CHAPTER 6

Pulp

CHAPTER CONTENTS

Anatomy 91
General features 91
Coronal pulp 91
Radicular pulp 91
Apical foramen 92
Accessory canals 92
Structural Features 92
Intercellular substance 93
Fibers 94
Cells of the pulp 94
Fibroblasts 94
Undifferentiated mesenchymal cells 95
Odontoblasts 95
Defense cells 97
Pulpal stem cells 98
Blood vessels 99
Lymph vessels 102
Nerves 103
Nerve endings 103
Functions 106
Inductive 106
 Formative 106
Nutritive 106
Protective 106
Defensive or reparative 106
Regressive Changes (Aging) 106
Development 107
Clinical Considerations 107
Pathologic considerations 107
Operative and endodontic considerations 108
Pulp chamber and its extensions 108
Pulpal response to restorative procedures and materials
109
Pulpal Pain 110
Vitality of Pulp 110
Summary 111
Review Questions 112

The term “pulpa,” derived from Latin primarily indicates animal or

plant tissues which are moist and soft, occurring in the form of a
cohering mass. Dental pulp can be defined as a richly vascularized
and innervated connective tissue of mesodermal origin enclosed by
dentin with communications to the periodontal ligament.
Anatomy
General features
The dental pulp occupies the center of each tooth and consists of soft
connective tissue. The pulp is housed in the pulp chamber of the
crown and in the root canal of the root. The pulp present in the crown
is called coronal pulp and the pulp present in the root is called
radicular pulp. The shape of the pulp therefore resembles the shape of
the tooth in which it is housed. The total volume of all the permanent
teeth pulp is 0.38 cm3, and the mean volume of a single adult human
pulp is 0.02 cm3. Molar pulps are three to four times larger than
incisor pulps. Table 6.1 gives the variation in the size of pulp in
different permanent teeth.

Table 6.1
Pulp Volumes for the Permanent Human Teeth
From a Preliminary Investigation of 160 Teetha
Maxillary (cm3) Mandibular (cm3)
Central incisor 0.012 0.006
Lateral incisor 0.011 0.007
Canine 0.015 0.014
First premolar 0.018 0.015
Second premolar 0.017 0.015
First molar 0.068 0.053
Second molar 0.044 0.032
Third molar 0.023 0.031
aFigures for volumes from Fanibunda KB: Personal communication, University of Newcastle
upon Tyne, Department of Oral Surgery, Newcastle upon Tyne, England.

Coronal pulp
The coronal pulp in young individuals resembles the shape of the
outer surface of the crown dentin. The coronal pulp has six surfaces:
the roof or occlusal, the mesial, the distal, the buccal, the lingual, and
the floor. It has pulp horns, which are protrusions that extend into the
cusps of each crown. The number of these horns thus depends on the
cuspal number. The cervical region of the pulp organs constricts as
does the contour of the crown, and at this zone the coronal pulp joins
the radicular pulp. Because of continuous deposition of dentin, the
pulp becomes smaller with age. This is not uniform through the
coronal pulp but progresses faster on the floor than on the roof or side
walls.

Radicular pulp
The radicular or root pulp is that pulp extending from the cervical
region of the crown to the root apex. In the anterior teeth, the
radicular pulps are single and in posterior ones multiple. They are not
always straight and vary in size, shape, and number. The radicular
portions of the pulp are continuous with the periapical connective
tissues through the apical foramen or foramina. The dentinal walls
taper and the shape of the radicular pulp is tubular. During root
formation, the apical root end is a wide opening limited by an
epithelial diaphragm (Fig. 6.1A). As growth proceeds, more dentin is
formed, so that when the root of the tooth has matured, the radicular
pulp is narrower. The apical pulp canal becomes smaller also because
of apical cementum deposition (Fig.6.1B).
 FIGURE 6.1 Development of apical foramen. (A) Undeveloped root
end. Wide opening at end of root, partly limited by epithelial diaphragm.
(B) Apical foramen fully formed. Root canal straight. Apical foramen
surrounded by cementum. (Source: From Coolidge ED: J Am Dent
Assoc 16:1456, 1929).

Apical foramen
The average size of the apical foramen of the maxillary teeth in the
adult is 0.4 mm. In the mandibular teeth, it is slightly smaller, being
0.3 mm in diameter.
The location and shape of the apical foramen may undergo changes
as a result of functional influences on the teeth. A tooth may be tipped
from horizontal pressure, or it may migrate mesially, causing the apex
to tilt in the opposite direction. Under these conditions, the tissues
entering the pulp through the apical foramen may exert pressure on
one wall of the foramen, causing resorption. At the same time,
cementum is laid down on the opposite side of the apical root canal,
resulting in a relocation of the original foramen (Fig. 6.2A).
 FIGURE 6.2 Variations of apical foramen. (A) Shift of apical foramen
by resorption of dentin and cementum on one surface and apposition of
cementum on the other. (B) Apical foramen on side of apex. (Source:
From Coolidge ED: J Am Dent Assoc 16:1456, 1929).

Sometimes the apical opening is found on the lateral side of the

apex (Fig. 6.2B), although the root itself is not curved. Frequently,
there are two or more foramina separated by a portion of dentin and
cementum or by cementum only.

Accessory canals
Accessory canals leading from the radicular pulp laterally through the
root dentin to the periodontal tissue may be seen anywhere along the
root but are most numerous in the apical third of the root (Fig. 6.3A–
C). They are clinically significant in spread of infection, either from
the pulp to the periodontal ligament or vice versa. The mechanism by
which they are formed is not known, but it is likely that they occur in
areas where there is premature loss of root sheath cells because these
cells induce the formation of the odontoblasts which form the dentin.
Accessory canals may also occur where the developing root
encounters a blood vessel. If the vessel is located in the area where the
dentin is forming, the hard tissue may develop around it, making a
lateral canal from the radicular pulp.

FIGURE 6.3 (A and B) Sections through teeth with accessory canals.

(A) Close to apex. (B) Close to bifurcation. (C) Radiograph of lower
molar with accessory canal filled. (Source: (C) From Johnston HB and
Orban B: J Endodont 3:21, 1948).
Structural features
The pulp is basically a loose connective tissue. Therefore, it contains a
ground substance (intercellular substance) in which are embedded
cells and fibres. Like other connective tissue, it contains supporting
elements—the blood vessels and nerves.
The central region of both the coronal and the radicular pulp
contains large nerve trunks and blood vessels. Peripherally, the pulp
is circumscribed by the specialized odontogenic region composed of
(1) the odontoblasts (the dentin-forming cells), (2) the cell-free zone
(Weil’s zone), and (3) the cell-rich zone (Fig. 6.4). The cell-free zone is
a space in which the odontoblast may move pulpward during tooth
development and later to a limited extent in functioning teeth. This
may be why the zone is inconspicuous during early stages of rapid
dentinogenesis since odontoblast migration would be greatest at that
time. The cell-rich layer composed principally of fibroblasts and
undifferentiated mesenchymal cells is restricted to the coronal
regions, as it is formed during the pre-eruptive phase of the tooth.
During early dentinogenesis, there are also many young collagen
fibers in this zone (Table 6.2).
 FIGURE 6.4 Diagram of pulp organ, illustrating architecture of large
central nerve trunks (dark) and vessels (light) and peripheral cell-rich,
cell-free, and odontoblast rows. Observe small nerves on blood
vessels.

Table 6.2
Zones of Pulp
Zone Major Component
Odontoblastic zone Odontoblast cells
Cell-free zone (Weil’s Relatively acellular, accommodate odontoblast during
zone) development and function of tooth
Cell-rich zone Fibroblasts, undifferentiated mesenchymal cells
(primarily coronal)
Pulp core Predominantly fibrous tissue, major vessels and nerves, fibroblasts

Intercellular substance
The intercellular substance is dense and gel like in nature, varies in
appearance from finely granular to fibrillar, and appears more dense
in some areas, with clear spaces left between various aggregates. It is
composed of both acid mucopolysaccharides and protein
polysaccharide compounds (glycosaminoglycans and proteoglycans).
During early development, the presence of chondroitin A, chondroitin
B, and hyaluronic acid has been demonstrated in abundance.
Glycoproteins are also present in the ground substance. The aging
pulp contains less of all of these substances. The ground substance
lends support to the cells of the pulp while it also serves as a means
for transport of nutrients from the blood vessels to the cells, as well as
for transport of metabolites from cells to blood vessels.
Glycosaminoglycans being hydrophilic, forms a gel and contributes
to high tissue fluid pressure of the pulp. Hyaluronan, in addition to
mechanical function helps in cell migration. Versican forms the bulk of
the proteoglycans. Syndecan, another important proteoglycan, attaches
to the cell and acts as an adhesion molecule between fibroblast and
collagen. It also binds signaling molecules like fibroblastic growth
factor. Tenascin and fibronectin, which promote cell adhesion and cell
migration are absent in areas of inflammation. Laminin, which is
present in the basement membrane of blood vessels, also coats the
odontoblast cell membrane. Integrins, the glycoproteins, which
interact to form cell surface adhesion receptors were found in pulp to
get attached to biologically active molecules like laminin and
fibronectin.

