These bacteria are nasty characters. Just listen to their names. Porphyromonas gingivalis. Campylobacter rectus. Tiny organisms surviving in a place that isn’t particularly friendly — the mouth.
“They’re constantly barraged with serum and white blood cells trying to kill them,” says Steven Offenbacher, professor of periodontology in the School of Dentistry. “But they have adapted to survive in that habitat. They have evolved just like an organism that lives in a hot spring or the bottom of the ocean.” That adaptation makes these bacteria hardy, and it makes them more able to spread.
No wonder then that these bacteria and the periodontal disease they cause are implicated as accomplices in some serious cases — premature birth and heart disease. The links to growth restriction and premature birth are well documented, while the link to heart disease is still controversial.
Periodontal disease begins when the bacteria in the sticky plaque on your teeth results in the gums becoming inflamed. That plaque can spread and grow below the gum line. Toxins produced by the bacteria stimulate inflammation, one of the body’s first lines of defense. But if that inflammation continues, the tissues and bone supporting the teeth break down, and the gums and supporting bone can separate from the teeth.
Most people have some gingivitis. But why do some of us go on to develop periodontal disease?
Poor oral hygiene is one contributor to periodontal disease, but it isn’t the only cause. Even in the United States where oral hygiene is advanced, the rate of the disease is about the same as in less-developed countries — one in five.
Another reason may be differences in the inflammatory response, says Patrick Flood, director of the Comprehensive Center for Inflammatory Disorders. Some people are genetically more susceptible to inflammation than others. James Beck, professor of dental ecology, says, “Two people could be exposed to the same organism, and one might have a really big reaction to it and the other might not have any at all.”
Inflammation starts when bacterial invaders encounter sentinel cells that patrol our bodies. These sentinels defend us by destroying the invaders, but they also call up reinforcements via release of chemical signals. Those chemicals help cause inflammation’s heat, itchiness, swelling, and pain. But what they are actually doing is signaling for help. Specialized defenses such as antibodies receive these signals and attempt to fight off the invader.
But just as important as the body’s signal to respond to invaders is the signal to “stand down.” Eventually, all the inflammatory cells must return to a state of surveillance or go through controlled cell death. If inflammation becomes chronic, then problems can start. For instance, once the body starts to respond to the bacteria in the mouth, inflammatory cells congregate and, if they don’t retreat, they can start to attack the support structures that the bacteria live on — your teeth.
Right now researchers are trying to learn exactly how the body regulates the inflammatory response so that we can learn to control it. At this stage we can do some systemic things to lessen the severity of arthritis or periodontal disease — take an antiinflammatory drug such as ibuprofen, for instance. But we don’t know enough about inflammation to target it in specific parts of the body. Flood says, “The key for us in biology will be to make smart bombs to go just where we want them to go and turn off just what we want them to turn off.”