Tokushima University / Educator and Researcher Directory --- Inagaki, Yuji

Personal Web Page

https://researchmap.jp/yujiinagaki (researchmap)

Field of Study

○	Periodontology
○	Endodontology

Subject of Study

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Book / Paper

Book:

1.	Yuji Inagaki, Jun-ichi Kido, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Mika Bandou, Koji Naruishi, Toshihiko Nagata and Hiromichi Yumoto : Gan-Lu-Yin (Kanroin), Traditional Chinese Herbal Extracts, Reduces Osteoclast Differentiation In Vitro and Prevents Alveolar Bone Resorption in Rat Experimental Periodontitis, Jul. 2021.

Academic Paper (Judged Full Paper):

1.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi, Kazuaki Kajimoto, Masatoshi Kataoka, Yasuo Shinohara and 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., Journal of Periodontal Research, Vol.58, No.2, 262-273, 2023. (Tokushima University Institutional Repository) ● Metadata: 119199 (Link to Publication Site) ● Publication site (DOI): 10.1111/jre.13088 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36579753 ● Search Scopus @ Elsevier (PMID): 36579753 ● Search Scopus @ Elsevier (DOI): 10.1111/jre.13088 (Tokushima University Institutional Repository: 119199, DOI: 10.1111/jre.13088, PubMed: 36579753)
2.	Yuta Uemura, Yuka Hiroshima, Ayano Tada, Keiji Murakami, Kaya Yoshida, Yuji Inagaki, Tomomi Kuwahara, Akikazu Murakami, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis Outer Membrane Vesicles Stimulate Gingival Epithelial Cells to Induce Pro-Inflammatory Cytokines via the MAPK and STING Pathways, Biomedicines, Vol.10, No.10, 2643, 2022. (Summary) () 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. -OMVs are involved in the pathogenesis of periodontitis. -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 -OMV-induced pro-inflammatory cytokines was investigated using Western blot analysis and specific pathway inhibitors. -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. -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 -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 -OMVs may play important roles in periodontitis exacerbation by stimulating various pathways. (Tokushima University Institutional Repository) ● Metadata: 117616 (Link to Publication Site) ● Publication site (DOI): 10.3390/biomedicines10102643 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36289904 ● Search Scopus @ Elsevier (PMID): 36289904 ● Search Scopus @ Elsevier (DOI): 10.3390/biomedicines10102643 (Tokushima University Institutional Repository: 117616, DOI: 10.3390/biomedicines10102643, PubMed: 36289904)
3.	Yuji Inagaki, Jun-ichi Kido, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Mika Bandou, Koji Naruishi, Toshihiko Nagata and Hiromichi Yumoto : Gan-Lu-Yin (Kanroin), traditional Chinese herbal extracts, reduces osteoclast differentiation in vitro and prevents alveolar bone resorption in rat experimental periodontitis, Journal of Clinical Medicine, Vol.10, No.3, 386, 2021. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 116745 (Link to Publication Site) ● Publication site (DOI): 10.3390/jcm10030386 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33498415 ● Search Scopus @ Elsevier (PMID): 33498415 ● Search Scopus @ Elsevier (DOI): 10.3390/jcm10030386 (Tokushima University Institutional Repository: 116745, DOI: 10.3390/jcm10030386, PubMed: 33498415)
4.	Tohru Hashimura, Jun-ichi Kido, Risa Matsuda, Miho Yokota, Hirokazu Matsui, Manami Inoue-Fujiwara, Yuji Inagaki, Mayumi Hidaka, Tamotsu Tanaka, Toshihiko Tsutsumi, Toshihiko Nagata and Akira Tokumura : A low level of lysophosphatidic acid in human gingival crevicular fluid from patients with periodontitis due to high soluble lysophospholipase activity: Its potential protective role on alveolar bone loss by periodontitis., Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1865, No.7, 158698, 2020. (Summary) We previously detected a submicromolar concentration of lysophosphatidic acid (LPA) in human saliva. Here, we compare LPA concentrations in human gingival crevicular fluid (GCF) from patients with periodontitis and healthy controls, and examine how the local LPA levels are regulated enzymatically. The concentrations of LPA and its precursor lysophospholipids in GCF was measured by liquid chromatography-tandem mass spectrometry. The LPA-producing and LPA-degrading enzymatic activities were measured by quantifying the liberated choline and free fatty acid, respectively. The concentration of LPA in GCF of periodontitis patients was lower than that of healthy controls, due to higher soluble lysophospholipase activity toward LPA. LPA was found to prevent survival of Sa3, a human gingival epithelium-derived tumor cell line, activate Sa3 through Ca mobilization, and release interleukin 6 from Sa3 in vitro. Furthermore, local injection of LPA into the gingiva attenuated ligature-induced experimental alveolar bone loss induced by oral bacteria inoculation in a rat model of periodontitis in vivo. A high concentration of LPA in human GCF is necessary to maintain normal gingival epithelial integrity and function, protecting the progression of periodontitis. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbalip.2020.158698 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32179099 ● Search Scopus @ Elsevier (PMID): 32179099 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbalip.2020.158698 (DOI: 10.1016/j.bbalip.2020.158698, PubMed: 32179099)
5.	Rie Kido, Yuka Hiroshima, Jun-ichi Kido, Takahisa Ikuta, Eijiro Sakamoto, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : Advanced glycation end-products increase lipocalin 2 expression in human oral epithelial cells., Journal of Periodontal Research, Vol.55, No.4, 539-550, 2020. (Tokushima University Institutional Repository) ● Metadata: 114681 (Link to Publication Site) ● Publication site (DOI): 10.1111/jre.12741 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32170733 ● Summary page in Scopus @ Elsevier: 2-s2.0-85081730917 (Tokushima University Institutional Repository: 114681, DOI: 10.1111/jre.12741, PubMed: 32170733, Elsevier: Scopus)
6.	Ryosuke Takagi, Eijiro Sakamoto, Jun-ichi Kido, Yuji Inagaki, Yuka Hiroshima, Koji Naruishi and Hiromichi Yumoto : S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells., BioMed Research International, Vol.2020, No.7149408, 2020. (Tokushima University Institutional Repository) ● Metadata: 114641 (Link to Publication Site) ● Publication site (DOI): 10.1155/2020/7149408 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32149126 ● Search Scopus @ Elsevier (PMID): 32149126 ● Search Scopus @ Elsevier (DOI): 10.1155/2020/7149408 (Tokushima University Institutional Repository: 114641, DOI: 10.1155/2020/7149408, PubMed: 32149126)
7.	Kohei Nonaka, Mika Bandou, Eijiro Sakamoto, Yuji Inagaki, Koji Naruishi, Hiromichi Yumoto and 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, Molecules, Vol.24, No.20, e3705, 2019. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 114673 (Link to Publication Site) ● Publication site (DOI): 10.3390/molecules24203705 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31619000 ● Summary page in Scopus @ Elsevier: 2-s2.0-85073474436 (Tokushima University Institutional Repository: 114673, DOI: 10.3390/molecules24203705, PubMed: 31619000, Elsevier: Scopus)
8.	Eijiro Sakamoto, Jun-ichi Kido, Ryosuke Takagi, Yuji Inagaki, Koji Naruishi, Toshihiko Nagata and Hiromichi Yumoto : Advanced glycation end-product 2 and Porphyromonas gingivalis lipopolysaccharide increase sclerostin expression in mouse osteocyte-like cells, Bone, Vol.122, 22-30, 2019. (Summary) Sclerostin is a secreted glycoprotein that is mainly expressed in osteocytes, exerts negative effects on bone formation, and is present at elevated levels in diabetes mellitus (DM). Periodontitis is an infectious disease caused by periodontopathic bacteria, a complication of DM, and sometimes associated with severe inflammation and alveolar bone resorption. Advanced glycation end-products (AGEs) are a major pathogen in DM complications and adversely influence periodontitis in DM patients. In the present study, the effects of AGE2 and Porphyromonas gingivalis lipopolysaccharide (P-LPS) on the expression of sclerostin in mouse osteocyte-like cells (MLO-Y4-A2 cells) and its function in osteoblast differentiation were investigated. AGE2 and P-LPS up-regulated the expressions of receptor of AGE (RAGE) and Toll-like receptor 2 (TLR2), respectively, and significantly up-regulated that of sclerostin and interleukin 6 (IL-6) in osteocytes. Sclerostin, RAGE and TLR2 levels were synergistically increased by AGE2 and P-LPS. The siRNAs of RAGE and TLR2 significantly inhibited AGE2- and P-LPS-induced sclerostin expression. AGE2 up-regulated sclerostin expression in osteocyte-like cells via the RAGE, ERK and JNK, and NF-κB signal pathways. On the other hand, P-LPS elevated sclerostin levels via the TLR2, JNK and p38, and NF-κB signal pathways. When osteocytes pre-treated with AGE2 and P-LPS and osteoblastic cells (MC3T3-E1) were co-cultured in the medium with a sclerostin-neutralizing antibody, AGE2- and P-LPS-induced decreases in alkaline phosphatase activity and Runx2 expression in osteoblastic cells were significantly inhibited by the sclerostin-neutralizing antibody. These results suggest that AGE2 and P-LPS influence bone metabolism and inflammation through the regulation of sclerostin expression, and may aggravate periodontitis with DM. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bone.2019.02.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30735798 ● Search Scopus @ Elsevier (PMID): 30735798 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bone.2019.02.001 (DOI: 10.1016/j.bone.2019.02.001, PubMed: 30735798)
