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Interleukin-29 modulates proinflammatory cytokine production in synovial inflammation of rheumatoid arthritis
Authors:Fang Wang  Lingxiao Xu  Xiaoke Feng  Dunming Guo  Wenfeng Tan  Miaojia Zhang
Institution:1. Center for Dentistry and Oral Hygiene, University of Groningen, University Medical Center Groningen, P.O. Box 30.001, 9700, RB, Groningen, The Netherlands
2. Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, P.O. Box 30.001, 9700, RB, Groningen, The Netherlands
3. Department of Oral and Maxillofacial Surgery, University of Groningen, University Medical Center Groningen, P.O. Box 30.001, 9700, RB, Groningen, The Netherlands
4. Department of Medical Microbiology, University of Groningen, University Medical Center Groningen, P.O. Box 30.001, 9700, RB, Groningen, The Netherlands
Abstract:

Introduction

The association between rheumatoid arthritis (RA) and periodontitis is suggested to be linked to the periodontal pathogen Porphyromonas gingivalis. Colonization of P. gingivalis in the oral cavity of RA patients has been scarcely considered. To further explore whether the association between periodontitis and RA is dependent on P. gingivalis, we compared host immune responses in RA patients with and without periodontitis in relation to presence of cultivable P. gingivalis in subgingival plaque.

Methods

In 95 RA patients, the periodontal condition was examined using the Dutch Periodontal Screening Index for treatment needs. Subgingival plaque samples were tested for presence of P. gingivalis by anaerobic culture technique. IgA, IgG and IgM antibody titers to P. gingivalis were measured by ELISA. Serum and subgingival plaque measures were compared to a matched control group of non-RA subjects.

Results

A higher prevalence of severe periodontitis was observed in RA patients in comparison to matched non-RA controls (27% versus 12%, p < 0.001). RA patients with severe periodontitis had higher DAS28 scores than RA patients with no or moderate periodontitis (p < 0.001), while no differences were seen in IgM-RF or ACPA reactivity. Furthermore, RA patients with severe periodontitis had higher IgG- and IgM-anti P. gingivalis titers than non-RA controls with severe periodontitis (p < 0.01 resp. p < 0.05), although subgingival occurrence of P. gingivalis was not different.

Conclusions

Severity of periodontitis is related to severity of RA. RA patients with severe periodontitis have a more robust antibody response against P. gingivalis than non-RA controls, but not all RA patients have cultivable P. gingivalis.
Keywords:
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