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Dentinal Caries Root Caries Microbiology of Dental Caries Mechanism of Adherence of Microorganisms to Tooth Surface Formation of Plaque Role of Saliva in Dental Caries
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Introduction Early Theories of Caries Aetiology Current Concepts of Caries Aetiology Classification of Dental Caries Clinical Manifestations of Dental Caries Process Caries of Enamel
Dental caries the disease of civilization, is affecting the mankind since the dawn of the time. Caries has also been noted in the fossil remains of Pithecanthropus erectus and Homo rhodesiensis, early ancestors of man. Caries seems to have increased considerably in Homo sapiens during Neolithic period when it was perhaps as high as that seen in many contemporary primitive people. In fact, in prehistoric skulls about 5% of the teeth exhibited caries. It is a chronic disease, a process that progresses very slowly in most individuals. The multifactorial aetiology of dental caries nowadays is relatively understood and the disease is therefore not only treatable but also most aspects of it, to an extent preventable infection. The carious lesion should be regarded not as a disease entity but as tissue damage caused by the dental caries. “Caries without cavitation”—caries should be considered as a process rather than simply as an event at a particular stage, i.e. a cavity requiring restoration. Evidence of frank cavitation was required for the diagnosis. There were two reasons for this; one being that from the public health standpoint there was little interest in lesions, which have no effect on the person in terms of requirements for treatment or restoration. When a caries-free individual is referred, it was found that such an individual had many pre-cavitational lesions approximally. However,
epidemiologically it was of little concern if that person went through life without frank cavitation. Tooth decay is an infectious disease generally affected by diet and the pattern of its consumption by the host. Its dependency on ingestion of fermentable dietary carbohydrate is beyond question. However caries does not occur in germ free animals, no matter what their diets are, thus establishing it as a fundamentally microbiological disease. Sound enamel demineralizes, if plaque bacteria are given with carbohydrate substrate and they produce acids, however, the presence of saliva in the mouth can act as a buffering agent which in turn to an extent can inhibit the demineralization process. The progression of carious lesion is not inevitable and disease can be controlled.
Salient Features of Carious Process
Salient features of carious process are listed below: 1. 2. 3. 4. 5. Carious process is spread over time Carious process does not have to progress The initial lesion can be arrested and reversed All ages are susceptible to caries Caries is the major cause of tooth loss in all age groups.
Dental caries is an infectious microbial disease that begins as demineralization of inorganic portion of tooth,
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A clinically well-known type of caries is characterized by extensive penetration into the dentin. leading to cavity formation. observed filamentous microorganisms. This theory was given by Melancholic Yellow bile Choleric Phlegm Blood Phlegmatic Black bile Sanguin FIGURE 30-1 Humour theory. • The Caries Process occurs as an interaction between the biofilm and the tooth surfaces: the caries lesion is the manifestation of the stage of the process at one point in time. (iii) black bile. These four fluids corresponds to the four humours: (i) phlegmatic. All diseases including caries were explained by an imbalance of these humours. Chemical Theory Chemical theory was given by Parmly (1819). 30. Humour Theory Ancient Greeks considered that relative proportions of four elementary fluids of the body determined a person’s physical and mental constitution: (i) blood. Guy de Cahuliac. Chemoparasitic Theory Chemoparasitic theory is the most accepted theory for the aetiology of dental caries. and (iv) yellow bile. the greatest Surgeon of the middle Ages believed that worming caused dental decay. According to this theory. Later. He stated that caries begin on the enamel surface in locations. toothache was caused by a worm that drank the blood of the teeth and fed on the roots of the jaws. but with a barely detectable catch in the fissure. and even into the pulp. Chapter-30. where food putrefied and acquired sufficient dissolving power to produce the disease chemically. analogous to bone gangrene.indd 322 6/1/2011 6:17:29 PM . onion and hyoscyamus. According to this theory. (ii) choleric (iii) sanguine. Vital Theory The vital theory regarded dental caries as originating within the tooth itself.322 PREVENTIVE DENTISTRY followed by destruction of organic portions. Ficinus. which he called denticolae in material taken from carious cavities. dental caries was caused by unidentified chemical agent.1). dental caries was caused by filamentous parasites present in the “surface membrane” (plaque?) of teeth. Parasitic or Septic Theory Parasitic or septic theory was given by Erdl (1843). (ii) phlegm. EARLY THEORIES OF CARIES AETIOLOGY Worm Theory According to an ancient Sumerian test. As a cure he advocated fumigation with seeds of leech. and (iv) melancholic (Fig.
