■慢性骨髓炎,包括植入物相关的人工关节感染,极难治愈。我们从聚(d,l-丙交酯(PDLLA)和聚(d,1-丙交酯-共-乙交酯)(PLGA)与β-磷酸三钙(β-TCP)的复合材料,用于治疗耐甲氧西林金黄色葡萄球菌骨髓炎。我们询问含有万古霉素的PDLLA/β-TCP和PLGA/β-TCP复合材料是否会阻止早期生物膜的形成,允许细胞增殖和成骨分化,并在不存在成骨培养基的情况下刺激成骨信号分子。
■制备复合材料并用扫描电子显微镜表征。评估体外万古霉素释放6周。通过结晶紫染色计算生物膜预防。用水溶性四唑盐和碱性磷酸酶(ALP)染色评估人骨髓间充质干细胞(hBM-MSCs)和骨肉瘤细胞(SaOS-2)的增殖和分化。实时定量聚合酶链反应定义了hBM-MSC的成骨信号分子。
■完全,从PDLLA/β-TCP和PLGA/β-TCP复合材料中释放出3.1±0.2mg和3.4±0.4mg万古霉素,分别,并抑制早期生物膜的形成。hBM-MSCs和SaOS-2细胞在复合物上增殖并刺激细胞的ALP活性。runt相关转录因子2(RUNX2)和SRY-Box转录因子9(SOX9)的表达,然而,与对照相比,复合材料的含量较低。
■含有PDLLA/β-TCP和PLGA/β-TCP复合物的万古霉素抑制早期生物膜形成和增殖分化的hBM-MSCs和SaOS-2细胞,但是在没有成骨培养基的情况下,成骨相关的RUNX2和SOX9转录因子在14天内没有强烈表达。
UNASSIGNED: Chronic osteomyelitis, including implant-related prosthetic joint infection, is extremely difficult to cure. We develop vancomycin containing release systems from poly(d,l-lactide) (
PDLLA) and poly(d,l-lactide-co-glycolide) (PLGA) composites with beta-tricalcium phosphate (β-TCP) to treat methicillin-resistant Staphylococcus aureus osteomyelitis. We ask whether vancomycin containing
PDLLA/β-TCP and PLGA/β-TCP composites will prevent early biofilm formation, allow cell proliferation and osteogenic differentiation, and stimulate osteogenic signaling molecules in the absence of an osteogenic medium.
UNASSIGNED: Composites were produced and characterized with scanning electron microscopy. In vitro vancomycin release was assessed for 6 weeks. Biofilm prevention was calculated by crystal violet staining. Human bone marrow-derived mesenchymal stem cells (hBM-MSCs) and osteosarcoma cell (SaOS-2) proliferation and differentiation were assessed with water soluble tetrazolium salt and alkaline phosphatase (ALP) staining. Real-time quantitative polymerase chain reaction defined osteogenic signaling molecules for hBM-MSCs.
UNASSIGNED: Totally, 3.1 ± 0.2 mg and 3.4 ± 0.4 mg vancomycin released from
PDLLA/β-TCP and the PLGA/β-TCP composites, respectively, and inhibited early biofilm formation. hBM-MSCs and SaOS-2 cells proliferated on the composites and stimulated ALP activity of cells. Runt-related transcription factor 2 (RUNX2) and SRY-Box transcription Factor 9 (SOX9) expressions were, however, lower with composites when compared with control.
UNASSIGNED: Vancomycin containing
PDLLA/β-TCP and PLGA/β-TCP composites inhibited early biofilm formation and proliferated and differentiated hBM-MSCs and SaOS-2 cells, but osteogenesis-related RUNX2 and SOX9 transcription factors were not strongly expressed in the absence of an osteogenic medium for 14 days.