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1. INTRODUCTION
Pain is one of the most commonly experienced symptoms in dentistry and, as such, is a major
concern to the dentist. It is often spoken of as a protective mechanism, since it is usually manifested
when an environment change occurs that causes injury to responsive tissue.
Historically, the pain of dental ill has been a constant tormentor since human beings arrived
on earth. Although everyone has experienced pain and described it as sharp, burning, aching,
cramping, dull, or throbbing, the actual pain experience varies greatly as a result of human
emotions. The ultimate purpose of pain response is to inform the patient of anatomic, physiologic,
or behavioral imbalances. These problems may range from mild to severe.
A patient’s oral and facial pain complaints may be based on a disorder in eight different
areas:
1. Periodontal tissue
2. Pulpal tissue
3. Tissue from adjacent sites (e.g. sinus, eye, ear, nose, throat, cervical spine, brain,
heart)
4. Neurologic system (e.g. peripheral, central)
5. Psychologic system
6. Vascular walls
7. Musculoskeletal tissue (i.e. temporomandibular,cervical) and
8. Idiopathic process (e.g. chronic atypical craniofacial pain).
The scope of this seminar is to elaborate in detail the pain of pulpal origin,
pain pathways, including its control and management.
DEFINITION AND CLASSIFICATION OF PAIN
DEFINITION:
The word “pain” was originated from Old French “peine”. Defined by ISAP, “Pain is an
unpleasant sensory and emotional experience associated with actual and potential tissue damage or
described in terms of such damage”. Pain is also defined as, “Pain is defined as an unpleasant
emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural
network to the central nervous system where it is interpreted as such”.
PAIN CLASSIFICATION:
The International Association for the Study of Pain (IASP) has categorized pain conditions
according to number of parameters: -
1. Axis I – Regions (The body region or site of reported pain).
2. Axis II− Systems (The body system whose abnormal functions produce pain).
3. Axis III – Temporal (Temporal characteristics of pain and pattern of occurrence).
4. Axis IV –Patient’s statement (Time since onset and intensity of pain).
5. Axis V – Etiology (The presumed etiology of pain problem)
NERVE CONDUCTION
Basic knowledge of pain comes from the understanding of nerve conduction and its self
propagated passage of an electrical current along nerve fibres.
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2. The conduction of an impulse by a nerve depends on the electrical potential that exists across
the nerve membrane. Although an electrical potential exists across the membrane of most cells in
the body, the nerve cell, being excitable, possesses the ability of transmitting or conducting
impulses along its length. The phenomenon is brought about by the flow of current across the
membrane during the transition of the nerve from the resting to the active state.
Nerve membrane is a thin elastic covering composed of a layer of lipid between two layers of
protein. Although the exact molecular structure of the membrane is in doubt, it is thought that the
membrane contains many minute pores through ions can diffuse under the proper circumstances.
Normally, electrolytic solutions containing an equal concentration (of approximately 155 mEq) of
anions and cations are present on the both side of cell membrane.
Resting state:
When the nerve is at rest, the greater number of anions (-) are present inside the cell
membrane, whereas an equal number of cations (+) are gathered outside the membrane. Thus
potassium ions are concentrated inside, while sodium and chloride ions are concentrated outside the
membrane. The difference in respective ion concentrations across the nerve membrane creates a
potential electrical difference between the inside negative and outside positive. The membrane
potential can develop by the creation of ionic imbalance. This can be accomplished by
1. An active diffusion of ions through the membrane and
2. A diffusion of ions across the membrane because of the gradient difference.
The electrochemical gradient between the inside of the nerve membrane and the outside is
approximately -70 to -90 mv, which indicates that the inside of membrane becomes 70 to 90 mv
more negative than the outside. Thus the unstimulated nerve or the nerve at rest is said to have
resting potential, during which time the membrane is polarized with the inside electrically negative
relative to outside. The polarized membrane is thus potential source of energy.
The resting potential of the nerve is assumed to result from and be maintained by the relative
permeability of the cell membrane to potassium and its relative impermeability to sodium ions.
Although the nerve membrane is freely permeable to potassium, this ion remains within the
asioplasm. Positively charged potassium ions are retained by the electrostatic attraction of the
negatively charged nerve membrane. Chloride on the other hand, remains outside the nerve
membrane as a result of the opposing electrostatic attraction of the negatively charged nerve
membrane. No chloride diffuses into the nerve membrane. The maintenance of the resting potential
is mainly a result of an active mechanism known as the “sodium pump,” which moves the sodium
from the area of lesser concentration inside the nerve to that of greater concentration outside.
Because of the greater concentration outside (142 mEq) and the lesser concentration inside the
nerve (10 mEq), the sodium tends to diffuse back across the membrane into the nerve as it is being
pumped out. This pumping action controls the concentration of sodium of both sides of the
membrane and thus maintains it in a polarized state. Both the concentration and the electrostatic
gradients for sodium favor its inward movement. It is relative impermeability of the nerve
membrane during the resting state that prevents a massive influx of this ion. Polarization of the
membrane will continue as long as the nerve remains undisturbed.
Depolarization:
When a stimulus of sufficient intensity to create an impulse is applied to the nerve, the
membrane is activated by an alteration in its permeability that permits sodium to increase its rate of
diffusion through the membrane into the nerve cell. It appears that initiation of changes in
membrane permeability to sodium occurs as a result of displacement of calcium ions from a
phospholipid-binding site. The marked increase in diffusion of sodium into the cell is followed by
the passage of potassium out of the cell. This action is said to abolish the resting potential and
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3. depolarized the membrane. It has been stated that the term depolarized is inaccurate, since a
reversal of polarity actually occurs, with the outside becoming negative relative to the inside,
resulting in a potential (reversal potential) of about twice that of the resting potential.
As the nerve is stimulated, there is a rapid (0.1 to 0.2 msec) passage of sodium into the cell
and a slower (1 to 2 msec) passage of potassium out of it. The alteration in the permeability of the
cell membrane that is initiated after an adequate stimulus is applied is believed to be the result of the
liberation of a transmitter substance, acetylcholine, at the site of stimulation. The passage of impulse
or the speed of the action potential is the result of a continuing stimulation or chain reaction, with
each area generating its own potential by the alteration of the permeability of the membrane to the
inward passage of sodium followed by the outward passage of potassium. In a larger myelinated
nerve, the stimulation takes place only at the nodes of Ranvier, with the impulse conducted along
the nerve fiber from node to node by its own energy source. The “jumping” of the impulse from
node to node through the surrounding interstitial tissue is called salutatory conduction, which
explains the greater rate of speed at which impulses are conducted by myelinated nerves.
Repolarization occurs rapidly after the passage of an impulse from node to node so that actually
only a small portion of nerve is depolarized at any one time.
Repolarization:
Following depolarization, the permeability of nerve membrane again decreases, while the
high permeability of potassium restored. Potassium moves freely out of the cell, thereby restoring
the original electrochemical equilibrium and restoring potential. Movement of both sodium ions into
the cell during depolarization and potassium out of cell during repolarization are passive (nonenergy
requiring) actions since each ion moves along its concentration gradient (for example from an area
of high concentration to an area of low concentration). The energy driven “sodium pump” then
actively transports sodium out of the nerve membrane against its concentration gradient while
simultaneously transporting potassium inward to reestablish the resting state. Adenosine
triphosphates (ATP) provide the energy source for the sodium pump.
The return of the resting potential occurs within 3 to 4 msec after initial stimulation, during
this 3 to 4 msec interval, the membrane has a reversal potential and cannot be stimulated. The nerve
is then in an absolute refractory period. When the normal ionic distribution pattern begins to return,
the nerve can be stimulated, but only by greater than usual stimulus. The nerve is then said to be
relatively refractory period.
When the pre-impulse concentration gradients of potassium inside the nerve and of sodium
outside are reached following the relative refractory period, the membrane is said to be normally
polarized and will react to a stimulus of normal intensity. However, during the relative refractory
period or the normal polarized state, a certain minimal stimulus is necessary to provoke a sufficient
ionic interchange to create an impulse. Once an impulse has been initiated within a particular nerve
fiber, the amplitude of electrical change as well as speed of nerve conduction remains constant
regardless of the quality or intensity of stimulus applied, which explains the all-or none law of nerve
action. At times this principle may seem unfounded; particularly when an exceptionally noxious
stimulus is applied to a nerve that may produce a much greater reaction. This greater response
stresses the multifiber composition of the nerve; whereas the weaker stimulus affects only a few
fibers, the more noxious or the stronger stimulus excites more or even all of the nerve fibers.
SENSORY RECEPTORS RELATED TO TOOTH
The dental pulp consists of well developed system of nerves. Thick nerve bundles or
fascicles enter the pulp by way of apical foramina and progress in a relatively straight course
towards the crown. These nerve fibers are myelinated and thought to function in a sensory capacity.
The unmyelinated fibers belong to the sympathetic nervous system, terminating on smooth muscle
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4. cells of blood vessels and controlling the constrictive activity of the vessels. In the crown portion,
the nerve divides into numerous fiber groups radiating towards the dentin, with the majority of the
fibers directed towards the pulp horns. These fibers or peripheral axons form a network, the
parietal layer or plexus of Raschkow before reaching the cell–rich zone. Both myelinated and
unmyelinated axons are present in the plexus. The axons pass through the cell-rich and cell-free
zones, losing their myelin sheath on the way. They then either terminate beneath or between the
odontoblasts or within the dentinal or predentinal tubules adjacent to the odontoblastic processes.
Other nerve fibers which appear to be embedded in the predentin or dentin form a loop and curve
back into the odontoblastic layer where they terminate in close contact with the odontoblast cell
proper. Many of these nerve endings terminate as round or oval swellings containing microvesicles
as well as other cellular organelles. These fibers end in extremely close proximity to the
odontoblastic cell membrane with a gap of only 200 A0
between the two. The further progression of
nerve fibers within dentin has been a subject of much controversy for many years. The nerve fibers
actually do enter dentinal tubules, the evidence indicating that nerve fibers progress deeply into the
dentin from the pulp is limited. The literature on this subject leads to the conclusion that a small
number of fibers enter the dentin and that these fibers penetrate only about one-third the distance to
the enamel.
Although the mechanism of dentinal sensitivity cannot be answered presently on the basis of
morphology, some of the current theories concerning stimulation of and impulse transduction
through dentin can be described:-
1) One of the most popular theory states that the odontoblast itself with its process extending
throughout the dentin, acts as a receptor cell, transmitting an impulse pulp ward to the nerve
endings which are found in close association with the odontoblastic cell body.
2) Another theory states that stimuli applied to dentin causes displacement of odontoblasts or
the contents of the dentinal tubules, which in turn excites nerve endings near the pulpal ends
of the tubules.
3) A third theory states that nerve endings within dentin respond directly to stimulation.
This requires either active or passive transmission of impulses through the dentinal tubule,
possibly by tissue fluid.
Unique feature of pulp and dentin is that whatever the stimulus (mechanical, thermal or
chemical) the only sensation elicits is one of pain. This is due to the fact that the pulp contains only
free nerve endings which are pain receptors and not other types of receptors that are sensitive in
perceiving other types of stimuli.
NEUROPHYSIOLOGY OF PAIN
Pain is a complex experience which includes not only the sensations evoked by tissue-
damaging or noxious stimuli but also the reactions or responses to such stimuli. Pain sensations
refer to our capacity to discriminate the quality of a noxious stimulus as well as location, intensity
and duration. Reactions to these sensations very from individual to individual and involve reflexive
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5. and more integrative motor responses. Intentional, cognitive, motivational and emotional variables
modify behaviors elicited by noxious stimuli.
Mechanisms of Pain:
The noxious mechanical and thermal stimuli applied to the extremities elicit in humans an
experience of two distinct types of pain. An early sharp, stinging, well localized sensation is
followed about 1 second later by a diffuse, burning sensation which often outlasts the stimulus. The
so called first and second pains have been shown to be correlated with conduction in small
myelinated (A delta) and unmyelinated (C) fibers. First and second pains are difficult to elicit on
