Osteoblastic ferroptosis inhibition by small-molecule promoting GPX4 activation for peri-prosthetic osteolysis therapy.

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Abstract

[Indexed for MEDLINE] Conflict of interest statement: Declarations. Ethics approval and consent to participate: Clinical samples were collected with permission of the Ethics Committee of the First Affiliated Hospital of Soochow University. All animal experiments were approved by the Ethics Committee of Soochow University. Consent for publication: All authors agree to be published. Competing interests: The authors declare no competing interests. 19. J Arthroplasty. 2004 Dec;19(8):1028-38. doi: 10.1016/j.arth.2004.03.024. Particle bioreactivity and wear-mediated osteolysis. Wang ML(1), Sharkey PF, Tuan RS. Author information: (1)Department of Orthopaedic Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. This review focuses on wear debris-mediated osteolysis, a major factor compromising the long-term success of total joint arthroplasty. Studies on retrieved implants and animal models, as well as in vitro studies on particle bioreactivity, suggest that wear-mediated periprosthetic osteolysis is unlikely to be caused solely by 1 particular cell type or particulate species, but is rather the cumulative consequence of a number of biological reactions. Our recent findings suggest 3 novel mechanisms of particle bioreactivity that may contribute to osteolysis: 1) exacerbated inflammation caused by elevated reactive oxygen species production by activated macrophages and osteoclasts, (2) impaired periprosthetic bone formation secondary to disrupted osteogenesis, and (3) compromised bone regeneration resulting from increased cytotoxic response of mesenchymal osteoprogenitor cells. Understanding the pathogenesis of wear-mediated osteolysis is needed to improve orthopedic implant biocompatibility and wear reduction, and to develop effective pharmacotherapies. DOI: 10.1016/j.arth.2004.03.024