C H APT E R

30

Dental Caries
SS Hiremath
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

CHAPTER OUTLINE
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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

INTRODUCTION
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 cavitationcaries 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.

Definition
Dental caries is an infectious microbial disease that begins as demineralization of inorganic portion of tooth,

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followed by destruction of organic portions, leading to cavity formation. 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.

Parasitic or Septic Theory

Parasitic or septic theory was given by Erdl (1843). According to this theory, dental caries was caused by filamentous parasites present in the surface membrane (plaque?) of teeth. Later, Ficinus, observed filamentous microorganisms, which he called denticolae in material taken from carious cavities.

EARLY THEORIES OF CARIES AETIOLOGY Worm Theory

According to an ancient Sumerian test, toothache was caused by a worm that drank the blood of the teeth and fed on the roots of the jaws. Guy de Cahuliac, the greatest Surgeon of the middle Ages believed that worming caused dental decay. As a cure he advocated fumigation with seeds of leech, onion and hyoscyamus.

Vital Theory
The vital theory regarded dental caries as originating within the tooth itself, analogous to bone gangrene. A clinically well-known type of caries is characterized by extensive penetration into the dentin, and even into the pulp, but with a barely detectable catch in the fissure.

Chemical Theory
Chemical theory was given by Parmly (1819). According to this theory, dental caries was caused by unidentified chemical agent. He stated that caries begin on the enamel surface in locations, where food putrefied and acquired sufficient dissolving power to produce the disease chemically.

Humour Theory
Ancient Greeks considered that relative proportions of four elementary fluids of the body determined a persons physical and mental constitution: (i) blood, (ii) phlegm, (iii) black bile, and (iv) yellow bile. These four fluids corresponds to the four humours: (i) phlegmatic, (ii) choleric (iii) sanguine, and (iv) melancholic (Fig. 30.1). All diseases including caries were explained by an imbalance of these humours.

Chemoparasitic Theory
Chemoparasitic theory is the most accepted theory for 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.

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Miller in 1890. In a series of experiments it was demonstrated that: 1. Acid was present within the deeper carious lesion, as shown by reaction on litmus paper. 2. Different kinds of foods (breads, sugar, but not meat) when mixed with saliva and incubated at 37C could decalcify the entire crown of the tooth. 3. Several types of mouth bacteria (at least 30 species are isolated) could produce enough acid to cause dental caries. 4. Lactic acid was an identifiable product in carbohydratesaliva, incubation mixtures. 5. Different microorganisms (filamentous, long and short bacilli and micrococci) invade carious dentin. Miller concluded that no single species of microorganism caused caries, but rather the process was mediated by oral microorganisms capable of producing acid and digesting protein.

meaning claw, and refers to compounds that are able to bind metallic ions such as calcium, iron, copper, zinc and other metals, by the secondary valence bonds.

CURRENT CONCEPTS OF CARIES AETIOLOGY

Caries is multifactorial disease mainly consisting of three parameters most commonly contributing for the initiation of dental caries namely, host factor (susceptible tooth surface), microorganism (Streptococcus mutans), and diet (sucrose), however the interplay between these factors has to take place in an appropriate time. 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). This factor has been added to emphasize the importance of time factor in the origin of the disease along with other three primary factors. Hence current concept of the aetiology of dental caries includes these important four factors as described in Keyes circle (Figs 30.230.4). There are various subfactors or cofactors contributing directly or indirectly in initiation of dental caries.

Critique of Chemoparasitic Theory

1. Millers chemoparasitic theory is unable to explain the predilection of specific sites on a tooth to dental caries. 2. The phenomenon of arrested caries is not explained by the chemoparasitic theory. 3. Millers theory does not explain why some populations are caries-free.

Keyes Circles
A carious lesion should be regarded not as a disease entity, but as tissue damage or a wound caused by the disease dental caries. The interaction of saliva, bacteria and microbial products in the production of biofilms on the tooth surface is an important factor to initiate dental caries. The susceptible host, cariogenic oral microbial flora and fermentable carbohydrate are important in the development of dental caries and they have been depicted through Keyes circles (Figs 30.3A, B). Each one of them is of equal importance in aetiology of the disease. However there are many secondary factors that either influence the progression or regression of dental caries (Fig. 30.4). Caries progression occurs when the demineralization and remineralization equilibrium is out of balance, leading to net mineral loss. Remineralization can arrest or reverse progression of disease and can lead to changes in mineral quality; 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. 1. Lesion detection: Implies an objective method of determining whether or not disease is present.