the face because of the reduced peripheral conduction time difference between A- delta and C fiber
discharge.
There are three major groups of nerve fibers, designated “A” “B” and “C”. The A group
includes all the myelinated axons of somatic nerves, varying in diameter from 22 µ to 2 µ with
conduction rates of 120 m/sec to 2.5 m/sec. These are further subdivided into alpha (α), beta (β) and
delta (δ). The B fibers are myelinated fibers of 3 µ diameters or less found in autonomic nerves.
The C fibers are all unmyelinated. The largest sensory fibers innervating the skin are in the A-beta
group, and conduct in the range of 40 to 80 m/sec. These are exclusively fibers which respond to
low threshold mechanical stimuli (Mechanoreceptive afferents), such as hair movement and
maintained light pressure. The other major myelinated groups of sensory fibers are A-delta fibers
conducting in range of 2.5 to 36 m/sec. This is functionally mixed group consisting of low threshold
mechanoreceptive afferents, fibers activated by cooling the skin (thermoreceptive afferents) and
fibers activated almost exclusively by intense forms of thermal and/or mechanical stimuli
(nociceptive afferents). Unmyelinated (C) fibers conducting in the 0.7 to 1.5 m/sec range are also a
mixed group functionally (mechanoreceptors, thermoreceptors and nociceptors).
Two major types of small myelinated A-delta fibers are found. One type high threshold
mechano-receptive afferents respond only to intense mechanical stimuli. The second type, A-delta
heat nociceptive afferents, responds to intense thermal and mechanical stimuli. Thus activation of
the terminals of A-delta heat nociceptive afferents only results in impulse discharges which
ultimately produce pain sensations.
The third major class of nociceptors is unmyelinated and is called C polymodal nociceptive
afferents. They constitute 80% to 90% or more of the C-fiber population innervating the face and
extremities. They are characterized by their high thresholds to thermal and mechanical stimuli and
their response to irritant chemicals applied to skin. Second pain produced by heat impulses occurs
even after blocking of activity in all myelinated fibers. Polymodal nociceptive afferents are the only
afferent group activated by this stimulus. Thus second pain is produced primarily due to activation
of these afferents.
A-Delta nerve fibers:
Most of the myelinated nerve fibers of the pulp are A-delta fibers. They are referred to as a
nociceptive fiber because of threat of tissue damage is the most effective stimulus. A-delta fibers are
relatively large fibers, with fast conduction velocities. They enter the root canal and divide into
smaller branches, coursing coronally through the pulp. Once beneath the odontoblastic layer, the A-
Delta fibers lose their myelin sheath and anastomose into a network of nerves referred to as the
plexus of Raschkow. This circumpulpal layer of nerves sends free nerve endings onto and through
the odontoblastic cell layer and dentin is referred to as the pulpodentinal complex. Researchers have
found that sensory innervation occurs only in dentinal tubules with viable odontoblasts, and that
odontoblast maintains their structural integrity only in innervated regions of a tooth.
Disturbances of the pulpodentinal complex in a vital tooth initially affect the low-threshold
A-delta fibers. Drilling, probing, drying with air and application of hyperosmotic solutions to
exposed dentin will cause pain. Movement of fluid in the dentinal tubules, known as hydrodynamic
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6. theory of dentin sensitivity, stimulates the A-delta fibers. The vital pulp responds immediately with
symptoms of dentinal pain. Application of some hyperosmotic agents to dentin does not cause pain
unless they are placed in a deep cavity preparation. This finding supports an additional mechanism
of dentin sensitivity the direct ionic theory.
Not all stimuli will reach the excitation threshold and generate a pain response. Irritants such
as incipient dental caries and mild periodontal disease are seldom painful. However, they can be
sufficiently irritating to stimulate the defensive formation of sclerotic or reparative dentin. The fact
that a pulp can become necrotic in the complete absence of pain indicates that there are peripheral
and central mechanisms that may control nociceptor sensitization and activation.
A-delta fiber pain must be provoked. Nociceptive signals, transmitted through fast
conducting myelinated pathways, are immediately perceived as a quick, sharp, momentary pain. The
sensation dissipates quickly upon removal of the inciting stimulus, such as drinking cold liquids or
probing exposed dentin. The clinical symptoms of A-delta fiber pain signify that the pulpodentinal
complex is intact and capable of responding to an external disturbance.
A-beta nerve fiber:
A-beta nerve fibers are among the fastest nerve fibers of all intradental nerves. They may
function as mechanoreceptors that trigger withdrawal reflexes so that potentially damaging forces
may be avoided. Intense cooling, serotonin, and hydrodynamic changes can also stimulate A-beta
fibers. Although studies suggested that they are capable of detecting prepain and pain, the role of A-
beta fibers is not clearly understood. However, future research should clarify their purpose.
C nerve fibers:
C fibers are small, unmyelinated nerves that innervate the pulp. They are high- threshold
fibers, course centrally in pulp stroma, and run subjacent to the A-delta fibers. Unlike A-delta fibers,
C fibers are not directly involved with the pulpodentinal complex and are less easily provoked. The
pain associated with C fibers is dull and poorly localized. In most cases, it occurs later, as a
secondary pain. C fibers have a high threshold and can be activated by intense heating or cooling of
the tooth crown or mechanical stimulation of the pulp. The receptive fields for these nerve fibers are
exclusively in the pulp proper. Once activated, the pain initiated by C fibers can radiate to
anywhere in the ipsilateral face and jaws.
C fiber pain is associated with tissue injury and is modulated by inflammatory mediators,
vascular changes in the blood volume and blood flow, and increases in tissue pressure. Stimulated C
fibers are capable of releasing inflammatory modulating neuropeptides, such as calcitonin gene-
related peptide (CGRP) and substance P. These neuropeptide enhance the inflammatory response by
stmulating the release of histamine and arachidonic acid metabolites.
When inflammation leads to pulp necrosis, a periradicular lesion may develop as extension of
the pulpal pathology. Even when a radiographic lesion is clearly visible, some nerve fibers may
respond to vitality testing. Both myelinated and unmyelinated nerves have been found in teeth with
necrotic pulp and periapical lesion. For this reason instrumentation of teeth with necrotic pulps may
cause pain. Because C fibers are more resistant than A-delta fibers to compromised blood flow and
hypoxic conditions, pain associated with necrotic pulp is more likely to be caused by C fiber
stimulation.
THEORIES OF PAIN
1. Specificity Theory-
In 1890’s Von Frey postulated that certain nerve endings in the skin were activated by tissue
damaging stimuli and gave rise to pain sensations. Histological identified receptor structures were
free nerve endings. Specific sensory fibers carry information related to specific modalities of
sensation. He also proposed that free nerve endings give rise to pain sensations in the brain.
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7. Shortcomings:
1) Major deficit of the theory is its inability to explain some of the characteristics of clinical
pain.
2) The specificity theory cannot explain all pathologic pains produced by mild non-noxious
stimuli.
3) The specificity theory also does not explain referred pain that can be triggered by mild
innocuous stimulation of normal skin.
4) This theory cannot explain the paroxysmal episodes of pain produced by mild stimulation of
trigger zones in trigeminal neuralgia.
The inadequacy of specifity theory is demonstrated further in analysis of central neurons
activated by noxious stimuli.
Specificity Theory
2. Central summation theory/Pattern theory-
Goldscheider proposed this theory. The intensive or summation theory proposes that pain is
not a separate modality but results from over stimulation of other primary sensations. Thus
stimulus intensity and central summation are critical determinants of pain. Excessive stimulation
activated all types of receptors resulting in convergence and summation of activity in the
brainstem and spinal cord. Pain resulted when activity exceeded a critical level due to excessive
activation of receptors normally responsive to non-noxious stimuli or when pathologic
conditions enhanced summation produced by such stimuli. This theory did not recognize the
importance of receptors specialization in response to noxious stimuli, its emphasis on central
summation and convergence was a valuable contribution to our understanding of pain
mechanisms.
Central Summation theory
3. Sensory interaction theory-
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8. Noordenbos proposed that rapidly conducting large fiber pathway inhibit or suppress activity in
slowly conducting small fiber pathways that convey noxious stimuli. A decrease in the ratio of
large to small fiber activity results in central summation and an increase in pain. An increase in
the ratio of large to small fiber activity results in more inhibition in nociceptive pathways and a
decrease in pain. Noordenbos also stressed the importance of a multisynaptic afferent system in
the spinal cord. Hyperalgesia following peripheral nerve injury can be explained by a greater
loss of large fibers than of small fibers. A reduction in large fiber activity would decrease the
ratio of large to small fiber activity resulting in more central summation an increase in pain.
Burning pain of slow onset in post herpetic neuralgia also can be understood on the basis of
large fiber destruction, a release of inhibitory mechanisms and central summation. Sensory
interaction theory stressed inhibition, an important physiologic mechanism in pain transmission.
Sensory Interaction Theory
4. Gate control theory-
In 1965 Melzack and Wall proposed this theory which combined the strengths of previous
theories and added some of its own. This theory provides a general conceptual framework for
viewing the multidimensionality of pain experience.
The basic tenets of this theory are:-
1) Nerve impulse from afferent fibers to spinal cord transmission or relay neurons are
modulated by a spinal gating mechanism, presumably in substantia gelatinosa layer of spinal
cord dorsal horn. The term “Gate” only refers to relative amount of inhibition or facilitation
that modulates the activity of the transmission cells carrying information about noxious
stimuli.
2) This gating mechanism is influenced by the relative activity in large diameter (A-beta) fibers
activated by low threshold non-noxious stimuli and small diameter (A-delta + C) fibers
activated in most cases by intense, noxious stimuli. Activity in large fibers tends to inhibit
transmission (close the gate); small fiber activity tends to facilitate transmission (open the
gate). Thus the theory recognizes receptor specificity and mechanism of convergence,
summation and inhibition.
3) This gating mechanism is influenced by descending control mechanisms from the brain
which relate to cognitive, motivational and affective processes. Large fibers, in particular,
activate central control mechanisms related to cognitive processing, which in turn modulate
the gating mechanism.
4) When the output of the transmission cells exceeds a critical level (central summation) neural
systems are activated which underlie the complex behaviours related to escape and avoidance
of tissue-damaging stimuli Melzack and Casey proposed that the output of the transmission
cells activated two major systems: One was a sensory-discriminative system involving
neospinothalamic fibers projecting into the ventroposterior thalamus and possibly the
somatosensory cortex. The second system was concerned with the unpleasant and aversive
aspects of pain sensations, and involves a reticular formation ascending pathway which
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9. projects to medial thalamic nuclei and the limbic system. A third system of descending
control exerted by neocortical activity is thought to modulate activity in sensory
discriminative and motivational–affective systems. All three systems ultimately influence the
motor mechanisms responsible for behaviours elicited by noxious stimuli.
The gate control theory and its recent modifications have stressed the importance of
descending control mechanisms in pain modulation. It also provides testable hypothesis about
pathways and mechanisms involved in the cognitive, motivational and affective component of the
pain experience.
Gate Control Theory
PERCEPTION AND SENSATION
A. Neospinothalamic system—three-neuron sequence
1. “First pain” pathway
a. Nociceptor
b. Sensory nerve
c. T cell
d. Thalamus
e. Sensory cortex
B. Paleospinothalamic system
1. “Second pain” pathway
a. Nociceptor
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10. b. Sensory nerve
c. Dorsal horn synapses
d. Surpaspinal networking
e. Sensory cortex
C. Sensory receptors
1. Special
a. Senses
b. Balance
2. Visceral
a. Hunger, nausea, distension
b. Visceral pain
3. Superficial
a. Transmit sensations
b. Cutaneous
c. Three categories based on type of stimuli to which they respond
4. Deep—tissue
a. Ligaments, muscles, and connective tissue
b. Supplied by mechanoreceptors and nociceptors.
D. Afferent (sensory) pathways—three types of first-order afferents (outside of central
nervous system) are relevant to pain transmission and are classified by structure,
degree of myelination, and function:
1. A-beta fibers—transmit sensory information regarding touch, vibration, hair
deflection
a. Large diameter; myelinated
b. Fast conducting; easily stimulated
2. A-delta fibers—respond to noxious mechanical stimulation (i.e., pinching,
prickling, crushing)
a. Small diameter; myelinated
b. Slower conduction velocity
3. C fibers—originate at deep receptors (ligaments, muscles, connective tissues)
a. Smallest of the three; myelinated
b. Slowest conduction velocity; require greater stimulation
E. Ascending pathways
1. Peripheral first-order afferent nerve enters spinal cord; synapses in dorsal horn
2. Second-order neuron transmits noxious information via lateral spinothalamic
tract of spinal cord to the thalamus
F. Supraspinal centers
1. Third-order neurons in thalamus; sensory information continues to be
organized
2. Thalamus relays sensory input to somatosensory cortex of the brain where
localization and discrimination of pain will occur
G. Descending pathways
10

