Tooth decay
Tooth decay | |
---|---|
Other names | Dental cavities, dental caries, cavities, caries |
Medication | Paracetamol (acetaminophen), ibuprofen[6] |
Frequency | 3.6 billion (2016)[7] |
Tooth decay, also known as cavities or caries, is the breakdown of
The cause of cavities is acid from bacteria dissolving the
Prevention of dental caries includes regular cleaning of the teeth, a diet low in sugar, and small amounts of
Worldwide, approximately 3.6 billion people (48% of the population) have dental caries in their
Signs and symptoms
A person experiencing caries may not be aware of the disease.[12] 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".[13] 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.[14]
As the
Dental caries can also cause
Cause
Four things are required for caries to form: a tooth surface (enamel or dentin), caries-causing bacteria, fermentable
Tooth decay is caused by
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.[25]
Bacteria
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.[26] This is driven by local environmental change, such as frequent sugar intake or inadequate biofilm removal (toothbrushing).[27] If left untreated, the disease can lead to pain, tooth loss and infection.[28]
The mouth contains a wide variety of
These bacterial strains, most notably S. mutans, can be inherited by a child from a caretaker's kiss or through feeding pre-masticated food.[29]
Dietary sugars
Bacteria in a person's mouth convert glucose, fructose, and most commonly sucrose (table sugar) into acids such as
Exposure
The frequency with which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development.[
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.[33] 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).
Teeth
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.
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.[41] In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.[42]
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.[43] These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5.[44] Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content.[45] 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;[46][47] 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
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
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.[51]
The use of
Intrauterine and neonatal
such as cadmium, mimic the calcium ion and therefore exposure to them may promote tooth decay.[65]Poverty is also a significant social determinant for oral health.[66] Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.[67]
Forms are available for risk assessment for caries when treating dental cases; this system using the evidence-based Caries Management by Risk Assessment (CAMBRA).[68] 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.[69]
Saliva also contains iodine and EGF. EGF results effective in cellular proliferation, differentiation and survival.[70] 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.[71]
Pathophysiology
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.[72][73] 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.[74]
Enamel
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.
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.[76] The translucent zone is the first visible sign of caries and coincides with a one to two percent loss of minerals.[77] 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.[78] 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
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.[79]
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.[75] The advancing front represents a zone of demineralized dentin due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentin caries has been reversibly attacked because the collagen matrix is not severely damaged, giving it potential for repair.
Sclerotic dentin
The structure of dentin is an arrangement of microscopic channels, called
In response, the fluid inside the tubules brings
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.[83] 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.
Tertiary dentin
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.[81] 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.[84] 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.
Cementum
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.[86]
Diagnosis
The presentation of caries is highly variable. However, the risk factors and stages of development are similar. Initially, it may appear as a small chalky area (smooth surface caries), which may eventually develop into a large cavitation. Sometimes caries may be directly visible. However other methods of detection such as X-rays are used for less visible areas of teeth and to judge the extent of destruction. Lasers for detecting caries allow detection without ionizing radiation and are now used for detection of interproximal decay (between the teeth).
Primary
Some dental researchers have cautioned against the use of dental explorers to find caries,[89] 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.[90] 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.[91]
The early carious lesion is characterized by demineralization of the tooth surface, altering the tooth's optical properties. Technology using
Classification
Caries can be classified by location, etiology, rate of progression, and affected hard tissues.[92] These forms of classification can be used to characterize a particular case of tooth decay to more accurately represent the condition to others and also indicate the severity of tooth destruction. In some instances, caries is described in other ways that might indicate the cause. The G. V. Black classification is as follows:
- Class I: occlusal surfaces of posterior teeth, buccal or lingual pits on molars, lingual pit near cingulum of maxillary incisors
- Class II: proximal surfaces of posterior teeth
- Class III: interproximal surfaces of anterior teeth without incisal edge involvement
- Class IV: interproximal surfaces of anterior teeth with incisal edge involvement
- Class V: cervical third of facial or lingual surface of tooth
- Class VI: incisal or occlusal edge is worn away due to attrition
Early childhood caries
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.[93] The teeth most likely affected are the maxillary anterior teeth, but all teeth can be affected.[94] 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.[95]
Another pattern of decay is "rampant caries", which signifies advanced or severe decay on multiple surfaces of many teeth.
