Dental caries

Dental caries, also known as tooth decay, cavities,or caries, is a breakdown of teeth due to activities ofbacteria.[1] The cavities may be a number of differentcolors from yellow to black.[2] Symptoms may includepain and difficulty with eating.[2][3] Complications mayinclude inflammation of the tissue around the tooth, toothloss, and infection or abscess formation.[4][2]

The cause of caries is bacterial break down of the hardtissues of the teeth (enamel, dentin and cementum). Thisoccurs due to acid made from food debris or sugar onthe tooth surface. Simple sugars in food are these bacte-ria’s primary energy source and thus a diet high in simplesugar is a risk factor. If mineral breakdown is greater thanbuild up from sources such as saliva, caries results. Riskfactors include conditions that result in less saliva suchas: diabetes mellitus, Sjogren’s syndrome and some med-ications. Medications that decrease saliva production in-clude antihistamines and antidepressants among others.[5]Caries is also associated with poverty, poor cleaning ofthe mouth, and receding gums resulting in exposure ofthe roots of the teeth.[1][6]

Prevention includes: regular cleaning of the teeth, a dietlow in sugar, and small amounts of fluoride.[3][5] Brush-ing the teeth two times per day and flossing between theteeth once a day is recommended by many.[1][5] Fluo-ride may be from water, salt or toothpaste among othersources.[3] Treating a mother’s dental caries may de-crease the risk in her children by decreasing the num-bers of certain bacteria.[5] Screening can result in earlierdetection.[1] Depending on the extent of destruction, var-ious treatments can be used to restore the tooth to properfunction or the tooth may be removed.[1] There is noknown method to grow back large amounts of tooth.[7]The availability of treatment is often poor in the develop-ing world.[3] Paracetamol (acetaminophen) or ibuprofenmay be taken for pain.[1]

Worldwide, approximately 2.43 billion people (36% ofthe population) have dental caries in their permanentteeth.[8] The World Health Organizations estimates thatnearly all adults have dental caries at some point intime.[3] In baby teeth it affects about 620 million peopleor 9% of the population.[8] They have becomemore com-mon in both children and adults in recent years.[9] Thedisease is most common in the developed world and lesscommon in the developing world due to greater simplesugar consumption.[1] Caries is Latin for “rottenness”.[4]

1 Signs and symptoms

(A) A small spot of decay visible on the surface of a tooth. (B)The radiograph reveals an extensive region of demineralizationwithin the dentin (arrows). (C) A hole is discovered on the sideof the tooth at the beginning of decay removal. (D) All decayremoved.

A person experiencing caries may not be aware of thedisease.[10] The earliest sign of a new carious lesion is theappearance of a chalky white spot on the surface of thetooth, indicating an area of demineralization of enamel.This is referred to as a white spot lesion, an incipient car-ious lesion or a “microcavity”.[11] As the lesion contin-ues to demineralize, it can turn brown but will eventu-ally turn into a cavitation (“cavity”). Before the cavityforms, the process is reversible, but once a cavity forms,the lost tooth structure cannot be regenerated. A lesionthat appears dark brown and shiny suggests dental carieswere once present but the demineralization process hasstopped, leaving a stain. Active decay is lighter in colorand dull in appearance.[12]

As the enamel and dentin are destroyed, the cavity be-comes more noticeable. The affected areas of the toothchange color and become soft to the touch. Once the de-cay passes through enamel, the dentinal tubules, whichhave passages to the nerve of the tooth, become exposed,resulting in pain that can be transient, temporarily wors-ening with exposure to heat, cold, or sweet foods anddrinks.[13] A tooth weakened by extensive internal decaycan sometimes suddenly fracture under normal chewingforces. When the decay has progressed enough to allowthe bacteria to overwhelm the pulp tissue in the center of

1

2 2 CAUSE

the tooth a toothache can result and the pain will becomemore constant. Death of the pulp tissue and infection arecommon consequences. The tooth will no longer be sen-sitive 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 thetooth to the surrounding soft tissues. Complications suchas cavernous sinus thrombosis and Ludwig angina can belife-threatening.[15][16][17]

2 Cause

Diagrammatic representation of acidogenic theory of causationof dental caries. Four factors, namely, a suitable carbohydratesubstrate (1), micro-organisms in dental plaque (2), a susceptibletooth surface (3) and time (4); must be present together for dentalcaries to occur (5). Saliva (6) and fluoride (7) are modifyingfactors

There are four main criteria required for caries formation:a tooth surface (enamel or dentin), caries-causing bac-teria, fermentable carbohydrates (such as sucrose), andtime.[18] However, it is also known that these four cri-teria are not always enough to cause the disease and asheltered environment promoting development of a cari-ogenic biofilm is required. The caries process does nothave an inevitable outcome, and different individualswill be susceptible to different degrees depending on theshape of their teeth, oral hygiene habits, and the bufferingcapacity of their saliva. Dental caries can occur on anysurface of a tooth that is exposed to the oral cavity, butnot the structures that are retained within the bone.[19]

Tooth decay is caused by specific types of bacteriathat produce acid in the presence of fermentablecarbohydrates such as sucrose, fructose, andglucose.[20][21]

Caries occur more often in people from the lower end ofthe socioeconomic scale than people from the upper endof the socioeconomic scale.[22]

A gram stain image of Streptococcus mutans.

