EFFECTS OF MAGNESIUM ON THE FORMATION OF CALCIUM-DEFICIENT HYDROXYAPATITE FROM CAHPO4-CENTER-DOT-2H(2)O AND CA-4(PO4)(2)O

Calcium-deficient hydroxyapatite (KA) with a Ca/P molar ratio of 1.50 was synthesized in various concentrations (0.01-75 mM) of MgCl2 at 37. 4 degrees C by reaction between particulate CaHPO4 . 2H(2)O and Ca-4(P O4)(2)O. The effects of magnesium on the kinetics of HA formation were determined using isothermal calorimetry. All reactions completely con sumed the precursor phases as indicated by X-ray diffraction analysis and a constant enthalpy of reaction (240 kJ/mol). Magnesium concentrat ions below 1 mM had no effect on the kinetics of HA formation. Magnesi um concentrations between 1 and 2.5 mM affected the reaction path but did not affect the time required for complete reaction. Higher concent rations extended the times of complete reaction due to magnesium adsor ption on the precursor phase(s) and HA nuclei, and stabilization of a noncrystalline calcium phosphate (NCP). HA formation in the presence o f magnesium resulted in separation of the following two events: initia l formation of HA nuclei and NCP, and consumption of CaHPO4 . 2H(2)O. This was indicated by the appearance of an additional calorimetric pea k. Variations in calcium, magnesium, and phosphate concentrations and pH with time were determined. Increasing the magnesium concentration r esulted in elevated calcium concentrations. After an initial decrease in magnesium owing to its adsorption onto PIA nuclei and precursor(s), a period of slow reaction al constant magnesium concentration was obs erved. Both the magnesium concentration in solution and the proportion s of precursors present decreased prior to any evidence of a crystalli ne product phase. This is attributed to the formation of NCP capable o f incorporating magnesium. This noncrystalline phase persisted for mor e than 1 year for reactions in magnesium concentrations about 2.5 mM. Its conversion to HA resulted in the release of magnesium to the solut ion. (C) 1997 John Wiley & Sons, Inc.