Periodontitis and rheumatoid arthritis are linked

Periodontitis and rheumatoid arthritis not only have common risk factors, but they also influence each other via enhanced inflammatory processes.

An old person showes its rheumatic hands

The clinical parallels between periodontitis and rheumatoid arthritis (RA) are clear: Both diseases are characterized by chronic inflammatory changes and subsequent tissue destruction. In rheumatoid arthritis, synovial membrane inflammation occurs first as a result of an immune system overreaction caused by highly regulated pro-inflammatory cytokines, culminating in tissue degeneration. Even though the etiology of rheumatoid arthritis is still unclear, similar risk factors are considered as triggers or drivers of the disease to those in periodontitis:

Studies show that the prevalence of rheumatoid arthritis is increased among periodontitis patients. Conversely, patients with rheumatoid arthritis are around 8x more likely to suffer concomitantly from periodontitis.

Periodontitis predisposes to rheumatoid arthritis

Various studies show that periodontitis-associated bacteria are detectable significantly more frequently in the gingival crevicular fluid, serum and synovial fluid of rheumatoid arthritis patients than in healthy individuals. The presence of periodontopathogenic bacteria also leads to increased production of inflammatory mediators such as interleukin-1. This causes a shift in bone homeostasis in the direction of catabolic processes. This acts as a driver not only for the progressive destruction of the periodontal apparatus but also joint degeneration in rheumatoid arthritis patients.

P. gingivalis citrullinates proteins

Some periodontitis-associated bacteria are very aggressive. P. gingivalis (Pg) is chiefly responsible, among other things, for the destruction of the periodontium. Pg also produces an enzyme that converts the amino acid arginine into citrulline, thereby changing the spatial arrangement of proteins. The result is that these proteins are no longer recognized by the immune system as endogenous and an immune response is triggered. Pg therefore further fuels the immune system’s autoimmune response and thereby further promotes rheumatoid arthritis.