1994 Fiscal Year Final Research Report Summary
Periodontal Disease and the Immune System.
| Project/Area Number |
05404066
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| Research Category |
Grant-in-Aid for General Scientific 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 | Niigata University |
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Principal Investigator |
HARA Kohji Niigata University School of Dentistry Professor, 歯学部, 教授 (20018419)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Tetsuo Niigata University School of Dentistry Associate, 歯学部, 助手 (00215344)
TAKEUCHI Yoshiharu Niigata University School of Dentistry Associate, 歯学部, 助手 (10236440)
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| Project Period (FY) |
1993 – 1994
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| Keywords | Local host immune response / Periodontitis / Host-parasite interaction / Biased host-defense network / Th cells / Polymorphonuclear leukocytes / Functional impairment / Eosinophil |
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| Research Abstract |
Periodontitis is acknowledged as a disease resulting from an imbalance the local immune system and pathogenic microbiota. We attempted to clarify the host-defense/immune network relevant to the pathogenesis and development of periodontitis by a series of experiments described herein. To clarify the pathway through which gingival tissue-borne T cells infiltrate the gingival crevice through the pocket epithelium, we quantitated CD4+, CD11a+and CD25+ cells in the area subjacent to the CD54+ pocket epithelium of gingival biopsies obtained from patients with periodontitis, and analyzed CD11a+CD25+CD4+ cells in GCF and venous blood by 3-color flow cytometry(FCM). The experiments demonstrated a correlation between the localization of CD54+ epithelial cells and that of CD11a+ T cells, which suggest an involvement of CD11a/CD54 molecules in T cell migration into gingival crevice. Then, because the afferent limb of the immune network is borne by effector cells, we assessed in vitro the extent in
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which neutrophil oxidative response can be depressed by exposure to P.gingivalisand compared the results with an in vivo quantitative analysis of the oxidative function of GCF neutrophil collected by crevicular washing from periodontal pockets with or without P.gingivalis. The in vitroexperiments showed that neutrophil incubated with P.gingivalis specifically reduced of DCF formation. The in vivo demonstrated a lower DCF formation by PMA and FMLP-stimulated GCF neutrophil from P.g.+sites than from P.g.-sites, suggesting that P.gingivalis depresses GCF neutrophil oxidative product formation. We then assessed the effect of P.gingivalis on neutrophil FcgammaRII and III mRNA levels by RT-PCR.Dialysates at different protein contents induced differential neutrophil Fcgamma mRNA levels, indicating the relevance of P.gingivalis to neutrophil functional impairment in periodontitis. IgE and sCD23 titer in GCF of AP patients reached ca.24-fold that in sera, but GCF of gingivitis patients contained no detectable sCD23. GCF from AP patients contained a high rate of activated cosinophils secreting ECP,while GCF of gingivitis patients did not. These imply that ECP-secreting activated eosinophils are relevant to the pathology of adult periodontitis. The above experiments show that periodontitis is a disease arising from a multiple biases and over-activation of the immune system, parts of them being elicited by periodontopathic bacterial species. A study combiningRNA seprotection assay and in situ hybridizationis underway to clarify the relationship between the cytokine production profile in periodontal lesions and the disease stata. Less
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Research Products
(4 results)
