Faculty Profiles - EKUNI Daisuke

MISC - EKUNI Daisuke

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ラット歯周炎モデルにおける肝病変に及ぼすブラッシングの影響

三部俊博, 友藤孝明, 江國大輔, 山中怜子, 東哲司, 玉木直文, 山本龍生, 渡邊達夫, 宮内睦美, 高田隆

日本歯周病学会会誌 49 ( 春季特別 ) 177 - 177 2007.4

ラット歯肉細胞の細胞増殖活性に対する通電刺激の影響

東哲司, 友藤孝明, 江國大輔, 三部俊博, 山本龍生, 渡邊達夫, 鼻戸由美

日本歯周病学会会誌 49 ( 春季特別 ) 163 - 163 2007.4

ラット歯槽骨の骨密度に及ぼす高コレステロール食摂取の影響

友藤孝明, 江國大輔, 東哲司, 三部俊博, 山本龍生, 渡邊達夫

日本歯周病学会会誌 49 ( 春季特別 ) 174 - 174 2007.4

Location of proliferating gingival cells following toothbrushing stimulation

T. Tomofuji, T. Sakamoto, D. Ekuni, T. Yamamoto, T. Watanabe

ORAL DISEASES 13 ( 1 ) 77 - 81 2007.1

Language：English Publisher：BLACKWELL PUBLISHING

OBJECTIVES: Mechanical stimulation by toothbrushing promotes healing of gingivitis through accelerating cell proliferation. Junctional epithelium proliferates at periodontal pocket formation. A question is arisen whether toothbrushing contributes to the repair of gingival inflammation or deterioration of pocket formation. The location of proliferating cells in gingiva stimulated mechanically by toothbrushing was investigated.
MATERIALS AND METHODS: A total of 24 teeth of dogs underwent daily plaque removal with a curette (plaque removal) or both plaque removal and toothbrushing (toothbrushing). Proliferative activity of gingival cells in six individual zones was evaluated by assaying expression of proliferating cell nuclear antigen (PCNA).
RESULTS: Toothbrushing increased densities of PCNA-positive basal cells in the junctional epithelium, connective tissues adjacent to the junctional epithelium, the alveolar bone of the oral epithelial side and the oral epithelium. However, the densities of PCNA-positive cells at the apical portion of the junctional epithelium, connective tissues adjacent to the cementum and the alveolar bone of the periodontal ligament side did not increase following toothbrushing.
CONCLUSIONS: Toothbrushing promotes proliferation of gingival cells other than fibroblasts in periodontium and basal cells in the apical portion of the junctional epithelium. The repair of periodontal tissues might be promoted by toothbrushing within the limit of the direct mechanical stimulation.

DOI： 10.1111/j.1601-0825.2006.01250.x

Location of proliferating gingival cells following toothbrushing stimulation

T. Tomofuji, T. Sakamoto, D. Ekuni, T. Yamamoto, T. Watanabe

ORAL DISEASES 13 ( 1 ) 77 - 81 2007.1

Language：English Publisher：BLACKWELL PUBLISHING

DOI： 10.1111/j.1601-0825.2006.01250.x

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歯周疾患と脂肪肝

山本龍生, 江國大輔, 友藤孝明

総合臨牀 56 ( 10 ) 2827 - 2876 2007

ラット歯周炎モデルに対するアミノ酸配合歯磨剤の効果

三部俊博, 草野弘揮, 江國大輔, 東哲司, 山中玲子, 友藤孝明, 山本龍生, 渡邊達夫

口腔衛生学会雑誌 = JOURNAL OF DENTAL HEALTH 56 ( 4 ) 453 - 453 2006.8

Regulation of epithelial cell growth factor receptor protein and gene expression using a rat periodontitis model

