A team of European researchers have shown a connection between the variance in the microbial composition in the mouths of people with early rheumatoid arthritis (ERA) and those at risk of developing the disease, compared with healthy individuals who were not at risk.
The findings come from a study published in Arthritis & Rheumatology titled, “The oral microbiome in early rheumatoid arthritis patients and individuals at risk differs from healthy controls.”
“Prevotella and Veillonella—both gram-negative anaerobes—were at higher relative abundance in saliva, and Veillonella was also at higher relative abundance in tongue coating, of both early rheumatoid arthritis patients and at-risk individuals compared to healthy controls,” the authors note. “Increased relative abundance of this potentially pro-inflammatory genus in ERA patients and at-risk individuals suggests a link between the oral microbiome and RA.”
The 50 participants in the study, all in their early 50s, include early rheumatoid arthritis (ERA) patients, at‐risk individuals with pain in their joints (arthralgia) or detectable autoantibodies, and healthy controls.
The authors led by Johanna Kroese, Ph.D., at the University of Amsterdam, conducted periodontal examinations scoring patients based on several periodontal variables including bleeding on probing (BOP), pocket probing depth (PPD), and periodontal inflamed surface area (PISA). Patients in the three groups show no differences in these scores.
The authors then conduct 16S rDNA amplicon sequencing to compare the microbial composition of subgingival dental plaque, saliva, and tongue coating. They find a difference in the microbial compositions of saliva and tongue coating between the ERA and at-risk groups, but no difference among the three groups in the microbial composition of dental plaque.
Earlier studies on new-onset RA and established RA patients have shown an increase in the Prevotella species of bacteria in the mouth and gut. Some strains of Prevotella can promote prolonged inflammation by stimulating local cytokine production and inducing mucosal inflammation. The local inflammation can lead to systemic dispersal of inflammatory mediators.
Although when RA is treated with medication, alterations in the mouth and gut microbiome are partially resolved, the biological mechanism that links the microbiome to the development of RA is not clearly understood.
The authors suggest larger cohort longitudinal studies with consistent methods of data collection, to aid the use of advanced methods such as artificial intelligence, to predict links between the oral microbiome and systemic inflammation.
