Porphyromonas gingivalisを口腔感染させたコラーゲン誘発関節炎モデルマウスの解析
目的 : 本研究は, Porphyromonas gingivalisの感染が関節リウマチ (RA) の増悪に与える影響について調べるため, RAモデルマウスとしてコラーゲン誘発関節炎モデルマウスを用いて検討した. 材料および方法 : RAモデルマウスとして, DBA/J1マウスの8週齢を用いた. 本マウスに, エマルジョンとしてウシⅡ型コラーゲンからなる抗原液とアジュバンドを調整後, 8週齢時に1回目, 11週齢時に2回目を感作させ関節炎を惹起させた. 実験群にはP. gingivalis ATCC33277株感染群 (n=12), ならびに対照群としてcarboxy methlcellul...
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| Published in | The Japanese Journal of Conservative Dentistry Vol. 61; no. 4; pp. 214 - 224 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | Japanese |
| Published |
特定非営利活動法人 日本歯科保存学会
2018
日本歯科保存学会 The Japanese Society of Conservative Dentistry |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0387-2343 2188-0808 |
| DOI | 10.11471/shikahozon.61.214 |
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| Abstract | 目的 : 本研究は, Porphyromonas gingivalisの感染が関節リウマチ (RA) の増悪に与える影響について調べるため, RAモデルマウスとしてコラーゲン誘発関節炎モデルマウスを用いて検討した. 材料および方法 : RAモデルマウスとして, DBA/J1マウスの8週齢を用いた. 本マウスに, エマルジョンとしてウシⅡ型コラーゲンからなる抗原液とアジュバンドを調整後, 8週齢時に1回目, 11週齢時に2回目を感作させ関節炎を惹起させた. 実験群にはP. gingivalis ATCC33277株感染群 (n=12), ならびに対照群としてcarboxy methlcellulose (CMC) 投与群 (n=12) の2群を設定した. P. gingivalisを2.5%CMCに懸濁して, 1日おきにマウスの口腔内に直接1×109CFU/mlの濃度で0.1ml投与した. 対照群は2.5%CMCを1日おきにマウスの口腔内に直接0.1ml投与した. 実験開始後から毎日, 関節炎臨床評価の経時的変化をSarkarらの方法を用いて評価した. また1週ごとに体重測定を行った. 42日目に下顎骨, 四肢の関節および血清を採取し, 以下の項目について検討した. P. gingivalisの感染を確認するために, 血清抗体価をELISAにて確認した. また, 関節リウマチの臨床マーカーであるmatrix metalloproteinase-3 (MMP-3), anti-cyclic citrullinated petide antibody (ACPA) 値をELISA法にて解析した. 下顎, 四肢のマイクロCTおよび組織学的形態を評価し, 膝関節はmatrix metalloproteinase-13 (MMP-13) 抗体を用い, 免疫組織染色を行った. 測定値は平均±標準偏差 (SD) で表し, 対照群と実験群間の有意差の検定にはMann-WhitneyのU検定を用い, p値が0.05未満で有意差ありと判定した. 結果 : 実験群においてP. gingivalisの血清抗体価は有意に増加し, 細菌感染を確認した. 実験群は対照群と比較し四肢末端の高度な発赤腫脹を認め, 関節炎臨床評価から42日後の実験群は対照群と比較し1.9倍関節炎Scoreの増加を認めた. マイクロCTによる解析では実験群において歯槽骨の骨吸収像を認め, 対照群と比較し有意に骨吸収の増加を認めた. 実験群の四肢末端の骨は腫脹, 変形および手根骨軟骨部の破壊, 膝関節表面と膝蓋骨の粗糙を呈した. また実験群のMMP-3値は, 対照群と比較し有意に増加した. 実験群のACPA活性値も, 対照群と比較し有意に増加した. 組織学的所見から, 実験群の膝関節組織は対照群と比較し高度な炎症性細胞の浸潤, 骨破壊像を認め, MMP-13による免疫染色においてパンヌスと関節半月にMMP-13陽性細胞を認めた. MMP-13陽性細胞数は対照群と比較して有意に増加した. 結論 : 本研究により, P. gingivalisによる口腔感染がコラーゲン誘発関節炎モデルマウスの組織破壊を促進することが示唆された. |
|---|---|
| AbstractList | 目的 : 本研究は, Porphyromonas gingivalisの感染が関節リウマチ (RA) の増悪に与える影響について調べるため, RAモデルマウスとしてコラーゲン誘発関節炎モデルマウスを用いて検討した. 材料および方法 : RAモデルマウスとして, DBA/J1マウスの8週齢を用いた. 本マウスに, エマルジョンとしてウシⅡ型コラーゲンからなる抗原液とアジュバンドを調整後, 8週齢時に1回目, 11週齢時に2回目を感作させ関節炎を惹起させた. 実験群にはP. gingivalis ATCC33277株感染群 (n=12), ならびに対照群としてcarboxy methlcellulose (CMC) 投与群 (n=12) の2群を設定した. P. gingivalisを2.5%CMCに懸濁して, 1日おきにマウスの口腔内に直接1×109CFU/mlの濃度で0.1ml投与した. 対照群は2.5%CMCを1日おきにマウスの口腔内に直接0.1ml投与した. 実験開始後から毎日, 関節炎臨床評価の経時的変化をSarkarらの方法を用いて評価した. また1週ごとに体重測定を行った. 42日目に下顎骨, 四肢の関節および血清を採取し, 以下の項目について検討した. P. gingivalisの感染を確認するために, 血清抗体価をELISAにて確認した. また, 関節リウマチの臨床マーカーであるmatrix metalloproteinase-3 (MMP-3), anti-cyclic citrullinated petide antibody (ACPA) 値をELISA法にて解析した. 下顎, 四肢のマイクロCTおよび組織学的形態を評価し, 膝関節はmatrix metalloproteinase-13 (MMP-13) 抗体を用い, 免疫組織染色を行った. 測定値は平均±標準偏差 (SD) で表し, 対照群と実験群間の有意差の検定にはMann-WhitneyのU検定を用い, p値が0.05未満で有意差ありと判定した. 結果 : 実験群においてP. gingivalisの血清抗体価は有意に増加し, 細菌感染を確認した. 実験群は対照群と比較し四肢末端の高度な発赤腫脹を認め, 関節炎臨床評価から42日後の実験群は対照群と比較し1.9倍関節炎Scoreの増加を認めた. マイクロCTによる解析では実験群において歯槽骨の骨吸収像を認め, 対照群と比較し有意に骨吸収の増加を認めた. 実験群の四肢末端の骨は腫脹, 変形および手根骨軟骨部の破壊, 膝関節表面と膝蓋骨の粗糙を呈した. また実験群のMMP-3値は, 対照群と比較し有意に増加した. 実験群のACPA活性値も, 対照群と比較し有意に増加した. 組織学的所見から, 実験群の膝関節組織は対照群と比較し高度な炎症性細胞の浸潤, 骨破壊像を認め, MMP-13による免疫染色においてパンヌスと関節半月にMMP-13陽性細胞を認めた. MMP-13陽性細胞数は対照群と比較して有意に増加した. 結論 : 本研究により, P. gingivalisによる口腔感染がコラーゲン誘発関節炎モデルマウスの組織破壊を促進することが示唆された. Purpose: This study examined the impact of Porphyromonas gingivalis infection on rheumatoid arthritis (RA) in collagen-induced arthritis model mice (RA model mice). Materials and methods: We used eight-week old DBA/J1 mice as the RA model mice. We prepared antigen solution and adjuvant from bovine type II collagen as an emulsion and sensitized the model mice at 8 and 11 weeks to induce arthritis. For the experimental group, we used a group infected with P. gingivalis ATCC33277 strain (n=12). For the control group, we used a carboxy methylcellulose (CMC) administered group (n=12). We suspended P. gingivalis in 2.5% CMC, and administered a 0.1 ml aliquot directly inside of the mouth of the mice every other day at the concentration of 1×109 