Blood vessel invasion at chondro-osseous interfaces is impaired in absence of Syndecan-1 in bone growth and fracture healing

Introduction: Neoangiogenesis drives the replacement of mineralized cartilage by trabecular bone during bone growth regulated by molecules like e.g. VEGF, OPG and RANKL. The Heparan sulfate proteoglycan Syndecan-1 (Sdc1) while interacting with VEGF and OPG, plays a role in the communication of osteoclasts and osteoblasts and in the development of blood vessels. To understand the function of Sdc1 in enchondral ossification we analysed bone structure and vessel development in bone growth and fracture healing in mice deficient in Sdc1.