PAIN MECHANISM1

Pain elicited by scraping of dentin or by application of cold or hypertonic solution

gives the impression that there may be a nerve pathway from CNS to DEJ.
However, no direct pathway has been identified. Applications of stimulants direct
to the dentin fail to produce pain. There are three mechanisms which may explain
about mechanism of pain: 1. direct innervations of dentin, 2. Odontoblasts as
receptor, 3. Hydrodynamic theory.
Direct innervations
Nerves are present in one third inner dentin and predentin. However, direct stimuli
to these nerves fail to produce pain. So, this theory is not the principal of pain
producing in dentin.
Odontoblasts as Receptor
This theory was considered because odontoblasts were of neural crest origin.
Transduction mechanism is the point of this theory. However, this theory is
controversial because in later research found that odontoblast process extends
only at partial dentin and it only has little potential membrane to do transduction.
In other hand, other research found that in some teeth the odontoblasts extend in
full thickness of the dentin and there is a gap junction between odontoblast and
possibly between odontoblast and nerves.
Hydrodinamic Theory
This theory postulated that the movement of fluid of dentinal tubules results in
distortion of nerve ending in the subodontoblastic nerve plexus (plexus of
Raschkow) that generates in neural impulse and a sensation of pain. In intact teeth
the application of hot and cold to the tooth surface produce different contraction
rates in dentin and dentinal fluid; this results fluid movement and initiation of
pain. This response is exaggerated when dentin is exposed. This theory has several
criticisms, first in the tooth whose pulp already damaged severely still can
experience dentin hypersensitivity, second the fluid in tubule is a little bit gelled
1 Walton and Torabinejad. Principles and Practice of Endodontics 3rd Edition. Sauders Co. 2008. Chapter 3.

with little hydraulic activity. Finally, the mechanism which explains the dentin
hypersensitivity is the combination between hydrodynamic theory and the thermal
receptors in the pulp, A-Delta and C nerve fibers.

Basically, there are 3 nerve fibers located in our oral region2:

a. A-fiber
b. A-fiber
c. C fiber
A-fiber
The rapidly conducting myelinated neurons that respond to light touch are called
A-beta fibers. Under normal conditions, activation of the A-beta fibers by highintensity stimulation results in low-frequency output in the central nervous
system. Activation of A-beta fibers normally is interpreted as nonpainful
mechanical stimulation or prepain. A-beta fibers have been shown to undergo
phenotypic changes that allow them to encode painful stimuli under inflammatory
conditions.

A-fiber & C fiber

2 Kenneth M. Hargreaves. Cohens Pathways of The Pulp 10th Edition.

Mosby Elsevier. 2011

A nociceptor is a sensory receptor that responds to potentially damaging stimuli

by sending nerve signals to the spinal cord and brain. This process, called
nociception, usually causes the perception of pain.
Nociceptor includes A-fiber & C fiber
- A fibers are myelinated and can allow an action potential to travel at a rate
of about 20 meters/second towards the CNS.
- C fibers are the unmyelinated and more slowly-conducting nerve axons. These
onlyconduct at speeds of around 2 meters/second.
As a result, pain comes in two phases. The first phase is mediated by the fastconducting A fibers and the second part due to (Polymodal) C fibers.

In short, comparison of the response characteristics of the pulp nerve fibres:

1) A-fiber Prepain sensations induced by electrical stimulation result from
activation of the lowest threshold A-fibres some of which can be classified as A
beta-fibres according to their conduction velocities,
2) A-fiber Responsible for the sensitivity of dentine and thus for the mediation
of the sharp pain induced by dentinal stimulation
3) Intradental C-fibres activated only if the external stimuli reach the pulp
proper. Their activation may contribute to the dull pain induced by intense thermal
stimulation of the tooth and to that associated with pulpal inflammation. The
smaller C fibres cause a slow, dull, crawling pain related to pulp tissue damage

and the inflammatory process due to their much higher treshold of excitability and
slow conduction.
Pulp nerves 3:

Sensory nerves which are branches of the maxillary and

mandibular divisions of the trigeminal nerve.