9.	Kohei Nonaka, Yukari Kajiura, Mika Bandou, Eijiro Sakamoto, Yuji Inagaki, JH Lew, Koji Naruishi, Takahisa Ikuta, Kaya Yoshida, Tesuo Kobayashi, Hiromasa Yoshie, Toshihiko Nagata and 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, Journal of Periodontal Research, Vol.53, No.3, 334-344, 2018. (Summary) 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. (Keyword) Antigens, Neoplasm / Diabetes Complications / Fibroblasts / Gingiva / Glycation End Products, Advanced / Humans / Intercellular Adhesion Molecule-1 / Interleukin-6 / MAP Kinase Signaling System / Mitogen-Activated Protein Kinase Kinases / Mitogen-Activated Protein Kinases / NF-kappa B / Periodontitis / Phosphorylation / Reactive Oxygen Species / THP-1 Cells (Tokushima University Institutional Repository) ● Metadata: 113617 (Link to Publication Site) ● Publication site (DOI): 10.1111/jre.12518 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29193068 ● Summary page in Scopus @ Elsevier: 2-s2.0-85036593558 (Tokushima University Institutional Repository: 113617, DOI: 10.1111/jre.12518, PubMed: 29193068, Elsevier: Scopus)
10.	Chie Wada -Mihara, Koji Naruishi, Mika Bandou, Yasufumi Nishikawa, Lew Jung-Hwan, Eijiro Sakamoto, Takahisa Ikuta, Kaoru Kono, Yukari Kajiura, Mari Hashimoto, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : 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, Vol.29, No.2, 49-53, 2017. (Tokushima University Institutional Repository) ● Metadata: 111059 (Link to Publication Site) ● Publication site (DOI): 10.20738/johb.29.2_49 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.20738/johb.29.2_49 (Tokushima University Institutional Repository: 111059, DOI: 10.20738/johb.29.2_49)
11.	Eijiro Sakamoto, Chie Wada -Mihara, Takahisa Ikuta, Yuji Inagaki, Jun-ichi Kido and Toshihiko 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, Journal of Periodontal Research, Vol.51, No.3, 313-320, 2016. (Summary) Diabetes is a major risk factor for periodontitis and there is a close relationship between the degree of hyperglycemia and the severity of periodontitis. Advanced glycation end-products (AGEs) accumulate in various tissues under diabetic conditions. AGEs in the periodontal tissues probably play a role in upregulating periodontal inflammation; however, the association of AGEs with the severity of periodontitis has not been fully clarified. Lipopolysaccharide from Porphyromonas gingivalis (P-LPS) is a potent pathogenic factor in periodontitis. Although the independent effect of AGE or P-LPS on osteoblastic cells has been reported in vitro, the effect of adding both has not been clearly elucidated. In this study, to explore factors aggravating diabetic periodontitis, we investigated the effects of AGE and P-LPS on the expression of osteoblastic markers and the expression of inflammation-related markers in vitro. Rat bone marrow cells were cultured, and alkaline phosphatase activity and bone nodule formation were evaluated as osteoblastic markers. Reverse transcription-polymerase chain reaction was performed to determine the mRNA expression of molecules associated with bone and inflammation. Protein levels of osteocalcin and interleukin-1β (IL-1β) were measured using enzyme-linked immunosorbent assay. AGEs and P-LPS independently reduced alkaline phosphatase activity and bone nodule formation. The addition of both AGE and P-LPS (AGE+P-LPS) further decreased these markers. Reverse transcription-polymerase chain reaction analysis revealed that AGE+P-LPS markedly decreased the mRNA expression of osteoblast-related molecules such as type 1 collagen, osteocalcin and Cbfa1, and markedly increased that of inflammation-related molecules such as IL1β and S100A8. AGE and P-LPS decreased the protein level of osteocalcin and increased that of IL-1β, and a further increase of IL-1β was detected for AGE+P-LPS. AGEs and P-LPS inhibited the expression of osteoblastic markers and increased the levels of inflammatory markers in rat bone marrow cells, suggesting that both AGE and P-LPS may be important factors associated with the aggravation of diabetic periodontitis. (Keyword) advanced glycation end products / diabetes / osteoblastic differentiation / periodontitis (Link to Publication Site) ● Publication site (DOI): 10.1111/jre.12310 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26223811 ● Summary page in Scopus @ Elsevier: 2-s2.0-84938353798 (DOI: 10.1111/jre.12310, PubMed: 26223811, Elsevier: Scopus)
12.	Yuka Hiroshima, Mika Bandou, Yuji Inagaki, Reiko Kido, Masatoshi Kataoka, Toshihiko Nagata and Jun-ichi Kido : Effect of Hangeshashinto on calprotectin expression in human oral epithelial cells., Odontology, Vol.104, No.2, 152-162, 2016. (Summary) Oral epithelial cells produce antimicrobial peptides (AMPs) to prevent microbial infection. Calprotectin (S100A8/S100A9) is one of these AMPs in oral epithelial cells, the expression of which is up-regulated by interleukin-1α (IL-1α). Hangeshashinto (HST) is a traditional Japanese herbal medicine that has anti-inflammatory effects. The purpose of this study was to investigate the effect of HST on the expression of calprotectin through the regulation of IL-1α in oral epithelial cells. Human oral epithelial cells (TR146) were cultured with HST in the presence or absence of anti-IL-1α antibody or IL-1 receptor antagonist, or with six major components of HST (3,4-dihydroxybenzaldehyde, baicalin, ginsenoside Rb1, glycyrrhizin, oleanolic acid and berberine). The expression of S100A8, S100A9, other AMPs and cytokine mRNAs was examined by RT-PCR and quantitative real-time PCR. Calprotectin expression and IL-1α secretion were investigated by ELISA. HST (6 μg/ml) increased the expression of S100A8/S100A9 mRNAs and calprotectin protein, and also up-regulated β-defensin 2 (DEFB4) and S100A7 expression. The expression of IL-1α mRNA and its protein was slightly but significantly increased by HST. A neutralizing antibody against IL-1α and IL-1 receptor antagonist inhibited HST-up-regulated S100A8/S100A9 mRNA expression. Although 3,4-dihydroxybenzaldehyde, baicalin and ginsenoside Rb1 as HST components increased S100A8/S100A9 expression, oleanolic acid and berberine decreased their expression. These results suggest that HST increases the expression of calprotectin, DEFB4 and S100A7 in oral epithelial cells. In response to HST, up-regulation of calprotectin expression may be partially induced via IL-1α. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-015-0196-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25649126 ● Search Scopus @ Elsevier (PMID): 25649126 ● Search Scopus @ Elsevier (DOI): 10.1007/s10266-015-0196-3 (DOI: 10.1007/s10266-015-0196-3, PubMed: 25649126)
13.	Jumpei Teramachi, Yuki Nagata, Khalid Mohammad, Yuji Inagaki, Yasuhisa Ohata, Theresa Guise, Laëtitia Michou, P Jacques Brown, J Jolene Windle, Noriyoshi Kurihara and David G Roodman : Measles virus nucleocapsid protein increases osteoblast differentiation in Paget's disease., The Journal of Clinical Investigation, Vol.126, No.3, 1012-1022, 2016. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1172/JCI82012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26878170 ● Summary page in Scopus @ Elsevier: 2-s2.0-84959912039 (DOI: 10.1172/JCI82012, PubMed: 26878170, Elsevier: Scopus)
14.	Jumpei Teramachi, Yuji Inagaki, Hiroki Shinohara, Hirohiko Okamura, Di Yang, Kazuhiko Ochiai, Ryoko Baba, Hiroyuki Morimoto, Toshihiko Nagata and Tatsuji Haneji : PKR regulates LPS-induced osteoclast formation and bone destruction in vitro and in vivo., Oral Diseases, 2016. (Summary) PKR plays a pivotal role in LPS-induced bone loss in PD, and, thus, has potential as a therapeutic target for PD. This article is protected by copyright. All rights reserved. (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.12592 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27718290 ● Search Scopus @ Elsevier (PMID): 27718290 ● Search Scopus @ Elsevier (DOI): 10.1111/odi.12592 (DOI: 10.1111/odi.12592, PubMed: 27718290)
