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Issue title: 3rd International Symposium on Mechanobiology of Cartilage and Chondrocyte. Brussels, May 16–17, 2003
Article type: Research Article
Authors: Day, J.S. | van der Linden, J.C. | Bank, R.A. | Ding, M. | Hvid, I. | Sumner, D.R. | Weinans, H.;
Affiliations: Erasmus Orthopaedic Research Lab, University Rotterdam, Rotterdam, The Netherlands | TNO Prevention and Health, Leiden, The Netherlands | Orthopaedic Research Laboratory, Aarhus University Hospital, Aarhus, Denmark | Department of Anatomy and Cell Biology, Rush Medical College, Chicago, IL, USA
Note: [] Address for correspondence: Harrie Weinans, Erasmus University Rotterdam, Erasmus Orthopaedic Research Lab, EE1614, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands. Tel.: +31 (0) 10 40 87367/87384; Fax: +31 (0) 10 40 89415; E‐mail: [email protected].
Abstract: Osteoarthritis is a chronic joint disease with pathological changes in the articulating cartilage and all other tissues that occupy the joint. Radin and coworkers have suggested the involvement of subchondral bone in the disease process. However, evidence for an essential role in the etiology has never been proven. Recent studies showing reduced chemical and mechanical properties of subchondral bone in various stages of the disease have invigorated interest in the role of subchondral bone in the development and progression of the disease. The current study showed that the concept of bone adaptation might explain subchondral stiffening, a process where subchondral bone becomes typically sclerotic in osteoarthritis. In addition, we report reduced mechanical matrix tissue properties as well as an increase in denatured collagen content. In conclusion, although osteoarthritic bone tissue contains increased denatured collagen and has reduced matrix mechanical properties, the widely accepted concept of subchondral stiffening is compatible with the process of normal bone adaptation.
Journal: Biorheology, vol. 41, no. 3‐4, pp. 359-368, 2004
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