D. Ekuni, J. D. Firth, E. E. Putnins

JOURNAL OF PERIODONTAL RESEARCH 41 ( 4 ) 340 - 349 2006.8

Language：English Publisher：BLACKWELL PUBLISHING

Background and Objective: Regulation of epithelial cell behavior associated with periodontitis is not well elucidated but many responses will ultimately be regulated by growth factor receptors. Using a rat experimental periodontitis model, protein and gene expression of select growth factor receptors in junctional and pocket epithelium were examined.
Material and Methods: Periodontal disease was induced by daily topical application of lipopolysaccharide using an established protocol. Animals were killed at time 0 (control), and at 2 and 8 wk. Frozen tissue samples were collected from the right palatal gingival soft tissue, and the left periodontal tissues were decalcified and embedded in paraffin. Laser microdissection and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to quantify keratinocyte growth factor receptor (KGFR), hepatocyte growth factor receptor (HGFR), epidermal growth factor receptor (EGFR) and fibroblast growth factor receptor 1 (FGFR1) gene expression, and in situ RT-PCR localized these increases to specific epithelial cells. Receptor protein expression was examined immunohistochemically. In cell culture, induction of HGFR and KGFR protein expression by serum, lipopolysaccharide and pro-inflammatory cytokines were examined using flow cytometry.
Results: Eight-week tissue samples exhibited histological changes consistent with periodontitis. KGFR and HGFR gene and protein expression were significantly induced at the 8 wk time point. KGFR expression was significantly up-regulated in basal and parabasal pocket epithelial cells, but HGFR was up-regulated throughout the pocket epithelium. In cell culture serum, lipopolysaccharide and pro-inflammatory cytokines, interleukin-1 beta and tumour necrosis factor-alpha significantly induced KGFR protein receptor expression, but HGFR expression was only induced by serum.
Conclusion: KGFR and HGFR are highly up-regulated in this model of periodontal disease and may play a significant role in regulating the proliferation and migration of pocket epithelium.

DOI： 10.1111/j.1600-0765.2006.00881.x

Oxidative damage of periodontal tissue in the rat periodontitis model: Effects of a high-cholesterol diet International journal

T Tomofuji, T Azuma, H Kusano, T Sanbe, D Ekuni, N Tamaki, T Yamamoto, T Watanabe

FEBS LETTERS 580 ( 15 ) 3601 - 3604 2006.6

Language：English Publisher：ELSEVIER SCIENCE BV

Studies suggest an association between consumption of a high-cholesterol diet and periodontitis. We addressed the mechanism by which high dietary cholesterol could be detrimental to periodontal health in a rat model. Feeding a high-cholesterol diet augmented the effects of bacterial pathogens and their products (e.g., lipopolysaccharide and proteases) on production of pro-inflammatory cytokines in fibroblasts. High dietary cholesterol also increased mitochondrial 8-hydroxydeoxyguanosine in the periodontal tissues. These results suggest that excessive tissue oxidative damage induced by high dietary cholesterol could potentiate pro-inflammatory cytokine production by fibroblasts stimulated with bacterial pathogens. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

DOI： 10.1016/j.febslet.2006.05.041

ラット歯周炎モデルのTNF-αとIL-1βの産生に対する高コレステロール食の影響

東哲司, 友藤孝明, 草野弘揮, 江國大輔, 山本龍生, 渡邊達夫

岡山歯学会雑誌 25 ( 1 ) 9 - 10 2006.6

A high cholesterol diet induces alveolar bone loss via RANKL expression and independent of the IL-1β and TNF-α signals in rats

EKUNI Daisuke, TOMOFUJI Takaaki, YAMANAKA Reiko, KUSANO Hiroki, AZUMA Tetsuji, SANBE Toshihiro, YAMAMOTO Tatsuo, WATANABE Tatsuo

48 ( 春季特別 ) 187 - 187 2006.3

Effects of toothbrushing on plasma lipopolysaccharide concentration in the rat periodontitis model

