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Background and aims: The present investigation was carried out to determine the levels of blood serum components and inflammatory cytokines in diabetic rat models [Goto-Kakizaki (GK), Zucker, and streptozotocin (STZ)-induced Sprague Dawley (SD) rats] which underwent abdominal Low-Power Laser Irradiation (LPLI) and compare them with non-irradiated controls. Methods: The animals were subdivided into the following groups: diabetic control rats (GK, Zucker, STZ) and diabetic rats treated with LPLI (GK + LPLI, Zucker + LPLI, and STZ + LPLI) (n = 7). The animals were irradiated three times weekly for 12 weeks in LPLI (830 nm) at a dose of 5 J/cm 2 for 500 s. Results: Body weight was significantly lowered in the Zucker-LPLI group compared to control at 10 weeks and this pattern was maintained until 12 weeks of age. TNF-α, IL-1I and IL-6 levels were significantly decreased (5.1 ± 1.1 vs 3.3 ± 0.5, p < 0.01; 43.6 ± 8.8 vs 27.1 ± 3.8, p < 0.01; 98.3 ± 15.8 vs 62.2 ± 12.1, p < 0.01) in the Zucker-LPLI group compared with the control rats. The small intestinal transit rates of charcoal meals were significantly decreased (58.1 ± 10.1 vs 73.4 ± 13.3, p < 0.05) in the Zucker-LPLI group compared with the control rats. Similarly, the serum levels of glucose, cholesterol and triglycerides of LPLI groups were decreased in comparison with that of diabetic control rats. Conclusions: We suggest that abdominal LPLI can reduce body weight and LPLI could be applicable for use against diabetic-induced inflammatory factors.

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The incidence of phenytoininduced gingival overgrowth is the highest among drugs that induce gingival overgrowth. Histological analysis has demonstrated that phenytoininduced gingival overgrowth is characterized by increased fibroblast proliferation and collagen formation in the gingiva. Cell cycle regulation, which induces cellular proliferation and division or apoptosis, is important to maintain fibroblast homeostasis in tissues. We previously demonstrated that gingival overgrowth is caused by the effect of phenytoin treatment to inhibit G 1 cell cycle arrest in gingival fibroblasts. In this study, we investigated the role of phenytoin in the apoptosis of human gingival fibroblasts to clarify the mechanism of phenytoininduced gingival overgrowth. Human gingival fibroblasts were cultured in DMEM and were treated with or without 0.25 µM phenytoin for 21 days. The following assays were then performed: 1) determination of the percentage of viable and dead cells by trypan blue staining, 2) determination of the relative amounts of apoptotic cells by absorptiometry, 3) nuclear staining using Hoechst 33258 for histological observation of apoptotic cells, and 4) RT -PCR analysis of mRNA expression levels of cyclin D and cyclin E. The results show that treatment with phenytoin decreased the number of apoptotic cells compared with the control. Phenytoin also increased the percentage of viable cells and decreased the percentage of dead cells compared with the control, and increased the cyclin D mRNA expression level compared to the control. We conclude that phenytoininduced gingival overgrowth results from the combined effects of those mechanisms to inhibit apoptosis in gingival fibroblasts. Keywords： drug-induced gingival overgrowth, phenytoin, gingival fibroblast, apoptosis

Tooth development is a multistage and multistep process involving fate determination and morphogenetic patterning events, epithelialmesenchymal interactions, and cell proliferation, differentiation, and migration. Animal model studies have shown that YAP and TAZ, effectors of the Hippo pathway, have a critical function in tooth morphogenesis. However, the function of YAP and TAZ in tooth development has not been well documented and its specific roles in tooth morphogenesis remain unclear. We used immunohistochemistry to examine the localization of YAP and TAZ in mouse mandibular first molar tooth germ. ICR mouse embryos on days E12, E14 and E18 were produced.Heads from these embryos were processed for paraffin embedding and prepared for immunohistochemistry. Immunostaining for YAP and TAZ showed different localization in tooth development. YAP was localized in the odontogenic epithelium from the early stages of tooth germ, but TAZ was not almost observed. YAP was also positive for preameloblasts or inner enamel epithelium, which were high columnar cells. On the other hand, TAZ localized to odontoblasts and preameloblasts or inner enamel epithelium. These results demonstrated functional differences between YAP and TAZ in tooth development, and suggested that these proteins were not only involved in cell proliferation, differentiation, and hard tissue formation, but also in threedimensional cusp morphogenesis during tooth development.