Introduction to Caries Process

Dental caries, commonly known as cavities, is a process that may take place on any tooth surface in the oral cavity where dental plaque is allowed to develop over a period of time 1. Dental caries is a bacterial infection, transmitted principally through the saliva, which leads to the destruction of enamel, dentin, and cementum. In dental caries, as in many other infectious diseases, there are three basic elements that must be present in order for this disease process to take place. These elements are the biologic agent, the host response, and the oral environment 2. The biological agents in dental caries are various bacteria common to plaque such as: Streptococcus mutans, Streptococcus sobrinus, Lactobacilli and other pathogens. The host refers to the immune response and saliva (quantity, quality and composition) and how they affect caries formation. The environment in dental caries consists of dietary intake of fermentable carbohydrates. When these three elements are present on any tooth surface, dental caries is the result. The hallmark clinical feature of dental caries is tooth demineralization and destruction.

Mineralization Equilibrium in Teeth

In order to understand why dental caries causes tooth destruction, we must first look at what teeth are composed of. The three basic tissues that compose teeth are enamel, dentin, and cementum.






Functional parts of a tooth. 3



All three of these tissues have high levels of calcium in their crystal structures and hence share the characteristic of being mineralized tissues. Because they are composed of mineralized tissues, teeth are subject to both demineralization (loss of calcium or other minerals from the crystal structure) and remineralization (addition of calcium or other minerals to the crystal structure).

Whether the tooth is remineralizing or demineralizing depends on the pH in the oral cavity. If the pH is above 5.5 (the critical pH for enamel 1) teeth will remineralize and tooth structure will be strengthened. When the pH falls below 5.5 teeth will undergo demineralization and weaken tooth structure (see photographs below). The rate of tooth destruction from demineralization is variable between individuals and is dependent on time, host immune response, location on the tooth, and other factors.



Smooth-surface caries. Clinical appearance of white "chalky" lesions of enamel demineralization (maxillary premolar and cuspid) and cavitation (lateral incisor) in a patient with rampant caries. 4



Pit and fissure caries.
A, Diagram of the characteristic shape of lesions demonstrating a small triangle-shaped lesion in the fissure of the occlusal enamel (brown) that appears narrow at the surface but wider at the dentoenamel junction to provide an even greater involvement of dentin (white). The pulp of the tooth reacts with the deposition of reparative dentin (blue).
B, Clinical appearance of molar with fissure caries, exhibiting the black areas of disintegration at the base of the fissure and the demineralized and undermined white opaque areas surrounding the enamel. 4


Biologic Agents: Plaque and Bacteria

Plaque
The agent in cariogenesis is plaque. Plaque is a biofilm composed of several different kinds of bacteria and their products that develop over the enamel on a layer known as pellicle. The process of plaque formation takes several days to weeks and will cause the surrounding environment to become acidic 5. The surface of enamel attracts salivary glycoproteins and bacterial products creating a layer known as pellicle. This thin layer forms on the surface of the enamel within minutes of its exposure. These glycoproteins include proline rich proteins that allow bacterial adhesion 7.

Colonizers
The first bacteria to attach to these pellicle glycoproteins are gram positive aerobic cocci such as Streptococcus sanguis 7. These bacteria are able to replicate in the oxygen rich environment of the oral cavity and form micro-colonies within minutes after attachment. Other bacteria including Strep mutans are able to grow in these colonies. Streptococcus mutans is important because it is associated with dental caries 10. These bacteria produce an enzyme known as glucosyl transferase. Glucosyl transferase converts sucrose into exopolysacharides. These exopolysacharides create a sticky environment that allows other bacteria to attach to the initial colonies and protect them from acidic environments.

As the plaque begins to develop and expand, oxygen can no longer diffuse into the colonies. After a few days anaerobic gram negative cocci, rods, and filaments begin to colonize the plaque 8. After several weeks the cocci, rods, and filaments grow together forming colonies known as corncobs. This anaerobic environment causes facultative anaerobes such as S. mutans and Lactobacilli to break down sucrose through fermentation pathways. These bacteria produce lactic acid as a metabolic byproduct 9. If the concentration of lactic acid becomes high enough it can cause the pH around the plaque to drop below 5.5 and demineralization will occur 10.

Changes in plaque composition over a 3-week period:
A, At 1 day. B, At 3 days, the cocci and a few filaments characterize the plaque. C, After 1 week, the filamentous organisms increase in number. D, By 3 weeks, the filamentous organisms predominate in the plaque. 6



Micrographs of (A) smooth-surface plaque showing the many relationships between different bacterial forms, including palisading and corn-cob formation and (B) mature plaque with compact bacteria and calcification at the base (approximately '5000). 5


Host Response: Saliva and Immune Response

Saliva
The ability of the oral cavity to protect itself comes in the form of saliva. Saliva is a complex oral fluid consisting of a mixture of secretions from the major salivary glands and the minor glands of the oral mucosa 1. Saliva is generated in glands and moved into the oral environment via ducts or openings. There are 3 major salivary glands; the parotid, submandibular, and the sublingual.

Major salivary glands of the oral cavity 11.

There are also numerous minor salivary glands found throughout the mouth and throat. Roughly 0.5 to 1.0 liters of saliva is produced per day with about 90% of that coming from the major glands 11. Most saliva production occurs with stimulation from food, but, there is also a steady slow amount of saliva that helps to moisten and protect the teeth, tongue and mucous membranes of the mouth and throat. Saliva functions to provide a healthy environment through physical, chemical and antibacterial properties 12:

• Physical: Due to its water content and the variations of flow rate saliva is able to physically cleanse the oral cavity of food and debris which will retard plaque formation. It also dilutes and removes organic acids from dental plaque 12.
  


