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2.4 Caries

Dental caries also known as tooth decay or a cavity, is aninfection,bacterial in origin,

that causes demineralization and destruction of the hard tissues of the teeth (enamel,dentin

and cementum). It is a result of the production of acid by bacterial fermentation of food

debris accumulated on the tooth surface. If demineralization exceeds saliva and other

remineralization factors such as from calcium and fluoridated toothpastes, these once hard

tissues progressively break down, producing dental caries (cavities or carious lesions, that is,

holes in the teeth). Today, caries remains one of the most common diseases throughout the

world. Cariology is the study of dental caries.

Depending on the extent of tooth destruction, various treatments can be used torestore

teeth to proper form, function, and aesthetics, but there is no known method to regenerate

large amounts of tooth structure. Instead, dental health organizations advocate preventive and

prophylactic measures, such as regularoral hygiene and dietary modifications, to avoid dental

caries.

2.4.1 Signs and Symptoms

A person experiencing caries may not be aware of the disease (Health Promotion

Board, 2006). The earliest sign of a new carious lesion is the appearance of a chalky 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" (Richie S.

King, 2011). 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 beregenerated.A lesion that appears dark brown

and shiny suggests dental caries were once present but the demineralization process has

stopped, leaving a stain. Active decay is lighter in color and dull in appearance (Clarke

Johnson, 2007).

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. Once the decay passes

through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become

exposed, resulting in pain that can be transient, temporarily worsening with exposure to heat,

cold, or sweet foods and drinks. A tooth weakened by extensive internal decay can sometimes

suddenly fracture under normal chewing forces. When the decay has progressed enough to

allow the bacteria to overwhelm the pulp tissue in the center of the tooth a toothache can

result and the pain will become more constant. Death of the pulp tissue and infection are
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common consequences. The tooth will no longer be sensitive to hot or cold, but can be very

tender to pressure.

Dental caries can also cause bad breath and foul tastes. In highly progressed cases,

infection can spread from the tooth to the surrounding soft tissues. Complications such as

cavernous sinus thrombosis and Ludwig angina can be life-threatening (Richard W

Hartmann, 2008).

2.4.2 Cause

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

(Southam, 1993). However, it is also known that these four criteria are not always enough to

cause the disease and a sheltered environment promoting development of a cariogenic biofilm

is required. 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 that is exposed to the oral cavity, but not the structures that are retained within the bone

(Smith B et al, 1990) .

The bacteria most responsible for dental cavities are the mutans streptococci, most

prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. If left

untreated, thedisease can lead to pain,tooth loss andinfection.Tooth decay disease is caused

by specific types of bacteria that produceacid in the presence of fermentablecarbohydrates

such as sucrose, fructose, and glucose (Rogers AH, 2008). The mineral content of teeth is

sensitive to increases in acidity from the production of lactic acid. To be specific, a tooth

(which is primarily mineral in content) is in a constant state of back-and-forth

demineralization and remineralizationbetween the tooth and surrounding saliva.For people

with little saliva, especially due to radiation therapies and autoimmune disorders, such as

Sjgren's syndrome, that may destroy thesalivary glands,there also exists therapies such as

saliva substitutes and remineralization products. These patients may be susceptible to dental

caries. When the pH at the surface of the tooth drops below 5.5, demineralization proceeds

faster than remineralization (meaning that there is a net loss of mineral structure on the

tooth's surface).

All caries occur from bacterial acid demineralization that exceeds saliva and fluoride

remineralization, and acid demineralization occurs where bacterial plaque is left on teeth.

Because most plaque-retentive areas are between teeth and inside pits and fissures on

chewing surfaces where brushing is difficult, over 80% of cavities occur inside pits and
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fissures. Areas that are easily cleansed with a toothbrush, such as the front and back surfaces

(facial and lingual), develop fewer cavities.

Some foods have an acidic pH of 5.5 or lower which can result in demineralisation in

the absence of bacteria. This is known as erosion, rather than caries, because the acid is not

bacterial in origin. Attack by acid from systemic complications such as bulimia and stomach

difficulties as well as vomiting can cause tooth erosion.

2.4.2.1 Teeth

There are certain diseases and disorders affecting teeth that may leave an individual at a

greater risk for cavities. 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. In both cases, teeth may be left more vulnerable

to decay because the enamel is not able to protect the tooth (Neville. et al, 2002).

In most people, disorders or diseases affecting teeth are not the primary cause of dental

caries. Approximately 96% of tooth enamel is composed of minerals. These minerals,

especially hydroxyapatite, will become soluble when exposed to acidic environments.

Enamel begins to demineralize at a pH of 5.5 (Dawes, 2003).Dentin andcementum are more

susceptible to caries thanenamelbecause they have lower mineral content (Mellberg, 1986).

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 evidence for linking malocclusion and/or crowding to the dental caries is weak

(Borzabadi-Farahani, A et al, 2011). However, the anatomy of teeth may affect the likelihood

of caries formation. Where the deep developmental grooves of teeth are more numerous and

exaggerated, pit and fissure caries are more likely to develop (see next section). Also, caries

are more likely to develop when food is trapped between teeth (Sherif Mohamed et al, 2012).

2.4.2.2 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. These organisms can produce high levels of lactic acid following 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 surfaces, a wider variety of bacteria can cause root caries including Lactobacillus

acidophilus, Actinomyces spp.,Nocardia spp., and Streptococcus mutans. Bacteria collect
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around the teeth and gums in a sticky, creamy-coloured mass calledplaque,which serves as a

biofilm.Some sites collect plaque more commonly than others, for example sites with a low

rate of salivary flow (molar fissures). Grooves on theocclusal surfaces ofmolar andpremolar

teeth provide microscopic retention sites for plaque bacteria, as do the interproximal sites.

