yujiinagaki/published_papers/52540168 Yukari Hatada Yuji Inagaki Daisuke Nakamura Minato Akizuki Yoshimune Iwata Rie Kido Mika Bando Hiromichi Yumoto Tryptanthrin, a constituent of Persicaria tinctoria, suppresses osteoclastogenesis and enhances the expression of tight junction proteins and cell adhesion molecules in gingival epithelial cells. Tryptanthrin, an ingredient of Persicaria tinctoria, has been reported to exhibit antioxidant and anti-inflammatory effects. To elucidate the potential role of tryptanthrin in periodontal disease, we investigated its effects on bone metabolism and innate immunity, including the epithelial barrier. RAW264.7 cells were cultured with soluble receptor activator of nuclear factor-κB ligand (sRANKL) and tryptanthrin, and stained with Tartrate-Resistant Acid Phosphatase (TRAP) to evaluate osteoclastgenesis. The expression of osteoclast differentiation markers was examined using western blot analysis. OBA-9 cells were cultured with tryptanthrin, and the expression of tight junction (TJ) proteins and cell adhesion molecules (CAMs) was examined by western blot analysis. We found that tryptanthrin significantly inhibited osteoclastgenesis and suppressed the expression of osteoclast differentiation markers. Further, tryptanthrin enhanced the expression of TJ proteins and CAMs. These results indicated that tryptanthrin inhibits osteoclastgenesis by downregulating the osteoclast differentiation markers and enhances cell-cell adhesion by upregulating TJ proteins and CAMs. Bioscience, biotechnology, and biochemistry null null 20260210 10.1093/bbb/zbag025 41665875 yujiinagaki/published_papers/52540592 Jun-Ichi Kido Rie Kido Sachiko Ando Atsuko Shinozaki Mika Bando Yuji Inagaki Yasuhiro Seki Yoshiyuki Ohiro Hiromichi Yumoto Evaluation of salivary calprotectin as a marker for screening periodontitis using a latex agglutination turbidimetric immunoassay system: a cross-sectional study. BACKGROUND: Biomolecules in body fluids such as gingival crevicular fluid and saliva are used for the diagnosis of periodontitis. Saliva is easy to collect and salivary biomarkers are useful in screening periodontitis. The suitable salivary biomarkers and their measuring system are important for screening periodontitis in mass dental examination. Therefore, this study examined the potential of few salivary biomarkers for screening and diagnosis of periodontitis and aimed to evaluate more effective biomarkers and their measuring methods in dental examination. METHODS: Ninety-three individuals with and without periodontitis participated in this clinical examination and were classified into the non-periodontal diseases or stage I periodontitis (control, n = 26) and stage II-IV periodontitis groups (periodontitis, n = 67) after periodontal examinations. Unstimulated saliva samples were collected from participants. The levels of salivary biomarkers including calprotectin, hemoglobin (Hb), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), alanine aminotransferase and aspartate aminotransferase (AST) were automatically measured using the latex agglutination turbidimetric immunoassay (LATIA) and enzyme assay systems. Differences in clinical indicator and biomarker levels in the control and periodontitis groups and their correlations were statistically analyzed. A receiver operating characteristic (ROC) analysis of the ability of salivary biomarkers to predict periodontitis was also performed. RESULTS: Salivary calprotectin, Hb, LDH, ALP and AST levels were significantly higher in the periodontitis group than that in the control group. At the initial stage of periodontitis, a significant difference was only observed in calprotectin levels. Calprotectin and LDH levels strongly correlated with clinical indicators including probing pocket depth, clinical attachment level, bleeding on probing, gingival index and periodontal inflamed surface area with high correlation coefficient (calprotectin: 0.582-0.660, LDH: 0.534-0.614). Calprotectin showed a higher area under the ROC curve value (0.894), with 91% sensitivity and 73% specificity, than the other salivary biomarkers. CONCLUSIONS: Salivary calprotectin showed a high effectiveness for the diagnosis of periodontitis, and the measurement of salivary calprotectin using the LATIA system that is a high throughput method is suitable for population-based screening of periodontal diseases. BMC oral health 26 1 240 240 20260107 10.1186/s12903-025-07622-7 41501804 yujiinagaki/published_papers/52515258 Raras Ajeng Enggardipta Minato Akizuki Mika Bando Yuji Inagaki Kazumitsu Sekine Kenichi Hamada Tomoko Sumitomo Kanta Sato Hiromichi Yumoto Trimethyl chitosan: Antibacterial activity on Enterococcus faecalis biofilm and cytocompatibility on human periodontal ligament fibroblasts cells BACKGROUND/PURPOSE: Effective disinfection of the root canal system remains a major challenge due to complex anatomy and the persistence of biofilm-forming bacteria such as Enterococcus faecalis. Trimethyl chitosan (TMC), a quaternized chitosan derivative, has shown promising antimicrobial properties but has not been extensively studied for endodontic use. This study aimed to evaluate the antibacterial and antibiofilm efficacy of TMC against E. faecalis and assess its cytocompatibility with human periodontal ligament fibroblasts (HPdLFs). MATERIALS AND METHODS: The E. faecalis biofilm formation in the presence of TMC and antibacterial activity of TMC against mature E. faecalis biofilms were evaluated using crystal violet staining, adenosine triphosphate assays, colony forming unit counting, scanning electron microscopy, and fluorescence microscopy. The expression of genes associated with E. faecalis biofilm formation, such as ace, esp, and gelE, was determined. Moreover, cytocompatibility of TMC with HPdLFs was assessed using a cell counting kit-8 assay. RESULTS: TMC significantly inhibited biofilm formation by E. faecalis and in the mature E. faecalis biofilm, TMC interfered with the total biofilm biomass, reduced bacterial numbers, weakened the biofilm structure, and upregulated ace, esp, and gelE expression. Furthermore, a lower concentration of TMC maintained HPdLFs viability. CONCLUSION: This study highlights the potential of TMC as a novel irrigating material owing to its antibacterial and antibiofilm activities against E. faecalis and its cytocompatibility with HPdLFs. Elsevier BV Journal of Dental Sciences 1991-7902 21 1 150 158 20250700 10.1016/j.jds.2025.06.022 41585173 yujiinagaki/published_papers/52541065 Rie Kido Yuka Hiroshima Jun-Ichi Kido Mika Bando Kaya Yoshida Yuji Inagaki Hiromichi Yumoto Lipocalin 2 inhibits the expressions of interleukin-8 and macrophage inflammatory protein-1α in human neutrophil-like cells. OBJECTIVES: Lipocalin 2 (LCN2) is a glycoprotein with multiple functions, including antimicrobial activity, inflammatory response modulation, and cell migration. LCN2 is expressed in some cells, such as epithelial cells and neutrophils, and its levels are increased in inflammatory diseases. This study investigated the presence of LCN2 receptor (24p3R) in cells around periodontal tissues and function of LCN2 in cells with a receptor to explore the role of LCN2 in periodontal diseases. METHODS: The presence of 24p3R was examined in periodontal cells, including human gingival fibroblasts, periodontal ligament fibroblasts, human oral epithelial cells (HOECs), and neutrophil-like cells (HL-60), by Western blotting. Changes in periodontal disease-associated proteins in the presence of recombinant LCN2 (rLCN2) were examined using a protein array in differentiated HL-60 (dHL-60) cells. Interleukin-8 (IL-8) and macrophage inflammatory protein-1α (MIP-1α) mRNA expressions were analyzed by qRT-PCR, and IL-8 and MIP-1α levels in dHL-60 cells treated with rLCN2 or Porphyromonas gingivalis-lipopolysaccaharide (P.g-LPS) were determined by enzyme-linked immunosorbent assay. RESULTS: We detected 24p3R in dHL-60 cells. IL-8 was highly expressed and MIP-1α was weakly expressed in dHL-60 cells using a protein array. rLCN2 significantly decreased IL-8 mRNA and protein levels and suppressed P.g-LPS-induced IL-8 production in dHL-60 cells. As dHL-60 cells were co-cultured with HOECs in which LCN2 was knocked down, IL-8 mRNA expression increased in dHL-60 cells. Furthermore, rLCN2 inhibited MIP-1α production in dHL-60 cells. CONCLUSION: LCN2 suppresses inflammatory responses by regulating IL-8 and MIP-1α expression in periodontal diseases. Journal of oral biosciences 67 1 100624 100624 20250300 10.1016/j.job.2025.100624 39892784 yujiinagaki/published_papers/48475605 Kenji Masutomi Mika Bando Yuji Inagaki Rie Kido Yuta Uemura Yukari Hatada Jun Ichi Kido Makoto Fukui Daisuke Hinode Hiromichi Yumoto Relationship between oral hypofunction and salivary biomarkers in older adults: a cross-sectional study BMC Oral Health 1472-6831 24 1 null null 20241200 10.1186/s12903-024-04556-4 38971720 2-s2.0-85197697204 yujiinagaki/published_papers/41825084 Jun-Ichi Kido Yuka Hiroshima Rie Kido Kaya Yoshida Yuji Inagaki Koji Naruishi Kazuaki Kajimoto Masatoshi Kataoka Yasuo Shinohara Hiromichi Yumoto Lipocalin 2, synthesized using a cell-free protein synthesis system and encapsulated into liposomes, inhibits the adhesion of Porphyromonas gingivalis to human oral epithelial cells. BACKGROUND AND OBJECTIVE: Lipocalin 2 (LCN2), a glycoprotein expressed in epithelial cells and leukocytes, has an antibacterial effect and plays a role in innate immunity. The delivery of LCN2 encapsulated in liposomes to oral epithelium may be useful to prevent oral infectious diseases. This study aimed to investigate the inhibitory effect of LCN2, artificially synthesized using a cell-free protein synthesis (CFPS) system, on the adhesion of Porphyromonas gingivalis to oral epithelial cells in order to approach oral healthcare using LCN2. METHODS: LCN 2 was synthesized using a CFPS system