Elucidation of the mechanism of inflammatory bone resorption embellished by mechanical stress

机械应力修饰下炎症性骨吸收机制的阐明

基本信息

批准号：
13672196
负责人：
TATSUMI Junichi
金额：
$ 1.92万
依托单位：
Meikai University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2003
项目状态：
已结题

项目摘要

Occlusal trauma causes alveolar bone resorption around the root in healthy periodontal tissue. In periodontitis tissue, occlusal trauma is also considered to be a factor that accelerates alveolar bone resorption caused by bacterial infection. In an experimental occlusal trauma model using the beagle dogs, the occurrence of thrombosis in microcirculation of periodontal ligament was demonstrated histopathologically. Thereby, occlusal trauma may cause hypoxia in the periodontal ligament. In the present study, the effects of hypoxia on the production of bone-resorbing factors from cultured human periodontal ligament cells were examined. Periodontal ligament culture cells were divided into 2 groups. One group was cultured under the hypoxic condition in 1% O2 (Hypoxia group), and the other was cultured in 20% O2 (Normoxia group). The concentrations of bone resorbing factors, vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-1β, tumor necrosis factor -α (TNF-α), and prostaglan … More din E2 (PGE_2) in the cell culture supernatants were determined by use of enzyme-linked immunosorbent assay. Expressions of the mRNAs concerned with these bone resorbing factors were detected by performing the reverse transcription-polymerase chain reaction. Hypoxia group showed higher concentrations of VEGF and IL-6 in their culture media than Normoxia group (p<0.01), and the observed expression of mRNAs for these proteins in the Hypoxia group was also higher than that of them in the Normoxia group. The expression of IL-1β was observed in only in the Hypoxia group. TNF-α and PGE_2 were undetectable in culture medium from both Hypoxia and Normoxia groups, whereas COX-2 mRNA was detected from the Hypoxia group. However, production of PGE_2 became discernible 3 hours after the addition of recombinant human VEGF even under normoxic condition. Similarly, PGE_2 became detectable in the culture medium 9 hours after the oxygen level had been elevated from hypoxic to normoxic. These results suggest that hypoxia induced by occlusal trauma may stimulate the periodontal ligament to produce bone resorbing factors, resulting in resorption of alveolar bone. Less

咬合创伤会导致健康牙周组织周围根部牙槽骨骨分辨率。在牙周炎组织中，咬合创伤也被认为是加速由细菌感染引起的肺泡骨溶解的因素。在使用Beagle狗的实验性咬合创伤模型中，在组织病理学上证明了血栓形成在牙周韧带微循环中的发生。因此，咬合创伤可能导致牙周韧带缺氧。在本研究中，检查了缺氧对培养的人牙周韧带细胞产生骨质化因子的影响。牙周韧带培养细胞分为两组。在1％O2（缺氧组）中，在低氧条件下培养了一组，另一组在20％O2（Normoxia组）中培养。 The concentrations of bone resorbing factors, vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-1β, tumor necrosis factor -α (TNF-α), and prostaglan … More din E2 (PGE_2) in the cell culture supernatants were determined by use of enzyme-linked immunosorbent assay.通过执行逆转录聚合酶链反应检测到与这些骨分辨因子有关的mRNA的表达。缺氧组在其培养基中显示出高于正常氧基团的VEGF和IL-6（p <0.01），并且在低氧组中观察到的这些蛋白的mRNA表达也高于正常氧组中的mRNA。仅在缺氧组中观察到IL-1β的表达。在缺氧和常氧基团的培养基中，无法检测到TNF-α和PGE_2，而从缺氧组中检测到COX-2 mRNA。但是，即使在常氧状态下，添加重组人VEGF 3小时后，PGE_2的产生也可辨别。同样，在氧气水平从低氧到常氧升高后9小时后，PGE_2在培养基中被检测到。这些结果表明，咬合创伤引起的缺氧可能会刺激牙周韧带产生骨分辨因子，从而导致牙槽骨的分辨率。较少的