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Textbook of Preventive and Community Dentistry, 2/e


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This book provides a comprehensive yet simple presentation of Preventive and Community Dentistry. Based on the syllabus prescribed by Dental Council of India, the book covers various aspects of public …

This book provides a comprehensive yet simple presentation of Preventive and Community Dentistry. Based on the syllabus prescribed by Dental Council of India, the book covers various aspects of public health, dental public health, preventive dentistry, and research methodology. An important feature of the book is inclusion of additional chapters on Forensic dentistry, Hospital administration, Occupational hazards, Nutrition and oral Health, Minimal invasive dentistry and Dental Practice management. These chapters are vital for richer understanding of community dentistry. Further, some useful information like facts about tobacco, fluorides and clinical cases proforma are included separately under the Appendices. All these features make the book quite comprehensive in scope and contemporary in approach.

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  • plz update it for chaper 27-consumer protection act from community dentistry by ss hiremath
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  • 1. C H APT E R 30 Dental Caries – SS Hiremath CHAPTER OUTLINE K Dentinal Caries K Root Caries K Introduction K Microbiology of Dental Caries K Early Theories of Caries Aetiology K Mechanism of Adherence of Microorganisms to K Current Concepts of Caries Aetiology Tooth Surface K Classification of Dental Caries K Formation of Plaque K Clinical Manifestations of Dental Caries Process K Role of Saliva in Dental Caries K Caries of Enamel epidemiologically it was of little concern if that person INTRODUCTION went through life without frank cavitation. Tooth decay is an infectious disease generally affected Dental caries the disease of civilization, is affecting the by diet and the pattern of its consumption by the host. mankind since the dawn of the time. Caries has also Its dependency on ingestion of fermentable dietary car- been noted in the fossil remains of Pithecanthropus erectus bohydrate is beyond question. However caries does not and Homo rhodesiensis, early ancestors of man. Caries occur in germ free animals, no matter what their diets seems to have increased considerably in Homo sapiens are, thus establishing it as a fundamentally microbiological during Neolithic period when it was perhaps as high disease. Sound enamel demineralizes, if plaque bacteria as that seen in many contemporary primitive people. are given with carbohydrate substrate and they produce In fact, in prehistoric skulls about 5% of the teeth exhib- acids, however, the presence of saliva in the mouth can act ited caries. as a buffering agent which in turn to an extent can inhibit It is a chronic disease, a process that progresses very the demineralization process. The progression of carious slowly in most individuals. The multifactorial aetiology lesion is not inevitable and disease can be controlled. 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 cari- Salient Features of Carious Process ous lesion should be regarded not as a disease entity but Salient features of carious process are listed below: as tissue damage caused by the dental caries. “Caries without cavitation”—caries should be consid- 1. Carious process is spread over time ered as a process rather than simply as an event at a par- 2. Carious process does not have to progress ticular stage, i.e. a cavity requiring restoration. Evidence 3. The initial lesion can be arrested and reversed of frank cavitation was required for the diagnosis. There 4. All ages are susceptible to caries were two reasons for this; one being that from the public 5. Caries is the major cause of tooth loss in all age groups. health standpoint there was little interest in lesions, which have no effect on the person in terms of requirements Definition for treatment or restoration. When a caries-free individ- ual is referred, it was found that such an individual had Dental caries is an infectious microbial disease that many pre-cavitational lesions approximally. However, begins as demineralization of inorganic portion of tooth,Chapter-30.indd 321 6/1/2011 6:17:29 PM
  • 2. 322 PREVENTIVE DENTISTRY followed by destruction of organic portions, leading to Parasitic or Septic Theory cavity formation. Parasitic or septic theory was given by Erdl (1843). • The Caries Process occurs as an interaction between According to this theory, dental caries was caused by the biofilm and the tooth surfaces: the caries lesion is filamentous parasites present in the “surface membrane” the manifestation of the stage of the process at one (plaque?) of teeth. Later, Ficinus, observed filamentous point in time. microorganisms, which he called denticolae in material taken from carious cavities. EARLY THEORIES OF CARIES AETIOLOGY Vital Theory The vital theory regarded dental caries as originating Worm Theory within the tooth itself, analogous to bone gangrene. A According to an ancient Sumerian test, toothache was clinically well-known type of caries is characterized by caused by a worm that drank the blood of the teeth and extensive penetration into the dentin, and even into the fed on the roots of the jaws. Guy de Cahuliac, the greatest pulp, but with a barely detectable catch in the fissure. Surgeon of the middle Ages believed that worming caused dental decay. As a cure he advocated fumigation with Chemical Theory seeds of leech, onion and hyoscyamus. Chemical theory was given by Parmly (1819). According to this theory, dental caries was caused by unidentified Humour Theory chemical agent. He stated that caries begin on the enamel Ancient Greeks considered that relative proportions of surface in locations, where food putrefied and acquired four elementary fluids of the body determined a person’s sufficient dissolving power to produce the disease physical and mental constitution: (i) blood, (ii) phlegm, chemically. (iii) black bile, and (iv) yellow bile. These four fluids cor- responds to the four humours: (i) phlegmatic, (ii) choleric Chemoparasitic Theory (iii) sanguine, and (iv) melancholic (Fig. 30.1). All dis- eases including caries were explained by an imbalance Chemoparasitic theory is the most accepted theory for of these humours. the aetiology of dental caries. This theory was given by Melancholic Yellow bile Choleric Phlegm Blood Phlegmatic Black bile Sanguin FIGURE 30-1 Humour theory.Chapter-30.indd 322 6/1/2011 6:17:29 PM
