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Dental Caries: Is Prolonged Breast-Feeding to Blame?


Josie Swan
P. Papathakis
FSN 310
3 December 2014

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Prolonged breast-feeding (after 12 months of age) provides the acquisition of the
cariogenic bacteria Streptococcus mutans, an energy source for this bacteria, and accelerated
growth due to common feeding habits (Li, Wang, and Caufield). All of these things can be
caused by something else, but the compilation of all three is unique to prolonged breastfeeding.
This paper will assess the ways that prolonged breastfeeding leads to dental caries, the likelihood
of attributing dental caries to prolonged breast-feeding, and the methods of prevention.
A significant factor in the correlation between breastfeeding and dental caries is the
transmission of Streptococcus mutans. This transmission is possible through many methods
including breast-feeding (Li, Wang, and Caufield). S. mutans contains an enzyme that cleaves
disaccharides. Disaccharides are two-part sugars that are made up of monosaccharides.
Monosaccharides are simple sugars. When disaccharides and S. mutans are simulataneously
present in the mouth, the enzyme breaks down disaccharides into monosaccharides. The
monosaccharides both contribute to the formation of plaque and are used as a carbon source to
decalcify enamel and create lactic acid (DenBesten and Berkowitz). It is important to note that
the transmission of S. Mutans is constant through the duration of breastfeeding. The significance
of duration, however, is the availability of sugar to S. mutans.
A study at the University of Minnesota provided that breast-milk in combination with
sucrose (a disaccharide) is more cariogenic than sucrose alone. Eighteen children between the
ages of twelve and twenty-four months were split into two groups. In the control group, the
children had exposure to sucrose and (similar to a prior study by the same researcher) developed
caries. In the experimental group, the children were exposed to human breast-milk and sucrose.
Caries developed much more rapidly for the experimental groupin 3.2 weeks (Erikson and
Mazhari). This study shows the significance of the duration of breast-feeding, as opposed to
whether the child is breast fed at all. This is because over time, a childs protein needs decrease;
the carbohydrate to protein ratio is significantly increased from infancy to toddlerhood. With the
increased carbohydrate intake in toddlerhood, the cariogenic effect of breast-milk is magnified.
Furthermore, the nutrient content of the breast-milk parallels the needs of the child. So as the
child grows and their carbohydrate needs increase, there are more disaccharides in the breastmilk (Brown, Isaacs, Krinke, Lechtenberg, and Murtaugh). The effect is intensified both by the
content of the breast-milk and the diet of the toddler.
After addressing the risk factors of breast-feeding in regard to dental caries, it is
imperative to express the likelihood of prolonged breastfeeding as the reason. This is because
prolonged breastfeeding is not the sole risk factor in dental caries. It is true that breastfeeding
transmits and supports S. mutans; but while prolonged breast-feeding is a compilation of risk
factors, these factors are achievable (each individually) in other ways (Li, Wang, and Caufield).
The transmission of S. mutans in combination with an adequate sugar intake promotes
decalcification of enamel; however, it is important to assess whether these are risks of prolonged
breast-feeding alone, or if they emerge with other origins (Erikson and Mazhari).
S. mutans can encounter a preferred environment within the mouth of a child who has
never breast-fed before. This is because there are other possible ways for the bacteria
transmission to occur. It can be transmitted at birth, though saliva, or though breast milk

