IntroductionLoss of tooth substance may result from the action of oral microorganisms as in dental caries, or be due to non-bacterial causes. The latter include mechanical factors associated with attrition and abrasion, chemical erosion, and pathological resorption.
Dental caries may be defined as a bacterial disease of the calcified tissues of the teeth characterized by demineralization of the inorganic and destruction of the organic substance of the tooth. It is a complex and dynamic process involving, for example, physicochemical processes associated with the movements of ions across the interface between the tooth and the external environment, as well as biological processes associated with the interaction of bacteria in dental plaque with host defence mechanisms.
Dental caries has been recognized throughout history and exists around the world, although the prevalence and severity varies in different populations. In western industrialized countries there was a sharp increase in disease activity in the first half of the twentieth century, but during the 1970s and 1980s the prevalence of dental caries in children fell steadily, particularly following the widespread use of fluoride-containing toothpastes. The reduction was much greater for smooth surface as opposed to occlusal caries, which now accounts for most of the lesions seen in children. Epidemiological studies have shown that the decline in prevalence is continued into adult life and, as a result, more people are retaining more teeth for much longer than before. This reflects the increase in the prevalence of root surface caries as people grow older.
Despite the encouraging and sustained reduction in dental caries in industrialized countries, the prevalence is increasing in certain developing countries and is associated with urbanization and the increased availability of refined carbohydrates.
Aetiology of dental caries
Introduction
Various theories for the aetiology of dental caries have been proposed, but there is now overwhelming support for the acidogenic theory. This theory, which has remained virtually unchanged since first postulated by W. D. Miller in 1889, proposes that acid formed from the fermentation of dietary carbohydrates by oral bacteria leads to a progressive decalcification of the tooth substance with a subsequent disintegration of the organic matrix. Some of the evidence supporting the acidogenic theory is discussed below.
Role of bacteria and dental plaque
Experiments with germ-free animals have shown that bacteria are essential for the development of dental caries. Bacteria are present in dental plaque which is found on most tooth surfaces. Dental plaque is a biofilm consisting of a variety of different species of bacteria embedded in a matrix derived from salivary mucins and extracellular polysaccharide polymers (glucans and fructans) synthesized by the organisms.
A clean enamel surface is covered in a few seconds by an adsorbed layer of molecules comprising mainly glycoproteins from saliva, the acquired pellicle, to which microorganisms initially adhere. As they multiply and synthesize extracellular matrix polymers other bacteria may bind to them, rather than to the pellicle, resulting in a complex biofilm of spatially arranged species. The close proximity of different species allows for a variety of synergistic or antagonistic interactions. In a healthy mouth the bacterial composition of the plaque varies at different sites on the teeth, reflecting the different microenvironments available for colonization.
Dietary sugars diffuse rapidly through plaque where they are converted to acids (mainly lactic acid but also acetic and propionic acids) by bacterial metabolism. The pH of the plaque may fall by as much as 2 units within 10 minutes after the ingestion of sugar, but over the next 30 to 60 minutes the pH slowly rises to its original figure, due to the diffusion of the sugar and some of the acid out of the plaque, and the diffusion into the plaque of buffered saliva which helps to dilute and neutralize the acid. At the critical pH of 5.5 mineral ions are liberated from the hydroxyapatite crystals of the enamel and diffuse into the plaque. The pH curves of plaque in response to sugar (Stephan's curves) are similar in shape in caries-free and caries-active individuals. However, since the starting pH may be lower in caries-active mouths, the reduction in pH will be greater and the pH will be depressed below the critical level for a greater period of time. At a neutral or slightly alkaline pH the plaque becomes supersaturated with mineral ions derived both from the saliva and from those released from the hydroxyapatite crystals. Ions may now diffuse back into enamel and be redeposited in the crystal structure and this reprecipitation of mineral is aided by fluoride ions.
There is, therefore, a see-sawing of ions across the plaque- enamel interface as the chemical environment within the plaque changes. However, mineral ions may be lost from the system by diffusion out of the plaque and into the saliva during the acid phase, and repeated episodes lead to an overall demineralization and the initiation of enamel caries. Obviously the frequency and duration of the acid phase of plaque will affect the rate of development of caries, and this is why the reduction of carbohydrate intake between meals has such a beneficial effect in caries prevention. Once enamel caries has progressed to cavity formation, the plaque becomes progressively more removed from saliva and probably remains acidic for longer periods. Many plaque bacteria store carbohydrate as an intracellular glycogen-like polysaccharide which may be formed from a variety of sugars, and this may be broken down to acid when other sources of carbohydrate are absent, such as between meals. In addition, as mentioned above, plaque organisms can synthesize extracellular glucans from dietary sugars which may also be metabolized to acid when other sources of carbohydrate are absent. However, abundant extracellular polysaccharides have other important consequences in that they markedly increase the bulk of the plaque, thereby interfering with the outward diffusion of acids and the inward diffusion of saliva and its buffering systems. Such plaques are likely to be more cariogenic because they favour retention of acid at the plaque-enamel interface.
Fluoride ions are present in relatively high concentration in plaque compared with saliva. Fluoride favours the precipitation of calcium and phosphate ions from solution, and so when present at the plaque-enamel interface the deposition of free mineral ions in the plaque as hydroxy- and fluorapatite on the remaining enamel crystals is encouraged. Fluorapatite crystals may also be formed during enamel development if fluorides have been administered systemically (for example by water fluoridation). Fluorapatite is less soluble in acid than hydroxyapatite. Systemic fluoride also promotes the formation of hydroxyapatite crystals with a more stable crystal lattice. Fluoride ions in plaque inhibit bacterial metabolism and this provides an additional mechanism for the preventive action of fluoride in enamel caries.
Experiments with germ-free animals have shown that bacteria are essential for the development of dental caries. Bacteria are present in dental plaque which is found on most tooth surfaces. Dental plaque is a biofilm consisting of a variety of different species of bacteria embedded in a matrix derived from salivary mucins and extracellular polysaccharide polymers (glucans and fructans) synthesized by the organisms.
A clean enamel surface is covered in a few seconds by an adsorbed layer of molecules comprising mainly glycoproteins from saliva, the acquired pellicle, to which microorganisms initially adhere. As they multiply and synthesize extracellular matrix polymers other bacteria may bind to them, rather than to the pellicle, resulting in a complex biofilm of spatially arranged species. The close proximity of different species allows for a variety of synergistic or antagonistic interactions. In a healthy mouth the bacterial composition of the plaque varies at different sites on the teeth, reflecting the different microenvironments available for colonization.
Dietary sugars diffuse rapidly through plaque where they are converted to acids (mainly lactic acid but also acetic and propionic acids) by bacterial metabolism. The pH of the plaque may fall by as much as 2 units within 10 minutes after the ingestion of sugar, but over the next 30 to 60 minutes the pH slowly rises to its original figure, due to the diffusion of the sugar and some of the acid out of the plaque, and the diffusion into the plaque of buffered saliva which helps to dilute and neutralize the acid. At the critical pH of 5.5 mineral ions are liberated from the hydroxyapatite crystals of the enamel and diffuse into the plaque. The pH curves of plaque in response to sugar (Stephan's curves) are similar in shape in caries-free and caries-active individuals. However, since the starting pH may be lower in caries-active mouths, the reduction in pH will be greater and the pH will be depressed below the critical level for a greater period of time. At a neutral or slightly alkaline pH the plaque becomes supersaturated with mineral ions derived both from the saliva and from those released from the hydroxyapatite crystals. Ions may now diffuse back into enamel and be redeposited in the crystal structure and this reprecipitation of mineral is aided by fluoride ions.
