作者: I. Aoyama , B. Calenic , T. Imai , H. Ii , K. Yaegaki
DOI: 10.1111/J.1600-0765.2011.01442.X
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摘要: Aoyama I, Calenic B, Imai T, Ii H, Yaegaki K. Oral malodorous compound causes caspase-8 and -9 mediated programmed cell death in osteoblasts. J Periodont Res 2012; 47: 365–373. © 2011 John Wiley & Sons A/S Background Objective: Hydrogen sulfide (H2S) is one of two volatile sulfur compounds that are known to be the main cause oral malodor; other methyl mercaptan. Other volatiles existing mouth air do not contribute significantly malodor originating cavity. also an etiological factor periodontal disease. However, effects H2S on alveolar bone remain unclear. The objectives this study were determine apoptotic osteoblasts verify molecular pathways. Material Methods: A clonal murine calvaria line was incubated with 50 ng/mL H2S. To detect apoptosis, cells analysed by flow cytometry ELISA. Mitochondrial membrane depolarization assessed using as well. ELISA used evaluate release cytochrome c into cytosol assess Fas ligand, p53, tumor necrosis factor α, interleukin IL1-α IL-β, IL-2, IL-4, IL-10, interferon-γ, granulocyte-colony stimulating granulocyte-macrophage colony factor. Caspase-3, -8 activities estimated. Expression BAX Bcl-2 real-time quantitative RT-PCR. DNA fragmentation detected single-cell gel electrophoresis. receptors evaluated western blotting. Results: After incubation, levels increased a time-dependent manner. depolarization, cytochrome c, p53 caspase-3, all greater. gene activity upregulated, whereas remained low. ligand/Fas receptor, factor α cytokines significant degree. Conclusion: At less-than-pathological concentrations gingival crevicular fluid, induces apoptosis mechanisms underlying process include mitochondrial pathway activation.