Applied Oral Physiology

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Pain

Publisher Summary

Pain is a symptom in the completely subjective sense. It is a complex experience that includes a sensory-discriminatory component. Pain also includes the accompanying responses or reactions elicited by the stimulus. The ability to diagnose and treat a patient suffering from pain depends largely on an intimate knowledge of the mechanisms and behavioral characteristics of pain. Pain intensity may provide an index of the urgency of treatment rather than the severity of its cause. Pain intensity is directly correlated with duration; the higher the intensity, the shorter the period of tolerance. The level of suffering may increase with the duration of pain, even though the input intensity remains either the same or actually decreases. All pains, regardless of initial type or aetiology, appear to take on the clinical characteristics of psychogenic intensification with time. The sensory pain receptors serving nociception may be divided into three main groups: exteroceptors, interoceptors, and proprioceptors.

Introduction

What is pain?

Terms used to describe pain

Neural pain mechanisms

Pain receptors

Exteroceptors

Interoceptors

Proprioceptors

Free (unencapsulated) receptors

Central connections for pain

Chemical mediators (transmitters)

Bradykinin

Histamine

Prostaglandins

Serotonin

Substance P

Other agents

Mechanics of pain

Gate theory

Orofacial pain

Secondary effects of pain

Pain aetiology (causes) Inflammation

Muscle pain

Vascular pain

Neural pain

Other causes of pain

Categories of facial pain

Somatic pain

Neurogenous pain

Psychogenic pain

Odontogenic pain (toothache)

Pain control

Conclusions

Review questions

References

Introduction

Dentistry owes its very beginnings to the quest for pain relief, and the identification, diagnosis and early elimination of pain remain important foundations to the dental profession.

Pain is a symptom in the completely subjective sense. It is a complex experience that includes a sensory–discriminatory component. Pain also includes the accompanying responses or reactions elicited by the stimulus. For instance, some of the reactions to a noxious stimulus include pain, startled response, muscle reflex, vocalization, sweating, increase in heart rate, in addition to blood pressure and behavioural changes. Such reactions will in turn be modified by a number of factors, including the emotional status of the patient, past experience and memories of pain, magnitude of tissue damage or stimulus, other concomitant sensory experiences, ability to comprehend the causes (aetiology) and consequences (pathogenesis) of the pain, and ethnic group and culture. Thus pain is both complex and multidimensional, with the result that accurate diagnosis and appropriate treatment is often difficult.

What is pain?

Neuroscience is characterized by two major rules:

(1) The more sensory nerves that supply a region of the body, the more acute the sensibility in the area.

(2) The higher the ratio of motor nerves to muscles, the greater the possible control finesse.

On both accounts, the oral cavity and face exceed most other bodily regions. The number of patients who have orofacial discomfort and pain is therefore not surprising. Unlike other sensations, however, pain is an experience that cannot be shared: it is wholly personal, belonging to the sufferer alone. Different individuals therefore feel and react to pain and suffering in different ways. One person cannot possibly sense exactly the feelings of another. Patients in pain therefore require individualized treatment.

The ability to diagnose and treat a patient suffering from pain depends largely on an intimate knowledge of the mechanisms and behavioural characteristics of pain. But here there is a problem, since much of our knowledge concerning the physiology of pain is largely conjectural. Nevertheless, acute pains are generally associated with tissue damage or threat of damage. By contrast, chronic pains may persist for long periods of time, and are often associated with a variety of factors, including:

(1) Some definite past event (e.g. accident, infection).

(2) Some ongoing disease process (e.g. rheumatoid arthritis, temporomandibular dysfunction).

(3) An unknown cause in many cases.