Proteolytic Theory
Proteolytic theory was given by Gottlieb in 1944. This theory suggested that the initial action was due to proteolylic enzymes attacking the lamellae, rod sheaths, tufts and walls of the dentinal tubules. Later a coccus, probably Staphylococcus aureus, was involved because of the yellow pigmentation that he considered pathognomonic of dental caries. Frisbie (1944) also described caries as a proteolytic process involving depolymerization and liquefaction of the organic matrix of enamel. Pincus (1949) contended that proteolytic organisms first attacked the protein elements, such as dental cuticle and then destroyed the prism sheaths.

ProteolysisChelation Theory
Proteolysischelation theory was proposed by Schatz et al (1955). It implies a simultaneous microbial degradation of the organic components (proteolysis), and dissolution of minerals of the tooth by the process of chelation. The word chelate is derived from the Greek chele

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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. from initial loss of mineral at the ultra structural level to total destruction of the tooth. However, caries lesion development is a highly dynamic process with alternating periods of progression and arrest/regression. Lesion progression may be arrested at any stage of lesion development, even at the stage of frank cavitation, provided the local environmental conditions, e.g. biofilm control and topical fluoride exposure, are favourable. Hence, the clinical stages of caries represent nothing but historical signs of the past caries experience. 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. Metabolic processes

2. Lesion assessment: Aims to characterize or monitor a lesion, once it has been detected. 3. Caries diagnosis: Implies a human, professional, summation of all available data. It is now appreciated that caries is initially reversible, chronic, disease process with known multifactorial aetiology. Dental caries progresses slowly in most of the individuals as chronic disease. The disease is seldom selflimiting and in the absence of treatment, a caries progress until the tooth is destroyed. The localized destruction of the hard tissues, often referred as the lesion, is the sign or symptom of the disease (Fezejerskov et al 2008). Lesion progression is often depicted on a linear scale ranging

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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

FIGURE 30-3

Keyes Circlecurrent concept of caries aetiology.

Microorganisms Strep. 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, 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).

are constantly taking place in the dental plaque as a result of microbial activity, and this is reflected by continuous, rapid fluctuations in plaque pH, both when the plaque is starved and fed. Hence, 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. The key point is, when the cumulative result of the de- and remineralization process is loss of mineral, caries lesion develop or progress. Caries lesions may be classified in various ways. Firstly, lesions can be classified according to their anatomical site and location. The lesions may be commonly found in pits and fissures, or

Classification Based on Morphology

This classification is according to anatomical site of the lesions.

Pit and Fissure Caries (Occlusal Caries)

Most common type of dental caries (Fig. 30.5). Occurs on the occlusal surfaces of molars and bicuspids.

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FIGURE 30-6

Cervical caries.

FIGURE 30-5

Pit and fissure caries.

Smooth surface caries. There are two variations of smooth surface caries. They are: (i) buccal and lingual surface 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. Proximal surfaces (interproximal) Interproximal cariesoccurring at mesial or distal contact points. Interproximal caries usually starts just cervical to the contact area (Fig. 30.7).

FIGURE 30-7

Proximal surfaces (interproximal).

Classification based on Severity and Progression

I. Rampant caries II. Early childhood caries (nursing caries) III. Radiation caries (xerostomia induced). Rampant caries. Rampant caries occurs as a sudden, rapid and almost uncontrollable destruction of teeth,

involving surfaces of teeth that are ordinarily relatively caries free (proximal and cervical surfaces of anterior teeth including the mandibular incisors get affected). A caries increment of 10 or more new lesions over a period of about a year is characteristic of a rampant caries attack (Fig. 30.8). Early childhood caries Early childhood caries is a specific form of rampant decay of the primary teeth of infants and toddlers. According to American Dental Association (ADA) it is defined as the presence of one or more decayed, missing or filled tooth surfaces in any primary tooth in a preschool age child between birth and 71 months of age.

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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. This is also named as baby bottle tooth decay. 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. 30.9). Radiation caries (xerostomia induced). This is a common complication of radiotherapy of oral cancer lesions and radiation-induced xerostomia (from the Greek, xeros = dry, stoma = mouth). Such patients develop rampant dental caries (Fig. 30.10). Xerostomia may be caused by factors other than radiation like Tumours of salivary glands Autoimmune diseases (e.g. Sjogrens syndrome)

Anti-sialagogue drugs Prolonged illness

Classification Based upon Part of Tooth Structure Involved

a. Enamel caries Incipient caries Linear enamel caries (odontoclasia) b. Dentinal caries c. Cemental caries

Enamel Caries
Incipient lesion: Incipient lesion is also called the early carious lesion. It manifests as a white, opaque region, which is best demarcated when the area is dried (Figs 30.11A, B).

