Glucocorticoids (GC) induce osteonecrosis (ON) and osteoporosis (OP); however, themechanism is complicated. While GCs may increase the risk of ON by reducing angiogenesis and vasoactivity, the reduction in bone strength that accompanies GC use is greater than can be explained by the loss of bone mass alone. To try to understand this discrepancy, we evaluated GC’s effects on novel bone quality measures, including bone bone hydration, bone blood flow, and bone angiogenesis gene expression. We performed two experiments. The first was to understand the role of GC on bone hydration, bone blood flow, and strength, and whether this is altered by anti-vascular endothelial growth factor (VEGF). In the second study we evaluated GC effects on bone vascularity by evaluating gene expression in bone, and if PTH, a known vasculoactive agent, influences this.
