Alkalay Ron N
Center for Advanced Orthopedic Studies, Department of Orthopedic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Clin Biomech (Bristol). 2015 Feb;30(2):121-8. doi: 10.1016/j.clinbiomech.2014.10.001. Epub 2014 Oct 12.
Pathologic vertebral fractures are associated with intractable pain, loss of function and high morbidity in patients with metastatic spine disease. However, the failure mechanisms of vertebrae with lytic defects and the failed vertebrae's ability to retain load carrying capacity remain unclear.
Eighteen human thoracic and lumbar vertebrae with simulated uncontained bone defects were tested under compression-bending loads to failure. Failure was defined as 50% reduction in vertebral body height. The vertebrae were allowed to recover under load and re-tested to failure using the initial criteria. Repeated measure ANOVA was used to test for changes in strength and stiffness parameters.
Vertebral failure occurred via buckling and fracture of the cortex around the defect, followed by collapse of the defect region. Compared to the intact vertebrae, the failed vertebrae exhibited a significant loss in compressive strength (59%, p<0.001), stiffness (53%, p<0.05) and flexion (70%, p<0.01) strength. Significant reduction in anterior-posterior shear (strength (63%, p<0.01) and stiffness (67%, p<0.01)) and lateral bending strength (134%, p<0.05) were similarly recorded. In the intact vertebrae, apart from flexion strength (r(2)=0.63), both compressive and anterior-posterior shear strengths were weakly correlated with their stiffness parameters (r(2)=0.24 and r(2)=0.31). By contrast, in the failed vertebrae, these parameters were strongly correlated, (r(2)=0.91, r(2)=0.86, and r(2)=0.92, p<0.001 respectively).
Failure of the vertebral cortex at the defect site dominated the initiation and progression of vertebral failure with the vertebrae failing via a consolidation process of the vertebral bone. Once failed, the vertebrae showed remarkable loss of load carrying capacity.
病理性椎体骨折与转移性脊柱疾病患者的顽固性疼痛、功能丧失及高发病率相关。然而，存在溶骨性缺损的椎体的失效机制以及失效椎体保持承载能力的能力仍不明确。
对18个模拟无包壳骨缺损的人胸椎和腰椎椎体进行压缩弯曲载荷试验直至失效。失效定义为椎体高度降低50%。让椎体在载荷下恢复，并使用初始标准重新测试直至失效。采用重复测量方差分析来检验强度和刚度参数的变化。
椎体失效通过缺损周围皮质的屈曲和骨折发生，随后缺损区域塌陷。与完整椎体相比，失效椎体的抗压强度（59%，p<0.001）、刚度（53%，p<0.05）和屈曲强度（70%，p<0.01）显著降低。前后剪切强度（63%，p<0.01）和刚度（67%，p<0.01）以及侧弯强度（134%，p<0.05）也有显著降低。在完整椎体中，除屈曲强度（r(2)=0.63）外，抗压强度和前后剪切强度与其刚度参数的相关性较弱（r(2)=0.24和r(2)=0.31）。相比之下，在失效椎体中，这些参数具有强相关性（分别为r(2)=0.91、r(2)=0.86和r(2)=0.92，p<0.001）。
缺损部位椎体皮质的失效主导了椎体失效的起始和进展，椎体通过椎骨的巩固过程而失效。一旦失效，椎体的承载能力会显著丧失。
