The Lack Of Estrogen Affected Osteoclasts’ Synthesis And Cytokines’ Secretion In Menopause Women

1. BackgroundPostmenopausal osteoporosis is a high incidence of elderly women systemic bone degenerative disease, manifested as loss of minerals, bone micro-structural damage, fragility, increased risk of fracture. Traditional methods focus from "lack of estrogen regulated by estrogen receptors on bone cells of bone metabolism," to explore the pathogenesis of this perspective, estrogen deficiency leads to a rapid increase in the number of osteoclast activity increased, while compensatory osteogenesis not enough to offset the rapid proliferation of bone loss, bone tissue "Reconstruction-absorb" the balance between break appears to accelerate bone loss, increased risk of fracture. However, the current focus of research in this area is to clarify how estrogen deficiency is osteoclast regulation of what specific ways by which to achieve this important factor involved in the adjustment process. In recent years, a large number of animal experiments reported in the immune system has a role in regulating bone metabolism, especially in activated T cells can produce large amounts of pro-osteoclast growth factor (osteoclastogenic cytokines), with the promotion of osteoclast differentiation, maturation and the role of regulatory activity. Estrogen deficiency can lead to osteoporosis in rats also accompanied by a significant change in immune function. This suggests that:estrogen deficiency leads to bone loss in immune cells and their secretion of cytokines may play an important regulatory role. Therefore, people start from a new angle-bone Immunology (osteoimmunology) investigate the pathogenesis of postmenopausal osteoporosis. But now a large number of experimental studies from animal experiments, the human body is the lack of experimental data, therefore, also the lack of estrogen after menopause is unclear what kind of environment on T cells and the secretion of pro-osteoclast growth factor production, the impact on the break bone cell differentiation, proliferation, maturation and apoptosis have any regulatory role. Therefore, from the perspective of T cells and their cytokine secretion of estrogen deficiency investigate mechanisms leading to bone loss, for our in-depth understanding of the pathogenesis of postmenopausal osteoporosis has very important significance. Immune theory is introduced into the bone and try to break the theories and methods of research in this field, so we further understand the molecular level in postmenopausal The pathogenesis of osteoporosis, and provide a new theoretical basis for active prevention of the disease.2. The purposeThis research synthesis of estrogen deficiency and cytokine secretion in postmenopausal women osteoclasts, to explore the molecular mechanisms of the pathogenesis of postmenopausal osteoporosis from immunology.3. MethodsThe subjects were 15 (mean 56.5 ± 5.9 years) with postmenopausal osteoporosis (postmenopausal osteoporosis, PostMO) and 15 (average 56.65±8.02 years) without postmenopausal osteoporosis (postmenopause, PostM) in older women. Subjects collected 5 ml isolated peripheral blood mononuclear cells were cultured osteoclasts; 5 ml serum samples were collected to detect TNF, IL-6, IL-7, RANKL and OPG levels, while the detection of peripheral blood T cells and TNF RANKL protein andmRNA expression. Data analysis using SAS9.2 software.4. ResultsPostmenopausal osteoporosis (PostMO) breaking number of women (118±17 OCs/ well) was significantly higher than that of postmenopausal bone cells without osteoporosis (PostM) women (34±5 OCs/well) (p<0.001), showed that osteoclasts increase the number of cells may be the main causes of osteoporosis in postmenopausal women. Lack of osteoclasts can significantly promote the synthesis of cytokine secretion of estrogen, PostMO serum TNF (p<0.001), IL-6 (p=0.048) and RANKL (p=0.006) were higher than women, while OPG and IL-There was no significant difference between the 7 groups. Flow cytometric analysis showed that PostMO group of women (38%) T cells expressed significantly higher levels of TNF PostM group of women (1.5%) (p<0.01), indicate a lack of T cells by stimulating the expression of TNF promote osteoclast differentiation and proliferation of estrogen. Meanwhile, PostMO group (3.1%) women RANKL mRNA expression was significantly higher than PostM group (1.2%) women (p<0.05).5. ConclusionsPostmenopausal women with estrogen deficiency leads to increased synthesis of osteoclasts, serum TNF, RANKL increased significantly, IL 6-secretion, but also a significant increase in TNF protein and RANKL/mRNA expression in T cells. Tip lack of estrogen significantly promote osteoclast synthesis and increased T cell secreted factors, which may be an important mechanism for postmenopausal osteoporosis disease.