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UofL study may help explain why gum disease is worse in smokers, but symptoms are fewer

by Julie Heflin last modified Dec 07, 2010 03:10 PM

Dec. 7, 2010            


           LOUISVILLE, Ky  - A study led by investigators at the University of Louisville School of Dentistry may provide a reason of how tobacco smoke contributes to gum disease. The results of the study were published early on-line in the November issue of the Journal of Dental Research. The study was funded by UofL.


“We have known that smokers are more likely to get gum disease and more likely to develop the plaque buildup that contributes to gum disease, but the clinical conundrum has always been why do they actually have less of the inflammation in and around their gums that we normally see in gum disease,” said David Scott, PhD, associate professor of oral health and systemic disease research at the UofL School of Dentistry and lead investigator on this study. “Our study sought the answer or answers to that question.”


The researchers obtained saliva samples from smokers and non-smokers both with periodontal, or gum, disease and without.


“We looked for molecules in the saliva samples that come from the bacteria that cause gum disease,” Scott said. “We found that tobacco smoke appears to induce changes to one of these molecules, lipopolysaccharide, or LPS. LPS normally induces inflammation in our gums but in smokers LPS is altered in such a way that fails to stimulate inflammation.”


When this happens, the inflammatory and immune system is less able to deal with these gum pathogens and so gum disease develops, Scott said.


Our bodies can recognize “foreign” compounds that are found on bacteria. LPS, present in bacteria such as the types that cause gum disease, is one of these foreign molecules and it acts as a stimulant of the immune system, Scott said. It is believed that the immune system’s ability to sense LPS is critical to the fighting off infection.


“The role of LPS is to trigger an immune response but we believe the interaction between bacteria and tobacco smoke makes bacteria produce LPS that we cannot recognize properly,” Scott said.


“In fact, by the time many of these patients start to have symptoms, their disease can be fairly advanced and may be less responsive to current treatments.”



The researchers compared saliva samples from 54 patients, including 22 smokers with periodontal disease, 15 smokers without periodontal disease, 15 non-smokers with the disease and 14 non-smokers without the disease.  The patients were treated at Ege University School of Dentistry in Izmir, Turkey. 


The next step will be to investigate why LPS from oral bacteria in smokers is not recognized and to see if gum disease may develop differently in smokers than nonsmokers. It may be that researchers will then be able to develop different prevention and treatment strategies for cigarette smokers. Scott and his team recently received a five-year, $1.8 million grant from the National Institutes of Health to continue the work.


            Other researchers involved in this project include Diane Renaud of UofL; Nurcan Buduneli and Basak Biyikoglu of the School of Dentistry at Ege University in Izmir, Turkey, and Lennart Larson of Lund University in Sweden.


            The abstract can be found on-line at .



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