5 things to consider regarding the connection between stroke and inflammation

The earliest study on the effect of inflammation on stroke was published in 1986. But while dental professionals are aware of this information, they may not always practice it, says Dr. Tim Donley, who specializes in periodontics, dental implants, gum disease and oral medicine at his practice in Bowling Green, Ky.

“If we, in dentistry, are indeed healers, which I know I signed up to become, it is imperative for us to take a different approach,” he says. “The key to the whole thing is to take more of a personalized dentistry approach to patient risk profiles as well as what treatments are provided and use our expertise to determine the next logical step based on those dynamics. The goal is to help patients become and remain inflammation-free.”

Here are five things to consider regarding this important connection between stroke and inflammation:

1. Effect on overall health. Bacteria accumulate between the soft tissue and the tooth. If not adequately removed on a frequent basis, bacteria start migrating deeper into the pocket, Donley says. Over time, bacteria initiate a host response that summons inflammatory cells, like white blood cells, to the area. The inflammatory cells release a variety of inflammatory mediators in an attempt to eliminate the causative bacteria. One of the untoward side effects is that the inflammatory mediators destruct collagen. When the collagen is destroyed, we lose integrity of the lining epithelium.

As it turns out, the mouth is indeed connected to the rest of the body. Once the lining epithelium is compromised (and this is the typical periodontal pocket in which we see bleeding when we probe it), bacteria, bacterial byproducts and inflammatory mediators release in response to the initiating bacteria, entering the blood stream daily and traveling wherever the blood flows. The important thing to realize from the outset is that the link between oral and overall health is inflammation-dependent. It is inflammation that results in collagen dissolution, loss of lining epithelium integrity as well as seepage of the bacteria, byproducts and inflammatory mediators into the systemic circulation. Inadequate removal of the initiating bacteria leads to inflammation, which can lead to outcomes far worse than tooth loss.

2. Role of cholesterol. In periodontal disease, simply having pathogens isn’t enough to cause disease-there needs to be a susceptible host, Donley says. Similarly, in cardiovascular disease, cholesterol alone does not cause disease.  The types of cholesterol that put a patient a risk for heart disease are well known.  But bad cholesterol numbers alone aren’t what cause the deleterious effect-it is inflammation. For a stroke to develop, the endothelium must fail twice, and inflammation plays an important role in this. First, the cholesterol is engulfed by the macrophage cells in the blood and goes through the endothelium, attaching to vessel walls. As the plaque starts to grow on the vessel wall, there is a fibrous cap that forms over the top of it. Inflammation causes the cap to disintegrate, allowing the plaque in the vessels to float downstream, which causes the stroke.

3. Increased risk. New sources of inflammation are being investigated in conjunction with the overall increased risk of stroke in our population. Certain conditions associated with arterial inflammation, such as lipid accumulation, tobacco use, insulin resistance, Vitamin D deficiency, diet, physical activity, psycho-social issues, oral health issues, chronic periapical infections around the teeth or systemic diseases, such as lupus, are responsible for causing the inflammation, Donley says.

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“Dentistry plays a role in a lot of these things,” he says. “It is time for dentists to realize they absolutely have to do more than just fix and clean teeth. They need to screen patients for some of these destructive lifestyle behaviors because they add to health problems such as stroke. There is evidence that strongly suggests periodontal disease contributes to these adverse outcomes.”

It is important to determine which patients have risk factors for periodontal diseases or risk factors for the systemic diseases potentially affected by periodontal inflammation. Then, giving these patients the tools to maximize the chance that they consistently remove the initiating bacterial biofilm is essential.

4. Uncertain “proof.” The precise nature of the relationship between periodontal and systemic diseases remains unclear. Thoughts on these challenges are often divided into distinctive groups, Donley says: Those who say in the age of evidence-based medicine, we need proof, and those who say part of an evidence-based approach includes clinical judgment. Donley is part of the latter group.  

“Proving that periodontal disease causes or contributes to the initiation and progression of the chronic diseases of aging will be difficult," he says. “Without question, inflammation has been identified as playing a key role in the development of stroke and other chronic diseases. The mouth is a significant source of this inflammation when periodontal disease persists.”

To combat oral inflammation, Donley recommends the Philips Sonicare FlexCare Platinum power toothbrush. His confidence in the brush is due to its clinically proven ability to remove seven times more plaque in-between teeth than a manual toothbrush. 

5. Role in other diseases. Inflammation is being investigated as playing a significant role in other diseases besides stroke, including cancer, diabetes, respiratory diseases, rheumatoid arthritis and Alzheimer’s.       

Periodontal diseases and a lot of systemic illnesses, such as stroke and cardiovascular disease,s are lifestyle diseases, which means they have factors that can be controlled and altered, Donley says.

“That’s where I think we’re doing patients a benefit in terms of oral health if we manage lifestyle factors,” he says. “There is a lot of information specifically looking at nutritional intervention, such as an inflammation-reducing diet, that benefits periodontal outcomes. That alone is great, but it is even better if we can help those at an elevated risk, those for whom reduction of inflammation is critical. We need to address not just what is presenting within the mouth but lifestyle factors so we can alter them to help in periodontal and systemic health.”          

Conclusion
When considering the link between inflammation and stroke, dental professionals must first determine what their desired endpoint of periodontal therapy is, Donley says.

“We need to determine if we are in the get-the-patient-out-of-pain business, the save-the-teeth business or the tooth-cleaning business,” he says. “At this point, based on the evidence, we should give great thought to becoming an inflammation-reduction business. The end point of periodontal therapy should be to achieve and maintain an oral cavity relatively free of inflammation over the patient’s lifespan. And only if the dental professional screens for inflammation, determines the treatment up to this point, identifies the risk factors, reassesses and develops an evidence-based approach can the patient be returned to inflammation-free status and have the appropriate tools to remain that way.”