15.	Jun-ichi Kido, Yukiko Bandou, Mika Bandou, Yukari Kajiura, Yuka Hiroshima, Yuji Inagaki, Hiromi Murata, Takahisa Ikuta, Reiko Kido, Koji Naruishi, Makoto Funaki and Toshihiko Nagata : YKL-40 level in gingival crevicular fluid from patients with periodontitis and type 2 diabetes, Oral Diseases, Vol.21, No.5, 667-673, 2015. (Summary) YKL-40 is a chitin-binding glycoprotein, the level of which increases in inflammatory diseases, diabetes mellitus (DM), cardiovascular diseases, and tumors. Gingival crevicular fluid (GCF) contains many proteins and markers of periodontitis. The purpose of this study was to investigate YKL-40 level in GCF from patients with periodontitis and DM and the association between YKL-40 level and chronic periodontitis (CP) or DM. The subjects were 121 patients with DM, CP, DM and periodontitis (DM-P), and healthy subjects (H). GCF was collected using paper strips after the sites for GCF collection were clinically evaluated for probing depth (PD), gingival index (GI), and bleeding on probing (BOP). YKL-40 in GCF was identified by Western blotting, and its level was determined by ELISA. YKL-40 was contained in GCF samples from H, DM, CP, and DM-P sites, and its levels (amount and concentration) in CP and DM-P were significantly higher than those in H and DM. GCF YKL-40 level significantly correlated with PD and GI, and its level in BOP-positive sites was significantly higher than that in BOP-negative ones. GCF YKL-40 level was elevated in periodontitis, but not DM. YKL-40 in GCF may be an inflammatory marker for periodontitis. (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.12334 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25740558 ● Summary page in Scopus @ Elsevier: 2-s2.0-84930271794 (DOI: 10.1111/odi.12334, PubMed: 25740558, Elsevier: Scopus)
16.	Takahisa Ikuta, Yuji Inagaki, Kazuya Tanaka, Tsuyoshi Saito, Yukiko Nakajima, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : Gene polymorphism of β-defensin-1 is associated with susceptibility to periodontitis in Japanese., Odontology, Vol.103, No.1, 66-74, 2015. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 106075 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-013-0139-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24276427 ● Summary page in Scopus @ Elsevier: 2-s2.0-84887927465 (Tokushima University Institutional Repository: 106075, DOI: 10.1007/s10266-013-0139-9, PubMed: 24276427, Elsevier: Scopus)
17.	Yuji Inagaki, Yukiko Nakajima, Masumi Horibe, 生田貴久, Yukari Kajiura, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : 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, Journal of the Japanese Association of Periodontology, Vol.67, No.4, 149-158, 2015. (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.57.149 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204416151552 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.57.149 (DOI: 10.2329/perio.57.149, CiNii: 1390001204416151552)
18.	Yukiko Nakajima, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : Advanced glycation end-products increase expression of S100A8 and A9 via RAGE-MAPK in rat dental pulp cells, Oral Diseases, Vol.21, No.3, 328-334, 2015. (Summary) Advanced glycation end products (AGE) are involved in the progression of diabetic complications. Although our previous reports show that AGE increased dental pulp calcification, AGE accumulation is also associated with inflammation. This study examined AGE effect on the expression of inflammation factors using rat dental pulp tissues and cell cultures. Receptor for AGE (RAGE), S100A8, S100A9, and interleukin (IL)-1β were selected as inflammation parameters. Rat dental pulp cells were cultured and treated with AGE, and the effects were determined by real-time PCR. An anti-RAGE antibody or MAPK pathway inhibitors (PD98059, SB203580, and SP60012) were used to investigate AGE signaling pathway. The mRNA levels of RAGE, S100A8, S100A9, and IL-1β were higher in diabetic pulp tissues. AGE increased mRNA expressions of S100A8, S100A9, and IL-1β in cultured dental pulp cells. In the presence of anti-RAGE antibody, AGE did not increase in S100A8 or S100A9 expressions. The AGE-induced increases in S100A8 and S100A9 were inhibited by PD98059 and SB203580, respectively. Advanced glycation end products increased mRNA expression of S100A8, S100A9, and IL-1β under diabetic pulp conditions, and AGE-induced increases in S100A8 and S100A9 expressions may be associated with the RAGE-MAPK signaling pathway. (Keyword) Advanced Glycosylation End Product-Specific Receptor / Animals / Antibodies / Calgranulin A / Calgranulin B / Cells, Cultured / Dental Pulp / Diabetes Mellitus / Flavonoids / Gene Expression / Glycosylation End Products, Advanced / Imidazoles / Interleukin-1beta / MAP Kinase Signaling System / Male / Mitogen-Activated Protein Kinases / Pyridines / RNA, Messenger / Rats (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.12280 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25098709 ● Summary page in Scopus @ Elsevier: 2-s2.0-84925124937 (DOI: 10.1111/odi.12280, PubMed: 25098709, Elsevier: Scopus)
19.	Yukari Kajiura, Mika Bandou, Yuji Inagaki, Toshihiko Nagata and Jun-ichi Kido : Glycated albumin and calprotectin levels in gingival crevicular fluid from patients with periodontitis and type 2 diabetes, Journal of Periodontology, Vol.85, No.12, 1667-1675, 2014. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 109408 (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2014.140241 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25126693 ● Search Scopus @ Elsevier (PMID): 25126693 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2014.140241 (Tokushima University Institutional Repository: 109408, DOI: 10.1902/jop.2014.140241, PubMed: 25126693)
20.	Naofumi Tamaki, Rita Cristina Orihuela Campos, Yuji Inagaki, Makoto Fukui, Toshihiko Nagata and 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., Free Radical Biology and Medicine, Vol.75, 222-229, 2014. (Summary) Oxidative stress is a key factor regulating the systemic pathophysiological effects associated with periodontitis. Resveratrol is a phytochemical with antioxidant and anti-inflammatory properties that can reduce oxidative stress and inflammation. We hypothesized that resveratrol may prevent the progression of periodontitis and reduce systemic oxidative stress through the activation of the Sirtuin1 (Sirt1)/AMP-activated protein kinase (AMPK) and the nuclear factor-E2 related factor 2 (Nrf2)/antioxidant defense pathways. Three groups of male Wistar rats (periodontitis treated with melinjo resveratrol, periodontitis without resveratrol, and control rats with no periodontitis or resveratrol treatment) were examined. A ligature was placed around the maxillary molars for 3 weeks to induce periodontitis, and the rats were then given drinking water with or without melinjo resveratrol. In rats with periodontitis, ligature placement induced alveolar bone resorption, quantified using three-dimensional images taken by micro-CT, and increased proinflammatory cytokine levels in gingival tissue. Melinjo resveratrol intake relieved alveolar bone resorption and activated the Sirt1/AMPK and the Nrf2/antioxidant defense pathways in inflamed gingival tissues. Further, melinjo resveratrol improved the systemic levels of 8-hydroxydeoxyguanosine, dityrosine, nitric oxide metabolism, nitrotyrosine, and proinflammatory cytokines. We concluded that oral administration of melinjo resveratrol may prevent the progression of ligature-induced periodontitis and improve systemic oxidative and nitrosative stress. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.freeradbiomed.2014.07.034 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25091897 ● Search Scopus @ Elsevier (PMID): 25091897 ● Search Scopus @ Elsevier (DOI): 10.1016/j.freeradbiomed.2014.07.034 (DOI: 10.1016/j.freeradbiomed.2014.07.034, PubMed: 25091897)
21.	Yukiko Nakajima, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Advanced glycation end-products enhance calcification in cultured rat dental pulp cells, Journal of Endodontics, Vol.39, 873-878, 2013. (Summary) 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. (Keyword) Alkaline Phosphatase / Animals / Cell Culture Techniques / Cells, Cultured / Dental Pulp / Dental Pulp Calcification / Fibroblasts / Gingiva / Glycosylation End Products, Advanced / Male / Osteocalcin / Osteopontin / Rats / Rats, Wistar / Receptors, Immunologic / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.joen.2012.11.027 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23791254 ● Summary page in Scopus @ Elsevier: 2-s2.0-84879412695 (DOI: 10.1016/j.joen.2012.11.027, PubMed: 23791254, Elsevier: Scopus)
22.	Yoshikazu Fukumoto, Masumi Horibe, Yuji Inagaki, Keiji Oishi, Naofumi Tamaki, Hiro-O Ito and Toshihiko Nagata : Association of gingival recession and other factors with the presence of dentin hypersensitivity., Odontology, 2013. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-012-0099-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23283584 ● Search Scopus @ Elsevier (PMID): 23283584 ● Search Scopus @ Elsevier (DOI): 10.1007/s10266-012-0099-5 (DOI: 10.1007/s10266-012-0099-5, PubMed: 23283584)