1. by the secondary valence bonds. sugar. B). probably Staphylococcus aureus. Later a coccus. Each one of them is of equal importance in aetiology of the disease. Thus the fourth factor has been considered either as independent factor or all the three primary factors have been put under time factor (outer ring). rod sheaths. This theory suggested that the initial action was due to proteolylic enzymes attacking the lamellae. The interaction of saliva. iron. tufts and walls of the dentinal tubules. and dissolution of minerals of the tooth by the process of chelation. Hence current concept of the aetiology of dental caries includes these important four factors as described in Keyes circle (Figs 30. and diet (sucrose). Several types of mouth bacteria (at least 30 species are isolated) could produce enough acid to cause dental caries. 3. CURRENT CONCEPTS OF CARIES AETIOLOGY Caries is multifactorial disease mainly consisting of three parameters most commonly contributing for the initiation of dental caries namely.4). 5. zinc and other metals.indd 323 6/1/2011 6:17:30 PM . but rather the process was mediated by oral microorganisms capable of producing acid and digesting protein. Acid was present within the deeper carious lesion.2–30. Proteolysis–Chelation Theory Proteolysis–chelation theory was proposed by Schatz et al (1955). bacteria and microbial products in the production of biofilms on the tooth surface is an important factor to initiate dental caries. incubation mixtures. In a series of experiments it was demonstrated that: 1. Lactic acid was an identifiable product in carbohydratesaliva. Proteolytic Theory Proteolytic theory was given by Gottlieb in 1944. Miller’s chemoparasitic theory is unable to explain the predilection of specific sites on a tooth to dental caries.3A. cariogenic oral microbial flora and fermentable carbohydrate are important in the development of dental caries and they have been depicted through Keyes circles (Figs 30. Lesion detection: Implies an objective method of determining whether or not disease is present. host factor (susceptible tooth surface). Miller concluded that no single species of microorganism caused caries. 4. microorganism (Streptococcus mutans). The word “chelate” is derived from the Greek “chele” Chapter-30. long and short bacilli and micrococci) invade carious dentin. • Remineralization can arrest or reverse progression of disease and can lead to changes in mineral quality. Different microorganisms (filamentous. 2. the understanding of the caries process has progressed far beyond the point of restricting the evidence of dental caries to the caries in enamel only or caries in enamel and dentin or levels of cavitation. The phenomenon of arrested caries is not explained by the chemoparasitic theory.DENTAL CARIES 323 Miller in 1890.4). copper. • Caries progression occurs when the demineralization and remineralization equilibrium is out of balance. and refers to compounds that are able to bind metallic ions such as calcium. Frisbie (1944) also described caries as a proteolytic process involving depolymerization and liquefaction of the organic matrix of enamel. however the interplay between these factors has to take place in an appropriate time. was involved because of the yellow pigmentation that he considered pathognomonic of dental caries. This factor has been added to emphasize the importance of time factor in the origin of the disease along with other three primary factors. leading to net mineral loss. Different kinds of foods (breads. The susceptible host. There are various subfactors or cofactors contributing directly or indirectly in initiation of dental caries. It implies a simultaneous microbial degradation of the organic components (proteolysis). such as dental cuticle and then destroyed the prism sheaths. Keyes Circles A carious lesion should be regarded not as a disease entity. meaning claw. Critique of Chemoparasitic Theory 1. Pincus (1949) contended that proteolytic organisms first attacked the protein elements. but not meat) when mixed with saliva and incubated at 37°C could decalcify the entire crown of the tooth. 30. as shown by reaction on litmus paper. However there are many secondary factors that either influence the progression or regression of dental caries (Fig. Miller’s theory does not explain why some populations are caries-free. 2. 3. but as tissue damage or a wound caused by the disease dental caries.
indd 324 6/1/2011 6:17:30 PM . are favourable. even at the stage of frank cavitation. a caries progress until the tooth is destroyed. What may be perceived clinically as an “incipient” or “early“ lesion may in reality turn out to be an age established lesion that has been present in the oral cavity for months or years and also from a biochemical point of view the caries process is much more complex. 3. It is now appreciated that caries is initially reversible. Lesion progression may be arrested at any stage of lesion development.g. professional. Lesion progression is often depicted on a linear scale ranging Chapter-30. biofilm control and topical fluoride exposure. from initial loss of mineral at the ultra structural level to total destruction of the tooth. e. provided the local environmental conditions. Hence. The localized destruction of the hard tissues. disease process with known multifactorial aetiology. However. chronic. The disease is seldom selflimiting and in the absence of treatment. Caries diagnosis: Implies a human. the clinical stages of caries represent nothing but historical signs of the past caries experience. summation of all available data. often referred as the lesion. is the sign or symptom of the disease (Fezejerskov et al 2008).324 PREVENTIVE DENTISTRY Absence of cariogenic plaque Microorganisms + Carbohydrates Acid production No caries Plaque + Sucrose + Cariogenic bacteria Cariogenic plaque + Cariogenic diet Acid production Subsurface demineralization Continuous sucrose consumption Initial lesion Repeated attack of cariogenic challenge Progression of carious lesion More of mineral loss Destruction of organic matrix Cavitation FIGURE 30-2 Flowchart depicting the caries process. Lesion assessment: Aims to characterize or monitor a lesion. Dental caries progresses slowly in most of the individuals as chronic disease. once it has been detected. Metabolic processes 2. caries lesion development is a highly dynamic process with alternating periods of progression and arrest/regression.
Caries lesions may be classified in various ways.and remineralization process is loss of mineral. and this is reflected by continuous.indd 325 6/1/2011 6:17:30 PM . 30. Pit and Fissure Caries (Occlusal Caries) • Most common type of dental caries (Fig. The key point is. concentration) Primary factors Secondary factors Age Fluorides Morphology Nutrition Trace elements Carbonate FIGURE 30-4 aetiology. Diagrammatic representation of interplay between primary and secondary factors in caries on smooth surfaces of the enamel (enamel caries) or on the exposed root cementum (root caries). • Occurs on the occlusal surfaces of molars and bicuspids. are constantly taking place in the dental plaque as a result of microbial activity. caries lesion develop or progress. Microorganisms Strep. rapid fluctuations in plaque pH. any clinically sound or carious tooth surface that is covered by an undisturbed plaque may experience minute mineral loses and mineral gains depending on the metabolic status of the microflora. lesions can be classified according to their anatomical site and location. when the cumulative result of the de.DENTAL CARIES 325 Microorganisms Microorganisms (cariogenic plaque) No Caries No Caries Time Time Host & teeth Caries Substrate Substrate (cariogenic diet) Caries Host (susceptible tooth surface) No Caries No Caries Time Time B A FIGURE 30-3 Keye’s Circle—current concept of caries aetiology. Hence.5). Chapter-30. both when the plaque is starved and fed. or Classification Based on Morphology This classification is according to anatomical site of the lesions. mutans (substrate) Oral hygiene Oral flora Fluoride in plaque Diet & nutrition Transmissibility Caries Substrate Host Oral clearance Oral hygiene Detergency of food Frequency of eating Carbohydrate (type. The lesions may be commonly found in pits and fissures. Firstly.
Buccal and lingual surface caries • Cervical caries (smooth surface caries)—occurring on buccal or lingual surfaces near the cementoenamel junction (Fig. A caries increment of 10 or more new lesions over a period of about a year is characteristic of a rampant caries attack (Fig. B FIGURE 30-7 Proximal surfaces (interproximal). Rampant caries II. b. They are: (i) buccal and lingual surface caries. 30.8). a. Proximal surfaces (interproximal) • Interproximal caries—occurring at mesial or distal contact points. rapid and almost uncontrollable destruction of teeth. Interproximal caries usually starts just cervical to the contact area (Fig.6). Chapter-30. Early childhood caries Early childhood caries is a specific form of rampant decay of the primary teeth of infants and toddlers.326 PREVENTIVE DENTISTRY A FIGURE 30-6 Cervical caries. missing or filled tooth surfaces in any primary tooth in a preschool age child between birth and 71 months of age”. Early childhood caries (nursing caries) III. Radiation caries (xerostomia induced). Rampant caries. involving surfaces of teeth that are ordinarily relatively caries free (proximal and cervical surfaces of anterior teeth including the mandibular incisors get affected). There are two variations of smooth surface caries. 30. Smooth surface caries.indd 326 6/1/2011 6:17:30 PM . Classification based on Severity and Progression I.7). Rampant caries occurs as a sudden. and (ii) proximal surfaces (interproximal). According to American Dental Association (ADA) it is defined as “the presence of one or more decayed. B A FIGURE 30-5 Pit and fissure caries. 30.
