Tokushima University / Educator and Researcher Directory --- Ozaki, Kazumi

Personal Web Page

https://researchmap.jp/read0017459 (researchmap)

Field of Study

○	Operative Dentistry, Periodontology

Subject of Study

○	象牙質齲蝕の発症機構に関する研究 (Streptococcus mutans, 齲蝕原性, 菌体内多糖)

Book / Paper

Book:

1.	Keiko Kataoka and Kazumi Ozaki : 太田敏子岡崎充宏金森政人古畑勝則松村充山本容正 (編集): メデイカルサイエンス微生物検査学第2版, 近代出版, Tokyo, Nov. 2016.
2.	Kazumi Ozaki : Chapter2 歯の硬組織欠損の種類, クインテッセンス株式会社, Tokyo, Sep. 2012.
3.	Kazumi Ozaki : Ⅳ感染症の検体検査 6. 口腔感染症, 近代出版, Tokyo, Sep. 2008.
4.	Kazumi Ozaki : 第Ⅱ部臨床編第5章壮・中年期(25∼64歳), 永末書店, Mar. 2008.
5.	蓮井義則 and Kazumi Ozaki : 歯科衛生士ポケットブック OSARAI, Dental Diamond Co., Tokyo, Mar. 2007.
6.	Kazumi Ozaki : 辺縁漏洩による細菌の侵入はどの程度問題か?, 永末書店, Kyoto, Jan. 2006.
7.	Kazumi Ozaki and : 取り残し細菌のアクティビティは?, 永末書店, Kyoto, Jan. 2006.
8.	今里聡 and Kazumi Ozaki : やさしい説明，上手な治療[4], 永末書店, Kyoto, Sep. 2004.
9.	Tadashi Nakanishi, Kanako Takahashi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Proceedings of the International Conference on Dentin/Pulp Complex 2001, --- An Immunohistologic Study on the Localization of Selected Bacteria and Chemokines in Human Deep-Carious Teeth ---, Quintessence Publishing CO.,Ltd., Tokyo, Jun. 2002.
10.	Takashi Matsuo, Masahiro Yoshiyama, Kazumi Ozaki and Hideaki Nakae : 第2章有髄歯への対応根面齲蝕への対応:シールドストレーションの応用, ヒョーロン·パブリッシャーズ, Tokyo, Aug. 2000. (Keyword) 象牙質齲蝕 / 先駆細菌 / シールドトリートメント / STOC / シールドストレーション

Academic Paper (Judged Full Paper):

