DENTAL CARIESDr. Ali Yaldrum

B.D.S, M.Sc (London)

Faculty of Dentistry, SEGi University

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Learning Objectives

• Define “Dental Caries”

• Describe classification of caries

• Describe progression of caries in enamel

• Describe progression of caries in dentin

• Describe progression of caries in root surface

• Analyze the fundamental differences of caries progression between enamel & dentin

• Develop holistic understanding of the disease

ContentsClick on the topic to jump

1. Dental Caries (definition)

2. Aetiology of Dental Caries

3. Biological Events initiating caries

4. Pathology of Caries

5. Enamel Caries

6. Cavity Formation

7. Caries in Dentine

8. Reactionary Changes in Dentin

9. Root surface caries

10. Arrested Caries & Remineralization

Dental Caries

It is bacterial disease of calcified tissue of the teeth characterized by demineralization of the inorganic and destruction of the organic substance of the tooth

Saliva

Saliva

Saliva

Saliva

Time

PlaqueBacteria

Susceptible Surface

Sugar

Caries

Aetiology of caries(fig.1)

EnamelBacterialEnzymes

Plaque

Polysaccharides

Polysaccharides

Sugar

Sugar

SalivaryBuffers

Ca+

Ca+

ACIDS

Plaque buffer

Plaque buffer

Biological events initiating Dental Caries (fig.2)

Pathology of Dental Caries

Dental caries can be classified into

• Site of attack

• Rate of attack

Site of Attack

• pits or fissure carries:1. Molars and premolar

2. Buccal and lingual surface of molars

3. Lingual surface of maxillary incisors

Site of Attack

• Smooth surface caries:1. Approximal surface (fig.3)

2. Gingival third of lingual and buccal surface

3. Choky white appearance of the enamel

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The main biochemical events in dental plaque in the devel-opment of dental caries are summarised diagrammatically in Figure 3.10.

PATHOLOGY OF ENAMEL CARIESEnamel is the usual site of the initial lesion unless dentine or cementum becomes exposed by gingival recession. Enamel, the hardest and densest tissue in the body, consists almost entirely of calcium apatite with only a minute organic con-tent. It therefore forms a formidable barrier to bacterial attack. However, once enamel has been breached, infection of dentine can spread with relatively little obstruction. Preventive meas-ures must therefore be aimed primarily at stopping the attack or at making enamel more resistant.

The essential nature of the carious attack on enamel is per-meation of acid into its substance. The crystalline lattice of calcium apatite crystals is relatively impermeable, but part of the organic matrix of enamel which envelops the apatite crys-tals has a relatively high water content and is permeable to hydrogen ions. Permeation of enamel by acid causes a series of submicroscopic changes. This process of enamel caries is a dynamic one and, initially at least, consists of alternating phases of demineralisation and remineralisation, rather than a continuous process of dissolution.

Enamel caries develops in four main phases (Box 3.12). These stages of enamel caries are distinguishable microscopically and are also clinically signifi cant. In particular, the early (white spot) lesion is potentially reversible, but cavity formation is irreversible and requires restorative measures to substitute for the lost tissue.

These initial changes are not due to bacterial invasion, but due to bacterial lactic or other acids causing varying degrees of demineralisation and remineralisation in the enamel. The features of these zones are summarised in Table 3.2.

The translucent zone is the fi rst observable change. The appearance of the translucent zone results from formation of sub-microscopic spaces or pores apparently located at prism bounda-ries and other junctional sites such as the striae of Retzius. When the section is mounted in quinoline, it fi lls the pores and, since it has the same refractive index as enamel, the normal structural features disappear and the appearance of the pores is enhanced (Fig. 3.13). Microradiography confi rms that the changes in the translucent zone are due to demineralisation.

Box 3.12 Stages of enamel caries

• The early (submicroscopic) lesion• Phase of non-bacterial enamel crystal destruction• Cavity formation• Bacterial invasion of enamel• Undermining of enamel from below after spread into dentine

The early lesion

The earliest visible changes are seen as a white opaque spot that forms just adjacent to a contact point. Despite the chalky appearance, the enamel is hard and smooth to the probe (Fig. 3.11). The microscopic changes under this early white spot lesion may be seen in undecalcifi ed sections but more readily when polarised light is used. Microradiography indicates the degree of demineralisation seen in the different zones.

