A study of the possibility of an aggravating factor for periodontal disease that excessive fructose intake in diabetes mellitus.
Project/Area Number |
18K09609
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 57030:Conservative dentistry-related
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Research Institution | Nihon University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
鈴木 直人 日本大学, 歯学部, 教授 (10226532)
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Project Period (FY) |
2018-04-01 – 2021-03-31
|
Project Status |
Completed (Fiscal Year 2020)
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Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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Keywords | 歯周病 / 糖尿病 / 骨芽細胞 / グルコーストランスポーター / 終末糖化産物 / GLUT4 / AGEs / COX2 / 炎症 |
Outline of Final Research Achievements |
The purpose of this study was to elucidate the causal relationship and molecular mechanism of the exacerbation of periodontal disease by excessive fructose intake in diabetes mellitus using osteoblasts by cell and molecular biology. As a result, fructose did not affect the progression of inflammation by fructose LPS in a hyperglycemic state. However, AGEs produced by hyperglycemia or glucose in the blood may exacerbate LPS-induced inflammation, which is one of the causes of inflammation in periodontal disease. In addition, related experiments showed that atmospheric pressure and cold nitrogen plasma could suppress the inflammation exacerbated by these AGEs.
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Academic Significance and Societal Importance of the Research Achievements |
糖尿病は歯周病増悪のリスクファクターとして疫学的及び動物実験においてもその相関が示されている。しかしながら,細胞・分子生物学的には明確な相関を示した報告は少ない。本研究の成果は,骨芽細胞に歯周病の炎症が進行する原因の一つあるLPSとグルコースまたは終末糖化産物で共刺激すると炎症性サイトカインや炎症性生理活性物質が増加するというものである。これは、糖尿病による高血糖状態における歯周病による炎症の進行の1つのメカニズムを細胞生物学的に明らかにしたものであると考えている。
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Report
(4 results)
Research Products
(4 results)