There is, therefore, a see-sawing of ions across the plaque- enamel interface as the chemical environment within the plaque changes. However, mineral ions may be lost from the system by diffusion out of the plaque and into the saliva during the acid phase, and repeated episodes lead to an overall demineralization and the initiation of enamel caries. Obviously the frequency and duration of the acid phase of plaque will affect the rate of development of caries, and this is why the reduction of carbohydrate intake between meals has such a beneficial effect in caries prevention. Once enamel caries has progressed to cavity formation, the plaque becomes progressively more removed from saliva and probably remains acidic for longer periods. Many plaque bacteria store carbohydrate as an intracellular glycogen-like polysaccharide which may be formed from a variety of sugars, and this may be broken down to acid when other sources of carbohydrate are absent, such as between meals. In addition, as mentioned above, plaque organisms can synthesize extracellular glucans from dietary sugars which may also be metabolized to acid when other sources of carbohydrate are absent. However, abundant extracellular polysaccharides have other important consequences in that they markedly increase the bulk of the plaque, thereby interfering with the outward diffusion of acids and the inward diffusion of saliva and its buffering systems. Such plaques are likely to be more cariogenic because they favour retention of acid at the plaque-enamel interface.
Fluoride ions are present in relatively high concentration in plaque compared with saliva. Fluoride favours the precipitation of calcium and phosphate ions from solution, and so when present at the plaque-enamel interface the deposition of free mineral ions in the plaque as hydroxy- and fluorapatite on the remaining enamel crystals is encouraged. Fluorapatite crystals may also be formed during enamel development if fluorides have been administered systemically (for example by water fluoridation). Fluorapatite is less soluble in acid than hydroxyapatite. Systemic fluoride also promotes the formation of hydroxyapatite crystals with a more stable crystal lattice. Fluoride ions in plaque inhibit bacterial metabolism and this provides an additional mechanism for the preventive action of fluoride in enamel caries.
Microbiology of dental caries
Acid is a general product of bacterial metabolism and no single bacterial species is uniquely associated with the development of enamel caries. Members of the 'mutans streptococci' group are the most efficient cariogenic organisms in animal experiments, and epidemiological data in humans indicates an association between the presence of S. mutans and S. sobrinus in plaque and the prevalence of caries. Some of the factors supporting an aetiological role for S. mutans in dental caries are summarized in. However, caries of enamel may develop in the absence of S. mutans and in some individuals high levels of S. mutans may be present on a tooth surface without the subsequent development of caries. Nevertheless, there is now a wealth of evidence from animal and human studies that the mutans streptococci, especially S. mutans, play a key role in the initiation of caries. Other bacteria, for example lactobacilli, may be important in the further progression of the lesion. Lactobacilli are also the pioneer organisms in dentine caries (see later).
Key points - In dental plaque
· cariogenic bacteria ferment carbohydrate to acid
· cariogenic bacteria can store carbohydrate intra and extracellularly
· extracellular polysaccharides increase plaque bulk
· bulky plaques interfere with outward diffusion of acid and inward diffusion of salivary buffers
· frequent intakes of carbohydrate can depress the pH below the critical level for long periods
Key points - Ionic exchanges in enamel caries
· ions see-saw across the plaque-enamel interface depending on pH
· ions in plaque can be redeposited into the enamel at a neutral pH or lost into the saliva
· enamel caries progresses when the net rate of loss of ions due to acid attack is greater than the net rate of gain due to remineralization
· fluoride ions encourage reprecipitation of minerals into enamel
· fluoride ions can replace hydroxyl ions in hydroxyapatite to form less acid-soluble fluorapatite
Key points - Microbiology of dental caries
· species that may be associated
- non-mutans streptococci, e.g. mitis group
- actinomycetes
· transmission of S. mutans occurs mainly from mother to child
· low plaque pH favours proliferation of mutans streptococci and lactobacilli
· level of mutans streptococci in plaque increased by sucrose consumption
Since caries occurs occasionally in the absence of S. mutans other bacteria can contribute to its development. A range of organisms has been isolated from such sites including several types of non-mutans streptococci, for example those belonging to the mitis, salivarius, anginosus, and sanguinis groups, and lactobacilli and actinomycetes. Although these organisms can induce experimental caries in animals their relative significance in the development of caries in humans is less clear. However, some are moderately acidogenic and as such may contribute to the acid pool of plaque as well as creating an environment favouring colonization by aciduric species such as mutans streptococci and lactobacilli. Because of the strong evidence that S. mutans and lactobacilli are major organisms associated with dental caries, simple screening tests to estimate the salivary levels of these bacteria have been developed as predictors of caries activity. However, the results from such tests need to be interpreted in conjunction with the assessment of other risk factors for caries in an individual patient. Infants become colonized by mutans streptococci from their mothers, and there is evidence that children of high-risk mothers become colonized at an earlier age and develop more carious lesions than children of low-risk mothers.
Role of carbohydrates
Numerous epidemiological studies have demonstrated a direct relationship between fermentable carbohydrate in the diet and dental caries. The evidence includes:
1. The increasing prevalence of dental caries in developing countries and previously isolated ethnic groups associated with westernization, urbanization, and the increasing availability of sucrose in their diet. Examples include Inuit, native North and South Americans, African tribes, and the rural population in countries in the Far East.
2. The decrease in the prevalence of caries during World War II because of sugar restriction, followed by a rise to previous levels when sucrose became available in the post-war period.
3. The Hopewood House study - a children's home in Australia where sucrose and white bread were virtually excluded from the diet. The children had low caries rates which increased dramatically when they moved out of the home.
Key points - Diet and dental caries
· caries prevalence increases when populations become exposed to sucrose-rich diets
· extrinsic sugars are more damaging than intrinsic sugars
· sucrose is the most cariogenic sugar
· frequency of sugar intake is of more importance than total amount consumed
Different carbohydrates have different cariogenic properties. Sucrose is significantly more cariogenic than other sugars, partly because it is readily fermented by plaque bacteria and partly because of its conversion by bacterial glucosyl transferase into extracellular glucans. Sucrose is also readily converted into intracellular polymers. Glucose, fructose, maltose, galactose, and lactose are also highly cariogenic carbohydrates in experimental caries in animals, but the principal carbohydrates available in human diets are sucrose and starches. Dietary sugars can be divided into intrinsic (mainly fruit and vegetables) and extrinsic sources (added sugars, milk, fruit juices). Dietary advice recommends that consumption of extrinsic sugars (except milk) should be reduced. Much of the epidemiological data incriminates sucrose. Its relative importance is also well illustrated in patients with hereditary fructose intolerance who cannot tolerate fructose or sucrose (ingestion may lead to coma and death) but who are able to consume starches. Such individuals have little or no caries. Starch solutions applied to bacterial plaque produce no significant depression in pH, due to the very slow diffusion of the polysaccharide into the plaque which must be hydrolysed by extracellular amylase before it can be assimilated and metabolized by plaque bacteria. However, cooked highly refined starches can cause caries, although much less than sucrose. The combination of cooked starch and sucrose together, such as in cakes and biscuits, is more cariogenic than sucrose alone. The main alternative non-sugar sweeteners, sorbitol and xylitol, are, to all intents and purposes, non-cariogenic. Xylitol is not fermented by oral bacteria and sorbitol is only fermented at a very slow rate.
