Linking rheumatoid arthritis and gum disease: Researchers find common bacterium

Researchers from Johns Hopkins Medicine have narrowed down the link between chronic gum disease and rheumatoid arthritis, identifying the common bacterium at play in both conditions.

An infection with this bacterium appears to trigger the complex cascade of events in the body that lead to chronic, joint-destroying rheumatoid arthritis, or RA.

"This research may be the closest we've come to uncovering the root cause of RA," says the study's lead author Maximilian Konig, a former Johns Hopkins School of Medicine fellow now at Massachusetts General Hospital.

The study's results were published this week in Science Translational Medicine.

The researchers discovered that a bacterium called Aggregatibacter actinomycetemcomitans is the common denominator between gum disease and RA. The clinical association between the two diseases has been known since the early 1900s, but most research in the past decade has focused on a different bacterium called Porphyromonas gingivalis. The Johns Hopkins research sought alternate explanations.

"This is like putting together the last few pieces of a complicated jigsaw puzzle that has been worked on for many years," says Felipe Andrade, the senior study investigator and associate professor at the Johns Hopkins University School of Medicine.

An estimated 1.5 people nationwide live with rheumatoid arthritis, according to the Centers for Disease Control and Prevention. The current treatment options of steroids, immunotherapy drugs, and physical therapy can help reduce or slow the painful joint deformities in some patients, but scientists have been looking for effective alternatives.

The research team, observing similar processes in the joints of RA patients and the gums of patients with periodontal disease, found an overlapping factor called hypercitrullination. That's an overactive version of citrullination, a protein conversion process that occurs naturally in everyone.

With abnormal accumulations of these types of proteins, the body produces antibodies that create inflammation and attack the body's own tissues—a hallmark feature of RA.

The researchers discovered that A. actinomycetemcomitans was the only bacterium capable of inducing hypercitrullination in the most abundant inflammatory cells found in both gum disease and RA.

The study used 196 samples from patients with RA, finding that more than half had evidence of infection by A. actinomycetemcomitans. The data was similar with the gum disease sample. Most striking, though, was that exposure to the bacterium appeared to be a major determinant in producing tissue-attacking antibodies in patients genetically susceptible to RA.

Konig cautioned that because more than half of the study participants with RA showed no evidence of A. actinomycetemcomitans, there could be other bacteria in the gut, lung, or elsewhere using a similar mechanism to induce hypercitrullination.

Andrade further noted that more research is necessary to track the role of the bacterium in the onset and evolution of RA, rather than when the disease is already established.