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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.

(For William's mother's story, see "Coping with Dental Caries.")

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.
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