This study tested the hypothesis that bioactive coating glass (SiO(2)-CaO-P(2)O(5)-MgO-K(2)O-Na(2)O system), used for implant coatings, enhanced the induction of collagen type 1 synthesis and in turn enhanced the expression of downstream markers alkaline phosphatase, Runx2 and osteocalcin during osteoblast differentiation. The ions from experimental bioactive glass (6P53-b) and commercial Bioglass(TM) (45S5) were added to osteoblast-like MC3T3-E1 subclone 4 cultures as a supplemented ion extract (glass conditioned medium (GCM)). Ion extracts contained significantly higher concentrations of Si and Ca (Si, 47.9+/-10.4 ppm; Ca, 69.8+/-14.0 for 45S5; Si, 33.4+/-3.8 ppm; Ca, 57.1+/-2.8 ppm for 6P53-b) compared with the control extract (Si<0.1 ppm, Ca 49.0 ppm in alpha-MEM) (ANOVA, p<0.05). Cell proliferation rate was enhanced (1.5x control) within the first 3 days after adding 45S5 and 6P53-b GCM. MC3T3-E1 subclone 4 cultures were then studied for their response to the addition of test media (GCM and control medium along with ascorbic acid (AA; 50 ppm)). Each GCM+AA treatment enhanced collagen type 1 synthesis as observed in both gene expression results (day 1, Col1alpha1, 45S5 GCM+AA: 3x control+AA; 6P53-b GCM+AA: 4x control+AA; day 5, Col1alpha2, 45S5 GCM+AA: 3.15x control+AA; 6P53-b GCM+AA: 2.35x control+AA) and in histological studies (Picrosirius stain) throughout the time course of early differentiation. Continued addition of each GCM and AA treatment led to enhanced expression of alkaline phosphatase (1.4x control+AA after 5 days, 2x control+AA after 10 days), Runx2 (2x control+AA after 7 days) and osteocalcin gene (day 3, 45S5 GCM+AA: 14x control+AA; day 5, 6P53-b GCM+AA: 19x control+AA) and protein expression (40x-70x control+AA after 6 days). These results indicated the enhanced effect of bioactive glass ions on key osteogenic markers important for the bone healing process.

Traumatic fractures cause structurally unstable sites due to severe bone loss. Such fractures generate a high yield of reactive oxygen species (ROS) that can lead to oxidative stress. Excessive and prolonged ROS activity impedes osteoblast differentiation and instigates long healing times. Stimulation of antioxidants such as superoxide dismutase (SOD1), are crucial to reduce ROS, stimulate osteogenesis, and strengthen collagen and mineral formation. Yet, no current fixative devices have shown an ability to enhance collagen matrix formation through antioxidant expression. This study reports plasma-enhanced chemical vapor deposition based amorphous silicon oxynitride (Si(ON)x) as a potential new fracture healing biomaterial that adheres well to the implant surface, releases Si(+4) to enhance osteogenesis, and forms a surface hydroxyapatite for collagen mineral attachment. These materials provide a sustained release of Si(+4) in physiological environment for extended times. The dissolution rate partially depends on the film chemistry and can be controlled by varying O/N ratio. The presence of Si(+4) enhances SOD1, which stimulates other osteogenic markers downstream and leads to rapid mineral formation. In vivo testing using a rat critical-sized calvarial defect model shows a more rapid bone-regeneration for these biomaterials as compared to control groups, that implies the clinical significance of the presented biomaterial.

Structurally unstable fracture sites require metal fixative devices, which have long healing times due to their lack of osteoinductivity. Bioactive glass coatings lack in interfacial bonding, delaminate, and have reduced bioactivity due to the high temperatures used for their fabrication. Here, we test the hypothesis that low-temperature PECVD amorphous silica can enhance adhesion to the underlying metal surface and that N incorporation enhances osteogenesis and rapid biomineralization. A model Ti/TiO2-SiOx interface was formed by first depositing Ti onto Si wafers, followed by surface patterning, thermal annealing to form TiO2, and depositing SiOx/Si(ON)x overlays. TEM micrographs showed conformal SiOx layers on Ti/TiO2 overlays while XPS data revealed the formation of an elemental Ti-O-Si interface. Nanoscratch testing verified strong SiOx bonding with the underlying TiO2 layers. In vitro studies showed that the surface properties changed significantly to reveal the formation of hydroxycarbonate apatite within 6 h, and Si(ON)x surface chemistry induced osteogenic gene expression of human periosteal cells and led to a rapid "bone-like" biomineral formation within 4 weeks. XANES data revealed that the incorporation of N increased the surface HA bioactivity by increasing the carbonate to phosphate ratio. In conclusion, silicon oxynitride overlays on bone-implant systems enhance osteogenesis and biomineralization via surface nitrogen incorporation.

a b s t r a c t a r t i c l e i n f o) after 30 days. In examining the extracellular matrix generated by cells when exposed to each GCM, it was found that 45S5 GCM had slightly elevated levels of mineral content within ECM as compared to 6P53-b GCM after 30 days while control treatments exhibited no mineral content. The formation of well-defined mineralized nodules (distinct PO 4 3− [960 cm