Neurophysiology of pain/Dental implant courses by Indian dental academy by indiandentalacademy

CONTENTS I. Introduction………………………………………………………………….3 II. Definition……………………………………………………………………..3 III. Nerve physiology……………………………………………….…………….3 1. Neurons 2. Structure of nerve fiber 3. Classification of neurons 4. Nerve impulse 5. Synapse 6. Neurotransmitters 7. The sensory System 8. The Receptors IV. Pain…………………………………………………………………………...….14 1. Receptors 2. Stimuli for pain 3. Characteristic of pain 4. Pain reaction 5. Pain pathway 6. Referred pain 7. Visceral pain 8. Trigeminal system 9. Theories of pain V. Management of dental pain……………………………………………………..30 o

Introduction and classification of pain

Examination and assessment of patient with Oro-facial pain

Determination of diagnosis

Management of dental pain 

Types of treatment

Somatic pain of Pulpal origin

Somatic pain from dental supporting tissue :

Pain disorders that mimic odontalagia

Atypical pain disorders that mimic odontalagia

Drug therapy 

Pain management principles



Non opioid analgesics



Opioid analgesics



Role of corticosteroids



New developments in pain management

VI. Conclusion……………………………………………………………....………54 VII. References…………………………………………………………….………..55

Introduction Pain is one of the most commonly experienced symptoms in dentistry and, as such is a major concern to the dentist. Pain is not a simple sensation but rather a complex neurobehavi oural event involving at least two components. First is an individual’s discernment or perception of the stimulation of specialized nerve endings designed to transmit information concerning potential or actual tissue damage .(nociception) Second is the individual’s reaction to this perceived sensation (pain behavior). Pain is a protective mechanism for the body; pain gives information about states of the body, but unlike other sensations, not about the nature of the stimulus. Definition The definition given by IASP (International Association for the study of pain)- “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. Pain is always subjective. Each individual learns the application of the word through experience related to injury in life. If is unquestionably a sensation in a part of body, but it is also always unpleasant and therefore also an emotional experience. Nerve physiology 1. Neurons: Nerve cells called neurons are responsible for conducting nerve impulse from one part of body to another. They are the structural and functional unit of the nervous system. Structure of a Neuron: Consist of three distinct portions 1. Cell body 2. Dendrites and 3. Axon 1. Cell body (soma or perikaryon) - contains, a well-defined nucleus and nucleolus

surrounded by a grander cytoplasm.

Within the cytoplasm are typical organelles such as lysosomes, mitochondria and Golgi complexes. Also in cytoplasm are located structures Characteristics of neurons; chromatophilic substance and neurofibrils. Chromatophilic substance (Nissl bodies) is an orderly arrangement of granular (rough) endoplasmic reticulum whose function is protein synthesis.

Neurofibrils are long, thin fibrils composed of in support and transportation of nutrients mature neurons do not contain a mitotic apparatus. 2. Neurons have two kinds of cytoplasmic process: Dendrites (dendro =tree) are usually highly branched, thick extensions of the cytoplasm of cell body. There function is to conduct nerve impulses towards the cell body. 3. Axon: is usually a single long thin process that is highly specialized and conducts nerve impulse away from the cell body to another neuron. It usually originates from the cell body as a small conical elevation called axon hillock. Its cytoplasm is called axoplasm and is surrounded by a plasma membrane known as the axolemma. Axon vary in length from a few millimeter in brain to a meter or more in spinal cord and toes. The distal ends of axon terminals are expanded into bulb like structures called synaptic end bulbs.

2. Structure of myelinated nerve fibre: The term nerve fibre may be applied to any process projecting from the cell body. More commonly it refers to an axon. A nerve fibre may be myelinated (or medullated) or non-myelinated (non-medullated). Myelin sheath is a multilayered, white phospholipid segmented covering. Axons with such a covering is called myelinated, where as those without it unmyelinated. The function of the myelin sheath is to increase the speed of nerve impulse conduction and to insulate and maintain the axon. Myelin is responsible for color of white matter in the nerves, brain and spinal cord.

The

myelin

sheath

axon

produced

flattened

cells,

called

Neurolemmocytes. (schwann cells) located along the axons. The peripheral nucleated cytoplasmic layer of neurolemmocyte is called the neurolemma (sheath of Schwann).

Between the segments of myelin sheath are unmyelinated gaps called neurofibral nodes. (Nodes of ranvier). At node of ranvier, there is no myelin sheath and the neurilemma is in direct contact with axis cylinder. The central core of the axon is called axoplasm; which is pasty in nature. The axoplasm is ensheathed by a membrane called axolemma.

Non myelinated nerve fibresAs there is no myelin sheath the diameter of these nerves are very small, and there is no node of ranvier. 3. Classification of neurons: 1. Structural classification: Based on number of processes extending from the cell body. 1. Multipolar neurons – several dendrites and one axon 2. Bipolar – one dendrite and one axon 3. Unipolar (pseudounipolar)- has only one process extending from the cell body, which divided into a central branch, which function as an axon, and a peripheral branch, which functions as a dendrite. 2. Functional classification: Based on the direction in which they transmit impulses. 1. Sensory (afferent) – transmit impulse from receptor in skin, sense organs, muscles, joints, viscera to brain and spinal cord. They are usually unipolar. 2. Motor (efferent) neurons – convey impulses from the brain and spiral cord to effectors, which may be either muscle or glands. 3. Other neurons called association neurons carry impulses from sensory to motor neurons and are located in brain and spinal cord. Eg,.stellate cells. The processes of afferent and efferent neurons are arranged into bundles called Nerves, if outside the CNS or fiber tracts if inside the CNS. The functional components of nerves are nerve fibres, which may be grouped according to following scheme. 1. General somatic afferent fibres 2. General somatic efferent fibres 3. General visceral afferent fibres 4. General visceral efferent fibres (autonomic) - Convey impulse from CNS to help control contractions of smooth and cardiac muscle and rate of secretion of salivary glands. 4. Nerve impulse The striking features of neurons is their highly developed ability to generate and conduct electrical messages called nerve impulse. Membrane potentials – In a resting neuron (one that is not conducting) there is a difference in electrical charges on either side of membrane. This difference is partly the result of unequal distribution of potassium (k+) ions and sodium ions (Na+) on either side of membrane. Even when a nerve cell is not conducting an impulse, it is active, transporting ions across its membrane. Na + ions are actively

transported out, and k+ transported in. The membrane system by which Na + and k+

ions are

actively transported simultaneously is called the sodium potassium pump. The sodium-potassium pump not only actively transports Na + and k+ ions, but also establishes concentration gradient for ions. The result is that there is difference in charge on either side of membrane, net positive outside and net negative inside. This difference in charge on either side of membrane of resting neuron is the resting membrane potential (RMP), such a membrane is said to be polarized. Electrical measurements of a polarized membrane indicate a voltage of about – 70 mV. Excitability The ability of nerve cells to respond to stimuli and convert them into nerve impulses is called excitability. A stimulus is any condition in the environment capable of altering the resting membrane potential. If an excitatory stimulus is of adequate strength, called a threshold stimulus, is applied to a polarized membrane, the membrane’s permeability to Na + ions greatly increases at the point of stimulation. The sodium channels open and permit the inflow of Na + ions by diffusion. As more Na+ ions enter the membrane then leave, the resting membrane potential begins to change. At first, the potential inside the membrane shift from −70 to zero, then to a positive value. This process is called Depolarization. Depolarization begins at −69 mV and from this point on the membrane is said to be depolarized. Throughout depolarization the Na + ions continue to rush inside until the RMP is reversed. Once the events of depolarization have occurred, we say that a nerve impulse (nerve action potential) is initiated.

An action potential is a rapid change in membrane potential that involves a depolarization followed by repolarization. The nerve impulse that is generated at any one point on membrane usually excites (depolarizes) adjacent portions of the membrane, causing the impulse to be propagated. By the time the nerve impulse has traveled from one point to the next, the previous point becomes Repolarized- its resting potential is restored. The repolarization period returns the cell to its resting membrane potential –70 mV. Refractory Period: When a nerve fibre is producing an action potential, the fibre becomes refractory to a second stimulus. The first phase of this refractory period is called Absolute Refractory period, i.e. no matter how strong is the stimulus, the fibre does not respond. During the later phase, only a very strong stimulus can produce a response, (i.e. the threshold is now higher than normal) this phase is called Relative refractory period.

