Oral bacteria may signal risk for pancreatic cancer
The amount of oral bacteria in the mouth may be associated with the risk of pancreatic cancer.
That’s according to a new study in the journal Gut, which found “significant associations” between antibodies for multiple oral bacteria and pancreatic cancer, which is difficult to detect and kills most patients within six months of diagnosis. Pancreatic cancer is responsible for 40,000 deaths a year in the United States.
This is an emerging issue in science, researchers say, but the importance of bacteria in cancer is growing.
“This is not an established risk factor,” said Brown University epidemiologist Dominique Michaud, Sc.D., the paper’s corresponding author. “But I feel more confident that there is something going on. It’s something we need to understand better.”
In a study of more than 800 European adults, Dr. Michaud and colleagues found that high antibody levels for one of the more infectious periodontal bacterium strains (Porphyromonas gingivalis) were associated with a two-fold risk for pancreatic cancer. In addition, subjects with high levels of antibodies for some kinds of harmless oral bacteria were associated with a 45-percent lower risk of pancreatic cancer—meaning the antibodies could have a protective effect.
The body generates antibodies as a response to foreign objects, like bacteria and viruses.
Other research has identified links between periodontal disease and pancreatic cancer, but Dr. Michaud’s Gut paper is the first study to test whether antibodies for oral bacteria are indicators of pancreatic cancer risk and the first to associate the immune response to harmless bacteria with pancreatic cancer risk. The physiological mechanism linking oral bacteria and pancreatic cancer remains unknown, but the study strengthens the suggestion that there is one.
“The impact of immune defense against both commensals and pathogenic bacteria undeniably plays a role,” said Jacques Izard, Ph.D., of the Forsyth Institute and Harvard University and co-lead author of the study. Commensal bacteria is harmless while pathogenic is harmful.
“We need to further investigate the importance of bacteria in pancreatic cancer beyond the associated risk,” said Dr. Izard.
Drs. Michaud and Izard researched data from the Imperial College-led European Prospective Investigation into Cancer and Nutrition Study, a massive dataset of more than 500,000 adults in 10 countries. From that population, they found 405 people who developed pancreatic cancer, but no other cancer, and who had blood samples available. The researchers also selected 416 demographically similar people who did not develop pancreatic cancer for comparison.
The researchers blinded themselves to which samples came from cancer patients and which didn’t during their analysis of the blood, which consisted of measuring antibody concentrations for 25 harmful and harmless oral bacteria. In their study design and analysis, they controlled for smoking, diabetes, body mass index and other risk factors.
An important element of the study design was that date of the blood samples preceded the diagnosis of pancreatic cancer by as much as a decade, meaning that the significant difference in antibody levels were likely not a result of cancer. Instead, the underlying mechanisms that link Porphyromonas gingivalis to pancreatic cancer could be causal, Dr. Michaud said, although much more research is needed to understand this association.
The researchers speculate that the association of high levels of antibodies for commensal bacteria and pancreatic cancer may indicate an innate, highly active immune response that is protective against cancer.
“Genetic determinants of immune surveillance clearly play a critical role in pancreatic cancer development,” the authors wrote. “Consequently, it is plausible that elevated levels of antibodies to oral bacteria in individuals serve as a marker for a genetically stronger immune response, providing protection against carcinogenesis.”
©2010 American Dental Association. All rights reserved. Reproduction or republication is strictly prohibited without the prior written permission from the American Dental Association.