2.1 Bacteria

The bacteria most responsible for dental cavities are themutans streptococci, most prominently Streptococcus mu-tans and Streptococcus sobrinus, and lactobacilli. If leftuntreated, the disease can lead to pain, tooth loss andinfection.[23]

The mouth contains a wide variety of oral bacteria,but only a few specific species of bacteria are be-lieved to cause dental caries: Streptococcus mutans andLactobacillus species among them. These organisms canproduce high levels of lactic acid following fermentationof dietary sugars, and are resistant to the adverse effectsof low pH, properties essential for cariogenic bacteria.[20]As the cementum of root surfaces is more easily deminer-alized than enamel surfaces, a wider variety of bacteriacan cause root caries including Lactobacillus acidophilus,Actinomyces spp., Nocardia spp., and Streptococcus mu-tans. Bacteria collect around the teeth and gums in asticky, creamy-colouredmass called plaque, which servesas a biofilm. Some sites collect plaque more commonlythan others, for example sites with a low rate of salivaryflow (molar fissures). Grooves on the occlusal surfacesof molar and premolar teeth provide microscopic reten-tion sites for plaque bacteria, as do the interproximal sites.Plaque may also collect above or below the gingiva whereit is referred to as supra- or sub-gingival plaque, respec-tively.These bacterial strains, most notably S. mutans can be in-herited by a child from a caretaker’s kiss or through feed-ing premasticated food.[24]

2.2 Dietary sugars

Bacteria in a person’s mouth convert glucose, fructose,and most commonly sucrose (table sugar) into acidssuch as lactic acid through a glycolytic process calledfermentation.[21] If left in contact with the tooth, theseacids may cause demineralization, which is the disso-lution of its mineral content. The process is dynamic,

2.4 Teeth 3

however, as remineralization can also occur if the acid isneutralized by saliva or mouthwash. Fluoride toothpasteor dental varnish may aid remineralization.[25] If dem-ineralization continues over time, enough mineral contentmay be lost so that the soft organic material left behinddisintegrates, forming a cavity or hole. The impact suchsugars have on the progress of dental caries is called cario-genicity. Sucrose, although a bound glucose and fructoseunit, is in fact more cariogenic than a mixture of equalparts of glucose and fructose. This is due to the bacte-ria utilising the energy in the saccharide bond betweenthe glucose and fructose subunits. S.mutans adheres tothe biofilm on the tooth by converting sucrose into an ex-tremely adhesive substance called dextran polysaccharideby the enzyme dextransucranase.[26]

2.3 Exposure

“Stephan curve”, showing sudden decrease in plaque pH follow-ing glucose rinse, which returns to normal after 30-60 min. Netdemineralization of dental hard tissues occurs below the criticalpH (5.5), shown in yellow.

The frequency of which teeth are exposed to cariogenic(acidic) environments affects the likelihood of cariesdevelopment.[27] After meals or snacks, the bacteria inthe mouth metabolize sugar, resulting in an acidic by-product that decreases pH. As time progresses, the pHreturns to normal due to the buffering capacity of salivaand the dissolved mineral content of tooth surfaces. Dur-ing every exposure to the acidic environment, portions ofthe inorganic mineral content at the surface of teeth dis-solves and can remain dissolved for two hours.[28] Sinceteeth are vulnerable during these acidic periods, the de-velopment of dental caries relies heavily on the frequencyof acid exposure.The carious process can begin within days of a tooth’serupting into the mouth if the diet is sufficiently richin suitable carbohydrates. Evidence suggests that theintroduction of fluoride treatments have slowed theprocess.[29] Proximal caries take an average of four yearsto pass through enamel in permanent teeth. Because the

cementum enveloping the root surface is not nearly asdurable as the enamel encasing the crown, root cariestends to progress much more rapidly than decay on othersurfaces. The progression and loss of mineralization onthe root surface is 2.5 times faster than caries in enamel.In very severe cases where oral hygiene is very poor andwhere the diet is very rich in fermentable carbohydrates,cariesmay cause cavities withinmonths of tooth eruption.This can occur, for example, when children continuouslydrink sugary drinks from baby bottles (see later discus-sion).

2.4 Teeth

There are certain diseases and disorders affecting teeththat may leave an individual at a greater risk for cavi-ties. Amelogenesis imperfecta, which occurs between 1in 718 and 1 in 14,000 individuals, is a disease in whichthe enamel does not fully form or forms in insufficientamounts and can fall off a tooth.[30] In both cases, teethmay be left more vulnerable to decay because the enamelis not able to protect the tooth.[31]

In most people, disorders or diseases affecting teeth arenot the primary cause of dental caries. Approximately96% of tooth enamel is composed of minerals.[32] Theseminerals, especially hydroxyapatite, will become solublewhen exposed to acidic environments. Enamel begins todemineralize at a pH of 5.5.[33] Dentin and cementumare more susceptible to caries than enamel because theyhave lower mineral content.[34] Thus, when root surfacesof teeth are exposed from gingival recession or periodon-tal disease, caries can develop more readily. Even in ahealthy oral environment, however, the tooth is suscepti-ble to dental caries.The evidence for linking malocclusion and/or crowdingto the dental caries is weak;[35][36] however, the anatomyof teeth may affect the likelihood of caries formation.Where the deep developmental grooves of teeth are morenumerous and exaggerated, pit and fissure caries is morelikely to develop (see next section). Also, caries is morelikely to develop when food is trapped between teeth.

2.5 Other factors

Reduced salivary flow rate is associated with increasedcaries since the buffering capability of saliva is notpresent to counterbalance the acidic environment cre-ated by certain foods. As a result, medical condi-tions that reduce the amount of saliva produced bysalivary glands, in particular the submandibular glandand parotid gland, are likely to dry mouth and thus towidespread tooth decay. Examples include Sjögren’ssyndrome, diabetes mellitus, diabetes insipidus, andsarcoidosis.[37] Medications, such as antihistamines andantidepressants, can also impair salivary flow. Stim-ulants, most notoriously methylamphetamine (“meth

4 3 PATHOPHYSIOLOGY

mouth”), also occlude the flow of saliva to an extremedegree. Tetrahydrocannabinol, the active chemical sub-stance in cannabis, also causes a nearly complete occlu-sion of salivation, known in colloquial terms as “cottonmouth”. Moreover, 63% of the most commonly pre-scribed medications in the United States list dry mouth asa known side-effect.[37] Radiation therapy of the head andneck may also damage the cells in salivary glands, some-what increasing the likelihood of caries formation.[38][39]

Susceptibility to caries can be related to alteredmetabolism in the tooth, in particular to fluid flow inthe dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet “significantly suppresses the rateof fluid motion” in dentin.[40]

The use of tobacco may also increase the risk for cariesformation. Some brands of smokeless tobacco containhigh sugar content, increasing susceptibility to caries.[41]Tobacco use is a significant risk factor for periodontaldisease, which can cause the gingiva to recede.[42] As thegingiva loses attachment to the teeth due to gingival reces-sion, the root surface becomes more visible in the mouth.If this occurs, root caries is a concern since the cementumcovering the roots of teeth is more easily demineralizedby acids than enamel.[43] Currently, there is not enoughevidence to support a causal relationship between smok-ing and coronal caries, but evidence does suggest a re-lationship between smoking and root-surface caries.[44]Exposed of children to secondhand tobacco smoke is as-sociated with tooth decay.[45]