All or None principle: A single nerve cell, transmits an action potential according to the all-or-none principle. Any stimulus strong enough to initiate a nerve impulse is referred to as Threshold (liminal) Stimulus. If a stimulus strong enough to initiate a nerve action potential, the impulse is conducted along the entire neuron at a constant and maximum strength. Any stimulus weaker than a threshold stimulus is termed a subthreshold stimulus. Such a stimulus, if occurring only is incapable of initiating a nerve impulse. If however, a second stimulus or a series of subthreshold stimuli is quickly applied to the neuron, the cumulative effect may be sufficient to initiate an impulse. This phenomenon is called ‘summation’. Saltatory Conduction: The step by step depolarization of each adjacent area of the axon or dendrite plasma membrane, is seen in unmyelinated fibres, the conduction called ‘continuous’. The myelin sheath surrounding a fibre does not conduct electric current. The myelin sheath is interrupted at various intervals called nodes of ranvier. At nodes, membrane depolarization can occur and nerve action potentials can be generated and conducted when a nerve impulse is conducted along a myelinated fiber, It moves from one node to another by ionic current flow through the surrounding extracellular fluid. Thus the impulse jumps from node to node. This type of conduction seen in myelinated fibers is called Saltatory conduction.

Speed of nerve conduction Nerve fibers having a greater diameter and those with a myelin sheath, conduct faster, than those with small ones. Based on their velocity of conductions Gasser and Erlanger made a classification in 1920 as below. Class of nerve

Diameter (in μm) thick or

Velocity of

Fibre

thin

conduction

22-12; thickest

(m/sec) 120-70

Aα /α

Heavily myelinated A

Aβ /β

Identity of nerves (where found)

Motor nerve (somatic) and proprioceptive (sensory)

12-6; thinner than α

70-30

Afferent for touch

30-15

Motor nerves to intrafusal muscle if

myelinated Aγ/γ

6-3; still more thin slightly myelinated

Aδ/δ

the spindle

5-2; still thinner <2 ;

30-12 10-3

Afferent for thermal senses Preganglionic fibres of ANS

myelinated 1.5- 0.3;

2-0.5

Afferent for pain ; post-ganglionic

Non-myelinated

(slowest)

sympathetic

Extremely thin

5. Synapse Impulses are conducted between one neuron to another across a synapse – a junction between two neurons. The synapse is essential for homoestasis because of its ability to transmit certain impulse and inhibit other. Within a synapse is a minute space, filled with extracellular fluid, about 20 nm across, called synaptic cleft. A presynaptic neuron is located before a synapse. A post synaptic nerve is located after a synapse. In the presynaptic bulb/knob there are small vesicles, each about 50nm diameter, containing a chemical substance, which acts as a synaptic transmitter called axodendritic, axosomatic and axoaxonic

Synaptic transmission Can be excitatory or inhibitory transmitter-receptor interaction. An excitatory receptor interaction is one that can lower the post synaptic neuronâ&#x20AC;&#x2122;s membrane potential so that a new nerve impulse can be generated across the synapse. As a result of combination of the chemical transmitter with the receptor, the post synaptic membrane is partially depolarized, i.e. there is a drop of potential across the membrane. This change from RMP level in the direction of threshold level is called EPSP. (Excitatory post-synaptic potential) Inhibitory transmitter receptor interaction : Is one that can inhibit nerve impulse generation at a synapse. The inhibitory transmitter receptor interactions make the post synaptic neuronâ&#x20AC;&#x2122;s RMP more negative. This is referred to as hyperpolarization. The alteration of the post synaptic membrane in which the resting membrane potential is made more negative is called the inhibitory post synaptic potential (IPSP).

Pre-synaptic inhibition. This occurs before a nerve impulse reaches a synapse. In this process, a synaptic end bulb of an inhibitory neuron synapses with the synaptic end bulb of a presynaptic neuron at an excitatory synapse. When inhibitory neuron releases neurotransmitter it depresses the release of

excitatory transmitter by presynaptic neuron. This, in turn decreases stimulation of the post synaptic neuron. Presynaptic inhibition occurs in many sensory pathways of nervous system and provides a means by which responses of post-synaptic neuron can be regulated. 6. Neurotransmittersare chemicals secreted by the nerve terminals1. ANS-fibers (sympathetic and parasympathetic) Eg. Acetylcholine. 2. Special

neuronal

tracts

the

brain.

(E.g.:

Noradrenergic/cholinergic/

serotininergic/histamineragic/GABAergic fibers) 3. Somatic Fibres (e.g. neuromuscular junction) 4. ENS (Enteric nervous fibres) and so on. 7. The sensory System: The sensory system brings information from the periphery to the CNS. The CNS requires a continual flow of information to maintain homeostasis and initiate appropriate responses to changes in the internal and external environments. Our ability to sense stimuli is vital to our survival. Conventionally the sensory system is divided into 1. General Senses 2. Special senses.

8. The Receptors: A receptor or sense organ may be viewed as a specialized nervous tissue that is extremely sensitive to certain type of changes in internal or external conditions. From the

receptors emerge, the afferent sensory nerve which eventually reaches the CNS. Thus receptor is the first structure in the sensory path. Receptors are also called as End organ. Classification: Types 1. Receptors of special senses- e.g. eye – rods and cones. 2. Receptors of somatic and visceral. 1. Touch , pressure - (i) Merkel’s disc (ii) Meissners corpuscle (iii) Pacinian corpuscle (iv) Ruffini end organ (v) Hair end organ (vi) Free nerve ending. 2. Pain- Free nerve ending 3. Cold-cold receptors. 4. Heat-free nerve ending 5. Proprioception and kinesthesia- muscle spindles; cristae and maculae of vestibular apparatus. 6. Interoception(a) Chemoreceptor (i) Carotid body chemoreceptor - blood O2 / CO2 tension, pH.

(ii) Central

chemoreceptor- detection CO2 (Brain Stem). (b) Baroreceptors: 1) Carotid Sinus (Blood Pressures) 2) Afferent arteriole of renal artery. 3) Left Ventricular mechanoreceptors. 4) Receptors of Hering Breuer reflex. 3. Can be classified as: (i) Mechanoreceptors (ii) Thermoreceptors (iii) Pain receptors (iv) Chemo receptors. IV. PAIN Pain is indispensable for normal life. It provides us with information about tissue damaging (noxious) stimuli and helps us to protect ourselves from greater damage. 1. Receptors for pain – Are called nociceptors, are simply free nerve endings, the branching ends of the dendrites of certain neurons. They are found in practically every tissue of the body. Other cutaneous receptors for touch, pressure, heat and cold when stimulated excessively may cause pain. 2. Stimulus for pain-

Stimulus may be Physical or chemical nature. Physical stimuli- pain is produced in the skin by many kinds of physical stimuli, thermal, mechanical and electrical stimuli; Chemical stimuli- it is possible that physical pain stimuli act via chemical mediators. The physical injury causes the release of certain chemical factors which are responsible for the lasting pain and hyperalgesia. Nature of chemical factors which produce pain : Many substances can arouse pain when applied to skin or mucous membrane or when infected into the body. They can be extrinsic alogenic substances or Intrinsic alogenic Substances. Extrinsic alogenic substances include strong irritants such as acids and alkalies, organic solvents, war gases and liquids which penetrate skin and mucous membrane. Also included are plant and animal stings and venoms. Intrinsic alogenic substances are the substances derived from living body, cells and fluids. It has been shown that many substances normally present inside body cells can cause pain when released into extracellular fluid. E.g. when blood platelets disintegrate they release 5HT (Serotonin) which produces pain. Erythrocytes have high k+ and ATP, which can evoke marked pain when the cell is lysed. Leucocytes have high cationic protein in their lysosomes, which produce pain. Mast cells contain histamine which in high concentration produces pain. Other substances include- acetylcholine. Plasma kinins: The plasma and ECF contains a protein system from which very active pain producing plasma kinins can be formed e.g. Bradykinin which is a nanopeptide and kallidin which is a decapeptide. They have actions like - cause vasodilatation, increase vascular permeability and pain. Pain produced by Bradykinin is enhanced by 5.HT. Studies have revealed that bradykinin is a physiological mediator of pain and patient receptors are selectively localized, to thin C unmyelinated ‘C’ fibers, along with other several sites. It is interesting to note that Myelinated Aδ fibers, showed no response to application of bradykinin. Allen M Lepinski et al in a in vivo study have found detected level of bradykinin in pulp tissue diagnosed with irreversible pulpitis when the patient had reported pain in the past, compared with patients who were in pain just before their visit to to endodontist. Harold Goodies et al in have developed the use of reverse phase , high performance liquid chromatography (HPLC) to identify and quantify bradykinin , substance p, and neurokinin A contained in dental pulp (Journal of Endodontics 1997; 23(4):210-204) Prostaglandin’s (PG’s)

Are capable of producing pain when present in high concentration (e.g.: 10µmol l -1) but lower concentration produce hyperalgesia. PG’s are formed from arachidonic acid, and since antiinflammatory drugs such as aspirin inhibit PG synthesis which may account for relief of pain. PG’s cause degranulation of mast cells which in turn release Histamine. The histamine then function as a chemotactic factor to which eosinophils respond. Eosinophils granules, contain eosinophilic cation protein (ECP) that has a great neurotoxic potential and is capable of damaging sensing nerve endings resulting in discharge of neuropeptides such as substance P and calcitonin gene related peptide.

