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Since the discovery of the Haversian system in human bone over three hundred years ago, researchers have been wondering about its mechanical advantages. Despite positive experimental evidences on the intervention of Haversian systems in the fracture process, the contributions of Haversian systems to bone fracture have been obscure. Here a unique microcracking process accompanying the inelastic deformation of Haversian bone is reported that may shine light on its structural advantages over other bones. When compressed transversely, the concentric bone lamellae surrounding each Haversian canal allow multiple radial microcracks and arc‐shaped cracks to develop intralamellarly. Groups of circumferential arc‐shaped microcracks develop in high shear zones and radiate out in oblique directions from each Haversian canal. At the cortical bone level, where the Haversian systems are randomly distributed within the interstitial matrix, multiple nucleations and stable development of such arc‐shaped cracks happen to most Haversian systems progressively. As a result, Haversian bone is not sensitive to the presence of Haversian canals and demonstrates high inelastic strains at macroscopic level.

Bone is a tough biological material. It is generally accepted that bone's toughness arises from its unique hierarchical structure, which in turn facilitates distributed microcracking prior to fracture. Yet, there has been limited progress on the detailed roles of the structural elements in the microcracking process. The present study examines the structure-microcracking relations at the lamellar and sub-lamellar levels of human cortical bone subjected to compressive loading. Laser scanning confocal microscopy revealed a clear influence of the local structure and porosity of the Haversian systems' lamellae on microcrack development. In particular, crack initiation and growth under transverse compression were associated with stress concentration at canaliculi. Later stages of microcracking showed extensive sub-lamellar cracks forming cross-hatched patterns and regularly spaced 0.5-1.7 μm apart. The density, size and regularity of the crack patterns suggest enhanced inelastic deformation capacity through cracking control at the level of mineralized collagen fibril bundles. The present study thus improves the current understanding of the nature of inelastic deformation and microcracking in bone and further suggests that bone's resistance to fracture is achieved through microcrack control at multiple length scales.