ArticleAdvanced healthcare materials2025
Si Inhibited Osteoclastogenesis: The Role of Fe and the Fenton Reaction.
Article in Advanced healthcare materials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- LincRNA-EPS alleviates osteoclastogenesis under inflammatory microenvironment through preventing excessive iron metabolism.Cell death & disease · 2026Article
- Si Inhibited Osteoclastogenesis: The Role of Fe and the Fenton Reaction.Advanced healthcare materials · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Soluble silicate species (Si) released from bioceramics have been reported to enhance bone regeneration and regulate bone remodeling, but their cellular mechanisms remain unclear. Here, we show that Si inhibited osteoclast (OC) formation and resorption (as determined by OC number, TRAP-5b expression, and volumetric resorption) in a concentration-dependent manner, in both primary OCs and an osteoclastic subclone of the RAW264.7 cell-line (p<0.001). We propose that Si‑mediated inhibition may be mediated via reduced reactive oxygen species (ROS) availability, due to iron‑silicate (Fe-O-Si) interactions. Biochemical assays demonstrated that Si decreased the availability of ROS, and decreased intracellular ROS concentrations in OCs, but only in the presence of Fe. Furthermore, Si-inhibited OC formation is restored by the addition of 10µM Fe (P<0.001). Fe-Si interactions were demonstrated by a reduction in Si and Fe concentrations (P<0.001) in solution (ICP-OES) and by Si─O─Fe bonds observed in precipitates (ATR-FTIR). These results suggest that that Si may inhibit OC activity by regulation of the Fenton reaction. Understanding the intracellular mechanisms of how Si interacts with OCs allows the development of new Si-releasing materials (e.g., bioactive glasses or bioceramics) with controlled release of Si to regulate osteoclastogenesis.
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Registered trials
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