Injuries to the intervertebral discs of the lumbosacral spine are invoked as a causative factor in one of the most common health problems in the United States — low back pain (LBP). Of the many possible etiologies of LBP, the intervertebral disc has been implicated as a more frequent source than muscular strain or ligamentous sprain. Although no single injury to the intervertebral disc has been unequivocally identified as a pain generator, theories of its involvement are common. [1, 2, 3, 4, 5, 6]
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The lifetime incidence of LBP has been reported to be 60-90% with an annual incidence of 5%. LBP affects men and women equally. Most people with LBP do not seek medical care, they do not have significant functional impairment, and they recover rapidly. Despite this fact, LBP accounts for 14.3% of new patient visits to physicians each year.
Back pain is the leading cause of lost work productivity and is second only to upper respiratory infection as a cause of time lost from work. Back pain is estimated to result in 175.8 million days of restricted activity in the United States annually. Nearly 2.5 million Americans are disabled by LBP, half of these chronically.
Interestingly, a review of research by Manek and MacGregor reveals that there is a significant genetic effect on LPB.  Data from candidate gene studies have shown an association between lumbosacral disc disease and mutations of genes encoding the alpha-2 and alpha-3 subunits of collagen IX.
In 1990, 400,000 industrial low back injuries resulted in disability in the United States.  This value accounts for approximately 22% of all workplace injuries, yet LBP represents 31% of all compensation payments. The total cost estimates of LBP range from $25-85 billion. 
The lumbar spine has an average of 5 vertebrae (normal range 4-6) with an intervertebral disc interposed between adjacent vertebral bodies. A cartilaginous endplate exists between the disc and the adjacent vertebral bodies and is considered part of the disc. The disc itself is composed of a central nucleus pulposus surrounded peripherally by the annulus fibrosis.
In normal young adults, the nucleus is a semifluid mass of mucoid material. The nucleus is composed of approximately 70-90% water in a young healthy disc, but this percentage generally decreases with age. The primary nuclear constituents include glycosaminoglycans, proteoglycans, and collagen. Type II collagen predominates in the nucleus. Proteoglycans are the largest molecules in the body and possess an enormous capacity to attract water through oncotic forces. These forces increase their weight by 250% and result in a gel-like composition. Biomechanically, the nucleus can display properties of either a solid or liquid substance depending on the transmitted loads and its posture.
The annulus fibrosis consists of 10-20 concentric collagen fiber layers that surround the nucleus. The layers are arranged in alternating orientation of parallel fibers lying approximately 65° from the vertical. The vertebral endplate is a thin layer of cartilage located between the vertebral body and the intervertebral disc. Although normally composed of both hyaline and fibrocartilage in youth, older endplates are virtually entirely fibrocartilage. Because the intervertebral disc is the largest avascular structure in the body, it is dependent on diffusion across the endplate for nutrition and waste removal. The endplate is considered part of the disc because the endplate almost always remains with the disc when the disc is displaced traumatically from the vertebral body.
The principal functions of the disc are to allow movement between vertebral bodies and to transmit loads from one vertebral body to the next. When axial loads are transmitted to the spine, the annulus and nucleus display a complex intertwined role, allowing for pressure dispersal. The nucleus has the capacity to sustain and transmit pressure. This ability is invoked principally during weight bearing. In this circumstance, the nucleus transmits loads and braces the annulus as described below.
The annular lamellae are capable of sustaining an axial load on the basis of its bulk. When an axial load is applied to the nucleus, it tends to shorten. The nucleus attempts to radially expand, thereby exerting pressure on the annulus. Annular resistance efficiently opposes this outward pressure, creating a hoop-tension effect. The intervertebral disc is so effective at resisting these axial loads that a 40-kg load to a disc causes only 1 mm of vertical compression and only 0.5 mm of radial expansion.
During movement, the annulus acts like a ligament to restrain movements and partially stabilize the interbody joint. The oblique orientation of the annular fibers provides resistance to vertical, horizontal, and sliding movement. The alternation in the direction of the annular fibers in consecutive lamellae causes the annulus to resist twisting motions poorly. When the segment twists one way, the fibers oriented in that direction are placed on stretch, whereas those fibers oriented in the opposite direction are placed on slack; therefore, the annulus resists the twisting motion with less than its full complement of fibers.
Intervertebral discs of the lumbosacral spine are susceptible to a variety of injuries, which may account for pain in the lower back. The central component to any injury involving the lumbosacral discs is the natural aging process of degeneration that Kirkaldy-Willis identified. The degenerative cascade describes this degenerative process of lumbosacral discs. Kirkaldy-Willis identified the following 3 phases of the degenerative cascade  :
The first phase, phase I, is known as the dysfunctional phase. This phase is characterized by circumferential tears or fissures in the outer annulus. In addition, endplate separation or failure can disrupt the blood supply, resulting in the loss of nutrition to the disc. These changes are thought to result from repetitive microtrauma. One hypothesis is that the discs' nuclear proteoglycans lose the capacity to absorb water and maintain their protective function.
Phase II, or the unstable phase, is characterized by multiple annular tears (both radial and circumferential), internal disc disruption, and resorption or loss of disc space height. This phase is thought to result from the progressive loss of the mechanical integrity of the 3-joint complex.
Phase III is also known as the stabilization phase. Further disc resorption, disc space narrowing, endplate destruction, disc fibrosis, and osteophyte formation are present. Disc injuries are more likely to occur in phase I or II of the degenerative process.
Various theories have been proposed as the sources of pain generation in disc injury, involving an intervertebral disc that is degenerative, bulging, or protruding. Mechanical compression and an immunologic or inflammatory response are possibly related to pain from a disc injury. Mechanical compression of a nerve alone is not necessarily painful; however, if that nerve is inflamed, it can produce severe pain with a small amount of mechanical compression.
The basis for an immunologic source for disc-related pain has been based upon the lack of blood supply to the nucleus pulposus, thus hiding it and its contents from the immune system. Injury to the disc would expose these foreign substances, initiating an autoimmune reaction. The nucleus pulposus has been shown to elicit an immune response. Various authors have reported that disc material can incite a leukocyte cell reaction, cytokine, and immunoglobulin response.
A second hypothesis that has gained support as initiating an inflammatory reaction may be the result of biochemical factors rather than an autoimmune response. Central to this idea is the arachidonic cascade. Phospholipase A2 (PLA2) is the rate-limiting step in this pathway, controlling the release of prostaglandins and leukotrienes. Saal showed that human PLA2 levels in the intervertebral disc are 20-10,000 times more active than the PLA2 found in other human tissues. [7, 8] This research led to the investigation of PLA2 and other biochemicals as putative mediators of the inflammatory response to intervertebral disc injury and, thus, inducing back pain.
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