| Abstract Scope |
A material’s capacity for limited deformation is a critical aspect of toughness as this enables the local dissipation of stresses that would otherwise cause fracture. Such inelastic deformation mechanisms are diverse; they include dislocation motion in crystalline materials, in-situ phase-transformations in certain metals and ceramics, sliding of collagen fibrils in bone, rotation of fibrils in skin, frictional motion between mineral “platelets” in seashells, and through mechanisms that also cause fracture such as shear-banding in glasses and microcracking in rocks. Resistance to fracture is thus a compromise: either a combination of the mutually exclusive properties of strength and deformability, as in intrinsic toughness, or between intrinsic and extrinsic (shielding) mechanisms that act to induce toughness, respectively, ahead or behind, the tip. We examine the interplay between such mechanisms in biological materials, including skin and bone, high-temperature materials, such as ceramic-matrix composites and nuclear graphite, and in bulk-metallic glasses and high-entropy alloys. |