MRI is the gold standard in assessing intervertebral disc generation (IDD), providing information of the integrity of the three components of the intervertebral disc (IVD). These include loss of signal intensity of the nucleus pulposus (NP), tears in the cartilage endplate (CEP) and annulus fibrosus (AF), and herniation through the AF, highlighting structural changes of the IVD leading to functional failure. Indeed, biochemical and mechanical studies support structural changes in relation to the extracellular matrix components and functional outcomes. However, these are endpoint assessments of a degenerated disc, and the processes leading to these outcomes are not clear, and difficult to assess in human. Thus, animal models for IDD are essential in understanding the biology.
While there are limitations in animal studies due to difference in disc size, mechanical load, cellular content and structural variations, the biology of IDD is likely to be conserved. Indeed, key insights into the cellular contribution and changes that could influence disc function have come from animal studies, in particular animals with natural “degeneration” of the IVD such as the mouse and dogs. A role of the notochordal-like cells, originating from the developing notochord is implicated, and onset of disc degeneration correlates with a decline of these cells in the disc. However, the cell biology of the disc is complex, and the cellular content is heterogeneous that changes with age. Much of the focus has been on cells of the NP with a general consensus that there is a gradual change from notochoral to notochordal-like cells, then chondrocyte-like cells and fibroblast-like cells.
However, the relationship between the different populations of cells is not clear, and what defines “functional” NP cells need to be addressed.
Recent advances for in vivo studies of cell biology, in particular, the mouse has enable the studied of cell fate of the IVD, providing insights of the original and fate of cells within the NP and AF, and the identification of potential stem/progenitor cells within the IVD that could be harnessed for repair or prevention of IDD.