CFU/ml. For the control group, we directly administered 0.1 ml of 2.5% CMC intraorally to the mice every other day. From the beginning of the experiment, we performed a clinical evaluation of arthritis every day using the method of Sarkar et al. Each week, we measured the body weight of the mice. On day 42, we sampled the mandible, joints from four limbs, and serum to examine the following items. To confirm P. gingivalis infection, we examined serum antibody titer with ELISA. We also analyzed MMP-3 and ACPA, which are clinical markers for rheumatoid arthritis, with ELISA. We evaluated micro CT images and the histological morphology of the mandibles and four limbs. The obtained results were statistically processed with Stat View software. Results: In the experimental group, serum antibody titer of P. gingivalis increased significantly, confirming the bacterial infection. The experimental group presented advanced redness and swelling in the extremities of four limbs compared to the control group. Forty-two days after the clinical evaluation of arthritis, the experimental group had an arthritis score that was 1.9 times greater than in the control group. The μCT analysis confirmed a significant increase in bone absorption in the experimental group compared to the control group through resorption images of alveolar bone. The experimental group exhibited swelling and bone deformation in the extremities of the four limbs, breaking of carpal cartilage, rough surface of knee joints, and rough surface of patella. MMP-3 values of the experimental group increased significantly compared to the control group. ACPA values of the experimental group also increased significantly compared to the control group. Knee joint tissues of the experimental group presented advanced invasion of inflammatory cells and damage to bones compared to the control group. MMP-13 immunostaining confirmed MMP-13 positive cells on the pannus and meniscus in the experimental group. The number of MMP-13 positive cells increased significantly compared to the control group. Conclusions: The results of this study suggested that oral infection of P. gingivalis accelerates destruction of the knee joints in collagen-induced arthritis model mice. 目的 : 本研究は, Porphyromonas gingivalisの感染が関節リウマチ (RA) の増悪に与える影響について調べるため, RAモデルマウスとしてコラーゲン誘発関節炎モデルマウスを用いて検討した. 材料および方法 : RAモデルマウスとして, DBA/J1マウスの8週齢を用いた. 本マウスに, エマルジョンとしてウシⅡ型コラーゲンからなる抗原液とアジュバンドを調整後, 8週齢時に1回目, 11週齢時に2回目を感作させ関節炎を惹起させた. 実験群にはP. gingivalis ATCC33277株感染群 (n=12), ならびに対照群としてcarboxy methlcellulose (CMC) 投与群 (n=12) の2群を設定した. P. gingivalisを2.5%CMCに懸濁して, 1日おきにマウスの口腔内に直接1×109CFU/mlの濃度で0.1ml投与した. 対照群は2.5%CMCを1日おきにマウスの口腔内に直接0.1ml投与した. 実験開始後から毎日, 関節炎臨床評価の経時的変化をSarkarらの方法を用いて評価した. また1週ごとに体重測定を行った. 42日目に下顎骨, 四肢の関節および血清を採取し, 以下の項目について検討した. P. gingivalisの感染を確認するために, 血清抗体価をELISAにて確認した. また, 関節リウマチの臨床マーカーであるmatrix metalloproteinase-3 (MMP-3), anti-cyclic citrullinated petide antibody (ACPA) 値をELISA法にて解析した. 下顎, 四肢のマイクロCTおよび組織学的形態を評価し, 膝関節はmatrix metalloproteinase-13 (MMP-13) 抗体を用い, 免疫組織染色を行った. 測定値は平均±標準偏差 (SD) で表し, 対照群と実験群間の有意差の検定にはMann-WhitneyのU検定を用い, p値が0.05未満で有意差ありと判定した. 結果 : 実験群においてP. gingivalisの血清抗体価は有意に増加し, 細菌感染を確認した. 実験群は対照群と比較し四肢末端の高度な発赤腫脹を認め, 関節炎臨床評価から42日後の実験群は対照群と比較し1.9倍関節炎Scoreの増加を認めた. マイクロCTによる解析では実験群において歯槽骨の骨吸収像を認め, 対照群と比較し有意に骨吸収の増加を認めた. 実験群の四肢末端の骨は腫脹, 変形および手根骨軟骨部の破壊, 膝関節表面と膝蓋骨の粗糙を呈した. また実験群のMMP-3値は, 対照群と比較し有意に増加した. 実験群のACPA活性値も, 対照群と比較し有意に増加した. 組織学的所見から, 実験群の膝関節組織は対照群と比較し高度な炎症性細胞の浸潤, 骨破壊像を認め, MMP-13による免疫染色においてパンヌスと関節半月にMMP-13陽性細胞を認めた. MMP-13陽性細胞数は対照群と比較して有意に増加した. 結論 : 本研究により, P. gingivalisによる口腔感染がコラーゲン誘発関節炎モデルマウスの組織破壊を促進することが示唆された. 「抄録」「目的」 : 本研究は, Porphyromonas gingivalisの感染が関節リウマチ (RA) の増悪に与える影響について調べるため, RAモデルマウスとしてコラーゲン誘発関節炎モデルマウスを用いて検討した. 「材料および方法」 : RAモデルマウスとして, DBA/J1マウスの8週齢を用いた. 本マウスに, エマルジョンとしてウシII型コラーゲンからなる抗原液とアジュバンドを調整後, 8週齢時に1回目, 11週齢時に2回目を感作させ関節炎を惹起させた. 実験群にはP. gingivalis ATCC33277株感染群 (n=12) , ならびに対照群としてcarboxy methlcellulose (CMC) 投与群 (n=12) の2群を設定した. P. gingivalisを2.5%CMCに懸濁して, 1日おきにマウスの口腔内に直接1×109CFU/mlの濃度で0.1ml投与した. 対照群は2.5%CMCを1日おきにマウスの口腔内に直接0.1ml投与した. 実験開始後から毎日, 関節炎臨床評価の経時的変化をSarkarらの方法を用いて評価した. また1週ごとに体重測定を行った. 42日目に下顎骨, 四肢の関節および血清を採取し, 以下の項目について検討した. P. gingivalisの感染を確認するために, 血清抗体価をELISAにて確認した. また, 関節リウマチの臨床マーカーであるmatrix metalloproteinase-3 (MMP-3) , anti-cyclic citrullinated petide antibody (ACPA) 値をELISA法にて解析した. 下顎, 四肢のマイクロCTおよび組織学的形態を評価し, 膝関節はmatrix metalloproteinase-13 (MMP-13) 抗体を用い, 免疫組織染色を行った. 測定値は平均±標準偏差 (SD) で表し, 対照群と実験群間の有意差の検定にはMann-WhitneyのU検定を用い, p値が0.05未満で有意差ありと判定した. 「結果」 : 実験群においてP. gingivalisの血清抗体価は有意に増加し, 細菌感染を確認した. 実験群は対照群と比較し四肢末端の高度な発赤腫脹を認め, 関節炎臨床評価から42日後の実験群は対照群と比較し1.9倍関節炎Scoreの増加を認めた. マイクロCTによる解析では実験群において歯槽骨の骨吸収像を認め, 対照群と比較し有意に骨吸収の増加を認めた. 実験群の四肢末端の骨は腫脹, 変形および手根骨軟骨部の破壊, 膝関節表面と膝蓋骨の粗ぞうを呈した. また実験群のMMP-3値は, 対照群と比較し有意に増加した. 実験群のACPA活性値も, 対照群と比較し有意に増加した. 組織学的所見から, 実験群の膝関節組織は対照群と比較し高度な炎症性細胞の浸潤, 骨破壊像を認め, MMP-13による免疫染色においてパンヌスと関節半月にMMP-13陽性細胞を認めた. MMP-13陽性細胞数は対照群と比較して有意に増加した. 「結論」 : 本研究により, P. gingivalisによる口腔感染がコラーゲン誘発関節炎モデルマウスの組織破壊を促進することが示唆された. |