23.	Yuka Hiroshima, Mika Bandou, Yuji Inagaki, Chie Wada -Mihara, Masatoshi Kataoka, Hiromi Murata, Yasuo Shinohara, Toshihiko Nagata and Jun-ichi Kido : Resistin in gingival crevicular fluid and induction of resistin release by Porphyromonas gingivalis lipopolysaccharide in human neutrophils, Journal of Periodontal Research, Vol.47, No.5, 554-562, 2012. (Summary) Resistin is an adipocytokine that induces insulin resistance and is predominantly expressed in adipocytes and peripheral blood mononuclear cells. Resistin expression increases in inflammatory diseases as well as diabetes mellitus, and is upregulated by bacterial pathogens and proinflammatory cytokines. The aim of this study was to identify resistin in human gingival crevicular fluid, to compare the resistin levels in gingival crevicular fluid between subjects with and without periodontitis and diabetes mellitus and to investigate the regulation of resistin release from human neutrophils by Porphyromonas gingivalis lipopolysaccharide (P-LPS). Gingival crevicular fluid samples were collected from patients with chronic periodontitis (n = 24), patients with diabetes mellitus-related periodontitis (n = 18) and healthy subjects (n = 21). Resistin in gingival crevicular fluid was determined using western blot analysis and an ELISA kit. The glycated hemoglobin (HbA(1c)) value was obtained from patients with diabetes mellitus-related periodontitis by a medical interview. Human neutrophils were cultured with P-LPS (0-1000 ng/mL), or incubated with inhibitors of actin or microtubule polymerization in the absence or presence of P-LPS. The medium and cellular fractions were used for determination of resistin by ELISA. The resistin level in gingival crevicular fluid from patients with periodontitis or diabetes mellitus-related periodontitis was significantly higher than that of healthy subjects. The resistin level in gingival crevicular fluid was correlated with gingival index score, but not blood HbA(1c) value. The P-LPS increased resistin release from human neutrophils, and its induction was decreased by actin polymerization inhibitors. We show, for the first time, the presence of resistin in gingival crevicular fluid. A high resistin level in gingival crevicular fluid samples from periodontitis patients may to some extent be related to P-LPS-induced resistin release from neutrophils. (Keyword) Actin Capping Proteins / Adult / Aged / Cell Culture Techniques / Chronic Periodontitis / Colchicine / Cytochalasin B / Cytochalasin D / Diabetes Complications / Female / Gingival Crevicular Fluid / Hemoglobin A, Glycosylated / Humans / Lipopolysaccharides / Male / Middle Aged / Neutrophils / Nocodazole / Nucleic Acid Synthesis Inhibitors / Periodontal Index / Periodontal Pocket / Periodontitis / Porphyromonas gingivalis / Resistin / Tubulin Modulators (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2011.01466.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22309231 ● Summary page in Scopus @ Elsevier: 2-s2.0-84865553635 (DOI: 10.1111/j.1600-0765.2011.01466.x, PubMed: 22309231, Elsevier: Scopus)
24.	Yuka Hiroshima, Mika Bandou, Masatoshi Kataoka, Yuji Inagaki, Mark C. Herzberg, Karen F. Ross, Kazuo Hosoi, Toshihiko Nagata and Jun-ichi Kido : Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α, Archives of Oral Biology, Vol.56, No.8, 761-767, 2011. (Summary) 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. (Keyword) Acute-Phase Proteins / Adolescent / Adult / Anti-Infective Agents / Antimicrobial Cationic Peptides / Blotting, Western / Calgranulin A / Calgranulin B / Cell Culture Techniques / Cystatin C / Female / Gene Expression Regulation / Gingiva / Humans / Immunity, Innate / Interleukin-1alpha / Keratinocytes / Lipocalins / Male / Oligonucleotide Array Sequence Analysis / Proline-Rich Protein Domains / Proto-Oncogene Proteins / S100 Proteins / Secretory Leukocyte Peptidase Inhibitor / Serine Proteinase Inhibitors / Up-Regulation / Young Adult / beta-Defensins (Link to Publication Site) ● Publication site (DOI): 10.1016/j.archoralbio.2011.01.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21316034 ● Search Scopus @ Elsevier (PMID): 21316034 ● Search Scopus @ Elsevier (DOI): 10.1016/j.archoralbio.2011.01.004 (DOI: 10.1016/j.archoralbio.2011.01.004, PubMed: 21316034)
25.	Yuji Inagaki, Mika Bandou, 中島由紀子, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Osmotic Stress Affects Calcium Deposition and Osteopontin Expression in Cultured Rat Dental Pulp Cells, The Japanese Journal of Conservative Dentistry, Vol.53, No.4, 367-375, 2010. (Summary) 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. (Keyword) Osmotic stress / Dental pulp cell / Mineralization / osteopontin (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205520972544 (CiNii: 1390001205520972544)
26.	Yuka Hiroshima, Mika Bandou, Masatoshi Kataoka, Yasuo Shinohara, MC Herzberg, KF Ross, Yuji Inagaki, Toshihiko Nagata and Jun-ichi Kido : Shosaikoto increases calprotectin expression in human oral epithelial cells., Journal of Periodontal Research, Vol.45, No.1, 79-86, 2010. (Summary) BACKGROUND AND OBJECTIVE: Oral epithelial cells help to prevent against bacterial infection in the oral cavity by producing antimicrobial peptides (AMPs). A broad-spectrum AMP, calprotectin (a complex of S100A8 and S100A9 proteins), is expressed by oral epithelial cells and is up-regulated by interleukin-1alpha (IL-1alpha). Shosaikoto (SST) is a traditional Japanese herbal medicine that has immunomodulatory effects and is reported to enhance the levels of IL-1alpha in epithelial cells. The purpose of this study was to investigate the effect of SST on the expression of calprotectin and other AMPs through the regulation of IL-1alpha in oral epithelial cells. MATERIAL AND METHODS: Human oral epithelial cells (TR146) were cultured with SST (at concentrations ranging from 10 to 250 microg/mL) in the presence or absence of anti-IL-1alpha or IL-1 receptor antagonist. The expression of S100A8- and S100A9-specific mRNAs was examined by northern blotting. Calprotectin expression and IL-1alpha secretion were investigated by immunofluorescent staining or ELISA. The expression of other AMPs and IL-1alpha was analyzed by RT-PCR and by quantitative real-time PCR. RESULTS: Shosaikoto (25 microg/mL) significantly increased the expression of S100A8- and S100A9-specific mRNAs and calprotectin protein. Shosaikoto increased S100A7 expression, but had no effect on the expression of other AMPs. The expression of IL-1alpha-specific mRNA and its protein were slightly increased by SST. A neutralizing antibody against IL-1alpha or IL-1 receptor antagonist inhibited SST up-regulated S100A8/S100A9 mRNA expression. CONCLUSION: These results suggest that SST increases the expression of calprotectin and S100A7 in oral epithelial cells. In response to SST, up-regulation of calprotectin may be partially induced via IL-1alpha. (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2009.01203.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19602113 ● Search Scopus @ Elsevier (PMID): 19602113 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2009.01203.x (DOI: 10.1111/j.1600-0765.2009.01203.x, PubMed: 19602113)
27.	Yuji Inagaki, Kaya Yoshida, Hirofumi Ohba, Hiroyuki Seto, Jun-ichi Kido, Tatsuji Haneji and Toshihiko Nagata : High glucose levels increase osteopontin production and pathologic calcification in rat dental pulp tissues., Journal of Endodontics, Vol.36, No.6, 1014-1020, 2010. (Summary) 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. (Keyword) Alkaline Phosphatase / Animals / Blood Glucose / Body Weight / Cell Culture Techniques / Cell Line / Dental Pulp / Dental Pulp Calcification / Dentin / Diabetes Mellitus, Type 2 / glucose / Hemoglobin A, Glycosylated / Male / Odontoblasts / osteopontin / Rats / Rats, Inbred OLETF / Rats, Long-Evans / Time Factors / Tooth Root (Link to Publication Site) ● Publication site (DOI): 10.1016/j.joen.2010.03.018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20478457 ● Summary page in Scopus @ Elsevier: 2-s2.0-77955303422 (DOI: 10.1016/j.joen.2010.03.018, PubMed: 20478457, Elsevier: Scopus)
28.	Yuka Hiroshima, Yuji Inagaki, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : Long-term Observation of Marked Overfilling in Root Canal Therapy : A Report of Three Cases, The Japanese Journal of Conservative Dentistry, Vol.51, No.5, 485-492, 2008. (Summary) 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. (Keyword) Endodontic therapy / Overfilling / Radiographic diagnosis (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680499131392 (CiNii: 1390282680499131392)
29.	S Kusunoki, K Takemura, K Takagi, Yuji Inagaki, J Asaka, T Ezaki and H Igimi : A new genetic assay for rifampicin susceptibility of Mycobacterium tuberculosis., 感染症学会雑誌, Vol.69, No.12, 1342-1347, 1995.
30.	Naoki Goshima, Yuji Inagaki, Hitoshi Otaki, Hiromitsu Tanaka, Naotaka Hayashi, Fumio Imamoto and Yasunobu Kano : Chimeric HU-IHF proteins that alter DNA-binding ability., Gene, Vol.118, No.1, 97-102, 1992.