Whilst there is no doubt that there is a direct relationship between dietary carbohydrates and caries, experimental evidence in humans has shown that the manner and form in which the carbohydrate is taken and the frequency of consumption are more important than the absolute amount of sugar consumed. The risk of caries is greatest if sugar is consumed between meals, thus supplying plaque bacteria with (in the case of habitual 'snackers') an almost constant supply of carbohydrate. It is also increased if the sugar is consumed in a sticky form likely to be retained on the surfaces of the teeth.
In children, prolonged sucking of a sweetened pacifier to about 2 years of age or beyond may be associated with rampant caries, involving particularly the smooth surfaces of the anterior maxillary teeth. A similar problem may also be seen in children given sweetened drinks in a nursing bottle, especially at night. Some studies have also shown an association between prolonged breast feeding beyond 2 years of age and extensive caries, but this is controversial as the results from different studies are conflicting.
Aetiological variables
Not all teeth or tooth surfaces are equally susceptible to caries, nor is the rate of progression of carious lesions constant. Factors influencing site attack and rates of progression in dental caries are largely unknown but may include:
Factors intrinsic to the tooth
Enamel composition - There is an inverse relationship between enamel solubility and enamel fluoride concentration. A graded increase in enamel resistance with age might account for selectivity of site attack.
Enamel structure - Developmental enamel hypoplasia and hypomineralization may affect the rate of progression but not the initiation of caries.
Tooth morphology - Deep, narrow pits and fissures favour the retention of plaque and food.
Tooth position - Malaligned teeth may predispose to the retention of plaque and food.
Factors extrinsic to the tooth
Saliva - Flow rate, viscosity, buffering capacity, availability of calcium and phosphate ions for mineralization, and the presence of antimicrobial agents such as immunoglobulins, thiocyanate ion, lactoferrin, and lysozyme may affect caries pattern.
Diet - The most important factor is the frequency of intake of sugary foods and drinks. Chewing sugar-free gum or eating a small portion of cheese after meals helps protect against dental caries. Phosphates in the diet, either organically bound or inorganic, may also reduce the incidence of caries.
Use of fluoride - In addition to an intrinsic effect, fluoride readily enters bacterial cells and can inhibit enzymes involved in the metabolism of sugar.
Immunity - See later.
Pathology of dental caries
Introduction
Clinically, dental caries may be classified according both to the location of the lesion on the tooth and to the rate of attack.
Classification by site of attack
Pit or fissure caries
Acid is a general product of bacterial metabolism and no single bacterial species is uniquely associated with the development of enamel caries. Members of the 'mutans streptococci' group are the most efficient cariogenic organisms in animal experiments, and epidemiological data in humans indicates an association between the presence of S. mutans and S. sobrinus in plaque and the prevalence of caries. Some of the factors supporting an aetiological role for S. mutans in dental caries are summarized in. However, caries of enamel may develop in the absence of S. mutans and in some individuals high levels of S. mutans may be present on a tooth surface without the subsequent development of caries. Nevertheless, there is now a wealth of evidence from animal and human studies that the mutans streptococci, especially S. mutans, play a key role in the initiation of caries. Other bacteria, for example lactobacilli, may be important in the further progression of the lesion. Lactobacilli are also the pioneer organisms in dentine caries (see later).
Key points - In dental plaque
· cariogenic bacteria ferment carbohydrate to acid
· cariogenic bacteria can store carbohydrate intra and extracellularly
· extracellular polysaccharides increase plaque bulk
· bulky plaques interfere with outward diffusion of acid and inward diffusion of salivary buffers
· frequent intakes of carbohydrate can depress the pH below the critical level for long periods
Key points - Ionic exchanges in enamel caries
· ions see-saw across the plaque-enamel interface depending on pH
· ions in plaque can be redeposited into the enamel at a neutral pH or lost into the saliva
· enamel caries progresses when the net rate of loss of ions due to acid attack is greater than the net rate of gain due to remineralization
· fluoride ions encourage reprecipitation of minerals into enamel
· fluoride ions can replace hydroxyl ions in hydroxyapatite to form less acid-soluble fluorapatite
Key points - Microbiology of dental caries
· species that may be associated
- non-mutans streptococci, e.g. mitis group
- actinomycetes
· transmission of S. mutans occurs mainly from mother to child
· low plaque pH favours proliferation of mutans streptococci and lactobacilli
· level of mutans streptococci in plaque increased by sucrose consumption
Since caries occurs occasionally in the absence of S. mutans other bacteria can contribute to its development. A range of organisms has been isolated from such sites including several types of non-mutans streptococci, for example those belonging to the mitis, salivarius, anginosus, and sanguinis groups, and lactobacilli and actinomycetes. Although these organisms can induce experimental caries in animals their relative significance in the development of caries in humans is less clear. However, some are moderately acidogenic and as such may contribute to the acid pool of plaque as well as creating an environment favouring colonization by aciduric species such as mutans streptococci and lactobacilli. Because of the strong evidence that S. mutans and lactobacilli are major organisms associated with dental caries, simple screening tests to estimate the salivary levels of these bacteria have been developed as predictors of caries activity. However, the results from such tests need to be interpreted in conjunction with the assessment of other risk factors for caries in an individual patient. Infants become colonized by mutans streptococci from their mothers, and there is evidence that children of high-risk mothers become colonized at an earlier age and develop more carious lesions than children of low-risk mothers.
Role of carbohydrates
Numerous epidemiological studies have demonstrated a direct relationship between fermentable carbohydrate in the diet and dental caries. The evidence includes:
1. The increasing prevalence of dental caries in developing countries and previously isolated ethnic groups associated with westernization, urbanization, and the increasing availability of sucrose in their diet. Examples include Inuit, native North and South Americans, African tribes, and the rural population in countries in the Far East.
2. The decrease in the prevalence of caries during World War II because of sugar restriction, followed by a rise to previous levels when sucrose became available in the post-war period.
3. The Hopewood House study - a children's home in Australia where sucrose and white bread were virtually excluded from the diet. The children had low caries rates which increased dramatically when they moved out of the home.