and assayed by Western blotting, mass spectrometry and enzyme-linked immunosorbent assay (ELISA). The bilayer liposomes were prepared by the spontaneous transfer method using 1,2-dioleoyl-sn-glycero-3 phosphocholine (DOPC), 3-sn-phosphatidylcholine from Egg Yolk (Egg-PC), and 1,2-dioleoyl-sn-glycero-3 phosphoethanolamine (DOPE). The cellular and medium fractions derived from the culture of oral epithelial cells with liposome-encapsulated LCN2 were assayed by Western blotting and ELISA. The effect of the synthesized LCN2 on adhesion of the labeled P. gingivalis to oral epithelial cells was investigated as an evaluation of its antibacterial activity. RESULTS: The synthesized LCN2 protein was identified by Western blotting; its amino acid sequence was similar to that of recombinant LCN2 protein. The additions of DOPE and octa-arginine in the outer lipid-layer components of liposome significantly increased the delivery of liposomes to epithelial cells. When oral epithelial cells were cultured with the synthesized and liposome-encapsulated LCN2, LCN2 was identified in the cellular and medium fractions by Western blotting and its concentration in the cellular fraction from the culture with the synthesized LCN2 was significantly higher than that of a template DNA-free protein. The synthesized LCN2 and liposome-encapsulated LCN2 significantly inhibited the adhesion of P. gingivalis to oral epithelial cells compared with template DNA-free protein. CONCLUSION: LCN2 was artificially synthesized by a CFPS system, encapsulated in liposomes, and delivered to oral epithelial cells, and demonstrated an antibacterial action against P. gingivalis. This approach may become a useful model for oral healthcare. Journal of periodontal research 58 2 262 273 20230400 10.1111/jre.13088 36579753 yujiinagaki/published_papers/40746397 Yuta Uemura Yuka Hiroshima Ayano Tada Keiji Murakami Kaya Yoshida Yuji Inagaki Tomomi Kuwahara Akikazu Murakami Hideki Fujii Hiromichi Yumoto Porphyromonas gingivalis Outer Membrane Vesicles Stimulate Gingival Epithelial Cells to Induce Pro-Inflammatory Cytokines via the MAPK and STING Pathways Porphyromonas gingivalis (Pg) is a keystone pathogen associated with chronic periodontitis and produces outer membrane vesicles (OMVs) that contain lipopolysaccharide (LPS), gingipains, and pathogen-derived DNA and RNA. Pg-OMVs are involved in the pathogenesis of periodontitis. Pg-OMV-activated pathways that induce the production of the pro-inflammatory cytokines, interleukin (IL)-6, and IL-8 in the human gingival epithelial cell line, OBA-9, were investigated. The role of mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB in levels of Pg-OMV-induced pro-inflammatory cytokines was investigated using Western blot analysis and specific pathway inhibitors. Pg-OMVs induced IL-6 and IL-8 production via the extracellular signal-regulated kinase (Erk) 1/2, c-Jun N-terminal kinase (JNK), p38 MAPK, and NF-κB signaling pathways in OBA-9 cells. In addition, the stimulator of interferon genes (STING), an essential innate immune signaling molecule, was triggered by a cytosolic pathogen DNA. Pg-OMV-induced IL-6 and IL-8 mRNA expression and production were significantly suppressed by STING-specific small interfering RNA. Taken together, these results demonstrated that Pg-OMV-activated Erk1/2, JNK, p38 MAPK, STING, and NF-κB signaling pathways resulting in increased IL-6 and IL-8 expression in human gingival epithelial cells. These results suggest that Pg-OMVs may play important roles in periodontitis exacerbation by stimulating various pathways. MDPI AG Biomedicines 2227-9059 10 10 2643 2643 20221020 10.3390/biomedicines10102643 yujiinagaki/published_papers/35026215 Yuji Inagaki Jun-Ichi Kido Yasufumi Nishikawa Rie Kido Eijiro Sakamoto Mika Bando Koji Naruishi Toshihiko Nagata Hiromichi Yumoto Gan-Lu-Yin (Kanroin), Traditional Chinese Herbal Extracts, Reduces Osteoclast Differentiation In Vitro and Prevents Alveolar Bone Resorption in Rat Experimental Periodontitis Gan-Lu-Yin (GLY), a traditional Chinese herbal medicine, shows therapeutic effects on periodontitis, but that mechanism is not well known. This study aims to clarify the precise mechanism by investigating the inhibitory effects of GLY extracts on osteoclastogenesis in vitro and on bone resorption in periodontitis in vivo. RAW264.7 cells are cultured with soluble receptor activator of nuclear factor-kappa B (sRANKL) and GLY extracts (0.01-1.0 mg/mL), and stained for tartrate-resistant acid phosphatase (TRAP) to evaluate osteoclast differentiation. Experimental periodontitis is induced by placing a nylon ligature around the second maxillary molar in rats, and rats are administered GLY extracts (60 mg/kg) daily for 20 days. Their maxillae are collected on day 4 and 20, and the levels of alveolar bone resorption and osteoclast differentiation are estimated using micro-computed tomography (CT) and histological analysis, respectively. In RAW264.7 cells, GLY extracts significantly inhibit sRANKL-induced osteoclast differentiation at a concentration of more than 0.05 mg/mL. In experimental periodontitis, administering GLY extracts significantly decreases the number of TRAP-positive osteoclasts in the alveolar bone on day 4, and significantly inhibits the ligature-induced bone resorption on day 20. These results show that GLY extracts suppress bone resorption by inhibiting osteoclast differentiation in experimental periodontitis, suggesting that GLY extracts are potentially useful for oral care in periodontitis. Journal of clinical medicine 10 3 null null 20210120 10.3390/jcm10030386 33498415 yujiinagaki/published_papers/34850612 Rie Kido Yuka Hiroshima Jun-ichi Kido Takahisa Ikuta Eijiro Sakamoto Yuji Inagaki Koji Naruishi Hiromichi Yumoto Advanced glycation end‐products increase lipocalin 2 expression in human oral epithelial cells Wiley Journal of Periodontal Research 1600-0765 55 4 539 550 20200800 10.1111/jre.12741 yujiinagaki/published_papers/28425723 Ryosuke Takagi Eijiro Sakamoto Jun-Ichi Kido Yuji Inagaki Yuka Hiroshima Koji Naruishi Hiromichi Yumoto S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells. Objective: Calprotectin is a heterocomplex of S100A8 and S100A9 and is mainly secreted from neutrophils, monocytes, and chondrocytes in inflammatory condition. Calprotectin binds to RAGE and TLR4 and induces the expression of proinflammatory chemokines and cytokines in various cells. Periodontitis is a chronic inflammatory disease that leads to gingival inflammation and alveolar bone resorption. Calprotectin levels in gingival crevicular fluid of periodontitis patients are higher than healthy patients. In the present study, the effects of S100A8 and S100A9 on the expressions of proinflammatory cytokines and bone metabolism-related factors in mouse osteocyte-like cells (MLO-Y4-A2) were investigated. Design: MLO-Y4-A2 cells were treated with S100A8 and S100A9, and the expressions of RAGE, TLR4, RANKL, and several inflammatory cytokines were analyzed by PCR and Western blotting or ELISA methods. To investigate the intracellular signaling pathways, phosphorylation of MAPK and STAT3 was determined by Western blotting, and chemical specific inhibitors and siRNAs were used. Results: Expressions of IL-6 and RANKL were increased by treatment with S100A9 but not S100A8. However, both S100A8 and S100A9 did not change expression of IL-1β, IL-8, and TNF-α. Although RAGE and TLR4 expressions were not upregulated by S100A9 treatment, transfection of siRNA for RAGE and TLR4 significantly decreased IL-6 and RANKL expressions. In addition, S100A9 activated p38, ERK, and STAT3 signaling pathways, and inhibitors for these factors significantly decreased S100A9-induced IL-6 and RANKL expressions. Conclusions: These results indicated that S100A9 induces IL-6 and RANKL production via engagement with RAGE and TLR4 signalings in osteocytes and suggested that S100A9 may play important roles in the periodontal alveolar bone destruction. BioMed research international 2020 7149408 7149408 20200000 10.1155/2020/7149408 32149126 yujiinagaki/published_papers/28425727 Kohei Nonaka Mika Bando Eijiro Sakamoto Yuji Inagaki Koji Naruishi Hiromichi Yumoto Jun-Ichi Kido 6-Shogaol Inhibits Advanced Glycation End-Products-Induced IL-6 and ICAM-1 Expression by Regulating Oxidative Responses in Human Gingival Fibroblasts. Advanced glycation end-products (AGEs) cause diabetes mellitus (DM) complications and accumulate more highly in periodontal tissues of patients with periodontitis and DM. AGEs aggravate periodontitis with DM by increasing the expression of inflammation-related factors in periodontal tissues. 6-Shogaol, a major compound in ginger, has anti-inflammatory and anti-oxidative activities. However, the influence of shogaol on DM-associated periodontitis is not well known. In this study, the effects of 6-shogaol on AGEs-induced oxidative and anti-oxidative responses, and IL-6 and ICAM-1 expression in human gingival fibroblasts (HGFs) were investigated. When HGFs were cultured with 6-shogaol and AGEs, the activities of reactive oxygen species (ROS) and antioxidant enzymes (heme oxygenase-1 [HO-1] and NAD(P)H quinone dehydrogenase 1 [NQO1]), and IL-6 and ICAM-1 expressions were investigated. RAGE expression and phosphorylation of MAPKs and NF-κB were examined by western blotting. 