Epigenetics, Inflammation, and Periodontal Disease

被引：12
作者：
Benakanakere M.R. [1 ]
Finoti L. [1 ]
Palioto D.B. [1 ,2 ]
Teixeira H.S. [3 ]
Kinane D.F. [4 ]
机构：
[1] Department of Periodontics, School of Dental Medicine, University of Pennsylvania, 240 South 40th street, Philadelphia, 19104, PA
[2] Department of OMS and Periodontology, University of São Paulo - School of Dentistry of Ribeirão, Preto
[3] Department of Orthodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, 19004, PA
[4] Division of Periodontology, School of Dental Medicine, University of Geneva Faculty of Medicine, Geneva
来源：
Current Oral Health Reports | 2019年 / 6卷 / 1期
基金：
美国国家卫生研究院;
关键词：
DNA methylation; Epigenetic regulation; Histone modifications; Immune regulation; Periodontal disease dysbiosis;
D O I：
10.1007/s40496-019-0208-4
中图分类号：
学科分类号：
摘要：
Purpose of the Review: The purpose is to provide current knowledge and recent development and understanding of periodontal disease dysbiosis in the perspective of epigenetic changes. Epigenetic changes, where environmental factors modify the gene expression network without changing the DNA sequence, may influence inflammatory diseases such as chronic periodontitis. These chemical modifications of DNA and histone proteins cause epigenetic changes that alter cellular function and host defenses. Recent Findings: Findings suggest that the methylation of cytosine residues on DNA particularly at CpG Islands is commonly associated with gene silencing, and covalent modifications on histones are associated with chromatin structural integrity and function that play crucial roles in gene expression. In periodontal immune dysbiosis, aberrant DNA methylation and/or histone modifications could potentially play a role in disease state. Summary: We broadly discuss epigenetic modifications related to immune regulation and comprehensively discuss recent developments in the dynamics of epigenetic changes pertaining to chronic inflammatory periodontal disease. © 2019, Springer Nature Switzerland AG.
引用
收藏
页码：37 / 46
页数：9
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