1997 Fiscal Year Final Research Report Summary
A study for establishment of judging periodontal disease activity
| Project/Area Number |
08672199
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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 |
Conservative dentistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
HARA Yoshitaka Nagasaki University, School of Dentistry, Associate Professor, 歯学部, 助教授 (60159100)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Yasuo Nagasaki University, School of Dentistry, Instructor, 歯学部, 助手 (90274670)
UKAI Takashi Nagasaki University, School of Dentistry, Instructor, 歯学部, 助手 (20295091)
ABE Yoshihiro Nagasaki University, School of Dentistry, Instructor, 歯学部, 助手 (70202687)
KATO Ihachi Nagasaki University, School of Dentistry, Professor, 歯学部, 教授 (30005087)
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| Project Period (FY) |
1996 – 1997
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| Keywords | IFN-gamma / IL-4 / periodontal disease / Immunohistological study |
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| Research Abstract |
The purpose of this study was to clarify the role of IFN-gamma and IL-4 in periodontal disease. Gingiva was biopsied at tooth extraction or periodontal surgery after examining clinical parameters. Serial paraffin sections were obtained and every five sections were stained immunohistologically with anti-IFN-gamma or IL-4 monoclonal antibody. The specimens were divided into three groups ; no treatment (NT) obtained at tooth extraction, treatment 1 (T1) obtained at periodontal surgery with deep pocket, and treatment 2 (T2) with shallow pocket. Then the number of IFN-gamma bearing cells was highest in NT and that in T2 was the next. When the specimens were grouped with bleeding on probing (Bop), the number of IFN-gamma bearing cells was higher in Bop+. Furthermore, the number of IFN-gamma bearing cells was higher in the gingiva with strong inflammatory cell infiltration than that with weak one. On the other hand, IL-4 bearing cells showed opposite tendency. These findings suggested that IFN-gamma is related with activation of periodontal disease and IL-4 plays the suppressive role in periodontal disease activity.
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