UWP 104F

Everybody Carries Dental Caries

Although largely preventable through practicing good oral hygiene, dental decay, also

known as caries, remains one of the most prevalent chronic diseases in children and adults

(NIDCR 2014). Caries may sometimes be used interchangeably with the term cavities, but it is

important to note that they are not the same. Whereas cavities are identified as discrete flaws in

normal tooth structure, dental caries is the process by which acidic metabolic byproducts of

bacteria lead to the gradual destruction of tooth structure. Cavities may or may not occur in the

presence of dental decay; many people experience dental decay without developing cavities. To

better understand the process, let us first discuss the composition and anatomy of the tooth.

At the center of the tooth is a soft gel-like core, called dental pulp. This area contains

blood vessels and nerves that allow for transportation of nutrients and sensation, respectively.

The pulp is also the home to specialized cells that can synthesize and secrete dentin, a calcified

tissue that surrounds the pulp. Besides protecting the core, dentin serves to provide shock

absorption and support to the outermost layer of the tooth known as the enamel. This exterior

level is composed primarily of a mineral compound called calcium hydroxyapatite. The chemical

structure of the mineral allows it to be compacted into elongated enamel rods consistent in both

shape and size (Selvig 1972). This feature is what makes enamel the hardest substance in the

human body.

Four elements lead to the production of caries. The first is the susceptibility of enamel

and dentin to acidic demineralization. These tooth structures will also serve as a platform for

which bacteria will stick to. The second component is the oral microbiome, which is estimated to

consist of 500 to 700 colonized bacterial species (Dewhirst 2010). However, only a couple of

UWP 104F these species are oral pathogens, namely Streptococcus mutans and lactobacilli. The third factor

is the presence of fermentable sugars, such as sucrose, which the bacteria will act on. Lastly, an

adequate amount of time for the above components to interact is necessary for producing the acid

that leads to dental decay.

The production of acid by bacteria is relatively complex and warrants a more detailed

explanation. Amongst the oral microbiome, Streptococcus mutans is particularly important

because studies have suggested that it is the chief pathogen. S. mutans exceptional ability to

adhere to the non-shedding tooth surface between adjacent teeth begins the disease process. In

the presence of sucrose, the pathogen will start to produce a sticky matrix of cells that houses a

community of different bacterial strains, known as biofilm. The buildup of biofilms allows the

persistent proliferation of bacteria. Sucrose serves a second purpose by fueling the metabolism of

the bacteria found in biofilms. During this process, a sucrose molecule is split into glucose and

fructose, which are both smaller sugar molecules. While fructose is fermented to provide energy

for growth, glucose molecules are used as a carbon source producing lactic acid as a byproduct

(Nishimura 2012). Since these metabolic processes are occurring within the biofilm matrix, the

increase in acid inevitably lowers the pH of the biofilm-covered tooth surface. In chemistry, pH

measures the acidity of an environment with lower pH values indicating higher acidity. As the

pH drops below 5.5 on the tooth surface, decalcification of the enamel occurs (Ubertalli 2012).

As mentioned previously, enamel and dentin are primarily composed of organized calcium

molecules. When the acid reacts with the mineral lattice, the solid tooth literally dissolves.

The reaction described above is reversible if the intake of sugar is halted. In this case,

acid buffers that are naturally found in human saliva help resist decreases in pH, which allow the

pH to rise back to a normal level. Saliva also contains mineral salts, such as calcium and

UWP 104F phosphate, both of which are necessary to remineralize the tooth. However, once bacteria have

dissolved enough enamel to reach the layer of dentin, irreversible decalcification has occurred.

These microorganisms may travel through the dentin to reach the pulpal nerves, causing pain and

temperature sensitivities for a person who is experiencing this degree of dental decay. If no

professional action is taken to remove and treat the infection, the decay may cause swelling that

cut off the blood supply in the pulp leading to possible toothaches or other complications.

Risk for this disease may stem from a variety of factors. Firstly, some teeth may

inherently have deep, narrow cracks extending from tooth surface to dentin. This flawed

anatomy allows bacteria to hide due to the inability of a tooth brush bristle to penetrate to their

narrow depths, decreasing cleansability while increasing susceptibility to caries. As expected,

certain foods or beverages, such as chewy candy and soda, are undoubtedly more likely to cause

dental decay due to high sugar content. Furthermore, the adhesive nature of these foods makes it

difficult for saliva to wash them off of enamel surfaces. The degree to which a person is exposed

to fluoride can also affect risk. Flouride actively promotes remineralization of enamel and helps

resist decalcification by the inhibition of bacterial metabolism of sugars.

Although dental caries is a common disease, it can be easily prevented or reversed by

adopting good oral hygiene. Brushing gently but thoroughly at least twice a day can help remove

dental plaque and prevent accumulation of oral pathogens and their acidic metabolic byproducts.

Since toothbrush bristles cannot effectively reach in between adjacent teeth, flossing at least once

per day is recommended to get rid of remaining plaque. As with any chronic disease, regular

visits to a health-care professional is recommended; people should visit a dentist twice a year for

oral cleanings that remove stubborn calculus (hard, mineralized plaque). This type of plaque may

accumulate despite a patients best efforts in brushing and flossing. If not enough attention is put

UWP 104F into taking good care of teeth, dental carries will surely continue to be one of the most prevalent

chronic diseases.

UWP 104F References:

Ubertalli, J., author. 2012 Caries [Internet]. Merck Sharp & Dohme Corp; [cited 2014 April 14]. Available from: http://www.merckmanuals.com/professional/dental_disorders/common_dental_disorders/caries.html?qt=caries&alt=sh Nishimura, J., author. 2012, Biofilm Formation by Streptococcus mutans and Related Bacteria [internet]. Scientific Research Publishing; [cited 2014 April 14]. Available from: http://dx.doi.org/10.4236/aim.2012.23025 Loesche, W. 1986. Role of Streptococcus mutans in Human Dental Decay. Microbiological Reviews. Dec. 1986: 353-380; [cited 2014 April 14].

NIDCR, 2014. Dental Caries (Tooth Decay) [Internet]. NIH; [cited 2014 April 15] Available from: https://www.nidcr.nih.gov/DataStatistics/FindDataByTopic/DentalCaries/DentalCariesAdults20to64.htm

Selvig, K. 1972. The Crystal Structure of Hydroxyapatite in Dental Enamel as Seen with the Electron Microscope. Journal of Ultrastructure Research [Internet]. [cited 2014 April 15]; 41(3-4): 369-375. Available from: http://www.sciencedirect.com/science/article/pii/S0022532072900767

Dewhirst, F. 2010. The Human Oral Microbiome. J. Bacteriology [Internet]. [cited 2014 April 15]; 192(19): 5002-5017. Available from: http://jb.asm.org/content/192/19/5002.full

NIDCR, 2014. Dental Caries (Tooth Decay) [Internet]. NIH; [cited 2014 April 15] Available from:Selvig, K. 1972. The Crystal Structure of Hydroxyapatite in Dental Enamel as Seen with the Electron Microscope. Journal of Ultrastructure Research [Internet]. [cited 2014 April 15]; 41(3-4): 369-375. Available from: http://www.sciencedirect.com/scienc...Dewhirst, F. 2010. The Human Oral Microbiome. J. Bacteriology [Internet]. [cited 2014 April 15]; 192(19): 5002-5017. Available from: http://jb.asm.org/content/192/19/5002.full