Abstract

BackgroundAccumulating evidence suggests that tobacco smoking affects the susceptibility to and severity of chronic periodontitis. Epigenetics may explain the role of smoking in the development and progress of periodontal disease. In this study, we performed transcriptomic and methylomic analyses of non-periodontitis and periodontitis-affected gingival tissues according to smoking status.MethodsHuman gingival tissues were obtained from 20 patients, including non-smokers with and without periodontitis (n = 5 per group) and smokers with and without periodontitis (n = 5 per group). Total RNA and genomic DNA were isolated, and their quality was validated according to strict standards. The Illumina NextSeq500 sequencing system was used to generate transcriptome and methylome datasets.ResultsComprehensive analysis, including between-group correlation, differential gene expression, DNA methylation, gene set enrichment, and protein-protein interaction, indicated that smoking may change the transcription and methylation states of extracellular matrix (ECM) organization-related genes, which exacerbated the periodontal condition.ConclusionsOur results suggest that smoking-related changes in DNA methylation patterns and subsequent alterations in the expression of genes coding for ECM components may be causally related to the increased susceptibility to periodontitis in smokers as they could influence ECM organization, which in turn may have an effect on disease characteristics.

Highlights

  • Accumulating evidence suggests that tobacco smoking affects the susceptibility to and severity of chronic periodontitis

  • Correlation of gene expression with smoking In the correlation analysis of the RNA sequencing (RNA-seq) data, we considered smoking (Fig. 1a) and periodontal condition as factors (Fig. 1b)

  • Our results indicate that smoking is closely associated with extracellular matrix (ECM) organization-related genes, which intensify the periodontal condition as indicated by Differentially expressed (DE) and Differentially methylated (DM) patterns, and proteinprotein interaction (PPI)-affected genes

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Summary

Introduction

Accumulating evidence suggests that tobacco smoking affects the susceptibility to and severity of chronic periodontitis. Epigenetics may explain the role of smoking in the development and progress of periodontal disease. Tobacco smoking is considered a major risk factor, and many studies have demonstrated that smoking alters the development and progression of periodontitis [3,4,5]. Epigenetic modifications include chemical alteration of DNA and associated proteins such as histones, which leads to chromatin remodeling and plays an important role in regulating gene expression [10]. Among these effects, DNA methylation is a common epigenetic mechanism observed in human cells [11]

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