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Exclusive preview pediatric dentistry principles and practice 2e by muthu

  1. 1. C h a p t e r Dental Caries MS Muthu, N Sivakumar CHAPTER OUTLINE Introduction Histopathology of Dental Caries Definition Enamel caries Etiology of Dental Caries Dentinal caries Dental plaque and dental caries Epidemiology of Dental Caries Theories Caries in the primary dentition Stephan curve Caries in the mixed dentition Role of saliva in dental caries Caries in the permanent dentition Socioeconomic factors Bilateral caries experience Hereditary factors Rampant Caries Clinical Classification of Dental Caries Sugar Substitutes According to location Fundamentals of artificial sweeteners According to rapidity Caries Vaccine According to whether lesion is a new one or not Suggested Reading Based on extent of damage Self-assessment Questions “The disease is painless; it’s the cure that hurts.” in Chapter 16 on Caries Risk Assessment and Caries —Katherine Whitehorn Activity Tests. Introduction Definition Dental caries remains as one of the most widespread Dental caries is a microbial disease of the calcified tissues diseases of mankind. It is the single most common of the teeth characterized by demineralization of the chronic childhood disease. It is five times more common inorganic portion and destruction of the organic sub- than asthma and seven times more common than hay stance of the tooth. fever. Nowadays, all experts on dental caries agree that Caries is a biofilm (plaque)-induced acid demineraliza- it is a multifactorial disease and also an infectious and tion of enamel or dentin, mediated by saliva—American communicable disease. Although there are effective ways Academy of Pediatric Dentistry. for prevention of this disease, the unmet needs remain large in developing and developed nations. This chapter Etiology of Dental Caries discusses the etiology of dental caries, histopathology of its spread and its pattern of occurrence in primary Dental Plaque and Dental Caries and permanent dentition. The various caries diagnos- Dental plaque plays a major role in the etiology of both tic methods and preventive measures are discussed periodontal disease and dental caries. Dental plaque isChapter-17.indd 195 11/08/11 7:20 PM
  2. 2. V 196 Pediatric Dentistry primarily composed of bacteria and lesser amounts of adherent debris during the usual masticatory move- bacterial extracellular products, food debris and desqua- ments. In the modern diet, soft and refined foods mated epithelial cells. The major determinant of plaque tend to cling tenaciously to the teeth and are not formation is the ability of certain microorganisms to removed because of the general lack of roughness. adhere to the tooth surface. This characteristic is a major The reduction of mastication due to the softness of factor influencing smooth surface caries. In contrast to diet also augments the clinging of food. Toffee and plaque on smooth surface, the ability of bacteria to adhere caramel adhere tenaciously to the tooth surface. is not a requisite for fissure caries. 2. The carbohydrate content of the diet has been almost Acid production by the oral microorganisms within universally accepted as one of the most important dental plaque is the most important determinant in patho- factors in the dental caries process. Sucrose is said genesis of dental caries. Simple sugars are easily converted to be the arch criminal of dental caries because by microorganisms to lactic acid. Demineralization of of its susceptibility of conversion to acids by oral enamel is a result of concentration of hydrogen ions present microorganisms. at the tooth surface and the amount of time for which 3. Animal studies have proven the fact that frequency of enamel is exposed to low pH conditions. Apart from the intake plays a major role in etiology of dental caries. acids, cariogenic microorganisms like S. mutans produce Individuals with more frequent intake of carbohy- large quantities of water insoluble glucan from sucrose. drates are more prone for dental caries than the indi- In addition to a role in bacterial attachment, the insoluble viduals taking the same quantity in a lesser frequency. extracellular polysaccharides are also believed to act as a Hence it can be said that “the most important thing barrier to the diffusion of acids away from the tooth and is not what we eat; but how we eat”. to the transport of salivary buffers into the plaque. For dental caries to occur, it is recognized to require a Host factor host (tooth), a dietary substrate (refined carbohydrates), Carbohydrates and microorganisms may be considered as aciduric bacteria (microorganisms). Given time, the inter- attack forces in caries etiology. Salivary secretion may be action of cariogenic microorganisms and fermentable considered an environmental force, capable of enhancing carbohydrates (sucrose) may induce demineralization, or detracting from the process and the enamel may be which can progress to loss of tooth structure/cavitation. viewed as a resistance force. Susceptibility of tooth can These three factors form the Keyes triad in the etiology of be attributed to certain physical and chemical changes dental caries (Fig. 17.1) and are discussed in detail below. in the enamel. These could be factors such as surface imperfections (hypoplasia, deep pits and fissures) that Dietary factor favor the accumulation of carbohydrates and microorgan- The role of the diet deserves special consideration because isms. Alterations in the tooth composition that predispose of the often observed differences in caries incidence of to destruction by cariogenic agents may occur prior to various populations who subsist on dissimilar diets. the eruption of teeth. 1. The physical nature of the diet has been suggested as one factor responsible for the difference in caries Microbial factor experience between individuals. The diet of the primi- Studies by Orland and Fitzgerald have demonstrated that tive man consisted of raw unrefined foods containing dental caries will not occur in the absence of microorgan- a great deal of roughage, which cleanses the teeth of isms. Animals maintained in a germ free environment did not develop caries even when fed a high carbohydrate diet. However, dental caries did develop in these animals when they were inoculated with microorganisms from Host caries-active animals and then fed cariogenic diets. Diet saliva Streptococcus mutans has been implicated as one of tooth the major and most virulent of the caries producing organisms. Streptococcus mutans is both acidogenic (acid producing) and aciduric (survives in acidic environ- Microflora ment). The other microorganisms attributed in etiology of dental caries are Lactobacillus acidophilus and Streptococcus sobrinus. These microorganisms convert the fermentable carbohydrates into acids which in turn dissolves the Figure 17.1 Keyes triad of dental caries. tooth structure.Chapter-17.indd 196 11/08/11 7:20 PM
