The direction of progressive herniation in porcine spine motion segments is influenced by the orientation of the bending axis.

BACKGROUND: It has been shown that disc herniations are a cumulative injury created by repetitive flexion motion while under modest compressive loads. There is a lack of data linking the direction of nucleus tracking to the orientation of the bending motion axis. Our purpose was to determine if the direction that the nucleus tracks through the annulus during progressive herniation is predictable from the direction of bending motion (i.e. a specific side with posterio-lateral herniation). METHODS: Matched cohorts (nu=16) of porcine cervical spine (C3/4 and C5/6) motion segments were potted in aluminum cups and bent at an angle of 30 degrees to the sagittal plane flexion axis while under a sustained compressive load of 1472 N. FINDINGS: The direction of bending motion affected the tracking pattern of the nucleus through the annular fibres in a predictable pattern. Specifically, bending the motion segments at an angle of 30 degrees to the left of the sagittal plane flexion axis biased the movement of the nucleus toward the posterior right side of the disc in 15 of the 16 specimens. INTERPRETATION: Based on this animal model, shown to have similar biomechanical behaviour to humans, the direction that the nucleus tracks through the annular fibres appears to be dependent upon the direction of bending motion. This may have implications on both herniation prevention and rehabilitation of posterio-lateral bulges and herniations.

The influence of static axial torque in combined loading on intervertebral joint failure mechanics using a porcine model.

BACKGROUND: The spine is routinely subjected to repetitive combined loading, including axial torque. Repetitive flexion-extension motions with low magnitude compressive forces have been shown to be an effective mechanism for causing disc herniations. The addition of axial torque to the efficacy of failure mechanisms, such as disc herniation, need to be quantified. The purpose of this study was to determine the role of static axial torque on the failure mechanics of the intervertebral joint under repetitive combined loading. METHODS: Repetitive flexion-extension motions combined with 1472 N of compression were applied to two groups of nine porcine motion segments. Five Nm of axial torque was applied to one group. Load-displacement behaviour was quantified, and planar radiography was used to document tracking of the nucleus pulposus and to identify fractures. FINDINGS: The occurrence of facet fractures was found to be higher (P=0.028) in the axial torque group (7/9), compared to the no axial torque group (2/9). More hysteresis energy was lost up to 3000 cycles of loading in the axial torque group (P<0.014). The flexion-extension cycle stiffness was not different between the two groups until 4000 cycles of loading, after which the axial torque group stiffness increased (P=0.016). The percentage of specimens that herniated after 3000 cycles of loading was significantly larger (P=0.049) for the axial torque group (71%) compared to the no axial torque group (29%). INTERPRETATION: Small magnitudes of static axial torque alter the failure mechanics of the intervertebral disc and vertebrae in combined loading situations. Axial torque appears to accelerate the susceptibility for injury to the intervertebral joint complex. This suggests tasks involving axial torque with other types of loading, apart from axial twist motion, should be monitored to assess exposure and injury risk.

Vascular biology of angiotensin and the impact of physical activity.

The renin-angiotensin system (RAS) is important for regulating blood pressure and extracellular fluid. The concept of the RAS has recently evolved from a classical systemic endocrine system to an appreciation of local RASs functioning in a paracrine manner, including in the vascular wall. Angiotensin II (AII), the main effector of the RAS, is a potent vasoconstrictor formed by the action of angiotensin-converting enzyme (ACE). ACE is multifunctional and also destroys the endogenous vasodilator bradykinin. A recently discovered novel ACE2 enzyme is responsible for forming a vasodilatory compound, angiotensin 1-7, from AII. Thus, the actions of ACE and ACE2 are antagonistic. Tissue actions of AII are mediated by specific receptors, AT1 and AT2, with AT1 mediating the classical actions. AT1-stimulated vasoconstricton occurs via phospholipase-D-mediated second messenger generation directly, and indirectly via the coupling of AT1 to the prooxidant enzyme NADPH oxidase. Since the vascular NADPH oxidase is a major source of vascular reactive oxygen species generation and is responsible for the breakdown of the vasodilator nitric oxide (NO), there is another potential link between RAS and regulation of vasodilatory pathways. AT2 signaling is antagonistic to AT1 signaling, and results in bradykinin and NO formation. Chronic AII signaling induces vascular dysfunction, whereas pharmacological management of the RAS can not only control blood pressure, but also correct endothelial dysfunction in hypertensives. Exercise training can also improve endothelial function in hypertensives, raising the question of whether there is a potential role for RAS in mediating the vascular effects of exercise training. Recent studies have demonstrated reductions in the expression of NADPH oxidase components in the vascular wall in response to exercise training, thus tempering one of the main cellular effectors of AII, and this is associated with reduced vascular ROS production and enhanced NO bioavailability. Importantly, it has now been demonstrated in human arteries that exercise training also tempers vascular AT1 receptor expression and AII-induced vasoconstriction, while enhancing endothelium-dependent dilation. The signals responsible for these chronic adaptations are not clearly understood, and may include changes in RAS components prompted by acute exercise. ACE genotype may have an effect on physical activity levels and on the cardiovascular responses to exercise training, and the II genotype (compared with ID and DD) is associated with the largest endothelium-dependent dilations in athletes compared with those in sedentary individuals. Thus, the tissue location of the RAS, the complement of ACE/ACE2, the receptor expression of AT1/AT2, and the ACE genotype are all variables that could impact the vascular responses to exercise training, but the responses of most of these variables to regular exercise training and the mechanisms responsible have not been systematically studied.

The effect of static torsion on the compressive strength of the spine: an in vitro analysis using a porcine spine model.

STUDY DESIGN: Matched porcine cervical spine motion segments were subjected to two main conditions and compared: axial compression and axial compression combined with varying axial torque. OBJECTIVES: To determine the effect of torsion on the acute compressive strength of the spine. SUMMARY OF BACKGROUND DATA: The spine is often subjected to compression together with axial torque as a component of complex loading, yet there is a lack of documentation on its effect on the compressive strength and injury mechanics. METHODS: Matched cohorts of porcine cervical spine (C5-C6) motion segments were compressed to failure at a rate of 3,000 N/s combined with 0 Nm, 5 Nm, 20 Nm, or 30 Nm of axial torque. Three "failure" points were recorded from the stress/strain association: the first "step" (initial microfracture), the initial slope change (yield point or "slow crush" mechanism), and the ultimate failure point (fracture). Furthermore, resultant injuries were documented using planar radiography and visual inspection following dissection of the motion segments. RESULTS: Axial torque affected the failure characteristics during acute compressive loading. The ultimate strength of the motion segments was significantly reduced with increasing static torques. The compressive load at which initial microfracture occurred, indicated by the first "step" in the load-deformation curve, was increased with 5 Nm, 10 Nm, and 20 Nm of applied torsion in comparison to no torque, but this effect was reduced with 30 Nm of torque. The "slow crush" mechanism of failure was not affected by the addition of axial torque. No radiographic gross injuries to the facet joints were observed. Damage appeared to be confined to the endplate and trabecular network of the vertebral body. CONCLUSIONS: Based on this animal model, shown to have similar biomechanical behavior to humans, axial torque appears to significantly reduce the compressive strength of the spine.