engleski

IGF-1 immunohistochemistry of the human osteosarcoma cells treated by the sera of patients with bone fractures, traumatic brain injury or combined injury associated with enhanced osteogenesis

Traumatic brain injury (TBI) is often associated with enhanced osteogenesis manifested as heterotopic ossifications or hypertrophic callus formation. Although there are several possible mechanisms involved in this phenomenon, the nature of humoral factors causing growth of mesenchymal (bone) cells after TBI is still uncertain. In our previous study we found the different patterns of post-traumatic changes of growth hormone (GH) and insulin-like growth factor type-1 (IGF-1) in patients with TBI, with bone fractures or with combined injury. That indicated involvement of GH/IGF-1 axis in post-traumatic stress response and in the phenomenon of enhanced osteogenesis in patients with TBI. It was also shown that these sera achieve different growth promoting activities in vitro, especially for human bone cells. The aim of this study was to analyse if sera of these patients would influence cellular IGF-1. Using sera of normal individuals as referral controls (N=15) we compared the in vitro influence on cellular IGF-1 presence of the sera of patients with isolated fractures (N=8), patients with TBI only (N=11) and combined TBI and fractures (N=10). The sera obtained were given at 1% concentration to human osteosarcoma cells (HOS) cultured under standard conditions for 24 hours. Immunocytochemical determination of IGF-1 was done using monoclonal antibodies. The incidence of IGF-1 positive cells was determined semiquantitatively. If the cells were cultured in the presence of normal human sera there were no IGF-1 positive cells noticed, while sera of patients with bone fracture induced IGF-1 in up to 10% of cells during the 2nd and 3rd week after injury. TBI-patients’ sera and those from patients with combined injury induced IGF-1 in HOS cells mostly during the 3rd (8/11 and 8/10 cases) and 4th week (8/11 and 5/10 cases). Induction of IGF-1 by the TBI-patients’ sera could be relevant for pathophysiology of enhanced osteogenesis, Finally, because the GH values in the sera of TBI patients decreased at the time of observed IGF-1 increase in vivo and in vitro, it seems that GH itself is not the trigger of the IGF-1 promoting activities of the TBI-patients’ sera.

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