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RANKL和OPG mRNA在牙周病中的表达:可能参与骨破坏过程。

Expression of RANKL and OPG mRNA in periodontal disease: possible involvement in bone destruction.

作者信息

Liu D, Xu J K, Figliomeni L, Huang L, Pavlos N J, Rogers M, Tan A, Price P, Zheng M H

机构信息

Department of Orthopaedic Surgery, Queen Elizabeth II Medical Centre, UWA, WA, Australia.

出版信息

Int J Mol Med. 2003 Jan;11(1):17-21. doi: 10.3892/ijmm.11.1.17.

DOI:10.3892/ijmm.11.1.17
PMID:12469211
Abstract

Periodontitis is a complex, multifactorial process affected by bacterial plaque-components and host defense mechanisms. Inflammation of the periodontitium may lead the destruction of the underlying ligament and alveolar bone. Receptor activator of NF-kappaB ligand (RANKL), a novel TNF receptor-related protein is an important factor for osteoclast differentiation and activation. Given osteolysis by osteoclast has been demonstrated in periodontitis, we hypothesized that RANKL expression may be associated with bone destruction in periodontitis. We used semi-quantitative RT-PCR to compare the gene expression of RANKL and osteoprogerin (OPG), a decoy receptor of RANKL, between moderate and advanced periodontitis, and healthy subjects. The level of RANKL mRNA was highest in advanced periodontitis. In contrast, the level of OPG mRNA in both advanced and moderate periodontitis was lower than that in the healthy group. It appears that the ratio of RANKL to OPG mRNA in periodontitis has increased. To determine the localization of RANKL gene transcripts in gingival tissue at the cellular level, in situ hybridization was performed using digoxigenin-labeled specific riboprobes. RANKL mRNA was expressed in inflammatory cells, mainly lymphocyte and macrophages. In addition, proliferating epithelium in the vicinity of inflammatory cells expressed high levels of RANKL mRNA. In short, our data suggest that up regulation of RANKL mRNA in both inflammatory cells and epithelium may be associated with the activation of osteoclastic bone destruction in periodontitis.

摘要

牙周炎是一个受细菌菌斑成分和宿主防御机制影响的复杂多因素过程。牙周组织的炎症可能导致其下方韧带和牙槽骨的破坏。核因子κB受体活化因子配体(RANKL)是一种新型的肿瘤坏死因子受体相关蛋白,是破骨细胞分化和活化的重要因素。鉴于破骨细胞引起的骨溶解在牙周炎中已得到证实,我们推测RANKL表达可能与牙周炎中的骨破坏有关。我们使用半定量逆转录聚合酶链反应(RT-PCR)比较中度和重度牙周炎患者以及健康受试者中RANKL和骨保护素(OPG,RANKL的诱饵受体)的基因表达。RANKL mRNA水平在重度牙周炎中最高。相反,重度和中度牙周炎患者的OPG mRNA水平均低于健康组。牙周炎中RANKL与OPG mRNA的比例似乎有所增加。为了在细胞水平上确定牙龈组织中RANKL基因转录本的定位,我们使用地高辛标记的特异性核糖探针进行了原位杂交。RANKL mRNA在炎症细胞中表达,主要是淋巴细胞和巨噬细胞。此外,炎症细胞附近增殖的上皮细胞表达高水平的RANKL mRNA。简而言之,我们的数据表明,炎症细胞和上皮细胞中RANKL mRNA的上调可能与牙周炎中破骨细胞性骨破坏的激活有关。

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