Bone and skeletal muscle loss after SCI

SCI 后骨和骨骼肌损失

基本信息

批准号：
6621335
负责人：
GARY A. DUDLEY
金额：
$ 7.02万
依托单位：
UNIVERSITY OF GEORGIA
依托单位国家：
美国
项目类别：
财政年份：
2002
资助国家：
美国
起止时间：
2002-02-01 至 2005-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/6621335
关键词：
atrophy bone density electrostimulus femur human subject human therapy evaluation magnetic resonance imaging musculoskeletal disorder therapy patient oriented research spinal cord injury striated muscles substantia spongiosa technology /technique development tibia

项目摘要

DESCRIPTION (provided by applicant): Loss of motor function in the lower limbs following spinal cord injury (SCI) results in a rapid reduction in bone mineral density (BMD), especially in trabecular regions, and a subsequent 5 to 23 fold increase in fracture risk. While BMD is currently the best in vivo surrogate for fracture risk widely available, knowledge of trabecular bone microarchitecture could explain substantial overlap in BMD observed in those who do and do not experience skeletal fracture. The PIs hypothesize that within one year of SCI trabecular bone microarchitecture will be impaired in the distal femur and proximal tibia - two common fracture sites. Irrespective of changes in trabecular bone microarchitecture, interventions that prevent rapid bone loss and reduce fracture incidence are needed. Because of the coordinating actions of skeletal muscle and bone, activities that promote skeletal muscle hypertrophy likely promote bone gain. This notion is supported by studies that demonstrate concomitant gains in muscle and bone following resistance training in able-bodied individuals. In clinically complete SCI patients, it has been recently shown that 8 weeks of electromyostimulation (EMS), which evoked high force contractions (simulatating resistance training), reversed the marked decrement of lower limb muscle evident 46 weeks after injury. Whether or not this novel application of EMS can also halt or reverse SCI-induced bone loss has not been determined. The PIs hypothesize that EMS evoked dynamic knee extension exercise will halt deterioration of trabecular bone microarchitecture and increase BMD, bone mineral content (BMC) and muscle mass in the lower limbs after SCI. To test these hypotheses, clinically complete SCI patients will be studied for 6 months starting 3 to 5 months after injury . The Specific Aims of this project are: 1) to determine if trabecular bone microarchitecture is compromised in the distal femur and proximal tibia after SCI; and 2) to determine if EMS evoked knee extension exercise has a positive impact on trabecular bone microarchitecture, BMD, BMC and muscle mass in the lower limbs after SCI. The significance of this research is that it will increase our current understanding of bone biology and potentially result in a novel application of EMS to control bone and muscle loss after SCI, both important secondary complications after injury.

描述（由申请人提供）：下肢运动功能丧失脊髓损伤（SCI）后的四肢会导致骨量迅速减少矿物质密度 (BMD)，特别是在小梁区域，以及随后的 5 至骨折风险增加 23 倍。而BMD是目前体内最好的广泛使用的骨折风险替代指标，骨小梁知识微结构可以解释在那些观察到的 BMD 的大量重叠谁经历过或没有经历过骨骼骨折。 PI 假设 SCI 后一年内，骨小梁微结构将受损股骨远端和胫骨近端——两个常见的骨折部位。不顾一切骨小梁微结构的变化，预防的干预措施需要快速骨质流失并减少骨折发生率。因为协调骨骼肌和骨骼的活动，促进骨骼肌肥大可能会促进骨增加。这个概念是得到证明肌肉和骨骼同时增长的研究的支持对身体健全的人进行阻力训练后。在临床上完全 SCI 患者，最近显示，8 周电肌刺激（EMS），引起强力收缩（模拟阻力训练），扭转了较低的明显下降受伤后 46 周肢体肌肉明显。不管这本小说应用 EMS 还可以阻止或逆转 SCI 引起的骨质流失，但尚未有研究证实决定。 PI 假设 EMS 引起动态膝关节伸展运动会阻止骨小梁微结构的恶化增加下肢 BMD、骨矿物质含量 (BMC) 和肌肉质量 SCI之后。为了检验这些假设，临床上完整的 SCI 患者将被研究从受伤后3至5个月开始，为期6个月。具体目标该项目的主要内容是： 1) 确定骨小梁微结构是否 SCI 后股骨远端和胫骨近端受损； 2) 到确定 EMS 诱发膝关节伸展运动是否对下肢骨小梁微结构、BMD、BMC 和肌肉质量 SCI之后。这项研究的意义在于它将提高我们的目前对骨生物学的理解并可能产生一种新颖的应用 EMS 控制 SCI 后骨质和肌肉损失，两者都很重要损伤后继发并发症。