The main cause for this type of caries is inappropriate feeding bottle or at will breastfeeding or combination of both and poor oral hygiene (Fig.9). Dentinal caries c. Such patients develop rampant dental caries (Fig. opaque region. This is a common complication of radiotherapy of oral cancer lesions and radiation-induced xerostomia (from the Greek. Sjogren’s syndrome) – – Anti-sialagogue drugs Prolonged illness Classification Based upon Part of Tooth Structure Involved a.10). stoma = mouth). Chapter-30. Xerostomia may be caused by factors other than radiation like – – Tumours of salivary glands Autoimmune diseases (e. Enamel caries • Incipient caries • Linear enamel caries (odontoclasia) b. Cemental caries Enamel Caries • Incipient lesion: Incipient lesion is also called the early carious lesion.11A. xeros = dry.DENTAL CARIES 327 ECG is a particularly virulant form of dental caries that is characterized by an overwhelming infections challenge and is associated with unusual dietary practices. It is a unique pattern of dental decay affecting maxillary primary incisors in young children due to prolonged nursing habit especially when the child is sleeping. Radiation caries (xerostomia induced). FIGURE 30-11 Incipient lesion. FIGURE 30-10 Radiation caries. FIGURE 30-8 Rampant caries. B). It manifests as a white. which is best demarcated when the area is dried (Figs 30. This is also named as baby bottle tooth decay. 30. 30.indd 327 6/1/2011 6:17:34 PM .g. Incipient lesion A A B B Incipient lesion FIGURE 30-9 Nursing caries.
in Latin America and Asian countries. This type of caries may result from: • • • • Poor cavity preparation Ditching around an amalgam restoration A defective restoration Or a combination of these factors. c. It is thought to result from the metabolic disturbances associated with trauma of birth and transient hypocalcaemia associated with transient hypoparathyroidism. Cemental caries. Recession of gingival margin is an inevitable process as a result of poor oral hygiene and loss of periodontal attachment with age. Primary caries Secondary caries (recurrent caries) Residual caries Arrested caries FIGURE 30-13 Arrested caries. The lesions predominate on the labial surfaces of the anterior maxillary teeth. which develop on the healthy enamel surface or on unrestored surfaces from those that develop adjacent to a filling.13). the shape and depth of the carious lesions can be scored on a four-point scale (D1 to D4): • D1—clinically detectable enamel lesions with intact (non-cavitated surfaces) • D2—clinically detectable cavities limited to the enamel • D3—clinically detectable lesions in dentin (with and without cavitation of dentin) • D4—lesions into pulp.328 PREVENTIVE DENTISTRY • Linear enamel caries (Odontoclasia): An atypical form of dental caries. the lesion establishes in dentin. Dentinal caries. Classification of Caries Based on Activity a. carious lesion involves dentin and over a period of time when the cariogenic challenge becomes more and more strong and along with other favourable factors. (The neonatal zone represents the demarcation between pre.5). Secondary caries. Residual caries is demineralised tissue that has been left behind before filling is placed (incomplete removal of carious dentin). Primary caries. There is clinical evidence that incipient and even more advanced carious lesions may become arrested if there is a significant shift in oral environmental conditions from those that predispose to caries to that tend to slow the caries process (Fig.15). remineralization and demineralization go hand in hand.and postnatal enamel and is a histologic feature of all primary teeth). in the region of neonatal line. called linear enamel caries. Chapter-30. At the same time. Arrested caries.2–5. however the repair process. CLINICAL MANIFESTATIONS OF DENTAL CARIES PROCESS Early Changes The earliest stage of caries is the first time demineralization of enamel which occurs after the plaque pH depression below the critical pH (5. 30. 30. d. FIGURE 30-12 Secondary caries. has been observed in the primary dentition of children.indd 328 6/1/2011 6:17:43 PM . outer layer of enamel might breakdown owing to progression of caries and leads to cavitation.14. 30. A carious lesion that develops at the interface of restoration and the cavosurface of the enamel is called secondary caries (Fig. and most of the time maintains the homeostasis (Figs 30. b. Primary caries is used to differentiate lesions.12). Subsequently the exposed root surface becomes more vulnerable to plaque accumulation and caries process might initiate involving cementum. On its way to progression. According to World Health Organization (WHO). This amount of demineralization cannot be detected clinically (they go unnoticed). Residual caries.
Frank Cavitation As the carious lesion progresses the subsurface lesion increases in dimension. subsurface to the surface and get added to the calcium and phosphate in dental plaque. The clinical appearance of white spot lesion is caused by subsurface enamel demineralization. Poor oral hygiene Frequent sugar exposure Continuous high cariogenic challenge Remineralization Demineralization Tooth FIGURE 30-15 Deranged equilibrium of demineralization and remineralization. Calcium and phosphate ions move from Chapter-30. White Spot Lesion The first visible clinical presentation of dental caries is referred to as white spot lesion. which are detectable only with the use of radiographs. even though caries are progressing at subsurface level. These occult lesions are usually seen with low caries rate which is suggestive of increased fluoride exposure. Later calcium and phosphate along with fluoride from saliva and biofilm helps in the precipitation on the superficial layer on the affected surface enamel. resulting in loss of translucency. Normally white spot lesion being smooth and having intact surface indicates that lesion is not active whereas lesions with rough surfaces because of increased porosity suggest that a lesion is active and progressing. This rapid precipitation of high levels of calcium and phosphate leads to occluding the pores that would further limit demineralization of the surface layer and limits remineralization of the underlying demineralized subsurface. White spot carious lesion does not necessarily progress to frank cavitation. Recently it has been observed that hidden caries may have origin as pre-eruptive defects. At this stage of carious process. eventually leading to collapse of the surface layer leading to cavitation. Arrested lesion may retain the appearance of white spots or acquire the appearance of brown spot.16). Therefore white spot can be referred as non-cavitated lesion. the lesion progression could be arrested or reversed by modifying any of the causative factors or application of appropriate preventive measures. demineralization commences on the subsurface. In this stage. Hidden or Occult Caries During the cariogenic challenge on account of fall of pH to a critical level. Caries progressing into dentin with intact surface is not clinically diagnosed but can be detected only in radiographs.indd 329 6/1/2011 6:17:45 PM .DENTAL CARIES 329 Demineralization Remineralization Tooth FIGURE 30-14 Equilibrium of demineralization and remineralization. tooth destruction progresses more rapidly because cavitation favours plaque accumulation and reduced salivary access.8 to 3%. which is not visible. The reversal of the white spot could be due to remineralization of the lesion subject to condition that surface layer is intact. 30. Hence there is an intact surface layer of the enamel. and most of the time they may not progress to frank cavitation in the absence of high cariogenic challenge (Fig. The prevalence of hidden caries ranges from 0.
