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Early Childhood Caries

William H. Bowen, MSc, PhD, DSc, discusses the possibility of preventing dental caries before it even begins.

Q What is the focus of your research on caries at the University of Rochester?

A. Many people think a cavity is the disease, dental caries. This is a misnomer. A cavity is the result of the disease that has been occurring on the tooth anywhere from months to years. The researchers at the University of Rochester Center for Oral Biology, myself included, are hoping to eventually be able to take a sample of saliva and identify those people who have the disease and, then if necessary, increase the level of prevention in those who are at risk to actually prevent cavities from forming. We are looking at how plaque is formed and the methods and techniques needed to prevent plaque from becoming virulent.

Q. What makes dental plaque so virulent?

A. The prime microbial culprit in the etiology of caries is Streptococcus mutans. What makes S. mutans so dangerous is that it produces a number of different enzymes that enable it to promote plaque formation. In addition, it is an extraordinarily potent producer of acid. The enzymes are known as glucosyltransferases. They synthesize a glue-like material called glucan from sugar and the combination of sugar and starch. The enzymes produce a glucan that makes up the bulk of dental plaque.

Dental plaque is a true biofilm. It uses three distinct enzymes. One enzyme adheres to the tooth surface. Bacteria in general do not stick very well to tooth surfaces—certainly not to naked tooth surfaces and not to surfaces covered in saliva. However, if a little of this glue-like material called glucan is present, then their ability to stick goes up 100 or 150 fold. Probably 20% to 30% of plaque is made up of glucan.

Q. Are there other bacteria responsible for caries?

A. Not all of the microorganisms in plaque are S. mutans. But S. mutans influence the other bacteria enormously. For example, the glucosyltransferase enzymes produced by S. mutans can adhere to the surface of other microorganisms and convert them into glucan producers. They produce so much of these other enzymes that they roam free in saliva. I can take saliva from some caries active people and add sugar to it and actually see glue-like material forming. The enzymes have remarkable properties in that they cling to a very diverse range of surfaces. I have already mentioned that one of the enzymes in plaque biofilm adheres to the tooth surface. Another enzyme attaches to a group of bacteria and converts them into glucan producers. In a transmission electron micrograph of dental plaque, you can see that there is a matrix material and that every organism is covered by the matrix. The microorganisms have absorbed the enzyme. But it’s a different enzyme so you have one enzyme that provides the binding surfaces to the tooth and another enzyme that provides the bulk of the plaque. The enzyme that makes up the plaque can also use starch to make the glucan as long as some sucrose is present. This explains the well-known phenomenon that combinations of sugar and starch are more cariogenic than either alone.

Q. Can these enzymes be stopped?

A. We’ve looked at a whole range of compounds that will inhibit these enzymes. The remarkable fact is that there are many compounds that will inhibit the enzymes in solution but when the enzymes are absorbed onto a surface, which is what happens in the mouth, the enzymes are extraordinarily difficult to inhibit.

The other area we’ve been actively pursuing is creating a saliva test. We’d like to be able to diagnose who has dental caries before lesions occur. This is particularly important in children at risk for childhood caries. Most kids don’t see a dental professional before age 2 and a half, 3, or 4. At the same time, many of these children have early childhood caries and by the time they see a dental professional, total devastation has occurred. Many of them end up having teeth removed and crowns placed. On the other hand, many babies go to well baby check ups with their physician as often as every 3 or 4 months. We would like to take a sample of saliva in the physician’s office to see if children have caries and then they can be referred to a dental professional for prevention.

THE SALIVA TEST

Q. Is the research on the saliva test moving forward?

A. What we’ve done so far is to use a monoclonal antibody to measure the amount of enzymes in the saliva. We’ve done a cross-sectional study and found that there is an enormous correlation between the amount of glucosyltransferase B in saliva and the prevalence of tooth decay. The next step we want to take is to determine whether this can be used to predict those who will develop cavities. This is extraordinarily promising and our goal is to end up with the equivalent of a pregnancy test. You take a drop of saliva, put it on a slide when you go to the physician’s office, and by the time you leave, you’re ready for a referral to a dental professional or not. This would be an enormous advancement in prevention, in reducing cost of dental care, and in improving access to care.

Q. How is the caries infection transferred?

A. The caries pattern in children follows that of the mother or the primary caregiver, more so than the father. This is most likely because the microorganisms are transmitted from mother to child and also the dietary patterns are mostly influenced by the mother.

The Caries Vaccine

Q Is a caries vaccine in development?

A. The caries vaccine is a futuristic concept. There are believers and nonbelievers and I’m somewhere in between. The premise of a caries vaccine is based on mucosal immunity. It’s the same kind of immunity that gives you protection against influenza and other diseases of the mucus membranes in various parts of the body. But the tooth is an inanimate object sticking out in a sea of saliva with plaque adhered to it. The problem is how to get a protective antibody on to the tooth surface in a very hostile environment.

Many researchers have used topical antibodies. For example, we’ve taken antibodies that inhibit glucosyltransferase prepared in eggs and given it to rats in their drinking water and seen a 30%-40% reduction in the number of carious lesions. The concept can work, the problem is in identifying the appropriate antigen in enough concentration in saliva to give protection. You can’t vaccinate into the salivary glands themselves because it will encourage inflammation. Without a blood supply on the surface of teeth, there isn’t a systemic delivery path.

Q. Are there are any other caries diagnostic devices being developed?

A. Currently, the disease dental caries is not being detected. We detect carious lesions, ie, loss of enamel. The disease dental caries occurs, within the milieu of dental plaque, on the tooth surface and may be active for as short as a few weeks or long as 18 months before a carious lesion appears. The traditional methods to detect carious lesions continue to be used in practices possibly with less emphasis on the use of a dental probe. Early white spot lesions may have the capacity to remineralize, which would be lost if a probe is placed in them. Methods to detect loss of enamel are in advanced stages of development but have not been introduced in large measure.

We think mechanical caries detection is comparatively late in the disease process. In order to detect carious lesions, some tooth loss is present. We would like to make a diagnosis long before any loss of tooth structure has occurred. This is why we’re working on the saliva test. There are some saliva tests now that are effective in looking for S. mutans but the problem is they take 48 to 72 hours to get results, creating a barrier between knowledge and action. We would like to get a diagnosis made in the physician’s office so action can take place immediately.

There’s little point in placing crowns and extracting teeth in children if action is not also taken with the rest of the family. So it’s important to evaluate the level of oral hygiene and the S. mutans levels of the main caretaker because if the same pattern continues, the child will be back in 6 months with the same number of lesions. So I regard early childhood caries as a family problem and one that should be treated as such. We’ve known that caries is an infectious and transmissible disease but we don’t really treat it as such do we?

From Dimensions of Dental Hygiene. March 2008;6(3): 20, 23.

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