Low-magnitude mechanical signals that stimulate bone formation in the ovariectomized rat are dependent on the applied frequency but not on the strain magnitude

被引:226
作者
Judex, Stefan [1 ]
Lei, Xin [1 ]
Han, Daniel [1 ]
Rubin, Clinton [1 ]
机构
[1] SUNY Stony Brook, Dept Biomed Engn, Stony Brook, NY 11794 USA
关键词
trabecular bone; ovariectomy; strain frequency; mechanical stimuli; bone formation; osteoporosis; bone strain; anabolic; skeleton; osteogenic; strain magnitude;
D O I
10.1016/j.jbiomech.2006.05.014
中图分类号
Q6 [生物物理学];
学科分类号
071011 [生物物理学];
摘要
There is growing evidence that extremely small mechanical signals, if applied at a sufficiently high frequency, can serve as anabolic signals to bone tissue. To determine if the responsiveness of bone to low-magnitude, high-frequency parameters is modulated by endocrine imbalance, ovariectomized (OVX) Sprague-Dawley rats were subjected to whole body vibrations (WBV, 0.15 g) at 45 Hz (n = 6) or 90 Hz (n = 6) for 10 min/day, and compared to OVX age-matched controls (it = 6). Five additional rats were used, in vivo, to establish the induced bone surface strain magnitudes (and strain rates). Following a 28 d protocol, bone formation rates in the metaphysis of the proximal tibia were 159% greater in 90 Hz rats when compared to age-matched controls, but 45 Hz rats were not significantly different from controls. Bone morphology of 90 Hz rats indicated significant], greater trabecular bone volume (22% and 25%) and thicker trabeculae (11% and 12%) over either controls or 45 Hz rats in the epiphysis of the distal femur, respectively. Despite the enhanced sensitivity of the skeleton towards the 90 Hz signal, the strain magnitudes and strain rates induced by this frequency were significantly lower than during 45 Hz vibration, suggesting that factors other than matrix strain are driving the anabolic response. Ideally, such mechanical signals represent a non-pharmacologic means of controlling bone mass and morphology in spite of systemic pressures for bone resorption. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1333 / 1339
页数:7
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