In contrast to acute pain, chronic pain, characteristically, serves no useful purpose in providing a warning of impending pathology. Rather the severity of chronic pain is more of a measure of the suffering it induces rather than the actual perception of noxious stimulation. For instance, low intensity pain may result from very serious causes, whereas excruciating pain may arise from some imperceptible cause, e.g. tic douloureux. Pain intensity may, therefore, provide an index of the urgency of treatment rather than the severity of its cause. Pain intensity is, however, directly correlated with duration. The higher the intensity, the shorter the period of tolerance: low-intensity pain can be sustained for several hours, whereas maximum-intensity pain can be tolerated for only a few seconds. Also, the higher the intensity of a pain, the more likely is the pain to be intermittent. In fact, intractable pain may not be pain in the true sense of the word but simply an unpleasant or unwanted sensation.¹

The onset of pain may be described by different characteristics. For instance, spontaneous pain occurs without provocation, whereas some provocative factor can usually be identified with induced pain. Alternatively, a pain may be triggered out of proportion to the actual stimulus. A single painful experience may last either for a few seconds or many months, during which time the pain may recur with sufficient frequency to establish a temporal relationship. Pains of short duration, separated by wholly pain-free periods, are defined as intermittent; pains of longer duration, even though variable in intensity, are termed continuous. A painful episode that lasts for several days is described as protracted, whereas intractable pain signifies that the symptoms do not respond to therapy. Two or more similar painful episodes signify recurrent pain, with intermittent pain-free intervals being termed remissions. Periodic pain is characterized by regularly recurring episodes.

A steady pain describes an unpleasant sensation, whereas paroxysmal pain comprises a volley of jabs. Bright pain has a stimulating quality, whereas dull pain is depressing. Both may be punctuated by sharp or radiating exacerbations. Pain may also be described as a function of the area where the symptom is felt, i.e. localized, spreading, migrating of referred.

Terms used to describe pain

The characteristics of a pain are difficult to define, although an ‘ache’ is the term most frequently used. Other terms include:

(1) Burning pain: a connotation of warmth.

(2) Deep pain: from deep visceral or somatic structures, with the symptoms being generally diffuse, often associated with symptom referral to other regions and/or muscle spasms.

(3) Itch: a subthreshold pain, which may have a warm or burning quality, but may become intractable.

(4) Pricking pain: a sharp intermittent character of short duration.

(5) Stinging pain: a more or less continuous high-intensity characteristic.

(6) Superficial pain: usually precisely localizable to a superficial lesion, with the timing, location and intensity of symptoms often being accurately described by the patient.

(7) Throbbing or pulsatile pain: an intermittent quality coincident with cardiac systoles.

(8) Tickle: a sensation induced by light superficial movement.

The level of suffering may increase with the duration of pain, even though the input intensity remains either the same or actually decreases. All pains, regardless of initial type or aetiology, appear to take on the clinical characteristics of psychogenic intensification with time, e.g. chronic orofacial pain syndromes are ultimately associated with chronic depression.

Somatic pain often reflects a pathological lesion in a specific organ or tissue, whereas neurogenous pain may indicate a disease process affecting a particular nerve fibre. The site where pain is felt, however, may or may not identify the location of the pain source. A primary nociceptive input characterizes pain emanating from the structures that hurt, whereas secondary pain may comprise pain felt some distance from the actual lesion, e.g. deep somatic pain input. All deep somatic pains are not alike, however, in that pain emanating from bones, joints, ligaments, muscles, soft connective tissues and tendons may be closely related to biomechanical functional demands. By contrast, high-threshold receptors innervate visceral structures so that pain is not usually felt until a certain threshold level is reached. Tissue injury (and healing) is generally associated with an inflammatory reaction that includes pain, although the symptoms depend on the location, type and phase of the inflammatory process. Most pains result from stimulation of nerves that innervate the site although some pains occur spontaneously apparently without stimulation. Pain is therefore a complex series of phenomena that may be described as unpleasant emotional and sensory experiences, associated with either actual or potential tissue damage or described in terms of such tissue damage.

Neural pain mechanisms

Classically, pain was considered a specific sensation with its own anatomically distinct receptors, primary afferent fibres, nerve tracts, relay systems and cortical reception areas. This theory contended that only free unmyelinated nerve endings in the orofacial area were activated by noxious stimuli. More recently, the anatomical specificity of receptors. has been discarded, as most receptors, if sufficiently stimulated, can respond to noxious irritation.

An alternative theory postulates that pain does not depend on specific pathways but on excessive stimulation involving all types of receptors, with the resultant central neural summation and/or convergence of activity. This summation theory was subsequently replaced by the pattern theory whereby the pattern of neural impulses set up by the noxious stimuli were considered important. Another theory (sensory interaction theory) contended that pain resulted from the interaction of both nociceptive and non-nociceptive afferent fibres on central neurones, the resulting excitatory or inhibitory interactions determining whether or not pain was perceived. Such a plethora of theories serves to emphasize the complexity of the neuronal components of pain sensation.

