A new strategy for the replacement therapy of dental caries.

The rationale of bacterial replacement therapy against dental caries is that relatively avirulent strains of Mutans Streptococi (MS) are most likely to occupy the same ecological niche in plaque as their more cariogenic counterparts. As known, lactate dehydrogenase (LDH) deficiency has been proposed as one aspect of a strategy to construct an effector strain because LDH-deficient mutants could affect acid production by MS so as to reduce their cariogenicity. Glucan-binding lectin (GBL) plays a very important role in the formation of dental plaque biomembrane and the adherence of S. mutans to teeth surface. The gcrR gene acts as a negative transcriptional regular of gbpc gene which encoded S. mutans GBL. We presume an LDH-deficient S. mutans mutants which harbours an insertion-deletion mutation in gcrR gene can result in overexpression of GBL and higher adherence to teeth than the wild-type S. mutans and will possess of both low-level acid production and strong colonization potential.