| Author | 安田, 忠司 澁谷, 俊昭 佐藤, 匠 松下, 至宏 |
| Author_FL | Yoshihiro MATSUSHITA Tadashi YASUDA Toshiaki SHIBUTANI Takumi SATO |
| Author_FL_xml | – sequence: 1 fullname: Tadashi YASUDA – sequence: 2 fullname: Takumi SATO – sequence: 3 fullname: Yoshihiro MATSUSHITA – sequence: 4 fullname: Toshiaki SHIBUTANI |
| Author_xml | – sequence: 1 fullname: 澁谷, 俊昭 organization: 朝日大学歯学部口腔感染医療学講座歯周病学分野 – sequence: 1 fullname: 佐藤, 匠 organization: 朝日大学歯学部口腔感染医療学講座歯周病学分野 – sequence: 1 fullname: 松下, 至宏 organization: 朝日大学歯学部口腔感染医療学講座歯周病学分野 – sequence: 1 fullname: 安田, 忠司 organization: 朝日大学歯学部口腔感染医療学講座歯周病学分野 |
| BackLink | https://cir.nii.ac.jp/crid/1390282763046545536$$DView record in CiNii |
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| Copyright | 2018 特定非営利活動法人日本歯科保存学会 |
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| DocumentTitleAlternate | Analysis of Collagen-induced Arthritis Model Mice Orally Infected with Porphyromonas gingivalis |
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| Language | Japanese |
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| MergedId | FETCHMERGED-LOGICAL-j3016-e9eca69e61b8144b0d1f605e5705a10b288c655fbc86ca5b05d3cb1ff31fb2573 |
| OpenAccessLink | https://www.jstage.jst.go.jp/article/shikahozon/61/4/61_214/_article/-char/ja |
| PageCount | 11 |
| ParticipantIDs | nii_cinii_1390282763046545536 medicalonline_journals_do1conde_2018_006104_002_0214_02243149552 jstage_primary_article_shikahozon_61_4_61_214_article_char_ja |
| PublicationCentury | 2000 |
| PublicationDate | 2018 |
| PublicationDateYYYYMMDD | 2018-01-01 |
| PublicationDate_xml | – year: 2018 text: 2018 |
| PublicationDecade | 2010 |
| PublicationTitle | The Japanese Journal of Conservative Dentistry |
| PublicationTitleAlternate | 日歯保存誌 |
| PublicationTitle_FL | Jpn J Conserv Dent 日歯保存誌 日本歯科保存学雑誌 |
| PublicationYear | 2018 |
| Publisher | 特定非営利活動法人 日本歯科保存学会 日本歯科保存学会 The Japanese Society of Conservative Dentistry |
| Publisher_xml | – name: 特定非営利活動法人 日本歯科保存学会 – name: 日本歯科保存学会 – name: The Japanese Society of Conservative Dentistry |
| References | 34) Larsen A, Dale K, Eek M. Radiographic evaluation of rheumatoid arthritis and related conditions by standard reference films. Acta Radiol Diagn. 1977; 8: 481-491. 21) 小林哲夫, 吉江弘正. 歯周炎と関節リウマチ 関連性と臨床対応 (総説). 日歯周誌 2012 ; 54 : 11-17. 47) Joe B, Griffiths MM, Remmers EF, Wilder RL. Animal models of rheumatoid arthritis and related inflammation. Curr Rheumatol Rep 1999; 1: 139-148. 28) 大山秀樹, 岡本慎治, 西村英紀, 新井英雄, 高柴正悟, 村山洋二. 歯周病原性細菌に対する血清IgG抗体を測定することによって集団検診で若年性歯周炎患者を検出する方法に関する研究. 岡山歯誌 2001 ; 20 : 181-191. 37) Klareskog L, Rönnelid J, Lundberg K, Padyukov L, Alfredsson L. Immunity to citrullinated proteins in rheumatoid arthritis. Annu Rev Immunol 2008; 26: 651-675. 22) Moore BA, Aznavoorian S, Engler JA, Windsor LJ. Induction of collagenase-3 (MMP-13) in rheumatoid arthritis synovial fibroblasts. Biochim Biophys Acta 2000; 1502: 307-318. 4) Bahekar AA, Singh S, Saha S, Molnar J, Arora R. The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis. Am Heart J 2007; 154: 830-837. 46) Kępczyńska MA, Zaibi MS, Alomar SY, Trayhurn P. PCR arrays indicate that the expression of extracellular matrix and cell adhesion genes in human adipocytes is regulated by IL-1β (interleukin-1β). Arch Physiol Biochem 2017; 123: 61-67. 5) Senba T, Kobayashi Y, Inoue K, Kaneto C, Inoue M, Toyokawa S, Suyama Y, Suzuki T, Miyano Y, Miyoshi Y. The association between self-reported periodontitis and coronary heart disease from MY Health Up Study. J Occup Health 2008; 50: 283-287. 7) Tomofuji T, Ekuni D, Sanbe T, Azuma T, Tamaki N, Irie K, Maruyama T, Yamamoto T, Watanabe T, Miyauchi M, Takata T. Effects of improvement in periodontal inflammation by toothbrushing on serum lipopolysaccharide concentration and liver injury in rats. Acta Odontol Scand 2009; 67: 200-205. 