A Biomechanical Assessment of Kyphoplasty as a Stand-Alone Treatment in a Human Cadaveric Burst Fracture Model

In vitro biomechanics study.To determine whether kyphoplasty is an adequate stand-alone treatment for restoring biomechanical stability in the spine after experiencing high-energy vertebral burst fractures.Kyphoplasty in the treatment of high-energy vertebral burst fractures has been shown by previous studies to significantly improve stiffness when used in conjunction with pedicle screw instrumentation. However, it is not known whether kyphoplasty as a stand-alone treatment may be an acceptable method for restoring biomechanical stability of a spinal motion segment post-burst fracture while allowing flexibility of the motion segment through the intervertebral discs.Young cadaveric spines (15-50 yr old; 3 males and 1 female; bone mineral density 0.27-0.31 gHA/cm) were divided into motion segments consisting of 3 intact vertebrae separated by 2 intervertebral discs (T11-L1 and L2-L4). Mechanical testing in axial, flexion/extension, lateral bending, and torsion was performed on each specimen in an intact state, after an experimentally simulated burst fracture and postkyphoplasty. Computed tomography was used to confirm the burst fractures and quantify cement placement.Between the intact and burst-fractured states significant decreases in stiffness were seen in all loading modes (63%-69%). Burst fracture increased the average angulation of the vertebral endplates 147% and decreased vertebral body height by an average of 40%. Postkyphoplasty, only small recoveries in stiffness were seen in axial, flexion/extension, and lateral bending (4%-12%), with no improvement in torsional stiffness. Large angular deformations (85%) and height loss (31%) remained postkyphoplasty as compared with the intact state.Lack of overall improvement in biomechanical stiffness indicates failure of kyphoplasty to sufficiently restore stability as a stand-alone treatment after high-energy burst fracture. The lack of stability can be explained by an inability to biomechanically repair the compromised intervertebral discs.3.