The dental patient is well equipped with oral sensory capacity. Touch, taste, and smell are all backed up and reinforced by sight and sound. To these five senses must be added several more, including pain. This rich, oral, sensory input has to be decoded and given meaning by the brain. The brain/mind may interpret the potentially fearful content of the incoming information as nonthreatening and ignore it. Or the sensory input may be magnified many times by stress, anxiety, and bad memories. Pain is not a direct sensory perception; it is an unpleasant emotional experience. Understanding pain would be impossible without joining up the sensations arising in the jaws and teeth with the patient’s brain/mind. The “hot tooth” is the result of neurogenic inflammation, the transport of inflammatory chemical messengers inside the axons of the nerve fibers from the peripheral nervous system into the pulp tissue.
The functions of chewing, swallowing, and speaking are complex and require a rich source of sensory input from a variety of receptor types in the muscles of the jaw, the periodontal ligament, and the soft tissues.
Several attempts have been made to define pain, none of which are entirely satisfactory. The definition adopted by the International Society of Pain Management is “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” Note that this definition includes an emotional component of pain which is always present and in fact defines pain from other sensations. We should never be tempted to describe pain without both its sensory and emotional components.
The relationship between an injury and the pain it causes is usually obvious. Banging your hand against a door may cause a twinge of pain, but it is not comparable to the pain you feel when your fingers are caught in the door as it slams closed. Usually, the worse the injury, the worse the pain. However, there are many occasions when this is not so. There are recorded cases of congenital analgesia in which there is a total absence of pain, without any physical abnormality of the nervous system. These poor individuals injure themselves without knowing it and die rather young from chronic tissue damage. From this example, we can conclude that pain has survival value. Congenital analgesia is a rare condition, but not infrequently, individuals have short periods or episodes of analgesia immediately following severe injury. This unexplained absence of pain has been observed during conflicts when badly wounded soldiers, brought from the battle front, appeared to be free of pain from their wounds. Episodic analgesia has also been observed in industrial accidents free of the diversions of war. The analgesia commonly does not last longer than 24 hours. During this time, it is confined to the injured part, so the patient may complain of some mild injury elsewhere, like the prick of an injection. From this example, we can surmise that if our survival depended on it, pain might be temporarily suppressed.
One of the puzzles of pain is that it may be felt even when there is little injury. Tension headaches and low back pain cause misery in many individuals, yet there is usually little injury or damage occurring. The passage of a kidney stone down the ureter does insignificant damage, but the slight stretching of the smooth muscle wall causes the patient to double up with excruciating pain. It is also puzzling that pain may appear long after healing has occurred to damaged or severed nerves. Months after the stump of an amputated limb has healed, a constant searing pain may appear wherever the limb used to be. This phantom limb pain responds poorly to analgesics. Pain without injury seems pointless and perverse of nature to inflict it on us.
Pain may be almost continuous or with only short remission for several years. It may be due to a chronic pathology (e.g., arthritis, vascular plaques around a ganglion) or a progressive cancer. However, the term chronic pain implies long-standing pain without any apparent organic cause which could account for its severity. The phantom limb pain mentioned above is an example. A similarly unpleasant cause of chronic pain is causalgia also known as complex regional pain syndrome. This pain is characterized by an intense burning pain in the area of a damaged peripheral nerve. It may result from trauma, such as a bullet wound, or fracture. Sometime after the injury, the skin becomes very tender to slight touching, which is followed after a slight delay by a most unpleasant burning or crushing pain over a wide area. The limb associated with the trauma may become swollen and stiff. Both phantom limb pain and causalgia are difficult to treat. Drugs and surgery, often performed at the request of the patient, are seldom successful.
We must avoid the temptation to assume that if we cannot find a cause for pain that it does not exist. Our ability to examine the nervous system is still very primitive. It is not like a network of telephone wires with direct links from receptors to a coordinating center. As more is understood about the complex changes in the nervous system following peripheral nerve damage, it becomes apparent that disruption in the central nervous system has also occurred.
