Master thesis : Micromechanical Investigation of Trabecular and Cortical Bone During Aging (including introduction to research methodology)

Abstract

Population ageing has become a major societal and healthcare challenge worldwide. As life expectancy increases, age-related deterioration of the musculoskeletal system becomes increasingly prevalent, leading to a progressive loss of bone strength and a higher risk of fragility fractures. Among the skeletal sites affected by age-related bone loss, the distal radius is particularly vulnerable, with wrist fractures frequently occurring early in the progression of skeletal fragility. Although age-related changes in trabecular and cortical bone microarchitecture have been extensively documented, their mechanical consequences and spatial distribution within the distal radius remain incompletely understood.

This thesis investigates how ageing affects the microstructure and local mechanical behaviour of the distal radius in postmenopausal women, with particular emphasis on the relationships between age-related morphological deterioration and deformation patterns within trabecular and cortical bone. To achieve this objective, a multiscale and region-specific approach combining high-resolution micro-computed tomography (micro-CT) and voxel-based micro-finite element (micro-FE) modelling was developed. Twelve distal radii from postmenopausal female donors were analysed and divided into middle-aged and old groups. Following micro-CT acquisition and image processing, trabecular and cortical morphometric parameters were quantified using image analysis techniques. In parallel, voxel-based micro-finite element models were generated directly from the segmented images and solved using the ParOSol solver under physiological loading conditions. The resulting strain and stress distributions were then compared with morphological parameters extracted from image analysis at several spatial scales. In particular, local trabecular analyses were performed using 5 mm cubic volumes of interest combined with numerical homogenization, while local cortical analyses were conducted by dividing the cortex into sixteen angular sectors to investigate the spatial relationships between cortical thickness and deformation.

The results obtained revealed a clear age-related deterioration of both trabecular and cortical bone microarchitecture. At the scale of the whole distal radius, older specimens exhibited lower trabecular bone volume fraction, reduced trabecular thickness, thinner cortices, smaller cortical areas and increased intracortical porosity. However, when the analysis was restricted to the clinically relevant region, age-related trabecular differences became negligible, suggesting that most trabecular deterioration is concentrated in the distal epiphyseal region. In contrast, cortical alterations remained pronounced and closely reflected those observed at the scale of the whole distal radius. In addition, mechanical analyses demonstrated higher deformation levels in older individuals in both compartments, with a proportionally greater age-related increase observed in cortical bone. At a more local scale, trabecular analyses further showed that effective strain could not be explained by the homogenized Young’s modulus alone. Although regions with higher bone volume fractions generally exhibited higher apparent stiffness, cubes displaying similar homogenized elastic properties often experienced markedly different deformation levels depending on their anatomical location within the trabecular compartment. Finally, the cortical sector-based analysis revealed strong spatial heterogeneity, with the anterior cortex consistently exhibiting the highest deformation levels despite remaining the thickest cortical region.

Overall, this work demonstrates that the mechanical consequences of ageing arise from complex interactions between trabecular deterioration, cortical degradation and whole-bone load redistribution mechanisms. Age-related fragility cannot be explained by a single morphological parameter or by the deterioration of a single anatomical region. Instead, the local mechanical response of the distal radius depends on the combined influence of bone microstructure, anatomical location and structural interactions occurring across multiple spatial scales. Taken together, these findings contribute to a better understanding of the mechanisms underlying distal radius fragility during ageing.