Dental caries

Dental caries, also known as tooth decay, cavities, or caries, is a breakdown of teeth due to
activities of bacteri .The cavities may be a number of different colors from yellow to black.
The cause of caries is bacterial break down of the hard tissues of the teeth .This occurs due to
acid made from food debris or sugar on the tooth surface. Simple sugarssimple suger in food are
these bacteria's primary energy source and thus a diet high in simple sugar is a risk factor. If mineral
breakdown is greater than build up from sources such as saliva, caries results. Risk factors include
conditions that result in less saliva such as: diabetes mellitus, Sjogren's syndrome and some
medications. Medications that decrease saliva production include antihistamines and
antidepressants among others.[5] Caries is also associated with poverty, poor cleaning of the mouth,
and receding gums resulting in exposure of the roots of the teeth.[1][6]
Prevention includes: regular cleaning of the teeth, a diet low in sugar, and small amounts of fluoride.
[3][5]
Brushing the teeth two times per day and flossing between the teeth once a day is recommended
by many.[1][5] Fluoride may be from water, salt or toothpasteamong other sources.[3] Treating a
mother's dental caries may decrease the risk in her children by decreasing the numbers of certain
bacteria.[5] Screening can result in earlier detection Depending on the extent of destruction, various
treatments can be used to restore the tooth to proper function or the tooth may be removed. There is
no known method to grow black large amounts of tooth. The availability of treatment is often poor in
the developing world.
Worldwide, approximately 2.43 billion people (36% of the population) have dental caries in their
permanent teeth .The World Health Organizations estimates that nearly all adults have dental caries
at some point in time. In baby teeth it affects about 620 million people or 9% of the population. They
have become more common in both children and adults in recent years.The disease is most
common in the developed world and less common in the developing world due to greater simple
sugar consumption.

Signs and symptoms

A person experiencing caries may not be aware of the disease.[10] 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".[11] 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. [12]
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.
[13]
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 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.[14] 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.[15][16][17]

Cause[edit]
There are four main criteria required for caries formation: a tooth surface (enamel or dentin), cariescausing bacteria, fermentablecarbohydrates (such as sucrose), and time.[18] 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.[19]
Tooth decay is caused by specific types of bacteria that produce acid in the presence
of fermentable carbohydrates such as sucrose,fructose, and glucose.[20][21]
Caries occur more often in people from the lower end of the socioeconomic scale than people from
the upper end of the socioeconomic scale.[22]

Bacteria[edit]
The bacteria most responsible for dental cavities are the mutans streptococci, most
prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. If left untreated,
the disease can lead to pain, tooth loss and infection.[23]
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 Lactobacillus species 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. [20] As the
cementum of root surfaces is more easily demineralized than enamel surfaces, a wider variety of
bacteria can cause root caries includingLactobacillus acidophilus, Actinomyces spp., Nocardia spp.,
and Streptococcus mutans. 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, for example sites with a low rate of salivary flow (molar fissures). Grooves on
the occlusal surfaces of molar and premolar 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.
These bacterial strains, most notably S. mutans can be inherited by a child from a caretaker's kiss or
through feeding premasticated food.[24]

Dietary sugars[edit]
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 calledfermentation.[21] 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. [25] 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.[26]

Teeth[edit]
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.[30] In both cases, teeth may be left more vulnerable to decay because the enamel
is not able to protect the tooth.[31]
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.[32] These minerals,
especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins
to demineralize at a pH of 5.5.[33] Dentin and cementum are more susceptible to caries
than enamel because they have lower mineral content.[34] 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; [35][36] 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 is more likely to
develop (see next section). Also, caries is more likely to develop when food is trapped between
teeth.

