Investigation of host factor in early-onset peiodontitis on people with Down syndrome.
Project/Area Number |
15591994
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pathobiological dentistry/Dental radiology
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Research Institution | Osaka University |
Principal Investigator |
MORISAKI Ichijiro Osaka University, Dental Hospital, Professor, 歯学部附属病院, 教授 (30116115)
|
Co-Investigator(Kenkyū-buntansha) |
AMANO Atsuo Osaka University, Graduate School of Dentistry, Professor, 大学院・歯学研究科, 教授 (50193024)
AKIYAMA Shigehisa Osaka University, Dental Hospital, Associate Professor, 歯学部附属病院, 助教授 (00283797)
MURAKAMI Jumpei Osaka University, Dental Hospital, Instructor, 歯学部附属病院, 助手 (70362689)
|
Project Period (FY) |
2003 – 2004
|
Project Status |
Completed (Fiscal Year 2004)
|
Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥2,500,000 (Direct Cost: ¥2,500,000)
|
Keywords | Down syndrome / peirodontitits / Porphyromonas gingivalis / adherence / invasion / gingival epithelial cell / gingival fibroblast / P.gingivalis / 歯肉 / 上皮細胞 |
Research Abstract |
Person with Down syndrome (DS) has been known to be vulnerable in defence mechanism against infection and susceptible to an early-onset as well as a severe adult periodontitis caused by Porphyromonas gingivalis which is the most relevant pathogen of the periodontal disease. Gingival epithelial cells (HGE) and fibroblasts (HGF) consisting of periodontal tissue are acting as a front barrier against invasion of pathogenic microorganisms including P.gingivalis. However, there is little study on the host responses of DS HGE to P.gingivalis infection. In this research project, we tried to develop the modified culture method for improving difficulty of HGE culture. Then we compared the susceptibility of HGE and HGF derived from both DS and normal subjects (NS) to P.gingivalis infection by invasion assay and confocal microscopic observasion. The HGE derived from DS could be cultured more selectively in the medium without serum compared to medium containing serum, however, it was still difficult
… More
to culture HGE in the serum free medium. This phenomenon seems to be due to an excess chromosome and reduced telomere in DS cells causing altered cell division and maintenance by deteriorated protein synthesis. Invasion assay showed HGE derived from DS was more susceptible to P.gingivalis infection in vitro than HGE from NS. Recently, it was reported that P.gingivalis could adhere and invade to HGF. In this study, we showed that greater number of P.gingivalis had adhered and invaded to HGF from DS than to HGF from NS. These finding indicated that not only HGE but DS-derived HGF, existing beneath the epithelial cell layer, was more susceptible to P.gingivalis than these from NS. Confocal microscopic observation showed that the numbers of P.gingivalis -invaded into both HGE and HGF from DS were grater than those incaded into HGE and HGF from NS, respectively, suggesting that the gingival cells from DS are more susceptible to P.gingivalis infection in vitro than those cells from NS. In conclusion, epithelial cells and fibroblasts of DS periodontal tissue are susceptible to P.gingivalis infection, and these altered defence mechanism could be responsible for early-onset severe periodontitis in DS. Less
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Report
(3 results)
Research Products
(24 results)