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ISSN 2007-4360 (Print)
Asociación Mexicana de Periodontología, Colegio de Periodoncistas A.C

2019, Number 3

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Rev Mex Periodontol 2019; 10 (3)

Relationship of periodontitis and rheumatoid arthritis through the IL-23/IL-17A axis

Rodríguez-Montaño R, Aguilar-Carrillo JA, Bernard-Medina AG, Martínez-Rodríguez VMC, Gómez-Meda BC, Guerrero-Velázquez C

Language: Spanish
References: 69
Page: 69-76
PDF size: 763.81 Kb.


ABSTRACT

Rheumatoid arthritis (RA) and periodontitis (P) are chronic inflammatory diseases. Recently it has been described that 90% of patients with RA present P. Both pathologies are characterized by the destruction of the joint and alveolar bone respectively. It is known that 1% of the population in the world presents artirits and in Mexico 1.6%. About periodontitis, its prevalence is 15 to 20% of the population in the world and in Mexico it is 60%. The etiology of these diseases is similar because they are multifactorial and the risk factors that can trigger them have them in common. Such as genetic, biological or environmental factors, within which one of the ones that keeps the relationship of these diseases closer is the biological one where a dysbiosis at the buccal or intestinal level can start with local and in turn systematic inflammation. The proinflammatory cytokines IL-23 and IL-17 and their receptors play a very important role in the immunopathology of these diseases. IL-23 activates and expands Th17 clones through IL-23R and promotes the production of IL-17 and RANKL, however, the soluble IL-23R receptor can block IL-23 by inhibiting its signaling. IL-17 through IL-17RA can activate fibroblasts and macrophages which express RANKL that activates osteoclast precursors and initiates bone erosion in joints and alveolar bone. Like the soluble receptor of IL-23R, IL-17RA being soluble can block IL-17A and inhibit its signaling.


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