Chronic pain sufferers tend to have signs of other conditions related to stress, such as depression, indigestion, constipation, and insomnia. Depression is a consistent feature of chronic pain. It may be argued that this is either secondary to the pain or that it is the primary condition and the most important to treat. The contribution made by physical and emotional factors to pain is illustrated by the Research Diagnostic Criteria classification of temporomandibular disorders (see Chapter 9.4.3 Research Diagnostic Criteria).
It is difficult to measure pain, because it is a private experience confined to the sufferer. We cannot examine the pain directly but have to rely on the patient’s version of it. Sometimes, it will seem that there is no cause for the pain and we might want to conclude that the patient is imagining it. However, all pain is real to the sufferer. The causes may lie too deep for us to find. We can get an idea of the nature of someone else’s pain by asking them to describe it. We will find it useful to pay close attention to the words they use. Some words may arise from a thoughtful, analytical process, so-called cognitive description. Other words which arise are an expression of emotions and from feelings, so-called affective descriptions. Examples of cognitive descriptive words are “sharp,” “burning,” “faint,” “mild,” and “intense” which suggest that the patient is describing the sensation of his or her pain. If affective words like “uncomfortable,” “miserable,” “unbearable,” and “awful” are used, we know the patient’s pain is affecting them emotionally.
A simpler, but less informative way of monitoring the levels of pain is by asking the patient to give it a rating on a scale from 1 (just perceptible) to 10 (unbearable). In experimental situations, the lowest intensity of a stimulus that produces pain is the pain threshold. The most intense stimulus that can be endured is the pain tolerance.
All pain has an emotional component. We have unhappy memories of being hurt and fear that pain may return. Pain is almost always unpleasant and we focus our efforts to avoid it. If we cannot avoid it, we want to make sure we get it under control as soon as possible. We usually welcome support from others who may help us to control our pain.
The attitudes to pain vary from one culture to another. Some individuals, such as the Native Americans, acquired a reputation for restraining their emotions, including pain. For them, it was not acceptable to show fear, suffering, or grief. These values became role models for the strong, silent cowboys, who the movies created into the heroes of the Wild West. In contrast, the individuals of the Mediterranean are less inhibited. It is not shameful for men to cry at the opera or for women to wail loudly in childbirth. Tests for pain threshold and tolerance for different cultural groups show marked differences, although the sensory threshold, that is, the ability to detect a stimulus such as a weak electric current or slight warmth is not different. This proves that the sensory apparatus of humans is essentially the same.
Attitudes to pain are shaped early in childhood by our parents’ response to minor cuts and bruises. Learning about pain also occurs after having suffered from it, so that it may be avoided in future. Many adult dental patients who are afraid of dental procedures are able to trace their fear back to painful experiences as children. On the other hand, pain-free experiences in childhood pave the way for an easy relationship with dentists and dentistry in adult life. The experience gained by pain and learning to avoid it reveal one of its main purposes, that is to prevent recurring injury.
Pain is more bearable when its cause can be understood and the threat identified. Pain near the heart is frightening because of the possibility that a heart attack is coming. If the doctor can assure us that the source of the pain is indigestion, as it often is, the pain may become quite insignificant. Reassurance by the doctor or dentist that pain is not a sign of a sinister illness, like cancer, immediately reduces the level of pain in the sufferer.
In some circumstances, pain may carry such positive associations as to be ignored. In a few cultures, the pain of childbirth is welcomed and celebrated as it brings promises of birth and new life. Such is the conviction of their women in labor that they laugh with pleasure and excitement at their birth pain.
