Degenerative disc disease (DDD) is an exceedingly common entity in the spine, encountered with increasing frequency throughout life and becoming almost universal in late adulthood to a varying degree. It is related to a combination biomechanical stresses and genetic predisposition which alter the metabolic and structural integrity of the intervertebral disc. These changes, in turn, modify the ability of the intervertebral disc to sustain and transmit forces, and subsequently, compensate for these alterations (or not) in a variety of ways, leading to billions of dollars in healthcare services and lost productivity every year due to associated morbidity from these conditions.
Wide variations exist in the reported prevalence of degenerative changes in the spine, likely related to differences in populations studied and variable definitions of what constitutes degenerative change. For example, is a Schmorl node a degenerative change? Additionally, because DDD encompasses such a wide variety of individually defined entities, it is hard to make broad statements about the incidence and related symptomatology.
Vertebral osteophytes, disc height loss, disc signal intensity loss, and disc bulging increase in frequency with age in a nearly linear fashion, but to different degrees, with disc signal loss and vertebral osteophytes increasing the most with age.
Below is a list of conditions that are frequently considered degenerative in nature, and their reported incidence is given in both asymptomatic and symptomatic adult populations 1:
- disc bulge: asymptomatic 10% to 81%, symptomatic 22% to 48%
- disc protrusion: asymptomatic 3% to 63%, symptomatic 0% to 79%
- disc extrusion: asymptomatic 0% to 24%, symptomatic 1% to 55%
- disc sequestration: 0% in asymptomatic subjects
- reduction in signal intensity of the disc: asymptomatic 20% to 83%, symptomatic 9% to 86%
- disc narrowing: asymptomatic 3-56%, symptomatic 15-53%
- annular tears (high intensity zones): asymptomatic 6-56%, symptomatic 15%
- Schmorl node: asymptomatic 8-19%, symptomatic 6-79%
Generally, degenerative changes of the disc affect hydration and elasticity of the cartilaginous endplate, annulus fibrosis and nucleus pulposus, with changes most pronounced in the nucleus pulposus. Within the nucleus pulposus, a loss of water-holding proteoglycans occurs, and within the annulus fibrosis type II collagen increases which reduce disc hydration as well. This makes the disc friable, precipitating fissures and progressive structural degradation. Nitrogen gas may be observed filling these defects as it is pulled from surrounding extracellular fluid, creating the vacuum cleft phenomenon.
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