Traumatic fracture accounts for about 50% of the total of traffic accidents. The incidence of fracture in postmenopausal women is significantly higher than that in men. About 5%-10% of patients with bone fracture will suffer from complications such as delayed union or nonunion, which seriously affects the recovery of patients after operation and increases the economic burden of families and society, however, the specific regulatory mechanism has not been fully defined. Immune cells play an important regulatory role in fracture healing, and innate immune response is the first to initiate and participate in fracture healing. Macrophages are innate immune cells which widely exist in various tissues of the body. They play a complex and precise regulatory role in fracture healing by participating in inflammatory response, osteogenic and osteoclast differentiation, mineralization and angiogenesis. Nevertheless, macrophages can be polarized into different subsets and perform different or even opposite functions under different immune microenvironments. At present, it is believed that there are three main polarization states of macrophages: non-activated M0 macrophages, classically activated M1 macrophages and selectively activated M2 macrophage. It has been shown that each subset was positively involved in the regulation process of fracture healing at different stages. Herein, in this paper, the role of different subsets of macrophages in different stages of fracture healing and the related experimental studies are reviewed, helpfully to clarify the immunological mechanism of fracture in-depth and provide new strategies for the research on the immunological intervention of fractures targeting macrophages.