depending on the site of origin and conditions in the mouth.1): a. f. The time for progression from incipient caries to clinical caries (cavitation) on smooth surfaces is estimated to be 18 months plus or minus 6 months. The progression of the carious lesion is variable. Radiation-induced xerostomia (dry mouth) can lead to clinical caries development as little as 3 months from the onset of the radiation. ‘U’ type. restricted intake of refined sugars and use of fluorides. Thus. Thus. ‘Y’-shaped divisions (5–10%). CARIES OF ENAMEL Macroscopic Changes of Enamel On smooth surfaces. d. Once the open carious lesion becomes self-cleansing. with improved oral hygiene measures. and extremely narrow slit (18–20%). ‘V’ type-wide at top and gradually narrowing towards the bottom (30–35%). 39. e. Chapter-30. Pit and fissure caries. almost the same width from top to bottom (12–15%).330 PREVENTIVE DENTISTRY Sound enamel Fluorides Good oral hygiene High cariogenic challenge Carious enamel Fermentable carbohydrates Cariogenic plaque Cavitation FIGURE 30-16 Schematic presentation of factors affecting sound and carious enamel.indd 330 6/1/2011 6:17:46 PM . the carious process is arrested and dentin becomes hard. Classification of fissure morphology is as follows (see Fig.18). On smooth enamel surfaces. dental caries is a damaging process. constricted hour glasses. can be arrested. multiple invaginations with inverted shape. The peak rate for the incidence of the new lesions occurs 3 years after the eruption of the tooth. ‘IK’ type. discoloured pigmentation of the enamel may be seen.17. b. Several morphological variations may be found along the length of the individual occlusal fissure as a result it Arrested Caries Caries lesion can become arrested at any stage of the caries process assuming that causal factors are changed or protective factors are increased. 30. c. ‘I’ type. resulting in an opaque chalky white lesion in location where caries progressed most probably are becoming arrested. they can be extremely diverse in shape and size and have been shown as broad or narrow funnels. extremely narrow slit with a larger space at bottom (24–26%). Occlusal pit and fissure lesions develop in less time than smooth surface caries lesion. Occlusal fissures are deep invagination of enamel. Using emerging technology we should be able to detect clinically the incipient dental caries lesion earlier. Other types (7–9%). The boundaries of caries diagnosis and caries intervention are changing dramatically. the earliest visible changes are usually manifested as a loss of translucency. which in its early stages is reversible and even in its more advanced stages. Smooth surface lesions when sectioned longitudinally are cone shaped with the apex directed towards the dentin (Figs 30. caries development and progression in healthy individuals is usually slow in comparison among compromised persons. Both poor oral hygiene and frequent exposure to sucrose containing diet can produce incipient lesions in as early as 3 weeks.
This lesion is commonly described as cone shaped with the base directed towards the dentin and apex towards the enamel surface. starting from the inner advancing front of the lesion. In newly erupted teeth. Furthermore. FIGURE 30-18 Smooth surface caries.DENTAL CARIES 331 Pulpal involvement Cavitation Irreversible Mineral loss Progression Clinical detectable level Microscopic level Reversible Ultra structural level FIGURE 30-17 Figure depicting progression of mineral loss in relation to time. 3.indd 331 6/1/2011 6:17:46 PM . Frequently. Many teeth have areas at the base of the fissures where a very thin enamel covers underlying dentin. FIGURE 30-19 Longitudinal sectional view of pit and fissure caries. Microscopic Changes of Carious Enamel Under microscope. Translucent zone Dark zone Body of the lesion Surface layer. look like inverted ‘Ys’. penetrating nearly perpendicularly towards the dentinoenamel junction. is not always possible to classify a tooth as having a particular type occlusal morphology. fissures having a broad base give rise to several pits. 2. Carious lesion more often starts at both sides of the fissure wall rather than at the base. Zone 1: translucent zone. Later these macroscopic changes of the enamel in initial caries proceed cavitation and occur without apparent break in the enamel surface. The zones are: 1. There is no sudden or dramatic change from zone to zone but there is a gradual series of changes within the lesion (Figs 30. 4. The translucent zone of enamel caries is not seen in all lesions. but when it is present it lies at the advancing front of the lesion and is Chapter-30.20A. which when sectioned. B). all zones may not be visible by polarized light microscopy. the enamel caries (initial caries) shows four zones. whereas in older individuals the lesions may be arrested or remineralised areas. brown stain or discoloured lesion is indicative of underlying decay.
