Department of Orthopedics, The First Affiliated Hospital of Xi' an Jiaotong University, Xi' An, China.
Department of Spine Surgery, The General Hospital of Ningxia Medical University.
Neurol Res. 2021 Jun;43(6):447-457. doi: 10.1080/01616412.2020.1866804. Epub 2021 Jan 17.
To establish an animal model of adjacent intervertebral disc degeneration by performing spinal fixation and fusion after percutaneous needle puncture and removal of the intervertebral disc or percutaneous needling of the vertebral body without removal of the intervertebral disc. We established a model of adjacent intervertebral disc degeneration after spinal fixation and fusion of rabbits maintained in upright feeding cages. Twenty-five healthy New Zealand rabbits were used. In the experimental group, the L3-4 intervertebral disc was percutaneously punctured with an 18-G needle under fluoroscopic guidance. Once degeneration occurred, the L3-4 disc was excised, and interbody fusion was performed. The changes in the adjacent intervertebral discs were observed periodically via X-ray and MRI. In the control group, the L3 vertebral body was percutaneously needled with an 18-G needle under fluoroscopic guidance. The changes in the adjacent intervertebral discs were observed on X-ray and MRI at 4, 8, and 12 weeks after puncture in both groups. At 12 weeks postoperatively, the animals were euthanized, and the histopathologic changes of the adjacent intervertebral discs were assessed using hematoxylin-eosin and TdT-mediated dUTP nick end labeling (TUNEL) staining. The mRNA and protein expressions of aggrecanase-1 were measured by real-time quantitative PCR and Western blot analysis. The product of aggrecan degradation, Aggrecan ARGxx, was measured by Western blot analysis. The degeneration of the intervertebral discs in the adjacent segments in the experimental group increased over time. The mRNA and protein expressions of aggrecanase-1 and the expression of Aggrecan ARGxx in the experimental group were significantly increased after puncture, fixation, and fusion (P<0.05). The adjacent intervertebral disc sections had a significantly lower cell density and significantly higher TUNEL-positive cell rate in the experimental group than the control group (P<0.05). The results suggest that the occurrence of intervertebral disc degeneration in adjacent segments may begin with the degeneration of the punctured intervertebral disc.
通过在经皮穿刺和去除椎间盘或不切除椎间盘而行经皮椎体穿刺后进行脊柱固定和融合,建立椎间盘相邻节段退变的动物模型。我们建立了一种在直立饲养笼中维持的兔脊柱固定和融合后椎间盘相邻节段退变的模型。使用 25 只健康的新西兰兔。实验组在透视引导下用 18-G 针经皮穿刺 L3-4 椎间盘。一旦发生退变,切除 L3-4 椎间盘,进行椎间融合。定期通过 X 线和 MRI 观察相邻椎间盘的变化。在对照组中,在透视引导下用 18-G 针经皮穿刺 L3 椎体。两组在穿刺后 4、8 和 12 周分别通过 X 线和 MRI 观察相邻椎间盘的变化。术后 12 周,处死动物,采用苏木精-伊红和 TdT 介导的 dUTP 缺口末端标记(TUNEL)染色评估相邻椎间盘的组织病理学变化。通过实时定量 PCR 和 Western blot 分析测量 aggrecanase-1 的 mRNA 和蛋白表达。通过 Western blot 分析测量 aggrecan 降解产物 Aggrecan ARGxx。实验组相邻节段椎间盘的退变随时间推移而增加。实验组穿刺、固定和融合后 aggrecanase-1 的 mRNA 和蛋白表达以及 Aggrecan ARGxx 的表达均显著增加(P<0.05)。实验组相邻椎间盘节段细胞密度明显降低,TUNEL 阳性细胞率明显高于对照组(P<0.05)。结果表明,相邻节段椎间盘退变的发生可能始于穿刺椎间盘的退变。