• Moritz Jokeit, Frédéric Cornaz, Jana F Schader, Cooper L Harshbarger, Anna-Katharina Calek, Sascha Jecklin, Jess G Snedeker, Mazda Farshad, and Jonas Widmer.
• Spine Biomechanics, Department of Orthopedics, Balgrist University Hospital, University of Zurich, Lengghalde 5, Zurich, CH-8008, Switzerland.
• Eur Spine J. 2025 Feb 6.

BackgroundDuring full flexion of the spine, the paraspinal muscles are largely inactive. This suggests that passive structures like the posterior osteoligamentous complex (POLC), consisting of interspinous and supraspinous ligaments and the spinous processes, play a key role in spinal stability and protection of the spinal column. The POLC, however, is often resected or damaged during spinal decompression surgeries, whereas the biomechanical implications of this resection or damage are not yet fully understood.MethodsA stepwise reduction study was performed on three fresh frozen cadaveric torsi (aged 30-78 years) using a custom setup which only allows sagittal plane motion. After preloading and locking in full flexion, the posterior lumbar structures were gradually resected in the following order: Skin, fascia, musculature, facet joints, ligamentum flavum, posterior ligamentous complex, and posterior longitudinal ligaments. Load cells measured force increase on the fixation frame after each resection step.ResultsThe load increased sequentially with each resection, demonstrating load transfer from the passive structures onto the fixation frame. The POLC, including the supraspinous and interspinous ligaments at L2-L5, accounted for 69 - 74% of the measured passive load resistance in full flexion, representing the largest contribution. Facet joints with their capsules contributed 10-18%, while muscular contributions were negligible (< 2%).ConclusionThe experiment indicates that the POLC is the primary passive stabilizer of the fully flexed lumbar spine. Surgical resection of this structure can redistribute loads and increase stresses on remaining spinal tissues, potentially leading to spinal instability, accelerated degeneration, and poor clinical long-term outcomes.© 2025. The Author(s).

6 keywords...

hide…