2003 Fiscal Year Final Research Report Summary
Effect of stress on the progression of periodontitis
| Project/Area Number |
14571984
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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 | KYUSHU UNIVERSITY |
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Principal Investigator |
GOTO Yasuharu KYUSHU UNIVERSITY, Faculty of Dentistry, Assistant, 大学院・歯学研究院, 助手 (00170473)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAZA Takayoshi KYUSHU UNIVERSITY, Faculty of Dentistry, Assistant, 大学院・歯学研究院, 助手 (80304814)
AKAMINE Akifumi KYUSHU UNIVERSITY, Faculty of Dentistry, Professor, 大学院・歯学研究院, 教授 (00117053)
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| Project Period (FY) |
2002 – 2003
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| Keywords | stress / periodontitis / substance P / junctional epithelium / neutrophils / migration / endocytotic ability / rat |
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| Research Abstract |
It has been suggested that, the link between inflammatory disease (such as periodontitis) and stress may lie in the release of neurotransmitters from sensory nerve fibers upon stimulation by external stimuli. Substance P(SP) has been implicated as one such neurotransmitter which may be associated with inflammation. The purpose of this study was to investigate the effect of SP on the progression of periodontitis. The effect of SP on junctional epithehal cells (JE cells) and neutrophils in the junctional epithelium (JE) was studied by light and electron microscopy using diaminobenzidine (DAB) reaction. Intravenous injection of SP (10μg/kg or 100μg/kg) or local application of SP at concentrations of 10^<-4> M for 15 min caused migration of neutrophils in the JE. Some of these migrating neutrophils released DAB-positive azurophil granules into the intercellular spaces of the JE cells. The JE cells at the coronal portion of the JE seemed to endocytose these granules and digest them in the cells. These findings suggest that SP released from nerve terminals in the JE enhances migration of neutrophils and endocytotic ability of neutrophils and JE cells to form a line of defense against harmful stimuli.
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