• Chemical: Saliva is able to regulate pH levels. Electrolytes and organic molecules found in saliva minimize the drop of pH due to demineralization and promote remineralization. For example, sodium phosphate acts as a neutralizer while sialin acts to raise pH to neutral levels. The calcium and phosphate dissolved in the saliva provide the building blocks for remineralization. It also provides minerals which are taken up by the incompletely formed enamel surface soon after eruption 1.
  


• Antibacterial: Saliva contains many antibacterial components including mucins, lysozymes, lactoferrin, perioxidase and most importantly immunoglobulins. These components inhibit bacterial replication and promote destruction of bacteria and their products 12.
  

Due to the fact that saliva plays such a significant role in keeping the oral environment healthy the occurrence of dry mouth, or xerostomia, can be very harmful. There are many causes of xerostomia but 3 in particular are the most effective at damaging salivary gland function. These are radiotherapy in the region of the glands, drugs and disease 1. Decreased salivary flow results in lower amount of mineral for remineralization and no liquid to buffer bacterial acid. This causes higher plaque accumulation which ultimately results in higher caries formation.

Carious lesions on teeth affected by xerostomia 1


Immune Response
The immune response to bacteria that cause caries is in the form of immunoglobulins (Ig). Immunoglobulins function by attaching to foreign objects, such as bacteria, and assist in destroying them. The effect of the following 2 immunoglobulins is the principal immune response in the oral cavity 12.

• Secretory Immunoglobulin A (S-IgA): This is the predominant Ig found in saliva. The main effect of S-IgA is inhibition of bacterial adhesion. This is done specifically by blocking bacterial adhesins, reducing their hydrophobicity and enhancing agglutination 11.
  
• Immunoglobulin G (IgG): IgG functions much IgA in that it inhibits bacterial adherence and enzyme function. However, while IgG is found in the oral cavity the exact role in host protection is uncertain 12.
  

Oral Environment

The component of the oral environment that promotes caries is the fermentable carbohydrate. These carbohydrates are introduced into the environment by the foods we eat, where they are broken down into simple sugars. These simple sugars, such as sucrose, are used by bacteria to produce lactic acid and exopolysacharides. These components allow the bacteria to thrive and develop plaque 12.

After eating a meal rich in fermentable carbohydrates, the pH in your mouth may drop for an hour or more. Although the mouth clears these sugars and equilibrates the pH through saliva production, this extended period of acidity can demineralize tooth structure. If the sugar and acidity remain on the teeth for a longer period, damage to tooth structure will be more critical. Some examples of this process are intermittently drinking soft drinks throughout the day, putting a baby to bed with a bottle of juice, or snacking between meals 12. Studies have shown that snacking between meals can increase your development of caries by 9 times, as opposed to eating meals without snacking in between 13.

These harmful effects can be counteracted and remineralization promoted. Refraining from snacking between meals, especially extremely acidic or sugary foods, will maintain the oral cavity at a more neutral pH. Chewing gum after meals will help stimulate saliva flow thus allowing it anti-cariogenic and buffering activities. Mechanical removal of plaque via brushing /flossing is the most efficient method of reducing cariogenic agents. Fluoride administration through topical applications, rinses, or water supply will help shift the oral cavity to conditions favorable of tooth remineralization 12.

References

1. Kidd, Edwina. Essentials of Dental Caries: The Disease and Its Management, 3rd Edition. 062005: Oxford University Press, USA, 062005. 1.1.

2. Burt BA, Ismail AL. Diet, nutrition and food Cariogenicity. Journal of Dental Research. 1986; 65: 1475-84.

3. Guyton, Arthur C.. Textbook of Medical Physiology, 11th Edition. 062005: Saunders Book Company, 062005. Chapter 79, figure 12.

4. Sapp, J. Philip. Contemporary Oral and Maxillofacial Pathology, 2nd Edition. 092003: Mosby, 092003

5. Samaranayake, Lakshman. Essential Microbiology for Dentistry, 3rd Edition. Churchill Livingstone, 092006.

6. Avery, James K.. Essentials of Oral Histology and Embryology: A Clinical Approach, 3rd Edition. C.V. Mosby, 012006.

7. Newman, Michael G.. Carranza's Clinical Periodontology, 10th Edition. Saunders Book Company, 072006. 9.4.2.

8. Harris, Norman O.. Primary Preventive Dentistry, 6th Edition. Prentice Hall, 082003. 2.4).

9. Miller, Chris H.. Infection Control and Management of Hazardous Materials for the Dental Team, 3rd Edition. Mosby, 092004. 2.3.3.3).

10. Roberson, Theodore. Sturdevant's Art and Science of Operative Dentistry, 5th Edition. C.V. Mosby, 042006. 3.2.2.

11. http://www.merck.com/media/mmhe2/figures/MMHE_08_111_01_eps.gif

12. Proctor and Gamble (2000). The Dental Caries Process and Prevention Strategies. [Interactive CD ROM]. Cincinnati: Bridge Integrated Communications

13. Gustafsson B, Quensel C, Swenander Lanke L, et al. The Vipeholm Dental Caries Study. Acta Odontol Scand. 1954; 11:232-364.