DYNAMIC PLASTICITY OF DENTAL SENSORY NERVE STRUCTURE AND CYTOCHEMISTRY
DYNAMIC PLASTICITY OF DENTAL SENSORY NERVE STRUCTURE AND CYTOCHEMISTRY
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DOI：
10.1016/0003-9969(94)90183-x
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发表时间：
1994-01-01
影响因子：
3
通讯作者：
BYERS, MR
中科院分区：
文献类型：
--
作者：
BYERS, MR
过敏性牙本质对正常的触摸或温度变化以及异常的痛感做出反应。本文综述了牙齿损伤后感觉神经结构、细胞化学和定位的动态变化，提示这些变化与牙本质过敏症的发生有关。含有降钙素基因相关肽(CGRP)的神经纤维是支配牙本质的主要感觉纤维。有证据表明许多牙本质神经末梢起源于细小的有髓纤维。CGRP神经末梢的位置与神经生长因子的牙髓梯度有关，这已通过原位杂交组织化学在正常牙齿中得到证实。当将浅洞钻入大鼠磨牙外牙本质时，牙髓神经生长因子增加了五到八倍，而损伤附近牙髓和牙本质中的感觉神经纤维发生了广泛的结构变化。如果愈合，这些神经生长因子和感觉神经反应最终会消退，但如果炎症继续下去，这两者都会继续。有关牙髓炎症与三叉神经中枢疼痛通路长期变化的证据进行了综述。牙齿损伤后可能存在广泛的神经可塑性，无论是在牙科疼痛纤维中还是在中枢疼痛通路中。这些神经结构、位置和细胞化学改变的时机与它们参与牙本质过敏症的机制是一致的。
Hypersensitive dentine responds to normal changes in touch or temperature with abnormal pain sensations. This paper reviews studies that have shown dynamic changes in sensory nerve structure, cytochemistry and location after tooth injury, suggesting that those changes contribute to dentine hypersensitivity. Nerve fibres containing calcitonin gene-related peptide (CGRP) are the main type of sensory fibre to innervate dentine. Evidence that many of those dentinal nerve endings originate from small myelinated fibres is presented here. The location of CGRP nerve terminals correlates with the pulpal gradients of nerve growth factor that have been demonstrated in normal teeth by in situ hybridization histochemistry. When shallow cavities are drilled into the outer dentine of rat molars a five-to-eight-fold increase in pulpal nerve growth factor precedes the extensive structural changes in the sensory nerve fibres in pulp and dentine near the injury. Those nerve growth factor and sensory nerve reactions eventually subside if healing occurs, but both continue if inflammation continues. Evidence correlating pulpal inflammation with long-term changes in central trigeminal pain pathways is reviewed. There can be extensive neuroplasticity after tooth injury, both within dental pain fibres and in central pain pathways. The timing of those alterations of nerve structure, location, and cytochemistry is consistent with their involvement in mechanisms of dentine hypersensitivity.