Abstract: Bone fracture is a significant economic and societal burden that continues to grow as the average age of our populations increases. Current therapies, particularly for fractures that are slow to heal, are suboptimal and are largely based on surgical interventions and implanted prostheses or biomaterials. We are investigating the alternative notion that fracture sites might be targeted systemically with drugs by using nanotechnology. We hypothesise that particular periods in fracture healing may be open to nanoparticle targeting due to vascular changes at the injury site. In this talk, I will present data from our group showing that temporally-controlled stimulation of the Wnt signalling pathway promotes increase in osteogenesis in human bone marrow isolates. In parallel, we have found that Wnt protein (Wnt3A) and Wnt pathway agonists (GSK3 inhibitors), which are unstable in aqueous medium, can be stably associated with liposomal and polymersome nanoparticles. These nanoparticles associate with human bone stem cells, elevate Wnt signalling and promote subsequent osteogenic differentiation. Finally dye labelling and whole-animal IVIS imaging shows that nanoparticles accumulate at bone fracture sites following administration after experimental bone fracture in cortical or segmental bone injury defects in mice. We continue to investigate this approach as a future clinical method for drugging of bone fracture repair.