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A hybrid hydrogel composed of gelatin and gold nanoparticles (GNPs) was designed to evaluate the effect of new bone formation and proves itself to be useful as an implant material for treating defected bone tissues.

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A significant problem that affects tissue-engineered electrospun nanofibrous scaffolds is poor infiltration of cells into the three-dimensional (3D) structure. Physical manipulation can enhance cellular infiltration into electrospun scaffolds. The porosity of electrospun nanofibers was highly enlarged by ultrasonication in an aqueous solution. The porosity and related property changes on a series of nanofibers were observed to be dependent on ultrasonication time and energy. To evaluate cell infiltration into the scaffold, fibroblasts were seeded onto these nanofibers and cultured for different lengths of time. The penetration levels of these cells into the scaffold were monitored using confocal lazer scanning microscopy. The cell infiltration potential was greatly increased with regard to an increase in pore size and porosity. These 3D nanofibrous scaffolds fabricated by an ultrasonication process allowed cells to infiltrate easily into the scaffold. This approach shows great promise for design of cell permeable nanofibrous scaffolds for tissue-engineering applications.

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Gold nanoparticles (GNPs) have been previously reported to inhibit osteoclast (OC) formation. However, previous research only confirmed the osteoclastogenesis inhibitory effect under in vitro conditions. The aim of this study was to develop a therapeutic agent for osteoporosis based on the utilization of GNPs and confirm their effect both in vitro and in vivo. We prepared β-cyclodextrin (CD) conjugated GNPs (CGNPs), which can form inclusion complexes with curcumin (CUR-CGNPs), and used these to investigate their inhibitory effects on receptor activator of nuclear factor-κb ligand (RANKL)-induced osteoclastogenesis in bone marrow-derived macrophages (BMMs). The CUR-CGNPs significantly inhibited the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cells in BMMs without inducing cytotoxicity. The mRNA expressions of genetic markers of OC differentiation including c-Fos, nuclear factor of activated T cells 1 (NFATc1), TRAP, and osteoclast associated receptor (OSCAR) were significantly decreased in the presence of CUR-CGNPs. In addition, the CUR-CGNPs inhibited OC differentiation of BMMs through suppression of the RANKL-induced signaling pathway. Additionally, CUR-CGNPs caused a decrease in RANKL-induced actin ring formation, which is an essential morphological characteristic of OC formation allowing them to carry out bone resorption activity. Furthermore, the in vivo results of an ovariectomy (OVX)-induced osteoporosis model showed that CUR-CGNPs significantly improved bone density and prevented bone loss. Therefore, CUR-CGNPs may prove to be useful as therapeutic agents for preventing and treating osteoporosis.

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