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Degenerative disc and impact on flexibility

Degenerative disc, flexibility, model

Aging and Degenerative Disc Changes of the IVD’s Impact on Spinal Flexibility

A publication reviewed several studies involving the biomechanics of the intervertebral discs (IVD) with macroscopic changes associated with degenerative disc disease with the aim of finding out how spinal flexibility was affected by dehydration, tears, fissures, osteophytes, and the inevitable collapse of the intervertebral space. The studies under review used cadavers and did not contribute to information about how degenerative disc disease may cause symptomatic back pain. However, the review can contribute to the understanding of disc degeneration disease and its progression, as well as offer insight into what surgical treatments could be beneficial in improving flexibility and spinal functionality in patients.

 

About Disc Degeneration

Degeneration of the IVD causes mechanical and biochemical changes in the disc and its surrounding structures. The space between the discs can collapse, and proteoglycan and water content can be greatly reduced, contributing to the damage of endplates and osteophytosis. The entire motion segment of the IVD is affected macroscopically and biomechanically by the degenerative process, and this can cause a loss of functionality and mobility that contributes to further progression of disc disease in the spine.

 

How the IVD Works

A properly functioning IVD evenly distributes weight-bearing loads across the spinal segments and allows the spine to suffer intense compressive loads without collapsing or losing its range of motion. Inside each IVD is a nucleus pulposus (NP)—a gelatinous substance with proteoglycans, elastin fibers, and Type II collagen. The NP is enclosed by the annulus fibrosis (AP)—a lamellar structure made up of Type I collagen fibers. The angle of the collagen fibers in the AP (30 degrees), alternates with that of the adjacent lamellae, which contain gel rich in proteoglycan and may be surrounded by connective bundles of collagen. Endplates connect the IVD to the surrounding vertebrae. The NP transitions to the AF in a transitional zone that is indicated by diverse types of tissue, rather than a distinct border. Negatively charged proteoglycans are balanced by positive cations within interstitial fluids, contributing to osmotic pressurization in response to its environment. Because of this, the IVD absorbs copious amounts of water, which helps the nucleus to adjust in reaction to high compressive forces.

The NP is bookended by the endplates and the AF, which allows the resulting hydrostatic pressure to balance any swelling pressure during active loading and at rest so that the disc will not bulge or collapse under compression. The structure of the lamellae in the AF is tension-loaded and assists with bending and shear. Vicious fluids flow through the permeable endplates, which help evenly distribute pressure within the nucleus or annular tension. The AF’s collagen bundles create an elasticity that absorbs compressive loads. The exchange of fluids within the IVD creates a balance between tension and flexibility that is integral to the function of the spinal unit.

Degenerative disc, flexibility, model

Degenerative disc model

 

Effects of Degenerative Disease and Aging on the IVD

 

  • Cellular/matrix alterations—Aging and degenerating IVD exhibit early changes in the endplates which in turn cause changes to the nucleus and annulus. A progressive reduction of cells begins in childhood and continues throughout a lifetime, decreasing and fragmenting the proteoglycan content in the nucleus and surrounding areas. In time, this leads to a reduction of the disc’s ability to repair itself. As the cells lose their ability to synthesize, there is further loss of proteoglycan content. Changes at the cellular level create biochemical alterations throughout the entire matrix. In time, the NP loses the ability to attract and retain adequate water and an increase in fibrous tissue takes place. A similar –though lesser—loss of water and collagen in the AF leads to reduced swelling pressure and contributes to the degenerative state.

 

  • Structural changes—Structural failures including tears and clefts follow (or are perhaps caused by) alterations in the NP and AF. Considered a symptom of degenerative disc disease, these changes are related to, but distinct from, the simple aging process. Endplate separations, radial tears, and rim lesions increase in the aging population, and approximately 50 percent of the cadaver specimens in one study showed evidence of IVD degeneration in subjects over 30. Calcification of the cartilaginous endplates cause biomechanical changes that reduce the flexibility of the endplates and make the IVD vulnerable to fracture, reduced water intake, and a lower solute exchange rate between the disc and vertebrae. Collapse of the intervertebral space occurs often in a degenerated IVD, though disc height reduction is not a common result of simple aging. In addition to a reduction in disc height, osteophytes may form around the affected vertebrae. Studies have suggested that these osteophytes may be the body’s attempt at providing supplemental stabilization in the degenerated spine segment.

 

  • Pain—A common cause of back pain, degenerative disc disease undermines the spine’s structural integrity and creates tension and spasms in the surrounding muscular structure. In severe cases of disc degeneration, disc prolapse, and collapse, radial tears that cause a leakage of collagen and fluids can increase the frequency and amount of back pain. Another common source of back pain is lesions or uneven loading in the endplates. When there is a reduction in disc height, nerve roots located in between the vertebrae may be squeezed or pinched into the space near the capsule joint, causing radicular pain. This type of pain can intensify with activity or prolonged sitting or standing. Facet join arthritis can cause a decrease in cartilage between the apophyseal or zygapophysial joints and may contribute to back pain.

 

  • Changes in Flexibility—When the IVD are in a degenerative state, the entire motion segment(s) can become more rigid and less flexible. Researchers have theorized that the spine loses its flexibility over time, triggered by an initial dysfunction and followed by instability, which leads to an attempt at stabilization. Thus, disc degeneration is a progressive event which is the result of the spine’s attempt to handle physiological loads. However, there is no evidence that shows a definitive connection between reduced range-of-motion therapies (such as surgical implants that inhibit the range-of-motion) and an improvement of disc degeneration.

 

 

Conclusions

Research into the biomechanics of the IVD systems clarifies some aspects of degenerative disc disease but offers little insight into the specific causes of lower back pain. Degenerative changes of the IVD systems cause changes to the functionality of the spine, with some inconclusive evidence of a loss of flexibility and increasing stiffening over time.  Further studies of the effects of disc degeneration and a possible link to spinal instability are recommended.

 

 

 

 

 

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