Bone defects arising from injury and/or disease are a common and debilitating clinical lesion. While the development of tissue microenvironments utilizing biomimetic constructs is an emerging approach for bone tissue engineering. In this context, bioactive glass nanoparticles (BGNPs) were embedded within polycaprolactone (PCL) scaffolds. The scaffolds exhibit an engineered unidirectional pore structure which are surface activated via oxygen plasma to allow immobilization of simvastatin (SIM) on the pore surface. Microscopic observation indicated the surface modification did not disturb the lamellar orientation of the pores improving the biomimetic formation of hydroxyapatite. Mathematically modelled release profiles reveal that the oxygen plasma pre-treatment can be utilized to modulate the release profile of SIM from the scaffolds. With the release mechanism controlled by the balance between the diffusion and erosion mechanisms. Computational modelling shows that Human Serum Albumin and Human α₂-macroglobulin can be utilized to increase SIM bioavailability for cells via a molecular docking mechanism. Cellular studies show positive MG-63 cell attachment and viability on optimized scaffolds with alkaline phosphatase activity enhanced along with enhanced expression of osteocalcoin biomarker.

由损伤和/或疾病引起的骨缺损是一种常见且使人衰弱的临床病变。而利用仿生结构开发组织微环境是骨组织工程的一种新兴方法。在这种情况下，生物活性玻璃纳米粒子 (BGNP) 被嵌入聚己内酯 (PCL) 支架内。该支架具有工程化的单向孔结构，通过氧等离子体进行表面活化，以将辛伐他汀 (SIM) 固定在孔表面。显微观察表明表面改性不会干扰孔的层状取向，从而改善羟基磷灰石的仿生形成。数学建模的释放曲线表明，氧等离子体预处理可用于调节 SIM 从支架中的释放曲线。释放机制由扩散和侵蚀机制之间的平衡控制。计算模型显示人血清白蛋白和人α_2-巨球蛋白可用于通过分子对接机制提高细胞的 SIM 生物利用度。细胞研究显示 MG-63 细胞在优化支架上的阳性附着和活力，碱性磷酸酶活性增强，骨钙生物标志物的表达增强。