ArticleJournal of cellular and molecular medicine2025
The Flavonoid Kaempferol Mitigates Periprosthetic Osteolysis by Regulating the NLRP3 Inflammasome and Balancing Bone Metabolism.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Reprogramming bone homeostasis: The recoupling-oriented framework of bidirectional regulation strategies for osteoporosis.iScience · 2026Review
- The "Tianyu" Formulation Alleviates Rheumatoid Arthritis by Modulating the NLRP3/Caspase-1/GSDMD-Mediated Pyroptosis Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Kaempferol Inhibits MMP-1-Mediated Migration and Invasion in Gemcitabine-Resistant Pancreatic Cancer Cells.Nutrients · 2026Article
- The Flavonoid Kaempferol Mitigates Periprosthetic Osteolysis by Regulating the NLRP3 Inflammasome and Balancing Bone Metabolism.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Total joint arthroplasty (TJA) is an effective intervention for end-stage arthritis; however, its long-term success is often compromised by wear particle-induced osteolysis, leading to aseptic loosening and implant failure. This study investigates the potential of kaempferol (Ka), a natural flavonoid with anti-inflammatory properties, to alleviate osteolysis by modulating NLRP3 inflammasome activation. In a murine calvarial osteolysis model, Ka administration significantly attenuated bone loss induced by CoCrMo alloy particles. Mechanistically, Ka dose-dependently inhibited NLRP3 inflammasome activation in macrophages, as evidenced by reduced IL-1β secretion, decreased ASC oligomerisation and suppressed GSDMD cleavage, ultimately leading to decreased pyroptosis. These effects were found to be partially mediated via GPR109a. Furthermore, Ka markedly suppressed osteoclast differentiation and activity both in vivo and in vitro while promoting osteoblast differentiation, thereby contributing to the restoration of bone remodelling balance. Taken together, our findings suggest that Ka exerts a protective effect against wear particle-induced osteolysis by targeting the NLRP3 inflammasome and modulating osteoimmune responses, which may offer a novel therapeutic strategy to manage periprosthetic osteolysis and prolong implant longevity.
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Registered trials
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