We have recently found that
17 beta-estradiol (E2) stimulates bone formation in rat cancellous bone, and that this bone formation is suppressed by (3-amino-1-hydroxypropylidene)-1-bisphosphonate (
AHPrBP). To analyse the relationship between
bone resorption and bone formation in the action of E2, we injected 13-week-old female rats sequentially with three
fluorochromes (
calcein,
tetracycline and
xylenol orange) at 7-day intervals. E2 (40 micrograms/kg) or vehicle was injected daily for 15 days, starting 24 hrs after the first
fluorochrome. A third group was injected with
AHPrBP (0.3 mg/kg) 24 hrs after the first two
fluorochromes. The rats were killed 48 hrs after the third
fluorochrome. We found that the perimeter of all three
fluorochrome labels was increased by E2. The entire perimeter of the first label was non-crenated. Since the first label was given before E2-administration, this suggests that label that would otherwise have been eluted from the bone surface had been fixed in bone by E2-induced bone formation, which might have occurred either through prolongation of pre-existing bone formation, or induction of bone formation on quiescent surfaces. In either case, our results suggest that resorption did not precede formation at the site of bone formation. Since induction of bone formation by E2 is suppressed by inhibition of
bone resorption, this suggests that the coupling of E2-induced formation to resorption in the rat does not necessarily require that formation occurs at the same site as
bone resorption.(ABSTRACT TRUNCATED AT 250 WORDS)