14) 松田剛正. 総論. 髙久史麿. 関節リウマチのトータルマネージメント. 1版. 医歯薬出版 : 東京 ; 2011. 16-19. 31) Maekawa T, Takahashi N, Tabeta K, Aoki Y, Miyashita H, Miyauchi S, Miyazawa H, Nakajima T, Yamazaki K. Chronic oral infection with Porphyromonas gingivalis accelerates atheroma formation by shifting the lipid profile. PLoS One 2011; 6: e20240. 54) Matsui T, Shimada K, Tohma S. Anti-cyclic citrullinated peptide antibody in rheumatic diseases other than rheumatoid arthritis. Clin Rheumatol 2006; 25: 610-611. 50) Yang CH, Huang F, Deng XH, Zhang JL, Zhang LY, Guo JH, Liang DF, Wang LS, Zhang YM. Effects of infliximab and etanercept, two types of anti-tumor necrosis factor-alpha inhibitor on serum level of matrix metalloproteinase 3 expression in patients with ankylosing spondylitis. Zhonghua Yi Xue Za Zhi 2006; 86: 2451-2454. 12) Hajishengallis G. Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response. Trends Immunol 2014; 35: 3-11. 2) 厚生労働省. 平成23年度歯科疾患実態調査. 2011.34-36. 9) Hasegawa K, Furuichi Y, Shimotsu A, Nakamura M, Yoshinaga M, Kamitomo M, Hatae M, Maruyama I, Izumi Y. Associations between systemic status, periodontal status, serum cytokine levels, and delivery outcomes in pregnant women with a diagnosis of threatened premature labor. J Periodontol 2003; 74: 1764-1770. 15) Shichikawa K, Inoue K, Hirota S, Maeda A, Ota H, Kimura M, Ushiyama T, Tsujimoto M. Changes in the incidence and prevalence of rheumatoid arthritis in Kamitonda, Wakayama, Japan, 1965-1996. Ann Rheum Dis 1999; 58: 751-756. 27) Murayama Y, Nagai A, Okamura K, Kurihara H, Nomura Y, Kokeguchi S, Kato K. Serum immunoglobulin G antibody to periodontal bacteria. Adv Dent Res 1988; 2: 339-345. 36) Kobayashi A, Naito S, Enomoto H, Shiomoi T, Kimura T, Obata K, Inoue K, Okada Y. Serum levels of matrix metalloproteinase 3 (stromelysin 1) for monitoring synovitis in rheumatoid arthritis. Arch Pathol Lab Med 2007; 131: 563-570. 48) Wang QH, Zhang SZ, Xue J, Wu HX. Serum metalloproteinase-3 levels in assessing efficacy of Etanercept in patients with ankylosing spondylitis. Zhejiang Da Xue Xue Bao Yi Xue Ban 2010; 39: 409-414. 52) Padyukov L, Seielstad M, Ong RT, Ding B, Rönnelid J, Seddighzadeh M, Alfredsson L, Klareskog L. Epidemiological Investigation of Rheumatoid Arthritis (EIRA) study group. A genome-wide association study suggests contrasting associations in ACPA-positive versus ACPA-negative rheumatoid arthritis. Ann Rheum Dis 2011; 70: 259-265. 49) Kawashiri SY, Kawakami A, Ueki Y, Imazato T, Iwamoto N, Fujikawa K, Aramaki T, Tamai M, Nakamura H, Origuchi T, Ida H, Eguchi K. Decrement of serum cartilage oligomeric matrix protein (COMP) in rheumatoid arthritis (RA) patients achieving remission after 6 months of etanercept treatment: comparison with CRP, IgM-RF, MMP-3 and anti-CCP Ab. Joint Bone Spine 2010; 77: 418-420. 55) Schmickler J, Rupprecht A, Patschan S, Patschan D, Müller GA, Haak R, Mausberg RF, Schmalz G, Kottmann T, Ziebolz D. Cross-sectional evaluation of periodontal status and microbiologic and rheumatoid parameters in a large cohort of patients with rheumatoid arthritis. J Periodontol 2017; 88: 368-379. 3) Mattila KJ, Nieminen MS, Valtonen VV, Rasi VP, Kesäniemi YA, Syrjälä SL, Jungell PS, Isoluoma M, Hietaniemi K, Jokinen MJ. Association between dental health and acute myocardial infarction. BMJ 1989; 298: 779-781. 17) De Pablo P, Chapple IL, Buckley CD, Dietrich T. Periodontitis in systemic rheumatic diseases. Nat Rev Rheumatol 2009; 5: 218-224. 8) Tomofuji T, Ekuni D, Yamanaka R, Kusano H, Azuma T, Sanbe T, Tamaki N, Yamamoto T, Watanabe T, Miyauchi M, Takata T. Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats. J Periodontol 2007; 78: 1999-2006. 41) McInnes IB, Buckley CD, Isaacs JD. Cytokines in rheumatoid arthritis―shaping the immunological landscape. Nat Rev Rheumatol 2016; 12: 63-68. 16) O’Reilly PG, Claffey NM. A history of oral sepsis as a cause of disease. Periodontol 2000 2000; 23: 13-18. 19) Lundberg K, Wegner N, Yucel-Lindberg T, Venables PJ. Periodontitis in RA―the citrullinated enolase connection. Nat Rev Rheumatol 2010; 6: 727-730. 