Caries Update

THE GENETIC FACTOR

Q. In the February 2004 issue of Dimensions of Dental Hygiene, you discussed the bacterial, carbohydrate,and salivary factors involved in the caries process. Do you think there is also a genetic component?

A. Researchers have been looking for a genetic component relating to caries for many years with very little success. However, this doesn’t mean that a genetic component does not exist. A group at the University of Pittsburgh is looking at twins in the United States and has found interesting results, but they haven’t yet been able to pin it down to a particular gene. Many differences exist in saliva from person to person and it is very likely with some of the new molecular biology techniques that differences in saliva canbe pinned down, which would then go back to some gene in the body that’s driving the salivary production process. I believe that in the future, tests will become available for particular salivary components that will point to some salivary deficiency.

The different bacteria that are passed on from mother or caregiver to a child are important. Some mothers have virulent strains and others don’t, so obviously a big genetic diversity exists in these particular strains of bacteria. Research is being done on this connection. It may turn out that the genetic factors in bacteria are more important than the genetic factors in the host. However, we do have our own immune systems and some seem to be more immune to the pathogenic bacteria than others.

If we go one step further, it should then be possible to engineer strains of bacteria that would be benign rather than pathogenic. Jeff Hillman, DMD, PhD, at the University of Florida School of Dentistry, has a genetically engineered version of Streptococcus mutans that does not produce lactic acid. In terms of reducing decay, trials in rats have been successful and he has now progressed to human trials. At the moment, it’s difficult to tell whether this will be a plus or not because so many other bacteria add to caries as well, it’s not just the S. mutans.

Q. What is the mechanism of action in genetically altered bacteria?

A. Hillman has a strain of bacteria that preferentially colonizes and it tends to stop the other pathogenic bacteria from colonizing. The genetically altered bacteria is very good at forming its own niche and not letting others come in. This is mechanism one. The second mechanism is when the bacteria takes the fermentable carbohydrates and instead of producing lactic acid, which is the strongest acid that S. mutans and S. sobrinus produce, it produces acetic acid that is weaker and it produces less of it. The problem is that if there are other bacteria around, such as Lactobacillus, that produce lactic acid, this may not be as beneficial as we had hoped.

Q. What are pathogenic bacteria and benign bacteria?

A. The pathogenic bacteria are mostly strains of S. mutans and S. sobrinus. Much work is being done on virulence factors. How much acid do they produce under certain conditions? Do they preferentially colonize? Do they live better under acid conditions? Can they produce more acid under acid conditions than other bacteria? And another whole group of pathogenic bacteria is, of course, the Lactobacillus species, that produce predominantly lactic acid. They can live under acid conditions where the benign bacteria tend to die off. So in a high caries situation, more and more of these so-called acidogenic and ciduric bacteria that survive and thrive at the expense of benign bacteria.

There are actually hundreds of other species in the mouth and millions of benign bacteria generally live in the mouth. Pathogenic bacteria are an absolute minority—generally less than 1% of the total flora. Some fraction of that 1% are the real troublemakers and they are specific strains of each species.

THE MOTHER/CHILD RELATIONSHIP

Q. Do people with a high caries index have a higher count of the pathogenic bacteria?

A. It comes down to the caries balance. In the caries process, bacteria, fermentable carbohydrates, and lack of salivary function are the predominant pathological factors. Research has shown that, in general, more cariogenic bacteria exist in a high caries individual.¹ Also certain strains tend to show up. Fairly new work is being done at the University of California, San Francisco, and at this point, it seems that if certain strains are present, then the caries rate increases. At some point in the future, probably when I’m retired, there will be some ability to test these bacteria and know that one patient has more virulent strains than another and that the patient has passed these strains down to his or her children.

Q. How is it possible that in the same family, one child may be caries free while the other has rampant caries?

A. Again, this is a matter of caries balance. However, there is still much that is unknown. Was child A more resistant than child B to virulent strains that were passed on from mother or caregiver? Undoubtedly there is something there, an immune response, that means that the particular child was not colonized so much or even at all by the specific pathogenic bacteria.

There is the old concept that child A has soft teeth and child B has hard teeth. I think there is some validity in this concept but it is nowhere as simple as that. Certainly in all the teeth we’ve looked at, there are no particular soft teeth and hard teeth or more resistant teeth and less resistant teeth unless you get gross developmental deficiencies where the teeth are indeed more soluble. This is very rare compared to many families with one child who has more caries than others. For example, a family was referred to us with two teenage girls. One had a lot of caries and the other did not have any. The differences in their bacteria were major. One had considerable genetic diversity and the other didn’t. Genetic diversity means the number of strains. The mother had no decay and the child with no decay had similar bacteria to her mother. The other child with a lot of decay had no similarities to her mother’s bacteria, which was very surprising.

Q. What is Xylitol’s role in prevention?

A. Xylitol is a non-cariogenic sweetener, meaning the bacteria cannot ferment it. They can’t eat it and produce acids. It is comparable to sucrose except that Xylitol has one carbon less and it’s not fermentable. Humans can absorb it and take some energy from it, but the bacteria can’t. Not only are the bacteria not able to produce acids and not able to metabolize it, Xylitol has an antibacterial effect. It seems to inhibit their ability to adhere and grow in the plaque. Two studies showed that if a mother takes Xylitol four times a day during the first years of herchild’s life, the child has much less cariogenic bacterial growth and a decreased incidence of caries later on. It is pretty amazing that a substance that tastes good enough to be used in confectionary and chewing gum is one that the bacteria can’t feed on and that also has antibacterial properties.

