STUDY DESIGN: Finite element study. OBJECTIVE: To analyze the effects of posterior shear loads, disc degeneration, and the combination of both on spinal torsion stiffness. SUMMARY OF BACKGROUND DATA: Scoliosis is a 3-dimensional deformity of the spine that presents itself mainly in adolescent girls and elderly patients. Our concept of its etiopathogenesis is that an excess of posteriorly directed shear loads, relative to the body's intrinsic stabilizing mechanisms, induces a torsional instability of the spine, making it vulnerable to scoliosis. Our hypothesis for the elderly spine is that disc degeneration compromises the stabilizing mechanisms. METHODS: In an adult lumbar motion segment model, the disc properties were varied to simulate different aspects of disc degeneration. These models were then loaded with a pure torsion moment in combination with either a shear load in posterior direction, no shear, or a shear load in anterior direction. RESULTS: Posteriorly directed shear loads reduced torsion stiffness, anteriorly directed shear loads increased torsion stiffness. These effects were mainly caused by a later (respectively earlier) onset of facet joint contact. Disc degeneration cases with a decreased disc height that leads to slackness of the annular fibers and ligaments caused a significantly decreased torsional stiffness. The combination of this stage with posterior shear loading reduced the torsion stiffness to less than half the stiffness of a healthy disc without shear loads. The end stage of disc degeneration increased torsion stiffness again. CONCLUSION: The combination of a decreased disc height, that leads to slack annular fibers and ligaments, and posterior shear loads very significantly affects torsional stiffness: reduced to less than half the stiffness of a healthy disc without shear loads. Disc degeneration, thus, indeed compromises the stabilizing mechanisms of the elderly spine. A combination with posteriorly directed shear loads could then make it vulnerable to scoliosis. LEVEL OF EVIDENCE: N/A.
STUDY DESIGN: Finite element study. OBJECTIVE: To analyze the effects of posterior shear loads, disc degeneration, and the combination of both on spinal torsion stiffness. SUMMARY OF BACKGROUND DATA: Scoliosis is a 3-dimensional deformity of the spine that presents itself mainly in adolescent girls and elderly patients. Our concept of its etiopathogenesis is that an excess of posteriorly directed shear loads, relative to the body's intrinsic stabilizing mechanisms, induces a torsional instability of the spine, making it vulnerable to scoliosis. Our hypothesis for the elderly spine is that disc degeneration compromises the stabilizing mechanisms. METHODS: In an adult lumbar motion segment model, the disc properties were varied to simulate different aspects of disc degeneration. These models were then loaded with a pure torsion moment in combination with either a shear load in posterior direction, no shear, or a shear load in anterior direction. RESULTS: Posteriorly directed shear loads reduced torsion stiffness, anteriorly directed shear loads increased torsion stiffness. These effects were mainly caused by a later (respectively earlier) onset of facet joint contact. Disc degeneration cases with a decreased disc height that leads to slackness of the annular fibers and ligaments caused a significantly decreased torsional stiffness. The combination of this stage with posterior shear loading reduced the torsion stiffness to less than half the stiffness of a healthy disc without shear loads. The end stage of disc degeneration increased torsion stiffness again. CONCLUSION: The combination of a decreased disc height, that leads to slack annular fibers and ligaments, and posterior shear loads very significantly affects torsional stiffness: reduced to less than half the stiffness of a healthy disc without shear loads. Disc degeneration, thus, indeed compromises the stabilizing mechanisms of the elderly spine. A combination with posteriorly directed shear loads could then make it vulnerable to scoliosis. LEVEL OF EVIDENCE: N/A.
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