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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

The aggravation of arthritis by periodontitis is dependent of IL-17 receptor A activation

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de Aquino, Sabrina G. [1, 2] ; Talbot, Jhimmy [3] ; Sonego, Fabiane [3] ; Turato, Walter M. [3] ; Grespan, Renata [3, 4] ; Avila-Campos, Mario J. [5] ; Cunha, Fernando Q. [3] ; Cirelli, Joni A. [1]
Total Authors: 8
[1] Univ Estadual Paulista UNESP, Sch Dent Araraquara, Dept Diag & Oral Surg, Araraquara - Brazil
[2] Univ Fed Paraiba, Hlth Sci Ctr, Dept Clin & Social Dent, Joao Pessoa, Paraiba - Brazil
[3] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pharmacol, Ribeirao Preto - Brazil
[4] Univ Fed Sergipe, Biol & Hlth Sci Ctr, Dept Physiol, Aracaju - Brazil
[5] Univ Sao Paulo, Inst Biomed Sci, Dept Microbiol, Ribeirao Preto - Brazil
Total Affiliations: 5
Document type: Journal article
Source: JOURNAL OF CLINICAL PERIODONTOLOGY; v. 44, n. 9, p. 881-891, SEP 2017.
Web of Science Citations: 11

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 C57BL/6 wild-type (WT) and IL-17 receptor A (IL-17RA)-knockout mice. Periodontal disease in naive 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-17RA-deficient mice. Conclusion: The effects of P. gingivalis-induced periodontitis on arthritis are dependent on Th17 expansion and IL-17RA signalling, which lead to increased neutrophil infiltration into the joints. (AU)

FAPESP's process: 09/00341-7 - Association between rheumatoid arthritis and periodontal disease: evaluation of the IL-23/IL-17 axis
Grantee:Joni Augusto Cirelli
Support Opportunities: Regular Research Grants
FAPESP's process: 08/08142-0 - Evaluation of rheumatoid arthritis and periodontal disease association. Study of IL-23/IL-17 axis in experimental model of rheumatoid arthritis and periodontal disease in mice.
Grantee:Sabrina Garcia de Aquino
Support Opportunities: Scholarships in Brazil - Doctorate