Other factors[edit]
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
the submandibular gland and parotid gland, are likely to dry mouth and thus to widespread tooth
decay. Examples include Sjgren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis.
[37]
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 in cannabis, 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 sideeffect.[37] Radiation therapy of the head and neck may also damage thecells in salivary glands,
somewhat increasing the likelihood of caries formation. [38][39]
Susceptibility to caries can be related to altered metabolism in the tooth, in particular to fluid flow in
the dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet "significantly
suppresses the rate of fluid motion" in dentin.[40]
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.[41] Tobacco use is a significant
risk factor for periodontal disease, which can cause the gingiva to recede.[42] 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.[43] 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.[44] Exposure of children to secondhand tobacco smoke is
associated with tooth decay.[45]

Intrauterine and neonatal lead exposure promote tooth decay.[46][47][48][49][50][51][52] Besides lead,
all atoms with electrical charge and ionic radius similar to bivalent calcium,[53]such as cadmium,
mimic the calcium ion and therefore exposure may promote tooth decay.[54]
Poverty is also a significant social determinant for oral health.[55] Dental caries have been linked with
lower socio-economic status and can be considered a disease of poverty.[56]
Forms are available for risk assessment for caries when treating dental cases; this system using the
evidence-based Caries Management by Risk Assessment (CAMBRA).[57] 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. [58]

Pathophysiology[edit]

The progression of pit and fissure caries resembles two triangles with their bases meeting along the junction of
enamel and dentin.

Teeth are bathed in saliva and have a coating of bacteria on them (biofilm) that continually forms.
The minerals in the hard tissues of the teeth (enamel, dentin and cementum) are constantly
undergoing processes of demineralization and remineralisation. Dental caries results when the
demineralization rate is faster than the remineralisation and there is net mineral loss. This happens
when there is an ecologic shift within the dental biofilm, from a balanced population of microorganisms to a population that produce acids and can survive in an acid environment. [59]

Enamel[edit]
Enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical process
brought on by the acidic environment produced by bacteria. As the bacteria consume the sugar and
use it for their own energy, they produce lactic acid. The effects of this process include the
demineralization of crystals in the enamel, caused by acids, over time until the bacteria physically

penetrate the dentin. Enamel rods, which are the basic unit of the enamel structure, run
perpendicularly from the surface of the tooth to the dentin. Since demineralization of enamel by
caries, in general, follows the direction of the enamel rods, the different triangular patterns between
pit and fissure and smooth-surface caries develop in the enamel because the orientation of enamel
rods are different in the two areas of the tooth.[60]
As the enamel loses minerals, and dental caries progresses, the enamel develop several distinct
zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface,
the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone.
[61]
The translucent zone is the first visible sign of caries and coincides with a one to two percent loss
of minerals.[62] A slight remineralization of enamel occurs in the dark zone, which serves as an
example of how the development of dental caries is an active process with alternating changes.
[63]
The area of greatest demineralization and destruction is in the body of the lesion itself. The
surface zone remains relatively mineralized and is present until the loss of tooth structure results in a
cavitation.

Dentin[edit]
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 byodontoblasts, which reside at the border between the
pulp and dentin. Since odontoblasts are present, a stimulus, such as caries, can trigger a biologic
response. These defense mechanisms include the formation of sclerotic and tertiary dentin. [64]
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. [60] The advancing front
represents a zone of demineralised dentine 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 dentine caries has been
reversibly attacked because the collage 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 dentine is irreversibly demineralised.
Sclerotic dentin[edit]
The structure of dentin is an arrangement of microscopic channels, called dentinal tubules, which
radiate outward from the pulp chamber to the exterior cementum or enamel border.[65] The diameter
of the dentinal tubules is largest near the pulp (about 2.5 m) and smallest (about 900 nm) at the
junction of dentin and enamel.[66] The carious process continues through the dentinal tubules, which
are responsible for the triangular patterns resulting from the progression of caries deep into the
tooth. The tubules also allow caries to progress faster.
In response, the fluid inside the tubules bring immunoglobulins from the immune system to fight the
bacterial infection. At the same time, there is an increase of mineralization of the surrounding
tubules.[67] This results in a constriction of the tubules, which is an attempt to slow 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.
According to hydrodynamic theory, fluids within dentinal tubules are believed to be the mechanism
by which pain receptors are triggered within the pulp of the tooth. [68] Since sclerotic dentin prevents
the passage of such fluids, pain that would otherwise serve as a warning of the invading bacteria
may not develop at first. Consequently, dental caries may progress for a long period of time without
any sensitivity of the tooth, allowing for greater loss of tooth structure. [citation needed]

