1999 Fiscal Year Final Research Report Summary
Establishment of molecular biological diagnostic strategies for periodontal diseases
| Project/Area Number |
09307043
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 | Osaka University |
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Principal Investigator |
OKADA Hiroshi Faculty of Dentistry, Osaka University Professor, 歯学部, 教授 (40038865)
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| Co-Investigator(Kenkyū-buntansha) |
KITAMURA Masahiro Dental Hospital, Osaka University Assistant Professor, 歯学部・附属病院, 講師 (10243247)
MURAKAMI Shinya Dental Hospital, Osaka University Assistant Professor, 歯学部・附属病院, 講師 (70239490)
SHIMAUCHI Hidetoshi Faculty of Dentistry, Osaka University Associate Professor, 歯学部, 助教授 (70187425)
NOZAKI Takenori Faculty of Dentistry, Osaka University Research Associate, 歯学部, 助手 (30263304)
SHIMABUKURO Yoshio Faculty of Dentistry, Osaka University Research Associate, 歯学部, 助手 (50231361)
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| Project Period (FY) |
1997 – 1999
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| Keywords | PERIODONTITIS / DIAGNOSIS / CYTOKINES / PCR / PERIODONTOPATHIC BACTERIA / SERUM ANTIBODY / GINGIVAL EPITHELIAL CELL / GINGIVAL FIBROBLAST |
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| Research Abstract |
In this study, we attempted to establish the strategies to diagnose the molecular pathogenesis of periodontal diseases. Genomic polymerase chain reaction (PCR) technique enabled us to sensitively and specifically detect Porphyromonas gingivalis (P.g.) and Actinobucillus actinomycetemcomitans (A.a.) in subgingival dental plaques. Furthermore, utilizing reverse transcription (RT)-PCR technique, we established the semiquantitative detection system of multiple cytokine mRNA in gingival specimens isolated by needle biopsy method. We then collected subgingival dental plaque, gingival specimens and serum from adult and early-onset periodontitis (EOP) patients at the times of first visit, reevaluation and supportive periodontal therapy (SPT) and analyzed those samples by molecular biological techniques described above. We observed the upregulated mRNA expression of a variety of inflammatory cytokines in inflamed periodontal lesions. Interestingly, we could statistically divide the multiple cyt
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okine mRNA expression profiles into 5 groups by cluster analysis. In particular, approximately 50% of the diseased sites from EOP were categorized into the groups showing relatively low expression of IL-8 and IFNィイD2γィエD2 mRNA.
In another study, serum levels of IgG subclass antibodies against P.g. were examined in relation to alveolar bone loss in periodontitis patients receiving SPT for 5 years. Statistically significant positive correlation was seen for the relationship between IgG2 levels and △bone loss score (p<0.001) in the SPT patients. This suggests that the prolonged IgG2 response observed after periodontal treatment may be associated with recurrent or persistent periodontal destruction.
In in vitro studies, we demonstrated that gingival epithelial cells preferentially secreted IL-8 and MCP-1 when stimulated with P.g. sonic extract. In addition, we clarified that adhesive interactions between lymphocytes and gingival fibroblasts induced inflammatory cytokine expression in the gingival fibroblasts. These results suggest that those resident cells actively participate in the cytokine network in inflamed periodontal lesions. Less
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