Cancel Mathilde, Grimard Guy, Thuillard-Crisinel Delphine, Moldovan Florina, Villemure Isabelle
Department of Mechanical Engineering, Ecole Polytechnique de Montréal, P.O. Box 6079, Station Centre-Ville, Montréal, Québec, Canada H3C 3A7.
Bone. 2009 Feb;44(2):306-15. doi: 10.1016/j.bone.2008.09.005. Epub 2008 Sep 24.
Mechanical loads are essential to normal bone growth, but excessive loads can lead to progressive deformities. In addition, growth plate extracellular matrix remodelling is essential to regulate the normal longitudinal bone growth process and to ensure physiological bone mineralization. In order to investigate the effects of static compression on growth plate extracellular matrix using an in vivo animal model, a loading device was used to precisely apply a compressive stress of 0.2 MPa for two weeks on the seventh caudal vertebra (Cd7) of rats during the pubertal growth spurt. Control, sham and loaded groups were studied. Growth modulation was quantified based on calcein labelling, and three matrix components (type II and X collagens, and aggrecan) were assessed using immunohistochemistry/safranin-O staining. As well, extracellular matrix components and enzymes (MMP-3 and -13, ADAMTS-4 and -5) were studied by qRT-PCR. Loading reduced Cd7 growth by 29% (p<0.05) and 15% (p=0.07) when compared to controls and shams respectively. No significant change could be observed in the mRNA expression of collagens and the proteolytic enzyme MMP-13. However, MMP-3 was significantly increased in the loaded group as compared to the control group (p<0.05). No change was observed in aggrecan and ADAMTS-4 and -5 expression. Low immunostaining for type II and X collagens was observed in 83% of the loaded rats as compared to the control rats. This in vivo study shows that, during pubertal growth spurt, two-week static compression reduced caudal vertebrae growth rates; this mechanical growth modulation occurred with decreased type II and X collagen proteins in the growth plate.
机械负荷对正常骨骼生长至关重要，但负荷过大可导致进行性畸形。此外，生长板细胞外基质重塑对于调节正常的纵向骨骼生长过程和确保生理性骨矿化至关重要。为了使用体内动物模型研究静态压缩对生长板细胞外基质的影响，在青春期生长突增期间，使用加载装置对大鼠的第七尾椎（Cd7）精确施加0.2 MPa的压缩应力，持续两周。对对照组、假手术组和加载组进行了研究。基于钙黄绿素标记对生长调节进行量化，并使用免疫组织化学/番红O染色评估三种基质成分（II型和X型胶原蛋白以及聚集蛋白聚糖）。此外，通过qRT-PCR研究细胞外基质成分和酶（MMP-3和-13、ADAMTS-4和-5）。与对照组和假手术组相比，加载分别使Cd7生长降低了29%（p<0.05）和15%（p=0.07）。胶原蛋白和蛋白水解酶MMP-13的mRNA表达未观察到显著变化。然而，与对照组相比，加载组中MMP-3显著增加（p<0.05）。聚集蛋白聚糖以及ADAMTS-4和-5的表达未观察到变化。与对照大鼠相比，83%的加载大鼠中观察到II型和X型胶原蛋白的低免疫染色。这项体内研究表明，在青春期生长突增期间，两周的静态压缩降低了尾椎生长速率；这种机械生长调节伴随着生长板中II型和X型胶原蛋白的减少而发生。