Tertiary dentin[edit]
In response to dental caries, there may be production of more dentin toward the direction of the pulp.
This new dentin is referred to as tertiary dentin.[66] Tertiary 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.[69] If the odontoblasts survive long enough to react to the dental caries, then
the dentin produced is called "reactionary" dentin. If the odontoblasts are killed, the dentin produced
is called "reparative" dentin.
In the case of reparative dentin, other cells are needed to assume the role of the destroyed
odontoblasts. Growth factors, especially TGF-,[69] are thought to initiate the production of reparative
dentin by fibroblasts and mesenchymal cells of the pulp.[70] Reparative dentin is produced at an
average of 1.5 m/day, but can be increased to 3.5 m/day. The resulting dentin contains irregularly
shaped dentinal tubules that may not line up with existing dentinal tubules. This diminishes the ability
for dental caries to progress within the dentinal tubules.

Cementum[edit]
The incidence of cemental caries increases in older adults as gingival recession occurs from either
trauma or periodontal disease. It is a chronic condition that forms a large, shallow lesion and slowly
invades first the roots cementum and then dentin to cause a chronic infection of the pulp (see further
discussion under classification by affected hard tissue). Because dental pain is a late finding, many
lesions are not detected early, resulting in restorative challenges and increased tooth loss. [71]

Prevention[edit]

Toothbrushes are commonly used to clean teeth.

Oral hygiene[edit]
Personal hygiene care consists of proper brushing and flossing daily. The purpose of oral hygiene is
to minimize any etiologic agents of disease in the mouth. The primary focus of brushing and flossing
is to remove and prevent the formation of plaque or dental biofilm. Plaque consists mostly of
bacteria.[82] As the amount of bacterial plaque increases, the tooth is more vulnerable to dental caries
when carbohydrates in the food are left on teeth after every meal or snack. A toothbrush can be used
to remove plaque on accessible surfaces, but not between teeth or inside pits and fissures on
chewing surfaces. When used correctly, dental floss removes plaque from areas that could otherwise
develop proximal caries but only if the depth of sulcus has not been compromised. Other adjunct
oral hygiene aids includeinterdental brushes, water picks, and mouthwashes.
However oral hygiene is probably more effective at preventing gum disease (periodontal disease)
than tooth decay. Food is forced inside pits and fissures under chewing pressure, leading to
carbohydrate-fueled acid demineralisation where the brush, fluoride toothpaste, and saliva have no

access to remove trapped food, neutralise acid, or remineralise demineralised tooth like on other
more accessible tooth surfaces food to be trapped. (Occlusal caries accounts for between 80 and
90% of caries in children (Weintraub, 2001).) Chewing fibre like celery after eating forces saliva
inside trapped food to dilute any carbohydrate like sugar, neutralise acid and remineralise
demineralised tooth. The teeth at highest risk for carious lesions are the permanent first and second
molars due to length of time in oral cavity and presence of complex surface anatomy.
Professional hygiene care consists of regular dental examinations and professional prophylaxis
(cleaning). Sometimes, complete plaque removal is difficult, and a dentist ordental hygienist may be
needed. Along with oral hygiene, radiographs may be taken at dental visits to detect possible dental
caries development in high risk areas of the mouth (e.g. "bitewing" x-rays which visualize the crowns
of the back teeth).