Academic Paper (Unrefereed Paper):

1.	Jun-ichi Kido, Mika Bandou, Yuji Inagaki, 生田貴久, Yukari Kajiura, Yukiko Nakajima, Eijiro Sakamoto, Chie Wada -Mihara, Masami Ninomiya, 西川泰史, Jung-Hwan Lew, Koji Naruishi and Toshihiko Nagata : Diagnosis of Periodontal Diseases using Biomarkers in Gingival Crevicular Fluid, Journal of Oral Health and Biosciences, Vol.29, No.1, 13-20, 2016. (Summary) 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. (Keyword) 歯周病診断 / バイオマーカー / 歯肉溝滲出液 (Tokushima University Institutional Repository) ● Metadata: 109875 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845763956844416 (Tokushima University Institutional Repository: 109875, CiNii: 1050845763956844416)

Proceeding of International Conference:

1.	E Sakamoto, Chie Wada -Mihara, T Ikuta, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : Age and LPS inhibit osteoblastic differentiation in rat bone marrow cells., international Associatuin of dental Research, Seattle,
2.	Yuka Hiroshima, Mika Bandou, Takahiro Hasegawa, Yuji Inagaki and Chie Wada -Mihara : Resistin release from neutrophils is induced by Porphyromonas gingivalis lipopolysaccharide., IADR (International Association of Dental Research) Barcelona, Spain, July 14-17, 2010,
3.	Eijiro Sakamoto, Yuji Inagaki, Ryosuke Takagi, Jun-ichi Kido and Hiromichi Yumoto : AGEs and LPS Inhibit Osteoblastic Differentiation via Sclerostin in Osteocytes, 96th General Session & Exhibition of the International Association of Dental Research, Jul. 2018.
4.	Yuji Inagaki, Kohei Nonaka, Ryosuke Takagi, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : Kanroin Extracts Prevent Alveolar Bone Resorption in Experimental Rat Periodontitis, 96th General Session & Exhibition of the International Association of Dental Research, Jul. 2018.
5.	Eijiro Sakamoto, Yuji Inagaki, Jun-ichi Kido, Takagi Ryosuke, Koji Naruishi and Toshihiko Nagata : AGE and Porphyromonas gingival is-LPS Increase Sclerostin Expression in Osteocytes, International Association for Dental Research, Mar. 2017. (Keyword) periodontitis / diabetes mellitus / bone and mineral metabolism
6.	T Ikuta, Yukari Kajiura, Mika Bandou, Yuji Inagaki, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : YKL-40 in gingival crevicular fluid from patients with periodontitis and diabetes., Euro Perio 2015, Jun. 2015.
7.	Yukari Kajiura, Mika Bandou, Jun-ichi Kido, Yuji Inagaki and Toshihiko Nagata : Determination of glycated albumin and calprotectin in gingival crevicular fluid from patients with periodontitis and diabetes., Euro Perio 2015, Jun. 2015.
8.	Yukari Kajiura, Mika Bandou, Yuji Inagaki, Hiromi Murata, Jun-ichi Kido and Toshihiko Nagata : Advanced glycation end-product increases oxidative stress in human gingival fibroblasts, 53th General Session of the Korean Academy of Periodontology Meeting, Seoul, Korea, Nov. 2013.
9.	Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata and Toshihiko Nagata : Effect of hypoxia on gene expression in human oral keratinocytes, 10th Asian Pacific Society of Periodontology Meeting, Nara, Sep. 2013.
10.	Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, 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 and Toshihiko Nagata : Diagnosis of diabetes-associated periodontitis using glycoalbumin and calprotectin in gingival crevicular fluid, 10th Asian Pacific Society of Periodontology Meeting, Nara, Sep. 2013.
11.	E Sakamoto, Chie Wada -Mihara, T Ikuta, Yuji Inagaki, Jun-ichi Kido and 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, May 2013.
12.	Toshihiko Nagata, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Yuji Inagaki, Hiromi Murata, Chie Wada -Mihara, Mika Bandou and 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, May 2013.
13.	Yukiko Nakajima, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and 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, May 2013.
14.	Eijiro Sakamoto, Chie Wada -Mihara, Takahisa Ikuta, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : Age and LPS inhibit osteoblastic differentiation in rat bone marrow cells., international Associatuin of dental Research, Seattle, Mar. 2013.
15.	Yukiko Nakajima, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and 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, 92, Dec. 2012.
16.	Mika Bandou, Yukari Kajiura, Jun-ichi Kido, Yuji Inagaki, Masatoshi Kataoka and 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, 79, Dec. 2012.
17.	Toshihiko Nagata, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Yuji Inagaki, Masami Ninomiya, Chie Wada -Mihara, Hiromi Murata, Yukiko Bandou and 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, Nov. 2012.
18.	Yuji Inagaki, Tsuyoshi Saito, Kazuya Tanaka, Takahisa Ikuta, Yukiko Nakajima, Toshikazu Yamaguchi, Jun-ichi Kido and Toshihiko Nagata : Gene polymorphisms of antimicrobial peptides in Japaneses periodontitis patients, Journal of the Japanese Association of Periodontology, Vol.54, No.3, 286, Sep. 2012.
19.	Yukiko Nakajima, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and 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, 73, Stockholm (Sweden), May 2012.
20.	Yuji Inagaki, Yukiko Nakajima, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and 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, 125, Stockholm (Sweden), May 2012.
21.	Yuka Hiroshima, Mika Bando, Takahiro Hasegawa, Yuji Inagaki, Eijiro Sakamoto, Yukiko Nakajima, Chie Mihara, Masatoshi Kataoka, Toshihiko Nagata, Kazuo Hosoi and Jun-ichi Kido : Resistin release from neutrophils is induced by Porphyromonas gingivalis lipopolysaccharide, 88th General Session & Exhibition of the International Association for Dental Research, Spain, Jul. 2010.
22.	Yuka Hiroshima, Mika Bando, Takahiro Hasegawa, Yuji Inagaki, Eijiro Sakamoto, Yukiko Nakajima, Chie Mihara, Masatoshi Kataoka, Toshihiko Nagata, Kazuo Hosoi and Jun-ichi Kido : Resistin release from neutrophils is induced by Porphyromonas gingivalis lipopolysaccharide, 88th General Session & Exhibition of the International Association for Dental Research, Spain, Jul. 2010.
23.	Yuji Inagaki, Hirofumi Ohba, Hiroyuki Seto, Masumi Horibe, Kaya Yoshida, Tatsuji Haneji and Toshihiko Nagata : Dental Pulp Calcification and Osteopontin Expression in Diabetic Rats, International Association for Dental Research, Brisbane, Australia, Jun. 2006.