has a pore volume of approximately 1%. Caries advances more rapidly in dentin than in enamel because dentin provides much less resistance to acid attack because of less mineralized content. When examined in ground section in water. cross-striations or along the striae of Retzius. which remain filled with air. The development and progression of caries in dentin is different from progression in the overlying enamel because of structural differences of dentin. which has an identical refractive index to that of enamel apatite giving translucent appearance. structural markings are lost. The dark zone is the most common feature of the carious lesion and it is the 2nd zone of alteration from normal enamel. the area appears translucent and the stria of Retzius may be well marked. DENTINAL CARIES the first recognizable alteration from the normal enamel. the surface layer is eventually destroyed and a cavity forms. the pores having been created by the demineralization process.3) is different to that of enamel (1. Caries in dentin produces variety of responses including sensitivity. The maximum amount of mineral loss is found in this zone. Because of this characteristics. due to penetration of the quinoline. however. Once these areas are filled with quinoline. hence allows for rapid lateral spreading once caries has penetrated the enamel. B FIGURE 30-20 Microscopic changes of initial caries. pain. the water molecules enter the pores in the tissue and since the refractive index of water (1. Zone 4: surface zone. It is shown that in this zone the pores are of varying sizes. Episodes of short duration pain may be felt occasionally during earlier stages of dentin caries. Quinoline is a large molecule and cannot enter the small pores. In longitudinal section with quinoline in polarized light microscopy. Macroscopic Changes of Dentin Dentin is the hard portion of the tooth that is covered by enamel on the crown and cementum on the root. with a pore volume of 2–4%. It is more porous than sound enamel. where it appears as a relatively unaffected area superficial to the body of the lesion. This zone lies superficial to dark zone and deep to the relatively unaffected surface layer of the lesion. Defence Reactions of Pulp-Dentin Complex Histopathology. Sound enamel has a pore volume of about 0. giving a dark appearance. the area appears dark.indd 332 6/1/2011 6:17:47 PM . increasing to 25% or more in the centre. demineralization and remineralization.1%. The zone has a pore volume of 1% but if the lesion progresses. The dentinoenamel junction (DEJ) has the least resistance to caries attack. The pores are probably located at junctional sites such as prism borders. The surface layer ranges between 30–100 mm thick and it is thinner in active lesions and thicker in inactive carious lesions. Dentin contains much less mineral and possesses microscopic tubules that provide the pathway for the ingress of acids and egress of mineral. The pore volume of this region is 5% at its periphery. These pains are due to stimulation of pulp tissue by movement of Chapter-30. Zone 2: dark zone. the translucent zone.62). This zone is more porous than translucent zone. The body of the lesion comprises the largest proportion of carious enamel in the small lesion. This zone is most clearly seen in polarized light microscope when the section is in water. It lies just superficial to the translucent zone and appears dark when the ground section is placed in quinoline. dentinal caries is ‘V’ shaped or cone shaped in cross-section with a wide base at the DEJ and the apex directed pulpally. large and small.332 PREVENTIVE DENTISTRY Plaque Demineralized zone Translucent zone A Zone 3: body of the lesion. These small pores could represent areas of repair where mineral has been re-deposited or they may have been created by demineralization that is by an opening up of sites not previously attacked.
The dentin can react defensively through repair to low and moderate intensity caries attack as long as pulp remains vital and has an adequate blood supply. toxins and few bacteria enter the pulp resulting in inflammation of the pulpal tissue. These hypermineralised or repaired areas may be seen as zones of increased porosity in radiographs. Initial pulpal inflammation is thought to be evident clinically by production of sharp pain (for few seconds) in response to a thermal stimulus. Once bacterial invasion of dentin is near to the pulp. The deepest area is normal dentin. FIGURE 30-21 Sclerosis dentin. Tubular Sclerosis within the Dentin Tubular sclerosis within the dentin is a process in which minerals are deposited within the lumina of the dentinal tubules. The success of dentinal reparative responses. depends on the severity of caries attack and ability of the pulp to respond. injurious agents will have reduced or no access to the pulp attack.DENTAL CARIES 333 fluid through dentinal tubules that have been exposed to the oral environment by cavitation. These dead empty tubules are termed as ‘dead tracts’. B). It may be acute or chronic. More intense caries activity results in bacterial invasion of the dentin. It represents an area of increased mineral content. The pulp-dentin complex reacts to caries attack by attempting to initiate remineralization and blocking off the open tissues. bacteria and bacterial cellular debris. which has tubules with odontoblastic process Chapter-30. 30. thermal stimulus will produce pain even after termination of stimulus typically for longer duration. abscess and death of the pulp. These cells produce repairable dentin (reactionary dentin) on affected portion of the pulpal wall. including high levels of acids. Dentin which has more mineral content than normal dentin is termed as ‘sclerotic dentin’ (Fig.indd 333 6/1/2011 6:17:48 PM . This material can cause degeneration and death of the odontoblasts as well as mild inflammation of the pulp.21). When the pulp becomes more severely inflamed.22A. Sclerotic dentin formation occurs ahead of the demineralization front of a slowly advancing lesion and may be seen under an old restoration. and it is the vascular response of the pulp tissue to injury. It is also called translucent zone. Reactionary Dentin (Reparative Dentin) Reactionary dentin is a layer of dentin formed at the interference between the dentin and pulp.20). Sclerotic dentin is usually shiny and discoloured but feels hard to the explorer’s tip (Fig. Inflammation of Pulp The third level of dentinal response is severe irritation. Reparative dentin is very effective barrier to diffusion of material through the tubules and is an important step in dentin repair. hydrolytic enzymes. Zones of Dentinal Caries Zone 1: Normal dentin. The blood supply of the pulp could be the most important limiting factor to the pulpal responses. It is formed in response to stimulus acting further peripherally and its distribution is limited to the area beneath the stimulus. The infected dentin contains a wide variety of pathogenic materials. like Acute and rapidly advancing caries with very high levels of acid production. Dentin responds to the stimulus of its caries demineralization episode by deposition of crystalline material in both the lumen of tubules and intertubular dentin of affected dentin in front of the infected dentin portion of the lesion. If dentinal sclerosis occurs. A short painful response to cold suggests reversible pulpitis or pulpal hyperaemia. overpowers dentinal responses and results in infection. The pulp may be irritated sufficiently from high acid levels or bacterial enzyme production to cause the formation of replacement odontoblasts (secondary odontoblasts). pulp extirpation and root canal treatment are necessary. It provides extra protection for the odontoblasts and other cells of the pulp by increasing the distance between them and the injurious stimulus (Figs 30. In slowly advancing caries vital pulp can repair demineralised dentin by remineralization of the intertubular dentin and by opposition of peritubular dentin. This suggests irreversible pulpitis and the pulp is unlikely to recover even after removing caries. This reaction results from odonto-blastic activity. 30. In such situations. The inflammation of the pulp is called pulpitis. either by remineralization of intertubular dentin and opposition of peritubular dentin or by reparative dentin. The degree of inflammatory response depends on the rapidity of caries.
