High-frequency, low-magnitude vibration does not prevent bone loss resulting from muscle disuse in mice following botulinum toxin injection.
High-frequency, low-magnitude vibration does not prevent bone loss resulting from muscle disuse in mice following botulinum toxin injection.
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DOI：
10.1371/journal.pone.0036486
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Boyd SK
中科院分区：
文献类型：
--
作者：
Manske SL;Good CA;Zernicke RF;Boyd SK
高频率、低幅度的振动表面上通过模仿正常的姿势肌肉活动来增强骨形成。我们通过研究每天暴露于低强度振动（VIB）是否会维持A型肉毒杆菌毒素（BTX）肌肉废用模型中的骨骼来验证这一假设。将雌性16-18周龄BALB/c小鼠（N = 36）分配至BTX-VIB、BTX-SHAM、VIB或SHAM。 向BTX小鼠的左后肢后部肌肉组织注射BTX（20 µL; 1 U/100 g体重）。所有小鼠麻醉20 min/d，5 d/wk，持续3 wk，左腿固定在保持器上。通过保持器，VIB小鼠接受45 Hz，±0.6 g的正弦加速度而不负重。SHAM小鼠不接受振动。在基线和3周时，通过体内micro-CT评估肌肉横截面积（MCSA）和胫骨骨特性（骨骺、干骺端和骨干）。BTX-VIB组和BTX-SHAM组干骺端骨体积分数分别降低12±9%和7±6%，而VIB组和SHAM组干骺端骨体积分数升高。BTX-VIB和BTX之间以及VIB和SHAM之间的动态组织形态计量学结果没有差异。因此，振动并不能防止肌肉活动迅速下降引起的骨质流失，也不能对正常小鼠产生合成代谢作用。每日负荷持续时间短于姿势性肌肉活动的预期，可能不足以防止骨丢失。基于本研究中使用的方法，在BTX诱导的肌肉活动不存在的情况下，振动不能防止骨丢失。
High-frequency, low-magnitude vibration enhances bone formation ostensibly by mimicking normal postural muscle activity. We tested this hypothesis by examining whether daily exposure to low-magnitude vibration (VIB) would maintain bone in a muscle disuse model with botulinum toxin type A (BTX). Female 16–18 wk old BALB/c mice (N = 36) were assigned to BTX-VIB, BTX-SHAM, VIB, or SHAM. BTX mice were injected with BTX (20 µL; 1 U/100 g body mass) into the left hindlimb posterior musculature. All mice were anaesthetized for 20 min/d, 5 d/wk, for 3 wk, and the left leg mounted to a holder. Through the holder, VIB mice received 45 Hz, ±0.6 g sinusoidal acceleration without weight bearing. SHAM mice received no vibration. At baseline and 3 wk, muscle cross-sectional area (MCSA) and tibial bone properties (epiphysis, metaphysis and diaphysis) were assessed by in vivo micro-CT. Bone volume fraction in the metaphysis decreased 12±9% and 7±6% in BTX-VIB and BTX-SHAM, but increased in the VIB and SHAM. There were no differences in dynamic histomorphometry outcomes between BTX-VIB and BTX nor between VIB and SHAM. Thus, vibration did not prevent bone loss induced by a rapid decline in muscle activity nor produce an anabolic effect in normal mice. The daily loading duration was shorter than would be expected from postural muscle activity, and may have been insufficient to prevent bone loss. Based on the approach used in this study, vibration does not prevent bone loss in the absence of muscle activity induced by BTX.
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