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重新审视多生牙:额外牙齿的流行病学和分子基础。

Revisiting the supernumerary: the epidemiological and molecular basis of extra teeth.

机构信息

Department of Orthodontics, East Kent Hospitals NHS Trust, London.

出版信息

Br Dent J. 2010 Jan 9;208(1):25-30. doi: 10.1038/sj.bdj.2009.1177.

DOI:10.1038/sj.bdj.2009.1177
PMID:20057458
Abstract

Supernumerary teeth are a common clinical and radiographic finding and may produce occlusal and dental problems. The aetiological basis of extra teeth is poorly understood in human populations; however, the mouse provides a useful model system to investigate the complex genetics of tooth development. This article describes recent advances in our understanding of the genetic basis of supernumerary teeth. We have reviewed biological evidence that provides insight into why supernumerary tooth formation may occur. Indeed, many of the molecular signalling pathways known to be involved in normal development of the tooth germ can also give rise to additional teeth if inappropriately regulated. These include components of the Hedgehog, FGF, Wnt, TNF and BMP families, which provide a useful resource of candidate genes that may potentially play a role in human supernumerary tooth formation.

摘要

额外牙是一种常见的临床和影像学表现,可能会导致咬合和牙齿问题。在人类中,额外牙的病因基础理解得还不够透彻;然而,老鼠为研究牙齿发育的复杂遗传学提供了一个有用的模型系统。本文描述了我们对额外牙遗传基础的理解的最新进展。我们综述了一些生物学证据,这些证据为我们理解额外牙形成的原因提供了一些线索。事实上,如果调控不当,许多已知参与牙原基正常发育的分子信号通路也可能导致额外牙的形成。这些信号通路包括 Hedgehog、FGF、Wnt、TNF 和 BMP 家族的成分,它们为候选基因提供了一个有用的资源,这些候选基因可能在人类额外牙形成中发挥作用。

相似文献

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Revisiting the supernumerary: the epidemiological and molecular basis of extra teeth.重新审视多生牙:额外牙齿的流行病学和分子基础。
Br Dent J. 2010 Jan 9;208(1):25-30. doi: 10.1038/sj.bdj.2009.1177.
2
[Recent advances in molecular mechanisms of supernumerary tooth formation].[多生牙形成分子机制的最新进展]
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Enhanced BMP signaling results in supernumerary tooth formation in USAG-1 deficient mouse.增强的骨形态发生蛋白(BMP)信号传导导致USAG-1基因缺陷小鼠出现多生牙。
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The epidemiology of supernumerary teeth and the associated molecular mechanism.多生牙的流行病学及其相关分子机制。
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A network of Wnt, hedgehog and BMP signaling pathways regulates tooth replacement in snakes.Wnt、Hedgehog 和 BMP 信号通路网络调节蛇的牙齿替换。
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Rudiment incisors survive and erupt as supernumerary teeth as a result of USAG-1 abrogation.由于USAG-1缺失,残留切牙作为多生牙存活并萌出。
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TNF signaling via the ligand-receptor pair ectodysplasin and edar controls the function of epithelial signaling centers and is regulated by Wnt and activin during tooth organogenesis.通过配体-受体对外胚层发育不良蛋白(ectodysplasin)和外胚层发育不良受体(edar)的肿瘤坏死因子(TNF)信号传导控制上皮信号中心的功能,并在牙齿器官发生过程中受Wnt和激活素调节。
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TNF signalling in tooth development.牙齿发育中的肿瘤坏死因子信号传导
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