Background/Purpose:

Periodontitis, a polymicrobial infectious and inflammatory disease of tooth-supporting structures, shares pathogenic mechanisms with rheumatoid arthritis (RA) and may trigger its onset. Most studies have focused on Porphyromonas gingivalis (Pg), and serologic responses to periodontal pathogens, rather than direct detection of organisms. One prior study by Scher et al. found enrichment of Prevotella and Leptotrichia species in the oral microbiota of new-onset RA patients, irrespective of periodontal disease status. Here we studied the subgingival plaque biofilm of patients with new-onset and chronic RA.

Methods:

43 subjects, 23 RA patients, all meeting 2010 ACR/EULAR criteria, and 20 age- and gender-matched healthy subjects without periodontitis or RA completed standardized dental examination performed by a single periodontist. Dental parameters were measured at 6 sites per tooth. A total of 86 subgingival plaque samples (2 per subject) were evaluated for the presence of 41 bacterial taxa associated with periodontitis biofilms by checkerboard DNA-DNA hybridization.

Results:

Typical of RA cohorts, the 23 patients were mainly female (87%) with median age of 48; 15 had DMARD-naive early disease. The majority (61%) was seropositive for ACPA, 43% were positive for rheumatoid factor, and they had a range of disease activity from mild to severe. None were current smokers. All but one patient received routine dental care with cleanings every 6 months.  

Of the 23 patients, 10 (43%) had gingivitis, a precursor of periodontitis, 9 (39%) had periodontitis, and only 4 patients (17%) had healthy periodontal tissue. Compared with the 20 healthy subjects, the 23 RA patients had significantly increased pocket depth (P<0.000001), clinical attachment loss (P=0.001), and bleeding on probing (P=0.0001). There were no differences in dental parameters between former vs. never smokers.

The RA patients had a distinct subgingival biofilm. Accounting for multiple comparisons, 10 of 41 pathogens had higher DNA probe counts (levels) in RA patients versus controls (P ≤0.002). Although RA patients had higher levels of classic “red-complex” pathogens (P. gingivalis, Tannerella forsythia, and Treponema denticola) than healthy controls, differences were not significant. Compared with chronic RA, new-onset patients had significantly higher levels of several pathogens, including Gemella morbillorum, Propionybacterium acnes, Streptococcus gordonii, and Leptotrichia buccalis (P≤0.05), regardless of whether they had periodontitis on examination. L. buccalis was present in 67% of new-onset RA patients versus only 13% of those with chronic RA (P=0.02). Finally, levels of L. buccalis and P. acnestended to correlate with multiple disease activity measures (P≤0.07).

Conclusion:

Despite routine dental care, most of our patients had gingivitis or periodontitis on examination and abundance of periodontal pathogens in subgingival plaque. Although P. gingivalis, a classic periodontal pathogen is of interest in RA pathogenesis, several other organisms including the previously implicated Leptotrichia species, may be more specifically associated with new-onset RA and may warrant further study as candidate triggers of RA.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/elevated-subgingival-levels-of-periodontal-pathogens-in-rheumatoid-arthritis-patients-particularly-leptotrichia-species-in-new-onset-disease/