Professor of Oral Biology
College of Dentistry
Richard Lamont’s research addresses fundamental questions in basic microbiology and pathogenesis and is pointing to new strategies to control infectious diseases. Periodontal diseases are among the most common bacterial infections of humans and almost all adults will experience some form of periodontal disease in their lifetime.
While severe periodontal disease is the major cause of tooth loss, it has recently become apparent that periodontal infections can also be associated with severe systemic conditions such as coronary artery disease and preterm delivery of low birth weight infants. Study of etiology of periodontal diseases is complicated by the fact that many of the bacterial pathogens are also present in healthy individuals. It seems that, over centuries of evolution, the bacteria and the host have learned to live together and inflict minimal harm on each other. Disease only occurs when this balance is upset.
Lamont’s research is focused on understanding the nature of the event or events that initiate the shift in personality of the bacteria from good guests to badly behaved ones. This involves global analyses of the nature of the adaptation that occurs when bacterial and host cells first encounter one another. By understanding the molecular and cellular processes that allow peaceful cohabitation or that trigger destructive consequences, it may be possible to identify targets for novel therapeutics designed to maintain the bacteria-host interactions in a state of harmony. As bacteria become increasingly resistant to conventional therapeutics, new treatments such as these are sorely needed. The work has resulted in over a hundred scholarly articles and several books and book chapters. Additionally, Lamont’s research has been featured in Science magazine and the Wall Street Journal. Over the next three years, Lamont intends to continue the molecular dissection of host-bacterial interactions in order to reconstruct a detailed picture of the sensing and response mechanisms that constrain bacterial pathogenic potential.