Differences in the salivary glycan pattern between children with high and low caries susceptibility.

Interactions between bacterial adhesins of lectin type and the oligosaccharide part of immobilised glycoconjugates on the tooth surface are involved in the specific colonisation of teeth. The specificity of the adhesion process is determined by the carbohydrate specificity of the bacterial lectins and the availability of the corresponding glycosylation pattern. On the other hand the same carbohydrate structures can specifically prevent the binding of bacteria by competitively blocking their adhesion, if sufficient amounts of this distinct carbohydrate structure are available in the secretion. Since carbohydrate binding receptors are also involved in the colonisation of tooth surfaces by cariogenic bacteria, it has been suggested that the architecture of the oligosaccharide portion of soluble glycoconjugates in saliva may play an important role as a constitutional host defence factor in the aetiology of dental caries. Characterising the availability of distinct carbohydrate patterns in saliva by using a pattern of well-described lectins in a competitive lectin inhibition assay we show that in children of a population-based sample a high caries susceptibility is associated with a reduced binding inhibition against the lectin peanut agglutinin (PNA). PNA is specific for the presence of terminal galactosyl residues and binds to the same O-glycan fractions as a surface lectin from Streptococcus mutans. The data suggest that a reduced availability of glycosylation patterns of galactosyl residues detected by the lectin PNA may act as an additional host-derived factor for an increased caries susceptibility.