基于磁性的光敏剂可提高针对成熟龋齿相关生物膜的抗菌光动力疗法的效率

Abdulrahman A. Balhaddad, Lamia Mokeem, Rashed Alsahafi, Michael D. Weir, Hockin H. K. Xu, Mary Anne S. Melo
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引用次数: 0

摘要

抗菌素光动力疗法(aPDT)在消除口腔病原体而不诱导微生物耐药性方面显示出前景。然而,光敏剂对生物膜的渗透有限,这阻碍了它对成熟、厚的生物膜的作用。本研究评估了磁性纳米颗粒和甲苯胺蓝矫形器(MagTBO)纳米平台对与龋齿相关的成熟变形链球菌生物膜的有效性。该研究采用恒深膜发酵(CDFF)模型,被称为“人工口腔”,来复制蛀牙过程,并允许生物膜在牙齿上生长。该方法能够在5天和10天内评估生物膜诱导的蛀牙性矿物质损失。研究表明,MagTBO在5天和10天内提高了aPDT对高度成熟和复杂生物膜的有效性。然而,生物膜的减少不影响下牙本质中的矿物质含量。这为临床aPDT方案提供了一种很有前途的方法。然而,重要的是要承认这些发现是基于体外研究,可能需要进一步的临床证实。总之,我们的数据表明,磁性光敏剂增强了aPDT对致病性口腔生物膜的调节,为临床aPDT方案提供了潜在的进步。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Magnetic-based photosensitizer to improve the efficiency of antimicrobial photodynamic therapy against mature dental caries-related biofilms

Magnetic-based photosensitizer to improve the efficiency of antimicrobial photodynamic therapy against mature dental caries-related biofilms

Antimicrobial photodynamic therapy (aPDT) shows promise in eliminating oral pathogens without inducing microbial resistance. Yet, it faces limited biofilm penetration by the photosensitizer, which hinders its efficacy against mature, thick biofilms. This study assesses the effectiveness of the MagTBO (magnetic nanoparticles and toluidine-blue ortho) nanoplatform against mature Streptococcus mutans biofilms associated with dental caries. The study employs constant-depth film fermenter (CDFF) models, known as “artificial mouth,” to replicate caries processes and allow biofilm growth over teeth. This method enables the evaluation of biofilm-induced mineral loss under cariogenic challenge over 5 and 10 days. The study shows that MagTBO improves aPDT's effectiveness against highly mature and complex biofilms over 5 and 10 days. However, the biofilm reduction unaffected the mineral content in the underlying dentin. This presents a promising approach for clinical aPDT protocols. However, it is crucial to acknowledge that these findings are based on in vitro studies and may necessitate further clinical confirmation. In summary, our data indicate that magnetic-based photosensitizers enhance the modulation of pathogenic oral biofilms by aPDT, offering potential advancements in clinical aPDT protocols.

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