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Manji M, Dahlen G and Fejerskov O. Caries Res 2018; 52: 548–564

Studies have identified the presence of around 700 microbial species in the oral microbiome, which, although variable between individuals, usually remains in a steady-state condition once teeth have erupted, unless disturbed by a challenge to the immune system. Many of these 700 species have not been isolated with common culture methods but are increasingly identifiable with new technologies.

The microbiome present within dental biofilm is metabolically active with constant small changes in pH, a higher pH favouring mineralisation and a more acidic pH favouring demineralisation. The presence of fermentable carbohydrate amplifies these fluctuations in favour of a lower pH at the tooth/biofilm interface. Cavitation may follow, but lesion development can be arrested at any stage by the regular removal of the microbial deposits.

If left undisturbed, the dental biofilm will also cause gingivitis, gradual buccal and lingual gingival recession over time and the formation of proximal periodontal pockets. However, only 10-15% of most populations worldwide suffer from severe attachment loss. This statistic has led to an unfruitful search for microbiological markers to identify those at risk but no study has been able to predict future development of either caries or periodontitis by the identification of single species of microbe.

Traditionally caries and periodontal disease have been considered separate diseases and their own specialties and research bases have developed. However, both diseases are associated with the same oral microbiome, consisting largely of commensal microbes.

The authors argue that these diseases can be understood better by considering the random metabolic processes which occur within the whole oral microbiome. These random processes result in alternating periods of de- and re-mineralisation at the tooth surface and are a result of the normal metabolic activity within the microbiome. Similarly with periodontal disease, the soft tissue response to these processes will be periods of inflammation and periods of recovery. Prolonged exposure to plaque reduces the ability to recover from the inflammatory phase. The progression of disease can be affected by other determinants, such as increased fermentable carbohydrate intake, diabetes and smoking, but cavitation and loss of attachment can still occur in the absence of these factors. The importance of regular plaque removal cannot be overemphasised.

Since the dental biofilm cannot be eliminated completely, the normal random processes within the microbiome will always continue, and the only difference between periodontal disease and dental caries is the function of how the host tissues respond to the normal metabolic activity of the commensal organisms in the biofilm.