Rheumatic Diseases Core Center

病理性脊椎骨折会导致大量小梁骨缺乏症患者的疼痛和残疾。增加癌症患者的预期寿命，允许骨转移和骨髓瘤进展，以及普通人群的老龄化，预计将导致高危人群的显着增加。我们假设，缺乏准确和可靠的病理性椎体骨折风险的临床预测指标是由于缺乏对潜在机制的了解。我们进一步假设，潜在的机制是在松质骨中积累了临界水平的损伤(微裂纹)。第三，我们假设在弥漫性骨丢失和局灶性骨丢失中损伤累积过程是不同的，导致在给定的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并更好地处理病理性脊椎骨折的临床问题。作为第一步，我们建议建立一个有限元分析(FEA)模型来研究椎体松质骨的损伤累积过程。我们将开发一个包含损伤效应的松质骨行为模型，其材料参数来自于椎骨标本的循环蠕变试验。该材料模型将在有限元模型中实现，以预测椎体松质骨标本对引导(拉伸、压缩、扭转)的响应。这些预测将与脊椎小梁标本的力学测试的实验结果进行比较。“病理”条件将使用有限元模型的“高”或“低”的密度和圆柱形的骨溶解缺陷的加载。具有“高”和“低”表观密度和模拟缺陷的试件的机械测试将被用来检验分析预测。这些损伤累积对椎体松质骨材料行为影响的检测将为椎体松质骨的材料行为提供重要的信息。更重要的是，它将为进一步研究解释骨小梁充分性的非侵入性临床测量以确定病理性脊柱骨折的长期可能性这一总体目标提供基础。

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.