6-Shogaol significantly inhibited AGEs-induced ROS activity, and increased HO-1 and NQO1 levels compared with the AGEs-treated cells. The AGEs-stimulated expression levels of receptor of AGE (RAGE), IL-6 and ICAM-1 and the phosphorylation of p38, ERK and p65 were attenuated by 6-shogaol. These results suggested that 6-shogaol inhibits AGEs-induced inflammatory responses by regulating oxidative and anti-oxidative activities and may have protective effects on periodontitis with DM. Molecules (Basel, Switzerland) 24 20 null null 20191015 10.3390/molecules24203705 31619000 yujiinagaki/published_papers/23493744 Sakamoto E Kido JI Takagi R Inagaki Y Naruishi K Nagata T Yumoto H Advanced glycation end-product 2 and Porphyromonas gingivalis lipopolysaccharide increase sclerostin expression in mouse osteocyte-like cells. Bone 8756-3282 122 22 30 20190500 10.1016/j.bone.2019.02.001 30735798 yujiinagaki/published_papers/26977866 Kohei Nonaka Yukari Kajiura Mika Bandou Eijiro Sakamoto Yuji Inagaki JH Lew Koji Naruishi Takahisa Ikuta Kaya Yoshida Tesuo Kobayashi Hiromasa Yoshie Toshihiko Nagata Jun-ichi Kido Advanced glycation end-products increase IL-6 and ICAM-1 expression via RAGE, MAPK and NF-kB pathways in human gingival fibroblasts Diabetes mellitus (DM) is a risk factor for periodontal diseases and may exacerbate the progression of the pathogenesis of periodontitis. Advanced glycation end-products (AGEs) cause DM complications relative to levels of glycemic control and larger amounts accumulate in the periodontal tissues of patients with periodontitis and DM. In the present study, we investigated the effects of AGEs on the expression of inflammation-related factors in human gingival fibroblasts (HGFs) to elucidate the impact of AGEs on DM-associated periodontitis. HGFs were cultured with or without AGEs. Cell viability was examined, and RNA and protein fractions were isolated from AGE-treated cells. The expression of interleukin (IL)-6, intercellular adhesion molecule-1 (ICAM-1), and the receptor for AGE (RAGE) was investigated using reverse transcription-polymerase chain reaction, quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay, and reactive oxygen species activity was measured using a kit with 2',7'-dichlorofluorescin diacetate. Human monocytic cells (THP-1) labeled with a fluorescent reagent were co-cultured with HGFs treated with AGEs and IL-6 siRNA, and the adhesive activity of THP-1 cells to HGFs was assessed. The expression of IL-6 and ICAM-1 was examined when HGFs were pretreated with recombinant human IL-6, the siRNAs of RAGE and IL-6, and inhibitors of MAPK and NF-κB, and then cultured with and without AGEs. The phosphorylation of MAPK and NF-κB was assessed using western blotting. AGEs increased the mRNA and protein expressions of RAGE, IL-6, ICAM-1 and reactive oxygen species activity in HGFs, and promoted the adhesion of THP-1 cells to HGFs, but had no effect on cell viability until 72 hours. Recombinant human IL-6 increased ICAM-1 expression in HGFs, while the siRNAs of RAGE and IL-6 inhibited AGE-induced IL6 and ICAM1 mRNA expression, and IL-6 siRNA depressed AGE-induced THP-1 cell adhesion. AGEs increased the phosphorylation of p38 and ERK MAPKs, p65 NF-κB and IκBα, while inhibitors of p38, ERK MAPKs and NF-κB significantly decreased AGE-induced IL-6 and ICAM-1 expression. AGEs increase IL-6 and ICAM-1 expression via the RAGE, MAPK and NF-κB pathways in HGFs and may exacerbate the progression of the pathogenesis of periodontal diseases. Journal of Periodontal Research 1600-0765 53 3 334 344 20180600 10.1111/jre.12518 29193068 yujiinagaki/published_papers/15560455 J. Teramachi Y. Inagaki H. Shinohara H. Okamura D. Yang K. Ochiai R. Baba H. Morimoto T. Nagata T. Haneji PKR regulates LPS-induced osteoclast formation and bone destruction in vitro and in vivo Blackwell Publishing Ltd Oral Diseases 1601-0825 23 2 181 188 20170301 10.1111/odi.12592 27718290 2-s2.0-85005966819 yujiinagaki/published_papers/15560452 Chie Mihara-Wada 美原(和田) 智恵 Koji Naruishi 成石 浩司 Mika Bandou 板東 美香 Nishikawa Yasufumi 西川 泰史 Jung-Hwan Lew Eijiro Sakamoto 坂本 英次郎 Ikuta Takahisa 生田 貴久 Kono Kaoru 河野 薫 Yukari Kajiura 梶浦 由加里 Hashimoto Mari 橋本 万里 Yukiko Nakajima 中島 由紀子 Yuji Inagaki 稲垣 裕司 Masami Ninomiya 二宮 雅美 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Post clinical clerkship-OSCEを見据えた歯周病科での模擬OSCEの概要 Journal of Oral Health and Biosciences 2188-7888 29 2 49 53 20170200 10.20738/johb.29.2_49 yujiinagaki/published_papers/15560473 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 生田 貴久 Yukari Kajiura 梶浦 由加里 Yukiko Nakajima 中島 由紀子 Eijiro Sakamoto 坂本 英次郎 Chie Mihara-Wada 美原(和田) 智恵 Masami Ninomiya 二宮 雅美 西川 泰史 Jung-Hwan Lew Koji Naruishi 成石 浩司 Toshihiko Nagata 永田 俊彦 Diagnosis of Periodontal Diseases using Biomarkers in Gingival Crevicular Fluid 歯肉溝滲出液中のバイオマーカーを用いた歯周病診断 Periodontal diseases cause an inflammation and degradation of periodontal tissues and missing of teeth. The incidence rate of periodontal diseases is high in middle-aged and elderly people.A reasonable diagnosis of periodontal diseases is very important to keep teeth, however, conventional examinations of periodontal diseases is not necessarily exact and objective. Gingival crevicular fluid (GCF) is an exudate secreted from periodontal tissues and contains many components including proteolytic enzymes, inflammatory cytokines, blood-associated proteins, cellular and bacterial fragments. Because some proteins in GCF are related to inflammation, tissue degradation and bone metabolism, those proteins have been studying as a diagnostic marker of periodontal diseases. GCF is noninvasively collected using a sterile paper strip and biomarkers are determined using enzyme-linked immunosorbent assay (ELISA) and enzyme activity assay. We identified calprotectin, an inflammationrelated protein, in GCF and calprotectin level in GCF from periodontitis sites was significantly higher than that of healthy control. Calprotectin level in GCF was positively correlated to gingival index and other biomarkers and decreased by periodontal treatments. Resistin is an adipocytokine and its level increases in some inflammatory diseases. Resistin level in GCF from periodontitis sites was high compared to the level of healthy control samples. Procollagen type I C-terminal peptide (PICP) is a biomarker for bone metabolism and its level was high in GCF collected from periodontitis sites. These results suggested that calprotectin, resistin and PICP are useful biomarkers for periodontal diseases. On the other hand, we showed that glycated albumin (GA), a marker of diabetes mellitus (DM), was contained in GCF and GA level in GCF from DM patients was significantly higher than that of non-DM individuals. Components in GCF may be biomarkers of systemic diseases as well as periodontal diseases and their determination will be useful diagnostic examination of some diseases. Recently, we have been studying the determining system of GCF calprotectin, including microchip ELISA, surface plasmon resonance assay and immuno-chromatography assay. When GCF biomarkers are determined using the determining systems, we will simply, exactly and objectively diagnose periodontal diseases at our dental offices. Journal of Oral Health and Biosciences 2188-7888 29 1 13 20 20161200 yujiinagaki/published_papers/15560453 E. Sakamoto C. Mihara T. Ikuta Y. Inagaki J. Kido T. Nagata Inhibitory effects of advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide on the expression of osteoblastic markers of rat bone marrow cells in culture Blackwell Munksgaard Journal of Periodontal Research 1600-0765 51 3 313 320 20160601 10.1111/jre.12310 26223811 2-s2.0-84938353798 yujiinagaki/published_papers/28188180 Yuka Hiroshima Mika Bando Yuji Inagaki Reiko Kido Masatoshi Kataoka Toshihiko Nagata Jun-ichi Kido Effect of Hangeshashinto on calprotectin expression in human oral epithelial cells ODONTOLOGY 1618-1255 104 2 152 162 20160500 10.1007/s10266-015-0196-3 yujiinagaki/published_papers/15560457 Yuka Hiroshima Mika Bando Yuji Inagaki Reiko Kido Masatoshi Kataoka Toshihiko Nagata Jun-ichi Kido Effect of Hangeshashinto on calprotectin expression in human oral epithelial cells Springer-Verlag Tokyo Odontology 1618-1255 104 2 152 162 20160501 10.1007/s10266-015-0196-3 25649126 2-s2.0-84922161650 yujiinagaki/published_papers/26880640 Jumpei Teramachi Yuki Nagata Khalid Mohammad Yuji Inagaki Yasuhisa Ohata Theresa Guise Laëtitia Michou Jacques P Brown Jolene J Windle Noriyoshi Kurihara G David Roodman Measles virus nucleocapsid protein increases osteoblast differentiation in Paget's disease. Paget's disease (PD) is characterized by focal and dramatic bone resorption and formation. Treatments that target osteoclasts (OCLs) block both pagetic bone resorption and formation; therefore, PD offers key insights into mechanisms that couple bone resorption and formation. Here, we evaluated OCLs from 3 patients with PD and determined that measles virus nucleocapsid protein (MVNP) was expressed in 70% of these OCLs. Moreover, transgenic mice with OCL-specific expression of MVNP (MVNP mice) developed PD-like bone lesions that required MVNP-dependent induction of high IL-6 expression levels in OCLs. In contrast, mice harboring a knockin of p62P394L (p62-KI mice), which is the most frequent PD-associated mutation, exhibited increased bone resorption, but not formation. Evaluation of OCLs from MVNP, p62-KI, and WT mice revealed increased IGF1 expression in MVNP-expressing OCLs that resulted from the high IL-6 expression levels in these cells. IL-6, in turn, increased the expression of coupling factors, specifically ephrinB2 on OCLs and EphB4 on osteoblasts (OBs). IGF1 enhanced ephrinB2 expression on OCLs and OB differentiation. Importantly, ephrinB2 and IGF1 levels were increased in MVNP-expressing OCLs from patients with PD and MVNP-transduced human OCLs compared with levels detected in controls. Further, anti-IGF1 or anti-IGF1R blocked Runx2 and osteocalcin upregulation in OBs cocultured with MVNP-expressing OCLs. These results suggest that in PD, MVNP upregulates IL-6 and IGF1 in OCLs to increase ephrinB2-EphB4 coupling and bone formation. The Journal of clinical investigation 0021-9738 126 3 1012 22 20160301 10.1172/JCI82012 26878170 yujiinagaki/published_papers/15560454 Jumpei Teramachi Yuki Nagata Khalid Mohammad Yuji Inagaki Yasuhisa Ohata Theresa Guise La?titia Michou P Jacques Brown J Jolene Windle Noriyoshi Kurihara David G Roodman Measles virus nucleocapsid