  • 3. DENTAL CARIES 323 Miller in 1890. In a series of experiments it was demon- meaning claw, and refers to compounds that are able to strated that: bind metallic ions such as calcium, iron, copper, zinc and 1. Acid was present within the deeper carious lesion, as other metals, by the secondary valence bonds. shown by reaction on litmus paper. 2. Different kinds of foods (breads, sugar, but not meat) when mixed with saliva and incubated at 37°C could CURRENT CONCEPTS OF CARIES decalcify the entire crown of the tooth. AETIOLOGY 3. Several types of mouth bacteria (at least 30 species are isolated) could produce enough acid to cause Caries is multifactorial disease mainly consisting of three dental caries. parameters most commonly contributing for the initia- 4. Lactic acid was an identifiable product in carbohydrate- tion of dental caries namely, host factor (susceptible tooth saliva, incubation mixtures. surface), microorganism (Streptococcus mutans), and diet 5. Different microorganisms (filamentous, long and (sucrose), however the interplay between these factors short bacilli and micrococci) invade carious dentin. has to take place in an appropriate time. Thus the fourth factor has been considered either as independent factor Miller concluded that no single species of microorgan- or all the three primary factors have been put under time ism caused caries, but rather the process was mediated factor (outer ring). This factor has been added to empha- by oral microorganisms capable of producing acid and size the importance of time factor in the origin of the digesting protein. disease along with other three primary factors. Hence current concept of the aetiology of dental caries includes Critique of Chemoparasitic Theory these important four factors as described in Keyes circle (Figs 30.2–30.4). There are various subfactors or co- 1. Miller’s chemoparasitic theory is unable to explain factors contributing directly or indirectly in initiation of the predilection of specific sites on a tooth to dental dental caries. caries. 2. The phenomenon of arrested caries is not explained by the chemoparasitic theory. Keyes Circles 3. Miller’s theory does not explain why some popula- A carious lesion should be regarded not as a disease entity, tions are caries-free. but as tissue damage or a wound caused by the disease dental caries. Proteolytic Theory The interaction of saliva, bacteria and microbial prod- ucts in the production of biofilms on the tooth surface is Proteolytic theory was given by Gottlieb in 1944. This an important factor to initiate dental caries. The suscep- theory suggested that the initial action was due to pro- tible host, cariogenic oral microbial flora and fermenta- teolylic enzymes attacking the lamellae, rod sheaths, tufts ble carbohydrate are important in the development of and walls of the dentinal tubules. Later a coccus, proba- dental caries and they have been depicted through Keyes bly Staphylococcus aureus, was involved because of the circles (Figs 30.3A, B). yellow pigmentation that he considered pathognomonic Each one of them is of equal importance in aetiology of dental caries. of the disease. However there are many secondary fac- Frisbie (1944) also described caries as a proteolytic tors that either influence the progression or regression of process involving depolymerization and liquefaction of dental caries (Fig. 30.4). the organic matrix of enamel. Pincus (1949) contended that proteolytic organisms • Caries progression occurs when the demineralization first attacked the protein elements, such as dental cuticle and remineralization equilibrium is out of balance, and then destroyed the prism sheaths. leading to net mineral loss. • Remineralization can arrest or reverse progression of disease and can lead to changes in mineral quality; Proteolysis–Chelation Theory the understanding of the caries process has progressed far beyond the point of restricting the evidence of Proteolysis–chelation theory was proposed by Schatz dental caries to the caries in enamel only or caries in et al (1955). It implies a simultaneous microbial degrada- enamel and dentin or levels of cavitation. tion of the organic components (proteolysis), and disso- lution of minerals of the tooth by the process of chelation. 1. Lesion detection: Implies an objective method of The word “chelate” is derived from the Greek “chele” determining whether or not disease is present.Chapter-30.indd 323 6/1/2011 6:17:30 PM
  • 4. 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 Destruction of More of mineral loss organic matrix Cavitation FIGURE 30-2 Flowchart depicting the caries process. 2. Lesion assessment: Aims to characterize or moni- from initial loss of mineral at the ultra structural level tor a lesion, once it has been detected. to total destruction of the tooth. However, caries lesion development is a highly dynamic process with alternat- 3. Caries diagnosis: Implies a human, professional, ing periods of progression and arrest/regression. summation of all available data. Lesion progression may be arrested at any stage of It is now appreciated that caries is initially reversible, lesion development, even at the stage of frank cavitation, chronic, disease process with known multifactorial provided the local environmental conditions, e.g. biofilm aetiology. control and topical fluoride exposure, are favourable. Dental caries progresses slowly in most of the indi- Hence, the clinical stages of caries represent nothing but viduals as chronic disease. The disease is seldom self- historical signs of the past caries experience. What may limiting and in the absence of treatment, a caries progress be perceived clinically as an “incipient” or “early“ lesion until the tooth is destroyed. The localized destruction of may in reality turn out to be an age established lesion the hard tissues, often referred as the lesion, is the sign or that has been present in the oral cavity for months or symptom of the disease (Fezejerskov et al 2008). Lesion years and also from a biochemical point of view the car- progression is often depicted on a linear scale ranging ies process is much more complex. Metabolic processesChapter-30.indd 324 6/1/2011 6:17:30 PM
  • 5. DENTAL CARIES 325 Microorganisms Microorganisms (cariogenic plaque) No No Caries Caries Time Time Host & Caries Substrate Caries teeth Substrate Host (cariogenic diet) (susceptible No No tooth surface) Caries Caries Time Time A B FIGURE 30-3 Keye’s Circle—current concept of caries aetiology. Microorganisms Strep. mutans (substrate) Oral hygiene Oral flora Fluoride in plaque Caries Diet & nutrition Transmissibility Substrate Host Oral clearance Oral hygiene Age Detergency of food Fluorides Frequency of eating Morphology Carbohydrate (type, Primary Secondary Nutrition concentration) factors factors Trace elements Carbonate FIGURE 30-4 Diagrammatic representation of interplay between primary and secondary factors in caries aetiology. are constantly taking place in the dental plaque as a on smooth surfaces of the enamel (enamel caries) or on result of microbial activity, and this is reflected by con- the exposed root cementum (root caries). tinuous, rapid fluctuations in plaque pH, both when the plaque is starved and fed. Hence, any clinically sound or Classification Based on Morphology carious tooth surface that is covered by an undisturbed plaque may experience minute mineral loses and min- This classification is according to anatomical site of the eral gains depending on the metabolic status of the lesions. microflora. The key point is, when the cumulative result of the de- and remineralization process is loss of mineral, Pit and Fissure Caries (Occlusal Caries) caries lesion develop or progress. Caries lesions may be classified in various ways. Firstly, lesions can be classi- • Most common type of dental caries (Fig. 30.5). fied according to their anatomical site and location. The • Occurs on the occlusal surfaces of molars and lesions may be commonly found in pits and fissures, or bicuspids.Chapter-30.indd 325 6/1/2011 6:17:30 PM