Following severe burns, the dead skin must be removed to allow healing. This wound debridement is very painful but is bearable if the patient can assist in the work of pulling away the dead tissue. The importance of control can be verified under experimental conditions. Volunteers allow themselves to be given an electric shock to find out how much they can tolerate. If they are able to manipulate the controls which increases the voltage, they are able to tolerate higher levels of stimulus than if this control is manipulated by anyone else. Some dental patients find that having their teeth cleaned with an ultrasonic scaler is uncomfortable and at times even painful; it helps the patient to put up with some discomfort, if there is some agreed way of giving the dentist a sign that the pain is more than the patient wants to tolerate.
One of the strategies for helping patients to deal with chronic pain is to give them control over their drug doses and to help them to take control of their lives rather than allow the pain to become their master.
It is possible to reduce awareness of pain for a while by diverting attention from it. Dancers and athletes are able to concentrate so fully on their performance that they can put pain out of their mind. Even mental arithmetic or visual and auditory distractions may for a while be effective in reducing pain.
Pains which are readily understood, and which over time are reduced, are reasonably well tolerated. Examples are birth pain and injury or inflammation, which are relatively short lived and can be reduced with suitable treatment. When the pain is out of the patient’s and the doctor’s or dentist’s control, it is said to be intractable and is highly distressing.
The mere suggestion that pain will be taken away has a powerful effect on the sufferer. So, a tablet which contains nothing more than flavoring, a placebo, often succeeds in reducing pain if the patient is told it is a powerful analgesic. It is still more effective if the tablet looks impressive (capsules are better that tablets) and if two are given. It is most important, though, for the therapist also to believe that the patient is being given an active analgesic, and that it is a strong one. When clinical trials are designed to compare an analgesic with a placebo, they are so-called “double-blind,” meaning neither the patient nor the doctor knows whether the tablet has the active ingredient or not. Under these conditions, 35% of patients given a placebo report that their pain goes away. The powerful effect of placebos extends to somatic illness. It does not imply that the patient’s complaint must be imagined but illustrates the complexity of illness, and how it is influenced by the reaction of both our minds and immune systems to it.
Experiencing pain and illness is worrying, and so it comes as a great relief to be in the care of someone who wants to help. It is likely that any benefit patients receive from homeopathic remedies is due to the care, compassion, and companionship, which the therapist provides.
The exact mental state during hypnosis is not clear, but it seems to be a sort of trance during which the subject is particularly susceptible to suggestion from the hypnotist, yet not under his or her control. Some individuals are unable to be hypnotized, but about 30% can be induced into a deep trance during which some painful surgery can be performed. These subjects are receptive to suggestion and also inclined to benefit most from placebos. Some individuals are able to induce trance-like states in themselves and then walk over hot coals or lie on beds of nails and even cut themselves without bleeding. An essential requirement of performing these challenges is training. So, these individuals do not possess some unusual physiological resistance to pain but must be trained to ignore it. Volunteers who are complete novices may be trained in a few days to walk over hot coals.
Unfortunately, many normal patients may have been told their pain is “psychological” because the doctor or dentist could not find a reason for it. All pain is strongly influenced by psychological factors; it is a highly emotion-filled experience, but what these therapists are really wanting to say is that the pain is imagined and not really there. As providers of health care, we have to be careful not to invest too much confidence in our own healing powers. We have some tools in our bag, but when it comes to management, particularly of chronic pain, the bag soon empties, and we may feel powerless and frustrated. Then, it is tempting to dismiss the problem by ruling that it does not really exist. All pain is real to the sufferer, whether or not the therapist can make any sense of it.
There are cases of patients who seem to need to have pain. They may be able to nurture it from within, or they may seek out painful operations, one after the other. The need for pain seems abnormal in any context, but particularly so when it becomes a feature of sexual pleasure. In the past, self-flagellation (whipping) was a well-recognized pathway to spiritual purity in Christian monks. Self-harming is sadly not uncommon among today’s troubled teenagers. There may be some sense of self-punishment in all these individuals, who feel better about themselves when some inner score is settled. However, the troubled mind of such individuals may work; it is probable that they have given pain a meaning, which somehow fulfils their emotional needs.