  3. 3. Dental Caries 197 17 Theories Oral Proteolytic Destruction The etiology of dental caries is considered to be a complex bacteria enzymes of problem complicated by many indirect factors which organic matrix of obscure the direct cause or causes. A number of theo- enamel ries of caries etiology exist. Some theories related to the etiology of caries, which have evolved through years of investigation and research will be discussed here. Loosening Acidogenic theory (chemico-parasitic theory) and (Fig. 17.2) loss of WD Miller, probably the best known of the early inves- apatite crystals tigators of dental caries, published extensively on the results of studies on dental caries since 1882. Miller Figure 17.3 Proteolysis theory. based his ideas on a series of experiments carried out in the laboratories of the famous German microbiolo- gist Robert Koch. He made the significant observation eventual loss, and collapse of the tissue (Fig. 17.3). This that many microorganisms could produce acid from the can be compared to the mortar softening and weakening fermentation of sugar. He showed that a number of oral in an old brick wall, the mortar being the organic matrix microorganisms had this property and that lactic acid was and the bricks representing the apatite crystals. Hence one of the major acids formed. He further showed that the initial attack on enamel might be proteolytic rather extracted human teeth could be demineralized by incu- than by acid. Frisbie in 1944 and Pincus in 1949 extended bating them in a mixture of bread or sugar with human the concept by proposing that sulfates of Gram-negative saliva. These findings were published in the book ‘The bacilli hydrolyzed the sulfated mucosubstances of the Microorganisms of Human Mouth’. matrix, liberating sulfuric acid, which then dissolved the In essence, the theory proposes that acids are produced mineral. Limitations of this theory are: at or near the tooth surface by bacterial fermentation of 1. Areas of enamel with a relatively high organic dietary carbohydrates (Fig. 17.2). The acids so formed content, such as tufts and lamellae do not show a are responsible for the dissolution of the apatite crystals greater susceptibility to caries. which forms the bulk of the enamel. The acids are held 2. It was not possible to simulate caries with proteolytic in close proximity to the tooth surface by dental plaque agents. which also serves to protect the acids from the washing 3. While there is no doubt that a wide variety of prote- and buffering effects of saliva. olytic enzymes are produced by dental plaque, they Bacteriologic studies have helped clarify the role of are more likely related to initiation of periodontal different microorganisms in the etiology of dental caries. disease. However, once enamel is collapsed and Two major microorganisms which are intimately associ- a cavity is formed, microorganisms can enter the ated with dental caries are Streptococcus mutans and Lactoba- tissue. Proteolysis will then play a significant role cillus acidophilus. It has also been reported that Streptococcus in tissue destruction especially in the dentin and mutans is related to the initiation of dental caries and cementum. Lactobacillus acidophilus is responsible for the progression of caries. Actinomyces species are also reported to be Proteolysis–chelation theory related to root caries formation. This theory was proposed by Schatz and Martin in 1955. The word chelation is derived from chelas—claw. Chela- Proteolysis theory tion is a process involving the complexing of a metallic This theory was proposed by Gottlieb in 1944. This ion to a complex substance through a coordinate covalent theory states that proteolytic enzymes liberated by oral bond which results in a highly stable, poorly dissociated bacteria could destroy the organic matrix of enamel, or weakly ionized compound. Chelates can be formed resulting in a loosening of the apatite crystals with their at neutral or alkaline pH values, the theory suggests the possibility that demineralization of enamel could Fermentation arise without acid formation. The proteolysis-chelation Sugar Acid theory of dental caries states that the bacterial attack on Bacteria the enamel, initiated by keratinolytic microorganisms, Figure 17.2 Acidogenic theory. results in a breakdown of the protein and other organicChapter-17.indd 197 11/08/11 7:20 PM
  4. 4. V 198 Pediatric Dentistry Keratinolytic Attack keratin Mutation of Abnormal mitotic Substances microorganisms and other odontoblasts control protein organic (MCP) components of enamel Form chelate Changes in Demineralization with calcified resistance of components enamel to acid of enamel attack Figure 17.4 Proteolysis–chelation theory. Figure 17.5 Autoimmunity theory. components of enamel, chiefly keratin (Fig. 17.4). This data collected during routine clinical examinations are results in the formation of substances which may form sufficiently accurate for mathematical analysis. soluble chelates with the mineralized components of the tooth and thereby decalcify the enamel at a neutral or even Sucrose–chelation theory alkaline pH. Enamel also contains other organic com- Eggers-Lura suggested that sucrose itself and not the acid ponents besides keratin, such as mucopolysaccharides, derived from it could cause the dissolution of enamel by lipid and citrate which may be susceptible to bacterial forming unionized calcium saccharates. The theory is that attack and act as chelators. The proteolysis–chelation calcium saccharates and calcium complexing intermedi- theory also states that both the organic and inorganic aries require inorganic phosphate which is subsequently portions of enamel are attacked simultaneously. Later removed from the enamel by phosphorylating enzymes research suggested that saliva and plaque do not contain (Fig. 17.6). Later, investigations failed to confirm this substances in sufficient concentrations to chelate calcium concept of caries formation. in detectable amounts from enamel. Stephan