Femoral bone loss in total knee arthroplasty. A review.

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Abstract

[Indexed for MEDLINE] 18. J Nanobiotechnology. 2024 Dec 18;22(1):758. doi: 10.1186/s12951-024-03049-4. Osteoblastic ferroptosis inhibition by small-molecule promoting GPX4 activation for peri-prosthetic osteolysis therapy. Liu X(#)(1), Wang W(#)(1), Zhu F(#)(1), Xu H(1), Ge G(1), Liang X(1), Yang H(1), Xu Y(1), Xu W(2), Wei M(3), Zhou Q(4), Geng D(5). Author information: (1)Department of Orthopaedic Surgery, Orthopaedic Institute, The First Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, Jiangsu, 215006, China. (2)Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215006, China. 13962157016@139.com. (3)Department of Traditional Chinese Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215006, China. weiminggang@suda.edu.cn. (4)Department of Orthopedics, Changzheng Hospital, Naval Medical University, Shanghai, 200070, China. zq590@sina.com. (5)Department of Orthopaedic Surgery, Orthopaedic Institute, The First Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, Jiangsu, 215006, China. szgengdc@suda.edu.cn. (#)Contributed equally Peri-prosthesis osteolysis (PPO) represents the most severe complication of total joint arthroplasty (TJA) surgery and imposes the primary cause of prosthesis failure and subsequent revision surgery. Antiresorptive therapies are usually prescribed to treat PPO, especially for elderly people. Nevertheless, the efficacy of anti-osteoporotic medications remains constrained. Recent therapeutic strategies to promote periprosthetic osseointegration by restoring osteoblast function are considered more effective approaches. However, the precise mechanism underlying the inhibition of osteogenesis triggered by wear particles remains enigmatic. Herein, we demonstrate that wear particles inhibit osteoblast function by inducing ferroptosis to sabotage extracellular mineralization and arouse periprosthetic osteolysis. The suppression of ferroptosis could significantly rescue osteogenesis thus alleviating PPO. Furthermore, Glutathione Peroxidase 4 (GPX4) has been identified as a key target in regulating osteoblastic ferroptosis. By utilizing virtual screening techniques, we have successfully conducted a comprehensive screening of a natural compound known as Urolithin A (UA), which exhibits remarkable inhibition of osteoblastic ferroptosis while simultaneously promoting the process of osteogenesis through its precise targeting mechanism on GPX4. Meanwhile, UA improves the osteolytic conditions significantly in vivo even when the adjunction of titanium (Ti) nanoparticles. This strategy has great potential in treating peri-prosthesis osteolysis and potentially broadens the scope of clinical therapy. © 2024. The Author(s). DOI: 10.1186/s12951-024-03049-4 PMCID: PMC11658433