Pathophysiology of Disc Degeneration and the Spondylotic Process

Lumbar spondylosis is not a pathologic process; it is but a manifestation of the wear and tear associated with aging, specifically the consequences of loading. It is defined as vertebral osteophytosis secondary to degenerative disc disease² and is not an inflammatory process. Noninfectious inflammatory processes are grouped together as arthritides and are excluded from this discussion.

Spondylosis and associated osteophytosis are universally accompanied by degeneration of the intervertebral disc. The intervertebral disc is an amphiarthrodial joint (no synovial membrane) with particular traits that result in a characteristic degeneration pattern. Conversely, arthritides classically involve the synovial membranes of diarthrodial joints (joints lined with synovium and lubricated with synovial fluid, such as facet joints). Facet joints, however, are also affected by the spondylotic process.^3,4

The degenerative process primarily involves the disc interspace and alters intradiscal dynamics that result in spine deformation. The resultant excessive motion and stresses cause extradiscal soft tissue proliferation. Finally, spine deformation predisposes to further deformation (see the section titled “Osteoporosis”). Osteoporosis contributes to the latter process, with a resultant asymmetrical vertebral body collapse.

Intradiscal Dynamics

Chronically elevated intradiscal pressure causes disc interspace narrowing (collapse), distorting the anulus fibrosus and the facet joint capsule. This in turn accelerates the degenerative process. If disc space degeneration progresses asymmetrically in the coronal plane, a scoliotic deformity may result.

The water content of the disc interspace gradually decreases throughout life, which contributes to alterations in the chemical and anatomic makeup of the disc. Fibroblasts become defective, and the desiccated disc is less effective as a cushion. Fissures then develop in the cartilaginous end plates. Schmorl nodes are manifestations of this pathologic process. Gas may accumulate in the disc (the vacuum phenomenon). An ingrowth of fibrocartilage (mucoid degeneration) with obliteration of the nucleus fibrosus ensues. Relative incompetence of the disc itself and relative instability result, and anulus fibrosus bulging and tension occur as a result of this process.³

Disc Deformation

Bulging of the anulus fibrosus results in periosteal elevation and subperiosteal bone formation. Spondylotic ridges (osteophytes) are laid down, and this can result in spinal canal encroachment. These ridges occur most commonly on the concave side of a curvature. Therefore, natural cervical and lumbar lordosis predisposes the spine to osteophyte formation toward the spinal canal, causing spinal canal encroachment. The thoracic region, by virtue of its intrinsic kyphotic posture, is relatively spared this process.

Form follows function, even during the process of degeneration. Therefore, osteophyte formation occurs predominantly on the concave side of a scoliotic curvature (where anulus fibrosus bulging is most significant), while disc herniation occurs commonly on the convex side of a spinal bend. The thin dorsal anulus fibrosus and relatively weak lateral aspect of the posterior longitudinal ligament combine with the migratory tendencies of the nucleus pulposus to encourage dorsolateral disc herniation.³

In the laboratory, (1) flexion (causing dorsal nucleus pulposus migration), (2) lateral bending away from the side of disc herniation (causing lateral nucleus pulposus migration), and (3) application of an axial load (causing an increase in intradiscal pressure) are required for the creation of a herniated lumbar disc. A degenerated disc is also necessary as a predisposing factor.⁵ This complex loading pattern results in the application of tension on the weakest portion of the anulus fibrosus (the dorsolateral position, the location of the herniation), migration of the nucleus pulposus toward this position, and an asymmetrical increase in intradiscal pressure. The age-related increased frequency of anulus fibrosus tears and a peaking of nucleus fibrosus pressures in people 35 to 55 years of age⁴ also predispose to an increased incidence of disc herniation. Asymmetrical collapse of the disc interspace is often a result of the disc degeneration process and places asymmetrical focal stresses on portions of the spine.

Extradiscal Soft Tissue Involvement

Hypertrophy and buckling of the ligamentum flavum, as well as other soft tissue proliferative processes, can result in spinal canal encroachment. Excessive pathologic segmental motion predisposes to this process and is a major factor related to the development of spinal stenosis.

Osteoporosis

Osteoporosis leads to a decrease in bony integrity, and this in turn leads to vertebral body collapse. The presence of thoracic kyphosis predisposes the thoracic spine to ventral vertebral body collapse, whereas asymmetrical disc interspace collapse (which is commonly associated with degenerative disc disease) predisposes to lateral vertebral body collapse. As the overall coronal and sagittal spinal balance worsens, the load shifts to more lateral and ventral supporting elements of the spine, respectively. This dislocation is progressive, subjecting the spine to longer and longer moment arms. Therefore, deformity begets deformity (deformity progression), creating a “vicious cycle” that perpetuates the process. Patients will often seek medical attention when the compensatory spondylotic processes have narrowed the neural canal or the spine has become so immobile that the patient can no longer compensate for the spinal imbalance.

