Tokushima University / Educator and Researcher Directory --- Nagata, Toshihiko

Personal Web Page

https://researchmap.jp/read0017481 (researchmap)

Field of Study

○	Periodontology
○	Endodontology

Subject of Study

○	骨代謝に視点をおいた歯周病の病態と治療, 薬物誘発性歯肉増殖症の病因と治療, 歯周病の新しい診断指標の開発 (periodontitis)
○	歯髄細胞の硬組織形成能と骨基質蛋白 (calcification)

Book / Paper

Book:

1.	Toshihiko Nagata : 先端医療シリーズ・歯科医学2 歯周病新しい治療を求めて, 先端医療技術研究所,
2.	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.
3.	Koji Naruishi and Toshihiko Nagata : 腎臓と他臓器連関を考える臓器連関の実態腎臓-口腔連関, Nankodo, Aug. 2020.
4.	Koji Naruishi and Toshihiko Nagata : ザ・ペリオドントロジー「歯周病と慢性腎臓病(CKD)」, 永末書店, Feb. 2019.
5.	Masami Ninomiya and Toshihiko Nagata : 臨床編歯周病の病因, 永末書店, Jan. 2016. (Keyword) periodontitis
6.	Masami Ninomiya and Toshihiko Nagata : 高齢者透析患者の口腔内病変はどのように発見し対策を立てますか?, 医歯薬出版株式会社, Sep. 2014. (Keyword) dialysis / 高齢者 / 歯周病
7.	Toshihiko Nagata and Masami Ninomiya : 口腔ケア実践上のノウハウ糖尿病になるとう蝕や歯周病になりやすい? 糖尿病患者の口腔ケアで注意点，強調すべき点は?, 医歯薬出版株式会社, Tokyo, Mar. 2013. (Keyword) diabetes mellitus / periodontitis / 口腔ケア
8.	Jun-ichi Kido and Toshihiko Nagata : 1型 2型糖尿病の患者から口臭と口腔乾燥症の相談を受けたらそれぞれどう指導する?, 医歯薬出版株式会社, Tokyo, 2013.
9.	Jun-ichi Kido and Toshihiko Nagata : 1型 2型糖尿病の患者から口臭と口腔乾燥症の相談を受けたらそれぞれどう指導する?, 医歯薬出版株式会社, 東京, 2013.
10.	Masami Ninomiya and Toshihiko Nagata : 歯周病治療の基礎と臨床臨床編 1章歯周病の病因, Mar. 2011.
11.	Toshihiko Nagata and Masami Ninomiya : 歯科衛生士教本·歯周病の治療, 永末書店, Kyoto, Dec. 2005.
12.	Toshihiko Nagata and Keiji Oishi : 「糖尿病の治療と看護」 3.糖尿病の合併症とその対策，看護 B.慢性合併症 9. 歯周病, Nankodo, Tokyo, Aug. 2003.
13.	Toshihiko Nagata and Jun-ichi Kido : プログレッシブテクニック臨床医のための歯周治療, 永末書店, 2001.

Academic Paper (Judged Full Paper):