Fibers
The collagen fibers in the pulp exhibit typical cross-striations at 64 nm
(640 Å) and range in length from 10 to 100 nm or more (Fig. 6.5). The
main type of collagen fiber in the pulp is type I. Type III collagen is
also present. Bundles of these fibers appear throughout the pulp. In
very young pulp, fine fibers ranging in diameter from 10 to 12 nm
(100 to 120 Å) have been observed. These fine fibers are called fibrillin.
Downregulation and degradation of fibrillin helps in release of TGF-β,
which in turn promotes the formation of a mineralized tissue barrier
in exposed pulps.
 FIGURE 6.5 Typical collagen fibers of the pulp with 640 Å banding.

Pulp collagen fibers do not contribute to dentin matrix production,

which is the function of the odontoblast. After root completion, the
pulp matures and bundles of collagen fibers increase in number. They
may appear scattered throughout the coronal or radicular pulp, or
they may appear in bundles. These are termed diffuse or bundle
collagen depending on their appearance, and their presence may
relate to environmental trauma. Fiber bundles are most prevalent in
the root canals, especially near the apical region.

Cells of the pulp

The predominant cell of the pulp is the fibroblast. The cells unique to
pulp are the odontoblasts. Apart from these cells, the pulp contains
defense cells, undifferentiated mesenchymal cells, and pulpal stem
cells.

Fibroblasts
The pulp organ is said to be consisting of specialized connective tissue
because it lacks elastic fibers. Fibroblasts are the most numerous cell
type in the pulp. As their name implies, they function in collagen fiber
formation throughout the pulp during the life of the tooth. They have
the typical stellate shape and extensive processes that contact and are
joined by intercellular junctions to the processes of other fibroblasts
(Fig. 6.6A). Under the light microscope, the fibroblast nuclei stain
deeply with basic dyes, and their cytoplasm is lighter stained and
appears homogeneous. Electron micrographs reveal abundant rough-
surfaced endoplasmic reticulum, mitochondria, and other organelles
in the fibroblast cytoplasm (Fig. 6.6B). This indicates that these cells
are active in pulpal collagen production. There is some difference in
appearance of these cells depending on the age of the pulp organ. In
the young pulp, the cells divide and are active in protein synthesis,
but in the older pulp, they appear rounded or spindle shaped with
short processes and exhibit fewer intracellular organelles. They are
then termed fibrocytes. In the course of development, the relative
number of cellular elements in the dental pulp decreases, whereas the
fiber population increases (Fig. 6.7). In the embryonic and immature
pulp, the cellular elements predominate, while in the mature pulp, the
fibrous components predominate. The fibroblasts of the pulp, in
addition to forming the pulp matrix, also have the capability of
ingesting and degrading this same matrix. These cells thus have a
dual function with pathways for both synthesis and degradation in
the same cell.
FIGURE 6.6 (A) Typical fibroblasts of pulp are stellate in shape with
long processes. (B) Electron micrograph of pulp fibroblast.
FIGURE 6.7 Age changes of dental pulp. Cellular elements decrease
and fibrous intercellular substance increases with advancing age. (A)
 Newborn infant. (B) Infant 9 months of age. (C) Adult.

Fibroblasts play an important role in inflammation and healing.

Fibroblasts secrete angiogenic factors like FGF-2 and VEGF, especially
after injury, which help in healing. They are also shown to secrete
colony-stimulating factors, which help in the migration of class II
major histocompatibility expressing cells into the pulp tissue. They
release inflammatory mediators cytokines and growth factors. In cell
cultures, they form mineralized tissue like bone on stimulation.

Undifferentiated mesenchymal cells

Undifferentiated mesenchymal cells are the primary cells in the very
young pulp, but a few are seen in the pulps after root completion.
They appear larger than fibroblasts and are polyhedral in shape with
peripheral processes and large oval staining nuclei. The latter are
distinctive because they lack a ribosome-studded endoplasmic
reticulum and have mitochondria with readily discernible cisternae.
They are found along pulp vessels, (Fig. 6.8) in the cell-rich zone and
scattered throughout the central pulp. Viewed from the side, they
appear spindle shaped. They are believed to be a totipotent cell and
when need arises they may become odontoblasts, fibroblasts, or
macrophages. They decrease in number in old age.
 FIGURE 6.8 Defense cells in pulp.

Odontoblasts
Odontoblasts, the second most prominent cell in the pulp, reside
adjacent to the predentin with cell bodies in the pulp and cell
processes in the dentinal tubules. The number of odontoblasts
corresponds to the number of dentinal tubules. They are
approximately 5–7 µm in diameter and 25–40 µm in length. They have
a constant location adjacent to the predentin, in what is termed the
“odontogenic zone of the pulp” (Fig. 6.9). The cell bodies of the
odontoblasts are columnar in appearance with large oval nuclei,
which fill the basal part of the cell (Fig. 6.9). Immediately adjacent to
the nucleus basally is rough-surfaced endoplasmic reticulum and the
Golgi apparatus. The cells in the odontoblastic row lie very close to
each other. Between odontoblasts gap, tight and desmosomal
junctions exist (Fig. 6.10). Further toward the apex of the cell appears
an abundance of rough-surfaced endoplasmic reticulum. Near the
pulpal–predentin junction, the cell cytoplasm is devoid of organelles.
Focal junctional complexes are present where the odontoblast cell
body gives rise to the process. Actin filaments are inserted into this
region. The clear terminal part of the cell body and the adjacent
intercellular junction is described by some as the terminal bar
apparatus of the odontoblast. At this zone, the cell constricts to a
diameter of 3–4 µm, where the cell process enters the predentinal
tubule (Fig. 6.9).
FIGURE 6.9 Diagram of odontogenic zone illustrating odontoblast,
cell-free, and cell-rich zones, with blood vessels and nonmyelinated
nerves among odontoblasts.
 FIGURE 6.10 Close relation of adjacent odontoblasts. Note junctional
complexes between cells (arrows).

The process of the cell contains no endoplasmic reticulum, but

during the early period of active dentinogenesis, it does contain
occasional mitochondria and vesicles. During the later stages of
dentinogenesis, these are less frequently seen.
The odontoblast morphology and its organelles vary with the
functional activity of the cell. An active cell is elongated whereas a
resting cell is stubby. The active cell has a basally placed nucleus and
a basophilic cytoplasm. The resting cell has little cytoplasm but a more
hematoxyphilic nucleus.
There is also a striking difference in the cytoplasm of the young cell
body, active in dentinogenesis, and the older cell. During this early
active phase, the Golgi apparatus is more prominent, the rough-
surfaced endoplasmic reticulum is more abundant, and numerous
mitochondria appear throughout the odontoblast. A great number of
vesicles are seen along the periphery of the process where there is
evidence of protein synthesis along the tubule wall. The cell actually
increases in size as its process lengthens during dentin formation.
When the cell process becomes 2 mm long, it is then many times
greater in volume than the cell body. While the active cell is rich in
organelles, the resting cell is devoid of organelles especially in the
supranuclear region, where mainly lipid-filled vacuoles are present.
Ultrastructurally, an intermediate stage between active and resting
called transitional stage is recognized. In this stage, the cells are
narrower with fewer organelles and with the presence of autophagic
vacuoles. Recently, primary cilia have been identified in odontoblast.
These cilia may play a role in response of odontoblasts to external
stimuli.
The form and arrangement of the bodies of the odontoblasts are not
uniform throughout the pulp. They are more cylindrical and longer
(tall columnar) in the crown (Fig. 6.11A) and more cuboid in the
middle of the root (Fig. 6.11B). Close to the apex of an adult tooth, the
odontoblasts are ovoid and spindle shaped, appearing more like
osteoblasts than odontoblasts, but they are recognized by their
processes extending into the dentin. The pseudostratified
arrangement seen in the coronal pulp is due to the crowding of cells in
this region (Fig. 6.11C). Ultrastructurally, ring-layered structures have
been observed between aging odontoblasts that might be
characteristic of aging teeth.
 FIGURE 6.11 Variation of odontoblasts in different regions of one
tooth. (A) High columnar odontoblasts in pulp chamber. (B) Low
columnar odontoblasts in root canal. (C) Flat odontoblasts in apical
region.

Collagen is assembled in the odontoblast similar to that occurring in

fibroblast. The noncollagenous proteins which are secreted by the
odontoblast may be present in the same secretory granule along with
the collagen.
Odontoblasts are end cells. They have lost the ability to divide.
When they die they have to be replaced by cells, which differentiate
from the cell-rich zone. Odontoblast and subodontoblastic cells have
been shown to undergo apoptotic cell death by apoptotic cell markers
like bcl-2.
Odontoblasts release inflammatory chemokine interleukin-8 which
is chemotactic for neutrophils. Nerve growth factor and its receptor
found in the odontoblasts are chemoattractants for neutrophils. Nitric
oxide synthetase are important enzymes for vasodilatation and blood
pressure regulation. These have been identified in odontoblasts and
endothelial cells of the pulp. This finding suggests that they may have
a role in mediating cell proliferation and vasodilatation.

