Pulpitis

https://en.wikipedia.org/wiki/Pulpitis. 14 Juli 2016/08:45

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Pulpitis
Classification and external resources

Pulpitis is inflammation of dental pulp tissue. The pulp contains the blood vessels the nerves
and connective tissue inside a tooth and provides the tooths blood and nutrients. Pulpitis is
mainly caused by bacteria infection which itself is a secondary development of caries (tooth
decay). It manifests itself in the form of a toothache. [1]

Symptoms

Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A
prolonged throbbing pain may be associated with the disease.[2] However, pulpitis can also
occur without any pain.[3]

Causes

Pulpitis may be caused by dental caries that penetrate through the enamel and dentin to reach
the pulp, or it may be a result of trauma, such as thermal insult from repeated dental
procedures.

Inflammation is commonly associated with a bacterial infection but can also be due to other
insults such as repetitive trauma or in rare cases periodontitis. In the case of penetrating
decay, the pulp chamber is no longer sealed off from the environment of the oral cavity.[4]

When the pulp becomes inflamed, pressure begins to build up in the pulp cavity, exerting
pressure on the nerve of the tooth and the surrounding tissues. Pressure from inflammation
can cause mild to extreme pain, depending upon the severity of the inflammation and the
body's response. Unlike other parts of the body where pressure can dissipate through the
surrounding soft tissues, the pulp cavity is very different. It is surrounded by dentin, a hard
tissue that does not allow for pressure dissipation, so increased blood flow, a hallmark of
inflammation, will cause pain.[5]

Pulpitis can often create so much pressure on the tooth nerve that the individual will have
trouble locating the source of the pain, confusing it with neighboring teeth, called referred
pain. The pulp cavity inherently provides the body with an immune system response
challenge, which makes it very difficult for a bacterial infection to be eliminated.[6]

If the teeth are denervated, this can lead to irreversible pulpitis, depending on the area, rate of
infection, and length of injury. This is why people who have lost their dental innervation have
a reduced healing ability and increased rate of tooth injury. Thus, as people age, their gradual
loss of innervation leads to pulpitis.[7]
Responses

Immune/inflammatory response

In the pulp, just as in other areas of the body, inflammation can be present. Inflammation of
the pulp does not take place only when the bacteria in the decay have reached the pulp.
Bacterial products may reach the pulp much earlier and begin the inflammatory response. The
inflammation may be acute or chronic because just like other tissues in the body, the pulp will
react to irritants with innate and/or adaptive immune responses.[8][9]

Innate immunity in the pulp is not specific but uses receptors to recognize molecular patterns
common to microbes to initiate bacterial killing (phagocytosis). The components of the innate
response of the dentin/pulp complex to caries include at least the following six: (1) outward
flow of dentinal fluid; (2) odontoblasts; (3) neuropeptides and neurogenic inflammation; (4)
innate immune cells, including immature dendritic cells (DCs), natural killer (NK) cells, and
T cells, as well as (5) their cytokines and (6) chemokines. Although the first two items are not
classic components of innate immunity, they are uniquely involved in the initial inflammatory
response to caries.[8]

Odontoblasts, (the cells that form dentin) have cellular processes that extend into dentinal
tubules and are the first to encounter the caries bacterial antigens. They express low levels of
interleukin 8 (IL-8) and genes related to chemokines and chemokine receptors. The
odontoblasts have been shown to attract immature dendritic cells.[8]

Dendritic cells (DCs) are a heterogeneous leukocyte (white blood cell) population. DCs in
healthy peripheral tissues (steady state) are in an immature state. The cells are capable of
sensing microbes as well as antigen capture and processing capabilities. A rapid accumulation
of pulpal DCs has been observed beneath cavity preparations, and an increased number of
DCs accumulated under caries. Immature DCs are therefore considered to be part of the
innate phase of pulpal immune response.[8]

Persistent infection leads to the activation of adaptive immunity. A transition to an adaptive

immune response will take place in the dental pulp as the caries and bacteria approach the
pulp. Antigens are recognized individually and lines of lymphocytes are developed to
produce specific antibodies which attach to the recognized cells and initiate their destruction.
Phagocytes remove the remains. B cells and T cells are the major lymphocytes involved.[10]

A variety of cytokines have been observed in the pulp. Patients with symptomatic and
asymptomatic irreversible pulpitis have been shown to have an almost 23-fold increase in the
cytokine IL-8 in the pulp. Cytokines in the pulp interact with each other. The ultimate effect
on pulpal inflammation and healing is dependent upon the integrated actions of these
inflammatory mediators.[11]

