Less Diffuse Damage was Observed in Osteogenesis Imperfecta Mice Femurs Than Wild-Type Controls

Accumulation of microdamage contributes to the deterioration of bone quality with aging among the elderly [1]. Microdamage formation in bone is dependent on its ultrastructural constituents. At the ultrastructural level, bone is a fiber-reinforced composite material in which mineral crystals are responsible for its stiffness and collagen fibrils offer its toughness [2]. Using animal models with distinct mineralization levels (BL6 and C3H mice), a previous study has demonstrated that highly mineralized bone tend to form linear microcracks whereas less mineralized bone is more likely to have diffuse damage [3]. To our knowledge, however, the effect of collagen phase on the microdamage formation of bone has not been well studied. Less collagen content [4] and smaller diameter [5] of collagen fibrils have been observed in bone with osteogenesis imperfecta (OI) disease, a mutation of a single nucleotide deletion in proα2(I) collagen gene. The oim mouse model has been widely used as animal models to study osteogenesis imperfecta disease. Consequently, the objective of current study was to determine the influence of collage phase alterations on microdamage formation in bone using oim mice.