Dental caries (version 2)

Dental Caries, its pathophysiology and progression in enamel, dentine and cementum. We will also look at different zones of caries existing within in enamel and dentine.

1. Dr. Ali Yaldrum
B.D.S, M.Sc (London)
get in touch
Dental Caries

2. 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
•Analyse the fundamental differences of caries progression
between enamel & dentin
•Develop holistic understanding of the disease

3. What are Caries?

4. 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

5. Sal
Sal
Sal
Sal
Time
Plaque
Bacteria
Susceptible
Surface
Sugar
Caries
Aetiology of caries
(fig.1)

6. EnamelBacterial
Enzymes
Plaque
Polysaccharides
Polysaccharides
Sugar
Sugar
Salivary
Buffers
Ca+
Ca+
ACIDS
Plaque buffer
Plaque buffer
Biological events initiating
Dental Caries (fig.2)

7. Pathology of Dental
Caries
Dental caries can be classified into
•Site of a"ack
•Rate of a"ack

8. Site of Attack
•Pits or fissure carries:
1.Molars and premolar
2.Buccal and lingual surface of molars
3.Lingual surface of maxillary incisors

9. 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

10. DENTAL CARIES
CHAPTER
3
49
The main biochemical events in dental plaque in the devel-
opment of dental caries are summarised diagrammatically in
Figure 3.10.
PATHOLOGY OF ENAMEL CARIES
Enamel 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. 3.11Early 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. 3.12Early 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.
HARD TISSUE PATHOLOGY
CHAPTER
3
52
Fig. 3.20Early 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. 3.18The organic matrix of developing enamel. An electronphotomicro-
graph of a section across the lines of the prisms before calcifi c a tion 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. 3.17Chalky 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 attack
on 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
AB
DENTINE
White spot
lesion
Early cavitation
(fig.3)

11. Site of Attack
•Cemental or root caries:
Root surface is exposed in the oral cavity
because of periodontal disease
•Recurrent caries:
#is occur around the margins or at the
base of a previously existing restoration.

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

13. DENTAL CARIES
CHAPTER
3
41
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. 3.2Extensive caries of decidous incisors and canines. This pattern of
caries is particularly associated with the use of sweetened dummies and
sweetened infant drinks.
Fig. 3.3The 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)

14. Rate of Attack
•Slowly progressive or chronic caries:
1.Progressive slowly and involve the pulp
2.Most common in adults

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

16. Caries in enamel

17. Enamel Caries
•#e 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)

18. Zones of Enamel Caries
1.Translucent Zone
2.Dark Zone
3.Body of Lesion
4.Surface Zone

19. 1
2
3
4
1: Translucent Zone
2: Dark Zone
3: Body of the lesion
4: Surface Zone
(fig.6)

20. Translucent Zone
•Earliest and deepest demineralization
•More pores than normal enamel
•Pores are more larger, approximately to the
size of water molecule
•#ere is a fall in magnesium and carbonate
mineral ions (1% mineral loss)

21. 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.

22. 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

23. Surface Zone
•1% mineral loss, about 40um thick
•Li"le change in early lesion

24. Surface Zone
•#e 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

25. HARD TISSUE PATHOLOGY
CHAPTER
3
50
Table 3.2 Key features of the enamel zones preceding cavity formation
Zone Key features Comments
Translucent zone 1% m ineral loss. Earliest and deepest demineralisation Broader in progressing caries, narrow or absent
in arrested or remineralised lesions
Dark zone 2–4% m ineral 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% m ineral loss Broader in progressing caries, replaced by a broad
dark zone in arrested or remineralised lesions
Surface zone 1% m ineral loss. A zone of remineralisation resulting Relat ively constant width, a little thicker in
from the d iffusion barrier and mineral content of plaque. arrested or rem ineralising lesions
Cav itation is loss of this layer, allowing bacteria
to enter the les ion
Fig. 3.13Early 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.
HARD TISSUE PATHOLOGY
CHAPTER
3
50
Table 3.2 Key features of the enamel zones preceding cavity formation
Zone Key features Comments
Translucent zone 1% m ineral loss. Earliest and deepest demineralisation Broader in progressing caries, narrow or absent
in arrested or remineralised lesions
Dark zone 2–4% m ineral 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% m ineral loss Broader in progressing caries, replaced by a broad
dark zone in arrested or remineralised lesions
Surface zone 1% m ineral loss. A zone of remineralisation resulting Relat ively constant width, a little thicker in
from the d iffusion barrier and mineral content of plaque. arrested or rem ineralising lesions
Cav itation is loss of this layer, allowing bacteria
to enter the les ion
Fig. 3.13Early 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.
DENTAL CARIES
CHAPTER
3
49
The main biochemical events in dental plaque in the devel-
opment of dental caries are summarised diagrammatically in
Figure 3.10.
PATHOLOGY OF ENAMEL CARIES
Enamel 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. 3.11Early 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. 3.12Early 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
polarised light
Water Quinoline Dry
(fig.7)

