A Pediatric Dentist's Perspective
Kevin J. Hale, D.D.S.
From: NEW BEGINNINGS, Vol. 14 No. 1, January-February 1997, pp. 11-12
We provide articles from our publications from previous years for reference for our Leaders and members. Readers are cautioned to remember that research and medical information change over time.
Few things are more disheartening
and frustrating to a pediatric dentist than to be confronted with a
very young patient with rampant decay. G.V. Black, a father of modern
dentistry, observed in the late 1800s that a child with decay before
age four had decay throughout life.
William's mother, Renee,
brought him to my office for an examination around one year of age.
Because she feared he might exhibit the same predisposition for decay
as his older sister, she had purposefully scheduled his first visit
early. I vividly recall the look of disappointment that flashed across
her eyes. She looked at me, reading my expression, and instantly knew
the news was not good. I explained that William had serious decay on
his top front four teeth. In the next courageous moment, Renee recovered.
Her look of disappointment was replaced with a posture of tenacious
determination. She and I had been down this road before. These previous
experiences had afforded us the opportunity to forge a strong relationship
of mutual empathy and respect. I believe that foundation of trust was
the pivotal element that allowed us to overcome William's decay issues.
It is important, at this
point, to review the causes of decay. William's mother and I had to
understand what we were up against in order to combat it effectively.
Dental decay (caries) is caused by bacteria that live in plaque on the
teeth. A tooth is essentially a hollow piece of bone with an enamel
cap. Enamel is just like glass. There are some species of bacteria,
of the many that live in the typical mouth, that produce more acids
than others. When acid meets glass, the glass is etched. The same process
occurs in the mouth. Bacteria eat sugars that pass through the mouth
and make acids. Acid then etches the tooth surface a little at a time
until the enamel is penetrated. Thus, a cavity is formed. This simple
explanation presents more questions than answers. One of those questions
is, "Why do some children have caries and others do not?"
The most common type of
decay is on the chewing surfaces of back teeth. This type of decay is
responsible for those silver fillings many of us have. It is caused
when the deep ditches and grooves at the base of the tooth form incompletely.
This tendency to have deep grooves in teeth may run in families. Sealants
are an early remedy for these types of cavities. Ask your dentist.
The type of decay found
in nursing caries occurs between and on the smooth surfaces of teeth.
This decay pattern is believed to be infectious. Certain strains of
high acid producing bacteria are passed from a caregiver to the infant
when teeth first erupt into the mouth. Interestingly, the child must
have teeth in order to support the organisms and the transfer occurs
through saliva-to-saliva contact. Therefore, if the mother has a history
of extensive dental decay between and on the smooth surfaces of her
teeth, she should not share spoons, clean pacifiers with her mouth,
or allow her saliva to contact her infant's mouth. Additionally, these
mothers should be seen by their dentist before the infant has teeth
in order to lower the proportion of high acid producing bacteria in
the mother's mouth, thereby lowering the probability of infecting the
infant. Once individuals are infected with these bacterial strains,
they will carry them throughout life or until they lose all their teeth.
The percentage of general population having relatively high levels of
high acid producing bacteria is estimated to be around 20 percent; therefore,
at least 80 percent of infants can and do sleep at the breast and with
bottles and have few problems. The key is to discern between infants
who carry these strains of "bad" bacteria and those that do not.
Ideally, foreknowledge could
prevent an infant from being infected with "bad" bacterial flora during
the first two to three years of life. However, when a child already
carries these bacteria, prevention is no longer possible, and management
of these bacterial populations becomes the chief concern. The goal is
to drive down the percentage of high acid producing bacteria while allowing
low acid producing bacteria to flourish.
William's mother and I discussed
at length the available options for management of his oral flora. Normally
I would recommend optimizing hygiene and fluoride exposure while curtailing
the frequency of carbohydrate exposure. Parents would brush their child's
teeth three to four times a day, massage a fluoride gel onto the teeth
at bedtime, and limit the child's access to the breast. In this case,
Renee explained that she would not limit William's feedings as it would
defeat integral nurturing and nutritional needs.
Frequency of feeding becomes
an issue when a child is a carrier of high acid producing bacteria.
These bacteria produce more acid than their "good" bacterial counterparts.
