Cortical Tissue Porosity of Brittle Osteogenesis Imperfecta Bone

INTRODUCTION There is currently no cure for the skeletal dysplasia osteogenesis imperfecta (OI), a debilitating disease that occurs in approximately 1 in every 20,000 human births. OI is caused by a genetic mutation that results in brittle bones and many fractures. In a mouse model of the disease, oim, we have characterized bone structure using X-ray microtomography, and found that oim bone has decreased bone volume, cortical area, cortical thickness, and moment of area compared to wild type (WT) bone [1]. In three-point bending tests, oim bone exhibited classic brittle behavior with fracture occurring just after the yield point of the tissue. In three-point bending, oim bones fractured obliquely at the distal end of the diaphysis, whereas WT bones fractured transversely under the midspan loading nose. To date, the role of porosity in determining OI bone fracture toughness is unknown. Because material structure at all hierarchical levels is critical in fracture mechanics, differences between oim bone and WT bone ultrastructure may explain the dramatic increase in fracture rates. The aim of this study was to quantitatively investigate the cortical tissue porosity in C57BL/6 (B6) WT mice and B6C3fe-a/acol1a2 brittle bone oim mice using synchrotron radiation-based computed tomography (SR CT).