摘要
Implant integration is severely impacted by diabetes mellitus impaired bone formation and chronic inflammation. Pronounced fluctuations in blood glucose levels further hinder therapeutic regulation, rendering static drug-release strategies inadequate. To address this issue, we developed a trabecular tantalum implant with a porous structure mimicking cancellous bone mechanics, coated with phenylboronic acid–modified mesoporous silica nanoparticles loaded with aspirin. This design enables dynamic, glucose-responsive, dual-mode drug delivery; under normoglycemia, aspirin is released slowly to promote osteogenesis, whereas under hyperglycemia, its release is accelerated to suppress inflammation. In vitro, the coating enhanced the osteogenic differentiation of stem cells and promoted M2 macrophage polarization. In a diabetic rat defect model, this system improved osseointegration and reduced inflammatory responses. These findings indicate that we developed a metabolically adaptive implant surface that integrates trabecular tantalum with glucose-responsive nanocarriers. By coupling drug release kinetics with the metabolic status, this strategy addresses the dual obstacles of impaired osteogenesis and inflammation in diabetes and advances the development of smart biomaterials for clinical translation.
危险品化学品经营许可证(带存储)