STUDY DESIGN: The progression of intervertebral disc degeneration (IDD) follows anterolateral stab of adult rabbit lumbar discs by 16-gauge hypodermic needle to a limited (5-mm) depth was studied for up to 24 weeks using magnetic resonance imaging (MRI).
OBJECTIVES: To develop a slowly progressive, reproducible rabbit model of IDD suitable for studying pathogenesis and pathopysiology of intervertebral disc degeneration. Moreover, to improve the MRI methods and achieve improved MRIs a custom quad coil tuned and matched for 3.0T was developed. Higher SNR achievable with this coil allowed the acquisition of higher resolution images.
METHODS: Part1 - The L2-L3, L3-L4, and L4-L5 lumbar intervertebral discs of 18 skeletally mature female New Zealand White (NZW) rabbits were stabbed by 16-gauge hypodermic needle to a depth of 5-mm in the left anterolateral annulus fibrosis (AF). Serial MRI scans of the stabbed discs and intact L1-2 and L5-6 control discs were performed at 3, 6, 12, and 24 weeks post surgery and compared with preoperative MRIs. Development of the quad coil at 3.0T was competed with reference phantom to demonstrate the advantages over the 5 inch surface coil at 1.5T. To further illustrate the coils advantages in-vivo rabbit MRIs were obtained with the custom coil and compared to the 5 inch surface coil at 1.5T
RESULTS: The stabbed discs exhibited a progressive decrease in MRI Index (the product of nucleus pulposus (NP) area and signal intensity from T2-weighted midsagittal plane images) starting at 3 weeks post stab and continuing through 24 weeks, with no evidence of spontaneous recovery or reversal of MRI changes. In addition, the constructed quad coil at 3.0T demonstrated the ability to obtain high resolution scans with SNR comparable to the 5 inch surface coil at 1.5T.
CONCLUSIONS: Stabbing the anterolateral AF of adult rabbit lumbar discs with a 16-gauge hypodermic needle to a limited (5-mm) depth results in a number of slowly progressive and reproducible MRI changes over 24 weeks that show a similarity to changes seen in human IDD. This model would appear suitable for studying pathogenesis and pathophysiology of IDD and testing safety and efficacy of novel treatments of IDD.
| Identifer | oai:union.ndltd.org:PITT/oai:PITTETD:etd-04062006-222447 |
| Date | 30 January 2008 |
| Creators | Kompel, John Francis |
| Contributors | Lars G. Gilbertson, Ph.D, Fernando Boada, Ph.D, James D. Kang, MD, Doug Robertson, MD, PhD |
| Publisher | University of Pittsburgh |
| Source Sets | University of Pittsburgh |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.library.pitt.edu/ETD/available/etd-04062006-222447/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Pittsburgh or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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