Senile kyphosis arises from anterior ‘wedge’ deformity of thoracolumbar vertebrae, often in the absence of trauma. It is difficult to reproduce these deformities in cadaveric spines, because a vertebral endplate usually fails first. We hypothesise that endplate fracture concentrates sufficient loading on to the anterior cortex that a wedge deformity develops subsequently under physiological repetitive loading. Thirty-four cadaveric thoracolumbar “motion segments,” aged 70–97 yrs, were overloaded in combined bending and compression. Physiologically-reasonable cyclic loading was then applied, at progressively higher loads, for up to 2 hrs. Before and after fracture, and again after cyclic loading the Introduction
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Osteoporotic vertebral fractures can cause severe vertebral wedging and kyphotic deformity. This study tested the hypothesis that kyphoplasty restores vertebral height, shape and mechanical function to a greater extent than vertebroplasty following severe wedge fractures. Pairs of thoracolumbar “motion segments” from seventeen cadavers (70–97 yrs) were compressed to failure in moderate flexion and then cyclically loaded to create severe wedge deformity. One of each pair underwent vertebroplasty and the other kyphoplasty. Specimens were then creep loaded at 1.0kN for 1 hour. At each stage of the experiment the following parameters were measured: vertebral height and wedge angle from radiographs, motion segment compressive stiffness, and stress distributions within the intervertebral discs. The latter indicated intra-discal pressure (IDP) and neural arch load-bearing (FN).Introduction
Methods
Senile kyphosis arises from anterior ‘wedge’ deformity of thoracolumbar vertebrae, often in the absence of trauma. It is difficult to reproduce these deformities in cadaveric spines, because a vertebral endplate usually fails first. We hypothesise that endplate fracture concentrates sufficient loading on to the anterior cortex that a wedge deformity develops subsequently under physiological repetitive loading. Thirty-four cadaveric thoracolumbar “motion segments,” aged 70–97 yrs, were overloaded in combined bending and compression. Physiologically-reasonable cyclic loading was then applied, at progressively higher loads, for up to 2 hrs. Before and after fracture, and again after cyclic loading the distribution of compressive loading on the vertebral body was assessed from recordings of compressive stress along the sagittal mid-plane of the adjacent intervertebral disc. Vertebral deformity was assessed from radiographs at the beginning and end of testing.Introduction
Methods
The feature of disc degeneration most closely associated with pain is a large fissure in the annulus fibrosus. Nerves and blood vessels are excluded from normal discs by high matrix stresses and by high proteoglycan (PG) content. However, they appear to grow into annulus fissures in surgically-removed degenerated discs. We hypothesize that anulus fissures provide a micro-environment that is mechanically and chemically conducive to the in-growth of nerves and blood vessels. 18 three-vertebra thoraco-lumbar spine specimens (T10/12 to L2/4) were obtained from 9 cadavers aged 68-92 yrs. All 36 discs were injected with Toluidine Blue so that leaking dye would indicate major fissures in the annulus. Specimens were then compressed at 1000 N while positioned in simulated flexed and extended postures, and the distribution of compressive stress within each disc was characterised by pulling a pressure transducer through it in various planes. After testing, discs were dissected and the morphology of fissures noted. Reductions in stress in the vicinity of fissures were compared with average pressure in the disc nucleus. Distributions of PGs and collagen were investigated in 16 surgically-removed discs by staining with Safranin O. Digital images were analysed in Matlab to obtain profiles of stain density in the vicinity of fissures.Introduction
Methods
In the annulus fibrosus of degenerated intervertebral discs, disruption to inter-lamellar cross-ties appears to lead to delamination, and the development of anulus fissures. We hypothesise that such internal disruption is likely to be driven by high gradients of compressive stress (i.e. large differences in stress from the nucleus to the mid anulus). Eighty-nine thoracolumbar motion segements, from T7/8 to L4/5, were dissected from 38 cadavers aged 42-96 yrs. Each was subjected to 1 kN compressive loading, while intradiscal compressive stresses were measured by pulling a pressure transducer along the disc's mid-sagittal diameter. Measurements were repeated in flexed and extended postures. Stress gradients were measured, in the anterior and posterior anulus of each disc, as the average rate of increase in stress (MPa/mm) between the nucleus and the region of maximum compressive stress in the anulus. Average nucleus pressure (IDP) was also recorded.Background
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