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. 2024 Sep 5;58(3):160-168.
doi: 10.26650/eor.20241423117.

Inflammatory mediators' essence in apical periodontitis

Affiliations

Inflammatory mediators' essence in apical periodontitis

Nikola Milojevic et al. Eur Oral Res. .

Abstract

Apical periodontitis (AP) represents chronic inflammatory reaction of periradicular tissues of teeth with necrotic pulp. Although AP has been considered as a multifactorial disease, different microorganisms and their virulence factors from infected root canals are considered to be the primary cause of periradicular inflammatory process. The interplay between microbes and host leads to an inflammatory cascade of events that includes activation of innate and adaptive components of immunity. Activation of different immune cells in AP is intermediated by different molecules known as mediators of inflammation. These molecules establish various network interrelationships in the inflamed periapical area and induce alveolar bone resorption. This narrative review aimed to explore and present the current knowledge of selected inflammatory mediators, including cytokines, matrix metalloproteinases, bone resorption regulators and components of oxidative stress involved in the alveolar bone resorption in AP.

Keywords: cytokines; Periapical periodontitis; bone resorption; matrix metalloproteinases; oxidative stress.

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Conflict of interest statement

Conflict of interest:The authors declared that they have no conflict of interest.

References

    1. Nair PN. On the causes of persistent apical periodontitis: a review. Int Endod J. 2006. Apr;39(4):249–81. 10.1111/j.1365-2591.2006.01099.x - DOI - PubMed
    1. Siqueira JF Jr, Rôças IN. Present status and future directions: microbiology of endodontic infections. Int Endod J. 2022. May;55(S3 Suppl 3):512–30. 10.1111/iej.13677 - DOI - PubMed
    1. Márton IJ, Kiss C. Overlapping protective and destructive regulatory pathways in apical periodontitis. J Endod. 2014. Feb;40(2):155–63. 10.1016/j.joen.2013.10.036 - DOI - PubMed
    1. Fouad AF. Molecular mediators of pulpal inflammation. In: Franklin RT, Seltzer S, Hargreaves KM, Goodis HE, editors. Seltzer and Bender’s Dental Pulp. Chicago: Quintessence Publishing; 2012. pp. 241–75.
    1. Liu C, Chu D, Kalantar-Zadeh K, George J, Young HA, Liu G. Cytokines: From Clinical Significance to Quantification. Adv Sci (Weinh). 2021. Aug;8(15):e2004433. 10.1002/advs.202004433 - DOI - PMC - PubMed

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