Proceeding of Domestic Conference:

1.	枡富健二, Mika Bandou, Yuji Inagaki, Rie Kido, 植村勇太, 畑田祐佳里, Jun-ichi Kido and Hiromichi Yumoto : 糖尿病関連歯周炎高齢患者のオーラルフレイルリスクバイオマーカーの探索, 第66回春季日本歯周病学会学術大会(高松), May 2023.
2.	西松佳苗, 清水日向, 中村大輔, 植村勇太, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido, Akikazu Murakami and Hiromichi Yumoto : Porphyromonas gingivalis由来OMVsは破骨細胞の分化と歯槽骨吸収に関与する, 四国歯学会第61回例会, Mar. 2023.
3.	Yuji Inagaki, Mika Bandou, Takahisa Ikuta, Jun-ichi Kido and Hiromichi Yumoto : 侵襲性歯周炎(ステージIII, グレードC)に対して歯周基本治療と歯周外科治療を行い奏功した一症例, 第65回秋季日本歯周病学会学術大会(仙台), Sep. 2022.
4.	Mika Bandou, Yuji Inagaki and Hiromichi Yumoto : Report of two cases of root coverage with connective tissue graft for patients suffering from gingival reccesion -Consideration of sufficient and insufficient case-, 第65回秋季日本歯周病学会学術大会, Sep. 2022.
5.	植村勇太, Yuji Inagaki, Yuka Hiroshima, 仲村大輔, Jun-ichi Kido and Hiromichi Yumoto : Porphyromonas gingivalis由来OMVs (Outer Membrane Vesicles)は破骨細胞の分化に関与する, 第65回秋季日本歯周病学会学術大会, Sep. 2022.
6.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : 人工合成したβ-defensin 2によるPorphyromonas gingivalisの付着抑制およびリポソーム封入と口腔上皮細胞への送達, 四国歯学会第60回例会, Jun. 2022.
7.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : 人工合成したbeta-defensin 2によるPorphyromonas gingivalisの付着抑制およびリポソーム封入と口腔上皮細胞への送達, 第65回春季日本歯周病学会学術大会, Jun. 2022.
8.	Rie Kido, Eijiro Sakamoto, Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Takahisa Ikuta, Masami Ninomiya, Yuji Inagaki, Yasufumi Nishikawa, Yoritoki Tomotake, Koji Naruishi and Hiromichi Yumoto : イムノクロマト法を用いたカルプロテクチン測定による歯周病およびインプラント疾患の診断, 四国歯学会第59回例会, Mar. 2022.
9.	Yuta Uemura, Yuka Hiroshima, 村上圭史, Yuji Inagaki, Hideki Fujii and Hiromichi Yumoto : Porphyromonas gingivalis OMVによる歯肉上皮細胞のサイトカイン産生機構, 四国歯学会第58回例会, Nov. 2021.
10.	Yuka Hiroshima, Rie Kido, Jun-ichi Kido, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : 人工合成したLopocalin 2はPorphyromonas gingivalisの口腔上皮細胞への付着を抑制する, 第64回秋季日本歯周病学会学術大会, Oct. 2021.
11.	Yuta Uemura, Yuka Hiroshima, Keiji Murakami, Yuji Inagaki, Hiromichi Yumoto and Hideki Fujii : ヒト歯肉上皮細胞におけるPorphyromonas gingivalis由来メンブレンベシクルの炎症性サイトカイン産生誘導機構の解明, 第19回四国免疫フォーラム, Jun. 2021.
12.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : リポソームに封入したリポカリン2の口腔上皮細胞への送達, 第64回春季日本歯周病学会学術大会, May 2021.
13.	Yuka Hiroshima, Yuta Uemura, Yuji Inagaki, Jun-ichi Kido and Hiromichi Yumoto : ヒト歯肉上皮細胞におけるPorphyromonas gingivalis由来メンブレンベシクルの炎症性サイトカイン産生誘導機構の解明, 第64回春季日本歯周病学会学術大会, May 2021.
14.	Yuta Uemura, Yuka Hiroshima, Yuji Inagaki and Hiromichi Yumoto : Porphyromonas gingivalis由来メンブレンベシクルがヒト歯肉上皮細胞に及ぼす影響, 日本歯科保存学会2020年度秋季学術大会(第153回), Nov. 2020.
15.	Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : 無細胞蛋白質合成系を用いた抗菌ペプチドの合成とリポソーム封入, 日本歯科保存学会2020年度春季学術大会(第152回)(神戸), Jun. 2020.
16.	Yuka Hiroshima, Jun-ichi Kido, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : オーラルケアへの応用に関連するリポソームのデリバリー法の検討, 第63回春季日本歯周病学会学術大会, May 2020.
17.	Rie Kido, Yuka Hiroshima, Takahisa Ikuta, Yuji Inagaki, Mika Bandou, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : 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, 第63回春季日本歯周病学会学術大会, May 2020.
18.	植村勇太, Masami Ninomiya, 和田明大, Rie Kido, 高木亮輔, 野中康平, 谷口裕哉, Takahisa Ikuta, Eijiro Sakamoto, Mika Bandou, Yuji Inagaki, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : 歯周病ならびに歯周組織再生療法に関する臨床研究について, 徳島県歯科医学大会・四国歯学会第56回例会, Feb. 2020.
19.	Kohei Nonaka, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Eijiro Sakamoto, Koji Naruishi and Hiromichi Yumoto : ショウガオールはヒト歯肉線維芽細胞においてAGEs誘導性の酸化ストレスを抑制する, 第62回秋季日本歯周病学会学術大会 (北九州), Oct. 2019.
20.	Yuka Hiroshima, Jun-ichi Kido, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto : オーラルケアへの応用を目指した抗菌ペプチド合成とリポソーム封入, 第62回秋季日本歯周病学会学術大会, Oct. 2019.
21.	Ryosuke Takagi, Eijiro Sakamoto, Yuji Inagaki, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : S100A9はMAPKおよびSTAT3経路を介して骨細胞におけるIL-6とRANKLの発現を調節する, 日本歯科保存学会 2019年度春季学術大会(第150回) (金沢), Jun. 2019.
22.	Yuji Inagaki, Takahisa Ikuta, Eijiro Sakamoto, Jun-ichi Kido and Hiromichi Yumoto : 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, 日本歯科保存学会2019年度春季学術大会(第150回), Jun. 2019.
23.	Rie Kido, Yuka Hiroshima, Takahisa Ikuta, Kaya Yoshida, Yuji Inagaki, Koji Naruishi, Kazumi Ozaki, Jun-ichi Kido and Hiromichi Yumoto : 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, May 2019.
24.	Yuji Inagaki, 高木亮輔, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : 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2018年度秋季学術大会(第149回), Nov. 2018.
25.	Nonaka Kohei, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Eijiro Sakamoto, Koji Naruishi and Hiromichi Yumoto : ショーガオールはヒト歯肉線維芽細胞におけるAGEs誘導性のIL-6およびICAM-1産生を抑制する, 第62回秋季日本歯周病学会学術大会, Oct. 2018.
26.	Eijiro Sakamoto, Takagi Ryosuke, Yuji Inagaki, Jun-ichi Kido and Hiromichi Yumoto : 最終糖化産物とLPSは骨細胞由来スクレロスチンを介して骨芽細胞分化を抑制する, 第148回日本歯科保存学会秋季学術大会, Jun. 2018.
27.	Yuji Inagaki, Kohei Nonaka, Ryosuke Takagi, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : 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, Jun. 2018.
28.	野中康平, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Eijiro Sakamoto, Koji Naruishi and Hiromichi Yumoto : 最終糖化産物はヒト歯肉線維芽細胞におけるIL-6とICAM-1の発現増加を介して単球との接着を誘導する, 第61回春季日本歯周病学会学術大会, Jun. 2018.
29.	Rie Kido, Eijiro Sakamoto, Mika Bandou, Yuji Inagaki, Masami Ninomiya, Chie Wada -Mihara, Takahisa Ikuta, Koji Naruishi, Toshihiko Nagata, Jun-ichi Kido and Hiromichi Yumoto : インプラント周囲溝滲出液中のカルプロテクチンとNTxを用いたインプラント疾患の診断, 第61回春季日本歯周病学会学術大会, Jun. 2018.
30.	Ryosuke Takagi, Eijiro Sakamoto, Yuji Inagaki, Yuka Hiroshima, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto : 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, Jun. 2018.
31.	Yuji Inagaki, Mika Bandou, 生田貴久 and Jun-ichi Kido : 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, Dec. 2017.
32.	Masami Ninomiya, Yuji Inagaki, Chie Wada -Mihara, Mika Bandou, Yukiko Nakajima, Eijiro Sakamoto, Ikuta Takahisa, Nishikawa Yasufumi, Jung-Hwan Lew, Rie Kido, Takagi Ryousuke, Nonaka Kouhei, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : 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, Jun. 2017. (Keyword) periodontitis / fibroblast growth factor 2 / periodontal regeneration / Regroth
33.	Chie Wada -Mihara, Koji Naruishi, Mika Bandou, 西川泰史, Hwan Jung Lew, Eijiro Sakamoto, 生田貴久, 河野薫, Yukari Kajiura, 橋本万里, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : アドバンスドOSCEを見据えた当科の模擬OSCEの概要, Shikoku Dental Research, Vol.29, No.2, 49-53, Jun. 2017.
34.	Eijiro Sakamoto, Yuji Inagaki, Jun-ichi Kido, Takagi Ryosuke, Koji Naruishi and Toshihiko Nagata : 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, May 2017. (Keyword) periodontitis / diabetes mellitus / bone and mineral metabolism / Advanced glycation end products / Lipopolysaccharide
35.	Eijiro Sakamoto, Yuji Inagaki, Jun-ichi Kido, 高木亮輔, 生田貴久, Koji Naruishi and Toshihiko Nagata : 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, Oct. 2016.
36.	Yukari Kajiura, Mika Bandou, Jun-ichi Kido, Yuji Inagaki and Toshihiko Nagata : 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, Oct. 2016.
37.	美原智恵, Koji Naruishi, Mika Bandou, 西川泰史, Jung-Hwan Lew, Eijiro Sakamoto, 生田貴久, 河野薫, Yukari Kajiura, 橋本万里, Yukiko Nakajima, Yuji Inagaki, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : 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, Jun. 2016.
38.	Yuji Inagaki, Eijiro Sakamoto, Jun-ichi Kido, Yukari Kajiura and Toshihiko Nagata : 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, May 2016.
39.	Eijiro Sakamoto, Yuji Inagaki, Jun-ichi Kido, Yukari Kajiura, Jung-Hwan Lew and Toshihiko Nagata : 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, May 2016.
40.	Jun-ichi Kido, Mika Bandou, Yukiko Nakajima, Yukari Kajiura, Yuji Inagaki, 生田貴久, Eijiro Sakamoto, Koji Naruishi and Toshihiko Nagata : 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, Nov. 2015.
41.	Yukari Kajiura, Jun-ichi Kido, Yukiko Nakajima, Mika Bandou, Yuji Inagaki, Koji Naruishi, Eijiro Sakamoto, Kaori Abe, Yuka Hiroshima and Toshihiko Nagata : 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, Sep. 2015.
42.	Eijiro Sakamoto, Jun-ichi Kido, Yukari Kajiura, Mika Bandou, Yuji Inagaki, Koji Naruishi, 生田貴久 and Toshihiko Nagata : 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, Sep. 2015.
43.	Yuji Inagaki : 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, Jul. 2015.
44.	橋村慧, 松田璃沙, Yuji Inagaki, 松井寛和, 横田美帆, Tamotsu Tanaka, Jun-ichi Kido, Toshihiko Nagata and Akira Tokumura : 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, 220, Nov. 2014.
45.	Jumpei Teramachi, 篠原宏貴, Yuji Inagaki, Di Yang, Hirohiko Okamura, Toshihiko Nagata and Tatsuji Haneji : PKRによる炎症性骨破壊制御, 日本解剖学会第69回中国・四国支部学術集会プログラム, Oct. 2014.
46.	Mika Bandou, Yukari Kajiura, Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Hiromi Murata and Toshihiko Nagata : 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, Oct. 2014.
47.	Yukari Kajiura, Yukiko Bandou, Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yukiko Nakajima, 生田貴久, Hiromi Murata, Yuka Hiroshima, Koji Naruishi and Toshihiko Nagata : 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, Oct. 2014.
48.	橋村慧, 松田璃沙, Yuji Inagaki, 松井寛和, 横田美帆, Tamotsu Tanaka, Jun-ichi Kido, Toshihiko Nagata and Akira Tokumura : 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, 55, Sep. 2014.
49.	Jumpei Teramachi, Yuji Inagaki, Hirohiko Okamura, Toshihiko Nagata and Tatsuji Haneji : 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, Jul. 2014.
50.	Mika Bandou, Yuka Hiroshima, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 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, Jun. 2014.
51.	Jun-ichi Kido, Yukiko Nakajima, Mika Bandou, Yuji Inagaki and Toshihiko Nagata : 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, Jun. 2014.
