Composite Containing Calcium Phosphate Particles Functionalized with 10-MDP

Abstract

The phosphate ester monomer 10-methacryloyloxydecyl dihydrogen phosphate (10-MDP) is capable of bonding to hydroxyapatite and, for this reason, is a key component of several self-etch adhesives. In this study, dicalcium phosphate dihydrate particles (DCPD; CaHPO4.2H2O) were functionalized with 10-MDP and used to formulate an experimental composite with 50 vol% inorganic content (3:1 DCPD:silanated barium glass ratio) dispersed in a BisGMA/TEGDMA matrix. The tested hypothesis was that DCPD functionalization would improve the composite’s mechanical performance without compromising Ca2+ release. Composites containing nonfunctionalized DCPD or only reinforcing glass (in both cases, with or without 10-MDP mixed in the resin phase) were used as controls. Materials were tested for degree of conversion (DC; by Fourier transform infrared spectroscopy), water sorption (WS) and solubility (SL; according to ISO 4049), biaxial flexural strength (BFS)/modulus (FM) after 24 h and 5 mo in water, and 28-d Ca2+ release in water (by plasma-coupled optical emission spectroscopy). Data were analyzed using analysis of variance/Tukey test (alpha: 5%). DCPD functionalization did not interfere with DC. The composite containing functionalized DCPD showed significantly lower WS and SL in comparison with the material formulated with nonfunctionalized particles. The presence of 10-MDP (as a functionalizing agent or dispersed in the resin phase) reduced the composite’s initial BFS and FM. After 5 mo in water, the composite with functionalized DCPD and both glass-only composites were able to maintain their mechanical properties at levels statistically similar to what was observed after 24 h. Ca2+ release was significantly reduced in both formulations containing 10-MDP. In conclusion, DCPD functionalization with 10-MDP increased the composite’s resistance to hydrolytic degradation, improving its mechanical stability after prolonged water storage. However, the impaired water transit at the particle-matrix interface led to a reduction in Ca2+ release.