11. 1. Noxious stimulation activates periaqueductal gray (PAG), which excites the
reticular formation, Raphe nucleus, and pituitary gland
2. Pain signals filtered out, lessening pain impulses sent to cognitive areas of the
brain cortex
3. Goal of pain management is to evoke these descending modulation areas,
which are at the subconscious level
a. Control of pain through activity modification (rest, splint)
b. Control through medication
c. Use of modalities
d. Reduction of stress
4. If not inhibited, affective-emotional pain response can be similar to shock
a. “Windup” phenomenon—pain syndrome resulting when noxious
stimulation spirals out of control
b. Pain stimulation continues to flow to cognitive areas and perception of
pain is increased
5. Proper treatment of acute injuries usually prevents this hyperstimulated state
TRIGEMINAL PAIN PATHWAY
Sensory messages from the mouth and face travel along peripheral nerve fibers which project
to a brainstem trigeminal nuclear complex that extends from the pons to the upper cervical segments
of the spinal cord. This core of neurons can be divided into subnuclei in the rostrocaudal direction
and each level consists of multiple neuronal cell types. Neurons that send direct projections to
ventrobasal thalamus are found at all levels. Neurons whose axons are confined to the trigeminal
brainstem nuclear complex and surrounding reticular formation also are very numerous. Their
intranuclear axonal projections ascend and descend throughout the body of the nucleus in distinct
fiber bundles. In addition there are projections to the trigeminal nuclei from the cerebral cortex, and
physiologic study suggest that activity in cerebral cortex and in other regions of the CNS can
ultimately modify sensory transmission in these brainstem nuclei. This complex structural
organization suggests that considerable modification of incoming sensory messages can take place
at this level of the trigeminal system.
A trigeminal tractotomy procedure (sjoquvist operation) which interrupts the trigeminal
brainstem nuclear complex in its more caudal extent near the obex, produces an almost complete
loss of pain and temperature sensibility in the oro-facial region, with minor effects on touch
sensation. This sensory dissociation in humans had led to two major hypotheses about the role of
the trigeminal brainstem nuclei in the transmission of nociceptive signals to other levels of the
neuraxis. One general hypothesis states that the caudal region, nucleus caudalis, exerts a
modulating influence on sensory transmission of pain and temperature signals through the more
rostral subdivisions of the nuclear complex via ascending intranuclear connections. Mechanisms of
summation, inhibition and facilitation are presumed to be critical determinants of the final output of
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12. trigeminothalamic projection neurons in the more rostral subdivisions. The second general
hypothesis considers nucleus caudalis to be the major component of the trigeminal nucleus
concerned with nociception. It receives noxious input and conveys this information to the thalamus
via a distinct primary afferent-projection neuron pathway which does not include the more rostral
subdivisions of the trigeminal brainstem nucleus. Mechanisms of summation and inhibition
influence the output of trigeminothalamic neurons in nucleus caudalis. Although these two
hypothesis are not mutually exclusive, recent anatomical and physiological studies provide strong
support for the second hypothesis.
The substantia gelatinosal layer (SG) and the marginal layer (MAR) of nucleus caudalis
receive an exclusive projection of small myelinated and unmyelinated axons whose receptor
terminals are activated primarily by noxious and thermal stimuli. These primary afferent neurons
terminate in the SG and MAR layers where they synapse on dendrites of neurons whose cell bodies
are located in the MAR and magnocellular (MAG) layers. There are two general categories of
trigemino–thalamic neurons in nucleus caudalis which ultimately receive input from these small
afferents and respond to noxious heat. The first type, referred to as nociceptive–specific neurons,
responds only to intense mechanical and thermal stimuli. Many are activated by non-noxious
intense pressure but respond maximally to pinch with serrated forceps. They appear to receive input
only from small myelinated and unmyelinated afferent fibers. The second type, wide–dynamic range
(WDR) neurons, is activated by hair movement and mechanical forces less than 1gm, but responds
maximally to pinch with serrated forceps. Many respond to noxious heat. They appear to receive
input from finely myelinated (A-delta) and unmyelinated (C) primary afferents. Their responses to
low threshold, light tactile input and their brief latency responses to electrical stimulation of facial
skin indicate that they also receive input from large (A-beta) myelinated afferents.
There is a third general category of trigemino–thalamic neurons in the nucleus caudalis
which responds to light touch, pressure or hair movement and appears to receive input exclusively
from large myelinated afferents. The low threshold mechanoreceptive neurons do not respond to
noxious heat or exhibit higher frequencies of impulses to noxious mechanical stimuli as opposed to
innocuous stimuli.
It is presumed that these neurons do not participate in mechanisms of pain sensations.
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13. Trigeminal Nociceptive Pathway
Nociceptive specific neurons are located mainly in the MAR layer. Wide –dynamic range (WAR)
neurons are found usually deep in the MAG layer and in the surrounding lateral reticular formation.
Low-threshold mechanoreceptive neurons, located usually in the superficial part of the MAG layer.
The neurons project directly to the thalamus in and near the ventro–posterior medial nucleus.
. .
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14. Location of neurons in nucleus caudalis
Inhibitory mechanisms modify transmission of impulses in trigeminothalamic neurons.
Activity in large myelinated, low-threshold mechanoreceptive afferents can inhibit or suppress the
response of nociceptive –specific and wide dynamic range neurons. This mechanism has led directly
to the use of transcutaneous electrical stimulation [TES] of large A-beta afferents as method of pain
relief. The output of these central nociceptive neurons also is suppressed or inhibited by electrical
stimulation of brain sites surroundings the cerebral aqueduct and third ventricle. Somatosensory
cortex neurons activated by oro-facial non-noxious input participate in a rapidly conducting
feedback loop between the trigeminal brainstem nuclei and the cortex. However, there is no direct
evidence that these cortical effects modify the activity of nociceptive neurons in nucleus caudalis.
Other investigators have shown that cortical and supraspinal influences inhibit activity of
spinal cord interneurons in the dorsal horn. More recently, it has been shown that spinothalamic low
threshold mechanoreceptive neurons are inhibited by cortical stimulation. However, nociceptive
neurons are not affected. The most powerful inhibition of nociceptive neurons in trigeminal nucleus
caudalis and spinal cord dorsal horn is produced by stimulation of midbrain periaqueductal gray and
diencephalic, periventricular regions. Heat induced responses of nociceptive–specific and wide–
dynamic range trigeminothalamic neurons can be suppressed for minutes by repetitive 10 to 30
seconds electrical stimulation of these midbrain and diencephalic regions. These descending
inhibitory mechanisms suppress the high–threshold responses to wide–dynamic range neurons more
effectively than the low –threshold component of their response. A similar preferential inhibitory
effect on responses evoked by tooth–pulp is observed in nucleus caudalis neurons activated by tooth
pulp and innocuous stimuli.
These inhibitory effects evoked by focal stimulation of midline midbrain and diencephalic
structures are particularly exciting because such stimulation also has profound antinociceptive
behavioural effects in humans. This stimulation produced inhibition shares common central nervous
mechanisms of action with analgesia produced by morphine and other narcotic analgesics.
Morphine micro-injected into these brain sites also produces inhibition of nociceptive neurons in the
spinal cord dorsal horn. Information about noxious stimuli is coded by the combined output of
nociceptive–specific and wide–dynamic range trigeminothalamic neurons located in the marginal
and magnocellular layers of nucleus caudalis and in the surrounding lateral reticular formation.
Both of these neurons are excellent candidates for the “pain” transmission cells. They receive input
from nociceptive and non–nociceptive afferents and mechanisms of convergence, central
summation, inhibition and descending control determine what sensory messages are relayed to the
thalamus by these neurons.
THALAMIC AND CORTICAL NOCICEPTIVE PATHWAYS
The ventroposterior nuclei and the posterior group of nuclei in thalamus receive projections
from three major ascending sensory pathways. The dorsal column-medial lemniscus system, the
spinocervical system and the spinothalamic system. All three pathways contain neurons that may be
involved in pain mechanisms, yet few neurons in these two thalamic nuclei have been found that
respond exclusively or maximally to nociceptive stimuli. A paucity of such neurons also is found in
14

