The extent of matrix damage and chondrocyte death in mechanically traumatized articular cartilage explants depends on rate of loading

Mechanical loads can lead to matrix damage and chondrocyte death in articular cartilage. This damage has been implicated in the pathogenesis of secondary ostecarthritis, Studies on cartilage explants with the attachment of underlying bone at high rates of loading have documented cell death adjacent to surface lesions. On the other hand, studies involving explants removed from bone at low rates of loading suggest no clear spatial association between cell death and matrix damage. The current study hypothesized that the observed differences in the distribution of cell death in these studies are attributed to the rate of loading. Ninety bovine cartilage explants were cultured for two days. Sixty explants were loaded in unconfined compression to 40 MPa in either a fast rate of loading experiment (similar to 900 MPa/s) or a low rate of loading experiment (40 MPa/s). The remaining 30 explants served as a control population. All explants were cultured for four days after loading. Matrix damage was assessed by measuring the total length and average depth of surface lesions and the release of glycosaminoglycans to the culture media. Explants;A ere sectioned and stained with calcein and ethidium bromide homodimer to document the number of live and dead cells. Greater matrix damage was documented in explants subjected to a high rate of loading, compared to explants exposed to a low rate of loading. The high rate of loading experiments resulted in cell death adjacent to fissures, whereas more dead cells were observed in the low rate of loading experiments and a more diffuse distribution of dead cells was observed away from the fissures. In Conclusion, this Study indicated that the rate of loading can significantly affect the degree of matrix damage, the distribution of dead cells, and the amount of cell death ill unconfined compression experiments on explants of articular cartilage. (C) 2001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.