In an in vitro study of human gingival tissue, researchers discovered that despite a plethora of antibodies present at the site of inflamed gum tissue, a protein called RANKL that is expressed by immune cells is able to override the body's method of defense.

"It's a groundbreaking discovery because it truly gives (us) a new understanding of periodontal disease," said lead author Dr. Toshihisa Kawai, an associate professor at the Forsyth Institute, an oral science research organization.

The study, which will be published in the September issue of the American Journal of Pathology, is the first experiment in human tissue to show that immune cells harm -- not help -- bones around the teeth. The research confirms similar findings from animal research.

However, Kawai does not know if results will hold true for people.

More than one in three Americans over 30, or almost 36 million people, have periodontitis, according to the American Academy of Periodontology. The disease begins mildly as a chronic bacterial infection, then leads to gingivitis, in which plaque inflames the gums. Left untreated, the plaque spreads below the gum line and spurs the growth of toxins, which in turn instigate an inflammatory response in the body -- the hallmark of periodontitis.

The progression of the disease can be gruesome, as the bones supporting the teeth slowly degrade and cause the gums to separate from the teeth. Gum disease is a major cause of tooth loss in Americans.

Yet for decades the exact pathology of periodontitis has remained out of reach for scientists. In recent years researchers have been working to explain why the bones of the jaw continue to break down despite the fact lymphocytes, or immune system white blood cells, are so abundant. These lymphocytes, which include T and B cells, produce hefty amounts of antibodies to act as weapons against the bacteria.

Usually, the immune system responds to bacteria by protecting the body against it. But in the case of periodontal disease, the opposite occurs: Kawai and colleagues found immune cells also produce an "unwanted pathogenic factor" -- the RANKL protein. This protein regulates osteoclasts, or cells that destroy bone.

In the laboratory culture, the RANKL proteins expressed on the immune cells were potent enough to activate the osteoclasts to disintegrate the bone.

Kawai's data suggests RANKL is a key player in bone loss and periodontal disease, said Dr. Denis Kinane, the associate dean for research at Kentucky's University of Louisville School of Dentistry.

"We don't really understand the path of periodontitis, but we're building up pieces up slowly that could be important in the jigsaw," he said.

Understanding RANKL -- and how to suppress it -- could aid doctors in detecting patients who are susceptible to the condition, Kinane said.

"If it's true that RANKL is pivotal in bone loss, it could give us a target," Kinane said. "We're always looking to understand the pathology of the disease and improve diagnosis."

Those particularly at risk for gum disease are smokers and diabetics. Risk factors include tobacco use, stress, genetics, hormonal changes and poor nutrition. Recent studies have also linked periodontitis to heart disease and low-birth-weight babies.

Kawai has now turned his focus on how to prevent immune cells from producing RANKL. In rat models he has been able to interrupt RANKL expression. Kawai hopes to find chemical compounds or other strategies to inhibit the production in diseased tissue.

"Teeth are very important to provide a joyful life. There is a huge demand to prevent periodontal disease," he said.

For more information: http://www.perio.org/consumer/disease_facts.htm

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