Stimulation of bone resorption in cultured mouse calvaria by Lys-bradykinin (kallidin), a potential mediator of bone resorption linking anaphylaxis processes to rarefying osteitis.

Lys-Bradykinin (kallidin) stimulated bone resorption in vitro as assessed by the release of 45Ca and 3H from mouse calvaria radiolabelled in vivo with [45Ca]CaCl2 and [3H]proline, respectively. The stimulatory effect of Lys-bradykinin was reduced by calcitonin, indicating that the bone resorptive effect of Lys-bradykinin was dependent on osteoclastic activity. Different inhibitors of arachidonic acid metabolism, including glucocorticoids, inhibited Lys-bradykinin stimulated mobilization of mineral, implicating the synthesis of prostaglandins as an intermediary step. Lys-Bradykinin enhanced the biosynthesis of PGE2 in osteoblast-like cells isolated from mouse calvaria. In view of these findings and the capacity of mast cells to generate kininogenase activity, resulting in formation of Lys-bradykinin and bradykinin, the role of these cells in the pathogenesis of bone loss in rheumatoid arthritis, mastocytosis and osteoporosis is discussed.