The systemic effect of local trauma in trabecular bone is observed as a global increase in bone formation potential and an elevated immune cell population, in the marrow of distant bones unrelated to the injury . Injuries have been shown to influence the expression of some immune cell markers in correlation with recovery outcome, for example, glucocorticoids (GCs) may be more or less imperative for healthy bone growth depending on the bone type . According to studies, a biomechanically stable bone healing in metaphysis remains unaffected by disruptions of osteoblast GC signaling, contrary to fractures in the diaphysis . Furthermore, it has been found that a therapy based on GCs paired with other antiinflammatory drugs may actually increase healing quality of metaphyseal fractures for patients with upregulated inflammatory response, but only if sufficient lymphocytes were present, aggregating osteoblast and osteocyte apoptosis, resulting in increased mechanical properties of the regenerated bone . This may be explained through biological differences between said bone fragments. Cortical bone healing depends on stem cells from distant sources, making inflammation a critical factor, in contrast to metaphyseal bone healing, which utilizes local abundance of stem cells, contributing to its independence from an inflammatory response . In consequence, a decreased signaling in inflammatory response hinders the cortical bone healing in diaphysis, due to insufficient MSC migration to the fracture. On the contrary, a decreased signaling is neutral or even beneficial for the trabecular healing in metaphysis, where the migration of MSCs is largely irrelevant for the process flow . The differences in cancellous and cortical bone healing are summarized in Table .