SUNFEST Report

نویسندگان

  • An Nguyen
  • Dawn M Elliott
چکیده

Background Context: In the United States, the most prevalent cause of disability of workers under 45 years of age is low back pain. Past research suggests that there is a link between low back pain and intervertebral disc degeneration. One of the earliest known components of disc degeneration is a decrease in proteoglycan content in the nucleus pulposus, which in turn leads to changes in mechanical properties. In this study, the effects of proteoglycan content and collagen cross-linking on swelling behavior were investigated. Study Design: Swelling pressure of the nucleus pulposus was measured in a confined compression experiment. The effects of two injectable agents were studied. The first was Chondroitinase ABC (ChABC), which is an enzyme that breaks down proteoglycan. ChABC was used to model disc degeneration. In addition, genipin -a cross-linking agent that promotes the cross-linking of fibers in the disc’s collagen network -was also used. Objectives: The main objective of this study was to determine the effects of cross-linking on the mechanical properties of degenerate nucleus pulposus. The first step was to determine baseline swelling pressure for control or normal sheep discs. The second was to determine the concentration of ChABC needed to mimic the degeneration found in human discs. The final step of the study was to investigate the potential of genipin required to restore the mechanical function in degenerate discs. Results: The average swelling pressure measured for normal sheep discs was 0.21 + 0.13 MPa. The optimal ChABC dose was 0.5 U with an average swelling pressure of 0.082 + 0.04 MPa. The average swelling pressure for the 0.5% genipin group and 0.5% genipin + 0.5 U ChABC were 0.15 + 0.07 MPa and 0.083 MPa, respectively. Conclusion: Though findings from this study were inconclusive, they do not eliminate the potential of genipin as a treatment for disc degeneration. This warrants further investigation into effects of cross-linking using genipin and the mechanisms by which genipin increases crosslinking.

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تاریخ انتشار 2006