33) Yamakawa M, Ouhara K, Kajiya M, Munenaga S, Kittaka M, Yamasaki S, Takeda K, Takeshita K, Mizuno N, Fujita T, Sugiyama E, Kurihara H. Porphyromonas gingivalis infection exacerbates the onset of rheumatoid arthritis in SKG mice. Clin Exp Immunol 2016; 186: 177-189. 35) Ribbens C, Martin y Porras M, Franchimont N, Kaiser MJ, Jaspar JM, Damas P, Houssiau FA, Malaise MG. Increased matrix metalloproteinase-3 serum levels in rheumatic diseases: relationship with synovitis and steroid treatment. Ann Rheum 2002; 61: 161-166. 13) Hajishengallis G, Darveau, RP, Curtis MA. The keystone-pathogenhypothesis. Nat Rev Microbiol 2012; 10: 717-725. 24) Martinez-Martinez RE, Abud-Mendoza C, Patiño-Marin N, Rizo-Rodríguez JC, Little JW, Loyola-Rodríguez JP. Detection of periodontal bacterial DNA in serum and synovial fluid in refractory rheumatoid arthritis patients. J Clin Periodontol 2009; 36: 1004-1010. 45) Takahashi S, Fukuda M, Mitani A, Fujimura T, Iwamura Y, Sato S, Kubo T, Sugita Y, Maeda H, Shinomura T, Noguchi T. Follicular dendritic cell-secreted protein is decreased in experimental periodontitis concurrently with the increase of interleukin-17 expression and the Rankl/Opg mRNA ratio. J Periodontal Res. 2014; 49: 390-397. 53) Daha NA, Toes RE. Rheumatoid arthritis: Are ACPA-positive and ACPA-negative RA the same disease?. Nat Rev Rheumatol 2011; 7: 202-203. 38) Uemura Y, Hayashi H, Takahashi T, Saitho T, Umeda R, Ichise Y, Sendo S, Tsuji G, Kumagai S. MMP-3 as a biomarker of disease activity of rheumatoid arthritis. Rinsho Byori 2015; 63: 1357-1364. 51) Anzilotti C, Merlini G, Pratesi F, Tommasi C, Chimenti D, Migliorini P. Antibodies to viral citrullinated peptide in rheumatoid arthritis. J Rheumatol 2006; 33: 647-651. 29) Sarkar S, Justa S, Brucks M, Endres J, Fox DA, Zhou X, Alnaimat F, Whitaker B, Wheeler JC, Jones BH, Bommireddy SR. Interleukin (IL)-17A, F and AF in inflammation: a study in collagen-induced arthritis and rheumatoid arthritis. Clin Exp Immunol 2014; 177: 652-661. 18) Okada Y, Suzuki A, Ikari K, Terao C, Kochi Y, Ohmura K, Higasa K, Akiyama M, Ashikawa K, Kanai M, Hirata J, Suita N, Teo YY, Xu H, Bae SC, Takahashi A, Momozawa Y, Matsuda K, Momohara S, Taniguchi A, Yamada R, Mimori T, Kubo M, Brown MA, Raychaudhuri S, Matsuda F, Yamanaka H, Kamatani Y, Yamamoto K. Contribution of a non-classical HLA gene, HLA-DOA, to the risk of rheumatoid arthritis. Am J Hum Genet 2016; 4: 366-374. 40) Graves DT, Li J, Cochran DL. Inflammation and uncoupling as mechanisms of periodontal bone loss. J Dent Res 2011; 90: 143-153. 43) Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman KS. Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontol 2000 1997; 14: 216-248. 39) Sommerfelt RM, Feuerherm AJ, Jones K, Johansen B. Cytosolic phospholipase A2 regulates TNF-induced production of joint destructive effectors in synoviocytes. PLoS One 2013; 12: e83555. 57) Hashimoto M, Yamazaki T, Hamaguchi M, Morimoto T, Yamori M, Asai K, Isobe Y, Furu M, Ito H, Fujii T, Terao C, Mori M, Matsuo T, Yoshitomi H, Yamamoto K, Yamamoto W, Bessho K, Mimori T. Periodontitis and Porphyromonas gingivalis in preclinical stage of arthritis patients. PLoS One 2015; 10: e0122121. 11) Hajishengallis G, Liang S, Payne MA, Hashim A, Jotwani R, Eskan MA, McIntosh ML, Alsam A, Kirkwood KL, Lambris JD, Darveau RP, Curtis MA. Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement. Cell Host Microbe 2011; 10: 497-506. 58) Shimada A, Kobayashi T, Ito S, Okada M, Murasawa A, Nakazono K, Yoshie H. Expression of anti-Porphyromonas gingivalis peptidylarginine deiminase immunoglobulin G and peptidylarginine deiminase-4 in patients with rheumatoid arthritis and periodontitis. J Periodontal Res 2016; 51: 103-111. 1) Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest 1976; 34: 235-249. 26) Chae P, Im M, Gibson F, Jiang Y |