1.	Mana Mekata, Kaya Yoshida, Takai Ayu, Yuka Hiroshima, Ayu Ikuta, Kayo Yoshida and Kazumi Ozaki : Porphyromonas gingivalis outer membrane vesicles increase vascular permeability by inducing stress fiber formation and degrading vascular endothelial-cadherin in endothelial cells., The FEBS Journal, Vol.in press,
2.	Risa Okamoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Keiichi Hosaka : Cardamonin inhibits the expression of inflammatory mediators in TNF-α-stimulated human periodontal ligament cells., Immunopharmacology and Immunotoxicology, 1-8, 2024. (Summary) We show that cardamonin reduces inflammatory mediator production by inhibiting the activation of several signaling pathways in this manuscript. (Link to Publication Site) ● Publication site (DOI): 10.1080/08923973.2024.2373217 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38918176 ● Search Scopus @ Elsevier (PMID): 38918176 ● Search Scopus @ Elsevier (DOI): 10.1080/08923973.2024.2373217 (DOI: 10.1080/08923973.2024.2373217, PubMed: 38918176)
3.	Risa Okamoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Keiichi Hosaka : Cardamonin decreases inflammatory mediator expression in IL-1β-stimulated human periodontal ligament cells., Molecular Biology Reports, Vol.51, No.1, 2024. (Summary) In this study, we found that cardamonin could suppress the production of inflammatory mediators in HPDLCs as well as the activation of several signaling pathways induced by IL-1β treatment. (Keyword) Chalcones / Interleukin-1beta / Periodontal Ligament / NF-kappa B / Cytokines / Cyclooxygenase 2 / Chemokines / Inflammation Mediators (Link to Publication Site) ● Publication site (DOI): 10.1007/s11033-023-09204-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38281189 ● Summary page in Scopus @ Elsevier: 2-s2.0-85183370663 (DOI: 10.1007/s11033-023-09204-8, PubMed: 38281189, Elsevier: Scopus)
4.	Kayo Yoshida, Kaya Yoshida, Yasuhiro Mouri, Ayu Takai, Mariko Seyama, Mana Mekata, Noriko Mizusawa, Keiko Miyoshi, Yasusei Kudo and Kazumi Ozaki : Porphyromonas gingivalis infection alters microRNA composition in extracellular vesicles., Journal of Oral Biosciences, Vol.66, No.2, 365-372, 2024.
5.	Kayo Yoshida, Kaya Yoshida, Mariko Seyama, Yuka Hiroshima, Mana Mekata, Natsumi Fujiwara, Yasusei Kudo and Kazumi Ozaki : Porphyromonas gingivalis outer membrane vesicles in cerebral ventricles activate microglia in mice, Oral Diseases, Vol.29, No.8, 3688-3697, 2023. (Summary) Objective: Porphyromonas gingivalis (Pg) is thought to be involved in the progression of Alzheimer's disease (AD). Whether Pg or its contents can reach the brain and directly affect neuropathology is, however, unknown. Here, we investigated whether outer membrane vesicles (OMVs) of Pg translocate to the brain and induce the pathogenic features of AD. Material and Methods: Pg OMVs were injected into the abdominal cavity of mice for 12 weeks. Pg OMV translocation to the brain was detected by immunohistochemistry using an anti-gingipain antibody. Tau protein and microglial activation in the mouse brain were examined by western blotting and immunohistochemistry. The effect of gingipains on inflammation was assessed by real-time polymerase chain reaction using human microglial HMC3 cells. Results: Gingipains were detected in the region around cerebral ventricles, choroid plexus, and ventricular ependymal cells in Pg OMV-administered mice. Tau and phosphorylated Tau protein increased and microglia were activated. Pg OMVs also increased the gene expression of proinflammatory cytokines in HMC3 cells in a gingipain-dependent manner. Conclusion: Pg OMVs, including gingipains, can reach the cerebral ventricle and induce neuroinflammation by activating microglia. Pg OMVs may provide a better understanding of the implications of periodontal diseases in neurodegenerative conditions such as AD. (Keyword) cerebral ventricle / gingipain / microglia / neuroinflammation / outer membrane vesicle / Porphyromonas gingivalis (Tokushima University Institutional Repository) ● Metadata: 118518 (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.14413 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36266256 ● CiNii @ National Institute of Informatics (CRID): 1050861074220169344 ● Summary page in Scopus @ Elsevier: 2-s2.0-85141542224 (Tokushima University Institutional Repository: 118518, DOI: 10.1111/odi.14413, PubMed: 36266256, CiNii: 1050861074220169344, Elsevier: Scopus)
6.	Yoshitaka Hosokawa, Ikuko Hosokawa, Masahiro Shimoyama, Risa Okamoto, Kazumi Ozaki and Keiichi Hosaka : The effects of berteroin on inflammatory mediators and antioxidant enzymes expression in human periodontal ligament cells., Naunyn-Schmiedeberg's Archives of Pharmacology, 2023. (Summary) Berteroin is a bioactive substance classified as an isothiocyanate found in cruciferous vegetables such as cabbage, arugula, and salad leaves. In this study, we aimed to determine whether berteroin exerts anti-inflammatory effects on human periodontal ligament cells (HPDLCs), a resident cells of periodontal tissue. Berteroin suppressed interleukin (IL)-1β or tumor necrosis factor (TNF)-α-induced chemokines (C-C motif chemokine ligand (CCL)2, CCL20, C-X-C motif chemokine ligand (CXCL)10, IL-8, and IL-6) production and intercellular adhesion molecule (ICAM)-1 expression in HPDLCs. In addition, berteroin inhibited phosphorylation of IκB kinase (IKK)- α/ β, nuclear factor (NF)- κB p65, and IκB- α and degradation of IκB- α in the NF-κB pathway induced by IL-1 β or TNF- α stimulation. Moreover, berteroin could inhibit signal transducer and activator of transcription (STAT)3 phosphorylation in TNF- α -stimulated HPDLC. Furthermore, berteroin increased the expression of the antioxidant enzymes, heme oxygenase (HO)-1 and NAD(P)H quinone dehydrogenase (NQO)1, in IL-1 β or TNF- α -stimulated HPDLCs. These results suggest that berteroin may decrease the production of inflammatory mediators in HPDLCs by suppressing the NF-κB pathway, and may also decrease the local reactive oxygen species (ROS) production in periodontal lesions by increasing the production of antioxidant enzymes. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-023-02761-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37804343 ● Search Scopus @ Elsevier (PMID): 37804343 ● Search Scopus @ Elsevier (DOI): 10.1007/s00210-023-02761-6 (DOI: 10.1007/s00210-023-02761-6, PubMed: 37804343)
7.	Masahiro Shimoyama, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Keiichi Hosaka : Effects of erucin on inflammatory mediators and antioxidant enzymes' expression in TNF-α-stimulated human oral epithelial cells., Immunopharmacology and Immunotoxicology, Vol.46, No.1, 49-54, 2023. (Summary) These results suggest that erucin may provide a new anti-inflammatory agent that can be used in the treatment of periodontitis. (Keyword) Humans / Tumor Necrosis Factor-alpha / Antioxidants / Inflammation Mediators / Epithelial Cells / NF-kappa B / Chemokines / Periodontitis / Sulfides / Thiocyanates (Tokushima University Institutional Repository) ● Metadata: 119317 (Link to Publication Site) ● Publication site (DOI): 10.1080/08923973.2023.2250551 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37624680 ● Search Scopus @ Elsevier (PMID): 37624680 ● Search Scopus @ Elsevier (DOI): 10.1080/08923973.2023.2250551 (Tokushima University Institutional Repository: 119317, DOI: 10.1080/08923973.2023.2250551, PubMed: 37624680)
8.	Natsumi Fujiwara, Shohei Yamashita, Motoki Okamoto, A Marion Cooley, Kazumi Ozaki, T Eric Everett and Maiko Suzuki : Perfluorooctanoic acid-induced cell death via the dual roles of ROS-MAPK/ERK signaling in ameloblast-lineage cells., Ecotoxicology and Environmental Safety, Vol.260, 2023. (Summary) Perfluorooctanoic acid (PFOA) is an artificial fluorinated organic compound that has generated increased public attention due to its potential health hazards. Unsafe levels of PFOA exposure can affect reproduction, growth and development. During tooth enamel development (amelogenesis), environmental factors including fluoride can cause enamel hypoplasia. However, the effects of PFOA on ameloblasts and tooth enamel formation remain largely unknown. In the present study we demonstrate several PFOA-mediated cell death pathways (necrosis/necroptosis, and apoptosis) and assess the roles of ROS-MAPK/ERK signaling in PFOA-mediated cell death in mouse ameloblast-lineage cells (ALC). ALC cells were treated with PFOA. Cell proliferation and viability were analyzed by MTT assays and colony formation assays, respectively. PFOA suppressed cell proliferation and viability in a dose dependent manner. PFOA induced both necrosis (PI-positive cells) and apoptosis (cleaved-caspase-3, γH2AX and TUNEL-positive cells). PFOA significantly increased ROS production and up-regulated phosphor-(p)-ERK. Addition of ROS inhibitor N-acetyl cysteine (NAC) suppressed p-ERK and decreased necrosis, and increased cell viability compared to PFOA alone, whereas NAC did not change apoptosis. This suggests that PFOA-mediated necrosis was induced by ROS-MAPK/ERK signaling, but apoptosis was not associated with ROS. Addition of MAPK/ERK inhibitor PD98059 suppressed necrosis and increased cell viability compared to PFOA alone. Intriguingly, PD98059 augmented PFOA-mediated apoptosis. This suggests that p-ERK promoted necrosis but suppressed apoptosis. Addition of the necroptosis inhibitor Necrostatin-1 restored cell viability compared to PFOA alone, while pan-caspase inhibitor Z-VAD did not mitigate PFOA-mediated cell death. These results suggest that 1) PFOA-mediated cell death was mainly caused by necrosis/necroptosis by ROS-MAPK/ERK signaling rather than apoptosis, 2) MAPK/ERK signaling plays the dual roles (promoting necrosis and suppressing apoptosis) under PFOA treatment. This is the initial report to indicate that PFOA could be considered as a possible causative factor for cryptogenic enamel malformation. Further studies are required to elucidate the mechanisms of PFOA-mediated adverse effects on amelogenesis. (Keyword) Mice / Animals / Reactive Oxygen Species / Ameloblasts / Cell Death / Necrosis (Tokushima University Institutional Repository) ● Metadata: 118930 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ecoenv.2023.115089 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37271104 ● Search Scopus @ Elsevier (PMID): 37271104 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ecoenv.2023.115089 (Tokushima University Institutional Repository: 118930, DOI: 10.1016/j.ecoenv.2023.115089, PubMed: 37271104)
9.	Natsumi Fujiwara, Mariko Seyama, Kayo Yoshida and Kazumi Ozaki : Oral exercise program to influence oral functions, health and oral literacy in the independent elderly., The Journal of Japan Society for Dental Hygiene, Vol.17, No.2, 49-59, 2023. (Keyword) 口腔体操 / 口腔機能 / 質問紙調査 / 行動変容 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520013962702282112 (CiNii: 1520013962702282112)
10.	Yoshitaka Hosokawa, Ikuko Hosokawa, Masahiro Shimoyama, Ayumi Fujii, Juri Sato, Kimitake Kadena, Kazumi Ozaki and Keiichi Hosaka : The Anti-Inflammatory Effects of Iberin on TNF-α-Stimulated Human Oral Epithelial Cells: In Vitro Research., Biomedicines, Vol.10, No.12, 2022. (Summary) Iberin is a bioactive chemical found in cruciferous plants that has been demonstrated to have anticancer properties. However, there have been no reports on its effects on periodontal resident cells, and many questions remain unanswered. The aim of this study was to examine whether iberin had anti-inflammatory effects on human oral epithelial cells, including influences on signal transduction pathway activation in TNF-α-στιμυλατεd χελλσ. Iberin inhibited the production of interleukin (IL)-6 and C-X-C motif chemokine ligand 10 (CXCL10), as well as the expression of vascular cell adhesion molecule (VCAM)-1, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2 in tumor necrosis factor (TNF)-α-stimulated TR146 cells, a human oral epithelial cell line. Moreover, iberin administration increased the expression of antioxidant signaling pathways, such as Heme Oxygenase (HO)-1 and NAD(P)H quinone dehydrogenase 1 (NQO1). Furthermore, we found that iberin could inhibit the activation of the nuclear factor (NF)-κB, signal transducer and activator of transcription (STAT)3, and p70S6 kinase (p70S6K)-S6 ribosomal protein (S6) pathways in TNF-α-stimulated TR146 cells. In conclusion, iberin reduced inflammatory mediator expression in human oral epithelial cells by preventing the activation of particular signal transduction pathways. (Tokushima University Institutional Repository) ● Metadata: 118001 (Link to Publication Site) ● Publication site (DOI): 10.3390/biomedicines10123155 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36551911 ● Search Scopus @ Elsevier (PMID): 36551911 ● Search Scopus @ Elsevier (DOI): 10.3390/biomedicines10123155 (Tokushima University Institutional Repository: 118001, DOI: 10.3390/biomedicines10123155, PubMed: 36551911)
11.	Masahiro Shimoyama, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Keiichi Hosaka : 6-(Methylsulfinyl) Hexyl Isothiocyanate Inhibits IL-6 and CXCL10 Production in TNF-α-Stimulated Human Oral Epithelial Cells., Current Issues in Molecular Biology, Vol.44, No.7, 2915-2922, 2022. (Summary) 6-(Methylsulfinyl) hexyl isothiocyanate (6-MSITC) is a bioactive substance found in wasabi (Wasabia japonica) and has been reported to have some bioactive effects including anticancer and antioxidant effects. However, there are no reports on its effects on periodontal resident cells, and many points remain unclear. In this study, we aimed to investigate whether 6-MSITC exerts anti-inflammatory effects on human oral epithelial cells, including effects on signal transduction pathway activation. 6-MSITC inhibited interleukin (IL)-6 and C-X-C motif chemokine ligand 10 (CXCL10) production in TNF-α-stimulated TR146 cells, which are a human oral epithelial cell line. Moreover, we found that 6-MSITC could suppress signal transducer and activator of transcription (STAT)3, nuclear factor (NF)-κB, and p70S6 kinase (p70S6K)-S6 ribosomal protein (S6) pathways activation in TNF-α-stimulated TR146 cells. Furthermore, STAT3 and NF-κB inhibitors could suppress IL-6 and CXCL10 production in TNF-α-treated TR146 cells. In summary, 6-MSITC could decrease IL-6 and CXCL10 production in human oral epithelial cell by inhibiting STAT3 and NF-κB activation. (Tokushima University Institutional Repository) ● Metadata: 117734 (Link to Publication Site) ● Publication site (DOI): 10.3390/cimb44070201 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35877425 ● Search Scopus @ Elsevier (PMID): 35877425 ● Search Scopus @ Elsevier (DOI): 10.3390/cimb44070201 (Tokushima University Institutional Repository: 117734, DOI: 10.3390/cimb44070201, PubMed: 35877425)
12.	Masato Tagi, Mari Tajiri, Yasuhiro Hamada, Yoshifumi Wakata, Xiao Shan, Kazumi Ozaki, Masanori Kubota, Sosuke Amano, Hiroshi Sakaue, Yoshiko Suzuki and Jun Hirose : Accuracy of an Artificial Intelligence-Based Model for Estimating Leftover Liquid Food in Hospitals: Validation Study., JMIR Formative Research, Vol.6, No.5, e35991, 2022. (Summary) An accurate evaluation of the nutritional status of malnourished hospitalized patients at a higher risk of complications, such as frailty or disability, is crucial. Visual methods of estimating food intake are popular for evaluating the nutritional status in clinical environments. However, from the perspective of accurate measurement, such methods are unreliable. The accuracy of estimating leftover liquid food in hospitals using an artificial intelligence (AI)-based model was compared to that of visual estimation. The accuracy of the AI-based model (AI estimation) was compared to that of the visual estimation method for thin rice gruel as staple food and fermented milk and peach juice as side dishes. A total of 576 images of liquid food (432 images of thin rice gruel, 72 of fermented milk, and 72 of peach juice) were used. The mean absolute error, root mean squared error, and coefficient of determination (R) were used as metrics for determining the accuracy of the evaluation process. Welch t test and the confusion matrix were used to examine the difference of mean absolute error between AI and visual estimation. The mean absolute errors obtained through the AI estimation approach were 0.63 for fermented milk, 0.25 for peach juice, and 0.85 for the total. These were significantly smaller than those obtained using the visual estimation approach, which were 1.40 (P<.001) for fermented milk, 0.90 (P<.001) for peach juice, and 1.03 (P=.009) for the total. By contrast, the mean absolute error for thin rice gruel obtained using the AI estimation method (0.99) did not differ significantly from that obtained using visual estimation (0.99). The confusion matrix for thin rice gruel showed variation in the distribution of errors, indicating that the errors in the AI estimation were biased toward the case of many leftovers. The mean squared error for all liquid foods tended to be smaller for the AI estimation than for the visual estimation. Additionally, the coefficient of determination (R) for fermented milk and peach juice tended to be larger for the AI estimation than for the visual estimation, and the R value for the total was equal in terms of accuracy between the AI and visual estimations. The AI estimation approach achieved a smaller mean absolute error and root mean squared error and a larger coefficient of determination (R) than the visual estimation approach for the side dishes. Additionally, the AI estimation approach achieved a smaller mean absolute error and root mean squared error compared to the visual estimation method, and the coefficient of determination (R) was similar to that of the visual estimation method for the total. AI estimation measures liquid food intake in hospitals more precisely than visual estimation, but its accuracy in estimating staple food leftovers requires improvement. (Tokushima University Institutional Repository) ● Metadata: 117555 (Link to Publication Site) ● Publication site (DOI): 10.2196/35991 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35536638 ● Search Scopus @ Elsevier (PMID): 35536638 ● Search Scopus @ Elsevier (DOI): 10.2196/35991 (Tokushima University Institutional Repository: 117555, DOI: 10.2196/35991, PubMed: 35536638)
13.	Yoshida Kayo, Kaya Yoshida, Natsumi Fujiwara, Mariko Seyama, Ono Kisho, Kawai Hotaka, Guo Jiajie, Wang Ziyi, Weng Yao, Yu Yaqiong, Uchida-Fukuhara Yoko, Ikegame Mika, Sasaki Akira, Nagatsuka Hitoshi, Kamioka Hiroshi, Hirohiko Okamura and Kazumi Ozaki : Extracellular vesicles of P. gingivalis-infected macrophages induce lung injury, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1867, No.11, 166236, 2021. (Summary) Periodontal diseases are common inflammatory diseases that are induced by infection with periodontal bacteria such as Porphyromonas gingivalis (Pg). The association between periodontal diseases and many types of systemic diseases has been demonstrated; the term "periodontal medicine" is used to describe how periodontal infection/inflammation may impact extraoral health. However, the molecular mechanisms by which the factors produced in the oral cavity reach multiple distant organs and impact general health have not been elucidated. Extracellular vesicles (EVs) are nano-sized spherical structures secreted by various types of cells into the tissue microenvironment, and influence pathophysiological conditions by delivering their cargo. However, a detailed understanding of the effect of EVs on periodontal medicine is lacking. In this study, we investigated whether EVs derived from Pg-infected macrophages reach distant organs in mice and influence the pathophysiological status. EVs were isolated from human macrophages, THP-1 cells, infected with Pg. We observed that EVs from Pg-infected THP-1 cells (Pg-inf EVs) contained abundant core histone proteins such as histone H3 and translocated to the lungs, liver, and kidneys of mice. Pg-inf EVs also induced pulmonary injury, including edema, vascular congestion, inflammation, and collagen deposition causing alveoli destruction. The Pg-inf EVs or the recombinant histone H3 activated the NF-κB pathway, leading to increase in the levels of pro-inflammatory cytokines in human lung epithelial A549 cells. Our results suggest a possible mechanism by which EVs produced in periodontal diseases contribute to the progression of periodontal medicine. (Tokushima University Institutional Repository) ● Metadata: 116182 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbadis.2021.166236 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34389473 ● Search Scopus @ Elsevier (PMID): 34389473 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbadis.2021.166236 (Tokushima University Institutional Repository: 116182, DOI: 10.1016/j.bbadis.2021.166236, PubMed: 34389473)
14.	Wenhua Shao, Natsumi Fujiwara, Yasuhiro Mouri, Satoru Kisoda, Kayo Yoshida, Kaya Yoshida, Hiromichi Yumoto, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : Conversion from epithelial to partial-EMT phenotype by Fusobacterium nucleatum infection promotes invasion of oral cancer cells., Scientific Reports, Vol.11, No.1, 14943, 2021. (Summary) The ability of cancer cells to undergo partial-epithelial mesenchymal transition (p-EMT), rather than complete EMT, poses a higher metastatic risk. Although Fusobacterium nucleatum mainly inhabits in oral cavity, attention has been focused on the F. nucleatum involvement in colorectal cancer development. Here we examined the p-EMT regulation by F. nucleatum in oral squamous cell carcinoma (OSCC) cells. We cultured OSCC cells with epithelial, p-EMT or EMT phenotype with live or heat-inactivated F. nucleatum. Expression of the genes involved in epithelial differentiation, p-EMT and EMT were examined in OSCC cells after co-culture with F. nucleatum by qPCR. Cell growth and invasion of OSCC cells were also examined. Both live and heat-inactivated F. nucleatum upregulated the expression of p-EMT-related genes in OSCC cells with epithelial phenotype, but not with p-EMT or EMT phenotype. Moreover, F. nucleatum promoted invasion of OSCC cells with epithelial phenotype. Co-culture with other strains of bacteria other than Porphyromonas gingivalis did not alter p-EMT-related genes in OSCC cells with epithelial phenotype. F. nucleatum infection may convert epithelial to p-EMT phenotype via altering gene expression in OSCC. Oral hygiene managements against F. nucleatum infection may contribute to reduce the risk for an increase in metastatic ability of OSCC. (Tokushima University Institutional Repository) ● Metadata: 116445 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-021-94384-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34294795 ● Summary page in Scopus @ Elsevier: 2-s2.0-85111135598 (Tokushima University Institutional Repository: 116445, DOI: 10.1038/s41598-021-94384-1, PubMed: 34294795, Elsevier: Scopus)
15.	Yoshitaka Hosokawa, Ikuko Hosokawa and Kazumi Ozaki : Nobiletin Decreases Inflammatory Mediator Expression in Tumor Necrosis Factor-Stimulated Human Periodontal Ligament Cells., Mediators of Inflammation, Vol.2021, No.5535844, 2021. (Summary) B and AKT1 activations and upregulating the NFE2L2 and HMOX1 expression. (Tokushima University Institutional Repository) ● Metadata: 116565 (Link to Publication Site) ● Publication site (DOI): 10.1155/2021/5535844 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34335088 ● Search Scopus @ Elsevier (PMID): 34335088 ● Search Scopus @ Elsevier (DOI): 10.1155/2021/5535844 (Tokushima University Institutional Repository: 116565, DOI: 10.1155/2021/5535844, PubMed: 34335088)
16.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Nobiletin Inhibits Inflammatory Reaction in Interleukin-1β-Stimulated Human Periodontal Ligament Cells., Pharmaceutics, Vol.13, No.5, 667, 2021. (Summary) The immune response in periodontal lesions is involved in the progression of periodontal disease. Therefore, it is important to find a bioactive substance that has anti-inflammatory effects in periodontal lesions. This study aimed to examine if nobiletin, which is found in the peel of citrus fruits, could inhibit inflammatory responses in interleukin (IL)-1β-stimulated human periodontal ligament cells (HPDLCs). The release of cytokines (IL-6, IL-8, CXCL10, CCL20, and CCL2) and matrix metalloproteinases (MMP-1 and MMP-3) was assessed by ELISA. The expression of cell adhesion molecules (ICAM-1and VCAM-1) and the activation of signal transduction pathways (nuclear factor (NF)-κB, mitogen-activated protein kinases (MAPKs) and protein kinase B (Akt)) in HPDLCs were detected by Western blot analysis. Our experiments revealed that nobiletin decreased the expression of inflammatory cytokines, cell adhesion molecules, and MMPs in IL-1β-stimulated HPDLCs. Moreover, we revealed that nobiletin treatment could suppress the activation of the NF-κB, MAPKs, and Akt pathways. These findings indicate that nobiletin could inhibit inflammatory reactions in IL-1β-stimulated HPDLCs by inhibiting multiple signal transduction pathways, including NF-κB, MAPKs, and Akt. (Tokushima University Institutional Repository) ● Metadata: 116619 (Link to Publication Site) ● Publication site (DOI): 10.3390/pharmaceutics13050667 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34066937 ● Search Scopus @ Elsevier (PMID): 34066937 ● Search Scopus @ Elsevier (DOI): 10.3390/pharmaceutics13050667 (Tokushima University Institutional Repository: 116619, DOI: 10.3390/pharmaceutics13050667, PubMed: 34066937)
17.	Natsumi Fujiwara, 久野恵, 田村真里奈, 篠永晴美, 迎美榛, Harumi Sakamoto, Mariko Seyama, Kazumi Ozaki and Daisuke Hinode : 歯科衛生士学生における摂食嚥下リハビリテーション臨床実習の有効性, The Journal of Japan Society for Dental Hygiene, Vol.15, No.2, 29-37, 2021. (Keyword) 歯科衛生士学生 / 臨床実習 / 摂食嚥下リハビリテーション / 多職種連携 / 専門性 / シカエイセイシガクセイ / リンショウジッシュウ / セッショクエンカリハビリテーション / タショクシュレンケイ / センモンセイ (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520854806140649088 (CiNii: 1520854806140649088)
18.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : The Polymethoxy Flavonoid Sudachitin Inhibits Interleukin-1 β-Induced Inflammatory Mediator Production in Human Periodontal Ligament Cells, BioMed Research International, Vol.2021, No.Article ID 8826586, 2021. (Tokushima University Institutional Repository) ● Metadata: 116275 (Link to Publication Site) ● Publication site (DOI): 10.1155/2021/8826586 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33575345 ● Search Scopus @ Elsevier (PMID): 33575345 ● Search Scopus @ Elsevier (DOI): 10.1155/2021/8826586 (Tokushima University Institutional Repository: 116275, DOI: 10.1155/2021/8826586, PubMed: 33575345)
19.	Natsumi Fujiwara, Naoya Kitamura, Kaya Yoshida, Tetsuya Yamamoto, Kazumi Ozaki and Yasusei Kudo : Involvement of Fusobacterium Species in Oral Cancer Progression: A Literature Review Including Other Types of Cancer, International Journal of Molecular Sciences, Vol.21, No.17, 6207, 2020. (Summary) Chronic inflammation caused by infections has been suggested to be one of the most important cause of cancers. It has recently been shown that there is correlation between intestinal bacteria and cancer development including metastasis. As over 700 bacterial species exist in an oral cavity, it has been concerning that bacterial infection may cause oral cancer. However, the role of bacteria regarding tumorigenesis of oral cancer remains unclear. Several papers have shown that species deriving the oral cavities, especially, play a crucial role for the development of colorectal and esophageal cancer. is a well-known oral bacterium involved in formation of typical dental plaque on human teeth and causing periodontal diseases. The greatest characteristic of is its ability to adhere to various bacteria and host cells. Interestingly, is frequently detected in oral cancer tissues. Moreover, detection of is correlated with the clinical stage of oral cancer. Although the detailed mechanism is still unclear, species have been suggested to be associated with cell adhesion, tumorigenesis, epithelial-to-mesenchymal transition, inflammasomes, cell cycle, etc. in oral cancer. In this review, we introduce the reports focused on the association of species with cancer development and progression including oral, esophageal, and colon cancers. (Keyword) Cell Adhesion / Colonic Neoplasms / Disease Progression / Epithelial-Mesenchymal Transition / Esophageal Neoplasms / Fusobacterium / Fusobacterium Infections / Humans / Inflammasomes / Mouth / Mouth Neoplasms (Tokushima University Institutional Repository) ● Metadata: 115246 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms21176207 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32867334 ● Summary page in Scopus @ Elsevier: 2-s2.0-85090108629 (Tokushima University Institutional Repository: 115246, DOI: 10.3390/ijms21176207, PubMed: 32867334, Elsevier: Scopus)
20.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo : Carnosic acid inhibits inflammatory cytokines production in human periodontal ligament cells., Immunopharmacology and Immunotoxicology, Vol.42, No.4, 373-378, 2020. (Summary) The results of this study suggest that CA has anti-inflammatory effects in human periodontal ligament cells by inhibiting JNK, NF-κB and STAT3 pathways. (Link to Publication Site) ● Publication site (DOI): 10.1080/08923973.2020.1782427 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32538208 ● Summary page in Scopus @ Elsevier: 2-s2.0-85087515653 (DOI: 10.1080/08923973.2020.1782427, PubMed: 32538208, Elsevier: Scopus)
21.	Natsumi Fujiwara, Keiji Murakami, Kaya Yoshida, Shunsuke Sakurai, Yasusei Kudo, Kazumi Ozaki, Katsuhiko Hirota, Hideki Fujii, Maiko Suzuki, Yoichiro Miyake and Hiromichi Yumoto : Suppresive effects of 2-methacryloyloxyethyl phosphorylcholine (MPC)-polymer on the adherence of Candida species and MRSA to acrylic denture resin., Heliyon, Vol.6, e04211, 2020. (Tokushima University Institutional Repository) ● Metadata: 115916 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.heliyon.2020.e04211 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32577575 ● Summary page in Scopus @ Elsevier: 2-s2.0-85086425832 (Tokushima University Institutional Repository: 115916, DOI: 10.1016/j.heliyon.2020.e04211, PubMed: 32577575, Elsevier: Scopus)
22.	Mariko Seyama, Kaya Yoshida, Kayo Yoshida, Natsumi Fujiwara, Kisho Ono, Takanori Eguchi, Hotaka Kawai, Jiajie Guo, Yao Weng, Yuan Haoze, Kenta Uchibe, Mika Ikegame, Akira Sasaki, Hitoshi Nagatsuka, Kuniaki Okamoto, Hirohiko Okamura and Kazumi Ozaki : Outer membrane vesicles of Porphyromonas gingivalis attenuate insulin sensitivity by delivering gingipains to the liver, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1866, No.6, 165731, 2020. (Summary) Outer membrane vesicles (OMVs) are nanosized particles derived from the outer membrane of gram-negative bacteria. Oral bacterium Porphyromonas gingivalis (Pg) is known to be a major pathogen of periodontitis that contributes to the progression of periodontal disease by releasing OMVs. The effect of Pg OMVs on systemic diseases is still unknown. To verify whether Pg OMVs affect the progress of diabetes mellitus, we analyzed the cargo proteins of vesicles and evaluated their effect on hepatic glucose metabolism. Here, we show that Pg OMVs were equipped with Pg-derived proteases gingipains and translocated to the liver in mice. In these mice, the hepatic glycogen synthesis in response to insulin was decreased, and thus high blood glucose levels were maintained. Pg OMVs also attenuated the insulin-induced Akt/ glycogen synthase kinase-3 (GSK-3 signaling in a gingipain-dependent fashion in hepatic HepG2 cells. These results suggest that the delivery of gingipains mediated by Pg OMV elicits changes in glucose metabolisms in the liver and contributes to the progression of diabetes mellitus. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbadis.2020.165731 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32088316 ● Search Scopus @ Elsevier (PMID): 32088316 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbadis.2020.165731 (DOI: 10.1016/j.bbadis.2020.165731, PubMed: 32088316)
23.	Natsumi Fujiwara, Hiromichi Yumoto, Koji Miyamoto, Katsuhiko Hirota, Hiromi Nakae, Saya Tanaka, Keiji Murakami, Yasusei Kudo, Kazumi Ozaki and Yoichiro Miyake : 2-Methacryloyloxyethyl phosphorylcholine (MPC)-polymer suppresses an increase of oral bacteria: a single-blind, crossover clinical trial, Clinical Oral Investigations, Vol.23, 739-746, 2019. (Summary) The biocompatible 2-methacryloyloxyethyl phosphorylcholine (MPC)-polymers, which mimic a biomembrane, reduce protein adsorption and bacterial adhesion and inhibit cell attachment. The aim of this study is to clarify whether MPC-polymer can suppress the bacterial adherence in oral cavity by a crossover design. We also investigated the number of Fusobacterium nucleatum, which is the key bacterium forming dental plaque, in clinical samples. This study was a randomized, placebo-controlled, single-blind, crossover study, with two treatment periods separated by a 2-week washout period. We conducted clinical trial with 20 healthy subjects to evaluate the effect of 5% MPC-polymer mouthwash after 5 h on oral microflora. PBS was used as a control. The bacterial number in the gargling sample before and after intervention was counted by an electronic bacterial counter and a culture method. DNA amounts of total bacteria and F. nucleatum were examined by q-PCR. The numbers of total bacteria and oral streptcocci after 5 h of 5% MPC-polymer treatment significantly decreased, compared to the control group. Moreover, the DNA amounts of total bacteria and F. nucleatum significantly decreased by 5% MPC-polymer mouthwash. We suggest that MPC-polymer coating in the oral cavity may suppress the oral bacterial adherence. MPC-polymer can be a potent compound for the control of oral microflora to prevent oral infection. (Keyword) 2-Methacryloyloxyethylphosphorylcholine / Clinical study / Oral infection / Oral bacteria / Fusobacterium nucleatum (Tokushima University Institutional Repository) ● Metadata: 113011 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00784-018-2490-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29766378 ● Summary page in Scopus @ Elsevier: 2-s2.0-85046904798 (Tokushima University Institutional Repository: 113011, DOI: 10.1007/s00784-018-2490-2, PubMed: 29766378, Elsevier: Scopus)
24.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Sudachitin Inhibits Matrix Metalloproteinase-1 and -3 Production in Tumor Necrosis Factor-α-Stimulated Human Periodontal Ligament Cells., Inflammation, Vol.42, No.4, 1456-1462, 2019. (Summary) Sudachitin, a polymethoxylated flavonoid found in the skin of Citrus sudachi, is a biologically active substance. The aim of this study was to examine whether sudachitin could be used to inhibit the expression of matrix metalloproteinase (MMP)-1 and MMP-3, which are involved in the destruction of periodontal tissues in periodontal lesions, in tumor necrosis factor (TNF)-α-stimulated human periodontal ligament cells (HPDLC). Sudachitin suppressed TNF-α-induced MMP-1 and MMP-3 production in HPDLC. On the other hand, it enhanced tissue inhibitor of metalloproteinase (TIMP)-1 expression. The level of Akt phosphorylation in the TNF-α-stimulated HPDLC was decreased by sudachitin treatment. Moreover, an Akt inhibitor reduced MMP-1 and MMP-3 production and increased TIMP-1 production. These findings indicate that sudachitin reduces MMP-1 and MMP-3 production in TNF-α-stimulated HPDLC by inhibiting the Akt pathway. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-019-01007-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30997585 ● Search Scopus @ Elsevier (PMID): 30997585 ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-019-01007-z (DOI: 10.1007/s10753-019-01007-z, PubMed: 30997585)
25.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo : Carnosic Acid Inhibits CXCR3 Ligands Production in IL-27-Stimulated Human Oral Epithelial Cells., Inflammation, Vol.42, No.4, 1311-1316, 2019. (Summary) Carnosic acid, which is a bioactive compound isolated from rosemary, has various pharmacological effects. However, the anti-inflammatory effect of carnosic acid on periodontitis is still unknown. The aim of this study was to investigate the effect of carnosic acid on CXC chemokine receptor 3 (CXCR3) ligands, which are involved in Th1 cells migration and accumulation, production in interleukin (IL)-27-stimulated human oral epithelial cells (TR146 cells). Carnosic acid decreased CXC chemokine ligand (CXCL)9, CXCL10, and CXCL11 production in IL-27-stimulated TR146 cells in a dose-dependent fashion. Moreover, we disclosed that carnosic acid could suppress signal transducer and activator of transcription (STAT)1, STAT3, and protein kinase B (Akt) phosphorylation in IL-27-stimulated TR146 cells. Furthermore, STAT1, STAT3, and Akt inhibitors could suppress CXCR3 ligands production in IL-27-treated TR146 cells. In summary, carnosic acid could reduce CXCR3 ligands production in human oral epithelial cell by inhibiting STAT1, STAT3, and Akt activation. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-019-00991-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30820808 ● Search Scopus @ Elsevier (PMID): 30820808 ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-019-00991-6 (DOI: 10.1007/s10753-019-00991-6, PubMed: 30820808)
26.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Honokiol and Magnolol Inhibit CXCL10 and CXCL11 Production in IL-27-Stimulated Human Oral Epithelial Cells., Inflammation, Vol.41, No.6, 2110-2115, 2018. (Summary) Honokiol and magnolol, which are lignans isolated from Magnolia quinquepeta, have some pharmacological effects. However, the anti-inflammatory effects of honokiol and magnolol on periodontal disease are still uncertain. The aim of this study was to examine the effect of honokiol and magnolol on CXC chemokine receptor 3 (CXCR3) ligands, which are related with Th1 cell migration, production in interleukin (IL)-27-stimulated human oral epithelial cells (TR146 cells). Honokiol and magnolol inhibited CXC chemokine ligand (CXCL)10 and CXCL11 production in IL-27-stimulated TR146 cells in a dose-dependent manner. Moreover, we revealed that honokiol and magnolol could suppress signal transducer and activator of transcription (STAT)3 and protein kinase B (Akt) phosphorylation in IL-27-stimulated TR146 cells though STAT1 phosphorylation was not suppressed by honokiol and magnolol treatment. Furthermore, STAT3 and Akt inhibitors could suppress CXCR3 ligand production in TR146 cells. In summary, honokiol and magnolol could reduce CXCR3 ligand production in oral epithelial cell by inhibiting STAT3 and Akt activation. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-018-0854-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30039429 ● Search Scopus @ Elsevier (PMID): 30039429 ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-018-0854-z (DOI: 10.1007/s10753-018-0854-z, PubMed: 30039429)
27.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Transforming growth factor-β1 increases C-C chemokine ligand 11 production in interleukin 4-stimulated human periodontal ligament cells., Cell Biology International, Vol.42, No.10, 1395-1400, 2018. (Summary) Transforming growth factor (TGF)-β1 is a multifunctional cytokine, which can control certain functions of various kinds of cells. However, it is unclear whether TGF-β1 affects T-cell migration in periodontal lesions. The aim of this study was to examine the effects of TGF-β1 on the production of C-C chemokine ligand (CCL)11, which is a T-helper 2-type chemokine, in human periodontal ligament cells (HPDLC). Interleukin (IL)-4 induced CCL11 production, but TGF-β1 did not, in HPDLC. However, TGF-β1 enhanced CCL11 production in IL-4-stimulated HPDLC. Western blot analysis showed that the signal transducer and activator of transcription 6 (STAT6) pathway was highly activated in HPDLC that had been stimulated with both IL-4 and TGF-β1. Mitogen-activated protein kinase activation did not differ between the HPDLC treated with a combination of IL-4 and TGF-β1 and those treated with IL-4 or TGF-β1 alone. Moreover, a STAT6 inhibitor significantly inhibited CCL11 production in HPDLC that had been stimulated with IL-4 and TGF-β1. The current study clearly demonstrated that TGF-β1 enhanced IL-4-induced CCL11 production in HPDLC. The STAT6 pathway is important for CCL11 production in IL-4- and TGF-β1-treated HPDLC. (Keyword) Cells, Cultured / Chemokine CCL11 / Chemokines, CC / cytokinesis / Humans / Interleukin-4 / Periodontal Ligament / phosphorylation / STAT6 Transcription Factor / signal transduction / Transforming Growth Factor beta1 (Tokushima University Institutional Repository) ● Metadata: 112813 (Link to Publication Site) ● Publication site (DOI): 10.1002/cbin.11030 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29993161 ● Search Scopus @ Elsevier (PMID): 29993161 ● Search Scopus @ Elsevier (DOI): 10.1002/cbin.11030 (Tokushima University Institutional Repository: 112813, DOI: 10.1002/cbin.11030, PubMed: 29993161)
28.	Kazumi Ozaki : A visualization system for supporting oral and nutritional care of the elderly., Journal of the Japanese Association of Periodontology, Vol.60, No.1, 35-43, 2018. (Keyword) oral healthcare / nutritional care / tacit knowledge / information and communications technology (Link to Publication Site) ● Publication site (DOI): 10.2329/perio.60.35 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679390528640 ● Search Scopus @ Elsevier (DOI): 10.2329/perio.60.35 (DOI: 10.2329/perio.60.35, CiNii: 1390282679390528640)
29.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Effects of Theaflavin on Chemokine Production in TNF-α-stimulated Oral Epithelial Cells, The Japanese Journal of Conservative Dentistry, Vol.61, No.1, 10-16, 2018. (Link to Publication Site) ● Publication site (DOI): 10.11471/shikahozon.61.10 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680499546240 ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.61.10 (DOI: 10.11471/shikahozon.61.10, CiNii: 1390282680499546240)
30.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : IL-27 Modulates Chemokine Production in TNF- -Stimulated Human Oral Epithelial Cells., Cellular Physiology and Biochemistry, Vol.43, No.3, 1198-1206, 2017. (Summary) IL-27 might control leukocyte migration in periodontal lesion by modulating chemokine production from epithelial cells. (Tokushima University Institutional Repository) ● Metadata: 112954 (Link to Publication Site) ● Publication site (DOI): 10.1159/000481760 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28977795 ● Search Scopus @ Elsevier (PMID): 28977795 ● Search Scopus @ Elsevier (DOI): 10.1159/000481760 (Tokushima University Institutional Repository: 112954, DOI: 10.1159/000481760, PubMed: 28977795)