The initial lesion is conical in shape with its apex towards the dentine and a series of four zones of differing translucency can be discerned. Working back from the deepest, advancing edge of the lesion, these zones consist fi rst of a translucent zone most deeply; immediately within this is a second dark zone; the third consists of the body of the lesion and the fourth consists of the surface zone (Fig. 3.12).

Fig. 3.11 Early enamel caries, a white spot lesion, in a deciduous molar. The lesion forms below the contact point and in consequence is much larger than an interproximal lesion in a permanent tooth (see Fig. 3.19).

Fig. 3.12 Early interproximal caries. Ground section in water viewed by polarised light. The body of the lesion and the intact surface layer are visible. The translucent and dark zones are not seen until the section is viewed immersed in quinoline.

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52 Fig. 3.20 Early cavitation in enamel caries. The surface layer of the white spot lesion has broken down, allowing plaque bacteria into the enamel.

Clinically, this is frequently evident when there is no more than a pinhole lesion in an occlusal pit, but cutting away the sur-rounding enamel shows it to be widely undermined.

As undermining of the enamel continues, it starts to collapse under the stress of mastication and to fragment around the edge of the (clinically obvious) cavity. By this stage, bacterial damage to the dentine is extensive.

The process of enamel caries is summarised in Box 3.13.

Fig. 3.18 The organic matrix of developing enamel. An electronphotomicro-graph of a section across the lines of the prisms before calcifi cation showing the matrix to be more dense in the region of the prism sheaths than in the prism cores or interprismatic substance. (By kind permission of Dr K Little.)

Fig. 3.17 Chalky enamel. An electronphotomicrograph of chalky enamel produced by the action of very dilute acid. The crystallites of calcium salts remain intact in the prism sheaths, while the prism cores and some of the interprismatic substance have been destroyed. The same appearance is seen in chalky enamel caused by early caries. (By kind permission of Dr K Little.)

Box 3.13 Process of enamel caries

• Permeation of the organic matrix by hydrogen ions causes submicroscopic changes

• The early damage is submicroscopic and seen as a series of zones of differing translucency

• Microradiography confi rms that these changes represent areas of increasing demineralisation

• The surface zone is largely formed by remineralisation• There is alternating demineralisation and remineralisation, but

demineralisation is predominant as cavity formation progresses• Bacteria cannot invade enamel until demineralisation provides

pathways large enough for them to enter (cavitation)

Fig. 3.19 Diagram summarising the main features of the precavitation phase of enamel caries as indicated here in this fi nal stage of acid attackon enamel before bacterial invasion, decalcifi cation of dentine has begun. The area (A) would be radiolucent in a bite-wing fi lm but the area (B) could be visualised only in a section by polarised light microscopy or microradi-ography. Clinically, the enamel would appear solid and intact but the sur-face would be marked by an opaque white spot over the area (A) as seen in Figure 3.11 (From McCracken AW, Cawson RA 1983 Clinical and oral microbiology. McGraw-Hill.)

ENAMEL

A B

DENTINE

White spot lesion

Early cavitation

(fig.3)

Site of Attack

• Cemental or root caries:Root surface is exposed in the oral cavity because of periodontal disease

• Recurrent caries:This occur around the margins or at the base of a previously existing restoration.

Rate of Attack

• Rampant caries:Rapidly progressing caries involving many or all of the erupted teeth (fig.4)

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Germ-free animals do not develop dental caries when fed a sucrose-rich diet which causes caries in animals with a nor-mal oral fl ora. Experiments using gnotobiotes have shown that the most potent causes of dental caries are a limited number of strains of the S. mutans group which are able to form cari-ogenic plaque.

S. mutans strains are a major component of plaque in human mouths, particularly in persons with a high dietary sucrose intake and high caries activity (Fig. 3.2). S. mutans isolated from such mouths are virulently cariogenic when introduced into the mouths of animals.

However, simple clinical observation of the sites (intersti-tially and in pits and fi ssures) where dental caries is active,

shows that the bacteria responsible are not those fl oating free in the saliva. Dental caries develops only at the interface between tooth surface and dental plaque in stagnation areas, particularly in occlusal fi ssures and approximally (Fig. 3.3).