Intrauterine and neonatal lead exposure promote toothdecay.[46][47][48][49][50][51][52] Besides lead, all atoms withelectrical charge and ionic radius similar to bivalentcalcium,[53] such as cadmium, mimic the calcium ion andtherefore exposure may promote tooth decay.[54]

Poverty is also a significant social determinant for oralhealth.[55] Dental caries have been linked with lowersocio-economic status and can be considered a diseaseof poverty.[56]

Forms are available for risk assessment for carieswhen treating dental cases; this system using theevidence-based Caries Management by Risk Assessment(CAMBRA).[57] It is still unknown if the identificationof high-risk individuals can lead to more effective long-term patient management that prevents caries initiationand arrests or reverses the progression of lesions.[58]

3 Pathophysiology

Teeth are bathed in saliva and have a coating of bacte-ria on them (biofilm) that continually forms. The min-erals in the hard tissues of the teeth (enamel, dentinand cementum) are constantly undergoing processes ofdemineralization and remineralisation. Dental caries re-sults when the demineralization rate is faster than theremineralisation and there is net mineral loss. This hap-

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

pens when there is an ecologic shift within the dentalbiofilm, from a balanced population of micro-organismsto a population that produce acids and can survive in anacid environment.[59]

3.1 Enamel

Enamel is a highly mineralized acellular tissue, and cariesact upon it through a chemical process brought on by theacidic environment produced by bacteria. As the bacteriaconsume the sugar and use it for their own energy, theyproduce lactic acid. The effects of this process includethe demineralization of crystals in the enamel, caused byacids, over time until the bacteria physically penetratethe dentin. Enamel rods, which are the basic unit of theenamel structure, run perpendicularly from the surface ofthe tooth to the dentin. Since demineralization of enamelby caries, in general, follows the direction of the enamelrods, the different triangular patterns between pit and fis-sure and smooth-surface caries develop in the enamel be-cause the orientation of enamel rods are different in the

3.2 Dentin 5

two areas of the tooth.[60]

As the enamel loses minerals, and dental caries pro-gresses, the enamel develop several distinct zones, visibleunder a light microscope. From the deepest layer of theenamel to the enamel surface, the identified areas are the:translucent zone, dark zones, body of the lesion, and sur-face zone.[61] The translucent zone is the first visible signof caries and coincides with a one to two percent loss ofminerals.[62] A slight remineralization of enamel occursin the dark zone, which serves as an example of how thedevelopment of dental caries is an active process with al-ternating changes.[63] The area of greatest demineraliza-tion and destruction is in the body of the lesion itself. Thesurface zone remains relatively mineralized and is presentuntil the loss of tooth structure results in a cavitation.

3.2 Dentin

Unlike enamel, the dentin reacts to the progression ofdental caries. After tooth formation, the ameloblasts,which produce enamel, are destroyed once enamel for-mation is complete and thus cannot later regenerateenamel after its destruction. On the other hand, dentinis produced continuously throughout life by odontoblasts,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 mech-anisms include the formation of sclerotic and tertiarydentin.[64]

In dentin from the deepest layer to the enamel, the distinctareas affected by caries are the advancing front, the zoneof bacterial penetration, and the zone of destruction.[60]The advancing front represents a zone of demineraliseddentine due to acid and has no bacteria present. The zonesof bacterial penetration and destruction are the locationsof invading bacteria and ultimately the decomposition ofdentin. The zone of destruction has a more mixed bacte-rial population where proteolytic enzymes have destroyedthe organic matrix. The innermost dentine caries hasbeen reversibly attacked because the collage matrix is notseverely damaged, giving it potential for repair. The outermore superficial zone is highly infected with proteolyticdegradation of the collagen matrix and as a result the den-tine is irreversibly demineralised.

3.2.1 Sclerotic dentin

The structure of dentin is an arrangement of microscopicchannels, called dentinal tubules, which radiate outwardfrom the pulp chamber to the exterior cementum orenamel border.[65] The diameter of the dentinal tubules islargest near the pulp (about 2.5 μm) and smallest (about900 nm) at the junction of dentin and enamel.[66] Thecarious process continues through the dentinal tubules,which are responsible for the triangular patterns resultingfrom the progression of caries deep into the tooth. The

The faster spread of caries through dentin creates this triangularappearance in smooth surface caries.

tubules also allow caries to progress faster.In response, the fluid inside the tubules bringimmunoglobulins from the immune system to fightthe bacterial infection. At the same time, there is anincrease of mineralization of the surrounding tubules.[67]This results in a constriction of the tubules, which is anattempt to slow the bacterial progression. In addition,as the acid from the bacteria demineralizes the hydrox-yapatite crystals, calcium and phosphorus are released,allowing for the precipitation of more crystals which falldeeper into the dentinal tubule. These crystals form abarrier and slow the advancement of caries. After theseprotective responses, the dentin is considered sclerotic.According to hydrodynamic theory, fluids within dentinaltubules are believed to be the mechanism by which painreceptors 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 in-vading bacteria may not develop at first. Consequently,dental caries may progress for a long period of time with-out any sensitivity of the tooth, allowing for greater loss

6 4 DIAGNOSIS

of tooth structure.

3.2.2 Tertiary dentin

In response to dental caries, there may be production ofmore dentin toward the direction of the pulp. This newdentin is referred to as tertiary dentin.[66] Tertiary dentinis produced to protect the pulp for as long as possiblefrom the advancing bacteria. As more tertiary dentin isproduced, the size of the pulp decreases. This type ofdentin has been subdivided according to the presence orabsence of the original odontoblasts.[69] If the odonto-blasts survive long enough to react to the dental caries,then the dentin produced is called “reactionary” dentin. Ifthe odontoblasts are killed, the dentin produced is called“reparative” dentin.In the case of reparative dentin, other cells are needed toassume the role of the destroyed odontoblasts. Growthfactors, especially TGF-β,[69] are thought to initiatethe production of reparative dentin by fibroblasts andmesenchymal cells of the pulp.[70] Reparative dentin isproduced at an average of 1.5 μm/day, but can be in-creased to 3.5 μm/day. The resulting dentin contains ir-regularly shaped dentinal tubules that may not line upwithexisting dentinal tubules. This diminishes the ability fordental caries to progress within the dentinal tubules.

