Abstract
Periodontitis (PD) is a common chronic infectious disease. The local inflammatory response in the host may cause the destruction of supporting periodontal tissue. Macrophages play a variety of roles in PD, including regulatory and phagocytosis. Moreover, under the induction of different factors, macrophages polarize and form different functional phenotypes. Among them, M1-type macrophages with proinflammatory functions and M2-type macrophages with anti-inflammatory functions are the most representative, and both of them can regulate the tendency of the immune system to exert proinflammatory or anti-inflammatory functions. M1 and M2 macrophages are involved in the destructive and reparative stages of PD. Due to the complex microenvironment of PD, the dynamic development of PD, and various local mediators, increasing attention has been given to the study of macrophage polarization in PD. This review summarizes the role of macrophage polarization in the development of PD and its research progress.
Highlights
PD is a chronic infectious disease caused by the chronic destruction of supporting periodontal tissue initiated by plaque biofilms and is characterized by microbial-related and host-mediated inflammation, leading to the loss of periodontal attachment [1]
PD, which occurs due to irreversible alveolar bone resorption and loss of attachment, is a problem that needs to be addressed in various oral treatments
From a cellular point of view, the activation of osteoclasts is the beginning of the progression of gingivitis to PD, and the gradual ascendance of osteoblasts in bone coupling is the beginning of chronic PD
Summary
PD is a chronic infectious disease caused by the chronic destruction of supporting periodontal tissue initiated by plaque biofilms and is characterized by microbial-related and host-mediated inflammation, leading to the loss of periodontal attachment [1]. As the core of LPS-induced cell activation and signal transduction, CD14 and TLR4 play a leading role in the inflammatory response of macrophages to endotoxin.
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