In fact, the central and peripheral mechanisms for pain (nociception) are both extremely complex and only partially understood. In fact, approximately 50% of sensory fibres and up to 20% of the spinal motor roots can transmit pain. Also, most pain receptors are poly- rather than unimodal. There is no central pain centre in the central nervous system analogous to the respiratory or vasomotor centres. This adds to the complexity of the nervous pathways serving pain.

The sensory (pain) receptors serving nociception may be divided into three main groups, although there is a considerable degree of functional overlap.

Pain receptors

Exteroceptors

These receptors are stimulated by the immediate external environment, with most of the impulses being sensed at conscious levels. Such receptors include:

(1) Free nerve endings: tactile and superficial pain.

(2) Krause’s corpuscles: cold receptors.

(3) Meissner’s corpuscles: tactile skin receptors.

(4) Merkels corpuscles: tactile receptors in the oral mucosa and submucosa of the tongue.

(5) Ruffini’s corpuscles: pressure and warmth receptors.

Interoceptors

Located in the body cavities, these serve involuntary bodily functions below conscious levels. These receptors include:

(1) Free nerve endings: perception of visceral pain and other sensations.

(2) Pacinian corpuscles: perception of pressure.

Proprioceptors

These receptors are chiefly involved in automatic functioning, and perceive movement, pressure and position. They include:

(1) Free nerve endings: perception of deep somatic pain and other sensations.

(2) Golgi tendon organs: mechanoreceptors in muscle tendons relaying data concerning muscle length and tension.

(3) Muscle spindles: mechanoreceptors between muscle fibres responsive to passive muscle stretch.

(4) Pacinian corpuscles: perception of pressure.

(5) Periodontal receptors: perception of tooth movement.

Free (unencapsulated) receptors

Free unencapsulated nerve endings are therefore the predominant form of nociceptor, especially in the cutaneous tissues, oral mucosa and periodontal tissues. But although these free nerve endings are associated with pain sensation, similar responses can also be elicited from other specialized nerve endings.

Central connections for pain

Oral or facial pain sensation is mediated centrally by afferent primary neurones that pass through the following:

(1) The posterior roots of the Vth (trigeminal), VIIth (facial), IXth (glossopharyngeal) and Xth (vagus) cranial nerves.

(2) The first, second and third cervical spinal nerves.

(3) The visceral afferents that descend through the cervical sympathetic chain to pass through the posterior roots of the upper thoracic spinal nerves.

The nerve cell bodies of the primary sensory neurones are located in the posterior root ganglion of the respective nerves through which they pass (with the exception of the proprioceptive fibres of the trigeminal, which are located in the mesencephalic nucleus in the midbrain).²

Subsequently, the pain fibres from the maxillofacial region terminate in the nucleus caudalis. This is the lower portion of the trigeminal spinal-tract nucleus.

The second order trigeminal neurones begin in the substantia gelatinosa of the nucleus caudalis and project to the thalamus. Third order neurones then project from the thalamus to the cerebral cortex. During this transition from first to second and from second to third-order neurones, considerable neural convergence occurs.

During the transmission of nerve impulses through these tracts, however, they are subjected to numerous inhibitory and facilitatory impulses from the higher cerebral centres. This is illustrated by the fact that the general intensity of suffering relates to a number of factors, including attention, attitude, preconditioning experience and temperament, all of which exert presynaptic inhibitory influences on the painful stimuli reaching the nucleus caudalis.³ Thus, pain transmission from the face and mouth is not just a simple neural pathway: a variety of intermediate influences may be exerted on the neural transmission. Such a modulating system may involve the following:

(1) A change in the character of the evoked discharge.

(2) Alteration of the modalities to which the neurone responds.

