Тіс эмалінің қышқылдануы және тіс шілуінің алдын алу жолдары

Deformation of teeth due to acids produced by bacteria

caries of bone
Prevention of dental caries includes regular cleaning of the teeth, a diet low in sugar, and small amounts of fluoride. The availability of treatment is often poor in the developing world. The World Health Organization 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 due to greater simple sugar consumption, but less common in the developing world.

A person experiencing caries may not be aware of the disease. 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 "micro cavity". As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated. A lesion that appears dark brown and shiny suggests dental caries were once present, but the demineralization process has stopped, leaving a stain. Active decay is lighter in color and dull in appearance. 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 the enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, resulting in pain that can be transient, temporarily worsening with exposure to heat, cold, or sweet foods and drinks. A tooth weakened by extensive internal decay can sometimes suddenly fracture under normal chewing forces. When the decay has progressed enough to allow the bacteria to overwhelm the pulp tissue in the center of the tooth, a toothache can result, and the pain will become more constant. Death of the pulp tissue and infection are common consequences. The tooth will no longer be sensitive to hot or cold but can be very tender to pressure. Dental caries can also cause bad breath and foul tastes. In highly progressed cases, an infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig angina can be life threatening.

Four things are required for caries to form: a tooth surface (enamel or dentin), caries causing bacteria, fermentable carbohydrates (such as sucrose), and time. This involves adherence of food to the teeth and acid creation by the bacteria that makes up the dental plaque. However, 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 disease 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. Tooth decay is caused by biofilm (dental plaque) lying on the teeth and maturing to become cariogenic (causing decay). Certain bacteria in the biofilm produce acids, primarily lactic acid, in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose. Caries occur more often in people from the lower end of the socio economic scale than people from the upper end of the socio economic scale, due to lack of education about dental care, and lack of access to professional dental care which may be expensive.

The most common bacteria associated with dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. However, cariogenic bacteria (the ones that can cause the disease) are present in dental plaque, but they are usually in too low concentrations to cause problems unless there is a shift in the balance. This is driven by local environmental change, such as frequent sugar intake or inadequate biofilm removal (toothbrushing). If left untreated, the disease can lead to pain, tooth loss and infection. 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. Streptococcus mutans are gram positive bacteria which constitute biofilms on the surface of teeth. 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.

Bacteria in a person's mouth convert glucose, fructose, and most commonly sucrose (table sugar) into acids, mainly lactic acid, through a glycolytic process called fermentation. 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 using 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 dextran sucranase.

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

There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities. Molar incisor hypo mineralization seems to be increasingly common. While the cause is unknown it is thought to be a combination of genetic and environmental factors. Possible contributing factors that have been investigated include systemic factors such as high levels of dioxins or polychlorinated biphenyl (PCB) in the mother's milk, premature birth and oxygen deprivation at birth, and certain disorders during the child's first 3 years such as mumps, diphtheria, scarlet fever, measles, hypoparathyroidism, malnutrition, malabsorption, hypo vitaminosis D, chronic respiratory diseases, or undiagnosed and untreated coeliac disease, which usually presents with mild or absent gastrointestinal symptoms. Amelogenesis imperfecta, which occurs in between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth. In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth. In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Approximately 96% of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. 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 dental caries is weak; 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.

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 lead to dry mouth and thus to widespread tooth decay. Examples include Sjögren syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. This is known as meth mouth. Tetrahydrocannabinol (THC), 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 side effect. 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. 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. Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede. As the gingiva loses attachment to the teeth due to gingival recession, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel. Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root surface caries. Exposure of children to secondhand tobacco smoke is associated with tooth decay. Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,
such as cadmium, mimic the calcium ion and therefore exposure to them may promote tooth decay. Poverty is also a significant social determinant for oral health. Dental caries have been linked with lower socio economic status and can be considered a disease of poverty. Forms are available for risk assessment for caries when treating dental cases; this system using the evidence based Caries Management by Risk Assessment (CAMBRA). It is still unknown if the identification of high risk individuals can lead to more effective long term patient management that prevents caries initiation and arrests or reverses the progression of lesions. Saliva also contains iodine and EGF. EGF results effective in cellular proliferation, differentiation and survival. Salivary EGF, which seems also regulated by dietary inorganic iodine, plays an important physiological role in the maintenance of oral (and gastro oesophageal) tissue integrity, and, on the other hand, iodine is effective in prevention of dental caries and oral health.

