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The aggravation of arthritis by periodontitis is dependent of IL ‐17 receptor A activation
Author(s) -
Aquino Sabrina G.,
Talbot Jhimmy,
Sônego Fabiane,
Turato Walter M.,
Grespan Renata,
AvilaCampos Mario J.,
Cunha Fernando Q.,
Cirelli Joni A.
Publication year - 2017
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12743
Subject(s) - arthritis , porphyromonas gingivalis , periodontitis , medicine , interleukin 17 , immunology , infiltration (hvac) , rheumatoid arthritis , cytokine , physics , thermodynamics
Aim To evaluate whether Porphyromonas gingivalis ‐induced periodontitis aggravates the antigen‐induced arthritis ( AIA ) model, and whether this effect is dependent on the Th17/ IL ‐17 signalling pathway. Materials and methods Antigen‐induced arthritis was triggered by local injection of methylated bovine serum albumin into the knee joint of previously immunized C57 BL /6 wild‐type ( WT ) and IL ‐17 receptor A ( IL ‐17 RA )‐knockout mice. Periodontal disease in naïve or arthritic mice was induced by oral infection with P. gingivalis . Animals were sacrificed 7, 15 and 30 days after infection. Alveolar bone loss, joint histopathology, articular hyperalgesia and joint cytokine production were assessed, in addition to the proportion of Th17 and Treg cells isolated from the inguinal lymph nodes. Results No influence of experimentally‐induced arthritis was found on the alveolar bone resorption induced by P. gingivalis . However , mice with experimentally‐induced arthritis that were exposed to P. gingivalis presented higher joint damage and Th17 frequencies when compared to non‐infected mice. The aggravation of arthritis by periodontitis was accompanied by increased TNF and IL ‐17 production and articular neutrophil infiltration, whereas arthritis aggravation and changes in neutrophil infiltration were absent in IL ‐17 RA ‐deficient mice. Conclusion The effects of P. gingivalis‐ induced periodontitis on arthritis are dependent on Th17 expansion and IL ‐17 RA signalling, which lead to increased neutrophil infiltration into the joints.