随着老龄化社会的到来，日益增加的原发性骨质疏松症及其相关的脆性骨折迅速成为一个全球性的医疗危机。低强度全身振动治疗骨质疏松，可明显增加骨密度和骨强度。 但力学刺激如何调控骨合成代谢的机理仍不清楚。因此，本研究假设： 在低强度全身振动的力学刺激下，1）BMSCs的成骨相关lnRNA表达上调，促进BMSCs的成骨细胞定向分化，增加骨形成；MMPCs的骨吸收相关lnRNA表达下调，抑制MMPCs的破骨细胞定向分化，降低骨吸收活性。2）成骨相关lnRNA表达上调，可经下游Canonical Wnt信号通路,促进骨形成；3）骨吸收相关lnRNA表达下调，可经下游OPG/RANKL/RANK信号通路，抑制破骨细胞形成。期望为临床原发性骨质疏松症的检测和诊断提供新的标志物，为其新药开发提供新的靶标，为预防和治疗原发性骨质疏松症提供一个非药理学的、有效的、无创性的、易于接受且可以长期坚持的治疗选项。

Osteoporosis is a systemic skeletal disease characterized by an unbalanced and/or uncoupled bone-remodeling activity leading to bone loss, microarchitectural deterioration of bone and ultimately fractures. And it is also predominantly a disease of aging, affecting particularly postmenopausal women, but also older men. This chronic disease represents a considerable medical and socioeconomic burden for modern societies. The options for the treatment of osteoporosis have so far comprised mostly antiresorptive drugs. These drugs have limitations, however, in particular the fact that they lead to a low turnover state where bone formation decreases with the decrease in bone-remodeling activity. Low-magnitude whole-body vibration therapy(LMWBVT), as an alternative option for osteoanabolic pathway, has received more and more attention. But, the mechanism how the mechanic stimuli regulate bone formation is still unclear. We hypothesis that LMWBVT can stimulate the proliferation of bone marrow –derived mesenchymal stem cells( BMSCs ) and the commitment of these cells into osteoblast by lncRNA and that LMWBVT can also inhibit the fusion of mononuclear cells and the commitment of these cells into osteoclasts by lncRNA. Meanwhile, lncRNA may modulate down-stream canonical Wnt signaling pathway and OPG/RANKL/RANK signaling pathway. So, the aim of the project is to investigate whether LMWBVT increase bone formation in rat osteoprotic model by lncRNA upregulating the BMSCs differentiation into osteoblast and inhibiting the mononuclear cells differentiation into osteoclasts.