Curve Autoimmunity theory Acidogenic bacteria in dental plaque can rapidly metabo- Burch and Jackson proposed this theory in 1966. This lize certain carbohydrates to acids. In the mouth, the theory is related to Burch’s theory of the cause of growth, resultant change in plaque pH over time is called a disease and aging in which the incidence of many diseases Stephan curve. During rest, the pH is fairly constant follow a mathematical pattern of random events. The although inter-subject differences between individuals random event which the theory requires is a mutation and between sites in one individual are found. Following in a cell concerned with the regulation of growth by exposure to fermentable refined carbohydrates, the pH synthesizing and releasing into the circulation a protein. reduces rapidly to reach a minimum in 5–20 minutes. Burch calls this protein a mitotic control protein (MCP) However, this returns to its starting value within 30–60 effective on highly specific targets such as a group of minutes. Stephan showed that within 2–4 minutes after cells in one tissue. rinsing with a solution of glucose or sucrose, plaque The authors of this theory quote studies of caries in pH was reduced from approximately 6.5 to about 5.5 twins which showed them that an individual inherits and gradually returned to the original pH value in 40 a genetic predisposition to caries. They suggested that minutes or so. Plotted graphically, this is known as the genes, partly inherited and partly as a result of mutations, determine whether a site on a tooth is at risk. In dental caries, the odontoblasts are the target cells and when the mutation occurs, an abnormal MCP is produced, leading Chelates Demineralization Sucrose with of enamel to disorders of the odontoblasts under its control. This calcium and in turn leads to changes in the resistance of the enamel phosphate to acid attack (Fig. 17.5). from enamel The limitation of this theory is that it is based on analysis of epidemiologic data. It is doubtful whether Figure 17.6 Sucrose–chelation theory.Chapter-17.indd 198 11/08/11 7:20 PM
  5. 5. Dental Caries 199 17 6.5 Buffering capacity of saliva has a tremendous influence on the carious process. The buffering capacity of saliva is primarily due to the presence of bicarbonate. The other 6.0 buffer of significance is phosphate. Individuals having pH salivary secretion with good buffering capacity could neutralize some of the acids that play an etiologic role 5.5 in tooth decay resulting in lesser caries. The presence of lysozyme, immunoglobulins and other antibacterial substances in saliva may also play a role in 5.0 5 1 0 15 20 caries formation. However, the exact manner in which these mechanisms work needs further research. Minutes after sucrose rinse Figure 17.7 Stephan curve. Socioeconomic Factors Since the socioeconomic conditions in various communi- Stephan curve after the Swedish dental scientist who first ties differ widely, knowledge of the possible relationship brought this into prominence (Fig. 17.7). of these factors to dental caries in children is advisable. Children living in the communities with higher economic Role of Saliva in Dental Caries levels had better access to dental care and had fewer lost teeth, but the total caries experience was unaffected by The fact that the teeth are in constant contact with and the level of dental care available. Though there are con- bathed by the saliva would suggest that this environmental flicting reports in this area, it appears that socioeconomic agent could profoundly influence the state of oral health conditions may affect the caries prevalence in the primary of a person. The complex nature of saliva and the great dentition more so than in the permanent dentition. The variation in composition makes it difficult to establish Surgeon General’s report from United States noted that the factors that may directly influence dental health. children and adolescents living in poverty suffer twice as The composition of stimulated and unstimulated saliva much tooth decay as their more affluent peers and that varies and is not particularly meaningful unless the their disease is more likely to go untreated. It is also men- exact conditions under which the saliva was collected tioned that although continuing reduction of dental caries are described. in permanent teeth have been achieved, caries prevalence Flow rate of saliva is an important factor in caries eti- in primary teeth has stabilized or possibly increased. ology. Individuals with greater salivary flow develop less However, the available data confirms that economically number of carious lesions than individuals with lesser poor children are at high risk for dental caries. salivary secretion. It is well known that in those instances in which normal salivary flow is greatly diminished, e.g. as the result of radiation therapy—rampant tooth decay Hereditary Factors may ensue. The importance of this possibility is easily It is clear from many dietary studies that variation in demonstrated in rodents. The total amount of saliva susceptibility to dental caries exists even under identi- secreted during sleep is negligible. As diminished salivary cal, controlled conditions. This implies that because of flow favors caries activity, the process of tooth decay genetic differences certain environmental influences are should be accelerated during nonwaking hours. During potentially more cariogenic for some people than for this period, the mechanical clearance of carbohydrates others. This is not to say that dental caries is an inherited and microorganisms would be minimal. disease; however, genetic influences may modify the overt The concentration of inorganic calcium and phos- expression of this disease in the individual. phorus shows considerable variation depending on the Most authors agree that genetic influences on dental rate of flow. The calcium and phosphorus in saliva is caries are relatively minor in comparison with the overall incorporated into the demineralized enamel surface under effect of environmental factors. This is supported by the appropriate conditions. It is reported that the calcium fact that children acquire their dietary habits, oral hygiene and phosphorus content of saliva is low in caries active habits and oral microflora from their parents. This makes persons. There are numerous other inorganic compo- dental caries more an environmental disease rather than nents of saliva such as sodium, magnesium, potassium, a hereditary disease. carbonate, fluoride and chloride. Some of the organic However, the authors are of opinion that genetics may constituents of saliva like ammonia, urea have been play a major role than what is thought of today. Their reported to decrease the caries incidence. views are based on the fact that children from some ofChapter-17.indd 199 11/08/11 7:20 PM
