Bioinspired Nacre-Like Alumina with a Metallic Nickel Compliant Phase Fabricated by Spark-Plasma Sintering.

Many natural materials present an ideal "recipe" for the development of future damage-tolerant lightweight structural materials. One notable example is the brick-and-mortar structure of nacre, found in mollusk shells, which produces high-toughness, bioinspired ceramics using polymeric mortars as a compliant phase. Theoretical modeling has predicted that use of metallic mortars could lead to even higher damage-tolerance in these materials, although it is difficult to melt-infiltrate metals into ceramic scaffolds as they cannot readily wet ceramics. To avoid this problem, an alternative ("bottom-up") approach to synthesize "nacre-like" ceramics containing a small fraction of nickel mortar is developed. These materials are fabricated using nickel-coated alumina platelets that are aligned using slip-casting and rapidly sintered using spark-plasma sintering. Dewetting of the nickel mortar during sintering is prevented by using NiO-coated as well as Ni-coated platelets. As a result, a "nacre-like" alumina ceramic displaying a resistance-curve toughness up to ≈16 MPa m½ with a flexural strength of ≈300 MPa is produced.

Bioinspired nacre-like alumina with a bulk-metallic glass-forming alloy as a compliant phase.

Bioinspired ceramics with micron-scale ceramic "bricks" bonded by a metallic "mortar" are projected to result in higher strength and toughness ceramics, but their processing is challenging as metals do not typically wet ceramics. To resolve this issue, we made alumina structures using rapid pressureless infiltration of a zirconium-based bulk-metallic glass mortar that reactively wets the surface of freeze-cast alumina preforms. The mechanical properties of the resulting Al2O3 with a glass-forming compliant-phase change with infiltration temperature and ceramic content, leading to a trade-off between flexural strength (varying from 89 to 800 MPa) and fracture toughness (varying from 4 to more than 9 MPa·m½). The high toughness levels are attributed to brick pull-out and crack deflection along the ceramic/metal interfaces. Since these mechanisms are enabled by interfacial failure rather than failure within the metallic mortar, the potential for optimizing these bioinspired materials for damage tolerance has still not been fully realized.

Alendronate treatment alters bone tissues at multiple structural levels in healthy canine cortical bone.

Bisphosphonates are widely used to treat osteoporosis, but have been associated with atypical femoral fractures (AFFs) in the long term, which raises a critical health problem for the aging population. Several clinical studies have suggested that the occurrence of AFFs may be related to the bisphosphonate-induced changes of bone turnover, but large discrepancies in the results of these studies indicate that the salient mechanisms responsible for any loss in fracture resistance are still unclear. Here the role of bisphosphonates is examined in terms of the potential deterioration in fracture resistance resulting from both intrinsic (plasticity) and extrinsic (shielding) toughening mechanisms, which operate over a wide range of length-scales. Specifically, we compare the mechanical properties of two groups of humeri from healthy beagles, one control group comprising eight females (oral doses of saline vehicle, 1 mL/kg/day, 3 years) and one treated group comprising nine females (oral doses of alendronate used to treat osteoporosis, 0.2mg/kg/day, 3 years). Our data demonstrate treatment-specific reorganization of bone tissue identified at multiple length-scales mainly through advanced synchrotron x-ray experiments. We confirm that bisphosphonate treatments can increase non-enzymatic collagen cross-linking at molecular scales, which critically restricts plasticity associated with fibrillar sliding, and hence intrinsic toughening, at nanoscales. We also observe changes in the intracortical architecture of treated bone at microscales, with partial filling of the Haversian canals and reduction of osteon number. We hypothesize that the reduced plasticity associated with BP treatments may induce an increase in microcrack accumulation and growth under cyclic daily loadings, and potentially increase the susceptibility of cortical bone to atypical (fatigue-like) fractures.