1.	Tsutsumi Toshihiko, Taira Satoshi, Matsuda Risa, Kageyama Chieko, Wada Mamiko, Kitayama Tomoya, Morioka Norimitsu, Morita Katsuya, Tsuboi Kazuhito, Naoshi Yamazaki, Jun-ichi Kido, Toshihiko Nagata, Dohi Toshihiro and Akira Tokumura : Lysophospholipase D activity on oral mucosa cells in whole mixed human saliva involves in production of bioactive lysophosphatidic acid from lysophosphatidylcholine., Prostaglandins & Other Lipid Mediators, Vol.174, 106881, 2024.
2.	Hiroshi Ito, Yukihiro Numabe, Shuichi Hashimoto, Satoshi Sekino, Etsuko Murakashi, Hitomi Ishiguro, Daisuke Sasaki, Takashi Yaegashi, Hideki Takai, Masaru Mezawa, Yorimasa Ogata, Hisashi Watanabe, Yuichi Izumi, Jun-ichi Kido, Yuka Hiroshima and Toshihiko Nagata : Utility of a haemoglobin test of gingival crevicular fluid: A multicentre, observational study., Oral Diseases, Vol.30, No.3, 1533-1542, 2024. (Tokushima University Institutional Repository) ● Metadata: 118968 (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.14536 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36790046 ● Summary page in Scopus @ Elsevier: 2-s2.0-85149959736 (Tokushima University Institutional Repository: 118968, DOI: 10.1111/odi.14536, PubMed: 36790046, Elsevier: Scopus)
3.	Koji Naruishi, Chie Wada -Mihara, Keiji Oishi and Toshihiko Nagata : Dental students' awareness after clinical training between dental treatment and systemic health: A questionnaire-based survey, Frontiers in Dental Medicine, 2022. (Link to Publication Site) ● Publication site (DOI): 10.3389/fdmed.2021.740441 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.3389/fdmed.2021.740441 (DOI: 10.3389/fdmed.2021.740441)
4.	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)
5.	Koji Inagaki, Takeshi Kikuchi, Toshihide Noguchi, Akio Mitani, Keiko Naruse, Tatsuaki Matsubara, Masamitsu Kawanami, Jun Negishi, Yasushi Furuichi, Eiji Nemoto, Satoru Yamada, Hiromasa Yoshie, Koichi Tabeta, Sachiyo Tomita, Atsushi Saito, Sayaka Katagiri, Yuichi Izumi, Hiroshi Nitta, Takanori Iwata, Yukihiro Numabe, Matsuo Yamamoto, Nobuo Yoshinari, Tsuyoshi Fujita, Hidemi Kurihara, Fusanori Nishimura, Toshihiko Nagata, Hiromichi Yumoto, Toru Naito, Kazuyuki Noguchi, Koichi Ito, Shinya Murakami, Rimei Nishimura and Naoko Tajima : A largescale observational study to investigate the current status of diabetic complications and their prevention in Japan (JDCP study 6): baseline dental and oral findings, Diabetology International, Vol.12, No.1, 52-61, 2020. (Summary) Japan Diabetes Complication and Prevention prospective (JDCP) study was conducted to examine the association between glycemic control and oral conditions in a large database of Japanese patients with diabetes. It included a total of 6099 patients with diabetes (range, 40-75 years) who had been treated as outpatients between 2007 and 2009. The mean number of present teeth at baseline was 19.8 and women with type 2 diabetes had fewer teeth than men with type 2 diabetes. Within the previous year, 17% of all patients had lost teeth. At baseline, 32% had experienced gingival swelling, 69% had brushed more than twice a day, 37% had used interdental cleaning aids, and 43% had undergone regular dental checkups. Multiple logistic regression analysis indicated that type 1 patients with HbA1c ≥ 7.0% were at higher risk of having fewer than 20 teeth (odds ratio [OR] 2.38; 95% confidence interval [CI] 1.25-4.78), and type 2 patients with HbA1c ≥ 8.0% also were at high risk of having fewer than 20 teeth (OR 1.16; 95% CI 1.00-1.34), after adjustment for nine possible confounding factors. In conclusion, patients with diabetes were found to be at high risk of tooth loss, and the poorer the glycemic control, the higher the risk of tooth loss in these patients. (Link to Publication Site) ● Publication site (DOI): 10.1007/s13340-020-00465-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33479579 ● Search Scopus @ Elsevier (PMID): 33479579 ● Search Scopus @ Elsevier (DOI): 10.1007/s13340-020-00465-3 (DOI: 10.1007/s13340-020-00465-3, PubMed: 33479579)
6.	稲垣幸司, 菊池毅, 野口俊英, 三谷章雄, 成瀬桂子, 川浪雅光, 根岸淳, 古市保志, 根本英二, 山田聡, 吉江弘正, 多部田康一, 富田幸代, 齊藤淳, 片桐さやか, 和泉雄一, 新田浩, 岩田隆紀, 沼部幸博, 山本松男, 吉成伸夫, 藤田剛, 栗原英見, 西村英紀, Toshihiko Nagata, Hiromichi Yumoto, Tohru Naito, 野口和行, 伊藤公一, 村上伸也, 西村理明, 田嶼尚子 and 糖尿病データベース構築委員会 : 糖尿病合併症の実態とその抑制に関する大規模観察研究ベースライン時の口腔所見JDCP study 6, Journal of the The Japan Diabetes Society, Vol.63, No.4, 195-205, 2020. (Link to Publication Site) ● Publication site (DOI): 10.11213/tonyobyo.63.195 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390566775131553664 ● Search Scopus @ Elsevier (DOI): 10.11213/tonyobyo.63.195 (DOI: 10.11213/tonyobyo.63.195, CiNii: 1390566775131553664)
7.	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)
8.	Masami Ninomiya, Mari Hashimoto, Kouji Yamanouchi, Yoshiaki Fukumura, Toshihiko Nagata and Koji Naruishi : Relationship of oral conditions to the incidence of infective endocarditis in periodontitis patients with valvular heart disease: a cross-sectional study., Clinical Oral Investigations, Vol.24, No.2, 833-840, 2020. (Summary) The patients with IE had fewer remaining teeth, more advanced bone resorption compared with those of patients without IE. These findings suggest a possible association between the occurrence of IE and periodontal infection. (Keyword) Infective endocarditis / Valvular heart disease / periodontitis (Tokushima University Institutional Repository) ● Metadata: 113773 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00784-019-02973-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31197658 ● Summary page in Scopus @ Elsevier: 2-s2.0-85067639107 (Tokushima University Institutional Repository: 113773, DOI: 10.1007/s00784-019-02973-2, PubMed: 31197658, Elsevier: Scopus)
9.	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)
10.	Jung-Hwan Lew, Koji Naruishi, Yukari Kajiura, Yasufumi Nishikawa, Takahisa Ikuta, Jun-ichi Kido and Toshihiko Nagata : High Glucose-Mediated Cytokine Regulation in Gingival Fibroblasts and THP-1 Macrophage: a Possible Mechanism of Severe Periodontitis with Diabetes., Cellular Physiology and Biochemistry, Vol.50, No.3, 973-986, 2018. (Summary) Diabetic conditions such as HG induce IL-1 and sIL-6R production from macrophages in inflammatory periodontal tissues and may exacerbate the periodontitis synergistically via MMP-1 production from HGFs. (Tokushima University Institutional Repository) ● Metadata: 113370 (Link to Publication Site) ● Publication site (DOI): 10.1159/000494481 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30355945 ● Search Scopus @ Elsevier (PMID): 30355945 ● Search Scopus @ Elsevier (DOI): 10.1159/000494481 (Tokushima University Institutional Repository: 113370, DOI: 10.1159/000494481, PubMed: 30355945)
11.	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)
12.	Kobayashi Tetsuo, Jun-ichi Kido, Yuichi Ishihara, K Omori, S Ito, T Matsuura, T Bando, J Wada, A Murasawa, K Nakazono, A Mitani, S Takashiba, Toshihiko Nagata and H Yoshie : The KCNQ1 gene polymorphism as a shared genetic risk for rheumatoid arthritis and chronic periodontitis in Japanese adults: A pilot case-control study, Journal of Periodontology, Vol.89, No.3, 315-324, 2018. (Summary) A number of studies have suggested a bidirectional relationship of periodontitis with rheumatoid arthritis (RA) and type 2 diabetes mellitus (T2DM). However, the genetic factors that underlie these relationships have not been elucidated. We conducted a multicenter case-control study that included 185 patients with RA and chronic periodontitis (CP), 149 patients with T2DM and CP, 251 patients with CP, and 130 systemically and periodontally healthy controls from a cohort of Japanese adults to assess the shared genetic risk factors for RA and CP as well as for T2DM and CP. A total of 17 candidate single nucleotide polymorphisms (SNPs) associated with RA, T2DM, and CP were genotyped. Multiple logistic regression analyses revealed that the KCNQ1 rs2237892 was significantly associated with comorbidity of RA and CP (P = 0.005) after adjustment for age, sex, and smoking status. The carriers of the T allele among patients with RA and CP showed significantly higher disease activity scores including 28 joints using C-reactive protein values than the non-carriers (P = 0.02), although the age, female percentage, and smoking status were comparable. Other SNPs were not associated with comorbidity of RA and CP, T2DM and CP, or susceptibility to CP. The results of the present pilot study suggest for the first time that the KCNQ1 rs2237892 may constitute a shared genetic risk factor for RA and CP, but not for T2DM and CP in Japanese adults. (Link to Publication Site) ● Publication site (DOI): 10.1002/JPER.17-0412 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29520783 ● Search Scopus @ Elsevier (PMID): 29520783 ● Search Scopus @ Elsevier (DOI): 10.1002/JPER.17-0412 (DOI: 10.1002/JPER.17-0412, PubMed: 29520783)
13.	Koji Naruishi, Yasufumi Nishikawa, Jun-ichi Kido, Akihiro Fukunaga and Toshihiko Nagata : Relationship of aspiration pneumonia to cognitive impairment and oral condition: a cross-sectional study., Clinical Oral Investigations, Vol.22, No.7, 2575-2580, 2018. (Summary) Early and simple evaluation of the oral condition and cognitive function can predict the risk of aspiration pneumonia. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00784-018-2356-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29388021 ● Summary page in Scopus @ Elsevier: 2-s2.0-85045039612 (DOI: 10.1007/s00784-018-2356-7, PubMed: 29388021, Elsevier: Scopus)
14.	Yukari Kajiura, Yasufumi Nishikawa, Hwan Jung Lew, Jun-ichi Kido, Toshihiko Nagata and Koji Naruishi : b-carotene suppresses Porphyromonas gingivalis lipopolysaccharide-mediated cytokine production in THP-1 monocytes cultured with high glucose condition., Cell Biology International, Vol.42, No.1, 105-111, 2018. (Summary) Periodontitis is associated with development of diabetes mellitus. Although lipopolysaccharide (LPS) of Porphyromonas gingivalis (Pg), a major pathogen of periodontitis, may lead the progression of diabetes complications, the precise mechanisms are unclear. We, therefore, investigated the effects of β-carotene on production of Pg LPS-induced inflammatory cytokines in human monocytes cultured high glucose (HG) condition. THP-1 cells were cultured under 5.5 mM or 25 mM glucose conditions, and cells were stimulated with Pg LPS. To investigate the productivity of TNF-α, IL-6, and MCP-1, cell supernatants were collected for ELISA. To examine the effects of NF-kB signals on cytokine production, Bay11-7082 was used. HG enhanced Pg LPS-induced production of TNF-α, IL-6, and MCP-1 via NF-kB signals in THP-1. β-carotene suppressed the enhancement of the Pg LPS-induced cytokine production in THP-1 via NF-κB inactivation. Our results suggest that β-carotene might be a potential anti-inflammatory nutrient for circulating Pg LPS-mediated cytokine production in diabetic patients with periodontitis. (Tokushima University Institutional Repository) ● Metadata: 112503 (Link to Publication Site) ● Publication site (DOI): 10.1002/cbin.10873 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28906038 ● Search Scopus @ Elsevier (PMID): 28906038 ● Search Scopus @ Elsevier (DOI): 10.1002/cbin.10873 (Tokushima University Institutional Repository: 112503, DOI: 10.1002/cbin.10873, PubMed: 28906038)
15.	Chie Wada -Mihara, Hiroyuki Seto, Hirofumi Ohba, Kaku Tokunaga, Jun-ichi Kido, Toshihiko Nagata and Koji Naruishi : Local administration of calcitonin inhibits alveolar bone loss in an experimental periodontitis in rats., Biomedicine & Pharmacotherapy, Vol.97, No.1, 765-770, 2018. (Summary) Calcitonin (CTN), a calcium regulatory hormone, promotes calcium diuresis from the kidney and suppresses bone resorption. The objective of this study was to evaluate whether the topical and intermittent application of CTN inhibits alveolar bone resorption using ligature-induced experimental periodontitis in rats. Experimental periodontitis was induced by placing a nylon ligature around maxillary molars of 8-week-old male Wistar rats for 20 days. Thirty-two rats were divided into four groups: basal sham control group, periodontitis group, periodontitis plus 0.2 U CTN (low dose), and periodontitis plus 1.0 U CTN (high dose) group. To investigate the effects of CTN on alveolar bone resorption, CTN was topically injected into the palatal gingivae every 2 days after ligature removal (day 0). Micro-computed tomography (CT) analysis was performed for linear parameter assessment of alveolar bone on day 5 and day 14. Periodontal tissues were examined histo-pathologically to assess the differences among the study groups. Micro-CT images showed that alveolar bone resorption was induced statistically around the molar of ligatured rats on day 5 and day 14. The amount of bone resorption was more severe on day 14 than that on day 5. On day 5, only high-dose CTN treatment significantly suppressed bone resorption. In addition, both doses of CTN significantly suppressed bone resorption on day 14. Histological examination clarified that there were fewer TRAP-positive cells in the CTN treatment groups than in the periodontitis group on day 5. Local administration of CTN decreased alveolar bone resorption by regulating osteoclast activation in rats with periodontitis. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2017.10.165 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29107933 ● Search Scopus @ Elsevier (PMID): 29107933 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2017.10.165 (DOI: 10.1016/j.biopha.2017.10.165, PubMed: 29107933)
16.	Jun-ichi Kido, Shinya Murakami, Masahiro Kitamura, Manabu Yanagita, Koichi Tabeta, Kazuhisa Yamazaki, Hiromasa Yoshie, Hisashi Watanabe, Yuichi Izumi, Reiko Suda, Matsuo Yamamoto, Hideki Shiba, Tsuyoshi Fujita, Hidemi Kurihara, Mitsuharu Mizuno, Akihiro Mishima, Nobumasa Kawahara, Kazuhiro Hashimoto, Koji Naruishi and Toshihiko Nagata : Useful Immunochromatographic Assay of Calprotectin in Gingival Crevicular Fluid for Diagnosis of Diseased Sites in Patients with Periodontal Diseases., Journal of Periodontology, 1-19, 2017. (Summary) Determination of GCF calprotectin using a novel IC chip system is useful for diagnosis of periodontal diseases. (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2017.170206 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28875823 ● Search Scopus @ Elsevier (PMID): 28875823 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2017.170206 (DOI: 10.1902/jop.2017.170206, PubMed: 28875823)
17.	Yukari Kajiura, Hwan Jung Lew, Takahisa Ikuta, Yasufumi Nishikawa, Jun-ichi Kido, Toshihiko Nagata and Koji Naruishi : Clinical Significance of GCF sIL-6R and Calprotectin to Evaluate the Periodontal Inflammation., Annals of Clinical Biochemistry, Vol.54, No.6, 664-670, 2017. (Summary) Both GCF sIL-6R and calprotectin levels are significant bio-markers to evaluate the periodontal inflammation. (Link to Publication Site) ● Publication site (DOI): 10.1177/0004563216680232 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27810997 ● Search Scopus @ Elsevier (PMID): 27810997 ● Search Scopus @ Elsevier (DOI): 10.1177/0004563216680232 (DOI: 10.1177/0004563216680232, PubMed: 27810997)
18.	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)
19.	Yasufumi Nishikawa, Yukari Kajiura, Hwan Jung Lew, Jun-ichi Kido, Toshihiko Nagata and Koji Naruishi : Calprotectin Induces IL-6 and MCP-1 Production via Toll-Like Receptor 4 Signaling in Human Gingival Fibroblasts., Journal of Cellular Physiology, Vol.232, No.7, 1862-1871, 2017. (Summary) Calprotectin, a heterodimer of S100A8 and S100A9 molecules, is associated with inflammatory diseases such as inflammatory bowel disease. We have reported that calprotectin levels in gingival crevicular fluids of periodontitis patients are significantly higher than in healthy subjects. However, the functions of calprotectin in pathophysiology of periodontitis are still unknown. The aim of this study is to investigate the effects of calprotectin on the productivity of inflammatory cytokines in human gingival fibroblasts (HGFs). The HGFs cell line CRL-2014® (ATCC) were cultured, and total RNAs were collected to examine the expression of TLR2/4 and RAGE mRNA using RT-PCR. After the cells were treated with S100A8, S100A9, and calprotectin, supernatants were collected and the levels of IL-6 and MCP-1 were measured using ELISA methods. To examine the intracellular signals involved in calprotectin-induced cytokine production, several chemical inhibitors were used. Furthermore, after the siRNA-mediated TLR4 down-regulated cells were treated with S100A8, S100A9, and calprotectin, the levels of IL-6 and MCP-1 were also measured. HGFs showed greater expression of TLR4 mRNA, but not TLR2 and RAGE mRNA compared with human oral epithelial cells. Calprotectin increased significantly the production of MCP-1 and IL-6 in HGFs, and the cytokine productions were significantly suppressed in the cells treated with MAPKs, NF-B, and TLR4 inhibitors. Furthermore, calprotectin-mediated MCP-1 and IL-6 production were significantly suppressed in TLR4 down-regulated cells. Taken together, calprotectin induces IL-6 and MCP-1 production in HGFs via TLR4 signaling that involves MAPK and NF-B, resulting in the progression of periodontitis. J. Cell. Physiol. 232: 1862-1871, 2017. © 2016 Wiley Periodicals, Inc. (Keyword) Antigens, Neoplasm / Cell Line, Tumor / cell proliferation and differentiation / Chemokine CCL2 / Down-Regulation / Fibroblasts / Gene Expression Regulation / Gingiva / Humans / Inflammation Mediators / Interleukin-6 / Intracellular Space / Leukocyte L1 Antigen Complex / Mitogen-Activated Protein Kinases / Models, Biological / NF-kappa B / Protein Kinase Inhibitors / RNA, Messenger / RNA, Small Interfering / Signal transduction of proinflammatory cytokine receptors / Sulfonamides / Toll-Like Receptor 4 / Transfection (Tokushima University Institutional Repository) ● Metadata: 111725 (Link to Publication Site) ● Publication site (DOI): 10.1002/jcp.25724 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27925202 ● Summary page in Scopus @ Elsevier: 2-s2.0-85008440585 (Tokushima University Institutional Repository: 111725, DOI: 10.1002/jcp.25724, PubMed: 27925202, Elsevier: Scopus)
20.	Hiroshi Ito, Yukihiro Numabe, Shuichi Hashimoto, Satoshi Sekino, Etsuko Murakashi, Hitomi Ishiguro, Daisuke Sasaki, Takashi Yaegashi, Hideki Takai, Masaru Mezawa, Yorimasa Ogata, Hisashi Watanabe, Satsuki Hagiwara, Yuichi Izumi, Yuka Hiroshima, Jun-ichi Kido, Toshihiko Nagata and Kazushi Kunimatsu : Correlation Between Gingival Crevicular Fluid Hemoglobin Content and Periodontal Clinical Parameters., Journal of Periodontology, Vol.87, No.11, 1314-1319, 2016. (Summary) Hb was observed in more than 60% of GCF samples in BOP(-) gingival sulci in both periodontally stable and periodontal-management-required groups. These results suggest inspection of Hb derived from microbleeding in gingival sulci may serve as an index for preclinical diagnosis. (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2016.160092 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27468797 ● Search Scopus @ Elsevier (PMID): 27468797 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2016.160092 (DOI: 10.1902/jop.2016.160092, PubMed: 27468797)
21.	Koji Naruishi, Keiji Oishi, Yuuji Inagaki, Masumi Horibe, Mika Bandou, Masami Ninomiya, K Kawahara, J Minakuchi, S Kawashima, K Shima, Jun-ichi Kido and Toshihiko Nagata : Association between Periodontal Condition and Kidney Dysfunction in Japanese Adults: A Cross-Sectional Study, Clinical and Experimental Dental Research, Vol.2, No.2, 1-8, 2016. (Tokushima University Institutional Repository) ● Metadata: 115061 (Link to Publication Site) ● Publication site (DOI): 10.1002/cre2.39 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1002/cre2.39 (Tokushima University Institutional Repository: 115061, DOI: 10.1002/cre2.39)
22.	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)
23.	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)
24.	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)
25.	Yumi Kuwamura, Sumikawa Masuko, Tetsuya Tanioka, Toshihiko Nagata, Eijiro Sakamoto, Hiromi Murata, Munehide Matsuhisa, Ken-ichi Aihara, Daisuke Hinode, Hirokazu Uemura, Hirokazu Ito, Yuko Yasuhara and Rozzano De Castro Locsin : Development of the Diabetes Oral Health Assessment Tool © for Nurses, Health, Vol.7, No.12, 1710-1720, 2015. (Keyword) diabetes mellitus / oral health behaviors / Oral Status / Nursing Assessment / Diabetes Nurse Specialist (Link to Publication Site) ● Publication site (DOI): 10.4236/health.2015.712186 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.4236/health.2015.712186 (DOI: 10.4236/health.2015.712186)
26.	Hiroki Shinohara, Jumpei Teramachi, Hirohiko Okamura, Di Yang, Toshihiko Nagata and Tatsuji Haneji : Double stranded RNA-dependent protein kinase is necessary for TNF--induced osteoclast formation in vitro and in vivo., Journal of Cellular Biochemistry, Vol.116, No.9, 1957-1967, 2015. (Summary) Double-stranded RNA-dependent protein kinase (PKR) is involved in cell cycle progression, cell proliferation, cell differentiation, tumorgenesis, and apoptosis. We previously reported that PKR is required for differentiation and calcification in osteoblasts. TNF- plays a key role in osteoclast differentiation. However, it is unknown about the roles of PKR in the TNF--induced osteoclast differentiation. The expression of PKR in osteoclast precursor RAW264.7 cells increased during TNF--induced osteoclastogenesis. The TNF--induced osteoclast differentiation in bone marrow-derived macrophages and RAW264.7 cells was markedly suppressed by the pre-treatment of PKR inhibitor, 2-aminopurine (2AP), as well as gene silencing of PKR. The expression of gene markers in the differentiated osteoclasts including TRAP, Calcitonin receptor, cathepsin K and ATP6V0d2 was also suppressed by the 2AP treatment. Bone resorption activity of TNF--induced osteoclasts was also supressed by 2AP treatment. Inhibition of PKR supressed the TNF--induced activation of NF-B and MAPK in RAW264.7 cells. 2AP inhibited both the nuclear translocation of NF-B and its transcriptional activity in RAW264.7 cells. 2AP inhibited the TNF--induced expression of NFATc1 and c-fos, master transcription factors in osteoclastogenesis. TNF--induced nuclear translocation of NFATc1 in mature osteoclasts was clearly inhibited by the 2AP treatment. The PKR inhibitor C16 decreased the TNF--induced osteoclast formation and bone resorption in mouse calvaria. The present study indicates that PKR is necessary for the TNF--induced osteoclast differentiation in vitro and in vivo. This article is protected by copyright. All rights reserved. (Tokushima University Institutional Repository) ● Metadata: 109478 (Link to Publication Site) ● Publication site (DOI): 10.1002/jcb.25151 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25739386 ● Search Scopus @ Elsevier (PMID): 25739386 ● Search Scopus @ Elsevier (DOI): 10.1002/jcb.25151 (Tokushima University Institutional Repository: 109478, DOI: 10.1002/jcb.25151, PubMed: 25739386)
27.	Koji Naruishi, Yukari Kajiura, 西川泰史, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : Inhibitory Effects of Cryptotanshinone on Inflammation-related Molecules in Human Gingival Fibroblasts, The Japanese Journal of Conservative Dentistry, Vol.58, No.3, 212-218, 2015. (Summary) Purpose: Cryptotanshinone (CPT) isolated from the root of an Asian medicinal plant, Salvia miltiorrhiza bunge, acts as a potent anti-tumor or anti-inflammatory agent in vitro. However, the effects of CPT on the progression of periodontitis are still unknown. This study investigated the effects of CPT on the production of inflammation-related molecules in human gingival fibroblasts. Methods: Human gingival fibroblasts (HGFs), CRL-2014TM (ATCC), were used. Cytotoxicity of the cells by CPT was examined. Dead cells stained by trypan blue were counted and analyzed. Next, the levels of IL-6 and VEGF in IL-1β-treated cells with or without CPT were measured using ELISA kits. The productivity of cathepsin L in IL-1β-treated cells with or without CPT was examined using Western blotting. Results: The ratio of viable cell numbers was significantly decreased by 100 μmol/l CPT. Next, the increase of IL-6 and cathepsin L induced by IL-1β was significantly suppressed by the pretreatment of 10 μmol/l CPT in HGFs. On the other hand, productivity of VEGF induced by IL-1β was not changed by the pretreatment of 10 μmol/l CPT. Conclusion: CPT suppresses IL-1β-induced IL-6 and cathepsin L production in HGFs, and might regulate the progression of periodontitis. (Keyword) IL-1β / cryptotanshinone / human gingival fibroblasts / IL-1β / periodontal inflammation (Link to Publication Site) ● Publication site (DOI): 10.11471/shikahozon.58.212 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205520665472 ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.58.212 (DOI: 10.11471/shikahozon.58.212, CiNii: 1390001205520665472)
28.	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)
29.	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)
30.	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)
31.	Hiromi Murata, T Hattori, H Maeda, S Takashiba, M Takigawa, Jun-ichi Kido and Toshihiko Nagata : Identification of transactivation-responsive DNA-binding protein 43 (TARDBP43; TDP-43) as a novel factor for TNF-a expression upon lipopolysaccharide stimulation in human monocytes., Journal of Periodontal Research, Vol.50, No.4, 452-460, 2015. (Summary) Tumor necrosis factor alpha (TNF-α) is a major cytokine implicated in various inflammatory diseases. The nature of the nuclear factors associated with human TNF-α gene regulation is not well elucidated. We previously identified a novel region located from -550 to -487 in human TNF-α promoter that did not contain the reported binding sites for nuclear factor kappa B (NF-κB) but showed lipopolysaccharide (LPS)-induced transcriptional activity. The purpose of this study is to identify novel factors that bind to the promoter region and regulate TNF-α expression. To identify DNA-binding proteins that bound to the target region of TNF-α promoter, a cDNA library from LPS-stimulated human monocytic cell line THP-1 was screened using a yeast one-hybrid system. Cellular localizations of the DNA-binding protein in the cells were examined by subcellular immunocytochemistry. Nuclear amounts of the protein in LPS-stimulated THP-1 cells were identified by western blot analysis. Expression of mRNA of the protein in the cells was quantified by real-time polymerase chain reaction. Electrophoretic mobility shift assays were performed to confirm the DNA-binding profile. Overexpression of the protein and knockdown of the gene were also performed to investigate the role for TNF-α expression. Several candidates were identified from the cDNA library and transactivation-responsive DNA-binding protein 43 (TARDBP43; TDP-43) was focused on. Western blot analysis revealed that nuclear TDP-43 protein was increased in the LPS-stimulated THP-1 cells. Expression of TDP-43 mRNA was already enhanced before TNF-α induction by LPS. Electrophoretic mobility shift assay analysis showed that nuclear extracts obtained by overexpressing FLAG-tagged TDP-43 bound to the -550 to -487 TNF-α promoter fragments. Overexpression of TDP-43 in THP-1 cells resulted in an increase of TNF-α expression. Knockdown of TDP-43 in THP-1 cells downregulated TNF-α expression. We identified TDP-43 as one of the novel TNF-α factors and found that it bound to the LPS-responsive element in the TNF-α promoter to increase TNF-α expression. (Link to Publication Site) ● Publication site (DOI): 10.1111/jre.12227 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25202836 ● Search Scopus @ Elsevier (PMID): 25202836 ● Search Scopus @ Elsevier (DOI): 10.1111/jre.12227 (DOI: 10.1111/jre.12227, PubMed: 25202836)
32.	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)
33.	Javkhlan Purevjav, Xu Guangfei, Chen Gang, Chenjuan Yao, Yuka Hiroshima, Hiroshi Yoshimura, Toshihiko Nagata and Kazuo Hosoi : Expression and LPS-Induced Elevation of Nod2 and Calprotectin in the Submandibular Gland of Wild-Type and TLR4-Knockout Male Mice, Journal of Research and Practice in Dentistry, Vol.2015, No.290259, 2015. (Link to Publication Site) ● Publication site (DOI): 10.5171/2015.290259 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.5171/2015.290259 (DOI: 10.5171/2015.290259)
34.	Koji Naruishi, Akiko Kunita, Katsuyuki Kubo, Toshihiko Nagata, Shogo Takashiba and Seiji Adachi : Predictors of improved functional outcome in elderly inpatients after rehabilitation: a retrospective study., Clinical Interventions in Aging, Vol.9, 2133-2141, 2014. (Summary) Age and disorder of oral function may be significant predictors of improved functional capacity after rehabilitation for elderly inpatients. (Link to Publication Site) ● Publication site (DOI): 10.2147/CIA.S73388 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25584025 ● Search Scopus @ Elsevier (PMID): 25584025 ● Search Scopus @ Elsevier (DOI): 10.2147/CIA.S73388 (DOI: 10.2147/CIA.S73388, PubMed: 25584025)
35.	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)
36.	Hiroshi Ito, Yukihiro Numabe, Satoshi Sekino, Etsuko Murakashi, Hitomi Iguchi, Shuichi Hashimoto, Daisuke Sasaki, Takashi Yaegashi, Kazushi Kunimatsu, Hideki Takai, Masaru Mezawa, Yorimasa Ogata, Hisashi Watanabe, Satsuki Hagiwara, Yuichi Izumi, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Evaluation of bleeding on probing and gingival crevicular fluid enzyme activity for detection of periodontally active sites during supportive periodontal therapy, Odontology, Vol.102, No.1, 50-56, 2014. (Summary) This study aimed to analyze the enzyme activity in gingival crevicular fluid (GCF) and its association with clinical parameters, especially bleeding on probing (BOP), and thus reconsider the significance and accuracy of recording BOP. A total of 184 patients who had entered supportive periodontal therapy were selected and GCF was collected from 401 sites before recording the clinical parameters, probing pocket depth (PPD), BOP, clinical attachment level, gingival index and plaque index. The enzyme activity of neutrophil elastase and aspartate aminotransferase and amount of protein in GCF were also analyzed. In the clinical parameters for biochemical data, amount of GCF showed the most correlation. A cut-off value for BOP and PPD were determined by the ROC curve and Youden index. Analysis was performed with all clinical parameters and biochemical data. Of the 401 sites, 51 were less than the cut-off value and were BOP-negative. On the other hand, 29 sites had values more than the cut-off value, with 14 BOP-negative sites and 15 BOP-positive sites. A conclusion is as follows: twenty-nine sites with values more than the cut-off value were diagnosed as sites requiring periodontal management, however, 14 of these were BOP-negative. These results suggest that combining other biochemical tests with examination of BOP and PPD may improve the validity of periodontal disease diagnosis. In future studies, it will be essential to find a marker that can precisely detect periodontal disease activity, and to develop a diagnostic tool for chair-side use. (Keyword) Aged / Female / Gingival Crevicular Fluid / Gingival Hemorrhage / Humans / Male / Middle Aged / Periodontal Pocket / periodontitis (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-012-0090-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23179356 ● Summary page in Scopus @ Elsevier: 2-s2.0-84892874741 (DOI: 10.1007/s10266-012-0090-1, PubMed: 23179356, Elsevier: Scopus)
37.	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)
38.	Toshio Takuma, Keiji Oishi, Tomofusa Manabe, Satoshi Yonada and Toshihiko Nagata : Buccal bone resorption around posterior implants after surgery: a 1-year prospective study., The International Journal of Oral & Maxillofacial Implants, Vol.29, No.3, 634-641, 2014. (Summary) This prospective study aimed to examine postoperative dimensional changes in the buccal bone and mucosa around single-stage implants placed in the posterior region. The dimensions of peri-implant tissue around screw-type implants placed in the posterior region were examined at surgery (baseline) and 6 months and 1 year after surgery. The lateral contour of the buccal bone and mucosa was horizontally measured at five vertical heights at 1-mm intervals (+1 to -3 mm from the implant platform) using custom-designed instruments. Bone resorption on the proximal sides was assessed on radiographs. Mucosal recession was measured on plaster casts of the dentition. Sixty-six implants placed in 30 patients were examined. All implants were clinically osseointegrated and stable throughout the study period. The buccal bone exhibited horizontal resorption throughout the study period, even at the most apical height measured. Assessed at each height, thicker bone (> 2 mm thick) tended to exhibit horizontal resorption during the first 6 months after surgery. However, the bone resorbed horizontally by approximately 0.4 mm during the final 6 months, irrespective of its contour. Vertical resorption of the buccal marginal bone was approximately 1 mm during the period from 6 months to 1 year. The bone-retaining group at the 1-year time point was found to have thicker bone walls at baseline compared with the bone-loss group. The thickness of the buccal mucosa showed little change. There was no obvious correlation between buccal bone resorption and mucosal recession. The buccal bone exhibited both horizontal and vertical resorption over the year after surgery. The initial contour of the bone was significantly associated with bone retention or loss at 1 year. However, mucosal recession was not directly affected by buccal bone resorption. (Keyword) Adult / Alveolar Bone Loss / Bone Resorption / Dental Implants, Single-Tooth / Female / Gingival Recession / Humans / Male / Middle Aged / Mouth Mucosa / Osseointegration / Prospective Studies / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.11607/jomi.3018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24818202 ● Summary page in Scopus @ Elsevier: 2-s2.0-84904428714 (DOI: 10.11607/jomi.3018, PubMed: 24818202, Elsevier: Scopus)
39.	Masami Ninomiya, Tomoko Azuma, Jun-ichi Kido, Shinya Murakami and Toshihiko Nagata : Successful case of periodontal tissue repair by fibroblast growth factor-2. -Long-term follow-up and comparison with enamel matrix derivative-, Clinical Advances in Periodontics, Vol.3, No.4, 216-221, 2013. (Link to Publication Site) ● Publication site (DOI): 10.1902/cap.2012.120014 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1902/cap.2012.120014 (DOI: 10.1902/cap.2012.120014)
40.	Mika Bandou, Xianqiong Zou, Yuka Hiroshima, Masatoshi Kataoka, Karen F. Ross, Yasuo Shinohara, Toshihiko Nagata, Mark C. Herzberg and Jun-ichi Kido : Mechanism of interleukin-1α transcriptional regulation of S100A9 in a human epidermal keratinocyte cell line, Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms, Vol.1829, No.9, 954-962, 2013. (Summary) S100A9 is a calcium-binding protein and subunit of antimicrobial calprotectin complex (S100A8/A9). Produced by neutrophils, monocytes/macrophages and keratinocytes, S100A9 expression increases in response to inflammation. For example, IL-1α produced by epithelial cells acts autonomously on the same cells to induce the expression of S100A8/A9 and cellular differentiation. Whereas it is well known that IL-1α and members of the IL-10 family of cytokines upregulate S100A8 and S100A9 in several cell lineages, the pathway and mechanism of IL-1α-dependent transcriptional control of S100A9 in epithelial cells are not established. Modeled using human epidermal keratinocytes (HaCaT cells), IL-1α stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor. Transcription of S100A9 in HaCaT cells depended on nucleotides -94 to -53 in the upstream promoter region, based upon the use of deletion constructs and luciferase reporter activity. Within the responsive promoter region, IL-1α increased the binding activity of CCAAT/enhancer binding protein β (C/EBPβ). Mutated C/EBPβ binding sequences or C/EBPβ-specific siRNA inhibited the S100A9 transcriptional response. Hence, IL-1α is strongly suggested to increase S100A9 expression in a human epidermal keratinocyte cell line by signaling through the IL-1 receptor and p38 MAPK, increasing C/EBPβ-dependent transcriptional activity. (Keyword) Base Sequence / Calgranulin B / Cell Line / DNA Primers / Epidermis / Humans / Interleukin-1alpha / Keratinocytes / Polymerase Chain Reaction / RNA Interference / Transcription, Genetic / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagrm.2013.03.010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23563247 ● Summary page in Scopus @ Elsevier: 2-s2.0-84880346974 (DOI: 10.1016/j.bbagrm.2013.03.010, PubMed: 23563247, Elsevier: Scopus)
41.	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)
42.	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)
43.	C Kudo, Koji Naruishi, H Maeda, Y Abiko, T Hino, M Iwata, C Mitsuhashi, S Murakami, T Nagasawa, Toshihiko Nagata, Satoshi Yoneda, Y Nomura, T Noguchi, Y Numabe, Y Ogata, T Sato, H Shimauchi, K Yamazaki, A Yoshimura and S Takashiba : Assessment of the plasma/serum IgG test to screen for periodontitis., Journal of Dental Research, Vol.91, No.12, 1190-1195, 2012. (Summary) Chronic periodontitis is a silent infectious disease prevalent worldwide and affects lifestyle-related diseases. Therefore, efficient screening of patients is essential for general health. This study was performed to evaluate prospectively the diagnostic utility of a blood IgG antibody titer test against periodontal pathogens. Oral examination was performed, and IgG titers against periodontal pathogens were measured by ELISA in 1,387 individuals. The cut-off value of the IgG titer was determined in receiver operating characteristic curve analysis, and changes in periodontal clinical parameters and IgG titers by periodontal treatment were evaluated. The relationships between IgG titers and severity of periodontitis were analyzed. The best cut-off value of IgG titer against Porphyromonas gingivalis for screening periodontitis was 1.682. Both clinical parameters and IgG titers decreased significantly under periodontal treatment. IgG titers of periodontitis patients were significantly higher than those of healthy controls, especially in those with sites of probing pocket depth over 4 mm. Multiplied cut-off values were useful to select patients with severe periodontitis. A blood IgG antibody titer test for Porphyromonas gingivalis is useful to screen hitherto chronic periodontitis patients. (Keyword) Actinobacillus actinomycetemcomitans / Adult / Antibodies, Bacterial / Case-Control Studies / Chronic Periodontitis / Eikenella corrodens / Female / Humans / Immunoglobulin G / Male / Mass Screening / Middle Aged / Porphyromonas gingivalis / Prevotella intermedia / Prospective Studies / ROC Curve / Reference Values / Reproducibility of Results / Sensitivity and Specificity (Link to Publication Site) ● Publication site (DOI): 10.1177/0022034512461796 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23018816 ● Search Scopus @ Elsevier (PMID): 23018816 ● Search Scopus @ Elsevier (DOI): 10.1177/0022034512461796 (DOI: 10.1177/0022034512461796, PubMed: 23018816)
44.	Chie Wada -Mihara, 徳永格, Hiroyuki Seto, Eijiro Sakamoto, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : Topical injection of osteoprotegerin prevents alveolar bone loss in rat experimental periodontitis, Journal of the Japanese Association of Periodontology, Vol.54, No.2, 167-174, 2012. (Keyword) osteoprotegerin / experimental periodontitis / alveolar bone / osteoclast (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.54.167 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679391110400 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.54.167 (DOI: 10.2329/perio.54.167, CiNii: 1390282679391110400)
45.	Jun-ichi Kido, Kaori Abe, Shouki Yatsushiro, Mika Bandou, Yuka Hiroshima, Toshihiko Nagata, Toshihiko Ooie, Masato Tanaka and Masatoshi Kataoka : Determination of calprotectin in gingival crevicular fluid by immunoassay on a microchip, Clinical Biochemistry, Vol.45, No.15, 1239-1244, 2012. (Summary) Gingival crevicular fluid (GCF) contains calprotectin, which appears to be a useful biomarker for periodontal diseases because of its high level in GCF from periodontally diseased pockets. To determine calprotectin in GCF that has a very small volume, sandwich enzyme-linked immunosorbent assay (ELISA) on a microchip was performed and its utility was estimated. Anti-calprotectin primary antibody was discharged on a microchip using a piezoelectric inkjet printing system. Calprotectin standard and calprotectin in GCF samples from eleven subjects were determined by the ELISA method with the prepared microchip and their values were compared with those obtained by conventional ELISA. Using the ELISA on a microchip, a reasonable standard curve of calprotectin protein (1.56-100 ng/mL) was obtained. Calprotectin in GCF samples was quantified and showed reasonable values in accordance with the condition of periodontal diseases. The values determined by the microchip method and conventional ELISA showed a significant linear relationship (R(2)=0.981). Calprotectin in GCF was determined using the ELISA on a microchip with high efficiency and this ELISA method for calprotectin determination may become a useful method for diagnosing periodontal diseases. (Keyword) Aged / Antibodies, Immobilized / calibration / Enzyme-Linked Immunosorbent Assay / Female / Gingival Crevicular Fluid / Humans / Lab-On-A-Chip Devices / Leukocyte L1 Antigen Complex / Linear Models / Male / Microfluidic Analytical Techniques / Middle Aged / Periodontal Diseases / Reference Standards / Reproducibility of Results / Sensitivity and Specificity (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clinbiochem.2012.05.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22609893 ● Search Scopus @ Elsevier (PMID): 22609893 ● Search Scopus @ Elsevier (DOI): 10.1016/j.clinbiochem.2012.05.009 (DOI: 10.1016/j.clinbiochem.2012.05.009, PubMed: 22609893)
46.	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)
47.	Jun-ichi Kido, Mika Bandou, Yuka Hiroshima, Hiroyuki Iwasaka, Keisuke Yamada, Naoto Ohgami, Toshiyuki Namubu, Masatoshi Kataoka, Takenori Yamamoto, Yasuo Shinohara, Ikuko Sagawa and Toshihiko Nagata : Analysis of proteins in human gingival crevicular fluid by mass spectrometry, Journal of Periodontal Research, Vol.47, No.4, 488-499, 2012. (Summary) Gingival crevicular fluid is a bodily fluid transuded from periodontal tissues into the gingival crevice and periodontal pocket, and contains many species of components. Proteins in gingival crevicular fluid have been studied as markers for periodontal diseases. Mass spectrometric analysis is used for the analyses of proteins, lipids, saccharides and metals, and expected as an approach for disease diagnosis. For better analysis of the protein components in gingival crevicular fluid, we investigated proteins in gingival crevicular fluid samples from the healthy gingival crevice and periodontal pocket using mass spectrometry. Gingival crevicular fluid samples were collected from subjects who gave their informed consent and were periodontally healthy or had diseased pockets. These samples were electrophoretically separated, and each fraction on the gels was analysed by nano liquid chromatography coupled with tandem mass spectrometry. Antimicrobial peptides detected in gingival crevicular fluid were confirmed by western blotting. One hundred and four proteins were detected in gingival crevicular fluid samples from both healthy sites and sites of periodontitis; 64 proteins were contained only in gingival crevicular fluid from healthy sites and 63 proteins were observed only in gingival crevicular fluid from periodontitis sites. These proteins were blood-, cytoskeleton-, immunity-, inflammation- and lipid-related proteins and enzymes. Some proteins, including ceruloplasmin, glycogen phosphorylase, glutathione S-transferase, phosphoglycerate mutase, psoriasin, S100A11 and resistin, were identified for the first time in gingival crevicular fluid. Antimicrobial peptides, such as lactoferrin, α1-antitrypsin, lipocalin, S100A7, S100A8, S100A9 and cathelicidin, were observed by mass spectrometry and western blotting. Multiple protein components in gingival crevicular fluid were analysed at the same time using mass spectrometry, and this approach may be useful for the diagnosis of periodontal diseases. (Keyword) Adult / Aged / Antimicrobial Cationic Peptides / Blotting, Western / Case-Control Studies / Ceruloplasmin / Chromatography, Liquid / Electrophoresis, Polyacrylamide Gel / Female / Gingival Crevicular Fluid / Glutathione Transferase / Glycogen Phosphorylase / Humans / Male / Middle Aged / Periodontal Pocket / periodontitis / Phosphoglycerate Mutase / Proteins / Resistin / S100 Proteins / Tandem Mass Spectrometry (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2011.01458.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22220998 ● Search Scopus @ Elsevier (PMID): 22220998 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2011.01458.x (DOI: 10.1111/j.1600-0765.2011.01458.x, PubMed: 22220998)
48.	Purevjav Javkhlan, Yuka Hiroshima, Ahmad Azlina, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Jun-ichi Kido, Toshihiko Nagata and Kazuo Hosoi : Lipopolysaccharide-mediated induction of calprotectin in the submandibular and parotid glands of mice, Inflammation, Vol.34, No.6, 668-680, 2011. (Summary) S100A8 and S100A9 constitute a heterodimeric protein, calprotectin. The mRNAs of S100A8 and S100A9, being expressed at minimal levels in the submandibular and parotid glands (SMG and PG, respectively) of C3H/HeN mice, were induced strongly and transiently by lipopolysaccharide (LPS). Among the mRNAs of members of the S100 protein family examined, those of S100A8 and S100A9 were specifically induced by LPS in the salivary glands. The induction was assumed to be mediated via toll-like receptor 4 (TLR4), since their elevation was limited in C3H/HeJ mice, a TLR4-mutant strain. These proteins became expressed in the granular convoluted tubular cells and striated duct cells in the SMG, and in both acinar and duct cells in the PG (all in the cytoplasm). The salivary calprotectin level was not increased by LPS treatment, implying that elevated calprotectin was not secreted into the saliva and that they may function in microcellular environment of the salivary gland. (Keyword) Animals / Calgranulin A / Calgranulin B / Leukocyte L1 Antigen Complex / Lipopolysaccharides / Mice / Parotid Gland / RNA, Messenger / Salivary Glands / Submandibular Gland / Transcriptional Activation (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-010-9277-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21125321 ● Search Scopus @ Elsevier (PMID): 21125321 ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-010-9277-1 (DOI: 10.1007/s10753-010-9277-1, PubMed: 21125321)
49.	Kaku Tokunaga, Hiroyuki Seto, Hirofumi Ohba, Chie Wada -Mihara, Hideki Hama, Masumi Horibe, Satoshi Yoneda and Toshihiko Nagata : Topical and intermittent application of parathyroid hormone recovers alveolar bone loss in rat experimental periodontitis., Journal of Periodontal Research, Vol.46, No.6, 655-662, 2011. (Summary) Periodontitis is characterized by periodontal tissue inflammation and alveolar bone loss. The intermittent administration of parathyroid hormone (PTH), a major regulator of bone remodeling, has been demonstrated to stimulate osteoblastic activity. Although the systemic administration of PTH has been reported to protect against periodontitis-associated bone loss, the effect of the topical administration of PTH is unclear. In this study, the effect of intermittent administration of PTH on osteoblastic differentiation was examined in cultured calvaria cells and then the effect of topical and intermittent administration of PTH was determined by measuring the recovery of alveolar bone loss after inducing experimental periodontitis in rats. Alkaline phosphatase activity and bone nodule formation were measured in fetal rat calvaria cells. Experimental periodontitis was induced by placing nylon ligature around rat maxillary molars for 20 d. After ligature removal (day 0), PTH was topically injected into buccal gingiva three times a week for 10 wk. Micro-computed tomography analysis and histological examination were performed on days 35 and 70. Intermittent exposure of PTH in calvaria cells increased alkaline phosphatase activity and bone nodule formation by 1.4- and 2.4-fold, respectively. Ligature procedures induced marked alveolar bone loss around the molars on day 0 and greater bone recovery was observed in the PTH-treated rats on day 70. An increase in osteoid formation on the surface of alveolar bone was detected in the PTH-treated rats. Intermittent treatment with PTH stimulated osteoblastic differentiation in fetal rat calvaria cell cultures, and topical and intermittent administration of PTH recovered alveolar bone loss in rat experimental periodontitis. (Keyword) Administration, Topical / Alkaline Phosphatase / Alveolar Bone Loss / Animals / Bone Regeneration / Cell Differentiation / Cells, Cultured / Drug Administration Schedule / Fetus / Image Processing, Computer-Assisted / Ligation / Osteoblasts / Parathyroid Hormone / Periodontitis / Rats / Rats, Inbred F344 / Rats, Wistar / Skull / X-Ray Microtomography (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2011.01386.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21722135 ● Search Scopus @ Elsevier (PMID): 21722135 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2011.01386.x (DOI: 10.1111/j.1600-0765.2011.01386.x, PubMed: 21722135)
50.	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)
51.	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)
52.	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)
53.	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)
54.	Mika Bandou, Yuka Hiroshima, Masatoshi Kataoka, MC Herzberg, KF Ross, Yasuo Shinohara, Takenori Yamamoto, Toshihiko Nagata and Jun-ichi Kido : Modulation of calprotectin in human keratinocytes by keratinocyte growth factor and interleukin-1alpha., Immunology and Cell Biology, Vol.88, No.3, 328-333, 2010. (Summary) Calprotectin is an antimicrobial complex composed of the S100A8 and S100A9 protein family subunits. Contributing to innate immunity, calprotectin expression is increased by interleukin-1alpha (IL-1alpha), which modulates keratinocyte differentiation. Keratinocyte growth factor (KGF) is produced by mesenchymal cells and has a mitogenic activity for epithelial cells. In this study, we investigated the effect of KGF on calprotectin expression in keratinocytes and modulation by IL-1alpha. Human keratinocytes were cultured with KGF in the presence or absence of a KGF receptor (KGFR) inhibitor or mitogen-activated protein kinase (MAPK) inhibitors. Calprotectin (S100A8/S100A9) expression was determined by northern blotting and enzyme-linked immunosorbent assay, respectively, whereas MAPK phosphorylation was analyzed by western blot analysis. KGF significantly decreased the expression of S100A8/S100A9-specific mRNAs and calprotectin protein. In the presence of KGF, KGFR inhibitor or extracellular-regulated kinase inhibitor restored KGF-downregulated expression of S100A8/S100A9. KGF increased IL-1alpha expression in keratinocytes, whereas IL-1alpha increased KGF expression in fibroblasts. Cocultured fibroblast and keratinocytes showed lower S100A8/S100A9 mRNA expression than keratinocytes alone in the presence or absence of IL-1alpha or KGF. These results suggest that fibroblast-derived KGF reduces or restricts calprotectin expression in keratinocytes, which supports our hypothesis that calprotectin expression in keratinocytes is modulated by factors associated with epithelial-mesenchymal interactions. (Link to Publication Site) ● Publication site (DOI): 10.1038/icb.2009.104 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20065999 ● Search Scopus @ Elsevier (PMID): 20065999 ● Search Scopus @ Elsevier (DOI): 10.1038/icb.2009.104 (DOI: 10.1038/icb.2009.104, PubMed: 20065999)