31.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : IL-29 Enhances CXCL10 Production in TNF--stimulated Human Oral Epithelial Cells., Immunological Investigations, Vol.46, No.6, 615-624, 2017. (Summary) Interleukin-29 (IL-29) is a cytokine belonging to the Type III interferon family. It was recently detected in the gingival crevicular fluid of periodontitis patients. However, the role of IL-29 in the pathogenesis of periodontal disease remains unknown. The aim of this study was to examine the effects of IL-29 on C-X-C motif chemokine ligand 10 (CXCL10) production in human oral epithelial cells. We measured CXCL10 production in TR146 cells, which is a human oral epithelial cell line, using an enzyme-linked immunosorbent assay. We used a Western blot analysis to detect IL-29 receptor expression and the phosphorylation levels of signal transduction molecules, including p38 mitogen-activated protein kinases (MAPK), signal transducer and activator of transcription 3 (STAT3), and nuclear factor (NF)- B p65, in the TR146 cells. The TR146 cells expressed the IL-29 receptor. IL-29 induced CXCL10 production in the TR146 cells. IL-29 significantly enhanced CXCL10 production in tumor necrosis factor (TNF)--stimulated TR146 cells. The p38 MAPK, STAT3, and NF-B pathways were found to be related to the IL-29-induced enhancement of CXCL10 production in TNF--stimulated TR146 cells. IL-29 promotes T helper 1-cell accumulation in periodontal lesions by inducing CXCL10 production in oral epithelial cells. (Tokushima University Institutional Repository) ● Metadata: 112817 (Link to Publication Site) ● Publication site (DOI): 10.1080/08820139.2017.1336176 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28753407 ● Search Scopus @ Elsevier (PMID): 28753407 ● Search Scopus @ Elsevier (DOI): 10.1080/08820139.2017.1336176 (Tokushima University Institutional Repository: 112817, DOI: 10.1080/08820139.2017.1336176, PubMed: 28753407)
32.	Natsumi Fujiwara, Keiji Murakami, Michiyasu Nakao, Munehisa Toguchi, Hiromichi Yumoto, Katsuhiko Hirota, Takashi Matsuo, Shigeki Sano, Kazumi Ozaki and Yoichiro Miyake : Antibacterial and antibiofilm effects of Reuterin-Related Compounds to periodontopathic bacteria, Journal of Oral Health and Biosciences, Vol.30, No.1, 8-17, 2017. (Tokushima University Institutional Repository) ● Metadata: 111063 (Link to Publication Site) ● Publication site (DOI): 10.20738/johb.30.1_8 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.20738/johb.30.1_8 (Tokushima University Institutional Repository: 111063, DOI: 10.20738/johb.30.1_8)
33.	Kaya Yoshida, Hirohiko Okamura, Yuka Hiroshima, Kaori Abe, Jun-ichi Kido, Yasuo Shinohara and Kazumi Ozaki : PKR induces the expression of NLRP3 by regulating the NF-κB pathway in Porphyromonas gingivalis-infected osteoblasts, Experimental Cell Research, Vol.354, No.1, 57-64, 2017. (Summary) The double-stranded RNA-dependent kinase (PKR), which is activated by double stranded RNA, induces inflammation by regulating NF-κB signaling. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome also modulates inflammation in response to infection. Porphyromonas gingivalis (P.gingivalis) is an oral bacterium which is implicated in the pathogenesis of periodontal diseases. We previously reported that PKR is a key modulator of bone metabolism and inflammation in the periodontal tissue. PKR was also reported to induce inflammation in response to microbes by regulating the NLRP3 inflammasome, suggesting that PKR could affect inflammation along with NLRP3 in periodontal diseases. In this study, we investigated the effects of PKR on NLRP3 expression and NF-κB activity in P. gingivalis infected osteoblasts. We first constructed a SNAP26b-tagged P.gingivalis (SNAP-P. g.) and traced its internalization into the cell. SNAP-P. g. increased the activity of PKR and NF-κB and also induced NLRP3 expression in osteoblasts. Inhibition of NF-κB attenuated SNAP-P. g.-induced NLRP3 expression. The knockdown of PKR using shRNA decreased both the activity of NF-κB and the expression of NLRP3 induced by SNAP-P.g.. We therefore concluded that in osteoblasts, P. gingivalis activated PKR, which in turn increased NLRP3 expression by activating NF-κB. Our results suggest that PKR modulates inflammation by regulating the expression of the NLRP3 inflammasome through the NF-κB pathway in periodontal diseases. (Keyword) 3T3 Cells / Animals / Gene Expression Regulation / Humans / Inflammasomes / Inflammation / Mice / NF-kappa B / NLR Family, Pyrin Domain-Containing 3 Protein / Osteoblasts / Periodontal Pocket / Porphyromonas gingivalis / Receptors, G-Protein-Coupled / Signal Transduction / Transcription Factor RelA (Tokushima University Institutional Repository) ● Metadata: 111349 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yexcr.2017.03.028 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28341446 ● Search Scopus @ Elsevier (PMID): 28341446 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yexcr.2017.03.028 (Tokushima University Institutional Repository: 111349, DOI: 10.1016/j.yexcr.2017.03.028, PubMed: 28341446)
34.	Natsumi Fujiwara, Keiji Murakami, Michiyasu Nakao, Munehisa Toguchi, Hiromichi Yumoto, Takashi Amoh, Katsuhiko Hirota, Takashi Matsuo, Shigeki Sano, Kazumi Ozaki and Yoichiro Miyake : Novel reuterin-related compounds suppress odour by periodontopathic bacteria, Oral Diseases, Vol.23, No.4, 492-497, 2017. (Summary) Halitosis is caused by volatile sulphur compounds including methyl mercaptan (CH3 SH) in the oral cavity and is a serious problem that limits interpersonal social communication. The aim of study was to evaluate the effects of reuterin-related compounds (RRCs) on halitosis-related periodontopathic bacteria in vitro. RRC-01, RRC-02 and RRC-03 (32 and 64 g ml(-1) ) in culture media containing Fusobacterium nucleatum JCM8523 and Porphyromonas gingivalis ATCC33277 were used. The effects of RRCs on CH3 SH production and detectable odour by F. nucleatum and P. gingivalis were examined by CH3 SH production assay and organoleptic test, respectively. The number of bacterial cells was also measured using an ATP assay. In P. gingivalis treated with RRCs, the expression of mgl gene, which is responsible for CH3 SH production, was examined by qRT-PCR. CH3 SH production and the score of detectable odour from F. nucleatum and P. gingivalis culture media containing RRCs were significantly lower than that without RRCs (P < 0.05). The expression of mgl gene in P. gingivalis was significantly downregulated by RRC-01 (P < 0.01), but not by RRC-02 or RRC-03. RRCs are potent oral care products for preventing halitosis via reducing CH3 SH production. (Link to Publication Site) ● Publication site (DOI): 10.1111/odi.12638 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28083982 ● Summary page in Scopus @ Elsevier: 2-s2.0-85015084211 (DOI: 10.1111/odi.12638, PubMed: 28083982, Elsevier: Scopus)
35.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : Gomisin N Decreases Inflammatory Cytokine Production in Human Periodontal Ligament Cells., Inflammation, Vol.40, No.2, 360-365, 2017. (Summary) Gomisin N, which is a lignan isolated from Schisandra chinensis, has some pharmacological effects. However, the anti-inflammatory effects of gomisin N on periodontal disease are uncertain. The aim of this study was to examine the effect of gomisin N on inflammatory mediator production in tumor necrosis factor (TNF)--stimulated human periodontal ligament cells (HPDLC). Gomisin N inhibited interleukin (IL)-6, IL-8, CC chemokine ligand (CCL) 2, and CCL20 production in TNF--stimulated HPDLC in a dose-dependent manner. Moreover, we revealed that gomisin N could suppress extracellular signal-regulated kinase (ERK) and c-Jun N terminal kinase (JNK) phosphorylation in TNF--stimulated HPDLC though protein kinase B (Akt) phosphorylation was not suppressed by gomisin N treatment. In summary, gomisin N might exert anti-inflammatory effects by attenuating cytokine production in periodontal ligament cells via inhibiting the TNF--stimulated ERK and JNK pathways activation. (Keyword) Anti-Inflammatory Agents / Cells, Cultured / Cyclooctanes / Cytokines / Dose-Response Relationship, Drug / Humans / Inflammation Mediators / Lignans / MAP Kinase Signaling System / Periodontal Ligament / Phosphorylation / Polycyclic Compounds / Tumor Necrosis Factor-alpha (Tokushima University Institutional Repository) ● Metadata: 112816 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-016-0482-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27896541 ● Search Scopus @ Elsevier (PMID): 27896541 ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-016-0482-4 (Tokushima University Institutional Repository: 112816, DOI: 10.1007/s10753-016-0482-4, PubMed: 27896541)
36.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Yoshihiro Ohta, Kazumi Ozaki and Takashi Matsuo : Alkannin inhibits CCL3 and CCL5 production in human periodontal ligament cells., Cell Biology International, Vol.40, No.12, 1380-1385, 2016. (Summary) Alkannin, which is found in Alkanna tinctoria, a member of the borage family, is used as a food coloring. Alkannin has recently been reported to have certain biological functions, such as anti-microbial and anti-oxidant effects. It is known that CC chemokine receptor (CCR) 5-positive leukocytes contribute to alveolar bone resorption in periodontal lesions. The aim of this study was to examine whether alkannin inhibits the production of CC chemokine ligand (CCL) 3 and CCL5, which are CCR5 ligands, in human periodontal ligament cells (HPDLC). Interleukin (IL)-1 induced CCL3 and CCL5 production in HPDLC. Alkannin inhibited IL-1-mediated CCL3 and CCL5 production in HPDLC in a dose-dependent manner. Moreover, we revealed that alkannin suppressed inhibitor of kappa B- degradation in IL-1-stimulated HPDLC. In addition, a nuclear factor (NF)-B inhibitor significantly inhibited CCL3 and CCL5 production in IL-1-stimulated HPDLC. These results demonstrate that alkannin inhibits CCR5 ligand production in IL-1-stimulated HPDLC by attenuating the NF-B signaling pathway. (Keyword) Cells, Cultured / Chemokine CCL3 / Chemokine CCL5 / Humans / I-kappa B Proteins / Interleukin-1beta / Ligands / Naphthoquinones / Periodontal Ligament / phosphorylation / Proteolysis / Transcription Factor RelA (Tokushima University Institutional Repository) ● Metadata: 112812 (Link to Publication Site) ● Publication site (DOI): 10.1002/cbin.10692 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27743458 ● Search Scopus @ Elsevier (PMID): 27743458 ● Search Scopus @ Elsevier (DOI): 10.1002/cbin.10692 (Tokushima University Institutional Repository: 112812, DOI: 10.1002/cbin.10692, PubMed: 27743458)
37.	Takamura Haruna, Kaya Yoshida, Hirohiko Okamura, Natsumi Fujiwara and Kazumi Ozaki : Porphyromonas gingivalis attenuates the insulin-induced phosphorylation and translocation of forkhead box protein O1 in human hepatocytes, Archives of Oral Biology, Vol.69, 19-24, 2016. (Tokushima University Institutional Repository) ● Metadata: 111993 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.archoralbio.2016.05.010 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84969142160 (Tokushima University Institutional Repository: 111993, DOI: 10.1016/j.archoralbio.2016.05.010, Elsevier: Scopus)
38.	Ikuko Hosokawa, Yoshitaka Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : Melatonin Inhibits CXCL10 and MMP-1 Production in IL-1-Stimulated Human Periodontal Ligament Cells., Inflammation, Vol.39, No.4, 1520-1526, 2016. (Summary) Melatonin is a hormone that is mainly secreted by the pineal gland and exhibits a wide spectrum of activities, including antioxidant functions. Melatonin has been detected in gingival crevicular fluid. However, the role of melatonin in periodontal tissue is still uncertain. The aim of this study was to examine the effects of melatonin on inflammatory mediator expression in human periodontal ligament cells (HPDLC). Interleukin (IL)-1 induced CXC chemokine ligand (CXCL)10, matrix metalloproteinase (MMP)-1, and tissue inhibitors of metalloproteinase (TIMP)-1 production in HPDLC. Melatonin decreased CXCL10 and MMP-1 production and increased TIMP-1 production in IL-1-stimulated HPDLC. Western blot analysis showed that melatonin inhibited p38 mitogen-activated protein kinase (MAPK) and c-jun N-terminal kinase (JNK) phosphorylation, and IkB- degradation and phosphorylation in IL-1-stimulated HPDLC. These results suggest that melatonin might inhibit Th1 cell migration by reducing CXCL10 production. Moreover, melatonin might inhibit soft tissue destruction by decreasing MMP-1 production in periodontal lesions. (Tokushima University Institutional Repository) ● Metadata: 112815 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-016-0386-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27271323 ● Search Scopus @ Elsevier (PMID): 27271323 ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-016-0386-3 (Tokushima University Institutional Repository: 112815, DOI: 10.1007/s10753-016-0386-3, PubMed: 27271323)
39.	Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Shikonin Inhibits Inflammatory Cytokine Production in Human Periodontal Ligament Cells., Inflammation, Vol.39, No.3, 1124-1129, 2016. (Summary) Shikonin, which is derived from Lithospermum erythrorhizon, a herb used in traditional medicine, has long been considered to be a useful treatment for various diseases in traditional oriental medicine. Shikonin has recently been reported to have several pharmacological properties, e.g., it has anti-microbial, anti-tumor, and anti-inflammatory effects. The aim of this study was to examine whether shikonin is able to influence the production of interleukin (IL)-6, IL-8, and/or chemokine C-C motif ligand (CCL)20, which contribute to the pathogenesis of periodontal disease, in human periodontal ligament cells (HPDLC). The production levels of IL-6, IL-8, and CCL20 in HPDLC were determined using an ELISA. Western blot analysis was used to detect nuclear factor kappa B (NF-B) pathway activation in HPDLC. Shikonin prevented IL-1- or tumor necrosis factor (TNF)--mediated IL-6, IL-8, and CCL20 production in HPDLC. Moreover, we found that shikonin suppressed the phosphorylation and degradation of inhibitor of kappa B-alpha (IB-) in IL-1- or TNF--stimulated HPDLC. These findings suggest that shikonin could have direct beneficial effects against periodontal disease by reducing IL-6, IL-8, and CCL20 production in periodontal lesions. (Tokushima University Institutional Repository) ● Metadata: 112814 (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-016-0344-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27072015 ● Search Scopus @ Elsevier (PMID): 27072015 ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-016-0344-0 (Tokushima University Institutional Repository: 112814, DOI: 10.1007/s10753-016-0344-0, PubMed: 27072015)
40.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : IL-4 Modulates CCL11 and CCL20 Productions from IL-1-Stimulated Human Periodontal Ligament Cells., Cellular Physiology and Biochemistry, Vol.38, No.1, 153-159, 2016. (Summary) These results mean that IL-4 enhanced Th2 cells migration in periodontal lesion to induce CCL11 production from HPDLCs. On the other hand, IL-4 inhibits Th17 cells accumulation in periodontally diseased tissues to inhibit CCL20 production. Therefore, IL-4 is positively related with the pathogenesis of periodontal disease to control chemokine productions in periodontal lesions. (Tokushima University Institutional Repository) ● Metadata: 112953 (Link to Publication Site) ● Publication site (DOI): 10.1159/000438617 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26765337 ● Search Scopus @ Elsevier (PMID): 26765337 ● Search Scopus @ Elsevier (DOI): 10.1159/000438617 (Tokushima University Institutional Repository: 112953, DOI: 10.1159/000438617, PubMed: 26765337)
41.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : Calcitriol Suppressed Inflammatory Reactions in IL-1-Stimulated Human Periodontal Ligament Cells., Inflammation, Vol.38, No.6, 2252-2258, 2015. (Summary) Vitamin D has important roles on control of calcium and phosphate levels in the body. However, the role of vitamin D on the pathogenesis of periodontal disease is still uncertain. Therefore, we examined the effect of the hormonal form of vitamin D, calcitriol, on inflammatory responses of human periodontal ligament cells (HPDLC). We detected vitamin D receptor expression in non-stimulated HPDLC. Calcitriol inhibited interleukin (IL)-6, IL-8, CC chemokine ligand (CCL) 20, CXC chemokine ligand (CXCL) 10, and matrix metalloproteinase (MMP)-3 release from IL-1-stimulated HPDLC. Tissue inhibitor of metalloproteinase (TIMP)-1 production did not change by calcitriol. Moreover, we found c-jun N-terminal kinase (JNK) phosphorylation and IB- degradation in IL-1-stimulated HPDLC were inhibited by calcitriol, and JNK and nuclear factor (NF)-B inhibitors could decrease IL-6, IL-8, CCL20, CXCL10, and MMP-3 productions in IL-1-treated HPDLC. These findings suggest that vitamin D could modulate inflammatory response in periodontal tissues. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-015-0209-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26156812 ● Summary page in Scopus @ Elsevier: 2-s2.0-84946497259 (DOI: 10.1007/s10753-015-0209-y, PubMed: 26156812, Elsevier: Scopus)
42.	Akiho MINATO, Kazumi Ozaki, Natsumi Fujiwara, Hiromi Nakae, Satsuki YABUUCHI and Miwa Matsuyama : Construction of test design for practical evaluation using OSCE method in the dental hygienist education, The Journal of Japan Society of Dental Hygiene Education, Vol.6, No.1, 30-39, 2015. (Keyword) 歯科衛生士教育 / 客観的臨床能力試験(OSCE) / 評価信頼性 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1522543656015655552 (CiNii: 1522543656015655552)
43.	Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Genipin inhibits MMP-1 and MMP-3 release from TNF--stimulated human periodontal ligament cells., Biochimie, Vol.107PB, 391-395, 2014. (Summary) Genipin, the aglycon of geniposide found in gardenia fruit has long been considered for treatment of inflammatory diseases in traditional oriental medicine. Genipin has recently been reported to have some pharmacological functions, such as antimicrobial, antitumor, and anti-inflammatory effects. The aim of this study was to examine whether genipin could modify matrix metalloproteinase (MMP)-1 and MMP-3, which are related to the destruction of periodontal tissues in periodontal lesion, expression in tumor necrosis factor (TNF)--stimulated human periodontal ligament cells (HPDLCs). Genipin prevented TNF--mediated MMP-1 and MMP-3 productions in HPDLCs. Moreover, genipin could suppress not only extracellular signal-regulated kinase (ERK) and Jun-N-terminal kinase (JNK) phosphorylations but also AMP-activated protein kinase (AMPK) phosphorylation in TNF--stimulated HPDLCs. Inhibitors of ERK and AMPK could inhibit both MMP-1 and MMP-3 productions. Moreover, we revealed the ERK inhibitor suppressed AMPK phosphorylation in TNF--stimulated HPDLCs. These data provide a new mechanism through which genipin could be used for the treatment of periodontal disease to prevent MMPs expression in periodontal lesion. (Tokushima University Institutional Repository) ● Metadata: 110103 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biochi.2014.10.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25457105 ● Summary page in Scopus @ Elsevier: 2-s2.0-84915753375 (Tokushima University Institutional Repository: 110103, DOI: 10.1016/j.biochi.2014.10.008, PubMed: 25457105, Elsevier: Scopus)
44.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : IL-22 Enhances CCL20 Production in IL-1-Stimulated Human Gingival Fibroblasts., Inflammation, Vol.37, No.6, 2062-2066, 2014. (Summary) CC chemokine ligand 20 (CCL20) is involved in the recruitment of Th17 cells and thus in the exacerbation of periodontal disease, but the effect of simultaneous interleukin (IL)-22 and IL-1 stimulation on CCL20 production in human gingival fibroblasts (HGFs) is uncertain. In this study, we investigated the mechanisms of IL-1- and/or IL-22-induced CCL20 production in HGFs. A single stimulation of IL-22 could not induce CCL20 production. On the other hand, IL-22 could increase CCL20 production from IL-1-stimulated HGFs in a dose-dependent manner. C-Jun N terminal kinase (JNK) and inhibitor of nuclear factor B (IB)- phosphorylation were increased in IL-1- and IL-22-stimulated HGFs. An inhibitor of nuclear factor (NF)-B decreased IL-1- and IL-22-induced CCL20 production, though an inhibitor of JNK did not modulate CCL20 production. These data suggest that IL-1 in cooperation with IL-22 could increase Th17 cell accumulation in periodontally diseased tissues to enhance CCL20 production in HGFs. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-014-9939-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24902798 ● Summary page in Scopus @ Elsevier: 2-s2.0-84937557635 (DOI: 10.1007/s10753-014-9939-5, PubMed: 24902798, Elsevier: Scopus)
45.	Natsumi Fujiwara, Shizuko Yanagisawa, Hiromi Nakae, Satsuki Yabuuchi, Yasuhiko Shirayama and Kazumi Ozaki : Qualitative analysis focused on the process of learning in clinical training for dental hygiene students, The Journal of Japan Society of Dental Hygiene Education, Vol.5, No.1, 39-45, 2014. (Keyword) 学習プロセス (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521136281135889280 (CiNii: 1521136281135889280)
46.	Masanori Nakano, Kazumi Ozaki, Yasuhiko Shirayama, Miwa Matsuyama, Akemi Nakagawa, Hiromi Nakae, Hiroki Iga, Ruri Ookuma and Ichiro fujishima : 要介護高齢者の口腔ケアを支援する簡易版アセスメントシートの開発, 日本摂食嚥下リハビリテーション学会誌, Vol.18, No.1, 3-12, 2014.
47.	Yoshitaka Hosokawa, Satoru Shindo, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : IL-6 trans-signaling enhances CCL20 production from IL-1-stimulated human periodontal ligament cells., Inflammation, Vol.37, No.2, 381-386, 2014. (Summary) CC chemokine ligand 20 (CCL20) plays a central role in the recruitment of CCR6-expressing cells, including Th17 cells which are related to bone resorption in periodontal lesions and thus in the development of periodontal disease. IL-6 is an important cytokine that is associated with the pathogenesis of periodontitis. However, the effect of IL-6 on CCL20 production is uncertain. The aim of this study was to examine whether IL-6 could modify CCL20 expression in human periodontal ligament cells (HPDLCs). HPDLCs expressed gp130 but did not express IL-6R on the surface of HPDLCs. So, IL-6 trans-signaling is important to recognize IL-6 by HPDLCs. IL-6/sIL-6R stimulation enhanced CCL20 production in IL-1-stimulated HPDLCs. IL-6 produced from IL-1-stimulated HPDLCs with sIL-6R could increase CCL20 production in HPDLCs with sIL-6R. Signal transducer and activator of transcription (STAT)3 activation was related to CCL20 production in IL-1 and IL-6/sIL-6R-stimulated HPDLCs. Our data suggests that HPDLCs, in response to IL-6, sIL-6R, and IL-1, may shift chemokine production to that favoring CCR6-expressing cells recruitment in periodontal lesions. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10753-013-9750-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24081898 ● Summary page in Scopus @ Elsevier: 2-s2.0-84896326562 (DOI: 10.1007/s10753-013-9750-8, PubMed: 24081898, Elsevier: Scopus)
48.	Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Genipin inhibits IL-1-induced CCL20 and IL-6 production from human periodontal ligament cells., Cellular Physiology and Biochemistry, Vol.33, No.2, 357-364, 2014. (Summary) These data provide a novel mechanism through which genipin could be used to provide direct benefits in periodontal disease to inhibit IL-6 and CCL20 productions in periodontal lesions. (Link to Publication Site) ● Publication site (DOI): 10.1159/000356675 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24557363 ● Summary page in Scopus @ Elsevier: 2-s2.0-84895641086 (DOI: 10.1159/000356675, PubMed: 24557363, Elsevier: Scopus)
49.	Ishikawa Makoto, Kaya Yoshida, Hirohiko Okamura, Kazuhiko Ochiai, Takamura Haruna, Natsumi Fujiwara and Kazumi Ozaki : Oral porphyromonas gingivalis translocates to the liver and regulates hepatic glycogen synthesis through the Akt/GSK-3b signaling pathway, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1832, No.12, 2035-2043, 2013. (Summary) Periodontal diseases are common chronic inflammatory disorders that result in the destruction of tissues around teeth. Many clinical studies suggest that periodontal diseases are risk factors for insulin resistance and diabetic mellitus development. However, the molecular mechanisms by which periodontal diseases regulate the progress of diabetes mellitus remain unknown. In this study, we investigated whether Porphyromonas gingivalis (P.g.), a major pathogen of periodontal diseases, present in the oral cavity, moves to the liver and affects hepatic glycogen synthesis. SNAP26b-tagged P.g. (SNAP-P.g.) was introduced into the oral cavity to induce periodontal disease in 4-week old female Balb/c mice. SNAP-P.g. was detected in the liver extracted from SNAP-P.g.-treated mice using nested PCR analysis. High blood glucose levels tended to promote SNAP-P.g. translocation from the oral cavity to the liver in mice. Periodic acid-Schiff staining suggested that hepatic glycogen synthesis decreased in SNAP-P.g.-treated mice. SNAP-P.g. was also internalized into the human hepatoma cell line HepG2, and this attenuated the phosphorylation of insulin receptor substrate (IRS)-1, Akt and glycogen synthase kinase-3β induced by insulin. Insulin-induced glycogen synthesis was suppressed by SNAP-P.g. in HepG2 cells. Our results suggest that P.g. translocation from the oral cavity to the liver may contribute to the progress of diabetes mellitus by influencing hepatic glycogenesis. (Keyword) periodontal disease / diabetes mellitus / Porphyromonas gingivalis / Hepatic glycogenesis / SNAP26b (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbadis.2013.07.012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23899607 ● Search Scopus @ Elsevier (PMID): 23899607 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbadis.2013.07.012 (DOI: 10.1016/j.bbadis.2013.07.012, PubMed: 23899607)
50.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : (-)-Epigallocatechin-3-Gallate Inhibits CC Chemokine Ligand 11 Production in Human Gingival Fibroblasts., Cellular Physiology and Biochemistry, Vol.31, No.6, 960-967, 2013. (Summary) Background: CC chemokine ligand 11 (CCL11) is related to Th2 cells migration via CC chemokine receptor 3 (CCR3). Th2 cells are involved in the etiology of periodontal disease. However, how the infiltration of Th2 cells is controlled in periodontally diseased tissues is unknown. (-)-Epigallocatechin gallate (EGCG), the major catechin in green tea, has multiple beneficial effects, but the effects of EGCG on CCL11 production are uncertain. In this study, we investigated whether cytokines could induce CCL11 production in human gingival fibroblasts (HGFs). Moreover, we examined the effects of EGCG on CCL11 production in HGFs. Methods and Results: ELISA analysis disclosed that interleukin (IL)-4 synergistically enhanced CCL11 production in IL-1 or tumor necrosis factor (TNF)--stimulated HGFs. EGCG prevented IL-1/ IL-4 or TNF-/IL-4-mediated CCL11 production in a concentration dependent manner. CCL11 production in HGFs was positively regulated by p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), and c-Jun N terminal kinase (JNK). Western blot analysis revealed that EGCG treatment prevented IL-1/IL-4 or TNF-/IL-4-induced ERK and JNK activation in HGFs. Conclusions: These data provide that CCL11 production in HGFs could be associated with Th2 cells infiltration in periodontal lesions. Moreover, EGCG is useful for periodontitis treatment to inhibit CCL11 production. (Link to Publication Site) ● Publication site (DOI): 10.1159/000350114 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23839108 ● Search Scopus @ Elsevier (PMID): 23839108 ● Search Scopus @ Elsevier (DOI): 10.1159/000350114 (DOI: 10.1159/000350114, PubMed: 23839108)
51.	Yasuhiko Shirayama, Kazumi Ozaki, Masanori Nakano, 薮内さつき, Hiromi Nakae, 那賀川明美 and Hiroki Iga : The usefulness of advising chart storage system for oral care which utilized cloud computing, General Rehabilitation, Vol.41, No.6, 569-572, 2013. (Keyword) 口腔保健業務支援システム / 口腔ケア / 要介護高齢者 / 参与観察 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390283684933932928 (CiNii: 1390283684933932928)
52.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : TLR3 agonist enhances CC chemokine ligand 20 production in IL-1-stimulated human gingival fibroblasts., Cellular Immunology, Vol.283, No.1-2, 8-11, 2013. (Summary) Viruses are related to the etiology of periodontitis. However, the role of viruses on Th17 cells infiltration in periodontitis lesions is unknown. Therefore, we examined the effects of TLR3 ligand on CCL20, which is related to Th17 cells migration, production in human gingival fibroblasts (HGFs). Polyinosinic-polycytidylic acid (Poly I:C), which is a TLR3 agonist, stimulation could moderately induce CCL20 production in HGFs. Poly I:C synergistically enhanced CCL20 expression from IL-1-stimulated HGFs. Inhibitors of p38 MAPK, extracellular signal-regulated kinase (ERK), c-Jun N terminal kinase (JNK), and NF-B significantly inhibited CCL20 production in Poly I:C/IL-1-stimulated HGFs. Western blot analysis disclosed phosphorylation of p38 MAPK, JNK, and IB- were enhanced in Poly I:C/IL-1-treated HGFs. These data suggested that virus infection is related to Th17 cells migration in periodontitis lesion to induce CCL20 production in HGFs via TLR3. Therefore, our results indicated that virus might be important pathogen in periodontal disease. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.cellimm.2013.05.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23850670 ● Search Scopus @ Elsevier (PMID): 23850670 ● Search Scopus @ Elsevier (DOI): 10.1016/j.cellimm.2013.05.005 (DOI: 10.1016/j.cellimm.2013.05.005, PubMed: 23850670)
53.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Tumor necrosis factor-like weak inducer of apoptosis increases CC chemokine ligand 20 production in interleukin 1-stimulated human gingival fibroblasts., Human Immunology, Vol.73, No.5, 470-473, 2012. (Summary) CC chemokine ligand 20 (CCL20) is related to T-helper (Th)-17 cell migration, and Th17 cells play important roles in exacerbation in periodontal disease. However, the effect of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) on CCL20 production is unknown. In this study, we examined the mechanisms of TWEAK in combination with interleukin (IL)-1-induced CCL20 production in human gingival fibroblasts (HGFs). TWEAK alone did not induce CCL20 production in HGFs. However, TWEAK enhanced CCL20 expression from IL-1-stimulated HGFs in a dose-dependent manner. Inhibitors of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase (ERK), protein kinase B (Akt), and nuclear factor B (NF-B) significantly inhibited CCL20 production in TWEAK and IL-1-stimulated HGFs. Western blot analysis revealed that phosphorylations of ERK, Akt, and inhibitor of NF-B were enhanced in TWEAK and IL-1-treated HGFs. These data suggest that TWEAK is positively related to Th17 cell migration in periodontally diseased tissues to enhance CCL20 production in IL-1-stimulated HGFs. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.humimm.2012.02.021 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22425737 ● Search Scopus @ Elsevier (PMID): 22425737 ● Search Scopus @ Elsevier (DOI): 10.1016/j.humimm.2012.02.021 (DOI: 10.1016/j.humimm.2012.02.021, PubMed: 22425737)
54.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Interleukin (IL)-17A synergistically enhances CC chemokine ligand 20 production in IL-1-stimulated human gingival fibroblasts., Human Immunology, Vol.73, No.1, 26-30, 2012. (Summary) CC chemokine ligand 20 (CCL20) plays a pivotal role in the recruitment of T-helper (Th)-17 cells and thus in the development of periodontal disease, but the effect of simultaneous interleukin (IL)-17A and IL-1 stimulation on CCL20 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms of IL-1- and IL-17A-induced CCL20 production in HGFs. IL-17A synergistically enhanced CCL20 production from IL-1-stimulated HGFs in a concentration-dependent manner. Extracellular signal-regulated kinase (ERK) and inhibitor of nuclear factor (NF)-B- phosphorylation were increased in IL-1- and IL-17A-stimulated HGFs. Inhibitors of or ERK and NF-B decreased IL-1- and IL-17A-induced CCL20 production. IL-1 stimulation elevated IL-17 receptor C expression on HGFs. These data suggest that IL-1 is actively related to Th17 cell migration into peripheral tissues to induce production of the Th17 chemokine, CCL20. Therefore, IL-1 might be a therapeutic target for Th17-related diseases, such as periodontal disease and arthritis. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.humimm.2011.10.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22019504 ● Search Scopus @ Elsevier (PMID): 22019504 ● Search Scopus @ Elsevier (DOI): 10.1016/j.humimm.2011.10.004 (DOI: 10.1016/j.humimm.2011.10.004, PubMed: 22019504)
55.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Black tea polyphenol inhibits CXCL10 production in oncostatin M-stimulated human gingival fibroblasts., International Immunopharmacology, Vol.11, No.6, 670-674, 2011. (Summary) CXC chemokine ligand 10 (CXCL10) plays an important role in the infiltration of Th1 cells and thus in the exacerbation of periodontal disease. Theaflavin-3,3'-digallate (TFDG), polyphenol in black tea, has some beneficial effects but the effect of TFDG on CXCL10 production from human gingival fibroblasts (HGFs) is uncertain. In this study, we investigated the mechanisms by which TFDG may inhibit oncostatin M (OSM)-induced CXCL10 production in human gingival fibroblasts. TFDG prevented OSM-mediated CXCL10 production by HGFs in a dose dependent manner. TFDG significantly inhibited OSM-induced phosphorylation of c-Jun N terminal kinase (JNK), protein kinase B (Akt) (Ser473) that are related to CXCL10 production from OSM-stimulated HGFs. In addition, TFDG suppressed OSM receptor (OSMR) β expression on HGFs. These data provide a novel mechanism where the black tea flavonoid, theaflavin, could provide direct benefits in periodontal disease. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.intimp.2011.01.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21255696 ● Search Scopus @ Elsevier (PMID): 21255696 ● Search Scopus @ Elsevier (DOI): 10.1016/j.intimp.2011.01.009 (DOI: 10.1016/j.intimp.2011.01.009, PubMed: 21255696)
56.	中江弘美, Daisuke Hinode, 薮内さつき, Yuko Takeuchi, Masami Yoshioka, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Kazumi Ozaki, Masaru Hada, Fumiaki Kawano and Katsuhiko Yoshimoto : 地域高齢者との福祉体験学習の教育効果と地域貢献事業としての評価, Journal of University Education Research, Vol.8, 17-24, 2011. (Summary) The purose of this study is to evaluate the educational effect by the welfare-experience learning program with aged people in community，and to evaluate this program as the regional contribution. This program is to aim at having a consciousness of becoming the dental professional in the University of Tokushima，Faculty of Dentistry，and they were carried out with 16 institutions (a total of 28 times).This program makes students accompany the oral health guidance"long-life oral healthy classroom"，and they carried out the experience study as on auxiliary person of the variaus functional oral-training for elderly people.By the investigation of the student's report, there are students who recognized the achievement objectives which are roles of the way concerning regional contribution as dental professionals in community. On the other hand，the questionnaire to the participating persoonnel was conducted in order to evalaote this program as the regional contrtbution. As a result，this program is useful to elderly people and the understanding of institution personnel is also deepened this practice. As mentioned above，the result of having is suitable for the educational goal "to have a consciousness of becoming the dental professional". Furthermore，this program was considered that future continuation is also expected by deepening of an understanding to the personnel's functional oral-training program.本研究の目的は，地域高齢者との福祉体験学習における学生への教育効果と，地域貢献事業としての評価をすることである．徳島大学歯学部では，医療人を志すものとしての自覚を持つことを目的とした取り組みを県内16カ所の施設で合計28回実施した．これは，学生が口腔保健指導「お口の健康長寿教室」において，高齢者を対象とした口腔機能訓練の補助者として体験学習するものである．学習後のレポートから，到達目標とした地域貢献の在り方や歯科専門職としての役割を認識する学生が多くを占めた．一方，地域貢献事業として評価するため，参加職員への調査を行った結果，利用者への役立ちに加え，多くの施設職員の理解も深まったとのアンケート結果が得られた．以上から，本取り組みは学生への教育目標「医療人としての自覚を持つ」に沿った成果が得られており，また，施設職員の口腔機能向上プ口グラムへの盤解の深まりから，今後の継続が期待される． (Keyword) 体験学習 / タイケンガクシュウ / 教育効果 / キョウイクコウカ / 地域貢献 / チイキコウケン / experience learning / experience learning / regional contribution / regional contribution / educational effects / educational effects (Tokushima University Institutional Repository) ● Metadata: 82982 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050564287417217536 (Tokushima University Institutional Repository: 82982, CiNii: 1050564287417217536)
57.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Oncostatin M synergistically induces CXCL10 and ICAM-1 expression in IL-1beta-stimulated-human gingival fibroblasts., Journal of Cellular Biochemistry, Vol.111, No.1, 40-48, 2010. (Summary) Periodontitis is a chronic bacterial infection of tooth-supporting structures. T-helper type 1 (Th1) cells are related to the exacerbation of periodontal disease. Human gingival fibroblasts (HGFs), the major cell type in periodontal connective tissues, are involved in immunological response in periodontal tissues. However, it is uncertain whether HGFs are related to Th1 response. Chemokine (C-X-C motif) ligand 10 (CXCL10) is a cytokine, that is related to Th1 cells migration. Intercellular adhesion molecule (ICAM)-1 is involved in Th1 cells retention and activation in inflamed tissue. The aim of this study is to examine the effect of oncostatin M (OSM) on CXCL10 and ICAM-1 expression in HGFs. OSM stimulation induced CXCL10 and ICAM-1 expression in HGFs. Moreover, the synergistic effects of CXCL10 release and ICAM-1 expression in HGFs were observed with combined stimulation of interleukin (IL)-1beta and OSM. OSM increased type 1 IL-1 receptor (IL-1R1) expression, and IL-1beta enhanced OSMRbeta expression on HGFs. IL-1beta + OSM stimulation enhanced the phosphorylation of inhibitor of nuclear factor kappaB (IkappaB)-alpha, signal transducer and activator of transcription (STAT)3, c-Jun N terminal kinase (JNK), and protein kinase B (Akt) compared to OSM or IL-1beta stimulation. CXCL10 production from OSM + IL-1beta stimulated HGFs was suppressed by nuclear factor (NF)-kappaB, STAT3, JNK, and phosphoinositide-3-kinase (PI3K) inhibitors. On the other hand, only NF-kappaB and STAT3 inhibitors suppressed ICAM-1 expression enhanced by OSM + IL-1beta treatment. These effects of OSM and IL-1beta may promote Th1 cells infiltration and retention in periodontally diseased tissues and be related to exacerbation of periodontal disease. J. Cell. Biochem. 111: 40-48, 2010. (c) 2010 Wiley-Liss, Inc. (Link to Publication Site) ● Publication site (DOI): 10.1002/jcb.22648 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20680966 ● Search Scopus @ Elsevier (PMID): 20680966 ● Search Scopus @ Elsevier (DOI): 10.1002/jcb.22648 (DOI: 10.1002/jcb.22648, PubMed: 20680966)
58.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Tea polyphenols inhibit IL-6 production in tumor necrosis factor superfamily 14-stimulated human gingival fibroblasts., Molecular Nutrition & Food Research, Vol.54 Suppl 2, S151-8, 2010. (Summary) IL-6 is well recognized to be a potent bone resorptive agent and thus in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins in green tea, and theaflavin-3,3'-digallate (TFDG), polyphenol in black tea, have multiple beneficial effects, but the effects of catechins and theaflavins on IL-6 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms by which EGCG, ECG, and TFDG inhibit tumor necrosis factor superfamily 14 (TNFSF14)-induced IL-6 production in HGFs. We detected TNFSF14 mRNA expression in human diseased periodontal tissues. TNFSF14 increased IL-6 production in HGFs in a concentration-dependent manner. EGCG, ECG, and TFDG prevented TNFSF14-mediated IL-6 production in HGFs. EGCG, ECG, and TFDG prevented TNFSF14-induced extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor-kappaB activation in HGFs. Inhibitors of ERK, JNK, and nuclear factor-kappaB decreased TNFSF14-induced IL-6 production. In addition, EGCG, ECG, and TFDG attenuated TNFSF14 receptor expression on HGFs. These data provide a novel mechanism through which the green tea and black tea polyphenols could be used to provide direct benefits in periodontal disease. (Link to Publication Site) ● Publication site (DOI): 10.1002/mnfr.200900549 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20461739 ● Search Scopus @ Elsevier (PMID): 20461739 ● Search Scopus @ Elsevier (DOI): 10.1002/mnfr.200900549 (DOI: 10.1002/mnfr.200900549, PubMed: 20461739)
59.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts, The Journal of Nutritional Biochemistry, Vol.21, No.7, 659-664, 2010. (Summary) CXC chemokine ligand 10 (CXCL10) plays a pivotal role in the recruitment of Th1 cells and, thus, in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins derived from green tea, have multiple beneficial effects, but the effects of catechins on CXCL10 production from human gingival fibroblasts (HGFs) is not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit oncostatin M (OSM)-induced CXCL10 production in HGFs. HGFs constitutively expressed glycoprotein 130 and OSM receptor beta (OSMR beta), which are OSM receptors. OSM increased CXCL10 production in a concentration-dependent manner. EGCG and ECG prevented OSM-mediated CXCL10 production by HGFs. Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription (STAT)3 decreased OSM-induced CXCL10 production. EGCG significantly prevented OSM-induced phosphorylation of JNK, Akt (Ser473) and STAT3 (Tyr705 and Ser727). ECG prevented phosphorylation of JNK and Akt (Ser473). In addition, EGCG and ECG attenuated OSMR beta expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids, catechins, can provide direct benefits in periodontal disease. (Keyword) Anti-Inflammatory Agents, Non-Steroidal / Antioxidants / Catechin / Cells, Cultured / Chemokine CXCL10 / Cytokine Receptor gp130 / Enzyme Inhibitors / Fibroblasts / Gene Expression Regulation / Gingiva / Humans / Oncostatin M / Oncostatin M Receptor beta Subunit / Osmolar Concentration / Periodontal Diseases / Phosphorylation / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jnutbio.2009.04.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19616927 ● Search Scopus @ Elsevier (PMID): 19616927 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2009.04.005 (DOI: 10.1016/j.jnutbio.2009.04.005, PubMed: 19616927)
