Abstract |
It is well known that the glucocorticoid suppresses the
osteoblast and the calcitonin suppresses the
osteoclast. If the calcitonin prevents the osteoporosis
with increased Tc-99m MDP uptake in the long-term use
of glucocorticoid, then the calcitonin has some
activating effect on the bone formation. The
immobilization operation was done on the left hind-leg
of 16 male Sprague-Dawley rats weighing aout 300 g
each. For 12 weeks after operation, 8 rats were
injected 0.5 mg/kg dexamethasone, and the other 8 rats
were injected 0.5 mg/kg dexamethasone and 1 u/kg eel
calcitonin. The bone mineraf contenf. was measured by
the single photon absorptiometry and the Tc-99m MDP
uptake was used as an index of the osteoblastic
activity. 1) The Tc-99m MDP uptakes in the
dexamethasone treated group were lower than those in
the dexamethasone and calcitonin treated group, and
there was no significant difference in Tc-99m MDP
uptakes between the immobilized and normal femurs. 2)
The bone rnineral contents in the dexamethasone treated
group were significantly lower than in the
dexamethasone and calcitonin treated group, and the
imrnobilized femurs had lower BMC than normal femurs.
3) The slope of regression between the BMC and Tc-99m
MDP uptake was stiff in the dexameth- asone treated
group, and flat in the dexamethasone and caicitonin
group, which shows discrepancy between the bone
resorption and formation resulting prevention of net
bone loss in the dexameth- asone and calcitonin treated
group. In conclusion, the calcitonin has some effect on
the bone forma- tion, and further studies with urinary
hydroxyproline and cyclic AMP are expected. |