| Project/Area Number |
16K11506
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
YOSHIDA Kaya 徳島大学, 大学院医歯薬学研究部(歯学域), 講師 (60363157)
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| Co-Investigator(Kenkyū-buntansha) |
岡村 裕彦 岡山大学, 医歯薬学総合研究科, 教授 (20380024)
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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 |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 歯周病 / 糖尿病 / ＰＫＲ / ＡＧＥｓ / 骨芽細胞 / 高血糖 / 破骨細胞分化 / PKR / AGEs / 歯周病マウス / PKR活性化 / AGEs合成 / 骨芽細胞分化 / 最終糖化産物 / 骨代謝 |
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| Outline of Final Research Achievements |
We investigated whether Porphyromonas gingivalis (Pg) and AGEs affect bone metabolisms by regulating PKR activation. The treatment with Pg induced and activated PKR in mouse osteoblastic MC3T3-E1 cells. The high glucose conditions by treating with glucose increased the effects of Pg on PKR activation, whereas it induced no change of Pg internalization and morphology of osteoblasts. The PKR activated by Pg induced the differentiation of osteoblasts but not osteoclasts. These results suggested that high glucose conditions might be result in the inhibition of osteoblast differentiation by accelerating PKR under Pg infection.
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| Academic Significance and Societal Importance of the Research Achievements |
歯周病原菌への感染（歯周病）は、PKRを誘導活性化して骨芽細胞分化を抑制することにより、歯槽骨吸収を引き起こす。この状況に高血糖（糖尿病）が加わると、PKRの誘導活性化はさらに増強され、歯槽骨は吸収されやすくなる。以上のような現象が、糖尿病関連歯周炎が重症化する機序の一端であると考えられる。
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