Apical periodontitis (AP) is a prevalent infectious and inflammatory disorder that involves inflammation of periapical tissues and the disintegration of alveolar bone. AP may eventually lead to tooth loss if not timely treated. This disease is caused by pathogenic bacteria in the necrotic pulps and root canals, thereby triggering responses from the innate and adaptive immune system of the periapical tissues. Regulatory T (Treg) cells play a major role in maintaining immune homoeostasis and immunological self-tolerance; however, these only account for roughly 5%-10% of human peripheral CD4(+) T cells. Several studies have examined the possible role and underlying mechanism of Treg cells in different inflammatory and autoimmune disorders to facilitate the development of novel treatments for these diseases. Recent studies have indicated that Treg cells may gather at the sites of infection, thus limiting the generation of immune responses and bone resorption in the periapical area. This review will summarize studies regarding the presence and regulatory role of Treg cells in AP.
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