Periodontitis is defined as an inflammatory condition caused by a dysbiotic microbiota that causes the periodontal ligament, cementum, and alveolar bone to gradually deteriorate. Rheumatoid arthritis is a chronic inflammatory autoimmune condition accompanied by persistent synovitis, systemic inflammation, and the production of autoantibodies.
Asymmetry between subgingival populations and host immune response is another dysbiotic characteristic of periodontitis. Synovial inflammation and hyperplasia in RA result in permanent damage to the bone and cartilage in the joints, loss of function, persistent discomfort, and functional limitations.
RA and periodontitis have distinct pathologies, but they share many pathological and immunological traits as well as a number of mediators, including the shared epitope (SE)-coding HLA-DRB1 allele, PAD, and collagenase, which may indicate either direct or indirect connections between these two conditions.
Interestingly, the bacteria present in the microbial biofilm causing periodontitis are the same as those found in the serum and synovial fluid of the joints of patients suffering from rheumatoid arthritis. In addition, collagenase, a kind of metalloproteinase, can be detected not only in the synovial fluid and serum of patients with RA but also in the gingival crevicular fluid (GCF) of patients with periodontitis.
The link between periodontitis and RA is undeniably significant due to the possible impact that treating or preventing periodontal disease may have on lowering the risk for RA. Therefore, additional clinical studies assessing the impact of periodontal therapy on RA episodes are required in the future.
Source: Rheumatoid arthritis risk in periodontitis patients: A systematic review and meta-analysis; https://www.sciencedirect.com/science/article/pii/S1297319X20301172
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