  6. 6. V 200 Pediatric Dentistry the rural or remote parts of India when examined seemed to have less dental decay or remain caries free. They have access to cheapest, stickiest toffees and chocolates and rarely do they perform proper oral hygiene measures. In spite of these detrimental environmental influences, they remain decay free beyond permanent dentition. Probably their teeth are less susceptible for dental caries because of inherent resistance. To summarize, susceptibility to Figure 17.8 Schematic diagram showing progress of pit and dental caries is influenced to a significant but minor fissure caries. degree by heredity. This genetic control is undoubtedly multifactorial in nature and such a polygenic background strongly implies considerable environmental influence. a pit or fissure and from a smooth surface is different, Specific types of dental caries susceptibility representing which is discussed in the next section on histopathology. the extremes of variation (caries free state or rampant Most of the pit and fissure caries develop with a narrow caries state) of this trait may ultimately prove to be penetration point and develop a large cavitation with monogenic traits, but at present the evidence is insuf- overhanging enamel. The lateral spread of the caries at ficient for a clear statement of such inheritance. More the dentinoenamel junction (explained in histopathology) research in the coming years with advanced molecular as well as penetration into the dentin along the dentinal techniques will elucidate this critical question. tubules may be extensive without fracturing away the overhanging enamel. Thus there may be a large carious Clinical Classification of lesion with only a tiny point of opening (Fig. 17.8). Dental Caries Smooth surface caries Dental caries can be classified clinically in a number of This type of caries is the one which develops on the ways depending upon the clinical features. proximal surfaces of teeth or on the gingival third of the buccal and lingual surfaces. This type of caries is entirely 1. According to location: dependent upon the development of recognizable plaque Pit and fissure caries for the initiation of caries. This ensures further reten- Smooth surface caries tion of carbohydrates and microorganisms on the tooth Root caries surface and subsequent production of acids to initiate the 2. According to rapidity with which it progresses: caries process. Proximal caries usually begins just below Acute dental caries the contact point and appears in the early stage as a faint Chronic dental caries white opacity of enamel (Fig. 17.9). 3. According to whether lesion is a new one or not: Root caries Primary caries Secondary caries Root caries is otherwise called root surface caries or caries of cementum. It is defined as a soft progressive 4. Based on extent of damage: lesion that is found anywhere on the root surface that has Incipient caries lost connective tissue attachment and is exposed to the Occult caries oral environment. The microorganisms involved in root caries are different from those involved in coronal caries. According to Location Pit and fissure caries These are the caries that occur on the pits and fissures of premolars and molars and on the lingual surface of incisors and canines. These are the most susceptible surfaces of tooth to develop caries. Deep pits and fissures favor food retention and are difficult to clean by routine brushing. Hence they provide a favorable environment for the oral microorganisms to thrive and convert the carbohydrates to acids continuously, leading to demin- Figure 17.9 Schematic diagram showing progress of smooth eralization of the enamel. The spread of caries through surface caries.Chapter-17.indd 200 11/08/11 7:20 PM
  7. 7. Dental Caries 201 17 Microorganisms appear to invade the cementum either along Sharpey’s fibers or between bundles of fibers, in a manner comparable to invasion along dentinal tubules. According to Rapidity with which it Progresses Acute dental caries This type of caries runs a rapid clinical course and results in early pulp involvement by the carious process. It occurs most often in children and young adolescents because the dentinal tubules are large and open and show no sclerosis. The process is so rapid that there is little or no time for deposition of secondary dentin. Early childhood caries caused by prolonged bottle feeding and on demand breast-feeding can be categorized into a form of acute Figure 17.10 Secondary caries around a filling. dental caries. Early childhood caries is dealt in Chapter 18. Chronic dental caries This form of caries progresses slowly and tends to involve the pulp much later than acute dental caries. It is seen most commonly in adults. The entrance to the lesion is almost invariably larger than that of acute caries. Because of this there is not only less food retention but also greater cleansing by saliva. The slow progress of the lesion often allows deposition of secondary dentin. According to Whether Lesion is a New One or Not Primary caries Figure 17.11 White spot lesions. Primary caries is the one which is occurring on the tooth for the first time. It can be any of the above mentioned type of caries. The physiochemical process of white spot lesions Secondary caries was difficult to understand until the Moreno model This type of caries occurs beneath or adjacent to an (Fig. 17.12) was described. In this model, acids formed existing restoration. This is most often due to inadequate by cariogenic bacteria dissolve the surface as well as caries removal prior to filling or because of poor margins subsurface enamel. The calcium and phosphate ions of restoration leading to leakage (Fig. 17.10). This allows from the subsurface dissolution diffuse outward toward both the bacteria and the substrate (carbohydrate) to enter the surface and reprecipitate on the surface making the and produce acids below or adjacent to the restorations enamel surface appear unaltered. Hence, the surface leading to secondary caries. enamel is in a type of chemical equilibrium with mineral being lost into the plaque due to low pH, but being Based on Extent of