Bone loss in postmenopausal women is explained by estrogen deficiency. Estrogen replacement therapies have been shown to reduce the postmenopausal bone loss. During pregnancy 17β-estradiol (E2) and progesterone (P) plasma levels rise up to 100-fold in the mother and the fetus. Delivery leads to a rapid decline in E2 and P plasma levels in the mother and the infant. In extremely low birthweigth infants (ELBW) postnatal bone demineralisation has been described, even in the condition of vitamin D- and adaequate mineral-supplementation. To study the effects of this early E2 and P withdrawal in ELBW-infants on postnatal bone mineralisation was the issue of this randomised controlled pilot study. Methods: Thirty infants with a median gestational age of 25,9 weeks (range 24-28) and birthweight of 708g(range 370-990) were enrolled. E2 and P supplementation was started in group A within the first postnatal hours via a lipid based intravenous solution containing different amounts of E2 and P. Supplementation was set to a transdermal application as soon as venous access was discontinued to a maximum of six weeks postnatally. Sequential blood samples were drawn in order to adjust the supplementation to intrauterine plasma levels of 2000-6000pg/mL E2 and 300-600ng/mL P. Bone mineral content (BMC) and bone width (BW) was measured after 1, 3 and 6 weeks using single photon adsorption densitometry. The three weekly changes of BMC/BW (dBMC/BW) were calculated at 3 and 6 weeks. Mineral supplementation was monitored individually via urinary calcium and phosphorus concentrations. Results: No differences in dBMC/BW could be found between group A and the control group B in general. However, a subgroup of group A infants fulfilling criteria of optimal E2 and P supplementation together with a sufficient mineral supply showed highest dBMC/BW. Conclusion: An E2 and P supplementation in ELBW infants showed no significant effects on postnatal bone mineralisation. Nevertheless, highest dBMC/BW were achieved in a subgroup of infants with optimal mineral- and E2- and P-supplementation.