Establishment of molecular biological diagnostic strategies for periodontal diseases

In this study，我们attempted to establish the strategies to diagnose the molecular pathogenesis of periodontal疾病。Genomic polymerase chain反应（PCR） technique enabled us to sensitively andspecifically detect Porphyromonas gingivalis (p.g.) and Actinobucillus actinomycetemcomitans （a.a.）in subgingival dental plaques. Furthermore, utilizing reverse transcription (RT)-PCR技术，我们established the semiquantitative detection system of multiple cytokine mRNA in gingival specimensisolated 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 offirst visit,reevaluation and supportive periodontal therapy (SPT) and analyzed those samples by molecular生物技术描述我们观察了一种多种mRNA表达式inflammatory cytokines in inflamed periodontal lesions. Interestingly，we could statistically divide the multiple cytokine mRNA表达式profiles into 5 groups by cluster analysis. In particular，approximately 50% of the diseased sites from EOP were categorized into the groups showing relativelylow expression of IL-8 and IFN - D2γ - D2 mRNA.In another study，serum levels of IgG subclass antibodies against p.g. were examined in relation to alveolar bone lossperiodontitis patients receiving SPT for 5 years. Statistically significant positive correlationwas seen for the relationship between IgG2 levels and△bone loss score (p<0.001) in the SPTpatients. This suggests that the prolonged IgG2 response observed after periodontal treatment可能beassociated with recurrent or persistent periodontal destruction.In体外研究，我们demonstrated that gingival epithelial cells preferentially secreted IL-8 and MCP-1 whenstimulated with p.g. sonic extract. In addition，we clarified that adhesive interactions between lymphocytes and gingival fibroblasts inducedinflammatory cytokine expression in the gingival fibroblasts.那些研究成果副细胞活动参与者in the cytokine network in inflamed periodontal lesions. Less

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 … More 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