Pelvic incidence-lumbar lordosis mismatch results in increased segmental joint loads in the unfused and fused lumbar spine.

Purpose: Symptomatic adjacent segment disease (ASD) has been reported to occur in up to 27 % of lumbar fusion patients. A previous study identified patients at risk according to the difference of pelvic incidence and lordosis. Patients with a difference between pelvic incidence and lumbar lordosis >15° have been found to have a 20 times higher risk for ASD. Therefore, it was the aim of the present study to investigate forces acting on the adjacent segment in relation to pelvic incidence-lumbar lordosis (PILL) mismatch as a measure of spino-pelvic alignment using rigid body modeling to decipher the underlying forces as potential contributors to degeneration of the adjacent segment.

Methods: Sagittal configurations of 81 subjects were reconstructed in a musculoskeletal simulation environment. Lumbar spine height was normalized, and body and segmental mass properties were kept constant throughout the population to isolate the effect of sagittal alignment. A uniform forward/backward flexion movement (0°-30°-0°) was simulated for all subjects. Intervertebral joint loads at lumbar level L3-L4 and L4-L5 were determined before and after simulated fusion.

Results: In the unfused state, an approximately linear relationship between sagittal alignment and intervertebral loads could be established (shear: 0° flexion r = 0.36, p < 0.001, 30° flexion r = 0.48, p < 0.001; compression: 0° flexion r = 0.29, p < 0.01, 30° flexion r = 0.40, p < 0.001). Additionally, shear changes during the transition from upright to 30° flexed posture were on average 32 % higher at level L3-L4 and 14 % higher at level L4-L5 in alignments that were clinically observed to be prone to ASD. Simulated fusion affected shear forces at the level L3-L4 by 15 % (L4-L5 fusion) and 23 % (L4-S1 fusion) more for alignments at risk for ASD.

Conclusion: Higher adjacent segment shear forces in alignments at risk for ASD already prior to fusion provide a mechanistic explanation for the clinically observed correlation between PILL mismatch and rate of adjacent segment degeneration.