Additive manufacturing (AM) technology has been broadly applied to the fabrication of metallic materials. However, current approaches consume either high energy or large investment that considerably elevates their entry threshold. An economic extrusion-based AM method followed by debinding and sintering could efficiently produce the metal part with relatively low cost and high material utilization. However, an in-depth analysis of the fatigue performance of the component built by such technology has been little documented in the literature so far. Herein, the 316L stainless steel was fabricated throughout the printing-debinding-sintering (PDS) pathway and its fatigue properties were comprehensively assessed. Tensile and flexural fatigue tests were conducted to reveal the fatigue strength and fractural behaviors under different loading conditions, while the fatigue crack growth (FCG) test was performed to quantify the crack propagation. The results indicated the number of 105 cycles can be reached for the tensile specimens under the fatigue loading of 120 MPa, whereas 1.37 × 105 cycles were endured by the flexural specimens under 150 MPa. The fractural morphology indicated an adverse impact of the pore-induced voids on the tensile fatigue crack propagation, but such a drawback could be alleviated in the flexural loading condition. The FCG test unveiled the crack growth rate with the number of cycles and determined the material-related coefficients in the fatigue crack growth model. The research findings provided valuable insights into the effects of the PDS process and microstructures on the fatigue properties of the metal component.

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Intramedullary stabilization is frequently used to treat long bone fractures. Since implant removal can become technically very challenging with the potential to cause further tissue damage, biodegradable materials are emerging as alternative options. Magnesium (Mg)-based biodegradable implants have a controllable degradation rate and good tissue compatibility, which makes them attractive for musculoskeletal research. Herein, the degradation of Mg and steel implants, the pathological characteristics and osteoblast differentiation in mice femora were examined. To investigate the molecular mechanism, we analyzed the differentially expressed long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) in Mg-implanted or stain-steel-implanted callus tissues. lncRNA LOC103691336 was upregulated in Mg-implanted tissues and most relevant to BMPR2, a kinase receptor of BMPs with an established role in osteogenesis. The knockdown of LOC103691336 attenuated Mg-mediated osteogenic differentiation. Furthermore, miR-138-5p, previously reported to inhibit osteogenic differentiation, could bind to LOC103691336 and BMPR2 in bone marrow stromal cells (BMSCs). LOC103691336 competed with BMPR2 for miR-138-5p binding in BMSCs to attenuate the inhibitory effect of miR-138-5p on BMPR2 expression. Finally, the effect of LOC103691336 knockdown on Mg-mediated osteogenic differentiation could be attenuated by miR-138-5p inhibition. In conclusion, we provided a novel mechanism of Mg implants mediating the osteogenesis differentiation and demonstrated that Mg implants may be promising for improving fracture healing.