Modulatory Mechanisms of Pathogenicity in Porphyromonas gingivalis and Other Periodontal Pathobionts

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.

Automated summary

The development of periodontitis is a result of the interaction between bacterial virulence factors and immune responses, leading to inflammation and tissue degradation. This disease is associated with a shift in the oral microbiome, where harmless bacteria become pathogenic and evade immune responses. This review focuses on the genetic, transcriptional, and post-translational mechanisms that mediate this commensal-pathogen transition, with a particular emphasis on Porphyromonas gingivalis.