Role of Hard Tissue Inelastic Properties in the Damage Behavior of Trabecular Bone

2000 ◽  
Author(s):  
Oscar C. Yeh ◽  
Tony M. Keaveny

Abstract Relatively little is known about the inelastic properties of trabecular hard tissue. In cortical tissue, age-related changes in mechanical properties were primarily observed in the postyield regime [1, 2]. Most notably, the ultimate strain was found to decrease by 9% per decade [1]. If similar changes in inelastic properties exist in trabecular tissue, there could be implications for the damage behavior of trabecular bone at the whole specimen “apparent” level. Understanding the role of these inelastic properties may help researchers identify which properties of trabecular tissue are vital to characterize and may improve understanding of age-related increases in skeletal fragility.

1991 ◽  
Vol 1 (4) ◽  
pp. 257-261 ◽  
Author(s):  
P. I. Croucher ◽  
N. J. Garrahan ◽  
R. W. E. Mellish ◽  
Juliette E. Compston

Author(s):  
Xiutao Shi ◽  
Xiang Wang ◽  
Glen L. Niebur

Osteoporosis is an age-related skeletal condition characterized by low bone mineral density and deterioration of the trabecular architecture leading to increased susceptibility to fracture [1]. Wolff hypothesized that trabecular architecture adapts to have its principal material axes aligned with the principal loading directions. Regions of experimentally labeled trabecular microdamage correspond to areas of high stress and strain calculated from FEA [2]. Studying the morphology of numerically predicted regions of tissue level yielding might provide insight into the role of trabecular architecture in the strength of trabecular bone.


Cytokine ◽  
2018 ◽  
Vol 111 ◽  
pp. 88-96 ◽  
Author(s):  
Rafaela Pravato Colato ◽  
Vânia Brazão ◽  
Gabriel Tavares do Vale ◽  
Fabricia Helena Santello ◽  
Pedro Alexandre Sampaio ◽  
...  

Endocrinology ◽  
2020 ◽  
Vol 161 (2) ◽  
Author(s):  
Işıl Kasapoğlu ◽  
Emre Seli

Abstract As women delay childbearing because of demographic and socioeconomic trends, reproductive aging and ensuing ovarian dysfunction become increasingly more prevalent causes of infertility. Age-related decline in fertility is characterized by both quantitative and qualitative deterioration of the ovarian reserve. Importantly, disorders of aging are frequently associated with mitochondrial dysfunction, as are impaired oogenesis and embryogenesis. Ongoing research explores the role of mitochondrial dysfunction in ovarian aging, and potential ways to exploit mitochondrial mechanisms to slow down or reverse age-related changes in female gonads.


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