Smoking Increases Risk of Oral Lesions, Delays Healing Following Periodontal Treatment

SAN ANTONIO -- Smoking can increase the chances of developing precancerous oral lesions and other types of tissue abnormalities, and can interfere with healing after treatment for gum disease, results of two studies conducted by researchers at the University at Buffalo School of Dental Medicine have shown.

The first study was presented today at the American Association of Dental Research meeting in San Antonio, Texas. The second study will be presented Friday.

In the first study, UB researchers sought to evaluate the impact of various risk factors on the development of oral lesions ranging from canker sores to tumors. These lesions can occur on the lips, tongue, cheeks, palate, floor of the mouth or any other soft tissue in the mouth.

A UB dental research team headed by Julie Cianciola, a dental student under the mentorship of Sara G. Grossi, D.D.S., UB clinical assistant professor of oral biology, assessed the impact of age, gender, education, subgingival microbial flora, smoking and alcohol on the development of lesions in 1,426 subjects.

Results showed that of all the variables examined, smoking was the only factor associated with all of the most frequently observed abnormalities.

The data showed that 37.6 percent of current smokers had oral lesions, compared to 29.3 percent of non-smokers and 34.5 percent of former smokers. The most frequently observed abnormalities were leukoplakia, benign lesions that can provide favorable conditions for the development of malignancy. Leukoplakia were found in 15.7 percent of current smokers, but in only 8.7 percent of non-smokers.

Oral varicose veins, another type of lesion, were present in 8.8 percent of smokers, but in only 3.1 percent of non-smokers. A third type of lesion, capillary haemangioma, also was seen more often in smokers than non-smokers.

"The finding that two types of vascular lesions were found more frequently in smokers adds to the evidence linking tobacco to vascular disease, both in microcirculation and macrocirculation," Grossi said.

Many types of lesions disappeared when subjects stopped smoking, but stopping smoking did not reverse the deepest tissue damage, Grossi noted.

Additional researchers on the study were Alex Ho, oral biology statistician; Robert Dunford, senior scientific programmer in oral biology, and Robert Genco, D.D.S., Ph.D., chair and SUNY Distinguished Professor in the UB Department of Oral Biology.

The research was supported in part by grants from the U.S. Public Health Service and the William E. and Grace S. Mabie Fund.

In addition to increasing the chances of developing oral lesions, smoking is a risk factor for periodontal disease, commonly known as gum disease. However, little is known about the effect of smoking on gum healing after treatment for periodontitis.

In the second study, designed to answer this question, a UB team headed by Grossi followed 55 smokers and 88 non-smokers diagnosed with substantial periodontitis and assessed them before and after treatment to determine the amount and rate of healing.

Results showed that although both groups had comparable disease and received the same treatment, the non-smokers healed better than the smokers.

"This finding has profound implications for the clinical management of periodontal disease," Grossi said. "Smokers do not respond as favorably to treatment as non-smokers.

"These were very conservative treatments," she added. "For more invasive procedures, such as surgery, the problems will be compounded. This is evidence of an adverse effect on the immune response."

Treatment for all participants in the study consisted of four to six sessions of subgingival scaling and root planing. The amount of healing was assessed three months after the last treatment.

The number of sites still prone to bleeding had decreased by 20 percent in non-smokers, compared to only 12 percent in smokers. Pocket depth, a measure of the amount of gum detachment at a tooth and a standard indicator of the seriousness of periodontal disease, also improved more in non-smokers than in smokers.

In addition, bacteria that cause periodontal disease were eliminated in non-smokers after treatment, but were still present in smokers.

Members of the research team, in addition to Grossi, were Joseph Zambon, D.D.S.; Eli Machtei, D.M.D.; Robert Schifferle, D.D.S.; Sebastiano Andreana, D.D.S.; Diane Cummins, Ph.D.; Godfrey Harrap, Ph.D., and Robert Genco, D.D.S., Ph.D., all of the UB Department of Oral Biology.

The study was supported in part by grants from the U.S. Public Health Service and Unilever Research.