Comparison of dynamic occlusal contacts during chewing between working and balancing sides

Objectives: Mastication is a crucial function for the elderly, and promotes oral health status, cognitive function and the physical constitution. Most reports about occlusion patterns and occlusal glide of adults have reported the jaw movement at the lower incisal point due to easiness of evaluating masticatory performance. The purpose of this study was to test the hypothesis that dynamic occlusal contact area (OCA) during chewing differ for each tooth on the working vs. the balancing chewing side. Design: In thirteen healthy Japanese females, OCA was estimated with a measurement system combining 3-D tracking of mandibular movements with 3-D digitization of tooth shape. Results: The starting of occlusal contact between teeth at working side and balancing side did not differ significantly. In contrast, ending of occlusal contact of teeth at balancing side were markedly longer than that of teeth at working side at lateral incisor, canine, and first premolar. The dynamic sum of OCAs for all teeth was symmetrical around maximum closed position (MCP) when chewing on the working side. In contrast, the dynamic sum of OCA peaked after MCP when chewing on the balancing side. In working and balancing side, sums of maximum OCA at all posterior teeth accounted for 93%, 86% of sum OCA for all teeth at working and balancing sides, respectively. Conclusion: Our result suggested that the hypothesis that dynamic OCA during chewing differ for each tooth on the working vs. the balancing chewing side was not accepted at molars

A new way of analyzing occlusion 3 dimensionally

This article introduces a new method for 3-dimensional dental cast analysis, by using a mechanical 3-dimensional digitizer, MicroScribe 3DX (Immersion, San Jose, Calif), and TIGARO software (not yet released, but available from the author at [email protected]). By digitizing points on the model, multiple measurements can be made, including tooth dimensions; arch length, width, and perimeter; curve of Spee; overjet and overbite; and anteroposterior discrepancy. The bias of the system can be evaluated by comparing the distance between 2 points as determined by the new system and as measured with digital calipers. Fifteen pairs of models were measured digitally and manually, and the bias was evaluated by comparing the variances of both methods and checking for the type of error obtained by each method. No systematic errors were found. The results showed that the method is accurate, and it can be applied to both clinical practice and research. Copyright © 2005 by the American Association of Orthodontists

Prevalence of molar incisor hypomineralization and regional differences throughout Japan

Abstract Background Molar incisor hypomineralization (MIH) frequently occurs in children worldwide. However, MIH prevalence throughout Japan has not yet been investigated. The purpose of this study was to clarify MIH prevalence rates and to consider potential regional differences throughout Japan. Methods A total of 4496 children aged 7–9 years throughout Japan were evaluated in this study. MIH prevalence rates among children were evaluated in eight regions throughout Japan. A child’s residence was defined as the mother’s residence during pregnancy. The localization of demarcated opacities and enamel breakdown was recorded on a standard code form using a guided record chart. Logistic regression analysis was used to evaluate whether MIH prevalence rates differed among age groups, sex, and regions. Results The overall prevalence of MIH in Japan was 19.8%. The prevalence of MIH was 14.0% in the Hokkaido region, 11.7% in the Tohoku region, 18.5% in the Kanto Shin-Etsu region, 19.3% in the Tokai Hokuriku region, 22.3% in the Kinki region, 19.8% in the Chugoku region, 28.1% in the Shikoku region, and 25.3% in the Kyushu region. These regional differences were statistically significant. Moreover, MIH prevalence rates decreased with age. No significant sex differences in MIH prevalence rates were demonstrated. Conclusions To our knowledge, this is the first MIH study carried out in several regions throughout Japan. Regional differences existed in MIH prevalence rates; particularly, MIH occurred more frequently in children residing in southwestern areas than those in northeastern areas of Japan

Tissue-Specific Stem Cells Obtained by Reprogramming of Non-Obese Diabetic (NOD) Mouse-Derived Pancreatic Cells Confer Insulin Production in Response to Glucose

<div><p>Type 1 diabetes occurs due to the autoimmune destruction of pancreatic β-cells in islets. Transplantation of islets is a promising option for the treatment of patients with type 1 diabetes that experience hypoglycemic unawareness despite maximal care, but the present shortage of donor islets hampers such transplantation. Transplantation of insulin-producing cells derived from the patients themselves would be one of the most promising approaches to cure type 1 diabetes. Previously, we demonstrated that insulin-producing cells could be produced by transfecting murine pancreatic cells with Yamanaka’s reprogramming factors. Non-obese diabetic (NOD) mice are naturally occurring mutant mice defective in insulin production due to autoimmune ablation of pancreatic β-cells. In this study, we showed that glucose-sensitive insulin-producing cells are successfully generated by transfecting primary pancreatic cells from NOD mice (aged 6 months old) with a plasmid harboring the cDNAs for Oct-3/4, Sox2, Klf4, and c-Myc. Transfection was repeated 4 times in a 2 day-interval. Sixty-five days after final transfection, cobblestone-like colonies appeared. They proliferated <i>in vitro</i> and expressed pluripotency-related genes as well as Pdx1, a transcription factor specific to tissue-specific stem cells for the β-cell lineage. Transplantation of these cells into nude mice failed to produce teratoma unlike induced pluripotent stem cells (iPSCs). Induction of these cells to the pancreatic β-cell lineage demonstrated their capability to produce insulin in response to glucose. These findings suggest that functional pancreatic β-cells can be produced from patients with type 1 diabetes. We call these resultant cells as “induced tissue-specific stem cells from the pancreas” (iTS-P) that could be valuable sources of safe and effective materials for cell-based therapy in type 1 diabetes.</p></div

Expression analysis in iTS-P.

