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Examining the Oral Systemic Connection: Series Part 1 - Biofilms and the Inflammatory Burden

Planktonic or not? That is the question that must be asked when treating microbial related diseases.

From the time that Robert Koch put out his famous Postulates in the late 1800’s, the fields of medicine and microbiology achieved great success in the identification and treatment of infectious diseases.  The identification of a number of specific microbes that were responsible for diseases of epidemic proportion became possible.(1)  The identification of the individual microbes that caused catastrophic infections led to successful treatments of these scourges of society.  In turn, countless numbers of lives were saved. Life expectancy was dramatically extended for those who had access to this medical care.

The individual microbes identified formed the initial foundations of microbiology, and were the targets of antibiotic treatment.  These contagious acute infections were studied as planktonic (free floating) organisms.  (See image courtesy of and with permission crom Center for BioFilm Engineering, MSU-Bozeman). They could be isolated and targeted with a wide array of chemotherapeutic agents.  Despite these successes, the development of antibiotic resistance and diseases of a more chronic nature continued to emerge.  According to the Centers of Disease Control and Prevention, up to 70% of human bacterial infections are caused by organized communities of bacteria called biofilms.(2)

Exactly what are biofilms and how are they important in the Oral/Systemic connection?

Biofilms are not the planktonic bacteria upon which the modern Germ Theory is based.  These are diverse communities of microbes which have the ability to adhere to surfaces both inside the human body and to other areas of our environment.  Biofilms are ubiquitous in nature and, in many instances, are quite beneficial.  When in proper balance and composition, these communities can aid in biological functions such as proper food processing in the human gut.  The bacteria in biofilms group together to enhance their own longevity and, in many instances, our own.

When biofilms form, the microbes have the ability to secrete extracellular polysaccharides (EPS) that are used to form a protective coat over the whole.  Within this protected antibiotic resistant community, genetic material may be exchanged and survival traits can be transferred from one species to the next. (3)  This process is known as Quorum Sensing, and is a very effective defense mechanism. (4)  If conditions around and in the biofilm remain the same, this homeostasis allows the nature and composition of the community to remain relatively static. If the stable biofilm is beneficial to the human host, no pathogenic diseases develop.  If the conditions (ecology) change, then the pathological nature of the biofilm can also change.

Dental Plaque is oral biofilm.  For it to change from commensal to pathogenic it takes complex interactions involving the host, the microbes, and the surrounding environment. (5) The process itself is time related, as the biofilm evolves.  Keeping the plaque young by disrupting its’ formation at least once in a 24 hour period is crucial in limiting the pathology associated with it.  Dental Plaque will always form, but allowing it to mature is what causes problems for the human host.

The role of the inflammatory burden in health.

Evidence can be found showing both the direct and indirect effects of oral biofilm on human health.  The most well known direct effect is Bacterial Endocarditis (BE).  Emerging evidence is showing that oral biofilm bacteria such as S. Sanguis and P. Gingivales have the ability to invade and injure endothelial cells lining arterial walls. (6) The resulting damage may provide a focal point for thrombus or atheroma formation.  It is, however, the indirect effects that are garnering the most attention in this evolving science.  Oral biofilm induced infections, such as periodontal disease, are able to activate a considerable cascade of inflammatory cytokines.  These cytokines can directly effect vessel walls or stimulate the liver to produce acute-phase proteins such as CRP. (7)

Human immune systems are best suited to protecting us from singular events.  The ensuing inflammatory response, in such cases, allows for a beginning and an end.  When dealing with low grade chronic infections, damage, depending on the host response, can occur.  Conditions such as periodontal disease evolve over the course of years.  Depending, again, on the susceptibility of the individual, a considerable amount inflammatory burden has been put in place.  It makes a strong case to include poor oral health as a risk factor for many chronic degenerative conditions.

References (#)

  • Castell JV, A. T. (1989). Interlukin-6. The major regulator of acute-phase protein synthesis in man and rat. Ann N Y Acad Sci , 557:87-99. (7)
  • Harold Marcotte, M. C. (1998). Oral Microbial Ecology and the Role of Salivary Immunoglobulin A. Microbiology and Molecular Biology Reviews , 71-109. (5)
  • Joe Harrison, R. T. (2005, November-December). Biofilms. American Scientist , p. 508. (4)
  • Joe Harrison, R. T. (2005). Biofilms. American Scientist , 508.  (1)
  • Prevention, C. f. (2005). Biofilms. American Scientist , 508.@ (2)
  • Proal, A. (2008). Understanding Biofilms. Bacteriality , 5-26. (3)
  • Talib Najjar, D. M. (2010, July 1). Bacterial Mouth Infections. Retrieved January 3, 2012, from Medscape Reference-Drugs, Diseases and Procedures: http://emedicine.medscape.com/article/1081424-overview (6)