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Background: Dental caries still appears at high prevalence worldwide. Disease distribution is skewed with more disease in socio-economically weak groups. However, also in populations considered as “low caries” there is a significant fraction with continuous disease development. Caries develops when the hard tissues of the tooth is demineralized, which occurs when pH drops below approximately 5.5 for enamel and 6.2 for dentine. The pH drop follows fermentation and acid production by tooth colonising bacteria upon dietary carbohydrate exposure. Thus, understanding the interactions between oral bacteria, diet and host factors is essential for managing the disease. The overall aim of this thesis was to study the oral microbiota in relation to caries and its association with sugar intake and driving forces behind sugar intake.

Material and method: Saliva and tooth biofilm samples, information on caries status, dietary habits and other lifestyle data were collected from 17-23 year old participants. The participants also carried out a tasting session for the tastes sour, sweet and bitter. Genomic DNA was extracted from saliva and tooth biofilm and analysed using 16S rDNA amplicon sequencing with two platforms. Taxa were classified against the eHOMD database. Taste gene genotyping was done by mass spectrometry. Data were compared by univariate and multivariate statistical methods.

Results: Oral microbiota was analysed in 64 adolescents. Streptococcus mutans, Scardovia wiggsiae, Bifidobacterium longum and Lepotrichia sp. HOT 498 displayed strong association with having caries, whereas Corynebacterium matruchotii and tooth brushing were associated with being caries-free. It was also confirmed that S.mutans was not compulsory for having caries. The oral microbiota in caries affected adolescents without S. mutans in was evaluated, and found to be characterised by a wide panel of saccharolytic non-S.mutans species. In contrast, tooth biofilms in individuals with caries and S. mutans were enriched for relatively few saccharolytic species in addition to S.mutans. Further, the overall microbiota pattern fell into four distinct clusters with deviating caries prevalence. The association with a set of lifestyle factors was searched, and sugar intake was found to differ between the groups. In the cluster with the highest sugar intake, the microbiota was less diverse and low sugar intake was characterized by enumeration of C. durum, C. matruchotiiand S. sanguinis. To deepen the knowledge on mechanisms behind sweet food intake, single nucleotide polymorphisms (SNP) genotyping in genes reported to be associated with taste regulation or sugar intake was done. SNPs in four genes were associated with sensitivity and preference for sweet taste and in the SLC2A2 gene also with caries.

Conclusions: This project confirmed that dental caries is not a single species disease, and in the present population S. mutans, S. wiggsiae, and B. longum were significant for having caries. It was also confirmed that S. mutans is not essential for having caries. Tooth biofilm microbiota in S. mutans free adolescents was characterised by a larger diversity of species than seen in those with caries and S. mutans. It may be hypothesised that sugar intake and associated pH drops alone or in interaction with host biology play a role in the differentiation of the microbiota into the distinct profiles. This was supported by the finding that sugar intake was related to microbiota clustering and less community diversity. In this perspective the genetically based influence on sugar preference should be taken into account in dietary counselling which is an important aspect in caries prevention and treatment.