Degenerative Lumbar Spondylolisthesis: Biochemical Aspects and Evaluation of Stabilization Surgery Extent in Terms of Adjacent Segment Disease Theory.

Abstract

In lumbar degenerative spondylolisthesis (DSL), the criteria and extent of surgical treatment have not been strictly defined owing to the adjacent segment disease theory and unclear molecular pathogenesis. The present study analyzed the clinical and radiographic findings of patients after lower lumbar fusion surgery with single and 2-level DSL and explored the inflammatory mediator's role in DSL evolution and symptoms. The prospective follow-up of patients with DSL, stratified by the stabilization extent (L4-L5, L5-S1, and L4-S1), included the Back Illness Pain and Disability 9-item questionnaire and native and dynamic radiographs to evaluate the intervertebral disc height and adjacent segments' angular motion. Follow-up examinations were performed at 3, 12, and 24 months. The pathological cytokine concentrations in the intervertebral disc and facet joints of the subchondral bone were assessed using the BioPlex assay in perioperatively collected patient samples and compared with those of control subjects obtained during multiorgan procurement. These findings were correlated with pain localization and severity. Statistical analysis of the questionnaire data revealed significant postoperative improvement in all patients, in particular, the L4-L5 group. Also, we found radiographic evidence of angular motion reduction in both adjacent segments near the limits of statistical significance and a meaningful correlation with subjective status improvement at 24 months. BioPlex analysis revealed platelet-derived growth factor 2 B subunits, interleukin-6, interleukin-8, and tumor necrosis factor-α were elevated in spinal unit segments and the interleukin-1β levels correlated significantly with the intensity of low backache. Our findings did not support the adjacent segment disease theory. However, later development of these changes could not be excluded. The cytokines, chemokines, and growth factors play a significant role in DSL pathogenesis and symptoms.