Spine Research Laboratory, Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan, USA.
J Neurosurg Spine. 2011 Oct;15(4):404-13. doi: 10.3171/2011.5.SPINE10811. Epub 2011 Jul 1.
In this study, the authors' goal was to investigate the long-term progression of disc degeneration and the participating mechanisms induced by needle puncture in a rat caudal disc model.
The C5-6 and C7-8 intervertebral discs of the caudal spine in rats were stabbed laterally using 21-gauge hypodermic needles to a depth of 5 mm from the subcutaneous surface with the aid of fluoroscopy. Signs of degeneration in the disc of the tail were analyzed from Day 1 to Week 30 by in vivo MR imaging, histology, and biochemical and/or molecular analyses.
Magnetic resonance imaging showed a progressive decrease in T2 density and MR imaging index throughout the entire investigation, starting at Day 1 after the needle puncture. However, histological scores revealed a bimodal pattern, showing that severity increased in the first 17 days, declined thereafter, and increased again by 30 weeks. Gene expression analysis showed a transient up-regulation in gene expression of aggrecan, type II collagen, and BMP-2, and inhibition of type I collagen. The MMP-3 mRNA levels were up-regulated at all tested time points within 6 weeks postinjury. Furthermore, the degenerated disc did not recover spontaneously, as shown by decreases in T2 density, MR imaging index, and sulfated glycosaminoglycan content in conjunction with increases in histological scores at 15 and 30 weeks postsurgery.
This study demonstrates that needle puncture into a tail disc in the rat induces a rapid and progressive disc degeneration process without spontaneous recovery. Changes in gene expression profiles of the disc matrix molecules as well as anabolic and catabolic factors at early time points further delineate the mechanism of disc degeneration in this newly developed animal model.
本研究旨在通过大鼠尾椎间盘中的针穿刺模型，探究椎间盘退变的长期进展及由此引发的参与机制。
借助透视，用 21 号皮下注射针从皮下表面侧向穿刺大鼠尾椎间盘中的 C5-6 和 C7-8 椎间盘，深度达 5mm。通过体内磁共振成像、组织学、生化和/或分子分析，从第 1 天到第 30 天分析尾部椎间盘退变的迹象。
磁共振成像显示，从针穿刺后第 1 天开始，整个研究过程中 T2 密度和磁共振成像指数逐渐降低，但组织学评分呈双峰模式，即前 17 天严重程度增加，随后下降，第 30 周再次增加。基因表达分析显示，聚集蛋白、II 型胶原和 BMP-2 的基因表达一过性上调，I 型胶原受到抑制。MMP-3mRNA 水平在损伤后 6 周内的所有测试时间点均上调。此外，退变的椎间盘不会自发恢复，这表现在 T2 密度、磁共振成像指数和硫酸化糖胺聚糖含量下降，以及手术后 15 周和 30 周组织学评分增加。
本研究表明，在大鼠尾椎间盘内进行针刺会导致快速进行性椎间盘退变过程，且无自发恢复。椎间盘基质分子以及合成代谢和分解代谢因子的基因表达谱在早期的变化进一步阐明了这种新开发的动物模型中椎间盘退变的机制。
