Some bacteria know more about your mouth than you do...


Bad breath, yellow teeth, decay and cavities that lead to hours in a chair with your mouth pried open at the dentist's office. It may seem unclear to many why we are taught to brush our teeth, floss and use fluoride toothpaste, but I assure you that there is good reason behind these activities. Bacteria colonize your oral cavity in enormous numbers. With a warm, nutrient rich environment, bacteria thrive. In particular, Streptococcus mutans is at the center of many common dental issues. Extensive research has shown that the metabolic activities of S. mutans and byproducts given off are majorly responsible for tooth decay. I will take you on a little trip through the biology and some other related topics of S. mutans so that you might be better equipped with the knowledge of this foe to our oral health.

Title: Streptococcus mutans and You; Home Sweet Home in your mouth.
Author: Jesse W. Manton
Date: 12/7/2010

The human body is made up of almost one trillion cells that are vastly outnumbered by bacteria living on and in many of our tissues. One of the major points of entry for bacteria after we have exited the womb is the oral cavity. As children, we undergo what Freudian psychosexual development declares, the oral stage. We experience the world through our mouth. We use our mouth to explore our fingers, toys, pets, dirt and far more foul things as well. The connection seems fairly obvious that by our exploration and food consumption, we have invited bacteria into us from day one. In the oral cavity, a warm, moist, nutrient rich medium correlates to bacterial growth like a tropical vacation might be to humans. Dental infections such as tooth decay and periodontal disease are some of the most common bacterial infections in humans, though non-life-threatening in nature, these infestations can have a significant effect on overall systemic health.3 Of the bacteria that gain residency and make up these infections in the oral cavity are various Streptococcal strains of bacteria. The best defined species among the oral streptococci that has shown cariogenicity is Streptococcus mutans¸ who prefer to colonize on the surface of teeth as opposed to other oral tissues.2 In the oral cavity there exists a dynamic ecosystem of interacting microbiota, metabolizing remnant nutrients as fuel sources and signaling through chemical messages. As formation of dental plaque begins to occur on erupted teeth, S. mutans and other bacteria are critical factors in the development of periodontal disease as well as the demineralization, degradation,decay of teeth and related tissues. To protect ourselves from the deleterious effects of our symbiotic oral microbial floral, proper dental hygiene is an essential part of our daily routine for prevention of infection and maintenance of oral tissue health and longevity.

