Operative Dentistry

Lecture (4)
Biologic Considerations of Dentin and its Clinical Significance in
Operative Dentistry
Dentin Formation Dentin is a mineralized connective tissue that is covered by
enamel in the crown and cementum in the root, as well as enclosing the innermost
pulp. Dentin formation, dentinogenesis, is accomplished by cells called
odontoblasts. Odontoblasts are considered part of pulp and dentin tissues because
their cell bodies are in the pulp cavity, but their long, slender cytoplasmic cell
processes (Tomes fibers) extend well (100–200 μm) into the tubules in the
mineralized dentin, Because of these odontoblastic cell processes, dentin is
considered a living tissue, with the capability of reacting to physiologic and
pathologic stimuli. These processes extend beyond the DEJ into the enamel forming
enamel spindles, which are responsible for sensitivity sensation during cavity
preparation in enamel.
Dentin formation begins immediately before enamel formation. The most
recently formed layer of dentin is always on the pulpal surface. Odontoblasts
generate an extracellular collagen matrix as they begin to move away from adjacent
ameloblasts. Mineralization of the collagen matrix, facilitated by modification of the
collagen matrix by various non-collagenous proteins, gradually follows its secretion
and deposition of intrafibrillar mineral crystals into the collagen fibrils. This
unmineralized zone of dentin is immediately next to the cell bodies of odontoblasts
and is called predentin
Dentinal tubules: The dentinal tubules are small canal that remain from the
process of dentinogenesis and extend through the entire width of dentin, from the
pulp to the DEJ. Each tubule contains the cytoplasmic cell process (Tomes fiber) of
an odontoblast and is lined with a layer of peritubular dentin, which is much more
mineralized than the surrounding intertubular dentin. The tubules comprise about
10% of dentin volume. In mature dentin, the odontoblastic process extends within
the dentinal tubule to about one-third the dentinal thickness.

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 The number of tubules increases from 15,000 to 20,000/mm2 at the DEJ to
45,000 to 65,000/mm2 at the pulp. The lumen of the tubules also varies from the
DEJ to the pulp surface. In coronal dentin, the average diameter of tubules at the
DEJ is 0.5 to 0.9 μm, but this increases to 2 to 3 μm near the pulp. Tubules are
generally oriented perpendicular to the DEJ. Along the tubule walls are small lateral
openings called canaliculi or lateral canals. The lateral canals are formed as a result
of the presence of secondary (lateral) branches of adjacent odontoblastic processes
during dentinogenesis.

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Dentinoenamel junction
It is the transition between the highly mineralized enamel and the collagen-
containing dentin. DEJ must resist fracture and separation under the extreme forces
from occlusal loading. DEJ width falls within a range of 2 to 15 μm. Some collagen
fibers from the dentinal material extend through this transitional area and are
embedded in the more highly mineralized enamel. These embedded collagen fibers
may also add to the overall strength and resilience of the junction between the two
tissues.

Dentin composition
Mature dentin is a crystalline material that is less hard than enamel but slightly
harder than bone. The odontoblast, with its cell body at the pulp periphery and its
extended process within the dentinal tubule, secretes the organic dentin matrix and
regulates mineralization. Mature dentin is 45% - 50% inorganic or mineralized
material, 30% organic material, and 25% water. The organic material is
approximately 90% type I collagen and 10% non-collagenous proteins.
The crystalline formation of mature dentin mainly consists of calcium
hydroxyapatite with the chemical formula of Ca10(PO4)6(OH)2. The calcium
hydroxyapatite found in dentin is similar to that found in a higher percentage in
enamel and in lower percentages in both cementum and bone tissue. In addition, the
crystals in dentin are platelike in shape and 30% smaller in size than those in enamel.

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The thickness of the apatite crystals varies from 3.5 nm near the DEJ to about 2 nm
close to the pulp. Small amounts of other minerals, such as carbonate and fluoride,
are also present. The mineral content of dentin increases with age.

Structurally there are two main types of dentin which are:

1. Intertubular dentin: the primary structural component of it is the
hydroxyapatite- embedded collagen matrix between tubules. Intertubular dentin
forming the bulk of dentin structure.
2. Peritubular dentin: it is the hypermineralized dentin limited to the walls of
dentinal tubules.
The walls of the dentinal tubules (peritubular dentin) in the primary dentin
gradually thicken, through ongoing mineral deposition, with age. The dentin
therefore becomes harder, denser, and, because tubular fluid low becomes more
restricted as the lumen spaces become smaller, less sensitive. The increased amount
of mineral in the primary dentin is defined as dentin sclerosis. Dentin sclerosis
resulting from aging is called physiologic dentin sclerosis. The dentinal tubules in
the Outer Dentin which is near the DEJ are relatively far apart and the Intertubular
dentin makes up 96% of the surface area. In the Inner Dentin, the tubules diameters
are larger and the distance between tubule centers is half that of tubules at DEJ. Thus,

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the intertubular matrix area is only 12% of the surface area, and the permeability of
inner dentin is about eight times more permeable than the dentin near DEJ.

