Abstract
Mechanical function and failure of intervertebral discs. In a healthy disc, the nucleus pulposus acts like a pressurised fluid which is restrained by tensile stress within the annulus. With increasing age, the nucleus becomes more fibrous, and biochemical changes cause the whole disc to become less elastic, and more yellow in colour. Mechanically, the hydrostatic nucleus shrinks with age, and concentrations of compressive stress appear in the posterior annulus. Experiments on cadaveric spines have shown that healthy discs can prolapse when loaded severely or repetitively in bending and compression, and that internal disruption of the disc probably follows damage to the vertebral endplates. However, mechanical loading is not necessarily harmful to living discs: on the contrary, moderate repetitive loading may lead to disc hypertrophy rather than injury.
Disc degeneration. Degeneration represents some mechanical or biological “insult” superimposed on normal ageing. A defining feature of “degeneration” should be structural failure of the annulus or endplate, because all degenerated discs exhibit structural failure whereas many old discs do not. Degeneration creates high stress concentrations within the annulus. Paradoxically, severe degeneration can lead to gross disc narrowing and reduced stresses in the annulus, presumably because it is “stress shielded” by the apophyseal joints. Animal experiments show that disc degeneration always follows mechanical disruption. In some cases, it may possibly precede it.
Disc degeneration and back pain. Pain-provocation studies have shown that severe and chronic back pain often originates in the posterior annulus fibrosus, and can be elicited by relatively moderate mechanical pressure. Anatomical studies indicate that the outer annulus is supplied with complex and free nerve endings from the mixed sinuvertebral nerve. MRI and discographic studies show that back pain is closely correlated with structural features of disc degeneration such as radial fissures and prolapse, although age-related changes in composition are clinically irrelevant. The stress-shielding of severely degenerated discs (see above) suggests that discogenic pain may be most closely associated with intermediate stages of degeneration. The localised stress concentrations found in degenerated cadaveric discs have been directly linked to low back pain in living people.
Medico-legal implications. The widely-held belief that a disc will not prolapse unless it is degenerated is no longer compatible with the scientific evidence. Severe loading, which in life usually arises from vigorous muscle contractions, can injure normal discs. On the contrary, it seems likely that severely degenerated discs are too fibrous to prolapse, and that many of the cell-mediated changes associated with disc prolapse occur after prolapse, rather than before. However, genetic inheritance is important in disc degeneration and prolapse, suggesting that some discs are more vulnerable than others to mechanical loading. The nature of this vulnerability is largely unknown, but is likely to involve genetic weaknesses in composition, and previous fatigue damage. It would be desirable to distinguish between these last two factors, but this is likely to prove difficult in practice.
The abstracts were prepared by Dr P Dolan. Correspondence should be addressed to him at the British Orthopaedic Association, Royal College of Surgeons, 35-43 Lincoln’s Inn Fields, London WC2A 3PN.
