Dictionary of dentistry‑No.1‑ "Dental caries"
Do you know the word "caries risk"? Caries risk refers to a susceptibility to dental cav‑
ities. Individuals with high caries risk are more likely to develop cavities despite fre‑quent brushing, while those with low caries risk are less likely to develop cavities de‑spite relatively infrequent brushing. What causes this difference? We'll begin byexplaining how dental caries begins.
Dental caries affects teeth, and its development involves the three factors of food, bac‑teria, and time.

TeethBacteria
CariesFoodTime

Factors underlying dental caries
Dental caries develops in the following stages:

C1

C1
C2
C3C4C2C3C4Caries localized in the enamel without subjective symptoms such as pain
Caries reaching the dentine; creating sensitivity to cold
Caries reaching the dental pulp; associated with sharp pain
Caries affecting the roots

Caries develops faster with deciduous teeth and newly erupted permanent teeth than withpermanent adult teeth. This is because the surface of a new tooth is soft and relatively
easily dissolved in acid, increasing susceptibility to caries.

Streptococcus mutans is a well‑known agent of caries, but just one of over 300 types ofbacteria found in the oral cavity. After a meal, Streptococcus mutans uses the sugars oc‑
curring in the food as an energy source to multiply, producing acid as a metabolic byprod‑
uct. This acid dissolves the surface of the tooth (decalcification equals caries). The
normal pH of the oral cavity is around 7. At a pH of 5.5 or below in an acid environment,
calcium and phosphate ions are released from the surface of the tooth. This pH is called
the critical pH. Since it takes about three minutes to reach the critical pH after foodfirst enters the mouth, thetooth surface begins to dis‑pH 8solve during the meal.
7critical pH

6←5decalcification

4
33分
0

And Streptococcus mutans produ‑
ces not just acids, but dex‑tran, a viscous substance thatallows bacteria to adhere tothe tooth surface and multi‑
ply, creating plaque. Althoughplaque looks like food resi‑timedue, it is actually a bacteri‑(minute)al mass; 1 mg of plaque con‑tains a few hundred million
bacteria.
The adhesion of plaque to the tooth sur‑face prevents acid diffusion, thereby
maintaining high concentrations of acids
within the plaque, facilitating decalci‑
fication and increasing caries risk.
Plaque is not water soluble and cannot
be eliminated by gargling, but is easily
removed by brushing. Brushing after
meals is important because it takes
around three hours for plaque to form.

recalcification

510Plaque15

As mentioned at the start, individual differences in caries risk are attributable to thequality and quantity of saliva. Sugar intake will lower pH below the critical level of
5.5 and initiate decalcification, but saliva makes teeth to recalcify as well as decalci‑
fy. The inorganic component of tooth enamel is hydroxyapatite (chemical formula: Ca10（P‑O4）6（OH）2), and the relationship between decalcification and recalcification can berepresented by the following chemical formula:
Ca10(PO4)6(OH)2 ＋ 8H＋Decalcification↓ ↑Recalcification
10Ca2＋ ＋ 6(HPO4)2− ＋ 2H2O
Saliva naturally contains the calcium and phosphate ions used to build hydroxyapatite.
Even when calcium and phosphate ions are released from the tooth surface, the supersatu‑
ration maintained by saliva promotes recalcification. This recalcification is facilitat‑ed by fluoride; when tooth crystals bind to fluoride, hydroxyapatite changes to fluoroa‑
patite, which is more acid resistant than ordinary hydroxyapatite. This is why fluoride
toothpaste is recommended. Saliva also contains bicarbonate, which neutralizes oral acid‑ity. Since more saliva is produced when the salivary glands are stimulated, chewing foodincreases bicarbonate levels and improves the quality and quantity of saliva, reducing
caries risk.