3. Characteristics of Pain 1. Threshold and intensity If the intensity of stimulus is below the threshold (subthreshold), pain is not felt. As the intensity increases more and more pain is felt. 2. Adaptation Pain receptors show no adaptation and so the pain continues as long as the receptors continue to be stimulated. This non-adapting nature of pain receptors keep the person apprised of a damaging stimulus. 3. Localization of pain Pain sensation is some what poorly localized. Pain is accurately localized in skin, but accuracy is lost as the source of pain sinks deeper into body. It may be said that pain is primarily localized to the segment corresponding to the stimulated nerves, and that accuracy of localization is superimposed on this segmental pattern. True visceral and deep somatic pain is sometimes felt at the site of primary stimulation and may or may not be associated wish pain, which is referred. 4. Emotional accompaniment Pain is commonly accompanied by emotions. These emotions are unpleasant. 5. Influence of rate of damage on intensity of pain. If the rate of tissue injury is high, intensity of pain also is high and vice versa. 6. Two types of pain Can be

(i) Fast Pain (ii) Slow Pain

After receiving a nociceptive stimulus, either Aδ or C type fiber or both may be stimulated. Adelta fibers are somewhat thick and finely myelinated with a faster rate of conduction, but C fibers are very thin and non-myelinated with a much slower rate of conduction. C type of fibers however outnumber A-delta fibers. Usually the pain due to C fibres stimulation is particularly unpleasant and outlasts the period of stimulation.

Fast pain is also described by many alternative names, such as sharp pain, pricking pain, acute pain and it is not felt in most of deeper tissues of body. Slow pain goes by multiple additional names burning pain, aching pain, throbbing pain nauseous pain and chronic pain. It can occur both in skin and in almost any deep tissue or organ. 4. Reactions of pain 1. Behavioral Crying, moaning screaming, rage, pain, frustration, mental irritation and depression can develop. 2. Muscular: Spasm of the skeletal muscles in the affected region develops. E.g. spasm of muscles around a fractured bone. 3. Changes in autonomic nervous system. Somatic pain is accompanied usually by signs of sympathetic overactivity. E.g.: rise in BP, tachycardia, pupillary dilatation. Conversely in visceral pain there is fall in BP, nauseating feeling, syncope. 4. Reflex response 5. Pain Pathway Fields divided the processing of pain from stimulation of primary afferent nociceptors to the subjective experience of pain in 4 steps : a. Transduction b. Transmission c.

Modulation and

d. Perception 1.Transduction: is the activation of the primary afferent nociceptor. Primary afferent nociceptors can be activated by various stimuli both intrinsic and extrinsic. Primary afferent nociceptors can be activated by intense thermal and mechanical stimuli, noxious chemicals and noxious cold. They are also activated by stimulation from endogenous algesic chemical substances (inflammatory mediators) produced by body in response to tissue injury. Damaged tissue or blood cells releases the polypeptide bradykinin, K +, histamine, serotonin and arachidonic acid. Arachidonic acid is processed by two different enzyme systems to produce prostaglandins and leukotrienes, which along with bradykinin, act as inflammatory mediators. The presence of such an ongoing inflammatory state courses physiologic sensitization of the primary afferent nociceptors. Sensitized nociceptors displays ongoing discharge, a lowered activation threshold to normally non painful stimuli and an exaggerated response to noxious stimuli. (Primary Hyperalgesia).

In addition to sending nociceptive impulses to synapse in dorsal horn of spinal cord, activation of cutaneous C fibers cause their cell bodies to synthesis the neuropeptides, substance P and calcitonin gene related peptide (CGRP). These neuropeptides are then antidromically transported along axon branches to periphery, where they induce further plasma extravasation and increase inflammation (produce flare) around injury site, referred to as neurogenic inflammation or axon reflex 2. Transmission Refers to the process by which peripheral nociceptive information is relayed to the central nervous system. The primary afferent nociceptors synapses with a second order pain transmitting neuron in the dorsal horn of the spinal cord where a new action potential heads towards higher brain structures. Dual pain pathways in spinal cord and brain stem On entering the spinal cord, the pain signals take two different pathways to brain, through the Neospinothalamic tract and the Paleospinothalamic tract.

The Neospinothalamic tract for fast pain The â&#x20AC;&#x2DC;fastâ&#x20AC;&#x2122; type AÎ´ pain fibers transmit mainly the mechanical and thermal pain. They terminate mainly in lamina I of dorsal horns, and there excite the second order neurons of the Neospinothalamic tract. These give rise to long fibers that cr side of the cord through the anterior commissure and then pass upwards to brain in the anterolateral columns. A few fibers of the Neospinothalamic tract terminate in the reticular area of brain stem, but most pass all the way to thalamus, terminating in the ventrobasal complex, along with cross immediately to the opposite dorsal column medial lemniscus tract. From these areas of the signals are transmitted to other basal areas of brain and to the somatic sensory cortex.

The Paleospinothalamic pathway for transmitting slow chronic pain. Transmits pain mainly carried in the peripheral slow suffering type C pain fibers. The C-fibers terminate almost entirely in the laminas II and III of dorsal horns, which together is called substantia gelationsa, the lateral most dorsal root fiber. Most of the signals then pass through one or more additional short fiber

neurons within dorsal horns themselves before

entering mainly lamina V, also in dorsal horn. Here the last neuron in the series give rise to long axons, that mostly join the fibers from the fast pathway, passing through the anterior commissure to opposite side of the cord, then upwards to brain in same anterolateral pathway. Termination: only one-tenth to one forth of the fibers pass all the way to thalamus. Instead they terminate principally in one of three different areas: 1. Reticular nuclei of medulla, pons and mesencephalon. 2. Tectal area of mesencephalon 3. Periacqueductal gray region surrounding the aqueduct of sylvius. These lower regions of brain appear to be very important in the appreciation of suffering type of pain.

From the reticular area of the brain stems, multiple short â&#x20AC;&#x201C; fiber neurons relay the pain signals upwards into the intralaminar nuclei of the thalamus and also into certain portions of hypothalamus. The neurotransmitters The sensory fibers (AÎ´ & C) transmit information by releasing excitatory amino acids, such as glutamate or neuropeptides (e.g.: substance P or Calcitonin gene related peptide (CGRP) Substance P is the probable neurotransmitter of type C nerve endings. It is slow to build up at synapse and also slow to be destroyed. After the pain is over, the substance P probably persists for many more seconds or perhaps minutes. This may explain at least partially the persistence of slow type of pain even after the painful stimuli is removed. (Note: In animal studies the administration of receptor antagonists to glutamate (in particular) and antagonists to substance P and CGRP (to lesser extent) has been shown to block hyperalgesia.) Evidence gathered in animal studies strongly implicates antagonists to the glutamate Nmethyl D-aspartate (NMDA) receptor as being effective in reducing hyperalgesia. These compounds are likely to serve as prototype for future classes of analgesic drugs. 3. Modulation:

Refers to mechanisms by which the transmission of noxious information to the brain is reduced. The endogenous pain inhibiting system consists of 3 major components and other accessory components. 1. The Periacqueductal gray area of the mesencephalon and upper pons surrounding the aqueduct of sylvius. Neurons from this area send signals to , 2. The Raphe magnus nucleus, a thin midline nucleus located in the lower pons and upper medulla. From here signals are transmitted down the dorsolateral columns in the spinal cord. 3. A pain-inhibiting complex located in the dorsal horns of the spinal cord. At this point the analgesia signals can block the pain before it is relayed on to the brain. Several different transmitter substances are involved in pain inhibition system, especially Enkephalin and serotonin. Many nerve fibers derived from both periventricular nuclei and the PAG area secrete Enkephalin at their endings. The endings of fibers of raphe magnus nucleus terminate in dorsal horns of the spinal cord, secrete serotonin at their endings. The serotonin in turn acts on still another set of local cord neurons that are believed to secrete enkephalin. Enkephalin is believed to cause presynaptic inhibition of both incoming type C and type Aδ pain fibers, where they synapse in dorsal horns. Thus, the pain inhibiting system can block pain signals at the initial entry point of the spinal cord. An endogenous opioid system for pain modulation also exists. Endogenous opioid peptides are naturally occurring pain dampening neurotransmitters and neuron modulators that are implicated in pain suppression and modulation e.g.: β-endorphin, met-enkephalin, leu-enkephalin and dynorphin. They reduce nociceptive transmission by preventing the release of excitatory neurotransmitter substance P from primary afferent nerve terminal. There are receptors called opiod receptors in brain (e.g. PAG) and SGR. These receptors are of 4 kinds i.e., K, μ,δ, σ, which can combine with endogenous opiod peptides, exogenous opiod alkaloids (morphine) and also with antagonists of opium. 4. Perception: the final step in the subjective experience of pain is perception. When nociceptive impulse reaches the cortex, perception occurs. It is at this point that suffering may occur. Suffering refers to the manner in which the patient responds to pain. How and where the brain perceives pain is still under investigation. Part of the difficulty lies in fact that pain experience has at least two components: (i)

The sensory discriminatory dimension

(ii)

The affective (emotional) dimension.

