The Perils of Inflammation
Thomas Van Dyke, the chair of the Department of Applied Oral Sciences at the Cambridge, Massachusetts-based Forsythe Institute, explains the role of oral inflammation on systemic health—and how a little aspirin could help save lives.
Thomas Van Dyke is chair of the Department of Applied Oral Sciences, vice president of clinical and translational research at the Cambridge, Massachusetts-based Forsyth Institute and a lecturer at the Harvard School of Dental Medicine. He studies the role of inflammation in gum disease and its impact on systemic health.
Scientific American Custom Media: What’s the relationship between gum disease and inflammation?
Thomas Van Dyke: The American Academy of Periodontology [now] categorizes periodontitis [gum disease] as an inflammatory disease induced by bacteria, rather than an infectious disease. It’s not like you catch periodontal disease. All the damage that’s caused is really not the bacteria destroying tissue—it’s the host’s response: inflammation. That creates an environment in which bacteria in the mouth overgrows: there’s a feedback [mechanism] that then develops more disease.
SACM: How does oral inflammation influence other medical conditions?
TVD: All of the diseases associated with periodontitis are inflammatory diseases. Some we didn’t used to think of as inflammatory, like cardiovascular disease. It’s been demonstrated epidemiologically that you have excess risk for cardiovascular disease if you have inflammatory disease. In animal models, there’s a pretty direct demonstration that having periodontal disease makes the [progression] of cardiovascular disease more rapid, and even possibly makes you susceptible to cardiovascular events—heart attacks—because gum inflammation elevates the systemic inflammatory response.
The same thing is true in type 2 diabetes. Basically, the pathogenesis is this: you get fat, you become inflamed, that causes insulin resistance so you have to make more insulin—to maintain your blood sugar, and eventually your pancreas stops producing insulin and you become diabetic. Diabetics are much more susceptible to developing periodontal disease because their inflammatory response has been heightened.
SACM: Is it correct that you believe aspirin can help with these conditions by fighting inflammation?
TVD: It’s not aspirin itself, it’s molecules called lipoxins and resolvins, compounds that regulate inflammation. Taking aspirin produces these molecules that then have a longer lifetime in the blood. Some of these compounds come from your own fatty acids, and others come from dietary omega 3 fatty acids [found in nuts and fish oil]. So if you actually take omega 3 fatty acids and baby aspirin at the same time, you get increased resolvins in the blood and this dampens the inflammatory response—which then dampens the cardiovascular disease process. There’s a lot of data that shows if you reduce inflammation, you reduce second heart attacks. Statins do that too, by the way.
SACM: Is this a proven treatment?
TVD: A lot of this stuff is still under investigation, but there has been significant progress in that direction. The role of inflammation in these diseases…has basically been strengthened over the past 10 years. The effects [of resolvins and lipoxins] in animal models are quite profound and are unlike anything we’ve been able to demonstrate with any other type of compound. But it still remains to be proven in humans.
SACM: How does taking care of oral health help fight other diseases?
TVD: “Every little bit helps” is a good way to look at it. If somebody has cardiovascular disease, it’s because they have a lot of risk factors. So you lower blood pressure, you lose weight, you exercise more, etc., etc. Each one of those that you do increases the chances for a better outcome, and periodontal disease is just one of the things on the list. If you take care of it, it increases your odds.
The Future of Oral Health was created by Scientific American Custom Media, a division separate from its board of editors, working in partnership with Colgate.