Aim:Most studies on fracture healing of traumatic brain injury focused on the mediators, hormones, and cytokines involved in this event, and no study has been conducted on how a damaged coordination center in the brain can play a role. The main objective of this research was to examine the effect of cerebellar damage on the process of fracture healing.Material and Methods:A total of forty-two male rats were selected at random and subsequently allocated into three distinct groups. The participants were divided into two subgroups within each group, with the intention of sacrificing them during the third and sixth weeks. Group 1 had isolated femoral fracture, Group 2 had femoral fracture after craniotomy, and Group 3 had femoral fracture accompanying cerebellar injury after craniotomy. Left femoral fractures in rats in all groups were treated using an intramedullary Kirschner wire. Radiological, histological, and biochemical evaluations were conducted at 3 and 6 weeks to assess the processes of fracture healing. To determine the effects of fracture healing and cerebellar injury on oxidant–antioxidant systems, catalase (CAT), malondialdehyde, superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities were measured.Results:Between the time frame of 3 to 6 weeks, Group 3 had higher radiography scores, alkaline phosphatase levels, callus/diaphyse ratio, callus improvement , and bone mineral density in comparison to the other groups. The levels of SOD were found to be statistically negligible in all groups, suggesting that SOD does not have a substantial impact on fracture healing in cerebellar injury. However, notable increases in the activity of GPx and CAT enzymes were observed, showing their considerable involvement in the process of fracture healing.Conclusion:Cerebellar injury reduces the oxidative stress in the fracture area and contributes positively to fracture healing both radiologically, biochemically and histopathologically.