3.3 Cementum

The incidence of cemental caries increases in older adultsas gingival recession occurs from either trauma or peri-odontal disease. It is a chronic condition that forms alarge, shallow lesion and slowly invades first the root’scementum and then dentin to cause a chronic infectionof the pulp (see further discussion under classification byaffected hard tissue). Because dental pain is a late finding,many lesions are not detected early, resulting in restora-tive challenges and increased tooth loss.[71]

4 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 sur-face caries), which may eventually develop into a largecavitation. Sometimes caries may be directly visible.However other methods of detection such as X-rays areused for less visible areas of teeth and to judge the extentof destruction. Lasers for detecting caries allow detectionwithout ionizing radiation and are now used for detectionof interproximal decay (between the teeth). Disclosingsolutions are also used during tooth restoration to mini-mize the chance of recurrence.Primary diagnosis involves inspection of all visible toothsurfaces using a good light source, dental mirror and

The tip of a dental explorer, which is used for caries diagnosis.

explorer. Dental radiographs (X-rays) may show dentalcaries before it is otherwise visible, in particular cariesbetween the teeth. Large dental caries are often apparentto the naked eye, but smaller lesions can be difficult toidentify. Visual and tactile inspection along with radio-graphs are employed frequently among dentists, in par-ticular to diagnose pit and fissure caries.[72] Early, uncav-itated caries is often diagnosed by blowing air across thesuspect surface, which removes moisture and changes theoptical properties of the unmineralized enamel.Some dental researchers have cautioned against the useof dental explorers to find caries,[73] in particular sharpended explorers. In cases where a small area of tooth hasbegun demineralizing but has not yet cavitated, the pres-sure from the dental explorer could cause a cavity. Since

4.2 Early childhood caries 7

the carious process is reversible before a cavity is present,it may be possible to arrest the caries with fluoride andremineralize the tooth surface. When a cavity is present,a restoration will be needed to replace the lost tooth struc-ture.At times, pit and fissure caries may be difficult to de-tect. Bacteria can penetrate the enamel to reach dentin,but then the outer surface may remineralize, especially iffluoride is present.[74] These caries, sometimes referredto as “hidden caries”, will still be visible on x-ray radio-graphs, but visual examination of the tooth would showthe enamel intact or minimally perforated.The differential diagnosis for dental caries includes dentalfluorosis and developmental defects of the tooth includ-ing hypomineralization of the tooth and hypoplasia of thetooth.[75]

4.1 Classification

G.V. Black Classification of Restorations

Caries can be classified by location, etiology, rate of pro-gression, and affected hard tissues.[76] These forms ofclassification can be used to characterize a particular caseof tooth decay in order to more accurately represent thecondition to others and also indicate the severity of toothdestruction. In some instances, caries are described inother ways that might indicate the cause. G.V. Black clas-sification:

• Class I - occlusal surfaces of posterior teeth, buccalor lingual pits on molars, lingual pit near cingulumof maxillary incisors

• Class II - proximal surfaces of posterior teeth

• Class III - interproximal surfaces of anterior teethwithout incisal edge involvement

• Class IV - interproximal surfaces of anterior teethwith incisal edge involvement

• Class V - cervical third of facial or lingual surfaceof tooth

• Class VI - incisal or occlusal edge worn away due toattrition

Rampant caries caused by methamphetamine abuse.

4.2 Early childhood caries

Early childhood caries (ECC) or "Baby bottle caries,”"baby bottle tooth decay,” or “Bottle Rot” is a patternof decay found in young children with their deciduous(baby) teeth. The teeth most likely affected are the max-illary anterior teeth, but all teeth can be affected.[77] Thename for this type of caries comes from the fact that thedecay usually is a result of allowing children to fall asleepwith sweetened liquids in their bottles or feeding childrensweetened liquids multiple times during the day.[78]

Another pattern of decay is “rampant caries”, which sig-nifies advanced or severe decay on multiple surfaces ofmany teeth.[79] Rampant caries may be seen in individ-uals with xerostomia, poor oral hygiene, stimulant use(due to drug-induced dry mouth[80]), and/or large sugarintake. If rampant caries is a result of previous radiationto the head and neck, it may be described as radiation-induced caries. Problems can also be caused by the self-destruction of roots and whole tooth resorption when newteeth erupt or later from unknown causes.

4.2.1 Rate of progression

Temporal descriptions can be applied to caries to indicatethe progression rate and previous history. “Acute” sig-nifies a quickly developing condition, whereas “chronic”describes a condition that has taken an extended time todevelop, in which thousands of meals and snacks, manycausing some acid demineralization that is not remineral-ized, eventually results in cavities.Recurrent caries, also described as secondary, are cariesthat appears at a location with a previous history of caries.This is frequently found on the margins of fillings andother dental restorations. On the other hand, incipientcaries describes decay at a location that has not experi-enced previous decay. Arrested caries describes a lesion

8 5 PREVENTION

on a tooth that was previously demineralized but was rem-ineralized before causing a cavitation. Fluoride treatmentcan help recalcification of tooth enamel as well as use ofAmorphous calcium phosphate.

4.2.2 Affected hard tissue

Depending on which hard tissues are affected, it is pos-sible to describe caries as involving enamel, dentin, orcementum. Early in its development, caries may affectonly enamel. Once the extent of decay reaches the deeperlayer of dentin, “dentinal caries” is used. Since cementumis the hard tissue that covers the roots of teeth, it is not of-ten affected by decay unless the roots of teeth are exposedto the mouth. Although the term “cementum caries” maybe used to describe the decay on roots of teeth, very rarelydoes caries affect the cementum alone. Roots have a verythin layer of cementum over a large layer of dentin, andthus most caries affecting cementum also affects dentin.

5 Prevention

Toothbrushes are commonly used to clean teeth.

