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Albeit researchers and scientists have been aware of a link between two highly common chronic inflammatory diseases, periodontal disease and rheumatoid arthritis (RA), the microbiological mechanisms have remained ambiguous.

In a recent article published in PLoS Pathogens, University of Louisville School of Dentistry Oral Health and Systemic Diseases group researcher Jan Potempa, PhD, DSc, and an international team of scientists from the European Union's Gums and Joints project have discovered how the bacterium that leads to periodontal disease, Porphyromonas gingivalis exacerbates RA by leading to earlier start, faster progression, and higher severity of the disease, including increased bone and cartilage erosion.

Scientists discovered that, Porphyromonas gingivalis produces a specific enzyme, peptidylarginine deiminanse (PAD) which then develops collagen-induced arthritis (CIA), a kind of arthritis resembling RA produced in the lab. PAD changes remains of certain proteins into citrulline, and the body recognizes citullinated proteins as trespassers, causing an immune attack. In RA patients, the succeeding result is chronic inflammation responsible for bone and cartilage deterioration within the joints.

Potempa and his team studied a second oral bacterium, Prevotella intermedia for the same affect, but learned it did not produce PAD, and consequently had no affect on CIA.

"Taken together, our results suggest that bacterial PAD 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," he said.

Potempa said he is hopeful these findings will shed new light on the treatment and prevention of RA.

“Studies indicate that compared to the general population, people with periodontal disease have an increased prevalence of RA and, periodontal disease is at least two times more prevalent in RA patients. Other research has shown that a P. gingivalis infection in the mouth will precede RA, and the bacterium is the likely culprit for onset and continuation of the autoimmune inflammatory responses that occur in the disease.”