Bone is the major sink and store for calcium and it fulfils essential roles in the maintenance of extracellular free ionised calcium concentration ([Ca2+e)within its homeostatic range (1.1 to 1.3mM). In response to acute hypercalcaemia or hypocalcaemia, Ca2+ is rapidly transported into or out of bone. Bone turnover (and therefore bone Ca2+ turnover) achieves the long term correction of the [Ca2+e] by the metabolic actions of osteoblasts (i.e., bone-forming cells) and osteoclasts (bone-resorbing cells), as they respectively incorporate or release Ca2+ from bone. These processes are regulated by the actions of hormones, such as parathyroid hormone (PTH), the release of which is a function of the [Ca2+]e, and is regulated by the action of the Ca2+e-sensing receptor (CaR) in the parathyroid gland. However, bone cells also directly respond to increasing and decreasing [Ca2+]e in their vicinity, independently of the systemic factors. Acute and long term local changes in [Ca2+]e affect bone cells and the physiological processes they are involved in but the molecular mechanisms which enable the bone cells to sense and respond to Ca2+e were not clear. Like the parathyroid cells, bone cells also express the CaR. This presentation will address how small deviations of [Ca2+]e from the physiological range have a significant impact on osteoblast function, proliferation and differentiation through the CaR and independently of other paracrine and endocrine factors.
22 - 24 Mar 2004
British Endocrine Societies