Hypertrophic callus formation and craniocerebral trauma: early diagnosis and behavior of basic fibroblast growth factor]

Hypertrophic callus formation in patients with severe head injury leads to an early fracture consolidation, whereas in joint fractures the enhanced ossification can even end in ankylosis of the injured joint. It is already known that these ossifications can be at least partly prevented by non-steroid anti-inflammatory drugs. Therefore, serum parameters have been determined that could predict this phenomenon. The mean values for alkaline phosphatase (ALP) and its bone isoenzyme were significantly increased in patients with severe head injury and bone fractures as soon as the 2nd week (reaching peak values in the 3rd week after injury) compared with patients with isolated fractures or head injury only and with normal healthy subjects. Procollagen I (PICP) was significantly increased even in the 1st week, reaching its peak during the 2nd week after injury. Compared with the callus volume at the time of fracture consolidation the size was determined from the X-rays--it was even possible to predict the volume of callus with the aid of these serum parameters as early as in the first few weeks after injury. A possible link between head injury and the increased bone formation could be the basic fibroblast growth factor (bFGF). In our study, bFGF was determined in serum by an immunoassay (ELISA), and an unusual pattern of dynamic change was observed in the patients with head injury and bone fractures. Compared with patients with isolated bone fractures bFGF immunoreactivity was significantly increased in patients with brain and bone lesions even in the 1st week after injury, with further peaks in the 2nd, 4th and 7th-8th weeks, with sudden decreases in between. In patients with isolated bone fractures a transient increase of bFGF was observed only during the 2nd week after injury. A similar increase was also determined in the sera of patients with head injury only, but it lasted longer. Thus, a posttraumatic increase of the serum bFGF was induced by bone as well as by brain injury, but was not causally related with the growth-promoting effects of the sera, as was proven by an in vitro analysis of the effects of the patients sera on L929 fibroblast growth.