2002 Fiscal Year Final Research Report Summary
Detection of bacterial species using 16S rDNA existed in deep layers of carious lesions with pulp exposure embedded with plastic material and analysis of the pathogenesis of pulpitis
| Project/Area Number |
13672000
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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 | The University of Tokushima |
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Principal Investigator |
OZAKI Kazumi Tokusima Univ., University Dental Hospital Assistant Professor, 歯学部附属病院, 講師 (90214121)
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| Co-Investigator(Kenkyū-buntansha) |
YUMOTOI Hiromichi Tokusiha Univ., School of Dentistry Instructor, 歯学部, 助手 (60284303)
KAWASAKI Akiko Tokusiha Univ., School of Dentistry Instructor, 歯学部, 助手 (60294708)
MATSUO Takashi Tokusiha Univ., School of Dentistry Professor, 歯学部, 教授 (30173800)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Dentinal caries / 16S rDNA / Embedding material for TEM / TEM-in situ hybridization / RT-PCR / Toll-like receptor |
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| Research Abstract |
Resin-embedded human carious dentin was used as template for polymerase chain reaction (PCR) detection of bacterial 16 rDNA existed in deep layers of carious lesions. A total of 34 bacterial spesies were detected from 39 human carious samples. 4.8 bacterial species per carious sample of coronal caries, 3.9 species of root caries were detected.
Characteristics of Toll-like receptor (TLR)-expressing cells in human dental pulp were studied. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis comfirmed the expression of TLR-2 Mrna in all of the inflamed pulps. In situ hybridization analysis using digoxigenin-labeled single strand Crna probe showed that TLR-2, 4 and 9 Mrna-expressing cells could be found in the inflamed pulps. Immunohistological analysis at a light microscopic level showed that TCR-2 and 4 protein in the cell body. In antigen-presenting cell (APC), dendritic cells were expressed TLR-2 protein, and macrophage-like cells were expressed TLR-4 protein in the cell body. These results suggested that TLR might be involved in the pathogenesis of pulpitis.
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