Periodontitis, a plethora of inflammatory conditions of the periodontium (the supporting teeth structures comprising gingiva, periodontal ligament and bone), is associated with a dysbiotic biofilm and dysregulation of the host immune response. The amount and composition of dysbiotic microbial biofilm that is formed on tooth surfaces, called dental plaque, is usually directly correlated with the amount of tissue destruction. However, both genetic and environmental host factors are associated with susceptibility to periodontitis, and several risk factors have already been established. Overactivation of the immune system caused by periodontal inflammation can contribute to the worsening of systemic diseases, such as diabetes, rheumatoid arthritis and atherosclerosis.
Experimental models that mimic periodontal disease in humans have been a valuable tool to understand the pathogenesis of periodontitis and propose new treatments, as well as to understand mechanisms involved in aggravation of systemic conditions caused by periodontal disease. Typically, periodontal destruction is induced in mice or rats by oral gavage with bacteria such as Porphyromonas gingivalis or Aggregatibacter Actinomycetemcomitans, by placement of silk ligatures for bacterial accumulation or by injection of heat killed bacteria or bacterial products such as LPS. With the emergence of novel genetically modified mouse models, mechanistic understanding of the disease has progressed immensely over the last decades.
Mouse models seem indispensable to study mechanistical effects on a whole organism. However, many laboratories are in the transition from animal models towards animal free models. In fact, this movement to reduce, refine and replace animal experiments is encouraged worldwide. Novel cell models to study mechanistical aspects of periodontitis are therefore important to establish. These could be tissue- or body-on-a-chip approaches that combine various cell types present in the periodontium together with a periodontitis specific challenge. These challenges could be defined bacteria or bacterial components, bacterial samples representing the microbiome from periodontitis patients or inflammatory cytokine(s).
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 immune system in periodontitis:
• Innovative approaches using animal models that address the participation of the host immune system in periodontal disease,
• Mechanistic studies combining cell culture and animal models to address inflammatory pathways activated during periodontal disease
• Mechanistic studies on the role of pathogen-associated molecular patterns (PAMPs) from periodontopathogenic bacteria in the pathogenesis of periodontal diseases
• Pharmacological interventions triggering the host immune system to treat periodontitis
• Regulation of osteoclastogenesis and osteoblastogenesis by periodontopathogenic bacteria PAMPs and host-derived factors released during periodontal diseases
• Novel cell biological approaches using periodontium derived cell cultures and patient materials such as sera before and after treatment
• Studies that are aimed at understanding immune system steered breakdown of soft or hard tissue due to activation of proteolytic pathways of immune cells, fibroblasts, or osteoclasts
• Reviews summarizing the current knowledge on the participation of the immune system or interventions aiming to treat periodontal diseases.
Periodontitis, a plethora of inflammatory conditions of the periodontium (the supporting teeth structures comprising gingiva, periodontal ligament and bone), is associated with a dysbiotic biofilm and dysregulation of the host immune response. The amount and composition of dysbiotic microbial biofilm that is formed on tooth surfaces, called dental plaque, is usually directly correlated with the amount of tissue destruction. However, both genetic and environmental host factors are associated with susceptibility to periodontitis, and several risk factors have already been established. Overactivation of the immune system caused by periodontal inflammation can contribute to the worsening of systemic diseases, such as diabetes, rheumatoid arthritis and atherosclerosis.
Experimental models that mimic periodontal disease in humans have been a valuable tool to understand the pathogenesis of periodontitis and propose new treatments, as well as to understand mechanisms involved in aggravation of systemic conditions caused by periodontal disease. Typically, periodontal destruction is induced in mice or rats by oral gavage with bacteria such as Porphyromonas gingivalis or Aggregatibacter Actinomycetemcomitans, by placement of silk ligatures for bacterial accumulation or by injection of heat killed bacteria or bacterial products such as LPS. With the emergence of novel genetically modified mouse models, mechanistic understanding of the disease has progressed immensely over the last decades.
Mouse models seem indispensable to study mechanistical effects on a whole organism. However, many laboratories are in the transition from animal models towards animal free models. In fact, this movement to reduce, refine and replace animal experiments is encouraged worldwide. Novel cell models to study mechanistical aspects of periodontitis are therefore important to establish. These could be tissue- or body-on-a-chip approaches that combine various cell types present in the periodontium together with a periodontitis specific challenge. These challenges could be defined bacteria or bacterial components, bacterial samples representing the microbiome from periodontitis patients or inflammatory cytokine(s).
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 immune system in periodontitis:
• Innovative approaches using animal models that address the participation of the host immune system in periodontal disease,
• Mechanistic studies combining cell culture and animal models to address inflammatory pathways activated during periodontal disease
• Mechanistic studies on the role of pathogen-associated molecular patterns (PAMPs) from periodontopathogenic bacteria in the pathogenesis of periodontal diseases
• Pharmacological interventions triggering the host immune system to treat periodontitis
• Regulation of osteoclastogenesis and osteoblastogenesis by periodontopathogenic bacteria PAMPs and host-derived factors released during periodontal diseases
• Novel cell biological approaches using periodontium derived cell cultures and patient materials such as sera before and after treatment
• Studies that are aimed at understanding immune system steered breakdown of soft or hard tissue due to activation of proteolytic pathways of immune cells, fibroblasts, or osteoclasts
• Reviews summarizing the current knowledge on the participation of the immune system or interventions aiming to treat periodontal diseases.