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 ... [Show full abstract] 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.