The effective dimension of pain is made up of feelings of unpleasantness and emotions associated with future implications related to pain. Although magnetic resonance imaging (MRI) studies have demonstrated the involvement of thalamus and multiple cortical areas in perception of pain, it is clear form the intersubject variability in the activation of any one of these areas that affective reactions and possibly motor responses are also involved. Of significance is the fact that with high level of modulation, or with damage in the pain transmission system. It is possible to have nociception without pain perception. Conversely, with certain types of damage to the nervous system, there may be an overreaction to pain stimuli or pain stimuli or pain perception without nociception.

6. Referred pain: Pain arising from deep tissue muscles ligaments, joints and viscera is often perceived at a site distant from the actual nociceptive source. This pain is called Referred pain. Mechanism of referred pain: Two most popular theories to explain referred pain are (i)

Convergence-projection theory

(ii)

Convergence- facilitation theory.

(i) Convergence-projection theory: Primary afferent nociception from both visceral and cutaneous neurons often converge onto the same second order pain transmission neuron in the spinal cord. The brain, having more awareness of cutaneous than visceral structures through the past experience, interprets the pain as coming from the regions sub served by the cutaneous afferent fibers.

(ii) Convergence- facilitation theory: This theory is similar to convergence-projection, except that the nociceptive input from the deeper structures causes the resting activity of second order pain transmission neuron in

spinal cord to increase or be “facilitated”. The resting activity is normally created by impulses from the cutaneous afferents. “Facilitation” from the deeper nociceptive impulses causes the pain to be perceived in the area that creates the normal resting background. 7. Visceral Pain: A viscous is insensitive to most sensory stimuli. However, pain sensation can, under some conditions arise from viscera. Characteristics: i)

As a rule, the visceral pain is ‘referred’

ii)

Often accompanied by vomiting and fall in BP

iii)

Drugs required to alleviate visceral pain are often sharply different from those required to alleviate the somatic pain.

iv)

Pain of a hollow viscus is often felt as colic, that is, it comes and goes to reappear again.

Causes: E.g. a. Ischemia e.g. Cardiac pain. b. Obstruction of hollow viscera – e.g. obstruction of segment of large intestine. c.

Inflammation- inflamed appendix.

d. Overdistension of hollow viscus. e. Severe vasodilatation- e.g. headache due to meaningful vasodilatation. Phantom limb pain: A kind of pain frequently experienced by patients who have had a limb amputated is called ‘phantom limb pain’. They still experience sensations such as itching, pressure, tingling or pain in extremity as if limb were still there. This probably occurs because the remaining proximal portions of sensory nerves that previously received impulse from limb are being stimulated by the trauma of amputation and brain interprets these stimuli from cut nerves, as if coming from non existing limb. 8. Trigeminal System: The primary afferent nociceptors from the maxillary and mandibular, branches of trigeminal nerve synapse in the nucleus caudalis of brain stem (at level of pons). The nucleus caudalis is the caudal portion of the trigeminal spinal tract nucleus and corresponds to the substantia gelatinosa of the rest of spinal dorsal horn. (Nucleus caudalis is the sensory nucleus of Trigeminal nerve)

From here the nociceptive input is transmitted to the higher centers via trigeminal lemniscus, to Postero-ventral nucleus of the thalamus & via connecting neurons to contralateral side of cortex of brain. Of significance is the arrangement of trigeminal nerve fibers within this nucleus and the fact that the nucleus descends as low as the 3-& 4 cervical vertebral (C-3, 4) in the spiral Cord. Fibers from all three trigeminal branches are found at all levels of nucleus caudalis arranged with the mandibular division highest & ophthalmic division lowest. In addition, they are arranged in such a manner that fibers closest to midline of face synapse in most cephalad portion of the tract. The more lateral the origin of fibres of face, the more caudal the synapse in the nucleus. Understanding this laminated arrangement helps to explain why a maxillary molar toothache may be perceived as pain in mandibular molar on same side (Referred) but not in an incisor.

Because the trigeminal nucleus descends to C3-4 level in spinal cord, primary afferent nociceptors from deep cervical structures synapse on same second order pain transmission neurons that subserve the fifth cranial nerve, this serves as a basis for understanding why cervical pain disorder may be perceived as pain in head & face, particularly in forehead & temple. 9. Theories of pain The precise mechanism for transmission of pain and the afferent efferent pathway itself are not completely understood and therefore subject to postulation. Two old but popular and one recent theory will be discussed 1. The specificity theory Advanced by von Frey in 1894, states that different sensory fibers mediates different sensory modalities such as pain, heat, cold touch & pressure. The receptors for pain are specific and mostly unmyelinated free nerve endings. When stimulated, these fibers transmit impulses along specific pathways. 2. The pattern theory In 1894 Goldscheider was the first to propose that stimulus intensity and central summation are the critical determinants of pain.

The theory proposes that pain is

generated by nonspecific receptors. It is assumed that all nerve fiber endings are alike and that the pattern for pain is produced by a more intense stimulation than for the other sensations.

The summation of the pain impulses produce a pattern that the brain

receives & recognizes.

3. Gate control theory The specific & pattern theories have been challenged by evidence from Melzack & Wall (1965) who introduced the Gate control theory of pain transmission. The actual mechanism is subject of controversy 1) Axons of large diameter afferent neurons (Aα, Aβ, Aγ) enter the Spinal Cord through dorsal root. The Principal branch of large- diameter axon enter dorsal horn, synapsing with T-cell (called Transmission cells, located adjacent to substantia gelatinosa). A collateral of some fiber enter the SG and another ascend to higher center. 2) Similarly Axon of small-diameter afferent neurons (C and Aδ) also enters the dorsal horn of spinal cord to synapse with T-cells. They also send collateral to SG. 3) The SG cells send branches to synapse with incoming axon (afferent) fiber entering T cell pool. Branches from SG cells do not contact the T cells directly but rather the terminal area of A and C axons. The only activity that can be performed by cells of SG is to send inhibition impulses to T-cell, preventing them from firing impulse.

4) Large diameter fibers can only excite the SG cells, which inturn send out inhibitory impulses to T-cells (Presynaptic inhibition). Since T cells are unable to transmit an impulse, the gate is closed to pain. 5) Messages (impulses) from the branches of smaller Aδ and C fibres can only inhibit the SG cells, stopping them from sending inhibitory impulses to T cells. This action opens the gate to pain. Since T cells are not receiving inhibitory impulses from SG cells, they are free to send a painful response when activated by the smaller when activated by the smaller C and Aδ fibers. Thus the small fibers Aδ and C fibers, open the gate to pain by inhibiting SG Cells; larger Aα, Aβ, Aγ fibers close the gate by exciting the SG cells. It is postulated that the gate control mechanism may be further modulated by intrinsic brain mechanism (Periacqueductal gray, reticular formation, thalamus) and through emotional, motivated, peripheral, psychic, and visual stimuli. Final response will depend on the balance or net result of the initial input from all three system; large diameter fibers, small diameter fibers and central control.

V .Management of Dental Pain Introduction Orofacial pain is the presenting symptom of a broad spectrum of diseases. As a symptom, it may be due to disease of Orofacial structures including teeth, generalized musculoskeletal or rheumatic disease, peripheral or central nervous system disease, or psychological abnormality; or the pain may be referred from other sources. (E.g.: Cervical muscles or intracranial pathologies). From a diagnostic perspective, the presence of absence of pain and its characteristics provides significant and reliable diagnostic information. From a practical perspective, most patients gauge the compliance of their dentist by how well the pain of dental procedures is controlled and how effectively conditions that cause pain are treated. Therefore pain is central diagnostic and therapeutic issue in the practice of dentistry. Definition of Pain The international Association of study of pain (IASP) defined pain as “An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. Classification of orofacial pain I.