Key points - Diet and dental caries
· caries prevalence increases when populations become exposed to sucrose-rich diets
· extrinsic sugars are more damaging than intrinsic sugars
· sucrose is the most cariogenic sugar
· frequency of sugar intake is of more importance than total amount consumed
Different carbohydrates have different cariogenic properties. Sucrose is significantly more cariogenic than other sugars, partly because it is readily fermented by plaque bacteria and partly because of its conversion by bacterial glucosyl transferase into extracellular glucans. Sucrose is also readily converted into intracellular polymers. Glucose, fructose, maltose, galactose, and lactose are also highly cariogenic carbohydrates in experimental caries in animals, but the principal carbohydrates available in human diets are sucrose and starches. Dietary sugars can be divided into intrinsic (mainly fruit and vegetables) and extrinsic sources (added sugars, milk, fruit juices). Dietary advice recommends that consumption of extrinsic sugars (except milk) should be reduced. Much of the epidemiological data incriminates sucrose. Its relative importance is also well illustrated in patients with hereditary fructose intolerance who cannot tolerate fructose or sucrose (ingestion may lead to coma and death) but who are able to consume starches. Such individuals have little or no caries. Starch solutions applied to bacterial plaque produce no significant depression in pH, due to the very slow diffusion of the polysaccharide into the plaque which must be hydrolysed by extracellular amylase before it can be assimilated and metabolized by plaque bacteria. However, cooked highly refined starches can cause caries, although much less than sucrose. The combination of cooked starch and sucrose together, such as in cakes and biscuits, is more cariogenic than sucrose alone. The main alternative non-sugar sweeteners, sorbitol and xylitol, are, to all intents and purposes, non-cariogenic. Xylitol is not fermented by oral bacteria and sorbitol is only fermented at a very slow rate.
Whilst there is no doubt that there is a direct relationship between dietary carbohydrates and caries, experimental evidence in humans has shown that the manner and form in which the carbohydrate is taken and the frequency of consumption are more important than the absolute amount of sugar consumed. The risk of caries is greatest if sugar is consumed between meals, thus supplying plaque bacteria with (in the case of habitual 'snackers') an almost constant supply of carbohydrate. It is also increased if the sugar is consumed in a sticky form likely to be retained on the surfaces of the teeth.
In children, prolonged sucking of a sweetened pacifier to about 2 years of age or beyond may be associated with rampant caries, involving particularly the smooth surfaces of the anterior maxillary teeth. A similar problem may also be seen in children given sweetened drinks in a nursing bottle, especially at night. Some studies have also shown an association between prolonged breast feeding beyond 2 years of age and extensive caries, but this is controversial as the results from different studies are conflicting.
Aetiological variables
Not all teeth or tooth surfaces are equally susceptible to caries, nor is the rate of progression of carious lesions constant. Factors influencing site attack and rates of progression in dental caries are largely unknown but may include:
Factors intrinsic to the tooth
Enamel composition - There is an inverse relationship between enamel solubility and enamel fluoride concentration. A graded increase in enamel resistance with age might account for selectivity of site attack.
Enamel structure - Developmental enamel hypoplasia and hypomineralization may affect the rate of progression but not the initiation of caries.
Tooth morphology - Deep, narrow pits and fissures favour the retention of plaque and food.
Tooth position - Malaligned teeth may predispose to the retention of plaque and food.
Factors extrinsic to the tooth
Saliva - Flow rate, viscosity, buffering capacity, availability of calcium and phosphate ions for mineralization, and the presence of antimicrobial agents such as immunoglobulins, thiocyanate ion, lactoferrin, and lysozyme may affect caries pattern.
Diet - The most important factor is the frequency of intake of sugary foods and drinks. Chewing sugar-free gum or eating a small portion of cheese after meals helps protect against dental caries. Phosphates in the diet, either organically bound or inorganic, may also reduce the incidence of caries.
Use of fluoride - In addition to an intrinsic effect, fluoride readily enters bacterial cells and can inhibit enzymes involved in the metabolism of sugar.
Immunity - See later.
Pathology of dental caries
Introduction
Clinically, dental caries may be classified according both to the location of the lesion on the tooth and to the rate of attack.
Classification by site of attack
Pit or fissure caries
This occurs on the occlusal surfaces of molars and premolars, on the buccal and lingual surfaces of molars, and the lingual surfaces of maxillary incisors. Early caries may be detected clinically by brown or black discoloration of a fissure in which a probe 'sticks'. The enamel directly bordering the pit or fissure may appear opaque, bluish-white as it becomes undermined by caries. Since the widespread use of fluoride-containing dentifrices early occlusal caries has become more difficult to diagnose. Apparently clinically sound enamel can overlay extensive dentine caries because of strengthening of the enamel by the formation of fluorapatite and the ability of fluoride to promote remineralization.
Smooth surface caries
This occurs on the approximal surfaces, and on the gingival third of the buccal and lingual surfaces. Approximal caries begins just below the contact point as a well-demarcated chalky-white opacity of the enamel . At this stage there is no loss of continuity of the enamel surface and the lesion cannot be detected by a probe or on routine radiographs. The white spot lesion may become pigmented yellow or brown and may extend buccally and lingually into the embrasures. As the caries progresses, the surrounding enamel becomes bluish-white. The surface of the lesion becomes roughened before frank cavitation occurs. There are no consistent radiographic features which enable unequivocal identification of enamel lesions that have cavitated from lesions where the surface is still intact. However, lesions with an underlying radiolucency involving half or more of the dentine thickness are always cavitated. For a radiolucency limited to the outer half of the dentine the probability of cavitation ranges from about 40 to 80 per cent in different studies. For radiolucencies limited to the enamel the probability of cavitation in most studies is low and such lesions should be treated by preventive measures and reviewed. Cervical caries extends occlusally from opposite the gingival margin on buccal and lingual tooth surfaces. It has a similar appearance to approximal caries, but almost always produces a wide open cavity.
Cemental or root caries
This occurs when the root face is exposed to the oral environment as a result of periodontal disease. The root face is softened and the cavities, which may be extensive, are usually shallow, saucer-shaped, with ill-defined boundaries.
Key points - Diagnosis of caries
· early occlusal caries may be difficult to detect
· radiolucencies in approximal enamel that do not reach the amelodentinal junction do not usually indicate enamel cavitation
· approximal lesions which on radiographs do not extend into dentine should be treated by preventive measures
Recurrent caries
This occurs around the margin or at the base of a previously existing restoration.
Classification by rate of attack
Rampant or acute caries
This is rapidly progressing caries involving many or all of the erupted teeth, often on surfaces normally immune to caries. The rapid coronal destruction and limited time for the protective responses of the pulpodentinal complex to occur lead to early involvement of the pulp.
Slowly progressive or chronic caries
This is caries that progresses slowly and involves the pulp much later than in acute caries. It is most common in adults and the slow progress allows time for defence reactions of the pulpodentinal complex (sclerosis and reactionary dentine formation) to develop.
Arrested caries
This is caries of enamel or dentine, including root caries, that becomes static and shows no tendency for further progression.
Enamel caries
Ground sections of teeth have been used extensively in histopathological studies of enamel caries and have been examined by transmitted and polarized light, and by microradiography. Electron microscopy and biochemical analysis of microdissected pieces of carious enamel have also been carried out. Most research has concentrated on smooth surface caries to avoid the problems of interpretation of histological features imposed by the anatomy of pits and fissures. However, the pathological features are essentially similar in both sites. The established early lesion (white spot lesion) in smooth surface enamel caries is cone-shaped, with the base of the cone on the enamel surface and the apex pointing towards the amelodentinal junction. The shape is modified in pit and fissure caries (see later). In ground sections it consists of a series of zones, the optical properties of which reflect differing degrees of demineralization. These zones are described below.
