The reduction in osteoblast number in turn contributes to decreased osteogenesis

Furthermore, we specifically labeled marrow vascular endothelial cells with Von Willbrand Factor and observed similar GC disruption of marrow microvessels as previously observed in rabbit femoral head. The disruption of marrow microvasculature would reduce the source of circulating progenitor cells LEE011 CDK inhibitor supporting osteogenesis. The reduction in local and circulating progenitors would then lead to reduce osteogenesis. Our findings suggest that bone formation, bone marrow fat metabolism and microcirculation are closely related to each other and confirm that the latter two factors also contribute significantly to the development of GC-induced bone loss and the decline in bone strength. Our data found weeks depressed adipogenesis LY2109761 TGF-beta inhibitor and stimulated angiogenesis and osteogenesis in GCtreated rats. The lower dose in GC treated rats only depressed adipogenesis and stimulated cancellous bone formation rate. The 40 mg dose also appeared to increase angiogenesis by enlarging marrow microvessels diameter but the observations were not statistically significant. The prevention of GC-stimulation of adipogenesis maintains marrow stromal and red marrow cell levels at control levels. Since osteogenesis and adipogenesis share common bone stromal progenitors, this means the pool of marrow progenitors available to differentiate into osteoblasts will be maintained and not be preferentially stimulated to form adipocytes by GC treatment.