15. medial thalamic nuclei which receive projections from spinoreticular and spinothalamic pathways.
The ventro-posterior nuclear region is involved in the localization and discrimination of pain.
Stimulation caudal and inferior to the ventroposterolateral nucleus results in localized pain in
conscious humans. These thalamic sites appear to receive direct input from spinothalamic tract
neurons.
The posterior nuclear group of the thalamus extends caudally from the caudal pole of the
ventroposterior nucleus to merge with the medial geniculate body and the midbrain tegmentum.
Most cells in this region responded only to noxious stimulation of large, bilateral receptive fields
including the face. Some neurons in the posterior group also responded to tooth –pulp stimulation
and this response is depressed after IV injection of morphine. Electrical impulses which are used to
stimulate tooth pulp may activate peripheral fibers that signal sensations other than pain. It is
possible that some central neurons may receive tooth –pulp input that is exclusively non –noxious in
character.
There is evidence that tooth pulp in humans project to the somatosensory cortex. Some of
these neurons respond exclusively to tooth–pulp electrical stimulation. The relationship of these
finding to pain mechanisms is unclear, tooth –pulp input may not be purely nociceptive in character.
LOCALIZATION OF PAIN DUE TO PERIODONTAL DISEASE
Localization of pain from the pulp is poor where as localization of pain from periodontal
disease is good. A difference in localization of pain from the pulp and periapical tissue might
depend on several neurological factors. The periodontium has mechanoreceptive fibres which pass
to principal nucleus and nucleus oralis of the trigeminal system. Here there are synapses which offer
a high degree of synaptic security and the secondary neurons carry the information to the
ventroposterior nucleus of the thalamus where the fibers are arranged in a somatotopic manner.
Tertiary fibers convey the information to the sensory part of the cerebral cortex where there is again
somatotopic representation. In other words the system allows recognition of the place of origin of
the neuronal information. On the other hand, neural impulses from the pulp go to the spinal nucleus
of the trigeminal nerve and thence to the reticular system. Here there is an opportunity for the
neural impulses to spread more widely in the brainstem so that the person is only able to form a
more generalized idea of the place of origin.
15

