Periodontitis: from microbial immune subversion to systemic inflammation

Abstract

Periodontitis is a dysbiotic inflammatory disease with an adverse impact on systemic health. Recent studies have provided insights into the emergence and persistence of dysbiotic oral microbial communities, which can mediate inflammatory pathology at local as well as distant sites. This Review discusses mechanisms of microbial immune subversion that tip the balance from homeostasis to disease in oral or extraoral sites.

GAS6 is a key homeostatic immunological regulator of host–commensal interactions in the oral mucosa

“…The teeth represent the only hard tissue in our body exposed to the hostile external environment, and bacteria colonize tooth enamel and adjacent soft tissues to form a persistent and chronic biofilm (5). An excessive inflammatory response against the oral biofilm results in periodontal diseases, and can facilitate intravascular dissemination of microorganisms throughout the body that is associated with adverse systemic conditions (6). Therefore, understanding the immune mechanisms engaged by the oral mucosal epithelium to maintain immunological homeostasis is of major importance for human health.…”

Presence of Porphyromonas and Prevotella species in the oral microflora of cattle with periodontitis

“…This investigation suggests the etiologic role of bacteria in bovine periodontitis, probably initiating the inflammatory response and leading to attachment bone loss derived from the action of mediated factors (IL-1, TNF, prostaglan-dins, complement, RANKL), as observed in human periodontitis (Hajishengallis 2015, Pandit et al 2015.…”

“…Periodontal breakdown in humans is strongly associated with dysbiosis of the periodontal microbiota, producing relevant changes in the relative abundance of individual components of the dental biofilm and modification in host-microbe relationship sufficient to mediate destructive inflammation and bone loss, which are linked to presence of black pigmented anaerobes, P. gingivalis in particular (Hajishengallis 2014, Hajishengallis 2015, Amaliya et al 2015. Other species such as P. intermedia, P. melaninogenica and P. loescheii have been isolated from healthy periodontal sites and their populations and occurrence are significantly higher in patients and periodontal sites presenting conjunctive attachment loss (Darout 2014, Dahlén et al 2014, Amaliya et al 2015.…”

Periodontal and inflammatory bowel diseases: Is there evidence for complex pathogenic interactions?

“…The inflammation evoked by periodontitis could result in low-grade systemic inflammation and thus it is plausible to speculate that periodontitis might influence IBD. Locally produced pro-inflammatory cytokines might enter the systemic circulation, induce an acutephase response in the liver, and contribute to several processes, such as an atherosclerotic process [63] . Also, as large quantities of oral bacteria are constantly swallowed via the saliva into the gut, it has been proposed that swallowed P. gingivalis may cause alterations to the gut microbiota, thereby leading to increased gut epithelial permeability and endotoxemia, which causes systemic inflammation [63] .…”

“…Locally produced pro-inflammatory cytokines might enter the systemic circulation, induce an acutephase response in the liver, and contribute to several processes, such as an atherosclerotic process [63] . Also, as large quantities of oral bacteria are constantly swallowed via the saliva into the gut, it has been proposed that swallowed P. gingivalis may cause alterations to the gut microbiota, thereby leading to increased gut epithelial permeability and endotoxemia, which causes systemic inflammation [63] . Arimatsu et al [64] have used a mouse model to evaluate whether endotoxemia is responsible for inflammation in several organs and tissues.…”