Premium
Necroptosis in the periodontal homeostasis: Signals emanating from dying cells
Author(s) -
Li J,
Ke X,
Yan F,
Lei L,
Li H
Publication year - 2018
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12722
Subject(s) - necroptosis , biology , programmed cell death , microbiology and biotechnology , ripk1 , proinflammatory cytokine , immune system , immunology , porphyromonas gingivalis , dysbiosis , pyroptosis , homeostasis , inflammasome , chemokine , inflammation , apoptosis , gut flora , biochemistry , genetics , bacteria
Periodontal tissues are constantly exposed to microbial stimuli. The equilibrium between microbes and host defense system helps maintain the homeostasis in the periodontal microenvironment. Growth of pathogenic bacteria in dental biofilms may induce proinflammatory cytokine production to recruit sentinel cells, mainly neutrophils and monocytes into the gingival sulcus or the periodontal pocket. Moreover, dysbiosis with overgrowth of anaerobic pathogens, such as Porphyromonas gingivalis and Tannerella forsythia , may induce death of both immune cells and host resident cells. Necroptosis is one newly characterized programmed cell death mediated by receptor‐interacting protein kinase ( RIPK )‐1, RIPK 3, and mixed lineage kinase like ( MLKL ). With its release of death‐associated molecular patterns ( DAMP s) into extracellular environment, necroptosis may help transmit the danger signal and amplify the inflammatory responses. In this review, we present recent advances on how necroptosis influences bacterial infection progression and what a role necroptosis plays in maintaining the homeostasis in the periodontal niche. Until we fully decipher the signals emanated from dying cells, we cannot completely understand the mechanism of disease progression.