It includes the superficial granular necrotic tissue. Zone 5: Infected dentin. Increasing frequent demineralization of the body of the enamel lesion over a period of time results in weakening and eventual collapse of the surface covering.indd 334 6/1/2011 6:17:48 PM . The dentin in this zone is capable of remineralization. In the outer carious dentin. Affected Dentin: This is softened. which are filled with bacteria. Weak organic acid demineralizes the dentin II. consists of decomposed dentin that is teeming with bacteria. which cannot be remineralized and must be removed during cavity preparation. Collagen fibres are believed to be important in the remineralization of carious dentin. The loss of structural integrity is followed by invasion of bacteria. protected dentin. degenerates and dissolves III. successful restorative procedures as well as prevention of spreading the infection. Less mineral is present in this zone and collagen in this zone will not self-repair. and should be preserved. Thus. This is the zone of demineralization of the intertubular dentin and initial formation of very fine crystals in the tubular lumen at the advancing front. A Crack (artefact) Primary dentin Reactive dentin Advanced Carious Lesions Secondary dentin Caries advancement in dentin proceeds through three changes: I.334 PREVENTIVE DENTISTRY of the intertubular dentin. This results in cavitation and provides an even more protective and retentive zone for the cariogenic plaque. Turbid dentin is the zone of bacterial invasion and is marked by widening and distortion of the dentinal tubules. Removal of infected dentin is essential to sound. a dragging instrument or desiccation from heat or air. a bur. Collagen (organic) content of the dentin is intact. the crosslinks decrease markedly and these biochemical findings suggest that remineralization can occur only in the inner carious dentin where the collagen denaturation is reversible depending on pH. There is no recognizable structure to the dentin. The organic material of the dentin. that are smooth and no crystals are in the lumen. Stimulation of dentin by osmotic gradient (from applied sucrose or salt). this region remains capable of self-repair provided the pulp remains vital. It is vital and no need to remove this dentin as it can be repaired. Stimulation of this region produces pain. particularly collagen. This zone of carious dentin is softer than normal dentin and shows further loss of mineral from the intertubular dentin. This zone cannot be remineralized and must be removed before restoration. which serves as a template for remineralization Chapter-30. and collagen and mineral seem to be absent. The outermost zone. thus helps in accelerating the caries progression. There is evidence that collagen fibres in the outer layer are irreversibly denatured. produces a sharp pain. Zone 4: Turbid dentin. There are no bacteria in the tubules. Subtransparent zone is seen next to normal dentin. There are no bacterial area found in this zone also. The zone of decomposed dentin (outer carious dentin) is soft infected dentin. Infected Dentin: This is both softened and contaminated with bacteria and dead (zones 4 and 5). Zone 2: Subtransparent dentin (zone of demineralization). demineralised dentin that is not yet invaded by bacteria (zones 2 and 3). Pulp tissue B FIGURE 30-22 Reactionary dentin. The inner layer of carious dentin although partially softened by demineralization contains only few bacteria. No bacteria are present in this zone either. because it can be remineralized. Zone 3: Transparent dentin. soft dry and leathery dentin.
Of the 200–300 species of microorganisms inhabited in the plaque. Two bacterial genera of special interest in cariogenesis are: (i) mutans streptococci. Acidogenic (acid producing) bacteria along with metabolic acids must be present to develop caries.indd 335 6/1/2011 6:17:51 PM . S. The mutans streptococci (MS) are a group of bacterial species previously considered to be serotypes of the single species.phosphotransferase mechanism 4. 4. Streptococcus sobrinus: It differs from S. It is claimed that root surface caries may occur within a deep periodontal pocket and lesion may be hidden in the pocket. Age Gender Fluoride exposure Systemic illness Medication Oral hygiene Diet Salivary changes. There are drastic changes in the salivary composition and flow rate this.e. the great majority are not directly involved in the caries process. Mutans streptococci and caries. use of fluoride toothpaste. in turn. Bacteria seem to penetrate into the tissue at an earlier stage in root caries than in coronal caries. Ability to stick to tooth surfaces and production of abundant quantity of insoluble extracellular polysaccharides from sucrose 2. Dental plaque fulfills both of these functions. Their ability to produce organic acid (lactic acid) from a number of sugar substrates 3. may get influenced and precipitated by medication due to chronic systemic illnesses in older people. during the cycles of either very low concentration of sugars (between meals) through to periods of excessive concentration of sugars. mutans in that it requires sucrose for attachment and growth in the plaque. with age. affect natural cleansing effect and protective properties of the saliva. which acts as a reserve substrate for bacteria. It is commonly seen in older people. mutans in that it lacks the adhesin required for sucrose-independent attachment and therefore only accumulates on smooth surfaces in the presence of sucrose rich diet. 5. The cemento-enamel junction is highly irregular and represents a particular bacterial retention site and majority of root caries lesions develops at this site. starts declining. These cariogenic features help MS to survive even in an unfriendly environment under the condition with or without sugar substrate. i. Gingival recession is a prerequisite for exposure of a root surface. It differs from S. Like enamel lesions. The byproducts of metabolism of sugars. And also the efficiency of the oral hygiene exercise by the older people is poor. Chapter-30. mutans is the most common of the human MS and has the greatest evidence implicating it as the most virulent odontopathogen in the aetiology of dental caries. Early diagnosis of such lesions is important because active lesions may become arrested following improved plaque control. acids are pumped out of the bacterial cells into plaque fluids. and care with diet. The transmissible nature of the disease in humans was demonstrated by the experiments of Keye’s. sometimes. This was clearly demonstrated that germ free Other Microbial Agents Responsible for Caries 1. Thus. Ability to resist aciduric and acidogenic environment because of phosphoenolpyruvate. Main reasons for Streptococcus mutans (MS) to be considered as a causative agent for dental caries are: 1. 7. Risk Factors for Root Caries The integrity of the periodontium as age advances.DENTAL CARIES 335 ROOT CARIES Recession of gingival margin is an inevitable reason for poor oral hygiene and loss of periodontal attachment. root surface caries lesions may be classified as active or arrested. 2. The risk factors for root caries are: 1. who showed that previously caries inactive hamsters developed caries after contact with caries active animals. Root lesions are very vulnerable to mechanical damage and probing should be avoided. 6. Hence all these factors might act as a risk factors directly or indirectly contributing for development of root caries in older people. and (ii) lactobacilli. MICROBIOLOGY OF DENTAL CARIES Cariogenic Bacteria Importance of bacteria for the initiation of dental caries was proved in animal experiment by Orland and colleagues in 1954. rats did not develop caries when fed cariogenic diet. 8. This. 3. Streptococcus mutans. on account of degenerative changes. The damage caused by MS is mainly due to lactic acid although other acids such as butyric and propionic present within the plaque. Production of intracellular polysaccharide.
