ArticleScientific reports2026
Circulating monocytes from aseptic loosening patients exhibit enhanced tropism toward periprosthetic tissues in NOD-SCID mouse model.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aseptic loosening (AL) remains the leading cause of implant failure after arthroplasty and is driven by chronic periprosthetic inflammation induced by particulate wear debris. Circulating monocytes contribute to this process by homing to inflamed periprosthetic tissues and propagating osteolytic inflammation. However, it remains unclear whether their enhanced recruitment reflects local chemoattractant signals alone or a state of systemic immune priming. To investigate the homing and migratory capacity of circulating monocytes from patients with aseptic loosening toward inflammatory periprosthetic tissues using a NOD-SCID xenograft model. Revision periprosthetic tissues (RPT) from AL patients and normal synovial tissues (NST) from anterior cruciate ligament reconstruction patients were implanted subcutaneously into contralateral quadriceps regions of NOD-SCID mice. Unrelated human peripheral blood monocytes (n = 6 each) were isolated from healthy volunteers (G1), primary arthroplasty patients (G2), and aseptic-loosened revision patients (G3), fluorescently labelled, and intravenously injected into mice. In vivo monocyte trafficking was quantified by serial fluorescence imaging at 1, 24, and 72 h. Monocyte infiltration into RPT was significantly greater than into control tissues across all groups. Recruitment was highest in G3, followed by G2 and G1 at 72 h (p < 0.05), with early migration evident by 24 h in all groups except G1. Multivariate regression identified patient group and implant duration as independent predictors of monocyte migration (R²=0.641, p < 0.001). Periprosthetic tissues are intrinsically chemotactic to circulating monocytes; however, monocytes from AL patients exhibit a markedly enhanced, hyper-responsive migratory phenotype consistent with systemic immune priming. These findings identify monocyte reprogramming as a previously underappreciated contributor to implant failure and suggest that targeting systemic innate immune activation may enable earlier risk stratification and novel therapeutic strategies to prevent or delay aseptic loosening.
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