HYPERTROPHIC CALLUS FORMATION AND SEVERE HEAD-INJURY - EARLY DIAGNOSTIC METHODS AND THE ROLE OF BASIC FIBROBLAST GROWTH-FACTOR

Hypertrophic callus formation in patients with severe head injury lead s to an early fracture consolidation, whereas in joint fractures the e nhanced ossification can even end in ankylosis of the injured joint. I t is already known that these ossifications can be at least partly pre vented by non-steroid anti-inflammatory drugs. Therefore, serum parame ters have been determined that could predict this phenomenon. The mean values for alkaline phosphatase (ALP) and its bone isoenzyme were sig nificantly increased in patients with severe head injury and bone frac tures as soon as the 2nd week (reaching peak values in the 3rd week af ter injury) compared with patients with isolated fractures or head inj ury only and with normal healthy subjects. Procollagen I (PICP) was si gnificantly increased even in the 1st week, reaching its peak during t he 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 the se serum parameters as early as in the first few weeks after injury. A possible link between head injury and the increased bone formation co uld be the basic fibroblast growth factor (bFGF). In our study, bFGF w as determined in serum by an immunoassay (ELISA), and an unusual patte rn of dynamic change was observed in the patients with head injury and bone fractures Compared with patients with isolated bone fractures bF GF immunoreactivity was significantly increased in patients with brain and bone lesions even in the Ist week after injury, with further peak s 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 increas e was also determined in the sera of patients with head injury only, b ut 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 r elated 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 fibr oblast growth.