Rodd H D, Morgan C R, Day P F, Boissonade F M
Dept. Oral Health and Development, School of Clinical Dentistry, University of Sheffield, Sheffield; England.
Eur Arch Paediatr Dent. 2007 Dec;8(4):184-8. doi: 10.1007/BF03262594.
This was to compare the pulpal expression of the transient receptor potential ion channel (TRPV1), a noxious heat receptor, in sound and hypomineralised human first permanent molars. The rationale for the investigation was to gain further insight into pulpal changes in hypomineralised teeth and the possible biological mechanisms underlying thermal hypersensitivity.
This was a laboratory study using a quantitative immuncocytochemical approach.
The experimental material comprised 17 sound and 18 hypomineralised molars (10 with intact enamel and 8 with enamel loss), obtained from children requiring dental extractions under general anaesthesia. Coronal pulps were removed and processed for indirect immunofluorescence using antibodies raised against TRPV1 and either the general neuronal marker, protein gene-product 9.5 or alpha smooth muscle actin in conjunction with Ulex europaeus agglutinin 1 lectin to fully label the pulp vasculature. Computerised image analysis was used to quantify the expression of TRPV1 in both pulpal nerves and blood vessels within different regions of the pulp including the pulp horn, subodontoblastic plexus and mid-coronal region.
Mean neuronal and vascular TRPV1 expression was significantly greater in some pulpal regions of hypomineralised teeth (both with and without enamel loss) than for sound samples (p<0.05, ANOVA).
Increased TRPV1 expression within the pulps of hypomineralised teeth may be indicative of an underlying pulpal inflammation and may help to explain the heat sensitivity experienced by some patients with this condition. However, future lines of enquiry should seek to correlate patient symptoms and responses to controlled hot and cold stimuli with pulpal expression of a variety of thermal receptors to gain further insight into dental pain mechanisms.
比较瞬时受体电位离子通道(TRPV1,一种伤害性热感受器)在健康和矿化不足的人类第一恒磨牙牙髓中的表达情况。开展此项研究的基本原理是进一步深入了解矿化不足牙齿的牙髓变化以及热过敏潜在的生物学机制。
这是一项采用定量免疫细胞化学方法的实验室研究。
实验材料包括从需要全身麻醉下拔牙的儿童获取的17颗健康磨牙和18颗矿化不足的磨牙(10颗釉质完整,8颗有釉质缺失)。去除冠髓,使用针对TRPV1以及一般神经元标志物蛋白基因产物9.5或α平滑肌肌动蛋白的抗体,结合荆豆凝集素1对牙髓血管进行全面标记,然后进行间接免疫荧光处理。利用计算机图像分析技术对牙髓不同区域(包括髓角、成牙本质细胞下丛和冠中部区域)的牙髓神经和血管中TRPV1的表达进行定量分析。
矿化不足牙齿(无论有无釉质缺失)的某些牙髓区域中,TRPV1在神经元和血管中的平均表达显著高于健康样本(p<0.05,方差分析)。
矿化不足牙齿牙髓中TRPV1表达增加可能表明存在潜在的牙髓炎症,这可能有助于解释部分患有这种情况的患者所经历的热敏感症状。然而,未来的研究方向应致力于将患者症状以及对可控冷热刺激的反应与多种热感受器的牙髓表达情况相关联,以进一步深入了解牙齿疼痛机制。