Endocrine Abstracts (2004) 7 S18

Extracellular calcium as direct modulator of bone function

D Riccardi1, MM Dvorak1, A Siddiqua1, DH Carter2 & SL Dallas3


1School of Biological Sciences, University of Manchester, G38 Stopford Building, Oxford Road, Manchester M13 9PT; 2Turner Dental School, University of Manchester, Manchester; 3University of Missouri at Kansas City, Kansas City, USA.


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.

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