and in some extent IL12 in smoking patients are responsible for higher tissue and bone degenerations and less treatment responses in smokers.
Highlights
Smoking acts as a natural and valuable model for studying the pathogenesis of periodontal patients
IL-1β gene expression in gingival tissue of non-smoker group with chronic periodontitis was significantly higher than non-smokerhealthy group (p=0.011)
IL-1β gene expression increases in gingival tissue of non-smoker-chronic periodontitis patients due to inflammatory processes but smoking reduces the expression of this cytokine in diseased periodontal tissues
Summary
Smoking acts as a natural and valuable model for studying the pathogenesis of periodontal patients. 596 The Open Dentistry Journal, 2017, Volume 11 in periodontitis incidence and severity between smokers and non-smokers have been well documented [1]. It has been proved that periodontal response in smokers compared to non-smokers is unfavorable [2 - 4]. A major portion of connective tissue and bone destruction, as a result of periodontitis, is due to pro-inflammatory cytokines originating from the host periodontal tissues. Reduced inflammatory cytokine level in smokers compared to periodontitis patients should be answered. The comparison of existing cytokines in the gingiva of healthy individuals, smoking and non-smoking patients might potentially offer valuable information regarding the primary mechanisms of connective tissue destruction and alveolar bone loss in periodontitis
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