S21_5

Bone mass and osteoarthritis

J. Dequeker, F.P. Luyten

Department of Rheumatology, University Hospitals, Leuven, Belgium.

ABSTRACT
There is now substantial evidence in human and experimental animal osteoarthritis (OA) that there is a change in the metabolism of the bony skeleton, and in particular at the subchondral area. Because these changes in bone density and metabolism precede cartilage fibrillation, it is likely that bone metabolism in general, and subchondral bone density in particular, are involved in the pathogenesis of osteoarthritis. The alteration in bone results in an increased pure and apparent density and low bone turnover. It does not appear to be the consequence of a change in serum levels of calcitropic hormones, but an alteration in local signals; in particular, growth factors such as TGF-b and IGF seem likely to play a role. In vitro studies suggest that the changes in bone matrix composition may be due to an altered osteoblast phenotype in OA.
The observation of important and consistent bone changes in OA lends further support to the hypothesis that this disease, or at least some subgroups of this heterogenous group of disorders, may primarily be a bone disorder in which more dense bone, with less shock-absorbing capacity, needs to transfer the stress of loading directly onto the articular surface, resulting in secondary changes in the cartilage.

Key words
Osteoarthritis, bone, osteoporosis, joint failure.

Please address correspondence and reprint requests to Prof. J. Dequeker, Department of Rheumatology, University Hospitals K.U. Leuven, B-3000 Leuven, Belgium.
E-mail: jan.dequeker@uz.kuleuven.ac.be