Effect of neuropeptides on the progression of stress-induced periodontitis

2005 Fiscal Year Final Research Report Summary

• Project/Area Number: 16592070
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Periodontal dentistry
• Research Institution: KYUSHU UNIVERSITY
• Principal Investigator: GOTO Yasuharu Kyushu University, Faculty of Dentistry, Research Associate, 大学院・歯学研究院, 助手 (00170473)
• Co-Investigator(Kenkyū-buntansha): AKAMINE Akifumi Kyushu University, Faculty of Dentistry, Professor, 大学院・歯学研究院, 教授 (00117053)
• Project Period (FY): 2004 – 2005
• Keywords: stress / periodontitis / neuropeptide / substance P / neutrophils / functional epithelium / 遊走 / 血管透過性

Research Abstract

The junctional epithelium (JE) is affected earlier than oral sulcular epithelium (OSE) and oral epithelium (OE) by stimuli that evoke periodontal inflammation. It has been suggested that the link between inflammatory disease and stress may lie in the release of neuropeptides from sensory nerve fibers upon stimulation by external stimuli. The purpose of this study was to investigate the effect of Substance P (SP) on the progression of periodontitis. The effect of SP on JE cells and neutrophils in the JE was studied by light and electron microscopy using diaminobenzidine (DAB) reaction. Topical application of SP at concentrations of 10^<-4> M into the rat molar gingival sulcus caused plasma extravasation in the sub-JE area. Intravenous injection of SP (10ug/kg or 100ug/kg) and local application of SP at concentrations of 10^<-4>M caused migration of neutrophils in the JE. Some of these migrating neutrophils released 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 in the JE enhances migration of neutrophils and endocytotic ability of neutrophils and JE cells to form a line of defense against harmful stimuli such as bacteria. Further research is needed to dissect the mechanisms involved in SP-induced neutrophil infiltration in the JE.