Polymicrobial communities in periodontal disease: Their quasi‐organismal nature and dialogue with the host

Abstract

In health, indigenous polymicrobial communities at mucosal surfaces maintain an ecological balance via both inter‐microbial and host‐microbial interactions that promote their own and the host's fitness, while preventing invasion by exogenous pathogens. However, genetic and acquired destabilizing factors (including immune deficiencies, immunoregulatory defects, smoking, diet, obesity, diabetes and other systemic diseases, and aging) may disrupt this homeostatic balance, leading to selective outgrowth of species with the potential for destructive inflammation. This process, known as dysbiosis, underlies the development of periodontitis in susceptible hosts. The pathogenic process is not linear but involves a positive‐feedback loop between dysbiosis and the host inflammatory response. The dysbiotic community is essentially a quasi‐organismal entity, where constituent organisms communicate via sophisticated physical and chemical signals and display functional specialization (eg, accessory pathogens, keystone pathogens, pathobionts), which enables polymicrobial synergy and dictates the community's pathogenic potential or nososymbiocity. In this review, we discuss early and recent studies in support of the polymicrobial synergy and dysbiosis model of periodontal disease pathogenesis. According to this concept, disease is not caused by individual “causative pathogens” but rather by reciprocally reinforced interactions between physically and metabolically integrated polymicrobial communities and a dysregulated host inflammatory response.

Combination of enamel matrix derivative and hyaluronic acid inhibits lipopolysaccharide-induced inflammatory response on human epithelial and bone cells

“…The application of EMD and HA as adjuvant chemotherapeutic bioagents in periodontal therapy is noteworthy; however, there are a limited number of studies investigating in vitro tissue wound healing response to typical pyrogen bacterial endotoxins, such as lipopolysaccharides (LPS), which induce detrimental biological responses and act as an important factor in periodontitis pathogenesis [28][29][30][31]. A number of other studies describe the use of HA and EMD in non-surgical and surgical periodontal therapy, with generally beneficial moderate effects on periodontal inflammation, on bleeding on probing, or residual pocket depth [11,14,20,[27][28][29][30][31]. Furthermore, different combinations of EMD and bone grafts and/or platelet growth factors have been used to regenerate intrabony defects [32].…”

“Submandibular Injection of Indoleamine 2,3-Dioxygenase Galectin-3 Fusion Protein Inhibits and Prevents Periodontal Disease Progression Over 12 Weeks”

“…The PD model used in these studies is dependent on a significant bacterial burden (18) and most bacterial species, including P. gingivalis , utilize tryptophan in their metabolism (19). Therefore, we next assessed the impact of IDO-Gal3 on bacterial burden.…”

Interdental and subgingival microbiota may affect the tongue microbial ecology and oral malodour in health, gingivitis and periodontitis

“…However, it was found that bacteria normally resident in the periodontal niches, increased in relative abundance on the tongue with higher plaque coverage and BOP values in the study population (Figure 1 & Figure 4). This suggests that the tongue dorsum may become a reservoir for periodontal bacteria possibly due to factors such as better nutrient availability resulting from periodontal inflammation and changes in redox potential could form part of the ecological pressures that could allow the tongue to support a more diverse and periodontopathic microbial population [42]. In turn, the tongue may also play a role in helping these microbial species in recolonising the subgingival and interdental niches.…”