Correction to the article “age-related changes in the collagen network and toughness of bone” [bone 31:1–7, 2002]

Wang, X; Shen, Xinmei; Li, X; Agrawal, C. Mauli

doi:10.1016/s8756-3282(03)00016-4

Cited by 12 publications

(4 citation statements)

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“…Secondary osteon concentration, bulk density, collagen properties, and increased bulk mineralization all appear to play an important role. 4,[14][15][16][17][18] Additional studies have examined the effect of crack velocity on fracture toughness. 8,19,20 However, these tests were performed at relatively low rates (crack velocities of 10 -5 -10 -3 m/s), and only more recently have more extreme loading rates been examined.…”

Section: Research Summary Biological Materials Sciencementioning

confidence: 99%

Aging and loading rate effects on the mechanical behavior of equine bone

Kulin

Jiang

Vecchio

2008

JOM

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Section: Research Summary Biological Materials Sciencementioning

confidence: 99%

Aging and loading rate effects on the mechanical behavior of equine bone

Kulin

Jiang

Vecchio

2008

JOM

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“…In this study, we quantitated five AGEs and five enzymatic crosslinks in 149 human cancellous bone samples by LC-QqTOF-MS to examine the patterns of AGEs accumulation, and to investigate whether pentosidine or tfAGEs more accurately reflects the actual AGEs status in bone collagen. As the clinical manifestations of AGEs accumulation include aging 12 , 37 , diabetes 38 and renal failure 39 , we also analyzed the association between AGEs and the clinical parameters such as age, gender, BMI, history of diseases, glycated hemoglobin (HbA1c) as the marker of blood glycemic status over several weeks to months 40 , tartrate-resistant acid phosphatase-5b (TRACP-5b) as the measure of bone resorption, and estimated glomerular filtration rate (eGFR).…”

Section: Introductionmentioning

confidence: 99%

Mass spectrometric quantitation of AGEs and enzymatic crosslinks in human cancellous bone

Arakawa

Suzuki

Kurosaka

et al. 2020

Sci Rep

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Advanced glycation end-products (AGEs) deteriorate bone strength. Among over 40 species identified in vivo, AGEs other than pentosidine were roughly estimated as total fluorescent AGEs (tfAGEs) due to technical difficulties. Using LC-QqTOF-MS, we established a system that enabled the quantitation of five AGEs (CML, CEL, MG-H1, CMA and pentosidine) as well as two mature and three immature enzymatic crosslinks. Human bone samples were collected from 149 patients who underwent total knee arthroplasty. Their clinical parameters were collected to investigate parameters that may be predictive of AGE accumulation. All the analytes were quantitated and showed significant linearity with high sensitivity and precision. The results showed that MG-H1 was the most abundant AGE, whereas pentosidine was 1/200–1/20-fold less abundant than the other four AGEs. The AGEs were significantly and strongly correlated with pentosidine, while showing moderate correlation with tfAGEs. Interestingly, multiple linear regression analysis revealed that gender contributed most to the accumulation of all the AGEs, followed by age, tartrate-resistant acid phosphatase-5b and HbA1c. Furthermore, the AGEs were negatively correlated with immature crosslinks. Mass spectrometric quantitation of AGEs and enzymatic crosslinks is crucial to a better understanding of ageing- and disease-related deterioration of bone strength.

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“…A significant difference in R-curve behavior expected when probing bones from varying ages [52]. As age increases, the crack growth resistance effectively disappears and work-to-fracture decrease [53]. Structurally this is due to both a degradation in collagen [54] and extensive remodeling in older bone manifested by increased cement lines.…”

Section: Nanofibril-bridged Crack Growth In Trabecular Bone Lamellaementioning

confidence: 99%

Nanofibril-mediated fracture resistance of bone

et al. 2021

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Natural hard composites like human bone possess a combination of strength and toughness that exceeds that of their constituents and of many engineered composites. This augmentation is attributed to their complex hierarchical structure, spanning multiple length scales; in bone, characteristic dimensions range from nanoscale fibrils to microscale lamellae to mesoscale osteons and macroscale organs. The mechanical properties of bone have been studied, with the understanding that the isolated microstructure at micro-and nano-scales gives rise to superior strength compared to that of whole tissue, and the tissue possesses an amplified toughness relative to that of its nanoscale constituents. Nanoscale toughening mechanisms of bone are not adequately understood at sample dimensions that allow for isolating salient microstructural features, because of the challenge of performing fracture experiments on small-sized samples.We developed an in-situ three-point bend experimental methodology that probes site-specific fracture behavior of micron-sized specimens of hard material. Using this, we quantify crack initiation and growth toughness of human trabecular bone with sharp fatigue pre-cracks and blunt notches. Our findings indicate that bone with fatigue cracks is two times tougher than that with blunt cracks. In-situ data-correlated electron microscopy videos reveal this behavior arises from crack-bridging by nanoscale fibril structure. The results reveal a transition between fibril-bridging (~1µm) and crack deflection/twist (~500µm) as a function of length-scale, and quantitatively demonstrate hierarchy-induced toughening in a complex material. This versatile approach enables quantifying the relationship between toughness and microstructure in various complex material systems and provides direct insight for designing biomimetic composites.

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Correction to the article “age-related changes in the collagen network and toughness of bone” [bone 31:1–7, 2002]

Cited by 12 publications

References 0 publications

Aging and loading rate effects on the mechanical behavior of equine bone

Aging and loading rate effects on the mechanical behavior of equine bone

Mass spectrometric quantitation of AGEs and enzymatic crosslinks in human cancellous bone

Nanofibril-mediated fracture resistance of bone

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