PURPOSEThis study was conducted to evaluate the effects of full-coverage all-ceramic zirconia, lithium disilicate glass-ceramic, leucite glass-ceramic, or stainless steel crowns on antagonistic primary tooth wear.MATERIALS AND METHODSThere were four study groups: the stainless steel (Steel) group, the leucite glass-ceramic (Leucite) group, the lithium disilicate glass-ceramic (Lithium) group, and the monolithic zirconia (Zirconia) group. Ten flat crown specimens were prepared per group; opposing teeth were prepared using primary canines. A wear test was conducted over 100,000 chewing cycles using a dual-axis chewing simulator and a 50 N masticating force, and wear losses of antagonistic teeth and restorative materials were calculated using a three-dimensional profiling system and an electronic scale, respectively. Statistical significance was determined using One-way ANOVA and Tukey's test (P<.05).RESULTSThe Leucite group (2.670±1.471 mm3) showed the greatest amount of antagonist tooth wear, followed by in decreasing order by the Lithium (2.042±0.696 mm3), Zirconia (1.426±0.477 mm3), and Steel groups (0.397±0.192 mm3). Mean volume losses in the Leucite and Lithium groups were significantly greater than in the Steel group (P<.05). No significant difference was observed between mean volume losses in the Zirconia and Steel groups (P>.05).CONCLUSIONLeucite glass-ceramic and lithium disilicate glass-ceramic cause more primary tooth wear than stainless steel or zirconia.

Mutations in a family with sequence similarity 83 member H (FAM83H) cause autosomal-dominant hypocalcification amelogenesis imperfecta (ADH CAI). All FAM83H ADHCAI-causing mutations terminate translation or shift the reading frame within the specific exon 5 segment that encodes from Ser(287) to Glu(694). Mutations near Glu(694) cause a milder, more localized phenotype. We identified disease-causing FAM83H mutations in two families with ADHCAI: family 1 (g.3115C>T, c.1993 C>T, p.Q665X) and family 2 (g.3151C>T, c.2029 C>T, p.Q677X). We also tested the hypothesis that truncation mutations alter the intracellular localization of FAM83H. Wild-type FAM83H and p.E694X mutant FAM83H fused to green fluorescent protein (GFP) localized in the cytoplasm of HEK293T cells, but the mutant FAM83H proteins (p.R325X, p.W460X, and p.Q677X) fused to GFP localized mainly in the nucleus with slight expression in the cytoplasm. We conclude that nuclear targeting of the truncated FAM83H protein contributes to the severe, generalized enamel phenotype.

The effect of epigallocatechin gallate (EGCG) on cell survival was studied by using serum-starved A549 non-small cell lung carcinoma (NSCLC) cells. A MTT assay showed that EGCG significantly increased the viability of serum-starved A549 cells compared to the control cells, though EGCG at high concentration (approximately 300 microM) had no protective effect against serum withdrawal-induced cell apoptosis. Western blots showed increased immunoreactivity for phospho-Akt and phospho-GSK3beta in EGCG-treated cells. To determine the mechanism for Akt phosphorylation, cells were pretreated with various kinase inhibitors before exposure to EGCG. Only LY294002 inhibited Akt activation induced by EGCG, implying that EGCG-induced Akt activation is PI3K dependent. Both phospho-Raf-1 and Raf-1 proteins were significantly decreased, whereas B-raf expression was not altered. This suggests that the Raf kinases have no role in the increased cell survival caused by EGCG. This study has shown that EGCG protects A549 cells from apoptosis induced by serum deprivation via Akt activation and this protective effect may limit the clinical use of EGCG in treating and preventing NSCLC.

In growing children it is frequently found that dental maturation is strongly influenced by the growth rate of maxilla or mandible. If there is evidence to prove this, it might be utilized as a criterion in the early diagnosis of skeletal malocclusion, even before the object's real skeletal features are yet revealed. The purpose of this study was to find out if the difference of dental maturation in over-grown mandible in children with skeletal Class III has any relationship with some skeletal features of mandible. 50 patients in Hellman dental age IIIA with normal occlusion and Class III malocclusion of mandibular overgrowth type respectively were selected as study objects. The age estimation was performed on maxillary and mandibular teeth, eruption rate of the 2nd molars of each group have been measured on panoramic radiography, and the differences in dental age of the upper and lower jaw were analyzed under Demirijian's method.The results were as follows:The difference of dental age of maxillary and mandibular teeth between the two groups was 0.66 and 1.20 years respectively, with a higher difference in the experimental group (p < 0.05). The difference of eruption rate of the maxillary and mandibular second molar was not found between two group (p >0.05).

For the resin repair in a resin-imbedded tooth cavity, AF spectrum produced by 405-nm wavelength could be a useful method in tracing the resin-tooth boundary if combined with conventional X-ray radiography.