Department of Kinesiology, University of Minnesota, Minneapolis, MN 55455, USA.
Neuromuscul Disord. 2011 Mar;21(3):183-93. doi: 10.1016/j.nmd.2010.12.002. Epub 2011 Jan 21.
The primary purpose of this study was to determine if tibial bone strength is compromised in dystrophic mice and if so, what geometric and material properties contribute. Results of three-point bending tests showed that tibia of mdx and dko (dystrophin- and utrophin-deficient) mice had up to 50% lower strength and stiffness compared to wild-type mice. Micro-computed tomography indicated that dystrophic tibia had reductions of 6-57% in cortical cross-sectional moment of inertia and cross-sectional area. Metaphyseal trabecular bone morphometry was also altered up to 78% in dystrophic mice. Bone-to-muscle functional ratios (i.e., three-point bending measures:muscle strength) indicated that bone strength was relatively high in 7-week-old dystrophic mice compared to muscle strength, but ratios were similar to wild-type mice by 24 months of age. Young dystrophic mice have compromised bone strength; these models may be useful for designing therapeutic regimens aimed at improving the skeleton.
本研究的主要目的是确定营养不良小鼠的胫骨骨强度是否受损，如果受损，哪些几何和材料特性会导致这种情况。三点弯曲试验的结果表明，mdx 和 dko（肌营养不良蛋白和 utrophin 缺乏）小鼠的胫骨强度和刚度比野生型小鼠低 50%。微计算机断层扫描表明，营养不良的胫骨的皮质横截面转动惯量和横截面面积减少了 6-57%。骺骨小梁骨形态计量学也发生了高达 78%的改变。骨-肌功能比（即三点弯曲测量：肌肉力量）表明，与肌肉力量相比，7 周龄营养不良小鼠的骨强度相对较高，但到 24 月龄时，与野生型小鼠相似。年轻的营养不良小鼠的骨强度受损；这些模型可能有助于设计旨在改善骨骼的治疗方案。
