N-Acetyl-l-cysteine-Derived Carbonized Polymer Dots with ROS Scavenging via Keap1-Nrf2 Pathway Regulate Alveolar Bone Homeostasis in Periodontitis

Periodontitis is a type of chronic inflammatory oral disease characterized by the destruction of periodontal connective tissue and progressive alveolar bone resorption. As oxidative stress is the key cause of periodontitis in the early periodontal microenvironment, antioxidative therapy has been con...

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Published in:Advanced healthcare materials 2023-10, Vol.12 (26), p.e2300890-e2300890
Main Authors: Liu, Xinchan, Hou, Yubo, Yang, Mingxi, Xin, Xirui, Deng, Yu, Fu, Ruobing, Xiang, Xingchen, Cao, Niuben, Liu, Xiaomeng, Yu, Weixian, Yang, Bai, Zhou, Yanmin
Format: Article
Language:English
Subjects:
Acetylcysteine
Alveolar bone
Antioxidants
Biocompatibility
Bone growth
Bone imaging
Bone resorption
Bone turnover
Cell differentiation
Connective tissue diseases
Connective tissues
Cysteine
Differentiation (biology)
Fluorescence
Gum disease
Homeostasis
Hydrogen peroxide
Microenvironments
Osteogenesis
Oxidative stress
Periodontal ligament
Periodontitis
Polymers
Protein L
Reactive oxygen species
Scavenging
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Summary:Periodontitis is a type of chronic inflammatory oral disease characterized by the destruction of periodontal connective tissue and progressive alveolar bone resorption. As oxidative stress is the key cause of periodontitis in the early periodontal microenvironment, antioxidative therapy has been considered a viable treatment for periodontitis. However, more stable and effective reactive oxygen species (ROS)-scavenging nanomedicines are still highly needed due to the instability of traditional antioxidants. Herein, a new type of N-acetyl-l-cysteine (NAC)-derived red fluorescent carbonized polymer dots (CPDs) has been synthesized with excellent biocompatibility, which can serve as an extracellular antioxidant to scavenge ROS effectively. Moreover, NAC-CPDs can promote osteogenic differentiation in human periodontal ligament cells (hPDLCs) under H O stimulation. In addition, NAC-CPDs are capable of targeted accumulation in alveolar bone in vivo, reducing the level of alveolar bone resorption in periodontitis mice, as well as performing fluorescence imaging in vitro and in vivo. In terms of mechanism, NAC-CPDs may regulate redox homeostasis and promote bone formation in the periodontitis microenvironment by modulating the kelch-like ECH-associated protein l (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. This study provides a new strategy for the application of CPDs theranostic nanoplatform for periodontitis.
ISSN:2192-2640
2192-2659
DOI:10.1002/adhm.202300890