FIGURE 30-10

Radiation caries.

FIGURE 30-8

Rampant caries.

Incipient lesion

A A

Incipient lesion

FIGURE 30-9

Nursing caries.

FIGURE 30-11

Incipient lesion.

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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 represents 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 hypocalcaemia associated with transient hypoparathyroidism. 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 establishes 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 a. b. c. d. Primary caries Secondary caries (recurrent caries) Residual caries Arrested caries FIGURE 30-13 Arrested caries.

FIGURE 30-12

Secondary caries.

According to World Health Organization (WHO), the shape and depth of the carious lesions can be scored on a four-point scale (D1 to D4): D1clinically detectable enamel lesions with intact (non-cavitated surfaces) D2clinically detectable cavities limited to the enamel D3clinically detectable lesions in dentin (with and without cavitation of dentin) D4lesions into pulp.

Primary caries. Primary caries is used to differentiate lesions, which develop on the healthy enamel surface or on unrestored surfaces from those that develop adjacent to a filling. Secondary caries. A carious lesion that develops at the interface of restoration and the cavosurface of the enamel is called secondary caries (Fig. 30.12). This type of caries may result from: Poor cavity preparation Ditching around an amalgam restoration A defective restoration Or a combination of these factors.

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 (5.25.5). This amount of demineralization cannot be detected clinically (they go unnoticed), however the repair process, remineralization and demineralization go hand in hand, and most of the time maintains the homeostasis (Figs 30.14, 30.15).

Residual caries. Residual caries is demineralised tissue that has been left behind before filling is placed (incomplete removal of carious dentin). Arrested 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. 30.13).

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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

The first visible clinical presentation of dental caries is referred to as white spot lesion. The clinical appearance of white spot lesion is caused by subsurface enamel demineralization, 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. White spot carious lesion does not necessarily progress to frank cavitation. In this stage, the lesion progression could be arrested or reversed by modifying any of the causative factors or application of appropriate preventive measures. Arrested lesion may retain the appearance of white spots or acquire the appearance of brown spot. The reversal of the white spot could be due to remineralization of the lesion subject to condition that surface layer is intact, and most of the time they may not progress to frank cavitation in the absence of high cariogenic challenge (Fig. 30.16). Therefore white spot can be referred as non-cavitated lesion.

subsurface to the surface and get added to the calcium and phosphate in dental plaque. Later calcium and phosphate along with fluoride from saliva and biofilm helps in the precipitation on the superficial layer on the affected surface enamel. 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. Hence there is an intact surface layer of the enamel, even though caries are progressing at subsurface level, which is not visible. Caries progressing into dentin with intact surface is not clinically diagnosed but can be detected only in radiographs. The prevalence of hidden caries ranges from 0.8 to 3%. These occult lesions are usually seen with low caries rate which is suggestive of increased fluoride exposure. Recently it has been observed that hidden caries may have origin as pre-eruptive defects, which are detectable only with the use of radiographs.

Frank Cavitation
As the carious lesion progresses the subsurface lesion increases in dimension, eventually leading to collapse of the surface layer leading to cavitation. At this stage of carious process, tooth destruction progresses more rapidly because cavitation favours plaque accumulation and reduced salivary access.

Hidden or Occult Caries

During the cariogenic challenge on account of fall of pH to a critical level, demineralization commences on the subsurface. Calcium and phosphate ions move from

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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.

The progression of the carious lesion is variable, 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 estimated to be 18 months plus or minus 6 months. The peak rate for the incidence of the new lesions occurs 3 years after the eruption of the tooth. Occlusal pit and fissure lesions develop in less time than smooth surface caries lesion. Both poor oral hygiene and frequent exposure to sucrose containing diet can produce incipient lesions in as early as 3 weeks. Radiation-induced xerostomia (dry mouth) can lead to clinical caries development as little as 3 months from the onset of the radiation. Thus, caries development and progression in healthy individuals is usually slow in comparison among compromised persons.