Chapter-30. as a general rule. Other bacteria particularly Actinomyces (A. the presence of insoluble glucans is an important factor in establishing the presence and virulence of an organism. However. And also S. casei) associated with progression. This is seen following irradiation for head and neck cancers. Thus. there will be a drop in pH of plaque to critical level. At the same time. sugar restriction has an influence to reduce the acidogenicity of dental plaque. consisting of one glucose and fructose unit (referred to as moieties) joined by a disaccharide bond. only to decrease in number as Lactobacillus population increases. S. they would be swept away by the salivary flow. Children who consume little or no sucrose. mutans in that it lacks the adhesion required for sucroseindependent attachment. Mutans streptococci are able to attach to the tooth surface by two mechanisms: i. The chains of glucose are called glucans and those of fructose are called fructans. Similarly those individuals receiving long-term nourishment via stomach tube have less plaque and very fewer S. MECHANISM OF ADHERENCE OF MICROORGANISMS TO TOOTH SURFACE Adherence by S. Subsequent growth of bacteria from small enamel defects and from cells initially attached to the tooth surface. Sucrose is a disaccharide sugar. ii. The plaque formation continues with the formation of extracellular polysaccharide chains via the breakdown of sucrose to glucose and fructose.23): 1. multiple carious lesions develop rapidly because of destruction of the salivary glands. and therefore it accumulates only on smooth surfaces in the presence of diet with FORMATION OF PLAQUE The initial colonization of microorganisms on the tooth surface probably begins with organisms other than Streptococcus mutans. Thus. Sometimes the enzyme may be altered resulting in the production of soluble glucan that does not support adherence to the tooth surface. mutans are implicated in the initiation of the lesion and Lactobacillus (specifically L. mutans number increases when sucrose is re-introduced into the diet. gelatinous substances that further enhance the bacterial ability to adhere to the tooth and to each other. mutans. odontolyticus) have also been associated with lesion progression including root surface caries. Thus. have a less cariogenic plaque. because of sucrose or fructose enzyme deficiencies. Adherence of bacteria to pellicle or the enamel surface 2. Otherwise. mutans in the plaque. Lactobacillus species have been shown that their numbers are so low so as to be incapable of producing range of pH values required for caries initiation. mutans appear. The individuals restricting their sucrose intake have a decreased proportion of S.indd 336 6/1/2011 6:17:52 PM . sucrose. Sucrose-dependent mechanisms: In this bacteria require the presence of sucrose to produce sticky extracellular polysaccharides or glucans. One of the key enzymes in conversion of glucose moiety of sucrose to glucan is glucosyltransferase. During the initial phases of the development of carious lesions. Adhesion between bacteria of the same or different species 3. The effect of sucrose dependency for production of glucans is seen in several clinical conditions. This leads to further accumulation of acids at the tooth-plaque interface and when sufficient amount of acids are produced. These mutant strains lacking the insoluble glucan are usually non-cariogenic. mutans decrease in number. It is considered as essential acidogenic bacteria causing caries. They have been shown to colonize white spot lesions before cavitation. At first bacteria must have to establish a strong foothold on the tooth surface and maintain their positions while continuing to colonize in protected areas provided by the interproximal space along the gingiva or in the regions of pit and fissures. wherein extensive. which allow attachment and accumulation.336 PREVENTIVE DENTISTRY 2. as teeth are lost throughout life and particularly disappear following full mouth extraction. mutans to the tooth surface is necessary both before and after colonization. more number of S. Streptococcus sobrinus differs from S. These extracellular polysaccharides are sticky. Sucrose-independent adsorption: In this. They also affect the rate at which saliva can enter the plaque to buffer the acids and reverse the demineralization process. Lactobacilli: Lactobacillus helps in progression of dental caries and it is aciduric and acidogenic in nature. 30. S. they have been associated in lesion development. They are also found in greater numbers in the more advanced smooth surface lesions. the bacteria attach to the acquired pellicle through specific extracellular proteins (adhering) located on the fimbriae of these organisms. The mechanism of initial colonization includes (Fig.
Saliva has many functions: cleansing effect. histatins. Lysozyme disrupts bacterial cell wall and leads to bacteriolysis. lactoferrin. The exposure to chewing forces and abrasion from foods 9. These properties and characteristics of saliva influence either progression or halting of carious process.24).9–7. 2. 3. The intake of fermentable carbohydrates 7. Lysozyme. providing an environment saturated with calcium and phosphate and antibacterial action. lactoperoxidase. The use of fluorides and other preventive products. The individual oral hygiene habits 12. ROLE OF SALIVA IN DENTAL CARIES Biological Role of Saliva Saliva is also called ‘liquid enamel’ as it is a rich source of various minerals. The quantity of plaque that forms on clean tooth surfaces during a given time represents the net result of interactions among aetiologic factors. 3. Chapter-30. it is not a prerequisite for caries initiation in the same sense that microorganisms. hemoprotein enzyme are present in saliva which play a role in the prevention of bacterial colonization on tooth surface.2. and protective factors: The total oral bacterial population The quantity of the oral bacterial flora The anatomy and surface morphology of the dentition The wettability and surface tension of the tooth surfaces 5. The mobility of the tongue and lips 8. The eruption stage of the teeth 10. a hydrolytic enzyme. Its pH is in the range of 6. secretory immunoglobulin A and bacteria derived glucosyl transferase (GTF). However important role saliva may play in dental caries. lactoperoxidase. The degree of gingival inflammation and volume of gingival exudate 11. sequestering iron away from bacteria and inhibits bacterial growth by both iron dependent and independent mechanisms. lysozyme. 4. such as chemical plaque control agents.indd 337 6/1/2011 6:17:52 PM . buffering capacity. Saliva-acquired components in the pellicle include cystatins. The composition of saliva and velocity of the salivary film can play a significant role in maintaining the integrity of the tooth tissues as teeth are bathed in saliva (direct contact) constantly.DENTAL CARIES 337 Flow rate Saliva Bacteria Tooth Enamel surface Flora Caries Composition pH Saliva Saliva Substrate Receptor on enamal surface Buffering capacity FIGURE 30-23 plaque. 1. 30. Mechanism of initial colonization of FIGURE 30-24 Diagrammatic representation of important role of saliva with other primary factors in caries aetiology. Lactoferrin binds iron. carbonic acid and phosphate buffer systems. amylase. 1. The salivary secretion rate and other properties of saliva 6. 2. These saliva-derived components attempt to negate deleterious by products of bacterial metabolism in the dental biofilm. many internal and external risk factors. substrate (sucrose) and tooth (host) are essential (Fig. The buffering effect of saliva is based mainly on bicarbonate.
