Background/Purpose: There is a proposed link between periodontal disease (PD) and rheumatoid arthritis (RA). A substantial, although not unanimous, body of epidemiological evidence indicates a bidirectional link, with patients with PD more likely to suffer RA and vice versa. Several mechanisms have been proposed to explain the relationship between PD and RA, including i) periodontal bacterial generating autoantigens, ii) local periodontal inflammation generating autoantigens, ii) direct bacterial insult to the joint, iv) systemic inflammation associated with periodontitis exacerbating inflammation at distant sites, and v) shared risk factors. Previous studies, using experimental models of later stages of arthritis and joint destruction, suggest that periodontal infection may exacerbate arthritis and vice versa. We sought to investigate whether periodontal infection may impact on the initiation of arthritis and therefore used an experimental model of breach of immune tolerance, generation of autoantibodies and synovitis. 

Methods: Mice were orally infected with P. gingivalis to initiate alveolar bone destruction, modeling human periodontal disease. Animals subsequently received Th1 polarized ovalbumin specific T cells by adoptive transfer, and were immunized, and then challenged in the footpad with ovalbumin. Paw swelling, joint histology, periodontal bone loss, responses of T cells from the draining lymph nodes, and serum antibody were assessed. 

Results: Animals developed footpad swelling and histological evidence of synovitis. Circulating anti-CCP antibodies were significantly elevated in experimental arthritis compared with control animals (arthritis: 1189 ± 25.56 ELISA units (EU), control: 934.1 ± 99.39 EU;  p<0.05), and a similar trend was observed for circulating anti-collagen antibodies, although this did not reach statistical significance (arthritis: 439.5 ± 124.2 EU, control: 224.0 ± 68.8 EU; p=0.19). Periodontal infection had no impact on any measures of this model of early arthritis. However, animals with periodontal infection and arthritis showed significantly more periodontal bone destruction (periodontal infection+arthritis: 0.44 ± 0.01 mm, periodontal infection: 0.40 ± 0.01 mm; p<0.05) compared with animals with periodontal infection alone. 

Conclusion:

These data suggest that periodontal infection may not be responsible for initiating the breach of tolerance associated with the initiation of arthritis. In this model system of breach of tolerance, oral infection made no impact on articular or autoantibody outcomes. Nonetheless, established periodontal inflammation may be detrimental to patients with RA and therefore further human and animal studies are required to unravel the mechanisms mediating the PD/RA relationship as understanding such a relationship offers potentially improved therapeutic strategies – for both PD and RA independently and in combination.  

This project was supported by EUFP7 ‘Gums and Joints’ Grant number 261460

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/experimental-arthritis-exacerbates-periodontal-disease-but-periodontal-infection-does-not-exacerbated-experimental-arthritis/