5.1 Oral hygiene

Personal hygiene care consists of proper brushing andflossing daily. The purpose of oral hygiene is to mini-mize any etiologic agents of disease in the mouth. Theprimary focus of brushing and flossing is to remove andprevent the formation of plaque or dental biofilm. Plaqueconsists mostly of bacteria.[81] As the amount of bacte-rial plaque increases, the tooth is more vulnerable to den-tal caries when carbohydrates in the food are left on teethafter everymeal or snack. A toothbrush can be used to re-move plaque on accessible surfaces, but not between teethor inside pits and fissures on chewing surfaces. Whenused correctly, dental floss removes plaque from areasthat could otherwise develop proximal caries but only if

the depth of sulcus has not been compromised. Other ad-junct oral hygiene aids include interdental brushes, waterpicks, and mouthwashes.However oral hygiene is probably more effective at pre-venting gum disease (periodontal disease) than tooth de-cay. Food is forced inside pits and fissures under chewingpressure, leading to carbohydrate-fueled acid demineral-isation where the brush, fluoride toothpaste, and salivahave no access to remove trapped food, neutralise acid,or remineralise demineralised tooth like on other moreaccessible tooth surfaces food to be trapped. (Occlusalcaries accounts for between 80 and 90% of caries in chil-dren (Weintraub, 2001).) Chewing fibre like celery af-ter eating forces saliva inside trapped food to dilute anycarbohydrate like sugar, neutralise acid and remineralisedemineralised tooth. The teeth at highest risk for cariouslesions are the permanent first and second molars due tolength of time in oral cavity and presence of complex sur-face anatomy.Professional hygiene care consists of regular dental exam-inations and professional prophylaxis (cleaning). Some-times, complete plaque removal is difficult, and a den-tist or dental hygienist may be needed. Along with oralhygiene, radiographs may be taken at dental visits to de-tect possible dental caries development in high risk areasof the mouth (e.g. "bitewing" x-rays which visualize thecrowns of the back teeth).

5.2 Dietary modification

For dental health, frequency of sugar intake is more im-portant than the amount of sugar consumed.[27] In thepresence of sugar and other carbohydrates, bacteria inthe mouth produce acids that can demineralize enamel,dentin, and cementum. The more frequently teeth areexposed to this environment the more likely dental cariesare to occur. Therefore, minimizing snacking is recom-mended, since snacking creates a continuous supply ofnutrition 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, arebest eaten as part of a meal. For children, the AmericanDental Association and the European Academy of Paedi-atric Dentistry recommend limiting the frequency of con-sumption of drinks with sugar, and not giving baby bot-tles to infants during sleep (see earlier discussion).[82][83]Mothers are also recommended to avoid sharing utensilsand cups with their infants to prevent transferring bacteriafrom the mother’s mouth.[84]

It has been found that milk and certain kinds of cheeselike cheddar cheese can help counter tooth decay if eatensoon after the consumption of foods potentially harmfulto teeth.[27] Also, chewing gum containing xylitol (a sugaralcohol) is widely used to protect teeth in many countriesnow. Xylitol’s effect on reducing dental biofilm is, it ispresumed, due to bacteria’s inability to utilize it like other

9

sugars.[85] Chewing and stimulation of flavor receptors onthe tongue are also known to increase the production andrelease of saliva, which contains natural buffers to pre-vent the lowering of pH in the mouth to the point whereenamel may become demineralized.[86]

5.3 Other measures

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.[87] Asealant is a thin plastic-like coating applied to the chewingsurfaces of the molars to prevent food from being trappedinside pits and fissures. This deprives resident plaque bac-teria carbohydrate preventing the formation of pit and fis-sure caries. Sealants are usually applied on the teeth ofchildren, as soon as the tooth erupt but adults are receiv-ing them if not previously performed. Sealants can wearout and fail to prevent access of food and plaque bacteriainside pits and fissures and need to be replaced so theymust be checked regularly by dental professionals.Calcium, as found in food such as milk and green veg-etables, is often recommended to protect against dentalcaries. Fluoride helps prevent decay of a tooth by bindingto the hydroxyapatite crystals in enamel.[88] The incorpo-rated calcium makes enamel more resistant to deminer-alization and, thus, resistant to decay.[89] Topical fluorideis more highly recommended than systemic intake suchas by tablets or drops to protect the surface of the teeth.This may include a fluoride toothpaste or mouthwash or

varnish.[90] After brushing with fluoride toothpaste, rins-ing should be avoided and the excess spat out.[91] Thisleaves a greater concentration of fluoride residue on theteeth. Many dental professionals include application oftopical fluoride solutions as part of routine visits and rec-ommend the use of xylitol and amorphous calcium phos-phate products. Silver diamine fluoride may work betterthan fluoride varnish to prevent cavities.[92]

Vaccines are also under development.[93]

6 Treatment

See also: Dental restoration and Tooth extractionMost importantly, whether the carious lesion is cavitated

An amalgam used as a restorative material in a tooth.

or noncavitated dictates the management. Clinical assess-ment of whether the lesion is active or arrested is alsoimportant. Noncavitated lesions can be arrested and rem-ineralization can occur under the right conditions. How-ever, this may require extensive changes to the diet (re-duction in frequency of refined sugars), improved oral hy-giene (toothbrushing twice per day with fluoride tooth-paste and daily flossing), and regular application of top-ical fluoride. Such management of a carious lesion istermed “non-operative” since no drilling is carried outon the tooth. Non-operative treatment requires excellentunderstanding and motivation from the individual, other-wise the decay will continue.Once a lesion has cavitated, especially if dentin is in-volved, remineralization is much more difficult and adental restoration is usually indicated (“operative treat-ment”). Before a restoration can be placed, all ofthe decay must be removed otherwise it will continueto progress underneath the filling. Sometimes a smallamount of decay can be left if it is entombed and the thereis a seal which isolates the bacteria from their substrate.This can be likened to placing a glass container over acandle, which burns itself out once the oxygen is usedup. Techniques such as stepwise caries removal are de-

10 7 EPIDEMIOLOGY

signed to avoid exposure of the dental pulp and overall re-duction of the amount of tooth substance which requiresremoval before the final filling is placed. Often enamelwhich overlies decayed dentin must also be removed as itis unsupported and susceptible to fracture. The moderndecision-making process with regards the activity of thelesion, and whether it is cavitated, is summarized in thetable.[94]

