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Ann Rheum Dis 2009;68:1902-1907 doi:10.1136/ard.2008.102392
  • Basic and translational research
  • Extended report

Effects of Porphyromonas gingivalis on cell cycle progression and apoptosis of primary human chondrocytes

  1. N Pischon1,
  2. E Röhner2,
  3. A Hocke3,
  4. P N’Guessan3,
  5. H C Müller3,
  6. G Matziolis4,
  7. V Kanitz1,
  8. P Purucker1,
  9. B-M Kleber1,
  10. J-P Bernimoulin1,
  11. G Burmester2,
  12. F Buttgereit2,
  13. J Detert2
  1. 1
    Department of Periodontology, Charité-Universitätsmedizin, Berlin, Germany
  2. 2
    Department of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin, Berlin, Germany
  3. 3
    Department of Infectious Diseases and Pneumology, Charité-Universitätsmedizin, Berlin, Germany
  4. 4
    Department of Orthopaedics, Charité-Universitätsmedizin, Berlin, Germany
  1. Correspondence to Dr N Pischon, Department of Periodontology, Charité-Universitätsmedizin, Berlin, Campus Virchow, Augustenburger Platz 1, 13353 Berlin, Germany; nicole.pischon{at}charite.de
  • Accepted 23 November 2008
  • Published Online First 3 December 2008

Abstract

Background: It has been suggested that bacterial infections have a role in the pathogenesis of rheumatoid arthritis (RA). P gingivalis, a Gram-negative, anaerobic rod, is one of the major pathogens associated with periodontal disease.

Objective: To examine P gingivalis infection and its effects on cell cycle progression and apoptosis of human articular chondrocytes.

Methods: Primary human chondrocytes cultured in monolayers were challenged with P gingivalis. Infection and invasion of P gingivalis into chondrocytes was analysed by scanning electron microscopy, double immunofluorescence and by antibiotic protection and invasion assay. Cell cycle progression of infected chondrocytes was evaluated by flow cytometry. Also, cell apoptosis was visualised by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) of DNA strand breaks and by western blot analysis.

Results: Data showed that P gingivalis could adhere and infect primary human chondrocytes. After chondrocyte infection, intracellular localisation of P gingivalis was noted. Flow cytometry analyses demonstrated affected cell cycle progression, with an increase of the G1 phase and a significant decrease of the G2 phase after infection. In addition, increased apoptosis of P gingivalis-infected chondrocytes was visualised by TUNEL assay and by upregulation of caspase-3 protein expression.

Conclusion: These data demonstrate that P gingivalis infects primary human chondrocytes and affects cellular responses, which might contribute to the tissue damage seen in the pathogenesis of rheumatoid arthritis.

Footnotes

  • NP and ER contributed equally to this work.

  • Funding This work was financially supported by DFG GK 325, Bonn, Germany, by DGP e.V., Germany and the support of GABA GmbH, Lörrach, Germany and by a Habilitation Fellowship from Charité-Universitätsmedizin Berlin, Germany to NP.

  • Competing interests None.

  • Ethics approval Approval from the ethics committee of the Universitaetsmedizin Charité, Berlin, Germany.

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