Mechanistic aspects of the fracture toughness of elk antler bone.

Bone is an adaptive material that is designed for different functional requirements; indeed, bones have a variety of properties depending on their role in the body. To understand the mechanical response of bone requires the elucidation of its structure-function relationships. Here, we examine the fracture toughness of compact bone of elk antler, which is an extremely fast-growing primary bone designed for a totally different function than human (secondary) bone. We find that antler in the transverse (breaking) orientation is one of the toughest biological materials known. Its resistance to fracture is achieved during crack growth (extrinsically) by a combination of gross crack deflection/twisting and crack bridging via uncracked "ligaments" in the crack wake, both mechanisms activated by microcracking primarily at lamellar boundaries. We present an assessment of the toughening mechanisms acting in antler as compared to human cortical bone, and identify an enhanced role of inelastic deformation in antler which further contributes to its (intrinsic) toughness.

Rising crack-growth-resistance behavior in cortical bone: implications for toughness measurements.

Fracture mechanics studies have characterized bone's resistance to fracture in terms of critical stress intensity factor and critical strain energy release rate measured at the onset of a fracture crack. This approach, although useful, provide a limited insight into fracture behavior of bone because, unlike classical brittle materials, bone is a microcracking solid that derives its resistance to fracture during the process of crack propagation from microfracture mechanisms occurring behind the advancing crack front. To address this shortfall, a crack propagation-based approach to measure bone toughness is described here and compared with crack initiation approach. Post hoc analyses of data from previously tested bovine and antler cortical bone compact specimens demonstrates that, in contrast to crack initiation approach, the crack propagation approach successfully identifies the superior toughness properties of red deer's antler cortical bone. Propagation-based slope of crack growth resistance curve is, therefore, a more useful parameter to evaluate cortical bone fracture toughness.

Experimental validation of a microcracking-based toughening mechanism for cortical bone.

It has been proposed that cortical bone derives its toughness by forming microcracks during the process of crack propagation (J. Biomech. 30 (1997) 763; J. Biomech. 33 (2000) 1169). The purpose of this study was to experimentally validate the previously proposed microcrack-based toughening mechanism in cortical bone. Crack initiation and propagation tests were conducted on cortical bone compact tension specimens obtained from the antlers of red deer. For these tests, the main fracture crack was either propagated to a predetermined crack length or was stopped immediately after initiating from the notch. The microcracks produced in both groups of specimens were counted in the same surface area of interest around and below the notch, and crack growth resistance and crack propagation velocity were analyzed. There were more microcracks in the surface area of interest in the propagation than in initiation specimens showing that the formation of microcracks continued after the initiation of a fracture crack. Crack growth resistance increased with crack extension, and crack propagation velocity vs. crack extension curves demonstrated the characteristic jump increase and decrease pattern associated with the formation of microcracks. The scanning electron micrographs of crack initiation and propagation displayed the formation of a frontal process zone and a wake, respectively. These results support the microcrack-based toughening mechanism in cortical bone. Bone toughness is, therefore, determined by its ability to form microcracks during fracture.

Tumor-like growth of antlers in castrated fallow deer: an electron microscopic study.

Male deer regenerate new sets of antlers each year. When fully grown, rising levels of testosterone promote antler ossification, cutting off the blood flow and causing the velvet integument to be shed. After the mating season, the old antlers fall off to be replaced by new ones. When the adult fallow deer is castrated in autumn or winter, its bony antlers are shed and replaced by usually shorter regenerates that remain permanently viable and in velvet. If prevented from winter freezing, these antlers continue to grow thicker each year, eventually giving rise to amorphous outgrowths, or antleromas, from their sides. These growths mushroom out from the antler as clusters of nodules, developing in unpredictable locations, but commonly at the bases and ends of the antlers. Their integument contains numerous hair follicles. Internally, antleromas are composed of masses of collagen together with fibroblasts actively engaged in ribonucleic acid and protein synthesis. Thin basal laminae surround the blood vessels, and in the skin separate the overlying epidermis from the collagenous substance of the antleroma. Despite their superficial resemblance to hypertrophic scars, antleromas lack many of the characters by which they are diagnosed. They may be classified as benign tumors, at least in the generic sense. Antleromas would appear to represent a sustained expression of antler regeneration uncoupled from those morphogenetic influences responsible for the configurations into which deer antlers normally develop.