Updated on 2022/11/02

写真a

 
YAMAMOTO Tadashi
 
Organization
Okayama University Hospital Professor
Position
Professor
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Degree

  • 博士(歯学) ( 岡山大学 )

Research Areas

  • Life Science / Conservative dentistry

Professional Memberships

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Committee Memberships

  • 日本歯周病学会   編集委員会 委員  

    2021   

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  • 岡山歯学会   評議員  

    2019   

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  • 日本歯周病学会   研究委員会 委員  

    2019 - 2020   

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  • 日本歯科保存学会   評議員  

    2017   

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  • 日本歯周病学会   評議員  

    2017   

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  • 日本歯科保存学会   医療合理化委員会 幹事  

    2017 - 2020   

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  • 日本歯周病学会   ペリオドンタルメディシン委員会 委員  

    2015   

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  • 広島大学   再生医療等委員会 3号委員  

    2015   

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  • 日本歯周病学会   若手研究者の集い合宿研修会WG 委員  

    2013   

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  • 日本歯科保存学会   編集委員会 幹事  

    2008 - 2011   

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  • 日本歯科保存学会   広報委員会 委員  

    2008 - 2011   

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Papers

  • Treatment resistance of rheumatoid arthritis relates to infection of periodontal pathogenic bacteria: a case-control cross-sectional study. International journal

    Kazu Takeuchi-Hatanaka, Yoshinobu Koyama, Kentaro Okamoto, Kyosuke Sakaida, Tadashi Yamamoto, Shogo Takashiba

    Scientific reports   12 ( 1 )   12353 - 12353   2022.7

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    Recent studies have shown that periodontitis is associated with rheumatoid arthritis (RA) and periodontal bacteria, such as Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg) are involved in the pathogenesis of RA via citrullinated proteins. Smoking has also been shown to be involved in the pathogenesis of RA; however, the extent of this involvement is still poorly understood. In addition, RA and polymyalgia rheumatica (PMR) are sometimes difficult to differentiate; however, the relationship between PMR and the factors from smoking and periodontal bacteria is unclear. The aim of this study was to clarify the relationship between periodontal pathogenic bacterial infections and smoking in patients with RA or PMR. This case-control study included 142 patients with untreated RA or PMR. This study evaluated the serum antibody titers against periodontal pathogenic bacterial antigens and an anti-citrullinated peptide antibody (ACPA). In patients with RA, the relationship between antibody titers and disease activity of RA and response after 3 months of treatment was also investigated. Additionally, the effects of smoking were evaluated. Although there was no significant difference in serum antibody titer against periodontal pathogenic bacteria between the ACPA-positive RA group and the ACPA-negative PMR group, we found an association between the elevated antibody titer against Pg and the degree of ACPA value, especially between negative group and high-value positive group (≥ 100 U/mL). The antibody titers against Aa and Pg did not differ depending on disease activity score 28 (DAS28) at baseline; however, patients with high antibody titers had poor RA therapeutic response as judged by DAS28 after 3 months. We could not find any association between smoking and any of these parameters. Periodontal pathogenic bacteria, especially Pg, are associated with elevated ACPA levels. Our findings suggest that Pg and Aa infections interfere with the therapeutic response of RA.

    DOI: 10.1038/s41598-022-16279-z

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  • Analysis of subgingival microbiota in monozygotic twins with different severity and progression risk of periodontitis. International journal

    Tadashi Yamamoto, Makoto Taniguchi, Kazuyuki Matsunaga, Yusuke Kawata, Mari Kawamura, Keisuke Okubo, Keisuke Yamashiro, Kazuhiro Omori, Shogo Takashiba

    Clinical case reports   10 ( 4 )   e05725   2022.4

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    The study aims to reveal the composition of subgingival bacteria in monozygotic twins with discordant in severity and progression risk of periodontitis. Microbiome analysis indicated that most bacteria were heritable but differed in their abundance and immune response. The dysbiotic bacteria can be considered as risk markers for periodontitis progression.

    DOI: 10.1002/ccr3.5725

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  • Estimation of periodontal pocket surface area in small to medium dogs: a proof-of-concept study. International journal

    Kazuya Tamura, Masako Tokuzen-Tai, Yasir Dilshad Siddiqui, Hitomi Tamura-Naito, Yoshiharu Nagahara, Kazu Hatanaka-Takeuchi, Tadashi Yamamoto, Shogo Takashiba

    BMC veterinary research   18 ( 1 )   13 - 13   2022.1

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    BACKGROUND: Periodontal disease is the most common dental disease in dogs. Although the systemic effects of periodontal disease have not been clarified in veterinary science, it is necessary to evaluate the effects of periodontal disease in clinical trials in the future. There have been a few clinical attempts made, however, to assess the severity of periodontal inflammation and its impact on the systemic health of dogs. Meanwhile, in the field of dentistry for humans, the periodontal inflamed surface area (PISA) and periodontal epithelial surface area (PESA) have been used to quantitatively assess the degree of periodontal disease affecting a single tooth as well as the overall extent of periodontitis. Recent studies have also suggested the use of these assessments to examine the relationship between periodontal inflammation and systemic health. RESULTS: The estimation formula for a dog's periodontal pocket surface area (PPSA), an alternative to PISA and PESA in humans, was established using body weight and periodontal pocket depth. Actual values were measured using extracted teeth from various dog breeds and sizes (2.3-25.0 kg of body weight) to obtain universal regression equations for PPSA. Altogether, 625 teeth from 73 dogs of 16 breeds were extracted and subsequently analyzed for morphological information. PPSA was measured in 61 dogs of 10 breeds with periodontal disease using the established estimation formulas, and the correlation between PPSA and preoperative blood chemistry data was analyzed accordingly. A strong correlation was found between PPSA and serum globulin (r = 0.71) while moderate correlations were found for C-reactive protein (r = 0.54) and serum albumin (r = -0.51). CONCLUSIONS: Estimation formulas using body weight and the 6-point probing depth were established for determining PPSA. Direct correlations between PPSA and several blood test results were observed in the study sample. Taken together, these results suggest that PPSA could be useful for evaluating the effects of periodontitis on systemic conditions in dogs.

    DOI: 10.1186/s12917-021-03116-0

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  • Enzymatic measurement of short-chain fatty acids and application in periodontal disease diagnosis. International journal

    Kazu Hatanaka, Yasushi Shirahase, Toshiyuki Yoshida, Mari Kono, Naoki Toya, Shin-Ichi Sakasegawa, Kenji Konishi, Tadashi Yamamoto, Kuniyasu Ochiai, Shogo Takashiba

    PloS one   17 ( 7 )   e0268671   2022

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    Periodontal disease is a chronic inflammatory condition caused by periodontal pathogens in the gingival sulcus. Short-chain fatty acids (SCFAs) produced by causal bacteria are closely related to the onset and progression of periodontal disease and have been reported to proliferate in the periodontal sulcus of patients experiencing this pathology. In such patients, propionic acid (C3), butyric acid (C4), isobutyric acid (IC4), valeric acid (C5), isovaleric acid (IC5), and caproic acid (C6), henceforth referred to as [C3-C6], has been reported to have a detrimental effect, while acetic acid (C2) exhibits no detrimental effect. In this study, we established an inexpensive and simple enzymatic assay that can fractionate and measure these acids. The possibility of applying this technique to determine the severity of periodontal disease by adapting it to specimens collected from humans has been explored. We established an enzyme system using acetate kinase and butyrate kinase capable of measuring SCFAs in two fractions, C2 and [C3-C6]. The gingival crevicular fluid (GCF) and saliva of 10 healthy participants and 10 participants with mild and severe periodontal disease were measured using the established enzymatic method and conventional gas chromatography-mass spectrometry (GC-MS). The quantification of C2 and [C3-C6] in human GCF and saliva was well correlated when using the GC-MS method. Furthermore, both C2 and [C3-C6] in the GCF increased with disease severity. However, while no significant difference was observed between healthy participants and periodontal patients when using saliva, [C3-C6] significantly differed between mild and severe periodontal disease. The enzymatic method was able to measure C2 and [C3-C6] separately as well as using the GC-MS method. Furthermore, the C2 and [C3-C6] fractions of GCF correlated with disease severity, suggesting that this method can be applied clinically. In contrast, the quantification of C2 and [C3-C6] in saliva did not differ significantly between healthy participants and patients with periodontal disease. Future studies should focus on inflammation rather than on tissue destruction.

    DOI: 10.1371/journal.pone.0268671

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  • Malnutrition delayed wound healing after tooth extraction by HMGB1-related prolonged inflammation. International journal

    Yao Zhang, Hidetaka Ideguchi, Hiroaki Aoyagi, Keisuke Yamashiro, Tadashi Yamamoto, Masahiro Nishibori, Shogo Takashiba

    International immunopharmacology   96   107772 - 107772   2021.7

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    Malnutrition causes prolonged inflammation, resulting in delayed wound healing. High mobility group box-1 (HMGB1) is a damage-associated molecular pattern that is present in the nuclei of macrophages and is secreted into the extracellular milieu in response to stimuli. It stimulates the production of interleukin-1β (IL-1β) through the receptors for advanced glycation end products (RAGE), inducing an inflammatory response, which is an essential response to initiate wound healing. We hypothesized that malnutrition may interfere with this cascade, causing abnormal inflammation and ultimately delaying wound healing. We used tooth-extracted mice with malnutrition fed with low-casein diet for two weeks. On days 3 and 7 after tooth extraction, the wound tissue was histologically observed and analyzed for several factors in the inflammation-regeneration lineage, including IL-1β, mesenchymal stem cells, myeloperoxidase activity, HMGB1, macrophage polarization, and adenosine 5-triphosphate (ATP). On day 7, delayed wound healing was observed with the following findings under malnutrition conditions: decreased mRNA expression of genes for regeneration and mesenchymal stem cell (MSC) accumulation, an obvious increase in myeloperoxidase and IL-1β mRNA expression, an increase in HMGB1 levels, and an increase in ATP concentration in tissues with elevated proportion of M2 macrophages. These results suggest that the significantly increased secretion of HMGB1 associated with the upregulated production of ATP and IL-1β secretion via the RAGE pathway may interfere with the resolution of inflammation and wound healing under the state of malnutrition.

    DOI: 10.1016/j.intimp.2021.107772

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  • The Fungal Metabolite (+)-Terrein Abrogates Ovariectomy-Induced Bone Loss and Receptor Activator of Nuclear Factor-κB Ligand-Induced Osteoclastogenesis by Suppressing Protein Kinase-C α/βII Phosphorylation. International journal

    Kyosuke Sakaida, Kazuhiro Omori, Masaaki Nakayama, Hiroki Mandai, Saki Nakagawa, Hidefumi Sako, Chiaki Kamei, Satoshi Yamamoto, Hiroya Kobayashi, Satoki Ishii, Mitsuaki Ono, Soichiro Ibaragi, Keisuke Yamashiro, Tadashi Yamamoto, Seiji Suga, Shogo Takashiba

    Frontiers in pharmacology   12   674366 - 674366   2021

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    Osteoporosis is a common disease characterized by a systemic impairment of bone mass and microarchitecture that results in fragility fractures. Severe bone loss due to osteoporosis triggers pathological fractures and consequently decreases the daily life activity and quality of life. Therefore, prevention of osteoporosis has become an important issue to be addressed. We have reported that the fungal secondary metabolite (+)-terrein (TER), a natural compound derived from Aspergillus terreus, has shown receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation by suppressing nuclear factor of activated T-cell 1 (NFATc1) expression, a master regulator of osteoclastogenesis. TER has been shown to possess extensive biological and pharmacological benefits; however, its effects on bone metabolism remain unclear. In this study, we investigated the effects of TER on the femoral bone metabolism using a mouse-ovariectomized osteoporosis model (OVX mice) and then on RANKL signal transduction using mouse bone marrow macrophages (mBMMs). In vivo administration of TER significantly improved bone density, bone mass, and trabecular number in OVX mice (p < 0.01). In addition, TER suppressed TRAP and cathepsin-K expression in the tissue sections of OVX mice (p < 0.01). In an in vitro study, TER suppressed RANKL-induced phosphorylation of PKCα/βII, which is involved in the expression of NFATc1 (p < 0.05). The PKC inhibitor, GF109203X, also inhibited RANKL-induced osteoclastogenesis in mBMMs as well as TER. In addition, TER suppressed the expression of osteoclastogenesis-related genes, such as Ocstamp, Dcstamp, Calcr, Atp6v0d2, Oscar, and Itgb3 (p < 0.01). These results provide promising evidence for the potential therapeutic application of TER as a novel treatment compound against osteoporosis.

    DOI: 10.3389/fphar.2021.674366

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  • Use of Highly Accurate Devices for a First Lower Premolar Endodontic Treatment with Multiple Root Canals.

    Zulema Arias Martinez, Jorge Lopez Videla, Keisuke Yamashiro, Yuki Shinoda-Ito, Tadashi Yamamoto, Shogo Takashiba

    Acta medica Okayama   75 ( 5 )   641 - 645   2021

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    This case report highlights the importance of using a dental operating microscope (DOM) and ultrasonic endodontic tips (UETs) to locate all root canals in the lower first premolar. A 53-year-old woman presented to our clinic with pain in the lower right first premolar. After a detailed search using a DOM and UETs, three root canals were found, prepared with rotary HyFlex endodontic files, and obturated using the lateral condensation technique. At the five-year follow-up after treatment, the tooth was completely restored and fulfilling its function, with no signs or symptoms of any post-treatment flare-up.

    DOI: 10.18926/AMO/62778

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  • Follistatin expressed in mechanically-damaged salivary glands of male mice induces proliferation of CD49f+ cells

    A. Ikeda, T. Yamamoto, J. Mineshiba, S. Takashiba

    Scientific Reports   10 ( 1 )   2020.12

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    <title>Abstract</title>Salivary glands (SGs) are very important for maintaining the physiological functions of the mouth. When SGs regenerate and repair from various damages, including mechanical, radiological, and immune diseases, acinar and granular duct cells originate from intercalated duct cells. However, the recovery is often insufficient because of SGs' limited self-repair function. Furthermore, the precise repair mechanism has been unclear. Here, we focused on CD49f, one of the putative stem cell markers, and characterized CD49f positive cells (CD49f+ cells) isolated from male murine SGs. CD49f+ cells possess self-renewal ability and express epithelial and pluripotent markers. Compared to CD49f negative cells, freshly isolated CD49f+ cells highly expressed inhibin beta A and beta B, which are components of activin that has anti-proliferative effects. Notably, an inhibitor of activin, follistatin was expressed in mechanically-damaged SGs, meanwhile no follistatin was expressed in normal SGs in vivo. Moreover, sub-cultured CD49f+ cells highly expressed both <italic>Follistatin</italic> and a series of proliferative genes, expressions of which were decreased by <italic>Follistatin</italic> siRNA. These findings indicated that the molecular interaction between activin and follistatin may induce CD49f+ cells proliferation in the regeneration and repair of mouse SGs.

    DOI: 10.1038/s41598-020-77004-2

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    Other Link: http://www.nature.com/articles/s41598-020-77004-2

  • 歯周組織の炎症と不妊の関連性を示唆する、ある侵襲性歯周炎患者の病態生理

    大森 一弘, 河野 隆幸, 小林 寛也, 新井 英雄, 山本 直史, 高柴 正悟

    日本歯科保存学雑誌   63 ( 5 )   451 - 460   2020.10

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    緒言:歯周病原細菌の感染と歯周組織の炎症が,妊娠に影響を与える可能性が報告されている.今回,不妊治療の経過が思わしくない侵襲性歯周炎患者に感染源除去の観点から専門的歯周治療を行い,自然妊娠から正常出産にいたった症例の経過をふまえ病態を考察する.症例:33歳,女性,既婚(不妊治療中).2016年9月,26の動揺および同部の自発痛を自覚し,かかりつけ歯科医院を受診した.同院でエックス線検査を受けて,重度の歯槽骨吸収があると説明された.早期の専門的歯周治療を勧められ,当科を紹介された.既往歴の特記事項はなく,不妊検査においても患者本人および夫ともに異常所見はなかった.歯周組織検査において,probing pocket depthが4mm以上の部位の割合は49.5%,bleeding on probingは47.9%,plaque control recordは3.1%,歯周炎症表面積(PISA)は2,392mm2であった.エックス線検査所見では,主訴部の26部を中心に根尖に及ぶ骨吸収像が多数存在した.歯周病原細菌に対する血清抗体価検査および歯周ポケット内細菌DNA検査ともに,Porphyromonas gingivalisの感染が強く疑われた.診断は広汎型侵襲性歯周炎(ステージIV,グレードC),二次性咬合性外傷とした.治療方針として,患者の妊娠希望に配慮して,できるかぎり早期(1年以内)の歯周環境の改善を目指すこととした.また,歯周外科治療が終了するまでの不妊治療を含めた妊娠活動を控える必要性について説明し,同意を得た.治療計画は,(1)歯周基本治療(患者教育,抜歯,局所抗菌療法を併用したスケーリング・ルートプレーニング,暫間固定),(2)歯周組織再生療法,(3)口腔機能回復治療,(4)歯周病安定期治療(SPT)とした.治療経過として,歯周治療に対する宿主反応性は非常に良く,炎症改善と歯槽骨の再生を確認した(歯周外科治療後PISA:43mm2).口腔機能回復治療中に自然妊娠し,35歳時に男児を正常出産(経腟分娩,3,240g,出産週数:38週+5日)した.考察および結論:重度のP. gingivalis感染および歯周炎症を伴う侵襲性歯周炎の罹患が,妊娠成立に影響を及ぼす可能性が示唆された.本症例のように不妊治療の経過が思わしくない場合には,歯周組織を含めた口腔状態を一度精査することが望まれる.(著者抄録)

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  • Isolation and identification of the antimicrobial substance included in tempeh using Rhizopus stolonifer NBRC 30816 for fermentation. Reviewed International journal

    Masahiro Ito, Takashi Ito, Hideyuki Aoki, Koshi Nishioka, Tsugumi Shiokawa, Hiroko Tada, Yuki Takeuchi, Nobuyuki Takeyasu, Tadashi Yamamoto, Shogo Takashiba

    International journal of food microbiology   325   108645 - 108645   2020.7

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    In this study, we focus on the antimicrobial properties of tempeh, a soybean fermented food, against oral bacteria. Tempeh showed antimicrobial activity against dental caries pathogenic bacterium Streptococcus mutans at a final concentration of 1 mg/mL. An antimicrobial substance contained in tempeh was present in the 100 kDa or greater fraction generated by ultrafiltration, but it was found not to be proteinaceous by native-PAGE, SDS-PAGE and protein degradation tests. Next, when the fraction was purified with an ODS column, the 80% and 100% methanol eluates showed antimicrobial activity against S. mutans. The 100% methanol eluate was further subjected to a 2nd column purification, and isolation of the target was confirmed by HPLC. When the isolated material was analyzed by ESI-MS, the m/z was 279.234. Further analysis by Raman spectroscopy revealed a peak similar to linoleic acid. This substance also possessed antimicrobial properties equivalent to linoleic acid.

    DOI: 10.1016/j.ijfoodmicro.2020.108645

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  • The fungal metabolite (+)-terrein abrogates osteoclast differentiation via suppression of the RANKL signaling pathway through NFATc1. Reviewed International journal

    Saki Nakagawa, Kazuhiro Omori, Masaaki Nakayama, Hiroki Mandai, Satoshi Yamamoto, Hiroya Kobayashi, Hidefumi Sako, Kyosuke Sakaida, Hiroshi Yoshimura, Satoki Ishii, Soichiro Ibaragi, Kimito Hirai, Keisuke Yamashiro, Tadashi Yamamoto, Seiji Suga, Shogo Takashiba

    International immunopharmacology   83   106429 - 106429   2020.6

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    Pathophysiological bone resorption is commonly associated with periodontal disease and involves the excessive resorption of bone matrix by activated osteoclasts. Receptor activator of nuclear factor (NF)-κB ligand (RANKL) signaling pathways have been proposed as targets for inhibiting osteoclast differentiation and bone resorption. The fungal secondary metabolite (+)-terrein is a natural compound derived from Aspergillus terreus that has previously shown anti-interleukin-6 properties related to inflammatory bone resorption. However, its effects and molecular mechanism of action on osteoclastogenesis and bone resorption remain unclear. In the present study, we showed that 10 µM synthetic (+)-terrein inhibited RANKL-induced osteoclast formation and bone resorption in a dose-dependent manner and without cytotoxicity. RANKL-induced messenger RNA expression of osteoclast-specific markers including nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), the master regulator of osteoclastogenesis, cathepsin K, tartrate-resistant acid phosphatase (Trap) was completely inhibited by synthetic (+)-terrein treatment. Furthermore, synthetic (+)-terrein decreased RANKL-induced NFATc1 protein expression. This study revealed that synthetic (+)-terrein attenuated osteoclast formation and bone resorption by mediating RANKL signaling pathways, especially NFATc1, and indicated the potential effect of (+)-terrein on inflammatory bone resorption including periodontal disease.

    DOI: 10.1016/j.intimp.2020.106429

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  • Evaluation of the simulator with automatic irrigation control system designed for countermeasures of internal contamination in dental unit water lines. Reviewed International journal

    Keisuke Okubo, Takashi Ito, Kentaro Okamoto, Ichiro Yamamoto, Hajime Mizutani, Yusuke Kawata, Yasuyoshi Shiota, Masahiro Ito, Shin Nakamura, Masako Tai, Tadashi Yamamoto, Shogo Takashiba

    Heliyon   6 ( 6 )   e04132   2020.6

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    The prevention of nosocomial infections is an imperative task. The dental chair unit (DCU) is an indispensable device used in dental treatment. However, it is known that the dental unit water line (DUWL) can become contaminated with biofilm, consisting mainly of heterotrophic bacteria (HB). Recently, the International Organization for Standardization specified the methods for testing DUWL contamination management. On these grounds, a simulator reproducing DUWL was prepared to standardize the examination method of the DUWL contamination. Objectives: To evaluate the reproducibility of the DUWL simulator, monitor the DUWL contamination states, and test the efficacy of a commercial decontaminant for DUWL. Methods: The DUWL simulator was assembled by a DCU manufacturing company. The simulator's DUWL was filled with tap water (TW), and left for approximately one year. Neutral electrolyzed water (NEW) was used as a decontaminant for DUWL. Both TW and NEW were passed through DUWL in a timely manner simulating daily dental treatment. Water was sampled from the air turbine hand piece weekly for 4 weeks and used for HB culture. Contamination status was evaluated by measuring bacterial adenosine triphosphate release and by culturing on Reasoner's 2A medium. Results: The DUWL released contaminated water had a bacterial count of over 6 × 104 cfu/mL. After passing NEW through DUWL for 1 week, the count drastically decreased to its basal level and remained steady for 4 weeks. However, TW showed no effect on DUWL decontamination throughout the examination periods. Conclusions: The DUWL simulator could be useful to examine the efficacy of the decontaminant for DUWL and development of new methods in DUWL contamination management.

    DOI: 10.1016/j.heliyon.2020.e04132

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  • Functionalized Graphene Oxide Shields Tooth Dentin from Decalcification Reviewed

    M. Z.I. Nizami, Y. Nishina, T. Yamamoto, Y. Shinoda-Ito, S. Takashiba

    Journal of Dental Research   99 ( 2 )   182 - 188   2020.2

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    © International & American Associations for Dental Research 2019. This in vitro study assessed the efficacy of functionalized graphene oxide (f-GO) nanocomposites on the decalcification of dentin, because dental caries of the root surface is becoming one of the new problems in aged society. Hydroxyapatite plates (HAP) and dentin slices were coated with f-GO nanocomposites by comparing them to silver diamine fluoride as a positive control, then treated with decalcification solutions such as ethylenediaminetetraacetic acid and citrate at 37°C for 24 h. Scanning electron microscopy (SEM) revealed significant protection of the surface morphology of HAP and dentin. On the other hand, a cariogenic Streptococcus mutans growth was inhibited by f-GO nanocomposites. In addition, cytotoxicity of them to epithelial cells was much less than that of povidone-iodine, which is commonly used for oral disinfectant. We synthesized 5 different f-GO nanocomposites such as GO–silver (Ag), GO-Ag–calcium fluoride (CaF2), GO-CaF2, GO-zinc, and GO–tricalcium phosphate (Ca3(PO4)2). They were standardized by evaluating under SEM, transmission electron microscopy (TEM), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), thermogravimetry analysis (TGA), and Raman spectra after being synthesized in an aseptic technique. The abilities of GO-Ag, GO-Ag-CaF2, and GO-CaF2 nanocomposites were most preventive for decalcification. In addition, GO-Ag and GO-Ag-CaF2 almost completely inhibited S. mutans growth. However, they did not exhibit cytotoxicity to epithelial cells except at the highest concentration (0.1 w/v%) of GO-Ag and GO-Ag-CaF2. Furthermore, these f-GO nanocomposites exhibited less or no discoloration of dentin, although commonly used silver diamine fluoride causes discoloration of dentin to black. Thus, these f-GO nanocomposites are useful to protect dental caries on the tooth root that becomes a social problem in aged society.