CARIES OF ENAMEL Macroscopic Changes of Enamel

On smooth surfaces. On smooth enamel surfaces, the earliest visible changes are usually manifested as a loss of translucency, resulting in an opaque chalky white lesion in location where caries progressed most probably are becoming arrested, discoloured pigmentation of the enamel may be seen. Smooth surface lesions when sectioned longitudinally are cone shaped with the apex directed towards the dentin (Figs 30.17, 30.18). Pit and fissure caries. Occlusal fissures are deep invagination of enamel, they can be extremely diverse in shape and size and have been shown as broad or narrow funnels, constricted hour glasses, multiple invaginations with inverted shape. Classification of fissure morphology is as follows (see Fig. 39.1): a. Y-shaped divisions (510%). b. V type-wide at top and gradually narrowing towards the bottom (3035%). c. U type, almost the same width from top to bottom (1215%). d. I type, and extremely narrow slit (1820%). e. IK type, extremely narrow slit with a larger space at bottom (2426%). f. Other types (79%). 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. Once the open carious lesion becomes self-cleansing, with improved oral hygiene measures, restricted intake of refined sugars and use of fluorides, the carious process is arrested and dentin becomes hard. The boundaries of caries diagnosis and caries intervention are changing dramatically. Using emerging technology we should be able to detect clinically the incipient dental caries lesion earlier. Thus, dental caries is a damaging process, which in its early stages is reversible and even in its more advanced stages, can be arrested.

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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.

FIGURE 30-18

Smooth surface caries.

FIGURE 30-19 Longitudinal sectional view of pit and fissure caries.

is not always possible to classify a tooth as having a particular type occlusal morphology. Frequently, fissures having a broad base give rise to several pits, which when sectioned, look like inverted Ys. Many teeth have areas at the base of the fissures where a very thin enamel covers underlying dentin. Carious lesion more often starts at both sides of the fissure wall rather than at the base, penetrating nearly perpendicularly towards the dentinoenamel junction. In newly erupted teeth, brown stain or discoloured lesion is indicative of underlying decay, whereas in older individuals the lesions may be arrested or remineralised areas. This lesion is commonly described as cone shaped with the base directed towards the dentin and apex towards the enamel surface. Later these macroscopic changes of the enamel in initial caries proceed cavitation and occur without apparent break in the enamel surface.

Microscopic Changes of Carious Enamel

Under microscope, the enamel caries (initial caries) shows four zones, starting from the inner advancing front of the lesion. The zones are: 1. 2. 3. 4. Translucent zone Dark zone Body of the lesion Surface layer.

There is no sudden or dramatic change from zone to zone but there is a gradual series of changes within the lesion (Figs 30.20A, B). Furthermore, all zones may not be visible by polarized light microscopy. Zone 1: translucent zone. 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

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Plaque Demineralized zone Translucent zone

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 this zone. In longitudinal section with quinoline in polarized light microscopy, the area appears translucent and 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 (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 30100 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 section 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.

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 been created by the demineralization process. Sound enamel has a pore volume of about 0.1%, the translucent zone, however, has a pore volume of approximately 1%. The pores are probably located at junctional sites such as prism borders, cross-striations or along the striae of Retzius. Once these areas are filled with quinoline, structural markings are lost, due to penetration of the quinoline, which has an identical refractive index to that of enamel apatite giving translucent appearance. Zone 2: dark zone. The dark zone is the most common feature of the carious lesion and it is the 2nd zone of alteration from normal enamel. It lies just superficial to the translucent zone and appears dark when the ground section is placed in quinoline. This zone is more porous than translucent zone, with a pore volume of 24%. It is shown that in this zone the pores are of varying sizes, large and small. Quinoline is a large molecule and cannot enter the small pores, which remain filled with air, giving a dark appearance. 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.

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. The development and progression of caries in dentin is different from progression in the overlying enamel because of structural differences of dentin. Dentin contains much less mineral and possesses microscopic tubules that provide the pathway for the ingress of acids and egress of mineral. The dentinoenamel junction (DEJ) has the least resistance to caries attack, hence allows for rapid lateral spreading once caries has penetrated the enamel. Because of this characteristics, dentinal caries is V shaped or cone shaped in cross-section with a wide base at the DEJ and the apex directed pulpally.

Defence Reactions of Pulp-Dentin Complex

Histopathology. Caries advances more rapidly in dentin than in enamel because dentin provides much less resistance to acid attack because of less mineralized content. Caries in dentin produces variety of responses including sensitivity, pain, demineralization and remineralization. Episodes of short duration pain may be felt occasionally during earlier stages of dentin caries. These pains are due to stimulation of pulp tissue by movement of

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fluid through dentinal tubules that have been exposed to the oral environment by cavitation. Once bacterial invasion 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 inflammatory response depends on the rapidity of caries. If dentinal 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 to low and moderate intensity caries attack as long as pulp remains vital and has an adequate blood supply. In slowly advancing caries vital pulp can repair demineralised dentin by remineralization of the intertubular dentin and by opposition of peritubular dentin. 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. These hypermineralised or repaired areas may be seen as zones of increased porosity in radiographs. A short painful response to cold suggests reversible pulpitis or pulpal hyperaemia. When the pulp becomes more severely inflamed, thermal stimulus will produce pain even after termination of stimulus typically for longer duration. This suggests irreversible pulpitis and the pulp is unlikely to recover even after removing caries. In such situations, pulp extirpation and root canal treatment are necessary.

