Projects per year
Abstract
Aim
To explore mechanistic links between rheumatoid arthritis (RA) and periodontitis (PD) through the lens of subgingival microbial dysbiosis–mediated inflammation.
Methods
Subgingival plaque from 100 volunteers with RA and PD (RAPD), 22 with RA (RAnoPD), 18 with PD (PDnoRA) and 19 healthy controls (noRAnoPD) was analysed using 16S-amplicon sequencing, semi-quantitative bead-based flow cytometry to measure crevicular fluid cytokines and ELISA to quantify antibodies to oral pathogens and systemic inflammatory markers in serum. The RAPD group had been randomised to receive intensive non-surgical periodontal therapy (PMPR) or oral hygiene alone and reviewed at 3 and 6 months in our previously reported study.
Results
Subgingival microbial dysbiosis, as evidenced by higher species richness, alpha-diversity and higher levels of known and putative periodontal pathobionts, was evident at baseline in RAnoPD, RAPD and PDnoRA. Higher serum antibodies to oral pathogens were recorded in RAPD. PMPR restored host–microbial homeostasis in RAPD within 3 months. Significant decreases in serum antibodies to microbial antigens and clinical measures of RA activity were seen after 3 and 6 months in the PMPR group but not controls.
Conclusions
We demonstrate a mutualistic influence of RA and PD, beginning with RA-induced dysbiosis of the periodontal microbiome, progressing to periodontal inflammation and culminating in PD-driven exacerbation of systemic inflammation.
To explore mechanistic links between rheumatoid arthritis (RA) and periodontitis (PD) through the lens of subgingival microbial dysbiosis–mediated inflammation.
Methods
Subgingival plaque from 100 volunteers with RA and PD (RAPD), 22 with RA (RAnoPD), 18 with PD (PDnoRA) and 19 healthy controls (noRAnoPD) was analysed using 16S-amplicon sequencing, semi-quantitative bead-based flow cytometry to measure crevicular fluid cytokines and ELISA to quantify antibodies to oral pathogens and systemic inflammatory markers in serum. The RAPD group had been randomised to receive intensive non-surgical periodontal therapy (PMPR) or oral hygiene alone and reviewed at 3 and 6 months in our previously reported study.
Results
Subgingival microbial dysbiosis, as evidenced by higher species richness, alpha-diversity and higher levels of known and putative periodontal pathobionts, was evident at baseline in RAnoPD, RAPD and PDnoRA. Higher serum antibodies to oral pathogens were recorded in RAPD. PMPR restored host–microbial homeostasis in RAPD within 3 months. Significant decreases in serum antibodies to microbial antigens and clinical measures of RA activity were seen after 3 and 6 months in the PMPR group but not controls.
Conclusions
We demonstrate a mutualistic influence of RA and PD, beginning with RA-induced dysbiosis of the periodontal microbiome, progressing to periodontal inflammation and culminating in PD-driven exacerbation of systemic inflammation.
| Original language | English |
|---|---|
| Number of pages | 12 |
| Journal | Journal of Clinical Periodontology |
| Early online date | 2 Dec 2025 |
| DOIs | |
| Publication status | E-pub ahead of print - 2 Dec 2025 |
Fingerprint
Dive into the research topics of 'Dysbiosis-Mediated Inflammation: A Pathophysiological Link Between Rheumatoid Arthritis and Periodontitis'. Together they form a unique fingerprint.Projects
- 2 Finished
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FP7_MC_ITN_RAPID: Rheumatoid Arthritis and Periodontal Inflammatory Disease
Dietrich, T. (Principal Investigator)
European Commission - Management Costs, European Commission
1/04/12 → 31/03/16
Project: Research
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FP7 COLLAB - GUMS & JOINTS: Protein Citrullination as a Link Between Periodontal Diseases and Rheumatoid Arthritis (RA) and Target for Development of Novel Drugs to Treat RA.
Dietrich, T. (Principal Investigator), Cooper, P. (Co-Investigator), De Pablo, P. (Co-Investigator), Scheel-Toellner, D. (Co-Investigator), Buckley, C. (Co-Investigator) & Chapple, I. (Co-Investigator)
European Commission - Management Costs, European Commission
1/11/10 → 31/10/14
Project: Research