    DOI: 10.1177/0022034519894583

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  • Induction of migration of periodontal ligament cells by selective regulation of integrin subunits Reviewed

    Mari Kawamura, Tadashi Yamamoto, Keisuke Yamashiro, Shinsuke Kochi, Chiaki Yoshihara-Hirata, Hidetaka Ideguchi, Hiroaki Aoyagi, Kazuhiro Omori, Shogo Takashiba

    Journal of Cellular and Molecular Medicine   23 ( 2 )   1211 - 1223   2020.2

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    © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. The recruitment of tissue-resident stem cells is important for wound regeneration. Periodontal ligament cells (PDL cells) are heterogeneous cell populations with stemness features that migrate into wound sites to regenerate periodontal fibres and neighbouring hard tissues. Cell migration is regulated by the local microenvironment, coordinated by growth factors and the extracellular matrix (ECM). Integrin-mediated cell adhesion to the ECM provides essential signals for migration. We hypothesized that PDL cell migration could be enhanced by selective expression of integrins. The migration of primary cultured PDL cells was induced by platelet-derived growth factor-BB (PDGF-BB). The effects of blocking specific integrins on migration and ECM adhesion were investigated based on the integrin expression profiles observed during migration. Up-regulation of integrins α3, α5, and fibronectin was identified at distinct localizations in migrating PDL cells. Treatment with anti-integrin α5 antibodies inhibited PDL cell migration. Treatment with anti-integrin α3, α3-blocking peptide, and α3 siRNA significantly enhanced cell migration, comparable to treatment with PDGF-BB. Furthermore, integrin α3 inhibition preferentially enhanced adhesion to fibronectin via integrin α5. These findings indicate that PDL cell migration is reciprocally regulated by integrin α3-mediated inhibition and α5-mediated promotion. Thus, targeting integrin expression is a possible therapeutic strategy for periodontal regeneration.

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  • Antimicrobial and antibiofilm effects of abietic acid on cariogenic Streptococcus mutans. Reviewed

    Yuki Ito, Takashi Ito, Keisuke Yamashiro, Fumi Mineshiba, Kimito Hirai, Kazuhiro Omori, Tadashi Yamamoto, Shogo Takashiba

    Odontology   108 ( 1 )   57 - 65   2020.1

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    Dental caries is a type of oral microbiome dysbiosis and biofilm infection that affects oral and systemic conditions. For healthy life expectancy, natural bacteriostatic products are ideal for daily and lifetime use as anti-oral infection agents. This study aimed to evaluate the inhibitory effects of abietic acid, a diterpene derived from pine rosin, on the in vitro growth of cariogenic bacterial species, Streptococcus mutans. The effective minimum inhibitory concentration of abietic acid was determined through observation of S. mutans growth, acidification, and biofilm formation. The inhibitory effects of abietic acid on the bacterial membrane were investigated through the use of in situ viability analysis and scanning electron microscopic analysis. Cytotoxicity of abietic acid was also examined in the context of several human cell lines using tetrazolium reduction assay. Abietic acid was found to inhibit key bacterial growth hallmarks such as colony forming ability, adenosine triphosphate activity (both planktonic and biofilm), acid production, and biofilm formation. Abietic acid was identified as bacteriostatic, and this compound caused minimal damage to the bacterial membrane. This action was different from that of povidone-iodine or cetylpyridinium chloride. Additionally, abietic acid was significantly less cytotoxic compared to povidone-iodine, and it exerted lower toxicity towards epithelial cells and fibroblasts compared to that against monocytic cells. These data suggest that abietic acid may prove useful as an antibacterial and antibiofilm agent for controlling S. mutans infection.

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  • High Mobility Group Box 1 Expression in Oral Inflammation and Regeneration. Reviewed International journal

    Keisuke Yamashiro, Hidetaka Ideguchi, Hiroaki Aoyagi, Chiaki Yoshihara-Hirata, Anna Hirai, Risa Suzuki-Kyoshima, Yao Zhang, Hidenori Wake, Masahiro Nishibori, Tadashi Yamamoto, Shogo Takashiba

    Frontiers in immunology   11   1461 - 1461   2020

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    High mobility group box 1 (HMGB1) is a non-histone DNA-binding protein of about 30 kDa. It is released from a variety of cells into the extracellular milieu in response to inflammatory stimuli and acts on specific cell-surface receptors, such as receptors for advanced glycation end-products (RAGE), Toll-like receptor (TLR)2, TLR4, with or without forming a complex with other molecules. HMGB1 mediates various mechanisms such as inflammation, cell migration, proliferation, and differentiation. On the other hand, HMGB1 enhances chemotaxis acting through the C-X-C motif chemokine ligand (CXCL)12/C-X-C chemokine receptor (CXCR)4 axis and is involved in regeneration. In the oral cavity, high levels of HMGB1 have been detected in the gingival tissue from periodontitis and peri-implantitis patients, and it has been shown that secreted HMGB1 induces pro-inflammatory cytokine expression, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, which prolong inflammation. In contrast, wound healing after tooth extraction or titanium dental implant osseointegration requires an initial acute inflammation, which is regulated by secreted HMGB1. This indicates that secreted HMGB1 regulates angiogenesis and bone remodeling by osteoclast and osteoblast activation and promotes bone healing in oral tissue repair. Therefore, HMGB1 can prolong inflammation in the periodontal tissue and, conversely, can regenerate or repair damaged tissues in the oral cavity. In this review, we highlight the role of HMGB1 in the oral cavity by comparing its function and regulation with its function in other diseases. We also discuss the necessity for further studies in this field to provide more specific scientific evidence for dentistry.

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  • Microbiome composition comparison in oral and atherosclerotic plaque from patients with and without periodontitis Reviewed

    Daichi Isoshima, Keisuke Yamashiro, Kazuyuki Matsunaga, Makoto Taniguchi, Takehiro Matsubara, Shuta Tomida, Shinzo Ota, Michiyoshi Sato, Yutaka Shimoe, Tatsuo Kohriyama, Zulema Arias, Kazuhiro Omori, Tadashi Yamamoto, Shogo Takashiba

    Odontology   2020

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    © 2020, The Society of The Nippon Dental University. There is no conclusive evidence regarding a causal relationship between periodontitis and atherosclerosis. In this study, we examined the microbiome in the oral cavity and atheromatous plaques from atherosclerosis patients with or without periodontitis to investigate the role of oral bacteria in the formation of atheromatous plaques. We chose four patients with and without periodontitis, who had undergone carotid endarterectomy. Bacterial samples were extracted from the tongue surface, from periodontal pocket (during the oral examination), and from the atheromatous plaques (APs). We investigated the general and oral conditions from each patient and performed next-generation sequencing (NGS) analysis for all bacterial samples. There were no significant differences between both groups concerning general conditions. However, the microbiome patterns of the gingival pocket showed differences depending on the absence or presence of periodontitis, while those of the tongue surface were relatively similar. The microbiome pattern of the atheromatous plaques was entirely different from that on the tongue surface and gingival pocket, and oral bacteria were seldom detected. However, the microbiome pattern in atheromatous plaques was different in the presence or absence of periodontitis. These results suggested that oral bacteria did not affect the formation of atheromatous plaques directly.

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  • 多施設後ろ向き観察研究による臨床指標としての歯周炎症表面積の基準値

    井上 裕貴, 畑中 加珠, 山本 直史, 平田 貴久, 三辺 正人, 山本 龍生, 内藤 徹, 山本 松男, 佐藤 秀一, 石幡 浩志, 稲垣 幸司, 三谷 章雄, 中島 啓介, 漆原 譲治, 高柴 正悟

    日本歯周病学会会誌   61 ( 4 )   159 - 167   2019.12

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    歯周炎症表面積(periodontal inflamed surface area:PISA)は,歯周組織の炎症部の面積を表す新たな歯周病の臨床指標である。従来伝わりづらかった歯周病の炎症程度を歯科以外の医療従事者が理解する上で,有用な指標であると考えられる。しかし,歯周病の程度や治療によるPISAの基準は未だ不明である。そこで,本研究は,日本歯周病学会が設ける歯周病専門医・認定医の電子申請書類のデータから各治療フェーズにおけるPISAの値を調べ,歯周病治療に伴う炎症度の基準値を提案することを目的とした。8施設で取得した113症例を用いて,Nesseらの方法によって歯周ポケット深さとプロービング時の出血からPISAを算出した。その結果,PISAの中央値は,初診時1,271.4mm2,歯周基本治療終了時211.8mm2,SPT移行時52.1mm2,そして最新SPT時30.0mm2であった。また,PISAはBOPと高い相関を示し(p<0.001),BOPよりも鋭敏に治療効果を反映した。以上から,中等度以上の歯周炎においてPISAを用いると,初診時は表面積約1,500mm2の歯周組織の炎症がSPT時は100mm2未満(初診時の約7%)に減少することが明らかになった。今後,更なるデータの蓄積および詳細な分析を行いながらPISAの使用を普及させると,PISAは医科歯科連携の際に歯周病炎症を伝える指標になり得ると考える。(著者抄録)

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  • 多施設後ろ向き観察研究による臨床指標としての歯周炎症表面積の基準値 Reviewed

    井上 裕貴, 畑中 加珠, 山本 直史, 平田 貴久, 三辺 正人, 山本 龍生, 内藤 徹, 山本 松男, 佐藤 秀一, 石幡 浩志, 稲垣 幸司, 三谷 章雄, 中島 啓介, 漆原 譲治, 高柴 正悟

    日本歯周病学会会誌   61 ( 4 )   159 - 167   2019.12

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:(NPO)日本歯周病学会  

    歯周炎症表面積(periodontal inflamed surface area:PISA)は,歯周組織の炎症部の面積を表す新たな歯周病の臨床指標である。従来伝わりづらかった歯周病の炎症程度を歯科以外の医療従事者が理解する上で,有用な指標であると考えられる。しかし,歯周病の程度や治療によるPISAの基準は未だ不明である。そこで,本研究は,日本歯周病学会が設ける歯周病専門医・認定医の電子申請書類のデータから各治療フェーズにおけるPISAの値を調べ,歯周病治療に伴う炎症度の基準値を提案することを目的とした。8施設で取得した113症例を用いて,Nesseらの方法によって歯周ポケット深さとプロービング時の出血からPISAを算出した。その結果,PISAの中央値は,初診時1,271.4mm2,歯周基本治療終了時211.8mm2,SPT移行時52.1mm2,そして最新SPT時30.0mm2であった。また,PISAはBOPと高い相関を示し(p<0.001),BOPよりも鋭敏に治療効果を反映した。以上から,中等度以上の歯周炎においてPISAを用いると,初診時は表面積約1,500mm2の歯周組織の炎症がSPT時は100mm2未満(初診時の約7%)に減少することが明らかになった。今後,更なるデータの蓄積および詳細な分析を行いながらPISAの使用を普及させると,PISAは医科歯科連携の際に歯周病炎症を伝える指標になり得ると考える。(著者抄録)

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  • Acceleration of bone regeneration of horizontal bone defect in rats using collagen-binding basic fibroblast growth factor combined with collagen scaffolds Reviewed International journal

    Shin Nakamura, Takashi Ito, Kentaro Okamoto, Takehiko Mima, Kentaro Uchida, Yasir D. Siddiqui, Masahiro Ito, Masako Tai, Keisuke Okubo, Keisuke Yamashiro, Kazuhiro Omori, Tadashi Yamamoto, Osamu Matsushita, Shogo Takashiba

    Journal of Periodontology   90 ( 9 )   1043 - 1052   2019.9

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    © 2019 The Authors. Journal of Periodontology published by Wiley Periodicals, Inc. on behalf of American Academy of Periodontology Background: Basic fibroblast growth factor (bFGF) has been applied for periodontal regeneration. However, the application depends on bone defect morphology because bFGF diffuses rapidly from defect sites. In a previous study, collagen-binding bFGF (CB-bFGF) has been shown to enhance bone formation by collagen-anchoring in the orthopedic field. The aim of this study is to demonstrate the efficacy of CB-bFGF with collagen scaffolds in bone regeneration of horizontal bone defect. Methods: Cell proliferation activity and collagen binding activity of CB-bFGF was confirmed by WST-8 assay and collagen binding assay, respectively. The retention of CB-bFGF in the collagen sheet (CS) was measured by fluorescence imaging. The rat horizontal alveolar bone defect model was employed to investigate the efficacy of CB-bFGF with collagen powder (CP). After 4 and 8 weeks, the regenerative efficacy was evaluated by microcomputed tomography, histological, and immunohistochemical analyses. Results: CB-bFGF had a comparable proliferation activity to bFGF and a collagen binding activity. CB-bFGF was retained in CS longer than bFGF. At 8 weeks postoperation, bone volume, bone mineral content, and new bone area in CB-bFGF/CP group were significantly increased compared with those in other groups. Furthermore, epithelial downgrowth was significantly suppressed in CB-bFGF/CP group. At 4 weeks, the numbers of osteocalcin, proliferating cell nuclear antigen, and osteopontin-positive cells at the regeneration site in CB-bFGF/CP group were greater than those in other groups. Conclusions: CB-bFGF/CP effectively promoted bone regeneration of horizontal bone defect possibly by sustained release of bFGF. The potential of CB-bFGF composite material for improved periodontal regeneration in vertical axis was shown.

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  • Effectiveness and safety of low-concentrated ozonized water for the reduction of contamination in dental unit water lines. Reviewed International journal

    Keisuke Okubo, Takashi Ito, Yasuyoshi Shiota, Yusuke Kawata, Tadashi Yamamoto, Shogo Takashiba

    Heliyon   5 ( 8 )   e02306   2019.8

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    Contamination of dental unit waterlines (DUWL) with heterotrophic bacteria can cause problems in immune compromised patients (aged, tumor and organ transplantation-patients). We focused on the use of low-concentrated ozonized water (OZW) as the biofilm formation restraint system for DUWL. Here, we examined the effects of low-concentrated OZW on the growth of bacteria and related biofilm formation and harmfulness to dental unit components (DUCs) in vitro. Objectives: To evaluate the bactericidal effects of OZW on biofilms in DUWL and DUC in vitro. Methods: Low-concentrated OZW (0.4 mg/L) was generated using an OZS-PTDX generator. Heterotrophic bacterial biofilms in old DUWL tubes and Candia albicans solution (control microbe) were treated with OZW for 1 h with gentle agitation before static culturing for 96 h in Reasoner's 2A liquid media. The control solutions were 0.1% cetylpyridinium chloride (CPC), chlorinated tap water (TW), and phosphate-buffered saline (PBS). Adenosine triphosphate (ATP) amounts of the microbes were measured and the biofilms of these microbes were observed using scanning electron microscopy (SEM). Moreover, surfaces of DUC soaked in OZW and TW were observed by SEM. Results: The OZW reduced ATP levels in microbes to 50% compared to TW and PBS treatment, although CPC reduced it below detection limits. SEM observation revealed deformation of microbes cultured with OZW, whereas no changes were seen on DUC surfaces. Conclusions: Low-concentrated OZW is bactericidal against heterotrophic bacteria biofilms and it is not harmful to DUC, suggesting that it might be useful in preventing DUWL contamination.

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  • Molecular imaging assessment of periodontitis lesions in an experimental mouse model Reviewed

    Hidetaka Ideguchi, Keisuke Yamashiro, Tadashi Yamamoto, Masayuki Shimoe, Shoichi Hongo, Shinsuke Kochi, Chiaki Yoshihara-Hirata, Hiroaki Aoyagi, Mari Kawamura, Shogo Takashiba

    Clinical Oral Investigations   23 ( 2 )   821 - 827   2019.2

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    © 2018, Springer-Verlag GmbH Germany, part of Springer Nature. Objective: We aimed to evaluate molecular imaging as a novel diagnostic tool for mice periodontitis model induced by ligature and Porphyromonas gingivalis (Pg) inoculation. Materials and methods: Twelve female mice were assigned to the following groups: no treatment as control group (n = 4); periodontitis group induced by ligature and Pg as Pg group (n = 4); and Pg group treated with glycyrrhizinic acid (GA) as Pg + GA group (n = 4). All mice were administered a myeloperoxidase (MPO) activity-specific luminescent probe and observed using a charge-coupled device camera on day 14. Image analysis on all mice was conducted using software to determine the signal intensity of inflammation. Additionally, histological and radiographic evaluation for periodontal inflammation and bone resorption at the site of periodontitis, and quantitative enzyme-linked immunosorbent assay (ELISA) were conducted on three mice for each group. Each experiment was performed three times. Results: Levels of serum IgG antibody against P. gingivalis were significantly higher in the Pg than in the Pg + GA group. Histological analyses indicated that the number of osteoclasts and neutrophils were significantly lower in the Pg + GA than in the Pg group. Micro-CT image analysis indicated no difference in bone resorption between the Pg and Pg + GA groups. The signal intensity of MPO activity was detected on the complete craniofacial image; moreover, strong signal intensity was localized specifically at the periodontitis site in the ex vivo palate, with group-wise differences. Conclusions: Molecular imaging analysis based on MPO activity showed high sensitivity of detection of periodontal inflammation in mice. Clinical relevance: Molecular imaging analysis based on MPO activity has potential as a diagnostic tool for periodontitis.

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  • Resolvin D2 induces resolution of periapical inflammation and promotes healing of periapical lesions in rat periapical periodotitis Reviewed

    Yasir Dilshad Siddiqui, Kazuhiro Omori, Takashi Ito, Keisuke Yamashiro, Shin Nakamura, Kentaro Okamoto, Mitsuaki Ono, Tadashi Yamamoto, Thomas E.Van Dyke, Shogo Takashiba

    Frontiers in Immunology   10 ( FEB )   307   2019

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    © 2019 Frew. Periapical periodontitis results from pulpal infection leading to pulpal necrosis and resorption of periapical bone. The current treatment is root canal therapy, which attempts to eliminate infection and necrotic tissue. But, in some cases periapical inflammation doesn't resolve even after treatment. Resolvins belongs to a large family of specialized pro-resolving lipid mediators that actively resolves inflammation signaling via specific receptors. Resolvin D2 (RvD2), a metabolite of docosahexaenoic acid (DHA), was tested as an intracanal medicament in rats in vivo. Mechanism was evaluated in rat primary dental pulp cells (DPCs) in vitro. The results demonstrate that RvD2 reduces inflammatory cell infiltrate, periapical lesion size, and fosters pulp like tissue regeneration and healing of periapical lesion. RvD2 enhanced expression of its receptor, GPR18, dentin matrix acidic phosphoprotein 1 (DMP1) and mineralization in vivo and in vitro. Moreover, RvD2 induces phosphorylation of Stat3 transcription factor in dental pulp cells. We conclude that intracanal treatment with RvD2 resolves inflammation and promoting calcification around root apex and healing of periapical bone lesions. The data suggest that RvD2 induces active resolution of inflammation with pulp-like tissue regeneration after root canal infection and thus maybe suitable for treating periapical lesions.

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  • Fungal metabolite (+)-terrein suppresses IL-6/sIL-6R-induced CSF1 secretion by inhibiting JAK1 phosphorylation in human gingival fibroblasts Reviewed International journal

    Satoshi Yamamoto, Kazuhiro Omori, Hiroki Mandai, Masaaki Nakayama, Saki Nakagawa, Hiroya Kobayashi, Tadashi Kunimine, Hiroshi Yoshimura, Kyosuke Sakaida, Hidefumi Sako, Soichiro Ibaragi, Tadashi Yamamoto, Hiroshi Maeda, Seiji Suga, Shogo Takashiba

    Heliyon   4 ( 11 )   e00979   2018.11

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    © 2018 The Authors Control of bacterial infection-induced inflammatory responses is one of the effective therapeutic approaches of periodontal diseases. Natural products such as lipid mediators and metabolites from microorganisms have been used for decreasing inflammation. We previously reported that (+)-terrein inhibited activation of STAT3 and ERK1/2 in interleukin-6 (IL-6) signaling cascade, leading to prevent vascular endothelial growth factor (VEGF) secretion in human gingival fibroblasts (HGFs). However, little is still known about the role of (+)-terrein on inflammatory responses. In this study, we provided the possibility of novel action that (+)-terrein inhibits activation of Janus-activated kinase 1 (JAK1), which has a central function in IL-6 signaling cascade, and alters expression of mRNAs and proteins induced by IL-6/soluble IL-6 receptor (sIL-6R) stimulation in HGFs. First, we performed PCR array to examine IL-6/sIL-6R-induced mRNA expression, and then expression of mRNA and protein of colony stimulating factor-1 (CSF1) and VEGF were clearly determined by quantitative RT-PCR and ELISA, respectively. Treatment with (+)-terrein suppressed expression of mRNA and protein of CSF1 and VEGF by IL-6/sIL-6R stimulation. Next, to test the effect of (+)-terrein on IL-6/sIL-6R signaling cascade, we demonstrated whether (+)-terrein affects phosphorylation of JAK1 and its downstream proteins, Akt and SHP-2. Western blotting revealed that (+)-terrein inhibited IL-6/sIL-6R-induced phosphorylation of JAK1, Akt, and SHP-2. Therefore, (+)-terrein suppresses IL-6/sIL-6R-induced expression of CSF1 and VEGF via inhibition of JAK1, Akt, and SHP-2. Based on our results, we suggest that (+)-terrein is a candidate compound for anti-inflammatory effect associated with IL-6 signaling.

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  • HMGB1-induced inflammatory response promotes bone healing in murine tooth extraction socket Reviewed

    Hiroaki Aoyagi, Keisuke Yamashiro, Chiaki Hirata-Yoshihara, Hidetaka Ideguchi, Mutsuyo Yamasaki, Mari Kawamura, Tadashi Yamamoto, Shinsuke Kochi, Hidenori Wake, Masahiro Nishibori, Shogo Takashiba

    Journal of Cellular Biochemistry   119 ( 7 )   5481 - 5490   2018.7

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    © 2018 Wiley Periodicals, Inc. High mobility group box 1 (HMGB1) is a non-histone DNA-binding protein that is secreted into the extracellular milieu in response to inflammatory stimuli. The secreted HMGB1 has been suggested to mediate various inflammatory diseases. However, it is still unknown whether HMGB1 is involved in a healing process in the tooth extraction socket, the tissue containing gingival epithelium, and alveolar bone that is exposed to oral bacteria. In this study, we constructed a murine tooth extraction model with anti-HMGB1 neutralization antibody administration and observed the inflammatory response and bone healing process in tooth extraction sockets by molecular imaging of myeloperoxidase (MPO) activity, histological analysis, and quantitative RT-PCR. The translocation of HMGB1 from the nucleus to the cytoplasm in gingival epithelial cells and inflammatory cells was inhibited by anti-HMGB1 antibody administration. The MPO activity around the tooth extraction socket was significantly reduced, and the numbers of CD31- and CD68-positive cells were significantly lower in the anti-HMGB1 antibody treatment samples than in the control samples. The TRAP-positive cells, osteocalcin positive cells, and the neoplastic bone area were significantly lower in anti-HMGB1 antibody treatment samples than in control samples. The expression levels of IL-1β and VEGF-A were also decreased in anti-HMGB1 antibody treatment samples compared to that in control samples. Secreted HMGB1 induced initial acute inflammation and inflammatory cells recruitment after tooth extraction. HMGB1 was associated with angiogenesis and bone remodeling by osteoclast and osteoblast activation and promoted bone healing in the tooth extraction socket.

