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

2019, Número 3

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Rev Mex Periodontol 2019; 10 (3)


Relación de la periodontitis y artritis reumatoide a través del eje IL-23/IL-17A

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

Idioma: Español
Referencias bibliográficas: 69
Paginas: 69-76
Archivo PDF: 763.81 Kb.


RESUMEN

La artritis reumatoide (AR) y la periodontitis (P) son enfermedades inflamatorias crónicas. De manera reciente, se ha descrito que 90% de los pacientes con AR presentan P. Ambas patologías se caracterizan por la destrucción de la articulación y el hueso alveolar, respectivamente. Se sabe que 1% de la población mundial presenta artilugios y en México es el 1.6%. Sobre la periodontitis, su prevalencia es de 15 a 20% de la población mundial y en México es de 60%. La etiología de ambas enfermedades es similar, ya que son multifactoriales y comparten varios factores de riesgo que pueden desencadenarlas, como lo son factores genéticos, biológicos o ambientales, dentro de los cuales uno de los que mantiene más cercana la relación de estas enfermedades es el factor biológico, donde una disbiosis a nivel bucal o intestinal puede comenzar con inflamación local y a su vez sistemática. Las citocinas proinflamatorias IL-23 e IL-17 y sus receptores juegan un papel muy importante en la inmunopatología de estas enfermedades. IL-23 activa y expande los clones Th17 a través de IL-23R y promueve la producción de IL-17 y RANKL; sin embargo, la IL-23R soluble puede bloquear el receptor de IL-23 al inhibir su señalización. IL-17 a través de IL-17RA puede activar fibroblastos y macrófagos que expresan RANKL que activa los precursores de osteoclastos e inicia la erosión ósea en las articulaciones y el hueso alveolar. Al igual que el receptor soluble de IL-23R, el ser soluble de IL-17RA puede bloquear a IL-17A e inhibir su señalización.


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