Enhancement of Bone-Forming Ability on Beta-Tricalcium Phosphate by Modulating Cellular Senescence Mechanisms Using Senolytics

• 資料種別: 博士論文
• タイトル: Enhancement of Bone-Forming Ability on Beta-Tricalcium Phosphate by Modulating Cellular Senescence Mechanisms Using Senolytics
• 著者・編者: 王, 欣琛
• 著者標目: 王, 欣琛
• 出版年月日等: 2022-03-04
• 出版年（W3CDTF）: 2022-03-04
• 並列タイトル等: セノリティクス薬を用いた細胞老化機序の制御によるβ型リン酸三カルシウムの骨形成能の向上
• 授与機関名: 大阪歯科大学
• 授与年月日: 2022-03-04
• 授与年月日（W3CDTF）: 2022-03-04
• 報告番号: 甲第923号
• 学位: 博士（歯学）
• 博論授与番号: 甲第923号
• 本文の言語コード: eng
• 件名標目: Cellular senescence｜Beta-tricalcium phosphate｜ Bone formation｜Senolytics
• 対象利用者: 一般
• 一般注記: Various stresses latently induce cellular senescence that occasionally deteriorates the functioning of surrounding tissues. Nevertheless, little is known about the appearance and function of senescent cells, caused by the implantation of beta-tricalcium phosphate (β-TCP)—used widely in dentistry and orthopedics for treating bone diseases. In this study, two varying sizes of β-TCP granules (<300 µm and 300–500 µm) were implanted, and using histological and immunofluorescent staining, appearances of senescent-like cells in critical-sized bone defects in the calvaria of Sprague Dawley rats were evaluated. Parallelly, bone formation in defects was investigated with or without the oral administration of senolytics (a cocktail of dasatinib and quercetin). A week after the implantation, the number of senescence-associated beta-galactosidase, p21-, p19-, and tartrate-resistant acid phosphatase-positive cells increased and then decreased upon administrating senolytics. This administration of senolytics also attenuated 4-hydroxy-2-nonenal staining, representing reactive oxygen species. Combining senolytic administration with β-TCP implantation significantly enhanced the bone formation in defects as revealed by micro-computed tomography analysis and hematoxylin-eosin staining. This study demonstrates that β-TCP granules latently induce senescent-like cells, and senolytic administration may improve the bone-forming ability of β-TCP by inhibiting senescence-associated mechanisms.; 2021年度; 機関リポジトリ記載の権利情報: CC BY-NC-ND
• 国立国会図書館永続的識別子: info:ndljp/pid/12296873; https://dl.ndl.go.jp/pid/12296873
• コレクション（共通）: 障害者向け資料
• コレクション（障害者向け資料：レベル1）: テキストデータ
• コレクション（個別）: 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• 収集根拠: 博士論文（自動収集）
• 受理日（W3CDTF）: 2022-06-05T18:01:14+09:00
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 掲載誌（URI）: http://id.nii.ac.jp/1392/00000300/
• 連携機関・データベース: 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

目次

2023-09-07 再収集