Dietary modification[edit]
For dental health, frequency of sugar intake is more important than the amount of sugar consumed.
[27]
In the presence of sugar and other carbohydrates, bacteria in the mouth produce acids that can
demineralize enamel, dentin, and cementum. The more frequently teeth are exposed to this
environment the more likely dental caries are to occur. Therefore, minimizing snacking is
recommended, since snacking creates a continuous supply of nutrition for acid-creating bacteria in
the mouth. Also, chewy and sticky foods (such as dried fruit or candy) tend to adhere to teeth longer,
and, as a consequence, are best eaten as part of a meal. For children, the American Dental
Association and the European Academy of Paediatric Dentistry recommend limiting the frequency of
consumption of drinks with sugar, and not giving baby bottles to infants during sleep (see earlier
discussion).[83][84] Mothers are also recommended to avoid sharing utensils and cups with their infants
to prevent transferring bacteria from the mother's mouth.[85]
It has been found that milk and certain kinds of cheese like cheddar cheese can help counter tooth
decay if eaten soon after the consumption of foods potentially harmful to teeth. [27] Also, chewing
gum containing xylitol (a sugar alcohol) is widely used to protect teeth in many countries now.
Xylitol's effect on reducing dental biofilm is, it is presumed, due to bacteria's inability to utilize it like
other sugars.[86] Chewing and stimulation of flavor receptors on the tongue are also known to
increase the production and release of saliva, which contains natural buffers to prevent the lowering
of pH in the mouth to the point where enamel may become demineralized. [87]

Other measures[edit]

Common dentistry trays used to deliver fluoride.

Fluoride is sold in tablets for cavity prevention.

The use of dental sealants is a means of prevention.[88] 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.
This deprives resident plaque bacteria carbohydrate preventing the formation of pit and fissure
caries. Sealants are usually applied on the teeth of children, as soon as the tooth erupt but adults
are receiving them if not previously performed. Sealants can wear out and fail to prevent access of
food and plaque bacteria inside pits and fissures and need to be replaced so they must be checked
regularly by dental professionals.
Calcium, as found in food such as milk and green vegetables, is often recommended to protect
against dental caries. Fluoride helps prevent decay of a tooth by binding to the hydroxyapatite
crystals in enamel.[89] The incorporated calcium makes enamel more resistant to demineralization
and, thus, resistant to decay.[90] Topical fluoride is more highly recommended than systemic intake
such as by tablets or drops to protect the surface of the teeth. This may include a
fluoride toothpaste or mouthwash or varnish.[91] After brushing with fluoride toothpaste, rinsing should
be avoided and the excess spat out.[92] This leaves a greater concentration of fluoride residue on the
teeth. Many dental professionals include application of topical fluoride solutions as part of routine
visits and recommend the use of xylitol andamorphous calcium phosphate products. Silver diamine
fluoride may work better than fluoride varnish to prevent cavities.[93] Water fluoridation also lowers the
risk of tooth decay.[94]
Vaccines are also under development.[95]

Treatment[edit]
See also: Dental restoration and Tooth extraction
No carious lesion

No treatment

Inactive lesion

Carious lesion

No treatment

Non-cavitated lesion

Non-operative treatment

Cavitated lesion

Operative treatment

Active lesion

Existing filling

No defect

Defective filling

No replacement

Ditching, overhang

No replacement

Fracture or food impaction

Repair or replacement of filling

Inactive lesion

No treatment

Non-cavitated lesion

Non-operative treatment

Cavitated lesion

Repair or replacement of filling

Active lesion

An amalgam used as a restorative material in a tooth.

