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Abdulkareem Al-Mezouri 201

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Caries of Dentin

Features and structure of dentin:

Dentin is the mineralized connective tissue that forms the largest portion of the
tooth structure, extending almost the full length of the tooth. Externally, dentin is covered
by enamel on the anatomic crown and cementum on the anatomic root. Internally, dentin
forms the walls of the pulp cavity (pulp chamber and pulp canals).

Dentin is less mineralized than enamel but more mineralized than cementum or
bone. The mineral content of dentin increases with age. Dentin has great tensile strength
and its flexibility prevents the brittle enamel fracturing. Its color is pale yellow and
provides color for enamel.

The composition of human dentin is approximately 70% inorganic material, 20%

organic material, and 10% water and other materials. The organic component of dentine
consists of collagen fibrils embedded in an amorphous ground substance. Because it is
softer than enamel, it decays more rapidly and is subject to severe cavities if not properly
treated.

Dentinal tubules

The basic repeatable unit in dentine is dentinal tubules. The dentinal tubules are
small canals that extend through the entire width of dentin, from the pulp to the DEJ and
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are widest at the pulp surface, with a diameter of about 3μm. Each tubule contains the
cytoplasmic cell process (Tomes fiber) of an odontoblast, afferent nerve terminals, and
each tubule is bathed in dentinal fluid. Each dentinal tubule is lined with a layer of
peritubular dentin, which is much more mineralized than the surrounding intertubular
dentin.

Peritubular and intertubular dentin

Caries of dentin:

Progression of caries in dentin is different from progression in the overlying

enamel because of the structural differences of 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 produces a variety of
responses in dentin, including pain, sensitivity, demineralization, and remineralization.

Often, pain is not reported even when caries invades dentin except 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
stimulation of pulp tissue by the movement of fluid through the dentinal tubules that have
been opened to the oral environment by cavitation. When bacterial invasion of the dentin
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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.

Levels of dentinal reaction to 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.
Three 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; and
3. Reaction to severe, rapidly advancing caries characterized by very high acid
levels.

Dentin can react defensively (by repair) to low-intensity and moderate-intensity

caries attacks as long as the pulp remains vital and has an adequate blood circulation.

First level:

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. 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. Dentin responds to the stimulus of its 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. Hypermineralized areas may be seen on radiographs as zones of increased
radiopacity (often S-shaped following the course of the tubules) ahead of the advancing,
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infected portion of the lesion. This repair occurs only if the tooth pulp is vital. Dentin that
has more mineral content than normal dentin is termed sclerotic dentin. Sclerotic dentin
formation occurs ahead of the demineralization front of a slowly advancing lesion and
may be seen under an old restoration. Sclerotic dentin is usually shiny and darker in color
but feels hard to the explorer tip.it appears transparent in transmitted light.

Sclerotic dentin

By contrast, normal, freshly cut dentin lacks Crystalline precipitates form in the
lumen of the dentinal tubules. When these affected tubules become completely occluded
by the mineral precipitate, they appear clear when a section of the tooth is evaluated.

Second level:

The second level of dentinal response is to moderate-intensity irritants. More

intense caries activity results in bacterial invasion of dentin. Infected dentin contains a
wide variety of pathogenic materials or irritants, including high acid levels, hydrolytic
enzymes, bacteria, and bacterial cellular debris. These materials can cause the
degeneration and death of odontoblasts and their tubular extensions below the lesion.
Empty tubule that result from degeneration of the odontoblastic processes called dead
tracts. These tracts extend from the external dentin surface to the pulp; the tubules are
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empty and thus appear black when ground sections of dentin are viewed microscopically
with transmitted light.

Dead tracts

The pulp may be irritated sufficiently from high acid levels or bacterial enzyme
production to cause the formation (from undifferentiated mesenchymal cells) of
replacement odontoblasts (secondary odontoblasts). These cells produce reparative dentin
(reactionary dentin) on the affected portion of the pulp chamber wall. This dentin is
different from the normal dentinal apposition that occurs throughout the life of the tooth
by primary (original) odontoblasts.

Reparative dentin
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The structure of reparative dentin varies from well-organized tubular dentin (less
often) to very irregular atubular dentin (more often), depending on the severity of the
stimulus. Reparative dentin is an effective barrier to diffusion of material through the
tubules and is an important step in the repair of dentin. Severe stimuli also can result in
the formation within the pulp chamber of unattached dentin, termed pulp stones, in
addition to reparative dentin.

Pulp stone

The success of dentinal reparative responses, either by remineralization of

intertubular dentin and apposition of peritubular dentin or by reparative dentin, depends
on the severity of the caries attack and the ability of the pulp to respond. The pulpal blood
supply may be the most important limiting factor to the pulpal responses.

Third level:

The third level of dentinal response is to severe irritation. Acute, rapidly

advancing caries with high levels of acid production overpowers dentinal defenses and
results in infection, abscess, and death of the pulp. Compared with other oral tissues, the
pulp is poorly tolerant of inflammation. Small, localized infections in the pulp produce an
inflammatory response involving capillary dilation, local edema, and stagnation of blood
flow.
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Because the pulp is contained in a sealed chamber, and its blood is supplied
through narrow root canals, any stagnation of blood flow can result in local anoxia and
necrosis. The local necrosis leads to more inflammation, edema, and stagnation of blood
flow in the immediately adjacent pulp tissue, which becomes necrotic in a cascading
process that rapidly spreads to involve the entire pulp.

Maintenance of pulp vitality depends on the adequacy of pulpal blood supply.

Recently erupted teeth with large pulp chambers and short, wide canals with large apical
foramina have a much more favorable prognosis for surviving pulpal inflammation than
fully formed teeth with small pulp chambers and small apical foramina.

Zones of Dentin Caries:

Caries advancement in dentin proceeds through three changes:

(1) weak organic acids demineralize dentin;

(2) the organic material of dentin, particularly collagen, degenerates and dissolves;
and
(3) the loss of structural integrity is followed by invasion of bacteria.

Three different zones have been described in carious dentin. The zones are most
clearly distinguished in slowly advancing lesions. In rapidly progressing caries, the
difference between the zones becomes less distinct.
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Zone 1: normal dentin:

The deepest area is normal dentin, which has tubules with odontoblastic processes
that are smooth, and no crystals are present in the lumens. The intertubular dentin has
normal cross-banded collagen and normal dense apatite crystals. No bacteria are present
in the tubules. Stimulation of dentin (e.g.,by osmotic gradient [from applied sucrose or
salt], a bur, a dragging instrument, or desiccation from heat or air) produces a sharp pain.

Zone 2: affected 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. Although organic acids attack the mineral and organic contents of dentin, 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.

The affected dentin zone can also be subclassified in three sub-zones:

(1) subtransparent dentin
(2) transparent dentin
(3) and turbid dentin.

Zone 3: infected dentin:

Also called outer carious dentin, this is the outermost carious layer, the layer that the
clinician would encounter first when opening a lesion. The infected dentin is the zone of
bacterial invasion and is marked by widening and distortion of the dentinal tubules,
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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.