Abstract

Background: Periodontitis (PD) is a chronic inflammatory disease that can eventually lead to tooth loss. Genetic and environmental factors such as smoking are involved in the pathogenesis of PD. The development of PD is potentiated by various pathogens that induce an immune response leading to the production of cytokines, such as interleukin (IL)-17. The synthesis of IL-17 is influenced genetically. The polymorphisms in IL-17 gene may affect the synthesis of IL-17. The aim of this study was to examine the association between the IL-17F rs763780 and IL-17A rs2275913 polymorphisms and PD in non-smoking and smoking patients to check if these polymorphisms could be a risk factor for PD. Methods: The study enrolled 200 patients with PD (130 non-smokers and 70 smokers) and 160 control subjects (126 non-smokers and 34 smokers). Periodontitis was diagnosed on the basis of 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. All samples were genotyped using allelic discrimination assays with TaqMan® probes on a Real-Time PCR Detection System. Results: There were no statistically significant differences in the distribution of the IL-17F rs763780 and IL-17A rs2275913 genotypes and alleles between patients with PD and control subjects, between smoking patients with PD and smoking control subjects, and between non-smoking patients with PD and non-smoking control subjects. Conclusions: The results of this study suggest a lack of statistically significant associations between IL-17F rs763780 and IL-17A rs2275913 polymorphisms and PD in Polish population.

Highlights

  • Introduction published maps and institutional affilPeriodontitis (PD) is characterized by inflammation and infiltration of inflammatory cells in periodontal tissue and continues to be a major public health problem [1]

  • We examined the polymorphisms of IL-17F rs763780 and IL-17A rs2275913 in PD patients to see if they could be a risk factor for the development of this disease in

  • We observed significantly increased values of approximal plaque index, sulcus bleeding index, probing pocket depth and clinical attachment loss in patients with periodontitis

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Summary

Introduction

Introduction published maps and institutional affilPeriodontitis (PD) is characterized by inflammation and infiltration of inflammatory cells in periodontal tissue and continues to be a major public health problem [1]. This disease is related to bacterial infections that induce an immune response [3,4]. Various factors induce an immune response leading to the production of inflammatory mediators, including proinflammatory cytokines, and subsequently to tissue destruction [5,6,7,8]. Smoking has been shown to affect the inflammatory response and synthesis of cytokines involved in inflammation in PD [9,10,11,12,13,14,15]. Genetic and environmental factors such as smoking are involved in the pathogenesis of PD. The development of PD is potentiated by various pathogens that induce an immune response leading to the production of cytokines, such as interleukin (IL)-17.

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