Damage remineralized from the ions diffusing out from the Incipient caries subsurface lesion. If the oral environment is maintained These are often called white spot lesions (Fig. 17.11). in a cariogenic state eventually the rate of transfer from Clinically, the surface of the lesion is intact and there the surface enamel into plaque becomes greater than the is subsurface demineralization. If the environment is rate of precipitation and the surface enamel collapses. favorable, these lesions can undergo remineralization. These lesions can be differentiated from developmental Occult caries defects by wetting the lesion. On wetting, these white Occult caries is used to describe a type of caries which spot lesions disappear; but the developmental defect is clinically not detected but seen on a radiograph. They persists. They can be diagnosed with a good bitewing are associated with pre-eruptive defects of enamel (which radiograph. occurs even before the tooth comes into the oral cavity) andChapter-17.indd 201 11/08/11 7:20 PM
  8. 8. V 202 Pediatric Dentistry ing of rods. Another change in early enamel caries is the Calcium Saliva Saliva accentuation of the incremental lines of Retzius. As this phosphates process advances and involves deeper layers of enamel, it forms a triangular or a cone-shaped lesion with the base toward the surface of the tooth. Pit and fissure caries have a different pattern of pro- gression. Often the enamel in the bottom of the pit is B−H+ Calcium phosphates Plaque very thin, so that early dentin involvement occurs. On the other hand, some pits and fissures are shallow and have a relatively thick layer of enamel covering their base. When caries occurs here, it follows the direction of enamel rods and characteristically forms a triangular cone-shaped lesion with its apex at the outer surface and Hydroxyapatite Surface its base towards the dentinoenamel junction. It should enamel be noted that the general shape of the lesion here is just opposite of that occurring on smooth surface caries. Fluorapatite This results in greater number of dentinal tubules being involved when the caries reaches the dentinoenamel Dicalcium phosphate dihydrate junction, causing greater cavitation with pit and fissure caries than smooth surface caries (Fig. 17.13). Inner enamel Dentinal Caries (Fig. 17.14) Demineralized Mutation of Once caries reaches the dentin, it progresses through Base enamel odontoblasts the open dentinal tubules. The speed at which various microorganisms travel depends upon a number of factors. Figure 17.12 Moreno model. Once microorganisms penetrate farther and farther into the dentinal tubules, they are separated more and more from the carbohydrate substrate upon which the bacte- seen only on radiographs. It is believed that increased fluo- ria responsible for the initiation of the disease depend. ride exposure encourages remineralization of the surface The high protein content of the dentin would favor the layer; but the cavitation continues in the dentin and the growth of those microorganisms which have the ability lesion is masked by an intact surface layer. These hidden to utilize this protein for metabolism. Thus proteolytic lesions are called fluoride bombs or fluoride syndrome. organisms would appear to predominate in deeper caries Histopathology of Dental Caries Amelodentinal Enamel junction surface Histopathological investigations have elucidated the prog- ress of caries in different tissues. For ease of understand- ing, the histopathology is discussed will be considered Translucent zone under the following headings: 1. Enamel caries 2. Dentinal caries Dark zone Enamel Caries Body of lesion The spread of caries in enamel varies for smooth surface caries and pit and fissure caries. In smooth surface caries, the earliest manifestation is the appearance beneath dental Surface zone plaque an area of decalcification which resembles a chalky white area. This is called incipient caries. At this stage, histologically, there is usually a loss of interprismatic or interrod substance of enamel with increased prominence Dentin Enamel of rods. In some instances, it consists of only roughen- Figure 17.13 Histopathology of enamel caries.Chapter-17.indd 202 11/08/11 7:20 PM
  9. 9. Dental Caries 203 17 Amelodentinal Enamel proximity to the ducts of the submandibular salivary junction surface gland, which means that they benefit from the diluting and buffering properties of saliva. Caries in Mixed Dentition Zone of fatty degeneration The newly erupted first permanent molars have areas Zone of bacterial that are susceptible to plaque retention and subsequent Zone of invasion development of caries. These are the occlusal surfaces decalcification of dentin in permanent molars, the lingual developmental pit and Zone of decomposed groove in maxillary permanent molars and the buccal Zone of dentin developmental groove in mandibular permanent molars. dentinal sclerosis Probably because of the depth, mandibular permanent molars decay more frequently than maxillary permanent molars. It is shown that the best predictor of caries in the permanent molars is the level of caries in the primary Dentin Enamel dentition. In addition to these areas, closing of proximal Figure 17.14 Histopathology of dentinal caries. contacts may result in the development of proximal lesions. The effect of fluoride has brought about a marked of the dentin, while acidogenic forms are prominent in decline in the number of interproximal lesions in the early caries. This substantiates the hypothesis that ini- mixed and young permanent dentition. This has occurred tiation and progression of dental caries are two distinct in both fluoridated and non-fluoridated communities and processes. As the carious lesion progresses towards the confirms the belief that occlusal pit and fissure caries is pulp, it tends to assume the shape of a triangle with the least influenced by fluoride. apex toward the pulp and the base toward the enamel. Caries in Early Permanent Dentition Various studies suggest that there is an unnecessarily high Epidemiology of Dental Caries incidence of caries in the young permanent dentition. The prevalence and incidence of a disease refers to the The order of susceptibility of teeth to caries in early number of individuals showing evidence of that disease permanent dentition is, first permanent molars (most either at one point in time (prevalence) or the change in susceptible), second permanent molars, premolars, maxil- the extent over a