52.	篠原宏貴, Jumpei Teramachi, Yuji Inagaki, Jun-ichi Kido, Toshihiko Nagata and Tatsuji Haneji : 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, Jun. 2014.
53.	橋村慧, 松田璃沙, Yuji Inagaki, 松井寛和, 横田美帆, Tamotsu Tanaka, Jun-ichi Kido, Toshihiko Nagata and Akira Tokumura : 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, 146, Jun. 2014.
54.	Yukari Kajiura, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, 生田貴久, 橋本万里, 篠原宏貴, Masami Ninomiya, Hiromi Murata, Yukiko Nakajima, Satoshi Yoneda, 美原智恵, Yuka Hiroshima, Keiji Oishi and Toshihiko Nagata : 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, May 2014.
55.	Yukiko Nakajima, Jun-ichi Kido, Mika Bandou, Yuji Inagaki and Toshihiko Nagata : 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, May 2014.
56.	篠原宏貴, Jumpei Teramachi, Yuji Inagaki, Jun-ichi Kido, Toshihiko Nagata and Tatsuji Haneji : 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, May 2014.
57.	Mika Bandou, Yukiko Nakajima, Yukari Kajiura, Jun-ichi Kido, Yuji Inagaki, Hiromi Murata and Toshihiko Nagata : 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, May 2014.
58.	Yukari Kajiura, Yukiko Bandou, Jun-ichi Kido, Mika Bandou, Yuji Inagaki, Yukiko Nakajima, 生田貴久, Hiromi Murata, Yuka Hiroshima, Koji Naruishi and Toshihiko Nagata : 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, May 2014.
59.	Jumpei Teramachi, 篠原宏貴, Yuji Inagaki, Hiroyuki Morimoto, Toshihiko Nagata and Tatsuji Haneji : The role of PKR on osteoclast formation in the microenvironment of periodontitis, 第119回日本解剖学会総会・全国学術集会, Feb. 2014.
60.	Jumpei Teramachi, 篠原宏貴, Yuji Inagaki, Toshihiko Nagata and Tatsuji Haneji : 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, Oct. 2013.
61.	Yuji Inagaki : 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, Oct. 2013.
62.	生田貴久, Yuji Inagaki, Yukiko Nakajima, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : 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, Oct. 2013.
63.	篠原宏貴, Jumpei Teramachi, Yuji Inagaki, Jun-ichi Kido, Toshihiko Nagata and Tatsuji Haneji : 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, Sep. 2013.
64.	Yukiko Nakajima, Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata and Toshihiko Nagata : 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, Sep. 2013.
65.	Yukiko Nakajima, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 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, Jun. 2013.
66.	梶浦由加里, Mika Bandou, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 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, Jun. 2013.
67.	Jun-ichi Kido, Mika Bandou, Yukiko Bandou, Yuji Inagaki, Yuka Hiroshima, 梶浦由加里, Chie Wada -Mihara, Hiromi Murata, 生田貴久, 篠原宏貴, Makoto Funaki and Toshihiko Nagata : 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, May 2013.
68.	坂本英次郎, 美原智恵, 生田貴久, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 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, May 2013.
69.	Jun-ichi Kido, Mika Bandou, Yukiko Bandou, Yuji Inagaki, Yuka Hiroshima, 梶浦由加里, 美原智恵, Hiromi Murata, 生田貴久, 篠原宏貴, 橋本万里, Makoto Funaki, Haruhiko Saito and Toshihiko Nagata : --, 第56回日本糖尿病学会年次学術集会, May 2013.
70.	Eijiro Sakamoto, Chie Wada -Mihara, 生田貴久, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 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, May 2013.
71.	坂本英次郎, Chie Wada -Mihara, 生田貴久, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 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, May 2013.
72.	Yuji Inagaki, 生田貴久, 中島由紀子, Jun-ichi Kido, Toshihiko Nagata, 齋藤剛 and 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, 64, Nov. 2012.
73.	Masumi Horibe, Yuji Inagaki, 中島由紀子, 生田貴久, Jun-ichi Kido and Toshihiko Nagata : 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, 157, Nov. 2012.
74.	中島由紀子, Yuji Inagaki, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 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, 97, Nov. 2012.
75.	坂本英次郎, Chie Wada -Mihara, 生田貴久, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 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, Nov. 2012.
76.	生田貴久, Yuji Inagaki, Eijiro Sakamoto, 中島由紀子, Jun-ichi Kido and Toshihiko Nagata : 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, Vol.54, 86, Sep. 2012.
77.	生田貴久, Yuji Inagaki, 坂本英次郎, 中島由紀子, Jun-ichi Kido and Toshihiko Nagata : 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, Vol.54, 86, Sep. 2012.
78.	Eijiro Sakamoto, Chie Wada -Mihara, 生田貴久, Yuji Inagaki, Jun-ichi Kido and Toshihiko Nagata : 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, 82, Jun. 2012.
79.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yukiko Bandou, Yuka Hiroshima, Hiromi Murata, Makoto Funaki, Haruhiko Saito and Toshihiko Nagata : 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, 186, May 2012.
80.	Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Yuka Hiroshima, Hiromi Murata, Takahisa Ikuta, 篠原宏貴, 橋本万里, 山田由加里, Yukiko Bandou, Haruhiko Saito and Toshihiko Nagata : 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, Vol.54, 112, May 2012.
81.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, Masami Ninomiya, Keiji Oishi, Eijiro Sakamoto, 中島由紀子, 生田貴久, 浅原洋士 and Toshihiko Nagata : 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, Vol.31, 86, Mar. 2012. (Keyword) *生物学的マーカー
82.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, Masami Ninomiya, Keiji Oishi, Eijiro Sakamoto, 中島由紀子, 生田貴久, 浅原洋士 and Toshihiko Nagata : 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, Vol.31, 86, Mar. 2012. (Keyword) *生物学的マーカー
83.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Hiromi Murata, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, Masami Ninomiya, Keiji Oishi, 坂本英次郎, 中島由紀子, 生田貴久, 浅原洋士 and Toshihiko Nagata : 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, Vol.31, 86, Mar. 2012. (Keyword) *生物学的マーカー
84.	Hiromi Murata, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Yuji Inagaki and Toshihiko Nagata : 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, 200, Oct. 2011.
85.	Yukiko Bandou, Jun-ichi Kido, Yuka Hiroshima, Mika Bandou, Yuji Inagaki, Hiromi Murata, Yosuke Shikama, Makoto Funaki and Toshihiko Nagata : 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, Vol.53, 106, Sep. 2011.
86.	Jun-ichi Kido, Kaori Abe, Masatoshi Kataoka, Mika Bandou, Yuka Hiroshima, Yuji Inagaki and Toshihiko Nagata : 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, Vol.53, 108, Sep. 2011.
87.	中島由紀子, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 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, 12, Jun. 2011.
88.	Mika Bandou, Yuji Inagaki, Jun-ichi Kido, Yuka Hiroshima, Masatoshi Kataoka, Hiromi Murata, Yukiko Bandou, Masami Ninomiya, Eijiro Sakamoto, 中島由紀子 and Toshihiko Nagata : 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, Vol.53, 119, May 2011. (Keyword) periodontitis / diabetes mellitus / 歯肉溝滲出液 / グリコアルブミン
89.	Mika Bandou, Yuji Inagaki, Jun-ichi Kido, Yuka Hiroshima, Masatoshi Kataoka, Hiromi Murata, Yukiko Bandou, Masami Ninomiya, 坂本英次郎, 中島由紀子 and Toshihiko Nagata : 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, Vol.53, 119, May 2011. (Keyword) periodontitis / diabetes mellitus / 歯肉溝滲出液 / グリコアルブミン
90.	Yukiko Nakajima, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 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), Oct. 2010.
91.	Yuji Inagaki, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima and Chie Wada -Mihara : 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, May 2010.
92.	Yuji Inagaki, Jun-ichi Kido, 板東美香, 廣島佑香, 片岡正俊, 美原智恵, 堀部ますみ, Satoshi Yoneda, Eijiro Sakamoto, 中島由紀子, Masami Ninomiya, 大石慶二, 浅原洋士 and Toshihiko Nagata : 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), May 2010.
93.	Yuji Inagaki, Jun-ichi Kido, 板東美香, 廣島佑香, 片岡正俊, 美原智恵, 堀部ますみ, Satoshi Yoneda, 坂本英次郎, 中島由紀子, Masami Ninomiya, 大石慶二, 浅原洋士 and Toshihiko Nagata : 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), May 2010.
94.	Jun-ichi Kido, Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Masatoshi Kataoka, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, 坂本英次郎, 中島由紀子, Masami Ninomiya, Keiji Oishi, 淺原洋士 and Toshihiko Nagata : 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, Vol.52, 97, May 2010.
95.	Yuji Inagaki, Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Masatoshi Kataoka, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, 坂本英次郎, 中島由紀子, Masami Ninomiya, Keiji Oishi, 淺原洋士 and Toshihiko Nagata : 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, Vol.53, No.Suppl.1, S-145, Apr. 2010. (Keyword) 生物学的マーカー
96.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Yuji Inagaki, Chie Wada -Mihara, Keiji Oishi, Masatoshi Kataoka and Toshihiko Nagata : 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, Oct. 2009.
97.	Yuji Inagaki, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 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, Oct. 2009.
98.	Mika Bandou, Yuka Hiroshima, Yuji Inagaki, Masatoshi Kataoka, Chie Wada -Mihara, Masumi Horibe, Satoshi Yoneda, Keiji Oishi, Masami Ninomiya, Javkhlan Purevjav, Jun-ichi Kido and Toshihiko Nagata : 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, Vol.51, 101, Oct. 2009.
99.	Yuji Inagaki, 大場博史, Hiroyuki Seto, Masumi Horibe, Kaya Yoshida and Toshihiko Nagata : 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, May 2006.
100.	大場博史, Hiroyuki Seto, 徳永格, 濱秀樹, Yuji Inagaki, Masumi Horibe and Toshihiko Nagata : 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, Apr. 2006.
101.	Hiroyuki Seto, 大場博史, 濱秀樹, Yuji Inagaki, Masumi Horibe and Toshihiko Nagata : 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, Mar. 2006.