16. PERIPHERAL NERVOUS SYSTEM AND ITS ROLE IN MEDIATING PAIN
Sensory inputs from various external stimuli are though to be received by specific peripheral
receptors that act as transducers and transmit by nerve action potentials along specific nerve
pathways towards CNS. Termed first–order afferents, these peripheral terminals of afferent nerve
fiber differ in the form of energy to which they respond at their respective lowest stimulus intensity.
The impulse is interpreted as nociceptive if it extends the pain threshold. Alternatively, there is
possible cellular damage accompanied by the release of endogenous pain-producing substances at
the receptor site which triggers a biochemical phenomenon causing pain. The terminals nervous
boutons, receptors or sensory end organs present the complex termination of sensory fibers
ultimately originating after many complex synapses from nerve nuclei or ganglia emanating from
the central or peripheral nervous system. Communication between the cell body and its terminal end
organ is by a phenomenon termed axoplasmic flow.
Thermal
↓
Biochemical →Stimulus ← Mechanical
↓
Sensory receptors
↓
Altered membrane conformation
↓
Change in membrane permeability
↓
Ionic flow transfer
|
16

17. ↓ ↓
Local Depolarization Depolarization without impulse
↓ ↓
Nerve action potential ← ← Neurotransmitter release
Thus the peripheral system comprises afferent neurons consisting of spinal and cranial
nerves. Their distal axonal branches end as free nerve endings or into receptors in body tissue where
their cell bodies reside in the sensory ganglia and their proximal axonal branches make contact with
second order neurons in the neuraxis.
NATURE OF PAIN:
Normally the pain experience begins with the peripheral nervous system. Nerve fibers have a
nucleus (i.e. the cell body) that is located either within the nervous system or in the ganglia located
in the peripheral tissues. Emanating from the cell body are long processes referred to as axis
cylinders. A single nerve is made up of hundreds of individual axis cylinders that are encased in a
fibrous capsule known as the “perineurium”. Each axis cylinder is ensheathed by specialized
‘Schwann cell’. Thus the peripheral nerve can be envisioned as a bundle of electric cables, all with
their own enveloping insulation.
Some axis cylinders, with their associated Schwann cells, have an additional insulating layer
known as myelin, a specialized lipid synthesized by the Schwann cells. Those fibers capable of
transmitting noxious stimulus (i.e. nociceptors) lack a myelin sheath. These nonmyelinated fibers
are also referred as C fibers, as apposed to certain A and B fibers that transmit nonpainful sensory
stimuli. The nerve endings of nociceptors C fibers are found in the skin and mucosa and, of course,
are prevalent throughout the jaws, teeth, and periodontal tissues. In the region of the jaws, the
nociceptor fibers are component of the trigeminal nerve. All of these nociceptors system in the
trigeminal system have their cell bodies located in the Gasserian ganglion and the afferent axis
cylinders that feed into these cell bodies exit the ganglion and extend towards the central nervous
system through the trigeminal trunk that enters the pons.
These fibers then progress from the pons into the upper aspect of the cervical region of the
spinal cord. It is in this location where the axis cylinders terminate in a region referred to as the
caudate nucleus of Vegus nerves that transmitting proprioceptive signals and light touch terminate
higher in the spinal cord (mesencephalic nucleus). Fibers that terminate in the caudate nucleus are
nociceptors that interdigitate with the secondary neurons. These secondary neurons then pass
(superiorly) into the brain itself. At this synapse in the caudate nucleus, neuropepties are secreted
that are capable of transmitting a noxious impulse from the C fibers across the synapse to the
secondary nerve fiber. In addition, other fibers have been identified that modulate this
neurotransmitters pathway. Interneurons also have fiber ending that contact the incoming nociceptor
fibers and are capable of secreting yet other neurotransmitters capable of inhibiting propogation of
the noxious stimuli. Many of these inhibitory neurosecretory molecules fall into a special class of
peptides known as endorphins.
17

18. Some times ago a theory was proposed to explain how noxious stimuli became consciously
identifiable in the higher centers of the brain. The gate control theory of pain is based on
observation of a variety of interconnections in the region of the synapse. As noxious stimuli became
more accentuated, the so-called gate would open and allow the impulses to be transmitted across the
synapse. Indeed, neuroscience researchers have provided evidence that the gatekeeper is, in fact,
represented by neurotransmitter molecules.
Once noxious stimuli, such as bacterial enzymes and toxins, as well as host mediators and
cytokines, accumulate in an acutely inflamed dental pulp, stimulate nociceptor fibers and the
impulse is transmitted across the synapse in the caudate nucleus, the signal is further propogated
through the secondary neuron to the midbrain. In the region the secondary fibers terminate in the
vicinity of the thalamus. This section of the midbrain, the periaqueductal gray matter, is under
significant neurosecretory molecular influences and is involved in variety of emotions. Thus it is
interesting to speculate how some pain syndromes may be modified by the patient’s psychologic
and emotional status. From this area of the brain, tertiary and quaternary neurons synapse and
transmit the nerve impulse to the cerebral cortex. It is at this level that the patient actually becomes
conscious of the pain symptom.
Nociceptor fibers are stimulated by a variety of physical and chemical stimuli. During an
infection or in face of trauma, the tissues release noxious chemicals, including both peptides and
lipids. In acute inflammation the pH often drops below 5, and it is well documented that both acidic
and alkaline solution stimulates firing of nocicepter fibers. Excessive heat, such as that from an
electrical burn or thermal injury, also stimulates nociceptor fibers. In the context of the
inflammatory reaction, kinins and prostaglandins, small vasoactive molecules, also have strong
nociceptor-stimulating effects. Acute compressive forces on nerve endings may also produce pain,
and this compression may be the result of cellular infiltrates into tissues and edema formation. As a
rule the patient is able to localize the specific region of pain where the tissue harbors the pathologic
process that has endangered the pain sensation. As clinician are well aware, severe may not always
be readily localized. The neuroanatomic basis for the inability to specifically localize severe pain is
not well understood. Eventually within several hours to several days, the pain becomes more
precisely localized.
Pathologic processes, such as acute infections or acute trauma, often precipitate complaints
of sharp, short- duration pain. Alternatively, low-grade or chronic inflammatory conditions are
frequently expressed as dull pain of longer duration. In addition, pain disorders that fail to show any
organic basis commonly surface as aching, chronic pains of longer duration. Therefore pain
symptoms must be precisely characterized before the clinician can arrive at a definitive diagnosis.
However, the clinician is often confronted with varied, multiple complaints for which more than one
diagnosis must be considered. This chapter will consider the facial pain disorders according to the
type of pain symptoms that the patient describes, thus constructing differential diagnoses for
specific types of complaints.
Pain may be classified as either typical (i.e., of expected character and duration) or atypical
(i.e. of unexpected character and often more chronic duration). Typical, acute pains are of shorter
duration, lasting seconds, minutes, hours, or even months depending on underling problem.
However, atypical, chronic pains arte of longer duration and may lasts from months to years, and
pain may be constant or intermittent. Some acute pains are singular in nature and nonrecurrent,
whereas other complaints are characterized by multiple occurrences. With chronic pain, the pain
experience frequently fluctuates, last beyond normal healing periods, and does not fit expected pain
patterns. Some patients may complain of chronic pain that begins as a mere nuisance in the morning
but builds to a more severe ache in the late afternoon.
Identification of precipitating, perpetuating, aggravating, or relieving factors is diagnostically
important. Sometimes gravity influences the severity of pain; simply by placing the head bellow the
knees, the patient may experience an exacerbation of pain. Exposure of tooth surfaces to both heat
18