Defense cells
In addition to fibroblasts, odontoblasts, and the cells that are a part of
the neural and vascular systems of the pulp, there are cells important
to the defense of the pulp. These are histiocytes or macrophages,
dendritic cells, mast cells, and plasma cells. In addition, there are the
blood vascular elements such as the neutrophils (PMNs), eosinophils,
basophils, lymphocytes, and monocytes. These latter cells emigrate
from the pulpal blood vessels and develop characteristics in response
to inflammation.
The histiocyte or macrophage is an irregularly shaped cell with
short blunt processes (Figs 6.8 and 6.12). In the light microscope, the
nucleus is somewhat smaller, more rounded, and darker staining than
that of fibroblasts, and it exhibits granular cytoplasm. When the
macrophages are inactive and not in the process of ingesting foreign
materials, one faces difficulty in distinguishing them from fibroblasts.
In the case of a pulpal inflammation, these cells exhibit granules and
vacuoles in their cytoplasm, and their nuclei increase in size and
exhibit a prominent nucleolus. Their presence is disclosed by
intravital dyes such as toluidine blue. These cells are usually
associated with small blood vessels and capillaries. Ultrastructurally,
the macrophage exhibits a rounded outline with short, blunt processes
(Fig. 6.12). Invaginations of the plasma membrane are noted, as are
mitochondria, rough-surfaced endoplasmic reticulum, free ribosomes,
and also a moderately dense nucleus. The distinguishing feature of
macrophages is aggregates of vesicles, or phagosomes, which contain
phagocytized dense irregular bodies (Fig. 6.12).
 FIGURE 6.12 (A) This histiocyte or macrophage is located adjacent to
capillary in peripheral pulp. Characteristic aggregation of vesicles,
vacuoles, and phagocytized dense bodies is seen to right of capillary
wall. (B) Multivesiculated body characteristic of macrophage. Note
typical invagination of cell plasma membrane (arrow). This cell is
located adjacent to group of nonmyelinated nerve fibers seen on left.

Dendritic cells were found in close relation to and in contact with

the cell membranes of the endothelial cell. These cells express
macrophage-related antigens (CD14 and CD68) and were identified
by their immunopositivity to HLA-DR monoclonal antibodies. These
cells are similar to Langerhans cells. They present the antigen to the T
cells. Some of these cells formed a reticular network in the connective
tissue. In deciduous teeth, these dendritic cells were shown to be
closely associated with odontoblasts. Their dendritic process
sometimes extended into the dentinal tubules and made contact with
the odontoblastic process. Their numbers were found to increase in
areas affected by caries, attrition, or restorative procedures. These
suggest that they have an important role to play in
immunosurveillance. In view of their close association with
odontoblasts, it is suggested that these cells may have some regulatory
function on the odontoblast. Immunocompetent cells present in
deciduous teeth increased in number during shedding.
Both lymphocytes and eosinophils are found extravascularly in the
normal pulp (Fig. 6.13), but during inflammation they increase
noticeably in number. Most of the lymphocytes present in the pulp are
T lymphocytes. Mast cells are also seen along vessels in the inflamed
pulp. They have a round nucleus and contain many dark-staining
granules in the cytoplasm, and their number increases during
inflammation.

FIGURE 6.13 (A) Small lymphocyte located in pulp. Cytoplasm forms

narrow rim around large oval-to-round nucleus. (B) Eosinophil in
extravascular location in pulp organ. Nucleus is polymorphic, and
granules in cytoplasm are characteristically banded.

The plasma cells are seen during inflammation of the pulp (Fig. 6.14).
With the light microscope, the plasma cell nucleus appears small and
concentric in the cytoplasm. The chromatin of the nucleus is adherent
to the nuclear membrane and gives the cell a cartwheel appearance.
The cytoplasm of this cell is basophilic with a light-stained Golgi zone
adjacent to the nucleus. Under the electron microscope, these cells
have a densely packed, rough-surfaced endoplasmic reticulum. Both
immature and mature cells may be found. The mature type exhibits a
typical small eccentric nucleus and more abundant cytoplasm (Fig.
6.14). The plasma cells function in the production of antibodies (Table
6.3).

FIGURE 6.14 Cluster of plasma cells in pulp with early caries pulpitis.
Observe dense peripheral nuclear chromatin and cytoplasm with
cisternae of rough endoplasmic reticulum. Source: (Courtesy C
Torneck, University of Toronto Dental School).

Table 6.3
Composition of Dental Pulp
Pulpal stem cells
Among the numerous stem cells that have been identified from dental
tissues and characterized, those from the pulpal tissues include dental
pulp stem cells (DPSCs) and stem cells from human exfoliated
deciduous teeth (SHED). Stem cells are found in higher concentration
in coronal pulp than in radicular pulp.
Pulpal stem cells express cytokeratin 18 and 19, indicating a
potential for odontoblast differentiation and dentin repair at sites of
injury. A comparative study of bone marrow and DPSCs indicates
that they are influenced by different regulatory mechanisms to engage
in bone and dentin formation, respectively. Dentin sialoprotein, a
marker for dentin synthesis has been observed in DPSC transplants,
while in bone marrow stem cell transplants expression of fibroblast
growth factor (FGF) and matrix metalloproteinase (MMP-9) have been
seen. Numerous growth factors including transforming growth factor
(TGF), bone morphogenetic protein (BMP-2) and dentin matrix
protein 1 (DMP-1) are capable of inducing proliferation and
differentiation of DPSCs. DMP-1 has been shown to induce formation
of dental pulp-like tissue in vivo.
Pulpal stem cells are pluripotential having the capacity for
angiogenic, chondrogenic, osteogenic, adipogenic, and neurogenic
differentiation, in some cases exceeding that of bone marrow stem
cells. The pulpal tissues of exfoliated deciduous teeth and permanent
third molars may serve as a suitable source of stem cells for future
stem cell–based therapies as they are found to be viable after
cryopreservation. The application of DPSCs in regenerative dentistry
and medicine (regeneration of bone and neural tissues) holds great
promise.

Blood vessels
The pulp organ is extensively vascularized. It is known that the blood
vessels of both the pulp and the periodontium arise from the inferior
or superior alveolar artery and also drain by the same veins in both
the mandibular and maxillary regions. The communication of the
vessels of the pulp with the periodontium, in addition to the apical
connections, is further enhanced by connections through the accessory
canals. These relationships are of considerable clinical significance in
the event of a potential pathologic condition in either the
periodontium or the pulp, because the infection has a potential to
spread through the accessory and apical canals. Although branches of
the alveolar arteries supply both the tooth and its supporting tissues,
those periodontal vessels entering the pulp change their structure
from the branches to the periodontium and become considerably
thinner walled than those surrounding the tooth.
Small arteries and arterioles enter the apical canal and pursue a
direct route to the coronal pulp (Fig. 6.15). Along their course they
give off numerous branches in the radicular pulp that pass
peripherally to form a plexus in the odontogenic region. Pulpal blood
flow is more rapid than in most areas of the body. This is perhaps
attributable to the fact that the pulpal pressure is among the highest of
body tissues. The flow of blood in arterioles is 0.3–1 mm per second,
in venules approximately 0.15 mm per second, and in capillaries about
0.08 mm per second. The largest arteries in the human pulp are 50–100
µm in diameter, thus equaling in size arterioles found in most areas of
the body. These vessels possess three layers. The first, the tunica
intima, consists of squamous or cuboid endothelial cells surrounded
by a closely associated basal lamina. Where the endothelial cells
contact, they appear overlapped to varying degrees. The second layer,
the tunica media, is approximately 5-µm thick and consists of one to
three layers of smooth muscle cells (Fig. 6.16). A basal lamina
surrounds and passes between these muscle cells and separates the
muscle cell layer from the intima. Occasionally, the endothelial cell
wall is in contact with the muscle cells. This is termed a
myoendothelial junction. The third and outer layer, the tunica
adventitia, is made up of a few collagen fibers forming a loose
network around the larger arteries. This layer becomes more
conspicuous in vessels in older pulps. Arterioles with diameters of 20–
30 µm with one or occasionally two layers of smooth muscle cells are
common throughout the coronal pulp (Fig. 6.17). The tunica adventitia
blends with the fibers of the surrounding intercellular tissue. Terminal
arterioles with diameters of 10–15 µm appear peripherally in the pulp.
The endothelial cells of these vessels contain numerous
micropinocytotic vesicles, which function in transendothelial fluid
movement. A single layer of smooth muscle cells surrounds these
small vessels. Occasionally, a fibroblast or pericyte lies on the surface
of these vessels. Pericytes are capillary-associated fibroblasts. They are
present partially encircling the capillaries. They have contractile
properties and they are capable of reducing the size of the capillary
lumen. Their nuclei can be distinguished as round or slightly oval
bodies closely associated with the outer surface of the terminal
arterioles or precapillaries (Fig. 6.18). Some authors call the smaller
diameter arterioles “precapillaries.” They are slightly larger than the
terminal capillaries and exhibit a complete or incomplete single layer
of muscle cells surrounding the endothelial lining. These range in size
from 8 to 12 µm.
FIGURE 6.15 Branching artery and nerve trunk in the pulp.
 FIGURE 6.16 Small arteriole near central pulp exhibiting relatively
thick layer of muscle cells. Dense basement membrane interspersed
between endothelial and muscle cells (arrow).
 FIGURE 6.17 Peripheral pulp and small arteriole or precapillary
exhibiting two thin layers of smooth muscle cells surrounding the
endothelial cell lining of vessel. Nucleus at bottom left of figure belongs
to a pericyte.

FIGURE 6.18 Area near subodontoblastic plexus showing both

myelinated and nonmyelinated axons adjacent to large capillary or
precapillary. Endothelial cell lining is surrounded by basement
membrane (arrow) and pericytes.

