Harmful oral bacteria linked to serious cancers

July 5, 2012, Featured in Complete Oral Care, 0 Comments

Everyone’s mouth is full of oral bacteria— most of them harmless. Beneficial Helpful Bacteria or Friendly Bacteria or Probiotic Bacteria or Probiotics or Oral Probiotics are live microorganisms thought to be beneficial, helpful, and friendly to the host organism. The vast majority of bacteria are actually helpful and even necessary for good health. From the mouth to the anus, these tiny life forms aid in breaking down and digesting food, converting nutrients and dietary fiber for absorption, synthesizing vitamins, and degrading toxins. They also aid the immune system to develop vigorous responses.

In a healthy mouth there is a natural balance of different bacterial species. This natural balance keeps the harmful bacteria from becoming too strong or out of balance so as to dominate. They join together to form communities so-called biofilms. Your body learns to live with them, because for most people, healthy biofilms keep the bad bacteria away. You can never completely get rid of all the bacteria in your mouth but brushing and flossing make sure the number of bacteria you do have is in a safe range. A common mistake many people make is to brush but not floss. This allows bacteria to build up to dangerous levels between the teeth where brushing alone cannot reach.

Many diseases are actually related to harmful oral bacteria. Treatment for numerous medical conditions such as cardiovascular disease, diabetes, kidney disease, rheumatoid arthritis, pulmonary disease, orthopedic replacement, cancer, and pregnancy may be complicated by bacteria from the mouth. When any one group of harmful bacteria begins to dominate, their levels of toxins increase to a point where they stimulate the immune system and cause an infection. Dental plaque is a biofilm which develops naturally on the teeth. Dental plaque consists of bacterial cells (60-70% the volume of the plaque), salivary polymers, and bacterial extracellular products. The dominant bacterial species in dental plaque are Streptococcus mutans and Streptococcus sanguis. They survive in the inner parts of the plaque where oxygen cannot reach them. In addition, large clumps of bacterial plaque at the gum line will prevent oxygen from reaching areas under the gum line. These oxygen poor regions are fertile environments for the more hostile anaerobic bacteria.

A build-up of dental plaque can lead to gum disease. Gum disease is a progressive inflammatory condition which affects the tissues and bone supporting the teeth. Gum disease causes bad breath, bleeding gums and, if untreated, cavities, receding gums and tooth loss. As gum disease progresses, bacterial enzymes break down the gum tissue, allowing bacteria to enter the circulatory system. They are measurable in the blood, so it becomes systemic and widely distributed. These circulating bacteria initiate a systemic inflammatory response. Individuals with gum disease have elevated serum biomarkers of systemic inflammation, such as CRP (C-reactive protein), and these may somehow contribute to the promotion of cancer cells.

Streptococcus mutans causes pneumonia, sinusitis, otitis media, and meningitis. The bacteria Streptococcus gordonii is a normal inhabitant of the mouth and contributes to dental plaque. If these bacteria enter into the blood stream through bleeding gums they can start to wreak havoc by masquerading as human proteins. The researchers have discovered that Streptococcus gordonii is able to produce a molecule on its surface that lets it mimic the human protein fibrinogen – a blood-clotting factor. This activates the platelets, causing them to clump inside blood vessels. These unwanted blood clots encase the bacteria, protecting them from the immune system and from antibiotics that might be used to treat infection. Platelet clumping can lead to growths on the heart valves (endocarditis), or inflammation of blood vessels that can block the blood supply to the heart or brain

A mixed-bacteria ecological approach to understanding the role of the oral bacteria in dental caries causation: an alternative to Streptococcus mutans and the specific-plaque hypothesis.

Tobacco smoking affects bacterial acquisition and colonization in oral biofilms.

The potential impact of periodontal disease on general health: a consensus view.

Low-grade inflammation in chronic infectious diseases: paradigm of periodontal infections.

Human platelets recognize a novel surface protein, PadA, on Streptococcus gordonii through a unique interaction involving fibrinogen receptor GPIIbIIIa.

Inflammation is a key element in gum disease caused by dental plaque. It is extremely well established that most cancers develop at sites of chronic inflammation. Chronic inflammation plays a critical role in the initiation, development, growth, and metastasis of cancer by inducing the release of a variety of cytokines and chemokines that alert the vasculature to release inflammatory cells and factors into the tissue milieu, thereby causing oxidative damage, DNA mutations, and other changes in the microenvironment, making it more conducive to cell transformation, increased survival and proliferation.

MicroRNAs (miRNAs) are a class of post-transcriptional regulators, and are associated with almost every normal cell function, including proliferation, differentiation and apoptosis. miRNAs have been demonstrated to regulate innate immune response to bacteria invasion. miRNAs could be potential bio-markers for severe periodontitis diagnosis. MicroRNA-155 (miR-155) recently has been identified with critical immune regulatory functions. Inflammation stimulates a rise in levels of miR-155, and that overexpression of miR-155 increases the spontaneous mutation rate, which can contribute to tumorigenesis. High levels of this molecule have been directly linked to the development of leukemias, and breast, lung and colon cancers.

Comparison of inflammatory microRNA expression in healthy and periodontitis tissues.

The role of microRNAs in normal and malignant hematopoiesis.

miR-155: on the crosstalk between inflammation and cancer.

Mutator activity induced by microRNA-155 (miR-155) links inflammation and cancer.

The Oncogenic Role of miR-155 in Breast Cancer.

miR-155 is up-regulated in primary and secondary glioblastoma and promotes tumour growth by inhibiting GABA receptors.

