Periodontitis and specifically infection with Porphyromonas gingivalis are associated with disease initiation of rheumatoid arthritis (RA) and may serve as targets for preventative intervention, according to study results published in JAMA Network Open.

RA can be detected via specific autoantibodies in the serum years before patients develop joint inflammation, which suggests that the joints may be a target rather than the primary cause of the disease. This also suggests that there may be a preclinical RA phase that could be targeted for disease prevention. Individuals at risk for RA have commonly shown serum samples enriched with IgA anti-citrulinated protein antibodies, implying that mucosal sites, like oral mucosa, may be important at the earliest stages of RA. Further, evidence suggests there is a clinical association between periodontitis and RA.

Periodontitis is associated with an abundance of the pathogenic organism P gingivalis, along with other anaerobic organisms; P gingivalis is capable of citrullinating local antigens and therefore potentially initiate anti-citrullinated protein antibodies. However, periodontitis and citrullinating bacteria have not been investigated in individuals at risk for RA. Therefore, this cross-sectional study examined periodontal disease and periodontopathic bacteria in individuals who were at risk for anti-cyclic citrullinated protein (anti-CCP) antibody-positive at-risk individuals without arthritis.

In total, 48 individual positive for anti-CCP who did not have arthritis were recruited nationally, 26 patients with early RA and 32 healthy control individuals were recruited locally and included in the study from 2015 to 2017. Using ultrasonography, periodontal assessments and the examinations of joints were performed. Individuals at risk for CCP+ were compared with patients with early RA and healthy individuals who were matched for age and smoking history in prevalence of diseased periodontal sites, periodontal inflamed surface area, and clinical periodontitis. Investigators profiled and analyzed DNA from subgingival plaque from both diseased and healthy periodontal sites.

Of the individuals at risk for CCP+, 65% were women and mean age was 51.9 years; of the patients with early RA, 54% were women and mean age was 54.4 years; of the healthy individuals, 59% were women and mean age was 49.4 years. Two individuals at risk for CCP+ had joint inflammation seen on ultrasonography. Further, 73% of the individuals at risk for CCP+, 54% of patients with early RA, and 38% of healthy individuals had clinical periodontitis. Individuals at risk for CCP+ had a greater median percentage of periodontal sites with disease when compared with healthy individuals (3.3% vs 0%) but was similar to patients with early RA (3.3% vs 1.1%). In a similar fashion, when compared with healthy individuals, CCP+ at-risk individuals had a higher median periodontal inflamed surface area (40 mm2 vs 221 mm2). With regard to healthy periodontal sites, individuals at risk for CCP+ had a greater relative abundance of P gingivalis compared with both healthy individuals and patients with early RA.

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Overall, the study authors concluded that, “In individuals at risk of RA, periodontitis and P gingivalis were increased before joint disease and may be a target for prevention.”

Reference

Mankia K, Cheng Z, Do T, et al. Prevalence of periodontal disease and periodontopathic bacteria in anti-cyclic citrullinated protein antibody-positive at-risk adults without arthritis. JAMA Network Open. 2019;2(6):e195394.