This work presents a strategy to augment the bioactivity of a new-generation metastable β-Ti–Nb–Sn alloy through surface severe plastic deformation. Foremost, the alloy was strengthened by precipitation of α phase using a well-designed thermo-mechanical processing route. Subsequently, the surface of the aged alloy was subjected to severe plastic deformation via surface mechanical attrition treatment (SMAT). Upon SMAT, a unique phenomenon of strain-induced precipitate coarsening was observed. A possible mechanism is proposed wherein the precipitates first dissolve due to significant slip transfer across the α/β-interface followed by reprecipitation along the other precipitates thereby leading to coarsening. Coarsening of the precipitates abrogated the strengthening caused by plastic deformation as a result of which the hardness did not increase significantly after SMAT in sharp contrast to other alloys. SMAT led to a decrease in the attachment of human mesenchymal stem cells because of an increase in the roughness-mediated surface hydrophobicity. On the other hand, an increase in the roughness led to the formation of more number of focal adhesions. This in turn enhanced the proliferation rate and more importantly, osteogenic differentiation of stem cells. Detailed investigation into the underlying mechanism revealed that an increase in focal adhesions activated the Akt-mediated mechano-transduction signaling pathway that enhanced the osteogenic differentiation. In summary, the potential of surface severe plastic deformation to impart bioactivity to the next-generation of orthopedic β-Ti alloys is underscored in this work.

中文翻译：

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整形外科Ti-Nb-Sn合金的表面严重塑性变形会引起异常的沉淀重塑并通过Akt信号支持干细胞成骨

这项工作提出了一种通过表面严重塑性变形来增强新一代亚稳态β-Ti-Nb-Sn合金的生物活性的策略。最重要的是，采用精心设计的热机械加工路线，通过沉淀出α相来增强合金强度。随后，通过表面机械磨损处理（SMAT）对时效合金的表面进行了严重的塑性变形。在SMAT上，观察到了应变引起的析出物粗化的独特现象。提出了一种可能的机制，其中沉淀物由于穿过α/β界面的明显滑移而首先溶解，然后沿其他沉淀物再沉淀，从而导致粗化。沉淀物的粗化消除了塑性变形引起的强化，因此与其他合金形成鲜明对比的是，SMAT处理后硬度并未显着提高。由于粗糙度介导的表面疏水性增加，SMAT导致人间充质干细胞的附着减少。另一方面，粗糙度的增加导致形成更多的粘连。这继而提高了干细胞的增殖速率，更重要的是提高了成骨细胞的分化。对潜在机制的详细研究表明，粘着斑的增加激活了Akt介导的机械传导信号通路，从而增强了成骨分化。总之，