Project/Area Number |
05671599
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Conservative dentistry
|
Research Institution | Kyushu University |
Principal Investigator |
KABASHIMA Hiroaki Kyushu Univ., Dentistry, Research Associate, 歯学部, 助手 (20214504)
|
Co-Investigator(Kenkyū-buntansha) |
HASHIGUCHI Isamu Kyushu Univ., Dentistry, Research Associate, 歯学部, 助手 (10150476)
HIROFUJI Takao Kyushu Univ., Dentistry, Assistant Professor, 歯学部, 講師 (10189897)
MAEDA Katsumasa Kyushu Univ., Dentistry, Professor, 歯学部, 教授 (00117243)
鳥谷 芳和 九州大学, 歯学部, 医員 (90211408)
|
Project Period (FY) |
1993 – 1995
|
Project Status |
Completed (Fiscal Year 1995)
|
Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
Keywords | Periodontal disease / GCF / IL-1alpha / IL-1beta / IL-1 Ra / IL-4 / CD4 positive cell / CD68 positive cell / IL‐1α / IL‐1β / IL‐1Ra / IL‐4 / 臨床的慢性状態 / IL-1alpha / IL-1receptor antagonist |
Research Abstract |
The gingival crevicular fluid (GCF) from moderate inflammation sites in patients with periodontal diseasepredominantly consisted of IL-alpha. Whereas, we found significantly higher level of IL-1beta in GCF from severe inflammation sites in patientswith complaints of spontaneous pain. This suggested that IL-beta is suspected to play an important role in theamplification of inflammatory process in periodontal disease. We detected IL-1 receptor antagonist (IL-1ra) and IL-4 existing in GCF by immunochemical method. However, we could not detect IL-4 in GCF from severe inflammation sites. In addition, we sought to detect whtich cells had produced cytokines in moderately inflamed gingival tissues by means of immunohistochemistry. The cells types expressing CD 68 were indentified as monocytes/macrophages and stained positive for IL-1ra. The helper T cells identified by immunostaining for CD4 stained positive for IL-4. These results suggested that IL-4 was to beone of mediators to regulate the degree of local inflammation in periodontal disease.
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