The mechanism of action of macrophage colony-stimulating factor (M-CSF) in osteoclast development was examined in a co-culture system of mouse osteoblastic cells and spleen cells.
The effect of local application of recombinant human basic fibroblast growth factor (rhbFGF) on fracture repair was examined using normal rats and streptozotocin-diabetic rats with impaired repairing ability. Immediately after fracturing the fibula, rhbFGF was applied by a single injection to the fracture site. Application of rhbFGF increased the volume and mineral content of callus in a dose-dependent manner in both normal and diabetic rats, and callus formation of diabetic rats was stimulated to levels similar to those in nontreated normal rats. The marked effect of rhbFGF on fracture repair was associated with an improvement in the mechanical properties of the healing fibula in both normal and diabetic rats. Immunohistochemical staining showed that endogenous bFGF was widely distributed in normal rats 1 and 3 weeks after fracture, especially in the soft callus and periosteum, whereas much less bFGF was detected in diabetic rats. Insulin treatment of diabetic rats restored the immunostaining for bFGF. These results demonstrate that bFGF is expressed during the early stage of fracture repair, and that the impaired fracture-repairing ability in diabetic rats is associated with reduced expression of bFGF at the fracture site. A single application of bFGF immediately after fracture not only facilitates the repair process in normal rats, but also recovers the impaired repairing ability in diabetic rats. These results suggest that local application of bFGF may facilitate bone union in patients with impaired as well as normal repairing ability.
The effects of a single local injection of recombinant human fibroblast growth factor-2 on the healing of segmental bone defects were evaluated in rabbits. One month after the external fixator originally designed for this experiment was installed in the tibia of the rabbit, a 3-mm bone defect was created by an osteotomy in the middle of the tibia and 0, 50, 100, 200, or 400 microg of fibroblast growth factor-2 in 100 microl of saline solution was injected into the defect. Injection of the growth factor increased the volume and mineral content of newly made bone at the defect in a dose-dependent manner with significant effects at concentrations of 100 microg or greater. These significant effects were observed at 5 weeks and later. One hundred micrograms of the growth factor increased the volume and mineral content of newly made bone by 95 and 36%, respectively, at 5 weeks. These results indicate that a single local injection of fibroblast growth factor-2 stimulates the healing of segmental defects. We speculate that such an injection could be clinically useful for the healing of fractures even when the fracture gap is rather large.
In 42% of the osteosarcomas, the tumor cells expressed ErbB-2. Expression of ErbB-2 was strongly correlated with early pulmonary metastasis and poor survival rate for the patient. These data suggest that ErbB-2 plays a significant role in aggressive tumor growth and in the promotion of metastatic potential in osteosarcomas. ErbB-2 in the osteosarcoma tissues would be a useful prognostic marker for patients.
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