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Rheumatoid arthritis and gum disease: what’s the link?

Posted Oct 27 2011 7:27am

Of the 50 million Americans—1 in 5 of the adult population—suffering from some form of arthritis, an estimated 1.5 million have the rheumatoid arthritis (RA) form source . RA is a progressively disabling autoimmune disease targeting the lining of joints, causing pain, stiffness, swelling and sometimes severe bone damage. Twenty six percent of Americans over 20 years old suffer from destructive periodontal (gum) disease (PD) source . PD typically results from untreated gingivitis, an inflammation of the gums caused by bacteria in the mouth gone awry, as well as other factors (genetic susceptibility, smoking, medications, illness, etc.). What’s intriguing is that these two prevalent chronic inflammatory diseases are sometimes linked, with RA sufferers being significantly more likely to experience PD. The biology of this association, however, remains unclear, with differing hypotheses on the direction of the link: does RA increase the risk of PD, or vice versa?

F1000 Member Robert Carter mentions one theory, that periodontal inflammation leads to citrullination (whereby arginine residues are converted to citrulline) in an evaluation of a paper from Celso Martins Queiroz-Junior and colleagues at the Universidade Federal de Minas Gerais, Brazil. This theory implicates an autoantibody response to citrullinated proteins, a common feature of RA, suggesting PD could increase the risk of developing RA. However, the paper by Queiroz-Junior et al. suggests the opposite: that arthritis can lead to gum disease.

Gum disease

from http://www.humanillnesses.com/

Queiroz-Junior et al. triggered arthritis in mice by injecting methylated BSA into knee joints, which led to periodontal disease 10.4049/​jimmunol.1101195 . Not only did these mice experience RA symptoms locally in the knee, they also had increased pro-inflammatory cytokines in the maxillae (upper jawbone). Furthermore, reducing joint disease in these mice by blocking tumour necrosis factor alpha (TNF-α) also reduced the PD. The paper also points to a lymph node-mediated pathway involved in spreading of immune disease throughout different parts of the body, as the induced arthritis in mice was associated with an increase in serum C-reactive protein levels and expression of transcription factors RORγ and Foxp3 in cervical lymph nodes. A 2005 review of the PD and RA link by Bartold, Marshall and Haynes discusses how a number of cytokines and matrix metalloproteinases (MMPs) are upregulated and common to both PD and RA pathogenesis. Determining the role of specific cytokines in RA and PD pathophysiology, and how they relate to the severity of each disease (among populations suffering both conditions), is clearly now an important research goal for medical research.

Mauro Perretti , in his evaluation of the Queiroz-Junior paper, writes:

Another elegant aspect of the study is the attention to the effect of the oral microbiota. Its removal by antiseptic also prevented PD in arthritic mice. The scenario that emerges is that of a ‘two-hit’ model, with a permissive – or more than permissive – effect of bacteria in the oral cavity.

This ‘two-hit’ model is further supported by the observation that no other joints in the infected mice were affected following induced arthritis in their knees. Perhaps then, this ‘two-hit’ hypothesis – that arthritis-induced PD is dependent on both TNF-α and on the oral microbiota (which is in our power to control) – could be the source of useful advice to RA sufferers: maintaining good dental hygiene practice might be enough for RA patients to keep gum disease at bay.

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