Physiologic and Tertiary Dentin

Some of the variations in the dentinal tissue occur during its natural sequence of
development or aging, while other variations result from the effects of external
factors on the tooth, such as caries, injury, or wear. An understanding of these
variations in the dentinal tissue is important because they are related to the long-term
success of dental procedures and therapies.
Physiologic dentin
Odontoblasts synthesize and secrete extracellular organic matrix, which,
following mineralization, forms the primary and secondary physiologic dentin.
1. Primary dentin: formed relatively quickly until root formation is completed by
odontoblasts. The first-formed, 150-μm-thick layer of primary dentin subjacent to
the enamel is termed mantle dentin. It differs from other primary dentin in that it is
4% less mineralized, and the collagen fiber orientation is perpendicular rather than
parallel to the DEJ. The odontoblasts produce primary dentin, mainly intertubular
dentin, at a rate of 4 to 8 μm/day. Approximately 2 to 3 years following tooth
eruption. The bulk of dentin surrounding the pulp chamber and canal systems,
termed circumpulpal dentin. The synthesis of dentin then slows to 1 to 2 μm/day,
decreasing in rate with age but continuing as long as the tooth is vital.
2. Secondary dentin: This is a slowly formed dentin of 1 to 2 μm/day, decreasing
in rate with age but continuing as long as the tooth is vital. This continued deposition
of secondary dentin led to constriction in the dimensions of the pulp chamber. In
response to mild occlusal stimulus, secondary dentin is mainly deposited in the pulp
horns and on the roof and floor of the pulp chamber so after many decades the

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chamber becomes quite narrow occluso-gingivally. This constriction in pulp
chamber size reduced the possibility of pulp exposure in old patients during cavity
or crown preparation. The dentist must pay attention for the size and location of the
pulp chamber to decide the design of the preparation and placement of retentive
features such as pins.

Sclerotic dentin (transparent or peritubular dentin)

This type of dentin results from aging or mild irritation (such as slow caries,
attrition, abrasion, erosion and occlusal trauma) and causes a change in the
composition of the primary dentin. The tubular content appears to be replaced by
calcified material that obliterates the tubules, progressing from the DEJ pulpaly. The
tubules become progressively hypermineralized and, with constriction of the lumen
and less permeable. The sclerotic dentin is harder, denser, less sensitive and more
protective of the pulp against subsequent irritation. Sclerosis resulting from aging is
(physiological dentin sclerosis) and that resulting from mild irritation called
(reactive dentine sclerosis). The combination of peritubular wall thickness and
intratubular crystals creates a zone of hypermineralized dentin beneath exposed or
carious dentin, the zone of sclerosis or translucent zone. Sclerotic dentin is
frequently found beneath both active caries lesions and restorations and is an

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important defense reaction of the hard tissues because it limits the permeability of
dentin.

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Reparative dentin (tertiary dentin)
Intense traumatic insult (injury) to the tooth, whether caused by bacterial
penetration associated with caries, or heat and trauma from a dental bur, may be
severe enough to destroy the supporting odontoblasts in the affected location. Within
3 weeks, fibroblasts or mesenchymal cells of the pulp are converted or differentiated
to simulate the activities of original odontoblast, and form irregularly organized
atubular dentin called reparative dentin.

Dentin Function
There are different functions of dentin which can be summarized as follow:
1. Structure: Dentin forms the bulk of the tooth (both in the crown and root). It
constitutes the largest percentage of tooth substrates.
2. Color: The coronal dentin (crown) provides color for the overlying enamel.
Because of the translucency of overlying enamel, the dentin of the tooth gives the
white enamel crown its underlying yellow hue, which is a deeper tone in permanent