Most importantly, whether the carious lesion is cavitated or noncavitated dictates the management.
Clinical assessment of whether the lesion is active or arrested is also important. Noncavitated
lesions can be arrested and remineralization can occur under the right conditions. However, this may
require extensive changes to the diet (reduction in frequency of refined sugars), improved oral
hygiene (toothbrushing twice per day with fluoride toothpaste and daily flossing), and regular
application of topical fluoride. Such management of a carious lesion is termed "non-operative" since
no drilling is carried out on the tooth. Non-operative treatment requires excellent understanding and
motivation from the individual, otherwise the decay will continue.
Once a lesion has cavitated, especially if dentin is involved, remineralization is much more difficult
and a dental restoration is usually indicated ("operative treatment"). Before a restoration can be
placed, all of the decay must be removed otherwise it will continue to progress underneath the filling.
Sometimes a small amount of decay can be left if it is entombed and the there is a seal which
isolates the bacteria from their substrate. This can be likened to placing a glass container over a
candle, which burns itself out once the oxygen is used up. Techniques such as stepwise caries
removal are designed to avoid exposure of the dental pulp and overall reduction of the amount of
tooth substance which requires removal before the final filling is placed. Often enamel which overlies
decayed dentin must also be removed as it is unsupported and susceptible to fracture. The modern
decision-making process with regards the activity of the lesion, and whether it is cavitated, is
summarized in the table.[96]
Destroyed tooth structure does not fully regenerate, although remineralization of very small carious
lesions may occur if dental hygiene is kept at optimal level. [13] For the small lesions, topical fluoride is
sometimes used to encourage remineralization. For larger lesions, the progression of dental caries
can be stopped by treatment. The goal of treatment is to preserve tooth structures and prevent
further destruction of the tooth. Aggressive treatment, by filling, of incipient carious lesions, places
where there is superficial damage to the enamel, is controversial as they may heal themselves, while
once a filling is performed it will eventually have to be redone and the site serves as a vulnerable site
for further decay.[11]
In general, early treatment is quicker and less expensive than treatment of extensive decay.
Local anesthetics, nitrous oxide ("laughing gas"), or other prescription medications may be required

in some cases to relieve pain during or following treatment or to relieve anxiety during treatment.
[97]
A dental handpiece ("drill") is used to remove large portions of decayed material from a tooth. A
spoon, a dental instrument used to carefully remove decay, is sometimes employed when the decay
in dentin reaches near the pulp.[98] Once the decay is removed, the missing tooth structure requires
a dental restoration of some sort to return the tooth to function and aesthetic condition.
Restorative materials include dental amalgam, composite resin, porcelain, and gold.[99] Composite
resin and porcelain can be made to match the color of a patient's natural teeth and are thus used
more frequently when aesthetics are a concern. Composite restorations are not as strong as dental
amalgam and gold; some dentists consider the latter as the only advisable restoration for posterior
areas where chewing forces are great.[100] When the decay is too extensive, there may not be enough
tooth structure remaining to allow a restorative material to be placed within the tooth. Thus,
a crown may be needed. This restoration appears similar to a cap and is fitted over the remainder of
the natural crown of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal.
For children, preformed crowns are available to place over the tooth. These are usually made of
metal (usually stainless steel but increasingly there are aesthetic materials). Traditionally teeth are
shaved down to make room for the crown but, more recently, stainless steel crowns have been used
to seal decay into the tooth and stop it progressing. This is known as the Hall Technique and works
be depriving the bacteria in the decay of nutrients and making their environment less favorable for
them. It is a minimally invasive method of managing decay in children and does not require local
anesthetic injections in the mouth.

A tooth with extensive caries eventually requiring extraction.

In certain cases, endodontic therapy may be necessary for the restoration of a tooth.[101] Endodontic
therapy, also known as a "root canal", is recommended if the pulp in a tooth dies from infection by
decay-causing bacteria or from trauma. During a root canal, the pulp of the tooth, including the nerve
and vascular tissues, is removed along with decayed portions of the tooth. The canals are
instrumented with endodontic files to clean and shape them, and they are then usually filled with a
rubber-like material called gutta percha.[102] The tooth is filled and a crown can be placed. Upon
completion of a root canal, the tooth is now non-vital, as it is devoid of any living tissue.
An extraction can also serve as treatment for dental caries. The removal of the decayed tooth is
performed if the tooth is too far destroyed from the decay process to effectively restore the tooth.
Extractions are sometimes considered if the tooth lacks an opposing tooth or will probably cause
further problems in the future, as may be the case for wisdom teeth.[103] Extractions may also be
preferred by people unable or unwilling to undergo the expense or difficulties in restoring the tooth.

