14.2 Caries

Caries (dental cavity, tooth decay) is a breakdown of teeth caused by bacteria. Symptoms include pain and difficulty with eating. Complications may include inflammation of the tissue around the tooth, tooth loss, and infection or abscess formation.

Cause

The cause of caries is acid from bacteria in dental plaque dissolving the hard tissues of the teeth (enamel, dentin and cementum). The acid is produced by the bacteria when they ferment food debris or sugar on the tooth surface. The mouth contains a wide variety of microorganisms but only a few bacteria are believed to cause dental caries infecting the enamel. Streptococcus mutans and Lactobacillus species among them.

Streptococcus mutans are gram-positive plaque builders and early colonizers of the dental pellicle. These organisms can produce high levels of lactic acid through fermentation of dietary sugars and are resistant to the adverse effects of low pH, properties essential for cariogenic bacteria. As the cementum of root surfaces is more easily demineralized than enamel on crown surfaces, a wider variety of bacteria can cause root caries, including Lactobacillus acidophilus, Actinomyces, Nocardia, and Streptococcus mutans.

Progression

A grows of plaque results in caries when it produced irreversible demineralization of the tooth. This can be very localized and some sites are more vulnerable than others. Sites with a low rate of salivary flow such as the grooves on the occlusal surfaces of molar and premolar teeth protect plaque from saliva and potentially from the tooth brush. Interproximal surfaces between teeth are another site where the plaque has a reduced likelihood of being removed.

Enamel

A person experiencing caries may initially not be aware of the disease. No pain is experienced and no reaction by the tooth is produced while only the enamel is being affected. The earliest sign of a new carious lesion is the appearance of an opaque white spot on the surface of the tooth, indicating an area of demineralization of enamel. This is referred to as a white spot lesion, an incipient carious lesion or a "microcavity".

As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated. A lesion that appears dark brown and shiny suggests dental caries were once present but the demineralization process stopped, leaving a stain. Active decay is initially light in color and opaque in appearance.

Enamel is a highly mineralized acellular tissue and caries act upon it through slowly through chemical demineralization. The hydroxyapatite crystals in enamel are organized in enamel rods which mostly run perpendicularly from the dentin to the surface of the tooth. Some curvature is added to this orientation, however, around surface features such as groves, ridges and pits. Demineralization of enamel by caries tends to follow the direction of the enamel rods. Knowledge of the patterns of orientation of enamel rods in the tooth, therefore, allows the dentist to predict the shape of the caries and facilitates its treatment.

Cementum

The protection that cementum offers to the tooth against caries is reduced in comparison to that offered by enamel. The roots are therefore more susceptible to caries than the crown. The incidence of cemental caries increases in older adults as gingival recession occurs from either trauma or periodontal disease.

Dentin

Once the infection reaches the dentin, it produces transient or constant pain which worsens upon exposure to heat, cold, or sweet foods and drinks. This is because the dentinal tubules, which extend into the pulp, transmit chemical and physical stimuli to the odontoblasts and pain receptors in the pulp.

Unlike enamel, the dentin reacts to the progression of dental caries. After tooth formation, the ameloblasts, which produce enamel, are destroyed once enamel formation is complete and thus cannot later regenerate enamel after its destruction. On the other hand, dentin is produced continuously throughout life by odontoblasts, which reside at the border between the pulp and dentin. After the tooth erupts, the odontoblasts greatly decelerate the speed of dentin production, switching from manufacturing primary to secondary dentin. Caries stimulate the odontoblasts to intensify the production of dentin. These defense mechanisms include the formation of sclerotic and tertiary dentin.

In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the advancing front, the zone of bacterial penetration, and the zone of destruction. The advancing front represents a zone of demineralised dentin due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentin caries has been reversibly attacked because the collagen matrix is not severely damaged, giving it potential for repair. The outer more superficial zone is highly infected with proteolytic degradation of the collagen matrix and as a result the dentin is irreversibly demineralized.

Sclerotic dentin

Dentinal tubules radiate outward from the pulp chamber to the cementum or enamel border. The diameter of the dentinal tubules is largest near the pulp (about 2.5 μm) and smallest (about 900 nm) at the junction of dentin and enamel. The carious process expands through the dentinal tubules. This gives rise to the triangular patterns shape of caries within dentin.

