Abstract
BACKGROUND Spinal burst fractures are pathologies that occur in spinal injuries and cause significant mortality and morbidity as a result. Burst fractures in spinal cord injuries can result in rapid and significant oxidative stress. In addition to the primary injury in severe spinal cord injuries, subsequent secondary lesions are mainly due to inflammatory cascade activation and excessive production of free radicals. This study evaluated oxidative stress and antioxidant enzyme levels in burst fractures. MATERIAL AND METHODS Twenty patients with burst fractures were diagnosed and underwent surgery and 20 healthy control subjects were included in the study. Neurological status was evaluated using the American Spine Injury Association Impairment Scale (ASIA) before and after surgery. Neurological function was scored as ASIA A: complete deficits, ASIA B-D: incomplete deficits, and ASIA E: neurologically intact. Spectrophotometry was performed to measure malondialdehyde (MDA) and low glutathione (GSH), glutathione peroxidase (GPx) levels, which represent lipid peroxide content. Evaluations were performed within 2 days after injury in the patients. RESULTS MDA levels were higher in the burst fracture group (p<0.001), whereas GSH and SOD activities were higher in the control group (both p<0.001). There was no statistically significant difference in GPx levels between the groups (p=0.482). CONCLUSIONS Oxidative stress appears to be related to burst fractures. Considering the importance of burst fractures in spinal cord injuries, a better understanding of these mechanisms may help in defining the role of oxidative stress after burst fractures. Prospective, randomized, controlled trials may reveal new therapeutic approaches that include antioxidants for explosive fractures focusing on oxidative stress.