2003 Fiscal Year Final Research Report Summary
Genetic risk factors for periodontitis in Japanese population
| Project/Area Number |
13672201
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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 | Fukuoka Dental College |
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Principal Investigator |
RIKIMARU Tetsuya Fukuoka Dental College, Faculty of Dentistry, Assistant Professor, 歯学部, 助手 (10299589)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAI Atsushi Fukuoka Dental College, Faculty of Dentistry, Associate Professor, 歯学部, 助教授 (70252989)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Periodontal disease / individual diversity in periodonto-pathogenesis / antigen presentation / inflammatory cytokines / genotyping / SNPs / HLA-DR / HLA-DQ |
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| Research Abstract |
Periodontal disease is one of choronic inflammatory disease caused by host-bacterial interactions. The most of the pathogenesis of this disease involved in individual diversity in host defense mechanisms against bacteria colonizing periodontal lesions. Head investigator had found remarkable individual differences in populations of stimulated peripheral blood T cells after co-culture with live periodontopathic bacteria, Porphyromonas gingivalis.
Taking into account of recent studies in periodontal pathogenesis have revealed that single polymorphisms (SNPs) might play an important role in periodonto-pathogenesis, by strengthening or weakening the reaction against bacterial lipopolysaccharides, therefore the head investigator aimed to investigate genetic backgrounds in Japanese populations, by comparing genetic markers between high responders and low responders.
The T cell response was clearly showed HLA-DR and HLA-DQ restriction but not HLA-DP, which had been reported to show genetically inequillibrium to TNF-A gene. Statistical skew in any 'susceptible' inflammatory cytokine SNPs nor subpopulational clustering with mitochondrial D-loop region analysis could not be found between subject groups.
The head investigator found that high responders bear susceptible HLA-DR and HLA-DQ genotype for early-onset periodontitis, but not susceptible inflammatory cytokine SNPs, suggesting that individual differences in T cell reactivity might reside in the process of antigen presentation and recognition rather than inflammatory cytokine production.
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