Lumbar degeneration or spondylosis is can be seen on the biochemical, cellular, and morphologic levels. The initial events of disc degeneration are related to many intrinsic and extrinsic factors, including cellular apoptosis or programmed cell death, mechanical disc injury, and genetic contributions.
The culprit event likely is related to compromise nutrient diffusion and disc hydration.
Subchondral sclerosis and an impaired vascular supply reduces porosity leading to shrinkage of pore sizes. This results in decrease in surface area which that markedly limits diffusion.
The cartilage calcifies and fissures. The end plate may separate from the vertebral body. Lactic acid production and accumulation increases with a tendency to a more acidic environment after diffusion is affected and disc relies on anaerobic metabolism.
Degraded waste accumulates and exceeds the diffusion capacity further. this leads to obstruction of waste clearance from the disc space. This in turn leads to diminished cellular metabolism and biosynthesis, resulting in impaired function.
Thus, a vicious cycle is formed which leads to destruction of collagen in end plates.
Prostaglandin content decreases and increased formation of nonaggregated prostaglamolecules increases. The ratio of chondroitin sulfate to keratan sulfate reverses with increased formation of the latter, which has less water-binding capacity.
An early adaptive increase in type II collagen production initially is found within the nucleus as well as in type I collagen fibers. Posttranslational modifications of collagen proteins also increase.
In the annulus, cell viability also eventually diminishes, with less extracellular matrix production and qualitative changes in collagen fibrils.
The extracellular matrix undergoes myxomatous degeneration and loss of normal organization of the collagen layers. The numbers of lamellae decrease, but the thickness of each layer and the spacing between the fiber bundles increase.
Clefts from within the anulus near the edge of the disc and progress toward the nucleus.
Catabolic mediators often are produced spontaneously within the degenerating disc and include degradative enzymes such as matrix metallo-proteinases (MMPs), oxygen free radicals, nitric oxide, interleukins, and prostaglandins.
MMPs are a family of enzymes synthesized by connective tissue cells. Degenerative changes occur within the disc, the inhibitors become dysfunctional and allow the activity of MMPs.
Interleukins are a family of inflammatory cytokines that have been shown to decrease cellular metabolism and PG synthesis. High levels of IL-1, IL-6, and prostaglandin E2 have been identified in herniated and degenerative disc tissue and may be capable of degradation by increasing the activity of other degenerative enzymes.
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