A. The intervertebral disk connects adjacent vertebral bodies.
B. The disk and the facet joints constitute the functional spinal unit that provides mechanical stability and allows physiologic motion.
A. Nucleus pulposus (
1. The nucleus pulposus is the central portion of the disk.
2. The hydrophilic matrix of the nucleus pulposus provides the swelling pressure that contributes to the normal height of the disk.
3. The matrix is viscoelastic and therefore dampens and distributes forces evenly across the end plate and anulus fibrosus.
4. The nucleus pulposus is hypoxic and relatively acidic. Nucleus pulposus cells are more synthetically active in this type of environment.
5. The nucleus pulposus has primarily type II collagen.
B. Anulus fibrosus
1. The anulus fibrosus surrounds and contains the centrally located nucleus pulposus.
2. The anulus fibrosus has high tensile strength and resists intervertebral distraction, but it is flexible enough to deform and allow intervertebral motion.
3. As the nucleus pulposus degenerates, the anulus fibrosus takes proportionately more axial load.
4. The annulus has primarily type I collagen.
C. End plates
1. The end plates form the interface between the vertebra and the disk and define the upper and lower boundaries of the disk.
2. The central portion of the end plate provides a major pathway for nutrients from the vertebral bodies to diffuse into the disk.
D. Vascular supply
1. In the adult, the disk is avascular. The blood supply ends at the bony end plate of the vertebral body and the outer anulus fibrosus. Thus most of the disk is considered immunologically isolated.
2. Because of this avascularity, the nutritional supply to the disk cells is primarily though diffusion (
Figure 2). As the disk gets larger, the distances nutrition must diffuse across become larger, further impeding nutritional supply to the disk cells.
1. The disk is minimally innervated. The sinuvertebral nerve (which arises from the dorsal root ganglion) innervates the outer anulus fibrosus. Nerve fibers do not penetrate beyond this superficial
[Figure 1. Sagittal section view of a motion segment comprising two vertebral bodies and an intervertebral disk forming a strong connection between the bones. The four regions of the disk are shown: cartilaginous end plate, outer anulus fibrosus, inner anulus fibrosus, and nucleus pulposus. The posterior articular and spinous processes and the articular surface of a facet joint are also shown.]
[Figure 2. Disk nutrition. The blood supply reaches the bony end plate but does not cross into the disk. The nutrients diffuse across the end plate to reach disk cells. The metabolic waste products leave the disk tissue by diffusing across the end plate and are carried away by blood flow.]
zone; therefore, most of the disk is not innervated.
2. Pain sensation from the disk arises only from the anulus fibrosus, but the nucleus pulposus can generate pain molecules that can stimulate the nerves found in the anulus fibrosus.
III. Biologic Activity
1. Disk cells are metabolically active, synthesizing disk matrix, catabolic enzymes, and growth factors (BMP-2, BMP-7, TGF-β, etc). Although disk cells constitute only a small proportion of the volume of the adult disk, they are responsible for maintaining the volume and composition of the disk matrix.
2. The normal turnover rate of the disk matrix is slow, but even a small deviation in the balance of disk homeostasis can result in disk degeneration over a period of years.
B. Cell characteristics by region
1. Nucleus pulposus cells are chondrocyte-like.
a. They exist in a hypoxic environment.
b. They characteristically synthesize proteoglycans (aggrecan, versican, and small leucine-rich proteoglycans [SLRPs]), collagen type II, and other matrix molecules.
2. Anulus fibrosus cells are fibroblast-like.
a. They characteristically produce type I collagen but also produce other matrix molecules, including proteoglycans.
b. The inner anulus cells produce relatively more proteoglycans than the outer anulus cells.
1. Disks undergo a natural degenerative process during aging that does not implicate a disease process.
2. In the young individual, the disk is tall, the nucleus pulposus is very watery, and the anulus fibrosus is intact. In the young child, the nucleus pulposus cells are mostly notochordal cells.
3. By age 10 years, notochordal cells have disappeared and are replaced by chondrocyte-like cells.
4. With increasing age, the disk cells produce less aggrecan and type II collagen, leading to decreases in proteoglycan and water content. As the nucleus pulposus desiccates, disk height is lost and the anulus fibrosus develops fissures.
5. 90% of asymptomatic individuals older than 60 years have MRI evidence of disk degeneration.
1. Strong evidence suggests that genetics plays an important role in disk degeneration. Twins studies have indicated that genetic factors are more important determinants of disk degeneration than factors such as lifetime occupation and leisure activities.
2. Mutations in the vitamin D receptor and COL9A2 genes have been implicated in disk degeneration.
3. A mutation in the cartilage intermediate layer protein (CILP) has been associated with an increased need for surgery to treat sciatica resulting from lumbar disk herniation.
1. Disk degeneration has been statistically associated with a higher incidence of low back pain, but the presence of one or more degenerated disks does not directly correlate with low back pain.
2. Despite improvements in imaging modalities such as MRI and CT, imaging studies remain unreliable in identifying a painful disk.
3. Diskography assesses disk morphology and may be helpful in identifying a painful disk (pain generator).
a. Diskography involves introducing a needle into the disk and injecting fluid under pressure.
b. Elicitation of the familiar, or concordant, pain is considered a positive test.
c. Diskography has been shown to have a high false-positive rate, especially in patients with chronic pain and abnormal psychometric testing results. There is a low predictive power for good results after fusion surgery.
A. Natural repair process—Perhaps because the disk is avascular, spontaneous biologic repair processes are quite limited and are thought to be ineffective.
B. Biologic therapy—Disk repair has been successful in some small animal experiments, but as of yet no credible report of success in humans has been published.
Top Testing Facts
1. The disk allows motion and provides mechanical stability of the functional spinal unit.
2. The disk is mostly avascular and depends on diffusion through pores in the end plate to provide nutrition to the disk cells.
3. Nucleus pulposus cells are more synthetically active in a hypoxic environment.
4. The nucleus pulposus is normally rich in aggregating proteoglycans (aggrecan and versican), which attract water and help maintain disk height. The nucleus pulposus has a higher concentration of type II collagen than the anulus fibrosus.
5. The anulus fibrosus is a well-organized laminated fibrous tissue composed primarily of type I collagen.
6. With increasing age, the disk cells produce less aggrecan and type II collagen, leading to decreases in proteoglycan and water content. As the nucleus pulposus desiccates, disk height is lost and the anulus fibrosus develops fissures.
7. Ninety percent of asymptomatic individuals older than 60 years have MRI evidence of disk degeneration.
8. Genetics plays a strong role in disk degeneration, but this seems to involve a multifactorial process that does not fit a Mendelian pattern.
9. Disk degeneration is not necessarily a painful condition.
10. Diskography has a high false-positive rate in patients with abnormal psychometric testing results.
Anderson DG, Tannoury C: Molecular pathogenic factors in symptomatic disc degeneration. Spine J 2005;5:260S-266S.
Battie MC, Videman T: Lumbar disc degeneration: Epidemiology and genetics. J Bone Joint Surg Am 2006;88(suppl 2): 3-9.
Park AE, Boden SD: Form and function of the intervertebral disk, in Einhorn TA, O'Keefe RJ, Buckwalter JA (eds): Orthopaedic Basic Science: Foundations of Clinical Practice, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, pp 259-264.