Department of Craniofacial Development, Dental Institute, King's College London, Guy's Hospital, London SE19RT, UK.
Semin Cell Dev Biol. 2010 May;21(3):314-24. doi: 10.1016/j.semcdb.2010.01.007. Epub 2010 Jan 18.
Teeth develop in the mammalian embryo via a series of interactions between odontogenic epithelium and neural crest-derived ectomesenchyme of the early jaw primordia. The molecular interactions required to generate a tooth are mediated by families of signalling molecules, which often act reiteratively in both a temporal and spatial manner. Whilst considerable information is now available on how these molecules interact to produce an individual tooth, much less is known about the processes that control overall tooth number within the dentition. However, a number of mouse models are now starting to provide some insight into the mechanisms that achieve this. In particular, co-ordinated restriction of signalling molecule activity is important in ensuring appropriate tooth number and there are different requirements for this suppression in epithelial and mesenchymal tissues, both along different axes of individual jaws and between the jaws themselves. There are a number of fundamental mechanisms that facilitate supernumerary tooth formation in these mice. A key process appears to be the early death of vestigial tooth primordia present in the embryo, achieved through the suppression of Shh signalling within these early teeth. However, restriction of WNT signalling is also important in controlling tooth number, with increased transduction being capable of generating multiple tooth buds from the oral epithelium or existing teeth themselves, in both embryonic and adult tissues. Indeed, uncontrolled activity of this pathway can lead to the formation of odontogenic tumours containing multiple odontogenic tissues and poorly formed teeth. Finally, disrupted patterning along the buccal-lingual aspect of the jaws can produce extra teeth directly from the oral epithelium in a duplicated row. Together, all of these findings have relevance for human populations, where supernumerary teeth are seen in association with both the primary and permanent dentitions. Moreover, they are also providing insight into how successional teeth form in both embryonic and post-natal tissues of the jaws.
哺乳动物胚胎中的牙齿通过牙原上皮和早期颌原基神经嵴衍生的中胚层之间的一系列相互作用而发育。产生牙齿所需的分子相互作用由信号分子家族介导，这些信号分子通常以时间和空间的方式反复作用。虽然现在已经有大量关于这些分子如何相互作用产生单个牙齿的信息，但对于控制牙列中牙齿总数的过程知之甚少。然而，现在有一些小鼠模型开始提供一些关于实现这一目标的机制的见解。特别是，信号分子活性的协调限制对于确保适当的牙齿数量很重要，并且上皮组织和间充质组织都有不同的要求，无论是在单个颌骨的不同轴线上，还是在颌骨本身之间。有许多基本机制可以促进这些小鼠中多余牙齿的形成。一个关键过程似乎是胚胎中存在的退化牙原基的早期死亡，这是通过抑制这些早期牙齿中的 Shh 信号来实现的。然而，WNT 信号的限制对于控制牙齿数量也很重要，增加转导能力能够从口腔上皮或现有的牙齿本身产生多个牙齿芽，无论是在胚胎组织还是成年组织中。事实上，该途径的不受控制的活性可导致形成包含多个牙源性组织和形态不良的牙齿的牙源性肿瘤。最后，沿着颌骨的颊舌方向的图案破坏可直接从口腔上皮产生多余的牙齿，形成重复的一行。总之，所有这些发现都与人类群体有关，在那里，多余的牙齿与乳牙和恒牙都有关。此外，它们还为胚胎和颌骨的产后组织中的继生牙形成提供了深入的了解。
