| Project/Area Number |
18K17204
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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 57060:Surgical dentistry-related
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | 薬剤関連顎骨壊死 / MRONJ / テリパラチド / TPTD / ビスフォスフォネート / ＭＲＯＮＪ / 薬剤関連性顎骨壊死 |
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| Outline of Final Research Achievements |
Serum receptor activator of NF-κB ligand (RANKL), osteocalcin (OC), and C-terminal crosslinking telopeptide of type I collagen (CTX) were also examined. TPTD administration reduced necrotic bone area of the mandibles and femurs in the BRON rat model and induced new bone formation. In addition, TPTD injection increased the number of osteoclasts. The suggested underlying mechanism is the induction of protein levels of RANKL by TPTD. Furthermore, the serum levels of bone metabolism biomarkers (OC and CTX) were upregulated in the TPTD injection group. In conclusion, ZOL has negative effects on osteoclasts. TPTD was found to be effective in eliminating the negative effects of ZOL. TPTD had positive effects in preventing bone resorption and promoting osteogenesis. In addition, TPTD improved osteoclastogenesis, which in turn led to the improvement of BRON.
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| Academic Significance and Societal Importance of the Research Achievements |
テリパラチド（TPTD）投与による壊死骨面積の減少および破骨細胞数の増加、RANKLとCTXの上昇から、MRONJによって形成された壊死骨が、破骨細胞により吸収されたことが推察された。MRONJに対するTPTD療法は、骨芽細胞による新生骨形成の促進だけでなく、破骨細胞の活性化による壊死骨の吸収よって、治療効果を発揮する可能性が示された。
これらは、MRONJに対するTPTDの有用性を示しただけでなく、破骨細胞の壊死骨吸収の促進が一因である可能性を示した画期的な報告であったと考える。
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