Thus. cariogenic bacteria. Buffering capacity of saliva d. Microbial flora of cariogenic plaque Chapter-30. when confronted with sufficient fermentable carbohydrate. At the same time. which leave the solution. The damage done to the tooth surface is caused by the intense localized production of acids by bacteria. Lactoperoxidase inhibits glucose metabolism. Rapid flow of highly buffered. 2. provided it is not acidified with dietary. protein rich glycoprotein bind to and protect hydroxyapapatite. 5. 5. Despite these buffering systems. Saliva is very important in the caries process. When a relatively soluble calcium phosphate mineral dissolves and equilibrium is attained with that mineral. three factors must be present simultaneously along with time factor. mobile saliva reduces the fall in plaque pH. so that the ion activity product increases with increasing flow rate. If under the influence of plaquecariogenic activity. The most prominent antibody found in the saliva is the SIgA. Write short notes on: a. Low viscosity is also associated with low caries activity due to rapid clearance of sugar from the oral cavity. Classify dental caries. antimicrobial actions and remineralization. Keyes circle b. Bicarbonates are the most important buffers of saliva. Define dental caries and discuss the early theories of caries aetiology. Most importantly. which breakdown the buffers and lead to dissolution of tooth minerals. and it may attempt to regrow using the remains of the original crystal as a template. CONCLUSION Dental caries is a multifactorial disease of bacterial origin. For caries to occur. Proteins can be disregarded as buffers. Radiation caries g. and sucrose containing dietary factors. Buffers work by converting any highly ionized acids or alkalis. These proteins also promote supersaturation of calcium phosphate ions in the fluid phase of the dental biofilm. unstimulated whole saliva is supersaturated with respect to hydroxyapatite and the level increases when the flow rate is stimulated. The development of carious lesion depends on structural factors of the tooth and also environmental factors. which tend to alter the pH of the solution into more weakly ionized substance. Thus less caries is associated with the rapid flow of saliva. both pH and calcium concentration increase with increasing flow rate. a small amount of high carbonate. it is clear that acid formation potential of plaque is such that. It is clear that enamel mineral does not dissolve in saliva under normal conditions. Discuss each type of dental caries. 3. low fluoride mineral of enamel dissolves then the enamel fluid at that site will be supersaturated with respect to low carbonate and/or high fluoride hydroxyapatite. Discuss the role of microbial agents responsible for caries. Iron is an essential element for bacterial metabolism. They are susceptible tooth surface. 4.338 PREVENTIVE DENTISTRY 4. Discuss the role of plaque in dental caries. Thus. the mechanism of caries process is relatively complex either in the enamel. Bicarbonates release the weak carbonic acid when an acid is added and since this acid is rapidly decomposed into water and carbon dioxide. Caries is an infectious disease caused by cariogenic plaque formation on the tooth which causes demineralization of the tooth. which tends to precipitate if suitable site is present. 6. the solution is often then supersaturated with respect to a less soluble calcium phosphate. The result is not the accumulation of a weaker acid but complete removal of acid. Root caries c. It is likely that hydroxyapatite crystals in the developing lesion will only be partly dissolved. 7. gastric or medicinal acids. which reflects the lifetime caries experience of the individual and may not have a protective function. the repaired section will contain less carbonate and will be less soluble and therefore much more resistant to future dissolution events. REVIEW QUESTIONS 1. Rampant caries e. In parotid secretion. This peroxidase protects salivary glycoprotein from degradation due to bacteria. Several of the proteins like statherin. the buffers are overcome within minutes. fluoride ions in solution (from the saliva) are likely to be incorporated so that repaired section will be not only lower in carbonate but richer in fluoride. Nursing caries f. Hidden caries h. Saliva contains considerable amounts of calcium and phosphate and is nearly always supersaturated with respect to enamel mineral and other biological appetites. Buffering Power of Saliva Diffusion of inorganic buffers from the saliva into the dental plaque plays an important part in reducing the effect of acids produced by the bacteria. The protective mechanisms of saliva include buffering actions.indd 338 6/1/2011 6:17:52 PM . dentin or cementum. (HAP). Phosphates also play some part.
Chemical and structural challenges in remineralization of the dental enamel lesions. Thylstrup A. Leach SA. Nyvad B. Possible physicochemical process in human dentin caries. Adv Dent Res 7: 4–14. 2. IRL Press. Fejerskov O.DENTAL CARIES 339 REFERENCES 1. Fejerskov O. Ogaard B. Artrun J. Some aspects of the ultra structure of early human enamel caries seen with the electron microscope. Dental plaque and caries on occlusal surfaces of first permanent molars in relation to stage of eruption. J Dent Res 68: 773–9. Textbook of Clinical Cariology (2nd edn). Chapter-30. Fejerskov O. 1967. 3. 9. Baelum V. Kerbel B. 7. Root caries in Scandinavia in the 1980 and future trend to be expected in dental caries experience in adults. Munksgaard. Active and inactive root surface caries— structural entities? In Thylstrup A. Thylstrup A. Kragh F . Scan J Dent Res 97: 285–96. Legerous KZ. Johnson NW. Qvist V (eds). Clinical and scanning electron microscopic study of surface changes of incipient enamel caries lesions after debonding. J Dent Res 66: 1356–9. Fejerskov O. Arch Oral Biol 12: 1505–21. 1986. 1987. Ekstrand KR. A scanning electron microscopic study of progressive stages of enamel caries in vivo. Caravalho JC. 8. 5. 1993. 1985. Daculci G. Caries Res 19: 355–67. Copenhagen. Scand J Dent Res 94: 193–210. 4. Jean A. Dentine and Dentin Reactions in the Oral Cavity. 1994.indd 339 6/1/2011 6:17:52 PM . Ostergaard ES. 6. 1989. Thylstrup A. 1989. 1987. Holmen L. Larsen MJ. Thylstrup A. Oxford 165–79.
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