55.	Akiko Yamada, Takenori Yamamoto, Yuya Yoshimura, Shunichi Gouda, Satoshi Kawashima, Naoshi Yamazaki, Kikuji Yamashita, Masatoshi Kataoka, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Ca2+-induced permeability transition can be observed even in yeast mitochondria under optimized experimental conditions., Biochimica et Biophysica Acta (BBA) - Bioenergetics, Vol.1787, No.12, 1486-1491, 2009. (Summary) Yeast mitochondria have generally been believed not to undergo the permeability transition (PT) by the accumulation of Ca(2+) within the mitochondrial matrix, unlike mammalian mitochondria. However, the reason why the yeast PT is not induced by Ca(2+) has remained obscure. In this study, we examined in detail the effects of Ca(2+) on yeast mitochondria under various conditions. As a result, we discovered that the PT could be induced even in yeast mitochondria by externally added Ca(2+) under optimized experimental conditions. The 2 essential parameters for proper observation of the PT-inducing effects of Ca(2+) were the concentrations of the respiratory substrate and that of inorganic phosphate (Pi) in the incubation medium. The yeast mitochondrial PT induced by Ca(2+) was found to be insensitive to cyclosporin A and suppressed in the presence of a high concentration of Pi. Furthermore, when the PT was induced in yeast mitochondria by Ca(2+), the release of cytochrome c from mitochondria was also observed. (Keyword) calcium / Cytochromes c / Mitochondrial Membrane Transport Proteins / Yeasts (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbabio.2009.07.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19616504 ● Search Scopus @ Elsevier (PMID): 19616504 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbabio.2009.07.001 (DOI: 10.1016/j.bbabio.2009.07.001, PubMed: 19616504)
56.	Hiroki Iga, Daisuke Hinode, Masanori Nakano, Hideo Yoshida, Kazumi Ozaki, Masaru Hada, Masami Yoshioka, Kaya Yoshida, Yuko Takeuchi, Yumi Hoshimo, Naoko Matsumoto and Toshihiko Nagata : 徳島大学パイロット事業支援プログラム「歯科医療系学生の口腔保健・福祉体験実習による健康長寿支援」, Journal of University Education Research, Vol.6, 108-114, 2009. (Keyword) oral health and welfare / health support program / hospitality mind (Tokushima University Institutional Repository) ● Metadata: 82696 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050302172854738944 (Tokushima University Institutional Repository: 82696, CiNii: 1050302172854738944)
57.	Akiko Yamada, Takenori Yamamoto, Naoshi Yamazaki, Kikuji Yamashita, Masatoshi Kataoka, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Differential permeabilization effects of Ca2+ and valinomycin on the inner and outer mitochondrial membranes as revealed by proteomics analysis of proteins released from mitochondria., Molecular & Cellular Proteomics, Vol.8, No.6, 1265-1277, 2009. (Summary) It is well established that cytochrome c is released from mitochondria when the permeability transition (PT) of this organelle is induced by Ca2+. Our previous study showed that valinomycin also caused the release of cytochrome c from mitochondria but without inducing this PT (Shinohara, Y., Almofti, M. R., Yamamoto, T., Ishida, T., Kita, F., Kanzaki, H., Ohnishi, M., Yamashita, K., Shimizu, S., and Terada, H. (2002) Permeability transition-independent release of mitochondrial cytochrome c induced by valinomycin. Eur. J. Biochem. 269, 5224-5230). These results indicate that cytochrome c may be released from mitochondria with or without the induction of PT. In the present study, we examined the protein species released from valinomycin- and Ca2+-treated mitochondria by LC-MS/MS analysis. As a result, the proteins located in the intermembrane space were found to be specifically released from valinomycin-treated mitochondria, whereas those in the intermembrane space and in the matrix were released from Ca2+-treated mitochondria. These results were confirmed by Western analysis. Furthermore to examine how the protein release occurred, we examined the correlation between the species of released proteins and those of the abundant proteins in mitochondria. Consequently most of the proteins released from mitochondria treated with either agent were highly expressed proteins in mitochondria, indicating that the release occurred not selectively but in a manner dependent on the concentration of the proteins. Based on these results, the permeabilization effects of Ca2+ and valinomycin on the inner and outer mitochondrial membranes are discussed. (Keyword) Amino Acid Sequence / Animals / Blotting, Western / Calcium / Cell Membrane Permeability / Electrophoresis, Polyacrylamide Gel / Intracellular Membranes / Microscopy, Electron, Transmission / Mitochondria, Liver / Molecular Sequence Data / Proteins / Proteomics / Rats / Valinomycin (Link to Publication Site) ● Publication site (DOI): 10.1074/mcp.M800377-MCP200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19218587 ● Search Scopus @ Elsevier (PMID): 19218587 ● Search Scopus @ Elsevier (DOI): 10.1074/mcp.M800377-MCP200 (DOI: 10.1074/mcp.M800377-MCP200, PubMed: 19218587)
58.	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)
59.	Yuka Hiroshima, Mika Bandou, Masatoshi Kataoka, Toshihiko Nagata and Jun-ichi Kido : Regulation of calprotectin expression in human keratinocytes in vitro, Journal of the Japanese Association of Periodontology, Vol.49, No.3, 224-232, 2007. (Summary) Calprotectin, a heterodimeric complex of S100A8 and S100A9, is an antimicrobial peptide (AMP) expressed in healthy or inflamed epithelium and epidermis. The expression of calprotectin and other AMPs in keratinocytes is regulated by proinflammatory cytokines, bacterial products and keratinocyte differentiation modulators. Interleukin-1α (IL-1α), an autonomous cytokine in keratinocytes, induces keratinocyte differentiation and up-regulates calprotectin expression. Since keratinocyte differentiation is also specified<KG>by interactions with the basement membrane and connective tissue proteins, we sought to learn whether calprotectin expression is affected by extracellular matrix (ECM) proteins in the presence or absence of IL-1α. Human immortalized epidermal keratinocytes (HaCaT cells) were grown in vitro on different ECM substrates including type I collagen (Col I), type IV collagen (Col IV), fibronectin (FN) and laminin (LM) with or without IL-1α and were then cultured in basement membrane extract (Matrigel)-coated dishes or on a feeder layer of fibroblasts. Calprotectin expression in the cultured cells was investigated using immunohistochemical and northern blot analyses, and an enzyme-linked immunosorbent assay. The four ECM proteins (Col I, Col IV, FN and LM) had little effect on calprotectin expression. IL-1α significantly increased the expression of S100A8/ S100A9 mRNAs and calprotecin protein in the cells cultured on each of the ECM(Col I, Col IV, FN and LM)-coated dishes,but these ECM protein substrates did not show a further effect on calprotectin expression in the presence of IL-1α. On the other hand, Matrigel and the fibroblast-feeder layer slightly decreased the expression of S100A8/S100A9 mRNAs in HaCaT cells. These results suggest that calprotectin expression in keratinocytes is regulated by cytokines during epithelial-mesenchymal interactions.<KG>Nihon Shishubyo Gakkai Kaishi (J Jpn Periodontol) 49 : 224-232,2007. (Keyword) calprotectin / interleukin-1α / extracellular matrix / keratinocyte (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.49.224 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679388561152 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.49.224 (DOI: 10.2329/perio.49.224, CiNii: 1390282679388561152)
60.	Hiroaki Tanaka, Kaya Yoshida, Hirohiko Okamura, Hiroyuki Morimoto, Toshihiko Nagata and Tatsuji Haneji : Calyculin A induces apoptosis and stimulates phosphorylation of p65NF-κB in human osteoblastic osteosarcoma MG63 cells, International Journal of Oncology, Vol.31, No.2, 389-396, 2007. (Summary) Previously, we reported that okadaic acid, a specific inhibitor of serine/threonine protein phosphatases, induced apoptosis in human osteoblastic cells. However, it is not clear whether calyculin A, another inhibitor of protein phosphatases, would induce apoptosis in human osteoblastic cells and if so, which mechanisms are involved and whether the phosphorylation status of NF-kappaB could be affected by the treatment with calyculin A. In this report, we demonstrate that calyculin A induced apoptosis in MG63 cells, as judged by WST-8 assay, nuclear fragmentation, and DNA ladder formation. Expression of PTEN, FasL, and FasR mRNA was stimulated by calyculin A treatment in MG63 cells. Calyculin A also enhanced the phosphorylation level of NF-kappaB, as judged from the results of Western blot analysis and an in vitro dephosphorylation assay. Western blot analysis with anti-phospho-p65NF-kappaB antibody disclosed that the NF-kappaB was phosphorylated on serine 536 in cytosol and translocated into nucleus with calyculin A-treatment. The phosphorylation status of p65NF-kappaB was further confirmed by using the phosphorylation site-mutated p65NF-kappaB gene transfected into HEK293 cells. Unlike TNF-alpha, calyculin A treatment did not degraded IkappaBalpha within 10 min, while it degraded IkappaBalpha at 2-h treatment. Our findings indicate that calyculin A elicit phosphorylation of NF-kappaB on serine 536 in MG63 cells, resulting in the translocation of phospho-NF-kappaB to the nucleus, thereby promoting transcriptional activity of NF-kappaB-related genes. (Keyword) Apoptosis / Binding Sites / Bone Neoplasms / Cell Line, Tumor / Cell Survival / Enzyme Inhibitors / Humans / Mutation / Osteoblasts / Osteosarcoma / Oxazoles / Phosphorylation / Serine / Transcription Factor RelA / Transcription, Genetic (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17611696 ● Search Scopus @ Elsevier (PMID): 17611696 (PubMed: 17611696)
61.	Mika Bandou, Yuka Hiroshima, Masatoshi Kataoka, Yasuo Shinohara, MC Herzberg, KF Ross, Toshihiko Nagata and Jun-ichi Kido : Interleukin-1alpha regulates antimicrobial peptide expression in human keratinocytes., Immunology and Cell Biology, Vol.85, No.7, 532-537, 2007. (Summary) Human epidermis and epithelium serve as physiologic barriers to protect against noxious and infectious agents. Contributing to the defense against infection, epithelial cells express antimicrobial peptides (AMPs). The expression of AMPs in keratinocytes is generally regulated directly by bacteria and indirectly by proinflammatory cytokines. Bacteria may also regulate AMP expression by inducing keratinocyte expression of the autonomous proinflammatory cytokine, interleukin-1alpha (IL-1alpha). To test the hypothesis that AMP expression may be regulated by cell autonomous cytokines, we investigated the effect of IL-1alpha on the expression of AMPs in human keratinocytes (HaCaT cells) by microarray, northern blot, reverse transcriptase (RT)-PCR and western blot analyses. IL-1alpha increased expression of mRNA in a dose- and time-dependent manner specific for lipocalin 2, S100A8, S100A9 and secretory leukocyte protease inhibitor (SLPI) more than twofold relative to nonstimulated cells (control), and slightly upregulated S100A7 and beta-defensin-2. Furthermore, the expression of lipocalin 2, S100A7, S100A8, S100A9 and SLPI proteins were upregulated by IL-1alpha. On the other hand, HaCaT cells expressed mRNA specific for other AMPs, including cystatin 3, adrenomedullin, RNase-7 and mucin 5, which were unaffected by IL-1alpha treatment. These results suggest that the autonomous keratinocyte cytokine, IL-1alpha, selectively upregulates the expression of AMPs which may modulate innate epithelial cell immunity in skin and mucosa. (Keyword) Immunity, Innate (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.icb.7100078 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17549071 ● Search Scopus @ Elsevier (PMID): 17549071 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.icb.7100078 (DOI: 10.1038/sj.icb.7100078, PubMed: 17549071)
62.	Kaori Abe, Keiko Miyoshi, Taro Muto, Ruspita Intan, Taigo Horiguchi, Toshihiko Nagata and Takafumi Noma : Establishment and characterization of rat dental epithelial derived ameloblast-lineage clones., Journal of Bioscience and Bioengineering, Vol.103, No.5, 479-485, 2007. (Summary) Teeth are the hardest tissues covered with enamel produced by ameloblasts. The ameloblast differentiation is controlled by sequential epithelial-mesenchymal interactions during tooth morphogenesis. However, the molecular mechanism of ameloblast differentiation remains unclear. To address this question, we developed an in vitro assay system to evaluate the molecular mechanism of amelogenesis. First, we established dental epithelium-derived clones from 6-day-old rat incisors and established that cells of the clone SRE-G5 were the largest producers of amelogenin mRNA. Next, we analyzed the effects of several chemicals on the amelogenin expression in SRE-G5 cells. Only mitogen-activated protein kinase (MAPK) activators enhanced amelogenin mRNA expression. This finding corresponded to the immunohistochemical data showing the presence of phosphorylated forms of p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) during ameloblast differentiation. To examine the roles of MAPK signals, we compared the effects of anisomycin and sodium salicylate on the expression of tooth-related differentiation markers. Both anisomycin and sodium salicylate induced amelogenin, Abcg2, and Bmp4 mRNA and down-regulated p75NGFR mRNA. On the other hand, ALP, ectodin, Bmp2 and Fgf8 mRNA were up-regulated only by anisomycin. These results indicate that MAPK signaling functions, at least in part, as the inducer of ameloblast differentiation. (Keyword) Ameloblasts / Amelogenesis / Amelogenin / Animals / cell differentiation / Cells, Cultured / Cloning, Molecular / Epithelial Cells / Incisor / Rats (Link to Publication Site) ● Publication site (DOI): 10.1263/jbb.103.479 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17609165 ● Summary page in Scopus @ Elsevier: 2-s2.0-34250827878 (DOI: 10.1263/jbb.103.479, PubMed: 17609165, Elsevier: Scopus)
63.	Noriko Hayashi, Jun-ichi Kido, (名) Suryono, Reiko Kido, Chie Wada -Mihara, Masatoshi Kataoka, Yasuo Shinohara and Toshihiko Nagata : Regulation of Calprotectin Expression by IL-1α and TGF-β in Human Gingival Keratinocytes, Journal of Periodontal Research, Vol.42, No.1, 1-7, 2007. (Summary) Calprotectin, a heterodimer of S100A8 and S100A9 with antimicrobial properties, is expressed in gingival keratinocytes and plays an important role in innate immunity. Because calprotectin expression is localized in the spinous cell layer of the gingival epithelium, we hypothesized that the expression of calprotectin in keratinocytes is related to the differentiation stage. The aim of the present study was to investigate the relationship between calprotectin expression and keratinocyte differentiation using some factors that regulated its differentiation. Normal human gingival keratinocytes were isolated from gingival tissues obtained at the extraction of wisdom teeth, and were cultured in serum-free keratinocyte medium supplemented with interleukin-1alpha or calcium, which promote keratinocyte differentiation, and transforming frowth factor-beta (TGF-beta) or retinoic acid, which suppress its differentiation. The expression of S100A8/A9 mRNA and the production of calprotectin in normal human gingival keratinocytes were examined by northern blotting and enzyme-linked immunosorbent assay, respectively. The expression of cytokeratin 14, involucrin and filaggrin (marker proteins of keratinocyte differentiation) was investigated by immunohistochemical staining, and the DNA-binding activity of CCAAT/enhancer binding protein alpha (C/EBPalpha), a transcription factor, was examined by electrophoretic mobility shift assay. The expression of S100A8/A9 mRNA and the production of calprotectin were increased by interleukin-1alpha and calcium, but decreased by TGF-beta. RA inhibited the expression of S100A8/A9 and keratinocyte differentiation, which were induced by interleukin-1alpha. C/EBPalpha DNA-binding activity in normal human gingival keratinocytes was enhanced by interleukin-1alpha and calcium, but suppressed by TGF-beta. The present study suggests that calprotectin expression is related to keratinocyte differentiation and that C/EBPalpha is a regulator of calprotectin expression in keratinocytes. (Keyword) calprotectin / gingival keratinocyte / differentiation / C/EBPα (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2005.00857.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17214633 ● Search Scopus @ Elsevier (PMID): 17214633 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2005.00857.x (DOI: 10.1111/j.1600-0765.2005.00857.x, PubMed: 17214633)
64.	Kaya Yoshida, Hiroyuki Shinohara, (名) Suryono, Tatsuji Haneji and Toshihiko Nagata : Arachidonic acid inhibits osteoblast differentiation through cytosolic phospholipase A2-dependent pathway., Oral Diseases, Vol.13, No.1, 32-39, 2007. (Summary) Arachidonic acid, a precursor of prostaglandins (PGs), is released by phospholipase A2 (PLA2) and plays an important role in biological reactions. We examined the roles of arachidonic acid on the pathway of PG synthesis and osteoblast differentiation by using clone MC3T3-E1 cells. The effect of arachidonic acid was evaluated by the measurement of alkaline phosphatase activity, cells shape, production of arachidonic acid and the expression of cyclooxygenase (COX). Arachidonic acid dose dependently decreased alkaline phosphatase activity and increased PGE2 production in MC3T3-E1 cells. The cell shape changed from polygonal to fibroblastic following treatment with arachidonic acid. These effects were recovered by the treatment of NS-398 and indomethacin. Arachidonic acid increased the expression of COX-2 mRNA and the PGE2 production. The exogenous arachidonic acid induced the release of cellular arachidonic acid in MC3T3-E1 cells. Moreover, methylarachidonyl fluorophosphonate suppressed the arachidonic acid release and the expression of COX-2 mRNA. The present results indicate that exogenous arachidonic acid stimulated the activity of PLA2, leading to the new release of membranous arachidonic acid. The amplified arachidonic acid enhanced PGE2 production by COX-2, which inhibits the differentiation of MC3T3-E1 cells. Our results provide a new insight into the molecular mechanisms by which exogenous arachidonic acid plays a role as a paracrine/autocrine amplifier of PGE2 biosynthesis by coupling with PLA2 and COX-2. (Keyword) 3T3 Cells / Alkaline Phosphatase / Animals / Arachidonic Acid / Arachidonic Acids / cell differentiation / Cell Shape / Clone Cells / Cyclooxygenase 2 / Cyclooxygenase 2 Inhibitors / Cyclooxygenase Inhibitors / Cytosol / Dinoprostone / Enzyme Inhibitors / Fibroblasts / Indomethacin / Mice / Nitrobenzenes / Osteoblasts / Phospholipases A / Phospholipases A2 / Phosphonic Acids / Prostaglandin-Endoperoxide Synthases / Prostaglandins / RNA, Messenger / Sulfonamides (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1601-0825.2006.01239.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17241427 ● Search Scopus @ Elsevier (PMID): 17241427 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1601-0825.2006.01239.x (DOI: 10.1111/j.1601-0825.2006.01239.x, PubMed: 17241427)
65.	Takenori Yamamoto, Akiko Yamada, Masahiro Watanabe, Yuya Yoshimura, Naoshi Yamazaki, Yoshiyuki Yoshimura, Takashi Yamauchi, Masatoshi Kataoka, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : VDAC1, having a shorter N-terminus than VDAC2 but showing the same migration in an SDS-polyacrylamide gel, is the predominant form expressed in mitochondria of various tissues., Journal of Proteome Research, Vol.5, No.12, 3336-3344, 2006. (Summary) The voltage-dependent anion channel (VDAC) is a pore-forming protein expressed in the outer membrane of eukaryotic mitochondria. Three isoforms of it, i.e., VDAC1, VDAC2, and VDAC3, are known to be expressed in mammals; however, the question as to which is the main isoform in mitochondria is still unanswered. To address this question, we first prepared standard VDACs by using a bacterial expression system and raised various antibodies against them by using synthetic peptides as immunogens. Of the three bacterially expressed VDAC isoforms, VDAC3 showed faster migration in SDS-polyacrylamide gels than VDAC1 and VDAC2, although VDAC2 is longer than VDAC1 and VDAC3, due to a 12-amino acid extension of its N-terminal region. Even with careful structural characterization of the expressed VDACs by LC-MS/MS analysis, serious structural modifications of VDACs causing changes in their migration in SDS-polyacrylamide gels were not detected. Next, immunoreactivities of the raised antibodies toward these bacterially expressed VDAC isoforms were evaluated. Trials to prepare specific antibodies against the three individual VDAC isoforms were not successful except in the case of VDAC1. However, using a synthetic peptide corresponding to the highly conserved region among the three VDACs, we were successful in preparing an antibody showing essentially equal immunoreactivities toward all three VDACs. When mitochondrial outer membrane proteins of various rat tissues were subjected to 2-dimensional electrophoresis followed by immunoblotting with this antibody, six immunoreactive protein spots were detected. These spots were characterized by LC-MS/MS analysis, and the signal intensities among the spots were compared. As a result, the signal intensity of the spot representing VDAC1 was the highest, and thus, VDAC1 was concluded to be the most abundantly expressed of the three VDAC isoforms in mammalian mitochondria. (Keyword) Amino Acid Sequence / Animals / Base Sequence / Chromatography, Liquid / DNA Primers / Electrophoresis, Gel, Two-Dimensional / Electrophoresis, Polyacrylamide Gel / Immunoblotting / Mass Spectrometry / Mitochondrial Proteins / Molecular Sequence Data / Protein Isoforms / Rats / Sequence Analysis, DNA / Voltage-Dependent Anion Channel 1 (Link to Publication Site) ● Publication site (DOI): 10.1021/pr060291w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17137335 ● Search Scopus @ Elsevier (PMID): 17137335 ● Search Scopus @ Elsevier (DOI): 10.1021/pr060291w (DOI: 10.1021/pr060291w, PubMed: 17137335)
66.	(名) Suryono, Jun-ichi Kido, Noriko Hayashi, Masatoshi Kataoka, Yasuo Shinohara and Toshihiko Nagata : Norepinephrine Stimulates Calprotectin Expression in Human Monocytic Cells, Journal of Periodontal Research, Vol.41, No.3, 159-164, 2006. (Summary) Calprotectin is composed of two proteins, S100A8 and S100A9, which are S100 family members, and is detected in gingival crevicular fluid and gingival tissue with inflammation. The release and production of calprotectin are regulated by lipopolysaccharides of periodontopathic bacteria and cytokines. Emotional or psychological stress, a risk factor of periodontal disease, is transmitted by stress modulators including norepinephrine and cortisol. The aim of the present study was to investigate the effect of stress on calprotectin expression using norepinephrine and cortisol. U-937 cells, a human monocytic cell line, were incubated with norepinephrine in the presence or absence of beta- or alpha-adrenergic receptor antagonists, or with cortisol. The expression of S100A8/S100A9 mRNAs was examined by northern blotting and the amount of calprotectin was measured by enzyme-linked immunosorbent assay (ELISA). The DNA binding activity of C/EBPalpha (CCAAT enhancing binding protein), a transcription factor, was examined by electrophoretic mobility shift assay. Norepinephrine stimulated the expression of S100A8/S100A9 mRNAs via beta-adrenergic receptors in U-937 cells and significantly increased calprotectin production to about 3.6-fold that of the control. However, cortisol had no effect on calprotectin expression at the mRNA and protein levels. Norepinephrine elevated C/EBPalpha DNA binding activity, but cortisol did not increase the activity. Norepinephrine, a stress modulator, stimulated calprotectin expression in human monocytic cells. Calprotectin expression may be regulated by stress in addition to inflammatory factors. (Keyword) Calprotectin / Norepinephrine / Cortisol / stress (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2005.00845.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16677282 ● Search Scopus @ Elsevier (PMID): 16677282 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2005.00845.x (DOI: 10.1111/j.1600-0765.2005.00845.x, PubMed: 16677282)
67.	Chie Wada -Mihara, Masatoshi Kataoka, Hiroyuki Seto, Noriko Hayashi, Jun-ichi Kido, Yasuo Shinohara and Toshihiko Nagata : High-turnover osteoporosis is induced by cyclosporin A in rats., Journal of Bone and Mineral Metabolism, Vol.24, No.3, 199-205, 2006. (Summary) Cyclosporin A (CsA) is used widely as an immunosuppressive agent, but it induces osteoporosis as a prominent side effect. To elucidate the mechanisms involved in CsA-induced osteoporosis, the effects of CsA on bone metabolism were investigated in a rat experimental model. Fifteen-day-old rats were fed a powdered diet containing or lacking CsA for 8-30 days. Analysis was performed by micro-computed tomography (muCT) and light microscopy to examine histomorphometric changes in rat tibiae on days 8, 16, and 30. Plasma parathyroid hormone (PTH) and osteocalcin (OCN) levels were determined by enzyme-linked immunosorbent assay (ELISA) on days 8, 16, and 30. The expression of OCN, osteopontin (OPN), and cathepsin K mRNAs in tibial bone marrow was examined by Northern blot analysis on days 8 and 16. Although no significant differences were observed in tibial length during the experimental periods, or in histomorphometric parameters on day 8, an apparent decrease in bone volume was observed in the CsA-treated group after day 16. Histologic analysis showed that the number of osteoblasts and osteoclasts on the surface of trabecular bone in the CsA-treated group had increased significantly on day 16. Plasma PTH and OCN levels in CsA-treated rats were significantly higher than those in control animals on day 8. Northern blot analysis revealed that the CsA-treated group showed an increase in the expression of OCN, OPN, and cathepsin K mRNAs on day 8 compared with the controls. These findings suggest that bone resorption in CsA-treated rats is induced by high-turnover osteoporosis and that bone remodeling activity may be activated by PTH. (Keyword) Animals / Bone Remodeling / Bone Resorption / Cyclosporine / Gingival Overgrowth / Immunosuppressive Agents / Male / Osteocalcin / Osteogenesis / Osteoporosis / Parathyroid Hormone / Rats / Rats, Inbred F344 / Tibia / Tomography, X-Ray Computed (Link to Publication Site) ● Publication site (DOI): 10.1007/s00774-005-0672-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16622732 ● Search Scopus @ Elsevier (PMID): 16622732 ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-005-0672-x (DOI: 10.1007/s00774-005-0672-x, PubMed: 16622732)
68.	Mari Ogino, Jun-ichi Kido, Mika Bando, Noriko Hayashi, Chie Wada -Mihara, Toshihiko Nagata, Fusanori Nishimura, Y. Soga, Shogo Takashiba, T. Kubota, M. Itagaki, Yasuko Shimada, H. Tai, Hiromasa Yoshie, Naoshi Yamazaki, Yasuo Shinohara and Masatoshi Kataoka : Alpha 2 integrin +807 polymorphism in drug-induced gingival overgrowth, Journal of Dental Research, Vol.84, No.12, 1183-1186, 2005. (Summary) Alpha2 integrin on fibroblasts is reported to play an important role in the induction of drug-induced gingival overgrowth, which is characterized by excessive accumulation of type I collagen in gingival connective tissue. Silent polymorphism 807 T/C within the alpha2 integrin gene is associated with high/low alpha2 integrin expression. The aim of this study was to test the hypothesis that expression of alpha2 integrin 807 T/C polymorphism correlates with drug-induced gingival overgrowth. A case-control study comparing 136 subjects taking calcium channel blockers (72 with vs. 64 without drug-induced gingival overgrowth) demonstrated that the frequency of the +807 C allele was significantly higher in the case group than in the controls (odds ratio, 3.61; 95% confidence interval, 2.14 - 6.10; P < 0.05). The present findings suggest that the alpha2 +807 C allele is one of the genetic risk factors for drug-induced gingival overgrowth. (Keyword) drug-induced gingival overgrowth / Alpha 2 integrin / SNP / collagen phagocytosis (Link to Publication Site) ● Publication site (DOI): 10.1177/154405910508401217 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16304451 ● Search Scopus @ Elsevier (PMID): 16304451 ● Search Scopus @ Elsevier (DOI): 10.1177/154405910508401217 (DOI: 10.1177/154405910508401217, PubMed: 16304451)
69.	Hiroyuki Seto, 和田智恵, Masumi Horibe and Toshihiko Nagata : ラット実験的歯周炎におけるアレンドロネートの歯槽骨吸収抑制作用, 日本歯周病学会誌, Vol.47, No.3, 153-160, 2005.
70.	Jun-ichi Kido, Noriko Hayashi, Masatoshi Kataoka and Toshihiko Nagata : Calprotectin expression in human monocytes: induction by porphyromonas gingivalis lipopolysaccharide, tumor necrosis factor-alpha, and interleukin-1beta, Journal of Periodontology, Vol.76, No.3, 437-442, 2005. (Summary) Calprotectin is a major cytosolic protein of monocytes and granulocytes. It is increased in inflammatory tissues and is detected at high levels in the gingival crevicular fluid (GCF) of periodontitis patients. We previously reported that lipopolysaccharide of Porphyromonas gingivalis (P-LPS) and cytokines induced the release of calprotectin from monocytes isolated from human peripheral blood. The mechanisms of calprotectin expression and presence of its regulation factors in periodontal disease are unknown. On the other hand, P-LPS and cytokines are significant etiologic factors in the initiation and progression of periodontal diseases. In this study, we investigated the expression and production of calprotectin from human monocytes by examining the effects of lipopolysaccharide of P-LPS, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). Monocytes were isolated from the peripheral blood of healthy donors and cultured in the presence or absence of P-LPS, TNF-alpha, or IL-1beta. The expressions of calprotectin mRNAs (MRP8 and MRP14) were detected by Northern blotting. The contents of calprotectin in the cells and medium fractions were determined by enzyme-linked immunosorbent assay (ELISA). The DNA binding activity of C/EBPalpha, a transcription factor of MRP14, was assessed by electrophoretic mobility shift DNA-binding assay (EMSA). P-LPS, TNF-alpha, and IL-1beta induced MRP8/14 mRNAs and calprotectin production in monocytes. These factors also induced DNA CEBPalpha binding activity in monocytes. P-LPS increased MRP14 mRNA expression in monocytes to the maximum level, about two times the control level after 24 hours treatment, but did not enhance the basal level of MRP8. When the effects of TNF-alpha and IL-1beta on those mRNAs were investigated, both MRP8 and MRP14 significantly increased to about 2- and 2.5-fold the control level, respectively. Increases of MRP8/14 mRNA expression were followed by their protein production at about 2-fold the basal amount. DNA binding activity of C/EBPalpha was increased in P-LPS, TNF-alpha, and IL-1beta-treated monocytes. These results demonstrate that P-LPS, TNF-alpha, and IL-1beta induce calprotectin production from human monocytes and that this production is associated with the activation of DNA C/EBPalpha binding complex. (Keyword) Calprotectin / interleukin-1beta / lipopolysaccharide / monocytes / porphyromonas gingivalis / tumor necrosis factor (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2005.76.3.437 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15857079 ● Search Scopus @ Elsevier (PMID): 15857079 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2005.76.3.437 (DOI: 10.1902/jop.2005.76.3.437, PubMed: 15857079)
71.	Toshiko Ohtake, Ryutaro Takahasi, Yasuhiko Ohyabu, Noriko Minamisono, Tsukasa Kuzuyama, Keiji Oishi and Toshihiko Nagata : A Study on Community Periodontal Index of Treatment Needs (CPITN) in Type 2 Diabetic Patients, Journal of the Japanese Association of Periodontology, Vol.47, No.1, 28-35, 2005. (Summary) Diabetic patients tend to suffer from severe periodontitls, which is aggravated in poorly controlled longterm diabetes. We calculated the community periodontal index of treatment needs (CPITN) and the number of missing teeth in 49 type 2 diabetic patients (DM group) and 30 nondiabetic patients (controls) . The DM group was further divided into 4 groups by HbA<1C>^^ score (DM1:<5.7, DM2:5.8-6.4,DM3:6.5-7.9,DM4:>8.O), and CPITN and the number of teeth lost were measured in each group. The CPITN for all diabetic patients ranged from I to 4, but no O, indicating required oral hygiene instruction. (Keyword) periodontal disease / type 2 diabetes mellitus / CPITN (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.47.28 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204413067776 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.47.28 (DOI: 10.2329/perio.47.28, CiNii: 1390001204413067776)
72.	Masumi Horibe, Takamasa Sawa, Masatoshi Kataoka, Jun-ichi Kido and Toshihiko Nagata : Regulation of tenascin expression in cultured rat dental pulp cells, Odontology, Vol.92, No.1, 22-26, 2004. (Summary) Tenascin (TN) is a glycoprotein of extracellular matrix abundantly present in embryonic mesenchymal tissues. Transforming growth factor-beta1 (TGF-beta1), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), hepatocyte growth factor (HGF), and retinoic acid (RA) are important regulators of dentinogenesis. Dental pulp cells have the capacity to differentiate into odontoblast-like cells. In this study, we investigated the effects of growth factors on TN expression and adhesive function using rat clonal dental pulp cells, RPC-C2A. Analyses of reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting revealed that RPC-C2A cells expressed TN molecules and that TGF-beta1, HGF, and RA increased expression of TN at the mRNA and protein level, while bFGF and EGF showed a weak effect. An adhesion assay revealed that treatment with TGF-beta1, HGF, and RA induced a marked reduction of cell attachment to fibronectin (FN)-coated surfaces, whereas there was no change with bFGF and EGF. Functional blocking of growth factor-stimulated TN protein by pretreating cells with anti-TN antibodies restored cell attachment to control levels. These findings suggest that TGF-beta1, HGF, and RA may regulate pulpal cell adhesion to FN-coated surfaces and that this effect is mediated by TN. (Keyword) Tenascin / dental pulp / growth factor / differentiation / Cell adhesion (Link to Publication Site) ● Publication site (DOI): 10.1007/s10266-004-0038-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15490301 ● Search Scopus @ Elsevier (PMID): 15490301 ● Search Scopus @ Elsevier (DOI): 10.1007/s10266-004-0038-1 (DOI: 10.1007/s10266-004-0038-1, PubMed: 15490301)
73.	Hideki Azuma, Jun-ichi Kido, Dai Ikedo, Masatoshi Kataoka and Toshihiko Nagata : Substance P Enhances the Inhibition of Osteoblastic Cell Differentiation Induced by Lipopolysaccharide From Porphyromonas gingivalis, Journal of Periodontology, Vol.75, No.7, 974-981, 2004. (Summary) Substance P (SP) is a multifunctional neuropeptide that transmits pain signals, regulates the immune system, and may modulate emotional stress. SP stimulates bone resorption activity of osteoclasts, and SP level in gingival crevicular fluid is correlated with the degree of periodontal inflammation. However, the exact roles of SP in bone metabolism and periodontal diseases are poorly understood. To elucidate the effect of stress on bone metabolism, we investigated the effect of SP on osteoblastic cell differentiation in the presence of lipopolysaccharide from Porphyromonas gingivalis (P-LPS). The primary osteoblastic cells were isolated from fetal rat calvaria (RC) and cultured with SP, P-LPS, and an SP antagonist (SPa). The effects of SP on bone nodule (BN), alkaline phosphatase (ALPase) activity, mRNA expressions of SP receptor, bone matrix proteins, and Cbfa 1 were investigated. SP stimulated the expression of SP receptor mRNA in RC cells and enhanced its expression in the presence of P-LPS (50 ng/ml). SP inhibited BN formation and ALPase activity in a dose-dependent manner (10(-7) to 10(-5) M) and further suppressed mRNA expression of bone sialoprotein, osteopontin, and osteocalcin but not of type I collagen mRNA. The inhibitory effects were enhanced in the presence of P-LPS and blocked by Spantide III. Furthermore, the expression of Cbfa 1 mRNA was also markedly suppressed in the presence of SP and P-LPS. These findings suggest that SP inhibits osteoblastic cell differentiation and may be related to bone metabolism in periodontal diseases under conditions of stress. (Keyword) Bone metabolism / cell differentiation / gingival crevicular fluid / lipopolysaccharides / osteoblasts / osteoclasts / periodontal diseases / Porphyromonas gingivalis / stress/adverse effects (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2004.75.7.974 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15341355 ● Search Scopus @ Elsevier (PMID): 15341355 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2004.75.7.974 (DOI: 10.1902/jop.2004.75.7.974, PubMed: 15341355)
74.	Jun-ichi Kido, R. Kido, (名) Suryono, Masatoshi Kataoka, M. K. Fagerhol and Toshihiko Nagata : Induction of calprotectin release by Porphyromonasgingivalis lipopolysaccharide in human neutrophils, Oral Microbiology and Immunology, Vol.19, No.3, 182-187, 2004. (Summary) Calprotectin, a major cytosolic protein of leukocytes, is detected in neutrophils, monocytes/macrophages, and epithelial cells. This protein is known to be a marker for several inflammatory diseases and is detected in inflammatory gingival tissue with periodontal disease. Recently, we found that the calprotectin level in gingival crevicular fluid from periodontitis patients was significantly higher than that of healthy subjects. However, the regulation of calprotectin in periodontal disease is unclear. In the present study, we investigated the effect of lipopolysaccharides of periodontopathic bacteria on calprotectin release from human neutrophils. Neutrophils from healthy donors were treated with lipopolysaccharides from Porphyromonas gingivalis (P-LPS), Actinobacillus actinomycetemcomitans, Prevotella intermedia, Fusobacterium nucleatum, and Escherichia coli. Calprotectin of neutrophil was identified by immunoblotting and calprotectin amount was determined by ELISA. Two subunits (10 and 14 kDa) of calprotectin were observed in the cell and medium fractions from neutrophils. P-LPS increased calprotectin release from seven to 16 times the control level after 30 min and its effect appeared in a dose-dependent manner (10-1000 ng/ml). Lipopolysaccharides from A. actinomycetemcomitans, P. intermedia, F. nucleatum, and E. coli also induced calprotectin release from neutrophils. These results suggest that lipopolysaccharides from periodontopathic bacteria induce calprotectin release from human neutrophils. (Keyword) calprotectin / lipopolysaccharide / neutrophil / periodontopathic bacteria (Link to Publication Site) ● Publication site (DOI): 10.1111/j.0902-0055.2004.00139.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15107070 ● Search Scopus @ Elsevier (PMID): 15107070 ● Search Scopus @ Elsevier (DOI): 10.1111/j.0902-0055.2004.00139.x (DOI: 10.1111/j.0902-0055.2004.00139.x, PubMed: 15107070)
75.	Masami Ninomiya, Nobuyuki Kamata, Masaru Nagayama and Toshihiko Nagata : エナメル基質タンパクの歯の移植への応用, the Quintessence, Vol.23, No.7, 89-96, 2004.
76.	(名) Suryono, Jun-ichi Kido, Noriko Hayashi, Masatoshi Kataoka and Toshihiko Nagata : Effect of Porphyromonas gingivalis lipopolysaccharide, tumor necrosis factor-alpha, and interleukin-1beta on calprotectin release in human monocytes, Journal of Periodontology, Vol.74, No.12, 1719-1724, 2003. (Summary) Calprotectin is a major cytosolic protein of monocytes, granulocytes, and epithelial cells. It is known that calprotectin is released in inflammatory tissues and detected in gingival crevicular fluid (GCF) of periodontitis patients at high levels. The origin of calprotectin in GCF and its regulation in periodontal disease are unknown. In this study, we investigated the distribution of calprotectin in gingival tissue with inflammation and the induction of calprotectin release from human monocytes by lipopolysaccharide of Porphyromonas gingivalis (P-LPS), tumor necrosis factor-alpha (TNF-alpha), or interleukin-1beta (IL-1beta). Gingival tissues were obtained from a healthy donor and a periodontitis patient and calprotectin in gingival tissues was examined by immunohistochemical staining. Monocytes were isolated from the peripheral blood of healthy donors and cultured with P-LPS, TNF-alpha or IL-1beta for 30 minutes to 4 hours. The content of calprotectin in the cell and medium fractions was determined by enzyme-linked immunosorbent assay (ELISA). Calprotectin was markedly detected at the epithelial and adjacent connective tissue with many inflammatory cells in the gingival tissue from the periodontitis patient. P-LPS increased calprotectin release from monocytes to the maximum level after 30 minutes of treatment and its level was elevated to about 2- to 3-fold of the control level in a dose-dependent manner (1 to 1,000 ng/ml). When the effect of TNF-alpha and IL-1beta on calprotectin release was investigated, calprotectin release significantly increased to about 2.2- and 1.5-fold that of the control level, respectively. These results demonstrate that calprotectin release from monocytes is induced by P-LPS, TNF-alpha, and IL-1beta, which in turn, cause and aggravate periodontal disease. (Keyword) calprotectin / gingival crevicular fluid/analysis / interleukin-1 / monocytes physiopathology / periodontitis/physiopatholoogy / Porphyromonas gingivalis / tumor necrosis factor (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2003.74.12.1719 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14974811 ● Search Scopus @ Elsevier (PMID): 14974811 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2003.74.12.1719 (DOI: 10.1902/jop.2003.74.12.1719, PubMed: 14974811)
77.	Jun-ichi Kido, Reiko Kido, (名) Suryono, Masatoshi Kataoka, Magne K. Fagerhol and Toshihiko Nagata : Calprotectin release from human neutrophils is induced by Porphyromonas gingivalis lipopolysaccharide via the CD-14-Toll-like receptor-nuclear factor kB pathway, Journal of Periodontal Research, Vol.38, No.6, 557-563, 2003. (Summary) Calprotectin is a cytosolic protein with antibacterial action in leukocytes and its level increases in some inflammatory diseases, including periodontal diseases, rheumatoid arthritis and ulcerative colitis. Recently, we found that the lipopolysaccharide of Porphyromonas gingivalis (P-LPS) induced calprotectin release from human neutrophils. P-LPS, a major virulence factor of periodontal pathogens, is known to induce the production and release of inflammatory cytokines through CD14, Toll-like receptor (TLR) and nuclear factor kappaB (NF-kappaB). In the present study, we investigated whether calprotectin release by P-LPS is induced via the CD14-TLR-NF-kappaB pathway and the cellular mechanism of calprotectin release in human neutrophils. Human neutrophils were isolated from the peripheral blood of healthy donors and pre-incubated in medium containing antibodies against CD14, TLR2 and TLR4, or several inhibitors of NF-kappaB, microtubules and microfilaments, and then incubated with P-LPS. The calprotectin amount in the culture medium was determined using ELISA, and the nuclear extracts from cells were used for the examination of NF-kappaB binding activity using electrophoretic mobility shift assays. P-LPS increased calprotectin release from neutrophils and its induction was inhibited by anti-CD14 and anti-TLR2 antibodies, but not by two anti-TLR4 antibodies. NF-kappaB inhibitors suppressed P-LPS-induced NF-kappaB binding activity and calprotectin release. The inhibitors of microtubule and microfilament polymerization significantly decreased P-LPS-induced calprotectin release. These results suggest that calprotectin release is induced by P-LPS via the CD14-TLR2-NF-kappaB signal pathway in human neutrophils and may be dependent on microtubule and microfilament systems. (Keyword) calprotectin / Porphyromonas gingivalis / lipopolysaccharide (Link to Publication Site) ● Publication site (DOI): 10.1034/j.1600-0765.2003.00691.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14632917 ● Search Scopus @ Elsevier (PMID): 14632917 ● Search Scopus @ Elsevier (DOI): 10.1034/j.1600-0765.2003.00691.x (DOI: 10.1034/j.1600-0765.2003.00691.x, PubMed: 14632917)
78.	Masatoshi Kataoka, Hiroyuki Seto, Chie Wada, Jun-ichi Kido and Toshihiko Nagata : Decreased expression of α2 integrin in fibroblasts isolated from cyclosporin A- induced gingival overgrowth in rats, Journal of Periodontal Research, Vol.38, No.5, 533-537, 2003. (Summary) Cyclosporin A (CsA), an immunosuppressive agent, induces fibrous gingival overgrowth through reduction of collagen phagocytosis by fibroblasts. Distinct receptors are involved in the binding of collagen to fibroblasts in collagen phagocytosis, and alpha2beta1 integrin serves as a specific receptor for type I collagen on fibroblasts. To elucidate the role of alpha2beta1 integrin in CsA-induced gingival overgrowth, we investigated collagen phagocytosis and alpha2beta1 integrin expression in rat gingival fibroblasts. Fibroblats were isolated from gingiva of rats fed a powdered diet containing or lacking CsA for 30 d. Flow cytometric analysis were performed to measure the collagen phagocytosis and the alpha2 integrin expression in fibroblasts. Furthermore, total RNAs were isolated from fibroblasts, and the reverse transcriptase-polymerase chain reaction was employed to investigate the mRNA levels of alpha2 integrin. In vitro collagen phagocytosis assay revealed that CsA-treated and control fibroblasts contained a mean of 13.5% and 36.1% phagocytic cells, respectively. CsA-treated fibroblasts had 28% lower expression of alpha2 integrin than that of control. and mRNA expression of alpha2 integrin in CsA-treated fibroblasts was apparently lower than in the controls, but the mRNA expression of beta1 integrin was not affected. These findings suggest that one etiological factor of gingival overgrowth may be inhibition of collagen phagocytosis by reducing alpha2 integrin expression in gingival fibroblasts. (Keyword) α2 integrin / collagen phagocytosis / cyclosporin A / gingival overgrowth (Link to Publication Site) ● Publication site (DOI): 10.1034/j.1600-0765.2003.00692.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12941079 ● Search Scopus @ Elsevier (PMID): 12941079 ● Search Scopus @ Elsevier (DOI): 10.1034/j.1600-0765.2003.00692.x (DOI: 10.1034/j.1600-0765.2003.00692.x, PubMed: 12941079)
79.	Masahiro Asano, Yoji Asahara, Akinori Kirino, Mika Oishi, Noriko Akimaru, Hideki Hama, (名) Suryono, Akemi Shionoya, Jun-ichi Kido and Toshihiko Nagata : Case Report of an Early-onset Periodontitis Patient Showing Self-Arrest of Alveolar Bone Loss after Puberty, Journal of the Japanese Association of Periodontology, Vol.45, No.3, 279-288, 2003. (Keyword) early-onset periodontitis / disease progression / self-arrest
80.	Kaya Yoshida, Hirohiko Okamura, Hiroyuki Morimoto, Toshihiko Nagata and Tatsuji Haneji : Okadaic acid stimulates the expression of receptor activator of nuclear factor-kappa B ligand RANKL in mouse osteoblastic cells, Biomedical Research (India), Vol.14, No.2, 126-132, 2003. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573950399828180096 ● Summary page in Scopus @ Elsevier: 2-s2.0-0344099417 (CiNii: 1573950399828180096, Elsevier: Scopus)
81.	Masami Ninomiya, Akane Takemura and Toshihiko Nagata : MMP 阻害剤の歯槽骨吸収抑制作用, the Quintessence, Vol.22, No.9, 41-47, 2003. (Keyword) マトリックスメタロプロテアーゼ(MMP) / MMPインヒビター / 歯周病
82.	Yasuki Shimizu, Masatoshi Kataoka, Hiroyuki Seto, Jun-ichi Kido and Toshihiko Nagata : Nifedipine induces gingival epithelial hyperplasia in rats through inhibition of apoptosis, Journal of Periodontology, Vol.73, No.8, 861-867, 2002. (Summary) Nifedipine is used as a long-acting vasodilator; one of its side effects is gingival overgrowth, characterized by an accumulation of collagenous components within the gingival connective tissue and epithelial hyperplasia with elongated, branched rete pegs penetrating into the connective tissue. We investigated the effect of nifedipine on apoptosis of gingival keratinocytes of rats to elucidate the mechanism of nifedipine-induced gingival epithelial hyperplasia. Twenty-day-old rats were fed a powdered diet containing or lacking nifedipine for 8 to 30 days. The mandibular gingiva and palatal mucosa were removed on days 8, 15, or 30, and epithelial thickness was examined by light microscopy. In situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay was used to examine apoptosis of keratinocytes in the epithelium. In addition, we examined the effects of nifedipine on proliferation of keratinocytes and epithelial cell life on day 8 by 5-bromo-2'-deoxyuridine (BrdU) staining. Microscopic examination showed gingival epithelial hyperplasia in nifedipine-treated rats after day 15. Apoptosis of gingival keratinocytes was seen to be inhibited in nifedipine-treated rats on day 8 and 15. Also, nifedipine did not induce an increase of keratinocyte proliferation activity in terms of the number of cells showing positive staining with BrdU. Prolongation of cell life by nifedipine was observed on day 8 in gingival epithelium through a delay of upward cell movement compared to controls. However, epithelial hyperplasia was not detected in palatal mucosa, and there were no significant differences in apoptotic rates of keratinocytes and cell life between nifedipine-treated rats and control rats. These results suggest that nifedipine induces epithelial hyperplasia in gingival overgrowth not by an increase in keratinocyte proliferation, but by prolongation of cell life through reduction of apoptosis before epithelial hyperplasia is detectable. (Keyword) animal studies / nifedipine/adverse effects / gingibal hyperplasia/physiology / cell survival / apoptosis / gingival overgrowth (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2002.73.8.861 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12211494 ● Search Scopus @ Elsevier (PMID): 12211494 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2002.73.8.861 (DOI: 10.1902/jop.2002.73.8.861, PubMed: 12211494)
83.	Nishikawa Hiroyuki, Akemichi Ueno, Taigo Horiguchi, Kikuji Yamashita, Inoue Hideo and Toshihiko Nagata : Effects of TGF-beta1 on Extracellular Matrix Formation in Rat Clonal Dental Pulp Cells, Dentistry in Japan, Vol.38, 44-50, 2002. (Keyword) TGF-beta1 / RPC-C2A cell / Dental pulp cell
84.	Masami Ninomiya, Nobuyuki Kamata, Ryoichi Fujimoto, Tomoko Ishimoto, (名) Suryono, Jun-ichi Kido, Masaru Nagayama and Toshihiko Nagata : Application of Enamel Matrix Derivative in Autotransplantation of an Impacted Maxillary Premolar, Journal of Periodontology, Vol.73, No.3, 346-351, 2002. (Summary) The success of tooth transplantation or replantation depends on the viability of periodontal ligament in the planted tooth. Mechanical injury to periodontal tissues frequently results in dental root resorption and dental ankylosis, which leads to the failure of transplantation or replantation. Enamel matrix derivative (EMD) has been recently used to induce periodontal regeneration. In this report, we show a clinical case of EMD application in the transplantation of an inversely impacted and immature tooth. An impacted second premolar was found in the right maxilla of a 16 year-old girl. The tooth was inversely impacted and the dental root was incomplete. When transplantation was carried out, EMD was applied to the periodontal tissues of the extracted premolar. The tooth was fixed at the correct position and the clinical condition was followed for evaluation for 6 months. Radiographs after 3 months exhibited new bone formation surrounding the transplanted tooth. After 6 months, considerable growth of dental root was evident, periodontal ligament-like radiolucency appeared, the vital reaction of the planted tooth was detected, and there were no signs of root resorption or ankylosis. Short-term results from this case indicate that EMD application was effective in the transplantation of an inversely impacted and immature tooth and that EMD might contribute to the growth of dental root and to the prevention of ankylosis. (Keyword) enamel matrix derivative / autotransplantation / periodontal membrane (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2002.73.3.346 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11922266 ● Search Scopus @ Elsevier (PMID): 11922266 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2002.73.3.346 (DOI: 10.1902/jop.2002.73.3.346, PubMed: 11922266)
