Porphyromonas gingivalis is considered a keystone pathogen in adult periodontitis but has also been associated with systemic diseases. It has a myriad of virulence factors that differ between strains. Genetic exchange and intracellular genome rearrangements may be responsible for the variability in the virulence of P. gingivalis. The present review discusses how the exchange of alleles can convert this bacterium from commensalistic to pathogenic and potentially shapes the host-microbe environment from homeostasis to dysbiosis. It is likely that genotypes of P. gingivalis with increased pathogenic adaptations may spread in the human population with features acquired from a common pool of alleles. The exact molecular mechanisms that trigger this exchange are so far unknown but they may be elicited by environmental pressure.
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