Hand pain, arthritis

(© ashtproductions - stock.adobe.com)

NEW YORK — It’s a strange phenomenon. Patients with gum disease often don’t respond to treatment for their rheumatoid arthritis, but doctors haven’t understood why — until now. A new study finds that treating gum disease first can help prevent arthritis flare-ups by eliminating mouth bacteria that leaks into the bloodstream.

Researchers from The Rockefeller University explain that rheumatoid arthritis is an autoimmune disease, meaning a condition causing the body to attack itself. For those with gum disease, bacteria seeping into the bloodstream activates an immune response which eventually pivots and targets the body’s healthy proteins — leading to a flare-up in the joints.

“If oral bacteria are getting in and repeatedly triggering immune responses relevant to rheumatoid arthritis, that could make it harder to treat,” says Dana Orange, a professor of clinical investigation in the laboratory of Robert B. Darnell, in a university release. “When doctors encounter arthritis patients who do not respond to treatment, it would be worth it to make sure they aren’t missing an underlying gum disease, which is quite treatable.”

blood vessels during an arthritis flare up
Blood vessels in the soft tissue between joints, during a rheumatoid arthritis flare-up. (Credit: ROCKEFELLER UNIVERSITY)

Gum disease is constantly triggering the immune system

The Darnell lab followed a small group of arthritis patients for several years, collecting blood samples weekly in the hopes of finding genetic changes which contribute to painful flare-ups. During the study, they noticed that two patients had moderate-to-severe periodontal disease. These patients had repeated episodes of oral bacteria making its way into their bloodstreams, even when they weren’t having dental surgery.

Orange notes that rheumatoid arthritis patients generally have autoantibodies in their bloodstream. In many cases, autoantibodies specifically target proteins which display the signs of citrullination, a process where one amino acid in the protein changes into a different one.

The new study found that oral bacteria in the blood also citrullinated in the mouth, just like the proteins autoantibodies target in arthritis patients. From there, the scientists demonstrated that the autoantibodies which attack citrullinated proteins in arthritis patients also activate when they detect citrullinated bacteria originating in the mouth.

Researchers believe this explains why arthritis treatments often fail for patients who also have gum disease. If the infected gums are continuously releasing bacteria that’s triggering an immune response, it makes it that much harder for arthritis medications to do their job. Simply put, study authors say not treating gum disease first would be like not plugging a hole in a sinking ship before you start scooping the water out.

Gum disease is quite curable; rheumatoid arthritis can be much more difficult to treat,” Orange says. “Our results indicate that periodontal disease leads to leaky gums that allow oral bacteria to enter the blood repeatedly. This level of oral bacteria in blood doesn’t cause obvious symptoms, so the patients were not aware this was happening, but they do trigger inflammatory and auto-antibody responses that are highly relevant to rheumatoid arthritis.”

The study is published in Science Translational Medicine.

About Chris Melore

Chris Melore has been a writer, researcher, editor, and producer in the New York-area since 2006. He won a local Emmy award for his work in sports television in 2011.

Our Editorial Process

StudyFinds publishes digestible, agenda-free, transparent research summaries that are intended to inform the reader as well as stir civil, educated debate. We do not agree nor disagree with any of the studies we post, rather, we encourage our readers to debate the veracity of the findings themselves. All articles published on StudyFinds are vetted by our editors prior to publication and include links back to the source or corresponding journal article, if possible.

Our Editorial Team

Steve Fink


Chris Melore


Sophia Naughton

Associate Editor