REPLACEMENT THERAPY OF DENTAL CARIES

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Lactate dehydrogenase (LDH)-deficient mutants of Streptococcus mutant strain BHT-2 proved well suited to serve as effector strains in the replacement therapy of dental caries in rodents. Attempts to extend their application to a primate model suffered from the drawbacks that mutants of strain BHT-2 were poor colonizers of the monkey's oral cavity and were prone to reversion during prolongee studies. Current work centers on constructing an effector strain better suited for use in monkeys and humans. Preliminary studies indicate that bacteriocin production may confer a selective advantage to Strep. mutans colonization. One strain has been isolated which produces a bacteriocin inhibitory8 to the growth of virtually all other strains. The bacteriocin is a small polypeptide. It will be purified from culture liquors, sequenced, and synthesized to provide a ready source of material for study. Aspects of this bacteriocin which will be investigated include the kinetics of its biosynthesis and its mode of action. High producing and deficient mutants will be tested in animal models in order to define the role of bacteriocins in colonization. The plasmid which codes for bacteriocin production in this strain will be transformed into a serogroup c strain of Strep. mutans. A non-reverting LDH-deficiency mutation present in a BHT-2 derivative will then be transformed into this strain. The resultant bacteriocin producing, LDH deficient strain will then be tested as an effector strain for use in the replacement therapy of dental caries.