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
t h e t e e t h c h a r a c t e r i z e d b y
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. e or
mel,
most
con-
ack.
tine
eas-
ack
per-
e of
t of
rys-
e to
ries
s is
ting
an a
hese
and
pot)
ible
ue.
features of these zones are summarised in Table 3.2.
The translucent zone is the first 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 fills 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 confirms that the changes in the
translucent zone are due to demineralisation.
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. 3.20 Early cavitation in enamel caries. The surface layer of the white
spot lesion has broken down, allowing plaque bacteria into the enamel.
ig. 3.18 The organic matrix of developing enamel. An electronphotomicro-
raph of a section across the lines of the prisms before calcification showing
he 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.)
nterprismatic substance have been destroyed. The same appearance is
een in chalky enamel caused by early caries. (By kind permission of
Dr K Little.)
Fig. 3.19 Diagram summarising the main features of the precavitation
phase of enamel caries as indicated here in this final stage of acid attack
on enamel before bacterial invasion, decalcification of dentine has begun.
The area (A) would be radiolucent in a bite-wing film 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.)
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. 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 fissures) where dental caries is active,
Bacterial polysaccharides
The ability of S. mutans to initiate sm
form large amounts of adherent plaqu
to polymerise sucrose into high-mol
like, extracellular polysaccharides (gl
cariogenicity of S. mutans depends as
form large amounts of insoluble extrac
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.
Box 3.2 Essential properties of cariogenic b
• Acidogenic
• Able to produce a pH low enough (usual
tooth substance
• Able to survive and continue to produce
• Possess attachment mechanisms for firm
tooth surfaces
• Able to produce adhesive, insoluble plaq
(glucans)
Glucans enable streptococci to adh
to the tooth surface, probably via spe
way, S. mutans and its glucans may ini
the teeth and enable critical masses o
Production of sticky, insoluble, extrac
by strains of S. mutans is strongly relate
The importance of sucrose in this
high energy of its glucose–fructose bon
thesis of polysaccharides by glucosyl
other source of energy. Sucrose is thus
such polysaccharides. Other sugars ar
less cariogenic (in the absence of pre
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.
• B e g i n n i n g o f e n a m e l c a r i e s ,
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. Body 5–25% mineral loss Broader in progressing car
dark zone in arrested or re
Surface zone 1% mineral loss. A zone of remineralisation resulting Relatively constant width,
from the diffusion barrier and mineral content of plaque. arrested or remineralising l
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 filled the larger pores,
causing most of the fine 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 3.1
ised light to show the full extent of demineralisa
kind permission of Professor Leon Silverstone
Update 1989;10:262.)
The dark zone is fractionally superficial to the translucent
zone. Polarised light microscopy shows that the volume of the
of new porosities but possibly also to
large pores of the translucent zone so th
Body 5–25% mineral loss Broader in progressing caries, replaced by a broa
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 filled the larger pores,
causing most of the fine 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 po
ised light to show the full extent of demineralisation. (Figs 3.12–3.14 b
kind permission of Professor Leon Silverstone and the Editor of Dental
Update 1989;10:262.)
The dark zone is fractionally superficial to the translucent of new porosities but possibly also to remineralisation of
49
11 Early enamel caries, a white spot lesion, in a deciduous molar. The
orms below the contact point and in consequence is much larger
interproximal lesion in a permanent tooth (see Fig. 3.19).
12 Early interproximal caries. Ground section in water viewed by
d light. The body of the lesion and the intact surface layer are
The translucent and dark zones are not seen until the section is
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. nphotomicrograph of chalky enamel
acid. The crystallites of calcium salts
hile the prism cores and some of the
estroyed. The same appearance is
y caries. (By kind permission of
• 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 final stage of acid attack
on enamel before bacterial invasion, decalcification of dentine has begun.
The area (A) would be radiolucent in a bite-wing film 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)

29. Interproximal caries on radiographs
(fig.9)

30. HARD TISSUE PATHOLOGY
CHAPTER
3
Fig. 3.24 This
marises the seq
enamel from th
lesion to early c
relates the diffe
development o
radiographic ap
clinical findings
lent by the late
and reproduced
Editor of the Br
1959; 107:27–
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
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

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.