CHICAGO – A causal relationship between rheumatoid arthritis and periodontal disease has not been confirmed, but recent data support the concept of a bi-directional relationship between the two.
In fact, a number of investigators have attempted to characterize the relationship between rheumatoid arthritis (RA) and periodontal disease. While most research confirms that one exists, the strength and extent of that relationship remain unclear, Michele Ravenel, D.M.D., said at the annual meeting of the American College of Rheumatology.
"Periodontal disease and RA do share similar pathologic mechanisms, and the relationship appears to be bi-directional," Dr. Ravenel said. But in her own review of the literature, the only consistency she found was inconsistency, said Dr. Ravenel.
In one recent case-control study involving 57 RA patients and 52 healthy subjects, those with RA were found to have significantly greater odds of having periodontitis after adjusting for a number of variables including RA status, age, sex, alcohol use, and body mass index (J. Periodontol. 2008;79:979-86).
"Periodontal disease and RA do share similar pathologic mechanisms, and the relationship appears to be bi-directional," said Michele Ravenel, D.M.D.
And in another recent study, 65 RA patients all were found to have some form of periodontal disease, which was moderate or severe in most cases. However, rheumatoid factor levels were not found to have any influence on oral bacterial composition and/or concentration – or on severity of periodontal disease (J. Periodontol. 2011;82:1424-32).
In yet another study of patients with both moderate to severe RA and severe periodontal disease, outcomes were compared in 10 patients on no treatment, 10 on periodontal therapy, 10 on anti-TNF-alpha therapy, and 10 on both periodontal therapy and anti-TNF-alpha therapy (J. Periodontol. 2009;80:535-40). Patients who were receiving treatment for periodontal disease – either with or without anti-TNF-alpha therapy for their RA – experienced significantly greater improvements in both the periodontal disease and the RA, compared with those not on periodontal therapy, said Dr. Ravenel of the Medical University of South Carolina, Charleston.
As for the role of periodontal pathogens in RA, findings from two recent case-control studies showed that serum antibodies to known periodontal pathogens were found more frequently in those with RA and periodontal disease than in controls (MedGenMed. 2005;7:2;Clin. Exp. Rheumatol. 2006;24:656-63).
In a cross-sectional study, bacterial DNA of some of the more virulent periodontal pathogens, including Porphyromonas gingivalis, Tannerella forsythia, and Prevotella intermedia, were identified in synovial fluid of RA-affected joints (J. Clin. Periodontol. 2009;1004-10).
In another study, which was presented separately at the 2011 annual meeting of the ACR, Dr. Jose U. Scher reported on a potentially important role for "a single species-level operational taxonomic unit belonging to the genus Porphyromonas and homologous to P. gingivalis," which he said could explain the link between RA and periodontal disease.
The particular Porphyromonas species was significantly more prevalent and more abundant in 25 patients with new-onset, never-treated RA, compared with 27 patients with established disease, and 14 healthy controls. That species accounted for nearly 10% of the bacteria in the new-onset RA patients, compared with about 3% and 4% of the bacteria in control patients and patients with chronic established disease, respectively, said Dr. Scher, of New York University Hospital for Joint Diseases.
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