| References_xml | – reference: 33) Yamakawa M, Ouhara K, Kajiya M, Munenaga S, Kittaka M, Yamasaki S, Takeda K, Takeshita K, Mizuno N, Fujita T, Sugiyama E, Kurihara H. Porphyromonas gingivalis infection exacerbates the onset of rheumatoid arthritis in SKG mice. Clin Exp Immunol 2016; 186: 177-189. – reference: 58) Shimada A, Kobayashi T, Ito S, Okada M, Murasawa A, Nakazono K, Yoshie H. Expression of anti-Porphyromonas gingivalis peptidylarginine deiminase immunoglobulin G and peptidylarginine deiminase-4 in patients with rheumatoid arthritis and periodontitis. J Periodontal Res 2016; 51: 103-111. – reference: 22) Moore BA, Aznavoorian S, Engler JA, Windsor LJ. Induction of collagenase-3 (MMP-13) in rheumatoid arthritis synovial fibroblasts. Biochim Biophys Acta 2000; 1502: 307-318. – reference: 30) Park CH, Abramson ZR, Taba M Jr, Jin Q, Chang J, Kreider JM, Goldstein SA, Giannobile WV. Three-dimensional micro-computed tomographic imaging of alveolar bone in experimental bone loss or repair. J Periodontol 2007; 78: 273-281. – reference: 13) Hajishengallis G, Darveau, RP, Curtis MA. The keystone-pathogenhypothesis. Nat Rev Microbiol 2012; 10: 717-725. – reference: 10) Ye C, Katagiri S, Miyasaka N, Bharti P, Kobayashi H, Takeuchi Y, Momohara Y, Sekiguchi M, Takamine S, Nagasawa T, Izumi Y. The anti-phospholipid antibody-dependent and independent effects of periodontopathic bacteria on threatened preterm labor and preterm birth. Arch Gynecol Obstet 2013; 288: 65-72. – reference: 7) Tomofuji T, Ekuni D, Sanbe T, Azuma T, Tamaki N, Irie K, Maruyama T, Yamamoto T, Watanabe T, Miyauchi M, Takata T. Effects of improvement in periodontal inflammation by toothbrushing on serum lipopolysaccharide concentration and liver injury in rats. Acta Odontol Scand 2009; 67: 200-205. – reference: 25) Okada M, Kobayashi T, Ito S, Yokoyama T, Abe A, Murasawa A, Yoshie H. Periodontal treatment decreases levels of antibodies to Porphyromonas gingivalis and citrulline in patients with rheumatoid arthritis and periodontitis. J Periodontol 2013; 84: 74-84. – reference: 28) 大山秀樹, 岡本慎治, 西村英紀, 新井英雄, 高柴正悟, 村山洋二. 歯周病原性細菌に対する血清IgG抗体を測定することによって集団検診で若年性歯周炎患者を検出する方法に関する研究. 岡山歯誌 2001 ; 20 : 181-191. – reference: 47) Joe B, Griffiths MM, Remmers EF, Wilder RL. Animal models of rheumatoid arthritis and related inflammation. Curr Rheumatol Rep 1999; 1: 139-148. – reference: 32) 後藤昌彦, 安田忠司, 澁谷俊昭. ニコチン経口摂取がラット歯槽骨に及ぼす影響. 岐歯学誌 2014 ; 41 : 128-136. – reference: 56) Nakamura H, Sato G, Hirata A, Yamamoto T. Immunolocalization of matrix metalloproteinase-13 on bone surface under osteoclasts in rat tibia. Bone 2004; 34: 48-56. – reference: 54) Matsui T, Shimada K, Tohma S. Anti-cyclic citrullinated peptide antibody in rheumatic diseases other than rheumatoid arthritis. Clin Rheumatol 2006; 25: 610-611. – reference: 31) Maekawa T, Takahashi N, Tabeta K, Aoki Y, Miyashita H, Miyauchi S, Miyazawa H, Nakajima T, Yamazaki K. Chronic oral infection with Porphyromonas gingivalis accelerates atheroma formation by shifting the lipid profile. PLoS One 2011; 6: e20240. – reference: 24) Martinez-Martinez RE, Abud-Mendoza C, Patiño-Marin N, Rizo-Rodríguez JC, Little JW, Loyola-Rodríguez JP. Detection of periodontal bacterial DNA in serum and synovial fluid in refractory rheumatoid arthritis patients. J Clin Periodontol 2009; 36: 1004-1010. – reference: 36) Kobayashi A, Naito S, Enomoto H, Shiomoi T, Kimura T, Obata K, Inoue K, Okada Y. Serum levels of matrix metalloproteinase 3 (stromelysin 1) for monitoring synovitis in rheumatoid arthritis. Arch Pathol Lab Med 2007; 131: 563-570. – reference: 41) McInnes IB, Buckley CD, Isaacs JD. Cytokines in rheumatoid arthritis―shaping the immunological landscape. Nat Rev Rheumatol 2016; 12: 63-68. – reference: 48) Wang QH, Zhang SZ, Xue J, Wu HX. Serum metalloproteinase-3 levels in assessing efficacy of Etanercept in patients with ankylosing spondylitis. Zhejiang Da Xue Xue Bao Yi Xue Ban 2010; 39: 409-414. – reference: 52) Padyukov L, Seielstad M, Ong RT, Ding B, Rönnelid J, Seddighzadeh M, Alfredsson L, Klareskog L. Epidemiological Investigation of Rheumatoid Arthritis (EIRA) study group. A genome-wide association study suggests contrasting associations in ACPA-positive versus ACPA-negative rheumatoid arthritis. Ann Rheum Dis 2011; 70: 259-265. – reference: 57) Hashimoto M, Yamazaki T, Hamaguchi M, Morimoto T, Yamori M, Asai K, Isobe Y, Furu M, Ito H, Fujii T, Terao C, Mori M, Matsuo T, Yoshitomi H, Yamamoto K, Yamamoto W, Bessho K, Mimori T. Periodontitis and Porphyromonas gingivalis in preclinical stage of arthritis patients. PLoS One 2015; 10: e0122121. – reference: 26) Chae P, Im M, Gibson F, Jiang Y, Graves DT. Mice lacking monocyte chemoattractant protein 1 have enhanced susceptibility to an interstitial polymicrobial infection due to impaired monocyte recruitment. Infect Immun 2002; 70: 3164-3169. – reference: 18) Okada Y, Suzuki A, Ikari K, Terao C, Kochi