(3) Alteration of the characteristics of its receptive field.⁴

There appears to be a general relationship between nerve fibre diameter and conduction velocity:⁵ large fibres conduct impulses more rapidly than small ones. There also appears to be some relationship between fibre size and the type of impulse transmitted, in that Aδ and C fibres appear to convey pain impulses, in addition to other sensory modalities, whereas the fast conducting Aα, β and γ fibres primarily convey tactile and propioceptive impulses but not pain. Aδ fibres also conduct warmth, touch and cold, whereas C fibres conduct itch, warmth and cold.⁶ It seems therefore that the larger peripheral nerve fibres have functional specificity that excludes pain, whereas pain sensations are predominantly carried by small fibres in addition to other sensations.⁷

Sensory information may be rapidly conducted to the CNS by transmission of nerve impulses, or more slowly by means of neurochemical substances passing through the axonal transport system.⁸ Nociceptive neurones range from high-threshold mechanosensitive and mechanothermoreceptive afferents to slowly adapting low-threshold polymodal afferents. Although a significant proportion of afferent fibres enter the central nervous system via the dorsal root ganglion and brain stem, a number also travel in the ventral root. For instance, approximately 20% of the fibres in the motor root of the trigeminal may be sensory and related to nociception.⁴

Chemical mediators (transmitters)

A number of biochemical factors are also associated with the transmission of pain, some act as algogenic agents, some as neurotransmitters and some in both capacities.

Bradykinin

Bradykinin is an endogenous polypeptide released from the inflammatory reaction or from ischaemic tissues. This serves as a powerful vasodilator in addition to increasing vascular permeability. Bradykinin also excites all types of receptors, sensitizing some high-threshold receptors to respond to otherwise innocuous stimuli.⁹ Bradykinin acts only in the presence of prostaglandins.¹⁰

Histamine

Histamine is a vasoactive amine that not only acts as a vasodilator but also increases small vessel permeability. Conceivably, histamine also functions as a central nervous system neurotransmitter.

Prostaglandins

Prostaglandins sensitize nociceptors to different types of stimuli, thus lowering their pain thresholds to all types of stimulation.¹¹ Prostaglandins are also required for the action of bradykinin;¹⁰ bradykinin also stimulates the release of prostaglandins.¹² In addition, prostaglandin E increases the response of slowly adapting Aδ mechanoreceptors to non-noxious stimuli.¹³

Serotonin

Peripherally, serotonin is associated with vascular pain syndromes as an algogenic agent.¹⁴ Centrally this monoamine appears to be an important endogenous antinociceptive mechanism.¹⁵

Substance P

This polypeptide acts centrally as an excitatory neurotransmitter for nociceptive impulses.¹⁶ It is also released from spinal cord cells by Aδ and C fibre afferent stimulation and excites dorsal horn neurones that are activated by noxious stimuli.¹⁷ Substance P modulating action on pain is both rapid and short-lived.¹⁸

Other agents

Acetylcholine⁴, potassium¹⁹ and a variety of endogenous toxic substances²⁰ serve as algogenic agents.

Mechanics of pain

At one time pain was considered to be evoked by noxious stimulation of neural structures, with the pain reaction involving a cerebral level modified by prior conditioning, memory, emotional response and evaluative significance of the pain. Pain is now considered to be a much more complex process, with neural impulses being altered, changed and modulated on passing to the higher centres, in addition to being affected by excitatory and inhibitory influences.

Gate theory

The gate control theory of pain is still the most accepted mechanistic theory of pain. It was devised by Melzack and Wall.²¹–²³ It proposed that noxious stimulation of the substantia gelantinosa functions as a gate control system that modulates the afferent patterns before they influence the transmission cells. The afferent patterns in the dorsal column system therefore function in part as a control trigger which activates selective brain processes that influence the modulating properties of the gate control system. The transmission cells activate neural mechanisms that comprise the action system responsible for response and perception.

On noxious stimulation of the skin, impulses are transmitted centrally by both large Aδ and small C fibres. The nerve impulses passing in the large Aδ fibres arrive at the substantia gelatinosa before those transmitted by the C fibres. These latter activate the transmission cells initially, in addition to activating a negative feedback mechanism which reduces their effect on the transmission cells. Nerve impulses in small C fibres therefore activate a positive feedback mechanism, which exaggerates the effect of impulses arriving on the transmission cells. Large-fibre impulses therefore close the gate, whereas small-fibre impulses open the gate.