In response to the caries, the fluid inside the tubules brings immunoglobulins (antibodies) from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the tubules. This results in a constriction of the tubules, which slows down the bacterial progression. In addition, as the acid from the bacteria demineralizes the hydroxyapatite crystals, calcium and phosphorus are released, allowing for the precipitation of more crystals which fall deeper into the dentinal tubule. These crystals form a barrier and slow the advancement of caries. After these protective responses, the dentin is considered sclerotic.

Since sclerotic dentin blocks the connection between the carious infection and the pulp pain that would otherwise serve as a warning of the invading bacteria may not develop. Consequently, dental caries may progress for a long period of time without any sensitivity of the tooth. Without pain, the caries may remain untreated for longer and result in greater loss of tooth structure.

Tertiary dentin

As another response to dental caries, odontoblasts may intensify the production of new dentin (tertiary dentin) toward the pulp. This additional dentin is produced to protect the pulp for as long as possible from the advancing bacteria. As more tertiary dentin is produced, the size of the pulp decreases. This type of dentin has been subdivided according to the presence or absence of the original odontoblasts. If it is produced by the original odontoblasts that formed the tooth the dentin produced is called reactionary dentin. If new odontoblasts differentiate in the pulp to produced it the dentin is called reparative dentin.

Pulp

When the caries reaches the pulp it causes inflammation of the pulpar tissue (pulpitis). Since the pulp is surrounded by hard tissue, the swelling caused by the inflammatory response causes a pressure build up in the pulpar chamber. This exerts pressure on the nerves of the tooth and can lead to intense pain and throbbing.

Pulpitis can also result from dental trauma or from exposure to heat. In such cases it can be reversible, but when caused by caries it almost always results in the death of tooth. The pressure build up and accompanying pain are relieved when the crown is opened (by the dentist or by the caries). If left untreated, the infection extends along the radicular pulp and passes through the apical foramina of the roots to enter the jaw bone. This forms an abscess (see chapter 15 Periodontal Disease). The abscess may form a fistula, a passage that extends from the abscess and opens at the surface of the gums or skin to relief the pressure and to drain the pus that is formed by the inflammation.

The infection can also expand from the abscess into other body tissues and become life-threatening. The tooth should be treated with root canal therapy, which involves removing all pulpar tissues, cleaning the pulp chamber and roots, filling them with a synthetic material and fitting a prosthetic crown to the tooth.

Diagnosis

The presentation of caries is highly variable. However, the risk factors and stages of development are similar. Initially, it may appear as a small chalky area (smooth surface caries), which may eventually develop into a large cavitation. As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch.

Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer. Visual and tactile inspection along with radiographs are employed frequently among dentists, in particular to diagnose pit and fissure caries. Early uncavitated caries is often diagnosed by blowing air across the suspect surface. This removes moisture and facilitates the detection of shine and texture differences between the unmineralized enamel and the surrounding healthy tissue. Dental radiographs (X-rays) may show dental caries before it is otherwise visible or when it is concealed as when it develops between the teeth. Laser imaging can also be used to reveal the shape and size of caries before initiating the treatment.

Classification

Caries are be classified by location, severity, and affected hard tissues. The G.V. Black classification is frequently used to indicate the type of tooth and position of the cavity:

• Class I. Occlusal surfaces of posterior teeth, buccal or lingual pits on molars, lingual pit near cingulum of maxillary incisors.

• Class II. Proximal surfaces of posterior teeth.

• Class III. Interproximal surfaces of anterior teeth without incisal edge involvement.

• Class IV. Interproximal surfaces of anterior teeth with incisal edge involvement.

• Class V. Cervical third of facial or lingual surface of tooth.

• Class VI. Incisal or occlusal edge is worn away due to attrition.
  
  

The severity of caries is described with four categories:

• Incipient. Caries advanced through less then half of the enamel cover.

• Moderate. Caries passed half of the enamel but did not reach the dentin.

• Advanced. Caries advanced through less then half of the dentin cover.

• Severe. Caries advanced through more then half of the dentin cover.

