Analysis of subgingival microbiome of periodontal disease and rheumatoid arthritis in Chinese: A case-control study Original paper
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Autoimmune Diseases
Autoimmune Diseases
Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.
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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.
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, 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.
What was studied?
This study investigated the subgingival microbiome in Chinese patients with rheumatoid arthritis (RA), periodontitis (PD), and healthy controls, aiming to explore potential microbial links between RA and PD. Using 16S rRNA Illumina MiSeq sequencing, the authors characterized bacterial composition and diversity in subgingival plaque, identifying differentially abundant taxa and evaluating whether oral microbiota might play a contributory role in RA pathogenesis via periodontal inflammation.
Who was studied?
A total of 143 participants were enrolled, comprising 54 RA patients, 45 PD patients, and 44 healthy controls, all recruited from Sichuan Provincial People’s Hospital. Inclusion criteria excluded individuals with systemic diseases other than RA or PD, and participants had not used antibiotics or immunosuppressive therapies in the preceding three months. Subgingival plaque samples were collected from six standardized index teeth for uniformity across groups.
What were the most important findings?
Although microbial richness (as measured by alpha diversity indices like Chao and Simpson) did not differ significantly among the RA, PD, and control groups, key compositional shifts were observed. Most notably, the phylum Spirochaetes—and its lineage down to the genus Treponema—was significantly enriched in RA patients at all taxonomic levels (P <0.008). These results were specific to RA; while PD patients showed a similar trend, the differences did not reach statistical significance.
Additionally, RA samples showed higher relative abundances of Porphyromonas, Prevotella, and Veillonella, which are consistent with previous literature identifying these as periodontopathogenic taxa. Conversely, Streptococcus and Gemella, both associated with a healthy oral microbiome, were significantly depleted in RA. Interestingly, Tannerella, another “red complex” pathogen, was also elevated in RA (P = 0.010), supporting a dysbiotic profile that overlaps with PD yet remains distinct.
From a microbiome signatures perspective, Treponema and Porphyromonas gingivalis are reaffirmed as Major Microbial Associations (MMAs) due to their consistent elevation and mechanistic links to citrullination and RA immunopathology. The study also reinforces the microbial overlap and divergence between RA and PD, highlighting subgingival niches as potential sources of systemic immune modulation.
What are the greatest implications of this study?
This study adds to a growing body of evidence implicating the oral microbiome—specifically the subgingival community—in the pathogenesis of rheumatoid arthritis. The consistent enrichment of Treponema across all taxonomic levels in RA patients suggests it may play a previously underappreciated role in RA, warranting mechanistic exploration, especially in relation to periodontal-immune crosstalk. The differential regulation of classic periodontal pathogens between RA and PD patients also underscores that, while these diseases share microbial risk factors, their oral dysbiosis patterns are not identical.
For clinical application, the identification of Treponema and Porphyromonas as MMAs provides potential microbial biomarkers for RA risk screening. Furthermore, the observation that RA patients without clinically diagnosed PD still harbor elevated pathobiont levels suggests that subclinical periodontal dysbiosis may be a risk modifier in RA development. This has implications for early intervention strategies and supports the integration of dental and rheumatologic care. For the Microbiome Signatures Database, this study strongly validates subgingival Treponema spp. as a population-specific MMA for RA and supports the prioritization of oral-microbiome-focused MBTIs.