  • 6. 326 PREVENTIVE DENTISTRY A FIGURE 30-6 Cervical caries. B A FIGURE 30-5 Pit and fissure caries. Smooth surface caries. There are two variations of smooth surface caries. They are: (i) buccal and lingual sur- face caries, and (ii) proximal surfaces (interproximal). a. Buccal and lingual surface caries • Cervical caries (smooth surface caries)—occurring on buccal or lingual surfaces near the cementoenamel junction (Fig. 30.6). B b. Proximal surfaces (interproximal) FIGURE 30-7 Proximal surfaces (interproximal). • Interproximal caries—occurring at mesial or distal contact points. Interproximal caries usually starts just involving surfaces of teeth that are ordinarily relatively cervical to the contact area (Fig. 30.7). caries free (proximal and cervical surfaces of anterior teeth including the mandibular incisors get affected). A caries Classification based on Severity and increment of 10 or more new lesions over a period of about a year is characteristic of a rampant caries attack (Fig. 30.8). Progression Early childhood caries Early childhood caries is a spe- I. Rampant caries cific form of rampant decay of the primary teeth of infants II. Early childhood caries (nursing caries) and toddlers. According to American Dental Association III. Radiation caries (xerostomia induced). (ADA) it is defined as “the presence of one or more decayed, Rampant caries. Rampant caries occurs as a sudden, missing or filled tooth surfaces in any primary tooth in rapid and almost uncontrollable destruction of teeth, a preschool age child between birth and 71 months of age”.Chapter-30.indd 326 6/1/2011 6:17:30 PM
  • 7. DENTAL CARIES 327 ECG is a particularly virulant form of dental caries that is – Anti-sialagogue drugs characterized by an overwhelming infections challenge and – Prolonged illness is associated with unusual dietary practices. It is a unique pattern of dental decay affecting maxillary primary incisors Classification Based upon Part of Tooth in young children due to prolonged nursing habit espe- Structure Involved cially when the child is sleeping. This is also named as baby bottle tooth decay. The main cause for this type of caries a. Enamel caries is inappropriate feeding bottle or at will breastfeeding or • Incipient caries combination of both and poor oral hygiene (Fig. 30.9). • Linear enamel caries (odontoclasia) b. Dentinal caries Radiation caries (xerostomia induced). This is a c. Cemental caries common complication of radiotherapy of oral cancer lesions and radiation-induced xerostomia (from the Greek, xeros = dry, stoma = mouth). Enamel Caries Such patients develop rampant dental caries (Fig. • Incipient lesion: Incipient lesion is also called the 30.10). Xerostomia may be caused by factors other than early carious lesion. It manifests as a white, opaque radiation like region, which is best demarcated when the area is – Tumours of salivary glands dried (Figs 30.11A, B). – Autoimmune diseases (e.g. Sjogren’s syndrome) FIGURE 30-10 Radiation caries. FIGURE 30-8 Rampant caries. Incipient lesion A A Incipient B B lesion FIGURE 30-9 Nursing caries. FIGURE 30-11 Incipient lesion.Chapter-30.indd 327 6/1/2011 6:17:34 PM
  • 8. 328 PREVENTIVE DENTISTRY • Linear enamel caries (Odontoclasia): An atypical form of dental caries, called linear enamel caries, has been observed in the primary dentition of children, in Latin America and Asian countries. The lesions predominate on the labial surfaces of the anterior maxillary teeth, in the region of neonatal line. (The neonatal zone repre- sents the demarcation between pre- and postnatal enamel and is a histologic feature of all primary teeth). It is thought to result from the metabolic disturbances associated with trauma of birth and transient hypocal- caemia associated with transient hypoparathyroidism. FIGURE 30-12 Secondary caries. Dentinal caries. On its way to progression, 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 lesion estab- lishes in dentin. At the same time, outer layer of enamel might breakdown owing to progression of caries and leads to cavitation. Cemental caries. Recession of gingival margin is an inevitable process as a result of poor oral hygiene and loss of periodontal attachment with age. Subsequently the exposed root surface becomes more vulnerable to plaque accumulation and caries process might initiate involving cementum. Classification of Caries Based on Activity FIGURE 30-13 Arrested caries. a. Primary caries b. Secondary caries (recurrent caries) According to World Health Organization (WHO), the c. Residual caries shape and depth of the carious lesions can be scored on d. Arrested caries a four-point scale (D1 to D4): Primary caries. Primary caries is used to differentiate • D1—clinically detectable enamel lesions with intact lesions, which develop on the healthy enamel surface or (non-cavitated surfaces) on unrestored surfaces from those that develop adjacent • D2—clinically detectable cavities limited to the to a filling. enamel Secondary caries. A carious lesion that develops at • D3—clinically detectable lesions in dentin (with and the interface of restoration and the cavosurface of the without cavitation of dentin) enamel is called secondary caries (Fig. 30.12). • D4—lesions into pulp. This type of caries may result from: • Poor cavity preparation • Ditching around an amalgam restoration CLINICAL MANIFESTATIONS OF DENTAL • A defective restoration CARIES PROCESS • Or a combination of these factors. Residual caries. Residual caries is demineralised Early Changes tissue that has been left behind before filling is placed The earliest stage of caries is the first time deminerali- (incomplete removal of carious dentin). zation of enamel which occurs after the plaque pH Arrested caries. There is clinical evidence that incipi- depression below the critical pH (5.2–5.5). This amount ent and even more advanced carious lesions may become of demineralization cannot be detected clinically (they arrested if there is a significant shift in oral environmen- go unnoticed), however the repair process, remineraliza- tal conditions from those that predispose to caries to that tion and demineralization go hand in hand, and most of tend to slow the caries process (Fig. 30.13). the time maintains the homeostasis (Figs 30.14, 30.15).Chapter-30.indd 328 6/1/2011 6:17:43 PM
  • 9. DENTAL CARIES 329 Demineralization Remineralization Tooth FIGURE 30-14 Equilibrium of demineralization and remineralization. Poor oral hygiene Frequent sugar exposure Continuous high cariogenic challenge Remineralization Demineralization Tooth FIGURE 30-15 Deranged equilibrium of demineralization and remineralization. White Spot Lesion subsurface to the surface and get added to the calcium and phosphate in dental plaque. Later calcium and The first visible clinical presentation of dental caries is phosphate along with fluoride from saliva and biofilm referred to as white spot lesion. The clinical appearance helps in the precipitation on the superficial layer on the of white spot lesion is caused by subsurface enamel affected surface enamel. This rapid precipitation of high demineralization, resulting in loss of translucency. levels of calcium and phosphate leads to occluding the Normally white spot lesion being smooth and having pores that would further limit demineralization of the intact surface indicates that lesion is not active whereas surface layer and limits remineralization of the underlying lesions with rough surfaces because of increased poros- demineralized subsurface. Hence there is an intact surface ity suggest that a lesion is active and progressing. layer of the enamel, even