The Effect Of Smoking On Il-6 Polymorphisms In Patients Suffering From Chronic Periodontitis

Research Article
Pavni Avasthy., Divya Tandon., Vivek Govila and Mona Sharma
Periodontitis, IL-6, polymorphism, SNP, clinical attachment loss, pocket probing depth.

Background & Objectives: Periodontitis is a multifactorial, inflammatory disease of supporting structures of the tooth. The complex pathogenesis of periodontitis implies the involvement of a susceptible host and a bacterial challenge. Many studies have provided a valuable contribution in understanding the genetic basis of periodontal disease, but the specific candidate genes of susceptibility are still unknown. The genome-wide studies and screening of Single Nucleotide Polymorphisms (SNPs) have yielded new genetic information but without a definitive solution for the management of periodontal disease. Methods: The present study was undertaken with the aim to evaluate the association of SNPs of IL6 gene with Chronic Periodontitis in smokers and nonsmokers. A total of 60 subjects aged between 25-60 years were selected for the study. They were divided into following groups as GROUP I Periodontally and systemically healthy individuals, GROUP II Chronic periodontitis subjects who were non-smokers and GROUP III Chronic Periodontitis subjects who were smokers. The clinical parameters: Plaque Index (PI), Gingival Index (GI), Probing Pocket Depth (PPD) and Clinical Attachment Level (CAL) were recorded and Blood samples were taken for genotyping. Results: The study thus demonstrated that for SNP IL-6 (rs 1800795), genotype GG (homozygous wild type) was significantly associated with Chronic Periodontitis. It also showed that there is an increased risk of association of disease severity with GC (heterozygous mutant) genotype i.e., an increased carriage rate of genotype GC was evident with the increase in severity of CP. Thus, highlighting an increase susceptibility to CP due to this gene polymorphism. There was no correlation with smoking in Test groups (II & III) seen, hence proving that the genotype frequencies are dependent on the severity of the disease rather than the risk factors involved.