Our Lady of Fatima University

COLLEGE OF DENTISTRY

Sharon Alvarez, DMD, Ph.D.

THE PATHOPHYSIOLOGY OF
CARIES

Clinical Characteristics of
the Caries Lesion
• When the tooth surface becomes cavitated, a more retentive surface area becomes
available to the biofilm community.
• The cavitation of the tooth surface produces a synergistic acceleration of the growth of
the cariogenic biofilm community and the expansion of the demineralization with
ensuing expanded cavitation.
• This situation results in a rapid and progressive destruction of the tooth structure.
• When enamel caries penetrates to the dentinoenamel junction (DEJ), rapid lateral
expansion of the caries lesion occurs because dentin is much less resistant to acid
demineralization.
• This sheltered, highly acidic, and anaerobic environment provides an ideal niche for cariogenic
bacteria.
 CLINIC AL SITES FOR C ARIES INITIATION

• three distinctly different clinical sites for caries initiation: EACH HAS distinct surface
topography and environmental conditions. Each area has distinct biofilm population.
(1) developmental pits and fissures of enamel, which are the most susceptible sites
(2) smooth enamel surfaces that shelter cariogenic biofilm
(3) the root surface
 CLINIC AL SITES FOR C ARIES INITIATION

• three distinctly different clinical sites for caries initiation: EACH HAS distinct surface
topography and environmental conditions. Each area has distinct biofilm population.
(1) developmental pits and fissures of enamel, which are the most susceptible sites
(2) smooth enamel surfaces that shelter cariogenic biofilm
(3) the root surface
 PITS AND FISSURE

• Bacteria rapidly colonize the pits and fissures of newly erupted teeth.
• The type and nature of the organisms prevalent in the oral cavity determine the
type of organisms colonizing pits and fissures and are instrumental in determining the
outcome of the colonization.
• Large variations exist in the microflora found in pits and fissures, suggesting that
each site can be considered a separate ecologic system.
• Numerous gram-positive cocci, especially S. sanguis, are found in the pits and fissures of
newly erupted teeth, whereas large numbers of MS usually are found in carious pits
and fissures.
 PITS AND FISSURE

The shape of the pits and fissures contributes to their high

susceptibility to caries.
• The long, narrow fissure prevents adequate biofilm removal
• Considerable morphologic variation exists in these structures
• Some pits and fissures end blindly, others open near the dentin, and others
penetrate entirely through the enamel.
 PITS AND FISSURE

• Pit-and-fissure caries expands as it penetrates into the enamel.

• The entry site may appear much smaller than the actual lesion, making clinical diagnosis
difficult.
 PITS AND FISSURE

• Caries lesions of pits and fissures develop from attack on their walls
• Progression of the dissolution of the walls of a pit-and-fissure lesion is similar in principle to
that of the smooth-surface lesion because a wide area of surface attack extends inward,
paralleling the enamel rods.
• A lesion originating in a pit or fissure affects a greater area of the DEJ than does a
comparable smooth-surface lesion.
• In cross-section, the gross appearance of a pit-and-fissure lesion is an inverted “V” with a
narrow entrance and a progressively wider area of involvement closer to the DEJ
 PITS AND FISSURE C ARIES

• Pit-and-fissure lesions have small sites of origin visible on the occlusal surface but have
a wide base
• Overall shape of a pit-and-fissure lesion is an inverted “V.” In contrast, a smooth-surface lesion
is V-shaped with a wide area of origin and apex of the V directed toward pulp
 PITS AND FISSURE C ARIES: PROGRESSION

PROGRESSION:
1. Demineralization follows the direction of the enamel
rods, spreading laterally as it approaches the
dentinoenamel junction (DEJ).
2. Soon after the initial enamel lesion occurs, a reaction
can be seen in the dentin and pulp. Forceful probing of
the lesion at this stage can result in damage to the
weakened porous enamel and accelerate the
progression of the lesion. Clinical detection at this
stage should be based on observation of discoloration
and opacification of the enamel adjacent to the fissure.
These changes can be observed by careful cleaning and
drying of the fissure.
3. Initial cavitation of the opposing walls of the fissure
cannot be seen on the occlusal surface. Opacification
can be seen that is similar to the previous stage.
Remineralization of the enamel because of trace
amounts of fluoride in the saliva may make progression
of pit-and-fissure lesions more difficult to detect
4. Extensive cavitation of the dentin and undermining of
the covering enamel darken the occlusal surface
 SMOOTH ENAMEL SURFACES

