The current concepts of fracture healing are mainly based on two variables: blood supply and stability. The effect of electricity on delayed union has not been explained. Possible individual differences in the primary osteogenetic activity and the effect of soft-tissue injuries are seldom considered. In recent years, interesting data have revealed how biomechanical forces and electric currents can be translated to biochemical mediators such as prostaglandins (PGE2), morphogens, and growth factors. It is likely that the fracture ends emit osteogenic signal substances (such as bone morphogenetic protein) to the exudate in addition to those mediators (interleukin-1, growth factors) which are released from the blood clot as in wound healing. Movement of the fragments increases the fracture exudate with its migrating cells and sprouting vessels, resulting in exuberant callus. Cartilage is formed in the well-vascularized granulation tissue due to its ability to repel vessels. Rigid fixation minimizes granulation tissue and external callus. Rigid plates may also retard effusion of morphogens and growth factors from bone ends. Reaming of the intramedullary canal and nailing may cause additional bone damage, which may increase the osteogenetic activity. Weight bearing stimulates growth factors and PGE2. The molecular activity of the fracture exudate is the most decisive factor for bone healing. This activity can be impeded by diastasis, infections, and soft-tissue crushing injuries that cause extensive activation of macrophages and activate mediators, disturbing the osteogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)