FIGURE 30-21

Sclerosis dentin.

The pulp may be irritated sufficiently from high acid levels or bacterial enzyme production to cause the formation of replacement odontoblasts (secondary odontoblasts).

Reactionary Dentin (Reparative Dentin)

Reactionary dentin is a layer of dentin formed at the interference between the dentin and pulp. It is formed in response to stimulus acting further peripherally and its distribution is limited to the area beneath the stimulus. It provides extra protection for the odontoblasts and other cells of the pulp by increasing the distance between them and the injurious stimulus (Figs 30.22A, B). These cells produce repairable dentin (reactionary dentin) on affected portion of the pulpal wall. Reparative dentin is very effective barrier to diffusion of material through the tubules and is an important step in dentin repair. The success of dentinal reparative responses, either by remineralization of intertubular dentin and opposition of peritubular dentin or by reparative dentin, depends on the severity of caries attack and ability of the pulp to respond. The blood supply of the pulp could be the most important limiting factor to the pulpal responses.

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. It is also called translucent zone. It represents an area of increased mineral content. Dentin which has more mineral content than normal dentin is termed as sclerotic dentin (Fig. 30.21). Sclerotic dentin formation occurs ahead of the demineralization front of a slowly advancing lesion and may be seen under an old restoration. Sclerotic dentin is usually shiny and discoloured but feels hard to the explorers tip (Fig. 30.20). More intense caries activity results in bacterial invasion of the dentin. The infected dentin contains a wide variety of pathogenic materials, including high levels of acids, hydrolytic enzymes, bacteria and bacterial cellular debris. This material can cause degeneration and death of the odontoblasts as well as mild inflammation of the pulp. These dead empty tubules are termed as dead tracts.

Inflammation of Pulp
The third level of dentinal response is severe irritation, like Acute and rapidly advancing caries with very high levels of acid production, overpowers dentinal responses and results in infection, abscess and death of the pulp. The inflammation of the pulp is called pulpitis. It may be acute or chronic, and it is the vascular response of the pulp tissue to injury.

Zones of Dentinal Caries

Zone 1: Normal dentin. The deepest area is normal dentin, which has tubules with odontoblastic process

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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 distortion of the dentinal tubules, which are filled with bacteria. Less mineral is present in this zone and collagen 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, protected dentin, consists of decomposed dentin that is teeming with bacteria. There is no recognizable structure to the dentin, and collagen and mineral seem to be absent. Removal of infected dentin is essential to sound, successful restorative procedures as well as prevention of spreading the infection.

A Crack (artefact) Primary dentin

Reactive dentin

Advanced Carious Lesions

Secondary dentin

Caries advancement in dentin proceeds through three changes: I. Weak organic acid demineralizes the dentin II. The organic material of the dentin, particularly collagen, degenerates and dissolves III. The loss of structural integrity is followed by invasion of bacteria. 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. This results in cavitation and provides an even more protective and retentive zone for the cariogenic plaque, thus 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 vital and no need to remove this dentin as it can be repaired. Infected Dentin: This is both softened and contaminated with bacteria and dead (zones 4 and 5). It includes the superficial granular necrotic tissue, soft dry and leathery dentin. The zone of decomposed dentin (outer carious dentin) is soft infected dentin, which cannot be remineralized and must be removed during cavity preparation. There is evidence that collagen fibres in the outer layer are irreversibly denatured. In the outer carious dentin, 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. Collagen fibres are believed to be important in the remineralization of carious dentin. The inner layer of carious dentin although partially softened by demineralization contains only few bacteria, and should be preserved, because it can be remineralized.

Pulp tissue

FIGURE 30-22

Reactionary dentin.

that are smooth and no crystals are in the lumen. There are no bacteria in the tubules. Stimulation of dentin by osmotic gradient (from applied sucrose or salt), a bur, a dragging instrument or desiccation from heat or air, produces a sharp pain. Zone 2: Subtransparent dentin (zone of demineralization). Subtransparent zone is seen next to normal dentin. 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. There are no bacterial area found in this zone also. The dentin in this zone is capable of remineralization. Zone 3: Transparent dentin. This zone of carious dentin is softer than normal dentin and shows further loss of mineral from the intertubular dentin. No bacteria are present in this zone either. Stimulation of this region produces pain. Collagen (organic) content of the dentin is intact, which serves as a template for remineralization

