Oral microbial dysbiosis linked to worsened periodontal condition in rheumatoid arthritis patients Original paper
Researched by:
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Kimberly Eyer
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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 impact of rheumatoid arthritis (RA) on subgingival microbial communities and its relationship to periodontal health, systemic inflammatory markers, and RA disease severity. Using 16S rRNA high-throughput sequencing, the researchers profiled the subgingival microbiota of RA patients and healthy controls, evaluating periodontal parameters, salivary cytokine concentrations, and the inflammatory potential of oral biofilms via in vitro PBMC assays.
Who was studied?
A total of 42 patients with RA and 47 matched healthy controls were recruited. Inclusion required RA diagnosis per ACR/EULAR criteria, no recent antibiotics or periodontal treatment, and no other rheumatic or immunosuppressive conditions. Half of each group had chronic periodontitis, allowing for comparative analysis of periodontal status. Clinical measures included probing depth, clinical attachment level, anti-citrullinated protein antibody (ACPA) levels, and cytokine profiling.
What were the most important findings?
RA patients exhibited a significantly altered subgingival microbiota characterized by increased bacterial load, alpha diversity, and enrichment of pathogenic taxa such as Prevotella spp., Parvimonas micra, and Anaeroglobus geminatus. These shifts occurred even in RA patients without clinical periodontitis, suggesting RA-induced systemic inflammation contributes to microbial dysbiosis. The presence of RA was also associated with elevated salivary levels of proinflammatory cytokines including IL-2, IL-6, IL-17, IL-33, TNF-α, and IFN-γ, many of which were positively correlated with disease severity and periodontal destruction. Pathogenic taxa correlated with tender and swollen joint counts and salivary cytokines, while commensals such as Actinomyces and Rothia aeria were depleted and negatively correlated with inflammation. PICRUSt-predicted metagenomic analysis revealed functional enrichment in genes associated with lipopolysaccharide biosynthesis, peptidases, and amino acid metabolism in RA microbiota. These functions likely contribute to heightened inflammatory responses, as confirmed by the significantly increased IFN-γ secretion from PBMCs exposed to RA-derived biofilm.
| Taxa or Parameter | Observation in RA Patients | Clinical or Functional Implication |
|---|---|---|
| Prevotella spp. | Increased even without periodontitis | Associated with RA severity and periodontal inflammation |
| Parvimonas micra | Elevated in RA with periodontitis | Correlated with tender/swollen joints and cytokines |
| Anaeroglobus geminatus | Enriched in RA subjects | Positively correlated with IL-17, TNF-α, IFN-γ |
| Selenomonas noxia | Increased in RA patients | Linked to salivary IL-6 and IL-33, and greater inflammatory potential |
| Actinomyces, Streptococcus, Rothia aeria | Depleted in RA | Negatively correlated with IL-17 and TNF-α, associated with oral health |
| Inflammatory cytokines | Elevated IL-2, IL-6, IL-17, IL-33, TNF-α, IFN-γ | Reflect systemic and local inflammation; linked to microbiota shifts |
| Functional pathways | Enrichment of peptidases, LPS biosynthesis, AA metabolism | Suggest microbial contribution to inflammation and tissue breakdown |
| IFN-γ secretion from PBMCs | Higher after RA biofilm exposure | Demonstrates heightened immunostimulatory potential of RA microbiota |
What are the greatest implications of this study?
This study provides compelling evidence that RA influences oral microbial ecology, driving dysbiosis that intensifies periodontal inflammation. The finding that RA patients without periodontitis still harbor enriched levels of periodontitis-associated taxa suggests that microbial dysbiosis may precede or exacerbate periodontal destruction through systemic inflammatory pathways. The identification of Prevotella spp., Selenomonas noxia, and Parvimonas micra as major microbial associations (MMAs) supports their role in RA-related oral pathology. These microbes may contribute to systemic autoimmunity through mechanisms like protein citrullination, thus implicating the oral microbiota as both a biomarker and a potential target for therapeutic intervention in RA. Importantly, the data support incorporating periodontal assessment and oral microbiota monitoring into RA management protocols and raise the potential for microbiome-based adjunctive therapies.