牙体缺损是口腔临床最常见的疾病，S.mutans致龋是其最主要的病因。S.mutans分泌GTF促进细菌的粘附、定植和产酸，从而破坏牙体硬组织，导致牙体缺损。如何在龋损早期特异性识别S.mutans、介入并中断其进一步发展，同时修复缺损具有重要的临床意义。本课题拟利用蔗糖类似物（3-脱氧蔗糖）为门控，以介孔硅为纳米载体，负载EGCG和PAH-ACP，构建GTF响应型智能药物控释系统。在龋损发生早期，口腔内微环境发生改变，S.mutans释放的GTF可特异性识别切断3-脱氧蔗糖，打开门控，释放能够高效杀菌并保护牙本质胶原的药物EGCG，并且释放矿化前驱体PAH-ACP促进牙本质再矿化。该系统具有特异性识别致龋菌、按需释放、原位修复的优点，将革新现有的缺损后修复策略，为早期预防龋损发生、修复继发龋坏、提高粘接修复耐久性等方面的探索提供新的技术支持和保障。

Tooth defect is the most common disease in dental treatment, and the dominant reason is believed to be the cariogenic effect of S. mutans. S. mutans could secrete an enzyme called GTF that facilitates the adherence, colonization and acid production of bacteria, thus leading to tooth defect. Therefore, there is high clinical significance in early specific recognition of S. mutans, early intervention and interruption of caries development and simultaneous repair of the tooth defect. Our study intends to establish the GTF-responsive drug controlled release system through using sucrose analogs (3-deoxysucrose) as the gatekeeper, and MSN as the nanocarrier for EGCG (antibacterial) and PAH-ACP (precursor of remineralization). During the early stage of caries development, the GTF secreted by S. mutans specifically recognizes and cuts 3-deoxysucrose to open the gate, releasing EGCG which could kill bacteria and protect dentin collagen effectively and PAH-ACP which facilitates the remineralization of demineralized dentin. The GTF-responsive drug controlled release system has various advantages, such as specific recognition of cariogenic bacteria, drug release as needed and in situ recovery. This system will renovate the existing defect repairing strategy, and provide new technical support and guarantee for the exploration of caries early prevention, secondary caries repair and prolongation of dentin bonding durability.