Initiation of Fracture Repair by Bone Morphogenetic Proteins

Publisher Website
Google Scholar
Abstract
The potential for regeneration and repair of bone is well known. This article conveys the current progress in the realm of bone morphogenetic proteins and their potential for initiating fracture repair cascade. Demineralized bone matrix induces bone formation and has served as a model for the bone repair cascade. A family of bone morphogenetic proteins has been identified, isolated, and cloned from the demineralized bone matrix. Bone morphogenetic proteins are pleiotropic regulators of chemotaxis, mitosis, and differentiation. The bone morphogenetic protein receptors, Types I and II, bind bone morphogenetic proteins and act in collaboration to transduce the phosphorylation of Smad 1 and Smad 5, which enter the nucleus in partnership with Smad 4 to initiate bone morphogenetic protein responses including fracture healing. The accumulated information on bone morphogenetic proteins may aid in accelerating fracture repair and the potential use of bone morphogenetic protein antibodies to inhibit heterotopic bone formation and fibrodysplasia ossificans progressiva.