Thoracolumbar burst fractures are severe spinal injuries which may result in neurological dysfunction. There is presently much controversy regarding the diagnosis of these injuries as clinically stable or unstable. Further, the injury mechanism of burst fractures has not been studied experimentally. The objectives of the present investigation were to determine the acute flexibility, alternatively the biomechanical instability, of thoracolumbar burst fractures and document the mechanism of injury for this spinal fracture.

Thirteen cadaveric three-vertebrae spine specimens from the thoracolumbar junction region were impacted in axial compression with ten specimens resulting in clinically relevant burst fractures. Impact loads and deformations were recorded during the trauma. Before and after the impact, the three-dimensional flexibility of the spine specimen was determined by applying loads individually (flexion/extension moment, axial torque, lateral bending moment, tension/compression force) and measuring total vertebral motion using stereophotogrammetry. X-rays and CT scans of the spine were obtained before and after injury and these radiographic images correlated to the spinal flexibility.

The burst fractures were found to be biomechanically unstable injuries with the greatest instabilities in axial torque and lateral bending. From lateral X-ray, the anterior unit height (vertebral height plus superior and inferior discs) had the highest correlations with the burst fracture flexibility. From the CT scans, the posterior vertebral body had the highest correlations with the burst fracture flexibility.

Measurements during impact suggested that the dynamic spinal canal encroachment averaged 300% more than the canal occlusion observed on the post-trauma CT scans. The average compressive force required to produce burst fracture was 6070N and was dependent on the age of the specimen.

Nonlinear axisymmetric finite element analyses were performed on the vertebral body to study the burst fracture injury mechanism. The primary injury mechanism was a multi-stage process, beginning with end-plate depression causing central cancellous bone fracture and ending with lateral expansion of the central core, resulting in failure of the peripheral cortical shell. The failure mechanism was found to be dependent on the compressive loading distribution on the vertebral body and the density of the vertebral cancellous bone.