The Journal of Bone and Joint Surgery, Vol 60, Issue 5 630-639, Copyright © 1978 by Journal of Bone and Joint Surgery, Inc
The role of mitochondria in growth plate calcification as demonstrated in a rachitic model
CT Brighton and RM Hunt
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.
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