A study on osteoclast-delivery therapy to anti-resorptive agent-related osteonecrosis of the jaw.
| Project/Area Number |
16K15832
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Surgical dentistry
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| Research Institution | Fukuoka Dental College |
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Principal Investigator |
Ikebe Tetsuro 福岡歯科大学, 口腔歯学部, 教授 (20202913)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | 顎骨壊死 / 破骨細胞 / 骨吸収抑制薬 / ARONJ / 細胞デリバリー / ＢＲＯＮＪ / DNAプロタミン |
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| Outline of Final Research Achievements |
The occurrence of anti-resorptive agent-related osteonecrosis of the jaw (ARONJ) is supposed to be due to the elimination of osteoclasts and suppression of bone turnover. Thus, the graft of exogenous osteoclasts or osteoblasts into the lesion may improve the symptom of ARONJ.I investigated two new materials, DNA/Protamine complex and DNA/polymer-coated carbon nanotubes complex as a carrier of delivering osteoclasts to the lesion. I confirmed that the mouse bone marrow cells derived osteoclasts and osteoblast cell lines could express their marker molecules in the cultures on both carrier materials. When both carrier materials containing osteoclasts or osteoblasts, which were grafted into the bone defect of calvaria as well as tooth extraction socket of mandible in the mice with or without the treatment of zoledronic acid, the new bone formation was promoted in the calvaria defect, but not extraction socket. The results of this project are promising for a new therapy of ARONJ.
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| Academic Significance and Societal Importance of the Research Achievements |
骨粗鬆症は高齢者の転倒に伴う骨折を増加させ、その結果寝たきりとなって生命予後を低下させる。ビスホスホネートやデノスマブなどの骨吸収抑制薬は、骨粗鬆症の治療に極めて有効であるが、一方、抜歯などを契機として難治性の顎骨壊死を引き起こし患者QOLの低下を招く。従って骨粗鬆症の治療を促進するためには顎骨壊死を制御することが重要である。本研究は顎骨壊死治療法の１つのアイデアとして、顎骨病巣に骨代謝関連細胞を移植して新生骨を誘導させるものであったが、その結果として細胞移植のための有効な担体を作製できた。本研究のこれからの展開は、顎骨壊死の治療を通じて健康寿命の延伸に寄与することが期待される。
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Report
(4 results)
Research Products
(3 results)
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[Presentation] サケDNAスカフォールドはリン酸輸送体の活性を介して骨形成を促進する2017
Author(s)
勝俣 由里, 鍛治屋 浩, 首藤 俊一, 池崎 晶二郎,田中 文恵, 永嶌 勝之, 永沼 香織, 見立 英史,米津 博文, 泉 喜和子, 平木 昭光, 池邉 哲郎
Organizer
第71回NPO法人日本口腔科学会学術集会
Place of Presentation
松山市
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