Destroyed tooth structure does not fully regenerate, al-though remineralization of very small carious lesions mayoccur if dental hygiene is kept at optimal level.[13] For thesmall lesions, topical fluoride is sometimes used to en-courage remineralization. For larger lesions, the progres-sion of dental caries can be stopped by treatment. Thegoal of treatment is to preserve tooth structures and pre-vent further destruction of the tooth. Aggressive treat-ment, by filling, of incipient carious lesions, places wherethere is superficial damage to the enamel, is controversialas they may heal themselves, while once a filling is per-formed it will eventually have to be redone and the siteserves as a vulnerable site for further decay.[11]

In general, early treatment is quicker and less expensivethan treatment of extensive decay. Local anesthetics,nitrous oxide (“laughing gas”), or other prescription med-ications may be required in some cases to relieve painduring or following treatment or to relieve anxiety dur-ing treatment.[95] A dental handpiece (“drill”) is used toremove large portions of decayed material from a tooth.A spoon, a dental instrument used to carefully removedecay, is sometimes employed when the decay in dentinreaches near the pulp.[96] Once the decay is removed, themissing tooth structure requires a dental restoration ofsome sort to return the tooth to function and aestheticcondition.Restorative materials include dental amalgam, compositeresin, porcelain, and gold.[97] Composite resin and porce-lain can be made to match the color of a patient’s naturalteeth and are thus used more frequently when aestheticsare a concern. Composite restorations are not as strongas dental amalgam and gold; some dentists consider thelatter as the only advisable restoration for posterior ar-eas where chewing forces are great.[98] When the decay istoo extensive, there may not be enough tooth structure re-maining to allow a restorative material to be placed withinthe tooth. Thus, a crown may be needed. This restorationappears similar to a cap and is fitted over the remainderof the natural crown of the tooth. Crowns are often madeof gold, porcelain, or porcelain fused to metal.For children, preformed crowns are available to placeover the tooth. These are usually made of metal (usuallystainless steel but increasingly there are aesthetic materi-als). Traditionally teeth are shaved down to make roomfor the crown but, more recently, stainless steel crownshave been used to seal decay into the tooth and stop itprogressing. This is known as the Hall Technique andworks be depriving the bacteria in the decay of nutrients

and making their environment less favorable for them. Itis a minimally invasivemethod ofmanaging decay in chil-dren and does not require local anesthetic injections in themouth.

A tooth with extensive caries eventually requiring extraction.

In certain cases, endodontic therapy may be necessary forthe restoration of a tooth.[99] Endodontic therapy, alsoknown as a “root canal”, is recommended if the pulp ina tooth dies from infection by decay-causing bacteria orfrom trauma. During a root canal, the pulp of the tooth,including the nerve and vascular tissues, is removed alongwith decayed portions of the tooth. The canals are instru-mented with endodontic files to clean and shape them,and they are then usually filled with a rubber-like mate-rial called gutta percha.[100] The tooth is filled and a crowncan be placed. Upon completion of a root canal, the toothis 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 thetooth is too far destroyed from the decay process to ef-fectively restore the tooth. Extractions are sometimesconsidered if the tooth lacks an opposing tooth or willprobably cause further problems in the future, as may bethe case for wisdom teeth.[101] Extractions may also bepreferred by people unable or unwilling to undergo theexpense or difficulties in restoring the tooth.

7 Epidemiology

Disability-adjusted life year for dental caries per 100,000inhabitants in 2004.[102]

Worldwide, approximately 2.43 billion people (36% ofthe population) have dental caries in their permanent

11

teeth.[8] In baby teeth it affects about 620 million peo-ple or 9% of the population.[8] The disease is most com-mon in Latin American countries, countries in theMiddleEast, and South Asia, and least prevalent in China.[103]In the United States, dental caries is the most commonchronic childhood disease, being at least five times morecommon than asthma.[104] It is the primary pathologicalcause of tooth loss in children.[105] Between 29% and59% of adults over the age of fifty experience caries.[106]

The number of cases has decreased in some developedcountries, and this decline is usually attributed to increas-ingly better oral hygiene practices and preventive mea-sures such as fluoride treatment.[107] Nonetheless, coun-tries that have experienced an overall decrease in casesof tooth decay continue to have a disparity in the distri-bution of the disease.[106] Among children in the UnitedStates and Europe, twenty percent of the population en-dures sixty to eighty percent of cases of dental caries.[108]A similarly skewed distribution of the disease is foundthroughout the world with some children having none orvery few caries and others having a high number.[106]Australia, Nepal, and Sweden (where children receivedental care paid for by the government) have a low inci-dence of cases of dental caries among children, whereascases are more numerous in Costa Rica and Slovakia.[109]

The classic DMF (decay/missing/filled) index is one ofthe most common methods for assessing caries preva-lence as well as dental treatment needs among popula-tions. This index is based on in-field clinical examinationof individuals by using a probe, mirror and cotton rolls.Because the DMF index is done without X-ray imag-ing, it underestimates real caries prevalence and treatmentneeds.[74]

Bacteria typically associated with dental caries have beenisolated from vaginal samples who have bacterial vagi-nosis.[110]

8 History

There is a long history of dental caries. Over a mil-lion years ago, hominins such as Australopithecus suf-fered from cavities.[111] The largest increases in theprevalence of caries have been associated with di-etary changes.[111][112] Archaeological evidence showsthat tooth decay is an ancient disease dating far intoprehistory. Skulls dating from amillion years ago throughthe neolithic period show signs of caries, including thosefrom the Paleolithic and Mesolithic ages.[113] The in-crease of caries during the neolithic period may be at-tributed to the increased consumption of plant foods con-taining carbohydrates.[114] The beginning of rice cultiva-tion in South Asia is also believed to have caused an in-crease in caries. Although there is also some evidencefrom sites in Thailand, such as Khok Phanom Di, thatshows a decrease in overall percentage of dental caries

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

with the increase in dependence on rice agriculture.[115]

