Phase transformations in a leucite-reinforced pressable dental ceramic.

The objectives of this study were to determine the conditions for the formation of sanidine in a pressable dental ceramic (OPC; Jeneric/Pentron). Ceramic discs (16 mm in diameter, 1.3 mm thick; n = 60) were pressed according to the manufacturer's recommendations. One group was left as pressed as the control; the other groups were further heat-treated at temperatures ranging from 700 degrees C to 1100 degrees C for times ranging from 10 min to 24 h. X-ray diffraction was performed on powdered specimens. The microstructure was investigated by scanning electron microscopy (SEM). X-ray diffraction showed that sanidine was the only crystalline phase present after heat treatment at 900 degrees C for 24 h, whereas a mix of tetragonal leucite and sanidine was found in the specimens heat-treated at 900 degrees C for 12 h and 800 degrees C for 24 h. Tetragonal leucite was the only phase present in the control specimens after heat treatment at 950 degrees C and higher, and in the specimens heat-treated up to 1 h at 850 degrees C or 900 degrees C. Tetragonal and cubic leucite were found in the specimens treated at 750 degrees C or 800 degrees C for 30, 60, and 180 min and 700 degrees C for 24 h. SEM confirmed the presence of sanidine in the specimens heat-treated at 900 degrees C for 24 h. All specimens treated for up to 20 min at temperatures ranging from 700 degrees C to 950 degrees CC contained only tetragonal leucite. The clinical significance of this study is that the formation of sanidine is unlikely to occur at the temperature and time ranges needed for the staining or veneering of this leucite-reinforced pressable dental ceramic.

Transmission electron microscopic investigation of high-palladium dental casting alloys.

OBJECTIVE: The purpose of this study was to use transmission electron microscopy to examine four representative high-palladium alloys and gain insight into possible strengthening mechanisms. METHODS: Castings of two Pd-Cu-Ga alloys and two Pd-Ga alloys were thinned by jet polishing and ion milling, followed by plasma cleaning, to yield foil specimens. Multiple specimens were prepared for each alloy. Bright-field images, dark-field images and selected-area electron diffraction patterns for the alloys in the as-cast condition, after simulated porcelain-firing heat treatment, and after annealing at 980 degrees C were analyzed by standard transmission electron microscope (TEM) techniques. The overall compositions of the ultrastructures for the specimen foils were determined by conventional standardless energy-dispersive spectroscopic analyses with the TEM, and mean values of the elemental compositions were compared to the nominal alloy compositions provided by the manufacturers. RESULTS: There was generally good agreement (differences less than 2 wt%) between the overall ultrastructure composition and each nominal alloy composition, except for Protocol from which in may have been lost during casting or formed intermetallic compounds that were not detected by TEM. The same fine-scale tweed structure within parallel bands of approximately 100-200 nm width was observed for all four alloys in the as-cast condition and after simulated porcelain-firing heat treatment. The persistence of the ultrastructure in the specimens of the two Pd-Cu-Ga alloys annealed at 980 degrees C and quenched in ice water indicated very rapid formation from the palladium solid solution. The presence of ¿100¿ and ¿110¿ forbidden reflections for the <001> zone suggested that the tweed structure is ordered, although further research is necessary to establish this conclusion. SIGNIFICANCE: The presence of a similar tweed structure in both the Pd-Cu-Ga alloys and the Pd-Ga alloys of substantially lower hardness shows that some other strengthening mechanism accounts for the high hardness and strength generally observed for Pd-Cu-Ga alloys.

Preparation of amorphous boron nitride and its conversion to a turbostratic, tubular form.

Amorphous boron nitride, BN, is obtained from the reaction of B-trichloroborazine, (BCINH)(3), with cesium metal. The amorphous product is converted to a turbostratic form upon heating to 1100 degrees C. Scanning electron microscopy reveals a previously unreported morphology composed of hollow tubular structures. The largest of these appear to be approximately 3 micrometers in external diameter and 50 to 100 micrometers in length. Transmission electron microscopy and selected-area electron diffraction also indicate the tube walls to be turbostratic in nature. The mechanism by which the tubes form is not known, although apparent sites of incipient tube growth have been observed.

Gastric mucosal calcinosis. Calcified aluminum phosphate deposits secondary to aluminum-containing antacids or sucralfate therapy in organ transplant patients.

We have noticed calcium deposits (gastric mucosal calcinosis, or GMC) in the superficial gastric mucosa of 28 organ transplant patients (OTPs) (11 liver, seven bone marrow, four kidney, three kidney/pancreas, two heart, and one each of liver and kidney transplant) who underwent endoscopic biopsies. The deposits were tinctorially similar to cytomegalovirus inclusions, ranged from 40 to 250 mu in diameter, and were present just beneath the surface epithelium at the tips of the foveolae. An x-ray microanalysis showed that these mucosal deposits contained the elements aluminum, phosphorus, calcium, and chlorine. Clinical chart review showed that all OTPs with GMC were taking aluminum-containing antacids or sucralfate. Review of biopsies from gastric ulcer patients found GMC in a significantly smaller percentage than in transplant patients (32.7% vs. 5.1%, p < 0.0002). In addition, all three ulcer patients with calcified deposits were chronic renal failure patients on long-term aluminum-containing antacid therapy. Gastric mucosal calcinosis appears to be caused by aluminum phosphate accumulation secondary to antacid or sucralfate therapy in organ transplant patients. The presence of GMC in OTPs and chronic renal failure patients rather than other gastric ulcer patients is most likely due to the longer duration of therapy with aluminum-containing compounds in the former two patient groups. The clinical relevance of GMC remains to be seen. In theory, however, accelerated bone demineralization via loss of phosphates and absorption of aluminum in the gastrointestinal tract may be a consequence of long-term aluminum-containing antacid or sucralfate therapy.