Could your ORAL HYGIENE have something to do with your CANCER?

The microbiome is a hot topic in modern medicine; research on its fundamental importance to human health is emerging almost daily. Today no one discredits the importance of the gastrointestinal microflora. However the understanding of which is most commonly localized to the small and large bowl.

Interestingly our perception of our oral environment and its microbiota is primarily limited to seemingly localized issues such as; dental carries, periodontitis and gingivitis. Yet with over 700 species of bacteria, fungi and viruses inhabiting the oral cavity can this merely be a localized situation? [1], [2].

Recently research began initially linking the presence of oral diseases such as dental carries, periodontitis and gingivitis to a wide range of extra-oral conditions. Since then research has found that certain strains of bacteria are in fact capable of extra-oral translocation resulting in systemic infections and inflammation. Finally research has begun linking particular bacterial strains to the increased prevalence and adverse health outcomes of individual diseases.

So far research has shown links between oral bacterial presence/translocation/overgrowth and the following conditions: cardiovascular disease, adverse pregnancy out-comes, rheumatoid arthritis, inflammatory bowel disease, colorectal cancer, pancreatic cancer, respiratory tract infections and organ inflammations. Bellow we will examine some of the effects oral bacteria may have on the extra oral environment (body).

Pancreatic Cancer: 

Researchers have identified two species of bacteria linked with periodontal disease in healthy individuals that are associated with a risk of developing pancreatic cancer. Porphyromonas gingivalis was associated with an 59% increased risk of pancreatic cancer and Aggregatibacter actinomycetemcomitans resulted in a shocking 119% increased risk [3], [4]

Atherosclerotic Disease (AD): 

Atherosclerotic disease, including myocardial infarction and stroke, is the leading cause of death worldwide. Although conditions such as smoking, obesity, high blood pressure, and diabetes are well known to contribute to AD, studies have rarely looked at the implication of oral bacteria in the initiation and progression of atherosclerosis.  Collectively, the following species have been detected: Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia, with some of the samples containing more than one type of bacteria [5], [6].

Adverse Pregnancy Outcomes (APO):

APO is a broad term including preterm labor, preterm premature rupture of membranes, preeclampsia, miscarriage, intra-uterine growth retardation, low birth weight, stillbirth, and neonatal sepsis. A recent review of epidemiologic and interventional studies on the link between periodontal infections and APO found F. nucleatum to be by far the most prevalent oral species associated with APO [7].  It was detected in a wide variety of placental and fetal tissues, including amniotic fluid, fetal membranes, cord blood, neonatal gastric aspirates, and fetal lung and stomach. It was directly associated with preterm birth, stillbirth, and early-onset neonatal sepsis [8]. P. gingivalis has also been associated with APO and specifically premature labor [9].

Rheumatoid Arthritis (RA):

RA is an autoimmune disease characterized by chronic inflammation of the joints and the surrounding tissues, leading eventually to destruction of the joint architecture and impaired function. Numerous clinical studies point toward a potential association between RA and chronic periodontitis [10], [11]. Treatment

of periodontal infections reduces the severity of active RA thereby suggesting periodontitis as a causal factor in the maintenance of the autoimmune inflammatory responses [11]. Prevotella intermedia and P. gingivalis as the most prevalent bacteria associated with RA and periodontitis [11].

Inflammatory Bowel Disease (IBD): 

IBD represents a group of chronic disorders of the gastrointestinal (GI) tract, including ulcerative colitis (UC) and Crohn’s disease (CD). Studies have shown that both genetic and environmental factors are involved in the development of IBD. Dysbiosis of intestinal microbiota has been shown to play a pivotal role in the pathogenesis of IBD. Oral bacteria; Fusobacterium nucleatum and

Campylobacter concisus, have recently been associated with IBD [12]. Invasive C. concisus oral strains were detected in 50% IBD patients, but none in the normal healthy controls.

Respiratory Tract Infections (RTI): 

Oral colonization by respiratory pathogens, due to poor oral hygiene and periodontal diseases, has been associated with pneumonia. Dental plaque has been shown to serve as a reservoir for respiratory pathogens [13].