protein increases osteoblast differentiation in Paget's disease. Paget's disease (PD) is characterized by focal and dramatic bone resorption and formation. Treatments that target osteoclasts (OCLs) block both pagetic bone resorption and formation; therefore, PD offers key insights into mechanisms that couple bone resorption and formation. Here, we evaluated OCLs from 3 patients with PD and determined that measles virus nucleocapsid protein (MVNP) was expressed in 70% of these OCLs. Moreover, transgenic mice with OCL-specific expression of MVNP (MVNP mice) developed PD-like bone lesions that required MVNP-dependent induction of high IL-6 expression levels in OCLs. In contrast, mice harboring a knockin of p62P394L (p62-KI mice), which is the most frequent PD-associated mutation, exhibited increased bone resorption, but not formation. Evaluation of OCLs from MVNP, p62-KI, and WT mice revealed increased IGF1 expression in MVNP-expressing OCLs that resulted from the high IL-6 expression levels in these cells. IL-6, in turn, increased the expression of coupling factors, specifically ephrinB2 on OCLs and EphB4 on osteoblasts (OBs). IGF1 enhanced ephrinB2 expression on OCLs and OB differentiation. Importantly, ephrinB2 and IGF1 levels were increased in MVNP-expressing OCLs from patients with PD and MVNP-transduced human OCLs compared with levels detected in controls. Further, anti-IGF1 or anti-IGF1R blocked Runx2 and osteocalcin upregulation in OBs cocultured with MVNP-expressing OCLs. These results suggest that in PD, MVNP upregulates IL-6 and IGF1 in OCLs to increase ephrinB2-EphB4 coupling and bone formation. The Journal of Clinical Investigation 1558-8238 126 3 1012 1022 20160215 10.1172/JCI82012 26878170 yujiinagaki/published_papers/15644908 Koji Naruishi Keiji Oishi Yuji Inagaki Masumi Horibe Mika Bando Masami Ninomiya Kazuhiko Kawahara Jun Minakuchi Shu Kawashima Kenji Shima Jun-Ichi Kido Toshihiko Nagata Association between periodontal condition and kidney dysfunction in Japanese adults: A cross-sectional study Wiley-Blackwell Clinical and Experimental Dental Research 2057-4347 2 3 200 207 20160000 10.1002/cre2.39 29744168 2-s2.0-85041411693 yujiinagaki/published_papers/15560456 Jun-Ichi Kido Y. Bando M. Bando Y. Kajiura Y. Hiroshima Y. Inagaki H. Murata T. Ikuta R. Kido K. Naruishi M. Funaki T. Nagata YKL-40 level in gingival crevicular fluid from patients with periodontitis and type 2 diabetes Blackwell Publishing Ltd Oral Diseases 1601-0825 21 5 667 673 20150701 10.1111/odi.12334 25740558 2-s2.0-84930271794 yujiinagaki/published_papers/15560460 Y. Nakajima Y. Inagaki J. Kido T. Nagata Advanced glycation end products increase expression of S100A8 and A9 via RAGE-MAPK in rat dental pulp cells Blackwell Publishing Ltd Oral Diseases 1601-0825 21 3 328 334 20150401 10.1111/odi.12280 25098709 2-s2.0-84925124937 yujiinagaki/published_papers/15560459 Yuji Inagaki 稲垣 裕司 Yukiko Nakajima 中島 由紀子 Masumi Horibe 堀部 ますみ 生田 貴久 Yukari Kajiura 梶浦 由加里 Koji Naruishi 成石 浩司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 肥満糖尿病ラット歯周炎の歯肉組織におけるオステオポンチンの局在 (NPO)日本歯周病学会 Journal of the Japanese Association of Periodontology 日本歯周病学会会誌 1880-408X 67 4 149 158 20150000 10.2329/perio.57.149 yujiinagaki/published_papers/15560461 Yukari Kajiura Mika Bandou Yuji Inagaki Toshihiko Nagata Jun-ichi Kido Glycated albumin and calprotectin levels in gingival crevicular fluid from patients with periodontitis and type 2 diabetes Patients with diabetes mellitus (DM) have a high prevalence of periodontitis. Periodontitis in these patients is characterized by severe inflammation and tissue breakdown, and its diagnosis is important for cures of periodontitis and DM. The purpose of this study is to investigate the levels of glycated albumin (GA), a DM marker, and calprotectin, an inflammatory marker, in gingival crevicular fluid (GCF) from patients with periodontitis and DM (DM-P). The 78 participants in this study were patients with DM, chronic periodontitis (CP), DM-P, and healthy individuals (H). GCF and blood were collected, and GA and calprotectin in GCF were analyzed using Western blotting and enzyme-linked immunosorbent assay. Levels were compared among H, DM, CP, and DM-P groups. Blood GA and glycated hemoglobin (HbA1c) were measured, and the correlation among GCF GA and blood HbA1c or GA levels was investigated. Receiver operating characteristic (ROC) analysis for GCF GA to predict DM was performed. GA was identified in GCF, and its amount/concentration in GCF samples from DM and DM-P were significantly higher than those of non-DM groups (H and CP). Calprotectin amounts in GCF from CP and DM-P were significantly higher than in H and DM groups. GCF GA level was positively correlated with blood HbA1c and GA level. ROC analysis of GCF GA showed an optimal cutoff value to predict DM. GA showed a high level in GCF from patients with DM. Examination of GA and calprotectin in GCF may be useful for predicting DM-P. Journal of Periodontology 1943-3670 85 12 1667 1675 20141200 10.1902/jop.2014.140241 25126693 yujiinagaki/published_papers/24815540 Fukumoto Y Horibe M Inagaki Y Oishi K Tamaki N Ito HO Nagata T Association of gingival recession and other factors with the presence of dentin hypersensitivity. 1 Odontology / the Society of the Nippon Dental University 1618-1247 102 42 49 20140100 10.1007/s10266-012-0099-5 23283584 yujiinagaki/published_papers/15560462 Naofumi Tamaki Rita Cristina Orihuela-Campos Yuji Inagaki Makoto Fukui Toshihiko Nagata Hiro-O Ito Resveratrol improves oxidative stress and prevents the progression of periodontitis via the activation of the Sirt1/AMPK and the Nrf2/antioxidant defense pathways in a rat periodontitis model Elsevier Inc. Free Radical Biology and Medicine 1873-4596 75 222 229 20140000 10.1016/j.freeradbiomed.2014.07.034 25091897 2-s2.0-84907345449 yujiinagaki/published_papers/24815534 Ikuta T Inagaki Y Tanaka K Saito T Nakajima Y Bando M Kido JI Nagata T Gene polymorphism of β-defensin-1 is associated with susceptibility to periodontitis in Japanese. Periodontitis is a multifactorial disease associated with genetic and environmental factors. Single-nucleotide polymorphisms (SNPs) are associated with susceptibility to common diseases such as diabetes and periodontitis. Although the oral cavity is exposed to various organisms, the conditions are well controlled by innate and acquired immune systems. Antimicrobial peptides (AMPs) play an important role in the innate immune system; however, the association of AMP-SNPs with periodontitis has not been fully elucidated. This study investigated the relationship between AMP-SNPs and periodontitis in Japanese. One hundred and five Japanese subjects were recruited, which included patients with aggressive, severe, moderate and mild periodontitis, and age-matched healthy controls. Genomic DNA was isolated from peripheral blood and genotypes of SNPs of β-defensin-1 and lactoferrin genes (DEFB1: rs1799946, rs1800972 and rs11362; and LTF: rs1126478) were investigated using the PCR-Invader assay. Protein level of AMPs in gingival crevicular fluid (GCF) was quantified by ELISA. Case-control studies revealed that the -44 CC genotype of DEFB1 (rs1800972) was associated with periodontitis (OR 2.51), particularly with severe chronic periodontitis (OR 4.15) and with combined severe and moderate chronic periodontitis (OR 4.04). No statistical differences were found in other genotypes. The β-defensin-1 concentrations in GCF were significantly lower in subjects with the -44 CC genotype of DEFB1 than in those without this genotype. No significant differences between GCF concentrations of AMPs and other genotypes were detected. The -44 CC genotype of the β-defensin-1 gene (DEFB1 rs1800972) may be associated with susceptibility to chronic periodontitis in Japanese. Odontology / the Society of the Nippon Dental University 1618-1247 103 1 66 74 20131100 10.1007/s10266-013-0139-9 24276427 yujiinagaki/published_papers/39576930 木戸 淳一 板東 美香 坂東 由記子 稲垣 裕司 廣島 佑香 梶浦 由加里 美原 智恵 村田 裕美 生田 貴久 篠原 宏貴 橋本 万里 船木 真理 齋藤 晴比古 永田 俊彦 糖尿病関連歯周炎の診断マーカーとしての歯肉溝滲出液中グリコアルブミンとカルプロテクチンの有用性 (一社)日本糖尿病学会 糖尿病 1881-588X 56 Suppl.1 S 220 20130400 yujiinagaki/published_papers/15560463 Yukiko Nakajima Yuji Inagaki Yuka Hiroshima Jun-ichi Kido Toshihiko Nagata Advanced glycation end-products enhance calcification in cultured rat dental pulp cells Amorphous calcification frequently appears in dental pulp tissues of diabetic patients; however, its pathologic process has not been fully elucidated. We previously found that pulp stones and thickened predentin occurred more frequently in diabetic rats. Recent findings demonstrated that accumulation of advanced glycation end-products (AGE) might be involved in vascular calcification complicated with diabetes. The aim of this study was to determine the effect of AGE on calcified nodule formation by rat dental pulp cells in culture. Rat dental pulp cells and gingival fibroblasts were independently cultured with 50 and 100 μg/mL AGE. Alkaline phosphatase activity and calcified nodule formation were measured. Expressions of receptor for AGE, osteopontin (OPN), and osteocalcin (OCN) mRNA were determined by quantitative real-time polymerase chain reaction. Protein levels of OPN and OCN secreted in culture medium were quantified by enzyme-linked immunosorbent assay. AGE (50 and 100 μg/mL) markedly increased both alkaline phosphatase activity and calcified nodule formation in dental pulp cells (P < .01), whereas it did not affect those in gingival fibroblasts. Real-time polymerase chain reaction analysis revealed that AGE increased mRNA expressions of receptor for AGE, OPN, and OCN in dental pulp cells (P < .05). Enzyme-linked immunosorbent assay analysis revealed that the protein levels of OPN and OCN produced by dental pulp cells were higher in AGE-treated than in untreated cells (P < .05). AGE enhanced the calcification potentials of rat