Teeth are bathed in saliva and have a coating of bacteria on them (biofilm) that continually forms. The development of biofilm begins with pellicle formation. Pellicle is an acellular proteinaceous film which covers the teeth. Bacteria colonize on the teeth by adhering to the pellicle coated surface. Over time, a mature biofilm is formed, creating a cariogenic environment on the tooth surface. The minerals in the hard tissues of the teeth enamel, dentin and cementum are constantly undergoing demineralization and remineralization. Dental caries result when the demineralization rate is faster than the remineralization, producing net mineral loss, which occurs when there is an ecologic shift within the dental biofilm from a balanced population of microorganisms to a population that produces acids and can survive in an acid environment.

Tooth 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 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. As the enamel loses minerals, and dental caries progresses, the enamel develops 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. The translucent zone is the first visible sign of caries and coincides with a one to two percent loss of minerals. 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. 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.

Unlike enamel, the dentin reacts to the progression of dental caries. After tooth formation, the ameloblasts, which produce enamel, are destroyed once enamel formation is complete and thus cannot later regenerate enamel after its destruction. On the other hand, dentin is produced continuously throughout life by odontoblasts, which reside at the border between the pulp and dentin. 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. In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the advancing front, the zone of bacterial penetration, and the zone of destruction. The diameter of the dentinal tubules is largest near the pulp (about 2.5 μm) and smallest (about 900 nm) at the junction of dentin and enamel. The carious process 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 brings immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules. 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. 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.

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. 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 β, Reparative dentin is produced at an average of 1.5 μm/day, but can be increased to 3.5 μm/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.

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 root's 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.

[[File:Lp473524f2 online. jpg|thumb|Tooth samples imaged with a non coherent continuous light source (row 1), LSI (row 2) and pseudo color visualization of LSI (row 3). Early, uncavitated caries is often diagnosed by blowing air across the suspect surface, which removes moisture and changes the optical properties of the unmineralized enamel. Some dental researchers have cautioned against the use of dental explorers to find caries, in particular sharp ended explorers. In cases where a small area of tooth has begun demineralizing but has not yet cavitated, the pressure from the dental explorer could cause a cavity. Since the carious process is reversible before a cavity is present, it may be possible to arrest caries with fluoride and remineralize the tooth surface. When a cavity is present, a restoration will be needed to replace the lost tooth structure. At times, pit and fissure caries may be difficult to detect. Bacteria can penetrate the enamel to reach dentin, but then the outer surface may remineralize, especially if fluoride is present. These caries, sometimes referred to as "hidden caries", will still be visible on X ray radiographs, but visual examination of the tooth would show the enamel intact or minimally perforated. The differential diagnosis for dental caries includes dental fluorosis and developmental defects of the tooth including hypomineralization of the tooth and hypoplasia of the tooth. The early carious lesion is characterized by demineralization of the tooth surface, altering the tooth's optical properties. Technology using laser speckle image (LSI) techniques may provide a diagnostic aid to detect early carious lesions.

right|thumb|alt=Photograph of teeth and gums on the lower right hand side of the mouth showing large caries lesions on all teeth at the level of the gum|Rampant caries caused by methamphetamine abuse. Early childhood caries (ECC), also known as "baby bottle caries," "baby bottle tooth decay" or "bottle rot," is a pattern of decay found in young children with their deciduous (baby) teeth. This must include the presence of at least one carious lesion on a primary tooth in a child under the age of 6 years. The teeth most likely affected are the maxillary anterior teeth, but all teeth can be affected. The name for this type of caries comes from the fact that the decay usually is a result of allowing children to fall asleep with sweetened liquids in their bottles or feeding children sweetened liquids multiple times during the day. Another pattern of decay is "rampant caries", which signifies advanced or severe decay on multiple surfaces of many teeth. Rampant caries may be seen in individuals with xerostomia, poor oral hygiene, stimulant use (due to drug induced dry mouth), and/or large sugar intake. If rampant caries is a result of previous radiation to 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 new teeth erupt or later from unknown causes. Children at 6–12 months are at increased risk of developing dental caries. For other children aged 12–18 months, dental caries develop on primary teeth and approximately twice yearly for permanent teeth. A range of studies have reported that there is a correlation between caries in primary teeth and caries in permanent teeth.