Bacterial polysaccharides

The ability of S. mutans to initiate smooth surface caries and form large amounts of adherent plaque depends on its ability to polymerise sucrose into high-molecular-weight, dextran-like, extracellular polysaccharides (glucans) (Box 3.2). The cariogenicity of S. mutans depends as much on its ability to form large amounts of insoluble extracellular glucans as on its ability to produce acid.

Fig. 3.2 Extensive caries of decidous incisors and canines. This pattern of caries is particularly associated with the use of sweetened dummies and sweetened infant drinks.

Fig. 3.3 The stagnation area in an occlusal pit. A ground section of a molar showing the size of the stagnation area in comparison with a toothbrush bristle placed above it. The complete inaccessibility of the stagnation area to cleaning is obvious.

Box 3.2 Essential properties of cariogenic bacteria

• Acidogenic• Able to produce a pH low enough (usually pH !5) to decalcify

tooth substance• Able to survive and continue to produce acid at low levels of pH• Possess attachment mechanisms for fi rm adhesion to smooth

tooth surfaces• Able to produce adhesive, insoluble plaque polysaccharides

(glucans)

Glucans enable streptococci to adhere to one another and to the tooth surface, probably via specifi c receptors. In this way, S. mutans and its glucans may initiate their attachment to the teeth and enable critical masses of plaque to be built up. Production of sticky, insoluble, extracellular glucan produced by strains of S. mutans is strongly related to their cariogenicity.

The importance of sucrose in this activity depends on the high energy of its glucose–fructose bond which allows the syn-thesis of polysaccharides by glucosyltransferase without any other source of energy. Sucrose is thus the main substrate for such polysaccharides. Other sugars are, to a variable degree, less cariogenic (in the absence of preformed plaque), partly because they are less readily formed into cariogenic glucans.

Plaque polysaccharides, synthesised by bacteria, play an essential role in the pathogenesis of dental caries. The propor-tions of the different types of polysaccharide, and the overall amounts formed, depend both on the kinds of bacteria present and the different sugars in the diet.

On a sucrose-rich diet, the main extracellular polysaccha-rides are glucans. Fructans formed from fructose are produced in smaller amounts. They are more soluble than glucans and less important in caries. Acid-producing microorganisms that do not produce insoluble polysaccharides do not appear to be able to cause caries of smooth surfaces. Even mutant strains of S. mutans which produce more soluble polysaccharides seem not to be cariogenic. Polysaccharides thus contribute to the adhesiveness, bulk and resistance to solution of plaque.

In the past, lactobacilli were thought to be the main cause of dental caries because they are numerous in the saliva and

Rampant caries(fig.4)

Rate of Attack

• Slowly progressive or chronic caries:1. Progressive slowly and involve the pulp

2. Most common in adults

Rate of Attack

• Arrested caries:Caries of enamel and dentine, including root caries.

Enamel Caries

• The pathological features are essentially similar in both sites.

• Enamel caries progression is a slow process.

• Beginning of enamel caries , microscopically four zones are seen (fig.6)

Zones of Enamel Caries

1. Translucent Zone2. Dark Zone3. Body of Lesion4. Surface Zone

EnamelDentin 12

3

4

1: Translucent Zone2: Dark Zone3: Body of the lesion4: Surface Zone

(fig.6)

Translucent Zone

• Earliest and deepest demineralization.

• More pores than normal enamel.

• Pores are more larger, approximately to the size of water molecule.

• There is a fall in magnesium and carbonate mineral ions (1% mineral loss)

Dark Zone

• 2-4% mineral loss

• Some of pores are larger, but other are smaller than those in translucent zone.

• Reminrelization has occurred due to reprecipitation of minerals lost from translucent zone.

Body of the lesion

• 5-25% mineral loss

• Apatite crystal are more larger than in normal enamel

• 5% demineralization shows that the area of radiolucency corresponds closely with the size and shape of the body

Surface Zone

• 1% mineral loss, about 40um thick

• Little change in early lesion

• The surface of normal enamel differs in composition from the deeper layer , being more highly mineralized so interpretation of possible chemical changes in this zone is difficult.