Somatic pain

Results from noxious stimulation of normal neural structures that innervate the body tissues. 1. superficial – E.g. : Cutaneous and mucogingival pain 2. Deep – visceral pain –E.g.: Pulpal dental pain Muculoskeletal – e.g. : TMJ pain, Muscle pain

II.

Neurogenic pain Is generated within the nervous system and is caused by an abnormality of the neural structure that innervates the body tissue. A – Paroxysysmal Pain E.g.: Idiopathic Neuralgia Symptomatic neuralgia B- Differentiation Pain – Results from interference with the transmission of afferent impulses by primary sensory neurons. E.g.: - traumatic neuroma, Post traumatic pain.

III.

Psychogenic Pain Has diffuse and vague distribution, no apparent cause or physical evidence of inflammation. E.g.: Chronic face pain Chronic structural pain Psychogenic pain Conversion hysteria Psychohoic hallucinations

Examination and assessment of patient with Oro-facial pain An accurate diagnosis of pain and effective treatment require an understanding of the patient’s subjective perception of the discomfort. A systemic approach for collecting diagnostic information is needed to minimized risk of missing critical information. History, physical examination and behavior assessment serve as the basis for diagnosis. History Evaluation of pain must intend all the standard component of a medical interview. Chief complaint, history of presenting illness past medical history, medications, review of system and family and social history. History of presenting illness HOPI should include a detailed description of pain and its location. Pain characteristics -

intensity

quality

location

onset

associated events at onset

duration and timing of pain

course of symptoms since onset

activities or experiences that increase pain or decrease pain

Associated symptoms (E.g.: altered sensation, swelling)

Previous treatment and their effects.

A Visual Analog Scale (VAS) or numeric scale can be used to assess intensity and a questionnaire such as the MPQ (McGill pain questionnaire) can capture the multidimensional experience of pain. Details of previous injuries, surgeries and radiation therapy should be obtained. Visual analog scale A visual analog scale is a line that represents a continuous of a particular experience such as pain. The most common form used pain is a 10 cm line, whether horizontal or vertical, with perpendicular stops at the ends. The ends are anchored by “No pain”and “Worst pain imaginable”. Patients are asked to place a slash mark somewhere along the line to indicate intensity of their current pain complaints. No pain ________________________________________ Worst pain imaginable

McGill pain questionnaire (MPQ) MPQ is a verbal pain scale that uses a vast array of words commonly used to describe a pain experience.Patients use different words to describe the affective component of their pain. To facilitate the use of these words in a systemic way. Melzack and Torgerson set about categorizing many of these verbal descriptors into classes and subclasses designed to describe these different aspects of the pain experience. The words are listed in 20 different categories. They are arranged in order of imagined from least intense to most intense and are grouped according to distinctly different qualities of pain. Patients are asked to circle only one word in each category that applies to them. The first 10 categories represent different sensory descriptors. The next five categories are effective or emotional descriptors, category 16 is evaluative, (i.e. intensity) and last four categories are grouped as miscellaneous. Changes in a patient’s pain experience can be monitored by administering the questionnaire at various time points during treatment and follow-up. Sample of McGill pain questionnaire

Past medical history and review of systems Helps to provide an insight into the general health of the patient and may provide clues regarding the present pain complaint. Patients use of medication should be recorded. Pain may be a presenting feature or an ongoing complaint in systemic disease. The diagnostician should ask supplemental questions in the following areas of concern. 1. Current medical conditions. 2. History of significant illness or serious injury 3. Prior hospitalization 4. Emotional and psychological history 5. Current medications 6. Habit (E.g.: alcohols , tobacco, drugs) 7. Any other noticeable sings or symptoms that may indicate an undiagnosed health problems. Dental history -Is most important aspect of diagnosis. Specific information regarding the age of previous dental work, as well as symptoms before and after the work was done, should be sought from the patient. Family, social and occupational history

Traumatic events or emotional distress prior to the onset of pain, a history of other close family members with chronic illness or pain, and any change in work should be explored because these can be significant stressors. Clinical examination Extra oral -

All patients should be examined for abnormal asymmetries, swelling, change in skin color, draining sinus tracts, or signs of trauma.

Extra oral examination includes visual examination and digital palpation of the face, lips and neck.

Extra oral swellings may indicate serious spreading of intraoral disease process.

Painful and enlarged lymph nodes are of particular importance, because they indicate spread of infection and the possibility of malignant disease.

The extent and manner of jaw opening can provide information regarding spread of infection and possible myofascial pain dysfunction. Intraoral examination - includes a visual inspection of hard and soft tissues of the oral cavity. An intraoral examination of oro-pharynx, cheeks alveolar mucosa, gingival, hard and soft plate, tongue and floor of mouth to identity possible areas of information, abrasion ulceration, neoplasm, or other abnormality To prevent missing any subtle lesions, soft tissues and teeth of the area to be examined should be made free of saliva. Dental examination - has two components 1. Physical inspection 2. Diagnostic tests Physical inspection -

Should include observation of periodontal health tissue color and tissue texture.

Any restorations, caries, tooth discoloration, erosion, fractures, swelling and sinus tract should be noted.

Any sings of periodontal disease must be considered in the differential diagnosis. Diagnosis tests: Enable the practitioner to: i.

Define the pain by evoking reproducible symptoms that, characterize the chief complaint.

ii.

Compare normal responses to abnormal responses which may be indicative of pathosis.

Diagnostic tests include the pulpal sensitivity tests- hot and cold thermal testing, as well as electric pulp testing.

Mechanical tests include the tooth percussion and tissue palpation. Transillumination and magnification, test cavity preparation and anesthetic tests are additional means of confirming a diagnosis Radiographic examination Radiographic view will contribute to the location and identification of patient problem. Changes in pulp chambers compared, often constitute a records of past pulpal insults, caries, secondary dentin under restorations, very large or narrow pulp chamber compared with adjacent teeth, deep bases, calcification and condensing osteitis can all indicate chronic inflammatory changes in the pulpal tissue. Periapical films, bitewing and other supplemental films like panorex may be used for radiographic examination. Determining the diagnosis The final phase of the diagnostic sequence require a systematic analysis of all pertinent data accumulated from the patients history as well as clinical, dental and radiographic evaluations. The first consideration when determining a diagnosis is whether the patient chief complaint is reproducible. Unless the symptoms can be duplicated, a diagnosis should not be made. Pulpal pain can be caused by caries, fractures, trauma and recent restorative treatment and less obvious cause such as developmental anomalies or orthodontic tooth moment. When a correct diagnosis has been made the cause of pain must be clearly understood; the diagnosis must be consistent with etiology. Treatment of pain Pain is the source of most chief complaints, which implies the expectation of expedient treatment and relief. Pain management can be approached in several different ways. -

Curative or definitive treatment â&#x20AC;&#x201C; provides relief by eliminating the cause. It is considered the optimal approach if a definitive diagnosis of the problems can be made and an effective treatment for the condition is available.

Palliative treatment â&#x20AC;&#x201C; Alleviate pain and other distressing symptoms without curing the condition. It is the appropriate approach to provide relief when no curative treatment is available for the condition. It is also useful in conjugation with curative treatment to provide relief until curative treatment eliminates the pain.

Symptomatic treatment â&#x20AC;&#x201C; Attempts to eliminate symptoms as they develop without specified consideration of their origin. It is an unsuitable approach , because , control of pain may allow the progression of potentially harmful undiagnosed diseases.

Most complaints directed to the dentist are related to somatic pain of inflammatory origin, which is usually controlled by curative dental procedures.

Somatic pain of Pulpal origin Toothache or odontalagia results in most instances from inflammatory stimulation of neural fibers of either the dental pulp or supportive alveolar tissues. Pulp pain or pulpalgia is by far the most commonly experienced pain in and near the oral cavity and may be classified according to degree of severity and the pathologic process present. 1. Hyperreactive pulpalgia a) Dentinal Hypersensitivity b) Hyperemia 2. Acute pulpalgia a) Incipient b) Moderate c) Advanced 3. Chronic pulpalgia 4. Hyperplasic pulpitis 5. Necrotic pulp 6. Internal resorption 7. Traumatic occlusion 8. Incomplete fracture 1) Hyperreactive pulpalgia : Characterized by short, sharp, shock that is “pain” best described as a sensation of sudden shock. The sensation is as sharp as it is sudden and elicited by some exciting factor. It is never spontaneous. Pain is of short duration, lasting only slightly longer than the time during which the irritating element is in contact with the tooth. Hyperreactive pulpalgia can be divided into: -

Hypersensitivity and

Hyperemia.

