The primary cause of cervical spondylosis is age-related degeneration. However, there are some exceptions where spinal injuries to the disc can augment the degenerative process in the younger patient. A secondary manifestation of spondylosis is related to the compression of the vascular and neural structures caused by a loss in the disc height and impinging osteophytes that contribute to the numbness, shock-like sensations, pain, and chronic motor and sensory affects, which if not corrected may lead to permanent disabilities.
It is this physiological degenerative cascade that contributes to the biomechanical changes that can cause neural and vascular compression, pain, and loss of function. illustrates the chain of events of cervical spondylosis starting with the biomechanical changes that can result in neural and vascular compression. Early changes in the proteoglycan matrix cause an increase in the ratio of keratin sulfate to chondroitin sulfate resulting in the loss of water within the disc. This desiccation causes the nucleus pulposus to lose elasticity, shrink in size, and lose the ability to bear axial loads. Since the dorsal fibers of the annulus are thinner than the ventral aspect, there is a path of least resistance through the annulus for a nucleus pulposus herniation. The annular fibers become mechanically compromised with further disc desiccation and are unable to effectively maintain axial loads, causing buckling of the spinal ligaments and annular fibers under compressive loads, which are further exacerbated with eccentric loads (i.e., flexion, torsion, and bending) [1
]. The resultant loss in disc height causes the discs to bulge, the ligamentous tissue to become lax and buckle, and the ventral aspect of the cervical spine to compress. At this point, there are significant alterations in the load distribution along the cervical spinal column, with an end result of kyphosis of the cervical spine. If not reversed, the kyphosis will continue to progress, the annular and Sharpey's fibers will separate from the vertebral periphery and bony endplates, resulting in reactive bone formation where the fibers have been separated. These resultant bone spurs can be formed along the ventral or dorsal margin of the cervical spine and within the canals in response to the altered biomechanical loads, causing compression of the neural and vascular structures.
Pathophysiological and biomechanical pathway of cervical spondylosis.
The unique properties of bone and soft tissue are the ability to regenerate and remodel the tissue along the lines of loading and stress application, thus regaining the structural integrity. However, if the load balance along the spinal column is altered and is not restored, the tissue will remodel along the altered load and stress planes, causing the tissue to remodel along new planes of loading. Since osteophyte or bone spur formation will occur in response to excessive eccentric loads, new bone will form in areas of greater stress and will be resorbed in areas of less stress.
The loss in the axial load bearing capabilities of the degenerative segment leads to a disruption in the load transfer along the neutral axis of the spinal column, also known as a change in the overall load balance, thereby transferring greater loads to the uncovertebral and facet joints, further accelerating the formation of spurs and osteophytes into the surrounding foramen, with greater angulation of the cervical spinal column ventrally. The ventral angulation along the cervical spine is a continuous cascade of mechanical events. As the lordotic angle is reduced, the moment arm about the center of rotation or instantaneous axis of rotation (IAR) is increased, therefore, changing the overall sagittal angulation and reducing the spinal canal diameter [1