The need for bone graft substitutes is increasing. The understanding of how these potential treatments exert their effect is lacking. Currently, BMPs are used clinically for augmentation of fracture healing and the exact mechanism(s) how they contribute bone healing is not clear. The literature show that demineralized bone matrix protein, OP-1, and IGF-1 are all factors which contribute to increased bone growth. The goal of this study was to determine if these factor signal through similar pathways that can affect bone growth. Our findings show upregulated intracellular MAPK and JAK STAT signaling by OP-1 as well as novel upregulated intracellular SMAD signaling by IGF-1. As expected, OP-1 signaled through the SMAD pathway and IGF-1 signaled through the MAPK and JAK STAT pathways. DBM which contains both OP-1 and IGF-1 signaled through all three pathways as well. The exact role of each of these factors needs to be further investigated to determine which pathway is crucial for normal bone formation and which pathways will be important for bone remodeling.
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