Role of complement in host–microbe homeostasis of the periodontium

Abstract

Complement plays a key role in immunity and inflammation through direct effects on immune cells or via crosstalk and regulation of other host signaling pathways. Deregulation of these finely balanced complement activities can link infection to inflammatory tissue damage. Periodontitis is a polymicrobial community-induced chronic inflammatory disease that can destroy the tooth-supporting tissues. In this review, we summarize and discuss evidence that complement is involved in the dysbiotic transformation of the periodontal microbiota and in the inflammatory process that leads to the destruction of periodontal bone. Recent insights into the mechanisms of complement involvement in periodontitis have additionally provided likely targets for therapeutic intervention against this oral disease.

A metalloproteinase mirolysin of Tannerella forsythia inhibits all pathways of the complement system

“…Recent advancement in periodontal studies finally refuted the perception of periodontitis as a classical infection, triggered by a single or limited number of microorganisms. Rather, periodontal disease is the result of dysbiosis in the oral microbiota, leading to the formation of pathogenic biofilm of altered composition and increased bacterial counts, which, in turn, causes complementdependent inflammation of periodontium and consequently bone loss (9,10). In contrast to the previous hypothesis implicating a crucial contribution of red complex species in the pathogenesis of periodontal disease, the new model of polymicrobial synergy and dysbiosis proposes a concept of low-abundant keystone pathogens capable of breaking down periodontal homeostasis and changing normal benign oral biofilm into a dysbiotic one (9).…”

Periodontal Disease: General Aspects from Biofilm to the Immune Response Driven by Periodontal Pathogens

“…Thus, the destruction of [73]. Some bacteria will also use surface molecules to escape the action of the complement system, as in the case of HRgpA gingipain from P. gingivalis [74].…”

“…Diet is also an important factor for disease prevention [74]. Nishida et al used a sample of 12,419 adults and showed that there was an increased risk of periodontal disease due to poor dietary intake of vitamin C. The authors also observed a dose-response relationship between vitamin C and disease severity [75].…”

“…Nishida et al used a sample of 12,419 adults and showed that there was an increased risk of periodontal disease due to poor dietary intake of vitamin C. The authors also observed a dose-response relationship between vitamin C and disease severity [75]. Vitamin C has antioxidant properties that help to reduce the production of reactive oxygen radicals formed during the inflammatory process [74]. Furthermore, a diet that is rich in fruits, vegetables and low fat and sugars contributes to maintain a healthy periodontal tissue, and low calorie intake reduce inflammatory changes, lowering the chances of tissue damage in periodontal disease [75].…”

Apolipoprotein E Related Co-Morbidities and Alzheimer’s Disease

“…Destruction of host gingival tissues is the consequence of this exposure [49,50]. Incidence of transient bacteraemia following chewing, tooth brushing and scaling in individuals with periodontal inflammation [51], enabling oral bacteria and bacterial components hematogenous to several systemic organs.…”