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While the osteopenia associated with oestrogen deficiency is thought to arise from a relative defect in bone formation with respect to resorption, oestrogen administration itself leads to a decrease, rather than an increase, in bone formation. This decrease in bone formation, which arises from oestrogen's inhibitory effect on bone turnover, presumably masks any underlying tendency of oestrogen treatment towards stimulation of bone formation. To investigate this further, we have examined the early effect of discontinuing the administration of oestradiol-17β (OE₂; 40 µg/kg on bone formation indices in ovariectomized 13-week-old rats, before the turnover-induced increase in formation occurs. Histomorphometric indices were assessed at the proximal tibial metaphysis 0, 7, 10, 13 and 16 days following discontinuation of OE₂ treatment. Measurements of body weight, uterine weight and longitudinal growth rate confirmed that there were rapid effects of OE₂ deficiency on these parameters.

We could detect no significant increase in bone resorption, as measured by osteoclast surface and number, until 16 days after ending treatment with OE₂; this was coincidental with a reduction in bone volume. Shorter periods of OE₂ deficiency were associated with a marked decrease in bone formation, as assessed by dynamic histomorphometric indices. This inhibition of bone formation was largely due to a reduction in double fluorochrome-labelled trabecular surfaces, which were decreased by approximately 70%. We conclude that ending OE₂ administration in ovariectomized rats caused a striking decrease in trabecular bone formation, if such indices are assessed prior to the subsequent turnover-induced increase in formation. This suggests that oestrogen treatment in ovariectomized rats is associated with a stimulatory effect on bone formation, in addition to its recognized anti-resorptive action.

Journal of Endocrinology (1993) 137, 497–503