Osteoporosis (OP) is a systemic metabolic bone disease with destruction of micro-structure, decreased bone mass and increasing risk of bone fracture. With the increase of population ageing, the prevalence of osteoporosis, especially postmenopausal osteoporosis, may increase, and the medical and socioeconomic influence may expand. Human osteoporosis mainly includes glucocorticoid-related osteoporosis, postmenopausal osteoporosis, disuse type, and senile osteoporosis. Glucocorticoid-related osteoporosis animal model is induced by using glucocorticoid. Glucocorticoids inhibit osteoblast activity and activate osteoclasts, leading to reduced bone formation and increased bone resorption. Animal model of postmenopausal osteoporosis is established by ovary resection. Estrogen reduction results in an enhancement in bone resorption and a decline in new bone formation, resulting in a decrease in bone mass. Estrogen receptor α induces osteoclast apoptosis, but the mechanism that blocks osteoblast function is currently unclear. SAM-P6 (senescence-accelerated mouse-P6) is an accelerated aging mouse with increased bone loss with age and is suitable for elderly osteoporosis animal models. The animal model of disuse osteoporosis is often established by sciatic nerve resection or suspension. The body is in a state of no gravity for a long time. The activity of osteoclasts is relatively increased, resulting in loss of bone mass. This review briefly summarizes the advantage and disadvantage of different types of osteoporosis animal model and their effects on different skeletal sites in postmenopausal osteoporosis. |