though caries are progressing White spot carious lesion does not necessarily progress at subsurface level, which is not visible. to frank cavitation. In this stage, the lesion progression Caries progressing into dentin with intact surface is not could be arrested or reversed by modifying any of the clinically diagnosed but can be detected only in radio- causative factors or application of appropriate preven- graphs. The prevalence of hidden caries ranges from tive measures. Arrested lesion may retain the appearance 0.8 to 3%. These occult lesions are usually seen with low of white spots or acquire the appearance of brown spot. caries rate which is suggestive of increased fluoride The reversal of the white spot could be due to reminer- exposure. Recently it has been observed that hidden car- alization of the lesion subject to condition that surface ies may have origin as pre-eruptive defects, which are layer is intact, and most of the time they may not progress detectable only with the use of radiographs. to frank cavitation in the absence of high cariogenic chal- lenge (Fig. 30.16). Therefore white spot can be referred as non-cavitated lesion. Frank Cavitation As the carious lesion progresses the subsurface lesion increases in dimension, eventually leading to collapse Hidden or Occult Caries of the surface layer leading to cavitation. At this stage During the cariogenic challenge on account of fall of pH of carious process, tooth destruction progresses more to a critical level, demineralization commences on the rapidly because cavitation favours plaque accumulation subsurface. Calcium and phosphate ions move from and reduced salivary access.Chapter-30.indd 329 6/1/2011 6:17:45 PM
  • 10. 330 PREVENTIVE DENTISTRY Sound enamel Fluorides High cariogenic challenge Good oral hygiene Carious enamel Fermentable carbohydrates Cariogenic plaque Cavitation FIGURE 30-16 Schematic presentation of factors affecting sound and carious enamel. The progression of the carious lesion is variable, CARIES OF ENAMEL depending on the site of origin and conditions in the mouth. The time for progression from incipient caries to clinical caries (cavitation) on smooth surfaces is esti- Macroscopic Changes of Enamel mated to be 18 months plus or minus 6 months. The On smooth surfaces. On smooth enamel surfaces, peak rate for the incidence of the new lesions occurs the earliest visible changes are usually manifested as a 3 years after the eruption of the tooth. Occlusal pit and loss of translucency, resulting in an opaque chalky white fissure lesions develop in less time than smooth surface lesion in location where caries progressed most probably caries lesion. Both poor oral hygiene and frequent expo- are becoming arrested, discoloured pigmentation of the sure to sucrose containing diet can produce incipient enamel may be seen. Smooth surface lesions when sec- lesions in as early as 3 weeks. Radiation-induced xero- tioned longitudinally are cone shaped with the apex stomia (dry mouth) can lead to clinical caries develop- directed towards the dentin (Figs 30.17, 30.18). ment as little as 3 months from the onset of the radiation. Thus, caries development and progression in healthy Pit and fissure caries. Occlusal fissures are deep individuals is usually slow in comparison among com- invagination of enamel, they can be extremely diverse in promised persons. shape and size and have been shown as broad or narrow funnels, constricted hour glasses, multiple invaginations with inverted shape. Arrested Caries Classification of fissure morphology is as follows (see Caries lesion can become arrested at any stage of the car- Fig. 39.1): ies process assuming that causal factors are changed or a. ‘Y’-shaped divisions (5–10%). protective factors are increased. Once the open carious b. ‘V’ type-wide at top and gradually narrowing lesion becomes self-cleansing, with improved oral hygiene towards the bottom (30–35%). measures, restricted intake of refined sugars and use c. ‘U’ type, almost the same width from top to bottom of fluorides, the carious process is arrested and dentin (12–15%). becomes hard. d. ‘I’ type, and extremely narrow slit (18–20%). The boundaries of caries diagnosis and caries inter- e. ‘IK’ type, extremely narrow slit with a larger space at vention are changing dramatically. Using emerging tech- bottom (24–26%). nology we should be able to detect clinically the incipient f. Other types (7–9%). dental caries lesion earlier. Thus, dental caries is a dam- aging process, which in its early stages is reversible and Several morphological variations may be found along even in its more advanced stages, can be arrested. the length of the individual occlusal fissure as a result itChapter-30.indd 330 6/1/2011 6:17:46 PM
  • 11. DENTAL CARIES 331 Pulpal involvement Cavitation Irreversible Progression Mineral loss Clinical detectable level Microscopic level Reversible Ultra structural level FIGURE 30-17 Figure depicting progression of mineral loss in relation to time. FIGURE 30-19 Longitudinal sectional view of pit FIGURE 30-18 Smooth surface caries. and fissure caries. is not always possible to classify a tooth as having a par- Microscopic Changes of Carious Enamel ticular type occlusal morphology. Frequently, fissures having a broad base give rise to several pits, which when Under microscope, the enamel caries (initial caries) shows sectioned, look like inverted ‘Ys’. Many teeth have areas four zones, starting from the inner advancing front of the at the base of the fissures where a very thin enamel covers lesion. The zones are: underlying dentin. 1. Translucent zone Carious lesion more often starts at both sides of the 2. Dark zone fissure wall rather than at the base, penetrating nearly 3. Body of the lesion perpendicularly towards the dentinoenamel junction. In 4. Surface layer. newly erupted teeth, brown stain or discoloured lesion is There is no sudden or dramatic change from zone to indicative of underlying decay, whereas in older indi- zone but there is a gradual series of changes within the viduals the lesions may be arrested or remineralised areas. lesion (Figs 30.20A, B). Furthermore, all zones may not This lesion is commonly described as cone shaped with be visible by polarized light microscopy. the base directed towards the dentin and apex towards the enamel surface. Later these macroscopic changes of the Zone 1: translucent zone. The translucent zone of enamel in initial caries proceed cavitation and occur with- enamel caries is not seen in all lesions, but when it is out apparent break in the enamel surface. present it lies at the advancing front of the lesion and isChapter-30.indd 331 6/1/2011 6:17:46 PM