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teeth. When the pulp undergoes infection or even dies, there is discoloration of the
dentin, which causes darkening of the clinical crown.
3. Elasticity: Dentin also has great tensile strength, providing an elastic basis for
the more brittle enamel. The tensile strength for enamel and dentin are 10 and 98
MPa, respectively. Although enamel is harder but enamel is very brittle and can be
fracture without support of dentin which characterized by elasticity to absorb the
heavy occlusal loads.
4. Support: Tooth strength and rigidity are provided by intact dentinal substrate.
Resistance of tooth to fracture is significantly lowered with increasing depth and
width of cavity preparation. For example, A posterior tooth with an endodontic
access preparation retains only a third of the fracture resistance of an intact tooth.
Therefore, a conservative initial approach that combines localized removal of
carious tooth structure, placement of a bonded restoration, and placement of sealant
is recommended. If large preparations are required, the dentist should consider
placement of inlays, onlay or crown. Also, higher concentrations of tooth-whitening
(bleaching) agents, may have adverse effects on the fracture toughness of dentin.
5. Protection: Protective encasement for the pulp. As a vital tissue without
vascular supply or innervation, it is nevertheless able to respond to thermal, chemical
or tactile external stimuli because of the presence of dentinal tubules that permit
stimuli transmission to the pulp
Dentin can be distinguished from enamel (during tooth preparation), by:
1. Color: Enamel is translucent in color depending on its thickness, while, dentin
is normally yellow-white and slightly darker than enamel. In older patient’s dentin
is darker and become brown or black in cases in which it has been exposed to oral
fluids, old restorative materials or slowly advancing caries.
2. Reflectance: dentin surfaces are opaquer and duller, being less reflective to
light than enamel surfaces, which appear shiny.
3. Hardness: dentin is softer than enamel, sharp explorer tends to catch and hold
in dentin. The hardness of dentin averages one fifth that of enamel, and its hardness
near the DEJ is about three times greater than near the pulp. Although dentin is a
hard, mineralized tissue, it is flexible. This flexibility helps support the more brittle,
less resilient enamel. Dentin is not as prone to fracture as is the enamel rod structure.
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 4. Sound: when moving an explorer tip over the tooth, enamel surfaces provide
a sharper, higher pitched sound than dentin surfaces.

Permeability of Dentin
The permeability of dentin can compromise its protective function because of the
presence of dentinal tubules, which are very important during formation of dentin,
however, when the external layer of enamel and cementum is lost from the periphery
of the dentinal tubules through caries, preparation with burs or abrasion and erosion,
the exposed dentinal tubules become channels between the pulp and the external oral
environment. However, in case of dentin cutting with bur, these exposed dentinal
tubules usually occluded by a layer of tenacious grinding debris called the smear
layer, which adheres to the surface and partially plugs the tubular orifices. However,
the removal of the smear layer with acid etching during dentin bonding procedures
causes an increase in the local dentinal permeability along with an outward fluid
movement from the tubules, which results in adverse conditions for adhesive
bonding by creating wet environment which may reduce bond strength of bonding
agent over time.
Also, the restored teeth are at risk of toxic leakage through the phenomenon of
microleakage (which is defined as diffusion of the bacteria, oral fluids, ions and
molecules into the tooth and the filling material interface) between the restorative
material and the cavity wall, through capillary action, and diffusion of fluids
containing various acidic and bacterial products can penetrate the gap between the
tooth and restoration and initiate secondary caries of the internal cavity walls.
Bacterial byproducts can continuously diffuse through permeable dentinal tubules to
reach the pulp, putting the tooth at risk for pulpal inflammation and sensitivity.

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 No restorative material or technique can ensure a complete hermetic seal of the
restoration-tooth interface, and leakage at the gingival (cementum or dentin) margins
of resin-bonded restorations is commonly reported. Dye experiment shows the
microleakage through restoration tooth interface.
Restorative techniques with varnishes, liners or dentin bonding resin adhesives
are effective to provide reliably sealed margins and sealed dentinal surface.
However, the remaining dentin thickness is the key determinant of the rate of
diffusion of gradient into the pulp, because thicker remaining dentin thickness with
provide both smaller tubular diameters and greater tubular lengths, therefore thicker
remaining dentin thickness can significantly reduce both the adverse toxic effect of
restorative materials and bacterial irritation to the pulp

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 There are also regional differences in dentinal permeability. Coronal dentin is
much more permeable than root dentin. The coronal occlusal dentin (pulpal floor of
a cavity preparation) is inherently less permeable than is the dentin around the pulp
horns or axial surfaces. As a result, only about 30% of the subjacent dentinal tubules
on occlusal surface are patent over their entire length. However, prepared proximal
boxes or gingival margins, which are relatively more susceptible to microleakage
and development of recurrent caries lesions, are located where the dentin is most
permeable.