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ROOT CARIES
Recession of gingival margin is an inevitable reason for poor oral hygiene and loss of periodontal attachment, with age. Gingival recession is a prerequisite for exposure of a root surface. It is commonly seen in older people. Bacteria seem to penetrate into the tissue at an earlier stage in root caries than in coronal caries. The cemento-enamel junction is highly irregular and represents a particular bacterial retention site and majority of root caries lesions develops at this site. It is claimed that root surface caries may occur within a deep periodontal pocket and lesion may be hidden in the pocket. Like enamel lesions, root surface caries lesions may be classified as active or arrested. Root lesions are very vulnerable to mechanical damage and probing should be avoided. Early diagnosis of such lesions is important because active lesions may become arrested following improved plaque control, use of fluoride toothpaste, and care with diet.

rats did not develop caries when fed cariogenic diet. The transmissible nature of the disease in humans was demonstrated by the experiments of Keyes, who showed that previously caries inactive hamsters developed caries after contact with caries active animals. Acidogenic (acid producing) bacteria along with metabolic acids must be present to develop caries. Dental plaque fulfills both of these functions. Of the 200300 species of microorganisms inhabited in the plaque, the great majority are not directly involved in the caries process. Two bacterial genera of special interest in cariogenesis are: (i) mutans streptococci, and (ii) lactobacilli. Mutans streptococci and caries. The mutans streptococci (MS) are a group of bacterial species previously considered to be serotypes of the single species, Streptococcus mutans. Main reasons for Streptococcus mutans (MS) to be considered as a causative agent for dental caries are: 1. Ability to stick to tooth surfaces and production of abundant quantity of insoluble extracellular polysaccharides from sucrose 2. Their ability to produce organic acid (lactic acid) from a number of sugar substrates 3. Ability to resist aciduric and acidogenic environment because of phosphoenolpyruvate- phosphotransferase mechanism 4. Production of intracellular polysaccharide, which acts as a reserve substrate for bacteria. These cariogenic features help MS to survive even in an unfriendly environment under the condition with or without sugar substrate, i.e. during the cycles of either very low concentration of sugars (between meals) through to periods of excessive concentration of sugars. The byproducts of metabolism of sugars, acids are pumped out of the bacterial cells into plaque fluids. The damage caused by MS is mainly due to lactic acid although other acids such as butyric and propionic present within the plaque. Thus, S. 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.

Risk Factors for Root Caries

The integrity of the periodontium as age advances, on account of degenerative changes, starts declining. And also the efficiency of the oral hygiene exercise by the older people is poor. There are drastic changes in the salivary composition and flow rate this, in turn, affect natural cleansing effect and protective properties of the saliva. This, sometimes, may get influenced and precipitated by medication due to chronic systemic illnesses in older people. Hence all these factors might act as a risk factors directly or indirectly contributing for development of root caries in older people. The risk factors for root caries are: 1. 2. 3. 4. 5. 6. 7. 8. Age Gender Fluoride exposure Systemic illness Medication Oral hygiene Diet Salivary changes.

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. This was clearly demonstrated that germ free

Other Microbial Agents Responsible for Caries

1. Streptococcus sobrinus: It differs from S. mutans in that it requires sucrose for attachment and growth in the plaque. It differs from S. 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.

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2. Lactobacilli: Lactobacillus helps in progression of dental caries and it is aciduric and acidogenic in nature. It is considered as essential acidogenic bacteria causing caries. 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. They have been shown to colonize white spot lesions before cavitation. Thus, as a general rule, they have been associated in lesion development. They are also found in greater numbers in the more advanced smooth surface lesions. This is seen following irradiation for head and neck cancers, wherein extensive, multiple carious lesions develop rapidly because of destruction of the salivary glands. During the initial phases of the development of carious lesions, more number of S. mutans appear, only to decrease in number as Lactobacillus population increases. Thus, S. mutans are implicated in the initiation of the lesion and Lactobacillus (specifically L. casei) associated with progression. Other bacteria particularly Actinomyces (A. odontolyticus) have also been associated with lesion progression including root surface caries.

sucrose. Thus, the presence of insoluble glucans is an important factor in establishing the presence and virulence of an organism. One of the key enzymes in conversion of glucose moiety of sucrose to glucan is glucosyltransferase. Sometimes the enzyme may be altered resulting in the production of soluble glucan that does not support adherence to the tooth surface. These mutant strains lacking the insoluble glucan are usually non-cariogenic. The effect of sucrose dependency for production of glucans is seen in several clinical conditions. Children who consume little or no sucrose, because of sucrose or fructose enzyme deficiencies, have a less cariogenic plaque. Similarly those individuals receiving long-term nourishment via stomach tube have less plaque and very fewer S. mutans. The individuals restricting their sucrose intake have a decreased proportion of S. mutans in the plaque. However, S. mutans number increases when sucrose is re-introduced into the diet. At the same time, sugar restriction has an influence to reduce the acidogenicity 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