  • 12. 332 PREVENTIVE DENTISTRY Zone 3: body of the lesion. The body of the lesion comprises the largest proportion of carious enamel in the small lesion. This zone lies superficial to dark zone and deep to the relatively unaffected surface layer of the lesion. The maximum amount of mineral loss is found in Plaque this zone. In longitudinal section with quinoline in polar- ized light microscopy, the area appears translucent and Demineralized zone Translucent zone the stria of Retzius may be well marked. When examined in ground section in water, the water molecules enter the pores in the tissue and since the refractive index of water A (1.3) is different to that of enamel (1.62), the area appears dark. The pore volume of this region is 5% at its periphery, increasing to 25% or more in the centre. Zone 4: surface zone. The surface layer ranges between 30–100 mm thick and it is thinner in active lesions and thicker in inactive carious lesions. This zone is most clearly seen in polarized light microscope when the sec- tion is in water, where it appears as a relatively unaffected area superficial to the body of the lesion. The zone has a pore volume of 1% but if the lesion progresses, the surface layer is eventually destroyed and a cavity forms. B FIGURE 30-20 Microscopic changes of initial caries. DENTINAL CARIES the first recognizable alteration from the normal enamel. It is more porous than sound enamel, the pores having Macroscopic Changes of Dentin been created by the demineralization process. Sound Dentin is the hard portion of the tooth that is covered by enamel has a pore volume of about 0.1%, the translucent enamel on the crown and cementum on the root. The zone, however, has a pore volume of approximately 1%. development and progression of caries in dentin is dif- The pores are probably located at junctional sites such ferent from progression in the overlying enamel because as prism borders, cross-striations or along the striae of of structural differences of dentin. Dentin contains much Retzius. less mineral and possesses microscopic tubules that pro- Once these areas are filled with quinoline, structural vide the pathway for the ingress of acids and egress of markings are lost, due to penetration of the quinoline, mineral. The dentinoenamel junction (DEJ) has the least which has an identical refractive index to that of enamel resistance to caries attack, hence allows for rapid lateral apatite giving translucent appearance. spreading once caries has penetrated the enamel. Because Zone 2: dark zone. The dark zone is the most com- of this characteristics, dentinal caries is ‘V’ shaped or mon feature of the carious lesion and it is the 2nd zone cone shaped in cross-section with a wide base at the DEJ of alteration from normal enamel. It lies just superficial and the apex directed pulpally. to the translucent zone and appears dark when the ground section is placed in quinoline. This zone is more Defence Reactions of Pulp-Dentin porous than translucent zone, with a pore volume of Complex 2–4%. It is shown that in this zone the pores are of varying Histopathology. Caries advances more rapidly in den- sizes, large and small. Quinoline is a large molecule and tin than in enamel because dentin provides much less resis- cannot enter the small pores, which remain filled with tance to acid attack because of less mineralized content. air, giving a dark appearance. Caries in dentin produces variety of responses including These small pores could represent areas of repair sensitivity, pain, demineralization and remineralization. where mineral has been re-deposited or they may have Episodes of short duration pain may be felt occasion- been created by demineralization that is by an opening ally during earlier stages of dentin caries. These pains up of sites not previously attacked. are due to stimulation of pulp tissue by movement ofChapter-30.indd 332 6/1/2011 6:17:47 PM
  • 13. DENTAL CARIES 333 fluid through dentinal tubules that have been exposed to the oral environment by cavitation. Once bacterial inva- sion of dentin is near to the pulp, toxins and few bacteria enter the pulp resulting in inflammation of the pulpal tissue. Initial pulpal inflammation is thought to be evident clinically by production of sharp pain (for few seconds) in response to a thermal stimulus. The degree of inflam- matory response depends on the rapidity of caries. If den- tinal sclerosis occurs, injurious agents will have reduced or no access to the pulp attack. The pulp-dentin complex reacts to caries attack by attempting to initiate remineralization and blocking off the open tissues. This reaction results from odonto-blastic activity. The dentin can react defensively through repair FIGURE 30-21 Sclerosis dentin. to low and moderate intensity caries attack as long as pulp remains vital and has an adequate blood supply. In The pulp may be irritated sufficiently from high acid levels slowly advancing caries vital pulp can repair demineral- or bacterial enzyme production to cause the formation of ised dentin by remineralization of the intertubular dentin replacement odontoblasts (secondary odontoblasts). and by opposition of peritubular dentin. Dentin responds to the stimulus of its caries deminer- alization episode by deposition of crystalline material Reactionary Dentin (Reparative Dentin) in both the lumen of tubules and intertubular dentin of Reactionary dentin is a layer of dentin formed at the affected dentin in front of the infected dentin portion of interference between the dentin and pulp. It is formed in the lesion. These hypermineralised or repaired areas may response to stimulus acting further peripherally and its be seen as zones of increased porosity in radiographs. distribution is limited to the area beneath the stimulus. It A short painful response to cold suggests reversible provides extra protection for the odontoblasts and other pulpitis or pulpal hyperaemia. When the pulp becomes cells of the pulp by increasing the distance between them more severely inflamed, thermal stimulus will produce and the injurious stimulus (Figs 30.22A, B). pain even after termination of stimulus typically for These cells produce repairable dentin (reactionary longer duration. This suggests irreversible pulpitis and dentin) on affected portion of the pulpal wall. Reparative the pulp is unlikely to recover even after removing caries. dentin is very effective barrier to diffusion of material In such situations, pulp extirpation and root canal treat- through the tubules and is an important step in dentin ment are necessary. repair. The success of dentinal reparative responses, either by remineralization of intertubular dentin and opposition Tubular Sclerosis within the Dentin of peritubular dentin or by reparative dentin, depends on the severity of caries attack and ability of the pulp to Tubular sclerosis within the dentin is a process in which respond. The blood supply of the pulp could be the most minerals are deposited within the lumina of the dentinal important limiting factor to the pulpal responses. tubules. It is also called translucent zone. It represents an area of increased mineral content. Dentin which has more mineral content than normal Inflammation of Pulp dentin is termed as ‘sclerotic dentin’ (Fig. 30.21). Sclerotic The third level of dentinal response is severe irritation, dentin formation occurs ahead of the demineralization like Acute and rapidly advancing caries with very high front of a slowly advancing lesion and may be seen under levels of acid production, overpowers dentinal responses an old restoration. Sclerotic dentin is usually shiny and dis- and results in infection, abscess and death of the pulp. coloured but feels hard to the explorer’s tip (Fig. 30.20). The inflammation of the pulp is called pulpitis. It may be More intense caries activity results in bacterial invasion acute or chronic, and it is the vascular response of the of the dentin. The infected dentin contains a wide variety pulp tissue to injury. of pathogenic materials, including high levels of acids, hydrolytic enzymes, bacteria and bacterial cellular debris. Zones of Dentinal Caries This material can cause degeneration and death of the odontoblasts as well as mild inflammation of the pulp. Zone 1: Normal dentin. The deepest area is normal These dead empty tubules are termed as ‘dead tracts’. dentin, which has tubules with odontoblastic processChapter-30.indd 333 6/1/2011 6:17:48 PM
