Periodontitis in established rheumatoid arthritis patients: a cross-sectional clinical, microbiological and serological study

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.

Figure 1

DAS28 scores and CRP levels in patients with rheumatoid arthritis and no (a), moderate (b), or severe (c) periodontitis. **P < 0.01. CRP, C-reactive protein; DAS28, disease activity score 28 tender and swollen joint count.

Figure 2

(A) IgM-RF and ACPA reactivity and (B) reactivity against five citrullinated (cit.) peptides in patients with rheumatoid arthritis and no (a), moderate (b), or severe (c) periodontitis. No significant differences were observed. ΔOD, optical density of the citrullinated form minus the native form of the peptide; ACPA, anti-citrullinated protein antibody; IgM-RF, immunoglobulin M-rheumatoid factor.

Figure 3

IgA, IgG, and IgM antibody response against Porphyromonas gingivalis in rheumatoid arthritis (RA) patients and non-RA controls with severe periodontitis as well as in healthy controls (HC). *P < 0.05. Ig, immunoglobulin.

Figure 4

Correlation of anti-citrullinated protein antibody (ACPA) in paired samples of serum and gingival crevicular fluid (GCF) of patients with rheumatoid arthritis (n = 45).