By Stephen T. Sinatra, M.D., F.A.C.C., F.A.C.N., C.N.S., C.B.T.
Cardiologists are especially aware of a connection between gum and heart health. Oftentimes patients with cardiovascular disease will also display symptoms of gum, or periodontal, disease such as missing and loose teeth, bleeding gums, and halitosis.
In 1998, the American Academy of Periodontology warned the public that gum infections pose more serious threats of systemic disease such as cardiovascular diseases, diabetes, and (respiratory diseases) pneumonia, to name a few.
Over the past two decades, various researchers have demonstrated that cardiovascular risks increase in tandem with the severity of gum infections. According to Thomas E. Rams, D.D.S., M.H.S., expert and author on the microbiology of gum disease, people, otherwise in good health who develop serious periodontal disease, double their risk of fatal heart attack and triple their risk of stroke. Since an estimated 54 million people have some form of periodontal disease, it’s no wonder cardiovascular disease is the number one killer in the U.S.!
Periodontal disease is characterized by inflammation of the gums caused by bacteria, spirochetes, and viruses growing in and around the teeth. Microbes in the mouth both directly and indirectly harm healthy tissues by causing inflammation. Enough oral bacteria will trigger an immune system response to get rid of the bacteria, which inflames the gums. When this condition becomes chronic, inflammation can spread through the body.
Infectious microbes, as well as the side products of the subsequent immune system response in the mouth, including inflammatory messengers and endotoxins from destroyed bacteria, travel through the bloodstream and circulate throughout the rest of the body. Chemicals our bodies produce during inflammation, such as CRP (C-reactive protein) and interleukin-6 damage other body tissues, creating more inflammation as the immune system is called to action again.
Additionally, antibodies in our bloodstreams, which normally counteract the bacteria, will eventually attack damaged, chronically inflamed tissues, causing more destruction within the body. Depending on how susceptible the person is to infection or tissue damage, the relocated toxins and inflammatory messengers can create a systemic inflammatory and hyper-immune state in the body.
Cardiovascular risk especially increases for a variety of reasons. Mouth microbes can eventually infect defective heart valves or arteries that have been eroded by other inflammatory substances. Rams suggests that this traveling and invasive bacteria can generate or add to inflammation in the arteries, which can lead to arterial disease. As well, some of these mouth bacteria can cause abnormal blood clotting. Some individuals also, for example, may produce excess levels of inflammatory markers which are known to be risk factors for heart disease.
The good news is that you can fight periodontal disease with good oral hygiene practices combined with a few common household staples. Rams recommends flossing and brushing your teeth often with baking soda, then swishing your mouth with apple cider vinegar; both products are antibacterial. Dr. Mark A. Breiner, D.D.S., who practices integrative dentistry, advocates, in addition to brushing with baking soda and salt, irrigating gums with hydrogen peroxide before brushing as an antibacterial strategy.
Taking antioxidants such as coenzyme Q10 and Vitamin C, essential fatty acids and magnesium can help support gum health from the inside by strengthening your immune system and reducing chronic inflammation. Remember that the situation in your mouth often reflects what is going on elsewhere in your body, and that local care, while important, is not enough. Strengthen your entire body through such healthy lifestyle practices as an anti-inflammatory diet and supplementation, exercise, as well as stress management.
- Scannapieco FA. Position Paper of the American Academy of Periodontology: Periodontal disease as a Potential Risk Factor for Systemic Diseases J. Periodontal. 1998 Jul;69(7)841-50.
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