Amelogenesis imperfecta (AI) is a collection of diverse inherited disorders featuring dental-enamel defects in the absence of significant nondental symptoms. AI phenotypes vary and are categorized as hypoplastic, hypocalcified, and hypomaturation types. Phenotypic specificity to enamel has focused research on genes encoding enamel-matrix proteins. We studied two families with autosomal-dominant hypocalcified AI and have identified nonsense mutations (R325X and Q398X) in the FAM83H gene on chromosome 8q24.3. The mutations perfectly cosegregate with the disease phenotype and demonstrate that FAM83H is required for proper dental-enamel calcification.

PURPOSE.The cortical bone thickness on the anterior region is important for achieving implant stability. The purpose of this study was to examine the thickness of the cortical and cancellous bones on the anterior region of the maxilla and mandible. MATERIALS AND METHODS. Twenty-five cadaver heads were used (16 male and 9 female; mean death age, 56.7 years). After the long axis of alveolar process was set up, it was measured in 5 levels starting from 2 mm below the cementoenamel junction (L1) at intervals of 3 mm. All data was analysed statistically by one-way ANOVA at the .05 significance level. RESULTS. The cortical bone thickness according to measurement levels in both the labial and lingual sides increased from L1 to L5, and the lingual side below L3 was significantly thicker than the labial side on the maxilla and mandible. In particular, the labial cortical bone thickness in the maxilla was the thinnest compared to the other regions. The cancellous bone thickness according to measurement levels increased from L1 to L5 on the maxilla, and on the mandible it was the thinnest at the middle level of the root. CONCLUSION. For implant placement on the anterior region, a careful evaluation and full knowledge on the thickness of the cortical and cancellous bone are necessary, therefore, these results may provide an anatomic guideline to clinicians.

The modiolus is strongly associated with facial expression, beauty, and aging, and so it is often viewed as the main facial landmark, both functionally and aesthetically. This study examined the modiolus and the surrounding structures histomorphologically with the aim of providing useful information for reconstructive and aesthetic surgery. Nineteen embalmed cadavers (38 hemifaces; 8 males and 11 females; mean age at death, 66.9 years) were examined in this study. For macroscopic observations, the modiolus and facial artery in the perioral region of 28 hemifaces were revealed by meticulous dissection. The modiolus and its surrounding structures were then prepared from 12 hemifaces for routine histology and stained with hematoxylin-eosin and Masson trichrome. A tendinous tissue nodule in the modiolus was found in 21.4% of cases (ie, 6 hemifaces). The facial artery passed approximately 1 mm lateral to the lateral border of the modiolus. In the central region of modiolus, which was an area of convergence of muscle fibers, the tendinous structure appeared as dense irregular collagenous connective tissue. Particularly in the middle layer between the skin and the oral mucosa, it appeared as a dense, compact, and prominent shape horizontally. The finding of the existence of a tendinous structure in the central region of the modiolus, which could act as an anchor for the converging facial muscles, is expected to provide critical information in the field of facial plastic surgery.

Resveratrol (trans-3,4',5,-trihydroxystilbene), a phytoalexin present in grape skin and red wine, suppresses many types of cancers by regulating cell proliferation and apoptosis through a variety of mechanisms. However, the effects of resveratrol on oral cancer are not completely understood. Thus, effects of resveratrol on cell growth and apoptosis induction were examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, DNA fragmentation, immunoblotting, and determination of caspase activation in KB human oral cancer cells. Treatment with resveratrol induced inhibition of cell growth depending on the resveratrol treatment time and concentration in KB cells. Treatment with resveratrol induced DNA ladder formation in KB cells and promoted proteolytic cleavage of procaspase-3 and procaspase-7 with increases in the amount of cleaved caspases-3 and -7. Proteolytic processing of caspase-9 in KB cells was increased by resveratrol treatment. Activation of caspase-3/-7 was detected in living KB cells by fluorescence microscopy. These results suggest that the resveratrol can suppress cell growth and induce cell apoptosis in KB human oral cancer cells, and may have potential as an anti-cancer drug.

Background: The light-emitting diode (LED) curing light used is presumed to be safe. However, the scientific basis for this is unclear, and the safety of LED curing light is still controversial. The purpose of this study was to investigate the effect of LED curing light irradiation according to the conditions applied for the polymerization of composite resins in dental clinic on the cell viability and inflammatory response in Raw264.7 macrophages and to confirm the stability of LED curing light. Methods: Cell viability and cell morphology of Raw264.7 macrophages treated with 100 ng/ml of lipopolysaccharide (LPS) or/and LED curing light with a wavelength of 440∼490 nm for 20 seconds were confirmed by methylthiazolydiphenyl-tetrazolium bromide assay and microscopic observation. The production of nitric oxide (NO) and prostaglandin E2 (PGE2) was confirmed by NO assay and PGE2 enzyme-linked immunosorbent assay kit. Expression of interleukin (IL)-1 and tumor necrosis factor (TNF)- in total RNA and protein was confirmed by reverse transcription polymerase chain reaction and Western blot analysis. Results: The LED curing light did not affect the viability and morphology of normal Raw264.7 cells but affected the cell viability and induced cytotoxicity in the inflammation-induced Raw264.7 cells by LPS. The irradiation of the LED curing light did not progress to the inflammatory state in the inflammation-induced Raw264.7 macrophage. However, LED curing light irradiation in normal Raw264.7 cells induced an increase in NO and PGE2 production and mRNA and protein expression of IL-1 and TNF-, indicating that it is possible to induce the inflammatory state. Conclusion: The irradiation of LED curing light in RAW264.7 macrophage may induce an excessive inflammatory reaction and damage oral tissues. Therefore, it is necessary to limit the long-term irradiation which is inappropriate when applying LED curing light in a dental clinic.