Biological Role of Calcium

FAO/WHO verbatim,

Calcium salts provide rigidity to the skeleton and calcium ions play a role in many if not most metabolic processes. In the primitive exoskeleton and in shells, rigidity is generally provided by calcium carbonate, but in the vertebrate skeleton it is provided by a form of calcium phosphate which approximates hydroxy-apatite [Ca10(OH)2(PO4)6] and is embedded in collagen fibrils.

Bone mineral serves as the ultimate reservoir for the calcium circulating in the ECF. Calcium enters the ECF from the gut by absorption and from bone by resorption. Calcium leaves the ECF via the gastrointestinal tract, kidneys, and skin and enters into bone via bone formation (Figure 13).

In addition, calcium fluxes occur across all cell membranes. Many neuro muscular and other cellular functions depend on the maintenance of the ionised calcium concentration in the ECF. Calcium fluxes are also important mediators of hormonal effects on target organs through several intracellular signalling pathways, such as the phosphoinositide and cyclic adenosine monophosphate systems.

Brown, E.M. & Hebert, S.C. 1997. Calcium-receptor-regulated parathyroid and renal function. Bone, 20: 303-309. 

The cytoplasmic calcium concentration is kept down by a series of calcium pumps, which concentrate calcium within the intracellular storage sites or extrude from the cells the calcium which flows in by diffusion. The physiology of calcium metabolism is primarily directed towards the maintenance of the concentration of ionised calcium in the ECF. 

This is protected and maintained by a feedback loop through calcium receptors in the parathyroid glands, which control the secretion of parathyroid hormone. This hormone increases the renal tubular re-absorption of calcium, promotes intestinal calcium absorption by stimulating the renal production of 1,25-dihyroxycolecaliferol [1,25(OH)2D], and, if necessary, resorbs bone.

Jones, G., Strugnell, S.A. & DeLuca, H.F. 1998. Current understanding of the molecular actions of vitamin D. Physiol. Revs., 78: 1193-1231. 

However, the integrity of the system depends critically on vitamin D status; if there is a deficiency of vitamin D, the loss of its calcaemic action

Nordin, B.E.C. 1960. Osteomalacia, osteoporosis and calcium deficiency. Clin. Orthop., 17: 235-258.

Wu, D.D., Boyd, R.D., Fix, T.J. & Burr, D.B. 1990. Regional patterns of bone loss and altered bone remodeling in response to calcium deprivation in laboratory rabbits. Calcif. Tissue Int., 47: 18-23.

leads to a decrease in the ionised calcium and secondary hyperparathyroidism and hypophosphataemia. This is why experimental vitamin D deficiency results in rickets and osteomalacia whereas calcium deficiency gives rise to osteoporosis.