Q. It’s an interesting concept to treat the child through the mother.

A. One of the concepts we need to push from an educational point of view is that mother and caregiver do pass on their bacteria to their children in the first several years of their lives and the earlier they colonize, then the more caries later. So if we can intervene with Xylitol, for example, or chlorhexidine treatments for mother or caregiver, this is an excellent way of stopping the infection.

AGE AND LIFESTYLE

Q. What role does age play in childhood caries?
A. The caries surveys show that around 12 years of age, there is a turning point toward more caries.² The percentage of caries-free children at the age of 12 is relatively high in the United States per the studies that had been published around 1989.2 At the age of 18, the number of caries-free young people has fallen to almost nothing. So during those teenage years, the incidence of caries skyrockets. The two highest caries groups are teenagers and people over 65.

Older people are more prone to root caries and their teeth are breaking down for various reasons and they are often changingtheir diet. With teenagers, once they hit puberty, their diet changes, they snack more frequently, and their hormones are changing drastically.

There are probably more pathogenic bacteria due to the diet change. Another large risk factor is orthodontic treatment. The moment those braces go on, the cariogenic bacteria population grows preferentially and the studies show this.³ Dramatic increases happen within months, which puts the teenage child at higher risk for caries. This continues until after the braces are removed. Hygienists can play a major role with these kids in terms of education and meticulous oral hygiene and increase fluoride treatments and antibacterial treatments.

TREATMENT

Q. Are antibacterial treatments effective?

A. When new caries arise in patients, fluoride usage is often increased to combat the caries challenge. This works to a point but eventually new caries occur in many patients. This is where antibacterial treatments play a role. The best option at the moment is chlorhexidine rinse. Rinses can be prescribed for kids and adults, with the recommendation of rinsing once a day for 1 week each month for up to 6 months, with a bacterial test before and after the 6 month period. Incorporating antibacterials swings the caries balance in the other direction toward halting the disease rather than letting it progress. Remineralization is great and it is the natural repair process, but it cannot overcome a severe bacterial challenge. I wish that dental hygienists were able to prescribe chlorhexidine rinse but they can recommend the prescription. Hygienists also play an incredibly important role in following up with the patient because a prescription is great, but if it is not used, it won’t work.

Q. What is the role of amorphous calcium phosphate in treating caries?

A. Our teeth are made of calcium phosphate, which is called carbonated hydroxyapatite, but it contains impurities that make it more soluble than pure hydroxypatite, which is one of the purest and least soluble forms of calcium phosphate. Amorphous calcium phosphate is non-crystalline, hence the name amorphous. It has a very simple chemical construction with calcium and phosphate ions together and it dissolves easily. When it dissolves, it produces calcium and phosphate that are available for remineralization. So theoretically, amorphous calcium phosphate could be applied and then it would slowly dissolve and slowly repair the tooth right there. For surface defects, such as initial stages of erosion or early surface decay, this really does work. In terms of remineralization of lesions below the surface—deep lesions that we know remineralize—I am not sure that amorphous calcium phosphates will play a big role.

Q. Is this more effective than fluoride?

A. With calcium and phosphate from the saliva and fluoride from a toothpaste or other topical source, they all have to diffuse down into the tooth and remineralize in the body of the lesion. With the amorphous calcium phosphate, theoretically at least, high calcium and phosphate concentrations are produced that precipitate material near or on the surface, which is good for surface defects, but it may not be useful for subsurface lesions.

Q. Some parts of the United States do not have fluoridated water and some communities want to end fluoridated water. How do you suggest oral health care professionals address this challenge?

A. What we need is fluoride coming from some topical source, including drinking water, in order to enhance remineralization. If we have a situation where people and families are using fluoride toothpaste twice a day, for example, we know this causes a dramatic reduction in dental decay. If we are trying to tip the caries balance, we can progressively add fluoride from various sources, including fluoride in drinking water. But the fluoride toothpaste, fluoride office topicals, fluoride mouth rinses, all work above and beyond the fluoride in the drinking water. If the drinking water is not fluoridated, then hygienists can recommend the daily use of fluoride in the home as a topical measure.
In high caries individuals, such as patients who come into the office with four cavities already, they are automatically at high risk for future caries. However, a caries bacterial test should be done as a baseline against which to measure the effectiveness of prescribed antibacterial treatments. The level of cariogenic bacteria must be reduced by using chlorhexidine mouthrinsing while the restorations are being programmed and completed. Also, to help swing the balance to stabilization, a high concentration prescription fluoride toothpaste (5,000 ppm fluoride) should be given for home use, as well as in-office fluoride treatment. Alternatively, for medium risk patients, all of the over-the-counter fluoride mouth rinses work as well in conjunction with daily use of a normal fluoride toothpaste.

REFERENCES

1. Leverett DH, Proskin HM, Featherstone JD, et al. Caries risk assessment in a longitudinal discrimination study. J Dent Res. 1993;72:538-543.
2. Kaste LM, Selwitz RH, Oldakowski RJ, Brunelle JA, Winn DM, Brown LJ. Coronal caries in the primary and permanent dentition of children and adolescents 1-17 years of age: United States, 1988-1991. J Dent Res. 1996;75(special issue):631-41.
3. Jordan C, LeBlanc DJ. Influences of orthodontic appliances on oral populations of mutans streptococci. Oral Microbiol Immunol. 2002;17:65-71.

From Dimensions of Dental Hygiene. February 2005;3(2):12, 14-15.