How do compression and flexion-compression injuries destabilize the spine? A novel in vitro protocol for analyzing three-dimensional biomechanical instability

Ann-Kathrin Greiner-PerthHans-Joachim Wilke^*Christian Liebsch

• Institute of Orthopeadic Research and Biomechanics, Trauma Centre Ulm, Ulm University Medical Centre, Ulm, Germany

Unstable traumatic spinal injuries require surgical stabilization. However, biomechanical instability of specific spinal injuries has been little investigated, although restoring stability represents a primary goal of surgical treatment. This study aimed (1) to develop an in vitro protocol to generate standardized spinal compression injuries, (2) to establish a three-dimensional flexibility analysis to identify relevant biomechanical instability parameters, and (3) to examine effects of person-specific factors on vertebral fragility. Mechanical fracture simulation was performed on twelve fresh-frozen human spine specimens (T9-11; 4 f / 8 m; 40-60 years) using a material testing machine. Pure compression trauma (n=6) was simulated by applying displacement-controlled axial compression at 300 mm/s until 20% compression of the T10 vertebral body height. Flexion-compression trauma (n=6) was achieved by additional flexural loading of 10 Nm. Pre-and post-traumatic pure moment testing with 5 Nm was performed in flexion/extension, lateral bending, and axial rotation using optical motion tracking to determine range of motion (ROM), neutral zone (NZ), coupled rotations, and coupled translations. Translations under shear loading of 100 N and axial deformation under 400 N compression were analyzed. All specimens exhibited AOSpine A1 injuries occurring at a median fracture load of 5.0 kN (2.4-9.2 kN). Pure compression generated isolated medial endplate fractures (n=5), while flexioncompression primarily provoked combined endplate and ventral compression injuries (n=3). Significant (p<0.05) increases were detected for all parameters except for coupled rotations and posterior (compression) and left shear translation (flexion-compression). Highest instability increases were determined for axial deformability (compression: +136% / flexion-compression: +200%) and NZ (flexion/extension: +177% / +188%; lateral bending: +174% / +126%). Mild to moderate disc degeneration and age did not correlate with fracture loads (p>0.05). In compression trauma, cortical bone mineral density (BMD) of T10 had no effect on fracture loads (p>0.05), whereas in flexioncompression trauma, a significant (p<0.05) linear correlation was found (Spearman's rs = 0.83). Relevant instability parameters of minor compression and flexion-compression injuries include axial deformability, NZ, ROM, and coupled translations. Cortical BMD of the target vertebra solely affect fracture generation in flexion-compression trauma. Consequently, risk factors for fracture development may vary between trauma mechanisms.