Ravosa Matthew J, Klopp Emily B, Pinchoff Jessie, Stock Stuart R, Hamrick Mark W
Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine, Columbia, Missouri 65212, USA.
J Morphol. 2007 Mar;268(3):275-82. doi: 10.1002/jmor.10517.
Compared with the normal or wild-type condition, knockout mice lacking myostatin (Mstn), a negative regulator of skeletal muscle growth, develop significant increases in relative masticatory muscle mass as well as the ability to generate higher maximal muscle forces. Wild-type and myostatin-deficient mice were compared to assess the postweaning influence of elevated masticatory loads because of increased jaw-adductor muscle and bite forces on the biomineralization of mandibular cortical bone and dental tissues. Microcomputed tomography (microCT) was used to quantify bone density at a series of equidistant external and internal sites in coronal sections for two symphysis and two corpus locations. Discriminant function analyses and nonparametric ANOVAs were used to characterize variation in biomineralization within and between loading cohorts. Multivariate analyses indicated that 95% of the myostatin-deficient mice and 95% of the normal mice could be distinguished based on biomineralization values at both symphysis and corpus sections. At the corpus, ANOVAs suggest that between-group differences are due to the tendency for cortical bone mineralization to be higher in myostatin-deficient mice, coupled with higher levels of dental biomineralization in normal mice. At the symphysis, ANOVAs indicate that between-group differences are related to significantly elevated bone-density levels along the articular surface and external cortical bone in the knockout mice. Both patterns, especially those for the symphysis, appear because of the postweaning effects of increased masticatory stresses in the knockout mice versus normal mice. The greater number of symphyseal differences suggest that bone along this jaw joint may be characterized by elevated plasticity. Significant differences in bone-density levels between normal and myostatin-deficient mice, coupled with the multivariate differences in patterns of plasticity between the corpus and symphysis, underscore the need for a comprehensive analysis of the plasticity of masticatory tissues vis-à-vis altered mechanical loads.
与正常或野生型情况相比,缺乏肌肉生长抑制素(Mstn,骨骼肌生长的负调节因子)的基因敲除小鼠,其咀嚼肌相对质量显著增加,产生最大肌肉力量的能力也显著增强。比较野生型和肌肉生长抑制素缺陷型小鼠,以评估由于咬肌和咬合力增加导致的咀嚼负荷升高对下颌皮质骨和牙齿组织生物矿化的断奶后影响。使用微型计算机断层扫描(microCT)对两个联合部位和两个体部位置的冠状切片中一系列等距的外部和内部位点的骨密度进行量化。判别函数分析和非参数方差分析用于描述负荷组内和组间生物矿化的变化。多变量分析表明,根据联合部位和体部切片的生物矿化值,可以区分95%的肌肉生长抑制素缺陷型小鼠和95%的正常小鼠。在体部,方差分析表明组间差异是由于肌肉生长抑制素缺陷型小鼠皮质骨矿化倾向较高,以及正常小鼠牙齿生物矿化水平较高。在联合部位,方差分析表明组间差异与基因敲除小鼠关节表面和外部皮质骨的骨密度水平显著升高有关。这两种模式,尤其是联合部位的模式,似乎是由于基因敲除小鼠与正常小鼠断奶后咀嚼应力增加的影响。联合部位更多的差异表明,该颌关节处的骨骼可能具有较高的可塑性。正常小鼠和肌肉生长抑制素缺陷型小鼠之间骨密度水平的显著差异,以及体部和联合部位之间可塑性模式的多变量差异,强调了需要全面分析咀嚼组织可塑性与机械负荷改变之间的关系。