The emergence of hospices followed the pioneering work of Cecily Saunders at St. Christopher’s Hospice in London. Now, we know there is much more that can be done to manage pain in the terminally ill, not the least of which is a willingness to use as much morphine as is necessary, without fear of tolerance or addiction. It is well proven that when addictive drugs are used to control pain, the dose does not have to be progressively increased to have the same effect (tolerance), nor are there withdrawal symptoms (addiction) should the medical condition make it possible to reduce the drug. While pain in the terminally ill can cast a heavy shadow over the last few months, or even years, it seems that when very close to death, there is eventually some respite. Animals normally sensitive to pain become quite peaceful and free of agony when massive injury and almost certain death are close at hand. There are also many cases recorded of humans who have been declared dead yet survived to tell their experience. These so-called near-death experiences are remarkably similar; the survivors recall being quite free of pain and surrounded by wonderful music and warm friendly individuals. It is as if, in the last act, the shadow of pain melts away, and death is a welcoming end.
While the brain or mind is the organ where pain is perceived, the tissue in which the pain originates makes a substantial difference to the experience. While some tissues have an unusual response to tissue damage, there are clinical types of pain which are common to all tissues.
Hyperalgesia: Tissues which have been subject to damage and painful for some time may become even more sensitive to stimulus than they were originally. An example of hyperalgesia is that experienced by light-skinned individuals, who have been sunburnt. The same day, they may feel pain getting into a hot bathtub. The next day they may feel pain in getting into even a slightly warm bathtub. The pain brought on by levels of a stimulus which are normally low enough not to cause pain is called allodynia. Both hyperalgesia and allodynia are brought about by an accumulation of pain and inflammation-stimulating chemicals in the damaged tissue and in the spinal cord. This is called peripheral and central sensitization and will be described in further detail below.
The pulp–dentin: The pulp–dentin is densely supplied with free nerve endings which are specialized (not specific) to conveying pain. The role of this sensitivity to pain is unclear. There are patients who feel very little pain during cavity preparation to remove dental caries, but most are only too happy to have as much anesthetic as is needed to ensure that cavity preparation is pain free.
The pulp–dentin is particularly sensitive to increase in pressure as it is a confined tissue space. Inflammation of the pulp rapidly causes a raise in tissue pressure, which leads to allodynia and hyperalgesia. In an allodynic condition, the pulp–dentin is sensitive to even slight changes in temperature, either hot or cold.
When enamel protection is lost or removed, the exposed dentin is sensitive to changes in osmotic pressure which may be brought about by sweet or sour foods. Pulp–dentin is also sensitive to electrical stimulation. The mechanisms which are thought to cause pulp–dentin pain are discussed in the next section.
Visceral pain: The gut and urogenital organs of the body are surprisingly insensitive to cutting or even burning but exquisitely sensitive to pressure or tension. As we have noted, the mild distension of the ureter, as a kidney stone is passed, causes severe pain. So does distension of the uterus during the contractions of menstruation or childbirth. Dilation of the cervix during childbirth may cause quite severe pain, but when the dilation is sudden, as may occur during rape, the pain is excruciating. If any of these organs is even slightly inflamed, the pain threshold to tension or pressure is very low.
Muscle pain: All types of muscle tissue are sensitive to ischemia. This is a reduced blood supply which may occur after sustained periods of muscle contraction which progressively interrupts the circulation. Ischemia causes a build up of metabolites, particularly lactic acid which may cause severe cramps and acute pain. A deeper and more diffuse muscle pain may occur after gradual and low-grade tissue damage to muscles. This damage may occur due to prolonged tension of the muscle, such as occurs with bad posture. For example, the neck muscles of dentists may ache after a day’s work, if the neck is not held in an upright posture at all times during operative procedures. There are usually tender areas of the back muscles, which are detectable as small lumps or ridges within the muscle mass. They have been called trigger points, as pressure on them triggers an episode of pain. Muscle pain is diffuse and may be felt some distance from the sight of a trigger point. Painful muscles of the jaw often refer pain to the area around the ear and the temporomandibular joint (TMJ) (see Chapter 10.4.8 Trigger Points in Muscles).