Translucent zone
This is the first recognizable histological change at the advancing edge of the lesion. It is more porous than normal enamel and contains 1 per cent by volume of spaces, the pore volume, compared with the 0.1 per cent pore volume in normal enamel. The pores are larger than the small pores in normal enamel which approximate to the size of a water molecule. Chemical analysis shows that there is a fall in magnesium and carbonate when compared with normal enamel, which suggests that a magnesium- and carbonate- rich mineral is preferentially dissolved in this zone. Dissolution of mineral occurs mainly from the junctional areas between the prismatic and interprismatic enamel. The prism boundaries, which are relatively rich in protein, allow ready ingress of hydrogen ions and the magnesium- and carbonate-rich mineral that is preferentially removed may represent the surface layers of crystallites at the prism boundaries. The translucent zone is sometimes missing, or present along only part of the lesion.
Dark zone
This zone contains 2-4 per cent by volume of pores. Some of the pores are large, but others are smaller than those in the translucent zone, suggesting that some remineralization has occurred due to reprecipitation of mineral lost from the translucent zone. It is thought that the dark zone is narrow in rapidly advancing lesions and wider in more slowly advancing lesions when more remineralization may occur.
Body of the lesion
This zone has a pore volume of between 5 and 25 per cent, and also contains apatite crystals larger than those found in normal enamel. It is suggested that these large crystals result from the reprecipitation of mineral dissolved from deeper zones. However, with continuing acid attack there is further dissolution of mineral both from the periphery of the apatite crystals and from their cores. The lost mineral is replaced by unbound water and to a lesser extent by organic matter, presumably derived from saliva and microorganisms. There is increased prominence of the striae of Retzius in the body of the lesion, the explanation for which is unknown.
Surface zone
This is about 40um thick and shows surprisingly little change in early lesions. The surface of normal enamel differs in composition from the deeper layers, being more highly mineralized and having, for example, a higher fluoride level and a lower magnesium level, and so interpretation of possible chemical changes in this zone is difficult. The surface zone remains relatively normal despite subsurface loss of mineral, because it is an area of active reprecipitation of mineral derived both from the plaque and from that dissolved from deeper areas of the lesion as ions diffuse outwards .
Histopathogenesis of the early lesion
The development of enamel caries can be traced through the following stages when ground sections are examined by transmitted light .
1. Development of a subsurface translucent zone, which is unrecognizable clinically and radiologically.
2. The subsurface translucent zone enlarges and a dark zone develops in its centre.
3. As the lesion enlarges more mineral is lost and the centre of the dark zone becomes the body of the lesion. This is relatively translucent compared with sound enamel and shows enhancement of the striae of Retzius, interprismatic markings, and cross-striations of the prisms. The lesion is now clinically recognizable as a white spot.
4. The body of the lesion may become stained by exogenous pigments from food, tobacco, and bacteria. The lesion is now clinically recognizable as a brown spot.
5. When the caries reaches the amelodentinal junction it spreads laterally, undermining the adjacent enamel, giving the bluish-white appearance to the enamel as seen clinically. Although lateral spread can occur before cavitation (see stage 6), it is more common and more extensive in lesions with cavity formation.
6. With progressive loss of mineral a critical point is reached when the enamel is no longer able to withstand the loads placed upon it and the structure breaks down to form a cavity. This stage may precede stage 5. Caries progression is a slow process and it usually takes several years before cavitation occurs.
Key points - Enamel caries
· a dynamic physicochemical process involving dissolution and repreciptation of mineral
· caries progression is usually a slow process
· zonation of the early (white spot) lesion reflects different degrees of demineralization
· four zones usually seen: translucent zone (1 per cent loss), dark zone (2-4 per cent loss), body (5-25 per cent loss), surface zone (intact)
· surface zone is an area of active remineralization
· the morphology of the lesion differs in pits and fissures compared with approximal surfaces
Caries in a fissure does not start at the base, but develops as a ring around the wall of the fissure, the histological features of the lesion being similar to those seen on smooth surfaces. As the caries progresses it spreads outwards into the surrounding enamel and downwards towards the dentine, and eventually coalesces at the base of the fissure. This produces a cone-shaped lesion, but the base of the cone is directed towards the amelodentinal junction and is not on the enamel surface as in smooth surface caries. The area of dentine ultimately involved is therefore larger than with smooth surface lesions.
Rampant or acute caries
This is rapidly progressing caries involving many or all of the erupted teeth, often on surfaces normally immune to caries. The rapid coronal destruction and limited time for the protective responses of the pulpodentinal complex to occur lead to early involvement of the pulp.
Slowly progressive or chronic caries
This is caries that progresses slowly and involves the pulp much later than in acute caries. It is most common in adults and the slow progress allows time for defence reactions of the pulpodentinal complex (sclerosis and reactionary dentine formation) to develop.
Arrested caries
This is caries of enamel or dentine, including root caries, that becomes static and shows no tendency for further progression.
Enamel caries
Ground sections of teeth have been used extensively in histopathological studies of enamel caries and have been examined by transmitted and polarized light, and by microradiography. Electron microscopy and biochemical analysis of microdissected pieces of carious enamel have also been carried out. Most research has concentrated on smooth surface caries to avoid the problems of interpretation of histological features imposed by the anatomy of pits and fissures. However, the pathological features are essentially similar in both sites. The established early lesion (white spot lesion) in smooth surface enamel caries is cone-shaped, with the base of the cone on the enamel surface and the apex pointing towards the amelodentinal junction. The shape is modified in pit and fissure caries (see later). In ground sections it consists of a series of zones, the optical properties of which reflect differing degrees of demineralization. These zones are described below.
Translucent zone
This is the first recognizable histological change at the advancing edge of the lesion. It is more porous than normal enamel and contains 1 per cent by volume of spaces, the pore volume, compared with the 0.1 per cent pore volume in normal enamel. The pores are larger than the small pores in normal enamel which approximate to the size of a water molecule. Chemical analysis shows that there is a fall in magnesium and carbonate when compared with normal enamel, which suggests that a magnesium- and carbonate- rich mineral is preferentially dissolved in this zone. Dissolution of mineral occurs mainly from the junctional areas between the prismatic and interprismatic enamel. The prism boundaries, which are relatively rich in protein, allow ready ingress of hydrogen ions and the magnesium- and carbonate-rich mineral that is preferentially removed may represent the surface layers of crystallites at the prism boundaries. The translucent zone is sometimes missing, or present along only part of the lesion.
Dark zone
This zone contains 2-4 per cent by volume of pores. Some of the pores are large, but others are smaller than those in the translucent zone, suggesting that some remineralization has occurred due to reprecipitation of mineral lost from the translucent zone. It is thought that the dark zone is narrow in rapidly advancing lesions and wider in more slowly advancing lesions when more remineralization may occur.
Body of the lesion
This zone has a pore volume of between 5 and 25 per cent, and also contains apatite crystals larger than those found in normal enamel. It is suggested that these large crystals result from the reprecipitation of mineral dissolved from deeper zones. However, with continuing acid attack there is further dissolution of mineral both from the periphery of the apatite crystals and from their cores. The lost mineral is replaced by unbound water and to a lesser extent by organic matter, presumably derived from saliva and microorganisms. There is increased prominence of the striae of Retzius in the body of the lesion, the explanation for which is unknown.
