Inhibition by thyrocalcitonin of estrogen-induced bone resorption in the mouse pubic symphysis.
A specific local erosion of the medial edges of the pubic bones is induced by administration of estradiol cyclopentylpropionate (ECP) to thyroparathyroidectomized mice. This paper presents both histochemical and biochemical evidence that porcine thyrocalcitonin (TCT) inhibits this estrogen-mediated resorption of the pubic symphysis. A marked increase in osteoclasts with a resultant increase in demonstrable sites of acid phosphatase (AcP) activity was observed in serial sections of resorbing pubic symphyses from ECP-treated animals. Bioassay of excised pubic symphyses revealed a concomitant increase in AcP activity. When mice were treated with TCT in combination with ECP, a marked decrease in osteoclasts with a resultant decrease in demonstrable sites of AcP activity and inhibition of the resorption process occurred. The mouse pubic symphysis thus appears to offer a model for exploring cellular mechanisms by which TCT regulates bone metabolism.
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D001862:Bone Resorption / Q000187:drug effects*; D002116:Calcitonin / Q000494:pharmacology*; D004958:Estradiol / Q000494:pharmacology*; D004965:Estrogen Antagonists; D005260:Female; D006651:Histocytochemistry; D051379:Mice; D010010:Osteoclasts / Q000187:drug effects; D010053:Ovary / Q000502:physiology; D010280:Parathyroid Glands / Q000502:physiology; D011631:Pubic Symphysis / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D013961:Thyroid Gland / Q000502:physiology
D004965:Estrogen Antagonists; D004958:Estradiol; D002116:Calcitonin; D000135:Acid Phosphatase