Peripheral nerve pain: Neuralgia is caused by viral infection or degeneration of peripheral nerves. Causalgia is more commonly caused by damage to peripheral nerves. During infection by the herpes zoster virus, inflammation of peripheral nerves occurs with blisters (shingles) on the skin over the affected nerve. During the active infection, a burning pain is felt, which usually subsides when the infection is resolved. In some patients, the pain persists (postherpetic neuralgia) and may become worse. This pain is similar to causalgia, in that the skin is hypersensitive to light stimulation, such as mild heat. For the first few seconds nothing is felt. Then a rush of burning pain follows which has a particularly unpleasant nature.
Trigeminal neuralgia is confined to the sensory distribution of the trigeminal nerve. Gentle stimulation of a usually well-defined trigger point on the face provokes a massive stabbing pain. Local anesthesia of the trigeminal nerve branches produces temporary relief. Other procedures which block the nerve for longer periods work temporarily, but the pain recurs. A frequent finding at autopsy or operation is a demyelination of the roots of the trigeminal nerve. This may be due to compression from the surrounding blood vessels. In many cases, relief is obtained by surgical decompression of the nerve roots. The pain may also be reduced by antiepileptic drugs (e.g., Tegretol), which decrease the firing of central brain cells.
An important factor which increases the response of all tissue to pain is inflammation. This is because many of the cytokines which promote inflammation such as prostaglandins, serotonin, substance P, and histamine all increase peripheral sensitization (see Chapter 10.4.6 Neurogenic Inflammation of the Pulp Tissue).
Brain and bone tissues. Neither the brain nor bone tissues perceive pain. It is the membranes around these tissues which are sensitive to pain. The clinical implications for dental surgeons are that an implant osteotomy may be prepared in alveolar bone, provided that a local infiltration of anesthesia is used to reduce sensations from the periosteum.
The interactions between sensory neurons in the spinal cord which influence the pain pathway, together with the influences on these neurons of a large family of neurochemicals, are complex. It is therefore not possible to present a comprehensive or succinct summary here. The reader interested to pursue a fuller understanding of pain mechanisms is referred to a group of reviews which present the latest levels of understanding.1,2 What follows is an abbreviated overview which is designed to provide the practitioner with a working understanding which will support clinical practice.
Nerve cells (neurons) in the peripheral and central nervous systems have a single thin axon which may be several centimeters long and transports electrical and chemical messages over long distances. Neurons also have hundreds of shorter projections called dendrites, which communicate with neighboring nerve cells. Bipolar neurons have two long axons, one receiving nerve impulses from the periphery and the other carrying impulses toward the central nervous system. The cell bodies of bipolar neurons are situated in peripheral nodes called ganglia. Nerve fibers serving the teeth and jaws have their cell bodies in the trigeminal ganglion.
There are three main chains of neurons carrying messages from the periphery to the brain. The neurons whose fibers carry impulses from receptors in the peripheral tissue are called first-order neurons. Their journey toward the central nervous system continues only as far as the dorsal horn of the spinal column or in the case of the trigeminal nerve to the subnucleus caudalis in the brainstem. Here, the central part of the axons of the first order neuron forms junctions with the second-order neurons of the trigeminal nucleus in the brainstem. These second-order neurons convey the impulses onward along their axons toward the third-order neurons in the thalamus from which axons project to the cortex (▶ Fig. 10.1). These are the three main levels in the pathways of the nervous system, but there are also interneurons, which carry impulses between the spinal neurons at each level and between each level in the main pathways.