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  • PET(18F-FDG)/CT検査を用いた慢性歯周炎患者における歯周組織炎症の評価

    井手口 英隆, 山城 圭介, 下江 正幸, 山本 直史, 長島 義之, 高柴 正悟

    日本歯周病学会会誌   60 ( 2 )   105 - 116   2018.6

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    歯周炎に対する検査方法は多数報告されているが、歯周組織炎症の程度を客観的に評価することが出来る方法は未だに確立されていない。我々は、医科領域で広く用いられているPET(18F-FDG)/CTが炎症組織の局在と炎症強度を可視化することができることに着目した。そして、乳がんの既往を有する慢性歯周炎患者に対する歯周治療の効果を、既存の歯周組織検査方法とPET(18F-FDG)/CTとで経時的に比較検討した。歯周治療が進むに従って歯周組織炎症は消失し、BOPの割合は56%から3%に、PISAは1143mm2から27mm2に改善した。さらに、歯周治療前にPET(18F-FDG)/CTで検出された18F-FDGの顕著な集積は歯周治療後には消失した。これらの結果から、PET(18F-FDG)/CTは炎症性口腔疾患に対する新規検査方法として有用と考えられる。すなわち本症例報告は、PET(18F-FDG)/CTが医科-歯科共通の検査項目となることによって、周術期の医科-歯科連携の強化や、全身疾患を有する多くの歯周炎患者に対してさらに効果的な歯周治療を行うことが出来る可能性を提案するものである。(著者抄録)

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  • Anti-HMGB1 neutralizing antibody attenuates periodontal inflammation and bone resorption in a murine periodontitis model Reviewed

    Chiaki Yoshihara-Hirata, Keisuke Yamashiro, Tadashi Yamamoto, Hiroaki Aoyagi, Hidetaka Ideguchi, Mari Kawamura, Risa Suzuki, Mitsuaki Ono, Hidenori Wake, Masahiro Nishibori, Shogo Takashiba

    Infection and Immunity   86 ( 5 )   2018.5

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    © 2018 American Society for Microbiology. High mobility group box 1 (HMGB1) is a non-histone DNA-binding protein that is secreted into the extracellular milieu in response to inflammatory stimuli. The secreted HMGB1 mediates various inflammatory diseases, including periodontitis; however, the underlying mechanisms of HMGB1-induced periodontal inflammation are not completely understood. Here, we examined whether anti-HMGB1 neutralizing antibody inhibits periodontal progression and investigated the molecular pathology of HMGB1 in vitro and in vivo. In vitro analysis indicated that HMGB1, granulocytemacrophage colony-stimulating factor (GM-CSF), and interleukin-1β (IL-1β) were secreted in response to tumor necrosis factor-α (TNF-α) stimuli in human gingival epithelial cells (HGECs) and human monocytic leukemia cells (THP-1) treated with phorbol myristate acetate. Increased levels of GM-CSF and IL-1β were observed in the conditioned media from TNF-α-stimulated HGECs and THP-1 in vitro. Simultaneous stimulation with TNF-α and anti-HMGB1 antibody significantly decreased TNF-α- induced inflammatory cytokine secretion. Experimental periodontitis was induced in mice using Porphyromonas gingivalis-soaked ligatures. The extracellular translocation was confirmed in gingival epithelia in the periodontitis model mice by immunofluorescence analysis. Systemic administration of anti-HMGB1 neutralizing antibody significantly inhibited translocation of HMGB1. The anti-HMGB1 antibody inhibited periodontal inflammation, expression of IL-1β and C-X-C motif chemokine ligand 1 (CXCL1), migration of neutrophils, and bone resorption, shown by bioluminescence imaging of myeloperoxidase activity, quantitative reverse transcription-PCR (RT-PCR), and micro-computed tomography analysis. These findings indicate that HMGB1 is secreted in response to inflammatory stimuli caused by periodontal infection, which is crucial for the initiation of periodontitis, and the anti-HMGB1 antibody attenuates the secretion of a series of inflammatory cytokines, consequently suppressing the progression of periodontitis.

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  • Correction to: Expression of optineurin isolated from rat-injured dental pulp and the effects on inflammatory signals in normal rat kidney cells (Odontology, (2018), 106, 2, (135-144), 10.1007/s10266-017-0314-5) Reviewed

    Kyoko Senoo, Keisuke Yamashiro, Tadashi Yamamoto, Fumio Myokai, Mari Kawamura, Shogo Takashiba

    Odontology   106 ( 2 )   223   2018.4

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    © 2017, The Society of The Nippon Dental University. In the original publication of the article, one of the author name was published incorrectly as “Keisuke Yamashairo” and correct name should be “Keisuke Yamashiro”.

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  • Modulation of microenvironment for controlling the fate of periodontal ligament cells: the role of Rho/ROCK signaling and cytoskeletal dynamics Reviewed

    Tadashi Yamamoto, Yuki Ugawa, Mari Kawamura, Keisuke Yamashiro, Shinsuke Kochi, Hidetaka Ideguchi, Shogo Takashiba

    Journal of Cell Communication and Signaling   12 ( 1 )   369 - 378   2018.3

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    © 2017, The International CCN Society. Cells behave in a variety of ways when they perceive changes in their microenvironment; the behavior of cells is guided by their coordinated interactions with growth factors, niche cells, and extracellular matrix (ECM). Modulation of the microenvironment affects the cell morphology and multiple gene expressions. Rho/Rho-associated coiled-coil-containing protein kinase (ROCK) signaling is one of the key regulators of cytoskeletal dynamics and actively and/or passively determines the cell fate, such as proliferation, migration, differentiation, and apoptosis, by reciprocal communication with the microenvironment. During periodontal wound healing, it is important to recruit the residential stem cells into the defect site for regeneration and homeostasis of the periodontal tissue. Periodontal ligament (PDL) cells contain a heterogeneous fibroblast population, including mesenchymal stem cells, and contribute to the reconstruction of tooth-supporting tissues. Therefore, bio-regeneration of PDL cells has been the ultimate goal of periodontal therapy for decades. Recent stem cell researches have shed light on intrinsic ECM properties, providing paradigm shifts in cell fate determination. This review focuses on the role of ROCK activity and the effects of Y-27632, a specific inhibitor of ROCK, in the modulation of ECM-microenvironment. Further, it presents the current understanding of how Rho/ROCK signaling affects the fate determination of stem cells, especially PDL cells. In addition, we have also discussed in detail the underlying mechanisms behind the reciprocal response to the microenvironment.

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  • 感染、炎症、機能の観点から見た口腔検査指標の歯周病治療に対する有用性 パイロット研究

    畑中 加珠, 片山 広大, 井上 裕貴, 坂井田 京佑, 清水 由梨香, 鈴木 里紗, 高木 美奈, 山本 直史, 高柴 正悟

    日本口腔検査学会雑誌   10 ( 1 )   58 - 63   2018.3

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    目的:歯周病治療の効果を「感染」、「炎症」、そして「機能」の3つの観点から評価して、治療効果を示す指標を探った。方法:歯周病治療を終えて安定期治療に至った7症例において、歯周局所の歯周病原細菌数と9菌種の血清IgG抗体価、歯周ポケット深さとプロービング時の出血から算出する歯周炎症表面積(PISA)、そして咀嚼機能の簡易指標として残存歯の動揺度を測定した。これら4つの指標の変動を治療時期の一定ポイントで調べ、それらの相互関係を検討した。結果:歯周治療が進むにしたがって、PISA、歯の動揺度およびPorphyromonas gingivalis(Pg)に対する抗体価の数値は低下し、7症例の各時期における平均値をとると、経時的な有意差が認められた(P<0.05)。しかしながら、他の菌種に対する抗体価や歯周局所の細菌数には増加するものもみられた。結論:「感染」、「炎症」、「機能」の3つの観点から歯周病治療の効果を評価する指標として、抗Pg抗体価、PISA、そして歯の動揺度を用いることは有用であった。(著者抄録)

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  • Effects of Lectins on initial attachment of cariogenic Streptococcus mutans Reviewed

    Takashi Ito, Yasuhiro Yoshida, Yasuyoshi Shiota, Yuki Ito, Tadashi Yamamoto, Shogo Takashiba

    Glycoconjugate Journal   35 ( 1 )   41 - 51   2018.2

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    © 2017, Springer Science+Business Media, LLC. Oral bacteria initiate biofilm formation by attaching to tooth surfaces via an interaction of a lectin-like bacterial protein with carbohydrate chains on the pellicle. This study aimed to find naturally derived lectins that inhibit the initial attachment of a cariogenic bacterial species, Streptococcus mutans (S. mutans), to carbohydrate chains in saliva in vitro. Seventy kinds of lectins were screened for candidate motifs that inhibit the attachment of S. mutans ATCC 25175 to a saliva-coated culture plate. The inhibitory effect of the lectins on attachment of the S. mutans to the plates was quantified by crystal violet staining, and the biofilm was observed under a scanning electron microscope (SEM). Surface plasmon resonance (SPR) analysis was performed to examine the binding of S. mutans to carbohydrate chains and the binding of candidate lectins to carbohydrate chains, respectively. Moreover, binding assay between the biotinylated-lectins and the saliva components was conducted to measure the lectin binding. Lectins recognizing a salivary carbohydrate chain, Galβ1-3GalNAc, inhibited the binding of S. mutans to the plate. In particular, Agaricus bisporus agglutinin (ABA) markedly inhibited the binding. This inhibition was confirmed by SEM observation. SPR analysis indicated that S. mutans strongly binds to Galβ1-3GalNAc, and ABA binds to Galβ1-3GalNAc. Finally, the biotinylated Galβ1-3GalNAc-binding lectins including ABA demonstrated marked binding to the saliva components. These results suggest that ABA lectin inhibited the attachment of S. mutans to Galβ1-3GalNAc in saliva and ABA can be useful as a potent inhibitor for initial attachment of oral bacteria and biofilm formation.

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  • IS1598 (IsPg4) distributed to abscess-forming strains of Porphyromonas gingivalis may enhance virulence through upregulation of nrdD-like gene expression Reviewed

    Norihiro Sonoi, Hiroshi Maeda, Toshimitsu Murauchi, Tadashi Yamamoto, Kazuhiro Omori, Susumu Kokeguchi, Koji Naruishi, Shogo Takashiba

    New Microbiologica   41 ( 1 )   52 - 60   2018.1

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    ©2018 by EDIMES-Edizioni Internazionali Srl. All rights reserved. An insertion sequence, IS1598 (IsPg4) has been found in virulent strains of Porphyromonas gingivalis in a murine abscess model. The present study was performed to investigate the effects of genetic rearrangements by IS1598 on the phenotypic characteristics of the virulent strains. For this purpose, we searched for a common insertion site of IS1598 among the virulent strains. Through cloning and database search, a common insertion site was identified beside an nrdD-like gene in the virulent FDC 381, W83 and W50 strains. In this region, predicted promoters of the nrdD-like gene and IS1598 are located in tandem, and accumulation of nrdD-like gene mRNA was 5-fold higher in virulent strains (W83, W50, FDC 381) than avirulent strains (ATCC33277, SU63, SUNY1021, ESO59 without IS1598). The role of the nrdD-like gene in virulence of P. gingivalis was investigated by constructing a nrdD-deficient mutant. In the murine abscess model, the parental W83 strain produced necrotic abscesses, while the nrdD-deficient mutant had almost lost this ability. Insertion of IS1598 into the nrdD-like gene promoter region may be related to the phenotypic differences in virulence among P. gingivalis strains through upregulation of the expression of this gene.

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  • Aggregatibacter actinomycetemcomitans regulates the expression of integrins and reduces cell adhesion via integrin alpha 5 in human gingival epithelial cells Reviewed

    Shinsuke Kochi, Keisuke Yamashiro, Shoichi Hongo, Tadashi Yamamoto, Yuki Ugawa, Masayuki Shimoe, Mari Kawamura, Chiaki Hirata-Yoshihara, Hidetaka Ideguchi, Hiroshi Maeda, Shogo Takashiba

    MOLECULAR AND CELLULAR BIOCHEMISTRY   436 ( 1-2 )   39 - 48   2017.12

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    Gingival epithelial cells form a physiological barrier against bacterial invasion. Excessive bacterial invasion destroys the attachment between the tooth surface and the epithelium, resulting in periodontitis. Integrins play a significant role in cell attachment; therefore, we hypothesized that bacterial infection might decrease the expressions of these integrins in gingival epithelial cells, resulting in reduced cell adhesion. Immortalized human gingival epithelial cells were co-cultured with Aggregatibacter actinomycetemcomitans Y4 (Aa Y4), and the gene expression levels of IL-8, proliferating cell nuclear antigen (PCNA), and integrins (alpha 2, alpha 3, alpha 5, beta 4, and beta 6) were measured using quantitative reverse transcription polymerase chain reaction. Expression of PCNA and integrins, except integrin alpha 5, was significantly downregulated, while expression of IL-8 and integrin alpha 5 was significantly upregulated in the cells co-cultured with Aa Y4. The number of adherent cells significantly decreased when co-cultured with Aa Y4, as determined using cell adhesion assays. In the cells co-cultured with Aa Y4 and an integrin alpha 5 neutralizing antibody, there was no effect on the expression of IL-8 and PCNA, while the expressions of integrins alpha 2, alpha 3, beta 4, and beta 6, and the number of adherent cells did not decrease. The number of invading bacteria in the cells was reduced in the presence of the antibody and increased in the presence of TLR2/4 inhibitor. Therefore, integrin alpha 5 might be involved in Aa Y4 invasion into gingival epithelial cells, and the resulting signal transduction cascade reduces cell adhesion by decreasing the expression of integrins, while the TLR2/4 signaling cascade regulates IL-8 expression.

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  • Assessment of pathogenesis of infective endocarditis by plasma IgG antibody titer test against periodontal bacteria. Reviewed International journal

    Isoshima D, Yamashiro K, Matsunaga K, Shinobe M, Nakanishi N, Nakanishi I, Omori K, Yamamoto T, Takashiba S

    Clinical case reports   5 ( 10 )   1580 - 1586   2017.10

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    Oral bacteria cause infective endocarditis (IE), so severe periodontitis is thought to be high risk for IE. We suggest the identification of high-risk patients by an IgG antibody titer test against periodontal bacteria might become common screening test.

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  • Rho-kinase regulates extracellular matrix-mediated osteogenic differentiation of periodontal ligament cells Reviewed

    Yuki Ugawa, Tadashi Yamamoto, Mari Kawamura, Keisuke Yamashiro, Masayuki Shimoe, Kazuya Tomikawa, Shoichi Hongo, Hiroshi Maeda, Shogo Takashiba

    CELL BIOLOGY INTERNATIONAL   41 ( 6 )   651 - 658   2017.6

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    The periodontal ligament (PDL) cells contain heterogeneous mesenchymal cell populations, which have the ability to differentiate into cells that produce adjacent mineralized tissues and abundant extracellular matrix (ECM). ECM is essential not only for the homeostasis of the periodontal tissue, but also for controlling the differentiation of the PDL cells. The process of differentiation involves mechanotransduction, which links the ECM to the cytoskeleton. The present study investigated the roles of Rho-associated coiled-coil containing protein kinase (ROCK) signaling, a crucial regulator of the cytoskeleton, during ECM-mediated osteogenic differentiation of PDL cells in vitro. The PDL cells were isolated from human periodontal ligaments of extracted teeth and cultured in osteogenic medium with or without Y-27632, a pharmacological inhibitor of ROCK. ECMcoated plates were used for ECM-mediated differentiation. The osteogenic phenotype was evaluated at different time points by real-time RT-PCR for the gene encoding alkaline phosphatase (ALP) and an ALP activity assay. The effects of ROCK on cytoskeletal changes and ECM synthesis were examined by immunofluorescence analysis. Y-27632 significantly inhibited ALP at the mRNA and protein activity levels in the late stage of differentiation; concomitantly, the actin filament content and the extracellular levels of collagen-I and fibronectin were markedly decreased by Y-27632. Exogenous collagen-I and fibronectin temporally increased ALP activity, with fibronectin showing a more pronounced effect. Importantly, ECM-mediated differentiation was almost completely inhibited by Y-27632. These findings indicated that ECM-mediated differentiation is dependent on ROCK signaling, and ROCK signaling contributes to the establishment of the ECM microenvironment for PDL cell differentiation.

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  • Smad2 overexpression enhances adhesion of gingival epithelial cells Reviewed

    Shoichi Hongo, Tadashi Yamamoto, Keisuke Yamashiro, Masayuki Shimoe, Kazuya Tomikawa, Yuki Ugawa, Shinsuke Kochi, Hidetaka Ideguchi, Hiroshi Maeda, Shogo Takashiba

    ARCHIVES OF ORAL BIOLOGY   71   46 - 53   2016.11

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    Objective: Gingival epithelial cells play an important role in preventing the initiation of periodontitis, by their hemidesmosomal adhesion to the tooth root surface. Adhesion requires integrin-extracellular matrix (ECM) interactions that are intricately regulated by transforming growth factor-beta (TGF-beta) signaling. However, the mechanisms underlying the interplay between adhesion molecules and TGF-beta, especially the respective roles of Smad2 and Smad3, remain elusive. In this study, we examined the effects of Smad overexpression on gingival epithelial cell adhesion and expression profiles of integrin and ECM-related genes.
    Methods: Human gingival epithelial cells immortalized by the SV40 T-antigen were transfected with Smad2- and Smad3-overexpression vectors. A cell adhesion assay involving fluorescence detection of attached cells was performed using the ArrayScan imaging system. Real-time PCR was performed to examine the kinetics of integrin and ECM gene expression. In vitro and in vivo localization of adhesion molecules was examined by immunofluorescence analysis.
    Results: By using SB431542, a specific inhibitor of the TGF-beta type I receptor, Smad2/3 signaling was confirmed to be dominant in TGF-beta 1-induced cell adhesion. The Smad2-transfectant demonstrated higher potency for cell adhesion and integrin expression (alpha 2, alpha 5, beta 4, and beta 6) than the Smad3-transfectant, whereas little or no change in ECM expression was observed in either transfectant. Moreover, the gingival epithelium of transgenic mice that overexpressed Smad2 driven by the keratin 14 promoter showed increased integrin alpha 2 expression.
    Conclusion: These findings indicate the crucial role of Smad2 in increased adhesion of gingival epithelial cells via upregulation of integrin alpha 2. (C) 2016 Elsevier Ltd. All rights reserved.

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  • Osteogenic differentiation regulated by Rho-kinase in periodontal ligament cells Reviewed

    Tadashi Yamamoto, Yuki Ugawa, Keisuke Yamashiro, Masayuki Shimoe, Kazuya Tomikawa, Shoichi Hongo, Shinsuke Kochi, Hidetaka Ideguchi, Hiroshi Maeda, Shogo Takashiba

    DIFFERENTIATION   88 ( 2-3 )   33 - 41   2014.9

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    The periodontal ligament is a multifunctional soft connective tissue, which functions not only as a cushion supporting the teeth against occlusal force, but is also a source of osteogenic cells that can regenerate neighboring hard tissues. Periodontal ligament cells (PDL cells) contain heterogeneous cell populations, including osteogenic cell progenitors. However, the precise mechanism underlying the differentiation process remains elusive. Cell differentiation is regulated by the local biochemical and mechanical microenvironment that can modulate gene expression and cell morphology by altering actin cytoskeletal organization mediated by Rho-associated, coiled-coil containing protein kinase (ROCK). To determine its role in PDL cell differentiation, we examined the effects of ROCK on cytoskeletal changes and kinetics of gene expression during osteogenic differentiation. PDL cells were isolated from human periodontal ligament on extracted teeth and cultured in osteogenic medium for 14 days. Y-27632 was used for ROCK inhibition assay. Osteogenic phenotype was determined by monitoring alkaline phosphatase (ALP) activity and calcium deposition by Alizarin Red staining. ROCK-induced cytoskeletal changes were examined by immunofluorescence analysis of F-actin and myosin light chain 2 (MLC2) expression. Real-time PCR was performed to examine the kinetics of osteogenic gene expression. F-actin and phospho-MLC2 were markedly induced during osteogenic differentiation, which coincided with upregulation of ALP activity and mineralization. Subsequent inhibition assay indicated that Y-27632 significantly inhibited F-actin and phospho-MLC2 expression in a dose dependent manner with concomitant partial reversal of the PDL cell osteogenic phenotype. PCR array analysis of osteogenic gene expression indicated that extracellular matrix genes, such as fibronectin 1, collagen type I and Ill, and biglycan, were significantly downregulated by Y27632. These findings indicated crucial effects of ROCK in cytoskeletal reorganization and differentiation of PDL cells toward osteogenic cells. ROCK contributes to induction of osteogenic differentiation by synergistic increases in extracellular matrix gene expression in PDL cells. (C) 2014 International Society of Differentiation, Published by Elsevier B.V. All rights reserved.

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  • Overexpression of Smad2 inhibits proliferation of gingival epithelial cells Reviewed

    M. Shimoe, T. Yamamoto, N. Shiomi, K. Tomikawa, S. Hongo, K. Yamashiro, T. Yamaguchi, H. Maeda, S. Takashiba

    JOURNAL OF PERIODONTAL RESEARCH   49 ( 3 )   290 - 298   2014.6

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    Background and Objective
    Spatiotemporal inhibition of apical migration and proliferation of gingival epithelium are significant factors involved in periodontal regeneration. Transforming growth factor beta (TGF-beta) is important in multiple aspects of wound healing, and Smad2, a downstream transcription factor of TGF-beta, has an inhibitory effect on re-epithelialization during gingival wound healing. Therefore, we investigated the effects on migration and proliferation status, and intra/extracellular signaling regulated by Smad2 overexpression in gingival epithelial cells.
    Material and Methods
    Gingival epithelial cells were isolated from the palatal gingival tissue of transgenic mice overexpressing Smad2 driven by the Keratin14 promoter. Smad2 expression was identified by western blotting and immunofluorescence analysis. Scratch assay and 5-bromo-2 '-deoxyuridine staining were performed to assess cell migration and proliferation. To inactivate TGF-beta type I receptor, the cultures were supplemented with SB431542. Secreted TGF-beta was quantified by ELISA. Smad2 target gene expression was examined by real-time RT-PCR and in vivo immunofluorescence analysis of gingival junctional epithelium.
    Results
    Smad2-overexpressing cells were confirmed to have significant phosphorylated Smad2 in the nucleus. Scratch assay and 5-bromo-2 '-deoxyuridine staining indicated that Smad2-overexpressing cells showed no significant differences in migration, but had reduced proliferation rates compared to wild-type controls. SB431542 significantly inhibited Smad2 phosphorylation, which coincided with restoration of the proliferation rate in Smad2-overexpressing cells. ELISA of TGF-beta release did not show any differences between genotypes. The cell cycle inhibitors, p15 and p21, showed significant upregulation in Smad2-overexpressing cells compared to wild-type controls. Moreover, junctional epithelium of the transgenic mice showed increased expression of P-Smad2, p15 and p21.
    Conclusion
    The signaling activation triggered by overexpression of Smad2 was dependent on TGF-beta type I receptor, and the activated Smad2 increased p15 and p21 expression, responsible for inhibiting cell cycle entry, resulting in antiproliferative effects on gingival epithelial cells. Understanding of Smad2-induced signaling would be useful for possible clinical application to regulate gingival epithelial downgrowth.

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  • 細菌感染度を評価しながら包括的歯周治療を行った広汎型侵襲性歯周炎患者の一症例

    冨川 和哉, 河野 隆幸, 山本 直史, 岩本 義博, 下江 正幸, 山口 知子, 本郷 昌一, 宮本 学, 前田 博史, 高柴 正悟

    日本歯周病学会会誌   55 ( 4 )   340 - 348   2013.12

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    歯周病に対する感受性が高い侵襲性歯周炎患者の治療においては、徹底した感染のコントロールによる疾患活動性の抑制が必要である。とりわけ、歯列不正を伴う歯周炎患者に矯正治療を行うことは、長期に渡る感染のコントロールを行う上で非常に有効である。しかし、歯周炎患者に矯正治療を行う場合に、感染がコントロールされている歯周状態かどうかを決定する基準は未だ明確でない。今回報告するのは、Agregatibacter actinomycetemcomitans(Aa)の感染が主な病態形成因子と考えられる、初診時22歳の広汎型侵襲性歯周炎患者に対して、矯正治療を含めた包括的歯周治療を行った症例である。初診以降、臨床計測値の変化に加えて、細菌DNA検査と歯周病原細菌に対する血清IgG抗体価検査を用いて、歯周病原細菌の感染度を評価した。その結果、歯周外科治療を含む感染源除去によって、細菌DNA検査でAaが検出されず、Aaに対する血清IgG抗体価が健常者レベルに推移したことを矯正治療移行前に確認した。すなわち、歯周病原細菌感染度が低下したと判断した後に、矯正治療を行うことで、現在まで良好なSPTを維持している。本症例においては、Aaの感染度の低下を細菌DNA検査と血清IgG抗体価を用いて評価することによって、客観的な根拠をもって矯正治療に移行できたと考える。(著者抄録)

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  • Serum antibody response to group II chaperonin from Methanobrevibacter oralis and human chaperonin CCT Reviewed

    Kimito Hirai, Hiroshi Maeda, Kazuhiro Omori, Tadashi Yamamoto, Susumu Kokeguchi, Shogo Takashiba

    PATHOGENS AND DISEASE   68 ( 1 )   12 - 19   2013.6

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    Both group I (HSP60) and group II (CCT) chaperonins are targets of autoantibodies. Autoimmune reactions to HSP60 have been well characterized, while immune reactions to group II chaperonin have not been clarified. Methanobrevibacter oralis is a suspected periodontal pathogen with group II chaperonin. In this study, serum responses to M.oralis chaperonin, human HSP60, and CCT subunits were examined using sera from patients with periodontitis and autoimmune diseases. In comparison with healthy controls, periodontitis patients showed significantly higher responses to CCT4 and CCT8 on dot blot analysis. Signals for CCT3 and CCT8 in autoimmune disease patients were significantly higher than in controls. Significant differences were also demonstrated by Western blotting in anti-CCT4 response in both patient groups. All subjects showed strong reactivity to M.oralis chaperonin and faint signals to human HSP60. Autoantibodies were raised against CCT rather than HSP60; and CCT3, CCT4, and CCT8 were shown to be the main targets. Host immune systems may be frequently exposed to chaperonins of Archaea in various habitats. Although further studies of the cross-reactivity between M.oralis chaperonin and human CCT are required, anti-CCT autoantibodies may be involved in the pathogenesis of periodontitis and autoimmune diseases.

