Unglaub F, Lorenz H, Nerlich A, Richter W, Kroeber M W
Stiftung Orthopädische Universitätsklinik, Heidelberg, Germany.
Z Orthop Ihre Grenzgeb. 2003 Jul-Aug;141(4):412-7. doi: 10.1055/s-2003-41567.
Degeneration of the intervertebral disc is a common disease in the adults, especially at advanced age. A causal therapy is not known, but the progress in new therapeutic strategies, for example in tissue engineering, shows new possibilities. The goal of our study was to develop a new animal model that stimulates a load induced degeneration of the disc. We used the New Zealand rabbit, because morphology is similar to the human intervertebral disc. The degeneration was induced by axial compression of the disc L4 - L5 with an external fixateur. After different loading intervals, the animals were sacrified and the discs examined by radiology, histology, apoptosis and biomechanical testing. Radiography showed a significant decrease of the disc thickness in all loaded groups. Morphologically the intervertebral discs of loaded rabbits showed degenerative changes which were comparable to those in humans. A significantly increased number of dead cells in the annulus occurred after 14 and 28 days loading compared to the controls. The bending stress measured as the load to failure was not significantly different between the unloaded discs and the 28 days loaded discs. The results show that our animal modell can create degeneration. Four weeks compression leads to significant degeneration. Degeneration of the discs persisted in animals that were allowed a recovery time of 28 days after 28 days of loading.
椎间盘退变是成年人的常见疾病，尤其是在老年人群中。目前尚不清楚其病因疗法，但新治疗策略（例如组织工程学）的进展展现了新的可能性。我们研究的目的是开发一种新的动物模型，以模拟负荷诱导的椎间盘退变。我们选用新西兰兔，因为其椎间盘形态与人的相似。通过外部固定器对L4 - L5椎间盘进行轴向压缩来诱导退变。在不同的加载时间间隔后，处死动物，并通过放射学、组织学、凋亡检测和生物力学测试对椎间盘进行检查。放射学检查显示，所有加载组的椎间盘厚度均显著降低。形态学上，加载兔的椎间盘呈现出与人类相似的退变变化。与对照组相比，加载14天和28天后，纤维环中死亡细胞数量显著增加。以破坏负荷衡量的弯曲应力在未加载椎间盘和加载28天的椎间盘之间无显著差异。结果表明，我们的动物模型能够引发退变。四周的压缩导致显著退变。在加载28天后给予28天恢复时间的动物中，椎间盘退变依然存在。
