Genetic, Cellular and Molecular Aspects involved in Apical Periodontitis

Abstract

The development, establishment and repair of apical periodontitis (AP) is dependent of several factors, which include host susceptibility, microbial infection, immune response, quality of root canal treatment and organism's ability to repair. The understanding of genetic contributions to the risk of developing AP and presenting persistent AP has been extensively explored in modern Endodontics. Thus, this article aims to provide a review of the literature regarding the biochemical mediators involved in immune response signaling, osteoclastogenesis and bone neoformation, as the genetic components involved in the development and repair of AP. A narrative review of the literature was performed through a PUBMED/MEDLINE search and a hand search of the major AP textbooks. The knowledge regarding the cells, receptors and molecules involved in the host's immune-inflammatory response during the progression of AP added to the knowledge of bone biology allows the identification of factors inherent to the host that can interfere both in the progression and in the repair of these lesions. The main outcomes of studies evaluated in the review that investigated the correlation between genetic polymorphisms and AP in the last five years, demonstrate that genetic factors of the individual are involved in the success of root canal treatment. The discussion of this review gives subsides that may help to glimpse the development of new therapies based on the identification of therapeutic targets and the development of materials and techniques aimed at acting at the molecular level for clinical, radiographic and histological success of root canal treatment.

Single nucleotide polymorphisms in inducible nitric oxide synthase gene are not associated with persistent apical periodontitis

“…AP is a complex pathology involving multiple factors, and various inflammatory and anti-inflammatory molecules may influence the state and progression of the disease [1]. The role of SNPs in the patient's response to root canal treatment, reflects the involvement of the heredity in the individual success of endodontic treatment [5], acting as a risk or a protective factor for the development and progression of AP [6].…”

“…The interactions between various inflammatory and anti‐inflammatory molecules can influence the disease state and progression [1]. The host susceptibility, microbial infection, immune response, quality of the endodontic treatment and organism's ability to repair are factors that may interfere with the development, establishment and repair of AP [5]. Although the presence of bacteria is the determining factor of PAP, heredity may be a significant contributor [6].…”

The effect of Nrf2 on bone resorption in chronic apical periodontitis

“…The pathological mechanism of CAP is still unclear. Microbial antigens from infected root canals can stimulate speci c in ammatory and nonspeci c immune responses in periapical tissues [6][7][8][9][10]. Gram negative bacteria is the main dominant bacterium in infected root canals and periapical tissue lesions.…”

Hypercitrullination and anti‐citrullinated protein antibodies in chronic apical periodontitis, a laboratory investigation. Does autoimmunity contribute to the pathogenesis?

“…In the course of the ongoing endodontic infection, microbes, their antigens and toxins reach the apical periodontal ligament and surrounding tissues through the apical foramen and trigger immunological defence mechanisms (Georgiou et al, 2019; Martinho et al, 2014). A delicate balance between protective and destructive reactions ultimately results in the formation of granulation tissue around the apical foramen, consisting of necrotic, exudative, granulomatous and fibrous zones (Márton & Kiss, 2000, 2014; Morse, 1977; Petean et al, 2022; Yanagisawa, 1980). In the necrotic and exudative zones, abundant neutrophils eliminate the majority of microbes rendering the granulomatous and fibrous zones sterile (Márton & Kiss, 2014).…”