Oral biofilm challenge regulates the RANKL-OPG system in periodontal ligament and dental pulp cells
Oral biofilm challenge regulates the RANKL-OPG system in periodontal ligament and dental pulp cells
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DOI：
10.1016/j.micpath.2010.11.002
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发表时间：
2011-01-01
影响因子：
3.8
通讯作者：
Bostanci, Nagihan
中科院分区：
文献类型：
--
作者：
Belibasakis, Georgios N.;Meier, Andre;Bostanci, Nagihan
口腔细菌引起的炎症性骨破坏是慢性和根尖牙周炎的一个标志。nf - κ B配体受体激活剂（RANKL）激活骨吸收，而骨保护素（OPG）阻断其作用。这些分别是肿瘤坏死因子配体和受体家族的成员。虽然已知单个口腔病原体可以调节与各自疾病相关的细胞（如牙周韧带（PDL）和牙髓（DP）细胞）中RANKL和OPG的表达，但多微生物口腔生物膜的作用尚不清楚。本研究旨在通过实时定量聚合酶链反应研究苏黎世离体龈上生物膜模型对人PDL和DP细胞培养中RANKL和OPG基因表达的影响。RANKL在DP细胞中的表达比PDL细胞明显上调（上调幅度是PDL细胞的4倍），而OPG的上调幅度相似。RANKL/OPG比值仅在DP细胞中增加，表明诱导骨吸收的能力增强。促炎细胞因子白细胞介素-1 β的表达在DP细胞中也增加，但在PDL细胞中没有。总的来说，DP细胞对龈上生物膜的高反应性，而不是PDL细胞对龈上生物膜的高反应性，可能构成了根尖牙周炎的一种假定的致病机制，这可能不是慢性牙周炎的关键。(C) 2010 Elsevier Ltd.版权所有。
Inflammatory bone destruction triggered by oral bacteria is a hallmark of chronic and apical periodontitis. Receptor activator of NF-kappa B ligand (RANKL) activates bone resorption, whereas osteoprotegerin (OPG) blocks its action. These are members of the tumor necrosis factor ligand and receptor families, respectively. Although individual oral pathogens are known to regulate RANKL and OPG expression in cells of relevance to the respective diseases, such as periodontal ligament (PDL) and dental pulp (DP) cells, the effect of polymicrobial oral biofilms is not known. This study aimed to investigate the effect of the Zurich in vitro supragingival biofilm model on RANKL and OPG gene expression, in human PDL and DP cell cultures, by quantitative real-time polymerase chain reaction. RANKL expression was more pronouncedly up-regulated in DP than PDL cells (4-fold greater), whereas OPG was up-regulated to a similar extent. The RANKL/OPG ratio was increased only in DP cells, indicating an enhanced capacity for inducing bone resorption. The expression of pro-inflammatory cytokine interleukin-1 beta was also increased in DP, but not PDL cells. Collectively, the high responsiveness of DP, but not PDL cells to the supragingival biofilm challenge could constitute a putative pathogenic mechanism for apical periodontitis, which may not crucial for chronic periodontitis. (C) 2010 Elsevier Ltd. All rights reserved.