Background: Intramedullary reaming and nailing of long bones impairs the endosteal circulation, often causing necrosis of the inner region of the bone cortex. We hypothesized that compensatory hypertrophy of the periosteal microcirculation may develop in response to mechanical destruction of the endosteum, and that this may affect bone survival in these circumstances. In these studies, nailing was performed with materials that affect regeneration of the endosteum differently, and the effects on the tibial periosteal microvasculatory organization were examined.
Methods: In male Wistar rats, the right tibia was reamed and implanted with an inert titanium nail or a less osseointegrative polyethylene nail; the contralateral tibial endosteum was destroyed by reaming. Reaming without nailing or sham operation was performed on both extremities in two other groups of rats. Twelve weeks later, the anteromedial and anterolateral surfaces of the tibias were exposed by a microsurgical technique. The structural characteristics of the periosteal microcirculation (vessel density and distribution of vessel diameters) were determined by intravital videomicroscopy and computer-assisted analysis. The stability of the implants was assessed on the basis of grades 0-2 on a qualitative scale.
Results: Tibial reaming alone caused significant increases in overall blood vessel and capillary densities in the periosteum compared with those of the intact tibias. Implantation with a titanium nail resulted in firm embedding of the nail and caused changes in the periosteal vasculature similar to those after reaming alone. In contrast, implantation of a polyethylene nail was followed by the development of marked instability of the endomedullary implant and significant increases in the percentage of capillaries and the vessel density in the periosteum.
Conclusions: Destruction of the endosteal microcirculation per se brings about an increase in periosteal vascular density, which is further augmented if implantation is performed with a material which delays regeneration of the endosteal circulation.