A fundamental question that needs to be addressed is
whether the dental pulp is necessary in a fully formed
tooth. One can argue that the tooth can continue to
function normally after the pulp is removed and
replaced with a root canal filling. In such situations, the
circulation of the periodontal ligament and the
surrounding tissues will support a pulpless or an
endodontically treated tooth.
A recent study on the bacterial invasion into dentinal
tubules of human teeth with or without viable pulp has
shown that teeth with pulps are much more resistant to
bacterial invasion into the dentinal tubules than are
teeth with root canal fillings.
In the latter, bacteria are
able to enter teeth and reach the root canal system in a
relatively short period of time.
Hence, the pulp plays
an important role in this defense process. In teeth with
pulps, the dentinal tubules are occupied by dentinal
fluid and odontoblastic processes, which may behave
collectively as a positively charged hydrogel.
The hydrogel is capable of arresting a great number of the
bacteria that enter the pulp. The outward flow of the
dentinal fluid is important in the pulp’s defense against
the entry of harmful substances because it affects the
rate at which toxic substances from the mouth diffuse
into the dentinal tubules.
Moreover, antibodies or
other antimicrobial agents may be present within the
dentinal fluid in response to bacterial infection of the
dentine.
The possible build-up of immune complexes
and the precipitation of high molecular weight plasma
proteins, such as fibrinogen, in the dentinal fluid may
reduce the functional radius of the dentinal tubules and
hence reduce the dentine permeability.
The pulp’s specialized cells, the odontoblasts, and
perhaps undifferentiated mesenchymal cells (which may
differentiate into dentine-forming cells if stimulated),
retain the ability to form dentine throughout life. This
enables the healthy pulp to partially compensate for the
loss of enamel or dentine caused by dental caries or
tooth wear through the formation of a hard tissue
barrier that isolates irritants from the remaining pulp
tissue. Secondary dentine is deposited circumferentially
at a very slow rate throughout the life of a normal
tooth. The odontoblasts secrete the dentinal matrix and
retreat toward the pulp center. They become crowded
and their direction can be altered. The dentine thus
produced is “wavier” and contains fewer tubules.
Odontoblasts may also form sclerotic dentine,
reactionary dentine and reparative dentine in response
to adverse stimuli, such as caries or operative
procedures. In sclerotic dentine, the dentinal tubules
become partially or completely filled with mineral
deposits consisting of hydroxyapatite and whitlockite
crystals, resulting in a decrease in the permeability of
the dentine. However, for sclerosis to occur, viable
odontoblast processes must be present within the
tubules. In reactionary dentine, the tubules are
continuous with the primary dentine and extend down
to the odontoblasts. Reparative dentine occurs at the
pulp surface of primary or secondary dentine and it will
be localized to the site of irritation. It forms
proportionally to the amount of primary dentine
destroyed. The rate seems to depend inversely on the
rate of carious attack; that is, more dentine is formed in
response to slowly progressing carious lesions. The
tubules in the reparative dentine are irregular or
frequently absent, which makes it less permeable to
external stimuli. Cells forming the reparative dentine
are thought not to be the primary odontoblasts but are
derived from the cells deeper in the pulp such as fibro
blasts in the cell-rich zone, endothelial cells or pericytes
of the blood vasculature which are differentiated upon
the stimulation by tissue growth factor- .
The reparative dentine, especially at the junctional zone
between primary and secondary dentine, has low
permeability and may block the ingress of irritants to
the pulp.
Pulp is equipped with the cellular components
necessary for the initial recognition and the subsequent
processing of antigens hence its ability to elicit an
immune defense reaction.
The main immune cells in
a normal pulp are peripheral T cells (helper/inducer and
cytotoxic/suppressor). The major antigen presenting
cells in the dental pulp are the dendritic cells located
primarily in the odontoblastic layer.
These cells
uptake, process, and present foreign antigens as
HLA-DR antigens on the cell surface to CD4 +
T-lymphocytes. Other antigen-presenting cells are
similar to macrophages and are located in the more
central portions of the pulp. In rat incisors, Class II
antigen activated macrophages are four times more
common than the dendritic cells.
It is noteworthy that
the normal dental pulp does not appear to have B
cells.
Pulp is also a sensory organ. Its sensitivity to thermal
stimuli is well recognized.
Regardless of the nature of
the sensory stimuli, such as thermal change, mechanical
deformation or trauma, the pulp registers different
impulses as a common sensation, i.e., pain. Such pain-registering
ability is important as part of the defense
mechanisms of the pulp. Patients with an inflamed pulp
tend to seek treatment earlier while the injury is
confined within the tooth, as opposed to those whose
teeth have been root-filled where the pain sensation will
not be experienced until substantial damage has
occurred in the tissues surrounding the root. In
addition, the proprioceptive function of the pulp limits
the load imposed on teeth by the masticatory muscles,
thus further protecting the tooth from injury.