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(Douglass, Douglass, and Silk). A child who has never breast-fed can harbor the same bacteria
without difficulty; however, it is likely a result of multiple factors as opposed to one.
If S. mutans is present in the mouth of a child and breast milk is not a source of nutrients,
the sugar intake is still a factor in cariogenicity. Though the common breast-feeding practices
harbor a very fertile environment for S. mutans, a similar sugar intake is very common in a child
who is not breast-fed (Mizoguchi, Kurumado, Tango and Minowa). The bacterias accessibility
to its energy source is the main factor. The frequency of eating is strongly correlated with dental
caries, though this outcome is reached in many different manners. The frequency of eating is
very high among children that are eating solid foods in addition to breast milk or artificial human
milk. However, it is important to recognize that these situations are virtually identical. The
demand for milk will be sporadic, and often children prefer to nurse before bed. The same is true
for a child going to bed with a bottle (Smith and Moffatt). The problem with the frequency of
eating is the amount of times per day the bacteria is encountering an energy source. This is
because when the food or milk is swallowed, the saliva in the mouth neutralizes the pH (reducing
lactic acid) and substantially decreases the amount of sugar in the mouth. When a child is eating
more often, the bacteria has an energy source more readily available. A similar situation is true
with eating at night. When a child falls asleep while drinking (regardless of whether it is breastmilk or cows milk) the milk will pool up in the mouth and saturate the surface of the teeth with
sugar. The child does not swallow so the saliva does not coat the mouth (Hallett and ORourke).
The accessibility of the sugar is the most significant factor if S. mutans is present. Along with
most, this risk factor is dependent on others. Because prolonged breast-feeding increase the
likelihood of many risk factors individually, it increases the likelihood of dental caries.
Though prolonged breast-feeding provides a compilation of risk factors for dental caries,
the prevention of such is becoming easier. Studies have shifted from fixing dental caries to
preventing them. Preventative measures include removing the energy source of the bacteria, or
simply decreasing the susceptibility of the enamel. A very simple method is drinking tap water.
Water rinses the sugars from the mouth, destroying the bacteria-prone environment mouth
(Hallett and ORourke). If the bacteria has no energy source, it cannot incubate nor produce
lactic acid. Also, the fluoride in tap water can prevent up to 60% of childhood caries. In 2010,
66.2% of the United States was receiving fluoridated water. This number is rising. Fluoride
protects teeth from decay by interacting with the enamel to strengthen it. This makes the enamel
less susceptible to the bacteria (Division of Oral Health).
This is another small distinction to note between the cariogenicity of human milk and
artificial human milk; the formula, when made with fluoridated tap water, contains preventative
properties. While there is no evidence that formula itself it a preventative strategy for dental
caries, the fluoride in the tap water has the same effect when mixed with artificial human milk
powder.
Another preventative measure is to remove the bacteria itself. Infant toothpaste can be
used as early as the teeth begin to come in (Dowshen). Toothpaste and toothbrushes remove the
bacteria from the surface of the teeth. Childrens diets should be decided by their nutritional
needs, not their enamels susceptibility to decay.

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Many things contribute to the risk of dental caries. Streptococcus mutans is the cariogenic
bacteria and its energy source is disaccharides. The disaccharides in breast-milk harbor a very
comfortable environment for the growth of S. mutans. This does not mean that the transmission
and growth are not possible through other manners. Prolonged breastfeeding provides a
collection of individual risks for dental caries. These are attained in other ways as well, but
prolonged breast-feeding has a distinctive accumulation of risk.

References
Brown, J. Isaacs, J. Krinke, U. Lechtenberg, E. and Murtaugh M. (2011) Chapter 6: Nutrition
During Lactation. Nutrition During the Life Cycle. Connecticut: Cengage Learning.
DenBesten, P. and Berkowitz R. (2003). Early Childhood Caries: An overview with reference to
our experience in California. Journal of the California Dental Association, 31(2), 139-142.
Division of Oral Health. (2010). Community Water Fluoridation. Centers for Disease Control
and prevention.
Douglass, J.M. Douglass, A.B. and Silk, H.J. (2004). A practical guide to infant oral health.
American Family Physician, 70(11), 2113-2122.
Dowshen, S. (2012). Keeping Your Kids Childs Teeth Healthy. Kids Health. The Nemours
Foundation.
Erikson, P. and Mazhari, E. (1999). Investigation of the role of human breast milk in caries
development. Pediatric Dentistry, 21(2), 86-90.
Hallett, K. and ORourke, P. (2002). Early child-hood caries and infant feeding practice.
Community Dental Health, 19, 237- 242.
Li, Y. Wang, W. and Caufield, P.W. (2000). The Fidelity of Mutans streptococci Transmission
and Caries Status. Caries Research, 34(20), 123-132.
Mizoguchi, K. Kurumado, K. Tango, T. and Minowa, M. (2003). Study on Factors for Caries and
Infant Feeding Characteristics in Children Aged 1.5-3 Years in a Kanto Urban Area.
Japanese Journal of Public Health, 50(9), 867-78.
Smith, P. and Moffatt M. (1998). Baby-bottle tooth decay: Are we on the right track?
International Journal of Circumpolar Health, 57(1), 155-62.

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