Plaque may also collect above or below the gingiva where it is referred to as supra- or sub-

gingival plaque, respectively (Rogers AH, 2008).

These bacterial strains, most notably S. mutans can be inherited by a child from a

caretaker's kiss or through feeding premasticated food (Douglass, JM, 2008). 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.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 isneutralizedby saliva or mouthwash. Fluoride toothpaste or dental

varnish may aid remineralization. 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

dextranpolysaccharide by the enzyme dextransucranase (Silverstone, 1983).

2.4.2.3 Exposure

The frequency of which teeth are exposed to cariogenic (acidic) environments affects

the likelihood of caries development. After meals or snacks, the bacteria in the mouth

metabolize sugar, resulting in an acidic by-product that decreases pH. As time progresses, the

pH returns to normal due to the buffering capacity ofsaliva 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.

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's 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

(Summit, James B. et al, 2001). Proximal caries take an average of four years to pass through

enamel in permanent teeth. Because thecementum enveloping the root surface is not nearly
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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 (see later discussion).

2.4.2.4 Other factors

Reduced salivary flow rate is associated with increased caries since the buffering

capability of saliva is not present to counterbalance the acidic environment created by certain

foods. As a result, medical conditions that reduce the amount of saliva produced by salivary

glands,in particular thesubmandibular gland andparotid gland,are likely todry mouth and

thus to widespread tooth decay. Examples include Sjgren's syndrome, diabetes mellitus,

diabetes insipidus,andsarcoidosis.Medications, such as antihistamines and antidepressants,

can also impair salivary flow. Stimulants, most notoriously methylamphetamine ("meth

mouth"), also occlude the flow of saliva to an extreme degree. Tetrahydrocannabinol, the

active chemical substance incannabis,also causes a nearly complete occlusion of salivation,

known in colloquial terms as "cotton mouth". Moreover, 63% of the most commonly

prescribed medications in the United States list dry mouth as a known side-effect. Radiation

therapy of the head and neck may also damage the cells in salivary glands, somewhat

increasing the likelihood of caries formation (Neville, B.W. et al, 2002).

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 (Neville,

B.W. et al, 2002). Tobacco use is a significant risk factor for periodontal disease, which can

cause thegingiva torecede (Anonim, 2007). As the gingiva loses attachment to the teeth due

to gingival recession, 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. 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 (Banting, 2006).

Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms

withelectrical charge andionic radius similar to bivalentcalcium,such ascadmium,mimic

the calciumion and therefore exposure may promote tooth decay (Arora M et al, 2008).
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Poverty is also a significant social determinant for oral health.[44] Dental caries have

been linked with lower socio-economic status and can be considered a disease of poverty.

(DYE, 2010).

Forms are available for risk assessment for caries when treating dental cases; this

system using the evidence-basedCaries Management by Risk Assessment (CAMBRA). It is

still unknown if the identification of high-risk individuals can lead to more effective long-

term patient management that prevents caries initiation and arrests or reverses the progression

of lesions (Tellez, 2012).

2.4.3 Classification

Caries can be classified by location, etiology, rate of progression, and affected hard

tissues. These forms of classification can be used to characterize a particular case of tooth

decay in order to more accurately represent the condition to others and also indicate the

severity of tooth destruction. In some instances, caries are described in other ways that might

indicate the cause. G.V. Black classification:

1. Class I - pit and fissure caries (anterior or posterior teeth)

2. Class II - approximal surfaces of posterior teeth

3.

Class III - approximal surfaces of anterior teeth without incisal edge involvement

4.

Class IV - approximal surfaces of anterior teeth with incisal edge involvement

5. Class V - gingival/cervical surfaces on the lingual or facial aspect (anterior or

posterior)

6. Class VI - incisal edge of anterior teeth or cusp heights of posterior teeth

According to the depth of the hole, caries can be grouped into:

1. Caries insipiens

Insipiens caries is caries that occurs on the surface of the tooth enamel. Usually in

these cases no pain tooth enamel appears only in black or brown stains.

2. Superficial caries

This is the caries has reached the inside of the tooth enamel. Sometimes a tooth ache.

3. Caries media

Caries Caries is a media that has reached the dentin (dental bone) or the mid-section

between the surface of the tooth and the pulp. At this stage, the tooth will be sore

when exposed to cold stimuli, sour and sweet foods.
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4. Caries profunda

It is close to or even caries reaches the pulp, causing inflammation of the pulp. At this

stage, the patient will usually feel pain when eating, and even the pain of a sudden

without any stimulation.

5. Radiographic Appearance of Dental Caries

6. Carious lesions are detected intraorally on the occlusal surfaces on posterior

teeth and interproximally on anterior teeth by the clinical examination techniques of

exploring and transillumination. Interproximal carious lesions between the posterior

teeth are not large enough to cause color changes at the marginal ridges are best

detected by bitewing radiographs and in some cases by properly paralleled periapical

radiographs. Facial and lingual caries can also be detected radiographically, but again,

loss of tooth structure must be sufficient to make the lession apparent (Bricker,

Langlais, and Miller, 2002).

7. Carious Lesion Detection

8. Dental caries often occurs bilaterally. Caries as a decay process does not

preferentially attack a molar on one side only. The process is not that specific. If

one discovers a cavity on one tooth in an arch, its counter-part on the opposite side

should be checked, or if. Once caries has been noticed on one proximal surface, it is

wise to check to adjacent surface for decay (Bricker, Langlais, and Miller, 2002) .

9.

10.


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11.

12.Figure 7. A to D, Several patterns of interproximal caries, E, Early interproximal carious lesions on the

lower second bicuspid and first molar (arrows) (Bricker, Langlais, and Miller, 2002).

caries profunda

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