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Impressively, that these decrements in osteoclastogenesis were evident even after 5 days of incubation of bone marrow Amyloid beta-Protein (1-15) with RANK-L and M-CSF suggested that the chronic absence of OT had induced a defect that did not reverse in culture. Together the results demonstrate that the osteoclastogenesis triggered in pregnant mice is, at least in part, dependent upon an intact OT axis. It is therefore likely that the increased serum levels of OT during pregnancy [8] drive the initial osteoclastogenesis that tends to mobilize maternal calcium towards fetal skeletogenesis. This response, we have shown, is attenuated in mice deficient in OT.
Considering that OT stimulates osteoblastogenesis as an anabolic hormone [12], we next examined whether osteoblast formation ex vivo was enhanced in pregnant wild type mice, and whether benthic zone response was attenuated in OT-deficiency. We studied the formation of both early, alkaline phosphatase-positive CFU-f, and late, mineralizing von Kossa-positive CFU-ob colonies. We found, as expected, that pregnancy strongly stimulated CFU-f formation ( Fig. 2A and B). This was mimicked by intraperitoneal OT injection, thrice weekly, as before, indicating that OT might, at least in part, mediate this increase ( Fig. 2C and D).