Continuous ongoing bombardment by afferent nerve impulses by C fibres serves to hold the gate in a relatively open position, i.e. pre-sets the gate before the arrival of noxious stimulation. This is a critical part of the gate control theory. If this activity is accentuated by inflammation or hyperaemia, the stimulus will stimulate the transmission cells more effectively. It will also be perceived as pain.

On noxious stimulation, the activity of the large fibres increases disproportionately to that of the small fibres, and the stimulus is received as pain. Large-fibre activity also partially closes the synaptic gate, thus shortening the transmission cell barrage. The perception of, and the reaction to, the noxious stimulus are thereby shortened and reduced, as the stimulus disproportionately affects the large fibres. Thus the synaptic gate, which permits the nerve impulses of the primary afferent neurones to fire the secondary transmission cells, is affected or reset by the noxious stimulus itself. With stimulation, more receptor fibre units will be recruited. This results in both counteractive positive and negative effects, and the transmission cell output slowly rises. Thus as the noxious stimulus is increased, pain perception and reaction slowly increase, although other factors modulate the response, i.e. the response is not necessarily proportionate to its cause. If the stimulation is prolonged, the large fibres begin to adapt, decreasing large-fibre activity. This will result in a shift in the balance in favour of small fibre activity, allowing the gate to open more widely. Thus, even though the intensity of the noxious stimulus may not increase, the fact that it is continuous tends to gradually increase the perception of the reaction to the stimulus. In effect, the duration of pain normally increases its intensity.

Large-fibre activity therefore modifies the degree of gate opening. Decreased large-fibre activity will result in gate opening, whereas there will be increased pain perception if there is disproportionate small-fibre activity. A critical level of gate activity is therefore set by the large-fibres. When this critical level is set high, pain is not perceived until the firing level is reached, causing a delay between stimulus and perception, termed temporal summation. After reaching this critical firing level, a transmission cell barrage may occur explosively, causing pain that is wholly disproportionate to stimulus intensity. This is termed spatial summation. Deficient large-fibre activity may therefore elevate the critical firing level of the gate control system reflected by summation effects. Deficiency in large-fibre activity may also result in the gate being opened, with the effect that lower-intensity stimulation is perceived as pain. Gate-setting and critical firing levels are therefore different facets of the pain mechanism, even though both affect the gate control system. Presetting of the gate is also determined by higher central nervous system centres, as illustrated by the following:

(1) Past experience.

(2) Conditioning.

(3) Attention directed to suffering.

(4) The emotional status of the individual at a given time.

Such inputs may individually or collectively serve to modulate the gate. When the gate is open, the patient will not only suffer more from the same noxious stimulus but may also perceive as pain stimuli those that normally should not be painful. A calm, placid and emotionally well-adjusted individual perceives and reacts to pain differently from a distraught, anxious, emotional patient.

Presetting of the gate is also dependent on the stimulus. When stimulation occurs, certain extremely fast-conducting fibres bypass the substantia gelantinosa to synapse first in the thalamus and then to the sensory cortex. These very rapidly transmitted impulses convey data concerning the location and nature of the noxious stimulus before the same stimulus reaches the synaptic gate. Such very rapid impulses have two effects:

(1) Setting the receptivity of cortical neurones for the subsequent afferent impulse volley from the transmission cells fired from the gate control system.

(2) Resetting the gate itself by nerve impulses transmitted by descending efferent fibres from the higher cortical centres to the gate control mechanism.

There may therefore be central modulation of the gate before the noxious impulses have had time to reach the gate. If such central inhibitory feedback control on the gate is total, no pain will be felt, regardless of the intensity of the noxious stimulus. If the central inhibitory system fails, however, all sensation may be perceived as pain.

Finally, the second-order neurones from the gate to the thalamus are another level where modulation may occur. These neurones may transmit data concerning the nature of the noxious stimulus resulting in activation of both motor and sensory cortices, i.e. leading to both reactionary and sensory responses to noxious stimulation. These will again be modulated by past experience and emotional states, etc. The role of the cerebral cortex in either sensory perception in general or pain perception in particular is, however, still uncertain. Undoubtedly the cortex and other parts of the forebrain, e.g. the limbic system, are implicated in motivation, emotion, and pain memory, although their exact involvement in pain mechanisms has yet to be defined.

