The role of blood supply to soft tissue in the healing of diaphyseal fractures. An experimental study.

It is the purpose of this paper to report experiments on revascularization of the fracture site in relation to the healing of fractures in rabbits and to suggest that devascularization of muscle should be considered as a significant cause of delay in the union of such fractures. The effect on fracture healing of damage to vessels in bone is dramatic, whether it be caused by experimental ligation of the nutrient vessels , or by the insertion of an intramedullary nail 8, or by peripheral vascular disease 2#{149} Vessels from the surrounding soft tissues (mainly the muscles) enlarge and new ones develop, penetrating the cortex and anastamosing with the remnants of the intramedullary vessels. The circulation through the cortex changes from a centrifugal one to a centripetal one. This may be regarded as a fundamental response of diaphyseal cortical bone to ischemia. Many simple undisplaced fractures leave the intramedullary vessels intact. During the healing of such fractures the intramedullary circulation proliferates and plays the dominant role in supplying vessels to the uniting callus and the necrotic bone ends of the fracture site There is little response from the vessels of the surrounding muscles or the periosteum. If the fracture is produced more violently or is displaced, and there is damage to the intramedullary vessels, then this precipitates the expected centripetal response from the vessels of the surrounding soft tissues. Gothman, in I 962, showed how in such fractures in a rabbit tibia the arterial reaction in the surrounding soft tissues appeared as early as four days following the injury and increased rapidly to a maximum in about two or three weeks. By far the greatest part of this arterial reaction came from the arteries in the surrounding muscles. After the fourth week the centripetal response subsided, coinciding with the reformation of an intramedullary circulation. The experiments to be reported were designed to show what happens when the fracture site is deprived of both intraniedullary and soft-tissue sources of revascularization at the same time.