Taiwanese Journal of Obstetrics and Gynecology · 2009 · 32 citations · 14 references
MedicineCell BiologyEndocrinologyBone MetabolismHormone BiochemistryReproductive EndocrinologyBone FormationOsteoclast BiologyOsteoclast FunctionOsteogenesisOsteoporosisSteroid Hormone SignalingBone Resorption InhibitionBone Resorption MarkersEstrogen Signaling In BoneHormonal Regulation Of OsteoclastsOsteoclast RegulationOsteoporosis In WomenPostmenopausal Bone Resorption
OBJECTIVE: Estrogen deficiency results in postmenopausal osteoporosis by increasing the rate of bone loss. The mechanism responsible for the effects of estrogen on osteoclasts is still unclear. MATERIALS AND METHODS: The potential of mononuclear cells from cord blood or bone marrow to differentiate into mature osteoclasts when co-cultured with human osteoblast cells was investigated. The effects of estrogen on osteoclastogenesis and osteoclast activity were also examined. RESULTS: Macrophage markers CD11b and CD14 were downregulated and vitronectin receptor was upregulated during 28 days' co-culture of mononuclear cells and human osteoblasts. Long-term co-culture resulted in the formation of numerous large tartrate-resistant acid phosphatase-positive multinucleated cells capable of resorption of bone slices. After incubation for 28 days, the addition of 17beta-estradiol caused a significant decrease in the expression of vitronectin receptor and tartrate-resistant acid phosphatase-positive multinucleated cells in cultures derived from both bone marrow and cord blood. A significant decrease in bone resorption was also noted in the presence of estrogen. CONCLUSION: Estrogen not only suppresses osteoclastogenesis but also inhibits the activity of osteoclasts.
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Estrogen promotes apoptosis of murine osteoclasts mediated by TGF–β
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