Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499679
Title: The response of articular cartilage to impact loading
Author: Jeffrey, Janet Elizabeth
ISNI:       0000 0004 0102 6253
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 2009
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Abstract:
In this study an in vitro model was used to simulate joint trauma by subjecting explants of articular cartilage to a single impact load using a specially designed drop-tower loading machine for which two different loading attachments were developed. The aim was to compare the biophysical effects of impact loading on bovine and human cartilage. The proteolytic lysomal enzyme, cathepsin B and the proinflammatory mediators, prostaglandin E2 (PGE2) and nitric oxide (NO) have been implicated in the degradation of cartilage following trauma. This study aimed to investigate the role of these degradatory mediators. Human cartilage was found to be less damaged than bovine after impact and the type of loading attachment affected the nature of the damage observed. Following an impact load on human cartilage explants, the levels of glycosaminoglycans (GAGs), a measure of cartilage breakdown, in the culture medium and the percentage of apoptotic chondrocytes were significantly increased. The levels of pro-cathepsin B were significantly increased in the culture medium compared to unloaded controls. Addition of human cystatin C and the synthetic cathepsin B inhibitor, CA-074Me, reduced this release. However these inhibitors had no effect on the release of GAGs or the levels of apoptosis following impact. A marked increase in PGE2 and NO was measured in the medium following an impact load, which was reduced by the selective cyclooxygenase-2 (COX-2) inhibitor, celecoxib, and the non-selective inhibitor, indomethacin. These inhibitors reduced chondrocyte apoptosis but no change was observed in the release of GAGs from the explants. This in vitro study indicates that cell viability and matrix degeneration are separately regulated and that it is unlikely that cathepsin B or COX-2 inhibition alone would slow down or prevent the development of secondary osteoarthritis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.499679  DOI: Not available
Keywords: Articular cartilage ; Osteoarthritis
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