Resorption of bone by mouse peritoneal macrophages.
An experimental system is described in which mononuclear phagocytes are shown to cause contact-dependent resorption of bone powder in vitro. Endotoxin, which is known to stimulate macrophage functions, and which has also been shown to increase bone resorption in organ culture, increased bone dissolution by mononuclear phagocytes. On the other hand, parathyroid hormone and prostaglandin E2, hormones which increase th number and activity of osteoclasts, had no effect on resorption of bone powder by mononuclear phagocytes. This suggests that the osteoclast, which is probably derived from mononuclear phagocytes, is induced to respond to these hormones indirectly, following a primary hormonal effect on osteoblasts.
D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D001862:Bone Resorption / Q000473:pathology*; D001842:Bone and Bones / Q000378:metabolism; D002478:Cells, Cultured; D015232:Dinoprostone; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000502:physiology*; D051379:Mice; D008903:Minerals / Q000378:metabolism; D010281:Parathyroid Hormone / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology
D008070:Lipopolysaccharides; D008903:Minerals; D010281:Parathyroid Hormone; D011458:Prostaglandins E; D015232:Dinoprostone