One of the key molecules mediating the inflammatory processes in tumor promotion is the cytokine, TNF (tumor necrosis factor). TNF is a biologically significant immune hormone which activates the immune response against pathogens, including cancer cells. Unfortunately, TNF can also be a growth factor for cancers at low concentrations. TNF is also produced by tumors and can act as an endogenous tumor promoter. The role of TNF has been linked to all steps involved in tumorigenesis, including cellular transformation, promotion, survival, proliferation, invasion, angiogenesis, and metastasis.

Inflammation, a key event in cancer development.

Inflammation and cancer: how hot is the link?

Roles of inflammation in cancer initiation, progression, and metastasis.

Inflammation and cancer: when NF-kappaB amalgamates the perilous partnership.

Cancer cell: using inflammation to invade the host.

Inflammation: a driving force speeds cancer metastasis.

TNF: a master switch for inflammation to cancer.

TNF-alpha/NF-kappaB/Snail pathway in cancer cell migration and invasion.

TNF-alpha in promotion and progression of cancer.

Tumour necrosis factor-alpha as a tumour promoter.

TNF promotes both necrosis and apoptosis. However, TNF-induced cell death plays only a minor role compared to its overwhelming functions in the inflammatory process. Its death-inducing capability is weak compared to other family members such as Fas. Whenever TNF is released, various cells with vastly diverse functions and conditions can all respond appropriately to inflammation. TNFAIP8 (TNF-alpha-induced protein 8 or TIPE) family is recently identified proteins which are important for maintaining immune homeostasis. TNFAIP8 is a suppressor of TNF-α mediated apoptosis, and its expression is induced by NF-κB activation. NF-kB, the pro-Inflammatory and pro-cancer molecule, promotes the survival of cancer cells. TNFAIP8 is considered to be associated with carcinogenesis. TNFAIP8 mediated rescue of pre-oncogenic cells enhances progression to oncogenic transformation.

The TIPE (TNFAIP8) family in inflammation, immunity, and cancer.

TIPE2, a negative regulator of innate and adaptive immunity that maintains immune homeostasis.

TNFAIP8 Overexpression: Clinical Relevance to Esophageal Squamous Cell Carcinoma.

TNFAIP8: a new effector for Galpha(i) coupling to reduce cell death and induce cell transformation.

Pancreatic cancer is one of the most aggressive human tumors and is virtually incurable. Little is known about what causes it. One established risk factor in pancreatic cancer is cigarette smoking; other links have been made to obesity, diabetes type 2 and insulin resistance. In a study, researchers found that gum disease was associated with an increased risk of pancreatic cancer. Nobody knows why gum disease may be linked with pancreatic cancer. It may be that chronic infection in the gums triggers inflammation throughout the body, which can fuel the growth of cancer. Recent research shows that TNFAIP8 may play important roles in the progression of pancreatic cancer.

Or it may be that oral bacteria trigger a chemical process in the body that results in high levels of nitrosamines, cancer-causing compounds that also are in tobacco smoke. Individuals with gum disease have higher levels of oral bacteria and higher levels of nitrosamines, which are carcinogens, in their oral cavity. Studies have shown that nitrosamines and gastric acidity may play a role in pancreatic cancer.

A prospective study of periodontal disease and pancreatic cancer in US male health professionals.

Expression of Tumor Necrosis Factor-alpha-induced Protein 8 in Pancreas Tissues and its Correlation with Epithelial Growth Factor Receptor Levels.

Etiology of pancreatic cancer, with a hypothesis concerning the role of N-nitroso compounds and excess gastric acidity.

The main risk factors for the development of oral cancer are tobacco and alcohol consumption, both of which are associated with dental hygiene and therefore likely to be confounders of an association with tooth loss. Smoking kills healthy oral bacteria and breeds the unhealthy bacteria. In addition, some studies have noted that infection with high-risk strains of Human Papillomavirus (HPV) is an independent risk factor for development of oral cancer, particularly in the tonsils, oropharynx, and oral cavity.

A review of the relationship between tooth loss, periodontal disease, and cancer.

Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study.

Chronic periodontitis and the incidence of head and neck squamous cell carcinoma.

Local Inflammation and Human Papillomavirus Status of Head and Neck CancersLocal Inflammation and HPV in Head and Neck Cancer.

It’s a fact that 90% of adults have active gum disease. Remember, most patients who present with gum disease are completely unaware of a gum problem being present in their mouth because it rarely causes pain until it becomes very severe, by which time it may be too late to save your teeth. If you have chronic gum disease, you need a more aggressive form of treatment, because even after a professional cleaning, they’re still at a very high risk for getting these pathogens back in your mouths right away.

If you suffer with chronic systemic inflammation or cancer, it may be worthwhile to use the active probiotic mouth rinse such as Oralzym-F. Many different oral problems may interfere with cancer treatment and diminish the patient’s quality of life. The blend of beneficial oral probiotics created in Oralzym-F crowd out the harmful bacteria by colonizing in the same places bad bacteria like to hide and by competing for the same nutrients. Within 4-5 days of using Oralzym-F three times daily, the natural healthy oral balance of bacteria will be greatly restored and you will begin to notice healthier gums. Active oral probiotics help you fight oral infections, inflammatory diseases, autoimmune diseases, viral diseases, HIV/AIDS, and cancer. They can line the teeth and the mucous membranes of the gum and the mouth, preventing or reducing tooth infection, abscess in gum and mouth abscess produced by harmful bacteria, viruses and fungi. 

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