In 1975, two of the five endorphins (morphine receptors in the central nervous system) were noted to be associated with antinociceptive mechanisms.²⁴ These polypeptides behave like morphine by binding to morphine receptors to obtund pain. Encephalin and β-endorphin may therefore act as chemical neuromodulators, influencing both pain threshold and pain tolerance,²⁵,26 further compounding the complexity of the mechanics of pain.

Orofacial pain

Orofacial pain may be carried by myelinated or unmyelinated afferents from a receptive field, with:

(1) High-threshold mechanoreceptive (A) afferent fibres activated only by intense mechanical stimuli.

(2) Heat nociceptive (A) afferents that respond to intense heat.

(3) Strong mechanical stimuli and polymodal nociceptive (C) afferents that are responsive to intense mechanical, thermal and chemical stimuli.

These afferents are conveyed to the trigeminal (gasserian) ganglion where their primary afferent cell bodies are located. They then enter the brain stem to traverse the trigeminal spinal tract before entering the trigeminal nuclear complex (primarily the nucleus caudalis). Within this nucleus caudalis there appear to be three general types of nociceptive neurones:

(1) Nociceptive-specific neurones that respond exclusively to noxious mechanical and thermal stimuli.

(2) Wide-dynamic range neurones that respond to non-noxious as well as noxious stimuli.

(3) Low-threshold mechanoreceptive neurones that respond to light touch, pressure or facial hair movement, rather than noxious mechanical or heat stimuli.

Some of the neurones project to the thalamus via a pathway that may cross in the brain stem to the contralateral side. Others traverse to the reticular formation, cranial nerve motor nuclei (e.g. subnucleus oralis and the main trigeminal sensory nucleus) or other subnuclei. Obviously, the somatosensory cerebral cortex is involved in both general sensory perception as well as pain perception, although the role of other cortical regions, e.g. limbic system, has yet to be defined.

Secondary effects of pain

There is generally a close segmental relationship between the primary initiating pain and secondary effects of the noxious stimulus. Most secondary symptoms occur in structures innervated by the same major nerve that mediates the primary pain. These secondary effects may include:

(1) Sensory effects resulting in referred pains and secondary hyperalgesias, e.g. angina pectoris radiates to the top of the left shoulder, left arm and left side of the neck. The exact mechanism of referred pain is unclear but appears to depend on convergence of afferent inputs to central neurones from both the source and the referral sites, in addition to central summation. For instance, afferent inputs from facial, tooth pulp, pharyngeal and laryngeal sites may converge on the trigeminal brain stem complex and underlie certain types of referred pain in the orofacial region.

(2) Autonomic effects resulting in vasomotor and glandular symptoms, e.g. facial flushing with a dental abscess.

(3) Motor effects resulting in trigger point and myospastic activity in segmentally related skeletal muscles, e.g. masseter muscle pain with temporomandibular joint malfunction. For instance, local occlusal interferences may trigger increased muscular activity, changes in jaw position, muscle fatigue and pain. Interestingly, there appear to be no significant differences between the occlusions of patients affected by this disorder and those without it, thereby throwing into question the over-reliance on occlusal rehabilitation as a treatment order of this condition.

Pain aetiology (causes)

No single noxious stimulus results specifically in pain. Pain is therefore stated to have a multimodal aetiology. Nevertheless, there are some specific pathological processes that are commonly associated with pain. A few are mentioned here, primarily to illustrate the complexity of pain. Much more information concerning these aetiologies may be found in standard textbooks of pathology.

Inflammation

Tissue injury initiates an inflammatory response. Such a response characteristically includes pain. Inflammatory pain is actually a reaction to the chemical inflammatory mediators of bradykinin and prostaglandins. These chemical mediators not only result in vasodilatation and increased capillary permeability but also alter local receptor sensitivity and receptivity.²⁷–³⁰ The pain threshold is lowered as a result of such mediator activity, the net result including increased nociceptor sensitivity to stimulation. Higher-threshold mechanoreceptors may also become sensitized to a wider variety of stimuli. As a result, spontaneous primary pain and stimulation-evoked primary hyperalgesia may occur. A prostaglandin-like substance may also be released in the central nervous system that sensitizes nociceptive interneurones to mechanical and chemical stimuli. The net result is that the neural pathways related to inflammatory pain become more sensitive to the action of opiates.³¹

Pain of inflammatory origin may involve different kinds of tissue innervated by receptors with different reactive responses. Superficial pain may be inflammatory in origin (e.g. gingivitis), whereas visceral inflammatory pain may result from inflammatory changes in the adjacent tissues, e.g. arteritis or lymphadenitis. Inflammatory pain is therefore but a component of a symptom complex.

