Current trends of genetics in apical periodontitis research

Abstract

Genetics is an emerging topic in endodontic research focusing on the host response regarding the pathogenesis of apical periodontitis (AP). A number of genetic epidemiological studies carried out by many investigators worldwide have shown evidence of an association between certain candidate genes and AP. Some studies have been conducted on knockout mice with a deficiency in certain proteins, leading to more or less severe AP, and thus suggesting a pivotal role of these genes in AP pathogenesis. Other research has evaluated the association between genetic polymorphisms in humans with different AP aspects; these studies pointed out that genetic polymorphisms in some candidate genes are involved in inter-individual variations in their response to AP. Therefore, the objective of this report was to provide an updated overview of the genes involved in AP pathogenesis, with a focus on the most relevant candidate genes.

Association of polymorphisms in TNF‐α, IL‐1β, GSTM and GSTT genes with apical periodontitis: is there a link with herpesviral infection?

“…Genetic polymorphisms may be considered as disease modifiers in AP, affecting its severity and clinical course (Aminoshariae & Kulild 2015, Salles et al 2017, 2018, Küchler et al 2018). It is also reasonable to assume that individuals are not equally prone to the development of AP.…”

“…It promotes osteoclastogenesis independently or in combination with other inflammatory mediators (Márton & Kiss 2014, Braz‐Silva et al 2019). The SNP at position −308 within the promoter is one of the best‐described polymorphisms in TNF gene, and the AA genotype is associated with high TNF production (Küchler et al 2018). In the present study, TNF‐α (−308 G >A) polymorphism appeared to be a strong risk factor for AP development, especially in AA homozygotes.…”

“…Heredity may also considerably affect the development, clinical course and severity of AP. Polymorphisms in genes encoding inflammatory cytokines associated with host immune response to microbial agents have been proposed as potential genetic markers of AP (Küchler et al 2018). This mostly refers to functional polymorphisms that alter the quantity or the structure of the encoded proteins and, therefore, presumably modulate an individual’s susceptibility to AP (Küchler et al 2018).…”

“…Polymorphisms in genes encoding inflammatory cytokines associated with host immune response to microbial agents have been proposed as potential genetic markers of AP (Küchler et al 2018). This mostly refers to functional polymorphisms that alter the quantity or the structure of the encoded proteins and, therefore, presumably modulate an individual’s susceptibility to AP (Küchler et al 2018). Thus far, three systematic reviews have provided a summary of the association studies on interleukin gene polymorphisms in AP (Aminoshariae & Kulild 2015, Salles et al 2017, 2018).…”

Aggregatibacter, a Low Abundance Pathobiont That Influences Biogeography, Microbial Dysbiosis, and Host Defense Capabilities in Periodontitis: The History of a Bug, and Localization of Disease

“…As such, host defense mechanisms that include coagulation factors (fibrin, Hageman factor, etc.) can act as a determinant in deterring systemic damage by localizing disease to the immediate area of challenge [107].…”