  • 14. 334 PREVENTIVE DENTISTRY of the intertubular dentin. Thus, this region remains capable of self-repair provided the pulp remains vital. Zone 4: Turbid dentin. Turbid dentin is the zone of bacterial invasion and is marked by widening and dis- tortion of the dentinal tubules, which are filled with bacteria. Less mineral is present in this zone and colla- gen in this zone will not self-repair. This zone cannot be remineralized and must be removed before restoration. Zone 5: Infected dentin. The outermost zone, pro- tected dentin, consists of decomposed dentin that is teem- ing with bacteria. There is no recognizable structure to the dentin, and collagen and mineral seem to be absent. A Removal of infected dentin is essential to sound, suc- cessful restorative procedures as well as prevention of Crack (artefact) Primary dentin spreading the infection. Reactive dentin Advanced Carious Lesions Caries advancement in dentin proceeds through three Secondary dentin changes: Pulp tissue I. Weak organic acid demineralizes the dentin II. The organic material of the dentin, particularly col- lagen, degenerates and dissolves III. The loss of structural integrity is followed by inva- sion of bacteria. Increasing frequent demineralization of the body of the enamel lesion over a period of time results in weak- ening and eventual collapse of the surface covering. This B results in cavitation and provides an even more protec- tive and retentive zone for the cariogenic plaque, thus FIGURE 30-22 Reactionary dentin. helps in accelerating the caries progression. Affected Dentin: This is softened, demineralised dentin that is not yet invaded by bacteria (zones 2 and 3). It is that are smooth and no crystals are in the lumen. There vital and no need to remove this dentin as it can be are no bacteria in the tubules. Stimulation of dentin by repaired. osmotic gradient (from applied sucrose or salt), a bur, Infected Dentin: This is both softened and contami- a dragging instrument or desiccation from heat or air, nated with bacteria and dead (zones 4 and 5). It includes produces a sharp pain. the superficial granular necrotic tissue, soft dry and leathery dentin. Zone 2: Subtransparent dentin (zone of deminer- The zone of decomposed dentin (outer carious dentin) alization). Subtransparent zone is seen next to normal is soft infected dentin, which cannot be remineralized and dentin. This is the zone of demineralization of the inter- must be removed during cavity preparation. There is evi- tubular dentin and initial formation of very fine crystals dence that collagen fibres in the outer layer are irrevers- in the tubular lumen at the advancing front. There are no ibly denatured. In the outer carious dentin, the crosslinks bacterial area found in this zone also. The dentin in this decrease markedly and these biochemical findings sug- zone is capable of remineralization. gest that remineralization can occur only in the inner Zone 3: Transparent dentin. This zone of carious carious dentin where the collagen denaturation is revers- dentin is softer than normal dentin and shows further ible depending on pH. Collagen fibres are believed to be loss of mineral from the intertubular dentin. No bacteria important in the remineralization of carious dentin. are present in this zone either. Stimulation of this region The inner layer of carious dentin although partially sof- produces pain. Collagen (organic) content of the dentin tened by demineralization contains only few bacteria, and is intact, which serves as a template for remineralization should be preserved, because it can be remineralized.Chapter-30.indd 334 6/1/2011 6:17:48 PM
  • 15. DENTAL CARIES 335 rats did not develop caries when fed cariogenic diet. The ROOT CARIES transmissible nature of the disease in humans was dem- onstrated by the experiments of Keye’s, who showed that Recession of gingival margin is an inevitable reason for previously caries inactive hamsters developed caries after poor oral hygiene and loss of periodontal attachment, contact with caries active animals. with age. Gingival recession is a prerequisite for expo- Acidogenic (acid producing) bacteria along with met- sure of a root surface. It is commonly seen in older peo- abolic acids must be present to develop caries. Dental ple. Bacteria seem to penetrate into the tissue at an plaque fulfills both of these functions. Of the 200–300 spe- earlier stage in root caries than in coronal caries. The cies of microorganisms inhabited in the plaque, the great cemento-enamel junction is highly irregular and repre- majority are not directly involved in the caries process. sents a particular bacterial retention site and majority of Two bacterial genera of special interest in cariogenesis root caries lesions develops at this site. It is claimed that are: (i) mutans streptococci, and (ii) lactobacilli. root surface caries may occur within a deep periodontal pocket and lesion may be hidden in the pocket. Like Mutans streptococci and caries. The mutans strepto- enamel lesions, root surface caries lesions may be classi- cocci (MS) are a group of bacterial species previously con- fied as active or arrested. Root lesions are very vulnera- sidered to be serotypes of the single species, Streptococcus ble to mechanical damage and probing should be mutans. avoided. Early diagnosis of such lesions is important Main reasons for Streptococcus mutans (MS) to be con- because active lesions may become arrested following sidered as a causative agent for dental caries are: improved plaque control, use of fluoride toothpaste, and 1. Ability to stick to tooth surfaces and production of care with diet. abundant quantity of insoluble extracellular poly- saccharides from sucrose Risk Factors for Root Caries 2. Their ability to produce organic acid (lactic acid) from a number of sugar substrates The integrity of the periodontium as age advances, on 3. Ability to resist aciduric and acidogenic environment account of degenerative changes, starts declining. And because of phosphoenolpyruvate- phosphotrans- also the efficiency of the oral hygiene exercise by the older ferase mechanism people is poor. There are drastic changes in the salivary 4. Production of intracellular polysaccharide, which composition and flow rate this, in turn, affect natural acts as a reserve substrate for bacteria. cleansing effect and protective properties of the saliva. This, sometimes, may get influenced and precipitated These cariogenic features help MS to survive even in by medication due to chronic systemic illnesses in older an unfriendly environment under the condition with or people. Hence all these factors might act as a risk factors without sugar substrate, i.e. during the cycles of either directly or indirectly contributing for development of root very low concentration of sugars (between meals) through caries in older people. to periods of excessive concentration of sugars. The by- The risk factors for root caries are: products of metabolism of sugars, acids are pumped out of the bacterial cells into plaque fluids. The damage 1. Age caused by MS is mainly due to lactic acid although other 2. Gender acids such as butyric and propionic present within the 3. Fluoride exposure plaque. Thus, S. mutans is the most common of the human 4. Systemic illness MS and has the greatest evidence implicating it as the 5. Medication most virulent odontopathogen in the aetiology of dental 6. Oral hygiene caries. 7. Diet 8. Salivary changes. Other Microbial Agents Responsible for Caries MICROBIOLOGY OF DENTAL CARIES 1. Streptococcus sobrinus: It differs from S. mutans in that it requires sucrose for attachment and growth in the Cariogenic Bacteria plaque. It differs from S. mutans in that it lacks the Importance of bacteria for the initiation of dental caries adhesin required for sucrose-independent attachment was proved in animal experiment by Orland and colleagues and therefore only accumulates on smooth surfaces in in 1954. This was clearly demonstrated that germ free the presence of sucrose rich diet.Chapter-30.indd 335 6/1/2011 6:17:51 PM