Veins and venules that are larger than the arteries also appear in the
central region of the root pulp. They measure 100–150 µm in diameter,
and their walls appear less regular than those of the arteries because
of bends and irregularities along their course. The microscopic
appearance of the veins is similar to that of the arteries except that
they exhibit much thinner walls in relation to the size of the lumen.
The endothelial cells appear more flattened, and their cytoplasm does
not project into the lumen. Fewer intracytoplasmic filaments appear in
these cells than in the arterioles. The tunica media consists of a single
layer or two of thin smooth muscle cells that wrap around the
endothelial cells and appear discontinuous or absent in the smaller
venules. The basement membranes of these vessels are thin and less
distinct than those of arterioles. The adventitia is lacking or appears as
fibroblasts and fibers are continuous with the surrounding pulp
tissue. Occasionally, two venous loops will be seen connected by an
anastomosing branch. Both venous-venous anastomosis and arteriole-
venous anastomosis occur in the pulp. The arteriole-venous shunts
may have an important role in regulation of pulpal blood flow.
Frequently arteriole or precapillary loops with capillaries are found
underlying the odontogenic zone in the coronal pulp.
Blood capillaries, which appear as endothelium-lined tubes, are 8–
10 µm in diameter. The nuclei of these cells may be lobulated and
have cytoplasmic projections into the luminal surface. The terminal
network of capillaries in the coronal pulp appears nearly
perpendicular to the main trunks. The vascular network passes among
the odontoblasts and underlies them as well. A few peripheral
capillaries found among the odontoblasts have fenestrations in the
endothelial cells. These pores are located in the thin part of the
capillary wall and are spanned only by the thin diaphragm of
contacting inner and outer plasma membranes of endothelial cells
(Fig. 6.19). These fenestrated capillaries are assumed to be involved in
rapid transport of metabolites at a time when the odontoblasts are
active in the process of dentinal matrix formation and its subsequent
calcification. Both fenestrated and continuous terminal capillaries are
found in the odontogenic region. During active dentinogenesis
capillaries appear among the odontoblasts adjacent to the predentin.
Later, after the teeth have reached occlusion and dentinogenesis slows
down, these vessels usually retreat to a subodontoblastic position
(Table 6.4).
 FIGURE 6.19 (A) Terminal capillary loops located among odontoblasts
may be fenestrated. These capillaries have both thick and thin
segments in their walls. (B) Endothelial cell wall bridges pores (arrows)
and is supported only by basement membrane (**).

Table 6.4
Microcirculation of Pulp
Arteries and arterioles thin walled
Pulpal arteries are as big as arterioles elsewhere
Do not branch in radicular pulp
Subodontoblastic plexus of capillaries seen
Presence of arteriole venous anastomosis
Pericytes in relation to smaller arterioles control blood flow
Sympathetic nerves also control blood flow
Higher capillary pressure
Rapid blood flow and fenestrated capillaries facilitate rapid metabolite transport
Veins and venules thin walled
Lymphatics follow course of blood vessels

Lymph vessels
Lymph capillaries are described as endothelium-lined tubes that join
thin-walled lymph venules or veins in the central pulp. The lymphatic
capillaries have thin walls. Cellular projections arise from the
endothelial cells. The cells contain multivesicular structures, Weibel–
Palade bodies, and paracrystalline inclusions. The lymphatic vessels
were more numerous in the central part of the pulp than in the
peripheral areas. The larger vessels have an irregular-shaped lumen
composed of endothelial cells surrounded by an incomplete layer of
pericytes or smooth muscle cells or both. Further, the lymph vessels
differ from venules in that their walls and basement membrane show
discontinuities, with the absence of RBCs but with the presence of
lymphocytes in the lumen. In inflamed pulps, due to increased
interstitial fluid pressure, gap junction develops between the
endothelial cells of the dilated lymph capillaries. Lymph vessels
draining the pulp and periodontal ligament have a common outlet.
Those draining the anterior teeth pass to the submental lymph nodes;
those of the posterior teeth pass to the submandibular and deep
cervical lymph nodes.

Nerves
The abundant nerve supply in the pulp follows the distribution of the
blood vessels. The majority of the nerves that enter the pulp are
nonmyelinated. Many of these gain a myelin sheath later in life. The
nonmyelinated nerves are found in close association with the blood
vessels of the pulp and many are sympathetic in nature. They have
terminals on the muscle cells of the larger vessels and function in
vasoconstriction (Fig. 6.18). Thick nerve bundles enter the apical
foramen and pass along the radicular pulp to the coronal pulp where
their fibers separate and radiate peripherally to the parietal layer of
nerves (Figs 6.20 and 6.21). The number of fibers in these bundles
varies greatly, from as few as 150 to more than 1200. The larger fibers
range between 5 and 13 µm, although the majority are smaller than 4
µm. The perineurium and the epineurium of the pulpal nerves are
thin. The large myelinated fibers mediate the sensation of pain that
may be caused by external stimuli. The peripheral axons form a
network of nerves located adjacent to the cell-rich zone. This is termed
the parietal layer of nerves, also known as the plexus of Raschkow
(Fig. 6.22). Both myelinated axons, ranging from 2 to 5 µm in
diameter, and minute nonmyelinated fibers of approximately 200–
1600 µm (2000–16,000 Å) in size make up this layer of nerves. The
parietal layer develops gradually, becoming prominent when root
formation is complete.
FIGURE 6.20 Major nerve trunks branch in pulp and pass to parietal
layer, which lies adjacent to cell-rich zone. Cell-rich zone curves
upward to right.

FIGURE 6.21 Parietal layer of nerves is composed of myelinated

nerve fibers. Cell-rich zone curves upward to right.
 FIGURE 6.22 Terminal nerve endings located among odontoblasts.
These arise from subjacent parietal layer.

Nerve endings
The mature deciduous teeth are well innervated, especially the
coronal pulp, have many nerve endings terminating in or near
odontoblast layer, with a few penetrating into the dentin. Nerve axons
from the parietal zone pass through the cell-rich and cell-free zones
and either terminate among or pass between the odontoblasts to
terminate adjacent to the odontoblast processes at the pulp–predentin
border or in the dentinal tubules. Nerve terminals consisting of round
or oval enlargements of the terminal filaments contain microvesicles,
small, dark, granular bodies, and mitochondria (Fig. 6.23). These
terminals are very close to the odontoblast plasma membrane,
separated only by a 20-µm (200 Å) cleft (Fig. 6.24). Many of these
indent the odontoblast surface and exhibit a special relationship to
these cells. Most of the nerve endings located among the odontoblasts
are believed to be sensory receptors. Some sympathetic endings are
found in this location as well. Whether they have some function
relative to the capillaries or the odontoblast in dentinogenesis is not
known. The nerve axons found among the odontoblasts and in the
cell-free and cell-rich zones are nonmyelinated but are enclosed in a
Schwann cell covering. It is presumed that these fibers lost their
myelin sheath as they passed peripherally from the parietal zone.
More nerve fibers and endings are found in the pulp horns than in
other peripheral areas of the coronal pulp.

FIGURE 6.23 Vesiculated nerve endings in predentin in zone adjacent

to odontoblast process.
 FIGURE 6.24 Vesiculated nerve ending partially surrounded by an
odontoblast process located adjacent to predentin. Note the uniform
cleft-like space between the nerve ending and the odontoblast process.
Gap junction appears between odontoblasts.

Recently a great deal of information has been reported regarding

the types of potential neurotransmitters that are present in the nerves
of the dental pulp. Substances such as substance P, 5-
hydroxytryptamine, vasoactive intestinal peptide, somatostatin, and
prostaglandins, as well as acetylcholine and norepinephrine have
been found throughout the pulp. The majority of these putative
transmitters have been shown to affect vascular tone and
subsequently modify the excitability of the nerve endings. Some of the
neuropeptides, like calcitonin gene–related peptide (CGRP) and
substance P are potent vasodilators, while others like norepinephrine
and neuropeptide Y are vasoconstrictors. Some neuropeptides like
substance P act as nociceptive transmitter, in that they help to transmit
pain sensation, while others like somatostatin act against them.
Further, it has been suggested that these changes in vascular tone can
also affect the incremental growth of dentin.
 It is a feature unique to dentin receptors that environmental stimuli
always elicit pain as a response. Sensory response in the pulp cannot
differentiate between heat, touch, pressure, or chemicals. This is
because the pulp organs lack those types of receptors that specifically
distinguish these other stimuli (Table 6.5).

Table 6.5
Nerves of the Pulp
Nerves follow the course of blood vessels
Very little branching in radicular pulp
Myelinated nerves lose myelin sheath and form plexus: plexus of Raschkow
Nerve fibers terminate adjacent to odontoblast or in dentinal tubules
Only free nerve endings in pulp: therefore, only pain sensation is felt
Myelinated/fast conducting: “a” delta fibers mediate sharp pain
Nonmyelinated/slow conducting: “c” fibers mediate dull pain
Sympathetic fibers end in blood vessels to control blood flow
Functions
Inductive
The primary role of the pulp anlage is to interact with the oral
epithelial cells, which leads to differentiation of the dental lamina and
enamel organ formation. The pulp anlage also interacts with the
developing enamel organ as it determines a particular type of tooth.

Formative
The pulp organ cells produce the dentin that surrounds and protects
the pulp. The pulpal odontoblasts develop the organic matrix and
function in its calcification. Through the development of the
odontoblast processes, dentin is formed along the tubule wall as well
as at the pulp–predentin front.

Nutritive
The pulp nourishes the dentin through the odontoblasts and their
processes and by means of the blood vascular system of the pulp.

Protective
The sensory nerves in the tooth respond with pain to all stimuli such
as heat, cold, pressure, operative cutting procedures, and chemical
agents. The nerves also initiate reflexes that control circulation in the
pulp. This sympathetic function is a reflex, providing stimulation to
visceral motor fibers terminating on the muscles of the blood vessels.

