Study design: This study analyzed the changes in the load-displacement behavior of lumbar spine segments caused by burst fractures that were experimentally produced in fresh human cadaveric spines. The effect of three transpedicular surgical constructs on stability was investigated in each specimen.
Objectives: To quantify the loss of mechanical stiffness caused by the injury, and to evaluate the stiffness of three transpedicular surgical constructs.
Summary of background data: Although various investigators have studied the biomechanical characteristics of the burst fracture and surgical stabilization techniques, few have reported quantitative data on the three-dimensional biomechanical instability of these fractures.
Methods: Load-displacement data were acquired in flexion, lateral bending, and axial rotation for intact specimens, after the L1 burst fracture was created and after the T12-L2 segments were stabilized using Luque plates, VSP plates, and Isola rods with one transverse connector.
Results: Spines with burst fractures showed a bilinear load-displacement behavior with significant instability (loss of stiffness relative to intact) at low loads (up to 3 N.m) in flexion, lateral bending, and axial rotation. The loss of stiffness was greatest in axial rotation over the entire load range (up to 10 N.m). If posterior element injury also was present, a significantly larger loss of stiffness was observed in flexion and axial rotation. The three transpedicular constructs improved the stability of the injured spine beyond that of the intact spine in flexion and lateral bending at low loads. At high loads, they restored the stiffness to intact levels. However, in axial rotation they did not restore the stiffness to pre-injury level, particularly when the posterior column was disrupted.
Conclusions: Reduction of the burst fracture returns the spine to its position of greatest inherent instability, essentially requiring the transpedicular instrumentation to be load bearing. To enhance mechanical stability, it may be necessary to augment the transpedicular construct, particularly when the posterior column is disrupted.