Scientists at the University of Louisville School of Dentistry report that they have discovered how the bacterium responsible for periodontal disease (PD) worsens rheumatoid arthritis. The link between gum disease and RA had previously been established but the new study revealed the specific interplay of the microbiological mechanisms that are involved.
“We showed that infection with viable periodontal pathogen Porphyromonas gingivalis strain W83 exacerbated collagen-induced arthritis (CIA) in a mouse model, as manifested by earlier onset, accelerated progression, and enhanced severity of the disease including significantly increased bone and cartilage destruction,” wrote the researchers in the current issue of PLOS Pathogens. “The ability of P. gingivalis to augment CIA was dependent on the expression of a unique P. gingivalis peptidylarginine deiminase (PPAD), which converts arginine residues in proteins to citrulline.”
According to Jan Potempa, Ph.D., D.Sc., oral health and systemic diseases group researcher, who worked with an international team of scientists from the European Union’s Gums and Joints project, the body recognizes citrullinated proteins as intruders, leading to an immune attack. In RA patients, the subsequent result is chronic inflammation responsible for bone and cartilage destruction within the joints.
“Taken together, our results suggest that bacterial [peptidylarginine deiminase] may constitute the mechanistic link between P. gingivalis periodontal infection and rheumatoid arthritis, but this ground-breaking conclusion will need to be verified with further research,” said Dr. Potempa.
He added that he hopes the study (“Porphyromonas gingivalis Facilitates the Development and Progression of Destructive Arthritis through Its Unique Bacterial Peptidylarginine Deiminase”) and its findings will shed new light on dealing with RA.
“High levels of citrullinated proteins in the chamber fluid suggests that PPAD contributes, at least partially, to the characteristic intensive citrullination of proteins in the periodontal stroma in PD,” continued the scientists in the PLOS article. “Together, it is tempting to hypothesize host proteins citrullinated by PPAD-producing P. gingivalis may contribute to a breach of immune tolerance in susceptible individuals that subsequently triggers an inappropriate immune response that exacerbates CIA. This knowledge may create new perspectives in the treatment and prevention of RA.”
