Researchers have long suspected that periodontal disease (gum disease) and rheumatoid arthritis (RA) may be triggered by a common factor. Now, a US study has uncovered new evidence that a bacterium known to cause chronic inflammatory gum infections also triggers the inflammatory “autoimmune” response characteristic of RA.
The researchers from Johns Hopkins Medicine say their findings have important implications for the prevention and treatment of RA.
For the study, the investigative team searched for a common denominator that may link both diseases. Initial clues came from the study’s analysis of periodontal samples, where they found that a similar process that had previously been observed in the joints of patients with RA was occurring in the gums of patients with periodontal disease. This common denominator is called hypercitrullination, Johns Hopkins Medicine explained.
The full findings, published in the journal Science Translational Medicine, demonstrate that a periodontal pathogen called Aggregatibacter actinomycetemcomitans (Aa) induces changes in neutrophil function, including hypercitrullination of host proteins, an abnormality that is also observed in the joints of patients with rheumatoid arthritis.
What’s more, the effect of an allele associated with increased risk of RA was only observed in patients exposed to Aa. This suggests that the results could eventually be used to identify and possibly treat high-risk patients.
“This is like putting together the last few pieces of a complicated jigsaw puzzle that has been worked on for many years,” commented senior study investigator Dr Felipe Andrade, associate professor of Medicine at the Johns Hopkins University School of Medicine.
“This research may be the closest we’ve come to uncovering the root cause of RA,” added first author Dr Maximilian F. Konig, a former Johns Hopkins University School of Medicine fellow now at Massachusetts General Hospital.
However, Konig also cautioned that more than half of the study participants who had RA had no evidence of infection with Aa, which may indicate that other bacteria in the gut, lung or elsewhere could be using a similar mechanism to induce hypercitrullination.