Introduction. Vertebral osteoporotic fracture increases both elastic and time-dependent ('creep') deformations of the fractured vertebral body during subsequent loading. The accelerated rate of creep deformation is especially marked in central and anterior regions of the vertebral body where bone mineral density is lowest. In life, subsequent loading of damaged vertebrae may cause anterior wedging of the vertebral body which could contribute to the development of kyphotic deformity. The aim of this study was to determine whether gradual creep deformations of damaged vertebrae can be reduced by vertebroplasty. Methods. Fourteen pairs of spine specimens, each comprising three vertebrae and the intervening soft tissue, were obtained from cadavers aged 67-92 yr. Specimens were loaded in combined bending and compression until one of the vertebral bodies was damaged. Damaged vertebrae were then augmented so that one of each pair underwent vertebroplasty with polymethylmethacrylate cement, the other with a resin (Cortoss). A 1kN compressive force was applied for 1 hr before fracture, after fracture, and after vertebroplasty, while creep deformation was measured in anterior, middle and posterior regions of each vertebral body, using a MacReflex optical tracking system. Results. Cement type had little influence on creep deformation, so data from all 28 specimens were pooled. After fracture, creep in the anterior vertebral body increased from 4,513 (STD 4766) to 54,107 (STD 54,845) microstrains (P<0.001), and creep in the central region of the vertebral body increased from 885 (STD 5,169) to 34,378 (STD 40,762) microstrain (P<0.001). (10,000 microstrains = 1% deformation.) Following vertebroplasty, creep deformations were reduced by 61% (P=0.002) and 66% (P=0.006) in anterior and central regions respectively. Conclusion. Creep deformations of the anterior and central regions of vertebral bodies increase markedly as a result of fracture but are then reduced by vertebroplasty. In life, vertebroplasty could help to slow or prevent the gradual development of kyphotic deformity following vertebral osteoporotic fracture, as well as increase vertebral stiffness and strength

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