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  • Medical microbiological approach to Archaea in oral infectious diseases Reviewed

    Hiroshi Maeda, Kimito Hirai, Junji Mineshiba, Tadashi Yamamoto, Susumu Kokeguchi, Shogo Takashiba

    Japanese Dental Science Review   49 ( 2 )   72 - 78   2013.5

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    Recent advances in molecular biological techniques have yielded large amounts of information regarding the oral microflora. The microbiological communities were shown to be more diverse than previously thought and to include a number of previously uncharacterized microorganisms. The range of research targets of microorganisms associated with oral diseases has been expanded to include these unknown or uncharacterized organisms. These organisms include the Archaea. A series of recent reports suggested these microorganisms to be potential pathogens involved in periodontitis and apical periodontitis mainly based on the detection frequency or their increased numbers in diseased sites in association with the severity or symptoms of disease. However, it cannot be concluded that Archaea are oral pathogens based on such circumstantial evidence. Further studies are required to investigate the potential pathogenic mechanisms of action of these organisms. This will require investigation of the antigenic properties of the Archaea and synergism with other established oral pathogens. Especially, studies of the host immune response will provide insight into the medical impact of Archaea as suspected pathogens. © 2013 Japanese Association for Dental Science.

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  • Smad2 Decelerates Re-epithelialization during Gingival Wound Healing Reviewed

    K. Tomikawa, T. Yamamoto, N. Shiomi, M. Shimoe, S. Hongo, K. Yamashiro, T. Yamaguchi, H. Maeda, S. Takashiba

    JOURNAL OF DENTAL RESEARCH   91 ( 8 )   764 - 770   2012.8

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    During periodontal regeneration, inhibition of gingival downgrowth is necessary to promote migration of mesenchymal cells into the defects. Transforming growth factor (TGF)-beta is a pleiotropic cytokine that has numerous cell functions, including regulation of epithelial growth. Recent studies have shown that Smad2, a downstream transcription factor of TGF-beta, plays crucial roles in wound healing in the epithelia. Therefore, we investigated the effects of Smad2 overexpression on re-epithelialization of gingival wounds. Transgenic mice overexpressing smad2 driven by the keratin 14 promoter (k14-smad2) were confirmed to have significant Smad2 phosphorylation in gingival basal epithelia. Punch wounds were made in the palatal gingiva, and wound healing was assessed histologically for 7 days. Re-epithelialization was significantly retarded on day 2, while collagen deposition was enhanced on day 7 in k14-smad2 compared with wild-type mice. Moreover, expression of keratin 16 (K16), an indicator of keratinocyte migration, was significantly inhibited in wound-edge keratinocytes in k14-smad2. The inhibition of K16 coincided with the induction of Smad2 in the corresponding epithelia, while BrdU incorporation was unaffected. These results indicated that Smad2 has inhibitory effects in regulating keratinocyte migration during gingival wound healing. TGF-beta/Smad2 signaling mediating alteration of K16 expression must be tightly regulated during periodontal regeneration.

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  • The promotional effect of IL-22 on mineralization activity of periodontal ligament cells Reviewed

    Nahoko Kato-Kogoe, Toshihiro Nishioka, Mutsuki Kawabe, Fusa Kataoka, Koji Yamanegi, Naoko Yamada, Masaki Hata, Tadashi Yamamoto, Keiji Nakasho, Masahiro Urade, Nobuyuki Terada, Hideki Ohyama

    CYTOKINE   59 ( 1 )   41 - 48   2012.7

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    Objectives: Interleukin (IL)-22 acts on non-immune cells to induce anti-microbial responses, protection from tissue damage, and enhance cell regeneration. However, little is known about the involvement of IL-22 in periodontal biology. This study investigated the biological effects of IL-22 on periodontal ligament (PDL) cells as part of studies to assess the involvement of IL-22 in periodontal disease.
    Materials and methods: Gene expression levels of IL-22 and its receptors in PDL cells and gingival tissue samples were evaluated by real-time PCR. Proliferative responses and mineralized-matrix forming activities of PDL cells were examined in the presence and absence of IL-22.
    Results: In contrast to the expression of IL-22 receptors detected in PDL tissues and their cell lines, gingival tissues showed modest or no gene expressions of IL-22. The production of several cytokines including IL-11, IL-8 and CCL2 was upregulated by IL-22 treatment of PDL cells in a dose-dependent manner. IL-22 treatment had no effect on the proliferative response in PDL cells. Meanwhile, IL-22 precipitated mineralized nodule formation and induced gene expressions of RUNX2,MSX2 and osteocalcin in PDL cells, suggesting that IL-22 enhances the mineralized matrix-forming activities of PDL cells.
    Conclusion: IL-22 has the potential to promote mineralizing activity in PDL cells and to develop appropriate regenerative therapy. (C) 2012 Elsevier Ltd. All rights reserved.

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  • 15-year Clinical Course of a Patient with Generalized Aggressive Periodontitis Followed with Regular examination of the serum titers of IgG antibodies against periodontal bacteria

    TOMIKAWA Kazuya, IWAMOTO Yoshihiro, OHE Hyogo, ARAI Hideo, YAMAMOTO Tadashi, MAEDA Hiroshi, TAKASHIBA Shogo

    Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology)   54 ( 2 )   193 - 202   2012.6

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    For the treatment of patients with aggressive periodontitis, a thorough control of the infection is required to reduce the disease activity. Detection of periodontal pathogens by a polymerase chain reaction-based method or measurement of the serum IgG antibody titers by enzyme-linked immunosorbent assay are now widely used for microbiological diagnosis and assessment of the disease activity. We report the case of a 25-year-old woman with impaired neutrophil phagocytosis ability who suffered from generalized aggressive periodontitis . After the initial periodontal treatment and periodontal regenerative surgery, she received the final prosthodontics, and supportive periodontal treatment (SPT) was initiated. For over a decade, from the beginning of the treatments, the clinical parameters and serum titers of IgG periodontal pathogens have been monitored, and the relationships between the twoanalyzed. During the SPT, recurrence and progression of periodontitis was seen around site 26, despite maintenance of a stable periodontal condition at other sites. The serum IgG antibody titers against periodontal pathogens were elevated in parallel with the progression of periodontitis at site 26. In the present case of generalized aggressive periodontitis, the serum IgG antibody titers reflected the disease activity of periodontitis even around a single tooth, suggesting the usefulness of the examination for assessment of the disease activity. Nihon Shishubyo Gakkai Kaishi(J Jpn Soc Periodontol)54(2):193-202, 2012

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  • Chronic periodontitis with multiple risk factor syndrome: a case report. Reviewed International journal

    Masayuki Shimoe, Tadashi Yamamoto, Yoshihiro Iwamoto, Nobuyuki Shiomi, Hiroshi Maeda, Fusanori Nishimura, Shogo Takashiba

    Journal of the International Academy of Periodontology   13 ( 2 )   40 - 7   2011.7

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    OBJECTIVE: Multiple risk factor syndrome is a clustering of cardiovascular risk factors, such as diabetes, dyslipidemia, hypertension, and obesity associated epidemiologically with insulin resistance. This report describes the clinical course of a patient suffering from severe periodontitis with multiple risk factor syndrome, and discusses the association between periodontal infection and systemic health. METHODS: The patient had a history of type 2 diabetes, dyslipidemia, and hypertension for over 10 years. At baseline, her hemoglobin A1 c was 8.1%. However, she had no diabetic complications except periodontitis. The IgG antibody titers against Porphyromonas gingivalis FDC 381 and SU63 were elevated above the mean of healthy subjects +2 standard deviations. Intensive periodontal treatment, including periodontal surgery, was performed to reduce periodontal infection and bacteremia. Her systemic and periodontal conditions were evaluated longitudinally for 10 years. RESULTS: Following periodontal treatment, antibody titers against Porphyromonas gingivalis and hemoglobin A1c values were significantly improved. The other clinical data and medication for her systemic condition also remained stable during supportive periodontal therapy. However, she developed myocardial infarction, and showed continuous deterioration of hemoglobin A1 c level and periodontitis. CONCLUSION: The long-term clustering of risk factors, such as diabetes, dyslipidemia, hypertension, and periodontitis, are associated with the development of myocardial infarction. Treatment of systemic conditions in combination with comprehensive periodontal treatment is important in management of patients with multiple risk factor syndrome.

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  • Inhibition of epithelial migration regulated by over-expressing Smad2 during gingival wound healing

    Tomikawa Kzauya, Yamamoto Tadashi, Shimoe Masayuki, Shiomi Nobuyuki, Mineshiba Jyunnji, Yamaguchi Tomoko, Hongo Shoichi, Maeda Hiroshi, Takashiba Shogo

    Program and Abstracts of Annual Meeting of the Japanese Society of Periodontology   2011   21 - 21   2011

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    DOI: 10.14833/amjsp.2011s.0.21.0

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    Other Link: http://search.jamas.or.jp/link/ui/2011257305

  • Rapid detection of mecA and spa by the loop-mediated isothermal amplification (LAMP) method. Reviewed International journal

    Y Koide, H Maeda, K Yamabe, K Naruishi, T Yamamoto, S Kokeguchi, S Takashiba

    Letters in applied microbiology   50 ( 4 )   386 - 92   2010.4

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    AIM: To develop a detection assay for staphylococcal mecA and spa by using loop-mediated isothermal amplification (LAMP) method. METHODS AND RESULTS: Staphylococcus aureus and other related species were subjected to the detection of mecA and spa by both PCR and LAMP methods. The LAMP successfully amplified the genes under isothermal conditions at 64 degrees C within 60 min, and demonstrated identical results with the conventional PCR methods. The detection limits of the LAMP for mecA and spa, by gel electrophoresis, were 10(2) and 10 cells per tube, respectively. The naked-eye inspections were possible with 10(3) and 10 cells for detection of mecA and spa, respectively. The LAMP method was then applied to sputum and dental plaque samples. The LAMP and PCR demonstrated identical results for the plaque samples, although frequency in detection of mecA and spa by the LAMP was relatively lower for the sputum samples when compared to the PCR methods. CONCLUSION: Application of the LAMP enabled a rapid detection assay for mecA and spa. The assay may be applicable to clinical plaque samples. SIGNIFICANCE AND IMPACT OF THE STUDY: The LAMP offers an alternative detection assay for mecA and spa with a great advantage of the rapidity.

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  • Highly expressed genes in a rough-colony-forming phenotype of Aggregatibacter actinomycetemcomitans: implication of a mip-like gene for the invasion of host tissue Reviewed

    Takemasa Maeda, Hiroshi Maeda, Kokoro Yamabe, Junji Mineshiba, Ichiro Tanimoto, Tadashi Yamamoto, Koji Naruishi, Susumu Kokeguchi, Shogo Takashiba

    FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY   58 ( 2 )   226 - 236   2010.3

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    Aggregatibacter actinomycetemcomitans, a potent pathogen of periodontitis, typically grows as a rough and adherent colony on primary isolated cultures. The colony transforms into a smooth phenotype during repeated subculture. In this study, we aimed to identify highly expressed genes in the rough-colony-forming phenotype for isolation of host-induced genes. Using a cDNA-subtractive hybridization technique, three genes, homologous to a macrophage infectivity potentiator gene (mip), peroxiredoxin gene (prx) and outer membrane protein gene (ompA), were identified. The expression levels of these genes in the rough-colony-forming phenotype were 4-10-fold higher as compared with the smooth-colony-forming phenotype. Attention was focused on the mip-like gene, and a recombinant protein and a deficient mutant were constructed. The recombinant protein reacted with sera from patients with periodontitis, suggesting the production of the Mip-like protein in periodontal lesions. Viable quantitative invasion assay demonstrated that the viable cell counts of the wild-type strain that invaded HeLa cells were more than fourfold as compared with the mip-deficient mutant. The expression of the mip-like gene, prx-like gene and ompA-like gene may be enhanced in the host, and the mip-like gene may play an important role in the infection of A. actinomycetemcomitans, especially in its invasion of the epithelium.

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  • Oligonucleotide array analysis of cyclic tension-responsive genes in human periodontal ligament fibroblasts Reviewed

    Keisuke Yamashiro, Fumio Myokai, Koichi Hiratsuka, Tadashi Yamamoto, Kyoko Senoo, Hideo Arai, Fusanori Nishimura, Yoshimitsu Abiko, Shogo Takashiba

    INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY   39 ( 5 )   910 - 921   2007

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    Mechanical stress results in differential gene expression that is critical to convert the stimulus into biochemical signals. Under physiological stress such as occlusal force, human periodontal ligament fibroblasts (HPLF) are associated with homeostasis of periodontal tissues however the changes in response to mechanotransduction remain uncharacterized. We hypothesized that cyclic tension-responsive (CT) genes may be used to identify a set of fundamental pathways of mechanotransduction. Our goal was to catalogue CT genes in cultured HPLE HPLF were subjected to cyclic tension up to 16 h, and total RNA was isolated from both tension-loaded and static HPLE The oligonucleotide arrays analysis revealed significant changes of mRNA accumulation for 122 CT genes, and their kinetics were assigned by the K-means clustering methods. Ingenuity Pathway Analysis was completed for HPLF mechanotransduction using 50 CT genes. This analysis revealed that cyclic tension immediately down-regulated all nuclear transcription factors except v-fos FBJ murine osteosarcoma viral oncogene homolog (FOS) reacting as an early responsive gene. In turn, transcription factors such as tumor protein p53 binding protein 2 (TP53BP2), and extra-nuclear molecules such as adrenergic receptor beta 2 (ADRB2) were up-regulated after 1-2 h, which may result in fundamental HPLF functions to adapt to cyclic tension. Subsequent inhibition assays using Y27632, a pharmacologic inhibitor of Rho-associated kinase (ROCK), suggested that HPLF has both ROCK-dependent and ROCK-independent CT genes. Mechanical stress was found to effect the expression of numerous genes, in particular, expression of an early responsive gene; FOS initiates alteration of HPLF behaviors to control homeostasis of the periodontal ligament. (C) 2007 Elsevier Ltd. All rights reserved.

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  • Inhibition of SMAD2 expression prevents murine palatal fusion Reviewed

    N Shiomi, XM Cui, T Yamamoto, T Saito, CF Shuler

    DEVELOPMENTAL DYNAMICS   235 ( 7 )   1785 - 1793   2006.7

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    Transforming growth factor (TGF)-beta 3 is known to regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Our previous studies showed that SMAD2, a TGF-beta signaling mediator, was expressed and phosphorylated primarily in the MEE and that SMAD2 phosphorylation in the MEE was temporospatially regulated by TGF-beta 3. The goal of this study was to examine the requirement for SMAD2 to complete the developmental events necessary for palatal fusion. SMAD2 expression was inhibited with Smad2 siRNA transfection into palatal tissues in vitro. The results showed that Smad2 siRNA transfection resulted in the maintenance of MEE cells in the palatal midline. Western blot and immunofluorescence analyses confirmed that the endogenous SAUD2 and phospho-SMAD2 levels were reduced following siRNA transfection. The SMAD3 level was not altered by the Smad2 siRNA transfection. The persistence of the MEE and the decreased SMAD2/phospho-SMAD2 levels were coincident with increased MEE cell proliferation. Addition of exogenous TGF-beta 3 increased p-SMAD2 level but not the total SMAD2 level. Therefore, exogenous TGF-beta 3 was not able to induce p-SMAD2 enough to rescue the palatal phenotype in the Smad2 siRNA group. The results indicated that the endogenous SMAD2 level is crucial in the regulation of disappearance of MEE during palatal fusion.

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  • Study on sgk Expression in Cultured Human Periodontal Ligament Fibroblasts Stimulated with Hyper Osmotic Stress

    MYOKAI Fumio, SENOO Kyoko, YAMASHIRO Keisuke, YAMAMOTO Tadashi, OYAIZU Kosuke, ARAI Hideo, NISHIMURA Fusanori, TAKASHIBA Shogo

    日本歯科保存学雑誌 = THE JAPANESE JOURNAL OF CONSERVATIVE DENTISTRY   48 ( 6 )   939 - 945   2005.12

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  • Effect of N '-nitrosonornicotine (NNN) on murine palatal fusion in vitro Reviewed

    T Saito, XM Cui, T Yamamoto, N Shiomi, P Bringas, CF Shuler

    TOXICOLOGY   207 ( 3 )   475 - 485   2005.2

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    Maternal smoking has been linked to an increased risk for orofacial clefts. N'-nitrosonornicotine (NNN) is one of the tobacco-specific nitrosamines that has been shown to be Linked to the deleterious effects of tobacco and could be linked to the formation of cleft palate birth defects. The effect of NNN on palatal fusion was examined using an in vitro organ culture model of palatal development. The organ cultures were exposed to NNN (0.0 1, 0. 1, 1, 10 and 100 mM) and the effects on palatal development characterized at defined points. Palatal fusion was evaluated at embryonic day 13 (E 13) + 72 h by characterizing the remaining medial edge epithelium (MEE) and determining the extent of fusion compared to controls. The NNN-treated group (I MM) had more MEE remaining in the palatal midline than the untreated group at E 13 + 72 h (P &lt; 0.05). Changes in cell proliferation in the MEE resulting from NNN exposure were examined by BrdU incorporation in replicating DNA. Changes in the pattern of MEE cell death were examined by TUNEL. BrdU incorporation and TUNEL staining showed that the NNN (1 mM)-treated palates had more MEE cell proliferation and less apoptosis than the untreated-palates at E 13 + 24 h (P &lt; 0.05). The mechanism altered by NNN was further evaluated by characterizations of extracellular signal-regulated kinase (ERK) 1/2, p38 and c-jun amino-terminal kinase (INK). NNN at I mM induced ERK1/2 phosphorylation, but reduced p38 phosphorylation (P&LT;0.05, P&LT; 0.01, respectively) in the MEE. The results suggest that NNN inhibited palatal fusion by effects on cell proliferation and MEE cell death. &COPY; 2004 Elsevier Ireland Ltd. All rights reserved.

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  • Overexpression of Smad2 in Tgf-beta 3-null mutant mice rescues cleft palate Reviewed

    XM Cui, N Shiomi, JC Chen, T Saito, T Yamamoto, Y Ito, P Bringas, Y Chat, CF Shuler

    DEVELOPMENTAL BIOLOGY   278 ( 1 )   193 - 202   2005.2

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    Transforming growth factor (TGF)-beta3 is an important contributor to the regulation of medial edge epithelium (MEE) disappearance during palatal fusion. SMAD2 phosphorylation in the MEE has been shown to be directly regulated by TGF-beta3. No phospho-SMAD2 was identified in the MEE in Tgf-beta3-null mutant mice (Tgf-beta(-1-)), which was correlated with the persistence of the MEE and failure of palatal fusion. In the present study, the cleft palate phenotype in Tgf-beta3(-/-) mice was rescued by overexpression of a Smad2 transgene in Keratin 14-synthesizing MEE cells following mating Tgf-beta3 heterozygous mice with Keratin 14 promoter directed Smad2 transgenic mice (K14-Smad2). Success of the rescue could be attributed to the elevated phospho-SMAD2 level in the MEE, demonstrated by two indirect evidences. The rescued palatal fusion in Tgf-beta3(-/-)/K14-Smad2 mice, however, never proceeded to the junction of primary and secondary palates and the most posterior border of the soft palate, despite phospho-SMAD2 expression in these regions at the same level as in the middle portion of the secondary palate. The K14-Smad2 transgene was unable to restore all the functional outcomes of TGF-beta3. This may indicate an anterior-posterior patterning in the palatal shelves with respect to TGF-beta3 signaling and the mechanism of secondary palatal fusion. (C) 2004 Elsevier Inc. All rights reserved.

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  • Identification of genes differentially regulated in rat alveolar bone wound healing by subtractive hybridization Reviewed

    T Ohira, F Myokai, N Shiomi, K Yamashiro, T Yamamoto, Y Murayama, H Arai, F Nishimura, S Takashiba

    JOURNAL OF DENTAL RESEARCH   83 ( 7 )   546 - 551   2004.7

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    Periodontal healing requires the participation of regulatory molecules, cells, and scaffold or matrix. Here, we hypothesized that a certain set of genes is expressed in alveolar bone wound healing. Reciprocal subtraction gave 400 clones from the injured alveolar bone of Wistar rats. Identification of 34 genes and analysis of their expression in injured tissue revealed several clusters of unique gene regulation patterns, including the up-regulation at 1 wk of cytochrome c oxidase regulating electron transfer and energy metabolism, presumably occurring at the site of inflammation; up-regulation at 2.5 wks of pro-alpha-2 type I collagen involving the formation of a connective tissue structure; and up-regulation at 1 and 2 wks and down-regulation at 2.5 and 4 wks of ubiquitin carboxyl-terminal hydrolase 13 involving cell cycle, DNA repair, and stress response. The differential expression of genes may be associated with the processes of inflammation, wound contraction, and formation of a connective tissue structure.

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  • Role of ERK1/2 signaling during EGF-induced inhibition of palatal fusion Reviewed

    T Yamamoto, XM Cui, CF Shuler

    DEVELOPMENTAL BIOLOGY   260 ( 2 )   512 - 521   2003.8

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    During mammalian palatal fusion, the medial edge epithelial (MEE) cells must stop DNA synthesis prior to the initial contact of opposing palatal shelves and thereafter selectively disappear from the midline. Exogenous EGF has been shown to inhibit the cessation of DNA synthesis and induce cleft palate; however, the precise intracellular mechanism has not been determined. We hypothesized that EGF signaling acting via ERK1/2 would maintain MEE DNA synthesis and cell proliferation and consequently inhibit the process of palatal fusion. Palatal shelves from E13 mouse embryos were maintained in organ cultures and stimulated with EGF. EGF-treated palates failed to fuse with intact MEE and had significant ERK1/2 phosphorylation. Both EGF-induced ERK1/2 phosphorylation and BrdU-incorporation were localized in the nucleus of MEE cells. Subsequent inhibition assays using U0126, a specific inhibitor of ERK1/2 phosphorylation, were conducted. U0126 inhibited EGF-induced ERK1/2 phosphorylation in a dose-dependent manner and consequently MEE cells stopped proliferation. The threshold of ERK1/2 inactivation to stop MEE DNA synthesis coincides with the level required to rescue the EGF-induced cleft palate phenotype. These results indicate that EGF-induced inhibition of palatal fusion is dependent on nuclear ERK1/2 activation and that this mechanism must be tightly regulated during normal palatal fusion. (C) 2003 Elsevier Inc. All rights reserved.

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  • Gene profiling in human periodontal ligament fibroblasts by subtractive hybridization Reviewed

    T Yamamoto, F Myokai, F Nishimura, T Ohira, N Shiomi, K Yamashiro, H Arai, Y Murayama, S Takashiba

    JOURNAL OF DENTAL RESEARCH   82 ( 8 )   641 - 645   2003.8

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    Genes expressed by human periodontal ligament fibroblasts (HPFs)are likely to be associated with specific functions of the ligament. The aim of this study is to profile genes expressed highly by HPFs. A library (6 x 103 pfu)was constructed, followed by subtraction of HPF cDNAs with human gingival fibroblast (HGF) cDNAs. Reverse-dot hybridization revealed that 33 clones expressed higher levels of specific mRNAs in HPFs than in HGFs. These were mRNAs for known genes including several associated with maturation and differentiation of cells. None had been reported in PFs. One clone, PDL-29 identified as a COX assembly factor, showed much stronger mRNA expression in HPFs than in HGFs in culture. In rat periodontium, however, PDL-29 mRNA expression was similar in PFs and GFs. These results suggest that HPFs express many previously unreported genes associated with maturation and differentiation, but expression can differ in vitro and in vivo.