Surface zone
This is about 40um thick and shows surprisingly little change in early lesions. The surface of normal enamel differs in composition from the deeper layers, being more highly mineralized and having, for example, a higher fluoride level and a lower magnesium level, and so interpretation of possible chemical changes in this zone is difficult. The surface zone remains relatively normal despite subsurface loss of mineral, because it is an area of active reprecipitation of mineral derived both from the plaque and from that dissolved from deeper areas of the lesion as ions diffuse outwards .
Histopathogenesis of the early lesion
The development of enamel caries can be traced through the following stages when ground sections are examined by transmitted light .
1. Development of a subsurface translucent zone, which is unrecognizable clinically and radiologically.
2. The subsurface translucent zone enlarges and a dark zone develops in its centre.
3. As the lesion enlarges more mineral is lost and the centre of the dark zone becomes the body of the lesion. This is relatively translucent compared with sound enamel and shows enhancement of the striae of Retzius, interprismatic markings, and cross-striations of the prisms. The lesion is now clinically recognizable as a white spot.
4. The body of the lesion may become stained by exogenous pigments from food, tobacco, and bacteria. The lesion is now clinically recognizable as a brown spot.
5. When the caries reaches the amelodentinal junction it spreads laterally, undermining the adjacent enamel, giving the bluish-white appearance to the enamel as seen clinically. Although lateral spread can occur before cavitation (see stage 6), it is more common and more extensive in lesions with cavity formation.
6. With progressive loss of mineral a critical point is reached when the enamel is no longer able to withstand the loads placed upon it and the structure breaks down to form a cavity. This stage may precede stage 5. Caries progression is a slow process and it usually takes several years before cavitation occurs.
Key points - Enamel caries
· a dynamic physicochemical process involving dissolution and repreciptation of mineral
· caries progression is usually a slow process
· zonation of the early (white spot) lesion reflects different degrees of demineralization
· four zones usually seen: translucent zone (1 per cent loss), dark zone (2-4 per cent loss), body (5-25 per cent loss), surface zone (intact)
· surface zone is an area of active remineralization
· the morphology of the lesion differs in pits and fissures compared with approximal surfaces
Caries in a fissure does not start at the base, but develops as a ring around the wall of the fissure, the histological features of the lesion being similar to those seen on smooth surfaces. As the caries progresses it spreads outwards into the surrounding enamel and downwards towards the dentine, and eventually coalesces at the base of the fissure. This produces a cone-shaped lesion, but the base of the cone is directed towards the amelodentinal junction and is not on the enamel surface as in smooth surface caries. The area of dentine ultimately involved is therefore larger than with smooth surface lesions.
Dentine caries
Dentine differs from enamel in that it is a living tissue and as such can respond to caries attack. It also has a relatively high organic content, approximately 20 per cent by weight, which consists predominantly of collagen. In dentine caries it is, therefore, necessary to consider both the defence reaction of the pulpodentinal complex and the carious destruction of the tissue which involves acid demineralization followed by proteolytic breakdown of the matrix. The defence reaction may begin before the carious process reaches the dentine, presumably because of irritation to the odontoblasts transmitted through the weakened enamel, and is represented by the formation of reactionary (or tertiary) dentine and dentinal sclerosis (see later). However, in progressive lesions the defence reaction is progressively overtaken by the carious process as it advances towards the pulp.
Key points - Processes in dentine caries
· defence reaction of pulpodentinal complex
- sclerosis
- reactionary dentine formation
- sealing of dead tracts
· carious destruction
- demineralization
- proteolysis
Caries of the dentine develops from enamel caries: when the lesion reaches the amelodentinal junction, lateral extension results in the involvement of great numbers of tubules .The early lesion is cone-shaped, or convex, with the base at the amelodentinal junction. Larger lesions may show a broadening of the apex of the cone as it approaches the circumpulpal dentine. In caries of dentine, demineralization by acid is always in advance of the bacterial front, the subsequent bacterial invasion being followed by breakdown of the collagenous matrix.
Because of the sequential nature of the changes, studies of ground and decalcified sections show a zoned lesion in which four zones are characteristically present.
Zone of sclerosis
The sclerotic or translucent zone is located beneath and at the sides of the carious lesion. It is almost invariably present, being broader beneath the lesion than at the sides, and is regarded as a vital reaction of odontoblasts to irritation. Two patterns of mineralization have been described. The first is the result of acceleration of the normal physiological process of centripetal deposition of peritubular dentine which eventually occludes the tubules. In the second, mineral first appears within the cytoplasmic process of the odontoblasts and the tubule is obliterated by calcification of the odontoblast process itself. Sclerosed dentine therefore has a higher mineral content.
Dead tracts may be seen running through the zone of sclerosis. They are the result of death of odontoblasts at an earlier stage in the carious process. The empty dentinal tubules contain air and the remains of the dead odontoblast process and such tubules can obviously not undergo sclerosis. However, they provide ready access of bacteria and their products to the pulp. To prevent this the pulpal end of a dead tract is occluded by a thin layer of hyaline calcified material, sometimes called eburnoid, which is derived from pulpal cells. Beyond this, further, often very irregular, reactionary dentine may form following differentiation of odontoblasts or odontoblast-like cells from the pulp.
Zone of demineralization
In the demineralized zone the intertubular matrix is mainly affected by a wave of acid produced by bacteria in the zone of bacterial invasion, which diffuses ahead of the bacterial front. The softened dentine in the base of a cavity is therefore sterile but, in clinical practice, it cannot be distinguished reliably from softened infected dentine (see later). It may be stained yellowish-brown as a result of the diffusion of other bacterial products interacting with proteins in dentine.
Zone of bacterial invasion
In this zone the bacteria extend down and multiply within the dentinal tubules, some of which may become occluded by bacteria .There are always, however, many empty tubules lying among tubules containing bacteria. The bacterial invasion probably occurs in two waves: the first wave consisting of acidogenic organisms, mainly lactobacilli, produce acid which diffuses ahead into the demineralized zone. A second wave of mixed acidogenic and proteolytic organisms then attack the demineralized matrix. The walls of the tubules are softened by the proteolytic activity and some may then be distended by the increasing mass of multiplying bacteria. The peritubular dentine is first compressed, followed by the intertubular dentine, resulting in elliptical areas of proteolysis-liquefaction foci. Liquefaction foci run parallel to the direction of the tubules and may be multiple, giving the tubule a beaded appearance . These changes are enhanced in the zone of destruction. The bacteria may show varying degrees of degeneration.
Zone of destruction
In the zone of destruction the liquefaction foci enlarge and increase in number. Cracks or clefts containing bacteria and necrotic tissue also appear at right angles to the course of the dentinal tubules forming transverse clefts. The mechanism of formation of transverse clefts is uncertain. They may follow the course of incremental lines, or result from the coalescence of liquefaction foci on adjacent tubules, or arise by extension of proteolytic activity along interconnecting lateral branches of odontoblast tubules. Bacteria are no longer confined to the tubules and invade both the peritubular and intertubular dentine. Little of the normal dentine architecture now remains and cavitation commences from the amelodentinal junction. In acute, rapidly progressing caries the necrotic dentine is very soft and yellowish-white; in chronic caries it has a brownish-black colour and is of leathery consistency.