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Table 3.2 Key features of the enamel zones preceding cavity formation

Zone Key features Comments

Translucent zone 1% mineral loss. Earliest and deepest demineralisation Broader in progressing caries, narrow or absent in arrested or remineralised lesions

Dark zone 2–4% mineral loss overall but a zone of remineralisation Broader in arrested or remineralised lesions, narrow just behind the advancing front in advancing lesions

Body 5–25% mineral loss Broader in progressing caries, replaced by a broad dark zone in arrested or remineralised lesions

Surface zone 1% mineral loss. A zone of remineralisation resulting Relatively constant width, a little thicker in from the diffusion barrier and mineral content of plaque. arrested or remineralising lesions Cavitation is loss of this layer, allowing bacteria to enter the lesion

Fig. 3.13 Early interproximal caries. Ground section viewed by polarised light after immersion in quinoline. Quinoline has fi lled the larger pores, causing most of the fi ne detail in the body of the lesion to disappear (Fig. 3.12), but the dark zone with its smaller pores is accentuated.

Fig. 3.14 The same lesion (Figs 3.12 and 3.13) viewed dry under polar-ised light to show the full extent of demineralisation. (Figs 3.12–3.14 by kind permission of Professor Leon Silverstone and the Editor of Dental Update 1989;10:262.)

The dark zone is fractionally superfi cial to the translucent zone. Polarised light microscopy shows that the volume of the pores in this zone has increased to 2–4% of the enamel vol-ume. This change is due mainly to formation of additional small pores. Two different-size pores thus coexist in the dark zone. The small ones are so minute that molecules of quinoline are unable to enter and the tissue has become transformed into a molecular sieve. The small pores therefore remain fi lled with air – this appears to produce the zone’s dark appearance.

Microradiography confi rms that the dark zone has suffered a greater degree of demineralisation. However, when the lesion is exposed to saliva or synthetic calcifying solutions in vitro, the dark zone actually extends further. This may indicate that the formation of the dark zone may be due not merely to creation

of new porosities but possibly also to remineralisation of the large pores of the translucent zone so that they become micro-pores impermeable to quinoline. It is widely believed therefore that these changes in the dark zone are evidence of reminerali-sation, as discussed later.

The body of the lesion forms the bulk of the lesion and extends from just beneath the surface zone to the dark zone. By transmitted light, the body of the lesion is comparatively trans-lucent compared with normal enamel and sharply demarcated from the dark zone. Within the body of the lesion, the striae of Retzius appear enhanced, particularly when mounted in quino-line and viewed under polarised light. Polarised light examina-tion (Fig. 3.14) also shows that the pore volume is 5% at the periphery but increases to at least 25% in the centre.

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Table 3.2 Key features of the enamel zones preceding cavity formation

Zone Key features Comments

Translucent zone 1% mineral loss. Earliest and deepest demineralisation Broader in progressing caries, narrow or absent in arrested or remineralised lesions

Dark zone 2–4% mineral loss overall but a zone of remineralisation Broader in arrested or remineralised lesions, narrow just behind the advancing front in advancing lesions

Body 5–25% mineral loss Broader in progressing caries, replaced by a broad dark zone in arrested or remineralised lesions

Surface zone 1% mineral loss. A zone of remineralisation resulting Relatively constant width, a little thicker in from the diffusion barrier and mineral content of plaque. arrested or remineralising lesions Cavitation is loss of this layer, allowing bacteria to enter the lesion

Fig. 3.13 Early interproximal caries. Ground section viewed by polarised light after immersion in quinoline. Quinoline has fi lled the larger pores, causing most of the fi ne detail in the body of the lesion to disappear (Fig. 3.12), but the dark zone with its smaller pores is accentuated.

Fig. 3.14 The same lesion (Figs 3.12 and 3.13) viewed dry under polar-ised light to show the full extent of demineralisation. (Figs 3.12–3.14 by kind permission of Professor Leon Silverstone and the Editor of Dental Update 1989;10:262.)

The dark zone is fractionally superfi cial to the translucent zone. Polarised light microscopy shows that the volume of the pores in this zone has increased to 2–4% of the enamel vol-ume. This change is due mainly to formation of additional small pores. Two different-size pores thus coexist in the dark zone. The small ones are so minute that molecules of quinoline are unable to enter and the tissue has become transformed into a molecular sieve. The small pores therefore remain fi lled with air – this appears to produce the zone’s dark appearance.

