Date Published: March 27, 2014
Publisher: Public Library of Science
Author(s): Sarah E. Whitmore, Richard J. Lamont, William E. Goldman.
Over a number of years, epidemiological studies established several well-defined risk factors for cancer, including age, heredity, diet, tobacco use, chronic viral infections, and inflammation. Paradoxically, the success of these studies left little room for incorporation of any new factors or causative agents, and, consequently, the idea that a bacterial infection could contribute to cancer was generally disregarded. However, landmark studies in the early 1990s established Helicobacter pylori as a causative agent of gastric cancers, resulting in a paradigm shift regarding the relationship between microbial agents and cancers . Indeed, in 1994, H. pylori became the first bacterial species to be officially recognized by the World Health Organization as a definite cause of cancer in humans. Since then, there has been a growing body of evidence supporting an association between specific microorganisms, including those in the oral cavity, and various types of cancers.
Epidemiological studies associate oral bacteria temporally and spatially with certain cancers and render involvement in the initiation or progression of the disease plausible. However, it is equally plausible that early undetected cancer, or precancerous lesions, facilitate the colonization and growth of oral bacteria. If these organisms are active participants in the disease process, then a mechanistic basis that would support an etiological role should exist.
Both P. gingivalis and F. nucleatum have attributes consistent with a role in cancer development and progression. The question then arises as to why the widespread infection with these organisms leads to disease in only a limited number of individuals. Part of the answer may relate to the community nature of oral infections and the potential constraining influence of other bacteria. However, another consideration is the multifactorial etiology of cancer, and, within this framework, specific oral bacteria and their associated inflammatory insults may play a contributory, but not exclusive, role.