| Project/Area Number |
05454516
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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 | Okayama University |
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Principal Investigator |
KURIHARA Hidemi Okayama Univ.Dent.Sch., Associat e Prof., 歯学部, 助教授 (40161765)
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| Co-Investigator(Kenkyū-buntansha) |
MYOUKAI Fumio Okayama Univ., Dent.Sch., Assistant Prof., 歯学部, 助手 (50263588)
HONGYO Hiroshi Okayama Univ., Dent.Sch., Assistant Prof., 歯学部, 助手 (80243476)
NAKAGAWA Masatsugu Okayama Univ., Dent.Sch., Assistant Prof., 歯学部, 助手 (80243468)
ISOSHIMA Osamu Okayama Univ., Dent.Sch., Assistant Prof., 歯学部・付属病院, 講師 (90176256)
宮本 学 岡山大学, 歯学部, 助手 (40252978)
小林 芳友 岡山大学, 歯学部, 助手 (90234856)
永井 淳 岡山大学, 歯学部附属病院, 講師 (70252989)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,100,000 (Direct Cost: ¥6,100,000)
Fiscal Year 1994: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1993: ¥3,800,000 (Direct Cost: ¥3,800,000)
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| Keywords | Protein kinase C / Cyclic AMP / CD18 / CD11 / Intracellular calucium ion / Phosphorylation / Leukotoxin / A.actinomycetemcomitans / 若年性歯周炎 / 好中球 / 走化能 / プロテインキナーゼC / LFA-1 / FMLP / cAMP |
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| Research Abstract |
In this project, we analyzed themechanism of depressed neutrophil chemotaxis in patients with early-onset periodontitis from the standpoint of intracellular signal transduction mechanism. We analyzed both of depressed chemotaxis mechanism in peripheral blood neutrophil, that genetically restricted, and in a study model that might be occurred in local periodontal region as the result of host-parasite interaction. Firstly, we evaluated the association between chemotaxis of peripheral neutrophils and the progression of periodontal disease with using a new clinical parameter. We could classify the patients into two groups ; 1) patients with depressed neutrophil chemotaxis and other abnormal reaction of neutrophil and 2) patients with normal neutrophil chemotaxis and severe A.actinomycetemcomitans (Aa) infection. Former is restricted genetically and later is the result from the interaction between Aa and neutrophils. Then, we analyzed 1) the abnormal reaction of peripheral neutrophils, that
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restricted genetically, from the stand points of intracellular signal transduction and 2) the influences on signal transduction of leukocytes by leukotoxin from Aa. The main project tittles were 1. the role of neutrophil chemotaxis on advanced periodontitis, 2. depressed neutrophil chemotaxis and the signal transduction mechanism in juvenile periodontitis, i) protein kinase C activity in neutrophils from juvenile periodontitis patients, ii) the change of intracellular concentration of calcium ion with stimulation of chemoattractant, iii) the deficient expression of CD18 molecule on cell surface in early-onset periodontitis, 3. the mechanism of cytotoxity of leukotoxin from Aa. Protein kinase C activity was low in the neutrophils from juvenile periodontitis patients. Deficient CD18 expression was not caused by anomaly on the genomic DNA.leukotoxin from Aa enhances the calcium dependent phosphorylation of 110 kDa protein of HL-60 cell. Periodontitis with similar clinical status not always have the same disorder of host defensive cells even in the same family. We have to further clarify the polymorphism on mechanism of development of periodontal disease at cellular functions, bioactive molecules, and genes. Less
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