Treatment Best treatment for hypersensitivity or hyperemia is prevention. Application of the resin adhesive or placement of an insulting base under metallic restorations will materially reduce most hypersensitivity. Recent methods: -

Physical methods- are remineralization of the dentinal tubuli from the “ calcium-phosphate protein complex” in saliva and/or from the formation of irritation dentin from the pulp

Chemical/mechanical obstruction: Use of materials like calcium hydroxide, formalin and silver nitrate. Agents that have

proved successful are potassium oxalate, strontium chloride, sodium and stannous fluoride and resins. Another approach, using potassium nitrate, blocks sensory nerve activity at the Pulpal ends of the tubules by altering the excitability of the nerves

2) Acute pulpalgia True pulpalgia begins with the development of pulp inflammation or pulpitis. It may be due to increased intrapulp tissue pressure. Treatment: In incipient cases of acute pulpalgia, removal of caries, followed by calcium hydroxide application and sedative cement for few days. For moderate cases, pulpectomy and Endodontic treatment may be required if the tooth can and should be saved, or extraction for hopeless tooth. 3) Chronic pulpalgia Pain is of long standing nature. Pain is quite diffuse, and the patient may hasve difficulty in locating the source. Chronic pulpalagia is likely to cause referred pain. Treatment: Pulp extirpation and endodontic therapy may be required. 4) Hyperplasic pulpitis (pulp polyp) The exposed tissue of hyperplasic pulp is practically free of symptoms unless stimulated directly. Differential diagnosis is concerned with only one problem, namely that of discerning whether the polyp is gingival or pulpal origin. Treatment: For tooth with hyperplasic pulpitis, if possible root canal should be carried out, or if the prognosis is poor, extraction is indicated. 5) Necrotic pulp There are no true symptoms of complete pulp necrosis, sine the pulp with its sensory nerves, is totally destroyed. Often, however, if only partial necrosis has occurred, and the patient has some vague, mild discomfort, as in chronic pulpalgia. Treatment: Endodontic therapy. 6) Internal resorption - is an insidious process when the afflicted pulp is completely free of symptoms. On the other hand, this condition has been known to mimic moderate acute pulpalgia in pain intensity. Treatment: Pulpectomy is the only treatment for resorption followed by Obturation with thermplasticized guttta percha. 7) Traumatic occlusion A tooth traumatized by bruxism or because of a restoration is in Hyperocclusion often responds much like the tooth with mild pulpalgia. Treatment:

Involves relieving the point of occlusal trauma by judicious grinding to reshape the involved tooth and its opponent. 8) Incomplete fracture or split tooth The symptoms range from those of a constant unexplained hypersensitive pulp to constant unexplained toothache. The most frequent complaint is that of a tooth painful to bite on, with an occasional mild ache. Treatment: If Incomplete fracture is suspected, but the pulp is not involved, full crown should be prepared. If an incomplete fracture has entered the pulp , then root canal treatment should be done first, followed by full coverage to prevent a total fracture. Somatic pain from dental supporting tissue : Periradicular pain â&#x20AC;&#x201C; may be almost as excruciating as pulp pain and often continue for longer period of time. 1) Symptomatic apical periodontitis: This acute form of periradicular pain can be most excruciating and sometimes lasts for days. The tooth is painful to touch, and even contacting the tooth in closure may bring a flood of tears. The pain has been described as constant, gnawing, throbbing and pounding. There is no overt swelling involved, just grossly painful tooth elevated in its socket. Treatment: -

To relive pain, an immediate injection of a long lasting local anesthetic should be given (Bupivacaine with epinephrine)

Occlusal corrections should be done to free the tooth completely from contact in closure in any excursion

Typically, symptomatic apical periodontitis follows initial Endodontic treatment

A rubber dam is placed, and temporary filling removed carefully,

Using paper points, the chamber and canal should be cleared of any liquid contents

Hydrocortisone,

combined

with

neomycin,

recommended

anti-

inflammatory/antibacterial medicament -

The canal is flooded with liquid suspension and then the fluid is teased out with a sterile file

A loose cotton pellet is then placed in chamber and a thin temporary filling placed without undue pressure

The patient should also be carried on systemic antibiotics and on anti-inflammatory drugs.

2) Acute apical abscess The pain of acute apical abscess, is similar to acute apical periodontitis, but somewhat lower in intensity. Treatment:

Drainage is established through the root canal , if abscess is in its

initial stage, or

by incision if abscess is fluctuant -

trephination may also be performed to establish drainage and relieve pressure

occlusion is relieved and a regimen of systemic antibiotics and either hot or cold rinses prescribed depending on the stage of development of abscess

Mild analgesics such as acetaminophen for pain or opiods or steroids if pain is severe.

Endodontic therapy or extraction, is completed after the acute symptoms have subsided. 3) Chronic apical periodontitis Is seldom painful and its management usually involves endodontic therapy for affected teeth. 4) Chronic apical abscess Is generally free of symptoms. There may be stages in the lonfg history of such lesion, when a draining fistula closes and mild swelling and discomfort ensue. Treatment: If the involved tooth can be saved, it may be retained by endodontic therapy. Periradicular surgery is sometimes indicated for these pathologic lesions. Pain disorders that mimic odontalagia Pain problems mimicking dental problems can be separated into two major categories: a) Typical pain disorders- those in which pathogenesis are known. b) Atypical pain disorders- have no established etiopathogenesis. Typical pain disorders 1) Neuralgias:

i) Trigeminal neuralgia ( Tic Douloureux) : Facial pain disorder with specific clinical features. The pain involves one or more of trigeminal nerve divisions. Precise cause unknown, empiric evidence suggests that the symptoms evolve as a consequence of vascular compression of gasserian ganglion. The character and duration of symptoms are unique, and a specific anatomic trigger point can be identified. Pain is severe and lancinating, shooting into bone and teeth. Treatment modalities are varied and include medical intervention and various surgical interventions.

Carbamazepine, the standard medical therapy for trigeminal neuralgia, is quite effective. Surgical modalities available are peripheral neurotomy, rhizotomy, alcohol injections, glycerol injections, cryotherapy, radiofrequency lesioning and laser therapy. Most widely accepted are the: surgical decompression and transcutaneous ganglionic neurolysis. (ii) Post-herpetic neuralgia: Primary infection with varicella zoster causes chicken pox, a disease that affects 95% of population during early childhood. In its secondary or recurrent form, the disease is refereed as herpes zoster or shingles. In the head and neck area, it is trigeminal ganglion that harbors the latent virus. The painful lesions of shingles cause a deep boring ache, involving not only the superficial mucosal and cutaneous tissue but also the maxillary and mandibular bones. Before the onset of vesicular eruption, it is common for the patient to experience prodromal pain, obscuring the diagnosis. Treatment: a variety of techniques used to manage pain, including transcutaneous electrical nerve stimulus, antiseizure drugs, analgesics and topical preparations. 2. Cluster headache (Sluders neuralgia) Cluster headaches derive their name from their temporal pattern. They tend to occur in â&#x20AC;&#x153;clusters,â&#x20AC;? a series of one to eight 20- to 180-minute attacks per day lasting for several weeks or months, followed by remissions of months or years. These headaches are found five to eight times more frequently in men than in women, particularly in men aged 20 to 50 years who smoke. The pain is a severe, unilateral, continuous, intense ache or burning that often occurs at night. Movements that increase blood flow to the head may result in throbbing. The most common sites are either around or behind the eye radiating to the forehead and temple or around and behind the eye radiating infraorbitally into the maxilla and occasionally into the teeth, rarely to the lower jaw and neck. Because of the oral symptoms, serious diagnostic errors are committed by dentists. Treatment includes: i)

vasoactive drugs- calcium channel blockers

ii)

prednisone

iii)

hyperbaric oxygen therapy

iv)

Vasoactive antimigrane drugs.

3. Otitis media The middle ear infection symptoms radiate from ear over the posterior aspects of maxilla and mandible. The definitive diagnosis is made by using an otoscope to examine the tympanic membrane.

