Glossitis of the tongue in iron deficiency anemia has been described as diffuse or patchy atrophy with tenderness or burning. One cause of iron deficiency anemia is sideropenic dysphagia (Plummer–Vinson or Paterson–Brown–Kelly syndrome) which is also characterized by esophageal webbing and dysphagia. Pernicious anemia is usually caused by autoimmune destruction of gastric parietal cells. Parietal cells secrete intrinsic factor which is required for the absorption of vitamin B12. Vitamin B12 deficiency results in megaloblastic anemia and may present as glossitis. The appearance of the tongue in vitamin B12 deficiency is described as "beefy" or "fiery red and sore". There may be
Inflammation to cease once the stimulus has been removed. As defined, acute inflammation is an immunovascular response to an inflammatory stimulus. This means acute inflammation can be broadly divided into a vascular phase that occurs first, followed by a cellular phase involving immune cells (more specifically myeloid granulocytes in the acute setting). The vascular component of acute inflammation involves the movement of plasma fluid, containing important proteins such as fibrin and immunoglobulins (antibodies), into inflamed tissue. Upon contact with PAMPs, tissue macrophages and mastocytes release vasoactive amines such as histamine and serotonin, as well as eicosanoids such as prostaglandin E2 and