Defensive or reparative
The pulp is an organ with remarkable reparative abilities. It responds
to irritation, whether mechanical, thermal, chemical, or bacterial, by
producing reparative dentin and mineralizing any affected dentinal
tubules. The changes in the odontoblast, subodontoblastic layer and
type of tertiary dentin formation varies with the extent of caries
exposing the dentin (open/closed lesion), its progression
(active/slowly progressive lesion). The reparative dentin was found to
be more atubular in closed/active lesions and more tubular in
open/slowly progressive lesions.
After injury to the mature tooth, the fate of the odontoblast can vary
according to the intensity of the injury. Milder injury can result in
functional activity leading to focal secretion of a reactionary dentin
matrix, called regeneration, while greater injury can lead to
odontoblast cell death. Induction of differentiation of a new
generation of odontoblast-like cells can then lead to reparative
dentinogenesis.
Both the reparative dentin created in the pulp and the calcification
of the tubules (sclerosis) are attempts to wall off the pulp from the
source of irritation. Also, the pulp may become inflamed due to
bacterial infection or by cutting action and placement of an irritating
restorative material. The pulp has macrophages, lymphocytes,
neutrophils, monocytes, and plasma and mast cells, all of which aid in
the process of repair of the pulp. Although the rigid dentinal wall has
to be considered as a protection of the pulp, it also endangers its
existence under certain conditions. During inflammation of the pulp,
hyperemia and edema may lead to the accumulation of excess fluid
outside the capillaries. An imbalance of this type, limited by the
unyielding enclosure, can lead to pressure on apical vessels and
ischemia, resulting in necrosis of the pulp. In most cases, if the
inflammation is not too severe, however, the pulp will heal since it has
excellent regenerative properties (Table 6.6).

Table 6.6
Functions of Pulp
Function Mode of Action
Inductive Differentiation of dental lamina and dental organ
 Determination of tooth morphology
Formative Production of dentin
Nutritive Nourishment of dentin
Protective/sensory Immune cells, pain perception
Defensive/reparative Production of reparative dentin
Regressive changes (aging)
The age changes in the dental pulp are dealt in Chapter 17, Age
Changes in Oral Tissues. Hence the age change in dental pulp is
briefly summarized in this chapter. The age changes in the pulp are
decrease in cellularity, increase of collagen fibres and their
aggregation into bundles, decrease in vascularity and appearance of
calcifications (Fig. 6.26A–D). The calcifications may be diffuse
calcifications or nodular calcifications, termed as pulp stones or
denticles. Pulp stones may lie free in the pulp, attached to dentinal
wall, or embedded in it. If pulp stones has the structure of dentin, it is
called true denticles, if not, false denticles.
Development
The tooth pulp is initially called the dental papilla. This tissue is
designated as “pulp” only after dentin forms around it. The dental
papilla controls early tooth formation. In the earliest stages of tooth
development, it is the area of the proliferating future papilla that
causes the oral epithelium to invaginate and form the enamel organs.
The enamel organs then enlarge to enclose the dental papillae in their
central portions (Fig. 6.25A). The dental papilla may play a role in
determining whether the forming enamel organ is to be an incisor or a
molar. Recent information indicates that the epithelium may have that
information. At the location of the future incisor, the development of
the dental pulp begins at about the 8th week of embryonic life in the
human. Soon thereafter the more posterior tooth organs begin
differentiating. The cell density of the dental papilla is great because
of proliferation of the cells within it (Fig. 6.25A). The young dental
papilla is highly vascularized, and a well-organized network of
vessels appears by the time dentin formation begins (Fig. 6.25B).
Capillaries crowd among the odontoblasts during this period of active
dentinogenesis. The cells of the dental papilla appear as
undifferentiated mesenchymal cells. Gradually these cells differentiate
into stellate-shaped fibroblasts. After the inner and enamel organ cells
differentiate into ameloblasts, the odontoblasts then differentiate from
the peripheral cells of the dental papilla and dentin production begins.
As this occurs, the tissue is no longer called dental papilla but is now
designated the pulp organ.
 FIGURE 6.25 (A) Young tooth bud exhibiting highly cellular dental
papilla. Compare dense cell population to that of adjacent connective
tissue. (B) Young tooth with blood vessels injected with India ink to
demonstrate extent of vascularity of pulp. Large vessels located
centrally and smaller ones peripherally among odontoblasts. Pulp
surrounded by dentin and enamel. (C) Young tooth stained with silver
to demonstrate neural elements. Myelinated nerves appear in pulp horn
only after considerable amount of dentin has been laid down.

Axons of developing nerves reach the jaws and form terminals near
sites of odontogenesis before tooth formation starts. Nerve fibers were
first seen in the dental follicle in the 11th week of intrauterine life. In
the 18th week, the nerve fibers were observed in the dental papilla. At
that time, the first layers of enamel and dentin were being formed. At
about 24th week, the nerve fibers reach the subodontoblastic region.
Subsequently, nerve fibers increase in number and those
accompanying blood vessels form neurovascular bundles in the
central portion of the developing pulp. During the fetal period, no
subodontoblastic plexuses or nerve fibers in the predentin or in the
dentin were observed. Few large myelinated nerves are found in the
pulp until the dentin of the crown is well advanced (Fig. 6.25C). At
that time nerves reach the odontogenic zone in the pulp horns. The
sympathetic nerves, however, follow the blood vessels into the dental
papilla as the pulp begins to organize. During development, dental
pulp cells produce nerve growth factor and semaphorin 7A as well as
brain-derived and glial cell line–derived neurotrophic factor, all of
which help to innervate the pulp. Growth factors like neurotrophin
and neurturin were shown not be involved in this process.
Clinical considerations
Pathologic considerations
Pulpal inflammation or pulpitis is a response of the traumatized pulp,
with trauma being a result of a bacterial infection as in dental caries or
physical trauma to the tooth structure. Pulpal inflammation in milder
forms could result in focal reversible pulpitis and may progress if left
unchecked to acute and chronic forms of pulpitis. Well-vascularized
pulpal tissues may at times in carious molar teeth of young adults and
children with open apex exhibit a form of hyperplasia, seen clinically
from an exposed pulp chamber as a protruding red mass of
granulation tissue called pulp polyp or chronic hyperplastic pulpitis. This
condition requires endodontic therapy or extraction of the tooth.
Inflammation within the pulp may also sometimes result in a
condition called internal resorption or pink tooth. The outward
resorption of dentinal walls by osteodentinoclasts (odontoclasts)
results in the pulpal tissue appearing pink through the thin
translucent enamel, hence the term pink tooth. This condition may
require endodontic therapy. Pulpal infection can spread apically into
the periodontal ligament causing granulomas, abscesses, and cysts.

Operative and endodontic considerations

Pulpal anatomy and the response of the pulp to the various filling
materials used for restoration of teeth are of utmost importance to all
practicing dentist.

Pulp chamber and its extensions

For all operative procedures, the shape of the pulp chamber and its
extensions into the cusps, the pulpal horns, are important to
remember. The wide pulp chamber in the tooth of a young person will
make a deep cavity preparation hazardous, and it should be avoided,
if possible. In some instances of developmental disturbances, the
pulpal horns project high into the cusps, and the exposure of a pulp
can occur when it is least anticipated. Sometimes, a radiograph will
help to determine the size of a pulp chamber and the extent of the
pulpal horns.
If opening a pulp chamber for treatment becomes necessary, its size
and variation in shape must be taken into consideration. With
advancing age, the pulp chamber becomes smaller (Fig. 6.26C), and
because of excessive dentin formation at the roof and floor of the
chamber, it is sometimes difficult to locate the root canals. In such
cases, it is advisable when one opens the pulp chamber to advance
toward the distal root in the lower molar and toward the lingual root
in the upper molar. In this region, one is most likely to find the
opening of the pulp canal without risk of perforating the floor of the
pulp chamber. In the anterior teeth, the coronal part of the pulp
chamber may be filled with secondary dentin, thus locating the root
canal is made difficult. Pulp stones lying at the opening of the root
canal may cause considerable difficulty when an attempt is made to
locate the canals.

FIGURE 6.26 These four diagrams depict pulp organ throughout life.
Observe first the decrease in size of pulp organ. (A–D) Dentin is
formed circumpulpally but especially in bifurcation zone. Note decrease
in cells and increase in fibrous tissue. Blood vessels (white) organize
early into odontoblastic plexus and later are more prominent in
subodontoblastic zone, indicating decrease in active dentinogenesis.
Observe sparse number of nerves in young pulp, organization of
 parietal layer of nerves. They are less prominent in aging pulp.
Reparative dentin and pulp stones are apparent in oldest pulp, (D).

The shape of the apical foramen and its location may play an
important part in the treatment of root canals. When the apical
foramen is narrowed by cementum, it is more readily located because
further progress of the broach will be stopped at the foramen. If the
apical opening is at the side of the apex, as shown in Fig. 6.2B, not
even radiographs will reveal the true length of the root canal, and this
may lead to misjudgment of the length of the canal and the root canal
filling.
Since accessory canals are rarely seen in radiographs, they are not
treated in root canal therapy. In any event, it would be mechanically
difficult or impossible to reach them. Fortunately, however, the
majority of them do not affect the success of endodontic therapy.
When accessory canals are located near the coronal part of the root
or in the bifurcation area (Fig. 6.3B), a deep periodontal pocket may
cause inflammation of the dental pulp. Thus periodontal disease can
have a profound influence on pulp integrity. Conversely, a necrotic
pulp can cause spread of disease to the periodontium through an
accessory canal. It is recognized that pulpal and periodontal disease
may spread by their common blood supply.

