Osteoarthritis (OA) is a chronic and degenerative joint disease. It is also known as degenerative arthritis. The main characteristics of OA are degeneration of articular cartilage and osteophyte formation, which eventually lead to joint deformity and loss of motor ability, and seriously affect the quality of life of the elderly. Although articular cartilage degeneration is the main pathological manifestation of OA, its pathological changes are not limited to the local cartilage, but affect all the tissues in the joint. Intercellular communication between osteocytes, chondrocytes and synovial cells is accomplished by releasing soluble mediators and mechanical signals. More and more studies have found that synovitis plays an important role in the occurrence and development of OA, and the key is the mixed inflammatory infiltration of macrophages in synovium of arthritis. Synovial macrophages are activated by microenvironment stimulation and differentiate into two functional polarization states: M1 subtype which produces proinflammatory factors and M2 subtype which produces anti-inflammatory factors. This process produces a series of dynamic changes among inflammatory factors. Because of the importance of the dynamic balance of macrophages in the development of diseases, macrophages have become a hot topic in the study of pathological mechanism and therapeutic strategies of OA. This review will review and summarize studies on synovitis and OA, which strongly suggest the importance of synovitis and activated synovial macrophages in promoting OA pathology. In particular, we will outline the role of synovial macrophages in promoting inflammation and destructive responses in OA and the potential role of cytokines produced by macrophages or macrophages as therapeutic strategies for the disease.