60.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo : Proinflammatroy effects of muramyldipeptide on human gingival fibroblasts, Journal of Periodontal Research, Vol.45, No.2, 193-199, 2010. (Summary) Because human gingival fibroblasts (HGFs) are the predominant cells in periodontal tissues, we hypothesized that HGFs are contributed to receptors for components of bacteria. In this study, we focused on expression and function of nucleotide binding oligomerization domain 2 (NOD2) in HGFs, which is a mammalian cytosolic pathogen recognition molecule. Expression of NOD2 in HGFs was examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry. Production of interleukin (IL)-6, IL-8, cc chemokine ligand2, cxc chemokine ligand10 (CXCL10) and CXCL11 from HGFs was examined by enzyme-linked immunosorbent assay (ELISA). We used RT-PCR and immunohistochemistry to detect the NOD2 expression in human gingival tissues. We found clear NOD2 expression in HGFs. Upon stimulation with NOD2 agonist, muramyldipeptide (MDP), production of proinflammatory cytokines was enhanced. Moreover, MDP-induced production of proinflammatory cytokines was inhibited in a different manner by mitogen-activated protein kinase inhibitors and phosphatidylinositol 3-kinase inhibitor. Furthermore, MDP enhanced CXCL10 and CXCL11 productions by tumor necrosis factor-alpha (TNF-alpha)- or interferon-gamma (IFN-gamma)-stimulated HGFs, although MDP alone did not induce these chemokines. TNF-alpha and IFN-gamma increased NOD2 expression in HGFs. In addition, we detected NOD2 expression in mononuclear cells and HGFs in periodontally diseased tissues. These findings indicate that MDP which induces production of cytokines and chemokines from HGFs is related to the pathogenesis of periodontal disease. (Keyword) Acetylmuramyl-Alanyl-Isoglutamine / Adult / Anthracenes / Calcium-Calmodulin-Dependent Protein Kinases / Cells, Cultured / Chemokine CCL2 / Chemokine CXCL10 / Chemokine CXCL11 / Chromones / Chronic Periodontitis / Enzyme Inhibitors / Female / Fibroblasts / Flavonoids / Gingiva / Humans / Imidazoles / Inflammation Mediators / Interferon-gamma / Interleukin-6 / Interleukin-8 / JNK Mitogen-Activated Protein Kinases / Male / Middle Aged / Morpholines / Nod2 Signaling Adaptor Protein / Periodontal Attachment Loss / Periodontal Pocket / Phosphatidylinositol 3-Kinases / Pyridines / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2009.01217.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20470259 ● Search Scopus @ Elsevier (PMID): 20470259 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2009.01217.x (DOI: 10.1111/j.1600-0765.2009.01217.x, PubMed: 20470259)
61.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : TNFSF14 coordinately enhances CXCL10 and CXCL11 production from IFN-gamma-stimulated human gingival fibroblasts, Molecular Immunology, Vol.47, No.4, 666-670, 2010. (Summary) TNFSF14 is involved in the pathogenesis of some inflammatory diseases such as arthritis. CXCL10 and CXCL11 recruit Th1 cells, and the productions of these chemokines are related to the exacerbation of some inflammatory diseases including arthritis and periodontal disease. We examined in vitro effects of TNFSF14 on IFN-gamma-induced CXCL10 and CXCL11 production in human gingival fibroblasts (HGFs). HGFs constitutively expressed TNFSF14 receptors, LTbetaR and HVEM. TNFSF14 enhanced IFN-gamma-induced secretion of CXCL10 and CXCL11 from HGFs. IFN-gamma treatment increased HVEM expression on HGFs. TNFSF14 in combination with IFN-gamma resulted in increased activation of p38 MAPK, ERK and IkappaB-alpha compared with TNFSF14 or IFN-gamma alone. Moreover, inhibitors of p38 MAPK, ERK and NF-kappaB abolished the CXCL10 and CXCL11 productions from TNFSF14 with IFN-gamma-stimulated HGFs. These effects of TNFSF14 may promote the infiltration of Th1 cells into lesions with inflammatory diseases. TNFSF14 might act as a proinflammatory cytokine in some inflammatory diseases thus is a candidate therapeutic target. (Keyword) Chemokine CXCL10 / Chemokine CXCL11 / Extracellular Signal-Regulated MAP Kinases / Fibroblasts / Gingiva / Humans / I-kappa B Proteins / Interferon-gamma / Lymphotoxin beta Receptor / MAP Kinase Kinase Kinases / Phosphorylation / Protein Kinase Inhibitors / Proto-Oncogene Proteins / RNA, Messenger / Receptors, Tumor Necrosis Factor, Member 14 / Signal Transduction / Tumor Necrosis Factor Ligand Superfamily Member 14 / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.molimm.2009.10.018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19939453 ● Search Scopus @ Elsevier (PMID): 19939453 ● Search Scopus @ Elsevier (DOI): 10.1016/j.molimm.2009.10.018 (DOI: 10.1016/j.molimm.2009.10.018, PubMed: 19939453)
62.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Catechins Inhibit CCL20 Production in IL-17A-stimulated Human Gingival Fibroblasts, Cellular Physiology and Biochemistry, Vol.24, No.5-6, 391-396, 2009. (Summary) CC chemokine ligand 20 (CCL20) plays a pivotal role in the recruitment of Th17 cells and thus in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins in green tea, have multiple beneficial effects, but the effects of catechins on CCL20 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit interleukin (IL)-17A-induced CCL20 production in human gingival fibroblasts. IL-17A increased CCL20 production in HGFs in a concentration-dependent manner. EGCG and ECG prevented IL-17A-mediated CCL20 production in HGFs. Inhibitors of p38 mitogen-activated protein kinase (MAPK) or extracellular signal-regulated kinase (ERK) decreased IL-17A-induced CCL20 production. EGCG and ECG prevented IL-17A-induced phosphorylation of p38 MAPK and ERK in HGFs. In addition, EGCG and ECG attenuated IL-17 receptor expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids catechins could be used to provide direct benefits in periodontal disease. (Keyword) Antioxidants / Catechin / Cells, Cultured / Chemokine CCL20 / Extracellular Signal-Regulated MAP Kinases / Fibroblasts / Gingiva / Humans / Interleukin-17 / Phosphorylation / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1159/000257431 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19910679 ● Search Scopus @ Elsevier (PMID): 19910679 ● Search Scopus @ Elsevier (DOI): 10.1159/000257431 (DOI: 10.1159/000257431, PubMed: 19910679)
63.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Human gingival fibroblasts express functional chemokine receptor CXCR6., Clinical and Experimental Immunology, Vol.156, No.3, 413-418, 2009. (Summary) We have reported that CXCL16, a recently discovered transmembrane chemokine, is expressed in human gingival fibroblasts (HGF). However, it is not known whether HGF express CXCR6, the receptor for CXCL16, or CXCL16 affects HGF biology. We have shown that HGF expressed CXCR6 by reverse transcription-polymerase chain reaction and flow cytometric analysis. Moreover, we elucidated that tumour necrosis factor (TNF)-alpha and cytosine-guanine dinucleotide (CpG) DNA (Toll-like receptor-9 ligand) treatment enhanced CXCR6 expression by HGF. Interleukin (IL)-4, IL-13 and CpG DNA up-regulated CXCR6 expression by TNF-alpha-stimulated HGF. On the other hand, IL-1beta and interferon-gamma inhibited CXCR6 expression on TNF-alpha-treated HGF. CXCL16 treatment induced HGF proliferation and phosphorylation of extracellular regulated kinase (ERK) and protein kinase B (AKT) in HGF. In conclusion, HGF expressed CXCR6 functionally, because CXCL16 induced HGF proliferation and ERK and AKT phosphorylation in HGF. These results indicate that CXCL16 may play an important role in the pathogenesis and remodelling in periodontally diseased tissues. (Keyword) Cell Proliferation / Cells, Cultured / Chemokines, CXC / CpG Islands / Cytokines / Extracellular Signal-Regulated MAP Kinases / Fibroblasts / Gingiva / Humans / Ligands / Proto-Oncogene Proteins c-akt / Receptors, Chemokine / Receptors, Scavenger / Receptors, Virus / Reverse Transcriptase Polymerase Chain Reaction / Toll-Like Receptors (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2009.03915.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19438592 ● Search Scopus @ Elsevier (PMID): 19438592 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2009.03915.x (DOI: 10.1111/j.1365-2249.2009.03915.x, PubMed: 19438592)
64.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Cytokines differentially regulate CXCL10 production by interferon-gamma-stimulated or tumor necrosis factor-alpha-stimulated human gingival fibroblasts., Journal of Periodontal Research, Vol.44, No.2, 225-231, 2009. (Summary) CXC chemokine 10 (CXCL10) activates CXC chemokine receptor 3 (CXCR3) and attracts activated T-helper 1 cells. In this study we examined the effects of cytokines on CXCL10 production by human gingival fibroblasts. Human gingival fibroblasts were exposed to pro-inflammatory cytokines (interleukin-1beta, tumor necrosis factor-alpha), a T-helper 1 cytokine (interferon-gamma), T-helper 2 cytokines (interleukin-4, interleukin-13), T-helper 17 cytokines (interleukin-17A, interleukin-22) and regulatory T-cell cytokines (interleukin-10, transforming growth factor-beta1) for 24 h. CXCL10 production by human gingival fibroblasts was examined by enzyme-linked immunosorbent assay. Human gingival fibroblasts produced CXCL10 protein upon stimulation with interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma. Treatment of human gingival fibroblasts with interferon-gamma in combination with tumor necrosis factor-alpha or interleukin-1beta resulted in a synergistic production of CXCL10. However, interleukin-4 and interleukin-13 inhibited CXCL10 production by interferon-gamma-stimulated or tumor necrosis factor-alpha-stimulated-human gingival fibroblasts. On the other hand, interleukin-17A and interleukin-22 enhanced CXCL10 production by human gingival fibroblasts treated with interferon-gamma and inhibited CXCL10 production by tumor necrosis factor-alpha-stimulated human gingival fibroblasts. Furthermore, the anti-inflammatory cytokine, interleukin-10, inhibited CXCL10 production by both interferon-gamma- and tumor necrosis factor-alpha-stimulated human gingival fibroblasts, but transforming growth factor-beta1 enhanced interferon-gamma-mediated CXCL10 production by human gingival fibroblasts. These results mean that the balance of cytokines in periodontally diseased tissue may be essential for the control of CXCL10 production by human gingival fibroblasts, and the production of CXCL10 might be important for the regulation of T-helper 1 cell infiltration in periodontally diseased tissue. (Keyword) Adult / Cells, Cultured / Chemokine CXCL10 / Cytokines / Female / Fibroblasts / Gingiva / Humans / Inflammation Mediators / Interferon-gamma / Interleukins / Periodontitis / Th1 Cells / Transforming Growth Factor beta1 / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2008.01124.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18973545 ● Search Scopus @ Elsevier (PMID): 18973545 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2008.01124.x (DOI: 10.1111/j.1600-0765.2008.01124.x, PubMed: 18973545)
65.	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) 口腔保健福祉 / コウクウホケンフクシ / 健康長寿支援 / ケンコウチョウジュシエン / ホスピタリティマインド / ホスピタリティマインド / oral health and welfare / oral health and welfare / health support program / health support program / hospitality mind / hospitality mind (Tokushima University Institutional Repository) ● Metadata: 82696 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050282812440496128 (Tokushima University Institutional Repository: 82696, CiNii: 1050282812440496128)
66.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : CC Chemokine ligand 17 in periodontal diseases: expression in diseased tissues and production by human gingival fibroblasts, Journal of Periodontal Research, Vol.43, No.4, 471-477, 2008. (Summary) It has been reported that T helper 2 (Th2) cells are related to exacerbation of periodontal disease. However, it is uncertain how the migration of Th2 cells is controlled. In this study, we examined the expression of CC chemokine ligand 17 (CCL17), which is a Th2 chemokine, in periodontal tissues. Moreover, we investigated the effects of cytokines and toll-like receptor (TLR) ligands on the production of CCL17 by human gingival fibroblasts (HGFs). We used immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) to detect CCL17 in periodontal tissues. HGFs were exposed to cytokines and TLR ligands. Expression of CCL17 was examined by RT-PCR and enzyme-linked immunosorbent assay. We used signal transduction inhibitors in some experiments. Both CCL17 and its receptor, CC chemokine receptor 4 (CCR4), were expressed in diseased periodontal tissues. A combination of tumour necrosis factor alpha (TNF-alpha) and interleukin (IL)-4/IL-13 increased CCL17 expression. Moreover, treatment of HGFs with a low dose of interferon-gamma (IFN-gamma) in combination with TNF-alpha and IL-4 or IL-13 had synergistic effects on the production of CCL17, whereas a high dose of IFN-gamma inhibited CCL17 production. Furthermore, Escherichia coli (E. coli) lipopolysaccharide (TLR4 ligand) and Pam3CSK4 (TLR2 ligand) inhibited CCL17 production by TNF-alpha + IL-4-stimulated HGFs, while CpG DNA (TLR9 ligand) enhanced TNF-alpha + IL-4 induced-CCL17 production by HGFs. Furthermore, a c-Jun NH2 terminal kinase (JNK) inhibitor, a phosphatidylinositol-3-kinase (PI3K) inhibitor and a nuclear factor kappa B (NF-kappa B) inhibitor inhibited CCL17 production by HGFs. These results suggest that the CCL17 produced by HGFs may be involved in the migration of Th2 cells into inflamed tissues, and provide evidence that CCL17 production is controlled by cytokines and TLR ligands in periodontal disease. (Keyword) Chemokine CCL17 / Cytokines / Escherichia coli / Fibroblasts / Gingiva / Humans / Interferon-gamma / Interleukin-13 / Interleukin-4 / JNK Mitogen-Activated Protein Kinases / Ligands / Lipopeptides / Lipopolysaccharides / NF-kappa B / Peptides / Periodontal Diseases / Phosphatidylinositol 3-Kinases / Receptors, CCR4 / Reverse Transcriptase Polymerase Chain Reaction / Th2 Cells / Toll-Like Receptor 2 / Toll-Like Receptor 4 / Toll-Like Receptor 9 / Toll-Like Receptors / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0765.2007.01080.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18557811 ● Search Scopus @ Elsevier (PMID): 18557811 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2007.01080.x (DOI: 10.1111/j.1600-0765.2007.01080.x, PubMed: 18557811)
67.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Adrenomedullin suppresses tumour necrosis factor alpha-induced CXC chemokine ligand 10 production by human gingival fibroblasts., Clinical and Experimental Immunology, Vol.152, No.3, 568-575, 2008. (Summary) Periodontal disease is an inflammatory disorder characterized by the involvement of chemokines that are important for the recruitment of leucocytes. Several cytokines, including tumour necrosis factor alpha (TNF-alpha), are involved in regulating levels of chemokines in periodontal disease. CXC chemokine ligand 10 (CXCL10) is a chemokine related to the migration of T helper 1 cells. In this study, we examined CXCL10 expression in human gingival fibroblasts (HGFs). Moreover, we investigated the effects of adrenomedullin (AM), which is a multi-functional regulatory peptide, on the production of CXCL10 by HGFs. We revealed that TNF-alpha stimulation induced CXCL10 production by HGFs. HGFs expressed AM and AM receptors, calcitonin-receptor-like receptor (CRLR) and receptor-activity-modifying protein (RAMP) 2, mRNAs constitutively. AM treatment supressed CXCL10 production by TNF-alpha-stimulated HGFs. Moreover, we elucidated that AM produced by HGFs inhibited CXCL10 production by HGFs, because AM antagonist enhanced CXCL10 production by HGFs. TNF-alpha treatment enhanced CRLR and RAMP2 mRNA expression in HGFs. Furthermore, AM is expressed in human periodontal tissues, including both inflamed and clinically healthy tissues. These results suggest that the CXCL10 produced by HGFs may be involved in the migration of leucocytes into inflamed tissues and related to exacerbation of periodontal disease. AM might be a therapeutic target of periodontal disease, because AM can inhibit CXCL10 production by HGFs. (Keyword) periodontal disease (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2008.03647.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18435806 ● Search Scopus @ Elsevier (PMID): 18435806 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2008.03647.x (DOI: 10.1111/j.1365-2249.2008.03647.x, PubMed: 18435806)
68.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : CXC chemokine ligand 16 in periodontal diseases: expression in diseased tissues and production by cytokine-stimulated human gingival fibroblasts., Clinical and Experimental Immunology, Vol.149, No.1, 146-154, 2007. (Summary) Periodontal disease is an inflammatory disorder characterized by the involvement of chemokines that are important for the recruitment of leucocytes. Several cytokines are involved in regulating levels of chemokines in periodontal disease. CXCL16 is a chemokine related to the migration of T helper 1 (Th1) cells and natural killer (NK) cells. In this study, we examined its expression in periodontal tissues. Moreover, we investigated the effects of cytokines on the production of CXCL16 by human gingival fibroblast (HGF). Reverse transcription-polymerase chain reaction (RT-PCR) analysis and immunohistochemistry revealed that CXCL16 and its receptor, CXCR6, were expressed at the mRNA and protein levels in diseased tissues. Proinflammatory cytokines [interleukin (IL)-1beta, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma] increased the mRNA expression and release of CXCL16 in a dose-dependent manner. Moreover, treatment of HGFs with IFN-gamma in combination with IL-1beta had a synergistic effect on the production of CXCL16. On the other hand, IL-4 and IL-13 inhibited the IL-1beta-induced CXCL16 production by HGFs. Inhibitors of A disintegrin and metalloprotease (ADAM)10 and ADAM17, a recently identified protease of CXCL16, reduced the amount of CXCL16 released from HGFs. These results suggest that the CXCL16 produced by HGFs may be involved in the migration of leucocytes into inflamed tissues, and provide evidence that CXCL16 production is controlled by cytokines in periodontal disease. (Keyword) Aged / Cells, Cultured / Chemokines, CXC / Chronic Disease / Cytokines / Female / Fibroblasts / Gene Expression / Gingiva / Humans / Interferon-gamma / Interleukin-13 / Interleukin-1beta / Interleukin-4 / Male / Metalloproteases / Middle Aged / Mitogen-Activated Protein Kinases / Periodontitis / RNA, Messenger / Receptors, Chemokine / Receptors, Scavenger / Receptors, Virus / Reverse Transcriptase Polymerase Chain Reaction (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2007.03398.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17459077 ● Search Scopus @ Elsevier (PMID): 17459077 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2007.03398.x (DOI: 10.1111/j.1365-2249.2007.03398.x, PubMed: 17459077)
69.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Proinflammatory effects of tumour necrosis factor-like weak inducer of apoptosis (TWEAK) on human gingival fibroblasts., Clinical and Experimental Immunology, Vol.146, No.3, 540-549, 2006. (Summary) Tumour necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), a member of the TNF family, is a multi-functional cytokine that regulates cellular proliferation, angiogenesis, inflammation and apoptosis. In this study, we investigated TWEAK expression in periodontally diseased tissues and the effect of TWEAK on human gingival fibroblasts (HGF). Reverse transcription-polymerase chain reaction (RT-PCR) analysis and immunohistochemistry revealed that TWEAK and the TWEAK receptor, fibroblast growth factor-inducible 14 (Fn14), mRNA and protein were expressed in periodontally diseased tissues. HGF expressed Fn14 and produced interleukin (IL)-8 and vascular endothelial growth factor (VEGF) production upon TWEAK stimulation in a dose-dependent manner. The IL-8 and VEGF production induced by TWEAK was augmented synergistically by simultaneous stimulation with transforming growth factor (TGF)-beta1 or IL-1beta. IL-1beta and TGF-beta1 enhanced Fn14 expression in a dose-dependent manner. Moreover, TWEAK induced intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression on HGF in a dose-dependent manner. The ICAM-1 expression induced by TWEAK was augmented by TGF-beta1. On the other hand, the TWEAK-induced VCAM-1 expression was inhibited by TGF-beta1. Phosphatidylinositol 3-kinase (PI3K) and nuclear factor-kappaB (NF-kappaB) inhibitor inhibit both ICAM-1 and VCAM-1 expression induced by TWEAK. However, mitogen-activated protein kinase (MEK) and c-Jun NH2-terminal kinase (JNK) inhibitor enhanced only VCAM-1 expression on HGF. These results suggest that TWEAK may be involved in the pathophysiology of periodontal disease. Moreover, in combination with IL-1beta or TGF-beta1, TWEAK may be related to the exacerbation of periodontal disease to induce proinflammatory cytokines and adherent molecules by HGF. (Keyword) Adult / Aged / Aged, 80 and over / Apoptosis / Cells, Cultured / Dose-Response Relationship, Immunologic / Female / Fibroblasts / Gene Expression / Gingiva / Humans / Intercellular Adhesion Molecule-1 / Interleukin-1beta / Interleukin-8 / Male / Middle Aged / Periodontitis / RNA, Messenger / Receptors, Tumor Necrosis Factor / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction / Transforming Growth Factor beta1 / Tumor Necrosis Factors / Vascular Cell Adhesion Molecule-1 / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2006.03233.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17100776 ● Search Scopus @ Elsevier (PMID): 17100776 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2006.03233.x (DOI: 10.1111/j.1365-2249.2006.03233.x, PubMed: 17100776)
70.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Cytokines differentially regulate ICAM-1 and VCAM-1 expression on human gingival fibroblasts., Clinical and Experimental Immunology, Vol.144, No.3, 494-502, 2006. (Summary) The expression of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) on human gingival fibroblasts (HGF) may be important for migration and retention of inflammatory cells in periodontally diseased tissue. This study aimed to assess which cytokines regulate ICAM-1 and VCAM-1 expression on HGF. Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma enhanced both ICAM-1 and VCAM-1 expression on HGF. Interleukin (IL)-1beta mainly up-regulated ICAM-1 expression. On the other hand, IL-4 and IL-13 enhanced only VCAM-1 expression on HGF. IL-10 did not modulate both ICAM-1 and VCAM-1 expression. Transforming growth factor (TGF)-beta1 enhanced ICAM-1 expression. However, TGF-beta1 inhibited the VCAM-1 expression induced by TNF-alpha or IL-4. Both ICAM-1 and VCAM-1 expression by HGF was inhibited by nuclear factor-kappaB (NF-kappaB) activation inhibitor (MG-132). Mitogen-activated protein kinases (MAPK) inhibitors did not influence ICAM-1 expression induced by TNF-alpha. Interestingly, VCAM-1 expression was enhanced by MEK inhibitor (PD98059) and c-Jun NH2-terminal kinase (JNK) inhibitor (SP600125). These results mean that the balance of cytokines in periodontally diseased tissue may be essential for control of ICAM-1 and VCAM-1 expression on HGF, and the balance of ICAM-1 and VCAM-1 expression might be important for regulation of leucocytes infiltration and retention in periodontally diseased tissue. (Keyword) Cells, Cultured / Cytokines / Drug Synergism / Enzyme Inhibitors / Fibroblasts / Flow Cytometry / Gene Expression Regulation / Gingiva / Humans / Imidazoles / Intercellular Adhesion Molecule-1 / Leupeptins / Mitogen-Activated Protein Kinase Kinases / NF-kappa B / Pyridines / RNA, Messenger / Recombinant Proteins / Reverse Transcriptase Polymerase Chain Reaction / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2006.03064.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16734619 ● Search Scopus @ Elsevier (PMID): 16734619 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2006.03064.x (DOI: 10.1111/j.1365-2249.2006.03064.x, PubMed: 16734619)
71.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Increase of CCL20 expression by human gingival fibroblasts upon stimulation with cytokines and bacterial endotoxin, Clinical and Experimental Immunology, Vol.142, No.2, 285-291, 2005. (Summary) We have demonstrated recently that CCL20 was expressed in periodontal diseased tissues and abundant CCR6 positive T cells infiltrated in periodontally diseased tissue. However, it is uncertain which cells can elicit CCL20 production. In the present study, we examined the properties of CCL20 production by human gingival fibroblasts (HGF) culture. Here, we report that interleukin-1 beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and Escherichia coli lipopolysaccharide (LPS) can significantly induce the production of CCL20 by HGF. We found that TNF-alpha and E. coli LPS enhanced the production of CCL20 by HGF treated with IL-1beta. In contrast, interferon-gamma (IFN-gamma) dramatically diminished CCL20 production induced by IL-1beta. Moreover, we demonstrated that nuclear factor-kappaB (NF-kappaB), p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK) play an important role in mediating the production of CCL20 induced by IL-1beta and TNF-alpha. On the other hand, we found that not only NF-kappaB, p38 MAPK and ERK but also c-Jun NH2-terminal kinase (JNK) are involved in CCL20 production induced by E. coli LPS. Finally, we found that HGF express CCR6, CCL20 receptor, and CCL20 induced vascular endothelial growth factor (VEGF) by HGF. Taken together, these findings that HGF will be a source of CCL20 in periodontal tissue, and the CCL20 production will be controlled by proinflammatory cytokine and bacterial LPS in periodontally diseased tissue. Thus, CCL20 by HGF might be involved in inflammatory cells infiltration, and promote the progression of periodontal disease. (Keyword) CCL20 / fibroblast / periodontal disease (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2005.02912.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16232215 ● Search Scopus @ Elsevier (PMID): 16232215 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2005.02912.x (DOI: 10.1111/j.1365-2249.2005.02912.x, PubMed: 16232215)
72.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae, Keiji Murakami, Yoichiro Miyake and Takashi Matsuo : CXCL12 and CXCR4 expression by human gingival fibroblasts in periodontal disease, Clinical and Experimental Immunology, Vol.141, No.3, 467-474, 2005. (Summary) CXCL12 is a CXC chemokine that is related to lymphocyte infiltration and angiogenesis in inflammatory sites such as arthritis. However, the expression and roles of CXCL12 in periodontal disease are uncertain. The aim of this study was to assess the expression of CXCL12 and its receptor, CXCR4, in periodontal tissue and to investigate the properties of CXCL12 and CXCR4 expression by human gingival fibroblasts (HGF). RT-PCR analysis revealed that CXCL12 and CXCR4 mRNA were expressed in both normal gingival tissues and periodontal diseased tissues. Immunohistochemistry disclosed that CXCL12 was expressed and CXCR4 positive cells were found in both normal and periodontal diseased gingival tissues. Our in vitro experiments elucidated that HGF constitutively produced CXCL12, and the levels were enhanced by stimulation with tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), regulated upon activation normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein 3(alpha) (MIP-3(alpha)). On the other hand, heat killed Porphyromonas gingivalis (P. gingivalis) and P. gingivalis LPS reduced the CXCL12 production by HGF. Flow cytometry analysis clarified that CXCR4 was highly expressed on HGF, and CXCR4 expression was abrogated by TNF-alpha, IFN-gamma and P. gingivalis LPS. Moreover, CXCL12 induced vascular endothelial growth factor (VEGF) production by HGF. Our results demonstrated that CXCL12 might be related to CXCR4+ cells infiltration and angiogenesis both in normal periodontal tissues and periodontal diseased tissue. P. gingivalis, a known periodontal pathogen, inhibits the production of CXCL12 and the expression of CXCR4 by HGF. This fact means that P. gingivalis may inhibit CXCR4+ cells infiltration and neovascularization in periodontal tissue and escape from the immune response. (Keyword) CXCL12 / CXCR4 / fibroblast / periodontal disease / Porphyromonas gingivalis (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2005.02852.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16045736 ● Search Scopus @ Elsevier (PMID): 16045736 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2005.02852.x (DOI: 10.1111/j.1365-2249.2005.02852.x, PubMed: 16045736)
73.	Akiko Kawasaki, Toshiyuki Suge, Kunio Ishikawa, Kazumi Ozaki, Takashi Matsuo and Shigeyuki Ebisu : Ammonium hexafluorosilicate increase acid resistance of bovine enamel and dentine, Journal of Materials Science. Materials in Medicine, Vol.16, No.5, 461-466, 2005. (Summary) Although diamine silver fluoride (AgF: (NH3)2AgF) stains teeth black, it is known as a very effective agent to prevent the dental caries progress. In order to find another fluoride that has a similar anticariogenic effect without changing tooth color, we prepared ammonium hexafluorosilicate (SiF: (NH4)2SiF6), in which the silver of AgF is replaced with silicon. In this study, the anticariogenic effect of SiF was evaluated using bovine teeth. Fluoride solutions, SiF, AgF, acidulated phosphate fluoride (APF), and sodium fluoride (NaF), were applied to bovine enamel and dentine blocks, and the depth of demineralization was measured after exposure to a demineralizing solution for 24 h. Also, fluoride was applied to a simulated dentine caries specimen to evaluate the caries progress-preventing ability. For the dentine specimens, mineral loss (Delta Z) was also measured with microradiography. We found that SiF treated enamel showed better acid resistance than specimens treated with NaF or APF. AgF treated enamel also showed similar acid resistance, but was stained black. SiF and AgF treated caries-affected dentine showed reduced demineralization when exposed to a demineralization solution for 24 h. Mineral loss (Delta Z) was reduced to 85% and 75%, respectively. Although the acid resistance of the SiF treated teeth was inferior to that of the AgF treated teeth, we consider that SiF has good potential as anticariogenic agent, since it increased acid resistance without changing tooth color. (Keyword) Acids / Animals / Biocompatible Materials / Calcification, Physiologic / Cattle / Dental Caries / Dental Enamel / Dentin / Drug Resistance / Fluorides / Hydrogen-Ion Concentration / Incisor / Silicic Acid (Link to Publication Site) ● Publication site (DOI): 10.1007/s10856-005-6987-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15875257 ● Search Scopus @ Elsevier (PMID): 15875257 ● Search Scopus @ Elsevier (DOI): 10.1007/s10856-005-6987-2 (DOI: 10.1007/s10856-005-6987-2, PubMed: 15875257)
74.	Takashi Matsuo, Toshiyuki Shirakami, Kazumi Ozaki, Tadashi Nakanishi, Hiromichi Yumoto and Shigeyuki Ebisu : An immunohistological study of the localization of bacteria invading root pulpal walls of teeth with periapical lesions, Journal of Endodontics, Vol.29, No.3, 194-200, 2003. (Summary) We immunohistologically examined the prevalence and localization of bacteria invading dentinal tubules of the roots of teeth with infected canals. Forty extracted teeth with apical lesions were selected and divided into two groups: a group of untreated teeth and a group of canal-enlarged teeth. The bacteria in the specimens were detected by Brown-Brenn stain and the labeled-streptavidin-biotin method with specific antisera for 16-bacteria. Seventy percent of the examined teeth showed bacteria invading the dentinal tubules of the roots. Fusobacterium nucleatum, Eubacterium alactolyticum, E. nodatum, Lactobacillus casei, and Peptostreptococcus micros were abundant. Even in the canal-enlarged group, invasion of bacteria was observed in 65% of teeth. This study revealed the actual condition of bacteria in infected root dentin and suggested that the canal-enlargement procedure could not completely remove all the bacteria in the infected dentinal tubules of the root. (Keyword) Adult / Aged / Bacteria / Coloring Agents / Dental Pulp / Dentin / Eubacterium / Fusobacterium nucleatum / Humans / Immune Sera / Immunoenzyme Techniques / Immunohistochemistry / Lactobacillus casei / Middle Aged / Peptostreptococcus / Periapical Diseases / Porphyromonas / Prevotella / Root Canal Preparation / Statistics, Nonparametric / Tooth Root (Link to Publication Site) ● Publication site (DOI): 10.1097/00004770-200303000-00008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12669880 ● Search Scopus @ Elsevier (PMID): 12669880 ● Search Scopus @ Elsevier (DOI): 10.1097/00004770-200303000-00008 (DOI: 10.1097/00004770-200303000-00008, PubMed: 12669880)
75.	Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Kanako Takahashi, Hiromichi Yumoto, Kazumi Ozaki and Takashi Matsuo : Macrophage Inflammatory Protein 3α-CC chemokine receptor 6 interactions play an important role in CD4⁺ T-cell accumulation in periodontal diseased tissue., Clinical and Experimental Immunology, Vol.128, No.3, 548-554, 2002. (Summary) The regulatory role of chemokines and chemokine receptors on specific lymphocyte recruitment into periodontal diseased tissue is poorly characterized. We observed that lymphocytes infiltrating inflamed gingival tissue expressed marked levels of CCR6. In periodontal diseased tissue, the expression of MIP-3alpha mRNA was detected by RT-PCR and further, MIP-3alpha was distributed in the basal layer of gingival epithelial cells, microvascular endothelial cells and the areas of inflammatory cells as shown by immunohistochemistry. Moreover, CCR6-expressing cells infiltrated into periodontal diseased tissue, and the proportion of CCR6-positive CD4+ T cells was significantly elevated in periodontal diseased tissue compared with peripheral blood in the same patients. Furthermore, gingival lymphocytes isolated from patients showed migration toward MIP-3alpha in an in vitro chemotaxis assay in which migration was abrogated by specific antibody to CCR6. Thus, these findings suggested that CCR6 and the corresponding chemokine, MIP-3alpha may have an important regulatory role in specific lymphocyte migration into inflamed periodontal tissue. (Keyword) CCR6 / MIP-3 alpha / periodontal disease / MONOCYTE CHEMOATTRACTANT PROTEIN-1 / INFLAMED HUMAN GINGIVA / IMMUNOHISTOLOGICAL ANALYSIS / SELECTIVE RECRUITMENT / INDUCIBLE EXPRESSION / BACTERIA / IMMUNITY / HEALTHY / LESIONS / SUBSETS (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1365-2249.2002.01865.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12067311 ● Search Scopus @ Elsevier (PMID): 12067311 ● Search Scopus @ Elsevier (DOI): 10.1046/j.1365-2249.2002.01865.x (DOI: 10.1046/j.1365-2249.2002.01865.x, PubMed: 12067311)
76.	Keiko Fujinaka, Akiko Kawasaki, Yoshiko YOSHIDA, Nozomi Matsuoka, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Immunohistological Studies on Localization of Selected Bacteria in Infected Root Canal Systems, The Japanese Journal of Conservative Dentistry, Vol.43, No.2, 407-416, 2000. (Keyword) 根尖性歯周炎 / 細菌 / 免疫染色
77.	綿城香, 石川利栄子, 蓮井義則, Kimiko Ueda Yamaguchi, Mizuho Nishino, Kazumi Ozaki and Takashi Matsuo : エナメル質形成不全症の1症例, The Japanese Journal of Pediatric Dentistry, Vol.37, No.3, 620-624, 1999.
78.	Akihisa Urayama, Masahiro Yoshiyama, Takeshi Kimochi, Nozomi Matsuoka, Kazumi Ozaki and Takashi Matsuo : Resin Infiltration into Artificial Carious Dentin, The Japanese Journal of Conservative Dentistry, Vol.42, No.3, 529-535, 1999. (Keyword) レジン / 浸透性 / 人工う蝕象牙質
79.	Masahiro Yoshiyama, 浦山明久, Takeshi Kimochi, Nozomi Matsuoka, Kazumi Ozaki and Takashi Matsuo : Resin Infiltration of Caries-infected Dentin, The Japanese Journal of Conservative Dentistry, Vol.42, No.1, 86-95, 1999. (Keyword) う蝕症 / レジン / 象牙質
80.	Yuichiro Noiri, Kazumi Ozaki, Hideaki Nakae, Takashi Matsuo and Shigeyuki Ebisu : An immunohistochemical study on the localization of Porphyromonas gingivalis, Campylobacter rectus and Actinomyces viscosus in human periodontal pockets, Journal of Periodontal Research, Vol.32, No.7, 598-607, 1997.
81.	Takashi Matsuo, Chisato Tagawa, Kazumi Ozaki, Yuichiro Noiri and Shigeyuki Ebisu : A Histological Analysis of T and B Cells in Periodontal Tissue Destruction, Oral Medicine & Pathology, Vol.1, No.2, 77-83, 1996. (Summary) We immunohistologically examined the cell densities and distribution of T and B cells in periodontitis and analyzed their relationship in terms of periodontal tissue destruction. Specimens were labeled with monoclonal antibodies for T cells (CD3) and B cells (CD20) and developed using the double staining technique. CD3^+ cells appeared in low density infiltrates and increased gradually with the number of total infiltrates; in contrast, CD20^+ cells did not appear in small infiltrates but increased rapidly with the number of infiltrates. The number of fibroblastic cells negatively correlated with that of the total infiltrates and CD20^+ cells, but it did not correlate with the number of CD3^+ cells. These findings suggest that the T cells infiltrated into the inflamed sites at the onset and increased gradually with the development of inflammation and that B cells infiltrated later than T cells and their number increased rapidly with inflammation. (Keyword) Immunohistology / T cell / B cell / tissue destruction / periodontal disease (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572824502001680896 (CiNii: 1572824502001680896)
82.	Yuichiro Noiri, Kazumi Ozaki, Keiko Fujinaka, Tae Okamoto, Takashi Matsuo and Shigeyuki Ebisu : A Study on Human Subgingival Plaque-Qualitative Analysis of Periodontal Disease associated Bacteria in Plaque-free Zones by a Scanning Immunoelectron Microscopy Method-, Journal of the Japanese Association of Periodontology, Vol.38, No.1, 60-68, 1996. (Keyword) Plaque-free zone / Periodontal disease-associated bacteria / Scanning immunoelectron microscopy method
83.	Yuichiro Noiri, Keiko Fujinaka, Tae Kondo, Kazumi Ozaki, Takashi Matsuo and Shigeyuki Ebisu : A Study on Human Subgingival Plaque-Participation of Bacterial Biofilms in the Colonization of Plaque Bacteria-, Journal of the Japanese Association of Periodontology, Vol.37, No.2, 329-336, 1995. (Keyword) Subgingival plaque / Bacterial biofilm / Scanning electron microscope
84.	Kazumi Ozaki, Takashi Matsuo, Hideaki Nakae, Yuichiro NOIRI, Masahiro YOSHIYAMA and Shigeyuki EBISU : A quantitative comparison of selected bacteria in human carious dentine by microscopic counts., Caries Research, Vol.28, No.3, 137-145, 1994. (Keyword) Actinomyces / Immunohistological stain / Microscopic counts / Mutans streptococci
85.	Yuichiro Noiri, Takashi Matsuo, Hideaki Nakae, Kazumi Ozaki and Shigeyuki Ebisu : A Study on Human Subgingival Plaque -Localization of Periodontopathic Bacteria in Human Periodontal Pockets-, Journal of the Japanese Association of Periodontology, Vol.36, No.2, 429-436, 1994. (Keyword) Periodontal poket / Periodontopathic bacteria / Localization / Immunohistochemical study
86.	Yuichiro Noiri, Takashi Matsuo, Hideaki Nakae, Kazumi Ozaki and Shigeyuki Ebisu : A Study on Human Subgingival Plaque Immunohistochemical Observation of Tooth Attached Subgingival Plaque, Journal of the Japanese Association of Periodontology, Vol.36, No.1, 223-232, 1994. (Keyword) Tooth-attached subgingival plaque / Periodontopathic bacteria / Immunohistochemical stain
87.	Kazumi Ozaki, Takashi Matsuo, Hideaki Nakae, Yuichiro Noiri, Reiko Oogimoto, Masahiro Yoshiyama and Shigeyuki Ebisu : Immunohistological Studies on the Localization of Selected Bacteria in Human Carious Dentin Located in Root Surfaces, The Japanese Journal of Conservative Dentistry, Vol.36, No.5, 1284-1291, 1993. (Keyword) 歯根部象牙質齲蝕 / 齲蝕関連細菌 / 光学顕微鏡的計測
88.	Kazumi Ozaki, Takashi Matsuo, Hideaki Nakae, Yuichiro Noiri, Reiko Oogimoto, Masahiro Yoshiyama and Shigeyuki Ebisu : Immunohistological Studies on the Localization of Selected Bacteria in Human Carious Dentin Located in Fissures and Smooth Surface Coronal Surfaces, The Japanese Journal of Conservative Dentistry, Vol.36, No.4, 1059-1069, 1993. (Keyword) 齲蝕関連細菌 / 酵素抗体法 / 光学顕微鏡的計測
89.	Masahiro Yoshiyama, Kazumi Ozaki and Shigeyuki Ebisu : Morphological characterization of hypersensitive human radicular dentin and the effect of a light-curing resin liner on tubular occlusion, Proceedings of the Finnish Dental Society, Vol.88, No.Suppl 1, 337-344, 1992. (Keyword) Root Hypersensitivity / SEM / Lamina Limitans / Dentin Biopsy
90.	Masahiro Yoshiyama, Kazumi Ozaki, Yuichiro Noiri, Kenya Kataoka, Tadashi Nakanishi, Reiko Ogimoto, Hideaki Nakae, Takashi Matsuo and Shigeyuki Ebisu : Treatment of Dentin Hypersensitivity-Effect of a Light-curing Resin Liner on Tubule Occlusion-, The Japanese Journal of Conservative Dentistry, Vol.34, No.1, 76-81, 1991. (Keyword) 象牙質知覚過敏症 / 象牙細管封鎖 / 光重合型レジンランナー
91.	yuichiro Noiri, Kazumi Ozaki, Tadashi Nakanishi, Kenya Ktaoka, Ichiro Amano and Masahiro Yoshiyama : Study on Adhesive Properties of Restorative Materials to Human Root Dentin, --- 1.Adhesive Properties of Resin Cement Used for Composite Resin Inlay Restoration to Human Coronal and Root Debtin ---, The Japanese Journal of Conservative Dentistry, Vol.33, No.3, 639-647, 1990. (Keyword) 歯根部象牙質 / 接着性 / レジセメント
92.	Masahiro Yoshiyama, Yuichiro Noiri, Kazumi Ozaki, Akitsugu Uchida, Yasuko Ishikawa and Hajime Ishida : Transmission electron microscopic characterization of hypersensitive human radicular dentin., Journal of Dental Research, Vol.69, No.6, 1293-1297, 1990. (Summary) Transmission electron microscopy (TEM) and x-ray microanalysis (XMA) were used for the study of the ultrastructure of the lumens of dentinal tubules in superficial layers of dentin specimens obtained by use of a new biopsy technique from both hypersensitive and naturally desensitized areas of exposed root surfaces, in vivo. The TEM images showed clearly that the lumens of most of the tubules were occluded with mineral crystals in naturally desensitized areas, but such lumens were empty and surrounded with peritubular and intertubular dentin in hypersensitive areas. Moreover, electron-dense structures that lined peritubular dentin were observed in the empty lumens of dentinal tubules. (Keyword) Dentin / Hypersensitivity (Link to Publication Site) ● Publication site (DOI): 10.1177/00220345900690061401 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 2355124 ● CiNii @ National Institute of Informatics (CRID): 1572543024127628672 ● Summary page in Scopus @ Elsevier: 2-s2.0-0025443224 (DOI: 10.1177/00220345900690061401, PubMed: 2355124, CiNii: 1572543024127628672, Elsevier: Scopus)
93.	Kazumi Ozaki, Yuichiro Noiri, Reiko Ogimoto, Jiro Masada, Masahiro Yoshiyama, Akitsugu Uchida and Hajime Ishida : FEffect of Tubulozole-C on the Dentin Formation of Rat Tooth, The Japanese Journal of Conservative Dentistry, Vol.32, No.5, 1490-1497, 1989. (Keyword) 歯牙象牙質 / 微小管 / ツブロゾールーC