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  • TGF-beta3-dependent SMAD2 phosphorylation and inhibition of MEE proliferation during palatal fusion

    CUI XM

    Dev Dyn   227 ( 3 )   387 - 394   2003.7

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  • Unique genes induced by mechanical stress in periodontal ligament cells Reviewed

    F Myokai, M Oyama, F Nishimura, T Ohira, T Yamamoto, H Arai, S Takashiba, Y Murayama

    JOURNAL OF PERIODONTAL RESEARCH   38 ( 3 )   255 - 261   2003.6

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    Objectives: The aim of this study is to isolate mechanical stress-induced genes (MSGens) from human periodontal ligament (PDL) cells and to analyze profiles of the mRNA expression of these genes.
    Background: Differential expression of genes in PDL cells under physiological stress such as occlusal force is thought to be orchestrated not only for the remodeling of PDL itself but also for the repair and regeneration of periodontal tissues. However, little is known about the genes expressed in PDL cells under mechanical stress.
    Methods: The cDNA from mechanical stress-applied human PDL cells was subtracted against the cDNA from static control cells. The subtracted cDNA was amplified by polymerase chain reaction (PCR) and cloned for further analysis.
    Results: Among 68 independent clones isolated, 15 contained DNA fragments greater than 250 bp. Reverse Northern analysis revealed a marked induction of MSGen-15 and MSGen-28 mRNA expression in the mechanical stress-applied cells. However, little difference in the magnitude of expression for the other MSGens was detected between the stress-applied cells and the control cells. After nucleotide sequencing and the analysis of homology with known genes, five clones were identified; ribosomal protein S27 (MSGen-9), MRG 15 (MSGen-15), androgen-binding protein (MSGen-18), cathepsin H (MSGen-28), and cytochrome c (MSGen-47). Interestingly, it has been reported that MRG 15 is a novel transcription factor involved in the regulation of cell growth and senescence. The remaining 10 clones, classified into six sequence types, had no significant homology with any known genes.
    Conclusions: These results suggest that many known and unknown genes are expressed in response to mechanical stress in PDL cells, and that a transcription factor, MRG 15, may be responsible for molecular events in PDL cells under mechanical stress.

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Books

  • Heat Shock Proteins in Inflammatory Diseases

    ( Role: Contributor ,  Heat Shock Proteins and Periodontitis – Cross-Reaction Between Bacterial and Human HSP in Periodontal Infection Linking with Cardiovascular Diseases)

    Springer Nature  2021.12 

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  • ザ・ペリオドントロジー = The periodontology

    沼部, 幸博, 梅田, 誠, 齋藤, 淳, 山本, 松男, 小方, 頼昌( Role: Contributor ,  歯周病の遺伝的背景)

    永末書店  2019.2  ( ISBN:9784816013584

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MISC

  • コラーゲン結合型塩基性線維芽細胞増殖因子を用いた水平性骨吸収に対する歯周組織再生療法の開発

    中村心, 伊東孝, 岡本憲太郎, 美間健彦, 内田健太郎, 山本直史, 松下治, 高柴正悟

    日本歯科医学会誌   40   2021

  • Control on Contamination in Dental Unit Water Lines (DUWL) using Neutral Electrolyzed Water

    伊東(信田)有希, 大森一弘, 伊東孝, 大久保圭祐, 平井公人, 山本直史, 高柴正悟

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   155th   2021

  • Isolation and identification of antibacterial substances contained in fermented soybean food Tempeh

    伊東昌洋, 伊東孝, 中村心, 青木秀之, 西岡功志, 塩川つぐみ, 多田宏子, 竹内祐貴, 武安伸幸, 山本直史, 高柴正悟

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   154th   2021

  • Endodontic Management of a Mandible Premolar with 3 root canals-A Case Report-

    ROSALIA Arias Martinez Zulema, YAMASHIRO Keisuke, SHINODA-ITO Yuki, YAMAMOTO Tadashi, TAKASHIBA Shogo

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   152nd   2020

  • Endodontic Management of a Bucco-Accessory Root Canal of a Maxillary Central Incisor: A Case Report

    ROSALIA Arias Martinez Zulema, SIDDIQUI Yasir Dilshad, YAMASHIRO Keisuke, SHINODA-ITO Yuki, YAMAMOTO Tadashi, TAKASHIBA Shogo

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   151st   2019

  • Functionalized Graphene Oxide Nanoparticles Protect Tooth Dentin from Decalcification besides Bactericidal Activity.

    ISLAM Nizami Mohammed Zahedul, NISHINA Yuta, YAMAMOTO Tadashi, SHINODA-ITO Yuki, TAKASHIBA Shogo

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   151st   2019

  • コラーゲン結合型塩基性線維芽細胞成長因子はコラーゲン基剤からの徐放によって歯周組織再生を促進する

    岡本憲太郎, 中村心, 伊東孝, SIDDIQUI Yasir Dilshad, 美間健彦, 内田健太郎, 大森一弘, 山本直史, 松下治, 高柴正悟

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   150th   2019

  • 歯周病の炎症度を示す臨床的検査基準値の検討

    井上 裕貴, 畑中 加珠, 大森 一弘, 山本 直史, 三辺 正人, 高柴 正悟, 平田 貴久, 山本 龍生, 内藤 徹, 山本 松男, 佐藤 秀一, 石幡 浩志, 稲垣 幸司, 三谷 章雄, 中島 啓介, 漆原 譲治

    日本未病システム学会学術総会抄録集   25回   108 - 108   2018.10

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  • 歯周病の炎症度を示す臨床的検査基準値の検討

    井上 裕貴, 畑中 加珠, 大森 一弘, 山本 直史, 三辺 正人, 高柴 正悟, 平田 貴久, 山本 龍生, 内藤 徹, 山本 松男, 佐藤 秀一, 石幡 浩志, 稲垣 幸司, 三谷 章雄, 中島 啓介, 漆原 譲治

    日本未病システム学会学術総会抄録集   25回   108 - 108   2018.10

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  • 2型糖尿病患者に対する歯周病治療時の課題を実感した1症例

    高橋 麻里子, 大森 一弘, 千神 八重子, 山本 直史, 高柴 正悟

    糖尿病   61 ( 5 )   359 - 359   2018.5

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  • 2型糖尿病患者に対する歯周治療の効果と課題を実感した一症例

    高橋 麻里子, 大森 一弘, 千神 八重子, 山本 直史, 高柴 正悟

    日本歯科評論   78 ( 1 )   141 - 150   2018.1

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  • 歯科用ユニット給水管路汚染対策に向けた自動注水型試験機の有効性評価

    岡本憲太郎, 大久保圭祐, 伊東孝, 伊東昌洋, 田井真沙子, 中村心, 山口唯菜, 塩田康祥, 河田有祐, 大森一弘, 山本直史, 高柴正悟

    岡山歯学会雑誌   37 ( 2 )   2018

  • 歯科用ユニット給水管路汚染対策用の注水制御シミュレータの評価

    岡本憲太郎, 大久保圭祐, 伊東孝, 山本一郎, 水谷元, 伊東昌洋, 田井真沙子, 中村心, 塩田康祥, 河田有祐, 大森一弘, 山本直史, 高柴正悟

    日本口腔機能水学会誌   19 ( 1 )   2018

  • コラーゲン結合型塩基性線維芽細胞成長因子とコラーゲン基剤を用いた複合剤の歯周組織再生への応用

    中村心, 伊東孝, 松下治, 岡本憲太郎, 美間健彦, 内田健太郎, SIDDIQUI Yasir Dilshad, 伊東昌洋, 田井真砂子, 大久保圭祐, 山城圭介, 大森一弘, 山本直史, 高柴正悟

    日本歯周病学会会誌(Web)   60   2018

  • 口腔バイオフィルム感染症を制御するパウダー状の天然食品の探索

    伊東昌洋, 伊東孝, 河田有祐, 塩田康祥, 大久保圭祐, 田井真砂子, 中村心, 岡本憲太郎, 青木秀之, 二井広平, 宮島彩, 大森一弘, 山本直史, 高柴正悟

    日本歯周病学会会誌(Web)   59   2017

  • 歯科用ユニット給水管路汚染対策用の自動注水制御シミュレータの評価

    大久保圭祐, 伊東孝, 山本一郎, 水谷元, 伊東昌洋, 田井真砂子, 中村心, 岡本憲太郎, 塩田康祥, 河田有祐, 大森一弘, 山本直史, 高柴正悟

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   147th   2017

  • 歯周病原細菌に対する指尖血漿IgG抗体価検査が感染性心内膜炎(IE)の起炎菌推定に繋がった症例

    磯島大地, 松永一幸, 工藤値英子, 伊東孝, 大森一弘, 山本直史, 高柴正悟

    日本歯科医師会雑誌   69 ( 5 )   2016

  • 口腔バイオフィルム抑制用の多糖誘導体リン酸化プルランにおける歯面への付着と薬剤徐放性効果の機序解明

    伊東孝, 塩田康祥, 河田有祐, 大久保圭祐, 伊東昌洋, 大森一弘, 山本直史, 高柴正悟

    日本歯周病学会会誌(Web)   58   2016

  • 海藻由来レクチンを用いた口腔バイオフィルム感染症の制御

    塩田康祥, 伊東孝, 河田有祐, 大久保圭祐, 伊東昌洋, 今村幸治, 大森一弘, 山本直史, 高柴正悟

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   144th   2016

  • 口腔細菌感染症を制御する機能性食品の探索

    伊東昌洋, 大久保圭祐, 伊東孝, 河田有祐, 塩田康祥, 大森一弘, 山本直史, 高柴正悟

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   145th   2016

  • 継続的な歯周支援治療が認知機能維持に及ぼす影響の検討-pilot study-

    大森一弘, 小林寛也, 伊東孝, 下江正幸, 畑中加珠, 園井教裕, 福家教子, 福家教子, 山本直史, 高柴正悟

    日本歯周病学会会誌(Web)   58   2016

  • 歯周病原細菌に対する指尖血漿IgG抗体価検査が感染性心内膜炎の起炎菌推定に繋がった一症例

    磯島大地, 松永一幸, 工藤値英子, 伊東孝, 大森一弘, 山本直史, 高柴正悟

    日本歯周病学会会誌(Web)   57   2015

  • 歯周病原細菌に対する指尖血漿IgG抗体価検査が感染性心内膜炎の起炎菌推定に繋がった症例

    磯島大地, 松永一幸, 工藤値英子, 伊東孝, 大森一弘, 山本直史, 高柴正悟

    岡山歯学会雑誌   34 ( 2 )   2015

  • マッシュルーム粗抽出物による口腔感染制御能を有した機能性食品の開発

    伊東孝, 今村幸治, 塩田康祥, 河田有祐, 大久保圭祐, 高知信介, 峯柴淳二, 山本直史, 前田博史, 高柴正悟

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   140th   2014

  • 海藻ミル由来のレクチンを用いた口腔感染制御システムの検討

    塩田康祥, 伊東孝, 河田有祐, 大久保圭祐, 今村幸治, 山本直史, 前田博史, 高柴正悟

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   141st   2014

  • 生体腎移植患者の周術期口腔感染管理を病病連携にて行った1例

    佐藤公麿, 河村麻里, 吉原千暁, 峯柴淳二, 山本直史, 高柴正悟, 曽我賢彦

    広島医学   66 ( 8 )   2013

  • 文献と臨床の橋わたし 血清抗体価を活用した歯周病診断(第2回) 血清抗体価の歯周治療への応用について

    山本 直史, 高柴 正悟

    日本歯科評論   70 ( 8 )   161 - 163   2010.8

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  • 特別養護老人ホームにおける口腔ケア

    鷲尾憲文, 澤田弘一, 金盛久展, 山本直史, 難波久美子, 奥典永

    地域医療(0289-9752)第46回特集   775 - 779   2007.10

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  • ラット創傷歯髄から単離したFIP-2が炎症制御因子と細胞死に与える影響について

    妹尾 京子, 山本 直史, 明貝 文夫, 山城 圭介, 新井 英雄, 西村 英紀, 高柴 正悟

    日本歯科保存学雑誌   50 ( 春季特別 )   45 - 45   2007.5

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  • 機械的刺激を与えた培養ヒト歯根膜線維芽細胞が発現する遺伝子の網羅的解析

    山城 圭介, 明貝 文夫, 妹尾 京子, 山本 直史, 新井 英雄, 西村 英紀, 高柴 正悟

    日本歯科保存学雑誌   47 ( 秋季特別 )   217 - 217   2004.10

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  • Study of Unique Genes Expressed by Mechanical Stress in Human Periodontal Ligament Fibroblasts

    MYOKAI Fumio, OHIRA Taisuke, YAMAMOTO Tadashi, MINESHIBA Junji, WASHIO Norifumi, NARUISHI Koji, ARAI Hideo, NISHIMURA Fusanori, TAKASHIBA Shogo, MURAYAMA Yoji

    Journal of the Japanese Association of Periodontology   40   108 - 108   1998.9

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  • Expression Pattern of Serum and Glucocorticoid-Inducible Kinase (sgk) during Rat Dental Hard Tissue Formation

    OHIRA Taisuke, MYOKAI Fumio, NARUISHI Koji, YAMAMOTO Tadashi, ARAI Hideo, NISHIMURA Fusanori, TAKASHIBA Shogo, MURAYAMA Yoji

    41   32 - 32   1998.5

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  • Genes Specifically Expressed by Fibroblasts Isolated from Periodontal Ligament

    YAMAMOTO Tadashi, TAKASHIBA Shogo, MYOKAI Fumio, TAKIGAWA Masayuki, WASHIO Norifumi, NISHIMURA Fusanori, ARAI Hideo, MURAYAMA Yoji

    Journal of the Japanese Association of Periodontology   40   114 - 114   1998.4

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  • A Case Study of family Members Manifesting Early-Onset Periodontitis with Gingival Overgrowth 〜Clinical, Microbiological, Immunological and Histological Observation〜

    OMURO Hiromasa, TAKIGAWA Masayuki, OKAMURA Kazunori, NISHIMURA Fusanori, NARUISHI Koji, SAWA Takamasa, YAMAMOTO Tadashi, OHIRA Taisuke, TAKAHASHI Keiso, JUAN Guo Shun, TAKASHIBA Shogo, MURAYAMA Yoji

    40   154 - 154   1997.5

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  • Chemotactic Event of Human Periodontal Ligament Fibroblasts are Dependent on Certain Phases of Cell Cycle

    Asahara Yoji, Nishimura Fusanori, Washio Norifumi, Chou Hsin-Hua, Yamamoto Tadashi, Arai Hideo, Takashiba Shogo, Murayama Yoji

    Journal of the Japanese Association of Periodontology   38   110 - 110   1996.3

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Presentations

  • Notchシグナル伝達経路を介した破骨細胞分化のメカニズム

    本行 令奈, 池田 淳史, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2021.10  (NPO)日本歯科保存学会

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  • 徹底した感染源除去が奏功した広汎型侵襲性歯周炎患者の15年臨床経過

    山本 直史, 小柳津 功介, 高柴 正悟

    日本歯周病学会会誌  2021.10  (NPO)日本歯周病学会

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  • RNAシャペロンであるHfqはAggregatibacter actinomycetemcomitansの病原因子を制御する

    尾内 千晃, 平井 公人, 池田 淳史, 伊東 昌洋, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2021.10  (NPO)日本歯周病学会

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  • 歯周感染が子宮組織に及ぼす影響のマウス絹糸結紮歯周炎モデルにおける免疫学的検討

    永田 千晶, 大森 一弘, 井手口 英隆, 佐光 秀文, 坂井田 京佑, 徳善 真砂子, 平井 公人, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2021.10  (NPO)日本歯周病学会

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  • 歯科ユニット給水管路(DUWL)内汚染の実際と電解機能水の効果

    伊東 有希[信田], 大森 一弘, 伊東 孝, 大久保 圭祐, 平井 公人, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2021.10  (NPO)日本歯科保存学会

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  • 歯内治療が原因で菌血症となった単心室症患者の症例報告とその対応策の提案

    児玉 加奈子, 井手口 英隆, 岡本 憲太郎, 佐光 秀文, 松本 俊樹, 大森 一弘, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2021.10  (NPO)日本歯科保存学会

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  • 短鎖脂肪酸は歯周炎症のバイオマーカーになり得るか

    児玉 加奈子, 畑中 加珠, 小西 健司, 白波瀬 泰史, 河野 麻理, 吉田 敏之, 戸谷 直樹, 酒瀬川 信一, 落合 邦康, 山本 直史, 高柴 正悟

    日本口腔検査学会総会・学術大会プログラム・抄録集  2021.8  (一社)日本口腔検査学会

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  • 人獣共通感染症の制御に向けたphytochemicalを利用したアプローチ

    松本 俊樹, 伊東 昌洋, 徳善 真砂子, 青木 秀之, 西岡 功志, 山本 直史, 高柴 正悟

    日本口腔検査学会総会・学術大会プログラム・抄録集  2021.8  (一社)日本口腔検査学会

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  • Resolvin D2 Promotes the Formation of Calcified Tissue on Pulp

    Yoneda Mitsuhiro, Yamamoto Tadashi, Takashiba Shogo, Arias Zulema, Nakamura Shin, Okamoto Kentarou, Ito Masahiro, Tamura Kazuya, Ideguchi Hidetaka, Yamashiro Keisuke, Omori Kazuhiro

    99th International Association for Dental Research  2021 

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  • Collagen-Binding Basic Fibroblast Growth Factor Promotes Horizontal Periodontal Regeneration

    Nakamura Shin, Yamamoto Tadashi, Matsushita Osamu, Takashiba Shogo, Okamoto Kentarou, Ito Takashi, Mima Takehiko, Uchida Kentaro, Ito Masahiro, Okubo Keisuke, Ideguchi Hidetaka, Omori Kazuhiro

    99th International Association for Dental Research  2021 

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  • ω-3脂肪酸誘導体の抗炎症作用による歯髄保存の試み

    米田 光宏, Zulema Rosalia Arias Martinez, 中村 心, 岡本 憲太郎, 伊東 昌洋, 田村 和也, 井手口 英隆, 大森 一弘, 山城 圭介, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2021.5  (NPO)日本歯科保存学会

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  • X連鎖性低リン血症性くる病を起因とした多発根尖性歯周炎に対し歯内療法を行った症例の病態考察

    佐光 秀文, 大森 一弘, 坂井田 京佑, 亀井 千晶, 小林 寛也, 井手口 英隆, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2021.5  (NPO)日本歯科保存学会

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  • Aggregatibacter actinomycetemcomitansに対し高い血清IgG抗体価反応を示す歯周炎患者の治療経過と病態考察

    岡本 憲太郎, 高知 信介, 小林 寛也, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2021.5  (NPO)日本歯周病学会

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  • 不妊治療中患者に対する血清IgG抗体価検査を用いた歯周病原細菌の感染度調査

    亀井 千晶, 大森 一弘, 佐光 秀文, 坂井田 京佑, 徳善 真砂子, 平井 公人, 小林 寛也, 山本 直史, 滝川 雅之, 三宅 貴仁, 高柴 正悟

    日本歯周病学会会誌  2021.5  (NPO)日本歯周病学会

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  • 大豆発酵食品テンペに含まれる抗菌性物質の単離と同定

    伊東 昌洋, 伊東 孝, 中村 心, 青木 秀之, 西岡 功志, 塩川 つぐみ, 多田 宏子, 竹内 祐貴, 武安 伸幸, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2021.5  (NPO)日本歯科保存学会

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  • HMGB1はM1マクロファージの分化を制御して歯周炎の進行に影響を及ぼす

    平井 杏奈, 井手口 英隆, 山城 圭介, Yao Zhang, 青柳 浩明, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2021.5  (NPO)日本歯科保存学会

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  • コラーゲン結合型塩基性線維芽細胞増殖因子を用いた水平性骨吸収に対する歯周組織再生療法の開発

    中村 心, 伊東 孝, 岡本 憲太郎, 美間 健彦, 内田 健太郎, 山本 直史, 松下 治, 高柴 正悟

    日本歯科医学会誌  2021.3  日本歯科医学会

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  • 侵襲性歯周炎の血液診断バイオマーカーとしての細胞外小胞由来マイクロRNAの探索

    河本 美奈, 山本 直史, 河村 麻理, 森 彩乃, 山城 圭介, 大森 一弘, 小野 喜章, 江口 傑徳, 十川 千春, 高柴 正悟

    岡山歯学会雑誌  2020.12  岡山歯学会

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  • 子宮内膜症の治療と妊娠を契機に進行したと疑われる慢性歯周炎患者の病態考察と治療経過

    坂井田 京佑, 大森 一弘, 小林 寛也, 山本 直史, 高柴 正悟

    岡山歯学会雑誌  2020.12  岡山歯学会

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  • Delayed Wound Healing after Tooth Extraction under Malnutrition

    Y. ZHANG, H. IDEGUCHI, H. AOYAGI, K. YAMASHIRO, T. YAMAMOTO, M. NISHIBORI, S. TAKASHIBA

    68th Japanese Association for Dental Research  2020 

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    Event date: 2020.11.7 - 2020.11.8

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  • 真菌代謝産物(+)-terreinがマウス骨粗鬆症モデルにおける骨代謝に及ぼす影響

    坂井田 京佑, 大森 一弘, 中川 沙紀, 佐光 秀文, 亀井 千晶, 山本 総司, 小林 寛也, 山城 圭介, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2020.11  (NPO)日本歯科保存学会

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  • High Mobility Group Box 1(HMGB1)はマクロファージからのCCL2分泌を制御して抜歯窩の歯周組織再生を促進する

    井手口 英隆, 平井 杏奈, 山城 圭介, 京嶌 里沙, 青柳 浩明, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2020.10  (NPO)日本歯周病学会

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  • ハンチントン舞踏病の広汎型慢性歯周炎患者への歯周病治療で感じた歯科衛生士の役割

    佐藤 由実, 伊藤 実有, 北村 彰子, よし田 亜紀, 苅田 奈生子, 磯島 大地, 伊東 昌洋, 長島 義之, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2020.10  (NPO)日本歯周病学会

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  • 歯の病的移動と歯周-歯内病変を併発した侵襲性歯周炎患者に対する歯周組織再生療法

    本行 令奈, 井手口 英隆, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2020.10  (NPO)日本歯周病学会

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  • High Mobility Group Box 1が抜歯窩治癒過程の間葉系幹細胞の遊走に及ぼす影響

    京嶌 里紗, 井手口 英隆, 山城 圭介, 平井 杏奈, 青柳 浩明, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2020.6  (NPO)日本歯科保存学会

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  • インテグリンα3の選択的阻害による微小環境の構築と歯槽骨再生

    森 彩乃, 山本 直史, 河村 麻理, 井手口 英隆, 青柳 浩明, 中村 心, 岡本 憲太郎, 平井 杏奈, 山城 圭介, 大森 一弘, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2020.6  (NPO)日本歯科保存学会

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  • 歯周組織再生療法の違いが歯肉縁下細菌叢に及ぼす影響 侵襲性歯周炎患者の一症例

    大森 一弘, 河野 隆幸, 新井 英雄, 小林 寛也, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2020.5  (NPO)日本歯周病学会

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  • 歯周病重症度マーカーとしての洗口液・唾液・歯肉溝滲出液中の短鎖脂肪酸

    畑中 加珠, 川瀬 貴博, 白波瀬 泰史, 河野 麻理, 吉田 敏之, 塚原 隆充, 落合 邦康, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2020.5  (NPO)日本歯周病学会

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  • 真菌二次代謝産物(+)-terreinはTNF-αの発現を抑制し歯周炎マウスモデルにおける歯槽骨吸収を抑制する

    佐光 秀文, 大森 一弘, 中川 沙紀, 亀井 千晶, 坂井田 京佑, 山本 総司, 井手口 英隆, 小林 寛也, 山城 圭介, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2020.5  (NPO)日本歯周病学会

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  • Functionalized Graphene Oxide Nanocomposites Protect Decalcification of Hydroxyapatite and Dentin

    Nizami MZI, Nishina Y, Yamamoto T, Shinoda-Ito Y, Takashiba S

    98th International Association for Dental Research  2020 

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    Event date: 2020.3.18 - 2020.3.21

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  • Involvement of HMGB1 in Delayed Wound Healing under Malnutrition

    Y. ZHANG, H. IDEGUCHI, H. AOYAGI, K. YAMASHIRO, T. YAMAMOTO, M. NISHIBORI, S. TAKASHIBA

    98th International Association for Dental Research  2020 

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  • Collagen-binding fibroblast growth factor-2 promotes periodontal regeneration by local retention

    Okamoto K, Yamamoto T, Takashiba S et al

    98th International Association for Dental Research  2020 

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    Event date: 2020.3.18 - 2020.3.21

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  • Periodontitis is Developed by HMGB1 Regulating Macrophage to M1 Polarization

    Hirai A, Ideguchi H, Yamamoto T, Takashiba S et al

    98th International Association for Dental Research  2020 

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    Event date: 2020.3.18 - 2020.3.21

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  • Functionalized Graphene Oxide Nanocomposites Prevent Tooth Dentin Decalcification

    N.M.Z. Islam, Y. Nishina, T. Yamamoto, Y. Shinoda-Ito, S. Takashiba

    第40回岡山歯学会学術集会  2019 

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    Event date: 2019.12.15

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  • 歯周組織の炎症と不妊との関連性を示唆する侵襲性歯周炎症例の病態生理~岡山大学病院・侵襲性歯周炎センターでの取り組み~

    亀井千晶,大森一弘,小林寛也,山本直史,高柴正悟

    第40回岡山歯学会学術集会  2019 

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  • 不妊と歯周組織の炎症との関連性を示唆する侵襲性歯周炎症例の病態生理

