Abstract

Bone fractures are repaired through the formation of new local bone (callus) at the fracture site, so that the supportive function of bone can be restored (Fig. 1). The underlying biological and biochemical events involved in bone repair have been major subjects of study in orthopedic science for many years. Although the molecular events await complete elucidation, the morphological changes associated with the repair process have been detailed and widely accepted. Following a fracture, young mesenchymal cells located in the periosteum, muscles, and marrow, adjacent to the fracture site, start to proliferate. Concomitantly, inflammatory cells migrate to the fracture site (inflammatory phase) over several days after the fracture has occurred. The mesenchymal cells then differentiate into chondrocytes or osteoblasts to form a new cartilage and bone mass, termed “soft callus.” The cartilage is then resorbed and replaced by new bone mass, through a process of endochondral bone formation. Thus, the fracture site becomes encased in newly formed fusiform bone mass (repairing phase), which is subsequently remodeled to restore the original osseous anatomy and function (remodeling phase). This cascade of biological reactions to fracture reflects the inherent regenerating potential of bone, and involvement of regulators or growth factor(s) that mediate the responses of local cells that contribute to the process of bone repair (1). The identification of the growth factors involved in this process may enable us to manipulate and augment bone regeneration. Bone morphogenetic proteins (BMPs) are examples of local factors that have the potential to promote the healing of bone injuries and restoration of bone defects.

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