Neutrophils are the overwhelming majority of immune cells responsible for antimicrobial defence of gingiva. Cases of neutropenia and leukocyte adhesion deficiencies are concomitant with severe early-onset periodontitis (earlier denoted chronic periodontitis). This indicates the indispensable role of neutrophils as a major antimicrobial defender in gingiva. In contrast, late-onset periodontitis is characterized by neutrophil hyper-responsiveness, massive neutrophil infiltration of gingiva, and exaggerated formation of crevicular neutrophil extracellular traps (NETs). The neutrophil response in the periodontal pocket is blown up due to both accumulations of neutrophils in the gingival epithelium and to neutrophil hyper-responsiveness. This issue suggests the crucial role of neutrophilic homeostasis for gingival health and neutrophil dysregulation as a major damaging factor of periodontitis pathology.
Up to date existing experimental periodontitis models, mostly based on the use of an excess of oral pathogens or their PAMPs, remain remote from the late-onset periodontitis in humans, which appears to be age-related. So, animal models of age-related periodontitis might be more useful. Die oral pathogens were mostly regarded as species and not as a biofilm and barely an animal model harboring dental biofilm (dental plaque) has been employed to study the oral neutrophil/biofilm interactions.
Another possibility to study oral neutrophil/biofilm interactions is to use ex vivo human cells from (liquid) biopsies and dental plaque from periodontitis patients. Non-invasive or little invasive approaches have some advantages insofar as human cells from patients with late-onset periodontitis, respectively human-harbored dental plaque can be utilized. Using such approaches might enable understanding the role of dental biofilm in periodontitis, which is frequently regarded as the pacemaker in the pathology development, unlike the common trend to consider the microbiota/host interactions as host-default.
In this Research Topic, we welcome Original Research, Systematic Review, Methods, Review, and Mini Review articles covering, but not limited to, the following subtopics on the involvement of the innate immune system in periodontitis:
• Mechanistic studies combining neutrophil culture inclusively NETs and genuine-grown dental plaque
• Pharmacological treatment modulating the neutrophil responsiveness in order to prevent or at least to attenuate periodontitis
• Studies on formation and effects of NETs within the crevice.
• Studies on patients with either neutropenia or leukocyte adhesion deficiencies or biopsies from them (also cell cultures and dental plaque).
• Reviews summarizing the current knowledge on the role of neutrophils and/or NETs and their interactions with dental plaque in periodontitis.
• Innovative approaches using animal models of age-related late-onset periodontitis
Neutrophils are the overwhelming majority of immune cells responsible for antimicrobial defence of gingiva. Cases of neutropenia and leukocyte adhesion deficiencies are concomitant with severe early-onset periodontitis (earlier denoted chronic periodontitis). This indicates the indispensable role of neutrophils as a major antimicrobial defender in gingiva. In contrast, late-onset periodontitis is characterized by neutrophil hyper-responsiveness, massive neutrophil infiltration of gingiva, and exaggerated formation of crevicular neutrophil extracellular traps (NETs). The neutrophil response in the periodontal pocket is blown up due to both accumulations of neutrophils in the gingival epithelium and to neutrophil hyper-responsiveness. This issue suggests the crucial role of neutrophilic homeostasis for gingival health and neutrophil dysregulation as a major damaging factor of periodontitis pathology.
Up to date existing experimental periodontitis models, mostly based on the use of an excess of oral pathogens or their PAMPs, remain remote from the late-onset periodontitis in humans, which appears to be age-related. So, animal models of age-related periodontitis might be more useful. Die oral pathogens were mostly regarded as species and not as a biofilm and barely an animal model harboring dental biofilm (dental plaque) has been employed to study the oral neutrophil/biofilm interactions.
Another possibility to study oral neutrophil/biofilm interactions is to use ex vivo human cells from (liquid) biopsies and dental plaque from periodontitis patients. Non-invasive or little invasive approaches have some advantages insofar as human cells from patients with late-onset periodontitis, respectively human-harbored dental plaque can be utilized. Using such approaches might enable understanding the role of dental biofilm in periodontitis, which is frequently regarded as the pacemaker in the pathology development, unlike the common trend to consider the microbiota/host interactions as host-default.
In this Research Topic, we welcome Original Research, Systematic Review, Methods, Review, and Mini Review articles covering, but not limited to, the following subtopics on the involvement of the innate immune system in periodontitis:
• Mechanistic studies combining neutrophil culture inclusively NETs and genuine-grown dental plaque
• Pharmacological treatment modulating the neutrophil responsiveness in order to prevent or at least to attenuate periodontitis
• Studies on formation and effects of NETs within the crevice.
• Studies on patients with either neutropenia or leukocyte adhesion deficiencies or biopsies from them (also cell cultures and dental plaque).
• Reviews summarizing the current knowledge on the role of neutrophils and/or NETs and their interactions with dental plaque in periodontitis.
• Innovative approaches using animal models of age-related late-onset periodontitis
