Descriptions of treatment for low back pain (LBP) date to Hippocrates (460-370 BCE), who reported joint manipulation and use of traction. Onset of LBP often is associated with bipedal ambulation. Theories propose that this transformation in the mechanics of locomotion is the inciting evolutionary event that made the lumbar spine susceptible to degenerative disease. Degeneration is universal to structures that comprise the functional spinal unit, composed of 2 adjacent vertebral bodies and the intervertebral disk. The disk and 2 zygapophyseal joints at the same level function as a trijoint complex.

As humans age, they endure both macrotraumas and microtraumas and undergo changes in body habitus that alter and redistribute biomechanical forces unevenly on the lumbar spine. Natural progression of degeneration of the lumbar segment with motion proceeds with characteristic anatomic, biomechanical, radiologic, and clinical findings in lumbar degenerative disk disease (LDDD).

ETIOLOGY
Traditionally, disk degeneration has been linked to mechanical loading. The importance of mechanical factors has been emphasized by experiments on cadaver spines with both a severe single event and relentless loading. Failure of disks is more common in areas where there are the heaviest mechanical stresses, such as the lower lumbar region. It has been suggested that mechanical factors produce endplate damage, the antecedent to disk degeneration.

The disk is metabolically active, and the metabolism is dependent on diffusion of fluid either from the marrow of the vertebral bodies across the subchondral bone and cartilaginous endplate or through the annulus fibrosus from the surrounding blood vessels. Morphologic changes in the vertebral bone and cartilaginous endplate, which occur with advancing age or degeneration, can interfere with normal disk nutrition and further the degenerative process. This disruption of the normal endplate results in deformation when under loading. This allows nuclear material to pass through the endplate, reducing intradiscal pressure with subsequent bulging and loss of height and adding more stress to the surrounding annulus. Compressive damage to the vertebral body endplate alters the distribution of stresses in the adjacent disk. Continual cyclic loading makes these changes worse. Diminished blood flow in the endplate initiates tissue breakdown first in the endplate and then in the nucleus. These altered stress distributions adversely affect disk cell metabolism. These changes then alter the integrity of the proteoglycans and water concentration, reducing the number of viable cells with subsequent alteration in the movement of solutes into and out of the disk.

The importance of normal blood flow to the homeostatic nutritional process in the intervertebral disk complex has been suggested to explain the association of atherosclerosis and aortic calcification with increased disk degeneration and subjective low back pain (10). As degeneration progresses, structures of the disk become more disarranged and greater stresses are placed on the annulus and facet joints. As increased forces are transmitted to the annulus, there may be fragmentation and fissuring. Disk degeneration involves structural disruption and cell-mediated changes in composition, but which occurs first is not clear. Biochemical factors can increase susceptibility to mechanical disruption, and this could adversely influence disk cell metabolism. Regardless of the initiating mechanism, these mechanisms would be interactive and additive, the end result being an altered functional ability of the disk to resist applied forces.

Mechanical load and injury
Abnormal mechanical loads are also thought to provide a pathway to disc degeneration. For many decades it was suggested that a major cause of back problems is injury, often work-related, which causes structural damage. It is believed that such an injury initiates a pathway that leads to disc degeneration and finally to clinical symptoms and back pain. Animal models have supported this finding. Although intense exercise does not appear to affect discs adversely and discs are reported to respond to some long-term loading regimens by increasing proteoglycan content, experimental overloading or injury to the disc can induce degenerative changes. Further support for the role of abnormal mechanical forces in disc degeneration comes from findings that disc levels adjacent to a fused segment degenerate rapidly.

This injury model is also supported by many epidemiological studies that have found associations between environmental factors and development of disc degeneration and herniation, with heavy physical work, lifting, truck-driving, obesity and smoking found to be the major risk factors for back pain and degeneration. As a result of these studies, there have been many ergonomic interventions in the workplace. However, the incidence of disc degeneration-related disorders has continued to rise despite these interventions. Over the past decade, as magnetic resonance imaging has refined classifications of disc degeneration, it has become evident that, although factors such as occupation, psychosocial factors, benefit payments and environment are linked to disabling back pain, contrary to previous assumptions these factors have little influence on the pattern of disc degeneration itself. This illustrates the tenuous relationship between degeneration and clinical symptoms.