85.	Teruo Nakamura, (名) Suryono, Jun-ichi Kido and Toshihiko Nagata : Quantitative Analyses of Propeptide of Type Procollagen and Osteocalcin in Gingival Crevicular Fluid of Periodontal Disease Patients, Journal of the Japanese Association of Periodontology, Vol.44, No.1, 73-81, 2002. (Summary) Biochemical markers in gingival crevicular fluid (GCF) have been studied to precisely and objectively diagnose periodontal disease. Carboxy terminal propeptide of type I procollagen (P I CP) and osteocalcin (OCN) are bone-related proteins produced by osteoblasts that are useful clinical indicators of metabolic bone diseases such as osteoporosis and hyperparathyroidism. To determine bone-related markers in GCF, we studied the presence of P I CP and OCN in GCF from periodontitis patients using immunoen-zymatic kits and the relationship between P I CP/OCN amounts and clinical parameters involving gingival index (GD, probing depth (PD) , and bleeding on probing (BOP). GCF samples were collected with paperstrips from 70 diseased sites (PD>4 mm) in 70 periodontitis patients and from 30 healthy sites (PD< 3 mm) in 30 healthy volunteers. A mean of 1.04 ng/site (0.91 ng/μl) P I CP was found at diseased sites and a mean of O . 17 ng/site (0.38 nglpl) at healthy sites, showing a 6 . 1-fold amount of P 1 CP at diseased sites. A mean of 56 .3 pg/site (47.6 pg/μl) OCN was found at diseased sites and a mean of 38.8 pg/site (1203.9 pg/μl) at healthy sites, showing a 1 .5-fold amount of OCN at diseased, sites. Both P 1 CP and OCN in GCF correlated positively with GI and PD, especially P 1 CP, P 1 CP greatly increased at BOP-positive sites (5.5-fold) , suggesting that P I CP may reflect disease activity in alveolar bone metabolism. These results indicate that P 1 C,P and OCN are present in GCF and that these molecules may be useful as a bone-related marker in periodontitis. P 1 CP may prove to be an especially potent marker for bone turnover in periodontitis. J Jpn Soc Periodontol, 44 : 73-81, 2002. (Keyword) gingival crevicular fluid / carboxy terminal propeptide of type procollagen / osteocalcin / periodontitis (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.44.73 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679388467456 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.44.73 (DOI: 10.2329/perio.44.73, CiNii: 1390282679388467456)
86.	Nobuyuki Kamata, Masami Ninomiya, Tomoko Azuma, Ryoichi Fujimoto, Mayumi Tomonari, Toshihiko Nagata and Masaru Nagayama : Autotransplantation of Impacted Teeth and Wisdom Teeth, Shikoku Dental Research, Vol.15, No.1, 205-213, 2002. (Keyword) 移植 / 智歯 / 埋伏歯
87.	Jun Tada, Toshimitsu Iwata and Toshihiko Nagata : Visiting service of oral health care for patients suffering from systemic diseases, Shikoku Dental Research, Vol.15, No.1, 215-218, 2002. (Keyword) 歯科訪問診療 / 口腔衛生指導 / QOL
88.	Jun-ichi Kido, Teruo Nakamura, Yoji Asahara, Takamasa Sawa, Kenjiro Kohri and Toshihiko Nagata : Osteopontin in gingival crevicular fluid, Journal of Periodontal Research, Vol.36, No.5, 328-333, 2001. (Summary) Osteopontin (OPN) is a major glycosylated phosphoprotein in bone matrix and is produced by several cells including osteoblasts, osteoclasts and macrophages. OPN levels increase in active sites of bone metabolism. Recently, several bone-related proteins were identified in gingival crevicular fluid (GCF) to seek markers of alveolar bone resorption in periodontal disease. In this study, we investigated the existence of OPN in GCF and the correlation between OPN level in GCF and probing depth (PD) of sampling sites in 98 periodontitis patients and 35 healthy subjects. An immunoblotting analysis using 10% polyacrylamide gel showed that two forms of OPN with molecular masses of 54 and 66 kDa and several degraded fragments were detected in most GCF samples from diseased sites (PD > 4 mm). In GCF samples from healthy sites (PD < or = 3 mm), only one form (54 kDa) was observed, but any degraded fragments were not detected. When OPN amounts in GCF samples were determined by ELISA, a weak. but significant correlation was observed between OPN amount in GCF and PD (r=0.32, p=0.0013). These results demonstrate that OPN exists in GCF and that OPN level in GCF increases with the progression of periodontal disease. (Keyword) osteopontin / gingival crevicular fluid / periodontal disease (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11585121 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035491642 (PubMed: 11585121, Elsevier: Scopus)
89.	Masatoshi Kataoka, Yasuki Shimizu, Kenji Kunikiyo, Yoji Asahara, Hideki Azuma, Takamasa Sawa, Jun-ichi Kido and Toshihiko Nagata : Nifedipine induces gingival overgrowth in rats through a reduction in collagen phagocytosis by gingival fibroblasts, Journal of Periodontology, Vol.72, No.8, 1078-1083, 2001. (Summary) Nifedipine is used as a long-acting vasodilator, and a primary side effect is the induction of gingival overgrowth, which is characterized by an accumulation of collagenous components within the gingival connective tissue. To elucidate the mechanisms of nifedipine-induced gingival overgrowth, we investigated the effect of nifedipine on Type I collagen metabolism in the gingiva of rats. Twenty-day-old rats were fed a powdered diet containing or lacking nifedipine for 3 to 55 days. Immunohistochemical analysis with anti-Type I collagen antibody was employed to examine the density of Type I collagen in the gingival connective tissue. Total RNAs were isolated from mandibular molar gingiva on days 0, 3, 15, 30, and 55, and reverse transcription polymerase chain reaction was performed to investigate the mRNA levels of Type I collagen. In addition, we performed a flow cytometric analysis with collagen-coated latex beads and cultured fibroblasts derived from rat gingiva to measure collagen phagocytosis. Immunohistochemical analysis revealed that Type I collagen was more prevalent in the connective tissue of nifedipine-treated gingiva than in controls on day 55. In the nifedipine-treated group, the expression of Type I collagen mRNA gradually decreased to 1.5% on day 55 compared to day 0. In the control group, Type I collagen mRNA also decreased to 32%; however, mRNA expression was significantly lower in the nifedipine-treated group than in the controls. When the rate of phagocytic cells derived from nifedipine-treated gingiva and controls was represented as the mean +/- SE of the percentage from 3 different experiments, the values were as follows: on day 15, 13.5 +/- 2.1% and 15.0 +/- 1.5%; on day 30, 12.2 +/- 4.3% and 34.5 +/- 6.7% in the nifedipine-treated and the control group, respectively, indicating that phagocytic cells were considerably fewer in the nifedipine-treated gingiva on day 30. This finding demonstrates that the decrease in phagocytosis caused by nifedipine appeared before the detection of severe macroscopic gingival overgrowth. These findings suggest that the decrease in collagen degradation due to lower phagocytosis is closely associated with the increase in Type I collagen accumulation in nifedipine-treated rat gingiva. (Keyword) animal studies / collagen/metabolism / gingival hyperplasia / etiology / nifedipine/adverse effects (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2001.72.8.1078 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11525441 ● Search Scopus @ Elsevier (PMID): 11525441 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2001.72.8.1078 (DOI: 10.1902/jop.2001.72.8.1078, PubMed: 11525441)
90.	Masami Ninomiya, Mika Oishi, Jun-ichi Kido, Yasuyoshi Ohsaki and Toshihiko Nagata : Immunohistochemical Localization of Osteopontin in human Pulp Stones., Journal of Endodontics, Vol.27, No.4, 269-272, 2001. (Summary) The organic matrix component of human pulp stones was investigated by immunohistochemistry. Two pulp stones were extracted from the upper molar teeth of two patients suffering from irreversible pulpitis. Both were formed in the center of the pulp cavity and located apart from the dentin walls. After demineralization, serial sections of the stones were prepared and subjected to immunohistochemical procedures using specific antibodies to type I collagen and noncollagenous proteins (osteopontin, osteonectin, and osteocalcin), which are reported to be involved in calcified matrix formation. Type I collagen was localized evenly in the stones, indicating that it is a major matrix component of pulp stones. Strong immunostaining of osteopontin appeared in the peripheral area of the stones, whereas osteonectin and osteocalcin were not detected. We previously reported that dental pulp cells produced osteopontin in vitro. Osteopontin has been commonly found in other pathological calcification, such as urinary stones, atherosclerotic plaques, and dental calculus. Taken together, the present findings suggest that osteopontin produced by dental pulp cells is possibly associated with calcification of the pulp stone matrix. (Keyword) osteopontin / pulp stone / calcification (Link to Publication Site) ● Publication site (DOI): 10.1097/00004770-200104000-00007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11485265 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035317644 (DOI: 10.1097/00004770-200104000-00007, PubMed: 11485265, Elsevier: Scopus)
91.	Jun-ichi Kido, Masatoshi Kataoka, Keiji Oishi, Yoji Asahara and Toshihiko Nagata : A Case Report on Gingival Overgrowth in a Patient Receiving Manidipine Hydrochloride, Journal of the Japanese Association of Periodontology, Vol.43, No.4, 388-395, 2001. (Keyword) drug-induced gingival overgrowth / manidipine hydrochloride / calcium channel blocker
92.	Masatoshi Kataoka, YASUKI SHIMIZU, KENJI KUNIKIYO, YOJI ASAHARA, Kikuji Yamashita, Masami Ninomiya, Ichijiro Morisaki, Yasuyoshi Ohsaki, Jun-ichi Kido and Toshihiko Nagata : Cyclosporin A Decreases the Degradation of Type I Collagen in Rat Gingival Overgrowth, Journal of Cellular Physiology, Vol.182, No.3, 351-358, 2000. (Summary) Cyclosporin A (CsA) is used as an immunosuppressive agent and its prominent side effect is the induction of fibrous gingival overgrowth. The purpose of this study was to investigate the effect of CsA on the type I collagen metabolism in the gingiva of rats fed a powdered diet either containing or lacking CsA. Immunohistochemical analysis revealed that type I collagen was more prevalent in the connective tissue of CsA-treated gingiva than in those of control rats on days 15, 30, and 55 after the start of feeding. Total RNAs were isolated from mandibular molar gingiva on days 0, 3, 8, 15, 30, and 55. Quantitative analysis of mRNA by reverse transcriptase-polymerase chain reaction revealed that the CsA-treated groups showed a gradual decrease in expression of type I collagen and collagenase mRNAs, 0.4% and 18.0% on day 55 compared with those on day 0, respectively. In the control groups, type I collagen and collagenase mRNAs also decreased to 19.7% and 63.0%, respectively, however, both mRNA expressions were significantly lower in the CsA-treated group than in the controls. An electron microscopic analysis of fibroblasts was performed to count the number of cells with collagen fibrils in the cytoplasm, a marker of phagocytosis of collagen by fibroblasts. The collagen fibrils were detected in 4.7% +/- 2.7% and 24.3% +/- 13.7% of fibroblasts in the overgrown gingiva treated with CsA rat for 8 days and 30 days, but in 57.0% +/- 5.3% and 81.3% +/- 9.2% of fibroblasts in the each control group gingiva, respectively. Furthermore, in vitro analysis was performed to measure the phagocytosis of cultured fibroblasts by flow cytometry using collagen-coated latex beads. Fibroblasts isolated from CsA-treated gingiva on day 8 and day 30 contained 5.7% +/- 0.6% and 9.9% +/- 1.5% phagocytic cells, whereas control fibroblasts contained 50.3% +/- 5.5% and 33.3% +/- 4.9% phagocytic cells, respectively. The inhibition rate of phagocytic activity was similar between in vivo and in vitro assays. These findings suggest that the decrease of the collagen degradation due to the lower phagocytosis and the lower collagenase mRNA expression are closely associated with the increase of type I collagen accumulation in CsA-treated rat gingiva. (Keyword) Animals / Cell Division / Cells, Cultured / Collagen / Collagenases / Cyclosporine / Fibroblasts / Gene Expression / Gingiva / Gingival Overgrowth / Immunosuppressive Agents / Latex / male / Microscopy, Electron / Microspheres / Phagocytosis / RNA, Messenger / Rats / Rats, Inbred F344 / Reverse Transcriptase Polymerase Chain Reaction / Specific Pathogen-Free Organisms (Link to Publication Site) ● Publication site (DOI): 10.1002/(SICI)1097-4652(200003)182:3<351::AID-JCP5>3.0.CO;2-U (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10653601 ● Summary page in Scopus @ Elsevier: 2-s2.0-0033957168 (DOI: 10.1002/(SICI)1097-4652(200003)182:3<351::AID-JCP5>3.0.CO;2-U, PubMed: 10653601, Elsevier: Scopus)
93.	Yoji Asahara, Fusanori Nishimura, Hisa Yamada, Koji Naruishi, Masatoshi Kataoka, Jun-ichi Kido, Toshihiko Nagata and Yoji Murayama : Mast cells are not involved in the development of cyclosporin A-induced gingival hyperplasia: a study with mast cell-deficient mice, Journal of Periodontology, Vol.71, No.7, 1117-1120, 2000. (Summary) A previous study suggested that mast cells (MC) are involved in the development of cyclosporin A-induced gingival hyperplasia, since an increased number of MC were observed in the tissue sections of enlarged gingiva. To determine the role of MC in gingival hyperplasia, an MC-deficient mouse model was used in the current study. MC-deficient mice (WBB6F1xW/Wv) and their littermates (+/+) were fed sucrose-containing diets supplemented with or without varying concentrations (300, 400, 500, 600 mg) of cyclosporin A/kg of diet. After 30 days, the mice were sacrificed and the degree of gingival hyperplasia was evaluated by the appearance of the gingiva. Tissue MC were stained with toluidine blue to confirm the presence or absence of MC in the enlarged gingiva. Both W/Wv and +/+ mice, when fed with 600 mg cyclosporin A/kg diet for 30 days, exhibited a similar degree of gingival hyperplasia, while other test mice or control mice did not. Toluidine blue staining of the tissue sections confirmed the presence of MC in the enlarged gingiva of the +/+ mice, but not the W/Wv mice. These results indicate that mast cells are not necessary in the development of cyclosporin A-induced gingival hyperplasia, and that the increased number of MC observed in the enlarged gingiva may be a secondary effect of gingival hyperplasia. We also conclude that a study of mice lacking certain molecules or cells would be quite useful in determining the molecules or cell types responsible for the pathogenesis of drug-induced gingival hyperplasia. (Keyword) Animals / Coloring Agents / Cyclosporine / Gingival Hyperplasia / Immunosuppressive Agents / Mast Cells / Mice / Mice, Mutant Strains / Specific Pathogen-Free Organisms / Tolonium Chloride (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2000.71.7.1117 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10960018 ● Search Scopus @ Elsevier (PMID): 10960018 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2000.71.7.1117 (DOI: 10.1902/jop.2000.71.7.1117, PubMed: 10960018)
94.	Hiroyuki Kadono, Jun-ichi Kido, Yoji Asahara, Takamasa Sawa, Masatoshi Kataoka and Toshihiko Nagata : Inhibition of Osteoblastic Cell Differentiation by Lipopolysaccharide from Porphyromonas gingivalis and Its Mechanism, The Japanese Journal of Conservative Dentistry, Vol.43, No.3, 592-601, 2000. (Keyword) Porphyromonas gingivalis / リポ多糖 / 骨芽細胞 / 分化 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1571980074485326848 (CiNii: 1571980074485326848)
95.	Hiroyuki Nishikawa, Akemichi Ueno, Seiji Nishikawa, Jun-ichi Kido, Mika Oishi, Hideo Inoue and Toshihiko Nagata : Sulfated glycosaminoglycan synthesis and its regulation by transforming growth factor-β in rat clonal dental pulp cells, Journal of Endodontics, Vol.26, No.3, 169-171, 2000. (Summary) Dental pulps contain sulfated glycosaminoglycans (GAGs), such as chondroitin 4-sulfate (CSA/4CS), dermatan sulfate (CSB/DS), and chondroitin 6-sulfate (CSC/6CS). Sulfated GAGs play important roles in mineralization and collagen fibrillogenesis during primary, secondary, and reparative dentin formations. Transforming growth factor-beta (TGF-beta) is a potent regulator for several extracellular matrix (ECM) components and modulates the proliferation and differentiation. Using rat clonal dental pulp cells (RPC-C2A), we investigated the constituents of GAGs synthesized by the cells and the effect of TGF-beta on their synthesis by measuring the radioactivity of [35S]sulfate incorporated into GAG fractions. Cellulose acetate electrophoresis analysis revealed that RPC-C2A cells synthesized CSA and CSB but not CSC and that 10 ng/ml of TGF-beta increased the production of CSA and CSB in the cell/ECM fraction. Measurement of [35S]sulfate incorporation showed a significant increase in the amount of GAGs by TGF-beta, 1.3-fold CSA, and 1.2-fold CSB in the cell/ECM fraction. In the medium fraction the most secreted GAG was CSA, whereas CSB was stored in the cell/ECM fraction. Secreted CSA in the medium was markedly increased by 10 ng/ml of TGF-beta (1.7-fold). These findings indicate that CSA and CSB are major sulfated GAGs synthesized by RPC-C2A cells and that TGF-beta acts as a stimulator of sulfated GAG synthesis in dental pulp cells. (Keyword) Animals / Cell Differentiation / Cell Division / Cells, Cultured / Chondroitin Sulfates / Clone Cells / Collagen / Dental Pulp / Dentin, Secondary / Dentinogenesis / Dermatan Sulfate / Electrophoresis, Cellulose Acetate / Extracellular Matrix / Radiopharmaceuticals / Rats / Statistics as Topic / Sulfur Radioisotopes / Tooth Calcification / Transforming Growth Factor beta (Link to Publication Site) ● Publication site (DOI): 10.1097/00004770-200003000-00010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11199713 ● Search Scopus @ Elsevier (PMID): 11199713 ● Search Scopus @ Elsevier (DOI): 10.1097/00004770-200003000-00010 (DOI: 10.1097/00004770-200003000-00010, PubMed: 11199713)
96.	Teruo Nakamura, Jun-ichi Kido, Reiko Kido, Keiji Oishi, Noriyuki Yamauchi, Masatoshi Kataoka and Toshihiko Nagata : The association of calprotectin level in gingival crevicular fluid with gingival index and the activities of collagenase and aspartate aminotransferase in adult periodontitis patients, Journal of Periodontology, Vol.71, No.3, 361-367, 2000. (Summary) Calprotectin, a major cytosol protein of leukocytes, exists in plasma and other body fluids of healthy human subjects. Since the calprotectin concentration rises markedly in some inflammatory diseases including rheumatoid arthritis, this protein has been thought to be a marker of inflammatory disease. Recently, we identified calprotectin in human dental calculus and gingival crevicular fluid (GCF), and found that the calprotectin concentration in GCF from patients with periodontitis was significantly higher than that in GCF from healthy subjects. In the present study, the association of GCF calprotectin level with GCF volume, gingival index (GI), and levels of biochemical markers including collagenase and aspartate aminotransferase (AST) in GCF was investigated to clarify the relationship between GCF calprotectin level and periodontal inflammation. Ninety GCF samples collected from periodontal pockets with a probing depth of more than 4 mm in 54 patients with adult periodontitis were used for these assays. The GCF volume was measured, and GI in each site was recorded. The calprotectin content in GCF samples was determined by ELISA using a specific antibody. The activity of collagenase or AST was measured by a respective assay kit. The total amount of calprotectin and GCF volume showed a highly significant correlation (r = 0.64, P <0.0001), whereas the calprotectin concentration had no correlation with the GCF volume (r = 0.01, P= 0.924). The mean calprotectin concentration in GCF increased with the degree of GI, and the concentration in individual samples was significantly correlated with the GI score (r = 0.56, P<0.0001). Significant positive correlations were observed in GCF calprotectin versus collagenase (r = 0.57, P <0.0001) and GCF calprotectin versus AST levels (r = 0.40, P <0.005). From the present results and our previous findings, it is shown that the GCF calprotectin level significantly correlates not only with clinical indicators but also with current biochemical marker levels and that calprotectin may be a useful marker for periodontal inflammation. (Keyword) calprotectin/analysis / dental calculus/analysis / gingival crevicular fluid/analysis / gingival index / periodontal diseases/diagnosis / collagenase / aspartate aminotransferase (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.2000.71.3.361 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10776922 ● Search Scopus @ Elsevier (PMID): 10776922 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2000.71.3.361 (DOI: 10.1902/jop.2000.71.3.361, PubMed: 10776922)
97.	Masami Ninomiya, 大場堂信, 二宮洋介, 中野恵子, Mika Oishi, 浅原洋士, Masatoshi Kataoka, 篠原啓之, Jun-ichi Kido and Toshihiko Nagata : ハムスター実験的歯周炎におけるプロスタグランディンE₂の歯槽骨吸収抑制効果, The Japanese Society of Conservative Dentistry, Vol.43, No.6, 1138-1144, 2000.
98.	Takanobu Ohba, Kayoko Akazawa, Yohsuke Ninomiya, Akinori Kirino, Noriko Akimaru, Tomoko Ishimoto, Sayuri Tono, Teruo Nakamura, Masatoshi Kataoka, Hiroyuki Shinohara, Jun-ichi Kido and Toshihiko Nagata : Epidemiologic Study of Periodontal Conditions in Patients Undergoing Renal Dialysis, Journal of the Japanese Association of Periodontology, Vol.42, No.4, 307-313, 2000. (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.42.307 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.2329/perio.42.307 (DOI: 10.2329/perio.42.307)
99.	Dai Ikedo, Yoji Asahara, Takamasa Sawa, Keiji Oishi, Noriyuki Yamauchi, Yasuki Shimizu, Mika Oishi, Masami Ninomiya, Masatoshi Kataoka, Hiroyuki Shinohara, Jun-ichi Kido and Toshihiko Nagata : Stimulatory Effects of Phenytoin on Osteoblastic Differentiation in Cultured MC3 T3-E1 Cells, Journal of the Japanese Association of Periodontology, Vol.42, No.2, 104-113, 2000. (Keyword) phenytoin / osteoblasts / differentiation / MC3 T3-E1
100.	D Ikedo, Keiji Oishi, N Yamauchi, Masatoshi Kataoka, Jun-ichi Kido and Toshihiko Nagata : Stimulatory effects of phenytoin on osteoblastic differentiation of fetal rat calvaria cells in culture., Bone, Vol.25, No.6, 653-660, 1999. (Summary) Phenytoin (diphenylhydantoin, DPH), an anticonvulsant drug for epileptic patients, has several adverse effects, including calvarial thickening and coarsening of the facial features, which occur with chronic DPH therapy. While previous studies have demonstrated that DPH has an anabolic action on bone cells in vivo and in vitro, the basis of these effects is not fully understood. In this study, the effect of DPH on osteoblastic differentiation of fetal rat calvaria (RC) cells in culture was investigated by measuring bone nodule (BN) formation, cell growth, alkaline phosphatase (ALPase) activity, collagen synthesis, and expression of osteocalcin (OC) and osteopontin (OP) mRNAs. Continuous treatment of RC cells with DPH for 18 days dose-dependently increased the mineralized BN number by 1.2-1.7-fold at concentrations of 12.5-200 micromol/L DPH. Cell growth was not affected at the same concentrations of DPH. ALPase activity was stimulated by DPH (1.1-1.9-fold) dose-dependently and was maintained at higher levels in DPH-treated cells throughout the experimental period. DPH increased mineralized and unmineralized BN formations both in the presence and the absence of 10(-8) mol/L dexamethasone (Dex). Expression of OC and OP mRNAs was markedly augmented by DPH on days 12-24 and on days 12-18, respectively. While control mRNA levels of OC and OP increased with time, the increases in DPH-treated cells were greater than those of the controls and the stimulatory effects were dose-dependent. Type I collagen was also influenced by DPH; mRNA level was enhanced and the percentage of collagen synthesized was increased significantly, by 200 micromol/L DPH. When DPH was added in three different culture stages, days 1-6 (growth), days 7-12 (matrix development), and days 13-18 (mineralization), BN formation was influenced primarily on days 1-6 and secondarily on days 7-12, but not on days 13-18, suggesting that DPH increased BN formation by enhancing not only the proportion of osteoprogenitor cells in the early stage but also the proportion of functional osteoblasts in the middle stage within mixed-cell populations. Moreover, such increases were detected in conditions of both Dex(+) and Dex(-). These findings demonstrate that DPH stimulates osteoblast-associated markers such as BNs, ALPase, OC, OP, and type I collagen by continuously affecting the stages of growth and matrix development in RC cells, and suggests that the stimulatory effects by DPH may possibly be induced independent of those by Dex. (Keyword) Alkaline Phosphatase / Animals / Anticonvulsants / Calcification, Physiologic / cell differentiation / cell division / Cells, Cultured / collagen / Dexamethasone / Fetus / Osteoblasts / Osteocalcin / osteopontin / Phenytoin / RNA, Messenger / Rats / Sialoglycoproteins / Skull / Stem Cells (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10593409 ● Search Scopus @ Elsevier (PMID): 10593409 (PubMed: 10593409)
101.	Jun-ichi Kido, T Nakamura, R Kido, Keiji Oishi, N Yamauchi, Masatoshi Kataoka and Toshihiko Nagata : Calprotectin in gingival crevicular fluid correlates with clinical and biochemical markers of periodontal disease., Journal of Clinical Periodontology, Vol.26, No.10, 653-657, 1999. (Summary) Clinical and biochemical markers of periodontal disease have been used for precise objective diagnosis of periodontal inflammation. Interleukin 1beta (IL-1beta) and prostaglandin E2 (PGE2), inflammatory factors, levels in gingival crevicular fluid (GCF) of patients with periodontal disease are elevated and have been studied as biochemical markers. The levels of calprotectin, a leukocyte protein, in body fluids of patients with some inflammatory diseases are raised. Recently, we detected calprotectin in GCF and its concentrations in periodontal pockets were higher than those in healthy gingival crevices. In this study, we investigated the correlations between GCF calprotectin levels and clinical indicators (probing depth and bleeding on probing, BOP), and the IL-1beta or PGE2 levels in GCE Probing depth and BOP at 130 sites of 110 subjects with periodontal or other oral diseases were examined, then GCF samples were collected and their calprotectin, IL-1beta and PGE2 were determined by ELISA. The calprotectin level correlated positively with the probing depth and was significantly higher at BOP-positive than BOP-negative sites. There were significant, positive correlations between the calprotectin and IL-1beta or PGE2 concentrations. These results indicate that the calprotectin level in GCF correlates well with clinical and biochemical markers of periodontal disease and suggest that calprotectin may be useful for evaluating the extent of periodontal inflammation. (Keyword) Adult / Aged / Aged, 80 and over / Aggressive Periodontitis / Biological Markers / Calcium-Binding Proteins / Dinoprostone / Enzyme-Linked Immunosorbent Assay / Female / Gingival Crevicular Fluid / Gingival Hemorrhage / Humans / Interleukin-1 / Leukocyte L1 Antigen Complex / Male / Membrane Glycoproteins / Middle Aged / Neural Cell Adhesion Molecules / Periodontal Diseases / Periodontal Pocket / periodontitis / Periodontium (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10522776 ● Search Scopus @ Elsevier (PMID): 10522776 (PubMed: 10522776)
102.	Keiji Oishi, Mika Oishi, Akira Takahashi, Jun-ichi Kido, Shuzaburo Uemura and Toshihiko Nagata : Examination of the roots of paramolar tuberoles with computed tomography: Report of 3 cases, Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology, Vol.88, No.4, 479-483, 1999.
103.	Mika Oishi, Masumi Horibe, Dai Ikedo, M Miyazaki, Keiji Oishi, Masatoshi Kataoka, Jun-ichi Kido and Toshihiko Nagata : Effect of retinoic acid on osteopontin expression in rat clonal dental pulp cells, Journal of Endodontics, Vol.25, No.10, 683-685, 1999.
104.	Hideki Sasaki, Dai Ikedo, Masatoshi Kataoka, Jun-ichi Kido, Seiichiro Kitamura and Toshihiko Nagata : Pronounced palatal and mandibular tori observed in a patient with chronic Phenytoin therapy, a case report, Journal of Periodontology, Vol.70, No.4, 445-448, 1999. (Summary) Phenytoin, an anticonvulsant drug for epileptic patients, has many adverse effects, including calvarial thickening and coarsening of the facial features. Previous studies have demonstrated that phenytoin has an anabolic action on bone cells. This report describes pronounced palatal and mandibular tori found in a 45-year-old Japanese man undergoing chronic phenytoin therapy. The tori were extremely large, lobular, and symmetrical. A palatal torus appeared along the middle of the hard palate and mandibular tori consisted of 2 pairs of nodular masses extensively filling the lingual floor of the oral cavity. Pronounced osseous outgrowth occurred for the duration of a dose-increase of phenytoin from 1985 to 1997. His parents did not have any palatal or mandibular tori. These facts suggest that these unusual tori may have been the result of chronic phenytoin therapy, rather than association with the familial background. (Keyword) Phenytoin/adverse effects / torus/palatal / torus/mandibular / osteogenesis (Link to Publication Site) ● Publication site (DOI): 10.1902/jop.1999.70.4.445 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10328658 ● Search Scopus @ Elsevier (PMID): 10328658 ● Search Scopus @ Elsevier (DOI): 10.1902/jop.1999.70.4.445 (DOI: 10.1902/jop.1999.70.4.445, PubMed: 10328658)
105.	Dai Ikedo, Keiji Ohishi, Masatoshi Kataoka, Jun-ichi Kido and Toshihiko Nagata : Stimulatory Effects of Phenytoin on Osteoblastic Differentiation of Fetal Rat Calvaria Cells in Culture, Bone, Vol.25, No.6, 653-660, 1999.
106.	Jun-ichi Kido, T Nakamura, R Kido, Keiji Oishi, N Yamauchi, Masatoshi Kataoka and Toshihiko Nagata : Calprotectin, a leukocyte protein related to inflammation, in gingival crevicular fluid., Journal of Periodontal Research, Vol.33, No.7, 434-437, 1998. (Keyword) Adult / Aged / Aged, 80 and over / Enzyme-Linked Immunosorbent Assay / Female / Gingival Crevicular Fluid / Humans / Leukocyte L1 Antigen Complex / Male / Membrane Glycoproteins / Middle Aged / Neural Cell Adhesion Molecules / periodontitis / Statistics, Nonparametric (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9842509 ● Search Scopus @ Elsevier (PMID): 9842509 (PubMed: 9842509)
107.	Keiko Nakano, Mika Oishi, Y Ogawa, T Ohba, Junichi Kido, Y Miyake and Toshihiko Nagata : Prostaglandin E2 inhibits alveolar bone resorption in experimantal periodontitis in hamster, Dentistry in Japan, Vol.34, 108-111, 1998.
108.	Akemichi Ueno, Kikuji Yamashita, Toshihiko Nagata, Chizuko Tsurumi, Yoshihiro Miwa, Seiichiro Kitamura and Hideo Inoue : cDNA cloning of bovine thrombospondin 1 and its expression in odontoblasts and predentin, Biochimica et Biophysica Acta (BBA) - Protein Structure and Molecular Enzymology, Vol.1382, No.1, 17-22, 1998. (Summary) The extracellular matrix protein thrombospondin 1 (TSP1) was cloned from odontoblasts of bovine mandibular teeth which participate in dentinogenesis. The 5289 bp cDNA contains a complete open reading frame of 1170 amino acids. Bovine TSP1 has high homologies to its human and mouse counterparts. In immunohistochemical analyses of bovine anterior teeth with anti-TSP1 monoclonal antibody, TSP1 was only detectable at the position of predentin, located between dentin and unmineralized dental pulp. Northern blot analysis showed high levels of two sizes of TSP1 mRNAs in odontoblasts but not dental pulp and gingiva. Previously we found that osteotropic factors such as calcitriol and TGF-beta induce TSP1 at the transcriptional level in clonal rat dental pulp cells. These results suggest a role of TSP1 in dentinogenesis and/or maintenance of dentin and dental pulp. (Keyword) Amino Acid Sequence / Animals / Base Sequence / Cattle / Chickens / Cloning, Molecular / DNA, Complementary / Dentinogenesis / Humans / Mice / Molecular Sequence Data / Odontoblasts / Rats / Recombinant Proteins / Sequence Alignment / Sequence Homology, Amino Acid / Thrombospondin 1 / Xenopus (Link to Publication Site) ● Publication site (DOI): 10.1016/S0167-4838(97)00188-X (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9507054 ● Search Scopus @ Elsevier (PMID): 9507054 ● Search Scopus @ Elsevier (DOI): 10.1016/S0167-4838(97)00188-X (DOI: 10.1016/S0167-4838(97)00188-X, PubMed: 9507054)
109.	山内規進, Jun-ichi Kido, Masatoshi Kataoka, Keiji Oishi, Seiji Nishikawa, Akemichi Ueno and Toshihiko Nagata : 前立腺癌細胞培養上清の骨芽細胞分化抑制作用とその性状, Shikoku Dental Research, Vol.10, No.2, 249-256, 1998. (Keyword) 骨芽細胞(細胞学,生理学)
110.	Jun-ichi Kido, N Yamauchi, Keiji Oishi, Masatoshi Kataoka, Seiji Nishikawa, T Nakamura, H Kadono, D Ikedo, Akemichi Ueno, N Nonomura, A Okuyama and Toshihiko Nagata : Inhibition of osteoblastic cell differentiation by conditioned medium derived from the human prostatic cancer cell line PC-3 in vitro., Journal of Cellular Biochemistry, Vol.67, No.2, 248-256, 1997. (Summary) Human prostatic carcinoma frequently metastasizes to bone tissue and activates bone metabolism, especially bone formation, at the site of metastasis. It has been reported that an extract of prostatic carcinoma and conditioned medium (CM) of a human prostatic carcinoma cell line, PC-3, established from a bone metastastic lesion, stimulate osteoblastic cell proliferation. However, there is little information about the effect of PC-3 CM on the differentiation of osteoblastic cells. In this study, we investigated the effect of PC-3 CM on the differentiation of two types of osteoblastic cells, primary fetal rat calvaria (RC) cells containing many undifferentiated osteoprogenitor cells, and ROS 17/2.8, a well-differentiated rat osteosarcoma cell line. PC-3 CM inhibited bone nodule formation and the activity of alkaline phosphatase (ALPase), an osteoblastic marker enzyme, on days 7, 14, and 21 (RC cells) or 3, 6, and 9 (ROS 17/2.8 cells) in a dose-dependent manner (5-30% CM). However, the CM did not affect cell proliferation or cell viability. PC-3 CM was found to markedly block the gene expression of ALPase and osteocalcin (OCN) mRNAs but had no effect on the mRNA expression of osteopontin (OPN), the latter two being noncollagenous proteins related to bone matrix mineralization. These findings suggest that PC-3 CM contains a factor that inhibits osteoblastic cell differentiation and that this factor may be involved in the process of bone metastasis from prostatic carcinoma. (Keyword) Alkaline Phosphatase / Animals / Bone and Bones / cell differentiation / cell division / Culture Media, Conditioned / Embryo, Mammalian / gene expression / Humans / Male / Osteoblasts / Osteocalcin / osteopontin / Osteosarcoma / Prostatic Neoplasms / RNA, Messenger / Rats / Sialoglycoproteins / Time Factors / Tumor Cells, Cultured (Link to Publication Site) ● Publication site (DOI): 10.1002/(SICI)1097-4644(19971101)67:2<248::AID-JCB10>3.0.CO;2-B (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9328830 ● Search Scopus @ Elsevier (PMID): 9328830 ● Search Scopus @ Elsevier (DOI): 10.1002/(SICI)1097-4644(19971101)67:2<248::AID-JCB10>3.0.CO;2-B (DOI: 10.1002/(SICI)1097-4644(19971101)67:2<248::AID-JCB10>3.0.CO;2-B, PubMed: 9328830)
111.	Jun-ichi Kido, S. Nishikawa, H. Ishida, Kikuji Yamashita, Seiichiro Kitamura, K. Kohri and Toshihiko Nagata : Identification of calprotein , a calcium binding leukocyte protein, In human dental calculus matrix, Journal of Periodontal Research, Vol.32, No.4, 335-361, 1997. (Summary) Calprotectin is a calcium binding protein produced by leukocytes, macrophages and epithelial cells, and its levels in several tissues increase during infections and in many inflamed areas, suggesting that it may be an indicator of inflammatory activity. Osteopontin is a prominent phosphorylated glycoprotein in bone matrix, having calcium binding capacity. Recently, it has been reported that calprotectin and osteopontin are present in urinary stones (pathological mineralized masses in the body), and that these proteins may be involved in their formation. Dental calculus formed by mineralization of dental plaque is an inflammatory factor which may contribute to periodontal disease. It contains many organic components involved in mineralization. We recently found osteopontin molecules in human dental calculus and suggested that the components of its matrix may be similar to those of urinary stones. In this study, we investigated the presence of calprotectin in human dental calculus by immunohistochemical and immunoblotting analyses using a specific antibody for calprotectin. After fixation and demineralization of dental calculi adhered to tooth roots, sections embedded in paraffin were immunoreacted with the antibody for calprotectin and positive immunostaining for calprotectin was observed. Dental calculus proteins were then extracted with EDTA and separated by electrophoresis on 15% polyacrylamide gels. By immunoblotting analysis, 3 or 4 bands were observed at 11, 14.5, 22-25, 28 or 36.5 kDa and these patterns corresponded to those of calprotectin subunits. When non-immune rabbit serum was used instead of calprotectin-specific antibody as a negative control, no immunoreactivity was observed. These findings indicate that calprotectin is associated not only with antibacterial action but also with calcium binding capacity during dental calculus formation. (Keyword) Calcium-Binding Proteins / Decalcification Technique / Dental Calculus / Electrophoresis, Polyacrylamide Gel / Humans / Immunoblotting / immunohistochemistry / Leukocyte L1 Antigen Complex / Neural Cell Adhesion Molecules (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.1997.tb00545.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9210089 ● Search Scopus @ Elsevier (PMID): 9210089 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.1997.tb00545.x (DOI: 10.1111/j.1600-0765.1997.tb00545.x, PubMed: 9210089)
112.	Noriyuki Yamauchi, Seiji Nishikawa, Jun-ichi Kido, Keiji Oishi, Toshihiko Nagata, Masatoshi Kataoka, Hiroyuki Shinohara and Hiroshi Ishida : Relationship between the expression of parathyroid hormone receptors and hormonal effect during rat osteoprogenitor cell differentiation, Journal of Bone and Mineral Metabolism, Vol.15, No.1, 17-22, 1997. (Keyword) hormone
113.	中野恵子, Keiji Oishi, 山内規進, Mika Oishi, 篠原啓之, Masatoshi Kataoka, Jun-ichi Kido, Seiji Nishikawa, 石田浩 and Toshihiko Nagata : ラット胎児頭蓋冠由来細胞培養系におけるプロスタグランディンE₂の石灰化促進作用, Journal of the Japanese Association of Periodontology, Vol.38, No.4, 484-492, 1996.
114.	Masami Ninomiya, Kikuji Yamashita, Toshihiko Nagata and Seiichiro Kitamura : ラット後肢の指骨切断後の治癒過程に及ぼすethane-1-hydroxy-1, 1-diphosphonateの影響—光学顕微鏡所見を中心に—, Shikoku Dental Research, Vol.8, No.2, 189-206, 1996.
115.	Jun-ichi Kido, C Kasahara, Keiji Oishi, Seiji Nishikawa, H Ishida, Kikuji Yamashita, Seiichiro Kitamura, K Kohri and Toshihiko Nagata : Identification of osteopontin in human dental calculus matrix., Archives of Oral Biology, Vol.40, No.10, 967-972, 1995. (Summary) Osteopontin is a prominent non-collagenous component of bone matrix, although it is expressed in several other tissues. Recently, osteopontin was reported to be involved in urinary stone formation and atherosclerotic lesions of the aorta, suggesting that it may be a key protein associated with these types of pathological mineralization. In this study, whether or not human dental calculus contains osteopontin was investigated by immunoblotting and immunohistochemical analyses. After extraction of calculus proteins with EDTA and separation of the proteins by electrophoresis, immunoblotting analysis revealed the presence of osteopontin. Two forms of osteopontin appeared at 61 and 68 kDa on 10% polyacrylamide gel and the proteins were digested with thrombin, a highly specific protease. Moreover, immunohistochemical analysis revealed that osteopontin was localized in dental calculus adherent to tooth roots. These findings indicate that osteopontin is, in fact, present in human dental calculus and may be involved in calculus formation as the stone matrix. (Keyword) Dental Calculus / Electrophoresis, Polyacrylamide Gel / Female / Humans / Immunoblotting / immunohistochemistry / Middle Aged / osteopontin / Sialoglycoproteins (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 8526807 ● Search Scopus @ Elsevier (PMID): 8526807 (PubMed: 8526807)
116.	Jun-ichi Kido, C. Kasahara, K. Ohishi, S. Nishikawa, H. Ishida, Kikuji Yamashita, Seiichiro Kitamura, K. Kohri and Toshihiko Nagata : Identification of osteopontin in human dental calculus matrix, Archives of Oral Biology, Vol.40, No.10, 967-972, 1995. (Keyword) dental calculus / mineralization / osteopontin (Link to Publication Site) ● Publication site (DOI): 10.1016/0003-9969(95)00056-U (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/0003-9969(95)00056-U (DOI: 10.1016/0003-9969(95)00056-U)
117.	Keiji Oishi, Seiji Nishikawa, Toshihiko Nagata, N Yamauchi, H Shinohara, Jun-ichi Kido and H Ishida : Physiological concentrations of retinoic acid suppress the osteoblastic differentiation of fetal rat calvaria cells in vitro., European Journal of Endocrinology, Vol.133, No.3, 335-341, 1995. (Summary) The effects of retinoic acid (RA) on osteoblastic differentiation and activity were studied in fetal rat calvaria cells cultured for up to 24 days. Fetal bovine serum used for the experiments was treated with an anion-exchange resin to remove endogenous RA. The depletion of RA in the treated serum was confirmed by high-performance liquid chromatography and tritiated RA tracing. Under the culture conditions employed, the continuous presence of RA for 14 days at 10(-9) mol/l or higher decreased both alkaline phosphatase (ALP) activity on day 12 and the number of bone nodules on day 14 in a dose-dependent manner. Short-term (24 h) exposure to RA at 10(-8) mol/l, which is a physiological concentration, decreased and increased the levels of ALP and osteopontin mRNA on day 6, respectively. Retinoic acid at 10(-8) mol/l also increased the level of osteocalcin mRNA on day 12. However, these effects were not obvious at later stages (days 18 and 24). At a high concentration (10(-6) mol/l), RA increased the level of osteopontin mRNA on day 6 and decreased the levels of ALP and osteocalcin mRNA irrespective of culture period. These results suggest that, at physiological concentrations, RA suppresses the differentiation of osteoprogenitor cells and regulates osteoblastic functions. (Keyword) Alkaline Phosphatase / Animals / Bone and Bones / Cattle / cell differentiation / Cells, Cultured / Chromatography, High Pressure Liquid / Fetal Blood / Ion Exchange Resins / Osteoblasts / Osteocalcin / osteopontin / RNA, Messenger / Rats / Sialoglycoproteins / Tretinoin (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 7581951 ● Search Scopus @ Elsevier (PMID): 7581951 (PubMed: 7581951)
118.	Toshihiko Nagata, Mika Yokota, Seiji Nishikawa, Hiroshi Ishida and Yoichi Wakano : Osteopontin expression in clonal dental pulp cells, Annals of the New York Academy of Sciences, Vol.760, 342-345, 1995.
119.	Jun-ichi Kido, 山内規進, 中野恵子, Keiji Oishi, Mika Oishi, 篠原啓之, Masatoshi Kataoka, Seiji Nishikawa, 石田浩 and Toshihiko Nagata : 株化ラット歯髄細胞培養上清がラット頭蓋冠由来骨原性細胞の石灰化骨様結節形成に及ぼす効果, The Japanese Journal of Conservative Dentistry, Vol.38, No.5, 1143-1148, 1995.
120.	Keiji Oishi, H Ishida, Toshihiko Nagata, N Yamauchi, C Tsurumi, Seiji Nishikawa and Y Wakano : Thyroid hormone suppresses the differentiation of osteoprogenitor cells to osteoblasts, but enhances functional activities of mature osteoblasts in cultured rat calvaria cells., Journal of Cellular Physiology, Vol.161, No.3, 544-552, 1994. (Summary) The effects of thyroid hormone on osteoblastic differentiation and activity were studied in fetal rat calvaria (RC) cells cultured for up to 30 days in medium supplemented with thyroid hormone-depleted serum. In this condition, the cells proliferated and differentiated to form mineralized bone nodules (BN) and expressed osteoblastic markers such as alkaline phosphatase (ALP), osteocalcin (OCN), and osteopontin (OPN). The continuous presence of triiodothyronine (T3) at 10(-9)-10(-8) M in the medium inhibited the osteoblastic differentiation: 34% decrease in ALP activity on day 12 and 60% decrease in BN formation on day 15 at 10(-8) M. T3 at these doses had no effect on the DNA content of RC cells at confluence (day 6). Short-term (48-h) exposure of T3 at 10(-9) M or higher decreased ALP activity when RC cells were differentiating (days 7-11). However, when BN formation by the cells had already reached a plateau (day 28), the activity was increased by treatment with T3 at 10(-7)-10(-6) M. OCN production was increased dose dependently by this treatment with T3 (2.1-fold and 1.3-fold of control at 10(-8) M on days 11 and 28, respectively). Similar increases were observed in the levels of OCN mRNA. In addition, increases in phosphorylated OPN in the medium (day 11) and mineralized matrix (day 28) were observed (1.5-fold at 10(-8)-10(-6) M), while OPN synthesis and the level of its mRNA were depressed by T3 (60-70% of control at 10(-8) M). These results suggest that T3 regulates osteoblastic differentiation and activity depending on the state of cell differentiation: T3 suppresses the differentiation of osteoprogenitor cells to osteoblasts, but enhances the functional activity of mature osteoblasts. (Keyword) Alkaline Phosphatase / Animals / Bone Development / cell differentiation / cell division / Cells, Cultured / gene expression / Osteoblasts / Osteocalcin / osteopontin / RNA, Messenger / Rats / Sialoglycoproteins / Skull / Time Factors / Triiodothyronine (Link to Publication Site) ● Publication site (DOI): 10.1002/jcp.1041610318 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 7962135 ● Search Scopus @ Elsevier (PMID): 7962135 ● Search Scopus @ Elsevier (DOI): 10.1002/jcp.1041610318 (DOI: 10.1002/jcp.1041610318, PubMed: 7962135)
121.	Toshihiko Nagata, Atsuko Kawahara, Chika Kasahara, Mika Yokota, Seiji Nishikawa, Yoichi Wakano and Hiroshi Ishida : Biochemical study on the tissue compartmentalization of phosphophoryn, osteopontin and bone sialoprotein (BSP) in rat incisor dentin, Journal of Bone and Mineral Metabolism, Vol.12, No.2, 7-13, 1994.
122.	Toshihiko Nagata, Mika Yokota, Keiji Oishi, Seiji Nishikawa, Hiroyuki Shinohara, Yoichi Wakano and Hiroshi Ishida : 1α,25-Dihydroxyvitamin D₃ stimulation osteopontin expression in rat clonal dental pulp cells, Archives of Oral Biology, Vol.39, No.9, 775-782, 1994.
123.	Noriyuki Yamauchi, Keiji Oishi, Seiji Nishikawa, Toshihiko Nagata, Masatoshi Kataoka, Hiroyuki Shinohara and Hiroshi Ishida : Expression and characterization of parathyroid hormone receptors on fetal rat calvaria cells in culture, Journal of Bone and Mineral Metabolism, Vol.12, No.Suppl.1, 33-37, 1994. (Keyword) osteoblast
124.	Shinji Kasahara, Chika KASAHARA, Seiji Nishikawa, Noriyuki YAMAUCHI, Keiji Oishi, Keiko KAHO, Toshihiko Nagata, Hiroshi ISHIDA and Yoichi WAKANO : Relationship between Calcium Binding Proteins Associated with Mineralized Bone Nodule and 5'-Methylthioadenosine Metabolism in Cultured Rat Calvaria Cells, Journal of the Japanese Association of Periodontology, Vol.35, No.1, 172-178, 1993. (Summary) 5'-Methylthioadenosine (MTA) is formed during the biosynthesis of polyamines. We previously reported that 5'-difluoromethylthioadenosine (DFMTA), a synthetic inhibitor of MTA phosphorylase, caused intracellular adenine depletion and inhibited both alkaline phosphatase activity and bone nodule formation in cultured rat calvaria cells. In addition, exogenous adenine enhanced these two markers and partially reversed the DFMTA-induced inhibition in this culture system. Osteopontin, a non-collagenous protein associated with matrix mineralization, has been reported to be predominantly incorporated into bone nodules in concert with the progresism of in vitro mineralization on rat calvaria cells. In this study, we examined the effects of adenine and DFMTA on osteopontin contents incorporated into mineralized nodules by using polyacrylamide gel electrophoresis and "Stains-All" staining. Adenine increased the accumulation of osteopontin into mineralized nodule whereas DFMTA inhibited it. Furthermore the osteopontin contents which had been decreased by DFMTA recovered with the addition of adenine. These results suggest that adenine formed from MTA is important in the mineralization process of rat calvaria cells. (Keyword) Rat calvaria cell / osteopontin / calcification / 5'-Methylthioadenosine / Adenine (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.35.172 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204410996736 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.35.172 (DOI: 10.2329/perio.35.172, CiNii: 1390001204410996736)
125.	Mika Yokota, Toshihiko Nagata, Hiroshi Ishida and Yoichi Wakano : Clonal dental pulp cells (RDP4-1, RPC-C2A) synthesize and secrete osteopontin (SPP1, 2ar), Biochemical and Biophysical Research Communications, Vol.189, No.2, 892-898, 1992.
126.	浜崎章弘, Toshihiko Nagata, 川人貴子, Keiji Oishi, 石田浩 and 若野洋一 : ヒト歯髄細胞培養系におけるインスリンとEGFの作用, The Japanese Journal of Conservative Dentistry, Vol.35, No.3, 724-730, 1992. (Keyword) Epidermal Growth Factor(薬理学)
127.	Shinji Kasahara, Seiji Nishikawa, H Ishida, Toshihiko Nagata, N Yamauchi, Keiji Oishi, Y Wakano and H Inoue : The role of 5'-methylthioadenosine on rat calvaria cell differentiation., Biochemical and Biophysical Research Communications, Vol.182, No.2, 817-823, 1992. (Summary) The role of 5'-methylthioadenosine (MTA), formed during the process of polyamine biosynthesis, on differentiation of osteoprogenitor cells was assessed by its effects on alkaline phosphatase (ALP) activity, bone nodule formation and osteopontin contents of cultured rat calvaria (RC) cells. These three markers were stimulated by exogenous MTA and were depressed by 5'-difluoromethylthioadenosine (DFMTA), a synthetic inhibitor of MTA phosphorylase, which cleaves MTA to adenine and 5-methylthioribose-1-phosphate. 5-Methylthioribose and 2-keto-4-methylthiobutyrate, metabolites of 5-methylthioribose-1-phosphate, had no effects on ALP activity and bone nodule formation in the presence or absence of DFMTA. On the other hand, adenine enhanced ALP activity, bone nodule formation and osteopontin contents in mineralized nodules and also partially reversed DFMTA-induced inhibition of these three markers. MTA, its metabolites and DFMTA did not affect the growth of RC cells under these culture conditions. These results suggest that adenine formed from MTA is important in the differentiation of RC cells. (Keyword) Adenine / Adenosine / Alkaline Phosphatase / Animals / Bone and Bones / cell differentiation / cell division / Cells, Cultured / Deoxyadenosines / Kinetics / osteopontin / Purine-Nucleoside Phosphorylase / Rats / Sialoglycoproteins / Thionucleosides (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 1734884 ● Search Scopus @ Elsevier (PMID): 1734884 (PubMed: 1734884)
128.	Shinji Kasahara, Seiji Nishikawa, Noriyuki YAMAUCHI, Keiji Oishi, Shigehito SUZUKI, Hiroshi II, Akihiro HAMASAKI, Toshihiko Nagata, Hiroshi ISHIDA and Yoichi WAKANO : Role of the Metabolism of 5'-Methylthioadenosine in the Proliferation and Differentiation of Osteoprogenitor Cells : Effects of an Inhibitor of Methylthioadenosine Phosphorylase on the Proliferation and Alkaline Phosphatase Activity of Fetal Rat Calvaria Cells, Journal of the Japanese Association of Periodontology, Vol.33, No.3, 632-638, 1991. (Summary) 5'-Methylthioadenosine (MTA) is formed during the biosynthesis of polyamines. This nucleoside is cleaved to adenine and 5'-methylthioribose-1-phosphate in mammalian cells by methylthioadenosine phosphorylase (MTA Pase). 5'-Difluoromethyl-thioadenosine (DFMTA), a synthetic analog of MTA is known to be an inhibitor of MTA Pase. In this study, we examined the effects of DFMTA on the cell proliferation and alkaline phosphatase (ALPase) activity of enzyme-released rat calvaria cells (RC cells). RC cells were isolated by collagenase digestion of 21-day fetal rat calvariae and cultured in the medium containing 15% NU serum, which was used because its MTA Pase activity is very low. Under the culture conditions employed, the ALPase activity of RC cells was low in the exponential growth phase, but markedly increased when the cells reached confluency (day 10). DFMTA strongly inhibited MTA Pase extracted from RC cells (Ki=0.60μM). DFMTA at low concentrations (5, 10μM) decreased the ALPase activity of RC cells measured on day 7 and 14, without affecting cell proliferation. At higher concentrations (≧25μM), this analog suppressed both ALPase activity and cell proliferation. These results suggested that the metabolism of MTA is involved in regulating cell proliferation and differentiation. (Keyword) Rat calvaria cell / cell proliferation and differentiation / cell differentiation / 5'-Methylthioadenosine (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.33.632 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679387895040 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.33.632 (DOI: 10.2329/perio.33.632, CiNii: 1390282679387895040)
129.	川原淳子, Mika Yokota, 安友美保子, 下保恵子, 浜崎章弘, Toshihiko Nagata, 石田浩 and 若野洋一 : ラット歯髄細胞が合成するタンパク質と石灰化の関連, 日本歯科保存学会雑誌, Vol.34, No.5, 1435-1441, 1991.
130.	Masami Ninomiya, Takanobu Ohba, Yohsuke Ninomiya, Keikko Nakano, Mika Oishi, Yoji Asahara, Masatoshi Kataoka, Hiroyuki Shinohara, Jun-ichi Kido and Toshihiko Nagata : Inhibitory Effects of Prostaglandin E2 on Alveolar Bone Resorption in Hamster Experimental Periodontitis, The Japanese Journal of Conservative Dentistry, Vol.43, No.6, 1138-1144, 1988.