dental pulp cells, suggesting that it may stimulate pathologic calcification of diabetic dental pulp tissues. Journal of Endodontics 1878-3554 39 873 878 20130116 10.1016/j.joen.2012.11.027 23791254 yujiinagaki/published_papers/15560464 Yoshikazu Fukumoto Masumi Horibe Yuji Inagaki Keiji Oishi Naofumi Tamaki Hiro-O Ito Toshihiko Nagata Association of gingival recession and other factors with the presence of dentin hypersensitivity. Dentin hypersensitivity (DH) may be present in association with gingival recession. The aim of this study was to determine quantitatively the association of gingival recession and other factors with the presence of DH. One hundred and four Japanese subjects with or without gingival recession were randomly selected. Intact canines and/or first premolars in both maxillary and mandibular quadrants were analyzed. Gingival recession was measured as a vertical length at the buccal site of the teeth. DH was recorded as an ordered categorical variable registering four increasing levels of pain after cold stimulation; from no discomfort to severe pain during and after stimulation (DH1, 2, 3, and 4). Association of DH with periodontal parameters and daily lifestyle was also investigated. Tooth-based analysis of 446 teeth from 104 subjects revealed that DH level was significantly higher in recessive teeth (1, 2, 3, and 4-8 mm) than in non-recessive teeth (0 mm). DH-positive rate in non-recessive teeth was only 18 % (DH1; 14 %, DH2; 3 %, and DH3; 1 %). Highest DH level was observed in teeth with severe recession (4-8 mm), showing DH0; 21 %, DH1; 33 %, DH2; 31 %, and DH3; 15 %. Recession-dependent increase in DH was observed, showing 18, 49, 52, 60, and 79 % DH-positive in teeth with 0, 1, 2, 3, and 4-8 mm recession, respectively. Plaque-free teeth showed a higher DH level than plaque-stained teeth, suggesting that good plaque control may be associated with the presence of DH. There were no significant differences in DH of teeth on the basis of smoking, probing depth, and bleeding on probing. Multiple logistic regression analysis revealed that gingival recession [odds ratio (OR) = 10.2, 95 % confidence interval (CI) = 5.5-18.9] and plaque deposition (OR = 0.3, 95 % CI = 0.2-0.5) were significant contributors to DH. Multilevel modeling analysis revealed that not only gingival recession and plaque deposition but also V-shaped cervical notch and tooth brushing frequency were associated with DH. These results demonstrate that the progression of gingival recession, plaque-free teeth, V-shaped cervical notch, and frequent brushing may be significant predictors of DH in canines and first premolars. Odontology 1618-1255 null null 20130103 10.1007/s10266-012-0099-5 23283584 yujiinagaki/published_papers/15560458 Takahisa Ikuta Yuji Inagaki Kazuya Tanaka Tsuyoshi Saito Yukiko Nakajima Mika Bando Mika Bandou Jun-ichi Kido Toshihiko Nagata Gene polymorphism of β-defensin-1 is associated with susceptibility to periodontitis in Japanese Gene polymorphism of β-defensin-1 is associated with susceptibility to periodontitis in Japanese. Springer Tokyo Odontology 1618-1255 103 1 66 74 20130000 10.1007/s10266-013-0139-9 24276427 2-s2.0-84887927465 yujiinagaki/published_papers/15560465 Y. Hiroshima M. Bando Y. Inagaki C. Mihara M. Kataoka H. Murata Y. Shinohara T. Nagata J. Kido Resistin in gingival crevicular fluid and induction of resistin release by Porphyromonas gingivalis lipopolysaccharide in human neutrophils Journal of Periodontal Research 0022-3484 47 5 554 562 20121000 10.1111/j.1600-0765.2011.01466.x 22309231 2-s2.0-84865553635 yujiinagaki/published_papers/15560466 Yuka Hiroshima Mika Bandou Masatoshi Kataoka Yuji Inagaki Mark C. Herzberg Karen F. Ross Kazuo Hosoi Toshihiko Nagata Jun-ichi Kido Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1α (IL-1α). IL-1α is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1α might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and β-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1α (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1α-inducible AMPs to provide a rapid and robust innate response to microbial infection. Archives of Oral Biology 1879-1506 56 8 761 767 20110211 10.1016/j.archoralbio.2011.01.004 21316034 yujiinagaki/published_papers/39306437 Bando Mika 板東 美香 Inagaki Yuji 稲垣 裕司 Kido Junichi 木戸 淳一 Hiroshima Yuka 廣島 佑香 Kataoka Masatoshi 片岡 正俊 Murata Hiromi 村田 裕美 Bando Yukiko 坂東 由記子 Ninomiya Masami 二宮 雅美 Sakamoto Eijiro 坂本 英次郎 Nakajima Yukiko 中島 由紀子 Nagata Toshihiko 永田 俊彦 Experimental method for measuring glycated albumin amount in gingival crevicular fluid 歯肉溝滲出液中のグリコアルブミン測定法の確立 JAPANESE SOCIETY OF PERIODONTOLOGY 特定非営利活動法人 日本歯周病学会 Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology 特定非営利活動法人 日本歯周病学会学術大会 プログラムおよび講演抄録集 2011 99 99 20110000 10.14833/amjsp.2011s.0.99.0 yujiinagaki/published_papers/15560467 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 中島 由紀子 Yuka Hiroshima 廣島 佑香 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Osmotic Stress Affects Calcium Deposition and Osteopontin Expression in Cultured Rat Dental Pulp Cells オスモティックストレスが培養歯髄細胞の硬組織形成能とオステオポンチン産生に及ぼす影響 Osmotic stress is a stimulus caused by osmotic pressure, which is known to affect physiological functions in various tissues and cells. However, there is little information on the effect of osmotic stress on dental pulp tissues and cells. In this study, we investigated the relationship between osmotic stress and calcium deposition in cultured rat dental pulp cells. We also analyzed the effect of osmotic stress on the expression and phosphorylation of osteopontin (OPN), a multi-functional bone matrix protein, in the dental pulp cells. Both hypo- and hyper-osmotic stress affected cell-shape and -growth, and decreased calcium deposition in cultured rat dental pulp cells. Hypoosmotic stress increased OPN secretion and its protein ratio in the culture medium. Also, the secreted OPN was highly phosphorylated. On the other hand, hyper-osmotic stress decreased OPN secretion and its protein ratio and most of the OPN in the hypertoinc medium was dephosphorylated. Both hypo- and hyper-osmotic stress decreased calcium deposition in the cultured rat dental pulp cells. However, the mechanism of the inhibitory action seemed to be different in the two groups, because the amount and phosphorylation pattern of OPN were not similar between the hypo- and hyper-osmotic conditions. We concluded that osmotic stress affects calcium deposition in cultured rat dental pulp cells and that OPN expression and its phosphorylation may be a control factor of osmotic stress-associated mineralization. 浸透圧変化が惹起する刺激源は一般にオスモティックストレス(osmotic stress)と呼ばれており,種々の組織や細胞に影響をもたらすことが知られている.しかし,オスモティックストレスが歯髄の組織や細胞にどのような影響を与えるのかを論じた成書や研究報告はぼとんどない.本研究ではラット由来の歯髄細胞培養系を用いて,オスモティックストレスと歯髄細胞の硬組織形成の関連性を検証した.また,オスモティックストレスによって硬組織形成関連タンパクであるオステオポンチン(OPN)の発現やリン酸化に変化が生じるかも検証した.その結果,歯髄細胞培養系においては,低張および高張のいずれのオスモティックストレスによっても細胞の形態や増殖に影響が認められ,硬組織形成も低下した.低張ストレスを付与するとOPNの発現量や総タンパク量に対するOPNの比率は上昇し,また発現したOPNはリン酸化されていた.一方,高張ストレスを付与するとOPNの発現量や総タンパク量に対するOPNの比率は低下し,脱リン酸化されたOPNが主に発現した.このように低張と高張のオスモティックストレスではOPNの発現量やリン酸化による修飾の程度が異なっていたことから,低張および高張のいずれのオスモティックストレスによっても石灰化は抑制されたが,その抑制のメカニズムは一様でないことが明らかとなった.以上より,オスモティックストレスは歯髄細胞の硬組織形成に影響を与え,OPNの発現およびそのリン酸化が制御因子として機能している可能性が示唆された. The Japanese Society of Conservative Dentistry 特定非営利活動法人日本歯科保存学会 The Japanese Journal of Conservative Dentistry 日本歯科保存学雑誌 0387-2343 53 4 367 375 20100831 10.11471/shikahozon.53.367 yujiinagaki/published_papers/28979573 Yuji Inagaki Kaya Yoshida Hirofumi Ohba Hiroyuki Seto Jun-ichi Kido Tatsuji Haneji Toshihiko Nagata High Glucose Levels Increase Osteopontin Production and Pathologic Calcification in Rat Dental Pulp Tissues JOURNAL OF ENDODONTICS 1878-3554 36 6 1014 1020 20100600 10.1016/j.joen.2010.03.018 yujiinagaki/published_papers/15560469 Yuji Inagaki Kaya Yoshida Hirofumi Ohba Hiroyuki Seto Jun-ichi Kido Tatsuji Haneji Toshihiko Nagata High glucose levels increase osteopontin production and pathologic calcification in rat dental pulp tissues. INTRODUCTION: Pulp stones are frequently formed as a pathologic calcification product in dental pulp tissues, but the pathogenesis is poorly understood. We previously found that osteopontin (OPN) was produced by dental pulp cells, and its expression was associated with formation of the pulp stone matrix. It was reported that amorphous calcification appeared in the dental pulp of diabetic patients. The aim of this study was to determine the relationship between OPN expression and pathologic calcification in rat diabetic pulp. METHODS: The effect of glucose on OPN production and alkaline phosphatase activity in cultured rat dental pulp cells (RPC-C2A) was investigated, and then dental pulp calcification and OPN expression in diabetic rats were determined and compared with those in healthy rats by histologic and immunohistochemical analyses. RESULTS: In RPC-C2A cells, biochemical analysis showed that a high concentration of glucose (50 mmol/L) increased OPN protein production and alkaline phosphatase activity 1.3-fold and 1.5-fold, respectively. Histologic observations showed more calcified particles in dental pulp tissues in diabetic than in nondiabetic rats. Moreover, a thickened layer of predentin was formed in the radicular pulp of diabetic rats. OPN was more strongly stained around the calcified particles and in the odontoblast zone under the thickened predentin in diabetic rats. CONCLUSIONS: OPN might be a key molecule involved in the increase of pathologic pulp calcifications, which are frequently observed in diabetic patients. Journal of Endodontics 1878-3554 36 6 1014 1020 20100424 10.1016/j.joen.2010.03.018 20478457 yujiinagaki/published_papers/15560468 Y. Hiroshima M. Bando M. Kataoka Y. Shinohara M. C. Herzberg K. F. Ross Y. Inagaki T. Nagata J. Kido Shosaikoto increases calprotectin expression in human oral epithelial cells Journal of Periodontal Research 