Abstract
OBJECTIVE: Previous studies found that Wnt7b played a unique and indispensable role in the process of osteoblast differentiation and could accelerate the repair of bone loss. However, what is the role of Wnt7B in osteogenesis? Is it possible to increase the expression of Wnt7b to promote the repair of skull defects? This study intends to provide the basic data for the application of Wnt7b in the treatment of craniomaxillofacial bone repair. METHODS: A calvarial defect mouse model that could induce Wnt7b overexpression was established. Three days after the operation, the mice in each group were intraperitoneally injected with tamoxifen (TAM) or oil eight times every other day. There were three groups. The TAMc group (R26(Wnt7b/Wnt7b)) was injected with tamoxifen. The Oil group (3.2 kb Col1-Cre-ER(T2); R26(Wnt7b/Wnt7b)) was injected with oil. The TAM group (3.2 kb Col1-Cre-ER(T2); R26(Wnt7b/Wnt7b)) was injected with tamoxifen. Four weeks after the surgery, micro-CT scanning was utilized to observe new bone formation and compare the ability to form new bone around the defect area. RESULTS: Four weeks after the operation, bone healing conditions were measured by using micro-CT scanning. The defect area of the TAM group was smaller than that of the other groups. Similarly, the bone volume fraction (BV/TV) significantly increased (p < 0.05), the trabecular number (Tb.N) increased, and the trabecular separation (Tb.Sp) decreased. CONCLUSIONS: Wnt7b participates in the bone formation process after calvarial damage, indicating the important role of Wnt7b in osteogenesis.