Epidemiology[edit]

Disability-adjusted life year for dental caries per 100,000 inhabitants in 2004.[104]
no data
<50
50-60
60-70
70-80
80-90
90-100

100-115
115-130
130-138
138-140
140-142
>142

Worldwide, approximately 2.43 billion people (36% of the population) have dental caries in their
permanent teeth.[8] In baby teeth it affects about 620 million people or 9% of the population.[8] The
disease is most common in Latin American countries, countries in the Middle East, and South Asia,
and least prevalent in China.[105] In the United States, dental caries is the most
common chronic childhood disease, being at least five times more common than asthma.[106] It is the
primary pathological cause of tooth loss in children.[107] Between 29% and 59% of adults over the age
of fifty experience caries.[108]
The number of cases has decreased in some developed countries, and this decline is usually
attributed to increasingly better oral hygienepractices and preventive measures such as fluoride
treatment.[109] Nonetheless, countries that have experienced an overall decrease in cases of tooth
decay continue to have a disparity in the distribution of the disease. [108] Among children in the United
States and Europe, twenty percent of the population endures sixty to eighty percent of cases of
dental caries.[110] A similarly skewed distribution of the disease is found throughout the world with
some children having none or very few caries and others having a high number.[108] Australia, Nepal,
and Sweden (where children receive dental care paid for by the government) have a low incidence
of cases of dental caries among children, whereas cases are more numerous in Costa
Rica and Slovakia.[111]
The classic DMF (decay/missing/filled) index is one of the most common methods for assessing
caries prevalence as well as dental treatment needs among populations. This index is based on infield clinical examination of individuals by using a probe, mirror and cotton rolls. Because the DMF
index is done without X-ray imaging, it underestimates real caries prevalence and treatment needs. [75]
Bacteria typically associated with dental caries have been isolated from vaginal samples who
have bacterial vaginosis.[112]

History[edit]

An image from Omne Bonum (14th century) depicting a dentist extracting a tooth with forceps.

