Dolph Houben

149 Viability and immune response to VCA 7 one each due to infection and rejection [30] . Neither prolonged immunosupression nor treatment of an acute rejection episodes with drug immunosupression proved successful. Thus, a different approach is necessary. In our eperimental study, all micorsurgically repaired bone vascular pedicles developed intimal hypertrophy and subsequently thrombosed 4-6 weeks after transplantation [33] . These changes were as expected after cessation of a 2-week period of immunosuppression and are consistent with vascular rejection [23] . Importantly, however, we were able to maintain bone viability despite rejection, made possible by the novel technique of autogenous neo-angiogenesis from an implanted autogenous AV-bundle. This success in a large animal model suggests possible future use in clinical practice. Conclusion Bone-only VCAs treated with short-term triple drug immunosuppression and intramedullary implantation of an arteriovenous (AV) bundle demonstrate improved osteocyte scores, diminished fibrosis and less inflammatory change than no-angiogenesis controls. Thrombosis of the allogeneic nutrient artery results from intimal hypertrophy, expected without immune modulation. Necrosis of the bone does not occur, due to development of a neoangiogenic autogenous blood supply during the initial period of drug therapy. In this study, there were no adverse systemic inflammatory effects of this process, studied by periodic peripheral blood cytokine determinations during a 20- week survival period. The bone allotransplants themselves demonstrated less inflammation and improved viability than no-angiogenesis controls, provided by the addition of an autogenous AV bundle. This novel approach to bone allotransplantation may have significant advantages over conventional methods in bone-only allotransplantation.