Abstract

: We evaluated the degenerative changes to rat tail vertebral discs induced by percutaneous needle puncture, and we compared 2 puncture styles for the depth of needle puncture and the rate of disc degeneration. : To develop a simple animal model of disc degeneration. : The study of biologically based treatments for degenerative disc disease depends largely on animal models. Annulus needle puncture in the lumbar spine inducing disc degeneration in rabbits has proven successful, but a similar method has not been evaluated in the tail discs of rats, even though it might produce a desirable model for disc repair studies. : Two consecutive rat tail vertebral discs, proximal and distal to the eighth coccygeal vertebra, were randomized for injury and control. The disc selected for injury was punctured percutaneously using a 20-gauge needle with either full penetration or half penetration. The discs were harvested 1, 2, and 4 weeks later. Measurements included disc height on molybdenum target digital radiographs, biochemistry (water content, glycosaminoglycans, and hydroxyproline), and histology. : Needle punctures with full or half penetration caused significant disc space narrowing and progressive histologic changes of degeneration as early as 1 and 2 weeks after injury, respectively. Significant decrease in glycosaminoglycan content was observed at 4 weeks in the half-penetration puncture discs and at 2 and 4 weeks in discs punctured penetratively. Penetrative puncture resulted in a faster decrease in disc height, lower glycosaminoglycan content, and higher grades of histologic degeneration. The water and hydroxyproline content of the discs did not change appreciably. : Tail disc percutaneous needle puncture is a simple method for inducing disc degeneration and the rate of degeneration is positively related to the depth of needle puncture. This model still has some limitations that should be taken into consideration when results of disc regeneration research in this model are interpreted and extrapolated to human.

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