19. and cold is well –recognized precipitating factors for pulpal pain. However, patient may relate
exacerbation of pain to emotional stress, jaw clenching, turning the head from left to right, or they
may note an increase in severity during mealtimes. Therefore is important to explore any factor that
could precipitate, perpetuate, aggravate or relieve symptoms and to evaluate these factors in the
context of the differential diagnosis.
Although most pain localized to teeth or jaw bones is odontogenic, anatomic considerations
are also important in the differential diagnosis of orofacial pains. The anatomic sites that must be
evaluated in patients who complain of pain that does not appear to be of an odontogenic origin
include the following:
Periodontium (periodontalgia)
Masticatory musculature (myaliga)
Jaw joints (arthralgia)
Salivary glands
Sinus linings
Middle ear(otalgia)
Pain disorders that mimic odontalgia:
The pain mimicking dental problems can be separated into two major categories:
 Typical pain disorders: those in which pathogenesis is known.
 Atypical pain disorders: have no established etiopathogenesis.
Differentiating typical and atypical orofacial pains that mimic odontalgia:
Condition Nature Triggers Duration
Odontalgia Stabbing, throbbing, nonepisodic Hot, cold, tooth percussion Hours,
days
Periodontalgia Deep aching, throbbing,
nonepisodic
Occlusion, percussion Hours,
days
Trigeminal
neuralgia
Lancinating, electrical, episodic 1mm to 2mm locus on skin or
mucosa, light touch triggers
pain
Seconds
Postherpetic Deep boring ache with burning
neuralgia
Spontaneous after facial
shingles
Weeks,
years
Cluster
headache
Severe ache, retroorbital
component, episodic
REM sleep, alcohol Minutes
Temporal
arterities
Trobbing, aching, erythema of
skin
Spontaneous Hours
Otitis media Severe ache, trobbing, deep to ear
nonepisodic, barometric pressure
Lowering head Hours days
Bacterial
sinusitis
Severe ache, trobbing in multiple
posterior maxillary teeth,
nonepisodic
Lowing head, tooth percussion Hours,
days
Allergic
sinusitis
Dull ache malar area, multiple
posterior maxillay teeth, seasonal
Lowering head Weeks,
months
Cardiogenic Short- lived ache in left posterior
mandible, episodic
Exertion Minutes
19

20. Sialolithiasis Sharp, drawing, salivary swelling,
episodic
Eating induced
salivation
Mintues
TMJ internal Dull ache, sharp episodes, derangments Opening chewing Weeks, years
Myalgia Dull ache, degree varies Stress clenching Weeks, years
Neoplastic Variable, motor deficit, paresthesia facial
pain
Spotaneous Days, months
Atypical
pain
Variable syndromes Nonspecific Seconds,
years
20

21. PHYSIOLOGY OF PULPAL PAIN
Hyperalgia and Allodynia:
Three characteristic define hyperalgia:
(1) spontaneous pain,
(2) a decreased pain threshold (i.e., allodynia), and
(3) An increased response to pain 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 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 increase sensitivity to the point where the arterial pressure wave of the
heartbeat stimulates the 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
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.
Inflammatory cycle:
To set the stage for repair of inflamed tissues, activated pulpal defenses must be able to
remove irritants hemodynamically and moderate the inflammatory process. Ideally the
inflammatory cycles of vascular stasis, capillary permeability, and chemotactic migration of
leucocytes to injured tissues are synchronized with the removal of irritants and drainage of exudate
from the area. With moderate to severe injury, an aberrant increase in capillary pressure can lead to
excessive permeability and fluid accumulation. A progressive pressure front builds and begins to
passively compress and collapse all local venules and lymphatic channels, outpacing the capacity of
the pulp to drain or shunt the exudates. Blood flow to the area ceases, and the injured tissue
undergoes necrosis. Leucocytes in the area degenerate and release intracellular lysosomal enzymes,
forming a microabscess.
Inflammatory mediators:
Inflammatory mediators, such as histamine, bradykinin, prostaglandin, serotonin, substance
P, CGRP and leukotrienes, can cause pain directly by activating or sensitizing pulpal nociceptors.
They also cause pain indirectly by initiating series of inflammatory events that result in increase in
vascular permeability, edema, and ultimately increased intrapulpal pressure. The renewed presence
of mediators sustains the inflammatory process beyond the initial traumatic event. Fluid leakage
diminishes blood flow and results in vascular stasis. Platelets aggregated in the vessels release the
neurochemical serotonin, which is leaked along with plasma, into the interstitial tissues. Serotonin
and other inflammatory mediators induce a state of hyperalgesia in the pulpal nociceptors.
The altered tissue conditions sensitize acute nociceptive activity and then activate initially
silent polymodal nociceptors. Nerve fibers that are activated by inflammation are termed silent or
21

22. sleeping, nociceptors. Acute nociceptors respond as soon as a stimulus reaches threshold levels,
whereas silent nociceptors are not activated until inflammation has been established. Inflammatory
mediators sensitize both types of nociceptors. When the dental pulp become inflamed, there is
significantly higher proportion of A-delta fibers responding to dentinal stimulation than in
uninflammed pulp. Additionally the respective field (i.e. the size of the area where a stimulus
activates a nerve fiber) becomes larger in inflamed pulps. This may be because of nerve sprouting or
activation, or it may be because of sensitization of silent nociceptors. When tissue becomes
inflamed, the polymodal nociceptive fibers initiate and enhance this process by neurogenic
inflammation. Substance P and calcitonin gene-related peptide (CGRP) can each contribute to the
inflammatory process, and research has shown that their vascular responses are potentiated with
coadministration. At the local level, neuropeptides stimulate the release of histamine, which refuels
the vascular inflammatory cycle. The sustained inflammatory cycle is detrimental in pulpal
recovery, terminating in the necrosis of the tissues.
ODONTOGENIC PAIN
I] Clinical characteristic of pain
1. Clinical characteristic of pulpal pain:
 The quality of the pain is dull, aching, throbbing, and occasionally sharp. The pain
quality varies according to status of the pulpal tissues (vital or nonvital).
 There is an identifiable condition that reasonably explains the symptoms (caries,
fracture, deep restoration).
 The response to local noxious stimulation is of threshold nature.
 Because pulpal pain is inflammatory, it tends to get better or worse but rarely stays the
over time.
 Local anesthesia of the affected tooth eliminates the pain.
2. Clinical characteristics of periodontal pain:
 The quality of the pain is dull, aching, or throbbing.
 There is an identifiable periodontal condition that reasonably explains the symptoms
(periodontal pockets abscess).
22

23.  The response to local mechanical pressure is proportionate to the amount of force
applied, rather than a threshold response as with pulpal pain.
 Under the load of occlusal pressure during chewing, the tooth feels sore or elongated.
Discomfort is often felt when biting pressure is released rather than while it is sustained.
 Local anesthesia of the affected periodontal tissue eliminates the pain.
Healthy pulp:
The healthy pulp is vital and free of inflammation. It is vital and free of inflammation. It is
stimulated by cold and hot sensitivity testing, responding with mild pain that lasts for no more than
1 to 2 seconds after the stimulus is removed. Mainly, myelinated (A-delta) and unmyelinated (C
fibers) afferent nerve fibers control the sensibility of the dental pulp. Operating under different
pathophysiologic capabilities, both sensory nerve fibers conduct nociceptive input to the brain.
Differences between the two sensory fibers enable the patient to discriminate and characterize the
quality, intensity, and duration of the pain response.
Normally dentin is sensitive to when exposed to irritants. The clinical symptoms of A-delta
fiber pain serve to signify that the pulpodentinal complex is intact and capable of responding to an
external disturbance. This is normal response of vital pulp. Many dentists have made the mistake of
interpreting this symptom of dentinal pain as an indication of reversible pulpitis. However, they are
not mutually exclusive. Thus dentinal sensitivity or pain should be distinguished from pulpal
inflammation.
Dentinal hypersensitivity:
The term dentin hypersensitivity has been used to describe a specific condition that is defined
as ‘pain arising from exposed dentin’. Typical this pain is in response to thermal, chemical, tactile,
or osmotic stimuli and is not caused by any other dental defect or pathology. The pain is consistent
with an exaggerated response of the normal pulpodentinal complex, and it is serve and sharp on
application of the stimulus to the exposed dentin. However, there is no lingering discomfort once
the stimulus is removed.
Dentin hypersensitivity is probably a symptom complex, rather than a true disease; it results
from stimulus transmission across exposed dentin. Although the precise mechanisms for dentin
sensitivity are not known, the hydrodynamic mechanism, as postulated by Brannstrom, is the theory
that is most commonly cited. In this mechanism sudden movements of fluid in the dentinal tubules
are believed to deform mechanosensitive nerve fiber at the pulp-dentin interface.
Scanning electron microscopic studies show that hypersensitive dentin has more than seven
times the number of surface tubules than insensitive dentin. Although dentinal tubules of insensitive
teeth are occluded, the apertures of the dentinal tubules in hypersensitive dentin are open, or widen.
Dye penetration studies indicate that the open tubules are patent to the pulp, and as a result, bacteria
or their toxic products can penetrate the dentin, causing inflammation.
When symptoms are associated with exposed dentin, the diagnosis is dentin hypersensitivity.
However when there is a specific etiologic factor causing the sensitivity, such as caries, fractures,
leaking restorations, or recent restorative treatment, teeth with vital pulps may exhibit symptoms
that are identical to dentin hypersensitivity. When symptoms develop in these situations, a diagnosis
of reversible pulpitis is appropriate.
Reversible pulpitis:
23

