Date Published: February 1, 2012
Publisher: Hindawi Publishing Corporation
Author(s): Lisa A. Ferrara.
Aging is the major risk factor that contributes to the onset of cervical spondylosis. Several acute and chronic symptoms can occur that start with neck pain and may progress into cervical radiculopathy. Eventually, the degenerative cascade causes desiccation of the intervertebral disc resulting in height loss along the ventral margin of the cervical spine. This causes ventral angulation and eventual loss of lordosis, with compression of the neural and vascular structures. The altered posture of the cervical spine will progress into kyphosis and continue if the load balance and lordosis is not restored. The content of this paper will address the physiological and biomechanical pathways leading to cervical spondylosis and the biomechanical principles related to the surgical correction and treatment of kyphotic progression.
Cervical spondylosis is a common progressive degenerative disorder of the human spine often caused by the natural aging process. It is defined as “vertebral osteophytosis secondary to degenerative disc disease” due to the osteophytic formations that occur with progressive spinal segment degeneration [1–3]. Early spondylosis is associated with degenerative changes within the intervertebral disc where desiccation of the disc occurs, thus causing overall disc height loss and a reduction in the ability of the disc to maintain or bear additional axial loads along the cervical spine [3, 4]. At birth, the intervertebral discs are healthy, with the proteoglycan matrix within the nucleus pulposus maintaining a 70% to 90% water content which declines with aging . As the water content declines within the nucleus pulposus, the once healthy glistening gelatinous appearance changes into a darkened and discolored fibrous “crabmeat” consistency with a loss in water content and a loss in the structural integrity.
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.
Elegant studies have been performed to characterize the histological and immunohistochemical differences between cervical disc herniation and spondylosis. Disc herniation can be an early contributor to spondylosis, as herniation creates a loss in the mechanical integrity of the intervertebral disc due to the extrusion or bulging of the nucleus pulposus through compromised annular fibers. The herniation often occurs dorsally, as the dorsal annular fibers are thinner and provide a less resistant pathway for the compromised nucleus pulposus matter. The intervertebral discs with surrounding tissues, subchondral vertebral bone, cartilaginous endplate, and posterior longitudinal ligaments were collected en bloc during decompression surgeries in 198 patients presenting with cervical intervertebral disc herniation resulting in 248 discs for evaluation. An additional 252 discs were harvested in a similar manner from 166 patients presenting with cervical spondylosis to provide a histological and immunohistochemical assessment between cervical spondylosis and disc herniation . The disc-herniated patients were younger (49.9 years, range 25–78 years) than the cervical spondylosis (mean age of 59.6 years, ranging from 32 to 83 years), with all patients presenting with signs and symptoms of radiculopathy, myelopathy, or myeloradiculopathy with an average duration of symptoms prior to surgery of 3.2 months. The control discs (free from cervical radiculopathy and myelopathy) were harvested during autopsies taken from eight donors with a mean age of 73 years. Chondrocyte proliferation, a change in the granular matrix, fibrocartilage degeneration of the annulus fibrosus and nucleus pulposus, cell proliferation, cartilage disorganization, cracks, microfractures, sclerotic endplates, and vascularization of the disc were parameters used to grade the level of disc degeneration. The herniated cervical discs demonstrated granulation tissue with new vascularization and an infiltration of CD68-positive macrophages surrounding the herniated tissue with greater advanced degeneration in the outer layer of the annulus . The spondylotic discs demonstrated thicker bony endplates and tumor necrosis factor and matrix metalloproteinase with greater advanced degeneration in the cartilaginous endplates and inner layer of the annulus. In essence, there were distinct differences and markers for distinguishing herniated discs from spondylotic discs.
Kyphotic deformity with neural and vascular compression often accompanies cervical spondylotic myelopathy. Initially the loss of disc height as a consequence of disc desiccation and altered load transmission along the cervical spine can lead to postural changes (Figure 3(b)). As spinal cycling continues during activities of daily living, the disc will continue to lose height ventrally. This altered posture will result in an increased moment arm about the point of central rotation or the IAR. In the healthy spine, axial loads are applied along the IAR and the loads are supported along the ventral column of the spine. However, with altered posture, the axial load profile along the cervical spine changes as the ventral column (vertebral bodies, disc, and ligamentous tissue) can no longer maintain these loads, and there is a transfer of the loads and stresses to the surrounding bony elements. Loss of the lordotic posture induces a greater moment arm at the point of rotation (point d in Figures 3(b) and 3(c)) when an axial load is applied. Without restoration of the native lordotic posture which will restore the “load balance” along the cervical spine, further axial loading will induce further progression of the kyphotic posture (Figure 3(c)).
Fusion of the degenerative unstable spine is often a final alternative to alleviate a painful spinal segment. Ventral interbody fusion is incorporated in a fusion construct to maximize the axial load bearing capacity of the spine while limiting the pathologic motion across a spinal segment. In situations such as kyphotic deformity correction, multisegmental ventral interbody fusions can provide the necessary ventral column support incorporating multiple points of fixation to resist the demanding translational, rotational, and bending loads placed upon on the degenerative kyphotic cervical spine and will provide ample strength to maintain the restored lordotic posture. Ventral support using multiple interbody fusion grafts supplemented with dorsal fixation across each level will also provide similar mechanical attributes as that of ventral support, where both approaches towards kyphotic deformity will allow for better force distribution across many points of fixation, thus minimizing the risk of stress risers that can cause graft subsidence, expulsion, screw loosening, or loss of fixation. Biomechanically, these strategies will improve the restoration of the lordotic posture for long-term fixation and stability. By restoring the lordotic posture of the cervical spine, the load balance is restored, where 80% of the axial loads transmitted along the ventral column is aligned at the IAR of the spinal column, effectively, halting the progression of the kyphotic curvature. Segmental fixation results in reduced localized forces and stresses at each spinal level and across the instrumentation, with reduced stresses on each screw and across each graft site for improved long-term fixation.