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): 1050020697877556480 (Tokushima University Institutional Repository: 109875, CiNii: 1050020697877556480)
2.	Toshihiko Nagata, Masumi Horibe, Keiji Oishi and Jun-ichi Kido : The close relationship between periodontitis and diabetes and the diagnosis of diabetes-associated periodontitis, Proceeding of 2013-Asian-Pacific Society of Periodontology Meeting, 89-95, 2014.
3.	Masami Ninomiya and Toshihiko Nagata : FGF-2による歯周組織再生療法, 歯の長期保存の臨床私はこうして歯を守る, Vol.38, No.6, 126-131, 2013. (Keyword) Periodontal regeneration / Fibroblast growth factor 2 / Clinical trial
4.	Masami Ninomiya, Kayoko Akazawa, Kazuhito Satomura, Nobuyuki Kamata, Masaru Nagayama, Keiji Moriyama, Jun-ichi Kido and Toshihiko Nagata : Hypercementosis with the progression of chronic apical periodontitis -A case report, Shikoku Dental Research, Vol.15, No.2, 263-269, 2003.
5.	Mika Oishi, 桐野晃教 and Toshihiko Nagata : 上顎側切歯にみられた歯内歯(Dens invaginatus/Dens in dente)における歯内治療の一例, Shikoku Dental Research, Vol.14, No.2, 301-307, 2002.