period of time (incidence). Dental caries lary anterior teeth, canine and mandibular incisors (least is measured in terms of decayed, missing and filled teeth susceptible). There is often a bilateral symmetry of caries or surfaces (DMFT or DMFS) for permanent teeth using attack in children which is discussed below. The occlusal capital letters. Dental caries in primary teeth is measured surfaces of recently erupted second molar and premolar as decayed, extracted (or indicated for extraction) and filled are susceptible to caries by virtue of their morphology. teeth or surfaces using lower case letters (deft or defs). There are more occlusal than interproximal lesions in the 12–13 years old due to the recent eruption and of Caries in Primary Dentition lack of establishment of proximal contacts on second Caries in children aged less than 3 years tend to involve molars and premolars. However, after the age 13 years, the occlusal surfaces of primary molars. In these children, there is an increased percentage of interproximal caries posterior contacts may not close until the age of 3 years compared to occlusal caries. which may explain this observation. However, once posterior contacts close, the prevalence of interproximal Bilateral Caries Experience caries increases. Secondly, primary molars have more The tendency for dental caries to occur bilaterally is a occlusal lesions than first primary molars; likewise the generally appreciated phenomenon. Based on studies mandibular molars have more than the maxillary because which investigated bilateral caries experience, the fol- of the depth and anatomy of the occlusal fissures. The lowing conclusions can be drawn: labial and lingual surfaces of primary incisors never decay, 1. It is said that 3 out of 4 cases in which dental caries except in cases of early childhood caries or nursing caries. occurs in a posterior tooth, the comparable tooth in Mandibular primary incisors seldom decay, probably the opposite arch will also be involved. because of the spacing that occurs in the area, protec- 2. In 4 out of 5 cases, caries will be on the same tion of the tongue (while bottle feeding) and their close surface.Chapter-17.indd 203 11/08/11 7:20 PM
  10. 10. V 204 Pediatric Dentistry may predispose an individual to rampant caries are as Rampant Caries follows: Rampant caries is defined as a “suddenly appearing, 1. Repressed emotions and fears widespread, rapidly burrowing type of caries, resulting 2. A traumatic school experience in early involvement of the pulp and affecting those 3. Dissatisfaction with achievement teeth usually regarded as immune to ordinary decay”. 4. Rebellion against a home situation (Massler, 1945). 5. Continuous general tension and anxiety. Winter et al in 1966 described it as a lesion of acute Such emotional disturbances may create an unusual onset involving many or all of the erupted teeth, rapidly craving for sweets or the habit of snacking which in turn destroying the coronal tissue, often on surfaces normally might influence the incidence of dental caries. A notice- immune to decay and leading to early involvement of able decrease in salivary flow is observed in individuals the dental pulp. with emotional disturbance which can increase their risk The mechanism of decay process in rampant caries is for caries. Radiation therapy for any tumor of head and similar to other types of caries explained above. However, neck also can lead to decreased salivary flow leading to it can occur suddenly in teeth that were previously rampant caries. sound for many years. Its sudden onset suggests that an overwhelming imbalance of the oral environment has occurred and some factors in the caries process seem Sugar Substitutes to accelerate it so that it becomes uncontrollable. This Artificial sweeteners are called sugar-substitutes. There type of rampant caries is seen in young teenagers though are two kinds of sweeteners—nutritive and non-nutritive. it is observed in children and adults (Fig. 17.15A, B). Nutritive sweeteners provide some calories; non-nutritive It is often associated with emotional disturbances. sweeteners typically provide zero calories. The ideal According to McDonald, some of the factors which sweetener should provide sweetness, with no unpleasant after-taste, have little or no calories, not be carcinogenic or mutagenic, be economical to produce and should not be degraded by heat when cooked. Fundamentals of Artificial Sweeteners I. Nutritive sweeteners As stated above, the terms ‘nutritive’ and ‘non-nutritive’ denote a difference in the amount of energy provided by sweeteners. Nutritive sweeteners include sugar sweet- eners (e.g. refined sugars, high fructose corn syrup, crystalline fructose, glucose, dextrose, corn sweeteners, honey, lactose, maltose, various syrups, invert sugars, (A) concentrated fruit juice) and reduced-energy polyols or sugar alcohols (e.g. sorbitol, mannitol, xylitol, isomalt, and hydrogenated starch hydrolysates). a. Sugar sweeteners: Most sugar sweeteners used as replacements for sugar contain about the same calories as sugar. So although there may be some differences in the way we metabolize sugar and nutritive sweeteners like sucrose and fructose, there is no obvious weight loss benefit. b. Polyols/sugar alcohols: Polyols offer less energy; and offer potential health benefits (e.g. reduced glycemic response and reduced dental caries risk). The polyols sorbitol, mannitol, and xylitol are found in plant products (B) such as fruits and berries. All polyols are absorbed slowly and incompletely from the intestine, therefore, an exces- Figure 17.15 Rampant caries. sive load may cause diarrhea. If polyols were completelyChapter-17.indd 204 11/08/11 7:20 PM