Treatment consist of antibiotic therapy usually penicillin with p-lactase inhibitor or clindamycin. Once diagnosis is established, referral to an otolaryngologist is recommended. 4. Sinogenic pain Acute Maxillary Sinusitis : Because the roots of the maxillary teeth extend to the sinus floor, it is axiomatic that acute infectious processes involving the sinus mucous membrane will simulate dental pain. Most forms of sinusitis are allergic and are characterized by dull pain complaints in the malar region and maxillary alveolus. When maxillary sinusitis is the consequence of an acute pyogenic bacterial infection, the symptoms are usually acute. The pain may be stabbing, with severe aching pressure and throbbing. Pain is frequently referred upward, under the orbit, and downward, over the maxillary posterior teeth. (Importantly, pain is not referred to a single tooth but is perceived in all teeth in the quadrant. Percussion sensitivity of the molar teeth is a common finding, and when the head is placed below the knees, the pain is often exacerbated.) Transillumination is a diagnostic aid that is easy to perform. Because maxillary root apices are separate from the antral floor by a few millimeters of bone. Hence it is essential to assess each maxillary tooth in patient with acute maxillary sinusitis, because treatment without management of the dental source will only result in recurrence of symptoms. Antibiotic therapy and induced sinus discharge recommended. Referral to otolaryngologist is recommended. 5) Cardiac jaw pain Vascular occlusive disease is one of the most common afflictions. The accumulation of atherosclerotic plaque in coronary vessels (in association with vasospasm) will lead to angina pectoris. The most common manifestation of coronary vascular occlusion, particularly in its acute manifestation, is substernal pair with reffered pain rotating over the left shoulder and down the arm. Occasionally angina pectoris is manifested as left shoulder and arm pain without a substernal component. Even less frequent is referral of pain up the neck into the left angle of the mandible. In these instances the referred pain may mimic odontalgia. When a patient reports left posterior mandibular pain and there is no obvious odontogenic source of infection, referred cardiogenic pain should be considered. Importantly, the patient should be questioned about the onset of the symptoms. If they occur after exercise or other exertion, then coronary vascular disease should be considered. Once suspected, referral to physician is recommended. 6) Sialolithiasis

Etiology is unknown. Desquamated epithelial cells from the major salivary ducts may accumulate and form complexes with salivary mucin to form nidus for calcification. Salivary stone evolves by sequential concretion of calcium phosphate salts, much like the growth rings of a tree. Once the stone reaches a critical size, the salivary duct becomes occluded and symptoms develop. Sialolithiasis is significantly more frequent in the submandibular duct; therefore pain associated with submandibular stones is more prone to mimic endodontic pain in the posterior aspect of the mandible. The occluded duct often leads to swelling of the submandibular area. Hence it may mimic lymphadenitis associated with an endodontic infection of a posterior mandibular tooth. Treatment consists of physical attempts to remove the stone by manipulating it with out the orifice. Larger stones will require a surgical cut down to the duct. 7) Abnormal joint function (Internal derangement) Internal derangement of the TMJ is often associated with localized joint area pain complaints. Internal derangements of the TMJ include meniscus displacement, formation of intraarticular adhesions, and various forms of arthritis. The chief findings associated with internal derangement include limitation of jaw opening, deviation on opening, joint clicking or crepitus, and pain directly localized to the joint region in front of the tragus of the ear. The pain associated with internal derangement is generally a boring ache, but it may be more acute when exacerbated by wide opening of the mandible or chewing. Pain is often referred into the temple, cheek and posterior dental areas of maxilla and mandible. In such instances the patient may perceive a joint problem as a dental problem or as a temple area headache. 8) Myalgia Myalgic pain disorders involving the masticatory musculature can be perceived as dental pain. These disorders appear to be the consequence of sustained muscle contraction usually associated with jaw clenching and bruxism. Myalgic pain is constant, variable in intensity, usually dull, aching and it involves multiple muscle areas. In general most patients complain of symptoms over the mandible and temple. Palpation of masticatory muscles will often reveal the presence of localized tender areas. Treatment is by physical therapy. 9) Myofascial pain - are characterized by continuous, dull pain of variable intensity, with localized tenderness in one or more muscles. Essential to the diagnosis of myofascial pain is discovery of localized hypersensitive areas (i.e., trigger points) Trigger points found in superficial aspect of masseter muscles have consistent referral patterns to the maxillary and mandibular teeth: tooth ache is the main problem

Temporalis muscle trigger point can refer pain to maxillary posterior and anterior teeth: headache and toothache are common associated complaints. Once trigger point has been located and a Myofascial disorder diagnosed, treatment can be instituted. Most common techniques for eliminating trigger point include: i)

Physical therapy

ii)

Spray and stretch therapy

iii)

Trigger point injections.

Atypical pain disorders that mimic odontalagia: Of all the facial pain syndromes, the group that most often simulates endodontic or odontogenic pain is â&#x20AC;&#x153;atypical facial painâ&#x20AC;?. Included in this are variety of disorders including phantom tooth pain, NICO- neuralgia inducing cavitatory osteonecrosis. CRPS- complex regional pain syndrome and causalgia. Atypical facial pain represents a pain syndrome that does not conform to specific organic disease and does not represent another well defined form of pain disorder. 1. Phantom tooth pain The term phantom tooth pain is used to describe pain that persists in teeth or the area of a specific tooth after the pulp has been extirpated. Phantom tooth pain is estimated to occur in less than 3% of patients undergoing root canal therapy. It has been suggested that surgical extirpation of the pulp results in damage to nerve fibers at the apex of the teeth and should be considered a traumatic neuralgia. Another possible mechanism is formation of a small traumatic neuroma in the apical periodontium. Although psychological factors have been suggested to be important in phantom tooth pain, there is not a great deal of evidence (on the basis of psychometric testing) that psychopathologic mechanisms are major factors. However it is suggested that phantom tooth pain is a deafferentation pain. 2. NICO- neuralgia inducing cavitatory osteonecrosisNeuralgia-inducing cavitational osteonecrosis (NICO) is an atypical orofacial pain localized to edentulous foci, which can sometimes be alleviated with a subperiosteal injection of local anesthetic. In such instances it has been proposed that small residual inflammatory, foci exist within endosteum and the focal necrosis occurs with neural damage. In selected cases surgical curettage has alleviated associated pain. Tissue curetted from these cavities often shows minor pathologic changes, such as fibrosis and mild inflammation. 3. CRPS- complex regional pain syndrome

Complex regional pain refers to pain complaints that have lasted longer than the normal healing period and have increased in complexity. Depending on the cause of the pain complaint, this diagnosis could be made in .4 to 6 weeks. A variety of factors can contribute to the perpetuation of pain complaints, including a lack of healing, inappropriate therapy, missed diagnosis, increase in psychologic involvement, and secondary gain. 4. Causalgia Causalgia pain can involve the jaws, head, and neck. When present, it may be confused with odontalagia. Causalgic pain is often associated with trauma, jaw fracture, or laceration and it may evolve after surgery. It has been hypothesized that in causalgia, nociceptor fibers become retracted in association with autonomic fiber. Patients have a tendency to rub and scratch the involved area, producing what are known as trophic foci; the skin can become encrusted and keratotic. The pain is characteristically paroxysmal and burning, and it may be both superficial and deep. When the predominant complaint is a deep component, it may be confused with toothache. To arrive at a definitive diagnosis of causalgia, historical trauma events and clinical features must be identified. When symptoms of orofacial pain are mild, the pain should be managed with analgesics and reassurance. Many patients with atypical facial pain respond favorably to tricyclic antidepressants, and particularly amitriptyline. In more severe cases, the therapy used for trigeminal neuralgia may be indicted. V . Drug therapy 1.Pain management principles Treatment of mild to moderate pain should begin with non-narcotic analgesic. If these drugs along are ineffective, intermediate potency opiods such as codeine or its derivatives are combined. Treatment of acute pain is directed towards the location, origin and cause of pain. opiates are often employed, but NSAIDâ&#x20AC;&#x2122;S are also staples of acute pain therapy because they can limit pain, swelling and erythema. other agents administered for acute pain include muscle relaxants and injectable local anesthetics. For server or chromic pain, analgesic should be given at regular intervals in adequate dose analgesic adjuvant such as tricyclic antidepressant is added to the drug regimen. Other adjunct include anticonvulsant, antiarrythmics, antihistamine or phenothiazines.

2. Non opiod analgesics: Non-steroidal anti-inflammatory drugs (NSAIDS ) this group drugs are used to treat mild to moderate acute or chronic pain from trauma, surgery or inflammatory conditions. -

Acetaminophen, although not an NSAID because it lacks anti- inflammatory properties, is the most commonly non-prescription pain reliever.

