Periodontal disease and the oral microbiota in new‐onset rheumatoid arthritis

Wiley - Tập 64 Số 10 - Trang 3083-3094 - 2012
Jose U. Scher1, Carles Úbeda2, Michele Equinda2, Raya Khanin2, Yvonne de Paiva Buischi3, Agnès Viale2, Lauren Lipuma2, Mukundan Attur4, Michael H. Pillinger4, Gerald Weissmann3, Dan R. Littman3, Eric G. Pamer2, Walter A. Bretz3, Steven B. Abramson4
1Division of Rheumatology, New York University and New York University Hospital for Joint Diseases, New York, New York 10003, USA.
2Memorial Sloan Kettering Cancer Center, New York, New York
3New York University, New York, New York.
4New York University and New York University Hospital for Joint Diseases; New York New York

Tóm tắt

AbstractObjective

To profile the abundance and diversity of subgingival oral microbiota in patients with never‐treated, new‐onset rheumatoid arthritis (RA).

Methods

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.

Results

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.

Conclusion

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.

Từ khóa


Tài liệu tham khảo

Lederberg J, 2001, 'Ome sweet 'omics—a genealogical treasury of words, The Scientist, 15, 8

10.1038/nature06244

10.1016/S0140-6736(09)60008-8

10.1038/ng.582

10.1136/bmj.324.7332.264

10.1038/nrrheum.2009.28

10.1016/j.mehy.2009.04.008

10.1002/art.27584

10.1902/annals.1999.4.1.1

10.1126/science.1177486

10.1172/JCI43918

10.1128/AEM.01541-09

10.1093/nar/gkm864

10.1101/gr.112730.110

10.1111/j.1462-2920.2010.02193.x

Magurran AE, 2004, Measuring biological diversity

10.1128/AEM.00062-07

10.1128/CVI.00272-09

10.1186/gb-2010-11-10-r106

10.1111/j.2517-6161.1995.tb02031.x

10.1002/art.1780380107

10.1902/jop.2005.76.8.1406

10.1128/JB.00542-10

10.1177/154405910808701104

10.1111/j.1600-051X.1998.tb02419.x

10.1111/j.0105-2896.2009.00850.x

10.1002/art.27552

10.1902/jop.2009.090309

10.1902/jop.2008.070501

10.1016/j.intimp.2008.09.008

10.3899/jrheum.091323

10.1902/jop.2011.100481

10.1111/j.1600-051X.2009.01496.x

Bingham CO, 2007, High prevalence of moderate to severe periodontal disease in rheumatoid arthritis patients, Arthritis Rheum, 56, S420

10.1016/S0140-6736(05)67728-8

10.1902/jop.2000.71.5.743

10.1002/art.20553

10.1371/journal.pone.0000161

10.1016/j.ijantimicag.2007.05.015

10.1128/AEM.01419-06

10.1128/JCM.01821-09

10.1099/ijs.0.02018-0

10.1128/JCM.43.8.3944-3955.2005

10.1099/ijs.0.02819-0

10.1002/art.24833

10.1136/ard.2010.139527

10.4049/jimmunol.1101195

10.1056/NEJMra1004965

10.1038/nrrheum.2011.121

10.1111/j.1365-3083.1994.tb03518.x

10.1016/j.immuni.2010.06.001