26. Cavity Formation
•Once bacteria have penetrated enamel,
they reach amelodentinal junction (ADJ)
and spread laterally to undermine the
enamel
•#is has 3 major effects

27. Cavity Formation
1.Enamel losses support of dentin thus
becoming weak
2.Enamel is a"acked from beneath
3.Spread along ADJ, allows them to a"ack
dentin over wide area (fig.8)

28. HARD TISSUE PATHOLOGY
CHAPTER
3
52
Fig. 3.20Early 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. 3.18The organic matrix of developing enamel. An electronphotomicro-
graph of a section across the lines of the prisms before calcifi c a tion 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. 3.17Chalky 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 attack
on 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
AB
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)

29. Interproximal caries on radiographs
(fig.9)

30. HARD TISSUE PATHOLOGY
CHAPTER
3
54
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 kindly
lent by the late Professor AI Darling
and reproduced by courtesy of the
Editor of the British Dental Journal
1959; 107:27–30.)
Fig. 3.25Infection 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. 3.26Caries 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)

31. Caries in dentine

32. Caries in Dentin
•Caries of the dentine develops from
enamel caries; when the lesion reaches
the amelodentinal junction.
•#e caries process in dentine is
approximately twice as rapid in enamel.

33. Zone of Dentin Caries
•Zone of Sclerosis
•Zone of Demineralization
•Zone of Bacterial invasion
•Zone of Destruction

34. Zone of Sclerosis
•#e 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.

35. 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.

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

37. Zone of Bacterial
Invasion
•In this zone bacteria extend down and
multiply within the dentinal tubules

38. Zone of Bacterial
Invasion
•#e 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 a"ack the
diminrelized matrix.

39. Zone of Bacterial
Invasion
•thickening of the dentinal tubule due to
the packing by microorganism
•Tiny “liquefaction foci” are formed by the
break down of the dentinal tubule
•#is focus is an ovoid area of destruction,
parallel to the course of the tubule and
filled with necrotic debris

40. Zone of Destruction
•In this zone of destruction, the
liquefaction foci enlarge and increase in
number.
•#is produces compression and distortion
of adjacent dentinal tubules.

41. Reactionary Changes in
Dentin
•Tubular Sclerosis
•Regular Reactionary Dentin
•Irregular Reactionary Dentin
•Dead Tracts

42. Secondary dentine carious development is
only slower because:
•fewer dentinal tubules
•with irregular course

43. Reactionary & Tertiary Dentin
•Eventually however the involvement of the
pulp results with ensuing inflammation
and necrosis.

44. Root surface caries
•Develops on exposed root surfaces due to
gingival recession
•Forms stagnation areas for plaque
•Cementum is readily decalcified

45. Root surface caries
•Cementum so %ens beneath the
accumulated plaque over a wide area
•Saucers shape cavity
•invaded along the direction of Sharpey’s
fibers

46. Root surface caries
(fig.10)

47. Root surface caries
•Spread between lamellae along the
incremental lines
•Dentin becomes split up & progressively
destroyed by combination of
demineralization and proteolysis

48. Arrested Caries &
Remineralization
Under favorable conditions, carious
demineralization can be reversed
1.Fluoride application
2.consumption of less cariogenic diet

49. Arrested Caries &
Remineralization
•white spot may become arrested
•adjacent teeth is removed resulting in
removal of stagnation area
•remineralized by minerals from enamel

50. 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

51. 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.