Pulpal response to restorative procedures and

materials
Pulp capping is successful, especially in noninfected or minimally
infected, accidentally exposed pulps in individuals of any age. In
these instances, dentin is formed at the site of the exposure; thus, a
dentin barrier or bridge is developed and the pulp retains vitality.
Dentin bridge forms an effective continuous barrier only if operative
debris and pulp capping material particles are removed.
All operative procedures cause an initial response in the pulp,
which is dependent on the severity of the insult. The pulp is highly
responsive to stimuli. Even a slight stimulus will cause inflammatory
cell infiltration (Fig. 6.27). A severe reaction is characterized by
increased inflammatory cell infiltration adjacent to the cavity site,
hyperemia, or localized abscesses. Hemorrhage may be present, and
the odontoblast layer is either destroyed or greatly disrupted. It is of
interest that most compounds containing calcium hydroxide readily
induce reparative dentin underlying a cavity (Fig. 6.28). Most
restorative materials also induce reparative dentin formations (Fig.
6.29). Usually, the closer a restoration is to the pulp, the greater will be
the pulp response. Though the high pH of calcium hydroxide is
bactericidal and promotes tertiary dentin formation, it has unstable
physical properties in that particles of calcium hydroxide get into pulp
causing pulpal inflammation. Newer composite resins used as pulp
capping agents showed better sealing properties than the earlier
composites and calcium hydroxide. Therefore, the bacterial leakage is
less compared to calcium hydroxide leading to a better dentin bridge
formation.

FIGURE 6.27 Mild pulp response with loss of odontoblast identity and
inflammatory cells obliterating cell-free zone.
FIGURE 6.28 Moderate cell response with formation of reparative
dentin underlying cavity. Note viable odontoblasts have deposited
tubular, reparative dentin.
 FIGURE 6.29 Diagram of reparative function of pulp organ to cavity
preparation and subsequent restoration. Reparative dentin is limited to
zone of stimulation.

More than calcium hydroxide, enamel matrix derivative was shown

to be more capable of promoting reparative process in the wounded
pulp. Mineral trioxide aggregate (MTA) has also been shown to be
more effective than calcium hydroxide as pulp capping agents.
Inflammation, hyperemia, and necrosis were less but more
odontoblasts and thicker dentin bridge formation was seen with MTA.
In future, incorporation of bioactive molecules like bone
morphogenetic protein, TGF-β1, or purified dentin protein fractions in
pulp capping materials, use of tissue-cultured dentin and stem cells to
produce dentin, may radically alter the present treatment approaches.
The thickness of remaining dentin was shown to be important factor
in maintaining the vitality of pulp. A minimum thickness of 5 mm or
greater has a powerful influence on pulp vitality but little effect on
reparative dentin formation and no effect on the intensity of
inflammation. The number of vital odontoblast remaining after cavity
preparation is a critical factor, apart from patient’s age which
determines the ability of the pulp to form reparative dentin. Pain may
be the only symptom in pulpitis and all other cardinal signs of
inflammation like rubor (redness), calor (heat), or tumor (swelling)
will not be appreciated clinically because pulp is situated deep within
the tooth and surrounded by hard tissues of the tooth. Since the pulp
contains only free nerve endings all forms of sensory stimuli like
touch, pressure, or temperature to the pulp result in causing pain
sensation only.

Pulpal pain
Pulpal pain worsens with the degree of inflammation. Stimuli causing
pain act through large diameter A-δ or smaller diameter C-fibers. A-δ
fibers are fast-conducting myelinated fibers and evoke a sharp pain,
while nonmyelinated C-fibers are slow-conducting fibers and produce
a dull pain on stimulation.
Changes occur in tissue fluid pressure in normal and inflamed
pulps, and this largely determines whether pulp necrosis occurs.
Tissue pressure is the hydrostatic pressure of the interstitial fluid
surrounding the pulpal cells. It increases due to increase in blood flow
and due to increased interstitial fluid; occurring as a result of
inflammation. This will cause increase in lymph flow and increased
absorption of fluid into the capillaries in the uninflamed area. This
will help in transport of fluid from the pulp and thereby reduces the
tissue fluid pressure to normal. Increased tissue pressure will promote
outward flow of dentinal fluid through the exposed dentinal tubule.
This serves to protect the pulp against entry of harmful substances. If
the compensatory mechanisms fail to reduce the tissue fluid pressure,
a sustained increase in the pressure occurs, and this will compress the
blood vessels causing ischemia and necrosis.
In response to orthodontic forces, the pulp shows cell damage,
inflammation, vasodilatation, and healing, all of which are associated
with increased vascularity due to release of angiogenic growth factors.
 Since dehydration causes pulpal damage, operative procedures
producing this condition should be avoided. When filling materials
contain harmful chemicals (e.g., acid in silicate cements and monomer
in the composites), an appropriate cavity liner should be used prior to
the insertion of restorations. Pulp has to be protected from damage
due to heat transmission especially by metallic restorations by the use
of bases.

Vitality of pulp
A vital pulp is essential to good dentition. Although modern
endodontic procedures can prolong the usefulness of a tooth, a
nonvital tooth becomes brittle and is subject to fractures. Therefore,
every precaution should be taken to preserve the vitality of a pulp.
In clinical practice, instruments called vitalometers, which test the
reaction of the pulp to electrical stimuli, or thermal stimuli (heat and
cold) are often used to test the “vitality” of the pulp. These methods
provide information about the status of the nerves supplying the
pulpal tissue and therefore check the “sensitivity” of the pulp and not
its “vitality.” The vitality of the pulp depends on its blood supply, and
one can have teeth with damaged nerve but normal blood supply (as
in cases of traumatized teeth). Such pulps do not respond to electrical
or thermal stimuli but are completely viable in every respect.
Laser Doppler flowmetry, an electro-optical technique used in the
recording of pulpal blood flow, has been found to be reliable in
assessing the vitality of traumatized teeth. Also, transmitted-light
photoplethysmography, which has been used to detect blood flow in
young permanent teeth, may be of use in the assessment of pulp
vitality.
The preservation of a healthy pulp during operative procedures and
successful management in cases of disease are two of the most
important challenges to the clinical dentist.
Summary
The pulp is a loose connective tissue occupying the pulp chamber in
the crown and root canal in the root. Pulp communicates with the
periodontal ligament through the apical foramen and through
accessory foramina.

Zones of the pulp

Pulp can be divided into different zones; the odontogenic zone close
to the pulp–dentin border, the cell-free zone of Weil beneath it, and
the parietal zone in the remaining area.

Cells of the pulp

Odontoblasts
The odontoblasts present in the odontogenic zone vary in size, shape,
and arrangement. In the coronal pulp, they are columnar in shape and
show a pseudostratified arrangement with an average diameter of 7.2
µm and 25–40 µm in length, becoming flatter and are arranged in a
single layer in the root. Odontoblasts have a basal polarized nucleus
and contact the adjacent cells focally with junctional complexes. The
odontoblast morphology and its organelles vary with functional
activity of the cell. In the active stage, as during the formation of
primary dentin formation, the cell is elongated with all the organelles
required for protein synthesis. In the resting stage, the cell is stubby
with fewer organelles. They are terminally differentiated so they have
to be replaced by undifferentiated mesenchymal cells when they die.
The cytoplasmic process extending from the apical cytoplasm is
usually devoid of organelles and extends to about two-third of the
lengths of the dentinal tubules. The cell-free zone contains
subodontoblastic plexus of nerves and vessels.
Fibroblasts and collagen fibers of the pulp
Pulp consists of fibroblasts, defense cells like histiocytes, plasma cells,
and pluripotent undifferentiated mesenchymal cells, and stem cells.
The fibroblasts are the most numerous of the pulpal cells. They are
star shaped and their process communicates with each other. They
form and degrade collagen fibers and the ground substance. Pulp
consists of loosely arranged type I fine collagen fibers. Their length
varies from 10 to 100 nm.

Defense cells
The histiocyte is an irregularly shaped cell and appears similar to
fibroblast. They are stained by vital dyes like toluidine blue.
Ultrastructurally, they show vesicles containing phagocytosed bodies.
Dendritic cells are antigen-presenting cells found in close relation to
or contact with their processes to odontoblast or endothelial cells.
The plasma cells are seen only during pulpal inflammation. They
are oval-shaped cells with eccentric nucleus. They produce antibodies.

Pulpal stem cells

These are pluripotent cells replacing injured odontoblast and produce
dentin. They can be induced to proliferate and differentiate by
numerous growth factors like TGF. Pulp of exfoliated deciduous teeth
and third molars are a good source of pulpal stem cells and they are
used in regeneration of dentin, bone, and neural tissues.

Pulpal blood vessels and circulation

The blood vessels are mainly arterioles of smaller size and thinner
walls than elsewhere, the capillaries have fenestrations and there are
arteriovenous communications. Blood flow in pulp is higher than in
most areas of the body, in capillaries is high—it is about 0.08 mm per
second. The circulation in pulp facilitates rapid transport of
metabolites. Pericytes are cells with contractile properties and are seen
on the surface of smaller arterioles. Blood vessels and nerves enter
and leave through apical foramen. Blood vessels in the pulp
communicate with the vessels in the periodontal ligament through
main and accessory canals. Lymph vessels also said to follow the
course of blood vessels. Lymph vessels draining anterior teeth drain
into submental lymph nodes and those from posterior teeth drain into
submandibular lymph nodes.

