Porphyromonas gingivalis Serum Antibody: Association With Rheumatoid Arthritis Disease Activity

Objectives: To determine the association of Porphyromonas gingivalis serum antibody and P. gingivalis counts in subgingival plaque with rheumatoid arthritis (RA) disease activity in established RA.
Methods: Subgingival plaque samples were collected from four sites/individual and pooled and serum was drawn from 256 RA patients. RA patients were categorized into low (DAS-28-CRP <3.2), moderate (DAS-28-CRP ≥ 3.2 and ≤5.1) and high (DAS-28-CRP >5.1) disease activity based on twenty-eight swollen and tender joint counts, patient global well-being scores, and serum C-reactive protein determination. Plaque samples were analyzed by 16S rRNA sequencing using the Illumina MiSeq platform. Serum antibody to P. gingivalis outer membrane antigen (OMA) was determined by ELISA. Normalized P. gingivalis and other Porphyromonas species bacterial counts in subgingival plaque were determined for each level of RA disease activity, using TMM and voom methods. Serum P. gingivalis antibody concentration and the ratio of antibody concentration to normalized bacterial counts were compared among RA disease activity groups using the non-parametric Kruskal-Wallis test.
Results: In the overall population, antibody to P. gingivalis OMA was associated with RA disease activity (p=0.02), with higher antibody concentrations in the high disease activity group. This association also was observed in non-smokers (p=0.03), but not in smokers. When evaluating serum P. gingivalis antibody concentration relative to bacterial counts in subgingival plaque in non-smokers, there was a significant association between RA disease activity and the ratio of P. gingivalis antibody to normalized P. gingivalis counts (p=0.02), but not to other Porphyromonas species. This significant association was not observed in smokers. TMM and voom normalization methods yielded similar results.
Conclusions: Antibody to P. gingivalis OMA is associated with RA disease activity. In non-smokers, this association persisted even after adjusting for P. gingivalis counts in subgingival plaque. These data suggest that infection with P. gingivalis may play a role in RA disease pathogenesis in non-smokers.