早期龋损的病理本质是相对完整釉质表层下的矿物丢失。成熟牙釉质缺乏成釉细胞及内源性再生能力，其治疗目标不应停留于表面矿物沉积，而应进一步指向表层下矿物恢复、晶体取向与多等级结构重建及长期力学功能恢复。近年来，钙磷离子簇或预成核簇、无定形磷酸钙前驱体、釉原蛋白来源肽及其他有机模板等策略，提高了矿物前驱体稳定性和有序结晶调控能力；牙面功能化、湿黏附、酸响应释放及靶向抗菌体系，也推动防龋与再矿化由简单功能叠加向时空协同发展。然而，现有证据多来自简化的体外脱矿或单菌生物膜模型，修复仍主要局限于表面数微米范围；对于真实早期龋损表层下矿物恢复、釉柱/釉柱间质重建、界面连续性，以及耐酸、耐磨和长期力学稳定性的证据仍不充分，非选择性抗菌还可能扰动口腔微生态。本文从早期龋损的病理基础和天然牙釉质多等级结构出发，围绕表面矿物沉积、表层下修复、结构与功能重建及抗菌与微生态调控等方面总结研究进展，并讨论临床转化瓶颈。未来应采用更接近真实口腔环境的表层下龋损及多菌种生物膜模型，将龋病响应与材料滞留相结合，并建立矿化深度、结构连续性与长期功能相互对应的评价体系。牙釉质防龋与再矿化的核心，是在维持口腔微生态稳态的前提下，实现早期龋损深部矿物恢复，并重建与天然牙釉质连续且可长期稳定的结构与功能。

Early enamel caries is characterized by mineral loss beneath a relatively intact surface. Because mature enamel lacks ameloblasts and endogenous regenerative capacity, therapeutic goals should extend beyond surface mineral deposition to subsurface mineral recovery, restoration of crystal orientation and hierarchical organization, and durable mechanical function. Recent strategies based on calcium-phosphate ionic or pre-nucleation clusters, amorphous calcium phosphate precursors, amelogenin-derived peptides, and other organic templates have improved precursor stabilization and the regulation of ordered crystallization. Tooth-surface functionalization, wet adhesion, pH-responsive release, and targeted antimicrobial systems are also promoting a transition from the simple combination of anticaries and remineralizing functions toward their spatial and temporal coordination. Nevertheless, most available evidence has been obtained from simplified in vitro demineralization or monospecies biofilm models, while repair remains largely confined to micrometer-scale surface layers. Robust evidence is still lacking for mineral recovery throughout clinically representative subsurface lesions, reconstruction of enamel rod/interrod architecture and interfacial continuity, and resistance to recurrent acid challenge, wear, and fatigue. Nonselective antimicrobial interventions may additionally disrupt oral microbial ecology. This expert perspective summarizes advances in surface mineral deposition, subsurface repair, structural and functional reconstruction, and antimicrobial and ecological regulation, while examining the major barriers to clinical translation. Future studies should employ clinically relevant subsurface caries lesions and multispecies biofilm models, integrate lesion-responsive activation and durable material retention with selective virulence control, and establish an evaluation framework linking mineralization depth, structural continuity, and long-term function. The central objective of enamel caries prevention and remineralization is to restore mineral within deep subsurface lesions and rebuild an enamel-continuous, hierarchically organized, and durable structure without compromising oral microbial homeostasis.