Authors
Cheng Zhu, Tiancheng Li, Yu Jin, Yixin Li, Qicheng Liu, Runzhe Fang, Luyao Qu, Xinyue Tang, Ruomei Li, Xiaoyue Zhao, Jin Hao, Bing Fang, Lunguo Xia
Published in
Advanced science (Weinheim, Baden-Wurttemberg, Germany). Pages e77247. Aug 18, 2026. Epub Aug 18, 2026.
Abstract
Periodontitis is a chronic inflammatory disease characterized by persistent inflammation and limited repair at sites of alveolar bone loss. Although excessive reactive oxygen species (ROS) are recognized drivers of periodontal tissue damage, oxidative stress alone does not fully explain the persistence of inflammation and the failure of regeneration. The immune and metabolic processes that cooperate with oxidative stress in sustaining this disease-supporting microenvironment remain incompletely defined. In this study, a pronounced TH17-skewed CD4+ T cell response is identified in experimental periodontitis, and enrichment of polyamine pathway activation is observed during TH17 differentiation, suggesting a candidate immunometabolic axis for intervention. Guided by this observation, difluoromethylornithine-loaded UiO-66(Ce)-Mn (DFMO@Ui-Mn) is developed as a nanozyme platform that integrates the cascade ROS-scavenging activity of UiO-66(Ce)-Mn with DFMO delivery for inhibition of polyamine metabolism. DFMO@Ui-Mn reduces TH17 polarization in vitro, alters polyamine-related metabolic profiles, attenuates inflammatory responses in vivo, lowers the TH17/Treg ratio, improves osteogenic readouts in a conditioned-medium model, and promotes alveolar bone repair in ligature-induced periodontitis. These findings support a therapeutic strategy that combines redox control with immunometabolic intervention to improve the periodontal microenvironment under inflammatory conditions.
PMID:
42610507
Bibliographic data and abstract were imported from PubMed on 18 Aug 2026.
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