Macrophages in periapical lesions

Abstract

Macrophages are major constituents of periapical granulomas. They have a central protective role in both innate immunity and adoptive, antigen-specific immune response. Macrophage activation may occur in periapical granulomas by cytokines produced by antigen-activated T-lymphocytes; by bacterial endotoxin, as part of the innate immunity; or by both these processes. Recent studies in athymic animals have shown that periapical granulomas may develop independently of T-lymphocytes. This observation reveals the major role that the activated macrophage may have in the formation of periapical lesions. Only a few of the macrophages in the periapical granuloma are activated. Current studies indicate that these activated cells are the source of the bone-resorbing cytokines in the periapical granuloma. Understanding the central role of the activated macrophage in the formation as well as the perpetuation of periapical lesions may lead to the development of new diagnostic and therapeutic tools in endodontics.

Histopathological study of radicular cysts diagnosed in a Brazilian population

“…These defense cells may also phagocytose cholesterol crystals and are called foamy macrophages (3,4,21). However, phagocytosis may not occur in the presence of some crystals exhibiting a large diameter, an event that induces the release of cytokines such as IL-1, impairing the repair process after endodontic treatment (3,6,(20)(21)(22)(23). Thus, the presence of cholesterol crystals is an important factor for lesion persistence (3,4,(20)(21)(22).…”

“…Macrophages are involved in the innate response of the periapical lesion, phagocytosing bacteria and preventing the dissemination of infection, as well as in the acquired response, presenting antigens to lymphocytes through the MHC II system, synthesizing cytokines and producing metalloproteinases (20). These defense cells may also phagocytose cholesterol crystals and are called foamy macrophages (3,4,21).…”

“…However, phagocytosis may not occur in the presence of some crystals exhibiting a large diameter, an event that induces the release of cytokines such as IL-1, impairing the repair process after endodontic treatment (3,6,(20)(21)(22)(23). Thus, the presence of cholesterol crystals is an important factor for lesion persistence (3,4,(20)(21)(22). These crystals may originate from the crystallization of lipids ingested from the vascular system itself, or may result from the production of local metabolites in the granulation tissue of the cystic wall and from the phagocytosis of the cell membranes of dead cells (21).…”

Association Between Apical Periodontitis and TNF-α -308 G>A Gene Polymorphism: A Systematic Review and Meta-Analysis

“…Apical periodontitis (AP) is generally a sequel of a root canal system infection, but even though microbial factors play a main role in the etiology of AP, the presence of lymphocytes, macrophages and neutrophils in periapical lesions indicates that the immune system is also involved in the process of pathogenesis (1,2). The main immunological constituents of periapical lesions are represented by macrophages and type 1 T helper cells (Th1).…”

Envolvimento de sinais coestimulatórios na periodontite apical crônica em humanos

“…Os macrófagos representam uma grande população de células nas lesões periapicais, atuando na imunidade inata como fagócitos e na adaptativa como células apresentadoras de antígeno contribuindo para iniciação e regulação do processo inflamatório (BAKER, 2000, METZGER, 2000LAPPIN, 2001, GRAVES;COCHRAN, 2003). Não parece haver diferença na quantidade e distribuição de macrófagos em cistos e granulomas periapicais.…”