Non-Collagenous Matrix Proteins and Post-Translational Modifications Explain Bone Toughness Loss in an Aging Mouse Model

Bone’s fracture resistance relies on its material properties, which can change with aging and disease. The material properties may be altered by changes in bone’s organic matrix via biochemical modifications of collagen, such as non-enzymatic glycation (NEG), which produces crosslinks known as advanced glycation end-products (AGEs). Alterations may also arise from the non-collagenous protein constituents, which compose 10% of bone’s organic matrix. Mice are frequently used as a model for osteoporosis research. Although studies demonstrate increased bone fragility with aging in human cadaveric models, very little information is available on mice bone material properties in the context of aging. Our goal was to use aging mice (21960 days old) and a novel fracture mechanics technique, that allows for measurement of bone’s fracture resistance at initiation and propagation, to investigate the relationship between the organic matrix of bone and bone fragility.