Oral bacteria have developed aggressive mechanisms to invade and persist in our cells, to escape immune detection and to adapt to niches at extra-oral sites. They are able to induce inflammatory responses leading to adverse systemic effects. Based on this evidence it is clear that the health of the oral environment is of pinnacle importance. Recommendations related to proper oral hygiene should become general practice for most health care providers (not merely Dentists) and the general consideration of dissemination of oral bacteria must be considered for each patient as a possible contributing cause for disease.

[1] J. He, Y. Li, Y. Cao, and J. Xue, “The oral microbiome diversity and its relation to human diseases,” Folia Microbiol., vol. 60, no. 1, pp. 69–80, 2015.

[2] K. T. Simpson and J. G. Thomas, “Oral Microbiome: Contributions to Local and Systemic Infections,” Curr. Oral Heal. Reports, vol. 3, no. 1, pp. 45–55, 2016.

[3] D. S. Michaud and J. Izard, “Microbiota, Oral Microbiome, and Pancreatic Cancer,” Cancer J., vol. 20, no. 3, pp. 203–206, 2014.

[4] I-Hsin Lin, J. Wu, S. M. Cohen, C. Chen, D. Bryk, M. Marr, M. Melis, E. Newman, H. L. Pachter, A. V. Alekseyenko, R. B. Hayes, and A. Jiyoung, “Pilot study of oral microbiome and risk of pancreatic cancer,” J. Cancer Res., vol. 73, no. 1, pp. 101–104, 2013.

[5] F. Pj, E. Gemmell, H. Sm, A. Hasan, W. Pj, W. Mj, C. Mp, M. P. Cullinan, and G. J. Seymour, “Cross-reactivity of GroEL antibodies with human heat shock protein 60 and quantification of pathogens in atherosclerosis,” Oral Microbiol. Immunol., pp. 296–302, 2005.

[6] F. Pj, E. Gemmell, A. Chan, C. Cl, W. Pj, B. Ps, W. Mj, C. Mp, M. P. Cullinan, and G. J. Seymour, “Inflammation , heat shock proteins and periodontal pathogens in atherosclerosis : an immunohistologic study,” pp. 206–211, 2006.

[7] Y. W. Han, “Oral Health and Adverse Pregnancy Outcomes – What’s Next?,” pp. 289–293, 2011.

[8] X. Wang, C. S. Buhimschi, S. Temoin, V. Bhandari, Y. W. Han, and I. A. Buhimschi, “Comparative Microbial Analysis of Paired Amniotic Fluid and Cord Blood from Pregnancies Complicated by Preterm Birth and Early-Onset Neonatal Sepsis,” vol. 8, no. 2, 2013.

[9] F. Tateishi, T. Nakamura, Y. Nakajima, K. Kawamata, Ó. J. Wiley, and A. S. Sons, “The possible mechanism of preterm birth associated with periodontopathic Porphyromonas gingivalis,” pp. 497–504, 2011.

[10] A. Dissick, R. S. Redman, M. Jones, B. V Rangan, A. Reimold, G. R. Griffiths, T. R. Mikuls, R. L. Amdur, J. S. Richards, and G. S. Kerr, “Association of Periodontitis With Rheumatoid Arthritis : A Pilot Study,” no. February, pp. 223–230, 2010.

[11] R. Jc, J. C. Rizo-rodrı, J. W. Little, and J. Pablo, “Detection of periodontal bacterial DNA in serum and synovial fluid in refractory rheumatoid arthritis patients,” pp. 1004–1010, 2009.

[12] J. Strauss, G. G. Kaplan, P. L. Beck, K. Rioux, R. Panaccione, R. Devinney, T. Lynch, and E. Allen-vercoe, “Invasive Potential of Gut Mucosa-derived Fusobacterium nucleatum Positively Correlates with IBD Status of the Host,” vol. 17, no. 9, pp. 1971–1978, 2011.

[13] A. S. Heo, E. M. Haase, A. J. Lesse, S. R. Gill, A. Frank, S. Heo, E. M. Haase, A. J. Lesse, S. R. Gill, and F. A. Scannapieco, “Genetic Relationships between Respiratory Pathogens Isolated from Dental Plaque and Bronchoalveolar Lavage Fluid from Patients in the Intensive Care Unit Undergoing Mechanical Ventilation Linked references are available on JSTOR for this article : Genetic Relationships between Respiratory Pathogens Isolated from Dental Plaque and Bronchoalveolar Lavage Fluid from Patients in the Intensive Care Unit Undergoing Mechanical Ventilation,” no. May, 2016.

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