ĭisc herniation can be an early precursor to the development of spondylosis. These degenerative changes lead to loss of cervical lordosis and movement, as well as a reduction in the spinal canal diameter. Furthermore, disruption in the load balance along the spinal column generates greater axial loads onto the uncovertebral and facet joints which triggers hypertrophy or enlargement of the joints and accelerates bony spur formation into the surrounding neural foramen. These bone spurs or osteophytes can form along the ventral or dorsal margins of the cervical spine, which can then project into the spinal canal and intervertebral foramina. Progression of the kyphosis causes the annular and Sharpey’s fibers to peel off from the vertebral body edges, resulting in reactive bone formation. The result is a reversal of the normal cervical lordosis. With further disc desiccation, the annular fibers become more mechanically compromised under compressive loads, producing significant alterations in the load distribution along the cervical spine. As the nucleus pulposus loses its ability to maintain weight-bearing loads effectively, it begins to herniate through the fibers of the annulus fibrosus and contributes to the loss of disc height, ligamentous laxity, and buckling, and compression of the cervical spine. Desiccation of the disc causes the nucleus pulposus to lose its elasticity as it shrinks and becomes more fibrous. An increase in the keratin-chondroitin ratio prompts changes to the proteoglycan matrix resulting in loss of water, protein, and mucopolysaccharides within the intervertebral disc. The pathogenesis of cervical spondylosis involves a degenerative cascade that produces biomechanical changes in the cervical spine, manifesting as secondary compression of neural and vascular structures.
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