Inflammatory and immune pathways in the pathogenesis of periodontal disease
By Ali Cekici, A. Kantarcı, H. Hasturk, T. V. Van Dyke. Periodontology 2000, 2014
1,256 citations recorded by the source corpus.
The pathogenesis of periodontitis involves a complex immune/inflammatory cascade that is initiated by the bacteria of the oral biofilm that forms naturally on the teeth. The susceptibility to periodontitis appears to be determined by the host response; specifically, the magnitude of the inflammatory response and the differential activation of immune pathways. The purpose of this review was to delineate our current knowledge of the host response in periodontitis. The role of innate immunity, the failure of acute inflammation to resolve (thus becoming chronic), the cytokine pathways that regulate the activation of acquired immunity and the cells and products of the immune system are considered. New information relating to regulation of both inflammation and the immune response will be reviewed in the context of susceptibility to, and perhaps control of, periodontitis.
Subfields: Immunology, Microbiology, Periodontics
View Paper: https://www.semanticscholar.org/paper/c3fc888e78412929aa058db83ac28ee0d7fec43e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
In Periodontics
Citations in the corpus
- Periodontitis: A Multifaceted Disease of Tooth-Supporting Tissues (2019, background): “Proinflammatory cytokines (IL-1β, IL-6, IL-23, TNF-α), chemokines (IL-8), and antimicrobial peptides produced by keratinocytes, fibroblasts, and dendritic cells are chemoattractant gradients for neutrophils, which migrate into inflamed tissues and stimulate the chemotaxis of nonresident cells (macro”
- Periodontitis: facts, fallacies and the future. (2017, background): “Hyperactive, as well as insufficient, immune responses are parts of the complex etiopathology of periodontitis (212) and may constitute potential therapeutic targets (35, 248).”
- Global burden of oral diseases: emerging concepts, management and interplay with systemic health. (2016, background): “…severity of periodontal disease are largely determined by the bacteriainitiated and dysregulated hyperimmuno-inflammatory response, modulated by various genetic, epigenetic, environmental and host factors such as tobacco use and uncontrolled DM (Page et al, 1997; Kornman, 2008; Cekici et al, 2014).”