1995 Fiscal Year Final Research Report Summary
Studies on the pathogenesis and the prevention of drug-induced gingival hyperplasia.
| Project/Area Number |
06454551
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Conservative dentistry
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| Research Institution | Osaka Dental University |
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Principal Investigator |
DOMAE Naochika Osaka Dental University, Medicine, Professor, 歯学部, 教授 (60115889)
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| Co-Investigator(Kenkyū-buntansha) |
UMEHARA Hisanori Osaka Dental Unviersity, Medicine, Instructor, 歯学部, 助手 (70247881)
MORIKUNI Tadahiro Osaka Dental University, Periodontology, Instructor, 歯学部, 助手 (60098027)
IMAI Hisao Osaka Dental University, Periodontology, Professor, 歯学部, 教授 (80067024)
HIGASHI Yoshikage Osaka Dental University, Oral Anatomy, Professor, 歯学部, 教授 (50066990)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Drug-induced gingival hyperplasia / Model animal having gingival hyperplasia / Calcium antagonist |
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| Research Abstract |
The gingival hyperplasia induced by various drugs (in especial Ca-antagonists) is one of the important and inveterate periodental disorders, but its pathogenesis is still unknown. The pathogenesis of gingival hyperplasia induced by Ca-antagonist (Nifedipine) and its possible prevention were studied in dogs. During about 6 months, one group of dogs was prevented any periodontal disorders by scaling and root planing and other group of dogs was permitted periodental diseases by infected plaque. After these pretreatment, both groups of dogs were treated with Nifedipine during about one and half years. The relation between the concentration of Nifedipine in plasma and plaque control record, probing depth, tooth mobility, bone loss, inflamation of gingiva, grade of gingival hyperplasia was examined in both groups.
We are now studing on the histopathology of hyperplastic gingiva and attempting to reveal whether various cytokines (IL-1, TNF,IL-4, & TGF-beta) and adohesion molecules (ICM-1, VCAM-1 & ECAM-1) have play a part in the pathogenesis of drug-induced gingival hyperplasia or not.
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