Repair of large bone defects resulting from trauma, tumors, and osteitis is a current challenge to surgeons. Adipose-derived adult stem cells (ASCs) are multipotent cells that are able to differentiate into osteoblasts in the presence of certain factors. In this study, the role of greater omentum as a scaffold incorporation of ASCs was evaluated in long-bone defect healing in dog model. Sixteen 3-4-year-old, male adult mongrel dogs, weighing 25.2 ± 3.5 kg, were used in this study. In the control group (n = 4), the defect was left empty. In the omental group (n = 4), the defect was filled with harvested omentum. In the omental-ASCs group (n = 4), the defect was filled with omentum and 1 mL of ASCs was injected into the grafted omentum. In the omental-culture medium group (n = 4), 1 mL of culture medium was injected into the grafted omentum. Finally, the injured radial bones were fixed with plate and screw. Radiographs of each forelimb was taken postoperatively on the first day and at the second, fourth, sixth, and eighth weeks postinjury to evaluate bone formation, union, and remodeling of the defect. The operated radii were removed on the 56th postoperative day and were histopathologically evaluated. In this study, both omental-culture medium and omental-ASCs groups demonstrated superior osteogenic potential in healing the radial bone defect. Compared to those of the omental and control groups, more advanced bone healing criteria were present in the omental-culture medium and omental-ASCs groups at radiological and histopathological levels at 8 weeks postsurgery.
To evaluate effects of different concentrations of nanosilver colloid on the cell culture of Sertoli cells, the proportion of lipid peroxidation, antioxidant capacity, nitric oxide (NO) production and genes expression of superoxide dismutases (SOD1 and SOD2) and nitric oxide synthases (eNOS and iNOS) were measured. Sertoli cells were incubated at concentrations of 25, 75 and 125 ppm nanosilver for 48 h. There was progressive lipid peroxidation in treatments according to increasing of nanosilver. Lipid peroxidation, as indicated by malondialdehyde levels, was significantly elevated by the highest concentration of silver colloid (125 ppm), although antioxidant capacity, as measured by ferric ion reduction, was unaffected. Nitrite, as an index of NO production was reduced only in 125 ppm of nanosilver. Expression of SOD1 gene was reduced in nanosilver-treated cells at all concentrations, whereas expression of SOD2 gene was reduced only in cells treated with 125 ppm nanosilver. Expression of iNOS gene was progressively increased with higher concentrations of nanosilver. Expression of eNOS gene was also increased in 125 ppm of nanosilver. In conclusion, toxic effects of nanosilver could be due to high lipid peroxidation and suppression of antioxidant mechanisms via reduced expression of SOD genes and increased expression of NOS genes.
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