In this study we investigated the expression of HIF-1ɑ in dental pulps of the teeth with severe periodontitis. The expression of HIF-1ɑ in dental pulps of the teeth with severe periodontitis was detected by immunohistochemistry, immunofluorescence and real-time PCR. Bone marrow macrophages (BMMs) were cultured under hypoxia in vitro. HIF-1ɑ, osteoclast-specific factors (NFATc1, CTSK and c-fos) and RANKL-induced osteoclastogenesis were evaluated by immunofluorescence, TRAP staining and western blotting. High levels of HIF-1ɑ protein were detected in dental pulps of teeth with severe periodontitis, whereas few positive HIF-1ɑ expressions were detected in healthy dental pulps. Hypoxia occurred in the dental pulps in response to heavy periodontitis. Many HIF-1ɑ-positive infiltratory inflammatory cells were observed around blood vessels. Tooth internal resorption was found in some teeth with severe periodontitis. The HIF-1ɑ levels were upregulated in BMMs under hypoxia, which also promoted osteoclast formation and resorption by NFATc1, CTSK and c-fos. Teeth with severe periodontitis show hypoxic dental pulps and increased potential of osteoclastic differentiation.

中文翻译：

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与严重牙周炎牙齿相关的缺氧牙髓中高水平的HIF-1ɑ。

在这项研究中，我们调查了HIF-1ɑ在患有严重牙周炎的牙齿的牙髓中的表达。通过免疫组织化学，免疫荧光和实时荧光定量PCR检测HIF-1ɑ在严重牙周炎牙齿牙髓中的表达。在缺氧条件下体外培养骨髓巨噬细胞（BMM）。通过免疫荧光，TRAP染色和蛋白质印迹法评估HIF-1ɑ，破骨细胞特异性因子（NFATc1，CTSK和c-fos）和RANKL诱导的破骨细胞生成。在患有严重牙周炎的牙齿的牙髓中检测到高水平的HIF-1ɑ蛋白，而在健康的牙髓中检测到很少的HIF-1ɑ阳性表达。牙髓缺氧是对重度牙周炎的反应。在血管周围观察到许多HIF-1β阳性浸润性炎症细胞。在一些患有严重牙周炎的牙齿中发现了牙齿内部吸收。低氧下BMMs中HIF-1ɑ水平上调，这也促进了破骨细胞的形成和NFATc1，CTSK和c-fos的吸收。患有严重牙周炎的牙齿显示出缺氧的牙髓并增加了破骨细胞分化的可能性。