A Sumerian text from 5000 BC describes a “tooth worm”as the cause of caries.[116] Evidence of this belief has alsobeen found in India, Egypt, Japan, and China.[112] Un-earthed ancient skulls show evidence of primitive dentalwork. In Pakistan, teeth dating from around 5500 BC to7000 BC show nearly perfect holes from primitive dentaldrills.[117] The Ebers Papyrus, an Egyptian text from 1550BC, mentions diseases of teeth.[116] During the Sargoniddynasty of Assyria during 668 to 626 BC, writings fromthe king’s physician specify the need to extract a toothdue to spreading inflammation.[112] In the Roman Em-pire, wider consumption of cooked foods led to a smallincrease in caries prevalence.[108] The Greco-Roman civ-ilization, in addition to the Egyptian, had treatments forpain resulting from caries.[112]

The rate of caries remained low through the Bronze Ageand Iron Age, but sharply increased during the MiddleAges.[111] Periodic increases in caries prevalence hadbeen small in comparison to the 1000 AD increase, whensugar cane became more accessible to theWestern world.Treatment consisted mainly of herbal remedies andcharms, but sometimes also included bloodletting.[118]The barber surgeons of the time provided services that in-cluded tooth extractions.[112] Learning their training fromapprenticeships, these health providers were quite suc-cessful in ending tooth pain and likely prevented sys-temic spread of infections in many cases. Among Ro-man Catholics, prayers to Saint Apollonia, the patronessof dentistry, were meant to heal pain derived from toothinfection.[119]

There is also evidence of caries increase in North Ameri-can Indians after contact with colonizing Europeans. Be-fore colonization, North American Indians subsisted onhunter-gatherer diets, but afterwards there was a greater

12 12 REFERENCES

reliance on maize agriculture, which made these groupsmore susceptible to caries.[111]

During the European Age of Enlightenment, the beliefthat a “tooth worm” caused caries was also no longer ac-cepted in the European medical community.[120] PierreFauchard, known as the father of modern dentistry, wasone of the first to reject the idea that worms caused toothdecay and noted that sugar was detrimental to the teethand gingiva.[121] In 1850, another sharp increase in theprevalence of caries occurred and is believed to be a re-sult of widespread diet changes.[112] Prior to this time,cervical caries was the most frequent type of caries, butincreased availability of sugar cane, refined flour, bread,and sweetened tea corresponded with a greater numberof pit and fissure caries.In the 1890s, W.D. Miller conducted a series of stud-ies that led him to propose an explanation for dentalcaries that was influential for current theories. He foundthat bacteria inhabited the mouth and that they producedacids that dissolved tooth structures when in the pres-ence of fermentable carbohydrates.[122] This explanationis known as the chemoparasitic caries theory.[123]Miller’scontribution, along with the research on plaque by G.V.Black and J.L. Williams, served as the foundation for thecurrent explanation of the etiology of caries.[112] Severalof the specific strains of lactobacilli were identified in1921 by Fernando E. Rodriguez Vargas.In 1924 in London, Killian Clarke described a sphericalbacterium in chains isolated from carious lesions whichhe called Streptococcus mutans. Although Clarke pro-posed this organism was the cause of caries the discov-ery was not followed up. Later, in the 1950s in the USA,Keyes and Fitzgerald working with hamsters showed thatcaries was transmissible and caused by an acid-producingStreptococcus. It was not until the late 1960s that it be-came generally accepted that the Streptococcus isolatedfrom hamster caries was the same as S. mutans describedby Clarke.[124]

Tooth decay has been present throughout human history,from early hominids millions of years ago, to modernhumans.[125] The prevalence of caries increased dramat-ically in the 19th century, as the Industrial Revolutionmade certain items, such as refined sugar and flour, read-ily available.[112] The diet of the “newly industrialized En-glish working class”[112] then became centered on bread,jam, and sweetened tea, greatly increasing both sugarconsumption and caries.

8.1 Etymology and usage

Naturalized from Latin into English (a loanword), cariesin its English form originated as a mass noun that means“rottenness”,[4][126] that is, “decay”. When used in thatsense, it takes singular verb inflections (just like the worddecay does). Thus caries was not traditionally a pluralword synonymous with holes or cavities; that is, it was not

the plural form of any singular form cary meaning holeor cavity. Nonetheless, the idea that it is such a plural is areanalysis that naturally occurs to most English speakers,and the reanalyzed sense is common enough to be enteredin various dictionaries and to exist in respectable usage.It still shows a hint of its reanalyzed origins in that it re-mains idiomatically limited to a plurale tantum sense—that is, like scissors or glasses, one speaks of plural cariesobligately in the plural—not of one scissor, glass, or cary.(This is why one can look for a singular count-noun formof dental cary in any of a dozen major medical and gen-eral dictionaries and not find it listed.) Many still use it inthe traditional sense (mass, singular), which is why theyspeak of carious lesions rather than just caries when theyintend the plural count sense.

9 Society and culture

It is estimated that untreated dental caries results inworldwide productivity losses in the size of about US$27billion yearly.[127]

10 Research

Cariology is the study of dental caries.

11 Other animals

Main article: Dental caries (non-human)

Dental caries is uncommon among companionanimals.[128]

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13 External links• Dental caries at DMOZ

• Centers for Disease Control, Dental Caries athttp://www.cdc.gov/healthywater/hygiene/disease/dental_caries.html

