Osteoporosis is a kind of brittle fracture as a significant manifestation of systemic, metabolic bone diseases. As a multifactorial diseases, the incidence of osteoporosis and related fractures will continue to increase, based on current epidemiological studies. This review focuses on progress of osteoporosis-related genes, signal transfer aspects of basic research and clinical treatment of secondary intertrochanteric fracture. Osteoblasts promote activation of osteoblast with Wnt pathway. By prostaglandin E2 (PGE2) bone cells promote the combination of receptor activator of NF-kB and receptor activator of nuclear factor κB ligand (RANK/RANKL), promoting osteoclast differentiation and bone absorption. Osteoblasts to the opposite. In the mitogen-activated protein kinase signaling pathway, ERK pathway, JNK pathway, P38 pathway and treatment of osteoporosis are closely linked. Through the JAK-STAT pathway, growth hormone and insulin-like growth factor-1 maintain the ratio osteoblasts and osteoclasts and then bone mass. Ratio imbalance leads osteoporosis. Based on the above basic research, more anti-osteoporosis drugs appear. Traditional surgical implants, such as dynamic hip screw, anatomical plate, gamma nail and proximal fermoral nail shrink, the use of PFNA/PFNA-Ⅱ gradually increases and becomes the first choice, which adheres to intramedullary fixation scientifically, compacts the femoral neck bone, increase the gripping, anti-rotation force and longitudinal stability.Although there are many shortcomings, hip replacement has become a remedial method effectively, songtimes the first options.