Academic Letter:

1.	Koji Naruishi, Akiko Kunita, Toshihiko Nagata, Shogo Takashiba and Seiji Adachi : Cut-off values of Functional Independence Measure scores for discharge destination., Geriatrics & Gerontology International, Vol.15, No.5, 670-671, 2015. (Link to Publication Site) ● Publication site (DOI): 10.1111/ggi.12430 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25899761 ● Summary page in Scopus @ Elsevier: 2-s2.0-84928136495 (DOI: 10.1111/ggi.12430, PubMed: 25899761, Elsevier: Scopus)
2.	Maki Hosoki, Takashi Matsuo, Toshihiko Nagata, Tetsuo Ichikawa, Yoshizo Matsuka and Eiji Tanaka : 徳島大学病院, Journal of Esthetic Dentistry, Vol.25, No.2, 196, 2013.
3.	徳永格, Hiroyuki Seto, 大場博史, 和田智恵, 濱秀樹, Masumi Horibe and Toshihiko Nagata : ラット実験的歯周炎における副甲状腺ホルモンの局所投与による歯槽骨形成作用, 第6回カルシトニン/副甲状腺ホルモン研究会記録集, 36, 2007.

Review, Commentary:

1.	Koji Naruishi and Toshihiko Nagata : Biological effects of interleukin-6 on Gingival Fibroblasts: Cytokine regulation in periodontitis., Journal of Cellular Physiology, Vol.233, No.9, 6393-6400, Mar. 2018. (Summary) Periodontitis is a bacterial infectious disease, and many inflammatory cytokines regulate periodontitis pathophysiology through a crosstalk between tissue cells and immune cells. Interleukin (IL)-6 is an important cytokine involved in the regulation of host response to bacterial infection. Human Gingival Fibroblasts (HGFs) are the most abundant cells in gingival connective tissues. Various HGF responses to periodontal pathogens or inflammatory cytokines contribute to the development of periodontitis. Lipopolysaccharide derived from Porphyromonas gingivalis (Pg LPS) and IL-1 significantly increase IL-6 production in HGFs. However, IL-6 cannot function in HGFs without the soluble form of the IL-6 receptor (sIL-6R), because HGFs do not express sufficient cell surface IL-6R to bind appreciable levels of IL-6. Importantly, sIL-6R is essential for IL-6 signaling in HGFs, and the sIL-6R is produced by differentiated THP-1 cells treated with IL-6. Calprotectin, a heterodimer of S100A8 and S100A9, is released during inflammation and significantly induces IL-6 production in HGFs via toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-B) signals. Calprotectin also induces sIL-6R production in differentiated THP-1 cells. IL-6 induces vascular endothelial growth factor (VEGF), matrix-metalloproteinase-1 (MMP-1), and cathepsin L production in HGFs in the presence of sIL-6R. Taken together, calprotectin-induced IL-6 production in HGFs may cause periodontitis progression through a crosstalk of fibroblasts and macrophages. There are many reports that examine how cytokines are released from HGFs to cause beneficial or harmful effects in inflamed periodontal lesions. This review explores the pathophysiology of periodontitis by focusing IL-6-mediated crosstalk of HGFs and macrophages. (Link to Publication Site) ● Publication site (DOI): 10.1002/jcp.26521 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29574949 ● Search Scopus @ Elsevier (PMID): 29574949 ● Search Scopus @ Elsevier (DOI): 10.1002/jcp.26521 (DOI: 10.1002/jcp.26521, PubMed: 29574949)
2.	Toshihiko Nagata, Masami Ninomiya, Chie Wada -Mihara, Jun-ichi Kido and Seiji Nishikawa : Etiology of drug-induced gingival overgrowth, Current Issues in Periodontics, 1-8, Oct. 2016. (Keyword) Drug-induced gingival overgrowth / epidemiology / Calcium-channel blocker
3.	Masami Ninomiya and Toshihiko Nagata : 全顎的な歯肉のびらん・接触痛, DENTAL DIAMOND, Vol.41, No.13, 19-20, Oct. 2016.
4.	Koji Naruishi and Toshihiko Nagata : 最新の知見から攻める!①歯周病と腎疾患はどう関係するの?, The Journal of Dental Hygiene, Vol.36, No.3, 304-305, Mar. 2016.
5.	Masami Ninomiya and Toshihiko Nagata : 下顎前歯部の動揺, DENTAL DIAMOND, Vol.40, No.15, 21-22, Nov. 2015. (Keyword) 侵襲性歯周炎 / 歯周治療
6.	Koji Naruishi and Toshihiko Nagata : 歯周病が生活習慣病に及ぼす影響, The Japanese Journal of Clinical Nutrition, Vol.126, No.3, 262-267, Mar. 2015.
7.	Jun-ichi Kido, Mika Bandou, E Sakamoto, Yukari Kajiura and Toshihiko Nagata : Effects of advanced glycation end-products on pathogenesis of diabetes-associated periodontitis, Journal of the Japanese Association of Periodontology, Vol.56, No.1, 17-24, 2014. (Keyword) 糖尿病関連歯周炎 / 最終糖化産物 / 歯周組織 (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.56.17 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204414873472 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.56.17 (DOI: 10.2329/perio.56.17, CiNii: 1390001204414873472)
8.	Masami Ninomiya and Toshihiko Nagata : 下顎前歯部の歯肉腫脹, DENTAL DIAMOND, Vol.38, No.8, 133-134, Jun. 2013. (Keyword) Gingival swelling / Pathologic examination / Radicular cyst
9.	Keiji Oishi and Toshihiko Nagata : Periodontal conditions in dialysis patients, The Japanese Journal of Clinical Dialysis, Vol.27, No.6, 55-62, Jun. 2011. (Keyword) periodontitis / 糖尿病性腎症 / 慢性炎症
10.	Toshihiko Nagata and Masami Ninomiya : 2.各論 1)歯周病 (特集透析患者の口腔衛生), 透析フロンティア, Vol.21, No.2, 12-16, May 2011.
11.	高柴正悟, 山田了, 伊藤公一, 高田隆, 島内英俊, Toshihiko Nagata, 吉江弘正 and 栗原英見 : Establishment of Examination for Judgment of Effects of Prevention and Treatment for Periodontal Treatment According to Clinical Database, Journal of the Japanese Association for Dental Science, Vol.30, 70-74, Mar. 2011. (Keyword) periodontitis / 細菌検査 / 臨床データベース / 予防・治療の効果判定 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572543025646375552 (CiNii: 1572543025646375552)
12.	Toshihiko Nagata : Drug-induced Disorders in Oral Tissues, Progress in Medicine, Vol.30, No.11, 2833-2838, Nov. 2010.
13.	Toshihiko Nagata : 糖尿病における歯周組織破壊の特徴, Diabetes Frontier, Vol.21, No.5, 542-548, Oct. 2010. (Keyword) periodontitis / 糖尿病関連歯周炎 / 歯槽骨 / 歯肉溝滲出液 / 診断マーカー
14.	Toshihiko Nagata and Youji Miyamoto : Bisphosphonate-related osteonecrosis of the jaws, Clinic All-Round, Vol.59, No.4, 540-543, Apr. 2010. (Keyword) 顎骨壊死 / ビスフォスフォネート / 副作用 / 骨粗鬆症 / 悪性腫瘍 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520854805754960640 (CiNii: 1520854805754960640)
15.	Keiji Oishi and Toshihiko Nagata : Root coverage procedures, Shikoku Dental Research, Vol.22, No.2, 185-190, Jan. 2010. (Tokushima University Institutional Repository) ● Metadata: 109797 (Tokushima University Institutional Repository: 109797)
16.	Toshihiko Nagata : Relationship between periodontal disease and renal disease, Journal of Clinical and Experimental Medicine, Vol.232, No.3, 190-193, Jan. 2010. (Keyword) 腎臓病 / periodontitis / 糖尿病腎症 / 人工透析 / 歯肉増殖症 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521980705428530304 (CiNii: 1521980705428530304)
17.	Hiroyuki Seto, Masami Ninomiya and Toshihiko Nagata : Alveolar bone resorption in animal models of periodontitis, CLINICAL CALCIUM, Vol.16, No.2, 24(248)-30(254), Jan. 2006.
18.	Hiroyuki Seto and Toshihiko Nagata : Ca拮抗薬による歯肉増殖症の治療, Dental Diamond, Vol.30, No.12, 118-119, Dec. 2005.
19.	Masatoshi Kataoka, Jun-ichi Kido, Yasuo Shinohara and Toshihiko Nagata : Drug-Induced Gingival Overgrowth a Review, Biological & Pharmaceutical Bulletin, Vol.28, No.10, 1817-1821, Oct. 2005. (Summary) Drug-induced gingival overgrowth is a side effect associated with 3 types of drugs: anticonvulsants (phenytoin), immunosuppressive agents (cyclosporine A), and various calcium channel blockers for cardiovascular diseases. Gingival overgrowth is characterized by the accumulation of extracellular matrix in gingival connective tissues, particularly collagenous components with various degrees of inflammation. Although the mechanisms of these disorders have not been elucidated, recent studies suggest that these disorders seem to be induced by the disruption of homeostasis of collagen synthesis and degradation in gingival connective tissue, predominantly through the inhibition of collagen phagocytosis of gingival fibroblasts. The integrins are a large family of heterodimeric transmembrane receptors for extracellular matrix molecules. alpha2beta1 integrin serves as a specific receptor for type I collagen on fibroblasts, and alpha2 integrin has been shown to play a crucial role in collagen phagocytosis. Actin filaments, which are assembled from monomers and oligomers, are involved in collagen internalization after binding to integrins. Furthermore, the implication of intracellular calcium in the regulation of integrin-mediated binding activity and gelsolin activity, known as a calcium-dependent actin-severing protein, is also described. In this review, we focus on collagen metabolism in drug-induced gingival overgrowth, focusing on the regulation of collagen phagocytosis in fibroblasts. (Keyword) drug-induced gingival overgrowth / collagen phagocytosis / α2β1 integrin / type I collagen / fibroblast (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.28.1817 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16204928 ● Search Scopus @ Elsevier (PMID): 16204928 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.28.1817 (DOI: 10.1248/bpb.28.1817, PubMed: 16204928)

