Age-related changes in the plasticity and toughness of human cortical bone at multiple length scales
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Age-related changes in the plasticity and toughness of human cortical bone at multiple length scales. / Zimmermann, Elizabeth A; Schaible, Eric; Bale, Hrishikesh; Barth, Holly D; Tang, Simon Y; Reichert, Peter; Busse, Bjoern; Alliston, Tamara; Ager, Joel W; Ritchie, Robert O.
in: P NATL ACAD SCI USA, Jahrgang 108, Nr. 35, 30.08.2011, S. 14416-21.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Age-related changes in the plasticity and toughness of human cortical bone at multiple length scales
AU - Zimmermann, Elizabeth A
AU - Schaible, Eric
AU - Bale, Hrishikesh
AU - Barth, Holly D
AU - Tang, Simon Y
AU - Reichert, Peter
AU - Busse, Bjoern
AU - Alliston, Tamara
AU - Ager, Joel W
AU - Ritchie, Robert O
PY - 2011/8/30
Y1 - 2011/8/30
N2 - The structure of human cortical bone evolves over multiple length scales from its basic constituents of collagen and hydroxyapatite at the nanoscale to osteonal structures at near-millimeter dimensions, which all provide the basis for its mechanical properties. To resist fracture, bone's toughness is derived intrinsically through plasticity (e.g., fibrillar sliding) at structural scales typically below a micrometer and extrinsically (i.e., during crack growth) through mechanisms (e.g., crack deflection/bridging) generated at larger structural scales. Biological factors such as aging lead to a markedly increased fracture risk, which is often associated with an age-related loss in bone mass (bone quantity). However, we find that age-related structural changes can significantly degrade the fracture resistance (bone quality) over multiple length scales. Using in situ small-angle X-ray scattering and wide-angle X-ray diffraction to characterize submicrometer structural changes and synchrotron X-ray computed tomography and in situ fracture-toughness measurements in the scanning electron microscope to characterize effects at micrometer scales, we show how these age-related structural changes at differing size scales degrade both the intrinsic and extrinsic toughness of bone. Specifically, we attribute the loss in toughness to increased nonenzymatic collagen cross-linking, which suppresses plasticity at nanoscale dimensions, and to an increased osteonal density, which limits the potency of crack-bridging mechanisms at micrometer scales. The link between these processes is that the increased stiffness of the cross-linked collagen requires energy to be absorbed by "plastic" deformation at higher structural levels, which occurs by the process of microcracking.
AB - The structure of human cortical bone evolves over multiple length scales from its basic constituents of collagen and hydroxyapatite at the nanoscale to osteonal structures at near-millimeter dimensions, which all provide the basis for its mechanical properties. To resist fracture, bone's toughness is derived intrinsically through plasticity (e.g., fibrillar sliding) at structural scales typically below a micrometer and extrinsically (i.e., during crack growth) through mechanisms (e.g., crack deflection/bridging) generated at larger structural scales. Biological factors such as aging lead to a markedly increased fracture risk, which is often associated with an age-related loss in bone mass (bone quantity). However, we find that age-related structural changes can significantly degrade the fracture resistance (bone quality) over multiple length scales. Using in situ small-angle X-ray scattering and wide-angle X-ray diffraction to characterize submicrometer structural changes and synchrotron X-ray computed tomography and in situ fracture-toughness measurements in the scanning electron microscope to characterize effects at micrometer scales, we show how these age-related structural changes at differing size scales degrade both the intrinsic and extrinsic toughness of bone. Specifically, we attribute the loss in toughness to increased nonenzymatic collagen cross-linking, which suppresses plasticity at nanoscale dimensions, and to an increased osteonal density, which limits the potency of crack-bridging mechanisms at micrometer scales. The link between these processes is that the increased stiffness of the cross-linked collagen requires energy to be absorbed by "plastic" deformation at higher structural levels, which occurs by the process of microcracking.
KW - Adult
KW - Aged
KW - Aged, 80 and over
KW - Aging
KW - Biomechanical Phenomena
KW - Bone and Bones
KW - Glycosylation End Products, Advanced
KW - Humans
KW - Middle Aged
KW - Tomography, X-Ray Computed
U2 - 10.1073/pnas.1107966108
DO - 10.1073/pnas.1107966108
M3 - SCORING: Journal article
C2 - 21873221
VL - 108
SP - 14416
EP - 14421
JO - P NATL ACAD SCI USA
JF - P NATL ACAD SCI USA
SN - 0027-8424
IS - 35
ER -