After completing his studies in biochemistry, biology and chemistry at Penn State University, Robert G. Quivey, Jr., continued there to earn his master’s degree in Genetics, and then a PhD in Microbiology at the University of Texas at Austin. He joined the University of Rochester in the mid 1980’s to work in the new field of bacterial molecular biology and the genetics of Streptococcus mutans. He was named the Center for Oral Biology’s director in 2009. Word of Mouth caught up with Dr. Quivey to learn what’s new in his lab.
Q. For those of us who are not dentists or scientists, what is Streptococcus mutans?
A. S. mutans is a bacterium that grows on the teeth of almost everyone’s mouth. W.D. Miller discovered the bacteria in 1890, but it was J. Kilian Clarke who named it S. mutans in 1924. S. mutans eats some of the sugar leftover on your teeth from your food, and also makes an acidic chemical called lactic acid. Without proper attention, dental plaque will accumulate and the S. mutans will eventually cause cavities, also known as dental caries. Caries is the Latin word for rottenness.
Q. Explain the process of how S. Mutans causes harm to our teeth.
A. Generally, the S. mutans, or this microbe or “bug” that grows on the teeth, is passed to babies after their teeth erupt. Most often, family members pass the microbe on to their children. The organism infects the mouth by using the sugars we eat in our diets to make two main products: 1) lactic acid, which causes tooth enamel to begin decaying, and 2) a gooey film on teeth that is also made of sugar that has been strung together to make the film. Almost everyone has felt that film on their teeth and it is because of S. mutans that the film is produced.
The film, which is really called dental plaque, or, the plaque matrix, is actually a very busy place. Many oral bacteria are captured in the matrix, as well as food particles, and S. mutans itself. In fact, after we are infected with S. mutans, it is there, in our mouths for virtually the rest of our lives. It’s a tough bug to get rid of. Our work is designed to find ways to reduce the ability of the organism to compete with the other bacteria in the mouth, or to stop its growth altogether, hopefully leading to the end of dental caries.
Q. Why does this topic interest you?
A. The work, as part of a large number of studies being conducted in labs around the world, has been a great deal of fun. We get to experience and observe biological events that have not been identified by anyone previously. The joy of discovery is profound. In addition, the real possibility of contributing to reducing the impact of a disease that is nearly universal, but also far more prevalent in those that cannot manage their own care or in those affected by severe or life-threatening disease, is greatly motivating. The opportunity to perform these studies with some very smart graduate students and outstanding technical assistants here at the University of Rochester, has made the job simply wonderful and a great gift in its own way.
I love the challenge of trying to outsmart a “bug” that has been around a long time, at least as far back as early-man, and one that has evolved to perfectly fit our lifestyle of eating a lot of sugary and starchy foods. The bacterium has also evolved ways to effectively compete with hundreds of other oral bacteria, so that in the plaque matrix, S. mutans is often the most dominant bacterium. The additional challenge is to find ways to eliminate S. mutans and maintain the “healthy” bacteria in the mouth that won’t cause disease.
Q. Describe your approach to this complex challenge.
A. The projects in our laboratory have focused on ways to prevent S. mutans from using its own tools that allow it to compete with other bacteria. These tools include proteins and fatty acids, which S. mutans uses to protect itself from its own lactic acid buildup and the toxic products that other bacteria produce. Every bacterium in the mouth has ways to carve out its own territory. Our approach to preventing dental disease, sometimes referred to as a probiotic approach, is to learn how to encourage these other non-pathogenic, or non-disease-producing bacteria to grow, in order to prevent S. mutans from growing.
Q. What have you learned?
A. We have made some progress on our goal of identifying key parts of the S. mutans strategy for infecting teeth and reducing the growth of healthy bacteria. Using tools that are common in molecular biology, we have identified genes in S. mutans that are important for the organism in its competition with healthy species of oral streptococci. We have shown that eliminating these genes from S. mutans results in a substantial loss of ability to cause disease, and in S. mutans ability to compete with the healthy oral streptococci.
The results of our experiments have been published in international scientific journals and we will continue to develop what we know into ways to prevent the disease from occurring in people.