Current concepts and an alternative perspective on periodontal disease

Abstract

Background: Epidemiological data from countries worldwide show a consistent pattern implying that a fraction of around 10% of those over 40-50 years in all populations will exhibit severe periodontitis with the potential risk of losing teeth during their life-time. The subgingival microbiota shows striking similarities between populations irrespective of disease severity and can only marginally explain the clinical pattern. It is also difficult to explain this pattern by genetic and acquired risk factors such as systemic disease (e.g. diabetes) or habits (e.g. smoking) even if they may have a confounding effect on the disease.

Main text: Inflammation of the gingiva appears to be a normal and physiological response to the presence of commensal bacteria along the gingival crevice and in the dental biofilm. Over many years of exposure to the dental biofilm, the chronic inflammation in the gingiva gradually results in a loss of attachment and bone loss. Numerous laboratory and clinical studies have provided insight into the potential role of determinants that are associated with periodontitis. However, it has been difficult to relate the findings to the pattern of the distribution of the disease observed in epidemiological studies. We propose a simple and parsimonious model that considers all the multitude of potential determinants as creating effectively random noise within the dental biofilm to which the tissues react by accumulating the effects of this noise.

Conclusions: We suggest that such a model can explain many of the epidemiological features of periodontal breakdown over time, and we discuss its clinical implications.

Keywords: Epidemiology; Host-pathogen response; Inflammation; Oral microbiome; Periodontitis.

Fig. 1

The symbiont-the host-parasite relationship in the interaction between the microbial community within the subgingival dental plaque/biofilm and the host tissue response in inflammation. The factors given within the microbial community represent those that have claimed to be of importance for the activities within the biofilm as well as exposing the host tissues [14, 16, 57]. Similarly, the factors given within the host tissue response are those usually claimed to participate in the inflammatory reaction or as host defence factors against infections. The subgingival microbial community (dysbiosis) is under influence of local environmental factors such as saliva, oral hygiene, diet, pocket depth, antiseptics, antibiotics (local) and probiotics. The composition and activity within the dental biofilm are highly dependent on the assay systems used for evaluation e.g. culture, microscopy DNA-probes, quantitative polymerase chain reaction (qPCR) or next generation sequencing (NGS), biochemical methods and sampling techniques and strategies. The host tissue response of each individual is influenced by population, age, gender and genetics [16]. Environmental host factors such as medicals (cytotoxic drugs, systemic antibiotics) and smoking [17] as well as internal host factor such as systemic diseases and conditions (e.g. diabetes, obesity) [59], psychic stress/allostatic load [60] The two systems are highly dynamic and constantly fluctuating in activity and characterized by temporality. Abbrevations: NH₃ ammonia, H₂S hydrogen sulphide, LPS lipopolysaccharide, OSCN- hypothiocyanite, H₂O₂ hydrogen peroxide, AI-2 Autoinducer-2, CSP Competence-stimulating peptide, GCF Gingival crevicular fluid, IL interleukins (IL-1beta, IL-6, IL-8, IL.-18), TNFalfa Tumor necrotic factor alfa, IFNgamma Interferon gamma, MMP’s Matrix Metalloproteinases, ROS reactive oxygen species, CRP C-reactive protein

Fig. 2

a-c. Three examples of a potentially infinite series showing erratic loss and gain of tissues caused by accumulation of (integrating the effects of small random fluctuations of activity (noise) within the dental biofilm. Adopted from Manji et al. [26, 61]