In addition to the lymphocytes, macrophages also provide defense against certain intracellular
pathogens. Activated macrophages can function as class II antigen-presenting cells, similar to
pulpal dendritic and B cells. In addition, activated macrophages secrete many inflammatory
mediators.[12]

Macrophages in the pulp become activated after receiving two signals. The first is a priming
stimulus and the second is an activating signal. The priming stimulus is secreted by activated
T-helper cells. The activating stimulus may include bacterial lipopolysaccharides, muramyl
dipeptide, and other chemical mediators.[12]

Macrophages are professional phagocytes in innate immune responses. Activated

macrophages are effective killers that eliminate pathogens in both innate and adaptive
immune responses, and are also important in tissue homeostasis, through the clearance of
senescent cells, and in remodeling and repair of tissue after inflammation. The number of
macrophages increases with the progression of caries and is always higher than that of DCs at
all stages of the caries invasion.[11]

Neurological responses

According to the Brnnstrm's hydrodynamic theory, activated nociceptors from fluid

movement and other irritants through the patent dentine tubules result in pulp pain.
Unmyelinated, slow conducting C-fibers aid in feeling a slowset, burning pain.[13] According
to neuronal studies, 70-80% of pulpal axons are unmyelinated.[14] Highly myelinated A-
fibers, which allow for fast conduction, are responsible for the sharp, shooting paining.[13]

Thus, the stimulus intensities are based on various fibers. Fast-conducting A and A-fibers
provide the lowest stimulus intensities (typically referred to as prepain sensations), and those
sensations eventually receive higher stimulation levels. The dull aches are associated with C-
fibers and slow A-fibers. As inflammation intensifies, the A-fibers are increasingly
activated. C-fiber innervation and A-fibers are polymodal receptors that are sensitive to
capsaicin and inflammatory mediators.[7]

The pain mechanisms associated with pulpitis are similar to those of the rest of the body (i.e.
receptors, intracellular signaling, transmitters, etc.). The inflammatory mediators act on
specific receptors relating to nociceptive neurons, leading to the production of second
messengers and activation of phospholipases and protein kinases. The second messengers
regulate receptors ion channels that deal with sensitization. The ion channels open based on
pain stimuli propagating action potentials in sensory neurons.[15]

In order for excitability and conduction to occur, voltage-gated sodium channels must be
activated. Changes in sodium channel (NaCH) expression occur after inflammatory lesions,
which may generate different pain states seen when neuronal fibers are activated. Studies
have been done on major NaCh isoforms to examine expression patterns. Nav1.6 nodal
accumulations do not vary in size or immunofluorescence staining activity in typical or
atypical nodal sites; however, the proportion of typical nodal sites decreases and increase in
atypical nodes in painful tooth samples compared to normal tooth samples. Nav1.7 has an
increased expression in typical and atypical nodal sites in painful samples. As a result, an
increased co-expression of multiple isoforms at demyelinating nodal sites in painful dental
pulp. This isoforms of sodium channels may be a main factor in pain sensations due to their
production of axonal excitability properties.[16]

Neuropeptides are increasingly being researched for having a role in molecular mechanisms
involved with pain, including ion channels and inflammation. Substance P (SP) is a
neuropeptide produced by capsaicin neuron cell bodies (localized in trigeminal ganglia and
dorsal root) and plays a major role in dental pain and inflammation. Other peptides include
cGRP, galanin, somatostatin, and neurokinin A-B. The biological effects of SP are expressed
by the binding of specific G protein-coupled NK receptors. Interaction with SP receptors
induces vasodilation and allows for plasma extravasation and mastocyte degranulation. SP is
highly expressed in dental pulp and dentin. When pain, thermal, and/or chemical stimulation
is present, SP production and release increases. Current studies focus on whether controlling
Substance P expression may control tooth pain.[15]

In addition, dental caries is more likely to develop pulpitis due to less time for the dental pulp
to react and protect itself by occluding the dentinal tubules.[13] Based on the tooth injury,
sensory nerve fibers react to pulpitis by growing terminal branches into the adjacent
surviving pulp, which also changes the cytochemical phenotype. This neural growth typically
lasts few a few days and function and form is retained.[7] Thus, pain is poorly localized, and
the level of pain stemming from pulpitis varies based on severity, quality, duration, onset,
trigger.

