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Periprosthetic bone loss is a major cause of aseptic loosening after joint replacement surgery, and the inflammation caused by wear particles disrupts bone metabolism. Currently, there aren’t effective non-surgical treatments available. In this study, we created a fused exosome, f‑exo, by combining M2 macrophage-derived exosomes with urine-derived stem cell exosomes. We used ultrasound combined with extrusion to fuse their membranes while keeping the proteins and biological activities of both exosomes. In vitro studies showed that f‑exo could work together to promote bone differentiation, inhibit osteoclast activation, and encourage new blood vessel formation.
Animal models showed that f‑exo, using surface molecules from M2 macrophage membranes, specifically targeted bone loss areas, stayed longer in circulation, effectively reduced titanium particle-induced bone damage, eased local inflammation, improved bone microstructure, and boosted both bone formation and H-type blood vessel formation. Proteomics suggested that it regulates bone metabolism through the HIF‑1, Wnt, and PI3K‑Akt pathways, with integrin αMβ2 involved in targeted adhesion. This fused exosome offers a new targeted strategy for treating periprosthetic bone loss, though scaling up production and ensuring long-term safety in the body still need further work.
References:
DOI: 10.1016/j.bioactmat.2025.04.006
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