Canals are the preferential sites for failure in cortical bone and their architecture is able to dictate the mechanical behaviour of the bone: smaller and branched canals generate a high volume of bone failure even at low apparent tissue strain. Osteogenesis imperfecta (OI), or brittle bone disease, is caused by mutations in the collagen genes and results in skeletal fragility. We recently showed that a mouse model of osteogenesis imperfecta (Summary
Introduction
Injury to muscles is very common. We have previously observed that basic fibroblast growth factor (b-FGF), insulin growth factor type 1 (IGF-1) and nerve growth factor (NGF) are potent stimulators of the proliferation and fusion of myoblasts in vitro. We therefore injected these growth factors into mice with lacerations of the gastrocnemius muscle. The muscle regeneration was evaluated at one week by histological staining and quantitative histology. Muscle healing was assessed histologically and the contractile properties were measured one month after injury. Our findings showed that b-FGF, IGF and to a less extent NGF enhanced muscle regeneration in vivo compared with control muscle. At one month, muscles treated with IGF-1 and b-FGF showed improved healing and significantly increased fast-twitch and tetanus strengths. Our results suggest that b-FGF and IGF-1 stimulated muscle healing and may have a considerable effect on the treatment of muscle injuries.
