Monocyte-mediated bone resorption involves release of nondialyzable substances in addition to prostaglandin.

Abstract

Human monocytes were stimulated by lectins to release prostaglandin and other factor(s) that induce bone resorption in vitro. High concentrations of indomethacin failed to inhibit production by stimulated monocytes of most of the bone-resorbing activity. This activity was retained in culture supernatants after extensive dialysis. These data demonstrate that monocytes are capable of the simultaneous production of prostaglandins and nondialyzable bone-resorbing factor(s). This (these) factor(s) may mediate localized bone resorption associated with certain chronic inflammatory diseases.