Abstract:

BACKGROUND: Recent studies have found that myostatin knockout mice showed a significant increase in muscle mass; the intensity and mineralization of the whole skeleton increase as well. Myostatin expression is found in the early stage of fracture repair.
OBJECTIVE: To explore the effects of myostatin applied at different stages on the callus amount and bone mineral density of fibula fractures in mice.
METHODS: Fibula fracture model was constructed in mice. The 48 model mice were randomly divided into three groups: control group (empty treatment other than model construction), 0 day group, 1 week group and 2 weeks group (mice in the latter three groups were injected with myostatin antibody of the same dose at different starting times after model construction). The callus amount of the fractures was measured in the 4th week after model construction. Myostatin content changes and muscle tissue changes were observed.
RESULTS AND CONCLUSION: The success rate of model construction was 80%. There was no significant difference in mouse body mass among groups (P > 0.05). The mass of gastrocnemius and the bone mineral density of the callus in the 0 day group were significantly higher than that in the other three groups (P < 0.01); there was no significant difference between the other three groups. Compared with the other groups, the tissue morphology of the myostatin content in the 0 day group also had an intuitive difference. These findings indicate that the early application of myostatin inhibitors after model construction can increase the bone mineral density and promote muscle proliferation in mouse fractures.