Alterations in microdamage morphology and accumulation are typically attributed to impaired remodeling, but may also result from changes in microdamage initiation and propagation. Such alterations are relevant for cancellous bone with high metabolic activity and numerous bone quality changes. This study investigates the role of trabecular microarchitecture on morphology and accumulation of microdamage in human cancellous bone. Trabecular bone cores from donors of varying ages and bone volume fraction (BV/TV) were separated into high and low BV/TV groups. Samples were subjected to no load or uniaxial compression to 0.6% (pre‐yield) or 1.1% (post‐yield) strain. Microdamage was stained with lead uranyl acetate and specimens were imaged via microcomputed tomography to quantify microdamage and determine its morphology in three‐dimensions (3D). Donors with high BV/TV had greater post‐yield strain and were tougher than low BV/TV donors. High BV/TV bone had less microdamage than low BV/TV bone under post‐ but not pre‐yield loading. Microdamage under both loading conditions showed significant correlations with microarchitecture and BV/TV, but the key predictor was structure model index (SMI). As SMI increased (more trabecular rods), microdamage morphology became crack‐like. Thus, low BV/TV and increased SMI have strong influences on microdamage accumulation in bone through altered initiation.
Keywords: microdamage; microarchitecture; trabecular bone; microcomputed tomography; lead uranyl acetate