Spinal Configuration

All aspects of spinal configuration should be considered carefully before determination of the surgical approach (which includes application of a spinal implant) for a spine disorder. The thoracic and lumbar regions are affected differently in this regard. Thoracic disc interspace height loss occurs predominantly in the ventral aspect of the disc. This loss results in progression of the natural kyphotic deformity as the degenerative process ensues, thus exaggerating propensities for deformity progression. The rib cage, however, substantially stabilizes the thoracic spine.

The coupling phenomenon (whereby one movement of the spine about or along an axis obligates another movement about or along another axis)³ plays a significant role in the development of degenerative spine deformations in the lumbar region (whereas it is of minimal significance regarding degenerative deformities in the thoracic region). This is because thoracic degenerative deformities are often oriented in the sagittal plane, whereas degenerative lumbar deformities are usually oriented in the coronal plane (excluding degenerative lumbar spondylolisthesis). The absence of uncovertebral joints (in contrast to the cervical region) and the sagittal orientation of the facet joints (in contrast to the cervical and thoracic regions) create a situation that causes obligatory rotation of the spine in response to lateral bending (coupling) and, commonly, a loss of normal lumbar lordosis. The progression of lateral bending deformities in the lumbar spine (scoliosis) thus predisposes to rotation of the spine (Fig. 85-1), and the influence of an uncompensated thoracic kyphosis predisposes the lumbar spine to greater “flattening” or loss of the normal lordotic curve.

FIGURE 85-1 Radiograph of the lumbar spine of a patient with degenerative rotatory scoliosis. This illustrates that, via the coupling phenomenon, the scoliosis is obligatorily associated with a rotatory deformation of the spine. Note that the spinous processes are rotated toward the concave side of the curvature, in contradistinction to the situation in the cervical spine, in which the coupling phenomenon results in an obligatory rotation of the spinous processes toward the convex side of the curvature.

Not all scoliotic curves are symptomatic, as patients may be able to compensate for these deformities by “rebalancing” the spine through other skeletal structures, such as pelvic tilt. When curve progression can no longer be compensated, the subsequent displacement of the load causes worsening of curve that caused it in the first place. Therefore, lateral bending deformation predisposes to lateral bending deformity progression in the lumbar spine, as the presence of kyphotic deformation predisposes to the progression of kyphotic deformation in the thoracic spine. An asymmetrical loss of height of the lumbar intervertebral disc may progress to an asymmetrical collapse of the vertebral body, as described previously in this chapter. As this scoliotic deformity progresses, it is obligatorily associated with rotation of the spine, with the spinous processes rotating toward the concave side of the curve (coupling).³ Of note is that because of the aforementioned osteophyte development propensities, osteophytes occur predominantly on the concave side of the curvature.

The obligatory association of rotation and loss of lordosis with lateral bending (coupling) complicates lumbar corrective and spinal instrumentation surgery. Transverse process exposure and dissection can cause injury to underlying nerve roots because of the relative dorsal migration of the root with respect to the transverse processes. Neuroforamina are considerably smaller on the concavity, and the neural structures within the spinal canal will naturally “hug” the lateral wall of the concave curve. This heightens the risk of neurologic injury during placement of instrumentation along the concavity. Therefore, care must be taken both during surgical exposure of the lumbar transverse processes and during placement of spinal instrumentation and subsequent correction.

Operative Treatment

The operative treatment of scoliosis is reserved for patients with refractory pain due to the scoliosis curve, significant curve progression, gait disturbance, and neurologic deficit all leading to a significant limitation of activities of daily living.^6,7 Preoperative preparation should include adequate imaging, as was already mentioned.

Any patient being considered for surgery not should only get detailed radiographic spine imaging but may also need a variety of complementary studies. A dual-energy x-ray absorptiometry scan can provide useful information about bone quality that may affect surgical planning. Patients with suspected pulmonary compromise should be sent for pulmonary function testing, although pulmonary compromise is rare in patients with curves less than 80 degrees.⁸ Medical and cardiac risk stratification should be obtained for anyone with a significant medical history. It should be noted that occult cardiac disease can be seen in adult scoliotic patients owing to severe deconditioning and the patient’s inability to experience exercise-related stress. Smoking cessation should be pursued, and a general rule of thumb is that elective surgery for deformity correction be offered to patients only after they have quit smoking.

The current approach to the surgical treatment of scoliosis is primarily pedicle screw and rod instrumentation. A recent report comparing hook-rod constructs and pedicle screw-rod constructs found that no pedicle screw patient required revision surgery for instrumentation-related complications and, overall, pedicle screw patients were 89% less likely to require revision surgery.⁹ These patients were also found to have better curve correction and maintenance of thoracic kyphosis, and pedicle screw-rod constructs often negated the need for ventral release surgery.¹⁰ However, hooks remain a valuable alternative when pedicle screws are contraindicated.

Goals of surgical correction of scoliosis are correction of coronal and sagittal balance to decrease pain, to decompress the neurologic elements, to correct balance so as to improve function, and to provide cosmesis.¹¹