  • 16. 336 PREVENTIVE DENTISTRY 2. Lactobacilli: Lactobacillus helps in progression of sucrose. Thus, the presence of insoluble glucans is an dental caries and it is aciduric and acidogenic in nature. important factor in establishing the presence and viru- It is considered as essential acidogenic bacteria causing lence of an organism. One of the key enzymes in conver- caries. Lactobacillus species have been shown that their sion of glucose moiety of sucrose to glucan is numbers are so low so as to be incapable of producing glucosyltransferase. Sometimes the enzyme may be range of pH values required for caries initiation. They altered resulting in the production of soluble glucan that have been shown to colonize white spot lesions before does not support adherence to the tooth surface. These cavitation. Thus, as a general rule, they have been asso- mutant strains lacking the insoluble glucan are usually ciated in lesion development. They are also found in non-cariogenic. greater numbers in the more advanced smooth surface The effect of sucrose dependency for production of lesions. This is seen following irradiation for head and glucans is seen in several clinical conditions. Children neck cancers, wherein extensive, multiple carious lesions who consume little or no sucrose, because of sucrose or develop rapidly because of destruction of the salivary fructose enzyme deficiencies, have a less cariogenic glands. During the initial phases of the development of plaque. Similarly those individuals receiving long-term carious lesions, more number of S. mutans appear, only to nourishment via stomach tube have less plaque and very decrease in number as Lactobacillus population increases. fewer S. mutans. The individuals restricting their sucrose Thus, S. mutans are implicated in the initiation of the intake have a decreased proportion of S. mutans in the lesion and Lactobacillus (specifically L. casei) associated plaque. However, S. mutans number increases when with progression. Other bacteria particularly Actinomyces sucrose is re-introduced into the diet. At the same time, (A. odontolyticus) have also been associated with lesion sugar restriction has an influence to reduce the acido- progression including root surface caries. genicity of dental plaque. And also S. mutans decrease in number, as teeth are lost throughout life and particularly disappear following full mouth extraction. MECHANISM OF ADHERENCE OF MICROORGANISMS TO TOOTH SURFACE FORMATION OF PLAQUE Adherence by S. mutans to the tooth surface is necessary The initial colonization of microorganisms on the tooth both before and after colonization. At first bacteria must surface probably begins with organisms other than have to establish a strong foothold on the tooth surface Streptococcus mutans. The mechanism of initial coloniza- and maintain their positions while continuing to colo- tion includes (Fig. 30.23): nize in protected areas provided by the interproximal 1. Adherence of bacteria to pellicle or the enamel space along the gingiva or in the regions of pit and fis- surface sures. Otherwise, they would be swept away by the sali- 2. Adhesion between bacteria of the same or different vary flow. species Mutans streptococci are able to attach to the tooth 3. Subsequent growth of bacteria from small enamel surface by two mechanisms: defects and from cells initially attached to the tooth i. Sucrose-independent adsorption: In this, the bacteria surface. attach to the acquired pellicle through specific extra- The plaque formation continues with the formation of cellular proteins (adhering) located on the fimbriae extracellular polysaccharide chains via the breakdown of these organisms. of sucrose to glucose and fructose. The chains of glu- ii. Sucrose-dependent mechanisms: In this bacteria require cose are called glucans and those of fructose are called the presence of sucrose to produce sticky extracel- fructans. These extracellular polysaccharides are sticky, lular polysaccharides or glucans, which allow gelatinous substances that further enhance the bacterial attachment and accumulation. ability to adhere to the tooth and to each other. They also Sucrose is a disaccharide sugar, consisting of one glu- affect the rate at which saliva can enter the plaque to cose and fructose unit (referred to as moieties) joined by buffer the acids and reverse the demineralization proc- a disaccharide bond. Streptococcus sobrinus differs from ess. This leads to further accumulation of acids at the S. mutans in that it lacks the adhesion required for sucrose- tooth-plaque interface and when sufficient amount of independent attachment, and therefore it accumulates acids are produced, there will be a drop in pH of plaque only on smooth surfaces in the presence of diet with to critical level.Chapter-30.indd 336 6/1/2011 6:17:52 PM
  • 17. DENTAL CARIES 337 Flow rate Saliva Bacteria Tooth Flora Composition Enamel surface pH Caries Saliva Saliva Substrate Receptor on enamal surface Buffering capacity FIGURE 30-23 Mechanism of initial colonization of FIGURE 30-24 Diagrammatic representation of plaque. important role of saliva with other primary factors in caries aetiology. The quantity of plaque that forms on clean tooth sur- The composition of saliva and velocity of the salivary faces during a given time represents the net result of film can play a significant role in maintaining the integrity interactions among aetiologic factors, many internal and of the tooth tissues as teeth are bathed in saliva (direct external risk factors, and protective factors: contact) constantly. Saliva has many functions: cleansing effect, buffering capacity, providing an environment 1. The total oral bacterial population saturated with calcium and phosphate and antibacterial 2. The quantity of the oral bacterial flora action. These properties and characteristics of saliva influ- 3. The anatomy and surface morphology of the dentition ence either progression or halting of carious process. 4. The wettability and surface tension of the tooth However important role saliva may play in dental caries, surfaces it is not a prerequisite for caries initiation in the same 5. The salivary secretion rate and other properties of sense that microorganisms, substrate (sucrose) and tooth saliva (host) are essential (Fig. 30.24). 6. The intake of fermentable carbohydrates Saliva-acquired components in the pellicle include 7. The mobility of the tongue and lips cystatins, histatins, lysozyme, amylase, lactoferrin, lac- 8. The exposure to chewing forces and abrasion from toperoxidase, secretory immunoglobulin A and bacteria foods derived glucosyl transferase (GTF). These saliva-derived 9. The eruption stage of the teeth components attempt to negate deleterious by products 10. The degree of gingival inflammation and volume of of bacterial metabolism in the dental biofilm. gingival exudate 11. The individual oral hygiene habits 1. The buffering effect of saliva is based mainly on 12. The use of fluorides and other preventive products, bicarbonate, carbonic acid and phosphate buffer such as chemical plaque control agents. systems. 2. Lysozyme, a hydrolytic enzyme, lactoperoxidase, hemoprotein enzyme are present in saliva which ROLE OF SALIVA IN DENTAL CARIES play a role in the prevention of bacterial colonization on tooth surface. 3. Lysozyme disrupts bacterial cell wall and leads to Biological Role of Saliva bacteriolysis. Lactoferrin binds iron, sequestering iron Saliva is also called ‘liquid enamel’ as it is a rich source away from bacteria and inhibits bacterial growth by of various minerals. Its pH is in the range of 6.9–7.2. both iron dependent and independent mechanisms.Chapter-30.indd 337 6/1/2011 6:17:52 PM
