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A Deadly Synergy

Periodontal disease might not just be a consequence of diabetes—but might also exacerbate the disease.

By Wendy Orent // Summer 2006
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Type 2 Diabetes, obesity, periodontal disease

Courtesy of J. Clifford Rigby

Periodontal disease, which destroys bone holding teeth in place, as in these X-rays, may also worsen diabetes or even help it develop.

The connection between periodontal disease and systemic illness, including cardiovascular disease and diabetes, has been known for some time. Louis Rose, professor of periodontics at the University of Pennsylvania School of Dental Medicine, even calls periodontal disease “the sixth complication of diabetes”—after heart disease, kidney disease, blindness, nerve damage and altered wound healing.

According to Rose, uncontrolled diabetes may lead to severe and rapidly progressive periodontal disease. Inflamed gum tissues form deep pockets brimming with pus and bacteria. Bone is absorbed; teeth lose their anchors in the jaw, get loose and may fall out. But this isn’t a one-way street. Of the numerous pathogens in gum tissue, Porphyromonas gingivalis—an invasive gram-negative anaerobic bacterium, a germ that grows under conditions of little or no oxygen—is the most prevalent and probably the most dangerous. It may also promote diabetes. (Christopher Cutler of the School of Dental Medicine, State University of New York at Stony Brook, says P. gingivalis has been found in atheromatous plaques in the blood vessels, and may play a role, along with other oral bacteria, in promoting heart disease as well.)

P. gingivalis grows in gum pockets and around teeth and releases a poison known as an endotoxin, or lipopolysaccharide. When the germs are in abundance, a high level of endotoxin accumulates in these gum pockets. Some is shed into the bloodstream and some is released when the bacterium dies.

This endotoxin, which forms the structural envelope of P. gingivalis, has a dual function. First, according to Cutler, the structure of the endotoxin tricks the body into not recognizing the germ as foreign, as an enemy. So the bacterium is less likely to be eliminated by scavenging immune cells. Second, the endotoxin produces inflammation by interacting with immune cells that release pro-inflammatory cytokines—the same chemicals pumped out by large, leaky fat cells.

Anthony M. Iacopino, associate dean for research and graduate studies at the Marquette University School of Dentistry, explains that when white blood cells such as monocytes, dendritic cells and polymorphonuclear leukocytes, all major components of cellular immunity, come into contact with the bacterial endotoxin, they release pro-inflammatory cytokines, and inflammation begins. “When the immune cells see lipid levels elevated,” says Iacopino, “they get very angry—and they release more pro-inflammatory cytokines. These, in turn, do just what all other pro-inflammatory cytokines do—they alter fatty acid metabolism. That releases more lipids; and lipids, in the bloodstream, do a lot of bad things, such as contributing to atherosclerosis.”

For the person already at risk for diabetes, the action of P. gingivalis may make matters worse. Though Iacopino and fellow researcher Cutler insist that neither existing experimental data nor clinical observations suggest that P. gingivalis and other gum pathogens actually cause diabetes, they have argued, in a series of compelling articles, that diabetes and gum disease exist in synergy.

One way to help apply the brakes to this cytokine/inflammation/lipid loop is to treat one of its causes—periodontal infection. Oral infections are chronic and long term, producing a constant inflammatory process that is slowly destructive. The persistent inflammation caused by elevated lipid levels has much the same effect, and putting these two systems together seems to produce a deadly combination.

What’s worse, this constant inflammation provides periodontal germs with exactly the environment they like. The immune cells that collect in the gums release cytokines that activate osteoclasts, a type of cell that absorbs bone. Cytokines also shut down the production of another type of bone cell, osteoblasts, which serve to build up bone. Meanwhile, marauding osteoclasts cause jaw destruction and loosen teeth, creating even deeper pockets—an environment in which the oxygen-hating P. gingivalis and other gum pathogens thrive. Perhaps disturbing the regulation of this entire system is the gum germ’s way of manipulating the body to produce a better environment for itself. Whether P. gingivalis has actually evolved such a strategy, or whether the whole inflammatory process is an incidental effect that happens to benefit gum pathogens, is impossible to say.

But the feedback loop between these twin inflammatory processes is clear. According to Cutler and Iacopino, treating gum disease helps control severe diabetes and controlling diabetes helps control gum disease. Rheumatoid arthritis and other long-term inflammatory conditions may show a similar kind of feedback loop, says Cutler.

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