Temporal descriptions can be applied to caries to indicate the progression rate and previous history. "Acute" signifies a quickly developing condition, whereas "chronic" describes a condition that has taken an extended time to develop, in which thousands of meals and snacks, many causing some acid demineralization that is not remineralized, eventually result in cavities. Recurrent caries, also described as secondary, are caries that appear at a location with a previous history of caries. This is frequently found on the margins of fillings and other dental restorations. On the other hand, incipient caries describes decay at a location that has not experienced previous decay. Arrested caries describes a lesion on a tooth that was previously demineralized but was remineralized before causing a cavitation. Fluoride treatment can help recalcification of tooth enamel as well as the use of amorphous calcium phosphate. Micro invasive interventions (such as dental sealant or resin infiltration) have been shown to slow down the progression of proximal decay.

Depending on which hard tissues are affected, it is possible to describe caries as involving enamel, dentin, or cementum. Early in its development, caries may affect only enamel. Once the extent of decay reaches the deeper layer of dentin, the term "dentinal caries" is used. Since cementum is the hard tissue that covers the roots of teeth, it is not often affected by decay unless the roots of teeth are exposed to the mouth. Although the term "cementum caries" may be used to describe the decay on roots of teeth, very rarely does caries affect the cementum alone.

right|thumb|alt=Head of a toothbrush|Toothbrushes are commonly used to clean teeth.

The primary approach to dental hygiene care consists of tooth brushing and flossing. The purpose of oral hygiene is to remove and prevent the formation of plaque or dental biofilm, although studies have shown this effect on caries is limited. While there is no evidence that flossing prevents tooth decay, the practice is still generally recommended. 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. Additional aids include interdental brushes, water picks, and mouthwashes. The use of rotational electric toothbrushes might reduce the risk of plaque and gingivitis, though it is unclear whether they are of clinical importance. However, oral hygiene is effective at preventing gum disease (gingivitis / periodontal disease). Food is forced inside pits and fissures under chewing pressure, leading to carbohydrate fuelled acid demineralisation where the brush, fluoride toothpaste, and saliva have no access to remove trapped food, neutralise acid, or remineralise tooth enamel. (Occlusal caries accounts for between 80 and 90% of caries in children (Weintraub, 2001).) Unlike brushing, fluoride leads to proven reduction in caries incidence by approximately 25%; higher concentrations of fluoride (>1,000 ppm) in toothpaste also helps prevents tooth decay, with the effect increasing with concentration up to a plateau. A randomized clinical trial demonstrated that toothpastes that contain arginine have greater protection against tooth cavitation than the regular fluoride toothpastes containing 1450 ppm alone. A Cochrane review has confirmed that the use of fluoride gels, normally applied by a dental professional from once to several times a year, assists in the prevention of tooth decay in children and adolescents, reiterating the importance of fluoride as the principal means of caries prevention. Another review concluded that the supervised regular use of a fluoride mouthwash greatly reduced the onset of decay in the permanent teeth of children. Professional hygiene care consists of regular dental examinations and professional prophylaxis (cleaning). Sometimes, complete plaque removal is difficult, and a dentist or dental 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). Alternative methods of oral hygiene also exist around the world, such as the use of teeth cleaning twigs such as miswaks in some Middle Eastern and African cultures. There is some limited evidence demonstrating the efficacy of these alternative methods of oral hygiene.

thumb|left|Annual caries incidence increases exponentially with annual per capita sugar consumption. Data based on 10,553 Japanese children whose individual lower first molar teeth were monitored yearly from the age of 6 to 11 years of age. Caries plotted on a logarithmic scale, so line is straight. People who eat more free sugars get more cavities, with cavities increasing exponentially with increasing sugar intake. Populations with less sugar intake have fewer cavities. In one population, in Nigeria, where sugar consumption was about 2g/day, only two percent of the population, of any age, had had a cavity. Chewy and sticky foods (such as candy, cookies, potato chips, and crackers) tend to adhere to teeth longer. However, dried fruits such as raisins and fresh fruit such as apples and bananas disappear from the mouth quickly, and do not appear to be a risk factor. Consumers are not good at guessing which foods stick around in the mouth. 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). Parents are also recommended to avoid sharing utensils and cups with their infants to prevent transferring bacteria from the parent's mouth. Xylitol is a naturally occurring sugar alcohol that is used in different products as an alternative to sucrose (table sugar). As of 2015 the evidence concerning the use of xylitol in chewing gum was insufficient to determine if it is effective at preventing caries.