Microradiography confi rms that the dark zone has suffered a greater degree of demineralisation. However, when the lesion is exposed to saliva or synthetic calcifying solutions in vitro, the dark zone actually extends further. This may indicate that the formation of the dark zone may be due not merely to creation

of new porosities but possibly also to remineralisation of the large pores of the translucent zone so that they become micro-pores impermeable to quinoline. It is widely believed therefore that these changes in the dark zone are evidence of reminerali-sation, as discussed later.

The body of the lesion forms the bulk of the lesion and extends from just beneath the surface zone to the dark zone. By transmitted light, the body of the lesion is comparatively trans-lucent compared with normal enamel and sharply demarcated from the dark zone. Within the body of the lesion, the striae of Retzius appear enhanced, particularly when mounted in quino-line and viewed under polarised light. Polarised light examina-tion (Fig. 3.14) also shows that the pore volume is 5% at the periphery but increases to at least 25% in the centre.

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The main biochemical events in dental plaque in the devel-opment of dental caries are summarised diagrammatically in Figure 3.10.

PATHOLOGY OF ENAMEL CARIESEnamel is the usual site of the initial lesion unless dentine or cementum becomes exposed by gingival recession. Enamel, the hardest and densest tissue in the body, consists almost entirely of calcium apatite with only a minute organic con-tent. It therefore forms a formidable barrier to bacterial attack. However, once enamel has been breached, infection of dentine can spread with relatively little obstruction. Preventive meas-ures must therefore be aimed primarily at stopping the attack or at making enamel more resistant.

The essential nature of the carious attack on enamel is per-meation of acid into its substance. The crystalline lattice of calcium apatite crystals is relatively impermeable, but part of the organic matrix of enamel which envelops the apatite crys-tals has a relatively high water content and is permeable to hydrogen ions. Permeation of enamel by acid causes a series of submicroscopic changes. This process of enamel caries is a dynamic one and, initially at least, consists of alternating phases of demineralisation and remineralisation, rather than a continuous process of dissolution.

Enamel caries develops in four main phases (Box 3.12). These stages of enamel caries are distinguishable microscopically and are also clinically signifi cant. In particular, the early (white spot) lesion is potentially reversible, but cavity formation is irreversible and requires restorative measures to substitute for the lost tissue.

These initial changes are not due to bacterial invasion, but due to bacterial lactic or other acids causing varying degrees of demineralisation and remineralisation in the enamel. The features of these zones are summarised in Table 3.2.

The translucent zone is the fi rst observable change. The appearance of the translucent zone results from formation of sub-microscopic spaces or pores apparently located at prism bounda-ries and other junctional sites such as the striae of Retzius. When the section is mounted in quinoline, it fi lls the pores and, since it has the same refractive index as enamel, the normal structural features disappear and the appearance of the pores is enhanced (Fig. 3.13). Microradiography confi rms that the changes in the translucent zone are due to demineralisation.

Box 3.12 Stages of enamel caries

• The early (submicroscopic) lesion• Phase of non-bacterial enamel crystal destruction• Cavity formation• Bacterial invasion of enamel• Undermining of enamel from below after spread into dentine

The early lesion

The earliest visible changes are seen as a white opaque spot that forms just adjacent to a contact point. Despite the chalky appearance, the enamel is hard and smooth to the probe (Fig. 3.11). The microscopic changes under this early white spot lesion may be seen in undecalcifi ed sections but more readily when polarised light is used. Microradiography indicates the degree of demineralisation seen in the different zones.

The initial lesion is conical in shape with its apex towards the dentine and a series of four zones of differing translucency can be discerned. Working back from the deepest, advancing edge of the lesion, these zones consist fi rst of a translucent zone most deeply; immediately within this is a second dark zone; the third consists of the body of the lesion and the fourth consists of the surface zone (Fig. 3.12).

Fig. 3.11 Early enamel caries, a white spot lesion, in a deciduous molar. The lesion forms below the contact point and in consequence is much larger than an interproximal lesion in a permanent tooth (see Fig. 3.19).

