Extracellular Ca2+ sensing by the osteoclast

Abstract An increasing number of cell types appear to detect changes in the extracellular Ca 2+ concentrationand and accordingly modify their function. We review recent evidence for the existence and function of such a mechanism in the osteoclast. Elevated external [Ca 2+ ] in the mM range reduces bone resorption and results in motile changes in the cells. These changes may partly result from elevations of cytosolic [Ca 2+ ] triggered through activation of a surface Ca 2+ receptor. Closer analyses of the increases in cytosolic [Ca 2+ ] associated with receptor activation are hindered by the action of this ion both as extracellular agonist and intracellular second messenger. Variations in the peak cytosolic [Ca 2+ ] response to external Ca 2+ with changes in cell membrane potential by K + and valinomycin establish a contribution from extracellular Ca 2+ . Use of CIO 4 − , Ni 2+ and Cd 2+ as surrogate activators in low extracellular [Ca 2+ ] indicate a contribution from Ca 2+ ] release from intracellular stores as well. Such agonists also modify Ca 2+ redistribution in other systems, such as skeletal muscle. Thus, we may gain insights into osteoclast extra-cellular Ca 2+ detection and transduction from known features of more well-characterised cell systems.