Nerves of the pulp

The nerves are of two types—the unmyelinated parasympathetic
nerves which are unbranched and end in blood vessels to control the
blood flow and the myelinated nerves and somatic nerves which lose
their myelin sheath before they branch and form plexus in the cell-free
zone. This plexus is often referred to as plexus of Raschkow. Some of
these extend to end below the odontoblast and form synapse while
others go up to predentin and loop backward while very few travel
within the dentin tubules spiraling around the odontoblastic process.
Since the pulp contains only free nerve endings, all forms of sensory
stimuli result in pain sensation.

Functions of the pulp

The functions of the pulp are to produce dentin (formative function),
nourish dentin (nutritive function), elicit pain to protect the tooth
(protective function), and to repair injured dentin or arrest caries
progression by forming reparative dentin (reparative function). In
early odontogenesis, the pulp anlage interacts with oral epithelial cells
to cause differentiation of enamel organ and dental lamina.

Development of pulp
The pulp is formed from dental papilla. After the peripheral cells of
dental papilla differentiate into odontoblast and produce dentin, the
rest of dental papilla becomes pulp. The earliest pulp of deciduous
teeth develops by 8th week of embryonic life. The developing pulp is
very cellular and very vascular. Nerves appear later (18th week),
reach subodontoblastic region by 24th week, the plexuses formation
occurring still later.