Fig. 3.12 Early interproximal caries. Ground section in water viewed by polarised light. The body of the lesion and the intact surface layer are visible. The translucent and dark zones are not seen until the section is viewed immersed in quinoline.

Interproximal caries viewed under polarized light

Water Quinoline Dry

(fig.7)

Cavity Formation

• Once bacteria have penetrated enamel, they reach amelodentinal junction (ADJ) and spread laterally to undermine the enamel

• This has 3 major effects

Cavity Formation

1. Enamel losses support of dentin thus becoming weak

2. Enamel is attacked from beneath3. Spread along ADJ, allows them to attack

dentin over wide area (fig.8)

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52 Fig. 3.20 Early cavitation in enamel caries. The surface layer of the white spot lesion has broken down, allowing plaque bacteria into the enamel.

Clinically, this is frequently evident when there is no more than a pinhole lesion in an occlusal pit, but cutting away the sur-rounding enamel shows it to be widely undermined.

As undermining of the enamel continues, it starts to collapse under the stress of mastication and to fragment around the edge of the (clinically obvious) cavity. By this stage, bacterial damage to the dentine is extensive.

The process of enamel caries is summarised in Box 3.13.

Fig. 3.18 The organic matrix of developing enamel. An electronphotomicro-graph of a section across the lines of the prisms before calcifi cation showing the matrix to be more dense in the region of the prism sheaths than in the prism cores or interprismatic substance. (By kind permission of Dr K Little.)

Fig. 3.17 Chalky enamel. An electronphotomicrograph of chalky enamel produced by the action of very dilute acid. The crystallites of calcium salts remain intact in the prism sheaths, while the prism cores and some of the interprismatic substance have been destroyed. The same appearance is seen in chalky enamel caused by early caries. (By kind permission of Dr K Little.)

Box 3.13 Process of enamel caries

• Permeation of the organic matrix by hydrogen ions causes submicroscopic changes

• The early damage is submicroscopic and seen as a series of zones of differing translucency

• Microradiography confi rms that these changes represent areas of increasing demineralisation

• The surface zone is largely formed by remineralisation• There is alternating demineralisation and remineralisation, but

demineralisation is predominant as cavity formation progresses• Bacteria cannot invade enamel until demineralisation provides

pathways large enough for them to enter (cavitation)

Fig. 3.19 Diagram summarising the main features of the precavitation phase of enamel caries as indicated here in this fi nal stage of acid attackon enamel before bacterial invasion, decalcifi cation of dentine has begun. The area (A) would be radiolucent in a bite-wing fi lm but the area (B) could be visualised only in a section by polarised light microscopy or microradi-ography. Clinically, the enamel would appear solid and intact but the sur-face would be marked by an opaque white spot over the area (A) as seen in Figure 3.11 (From McCracken AW, Cawson RA 1983 Clinical and oral microbiology. McGraw-Hill.)

ENAMEL

A B

DENTINE

Main features of the precavitation phase of enamel caries. The area (A) would be radiolucent in a bite-wing film but the area (B) could be visualized only in a section by polarised light microscopy or microradiography.

(fig.8)

Interproximal caries on radiographs(fig.9)

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Reactionary changes in dentine are summarised in Table 3.3.These reactionary changes start to develop early but at best

can only slow the advance of dental caries. Even sclerotic den-tine is vulnerable to bacterial acid and proteolysis and once bacteria have penetrated the normal dentine they can invade any reactionary dentine to reach the pulp (Figs 3.29–3.32).

Root surface caries

When the neck of the tooth becomes exposed by recession of the gingival margin in later life, a stagnation area may be formed and the cementum attacked. Cementum is readily

decalcifi ed and presents little barrier to infection. The cemen-tum therefore softens beneath the plaque over a wide area, producing a saucer-shaped cavity and the underlying dentine is soon involved. Cementum is invaded along the direction of Sharpey’s fi bres. Infection spreads between the lamellae along the incremental lines, with the result that the dentine becomes split up and progressively destroyed by a combination of

Fig. 3.24 This diagram sum-marises the sequential changes in enamel from the stage of the initial lesion to early cavity formation and relates the different stages in the development of the lesion with the radiographic appearances and clinical fi ndings. (Diagram kindlylent by the late Professor AI Darling and reproduced by courtesy of the Editor of the British Dental Journal 1959; 107:27–30.)