<p>(A) RT-PCR analysis for mRNA expression of pluripotency-related markers (Oct3/4, Sox2, Klf4, c-Myc, Esg1, and Rex1) and the pancreas-related marker (Pdx1) in the pancreatic tissue of NOD mice (Panc), the ES cells (ES), and the iTS-P lines (4–2, 4–3, 4–4, 4–7, 4–9 and 4–11). Abbreviations: Oct3/4, octamer-binding transcription factor 3/4; Sox2, SRY (sex determining region Y)-box 2; Klf4, Kruppel-like factor 4; c-Myc, proto-oncogene for avian myelocytomatosis viral oncogene homolog; Esg1, embryonic stem cell-specific gene 1; Rex1, RNA exonuclease 1 homolog; Pdx1, pancreatic and duodenal homeobox 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase. (B) PCR analysis of genomic DNA isolated from the pancreatic tissue of NOD mice (Panc), ES cells (ES), iTS-P lines (4–2, 4–3, 4–4, 4–7, 4–9, and 4–11) to detect the presence of FUW-OSKM integrated into the chromosomes of iTS-P lines. Primers 2 (O-1), 3 (O-2), and 4 (K) correspond to the cDNA for each protein in FUW-OSKM (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0163580#pone.0163580.g001" target="_blank">Fig 1A</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0163580#pone.0163580.s001" target="_blank">S1 Table</a>). When genomic PCR is performed using these primers, the size of the amplified endogenous gene (Endo; shown by open arrowheads) is always larger than that of the cDNA (Tg; shown by solid arrowheads) in FUW-OSKM, since the former products contain intronic sequences. Since primers 1 and 5 are specific to FUW-OSKM, the samples showing amplification with these primers are thought to be the ones carrying FUW-OSKM in their genome. Lane OSKM shows FUW-OSKM plasmid (~10 ng) amplified as a positive control.</p

Immunostaining of differentiated iTS-P and insulin response upon glucose-stimulation.

<p>(A) Immunostaining of islet cells and insulin-producing cells (corresponding to Stage 4–5) derived from iTS-P 4–2 line using anti-insulin or anti-C-peptide antibodies. Scale bar = 100 μm. (B) Insulin release assay. (a) Release of insulin upon glucose-stimulation. Insulin response of iTS-P 4–2 (corresponding to Stages 4–5) was higher than that of differentiated ES cells (corresponding to Stages 4–5) upon stimulation with 2.8 and 20 mM D-glucose. The amount of insulin released into the culture medium was measured by ELISA. (b) Stimulation index (SI) upon glucose-stimulation. The SI of iTS-P 4–2 Stages 4–5 was higher than that of Stages 4–5 ES cells. (c) SI at phase I and II. The SI of iTS-P 4–2 Stages 4–5 at phase I (within 10 min after stimulation) and phase II (10 to 60 min after stimulation) was 1.1 and 2.2, respectively.</p

Characterization of iTS-P as pancreatic progenitors.

<p>(A) Teratoma/tumorigenic Assay. One Balb/c-nude mouse approximately 1.5 months after grafting is shown as an example. The site into which ES cells (indicated by “ES cell”) were inoculated exhibited the presence of a solid tumor, whereas the site into which iTS-P (indicated by “iTS-P 4–2”) were inoculated did not show any sign of solid tumor generation. (B) RT-PCR analysis for mRNA expression of endodermal cell markers (Hnf1, Hnf4, Hnf6, Foxa2, Sox17, and HB9) in iTS-P lines (4–2, 4–3, and 4–7) and differentiated ES cells at Stages 1 to 3 (Stage 1–3 ES; used as a positive control). Abbreviations: Hnf1, hepatocyte nuclear factor-1-; Hnf4, hepatocyte nuclear factor-4-; Hnf6, hepatocyte nuclear factor-6; Foxa2, forkhead box protein A2; Sox17, SRY (sex determining region Y)-box 17; HB9, homeobox protein HB9. (C) Immunostaining of iTS-P 4–2 Stages 4–5 using anti-Pdx1 antibody. Scale bar = 100 μm. (D) Electron microscopy of dense-core vesicles (arrows) in iTS-P 4–2 Stages 4–5. Scale bar = 5 μm. (E) Schematic representation of stepwise differentiation of ES cells towards insulin-producing cells. Cells of the definitive endoderm (DE) express Foxa2 and Sox17; cells of gut tube endoderm (GTE) express Hnf1β and Hnf4α; cells of pancreatic progenitors (PP) express Pdx1 and Hnf6; and insulin-producing cells (IPC) express insulin (Ins), glucose transporter 2 (Glut2), and glucokinase (GK). Abbreviations: KAAD-cyclopamine, 3-keto-N-aminoethyl-N'-aminocaproyldihydrocinnamoyl cyclopamine; FGF10, fibroblast growth factor 10; DAPT, N-(S)-phenyl-glycine-t-butyl ester; IFG-1, insulin-like growth factor 1.</p

Differentiation of iTS-P into insulin-producing cells.

<p>(A) RT-PCR analysis for mRNA expression of pancreatic β-cell markers in differentiated iTS-P cells (iTS-P 4–2 Stages 1–5 and iTS-P 4–2 Stages 4–5) and ES cells (Stages 1–5 ES and Stages 4–5 ES). Isolated islets were used as the positive control. Abbreviations: Nkx2.2, NK2 homeobox 2; Nkx6.1, NK6 homeobox 1; Pax4, paired box protein 4; Pax6, paired box protein 6; Ins1, insulin 1; Ngn3, neurogenin 3; NeuroD, neurogenic differentiation. (B) Quantitative RT-PCR analysis of insulin-1 (upper panel) and -2 (lower panel) mRNA in differentiated iTS-P and ES cells. Isolated islets were used as the positive control. *<i>P</i><0.05 between two groups.</p