Fig. 10.1 A diagrammatic representation of the three orders of neurons in the nerve pathways of the trigeminal nerve. The nerves of the dental pulp have their cell bodies in the trigeminal ganglion. These first-order nerve cells (1st or) are bipolar, that is they have two axons, one leading toward the periphery, in this case, the dental pulp, the other leading toward the brainstem, where they synapse with the second-order (2nd or) nociceptive specific neurons (NS) of the trigeminal nucleus. Should the membrane of the NS depolarize, an impulse will travel along the cell’s axon to the next level, a synapse in a third-order neuron (3rd or) of the thalamus. If this neuron depolarizes, an electrical impulse travels down its axon to synapses in the cortex. The route for a single nerve impulse from a receptor in the dental pulp must then pass through three orders of neuron. These synapses may be likened to gates, which may or may not transmit the impulse onward.
Nociceptors are sensory nerve cells with receptors which detect tissue damage and are responsible for transmitting pain impulses to the brain. The cell bodies of nociceptors are the first-order, bipolar neurons located in the dorsal root ganglia of the spinal cord and the trigeminal ganglia of the trigeminal nerve.
There are other fiber types (Aβ), mainly concerned with nonpain sensation such as mechanoreception and proprioception which are up to 50 times faster than fibers which convey pain impulses. They are of importance in the pathway of pain as they may modulate pain transmission.
The first sharp stinging pain after injury (such as touching a hot cooking pan) lasts a few seconds only and is carried fast enough along myelinated Aβ fibers to ensure a rapid response (withdrawal). This first pain is followed by a poorly localized deeper pain which is carried by the nonmyelinated, C fibers. The impulses carried by C fibers also alert the slower metabolic responses required for inflammation and healing. The pain response to sudden injury changes in the seconds, hours, and days after tissue damage.
Nerve axons are two-way transporters of both electrical and chemical messages. They carry electrical impulses toward and away from the nerve cell. Nerve cells are polarized, the outside of the cell membrane being relatively positively charged. The nerve impulses start as a reverse in the polarity, just at one site of the membrane. This reversal of polarity triggers a cascade of depolarization events along the nerve axon, and like a wave, this electrical pulse passes down the nerve axon (▶ Fig. 10.2). The electrical potential of this depolarization is constant in the peripheral nerve axons, but the frequency of the impulses varies, and it is this variation which conveys the nature of the information being carried.
Fig. 10.2 A diagrammatic representation of a nerve impulse propagated by depolarization of the axon membrane. (a) The nerve cell membrane and its axon are highly polarized. Stimulation of a nerve ending sends a wave of electrical depolarization caused by the rapid exchange of sodium (Na) and potassium (K) ions through channels in the cell membrane. The wave of depolarization moves toward a nociceptive specific (NS) neuron in the spinal cord or brainstem. (b) At the NS neuron, the electrical impulse causes the release of neurotransmitter substances into the synapse gap. If the concentration of these chemicals reaches a critical level, and if the NS neuron is already in an excited state, its membrane may depolarize and send an impulse toward the brain. The NS neuron also secretes deactivators into the synaptic gap which break down the neurotransmitters and deactivate them. It is here that opiates and serotonin reduce the influence of the neurotransmitter substances. Here, even at the first synaptic junction, there are neurochemicals which are associated with emotions, fatigue, or anxiety, which influence the excitability of the NS neuron.
If the axon is more than 1 µm in diameter, it is covered by a sheath of myelin, an insulating material. This material is formed by a glial (nerve-supporting) cell, called a Schwann cell. These cells wrap their cell membranes, which contain myelin around the nerve axon. There are gaps in the myelin between each cell, called nodes of Ranvier, which allow the nerve impulse to jump across from one node in the myelin sheath to the next, thereby increasing its speed of conduction several times.
