Abstract

The degenerative response of rat tail and lumbar intervertebral discs to a stab incision was evaluated. To examine and compare the postinjury degenerative response of lumbar and tail discs. Although successful in larger animals, a stab incision for inducing disc degeneration in rats has not been evaluated. Rodents are desirable models for disc repair studies due to their low cost, ease of care, and fast healing times. Lumbar and tail discs were exposed surgically and stabbed with a number 11 blade. Disc architecture, levels of IL-1beta, IL-6, and TNF-alpha, and biomechanical properties were analyzed. A functional disability secondary to multilevel lumbar disc injury was quantified and compared with that of rats undergoing sham surgery. Histologic evaluation of stabbed tail discs demonstrated a nucleus pulposus size decrease, anular collagen layer disorganization, and cellular metaplasia of anular fibroblasts to chondrocyte-appearing cells. Besides the continued presence of the stab injury tract, few changes were observed in the lumbar disc histology. Cytokine measurements indicated a transient peak in IL-1beta in tail discs 4 days following injury. No significant changes in IL-1beta, IL-6, or TNF-alpha were measured. No significant differences in biomechanical properties were observed between stab injury and sham surgery discs. Yet, despite insignificant differences in histologic, cytochemical, or biomechanical properties in the lumbar discs, the rats with lumbar stab injury had a significant decrease in walking ability 28 days after surgery. Tail disc stab injury was successful in creating morphologic signs of degeneration and transient high concentrations of IL-1beta. However, the degenerative response in the lumbar discs was much slower, suggesting that site-specific factors, such as increased stability due to posterior elements and torso musculature, helped facilitate healing. Yet, functional assessment indicated that the rats were partially disabled by multiple lumbar injuries.

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