Fig. 3.25 Infection of the dentinal tubules. This electronphotomicrograph shows bacteria in the lumen of the tubules. Between the tubules is the collagenous matrix of the dentine. (By kind permission of K Little.)

Fig. 3.26 Caries of dentine. Infected tubules and fusiform masses of bac-teria have expanded into the softened tissue. Adjacent tubules in the dem-ineralised dentine have been bent and pushed aside by these masses.

Sequential changes in enamel from the stage of the initial lesion to early cavity formation

(fig.10)

Caries in Dentin

• Caries of the dentine develops from enamel caries; when the lesion reaches the amelodentinal junction.

• The caries process in dentine is approximately twice as rapid in enamel.

Zone of Dentin Caries

• Zone of Sclerosis

• Zone of Demineralization

• Zone of Bacterial invasion

• Zone of Destruction

Zone of Sclerosis

• The sclerotic or translucent zone is located beneath and at the sides of the carious lesion.

• Dead tract may be seen running through the zone of sclerosis because the death of odontoblast at an earlier stage in the process of caries.

Zone of Demineralization

• In the demineralization zone the intratubular matrix is mainly affected by a wave of acid produced by bacteria in the zone of bacterial zone.

• It may be stained yellowish –brown as a result of the diffusion of other bacterial products interacting with proteins in dentine.

Zone of Bacterial Invasion

• In this zone bacteria extend down and multiply within the dentinal tubules

• The bacterial invasion probably occurs in two waves:i. 1st wave consist of acidogenic organism, mainly

lactobacilli , produce acid which diffuses ahead into the deminrelized zone.

ii. 2nd wave of mixed acidogenic and proteolytic organism then attack the diminrelized matrix.

Zone of Bacterial Invasion

• In addition thickening of the dentinal tubule due to the packing of the tubules by microorganism.

• Tiny “liquefaction foci” are formed by the break down of the dentinal tubule.

• This focus is an ovoid area of destruction , parallel to the course of the tubule and filled with necrotic debris.

Zone of Destruction

• In th is zone of destruct ion, the liquefaction foci enlarge and increase in number.

• Th is produces compress ion and distortion of adjacent dentinal tubules.

Reactionary Changes in Dentin

• Tubular Sclerosis

• Regular Reactionary Dentin

• Irregular Reactionary Dentin

• Dead Tracts

Reactionary Changes in Dentin

The carious involvement of secondary dentine does not differ remarkably from the involvement of the primary dentine , except that is usually somewhat slower because the dentinal tubule are fewer in number and more irregular in their course , thus delaying penetration of the invading microorganism.

Reactionary & Tertiary Dentin

• Eventually however the involvement of t h e p u l p r e s u l t s w i t h e n s u i n g inflammation and necrosis.

Root surface caries

• Develops on exposed root surfaces due to gingival recession

• Forms stagnation areas for plaque

• Cementum is readily decalcified

Root surface caries

• Cementum softens beneath the accumulated plaque over a wide area

• Saucers shape cavity

• invaded along the direction of Sharpey’s fibers

Root surface caries

(fig.10)

Root surface caries

• Spread between lamellae along the incremental lines

• Dentin becomes split up & progressively d e s t r o y e d b y c o m b i n a t i o n o f demineralization and proteolysis

Arrested Caries & Remineralization

Under favorable conditions, carious demineralization can be reversed1. Fluoride application 2. consumption of less cariogenic diet

Arrested Caries & Remineralization

• white spot may become arrested

• adjacent teeth is removed resulting in removal of stagnation area

• remineralized by minerals from enamel

Arrested Caries & Remineralization

• Dentin caries may be occasionally be arrested as a result of extensive destruction of enamel resulting in wider area of dentin becoming involved

References

• J. V. Soames, J. C. Southam, “Dental Caries” in Oral Pathology, 4th Edition, Oxford University Press, 2007 pp 19-31.

• R. A. Cawson, E. W. Odell, “Dental Caries” in Cawson’s Essential of Oral Pathology and Oral Medicine, Eighth Edition, Churchill Livingstone Elsevier, 2008 pp 40-59.