Adherence by S. mutans to the tooth surface is necessary both before and after colonization. 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. Otherwise, they would be swept away by the salivary flow. Mutans streptococci are able to attach to the tooth surface by two mechanisms: i. Sucrose-independent adsorption: In this, the bacteria attach to the acquired pellicle through specific extracellular proteins (adhering) located on the fimbriae of these organisms. ii. Sucrose-dependent mechanisms: In this bacteria require the presence of sucrose to produce sticky extracellular polysaccharides or glucans, which allow attachment and accumulation. Sucrose is a disaccharide sugar, consisting of one glucose and fructose unit (referred to as moieties) joined by a disaccharide bond. Streptococcus sobrinus differs from S. mutans in that it lacks the adhesion required for sucroseindependent attachment, 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. The mechanism of initial colonization includes (Fig. 30.23): 1. Adherence of bacteria to pellicle or the enamel surface 2. Adhesion between bacteria of the same or different species 3. Subsequent growth of bacteria from small enamel defects and from cells initially attached to the tooth surface. The plaque formation continues with the formation of extracellular polysaccharide chains via the breakdown of sucrose to glucose and fructose. The chains of glucose are called glucans and those of fructose are called fructans. These extracellular polysaccharides are sticky, gelatinous substances that further enhance the bacterial ability to adhere to the tooth and to each other. They also affect the rate at which saliva can enter the plaque to buffer the acids and reverse the demineralization process. This leads to further accumulation of acids at the tooth-plaque interface and when sufficient amount of acids are produced, there will be a drop in pH of plaque to critical level.

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Flow rate

Saliva

Bacteria

Tooth
Enamel surface

Flora Caries

Composition

pH

Saliva

Saliva

Substrate

Receptor on enamal surface

Buffering capacity

FIGURE 30-23 plaque.

Mechanism of initial colonization of

FIGURE 30-24 Diagrammatic representation of important role of saliva with other primary factors in caries aetiology. 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. Saliva has many functions: cleansing effect, buffering capacity, providing an environment saturated with calcium and phosphate and antibacterial action. These properties and characteristics of saliva influence either progression or halting of carious process. However important role saliva may play in dental caries, it is not a prerequisite for caries initiation in the same sense that microorganisms, substrate (sucrose) and tooth (host) are essential (Fig. 30.24). Saliva-acquired components in the pellicle include cystatins, histatins, lysozyme, amylase, lactoferrin, lactoperoxidase, secretory immunoglobulin A and bacteria derived glucosyl transferase (GTF). These saliva-derived components attempt to negate deleterious by products of bacterial metabolism in the dental biofilm. 1. The buffering effect of saliva is based mainly on bicarbonate, carbonic acid and phosphate buffer systems. 2. Lysozyme, a hydrolytic enzyme, lactoperoxidase, hemoprotein enzyme are present in saliva which play a role in the prevention of bacterial colonization on tooth surface. 3. Lysozyme disrupts bacterial cell wall and leads to bacteriolysis. Lactoferrin binds iron, sequestering iron away from bacteria and inhibits bacterial growth by both iron dependent and independent mechanisms.

The quantity of plaque that forms on clean tooth surfaces during a given time represents the net result of interactions among aetiologic factors, many internal and external risk factors, 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 salivary secretion rate and other properties of saliva 6. The intake of fermentable carbohydrates 7. The mobility of the tongue and lips 8. The exposure to chewing forces and abrasion from foods 9. The eruption stage of the teeth 10. The degree of gingival inflammation and volume of gingival exudate 11. The individual oral hygiene habits 12. The use of fluorides and other preventive products, such as chemical plaque control agents. 1. 2. 3. 4.

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. Its pH is in the range of 6.97.2.

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4.

5.

6.

7.

Iron is an essential element for bacterial metabolism. Lactoperoxidase inhibits glucose metabolism. This peroxidase protects salivary glycoprotein from degradation due to bacteria. Several of the proteins like statherin, protein rich glycoprotein bind to and protect hydroxyapapatite. (HAP). These proteins also promote supersaturation of calcium phosphate ions in the fluid phase of the dental biofilm. The most prominent antibody found in the saliva is the SIgA, which reflects the lifetime caries experience of the individual and may not have a protective function. Rapid flow of highly buffered, mobile saliva reduces the fall in plaque pH. Thus less caries is associated with the rapid flow of saliva. Low viscosity is also associated with low caries activity due to rapid clearance of sugar from the oral cavity.

