The researchers explained that it is because autoimmunity in RA is characterised by an antibody response to citrullinated proteins and the oral bacterium Porphyromonas gingivalis (Pg) is the only human pathogen known to express an enzyme that can generate citrullinated proteins.
"Our results support the hypothesis that local inflammation at mucosal surfaces, such as the gums in this case, may provide the primary trigger for the systemic autoimmunity seen in RA," said co-author Kulveer Mankia of Leeds Institute of Rheumatic and Musculoskeletal Medicine.
"It has been shown that RA-associated antibodies, such as anti-citrullinated protein antibodies, are present well before any evidence of joint disease. This suggests they originate from a site outside of the joints," Mankia added.
RA is a chronic inflammatory disease that affects a person's joints, causing pain and disability and can also affect internal organs.
The study, presented at the Annual European Congress of Rheumatology (EULAR 2018), included 48 at-risk individuals who were tested positive for anti-citrullinated protein antibodies and had musculoskeletal symptoms but no clinical synovitis, 26 patients with RA and 32 healthy controls.
DNA was isolated from the subgingival plaque, next to the gums, of each participant and used to measure the levels of three types of bacteria -- Pg, Aggregatibacter actinomycetemcomitans (Aa) and Filifactor Alocis, the researchers said.
The results showed that there was increased abundance of both Pg and Aa in at-risk individuals. However, in at-risk individuals, only Pg was significantly increased at healthy dental sites and was associated with the overall extent of gum disease.
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