Age changes in the pulp

The age changes in the pulp include decreased cellularity, increase in
fibers with bundle formation, degeneration of nerves and
calcifications. Pulp arterioles are end arteries and as pulp circulation is
not collateral, inflammation of pulp results in necrosis. The age
changes of the pulp are dealt in detail in Chapter 17, Age Changes in
Oral Tissues.
Review questions
1. Describe the cells of the pulp.
2. What are the types of stem cells present in the pulp and their
potential applications?
3. Describe the vasculature of the pulp.
4. What does cell-free zone contain?
5. List out the differences between coronal and radicular pulp.
6. Why all types of sensory stimuli to the pulp are felt as pain?
7. What are the functions of pulp?
8. What are the peculiarities of pulpal inflammation?
References
A complete list of references is available at [Link]
Suggested reading
1. Berkovitz BK, Holland GH, Moxham BJ. Oral
Anatomy. Histology and Embryology, ed 4, St
Louis:, Mosby. 2009;152-168.
2. Fried K, Nosrat C, Lillesaar C. Molecular
signaling and pulpal nerve development. Crit
Rev Oral Biol Med. 2000;11(3):318.
3. Murray PE, Windsor LJ, Smyth TW. Analysis
of pupal reactions to restorative procedures.
materials, pulp capping and future therapies, Crit
Rev Oral Biol Med. 2002;13(6):509.
4. Nanci A. Dentin. Pulp Complex. In Ten
Cate’s Oral Histology Development, Structure
and Function, ed 1 South Asia, St Louis/New
Delhi:. Elsevier /Relx. 2018;157-192.
References
1. Aeinechi M, Eslami B, Ghanbariha M.
Mineral trioxide aggregate (MTA) and
calcium hydroxide and pulp—capping agents
in human teeth: a preliminary report. Int
Endod J. 2003;36(3):225.
2. Angelova A, Takagi Y, Kaneko T.
Immunocompetent cells in the pulp of human
deciduous teeth. Arch Oral Biol. 2004;49(1):29.
3. Avery JK. Siskin M The biology of the
human dental pulp (Available only through
American Association of Endodontists,
Atlanta, Ga.) Structural elements of the young
normal human pulp. St Louis: The CV Mosby
Co. 1973.
4. Avery JK, Han SS. The formation of collagen
fibrils in dental pulp. J Dent Res.
1961;40(6):1248.
5. Batouli S, Miura M, Brahim J. Comparison of
stem cell-mediated osteogenesis and
dentinogenesis. J Dent Res. 2003;82(12):976.
6. Bender IB. Pulpal pain diagnosis—a review.
J Endod. 2000;26(3):175.
7. Berkovitz BK, Holland GH, Moxham BJ. Oral
Anatomy. Histology and Embryology, ed 3, St
Louis: Mosby. 2002;149-167.
 8. Beveridge EE, Brown AC. The measurement
of human dental intrapulpal pressure and its
response to clinical variables. Oral Surg.
1965;19(5):655.
9. Bhussry BR. Biology of the dental pulp organ
a symposium Modification of the dental pulp
organ during development and aging. In Finn SB:.
University of Alabama: University of
Alabama Press. 1968.
10. Biorndal L, Darvann T. A light microscopic
study of odontoblastic and non-odontoblastic
cells involved in tertiary dentinogenesis in
well-defined cavitated carious lesions. Caries
Res. 1999;33(1):50.
11. Casagrande L, Mattuella LG, De Arauio FB.
Stem cells in dental practice: perspectives in
conservative pulp therapies. J Clin Pediatr
Dent. 2006;31(1):.
12. Corpron RE, Avery JK. The ultrastructure of
intradental nerves in developing mouse
molars. Anat Rec. 1973;175(3):585.
13. Corpron RE, Avery JK, Lee SD. Ultrastructure
of terminal pulpal blood vessels in mouse
molars. Anat Rec. 1974;179(4):527.
14. Dahl E, Mjör IA. The fine structure of the
vessels in the human dental pulp. Acta
Odontol Scand. 1973;31(4):223.
15. Derringer KA, Jaggers DC, Linden RW.
Angiogenesis in human dental pulp following
orthodontic tooth movement. J Dent Res.
1996;75(10):1761.
16. Edds AC, Walden JE, Scheetz JP. Pilot study
of correlation of pulp stones with
cardiovascular disease. J Endod.
2005;31(7):504.
17. Egan CA, Hector MP, Bishop MA. On the
pulpal nerve supply in primary human teeth:
evidence for the innervation of primary
dentine. Int J Paediater Dent. 1999;9(1):57.
18. Espina AT, Castellanos AV, Fererira JL. Age
related changes in blood capillary
endothelium of human dental pulp: an
ultrastructural study. Int Endod J.
2003;36(6):395.
19. Evans D, Reid J, Strang R. A comparison of
laser Doppler flowmetry with other methods
of assessing the vitality of traumatized
anterior teeth. Endod Dent Traumatol.
1999;15(6):284.
20. Fanibunda KB. Volume of the dental pulp
cavity-method of measurement. British IADR
Abstr No 150. J Dent Res. 1973;52(Suppl):971.
21. Fanibunda KB. A preliminary study of the
volume of the pulp in the permanent human
 teeth. Unpublished personal communication:.
1975.
22. Fearnhead RW. Pergamon Press Anderson DJ
Sensory mechanisms in dentin The histological
demonstration of nerve fibers in human dentin.
Oxford, England: Anderson DJ. 1963.
23. Felaco M, Di Maio FD, De Fazio P.
Localization of the e-NOS enzyme in
endothelial cells and odontoblasts of healthy
human dental pulp. Life Sci. 2000;68(3):297.
24. Finn SB. Biology of the dental pulp organ a
symposium :. University of Alabama:,
University of Alabama Press. 1968.
25. Fried K, Nosrat C, Lillesaar C. Molecular
signaling and pulpal nerve development. Crit
Rev Oral Biol Med. 2000;11(3):318.
26. Griffin CJ, Harris R. The ultrastructure of the
blood vessels of the human dental pulp
following injury. Aust Dent J. 1972;17:303.
27. Griffin CJ, Harris R. The ultrastructure of the
blood vessels of the human dental pulp
following injury. Aust Dent J. 1973;18:88.
28. Gronthos S, Brahim J, Li W. Stem cell
properties of human dental pulp stem cells. J
Dent Res. 2002;81(8):531.
29. Han SS, Avery JK. The ultrastructure of
capillaries and arterioles of the hamster dental
 pulp. Anat Rec. 1963;145(4):549.
30. Han SS, Avery JK. The fine structure of
intercellular substances and rounded cells in
the incisor pulp of the guinea pig. Anat Rec.
1965;151(1):41.
31. Han SS, Avery JK, Hale LE. The fine structure
of differentiating fibroblasts in the incisor
pulp of the guinea pig. Anat Rec.
1965;153(2):187.
32. Harrop TJ, MacKay B. Electron microscopic
observations of healing in dental pulp in the
rat. Arch Oral Biol. 1968;13(43):365.
33. Heveraas KJ, Berggreen E. Interstitial fluid
pressure in normal and inflamed pulp. Crit
Rev Oral Boil Med. 1999;10(3):328.
34. Huang GT, Gronthos S, Shi S. Mesenchymal
stem cells derived from dental tissues vs.
those from other sources: their biology and
role in regenerative medicine. J Dent Res.
2009;88(9):792.
35. Ikawa M, Komatsu H, Ikawa K. Age-related
change in the human pulpal blood flow
measured by laser Doppler flowmetry. Dent
Traumatol. 2003;19(1):36.
36. Kaneko T, Arayatrakoollikit U, Yamanaka Y.
Immunohistochemical and gene expression
analysis of stem-cell-associated markers in rat
 dental pulp. Cell Tissue Res. 2013;351(3):425.
37. Kannari N, Ohshima H, Maeda T. Class II
MHC antigen-expressing cells in the pulp
tissue of human deciduous teeth prior to
shedding. Arch Histol Cytol 61(1):. 1998.
38. Kim S. Regulation of blood flow of the dental
pulp of dogs macrocirculation and
microcirculation studies :. Thesis, New York:,
Columbia University. 1981.
39. Klinge RF. A microradiographic and electron
microscopic study of tertiary dentin in human
deciduous teeth. Acta Odontol Scand.
1999;57(2):87.
40. Kollar EJ, Baird GR. The influence of the
dental papilla on the development of tooth
shape in embryonic mouse tooth germs. J
Embryol Exp Morphol. 1969;21:131.
41. Kollar EJ, Baird GR. Tissue interactions in
embryonic mouse tooth germs. II. The
indicative role of the dental papilla. J Embryol
Exp Morphol. 1970;24:173.
42. Kollar EJ, Baird GR. Tissue interactions in
embryonic mouse tooth germs. I.
Reorganization of the dental epithelium
during tooth-germ reconstruction. J Embryol
Exp Morphol. 1970;24:159.
43. Kovacs I. Dahlberg AA Dental morphology
 and evaluation A systematic description of dental
roots. Chicago:, University of Chicago Press.
1971.
44. Liu H, Li W, Gao C. Dentonin. a fragment of
MEPE, enhanced dental pulp stem cell
proliferation, J Clin Pediatr Dent. 2003;27(3):277.
45. Marchetti C, Pogai P, Calligaron A.
Lymphatic vessels in the healthy human
dental pulp. ActaAnat (Bassel). 1991;140(4):329.
46. Marchetti C, Pogai P, Calligaron A.
Lymphatic vessels of the human dental pulp
in different conditions. Anat Rec.
1992;234(1):27.
47. Maroto M, Barberia E, Planelis P. Dentin
bridge formation after mineral trioxide
aggregate (MTA) pulpotomies in primary
teeth. Am J Dent. 2005;18(3):151.
48. Martinez EF, Machado de Souza SO, Correa
L. Immunohistochemical localization of
tenascin. fibronectin, and type III collagen in
human dental pulp, J Endod. 2000;26(12):708.
49. Mathieu S, EL-Battari A, Dejou J. Role of
injured endothelial cells in the recruitment of
human pulp cells. Arch Oral Biol.
2005;50(2):109.
50. Matsumoto Y, Zhano B, Kato S. Lymphatic
networks in the periodontal tissues and dental
 pulp as revealed by histochemical study.
Microsc Res Tech. 2002;56(1):50.
51. Maurin JC, Delorme G, Machuca-Gavet I.
Odontoblast expressions of semaphorin 7A
during innervation of human dentin. Matrix
Biol. 2005;24(3):232.
52. Misako Nakashima, KoichiroIohara, Masashi
Murakami. Dental pulp stem cells and
regeneration. Endodontic Topics. 2013;28(1):38.
53. Mitsiadis TA, Rahiotis C. Parallels between
tooth development and repair: conserved
molecular mechanisms following carious and
dental injury. J Dent Res. 2004;83(12):896.
54. Miwa Z, Ikawa M, Iijima H. Pulpal blood
flow in vital and nonvital young permanent
teeth measured by transmitted-light photo
plethysmography: a pilot study. Pediatr Dent.
2002;24(6):594.
55. Mjör IA, Pindborg JJ. Histology of the human
tooth. Copenhagen:, Munksgaard, Interna
tional Booksellers & Publishers, Ltd. 1973.
56. Murray PE, About I, Lumley PJ. Human
odontoblast cell numbers after dental injury. J
Dent. 2000;28(4):277.
57. Murray PE, Windsor LJ, Smyth TW. Analysis
of pupal reactions to restorative procedures,
materials, pulp capping and future therapies.
 Crit Rev Oral Biol Med. 2002;13(6):509.
58. Murray PE, Smith AJ, Windsor LJ. Remaining
dentine thickness and human pulp responses.
Int Endod J. 2003;36(1):33.
59. Nakamura Y, Hammarstrom L, Lundberg E.
Enamel matrix deriv-ative promotes
reparative processes in the dental pulp. Adv
Dent Res. 2001;15:105.
60. Nanci A. Dentin, Pulp Complex. In Ten
Cate’s Oral Histology Develop-ment,
Structure and Function, ed 6, St Louis.:
Elsevier. 2005;198-239.
61. Nishijima S, Imanishi I, Aka M. An
experimental study on the lymph circulation
in dental pulp. J Osaka Dent School. 1965;5:45.
62. Nosrat IV, Widenfalk J, Oison L. Dental pulp
cells produce neurotrophic factors. interact
with trigeminal neurons in vitro, and rescue motor
neurons after spinal cord injury, Dev Biol.
2001;238(1):120.
63. Nygaard-Ostby B, Hjortdal O. Tissue
formation in the root canal following pulp
removal. Scand J Dent Res. 1971;79:333.
64. Okiji T, Jontell M, Belichenko P. Perivascular
dendritic cells of the human dental pulp. Acta
Physiol Scand. 1997;159(2):163.
65. Ogilvie AL, Ingle JE. An atlas of pulpal and
 periapical biology. Philadelphia:, Lea
&Febiger. 1965.
66. Ohshima H, Maeda T, Takano Y. The
distribution and ultrastructure of class II
MHC-positive cells in human dental pulp.
Cell Tissue Res. 1999;295(1):151.
67. Oyama M, Myokai F, Ohira T. Isolation and
expression of FIP-2 in wounded pulp of the
rat. J Dent Res. 2005;84(9):842.
68. Piattelli A, Rubini C, Floroni M. bci-2. p. 53,
and MIB -1 in human adult dental pulp, Endod.
2000;26(4):225.
69. Rapp R, Avery JK, Strachan DS. The
distribution of nerves in human primary
teeth. Anat Rec. 1967;159(1):89.
70. Rebecca S. Prescott, RajaaAlsanea, Mohamed
I, Fayad. In-vivo Generation of Dental Pulp-
Like Tissue Using Human Pulpal Stem Cells.
a Collagen Scaffold and Dentin Matrix Protein 1
Following Subcutaneous Transplantation in Mice,
J Endod. 2008;34(4):421.
71. Saunders RL, de CH, Röckert H√òE. vol 1
Miles AEW Structural and chemical
organization of teeth Vascular supply of dental
tissues, including lymphatics. New York:
Academic Press, Inc. 1967.
72. Sawa Y, Horie Y, Yamaoka Y. Production of
 colony-stimulating factor in human dental
pulp fibroblasts. Jent Dent Res. 2003;82(2):96.
73. Shizhu Z, Dongchuan W, Xianzhi Z. Age-
related changes of the ultrastructures in
dental pulp-dentine complex. Chinese J
Geriatrics 5:. 1996.
74. Smith AJ, Lesot H. Induction and regulation
of crown dentinogenesis: embryonic events as
a template for dental tissue repair. Crit Rev
Oral Biol. 2001;12(5):425.
75. Stanley HR, Rainey RR. Age changes in the
human dental pulp. Oral Surg. 1962;15:1396.
76. Takahashi K, Yoshiaki K, Kim S. A scanning
electron microscope study of the blood vessels
of dog pulp using corrosion resin casts. J
Endod. 1982;8(3):131.
77. Tecles O, Laurent P, Zvgouritsas S.
Activation of human dental pulp
progenitor/stem cells in response to
odontoblast injury. Arch Oral Biol.
2005;50(2):103.
78. Torneck CD. Changes in the fine structure of
the dental pulp in human caries pulpitis. I.
Nerves and blood vessels. J Oral Pathol.
1974;3:71.
79. Torneck CD. Changes in the fine structure of
the dental pulp in human caries pulpitis. II.
 Inflammatory infiltration. J Oral Pathol.
1974;3:83.
80. Tran-Hung L, Mathieu S, About I. Role of
human pulp fibroblasts in angiogenesis. J
Dent Res. 2006;85(9):819.
81. Weinstock M, Leblond CP. Formation of
collagen. Fed Proc. 1974;33(5):1205.
82. Weinstock M, Leblond CP. Synthesis.
migration and release of precursor collagen by
odontoblasts as visualized by radioautography
after [3H] proline administration, J Cell Biol.
1974;60:92.
83. Wong VS, Freer TJ, Joseph BK. Tooth.
movement and vascularity of the dental pulp: a
pilot study, Aust Orthod J. 1999;15(4):246.
84. YoshibaN, Yoshiba K, Ohkura N.
Expressional alterations of fibrillin-1 during
wound healing of human dental pulp. J
Endod. 2012;38(2):177.
85. Zachrisson BV. Mast cells in human dental
pulp. Arch Oral Biol. 1971;16:555.
86. Zerlotti E. Histochemical study of the
connective tissue of the dental pulp. Arch Oral
Biol. 1964;9:149.
87. Zhang W, Walboomers XF, Shi S, et al:
Multilineage differentiation potential of stem
cells derived from human dental pulp after
 cryopreservation, Tissue Eng Sep 1: (Epub
Ahead of Print).
88. Zhu O, Safavi KE, Spanoberg LS. Integrin
expression in human dental pulp cells and
their role in cell attachment on extracellular
matrix proteins. J Endod. 1998;24(10):641.
89. Zmijiewska C, Surkyk-Zasada J, Zabel M.
Development of innervation in primary
incisors in the foetal period. Arch Oral Biol.
2003;48(11):745.