Review, Commentary:

1.	Kazumi Ozaki : 【第10章】テーラーメイド医療としてのう蝕予防管理, 歯科衛生士のう蝕予防管理テキストブックーバイブルとして,認定資格取得をめざしてー, 105-115, Jul. 2021.
2.	Kaya Yoshida, Kayo Yoshida, Mariko Seyama, Kazumi Ozaki and Hirohiko Okamura : Extracellular Vesicles in Periodontal Medicine: The Candidates Linking Oral Health to General Health, Journal of Oral Health and Biosciences, Vol.33, No.1, 15-23, Jun. 2020. (Tokushima University Institutional Repository) ● Metadata: 114869 (Link to Publication Site) ● Publication site (DOI): 10.20738/johb.33.1_15 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.20738/johb.33.1_15 (Tokushima University Institutional Repository: 114869, DOI: 10.20738/johb.33.1_15)
3.	Yasuhiko Shirayama, Tetsuo Ichikawa, Kazumi Ozaki and Shizuko Yanagisawa : 徳島県地域包括ケアシステム学会, 月刊介護保険, No.264, 28, Feb. 2018.
4.	Yasuhiko Shirayama, Tetsuo Ichikawa, Shizuko Yanagisawa and Kazumi Ozaki : 離島における福祉崩壊の危機, 月刊介護保険, No.249, 23, Nov. 2016.
5.	Takashi Matsuo, Kazumi Ozaki, Tadashi Nakanishi, Hiromichi Yumoto, Kanako Takahashi, Kouji Hirao and Daisuke Takegawa : Pulp pathosis and its diagnosis, The Journal of Japan Endodontic Association, Vol.34, No.2, 67-76, May 2013. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680166022016 (CiNii: 1390282680166022016)
6.	Tadashi Nakanishi, Kanako Takahashi, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo : Bacterial irritation and pulpal response in pulpitis, Shikoku Dental Research, Vol.14, No.2, 255-263, 2002. (Keyword) 歯髄炎 / う蝕関連細菌 / 免疫担当細胞 / プロスタグランディン / cytokine
7.	Takashi Matsuo, Kazumi Ozaki, Hiromichi Yumoto and Masahiro Yoshiyama : Caries-A disease of bacteria infection, Caries Preventive restoration, 1-8, 2001.
8.	Masahiro Yoshiyama, Takashi Matsuo and Kazumi Ozaki : Possibility of Sealed Restoration to Carious Dentine:Treatment of Embeddding Bacteria and the Present Statue, the Quintessence, Vol.18, No.1, 77-89, Jan. 1999. (Keyword) 象牙質齲蝕 / シールド·レストレーション / 接着性レジン