  11. 11. Dental Caries 205 17 absorbed, then like sugar they would provide the usual 2. Disaccharide polyols or novel sugars 4 calories per gram. The FDA allows these nutritive Isomalt: It gives 2 cal/g energy, 45–65% as sweet as sweeteners to be labeled as having fewer calories per sucrose and used as a bulking agent. gram than other nutritive sweeteners. Lactitol: It gives 2 cal/g energy, 30–40% as sweet as Approved nutritive sweeteners sucrose and used as a bulking agent. 1. Monosaccharide polyols or novel sugars Maltitol: It gives 2.1 cal/g energy, 90% as sweet as sucrose and used as a bulking agent. Sorbitol: Sorbitol is a sugar alcohol that occurs natu- Trehalose: It gives 4 cal/g energy. It is 45% as sweet rally in many fruits and berries. It is produced com- as sucrose. mercially from glucose, but is expensive to manufacture. Sorbitol is often used as a ‘bulk’ sweetener in a variety 3. Polysaccharide polyols of food substances such as chewing gum, chocolates HSH (hydrogenated starch hydrolysates): It gives and confectioneries. It is half as sweet as sucrose and 3 cal/ g energy and 25–50% as sweet as sucrose (depend- is considered non-cariogenic, although in solution it ing on the monosaccharide composition). can be fermented slowly by mutans streptococci. Sor- bitol has been shown to be cariogenic with prolonged II. Non-nutritive sweeteners use by patients with reduced salivary gland function. Non-nutritive artificial sweeteners are intensely sweet— Sorbitol is not easily metabolized or absorbed from the between 200 and 700 times sweeter than sugar. They add gastrointestinal tract and can cause diarrhea, if ingested sweetness to foods for people (like diabetics) who need in large quantities. to limit their intake of sugar. They contain little or no Sorbitol gives 2.6 cal/g energy. Generally recognized as calories or glycemic response (impact on blood sugar Safe (GRAS)—label must warn about a laxative effect. It levels). The United States lead the world in consumption is 50–70% as sweet as sucrose; some individuals experi- of high-intensity sweeteners, consuming approximately ence a laxative effect from a load of > 50 gm. 50% of the world demand. Non-nutritive sweeteners may Mannitol: It gives 1.6 cal/g energy. Approved food assist in weight management, control of blood glucose additive; the label must warn about a laxative effect. It is and prevention of dental caries. But most non-nutritive 50–70% as sweet as sucrose; some individuals experience sweeteners come with health warnings because of the a laxative effect from a load of > 20 gm. lack of clinical tests on their long-term use. FDA has approved four non-nutritive sweeteners and Xylitol: Xylitol was discovered in wood chips in 1890 regulates them as food additives— saccharin, aspar- and in wheat and oat straw in 1891. It is a non-ferment- tame, acesulfame potassium (or acesulfame-K) and able, pleasant tasting, noncariogenic polyol derived from sucralose. Nutritive sweeteners provide a sweet taste pentose sugar xylose and is relatively expensive to manu- and a source of energy; non-nutritive sweeteners are facture. Xylitol is as sweet as sucrose and was approved sweet without energy. The ideal agent should provide as safe for use in humans in 1986. It is used primarily sweetness, but with no unpleasant after-taste, have little in chewing gum and possesses approximately the same or no calories, not be carcinogenic or mutagenic, be sweetness potency as sucrose. Studies have suggested economical to produce, and should not be degraded by that the regular use of xylitol containing chewing gum heat when cooked. reduces the amount of dental plaque as well as increase saliva flow. A significant reduction in caries incidence Non-nutritive sweetening agents or noncaloric has been reported in caries active age groups when sweeteners xylitol containing gum was chewed regularly. Recently, The US Food and Drug Administration (FDA) approved xylitol has been credited in reducing the transmission of non-caloric sweeteners to date are aspartame, acesulfame cariogenic bacteria from mother to infant and has been potassium, saccharin, sucralose and neotame. Non-nutri- shown to have bactericidal qualities. The FDA has not tive sweeteners offer no energy (or insignificant energy yet approved additional uses of xylitol as a sweetener. in the case of aspartame) and, because they sweeten However, numerous European studies have established with little volume, they can also be referred to as high- the safety for human consumption. An additional reported intensity sweeteners. benefit of chewing gum containing xylitol is reduced ear infection in young children at day-care centers. 1. Aspartame (Nutrasweet, Equal, Sugar Twin): Aspar- It gives 2.4 cal/g energy. It is an approved food additive tame (Equal) is a dipeptide methyl ester, discovered in used in foods for special dietary use. 1965 and is approximately 200 times sweeter than sucrose.Chapter-17.indd 205 11/08/11 7:20 PM
  12. 12. V 206 Pediatric Dentistry Aspartame was approved in 1981 for limited use as a 4. Sucralose (splenda): Sucralose is a non-nutritive, sweetener in the US, and extended to a larger market noncaloric trichlorinated derivative of sucrose. It is not in 1983. Its nutritive value is 4 cal/g energy. metabolized by the body and has been shown to be non- Aspartame is the most widely used non-cariogenic artifi- cariogenic. Sucralose is widely used throughout the world cial sweetener. Its primary use is in diet, soft drinks, yogurt, in many food products such as tea and coffee sweetener, puddings, gelatin and snack foods. Aspartame has been carbonated and non-carbonated beverages, baked goods, shown to have a protective effect against some mycotoxins chewing gum and frozen desserts. No health concerns and is claimed to be safe for use by type 2 diabetics. have been reported with sucralose. Mycotoxins are toxic metabolic products of some fungi Sucralose is approved as a general-purpose sweetener. and can result in mycotoxicosis in humans. Mycotoxins It is 600 times sweeter than sucrose; non-cariogenic and can be found in contaminated cereals and foods obtained produces no glycemic response; sweetening power is not from animals that ingested a mycotoxin contained diet. reduced with heating. Nutritive value is zero calories. Oral ingestion of 6 mg/kg of aspartame has been 5. Neotame: Neotame is approved as general-purpose reported to reduce the number of sickle cells in the blood sweetener. It is 8,000 times sweeter than sucrose; non- of patients with homogenous sickle cell anemia. cariogenic and produces no glycemic response; sweeten- There have been concerns raised relative to toxic effects ing power is not reduced with heating. This sweetener on growth, glucose homeostasis and liver functions with does provide energy; however, because of the intense long-term usage. People with phenylketonuria should sweetness, the amount of energy derived from it is neg- avoid aspartame as they cannot metabolize phenylalanine, ligible. Nutritive value is zero calories. a component of aspartame. 