Muscle pain

Most muscle pain is noninflammatory in origin. Sometimes it results from muscle spasm, sometimes it is reactive, and sometimes it is protective. For example, muscle splinting is a temporary protective mechanism resulting in muscle pain and weakness. As a consequence, such muscle splinting serves to rest the muscle until the symptoms have disappeared.

Vascular pain

Patients with vascular pain (e.g. migraine) frequently display a characteristic emotional overlay with personality features of insecurity and tension. Four possible conditions have been associated with vascular pain discomfort:³²

(1) Vasodilatation and increased vascular permeability.

(2) Tissue oedema at the painful site.

(3) Oedema of the vessel wall and perivascular tissues.

(4) Associated muscle pain.

Thus, whereas vascular spasm and associated ischaemia contribute to the aetiology of vascular pain, other features may also occur.

Neural pain

Cutting or crushing a peripheral nerve induces anaesthesia due to afferent impulse interruption. Other symptoms may also occur, including paraesthesia, hyperaesthesia, hyperanalgesia or spontaneous pain. These symptoms may characterize the local area supplied by the nerve or may radiate to a much larger area.

Short term neural compression is usually painless, and/or results in anaesthesia. Chronic neural compression, however, ultimately leads to myelin nerve sheath degeneration. Loss of the myelin sheath may result in impulses travelling through the demyelinated region passing (shorting) to adjacent nerve fibres in a random manner, often reflected as pain, e.g. trigeminal neuralgia.³³

Trauma, bacterial infection and inflammation may result in inflammatory changes of the nerve fibre itself.¹ As a result the threshold of C fibres may be lowered, thus making them more sensitive to nociceptive stimuli and there may be partial or complete abolition of the reactivity of the Aδ fibres.³⁴ Thus the peripheral inhibitory mechanisms of pain modulation may be reduced, leading to the net neural activity being perceived as pain.²¹

Other causes of pain

Pain may result from a variety of pathological events, including:

(1) Spontaneous events, without obvious cause.

(2) Elevation of body temperature, e.g. fever.

(3) A general response to abnormal allergic, emotional, endocrine, metabolic or toxic conditions.

(4) Direct noxious chemical, mechanical or thermal insults.

Categories of facial pain

Pain from the face or oral cavity may be classified into three general categories: somatic, neurogenous or psychogenic.

Somatic pain

Somatic pain may result from stimulation of neural receptors or peripheral nerves. If superficial in origin, the clinical characteristics include:

(1) Bright pain with a stimulating quality.

(2) Accurate pain localization.

(3) Accurate correlation between lesional site and pain source.

(4) Temporary pain abolition by topical anaesthetic application to the site.

If deep in origin, the clinical characteristics include:

(1) Dull pain, depressing in quality.

(2) Variable localization of diffuse pain.

(3) Site of pain may/may not correlate with lesional site.

(4) Frequent display of secondary central excitatory effects.

Neurogenous pain

As neurogenous pains are generated within the nervous system itself, nerve receptor or fibre stimulation is unnecessary. The clinical characteristics of such neurogenous pains include:

(1) Bright, burning pains with a stimulating quality.

(2) Good localization.

(3) Close correlation between site of pain and lesion.

(4) Possible accompaniment by other sensory, motor and/or autonomic symptoms.

Psychogenic pain

Psychogenic pain may reflect somatic or neurogenous pain intensification, or may be a psychoneurotic manifestation. The characteristics of psychogenic pain include:

(1) The site of pain often has no correlation with a possible cause.

(2) The clinical behaviour and/or response to therapy may be non-physiological, unexpected or unusual.