Proceeding of International Conference:

1.	Kaya Yoshida, Mariko Seyama, Natsumi Fujiwara, Hirohiko Okamura and Kazumi Ozaki : The effects of outer membrane vesicles delived from Porphyromonas gingivalis on hepatic glucose metabolisms., International Society for ExtracellularVesicles 2019 Annual Meeting, Kyoto, Apr. 2019.
2.	Natsumi Fujiwara, Hiromichi Yumoto, Keiji Murakami, Yasusei Kudo, Hiromi Nakae, Katsuhiko Hirota, Kazumi Ozaki and Yoichiro Miyake : 2-methacryloyloxyethyl-phosphorylcholine (MPC)-polymer suppresses the adherence of oral bacteria, 2018 IADR/PER General Session (ExCel London Convention Center, London, England) 25-28th July, 2018, Jul. 2018.
3.	Shindo Satoru, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : The effect of genipin on dendritic cells activation, 93rd General Session & Exhibition of the IADR, Boston, Mar. 2015.
4.	Ikuko Hosokawa, Yoshitaka Hosokawa, Shindo Satoru, Kazumi Ozaki and Takashi Matsuo : Melatonin inhibits inflammatory mediators productions in human periodontal ligament cells, 93rd General Session & Exhibition of the IADR, Boston, Mar. 2015.
5.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : IL-4 modulates chemokine productions from IL-1-stimulated human periodontal ligament cells, 93rd General Session & Exhibition of the IADR, Boston, Mar. 2015.
6.	Kaya Yoshida, Haruna Takamura, Hirohiko Okamura, Natsumi Fujiwara and Kazumi Ozaki : Oral porphyromonas gingivalis translocates to liver and regulates hepatic glycogen metabolisms by attenuating insulin signaling, 10 th Asian Pacific Society of Periodontology Meeting, Nara, Japan, Sep. 2013.
7.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo : Pro-inflammatory Roles of NOD2 in Human Gingival Fibroblasts, The 3rd International Symposium on "Oral Sciences to Improve the Quality of Life", Tokushima, Sep. 2008.
8.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo : Pro-inflammatory Roles of NOD2 in Human Gingival Fibroblasts, 86th General Session and Exhibition of the International Association for Dental Research, Toronto, Jul. 2008.
9.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Th17 cytokines enhance CCL20 production by human gingival fibroblasts., 86th General Session and Exhibition of the International Association for Dental Research, Toronto, Jun. 2008.
10.	Tomoko Kimura, Kazumi Ozaki, Keiji Murakami, Kikumi Fujisaka and Takashi Matsuo : The Analysis of role of Phosphoenolpyruvate-Dependent Sucrose Phosphotransferase System in pathogenicity of Streptococcus mutans., 第1回国際シンポジウム・FDワークショップ, Awaji, Mar. 2007.
11.	Natsuko Ida, Kazumi Ozaki, Shinji Suenobu, Kanako Takahashi, Daisuke Yamaguchi and Takashi Matsuo : Opsonized Streptococcus mutans influences maturation of human dendritic cells, The 82nd General Session of IADR Meeting, Hawaii, Mar. 2004.
12.	Kazumi Ozaki and Takashi Matsuo : Expression of adrenomedullin and its receptors in inflamed gingival tissue, The 82nd General Session of IADR Meeting, Hawaii, Mar. 2004.
13.	Natsuko Ida, Kazumi Ozaki, Shinji Suenobu, Kanako Takahashi, Daisuke Yamaguchi and Takashi Matsuo : Opsonized Streptococcus mutans influences maturation of human dendritic cells., Seoul, Nov. 2003.
14.	Takuya Shibutani, Kazumi Ozaki and Takashi Matsuo : Comparison of root canal preparation by three Ni-Ti instruments, Seoul, Nov. 2003.
15.	Kazumi Ozaki, Shinji Suenobu, Natsuko Ida and Takashi Matsuo : Bacterial Viability Assay at an Electron Microscopic Leved, The 81th General Session of IADR Meeting, Goteborg, Sweden, Jun. 2003.
16.	Shinji Suenobu, Kazumi Ozaki and Takashi Matsuo : The Analysis of mRNA Expression of Glucosyltransferases and Dextranase A from Streptococcs mutans Adhered to the Dentin, The 81th General Session of IADR Meeting, Goteborg, Sweden, Jun. 2003.
17.	Takuya Shibutani, Kazumi Ozaki and Takashi Matsuo : Comparison of the Effects of Three Ni-Ti Preparation Techniques by Micro-computed Tomography, The 81th General Session of IADR Meeting, Goteborg, Sweden, Jun. 2003.
18.	Akiko Kawasaki, Toshiyuki Suge, Kunio Ishikawa, Kazumi Ozaki, Takashi Matsuo and Shigeyuki Ebisu : Ammonium hexafluorosilicate increase acid resistance of bovine enamel and dentin, Journal of Dental Research, Vol.82, No.Special Issue B, B-71, Goteborg, Jun. 2003.
19.	Akiko Kawasaki, Toshiyuki Suge, Kunio ISHIKAWA, Kazumi Ozaki and Takashi Matsuo : Ammonium hexafluorosilicate increased acid resistance of bovine enamel and dentin, Transactions of the fourth international congress on dental materials, Vol.16, 195, Honolulu, Jan. 2002.
20.	Takashi Matsuo, Keiko Fujinaka, Yoshiko Yoshida and Kazumi Ozaki : Scanning electron microscope observations in the apices of roots with refractory apical periodontitis, The 3rd Joint Scientific Meeting between KACD and JSCD, Seoul, Nov. 2001.
21.	Tadashi Nakanishi, Kanako Takahashi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : An immunohistological study on the localization of selected bacteria and chemokines in human deep-carious teeth, The International Conference on Dentin/Pulp complexs, Chiba, Jul. 2001.
22.	Kazumi Ozaki and Takashi Matsuo : A three-dimensional examination of morphological changes in experimental cementum caries lesions, 77th General Session of IADR Meeting, Vancouver, Mar. 1999.
23.	Kazumi Ozaki, Yuichirou Noiri, Hideaki Nakae, Takashi Matsuo and Shigeyuki Ebisu : A histopathological and microbiological study on experimental root-surface caries in humans, 74th General Session of IADR Meeting, San Francisco, Mar. 1996.
24.	Yuichirou Noiri, Kazumi Ozaki, Tae Okamoto, Keiko Fujinaka, Takashi Matsuo and Shigeyuki Ebisu : Localization of periodontal disease-associated bacteria in human periodontal pockets, 74th General Session of IADR Meeting, San Francisco, Mar. 1996.
25.	Masahiro Yoshiyama, Kazumi Ozaki and Shigeyuki Ebisu : Morphological characterization of hypersensitive human radicular dentin and the effect of a light-curing resin liner on tubular occlusion, International Conference Pathobiology of Dentin/Pulp Complex, May 1991.

Proceeding of Domestic Conference:

