MULTISCALE MODELLING OF ENAMEL DEMINERALISATION AND ACELLULAR REPAIR

牙釉质脱矿和脱细胞修复的多尺度建模

• 批准号: 2739353
• 金额: --
• 依托单位: King's College London
• 依托单位国家: 英国
• 项目类别: Studentship
• 财政年份: 2022
• 资助国家: 英国
• 起止时间: 2022 至 无数据
• 项目状态: 未结题
• 来源: https://gtr.ukri.org/projects?ref=studentship-2739353
• 关键词: MULTISCALE; MODELLING; ENAMEL; DEMINERALISATION; ACELLULAR

Dental erosion is defined as the loss of dental hard tissues through chemical dissolution of the tooth structure without bacterial involvement [1]. Erosion is classically defined as having an intrinsic aetiology (due to exposure of tooth surfaces to gastro-intestinal acids) or extrinsic aetiology [2] (due to exposure of the teeth to dietary/environmental acids). Dental erosion has an increasing prevalence in the developed world and represents a significant challenge to dental practitioners in terms of the predictable management of the damaged dentition. As a progressive condition (due to the lack of intrinsic biological repair mechanisms for dental enamel), dental erosion is of relevance to our ageing population. Prevention therefore remains key, and whilst behavioural change (diet or amelioration of intrinsic factors) is essential, consumer products to delay, prevent and reverse early demineralisation are urgently sought. There have been considerable efforts to model dental erosion ex-vivo. These approaches typically expose animal or human tooth surfaces to an acid challenge and measure the resultant surface changes qualitatively through imaging [3, 4] or quantitatively through metrology and characterisation of surface micromechanical properties [5-8]. The two main limitations are (i) an inability to relate the specific variability of the hierarchically organised mineralised tooth structure (enamel prism orientation, size, hydroxyapatite crystallite size and texture, presence of substitutional ions within the mineralized tooth structure) (ii) difficulties in monitoring the sequence of dissolution and its impact on structural integrity in real-time.

牙齿侵蚀是指牙齿硬组织在没有细菌参与的情况下通过牙齿结构的化学溶解而丧失[1]。侵蚀通常被定义为具有内在病因（由于牙齿表面暴露于胃肠道酸）或外在病因[2]（由于牙齿暴露于饮食/环境酸）。牙齿侵蚀在发达国家的发病率越来越高，在受损牙列的可预测管理方面对牙科医生提出了重大挑战。作为一种渐进性疾病（由于缺乏牙釉质的内在生物修复机制），牙齿侵蚀与我们的老龄化人口有关。因此，预防仍然是关键，虽然行为改变（饮食或改善内在因素）是必不可少的，但迫切需要延迟，预防和逆转早期脱矿作用的消费品。已经有相当大的努力来模拟离体牙侵蚀。这些方法通常将动物或人类牙齿表面暴露于酸挑战，并通过成像[3，4]定性测量所得表面变化，或通过计量学和表面微机械特性表征[5-8]定量测量所得表面变化。两个主要限制是（i）无法将分层组织的矿化牙齿结构的特定可变性（牙釉质棱柱取向、尺寸、羟基磷灰石微晶尺寸和纹理、矿化牙齿结构内替代离子的存在）联系起来（ii）难以实时监测溶解顺序及其对结构完整性的影响。