Biochemical and biophysical research communications · 2025
Maltol promotes osteoclastogenesis and exacerbates periodontitis via TRAF6/JNK/Nfatc1 pathway.
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Zhao Rui, Fu Jingfei, Jiang Yiyang, Wu Lili, Yan Ziqi, Liu Yi
Аннотация
OBJECTIVE: The aim of this study was to investigate the role of maltol in osteoclast differentiation and its mechanism, and to provide evidence for the effect of common sweeteners on periodontal tissue destruction and the prevention of periodontitis.
METHODS: BMMNCs were treated with maltol, M-CSF and RANKL to observe their osteoclast potential. The differentiation of osteoclasts was observed by TRAP staining, Western blotting and RT-PCR analysis. Further investigations into the relevant signaling pathways were carried out. In vivo, periodontitis was established by ligating the maxillary second molars of mice with silk thread (n = 8 in each group). After that, we evaluated the effect of maltol on bone resorption by oral gavage.
RESULTS: Maltol significantly promoted osteoclast differentiation of rankl stimulated BMMNCs. This is mediated by modulation of the tumor necrosis factor receptor-related factor 6 (TRAF6)/C-Jun n-terminal kinase (JNK)/activated T cell nuclear factor 1 (Nfatc1) signaling pathway. In addition, maltol can significantly promote bone resorption in animal models of periodontitis.
CONCLUSIONS: Maltol promotes OC differentiation of bone marrow mesenchymal stem cells induced by rankl through TRAF/JNK pathway and upregulates NFATc1 expression. Maltol promotes bone resorption by promoting osteoclast differentiation in experimental periodontitis model of mice.
METHODS: BMMNCs were treated with maltol, M-CSF and RANKL to observe their osteoclast potential. The differentiation of osteoclasts was observed by TRAP staining, Western blotting and RT-PCR analysis. Further investigations into the relevant signaling pathways were carried out. In vivo, periodontitis was established by ligating the maxillary second molars of mice with silk thread (n = 8 in each group). After that, we evaluated the effect of maltol on bone resorption by oral gavage.
RESULTS: Maltol significantly promoted osteoclast differentiation of rankl stimulated BMMNCs. This is mediated by modulation of the tumor necrosis factor receptor-related factor 6 (TRAF6)/C-Jun n-terminal kinase (JNK)/activated T cell nuclear factor 1 (Nfatc1) signaling pathway. In addition, maltol can significantly promote bone resorption in animal models of periodontitis.
CONCLUSIONS: Maltol promotes OC differentiation of bone marrow mesenchymal stem cells induced by rankl through TRAF/JNK pathway and upregulates NFATc1 expression. Maltol promotes bone resorption by promoting osteoclast differentiation in experimental periodontitis model of mice.