上睑下垂
骨溶解
炎症
骨吸收
假体周围
破骨细胞
机制(生物学)
医学
炎症体
免疫学
关节置换术
外科
内科学
哲学
受体
认识论
作者
Jian Yin,Zhaoyang Yin,Lai Peng,Xinhui Liu,Jinzhong Ma
出处
期刊:Biomolecules
[MDPI AG]
日期:2022-11-23
卷期号:12 (12): 1733-1733
被引量:10
摘要
Periprosthetic osteolysis (PPO) along with aseptic loosening (AL) caused by wear particles after artificial joint replacement is the key factor in surgical failure and subsequent revision surgery, however, the precise molecular mechanism underlying PPO remains unclear. Aseptic inflammation triggered by metal particles, resulting in the imbalance between bone formation by osteoblasts and bone resorption by osteoclasts may be the decisive factor. Pyroptosis is a new pro-inflammatory pattern of regulated cell death (RCD), mainly mediated by gasdermins (GSDMs) family, among which GSDMD is the best characterized. Recent evidence indicates that activation of NLRP3 inflammasomes and pyroptosis play a pivotal role in the pathological process of PPO. Here, we review the pathological process of PPO, the molecular mechanism of pyroptosis and the interventions to inhibit the inflammation and pyroptosis of different cells during the PPO. Conclusively, this review provides theoretical support for the search for new strategies and new targets for the treatment of PPO by inhibiting pyroptosis and inflammation.
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