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Introduction and Aims: Assessment of the metabolic state of articular cartilage (AC) is important in understanding the initiation and progression of osteoarthritis (OA). The purpose of this study was to evaluate changes in gene expression of the major AC extracellular matrix (ECM) components, in addition to a number of molecules involved in OA, including the novel glycoprotein lubricin, following lateral meniscectomy in a sheep model of OA.

Method: AC tissue from both medial (MTP) and lateral (LTP) tibial plateaux were collected from six non-operated control (NOC) and six lateral meniscectomised (MEN) pure-bred Merino sheep six months post-surgery for semi-quantitative RT-PCR to assess patterns of mRNA expression (relative to GAPDH). Histological evaluation using a modified Mankin score was undertaken in the same sheep to grade the AC and immunohistochemical localisation of gene products was performed.

Results: Cartilage degeneration was evident both macroscopically and histologically in the LTP following MEN, with less marked changes appearing in the MTP. The mean total tissue RNA increased greater than five-fold in the LTP following MEN (p< 0.01). Expression of aggrecan (p< 0.01) and collagen type II (p< 0.01) were found to be significantly elevated in LTP AC following MEN. Increased expression of biglycan (p< 0.01) was observed in LTP AC following MEN, whereas conversely, there was a decreased expression of decorin (p< 0.01), the other fibril associated small leucine rich proteoglycan. Expression of both lubricin (p< 0.01) and connective tissue growth factor (CTGF) (p< 0.05) were also found to decrease following MEN in LTP AC. TGFβ demonstrated no change in expression following MEN. Significant changes in gene expression were generally not seen in the MTP following MEN; however trends were observed reflecting similar gene profile changes to those occurring in the LTP.

Conclusion: Strong up-regulation in gene expression of the major cartilage ECM components was found, reflecting an anabolic response and attempted tissue repair. Significant changes were also observed for other ECM macromolecules thought to be involved in degenerative joint disease, contributing to alterations in the gene expression profile associated with OA.

These abstracts were prepared by Editorial Secretary, George Sikorski. Correspondence should be addressed to Australian Orthopaedic Association, Ground Floor, The William Bland Centre, 229 Macquarie Street, Sydney, NSW 2000, Australia.

One or more of the listed authors are receiving or have received benefits or support from a recognised academic body for the pursuance of the study.