Article: Torres, AM; Matheny, JB; Keaveny, TM; Taylor, D; Rimnac, CM; Hernandez, CJ; (2016) “Material Heterogeneity in Cancellous Bone Promotes Deformation Recovery After Mechanical Failure”, Proceedings of the National Academy of Sciences of the United States of America, 113(11):2892-2897
Abstract: Many natural structures use a foam core and solid outer shell to achieve high strength and stiffness with relatively small amounts of mass. Biological foams, however, must also resist crack growth. The process of rack propagation within the struts of a foam is not well understood and is complicated by the foam microstructure. We demonstrate that in cancellous bone, the foam-like component of whole bones, damage propagation during cyclic loading is dictated not by local tissue stresses but by heterogeneity of material properties associated with increased ductility of strut surfaces. The increase in surface ductility is unexpected because it is the opposite pattern generated by surface treatments to increase fatigue life in man-made materials, which often result in reduced surface ductility. We show that the more ductile surfaces of cancellous bone are a result of reduced accumulation of advanced glycation end products compared with the strut interior. Damage is therefore likely to accumulate in strut centers making cancellous bone more tolerant of stress concentrations at strut surfaces. Hence, the structure is able to recover more deformation after failure and return to a closer approximation of its original shape. Increased recovery of deformation is a passive mechanism seen in biology for setting a broken bone that allows for a better approximation of initial shape during healing processes and is likely the most important mechanical function. Our findings suggest a previously unidentified biomimetic design strategy in which tissue level material heterogeneity in foams can be used to improve deformation recovery after failure.
Funding Acknowledgement: National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health Award [AR057362]; National Institutes of Health (NIH) [8U42OD011158-22]; Cornell’s National Science Foundation (NSF) [DGE-1144153]; NSF Graduate Research Fellowship Program (GRFP); NSF GRFP; Cornell Colman fellowship; NIH [S10RR025502]
Funding Text: We thank Christopher Chapa and Floor Lambers for assistance with specimen preparation. We thank Matthew Goff for assistance with finite element models. This work was supported by National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health Award AR057362 (principal investigator, C.J.H.). We acknowledge use of human vertebral bodies provided by the National Disease Research Interchange, with support from National Institutes of Health (NIH) Grant 8U42OD011158-22, Cornell’s National Science Foundation (NSF) Grant DGE-1144153, NSF Graduate Research Fellowship Program (GRFP) (to A.M.T.), NSF GRFP (to J.B.M.), and a Cornell Colman fellowship (to A.M.T.). Imaging data were acquired in the Cornell Biotechnology Resource Center (BRC)-Imaging Facility using the shared, NIH-funded (S10RR025502) Zeiss LSM 710 Confocal.