0022-3484 45 1 79 86 20100200 10.1111/j.1600-0765.2009.01203.x 19602113 2-s2.0-74549212506 yujiinagaki/published_papers/29808038 T. Kobayashi T. Nagata S. Murakami S. Takashiba H. Kurihara Y. Izumi Y. Numabe H. Watanabe M. Kataoka A. Nagai J. Hayashi H. Ohyama Y. Okamatsu Y. Inagaki H. Tai H. Yoshie Genetic risk factors for periodontitis in a Japanese population Journal of Dental Research 0022-0345 88 12 1137 1141 20091200 10.1177/0022034509350037 19892918 2-s2.0-70450168967 yujiinagaki/published_papers/15560470 Yuka Hiroshima 廣島 佑香 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Long-term Observation of Marked Overfilling in Root Canal Therapy : A Report of Three Cases 著明な過剰根管充填の経過を長期観察した3症例 In endodontic therapy, overfilling of gutta-percha point in root canals sometimes occurs due to wrong measurement of working length and overextension of gutta-percha point. Although a slight overfilling to periapical tissues (within 2 mm past the apical foramen) is tolerable, marked overfilling should be checked by postoperative recheck radiographs and/or clinical symptoms. In this report, three clinical cases of marked overfilling are described and long-term radiographic observation (6-14 years) was continued. Overfilled gutta-percha points on the radiographic observation were 3.0 (case 1), 2.5 (case 2), and 3.5 mm (case 3) in the left maxillary molar of a 47-year-old woman, in the left mandibular molar of a 45-year-old woman, and in the left mandibular premolar of a 39-year-old woman, respectively. In case 1, an overfilled point was cut after 1.5 years and disappeared after 3.5 years, and then apical radiolucency was improved after 6 years. In case 2, overfilled points started to minimize after 3 years and disappeared after 14 years. In case 3, an overfilled point was minimized after 13 years accompanied with improvement of apical lesion. None of the cases showed any significant clinical symptoms after the overfilling. These observations are interesting to longitudinally evaluate the disappearance of overfilled gutta-percha and the improvement of apical lesion. 歯内治療において,ときどき過剰根管充填(過剰根充)に遭遇する.一般に,過剰根充は作業長の測定ミスや根充操作時のガッタパーチャポイントの根尖孔外への突き出しが主な原因であるといわれている.根尖孔から2mm以内のわずかな過剰根充であれば根尖歯周組織に為害性はないが,それ以上の著しい過剰根充の場合は,術後の症状やX線写真によるチェックを行い注意深く対応する必要がある.本報告では,X線写真上で2.5?3.5mmのポイントの突出が認められた3症例(症例1:上顎第二大臼歯,3.0mm,症例2:下顎第一大臼歯,2.5mm,症例3:下顎第一小臼歯,3.5mm)について,最長6?14年の経過観察を行った結果を提示した.症例1では,突出ポイントは1年5カ月後に切断され3年8カ月後に消失し,6年8カ月後に根尖透過像も改善した.症例2では,突出ポイントは3年後に縮小傾向を示し,14年7カ月後には消失しており,根尖透過像の消失,歯槽硬線の明瞭化が観察された.症例3では,突出ポイントは13年6カ月後にわずかな部分を残して,ほとんどが吸収しており,同時に根尖透過像も消失していた.臨床症状は,症例1で打診痛が長期残存したほかには特記事項はほとんど認められなかった.当該歯は現在も健常に機能している.今回の症例は,術前診断,術中術後の情報を詳細に提示しながら過剰根充されたガッタパーチャポイントの経過と根尖病巣の治癒経過を長期間追跡したものであり,過剰根充の転帰を知るうえで興味深い臨床報告である. The Japanese Society of Conservative Dentistry 特定非営利活動法人日本歯科保存学会 The Japanese Journal of Conservative Dentistry 日本歯科保存学雑誌 0387-2343 51 5 485 492 20081031 10.11471/shikahozon.51.485 yujiinagaki/published_papers/15560471 S Kusunoki K Takemura K Takagi Yuji Inagaki 稲垣 裕司 J Asaka T Ezaki H Igimi A new genetic assay for rifampicin susceptibility of Mycobacterium tuberculosis. 日本感染症学会 感染症学会雑誌 0387-5911 69 12 1342 1347 19951200 10.11150/kansenshogakuzasshi1970.69.1342 yujiinagaki/published_papers/15560472 N GOSHIMA Y INAGAKI H OTAKI H TANAKA N HAYASHI F IMAMOTO Y KANO CHIMERIC HU-IHF PROTEINS THAT ALTER DNA-BINDING ABILITY GENE 0378-1119 118 1 97 102 19920900 10.1016/0378-1119(92)90254-M yujiinagaki/misc/48475577 廣島佑香 木戸理恵 木戸淳一 稲垣裕司 成石浩司 湯本浩通 人工合成したLipocalin 2はPorphyromonas gingivalisの口腔上皮細胞への付着を抑制する 日本歯周病学会会誌(Web) 1880-408X 63 null null 20210000 yujiinagaki/misc/48475593 木戸理恵 廣島佑香 生田貴久 稲垣裕司 板東美香 成石浩司 木戸淳一 湯本浩通 最終糖化産物による口腔上皮細胞のLipocalin2発現誘導は好中球の遊走性とサイトカイン発現を調節する 日本歯周病学会会誌(Web) 1880-408X 62 null null 20200000 yujiinagaki/misc/48475584 木戸理恵 廣島佑香 生田貴久 吉田賀弥 稲垣裕司 成石浩司 尾崎和美 木戸淳一 湯本浩通 最終糖化産物はヒト口腔上皮細胞のリポカリン2発現を増加する 日本歯周病学会会誌(Web) 1880-408X 61 null null 20190000 yujiinagaki/misc/35026273 稲垣裕司 野中康平 高木亮輔 西川泰史 木戸理恵 坂本英次郎 成石浩司 木戸淳一 湯本浩通 甘露飲エキス配合製剤はラット実験的歯周炎において歯槽骨吸収を抑制する 日本歯周病学会会誌(Web) 1880-408X 60 null null 20180000 yujiinagaki/misc/35026268 稲垣裕司 高木亮輔 西川泰史 木戸理恵 坂本英次郎 成石浩司 木戸淳一 湯本浩通 甘露飲エキスは破骨細胞と骨芽細胞の分化制御を介してラット実験的歯周炎の歯槽骨吸収を抑制する 日本歯科保存学会学術大会プログラムおよび講演抄録集(Web) 149th null null 20180000 yujiinagaki/misc/35026281 美原智恵 成石浩司 板東美香 西川泰史 LEW Jung Hwan 坂本英次郎 生田貴久 河野薫 梶浦由加里 橋本万里 中島由紀子 稲垣裕司 二宮雅美 木戸淳一 永田俊彦 アドバンスドOSCEを見据えた当科の模擬OSCEの概要 Journal of Oral Health and Biosciences 2188-7888 29 2 null null 20170000 yujiinagaki/misc/38520154 INAGAKI Yuji 稲垣 裕司 OHBA Hirofumi 大場 博史 NAGATA Toshihiko 永田 俊彦 Mineralized Tissue Formation and Osteopontin Expression in Cultured Dental Pulp Cells Derived from Type 2-Diabetes Rat 2型糖尿病ラット由来歯髄細胞培養系における石灰化物形成とオステオポンチン産生 日本歯科保存学雑誌 0387-2343 51 138 138 20080507 yujiinagaki/misc/39382307 INAGAKI Yuji 稲垣 裕司 OHBA Hirofumi 大場 博史 NAGATA Toshihiko 永田 俊彦 Study on Vascular Complication and Osteopontin Expression in Dental Pulp Tissues of Rats with Type 2 Diabetes Mellitus 2型糖尿病モデルラットにおける歯髄内動脈硬化巣の同定とオステオポンチンの関与 日本歯科保存学雑誌 = THE JAPANESE JOURNAL OF CONSERVATIVE DENTISTRY 0387-2343 50 191 191 20071005 yujiinagaki/misc/38324406 INAGAKI Yuji 稲垣 裕司 OHBA Hirofumi 大場 博史 SETO Hiroyuki 瀬戸 浩行 HORIBE Masumi 堀部 ますみ YOSHIDA Kaya 吉田 賀弥 NAGATA Toshihiko 永田 俊彦 Mineralized Tissue Formation and Osteopontin Expression in Dental Pulp Tissues of Rats with Type 2 Diabetes Mellitus 2型糖尿病モデルラットにおける歯髄内石灰化物形成とオステオポンチンの関与 日本歯科保存学雑誌 = THE JAPANESE JOURNAL OF CONSERVATIVE DENTISTRY 0387-2343 49 131 131 20060421 yujiinagaki/misc/39039290 OHBA Hirofumi 大場 博史 SETO Hiroyuki 瀬戸 浩行 TOKUNAGA Kaku 徳永 格 HAMA Hideki 濱 秀樹 INAGAKI Yuji 稲垣 裕司 HORIBE Masumi 堀部 ますみ NAGATA Toshihiko 永田 俊彦 The Stimulatory Effect of Simvastatin on Bone Mineralization in Rat Calvarial Defects ラット頭蓋骨骨欠損部におけるシンバスタチンの石灰化促進作用 日本歯周病学会会誌 0385-0110 48 185 185 20060331 yujiinagaki/misc/39312378 YOSHIDA Kaya 吉田 賀弥 HORIBE Masumi 堀部 ますみ OGINO Mari 荻野 真理 INAGAKI Yuji 稲垣 裕司 KIDO Jun-ichi 木戸 淳一 NAGATA Toshihiko 永田 俊彦 Effect of Glucose on the Production of Osteopontin in Cultured Dental Pulp Cells 歯髄オステオポンチンの産生に及ぼすグルコースの影響 日本歯科保存学雑誌 = THE JAPANESE JOURNAL OF CONSERVATIVE DENTISTRY 0387-2343 47 21 21 20041018 yujiinagaki/presentations/14829645 稲垣 裕司 生田 貴久 坂本 英次郎 木戸 淳一 湯本 浩通 全顎的歯周治療に伴って関節リウマチの状態が改善した一症例 第150回日本歯科保存学会春季学術大会 20190627 yujiinagaki/presentations/14829643 木戸 理恵 廣島 佑香 生田 貴久 吉田 賀弥 稲垣 裕司 成石 浩司 尾崎 和美 木戸 淳一 湯本 浩通 最終糖化産物はヒト口腔上皮細胞のリポカリン2発現を増加する 第62回春季日本歯周病学会学術大会 20190524 yujiinagaki/presentations/2699433 稲垣裕司 高木亮輔 西川泰史 木戸理恵 坂本英次郎 成石浩司 木戸淳一 湯本浩通 甘露飲エキスは破骨細胞と骨芽細胞の分化制御を介してラット実験的歯周炎の歯槽骨吸収を抑制する 第149回日本歯科保存学会秋季学術大会 20181101 yujiinagaki/presentations/4504122 Eijiro Sakamoto Yuji Inagaki Ryosuke Takagi Jun-ichi Kido Hiromichi Yumoto AGE and LPS Inhibit Osteoblastic Differentiation via Sclerostin in Osteocyte. International Association for Dental Research, 96th General Session & Exhibition, London, England 20180728 yujiinagaki/presentations/2699449 Yuji Inagaki Kohei Nonaka Ryosuke Takagi Yasufumi Nishikawa Rie Kido Eijiro Sakamoto Koji Naruishi Jun-ichi Kido Hiromichi Yumoto Kanroin Extracts Prevent Alveolar Bone Resorption in Experimental Rat Periodontitis. International Association for Dental Research, 96th General Session & Exhibition, London, England 20180726 yujiinagaki/presentations/2699428 稲垣裕司 野中康平 高木亮輔 西川泰史 木戸理恵 坂本英次郎 成石浩司 木戸淳一 湯本浩通 甘露飲エキス配合製剤はラット実験的歯周炎において歯槽骨吸収を抑制する 第61回春季日本歯周病学会学術大会 20180601 yujiinagaki/presentations/2699144 Ryosuke Takagi 高木 亮輔 Eijiro Sakamoto 坂本 英次郎 Yuji Inagaki 稲垣 裕司 Yuka Hiroshima 廣島 佑香 Koji Naruishi 成石 浩司 Jun-ichi Kido 木戸 淳一 Hiromichi Yumoto 湯本 浩通 カルプロテクチンはマウス骨細胞の炎症および骨代謝関連因子の発現を制御する 第61回春季日本歯周病学会学術大会 20180601 yujiinagaki/presentations/2699145 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 生田 貴久 Jun-ichi Kido 木戸 淳一 歯肉退縮に対して異なる術式を用いて根面被覆を行った一症例 日本歯周病学会60周年記念大会 20171217 yujiinagaki/presentations/2699146 Masami Ninomiya 二宮 雅美 Yuji Inagaki 稲垣 裕司 Chie Mihara-Wada 美原(和田) 智恵 Mika Bandou 板東 美香 Yukiko Nakajima 中島 由紀子 Eijiro Sakamoto 坂本 英次郎 Ikuta Takahisa 生田 貴久 Nishikawa Yasufumi 西川 泰史 Jung-Hwan Lew Kido Rie 木戸 理恵 Takagi Ryousuke 高木 亮輔 Nonaka Kouhei 野中 康平 Koji Naruishi 成石 浩司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 新規歯周組織再生剤「リグロス歯科用液キット」の有効性 四国歯学会 第51回例会 20170629 yujiinagaki/presentations/2699147 Chie Mihara-Wada 美原(和田) 智恵 Koji Naruishi 成石 浩司 Mika Bandou 板東 美香 西川 泰史 Hwan Jung Lew Eijiro Sakamoto 坂本 英次郎 生田 貴久 河野 薫 Yukari Kajiura 梶浦 由加里 橋本 万里 Yukiko Nakajima 中島 由紀子 Yuji Inagaki 稲垣 裕司 Masami Ninomiya 二宮 雅美 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 アドバンスドOSCEを見据えた当科の模擬OSCEの概要 Shikoku Dental Research 四国歯学会雑誌 20170623 yujiinagaki/presentations/2699148 Eijiro Sakamoto 坂本 英次郎 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Takagi Ryosuke 高木 亮輔 Koji Naruishi 成石 浩司 Toshihiko Nagata 永田 俊彦 最終糖化産物とLPSはMAPKおよびNF-kBを介してマウス骨細胞のスクレロスチンの発現を調節する 第60回春季日本歯周病学会学術大会 20170500 yujiinagaki/presentations/2699128 Eijiro Sakamoto Yuji Inagaki Jun-ichi Kido Takagi Ryosuke Koji Naruishi Toshihiko Nagata AGE and Porphyromonas gingival is-LPS Increase Sclerostin Expression in Osteocytes International Association for Dental Research 20170321 yujiinagaki/presentations/2699149 Eijiro Sakamoto 坂本 英次郎 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 高木 亮輔 生田 貴久 Koji Naruishi 成石 浩司 Toshihiko Nagata 永田 俊彦 マウス骨細胞株MLO-Y4-A2のスクレロスチン発現における最終糖化産物およびLPSの影響 第145回日本歯科保存学会秋季学術大会 20161028 yujiinagaki/presentations/2699150 Yukari Kajiura 梶浦 由加里 Mika Bandou 板東 美香 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Toshihiko Nagata 永田 俊彦 歯肉溝滲出液を用いた糖尿病関連歯周炎の新規診断法の確立 第23回日本歯科医学会総会 20161021 yujiinagaki/presentations/2699151 美原 智恵 Koji Naruishi 成石 浩司 Mika Bandou 板東 美香 西川 泰史 Jung-Hwan Lew Eijiro Sakamoto 坂本 英次郎 生田 貴久 河野 薫 Yukari Kajiura 梶浦 由加里 橋本 万里 Yukiko Nakajima 中島 由紀子 Yuji Inagaki 稲垣 裕司 Masami Ninomiya 二宮 雅美 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 アドバンスOSCEを見据えた当科の模擬OSCEの概要 第49回四国歯学会例会 20160623 yujiinagaki/presentations/2699152 Yuji Inagaki 稲垣 裕司 Eijiro Sakamoto 坂本 英次郎 Jun-ichi Kido 木戸 淳一 Yukari Kajiura 梶浦 由加里 Toshihiko Nagata 永田 俊彦 骨細胞培養系におけるAGEとLPS刺激によるスクレロスチンの発現上昇 