1.	Kaya Yoshida, Yuka Hiroshima, Ayu Takai, 生田あゆ, Kayo Yoshida and Kazumi Ozaki : 歯周病菌外膜小胞が血管透過性を亢進する機構, 第11回日本細胞外小胞学会学術集会, Oct. 2024.
2.	MEKATA Mana, Kaya Yoshida, Ayu Takai, SEYAMA Mariko, IKUTA Ayu and Kazumi Ozaki : Porphyromonas gingivalisのOuter membrane vesiclesが血管透過性に与える影響, 第67回春季日本歯周病学会学術大会, May 2024.
3.	Ayu Takai, Kaya Yoshida, IKUTA Ayu, SEYAMA Mariko, MEKATA Mana and Kazumi Ozaki : Porphyromonas gingivalis由来OMVsによるアストロサイトのNLRP3インフラマソーム活性化機構, 第67回春季日本歯周病学会学術大会, May 2024.
4.	Ayu Takai, Kaya Yoshida, HAMAE Yumi, MIYAKURA Yoshino, IKUTA Ayu, 瀬山真莉子, MEKATA Mana, YOSHIDA Kayo and Kazumi Ozaki : 要介護高齢者の認知機能と口腔機能の関係, 第 268 回徳島医学会学術集会(令和5年度冬期), Mar. 2024.
5.	Okamoto Risa, Yoshitaka Hosokawa, Ikuko Hosokawa, Shimoyama Masahiro, Kazumi Ozaki and Keiichi Hosaka : TNF-αで刺激されたヒト歯根膜由来細胞の炎症性メディエーター発現に与えるcardamoninの影響, 日本歯科保存学会2023年度秋季学術大会(第159回), Nov. 2023.
6.	Jin Shengjian, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Noriko Mizusawa, Hagita Hiroko, Sarubo Motoharu, Yoshida Kayo, Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : The role of deubiquitinating enzyme, OTUB1 in head and neck squamous cell carcinoma (HNSCC) progression, 第82回日本癌学会学術集会, Sep. 2023.
7.	YOSHIDA Kayo, Kaya Yoshida, Mariko Seyama, MEKATA Mana, Natsumi Fujiwara, Noriko Mizusawa, Yasuhiro Mouri, Yasusei Kudo and Kazumi Ozaki : 歯周病原菌由来細胞外小胞を介した肺炎発症メカニズムの解明, 第66回春季日本歯周病学会学術大会, May 2023.
8.	Mariko Seyama, Natsumi Fujiwara, Ayu Takai, MEKATA Mana, YOSHIDA Kayo, Kaya Yoshida and Kazumi Ozaki : 認知・口腔機能管理のためのWebシステムの可用性に関する研究, 第66回春季日本歯周病学会学術大会, May 2023.
9.	Shizuko Yanagisawa and Kazumi Ozaki : ICTを用いた口腔機能維持管理システムの開発に向けた口腔機能調査, 第72回日本口腔衛生学会総会, May 2023.
10.	Mariko Seyama, Natsumi Fujiwara, Ayu Takai, MEKATA Mana, YOSHIDA Kayo, Kaya Yoshida and Kazumi Ozaki : 認知機能評価Webシステムの有用性に関する研究, 第20回日本口腔ケア学会/第3回国際口腔ケア総会・学術大会, Apr. 2023.
11.	Jin Shengjian, Takaaki Tsunematsu, Taigo Horiguchi, Yasuhiro Mouri, Wenhua Shao, Keiko Miyoshi, Noriko Mizusawa, Hiroko Hagita, YOSHIDA Kayo, Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : The role of Deubiquitinating enzyme, OTUB1 in head and neck squamous cell carcinoma (HNSCC) progression, 第61回四国歯学会, Mar. 2023.
12.	Kayo Yoshida, Kaya Yoshida, Mariko Seyama and Kazumi Ozaki : 歯周病原菌の外膜小胞がもたらすアルツハイマー型認知症発症機構の解明, Journal of Oral Biosciences Supplement 2022, 263, Sep. 2022.
13.	Masato Tagi, 田尻真梨, Yasuhiro Hamada, Yoshifumi Wakata, Xiao Shan, Kazumi Ozaki, 久保田雅則, 天野宗佑 and Jun Hirose : Clinical validation of an AI-based system for estimating intake hospital liquid food, 第41回医療情報学連合大会, Nov. 2021.
14.	Masato Tagi, 田尻真梨, Yasuhiro Hamada, Yoshifumi Wakata, Xiao Shan, Kazumi Ozaki, 久保田雅則, 天野宗佑 and Jun Hirose : Validation of an AI-based model for estimating leftover liquid food in hospitals, 日本医療情報学会春季学術大会, Vol.25, 70-71, Jun. 2021.
15.	Yoshitaka Hosokawa, Ikuko Hosokawa and Kazumi Ozaki : The effect of nobiletin on inflammatory mediator production in IL-1β-stimulated human periodontal ligament cells, 2021年度日本歯科保存学会春季学術大会(第154回), Jun. 2021.
16.	Mariko Seyama, Kayo Yoshida, Natsumi Fujiwara and Kazumi Ozaki : ライブ配信による臨床系基礎実習に関する一考察, 四国歯学会第57回例会, Mar. 2021. (Keyword) オンライン授業 / 臨床系基礎実習
17.	Minami Itoh, Kazumi Ozaki, Hijiri Kobayashi, Sayaka Matsumoto, Kayo Yoshida and Mariko Seyama : 継続可能性を高める簡易認知機能評価の確立に関する研究, 四国歯学会第57回例会, Mar. 2021. (Keyword) cognitive function / ICT
18.	Kayo Yoshida, Kaya Yoshida, Mariko Seyama and Kazumi Ozaki : 歯周病原菌感染マクロファージの細胞外小胞が肺に線維化を誘導する可能性の検証, 第62回秋季日本歯周病学会学術大会, Oct. 2020.
19.	Ikuko Hosokawa, Yoshitaka Hosokawa and Kazumi Ozaki : The effect of Carnosic Acid on inflammatory cytokine production in IL-1β-stimulated human periodontal ligament cells, 日本歯科保存学会2020年度春季学術大会, Jun. 2020.
20.	Yoshitaka Hosokawa, Ikuko Hosokawa and Kazumi Ozaki : The effect of Sudachitin on inflammatory mediator production in IL-1β-stimulated human periodontal ligament cells, 日本歯科保存学会2020年度春季学術大会, Jun. 2020.
21.	Kayo Yoshida, Kazumi Ozaki, Mariko Seyama, Yuko Takeuchi, Shizuko Yanagisawa and Miwa Matsuyama : クラウドコンピューティングを利用した多職種経口摂取支援の体制づくりに向けて∼嚥下時産生音の有用性に関する検証∼, 第2回徳島県歯科医学大会(徳島県徳島市), Feb. 2020.
22.	Kazumi Ozaki, Mariko Seyama, Kayo Yoshida, Yuko Takeuchi, Shizuko Yanagisawa and Miwa Matsuyama : 地域住民の包括的支援に資する情報共有体制の構築 ∼オーラルフレイル予防対策を起点とした``見える化''と``つなぐ化''∼, 第2回徳島県歯科医学大会(徳島県徳島市), Feb. 2020.
23.	Kayo Yoshida, Natsumi Fujiwara, Akari Watanabe, Miwa Matsuyama and Kazumi Ozaki : ヘッドマウントディスプレイのマイクロスコープへの応用に関する研究, 第10回日本歯科衛生教育学会総会・学術大会(福岡県福岡市), Dec. 2019.
24.	Kaya Yoshida, 吉田佳世, Kazumi Ozaki and Hirohiko Okamura : Porphyromonas gingivalis感染マクロファージの細胞外小胞が多臓器に及ぼす影響, 第6回日本細胞外小胞学会, Oct. 2019.
25.	Kayo Yoshida, Kazumi Ozaki, 中野明加里, Natsumi Fujiwara, Yuko Takeuchi and Shizuko Yanagisawa : ミールラウンドの遠隔支援における一評価指標としての嚥下時産生音の可能性, 日本歯科衛生学会第14回学術大会(愛知県名古屋市), Sep. 2019.
26.	久野恵, Natsumi Fujiwara, 篠永晴美, 迎美榛, Harumi Sakamoto, 田村真里奈, Akari Watanabe, Miwa Matsuyama, Kazumi Ozaki and Daisuke Hinode : 摂食・嚥下リハビリテーション臨床実習における歯科衛生士学生の学びと教育的効果, 日本歯科衛生学会第14回学術大会(愛知県名古屋市), Sep. 2019.
27.	Natsumi Fujiwara, Kazumi Ozaki, Kayo Yoshida, Yuko Takeuchi and Shizuko Yanagisawa : 口腔体操プログラム実施が自立高齢者の口腔機能および口腔リテラシーに与える効果, 日本歯科衛生学会第14回学術大会(愛知県名古屋市), Sep. 2019.
28.	Kayo Yoshida, Natsumi Fujiwara, Yuko Takeuchi, Shizuko Yanagisawa and Kazumi Ozaki : 健口体操プログラムは自立高齢者の口腔セルフケア行動と口腔衛生に影響を与える, 第3回徳島県地域包括ケアシステム学会学術集会(徳島県徳島市), Aug. 2019.
29.	Natsumi Fujiwara, Kayo Yoshida, Yuko Takeuchi, Shizuko Yanagisawa and Kazumi Ozaki : 健口体操プログラムは自立高齢者の口腔機能向上に影響を与える, 第3回徳島県地域包括ケアシステム学会学術集会(徳島県徳島市), Aug. 2019.
30.	Kaya Yoshida, Kayo Yoshida, Natsumi Fujiwara, Kazumi Ozaki and Hirohiko Okamura : 感染マクロファージの膜小胞は歯周病関連疾患発症に関与するか?, 第38回分子病理学研究会淡路島シンポジウム, Jul. 2019.
31.	湯浅雅志 and Kazumi Ozaki : 広域で社会資源の少ない地域でのICT活用とアナログミーティングの融合による地域ケア会議の効用, 第18回日本ケアマネジメント学会研究大会 in 仙台, Jun. 2019.
32.	Rie Kido, Yuka Hiroshima, Takahisa Ikuta, Kaya Yoshida, Yuji Inagaki, Koji Naruishi, Kazumi Ozaki, Jun-ichi Kido and Hiromichi Yumoto : 最終糖化産物はヒト口腔上皮細胞のリポカリン2発現を増加する, 第62回春季日本歯周病学会学術大会, May 2019.
33.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo : Carnosic acidはヒト口腔上皮細胞のIL-27誘導CXCR3リガンド産生を抑制する, 日本歯科保存学会2018年度秋季学術大会, Nov. 2018.
34.	Kaya Yoshida, Mariko Seyama, Natsumi Fujiwara and Kazumi Ozaki : Porphyromonas gingivalis感染したマクロファージが由来の膜小胞が肝臓糖代謝に及ぼす影響, 第61回秋季日本歯周病学会学術大会 2018年10月26日(大阪市), Vol.60, 115, Oct. 2018.
35.	Kazumi Ozaki, 濵田邦美, 湯浅雅志 and Natsumi Fujiwara : 要援護者の個別課題を共有・管理するICTシステムの開発, Journal of the Japanese Association of Periodontology, Vol.60, 135, Oct. 2018. (Keyword) クラウド型Webアプリケーションシステム / 地域ケア会議 / タイムライン機能 / 医療・介護・福祉連携
36.	Kumiko Miura, Kazumi Ozaki, Shizuko Yanagisawa, Yasuhiko Shirayama and Natsumi Fujiwara : ICTを活用した歯科衛生士による要介護高齢者の口腔健康管理について, Journal of the Japanese Association of Periodontology, Vol.60, 135, Oct. 2018. (Keyword) 口腔健康管理 / クラウド型Webアプリケーションシステム / 医療・介護連携
37.	Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, 内部健太, 池亀美華 and Hirohiko Okamura : Porphyromonas gingivalis感染したマクロファージが産生する膜小胞が肝臓糖代謝に及ぼす影響, 第60回日本歯科基礎医学会学術大会 2018年9月5-7日(九州大学病院キャンパス百年講堂, 福岡市), Sep. 2018.
38.	Natsumi Fujiwara, Keiji Murakami, Kaya Yoshida, Yasusei Kudo, Katsuhiko Hirota, Kazumi Ozaki, Hideki Fujii and Hiromichi Yumoto : MPCポリマーコーティングによる義歯用レジンのカンジダ付着(撥菌)効果, 第60回日本歯科基礎医学会学術大会 2018年9月5-7日(九州大学病院キャンパス百年講堂, 福岡市), Sep. 2018.
39.	Kaya Yoshida, Natsumi Fujiwara, Kazumi Ozaki, 内部健太, 池亀美華 and Hirohiko Okamura : Extracellular vesicles from Porphyromonas gingivalis-infected macrophages include histone proteins and translocate to the liver, 第10回日本RNAi研究会・第5回日本細胞外小胞学会 (グランドプリンスホテル広島・広島市), Aug. 2018. (Keyword) osteoblast
40.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : IL-27 induces CXCR3 ligands production in human oral epithelial cells, 第61回日本歯周病学会春季学術大会, Jun. 2018.
41.	Mariko Seyama, Kaya Yoshida, Natsumi Fujiwara and Kazumi Ozaki : Porphyromonas gingivalisの分泌小胞は肝臓の糖代謝に影響を与える, 第61回日本歯周病学会学術大会, Vol.60, 128, Jun. 2018.
42.	Natsumi Fujiwara, Kazumi Ozaki, Shizuko Yanagisawa, Mariko Seyama, Yuki Matsumura, Rika Kawano and Yasuhiko Shirayama : 徳島県那賀町における口腔ケア実施の実態調査と支援職員への口腔ケア研修会の取り組み, 第67回日本口腔衛生学会・総会_平成30年5月18-20日_北海道札幌市, Vol.68, 165, May 2018.
43.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : IL-29 enhances CXCL10 production in TNF-alpha-stimulated human oral epithelial cells, 第60回日本歯周病学会秋季学術大会, Dec. 2017.
44.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : IL-29 enahances CXCL10 production in human oral epithelial cells, 第60回日本歯周病学会春季学術大会, Oct. 2017.
45.	Natsumi Fujiwara, Hiromichi Yumoto, Katsuhiko Hirota, Keiji Murakami and Kazumi Ozaki : Suppression of oral bacteria by 2-methacryloyloxyethyl-phosphorylcholine-polymer, 第59回歯科基礎医学会学術大会プログラム・抄録集平成29年9月16-18日(松本歯科大学，長野県塩尻市), 341, Sep. 2017.
46.	Natsumi Fujiwara, Tokiko Doi, Hiromi Nakae, Yuka Sogawa, Masami Yoshioka, 高橋侑子, 幸江真杉, Kazumi Ozaki and Daisuke Hinode : 本学歯科衛生学生の病棟口腔ケア臨床実習の取り組みとその効果, 第14回日本口腔ケア学会総会・学術大会プログラム・抄録集, 208, Apr. 2017.
47.	Shindo Satoru, Ikeda Atsushi, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Citrullinated vimentin promotes osteoclastgenesis, 日本歯科保存学会2016年度秋季学術大会, Oct. 2016.
48.	Yoshitaka Hosokawa, Ikuko Hosokawa, Shindo Satoru, Kazumi Ozaki and Takashi Matsuo : The effect of Gominsin N on inflammatory cytokine production in human periodontal ligament cells, 日本歯科保存学会2016年度秋季学術大会, Oct. 2016.
49.	池田真己, 中上久美子, 三野聖子, 榎恵子, 一宮麗子, 井手口英章, Natsumi Fujiwara, Kazumi Ozaki and Takashi Iwata : スキルス・ラボを活用した歯科衛生士の教育効果, 日本歯科衛生教育学会, Vol.7, No.2, 197, Oct. 2016.
50.	Natsumi Fujiwara, Hiromi Nakae, Masami Yoshioka, Yuka Sogawa, 高橋侑子, 田口侑子, Akari Watanabe, Tokiko Doi, Kazumi Ozaki and Daisuke Hinode : 某大学における周術期口腔機能管理の臨床実習の取り組みとその効果, 日本歯科衛生学会第11回学術大会 2016年9/17日~19日広島県広島市広島国際会議場, Vol.11, No.1, 174, Sep. 2016.
51.	Natsumi Fujiwara, Keiji Murakami, Hiromichi Yumoto, Katsuhiko Hirota, Kazumi Ozaki and Yoichiro Miyake : Effects of novel compounds on periodontopathic bacteria, 第58回歯科基礎医学会学術大会北海道札幌市 2016年8月24-26日, Aug. 2016.
52.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : The effect of alkannin on IL-6 and CCL20 production in human periodontal ligament cells, 第59回春季日本歯周病学会学術大会, May 2016.
53.	Kaya Yoshida, Natsumi Fujiwara, Yuka Hiroshima, Kaori Abe, Jun-ichi Kido and Kazumi Ozaki : Porphyhepatic cellsromonas gingivalis inhibits insulin signaling by regulating SOCS3 and IRS-1 in, 第59回春季日本歯周病学会学術大会, May 2016.
54.	Hiromi Nakae, 薮内さつき, Natsumi Fujiwara, Shizuko Yanagisawa, Masami Yoshioka, Kaya Yoshida, Yuko Takeuchi, Akari Watanabe, Tokiko Doi, Miwa Matsuyama, Hiroki Iga, Kazumi Ozaki, Daisuke Hinode, Masanori Nakano and Yasuhiko Shirayama : 健口体操ポスターを活用した口腔機能向上の取り組み, 第13回日本口腔ケア学会総会・学術大会, Apr. 2016.
55.	Shizuko Yanagisawa, Yasuhiko Shirayama, Masami Yoshioka, 高村春菜, Kazumi Ozaki and Masanori Nakano : 老人福祉施設における食形態決定に関する観察項目の検討, 第13回日本口腔ケア学会総会, Apr. 2016.
56.	濱本恵, Yasuhiko Shirayama, 中野渡有香, 中原恵子, Nori Sato, Kazumi Ozaki and Shinsuke Katoh : 重なり五角形を用いた高次脳機能スクリーニング検査の検討(第2報), 第39回日本高次脳機能障害学会学術集会, Dec. 2015.
57.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : The effects of alkannin on CCR5 ligands production from human periodontal ligament cells, 日本歯科保存学会2015年度秋季学術大会, Nov. 2015.
58.	Shizuko Yanagisawa, Yasuhiko Shirayama, Masami Yoshioka, 高村春菜, Kazumi Ozaki, Yuko Takeuchi and Masanori Nakano : 常食化に向けた食物形態と口腔評価との関連に関する研究-口腔評価の精度向上と「不適合」要因の解明-, 平成27年度全国老人福祉施設研究会議, Oct. 2015.
59.	Kaya Yoshida, Hirohiko Okamura and Kazumi Ozaki : PKRやインフラマソームがP. gingivalisを感染させた骨芽細胞において骨吸収に関連する因子の発現に与える影響, 第57回歯科基礎医学会学術大会, Sep. 2015.
60.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : Effects of IL-4 on CCL11 and CCL20 productions in human periodontal ligament cells, 第58回秋季日本歯周病学会学術大会, Sep. 2015.
61.	薮内さつき, Hiromi Nakae, Daisuke Hinode, Hiroki Iga, Kazumi Ozaki, Yasuhiko Shirayama, Miwa Matsuyama, Masami Yoshioka, Shizuko Yanagisawa, Natsumi Fujiwara, Akari Watanabe, Tokiko Doi, Fumiaki Kawano and Katsuhiko Yoshimoto : 歯学部学生の情動知能に対する高齢者交流学習の効果, 第34回日本歯科医学教育学会総会および学術大会鹿児島市, Jul. 2015.
62.	Natsumi Fujiwara, Hiromi Nakae, 薮内さつき and Kazumi Ozaki : 歯科衛生士学生の自己教育力に関する実態について, The Journal of Japanese Dental Education Association, Jul. 2015.
63.	Shizuko Yanagisawa, Yasuhiko Shirayama, Masami Yoshioka, 高村春菜, Kazumi Ozaki, Yuko Takeuchi and Masanori Nakano : 施設介護職員における口腔評価の精度向上の検討, 第12回日本口腔ケア学会総会, Jun. 2015.
64.	薮内さつき, Hiromi Nakae, Daisuke Hinode, Yuko Takeuchi, Hiroki Iga, Kazumi Ozaki, Yasuhiko Shirayama, Miwa Matsuyama, Shizuko Yanagisawa, Masami Yoshioka, Kaya Yoshida, Natsumi Fujiwara, Akari Watanabe, Tokiko Doi, Masanori Nakano, Fumiaki Kawano and Katsuhiko Yoshimoto : 地域育成型歯学教育プログラムの評価(第2報)地域福祉体験学習における教育効果の変化, 平成26年度FD推進プログラム大学教育カンファレンスin徳島, 62-63, Dec. 2014.
65.	Shindo Satoru, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : Shikoninがヒト歯根膜由来細胞のIL-6およびIL-8産生に与える影響, 第141回日本歯科保存学会秋季学術大会, Oct. 2014.
66.	Yumi Hoshimo, 溝部潤子, 中道敦子, Akari Watanabe, Natsumi Fujiwara, Kazumi Ozaki, Daisuke Hinode, Hiroki Iga, 岩城重次 and 菅武雄 : 口腔ケアシミュレータを応用したリカレント教育の試み -学生実習との比較- ・北九州, 第33回日本歯科医学教育学会, Jul. 2014.
67.	薮内さつき, Hiromi Nakae, Daisuke Hinode, Hiroki Iga, Kazumi Ozaki, Yasuhiko Shirayama, Miwa Matsuyama, Shizuko Yanagisawa, Masami Yoshioka, Yumi Hoshimo, Natsumi Fujiwara, Akari Watanabe, Fumiaki Kawano and Katsuhiko Yoshimoto : 高齢者交流学習後の歯学部生の高齢者イメージの変化・北九州, The Journal of Japanese Dental Education Association, 105, Jul. 2014.
68.	Shizuko Yanagisawa, Yasuhiko Shirayama, Masanori Nakano, Kazumi Ozaki and Hiroki Iga : 口腔保健業務支援システムを用いた離島高齢者福祉施設における連携体制の構築, 第11回日本口腔ケア学会総会, Jun. 2014.
69.	Shindo Satoru, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : GenipinはE.coli LPSが誘導するヒト歯根膜細胞のIL-6およびIL-8産生を抑制する, 第140回日本歯科保存学会春季学術大会, Jun. 2014.
70.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : 活性型ビタミンDはIL-1β刺激ヒト歯根膜細胞の炎症性サイトカイン産生を抑制する, 第140回日本歯科保存学会春季学術大会, Jun. 2014.
71.	Kitanaka Yutaro, Yoshitaka Hosokawa, Ikuko Hosokawa, Shindo Satoru, Kazumi Ozaki and Takashi Matsuo : genipinはTNF-αが誘導するヒト歯根膜由来細胞のIL-6産生を抑制する, 第57回春季歯周病学会学術大会, May 2014.
72.	Yumi Hoshimo, Atsuko Nakamichi, 管武雄, Akari Watanabe, Natsumi Fujiwara, Miwa Matsuyama, Kazumi Ozaki, 岩城重次, Daisuke Hinode and Hiroki Iga : 歯科衛生士学生を対象とした新しい口腔ケア教育の取り組み-口腔ケアシミュレータを応用したケア実習の効果-, 日本歯科衛生教育学会雑誌, Vol.14, No.2, 109, Dec. 2013. (Keyword) 歯科衛生士教育 / 口腔ケア / シミュレータ
73.	Tomoko Kimura, Kazumi Ozaki, Hiromichi Yumoto, Keiji Murakami, Chieko Sugawara, Chihiro Shinohara, Emi Takegawa, Yoichiro Miyake, Takashi Matsuo and Fumiaki Kawano : Roles of scrA gene in pathogenicity of Streptococcus mutans, 第6回日本総合歯科学会総会・学術大会, 38, Nov. 2013.
74.	進藤智, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : GenipinはIL-1betaが誘導するヒト歯根膜細胞のCCL20およびIL-6 産生を抑制する, 第139回日本歯科保存学会秋季学術大会, Oct. 2013.
75.	Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo : The effect of genipin on CCL20 and IL-6 productions from IL-1beta-stimulated human periodontal ligament cells, The Japanese Journal of Conservative Dentistry, 70, Oct. 2013.
76.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo : IL-6 enhances CCL20 production from IL-1-stimulated human periodontal ligament cells, Journal of the Japanese Association of Periodontology, 97, May 2013.
77.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo : The effect of adrenomedullin on Th17-related cytokines production from human dendrtic cells, The Japanese Journal of Conservative Dentistry, Nov. 2012.
78.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : The effect of IL-17A on CCL20 production from TNF-a-stimulated human gingival fibroblasts, 日本歯科保存学雑誌, Nov. 2012.
79.	石川真琴, Kaya Yoshida, Natsumi Fujiwara, Yoshitaka Hosokawa, Ikuko Hosokawa and Kazumi Ozaki : 歯周病原性細菌Porphyromonas gingivalis感染が肝臓糖代謝に及ぼす影響, 日本歯科保存学雑誌, 155, Nov. 2012.
80.	Kazumi Ozaki, 那賀川明美, Masanori Nakano, Yasuhiko Shirayama, Miwa Matsuyama, Daisuke Hinode, Masaru Hada, Masami Yoshioka, Atsuko Nakamichi, Kaya Yoshida, Yuko Takeuchi, Yumi Hoshimo, Natsumi Fujiwara, Hiromi Nakae, 薮内さつき, Hiroki Iga, Fumiaki Kawano and Tetsuo Ichikawa : 社会福祉施設での訪問口腔ケアを支援する包括ケア型地域ICTシステムについて, 第22回日本歯科医学会総会プログラム・事前抄録集, 163, Nov. 2012.
81.	Yumi Hoshimo, Atsuko Nakamichi, Shigetsugu Iwaki, Takeo Suga, Yayoi Kanehisa, Daisuke Hinode and Kazumi Ozaki : development and evaluation of a novel oral hygiene simulator for dental hygienists education, The Journal of Japan Societty of Dental Hygiene Education, Vol.3, No.1, 63, Nov. 2012. (Keyword) Professional Oral Heaalth Care / OralCcare Simulator / Education for Dental Hygienists
82.	Yumi Hoshimo, Atsuko Nakamichi, Takeo Suga, Shigetsugu Iwaki, Yayoi Kanehisa, Daisuke Hinode and Kazumi Ozaki : The Educational Effects of Practice for Skill Acquirement of Oral Care with a Novel Simulator on a Ventilator, The Journal of Japan Societty of Dental Hygiene Education, Vol.3, No.1, 78, Nov. 2012. (Keyword) Professional Oral Heaalth Care / OralCcare Simulator / Education for Dental Hygienists
83.	Natsumi Fujiwara, Yasuhiko Shirayama, Atsuko Nakamichi, Yumi Hoshimo and Kazumi Ozaki : The Qualitative Study on the Evaluation of Dental Hygiene Students' Growth by Clinical Training, The Journal of Japan Society of Dental Hygiene Education, Vol.3, No.1, 54, Nov. 2012. (Keyword) Dental Hygienist / Clinical Training / M-GTA
84.	薮内さつき, Hiromi Nakae, Daisuke Hinode, Yuko Takeuchi, Hiroki Iga, Kazumi Ozaki, Masaru Hada, Yasuhiko Shirayama, Miwa Matsuyama, Masami Yoshioka, Atsuko Nakamichi, Yumi Hoshimo, Natsumi Fujiwara, Masanori Nakano, Fumiaki Kawano and Katsuhiko Yoshimoto : 高齢社会を担う地域育成型歯学教育:専門教育終了時の授業アンケートから考察される教育効果, 第31回日本歯科医学教育学会総会および学術大会プログラム・抄録集, 124, Jul. 2012.
85.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : The effect of catechin on CCL11 production from TNF-alpha -stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Jun. 2012.
86.	薮内さつき, Hiroki Iga, Masanori Nakano, Kazumi Ozaki, Hiromi Nakae, 石川真琴 and 江頭陽子 : 介護施設職員のための口腔ケアセミナープログラム構築の試み, 第9回日本口腔ケア学会総会学術大会プログラム・抄録集, 106, Jun. 2012. (Keyword) 口腔ケア / 介護施設職員
87.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : The effect of IL-22 on CCL20 production in IL-1beta-stimulated human gingival fibroblasts, Journal of the Japanese Association of Periodontology, May 2012.
88.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi and Takashi Matsuo : The effect of TWEAK on CCL20 production on IL-1beta-stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Oct. 2011.
89.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : The effect of theaflavin on IL-6 production in TNFSF14-stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Jun. 2011.
90.	Kazumi Ozaki, Natsumi Fujiwara, 石川真琴, Ikuko Hosokawa, Yoshitaka Hosokawa and Hiromichi Yumoto : う蝕関連細菌の家族内伝播と生活習慣による影響に関する研究 ―兄弟姉妹間の差異について―, 134回日本歯科保存学会春季学術大会, Jun. 2011.
91.	Kazumi Ozaki, Natsumi Fujiwara, 石川真琴, 細川育子, Yoshitaka Hosokawa and Hiromichi Yumoto : う蝕関連細菌の家族内伝播と生活習慣による影響に関する研究 ―兄弟姉妹間の差異について―, 134回日本歯科保存学会春季学術大会, Jun. 2011.
92.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : TLR3 ligandがヒト歯肉線維芽細胞のIL-1beta誘導CCL20産生に与える影響, Journal of the Japanese Association of Periodontology, May 2011.
93.	Shindo Satoru, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Oncostatin Mが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす紅茶ポリフェノールの影響, Journal of the Japanese Association of Periodontology, May 2011.
94.	Shindo Satoru, Yoshitaka Hosokawa, Hosokawa Ikuko, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Oncostatin Mが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす紅茶ポリフェノールの影響, Journal of the Japanese Association of Periodontology, May 2011.
95.	Hisahiro Takeuchi, Toshiyuki Suge, Yukihiro Momota, Kazumi Ozaki, Atsuko Nakamichi, Yoichiro Miyake, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 日本歯科大学臨床実習視察報告, 第38回四国歯学会例会, Mar. 2011.
96.	薮内さつき, 中江弘美, Daisuke Hinode, Yuko Takeuchi, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Kaya Yoshida, Atsuko Nakamichi, Yumi Hoshimo, Natsumi Fujiwara, Fumiaki Kawano and Katsuhiko Yoshimoto : 徳島大学教育GP「高齢社会を担う地域育成型歯学教育」授業アンケートから考察される教育効果, 平成22年度全学FD大学教育カンファレンス in 徳島, Jan. 2011.
97.	中江弘美, Daisuke Hinode, 薮内さつき, Hiroki Iga, Masami Yoshioka, Masanori Nakano, Hideo Yoshida, Kazumi Ozaki, Masaru Hada and Atsuko Nakamichi : 地域高齢者との福祉体験学習の教育効果と地域貢献事業としての評価, 第7回日本口腔ケア学会学術大会, Nov. 2010.
98.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : The effect of catechin on IL-6 production from TNFSF14-stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Oct. 2010.
99.	Yoshitaka Hosokawa, Hosokawa Ikuko, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : The effect of catechin on IL-6 production from TNFSF14-stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Oct. 2010.
100.	Hashimoto Reina, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : IL-1betaが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす緑茶カテキンの影響, Journal of the Japanese Association of Periodontology, Sep. 2010.
101.	Hashimoto Reina, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : IL-1betaが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす緑茶カテキンの影響, Journal of the Japanese Association of Periodontology, Sep. 2010.
102.	Hashimoto Reina, Yoshitaka Hosokawa, Hosokawa Ikuko, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : IL-1betaが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす緑茶カテキンの影響, Journal of the Japanese Association of Periodontology, Sep. 2010.
103.	薮内さつき, Hiroki Iga, 中江弘美, Daisuke Hinode, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Atsuko Nakamichi, Yumi Hoshimo, Fumiaki Kawano and Katsuhiko Yoshimoto : 「人間力の向上」を目指した教育プログラム-「高齢者交流学習」-, 第29回日本歯科医学教育学会, Jul. 2010.
104.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : IL-17A enhances CCL20 production in IL-1beta-stimulated human gingival fibroblasts, Journal of the Japanese Association of Periodontology, May 2010.
105.	Yoshitaka Hosokawa, Hosokawa Ikuko, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : IL-17A enhances CCL20 production in IL-1beta-stimulated human gingival fibroblasts, Journal of the Japanese Association of Periodontology, May 2010.
106.	Tomoko Kimura, Kazumi Ozaki, Hiromichi Yumoto, Keiji Murakami, Shizuo Kayama, 藤坂菊美, Kanako Takahashi and Yoichiro Miyake : Roles and virulence of scrA and htrA genes in Streptococcus mutans, 第83回日本細菌学会総会, Mar. 2010.
107.	Hiroki Iga, Masanori Nakano, Daisuke Hinode, Kazumi Ozaki, Hisahiro Takeuchi, Katsuhiko Yoshimoto and Yoshio Hayashi : 口腔保健学を基軸とした国際的社会福祉教育プログラムの構築に向けて, 平成21年度全学FD 徳島大学教育カンファレンス, Mar. 2010.
108.	中江弘美, Daisuke Hinode, 薮内さつき, Yuko Takeuchi, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Atsuko Nakamichi, Yumi Hoshimo, Naoko Matsumoto, Fumiaki Kawano and Katsuhiko Yoshimoto : 地域育成型歯学教育プログラムの評価 -地域福祉体験学習の取り組みを通して-, 平成21年度全学FD 徳島大学教育カンファレンス, Mar. 2010.
109.	Daisuke Hinode, 中江弘美, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Atsuko Nakamichi, Yumi Hoshimo, Naoko Matsumoto, Fumiaki Kawano and Katsuhiko Yoshimoto : 「高齢社会を担う地域育成型歯学教育」—地域福祉体験学習の取り組みと教育効果—, 第28回日本歯科医学教育学会総会および学術大会, Nov. 2009.
110.	Daisuke Hinode, Yuko Takeuchi, Hiroki Iga, Masanori Nakano, Hideo Yoshida, Masaru Hada, Kazumi Ozaki, Masami Yoshioka, Kaya Yoshida, Yumi Hoshimo, Naoko Matsumoto, Fumiaki Kawano and Katsuhiko Yoshimoto : 高齢社会を担う地域育成型歯学教育 -初年次教育における達成課題-, 平成20年度全学FD 徳島大学教育カンファレンス, Jan. 2009.
111.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Adrenomedullin inhibits CXCL10 production by human gingival fibroblasts, 56th Annual Meeting of Japanese Association for Dental Research, Nov. 2008.
112.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Toll-like Receptor Ligands刺激が誘導する単球のCCL20産生に及ぼすAdrenomedullinの影響, 第128回日本歯科保存学会秋季学術大会, Nov. 2008.
113.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : ヒト歯肉線維芽細胞におけるTLR4 ligandが誘導するCXCL10産生に及ぼすAdrenomedullinの影響, 第51回日本歯周病学会秋季学術大会, Oct. 2008.
114.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Toll-like Receptor Ligands刺激が誘導する単球のIL-1beta産生に及ぼすAdrenomedullinの影響, 第128回日本歯科保存学会春季学術大会, Jun. 2008.
115.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Flagellinがヒト歯肉線維芽細胞のサイトカイン産生および接着分子発現に与える影響, 第128回日本歯科保存学会春季学術大会, Jun. 2008.
116.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Adrenomedullinがヒト歯肉線維芽細胞のToll-like Receptor Ligands誘導サイトカイン産生に与える影響, 第51回日本歯周病学会春季学術大会, Apr. 2008.
117.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Toll-like receptor ligandsがヒト歯肉線維芽細胞のCXCL10産生に与える影響, 第51回日本歯周病学会春季学術大会, Apr. 2008.
118.	木村智子, Kazumi Ozaki, Shizuo Kayama, 藤坂菊美, Hiromichi Yumoto and Yoichiro Miyake : Streptococcus mutansの病原性におけるスクロース輸送系遺伝子の役割について, 第81回日本細菌学会総会, Mar. 2008.
119.	木村智子, Kazumi Ozaki, Shizuo Kayama, 藤坂菊美 and Yoichiro Miyake : Streptococcus mutansの病原性におけるスクロース輸送系遺伝子の役割について, 第81回日本細菌学会総会, Mar. 2008.
120.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Adrenomedulinがヒト歯肉線維芽細胞のサイトカイン産生に与える影響の解析, 第127回日本歯科保存学会秋季学術大会, Nov. 2007.
121.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo : Proinflammatory Roles of NOD2 in Human Gingival Fibroblasts, 第55回国際歯科研究学会日本部会(JADR)総会・学術大会, Nov. 2007.
122.	Yumi Hoshimo, Kazumi Ozaki, Naoko Matsumoto, Kaya Yoshida, Masami Yoshioka, Yuko Takeuchi, Hideo Yoshida, Daisuke Hinode, Masanori Nakano, Hiroki Iga and Masaru Hada : 歯科衛生士教育の4年生教育に関するニーズ, 第2回日本衛生士教育学術大会, Nov. 2007.
123.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo : Proinflammatory Roles of NOD2 in Human Gingival Fibroblasts, 第55回国際歯科研究学会日本部会(JADR)総会・学術大会, Nov. 2007.
124.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : サイトカインがヒト歯肉線維芽細胞のCXCL10産生に与える影響, 日本歯周病学会50周年記念学術大会, Sep. 2007.
125.	木村智子, Kazumi Ozaki, 藤坂菊美 and Takashi Matsuo : Streptococcus mutans の病原性におけるスクロース輸送系遺伝子の役割について, 第126回日本歯科保存学会春季学術大会, Jun. 2007.
126.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : ヒト歯肉線維芽細胞におけるCCL17産生の解析, 第50回春季日本歯周病学会学術大会, May 2007.
127.	Yoshitaka Hosokawa, 細川育子, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : ヒト歯肉線維芽細胞におけるCCL17産生の解析, 第50回春季日本歯周病学会学術大会, May 2007.
128.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : サイトカイン刺激によるヒト歯肉線維芽細胞におけるCXCL16産生の解析, 第36回日本免疫学会総会・学術集会, Dec. 2006.
129.	Yoshitaka Hosokawa, 細川育子, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : サイトカイン刺激によるヒト歯肉線維芽細胞におけるCXCL16産生の解析, 第36回日本免疫学会総会・学術集会, Dec. 2006.
130.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : サイトカインがヒト歯肉線維芽細胞上のICAM-1およびVCAM-1発現に与える影響, 第49回秋季日本歯周病学会学術大会, Oct. 2006.
131.	Yoshitaka Hosokawa, 細川育子, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : サイトカインがヒト歯肉線維芽細胞上のICAM-1およびVCAM-1発現に与える影響, 第49回秋季日本歯周病学会学術大会, Oct. 2006.
132.	木村智子, Kazumi Ozaki, 藤坂菊美, Keiji Murakami and Yoichiro Miyake : Streptococcus mutansの病原性におけるスクロース輸送系遺伝子の役割について, 第59回日本細菌学会中国・四国支部総会, Oct. 2006.
133.	藤坂菊美, Kazumi Ozaki and Takashi Matsuo : S. mutans com遺伝子の象牙質への侵入に及ぼす影響について, 第124回日本歯科保存学会春季学会, May 2006.
134.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : TWEAKがヒト歯肉線維芽細胞における炎症性サイトカイン産生ならびに接着分子発現に与える影響の解析, 第49回春季日本歯周病学会学術大会, Apr. 2006.
135.	Yoshitaka Hosokawa, 細川育子, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : TWEAKがヒト歯肉線維芽細胞における炎症性サイトカイン産生ならびに接着分子発現に与える影響の解析, 第49回春季日本歯周病学会学術大会, Apr. 2006.
136.	菅悦子, 三木千津, 石川清美, 大森幸子, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 患者のコンプライアンスに配慮した歯周治療について, 第49回春季日本歯周病学会学術大会, Apr. 2006.
137.	Yoshitaka Hosokawa, Ikuko Hosokawa, Hideaki Nakae, Kazumi Ozaki and Takashi Matsuo : 炎症性サイトカインおよびLPSはヒト歯肉線維芽細胞のCCL20産生を誘導する, 第48回秋季日本歯周病学会学術大会, Sep. 2005.
138.	Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo : Langerhans細胞における抗菌ペプチドの発現について, 第48回秋季日本歯周病学会学術大会, Sep. 2005.
139.	大森幸子, 三木千津, 石川清美, 菅悦子, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 咬合に問題を有する歯周病患者の治療経過について, 第48回秋季日本歯周病学会学術大会, Sep. 2005.
140.	Yoshitaka Hosokawa, 細川育子, Hideaki Nakae, Kazumi Ozaki and Takashi Matsuo : 炎症性サイトカインおよびLPSはヒト歯肉線維芽細胞のCCL20産生を誘導する, 第48回秋季日本歯周病学会学術大会, Sep. 2005.
141.	細川育子, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo : Langerhans細胞における抗菌ペプチドの発現について, 第48回秋季日本歯周病学会学術大会, Sep. 2005.
142.	菅悦子, 三木千津, 石川清美, 大森幸子, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 糖尿病を有する患者の歯周治療における管理の重要性, 第48回秋季日本歯周病学会学術大会, Apr. 2005.
143.	末延慎司, 藤坂菊美, Kazumi Ozaki and 大嶋隆 : 培養条件変化によるStreptococcus mutansの動態に関する解析, 第78回日本細菌学会総会, Apr. 2005.
144.	藤坂菊美, 末延慎司, Kazumi Ozaki and Takashi Matsuo : 培養条件変化によるStreptococcus mutansの動態に関する解析, 第121回日本歯科保存学会秋季学会, Nov. 2004.
145.	末延慎司, 藤坂菊美, Kazumi Ozaki and Takashi Matsuo : 培養条件変化によるStreptococcus mutansの動態に関する解析, 第121回日本歯科保存学会秋季学会, Nov. 2004.
146.	三木千津, 石川清美, 菅悦子, 大森幸子, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 口腔癌患者における歯周治療および長期的管理の重要性, 第47回秋季日本歯周病学会学術大会, Oct. 2004.
147.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : ヒト歯肉線維芽細胞におけるCXCL12産生ならびに機能的解析, 第47回秋季日本歯周病学会学術大会, Oct. 2004.
148.	Yoshitaka Hosokawa, 細川育子, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : ヒト歯肉線維芽細胞におけるCXCL12産生ならびに機能的解析, 第47回秋季日本歯周病学会学術大会, Oct. 2004.
149.	菅悦子, 三木千津, 石川清美, 大森幸子, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 歯周治療中に発見した口腔粘膜疾患の一例, 第47回春季日本歯周病学会学術大会, May 2004.
150.	末延慎司, 藤坂菊美, Kazumi Ozaki and 大嶋隆 : Streptococcus mutansの象牙質への付着とグルカン合成量の関係, 第77回日本細菌学会, Apr. 2004.
151.	渋谷拓也, Kazumi Ozaki, Takashi Matsuo, 石川邦夫 and 恵比須繁之 : マイクロCTによる3種Ni-Ti製ロータリーファイルの比較, 第119回日本歯科保存学会秋季大会, Nov. 2003.
152.	Harumi Sakamoto, Kazumi Ozaki, Keiji Oishi, Akiko Kawasaki, Nozomi Yokoyama and Takashi Matsuo : 大規模ネットワークにおける歯周病検査・歯科保健指導の電子記録ならびにその運用について, Journal of the Japanese Association of Periodontology, Vol.45, 197, Oct. 2003.
153.	大森幸子, 渡邊久恵, 三木千津, 石川清美, 山下美由紀, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 歯肉退縮にともなう発音及び審美障害に対する対応, 第46回秋季日本歯周病学会学術大会, Oct. 2003.
154.	末延慎司 and Kazumi Ozaki : 浮遊，付着状態におけるStreptococcus mutansのglucosyltransferaseならびにdextranase遺伝子発現の解析, 第56回日本細菌学会中国四国支部総会, Oct. 2003.
155.	Toshiyuki Suge, Akiko Kawasaki, Kazumi Ozaki, Takashi Matsuo, 石川邦夫 and 恵比須繁之 : Effects of ammonium hexafluorosilicate on acid resistance of bovine teeth, 第118回日本歯科保存学会春季学会, Jun. 2003.
156.	位田夏子, Kazumi Ozaki, 末延慎司, Kanako Takahashi, Daisuke Yamaguchi and Takashi Matsuo : S.mutans刺激によるヒト樹状細胞の成熟化の異差について, 第118回日本歯科保存学会春季学会, Jun. 2003.
157.	渡邊久恵, 三木千津, 石川清美, 山下美由紀, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 歯周治療におけるリコールシステムの現状, 第46回春季日本歯周病学会学術大会, Apr. 2003.
158.	末延慎司, 位田夏子 and Kazumi Ozaki : Streptococcus mutansの環境変化におけるGlucosyltransferase関連遺伝子発現の解析, 第76回日本細菌学会, Apr. 2003.
159.	Kanako Takahashi, Tadashi Nakanishi, Daisuke Yamaguchi, Yoshitaka Hosokawa, Hiromichi Yumoto, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 歯髄炎の病態形成におけるLARCおよびCCR6の役割, 第32回日本免疫学会, Dec. 2002.
160.	蓮井義則, 荒木哲也, Kazumi Ozaki and 篠崎文彦 : 小学生の咬合力と新スポーツテストの比較検討, 第14回日本小児口腔外科学会, Nov. 2002.
161.	Kazumi Ozaki : 象牙細管内細菌の挙動, 第117回日本歯科保存学会秋季学会, Vol.45, 4, Nov. 2002.
162.	石川清美, 渡邊久恵, 三木千津, 久保万友美, 山下美由紀, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 小学校全児童を対象にした経年的な歯科検診・検査の解析, 第45回秋季日本歯周病学会学術大会, Vol.44, 209, Oct. 2002.
163.	Kazumi Ozaki, 木持健, 末延慎司 and Takashi Matsuo : 象牙細管に侵入させた細菌の超微組織学的検索, 第116回日本歯科保存学会春季学会, Vol.45, 46, May 2002.
164.	Chihiro Shinohara, Tadashi Nakanishi, 末延慎司, Kazumi Ozaki and Takashi Matsuo : 抜歯に至った難治性根尖性歯周炎の1症例, 第116回日本歯科保存学会春季学会, Vol.45, 114, May 2002.
165.	Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Hirotoshi Shimizu, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 歯周炎病変局所におけるLARCおよびCCR6の発現, 第31回日本免疫学会, Dec. 2001.
166.	末延慎司, Kazumi Ozaki, 位田夏子, Akiko Kawasaki, Toshiyuki Suge and Takashi Matsuo : 銀担持シリカを添加した合着用グラスアイオノマーセメントの諸性質, 第115回秋季日本歯科保存学会, Nov. 2001.
167.	Kanako Takahashi, Tadashi Nakanishi, Yoshitaka Hosokawa, Chihiro Shinohara, Hiromichi Yumoto, Kazumi Ozaki and Takashi Matsuo : 炎症歯髄におけるLARCおよびCCR6の発現, 第115回秋季日本歯科保存学会, Nov. 2001.
168.	Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Hirotoshi Shimizu, Hiromichi Yumoto, Kazumi Ozaki and Takashi Matsuo : 歯周炎病変局所におけるLARCおよびCCR6の発現, 第44回秋季日本歯周病学会学術大会, Oct. 2001.
169.	Keiko Fujinaka, Akiko Kawasaki, 吉田佳子, Kazumi Ozaki and Takashi Matsuo : 難治性根尖性歯周における根尖部の走査型電子顕微鏡による検索, 第114回日本歯科保存学会, Jun. 2001.
170.	Takashi Matsuo, Tadashi Nakanishi, Kanako Takahashi, Kazumi Ozaki and Hideaki Nakae : 歯髄炎の不可逆性化に関する臨床的および病理学的考察, 第14回「歯内療法の集い」, May 2001.
171.	Tadashi Nakanishi, Nozomi Matsuoka, Kanako Takahashi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 深在う蝕における侵入細菌の局所と歯髄反応, 第113回秋季日本歯科保存学会, Nov. 2000.
172.	Kazumi Ozaki, Hiromichi Yumoto, Chihiro Shinohara, 木持健 and Takashi Matsuo : 象牙質齲蝕に侵入した細菌種の同定, 第113回日本歯科保存学会秋季学会, Nov. 2000.
173.	Yoshitaka Hosokawa, 山口大輔, 清水洋利, Tadashi Nakanishi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 歯周炎の病巣局所におけるケモカインおよびケモカイン受容体の発現, 第30回日本免疫学会総会, Nov. 2000.
174.	渡邊久恵, 三木千津, 石川清美, 久保万友美, 石丸毅, 石川利栄子, 蓮井義則, Kazumi Ozaki and Takashi Matsuo : 口腔ケアで完治した難治性の口角ビランの一例, 第43回春季日本歯周病学会学術大会, May 2000.
175.	Hirotoshi Shimizu, Yoshitaka Hosokawa, Daisuke Yamaguchi, Tadashi Nakanishi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 歯周炎の病巣局所におけるリンパ球浸潤に対するケモカインの関与, 第29回日本免疫学会総会, Dec. 1999.
176.	Kazumi Ozaki, Tadashi Nakanishi, Keiko Fujinaka and Takashi Matsuo : 歯根部象牙質齲蝕誘発モデルの細菌学ならびに形態学的検索, 第110回日本歯科保存学会春季学会, May 1999.
177.	Akihisa Urayama, Takeshi Kimochi, Nozomi Matsuoka, Kazumi Ozaki, Masahiro Yoshiyama and Takashi Matsuo : Resin Infiltration into Artificial Carious Dentin, 第110回日本歯科保存学会春季学会, May 1999.
178.	Hirotoshi Shimizu, Yoshitaka Hosokawa, Tadashi Nakanishi, Kazumi Ozaki and Hideaki Nakae : 歯周炎の病巣局所におけるVCAM-1,VLA-4を介する接着系の解析, 第28回日本免疫学会, Dec. 1998.
179.	木持健, Akihisa Urayama, Kazumi Ozaki, 吉山昌宏 and Takashi Matsuo : 齲蝕象牙質へのレジン浸透性, 第109回日本歯科保存学会春季学会, Nov. 1998.
180.	Akihisa Urayama, Kazumi Ozaki, 吉山昌宏 and Takashi Matsuo : 人工齲蝕象牙質へのレジン浸透性, 第108回日本歯科保存学会春季学会, Jun. 1998.
181.	Kazumi Ozaki, Keiko Fujinaka, 糸田川徳則 and Takashi Matsuo : 歯根部齲蝕誘発モデルの細菌学ならびに形態学検索, 第107回日本歯科保存学会秋季学会, Nov. 1997.
182.	吉山昌宏, 糸田川徳則, Kazumi Ozaki and Takashi Matsuo : 齲蝕象牙質へのレジン浸透性, 第107回日本歯科保存学会秋季学会, Nov. 1997.
183.	向井知里, 吉田佳子, Kazumi Ozaki, 野杁由一郎 and Takashi Matsuo : ヒト感染根管における細菌侵入に免疫組織学的解析, 第106回日本歯科保存学会春季学会, Jun. 1997.
184.	吉山昌宏, Kazumi Ozaki and Takashi Matsuo : 齲蝕象牙質へのレジン浸透性, 第106回日本歯科保存学会春季学会, Jun. 1997.
185.	Tadashi Nakanishi, Hirotoshi Shimizu, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 多形核白血球の集積化による歯髄組織破壊機構の解析, 第105回日本歯科保存学会春秋季学会, Nov. 1996.
186.	Kazumi Ozaki, 川戸純奈, 野杁由一郎, Takashi Matsuo and 恵比須繁之 : 歯根部齲蝕誘発モデルにおける齲蝕関連細菌の免疫電顕による検索, 第104回日本歯科保存学会春季学会, May 1996.
187.	平尾清司, Hideaki Nakae, Kazumi Ozaki, Takashi Matsuo and 恵比須繁之 : 歯周病原細菌の付着を促進させるヒト顎舌下腺唾液糖蛋白に対するモノクロナール抗体の作製, 第39回春季日本歯周病学会学術大会, Apr. 1996.
188.	Kazumi Ozaki, 川戸純奈, 野杁由一郎, Takashi Matsuo and 恵比須繁之 : ヒト口腔内における歯根部齲蝕誘発モデルの細菌学ならびに形態学的検索, 第103回日本歯科保存学会秋季学会, Oct. 1995.
189.	野杁由一郎, Keiko Fujinaka, 岡本妙, Kazumi Ozaki, Takashi Matsuo and 恵比須繁之 : ヒト歯周ポケット底部における歯周関連細菌の免疫電顕法による検索, 第38回秋季日本歯周病学会学術大会, Oct. 1995.
190.	白神俊之, Kazumi Ozaki, Takashi Matsuo and 恵比須繁之 : 感染根管処置に反応せず，抜歯に至った1症例, 第2回「歯内療法の集い」, Jun. 1995.
191.	Kazumi Ozaki : 歯根部齲蝕に関する基礎的研究, 平成6年度徳島県歯科医学大会, Jan. 1995.
192.	白神俊之, Takashi Matsuo, Kazumi Ozaki, 野杁由一郎 and 恵比須繁之 : 根尖病巣を有する歯の歯根部象牙細管侵入細菌の免疫組織学的検索, 第101回日本歯科保存学会秋季学会, Nov. 1994.
193.	野杁由一郎, 近藤妙, Kazumi Ozaki, Hideaki Nakae, Takashi Matsuo and 恵比須繁之 : ヒト歯周ポケットにおける異種菌体間相互作用の形態学的検索, 第37回日本歯周病学会秋季学会, Oct. 1994.
194.	野杁由一郎, Takashi Matsuo, Hideaki Nakae, Kazumi Ozaki and 恵比須繁之 : ヒト歯肉縁下プラークの研究, 第17回四国歯学会, Jul. 1994.
195.	Kazumi Ozaki, 野杁由一郎 and 恵比須繁之 : ヒト歯根部齲蝕病巣の超微細形態学的検索, 第100回日本歯科保存学会春季学会, May 1994.
196.	野杁由一郎, 近藤妙, Kazumi Ozaki, Hideaki Nakae, Takashi Matsuo and 恵比須繁之 : ヒト歯周ポケットにおける歯周病関連細菌の免疫組織学的2重染色法による検索, 第36回秋季日本歯周病学会学術大会, Oct. 1993.
197.	白神俊之, Takashi Matsuo, Kazumi Ozaki, 野杁由一郎 and 恵比須繁之 : 歯根部象牙細管に侵入した細菌の免疫組織学的検索, 第98回日本歯科保存学会春季学会, Jun. 1993.
198.	野杁由一郎, Kazumi Ozaki, Hideaki Nakae, Takashi Matsuo and 恵比須繁之 : ヒト歯周ポケットにおける歯周病関連細菌の局在性の検索, 第36回春季日本歯周病学会学術大会, May 1993.
199.	Kazumi Ozaki, Takashi Matsuo, Hideaki Nakae, 吉山昌宏 and 恵比須繁之 : 象牙質齲蝕病巣における侵入細菌の免疫組織学的検索, 第15回四国歯学会, Jun. 1992.
200.	Kazumi Ozaki, Takashi Matsuo, Hideaki Nakae, 吉山昌宏 and 恵比須繁之 : 象牙質齲蝕における侵入細菌の免疫組織学的検索, 第96年日本歯科保存学会春季学会, Jun. 1992.
201.	吉山昌宏, Toshiyuki Suge, 白神俊之, Kazumi Ozaki and 恵比須繁之 : 象牙質知覚過敏症の発症機構, 硬組織研究技術談話会, Mar. 1992.
202.	Kazumi Ozaki, Takashi Matsuo, Hideaki Nakae, 吉山昌宏 and 恵比須繁之 : 齲蝕における象牙質侵入細菌の動態に関する免疫組織化学的検討, 第95回日本歯科保存学会秋季学会, Nov. 1991.
203.	吉山昌宏, Toshiyuki Suge, Kazumi Ozaki and 恵比須繁之 : 象牙質知覚過敏症の発症機構, 第95回日本歯科保存学会秋季学会, Nov. 1991.
204.	Takashi Matsuo, Tadashi Nakanishi, 片岡健哉, Kazumi Ozaki, 野杁由一郎, 大木元玲子, Hideaki Nakae, 吉山昌宏 and 恵比須繁之 : 覆髄法の適応範囲の拡大に関する臨床的検討, 第14回四国歯学会, Jul. 1991.
205.	Masahiro Yoshiyama, Kazumi Ozaki, Yuichiro Noiri, Kenya Kataoka, Tadashi Nakanishi, Reiko Ogimoto, Hideaki Nakae, Takashi Matsuo and Shigeyuki Ebisu : Treatment of Dentin Hypersensitivity, --- Effect of a Light-curing Resin Liner on Tubule Occlusion ---, 第93回日本歯科保存学会秋季学会, Sep. 1990.
206.	Kazumi Ozaki, 野杁由一郎, Tadashi Nakanishi, 片岡健哉 and 吉山昌宏 : コンポジットレジンの歯根部象牙質に対する接着性, 第92回日本歯科保存学会春季学会, Jun. 1990.

