Osteoporosis is a common bone metabolic disease in postmenopausal women, diabetic patients and obese patients and is characterized by an imbalance in bone formation and resorption. Current studies have conducted in-depth research on these groups and revealed their respective pathogenesis and treatment measures. However, the causes of osteoporosis in patients are complex, usually combining multiple factors. Unifying the same pathway that induces bone loss in various pathological states will greatly facilitate the diagnosis and treatment of osteoporosis. Purine metabolism is an important biological process in determining genetic orientation and functional performance. Adequate evidence confirms the widespread existence of purine metabolism disorders in various types of osteoporosis. Purine metabolism plays an important role in the process of bone remodeling. The aim of the present study was to determine changes in purine metabolism in high-risk populations with various types of osteoporosis and the pathogenesis of bone loss caused by abnormal purine metabolism. Two states of balance are maintained in the process of bone remodeling including osteogenesis and adipogenesis and osteoblasts and osteoclasts. Abnormal purine metabolism induces hyperuricemia and the accumulation of reactive oxygen species (ROS). Monosodium urate (MSU), ROS and ROS-induced inflammation inhibit the expression of osteogenic turnover indicators and promote osteoclast differentiation. ADA, ADCY, ENPP1 and PDE are the genes involved in purine metabolism most strongly associated with bone remodeling. Constructing a network between purine metabolism and bone metabolism and mining the core regulatory mechanism will contribute to revealing the pathogenesis and optimizing the treatment of osteoporosis.