AZUMA Tetsuji, TOMOFUJI Takaaki, EKUNI Daisuke, YAMANAKA Reiko, KUSANO Hiroki, SANBE Toshihiro, YAMAMOTO Tatsuo, WATANABE Tatsuo

48 ( 春季特別 ) 175 - 175 2006.3

RNA integrity and in situ RT-PCR in dento-alveolar tissues after microwave accelerated demineralisation International journal

D Ekuni, JD Firth, EE Putnins

ARCHIVES OF ORAL BIOLOGY 51 ( 2 ) 164 - 169 2006.2

Language：English Publisher：PERGAMON-ELSEVIER SCIENCE LTD

Objective: The structural organization of oral soft tissue and its relationship with highly calcified teeth are difficult to preserve unless tissues are decalcified, paraffin embedded and subsequently sectioned. However, enamel decalcification time and its negative impact on RNA integrity makes it difficult to effectively analyse in situ gene expression. This study examined the impact of microwave-enhanced decalcification on processing time, RNA integrity and detection of in situ mRNA expression in hard and soft tissue for cell type specific markers of Keratinocyte growth factor receptor, Scleraxis and Osteonectin.
Design: Maxillas and mandibles were obtained from three mate Wistar strain rats. Right side tissues were decalcified using a microwave plus 10% EDTA solution (M+) while left side tissues were decalcified in 10% EDTA solution alone (M-).
Results: Microwave use reduced decalcification time by up to 50% and had no significant impact on morphology, RNA quality and in situ detection of gene expression relative to the M-group.
Conclusions: In situ RT-PCR gene expression of microwave decalcified paraffin-embedded oral tissues is an effective technique to localize in situ gene expression while maintaining excellent soft and hard tissue architecture. (c) 2005 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.archoralbio.2005.06.010

Spatial extent of proliferation of oral sulcular epithelium by toothbrushing

Sakamoto T, Horiuchi M, Tomofuji T, Ekuni D, Yamamoto T, Watanabe T

Int J Oral Health 2006

ラット歯周炎モデルに対するビタミンC配合歯磨剤の効果

友藤孝明, 草野弘揮, 東哲司, 三部俊博, 山中玲子, 江國大輔, 山本龍生, 渡邊達夫

日本歯周病学会会誌 48 ( 3 ) 201 - 207 2006

Language：Japanese Publisher：(NPO)日本歯周病学会

ビタミンCの経口摂取が歯周炎に有効であることが疫学研究により報告されている。ビタミンCによる歯周炎の組織変化を知ることは、歯周炎の予防・治療を考える上で有用である。本研究では、ビタミンC配合歯磨剤の効果を、ラット歯周炎モデルを用いて組織学的に検討した。8週齢のラット50匹を用いた。ラットの上顎第一臼歯の歯肉溝に、1日1回、歯周炎誘発物質(リポポリサッカライドとプロテアーゼ)を塗布し、歯周炎を惹起した。塗布開始4週後にラットを5群に分け、歯周炎誘発物質に加えて0%(基材のみ:歯周炎群)、1%、2%、3%または5%のビタミンCを配合した歯磨剤を3週間塗布した。その結果、3%と5%のビタミンC配合群は歯周炎群よりも、結合組織の好中球数が有意に減少し、コラーゲン密度が著明に増加した。また、歯周組織における8-ヒドロキシデオキシグアノシン(酸化ストレスの指標)の発現は、歯周炎群よりもビタミンC配合群において有意に低かった。これらの結果から、3%以上のビタミンCを配合した歯磨剤は、歯周炎組織において好中球浸潤を軽減し、コラーゲン合成を促すことで炎症を軽減させること、また、1%以上のビタミンC配合歯磨剤は歯周炎における酸化ストレスを低下させることが示唆された。(著者抄録)

DOI： 10.2329/perio.48.201

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Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2006&ichushi_jid=J01095&link_issn=&doc_id=20061012330005&doc_link_id=%2Fcp9perlo%2F2006%2F004803%2F006%2F0201-0207%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcp9perlo%2F2006%2F004803%2F006%2F0201-0207%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Effects of a high-cholesterol diet on cell behavior in rat periodontitis

