DAMAGE AND PATHOLOGIC FRACTURE IN VERTEBRAL BODIES

病理性椎体骨折导致疼痛和残疾的大量患者与骨小梁缺乏症。癌症患者的预期寿命增加，导致骨骼转移和骨髓瘤进展以及一般人群的老龄化，预计将导致高危人群的显着增加。我们假设缺乏准确可靠的病理性椎骨骨折风险的临床预测因素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小梁骨中积累了临界水平的损伤（微裂）。第三，我们假设弥漫性骨损失和局灶性骨损失的损伤积累过程不同，导致在给定骨量损失下的不同骨折风险水平。我们的长期目标是更好地理解并因此更好地处理病理性椎体骨折的临床问题。作为第一步，我们建议建立一个有限元分析（FEA）模型来研究椎小骨的损伤积累过程。我们将开发一个小梁骨行为模型，包括从椎骨标本的循环蠕变试验中得出的材料参数的损伤效应。该材料模型将在FEA模型中实现，以预测椎小梁骨标本对牵引（张力，压缩，扭转）的响应。这些预测将与脊椎小梁标本力学测试的实验结果进行比较。“病理”条件将使用具有“高”或“低”密度和圆柱形骨溶解缺陷的标本在加载下的有限元模型进行研究。具有“高”和“低”表观密度和受激缺陷的试样的力学试验将用于检验分析预测。这些损伤累积对椎体骨小梁材料行为影响的研究将提供有关椎体骨小梁行为的重要信息。更重要的是，它将为进一步研究提供基础，以实现解释小梁骨充足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.