Odontogenic pain (toothache)

A tooth is primarily innervated from the maxillary or mandibular division of the trigeminal nerve that pass essentially through the apical foramen. These nerve fibres are evident at the cap stage of odontogenesis.³⁵ Whereas in the fully developed tooth, some nerves terminate in the pulp proper, the majority pass towards the coronal pulpal walls and roof to form the subodontoblastic nerve plexus. Nerve fibres from this plexus then pass into the overlying odontoblastic layer, and comprise both myelinated and unmyelinated nerve fibres (some of which may be autonomic in origin). Thermal, osmotic, electrical, therapeutic and pharmacolgical stimuli result in pulpal nerve excitation,³⁶ although the degree of specificity remains obscure. In fact both myelinated (A) and unmyelinated (C) fibres pass through the apical foramen into the root canal and generally branch infrequently until the coronal aspect where they fan out towards the pulpal dentine border as Rashkow’s plexus. The density of this plexus varies, tending to be greater at the tips of the coronal pulp horns. From this subodontoblastic nerve plexus, nerve fibres are distributed in the pulpodentinal border zone, with terminals showing a characteristic head-like structure.

Some of the small (<1 μm diameter) nerve fibres in the odontoblastic zone are closely applied to the odontoblasts, and others enter the predentine to pass in the dentinal tubules for variable distances.³⁷–³⁹ Some of these nerve fibres may, however, have an autonomic efferent rather than nociceptive afferent function. Also, there is little evidence that these fibres pass to the amelocemental junction (clinically the most sensitive region of the tooth). Thus, although these nerve fibres may be associated with tooth-ache, other mechanisms may also be responsible.

The odontoblastic transduction theory contends that a dental stimulus excites either an odontoblast or its process which then transmits the excitation to adjacent nerve fibres. Such a view is supported by the close association between odontoblasts and subodontoblastic nerve plexus, in addition to the neural crest origin of the odontoblasts themselves. The hydrodynamic theory contends that enamel or dentinal stimulation causes an outward or inward flow of dentinal tubular contents, the resultant disturbances being translated as pulpal nerve excitation.⁴⁰ Conceivably, more than one mechanism may be involved.

The innervation of the pulp includes both afferent neurones that conduct sensory impulses and efferent autonomic neurones that principally provide neurogenic modulation of the blood flow in the pulp. Myelinated axons appear mostly associated with pain sensory function and have the following properties:

(1) Relatively fast conduction velocity.

(2) Relatively slow stimulation threshold.

(3) Considered to convey impulses conceived as sharp and penetrating.

The pain sensory unmyelinated nerve fibres passing into the pulp tissue are generally considered to exhibit the following properties:

(1) Relatively slow conduction velocity.

(2) Relatively high stimulation threshold.

(3) Considered to convey impulses conceived as dull and lingering.

Pulpal (including nociceptive) stimuli result in neuronal activity in widely dispersed CNS regions, including:

(1) Trigeminal brain stem sensory nuclei.

(2) Cranial nerve motor nuclei.

(3) Cerebellum.

(4) Reticular formation.

(5) Ventrobasal thalamus.

(6) Hypothalamus.

(7) Somatosensory cerebral cortex.

(8) Orbital cerebral cortex.

Pulpal stimulation thereby produces emotional, motivational and other behavioural changes, in addition to the appropriate reflex responses. The innervation of tooth pulps exhibits marked ariability, with an increase in the number of myelinated axons from the time of first eruption to some time after eruption. This correlates with newly erupted healthy teeth being less sensitive than older healthy teeth. With aging, however, the number of axons entering a tooth generally decreases. This again correlates well with clinical findings of a reduction in pulpal sensitivity with increasing age.

Pain control

Many procedures are available for the control of pain. These include:

(1) Pharmacological agents: local and general anaesthetic agents, analgesic drugs, e.g. morphine.

(2) Therapeutic procedures: acupuncture, transcutaneous electrical stimulation, audioanalgesia, hypnosis.

(3) Psychiatric counselling.

(4) Neurosurgery.

All these methods are directed toward blocking pain transmission either at the periphery before the impulses enter the brain or within the brain.

The reader is referred to more clinically oriented textbooks for a more detailed exposition of these