18 14 TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES

14 Text and image sources, contributors, and licenses

14.1 Text• Dental caries Source: https://en.wikipedia.org/wiki/Dental_caries?oldid=688592384 Contributors: RoseParks, Alex.tan, Ewen,Kchishol1970, Michael Hardy, Booyabazooka, Fred Bauder, Lousyd, Ellywa, Ronz, Samw, Raven in Orbit, Ike9898, WhisperToMe,Furrykef, Tempshill, HarryHenryGebel, Renato Caniatti~enwiki, Owen, Robbot, Davodd, Diberri, Alan Liefting, Dave6, KMT, Gua-naco, Jason Quinn, Jackol, Glengarry, Andycjp, Xmnemonic, PDH, TonyW, Marine 69-71, Mike Rosoft, A-giau, Discospinster, RichFarmbrough, Vsmith, Xezbeth, Dbachmann, Mykhal, Plugwash, CanisRufus, Pjf, El C, Fenevad, Rgdboer, Sihaya~enwiki, Bobo192,Smalljim, Nectarflowed, Garlics82, Arcadian, Jumbuck, Alansohn, Eric Kvaalen, Atlant, Jlockhart, Wouterstomp, Axl, Goldom, Pion,Phyllis1753, Snowolf, Radical Mallard, Velella, Pablo Alcayaga, Zantastik, Dalillama, Runtime, ReubenGarrett, SteinbDJ, Forteblast,Mel Etitis, Woohookitty, 2004-12-29T22:45Z, Jersyko, Dozenist, CiTrusD, Dzordzm, Pufferfish101, Eras-mus, Prashanthns, Graham87,Teknic, Imersion, FreplySpang, Jclemens, BorgHunter, Josh Parris, Rjwilmsi, Seraphimblade, ElKevbo, StephanieM, The wub, Scor-pionman, FlaBot, WWC, AED, JdforresterBot, Alexkasper, Kolbasz, YurikBot, Wavelength, Ste1n, Phantomsteve, Lexi Marie, ChrisCapoccia, JabberWok, Gaius Cornelius, Wimt, Smash, Dialectric, Mike18xx, Blur4760~enwiki, Rmky87, Titototito, Zwobot, AaronSchulz, PrimeCupEevee, Mysid, DRosenbach, Lycaon, Lt-wiki-bot, Ageekgal, Closedmouth, Wikiwawawa, GraemeL, Ilmari Karonen,Kungfuadam, Kellypk, Settingprecedent, Brentt, SmackBot, TomGreen, Tomer yaffe, Jagged 85, Eskimbot, Geoff B, Gilliam, Chris thespeller, Rakela, RDBrown, Tito4000, Isaacsurh, Moshe Constantine Hassan Al-Silverburg, DHN-bot~enwiki, Colonies Chris, Can't sleep,clown will eat me, Morphax, Rrburke, Lord Vader, Drphilharmonic, Autodmc, Sayden, Vina-iwbot~enwiki, Clicketyclack, Bouncingmo-lar, SashatoBot, Gloriamarie, Harryboyles, Mouse Nightshirt, SS2005, Euchiasmus, Littleman TAMU, 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JhsBot, יכול ,כל Blurpeace, Pnswmr, Tomaxer, Enviroboy, Jcdi-etz03, Temporaluser, Doc James, Brendog69, Gbawden, Bfpage, SieBot, Brenont, Sebastiano venturi, Ellielancaster, Lucasbfrbot, Super-tooth, Flyer22 Reborn, JetLover, Ideaslondon, Lightmouse, Drjerrygordon, Onebadtown, Fsicar, Fuzzycloud, DrATty, Joedoedoe, Touch-stone42, Sfan00 IMG, ClueBot, Rustic, EoGuy, Piabrown, ImperfectlyInformed, Gonzomalan, Sassf, Neverquick, DragonBot, Ktr101,Kjramesh, Bobby Tables, Sun Creator, NuclearWarfare, Lunchscale, Tuchomator, Iohannes Animosus, Singhalawap, Achilles.g, MuroBot, Ra2007, Versus22, Kubek15, Danep2, Johnuniq, Wnt, Vanished user uih38riiw4hjlsd, Behdentresources, Jupiter849, Life of Riley,CynRN, XLinkBot, Tarheel95, Reggaejessie, Facts707, SilvonenBot, Badgernet, D.M. from Ukraine, Addbot, Wakablogger2, Fyrael,Midgette, TutterMouse, Lenwbrown, Gkopjar, Dentdude, MrOllie, Download, Glane23, LinkFA-Bot, Quercus solaris, Interwebs, Black-socks4, Tide rolls, Verazzano, MuZemike, Jarble, Eleutherian, AKFORTYS3V3N, Luckas-bot, Yobot, Fraggle81, Oral BioTech, Udaza,AnomieBOT, Archon 2488, Fivestar51, Materialscientist, Citation bot, ArthurBot, LilHelpa, TheAMmollusc, Capricorn42, Anna Frode-siak, Jhirsch1971, J04n, GrouchoBot, Gangasrotogati, Mdewman6, RibotBOT, Ninjafusion, Whocares30, Doodleping, Crazysissycat,Hspatel, LucienBOT, Wikiphile1603, Saimondo, Tetraedycal, Turki-almutarir, OgreBot, Citation bot 1, Galmicmi, Simple Bob, Elec-tricMuffin, MastiBot, SpaceFlight89, Punker2550, PeggyDoll, Fitdent, Leasnam, Orenburg1, TobeBot, Trappist the monk, Thedentist-mod, S charm, Reaper Eternal, DARTH SIDIOUS 2, Norlesh, EmausBot, GoingBatty, Slightsmile, K6ka, LFlagg, ZéroBot, Jeanpetr,Geordielass86, A930913, Ebrambot, Aeonx, Furries, Chezi-Schlaff, JoeSperrazza, L Kensington, Puffin, Dds7777, GarethOwens, Clue-Bot NG, Erasistratus1, Omair00, Chattaranga, Primergrey, Widr, Mars Cadbury, Sssbbbrrr, Helpful Pixie Bot, Cavityfree, Mindstormer12,BG19bot, Godimas, SharkinthePool, Alin211, CatPath, Uglybetty56, Saurabhahujadr, Ljaic, Ladeeda123, Loriendrew, Digantatalukdar,BattyBot, Biosthmors, Bellechic, Piet De Vaere, Abeydoun1104, ChrisGualtieri, GoShow, BrightStarSky, Dexbot, SantoshBot, Nee-talia Jones, Mogism, Landindmd, Claireshepherd, Graphium, Yannsolo, Fedelis4198, Malaysiaboy, Moony22, Only1tomfriar, Flagators,Doychin90, François Robere, Ecosarah, Blackbombchu, Ginsuloft, BruceBlaus, Scl120, Spardue13, RhinoMind, Dr.bilalradwan, Czech-mateVV, Suyash.dwivedi, WagnerDentalDDS, Monkbot, Monopoly31121993, Lizzy8127, Hurlej, Dabumtis, Njord njord n, Matthew Fer-guson 57, Conkle.30, Rainydays404, Gamingforfun365, Justin Jameson, Ap1948 and Anonymous: 516

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