Re-Opening the Connection Between RA and Gum Disease

It may not come as a surprise to learn that many individuals struggling with RA also report higher incidences of gum or mouth conditions. You may have even experienced some of these yourself, or are currently dealing with them. Struggles can range from dry mouth leading to tooth decay, gingivitis, and thrush; to medications like methotrexate causing oral ulcers. However, one of the most severe conditions that often accompanies RA is a periodontal disease. Periodontal disease comes from inflammation in the mouth that can lead to tissue and tooth destruction.

For years, the link between RA and periodontal disease has been researched, and speculations have centered around a bacterium called porphyromonas gingivitis. However, after much study, a definitive link between the bacterium and the mechanisms behind RA and periodontal disease has yet to be found. Although recently, a new study indicates that the proposed link may not have been the most crucial.

A study published this December in Science Translational Medicine from researchers at Johns Hopkins University School of Medicine in Baltimore, Maryland, has potentially found the true missing piece behind the RA and periodontal disease connection. This crucial link comes in the form of a different bacterium, aggregatibacter actinomycetemcomitans. Although the name may sound other-worldly, the mechanism behind it isn’t terribly complex.

The A. actinomycetemcomitans bacteria secretes a leukotoxin, killing host immune cells, and inducing the production of special proteins, known as citrullinated proteins. These proteins then cause the body to make a slew of antibodies in response, thus, leading to the inflammation we all know to be a staple of RA (and periodontal disease). This specific bacterium is unlike any of the others once considered to be at work in both RA and gum disease because it specifically causes the hypercitrullination phenomenon (making excess citrullinated proteins).

The researchers studied 196 individuals with RA and found that nearly half had gum disease, and tested positive for the A. actinomycetemcomitans bacterium (as compared to roughly 10% of the control population). It was also determined that a risk factor for the development of RA was prior exposure to the bacterium.

While a specific cause-and-effect relationship cannot be drawn from these results alone, it does indicate a new potential direction for research to take. Not only could it be possible to integrate antibiotics into the treatment regimens of individuals with RA, but there is also a chance that those who are at risk for RA or have been exposed to the bacterium could receive directed therapies early on to delay the onset of RA or to slow the progression of initial symptoms. There is still much work to be done to further characterize the connection between RA and gum disease, however, more doors are opening with new paths behind them with potential answers!

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