    大森一弘,小林寛也,山本直史,高柴正悟

    日本歯周病学会中国四国三大学日本臨床歯周病学会中国支部合同研修会  2019 

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    Event date: 2019.12.1

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  • 歯周組織の炎症と不妊との関連性を示唆する侵襲性歯周炎症例の病態生理 岡山大学病院・侵襲性歯周炎センターでの取り組み

    亀井 千晶, 大森 一弘, 小林 寛也, 山本 直史, 高柴 正悟

    岡山歯学会雑誌  2019.12  岡山歯学会

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  • 真菌二次代謝産物terreinはマウス歯周病モデルにおける歯槽骨吸収を抑制する

    佐光 秀文, 大森 一弘, 中川 沙紀, 坂井田 京佑, 山本 総司, 青柳 浩明, 小林 寛也, 大野 充昭, 平井 公人, 山城 圭介, 山本 直史, 高柴 正悟

    有病者歯科医療  2019.12  (一社)日本有病者歯科医療学会

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  • Identification of Circulating Exosome-derived microRNA as a Diagnostic Biomarker for Aggressive Periodontitis

    Takaki M, Yamamoto T, Kawamura M, Mori A, Eguchi T, Sogawa C, and Takashiba S

    The 1st international symposium for intercellular communication and extracellular vesicles  2019 

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    Event date: 2019.11.21

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  • 真菌二次代謝産物terreinはマウス骨粗鬆症モデルにおいて大腿骨吸収を抑制する

    坂井田 京佑, 大森 一弘, 中川 沙紀, 佐光 秀文, 山本 総司, 小林 寛也, 平井 公人, 山城 圭介, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2019.10  (NPO)日本歯周病学会

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  • High Mobility Group Box 1(HMGB1)は間葉系幹細胞の遊走を介して抜歯窩の創傷治癒を促進する

    平井 杏奈, 井手口 英隆, 山城 圭介, 青柳 浩明, 鈴木 里紗, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2019.10  (NPO)日本歯周病学会

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  • 二次性咬合性外傷を伴う重度慢性歯周炎患者への歯周組織再生治療の成功要因

    山本 直史, 新井 英雄, 高柴 正悟

    日本歯周病学会会誌  2019.10  (NPO)日本歯周病学会

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  • 広汎型中等度慢性歯周炎患者の24年経過からみたSPTの重要性

    福家 教子, 佐藤 佐智子, 新井 英雄, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2019.10  (NPO)日本歯周病学会

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  • Resolvin-D2 Bridges Resolution of Periapical Inflammation to Tissue Regeneration

    Siddiqui Yasir, Omori Kazuhiro, Ito Takashi, Yamashiro Keisuke, Yamamoto Tadashi, Van Dyke Thomas, Takashiba Shogo

    97th International Association for Dental Research  2019 

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    Event date: 2019.7.26 - 2019.7.29

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  • Identification of an Antimicrobial Substance from Soybean Fermented "Tempeh"

    Ito Masahiro, Tai Masako, Okamoto Kentaro, Omori Kazuhiro, Yamamoto Tadashi, Takashiba Shogo, Ito Takashi, Aoki Hideyuki, Nishioka Koshi, Shiokawa Tsugumi, Tada Hiroko, Takeuchi Yuki, Takeyasu Nobuyuki, Nakamura Shin

    97th International Association for Dental Research  2019 

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  • Collagen-binding Basic Fibroblast Growth Factor Regenerates Horizontal Alveolar Bone Defect

    Nakamura Shin, Yamashiro Keisuke, Omori Kazuhiro, Yamamoto Tadashi, Matsushita Osamu, Takashiba Shogo, Ito Takashi, Okamoto Kentaro, Mima Takehiko, Uchida Kentaro, Siddiqui Yasir, Ito Masahiro, Tai Masako, Okubo Keisuke

    97th International Association for Dental Research  2019 

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  • Phytochemicalによる口腔感染症の制御に向けて

    山本直史,伊東昌洋、高柴正悟、

    2019年度中四国乳酸菌研究会研究発表会  2019 

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    Event date: 2019.6.21

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  • 子宮全摘出・卵巣片側摘出直後から急性化した重度慢性歯周炎症例の治療と病態考察

    坂井田 京佑, 大森 一弘, 佐光 秀文, 小林 寛也, 高知 信介, 河野 隆幸, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2019.5  (NPO)日本歯周病学会

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  • 徹底した感染管理が垂直性骨欠損を改善する要因であった重度慢性歯周炎症例

    大久保 圭祐, 高知 信介, 本郷 昌一, 河野 隆幸, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2019.5  (NPO)日本歯周病学会

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  • コラーゲン結合型塩基性線維芽細胞成長因子はコラーゲン基剤からの徐放によって歯周組織再生を促進する

    岡本 憲太郎, 中村 心, 伊東 孝, Siddiqui Yasir Dilshad, 美間 健彦, 内田 健太郎, 大森 一弘, 山本 直史, 松下 治, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2019.5  (NPO)日本歯科保存学会

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  • 歯周組織の炎症と不妊の関連性を示唆するある侵襲性歯周炎患者の病態生理

    大森 一弘, 河野 隆幸, 小林 寛也, 新井 英雄, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2019.5  (NPO)日本歯科保存学会

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  • 真菌二次代謝産物terreinはマウス歯周病モデルにおける歯槽骨吸収を抑制する

    佐光 秀文, 大森 一弘, 中川 沙紀, 坂井田 京佑, 山本 総司, 青柳 浩明, 小林 寛也, 大野 充昭, 平井 公人, 山城 圭介, 山本 直史, 高柴 正悟

    歯科薬物療法  2019.3  (一社)日本歯科薬物療法学会

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  • 当院における成人先天性心疾患患者の口腔状態の現況(Current Oral Condition of Patients with Adult Congenital Heart Disease in ACHD Center/Okayama University Hospital)

    大森 一弘, 杜 徳尚, 高知 信介, 山本 直史, 赤木 禎治, 伊藤 浩, 高柴 正悟

    日本成人先天性心疾患学会雑誌  2019.1  日本成人先天性心疾患学会

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  • 歯科用ユニット給水管路汚染対策に向けた自動注水型試験機の有効性評価

    岡本 憲太郎, 大久保 圭祐, 伊東 孝, 伊東 昌洋, 田井 真沙子, 中村 心, 山口 唯菜, 塩田 康祥, 河田 有祐, 大森 一弘, 山本 直史, 高柴 正悟

    岡山歯学会雑誌  2018.12  岡山歯学会

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  • 岡山大学病院・糖尿病教育入院患者を対象とした医科歯科連携システムの概況

    清水 由梨香, 大森 一弘, 利根 淳仁, 高知 信介, 山本 直史, 和田 淳, 高柴 正悟

    岡山歯学会雑誌  2018.12  岡山歯学会

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  • 侵襲性歯周炎患者の専門外来部門連携による包括的な治療と病態解析

    高知 信介, 久保 克行, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2018.10  (NPO)日本歯周病学会

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  • 歯周病原細菌によるヒトと伴侶動物イヌとの人獣共通感染症検査の研究

    田井 真砂子, 伊東 孝, 平山 晴子, 矢田 範夫, 小川 寛人, 田村 和也, 伊東 有希, 大久保 圭祐, 伊東 昌洋, 中村 心, 岡本 憲太郎, 平井 公人, 山城 圭介, 大森 一弘, 山本 直史, 樅木 勝巳, 高柴 正悟

    日本歯周病学会会誌  2018.10  (NPO)日本歯周病学会

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  • 侵襲性歯周炎患者の血漿エクソソーム由来microRNAの発現解析

    高木 美奈, 山本 直史, 河村 麻理, 高知 信介, 山城 圭介, 大森 一弘, 江口 傑徳, 十川 千春, 高柴 正悟

    日本歯周病学会会誌  2018.10  (NPO)日本歯周病学会

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  • コラーゲン結合型塩基性線維芽細胞成長因子とコラーゲン基剤を用いた複合剤の歯周組織再生への応用

    中村 心, 伊東 孝, 松下 治, 岡本 憲太郎, 美間 健彦, 内田 健太郎, Siddiqui Yasir Dilshad, 伊東 昌洋, 田井 真砂子, 大久保 圭祐, 山城 圭介, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2018.10  (NPO)日本歯周病学会

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  • 歯周病の炎症度を示す臨床的検査基準値の検討

    井上 裕貴, 畑中 加珠, 大森 一弘, 山本 直史, 三辺 正人, 高柴 正悟, 平田 貴久, 山本 龍生, 内藤 徹, 山本 松男, 佐藤 秀一, 石幡 浩志, 稲垣 幸司, 三谷 章雄, 中島 啓介, 漆原 譲治

    日本未病システム学会学術総会抄録集  2018.10  (一社)日本未病学会

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  • 真菌二次代謝産物(+)-terreinはマウス実験的歯周炎モデルにおける歯槽骨吸収を抑制する

    佐光 秀文, 大森 一弘, 中川 沙紀, 坂井田 京佑, 山本 総司, 青柳 浩明, 小林 寛也, 山城 圭介, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2018.10  (NPO)日本歯科保存学会

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  • HMGB1-induced inflammatory response promotes bone regeneration in murine tooth extraction socket

    Aoyagi H, Yamashiro K, Hirata-Yoshihara C, Ideguchi H, Kawamura M, Wake H, Yamasaki M, Suzuki R, Kochi S, Yamamoto T, Nishibori M, Takashiba S

    96th International Association for Dental Research  2018 

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  • Resolvin-D2 reduced inflammation and induces calcification periapical lesion.

    Siddiqui DY, Omori K, Ito T, Yamashiro K, Yamamoto T, Takashiba S

    96th International Association for Dental Research  2018 

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  • 歯科治療介入が生活習慣の改善につながった糖尿病関連性歯周炎患者の一症例

    志茂 加代子, 河村 麻理, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2018.5  (NPO)日本歯周病学会

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  • High Mobility Group Box 1(HMGB1)誘導性の炎症反応はマウス抜歯窩の骨治癒を促進する

    青柳 浩明, 山城 圭介, 平田 千暁, 井手口 英隆, 山崎 睦代, 河村 麻理, 鈴木 里紗, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2018.5  (NPO)日本歯科保存学会

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  • 上顎中切歯の歯内-歯周病変に対して部分矯正治療と自家骨移植術を行い歯科インプラント治療を回避した一症例

    鈴木 里紗, 井手口 英隆, 本郷 昌一, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2018.5  (NPO)日本歯周病学会

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  • 性別と年齢で層別した東日本大震災後の心理社会的要因と口腔内環境との関連 福島県「県民健康調査」

    坪井 綾香, 江口 依里, 大森 一弘, 山本 直史, 伊藤 達男, 長岡 憲次郎, 大平 哲也, 荻野 景規, 高柴 正悟

    日本歯周病学会会誌  2018.5  (NPO)日本歯周病学会

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  • 真菌二次代謝産物(+)-terreinはヒト歯肉上皮細胞におけるAggregatibacter actinomycetemcomitans刺激による細胞間接着分子の発現低下を抑制する

    中村 亜里紗, 大森 一弘, 小林 寛也, 冨川 知子, 山本 総司, 中川 沙紀, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2018.5  (NPO)日本歯科保存学会

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  • 歯科用ユニット給水管路汚染対策用の注水制御シミュレータの評価

    岡本 憲太郎, 大久保 圭祐, 伊東 孝, 山本 一郎, 水谷 元, 伊東 昌洋, 田井 真沙子, 中村 心, 塩田 康祥, 河田 有祐, 大森 一弘, 山本 直史, 高柴 正悟

    日本口腔機能水学会誌  2018.3  日本口腔機能水学会

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  • 岡山大学病院・侵襲性歯周炎センターの概要と取り組み例

    小林寛也,大森一弘,山本直史,高柴正悟

    日本歯周病学会中国四国三大学日本臨床歯周病学会中国支部合同研修会  2017 

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    Event date: 2017.11.12

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  • 2型糖尿病患者に対する歯周病治療時の課題を実感した一症例

    ?橋麻里子,大森一弘,千神八重子,山本直史,高柴正悟

    日本糖尿病学会中国四国 地方会第55回総会  2017 

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    Event date: 2017.11.11

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  • 口腔バイオフィルム感染症を制御するパウダー状の天然食品の探索

    伊東 昌洋, 伊東 孝, 河田 有祐, 塩田 康祥, 大久保 圭祐, 田井 真砂子, 中村 心, 岡本 憲太郎, 青木 秀之, 二井 広平, 宮島 彩, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.11  (NPO)日本歯周病学会

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  • 家族性リポ蛋白リパーゼ欠損症および2型糖尿病に罹患した重度慢性歯周炎患者に対する非外科的歯周治療の効果を実感した一症例

    千神 八重子, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.11  (NPO)日本歯周病学会

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  • 人工関節置換術の周術期における早期からの口腔感染管理が奏功した慢性歯周炎患者の一症例

    小川 侑子, 山本 総司, 佐藤 公麿, 峠 亜也香, 宮岡 満奈, 向井 麻里子, 児玉 由佳, 竹本 奈奈, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.11  (NPO)日本歯周病学会

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  • 血清IgG抗体価検査がスクリーニング、早期診断および管理につながった侵襲性歯周炎患者の22年間経過症例

    大森 一弘, 大山 秀樹, 河野 隆幸, 冨川 知子, 清水 明美, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.11  (NPO)日本歯周病学会

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  • 咬合挙上と自家骨移植が治療ポイントとなった重度慢性歯周炎患者症例

    中村 心, 井手口 英隆, 佐々木 禎子, 峯柴 淳二, 下江 正幸, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.11  (NPO)日本歯周病学会

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  • 口腔細菌の特定と口腔治療が急性椎前部膿瘍の治癒に奏功した症例

    松永 一幸, 山城 圭介, 平田 千暁, 猪原 健, 大久保 圭祐, 磯島 大地, 坂井田 京佑, 大森 一弘, 山本 直史, 高柴 正悟, 竹丸 誠, 下江 豊, 栗山 勝

    日本歯周病学会会誌  2017.11  (NPO)日本歯周病学会

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  • Resolvin D2 induces root apex calcification via enhancing DMP-1 expression in rat periapical periodontitis model.

    Kawamura M, Yamamoto T, Yamashiro K, Shimoe M., Yoshihara C, Ideguchi H, Aoyagi H, Omori K, Takashiba S

    65th Japanese Association for Dental Research  2017 

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  • 歯科用ユニット給水管路汚染対策用の自動注水制御シミュレータの評価

    大久保 圭祐, 伊東 孝, 山本 一郎, 水谷 元, 伊東 昌洋, 田井 真砂子, 中村 心, 岡本 憲太郎, 塩田 康祥, 河田 有祐, 大森 一弘, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2017.10  (NPO)日本歯科保存学会

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  • 歯周病罹患の有無によるアテローム性動脈硬化病変の細菌叢のメタゲノム解析

    磯島 大地, 山城 圭介, 松永 一幸, 大森 一弘, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2017.10  (NPO)日本歯科保存学会

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  • 真菌二次代謝産物(+)-terreinはRANKL誘導性破骨細胞分化におけるNFATc1の発現を抑制する

    中川 沙紀, 大森 一弘, 山本 総司, 小林 寛也, 河村 麻理, 中村 亜里紗, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2017.5  (NPO)日本歯科保存学会

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  • インテグリンサブユニットの選択的制御による歯根膜細胞の遊走促進

    河村 麻理, 山本 直史, 山城 圭介, 平田 千暁, 青柳 浩明, 井手口 英隆, 大森 一弘, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2017.5  (NPO)日本歯科保存学会

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  • 患者視点からの歯周組織再生療法の選択基準

    畑中 加珠, 下江 正幸, 大森 一弘, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2017.5  (NPO)日本歯科保存学会

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  • 歯周病罹患の有無によるアテローム性動脈硬化病変部のマイクロバイオームの違い

    磯島 大地, 山城 圭介, 松永 一幸, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.4  (NPO)日本歯周病学会

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  • 真菌代謝産物terreinはAggregatibacter actinomycetemcomitans歯肉上皮感染時のIL-8産生を抑制する

    中村 亜里紗, 大森 一弘, 小林 寛也, 山本 総司, 中川 沙紀, 冨川 知子, 峯柴 史, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.4  (NPO)日本歯周病学会

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  • HMGB1が歯槽骨治癒に及ぼす影響

    青柳 浩明, 山城 圭介, 井手口 英隆, 平田 千暁, 河村 麻理, 下江 正幸, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.4  (NPO)日本歯周病学会

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  • 2型糖尿病患者に対する歯周治療の効果とSPT時の課題を実感した一症例

    高橋 麻里子, 大森 一弘, 千神 八重子, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2017.4  (NPO)日本歯周病学会

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  • Role of integrin isoforms during migration of periodontal ligament cells

    Kawamura M, Yamamoto T, Yamashiro K, Shimoe M., Yoshihara C, Ideguchi H, Aoyagi H, Omori K, Takashiba S

    95th International Association for Dental Research  2017 

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  • Fungal metabolite terrein suppresses IL-6/sIL-6R-induced CSF1 secretion in gingival fibroblasts.

    Yamamoto S, Omori K, Goto A, Kobayashi H, Nakagawa S, Nakamura A, Yamamoto D, Yamamoto T, Takashiba S

    95th International Association for Dental Research  2017 

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  • Osteogenic Differentiation Regulated by Rho-kinase in Periodontal Ligament Cells

    山本直史

    第37回岡山歯学会学術集会,岡山歯学会受賞講演  2016 

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    Event date: 2016.10.16

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  • 口腔細菌感染症を制御する機能性食品の探索

    伊東 昌洋, 大久保 圭祐, 伊東 孝, 河田 有祐, 塩田 康祥, 大森 一弘, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2016.10  (NPO)日本歯科保存学会

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  • 6根管を有する下顎第一大臼歯の根管治療と歯科用コーンビームCTの有用性

    海老沼 孝至, 坪井 綾香, 大久保 圭祐, 下江 正幸, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2016.10  (NPO)日本歯科保存学会

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  • 口腔バイオフィルム抑制用の多糖誘導体リン酸化プルランにおける歯面への付着と薬剤徐放性効果の機序解明

    伊東 孝, 塩田 康祥, 河田 有祐, 大久保 圭祐, 伊東 昌洋, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2016.9  (NPO)日本歯周病学会

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  • 薬剤性歯肉増殖の病態に酸化ストレスが及ぼす影響

    坪井 綾香, 大森 一弘, 下江 正幸, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2016.9  (NPO)日本歯周病学会

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  • 継続的な歯周支援治療が認知機能維持に及ぼす影響の検討 pilot study

    大森 一弘, 小林 寛也, 伊東 孝, 下江 正幸, 畑中 加珠, 園井 教裕, 福家 教子, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2016.9  (NPO)日本歯周病学会

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  • 抗Porphyromonas gingivalis IgG血症の診断に関わる抗原タンパク質の選定

    田井 真砂子, 冨川 知子, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯科医師会雑誌  2016.8  (公社)日本歯科医師会

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  • 男女・年齢別歯科関連行動と歯周病原細菌の感染度との関連

    坪井 綾香, 江口 依里, 畑中 加珠, 大森 一弘, 山本 直史, 荻野 景規, 高柴 正悟

    日本歯科医師会雑誌  2016.8  (公社)日本歯科医師会

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  • 歯周病原細菌に対する指尖血漿IgG抗体価検査が感染性心内膜炎(IE)の起炎菌推定に繋がった症例

    磯島 大地, 松永 一幸, 工藤 値英子, 伊東 孝, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯科医師会雑誌  2016.8  (公社)日本歯科医師会

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  • Type-I Pepsin-Solubilized Collagen from Bohadschia Bivittata Enhanced hPDLFs Cells Viability

    Siddiqui DY, Omori K, Ito T, Yamamoto T, Arief ME, Takashiba S

    94th International Association for Dental Research  2016 

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  • Anti-HMGB1 neutralization antibody attenuates inflammatory cytokine secretion and progression of periodontitis

    Yoshihara C, Yamashiro K, , Yamamoto T, Ideguchi H, Aoyagi H, Shimoe M., Hongo S, Kawamura M, Ryu M, Nishibori M, Takashiba S

    94th International Association for Dental Research  2016 

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  • Effects of Zoledronic Acid in Periodontitis by Molecular Imaging

    Ideguchi H, Yamamoto T, Yamashiro K, Shimoe M., Hongo S, Yoshihara C, Aoyagi H, Kawamura M, Takashiba S

    94th International Association for Dental Research  2016 

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    Event date: 2016.6.22 - 2016.6.24

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  • 海藻由来レクチンを用いた口腔バイオフィルム感染症の制御

    塩田 康祥, 伊東 孝, 河田 有祐, 大久保 圭祐, 伊東 昌洋, 今村 幸治, 大森 一弘, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2016.6  (NPO)日本歯科保存学会

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  • 歯根・歯槽骨が吸収した下顎第二大臼歯に対する智歯移植前の根管処置症例の考察

    海老沼 孝至, 大森 一弘, 前田 博史, 下江 正幸, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2016.6  (NPO)日本歯科保存学会

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    Event date: 2016.6

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  • 口唇閉鎖不全を有する元ハンセン病患者の嚥下時の舌運動に関する研究

    高知 信介, 宮崎 みづき, 園井 教裕, 山本 直史, 高柴 正悟

    日本ハンセン病学会雑誌  2016.4  日本ハンセン病学会

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    Event date: 2016.4

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  • 先天性ネフローゼ症候群患者の薬物性歯肉増殖症への対応

    梶谷 明子, 下江 正幸, 井手口 英隆, 峯柴 淳二, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2016.4  (NPO)日本歯周病学会

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    Event date: 2016.4

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  • 実験的歯周炎モデルマウスにおける抗HMGB1抗体の歯周炎抑制効果

    吉原 千暁, 山城 圭介, 山本 直史, 井手口 英隆, 青柳 浩明, 下江 正幸, 本郷 昌一, 河村 麻理, 高柴 正悟

    日本歯周病学会会誌  2016.4  (NPO)日本歯周病学会

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  • 真菌由来代謝産物(+)-terreinはヒト歯肉線維芽細胞におけるinterleukin-6誘導性SHP2-Aktシグナル活性を抑制する

    山本 総司, 大森 一弘, 後藤 絢香, 小林 寛也, 中川 沙紀, 中村 亜里紗, 冨川 知子, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2016.4  (NPO)日本歯周病学会

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    Event date: 2016.4

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  • インテグリン発現による歯根膜細胞の遊走制御

    河村 麻理, 山本 直史, 山城 圭介, 吉原 千暁, 本郷 昌一, 下江 正幸, 大森 一弘, 高柴 正悟

    日本歯周病学会会誌  2016.4  (NPO)日本歯周病学会

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  • 細菌感染度を指標とした包括的歯周治療中の広汎型重度慢性歯周炎患者の免疫反応性

    本郷 昌一, 冨川 和哉, 下江 正幸, 青柳 浩明, 河野 隆幸, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2016.4  (NPO)日本歯周病学会

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  • 多血小板血漿を併用した自家骨移植が奏功した重度慢性歯周炎患者症例の考察

    大森 一弘, 河野 隆幸, 下江 正幸, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2016.4  (NPO)日本歯周病学会

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  • 歯周病細菌に対する指尖血漿IgG抗体価検査が感染性心内膜炎の起炎菌推定に繋がった症例

    磯島 大地, 松永 一幸, 工藤 値英子, 伊東 孝, 大森 一弘, 山本 直史, 高柴 正悟

    岡山歯学会雑誌  2015.12  岡山歯学会

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    Event date: 2015.12

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  • 真菌由来代謝産物(+)-terreinはRANKL誘導性破骨細胞分化を抑制する

    中川 沙紀, 大森 一弘, 山本 総司, 小林 寛也, 後藤 絢香, 中村 亜里紗, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2015.11  (NPO)日本歯科保存学会

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    Event date: 2015.11

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  • Smad2 and ROCK signaling as Potential Therapeutic Targets for Periodontal Regeneration

    Yamamoto T

    63rd Japanese Association for Dental Research  2015 

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    Event date: 2015.10.30 - 2015.10.31

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  • 咬合崩壊した慢性歯周炎患者における口腔機能回復治療時の留意点

    佐藤公麿,佐藤毅,下江正幸,山本直史,高柴正悟

    日本歯周病学会中国四国三大学日本臨床歯周病学会中国支部合同研修会  2015 

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    Event date: 2015.10.12

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  • 歯周病原細菌に対する指尖血漿IgG抗体価検査が感染性心内膜炎の起炎菌推定に繋がった一症例

    磯島 大地, 松永 一幸, 工藤 値英子, 伊東 孝, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2015.8  (NPO)日本歯周病学会

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  • 悪習癖の除去によって歯周状態を著しく改善できた中等度慢性歯周炎患者の一症例

    高知 信介, 峯柴 淳二, 下江 正幸, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2015.8  (NPO)日本歯周病学会

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  • 自家歯牙移植を応用した口腔機能回復治療症例の臨床的考察

    佐藤 公麿, 田井 真砂子, 吉原 千暁, 本郷 昌一, 山本 直史, 高柴 正悟

    広島医学  2015.8  広島医学会

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  • 高齢者に対してライフステージを考慮したインプラントメインテナンスを行っている一症例

    向井 麻理子, 佐藤 公麿, 小川 侑子, 田中 亜也香, 宮岡 満奈, 兒玉 由佳, 竹本 奈奈, 山本 直史, 高柴 正悟

    日本歯科衛生学会雑誌  2015.8  日本歯科衛生学会

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  • 骨格性下顎前突症を伴う広汎型重度慢性歯周炎患者に対し外科的矯正治療を併用した包括的歯周治療を行った一症例

    佐藤 公麿, 下江 正幸, 河野 隆幸, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2015.8  (NPO)日本歯周病学会

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  • ハンセン病元患者の歯周管理に関する考察

    園井 教裕, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2015.8  (NPO)日本歯周病学会

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  • 上顎切歯歯冠部に発症した内部吸収の一症例

    青柳 浩明, 下江 正幸, 峯柴 淳二, 山本 直史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2015.6  (NPO)日本歯科保存学会

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    Event date: 2015.6

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  • ROCK阻害剤は歯根膜細胞の遊走を促進する

    河村 麻理, 山本 直史, 吉原 千暁, 松永 一幸, 井手口 英隆, 本郷 昌一, 下江 正幸, 大森 一弘, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2015.6  (NPO)日本歯科保存学会

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  • 骨吸収抑制剤としてのビスフォスフォネート製剤が歯周炎組織へ及ぼす影響

    井手口 英隆, 山本 直史, 下江 正幸, 本郷 昌一, 青柳 浩明, 吉原 千暁, 河村 麻里, 高柴 正悟

    日本歯周病学会会誌  2015.4  (NPO)日本歯周病学会

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    Event date: 2015.4

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  • 生体の反応を確認しつつ歯周-矯正-補綴治療を行った広汎型侵襲性歯周炎の一症例

    下江 正幸, 岩本 義博, 冨川 和哉, 大森 一弘, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2015.4  (NPO)日本歯周病学会

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  • 真菌由来代謝産物(+)-terrein誘導体がIL-6誘導性VEGFおよびCSF-1の産生に及ぼす影響の検討

    山本 総司, 大森 一弘, 後藤 絢香, 池田 淳史, 小林 寛也, 中川 沙紀, 山本 大介, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2015.4  (NPO)日本歯周病学会

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  • IL-6/sIL-6R Enhances Cathepsin-B Secretion via Caveolin-1-mediated ERK1/2 in Gingival Fibroblasts

    Goto A, Omori K, Yamaguchi T, Kobayashi T, Yamamoto T, Maeda H, Takashiba S

    93th International Association for Dental Research  2015 

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    Event date: 2015.3.11 - 2015.3.14

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  • Follistatin induces proliferation of CD49f+ cells isolated from Salivary Glands

    Ikeda A, Yamamoto T, Mineshiba J, Takashiba S.