Additionally, these "bad" bacteria can tolerate higher levels of acid
in their environment. With constant feedings and constant sugar exposure,
the ecology of the mouth changes to actually select for the "bad" bacteria,
while selectively killing off the "good" guys. Within three months of
this pattern being established, the "bad" bacteria can account for 75
percent of the flora of the mouth. At that point, every exposure to
any sugar source proliferates this established ecosystem while producing
very high levels of tooth dissolving acids. The trick is to reverse
the entire process.
We did manage to reverse
the increased proportion of high acid producing bacteria in William's
mouth. Our success came as a result of Renee's understanding of this
complex process and her adherence to management regimens.
The management of a micro-ecosystem
of a mouth gone bad involves the control of three components. Those
are the diet of the oral flora, hygiene, and fluoride exposure. As we
discussed earlier, frequency of feeding becomes an issue because increased
feedings increase the overall amount of time the bacteria in the mouth
are exposed to sugars. Therefore, as far as the teeth are concerned,
it would be better for an infant to consume a large amount in one fast
feeding rather than graze on small amounts all day long. Reality usually
places a nursing child somewhere in the middle of these extremes. When
trying to control simple carbohydrate exposure, we normally attempt
to negotiate a movement toward optimized feeding patterns rather than
change them completely. Our experience has been that infants are usually
recalcitrant about changing their feeding schedules.
All this means that of the
three components to be controlled in a breastfeeding infant, diet or
frequency is probably not going to change significantly. Therefore,
paramount efforts must be placed on hygiene and fluoride. Hygiene is
the simpler of the two. Teeth should be brushed as soon as they erupt.
Since the bacteria are being fed constantly, they are capable of creating
large amounts of plaque (their house), acid (bacterial poop), and many
other bacteria. An infant who feeds throughout the day and night needs
to have his teeth brushed frequently. This can be accomplished with
a small head, soft bristle brush, and a damp washcloth. The brush will
do a better job of breaking up and removing the plaque, but at a minimum
the teeth should be wiped with a washcloth after each feeding, if possible.
The last component to be
considered are fluorides. Some caution must be exercised with these
agents. If a child swallows any form of fluoride it is quickly absorbed
and a corresponding spike in fluoride blood levels will occur. These
relatively short lived elevations in plasma fluoride are usually harmless
to the child but repeated exposures have been linked to dental fluorosis,
which can cause a chalky speckling on the front, permanent teeth. We
have found the best way to optimize topical fluoride exposure is for
an adult to massage a small amount of fluoride gel onto the child's
teeth with their fingers and wipe out the excess upon completion. The
effect of increasing the fluoride exposure is twofold. First, it greatly
enhances remineralization of the starts of little cavities. Second,
fluoride disrupts the enzymes that the "bad" bacteria use to move sugars
intracellularly. This action makes it tough for them to live and reproduce.
Therefore, topical fluoride will actually select for the "good" bacteria
while inhibiting the "bad" bacteria.
A combination of measures
reached through a give and take spirit allowed us to stop William's
decay process. Because Renee felt comfortable enough to describe William's
feeding habits accurately, and because I respected her judgment of what
was best for her child, we were able to function as a team. What could
have been a potentially frustrating and disappointing experience with
a disastrous outcome became an opportunity for growth and development.
References
Aaltonen, A.S. and Tenovuo,
J. Association between mother-infant salivary contacts and caries resistance
in children: a cohort study. Ped Dentistry 1994; 16(2):110-16.
Alaluusua, S. et al. Prevalence
of caries and salivary levels of mutans streptococci in 5-year-old children
in relation to duration of breastfeeding. Scan J Dent Res 1990;
98(3):193-96.
Arnold, R.R. et al. A bactericidal
effect for human lactoferrin. Science 1977; 197:263-65.
Roberts, G.J. et al. Patterns
of breast and bottle feeding and their association with dental caries
in 1- to 4-year-old South African children. 1. Dental caries prevalence
and experience. Comm Dent Hlth 1993; 10:405-13.
Roberts, G.J. et al. Patterns
of breast and bottle feeding and their association with dental caries
in 1- to 4-year-old South African children. 2. A case control study
of children with nursing caries. Comm Dent Hlth 1994; 11:38-41.
Torney, RH. Prolonged, on-demand
breastfeeding and dental caries--an investigation. M.Dent.Sc.
thesis 1992.
Wendt, L.K. et al. Analysis
of caries-related factors in infants and toddlers living in Sweden.
Acta Odont Scand 1996; 54(2):131-37.
Last updated Friday, October 13, 2006 by njb.
Page last edited Sun Oct 14 09:30:18 UTC 2007.
