Abstract
The pathogenesis of periodontitis depends on a sustained feedback loop where bacterial virulence factors and immune responses both contribute to inflammation and tissue degradation. Periodontitis is a multifactorial disease that is associated with a pathogenic shift in the oral microbiome. Within this shift, low-abundance Gram-negative anaerobic pathobionts transition from harmless colonisers of the subgingival environment to a virulent state that drives evasion and subversion of innate and adaptive immune responses. This, in turn, drives the progression of inflammatory disease and the destruction of tooth-supporting structures. From an evolutionary perspective, bacteria have developed this phenotypic plasticity in order to respond and adapt to environmental stimuli or external stressors. This review summarises the available knowledge of genetic, transcriptional, and post-translational mechanisms which mediate the commensal-pathogen transition of periodontal bacteria. The review will focus primarily on Porphyromonas gingivalis.
Subject
Virology,Microbiology (medical),Microbiology
Reference117 articles.
1. Beyond the red complex and into more complexity: The polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology;Hajishengallis;Mol. Oral Microbiol.,2012
2. Suzuki, N., Yoneda, M., and Hirofuji, T. (2013). Mixed red-complex bacterial infection in periodontitis. Int. J. Dent., 587279.
3. Complement and dysbiosis in periodontal disease;Hajishengallis;Immunobiology,2012
4. Low-Abundance Biofilm Species Orchestrates Inflammatory Periodontal Disease through the Commensal Microbiota and Complement;Hajishengallis;Cell Host Microbe,2011
5. Pathogens, Commensal Symbionts, and Pathobionts: Discovery and Functional Effects on the Host;Hornef;ILAR J.,2015
Cited by
8 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献