Escape from Inhibition of Resorption in Cultures of Fetal Bone Treated with Calcitonin and Parathyroid Hormone

Initially calcitonin (CT) could completely inhibit the increase in bone resorption produced by parathyroid hormone (PTH) or 25-hydroxycholecalciferol (HCC) in fetal rat long bone shafts in tissue culture, but this effect was transient. After a period of inhibition varying from less than 36 hr to several days there was escape, that is, resorption began to increase despite the addition of fresh CT. This occurred with salmon calcitonin and human calcitonin as well as rat calcitonin at doses which were maximal or supramaximal for initial inhibition. Escape did not occur when spontaneous resorption in control untreated bones was blocked by CT, or when CT inhibited resorption produced by vitamin A, prostaglandin E, or dibutyryl- cyclic AMP. It was seen with calvaria as well as long bones stimulated with PTH. Escape could occur in the absence of PTH or 25-HCC if the bones were pretreated with maximal doses of these stimulators to induce resorption, and then treated with CT. Escape was prevented or delayed by decreasing the concentrations of calcium or phosphate in the medium. (Endocrinology90: 752, 1972)