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.	Yumi Kuwamura, Masuko Sumikawa, Eijiro Sakamoto, Ineko Takikawa, Hikari Yamako, Hirokazu Uemura, Sachi Kishida, Toshihiko Nagata and Munehide Matsuhisa : Nurses' Implementation and Opinion of Assessment of Oral Health Behavior in Patients with Diabetes, Journal of Diabetes Investigation, Vol.8, No.Supplement S1 May, 50, Nagoya, May 2017. (Keyword) Nurse / oral health behaviors / diabetes
3.	Yuka Hiroshima, Eijiro Sakamoto, Kaori Abe, Kaya Yoshida, Koji Naruishi, Toshihiko Nagata, Yasuo Shinohara, Geczy Carolyn and Jun-ichi Kido : Advanced Glycation End-Products Increase Calprotectin in Human Gingival Epithelial Cells, The 95th General Session & Exhibition of the International Association for Dental Research (IADR), San Francisco, Mar. 2017.
4.	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
5.	Jung-Hwan Lew, Koji Naruishi, Yukari Kajiura, Yasufumi Nishikawa, Jun-ichi Kido and Toshihiko Nagata : High glucose enhances IL-6-induced protease production in gingival fibroblasts, 94th General Session & Exhibition, International Association for Dental Research, Seoul, Jun. 2016.
6.	Yasufumi Nishikawa, Koji Naruishi, Yukari Kajiura, Jung-Hwan Lew, Jun-ichi Kido and Toshihiko Nagata : Calprotectin induced the expression of inflammation-related molecules in gingival fibroblasts, 94th General Session & Exhibition, International Association for Dental Research, Seoul, Jun. 2016.
7.	Yukari Kajiura, Koji Naruishi, Yukiko Nakajima, Yasufumi Nishikawa, Jung-Hwan Lew, Jun-ichi Kido and Toshihiko Nagata : High glucose enhaces P. gingivalis-induced cytokine production in THP-1 monocytes, 94th General Session & Exhibition, International Association for Dental Research, Seoul, Jun. 2016.
8.	Syotaro Yoshioka, Yoshiteru Tada, Junichiro Satomi, Kenji Yagi, Koji Naruishi, Kazuyuki Kuwayama, Keiko Kitazato, Takeshi Miyamoto, Yasuhisa Kanematsu, Masafumi Harada, Toshihiko Nagata and Shinji Nagahiro : Impact of Periodontal Disease and Bacteria on Intracranial Aneurysms, International Stroke Conference 2016, Los Angeles, Feb. 2016.
9.	Masami Ninomiya, Keiji Oishi, Hashimoto Mari, Koji Naruishi, Yamanouchi Kouji, Fukumura Yoshiaki and Toshihiko Nagata : A Cross-Sectional Study on the Severity of Periodontitis in Infective Endocarditis Patients, 11th Asian Pacific Society of Periodontology Meeting, Oct. 2015. (Keyword) infective endocarditis / periodontitis / bone resorption / serum antibody titer / epidemiology
10.	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.
11.	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.
12.	Hiromi Murata, H Maeda, S Takashiba, Jun-ichi Kido and Toshihiko Nagata : Screening of novel factors for TNF-a expression in LPS-stimulated macrophages., 93rd General Session & Exhibition of the IADR, Mar. 2015.
13.	Koji Naruishi and Toshihiko Nagata : HGFs-macrophage crosstalk: sIL-6R secretion in THP-1 macrophages, 62th Annual Meeting of Japanese Association for Dental Reserch Abstract, Dec. 2014.
14.	Toshihiko Nagata : Diabetes-associated periodontitis and biomarkers., The Tomas Van Dyke Symposium on Periodontal Medicine, Howard Plaza Hotel Taipei, Taipei, Feb. 2014. (Keyword) diabetes / periodontitis / diagnosis
15.	Toshihiko Nagata : The relationship between periodontitis and diabetes and the diagnosis of diabetes-asociated periodontitis., 2013 Special Lecture The 53rd General Session of Korean Academy of Periodontology, Seoul, Nov. 2013. (Keyword) diabetes / periodontitis / diagnosis
16.	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.
17.	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.
18.	Toshihiko Nagata : The close relationship between periodontitis and diabetes and the diagnosis of diabetes-associated periodontitis, 10th Asian Pacific Society of Periodontology, 21, Sep. 2013. (Keyword) periodontitis / diabetes
19.	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.
20.	Hiromi Murata, Masami Ninomiya, Takashiba Shogo, Maeda Hiroshi, Jun-ichi Kido and Toshihiko Nagata : A major neurodegenerative disease protein TDP-43 enhances TNF- transcriptional regulation in human monocyte-derived macrophage-like cells, 10th Asian Pacific Society of Periodontology Meeting, 42, Sep. 2013.
21.	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.
22.	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.
23.	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.
24.	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.
25.	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.
26.	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.
27.	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.
28.	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.
29.	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.
30.	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.
31.	Masami Ninomiya, Satoshi Yoneda, Jun-ichi Kido and Toshihiko Nagata : Successful periodontal regeneration by FGF2. -A long-term follow-up case report-, The 96th Annual Meeting of American Academy of Periodontology in collaboration with the Japanease Society of Periodontology, USA, Hawaii, Oct. 2010.
32.	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.
33.	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.
34.	Mika Bando, Jun-ichi Kido, Yuka HIroshima, Hiroyuki Iwasaka, Keisuke Yamada, Toshiyuki Nanbu, Masatoshi Kataoka and Toshihiko Nagata : Analysis of proteins in gingival crevicular fluid by mass spectrometry, 88th General Sesseion & Exhibition of the International Association for Dental Research, Spain, Jul. 2010.
35.	Purevjav Javkhlan, Yuka Hiroshima, Azlina Ahmad, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Jun-ichi Kido, Toshihiko Nagata and Kazuo Hosoi : Induction of calprotectin mRNAs by lipopolysaccharide in the salivary gland of mice, The Journal of Medical Investigation : JMI, Vol.56, No.Suppl, 287-289, Tokushima, Dec. 2009. (Summary) Calprotectin is a major cytosolic calcium-binding protein of leukocytes which belongs to the S100 protein family. S100A8 and S100A9, major types of calprotectin are heterodimeric complexes being composed of light- and heavy-chain subunits. The calprotectin levels in the plasma, feces, synovial fluid, gingival crevicular fluid, dental calculus and saliva change when the host animal suffers from several inflammatory diseases. Members of Toll-like receptor (TLR) family are pattern-recognition receptors for lipopolysaccharide (LPS) and other pathogens. Here we examined if the biological role of TLR receptor is reflected to the calprotectin expression in the salivary gland. Time course study by using real-time RT-PCR detected higher levels of S100A8 and S100A9 mRNA at 1.5-3 h after injection of LPS in both the submandibular gland (SMG) and parotid gland (PG) of C3H/HeN mice but not in the same tissues of C3H/HeJ, a TLR-4 mutant strain, indicating that this induction is mediated via the TLR-4. These results indicate that, an inflammatory marker, calprotectin, is expressed in the mouse salivary gland and that LPS stimulated its synthesis. Calprotectin (S100A8/A9) showed minimum expression in all cellular segments in the SMG except excretory duct cells, which showed strong signal at the cytoplasm. LPS induced their expressions in the granular convoluted tubular cells and striated duct cells. In the PG, these proteins were expressed very weakly in both duct and acinar cells with a little stronger staining for the former cells. LPS injection induced calprotectin (S100A8/A9) in both duct and acinar cells especially in the former cells. (Keyword) Animals / Calgranulin A / Calgranulin B / Leukocyte L1 Antigen Complex / Lipopolysaccharides / Mice / Mice, Inbred C3H / Mice, Mutant Strains / Parotid Gland / RNA, Messenger / salivary glands / Submandibular Gland / Toll-Like Receptor 4 (Tokushima University Institutional Repository) ● Metadata: 111354 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.56.287 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20224205 ● Search Scopus @ Elsevier (PMID): 20224205 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.56.287 (Tokushima University Institutional Repository: 111354, DOI: 10.2152/jmi.56.287, PubMed: 20224205)
36.	Hiroaki Tanaka, Hirohiko Okamura, Kaya Yoshida, Toshihiko Nagata and Tatsuji Haneji : Phosphorylation of p65NF-kB and degradation of IkB in Calyculin-A-induced apoptotic cells, The 2nd international symposium on and workshop ''The Future Direction of Oral Sciences in the 21st century'' -Oral Sciences for Our Healthy Life-, Tokushima, Japan, Dec. 2007.
37.	Hiroaki Tanaka, Kaya Yoshida, Hirohiko Okamura, Toshihiko Nagata and Tatsuji Haneji : Phosphorylation of NF-kB in calyculin A-induced apoptotic cells, 21st International Association for Dental Research - South East Asia Division, Bali, Indonesia, Sep. 2007.
38.	Hiroaki Tanaka, Hirohiko Okamura, Kaya Yoshida, Toshihiko Nagata and Tatsuji Haneji : Calyculin A induces apoptosis and phosphorylation of p65NF-kB, The 1st international symposium and workshop ''The Future Direction of Oral Sciences in the 21st century'', Awajishima, Mar. 2007.
39.	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.
40.	Akiko Yamada, Takenori Yamamoto, Masatoshi Kataoka, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Induction of Permeability Transition in Yeast Mitochondria Causes Release of Mitochondrial Cytochrome c, 45th American Society for Cell Biology Annual Meeting, San Francisco, Dec. 2005.
41.	Kaya Yoshida, Hiroyuki Shinohara, (名) Suryono, Tatsuji Haneji and Toshihiko Nagata : Inhibition of osteoblastic differentiation by arachidonic acid treatment through increase of prostaglandin E2 in MC3T3-E1 cells, The 1st Joint Meeting of the International Bone and Mineral Society, Osaka, Jun. 2003.

Proceeding of Domestic Conference:

