Integrated hypothesis of dental caries and periodontal diseases

Abstract

This review considers an integrated hypothesis of dental caries and periodontal diseases that builds on theoretical ecological principles. The backbone of the hypothesis is based on the dynamic stability stage of the oral microbiota, at which intrinsic (mainly saliva and gingival crevicular fluid) and bacterial (mainly metabolic) resilience factors maintain ecological dynamic stability, compatible with clinical health. However, loss of intrinsic resilience factors and/or prolonged changes in the availability of microbial metabolic substrates may shift the ecological balance of the microbiota into either saccharolytic (acidogenic) or amino acid-degrading/proteolytic (alkalinogenic) stages, depending on the nature of the predominant substrates, leading to clinical diseases. Therefore, to maintain and restore the dynamic stability of the oral microbiota, it is necessary to control the drivers of disease, such as salivary flow and influx of bacterial nutrients into the oral cavity. Contrary to conventional wisdom, excessive intake of fermentable carbohydrates may contribute to inflammation in periodontal tissues resulting from hyperglycaemia. An integrated hypothesis emphasizes that both dental caries and periodontal diseases originate in the dynamic stability stage and emerge in response to nutritional imbalances in the microbiota. Periodontal diseases may belong to the sugar driven inflammatory diseases, similar to diabetes, obesity, and cardiovascular diseases.

Keywords: Dental caries; carbohydrates; dynamic stability stage; ecological hypothesis; ecosystem; gingival crevicular fluid; microbiota; periodontal diseases; resilience factor.

Figure 1.

Illustration of three theoretical pH response patterns in the integrated hypothesis of dental caries and periodontal diseases. The green curve illustrates pH fluctuations of the microbiota at the dynamic stability stage associated with clinical health, at which pH fluctuations are balanced over time due to infrequent nutrient exposures. The red and blue curves show pH fluctuations of the microbiota at subgingival and supragingival sites in response to increasing exposure microbial nutrients, respectively. When GCF/inflammatory nutrients are intense and prolonged, pH of the microbiota may drift from the dynamic stability stage into proteolytic/amino-acid degrading and inflammatory stages associated with gingivitis and periodontitis (red curve), whereas intense and prolonged increases in exposure to dietary carbohydrates promotes a drift of pH into acidogenic and aciduric stages associated with caries (blue curve). For further details, see text

Figure 2.

Overview of intrinsic and bacterial metabolic resilience factors operating at the dynamic stability stage. Bacterial metabolic resilience comprises two categories: bi-directional pH metabolic regulation and autonomic metabolic repression. Resilience factor marked in red = acidification factor, which is more active under alkaline than under acidic conditions. Resilience factors marked in blue = acid-neutralization/alkalization factors, some of which are more active under acidic than under alkaline conditions or active at a wide range of pH. Some bacterial metabolites, such as NH₃ and sulfur compounds are inflammatory factors. For detailed description, see text