This thesis is unified around the theme of disc height loss. Current knowledge in the area of spine research identifies mechanical overload as the culprit for the initiation of injury to the spine. While genetic predispositions may play a factor in the severity of spine degeneration or in the resiliency to applied load, ultimately, injury occurs when a load exceeds a tissue’s tolerance.

Disc height loss has the potential to be a primary factor in the progression of spinal degeneration. For example, disc height has been touted as a major component for the initiation of pathological and degenerative changes to the spine. Pathologic, non-recoverable disc height loss can occur through herniation or endplate fracture and could result in a degenerative cascade of injury that eventually involves the facet joints, narrows nerve root space, and increases stress at adjacent segments. What is not known is the degree to which disc height affects the degenerative cascade;​ that is, there is no quantitative data outlining the progression of mechanical consequences at adjacent segments or at the injured segment itself during disc height loss. Further, the degree to which restoring disc height, if even possible, will reverse the process of degeneration is not entirely clear. There is data which suggests that nucleus replacement can restore stress distributions within an injured disc, but the extent of repair material survivability is unknown. Finally, clinical categories of measuring spinal degeneration are based on visual cues and features from medical imaging. Understanding the links between joint visual cues and aberrant movement may help to guide clinical practice;​ researchers will gain greater insight into the mechanical consequences of anatomical features associated with degeneration.

This thesis was comprised of three studies. Study 1 examined the effect of disc height loss and subsequent restoration using an injectable hydrogel on the relative kinematics of a segment with height loss and an adjacent segment. It was found that disc height loss produced an immediate effect, where relative angular displacement was reduced in the segment with height loss and increased in the adjacent segment. Restoring disc height with an injectable hydrogel brought the relative angular displacement of both segments back to their initial values. This study is the first of its kind to examine the immediate effects of disc height loss via loss of nucleus pulposus and restoration. Whether these effects are as clear in-vivo remains to be seen.

Study 2 evaluated the efficacy of a novel repair strategy to restore the mechanical profile of a spine segment with disc height loss initiated via compressive fracture. The strategy employed the use of PMMA injected into the vertebral body to attempt to seal a fracture from above the disc, and an injectable hydrogel to restore disc height. The use of PMMA was found to restore the compressive stiffness of the injured segment to within approximately 20% of its initial value, while the use of the injectable hydrogel restored the sagittal plane rotational stiffness to within approximately 50-80% of its initial value. After further repetitive compression had been applied to the spine segment however, the restorative influence of both interventions was lost in terms of rotational and compressive stiffness. It was found that large cracks in the endplate prevented the hydrogel from being contained and quickly returned the segment back to its injured profile. Future efforts at restoring the disc while maintaining its anatomical structures need better methods of creating a sufficient seal inside the disc to allow it to re-pressurize and sustain the stresses encountered on a daily basis.

Study 3 employed the use of a novel spine tracking algorithm developed as part of this thesis to evaluate sagittal plane cervical spine motion of a series of patient image sequences who had experienced trauma and had a chief complaint related to their neck, head, or shoulders. Some patients had evidence of disc height loss while others did not. Clinical subgroups were created that classified disc height loss as either moderate/severe (3 cases), mild (8 cases), or non-existent (9 cases). When normalized angular displacement of the C5/C6 segment in a group with moderate to severe height loss was compared to the same level in a group with no height loss, there was a statistically significant difference in angular displacement between the two groups (p = 0.004). Angular displacement at C5/C6 was 20.2% ± 2.3% of total measured neck angular displacement in the moderate/severe height loss group compared to 30.6% ± 4.0% of total measured neck angular displacement in the group without height loss. Based on the limited sample size of this study it would appear that disc height loss creates a loss in range of motion. This work has further revealed the heterogeneous nature of individual segmental movement patterns. However, in the group without height loss, there was a systematic trend seen of an increasing angular displacement with descending segmental level. This was not observed in those with moderate to severe disc height loss.

The broad implications of this work are that disc height loss influences spine kinematics, which has implications with respect to further injury propagation through the spinal linkage. Angular displacement of a spine segment appears to be governed by its local stiffness. Restoration of disc height under real injury scenarios is a difficult proposition and any attempts at repair need to sufficiently seal the disc space and prevent extrusion of nucleus pulposus or hydrogel-based implants. We now appreciate the difficulty in this objective. Further, repeating the mechanism of injury will reduce the mechanical effects of the restorative intervention, preventing this is highly important.