24. An external irritant of significant magnitude or duration injures the pulp. Although a
localized injury initiates tissue inflammation, the nature and extend of pulp injury and the dynamics
of the inflammatory response will determine whether the process can be confined and the tissue
repaired to restore pulpal homeostasis. Reversible pulpitis implies that from the clinical signs,
symptoms, and diagnostic tests, the pulp is vital and inflamed but posses the repairative capacities to
return to health on removal of irritant.
Pulpal pain is common after restorative treatment. Procedure such as cavity and crown
preparations can make teeth feel especially sensitive. Damage to the pulp is caused by heat
generation, pressure, and dentin desiccation, toxic component of the restorative material and
restorative materials, and especially marginal leakage of bacterial colonization of the dentin-
restorative interface. Often the histologic response to caries or restoration is chronic inflammation.
When a new operative procedure is performed on such teeth, the ensuing pain is in most cases,
related to an acute exacerbation of a previously existing, asymptomatic chronic pulpitis.
Irriversible pulpitis:
The pulp is enclosed in a rigid, mineralized environment and has a very limited ability to
increase its volume during episodes of inflammation. In this low compliance environment, an
intense inflammatory response can lead to adverse increases in tissue pressure, outpacing the pulps
compensatory mechanisms to reduce it. The inflammatory process spreads circumferentially and
increamentally through the pulp, perpetuating the destructive cycle.
With provocation, an injured vital pulp with established local inflammation, the response is
exaggerated and out of character with the challenging stimulus, which is often thermal.
Inflammatory mediators induce this type of hyperalgesia, and one of the classic symptoms of
irreversible pulpitis is lingering pain through thermal stimuli. As the exaggerated A-delta fiber pain
subsides, a dull, throbbing ache may persist. This second pain symptom signifies the inflammatory
of nociceptive C nerve fibers.
With increasing inflammation of pulp tissues, C fiber pain becomes the only pain feature.
Pain that may begin as a short, lingering discomfort can escalate to an intensely prolonged episode
or a constant, diffuse, throbbing pain. Spontaneous pain is another hallmark of irreversible pulpitis.
If the pulpal pain is prolonged and intense, central excitatory effects may produce pain referral to
distant site or to other teeth. When C fiber pain dominates A-delta fiber pain, pain is more diffuse
and dentist’s ability to identifying the offending tooth, through provocation is reduced. Often
clinician may have found that pulp afflicted with irreversible pulpitis without periradicular pathosis
are the most difficult to diagnose. If the periradicular proprioceptive nerve fibers are not inflamed,
then the tooth will not be tender to percussion and the symptoms may difficult to localize.
C fiber pain is an ominous symptom that signifies that irreversible local tissue damage has
occurred. Irreversible pulpitis is clinical term that implies that the inflamed, vital pulp lacks the
reparative ability to return to health.
Pulpal necrosis:
There are no true symptoms of pulpal necrosis, because sensory nerves have been destroyed.
However, pain may arise from the periradicular tissues that may be inflamed because of pulpal
degeneration. Necrosis may be complete or partial, in which case various symptoms are present.
This can be confusing, because of the presence of some remaining vital tissue in apportion of the
root canal system. This condition is most common in multirooted teeth. In most case there is no
response to thermal or electric pulp sensitivity testing, however vital response is sometimes
encountered.
Acute apical periodontitis:
24

25. In most cases, acute apical periodontitis arises as a sequel to irreversible pulpitis, or it arises
after endodontic treatment. The inflammatory process leading to irreversible pulpitis may extend in
the periradicular tissues, resulting in localized inflammation of the periodontal ligament. When the
transition of the pulpal inflammation to periradicular inflammation is rapid, the patients’ pain
experience is severe because of the simultaneous occurrence of the irreversible pulpitis, and the
tooth is extremely painful to touch, with a dull, constant, throbbing pain. Often the cause of acute
apical periodontitis is obvious, and the symptoms are readily explained.
In most cases postoperative pain following endodontic treatment is caused by acute apical
periodontitis. Root canal instrumentation, beyond the apex or extrusion of debris from the root into
the periodontal tissues, can produce an acute apical inflammatory reaction. In this situation the
clinical differentiation between an acute apical periodontitis and a developing acute periradicular
abscess is difficult.
Acute periradicular abscess:
Extention of pulpal disease into the surrounding periapical tissues may result in periapical
infection. The acute periradicular abscess is an inflammatory reaction to pulpal infection and
necrosis, characterized by rapid onset, spontaneous pain, and tenderness of tooth to pressure, pus
formation and eventual swelling of associated tissues. The abscess may develop from a pulp that
undergoes rapid degeneration from pulpitis to necrosis with spread of infection into periradicular
tissues. Alternatively it may arise as an exacerbation of the chronic apical periodontitis (i.e. phoenix
abscess). Although the pulp is necrotic and not sensitive to thermal testing, the initial pain from an
acute radicular abscess can be intense. As bone resorption occurs, purulent drainage into the
surrounding tissue spaces and swelling occurs. However an intrabony pressure is reduced, the pain
may subside slightly.
If the swelling associated with an acute periradicularabscess begins to drain through an
intraoral or an extraoral sinus tract, the painful symptoms will diminish as the pus discharges. Thus
the acute periradicuilar abscess may subside into a suppurating chronic apical periodontitis.
Periodontal abscess:
The acute periodontal abscess is an inflammatory reaction originating in the periodontium. It
is usually characterized by rapid onset, spontaneous tenderness of the tooth to pressure, pus
formation, and swelling. Frequently it is caused body entrapment and associated with a tooth with
vital pulp. The abscess develops from an infection from an infection of an existing periodontal
pocket, or it develops as an apical extension of infection from a gingiva pocket. The pain of a
periodontal abscess is similar in nature to that of acute periodontal abscess. However it is often not
as severe. A deep periodontal pocket is always associated with the tooth, and localized swelling is
often present.
Referred pain:
Pain may be referred from teeth to other orofacial structures, or it may be referred from
distant anatomic sites to teeth. Acute odontogenic pain often has a component that is felt in one or
more adjacent teeth, of the same arch, in teeth of the opposite arch, or in both locations. Clinically,
it is rare for pain from pulpally involved teeth to be referred across the midline, except when the site
of primary a primary pain is located close to the midline. Referred odontogenic a pain is most
commonly associated with irreversible pulpitis, and it is frequently felt as a headache. The variable,
spontaneous, unlocalized and pulsatile qualities of the pain associated with irreversible pulpitis,
together with its referral patterns, can intimate almost every pain disorder of the face and head.
25

26. CONTROL AND MANAGEMENT OF PAIN IN DENTISTRY
Pain can be modified by cognitive, emotional and symbolic factors, all of which are
interrelated. Management of pain therefore requires more than providing things that can be
swallowed, injected or inhaled. It also demands the modification of the pain experience through an
understanding of the individual patient and his or her psychology. While some management
suggestions have been incorporated throughout, what follows a few general principles may be
useful.
Management Principles:
1. Each patient should be attended to as an individual.
2. Give patients an accurate description of what will be experienced during a procedure.
3. Give patients a feeling of some control.
4. Try to establish a relaxed environment.
5. Pay attention to the patient.
26

