Several investigations have demonstrated a precise balance to exist between bone morpho-genetic protein (BMP) agonists and antagonists, dictating BMP signaling and osteogenesis. Using RNA interference, we have previously reported that reduction of noggin enhanced BMP signaling and in vitro osteoblast bone formation. This study examined the in vivo biology of noggin-suppressed osteoblasts, in the setting of critical-sized defects in mice. Radiographic and histological analyses were employed to evaluate differences in bone regeneration across the region of injury. Skeletal homeostasis involves a dynamic interplay of multiple factors, each influencing the metabolic activity of local bone forming cells. Alteration in the capacity of these cells to deposit a mineralized extracellular matrix occurs not only in disease states and aging, but also during bone repair and natural growth. A multitude of cytokines with the capacity to regulate recruitment and differentiation of osteo-progenitors have already been identified
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