Abstract
Neutrophils are key cells of the immune system and have a decisive role in fighting foreign pathogens in infectious diseases. Neutrophil extracellular traps (NETs) consist of a mesh of DNA enclosing antimicrobial peptides and histones that are released into extracellular space following neutrophil response to a wide range of stimuli, such as pathogens, host-derived mediators and drugs. Neutrophils can remain functional after NET formation and are important for periodontal homeostasis. Periodontitis is an inflammatory multifactorial disease caused by a dysbiosis state between the gingival microbiome and the immune response of the host. The pathogenesis of periodontitis includes an immune-inflammatory component in which impaired NET formation and/or elimination can be involved, contributing to an exacerbated inflammatory reaction and to the destruction of gingival tissue. In this review, we summarize the current knowledge about the role of NETs in the pathogenesis of periodontitis.
Highlights
Pathology Department, School of Medicine (IBIMER, CIBM), University of Granada, 18071 Granada, Spain; Biosanitary Research Institute (IBS-GRANADA), University of Granada, 18012 Granada, Spain
While the investigations appreciated that the removal of Neutrophil extracellular traps (NETs) is essential for tissue homeostasis, the processes involved and time required in removing NETs are not well understood
NET formation has been associated with different diseases, such as inflammatory diseases including periodontitis and autoimmune diseases such as rheumatoid arthritis (RA)
Summary
Periodontitis is a chronic inflammatory disease that affects the tooth-supporting tissues and exhibits a wide range of clinical, microbiological and immunological manifestations It is associated with, and caused by, a multifaceted dynamic interaction among specific infectious agents, host immune responses, hazardous environmental exposure and genetic propensity [1]. In a susceptible host in which neutrophils do not properly contribute to the restraint of the invading bacteria, the homeostasis between the biofilm and the host response is altered, leading to an increase in tissue destruction [12,13] Due to this immune-inflammatory component, periodontitis has been related to several systemic diseases, including rheumatoid arthritis (RA) [14]. Previous studies have indicated that neutrophils derived from patients with periodontitis are hyperactive and have an increased activity and production of reactive oxygen species (ROS) in response to a microbial invasion [15]
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