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BioMed Research International
Volume 2016 (2016), Article ID 5952165, 14 pages
http://dx.doi.org/10.1155/2016/5952165
Review Article

A Review of Animal Models of Intervertebral Disc Degeneration: Pathophysiology, Regeneration, and Translation to the Clinic

1The Ritchie Centre, Hudson Institute of Medical Research, Clayton, VIC 3168, Australia
2Department of Neurosurgery, Monash Medical Centre, Clayton, VIC 3168, Australia
3Department of Surgery, Monash University, Clayton, VIC 3168, Australia
4Proteobioactives, Pty. Ltd., Balgowlah, NSW 2093, Australia
5Department of Neurosurgery, St Vincent’s Private Hospital, Fitzroy, VIC 3065, Australia

Received 18 March 2016; Accepted 3 May 2016

Academic Editor: Oreste Gualillo

Copyright © 2016 Chris Daly et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lower back pain is the leading cause of disability worldwide. Discogenic pain secondary to intervertebral disc degeneration is a significant cause of low back pain. Disc degeneration is a complex multifactorial process. Animal models are essential to furthering understanding of the degenerative process and testing potential therapies. The adult human lumbar intervertebral disc is characterized by the loss of notochordal cells, relatively large size, essentially avascular nature, and exposure to biomechanical stresses influenced by bipedalism. Animal models are compared with regard to the above characteristics. Numerous methods of inducing disc degeneration are reported. Broadly these can be considered under the categories of spontaneous degeneration, mechanical and structural models. The purpose of such animal models is to further our understanding and, ultimately, improve treatment of disc degeneration. The role of animal models of disc degeneration in translational research leading to clinical trials of novel cellular therapies is explored.