Reactionary (or tertiary) dentine
A layer of reactionary (or tertiary) dentine is often formed at the surface of the pulp chamber deep to the dentine caries, this dentine being localized to the irritated odontoblasts. It varies in structure but the tubules are generally irregular, tortuous, and fewer in number than in primary dentine, or may even be absent. Microradiography shows variations in mineralization, but areas of hypermineralization when compared with primary dentine may be present. Its formation effectively increases the depth of tissue between the carious dentine and the pulp, and in this way delays involvement of the pulp.
Reactionary dentine is a non-specific response to odontoblast irritation, also being formed in reaction to tooth wear and cavity and crown preparations.
Key points - Dentine caries
· zoned lesion but zones not well demarcated
· demineralization precedes bacterial invasion
· bacterial invasion of tubules; acid produced by acidogenic organisms diffuses ahead
· proteolytic organisms in tubules break down demineralized dentine
· histological evidence of proteolysis - liquefaction foci, transverse clefts
· in the base of a cavity soft dentine must be removed; stained hard dentine can be retained
Clinical aspects of dentine caries
The dentine at the base of a cavity may be soft, hard, stained, or unstained. Excavation of the softened dentine removes the great majority of cariogenic bacteria. Hard stained dentine may harbour small numbers of bacteria but these are of no consequence. There is no need to remove hard stained dentine. Follow-up studies have shown that lesions treated in this way and then sealed do not progress, providing the seal remains intact, even though some infected dentine may remain. Various caries-detector dyes have been developed with the aim of distinguishing between infected and sterile dentine but their validity and reliability require further study and, at present, they are not recommended for routine use.
The technique of stepwise excavation of a deep carious lesion takes advantage of the fact that progression of caries can be prevented even if some bacteria still remain. The aim of the technique is to remove as much infected dentine as is safely possible at the first excavation, without risking pulpal exposure, in order to reduce the rate of progression. The tooth is then sealed for an interval (from 4 to 6 months in different studies) to allow time for the defence reactions of the pulpodentinal complex to develop, before final excavation.
Chemomechanical methods of removal of carious dentine have also been developed. Although these reduce the amount of cavity preparation and removal of sound tooth tissue that would have been required for access using conventional excavation, the early techniques were time-consuming and relatively inefficient. However, the recently introduced reagent Carisolv (Medi Team) appears more promising. Essentially, chemomechanical techniques involve the application of reagents to carious dentine which chlorinate degraded collagen, disrupting and softening it, facilitating its removal.
Dentine differs from enamel in that it is a living tissue and as such can respond to caries attack. It also has a relatively high organic content, approximately 20 per cent by weight, which consists predominantly of collagen. In dentine caries it is, therefore, necessary to consider both the defence reaction of the pulpodentinal complex and the carious destruction of the tissue which involves acid demineralization followed by proteolytic breakdown of the matrix. The defence reaction may begin before the carious process reaches the dentine, presumably because of irritation to the odontoblasts transmitted through the weakened enamel, and is represented by the formation of reactionary (or tertiary) dentine and dentinal sclerosis (see later). However, in progressive lesions the defence reaction is progressively overtaken by the carious process as it advances towards the pulp.
Key points - Processes in dentine caries
· defence reaction of pulpodentinal complex
- sclerosis
- reactionary dentine formation
- sealing of dead tracts
· carious destruction
- demineralization
- proteolysis
Caries of the dentine develops from enamel caries: when the lesion reaches the amelodentinal junction, lateral extension results in the involvement of great numbers of tubules .The early lesion is cone-shaped, or convex, with the base at the amelodentinal junction. Larger lesions may show a broadening of the apex of the cone as it approaches the circumpulpal dentine. In caries of dentine, demineralization by acid is always in advance of the bacterial front, the subsequent bacterial invasion being followed by breakdown of the collagenous matrix.
Because of the sequential nature of the changes, studies of ground and decalcified sections show a zoned lesion in which four zones are characteristically present.
Zone of sclerosis
The sclerotic or translucent zone is located beneath and at the sides of the carious lesion. It is almost invariably present, being broader beneath the lesion than at the sides, and is regarded as a vital reaction of odontoblasts to irritation. Two patterns of mineralization have been described. The first is the result of acceleration of the normal physiological process of centripetal deposition of peritubular dentine which eventually occludes the tubules. In the second, mineral first appears within the cytoplasmic process of the odontoblasts and the tubule is obliterated by calcification of the odontoblast process itself. Sclerosed dentine therefore has a higher mineral content.
Dead tracts may be seen running through the zone of sclerosis. They are the result of death of odontoblasts at an earlier stage in the carious process. The empty dentinal tubules contain air and the remains of the dead odontoblast process and such tubules can obviously not undergo sclerosis. However, they provide ready access of bacteria and their products to the pulp. To prevent this the pulpal end of a dead tract is occluded by a thin layer of hyaline calcified material, sometimes called eburnoid, which is derived from pulpal cells. Beyond this, further, often very irregular, reactionary dentine may form following differentiation of odontoblasts or odontoblast-like cells from the pulp.
Zone of demineralization
In the demineralized zone the intertubular matrix is mainly affected by a wave of acid produced by bacteria in the zone of bacterial invasion, which diffuses ahead of the bacterial front. The softened dentine in the base of a cavity is therefore sterile but, in clinical practice, it cannot be distinguished reliably from softened infected dentine (see later). It may be stained yellowish-brown as a result of the diffusion of other bacterial products interacting with proteins in dentine.
Zone of bacterial invasion
In this zone the bacteria extend down and multiply within the dentinal tubules, some of which may become occluded by bacteria .There are always, however, many empty tubules lying among tubules containing bacteria. The bacterial invasion probably occurs in two waves: the first wave consisting of acidogenic organisms, mainly lactobacilli, produce acid which diffuses ahead into the demineralized zone. A second wave of mixed acidogenic and proteolytic organisms then attack the demineralized matrix. The walls of the tubules are softened by the proteolytic activity and some may then be distended by the increasing mass of multiplying bacteria. The peritubular dentine is first compressed, followed by the intertubular dentine, resulting in elliptical areas of proteolysis-liquefaction foci. Liquefaction foci run parallel to the direction of the tubules and may be multiple, giving the tubule a beaded appearance . These changes are enhanced in the zone of destruction. The bacteria may show varying degrees of degeneration.
Zone of destruction
In the zone of destruction the liquefaction foci enlarge and increase in number. Cracks or clefts containing bacteria and necrotic tissue also appear at right angles to the course of the dentinal tubules forming transverse clefts. The mechanism of formation of transverse clefts is uncertain. They may follow the course of incremental lines, or result from the coalescence of liquefaction foci on adjacent tubules, or arise by extension of proteolytic activity along interconnecting lateral branches of odontoblast tubules. Bacteria are no longer confined to the tubules and invade both the peritubular and intertubular dentine. Little of the normal dentine architecture now remains and cavitation commences from the amelodentinal junction. In acute, rapidly progressing caries the necrotic dentine is very soft and yellowish-white; in chronic caries it has a brownish-black colour and is of leathery consistency.
