Is kyphoplasty better than vertebroplasty at restoring form and function after severe vertebral wedge fractures?

BACKGROUND CONTEXT: The vertebral augmentation procedures, vertebroplasty and kyphoplasty, can relieve pain and facilitate mobilization of patients with osteoporotic vertebral fractures. Kyphoplasty also aims to restore vertebral body height before cement injection and so may be advantageous for more severe fractures. PURPOSE: The purpose of this study was to compare the ability of vertebroplasty and kyphoplasty to restore vertebral height, shape, and mechanical function after severe vertebral wedge fractures. STUDY DESIGN/SETTING: This is a biomechanical and radiographic study using human cadaveric spines. METHODS: Seventeen pairs of thoracolumbar "motion segments" from cadavers aged 70-98 years were injured, in a two-stage process involving flexion and compression, to create severe anterior wedge fractures. One of each pair underwent vertebroplasty and the other kyphoplasty. Specimens were then compressed at 1 kN for 1 hour to allow consolidation. Radiographs were taken before and after injury, after treatment, and after consolidation. At these same time points, motion segment compressive stiffness was assessed, and intervertebral disc "stress profiles" were obtained to characterize the distribution of compressive stress on the vertebral body and neural arch. RESULTS: On average, injury reduced anterior vertebral body height by 34%, increased its anterior wedge angle from 5.0° to 11.4°, reduced intradiscal (nucleus) pressure and motion segment stiffness by 96% and 44%, respectively, and increased neural arch load bearing by 57%. Kyphoplasty caused 97% of the anterior height loss to be regained immediately, although this reduced to 79% after consolidation. Equivalent gains after vertebroplasty were significantly lower: 59% and 47%, respectively (p<.001). Kyphoplasty reduced vertebral wedging more than vertebroplasty (p<.02). Intradiscal pressure, neural arch load bearing, and motion segment compressive stiffness were restored significantly toward prefracture values after both augmentation procedures, even after consolidation, but these mechanical effects were similar for kyphoplasty and vertebroplasty. CONCLUSIONS: After severe vertebral wedge fractures, vertebroplasty and kyphoplasty were equally effective in restoring mechanical function. However, kyphoplasty was better able to restore vertebral height and reverse wedge deformity.

Pathogenesis of Vertebral Anterior Wedge Deformity: A 2-Stage Process?

STUDY DESIGN: Biomechanical and radiographical study on cadaveric spines. OBJECTIVE: To explain the pathogenesis of vertebral "anterior wedge" deformity, which causes senile kyphosis. SUMMARY OF BACKGROUND DATA: This deformity arises with minimal trauma and is difficult to reproduce in cadaveric spines. We hypothesize that wedging is created by a 2-stage process. First, excessive loading damages a vertebral endplate and decompresses the adjacent intervertebral disc. This alters load sharing between the vertebral body cortex and trabeculae so that subsequent cyclic loading causes progressive collapse of the unsupported anterior cortex. METHODS: Thirty-four cadaveric thoracolumbar "motion segments," aged 70 to 98 years, were positioned in flexion and overloaded in compression. Physiologically reasonable cyclic compressive loading was then applied to each flexed specimen, at progressively higher loads, for up to 2 hours. Before and after initial overload and again after cyclic loading, the distribution of loading on the vertebra was assessed from measurements of compressive stress within the adjacent disc. These "stress profiles" were repeated in the neutral, flexed, and extended postures. Progressive vertebral body deformity was assessed radiographically. RESULTS: Compressive overload induced endplate fracture at an average force of 2.31 kN. There was minimal anterior wedging, but pressure in the adjacent disc nucleus (in flexion) fell by an average of 55% and neural arch load bearing increased by 166%. Subsequent cyclic loading exaggerated these changes and concentrated compressive stress within the anterior annulus. After both stages, height of the anterior and posterior vertebral cortexes was reduced by 32% and 12%, respectively, so that anterior wedging of the vertebral body increased from 5.0° to 11.4° on average. All changes were highly significant (P < 0.001). CONCLUSION: Anterior wedge deformities can be created consistently by a 2-stage process involving initial endplate damage, followed by progressive collapse of the anterior cortex. Detecting initial endplate damage may be important to minimize vertebral deformity in patients with osteoporosis. LEVEL OF EVIDENCE: N/A.