Associate ProfessorAaron Schindeler

Aaron Schindeler’s published work spans musculoskeletal regeneration, genetic bone disease, and gene-therapy delivery: early, highly cited contributions helped define the cellular and remodeling biology of fracture repair, including how periosteal and other lineages coordinate healing. He then pushed into translational orthopaedics - testing biologics and biomaterials to enhance repair (e.g., BMP-2 strategies and advanced ceramic scaffold systems such as 3D-printed Baghdadite constructs). A major ongoing theme has been skeletal and soft-tissue manifestations of neurofibromatosis type 1 (including mechanistic and intervention-focused studies of NF1-related muscle and bone phenotypes). More recently, his work has converged on curative molecular therapies for heritable disorders - developing bone-targeted AAV tools and articulating/advancing cell and gene therapy strategies for osteogenesis imperfecta and related conditions. His current focus extends this trajectory into precision genome surgery, including in vivo base editing in disease models and the broader opportunities/hurdles for NF gene therapy.Aaron Schindeler’s published work spans musculoskeletal regeneration, genetic bone disease, and gene-therapy delivery: early, highly cited contributions helped define the cellular and remodeling biology of fracture repair, including how periosteal and other lineages coordinate healing. He then pushed into translational orthopaedics—testing biologics and biomaterials to enhance repair (e.g., BMP-2 strategies and advanced ceramic scaffold systems such as 3D-printed Baghdadite constructs). A major ongoing theme has been skeletal and soft-tissue manifestations of neurofibromatosis type 1 (including mechanistic and intervention-focused studies of NF1-related muscle and bone phenotypes). More recently, his work has converged on curative molecular therapies for heritable disorders - developing bone-targeted AAV tools and articulating/advancing cell and gene therapy strategies for osteogenesis imperfecta and related conditions. His current focus extends this trajectory into precision genome surgery, including in vivo base editing in disease models and the broader opportunities/hurdles for NF gene therapy.

“Looking back, I’m proudest of the moments when our work has crossed the bridge from bench to bedside. In neurofibromatosis type 1 (NF1), my lab has focused on the complications that steal function from children - particularly tibial pseudarthrosis and muscle weakness - and we’ve worked with clinical colleagues to translate mechanistic insights into practical interventions that can be applied in real patients. That translational arc - finding something true about disease biology, turning it into something actionable, and seeing it make a measurable difference in a child’s life - is why I got into research in the first place.

“That drive has always been powered by a fascination with genetics. My PhD work in reverse genetics and heart development taught me how deeply genotype shapes biology, but also how hard it was to move from ‘cause’ to ‘cure.’ Today, the landscape is changing fast. CRISPR, gene therapy, and the broader toolkit of precision medicine are turning what used to be distant hopes into plausible treatment strategies for children born with severe genetic disorders. The pace of progress is exhilarating, and I’m excited to help build the next generation of therapies - because I genuinely believe the coming decade will deliver major improvements in quality of life for families living with genetic disease.”