ABSTRACT
In situations of pathological localized bone destruction, from which a great deal of our knowledge on the subject has come, there is often fairly clear evidence of the cellular source of the prostaglandins (PGs) implicated in the resorption. Starting with a relatively simple concept, the cells which produce the PGs can be classified as “resident” to bone and surrounding connective tissues, or as “nonresident”. During the 1970s the involvement of PGs with several aspects of inflammation (notably vasodilation, edema, and pain) led to much interest in their production by inflammatory cells. The monocyte-macrophage as a source for bone-resorbing PGs was a popular concept. It fit several pertinent observations, such as the presence of mononuclear phagocytes in healthy bone induced to resorb in tissue cultures, the characteristic infiltration by macrophages of chronically inflamed tissues associated with bone resorption, and the presence in inflamed tissues of many agents which are capable of stimulating PG synthesis in macrophages.
