Frontiers in bioengineering and biotechnology · 2026
Biomechanical analysis of T10-T11 vertebrae under the combined effects of osteoporosis and L4 spondylolisthesis: a finite element analysis based on computed tomography.
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Yang Zhizhou, Lian Xiaowei, Wang Yunsheng, Xiong Xiao, Wang Zimo, Wang Linfeng, Wang Xiaobin, Wang Feng
Аннотация
AIMS: Osteoporotic vertebral compression fractures are common; however, the biomechanical link between L4 spondylolisthesis and non-adjacent thoracic fractures remains unclear. This study used 3D finite element (FE) analysis to assess the biomechanical effects of L4 spondylolisthesis and osteoporosis on T10-T11.
METHODS: Four FE models of T10-L5 were reconstructed from CT images of a healthy adult male: normal (A), isolated spondylolisthesis (B), isolated osteoporosis (C), and combined (D). A 500-N axial load and 10-N·m moments simulated six motions. Maximum von Mises stresses of whole vertebra and cancellous bone, and segmental ROM at T10-T11, were compared.
RESULTS: L4 spondylolisthesis alone increased T10-T11 ROM (4.5%-24.7%) and stress versus normal. Osteoporosis alone markedly raised T10 overall stress (+73.9%) and cancellous stress (+19.6%) during flexion. The combined model showed the worst deterioration: peak overall stress 59.07 MPa (flexion) and cancellous stress 1.06 MPa (lateral bending). Stress nephograms confirmed concentration at the anterocentral body and pedicles, with wider distribution and higher magnitudes in pathological models. The isolated spondylolisthesis effect on stress (0.4%-15.1%) was far smaller than osteoporosis alone, and combined elevation was predominantly driven by osteoporosis. Yet synergy was most pronounced in cancellous bone-the primary load-bearing structure-where combined effects exceeded the sum of individual ones by up to 7.6 percentage points, highlighting spondylolisthesis as a critical amplifier of fracture-relevant stress in osteoporotic vertebrae.
CONCLUSION: L4 spondylolisthesis moderately increases thoracic stress and ROM, but osteoporosis remains the main determinant of T10-T11 stress. Spondylolisthesis acts as a secondary modifier that synergistically amplifies cancellous bone stress beyond additive expectations once osteoporosis compromises vertebral strength. This synergy is the key biomechanical link between lumbar spondylolisthesis and the clinically observed rise in thoracic fracture risk. Osteoporosis worsens this effect, deteriorating the upper thoracic biomechanical environment and increasing susceptibility to secondary fractures. Clinically, concomitant lumbar spondylolisthesis in osteoporotic patients should be recognized as a key biomechanical marker for thoracic fracture risk.
METHODS: Four FE models of T10-L5 were reconstructed from CT images of a healthy adult male: normal (A), isolated spondylolisthesis (B), isolated osteoporosis (C), and combined (D). A 500-N axial load and 10-N·m moments simulated six motions. Maximum von Mises stresses of whole vertebra and cancellous bone, and segmental ROM at T10-T11, were compared.
RESULTS: L4 spondylolisthesis alone increased T10-T11 ROM (4.5%-24.7%) and stress versus normal. Osteoporosis alone markedly raised T10 overall stress (+73.9%) and cancellous stress (+19.6%) during flexion. The combined model showed the worst deterioration: peak overall stress 59.07 MPa (flexion) and cancellous stress 1.06 MPa (lateral bending). Stress nephograms confirmed concentration at the anterocentral body and pedicles, with wider distribution and higher magnitudes in pathological models. The isolated spondylolisthesis effect on stress (0.4%-15.1%) was far smaller than osteoporosis alone, and combined elevation was predominantly driven by osteoporosis. Yet synergy was most pronounced in cancellous bone-the primary load-bearing structure-where combined effects exceeded the sum of individual ones by up to 7.6 percentage points, highlighting spondylolisthesis as a critical amplifier of fracture-relevant stress in osteoporotic vertebrae.
CONCLUSION: L4 spondylolisthesis moderately increases thoracic stress and ROM, but osteoporosis remains the main determinant of T10-T11 stress. Spondylolisthesis acts as a secondary modifier that synergistically amplifies cancellous bone stress beyond additive expectations once osteoporosis compromises vertebral strength. This synergy is the key biomechanical link between lumbar spondylolisthesis and the clinically observed rise in thoracic fracture risk. Osteoporosis worsens this effect, deteriorating the upper thoracic biomechanical environment and increasing susceptibility to secondary fractures. Clinically, concomitant lumbar spondylolisthesis in osteoporotic patients should be recognized as a key biomechanical marker for thoracic fracture risk.