Brighton C T, Hunt R M
J Bone Joint Surg Am. 1978 Jul;60(5):630-9.
In a phosphate-vitamin D-deficiency rachitic model in rats, potassium pyroantimonate was employed as a histochemical stain for calcium at the ultrastructural level in the costochondral growth plates. In the control plates, there was a shift of calcium from an intracellular, mainly mitochondrial location in the top part of the zone of hypertrophic cells to an extracellular, mainly matrix-vesicle location in the bottom part of the zone of hypertrophic cells. In the rachitic plates, mitochondria and cell membranes throughout the bottom of the hypertrophic zone remained heavily loaded with calcium. After treatment with phosphate was started, the mitochondria and cell membranes at the bottom of the hypertrophic zone rapidly lost calcium and matrix calcification began. Thus, in the normal growth plate, matrix calcification begins at the level in the plate where mitochondria lose calcium; in rickets, the matrix does not calcify and mitochondria do not lose calcium; and in healing rickets, calcification begins in the matrix at the bottom of the hypertrophic zone as the mitochondria at that level lose calcium. These findings support the hypothesis that mitochondria play an important role in matrix calcification.
在大鼠的磷酸盐 - 维生素D缺乏性佝偻病模型中，焦锑酸钾被用作超微结构水平下肋软骨生长板中钙的组织化学染色剂。在对照生长板中，钙从肥大细胞区顶部细胞内（主要在线粒体）位置转移至肥大细胞区底部细胞外（主要在基质小泡）位置。在佝偻病生长板中，肥大区底部的线粒体和细胞膜仍大量负载钙。开始用磷酸盐治疗后，肥大区底部的线粒体和细胞膜迅速失去钙，基质钙化开始。因此，在正常生长板中，基质钙化始于线粒体失去钙的生长板水平；在佝偻病中，基质不钙化且线粒体不失去钙；而在愈合期佝偻病中，随着肥大区底部该水平的线粒体失去钙，基质钙化在该区域底部的基质中开始。这些发现支持线粒体在基质钙化中起重要作用这一假说。