T Tomofuji, H Kusano, T Azuma, D Ekuni, T Yamamoto, T Watanabe

JOURNAL OF DENTAL RESEARCH 84 ( 8 ) 752 - 756 2005.8

Language：English Publisher：INT AMER ASSOC DENTAL RESEARCHI A D R/A A D R

Studies have shown an association between periodontitis and serum cholesterol levels. We hypothesized that high dietary cholesterol could influence periodontitis as a result of proliferation of the junctional epithelium. Rats were divided into 4 groups. Two groups were fed a regular diet, and 2 groups were fed a high-cholesterol diet. One of each dietary group was treated with periodontitis-inducing agents ( lipopolysaccharide and proteases), while the other was treated with pyrogen-free water. Feeding rats with a high-cholesterol diet induced an increase in blood total cholesterol and a decrease in high-density lipoprotein cholesterol. Proliferation of the junctional epithelium with increasing bone resorption was promoted by the consumption of a high-cholesterol diet. High dietary cholesterol further increased the cell-proliferative activity of the junctional epithelium induced by lipopolysaccharide and proteases. These results suggest that high dietary cholesterol can initiate and augment periodontitis in the rat periodontitis model.

DOI： 10.1177/154405910508400813

高コレステロール食がラット付着上皮の根尖側移動に与える影響

草野弘揮, 友藤孝明, 東哲司, 江國大輔, 山本龍生, 渡邊達夫

岡山歯学会雑誌 24 ( 1 ) 11 - 11 2005.6

歯肉溝へのLipopolysaccharideおよびプロテアーゼ投与によるラット肝組織の変化

友藤孝明, 東哲司, 草野弘揮, 江國大輔, 山本龍生, 渡邊達夫

日本歯周病学会会誌 47 ( 春季特別 ) 82 - 82 2005.3

Initial apical migration of junctional epithelium in rats following application of lipopolysaccharide and proteases International journal

D Ekuni, T Tomofuji, R Yamanaka, K Tachibana, T Yamamoto, T Watanabe

JOURNAL OF PERIODONTOLOGY 76 ( 1 ) 43 - 48 2005.1

Language：English Publisher：AMER ACAD PERIODONTOLOGY

Background: Apical migration of junctional epithelium (JE) occurs in association with periodontal pocket formation. The aim of this study was to investigate the gingival changes occurring during apical migration of the JE following application of factors associated with inflammatory periodontal disease pathogenesis.
Methods: Six-week-old male Wistar rats were divided into six groups: three experimental groups to investigate gingival changes following 2, 4, and 8 weeks topical application of lipopolysaccharide (LPS) and proteases and three control groups using pyrogen-free water. After 2, 4 or 8 weeks, nuclear DNA fragmentation was detected in periodontal ligament (PDL) fibroblasts using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method, and proliferative activities of the basal cells and fibroblasts were evaluated through expression of proliferating cell nuclear antigen (PCNA). Collagen destruction was examined histologically.
Results: Gingiva treated with LPS and proteases showed an increase in PCNA-positive basal cells but not the fibroblasts. Collagen destruction was observed at 2 weeks; apical migration of the JE and TUNEL-positive fibroblasts was seen at 4 weeks.
Conclusions: Following application of LPS and proteases to rat gingival sulci, the apical migration of the JE appears to occur simultaneously with the apoptosis of PDL fibroblasts, which in turn follows proliferation of the basal cells and collagen destruction.

DOI： 10.1902/jop.2005.76.1.43

Fibroblast proliferation and resultant increase in gingival tissue volume in rats fed a high-cholesterol diet.

Tomofuji T, Azuma T, Kusano H, Ekuni D, Sanbe T, Yamamoto T, Watanabe T

Int J Oral Health 2005

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