Parathormone-stimulated resorption of devitalised bone by cultured osteoclast-type bone cells.

Abstract

WE recently reported the isolation from mouse calvaria of two different bone cell populations that express unique changes in metabolism when exposed in culture to parathormone and calcitonin1–3. In one cell type, termed CT, parathormone increased the synthesis of hyaluronate and the activity of acid phosphatase. In the second cell type, termed PT, parathormone inhibited citrate decarboxylation and decreased the activities of prolyl hydroxylase and alkaline phosphatase. Calcitonin blocked the effects of parathormone in the CT cells but not in the PT cells. Since the changes elicited in the separate populations by parathormone closely resembled those exhibited by calvaria maintained in organ culture4, it seemed probable that the isolated cells retained unique properties in culture that are characteristic of their function in the intact tissue. On the basis of these results the CT cells were provisionally identified as osteoclasts and the PT cells as osteoblasts3. The major physiological result of the action of parathormone on bone in vivo or in culture is resorption of the calcified extracellular matrix, so we evaluated this function in the isolated bone cells. Should either the CT or PT cells promote resorption in vitro, this would further demonstrate that they retain differentiated function in culture and would aid in establishing their identity. We describe here a procedure which allowed us to test for resorptive properties of our isolated bone cell populations. We found that parathormone markedly stimulated the capacity of CT, but not PT, cells to resorb a calcified bone matrix substrate—a property in keeping with the identification of the CT cells as osteoclasts.