In patients with severe traumatic brain injury (TBI), healing of a fracture of long or large bone has been observed to be accelerated with excessive callus formation and united at a faster rate. It seems that the enhanced osteogenesis in patients strongly promotes the growth of osteoblast cells. The existing hypothesis is not convincing in explaining the mechanisms of this problem. Craniocerebral trauma patients present a state of hypercoagulability at early stage and thrombin content was very high level at the site of injury. Thrombin is an important link between coagulation and inflammation, and exerts multiple effects upon osteoblasts including stimulating proliferation and inhibiting osteoblast differentiation and apoptosis. Whether this rapidly forming new bone is caused by thrombin has not yet been identified. We hypothesize that in the case of an individual with a head injury, thrombin might be a potential regulator of early fracture healing, which result in accelerated bone healing and hypertrophic callus. If this hypothesis is verified, it will be helpful for the understanding of the basic mechanisms involved in control of bone repair and potential for the development of new novel therapeutic agents.