There is a long history of dental caries. Over a million years ago, hominins such
as Australopithecus suffered from cavities.[113] The largest increases in the prevalence of caries have
been associated with dietary changes.[113][114] Archaeological evidence shows that tooth decay is an
ancient disease dating far into prehistory. Skulls dating from a million years ago through
the neolithic period show signs of caries, including those from the Paleolithic and Mesolithic ages.
[115]
The increase of caries during the neolithic period may be attributed to the increased consumption
of plant foods containing carbohydrates.[116] The beginning of rice cultivation in South Asia is also
believed to have caused an increase in caries. Although there is also some evidence from sites in
Thailand, such as Khok Phanom Di, that shows a decrease in overall percentage of dental caries
with the increase in dependence on rice agriculture. [117]
A Sumerian text from 5000 BC describes a "tooth worm" as the cause of caries.[118] Evidence of this
belief has also been found in India,Egypt, Japan, and China.[114] Unearthed ancient skulls show
evidence of primitive dental work. In Pakistan, teeth dating from around 5500 BC to 7000 BC show
nearly perfect holes from primitive dental drills.[119] The Ebers Papyrus, an Egyptian text from 1550
BC, mentions diseases of teeth.[118] During the Sargonid dynasty of Assyria during 668 to 626 BC,
writings from the king's physician specify the need to extract a tooth due to spreading inflammation.
[114]
In the Roman Empire, wider consumption of cooked foods led to a small increase in caries
prevalence.[110] The Greco-Roman civilization, in addition to the Egyptian, had treatments for pain
resulting from caries.[114]
The rate of caries remained low through the Bronze Age and Iron Age, but sharply increased during
the Middle Ages.[113] Periodic increases in caries prevalence had been small in comparison to the
1000 AD increase, when sugar cane became more accessible to the Western world. Treatment
consisted mainly of herbal remedies and charms, but sometimes also included bloodletting.
[120]
The barber surgeons of the time provided services that included tooth extractions.[114]Learning
their training from apprenticeships, these health providers were quite successful in ending tooth pain
and likely prevented systemic spread of infections in many cases. Among Roman Catholics, prayers
to Saint Apollonia, the patroness of dentistry, were meant to heal pain derived from tooth infection. [121]
There is also evidence of caries increase in North American Indians after contact with colonizing
Europeans. Before colonization, North American Indians subsisted on hunter-gatherer diets, but
afterwards there was a greater reliance on maize agriculture, which made these groups more
susceptible to caries.[113]
During the European Age of Enlightenment, the belief that a "tooth worm" caused caries was also no
longer accepted in the European medical community.[122] Pierre Fauchard, known as the father of
modern dentistry, was one of the first to reject the idea that worms caused tooth decay and noted
that sugar was detrimental to the teeth and gingiva.[123]In 1850, another sharp increase in the
prevalence of caries occurred and is believed to be a result of widespread diet changes. [114] Prior to
this time, cervical caries was the most frequent type of caries, but increased availability of sugar
cane, refined flour, bread, and sweetened tea corresponded with a greater number of pit and fissure
caries.
In the 1890s, W.D. Miller conducted a series of studies that led him to propose an explanation for
dental caries that was influential for current theories. He found that bacteria inhabited the mouth and
that they produced acids that dissolved tooth structures when in the presence of fermentable
carbohydrates.[124] This explanation is known as the chemoparasitic caries theory.[125] Miller's
contribution, along with the research on plaque by G.V. Black and J.L. Williams, served as the
foundation for the current explanation of the etiology of caries. [114] Several of the specific strains of
lactobacilli were identified in 1921 by Fernando E. Rodriguez Vargas.
In 1924 in London, Killian Clarke described a spherical bacterium in chains isolated from carious
lesions which he called Streptococcus mutans. Although Clarke proposed this organism was the
cause of caries the discovery was not followed up. Later, in the 1950s in the USA, Keyes and
Fitzgerald working with hamsters showed that caries was transmissible and caused by an acid-

producing Streptococcus. It was not until the late 1960s that it became generally accepted that
the Streptococcus isolated from hamster caries was the same as S. mutans described by Clarke.[126]
Tooth decay has been present throughout human history, from early hominids millions of years ago,
to modern humans.[127] The prevalence of caries increased dramatically in the 19th century, as
the Industrial Revolution made certain items, such as refined sugar and flour, readily available.
[114]
The diet of the newly industrialized English working class[114] then became centered on bread,
jam, and sweetened tea, greatly increasing both sugar consumption and caries.

Etymology and usage[edit]

Naturalized from Latin into English (a loanword), caries in its English form originated as a mass
noun that means "rottenness",[4][128] that is, "decay". When used in that sense, it takes singular
verb inflections (just like the word decay does). Thus caries was not traditionally a plural word
synonymous with holes or cavities; that is, it was not the plural form of any singular
form cary meaning hole or cavity. Nonetheless, the idea that it is such a plural is
a reanalysis that naturally occurs to most English speakers, and the reanalyzed sense is common
enough to be entered in various dictionaries and to exist in respectable usage. It still shows a hint of
its reanalyzed origins in that it remains idiomatically limited to a plurale tantum sensethat is,
like scissors or glasses, one speaks of plural caries obligately in the pluralnot of one scissor,
glass, or cary. (This is why one can look for a singular count-noun form of dental cary in any of a
dozen major medical and general dictionaries and not find it listed.) Many still use it in the traditional
sense (mass, singular), which is why they speak of carious lesions rather than just caries when they
intend the plural count sense.