At the end of this lecture, the student should be able to: Develop understanding of the classification Describe how a cyst develops. Describe the origin and identifying characteristics of the radicular cyst. Describe the origin and identifying characteristics of the Dentigerous cyst. Describe the origin and identifying characteristics of the Odontogenic Keratocyst cyst. Describe the radiographic characteristics of the dentigerous cyst and the odontogenic keratocyst. Discuss the radiographic appearance of the lateral periodontal cyst. 8. List the factors involved in the nevoid basal cell carcinoma syndrome. State the histologic finding that is a key diagnostic feature of Radicular, Dentigerous & Keratocysts. Describe the origin and identifying characteristics of non odontogenic cysts. Describe different treatment options available, and their clinical importance.

1. DENTAL CARIES
Dr. Ali Yaldrum
B.D.S, M.Sc (London)
Faculty of Dentistry, SEGi University
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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
• Analyze the fundamental differences of caries progression
between enamel & dentin
• Develop holistic understanding of the disease

3. Contents
Click on the topic to jump
1. Dental Caries (definition)
2. Aetiology of Dental Caries
8. Reactionary Changes in
3. Biological Events initiating
Dentin
caries
9. Root surface caries
4. Pathology of Caries
10. Arrested Caries &
5. Enamel Caries
Remineralization
6. Cavity Formation
7. Caries in Dentine

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

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

7. Pathology of Dental Caries
Dental caries can be classified into
• Site of attack
• Rate of attack

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. nterprismatic substance havezonesdestroyed. The same appearance is
features of these been are summarised in Table 3.2.
een in chalky enamel caused by early caries. (By kind permission of
Dr K Little.)
The translucent zone is the first observable change. The
appearance of the translucent zone results from formation of sub-
e or microscopic spaces or pores apparently located at prism bounda- 3.19 Diagram summarising the main features of the precavitation
Fig.
mel, phase of enamel caries as indicated here in this final stage of acid attack
ries and other junctional sites such as the striae of Retzius. When
most the section is mounted in quinoline, it fills the pores and, since enamel before bacterial invasion, decalcification of dentine has begun.
on
The area (A) would be radiolucent in a bite-wing film but the area (B) could
con- it has the same refractive index as enamel, the normal structural visualised only in a section by polarised light microscopy or microradi-
be
ack. features disappear and the appearance of the pores is enhanced ography. Clinically, the enamel would appear solid and intact but the sur-
tine (Fig. 3.13). Microradiography confirms that the changes in the would be marked by an opaque white spot over the area (A) as seen
face
in Figure 3.11 (From McCracken AW, Cawson RA 1983 Clinical and oral
eas- translucent zone are due to demineralisation. microbiology. McGraw-Hill.)
tack
per-
e of
t of
rys-
e to
ries
s is
ting
an a
hese
and
ig. 3.18 The organic matrix of developing enamel. An electronphotomicro-
pot) of a section across the lines of the prisms before calcification showing
raph
he matrix to be3.11 dense in thecaries, aof the prism sheaths than in the
ible Fig. more Early enamel region white spot lesion, in a deciduous molar. The 3.20 Early cavitation in enamel caries. The surface layer of the white
Fig.
Early cavitation
prism cores or interprismatic substance. (By kind permission of Dr Kis much larger spot lesion has broken down, allowing plaque bacteria into the enamel.
lesion forms below the contact point and in consequence Little.)
ue.
White spot
than an interproximal lesion in a permanent tooth (see Fig. 3.19).
lesion
(fig.3)

11. 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.

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 Bacterial polysaccharides
mouths, particularly in persons with a high dietary sucrose The ability of S. mutans to initiate sm
intake and high caries activity (Fig. 3.2). S. mutans isolated form large amounts of adherent plaque
from such mouths are virulently cariogenic when introduced to polymerise sucrose into high-mol
into the mouths of animals. like, extracellular polysaccharides (gl
However, simple clinical observation of the sites (intersti- cariogenicity of S. mutans depends as
tially and in pits and fissures) where dental caries is active, form large amounts of insoluble extrac
ability to produce acid.
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 adhe
to the tooth surface, probably via spe
way, S. mutans and its glucans may init
Fig. 3.2 Extensive caries of decidous incisors and canines. This pattern of the teeth and enable critical masses of
caries is particularly associated with the use of sweetened dummies and
Rampant caries
sweetened infant drinks. Production of sticky, insoluble, extrace
by strains of S. mutans is strongly relate
The importance of sucrose in this a
high energy of its glucose–fructose bon
(fig.4)
thesis of polysaccharides by glucosylt
other source of energy. Sucrose is thus
such polysaccharides. Other sugars are
less cariogenic (in the absence of pre

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. 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)

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

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

19. 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)

20. 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.

