The metabolic effects of phoshate on bone - abstract

ABSTRACT

The therapeutic role of phosphate solutions in the management of hypercalcemic states has been well established, but the mechanism by which phosphate lowers the serum calcium is unclear. The two major possibilities are that phosphate produces its effect by inhibiting bone resorption or stimulating bone formation. Total urinary hydroxyproline (OHPr) is an index of collagen metabolism and rises when there is excessive bone resorption. The effect of the phosphate on urinary OHPr excreation in patients with such metabolic bone diseases as Paget's disease, secondary hyperparathyroidism, osteogenesis imperfecta and osteoporosis was studied, and in all these conditions, oral phosphate supplementation reduced urinary OHPr and a cessation of phosphate was immediately followed by a rise in urinary OHPr levels. In further studies on dogs the effect of phosphate supplementation on collagen synthesis in vivo was estimated by measuring the incorporation of labelled proline into bone collagen. The results show that phosphate supplementation increased the rate of collagen synthesis but resorption was little influenced. It is proposed that phosphate lowers the serum calcium by promoting collagen synthesis and stimulating new bone formation (AU)