Basic science of spinal degeneration

This article summarizes recent advances in our understanding of spinal pathology and pain. Degeneration appears to start in the intervertebral discs, often before age 20 years, and can be distinguished from ‘normal’ ageing by the presence of physical disruption, typically in the form of annulus fissures, prolapse or endplate fracture. Disruption is ultimately mechanical, but frustrated attempts by a small population of disc cells to heal a large avascular matrix give rise to the typical biological features of disc degeneration. Genetic inheritance and ageing are important risk factors for disc degeneration because they can weaken the disc matrix, and hinder repair processes. Discogenic pain appears to arise from the disc periphery as a result of in-growing nerves being sensitized by soluble factors from activated disc and blood cells. A degenerated disc loses pressure in the nucleus and bulges radially outwards, like a flat tyre. This often leads to a transient segmental instability, which can be reversed by the growth of osteophytes around the margins of the vertebral body. Annulus collapse in severe disc degeneration transfers compressive load-bearing to the neural arch, leading to facet joint osteoarthritis, and possibly to degenerative scoliosis. The anterior vertebral body then becomes relatively unloaded, and consequent focal bone loss (exacerbated by systemic osteoporosis) increases the risk of anterior wedge deformities, and senile kyphosis. Future interventions may include physical therapy to aid disc healing, disc prostheses with no moving parts, and injection therapies to block pain pathways.