1.	Takekawa Kaori, Masami Ninomiya, Toshihiko Nagata and Hiromichi Yumoto : A case report of initial periodontal therapy for severe drug-induced gingival overgrowth with cardiovascular disease, Journal of the Japanese Association of Periodontology, Vol.60, 162, Jun. 2018. (Keyword) Drug-induced gingival overgrowth / Initial periodontal therapy / Cardiovascular disease
2.	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.
3.	Chie Wada -Mihara, Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : 降圧薬由来の歯肉増殖を伴う重度歯周炎患者に対する歯周治療の効果, 日本歯周病学会中国四国3大学・日本臨床歯周病学会中国四国支部合同研修会, Nov. 2017. (Keyword) Antihypertensive drug / Drug-induced gingival hyperplasia / periodontitis
4.	Yukari Kajiura, Masami Ninomiya, Ikuta Takahisa, HWAN JUNG LEW, Jun-ichi Kido and Toshihiko Nagata : A case report of radicular cysts in maxillary both lateral incisors, 日本歯科保存学会2017年度秋季学術大会(第147回), Oct. 2017. (Keyword) Radicular cyst / Chronic apical periodontitis / Cystectomy / multiple
5.	Yumi Kuwamura, Eijiro Sakamoto, 澄川真珠子, 大和光, 瀧川稲子, Hiromi Murata and Toshihiko Nagata : DiOHAT(Diabetes Oral Health Assessment Tool for Nurses)臨床版を用いた看護アセスメント結果の実態, The Journal of Japan Academy of Diabetes Education and Nursing, Vol.21, 119, Sep. 2017.
6.	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
7.	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.
8.	小林哲夫, Jun-ichi Kido, 石原裕一, 大森一弘, 三谷章雄, 高柴正悟, Toshihiko Nagata and 吉江弘正 : 歯周炎と全身疾患(糖尿病・関節リウマチ)に共通するリスク遺伝子の解析, 第60回春季日本歯周病学会学術大会, May 2017.
9.	Masami Ninomiya, Yukari Kajiura and Toshihiko Nagata : A case report of comprehensive periodontal treatment of severe drug-induced gingival overgrowth with malaligned teeth, 日本歯周病学会雑誌, Vol.59, 158, May 2017. (Keyword) drug-induced gingival overgrowth / calcium channel blocker
10.	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
11.	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.
12.	Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : Long-term follow-up case reports for over 10-year after periodontal regeneration by FGF-2, The Journal of the Japan Dental Association, Vol.69, No.5, 137, Oct. 2016. (Keyword) fibroblast growth factor 2 / periodontal regeneration / long-term follow-up case
13.	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.
14.	Chie Wada -Mihara, Jun-ichi Kido and Toshihiko Nagata : A case report of severe periodontitis with tooth movement induced by gingival overgrowth, Journal of the Japanese Association of Periodontology, Vol.58, No.9, 145, Oct. 2016.
15.	Mika Bandou, Yukari Kajiura, 野中康平, Eijiro Sakamoto, Koji Naruishi, Jun-ichi Kido and Toshihiko Nagata : 最終糖化産物はヒト歯肉線維芽細胞におけるIL-6およびICAM-1の発現を増加する, 第59回秋季日本歯周病学会学術大会, Oct. 2016.
16.	Yuka Hiroshima, Jun-ichi Kido, Eijiro Sakamoto, 阿部佳織, Kaya Yoshida, Toshihiko Nagata and Yasuo Shinohara : 最終糖化産物はヒト歯肉上皮細胞におけるS100A8およびS100A9発現を上昇する, 第59回秋季日本歯周病学会学術大会, Oct. 2016.
17.	Yumi Kuwamura, 澄川真珠子, 瀧川稲子, 大和光, Eijiro Sakamoto and Toshihiko Nagata : 糖尿病口腔保健行動アセスメントシートDiOHAT実用版の臨床使用の試みと実用化に向けた課題, The Journal of Japan Academy of Diabetes Education and Nursing, Vol.20, No.Sep., 145, Sep. 2016. (Keyword) diabetes mellitus / oral health behaviors / nursing / assessment
18.	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.
19.	西川泰史, Koji Naruishi, Yukari Kajiura, Jung-Hwan Lew, Jun-ichi Kido and Toshihiko Nagata : カルプロテクチンはヒト歯肉線維芽細胞のTLR4を介して炎症性関連因子の発現を亢進する, 第144回日本歯科保存学会春季学術大会, Jun. 2016.
20.	Yukari Kajiura, Masami Ninomiya, Kono Kaoru and Toshihiko Nagata : The evaluation of periodontal pathogens in a patient with localized aggressive periodontitis which progressed after the childbirth, Journal of the Japanese Association of Periodontology, Vol.58, 161, May 2016. (Keyword) aggressive periodontitis / bacteriological examination / serum antibody titer / periodontal surgery
21.	Jung-Hwan Lew, Koji Naruishi, Yukari Kajiura, 西川泰史, Jun-ichi Kido and Toshihiko Nagata : カロテノイドは高グルコース下で培養したヒト歯肉線維芽細胞のIL-6誘導性タンパク分解酵素産生を抑制する, 第59回春季日本歯周病学会学術大会, May 2016.
22.	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.
23.	Yuka Hiroshima, Jun-ichi Kido, Kaya Yoshida, Kaori Abe, Yasuo Shinohara and Toshihiko Nagata : Hypoxic condition down-regulates S100A8 expression in human oral epithelial cells, 第59回春季日本歯周病学会学術大会, May 2016.
24.	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.
25.	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.
26.	吉岡正太郎, Yoshiteru Tada, Kazuyuki Kuwayama, Kenji Yagi, Junichiro Satomi, 宮本健志, 北里慶子, Koji Naruishi, Toshihiko Nagata, Masafumi Harada and Shinji Nagahiro : 歯周病の重症度および原因菌は脳動脈瘤の発生と破裂に関与する, 一般社団法人日本脳神経外科学会第74回学術総会, Oct. 2015.
27.	Hashimoto Mari, Masami Ninomiya, Tetsuya Kitagawa and Toshihiko Nagata : 感染性心内膜炎の既往のある慢性歯周炎患者に対して歯周治療によりQOL向上を図った症例, 日本歯周病学会中国四国3大学・日本臨床歯周病学会中国四国支部合同研修会, Oct. 2015. (Keyword) Infective endocarditis / periodontitis / Periodontal bacteria / Serum antibody titer
28.	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.
29.	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.
30.	Koji Naruishi, Yukari Kajiura, 西川泰史, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : 培養歯肉線維芽細胞におけるクリプトタンシノンによる炎症関連分子の生産抑制効果, 第142回日本歯科保存学会春季学術大会, Jun. 2015.
31.	Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液中のバイオマーカーを用いた歯周病診断(臨床教育講演), 四国歯学会第47回例会, Jun. 2015.
32.	Yumi Kuwamura, 澄川真珠子, Hiromi Murata, 瀧川稲子, 大和光, 石田伸子, 菊井聡子, Yasuhiro Hamada, Hirokazu Ito, Yuko Yasuhara, Daisuke Hinode, Hirokazu Uemura, Ken-ichi Aihara, Munehide Matsuhisa, Tetsuya Tanioka and Toshihiko Nagata : 多職種協働での糖尿病患者の口腔保健行動支援:口腔保健行動を査定するための査定シート案についての糖尿病看護の専門家の評価と実施状況, Journal of the The Japan Diabetes Society, Vol.58, No.supplement 1, S290, May 2015. (Keyword) diabetes / oral health behaviors / nursing
33.	Masami Ninomiya, Hashimoto Mari and Toshihiko Nagata : A case report that improved the quality of life by comprehensive periodontal treatment for a hemodialysis patient with severe chronic periodontitis, 第58回春季日本歯周病学会学術大会, Vol.57, No.May, 139, May 2015. (Keyword) Renal failure / Hemodialysis / Chronic periodontitis
34.	西川泰史, Koji Naruishi, Yukari Kajiura, Mika Bandou, Jun-ichi Kido and Toshihiko Nagata : カルプロテクチンがヒト歯肉線維芽細胞の炎症関連因子の発現に及ぼす影響, 第58回春季日本歯周病学会学術大会, May 2015.
35.	Jun-ichi Kido, Toshihiko Nagata, Koji Naruishi, 多部田康一, 山崎和久, 吉江弘正, 渡邊久, 和泉雄一, 須田玲子, 山本松男, 柴秀樹, 栗原英見, 柳田学, 北村正博, 三島昭宏, 水野光春 and 村上伸也 : イムノクロマト法を用いた歯肉溝滲出液中のカルプロテクチン測定による歯周病診断ー第2報ー, 第58回春季日本歯周病学会学術大会, May 2015.
36.	Masuda Yuri, Inagaki Koji, Masami Ninomiya, Kono Takayuki, Toshihiko Nagata and Mitani Akio : A team approach to a case of aggressive periodontitis with pregnancy, 第9回日本歯周病学会中部地区大学・日本臨床歯周病学会中部支部合同研究会, Nov. 2014. (Keyword) aggressive periodontitis / periodontal initial treatment / pregnancy / team approach
37.	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.
38.	Masami Ninomiya and Toshihiko Nagata : HIV/HCV重複感染血友病患者に対する包括的歯周治療によりQOL向上を図った一症例, 日本歯周病学会中国四国3大学・日本臨床歯周病学会中国四国支部合同研修会, Nov. 2014. (Keyword) HIV/HCV重複感染 / 血友病 / 包括的歯周治療 / ペリオドンタルメディシン
39.	Masami Ninomiya, Keiji Oishi, Hashimoto Mari, Koji Naruishi and Toshihiko Nagata : A Cross-Sectional Study on the Progression of Periodontitis in Infective Endocarditis Patients, 日本歯科保存学会 2014年度秋季学術大会(第141回), Oct. 2014. (Keyword) Infective Endocarditis / periodontitis / epidemiology
40.	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.
41.	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.
42.	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.
43.	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.
44.	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.
45.	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.
46.	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.
47.	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.
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 : 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.
49.	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.
50.	Hashimoto Mari, Masami Ninomiya and Toshihiko Nagata : A case report of chronic periodontitis with the history of infective endocariditis, Journal of the Japanese Association of Periodontology, Vol.56, 51, May 2014. (Keyword) Infective endocariditis / Chronic periodontitis / Serum antibody
51.	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.
52.	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.
53.	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.
54.	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.
55.	Hiromi Murata, Masami Ninomiya and Toshihiko Nagata : 侵襲性歯周炎患者に対して自家歯牙移植による咬合の回復を行った一症例, 日本歯周病学会第3回四国地区臨床研修会, 39, Apr. 2014. (Keyword) 侵襲性歯周炎 / 自家歯牙移植 / 歯周治療
56.	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.
57.	Masami Ninomiya and Toshihiko Nagata : A case report of generalized aggressive periodontitis in two sisters, 日本歯周病学会中国四国3大学・日本臨床歯周病学会中国四国支部合同研修会, Oct. 2013. (Keyword) Aggressive periodontitis / family / Comprehensive treatment / 細菌検査 / 血清抗体価検査
58.	小原真純, Eijiro Sakamoto, Tamotsu Tanaka, Jun-ichi Kido, Toshihiko Nagata and Akira Tokumura : 骨髄幹細胞から骨芽細胞への分化におけるリゾホスファチジン酸およびその産生酵素の役割, 第52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, Oct. 2013.
59.	小原真純, 坂本英次郎, Tamotsu Tanaka, Jun-ichi Kido, Toshihiko Nagata and Akira Tokumura : 骨髄幹細胞から骨芽細胞への分化におけるリゾホスファチジン酸およびその産生酵素の役割, 第52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, Oct. 2013.
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.	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.
62.	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.
63.	Hiromi Murata, 前田博史, 高柴正悟, Jun-ichi Kido and Toshihiko Nagata : 神経変性疾患関連因子TDP-43は単球におけるLPS誘導性TNF-a転写調節に関与する, 第56回秋季日本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.	Jun-ichi Kido, Toshihiko Nagata, 多部田康一, 山崎和久, 吉江弘正, 渡辺久, 和泉雄一, 須田玲子, 山本松男, 柴秀樹, 栗原英見, 柳田学, 北村正博, 南部敏之, 水野光春 and 村上伸也 : イムノクロマト法を用いた歯肉溝滲出液中のカルプロテクチン測定による歯周病診断, 第56回秋季日本歯周病学会学術大会, Sep. 2013.
66.	Hiromi Murata, 生田貴久, Jun-ichi Kido and Toshihiko Nagata : 神経変性疾患関連因子TDP-43はマクロファージ様細胞のTNF-a転写調節に関与する, 第138回日本歯科保存学会春季学術大会, Jun. 2013.
67.	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.
68.	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.
69.	Masami Ninomiya, Mika Bandou, Hiromi Murata, Takahisa Ikuta, Jun-ichi Kido and Toshihiko Nagata : A case report of comprehensive periodontal treatments for generalized aggressive periodontitis in two sisters, Journal of the Japanese Association of Periodontology, Vol.55, Jun. 2013. (Keyword) Aggressive periodontitis / family / Periodontal Treatment
70.	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.
71.	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.
72.	Keiji Oishi, 詫間俊夫, Satoshi Yoneda and Toshihiko Nagata : 臼歯部インプラントの頬側歯槽骨及び軟組織の形態変化∼前向き臨床研究∼ (第3報), 日本歯周病学会会誌第56回秋季学術大会特別号, Vol.55, 113, May 2013.
73.	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.
74.	Toshihiko Nagata : 糖尿病と歯周病糖尿病関連歯周炎の病態と診断糖尿病学会シンポジウム19「新たに注目される糖尿病関連疾患」, 第56回日本糖尿病学会年次学術集会(熊本), May 2013.
75.	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.
76.	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.
77.	Masami Ninomiya and Toshihiko Nagata : A long-term follow-up case report of drug-induced gingival overgrowth appeared in a renal transplant recipient, 日本歯科保存学会2012年度秋季学術大会(第137回), 135, Nov. 2012. (Keyword) Drug-induced gingival overgrowth / Renal transplant / Cyclosporin
78.	伊藤弘, 沼部幸博, 関野愉, 村樫悦子, 井口一美, 戸円智幸, 橋本修一, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性 -歯周病迅速診断キット開発に向けて-(第六報), 日本歯科保存学雑誌第137回秋季学術大会講演抄録集, 65, Nov. 2012.
79.	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.
80.	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.
81.	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.
82.	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.
83.	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.
84.	Keiji Oishi, 詫間俊夫, Satoshi Yoneda and Toshihiko Nagata : 臼歯部インプラントの頬側歯槽骨及び軟組織の形態変化∼前向き臨床研究∼ (第2報), 日本歯周病学会会誌第55回秋季学術大会特別号, Vol.54, 82, Sep. 2012.
85.	福本善和, Masumi Horibe, Keiji Oishi and Toshihiko Nagata : 象牙質知覚過敏と歯肉退縮の関連についての臨床疫学研究(第2報), 日本歯周病学会会誌第55回秋季学術大会特別号, Vol.54, 82, Sep. 2012.
86.	伊藤弘, 関野愉, 村樫悦子, 井口一美, 橋本修一, 沼部幸博, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性-歯周病迅速診断キット開発に向けて-(第五報), 日本歯周病学会会誌第55回学術大会秋季特別号, Vol.54, 83, Sep. 2012.
87.	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.
88.	Tomoko Azuma, 東秀樹, Masami Ninomiya and Toshihiko Nagata : A case report of periodontal surgery and orthodontic therapy for severe chronic periodontitis with flared anterior teeth, Journal of the Japanese Association of Periodontology, Vol.54, Sep. 2012. (Keyword) Severe periodontitis / Periodontal surgery / Orthodontic therapy
89.	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.
90.	Masami Ninomiya, Ikuta Takahisa and Toshihiko Nagata : A Case Report of Expanded Radicular Cyst in Mandible Anterior Teeth, 日本歯科保存学会 2012年度春季学術大会(第136回), Jun. 2012. (Keyword) Radicular Cyst / Biopsy / 嚢胞摘出術
91.	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.
92.	薫廣瀬, Masami Ninomiya and Toshihiko Nagata : Oral care management of a mentally retarded patient with the history of infective endocarditis, Journal of the Japanese Association of Periodontology, Vol.54, May 2012. (Keyword) Infective endocarditis / Mentally retarded patient / Periodontal initial therapy
93.	Hiromi Murata, Masami Ninomiya and Toshihiko Nagata : A successful case of autotransplantation and flap surgery performed to generalized aggressive periodontitis, Journal of the Japanese Association of Periodontology, Vol.54, May 2012. (Keyword) Aggressive periodontitis / Autotransplantation / Periodontal surgery
94.	Yuka Hiroshima, Mika Bandou, Masatoshi Kataoka, Jun-ichi Kido and Toshihiko Nagata : ヒト口腔上皮細胞のカルプロテクチン発現に及ぼす半夏瀉心湯の影響, 日本歯周病学会会誌第55回春季学術大会特別号, Vol.54, 131, May 2012.
95.	伊藤弘, 関野愉, 村樫悦子, 井口一美, 橋本修一, 沼部幸博, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡辺久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性 -歯周病迅速診断キット開発に向けて-(第四報), 日本歯周病学会会誌第55回春季学術大会特別号, Vol.54, 126, May 2012.
96.	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.
97.	畑中加珠, 安田多賀子, 福家教子, Jun-ichi Kido, Keiji Oishi, 田中敬子, 須田智也, 佐保輝之, 市川朋生, 鈴木丈一郎, 八島章博, 橘亜希, Toshihiko Nagata, 和泉雄一, 村上伸也, 五味一博 and 高柴正悟 : SPT期間中の歯周組織の維持・改善に対する塗布用ブラシ一体型一般用歯周病薬(MC2)の多施設臨床試験, 日本歯周病学会会誌第55回春季学術大会特別号, Vol.54, 130, May 2012.
98.	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
99.	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
100.	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
101.	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.
102.	中島由紀子, 稲垣裕司, Mika Bandou, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 最終糖化産物(AGEs)がラット培養歯髄細胞の石灰化物形成と抗菌ペプチド発現に及ぼす影響, 日本歯科保存学会雑誌第135回秋季学術大会プログラム, 46, Oct. 2011.
103.	伊藤弘, 沼部幸博, 関野愉, 村樫悦子, 井口一美, 橋本修一, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性-歯周病迅速診断キット開発に向けて- 第二報, 日本歯周病学会会誌秋季特別号, Vol.53, 107, Sep. 2011.
104.	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.
105.	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.
106.	Mika Oishi, Chihiro Shinohara, Takahisa Ikuta and Toshihiko Nagata : The case report Cowden disease with multiple papillomas in mouth, 第54回日本歯周病学会秋季学術大会, Sep. 2011.
107.	Masami Ninomiya and Toshihiko Nagata : A case report of comprehensive treatment focusing on initial periodontal therapy for a patient with hemophilia B and HIV/HCV co-infection, Journal of the Japanese Association of Periodontology, Vol.53, 139, Sep. 2011. (Keyword) HIV/HCV co-infection / hemophilia / periodontal disease
108.	詫間俊夫, Keiji Oishi and Toshihiko Nagata : 臼歯部インプラントの頬側歯槽骨及び軟組織の形態変化前向き臨床研究, Journal of the Japanese Association of Periodontology, Vol.53, 103, Sep. 2011. (Keyword) *歯科インプラント
109.	福本善和, Masumi Horibe, Keiji Oishi and Toshihiko Nagata : 象牙質知覚過敏と歯肉退縮の関連についての臨床疫学研究, Journal of the Japanese Association of Periodontology, Vol.53, 104, Sep. 2011. (Keyword) *歯肉後退(合併症)
110.	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.
111.	美原智恵, Jun-ichi Kido, Satoshi Yoneda, Yuka Hiroshima, Hiroyuki Seto and Toshihiko Nagata : 上顎前歯の著しいフレアアウトを伴った薬物性歯肉増殖症の一症例, 日本歯周病学会会誌春季特別号, Vol.53, 139, May 2011. (Keyword) periodontitis / 薬物性歯肉増殖症
112.	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
113.	伊藤弘, 関野愉, 村樫悦子, 井口一美, 沼部幸博, 橋本修一, 佐々木大輔, 八重柏隆, 國松和司, 高井英樹, 目澤優, 小方頼昌, 渡邊久, 萩原さつき, 和泉雄一, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : 歯肉溝滲出液(GCF)を用いた歯周病罹患部位の診断と治療効果のモニタリングの有用性 -歯周病迅速診断キット開発に向けて- 第1報, 日本歯周病学会会誌春季特別号, Vol.53, 121, May 2011.
114.	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
115.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Masatoshi Kataoka and Toshihiko Nagata : ヒト口腔上皮細胞におけるカルプロテクチン発現に及ぼす半夏瀉心湯の影響, 日本歯周病学会会誌春季特別号, Vol.53, 114, May 2011. (Keyword) periodontitis / 口腔上皮細胞 / 半夏瀉心湯 / カルプロテクチン
116.	Masumi Horibe, Keiji Oishi, Jun-ichi Kido and Toshihiko Nagata : 歯周病治療によってHbA1cが改善した2症例, 日本糖尿病学会第54回年次学術集会プログラム, 150, May 2011.
117.	Chie Wada -Mihara, Jun-ichi Kido, Satoshi Yoneda, Yuka Hiroshima, Hiroyuki Seto and Toshihiko Nagata : 上顎前歯の著しいフレアアウトを伴った薬物性歯肉増殖症患者の一症例, Journal of the Japanese Association of Periodontology, May 2011.
118.	Masumi Horibe, Keiji Oishi, Jun-ichi Kido and Toshihiko Nagata : 歯周病治療によってHbA1cが改善した2症例, Journal of the The Japan Diabetes Society, Vol.54, No.Suppl.1, S-353, Apr. 2011. (Keyword) Glycosylated Hemoglobin A
119.	Yuka Sogawa, Masami Ninomiya, Tomoko Azuma and Toshihiko Nagata : 急性骨髄性白血病の骨髄移植後に発症した移植片対宿主病患者に対し口腔衛生管理を行った一症例, 日本歯周病学会雑誌, Vol.53, 149, Apr. 2011. (Keyword) 急性骨髄性白血病 / 移植片対宿主病(GVHD) / 口腔衛生管理
120.	Eijiro Sakamoto, Masami Ninomiya, Satoshi Yoneda, Tokunaga Kaku, Nakajima Yukiko, Javkhlan Purevjav, Takeda Yoko, Takemura Akane and Toshihiko Nagata : Inhibitory Effects of L-Cysteine on Alveolar Bone Resorption in Hamster Experimental Periodontitis, Shikoku Dental Research, Vol.23, No.2, 141, Jan. 2011. (Keyword) periodontal disease / L-Cysteine / Alveolar Bone
121.	Sakamoto Eijiro, Masami Ninomiya, Satoshi Yoneda, Tokunaga Kaku, Nakajima Yukiko, Javkhlan Purevjav, Takeda Yoko, Takemura Akane and Toshihiko Nagata : Inhibitory Effects of L-Cysteine on Alveolar Bone Resorption in Hamster Experimental Periodontitis, Shikoku Dental Research, Vol.23, No.2, 141, Jan. 2011. (Keyword) periodontal disease / L-Cysteine / Alveolar Bone
122.	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.
123.	Purevjav Javkhlan, Yuka Hiroshima, Ahmad Azlina, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Toshihiko Nagata and Kazuo Hosoi : Calprotectin expression in the mouse salivary gland: Induction by lipopolysaccharide, 第52回歯科基礎医学会(2010年9月20-22日), Sep. 2010.
124.	Eijiro Sakamoto, 美原智恵, 徳永格, 瀬戸浩行, 廣島佑香, Jun-ichi Kido and Toshihiko Nagata : ラット実験的歯周炎におけるオステオプロテジェリンの影響, 第53回日本歯周病学会秋季学術大会(高松), Sep. 2010.
125.	浅原洋士, Keiji Oishi, Jun-ichi Kido and Toshihiko Nagata : II型糖尿病コントロール不良を伴った重度慢性歯周炎患者の治療例, Journal of the Japanese Association of Periodontology, Vol.52, 120, Sep. 2010.
126.	坂本英次郎, 美原智恵, 徳永格, 瀬戸浩行, 廣島佑香, Jun-ichi Kido and Toshihiko Nagata : ラット実験的歯周炎におけるオステオプロテジェリンの影響, 第53回日本歯周病学会秋季学術大会(高松), Sep. 2010.
127.	Purevjav Javkhlan, Yuka Hiroshima, Ahmad Azlina, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Toshihiko Nagata and Kazuo Hosoi : Calprotectin expression in the mouse salivary gland: Induction by lipopolysaccharide, Journal of Oral Biosciences, Vol.52, No.supplement, 94, Sep. 2010.
128.	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.
129.	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.
130.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Eijiro Sakamoto, 中島由紀子, Masatoshi Kataoka and Toshihiko Nagata : Porphyromonas gingivalis由来LPSはヒト好中球からのレジスチンの遊離を促進する, 第53回春季日本歯周病学会学術大会, Vol.52, 105, May 2010.
131.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, 坂本英次郎, 中島由紀子, Masatoshi Kataoka and Toshihiko Nagata : Porphyromonas gingivalis由来LPSはヒト好中球からのレジスチンの遊離を促進する, 第53回春季日本歯周病学会学術大会, Vol.52, 105, May 2010.
132.	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.
133.	Masami Ninomiya, Satoshi Yoneda, 坂本英次郎, 中島由紀子, 徳永格, Javkhlan Purevjav, 竹田洋子, 江口徹, 武村あかね and Toshihiko Nagata : ハムスター実験的歯周炎モデルにおけるL-システインの歯槽骨吸収抑制効果, 日本歯科保存学会雑誌, Vol.53, 42, May 2010.
134.	Masami Ninomiya, Satoshi Yoneda and Toshihiko Nagata : A case report of comprehensive treatment with FGF-2 periodontal regenerative therapy and autotransplantation for chronic periodontitis, 日本歯周病学会雑誌, Vol.52, 132, May 2010. (Keyword) 慢性歯周炎 / 歯周組織再生療法 / 自家歯牙移植
135.	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
136.	Keiji Oishi, Masumi Horibe, Masami Ninomiya and Toshihiko Nagata : Usefulness of a new parameter "Total Bone Resorption" representing the severity of periodontal tissue breakdown: the association with the severity of diabetes, Journal of the Japanese Association of Periodontology, Vol.52, 119, Apr. 2010.
137.	Eijiro Sakamoto, Masami Ninomiya, Satoshi Yoneda, 徳永格, 中島由紀子, フルジャフジャフラン, Katsuhiko Hirota, Yoichiro Miyake, 竹田洋子, 武村あかね and Toshihiko Nagata : ハムスター実験的歯周炎におけるL-Cysteinの歯槽骨吸収抑制効果, 四国歯学会第36回例会, Mar. 2010.
138.	坂本英次郎, Masami Ninomiya, Satoshi Yoneda, 徳永格, 中島由紀子, フルジャフジャフラン, Katsuhiko Hirota, Yoichiro Miyake, 竹田洋子, 武村あかね and Toshihiko Nagata : ハムスター実験的歯周炎におけるL-Cysteinの歯槽骨吸収抑制効果, 四国歯学会第36回例会, Mar. 2010.
139.	Keiji Oishi and Toshihiko Nagata : 歯根尖切除術について, Shikoku Dental Research, Vol.22, No.2, 201-202, 2010. (Keyword) *歯根尖切除術
140.	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.
141.	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.
142.	Keiji Oishi, Yuka Hiroshima and Toshihiko Nagata : 著明な歯肉増殖を伴う慢性歯周炎患者の一症例, Journal of the Japanese Association of Periodontology, Vol.51, 106, Oct. 2009.
143.	Chie Wada -Mihara, 徳永格, 瀬戸浩行, 大場博史, Yuka Hiroshima, Jun-ichi Kido and Toshihiko Nagata : ラット実験的歯周炎におけるオステオプロテジェリンの骨吸収と炎症におよぼす効果, 第52回秋季日本歯周病学会学術大会, Vol.51, 93, Oct. 2009.
144.	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.
145.	Yuka Hiroshima, Mika Bandou, Jun-ichi Kido, Masatoshi Kataoka and Toshihiko Nagata : ヒト歯肉上皮細胞における抗菌ペプチド遺伝子発現のマイクロアレイ法による解析, 第52回秋季日本歯周病学会学術大会, Vol.51, 90, Oct. 2009.
146.	Jun-ichi Kido, Masatoshi Kataoka, 日野真美, Mika Bandou, Yuka Hiroshima and Toshihiko Nagata : 歯周病バイオマーカーのマイクロチップ基板を用いた測定と歯周病診断への応用, 第2回日本口腔検査学会, 28, Oct. 2009.
147.	Javkhlan Purevjav, Yuka Hiroshima, Ahmad Azlina, Takahiro Hasegawa, Chenjuan Yao, Tetsuya Akamatsu, Toshihiko Nagata and Kazuo Hosoi : Calprotectin induction by lipopolysaccharide in the salivary gland of mice, 第51回歯科基礎医学会, Sep. 2009.
148.	Jun-ichi Kido, Masatoshi Kataoka, Mika Bandou, Yuka Hiroshima, Chie Wada -Mihara and Toshihiko Nagata : マイクロチップ基板を用いたカルプロテクチンの測定‐歯周病診断法への応用の可能性について‐, 第52回春季日本歯周病学会学術大会, Vol.51, 114, May 2009.
149.	Keiji Oishi and Toshihiko Nagata : 根面被覆術について, Shikoku Dental Research, Vol.21, No.2, 428, 2009. (Keyword) *歯周療法
150.	下川洋介, Masumi Horibe, Keiji Oishi and Toshihiko Nagata : ステロイド剤長期服用患者に見られた象牙質知覚過敏症の一症例, The Japanese Journal of Conservative Dentistry, Vol.51, 121, Oct. 2008. (Keyword) *Prednisolone(治療的利用,毒性・副作用)
151.	Keiji Oishi, 徳永格, Satoshi Yoneda, Mika Oishi and Toshihiko Nagata : CTによって診断された歯根破折の一症例, The Japanese Journal of Conservative Dentistry, Vol.51, 154, Oct. 2008. (Keyword) *歯牙破折(X線診断,治療)
152.	Ruspita Ita, Keiko Miyoshi, Taro Muto, Taigo Horiguchi, Kaori Abe, Takafumi Noma and Toshihiko Nagata : A possible role of Sp6 in Amelogenesis, 「魅力ある大学院教育」イニシアティブ「21世紀の口腔科学が目指すべき方向性」, Dec. 2007.
153.	Takenori Yamamoto, Akiko Yamada, Naoshi Yamazaki, Kikuji Yamashita, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : シトクロムcと伴にミトコンドリアから放出されるタンパク質のプロテオーム解析, 第29回生体膜と薬物の相互作用シンポジウム, Nov. 2007.
154.	Kaori Abe, Keiko Miyoshi, Taro Muto, Taigo Horiguchi, Ruspita Intan, Toshihiko Nagata and Takafumi Noma : Redox regulation of amelogenin gene expression, 第49回歯科基礎医学学術大会, Aug. 2007.
155.	田中宏明, Hirohiko Okamura, Kaya Yoshida, Toshihiko Nagata and Tatsuji Haneji : カリクリンA 誘導アポトーシス細胞によおけるIkB の分解とNF-kB のリン酸化, 第49 回歯科基礎医学会総会, Aug. 2007.
156.	Keiji Oishi and Toshihiko Nagata : 下顎前歯に限局して生じた歯肉退縮の2症例について, Journal of the Japanese Association of Periodontology, Vol.49, 190, Apr. 2007. (Keyword) *下顎疾患
157.	Kaori Abe, Keiko Miyoshi, Taro Muto, Taigo Horiguchi, Ruspita Ita, Takafumi Noma and Toshihiko Nagata : MAPK activation via ROS induces amelognin expression in the ameloblast-lineage cells, 「魅力ある大学院教育」イニシアティブ「21世紀の口腔科学が目指すべき方向性」, 2007.
158.	Akiko Yamada, Takenori Yamamoto, Naoshi Yamazaki, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Differential protein release from mitochondria induced by Ca²⁺ and valinomycin as revealed by immunological and proteomics techniques, 第6回ミトコンドリア学会, Dec. 2006.
159.	Takenori Yamamoto, Akiko Yamada, masahiro watanabe, yuya yoshimura, Naoshi Yamazaki, Yoshiyuki Yoshimura, Takashi Yamauchi, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Expression levels of voltage-dependent anion channel (VDAC) isoforms in mitochondrial outer membrane revealed by immunological and proteomics techniques, 第28回生体膜と薬物の相互作用シンポジウム, Nov. 2006.
160.	Masahiro Asano, Keiji Oishi and Toshihiko Nagata : 原因不明の歯髄炎様疼痛および抜歯後疼痛が長期間持続した1症例, The Japanese Journal of Conservative Dentistry, Vol.49, 203, Oct. 2006. (Keyword) *歯髄炎(病因)
161.	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.
162.	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.
163.	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.
164.	Akiko Yamada, Takenori Yamamoto, Masatoshi Kataoka, Toshihiko Nagata, Hiroshi Terada and Yasuo Shinohara : Permeability transition induced in yeast mitochondria also causes release of cytochrome c from mitochondria, 第78回日本生化学会大会, Oct. 2005.
165.	大場博史, Hiroyuki Seto, 和田智恵, 濱秀樹, Masumi Horibe, Jun-ichi Kido and Toshihiko Nagata : ラット実験的歯周炎における乳塩基性タンパク質の歯槽骨吸収改善効果, 第48回秋季日本歯周病学会学術大会, Sep. 2005.
166.	和田智恵, Masumi Horibe, Hiroyuki Seto, Jun-ichi Kido and Toshihiko Nagata : サイクロスポリンAがラット歯槽骨骨代謝に及ぼす影響, 第48回秋季日本歯周病学会学術大会, Sep. 2005.
167.	Keiji Oishi and Toshihiko Nagata : 喫煙している慢性歯周炎患者に外科的歯周治療を行なった一症例, Journal of the Japanese Association of Periodontology, Vol.47, 241, Sep. 2005. (Keyword) 喫煙
168.	田中宏明, Hirohiko Okamura, Katsuhiko Hirota, 尾崎明子, Bruna Rabelo Amorim, Kaya Yoshida, 長宗秀明, Yoichiro Miyake, Toshihiko Nagata and Tatsuji Haneji : Streptococcus Intermedius由来毒素intermedilysin処理細胞におけるPTEN, Akt, 及びPDK-1の発現, 第47回歯科基礎医学会総会, Sep. 2005.
169.	Hideki Hama, Hideki Azuma, Hiroyuki Seto and Toshihiko Nagata : Effect of Enamel Matrix Derivative on Osteoblastic Differentiation of Rat Calvaria Cells in Culture, 2nd Joint Meeting of ECTS and IBMS, Jun. 2005.
170.	Hiroyuki Seto, Hiroshi Oba, Hideki Hama, Masumi Horibe and Toshihiko Nagata : Statin Induces Mineralized Tissue Formation in Cultured Rat Dental Pulp Cells, 2nd Joint Meeting of ECTS and IBMS, Jun. 2005.
171.	Chie Wada, Hiroyuki Seto and Toshihiko Nagata : Effects of Cyclosporine A on the Remodeling of alveoalr Bone in Rats, 2nd Joint Meeting of ECTS and IBMS, Jun. 2005.
172.	Masami Ninomiya and Toshihiko Nagata : Two Case Reports of Excessive Hypercementosis Associated with Chronie Apieal Periodontitis, 日本歯科保存学会2005年度春季学会(第122回), Vol.48, 197, Jun. 2005.
173.	Masami Ninomiya and Toshihiko Nagata : Two Case Reports of Autotransplantation Using Enamel Matrix Derivative, 日本歯科保存学会2004年度秋季学会(第121回), Vol.47, 228, Nov. 2004.
174.	Keiko Tsuji, Shinya Horiuchi, Masami Ninomiya, Toshihiko Nagata and Keiji Moriyama : A case of bilateral cleft lip and palate patient with osteoporosis treated by orthodonticperiodontic approach, 第63回日本矯正歯科学会大会, 302, Nov. 2004.
175.	Hiroyuki Seto, Masami Ninomiya, 和田智恵, 福本善和, 片岡正俊, Jun-ichi Kido and Toshihiko Nagata : Ca拮抗薬による歯肉増殖症の病態と治療, 第20回日本歯科医学会総会, Vol.57, No.4, 99, Oct. 2004.
176.	Tomoko Azuma, Masami Ninomiya, Hideki Azuma and Toshihiko Nagata : A case report of a tooth replantation using Emdogain Gel, 第47回秋季日本歯周病学会学術大会, 164, Oct. 2004. (Keyword) 再植 / エムドゲインゲル / 歯根膜
177.	Masami Ninomiya, Hiroyuki Seto, Jun-ichi Kido and Toshihiko Nagata : Phase \|\| Clinical Trial of Periodontal Regenerarion by KCB-1D(FGF-2), --- A Successful Case Report of Periodontal Regeneration by KCB-1D(FGF-2) ---, 第47回秋季日本歯周病学会学術大会, Oct. 2004. (Keyword) 塩基性線維芽細胞増殖因子(FGF-2) / 歯周組織再生 / 治験
178.	Keiji Oishi, Mika Oishi and Toshihiko Nagata : 培養ヘルトビッヒ上皮鞘細胞の形成する細胞外基質の検索, Journal of the Japanese Association of Periodontology, Vol.46, 81, Sep. 2004. (Keyword) *細胞外基質
179.	Hideki Hama, Hideki Azuma, Hiroyuki Seto, Masami Ninomiya, Keiji Oishi, Jun-ichi Kido and Toshihiko Nagata : エナメルマトリックス蛋白による骨芽細胞分化抑制作用および活性型TGF-βの関与, Journal of the Japanese Association of Periodontology, Vol.46, 114, May 2004. (Keyword) エナメルマトリックス蛋白 / osteoblast / differentiation / 活性型TGF-β
180.	Nobuyuki Kamata, Satoshi Tutumi, Yutaka Maruoka, Koichi Nakakuki, Masami Ninomiya, Yuji Kabasawa, Syunpei Yamada, Kazuto Kurohara, Ken Omura, Teruo Amagasa, Toshihiko Nagata, Masaru Nagayama and Mitsuo Itakura : 顎骨の骨およびセメント質形成病変における遺伝子変異検索, The 58th Annual Meeting of The Japanese Stomatological Society, 132, May 2004.
181.	Masahiro Asano, Keiji Oishi and Toshihiko Nagata : 大理石骨病を有する慢性歯周炎患者の1症例, Journal of the Japanese Association of Periodontology, Vol.46, 180, May 2004. (Keyword) *歯周炎(合併症)
182.	Masami Ninomiya, Jun-ichi Kido and Toshihiko Nagata : A Case Report of Cyclosporin A-induced Gingival Overgrowth Observed in a Patient with Aplastic Anemia, 日本歯科保存学会2003年度秋季学会(第119回), Vol.46, 206, Nov. 2003.
183.	Kaya Yoshida, Toshihiko Nagata and Tatsuji Haneji : アラキドン酸がプロスタグランジンE2合成経路に与える影響について, 第45回歯科基礎医学会総会, Sep. 2003.
184.	Tomoko Azuma, Gota Cho, Keizo Suzuki, Kaya Yoshida, Masumi Horibe, Teruo Nakamura, Masami Ninomiya, Keiji Oishi, Jun-ichi Kido and Toshihiko Nagata : 糖尿病性腎症患者の歯周病罹患に関する疫学的研究, Journal of the Japanese Association of Periodontology, Apr. 2003. (Keyword) 糖尿病性腎症 / 人工透析 / CPITN
185.	Masami Ninomiya and Toshihiko Nagata : A Case of the Patient with Malalignment Following Severe Nifedipine-induced Gingival Overgrowth, 第46回秋季日本歯周病学会学術大会, 170, Apr. 2003. (Keyword) ニフェジピン歯肉増殖症 / 歯周外科 / MTM
186.	Masami Ninomiya, Akane Takemura and Toshihiko Nagata : 骨代謝に視点をおいた歯周病治療薬の開発と展望, 第46回秋季日本歯周病学会学術大会, 47, Apr. 2003.
187.	Tae Usami, Masami Ninomiya and Toshihiko Nagata : A Study on the Surface Scratch of Ceramic Sharpening Stones, 第45回秋季日本歯周病学会学術大会, 215, Oct. 2002. (Keyword) セラミックストーン / シャープニング / 器具のメインテナンス
188.	Hirohiko Okamura, Kaya Yoshida, Hiroyuki Morimoto, Toshihiko Nagata, Seiichiro Kitamura and Tatsuji Haneji : 薬剤感受性の異なる口腔扁平上皮癌細胞におけるMDR1の発現と転写調節, 第44回歯科基礎医学会総会, Oct. 2002.
189.	Kaya Yoshida, Hirohiko Okamura, Toshihiko Nagata and Tatsuji Haneji : マウス骨芽細胞様細胞MC3T3-E1においてオカダ酸はRANKLの発現を促進する, 第44回歯科基礎医学会総会, Oct. 2002.
190.	Keiji Oishi, Mika Oishi, Jun-ichi Kido and Toshihiko Nagata : ヘルトビッヒ上皮鞘細胞と歯根膜細胞の共存培養における形質の変化, Journal of the Japanese Association of Periodontology, Vol.44, 128, Apr. 2002. (Keyword) 細胞
191.	Masami Ninomiya, Noriyuki Yamauchi, Jun-ichi Kido and Toshihiko Nagata : A case Report of Multiple Hypercementosis Observed in Whole Mandibular Teeth, 第44回秋季日本歯周病学会学術大会, 176, Oct. 2001. (Keyword) セメント質過形成 / 家族性疾患 / 骨系統疾患
192.	A Takemura, Masami Ninomiya, T ohba, K Kunikiyo, H Azuma, H Hama, (名) Suryono, H Shinohara, Jun-ichi Kido and Toshihiko Nagata : Effects of novel MMP inhibitor on experimental periodontitis in hamsters, 79th International Association for Dental Research(LADR), Jun. 2001.
193.	Nobuyuki Kamata, Masami Ninomiya, Tomoko Azuma, 藤本良一, Toshihiko Nagata and Masaru Nagayama : 智歯·埋伏歯の移植歯への応用, 四国歯学会第25回例会·第20回総会, Jun. 2001.
194.	Nobuyuki Kamata, Masami Ninomiya, 藤本良一, 友成真弓, Toshihiko Nagata and Masaru Nagayama : 智歯·埋伏歯の移植術へのエムドゲインの応用, 第55回日本口腔科学会総会, Apr. 2001.
195.	Keiji Oishi, M. Zeichner-David, Jun-ichi Kido and Toshihiko Nagata : ヘルトビッヒ上皮鞘細胞の分離培養とその性質, Journal of the Japanese Association of Periodontology, Vol.43, 98, Apr. 2001. (Keyword) エナメル質蛋白質
196.	Mika Oishi, Keiji Oishi, Jun-ichi Kido and Toshihiko Nagata : 上顎臼傍結節内にみられた歯髄腔の存在について, The Japanese Journal of Conservative Dentistry, Vol.41, 169, Oct. 1998. (Keyword) 過剰歯(病理学)
197.	池戸大, Keiji Oishi, 山内規進, Masatoshi Kataoka, Jun-ichi Kido and Toshihiko Nagata : フェニトインが骨芽細胞の分化に及ぼす影響, Journal of the Japanese Association of Periodontology, Vol.40, 113, Sep. 1998. (Keyword) Phenytoin(薬理学)
198.	Teruo Nakamura, Jun-ichi Kido, Reiko Kido, Keiji Oishi, Noriyuki Yamauchi, Masatoshi Kataoka and Toshihiko Nagata : Usefulness of Calprotectin as a Marker for Periodontal Disease Activity, Journal of the Japanese Association of Periodontology, Vol.40, No.0, 87, Apr. 1998. (Keyword) Calprotectin / 歯肉溝滲出液 / 歯周疾患活動性指標 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570291227392919808 (CiNii: 1570291227392919808)
199.	Dai Ikedo, Keiji Oishi, Teruo Nakamura, Jun-ichi Kido and Toshihiko Nagata : Role of Bone Sialoprotein in Osteoblasts : Supression of BSP Expression by Anti-senseDNA, Journal of the Japanese Association of Periodontology, Vol.39, No.0, 106, Sep. 1997. (Keyword) 骨シアロ蛋白 / osteoblast / アンチセンスDNA (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572261552228572288 (CiNii: 1572261552228572288)
200.	Keiko NAKANO, Noriyuki YAMAUCHI, Keiji Oishi, Masatoshi Kataoka, Jun-ichi Kido, Seiji Nishikawa and Toshihiko Nagata : The Effect of Prostagladin E_2 on the Mineralization in Cultured Fetal Rat Calvaria Cells, Journal of the Japanese Association of Periodontology, Vol.38, No.0, 111, Sep. 1996. (Keyword) プロスタグランディンE 2 / 骨原性細胞 / calcification (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573387452136227456 (CiNii: 1573387452136227456)
201.	Jun-ichi Kido, Noriyuki YAMAUCHI, Keiji Oishi, Seiji Nishikawa, Hiroshi ISHIDA, Toshihiko Nagata and Akemichi Ueno : Regulatory Factor on Osteoblastic Differentiation Derived from Human Prostatic Cancer Cells, Journal of the Japanese Association of Periodontology, Vol.38, No.0, 146, Mar. 1996. (Keyword) ヒト前立腺癌細胞 / 骨原性細胞 / 分化調節因子 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570854177345162240 (CiNii: 1570854177345162240)
202.	Jun-ichi Kido, Keiji Oishi, Noriyuki YAMAUCHI, Hiroyuki SHINOHARA, Seiji Nishikawa, Hiroshi ISHIDA and Toshihiko Nagata : Study of calcium binding proteins in dental calculus : Identifications of osteopontin and calprotectin, Journal of the Japanese Association of Periodontology, Vol.37, No.0, 102, Sep. 1995. (Keyword) 歯石 / osteopontin / カルプロテクチン (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570009752415932288 (CiNii: 1570009752415932288)
203.	Noriyuki YAMAUCHI, Keiji Oishi, Jun-ichi Kido, Seiji Nishikawa, Toshihiko Nagata, Hiroshi ISHIDA, Akemichi Ueno, Norio NONOMURA, Yasuyuki KOJIMA, Kouji MIKI and Akihiko OKUYAMA : Suppresive Factor on Osteoblastic Differentiation Dervied from Human Prostatic Tumor Cells, The Japanese Journal of Conservative Dentistry, Vol.38, No.0, 59, Sep. 1995. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1571135649334456704 (CiNii: 1571135649334456704)
204.	Keiji Oishi, 山内規進, Mika Oishi, Jun-ichi Kido, Seiji Nishikawa, 石田浩 and Toshihiko Nagata : レチノイン酸が骨芽細胞の分化に及ぼす影響細胞の分化段階で異なる作用について, Journal of the Japanese Association of Periodontology, Vol.37, 105, Sep. 1995. (Keyword) Retinoic Acid(薬理学)
205.	Noriyuki YAMAUCHI, Keiji Oishi, Seiji Nishikawa, Toshihiko Nagata, Hiroshi ISHIDA and Yoichi WAKANO : The relationship between changes in the number of parathyroid hormone(PTH) receptors and PTH action during osteoblastic differentiation in rat calvaria cells, Journal of the Japanese Association of Periodontology, Vol.36, No.0, 68, Sep. 1994. (Keyword) 骨原性細胞 / PTH受容体 / cell differentiation (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572543027206386048 (CiNii: 1572543027206386048)
206.	Keiji Oishi, 山内規進, Seiji Nishikawa, Toshihiko Nagata, 石田浩 and 若野洋一 : レチノイン酸がラット胎仔頭蓋冠由来骨原性細胞の分化に及ぼす影響について, The Japanese Journal of Conservative Dentistry, Vol.37, 70, Apr. 1994. (Keyword) Retinoic Acid(薬理学)
207.	Keiko KAHO, Noriyuki YAMAUTI, Keiji Oishi, Seiji Nishikawa, Toshihiko Nagata, Hiroshi ISHIDA and Yoichi WAKANO : Effect of prostaglandin E_2 on the formation of bone nodules in fetal rat calvarial cells in culture, Journal of the Japanese Association of Periodontology, Vol.35, No.0, 128, Sep. 1993. (Keyword) プロスタグランディンE 2 / 骨原性細胞 / 骨形成 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573950402089009024 (CiNii: 1573950402089009024)
208.	Keiji Oishi, 山内規進, Toshihiko Nagata, 石田浩 and 若野洋一 : 骨原性細胞の分化に及ぼす甲状腺ホルモンの影響, Journal of the Japanese Association of Periodontology, Vol.35, 94, Apr. 1993. (Keyword) 甲状腺ホルモン(薬理学)
209.	Keiji Oishi, 山内規進, Toshihiko Nagata, 石田浩 and 若野洋一 : ラット胎仔頭蓋骨由来骨芽細胞に対する甲状腺ホルモンの作用について, Japanese Journal of Bone and Mineral Metabolism, Vol.10, No.3, 348, Jul. 1992. (Keyword) 甲状腺ホルモン(薬理学)

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 and Toshihiko Nagata : 歯根側面に認められたX線透過像, DENTAL DIAMOND, Vol.37, No.5, 119-120, Apr. 2012. (Keyword) Root Flacture / diagnostic imaging
4.	Masami Ninomiya and Toshihiko Nagata : FGF-2による再生療法, 臨床歯科を語る会シンポジウム, Jul. 2011. (Keyword) FGF-2 / 歯周組織再生療法 / 治験
5.	Masami Ninomiya and Toshihiko Nagata : 口腔内全体にわたる歯肉のびらん, Dental Diamond, Vol.36, No.5, 139-140, Apr. 2011.
6.	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
7.	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.
8.	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)

Diagnosis of peri-implant diseases by cellular biomarkers and development of diagnostic device (Project/Area Number: 15K15767 )
Analysis of the disorder on cell function induced by advanced glycation end-product (AGE) in dental pulp, gingival and alveolar bone tissues (Project/Area Number: 15K15701 )
Role of periodontal disease in the rupture of intracranial aneurysms (Project/Area Number: 15K10305 )
Pathophysiology of diebetes-associated periodontitis and establishment of novel diagnosis system of diabetes-associated periodontitis (Project/Area Number: 15H05054 )
Development of the diabetes oral health assessment tool for nurses to help the patients with diabetes with their oral health behaviors simply (Project/Area Number: 26463305 )
Relationship of periodontal infection and inflammatory cytokine to the incidence of infective endocarditis (Project/Area Number: 26463135 )
Effect of pressure change and simulated microgravity on the expression of pain receptors in cultured dental pulp cells (Project/Area Number: 25670810 )
An analysis of shared risk cytokine gene for periodontitis, diabetes mellitus, and rheumatoid arthritis (Project/Area Number: 25253104 )
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 )
Study on the risk of infective endocarditis accompanied with the progression of periodontitis (Project/Area Number: 23593063 )
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 )
Development of the diagnostic method for periodontal diseases Using a microdevice to determine calprotectin (Project/Area Number: 21592625 )
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 )
Mail Medicine using Fingertip Plasma for Screening and Monitoring Periodontitis (Project/Area Number: 18209061 )
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 )
歯周病細菌に対する血清抗体価測定法の標準化に関する調査研究 (Project/Area Number: 17639021 )
α2 integrin +807 polymorphism in drug-induced gingival overgrowth (Project/Area Number: 16592068 )
Diagnostic approaches by a susceptibility determination based on gene polymorphism in Japanese periodontitis patients. (Project/Area Number: 16209062 )
Clinical research for relationship between periodontal disease and systemic disease (Project/Area Number: 15209071 )
歯周炎感受性における各種遺伝子多型の寄与率に関する総合研究の企画調査 (Project/Area Number: 14607021 )
Resolution of the wound healing mechanism of dertin-pulp complex and application of the knowledge on it to regenerative medicine (Project/Area Number: 14207082 )
全身疾患と歯周病罹患に関する疫学調査 (Project/Area Number: 13897019 )
ストレスが歯周病の危険因子であるかどうかの直接的証明 (Project/Area Number: 13877358 )
Study on pathogenesis and treatment of periodontal disease which is focused in bone metabolism (Project/Area Number: 13307059 )
発生工学に基づいた歯周組織再生療法の確立について (Project/Area Number: 12897020 )
腎透析患者におけるカルシウム代謝異常と歯周疾患罹患度との相関 (Project/Area Number: 11877367 )
Developmental trial of a diagnosis kit on the disease activity of alveolar bone resofptibn in periodontitis patients. (Project/Area Number: 11557168 )
Molecular biology of pathological conditions and diagnosis in dental pulp disorder and periodontal disease. (Project/Area Number: 10307047 )
Study of aging system in Pulpal and periodontal tissue (Project/Area Number: 09307042 )
Possibility of Prostaglandin E_2 as a drug for periodontal disease. (Project/Area Number: 07457458 )
骨原性細胞が合成するカルシウム結合性蛋白質とメチルチオアデノシン代謝との関連 (Project/Area Number: 04671163 )
Study of osteopontin synthesis and the expression during dentinogenesis (Project/Area Number: 03670893 )
Study of localization and significance of phospholipase A2 in periodontitis. (Project/Area Number: 03454442 )
Search by Researcher Number (10127847)

Professor Emeritus : Nagata, Toshihiko

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