    93th International Association for Dental Research  2015 

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    Event date: 2015.3.11 - 2015.3.14

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  • 血清中ビタミンCの欠乏が原因の一つと考える歯肉増殖症患者の歯周治療経過

    河村 麻理, 大森 一弘, 秋山 謙太郎, 下江 正幸, 山本 直史, 高柴 正悟

    岡山歯学会雑誌  2014.12  岡山歯学会

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  • 細菌感染度を指標にした包括的歯周治療による広汎型重度慢性歯周炎患者の治療経過

    塩田康祥,伊東孝,河田有祐,大久保圭祐,今村幸治,山本直史,前田博史,高柴正悟

    日本歯周病学会中国四国三大学日本臨床歯周病学会中国支部合同研修会  2014 

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    Event date: 2014.11.9

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  • 海藻ミル由来のレクチンを用いた口腔感染制御システムの検討

    塩田 康祥, 伊東 孝, 河田 有祐, 大久保 圭祐, 今村 幸治, 山本 直史, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2014.10  (NPO)日本歯科保存学会

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  • 真菌由来代謝産物(+)-terreinはinterleukin-6誘導性colony stimulating factor-1の遺伝子発現を抑制する

    山本 総司, 大森 一弘, 後藤 絢香, 池田 淳史, 松永 一幸, 山本 大介, 山本 直史, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2014.10  (NPO)日本歯科保存学会

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  • 下顎に破壊的な歯槽骨吸収を伴う広汎型重度慢性歯周炎患者に対して歯周外科と歯周補綴を行った一症例

    本郷 昌一, 冨川 和哉, 下江 正幸, 山本 直史, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2014.9  (NPO)日本歯周病学会

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    Event date: 2014.9

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  • 歯周組織再生療法と口腔機能回復治療が奏功した咬合崩壊の過程にあった慢性歯周炎患者の一症例

    佐藤 公麿, 冨川 和哉, 冨川 知子, 山本 直史, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2014.9  (NPO)日本歯周病学会

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    Event date: 2014.9

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  • HMGB1は歯肉上皮細胞におけるE-Cadherinの発現を抑制する

    吉原 千暁, 山城 圭介, 山本 直史, 下江 正幸, 本郷 昌一, 高知 信介, 井手口 英隆, 河村 麻里, 青柳 浩明, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2014.9  (NPO)日本歯周病学会

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    Event date: 2014.9

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  • マッシュルーム粗抽出物による口腔感染制御能を有した機能性食品の開発

    伊東 孝, 今村 幸治, 塩田 康祥, 河田 有祐, 大久保 圭祐, 高知 信介, 峯柴 淳二, 山本 直史, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2014.6  (NPO)日本歯科保存学会

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    Event date: 2014.6

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  • 歯周病安定期治療中に心筋梗塞を発症したマルチプルリスクファクターシンドロームを有する慢性歯周炎患者の一症例

    山本総司,下江正幸,山本直史,岩本義博,前田博史,高柴正悟

    第3回日本歯周病学会四国地区臨床研修会  2014 

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    Event date: 2014.4.6

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  • 脆弱な歯肉を有する侵襲性歯周炎患者の治療例とリスク因子の考察

    青柳浩明,前田博史,小林芳友,澤田弘一,河野隆幸,清水明美,大森一弘,峯柴淳二,山本直史,下江正幸,高柴正悟

    第3回日本歯周病学会四国地区臨床研修会  2014 

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    Event date: 2014.4.6

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  • グリチルリチン酸経口投与によるin vivo歯周組織治癒効果

    井手口 英隆, 山城 圭介, 山本 直史, 本郷 昌一, 下江 正幸, 高知 信介, 青柳 浩明, 吉原 千暁, 河村 麻里, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2014.4  (NPO)日本歯周病学会

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    Event date: 2014.4

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  • 薬物性歯肉増殖症を併発した慢性歯周炎患者の感染制御による管理

    冨川 知子, 後藤 絢香, 下江 正幸, 峯柴 淳二, 山本 直史, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2014.4  (NPO)日本歯周病学会

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    Event date: 2014.4

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  • 侵襲性歯周炎患者に対しての感染モニタリングによる長期間管理症例

    山城 圭介, 杉 典子, 下江 正幸, 山本 直史, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2014.4  (NPO)日本歯周病学会

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  • Oral biofilm inhibition effect and the cytotoxicity test of codium fragile extract

    Shiota Y, Ito T, Yoshida Y, Mineshiba J, Yamamoto T, Omori K, Kawata Y, Yamamoto D, Kochi S, Nakamura A, Okubo K, Imamura K, Takeuchi H, Takashiba S

    10th Asian Pacific Society of Periodontology Meeting  2013 

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    Event date: 2013.9.3

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  • Aggregatibacter actinomycetemcomitans Y4はintegrin α5を介して細胞内に侵入する

    高知 信介, 山城 圭介, 山本 直史, 本郷 昌一, 下江 正幸, 冨川 和哉, 鵜川 祐樹, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2013.9  (NPO)日本歯周病学会

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  • 生体腎移植患者の周術期口腔感染管理を病病連携にて行った1例

    佐藤 公麿, 河村 麻里, 吉原 千暁, 峯柴 淳二, 山本 直史, 高柴 正悟, 曽我 賢彦

    広島医学  2013.8  広島医学会

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  • 歯肉上皮においてSmad2はintegrin発現を促進する

    本郷 昌一, 山城 圭介, 山本 直史, 高知 信介, 下江 正幸, 冨川 和哉, 鵜川 祐樹, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2013.5  (NPO)日本歯科保存学会

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    Event date: 2013.5

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  • Methanobrevibactor oralisおよびヒトのグループIIシャペロニンに対する免疫応答の解析

    平井 公人, 前田 博史, 山城 圭介, 大森 一弘, 峯柴 淳二, 山本 直史, 苔口 進, 高柴 正悟

    日本歯周病学会会誌  2013.4  (NPO)日本歯周病学会

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  • Overexpression of Smad2 Enhances FGF2 Expression in Periodontal Ligament Cells

    Ugawa Y, Yamamoto T, Yamashiro K, Hongo S, Ideguchi H, Shimoe M, Tomokawa K, Kochi S, Maeda H, Takashiba S

    91th International Association for Dental Research  2013 

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    Event date: 2013.3.22 - 2013.3.24

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  • Integrin α5 Regulates Cell Adhesion in Gingival Epithelium during Infection

    Kochi S, Yamashiro K, Yamamoto T, Hongo S, Shimoe M, Tomikawa K, Ugawa Y, Maeda H, Takashiba S

    91th International Association for Dental Research  2013 

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    Event date: 2013.3.22 - 2013.3.24

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  • TGF-β Signaling Enhances Cell Adhesion in Gingival Epithelial Cells

    Hongo S, Yamashiro K, Yamamoto T, Kochi S, Shimoe M, Tomikawa K, Ugawa Y, Maeda H, Takashiba S

    91th International Association for Dental Research  2013 

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    Event date: 2013.3.22 - 2013.3.24

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  • ROCK regulates extracellular matrix-mediated osteogenic differentiation of periodontal ligament cells

    Y. UGAWA*, T. YAMAMOTO, K. YAMASHIRO, M. SHIMOE, K. TOMIKAWA, S. HONGO, S. KOCHI, H. MAEDA, and S. TAKASHIBA

    60th Japanese Association for Dental Research  2012 

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    Event date: 2012.12.14 - 2012.12.15

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  • Smad2過剰発現が歯根膜線維芽細胞に及ぼす影響

    井手口 英隆, 山本 直史, 山城 圭介, 鵜川 祐樹, 本郷 昌一, 下江 正幸, 高知 信介, 前田 博史, 高柴 正悟

    岡山歯学会雑誌  2012.12  岡山歯学会

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    Event date: 2012.12

    Language:Japanese  

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  • 歯根膜線維芽細胞においてSmad2はFGF2遺伝子発現を促進する

    鵜川 祐樹, 山本 直史, 山城 圭介, 下江 正幸, 冨川 和哉, 本郷 昌一, 高知 信介, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2012.10  (NPO)日本歯科保存学会

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    Event date: 2012.10

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  • 人工骨移植を行い長期間安定した予後が得られた広汎型侵襲性歯周炎の症例

    前田 博史, 清水 明美, 澤田 弘一, 峯柴 淳二, 山本 直史, 高柴 正悟

    日本歯周病学会会誌  2012.9  (NPO)日本歯周病学会

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    Event date: 2012.9

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  • 外科的矯正治療を併用した包括的歯周治療を行っている重度広汎型慢性歯周炎患者の一症例

    佐藤公麿,下江正幸,山口知子,峯柴淳二,山本直史,前田博史,高柴正悟

    日本歯周病学会中国地区臨床研修会  2012 

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    Event date: 2012.7.8

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  • 自家骨移植にPRPを応用した歯周組織再生療法を行い良好に経過している重度広汎型慢性歯周炎患者の一症例

    井手口英隆,下江正幸,山本直史,岩本義博,冨川和哉,山城圭介,前田博史,高柴正悟

    日本歯周病学会中国地区臨床研修会  2012 

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    Event date: 2012.7.8

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  • Aggregatibacter actinomycetemcomitansおよび抗菌薬添加がヒト歯肉上皮細胞の細胞接着因子に及ぼす影響

    高知 信介, 山城 圭介, 山本 直史, 本郷 昌一, 下江 正幸, 冨川 和哉, 鵜川 祐樹, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2012.5  (NPO)日本歯科保存学会

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    Event date: 2012.5

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  • 歯肉上皮細胞においてSmad2/3は細胞接着分子と細胞外基質の発現を促進する

    本郷 昌一, 山城 圭介, 山本 直史, 高知 信介, 下江 正幸, 冨川 和哉, 鵜川 祐樹, 塩見 信行, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2012.4  (NPO)日本歯周病学会

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    Event date: 2012.4

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  • アクチン細胞骨格を制御するRho kinaseが歯根膜線維芽細胞の硬組織形成細胞への分化に及ぼす影響

    鵜川 祐樹, 山本 直史, 山城 圭介, 下江 正幸, 冨川 和哉, 本郷 昌一, 高知 信介, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2012.4  (NPO)日本歯周病学会

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    Event date: 2012.4

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  • 歯周病細菌感染度を評価しながら包括的歯周治療を行った広汎型侵襲性歯周炎患者の一症例

    冨川 和哉, 河野 隆幸, 山本 直史, 岩本 義博, 下江 正幸, 鵜川 祐樹, 本郷 昌一, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2011.9  (NPO)日本歯周病学会

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    Event date: 2011.9

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  • 再生療法と骨整形術を併用して臼歯部に限局した不整な骨吸収に対応した慢性歯周炎の症例

    高知 信介, 冨川 和哉, 岩本 義博, 山本 直史, 宮本 学, 山城 圭介, 峯柴 淳二, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2011.9  (NPO)日本歯周病学会

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    Event date: 2011.9

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  • 歯肉上皮細胞において外因性Smad2は細胞接着分子の発現を促進する

    本郷 昌一, 山城 圭介, 山本 直史, 下江 正幸, 冨川 和哉, 鵜川 祐樹, 高知 信介, 塩見 信行, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2011.9  (NPO)日本歯周病学会

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    Event date: 2011.9

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  • Aggregatibacter actinomycetemcomitansがヒト歯肉上皮細胞の細胞接着因子に及ぼす影響

    高知 信介, 山城 圭介, 山本 直史, 本郷 昌一, 下江 正幸, 冨川 和哉, 鵜川 祐樹, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2011.9  (NPO)日本歯科保存学会

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    Event date: 2011.9

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  • 歯根膜細胞の分化過程におけるBMPとWntシグナルへのRho kinasesの影響

    鵜川 祐樹, 山本 直史, 山城 圭介, 下江 正幸, 冨川 和哉, 本郷 昌一, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2011.5  (NPO)日本歯科保存学会

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    Event date: 2011.5

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  • Smad2による歯肉創傷治癒の再上皮化抑制

    冨川 和哉, 山本 直史, 下江 正幸, 塩見 信行, 峯柴 淳二, 山口 知子, 本郷 昌一, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2011.4  (NPO)日本歯周病学会

  • Cell proliferation regulated by over-expressing Smad2 in gingival epithelial cells in vitro

    Shimoe M, Yamamoto T, Shiomi N, Tomikawa K, Ugawa Y, Hongo S, Yamaguchi T, Mineshiba J, Maeda H, Takashiba S

    96th American Academy of Periodontology  2010 

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    Event date: 2010.10.31

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  • 生活習慣病と歯周病の重症度との関連性

    本郷昌一,目黒道生,畑中加珠,冨川和哉,山本直史,前田博史,高柴正悟

    岡山歯学会  2010 

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    Event date: 2010.9.26

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  • 歯周病原細菌に対して高応答性の広汎型侵襲性歯周炎患者の治療経過と病態考察

    下江 正幸, 山本 直史, 岩本 義博, 冨川 和哉, 前田 博史, 高柴 正悟

    日本歯周病学会会誌  2010.9  (NPO)日本歯周病学会

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  • Osteogenic differentiation regulated by Rho kinase in periodontal ligament cells

    Yamamoto T, Ugawa U, Senoo K, Shimoe M, Tomikawa K, Hongo S, Maeda H, Takashiba S

    88th International Association for Dental Research  2010 

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    Event date: 2010.7.15

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  • ショットガンクローニング法によるPorphyromonas gingivalisからのsmall noncoding RNAの同定

    山部 こころ, 前田 博史, 樋口 彩子, 園井 教裕, 目黒 道生, 谷本 一郎, 山本 直史, 成石 浩司, 苔口 進, 高柴 正悟

    日本歯周病学会会誌  2009.9  (NPO)日本歯周病学会

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  • 根尖性歯周炎が易感染性患者の敗血症に関与することが示唆された一例

    目黒 道生, 曽我 賢彦, 工藤 値英子, 山本 直史, 前田 博史, 西村 英紀, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2009.5  (NPO)日本歯科保存学会

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    Event date: 2009.5

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  • Rho kinasesによる歯根膜細胞の分化制御

    山本 直史, 鵜川 祐樹, 妹尾 京子, 峯柴 淳二, 前田 博史, 高柴 正悟

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2009.5  (NPO)日本歯科保存学会

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  • 酵母one-hybrid法によるTNF-α発現を制御する新規転写因子の検索

    村田 裕美, 山本 直史, 明貝 文夫, 小柳津 功介, 清水 明美, 前田 博史, 新井 英雄, 高柴 正悟

    日本歯周病学会会誌  2007.8  (NPO)日本歯周病学会

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  • Effects of FIP-2 Isolated from Rat Wounded Pulp on Inflammatory Regulators and Cell Death

    SENOO Kyoko, YAMAMOTO Tadashi, MYOKAI Fumio, YAMASHIRO Keisuke, ARAI Hideo, NISHIMURA Fusanori, TAKASHIBA Shogo

    日本歯科保存学雑誌 = THE JAPANESE JOURNAL OF CONSERVATIVE DENTISTRY  2007.5.7 

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    Event date: 2007.5.7

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  • Effects on Inflammatory Signals by rFIP-2 Induced in Wounded Pulp

    Senoo K, *Yamamoto T, Myokai F, Yamashiro K, Arai H, Nishimura F, Takashiba S

    85th International Association for Dental Research  2007 

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    Event date: 2007.3.20 - 2007.3.22

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  • Transcription of rFIP-2 is Regulated by Alternative Use of Promoters

    *Yamamoto T, Myokai F, Senoo K, Yamashiro K, Arai H, Nishimura F, Takashiba S

    84th International Association for Dental Research  2006 

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    Event date: 2006.6.28 - 2006.6.30

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  • Characterization of hNIP-7 Isolated from Stretch-Stressed Human Periodontal Ligament Fibroblasts

    Senoo K, Myokai F, *Yamashiro K, Yamamoto T, Nishimura F, Takashiba S

    84th International Association for Dental Research  2006 

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    Event date: 2006.6.28 - 2006.6.30

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  • 大島青松園における口腔ケアの現状および今後の課題

    福家教子, *山本直史, 岩田梢, 平田千津留, 大藪美久仁, 山下満徳, 市原新一郎, 木村龍二, 新盛英世, 長尾榮治

    第8回病院歯科介護研究会総会・学術講演会  2005 

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    Event date: 2005.10.9

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  • 大島青松園におけるHCV感染の現状と対策(第二報)

    市原新一郎, 長尾榮治, 小林一夫, 長町典夫, 河西純, 十河英世, 福家教子, *山本直史, 新盛英世

    第74回瀬戸内集談会  2005 

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    Event date: 2005.7.21

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  • Inhibition of Smad2 expression affects palatal fusion

    Shiomi N, Cui XM, Saito T, *Yamamoto T, Shuler CF

    83rd International Association for Dental Research  2005 

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    Event date: 2005.3.9 - 2005.3.11

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  • MAP kinases mediate NNN-induced inhibition of palatal fusion

    Saito T, Cui XM, *Yamamoto T, Shiomi N, Shuler CF

    83rd International Association for Dental Research  2005 

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    Event date: 2005.3.9 - 2005.3.11

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  • Co-localization of phospho-Smad2 and p66shc in MEE during palatal fusion

    *Yamamoto T, Cui XM, Lee MK, Smith SM, Takashiba S, Shuler CF

    83rd International Association for Dental Research  2005 

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    Event date: 2005.3.9 - 2005.3.11

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  • Overexpression of Smad2 in Tgf-&#61538;3-null mutant mice rescues cleft palat

    Cui XM, Shiomi N, Saito T, *Yamamoto T, Chai Y, Shuler CF

    83rd International Association for Dental Research  2005 

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    Event date: 2005.3.9 - 2005.3.11

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  • Exhaustive Gene Expression Analysis in Cultured Human Periodontal Ligament Fibroblasts by Mechanical Stress

    YAMASHIRO Keisuke, MYOKAI Fumio, SENOO Kyoko, YAMAMOTO Tadashi, ARAI Hideo, NISHIMURA Fusanori, TAKASHIBA Shogo

    日本歯科保存学雑誌 = THE JAPANESE JOURNAL OF CONSERVATIVE DENTISTRY  2004.10.18 

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    Event date: 2004.10.18

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  • Generation of a transgenic mouse model expressing TGF-b3 inducible GFPcre

    *Yamamoto T, Kwang S, Cui XM, Shuler CF

    82nd International Association for Dental Research  2004 

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    Event date: 2004.3.11 - 2004.3.13

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  • Effect of N'-nitrosonornicotine (NNN) on murine palatal fusion in vitro

    Saito T, Cui XM, *Yamamoto T, Schmid D, Shiomi N, Shuler CF

    82nd International Association for Dental Research  2004 

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    Event date: 2004.3.11 - 2004.3.13

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  • Role of ERK1/2 signaling during EGF-induced inhibition of palatal fusion

    *Yamamoto T, Cui XM, Shuler CF

    81st International Association for Dental Research  2003 

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    Event date: 2003.6.25 - 2003.6.27

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  • Regulation of palatal fusion

    Shuler CF, Cui XM, Mogass M, Schmid D, Chen JC, Beak SH, Nakajima A, Yamazaki K, Yamamoto T, Bahiri N, Dalrymple K

    The Proceedings of International Symposium of Oral Science in Tsurumi University School of Dental Medicine  2001 

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    Event date: 2001.7.1

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  • TGF-beta3 intracellular signaling is required for inhibition of MEE proliferation

    Cui XM, Chen J, Yamamoto T, Mogass M, Chai Y, Shuler CF

    79th International Association for Dental Research  2001 

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    Event date: 2001.6.30

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  • Periodontal conditions of patients with severe compromised hosts

    Sawada S, 84th American Academy of Periodontology A, Fujimoto C, Mineshiba J, Kurihara M, Yamamoto T, Katayama T, Sugi N, Fujinami M, Sawada K, Kokeguchi S, Nishimura F, Takashiba S, Murayama Y

    2000 

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    Event date: 2000.9.17

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  • Differentially expressed gene induced by mechanical stress in periodontal ligament cells

    Myokai F, Ohira T, Yamamoto T, Nishimura F, Arai H, Takashiba S, Murayama Y

    78th International Association for Dental Research  2000 

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    Event date: 2000.4.5

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  • Unique genes expressed in fibroblasts from human periodontal ligament in vitro

    Yamamoto T, Takashiba S, Myokai F, Ohira T, Wasio N, Nishimura F, Arai H, Murayama Y

    11th International Conference on Periodontal Research  1999 

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    Event date: 1999.6.17

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  • Possible role of serum and glucocorticoid-lnducible kinase during craniofacial-oral-dental development.

