Bone fractures are a common injury that is often accompanied by ischemia or broken blood vessels. Blood vessels are essential for bone repair as they supply oxygen to surrounding cells. Thrombospondin-1 (TSP1) is understood to inhibit angiogenesis (blood vessel development). However, the effects of directly inducing blood vessels in an ischemic callus is not fully understood. This study aimed to develop a profile of an ischemic fracture callus in TSP1’s absence. We hypothesized that TSP1 inhibition would increase blood vessel density, thus increasing the callus size because fibrosis tissue develops first (before cartilage and bone) and simultaneously with blood vessels. Previously harvested ischemic fracture callus of mice from days 4 were tested for CD31+ (blood vessels). Days 7 and 15, tissues were examined for callus size and matrix (fibrosis tissue, cartilage, and bone formation). Results indicated that TSP1 inhibition was positive for blood vessel, bone, cartilage, and fibrous tissue development within the callus. However, there was a large development of fibrosis tissue on day 7 post-fracture which signified blood vessel development but also the reason for cartilage and bone being delayed at day 15 due to limited space. This study has provided insights into the underlying profile of a fracture callus in TSP1’s absence, prompting future research to investigate treatments to prevent heavy fibrosis tissue development for maximum bone healing.

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