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Background: Scaffold (SCA) functionalization with aptamers (APT) provides adsorption of specific bioactive molecules on biomaterial surfaces. The aim of this study was to observe if SCA enriched with anti-fibronectin APT can favor coagulum (PhC) and osteoblasts (OSB) differentiation. Methods: 20 μg of APT was functionalized on SCA by simple adsorption. For PhC formation, SCAs were inserted into rat calvaria defects for 17 h. Following proper transportation (buffer solution PB), OSBs (UMR-106 lineage) were seeded over PhC + SCAs with and without APT. Cells and PhC morphology, PhC cell population, protein labeling and gene expression were observed in different time points. Results: The APT induced higher alkaline phosphatase and bone sialoprotein immunolabeling in OSB. Mesenchymal stem cells, leukocytes and lymphocytes cells were detected more in the APT group than when scaffolds were not functionalized. Additionally, an enriched and dense fibrin network and different cell types were observed, with more OSB and white blood cells in PhC formed on SCA with APT. The gene expression showed higher transforming growth factor beta 1 (TGF-b1) detection in SCA with APT. Conclusions: The SCA functionalization with fibronectin aptamers may alter key morphological and functional features of blood clot formation, and provides a selective expression of proteins related to osteo differentiation. Additionally, aptamers increase TGF-b1 gene expression, which is highly associated with improvements in regenerative therapies. [ABSTRACT FROM AUTHOR]

Aluminum (Al) is the most abundant metal in the earth's crust and is found naturally in the air, water, and soil. Al may pose a major threat to humans, causing diseases and bone disorders. Nevertheless, the effects of Al on alveolar bone are not reported in the literature. Here, we investigated the effects of sub-chronic intoxication with Al citrate in a model of alveolar bone loss, induced by ligature, in male Wistar rats. The animals were exposed to Al citrate (100 mg/kg/day), by gavage, for 30 days. We used 40 rats equally divided into four groups: Control; Experimental Periodontitis (EPeriodontitis); Al; Al+EPeriodontitis. After exposure period, we evaluated the concentration of Al in the blood and alveolar bone, as well as the Al measurement in alveolar bone. The results showed that the Al exposure promoted distribution of Al in blood serum and in the alveolar bone. The Al exposure per si results in alveolar bone loss as well as potentiates damages of periodontitis induced cases. These results suggest that levels aluminum in the blood and alveolar bone induce alveolar bone loss, besides present aggravating effect in the presence of induced periodontitis. [ABSTRACT FROM AUTHOR]