第59回春季日本歯周病学会学術大会 20160520 yujiinagaki/presentations/2699153 Eijiro Sakamoto 坂本 英次郎 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Yukari Kajiura 梶浦 由加里 Jung-Hwan Lew Toshihiko Nagata 永田 俊彦 糖尿病関連歯周炎の歯槽骨破壊におけるスクレロスチンの役割 第59回日本糖尿病学会年次学術集会 20160519 yujiinagaki/presentations/2699210 Jumpei Teramachi 寺町 順平 篠原 宏貴 Yuji Inagaki 稲垣 裕司 Hirohiko Okamura 岡村 裕彦 Toshihiko Nagata 永田 俊彦 炎症性骨破壊におけるPKRの枢軸的役割 第135回徳島生物学会 20151223 yujiinagaki/presentations/2699211 Yuji Inagaki 稲垣 裕司 Jumpei Teramachi 寺町 順平 Tatsuji Haneji 羽地 達次 Toshihiko Nagata 永田 俊彦 歯周炎局所の破骨細胞形成における二本鎖RNA依存性プロテインキナーゼ(PKR)の役割 徳島骨代謝研究会 20151119 yujiinagaki/presentations/2699154 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yukiko Nakajima 中島 由紀子 Yukari Kajiura 梶浦 由加里 Yuji Inagaki 稲垣 裕司 生田 貴久 Eijiro Sakamoto 坂本 英次郎 Koji Naruishi 成石 浩司 Toshihiko Nagata 永田 俊彦 ヒト口腔上皮細胞と歯肉線維芽細胞において低酸素環境が誘導する遺伝子発現の比較 第143回日本歯科保存学会秋季学術大会 20151112 yujiinagaki/presentations/2699156 Eijiro Sakamoto 坂本 英次郎 Jun-ichi Kido 木戸 淳一 Yukari Kajiura 梶浦 由加里 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Koji Naruishi 成石 浩司 生田 貴久 Toshihiko Nagata 永田 俊彦 最終糖化産物はヒト口腔上皮細胞の遺伝子発現を調節する 第58回秋季日本歯周病学会学術大会 20150912 yujiinagaki/presentations/2699155 Yukari Kajiura 梶浦 由加里 Jun-ichi Kido 木戸 淳一 Yukiko Nakajima 中島 由紀子 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Koji Naruishi 成石 浩司 Eijiro Sakamoto 坂本 英次郎 Kaori Abe 阿部 佳織 Yuka Hiroshima 廣島 佑香 Toshihiko Nagata 永田 俊彦 低酸素環境が誘導するヒト口腔上皮細胞における遺伝子発現の解析 第58回秋季日本歯周病学会学術大会 20150912 yujiinagaki/presentations/2699157 Yuji Inagaki 稲垣 裕司 Role of TAF12 in the Increased VDR Activity in Paget's Disease of Bone 第33回日本骨代謝学会学術集会 20150725 yujiinagaki/presentations/2699130 Yukari Kajiura Mika Bandou Jun-ichi Kido Yuji Inagaki Toshihiko Nagata Determination of glycated albumin and calprotectin in gingival crevicular fluid from patients with periodontitis and diabetes. Euro Perio 2015 20150603 yujiinagaki/presentations/2699129 T Ikuta Yukari Kajiura Mika Bandou Yuji Inagaki Koji Naruishi Jun-ichi Kido Toshihiko Nagata YKL-40 in gingival crevicular fluid from patients with periodontitis and diabetes. Euro Perio 2015 20150603 yujiinagaki/presentations/2699158 橋村 慧 松田 璃沙 Yuji Inagaki 稲垣 裕司 松井 寛和 横田 美帆 Tamotsu Tanaka 田中 保 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Akira Tokumura 徳村 彰 歯周病におけるリゾホスファチジン酸の役割 第53回 日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, プログラム 20141109 yujiinagaki/presentations/2699159 Jumpei Teramachi 寺町 順平 篠原 宏貴 Yuji Inagaki 稲垣 裕司 Di Yang 楊 諦 Hirohiko Okamura 岡村 裕彦 Toshihiko Nagata 永田 俊彦 Tatsuji Haneji 羽地 達次 PKRによる炎症性骨破壊制御 The Japanese Association of Anatomists 社団法人 日本解剖学会 日本解剖学会 第69回中国・四国支部学術集会プログラム 20141025 yujiinagaki/presentations/2699161 Yukari Kajiura 梶浦 由加里 Yukiko Bandou 坂東 由記子 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Yukiko Nakajima 中島 由紀子 生田 貴久 Hiromi Murata 村田 裕美 Yuka Hiroshima 廣島 佑香 Koji Naruishi 成石 浩司 Toshihiko Nagata 永田 俊彦 歯周病および糖尿病患者の歯肉溝滲出液中のYKL-40レベルの検討 第57回秋季日本歯周病学会学術大会 20141019 yujiinagaki/presentations/2699160 Mika Bandou 板東 美香 Yukari Kajiura 梶浦 由加里 Yukiko Nakajima 中島 由紀子 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Hiromi Murata 村田 裕美 Toshihiko Nagata 永田 俊彦 最終糖化産物は口腔由来線維芽細胞・上皮細胞での炎症関連因子と酸化ストレス因子の発現に影響する 第57回秋季日本歯周病学会学術大会 20141019 yujiinagaki/presentations/2699162 橋村 慧 松田 璃沙 Yuji Inagaki 稲垣 裕司 松井 寛和 横田 美帆 Tamotsu Tanaka 田中 保 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Akira Tokumura 徳村 彰 大豆由来リゾホスファチジン酸の歯周病抑制効果 日本農芸化学会中四国支部第 40回講演会, 講演要旨集 20140927 yujiinagaki/presentations/2699163 Jumpei Teramachi 寺町 順平 Yuji Inagaki 稲垣 裕司 Hirohiko Okamura 岡村 裕彦 Toshihiko Nagata 永田 俊彦 Tatsuji Haneji 羽地 達次 PKRは歯周病変における破骨細胞形成及び骨吸収を制御する 第32回日本骨代謝学会学術集会 20140725 yujiinagaki/presentations/2699166 篠原 宏貴 Jumpei Teramachi 寺町 順平 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Tatsuji Haneji 羽地 達次 PKR阻害によるTNF-α誘導性骨吸収の抑制 第140回日本歯科保存学会春季学会学術大会 20140620 yujiinagaki/presentations/2699165 Jun-ichi Kido 木戸 淳一 Yukiko Nakajima 中島 由紀子 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Toshihiko Nagata 永田 俊彦 低酸素環境とP.gingivalis由来リポ多糖はヒト口腔上皮細胞での炎症関連因子および血管関連因子の発現を調節する 第140回日本歯科保存学会春季学術大会 20140620 yujiinagaki/presentations/2699164 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 ヒト上皮細胞におけるInterleukin-1aによるS100A9遺伝子の転写調節 第140回日本歯科保存学会春季学術大会 20140620 yujiinagaki/presentations/2699167 橋村 慧 松田 璃沙 Yuji Inagaki 稲垣 裕司 松井 寛和 横田 美帆 Tamotsu Tanaka 田中 保 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Akira Tokumura 徳村 彰 歯周病の進行に及ぼす口腔内リゾホスファチジン酸の抑制効果 第56回 日本脂質生化学会, 講演要旨集 20140607 yujiinagaki/presentations/2699168 Yukari Kajiura 梶浦 由加里 Mika Bandou 板東 美香 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 生田 貴久 橋本 万里 篠原 宏貴 Masami Ninomiya 二宮 雅美 Hiromi Murata 村田 裕美 Yukiko Nakajima 中島 由紀子 Satoshi Yoneda 米田 哲 美原 智恵 Yuka Hiroshima 廣島 佑香 Keiji Oishi 大石 慶二 Toshihiko Nagata 永田 俊彦 歯肉溝滲出液中のグリコアルブミンおよびカルプロテクチンを指標とした糖尿病関連歯周炎の診断 第57回春季日本歯周病学会学術大会 20140524 yujiinagaki/presentations/2699170 篠原 宏貴 Jumpei Teramachi 寺町 順平 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Tatsuji Haneji 羽地 達次 TNF-α誘導性破骨細胞形成におけるPKRの役割 第57回春季歯周病学会学術大会 20140523 yujiinagaki/presentations/2699169 Yukiko Nakajima 中島 由紀子 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Toshihiko Nagata 永田 俊彦 Effect of hypoxia and P. gingivalis-lipopolysaccharide on the expression of inflammation-related molecules in human oral keratinocytes 第57回春季日本歯周病学会学術大会 20140523 yujiinagaki/presentations/2699171 Mika Bandou 板東 美香 Yukiko Nakajima 中島 由紀子 Yukari Kajiura 梶浦 由加里 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Hiromi Murata 村田 裕美 Toshihiko Nagata 永田 俊彦 最終糖化産物は歯周組織細胞での炎症性関連因子と酸化ストレス因子の発現に影響する 第57回日本糖尿病学会年次学術集会 20140522 yujiinagaki/presentations/2699172 Yukari Kajiura 梶浦 由加里 Yukiko Bandou 坂東 由記子 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Yukiko Nakajima 中島 由紀子 生田 貴久 Hiromi Murata 村田 裕美 Yuka Hiroshima 廣島 佑香 Koji Naruishi 成石 浩司 Toshihiko Nagata 永田 俊彦 歯周病および糖尿病患者の歯肉溝滲出液中のYKL-40レベルの検討 第57回日本歯周病学会秋期学術大会抄録集 20140500 yujiinagaki/presentations/2699173 Jumpei Teramachi 寺町 順平 篠原 宏貴 Yuji Inagaki 稲垣 裕司 Hiroyuki Morimoto 森本 景之 Toshihiko Nagata 永田 俊彦 Tatsuji Haneji 羽地 達次 The role of PKR on osteoclast formation in the microenvironment of periodontitis 歯周病微小環境での破骨細胞形成におけるPKRの役割 第119回日本解剖学会総会・全国学術集会 20140228 yujiinagaki/presentations/2699131 Yukari Kajiura Mika Bandou Yuji Inagaki Hiromi Murata Jun-ichi Kido Toshihiko Nagata Advanced glycation end-product increases oxidative stress in human gingival fibroblasts 53th General Session of the Korean Academy of Periodontology Meeting 20131122 yujiinagaki/presentations/2699174 Jumpei Teramachi 寺町 順平 篠原 宏貴 Yuji Inagaki 稲垣 裕司 Toshihiko Nagata 永田 俊彦 Tatsuji Haneji 羽地 達次 歯周病変における破骨細胞形成における日本鎖RNA依存性プロテインキナーゼの役割 日本解剖学会 第68回中国・四国支部学術集会 20131020 yujiinagaki/presentations/2699175 Yuji Inagaki 稲垣 裕司 象牙質知覚過敏の発現に及ぼす 歯肉退縮および生活習慣因子の影響 第139回日本歯科保存学会秋季学術大会 20131018 yujiinagaki/presentations/2699176 生田 貴久 Yuji Inagaki 稲垣 裕司 Yukiko Nakajima 中島 由紀子 Mika Bandou 板東 美香 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 日本人歯周病患者を対象とした抗菌ペプチド遺伝子のSNPs解析と疾患感受性の検討 第139回日本歯科保存学会秋季学術大会 20131017 yujiinagaki/presentations/2699178 Yukiko Nakajima 中島 由紀子 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Hiromi Murata 村田 裕美 Toshihiko Nagata 永田 俊彦 低酸素環境がヒト口腔上皮細胞の各種遺伝子発現に及ぼす影響 第56回秋季日本歯周病学会学術大会 20130922 yujiinagaki/presentations/2699177 篠原 宏貴 Jumpei Teramachi 寺町 順平 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 Tatsuji Haneji 羽地 達次 歯周病変における破骨細胞形成に二本鎖RNA依存性プロテインキナーゼが関与する 第56回秋季歯周病学会学術大会 20130922 yujiinagaki/presentations/2699132 Yukiko Nakajima Jun-ichi Kido Yuji Inagaki Mika Bandou Yuka Hiroshima Hiromi Murata Toshihiko Nagata Effect of hypoxia on gene expression in human oral keratinocytes 10th Asian Pacific Society of Periodontology Meeting 20130904 yujiinagaki/presentations/2699133 Jun-ichi Kido Mika Bandou Yuji Inagaki Yuka Hiroshima Hiromi Murata Chie Mihara-Wada 梶浦 由加里 生田 貴久 篠原 宏貴 橋本 万里 Yukiko Nakajima Yukiko Bandou Makoto Funaki Haruhiko Saito Toshihiko Nagata Diagnosis of diabetes-associated periodontitis using glycoalbumin and calprotectin in gingival crevicular fluid 10th Asian Pacific Society of Periodontology Meeting 20130903 yujiinagaki/presentations/2699179 Yukiko Nakajima 中島 由紀子 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 最終糖化産物(AGE)はRAGE-MAPK経路を介してラット培養歯髄細胞の石灰化物形成を促進する 第138回日本歯科保存学会春季学術大会 20130627 yujiinagaki/presentations/2699180 梶浦 由加里 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 最終糖化産物が歯肉線維芽細胞における酸化ストレス反応に及ぼす影響 第56回春季日本歯周病学会学術大会 20130601 yujiinagaki/presentations/2699181 坂本 英次郎 美原 智恵 生田 貴久 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 ラット骨芽細胞の分化に及ぼす最終糖化産物とリポ多糖の影響 第56回春季日本歯周病学会学術大会 20130531 yujiinagaki/presentations/2699135 Toshihiko Nagata Jun-ichi Kido Mika Bandou Yuka Hiroshima Yuji Inagaki Hiromi Murata Chie Mihara-Wada Mika Bandou Makoto Funaki Diagnosis of diabetes-associated periodontitis using biomarkers in gingival crevicular fluid 91th General Session & Exhibition of the International Association for Dental Research. Seattle, USA 20130522 yujiinagaki/presentations/2699134 E Sakamoto Chie Mihara-Wada T Ikuta Yuji Inagaki Jun-ichi Kido Toshihiko Nagata AGE and LPS inhibits osteoblastic differentiation in rat bone-marrow cells 91th General Session & Exhibition of the International Association for Dental Research, Settle, USA 20130522 yujiinagaki/presentations/2699136 Yukiko Nakajima Yuji Inagaki Yuka Hiroshima Jun-ichi Kido Toshihiko Nagata AGE induces calcification and inflammatory factors in dental pulp tissues 91th General Session & Exhibition of the International Accociation for Dental Research, Seattle, USA 20130521 yujiinagaki/presentations/2699182 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yukiko Bandou 坂東 由記子 Yuji Inagaki 稲垣 裕司 Yuka Hiroshima 廣島 佑香 梶浦 由加里 美原 智恵 Hiromi Murata 村田 裕美 生田 貴久 篠原 宏貴 橋本 万里 Makoto Funaki 船木 真理 Haruhiko Saito 齋藤 晴比古 Toshihiko Nagata 永田 俊彦 糖尿病関連歯周炎の診断マーカーとしての歯肉溝滲出液中グリコアルブミンとカルプロテクチンの有用性, 第56回日本糖尿病学会年次学術集会 20130517 yujiinagaki/presentations/2699183 Eijiro Sakamoto 坂本 英次郎 Chie Mihara-Wada 美原(和田) 智恵 生田 貴久 