Intervertebral Disc Degeneration
What is Intervertebral Disc Degeneration, and What Causes It?
From: Spine Volume 31, Number 18, pp 2151–2161, 2006
Study Design. Review and reinterpretation of existing literature.
Objective. To suggest how intervertebral disc degeneration might be distinguished from the physiologic processes of growth, aging, healing, and adaptive remodeling. Summary of Background Data. The research literature concerning disc degeneration is particularly diverse, and there are no accepted definitions to guide biomedical research, or medicolegal practice.
Definitions. The process of disc degeneration is an aberrant, cell-mediated response to progressive structural failure. A degenerate disc is one with structural failure combined with accelerated or advanced signs of aging. Early degenerative changes should refer to accelerated age-related changes in a structurally intact disc. Degenerative disc disease should be applied to a degenerate disc that is also painful.
Justification. Structural defects such as endplate fracture, radial fissures, and herniation are easily detected, unambiguous markers of impaired disc function. They are not inevitable with age and are more closely related to pain than any other feature of aging discs. Structural failure is irreversible because adult discs have limited healing potential. It also progresses by physical and biologic mechanisms, and, therefore, is a suitable marker for a degenerative process. Biologic progression occurs because structural failure uncouples the local mechanical environment of disc cells from the overall loading of the disc, so that disc cell responses can be inappropriate or “aberrant.” Animal models confirm that cell-mediated changes always follow structural failure caused by trauma. This definition of disc degeneration simplifies the issue of causality: excessive mechanical loading disrupts a disc’s structure and precipitates a cascade of cell-mediated responses, leading to further disruption. Underlying causes of disc degeneration include genetic inheritance, age, inadequate metabolite transport, and loading history, all of which can weaken discs to such an extent that structural failure occurs during the activities of daily living. The other closely related definitions help to distinguish between degenerate and injured discs, and between discs that are and are not painful.
The purpose of the present article is to propose and justify a working definition of intervertebral disc degeneration, and show how it facilitates interpretation of the diverse research literature. Initial sections review the evidence concerning intervertebral disc functional anatomy, metabolism, aging, structural failure, and pain. This review is followed by an account of disc degeneration as suggested by animal models and epidemiology. Finally, 2 “interpretation” sections consider what disc degeneration is and what causes it.
- Disc degeneration is an aberrant cell-mediated response to progressive structural failure.
- Disc structural failure is irreversible, always progresses by physical and biologic mechanisms, and is closely associated with mechanical dysfunction and pain.
- Genetic inheritance, age, inadequate metabolite transport, and loading history can weaken discs to such an extent that structural failure occurs during the activities of daily living.
Plainly, excessive mechanical loading causes a disc to degenerate by disrupting its structure and precipitating a cascade of nonreversible cell-mediated responses leading to further disruption. As discussed previously, and in detail elsewhere, cadaveric experiments and mathematical models show how various combinations of compression, bending, and torsion can cause all the major structural features of disc degeneration, including endplate defects, radial fissures, radial bulging, disc prolapse, and internal collapse of the anulus. Injury or wear and tear “fatigue” loading can create damage. Animal experiments confirm that structural disruption to disc or endplate always leads to cell-mediated degenerative changes.
Although we suggest that mechanical loading precipitates degeneration, the most important cause of degeneration could be the various processes that weaken a disc before disruption, or that impair its healing response. The combined effects of an unfavorable inheritance, middle age, inadequate metabolite transport, and loading history appear to weaken some discs to such an extent that physical disruption follows some minor incident. A common example is that of disc herniation following a cough or sneeze. It could be argued that such a weakened disc should be considered degenerated, even if it remains structurally sound. However, a disc is unlikely to become painful until it becomes disrupted, so there is little to be gained by anticipating future events and applying the term “degeneration” before this crucial nonreversible event actually occurs. As suggested previously, accelerated biochemical or cellular events in a structurally sound disc could be designated “early degenerative changes” to distinguish them from changes that are entirely typical of the disc’s age. The multifactorial nature of disc weakening suggests that, from a medicolegal standpoint, all discs are “vulnerable” to a greater or lesser extent, and the vulnerability can only be gauged from the violence, or otherwise, required to disrupt the disc and initiate degeneration.
The process of disc degeneration should be defined as an aberrant, cell-mediated response to progressive structural failure. Definitions of a degenerated disc and early degenerative changes should also refer to structural failure, whereas degenerative disc disease should apply to a degenerated disc, which is also painful. The underlying cause of disc degeneration is tissue weakening occurring primarily from genetic inheritance, aging, nutritional compromise, and loading history. The precipitating cause is structural disruption occurring from injury or fatigue failure.
