Drs. Scher and Ubeda contributed equally to this work.
Periodontal disease and the oral microbiota in new-onset rheumatoid arthritis†
Article first published online: 27 SEP 2012
Copyright © 2012 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 64, Issue 10, pages 3083–3094, October 2012
How to Cite
Scher, J. U., Ubeda, C., Equinda, M., Khanin, R., Buischi, Y., Viale, A., Lipuma, L., Attur, M., Pillinger, M. H., Weissmann, G., Littman, D. R., Pamer, E. G., Bretz, W. A. and Abramson, S. B. (2012), Periodontal disease and the oral microbiota in new-onset rheumatoid arthritis. Arthritis & Rheumatism, 64: 3083–3094. doi: 10.1002/art.34539
ClinicalTrials.gov identifier: NCT01198509.
- Issue published online: 27 SEP 2012
- Article first published online: 27 SEP 2012
- Accepted manuscript online: 10 MAY 2012 01:40PM EST
- Manuscript Accepted: 3 MAY 2012
- Manuscript Received: 29 SEP 2011
- NIH (National Center for Research Resources KL2 Program in Translational Research). Grant Number: 1 UL1-RR-029893
- National Institute of Arthritis and Musculoskeletal and Skin Diseases, through the American Recovery and Reinvestment Act of 2009. Grant Number: RC2-AR-058986
- Tow Foundation
To profile the abundance and diversity of subgingival oral microbiota in patients with never-treated, new-onset rheumatoid arthritis (RA).
Periodontal disease (PD) status, clinical activity, and sociodemographic factors were determined in patients with new-onset RA, patients with chronic RA, and healthy subjects. Multiplexed-454 pyrosequencing was used to compare the composition of subgingival microbiota and establish correlations between the presence/abundance of bacteria and disease phenotypes. Anti–Porphyromonas gingivalis antibody testing was performed to assess prior exposure to the bacterial pathogen P gingivalis.
The more advanced forms of periodontitis were already present at disease onset in patients with new-onset RA. The subgingival microbiota observed in patients with new-onset RA was distinct from that found in healthy controls. In most cases, however, these microbial differences could be attributed to the severity of PD and were not inherent to RA. The presence and abundance of P gingivalis were also directly associated with the severity of PD and were not unique to RA. The presence of P gingivalis was not correlated with anti–citrullinated protein antibody (ACPA) titers. Overall exposure to P gingivalis was similar between patients with new-onset RA and controls, observed in 78% of patients and 83% of controls. The presence and abundance of Anaeroglobus geminatus correlated with the presence of ACPAs/rheumatoid factor. Prevotella and Leptotrichia species were the only characteristic taxa observed in patients with new-onset RA irrespective of PD status.
Patients with new-onset RA exhibited a high prevalence of PD at disease onset, despite their young age and paucity of smoking history. The subgingival microbiota profile in patients with new-onset RA was similar to that in patients with chronic RA and healthy subjects whose PD was of comparable severity. Although colonization with P gingivalis correlated with the severity of PD, overall exposure to P gingivalis was similar among the groups. The role of A geminatus and Prevotella/Leptotrichia species in this process merits further study.