Spaceflight inhibits bone formation independent of corticosteroid status in growing rats

Bone formation and structure have been shown repeatedly to be altered after spaceflight, However, it is not known whether these changes are related to a stress-related altered status of the corticosteroid axis, We investigate d the role of corticosteroids on spaceflight-induced effects in rat pelvis and thoracic vertebrae, Thirty-six male Sprague-Dawley rats were assigned t o a flight, flight control, or vivarium group (n = 12/group). Bilateral adr enalectomy was performed in six rats per group, the additional six rats und ergoing sham surgery. Adrenalectomized (ADX) rats were implanted with corti costeroid pellets. On recovery from spaceflight, thoracic vertebrae and the whole pelvis were removed and processed for biochemistry, histomorphometry , or bone cell culture studies, The 17-day spaceflight resulted in decrease d bone volume (BV) in the cotyle area of pelvic bones (-12%; p < 0.05) asso ciated with similar to 50% inhibition of bone formation in the cancellous a rea of pelvic metaphyses and in thoracic vertebral bodies, The latter effec t was associated with a decreased number of endosteal bone cells isolated f rom the bone surface (BS) in these samples (-42%; p < 0.05), This also was associated with a decreased number of alkaline phosphatase positive (ALP+) endosteal bone cells at 2 days and 4 days of culture, indicating decreased osteoblast precursor cell recruitment, Maintaining basal serum corticostero ne levels in flight-ADX rats did not counteract the impaired bone formation in vertebral or pelvic bones. Moreover, the decreased ex vivo number of to tal and ALP+ endosteal bone cells induced by spaceflight occurred independe nt of endogenous corticosteroid hormone levels. These results indicate that the microgravity-induced inhibition of bone formation and resulting decrea sed trabecular bone mass in specific areas of weight-bearing skeleton in gr owing rats occur independently of endogenous glucocorticoid secretion.