Periodontal disease and the oral microbiota in new-onset rheumatoid arthritis Original paper
Researched by:
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Kimberly Eyer
ID
Kimberly Eyer
Kimberly Eyer, a Registered Nurse with 30 years of nursing experience across diverse settings, including Home Health, ICU, Operating Room Nursing, and Research. Her roles have encompassed Operating Room Nurse, RN First Assistant, and Acting Director of a Same Day Surgery Center. Her specialty areas include Adult Cardiac Surgery, Congenital Cardiac Surgery, Vascular Surgery, and Neurosurgery.
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Rheumatoid Arthritis
Rheumatoid Arthritis
OverviewRheumatoid arthritis (RA) is a systemic autoimmune disease marked by chronic joint inflammation, synovitis, and bone erosion, driven by Treg/Th17 imbalance, excessive IL-17, TNF-α, and IL-1 production, and macrophage activation. Emerging evidence links microbial dysbiosis and heavy metal exposure to RA, [1][2] with gut microbiota influencing autoimmune activation via Toll-like receptor (TLR) signaling, inflammasome activation, […]
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Kimberly Eyer
Researched by:
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Kimberly Eyer
ID
Kimberly Eyer
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Kimberly Eyer
What was studied?
This study investigated the composition and diversity of the subgingival oral microbiota in patients with new-onset rheumatoid arthritis (RA), patients with chronic RA, and healthy controls. Using high-throughput 16S rRNA pyrosequencing, the authors aimed to determine whether microbial shifts in the oral cavity are associated with RA development. By focusing on treatment-naïve individuals with early RA, the study sought to eliminate confounding effects from immunosuppressive drugs, highlighting early microbial features that may precede or trigger RA onset.
Who was studied?
The study enrolled 31 patients with new-onset RA (defined as disease duration between 6 weeks and 6 months, and no history of steroid or disease-modifying antirheumatic drug use), 34 patients with chronic RA, and 18 age-, sex-, and ethnicity-matched healthy controls. All participants underwent periodontal examinations, subgingival sampling, and serological testing for rheumatoid factor (RF), anti-citrullinated protein antibodies (ACPA), and Porphyromonas gingivalis-specific antibodies.
What were the most important findings?
Patients with new-onset RA showed a significantly higher prevalence of moderate-to-severe periodontitis (PD) compared to controls, despite being younger and having low rates of smoking—suggesting that PD may be a distinct comorbidity or preclinical feature of RA. Although global oral microbial diversity did not differ significantly across groups, the presence of certain bacterial taxa such as Prevotella (OTU60) and Leptotrichia (OTU87) was unique to new-onset RA patients, regardless of PD status. Anaeroglobus geminatus (OTU99) was found to correlate with ACPA and RF titers and was significantly more prevalent in RA patients, highlighting it as a potential microbial biomarker of autoimmune activation. While P. gingivalis was more abundant in subjects with severe PD, its presence was not uniquely associated with RA, nor did it correlate with autoantibody levels.
Structured Table:
| Key Findings | Microbial Associations | Implications |
|---|---|---|
| Higher prevalence of periodontitis in new-onset RA | Porphyromonas, Tannerella, Treponema (red complex) | Reflects shared pathology, not RA specificity |
| Unique taxa in new-onset RA | Prevotella (OTU60), Leptotrichia (OTU87) | Potential early biomarkers, independent of PD |
| Immune correlation | Anaeroglobus geminatus (OTU99) ↔ ACPA/RF levels | Suggests microbial modulation of systemic autoimmunity |
| Exposure to P. gingivalis not RA-specific | Detected in ~80% of all groups | Challenges specificity of P. gingivalis as sole RA microbial trigger |
What are the greatest implications of this study?
The study demonstrates that specific oral microbial shifts precede or coincide with RA onset and may contribute to immune dysregulation. The detection of Prevotella, Leptotrichia, and Anaeroglobus geminatus as uniquely enriched in new-onset RA patients suggests that the subgingival microbiome could be involved in initiating or perpetuating systemic autoimmunity. Importantly, the lack of specificity of P. gingivalis to RA patients—despite its known peptidylarginine deiminase (PAD) activity—challenges its role as a singular microbial trigger. Instead, the data support a more nuanced model where periodontopathic bacteria and dysbiosis act in concert with genetic and environmental factors to promote RA. These findings underscore the importance of evaluating the oral microbiome as both a biomarker reservoir and a potential target for microbiome-modulating interventions in early RA.