Pain Cognitive Function Research Center, Dental Research Institute and Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul 110-749, Republic of Korea.
J Dent Res. 2013 Nov;92(11):948-55. doi: 10.1177/0022034513501877. Epub 2013 Aug 16.
Due, in part, to the unique structure of the tooth, dental pain is initiated via distinct mechanisms. Here we review recent advances in our understanding of inflammatory tooth pain and discuss 3 hypotheses proposed to explain dentinal hypersensitivity: The first hypothesis, supported by functional expression of temperature-sensitive transient receptor potential channels, emphasizes the direct transduction of noxious temperatures by dental primary afferent neurons. The second hypothesis, known as hydrodynamic theory, attributes dental pain to fluid movement within dentinal tubules, and we discuss several candidate cellular mechanical transducers for the detection of fluid movement. The third hypothesis focuses on the potential sensory function of odontoblasts in the detection of thermal or mechanical stimuli, and we discuss the accumulating evidence that supports their excitability. We also briefly update on a novel strategy for local nociceptive anesthesia via nociceptive transducer molecules in dental primary afferents with the potential to specifically silence pain fibers during dental treatment. Further understanding of the molecular mechanisms of dental pain would greatly enhance the development of therapeutics that target dental pain.
部分由于牙齿的独特结构，牙痛是通过不同的机制引发的。在这里，我们回顾了我们对炎性牙痛理解的最新进展，并讨论了三个用来解释牙本质过敏的假说：第一个假说，由温度敏感瞬时受体电位通道的功能表达支持，强调了牙髓传入神经元对有害温度的直接转导。第二个假说，即流体动力理论，将牙痛归因于牙本质小管内的流体运动，我们讨论了几个候选细胞机械换能器来检测流体运动。第三个假说集中在成牙本质细胞探测热或机械刺激的潜在感觉功能上，我们讨论了支持其兴奋性的累积证据。我们还简要介绍了一种通过牙髓传入神经中伤害感受器转导分子来实现局部伤害性麻醉的新策略，这种策略有可能在牙科治疗期间特异性地使疼痛纤维沉默。进一步了解牙痛的分子机制将极大地促进针对牙痛的治疗方法的发展。