Prevention

Oral hygiene

The risk of caries can be reduced with proper brushing and flossing daily. The goal is to remove all plaque from the surfaces of the teeth. Plaque growths faster and produces more acid when carbohydrates in the food are left on teeth after every meal or snack. The toothbrush is highly effective at removing plaque on accessible surfaces, but it is not as useful between teeth. When used correctly, dental floss removes plaque between teeth. Additional aids include interdental brushes, water picks, and mouthwashes.

Daily brushing prevents periodontal disease more than tooth decay. This is because food forced inside pits and fissures of posterior teeth cannot be removed by the brush or the floss and it is not exposed enough to the protective action of saliva. The majority of caries in children occur on the oclusal surfaces of posterior teeth. The teeth at highest risk for carious lesions are the permanent first molars in part because they are the first permanent teeth to erupt and they frequently do so before children become effective and performing their oral hygiene.

Professional dental hygiene involves regular examination and cleaning. Examination includes both visual and x-ray screening whereas cleaning targets the removal of plaque and calculus.

Diet

The risk of cavities increases with the frequency of sugar consumption. Minimizing snacking is recommended, especially with chewy and sticky sweets (candy, cookies, potato chips, and crackers) that tend to adhere to teeth for long. Parents should limit the frequency of consumption of drinks with sugar by children.

Other measures

Dental sealants are frequently used to prevent cavities in the occlusal surfaces of posterior teeth. A sealant is a thin plastic-like coating applied to the chewing surfaces of the molars to prevent food from being trapped inside pits and fissures. Sealants are usually applied on the teeth of children, as soon as the teeth erupt. They are effective but they can wear out and fail, so regular inspection is important.

Fluoride binds to the hydroxyapatite crystals in enamel and hinders demineralization while also inhibiting the attachment of bacteria to the tooth. Topical fluoride can be found in some treated tap water (varies with city), toothpaste, mouthwash and fluoride tablets. It can also be applied as a varnish by dental professionals.

Summary

The acid produced by bacteria in plaque through lactic fermentation causes gradual demineralization of the enamel. As it progresses deeper, the infection forms a cavity and the structural damage cannot be reversed anymore. Pain starts when the infection reaches the dentin. The pulp reacts making the dentin sclerotic at the site of the infection and this may stop the pain temporarily. The pulp also responds producing tertiary dentin. Infection of the pulp causes pulpitis and can produce intense pain. The infection can extend through the roots and form an abscess in the jaw bone.

Key terms

Dental cavity, tooth decay, caries, Streptococcus, Lactobacillus, Stephen curve, demineralization, smooth surface cavity, pit and fissure cavity, root cavity, enamel rod, dentinal tubule, odontoblast, sclerotic dentin, tertiary dentin, reparative dentin, reactionary dentin, dental explorer, laser speckle imaging, toothbrushing, flossing, fluoride, pulpitis, dental abscess, fistula, root canal therapy.

Figure credits

Figure 1 by Suyash.dwivedi - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=40104921

Figure 2 by Lesion - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=31848724

Figure 3 by Photo Credit:Content Providers(s): Streptococcus mutansTranswiki approved by: w:en:User:Dmcdevit - Centers for Disease Control and Prevention's Public Health Image Library (PHIL) #1043 (https://phil.cdc.gov/details.aspx?pid=1043). Wikipedia:en., Public Domain, https://commons.wikimedia.org/w/index.php?curid=2740715

Figure 4 by KDS4444 - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=52526358

Figure 5a by I, ADuran, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2306956

Figure 5b by ADuran - self-made; tooth is GFDL, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2298759

Figure 6 by Dozenist - Self-retouched, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=4078391

Figure 7 by Amdeana - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=44830307

Figure 8 by Jessr6544 (Jessr65444) - Own work, Public Domain, https://commons.wikimedia.org/w/index.php?curid=3662447

Figure 9 by Jonas Bergsten - Photo taken by Jonas Bergsten using a Canon PowerShot G3., Public Domain, https://commons.wikimedia.org/w/index.php?curid=228100

Figure 10 by Mysid - Own work, Public Domain, https://commons.wikimedia.org/w/index.php?curid=1580982

Figure 11 by Dozenist – CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=212658