Ischemia‐reperfusion injury. A phenomenon, that also occurs in the bone

Ischemia‐reperfusion injury of the bone occurs due to traumatic and non‐traumatic alterations affecting blood supply to the bone. It is likely to occur also upon insertion of an implant. Ischemia‐reperfusion injury of the bone has been studied by interruption of blood supply in situ , in limb replantation/transplantation models, in revascularized bone grafts and non‐vascularized bone fragments, as well as in isolated cultured cells. All cells of the bone are affected, including osteoblasts, osteocytes, osteoclasts, chondrocytes, and bone marrow cells. Critical ischemia times for induction of bone cell death, either in the ischemic period or following reperfusion, are in the range of 3 to 7 h. These critical ischemia times are significantly increased by decreasing the temperature from 37 °C to 0–4 °C. Anoxia is the most likely trigger of cell injury in the ischemic phase. In the reperfusion phase, reactive oxygen species are decisively involved in the injurious process. In general, however, the available information on the mechanism of ischemia‐reperfusion injury of the bone is relatively sparse. On the other hand, there are clear similarities to the mechanisms of ischemia‐reperfusion injury known from other organs, and there is a clear potential for protection against ischemia‐reperfusion injury of the bone.