Et cetera, Workshop:

1.	Natsumi Fujiwara, Wenhua Shao, Kaya Yoshida, Rieko Arakaki, Kazumi Ozaki, Naozumi Ishimaru and Yasusei Kudo : Fusobacterium nucleatumが与える口腔癌細胞への影響, 第38回分子病理学研究会淡路島シンポジウム(兵庫県) 2019年7月19-20日, Jul. 2019.
2.	Natsumi Fujiwara, Kazumi Ozaki, Kayo Yoshida, Yuko Takeuchi and Shizuko Yanagisawa : 口腔ケア支援体制づくりを目指した研修会の取り組みと介護関係職員の口腔ケア実施状況, 第54回日本理学療法学術研修大会in徳島2019 総合事業実践報告会 2019年5月25日(徳島県徳島市), May 2019.
3.	Kaya Yoshida, Mariko Seyama, Natsumi Fujiwara, Kazumi Ozaki, 内部健太, 池亀美華 and Hirohiko Okamura : 歯周病が糖尿病を重症化する機序について, 2018 Bioscience retreat in Awaji, Nov. 2018.
4.	Natsumi Fujiwara, Miki Tsurukuma, Kaya Yoshida, Keiji Murakami, Kazumi Ozaki, Hideki Fujii and Hiromichi Yumoto : MPCポリマーコーティングによる義歯用レジンのカンジダ付着抑制効果, 2018 Bioscience retreat in Awaji, Nov. 2018.
5.	Mariko Seyama, Kaya Yoshida, Natsumi Fujiwara and Kazumi Ozaki : Porphyromonas gingivalisの分泌小胞が肝臓インスリンシグナルに及ぼす影響について, 2017 Bioscience Retreat in Tosa, Dec. 2017.
6.	Kaya Yoshida, Mariko Seyama, Natsumi Fujiwara, Kazumi Ozaki, 内部健太, 池亀美華 and Hirohiko Okamura : Porphyromonas gingivalis感染したマクロファージはインスリンシグナル抑制因子を含むエクソソームを産生する, 2017 Bioscience Retreat in Tosa, Dec. 2017.
7.	Hisahiro Takeuchi, Toshiyuki Suge, Yukihiro Momota, Kazumi Ozaki, Atsuko Nakamichi, Yoichiro Miyake, Katsuhiko Yoshimoto and Tetsuo Ichikawa : 日本歯科大学臨床実習視察報告, Shikoku Dental Research, Vol.24, No.2, 85-94, Jan. 2012. (Tokushima University Institutional Repository) ● Metadata: 109821 (Tokushima University Institutional Repository: 109821)

Report:

1.	Yoshihiko Ueno, Yosuke Seki, Chigusa Uchiumi, Takeshi Iwasa, Akira Takahashi, Toshiyuki Yasui, Shinji Kawahito, Kazumi Ozaki, Hiromichi Fujino, Toshio Takayanagi, Takefumi Hattori, Takahito Saito and Maiko Kamioka : 令和5年度徳島大学高等教育研究センターアドミッション部門報告書, 令和5年度徳島大学高等教育研究センターアドミッション部門報告書, Mar. 2024.
2.	Yoshihiko Ueno, Yosuke Seki, Satoshi Kinugawa, Hisayoshi Morioka, Akira Takahashi, Kenji Mori, Naozumi Ishimaru, Kazumi Ozaki, Tetsuo Yamazaki, Atsushi Takada, Yoshihiro Uto, Takahito Saito and Maiko Kamioka : 令和4年度徳島大学高等教育研究センターアドミッション部門報告書, 令和4年度徳島大学高等教育研究センターアドミッション部門報告書, Mar. 2023.
3.	Kazumi Ozaki, Mariko Seyama and Kayo Yoshida : 公益財団法人 e-とくしま推進財団令和3年度調査·研究事業助成事業「認知・口腔機能同時モニタリングWebシステムの地域展開による健口・健康長寿実現戦略」報告書, 1-19, Mar. 2022. (Keyword) ICT / かなひろいテスト / オーラルディアドコキネシス
4.	Yoshihiko Ueno, Yosuke Seki, Ryuji Yorioka, Yuishin Izumi, Takeshi Nikawa, Reiko Okahisa, Naozumi Ishimaru, Kazumi Ozaki, Hideji TANAKA, Kenji Terada, Tamotsu Tanaka, Ray S. Furuya and Maiko Kamioka : 令和3年度徳島大学高等教育研究センターアドミッション部門報告書, 令和3年度徳島大学高等教育研究センターアドミッション部門報告書, Mar. 2022.
5.	Kazumi Ozaki, Yasuhiko Shirayama, Tetsuo Ichikawa, Miwa Matsuyama, Yasuhiro Hamada, Shinsuke Katoh, 濱田邦美, Teruyoshi Kageji, 藤原真治, Shizuko Yanagisawa, Akari Watanabe, Mariko Seyama and Yuko Takeuchi : 中山間地域の通いの場におけるオーラルフレイル予防対策を起点とした地域住民の包括的支援に関する調査研究事業∼``見える化''・``つなぐ化''プロジェクト∼, 令和2年度厚生労働省老人保健事業推進費等補助金(老人保健健康増進等事業) 報告書, 1-98, Mar. 2021. (Keyword) ICT / オーラルフレイル / 高齢者サロン
6.	Kazumi Ozaki, Yasuhiko Shirayama, Shizuko Yanagisawa and Yuko Takeuchi : 公益社団法人全国老人福祉施設協議会令和元年度調査研究助成事業「ICT システムを用いた多職種による遠隔モニタリングがもたらす食支援業務の質向上および効率化に関する実証研究」報告書, 1-63, Apr. 2020. (Keyword) ICT / 多職種連携 / 食支援
7.	Kazumi Ozaki, Yasuhiko Shirayama, Shizuko Yanagisawa, Natsumi Fujiwara and Yuko Takeuchi : 「ICTシステムを用いた多職種による遠隔モニタリングがもたらす食支援業務の質向上および効率化に関する実証研究」報告書, 公益社団法人全国老人福祉施設協議会(令和元年度調査研究助成事業), Apr. 2020.
8.	Kazumi Ozaki, Yasuhiko Shirayama, Tetsuo Ichikawa, Miwa Matsuyama, Yasuhiro Hamada, Shinsuke Katoh, 濵田邦美, Teruyoshi Kageji, 藤原真治, Shizuko Yanagisawa, Natsumi Fujiwara and Yuko Takeuchi : 令和元年度老人保健事業推進費等補助金(老人保健健康増進等事業)中山間地域における地域住民との連携によるオーラルフレイル予防のためのICT利活用の強化・進展に関する調査研究事業「とくしま助INTプロジェクト」報告書, 1-94, Mar. 2020.
9.	Kazumi Ozaki, Yasuhiko Shirayama, Shinsuke Katoh, Tetsuo Ichikawa, Yasuhiro Hamada, Shizuko Yanagisawa, Natsumi Fujiwara and Yuko Takeuchi : 平成30年度老人保健事業推進費等補助金(老人保健健康増進等事業)中山間地域におけるICT利活用によるフレイル・オーラルフレイル予防のためのベストプラクティス確立・普及に関する調査研究事業「阿波なかつむぎプロジェクト」報告書, 1-92, Mar. 2019.
10.	Yasuhiko Shirayama, Kazumi Ozaki, Shinsuke Katoh, Tetsuo Ichikawa, Saori Iwamoto, Shinji Nagahiro, Shizuko Yanagisawa and Natsumi Fujiwara : 「那賀イ∼と，つながる・みまもるプロジェクト」報告書, 平成29年度老人保健事業推進費等補助金中山間地域の地域包括ケアシステム構築における食支援連携促進に資するICT利活用に関する調査研究事業「那賀イーと,つながる・みまもるプロジェクト」報告書, 1-86, Mar. 2018.
11.	Kazumi Ozaki, Natsumi Fujiwara, Shizuko Yanagisawa and Yasuhiko Shirayama : 口腔ケア関連ICTツールを併用した経口摂取支援業務運用ガイドラインの策定に関する研究, 公益財団法人全国老人福祉施設協議会平成29年度全国老人福祉施設研究会議高知会議要覧, 247-252, Oct. 2017. (Keyword) 口腔健康管理 / ICTシステム / CAPDo
12.	Kazumi Ozaki : 象牙細管侵入細菌の菌体内多糖合成に関する動的解析, 平成17年度∼平成18年度科学研究費補助金(基盤研究(C))研究成果報告書, Tokushima, Mar. 2007.
13.	Kazumi Ozaki and Takashi Matsuo : Bacterial Viability Assay at an Electron Microscopic Leved, カリオロージに基づく齲蝕の診断法および治療法の開発, 51-58, Mar. 2005.
14.	Kazumi Ozaki and Takashi Matsuo : PCR Amplificcation of Target DNA Extracted From Bacterial Cells Embedded in Plastic Material for Electron Microscopy, カリオロージに基づく齲蝕の診断法および治療法の開発, 29-49, Mar. 2005. (Keyword) Bactrerial DNA / Semiquantitative PCR / Embedding-Material
15.	Kazumi Ozaki and Takashi Matsuo : 電顕用樹脂埋試料から抽出した細菌の16SrDNAを利用した象牙齲蝕病巣深部の細菌の同定, カリオロジーに基づく齲蝕の診断法および治療法の開発, 15-27, Mar. 2005.
16.	Kazumi Ozaki : 齲蝕象牙質の細管侵入細菌におけるスクロース代謝の動的解析, 平成15年度∼平成16年度科学研究費補助金(基盤研究(C)(2))研究成果報告書, Mar. 2005.
17.	Kazumi Ozaki : 微小組織切片中の核酸を利用した露髄部の細菌種の同定および炎症歯髄の病態解析, 平成13年度∼平成14年度科学研究費補助金(基盤研究(C)(2))研究成果報告書, Mar. 2003.
18.	Kazumi Ozaki : 象牙細管内の環境をシミュレーションした露出歯根象牙の齲蝕の誘発モデルの確立, 平成11年度∼平成12年度科学研究費補助金(基盤研究(C)(2))研究成果報告書, Mar. 2001.
19.	Kazumi Ozaki : In situにおける露出歯根象牙質での齲蝕誘発とその細菌学的および形態学的解析, 研究報告書 [第13回]平成8年度助成事業, 37-48, 東京, Feb. 1999.

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

再生環境下での休眠状態・若返り間葉系幹細胞の歯周組織再生療法と全身疾患への応用 (Project/Area Number: 24K12913 )
The role of DNA of Periodontal bacterium OMVs in Alzheimer's diseases. (Project/Area Number: 23K09505 )
口腔・認知機能Web評価システムの地域展開による健口・健康長寿実現戦略 (Project/Area Number: 22K10078 )
ポリフェノール内包キトサンナノカプセルを用いた口腔バイオフィルム抑制技術の開発 (Project/Area Number: 22K09967 )
歯周医学における歯周病原細菌由来ベシクルの役割解明と歯周病重症化予防剤の開発 (Project/Area Number: 21K09896 )
Study of the inhibitory effects of polyphenol loaded titania nanotubes on bacterial growth and biofilm formation (Project/Area Number: 19K10132 )
Development and construction of a database for maintenance and management of oral functions in the elderly (Project/Area Number: 17K11754 )
Study of the effects of polyphenol-silver nanoparticles complex upon oral biofilm formation and antimicrobial activity (Project/Area Number: 16K11554 )
Development of oral probiotics using multi-bacteria (Project/Area Number: 25670886 )
Study of the effects of serine proteases on the cariogenicity of Streptococcus mutans (Project/Area Number: 25462962 )
Development of extracellular DNA-protein complex-targeting novel treatments and prevention for oral biofilm-related infectious diseases (Project/Area Number: 24592872 )
Study of the effects of adrenomedullin upon oral biofilm formation (Project/Area Number: 22592122 )
Endodontic therapeutic application of electro-magnetic wave irradiation for refractory periapical periodontitis and periapical biofilm (Project/Area Number: 21592423 )
Development of the diagnosis and treatment of root caries on its pathosis and pathogenesis (Project/Area Number: 20592229 )
Study of quorum-sensing system of invading bacteria in dentinal caries (Project/Area Number: 19592204 )
Clarification of the mechanism of periodontitis-initiated/accelerated atheroacleicsis and identification of its causal components (Project/Area Number: 18592263 )
Study on synthesizing of intracellular polysaccharide by Streptococcus mutans in dentinal tubules. (Project/Area Number: 17591993 )
Analysis of the role of pulp fibroblasts on lymphocytes infiltration in pulpitis (Project/Area Number: 16591915 )
Study on Streptococcus mutans sucrose-dependent adherence and cariogenesis. (Project/Area Number: 15592021 )
Development of the new diagnostic methods and treatments of dental caries based upon caliology (Project/Area Number: 14207081 )
Detection of bacterial species using 16S rDNA existed in deep layers of carious lesions with pulp exposure embedded with plastic material and analysis of the pathogenesis of pulpitis (Project/Area Number: 13672000 )
Examination of the histological and bacteriological features of the interface between bacterial deposits and root dentin using a device that included exposed root dentin reproduced pulpal pressure in vitro. (Project/Area Number: 11671896 )
Bacterial Invasion of Infected Canals and Root Dentin of Human Teeth and Analysis of the Host-parasite Interaction at the Apex. - Elucidation of Pathogenesis of Refractory Cases-. (Project/Area Number: 10470406 )
歯根部象牙質齲蝕発症おける齲蝕原性細菌の動態の三次元的解析 (Project/Area Number: 09771621 )
In situにおける露出歯根象牙質で齲蝕誘発とその細菌学的および形態学的解析 (Project/Area Number: 08771700 )
歯根部象牙質齲蝕の進行と防御に関する免疫組織学的研究 (Project/Area Number: 07771764 )
In vivoにおける歯根部齲蝕の誘発とその細菌学的ならびに形態学的解析 (Project/Area Number: 07672078 )
非進行性の歯根部齲蝕の診断に関する細菌学的および形態学的研究 (Project/Area Number: 06771720 )
Localization of periodontal disease-associated bacteria in human periodontal pockets and its relationship to tissue destruction (Project/Area Number: 04454472 )
象牙質知覚過敏症における象牙細管の石灰化を阻害する物質の同定とその局在 (Project/Area Number: 03670894 )
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Professor : Ozaki, Kazumi

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