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 tissue3. Tissue from adjacent sites (e.g. sinus, eye, ear, nose, throat, cervical spine, brain,

heart)4. Neurologic system (e.g. peripheral, central)5. Psychologic system6. Vascular walls7. Musculoskeletal tissue (i.e. temporomandibular,cervical) and8. 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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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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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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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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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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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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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 Theory2. 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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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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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 sequence1. “First pain” pathway

a. Nociceptorb. Sensory nerve

c. T celld. Thalamus

e. Sensory cortexB. Paleospinothalamic system

1. “Second pain” pathwaya. Nociceptor

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b. Sensory nervec. Dorsal horn synapses

d. Surpaspinal networkinge. Sensory cortex

C. Sensory receptors1. Special

a. Sensesb. Balance

2. Viscerala. Hunger, nausea, distension

b. Visceral pain3. Superficial

a. Transmit sensationsb. Cutaneous

c. Three categories based on type of stimuli to which they respond4. Deep—tissue

a. Ligaments, muscles, and connective tissueb. 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 stimulated2. A-delta fibers—respond to noxious mechanical stimulation (i.e., pinching,

prickling, crushing)a. Small diameter; myelinated

b. Slower conduction velocity3. C fibers—originate at deep receptors (ligaments, muscles, connective tissues)

a. Smallest of the three; myelinatedb. Slowest conduction velocity; require greater stimulation

E. Ascending pathways1. 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 centers1. Third-order neurons in thalamus; sensory information continues to be

organized2. Thalamus relays sensory input to somatosensory cortex of the brain where

localization and discrimination of pain will occurG. Descending pathways

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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 modalitiesd. Reduction of stress

4. If not inhibited, affective-emotional pain response can be similar to shocka. “Windup” phenomenon—pain syndrome resulting when noxious

stimulation spirals out of controlb. Pain stimulation continues to flow to cognitive areas and perception of

pain is increased5. 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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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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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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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

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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.

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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

|

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↓ ↓

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.

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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

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 liningsMiddle 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 DurationOdontalgia Stabbing, throbbing, nonepisodic Hot, cold, tooth percussion Hours,

daysPeriodontalgia Deep aching, throbbing,

nonepisodicOcclusion, percussion Hours,

daysTrigeminal 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

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Sialolithiasis Sharp, drawing, salivary swelling, episodic

Eating induced salivation

Mintues

TMJ internal Dull ache, sharp episodes, derangments Opening chewing Weeks, yearsMyalgia Dull ache, degree varies Stress clenching Weeks, yearsNeoplastic Variable, motor deficit, paresthesia facial

painSpotaneous Days, months

Atypical pain

Variable syndromes Nonspecific Seconds, years

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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

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 pain1. 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).

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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:

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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

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.

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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.

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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.

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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)

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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, Diflunisal2. Pyrazolone derivatives- Phenyl butazone, Oxyphenbutazone3. Indole derivatives- Indomethacin, Sulindac4. Propionic acid derivatives-Ibuprofen, Naproxen, Ketoprofen, Flurbiprofen5. Anthranilic acid derivatives- Mephenamic acid6. Aryl –acetic acid derivatives- Diclofenac7. Oxicam derivatives- Piroxicam, Tenoxicam8. 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 AnalgesicsThe 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

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, Codeine2. Semi synthetic opiates - Diacetylmorphine (Heroine), Pholcodeine3. 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 depression2. Blurring of vision3. Urinary retention4. Idiosyncrasy and Allergy5. Apnoea6. Acute morphine poisoning7. 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 Vertigo2. Ataxia3. Impairment of psychomotor skill4. Tolerance

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5. Paradoxical stimulation6. Irritability and sweating.

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