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纳米酶应对牙周生物膜相关挑战:机制、平台与转化前景

Nanozymes for periodontal biofilm-associated challenges: mechanisms, platforms, and translational perspectives.

综述 Meta鼻科IF 6.2Q1

文献信息

中文摘要

牙周炎是一种由失调的龈下生物膜驱动的慢性炎症性疾病,其胞外聚合物(EPS)基质赋予其对常规疗法和宿主免疫的显著抵抗力,抗生素耐药性进一步加剧了这一挑战。纳米酶作为具有内在酶样催化活性的纳米材料,因其催化效率、稳定性和多功能性而提供了一种有前景的替代方案。本叙述性综述综合了当前关于纳米酶应用于克服牙周炎生物膜相关挑战的证据,重点关注抗生物膜机制、代表性平台、递送策略和转化障碍。通过PubMed、Web of Science和Scopus进行了文献检索,关键词包括“纳米酶”、“牙周炎”和“生物膜”。纳米酶通过互补机制对抗牙周生物膜:通过过氧化物酶和氧化酶样活性产生活性氧(ROS)以杀死生物膜内细菌;降解EPS成分包括多糖、蛋白质和胞外DNA;破坏细菌粘附和群体感应;以及通过过氧化氢酶和超氧化物歧化酶样活性清除ROS来调节炎症。代表性平台已在多种临床前模型中进行了评估,包括边缘性牙周炎、根尖周炎和其他生物膜相关感染,每个模型具有不同程度的直接牙周相关性。虽然一些平台已直接在牙周炎模型中得到验证,但其他平台提供间接证据或机制见解,为其转化潜力提供信息。这些包括Ru-C3N4单原子纳米酶(在中耳炎模型中测试)、含益生菌的AgAu-CeO2异质结纳米酶、ferumoxytol(在根尖周炎中测试)、线粒体靶向铁蛋白纳米酶和Ru@COF纳米酶。尽管临床前证据令人鼓舞,但长期生物安全性、金属离子积累和临床转化方面的挑战仍然存在。未来研究应优先考虑标准化安全评估、可生物降解设计和临床验证,以将基于纳米酶的疗法从实验室转化为临床。

英文摘要

Periodontitis is a chronic inflammatory disease driven by dysbiotic subgingival biofilms whose extracellular polymeric substance (EPS) matrix confers marked resistance to conventional therapies and host immunity, with antibiotic resistance further compounding the challenge. Nanozymes, as nanomaterials with intrinsic enzyme-like catalytic activities, offer a promising alternative due to their catalytic efficiency, stability, and multifunctionality. This narrative review synthesizes current evidence on nanozyme applications for overcoming biofilm-associated challenges in periodontitis, focusing on antibiofilm mechanisms, representative platforms, delivery strategies, and translational hurdles. A literature search was conducted across PubMed, Web of Science, and Scopus using keywords including "nanozyme," "periodontitis," and "biofilm." Nanozymes combat periodontal biofilms through complementary mechanisms: reactive oxygen species (ROS) generation via peroxidase- and oxidase-like activities to kill biofilm-embedded bacteria; degradation of EPS components including polysaccharides, proteins, and extracellular DNA; disruption of bacterial adhesion and quorum sensing; and modulation of inflammation via ROS scavenging through catalase- and superoxide dismutase-like activities. Representative platforms have been evaluated in diverse preclinical models including marginal periodontitis, apical periodontitis, and other biofilm-associated infections each with distinct levels of direct periodontal relevance. While some platforms have been validated directly in periodontitis models, others provide indirect evidence or mechanistic insights that inform translational potential. These include Ru-C3N4 single-atom nanozymes (tested in otitis media models), AgAu-CeO2 heterojunction nanozymes with probiotics, ferumoxytol (tested in apical periodontitis), mitochondria-targeted ferritin nanozymes, and Ru@COF nanozymes. Despite encouraging preclinical evidence, challenges in long-term biosafety, metal-ion accumulation, and clinical translation persist. Future research should prioritize standardized safety evaluation, biodegradable designs, and clinical validation to translate nanozyme-based therapies from bench to bedside.