Intersection between macrophages and periodontal pathogens in periodontitis

Abstract

Periodontitis is a chronic infectious disease characterized by loss of periodontal attachment and resorption of alveolar bone. Dysregulated oral microbial community is the initial factor of periodontitis and causes excessive infiltration of immune cells in periodontal tissues. Macrophage, as an important part of the innate immune system, interacts continually with oral pathogens. Macrophages can recognize and phagocytize pathogens and apoptotic neutrophils and produce the specialized pro‐resolving mediators (SPMs) playing an important role in maintaining the homeostasis of tissue microenvironment. However, macrophages may also induce abnormal immune responses with the overstimulation from pathogens, leading to the destruction of periodontal tissues and alveolar bone. Looking for targeted drugs that can regulate the activities of oral pathogens and the functions of macrophages provides a new idea for periodontitis treatment. This review summarizes the interaction between macrophages and periodontal pathogens in periodontitis, focusing on the pro‐inflammation and anti‐inflammation phenotypes of macrophages, and briefly concludes potential new methods of periodontitis therapy targeted at oral pathogens and macrophages.

Eriodictyol Suppresses Porphyromonas gingivalis-Induced Reactive Oxygen Species Production by Gingival Keratinocytes and the Inflammatory Response of Macrophages

“…Macrophages, which are key cells of the innate immune system, play an essential role in the overall inflammatory response. During the onset and progression of periodontitis, macrophages are found in high numbers in diseased periodontal sites [ 9 , 10 ]. These leukocytes modulate the inflammation process by secreting a variety of chemical agents, including cytokines, that can amplify the inflammatory response [ 9 , 10 ].…”

“…During the onset and progression of periodontitis, macrophages are found in high numbers in diseased periodontal sites [ 9 , 10 ]. These leukocytes modulate the inflammation process by secreting a variety of chemical agents, including cytokines, that can amplify the inflammatory response [ 9 , 10 ]. We showed that eriodictyol attenuates the production of IL-1β, IL-6, IL-8, and TNF-α by P. gingivalis -stimulated macrophages.…”

“…Macrophages, which make up an important part of the inflammatory infiltrate in active periodontal lesions, are major producers of MMPs when they are triggered by periodontal pathogens [ 10 ]. Given their action on a large array of extracellular matrix proteins such as laminin, fibronectin, and collagen, MMPs contribute to periodontal tissue destruction [ 47 , 48 ].…”

“…In a healthy periodontium, the immune response of mucosal and infiltrating immune cells triggered by periodontal pathogens in the dental biofilm is moderate and protective [ 7 , 8 ]. More specifically, macrophages and monocytes play a key role in host defenses against periodontal infections and contribute to the initiation of an adaptive immune response to periodontal pathogens such as P. gingivalis [ 9 , 10 ]. However, if periodontal pathogens proliferate and increase in number, a state of dysbiosis develops in the subgingival sites, inducing an exaggerated inflammatory response, which leads to the secretion of cytokines and matrix metalloproteinases (MMPs) that sustain the chronic inflammatory reaction and modulate connective tissue and alveolar bone destruction [ 11 ].…”

Polarized Macrophages in Periodontitis: Characteristics, Function, and Molecular Signaling

“…Li et al (162) found that inhibition of NF-kB and JAK1/STAT1/3 signaling pathway is the main mechanism by which Mangiferin ameliorates experimental periodontitis in mice. Efforts to maintain the balance of the local microenvironment and search for targeted drugs that can regulate the activity of oral pathogens and the function of macrophages are continuing, providing new ideas for the treatment of PD (163).…”