Oxidized low density lipoproteins (oLDL) are products of systemic oxidative stress initiated by the mechanism of free radical induced lipid peroxidation. Oxidatively modified epitopes on LDL molecules are immunogenic and antibodies against such epitopes are generated. The aim of the study was to determine whether traumatic injury and consequent oxidative stress are accompanied by changes in the titer of autoantibodies against oLDL, and to determine whether patients with different injuries can be distinguished by measuring their anti-oLDL titer. Sera of twenty-four patients divided into three groups of eight subjects each were investigated by an anti-oLDL ELISA immunoassay: 1) patients with bone fractures, 2) with traumatic brain injury (TBI) and 3) with both bone fractures and TBI. The patients were followed during four weeks after injury and anti-oLDL titers were determined on a weekly basis. The control group consisted of 22 healthy persons. The lowest antibody titer was measured in all groups during the 1st week after injury. While the serum levels of patients with combined injury did not differ from those of the other two groups, the levels of patients with TBI were significantly higher than those of patients with isolated bone fractures. During the four-week convalescence, a gradual and significant increase in the anti-oLDL titer was observed in all patients. However, this value was increased above normal values only in the sera of patients with TBI during the third and the fourth week after injury. Reactive oxygen species (ROS) play an important role in the regulation of bone synthesis and remodelling. Therefore, we assume that the combination of a fracture with TBI-mediated post-traumatic stress response might be related to the altered fracture healing (enhanced osteogenesis) frequently observed in these patients.