Phillips F M, Reuben J, Wetzel F T
Section of Orthopaedic Surgery and Rehabilitation Medicine, Spine Centre, University of Chicago, Illinois 60640, USA.
J Bone Joint Surg Br. 2002 Mar;84(2):289-94. doi: 10.1302/0301-620x.84b2.11937.
Our study establishes a rabbit model of disc degeneration which requires neither a chemical nor physical injury to the disc. Disc degeneration similar to that seen in man was created at levels proximal (L4-L5) and caudal (L7-S1) to a simulated lumbar fusion and was studied for up to nine months after arthrodesis. Loss of the normal parallel arrangement of collagen bundles within the annular lamellae was observed in intervertebral discs adjacent to the fusion at three months. By six months there was further disorganisation as well as loss of distinction between the lamellae themselves. By nine months the structure of the disc had been replaced by disorganised fibrous tissue, and annular tears were seen. There was an initial cellular proliferative response followed by loss of chondrocytes and notochordal cells in the nucleus pulposus. Degeneration was accompanied by a decrease in the monomer size of proteoglycans. Narrowing of the disc space, endplate sclerosis and the formation of osteophytes at adjacent disc spaces were observed radiologically.
我们的研究建立了一种椎间盘退变的兔模型,该模型既不需要对椎间盘进行化学损伤也不需要物理损伤。在模拟腰椎融合的近端(L4-L5)和尾端(L7-S1)节段产生了与人相似的椎间盘退变,并在关节融合术后长达九个月的时间内进行了研究。在融合相邻的椎间盘内,三个月时观察到纤维环板层内胶原束正常平行排列的丧失。到六个月时,纤维环进一步紊乱,并且板层之间的区分也丧失。到九个月时,椎间盘结构已被紊乱的纤维组织取代,并可见环状撕裂。髓核中最初有细胞增殖反应,随后软骨细胞和脊索细胞丢失。退变伴随着蛋白聚糖单体大小的减小。影像学观察到椎间盘间隙变窄、终板硬化以及相邻椎间盘间隙处骨赘形成。