Y, Ohmura K, Higasa K, Akiyama M, Ashikawa K, Kanai M, Hirata J, Suita N, Teo YY, Xu H, Bae SC, Takahashi A, Momozawa Y, Matsuda K, Momohara S, Taniguchi A, Yamada R, Mimori T, Kubo M, Brown MA, Raychaudhuri S, Matsuda F, Yamanaka H, Kamatani Y, Yamamoto K. Contribution of a non-classical HLA gene, HLA-DOA, to the risk of rheumatoid arthritis. Am J Hum Genet 2016; 4: 366-374. – reference: 17) De Pablo P, Chapple IL, Buckley CD, Dietrich T. Periodontitis in systemic rheumatic diseases. Nat Rev Rheumatol 2009; 5: 218-224. – reference: 49) Kawashiri SY, Kawakami A, Ueki Y, Imazato T, Iwamoto N, Fujikawa K, Aramaki T, Tamai M, Nakamura H, Origuchi T, Ida H, Eguchi K. Decrement of serum cartilage oligomeric matrix protein (COMP) in rheumatoid arthritis (RA) patients achieving remission after 6 months of etanercept treatment: comparison with CRP, IgM-RF, MMP-3 and anti-CCP Ab. Joint Bone Spine 2010; 77: 418-420. – reference: 43) Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman KS. Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontol 2000 1997; 14: 216-248. – reference: 34) Larsen A, Dale K, Eek M. Radiographic evaluation of rheumatoid arthritis and related conditions by standard reference films. Acta Radiol Diagn. 1977; 8: 481-491. – reference: 39) Sommerfelt RM, Feuerherm AJ, Jones K, Johansen B. Cytosolic phospholipase A2 regulates TNF-induced production of joint destructive effectors in synoviocytes. PLoS One 2013; 12: e83555. – reference: 50) Yang CH, Huang F, Deng XH, Zhang JL, Zhang LY, Guo JH, Liang DF, Wang LS, Zhang YM. Effects of infliximab and etanercept, two types of anti-tumor necrosis factor-alpha inhibitor on serum level of matrix metalloproteinase 3 expression in patients with ankylosing spondylitis. Zhonghua Yi Xue Za Zhi 2006; 86: 2451-2454. – reference: 16) O’Reilly PG, Claffey NM. A history of oral sepsis as a cause of disease. Periodontol 2000 2000; 23: 13-18. – reference: 19) Lundberg K, Wegner N, Yucel-Lindberg T, Venables PJ. Periodontitis in RA―the citrullinated enolase connection. Nat Rev Rheumatol 2010; 6: 727-730. – reference: 40) Graves DT, Li J, Cochran DL. Inflammation and uncoupling as mechanisms of periodontal bone loss. J Dent Res 2011; 90: 143-153. – reference: 15) Shichikawa K, Inoue K, Hirota S, Maeda A, Ota H, Kimura M, Ushiyama T, Tsujimoto M. Changes in the incidence and prevalence of rheumatoid arthritis in Kamitonda, Wakayama, Japan, 1965-1996. Ann Rheum Dis 1999; 58: 751-756. – reference: 12) Hajishengallis G. Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response. Trends Immunol 2014; 35: 3-11. – reference: 11) Hajishengallis G, Liang S, Payne MA, Hashim A, Jotwani R, Eskan MA, McIntosh ML, Alsam A, Kirkwood KL, Lambris JD, Darveau RP, Curtis MA. Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement. Cell Host Microbe 2011; 10: 497-506. – reference: 2) 厚生労働省. 平成23年度歯科疾患実態調査. 2011.34-36. – reference: 35) Ribbens C, Martin y Porras M, Franchimont N, Kaiser MJ, Jaspar JM, Damas P, Houssiau FA, Malaise MG. Increased matrix metalloproteinase-3 serum levels in rheumatic diseases: relationship with synovitis and steroid treatment. Ann Rheum 2002; 61: 161-166. – reference: 1) Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest 1976; 34: 235-249. – reference: 37) Klareskog L, Rönnelid J, Lundberg K, Padyukov L, Alfredsson L. Immunity to citrullinated proteins in rheumatoid arthritis. Annu Rev Immunol 2008; 26: 651-675. – reference: 14) 松田剛正. 総論. 髙久史麿. 関節リウマチのトータルマネージメント. 1版. 医歯薬出版 : 東京 ; 2011. 16-19. – reference: 29) Sarkar S, Justa S, Brucks M, Endres J, Fox DA, Zhou X, Alnaimat F, Whitaker B, Wheeler JC, Jones BH, Bommireddy SR. Interleukin (IL)-17A, F and AF in inflammation: a study in collagen-induced arthritis and rheumatoid arthritis. Clin Exp Immunol 2014; 177: 652-661. – reference: 44) Assuma R, Oates T, Cochran D, Amar S, Graves DT. IL-1 and TNF antagonists inhibit the inflammatory response and bone loss in experimental periodontitis. J Immunol 1998; 160: 403-409. – reference: 9) Hasegawa K, Furuichi Y, Shimotsu A, Nakamura M, Yoshinaga M, Kamitomo M, Hatae M, Maruyama I, Izumi Y. Associations between systemic status, periodontal status, serum cytokine levels, and delivery outcomes in pregnant women with a diagnosis of threatened premature labor. J Periodontol 2003; 74: 1764-1770. – reference: 20) Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nat Rev Immunol 2015; 15: 30-44. – reference: 3) Mattila KJ, Nieminen MS, Valtonen VV, Rasi VP, Kesäniemi YA, Syrjälä SL, Jungell PS, Isoluoma M, Hietaniemi K, Jokinen MJ. Association between dental health and acute myocardial infarction. BMJ 1989; 298: 779-781. – reference: 8) Tomofuji T, Ekuni D, Yamanaka R, Kusano H, Azuma T, Sanbe T, Tamaki N, Yamamoto T, Watanabe T, Miyauchi M, Takata T. Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats. J Periodontol 2007; 78: 1999-2006. – reference: 55) Schmickler J, Rupprecht A, Patschan S, Patschan D, Müller GA, Haak R, Mausberg RF, Schmalz G, Kottmann T, Ziebolz D. Cross-sectional evaluation of periodontal status and microbiologic and rheumatoid parameters in a large cohort of patients with rheumatoid arthritis. J Periodontol 2017; 88: 368-379. – reference: 6) Grossi SG, Genco RJ. Periodontal disease and diabetes mellitus: a two-way relationship. Ann Periodontol 1998; 3: 51-61. – reference: 21) 小林哲夫, 吉江弘正. 歯周炎と関節リウマチ 関連性と臨床対応 (総説). 日歯周誌 2012 ; 54 : 11-17. – reference: 53) Daha NA, Toes RE. Rheumatoid arthritis: Are ACPA-positive and ACPA-negative RA the same disease?. Nat Rev Rheumatol 2011; 7: 202-203. – reference: 42) Kobayashi T, Yoshie H. Host responses in the link between periodontitis and rheumatoid arthritis. Curr Oral Health Rep 2015; 2: 1-8. – reference: 45) Takahashi S, Fukuda M, Mitani A, Fujimura T, Iwamura Y, Sato S, Kubo T, Sugita Y, Maeda H, Shinomura T, Noguchi T. Follicular dendritic cell-secreted protein is decreased in experimental periodontitis concurrently with the increase of interleukin-17 expression and the Rankl/Opg mRNA ratio. J Periodontal Res. 2014; 49: 390-397. – reference: 23) Témoin S, Chakaki A, Askari A, El-Halaby A, Fitzgerald S, Marcus RE, Han YW, Bissada NF. Identification of oral bacterial DNA in synovial fluid of patients with arthritis with native and failed prosthetic joints. J Clin Rheumatol 2012; 18: 117-121. – reference: 38) Uemura Y, Hayashi H, Takahashi T, Saitho T, Umeda R, Ichise Y, Sendo S, Tsuji G, Kumagai S. MMP-3 as a biomarker of disease activity of rheumatoid arthritis. Rinsho Byori 2015; 63: 1357-1364. – reference: 4) Bahekar AA, Singh S, Saha S, Molnar J, Arora R. The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis. Am Heart J 2007; 154: 830-837. – reference: 5) Senba T, Kobayashi Y, Inoue K, Kaneto C, Inoue M, Toyokawa S, Suyama Y, Suzuki T, Miyano Y, Miyoshi Y. The association between self-reported periodontitis and coronary heart disease from MY Health Up Study. J Occup Health 2008; 50: 283-287. – reference: 51) Anzilotti C, Merlini G, Pratesi F, Tommasi C, Chimenti D, Migliorini P. Antibodies to viral citrullinated peptide in rheumatoid arthritis. J Rheumatol 2006; 33: 647-651. – reference: 27) Murayama Y, Nagai A, Okamura K, Kurihara H, Nomura Y, Kokeguchi S, Kato K. Serum immunoglobulin G antibody to periodontal bacteria. Adv Dent Res 1988; 2: 339-345. – reference: 46) Kępczyńska MA, Zaibi MS, Alomar SY, Trayhurn P. PCR arrays indicate that the expression of extracellular matrix and cell adhesion genes in human adipocytes is regulated by IL-1β (interleukin-1β). Arch Physiol Biochem 2017; 123: 61-67. |
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| Snippet | 目的 : 本研究は, Porphyromonas gingivalisの感染が関節リウマチ (RA) の増悪に与える影響について調べるため, RAモデルマウスとしてコラーゲン誘発関節炎モデルマウスを... 「抄録」「目的」 : 本研究は, Porphyromonas gingivalisの感染が関節リウマチ (RA) の増悪に与える影響について調べるため, RAモデルマウスとしてコラーゲン誘発関節... Purpose: This study examined the impact of Porphyromonas gingivalis infection on rheumatoid arthritis (RA) in collagen-induced arthritis model mice (RA model... |
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| StartPage | 214 |
| SubjectTerms | collagen-induced arthritis model mouse Porphyromonas gingivalis rheumatoid arthritis コラーゲン誘発関節炎モデルマウス 関節リウマチ |
| Title | Porphyromonas gingivalisを口腔感染させたコラーゲン誘発関節炎モデルマウスの解析 |
| URI | https://www.jstage.jst.go.jp/article/shikahozon/61/4/61_214/_article/-char/ja http://mol.medicalonline.jp/en/journal/download?GoodsID=do1conde/2018/006104/002&name=0214-0224j https://cir.nii.ac.jp/crid/1390282763046545536 |
| Volume | 61 |
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| ispartofPNX | 日本歯科保存学雑誌, 2018, Vol.61(4), pp.214-224 |
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