Elucidation of mechanism of drug-induced gingival overgrowth and search for its therapeutic drugs
| Project/Area Number |
22592321
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ARA Toshiaki 松本歯科大学, 歯学部, 助教 (90387423)
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| Research Collaborator |
KAWAKAMI Toshiyuki 松本歯科大学, 総合歯科医学研究所, 教授 (80104892)
NAKANO Keisuke 松本歯科大学, 総合歯科医学研究所, 准教授 (10325095)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 歯肉増殖症 / ニフェジピン / フェニトイン / カルシウム感知受容体 / TRPV1 チ ャネル / 細胞内カルシウム濃度 / TRPV1チャネル / 細胞内カルシウム / CaSR / TRPチャネル |
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| Research Abstract |
It was elucidated the mechanism of gingival overgrowth as described below. Nifedipine (an anti-hypertension drug) and phenytoin (an antiepileptic drug) directly act on calcium-sensing receptors, which elevate the intracellular Ca2+ concentration ([Ca2+]i) by enhancing the Ca2+ release from intracellular Ca2+ stores and Ca2+ entry through transient receptor potential V1 channels. The [Ca2+]i elevation becomes a trigger of evocation of gingival overgrowth (Modified Ca2+ trigger theory).
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Report
(4 results)
Research Products
(17 results)
