中性粒细胞胞外陷阱
牙周炎
破骨细胞
发病机制
牙槽
S100A9型
免疫系统
基因剔除小鼠
炎症
下调和上调
免疫学
自噬
医学
骨吸收
骨重建
平衡
机制(生物学)
癌症研究
细胞外
化学
牙龈炎
单核细胞
巨噬细胞
骨免疫学
免疫失调
细胞分化
作者
Y.Y. Wei,J.Q. Zheng,Y.L. Zhou,Zhigang Wu,X.Z. Liu,H.Y. Yang,F.F. Song,C. Huang
标识
DOI:10.1177/00220345251413516
摘要
deficiency mice upon rapamycin-induced autophagy restoration. Therapeutic intervention with the S100A9-specific inhibitor tasquinimod effectively inhibited osteoclastic differentiation of macrophages and mitigated bone loss. In conclusion, our findings reveal the mechanism by which S100A9 regulates osteoclast differentiation via NETosis, providing insights into osteoimmunological regulation in the pathogenesis of periodontitis.
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