Disc degeneration starts early in life and frequently progresses relentlessly. By the eighth decade the majority of individuals have diffuse disc degeneration throughout their spine. Although it is clear that disc degeneration is not synonymous with spine pain, it is well accepted that degenerative disc disease brings about a cascade of anatomic changes that play a major role in the pathophysiology of well-described clinical entities.
The pathogenesis of disc degeneration has not been completely elucidated. Multiple factors, working separately or in combination, contribute to disc degeneration. Being the largest avascular structures in the body, the discs depend on a tenuous nutritional supply that predisposes them to early degeneration. Heredity is another important factor that may contribute to disc degeneration under normal physiological conditions. Aging also plays a significant role in disc degeneration. Age-related vascular changes such as atherosclerosis and decreased vascular density, and vertebral endplate changes such as calcification, compromise discal nutrition and contribute to disc degeneration.
Mechanical factors such as repetitive trauma due to sports or occupation may also adversely affect the discs. Smoking has a negative impact on the metabolic processes within the discs, as nicotine-mediated vasoconstriction interferes with the discs' oxygen supply and nutrition.
During the degenerative process the disc undergoes both biochemical and biomechanical changes. Due to the compromised nutrition, increased lactic acid concentration, and low pH, the number of cells within the discs decreases and matrix synthesis diminishes. The proteoglycans and the water-retaining capacity of the disc decrease as well. Decreased discal height alters the load distribution in the motion segment and decreases the ability of the discs to withstand shear stress.
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