Abstract
Despite a number of reports in the literature on the role of epigenetic mechanisms in periodontal disease, a thorough assessment of the published studies is warranted to better comprehend the evidence on the relationship between epigenetic changes and periodontal disease and its treatment. Therefore, the aim of this systematic review is to identify and synthesize the evidence for an association between DNA methylation/histone modification and periodontal disease and its treatment in human adults. A systematic search was independently conducted to identify articles meeting the inclusion criteria. DNA methylation and histone modifications associated with periodontal diseases, gene expression, epigenetic changes after periodontal therapy, and the association between epigenetics and clinical parameters were evaluated. Sixteen studies were identified. All included studies examined DNA modifications in relation to periodontitis, and none of the studies examined histone modifications. Substantial variation regarding the reporting of sample sizes and patient characteristics, statistical analyses, and methodology, was found. There was some evidence, albeit inconsistent, for an association between DNA methylation and periodontal disease. IL6, IL6R, IFNG, PTGS2, SOCS1, and TNF were identified as candidate genes that have been assessed for DNA methylation in periodontitis. While several included studies found associations between methylation levels and periodontal disease risk, there is insufficient evidence to support or refute an association between DNA methylation and periodontal disease/therapy in human adults. Further research must be conducted to identify reproducible epigenetic markers and determine the extent to which DNA methylation can be applied as a clinical biomarker.
Highlights
Periodontitis is a destructive disease of tooth-supporting tissues, induced by bacterial biofilm [1], which consists mainly of gram-negative, anaerobic, and micro-aerophilic bacteria that can colonize the sub-gingival areas [2,3]
Zhang’s group (2010) found an inverse association between PTGS2 methylation and PTGS2 expression with higher methylation levels and lower gene expression in the chronic periodontitis (CP) group compared to healthy controls [21]
De Faria’s group (2013) reported a hypermethylated TLR2 profile in the CP group compared to controls and higher TLR2 transcription in the control group; no statistically significant difference was found in TLR2 transcript levels and the number of inflammatory cells in either group [34]
Summary
Periodontitis is a destructive disease of tooth-supporting tissues, induced by bacterial biofilm [1], which consists mainly of gram-negative, anaerobic, and micro-aerophilic bacteria that can colonize the sub-gingival areas [2,3] This bacterial biofilm triggers an inflammatory host response influenced by environmental, genetic, and epigenetic factors [4,5,6]. Epigenetic modifications are chemical alterations to DNA and its associated histone proteins, which alter gene expression, but are not encoded in the DNA sequence. Histone acetylation is controlled by histone acetyltransferases (HATs), which add acetyl groups to histones, and histone deacetylases (HDACs), which remove the acetyl groups [12] Both DNA methylation and histone modifications are reversible [13] and linked [10,12]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