NSAIDS differ from opioid analgesics in that they are antipyretics and do not induce physical or psychological dependence

NSAIDS work primarily at the site of injury by inhibiting the enzyme cyclo-oxygenase (cox), which is required for the synthesis of prostaglandins, substances that sensitize peripheral sensory nerves and contribute to experience of pain.

Patients may vary in their response to NSAIDS produce an analgesic effect after several days different NSAID

It is Inadvisable to prescribe two different NSAID at the same time, rather , one NSAID should be used and its dose and timing adjusted for maximum analgesic effect.

Combinations of NSAID increase the risk of side effects

Because of extensive side effects profiles, long term use of NSAID must be carefully weighted against the clinical response of each patient for whom they are prescribed.

The most serious adverse reactions involving the GIT , include dyspepsia at one extreme to potentially serious bleeding ulcers at the other

Other adverse events attributed to NSAIDS are kidney dysfunction or failure, dermatologic reactions such as rash, drowsiness or dizziness, excessive bleeding or bruising because of inhibition of prated activity and increased risk of an asthamatic episode

While all NSAID pose a risk of a bleeding, ibuprofen and diclofenac are considered to pose a lower risk and ketoprofen and piroxicam considered to pose a high risk.

With any NSAID the risk increase when high doses are prescribed.

NSAID are available that selectively inhibit only one of isoforms of Cox, namely Cox-2. The inhibition of Cox-2 seems to the related to the anti-inflammatory and analgesic effect, whereas the inhibition of cox-1 is thought to be responsible for many of the side effects.

The cox-2 inhibitor colecoxib and rofecoxib pose less risk of GI bleeding and do not inhibit platelet aggregation.

NSAID have a significant number of drug interactions. The most troublesome of these are exacerbation of bleeding disorders in patient taking anticoagulants such as warfarin, and antagonism of agents used in treatment of high blood pressure.

3.Opioid analgesics The largest group of opioids that are used for analgesia consist of morphine like agonists. opioids included bath natural and synthetic agents. They are unique in their ability to reduce moderate to severe pain without producing loss if consciousness. There are three classes of opiods 1. The phenanthrenes – Eg: morphine, codeine, oxycodone 2. The phenylpiperidine derivatives – Eg: Meperidine, fentanyl 3. Dipheyl heptane derivative eg: methandone and propoxyphene. -

Required doses of opioids vary according to patients prior exposure, severity of pain, hepatic or renal function, and rate of administration

Most clinically available opioids activate the µ opioid receptor. This opioid receptor is located at several important site in brain and is activation inhibits the transmission of nociceptive signals

Although opiod are effective as analgesics for moderate to server pain there use is generally limited by their adverse effects.

Opiod include numbers side effects including nausea, emesis, dizziness, drowsiness and the potential for respiratory depression and constipation. Chronic use is associated with tolerance and dependence. Analgesic doses of representative opiods Drug

Dose equivalent to codeine (60 mg)

Codeine

Oxycodeine

5-6

Hydrocodone

Proxyphene IV

146

Meperidine

Tramadol

Role of corticosteroids The cause of postoperative pain or flare-up after endodontic treatment can be attributed to inflammation or infection or both occurring in the periradicular tissue. The act of establishing patency and subsequently debriding and shaping the root canal system directly irritates the periradicular tissues and inadvertently introduces bacteria. Bacterial products, necrotic pulpal tissue, or caustic irrigating solution through apical foramen Glulocorticosteroids are known to reduce the acute inflammatory response. They inhibit the formation of arachidonic acid from neutrophil and macrophage cell membrane phospholipids: thus blocking the cycloxygenase and lipoxygenase pathways and respective synthesis of prostaglandin and leukotriens. Antidepressants Tricyclic antidepressants, which inhibit the reuptake and storage of the neurogenic amines serotonin and norepinephrine, have analgesic properties related to their ability to increase pain tolerance. The antidepressants include several classes of agents, which can be organized into three categories: tricyclic antidepressants, monoamine oxidase inhibitors, and newer heterocyclic compounds.

Clinical effects include improvement in mood and sleep, anxiety reduction, and a decreased perception of pain. The tricyclic agents are commonly employed in the management of neurogenic pain conditions. The tricyclic antidepressants are available as either tertiary or secondary amine structures; the former agents produce more frequent and more intense side effects than the latter. Monoamine oxidase inhibitors have been used infrequently for treatment of painful conditions such as migraine and are reserved for patients refractory to the tricyclic antidepressants. Most commonly employed antidepressed for painful conditions is amitriptyline in doses of 25-150 mg/day. Anticonvulsants The mechanism of action of carbamazepine and valproate is suppression spontaneous neuronal firing. Lancinating or Buffering pains are best treated these agents, and they are prescribed for trigeminal neuralgia, cranial nerve disorders, deafferentation pains (e.g., phantom tooth pain), and other neuralgic syndromes. Typical adult doses of carbamazepine are 200 to 400 mg to four times daily, and valproate is usually dosed as 250 to 750 mg two to three times daily. A sustained-release carbamazepine product that allows twice-d dosing is also available. Plasma levels should be monitored because side effect may include ataxia, diplopia, nausea, and emesis. Antiarrhythmics and Local Anesthetics Lidocaine is also given for neuropathic syndromes, and similar to all local anesthetics, enters the central and peripheral nervous systems after administration. Mexiletine has been used in lidocaine-responsive patients requiring longer-acting substitute because both agents reduce neuronal firing. Dose- 10 mg/kg/day. Adjuntive medications: Benzodiapenes such as diazepam are useful foe skeletal muscle relaxation and anxiolysis in the treatment of acute pain, and clonazepam has been used in the management of neuropathic and atypical facial pain. Antihistaminics - such as hydrazine and promethazine have been used to augment sedation and reduce itching associated with opioids administration. They may have some analgesic activity by virtue of reduction of histamine release in areas of inflammation. New developments in pain management -

N methyl-D-aspartate (NMDA) is an excitatory amino acid that was discovered to produces hyperalgesia of CNS origin. Glutamate may also play a similar role in activating pain system.

Research into NMDA receptor antagonist offer an exciting hint at the future of pharmacologic agents for pain management. Ketamine, a commercially available anesthetic is one such NMDA antagonist, but is available only parentally and produces adverse reactions such as dysphoria and hallucinations. -

Dextrorphan, the demethylated metabolite of dextromethorphan (a cough suppressant) is another agent undergoing investigation.

Calcium channel blockers used in the treatment of hypertension may also potentiate morphine analgesia by modulation of calcium availability to the cell. These drugs are devoid of any analgesic activity when given alone.

Opioid peptides such as enkephalin analogues show promise as therapeutic agents because they differ from opioids in several ways. One advantage the peptides may have over their opioid counterparts is degradation to constituent amino ands instead of active and possible toxic metabolites.

VI. Conclusion Pain is mainly a protective mechanism for the body; it occurs whenever any tissues are being damaged, and it causes the individual to react to remove the pain stimulus. This basic nervous and defense function is applicable to the dental pulp. A conscious recognition of irritants to the tooth gives the patient an opportunity to have the problem corrected before irreversible effects can occur. In evaluating pulpal and periapical pain, other disorders must be considered in the differential diagnosis. Pain management has progressed a great deal scientifically throughout the last century, in part as a result of the introduction of more effective pharmacologic agents and development of better understanding of the molecular biologic principles that govern their use.

VII. Reference 1. Guyton and Hall. Textbook of Medical physiology – 10th Edition 2. Gerald J Tortora and Nicholas P.Anagnostakos. Principles of Anatomy and Physiology- 6th Edition 3. Cyril A.Keele, Eric Neil ,and Norman Joels. Samson Wright’s Applied physiology- 13th Edition 4. Pathways of pulps – 8th edition, Stephen Cohen, Richard.C.Burns 5. Ingle and Bakland. Endodontics 5-th edition 6. Franklin S. weine - Endodontic Therapy 5th edition. 7. Local anesthesia- Monheim’s

8. Lori A Reisner-Keller. Pharmacotherapeutics in the management of Orofacial pain. Dent Clin N Am (DCNA) 1997; 41(2): 259-278 9. Greenberg and Glick. Burketâ&#x20AC;&#x2122;s Oral medicine Diagnosis and Treatment. 10 th Edition 10. Allen M Lepinski, Kenneth M .Hargreaves, Harold E. Goodies and Walter R. Bowles. Bradykinin levels in Dental pulp by microanalysis. J Endodon 2000; 26(12):744-747 11. Harold Goodies and Kuniko Saeki. Identification of Bradykinin, Substance P and Neurokinin A in Human dental pulp. J endodon 1997;23(4):201-204