The etiology of rheumatoid arthritis (RA), a chronic inflammatory systemic disease, remains unclear. It is characterized by symmetrical and invasive joint inflammation, primarily affecting distal small joints such as those in the hands and feet. This inflammation can lead to joint deformity and loss of function, and often accompanied by involvement of extra-articular organs like the lungs and heart. Currently, anti-rheumatic drugs only provide symptom improvement but have toxic side effects that require optimization. Therefore, it is crucial to thoroughly analyze the mechanisms underlying RA development for the identification of new drug targets. Programmed cell death (PCD) has been extensively studied in recent years and proved to be one of the key pathogenic factors in RA. Dysregulation of PCD is particularly evident in synoviocytes, immune cells, and osteocytes. This review summarizes various forms of PCD including apoptosis, NETosis, autophagy, pyroptosis, necroptosis, ferroptosis, cuproptosis, as well as their regulatory roles in fibroblast synoviocytes, immune cells and osteocytes. These findings hold significant theoretical implications for optimizing clinical treatment options for RA and developing new target drugs.