Disc Degeneration and Aging
This is a complex issue. Normal ageing processes lead to changes in the motion segment. These occur to different degrees in different people and the rate is related to:
- Intrinsic factors (e.g. genetic makeup)
- Extrinsic factors (e.g. injury, smoking, occupation)
It is difficult to distinguish between what is normal and what is pathological. A simplified view is presented below.
This was first described by Kirkaldy-Willis. The primary concept is of three stages - dysfunction, instability and stabilisation. My interpretation is as follows.
The primary initiator is the disc. It is unable to regenerate as it has no direct blood supply. The water content of the disc decreases and the chemical structure (of the mucopolysaccharides) changes. The result is that the disc loses turgor, height and elasticity. It allows excessive movement at the motion segment. This is the phase of dysfunction. This results in small tears in the disc. Initially these are circumferential but with time, the tears can coalesce and become radial. The next step is resorption of the disc. The process of desiccation (drying out) is accelerated by the presence of radial tears. Abnormal movement is allowed by degeneration of the disc. This is the phase of instability. The final step is formation of osteophytes in an attempt to decrease this abnormal movement. This is the phase of stabilization.
There are corresponding changes in the facet joints. As the disc loses turgor and height during the phase of dysfunction, there is increased load on the facet joint and synovitis results. During the phase of instability, there is increased movement at the facet joints due to capsular instability and joint degeneration. With stabilization, there is osteophyte formation and enlargement of the articular processes.
During the dysfunctional and unstable phases, radial tears can become large enough to allow the nucleus pulposus to herniate through the tear in the annulus fibrosis into the spinal canal. They usually occur in a posterolateral direction. This focal prolapse differs from the generalized bulge that is part of the normal degenerative process.
The phase of instability can be asymptomatic, or sometimes be associated with back pain. The exact cause is unclear but it is presumably due to minor subluxations of the facet joints and abnormal movement at the intervertebral disc.
The disc degeneration during dysfunction and instability is associated with ingrowth of blood vessels and nerve endings. There is venous hypertension in the region of the end-plate. The exact cause is unclear but the result is pain arising from the disc itself.
Encroachment upon the neural contents of the spinal canal occurs in the phase of stability due to:
- Bulging of the disc into the canal with enlargement of the facet joints again into the canal causing narrowing of the central spinal canal (central stenosis)
- Enlargement of the facet joints in the region of the path of the nerve roots in the spinal canal (lateral stenosis)
- Narrowing of the disc and thus the exit foramen between the vertebral bodies (foraminal stenosis)
Facet joint degeneration during the phase of instability can lead to joint destruction. The joint becomes incompetent and together with the increased movement possible at the disc, one vertebra is able to slip forward on the one below. This is often associated with stenosis in the phase of stabilization. The slip together with reactive osteophyte formation lead to narrowing of the central canal.
The process is similar to degenerative spondylolisthesis. In this case, the facet degeneration allows lateral slip and tilt of one vertebra on another. Again this is often associated with stenosis.