Periodontitis is a collection of diseases where microorganisms cause destruction of the tooth-supporting structures through poorly controlled inflammatory responses. A world workshop held in 2017 distinguished periodontitis in three clinical forms: necrotizing periodontitis, periodontitis as a manifestation of systemic disease, and the forms of the disease previously recognized as chronic or aggressive, now grouped under a single category, periodontitis [
1].
The oral cavity contains up to 1000 different bacteria localized in different niches, each with a characteristic microbiota [
2]. A homeostatic balance exists most of the time between host and oral microbes, but this can be tipped towards disease. Traditional culture-based methods emphasized the anaerobic Gram-negative rods
Porphyromonas gingivalis,
Tannerella forsythia, and
Treponema denticola (the red complex) as the major pathogens of periodontitis [
3]. Culture-independent methods have extended this list to comprise both Gram-positive and Gram-negative bacteria (reviewed by Lamont et al. [
4]). Among all these species
P. gingivalis has emerged as a keystone bacterium in periodontitis [
5,
6].
In periodontitis, polymicrobial communities initiate a dysregulated host response through polymicrobial synergy and dysbiosis [
7]. As a keystone pathogen,
P. gingivalis increases the nososymbiosity of subgingival microbial communities and drives periodontitis pathogenicity, remarkably, even at a low abundance [
5]. In this interplay, inflammation is an important ecological factor that can stimulate outgrowth of periodontitis-associated microorganisms by tissue destruction releasing nutrients (e.g., degraded collagen, haeme-containing complexes, amino acids, and iron). The nutrients are transferred to the subgingival bacteria, to which
P. gingivalis belongs, by the inflammatory exudate of the gingival crevicular fluid. Also increase in genes important for the pathogenesis of periodontitis such as proteolysis-related genes and genes for peptide transport and acquisition of iron and genes for synthesis of lipopolysaccharides (LPSs) have been detected. These genes elevate the proinflammatory potential of the microbial community [
8]. Remodeling of the original biofilm into a dysbiotic one increases the capability of the biofilm to release proinflammatory cytokines from host cells [
9].
P. gingivalis also uncouples inflammation from the bactericidal activity of leukocytes [
5]. This subversive action disrupts the microbial homeostasis and contributes to development of a dysbiotic microbiota and periodontitis. Furthermore,
P. gingivalis selectively suppresses IL-8 and T helper 1 cell-biasing chemokines (CXCL9, CXCL10, and CXCL11) [
10]. By manipulating host immunity and keeping bactericidal and inflammatory activities apart,
P. gingivalis increases the adaptive fitness of the entire microbial community [
4].