UCSF

Low back pain may be caused by disc degeneration and is a prevalent problem in the United States affecting thirty-one million Americans at any given time. While the etiology is unknown, it has been hypothesized that poor disc nutrition triggered by sclerosis in the vertebral endplate and/or calcification of the cartilaginous endplate is a leading factor in disc degeneration. The objective of this study was to better understand these phenomena by measuring endplate permeability and vertebral endplate bone microstructure and correlating these parameters with disc degeneration parameters.

Intervertebral cores including the subchondral bone, cartilage endplate and adjacent nucleus were harvested from human cadaveric lumbar spines and used for permeability and morphology assessments. The endplate permeability was measured using a custom made, validated permeameter device and the morphology of the vertebra was analyzed using a MicroCT device. The individual relationships between endplate permeability, vertebral endplate morphological changes and disc degeneration parameters was analyzed.

Contrary to previous findings, bone permeability was observed to increase with disc degeneration. Vertebral endplate porosity increased and trabecular thickness decreased as the bony endplate became more homogeneous with disc degeneration. Cartilage permeability was not correlated with disc degeneration, but cell density increased, GAGs decreased and GAGs/cell decreased with degeneration.

The correlation between bone permeability, porosity and degeneration suggest that sclerosis at the vertebral endplate was not present. These results in combination with those found for cartilage permeability, cell density and GAGs in the disc imply that cell dysfunction and a decrease of nutrient availability through the capillaries, rather than physical barriers to transport, accelerate disc disease.