The Potential Role of Epigenetic Modifications on Different Facets in the Periodontal Pathogenesis

Abstract

Periodontitis is a chronic inflammatory disease that affects the supporting structures of teeth. In the literature, the association between the pathogenicity of bacteria and environmental factors in this regard have been extensively examined. In the present study, we will shed light on the potential role that epigenetic change can play on different facets of its process, more particularly the modifications concerning the genes involved in inflammation, defense, and immune systems. Since the 1960s, the role of genetic variants in the onset and severity of periodontal disease has been widely demonstrated. These make some people more susceptible to developing it than others. It has been documented that the wide variation in its frequency for various racial and ethnic populations is due primarily to the complex interplay among genetic factors with those affecting the environment and the demography. In molecular biology, epigenetic modifications are defined as any change in the promoter for the CpG islands, in the structure of the histone protein, as well as post-translational regulation by microRNAs (miRNAs), being known to contribute to the alteration in gene expression for complex multifactorial diseases such as periodontitis. The key role of epigenetic modification is to understand the mechanism involved in the gene-environment interaction, and the development of periodontitis is now the subject of more and more studies that attempt to identify which factors are stimulating it, but also affect the reduced response to therapy.

The Genetic Aspects of Periodontitis Pathogenesis and the Regenerative Properties of Stem Cells

“…Periodontitis is a state of permanent inflammation in the periodontium. Microbial biofilm and their metabolism cause host cell death and increased turnover, and increased regeneration affects defense responses and epigenetic alterations [6]. Gingival crevicular fluid (GCF) is derived from the periodontal tissue, and its production increases in PD [7].…”

“…Gingival crevicular fluid (GCF) is derived from the periodontal tissue, and its production increases in PD [7]. It consists of many different cells stimulated by interleukin 8, which aimed to produce antimicrobial peptides (AMPs) to control the immune response [6,7]. In PD, the expression of AMPs can be dysregulated [8], and upregulation could suggest an engaged immune response to control pathogen-induced inflammation.…”

Impact of Non-Surgical Periodontal Treatment on the Concentration and Level of MRP-8/14 (Calprotectin) as an Inflammatory Biomarker in Women with Periodontitis and Rheumatoid Arthritis: A Quasi-Experimental Study

“…The main risk factors for periodontal disease are poor oral hygiene and tobacco use. The origin of periodontitis is multifactorial and involves multiple component causes, genetics, epigenetic influences, and modifiable factors such as environmental factors, habits, and medications that establish and propagate periodontitis lesions [5,6]. The appearance of dysbiosis of the subgingival microbiome triggers an inflammatory response.…”