BASIC FIBROBLAST GROWTH-FACTOR (BFGF) IMMUNOREACTIVITY AS A POSSIBLE LINK BETWEEN HEAD-INJURY AND IMPAIRED BONE-FRACTURE HEALING

Citation
R. Wildburger et al., BASIC FIBROBLAST GROWTH-FACTOR (BFGF) IMMUNOREACTIVITY AS A POSSIBLE LINK BETWEEN HEAD-INJURY AND IMPAIRED BONE-FRACTURE HEALING, Bone and mineral, 27(3), 1994, pp. 183-192
Citations number
25
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
01696009
Volume
27
Issue
3
Year of publication
1994
Pages
183 - 192
Database
ISI
SICI code
0169-6009(1994)27:3<183:BFG(IA>2.0.ZU;2-E
Abstract
Healing of fractures of long bones or large joints is often accelerate d in patients with severe traumatic brain injury (TBI). However, in th ese patients an early fracture healing is accompanied by hypertrophic callus formation or heterotopic ossifications which might even result in an ankylosis of the affected joints. It seems that enhanced osteoge nesis in patients suffering from TBI could be caused by some humoral f actors, since the sera of these patients strongly promote the growth o f osteoblast cells in vitro. However, humoral growth promoting factors which could perhaps induce enhanced osteogenesis are not yet identifi ed. Hence, the aim of this study was to analyse if basic fibroblast gr owth factor (bFGF) could be related to the phenomenon of enhanced oste ogenesis, since bFGF stimulates the growth of osteoblasts in vitro and could be found both in the brain and the bone tissue. For that purpos e the values of bFGF immunoreactivity were determined in the sera of p atients with TBI and bone fractures (n = 8) as well as in the sera of patients with either TBI alone (n = 10) or bone fractures alone (n = 7 ), during a period of three months after injury. Quantification of the bFGF immunoreactivity was done using the ELISA based on monoclonal an tibodies raised against the recombinant human bFGF. The bFGF immunorea ctivity values obtained were also compared with the values determined in the sera of normal, healthy persons (n = 9). In the group of patien ts with bone fractures alone only a transient increase of bFGF immunor eactivity (threefold above the normal values) was observed in the seco nd week after injury. A similar increase of the values of bFGF immunor eactivity was also determined in the sera of patients with TBI only, b ut it lasted longer (from the Ist until the 7th to 8th week after inju ry). In the case of patients with TBI and bone fractures a specific pa ttern of post-traumatic dynamic change of the values of serum bFGF imm unoreactivity was observed. Namely, the increase of bFGF immunoreactiv ity (up to seven-fold above the normal values) was determined even dur ing the first week after injury. Afterwards, periods of high values of bFGF immunoreactivity observed during the 2nd, 4th and the 7-10th wee ks after injury were interrupted by sudden decreases even to the norma l values (during the 3rd and the 5-6th week after injury). Thus, post- traumatic increase of the serum bFGF immunoreactivity was induced both by bone fractures and TBI, while the unusual pattern of its changes c ould be related to the phenomenon of enhanced osteogenesis in the pati ents with brain injury.