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Bone metabolism is altered in preclinical rheumatoid arthritis
  1. Dirkjan van Schaardenburg1,2,
  2. Markus M J Nielen1,
  3. Willem F Lems1,2,
  4. Jos W R Twisk3,
  5. Henk W Reesink4,
  6. Rob J van de Stadt1,
  7. Irene E van der Horst-Bruinsma2,
  8. Margret H M T de Koning1,
  9. Moud R Habibuw4,
  10. Ben A C Dijkmans1,2
  1. 1Jan van Breemen Institute, Amsterdam, The Netherlands
  2. 2Department of Rheumatology, VU University Medical Centre, Amsterdam, The Netherlands
  3. 3Department of Clinical Epidemiology and Biostatistics, VU University Medical Centre, Amsterdam, The Netherlands
  4. 4Sanquin Blood Bank North West Region, Amsterdam, The Netherlands
  1. Correspondence to Dr Dirkjan van Schaardenburg, Jan van Breemen Institute, Jan van Breemenstraat 2, Amsterdam 1056AB, The Netherlands; d.v.schaardenburg{at}janvanbreemen.nl

https://doi.org/10.1136/ard.2010.135723

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    Radiographic damage and its progression in early rheumatoid arthritis (RA) can be predicted by markers and regulators of bone metabolism. Studies of bone formation in RA patients measuring osteocalcin or the N-terminal telopeptide of type I procollagen (P1NP) have produced varying results, whereas measurements of bone resorption using serum or urine C-terminal crosslink of type I collagen (β-CTX) mostly show increased values.1,–,3 RA patients often have elevated serum levels of the osteoclast-activating cytokine receptor activator of nuclear factor κB ligand (RANKL), as well as of osteoprotegerin, which prevents osteoclast activation.4

    We previously reported increased levels of autoantibodies and acute phase reactants …

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    Footnotes

    • Funding This study was funded by the Dutch Arthritis Association.

    • Competing interests None.

    • Ethics approval This study was conducted with the approval of Slotervaart Hospital, Amsterdam, The Netherlands.

    • Provenance and peer review Not commissioned; externally peer reviewed.