It’s one of the easiest ways to care for your health, a ritual we participate in daily: brushing those osseous outcroppings, our teeth. For those of us who heed the pleas of our dentists, flossing is a part of our routines, too. But the state of affairs of our glistening maws – the density of plaque, the presence of gingivitis, a full set of chompers – is important beyond mere aesthetics. Good oral fitness, particularly steps taken to limit the bacterial status quo, plays an important role in the goings-on of our body as a whole; a dirty mouth – and not the kind prone to sailor-like profanity – can provide important clues as to how susceptible you are to heart attacks and strokes.
Periodontitis is a chronic bacterial infection of the scaffolding of teeth, including the gums, connective tissue, and jawbone that surround and encapsulate a tooth. It may well be one of the most common diseases of man: in the United States, anywhere from 30 to 50% of the adult population has a mild form of the disease, while an additional 5 to 15% suffers from a severe form (1).
That disease begins with dental plaque or calculus, a layering and mineralization of pathogenic microbes that thrive in the dark, wet, and (occasionally) nutrient-rich crevices of our mouth. Over 500 microbes have been implicated as residents of these so-called periodontal pockets, those clefts and rifts between tooth and gum, forming complex biofilms and microbiotic communities of Gram negative rods, Gram positive cocci and rods, and spirochetes (2). Periodontitis can incite additional infections: burrowing tooth cavities or caries; gingivitis, an infection of the fleshy gums; and, most severely, destruction of the alveolar jawbone that props the teeth (3).
But periodontitis is not just a local infection, limited in its effects to the body’s entranceway. It goes beyond the pearly whites and has the potential to wreak havoc farther afield, upon our thrumming arteries, heart, and brain (3). The microbes responsible for periodontal disease assist in forming atherosclerotic plaques, which travel in the blood and set up shop in arteries (4)(5). One bacteria commonly found in our mouths and which is responsible for oral disease is Porphyromonas gingivalis. But outside the oral cavity, this bacteria can attract vital cells responsible for blood clotting, platelets, which in turn can form thromboses, leading to the embolisms responsible for heart attacks and strokes (6).
When the severity of periodontal disease was directly measured in a 2006 Swedish study by counting existing pockets of infection and decay, it was found to be associated with hypertension in a dose-dependent manner (7). In other words, the lack of oral maintenance that allows build-up of bacteria on our chompers allows a similar build-up in less visible but far more life-threatening locales as well.
Sometimes it really is just a matter of numbers. A study in 2006 found that the number of teeth remaining after periodontal disease was related to the prevalence of both heart attacks and hypertension (7). A similar study in Iran found that the magic number was ten: a loss of more than ten teeth resulted in more than a 250% increase in risk of myocardial infarction (5). In that sad countdown from a Cheshire Cat grin to a gap-toothed grimace, there’s a corresponding increase in risk of heart attack and high blood pressure.
As with any infectious disease process, there is the tug-of-war balance between our immune response and the infection in question. It is a battle of cells. On one side, our white blood cells issue forth inflammatory signals and antimicrobial compounds; on the other, single-celled pathogens seditiously destroy tissues with their own equally destructive and inflammatory signals.
For over a decade now, patients with periodontal disease have consistently shown elevated systemic levels of an inflammatory marker known as C-reactive protein (CRP). This protein is a key player in the body’s innate immunity, neutralizing microbial interlopers such as bacteria, viruses, and fungi, as well as other forms of damage or malignancy. It is commonly measured in the blood to assess an ongoing inflammation, and high levels of CRP have long been positively associated with cardiovascular disease (8). The long-standing chronic infection and “microbial burden” that is periodontitis is considered to be a risk factor that predisposes those with bad oral health to cardiovascular disease (9)(10).
What kind of causality exists between both the risks and outcomes of the two diseases, that of the mouth and the heart, is unclear. All research points to correlations and associations, while the actual relationship between these diseases, if there is any to be found, requires more teasing out.
Though pathogenic bacteria in the mouth can form atherosclerotic plaques and emboli, the relationship between periodontitis and heart disease may represent an overall systemic failure, an immune system deficient in controlling disease and decay or perhaps a failure of repair. Both periodontitis and heart disease could be two sides of the same coin, representing a malfunctioning immune system, the coincident effects of an identical disease process (3).
The association between our chompers, the dark tickings of our heart and the often obscure workings of our complex, omnipresent immune system highlight the blurring boundary of the body’s internal ecosystems. Are tooth tartar and clogging arterial plaques really so different? Can decay and inflammation be contained? Is one type of inflammation any different from another? Everything is interrelated: the human body is more than just an assortment of individual working parts. An ear here, a pancreas there, ten toes below. What grows and replicates and harms in the mouth, in one circumscribed bodily locale, has the potential to morph and move and adapt.
1) VD Friedewald et al. (2009) Periodontitis and atherosclerotic cardiovascular disease. J Periodontol. 80: 1021-32
2) KE Fenesy (1998). Periodontal disease: an overview for physicians. Mt Sinai J of Med . 65: 362-9
3) G Pendyala et al. (2013 ) Links demystified: Periodontitis and cancer. Dent Res J (Isfahan). 10(6): 704–712.
4) B Söder et al. (2007) Periodontitis and premature death: a 16-year longitudinal study in a Swedish urban population. J Periodontal Res.42(4):361-6.
5) MK Samani et al. (2013) The relationship between acute myocardial infarction and periodontitis. Caspian J Intern Med. 4(2): 667-671
6) M Herzberg et al. (1998) Dental plaque, platelets, and cardiovascular disease. Ann Periodontol. 3: 152-58
7) A Holmlund et al. (2006) Severity of periodontal disease and number of remaining teeth are related to the prevalence of myocardial infarction and hypertension in a study based on 4,254 subjects. <>emJ Periodontal. 77(7):1173-8.
8) Noack B1 et al (2001) Periodontal infections contribute to elevated systemic C-reactive protein level. J of Periodontal. 72(9):1221-7.
9) DF Kinane & GJ Marshall (2001) Periodontal manifestations of systemic disease. Aust Dent J. 46(1):2-12.
10) SO Geerts et al (2004) Further evidence of the association between periodontal conditions and coronary artery disease. J Periodontol. 75(9):1274-80.