Service Communautaire d'Information sur la Recherche et le Développement - CORDIS

Histology and pathology of the human intervertebral disc

Histology of the intervertebral disc shows it to be a highly organized matrix, laid down by relatively few cells in a very specific manner. The central gelatinous nucleus pulposus is contained within the more collagenous anulus fibrosus laterally and the cartilage endplates inferiorly and superiorly. The anulus consists of concentric rings or lamellae, with fibers in the outer ones continuing into the longitudinal ligaments and vertebral bodies. This arrangement allows the discs to facilitate movement and flexibility within what would be an otherwise rigid spine. The human disc begins life with some vascular supply, both within the cartilage endplates and the anulus fibrosus. These vessels recede soon after birth, leaving the disc with very little direct blood supply in the healthy adult.

With increasing age, changes occur to both the cellular and matrix components of the disc. Water is lost from the matrix, and proteoglycan content also changes and diminishes. Morphologically the disc particularly the nucleus becomes less gelatinous and more fibrous; eventually cracks and fissures form. More blood vessels begin to grow into the disc via the outer anulus. Cellular changes include not only an increase in cell proliferation and the formation of cell clusters, but also increased cell death. The cartilage endplate also undergoes changes with age, including thinning, altered cell density, formation of fissures, and sclerosis of the subchondral bone. These changes are similar to those seen in degenerative disc disease, resulting in much discussion as to whether aging and degeneration are two separate processes, or the same process occurring over a different timescale.

Additional disorders involving the intervertebral disc can demonstrate other changes in morphology. Discs from patients with spinal deformities, e.g., scoliosis, have ectopic calcification in the cartilage endplate and sometimes in the disc itself. Cells in these discs and also those from patients with spondylolisthesis have been demonstrated to have some very long cell processes. Disc cells in herniated discs show some further differences; for example, they appear to have a higher degree of cellular senescence than nonherniated discs and produce a greater abundance of matrix metalloproteinases. The role that abnormalities such as these play in the etiopathogenesis of the different disorders is not always clear. They may be due to a genetic predisposition or a response of the tissue to some insult or to an altered mechanical environment. Whatever the initial cause, if the morphology of the tissue changes, it is likely to alter the physiologic and mechanical functioning of the tissue.

Reported by

THE ROBERT JONES AND AGNES HUNT ORTHOPAEDIC AND DISTRICT HOSPITAL NHS TRUST
Shropshire
SY10 7AG OSWESTRY
United Kingdom