A nerve impulse that originates from the periphery travels as far as the spinal cord where it has to be carried across a space between the nerve axon and the cell membrane of the spinal cord cell. This space is called a synapse. The synaptic space is crossed, not by an electrical discharge, but by chemical transmitters released from the end terminal of the axon. These neurotransmitters accumulate in the narrow synaptic space, and when the concentration is high enough, they cause the adjacent cell membrane of the spinal cord cell to depolarize and send an electrical impulse along its own axon.
Impulses from pain receptors traveling along C fibers or Aδ fibers synapse with nociceptive specific (NS) neurons in the spinal cord. These neurons are dedicated to pain impulses. There is a second type of neuron in the spinal cord which receives pain and non-pain impulse of varying ranges of impulse intensities. This is a called a wide dynamic range (WDR) neuron.
These WDR neurons also receive impulses from viscera. This association is thought to account for the pain, for example, from angina (visceral) which may become associated with somatic tissues (the shoulder) and produce the sensation of shoulder pain, which actually originates from the heart. This is called referred pain.
Nerve axons not only transmit electrical impulses but also carry chemical messengers. These messengers are neuropeptides, protein-like molecules used by neurons to communicate with each other. Neuropeptides are carried in both directions within the axon along a transport route of microtubules. This transport may take days, whereas the nerve impulse takes a few seconds. Some of the neuropeptides are transported from the ganglion cell to the synapses with the spinal cord NS neuron. Neuropeptides are also transported toward the peripheral nerve endings and released into the tissue where they mediate inflammation and lower the threshold of the receptor to excite further depolarization. The inflammation mediated by this release of neuropeptides into the tissue is known as neurogenic inflammation. The influence of released neuropeptides on the threshold of the receptor is one of the causes of peripheral sensitization.
Pain fibers not only transport peptides to the peripheral end of the nerve axon but also to the central end where they increase the excitability of the spinal nociceptive neuron. This process is called central sensitization (see Appendix G .1 Peripheral Sensitization and G.2 Central Sensitization). The clinical manifestation of peripheral and central sensitization is hyperalgesia. Hyperalgesia is an increased sensitivity to pain caused by heat, chemicals, or mechanical trauma.
The pathway of pain impulses toward the brain is complex. There are many levels through the brainstem and midbrain where impulses are diverted and subject to modification before continuing eventually to the cortex. The simple observation which can be made is that there is no center in the brain or brainstem where pain is specifically experienced (see Appendix G.3 Central Connections of Pain Impulses).
The pulp is extremely highly innervated. Beneath the layer of odontoblasts there is a rich plexus of nerves described by Rashkow. Nerves which are continuous with this plexus penetrate into the dentinal tubule for a short distance (about 100 µm). If cross-sections of dentin are viewed using a transmission electron microscope (TEM), the unmyelinated nerves can be seen lying next to the odontoblast’s process (▶ Fig. 10.3). At those places, where the nerve and process are close, there is evidence of a gap junction which would allow electrical communication between the two membranes but no synapse between the nerve and odontoblast. The nerve axons contain mitochondria and microfilaments and both these can be observed to disappear after experimental inferior alveolar nerve section. Not every tubule has a nerve, only about 40% do in the densest areas around the pulp horn. The incidence of nerves in tubules falls to 5% around the sides of the pulp chamber and drops to less than 1% in root dentin.
Dentinal tubules contain fluid in the periodontoblastic space. This fluid is probably derived from pulp capillaries but may arrive via the odontoblast. According to the hydrodynamic theory, a stimulus applied to the dentin surface induces fluid flow in the dentinal tubules (▶ Fig. 10.4). This flow causes distortion of the peripheral pulp tissue and consequent activation of nerve endings at the pulp–dentin border. The theory is supported by a number of in vivo observations. If the passage of fluid is blocked, then dentin sensitivity is reduced. This happens if after cutting dentin with a bur, the layer of smeared debris is left on the dentin surface. Reduced sensitivity also occurs if the flow of fluid is reduced by the deposition of peritubular (intratubular) dentin. If, on the other hand, the passage of fluid is increased, so is dentin sensitivity. This occurs if the surface of the dentin is etched with acid, which opens up the tubule.