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 ラット骨芽細胞の分化発現に及ぼす最終糖化産物とリポ多糖の影響 第56回春季歯周病学会 20130500 yujiinagaki/presentations/2699126 E Sakamoto Chie Mihara-Wada T Ikuta Yuji Inagaki Jun-ichi Kido Toshihiko Nagata Age and LPS inhibit osteoblastic differentiation in rat bone marrow cells. international Associatuin of dental Research 20130300 yujiinagaki/presentations/2699138 Mika Bandou Yukari Kajiura Jun-ichi Kido Yuji Inagaki Masatoshi Kataoka Toshihiko Nagata Lipopolysaccharide induces oxidative stress and antioxidant responses in gingival fibroblasts The 60th Annual Meeting of Japanese Association for Dental Research, Program and abstracts of papers 20121214 yujiinagaki/presentations/2699137 Yukiko Nakajima Yuji Inagaki Yuka Hiroshima Jun-ichi Kido Toshihiko Nagata AGE induces calcification- and inflammation-related factors in dental pulp cells The 60th Annual Meeting of Japanese Association for Dental Research, Program and abstracts of papers 20121214 yujiinagaki/presentations/2699139 Toshihiko Nagata Jun-ichi Kido Mika Bandou Yuka Hiroshima Yuji Inagaki Masami Ninomiya Chie Mihara-Wada Hiromi Murata Yukiko Bandou Makoto Funaki Diagnosis of diabetes-associated periodontitis by measuring biomarkers in gingival crevicular fluid The 9th International Diabetes Federation Western Pacific Region Congress/ The 4th AASD Scientific Meeting 20121124 yujiinagaki/presentations/2699184 Yuji Inagaki 稲垣 裕司 生田 貴久 中島 由紀子 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 齋藤 剛 田中 和也 日本人歯周病患者を対象として抗菌ペプチド遺伝子のSNPs解析と疾患感受性の検討 日本歯科保存学雑誌 第137回秋季学術大会講演抄録集 20121123 yujiinagaki/presentations/2699186 中島 由紀子 Yuji Inagaki 稲垣 裕司 Yuka Hiroshima 廣島 佑香 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 最終糖化産物(AGE)はラット歯髄における石灰化物形成と炎症反応を進展させる 日本歯科保存学雑誌 第137回秋季学術大会講演抄録集 20121122 yujiinagaki/presentations/2699185 Masumi Horibe 堀部 ますみ Yuji Inagaki 稲垣 裕司 中島 由紀子 生田 貴久 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 糖尿病ラットの実験的歯周炎における歯周組織破壊とオステオポンチンの局在 日本歯科保存学雑誌 第137回秋季学術大会講演抄録集 20121122 yujiinagaki/presentations/2699187 坂本 英次郎 Chie Mihara-Wada 美原(和田) 智恵 生田 貴久 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 ラット骨芽細胞の分化に及ぼす最終糖化産物とリポ多糖の影響 第19回 徳島骨代謝研究会 20121100 yujiinagaki/presentations/2699140 Yuji Inagaki Tsuyoshi Saito Kazuya Tanaka Takahisa Ikuta Yukiko Nakajima Toshikazu Yamaguchi Jun-ichi Kido Toshihiko Nagata Gene polymorphisms of antimicrobial peptides in Japaneses periodontitis patients Journal of the Japanese Association of Periodontology 20120929 yujiinagaki/presentations/2699188 生田 貴久 Yuji Inagaki 稲垣 裕司 Eijiro Sakamoto 坂本 英次郎 中島 由紀子 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 模擬無重力下での培養骨芽細胞の分化発現に及ぼす歯周病原因子の影響 日本歯周病学会会誌 第55回秋季学術大会特別号 20120923 yujiinagaki/presentations/2699189 Eijiro Sakamoto 坂本 英次郎 美原 智恵 生田 貴久 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 ラット骨芽細胞の分化発現に及ぼす最終糖化産物及びリポ多糖の影響 日本歯科保存学雑誌 第136回春季学術大会講演抄録集 20120629 yujiinagaki/presentations/2699190 坂本 英次郎 Chie Mihara-Wada 美原(和田) 智恵 生田 貴久 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 ラット骨芽細胞の分化発現に及ぼす最終糖化産物及びリポ多糖の影響 第136回 春季日本歯周病学会 20120600 yujiinagaki/presentations/2699191 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 Yukiko Bandou 坂東 由記子 Yuka Hiroshima 廣島 佑香 Hiromi Murata 村田 裕美 Makoto Funaki 船木 真理 Haruhiko Saito 齋藤 晴比古 Toshihiko Nagata 永田 俊彦 歯肉溝滲出液中のバイオマーカーを用いた糖尿病関連歯周炎の診断 第55回日本糖尿病学会年次学術集会 抄録集 20120519 yujiinagaki/presentations/2699142 Yuji Inagaki Yukiko Nakajima Mika Bandou Yuka Hiroshima Jun-ichi Kido Toshihiko Nagata Relationship between pathologic calcification and osteopontin expression in dental pulp tissues of diabetic rats European Calcified Tissue Society, 39th Annual Congress, Final Programme 20120519 yujiinagaki/presentations/2699141 Yukiko Nakajima Yuji Inagaki Mika Bandou Yuka Hiroshima Jun-ichi Kido Toshihiko Nagata Advanced glycation end-product increase calcification and inflammatory factors in cultured rat dental pulp cells European Calcified Tissue Society, 39th Annual Congress Final programme 20120519 yujiinagaki/presentations/2699192 Mika Bandou 板東 美香 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Yuka Hiroshima 廣島 佑香 Hiromi Murata 村田 裕美 Takahisa Ikuta 生田 貴久 篠原 宏貴 橋本 万里 山田 由加里 Yukiko Bandou 坂東 由記子 Haruhiko Saito 齋藤 晴比古 Toshihiko Nagata 永田 俊彦 糖尿病関連歯周炎の診断指標スクリーニングに向けた医科・歯科連携研究 日本歯周病学会会誌 第55回春季学術大会特別号 20120518 yujiinagaki/presentations/2699193 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Hiromi Murata 村田 裕美 Chie Mihara-Wada 美原(和田) 智恵 Masumi Horibe 堀部 ますみ Satoshi Yoneda 米田 哲 Masami Ninomiya 二宮 雅美 Keiji Oishi 大石 慶二 Eijiro Sakamoto 坂本 英次郎 中島 由紀子 生田 貴久 浅原 洋士 Toshihiko Nagata 永田 俊彦 バイオマーカーを用いた糖尿病関連歯周炎の診断研究 Journal of the Japanese Association for Dental Science 日本歯科医学会誌 20120300 yujiinagaki/presentations/2699194 Hiromi Murata 村田 裕美 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Yuji Inagaki 稲垣 裕司 Toshihiko Nagata 永田 俊彦 最終糖化産物はマクロファージ様細胞の炎症関連因子の発現を調節する 日本歯科保存学会雑誌 第135回秋季学術大会プログラム 20111021 yujiinagaki/presentations/2699196 Jun-ichi Kido 木戸 淳一 Kaori Abe 阿部 佳織 Masatoshi Kataoka 片岡 正俊 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Yuji Inagaki 稲垣 裕司 Toshihiko Nagata 永田 俊彦 マイクロチップELISA法による歯肉溝滲出液中のカルプロテクチン測定 日本歯周病学会 秋季特別号 20110924 yujiinagaki/presentations/2699195 Yukiko Bandou 坂東 由記子 Jun-ichi Kido 木戸 淳一 Yuka Hiroshima 廣島 佑香 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Hiromi Murata 村田 裕美 Yosuke Shikama 四釜 洋介 Makoto Funaki 船木 真理 Toshihiko Nagata 永田 俊彦 歯肉溝滲出液中のNKL-40の分析 日本歯周病学会会誌 秋季特別号 20110924 yujiinagaki/presentations/2699197 中島 由紀子 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 ラット培養歯髄細胞における最終糖化産物(AGEs)の石灰化促進作用 日本歯科保存学会雑誌 第134回春季学術大会プログラム 20110609 yujiinagaki/presentations/2699198 Mika Bandou 板東 美香 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Yuka Hiroshima 廣島 佑香 Masatoshi Kataoka 片岡 正俊 Hiromi Murata 村田 裕美 Yukiko Bandou 坂東 由記子 Masami Ninomiya 二宮 雅美 Eijiro Sakamoto 坂本 英次郎 中島 由紀子 Toshihiko Nagata 永田 俊彦 歯肉溝滲出液中のグリコアルブミン測定法の確立 日本歯周病学会会誌 春季特別号 20110527 yujiinagaki/presentations/2699212 Masami Ninomiya 二宮 雅美 Satoshi Yoneda 米田 哲 Masumi Horibe 堀部 ますみ 美原 智恵 Yuji Inagaki 稲垣 裕司 Keiji Oishi 大石 慶二 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 FGF-2による歯周組織再生療法 第10回 徳島Bone Forum 20101202 yujiinagaki/presentations/2699199 Yukiko Nakajima 中島 由紀子 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 グルコースが糖尿病ラット由来歯髄細胞の石灰化物形成とオステオポンチン産生に及ぼす影響 第133回日本歯科保存学会秋季学術大会(岐阜) 20101028 yujiinagaki/presentations/2699127 Yuka Hiroshima Mika Bandou Takahiro Hasegawa Yuji Inagaki Chie Mihara-Wada Resistin release from neutrophils is induced by Porphyromonas gingivalis lipopolysaccharide. IADR (International Association of Dental Research) Barcelona, Spain, July 14-17, 2010 20100720 yujiinagaki/presentations/2699213 Yuji Inagaki 稲垣 裕司 Kaya Yoshida 吉田 賀弥 大場 博史 中島 由紀子 瀬戸 浩行 Jun-ichi Kido 木戸 淳一 羽地 達次 Toshihiko Nagata 永田 俊彦 高血糖は歯髄組織におけるオステオポンチン産生と病的石灰化を促進する 第1回骨バイオサイエンス研究会 (岡山) 20100612 yujiinagaki/presentations/2699201 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 板東 美香 廣島 佑香 片岡 正俊 美原 智恵 堀部 ますみ Satoshi Yoneda 米田 哲 Eijiro Sakamoto 坂本 英次郎 中島 由紀子 Masami Ninomiya 二宮 雅美 大石 慶二 浅原 洋士 Toshihiko Nagata 永田 俊彦 糖尿病関連歯周炎における歯肉溝滲出液中のバイオマーカーの分析 第53回日本糖尿病学会年次学術集会 (岡山) 20100527 yujiinagaki/presentations/2699202 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Masatoshi Kataoka 片岡 正俊 Chie Mihara-Wada 美原(和田) 智恵 Masumi Horibe 堀部 ますみ Satoshi Yoneda 米田 哲 坂本 英次郎 中島 由紀子 Masami Ninomiya 二宮 雅美 Keiji Oishi 大石 慶二 淺原 洋士 Toshihiko Nagata 永田 俊彦 歯肉溝浸出液中の糖尿病関連歯周炎バイオマーカーの検索 Journal of the Japanese Association of Periodontology 日本歯周病学会会誌 20100514 yujiinagaki/presentations/2699200 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Chie Mihara-Wada 美原(和田) 智恵 糖尿病関連歯周炎における歯肉溝浸出液中のバイオマーカーの分析 第53回 日本糖尿病学会 20100500 yujiinagaki/presentations/2699203 Yuji Inagaki 稲垣 裕司 Jun-ichi Kido 木戸 淳一 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Masatoshi Kataoka 片岡 正俊 Chie Mihara-Wada 美原(和田) 智恵 Masumi Horibe 堀部 ますみ Satoshi Yoneda 米田 哲 坂本 英次郎 中島 由紀子 Masami Ninomiya 二宮 雅美 Keiji Oishi 大石 慶二 淺原 洋士 Toshihiko Nagata 永田 俊彦 糖尿病関連歯周炎における歯肉溝滲出液中のバイオマーカーの分析 Journal of the The Japan Diabetes Society 糖尿病 20100425 yujiinagaki/presentations/2699204 Yuka Hiroshima 廣島 佑香 Mika Bandou 板東 美香 Jun-ichi Kido 木戸 淳一 Yuji Inagaki 稲垣 裕司 Chie Mihara-Wada 美原(和田) 智恵 Keiji Oishi 大石 慶二 Masatoshi Kataoka 片岡 正俊 Toshihiko Nagata 永田 俊彦 ヒト口腔上皮細胞における抗菌ペプチド遺伝子発現に及ぼす小柴胡湯の影響 第131回日本歯科保存学会秋季学術大会 20091030 yujiinagaki/presentations/2699205 Yuji Inagaki 稲垣 裕司 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 オスモティックストレスが歯髄細胞の硬組織形成能とオステオポンチン産生に及ぼす影響 第131回日本歯科保存学会秋季学術大会 20091029 yujiinagaki/presentations/2699206 Mika Bandou 板東 美香 Yuka Hiroshima 廣島 佑香 Yuji Inagaki 稲垣 裕司 Masatoshi Kataoka 片岡 正俊 Chie Mihara-Wada 美原(和田) 智恵 Masumi Horibe 堀部 ますみ Satoshi Yoneda 米田 哲 Keiji Oishi 大石 慶二 Masami Ninomiya 二宮 雅美 Javkhlan Purevjav Jun-ichi Kido 木戸 淳一 Toshihiko Nagata 永田 俊彦 糖尿病関連歯周炎における歯肉溝浸出液中バイオマーカーの分析 Journal of the Japanese Association of Periodontology 日本歯周病学会会誌 20091011 yujiinagaki/presentations/2699143 Yuji Inagaki Hirofumi Ohba Hiroyuki Seto Masumi Horibe Kaya Yoshida Tatsuji Haneji Toshihiko Nagata Dental Pulp Calcification and Osteopontin Expression in Diabetic Rats International Association for Dental Research 20060629 yujiinagaki/presentations/2699207 Yuji Inagaki 稲垣 裕司 大場 博史 Hiroyuki Seto 瀬戸 浩行 Masumi Horibe 堀部 ますみ Kaya Yoshida 吉田 賀弥 Toshihiko Nagata 永田 俊彦 2型糖尿病モデルラットにおける歯髄内石灰化物形成とオステオポンチンの関与 第124回春季日本歯科保存学会学術大会 20060526 yujiinagaki/presentations/2699208 大場 博史 Hiroyuki Seto 瀬戸 浩行 徳永 格 濱 秀樹 Yuji Inagaki 稲垣 裕司 Masumi Horibe 堀部 ますみ Toshihiko Nagata 永田 俊彦 ラット頭蓋骨骨欠損におけるシンバスタチンの石灰化促進作用 第49回春季日本歯周病学会学術大会 20060428 yujiinagaki/presentations/2699209 Hiroyuki Seto 瀬戸 浩行 大場 博史 濱 秀樹 Yuji Inagaki 稲垣 裕司 Masumi Horibe 堀部 ますみ Toshihiko Nagata 永田 俊彦 スタチンによるラット骨欠損部の石灰化促進作用について 第4回日本歯科骨粗鬆症研究会学術大会 20060305 Yuji Inagaki 稲垣 裕司 The Japanese Society of Periodontology 日本歯周病学会 第14回会誌賞(2015年度) 肥満糖尿病ラット歯周炎の歯周組織におけるオステオポンチンの局在 20161007 稲垣 裕司 日本歯周病学会 第98回アメリカ歯周病学会共催日本歯周病学会2012年度大会JSPポスター賞 20130500 Yuji Inagaki 稲垣 裕司 The Koraku Foundation 財団法人 三木康楽会 康楽賞 20040100