Parathyroid hormone and calcitonin interactions in bone: Irradiation-induced inhibition of escape in vitro

• Published in: Calcified tissue international Vol. 34; no. 1; pp. 197 - 203
• Main Authors: Krieger, Nancy S., Feldman, Roy S., Tashjian, Armen H.
• Format: Journal Article
• Language: English
• Published: 01-12-1982
• ISSN: 0171-967X; 1432-0827
• DOI: 10.1007/BF02411233

Calcitonin (CT) inhibits hormonally stimulated bone resorption only transiently in vitro. This phenomenon has been termed "escape," but the mechanism for the effect is not understood. One possible explanation is that bone cell differentiation and recruitment of specific precursor cells, in response to stimulators of resorption, lead to the appearance of osteoclasts that are unresponsive to CT. To test this hypothesis, cell proliferation in neonatal mouse calvaria in organ culture was inhibited by irradiation from a cobalt-60 source. At a dose of 6000 R, ( super(3)H)thymidine incorporation into intact calvaria was nhibited approximately 90%. Irradiation had no effect on the resorptive response to 0.1 U/ml parathyroid hormone (PTH). However, irradiation induced a dose-dependent inhibition of the escape response which was maximal at 6000 R. A dose of 6000 R did not affect the binding of super(125)I-salmon CT to calvaria and decreased PTH stimulation of cyclic AMP release from bone without affecting the cyclic AMP response to CT.