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RANKL在人乳牙生理性牙根吸收过程中牙周膜细胞中的表达及作用

Expression and role of RANKL in periodontal ligament cells during physiological root-resorption in human deciduous teeth.

作者信息

Fukushima Hidefumi, Kajiya Hiroshi, Takada Keisuke, Okamoto Fujio, Okabe Koji

机构信息

Department of Oral Growth and Development and Physiological Science and Molecular Biology, Fukuoka Dental College, Fukuoka, Japan.

出版信息

Eur J Oral Sci. 2003 Aug;111(4):346-52. doi: 10.1034/j.1600-0722.2003.00051.x.

DOI:10.1034/j.1600-0722.2003.00051.x
PMID:12887401
Abstract

Although important roles of receptor activator of NF-kappaB ligand (RANKL) and its receptor (RANK) have been established for osteoclastogenesis and bone resorption, their expression and roles during physiological root resorption remain uncertain. Physiological root resorption for shedding of human deciduous teeth is mediated by osteoclast-like cells (odontoclasts). In this study, we examined the expression of RANKL and osteoprotegerin (OPG), a decoy receptor that prevents RANKL from binding to RANK in human periodontal ligament (PDL) cells during physiological root resorption using immunocytochemistry and reverse transcriptase polymerase chain reaction. The effect of RANKL on root resorbing activity of odontoclasts was evaluated by measuring the size of dissolved area on calcium phosphate-coated coverslips. The PDL cells isolated from either non-resorbing deciduous teeth or permanent teeth abundantly expressed OPG, but not RANKL. In contrast, PDL cells derived from resorbing deciduous teeth dominantly expressed RANKL. Human odontoclasts derived from resorbing deciduous teeth expressed both RANKL and RANK. It was observed that RANKL increased odontoclast actin ring formation and resorbing activity in a dose-dependent manner. These results indicate that PDL cells during the root-resorbing state express RANKL but decrease OPG expression. Expression of RANKL likely participates in odontoclastogenesis and activates physiological root resorption.

摘要

尽管核因子κB受体活化因子配体(RANKL)及其受体(RANK)在破骨细胞生成和骨吸收中所起的重要作用已得到证实,但其在生理性牙根吸收过程中的表达及作用仍不明确。人类乳牙脱落的生理性牙根吸收是由破骨细胞样细胞(破牙细胞)介导的。在本研究中,我们运用免疫细胞化学和逆转录聚合酶链反应,检测了生理性牙根吸收过程中人类牙周膜(PDL)细胞中RANKL和骨保护素(OPG,一种阻止RANKL与RANK结合的诱饵受体)的表达情况。通过测量磷酸钙包被盖玻片上溶解区域的大小,评估了RANKL对破牙细胞牙根吸收活性的影响。从未发生吸收的乳牙或恒牙中分离出的PDL细胞大量表达OPG,但不表达RANKL。相反,来自发生吸收的乳牙的PDL细胞主要表达RANKL。来自发生吸收的乳牙的人类破牙细胞同时表达RANKL和RANK。观察发现,RANKL以剂量依赖的方式增加破牙细胞肌动蛋白环的形成和吸收活性。这些结果表明,处于牙根吸收状态的PDL细胞表达RANKL,但OPG表达降低。RANKL的表达可能参与破牙细胞生成并激活生理性牙根吸收。

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