1995 Fiscal Year Final Research Report Summary
The immunologically and molecular biologically investigation for diagnostic methods of periodontal disease activity
| Project/Area Number |
06304041
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Conservative dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
OKADA Hiroshi Osaka Univ.Fac.of Dentistry, Dept.of Periodontol.and Endodontol., Professor., 歯学部, 教授 (40038865)
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| Co-Investigator(Kenkyū-buntansha) |
MAITA Eikichi Tohoku Univ.School of Dentistry, Dept.of Endodontol.and Periodontol., Associate, 歯学部, 助教授 (80108547)
KATO Ihachi Nagasaki Univ.School of Dentistry, Dept.of Periodontol., Professor., 歯学部, 教授 (30005087)
MAEDA Katumasa Kyusyu Univ.Fac.of Dentistry, Dept.of Periodontol.and Endodontol., Professor., 歯学部, 教授 (00117243)
MURAYAMA Youji Okayama Univ.Dental School, Dept.of Periodontol.and Endodontol., Professor., 歯学部, 教授 (50029972)
MURAI Seidai Nihon Univ.Fac.of Dentistry, Dept.of Periodontol., Professor., 歯学部, 教授 (50059185)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Periodontal disease activity / Inflammatory cytokine / Alkaline phosphatase / Periodontopathic bacteria / Polymerase chain reaction / Neutrophil lysosomal proteinase / PH in periodontal pockets / Secretory leukocyte protease inhibitor |
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| Research Abstract |
This study was designed to immunologically and molecular biologically evaluate the diseased conditions of periodontitis and develop procedures to diagnose active lesions and susceptible patients. The techniques utilizing DNA probes and polymerase chain reaction were introduced to sensitively detect and identify periodontopathic bacteria in subgingival plaque. It was shown that P.gingivalis (Pg) was frequently detected in active diseased lesions. Additionally, T.denticola (Td) was always found in the unsuccessfully treated periodontal lesions but not in the successfully treated lesions, suggesting that Td would be a diagnostic indicator of the diseased conditions in the lesions after periodontal treatments. It was also suggested that Vgamma9/Vdelta2 T cells may play an important role in prevention of bacterial infection or tissue destruction. Futhermore, immune response against heat shock protein (HSP) 60 may react with both periodontitis-associated microorganisms and host cells because
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HSP 60 specific antibodies of periodontitis patients crossreact to proteins isolated from gingival fibroblast. In addition, it was also indicated that the levels of serum actibodies specific to Pg could be used as a risk indicator for the progression of periodontal diseases, because the susceptible patients to periodontal diseases exhibited significantly higher anti-Pg antibody levels than the resistant patients. Furthermore, the high levels of polyamines, alkaline phosphatase, platelet-activating factor activities, neutrophil lysosomal proteinase (medullasin and cathepsin G), secretory leukocyte protease inhibitor (SLPI), inflammatory cytokines (IL-1, IL-6, Il-8) and prostaglandin E_2 were frequently observed in gingival crevicular fluid. Also pH in periodontal pockets was significantly high in the sites with deep probing depth. Parameters showing above seem to be useful to diagnose active periodontal diseases. In conclusion, it was suggested that the combining host immune responses, inflammatory cytokines and mediators in local diseased sites examined in this study may enable us to diagnose periodontal dosease activity. Less
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