Affiliations: Collagen Research Group, University of Bristol, Bristol, UK | Oral and Dental Science, University of Bristol, Bristol, UK | Academic Rheumatology Unit, Southmead Hospital, Bristol, UK | Orthopaedic Research Laboratory, University of Louvain, Brussels, Belgium
Note: [] Address for correspondence: Professor Allen J. Bailey, Collagen Research Group, University of Bristol, Bristol BS40 5DS, UK. E‐mail: A.J.Bailey@bristol.ac.uk.
Abstract: The subchondral bone has long been known to thicken in osteoarthritis. However, recent evidence has demonstrated that the turnover of the bone is increased several fold, and further suggests that the thickening occurs prior to degradation of the articular cartilage, indicating that it plays a role in the pathogenesis of osteoarthritis. The mechanical and biochemical properties of the subchondral bone are therefore of particular interest in any attempt to determine the nature of the factors initiating osteoarthritis. We have shown that the subchondral bone collagen of the femoral head possessed a 20‐fold increase in turnover, as assessed by procollagen rate of synthesis and metalloproteinase degradation, and a 25% decrease in mineralisation. This increased metabolism and high lysyl hydroxylation leads to narrower and weaker fibres. Additionally the phenotypic expression of the osteoblasts is modified to produce increasing proportions of type I homotrimer in addition to the normal type I heterotrimer, which further reduces the mechanical strength of the bone. Overall, the narrow immature collagen fibres, the reduction in pyrrole cross‐linking, decreased mineralisation, and increased amounts of type I homotrimer, all contribute to a weakening of the mechanical properties of the subchondral bone.
