High-strength bioactive glass-ceramic A-W was soaked in various acellular aqueous solutions different in ion concentrations and pH. After soaking for 7 and 30 days, surface structural changes of the glass-ceramic were investigated by means of Fourier transform infrared reflection spectroscopy, thin-film x-ray diffraction, and scanning electronmicroscopic observations, in comparison with in vivo surface structural changes. So-called Tris buffer solution, pure water buffered with trishydroxymethyl-aminomethane, which had been used by various workers as a "simulated body fluid," did not reproduce the in vivo surface structural changes, i.e., apatite formation on the surface. A solution, ion concentrations and pH of which are almost equal to those of the human blood plasma--i.e., Na+ 142.0, K+ 5.0, Mg2+ 1.5, Ca2+ 2.5, Cl- 148.8, HCO3- 4.2 and PO4(2-) 1.0 mM and buffered at pH 7.25 with the trishydroxymethyl-aminomethane--most precisely reproduced in vivo surface structure change. This shows that careful selection of simulated body fluid is required for in vitro experiments. The results also support the concept that the apatite phase on the surface of glass-ceramic A-W is formed by a chemical reaction of the glass-ceramic with the Ca2+, HPO4(2-), and OH- ions in the body fluid.

Glass-ceramic A-W, containing crystalline apatite and wollastonite in a MgO-CaO-SiO2 glassy matrix shows high bioactivity as well as high mechanical strength, but other ceramics containing the same kinds of crystalline phases in different glassy matrices do not show the same bioactivity. In order to investigate the bone-bonding mechanism of this type of glass-ceramic, surface structural changes of the glass-ceramics after exposure to simulated body fluid were analyzed with various techniques. A solution with ion concentrations which are almost equal to those of the human blood plasma was used as the simulated body fluid, instead of Tris-buffer solution hitherto used. For analyzing the surface structural changes, thin-film x-ray diffraction was used in addition to conventional techniques. It was found that a bioactive glass-ceramic forms a Ca, P-rich layer on its surface in the fluid but nonbioactive ones do not, and that the Ca, P-rich layer consists of carbonate-containing hydroxyapatite of small crystallites and/or defective structure. These findings were common to those of Bioglass-type glasses. So, we conclude that the essential condition for glass and glass-ceramic to bond to bone is the formation of the surface apatite layer in the body environment but it is not essential to contain apatite within the material. Bioactivity of glass and glass-ceramic can be evaluated in vitro by examining the formation of the surface apatite layer in the simulated body fluid described above.

The prerequisite for glasses and glass-ceramics to bond to living bone is the formation of biologically active bonelike apatite on their surfaces in the body. Our previous study showed that a silica gel prepared by hydrolysis and polycondensation of tetraethoxysilane in aqueous solution containing poly(ethy1ene glycol) induces apatite nucleation on its surface in a simulated body fluid. In the present study, the effects of heat treatment of silica gel on its catalytic effects in apatite nucleation was investigated in a simulated body fluid. It was found that apatite forms on the surfaces of silica gels heat-treated below 8OO"C, but not on those heat-treated above 900°C. The volume of nanometer-range pores in the gel remarkably decreased by heat treatment above 900°C. The concentration of silanol groups in the silica gels gradually decreased with increasing heat treatment temperature. The rate of silica dissolution from the gel into the simulated body fluid decreased remarkably by heat treatment above 900°C. This suggested that a special type of silanol group which is formed by soaking the gel treated below 800°C into the simulated body fluid is responsible for apatite nucleation.

It has been proposed that the formation of a surface apatite layer in vivo on surface active ceramics is an essential condition for chemical bonding between ceramics and bone tissue. To clarify the difference in bone-bonding mechanisms between surface active ceramics and bioresorbable ceramics, two experiments were performed using plates of dense beta-tricalcium phosphate (beta-TCP). First, plates of beta-TCP were implanted subcutaneously in rats for 8 weeks. Surface change due to bioresorption was observed with scanning electron microscopy. Formation of the apatite layer on the surface was investigated using thin-film x-ray diffraction and Fourier transform infrared reflection spectroscopy. Second, plates of beta-TCP were implanted in tibiae of rabbits for 8 and 25 weeks and subjected to the detaching test to measure bone-bonding strength. beta-TCP bonded strongly to bone. Undecalcified sections of the interface of bone and beta-TCP were examined with SEM-EPMA. However, by physicochemical methods, no formation of surface apatite layer was observed. These results suggest that beta-TCP bonds to bone through microanchoring between bone and rough surface of resorbed beta-TCP.

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