Periodontal Disease and Rheumatoid Arthritis

The Evidence Accumulates for Complex Pathobiologic Interactions

Clifton O. Bingham III; Malini Moni


Curr Opin Rheumatol. 2013;25(3):345-353. 

In This Article

Clinical Studies of P. gingivalis in Rheumatoid Arthritis

A number of studies[26,58,59,60] have evaluated whether exposure to Pg is seen in rheumatoid arthritis and whether exposure is associated with rheumatoid arthritis autoantibodies. Using an antibody against Pg, Mikuls et al.[58] demonstrated that anti-Pg presence and titers were higher in rheumatoid arthritis than controls. They also showed that Pg titers were associated with anticyclic citrullinated protein (anti-CCP) antibodies of the IgM and IgG2 isotypes. Recent studies have also studied relationships between anti-Pg and rheumatoid arthritis antibodies, though in a recent study[59] of Japanese rheumatoid arthritis patients, anti-Pg was associated with rheumatoid factors, but not with anti-CCP. In another study[60] that examined 11 periodontal pathogens in subgingival plaque profile from rheumatoid arthritis patients, there was no association of the presence or abundance of Pg with rheumatoid factors, but ACPA results were not reported, and rheumatoid factor seropositivity in the population was very low. And in another study,[61] antibodies to Pg were associated with worse periodontal disease parameters in rheumatoid arthritis patients but not with five different specific ACPA from enolase, fibrinogen, and vimentin.

Two recent studies have further examined relationships between Pg exposure and rheumatoid arthritis antibodies in two important populations. The first of these examined ACPA and antibodies against three different periodontopathic bacteria, including Pg, in individuals at risk for developing rheumatoid arthritis (HLA-DR4 and/or being a first-degree relative of a person with rheumatoid arthritis).[62] Similarly to earlier reports in another high-risk cohort of native Americans,[63] they showed anti-Pg as a marker of potential periodontal disease was associated with ACPA and rheumatoid factors. In the recent study, this relationship was seen with anti-Pg but not with the other oral bacteria tested, suggesting that Pg exposure was permissive in the development of rheumatoid arthritis antibodies, even before the presence of any clinical arthritis.

The second study by Scher et al.[64] examined anti-Pg and added sophisticated multiplex pyrosequencing to evaluate the oral microbiome in groups of individuals with early rheumatoid arthritis, established rheumatoid arthritis, and healthy adults. Prior studies had been cross-sectional but had not addressed associations at the inception of rheumatoid arthritis. These investigators showed that periodontal disease was present and frequently severe in the early and established rheumatoid arthritis groups, more than that in controls (62%, 52%, 22% with severe periodontal disease, respectively). In contrast to other reports, neither anti-Pg nor the abundance of Pg organisms was higher in rheumatoid arthritis patients compared with controls, nor was there a relationship between anti-Pg or Pg abundance and the presence of rheumatoid arthritis autoantibodies; however, they identified additional bacterial species apart from Pg that were associated with rheumatoid arthritis autoantibodies (Anaeroglobus geminatus) and new-onset rheumatoid arthritis (Prevotella and Leptrotrichia species).