4.7 Article

Epigallocatechin gallate-based nanoparticles with reactive oxygen species scavenging property for effective chronic periodontitis treatment

Journal

CHEMICAL ENGINEERING JOURNAL
Volume 433, Issue -, Pages -

Publisher

ELSEVIER SCIENCE SA
DOI: 10.1016/j.cej.2021.132197

Keywords

Epigallocatechin gallate; Nanoparticles; Reactive oxygen species; Anti-inflammation; Chronic periodontitis

Funding

  1. National Natural Science Foundation of China [81671021, 31872750, 51373106]
  2. National Clinical Research Center for Oral Diseases of Sichuan University

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Chronic periodontitis, a common oral disease, is aggravated by excessive levels of reactive oxygen species (ROS), which leads to tissue destruction. Tea polyphenol-derived nanoparticles can effectively scavenge ROS, reduce inflammation, and inhibit bone loss in chronic periodontitis through reprogramming macrophages. These nanoparticles have the potential to be a promising therapy for periodontitis.
Chronic periodontitis is one of the most common oral diseases worldwide and the excessive local reactive oxygen species (ROS) level of periodontitis aggravates the destruction of periodontal tissue. Scavenging of ROS to remodel the periodontal microenvironment and relieve inflammatory response may be an effective strategy for periodontal therapy. Tea polyphenol-derived functional nanomaterials often serve as ROS scavenger in inflammatory disease for their antioxidant and anti-inflammation ability. However, the therapeutic effect of tea polyphenol resources remains unsatisfactory due to the tedious encapsulation, poor stability, and low operational bioactivities. In this work, functionalized epigallocatechin-3-gallate (EGCG, green tea derivative) nanoparticles (NPs) were developed via a one-step polyphenolic condensation reaction. The resulting polyphenol-based nanoparticles with potent antioxidant capacity improved the chemical stability of epigallocatechin gallate. The EGCG NPs can scavenge ROS effectively, and down-regulate the expression of pro-inflammatory cytokines by reprograming macrophages from M1 to M2 phenotype. In vivo results illustrate that EGCG NPs can inhibit the alveolar bone loss from 1346.8 +/- 244.9 mu m to 596.1 +/- 92.1 mu m via decreasing ~ 50% ROS level, as well as reduce osteoclastic activity in a rat model of chronic periodontitis. Therefore, the biosafe EGCG NPs have great potential in ROS-scavenging and provide a promising strategy to remodel the inflammatory microenvironment by inducing the polarization of macrophages from M1 toward M2 phenotype for efficient periodontitis therapy.

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