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 main pathological changes of SSc are inflammatory cell infiltration of connective tissue, intimal hyperplasia, vascular occlusion, fibrous tissue proliferation and sclerotic atrophy. In the initial stage of skin lesions (inflammatory phase), interstitial edema of the dermis, separation of collagen fibers, perivascular lymphocytic infiltration of small vessels, edema of the vessel wall, and breakage of elastic fibers. Thereafter, the perivascular inflammatory cell infiltrate subsides, collagen swells, and acidic mucopolysaccharides and their collagen increase around the small vessel fibers. In the later stage (sclerotic phase), collagen fibers homogenize, collagen fiber bundles parallel to the epidermis increase, and collagen fibers proliferate and extend deeper. Small vessel walls thicken and the lumen becomes smaller to the point of occlusion. Late changes continue to occur, leading to epidermal and appendage atrophy, calcium salt deposition, and sclerotic atrophy of fascial muscles. (A) limited scleroderma needs to be distinguished from the following diseases: 1, spot atrophy Early damage is of different sizes, skin-colored or greenish white, slightly concave or elevated, surface wrinkled, not hard to touch. 2, atrophic sclerosing moss skin lesions are lavender shiny flat papules, varying in size, often aggregated distribution, but not fused with each other, the surface of the hair follicle keratin plugs, sometimes blistering, and gradually appear skin atrophy. (B) Systemic sclerosis needs to be differentiated from the following diseases: 1. Adult sclerosis: The lesions mostly develop from the head and neck to the back of the shoulders, with deep dermal swelling and stiffness. There is no local pigmentation, atrophy or hair loss, and there is a tendency for self-healing. 2. Mixed connective tissue disease: Patients have mixed manifestations of SLE, scleroderma, dermatomyositis or polymyositis, including Raynaud’s phenomenon, non-depressed puffiness of the face and hands, salami-like swelling of the fingers, fever, non-destructive polyarthritis, muscle weakness or myalgia. Antibodies to both leaching nuclear antigen (ENA) and RNP may show high titers of positive reactions. 3. Scleroderma-like syndrome due to chemicals and toxins: People who are exposed to chemicals such as polyvinyl chloride and benzene, as well as those who consume toxic oils or certain drugs and those who undergo silicone breast augmentation can develop scleroderma as well as certain other symptoms of scleroderma. However, these people do not have typical clinical manifestations of scleroderma, and there are no specific autoantibodies in the serum. When exposure is stopped, symptoms can gradually disappear and are easily distinguished from scleroderma.