H. Nagai et al., Systemic injection of FGF-2 stimulates endocortical bone modelling in SAMP6, a murine model of low turnover osteopenia, J VET MED S, 61(8), 1999, pp. 869-875
The effects of systemically administered fibroblast growth factor-a (FGF-2)
at doses of 0.1 and 0.3 mg/kg/day for 7 days were investigated 5-week-old
male SAMP6 mice, a model of low turnover osteopenia. The bone histomorphome
try in the distal epiphyseal growth plate of the femur showed that 0.3 mg/k
g/day of FGF-2 decreased the longitudinal growth rate and cartilage cell pr
oduction rate and increased the growth plate width. Growth plate chondrocyt
es showed the features of defective endochondral ossification at the same d
osage level. In the distal one third of the femur, the marrow trabecular ar
ea, endocortical mineral apposition rate and/or bone formation rate were in
creased in both the SAMP6 mice given 0.1 and 0.3 mg of FGF-2/kg/day. In thi
s region, the endocortical osteoblasts were hypertrophied with some layers
of overlying proliferated fibroblastic mesenchymal cells. The presence of s
mall foci of bone formation within the layers of these mesenchymal cells in
dicates their osteogenic potential. On the other hand, the periosteal bone
formation rate in the mid-shaft of the femur was depressed in the 0.3 mg/kg
/day group. These results suggest that systemically administered FGF-2 may
have the possibility to increase the peak bone mass in SAMP6 by stimulating
the osteoprogenitor cells to proliferate and differentiate into osteoblast
s and enhancing endocortical bone modelling. The higher dose of FGF-2, howe
ver, inhibited both endochondral and periosteal bone formation.