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Osteogenesis imperfecta (OI) is a disease attributable to any of a large number of possible mutations of type I collagen. The disease is clinically characterized in part by highly brittle bone, the cause of this feature being unknown. Recently a mouse model of OI, designated as osteogenesis imperfecta murine (oim), and having a well defined genetic mutation, has been studied and found to contain mineral crystals different in their alignment with respect to collagen and in their size. These observations are consistent with those reported in human OI and the unusual crystal alignment and size undoubtedly contribute to the reduced mechanical properties of OI bone. While the mineral has been investigated, no information is available on the tensile properties of oim collagen. In this study, the mechanical properties of tendon collagen under tension have been examined for homozygous (oim/oim), heterozygous (+/oim), and control (+/+) mice under native wet conditions. The ultimate stress and strain found for oim/oim collagen were only about half the values for control mice. Assuming that prestrained collagen molecules carry most of the tensile load in normal bone while the mineral confers rigidity and compression stability, the reported results suggest that the brittleness of OI bone in the mouse model may be related to a dramatic reduction of the ultimate tensile strain of the collagen.

Collagen from the osteogenesis imperfecta mouse model (oim) shows reduced resistance against tensile stress.