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.