Maurin Jean-Christophe, Couble Marie-Lise, Thivichon-Prince Béatrice, Magloire Henri
EA 4691 biomatériaux et inflammation en site osseux, SFR CAP-Santé, université Reims Champagne-Ardenne, UFR d'odontologie, 2, rue du Général Koenig, 51100 Reims, France.
Med Sci (Paris). 2013 Mar;29(3):293-9. doi: 10.1051/medsci/2013293016. Epub 2013 Mar 27.
Dentinal sensitivity is a clinical condition daily encountered by practitioners and constitutes the symptoms of dentinal hypersensitivity, a common dental pain affecting on average 30% of the population. However, the management of this pathology is not always effective due to the lack of knowledge particularly concerning the means by which dental nociceptive signals are transduced. The mechanisms underlying dentin sensitivity still remain unclear probably due to the structural and functional complexity of the players including odontoblasts, nerve endings and dentinal fluid running in the dentinal tubules. The unique spatial situation of odontoblasts, ciliated cells in close relationship with nerve terminals, suggests that they could play a pivotal role in the transduction of sensory events occurring within the dentin tissue. Our studies have identified mechano-thermosensitive transient receptor potential ion channels (TRPV1-4, TRPA8, TRPM3, KCa, TREK-1, PC1, PC2) localised on the odontoblastic membrane and at the base of the cilium. They could sense temperature variations or movements of dentinal fluid within tubules. Moreover, several voltage-gated sodium channels confer excitable properties to odontoblasts in response to injection of depolarizing currents. In vivo, these channels co-localize with nerve endings at the apical pole of odontoblasts, and their expression pattern seems to be correlated with the spatial distribution of stretch-activated KCa channels. All these data strengthen the hypothesis that odontoblasts could act as sensor cells able to transmit nociceptive signals. However, how cells sense signals and how the latter are transmitted to axons represent the main issue to be solved.
牙本质敏感是临床医生日常遇到的一种情况,它构成了牙本质过敏症的症状,这是一种常见的牙齿疼痛,平均影响30%的人群。然而,由于缺乏相关知识,特别是关于牙齿伤害性信号传导方式的知识,这种病理状况的治疗并不总是有效。牙本质敏感的潜在机制仍然不清楚,这可能是由于包括成牙本质细胞、神经末梢和牙本质小管内流动的牙本质液等相关因素在结构和功能上的复杂性所致。成牙本质细胞的独特空间位置,即与神经末梢密切相关的纤毛细胞,表明它们可能在牙本质组织内发生的感觉事件的传导中起关键作用。我们的研究已经确定了机械热敏感瞬时受体电位离子通道(TRPV1 - 4、TRPA8、TRPM3、KCa、TREK - 1、PC1、PC2)定位于成牙本质细胞膜和纤毛基部。它们可以感知牙本质小管内牙本质液的温度变化或运动。此外,几种电压门控钠通道在注射去极化电流时赋予成牙本质细胞兴奋性特性。在体内,这些通道与成牙本质细胞顶端极的神经末梢共定位,并且它们的表达模式似乎与牵张激活的KCa通道的空间分布相关。所有这些数据强化了成牙本质细胞可能作为能够传递伤害性信号的感觉细胞的假设。然而,细胞如何感知信号以及信号如何传递到轴突是有待解决的主要问题。