    F Myokai, T Ohira, T Yamamoto, K Naruishi, F Nishimura, H Arai, S Takashiba, Y Murayama

    JOURNAL OF DENTAL RESEARCH  1999.5  AMER ASSOC DENTAL RESEARCH

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    Event date: 1999.5

    Language:English  

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  • Role of serum and glucocorticoid-inducible kinase during craniofacial-oral-dental development

    Myokai F, Ohira T, Yamamoto T, Naruishi K, Nishimura F, Arai H, Takashiba S, Murayama Y

    46th Japanese Association for Dental Research  1998 

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    Event date: 1998.12.28

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  • Study of Unique Genes Expressed by Mechanical Stress in Human Periodontal Ligament Fibroblasts

    MYOKAI Fumio, OHIRA Taisuke, YAMAMOTO Tadashi, MINESHIBA Junji, WASHIO Norifumi, NARUISHI Koji, ARAI Hideo, NISHIMURA Fusanori, TAKASHIBA Shogo, MURAYAMA Yoji

    Journal of the Japanese Association of Periodontology  1998.9.15  The Japanese Society of Periodontology

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    Event date: 1998.9.15

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  • Expression Pattern of Serum and Glucocorticoid-Inducible Kinase (sgk) during Rat Dental Hard Tissue Formation

    OHIRA Taisuke, MYOKAI Fumio, NARUISHI Koji, YAMAMOTO Tadashi, ARAI Hideo, NISHIMURA Fusanori, TAKASHIBA Shogo, MURAYAMA Yoji

    日本歯科保存学雑誌  1998.5.1 

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    Event date: 1998.5.1

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  • Genes Specifically Expressed by Fibroblasts Isolated from Periodontal Ligament

    YAMAMOTO Tadashi, TAKASHIBA Shogo, MYOKAI Fumio, TAKIGAWA Masayuki, WASHIO Norifumi, NISHIMURA Fusanori, ARAI Hideo, MURAYAMA Yoji

    Journal of the Japanese Association of Periodontology  1998.4.15  The Japanese Society of Periodontology

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    Event date: 1998.4.15

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  • Chemotactic Event of Human Periodontal Ligament Fibroblasts are Dependent on Certain Phases of Cell Cycle

    Asahara Yoji, Nishimura Fusanori, Washio Norifumi, Chou Hsin-Hua, Yamamoto Tadashi, Arai Hideo, Takashiba Shogo, Murayama Yoji

    Journal of the Japanese Association of Periodontology  1996.3.25  The Japanese Society of Periodontology

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    Event date: 1996.3.25

    Language:Japanese  

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  • 歯科ユニット給水管路(DUWL)内汚染の実際と電解機能水の効果

    上田 彩華, 伊東-信田 有希, 大森 一弘, 伊東 孝, 大久保 圭祐, 平井 公人, 山本 直史, 高柴 正悟

    第42回 岡山歯学会学術集会  2021.11.28 

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  • ⼦宮全摘出・卵巣⽚側摘出直後から急性化した 重度慢性⻭周炎症例の病態考察

    坂井田京佑, 大森一弘, 佐光秀文, 永田千晶, 山本直史, 高柴正悟

    ⽇本⻭周病学会中国四国3⼤学・ ⽇本臨床⻭周病学会中国四国⽀部合同研修会  2021.11.28 

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  • 歯内治療が原因で菌血症となった単心室症患者の症例報告とその対応策の提案

    児玉 加奈子, 井手口 英隆, 岡本 憲太郎, 佐光 秀文, 松本 俊樹, 大森 一弘, 山本 直史, 高柴 正悟

    第42回 岡山歯学会学術集会  2021.11.28 

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  • 大豆発酵食品テンペによる口腔感染症の制御

    伊東 昌洋、伊東 孝、中村 心、青木 秀之、西岡 功志、塩川 つぐみ、多田 宏子、竹内 祐貴、武安 伸幸、山本 直史、高柴 正悟

    第28回日本未病学会学術総会  2021.11.21 

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  • 不妊治療中患者における歯周病原細菌の感染度調査 ―血清IgG抗体価検査を応用したパイロット研究―

    永田千晶, 大森一弘, 佐光秀文, 坂井田京佑, 井手口英隆, 池田淳史, 徳善真砂子, 平井公人, 畑中加珠, 山本直史, 滝川雅之, 三宅貴仁, 高柴正悟

    第28回日本未病学会学術総会  2021.11.20 

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  • 侵襲性歯周炎の血液診断マーカー候補となる細胞外小胞由来マイクロRNAとその炎症誘導機構

    森彩乃, 山本直史, 井手口英隆, 河村麻理, 河本美奈, 伊東昌洋, 小野喜章, 中山真彰, 山城圭介, 大森一弘, 高柴正悟

    第42回日本炎症・再生医学会  2021.7.7 

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  • 歯肉増殖を伴う早期発症型歯周炎の家族症例 ~臨床的, 細菌学的免疫学的, 病理学的観察~

    大室博正, 滝川雅之, 岡村和則, 西村英紀, 成石浩司, 澤孝賢, 山本直史, 大平泰資, 高橋慶壮, 郭淑娟, 高柴正悟, 村山洋二

    第106回日本歯科保存学会春季大会  1997.6.6 

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Awards

  • IADR/AADR William J. Gies Awards

    2021.7   Functionalized Graphene Oxide Shields Tooth Dentin from Decalcification

    Nizami MZI, Nishina Y, Yamamoto T, Shinoda-Ito Y, Takashiba S

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  • 岡山歯学会優秀論文賞

    2015.9   岡山歯学会  

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  • 日本歯周病学会奨励賞

    2004.5   日本歯周病学会  

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Research Projects

  • 細胞外小胞の口腔トロピズムを基軸とする侵襲性歯周炎の病態解明と診断への応用展開

    Grant number:21H03119  2021.04 - 2025.03

    日本学術振興会  科学研究費助成事業 基盤研究(B)  基盤研究(B)

    山本 直史

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    Grant amount:\16900000 ( Direct expense: \13000000 、 Indirect expense:\3900000 )

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  • 患者自身が管理するPHR を活用した安全安心な歯科医療環境の構築

    2020

    日本歯科医学会  プロジェクト研究費 

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  • Development of periodontal tissue regeneration therapy for horizontal alveolar bone resorption with collagen-binding FGF-2

    Grant number:19H03831  2019.04 - 2023.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

    高柴 正悟, 松下 治, 平山 晴子, 山本 直史, 美間 健彦

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    Grant amount:\17030000 ( Direct expense: \13100000 、 Indirect expense:\3930000 )

    本研究は,水平性骨吸収に対する歯周組織再生療法を実現するために,既に歯科臨床で応用されている塩基性線維芽細胞増殖因子(bFGF)と細菌由来のコラーゲン結合ドメイン(CBD)を組み合わせた融合タンパク質(CBFGF)を用いた研究である。本研究の目的は,CBFGFの最適化とイヌを用いた実験モデルによる非臨床試験データの取得である。2019年度は,認可済みのbFGF製剤に合わせて,CBFGFを組換融合型から架橋型へ変更するための実験とイヌの骨欠損モデルを用いた実験を実施した。まず,CBFGFの最適化について,架橋反応の比率・濃度などの反応条件を決定するために,多量のbFGFとCBDを要した。そこで,大腸菌生産系を用いてbFGFとCBDを精製し,実験効率の改善を図った。現在は,CBDとbFGFを架橋する適切な条件を探索しているところである。また,イヌを用いた実験モデルでは,歯周組織再生療法の適応症である垂直性骨欠損(2壁性)で組換融合型CBFGFの有効性を実証し,水平性骨欠損および垂直性骨欠損(1壁性)を作製して,組換融合型CBFGFを投与した。現在,動物へのタンパク質の投与は終了し,一部のサンプルはCT撮影まで行っている。
    また,組換融合型CBFGFについてこれまでに得られたデータについては,研究発表(Takashiba S, International Academy of Periodontology, 2019;Nakamura S, et al, International Association of Dental Research, General Session & Exhibition, 2019;岡本ら,日本歯科保存学会,2019;高柴,BioJapan 2019)を行って,今後の研究の進め方やCBFGFの製剤化に関して,様々な研究者や企業と情報交換を行った。

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  • 細胞外小胞による生体ネットワークの解明と医療への応用

    2019

    岡山大学  次世代研究育成グループ事業 

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  • 幹細胞ニッチの制御を目指したインテグリンペプチド療法の開発

    Grant number:18K09576  2018.04 - 2021.03

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    山本 直史, 小林 寛也, 山城 圭介, 高柴 正悟

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    Grant amount:\4420000 ( Direct expense: \3400000 、 Indirect expense:\1020000 )

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  • Inflamm-agingを中心とした歯周病,サルコペニア,糖尿病の病態解明

    Grant number:18K09598  2018.04 - 2021.03

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    小林 寛也, 山本 直史, 山城 圭介, 高柴 正悟

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    Grant amount:\4420000 ( Direct expense: \3400000 、 Indirect expense:\1020000 )

    サルコペニア予防は高齢者の要介護度を低下させるために重要な課題である。申請者らは,近年提唱されている炎症性老化の概念に着目し,慢性炎症性疾患である歯周病が,筋組織の治癒過程,インスリン抵抗性に及ぼす影響とその制御メカニズムの一端を,老齢マウスを用いた歯周炎モデルに用いて明らかにすることを目的に研究を行なっている。平成30年度に行った研究成果は以下の通りである。
    ①歯周炎/筋損傷モデルマウスの作製:C57BL/6J(健康)とTALLYHO/JngJ(糖尿病)の老齢マウスの第二大臼歯に歯周病原細菌Porphyromonas gingivalis(P.g.)を浸漬させた絹糸を3週間結紮した後に,前脛骨筋に筋損傷を惹起させる塩化バリウムを注射した。
    ②歯槽骨吸収量の定量:小動物用マイクロスX線スキャナを用いて調べた。
    ③マウスの炎症状態のモニタリング:好中球に特異的なミエロペルオキシダーゼ(MPO)活性に反応して発光するXenolight Redject Inflammation Probeを使用したin vivoイメージングシステム(IVIS)を用いて解析した。
    研究を開始した平成30年度は,上記事項に加えて筋損傷後の血清中の炎症性サイトカインを網羅的に解析し,歯周病または糖尿病の有無で発現パターンを比較する予定であったが,まだ開始できていない。理由としては,筋損傷モデルマウスの確立が不完全なためである。引き続きモデルマウスの確立を進めていくが,時間を要するようであれば,確立方法を変更することも検討していく。

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  • Functional analysis of HMGB1 as an inflammatory mediator in periodontitis

    Grant number:16K20670  2016.04 - 2018.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)  Grant-in-Aid for Young Scientists (B)

    YAMASHIRO KEISUKE, AOYAGI Hiroaki, IDEGUCHI Hidetaka, KOCHI Shinsuke, YAMAMOTO Tadashi, TAKASHIBA Shogo, WAKE Hidenori, NISHIBORI Masahiro

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    Grant amount:\3900000 ( Direct expense: \3000000 、 Indirect expense:\900000 )

    High mobility group box 1 (HMGB 1) is a DNA binding protein, but it plays as an inflammatory mediator when it is secreted extracellularly due to tissue damage or necrosis. The detailed mechanism of how HMGB1 affects the progress of periodontitis has not been elucidated. As a result of this study, it was revealed that HMGB1 was produced from gingival epithelial cells, macrophage-like cells by inflammatory stimulation. In addition, by administering anti-HMGB 1 antibody to periodontitis model mice, inflammation due to periodontitis is suppressed. As a result, migration of neutrophils, production of IL-1βwere suppressed and the bone resorption by periodontitis was suppressed.

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  • Inflamm-agingとして歯周病が及ぼすサルコペニアへの影響の解明

    2015

    小林孫兵衛記念医学振興財団  研究助成金 

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  • Induction of Migration of Periodontal Ligament Cells by Selective Regulation of Integrin Expression

    Grant number:26463134  2014.04 - 2017.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    Yamamoto Tadashi

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    Grant amount:\4810000 ( Direct expense: \3700000 、 Indirect expense:\1110000 )

    Periodontal ligament cells (PDLCs) are multipotent cells that can differentiate into osteogenic cells. It is necessary to induce migration of PDLCs for regeneration and homeostasis of periodontal tissue. Cell migration is regulated by local microenvironment, defined by coordination between soluble factors and extracellular matrix (ECM). Integrin-mediated cell adhesion to ECM provides essential signals for cell migration. To determine adhesion molecules responsible for migration of PDLCs, we examined expression profiles of integrin and ECM, and the integrin isoform-specific regulation of migration of PDLCs. The array analysis indicated that mRNA of integrin α2, α3, α4, and α5 were increased in migrating PDLCs. Anti-integrin α3 antibody and blocking peptides significantly increased migration of PDLCs, conversely anti-integrin α5 antibody decreased. Therefore, specific inhibition of integrin α3 may be useful to induce migration of PDLCs during regeneration of periodontal tissue.

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  • 唾液腺体性幹細胞とiPS細胞を用いた唾液腺機能再生に関する研究

    Grant number:25463217  2013.04 - 2014.03

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    峯柴 淳二, 大森 一弘, 山本 直史, 高柴 正悟

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    Grant amount:\4940000 ( Direct expense: \3800000 、 Indirect expense:\1140000 )

    【研究の目的】唾液は,口腔感染制御を含めて口腔内環境を保つ重要な働きを持つ。しかし唾液を分泌する唾液腺は,自己再生能が低く,障害後の機能回復は難しい。我々は,CD49F+細胞がin vitroではINHIBIN βA,INHIBIN βB,FOLLISTATINを発現することを報告している。INHIBINのβ鎖はホモ二量体を構成し,ACTIVIN分子と成る。一方FOLLISTATINは,ACTIVINに特異的に結合し,その受容体への結合を阻害する。本研究は,マウス顎下腺の主排泄導管を結紮後に解除すると顎下腺が再生することを利用し,in vivoにおいて唾液腺組織再生中のCD49F,INHIBIN βA,INHIBIN βB,そしてFOLLISTATINの発現局在の解明を目的とした。
    【研究実施計画および結果】
    マウス顎下腺の片側の排泄導管を血管結紮用クリップで結紮,他方は対照とし,6日後に結紮を解除した。結紮解除1,2,4,8,16日後の顎下腺を摘出し,パラフィン包埋切片作製の後,INHIBIN βA,INHIBIN βB,CD49FそしてFOLLISTATINの局在を免疫組織染色法で検討した。その結果,結紮解除後のどの日数でもINHIBIN βAは染色されず,INHIBIN βBとCD49fは染色された。また,結紮解除後8日目にはFOLLISTATINが染色された。さらに連続切片上で,CD49F,INHIBIN βB,そしてFOLLISTATINが同部位で染色された。以上から,結紮解除後8日目以降の唾液腺組織再生に,CD49F+細胞でのactivin-follistatin相互作用の関与を想定できる。
    以上から本研究を行った結果,マウス顎下腺主排泄導管結紮解除後8日目の導管上皮細胞で,CD49F,INHIBIN βB,FOLLISTATINが発現していることが解明された。

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  • 「分子イメージング・マイクロドーズ(第0相)臨床試験体制を擁する分子標的治療研究・教育拠点の構築」事業

    2013

    岡山大学  特別経費(プロジェクト分) 

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  • Construction of the prevention system of a Bisphosphonate-Related Osteonecrosis of the Jaw judging from an intraoral infection degree

    Grant number:23593058  2011 - 2013

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    HATANAKA KAZU, TAKASHIBA Shogo, YAMAMOTO Todashi, YAMASHIRO Keisuke

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

    The phenomenon of osteonecrosis of the jaw (ONJ) has been reported in the cancer patient who has received medication of the bisphosphonate (BP) to bone metastases. In Okayama University Hospital, the oral hygienist has been stationed in the Center for Clinical Oncology, and investigated the intraoral trouble. As a result, the Center use patients and the number of interviews by oral hygienist are increasing year by year, and were able to find six ONJ newly in three years. Those patients are followed up in the Department of Periodontics and Oral Surgery. Moreover, many of other chemotherapy patients had the symptom of stomatitis.

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  • Cell cycle atlas of periodontium

    Grant number:23659977  2011 - 2013

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research  Grant-in-Aid for Challenging Exploratory Research

    YAMAMOTO Tadashi, TAKASHIBA Shogo, HATANAKA Kazu, YAMASHIRO Keisuke, YAMAGUCHI Tomoko

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    Grant amount:\3510000 ( Direct expense: \2700000 、 Indirect expense:\810000 )

    Fucci transgenic mice constitutively expressing cell-cycle probes are important tools to analyze the spatiotemporal transition of the cell-cycles in periodontium, especially, are useful to visualize the cell-cycles of undifferentiated mesenchymal cells and gingival epithelial cells. The molecular imaging employing Fucci technology demonstrated that a series of active enzymes produced by neutrophil during periodontal inflammation would induce G1-arrest of the cell-cycle of periodontal cells.

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  • The molecular biological analysis of the mechanism for cell adhesion mediated by growth factor in human gingival epithelial cells

    Grant number:22890119  2010 - 2011

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Research Activity start-up  Grant-in-Aid for Research Activity start-up

    YAMASHIRO Keisuke, YAMAMOTO Tadashi, TAKASHIBA Shogo

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    Grant amount:\2977000 ( Direct expense: \2290000 、 Indirect expense:\687000 )

    Periodontal disease, chronic inflammation disease, is caused by infection of periodontal pathogen. It is thought that about 80% of Japanese are affected and it is a major cause of tooth loss. It is still unknown that the difference of progression of periodontal disease for each patient. It is thought that the attachment between gingival epithelial cells and tooth is a physical barrier from infection, and this attachment is important for prevention of periodontal disease. In this study, we hypothesis that growth factors secretes from gingival epithelial cells regulate the attachment between gingival epithelial cells and tooth, and we investigate the mechanism about the regulation.

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  • 細胞骨格分子を介した歯根膜幹細胞の増殖・分化制御に関する研究

    2010

    両備てい園記念財団  生物学研究助成 

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  • Healing mechanism of rat experimental periapical lesions targeting laminin γ2 expression

    Grant number:20592226  2008 - 2010

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    HATANAKA Kazu, YAMAMOTO Tadashi, TAKASHIBA Shougo, SHIMOE Masayuki, YAMAGUCHI Tomoko, NARUISHI Koji, KAKO Aya

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    Grant amount:\4420000 ( Direct expense: \3400000 、 Indirect expense:\1020000 )

    We have previously reported that cellular matrix laminin and inflammatory cytokine IL-1αgenes increased during periapical healing phase in a rat periapical periodontitis. In this study, we investigated the effect of these molecules to osteoblast that play a central role in bone formation. Our findings the enhancement of integrin α3 expression by IL-1α and the attachment of osteoblasts to laminin after stimulation with IL-1α suggest an important mechanism for adherence of osteoblasts in periapical healing.

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  • Investigation of the mechanisms of osteogenic differentiation by RhoA in periodontal ligament cells for cell transplantation

    Grant number:20592429  2008 - 2010

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    YAMAMOTO Tadashi, TAKASHIBA Shogo, MINESHIBA Junji, YAMASHIRO Keisuke, NARUISHI Koji, SHIOMI Nobuyuki, SONOYAMA Wataru

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

    In periodontal ligament cells (PDL cells), cytoskeletal signaling regulated by Rho-ROCK is critical in the differentiation process, and the expression of osteogenic genes such as BMP-4, Wnt3a, and Wnt5a. Meanwhile over-expression of RhoA or ROCK showed significant low cell proliferation, suggesting that PDL cells differentiation is coordinately regulated by Rho-ROCK induced cytoskeletal molecules, as well as soluble growth factors and extracellular matrix.

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  • Smad2 transgenic miceを用いた歯肉上皮創傷治癒に関する研究

    2008

    岡山大学大学院GP(医療系大学院高度臨床専門医養成コース)  研究計画に基づく研究費 

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  • 創傷歯髄から単離した新規遺伝子FIP-2による歯髄炎症のコントロール法の探索

    Grant number:18799006  2006 - 2007

    日本学術振興会  科学研究費助成事業 若手研究(B)  若手研究(B)

    山本 直史

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    Grant amount:\3200000 ( Direct expense: \3200000 )

    歯髄組織の保存および象牙質の再生を促進するためには,歯髄炎症を分子生物学的アプローチからコントロールすることが有効であると考えられる。本年度は,ラット創傷歯髄から単離した新規遺伝子FIP-2の発現抑制による歯髄炎症のコントロールを目標として,FIP-2が制御する炎症性シグナル分子機構および細胞死への影響を調べた。
    FIP-2に特異的なsiRNAを含む発現ベクターをラット腎臓細胞に遺伝子導入・薬剤選択培養し,FIP-2を発現抑制した細胞株(FIP-2KD)を確立した。FIP-2-KDおよびMockの細胞株をそれぞれ無刺激または過酸化水素にて刺激し,細胞内蛋白の発現変化を抗体アレイで解析し,制御因子の相互関係をIngenuity Signaling Pathways Knowledge Baseを用いてパスウェイ解析を行った。
    Mockに比較してFIP-2-KDでは,一連の細胞増殖因子mitogen activated protein kinase(MAPKS),myelocytosis(MYC),細胞周期制御因子cyclin dependent kinase(CDKS),そしてcell division cycle(CDCS)のシグナルが増強していた。また,細胞死制御因子であるCaspasesのシグナルが減弱していた。一方,過酸化水素で刺激下では,一連の細胞周期制御因子,細胞増殖因子,そして細胞死制御因子の発現が,顕著に抑制されており,DNAの断片化を示すTUNEL陽性細胞はFIP-2-KDにおいて著しく少なかった。
    以上の結果から,FIP-2は,炎症性反応のなかで発現増加し,細胞死を促進させる因子であることが示唆された。FIP-2を局所的に発現抑制することは歯髄の炎症反応の改善に役立つ可能性がある。

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  • エクソソームによる侵襲性歯周炎患者の病態解析 ~パイロット研究~

    The Japanese Society of Periodontology  2017 JSP Planning survey Research 

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  • 幹細胞ニッチを制御する歯科再生材料の開発

    Japan Agency for Medical Research and Development  AMED under Grant Number JP18lm0203008 

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  • 血中エクソソームを標的とした侵襲性歯周炎のナノ診断システムの開発

    Japan Agency for Medical Research and Development  AMED under Grant Number JP19lm0203008 

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Class subject in charge

  • Periodontal/Oral Medicine (2022academic year) 1st semester  - 木3,木4

  • Periodontal/Oral Medicine (2022academic year) 1st semester  - 木3~4

  • Clinical training:Pathophysiology of Oral Infection and Inflammation (2022academic year) special  - その他

  • Lecture and Research Projects:Pathophysiology of Oral Infection and Inflammation (2022academic year) special  - その他

  • Oral Infection and Immunology (2022academic year) Third semester  - 火2~3

  • Research Projects and Practice: Periodontal Science I (2022academic year) special  - その他

  • Lecture and Research Projects: Periodontal Science I (2022academic year) special  - その他

  • Research Projects and Practice: Periodontal Science II (2022academic year) special  - その他

  • Lecture and Research Projects: Periodontal Science II (2022academic year) special  - その他

  • Periodontology and Periodontics (2022academic year) Fourth semester  - 火2,火3

  • Clinical training:Specialty Training for Advanced Periodontics (2022academic year) special  - その他

  • Lecture and Research Projects:Specialty Training for Advanced Periodontics (2022academic year) special  - その他

  • Clinical training:Specialty Training for Advanced Endodontics (2022academic year) special  - その他

  • Lecture and Research Projects:Specialty Training for Endodontics (2022academic year) special  - その他

  • Endodontology and Endodontics (2022academic year) Fourth semester  - 木4

  • Periodontal/Oral Medicine (2021academic year) Fourth semester  - 木3,木4

  • Clinical training:Pathophysiology of Oral Infection and Inflammation (2021academic year) special  - その他

  • Lecture and Research Projects:Pathophysiology of Oral Infection and Inflammation (2021academic year) special  - その他

  • Interdisciplinary Research and Clinic (2021academic year) Third semester  - 月1,月2

  • Research Projects and Practice: Periodontal Science I (2021academic year) special  - その他

  • Lecture and Research Projects: Periodontal Science I (2021academic year) special  - その他

  • Research Projects and Practice: Periodontal Science II (2021academic year) special  - その他

  • Lecture and Research Projects: Periodontal Science II (2021academic year) special  - その他

  • Periodontology and Periodontics (2021academic year) Fourth semester  - 火3,火4

  • Periodontology and Periodontics (2021academic year) Fourth semester  - 火2,火3

  • Periodontology and Periodontics (2021academic year) Fourth semester  - 火3,火4

  • Clinical training:Specialty Training for Advanced Periodontics (2021academic year) special  - その他

  • Lecture and Research Projects:Specialty Training for Advanced Periodontics (2021academic year) special  - その他

  • Clinical training:Specialty Training for Advanced Endodontics (2021academic year) special  - その他

  • Lecture and Research Projects:Specialty Training for Endodontics (2021academic year) special  - その他

  • Endodontology and Endodontics (2021academic year) Fourth semester  - 木4

  • Clinical training:Pathophysiology of Oral Infection and Inflammation (2020academic year) special  - その他

  • Lecture and Research Projects:Pathophysiology of Oral Infection and Inflammation (2020academic year) special  - その他

  • Interdisciplinary Research and Clinic (2020academic year) Third semester  - 月1,月2

  • Periodontology and Periodontics (2020academic year) Fourth semester  - 火3,火4

  • Periodontology and Periodontics (2020academic year) Fourth semester  - 火2,火3

  • Clinical training:Speciality Training of Periodontics for Periodontal Disease an (2020academic year) special  - その他

  • Lecture and Research Projects:Speciality Training of Periodontics for Periodonta (2020academic year) special  - その他

  • Clinical training:Speciality Training of Endodontics for Pulpal and Endodotinc L (2020academic year) special  - その他

  • Lecture and Research Projects:Speciality Training of Endodontics for Pulpal and (2020academic year) special  - その他

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