27. MANAGEMENT OF PAIN
Management of acute pain based on knowledge of peripheral and central mechanisms pain
involves a three-pronged approach: inhibition of biochemical processes signaling tissue injury,
blockage of nociceptive impulses in the peripheral nerves, and activation of opoid analgesic
mechanisms in the CNS. Each of these approaches can be simultaneously employed to result in
additive analgesia with the potential for increased side effects. To minimize the perception of pain
and the experience of side effects, a flexible prescription strategy is required, which begins with the
single drug entity.
Management of mild pain:
Oral administration of 650 mg of aspirin or 200 mg of every 4 hours as needed is more than
adequate for the management of mild pain chrematistic of most dental therapy, or a previously
asymptomatic tooth or periodontal scaling should be responsive to aspirin or ibuprofen at these
doses with a minimal potential for side effect. For patients for whom the use of aspirin–like drugs is
contraindicated, oral administration of 600 to 1000 mg acetaminophen should provide comparable
analgesic effect.
Management of moderate pain:
Pain that is unrelieved by this treatment or is sufficiently traumatic to predict the likelihood
of moderate pain, can usually be managed with 400 to 600 mg of ibuprofen every 4 to 6 hours.
Preoperative administration of ibuprofen combined with postoperative administration has proved
effectively to delay the onset of postoperative pain and lessen its severity when it does occur. Such
prophylactic treatment can provide a relatively pain-free period following the dental procedure and
possibly obtund postoperative swelling associated with surgical procedures. Failure to obtain
adequate relief with ibuprofen alone may require the addition of 60 to 90 mg codeine but with a
predictable increase in opoid side effects. Patient must be explicitly instructed in order to ensure
compliance and monitored to balance relief of pain against side-effect liability.
Acetaminophen, combined with either 60 mg codrinr or 5mg of oxycodone, should provide
somewhat comparable analgesic effect in aspirin-intolerant patient but at the expense of opoid side
effects in a substantial number of patients.
Management of severe pain:
The onset of severe pain following a particular traumatic dental procedure surgical removal
of bony impactions, osseous periodontal surgery) can be etidocaine, in combination with an NSAID.
Subsequent postoperative pain following offset of anesthesia that is not relieved by the NSAID
alone can be managed with a combination of an NSAID and 10 mg oxycodone but, again, with a
substantial incidence of opoid side effects.
Pain that is not adequately managed by these combinations should the need to re-evaluate
possible etiological factors. Pain secondary to infection requires drainage and antibiotic therapy as a
primary mode of therapy and adjunctive analgesic therapy. Pain that continues beyond the normal
time course of the inflammatory process may reflect deficits in healing such as alveolar osteitis,
damage to associated structures such as peripheral nerve or to maxillary sinus, or an acute
manifestation of a pre-existing chronic pain syndrome.
27

28. Basis for selecting rational analgesic treatment:
the selection of appropriate analgesic therapy should be based on the results of scientifically
controlled clinical trials using dental outpatients. A large body of adata that has appeared in the
dental literature in the past decade supports the use of NSAID as the agent of choice for moderate
pain with minimal potential for side effects. Additional literature supports the use of a long-acting
anesthetic in combination with NSAID pretreatment for preventing the onset and intensity of
postoperative pain. Owing to limited efficacy and substantial side effects, the use of oral opoids
should be limited to patients whose pain is unrelieved by nonopoid therapy. Other adjunctive agents
(barbiturates, caffeine, phenothiazines) provide little analgesic activity. In the absence of strong
scientific evidence that has yet to be demonstrated, combination analgesics containing these
adjunctive agents do not represent.
Pharmacotherapy:
I]. Non-steroidal Anti-inflammatory Drugs and Antipyretics-Analgesics (NSAIDs)
28

29. All drugs grouped in this class have analgesic, antipyretic and anti-inflammatory actions in
different measures. Compare to morphine they are weaker analgesics (except for inflammatory pain)
do not depress CNS, do not produce physical dependence and have no abuse liability. They are also
called non-narcotic, non-opoid or aspirin like analgesic. They act primarily on peripheral pain
mechanisms but also in CNS to raise pain threshold.
Classification:
Non-selective Cox inhibitors (Conventional NSAIDS)
1. Salicylates- Aspirin, Diflunisal
2. Pyrazolone derivatives- Phenyl butazone, Oxyphenbutazone
3. Indole derivatives- Indomethacin, Sulindac
4. Propionic acid derivatives-Ibuprofen, Naproxen, Ketoprofen, Flurbiprofen
5. Anthranilic acid derivatives- Mephenamic acid
6. Aryl –acetic acid derivatives- Diclofenac
7. Oxicam derivatives- Piroxicam, Tenoxicam
8. Pyrrolo -Pyrrolo derivatives- Ketorolac
Preferential COX-2 inhibitors- Nimesulide, Meloxicam, Nabumetone
C) Selective COX-2 inhibitors- Celecoxib, Rofecoxib, Valdecoxib
D) Analgesics – Antipyretics with poor anti–inflammatory action-
Para aminophenol derivatives - Paracetamol (Acetaminophen)
Pyrazolone derivatives - Metamizol (Dipyrone),
Benzoxacaine derivatives - Nefopam.
Mechanism of Action:
Prostaglandins (PGs) induce hyperalgesia by affecting the transducing property of free nerve
endings; stimuli that normally do not elicit pain are able to do so. NSAID’s do not affect the
tenderness induced by direct application of PG’s but block the pain sensitizing mechanism induced
by bradykinin, TNF α, interleukins (ILs) and other algesic substances. They are therefore more
effective against inflammation associated pain.
Adverse effects of NSAIDs:
Gastrointestinal-
Gastric irritation, Erosions, Peptic ulceration, Gastric bleeding/perforation, esophagitis.
Renal-
Na+
& water retention, chronic renal failure, interstitial nephritis, papillary necrosis.
Hepatic-
Raised transaminases, hepatic failure (rare).
CNS-
Headache, mental confusion, behavioural disturbance, seizure precipitation.
Haemotological-
Bleeding, thrombocytopenia, haemolytic anemia, agranulocytosis.
Others-
Asthma exacerbation, nasal polyposis, skin rashes, pruritus, angioedema.
II) Opoid Analgesics
The narcotic agents are those compounds related to opium which have a central action and an
abuse potential by virtue of addiction liability. Narcotics do not necessarily abolish pain but produce
29

30. relief by altering our reaction to it. The analgesic property of morphine can be summarized into
three distinct actions:-
Elevation of pain threshold.
Modifying the reaction to pain.
Induction of lethargy and sleep.
Classification:
1. Natural opium alkaloids - Morphine, Codeine
2. Semi synthetic opiates - Diacetylmorphine (Heroine), Pholcodeine
3. Synthetic Opoid - Pethidine, Fentanyl, Methadone,
Dextropropoxyphene, Tramadol, Ethoheptazine.
Mechanism of Actions:
The analgesic action of morphine has spinal and supraspinal components. It acts in the
substantia gelatinosa of dorsal horn to inhibit release of excitatory transmitters from primary
afferents carrying pain impulses. The action appears to be exerted through interneuron’s which are
involved in the ‘gating’ of pain impulses. Release of substance P from primary pain afferents in the
spinal cord and its post-synaptic action on dorsal horn neurons is inhibited by morphine. Action at
supraspinal sites in medulla, mid-brain, limbic and cortical areas may alter processing and
interpretation of pain impulses as well as send inhibitory impulses through descending pathways to
the spinal cord. Several aminergic and other neuronal systems appear to be involved in the action of
morphine and simultaneous action at spinal and supraspinal sites greatly amplifies the analgesic
action.
Adverse effects:
1. Respiratory depression
2. Blurring of vision
3. Urinary retention
4. Idiosyncrasy and Allergy
5. Apnoea
6. Acute morphine poisoning
7. Tolerance and dependence.
III) Tranquilizers:
Anxiety is an important factor in reducing pain tolerance or producing greater pain
Tranquilization diminish the patient’s fear and apprehension and produce some degree of cortical
depression of the CNS, ranging from mild sedation to sleep. Sedative–antianxiety (anxiolytic) is
prescribed more frequently for management of anxiety states. The most widely used class is the
benzodiazapenes (Diazepam, Oxazepam, Chlordiazepoxide, Lorazepam, and Alprazolam).
Mechanism of Action:
Benzodiazapenes (BZD) act by enhancing pre-synaptic post-synaptic inhibition through a
specific BZD receptor which is an integral part of the GABA-receptor-Cl-
-channel complex. BZDs
have only GABA facilitatory but not GABA mimetic action.
Adverse effects:
1. Dizziness and Vertigo
2. Ataxia
3. Impairment of psychomotor skill
4. Tolerance
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31. 5. Paradoxical stimulation
6. Irritability and sweating.
31