Phosphate modulation of calcium transport by a calcium-phospholipid-phosphate complex of calcifying tissues.

The ionophoretic activities of a stable Ca-PS-Pi complex were examined in a three-compartment lipid-aqueous phase transport system. It was found that the complex transported Ca2+ at a slower rate than free PS. Analysis of the transport process, using an equilibrium partitioning model, revealed that Ca2+ binding to the complex was the rate-limiting step. This inhibition was overcome by the addition of exogeneous Pi. It was concluded that the complex acted as an ionophore and that the presence of coordinated Ca and P atoms facilitated Pi modulation of Ca2+ transport.

Effect of fluoride on phosphatidylserine-mediated calcium transport.

Experiments to study the effect of F- on phosphatidylserine-mediated Ca2+ transport were performed utilizing two and three compartment lipid-aqueous phase model systems. Using the three compartment model, it was shown that F- modulated the rate of Ca2+ transport in a biphasic manner. Low concentrations of F- enhanced the Ca2+ translocation rate and high levels of F- inhibited the rate of Ca2+ transport. To determine whether the enhancement or inhibition of Ca2+ transport rate by F- was due to an increase in the uptake of Ca2+ into the lipid phase, or to an increase in the ability of the lipid phase to release Ca2+, a two compartment model was used. It was found that the ability of the phosphatidylserine phase to take up Ca2+ increased as the F- concentration of the aqueous donor phase was raised. In addition, Ca2+ release from the phosphatide was also modulated by F-. High F- levels inhibited the release of Ca2+ from the lipid, while low levels of F- did not retain Ca2+ in the lipid phase. Thus, it was concluded that F- enhanced the interaction between Ca2+ and phosphatidylserine, possibly by forming a phosphatidylserine-Ca-F complex. Once this interaction had taken place, Ca2+ release into the aqueous receiver compartment was dependent on the F- concentration. Thus, low F- levels induced a net increase in Ca2+ transport, while high F- levels inhibited Ca2+ translocation rates.

Bone solubilization by mononuclear cells.

Mononuclear cells derived from chicken peripheral blood or from thioglycollate-induced mouse peritoneal exudates were found to cause calcium release from devitalized homologous bone in vitro. These mononuclear cells with osteolytic activity were adherent to plastic surfaces and were identified as being macrophages by cell surface markers and histochemical staining. Other mononuclear cells such as chicken thymocytes, nonadherent peripheral blood mononuclear cells, and chick embryo fibroblasts did not cause bone dissolution. In parallel with the active solubilization of bone mineral, 14C-label was also released from devitalized calvaria prelabeled with 14C-proline. Macrophages, inactivated by repeated freezing and thawing as well as those cultured in the presence of iodoacetate, did not solubilize bone in vitro. The degree of bone solubilization was directly related to the numbers of macrophages per culture as well as the duration of the culture period. Powdered devitalized homologous bone was used in most experiments, but macrophages were also able to solubilize bone material in vitro from devitalized calvaria and bone slabs. The addition of Escherichia coli lipopolysaccharide to cultures of bone and macrophages significantly increased the levels of calcium released from bone. The addition of parathyroid hormone and calcitonin had no effect on macrophage-mediated bone dissolution. These results suggest that viable macrophages have osteolytic activity and that this activity is modulated by an inflammatory mediator, endotoxin.

An improved technique for the retention of polycarbonate crowns.

The following conclusions may be drawn from this study: Composite resins do not bond to polycarbonate crowns. A technique for priming the internal surfaces of polycarbonate crowns is indicated, in order to create such a bond. Priming the polycarbonate crown with methyl methacrylate monomer alone produces a bond with composite resins. Priming the polycarbonate crown with a syrup of methyl methacrylate monomer and (poly) methyl methacrylate powder appears to produce a stronger bond with composite resins than the monomer alone.