Individual and combined effects of OA-related subchondral bone alterations on proximal tibial surface stiffness: a...

The role of subchondral bone in OA pathogenesis is unclear. While some OA-related changes to morphology and material properties in different bone regions have been described, the effect of these alterations on subchondral bone surface stiffness has not been investigated. The objectives of this study were to characterize the individual (Objective 1) and combined (Objective 2) effects of OA-related morphological and mechanical alterations to subchondral and epiphyseal bone on surface stiffness of the proximal tibia. We developed and validated a parametric FE model of the proximal tibia using quantitative CT images of 10 fresh-frozen cadaveric specimens and in situ macro-indentation testing. Using this validated FE model, we estimated the individual and combined roles of OA-related alterations in subchondral cortical thickness and elastic modulus, and subchondral trabecular and epiphyseal trabecular elastic moduli on local surface stiffness. A 20% increase in subchondral cortical or subchondral trabecular elastic moduli resulted in little change in stiffness (1% increase). A 20% reduction in epiphyseal trabecular elastic modulus, however, resulted in an 11% reduction in stiffness. Our parametric analysis suggests that subchondral bone stiffness is affected primarily by epiphyseal trabecular bone elastic modulus rather than subchondral cortical and trabecular morphology or mechanical properties. Our results suggest that observed OA-related alterations to epiphyseal trabecular bone (e.g., lower mineralization, bone volume fraction, density and elastic modulus) may contribute to OA proximal tibiae being less stiff than normal.