S. mutans are nonmotile, catalse-negative, gram-positive streptococci that exist in the oral cavity with such other streptococci as S. sanguis, S. minitor, S. salivarius and S. milleri. Each of these bacteria has their own distinctive preferred micro habitat including a particular surface that they prefer to colonize. The colonization of the mouth by bacteria begins before the eruption of teeth in newborns. With the eruption of teeth, this provides another surface upon which bacteria can attach and plaque formation may occur. The number of bacteria that can exist in dental plaque has been recorded to reach 108 per mg (wet weight).2 Clinical studies have shown that plaque adherence to teeth is a critical factor in both dental caries and in periodontal disease. By chemical signaling and the production of dextrin, bacteria can clump together into biofilms on the surface of the teeth. When these bacteria have a source of carbohydrates such as glucose, sucrose or fructose, they are capable of synthesizing polysaccharide that allow this adherence to teeth surfaces and to one another. The location of predominant plaque adhesion on the tooth surface has been shown to be greatest on the crownal surfaces along the gum line and in-between adjacent teeth.3 Understandably, this can be predicted and is observed as the location of caries in many individuals.
In the oral cavity, humans produce salivary glycoprotein that coats the teeth in with a thin layer of negatively charged invisible film called the Acquired Enamel Pellicle (AEP). This is one of the initial protective mechanisms we use to resist adherence of the outwardly negatively charged invading bacteria.3 The build-up of plaque on the surface of teeth overcomes this protective mechanism. Some research suggests that S. mutans acts like a negative charged particle and the presence of calcium and protamine phosphate significantly increased the uptake of bacteria, whereas fluorides and phosphates present in our saliva decreased the uptake of cells based upon their electrostatic nature and the interactions of charged particles.2
Some of the metabolic byproducts that S. mutans produces include ethanol, formate, acetic acid and majorly lactic acid in the presence of excess glucose. Reported as a homofermentative lactic acid bacterium, S. mutans' metabolic mechanisms have been shown to vary regarding environmental conditions, which leads to utilization of various carbohydrate nutrient sources and a variety of acidic products. Acid is very rapidly produced by S. mutans metabolism, having been shown to give a pH drop from 7 to 4.2 in only 24 hours.2 S. mutans can ferment glucose, lactose, raffinose, mannitol, lnulin and salicin with production of acid. Glucose and sucrose have been experimentally shown to support equally exponential rates of cell growth when using as the energy source for S. mutans metabolism, with sucrose playing a vital role in adherence to teeth and cariogenisis.2 These same polysaccharides as well as other nutrients required for these microbes to live in the oral cavity are found in the food from human diets.
Glucose is the predominate carbohydrate monomer that is used by almost every living organism in the synthesis of energy storage molecules as well as structural components of cells. Many of these polysaccharides that are built from glucose are used as a human sources of energy.4 Humans consume carbohydrate rich pastas, sweets, beverages et cetera that begin their digestion in our oral cavity with salivary amylase hydrolyzing oligosaccharides and polysaccharides into smaller carbohydrate units. Since glucose is universal in its utilization by life forms, S. mutans in the oral cavity that find remnant carbohydrates lingering from mastication, will use those remnants as a nutrient source for their survival and reproduction.
Cariology is the study of dental caries and cariogenesis.1 This refers to the formation of cavities in the tissues of teeth and how they progress. Through extensive research with strains of streptococci and lab animals, S. mutans has been proven to be one the prime offenders in cariogenesis. Strains of S. mutans tend to cause smooth-surface and pit-and-fissure caries in animals, however there is variation in the pattern and severity of the induced carious lesions. Dietary factors are critical in this variation, with sucrose-rich diets demonstrating to be the most cariogenic and supportive of the most rapid progressive pathogenesis.2
Direct methods of controlling S. mutans presence in the oral cavity have been experimentally approached. Use of antimicrobial agents has proven quite successful for maintenance and improvement of oral health. S. mutans is very susceptible to penicillin G, sulfadiazine, ampicillin, erythromycin, cephalothin, methicillin, vancomycin, kanamycin and iodine to name a few.2 Research in the realm of immunization against S. mutans has been explored. Serum antibodies for S. mutans have been shown to play a protective role. Patients with immunoglobulin dysfunction have been found to have a greater susceptibility to dental caries.2 The importance of saliva and its components to maintain oral health is paramount. Salivary antibodies that recognize common antigenic bacteria of the oral cavity have been identified as a key component of protection. When a human has low levels of salivary immunoglobulin, there is a heightened risk of developing caries via bacteria. By increasing the local immune response, S. mutans shows a direct reduction of carious lesion formation.2 These reductions were greater on smooth surfaces which are easier to access, than on occlusal surfaces which have high levels of adherence and difficult accessibility.
Salivary pH and fluoride have a critical role in preventing infection by S. mutans. Fluoride ion is an important sugar transport and metabolism inhibitor used by humans. Uncharged HF molecules are taken into a bacterial cell and will dissociate into fluoride ion with a lowered pH environment. Fluoride toxicity to S. mutans is derived from fluoride’s ability to inhibit glycolysis metabolism in the step requiring enolase.3 Optimal levels of drinking water fluoridation as well as fluoride toothpaste and topical fluoride treatment by dental professionals are means taken to prevent infestation and tooth decay by S. mutans on a public health level. Saliva helps maintains the pH of the oral cavity and combats bacterial inhabitants. Many proteins are secreted by salivary glands, including lysozyme and other macromolecules which have antibacterial properties, acting as part of the human non-specific immune defense. Balancing the pH changes that follow mastication of various pH foods and consumption of beverages as well as yielded effects of the byproducts from fermentative action by S. mutans et cetera is an important part of the constant war over your oral health.
The pH of the oral cavity also affects the demineralization and remineralization of tooth tissues. The early characterization of an enamel lesion is an intact surface with a subsurface that has experienced the effects of demineralization. Diffusion of organic acids from aciduric S. mutans and other aciduric microbes into the enamel creates a decreased pH environment and is the beginning of the demineralization process. As the pH in the oral cavity returns to a more neutral environment, remineralization of the enamel can occur via saliva and its constituents. Restriction of plaque acid, introduced dietary acids as well as fluoride treatment can assist in the process of remineralization.3 When the system of demineralization of the tooth by S. mutans’ acidic byproducts and the remineralization by saliva is interfered with, the enamel subsurface is weakened and this contributes the progression toward clinical decay.3

Dental caries can primarily be prevented or controlled by understanding the dynamics of our oral bacteria, especially S. mutans. In addition to reduced colonization, dietary and consumption routine changes as well as fluoride treatment of teeth can beneficially affect the longevity and health of these tissues. Reducing the colonization of S. mutans can be accomplished with a robust oral hygiene regiment including regular brushing, flossing, mouthwash use, fluoride treatment and biannual dental professional check-ups. As individuals in a first world country, we have immediate access to oral health care and hygienic products useful in preventing S. mutans caused tooth decay. A future look at the possibilities of combating S. mutans and other decay-promoting oral bacteria requires a vision that can see the wide spread treatment of this extremely common human disease throughout the world and its underserved populations. With effective and progressive research to find low cost solutions for preventative care, perhaps we may be able to take tooth decay off the list of most common bacterial infections once and for all.

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