  • 18. 338 PREVENTIVE DENTISTRY Iron is an essential element for bacterial metabolism. When a relatively soluble calcium phosphate mineral Lactoperoxidase inhibits glucose metabolism. This dissolves and equilibrium is attained with that mineral, peroxidase protects salivary glycoprotein from degra- the solution is often then supersaturated with respect to a dation due to bacteria. less soluble calcium phosphate, which tends to precipitate 4. Several of the proteins like statherin, protein rich if suitable site is present. If under the influence of plaque- glycoprotein bind to and protect hydroxyapapatite. cariogenic activity, a small amount of high carbonate, low (HAP). These proteins also promote supersaturation fluoride mineral of enamel dissolves then the enamel of calcium phosphate ions in the fluid phase of the fluid at that site will be supersaturated with respect to dental biofilm. low carbonate and/or high fluoride hydroxyapatite. 5. The most prominent antibody found in the saliva is It is likely that hydroxyapatite crystals in the developing the SIgA, which reflects the lifetime caries experience lesion will only be partly dissolved, and it may attempt of the individual and may not have a protective to regrow using the remains of the original crystal as a function. template. Thus, the repaired section will contain less car- 6. Rapid flow of highly buffered, mobile saliva reduces bonate and will be less soluble and therefore much more the fall in plaque pH. Thus less caries is associated resistant to future dissolution events. At the same time, with the rapid flow of saliva. fluoride ions in solution (from the saliva) are likely to be 7. Low viscosity is also associated with low caries activ- incorporated so that repaired section will be not only ity due to rapid clearance of sugar from the oral lower in carbonate but richer in fluoride. cavity. Buffering Power of Saliva CONCLUSION Dental caries is a multifactorial disease of bacterial ori- Diffusion of inorganic buffers from the saliva into the gin. For caries to occur, three factors must be present dental plaque plays an important part in reducing the simultaneously along with time factor. They are suscep- effect of acids produced by the bacteria. Bicarbonates are tible tooth surface, cariogenic bacteria, and sucrose con- the most important buffers of saliva. Phosphates also taining dietary factors. Caries is an infectious disease play some part. Proteins can be disregarded as buffers. caused by cariogenic plaque formation on the tooth Buffers work by converting any highly ionized acids or which causes demineralization of the tooth. Saliva is alkalis, which tend to alter the pH of the solution into very important in the caries process. The protective more weakly ionized substance. Bicarbonates release the mechanisms of saliva include buffering actions, antimi- weak carbonic acid when an acid is added and since this crobial actions and remineralization. The development acid is rapidly decomposed into water and carbon dioxide, of carious lesion depends on structural factors of the which leave the solution. The result is not the accumula- tooth and also environmental factors. Thus, the mecha- tion of a weaker acid but complete removal of acid. nism of caries process is relatively complex either in the Despite these buffering systems, it is clear that acid enamel, dentin or cementum. formation potential of plaque is such that, when con- fronted with sufficient fermentable carbohydrate, the buffers are overcome within minutes. The damage done REVIEW QUESTIONS to the tooth surface is caused by the intense localized production of acids by bacteria, which breakdown the 1. Define dental caries and discuss the early theories of buffers and lead to dissolution of tooth minerals. caries aetiology. 2. Classify dental caries. Discuss each type of dental caries. Saliva contains considerable amounts of calcium and 3. Discuss the role of plaque in dental caries. phosphate and is nearly always supersaturated with 4. Discuss the role of microbial agents responsible for respect to enamel mineral and other biological appetites. caries. In parotid secretion, both pH and calcium concentration 5. Write short notes on: increase with increasing flow rate, so that the ion activity a. Keyes circle product increases with increasing flow rate. Most impor- b. Root caries tantly, unstimulated whole saliva is supersaturated with c. Buffering capacity of saliva d. Rampant caries respect to hydroxyapatite and the level increases when e. Nursing caries the flow rate is stimulated. It is clear that enamel mineral f. Radiation caries does not dissolve in saliva under normal conditions, pro- g. Hidden caries vided it is not acidified with dietary, gastric or medicinal h. Microbial flora of cariogenic plaque acids.Chapter-30.indd 338 6/1/2011 6:17:52 PM
  • 19. DENTAL CARIES 339 5. Holmen L, Thylstrup A, Ogaard B, Kragh F A scanning electron . REFERENCES microscopic study of progressive stages of enamel caries in vivo. 1. Artrun J, Thylstrup A. Clinical and scanning electron micro- Caries Res 19: 355–67, 1985. scopic study of surface changes of incipient enamel caries 6. Johnson NW. Some aspects of the ultra structure of early lesions after debonding. Scand J Dent Res 94: 193–210, human enamel caries seen with the electron microscope. Arch 1986. Oral Biol 12: 1505–21, 1967. 2. Caravalho JC, Ekstrand KR, Thylstrup A. Dental plaque and 7. Larsen MJ, Fejerskov O. Chemical and structural challenges in caries on occlusal surfaces of first permanent molars in relation remineralization of the dental enamel lesions. Scan J Dent Res to stage of eruption. J Dent Res 68: 773–9, 1989. 97: 285–96, 1989. 3. Daculci G, Legerous KZ, Jean A, Kerbel B. Possible physico- 8. Nyvad B, Fejerskov O. Active and inactive root surface caries— chemical process in human dentin caries. J Dent Res 66: structural entities? In Thylstrup A, Leach SA, Qvist V (eds). 1356–9, 1987. Dentine and Dentin Reactions in the Oral Cavity. IRL Press, 4. Fejerskov O, Baelum V, Ostergaard ES. Root caries in Scandinavia Oxford 165–79, 1987. in the 1980 and future trend to be expected in dental caries 9. Thylstrup A, Fejerskov O. Textbook of Clinical Cariology (2nd experience in adults. Adv Dent Res 7: 4–14, 1993. edn). Munksgaard, Copenhagen, 1994.Chapter-30.indd 339 6/1/2011 6:17:52 PM