The Dental Caries Process

The classic Keyes model suggests that dental caries result from bacterial fermentation of carbohydrates at the tooth surface (Figure 1). Acid produced as a byproduct of fermentation erodes the enamel in a site-specific manner. The removal of the outer mineral component of the enamel is termed demineralization. Between periods of acid production leading to demineralization, minerals including fluoride from saliva, the diet, and/or water are added back to the enamel. The uptake of minerals into the enamel tissue is called remineralization. The development of a carious lesion reflects an imbalance between demineralization and remineralization when mineral removal outpaces mineral uptake. A cavity is formed when sufficient enamel is removed to create a hole.

Figure 1. Classic Keyes model

Figure 1. Classic Keyes model

The oral microbiome refers to the diverse community of microorganisms that live within the oral cavity. The presence of caries reflects a loss of healthy bacteria and an increase in cariogenic bacteria. S. mutans were initially thought responsible for the caries process. However, our current understanding suggests that S. mutans is one of several bacteria responsible for the initiation of caries, and a host of bacteria and fungi support the progression of the caries process.³ The bacterial composition of the oral microbiome changes throughout the caries process. Oral hygiene behaviors including brushing and flossing disrupt the oral microbiome, and fluoride can both interfere with bacterial growth and remineralize the tooth surface.

The tooth is composed of several layers – the inner pulp, the dentin, and the outer enamel surface. Although the enamel is relatively inert once it’s developed, the enamel is susceptible to insults during development. The insults can increase susceptibility to bacterial colonization and/or bacterial acid attack. Enamel hypoplasia and hypomineralization are enamel defects associated with vitamin A, vitamin D, calcium, and phosphorous deficiencies and/or other environmental exposures during tooth development.⁴ Lower maternal serum concentrations of vitamin D have been associated with early childhood caries in their infants at one year of age (Figure 2).⁵ Lower overall diet quality and/or malnutrition have been also associated with an increased risk of severe early childhood caries.^6-8

Figure 2. Prenatal vitamin D & ECC⁵

Figure 2. Prenatal vitamin D & ECC⁵

Caries is a diet-dependent disease; without fermentable carbohydrates, caries do not occur. While sugars are the primary substrate for oral bacteria, starches are also fermentable with modified starches more easily fermented. The nature of carbohydrate might influence the length of time the carbohydrate spends in the mouth. For example, baked starches with sugars are considered more cariogenic than either starches or sugars as they are more retentive. The form (i.e., liquid vs. solid) or texture (i.e., processed snack foods) of the carbohydrate might also influence the time spent in the mouth, particularly if the composition is sticky.

When considering caries risk, we often talk about the frequency or quantity of carbohydrate intake. However, the length of exposure to the carbohydrate is more relevant to caries risk. Exposure is a function of the frequency and duration of the eating or drinking event. For example, a 12 oz sugar sweetened beverage might be consumed in 20 minutes or over four hours. While it’s the same quantity and the same frequency, the exposure times are very different. Individuals with oral motor skill deficiencies that result in pocketing of foods and/or reduced clearance might have extended exposure times which increases their caries risk.