2. Acesulfame potassium or acesulfame K (Sunett, Sweet and Safe, Sweet One): Acesulfame potassium, a Caries Vaccine non-nutritive product, was approved by the FDA in 1988 A vaccine is defined as ‘a suspension of attenuated or for use as a sweetener in dry food products. In 1994, killed microorganisms administered for the prevention, yogurt, refrigerated desserts, syrups and baked goods amelioration or treatment of infectious diseases’. were added to the approved list. The use of acesulfame A vaccine to prevent the disease of dental caries has potassium is approved for use in foods, beverages, cos- been an anticipated scientific breakthrough since 1940s metics and pharmaceuticals in more than 30 countries. even though the etiological agents were thought to Although considered safe for consumption by humans be lactobacilli. With the recognition of mutans strep- there have been some health issues raised relative to tococci (Streptococcus mutans and Streptococcus sobrinus dose-dependent cytogenetic toxicity. and their relatives) as the key organisms in the dental Acesulfame K is approved as a general-purpose sweet- caries process, the method of immunization specially ener 200 times sweeter than sucrose; non-cariogenic and targeted at neutralizing S. mutans has been a thrust in produces no glycemic response; synergizes the sweetening caries vaccine research. The efforts have thus been power of nutritive and non-nutritive sweeteners; sweet- directed against colonization of these organisms in ening power is not reduced with heating. Its nutritive the oral cavity. Considerable progress has been made value is zero calories. in elucidating the factors involved in their pathogenic 3. Saccharin: Saccharin is 200 to 700 times sweeter than activity, culminating recently in the sequencing of the sucrose and is the oldest of the artificial sweeteners used entire S. mutans genome. in the United States. It is non-cariogenic and non-caloric Likewise, enormous strides have been made in com- and is available in liquid and tablet forms as a tabletop prehending the workings of the mucosal immune system sweetener but has a slightly bitter after-taste. In 1970, by which secretory IgA (S-IgA) antibodies are generated saccharin was identified as a potential bladder carcinogen. in saliva and other secretions. The mechanisms of action A warning label is required on all food products in the of salivary IgA antibodies against mutans streptococci US that contain saccharin. include interference with their sucrose-independent and It is approved as a sweetener for beverages and as sucrose-dependent attachment to and accumulation on, a tabletop sweetener in foods with specific maximum tooth surfaces, as well as possible inhibition of their amounts allowed and 200–700 times sweeter than sucrose; metabolic activities. non-cariogenic and produces no glycemic response; syn- The goal of immunizing infants and young children ergizes the sweetening power of nutritive and non- against colonization by mutans streptococci and hence nutritive sweeteners; sweetening power is not reduced diminishing the development of caries might be accom- with heating and has a nutritive value of zero calories. plished by applying new strategies of mucosal vaccinationChapter-17.indd 206 11/08/11 7:20 PM
  13. 13. Dental Caries 207 17 that would induce salivary IgA antibodies without the where mutans streptococci is not yet a permanent member complications of parenteral injection. of the dental biofilm. The most recent research is directed towards a greater Passive immunization: Passive antibody administra- understanding of the immune system and specifically tion has also been examined for effects on indigenous of the immune responses to mutans streptococci. The mutans streptococci. Strategies include, development route of administration of the vaccine is usually mucosal of antibodies to mutans streptococcal antigens in cow’s absorption by intraoral or intranasal tissues. milk and hen’s eggs, and the genetic engineering of Active immunization: Enteric coated capsules filled human like S-IgA antibodies in plants. Mouth rinses with crude S.mutans GS-5 GTF antigen preparation containing bovine milk or hen egg yolk IgY antibody in lysosomes were used to immunize adults. Parotid to S.mutans cells led to modest short-term decreases salivary IgA antibody responses were induced with this in the numbers of indigenous mutans streptococci in application. This delayed the colonization of S.mutans saliva or dental plaque. in the oral cavity. Elaborate discussion on caries vaccine is beyond the Mucosal immunization with dental caries vaccines scope of this textbook. Hence readers are suggested to could be protective, especially in pediatric populations refer to appropriate resources for the same. SUGGESTED READING 1. Braham RL, Morris ME. Textbook of Pediatric Dentistry (2nd edn). New Delhi, CBS Publishers, 1980. 2. Edgar WM, Mullane DMO. Saliva and Oral Health (2nd edn). London, British Dental Association, 1996. 3. Finn SB. Clinical Pedodontics (4th edn). Philadelphia, Saunders, 1991. 4. Fitzgerald RJ et al. Dental caries in gnotobiotic rats infected with a variety of Lactobacillus acidophilus. Arch Oral Biol 11: 473–76, 1966. 5. Kennedy DB et al. Pediatric Operative Dentistry (4th edn). Great Britain, Wright, 1996. 6. McDonald RE, Avery DR, Dean JA. Dentistry for the Child and Adolescent (8th edn). St.Louis, Mosby, 2004. 7. Moreno EC, Zahradnik RT. Chemistry of enamel subsurface demineralization in vitro. J Dent Res 53: 226, 1974. 8. Orland FJ. Bacteriology of dental caries: formal discussion. J Dent Res 43: 1045–47, 1964. 9. Stephan RM. Changes in the hydrogen ion concentration on tooth surfaces and in carious lesions. J Am Dent Assoc 27: 718, 1940. 10. Stephen HYW: Pediatric Dentistry: Total Patient Care. Philadelphia, Lea and Febiger, 1988. 11. Stewart RE, Barber TK, Troutman KC et al. Pediatric Dentistry: Scientific Foundations and Clinical Practice. St. Louis, Mosby, 1982. 12. Tandon S. Textbook of Pedodontics (2nd edn). Hyderabad, Paras Publishing, 2003. SELF-ASSESSMENT QUESTIONS Essay Type 1. Define dental caries. Classify types of caries and describe the role of plaque in caries formation. 2. Enumerate the theories on dental caries. Write about the acidogenic theory. 3. Sugar substitutes. 4. Caries vaccine. Short Notes 1. Rampant caries 8. Pit and fissure caries 2. Acidogenic theory 9. Smooth surface caries 3. Proteolysis-chelation theory 10. Secondary caries 4. White spot lesion and Moreno’s model 11. Root caries 5. Aspartame 12. Stephan’s curve 6. Xylitol 13. Autoimmunity theory of caries formation 7. Occult caries or fluoride bombChapter-17.indd 207 11/08/11 7:20 PM
  14. 14. Chapter-17.indd 208 11/08/11 7:20 PM