Reactionary (or tertiary) dentine
A layer of reactionary (or tertiary) dentine is often formed at the surface of the pulp chamber deep to the dentine caries, this dentine being localized to the irritated odontoblasts. It varies in structure but the tubules are generally irregular, tortuous, and fewer in number than in primary dentine, or may even be absent. Microradiography shows variations in mineralization, but areas of hypermineralization when compared with primary dentine may be present. Its formation effectively increases the depth of tissue between the carious dentine and the pulp, and in this way delays involvement of the pulp.
Reactionary dentine is a non-specific response to odontoblast irritation, also being formed in reaction to tooth wear and cavity and crown preparations.
Key points - Dentine caries
· zoned lesion but zones not well demarcated
· demineralization precedes bacterial invasion
· bacterial invasion of tubules; acid produced by acidogenic organisms diffuses ahead
· proteolytic organisms in tubules break down demineralized dentine
· histological evidence of proteolysis - liquefaction foci, transverse clefts
· in the base of a cavity soft dentine must be removed; stained hard dentine can be retained
Clinical aspects of dentine caries
The dentine at the base of a cavity may be soft, hard, stained, or unstained. Excavation of the softened dentine removes the great majority of cariogenic bacteria. Hard stained dentine may harbour small numbers of bacteria but these are of no consequence. There is no need to remove hard stained dentine. Follow-up studies have shown that lesions treated in this way and then sealed do not progress, providing the seal remains intact, even though some infected dentine may remain. Various caries-detector dyes have been developed with the aim of distinguishing between infected and sterile dentine but their validity and reliability require further study and, at present, they are not recommended for routine use.
The technique of stepwise excavation of a deep carious lesion takes advantage of the fact that progression of caries can be prevented even if some bacteria still remain. The aim of the technique is to remove as much infected dentine as is safely possible at the first excavation, without risking pulpal exposure, in order to reduce the rate of progression. The tooth is then sealed for an interval (from 4 to 6 months in different studies) to allow time for the defence reactions of the pulpodentinal complex to develop, before final excavation.
Chemomechanical methods of removal of carious dentine have also been developed. Although these reduce the amount of cavity preparation and removal of sound tooth tissue that would have been required for access using conventional excavation, the early techniques were time-consuming and relatively inefficient. However, the recently introduced reagent Carisolv (Medi Team) appears more promising. Essentially, chemomechanical techniques involve the application of reagents to carious dentine which chlorinate degraded collagen, disrupting and softening it, facilitating its removal.
Root caries
The primary tissue affected in root caries is usually the cementum. The development of cemental caries is preceded by exposure of the root to the oral environment as a result of periodontal disease followed by bacterial colonization. Although Actinomyces species are present in large numbers and have been implicated in the disease, other organisms, including mutans streptococci and lactobacilli, are also associated with root caries.
Microradiographs of developing lesions show subsurface demineralization of the root which may extend into dentine. The surface layer is hypermineralized and is analogous to that seen in the early enamel lesion. It represents a zone of reprecipitation of mineral removed from the subsurface and of remineralization from minerals present in plaque/saliva. Fluoride is readily taken up by carious root surfaces and this enhances remineralization.
Despite the initial hypermineralization of the surface, progressive softening occurs with time in active lesions. Root caries is clinically diagnosed by a softening and brownish discoloration of the tissues. Demineralization is rapidly followed by bacterial invasion along the exposed collagen fibres and fracture and loss of successive layers of cementum. These fractures frequently occur parallel to the root surface and are associated with invasion of bacteria along the incremental bands in cementum which run as concentric layers around the root. This extension results in lesions that spread laterally around the root and often coalesce with other lesions so that eventually the carious process may encircle the root.
As the cementum is lost the peripheral dentine is exposed. The basic reactions and carious destruction of this tissue are the same as those described previously. Sclerosis may lead to arrested lesions and the surface of the exposed dentine may be covered by a hypermineralized layer.
Arrested caries
Enamel
Arrest of an approximal smooth surface lesion prior to cavity formation can occur when the adjacent tooth is lost so that the lesion becomes accessible to plaque control. Remineralization may then occur from saliva or from the topical application of calcifying solutions, but a normal crystalline structure is not necessarily reformed.
Dentine
Arrest of coronal dentinal caries may occur in lesions characterised by marked early dentinal sclerosis which limits the rate of inward spread of the caries. (In contrast, teeth involved by rampant caries show a minimal protective response.) As a result, there is extensive lateral spread of caries along the zone of the amelodentinal junction, which undermines the surface enamel. Fracture and loss of this unsupported enamel exposes the superficially softened carious dentine to the oral environment and it is then removed by attrition and abrasion, leaving a hard, polished surface. Such dentine is deeply pigmented brown-black in colour. Its surface is hypermineralized due to remineralization from oral fluids and has a high fluoride content.
Arrested lesions of root caries have a similar clinical appearance and develop in a similar manner following loss of the superficially softened cementum.
Immunological aspects of dental caries
Caries in man is associated with the development of serum and salivary antibodies against S. mutans, but in almost all individuals this natural active immunity appears to have little effect as caries is virtually universal in Western populations. This may be because S. mutans is only weakly antigenic.
However, artificial active immunity following experimental immunization in animal models has been shown to produce a significant reduction in caries. Early experiments used vaccines composed of whole cells of S. mutans, but these could induce antibodies in humans which cross-react with heart tissue. Subsequently, various subunits of the organism have been investigated, especially surface antigens involved in the attachment of the organism to tooth surfaces, which still confer protection against caries but without the risk of cross-reactivity.
Immunization evokes a humoral response and protection against S. mutans is provided largely by secretory IgA antibodies in saliva, although IgG and IgM class antibodies can also gain access to the mouth via the crevicular fluid. The salivary IgA antibodies act mainly by interfering with the attachment of the organism to tooth surfaces. In addition to active immunity, the development of genetically engineered antibodies (monoclonal antibodies) against specific mutans streptococcal antigens offer the prospect of passive immunization as a preventive strategy for the future.
Caries in man is associated with the development of serum and salivary antibodies against S. mutans, but in almost all individuals this natural active immunity appears to have little effect as caries is virtually universal in Western populations. This may be because S. mutans is only weakly antigenic.
However, artificial active immunity following experimental immunization in animal models has been shown to produce a significant reduction in caries. Early experiments used vaccines composed of whole cells of S. mutans, but these could induce antibodies in humans which cross-react with heart tissue. Subsequently, various subunits of the organism have been investigated, especially surface antigens involved in the attachment of the organism to tooth surfaces, which still confer protection against caries but without the risk of cross-reactivity.
Immunization evokes a humoral response and protection against S. mutans is provided largely by secretory IgA antibodies in saliva, although IgG and IgM class antibodies can also gain access to the mouth via the crevicular fluid. The salivary IgA antibodies act mainly by interfering with the attachment of the organism to tooth surfaces. In addition to active immunity, the development of genetically engineered antibodies (monoclonal antibodies) against specific mutans streptococcal antigens offer the prospect of passive immunization as a preventive strategy for the future.
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