Lipson S J, Muir H
Spine (Phila Pa 1976). 1981 May-Jun;6(3):194-210. doi: 10.1097/00007632-198105000-00002.
An animal model of intervertebral disc degeneration induced surgically by ventral nuclear herniation in the rabbit produces morphologic changes of disc degeneration. Histologic characteristics and proteoglycan changes have been studied at various times after herniation. After injury, there was metaplasia into fibrocartilage originating from the cells along the margins of the annular wound, with proliferation of cells changing almost the entire disc space into fibrocartilage. A vertebral osteophyte occurred through an endochondral ossification sequence. Aggregating proteoglycans had two periods of repletion in the early course of degeneration. The water content of the disc was rapidly but only transiently restored in the first two days after herniation, whilst the changes in the total proteoglycan content of the disc paralleled these changes. Hyaluronic acid content decreased rapidly after herniation, but the size of the proteoglycan monomers did not change with degeneration. It is suggested that loss of confined fluid mechanics signals an abortive repair attempt rather than that of biochemical changes in proteoglycans initiate disc degeneration.
通过兔腹侧核突出手术诱导的椎间盘退变动物模型会产生椎间盘退变的形态学变化。在突出后的不同时间研究了组织学特征和蛋白聚糖变化。损伤后，沿环形伤口边缘的细胞发生化生形成纤维软骨，细胞增殖几乎将整个椎间盘间隙转变为纤维软骨。椎体骨赘通过软骨内成骨序列形成。聚集蛋白聚糖在退变早期有两个补充期。椎间盘的含水量在突出后的前两天迅速但只是短暂恢复，而椎间盘总蛋白聚糖含量的变化与这些变化平行。透明质酸含量在突出后迅速下降，但蛋白聚糖单体的大小不会随退变而改变。有人认为，受限流体力学的丧失表明修复尝试失败，而非蛋白聚糖的生化变化引发椎间盘退变。
