Variation in Gene for Fibrinogen Associated With Severe Gum Disease, UB Oral Biologists Show

CHICAGO -- A variation in the gene that expresses fibrinogen, a protein that aids coagulation and accumulates in the blood stream in response to infection, may help to explain why some people develop severe gum disease while others do not.

In findings presented here today (March 10, 2001) at the annual meeting of the American Association for Dental Research, oral biologists from the University at Buffalo School of Dental Medicine reported that adults with severe gum disease, or periodontitis, were more likely to exhibit a genotype associated with high plasma fibrinogen levels than healthy controls.

Blood sample analysis also showed that the periodontitis patients had significantly higher levels of fibrinogen in their blood than did persons without gum disease.

"Most diseases, especially infectious diseases, are associated with a complex array of risk factors, any one of which increases the chances of a person developing the disease," said Ernesto De Nardin, Ph.D., UB associate professor of oral biology and microbiology and senior author on the study.

"Persons with the rare form of the fibrinogen gene would add that risk factor to any others associated with the development of periodontal disease. They should pay particular attention to their oral hygiene and perhaps visit their dentist more often than normal."

De Nardin and colleagues previously demonstrated that the presence of the rare H2H2 fibrinogen genotype in persons with periodontal disease provided one possible explanation for the known relationship between poor oral health and heart disease.

Elevated plasma fibrinogen levels are known to be an independent risk factor for cardiovascular disease by increasing the propensity for blood clots. In the current study, UB oral biologists took this research further, studying the incidence of the rarer fibrinogen genotype in persons with periodontal disease in an effort to explain in part the variance of the disease in adults.

Besides its role in blood clotting, De Nardin noted, fibrinogen also can increase inflammation in three ways: by providing a framework for the accumulation of inflammatory cells, promoting the immune response and aiding in bacterial colonization, adhesion and invasion.

For this study, the researchers investigated the distribution of the two abnormal fibrinogen genotypes -- termed H1H2 and H2H2 -- and assessed fibrinogen levels in 79 persons with periodontitis and 75 persons without the disease.

Results showed that 51 percent of the periodontal patients had one of the abnormal genotypes, compared to 30 percent of the healthy controls. Further, risk of periodontal disease was found to be three times greater in persons with the H1H2 gene and six times greater in those with the H2H2 gene, compared to persons with the normal gene type.

The amount of fibrinogen in the blood stream also was about 10 percent higher in the periodontal group than in the healthy controls, De Nardin said.

Also contributing to the research were S.E. Sahingur, Ph.D., a student researcher in De Nardin's laboratory; A. Sharma, Ph.D., assistant professor of oral biology; Alex Ho, UB statistician, and Robert J. Genco, D.D.S., Ph.D., SUNY Distinguished Professor and chair of the UB Department of Oral Biology.

The study was funded by a grant from the National Institutes of Health.