Rheumatic Diseases Core Center

病理性椎体骨折导致大量骨小梁缺损患者的疼痛和残疾。癌症患者预期寿命的增加，允许骨转移和骨髓瘤进展以及一般人群的老龄化，预计将导致风险人群的显著增加。我们推测，缺乏准确可靠的病理椎骨骨折风险的临床预测是由于缺乏对潜在机制的理解。我们进一步假设，潜在的机制是在骨小梁中累积临界水平的损伤（微裂纹）。第三，我们假设损伤累积过程在弥漫性骨丢失与局灶性骨丢失中是不同的，导致在给定骨量丢失时不同程度的骨折风险。我们的长期目标是更好地了解和更好地管理病理性椎体骨折的临床问题。作为第一步，我们建议开发一个有限元分析（FEA）模型，以调查在椎体松质骨的损伤累积过程。我们将建立一个骨小梁行为的模型，包括损伤效应和来自椎骨样本循环蠕变试验的材料参数。该材料模型将在FEA模型中实施，以预测椎体松质骨样本对引导（拉伸、压缩、扭转）的反应。这些预测将与椎骨小梁标本的力学测试的实验结果进行比较。将使用具有“高”或“低”密度和圆柱形溶骨性缺损的样本在载荷下的FEA模型研究“病理”条件。将使用具有“高”和“低”表观密度和刺激缺陷的试样的机械测试来检查分析预测。研究损伤累积对脊柱松质骨材料行为的影响，将为松质骨的力学行为提供重要的信息。更重要的是，它将为进一步研究提供基础，以实现解释骨小梁充分性的非侵入性临床测量的总体目标，以确定病理性椎体骨折的长期可能性。

Pathologic vertebral fractures result in pain and disability in a large population of patients with trabacular bone deficiencies. Increasing life expectancy of cancer patients allowing skeletal metastatic and myeloma progression and aging of the general population is expected to lead to a significant increase in the at risk population. We hypothesize that the lack of accurate and reliable clinical predictors of fracture risk in pathologic vertebrae is due to a lack of understanding of the underlying mechanisms. We further hypothesize that the underlying mechanism is the accumulation of a critical level of damage (microcracking) in trabecular bone. Thirdly, we hypothesize that the damage accumulation process is different in diffuse loss of bone versus focal loss of bone, leading to different levels of fracture risk at a given loss of bone mass. Our long term goal is to better understand and thereby better manage the clinical problem of pathologic vertebral fractures. As a first step, we propose to develop a Finite Element Analysis (FEA) model to investigate the damage accumulation process in vertebral trabacular bone. We will develop a model of trabecular bone behavior including damaging effects with material parameters derived from cyclic creep tests of vertebral bone specimens. This material model will be implemented within a FEA model to predict the response of vertebral trabecular bone specimens to leading (tension, compression, torsion). These predictions will be compared with experimental results from mechanical tests of vertebral trabecular specimens. "Pathologic" conditions will be investigated using FEA models of specimens with "high" or "low" densities and cylindrical osteolytic defects under loading. Mechanical testing of specimens with "high" and "low" apparent densities and stimulated defects will be used to examine the analytical predictions. These examinations of the effects of damage accumulation on the material behavior of vertebral trabacular bone will provide significant information on trabacular bone behavior. More importantly, it will provide the basis for further investigations towards the overall goal of interpreting non-invasive clinical measures of trabecular bone adequacy to determine long-term likelihood of pathologic vertebral fracture.