As caries invades dentin, the number of permeable dentinal tubules correlates with the degree
of pain. Intrapulp pressure have an effect on the sensory nerves of varying diameters:
blocking larger diameter A-fibres and activating smaller C-fibers. Under hypoxic
environments and pulp degeneration (symptom of pulpitis), C-fibers may still function.[13]
Once reparative dentin forms, odontoblasts associated with the dentin change, and the pulpal
fibroblasts lose p75 expression, which is a neurotrophin receptor.[7]

Cells involved in immune response

Cell Type Function
Mast Cells Rapid release of granules rich in histamine and heparin, along with
various hormonal mediators and chemokines
Macrophages Phagocytic leukocytes that engulf and destroy bacteria
Neutrophils Contain a variety of toxic substances that kill or inhibit growth of bacteria
and fungi
Dendritic Cells Antigen presentation
Basophils Release histamine, which is important in allergic reactions and defense
against parasites.
Eosinophils Secrete a range of highly toxic proteins and free radicals that are highly
effective in killing bacteria and parasites
Natural Killer Destroy compromised host cells, such as tumor cells or virus-infected
Cells cells

Pulp sensibility tests

Pulp sensibility tests are routinely used in the diagnosis of dental disease. There are 2 general
types:

Thermal-- most commonly, ethyl chloride sprayed onto a small ball of cotton wool,
which produces intense cold. Alternatively gutta percha can be heated to produce heat.
Electrical pulp test-- electric pulp testing (EPT) has been available for over a century
and used by dentists worldwide. It is used to determine the health of the pulp and
pulp-related pain. It does not provide information on vascular supply to the pulp. EPT
produces electrical stimuli that cause an ionic change across the neural membrane,
inducing an action potential in myelinated nerves. The threshold of pain level will be
determined by increasing the voltage. The requirements of an EPT are appropriate
application method, careful interpretation of the results, and an appropriate stimulus.
The tests must be done with tooth isolation and conduction media. EPT is not
 recommended for patients with orthodontic bands or crowned teeth. Key factors in
testing are the enamel and dentine thickness and the number of nerve fibers
underlying the pulp. Pulp nerve fibers respond to lower current intensities and a small
number of pulpal afferents, creating neural responses when electrical stimulation is
applied. EPTs may be unreliable and lead to false-positive and false-negative results.
False-positive responses in teeth may be attributed to pulpal necrosis. Also, since
pulpal and periodontal nerve thresholds may overlap, the periodontal nerves may give
a false indication in tooth sensibility.[17][18]

Possible explanations for false-positives include:

Response caused by conduction of the current because of periodontal or gingival

issues
Breakdown products associated with pulp necrosis may be able to conduct electric
current next to infected and hypersensitive pulp tissue
Inflamed pulp tissue may still be present
Metallic restorations or orthodontic gear are still present

Studies have indicated that there is little correlation between histopathological status of the
pulp and clinical information. A negative EPT response showed localized necrosis in 25.7%
of cases and 72% of cases. Thus, 97.7% of cases with a negative response to EPT indicated
that a root canal treatment should be carried out.[18]

Treatment

Once the pulp has become inflamed, the tooth can be diagnostically divided into two
categories.

Reversible pulpitis
Irreversible pulpitis

Reversible pulpitis

This is the condition where the pulp is inflamed and is actively responding to an irritant. This
may include a carious lesion that has not reached the pulp.

Symptoms include transient pain or sensitivity resulting from many stimuli, notably hot, cold,
sweet,[19] water and touch. The pulp is still considered to be vital. This means that once the
irritant is eliminated, usually by removal of decay and the placement of a restoration, that the
pulp will return to its normal, healthy state.[6]

Irreversible pulpitis

This is the condition where the pulp is irreversibly damaged. The pulp can not recover from
the insult and damage. For example, decay that has reached the pulp of the tooth introduces
bacteria into the pulp. The pulp is still alive, but the introduction of bacteria into the pulp will
not allow the pulp to heal and it will ultimately result in necrosis, or death, of the pulp tissue.
[6]
Symptoms associated with irreversible pulpitis may include dull aching, pain from hot or cold
(though cold may actually provide relief) lingering pain after removal of a stimulus,
spontaneous pain, or referred pain.[19][20]

Clinical signs may include reduced response to electronic pulp testing and painful response to
thermal stimuli.[19] Today electronic pulp testers are rarely used for diagnosis of the
reversibility of pulpitis due to their unreliable nature. Instead they should only be used to test
the vitality of teeth.

The pulp of a tooth with irreversible pulpitis may not be left alone to heal. That is at least the
general viewpoint of the dental profession, and not every dentist would agree that a dead
tooth must be treated. No statistics are known but it is possible to have a trouble-free tooth
after irreversible pulpitis, albeit a dead tooth. The tooth may be endodontically treated
whereby the pulp is removed and replaced by gutta percha. An alternative is extraction of the
tooth. This may be required if there is insufficient coronal tissue remaining for restoration
once the root canal therapy has been completed.[6]

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