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.[98]
A range of studies have reported that there is a correlation between caries in primary teeth and caries in permanent teeth.[99][100]
Rate of progression
This section needs additional citations for verification. (November 2016) |
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.[101]
Affected hard tissue
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.
Prevention
Oral hygiene
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,[102] although studies have shown this effect on caries is limited.[103] While there is no evidence that flossing prevents tooth decay,[104] the practice is still generally recommended.[5]
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
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.[106] 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.[107] 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.[108] Another review concluded that the supervised regular use of a fluoride mouthwash greatly reduced the onset of decay in the permanent teeth of children.[109]
Professional hygiene care consists of regular dental examinations and professional prophylaxis (cleaning). Sometimes, complete plaque removal is difficult, and a dentist or
Alternative methods of oral hygiene also exist around the world, such as the use of
Dietary modification
People who eat more
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.[112]
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).[113][114] Parents are also recommended to avoid sharing utensils and cups with their infants to prevent transferring bacteria from the parent's mouth.[115]
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.[116][117][118]
Other measures
The use of dental sealants is a means of prevention.[119] 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.[120][needs update]
Calcium, as found in food such as milk and green vegetables, is often recommended to protect against dental caries.
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.[131] To further increase a child's cooperation in caries management, good communication by the dentist and the rest of the staff of a dental practice should be used. This communication can be improved by calling the child by their name, using eye contact and including them in any conversation about their treatment.[131]
Vaccines are also under development.[132]
Treatment
No carious lesion | No treatment | ||
Carious lesion | Inactive lesion | No treatment | |
Active lesion | Non-cavitated lesion | Non-operative treatment | |
Cavitated lesion | Operative treatment | ||
Existing filling | No defect | No replacement | |
Defective filling | Ditching, overhang | No replacement | |
Fracture or food impaction | Repair or replacement of filling | ||
Inactive lesion | No treatment | ||
Active lesion | Non-cavitated lesion | Non-operative treatment | |
Cavitated lesion | Repair or replacement of filling |
Most importantly, whether the carious lesion is cavitated or non-cavitated 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. More recently, Immunoglobulin Y specific to Streptococcus mutans has been used to suppress growth of S. mutans.[133] 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 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.[134]
Destroyed tooth structure does not fully regenerate, although remineralization of very small carious lesions may occur if dental hygiene is kept at optimal level.[15] 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.[13]
In general, early treatment is quicker and less expensive than treatment of extensive decay.
Restorative materials include dental
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 by 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.
In certain cases,
An
Epidemiology
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 3.6 billion people have dental caries in their permanent teeth.
Treating dental cavities costs 5–10% of health-care budgets in industrialized countries, and can easily exceed budgets in lower-income countries.[150]
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.[151] Nonetheless, countries that have experienced an overall decrease in cases of tooth decay continue to have a disparity in the distribution of the disease.[149] Among children in the United States and Europe, twenty percent of the population endures sixty to eighty percent of cases of dental caries.[152] 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.[149] 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.[153]
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.[90]
Bacteria typically associated with dental caries have been isolated from vaginal samples from females who have bacterial vaginosis.[154]
History
There is a long history of dental caries. Over a million years ago,
Archaeological evidence shows that tooth decay is an ancient disease dating far into
A
The rate of caries remained low through the
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.[156]
During the European Age of Enlightenment, the belief that a "tooth worm" caused caries was also no longer accepted in the European medical community.[166] 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.[167] In 1850, another sharp increase in the prevalence of caries occurred and is believed to be a result of widespread diet changes.[157] 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.[168] This explanation is known as the chemoparasitic caries theory.[169] 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.[157] Several of the specific strains of lactobacilli were identified in 1921 by Fernando E. Rodríguez 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 that this organism was the cause of caries, the discovery was not followed up. Later, in 1954 in the US, Frank Orland working with hamsters showed that caries was transmissible and caused by acid-producing Streptococcus thus ending the debate whether dental caries were resultant from bacteria. 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.[170]
Tooth decay has been present throughout human history, from early
Etymology and usage
Naturalized from Latin into English (a
Cariesology[173][174] or cariology[175] is the study of dental caries.
Society and culture
It is estimated that untreated dental caries results in worldwide productivity losses in the size of about US$27 billion yearly.[176]
Other animals
Dental caries are uncommon among companion animals.[177]
See also
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General and cited sources
- Nanci, A. (2013). Ten Cate's Oral Histology (8th ed.). St. Louis, MO: Elsevier. ISBN 978-0-323-07846-7.