Pathogenetically, we can distinguish 2 main groups of microangiopathic ulcers (MUs): (1) ulcers due to inflammatory microangiopathy, mainly including cutaneous small and medium vessel vasculitis (VS), pyoderma gangrenosum (PG), and connective tissue disease (CTD), and (2) ulcers due to occlusive microangiopathy. The group of microangiopathic occlusive ulcers is more heterogeneous and includes very poorly understood disturbances (such as livedo vasculopathy and calciphylaxis), still-debated ulcerative diseases (such as hypertensive ulcers), recently described iatrogenic ulcers (ie, during hydroxyurea therapy), ulcers due to cryoprotein deposition, ulcers linked to clot formation (ie, antiphospholipid antibodies) or microembolization (ie, cholesterol emboli and injected substances), and metabolic anomalies. These conditions can induce thromboses or anatomo-functional occlusion of cutaneous microvessels (Figures 1-3). A consistent number of inflammatory MUs are the result of skin necrosis due to a VS. VS is an immunologically mediated angiocentric inflammation, characterized by neutrophils and lymphomonocyte infiltration of the vessel wall, which induces fibrinoid necrosis, reduction of blood supply, and ischemia. The result may be frequently a chronic ulcer