Reasearch Awards nomination

Email updates

Keep up to date with the latest news and content from Arthritis Research & Therapy and BioMed Central.

Open Access Highly Accessed Research article

Porphyromonas gingivalis and the pathogenesis of rheumatoid arthritis: analysis of various compartments including the synovial tissue

Michele Ciro Totaro1, Paola Cattani2, Francesco Ria3, Barbara Tolusso1, Elisa Gremese1, Anna Laura Fedele1, Sara D'Onghia2, Simona Marchetti2, Gabriele Di Sante3, Silvia Canestri1 and Gianfranco Ferraccioli1*

Author Affiliations

1 Division of Rheumatology, Institute of Rheumatology and Affine Sciences, Catholic University of the Sacred Heart, Via G. Moscati 31, Rome, 00168, Italy

2 Laboratory of Clinical analyses, Association Columbus, Catholic University of the Sacred Heart, Via G. Moscati 31, Rome, 00168, Italy

3 Institute of General Pathology, Catholic University of the Sacred Heart, Largo F. Vito 1, Rome, 00168, Italy

For all author emails, please log on.

Arthritis Research & Therapy 2013, 15:R66  doi:10.1186/ar4243

Published: 18 June 2013

Abstract

Introduction

We evaluated the presence of Porphyromonas gingivalis (Pg) DNA in the synovial tissue through synovial biopsy and in other compartments of rheumatoid arthritis (RA) patients in comparison with patients affected by other arthritides. Possible links with clinical, immunologic and genetic features were assessed.

Methods

Peripheral blood (PB), sub-gingival dental plaque, synovial fluid (SF) and synovial tissue samples were collected from 69 patients with active knee arthritis (32 with RA and 37 with other arthritides, of which 14 had undifferentiated peripheral inflammatory arthritis - UPIA). Demographic, clinical, laboratory and immunological data were recorded. The presence of Pg DNA was evaluated through PCR. The HLA-DR haplotype was assessed for 45 patients with RA and UPIA.

Results

No differences arose in the positivity for Pg DNA in the sub-gingival plaque, PB and SF samples between RA and the cohort of other arthritides. Full PB samples showed a higher positivity for Pg DNA than plasma samples (11.8% vs. 1.5%, P = 0.04). Patients with RA showed a higher positivity for Pg DNA in the synovial tissue compared to controls (33.3% vs. 5.9%, P <0.01). UPIA and RA patients carrying the HLA DRB1*04 allele showed a higher positivity for Pg DNA in the synovial tissue compared to patients negative for the allele (57.1% vs. 16.7%, P = 0.04). RA patients positive for Pg DNA in the sub-gingival plaque had a lower disease duration and a higher peripheral blood leucocyte and neutrophil count. The presence of Pg DNA did not influence disease activity, disease disability or positivity for autoantibodies.

Conclusions

The presence of Pg DNA in the synovial tissue of RA patients suggests a pathogenic role of the bacterium. The higher positivity of Pg DNA in full peripheral blood and synovial tissue samples compared to plasma and synovial fluid suggests a possible intracellular localization of Pg, in particular in patients positive for HLA-DR4.