No. Not really. At least, not everybody. But which of us?
It has been known for the last hundred years that the mouth—the oral cavity—is the site of many infectious and inflammatory pathogens. The connection to system-wide infections isn’t that old, though. Periodontitis is one of the prime suspects in the pathogenesis of a number of illnesses that include cardiovascular disease, bacterial pneumonia and diabetes mellitus. Poor oral hygiene, which is more common than we think, leads to the bacterial colonization of teeth and possibly an even greater introduction of bacteria into the blood stream (Rai, 2007).
Oral infections are predominantly anaerobic gram-negative bacteria, meaning that they can survive for a long time on a moist surface. This is antipodal to the gram-positive kinds that are tougher and can live on dry surfaces. Three out of four American adults are believed to suffer mild periodontal disease, with almost a third having chronic activity. This bodes terribly for long-term health. Oral disease may affect overall health in a few ways. First, bacteria from the gums enter saliva, where they can cling to moisture droplets that are inspired from the air. These can cause respiratory issues. Second, the bacteria associated with periodontal disease can get into the circulatory system via the spaces around the gums. These can travel the body and cause illness in other organs. Third, inflammation from periodontal disease may incite another systemic inflammatory response and contribute to other conditions that have an inflammatory component, such as cardiovascular disease, diabetes or kidney disease. Whatever the case may be, it’s in our best interest to keep the mouth as clean as we can to reduce disease potential (Han, 2013).
In periodontal disease, pro-inflammatory substances called cytokines can reach high tissue concentrations. Here, the periodontium acts like a reservoir, from which place a systemic attack can be launched. One of these cytokines, an interleukin named IL-1β, favors coagulation and thrombosis while inhibiting the breakdown of fibrin, the protein that forms a clot (Clinton, 1991). It sounds odd, but these same mediators are felt to cause preterm labor and low birth weight (Page, 1998). As far back as the 1890’s, medical practitioners thought a relationship of the mouth to the rest of the body existed. In 1891 a dentist named Willoughby Dayton Miller wrote a piece titled “The Human Mouth as a Focus of Infection.” His work associated mouth conditions with serious conditions elsewhere in the body, including the brain, lungs and digestive system. His treatise may be found here:
http://www-personal.umich.edu/~pfa/denthist/articles/Miller1891.html , which cites the 1891 issue of Dental Cosmos.
One of the most obdurate villains in this drama is Streptococcus sanguinis, formerly known as S. sanguis. This one is gram positive and is a normal inhabitant of a healthy mouth, where it is particularly found in plaque. It forms a biofilm, characteristic of the plaque, and has the uncanny ability to modify its environment to make it less hospitable to other strains of streptococcus that may cause cavities. But it also has the wherewithal to get into the bloodstream and take up residence in heart valves—namely the mitral and aortic—and cause subacute bacterial endocarditis (inflammation of the thin membrane that lines the interior of the heart). Guess how this might happen. Vigorous dental cleanings that draw blood and oral surgeries are causes. This is why an extraction or other oral surgery practically demands a course of antibiotics before and after the procedure. An infection is harder to treat than to prevent.
Biofilms are tenaciously adhesive and protective of the pathogens that live within. Plaque is an accumulation of saliva bacteria, which colonize the spaces and fissure between teeth. These bacteria use dietary sucrose to make acidic chemicals that help them stick to the teeth. The acids eat through tooth enamel, and the caries life cycle begins. Planktonic bacteria are those which float freely in their environment, while sessile are those which are firmly attached to something else. Mouth bacteria, and perhaps others, seem to have the means to switch back and forth between these states, dissolving their biofilms to become mobile. This tells scientists that bacteria communicate among themselves, perhaps by using protein mediators (Macedo, 2009) (Abraham, 2006). Once these communication media are identified, science will be able to control biofilms and halt the virulence that besets us.
There is frustration that dental biofilms cannot be eliminated because of their diversity and numbers, but their control can be realized along a few avenues, including anti-plaque surfactants and essential oils, and anti-microbial agents that include metal ions, phenols and quaternary ammonia compounds formulated into dental care products (Mash, 2010). Mechanical hygiene methods—brushing and flossing—are first steps in controlling oral bacteria colonies because, if they are not regularly removed, they will mature into pathogenic, albeit microscopic, Mongols. Teeth comprise only twenty percent of the oral surface, so mouth rinses are needed to reach the spots a brush doesn’t (Gurenlian, 2012) and help to reduce risk factors for systemic disease (Lockhart, 2009).
The chemistry of mouth rinses is expanding its purview beyond halitosis to include novel ingredients that kill biofilm bacteria. Low amounts of levulinic acid and sodium compounds have surpassed Listerine in efficacy (Wang, 2012), and herbal extracts were found to kill oral bacteria immediately upon contact, compared with chlorhexidine (Verkaik, 2011), a mouthwash component also used by surgeons to wash their hands prior to an operation.
Preventing systemic infection with good oral hygiene is a worthwhile endeavor. The need for prophylactic antibiotics before visiting the dentist may be restricted to those with artificial heart valves, a history of infective endocarditis, serious congenital heart defects, and other cardiac abnormalities. In general, the American Heart Association suggests there be no antibiotic prophylaxis based solely on lifetime risk of acquisition of infective endocarditis, it being reasonable only for patients with underlying cardiac conditions associated with high risk of adverse outcome (Taubert et al, 2007).
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