Et cetera, Workshop:

1.	Jumpei Teramachi, 篠原宏貴, Yuji Inagaki, Hirohiko Okamura and Toshihiko Nagata : 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, Dec. 2015.
2.	Yuji Inagaki, Jumpei Teramachi, Tatsuji Haneji and Toshihiko Nagata : 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, Nov. 2015.
3.	Masami Ninomiya, Satoshi Yoneda, Masumi Horibe, 美原智恵, Yuji Inagaki, Keiji Oishi, Jun-ichi Kido and Toshihiko Nagata : FGF-2による歯周組織再生療法, 第10回徳島Bone Forum, Dec. 2010. (Keyword) FGF-2 / 歯周組織再生療法 / 治験
4.	Yuji Inagaki, Kaya Yoshida, 大場博史, 中島由紀子, 瀬戸浩行, Jun-ichi Kido, 羽地達次 and Toshihiko Nagata : 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), Jun. 2010.
5.	Yuji Inagaki, 吉田賀弥, 大場博史, 中島由紀子, 瀬戸浩行, Jun-ichi Kido, 羽地達次 and Toshihiko Nagata : 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), Jun. 2010.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

ロバストネス最適化を基盤とした天然物由来アルカロイドを用いた歯周治療の開発 (Project/Area Number: 24K12931 )
歯周医学における歯周病原細菌由来ベシクルの役割解明と歯周病重症化予防剤の開発 (Project/Area Number: 21K09896 )
Study of exosomes from cells in periodontal tissues with diabetes-associated periodontitis (Project/Area Number: 21K09895 )
スクレロスチンを新規標的マーカーとした糖尿病関連歯周炎の非侵襲的診断法の開発 (Project/Area Number: 21K09874 )
高齢者糖尿病関連歯周炎患者のオーラルフレイルリスクバイオマーカーの探索 (Project/Area Number: 20K09957 )
Elucidation of the roles in the dental pulp of the innate immune receptor, Mincle, which recognizes dead cells by bacterial infection (Project/Area Number: 18K09577 )
Basic study for oral care system using an artificial cell (Project/Area Number: 17H04418 )
Development of a new periodontal treatment targeting the cross talk between osteoclast and osteoblast (Project/Area Number: 16K11833 )
Effect of hypoxia inducible factor on periodontal diseases and possibility of HIF inhibition as therapeutic drug (Project/Area Number: 24593125 )
糖尿病歯髄の病的石灰化および炎症反応に及ぼす最終糖化産物（ＡＧＥｓ）の影響 (Project/Area Number: 24592869 )
Effect of periodontopathic factors on osteoblastic differentiation of rat bone-marrow cells cultured under simulated microgravity (Project/Area Number: 23659979 )
Significance of osteopontin in gingival crevicular fluid of diabetes-associated periodontitis patients. (Project/Area Number: 22592314 )
Analysis of association between gene polymorphisms of antimicrobial peptides and periodontitis among Japanese patients (Project/Area Number: 21592626 )
歯髄細胞におけるオスモティックストレスと硬組織形成能に関する細胞生物学的解析 (Project/Area Number: 19659498 )
糖尿病性動脈硬化は歯髄石灰化の誘発因子となるか? (Project/Area Number: 17659597 )
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Associate Professor : Inagaki, Yuji

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)