• The smooth enamel surfaces of teeth present a less favorable site for cariogenic biofilm
attachment.
• Cariogenic biofilm usually develops only on the smooth surfaces that are near the gingiva or
are under proximal contacts.
• The proximal surfaces are particularly susceptible to caries because of the extra shelter
provided to resident cariogenic biofilm owing to the proximal contact area immediately
occlusal to it
 SMOOTH ENAMEL SURFACES

• The smooth enamel surfaces of teeth present a less favorable site for cariogenic biofilm
attachment.
• Cariogenic biofilm usually develops only on the smooth surfaces that are near the gingiva
or are under proximal contacts.
• The proximal surfaces are particularly susceptible to caries because of the extra shelter
provided to resident cariogenic biofilm owing to the proximal contact area immediately
occlusal to it
 SMOOTH ENAMEL SURFACES

• the path of ingress of the lesion is roughly parallel to the long axis of the enamel rods in
the region
• . A cross-section of the enamel portion of a smooth-surface lesion shows a V-shape, with a
wide area of origin and the apex of the V directed toward the DEJ. After caries penetrates the
DEJ, softening of dentin spreads rapidly laterally and pulpally
 SMOOTH ENAMEL SURFACES: PROGRESSION

1. Initial demineralization (indicated by the shading in the enamel) on the proximal surfaces is
not detectable clinically or radiographically.
2. All proximal surfaces are demineralized to some degree, but most are remineralized and
become immune to further attack.
3. When proximal caries first becomes detectable radiographically, the enamel surface is likely
still to be intact. An intact surface is essential for successful remineralization and arrest of the
lesion.
 SMOOTH ENAMEL SURFACES: PROGRESSION

3. Demineralization of the dentin (indicated by the shading in the dentin) occurs before
cavitation of the surface of the enamel. Treatment designed to promote remineralization can be
effective up to this stage.
4. Cavitation of the enamel surface is a critical event in the caries process in proximal surfaces.
Cavitation is an irreversible process and requires restorative treatment and correction of the
damaged tooth surface. Cavitation can be diagnosed only by clinical observation. The use of a
sharp explorer to detect cavitation is problematic because excessive force in application of the
explorer tip during inspection of the proxi- mal surfaces can damage weakened enamel and
accelerate the caries process by creating cavitation. Separation of the teeth can be used to
provide more direct visual inspection of suspect surfaces. Fiberoptic illumination and dye
absorption also are promising new evaluation procedures, but neither is specific for cavitation. D,
Advanced cavitated lesions require prompt restorative intervention to prevent pulpal disease,
limit tooth structure loss, and remove the nidus of infection of odontopathic organisms.
 SMOOTH ENAMEL SURFACES: PROGRESSION

Cavitation is an irreversible process and requires restorative treatment and

correction of the damaged tooth surface.
• Cavitation can be diagnosed only by clinical observation. The use of a sharp explorer to detect
cavitation is problematic because excessive force in application of the explorer tip during
inspection of the proximal surfaces can damage weakened enamel and accelerate the caries
process by creating cavitation.
• Separation of the teeth can be used to provide more direct visual inspection of suspect surfaces.
• Fiberoptic illumination and dye absorption are new evaluation procedures, but neither is specific for
cavitation.
• Advanced cavitated lesions require prompt restorative intervention to prevent pulpal disease,
limit tooth structure loss, and remove the nidus of infection of odontopathic organisms.
 ROOT SURFACES

• the proximal root surface, particularly near the cemento- enamel junction (CEJ),
often is unaffected by the action of hygiene procedures such as flossing because it
may have concave anatomic surface contours (fluting) and occasional roughness at
the termination of the enamel.
 ROOT SURFACES

• exposure to the oral environment (as a result of gingival recession), favor the
formation of mature, cariogenic biofilm and proximal root-surface caries.
• Likewise, the facial or lingual root surfaces (particularly near the CEJ), when exposed
to the oral environment (because of gingival recession), are often both neglected in
hygiene procedures and usually not rubbed by the bolus of food
 ROOT SURFACES

• Consequently, these root surfaces also frequently harbor cariogenic biofilm.

• Root-surface caries is more common in older patients because of niche availability
and other factors sometimes associated with senescence, such as decreased
salivary flow and poor oral hygiene as a result of lowered digital dexterity and
decreased motivation.
 ROOT SURFACES

Caries originating on the root is alarming because

(1) it has a comparatively rapid progression
(2) it is often asymptomatic
(3) it is closer to the pulp,
(4) it is more difficult to restore.
 ROOT SURFACE C ARIES

• Root caries begins directly on dentin.

