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Molecular mechanisms of cartilage and bone destruction
Type II collagen degradation and its regulation in articular cartilage in osteoarthritis
  1. A R Poole1,
  2. M Kobayashi1,2,
  3. T Yasuda1,2,
  4. S Laverty1,3,
  5. F Mwale4,
  6. T Kojima1,5,
  7. T Sakai1,
  8. C Wahl1,
  9. S El-Maadawy1,
  10. G Webb6,
  11. E Tchetina1,
  12. W Wu7
  1. 1Shriners Hospitals for Children, Departments of Surgery and Medicine, McGill University, Montreal, Quebec, Canada
  2. 2Department of Orthopaedic Surgery, Kyoto University Medical School, Kyoto, Japan
  3. 3Faculty of Veterinary Medicine, Department of Clinical Sciences, University of Montreal, Ste-Hyacinthe, Quebec, Canada
  4. 4Department of Orthopaedic Surgery, Jewish General Hospital, Montreal, Quebec, Canada
  5. 5Department of Orthopaedic Surgery, Nagoya University School of Medicine, Nagoya, Japan
  6. 6Molecular Cell Biology Unit, Glaxo Wellcome Research, Stevenage, Hertfordshire, UK
  7. 7Arthritis Unit, Massachusetts General Hospital, Boston, MA, USA
  1. Correspondence to:
    Dr A R Poole;
    rpoole{at}shriners.mcgill.ca

https://doi.org/10.1136/ard.61.suppl_2.ii78

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    The progressive degeneration of articular cartilage is an underlying problem in the pathogenesis of osteoarthritis (OA) as well as in rheumatoid arthritis (RA) and other inflammation arthritides. It leads to a loss of joint function, frequently accompanied by debilitating pain.

    In idiopathic OA this is a degenerative process that may cover a period of 20–30 years, culminating in clinical presentation and a need for joint replacement as the only effective means of managing this condition. There are as yet no recognisable disease modifying treatments for OA; only symptomatic treatment (pain relief) is possible.

    The physical and economic burden of OA is enormous, affecting up to 15% of the total population (>50% of the aging population over 60 years of age). We face an enormous challenge in the management of this condition. Yet with recent progress in reaching an improved understanding of the pathobiology of this condition there is a realisation that there are recognisable targets for treatment. With the advent and promise of new methodologies to detect early disease and predict its progression, there are new opportunities for its future management.

    In this paper we review what we know about the pathobiology of OA and how it can be investigated, focusing on the chondrocyte and the collagen fibrils that it produces which form the endoskeletal backbone of the extensive extracellular matrix.

    STRUCTURE AND ORGANISATION OF ARTICULAR CARTILAGE

    Articular cartilage contains only one cell type, the chondrocyte. In the adult this occupies <5% of the cartilage volume: the remainder is occupied by an extensive extracellular matrix. The structural backbone of this matrix is the collagen fibril (fig 1). This is composed mainly of type II collagen. It also contains type IX collagen on the surface of the fibril.1 Immunological methods have been developed to determine the contents and measure the turnover of these molecules.2 These …

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