| Project/Area Number |
18K16605
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56020:Orthopedics-related
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 骨端線損傷 / 成長板 / 成長板軟骨損傷 / ガングリオシド / 糖脂質 / 整形外科 / 成長板損傷 / 動物モデル / 成長板修復 |
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| Outline of Final Research Achievements |
The purpose of the current study was to clarify the roles of ganglioside series after growth plate (GP) injury. 5 weeks postoperatively, the length of operated tibia was significantly shortened compared to those of sham operated tibia in WT mice. The drop ratio in KO mice significantly decreased compared to those in WT mice. The height of growth plate in KO mice were significantly higher than those in WT mice. Bone volume of the physeal bridge and BMD of the subchondral area in KO mice were almost equal to those in WT mice.
The current study demonstrated that b-series gangliosides were most abundant gangliosides series in physeal chondrocyte and depletion of b-series gangliosides inhibited growth imbalance in mice. The treatment strategy that enhances viability of remaining cartilage via b-series gangliosides pathway may be future directions for the growth plate injury.
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| Academic Significance and Societal Importance of the Research Achievements |
成長板軟骨損傷に対して四肢変形の主因となる損傷部位の骨性癒合に対して、骨性架橋の切除に加えて骨セメント移植や自家脂肪組織移植などが試みられている。しかし、成長板障害に続発する骨性癒合を抑制する治療法は未だ存在しない。我々はこの点に着目し、内軟骨性骨化を制御することで骨性架橋形成の抑制を目指している。本コンセプトは、今まで骨性架橋を侵襲的に切除するしかなかった治療法とは異なり、成長板軟骨板損傷に対する非侵襲的治療法の開発という新たな方向性を示している。
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