Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

Abstract

Late-onset periodontitis is associated with a series of inflammatory reactions induced by periodontal pathogens, such as Porphyromonas gingivalis, a keystone pathogen involved in periodontitis. Neutrophils are the most abundant leukocytes in the periodontal pocket/gingival crevice and inflamed periodontal tissues. They form a “wall” between the dental plaque and the junctional epithelium, preventing microbial invasion. The balance between neutrophils and the microbial community is essential to periodontal homeostasis. Excessive activation of neutrophils in response to periodontal pathogens can induce tissue damage and lead to periodontitis persistence. Therefore, illuminating the interactions between neutrophils and periodontal pathogens is critical for progress in the field of periodontitis. The present review aimed to summarize the interactions between neutrophils and periodontal pathogens in late-onset periodontitis, including neutrophil recruitment, neutrophil mechanisms to clear the pathogens, and pathogen strategies to evade neutrophil-mediated elimination of bacteria. The recruitment is a multi-step process, including tethering and rolling, adhesion, crawling, and transmigration. Neutrophils clear the pathogens mainly by phagocytosis, respiratory burst responses, degranulation, and neutrophil extracellular trap (NET) formation. The mechanisms that pathogens activate to evade neutrophil-mediated killing include impairing neutrophil recruitment, preventing phagocytosis, uncoupling killing from inflammation, and resistance to ROS, degranulation products, and NETs.

The influence of chronic hyper-homocysteinemia on characteristics of peripheral neutrophils’ programmed death in lipo-polysaccharide-induced periodontitis

“…At the same time, excessive activation of neutrophils and ROS hyper-production as a reaction to periodontal pathogens can induce periodontium damage, and lead to the persistence of periodontitis [27]. Our results showed the significant increase of ROS generation by peripheral blood neutrophils, decrease of their ΔΨm as well as the increase of the number of cells with signs of apoptosis in case of LPS-induced periodontitis.…”

“…Of all PMNs in the periodontal pocket and gingival crevice, neutrophils comprise the largest fraction. Since neutrophils are also the largest leukocyte group in inflamed periodontal tissues, they act as a barrier preventing micro-organism ingress between dental plaque and junctional epithelium [27]. Neutrophils produce marked bactericidal effect; they neutralize pathogens by releasing free radicals (in so called 'respiratory burst'), and then absorbing them through phagocytosis [28].…”

The effect of complex treatment on some hematological and hemostasiological indicators during the treatment of generalized periodontitis in patients with different blood group affiliation

“…The total blood test was determined using an automatic hematology analyzer "Sysmex KX-21" from Roche (Japan) using a commercial kit of reagents from Roche (Germany), which counts the number of blood cells using conductometric detection. Differentiated calculation of the expanded leukocyte formula was performed using a Zeiss light microscope according to a unified method (Jiang et al 2021), the principle of which is microscopy of stained blood smears with differentiation of different forms of leukocytes. The index of leukocyte intoxication (Kolte et al 2014) was calculated by the formula I.I.…”

Porphyromonas gingivalis and dental stem cells crosstalk amplify inflammation and bone loss in the periodontitis niche

“…Histological evidence suggests that neutrophils can create a "wall" like barrier between pathogen-rich dental plaque and junctional epithelium, thus providing antimicrobial support to the host epithelial cells (Cortés-Vieyra et al, 2016). Neutrophil functions are essential for periodontal homeostasis (Jiang et al, 2021). In the periodontitis niche, dental stem cells interact with neutrophils.…”