Cortical tibial bone volume in two strains of mice: effects of sciatic neurectomy and genetic regulation of bone response to mechanical loading.

Cortical tibial bone volume in two strains of mice: effects of sciatic neurectomy and genetic regulation of bone response to mechanical loading.
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DOI:
10.1016/s8756-3282(99)00155-6
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发表时间:
1999-08
期刊:
影响因子:
4.1
通讯作者:
Y. Kodama;H. Dimai;J. Wergedal;M. Sheng;R. Malpe;Š. Kutílek;W.G Beamer;L. Donahue;C.J Rosen;D. J. Baylink;John R. Farley
Y. Kodama;H. Dimai;J. Wergedal;M. Sheng;R. Malpe;Š. Kutílek;W.G Beamer;L. Donahue;C.J Rosen;D. J. Baylink;John R. Farley
中科院分区:
医学2区
文献类型:
--
作者:
Y. Kodama;H. Dimai;J. Wergedal;M. Sheng;R. Malpe;Š. Kutílek;W.G Beamer;L. Donahue;C.J Rosen;D. J. Baylink;John R. Farley

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尽管C3H/HeJ (C3H)和C57BL/6J (B6)小鼠的体型(和成年体重)相似,骨骼外形尺寸也相似,但C3H小鼠的峰值骨密度高于B6小鼠(例如,股骨峰值骨密度比B6小鼠高53%)。目前的研究旨在评估机械加载/卸载作为这些近交系小鼠之间骨密度差异的可能决定因素的作用,特别是评估坐骨神经切除术对雌性C3H和B6小鼠胫骨骨形成和吸收的组织形态学指标的影响。每组10只小鼠进行左侧坐骨神经切除术(左后肢固定)或假手术。每只小鼠的对侧(右)腿作为对照。固定4周后,两种小鼠的骨形成指标均未发生系统性变化(即血清碱性磷酸酶和血清骨钙素均未发生变化)。然而,在胫腓连接处的组织形态学评估显示,4周的固定导致B6小鼠骨内骨形成周长的时间依赖性减少(例如,4周时,14%的对照单标记,未侵蚀表面,p < 0.005),同时骨内骨吸收周长增加(即,424%的对照侵蚀表面,p < 0.005)。这些作用与B6小鼠该部位的髓质面积增加(为对照组的132%,p < 0.05)有关。C3组小鼠胫骨的反应模式有所不同——骨形成周长减少幅度小得多(4周时为对照组的88%,p < 0.05),骨吸收周长没有增加,髓质面积也没有变化。在胫骨近端,在第二个横断面取样点也观察到类似的效果。综上所述,这些发现表明B6小鼠比C3H小鼠对后肢固定化后的骨内丢失更敏感。
Although C3H/HeJ (C3H) and C57BL/6J (B6) mice are similar in body size (and adult weight), and have bones of similar external size, C3H mice have higher peak bone densities than B6 mice (e.g., 53% higher peak bone density in the femora). The current studies were intended to assess the role of mechanical loading/unloading as a possible determinant of the bone density difference between these inbred strains of mice and, specifically, to assess the effect of sciatic neurectomy on histomorphometric indices of bone formation and resorption in the tibiae of female C3H and B6 mice. Groups of 10 mice of each strain were subjected to left-side sciatic neurectomy (left hindlimb immobilization) or a sham procedure. The contralateral (right) legs of each mouse were used as controls. Four weeks of immobilization produced no systemic changes in bone formation indices in either strain of mice (i.e., no change in serum alkaline phosphatase or serum osteocalcin). However, histomorphometric assessments at the tibiofibular junction showed that 4 weeks of immobilization caused a time-dependent decrease in the length of the endosteal bone forming perimeter (e.g., 14% of control single-labeled, noneroded surface at 4 weeks, p < 0.005) with a concomitant increase in the length of the endosteal bone resorbing perimeter (i.e., 424% of control eroded surface at 4 weeks, p < 0.005), in the B6 mice. These effects were associated with an increase in medullary area (132% of control, p < 0.05) at this site, in the B6 mice. The pattern of response was different in the tibiae of the C3 mice—a much smaller decrease in bone forming perimeter (88% of control at 4 weeks, p < 0.05), with no associated increase in bone resorbing perimeter, and no change in medullary area. Similar effects were seen at a second cross-sectional sampling site, in the proximal tibia. Together, these findings indicate that B6 mice are more sensitive to endosteal bone loss from hindlimb immobilization than C3H mice.