Background: Dental caries is an infectious disease, and it affects 90 percent of late adolescents and young adults in the United States. It is a complex disease that occurs along the interface between the dental biofilm and the enamel surface.
Results: Many components in saliva are taken up by dental biofilm and protect the enamel surface. On the other hand, newly erupted teeth depend on the enamel pellicle for posteruption maturation of acid-susceptible substituted hydroxyapatite. When Streptococcus mutans colonizes dental biofilm, it depends on vertical transmission, horizontal transmission or both. These acidogenic, aciduric bacteria are considered to be the primary organisms responsible for enamel caries. The ability of the biofilm to sequester calcium, phosphate and fluoride from the saliva, as well as from sources outside the oral cavity allows enamel to undergo remineralization after demineralization. Optimal remineralization depends on the enamel surface's being exposed to low concentrations of calcium, phosphate and fluoride for prolonged periods. Outside sources of bioavailable calcium, phosphate and fluoride can alter dental biofilm's cariogenicity.
Clinical implications: The use of sugar alcohols, povidone-iodine, delmopinol, triclosan and chlorhexidine may modulate the caries process. In addition, studies involving probiotics and molecular genetics have provided results showing that these methods can replace and displace cariogenic bacteria with noncariogenic bacteria, while maintaining normal oral homeostasis.