Introduction. 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. Methods. 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 (F. N. ). Results. Fracture and cyclic loading reduced anterior vertebral height by 34%, increased wedge angle from 5.0° to 11.4°, increased F. N. by 58% and reduced IDP and compressive stiffness by 96% and 44% respectively. Kyphoplasty restored anterior height to a greater extent than vertebroplasty (p<0.001), by 96% versus 59% immediately after augmentation, and by 79% versus 47% after subsequent creep loading. Wedge angle was also reduced to a greater extent following kyphoplasty than vertebroplasty (p<0.02) by 7.2° vs 4.2° after augmentation and 6.6° vs 4.0° after creep loading. IDP, F. N. and compressive stiffness were restored to a similar extent by both procedures. Conclusion. Kyphoplasty and vertebroplasty were equally effective in restoring mechanical function following severe wedge fractures, but kyphoplasty was better able to correct deformity by restoring vertebral height and reducing wedging. No conflicts of interest. Sources of funding: Funding was provided by a Royal College of Surgeons of England Research Fellowship and the Gloucestershire Arthritis Trust. Materials were provided by Medtronic and Depuy. This abstract has not been previously published in whole or substantial part nor has been presented previously at a national meeting

Introduction. 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. Methods. 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. Results. Initial overload usually fractured a vertebral endplate, at 2.31 kN (STD 0.85). There was minimal anterior wedging, but pressure in the nucleus of the adjacent disc was reduced by 65.2% on average, and relatively elevated in the annulus and neural arch. Subsequent cyclic loading then caused anterior wedge deformity of the vertebral body, with the height of the anterior and posterior cortex decreasing by 34.3% (13.2) and 12.7% (7.5) respectively, and wedge angle increasing from 5.0° (3.76) to 11.4° (3.93) (all p<0.001). Discussion and Conclusion. Our hypothesis is supported: initial minor damage facilitates progressive anterior wedge deformity by transferring compressive loading on to the anterior cortex. Detecting initial endplate damage is important to minimise subsequent vertebral deformity in patients with osteoporosis. No conflicts of interest. Sources of funding: Funding was provided by a Royal College of Surgeons of England Research Fellowship and by the Gloucestershire Arthritis Trust. This work was presented at the British Orthopaedic Research Society Meeting

Introduction. 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. Methods. 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. Results. Initial overload usually fractured a vertebral endplate, at 2.31 kN (STD 0.85). There was minimal anterior wedging, but pressure in the nucleus of the adjacent disc was reduced by 65.2% on average, and relatively elevated in the annulus and neural arch. Subsequent cyclic loading then caused anterior wedge deformity of the vertebral body, with the height of the anterior and posterior cortex decreasing by 34.3% (13.2) and 12.7% (7.5) respectively, and wedge angle increasing from 5.0° (3.76) to 11.4° (3.93) (all p<0.001). Discussion and Conclusion. Our hypothesis is supported: initial minor damage facilitates progressive anterior wedge deformity by transferring compressive loading on to the anterior cortex. Detecting initial endplate damage is important to minimise subsequent vertebral deformity in patients with osteoporosis. 256 words (250 excluding section headings) Acknowledgements Funding was provided by a Royal College of Surgeons of England Research Fellowship and by the Gloucestershire Arthritis Trust