Causes

There are four main criteria required for caries formation: a tooth surface (enamel or dentin); caries-causing bacteria; fermentable carbohydrates (such as sucrose); and time.[24] The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth which is exposed to the oral cavity, but not the structures which are retained within the bone.[25]

Teeth

There are certain diseases and disorders affecting teeth which may leave an individual at a greater risk for caries. Amelogenesis imperfecta, which occurs between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth.[26] In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.[27]
In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Ninety-six percent of tooth enamel is composed of minerals.[28] These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5.[29] Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content.[30] Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.
The anatomy of teeth may affect the likelihood of caries formation. Where the deep grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop. Also, caries are more likely to develop when food is trapped between teeth.
A gram stain image of Streptococcus mutans.

Bacteria

The mouth contains a wide variety of oral bacteria, but only a few specific species of bacteria are believed to cause dental caries: Streptococcus mutans and Lactobacilli among them.[3][5] Lactobacillus acidophilus, Actinomyces viscosus, Nocardia spp., and Streptococcus mutans are most closely associated with caries, particularly root caries. Bacteria collect around the teeth and gums in a sticky, creamy-coloured mass called plaque, which serves as a biofilm. Some sites collect plaque more commonly than others. The grooves on the biting surfaces of molar and premolar teeth provide microscopic retention, as does the point of contact between teeth. Plaque may also collect along the gingiva.

Fermentable carbohydrates

Bacteria in a person's mouth convert glucose, fructose, and most commonly sucrose (table sugar) into acids such as lactic acid through a glycolytic process called fermentation.[4] If left in contact with the tooth, these acids may cause demineralization, which is the dissolution of its mineral content. The process is dynamic, however, as remineralization can also occur if the acid is neutralized by saliva or mouthwash. Fluoride toothpaste or dental varnish may aid remineralization.[31] If demineralization continues over time, enough mineral content may be lost so that the soft organic material left behind disintegrates, forming a cavity or hole. The impact such sugars have on the progress of dental caries is called cariogenicity. Sucrose, although a bound glucose and fructose unit, is in fact more cariogenic than a mixture of equal parts of glucose and fructose. This is due to the bacteria utilising the energy in the saccharide bond between the glucose and fructose subunits. S.mutans adheres to the biofilm on the tooth by converting sucrose into an extremely adhesive substance called dextran polysaccharide by the enzyme dextransucranase.[32]

Time

The frequency of which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development.[33] After meals or snacks, the bacteria in the mouth metabolize sugar, resulting in an acidic by-product which decreases pH. As time progresses, the pH returns to normal due to the buffering capacity of saliva and the dissolved mineral content of tooth surfaces. During every exposure to the acidic environment, portions of the inorganic mineral content at the surface of teeth dissolves and can remain dissolved for two hours.[34] Since teeth are vulnerable during these acidic periods, the development of dental caries relies heavily on the frequency of acid exposure.
The carious process can begin within days of a tooth erupting into the mouth if the diet is sufficiently rich in suitable carbohydrates. Evidence suggests that the introduction of fluoride treatments have slowed the process.[35] Proximal caries take an average of four years to pass through enamel in permanent teeth. Because the cementum enveloping the root surface is not nearly as durable as the enamel encasing the crown, root caries tends to progress much more rapidly than decay on other surfaces. The progression and loss of mineralization on the root surface is 2.5 times faster than caries in enamel. In very severe cases where oral hygiene is very poor and where the diet is very rich in fermentable carbohydrates, caries may cause cavities within months of tooth eruption. This can occur, for example, when children continuously drink sugary drinks from baby bottles.

Other risk factors

Reduced saliva is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As result, medical conditions that reduce the amount of saliva produced by salivary glands, particularly the submandibular gland and parotid gland, are likely to lead to widespread tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis.[36] Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. Abusers of stimulants tend to have poor oral hygiene. Tetrahydrocannabinol, the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known colloquially as "cotton mouth". Moreover, sixty-three percent of the most commonly prescribed medications in the United States list dry mouth as a known side effect.[36] Radiation therapy of the head and neck may also damage the cells in salivary glands, increasing the likelihood of caries formation.[37]
The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries.[38] Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede.[39] As the gingiva loses attachment to the teeth, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel.[15] Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries.[40]
Intrauterine and neonatal lead exposure promote tooth decay.[41][42][43][44][45][46][47] Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,[48] such as cadmium, mimic the calcium ion and therefore exposure may promote tooth decay.[49]
Salivary and dietary iodine seems to play an important role in pathogenesis of dental caries and in salivary glands physiology. Saliva is rich in peroxidase enzymes and has high secretion of iodides. Iodine is able to penetrate directly through intact enamel in dentine, pulp and periodontal tissues and according to some researchers it is able to prevent some dental pathologies directly with antibacterial action, and also indirectly with an antioxidant mechanism.
- Venturi S, Venturi M. (2009). Iodine in evolution of salivary glands and in oral health. Nutr Health. 2009;20(2):119-34.
- Banerjee, R.K. and Datta, A.G. (1986). Salivary peroxidases. Mol Cell Biochem, 70, 21-9.
- Hardgrove, T.A.: ADA Booklet (1939). “Dental Caries” published in 1939 by the American Dental Association (ADA). (Lynch, Kettering, Gies, eds.).
- Bartelstone, H. J. (1951). Radioiodine penetration through intact enamel with uptake by bloodstream and thyroid gland. J Dent Res., 5, 728–33.
- Bartelstone, H.J., Mandel, I.D., Oshry, E. and Seidlin, S.M. (1947). Use of Radioactive Iodine as a Tracer in the Study of the Physiology of Teeth.