Sensitivity of Dentin
Although dentin is sensitive to thermal, tactile and osmotic stimuli across its (3-
3.5 mm) thickness. Dentin is neither vascularized nor innervated, except for about
20% of tubules that have nerve fibers penetrating inner dentin by few microns. Also,
odontoblastic processes in the dentinal tubules reach only the inner third of dentin
and their cell membrane is not conductive, however recent studies suggest that
odontoblasts could possibly be directly involved in the sensory transduction process
of the tooth through some form of mechanosensory system.

Theories of Dentin Sensitivity

There are many theories proposed to explain dentin sensitivity
1. Direct innervation theory:
According to direct innervation theory, nerve endings penetrate dentine and
extend to the dentino-enamel junction. Direct mechanical stimulation of these nerves
will initiate an action potential. There are many shortcomings of this theory. There
is lack of evidence that outer dentin, which is usually the most sensitive part, is
innervated. Developmental studies have shown that the plexus of Rashkow and
intratubular nerves do not establish themselves until the tooth has erupted; yet, newly
erupted tooth is sensitive. Moreover, pain inducers such as bradykinin fail to induce
pain when applied to dentine, and bathing dentine with local anesthetic solutions
does not prevent pain, which does so when applied to skin.
2. Odontoblast receptor theory:
Odontoblast receptor theory states that odontoblasts act as receptors by
themselves and relay the signal to a nerve terminal. But majority of studies have

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shown that odontoblasts are matrix forming cells and hence they are not considered
to be excitable cells, and no synapses have been demonstrated between odontoblasts
and nerve terminals
3. Theory of thermal shock:
This states that sensitivity is the result of direct thermal shock (temperature
change) to the pulp via temperature changes transferred from the oral cavity through
the tooth or restorative material, especially when the remaining dentin is thin.
Protection from this insult would then be provided by an adequate thickness of an
insulating material such as cements.
4. The hydrodynamic theory:
This theory based on the capillary flow dynamics of the fluid-filled dentinal
tubule. In a vital tooth with exposed dentin there is a constant slow movement of
fluid outward through the dentinal tubules. The hydrodynamic theory proposed that
when a stimulus such as air evaporation, cold or heat (i.e. generated from dental bur)
or tactile pressure with probe cause the slow fluid movement to become more rapid
causing displacement in the odontoblastic cell bodies and stretches the intertwined
terminal branches of the nerve plexus to allow the entry of sodium to initiate
depolarization and the perception of pain.
As dentin near the pulp, tubule density and diameter increase also the
permeability increase, thus increasing both the volume and flow of fluid. This
explains why deeper restorations are associated with more problems of sensitivity.
In root dentin hypersensitivity the degree of tubule closure from intratubular crystals
was directly correlated with decreased sensitivity to touch, air, or temperature
stimuli. Tooth pastes that contain strontium chloride, oxalates can promote
intratubular crystallization and desensitize dentin. Resin bonding agents, fluoride
varnishes and potassium and silver nitrate can also reduce dentin hypersensitivity by
occluding dentinal tubules or nerve desensitization. Calcium silicate cements can
reduce dentin hypersensitivity by remineralization as well.

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Comparison between thermal shock and hydrodynamic theories:
According to hydrodynamic theory, during temperature change, if the tubules can
be occluded, rapid outward fluid flow is prevented and temperature do not induce
pain. Therefore, reducing dentin sensitivity to thermal changes is by effective sealing
of the dentinal tubules rather than placement of an insulating material (according to
thermal shock theory). The hydrodynamic theory has gained general acceptance in
recent years and has changed the direction of restorative procedures away from
thermal insulation and toward dentinal sealing. Thus, there is increasing emphasis
on the integrity of the interface between restorative material and cavity preparation
in adhesive restorations.
Also, it is worth noting that when the tooth exposed to thermal, mechanical and
chemical stimuli for a long time, the rate of formation and the thickness and
organization of reactionary dentin (as a response of pulp to stimuli) depend on the
intensity and duration of the stimulus. The barrier of reactionary dentin is superior
because there is no continuity between the affected permeable tubules of the regular
primary dentin and those within the reactionary dentin. The tooth will be able to
compensate for the traumatic or carious loss of peripheral dentin with deposition of
new dentin substrate and reduction of pulpal irritation from tubule permeability.
Unless the lesion is either arrested or removed and a restoration placed, the diffusion
of bacterial toxins reaching the pulp and initiate strong inflammatory response and
result in pulpal necrosis.

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