• Root-surface lesions can progress rapidly because dentin is less resistant to caries attack.
PROGRESSION OF CARIOUS
LESION
 ENAMELC ARIES

• progression and morphology of the caries lesion vary,

depending on the site of origin and the conditions in the
mouth
• The time for progression from non-cavitated caries to clinical
caries (cavitation) on smooth surfaces is estimated to be 18
months ± 6 months.
• Peak rates for the incidence of new lesions occur 3 years after
the eruption of the tooth. Occlusal pit-and-fissure lesions
develop in less time than smooth-surface caries.
• Poor oral hygiene and frequent exposures to sucrose-
containing or acidic food can produce noncavitated (“white
spot”) lesions (first clinical evidence of demineralization) in 3
weeks.
• Radiation-induced xerostomia (dry mouth) can lead to clinical
caries development in 3 months from the onset of the
radiation.
• Caries development in healthy individuals is usually slow
compared with the rate possible in compromised persons.
 ENAMEL C ARIES

WHITE SPOT LESIONS HYPOCALCIFICATION

• Noncavitated caries partially or • hypocalcified enamel is affected less by

totally disappears visually when the drying and wetting
enamel is hydrated (wet)
 ENAMEL C ARIES

WHITE SPOT LESIONS HYPOCALCIFICATION

• Noncavitated caries partially or • hypocalcified enamel is affected less by

totally disappears visually when the drying and wetting
enamel is hydrated (wet)

Softened chalky enamel that can be chipped away

with an explorer is a sign of active caries.
Injudicious use of an explorer tip can cause actual
cavitation n a previously noncavitated area,
requiring, in most cases, restorative intervention
ENAMEL C ARIES
 ENAMEL CARIES
• First clinical sign of caries induced demineralization is the white
spot lesion
• usually are observed on the facial and lingual surfaces of teeth.
• White spots are chalky white, opaque areas that are revealed only
when the tooth surface is desiccated and are termed noncavitated
enamel caries lesions.
 ENAMEL CARIES

• These areas of enamel lose their translucency because of

the extensive subsurface porosity caused by
demineralization.
 ENAMEL CARIES
ACTIVE CARIES
• A more advanced lesion develops a rough surface that is softer than the unaffected, normal
enamel.
• Softened chalky enamel that can be chipped away with an explorer is a sign of active
caries.
• Injudicious use of an explorer tip can cause actual cavitation in a previously noncavitated
area, requiring, in most cases, restorative intervention.
• Noncavitated enamel lesions retain most of the original crystalline framework of the
enamel rods, and the etched crystallites serve as nucleating agents for remineralization.
• Calcium and phosphate ions from saliva can penetrate the enamel surface and precipitate
on the highly reactive crystalline surfaces in the enamel lesion.
• The supersaturation of saliva with calcium and phosphate ions serves as the driving force
for the remineralization process.
•
 ENAMEL CARIES
CAVITATED ENAMEL LESIONS
• Cavitated enamel lesions can be initially detected as subtle breakdown of the enamel
surface.
• These lesions are very sensitive to probing, and can be easily enlarged by using sharp
explorers and excessive probing force.
• More advanced cavitated enamel lesions are more obviously detected as enamel
breakdown.
• Although some cavitated enamel lesions can be arrested and may not progress to larger
lesions, most cavitated caries lesions require restorative treatment.
•
 ENAMEL CARIES
INACTIVE CARIES
• Remineralized (arrested) lesions can be observed clinically as intact, but discolored, usually
brown or black, spots
• The change in color is presumably caused by trapped organic debris and metallic ions
within the enamel.
• These discolored, remineralized, arrested caries areas are intact and are more resistant to
subsequent caries attack than the adjacent unaffected enamel.
• They should not be restored unless they are esthetically objectionable.
 ZONES OF INCIPIENT ENAMEL
CARIES
1. Surface Zone – intact hypermineralized zone.
• Surface layer
• Reprecipitation of minerals
• Pore volume (PV) is < 5%
2. Body of the lesion – porous and soft. Striae of
Retzius is enhance.
subsurface
• PV is 5 - 25%
3. Dark Zone – a “dark” area surrounds
the body of the lesion due to deposition of
ions in previously empty pores. PV is 2-4%
4. Translucent Zone – the advancing front of
lesions.
• Zone of reaction or limiting zone
PV is 1% or 10X of sound enamel
ZONES OF INCIPIENT ENAMEL
CARIES

Surface Zone

Body of the Lesion

Dark Zone

Translucent Zone

Ground section viewed with

transmitted polarized light
with a Red 1 filter
 MICRORADIOGRAPH OF
INCIPIENT ENAMEL CARIES
 HISTOPATHOLOGY OF CARIES

ENAMEL CARIES

• The mineralization process is apparently some what discontinuous and is

characterized by alternating phases of high and low activity.
• Thus enamel, is capable of acting as a molecular sieve like by allowing free
movement of small molecules and blocking the passage of larger
molecular and ions.

