Affiliations: MSTP, Baylor College of Medicine, Houston, TX, USA | Department of Biomedical Engineering, University of California Davis, Davis, CA, USA
Note: [] Address for correspondence: Kyriacos A. Athanasiou, Department of Biomedical Engineering, University of California Davis, One Shields Avenue, Davis, CA 95616, USA. Tel.: +1 530 754 6645; Fax: +1 530 754 8375; E-mail: [email protected].
Abstract: This review discusses a framework for studying injurious loading of articular cartilage, which can lead to post-traumatic osteoarthritis. The framework separates the mechanical from the biological response of the tissue to injury. The mechanical response is governed by the tissue's biomechanical behavior and sets off mechano-transductive pathways. These pathways then determine the biological response. The mechanical response of cartilage to injury has been studied by analytical and computational models of injurious loading, joint contact, and surface fissuring. These models have identified shear and tensile stresses as important parameters governing articular cartilage failure in response to mechanical injury. Further, measurement of cartilage's material properties during impact loading has shown that the tissue is significantly stiffer than predicted from quasi-static testing. In terms of the biological response, cell death and sulfated glycosaminoglycan (sGAG) loss from the tissue are early degradative changes that lead to decreased tissue function. These biological sequelae have also been the subject of targeted intervention strategies post-injury. Some success has been found for decreasing cell death and sGAG loss using various bioactive agents. The framework and treatments reviewed here may be useful starting points in the study of mechanical injury to other tissues.