Fig. 10.4 Diagrammatic representation of flow in the dentinal tubule. (a) In the young tooth, dentinal fluid flows back and forth in the tubule in response to mechanical and thermal stimuli causing stimulation of pain receptors in the dentin and pulp. (b) In the older tooth, the tubules become narrower and are eventually blocked with peritubular dentin and secondary dentin, which progressively reduce the flow of the dentinal fluid and reduce the sensitivity of dentin to mechanical stimuli.
The flow of fluid in the dentin tubule can be measured in vitro and can be experimentally increased by applying a strong osmotic solution to an exposed dentin surface. This experimental observation may explain the pain which occurs when cement-denuded root surfaces are in contact with sweet food which has a high osmotic pressure. Although the initial stimulus to the dentin may be sensed by mechanical displacement of fluid in the tubule, it must eventually be transcribed into a nerve impulse. How and exactly where this occurs is not certain, although the rich nerve plexus of Raschkow just beneath the layer of odontoblasts must be involved. What is evident is that dentin sensitivity is dependent on the condition of the pulp. Hence, some patients are able to tolerate tooth preparation without an anesthetic, and on the other extreme, a tooth whose pulp is already inflamed may be so hypersensitive that pain is felt in spite of several injections of local anesthetic. There is no proof of the hydrodynamic theory, but it fits the observations better than any other at present.
A knowledge of the mechanisms and pathways of dentinal pain allows dentists to take rational clinical steps to reduce dentinal sensitivity. The main thrust is twofold. Firstly, to reduce fluid movement and secondly to reduce inflammation of the pulp. The dentist can reduce root dentin sensitivity by applying adhesives which will block the exposed dentinal tubules. At present, there is no medication that has been found to be reliably successful for home use, although toothpastes containing potassium oxalate and stannous fluoride are available. The response of the pulp can be reduced by applying sedative dressings to the floor of deep cavities. Eugenol causes reversible sedation of the pulp.
Dentin which has been recently exposed is usually sensitive to a variety of stimuli, heat, cold, osmotic pressure, drying, and mechanical stimulation. These stimuli all cause pain, no other sensation. Dentin which has been exposed for some time, such as might occur after gradual tooth wear, is not sensitive. However, root dentin often is sensitive (one in seven complaints). The root dentin is covered with only a thin (100 µm) layer of cement which may be removed during periodontal surgery or by incorrect tooth brushing. The exposed root dentin is sensitive to brushing, cold and sweet foods.
Bacteria in carious lesions produce acids, which diffuse through sound dentin to reach the pulp tissue. The acid irritation causes pain and inflammation of the pulp and increased sensitivity to stimuli which would not normally cause pain, such as hot or cold beverages. If bacteria in dentin continue to advance toward the pulp, inflammation progresses and the tooth begins to ache continuously. Other nearby teeth may also ache. This is the typical response of C fibers in promoting further inflammation, sensitivity, and healing. In softer tissues, these responses produce the cardinal signs of inflammation, redness, swelling, heat, and pain. However, in the pulp chamber, no swelling is possible. The pulp tissue pressure increases, as the inflammatory exudate accumulates in the confined space of the pulp chamber. The increased pressure causes further pain. At this point, the pulpal damage may be considered irreversible; the pulp tissue must be removed by root canal treatment.
The dentist and patient are concerned with reducing dentinal pain during cavity preparation. This is usually successfully achieved by blocking the nerve impulse on its way to the trigeminal nucleus using a local anesthetic. Not everyone finds an injection of local anesthetic essential, even though they have a normal pain response elsewhere. On the other hand, sometimes it is difficult for the dentist to achieve anesthesia, even after several injections. It does not help to apply the local anesthetic directly to the dentin, but it may be applied under some circumstances directly to an exposed pulp.