Endochondral ossification is recapitulated during long-bone repair. Although the β-catenin pathway has been investigated in the context of bone development and skeletogenesis, its role in the bone regeneration processes is not clear. Using pharmalogical reagents, we are able to augment β-catenin signaling during bone repair and have observed substantially improved healing in various pathological conditions. Deficiencies seen in bone regeneration with age are (in part) mediated by the β-catenin pathway. Our models which are able to “rejuvenate” aged bone regeneration do so in a β-catenin dependent manner. Mutation in the FGFR3 gene (achondroplasia) results in augmented bone repair and cellular differentiation. We are currently investigating the impact of FGFR3 signalling on osteoblast differentiation. Furthermore, we are also investigating how glucocorticoids induce osteoporosis in chronic paediatric diseases such as Acute Lymphoblastic Leukemia and Duchene Muscular Dystrophy. Insights into these pathways and diseases may offer new therapeutic options with which to enhance bone regeneration or fracture repair. Team Members (Left to Right): Puviindran Nadesan, Linda Vi, Farasat Zaman, Gurpreet Baht, Saber Ghadakzadeh, Heather Whetstone, Chunying Yu and Simon Kelley.