AI Article Synopsis
- Periprosthetic osteolysis (PPO) and aseptic loosening (AL) are major causes of failure in artificial joint replacements, primarily caused by wear particles leading to inflammation and bone resorption imbalance.
- The process of pyroptosis, a type of regulated cell death, is significantly involved in PPO, particularly through the activation of NLRP3 inflammasomes and gasdermins like GSDMD.
- This review explores the molecular mechanisms behind PPO and pyroptosis, suggesting potential interventions to reduce inflammation and offers new strategies for treatment.
Article Abstract
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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9775904 | PMC |
| http://dx.doi.org/10.3390/biom12121733 | DOI Listing |
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