21. 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

22. 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.

23. Body 5–25% mineral loss
Body 5–25% mineral loss Broader in progressing caries, replaced by a broa
Broader in progressing car
dark zone in arrested ordark zone in arrested or re
remineralised lesions
Interproximal caries viewed under
Surface zone Surface zone loss. A zone of remineralisation resultingremineralisation resulting constant width, a little thicker in width, a
1% mineral 1% mineral loss. A zone of
from the diffusion barrier frommineral content of plaque.
Relatively Relatively constant
and the diffusion barrier and mineral content of plaque. remineralising lesions remineralising le
arrested or arrested or
polarized light
11 Early enamel caries, a white spot lesion, in a deciduous molar. The loss of this layer, allowingloss of this layer, allowing bacteria
Cavitation is Cavitation is bacteria
orms below the contact point and in consequence is much larger lesion
to enter the to enter the lesion
interproximal lesion in a permanent tooth (see Fig. 3.19).
12 Early interproximal caries. Ground section in Fig. 3.13 Early interproximal caries. Ground section viewed by polarisedsame lesion 3.14 3.12 and 3.13) viewed dry under3.1
water viewed by Fig. 3.14 The
Fig. The same lesion (Figs 3.12 and
(Figsto show the full extent of demineralisa
po
Fig. 3.13 Early intact surfaceafter immersion in quinoline. Quinoline has ised light
d light. The body of the lesion and the interproximal caries. Ground section viewed by polarisedfilled theised light to show the full extent of demineralisation. (Figs 3.12–3.14 b
Water Quinoline Dry
light layer are larger pores,
kind permission of Professor Leon Silverstone a
The translucent and dark zones immersion in quinoline. Quinoline hasnelled thein the body of the lesion to disappear (Fig.of Professor Leon Silverstone and the Editor of Dental
light after are not seen until the sectionof the fi fi detail larger pores,
causing most is kind permission
49
causing most of the fine detail inbut the dark zonelesionits smaller pores is accentuated. Update 1989;10:262.)
immersed in quinoline. 3.12), the body of the with to disappear (Fig. Update 1989;10:262.)
3.12), but the dark zone with its smaller pores is accentuated.
The dark zone is fractionally superficial to the translucent of new porosities but possibly also to
(fig.7)
The dark zone is fractionally superficial to the translucent of new porosities but possibly also to remineralisation of
zone. Polarised light microscopy shows that the volume of the large pores of the translucent zone so th

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

25. Cavity Formation
1. Enamel losses support of dentin thus
becoming weak
2. Enamel is attacked from beneath
3. Spread along ADJ, allows them to attack
dentin over wide area (fig.8)

26. • 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)
DENTINE
ENAMEL
A B
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
(fig.8)
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
Main features of the precavitation phase of enamel caries. The area
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
(A) would be radiolucent in a bite-wing film but the area (B) could be
be visualised only in a section by polarised light microscopy or microradi-
ography. Clinically, the enamel would appear solid and intact but the sur-
visualized only in a section by polarised light microscopy or
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
microradiography. microbiology. McGraw-Hill.)

27. Interproximal caries on radiographs
(fig.9)

28. HARD TISSUE PATHOLOGY
CHAPTER
3
Fig. 3.24 This
marises the seq
enamel from th
lesion to early c
relates the diffe
development o
Sequential changes in enamel from the stage of the radiographic ap
initial lesion to early cavity formation clinical findings
lent by the late
and reproduced
Editor of the Br
(fig.10) 1959; 107:27–

29. 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.

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

31. 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.

32. 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.

33. 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.

34. 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.

35. Zone of Destruction
• In th is zone of d e s t r u c t i o n , t h e
liquefaction foci enlarge and increase in
number.
• T h i s p ro d u c e s c o m p re s s i o n a n d
distortion of adjacent dentinal tubules.

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

37. 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.

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

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

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

41. Root surface caries
(fig.10)

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

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

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

45. 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

46. 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.