牙本质过敏的病因学。

M Brännström
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引用次数: 0

摘要

过敏的牙本质似乎主要是牙髓壁上的牙本质疼痛纤维(a -纤维)激活的结果。激活这些神经的刺激主要是那些从牙本质小管中清除液体并调动毛细血管力,导致快速向外流动的刺激。施加冷刺激使液体收缩,在小管的牙髓区域产生类似的快速向外流动。当牙齿中充满细菌的间隙充满液体时,对寒冷过敏也很明显。实验表明,具有专利小管的新暴露的牙本质表面比被涂抹层污染的表面更敏感。邻近牙髓区的炎症也会增加敏感性。颈椎和咬合表面过敏的发生是由于口腔环境的机械和酸性作用、牙刷磨损、饮食中的侵蚀成分、牙本质的菌斑和细菌侵入。有时牙本质通过修复治疗暴露,偶尔偏心的咬合负荷会导致过敏。除非打开的管状孔被密封,否则灵敏度可能持续存在。
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Etiology of dentin hypersensitivity.

Hypersensitive dentin appears to be mainly the result of an activation of the dentinal pain fibres, the A-fibres, at the pulpal wall. The stimuli which activate these nerves are primarily those which remove fluid from the dentinal tubules and mobilize capillary forces, causing a rapid outward flow. Application of a cold stimulus causes the fluid to contract, resulting in a similar rapid outward flow in the pulpal region of the tubules. Hypersensitivity to cold is also marked when there is a fluid-filled gap containing bacteria in the tooth. Experiments have shown that a freshly exposed dentin surface with patent tubules is more sensitive than a surface contaminated by a smear layer. Inflammation in the adjacent pulpal region can also increase sensitivity. The development of hypersensitive cervical and occlusal surfaces is due to mechanical and acidic effects from the oral environment, toothbrush abrasion, erosive components in the diet, plaque and bacterial invasion of dentin. Sometimes dentin is exposed by restorative therapy and occasionally eccentric occlusal loads can contribute to hypersensitivity. The sensitivity may persist unless the open tubular apertures are sealed.

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