• The movement of ions through carious enamel can result in acid dissolution
of the underlying dentin before actual cavitations of the enamel surface.
 PIT & FISSURE ENAMEL C ARIES

Compare thickness of
enamel below base of pit
ADVANCED PIT & FISSURE
C ARIES
DENTINAL CARIES
 DENTIN

• Dentin contains much less mineral and possesses microscopic tubules that
provide a pathway for the ingress of bacteria and egress of minerals.
• The DEJ has the least resistance to caries attack and allows rapid lateral
spreading when caries has penetrated the enamel
• Because of these characteristics, dentinal caries is V-shaped in cross-section
with a wide base at the DEJ and the apex directed pulpally.
• Caries advances more rapidly in dentin than in enamel because dentin
provides much less resistance to acid attack owing to less mineralized
content.
• Caries produces a variety of responses in dentin, including pain, sensitivity,
demineralization, and remineralization.
 D E N T I N C A R I E S A N D PA I N

• Pain is commonly reported when deep lesions bring the bacterial infection
close to the pulp.
• Episodes of short-duration pain may be felt occasionally during earlier
stages of dentin caries.
• The pain is caused by
1. stimulation of pulp tissue by the movement of fluid through the
dentinal tubules that have been opened to the oral environment by
cavitation.
2. When bacterial invasion of the dentin is close to the pulp, toxins and
possibly a few bacteria enter the pulp, resulting in inflammation of
the pulpal tissues and, thus, pulpal pain.
 DENTINAL CARIES

The pulp–dentin complex reacts to caries attacks by attempting to initiate

remineralization and blocking off the open tubules. These reactions result
from odontoblastic activity and the physical process of demineralization and
remineralization.
3 levels of dentinal reaction to caries can be recognized
(1) reaction to a long-term, low-level acid demineralization associated with a
slowly advancing lesion
(2) reaction to a moderate-intensity attack
(3) reaction to severe, rapidly advancing caries characterized by very high
acid levels
 DENTINAL CARIES

• In slowly advancing caries, a vital pulp can repair

demineralized dentin by remineralization of the
intertubular dentin and by apposition of
peritubular dentin.
• Early stages of caries or mild caries attacks
produce long-term, low-level acid
demineralization of dentin.
• Direct exposure of the pulp tissue to
microorganisms is not a prerequisite for an
inflammatory response. Toxins and other
metabolic byproducts, especially hydrogen ion,
can penetrate via the dentinal tubules to the
pulp.
• Even when the lesion is limited to enamel, the
pulp can be shown to respond with inflammatory
cells
• first caries demineralization episode by
deposition of crystalline material in the lumen of
the tubules and the intertubular dentin of
affected dentin in front of the advancing infected
dentin portion of the lesion
 DENTINAL CARIES

• More intense caries activity results in bacterial invasion of dentin.

• Irritants can cause the degeneration and death of odontoblasts and their tubular extensions
below the lesion and a mild inflammation of the pulp.
• pulp may be irritated sufficiently from high acid levels or bacterial enzyme production to
cause the formation of replacement odontoblasts (secondary odontoblasts). These cells
produce reparative dentin (reactionary dentin) on the affected portion of the pulp chamber
wall
• Reparative dentin is an effective barrier to diffusion of material through the tubules
and is an important step in the repair of dentin.
 DENTINAL CARIES

• Acute, rapidly advancing caries with high levels of acid production overpowers dentinal
defenses and results in infection, abscess, and death of the pulp.
 ZONES OF
DENTINAL
CARIES

Caries advancement in dentin proceeds through three

changes:
1. Weak organic acid demineralized dentin.
2.Organic material of dentin particularly collagen is degenerated
and dissolution.
3.loss of structural integrity is followed by invasion of bacteria.
 ZONES OF DENTINAL CARIES