The small branches enter the apical foramina following the route of

the blood vessels.

A- and A- fibres produce initial rapid sharp pain in response to
external stimuli without the presence of tissue injury because of
their peripheral location, low treshold of excitability and fast
conduction (mostly located in the coronal portion, greatest nerve

density in the pulp horns).

Sympathetic nerve fibres originate from the cervical sympathetic
ganglion, joining the trigeminal nerve and follow the

sensory

nerves to the teeth.

Sympathetic nerves mediator are noradrenaline and neuropeptide

Y.
Sympathetic vasoconstriction is activated by stress and painful
stimuli, and may modulate the excitability of the sensory nerves.

Pain Processing4
Pain is perceived and recognized in the cortex because of incoming
nociceptive (i.e., noxious stimulus) input. In most cases the input from the pulpal
and periradicular tissues is transmitted through the maxillary or mandibular
branches of the trigeminal nerve toward the central nervous system (CNS) for
processing.
A-delta neurons pass to the thalamus directly, by way of the
neospinothalamic tract. The pathway ascends to the thalamus directly and is said
3 Walton and Torabinejad. Principles and Practice of Endodontics 3rd
Edition. Sauders Co. 2008. Chapter 3.
4 Cohen, Stephen & Richard C. Burns. Pathways of The Pulp 8thedition.
St Louis Missouri: Mosby, 2002

to carry fast pain. The second-order C-fiber neuron carries impulses via the
paleospinothalamic tract. Because the impulses take longer to reach the thalamus,
this type of pain is called slow pain. Fast pain tends to be sharp and easy to
localize; slow pain tends to be dull and aching.
Once the nociceptive input reaches the higher centers of the brain, there
are further interactions of neurons between the thalamus, cortex, and the limbic
system. The CNS has the ability to control or modulate the pain-transmitting
neurons. Several areas of the cortex and brain stem have been identified that can
either enhance or reduce nociceptive input arriving by way of the transmitting
neurons. When the impulses reach the sensory cortex, pain recognition occurs.
Physiology of Pulpal Pain (Hyperalgesia and Allodynia)5
Three characteristics define hyperalgesia: (1) spontaneous pain, (2) a
decreased pain threshold (i.e., allodynia), and (3) an increased response to painful
stimuli. The symptoms of hyperalgesia are frequently encountered in dental
patients. Spontaneous pain usually indicates the presence of irreversible pulpitis
or pulpal necrosis. The pulpal and periradicular tissues may have become
sensitized during the inflammatory process, leading to a state of allodynia in
which innocuous stimuli are perceived as painful.
Because of allodynia, spontaneous pain can arise from a reduced thermal
threshold, causing pulpal nociceptors to be activated by the body temperature.
Patients may describe sensitivity to heat and relief from cold, and they may sip a
large cup of ice water to reduce discomfort. Some patients complain of a
throbbing, pulsating pain, which is probably caused by a reduced threshold
of mechanoreceptors that increases sensitivity to the point where the arterial
pressure wave of the heartbeat stimulates perivascular nociceptors in the
pulp. Like pulpal nociceptors, periodontal mechanoreceptors acquire lower
thresholds and increased firing frequencies. Therefore performing diagnostic tests,
such as percussion and palpation, in the presence of allodynia can create painful
5 Cohen, Stephen & Richard C. Burns. Pathways of The Pulp 8thedition.
St Louis Missouri: Mosby, 2002. Chapter 2

responses. Similarly, performing pulp sensitivity tests can produce painful

responses, because the pulpal nociceptors are sensitized.
These signs and symptoms indicate that the pulpal and/or periradicular
tissues are in a state of hyperalgesia. A combination of neuroinflammatory
mechanisms can induce hyperalgesia, some occurring at the site of inflammation
and others occurring in the CNS.