Acid Stress Survival Mechanisms of the Cariogenic Bacterium Streptococcus mutans

Abstract

Streptococcus mutans, the major etiological agent in human dental caries, is capable of forming a biofilm, or dental plaque, on the tooth surface (Loesche, 1986; Tanzer et al., 2001). S. mutans generates large amounts of acid within dental plaque from fermentable dietary carbohydrates. During meals, the ingestion of carbohydrates causes the pH of the dental plaque to fall below 4.0. Acid accumulation can eventually destroy the crystalline structure of teeth that is the hardest tissue in the human body, leading to the formation of a carious lesion (Quivey et al., 2001). The ability of S. mutans to survive in such a severe environment represents one of the most important virulence factors of this microorganism. The mechanisms of acid tolerance that are most common among Gram-positive bacteria have been proposed to be: i) proton pumps; ii) protection and/or repair of macromolecules; iii) cell-membrane changes; iv) production of alkali; v) regulators; vi) cell density and biofilms; and vii) alteration of metabolic pathways (Fig. 1) (Cotter & Hill, 2003). Many researchers have sought to explain the mechanisms of acid tolerance in S. mutans, and various genes contributing to aciduricity in S. mutans have been identified. In this chapter, we review those genes that have been reported to be involved in S. mutans aciduricity, including those participating in two-component systems and others, especially targeting the dgk homolog.