Limb ulcers are an important complication of systemic scleroderma, and persistent and recurrent ulcers can cause severe pain, infection, gangrene, functional impairment, and decreased quality of life, causing great suffering to patients. Because of this, the study of scleroderma extremity ulcers has become a hot issue for research in recent years. The causes of its pathogenesis are still unclear and are summarized in the following aspects: 1, genetic factors According to the obvious family history of some patients, the increased incidence of HLA-B8 in patients with severe disease and chromosomal abnormalities in the relatives of patients, it is believed that the characteristics of the genetic type may be on the dominant allele of the X chromosome. 2. Infectious factors Many patients often have acute infections before the onset of the disease, including pharyngitis, tonsillitis, pneumonia, scarlet fever, measles, sinusitis, etc. Paramyxovirus-like inclusion bodies have been found in the transverse muscle and kidney of patients. 3. Abnormalities in connective tissue metabolism Patients show extensive connective tissue lesions with significantly increased collagen content in the skin and the presence of more soluble collagen and unstable intermolecular side chains within the skin damage during the live phase of the virus. Cultures of fibroblasts from patients show significantly increased activity of collagen synthesis. 4, vascular abnormalities Patients mostly have Raynaud’s phenomenon, not only limited to the extremities, but also occur in the visceral vessels; histopathology shows that the skin lesions and viscera can have small vessel (artery) contracture and endothelial hyperplasia, so some people believe that the disease is a primary vascular disease, but because vascular lesions are not seen in all patients, it is also believed that vascular lesions are not the only pathogenic factors of the disease. 5, immune abnormalities This is one of the most important views in recent years. A variety of autoantibodies (such as anti-nuclear antibodies, anti-DNA antibodies, anti-ssRNA antibodies, anti-scleroderma skin extract antibodies, etc.) can be measured in the patient’s body; the number of B cells in the patient’s body is increased, and humoral immunity is obviously enhanced, and the positive rate of circulating immune complex determination is up to 50% or more in systemic patients, and most patients have hypergammaglobulinemia; some cases are often associated with lupus erythematosus, dermatomyositis, rheumatoid arthritis, and dry syndrome. Some cases are often complicated by lupus erythematosus, dermatomyositis, rheumatoid arthritis, dry syndrome, or Hashimoto’s thyroiditis. It is now mostly believed that the disease may be an autoimmune disease caused by a persistent chronic infection on top of a certain genetic background.