Abstract
Arthroplasty is the most effective method for treating end-stage bone and joint disease in the world. However, the artificial joint prosthesis has a limited service life. It is known that wear particles could stimulate macrophages to produce proinflammatory cytokine, which activates the osteoclasts around the prosthesis, and play the most important role in aseptic loosening. The particles can activate pattern recognition receptors (PRRs) of macrophages to produce pro-inflammatory factors such as TNF-α and IL-1β, and induce osteolysis around the prosthesis. Based on previous research, we found that in mouse macrophages with the RIPK3 gene inhibited, the expression of proinflammatory factors induced by wear particles was significantly reduced, and the assembly of NLRP3 inflammatory bodies was limited. At the same time, it was found that the effects of cranium lysis were weakened in mice injected with lentivirus targeting to inhibit RIPK3. This study shows that RIPK3 plays a positive regulatory role in the inflammatory response caused by wear particles activating macrophage PRRs/NLRP3 signaling pathway.
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