Sclerostin is a secreted glycoprotein that inhibits the intracellular Wnt signaling pathway, which when inactivated bone formation is stimulated. This stimulation has been proven in fracture studies, showing larger and stronger calluses with accelerated fracture healing, both in sclerostin knockout and sclerostin antibody injection models. The effects of these two mechanisms have not been compared to assess the accurate effect of the Scl-Ab injections. Therefore we designed a study to compare the effect of sclerostin depletion (sclerostin knockout) and inhibition (Scl-Ab injection). 10-week-old male SOST knockout (KO) (N=20) and Wild-type (WT) (N=40) mice underwent insertion of a tibial intramedullary pin after which a mid-shaft tibial osteotomy was performed. The mice were divided into three groups: SOST KO (N=20), WT with Scl-Ab injection “intravenous dose of 100mg/kg weekly” (N=20) and WT with saline injection (N=20). Each group was managed and sacrificed according to the specified protocol.Background
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