thumb|alt=Refer to caption|Common dentistry trays used to deliver fluoride. thumb|Fluoride is sold in tablets for cavity prevention. The use of dental sealants is a means of prevention. 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 of carbohydrate, preventing the formation of pit and fissure caries. Sealants are usually applied on the teeth of children, as soon as the teeth 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. Dental sealants have been shown to be more effective at preventing occlusal decay when compared to fluoride varnish applications. 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. Streptococcus mutans is the leading cause of tooth decay. Low concentration fluoride ions act as bacteriostatic therapeutic agent and high concentration fluoride ions are bactericidal. The incorporated fluorine makes enamel more resistant to demineralization and, thus, resistant to decay. Fluoride can be found in either topical or systemic form. Topical fluoride is more highly recommended than systemic intake to protect the surface of the teeth. Topical fluoride is used in toothpaste, mouthwash and fluoride varnish. It is recommended that all adult patients to use fluoridated toothpaste with at least 1350ppm fluoride content, brushing at least 2 times per day and brush right before bed. For children and young adults, use fluoridated toothpaste with 1350ppm to 1500ppm fluoride content, brushing 2 times per day and also brush right before bed. American Dental Association Council suggest that for children <3 years old, caregivers should begin brushing their teeth by using fluoridated toothpaste with an amount no more than a smear. Supervised toothbrushing must also be done to children below 8 years of age to prevent swallowing of toothpaste. After brushing with fluoride toothpaste, rinsing should be avoided and the excess spat out. Many dental professionals include application of topical fluoride solutions as part of routine visits and recommend the use of xylitol and amorphous calcium phosphate products. Silver diamine fluoride may work better than fluoride varnish to prevent cavities. Systemic fluoride is found as lozenges, tablets, drops and water fluoridation. These are ingested orally to provide fluoride systemically. An oral health assessment carried out before a child reaches the age of one may help with management of caries. The oral health assessment should include checking the child's history, a clinical examination, checking the risk of caries in the child including the state of their occlusion and assessing how well equipped the child's parent or carer is to help the child prevent caries. Vaccines are also under development.

thumb|upright=1.3|alt=Color coded map displaying caries experience throughout the world.|Disability adjusted life year for dental caries per 100,000 inhabitants in 2004. Worldwide, approximately 3.6 billion people have dental caries in their permanent teeth. In the United States, dental caries is the most common chronic childhood disease, being at least five times more common than asthma. It is the primary pathological cause of tooth loss in children. Between 29% and 59% of adults over the age of 50 experience caries. Treating dental cavities costs 5–10% of health care budgets in industrialized countries, and can easily exceed budgets in lower income countries. The number of cases has decreased in some developed countries, and this decline is usually attributed to increasingly better oral hygiene practices and preventive measures such as fluoride treatment. Nonetheless, countries that have experienced an overall decrease in cases of tooth decay continue to have a disparity in the distribution of the disease. 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 in field 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.

thumb|right|alt=Refer to caption|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 Paranthropus had cavities. The largest increases in the prevalence of caries have been associated with dietary changes. 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. The increase of caries during the Neolithic period may be attributed to the increased consumption of plant foods containing carbohydrates. The beginning of rice cultivation in South Asia is also believed to have caused an increase in caries especially for women, 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. A Sumerian text from 5000 BC describes a "tooth worm" as the cause of caries. Evidence of this belief has also been found in India, Egypt, Japan, and China. The Ebers Papyrus, an Egyptian text from 1550 BC, mentions diseases of teeth. The Greco Roman civilization, in addition to the Egyptian civilization, had treatments for pain resulting from caries. The barber surgeons of the time provided services that included tooth extractions. There is also evidence of caries increase when Indigenous people in North America changed from a strictly hunter gatherer diet to a diet with maize. Rates also increased after contact with colonizing Europeans, implying an even greater dependence on maize. 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. In 1850, another sharp increase in the prevalence of caries occurred and is believed to be a result of widespread diet changes. This explanation is known as the chemoparasitic caries theory. 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. Tooth decay has been present throughout human history, from early hominids millions of years ago, to modern humans. 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. that is, 'decay'. The word is an uncountable noun. Cariesology or cariology is the study of dental caries.

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

Dental caries are uncommon among companion animals.