Bone and mineral最新文献

Maintaining bone mass after extraction of teeth is a major problem in the prevention of oral disease. Maintenance theoretically could be enhanced by immediate implantation of submerged ceramic hydroxyapatite (HA) implants releasing the bone resorption-inhibiting agent bisphosphonate (P-C-P). Four different types of ceramic HA implants were designed as release systems for an in vitro study and assayed in saline at a temperature of 37°C during 3 months. The implants were either rod- or tube-shaped, with densities of 3.104 g/cm³ and 1.408 g/cm³ (microporous) or 2.369 g/cm³ (macro/microporous). Loading of the implants with the P-C-P was done by adsorption into the ceramic (rod-shaped implants) or by filling the reservoir of the implant (tube-shaped implants). Despite the fact that P-C-P has a high bonding affinity to HA it appeared that the release of adsorbed P-C-P from the ceramic HA occurred steady, controlled and over a long period of time. The rod-shaped implants had much better release properties than the tube-shaped implants. Microporous ceramic HA rods sintered at 800°C and macro/microporous rods sintered at 1300°C are considered to be promising release systems for P-C-Ps.

The bone mineral content (BMC) and bone mineral density (BMD) of the femoral midshaft from 15 skeletally mature male rats were measured by Single Photon Absorptiometry (SPA), and comparisons made to fracture strength of the femoral diaphysis and the femoral neck. In stepwise regression the factors contributing significantly to the ultimate bending moment of the shaft were BMC and femoral length. BMC correlated strongly with the ultimate bending moment of the femoral diaphysis (r² = 0.63, P < 0.01). The correlation between BMC and ultimate moment of the femoral neck was moderate (r² = 0.51, P < 0.01). The correlations between BMD and mechanical parameters were lower than the corresponding values for BMC, with a significant result only for the bending moment of the femoral diaphysis (r² = 0.48, P < 0.01). In conclusion, BMC rather than BMD, is most predictive for fracture strength of the femur in rats.

The effects of gallium nitrate (GN) were evaluated on osteopenia induced by ovariectomy (OVX) and a low-calcium diet (LCD) in Sprague-Dawley rats. Twenty-five rats (300–400 g) were randomized into four groups of 5–7 animals: (I) OVX LCD treated with GN for 22 weeks; (II) OVX LCD treated with GN for 10 weeks; (III) OVX LCD treated with saline; and (IV) sham-operated (SO), normal diet, treated with saline. GN-treated rats received a 30-mg/kg subcutaneous single dose of elemental gallium, followed by 10 mg/kg per week, whereas control animals received an equal volume of saline. All animals were euthanized at 22 weeks. Measurements of bone density and histomorphometry, performed on the proximal portion of the tibia, indicated significant bone loss in all OVX LCD animals. GN-treated rats in group I gained significantly less weight than those in the other groups, and their blood urea nitrogen increased, suggesting a nephrotoxic effect. After discontinuation of GN, rats in group II gained weight at the same rate as those which had received only saline. Bone formation rates in the GN-treated rats were double those of the saline-treated OVX animals and more than 10 times those of SO controls. Although the bone formation rate in GN-treated rats increased, GN had no effect in preventing the loss of bone surface, density and volume induced by OVX LCD. These findings suggest that although GN may enhance osteoblastic activity, this agent alone does not appear effective in the prevention of bone loss induced by OVX LCD.

Human cancellous bone was imaged and its absorptive density accurately measured in three dimensions (3D), nondestructively and at high spatial resolution by means of computerized microtomography (μCT). Essential for achieving the resolution and accuracy was the use of monoenergetic synchrotron radiation (SR) which avoided beam hardening effects, secured excellent contrast conditions including the option of energy-modulated contrast, and yet provided high intensity. To verify the resolution, we selected objects of ~ 8 μm size that could be observed on tomograms and correlated them in a unique manner to their counter images seen in histological sections prepared from the same specimen volume. Thus we have shown that the resolution expected from the voxel size of 8 μm used in the μCT process is in effect also attained in our results. In achieving the present results no X-ray-optical magnification was used. From μCT studies of composites (Bonse et al., X-ray tomographic microscopy (XTM) applied to carbon-fibre composites. In: Materlik G, ed. HASYLAB Jahresbericht 1990. Hamburg: DESY, 1990;567–568) we know that by including X-ray magnification a resolution below 2 jim is obtained. Therefore, with foreseeable development of our μCT method, the 3D and nondestructive investigation of structures in mineralized bone on the 2 μm level is feasible. For example, it should be possible to study tomographically the 3D distribution and amount of osteoclastic resorption in the surrounding bone structure.

The effect of paraformaldehyde-fixed murine macrophage P388D₁ cells on osteoclast-like cell formation was investigated in mouse marrow cultures. When mouse marrow cells were cocultured for 8 days with paraformaldehyde-fixed P388D₁ cells stimulated with lipopoly-saccaride (LPS), many tartrate-resistant acid phosphatase (TRACP)-positive multinucleated cells were formed. Non-stimulated, and paraformaldehyde-fixed P388D₁ cells did not induce the formation of TRACP-positive multinucleated cells. Salmon calcitonin and indomethacin strongly inhibited the paraformaldehyde-fixed, LPS-stimulated P388D₁ cells-induced TRACP-positive multinucleated cell formation. Monospecific anti-mouse recombinant IL-lα serum inhibited TRACP-positive multinucleated cell formation in the presence of paraformaldehyde-fixed P388D₁ cells stimulated with LPS. These results suggest that membrane-associated IL-1 on macrophages is responsible for the resorptive effect of paraformaldehyde-fixed P388D₁ cells stimulated with LPS.