When a relatively soluble calcium phosphate mineral dissolves and equilibrium is attained with that mineral, the solution is often then supersaturated with respect to a less soluble calcium phosphate, which tends to precipitate if suitable site is present. If under the influence of plaquecariogenic activity, a small amount of high carbonate, 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. It is likely that hydroxyapatite crystals in the developing lesion will only be partly dissolved, and it may attempt to regrow using the remains of the original crystal as a template. Thus, the repaired section will contain less carbonate and will be less soluble and therefore much more resistant to future dissolution events. At the same time, 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.

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. Bicarbonates are the most important buffers of saliva. Phosphates also play some part. Proteins can be disregarded as buffers. Buffers work by converting any highly ionized acids or alkalis, which tend to alter the pH of the solution into more weakly ionized substance. Bicarbonates release the weak carbonic acid when an acid is added and since this acid is rapidly decomposed into water and carbon dioxide, which leave the solution. The result is not the accumulation of a weaker acid but complete removal of acid. Despite these buffering systems, it is clear that acid formation potential of plaque is such that, when confronted with sufficient fermentable carbohydrate, the buffers are overcome within minutes. The damage done to the tooth surface is caused by the intense localized production of acids by bacteria, which breakdown the buffers and lead to dissolution of tooth minerals. Saliva contains considerable amounts of calcium and phosphate and is nearly always supersaturated with respect to enamel mineral and other biological appetites. In parotid secretion, both pH and calcium concentration increase with increasing flow rate, so that the ion activity product increases with increasing flow rate. Most importantly, unstimulated whole saliva is supersaturated with respect to hydroxyapatite and the level increases when the flow rate is stimulated. It is clear that enamel mineral does not dissolve in saliva under normal conditions, provided it is not acidified with dietary, gastric or medicinal acids.

CONCLUSION
Dental caries is a multifactorial disease of bacterial origin. For caries to occur, three factors must be present simultaneously along with time factor. They are susceptible tooth surface, cariogenic bacteria, and sucrose containing dietary factors. Caries is an infectious disease caused by cariogenic plaque formation on the tooth which causes demineralization of the tooth. Saliva is very important in the caries process. The protective mechanisms of saliva include buffering actions, antimicrobial actions and remineralization. The development of carious lesion depends on structural factors of the tooth and also environmental factors. Thus, the mechanism of caries process is relatively complex either in the enamel, dentin or cementum.

REVIEW QUESTIONS
1. Define dental caries and discuss the early theories of caries aetiology. 2. Classify dental caries. Discuss each type of dental caries. 3. Discuss the role of plaque in dental caries. 4. Discuss the role of microbial agents responsible for caries. 5. Write short notes on: a. Keyes circle b. Root caries c. Buffering capacity of saliva d. Rampant caries e. Nursing caries f. Radiation caries g. Hidden caries h. Microbial flora of cariogenic plaque

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REFERENCES
1. Artrun J, Thylstrup A. Clinical and scanning electron microscopic study of surface changes of incipient enamel caries lesions after debonding. Scand J Dent Res 94: 193210, 1986. 2. Caravalho JC, Ekstrand KR, Thylstrup A. Dental plaque and caries on occlusal surfaces of first permanent molars in relation to stage of eruption. J Dent Res 68: 7739, 1989. 3. Daculci G, Legerous KZ, Jean A, Kerbel B. Possible physicochemical process in human dentin caries. J Dent Res 66: 13569, 1987. 4. Fejerskov O, Baelum V, Ostergaard ES. Root caries in Scandinavia in the 1980 and future trend to be expected in dental caries experience in adults. Adv Dent Res 7: 414, 1993.

5. Holmen L, Thylstrup A, Ogaard B, Kragh F . A scanning electron microscopic study of progressive stages of enamel caries in vivo. Caries Res 19: 35567, 1985. 6. Johnson NW. Some aspects of the ultra structure of early human enamel caries seen with the electron microscope. Arch Oral Biol 12: 150521, 1967. 7. Larsen MJ, Fejerskov O. Chemical and structural challenges in remineralization of the dental enamel lesions. Scan J Dent Res 97: 28596, 1989. 8. Nyvad B, Fejerskov O. Active and inactive root surface caries structural entities? In Thylstrup A, Leach SA, Qvist V (eds). Dentine and Dentin Reactions in the Oral Cavity. IRL Press, Oxford 16579, 1987. 9. Thylstrup A, Fejerskov O. Textbook of Clinical Cariology (2nd edn). Munksgaard, Copenhagen, 1994.

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