1. Infected zone
2. Turbid zone
3. Transparent dentin
4. Subtransparent dentin
5. Normal dentin
Infected Zone

Turbid Zone

Transparent dentin
Subtransparent
dentin
Normal dentin
 ZONES OF DENTINAL CARIES

ZONE 1 NORMAL DENTIN

• Deepest area
• Has a tubule with odontoblastics rocesses that are smooth and no crystals
in the lumen
• intertubular dentin has normal cross-banded collagen and normal dense
apatite crystals.
• No bacteria are present in the tubules.
• Stimulation of dentin produces a sharp pain.
• There are no bacteria in the tubules
 ZONES OF DENTINAL CARIES

ZONE 2 SUB TRANSPARENT DENTIN

Zone of demineralized (by acid from caries) of the intertubular dentin and
initial formation of very fine crystals in the tubules and lumen at the
advancing prone.
Damage to the odontoblastic process is ended, however no bacteria are
founf in this zone.
 ZONES OF DENTINAL CARIES

ZONE 3 TRANSPARENT DENTIN

Zone of carious dentin that is softer than normal dentin.
Shows further loss of mineral from intertubular dentin and many large crystals
in the lower of dentinal tubules
 ZONES OF DENTINAL CARIES

• ZONE 4 TURBID DENTIN

• Zones of bacterial invasion marked by widening and distortion of dentinal
tubules w/c filled with bacteria.
• Dentin in this zone will not self repair.
 ZONES OF DENTINAL CARIES

ZONE 5 INFECTED DENTIN

Outermost zone of infected dentin
Decomposed dentin that is teeming with bacteria.
No recognizable structure to dentin, seems to be absent of collagen and
mineral.
 ZONES OF DENTINAL CARIES

NECROTIC DENTIN

• It recognized clinically, as a wet, mushy, easily

removable mass.
• This is structure less/ granular in histologic
appearance and contain masses of bacteria.
• Removal of the necrotic material uncovers
deeper infected dentin (turbid dentin), which
appears dry and leathery.
 ZONES OF DENTINAL CARIES

Sensitivity Presence of Capacity to

to stimuli bacteria remineralize
Zone 1, IZ
- + -
Zone 2, TZ
- + -
Zone 3, TrD
+ - +
Zone 4, STrD
+ - +
Zone 5, ND
+ - +
 ZONES OF DENTINAL CARIES
INFECTED AND AFFECTED DENTIN
Affected dentin =turbid, transparent and subtransparent dentin
• Also called inner carious dentin
• affected dentin is a zone of demineralization of intertubular dentin and of initial formation of fine
crystals in the tubule lumen at the advancing front.
• Damage to the odontoblastic process is evident
• Affected dentin is softer than normal dentin and shows loss of mineral from intertubular dentin and
many large crystals in the lumen of the dentinal tubules.
• Stimulation of affected dentin produces pain.
• the collagen cross-linking remains intact in this zone.
The intact collagen can serve as a template for remineralization of intertubular dentin, and this region
remains capable of self-repair, provided that the pulp remains vital.
 ZONES OF DENTINAL CARIES
INFECTED AND AFFECTED DENTIN
Infected dentin =turbid, transparent and subtransparent dentin
• Also called outer carious dentin: DRY AND LEATHERY
• the outermost carious layer
• the zone of bacterial nvasion
• widening and distortion of the dentinal tubules, which are filled with bacteria.
• Little mineral is present, and the collagen in this zone is irreversibly denatured.
• The dentin in this zone does not self-repair. This zone cannot be remineralized, and its
removal is essential to sound, successful restorative procedures and the prevention of
spreading the infection.
 ZONES OF DENTINAL CARIES

INFECTED AND AFFECTED

DENTIN

In a tooth with a deep caries lesion, no history of spontaneous pain, normal

responses to thermal stimuli, and a vital pulp, a deliberate, incomplete caries
excavation may be indicated. This procedure is termed indirect pulp capping
(also referred to as stepwise caries excavation or partial caries excavation)
 ZONES OF DENTINAL CARIES

ADVANCED C ARIOUS LESIONS

Increasing demineralization of the body of the enamel lesion results in the weakening
and eventual collapse of the surface enamel.
The resulting cavitation provides an even more protective and retentive habitat for the
cariogenic biofilm, accelerating the progression of the lesion.
 REFERENCES

• Heymann, H., Swift, E. J., Ritter, A. V., & Sturdevant, C. M.

(2013). Sturdevant's art and science of operative dentistry.
St. Louis, Mo: Elsevier/Mosby.
• Schüpbach P, Guggenheim B, Lutz F. Human root caries:
histopathology of initial lesions in cementum and dentin. J
Oral Pathol Med. 1989;18(3):146-156. doi:10.1111/j.1600-
0714.1989.tb00753.x