There are several reasons to research the effects of axial twist exposures and the resulting loading on the spine. The lack of consensus from the limited work that has previously examined the role of axial twist moments and motions in the development of spine injuries or generation of low back pain is the primary reason. From recently published works, axial twist moments appear to represent an increased risk for injury development when it acts in concert with loading about other physiological axes (i.e. flexion, extension, and compression). However, there is a large body of epidemiologic data identifying axial twist moments and/or motion as risk factors for low back disorders and pain, demonstrating the need for this series of investigations. It is likely that these combined exposures increase risk through altering the spine’s load distribution (passive resistance) by modifying the mechanics, but this deduction and related causal mechanism need to be researched.

The global objective of this research was focused on determining whether there is evidence to support altered load distribution in the spine, specifically between the intervertebral disc and facets, in response to applied axial twist moments (when added in combination with one and two axes of additional loading). Also included was whether these modes of loading can modify spine mechanics and contribute and/or alter the development of damage and pain. This objective was addressed through one in-vivo (Drake and Callaghan, 2008a– Chapter #2) and three in-vitro (Drake et al., 2008– Chapter #4;​ Drake and Callaghan, 2008b– Chapter #5;​ Drake and Callaghan, 2008c– Chapter #6) studies that:​ (1) Quantified the amount of passive twist motion in the lumbar spine when coupled with various flexionextension postures;​ (2) Documented the effects of flexion-extension postures and loading history on the distance between the facet articular surfaces;​ (3) Evaluated the result of axial twist rotation rates on acute failure of the spine in a neutral flexion posture;​ and (4) Explored whether repetitive combined loading has the ability to cause enough deformation to the spine to generate pain.

Through the combination of findings previously reported in the literature and the outcomes of Drake and Callaghan (2008a– Chapter #2) and Drake et al. (2008– Chapter #4), a postural mediated mechanism was hypothesized to be responsible for governing the load distribution between the facet joints and other structures of the spine (i.e. disc, ligaments). Increased flexed postures were found to decrease the rotational stiffness by resulting in larger twist angles for the same applied twist moment in-vivo relative to a neutral flexion posture (Drake and Callaghan, 2008a– Chapter #2). This suggested there might be an increased load on the disc due to a change in facet coupling in these combined postures. Similarly, increased angles were observed in flexed and twisted postures for in-vitro specimens relative to a neutral flexion posture. These observed differences were found to correspond with altered facet joint mechanics. Specifically that flexed twisted postures increased the inter-facet spacing relative to the initial state of facet articulation (Drake et al., 2008– Chapter #4). These finding supported the postulated postural mechanism. Therefore, in a neutral posture the facet joints likely resisted the majority of any applied twist moment based on the limited range of motion and higher axial rotational stiffness responses observed. It was suspected that the changes in mechanics would likely cause a change in the load distribution however the magnitude of change in load distribution remains to be quantified.

Further support for this postulated postural mechanism comes from the mode of failure for specimens that were exposed to 10,000 cycles of 5° axial twist rotation while in a static flexed posture (Drake and Callaghan, 2008c– Chapter #6), and neutrally flexed specimens exposed to 1.5° of rotation for 10,000 cycles reported in the literature. Without flexion, the failure patterns were reported to occur in the endplates, facets, laminae and capsular ligaments, but not the disc. However, with flexion the repetitive axial twist rotational displacements caused damage primarily to the disc. If the load distribution was unchanged, the higher axial rotation angle should have caused the specimen to fail in less cycles of loading, and the failure pattern should not have changed. Modulators of this hypothesized mechanism include the velocity of the applied twist moment and the effects these have on the failure parameters and injury outcomes. The three physiologic loading rates investigated in this work were not shown to affect the ultimate axial twist rotational failure angle or moment in a neutral flexion/extension posture, but were shown to modify flexionextension stiffness (Drake and Callaghan, 2008b– Chapter #5). All of the flexion-extension stiffness values post failure, from a one-time axial twist exposure, was less than those from a repetitive combined loading exposure that has been established to damage the intervertebral disc but not the facets. Therefore, it is likely that the facet joint provides the primary resistance to acute axial twist moments when the spine is in a neutral flexion posture, but there appears to be a redistribution of the applied load from the facets to the disc in repetitive exposures.

The aforementioned studies determined there are changes in load distribution and load response caused by altered mechanics resulting from twist loading, but whether the exposures could possibly produce pain needed to be addressed. Previous research has determined that the disc has relatively low innervation in comparison to the richly innervated facet capsule and vertebra, with only the outer regions being innervated. Likewise, it is assumed that pain could be directly generated as the nucleus pulposus disrupted the innervated outer annular fibres in the process of herniation. Also, direct compression of the spinal cord or nerve roots has been shown to occur from the extruded nucleus and result in the generation of pain responses. Additionally, the nucleus pulposus has been shown to be a noxious stimulus that damages the function and structure of nerves on contact. The other source of nerve root compression commonly recognized is a decrease in intervertebral foramina space, which was previously believed to only be caused through losses in disc height. However, decreased intervertebral foramina space due to repetitive motions appears to be a viable pain generating pathway that may not directly correspond to simply a loss of specimen or disc height (Drake and Callaghan, 2008c– Chapter #6). This is new evidence for combined loading to generate pain through spinal deformation. The objective of many traditional treatments for nerve root compression focus on restoring lost disc height to remove the nerve root compression. Unfortunately, nerve root compression caused by repetitive loading may not be alleviated through this approach.

This collection of studies was focused on determining whether altered load distribution in the spine, specifically between the intervertebral disc and facets, in response to applied axial twist loading (when added in combination with one and two axes of additional loading) was occurring, and examining how these modes of loading can contribute and/or alter the development of injury and pain. Therefore, findings generated from this thesis may have important implications for clinicians, researchers, and ergonomists.