Dental caries, also known as tooth decay or a cavity, is an infection, bacterial in origin, that causes demineralization and destruction of the hard tissues (enamel, dentin and cementum), usually by production of acid by bacterial fermentation of the food debris accumulated on the tooth surface.
If demineralization exceeds saliva and other remineralization factors such as from calcium and fluoridated toothpastes, these hard tissues progressively break down, producing dental caries (cavities, holes in the teeth). The bacteria most responsible for dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. If left untreated, the disease can lead to pain, tooth loss and infection.
Today, caries remain one of the most common diseases throughout the world. Cariology is the study of dental caries.
he 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 radiation and are now used for detection of interproximal decay (between the teeth). Disclosing solutions are also used during tooth restoration to minimize the chance of recurrence.
Tooth decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose. The mineral content of teeth is sensitive to increases in acidity from the production of lactic acid. To be specific, a tooth (which is primarily mineral in content) is in a constant state of back-and-forth demineralization and remineralization between the tooth and surrounding saliva. For people with little saliva, especially due to radiation therapies that may destroy the salivary glands, there also exists remineralization gel. These patients are particularly susceptible to dental caries. When the pH at the surface of the tooth drops below 5.5, demineralization proceeds faster than remineralization (meaning that there is a net loss of mineral structure on the tooth's surface). Most foods are in this acidic range and without remineralization, this results in the ensuing decay. Depending on the extent of tooth destruction, various treatments can be used to restore teeth to proper form, function, and aesthetics, but there is no known method to regenerate large amounts of tooth structure. Instead, dental health organizations advocate preventive and prophylactic measures, such as regular oral hygiene and dietary modifications, to avoid dental caries.
Signs and symptoms
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 an incipient carious lesion or "microcavity". 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 brown and shiny suggests dental caries was once present but the demineralization process has stopped, leaving a stain. A brown spot that is dull in appearance is probably a sign of active caries.
As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, resulting in a toothache. The pain may worsen with exposure to heat, cold, or sweet foods and drinks. Dental caries can also cause bad breath and foul tastes. In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig's angina can be life-threatening
Causes
There are four main criteria required for caries formation: a tooth surface (enamel or dentin); caries-causing bacteria; fermentable carbohydrates (such as sucrose); and time. The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone. All caries occur from acid demineralization that exceeds saliva and fluoride remineralization, and almost all acid demineralization occurs where food (containing carbohydrate like sugar) is left on teeth. Because most trapped food is left between teeth, over 80% of cavities occur inside pits and fissures on chewing surfaces where brushing, fluoride, and saliva cannot reach to remineralize the tooth as they do on easy-to-reach surfaces that develop few cavities.
In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Ninety-six percent 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 the dental caries is weak; however,the anatomy of teeth may affect the likelihood of caries formation. Where the deep grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop. Also, caries are more likely to develop when food is trapped between teeth.
The progression of pit and fissure caries resembles two triangles with
their bases meeting along the junction of enamel and dentin.
As the enamel loses minerals, and dental caries progresses, the enamel develop several distinct zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone. 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.
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 advancing front represents a zone of demineralised dentine due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentine caries has been reversibly attacked because the collage matrix is not severely damaged, giving it potential for repair. The outer more superficial zone is highly infected with proteolytic degradation of the collagen matrix and as a result the dentine is irreversibly demineralised.
The faster spread of caries through dentin creates this triangular appearance in smooth surface caries.
In response, the fluid inside the tubules bring immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules 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.
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. Consequently, dental caries may progress for a long period of time without any sensitivity of the tooth, allowing for greater loss of tooth structure.
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, are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp. 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.
If demineralization exceeds saliva and other remineralization factors such as from calcium and fluoridated toothpastes, these hard tissues progressively break down, producing dental caries (cavities, holes in the teeth). The bacteria most responsible for dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. If left untreated, the disease can lead to pain, tooth loss and infection.
Today, caries remain one of the most common diseases throughout the world. Cariology is the study of dental caries.
he 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 radiation and are now used for detection of interproximal decay (between the teeth). Disclosing solutions are also used during tooth restoration to minimize the chance of recurrence.
Tooth decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose. The mineral content of teeth is sensitive to increases in acidity from the production of lactic acid. To be specific, a tooth (which is primarily mineral in content) is in a constant state of back-and-forth demineralization and remineralization between the tooth and surrounding saliva. For people with little saliva, especially due to radiation therapies that may destroy the salivary glands, there also exists remineralization gel. These patients are particularly susceptible to dental caries. When the pH at the surface of the tooth drops below 5.5, demineralization proceeds faster than remineralization (meaning that there is a net loss of mineral structure on the tooth's surface). Most foods are in this acidic range and without remineralization, this results in the ensuing decay. Depending on the extent of tooth destruction, various treatments can be used to restore teeth to proper form, function, and aesthetics, but there is no known method to regenerate large amounts of tooth structure. Instead, dental health organizations advocate preventive and prophylactic measures, such as regular oral hygiene and dietary modifications, to avoid dental caries.
Signs and symptoms
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 an incipient carious lesion or "microcavity". 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 brown and shiny suggests dental caries was once present but the demineralization process has stopped, leaving a stain. A brown spot that is dull in appearance is probably a sign of active caries.
As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, resulting in a toothache. The pain may worsen with exposure to heat, cold, or sweet foods and drinks. Dental caries can also cause bad breath and foul tastes. In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig's angina can be life-threatening
Causes
There are four main criteria required for caries formation: a tooth surface (enamel or dentin); caries-causing bacteria; fermentable carbohydrates (such as sucrose); and time. The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone. All caries occur from acid demineralization that exceeds saliva and fluoride remineralization, and almost all acid demineralization occurs where food (containing carbohydrate like sugar) is left on teeth. Because most trapped food is left between teeth, over 80% of cavities occur inside pits and fissures on chewing surfaces where brushing, fluoride, and saliva cannot reach to remineralize the tooth as they do on easy-to-reach surfaces that develop few cavities.
Teeth
There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for caries. Amelogenesis imperfecta, which occurs between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth.In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Ninety-six percent 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 the dental caries is weak; however,the anatomy of teeth may affect the likelihood of caries formation. Where the deep grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop. Also, caries are more likely to develop when food is trapped between teeth.
Pathophysiology
Enamel
Enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical process brought on by the acidic environment produced by bacteria. As the bacteria consume the sugar and use it for their own energy, they produce lactic acid. The effects of this process include the demineralization of crystals in the enamel, caused by acids, over time until the bacteria physically penetrate the dentin. Enamel rods, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin. Since demineralization of enamel by caries, in general, follows the direction of the enamel rods, the different triangular patterns between pit and fissure and smooth-surface caries develop in the enamel because the orientation of enamel rods are different in the two areas of the tooth.As the enamel loses minerals, and dental caries progresses, the enamel develop several distinct zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone. 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.
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.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 advancing front represents a zone of demineralised dentine due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentine caries has been reversibly attacked because the collage matrix is not severely damaged, giving it potential for repair. The outer more superficial zone is highly infected with proteolytic degradation of the collagen matrix and as a result the dentine is irreversibly demineralised.
Sclerotic dentin
The structure of dentin is an arrangement of microscopic channels, called dentinal tubules, which radiate outward from the pulp chamber to the exterior cementum or enamel border. 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 bring immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules 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.
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. Consequently, dental caries may progress for a long period of time without any sensitivity of the tooth, allowing for greater loss of tooth structure.
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. 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.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, are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp. 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.
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