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RANKL-OPG 系统受龈上和龈下生物膜上清液的差异调节。

The RANKL-OPG system is differentially regulated by supragingival and subgingival biofilm supernatants.

机构信息

Oral Microbiology and Immunology, Institute of Oral Biology, Center of Dental Medicine, University of Zürich, Plattenstrasse 11, 8032 Zürich, Switzerland.

出版信息

Cytokine. 2011 Jul;55(1):98-103. doi: 10.1016/j.cyto.2011.03.009. Epub 2011 Apr 6.

DOI:10.1016/j.cyto.2011.03.009
PMID:21474331
Abstract

Periodontitis is an inflammatory condition that destroys the tooth supporting tissues, including the alveolar bone. It is triggered by polymicrobial biofilms attaching on tooth surfaces, which can be supragingival or subgingival. Bone resorption is triggered by receptor activator of NF-κB ligand (RANKL) and blocked by its soluble decoy receptor osteoprotegerin (OPG), which are cytokines of the tumor necrosis factor ligand and receptor families, respectively. The present study aimed to comparatively investigate the effects of the Zürich in vitro supragingival and subgingival biofilm models, on RANKL and OPG gene expression in primary human gingival fibroblasts (GF) cultures. The cells were challenged with biofilm culture supernatants for up-to 24h. RANKL and OPG gene expression in the cells was analyzed by quantitative real-time polymerase chain reaction (qPCR) and their relative RANKL/OPG ratio was calculated. Both biofilm supernatants induced RANKL expression, but the subgingival caused a more pronounced up-regulation compared to the supragingival (10-fold at 6h and 100-fold at 24h). Changes in OPG expression in response to either biofilm were more limited. Accordingly, the subgingival biofilm caused a greater enhancement of the relative RANKL/OPG ratio (4-fold at 6h and 110-fold 24h). In conclusion, subgingival biofilms exhibit a stronger potency for inducing molecular mechanisms of bone resorption than supragingival biofilms, in line with their higher virulence nature for the development of periodontitis.

摘要

牙周炎是一种炎症性疾病,会破坏牙齿支持组织,包括牙槽骨。它是由附着在牙齿表面的多微生物生物膜引发的,可以是龈上或龈下的。破骨细胞激活受体配体(RANKL)触发骨吸收,并被其可溶性诱饵受体骨保护素(OPG)阻断,它们分别是肿瘤坏死因子配体和受体家族的细胞因子。本研究旨在比较苏黎世体外龈上和龈下生物膜模型对原代人牙龈成纤维细胞(GF)培养物中 RANKL 和 OPG 基因表达的影响。用生物膜培养上清液刺激细胞长达 24 小时。通过实时定量聚合酶链反应(qPCR)分析细胞中 RANKL 和 OPG 基因的表达,并计算其相对 RANKL/OPG 比值。两种生物膜上清液均诱导 RANKL 表达,但龈下生物膜引起的上调更为明显(6 小时时为 10 倍,24 小时时为 100 倍)。对任一生物膜的 OPG 表达变化更为有限。因此,龈下生物膜引起的相对 RANKL/OPG 比值增加(6 小时时为 4 倍,24 小时时为 110 倍)更大。总之,龈下生物膜在诱导骨吸收的分子机制方面比龈上生物膜具有更强的效力,这与它们在牙周炎发展中的更高毒力特性一致。

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