AUGMENTATION OF TRABECULAR BONE BY LOW MAGNITUDE STRAIN

这个实验室的初步工作表明，极低的 大小(&lt；30微应变)机械信号可以是成骨的，如果 应用于高频(5至50赫兹)。如此高频率的低频 大小应变是骨骼应变的重要组成部分 历史表明，这些机械事件可能代表着 骨骼形态的重要决定因素。我们假设很小 高频负载增加，以非侵入性方式引入 骨骼通过振动，会刺激骨量的增加而不会 牺牲骨骼质量。考虑到这些压力水平远远低于 (&lt；1/100)那些可能对组织造成损害的，我们相信这些 Signals作为一种机械预防骨量减少症的方法具有巨大的潜力。 使用骨骼成熟的绵羊，随机、部分5x4x3因子 实验设计，评估频率(7.5、15、30、60或120赫兹)， 持续时间(5、10、20或40分钟)和强度(0.1、0.2或0.4g)将为 用于确定非侵入性机械装置的疗效 增加胫骨和股骨的骨小梁。一系列体内和 体外方案将被用来量化这12个人的能力 进行一个月的机械干预，以影响骨量和骨形态。 双能x射线吸收测量法将确定密度的变化 时间的函数，动态和静态的组织形态计量学将量化 站点-响应的专一性、质量和程度，以及机械性 测试将被用来确定这种治疗是否影响力量 和骨骼处理区域的硬度。最后，最重要的 成骨机械信号将被用来确定骨密度， 在骨质疏松的骨骼中可以恢复强度和刚度。 这些实验可能会对这种机制产生新的见解。 力学因素控制着骨骼的形态，也导致了一种新的 治疗骨质疏松症。

Preliminary work in this laboratory has demonstrated that extremely low magnitude (<30 Microstrain) mechanical signals can be osteogenic if applied at a high frequency (5 to 50 Hz). Such high frequency low magnitude strains comprise an important constituent of a bone's strain history, suggesting that these mechanical events could represent a significant determinant of bone morphology. We hypothesize that small increases in high frequency loading, introduced non-invasively into the skeleton via vibration, will stimulate an increase in bone mass without sacrificing bone quality. Considering these strain levels are well below (<1/100th) those which may cause damage to the tissue, we believe these signals hold great potential as a mechanical prophylaxis for osteopenia. Using skeletally mature sheep, a randomized, partial 5x4x3 factorial experimental design, evaluating frequency (7.5, 15, 30, 60 or 120 Hz), duration (5, 10, 20 or 40 min), and intensity (0.1, 0.2 or 0.4g) will be used to determine the efficacy of a non-invasive mechanical device to augment the trabeculae of the tibia and femur. A series of in vivo and ex vivo protocols will be used to quantify the ability of this twelve month mechanical intervention to affect both bone mass and morphology. Dual energy x-ray absorptiometry will determine changes in density as a function of time, dynamic and static histomorphometry will quantify the site-specificity, quality, and extent of the response, and mechanical testing will be used to determine if this treatment influences strength and stiffness of the treated regions of the skeleton. Finally, the most osteogenic mechanical signals will be used to determine if bone density, strength, and stiffness can be recovered in the osteopenic skeleton. These experiments may yield new insights into the mechanisms by which mechanical factors control bone morphology, as well as lead to a novel treatment for osteoporosis.