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Stepwise reduction experiment reveals POLC as primary passive stabilizer in lumbar spine during flexion, suggesting surgical disruption may lead to instability.
In full spinal flexion, paraspinal muscle activity is minimal, suggesting that passive structures, particularly the posterior osteoligamentous complex (POLC), are crucial for spinal stability. The POLC comprises interspinous and supraspinous ligaments and spinous processes, which are often resected or impaired during spinal decompression procedures. However, the biomechanical consequences of POLC disruption remain poorly understood. We conducted a stepwise reduction experiment using three fresh frozen cadaveric torsi (age range: 30–78 years). Using a custom setup restricting motion to the sagittal plane, specimens were preloaded and locked in full flexion. Sequential resection of posterior lumbar structures was performed in the following order: skin, fascia, musculature, posterior ligamentous complex, facet joints, laminae, and posterior longitudinal ligaments. Load cells monitored force changes on the fixation frame following each resection step. Sequential increases in load were observed with each resection, indicating load transfer from resected passive structures to the fixation frame. The POLC (supraspinous and interspinous ligaments at L2-L5) provided the dominant contribution to passive load resistance in full flexion, accounting for 69–74% of the total measured resistance. Facet joints and their capsules contributed 10–18%, while muscular tissue contribution was minimal (<2%). This study demonstrates that the POLC serves as the primary passive stabilizer in the fully flexed lumbar spine. Surgical disruption of this complex may result in load redistribution and increased stress on remaining spinal structures, potentially contributing to spinal instability, accelerated degenerative changes, and compromised long-term clinical outcomes.
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Jokeit et al. (2025) studied this question.
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