Inflammatory profile of chronic apical periodontitis: a literature review

Abstract

Apical periodontitis caused by root canal infection is the most frequent pathological lesion in the jaws, mainly manifested as periapical granulomas and cysts. Understanding of the formation and progression of apical periodontitis as well as the identification of inflammatory biomarkers can help increase the knowledge of pathogenic mechanisms, improve the diagnosis and provide support for different therapeutic strategies. The objective of the present article is to review inflammatory biomarkers such as cytokines, chemokines, inflammatory cells, neuropeptides, RANK/RANKL/OPG system and other inflammatory markers and to relate these systems to the development and progression of pathological conditions related to apical periodontitis.

Effect of intercellular adhesion molecule 1 deficiency on the development of apical periodontitis

“…On the other hand, a cell culture study demonstrated that the RANK and RANKL factors are not sufficient for the firm and static union between osteoblasts and osteoclasts and that the ICAM‐1/LFA molecules are necessary to the effective adhesion between these cells during the osteoclastogenesis (Okada et al ). However, those present in vivo findings confirm the requirement of RANKL expressed on osteoblasts for osteoclasts maturation and the crucial involvement of the RANK and RANKL in periapical lesion development, as previously described (Vernal et al , Bezerra da Silva et al , Braz‐Silva et al , Francisconi et al . , Howait et al , Jakovljevic et al ).…”

“…In the present study, a lower level of INF‐γ and higher level of IL‐10 in the ICAM‐1 KO mice was observed, while the expression of TNF‐α and OPG was equal to both groups. Although the main cytokines secreted by neutrophils are IL‐1, IL‐6 and TNF‐α (Márton & Kiss , Reinke & Sorg ), the pathogenesis of the biochemical network is not so obvious and occurs in a very complex and dynamic way (Braz‐Silva et al ). These cytokines are also produced by other inflammatory cells and show different behaviours, depending on the immunopathological micro‐environment.…”

“…Apical periodontitis results from polymicrobial infection of the dental pulp and root canal system leading to a progressive destruction of periodontal ligament, cementum, and alveolar bone. The destruction of apical and periapical tissues is mediated by a complex network of cellular and molecular mechanisms, which includes migration of inflammatory cells to the sites of infection and osteoclastogenesis (Wang & Stashenko , Stashenko et al , Nair , De Rossi et al , Fukada et al , da Silva et al , de Oliveira et al , De Rossi et al , Braz‐Silva et al , Jakovljevic et al , Howait et al ). The knowledge of regulatory mechanisms that control the host immune system response to infection is important for a better understanding of the aetiopathogenesis and treatment of immunoinflammatory diseases.…”

The Presence and involvement of interleukin‐17 in apical periodontitis

“…, Braz‐Silva et al . ). Cytokines play an important role in innate and adaptive immunity and have a substantial role in managing the orientation, intensity and persistence of the inflammatory reaction (Roescher et al .…”

“…Chronic inflammatory lesions and destruction of alveolar bone structures are the result of the failure of host defence mechanisms to eradicate infection ). Although many experimental and clinical studies have been reported over the past decades to explore the pathogenesis and much is already known about the process, the exact role of immune cells, cytokines and other inflammatory mediators associated with the persistence and resolution of periapical lesions (PLs) is not completely understood (Marton & Kiss 2000, Nair 2004, Belibasakis et al 2013, Braz-Silva et al 2018. Cytokines play an important role in innate and adaptive immunity and have a substantial role in managing the orientation, intensity and persistence of the inflammatory reaction (Roescher et al 2009).…”